amId	assignedId	sdocId	userId	editorUserId	indexActionMentionId	external_id	dbActionMentionId	entity1	semantic_class_entity1	modifier_entity1	actionType	semantic_class_actionType	modifier_actionType	protein_domain_entity1	gene_region_entity1	entity2	semantic_class_entity2	modifier_entity2	protein_domain_entity2	gene_region_entity2	topic	statement_context	negative	certainty_level	derived_certainty_level	applied_rule	indexSentenceId	pmid	sentenceText	procset
44403	2	12	6	10	NULL	0	NULL	asd	NULL		asd	NULL				asd	NULL				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_295_4_1027_s_40	12127999	"`Microsomal"` membrane prepared as described from fresh bovine lens epithelia bound progesterone and corticosterone with high affinity ( Kd 75 nM) ( Fig. 2).	bind
1040	3	12	7	10	NULL	0	NULL	testing	NULL		action test	NULL	mod action 			dfgf	NULL			fgdsg	NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_295_4_1027_s_40	12127999	"`Microsomal"` membrane prepared as described from fresh bovine lens epithelia bound progesterone and corticosterone with high affinity ( Kd 75 nM) ( Fig. 2).	bind
57771	1	201	5	NULL	NULL	0	NULL	Amph2	GP		bind			SH3		dynamin	GP				NULL		0	NULL	NULL	NULL	gw60_embo_17_18_5273_s_218	9736607	( A) Amph2 SH3 and Amph2-SH3deltaDAPS domains bind equally well to dynamin.	bind
57772	2	201	5	NULL	NULL	0	NULL	Amph2	GP		bind			SH3deltaDAPS		dynamin	GP				NULL		0	NULL	NULL	NULL	gw60_embo_17_18_5273_s_218	9736607	( A) Amph2 SH3 and Amph2-SH3deltaDAPS domains bind equally well to dynamin.	bind
1108	1	201	6	NULL	NULL	0	NULL	Amph2	GP		bind			SH3 domain		dynamin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_18_5273_s_218	9736607	( A) Amph2 SH3 and Amph2-SH3deltaDAPS domains bind equally well to dynamin.	bind
1109	2	201	6	NULL	NULL	0	NULL	Amph2	GP		bind			SH3deltaDAPS		dynamin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_18_5273_s_218	9736607	( A) Amph2 SH3 and Amph2-SH3deltaDAPS domains bind equally well to dynamin.	bind
57773	1	212	5	NULL	NULL	0	NULL	Bcl-2	GP	deletion mutant	retains			1-82		Bax	GP	binding activity of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_20_11962_s_8	7744846	( A) and an NH -terminal deletion mutant  Bcl-2( 1-82) retained Bax binding activity  in vitro  but failed to suppress Bax-mediated cytotoxicity in yeast.	bind
57774	2	212	5	NULL	NULL	0	NULL	Bax	GP		mediates					cytotoxicity	Process				NULL	yeast	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_20_11962_s_8	7744846	( A) and an NH -terminal deletion mutant  Bcl-2( 1-82) retained Bax binding activity  in vitro  but failed to suppress Bax-mediated cytotoxicity in yeast.	bind
57775	3	212	5	NULL	NULL	0	NULL	Bcl-2	GP	deletion mutant	does not suppress			1-82		statement 2	Process				NULL	yeast	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_20_11962_s_8	7744846	( A) and an NH -terminal deletion mutant  Bcl-2( 1-82) retained Bax binding activity  in vitro  but failed to suppress Bax-mediated cytotoxicity in yeast.	bind
1110	1	212	6	NULL	NULL	0	NULL	Bcl-2	GP		bind			NH -terminal deletion mutant		Bax	GP				NULL	In vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_20_11962_s_8	7744846	( A) and an NH -terminal deletion mutant  Bcl-2( 1-82) retained Bax binding activity  in vitro  but failed to suppress Bax-mediated cytotoxicity in yeast.	bind
1111	3	212	6	NULL	NULL	0	NULL	Bcl-2	GP		does not supress			NH -terminal deletion mutant		Statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_20_11962_s_8	7744846	( A) and an NH -terminal deletion mutant  Bcl-2( 1-82) retained Bax binding activity  in vitro  but failed to suppress Bax-mediated cytotoxicity in yeast.	bind
1112	2	212	6	NULL	NULL	0	NULL	Bax	GP		mediates					cytotoxicity	Process				NULL	yeast	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_20_11962_s_8	7744846	( A) and an NH -terminal deletion mutant  Bcl-2( 1-82) retained Bax binding activity  in vitro  but failed to suppress Bax-mediated cytotoxicity in yeast.	bind
57776	1	218	5	NULL	NULL	0	NULL	cephalexin	GP		bind					BcII	GP	WT			NULL		0	NULL	NULL	NULL	gw70_pnas_102_39_13761_s_140	16172409	( A) and cephalexin ( B) binding to WT BcII (filled circles) and M5 (open circles).	bind
57777	2	218	5	NULL	NULL	0	NULL	cephalexin	GP		bind					M5	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_102_39_13761_s_140	16172409	( A) and cephalexin ( B) binding to WT BcII (filled circles) and M5 (open circles).	bind
1113	1	218	6	NULL	NULL	0	NULL	cephalexin	Chemical		bind					BcII	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13761_s_140	16172409	( A) and cephalexin ( B) binding to WT BcII (filled circles) and M5 (open circles).	bind
1114	2	218	6	NULL	NULL	0	NULL	cephalexin	Chemical		bind					M5	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13761_s_140	16172409	( A) and cephalexin ( B) binding to WT BcII (filled circles) and M5 (open circles).	bind
57778	1	219	5	NULL	NULL	0	NULL	V2R-pp	GP		bind					beta-arrestin 2	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_53_55744_s_141	15501822	( A) and competitive binding of V2R-pp and V2R-np to beta-arrestin 2 ( B).	bind
57779	2	219	5	NULL	NULL	0	NULL	V2R-np	GP		bind					beta-arrestin 2	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_53_55744_s_141	15501822	( A) and competitive binding of V2R-pp and V2R-np to beta-arrestin 2 ( B).	bind
57780	3	219	5	NULL	NULL	0	NULL	statement 1	Process		competes with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_53_55744_s_141	15501822	( A) and competitive binding of V2R-pp and V2R-np to beta-arrestin 2 ( B).	bind
1115	1	219	6	NULL	NULL	0	NULL	V2R-pp	GP		bind					beta-arrestin 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_53_55744_s_141	15501822	( A) and competitive binding of V2R-pp and V2R-np to beta-arrestin 2 ( B).	bind
1116	2	219	6	NULL	NULL	0	NULL	V2R-np	GP		bind					beta-arrestin 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_53_55744_s_141	15501822	( A) and competitive binding of V2R-pp and V2R-np to beta-arrestin 2 ( B).	bind
51765	3	219	6	NULL	NULL	0	NULL	statement 1	process		compete with					statement 2	process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_53_55744_s_141	15501822	( A) and competitive binding of V2R-pp and V2R-np to beta-arrestin 2 ( B).	bind
57781	1	233	5	NULL	NULL	0	NULL	platelets	Cell		is stimulated by					thrombin	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_12_7004_s_178	8636130	( A) and irreversible ( B) binding of PAC-1  to thrombin-stimulated platelets.	bind
57782	2	233	5	NULL	NULL	0	NULL	PAC-1	GP		bind		irreversibly			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_12_7004_s_178	8636130	( A) and irreversible ( B) binding of PAC-1  to thrombin-stimulated platelets.	bind
1117	2	233	6	NULL	NULL	0	NULL	PAC-1	GP		bind		irreverrsible			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_12_7004_s_178	8636130	( A) and irreversible ( B) binding of PAC-1  to thrombin-stimulated platelets.	bind
51766	1	233	6	NULL	NULL	0	NULL	thrombin	GP		stimulate					platelets	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_12_7004_s_178	8636130	( A) and irreversible ( B) binding of PAC-1  to thrombin-stimulated platelets.	bind
57840	1	235	5	NULL	NULL	0	NULL	mAb	GP		bind					TPO	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_50_35313_s_146	10585396	( A) and mAb 47 binding to untreated TPO and TPO treated by CaCl2 (8 x 10 6M) with or without EDTA (1.6 x 10 4M) ( B).	bind
57841	2	235	5	NULL	NULL	0	NULL	TPO	GP		treated with					CaCl2	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_50_35313_s_146	10585396	( A) and mAb 47 binding to untreated TPO and TPO treated by CaCl2 (8 x 10 6M) with or without EDTA (1.6 x 10 4M) ( B).	bind
57842	3	235	5	NULL	NULL	0	NULL	mAb	GP		bind					statement 1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_50_35313_s_146	10585396	( A) and mAb 47 binding to untreated TPO and TPO treated by CaCl2 (8 x 10 6M) with or without EDTA (1.6 x 10 4M) ( B).	bind
1118	1	235	6	NULL	NULL	0	NULL	mAb 47	AminoAcid		bind					TPO	GP	untreated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_50_35313_s_146	10585396	( A) and mAb 47 binding to untreated TPO and TPO treated by CaCl2 (8 x 10 6M) with or without EDTA (1.6 x 10 4M) ( B).	bind
1119	2	235	6	NULL	NULL	0	NULL	mAb 47	AminoAcid		bind					TPO 	GP	CaCl2 treated 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_50_35313_s_146	10585396	( A) and mAb 47 binding to untreated TPO and TPO treated by CaCl2 (8 x 10 6M) with or without EDTA (1.6 x 10 4M) ( B).	bind
57783	1	237	5	NULL	NULL	0	NULL	FV	GP		bind					PS	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_49_51466_s_103	15452129	( A) and MMRN1 did not significantly inhibit FV binding to PS ( B).	bind
57784	2	237	5	NULL	NULL	0	NULL	MMRN1	GP		does not inhibit		significantly			statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_49_51466_s_103	15452129	( A) and MMRN1 did not significantly inhibit FV binding to PS ( B).	bind
1122	1	237	6	NULL	NULL	0	NULL	FV	GP		bind					PS	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51466_s_103	15452129	( A) and MMRN1 did not significantly inhibit FV binding to PS ( B).	bind
1123	2	237	6	NULL	NULL	0	NULL	MMRN1	GP		does not inhibit		significantly 			Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51466_s_103	15452129	( A) and MMRN1 did not significantly inhibit FV binding to PS ( B).	bind
57794	1	243	5	NULL	NULL	0	NULL	protein phosphatase 1	GP		bind					Yotiao	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_36_31347_s_28	16002409	( A) and protein phosphatase 1 ( 1) are shown bound to Yotiao.	bind
1124	1	243	6	NULL	NULL	0	NULL	protein phosphatase 1	GP		bind					Yotiao	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31347_s_28	16002409	( A) and protein phosphatase 1 ( 1) are shown bound to Yotiao.	bind
57795	1	248	5	10	NULL	0	NULL	SLV	CellComponent		contains					PS	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_16_11013_s_212	10196183	( A) and TGase 1 bound to SLV containing 15% PS ( B).	bind
57796	2	248	5	NULL	NULL	0	NULL	TGase 1	GP		bind					statement 1	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_16_11013_s_212	10196183	( A) and TGase 1 bound to SLV containing 15% PS ( B).	bind
1125	1	248	6	NULL	NULL	0	NULL	TGase 1	GP		bind					SLV	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_16_11013_s_212	10196183	( A) and TGase 1 bound to SLV containing 15% PS ( B).	bind
57797	1	258	5	NULL	NULL	0	NULL	AP4	GP		bind					PAHX-AP1	GP			PRE	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_35_13074_s_36	16924111	( A) AP4 binds to the PAHX-AP1 PRE, but Gem does not.	bind
57798	2	258	5	NULL	NULL	0	NULL	Gem	GP		does not bind					PAHX-AP1	GP			PRE	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_35_13074_s_36	16924111	( A) AP4 binds to the PAHX-AP1 PRE, but Gem does not.	bind
1126	1	258	6	NULL	NULL	0	NULL	AP4	GP		bind					PAHX-AP1	GP			PRE	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_35_13074_s_36	16924111	( A) AP4 binds to the PAHX-AP1 PRE, but Gem does not.	bind
1127	2	258	6	NULL	NULL	0	NULL	Gem	GP		does not bind					PAHX-AP1	GP			PRE	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_35_13074_s_36	16924111	( A) AP4 binds to the PAHX-AP1 PRE, but Gem does not.	bind
57799	1	260	5	NULL	NULL	0	NULL	Arp2/3	GP		bind					VCA domain	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_science_290_5492_801_s_73	11052943	( A) Arp2/3  binding to the VCA domain is not blocked by the GBD (residues 196-274)  or control region (178-274).	bind
57800	2	260	5	NULL	NULL	0	NULL		AminoAcid		does not block			GBD (residues 196-274)		statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_science_290_5492_801_s_73	11052943	( A) Arp2/3  binding to the VCA domain is not blocked by the GBD (residues 196-274)  or control region (178-274).	bind
57801	3	260	5	NULL	NULL	0	NULL		AminoAcid		does not block			control region (178-274)		statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_science_290_5492_801_s_73	11052943	( A) Arp2/3  binding to the VCA domain is not blocked by the GBD (residues 196-274)  or control region (178-274).	bind
1128	1	260	6	NULL	NULL	0	NULL	Arp2/3	GP		bind						AminoAcid		VCA domain		NULL		NULL	NULL	NULL	NULL	gw60_science_290_5492_801_s_73	11052943	( A) Arp2/3  binding to the VCA domain is not blocked by the GBD (residues 196-274)  or control region (178-274).	bind
1129	2	260	6	NULL	NULL	0	NULL		AminoAcid		does not block			GBD (residues 196-274)		Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_290_5492_801_s_73	11052943	( A) Arp2/3  binding to the VCA domain is not blocked by the GBD (residues 196-274)  or control region (178-274).	bind
1130	3	260	6	NULL	NULL	0	NULL		AminoAcid		does not block			control region (178-274)		Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_290_5492_801_s_73	11052943	( A) Arp2/3  binding to the VCA domain is not blocked by the GBD (residues 196-274)  or control region (178-274).	bind
57802	1	261	5	NULL	NULL	0	NULL	Noxa m3	GP		bind					Mcl-1	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_196	15901672	( A) As Noxa m3 binds Mcl-1, Bcl-xL, and Bcl-w but not Bcl-2, targeting of these prosurvival proteins suffices for Bak-mediated  apoptosis, whereas neutralization of Bcl-2 is not required.	bind
57803	2	261	5	NULL	NULL	0	NULL	Noxa m3	GP		bind					Bcl-xL	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_196	15901672	( A) As Noxa m3 binds Mcl-1, Bcl-xL, and Bcl-w but not Bcl-2, targeting of these prosurvival proteins suffices for Bak-mediated  apoptosis, whereas neutralization of Bcl-2 is not required.	bind
57804	3	261	5	NULL	NULL	0	NULL	Noxa m3	GP		bind					Bcl-w	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_196	15901672	( A) As Noxa m3 binds Mcl-1, Bcl-xL, and Bcl-w but not Bcl-2, targeting of these prosurvival proteins suffices for Bak-mediated  apoptosis, whereas neutralization of Bcl-2 is not required.	bind
57805	4	261	5	NULL	NULL	0	NULL	Noxa m3	GP		does not bind					Bcl-2	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_196	15901672	( A) As Noxa m3 binds Mcl-1, Bcl-xL, and Bcl-w but not Bcl-2, targeting of these prosurvival proteins suffices for Bak-mediated  apoptosis, whereas neutralization of Bcl-2 is not required.	bind
57806	5	261	5	NULL	NULL	0	NULL	Bak	GP		mediates					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_196	15901672	( A) As Noxa m3 binds Mcl-1, Bcl-xL, and Bcl-w but not Bcl-2, targeting of these prosurvival proteins suffices for Bak-mediated  apoptosis, whereas neutralization of Bcl-2 is not required.	bind
57807	6	261	5	NULL	NULL	0	NULL	Mcl-1	GP		is a type of					prosurvival protein	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_196	15901672	( A) As Noxa m3 binds Mcl-1, Bcl-xL, and Bcl-w but not Bcl-2, targeting of these prosurvival proteins suffices for Bak-mediated  apoptosis, whereas neutralization of Bcl-2 is not required.	bind
57808	7	261	5	NULL	NULL	0	NULL	Bcl-xL	GP		is a type of					prosurvival protein	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_196	15901672	( A) As Noxa m3 binds Mcl-1, Bcl-xL, and Bcl-w but not Bcl-2, targeting of these prosurvival proteins suffices for Bak-mediated  apoptosis, whereas neutralization of Bcl-2 is not required.	bind
57809	8	261	5	NULL	NULL	0	NULL	Bcl-w	GP		is a type of					prosurvival protein	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_196	15901672	( A) As Noxa m3 binds Mcl-1, Bcl-xL, and Bcl-w but not Bcl-2, targeting of these prosurvival proteins suffices for Bak-mediated  apoptosis, whereas neutralization of Bcl-2 is not required.	bind
57810	9	261	5	NULL	NULL	0	NULL	Bcl-2	GP		is a type of					prosurvival protein	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_196	15901672	( A) As Noxa m3 binds Mcl-1, Bcl-xL, and Bcl-w but not Bcl-2, targeting of these prosurvival proteins suffices for Bak-mediated  apoptosis, whereas neutralization of Bcl-2 is not required.	bind
57811	10	261	5	NULL	NULL	0	NULL	Mcl-1	GP	targeting of	suffices for					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_196	15901672	( A) As Noxa m3 binds Mcl-1, Bcl-xL, and Bcl-w but not Bcl-2, targeting of these prosurvival proteins suffices for Bak-mediated  apoptosis, whereas neutralization of Bcl-2 is not required.	bind
57812	11	261	5	NULL	NULL	0	NULL	Bcl-xL	GP		suffices for					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_196	15901672	( A) As Noxa m3 binds Mcl-1, Bcl-xL, and Bcl-w but not Bcl-2, targeting of these prosurvival proteins suffices for Bak-mediated  apoptosis, whereas neutralization of Bcl-2 is not required.	bind
57813	12	261	5	NULL	NULL	0	NULL	Bcl-w	GP		suffices for					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_196	15901672	( A) As Noxa m3 binds Mcl-1, Bcl-xL, and Bcl-w but not Bcl-2, targeting of these prosurvival proteins suffices for Bak-mediated  apoptosis, whereas neutralization of Bcl-2 is not required.	bind
1131	1	261	6	NULL	NULL	0	NULL	Noxa m3	GP		bind					Mcl-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_196	15901672	( A) As Noxa m3 binds Mcl-1, Bcl-xL, and Bcl-w but not Bcl-2, targeting of these prosurvival proteins suffices for Bak-mediated  apoptosis, whereas neutralization of Bcl-2 is not required.	bind
1132	2	261	6	NULL	NULL	0	NULL	Noxa m3	GP		bind					Bcl-xL	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_196	15901672	( A) As Noxa m3 binds Mcl-1, Bcl-xL, and Bcl-w but not Bcl-2, targeting of these prosurvival proteins suffices for Bak-mediated  apoptosis, whereas neutralization of Bcl-2 is not required.	bind
1133	3	261	6	NULL	NULL	0	NULL	Noxa m3	GP		bind					Bcl-w	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_196	15901672	( A) As Noxa m3 binds Mcl-1, Bcl-xL, and Bcl-w but not Bcl-2, targeting of these prosurvival proteins suffices for Bak-mediated  apoptosis, whereas neutralization of Bcl-2 is not required.	bind
1134	4	261	6	NULL	NULL	0	NULL	Noxa m3	GP		does not bind					Bcl-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_196	15901672	( A) As Noxa m3 binds Mcl-1, Bcl-xL, and Bcl-w but not Bcl-2, targeting of these prosurvival proteins suffices for Bak-mediated  apoptosis, whereas neutralization of Bcl-2 is not required.	bind
1135	5	261	6	NULL	NULL	0	NULL	Bak	GP		mediates					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_196	15901672	( A) As Noxa m3 binds Mcl-1, Bcl-xL, and Bcl-w but not Bcl-2, targeting of these prosurvival proteins suffices for Bak-mediated  apoptosis, whereas neutralization of Bcl-2 is not required.	bind
57814	1	262	5	NULL	NULL	0	NULL	SeqA	GP		bind					GATC sequences within oriC	NucleicAcid	newly generated;;hemimethylated			NULL		NULL	NULL	NULL	NULL	gw70_embo_24_8_1502_s_235	15933720	( A) As replication initiates, SeqA binds newly generated hemimethylated GATC sequences  within  oriC, triggering origin sequestration.	bind
57815	2	262	5	NULL	NULL	0	NULL	statement 1	Process		triggers					origin sequestration	Process				NULL		0	NULL	NULL	NULL	gw70_embo_24_8_1502_s_235	15933720	( A) As replication initiates, SeqA binds newly generated hemimethylated GATC sequences  within  oriC, triggering origin sequestration.	bind
1136	1	262	6	NULL	NULL	0	NULL	SeqA	NucleicAcid		bind					oriC	NucleicAcid	newly generated;;hemimethylated		GATC 	NULL		NULL	NULL	NULL	NULL	gw70_embo_24_8_1502_s_235	15933720	( A) As replication initiates, SeqA binds newly generated hemimethylated GATC sequences  within  oriC, triggering origin sequestration.	bind
1137	2	262	6	NULL	NULL	0	NULL	Statement 1	Process		triggers					origin 	NucleicAcid	sequestration of			NULL		NULL	NULL	NULL	NULL	gw70_embo_24_8_1502_s_235	15933720	( A) As replication initiates, SeqA binds newly generated hemimethylated GATC sequences  within  oriC, triggering origin sequestration.	bind
51767	3	262	6	NULL	NULL	0	NULL	statement 1	Process		occurs after					replication	Process	initiation of			NULL		NULL	NULL	NULL	NULL	gw70_embo_24_8_1502_s_235	15933720	( A) As replication initiates, SeqA binds newly generated hemimethylated GATC sequences  within  oriC, triggering origin sequestration.	bind
57843	1	262	7	NULL	NULL	0	NULL	GATC sequences	GP	hemimethylated	present within					oriC	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_8_1502_s_235	15933720	( A) As replication initiates, SeqA binds newly generated hemimethylated GATC sequences  within  oriC, triggering origin sequestration.	bind
57844	2	262	7	NULL	NULL	0	NULL	SeqA	GP		bind					statement 1	GP	newly generated			NULL		0	NULL	NULL	NULL	gw70_embo_24_8_1502_s_235	15933720	( A) As replication initiates, SeqA binds newly generated hemimethylated GATC sequences  within  oriC, triggering origin sequestration.	bind
57845	3	262	7	NULL	NULL	0	NULL	statement 2	Process		occur during					replication	Process	initiation of			NULL		0	NULL	NULL	NULL	gw70_embo_24_8_1502_s_235	15933720	( A) As replication initiates, SeqA binds newly generated hemimethylated GATC sequences  within  oriC, triggering origin sequestration.	bind
57846	4	262	7	NULL	NULL	0	NULL	statement 2	Process		trigger					origin sequestration	Process				NULL		0	NULL	NULL	NULL	gw70_embo_24_8_1502_s_235	15933720	( A) As replication initiates, SeqA binds newly generated hemimethylated GATC sequences  within  oriC, triggering origin sequestration.	bind
57816	1	349	5	NULL	NULL	0	NULL	SRC1	GP		bind					FXR	GP				NULL		0	NULL	NULL	NULL	gw60_science_284_5418_1365_s_63	10334993	( A) CDCA and its conjugates increase SRC1 binding to FXR.	bind
57817	2	349	5	NULL	NULL	0	NULL	CDCA	GP		increases					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_science_284_5418_1365_s_63	10334993	( A) CDCA and its conjugates increase SRC1 binding to FXR.	bind
1138	1	349	6	NULL	NULL	0	NULL	SRC1	GP		bind					FXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5418_1365_s_63	10334993	( A) CDCA and its conjugates increase SRC1 binding to FXR.	bind
1139	2	349	6	NULL	NULL	0	NULL	CDCA	Chemical		increase					Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5418_1365_s_63	10334993	( A) CDCA and its conjugates increase SRC1 binding to FXR.	bind
57818	1	351	5	NULL	NULL	0	NULL	CED-4	GP		bind					CED-9	GP				NULL		0	NULL	NULL	NULL	gw60_science_275_5303_1122_s_90	9027312	( A) CED-4 binds CED-9.	bind
1140	1	351	6	NULL	NULL	0	NULL	CED-4	GP		bind					CED-9	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_275_5303_1122_s_90	9027312	( A) CED-4 binds CED-9.	bind
57819	1	354	5	NULL	NULL	0	NULL	Cellular proteins	GP		is associated with					Grb2	GP				NULL		0	NULL	NULL	NULL	gw60_embo_20_22_6337_s_167	11707405	( A) Cellular proteins associated with Grb2 bound to MT mutants.	bind
57820	2	354	5	NULL	NULL	0	NULL	statement 1	GP		bind					MT	GP	mutant			NULL		0	NULL	NULL	NULL	gw60_embo_20_22_6337_s_167	11707405	( A) Cellular proteins associated with Grb2 bound to MT mutants.	bind
1141	1	354	6	NULL	NULL	0	NULL	Grb2	GP		bind					MT	CellComponent	mutant			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_22_6337_s_167	11707405	( A) Cellular proteins associated with Grb2 bound to MT mutants.	bind
51768	2	354	6	NULL	NULL	0	NULL	Cellular proteins	GP		associate with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_22_6337_s_167	11707405	( A) Cellular proteins associated with Grb2 bound to MT mutants.	bind
1207	1	370	6	NULL	NULL	0	NULL	dopamine	Chemical		compete with					E-HRP	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_155	11027358	( A) Competition of E-HRP binding by the catecholamines dopamine (Dpn), NE, and epinephrine (E) and the catecholestrogen 2-hydroxyestradiol.	bind
1208	2	370	6	NULL	NULL	0	NULL	NE	Chemical		compete with					E-HRP	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_155	11027358	( A) Competition of E-HRP binding by the catecholamines dopamine (Dpn), NE, and epinephrine (E) and the catecholestrogen 2-hydroxyestradiol.	bind
1209	3	370	6	NULL	NULL	0	NULL	epinephrine	Chemical		compete with					E-HRP	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_155	11027358	( A) Competition of E-HRP binding by the catecholamines dopamine (Dpn), NE, and epinephrine (E) and the catecholestrogen 2-hydroxyestradiol.	bind
1210	4	370	6	NULL	NULL	0	NULL	2-hydroxyestradiol	Chemical		compete with					E-HRP	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_155	11027358	( A) Competition of E-HRP binding by the catecholamines dopamine (Dpn), NE, and epinephrine (E) and the catecholestrogen 2-hydroxyestradiol.	bind
51769	5	370	6	NULL	NULL	0	NULL	Dpn	Chemical		is					dopamine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_155	11027358	( A) Competition of E-HRP binding by the catecholamines dopamine (Dpn), NE, and epinephrine (E) and the catecholestrogen 2-hydroxyestradiol.	bind
51770	6	370	6	NULL	NULL	0	NULL	E	Chemical		is 					epinephrine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_155	11027358	( A) Competition of E-HRP binding by the catecholamines dopamine (Dpn), NE, and epinephrine (E) and the catecholestrogen 2-hydroxyestradiol.	bind
51771	7	370	6	NULL	NULL	0	NULL	dopamine	Chemical		is a type of					catecholamine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_155	11027358	( A) Competition of E-HRP binding by the catecholamines dopamine (Dpn), NE, and epinephrine (E) and the catecholestrogen 2-hydroxyestradiol.	bind
51772	8	370	6	NULL	NULL	0	NULL	NE	Chemical		is a type of					catecholamine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_155	11027358	( A) Competition of E-HRP binding by the catecholamines dopamine (Dpn), NE, and epinephrine (E) and the catecholestrogen 2-hydroxyestradiol.	bind
51773	9	370	6	NULL	NULL	0	NULL	E	Chemical		is a type of					catecholamine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_155	11027358	( A) Competition of E-HRP binding by the catecholamines dopamine (Dpn), NE, and epinephrine (E) and the catecholestrogen 2-hydroxyestradiol.	bind
51774	10	370	6	NULL	NULL	0	NULL	2-hydroxyestradiol	Chemical		is a type of					catecholestrogen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_155	11027358	( A) Competition of E-HRP binding by the catecholamines dopamine (Dpn), NE, and epinephrine (E) and the catecholestrogen 2-hydroxyestradiol.	bind
57821	1	371	5	NULL	NULL	0	NULL	hnRNP A1	GP	endogenous	bind					MHV RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4701_s_177	10970862	( A) Competition of the binding of endogenous hnRNP A1 to MHV RNA by hnRNP A1deltaC.	bind
57822	2	371	5	NULL	NULL	0	NULL	hnRNP A1deltaC	GP		bind					MHV RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4701_s_177	10970862	( A) Competition of the binding of endogenous hnRNP A1 to MHV RNA by hnRNP A1deltaC.	bind
57823	3	371	5	NULL	NULL	0	NULL	statement 2	Process		competes with					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4701_s_177	10970862	( A) Competition of the binding of endogenous hnRNP A1 to MHV RNA by hnRNP A1deltaC.	bind
1211	1	371	6	NULL	NULL	0	NULL	hnRNP A1	GP	endogenous	bind					MHV RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4701_s_177	10970862	( A) Competition of the binding of endogenous hnRNP A1 to MHV RNA by hnRNP A1deltaC.	bind
1212	2	371	6	NULL	NULL	0	NULL	hnRNP A1deltaC	GP		bind					MHV RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4701_s_177	10970862	( A) Competition of the binding of endogenous hnRNP A1 to MHV RNA by hnRNP A1deltaC.	bind
51775	3	371	6	NULL	NULL	0	NULL	statement 1	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4701_s_177	10970862	( A) Competition of the binding of endogenous hnRNP A1 to MHV RNA by hnRNP A1deltaC.	bind
57824	1	377	5	NULL	NULL	0	NULL	E1	GP		bind		cooperatively	DBD		E2	GP		DBD		NULL		0	NULL	NULL	NULL	gw60_embo_19_12_3069_s_187	10856250	( A) Cooperative binding of E1 and E2 DBDs is disrupted by a double point mutation between the two sites.	bind
1213	1	377	6	NULL	NULL	0	NULL	E1	GP		bind		cooperatively	DBD		E2	GP		DBD		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_12_3069_s_187	10856250	( A) Cooperative binding of E1 and E2 DBDs is disrupted by a double point mutation between the two sites.	bind
57825	1	378	5	NULL	NULL	0	NULL	capsids	GP	CPV	bind					TfR	GP	feline			NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_553_s_287	16153179	( a) CPV and FPV capsids bind to the feline TfR, but only CPV capsids bind the canine  TfR.	bind
57826	2	378	5	NULL	NULL	0	NULL	capsids	GP	FPV	bind					TfR	GP	feline			NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_553_s_287	16153179	( a) CPV and FPV capsids bind to the feline TfR, but only CPV capsids bind the canine  TfR.	bind
57827	3	378	5	NULL	NULL	0	NULL	capsids	GP	CPV	bind					TfR	GP	canine			NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_553_s_287	16153179	( a) CPV and FPV capsids bind to the feline TfR, but only CPV capsids bind the canine  TfR.	bind
1215	1	378	6	NULL	NULL	0	NULL	CPV capsid	CellComponent		bind					TfR	GP	feline			NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_553_s_287	16153179	( a) CPV and FPV capsids bind to the feline TfR, but only CPV capsids bind the canine  TfR.	bind
1216	2	378	6	NULL	NULL	0	NULL	FPV capsid	CellComponent		bind					TfR	GP	feline			NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_553_s_287	16153179	( a) CPV and FPV capsids bind to the feline TfR, but only CPV capsids bind the canine  TfR.	bind
1217	3	378	6	NULL	NULL	0	NULL	CPV capsid	CellComponent		bind					TfR	GP	canine			NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_553_s_287	16153179	( a) CPV and FPV capsids bind to the feline TfR, but only CPV capsids bind the canine  TfR.	bind
57828	1	386	5	NULL	NULL	0	NULL	GAPDH	GP		bind					Siah1	GP				NULL	in vitro	0	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_35	16505364	( a) Deprenyl (DEP) inhibits the binding of GAPDH and Siah1  in vitro.	bind
57829	2	386	5	NULL	NULL	0	NULL	DEP	Chemical		is					Deprenyl	Chemical				NULL		0	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_35	16505364	( a) Deprenyl (DEP) inhibits the binding of GAPDH and Siah1  in vitro.	bind
57830	3	386	5	NULL	NULL	0	NULL	DEP	Chemical		inhibits					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_35	16505364	( a) Deprenyl (DEP) inhibits the binding of GAPDH and Siah1  in vitro.	bind
1218	1	386	6	NULL	NULL	0	NULL	GAPDH	GP		bind					Siah1	GP				NULL	In vitro	NULL	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_35	16505364	( a) Deprenyl (DEP) inhibits the binding of GAPDH and Siah1  in vitro.	bind
1219	2	386	6	NULL	NULL	0	NULL	Deprenyl 	Chemical		inhibits					Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_35	16505364	( a) Deprenyl (DEP) inhibits the binding of GAPDH and Siah1  in vitro.	bind
51776	3	386	6	NULL	NULL	0	NULL	DEP	Chemical		is					Deprenyl	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_35	16505364	( a) Deprenyl (DEP) inhibits the binding of GAPDH and Siah1  in vitro.	bind
57831	1	387	5	NULL	NULL	0	NULL	IDH2	GP		bind			catalytic site		isocitrate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_15_12864_s_267	12562755	( A) Despite residue differences in the isocitrate binding sites, the catalytic site in IDH2 and the regulatory site in IDH1 bind isocitrate with similar affinity.	bind
57832	2	387	5	NULL	NULL	0	NULL	IDH1	GP		bind			regulatory site		isocitrate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_15_12864_s_267	12562755	( A) Despite residue differences in the isocitrate binding sites, the catalytic site in IDH2 and the regulatory site in IDH1 bind isocitrate with similar affinity.	bind
57833	3	387	5	NULL	NULL	0	NULL	statement 1	Process	affinity of	is similar to					statement 2	Process	affinity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_15_12864_s_267	12562755	( A) Despite residue differences in the isocitrate binding sites, the catalytic site in IDH2 and the regulatory site in IDH1 bind isocitrate with similar affinity.	bind
1220	1	387	6	NULL	NULL	0	NULL	IDH2	GP		bind			catalytic site		isocitrate	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_12864_s_267	12562755	( A) Despite residue differences in the isocitrate binding sites, the catalytic site in IDH2 and the regulatory site in IDH1 bind isocitrate with similar affinity.	bind
1221	2	387	6	NULL	NULL	0	NULL	IDH1	GP		bind			regulatory site		isocitrate	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_12864_s_267	12562755	( A) Despite residue differences in the isocitrate binding sites, the catalytic site in IDH2 and the regulatory site in IDH1 bind isocitrate with similar affinity.	bind
51777	3	387	6	NULL	NULL	0	NULL	statement 1	Process	affinity of	is similar to					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_12864_s_267	12562755	( A) Despite residue differences in the isocitrate binding sites, the catalytic site in IDH2 and the regulatory site in IDH1 bind isocitrate with similar affinity.	bind
57834	1	391	5	NULL	NULL	0	NULL	Dsk2p	GP		bind		directly			tetra-Ub	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_745_s_133	11805328	( A) Direct binding of Dsk2p to tetra-Ub.	bind
1222	1	391	6	NULL	NULL	0	NULL	Dsk2p	GP		bind		directly			tetra-Ub	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_745_s_133	11805328	( A) Direct binding of Dsk2p to tetra-Ub.	bind
57835	1	392	5	NULL	NULL	0	NULL	Hsps	GP		bind					Tdag51	GP				NULL		0	NULL	NULL	NULL	gw70_embo_25_20_4773_s_112	17024176	( A) Direct binding of Hsps with Tdag51.	bind
1223	1	392	6	NULL	NULL	0	NULL	Hsps	GP		bind		directly			Tdag51	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_20_4773_s_112	17024176	( A) Direct binding of Hsps with Tdag51.	bind
57836	1	393	5	NULL	NULL	0	NULL	TLP	GP		bind					TFIIA	GP				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_8_2127_s_168	12682363	( A) Direct binding of TLP and TFIIA.	bind
1224	1	393	6	NULL	NULL	0	NULL	TLP	GP		bind		directly			TFIIA	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_8_2127_s_168	12682363	( A) Direct binding of TLP and TFIIA.	bind
57837	1	398	5	NULL	NULL	0	NULL	NCI-65828	Chemical		docks					AccD5	GP		acyl-CoA-binding pocket		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_9_3072_s_149	16492739	( A) Docking of NCI-65828 in the acyl-CoA-binding pocket of AccD5 matches the binding  motif of an acyl-CoA, in which the anionic sulfate of NCI-65828 binds the entrance  of the CoA pocket and the hydrophobic moiety binds the hydrophobic interior of the  CoA pocket.	bind
57838	2	398	5	NULL	NULL	0	NULL	NCI-65828	Chemical	anionic sulfate of	bind					CoA pocket	AminoAcid	entrance of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_9_3072_s_149	16492739	( A) Docking of NCI-65828 in the acyl-CoA-binding pocket of AccD5 matches the binding  motif of an acyl-CoA, in which the anionic sulfate of NCI-65828 binds the entrance  of the CoA pocket and the hydrophobic moiety binds the hydrophobic interior of the  CoA pocket.	bind
57839	3	398	5	NULL	NULL	0	NULL	NCI-65828	Chemical	hydrophobic moiety of	bind					CoA pocket	AminoAcid	hydrophobic interior of			NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3072_s_149	16492739	( A) Docking of NCI-65828 in the acyl-CoA-binding pocket of AccD5 matches the binding  motif of an acyl-CoA, in which the anionic sulfate of NCI-65828 binds the entrance  of the CoA pocket and the hydrophobic moiety binds the hydrophobic interior of the  CoA pocket.	bind
1225	1	398	6	NULL	NULL	0	NULL	NCI-65828 	Chemical		bind			anionic sulfate		AccD5	GP		entrance of the CoA pocket		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_9_3072_s_149	16492739	( A) Docking of NCI-65828 in the acyl-CoA-binding pocket of AccD5 matches the binding  motif of an acyl-CoA, in which the anionic sulfate of NCI-65828 binds the entrance  of the CoA pocket and the hydrophobic moiety binds the hydrophobic interior of the  CoA pocket.	bind
1226	2	398	6	NULL	NULL	0	NULL	NCI-65828 	Chemical		bind			hydrophobic moiety		AccD5	GP		hydrophobic interior of the CoA pocket		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_9_3072_s_149	16492739	( A) Docking of NCI-65828 in the acyl-CoA-binding pocket of AccD5 matches the binding  motif of an acyl-CoA, in which the anionic sulfate of NCI-65828 binds the entrance  of the CoA pocket and the hydrophobic moiety binds the hydrophobic interior of the  CoA pocket.	bind
57920	1	401	5	NULL	NULL	0	NULL	anti-CD81	GP		bind					B cells	Cell				NULL		0	NULL	NULL	NULL	gw60_science_282_5390_938_s_43	9794763	( A) Dose-dependent inhibition of anti-CD81 binding to B cells by recombinant E2.	bind
57921	2	401	5	NULL	NULL	0	NULL	E2	GP	recombinant	inhibits		dose dependently			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_science_282_5390_938_s_43	9794763	( A) Dose-dependent inhibition of anti-CD81 binding to B cells by recombinant E2.	bind
1227	1	401	6	NULL	NULL	0	NULL	anti-CD81	GP		bind					B cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_science_282_5390_938_s_43	9794763	( A) Dose-dependent inhibition of anti-CD81 binding to B cells by recombinant E2.	bind
1228	2	401	6	NULL	NULL	0	NULL	E2	GP	recombinant	inhibits		dose-dependently			Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_282_5390_938_s_43	9794763	( A) Dose-dependent inhibition of anti-CD81 binding to B cells by recombinant E2.	bind
57922	1	403	5	NULL	NULL	0	NULL	Notch1	GP	activated	down-modulates					Wnts gene	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_genesdev_19_12_1485_s_64	15964998	( A) Down-modulation of  Wnts gene expression by activated Notch1.	bind
1229	1	403	6	NULL	NULL	0	NULL	Notch1	GP	activated	downregulates					Wnts gene	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_12_1485_s_64	15964998	( A) Down-modulation of  Wnts gene expression by activated Notch1.	bind
57923	1	405	5	NULL	NULL	0	NULL	dsDNA	NucleicAcid		bind					Cdc6-1 proteins	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_15_4940_s_135	16150924	( A) dsDNA binding of Cdc6-1 proteins; ( B) ssDNA binding of Cdc6-1 proteins; ( C) dsDNA binding of Cdc6-2 proteins; ( D) ssDNA binding of Cdc6-2 proteins.	bind
57924	2	405	5	NULL	NULL	0	NULL	ssDNA	NucleicAcid		bind					Cdc6-1 proteins	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_15_4940_s_135	16150924	( A) dsDNA binding of Cdc6-1 proteins; ( B) ssDNA binding of Cdc6-1 proteins; ( C) dsDNA binding of Cdc6-2 proteins; ( D) ssDNA binding of Cdc6-2 proteins.	bind
57925	3	405	5	NULL	NULL	0	NULL	dsDNA	NucleicAcid		bind					Cdc6-2 proteins	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_15_4940_s_135	16150924	( A) dsDNA binding of Cdc6-1 proteins; ( B) ssDNA binding of Cdc6-1 proteins; ( C) dsDNA binding of Cdc6-2 proteins; ( D) ssDNA binding of Cdc6-2 proteins.	bind
57926	4	405	5	NULL	NULL	0	NULL	ssDNA	NucleicAcid		bind					Cdc6-2 proteins	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_15_4940_s_135	16150924	( A) dsDNA binding of Cdc6-1 proteins; ( B) ssDNA binding of Cdc6-1 proteins; ( C) dsDNA binding of Cdc6-2 proteins; ( D) ssDNA binding of Cdc6-2 proteins.	bind
1230	1	405	6	NULL	NULL	0	NULL	dsDNA	NucleicAcid		bind					Cdc6-1 proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_15_4940_s_135	16150924	( A) dsDNA binding of Cdc6-1 proteins; ( B) ssDNA binding of Cdc6-1 proteins; ( C) dsDNA binding of Cdc6-2 proteins; ( D) ssDNA binding of Cdc6-2 proteins.	bind
1231	2	405	6	NULL	NULL	0	NULL	ssDNA	NucleicAcid		bind					Cdc6-1 proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_15_4940_s_135	16150924	( A) dsDNA binding of Cdc6-1 proteins; ( B) ssDNA binding of Cdc6-1 proteins; ( C) dsDNA binding of Cdc6-2 proteins; ( D) ssDNA binding of Cdc6-2 proteins.	bind
1232	3	405	6	NULL	NULL	0	NULL	dsDNA	NucleicAcid		bind					cdc6-2 proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_15_4940_s_135	16150924	( A) dsDNA binding of Cdc6-1 proteins; ( B) ssDNA binding of Cdc6-1 proteins; ( C) dsDNA binding of Cdc6-2 proteins; ( D) ssDNA binding of Cdc6-2 proteins.	bind
1233	4	405	6	NULL	NULL	0	NULL	ssDNA	NucleicAcid		bind					Cdc6-2 proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_15_4940_s_135	16150924	( A) dsDNA binding of Cdc6-1 proteins; ( B) ssDNA binding of Cdc6-1 proteins; ( C) dsDNA binding of Cdc6-2 proteins; ( D) ssDNA binding of Cdc6-2 proteins.	bind
57927	1	407	5	NULL	NULL	0	NULL	Fos/Jun heterodimers	GP		bind					TNF	GP			TRE site in promoter	NULL		0	NULL	NULL	NULL	gw60_jclininvest_104_4_503_s_210	10449442	( a) E2 decreases the binding of Fos/Jun heterodimers to the TRE site in the TNF promoter.	bind
57928	2	407	5	NULL	NULL	0	NULL	E2	GP		decreases					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jclininvest_104_4_503_s_210	10449442	( a) E2 decreases the binding of Fos/Jun heterodimers to the TRE site in the TNF promoter.	bind
1234	1	407	6	NULL	NULL	0	NULL	Fos/Jun heterodimer	GP		bind					TNF 	GP			TRE site in promoter	NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_4_503_s_210	10449442	( a) E2 decreases the binding of Fos/Jun heterodimers to the TRE site in the TNF promoter.	bind
1235	2	407	6	NULL	NULL	0	NULL	E2	GP		decreases 					Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_4_503_s_210	10449442	( a) E2 decreases the binding of Fos/Jun heterodimers to the TRE site in the TNF promoter.	bind
1236	1	408	6	NULL	NULL	0	NULL	E2F-1-ER	GP		bind					BMI1 	GP			Promoter	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_6_1745_s_147	16582100	( A) E2F-1-ER binds to the  BMI1 promoter upon activation by 4-OHT. Crosslinked chromatin was isolated from untreated  and 4-OHT treated 1A3 cells and precipitated with an E2F-1 specific antibody or a  control antibody.	bind
1507	2	408	6	NULL	NULL	0	NULL	4-OHT	Chemical		activates					Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_6_1745_s_147	16582100	( A) E2F-1-ER binds to the  BMI1 promoter upon activation by 4-OHT. Crosslinked chromatin was isolated from untreated  and 4-OHT treated 1A3 cells and precipitated with an E2F-1 specific antibody or a  control antibody.	bind
1508	4	408	6	NULL	NULL	0	NULL	chromatin	Chromosome	crosslinked	precipates					E2F-1 specific antibody	GP				NULL	untreated 1A3 cells	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_6_1745_s_147	16582100	( A) E2F-1-ER binds to the  BMI1 promoter upon activation by 4-OHT. Crosslinked chromatin was isolated from untreated  and 4-OHT treated 1A3 cells and precipitated with an E2F-1 specific antibody or a  control antibody.	bind
1509	5	408	6	NULL	NULL	0	NULL	chromatin	Chromosome	crosslinked	precipates					E2F-1 specific antibody	GP				NULL	4-OHT treated 1A3 cells	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_6_1745_s_147	16582100	( A) E2F-1-ER binds to the  BMI1 promoter upon activation by 4-OHT. Crosslinked chromatin was isolated from untreated  and 4-OHT treated 1A3 cells and precipitated with an E2F-1 specific antibody or a  control antibody.	bind
57929	1	409	5	NULL	NULL	0	NULL	E2F7	GP		bind					E2F sites	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_embo_22_23_6289_s_118	14633988	( A) E2F7 binds E2F sites.	bind
1237	1	409	6	NULL	NULL	0	NULL	E2F7	GP		bind						GP			E2F site	NULL		NULL	NULL	NULL	NULL	gw70_embo_22_23_6289_s_118	14633988	( A) E2F7 binds E2F sites.	bind
57930	1	410	5	NULL	NULL	0	NULL	Ebp1	GP		bind					Akt	GP				NULL	nuclear extract	0	NULL	NULL	NULL	gw70_embo_25_10_2083_s_132	16642037	( A) Ebp1 binds Akt in the nuclear extract.	bind
1238	1	410	6	NULL	NULL	0	NULL	Ebp1	GP		bind					Akt	GP				NULL	nuclear extract	NULL	NULL	NULL	NULL	gw70_embo_25_10_2083_s_132	16642037	( A) Ebp1 binds Akt in the nuclear extract.	bind
57931	1	411	5	NULL	NULL	0	NULL	rapamycin	Chemical		effects		possibly			eIF2alpha	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_genesdev_17_7_859_s_73	12654728	( A) Effect of rapamycin on phosphorylation of eIF2alpha is strongly dependent on dephosphorylation of Ser 577 and the tRNA binding activity of GCN2.	bind
57932	2	411	5	NULL	NULL	0	NULL	statement 1	Process		is dependent on		strongly			Ser 577	AminoAcid	dephosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_7_859_s_73	12654728	( A) Effect of rapamycin on phosphorylation of eIF2alpha is strongly dependent on dephosphorylation of Ser 577 and the tRNA binding activity of GCN2.	bind
57933	3	411	5	NULL	NULL	0	NULL	GCN2	GP		bind					tRNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_genesdev_17_7_859_s_73	12654728	( A) Effect of rapamycin on phosphorylation of eIF2alpha is strongly dependent on dephosphorylation of Ser 577 and the tRNA binding activity of GCN2.	bind
57934	4	411	5	NULL	NULL	0	NULL	statement 1	Process		is dependent on		strongly			statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_genesdev_17_7_859_s_73	12654728	( A) Effect of rapamycin on phosphorylation of eIF2alpha is strongly dependent on dephosphorylation of Ser 577 and the tRNA binding activity of GCN2.	bind
1503	1	411	6	NULL	NULL	0	NULL	rapamycin	Chemical		effects					eIF2alpha	GP	phosphorylation of 			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_7_859_s_73	12654728	( A) Effect of rapamycin on phosphorylation of eIF2alpha is strongly dependent on dephosphorylation of Ser 577 and the tRNA binding activity of GCN2.	bind
1504	2	411	6	NULL	NULL	0	NULL	GCN2	GP		bind					tRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_7_859_s_73	12654728	( A) Effect of rapamycin on phosphorylation of eIF2alpha is strongly dependent on dephosphorylation of Ser 577 and the tRNA binding activity of GCN2.	bind
1505	3	411	6	NULL	NULL	0	NULL	Statement 1	Relationship		dependent on		strongly			Ser 577	AminoAcid	dephosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_7_859_s_73	12654728	( A) Effect of rapamycin on phosphorylation of eIF2alpha is strongly dependent on dephosphorylation of Ser 577 and the tRNA binding activity of GCN2.	bind
1506	4	411	6	NULL	NULL	0	NULL	Statement 1	Relationship		dependent on		strongly			Statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_7_859_s_73	12654728	( A) Effect of rapamycin on phosphorylation of eIF2alpha is strongly dependent on dephosphorylation of Ser 577 and the tRNA binding activity of GCN2.	bind
1070	1	415	5	NULL	NULL	0	NULL	eIF2B	GP		does not catalyze					GDP	Chemical	exchange of			NULL	on eIF2(alphaP)	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_12841_s_158	9582312	( a) eIF2B reportedly does not catalyze GDP exchange on eIF2(alphaP) ( 15); ( b) eIF2(alphaP) displaces unphosphorylated eIF2 bound to eIF2B but unphosphorylated eIF2 does not ( 16); and ( c) eIF2(alphaP) inhibits the activity of eIF2B in the presence of low concentrations of substrate ( i.e. <10-fold molar excess of eIF2.GDP to eIF2(alphaP)) but at higher substrate concentrations the inhibition caused by eIF2(alphaP) is negligible ( 15), suggesting that eIF2(alphaP) is acting as a competitive inhibitor of eIF2B.	bind
1071	2	415	5	NULL	NULL	0	NULL	eIF2	GP	unphosphorylated	bind					eIF2B	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_12841_s_158	9582312	( a) eIF2B reportedly does not catalyze GDP exchange on eIF2(alphaP) ( 15); ( b) eIF2(alphaP) displaces unphosphorylated eIF2 bound to eIF2B but unphosphorylated eIF2 does not ( 16); and ( c) eIF2(alphaP) inhibits the activity of eIF2B in the presence of low concentrations of substrate ( i.e. <10-fold molar excess of eIF2.GDP to eIF2(alphaP)) but at higher substrate concentrations the inhibition caused by eIF2(alphaP) is negligible ( 15), suggesting that eIF2(alphaP) is acting as a competitive inhibitor of eIF2B.	bind
1072	3	415	5	NULL	NULL	0	NULL	eIF2(alphaP)	GP		displaces					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_12841_s_158	9582312	( a) eIF2B reportedly does not catalyze GDP exchange on eIF2(alphaP) ( 15); ( b) eIF2(alphaP) displaces unphosphorylated eIF2 bound to eIF2B but unphosphorylated eIF2 does not ( 16); and ( c) eIF2(alphaP) inhibits the activity of eIF2B in the presence of low concentrations of substrate ( i.e. <10-fold molar excess of eIF2.GDP to eIF2(alphaP)) but at higher substrate concentrations the inhibition caused by eIF2(alphaP) is negligible ( 15), suggesting that eIF2(alphaP) is acting as a competitive inhibitor of eIF2B.	bind
1073	4	415	5	NULL	NULL	0	NULL	eIF2	GP	unphosphorylated	does not displace					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_12841_s_158	9582312	( a) eIF2B reportedly does not catalyze GDP exchange on eIF2(alphaP) ( 15); ( b) eIF2(alphaP) displaces unphosphorylated eIF2 bound to eIF2B but unphosphorylated eIF2 does not ( 16); and ( c) eIF2(alphaP) inhibits the activity of eIF2B in the presence of low concentrations of substrate ( i.e. <10-fold molar excess of eIF2.GDP to eIF2(alphaP)) but at higher substrate concentrations the inhibition caused by eIF2(alphaP) is negligible ( 15), suggesting that eIF2(alphaP) is acting as a competitive inhibitor of eIF2B.	bind
1074	5	415	5	NULL	NULL	0	NULL	eIF2(alphaP)	GP		inhibit 					eIF2B	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_12841_s_158	9582312	( a) eIF2B reportedly does not catalyze GDP exchange on eIF2(alphaP) ( 15); ( b) eIF2(alphaP) displaces unphosphorylated eIF2 bound to eIF2B but unphosphorylated eIF2 does not ( 16); and ( c) eIF2(alphaP) inhibits the activity of eIF2B in the presence of low concentrations of substrate ( i.e. <10-fold molar excess of eIF2.GDP to eIF2(alphaP)) but at higher substrate concentrations the inhibition caused by eIF2(alphaP) is negligible ( 15), suggesting that eIF2(alphaP) is acting as a competitive inhibitor of eIF2B.	bind
1075	6	415	5	NULL	NULL	0	NULL	eIF2(alphaP)  	GP		inhibit		negligible			eIF2B	GP	activity			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_12841_s_158	9582312	( a) eIF2B reportedly does not catalyze GDP exchange on eIF2(alphaP) ( 15); ( b) eIF2(alphaP) displaces unphosphorylated eIF2 bound to eIF2B but unphosphorylated eIF2 does not ( 16); and ( c) eIF2(alphaP) inhibits the activity of eIF2B in the presence of low concentrations of substrate ( i.e. <10-fold molar excess of eIF2.GDP to eIF2(alphaP)) but at higher substrate concentrations the inhibition caused by eIF2(alphaP) is negligible ( 15), suggesting that eIF2(alphaP) is acting as a competitive inhibitor of eIF2B.	bind
1076	7	415	5	NULL	NULL	0	NULL	eIF2(alphaP)	GP		inhibit		competitively			eIF2B	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_12841_s_158	9582312	( a) eIF2B reportedly does not catalyze GDP exchange on eIF2(alphaP) ( 15); ( b) eIF2(alphaP) displaces unphosphorylated eIF2 bound to eIF2B but unphosphorylated eIF2 does not ( 16); and ( c) eIF2(alphaP) inhibits the activity of eIF2B in the presence of low concentrations of substrate ( i.e. <10-fold molar excess of eIF2.GDP to eIF2(alphaP)) but at higher substrate concentrations the inhibition caused by eIF2(alphaP) is negligible ( 15), suggesting that eIF2(alphaP) is acting as a competitive inhibitor of eIF2B.	bind
52129	8	415	5	NULL	NULL	0	NULL	statement 5	Process		in the presence of					substrate	GP	low concentration of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_12841_s_158	9582312	( a) eIF2B reportedly does not catalyze GDP exchange on eIF2(alphaP) ( 15); ( b) eIF2(alphaP) displaces unphosphorylated eIF2 bound to eIF2B but unphosphorylated eIF2 does not ( 16); and ( c) eIF2(alphaP) inhibits the activity of eIF2B in the presence of low concentrations of substrate ( i.e. <10-fold molar excess of eIF2.GDP to eIF2(alphaP)) but at higher substrate concentrations the inhibition caused by eIF2(alphaP) is negligible ( 15), suggesting that eIF2(alphaP) is acting as a competitive inhibitor of eIF2B.	bind
52130	9	415	5	NULL	NULL	0	NULL	statement 6	Process		in the presence of					substrate	GP	high concentration of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_12841_s_158	9582312	( a) eIF2B reportedly does not catalyze GDP exchange on eIF2(alphaP) ( 15); ( b) eIF2(alphaP) displaces unphosphorylated eIF2 bound to eIF2B but unphosphorylated eIF2 does not ( 16); and ( c) eIF2(alphaP) inhibits the activity of eIF2B in the presence of low concentrations of substrate ( i.e. <10-fold molar excess of eIF2.GDP to eIF2(alphaP)) but at higher substrate concentrations the inhibition caused by eIF2(alphaP) is negligible ( 15), suggesting that eIF2(alphaP) is acting as a competitive inhibitor of eIF2B.	bind
1512	1	415	6	NULL	NULL	0	NULL	eIF2	GP	unphosphorylated	bind					eIF2B	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_12841_s_158	9582312	( a) eIF2B reportedly does not catalyze GDP exchange on eIF2(alphaP) ( 15); ( b) eIF2(alphaP) displaces unphosphorylated eIF2 bound to eIF2B but unphosphorylated eIF2 does not ( 16); and ( c) eIF2(alphaP) inhibits the activity of eIF2B in the presence of low concentrations of substrate ( i.e. <10-fold molar excess of eIF2.GDP to eIF2(alphaP)) but at higher substrate concentrations the inhibition caused by eIF2(alphaP) is negligible ( 15), suggesting that eIF2(alphaP) is acting as a competitive inhibitor of eIF2B.	bind
1513	2	415	6	NULL	NULL	0	NULL	eIF2(alphaP)	GP		inhibits					eIF2B	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_12841_s_158	9582312	( a) eIF2B reportedly does not catalyze GDP exchange on eIF2(alphaP) ( 15); ( b) eIF2(alphaP) displaces unphosphorylated eIF2 bound to eIF2B but unphosphorylated eIF2 does not ( 16); and ( c) eIF2(alphaP) inhibits the activity of eIF2B in the presence of low concentrations of substrate ( i.e. <10-fold molar excess of eIF2.GDP to eIF2(alphaP)) but at higher substrate concentrations the inhibition caused by eIF2(alphaP) is negligible ( 15), suggesting that eIF2(alphaP) is acting as a competitive inhibitor of eIF2B.	bind
1514	3	415	6	NULL	NULL	0	NULL	eIF2(alphaP)	GP		inhibit		competitively			eIF2B	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_12841_s_158	9582312	( a) eIF2B reportedly does not catalyze GDP exchange on eIF2(alphaP) ( 15); ( b) eIF2(alphaP) displaces unphosphorylated eIF2 bound to eIF2B but unphosphorylated eIF2 does not ( 16); and ( c) eIF2(alphaP) inhibits the activity of eIF2B in the presence of low concentrations of substrate ( i.e. <10-fold molar excess of eIF2.GDP to eIF2(alphaP)) but at higher substrate concentrations the inhibition caused by eIF2(alphaP) is negligible ( 15), suggesting that eIF2(alphaP) is acting as a competitive inhibitor of eIF2B.	bind
1516	4	415	6	NULL	NULL	0	NULL	eIF2B	GP		does not catalyze					GDP	Chemical	exchange of			NULL	on eIF2(alphaP)	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_12841_s_158	9582312	( a) eIF2B reportedly does not catalyze GDP exchange on eIF2(alphaP) ( 15); ( b) eIF2(alphaP) displaces unphosphorylated eIF2 bound to eIF2B but unphosphorylated eIF2 does not ( 16); and ( c) eIF2(alphaP) inhibits the activity of eIF2B in the presence of low concentrations of substrate ( i.e. <10-fold molar excess of eIF2.GDP to eIF2(alphaP)) but at higher substrate concentrations the inhibition caused by eIF2(alphaP) is negligible ( 15), suggesting that eIF2(alphaP) is acting as a competitive inhibitor of eIF2B.	bind
1517	5	415	6	NULL	NULL	0	NULL	Statement 2	Process		occurs in presence of					substrate	GP	low concentration			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_12841_s_158	9582312	( a) eIF2B reportedly does not catalyze GDP exchange on eIF2(alphaP) ( 15); ( b) eIF2(alphaP) displaces unphosphorylated eIF2 bound to eIF2B but unphosphorylated eIF2 does not ( 16); and ( c) eIF2(alphaP) inhibits the activity of eIF2B in the presence of low concentrations of substrate ( i.e. <10-fold molar excess of eIF2.GDP to eIF2(alphaP)) but at higher substrate concentrations the inhibition caused by eIF2(alphaP) is negligible ( 15), suggesting that eIF2(alphaP) is acting as a competitive inhibitor of eIF2B.	bind
1869	6	415	6	NULL	NULL	0	NULL	eIF2(alphaP)	GP		displaces					Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_12841_s_158	9582312	( a) eIF2B reportedly does not catalyze GDP exchange on eIF2(alphaP) ( 15); ( b) eIF2(alphaP) displaces unphosphorylated eIF2 bound to eIF2B but unphosphorylated eIF2 does not ( 16); and ( c) eIF2(alphaP) inhibits the activity of eIF2B in the presence of low concentrations of substrate ( i.e. <10-fold molar excess of eIF2.GDP to eIF2(alphaP)) but at higher substrate concentrations the inhibition caused by eIF2(alphaP) is negligible ( 15), suggesting that eIF2(alphaP) is acting as a competitive inhibitor of eIF2B.	bind
1870	7	415	6	NULL	NULL	0	NULL	eIF2	GP	unphosphorylated	does not displace					Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_12841_s_158	9582312	( a) eIF2B reportedly does not catalyze GDP exchange on eIF2(alphaP) ( 15); ( b) eIF2(alphaP) displaces unphosphorylated eIF2 bound to eIF2B but unphosphorylated eIF2 does not ( 16); and ( c) eIF2(alphaP) inhibits the activity of eIF2B in the presence of low concentrations of substrate ( i.e. <10-fold molar excess of eIF2.GDP to eIF2(alphaP)) but at higher substrate concentrations the inhibition caused by eIF2(alphaP) is negligible ( 15), suggesting that eIF2(alphaP) is acting as a competitive inhibitor of eIF2B.	bind
57935	1	416	5	NULL	NULL	0	NULL	eIF3	GP		bind					48S preinitiation complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_6_1381_s_257	14988734	( A) eIF4B, in concert with eIF4F (4E/4G/4A) or eIFiso4F, interacts with eIF3 bound to  the 48S preinitiation complex.	bind
57936	2	416	5	NULL	NULL	0	NULL	eIF4B	GP		interacts with					statement 1	GP				NULL		0	NULL	NULL	NULL	gw70_embo_23_6_1381_s_257	14988734	( A) eIF4B, in concert with eIF4F (4E/4G/4A) or eIFiso4F, interacts with eIF3 bound to  the 48S preinitiation complex.	bind
57937	3	416	5	NULL	NULL	0	NULL	eIF4F (4E/4G/4A)	GP		interacts with					statement 1	GP				NULL		0	NULL	NULL	NULL	gw70_embo_23_6_1381_s_257	14988734	( A) eIF4B, in concert with eIF4F (4E/4G/4A) or eIFiso4F, interacts with eIF3 bound to  the 48S preinitiation complex.	bind
57938	4	416	5	NULL	NULL	0	NULL	eIFiso4F	GP		interacts with					statement 1	GP				NULL		0	NULL	NULL	NULL	gw70_embo_23_6_1381_s_257	14988734	( A) eIF4B, in concert with eIF4F (4E/4G/4A) or eIFiso4F, interacts with eIF3 bound to  the 48S preinitiation complex.	bind
57939	5	416	5	NULL	NULL	0	NULL	statement 2	Process		in concert with					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_embo_23_6_1381_s_257	14988734	( A) eIF4B, in concert with eIF4F (4E/4G/4A) or eIFiso4F, interacts with eIF3 bound to  the 48S preinitiation complex.	bind
57940	6	416	5	NULL	NULL	0	NULL	statement 2	Process		in concert with					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_embo_23_6_1381_s_257	14988734	( A) eIF4B, in concert with eIF4F (4E/4G/4A) or eIFiso4F, interacts with eIF3 bound to  the 48S preinitiation complex.	bind
1518	1	416	6	NULL	NULL	0	NULL	eIF3	GP		bind					48S preinitiation complex	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_6_1381_s_257	14988734	( A) eIF4B, in concert with eIF4F (4E/4G/4A) or eIFiso4F, interacts with eIF3 bound to  the 48S preinitiation complex.	bind
1519	2	416	6	NULL	NULL	0	NULL	eIF4B	GP		interacts with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_6_1381_s_257	14988734	( A) eIF4B, in concert with eIF4F (4E/4G/4A) or eIFiso4F, interacts with eIF3 bound to  the 48S preinitiation complex.	bind
1520	3	416	6	NULL	NULL	0	NULL	eIF4F (4E/4G/4A)	GP		interacts with					Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_6_1381_s_257	14988734	( A) eIF4B, in concert with eIF4F (4E/4G/4A) or eIFiso4F, interacts with eIF3 bound to  the 48S preinitiation complex.	bind
51778	4	416	6	NULL	NULL	0	NULL	eIFiso4F	GP		interacts with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_6_1381_s_257	14988734	( A) eIF4B, in concert with eIF4F (4E/4G/4A) or eIFiso4F, interacts with eIF3 bound to  the 48S preinitiation complex.	bind
51779	5	416	6	NULL	NULL	0	NULL	statement 2	Process		 in concert with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_6_1381_s_257	14988734	( A) eIF4B, in concert with eIF4F (4E/4G/4A) or eIFiso4F, interacts with eIF3 bound to  the 48S preinitiation complex.	bind
51780	6	416	6	NULL	NULL	0	NULL	statement 2	Process		in concert with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_6_1381_s_257	14988734	( A) eIF4B, in concert with eIF4F (4E/4G/4A) or eIFiso4F, interacts with eIF3 bound to  the 48S preinitiation complex.	bind
57941	1	421	5	NULL	NULL	0	NULL	DLX1	GP	recombinant	bind					Dlx5/ Dlx6 	GP			intergenic enhancer	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_3_884_s_172	14769946	( a) Electrophoretic mobility shift assays (EMSA) demonstrate recombinant DLX1 and DLX2  bind to the  Dlx5/ Dlx6 intergenic enhancer  in vitro.	bind
57942	2	421	5	NULL	NULL	0	NULL	DLX2	GP	recombinant	bind					Dlx5/ Dlx6	GP			intergenic enhancer	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_3_884_s_172	14769946	( a) Electrophoretic mobility shift assays (EMSA) demonstrate recombinant DLX1 and DLX2  bind to the  Dlx5/ Dlx6 intergenic enhancer  in vitro.	bind
1239	1	421	6	NULL	NULL	0	NULL	Dlx1	GP		bind					Dlx5/ Dlx6 	GP			intergenic enhancer	NULL	In vitro	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_3_884_s_172	14769946	( a) Electrophoretic mobility shift assays (EMSA) demonstrate recombinant DLX1 and DLX2  bind to the  Dlx5/ Dlx6 intergenic enhancer  in vitro.	bind
1240	2	421	6	NULL	NULL	0	NULL	DLX2	GP		bind					Dlx5/ Dlx6 	GP			intergenic enhancer	NULL	In vitro	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_3_884_s_172	14769946	( a) Electrophoretic mobility shift assays (EMSA) demonstrate recombinant DLX1 and DLX2  bind to the  Dlx5/ Dlx6 intergenic enhancer  in vitro.	bind
57943	1	423	5	NULL	NULL	0	NULL	Cdc20	GP		associates with					APC	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_24_3278_s_98	11751633	( A) Emi1 can bind Cdc20 and Cdh1 already associated with the APC.	bind
57944	2	423	5	NULL	NULL	0	NULL	Cdh1	GP		associates with					APC	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_15_24_3278_s_98	11751633	( A) Emi1 can bind Cdc20 and Cdh1 already associated with the APC.	bind
57945	3	423	5	NULL	NULL	0	NULL	Emi1	GP		bind					statement 1	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_15_24_3278_s_98	11751633	( A) Emi1 can bind Cdc20 and Cdh1 already associated with the APC.	bind
57946	4	423	5	NULL	NULL	0	NULL	Emi1	GP		bind					statement 1	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_15_24_3278_s_98	11751633	( A) Emi1 can bind Cdc20 and Cdh1 already associated with the APC.	bind
1282	1	423	6	NULL	NULL	0	NULL	Cdc20	GP		associates					APC	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_24_3278_s_98	11751633	( A) Emi1 can bind Cdc20 and Cdh1 already associated with the APC.	bind
1283	2	423	6	NULL	NULL	0	NULL	Cdh1	GP		associates					APC	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_24_3278_s_98	11751633	( A) Emi1 can bind Cdc20 and Cdh1 already associated with the APC.	bind
1285	4	423	6	NULL	NULL	0	NULL	Emi1	GP		bind					Statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_24_3278_s_98	11751633	( A) Emi1 can bind Cdc20 and Cdh1 already associated with the APC.	bind
1286	3	423	6	NULL	NULL	0	NULL	Emi1	GP		bind					Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_24_3278_s_98	11751633	( A) Emi1 can bind Cdc20 and Cdh1 already associated with the APC.	bind
57947	1	425	5	NULL	NULL	0	NULL	p53	GP		bind					p53-responsive gene sequence	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_pnas_99_22_14548_s_109	12357032	( A) EMSA showing binding of p53 to a p53-responsive gene sequence.	bind
1289	1	425	6	NULL	NULL	0	NULL	p53	GP		bind					p53	GP			responsive gene sequence	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_22_14548_s_109	12357032	( A) EMSA showing binding of p53 to a p53-responsive gene sequence.	bind
57948	1	426	5	NULL	NULL	0	NULL	RARalpha1deltaBC	GP	recombinant;;purified	does not bind					DR5	GP			RARE	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4901_s_190	11812818	( A) EMSA using purified recombinant proteins (RARalpha1, RXRalpha and RARalpha1deltaBC) shows that RARalpha1deltaBC does not bind the RARE DR5 (lane 2), unlike RARalpha1 and RXRalpha (lanes 3 and 4, respectively).	bind
57949	2	426	5	NULL	NULL	0	NULL	RARalpha1	GP	recombinant;;purified	bind					DR5	GP			RARE	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4901_s_190	11812818	( A) EMSA using purified recombinant proteins (RARalpha1, RXRalpha and RARalpha1deltaBC) shows that RARalpha1deltaBC does not bind the RARE DR5 (lane 2), unlike RARalpha1 and RXRalpha (lanes 3 and 4, respectively).	bind
57950	3	426	5	NULL	NULL	0	NULL	RXRalpha	GP	recombinant;;purified	bind					DR5	GP			RARE	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4901_s_190	11812818	( A) EMSA using purified recombinant proteins (RARalpha1, RXRalpha and RARalpha1deltaBC) shows that RARalpha1deltaBC does not bind the RARE DR5 (lane 2), unlike RARalpha1 and RXRalpha (lanes 3 and 4, respectively).	bind
1291	1	426	6	NULL	NULL	0	NULL	RARalpha1deltaBC	GP	purified;;recombinant	does not bind					DR5	GP			RARE 	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4901_s_190	11812818	( A) EMSA using purified recombinant proteins (RARalpha1, RXRalpha and RARalpha1deltaBC) shows that RARalpha1deltaBC does not bind the RARE DR5 (lane 2), unlike RARalpha1 and RXRalpha (lanes 3 and 4, respectively).	bind
1293	2	426	6	NULL	NULL	0	NULL	RXRalpha	GP		bind					DR5	GP			RARE 	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4901_s_190	11812818	( A) EMSA using purified recombinant proteins (RARalpha1, RXRalpha and RARalpha1deltaBC) shows that RARalpha1deltaBC does not bind the RARE DR5 (lane 2), unlike RARalpha1 and RXRalpha (lanes 3 and 4, respectively).	bind
1294	3	426	6	NULL	NULL	0	NULL	RARalpha1	GP		bind					DR5	GP			RARE 	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4901_s_190	11812818	( A) EMSA using purified recombinant proteins (RARalpha1, RXRalpha and RARalpha1deltaBC) shows that RARalpha1deltaBC does not bind the RARE DR5 (lane 2), unlike RARalpha1 and RXRalpha (lanes 3 and 4, respectively).	bind
57951	1	427	5	NULL	NULL	0	NULL	Apaf-1	GP	endogenous	bind					Apaf-1	GP		1-570		NULL		0	NULL	NULL	NULL	gw60_embo_18_13_3586_s_114	10393175	( A) Endogenous Apaf-1 binds Apaf-1(1-570) in the presence of cytochrome  c and dATP.	bind
57952	2	427	5	NULL	NULL	0	NULL	statement 1	Process		in the presence of					cytochrome c	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_13_3586_s_114	10393175	( A) Endogenous Apaf-1 binds Apaf-1(1-570) in the presence of cytochrome  c and dATP.	bind
57953	3	427	5	NULL	NULL	0	NULL	statement 1	GP	endogenous	in the presence of					dATP	Chemical				NULL		0	NULL	NULL	NULL	gw60_embo_18_13_3586_s_114	10393175	( A) Endogenous Apaf-1 binds Apaf-1(1-570) in the presence of cytochrome  c and dATP.	bind
1295	1	427	6	NULL	NULL	0	NULL	Apaf-1	GP	endogenous	bind					Apaf-1	GP		1-570		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_13_3586_s_114	10393175	( A) Endogenous Apaf-1 binds Apaf-1(1-570) in the presence of cytochrome  c and dATP.	bind
1296	2	427	6	NULL	NULL	0	NULL	Statement 1	Process		occurs in presence of					cytochrome c	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_13_3586_s_114	10393175	( A) Endogenous Apaf-1 binds Apaf-1(1-570) in the presence of cytochrome  c and dATP.	bind
1297	3	427	6	NULL	NULL	0	NULL	Statement 1	Process		occurs in presence of					dATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_13_3586_s_114	10393175	( A) Endogenous Apaf-1 binds Apaf-1(1-570) in the presence of cytochrome  c and dATP.	bind
57954	1	428	5	NULL	NULL	0	NULL	CREB	GP		bind					CART	GP			promoter	NULL		0	NULL	NULL	NULL	gw70_pnas_103_39_14489_s_93	16971488	( A) Estradiol increases CREB binding to CART promoter DNA.	bind
57955	2	428	5	NULL	NULL	0	NULL	Estradiol	GP		increases					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_103_39_14489_s_93	16971488	( A) Estradiol increases CREB binding to CART promoter DNA.	bind
1299	1	428	6	NULL	NULL	0	NULL	CREB	GP		bind					CART	GP			promoter DNA	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_39_14489_s_93	16971488	( A) Estradiol increases CREB binding to CART promoter DNA.	bind
1300	2	428	6	NULL	NULL	0	NULL	Estradiol	Chemical		increases					Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_39_14489_s_93	16971488	( A) Estradiol increases CREB binding to CART promoter DNA.	bind
57956	1	429	5	NULL	NULL	0	NULL	CITED1	GP		bind					ERalpha	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_15_19_2598_s_144	11581164	( A) Estrogen-dependent binding of CITED1 to ERalpha.	bind
57957	2	429	5	NULL	NULL	0	NULL	statement 1	Process		is dependent on					Estrogen	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_15_19_2598_s_144	11581164	( A) Estrogen-dependent binding of CITED1 to ERalpha.	bind
1302	1	429	6	NULL	NULL	0	NULL	CITED1	GP		bind					ERalpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_19_2598_s_144	11581164	( A) Estrogen-dependent binding of CITED1 to ERalpha.	bind
1303	2	429	6	NULL	NULL	0	NULL	Statement 1	Process		dependent on					Estrogen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_19_2598_s_144	11581164	( A) Estrogen-dependent binding of CITED1 to ERalpha.	bind
57958	1	430	5	NULL	NULL	0	NULL	Sema4D	GP		bind					plexin-B1	GP				NULL	COS-7 cells	0	NULL	NULL	NULL	gw60_genesdev_16_7_836_s_67	11937491	( A) Expression of RacL61 enhances the binding of Sema4D to plexin-B1 in COS-7 cells.	bind
57959	2	430	5	NULL	NULL	0	NULL	RacL61	GP	expression of	enhances					statement 1	Process				NULL	COS-7 cells	NULL	NULL	NULL	NULL	gw60_genesdev_16_7_836_s_67	11937491	( A) Expression of RacL61 enhances the binding of Sema4D to plexin-B1 in COS-7 cells.	bind
1306	1	430	6	NULL	NULL	0	NULL	Sema4D	GP		bind					plexin-B1	GP				NULL	Cos-7 cells	NULL	NULL	NULL	NULL	gw60_genesdev_16_7_836_s_67	11937491	( A) Expression of RacL61 enhances the binding of Sema4D to plexin-B1 in COS-7 cells.	bind
1308	2	430	6	NULL	NULL	0	NULL	RacL61	GP	expression of	enhances					Statement 1	Process				NULL	COS-7 cells	NULL	NULL	NULL	NULL	gw60_genesdev_16_7_836_s_67	11937491	( A) Expression of RacL61 enhances the binding of Sema4D to plexin-B1 in COS-7 cells.	bind
57960	1	434	5	NULL	NULL	0	NULL	scFv	GP		bind					BMS	Cell				NULL	human plasma	NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_166	15563590	( A) Flow cytometric analysis of scFv binding to BMS breast cancer cells in human plasma  anticoagulated with 50 nM PPACK.	bind
57961	2	434	5	NULL	NULL	0	NULL	BMS	Cell		is a type of					breast cancer cells	Cell				NULL		0	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_166	15563590	( A) Flow cytometric analysis of scFv binding to BMS breast cancer cells in human plasma  anticoagulated with 50 nM PPACK.	bind
1310	1	434	6	NULL	NULL	0	NULL	scFv	GP		bind					BMS breast cancer cells	Cell				NULL	human plasma	NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_166	15563590	( A) Flow cytometric analysis of scFv binding to BMS breast cancer cells in human plasma  anticoagulated with 50 nM PPACK.	bind
57962	1	435	5	NULL	NULL	0	NULL	mAb 38C2	GP		bind					M21 cells	Cell				NULL		0	NULL	NULL	NULL	gw70_pnas_100_9_5396_s_92	12702756	( A) Flow cytometry histogram showing the binding of mAb 38C2 to human melanoma M21 cells  in the presence of a twice equimolar concentration of SCS-873 (red).	bind
57963	2	435	5	NULL	NULL	0	NULL	M21 cells	Cell		is a type of					human melanoma cells	Cell				NULL		0	NULL	NULL	NULL	gw70_pnas_100_9_5396_s_92	12702756	( A) Flow cytometry histogram showing the binding of mAb 38C2 to human melanoma M21 cells  in the presence of a twice equimolar concentration of SCS-873 (red).	bind
57964	3	435	5	NULL	NULL	0	NULL	statement 1	Process		in the presence of					SCS-873	Chemical				NULL		0	NULL	NULL	NULL	gw70_pnas_100_9_5396_s_92	12702756	( A) Flow cytometry histogram showing the binding of mAb 38C2 to human melanoma M21 cells  in the presence of a twice equimolar concentration of SCS-873 (red).	bind
1327	1	435	6	NULL	NULL	0	NULL	mAb 38C2	AminoAcid		bind					melanoma M21 cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_9_5396_s_92	12702756	( A) Flow cytometry histogram showing the binding of mAb 38C2 to human melanoma M21 cells  in the presence of a twice equimolar concentration of SCS-873 (red).	bind
1328	2	435	6	NULL	NULL	0	NULL	Statement 1	Process		occurs in presence of					SCS-873	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_9_5396_s_92	12702756	( A) Flow cytometry histogram showing the binding of mAb 38C2 to human melanoma M21 cells  in the presence of a twice equimolar concentration of SCS-873 (red).	bind
57965	1	438	5	NULL	NULL	0	NULL	FMRP	GP		bind					MBP	GP			3''-UTR	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2276_s_200	11376146	( A) FMRP binds to the MBP 3''-UTR.	bind
1329	1	438	6	NULL	NULL	0	NULL	FMRP	GP		bind					MBP	GP			3''-UTR	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2276_s_200	11376146	( A) FMRP binds to the MBP 3''-UTR.	bind
57966	1	442	5	NULL	NULL	0	NULL	c-Myc	GP	full-length;;35S-labeled	bind					GST-cdr2					NULL	in vitro	0	NULL	NULL	NULL	gw60_genesdev_13_16_2087_s_47	10465786	( A) Full-length 35S-labeled c-Myc binds to GST-cdr2 in vitro.	bind
1330	1	442	6	NULL	NULL	0	NULL	c-Myc	GP	Full-length;;35S-labeled	bind					GST-cdr2	GP				NULL	In vitro	NULL	NULL	NULL	NULL	gw60_genesdev_13_16_2087_s_47	10465786	( A) Full-length 35S-labeled c-Myc binds to GST-cdr2 in vitro.	bind
57967	1	444	5	NULL	NULL	0	NULL	FWD1	GP		bind					Skp1	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_7_3859_s_73	10097128	( A) FWD1 binds to Skp1.	bind
1331	1	444	6	NULL	NULL	0	NULL	FWD1	GP		bind					Skp1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_7_3859_s_73	10097128	( A) FWD1 binds to Skp1.	bind
57968	1	445	5	NULL	NULL	0	NULL	GA	GP		bind					TfR	GP				NULL	in vitro	0	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_126	16103367	( A) GA binds TfR  in vitro.	bind
1332	1	445	6	NULL	NULL	0	NULL	GA	GP		bind					TfR	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_126	16103367	( A) GA binds TfR  in vitro.	bind
57969	1	446	5	NULL	NULL	0	NULL	GA	GP		induce					Cbl	GP	phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw70_pnas_103_30_11318_s_90	16844778	( A) GA induces Cbl tyrosine phosphorylation and PI3-kinase p85 binding to Cbl in an  Src-dependent manner.	bind
57970	2	446	5	NULL	NULL	0	NULL	PI3-kinase	GP		bind			p85		Cbl	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_30_11318_s_90	16844778	( A) GA induces Cbl tyrosine phosphorylation and PI3-kinase p85 binding to Cbl in an  Src-dependent manner.	bind
57971	3	446	5	NULL	NULL	0	NULL	GA	GP		induce					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_103_30_11318_s_90	16844778	( A) GA induces Cbl tyrosine phosphorylation and PI3-kinase p85 binding to Cbl in an  Src-dependent manner.	bind
57972	4	446	5	NULL	NULL	0	NULL	statement 1	Process		is dependent on					Src	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_30_11318_s_90	16844778	( A) GA induces Cbl tyrosine phosphorylation and PI3-kinase p85 binding to Cbl in an  Src-dependent manner.	bind
57973	5	446	5	NULL	NULL	0	NULL	statement 3	Process		is dependent on					Src	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_30_11318_s_90	16844778	( A) GA induces Cbl tyrosine phosphorylation and PI3-kinase p85 binding to Cbl in an  Src-dependent manner.	bind
1336	1	446	6	NULL	NULL	0	NULL	PI3-kinase p85	GP		bind					Cbl	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_30_11318_s_90	16844778	( A) GA induces Cbl tyrosine phosphorylation and PI3-kinase p85 binding to Cbl in an  Src-dependent manner.	bind
1337	2	446	6	NULL	NULL	0	NULL	GA	Chemical		induce					Cbl	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_30_11318_s_90	16844778	( A) GA induces Cbl tyrosine phosphorylation and PI3-kinase p85 binding to Cbl in an  Src-dependent manner.	bind
1338	3	446	6	NULL	NULL	0	NULL	GA	Chemical		induce					Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_30_11318_s_90	16844778	( A) GA induces Cbl tyrosine phosphorylation and PI3-kinase p85 binding to Cbl in an  Src-dependent manner.	bind
1339	4	446	6	NULL	NULL	0	NULL	Statement 1	Process		depend on					Src	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_30_11318_s_90	16844778	( A) GA induces Cbl tyrosine phosphorylation and PI3-kinase p85 binding to Cbl in an  Src-dependent manner.	bind
57974	1	448	5	NULL	NULL	0	NULL	GAPDH	GP		bind					Htt	GP				NULL	in vitro	0	NULL	NULL	NULL	gw70_pnas_103_9_3405_s_29	16492755	( A) GAPDH binds to Htt  in vitro.	bind
1340	1	448	6	NULL	NULL	0	NULL	GAPDH	GP		bind					Htt	GP				NULL	In vitro	NULL	NULL	NULL	NULL	gw70_pnas_103_9_3405_s_29	16492755	( A) GAPDH binds to Htt  in vitro.	bind
57978	1	449	5	NULL	NULL	0	NULL	nuclear extracts	CellComponent	zebrafish;;eye	bind					AP-1 oligonucleotides	GP	consensus			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_29_10194_s_51	16000406	( A) Gel mobility-shift assay of zebrafish eye nuclear extracts binding to consensus  AP-1 or CRE oligonucleotides.	bind
57979	2	449	5	NULL	NULL	0	NULL	nuclear extracts	CellComponent	zebrafish;;eye	bind					CRE oligonucleotides	GP	consensus			NULL		0	NULL	NULL	NULL	gw70_pnas_102_29_10194_s_51	16000406	( A) Gel mobility-shift assay of zebrafish eye nuclear extracts binding to consensus  AP-1 or CRE oligonucleotides.	bind
1341	1	449	6	NULL	NULL	0	NULL	eye nuclear extracts	OrganismPart	zebrafish	bind					consensus AP-1 oligonucleotides	NucleicAcid			site	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_29_10194_s_51	16000406	( A) Gel mobility-shift assay of zebrafish eye nuclear extracts binding to consensus  AP-1 or CRE oligonucleotides.	bind
1343	2	449	6	NULL	NULL	0	NULL	eye nuclear extracts	OrganismPart	zebrafish	bind					CRE oligonucleotides	NucleicAcid			site	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_29_10194_s_51	16000406	( A) Gel mobility-shift assay of zebrafish eye nuclear extracts binding to consensus  AP-1 or CRE oligonucleotides.	bind
57980	1	451	5	NULL	NULL	0	NULL	C/EBP	GP		bind					C/EBP-binding site	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_24_3_475_s_178	12663507	( A) Gel shift analysis of C/EBP binding to the C/EBP-binding site.	bind
1345	1	451	6	NULL	NULL	0	NULL	C/EBP	GP		bind						NucleicAcid			C/EBP-binding site	NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_24_3_475_s_178	12663507	( A) Gel shift analysis of C/EBP binding to the C/EBP-binding site.	bind
57981	1	455	5	NULL	NULL	0	NULL	ChREBP	GP		bind					LPK	GP			ChRE	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_44_15597_s_128	15496471	( A) Gel-shift analysis of ChREBP bound to ChREs of LPK, ACC1, and FAS.	bind
57982	2	455	5	NULL	NULL	0	NULL	ChREBP	GP		bind					ACC1	GP			ChRE	NULL		0	NULL	NULL	NULL	gw70_pnas_101_44_15597_s_128	15496471	( A) Gel-shift analysis of ChREBP bound to ChREs of LPK, ACC1, and FAS.	bind
57983	3	455	5	NULL	NULL	0	NULL	ChREBP	GP		bind					FAS	GP			ChRE	NULL		0	NULL	NULL	NULL	gw70_pnas_101_44_15597_s_128	15496471	( A) Gel-shift analysis of ChREBP bound to ChREs of LPK, ACC1, and FAS.	bind
1346	1	455	6	NULL	NULL	0	NULL	ChREBP	GP		bind					LPK	GP			ChRE	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_44_15597_s_128	15496471	( A) Gel-shift analysis of ChREBP bound to ChREs of LPK, ACC1, and FAS.	bind
1347	2	455	6	NULL	NULL	0	NULL	ChREBP	GP		bind					ACC1	GP			ChRE	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_44_15597_s_128	15496471	( A) Gel-shift analysis of ChREBP bound to ChREs of LPK, ACC1, and FAS.	bind
1348	3	455	6	NULL	NULL	0	NULL	ChREBP	GP		bind					FAS	GP			ChRE	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_44_15597_s_128	15496471	( A) Gel-shift analysis of ChREBP bound to ChREs of LPK, ACC1, and FAS.	bind
57984	1	458	5	NULL	NULL	0	NULL	Gic2p	GP		bind					Cdc42p-GTP	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_11_22_2972_s_66	9367980	( A) Gic2p binds to Cdc42p-GTP.	bind
1349	1	458	6	NULL	NULL	0	NULL	Gic2p	GP		bind					Cdc42p-GTP	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_22_2972_s_66	9367980	( A) Gic2p binds to Cdc42p-GTP.	bind
57985	1	459	5	NULL	NULL	0	NULL	Gp33	GP		bind					RNAP	GP		core subunits		NULL		0	NULL	NULL	NULL	gw70_pnas_101_50_17365_s_83	15574501	( A) Gp33 binding to individual RNAP core subunits.	bind
1351	1	459	6	NULL	NULL	0	NULL	Gp33	GP		bind					 RNAP 	GP		individual core subunits		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_50_17365_s_83	15574501	( A) Gp33 binding to individual RNAP core subunits.	bind
57986	1	460	5	NULL	NULL	0	NULL	GTP	Chemical		bind					heterotrimeric G proteins	GP	a subunit of			NULL		0	NULL	NULL	NULL	gw60_science_294_5548_1845_s_25	11729293	( A) GPCRs promote binding of GTP to the a subunit of heterotrimeric G proteins.	bind
57987	2	460	5	NULL	NULL	0	NULL	GPCRs	GP		promotes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_science_294_5548_1845_s_25	11729293	( A) GPCRs promote binding of GTP to the a subunit of heterotrimeric G proteins.	bind
1354	1	460	6	NULL	NULL	0	NULL	GTP	Chemical		bind					heterotrimeric G proteins	GP		subunit		NULL		NULL	NULL	NULL	NULL	gw60_science_294_5548_1845_s_25	11729293	( A) GPCRs promote binding of GTP to the a subunit of heterotrimeric G proteins.	bind
1355	2	460	6	NULL	NULL	0	NULL	GPCRs	GP		promote					Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_294_5548_1845_s_25	11729293	( A) GPCRs promote binding of GTP to the a subunit of heterotrimeric G proteins.	bind
57988	1	463	5	NULL	NULL	0	NULL	GST-Ebp1	GP		bind					HDAC	GP	activity of			NULL	Hela cells	0	NULL	NULL	NULL	gw60_nucleicacidsres_31_8_2168_s_201	12682367	( A) GST-Ebp1 binds HDAC activity from Hela cells.	bind
1356	1	463	6	NULL	NULL	0	NULL	GST-Ebp1	GP		bind					HDAC	GP				NULL	Hela cells	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_8_2168_s_201	12682367	( A) GST-Ebp1 binds HDAC activity from Hela cells.	bind
57989	1	465	5	NULL	NULL	0	NULL	stargazin	GP	point mutant	does not bind			T321F		PSD-95	GP	WT			NULL		0	NULL	NULL	NULL	gw60_pnas_99_21_13902_s_149	12359873	( A) GST-fusion proteins show that stargazin with a point mutation in its PDZ-binding region (T321F) does not bind WT PSD-95, but does bind PSD-95 bearing a compensatory point mutation (H225V) in its second PDZ domain.	bind
57990	2	465	5	NULL	NULL	0	NULL	stargazin	GP	point mutant	bind			T321F		PSD-95	GP	compensatory point mutant	H225V		NULL		0	NULL	NULL	NULL	gw60_pnas_99_21_13902_s_149	12359873	( A) GST-fusion proteins show that stargazin with a point mutation in its PDZ-binding region (T321F) does not bind WT PSD-95, but does bind PSD-95 bearing a compensatory point mutation (H225V) in its second PDZ domain.	bind
1357	1	465	6	NULL	NULL	0	NULL	stargazin	GP	mutant	does not bind			 PDZ-binding region (T321F)		PSD-95	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_21_13902_s_149	12359873	( A) GST-fusion proteins show that stargazin with a point mutation in its PDZ-binding region (T321F) does not bind WT PSD-95, but does bind PSD-95 bearing a compensatory point mutation (H225V) in its second PDZ domain.	bind
1359	2	465	6	NULL	NULL	0	NULL	stargazin	GP	mutant	bind			 PDZ-binding region (T321F)		PSD-95	GP	mutant	 PDZ domain (H225V)		NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_21_13902_s_149	12359873	( A) GST-fusion proteins show that stargazin with a point mutation in its PDZ-binding region (T321F) does not bind WT PSD-95, but does bind PSD-95 bearing a compensatory point mutation (H225V) in its second PDZ domain.	bind
57991	1	469	5	NULL	NULL	0	NULL	Hesx1	GP		bind					TLE family corepressors	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_15_23_3193_s_104	11731482	( A) Hesx1 binds TLE family corepressors.	bind
1362	1	469	6	NULL	NULL	0	NULL	Hesx1	GP		bind					TLE family corepressors	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_23_3193_s_104	11731482	( A) Hesx1 binds TLE family corepressors.	bind
57992	1	471	5	NULL	NULL	0	NULL	His6CED-9	GP		bind			(68-251; G169E)		GST-CED-4	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_11916_s_75	11027303	( A) His6CED-9(68-251; G169E) binds GST-CED-4 as well as His6CED-9(68-251).	bind
57993	2	471	5	NULL	NULL	0	NULL	His6CED-9	GP		bind			(68-251; G169E)		His6CED-9	GP		(68-251)		NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_22_11916_s_75	11027303	( A) His6CED-9(68-251; G169E) binds GST-CED-4 as well as His6CED-9(68-251).	bind
1521	1	471	6	NULL	NULL	0	NULL	His6CED-9	GP		bind			68-251; G169E		GST-CED-4	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_22_11916_s_75	11027303	( A) His6CED-9(68-251; G169E) binds GST-CED-4 as well as His6CED-9(68-251).	bind
1522	2	471	6	NULL	NULL	0	NULL	His6CED-9	GP		bind			(68-251; G169E)		His6CED-9	GP		(68-251)		NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_22_11916_s_75	11027303	( A) His6CED-9(68-251; G169E) binds GST-CED-4 as well as His6CED-9(68-251).	bind
57994	1	474	5	NULL	NULL	0	NULL	HTm4	GP		bind					KAP-CDK2	GP				NULL		0	NULL	NULL	NULL	gw60_jclininvest_109_1_51_s_186	11781350	( a) HTm4 binds to KAP-CDK2 under normal physiological conditions.	bind
1523	1	474	6	NULL	NULL	0	NULL	HTm4	GP		bind					KAP-CDK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_109_1_51_s_186	11781350	( a) HTm4 binds to KAP-CDK2 under normal physiological conditions.	bind
57995	1	475	5	NULL	NULL	0	NULL	Cds1	GP		bind					GST:Wee170	GP				NULL		0	NULL	NULL	NULL	gw60_science_280_5365_909_s_110	9572736	( A) HU stimulates Cds1 binding to GST:Wee170.	bind
57996	2	475	5	NULL	NULL	0	NULL	HU	Chemical		stimulates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_science_280_5365_909_s_110	9572736	( A) HU stimulates Cds1 binding to GST:Wee170.	bind
1524	1	475	6	NULL	NULL	0	NULL	Cds1	GP		bind					GST:Wee170	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_280_5365_909_s_110	9572736	( A) HU stimulates Cds1 binding to GST:Wee170.	bind
1525	2	475	6	NULL	NULL	0	NULL	HU	GP		stimulates					Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_280_5365_909_s_110	9572736	( A) HU stimulates Cds1 binding to GST:Wee170.	bind
57997	1	477	5	NULL	NULL	0	NULL	PABP	GP	human	does not bind			RRM2		eIF4G	GP	yeast			NULL		0	NULL	NULL	NULL	gw60_embo_18_11_3153_s_284	10357826	( A) Human PABP RRM2 cannot bind to yeast eIF4G.	bind
1526	1	477	6	NULL	NULL	0	NULL	PABP	GP	human	does not bind			RRM2		eIF4G	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_11_3153_s_284	10357826	( A) Human PABP RRM2 cannot bind to yeast eIF4G.	bind
57998	1	478	5	NULL	NULL	0	NULL	PAHX	GP	human	bind		specifically			FKBP52	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_96_5_2104_s_149	10051602	( A) Human PAHX specifically binds FKBP52  in vitro.	bind
1527	1	478	6	NULL	NULL	0	NULL	PAHX	GP	human	bind		specifically			FKBP52	GP				NULL	In vitro	NULL	NULL	NULL	NULL	gw60_pnas_96_5_2104_s_149	10051602	( A) Human PAHX specifically binds FKBP52  in vitro.	bind
57999	1	479	5	NULL	NULL	0	NULL	VHL	GP	human	bind					peptide substrates	GP	hydroxylated			NULL		0	NULL	NULL	NULL	gw60_science_294_5545_1337_s_80	11598268	( A) Human VHL binds to all hydroxylated peptide substrates.	bind
1528	1	479	6	NULL	NULL	0	NULL	VHL	GP	human	bind					peptide substrate	GP	hydroxylated			NULL		NULL	NULL	NULL	NULL	gw60_science_294_5545_1337_s_80	11598268	( A) Human VHL binds to all hydroxylated peptide substrates.	bind
58000	1	486	5	NULL	NULL	0	NULL				bind				IGR	Clr3-myc/high H3K14Ac	GP				NULL	clr3delta	NULL	NULL	NULL	NULL	gw70_embo_24_16_2906_s_181	16079916	( A) IGR binding of Clr3-myc/high H3K14Ac in  clr3delta; ( B) ORF binding of Clr3-myc high H3K14Ac in  clr3delta; ( C) IGR binding of Sir2-myc/H3K9Ac in  sir2delta; ( D) ORF binding of Sir2-myc/high H3K9Ac in  sir2delta.	bind
58001	2	486	5	NULL	NULL	0	NULL				bind				ORF	Clr3-myc high H3K14Ac	GP				NULL	clr3delta	NULL	NULL	NULL	NULL	gw70_embo_24_16_2906_s_181	16079916	( A) IGR binding of Clr3-myc/high H3K14Ac in  clr3delta; ( B) ORF binding of Clr3-myc high H3K14Ac in  clr3delta; ( C) IGR binding of Sir2-myc/H3K9Ac in  sir2delta; ( D) ORF binding of Sir2-myc/high H3K9Ac in  sir2delta.	bind
58002	3	486	5	NULL	NULL	0	NULL				bind				IGR	Sir2-myc/H3K9Ac	GP				NULL	sir2delta	0	NULL	NULL	NULL	gw70_embo_24_16_2906_s_181	16079916	( A) IGR binding of Clr3-myc/high H3K14Ac in  clr3delta; ( B) ORF binding of Clr3-myc high H3K14Ac in  clr3delta; ( C) IGR binding of Sir2-myc/H3K9Ac in  sir2delta; ( D) ORF binding of Sir2-myc/high H3K9Ac in  sir2delta.	bind
58003	4	486	5	NULL	NULL	0	NULL				bind				ORF	Sir2-myc/high H3K9Ac	GP				NULL	sir2delta	0	NULL	NULL	NULL	gw70_embo_24_16_2906_s_181	16079916	( A) IGR binding of Clr3-myc/high H3K14Ac in  clr3delta; ( B) ORF binding of Clr3-myc high H3K14Ac in  clr3delta; ( C) IGR binding of Sir2-myc/H3K9Ac in  sir2delta; ( D) ORF binding of Sir2-myc/high H3K9Ac in  sir2delta.	bind
1529	1	486	6	NULL	NULL	0	NULL		NucleicAcid		bind				IGR	Clr3-myc/high H3K14Ac	GP				NULL	clr3delta	NULL	NULL	NULL	NULL	gw70_embo_24_16_2906_s_181	16079916	( A) IGR binding of Clr3-myc/high H3K14Ac in  clr3delta; ( B) ORF binding of Clr3-myc high H3K14Ac in  clr3delta; ( C) IGR binding of Sir2-myc/H3K9Ac in  sir2delta; ( D) ORF binding of Sir2-myc/high H3K9Ac in  sir2delta.	bind
1530	2	486	6	NULL	NULL	0	NULL		NucleicAcid		bind				ORF	Clr3-myc high H3K14Ac	GP				NULL	clr3delta	NULL	NULL	NULL	NULL	gw70_embo_24_16_2906_s_181	16079916	( A) IGR binding of Clr3-myc/high H3K14Ac in  clr3delta; ( B) ORF binding of Clr3-myc high H3K14Ac in  clr3delta; ( C) IGR binding of Sir2-myc/H3K9Ac in  sir2delta; ( D) ORF binding of Sir2-myc/high H3K9Ac in  sir2delta.	bind
1531	3	486	6	NULL	NULL	0	NULL		NucleicAcid		bind				IGR	Sir2-myc/H3K9Ac	GP				NULL	sir2delta	NULL	NULL	NULL	NULL	gw70_embo_24_16_2906_s_181	16079916	( A) IGR binding of Clr3-myc/high H3K14Ac in  clr3delta; ( B) ORF binding of Clr3-myc high H3K14Ac in  clr3delta; ( C) IGR binding of Sir2-myc/H3K9Ac in  sir2delta; ( D) ORF binding of Sir2-myc/high H3K9Ac in  sir2delta.	bind
1532	4	486	6	NULL	NULL	0	NULL		NucleicAcid		bind				ORF	Sir2-myc/high H3K9Ac	GP				NULL	sir2delta	NULL	NULL	NULL	NULL	gw70_embo_24_16_2906_s_181	16079916	( A) IGR binding of Clr3-myc/high H3K14Ac in  clr3delta; ( B) ORF binding of Clr3-myc high H3K14Ac in  clr3delta; ( C) IGR binding of Sir2-myc/H3K9Ac in  sir2delta; ( D) ORF binding of Sir2-myc/high H3K9Ac in  sir2delta.	bind
58004	1	487	5	NULL	NULL	0	NULL	clathrin-adaptor	GP		bind					GST-CI-MPR	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_16_9047_s_97	10908666	( A) Immunoblot analysis of clathrin-adaptor binding to GST-CI-MPR constructs confirms the recognition of tyrosine and/or dileucine motifs by AP-1 and AP-2.	bind
58005	2	487	5	NULL	NULL	0	NULL	AP-1	GP		recognizes								tyrosine;;dileucine motifs		NULL		0	NULL	NULL	NULL	gw60_pnas_97_16_9047_s_97	10908666	( A) Immunoblot analysis of clathrin-adaptor binding to GST-CI-MPR constructs confirms the recognition of tyrosine and/or dileucine motifs by AP-1 and AP-2.	bind
58006	3	487	5	NULL	NULL	0	NULL	AP-2	GP		recognizes								tyrosine;;dileucine motifs		NULL		0	NULL	NULL	NULL	gw60_pnas_97_16_9047_s_97	10908666	( A) Immunoblot analysis of clathrin-adaptor binding to GST-CI-MPR constructs confirms the recognition of tyrosine and/or dileucine motifs by AP-1 and AP-2.	bind
58007	4	487	5	NULL	NULL	0	NULL	statement 1	Process		confirms					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_97_16_9047_s_97	10908666	( A) Immunoblot analysis of clathrin-adaptor binding to GST-CI-MPR constructs confirms the recognition of tyrosine and/or dileucine motifs by AP-1 and AP-2.	bind
58008	5	487	5	NULL	NULL	0	NULL	statement 1	Process		confirms					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_97_16_9047_s_97	10908666	( A) Immunoblot analysis of clathrin-adaptor binding to GST-CI-MPR constructs confirms the recognition of tyrosine and/or dileucine motifs by AP-1 and AP-2.	bind
1533	1	487	6	NULL	NULL	0	NULL	clathrin-adaptor 	GP		bind					GST-CI-MPR	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_16_9047_s_97	10908666	( A) Immunoblot analysis of clathrin-adaptor binding to GST-CI-MPR constructs confirms the recognition of tyrosine and/or dileucine motifs by AP-1 and AP-2.	bind
1534	2	487	6	NULL	NULL	0	NULL	AP1	GP		recognizes						AminoAcid		tyrosine and/or dileucine motifs		NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_16_9047_s_97	10908666	( A) Immunoblot analysis of clathrin-adaptor binding to GST-CI-MPR constructs confirms the recognition of tyrosine and/or dileucine motifs by AP-1 and AP-2.	bind
1535	3	487	6	NULL	NULL	0	NULL	AP2	GP		recognizes						AminoAcid		tyrosine and/or dileucine motifs		NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_16_9047_s_97	10908666	( A) Immunoblot analysis of clathrin-adaptor binding to GST-CI-MPR constructs confirms the recognition of tyrosine and/or dileucine motifs by AP-1 and AP-2.	bind
1536	4	487	6	NULL	NULL	0	NULL	Statement 1	Process		confirms					Statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_16_9047_s_97	10908666	( A) Immunoblot analysis of clathrin-adaptor binding to GST-CI-MPR constructs confirms the recognition of tyrosine and/or dileucine motifs by AP-1 and AP-2.	bind
1537	5	487	6	NULL	NULL	0	NULL	Statement 1	Process		confirms					Statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_16_9047_s_97	10908666	( A) Immunoblot analysis of clathrin-adaptor binding to GST-CI-MPR constructs confirms the recognition of tyrosine and/or dileucine motifs by AP-1 and AP-2.	bind
58009	1	491	5	NULL	NULL	0	NULL	gD	GP	soluble	bind					GST-PFD	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_102_26_9323_s_166	15972328	( A) Immunoblots of soluble forms of gD bound by GST-PFD fusion proteins.	bind
58010	2	491	5	NULL	NULL	0	NULL	GST-PFD	GP		is a type of					fusion protein	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_102_26_9323_s_166	15972328	( A) Immunoblots of soluble forms of gD bound by GST-PFD fusion proteins.	bind
1538	1	491	6	NULL	NULL	0	NULL	gD	GP	soluble	bind					GST-PFD	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_26_9323_s_166	15972328	( A) Immunoblots of soluble forms of gD bound by GST-PFD fusion proteins.	bind
51782	2	491	6	NULL	NULL	0	NULL	GST-PFD	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_26_9323_s_166	15972328	( A) Immunoblots of soluble forms of gD bound by GST-PFD fusion proteins.	bind
58011	1	492	5	NULL	NULL	0	NULL	calstabin2	GP		bind			D37V		RyR2	GP		S2808D		NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_73	16481613	( A) Immunoblots showing that calstabin2 - D37V bound to RyR2 - S2808D (which mimics  chronically PKA-phosphorylated RyR2), whereas WT calstabin2 and mutants F36Y and  F99Y did not.	bind
58012	2	492	5	NULL	NULL	0	NULL	calstabin2	GP	WT	does not bind					RyR2	GP		S2808D		NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_73	16481613	( A) Immunoblots showing that calstabin2 - D37V bound to RyR2 - S2808D (which mimics  chronically PKA-phosphorylated RyR2), whereas WT calstabin2 and mutants F36Y and  F99Y did not.	bind
58013	3	492	5	NULL	NULL	0	NULL	calstabin2	GP	mutant	does not bind			F36Y 		RyR2	GP		S2808D		NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_73	16481613	( A) Immunoblots showing that calstabin2 - D37V bound to RyR2 - S2808D (which mimics  chronically PKA-phosphorylated RyR2), whereas WT calstabin2 and mutants F36Y and  F99Y did not.	bind
58014	4	492	5	NULL	NULL	0	NULL	calstabin2	GP	mutant	does not bind			F99Y		RyR2	GP		S2808D		NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_73	16481613	( A) Immunoblots showing that calstabin2 - D37V bound to RyR2 - S2808D (which mimics  chronically PKA-phosphorylated RyR2), whereas WT calstabin2 and mutants F36Y and  F99Y did not.	bind
58015	5	492	5	NULL	NULL	0	NULL	PKA	GP		phosphorylates					RyR2	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_73	16481613	( A) Immunoblots showing that calstabin2 - D37V bound to RyR2 - S2808D (which mimics  chronically PKA-phosphorylated RyR2), whereas WT calstabin2 and mutants F36Y and  F99Y did not.	bind
58016	6	492	5	NULL	NULL	0	NULL	RyR2	GP		mimics		chronically	S2808D		statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_73	16481613	( A) Immunoblots showing that calstabin2 - D37V bound to RyR2 - S2808D (which mimics  chronically PKA-phosphorylated RyR2), whereas WT calstabin2 and mutants F36Y and  F99Y did not.	bind
1539	1	492	6	NULL	NULL	0	NULL	calstabin2	GP		bind			D37V		RyR2	GP		S2808D		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_73	16481613	( A) Immunoblots showing that calstabin2 - D37V bound to RyR2 - S2808D (which mimics  chronically PKA-phosphorylated RyR2), whereas WT calstabin2 and mutants F36Y and  F99Y did not.	bind
1540	2	492	6	NULL	NULL	0	NULL	calstabin2	GP	wild type	does not bind					RyR2	GP		S2808D		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_73	16481613	( A) Immunoblots showing that calstabin2 - D37V bound to RyR2 - S2808D (which mimics  chronically PKA-phosphorylated RyR2), whereas WT calstabin2 and mutants F36Y and  F99Y did not.	bind
1541	3	492	6	NULL	NULL	0	NULL	calstabin2	GP	mutant	does not bind			F36Y		RyR2	GP		S2808D		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_73	16481613	( A) Immunoblots showing that calstabin2 - D37V bound to RyR2 - S2808D (which mimics  chronically PKA-phosphorylated RyR2), whereas WT calstabin2 and mutants F36Y and  F99Y did not.	bind
1542	4	492	6	NULL	NULL	0	NULL	calstabin2	GP	mutant	does not bind			F99Y		RyR2	GP		S2808D		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_73	16481613	( A) Immunoblots showing that calstabin2 - D37V bound to RyR2 - S2808D (which mimics  chronically PKA-phosphorylated RyR2), whereas WT calstabin2 and mutants F36Y and  F99Y did not.	bind
1543	6	492	6	NULL	NULL	0	NULL	RyR2	GP		mimics 		chronically	S2808D		statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_73	16481613	( A) Immunoblots showing that calstabin2 - D37V bound to RyR2 - S2808D (which mimics  chronically PKA-phosphorylated RyR2), whereas WT calstabin2 and mutants F36Y and  F99Y did not.	bind
51783	5	492	6	NULL	NULL	0	NULL	PKA	GP		phosphorylate					RyR2	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_73	16481613	( A) Immunoblots showing that calstabin2 - D37V bound to RyR2 - S2808D (which mimics  chronically PKA-phosphorylated RyR2), whereas WT calstabin2 and mutants F36Y and  F99Y did not.	bind
58017	1	494	5	NULL	NULL	0	NULL	SecA	GP	cytoplasmic				C-domain		SecA	GP	cytoplasmic	N-domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13724_s_342	11825907	( a) In cytoplasmic SecA, binding of the C-domain to the N-domain represses both ATP hydrolysis and preprotein binding.	bind
58018	2	494	5	NULL	NULL	0	NULL	statement 1	Process		repress					ATP hydrolysis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13724_s_342	11825907	( a) In cytoplasmic SecA, binding of the C-domain to the N-domain represses both ATP hydrolysis and preprotein binding.	bind
58019	3	494	5	NULL	NULL	0	NULL	statement 1	Process		repress					preprotein binding	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13724_s_342	11825907	( a) In cytoplasmic SecA, binding of the C-domain to the N-domain represses both ATP hydrolysis and preprotein binding.	bind
1544	1	494	6	NULL	NULL	0	NULL		AminoAcid		bind			C-domain			AminoAcid		N-domain		NULL	cytoplasmic SecA	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13724_s_342	11825907	( a) In cytoplasmic SecA, binding of the C-domain to the N-domain represses both ATP hydrolysis and preprotein binding.	bind
1545	2	494	6	NULL	NULL	0	NULL	Statement 1	Process		repress					ATP	Chemical	hydrolysis of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13724_s_342	11825907	( a) In cytoplasmic SecA, binding of the C-domain to the N-domain represses both ATP hydrolysis and preprotein binding.	bind
1546	3	494	6	NULL	NULL	0	NULL	Statement 1	Process		repress					preprotein	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13724_s_342	11825907	( a) In cytoplasmic SecA, binding of the C-domain to the N-domain represses both ATP hydrolysis and preprotein binding.	bind
58020	1	496	5	NULL	NULL	0	NULL	adenosine nucleotide	NucleicAcid		bind					NifL	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_46_16316_s_182	15534211	( A) In the absence of 2-oxoglutarate, both the reduced and oxidized forms of NifL inhibit  the activity of NifA, provided that adenosine nucleotide is bound to NifL ( ,  ,  ).	bind
58021	2	496	5	NULL	NULL	0	NULL	NifL	GP	oxidized	inhibits					NifA	GP	activity of			NULL		0	NULL	NULL	NULL	gw70_pnas_101_46_16316_s_182	15534211	( A) In the absence of 2-oxoglutarate, both the reduced and oxidized forms of NifL inhibit  the activity of NifA, provided that adenosine nucleotide is bound to NifL ( ,  ,  ).	bind
58022	3	496	5	NULL	NULL	0	NULL	statement 2	Process		in the absence of					2-oxoglutarate	Chemical				NULL		0	NULL	NULL	NULL	gw70_pnas_101_46_16316_s_182	15534211	( A) In the absence of 2-oxoglutarate, both the reduced and oxidized forms of NifL inhibit  the activity of NifA, provided that adenosine nucleotide is bound to NifL ( ,  ,  ).	bind
58023	4	496	5	NULL	NULL	0	NULL	NifL	GP	reduced	inhibit					NifA	GP	activity of			NULL		0	NULL	NULL	NULL	gw70_pnas_101_46_16316_s_182	15534211	( A) In the absence of 2-oxoglutarate, both the reduced and oxidized forms of NifL inhibit  the activity of NifA, provided that adenosine nucleotide is bound to NifL ( ,  ,  ).	bind
58024	5	496	5	NULL	NULL	0	NULL	statement 4	Process		in the absence of					2-oxoglutarate	Chemical				NULL		0	NULL	NULL	NULL	gw70_pnas_101_46_16316_s_182	15534211	( A) In the absence of 2-oxoglutarate, both the reduced and oxidized forms of NifL inhibit  the activity of NifA, provided that adenosine nucleotide is bound to NifL ( ,  ,  ).	bind
58025	6	496	5	NULL	NULL	0	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_46_16316_s_182	15534211	( A) In the absence of 2-oxoglutarate, both the reduced and oxidized forms of NifL inhibit  the activity of NifA, provided that adenosine nucleotide is bound to NifL ( ,  ,  ).	bind
58026	7	496	5	NULL	NULL	0	NULL	statement 1	Process		leads to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_46_16316_s_182	15534211	( A) In the absence of 2-oxoglutarate, both the reduced and oxidized forms of NifL inhibit  the activity of NifA, provided that adenosine nucleotide is bound to NifL ( ,  ,  ).	bind
1551	1	496	6	NULL	NULL	0	NULL	adenosine nucleotide	NucleicAcid		bind					NifL	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_46_16316_s_182	15534211	( A) In the absence of 2-oxoglutarate, both the reduced and oxidized forms of NifL inhibit  the activity of NifA, provided that adenosine nucleotide is bound to NifL ( ,  ,  ).	bind
1552	3	496	6	NULL	NULL	0	NULL	NifL	GP	reduced	inhibit 					NifA	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_46_16316_s_182	15534211	( A) In the absence of 2-oxoglutarate, both the reduced and oxidized forms of NifL inhibit  the activity of NifA, provided that adenosine nucleotide is bound to NifL ( ,  ,  ).	bind
1553	2	496	6	NULL	NULL	0	NULL	NifL	GP	oxidized	inhibit					NifA	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_46_16316_s_182	15534211	( A) In the absence of 2-oxoglutarate, both the reduced and oxidized forms of NifL inhibit  the activity of NifA, provided that adenosine nucleotide is bound to NifL ( ,  ,  ).	bind
1582	4	496	6	NULL	NULL	0	NULL	statement 2	Process		occurs in absence of					2-oxoglutarate	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_46_16316_s_182	15534211	( A) In the absence of 2-oxoglutarate, both the reduced and oxidized forms of NifL inhibit  the activity of NifA, provided that adenosine nucleotide is bound to NifL ( ,  ,  ).	bind
1589	5	496	6	NULL	NULL	0	NULL	Statement 3	Process		occurs in absence of					2-oxoglutarate	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_46_16316_s_182	15534211	( A) In the absence of 2-oxoglutarate, both the reduced and oxidized forms of NifL inhibit  the activity of NifA, provided that adenosine nucleotide is bound to NifL ( ,  ,  ).	bind
1593	6	496	6	NULL	NULL	0	NULL	statement 2	Process		dependent on					Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_46_16316_s_182	15534211	( A) In the absence of 2-oxoglutarate, both the reduced and oxidized forms of NifL inhibit  the activity of NifA, provided that adenosine nucleotide is bound to NifL ( ,  ,  ).	bind
1594	7	496	6	NULL	NULL	0	NULL	Statement 3	Process		dependent on					Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_46_16316_s_182	15534211	( A) In the absence of 2-oxoglutarate, both the reduced and oxidized forms of NifL inhibit  the activity of NifA, provided that adenosine nucleotide is bound to NifL ( ,  ,  ).	bind
58027	1	498	5	NULL	NULL	0	NULL	GST-BAK	GP		bind					BCL-XL	GP	IVT			NULL	in vitro	0	NULL	NULL	NULL	gw60_genesdev_14_16_2060_s_136	10950869	( A) In vitro binding between GST-BAK and IVT BCL-XL, p15 BID, and BIDalpha345/TM, but not p15 BID mIII.4 or BIDalpha345/TM mIII.4 (lanes  1-5).	bind
58028	2	498	5	NULL	NULL	0	NULL	GST-BAK	GP		bind					p15 BID	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_14_16_2060_s_136	10950869	( A) In vitro binding between GST-BAK and IVT BCL-XL, p15 BID, and BIDalpha345/TM, but not p15 BID mIII.4 or BIDalpha345/TM mIII.4 (lanes  1-5).	bind
58029	3	498	5	NULL	NULL	0	NULL	GST-BAK	GP		bind					BIDalpha345/TM	GP				NULL	in vitro	0	NULL	NULL	NULL	gw60_genesdev_14_16_2060_s_136	10950869	( A) In vitro binding between GST-BAK and IVT BCL-XL, p15 BID, and BIDalpha345/TM, but not p15 BID mIII.4 or BIDalpha345/TM mIII.4 (lanes  1-5).	bind
58030	4	498	5	NULL	NULL	0	NULL	GST-BAK	GP		does not bind					p15 BID mIII.4	GP				NULL	in vitro	0	NULL	NULL	NULL	gw60_genesdev_14_16_2060_s_136	10950869	( A) In vitro binding between GST-BAK and IVT BCL-XL, p15 BID, and BIDalpha345/TM, but not p15 BID mIII.4 or BIDalpha345/TM mIII.4 (lanes  1-5).	bind
58031	5	498	5	NULL	NULL	0	NULL	GST-BAK	GP		does not bind					BIDalpha345/TM mIII.4	GP				NULL	in vitro	0	NULL	NULL	NULL	gw60_genesdev_14_16_2060_s_136	10950869	( A) In vitro binding between GST-BAK and IVT BCL-XL, p15 BID, and BIDalpha345/TM, but not p15 BID mIII.4 or BIDalpha345/TM mIII.4 (lanes  1-5).	bind
1895	1	498	6	NULL	NULL	0	NULL	GST-BAK	GP		bind					BCL-XL	GP	IVT			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_14_16_2060_s_136	10950869	( A) In vitro binding between GST-BAK and IVT BCL-XL, p15 BID, and BIDalpha345/TM, but not p15 BID mIII.4 or BIDalpha345/TM mIII.4 (lanes  1-5).	bind
1896	2	498	6	NULL	NULL	0	NULL	GST-BAK	GP		bind					p15 BID	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_14_16_2060_s_136	10950869	( A) In vitro binding between GST-BAK and IVT BCL-XL, p15 BID, and BIDalpha345/TM, but not p15 BID mIII.4 or BIDalpha345/TM mIII.4 (lanes  1-5).	bind
1897	3	498	6	NULL	NULL	0	NULL	GST-BAK	GP		bind					BIDalpha345/TM	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_14_16_2060_s_136	10950869	( A) In vitro binding between GST-BAK and IVT BCL-XL, p15 BID, and BIDalpha345/TM, but not p15 BID mIII.4 or BIDalpha345/TM mIII.4 (lanes  1-5).	bind
1898	4	498	6	NULL	NULL	0	NULL	GST-BAK	GP		does not bind					p15 BID mIII.4	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_14_16_2060_s_136	10950869	( A) In vitro binding between GST-BAK and IVT BCL-XL, p15 BID, and BIDalpha345/TM, but not p15 BID mIII.4 or BIDalpha345/TM mIII.4 (lanes  1-5).	bind
1899	5	498	6	NULL	NULL	0	NULL	GST-BAK	GP		does not bind					BIDalpha345/TM mIII.4	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_14_16_2060_s_136	10950869	( A) In vitro binding between GST-BAK and IVT BCL-XL, p15 BID, and BIDalpha345/TM, but not p15 BID mIII.4 or BIDalpha345/TM mIII.4 (lanes  1-5).	bind
58032	1	499	5	NULL	NULL	0	NULL	Eps15	GP		bind					EH-binding proteins	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_11_17_2239_s_102	9303539	( A) In vitro binding of Eps15 to Gst fusions of EH-binding proteins.	bind
58033	2	499	5	NULL	NULL	0	NULL	EH-binding proteins	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_17_2239_s_102	9303539	( A) In vitro binding of Eps15 to Gst fusions of EH-binding proteins.	bind
1596	1	499	6	NULL	NULL	0	NULL	Eps15	GP		bind					EH-binding proteins	GP				NULL	In vitro	NULL	NULL	NULL	NULL	gw60_genesdev_11_17_2239_s_102	9303539	( A) In vitro binding of Eps15 to Gst fusions of EH-binding proteins.	bind
58034	1	500	5	NULL	NULL	0	NULL	Trn2	GP		is					transportin 2	GP				NULL		0	NULL	NULL	NULL	gw60_science_294_5548_1895_s_152	11729309	( A) In vitro binding of transportin 2 (Trn2)  to HuR is mediated by HNS.	bind
58035	2	500	5	NULL	NULL	0	NULL	Trn2	GP		bind					HuR	GP				NULL	in vitro	0	NULL	NULL	NULL	gw60_science_294_5548_1895_s_152	11729309	( A) In vitro binding of transportin 2 (Trn2)  to HuR is mediated by HNS.	bind
58036	3	500	5	NULL	NULL	0	NULL	statement 1	Process		is mediated by					HNS	GP				NULL	in vitro	0	NULL	NULL	NULL	gw60_science_294_5548_1895_s_152	11729309	( A) In vitro binding of transportin 2 (Trn2)  to HuR is mediated by HNS.	bind
1620	1	500	6	NULL	NULL	0	NULL	Trn2	GP		bind					HuR	GP				NULL	In vitro	NULL	NULL	NULL	NULL	gw60_science_294_5548_1895_s_152	11729309	( A) In vitro binding of transportin 2 (Trn2)  to HuR is mediated by HNS.	bind
1621	2	500	6	NULL	NULL	0	NULL	HNS	AminoAcid		mediates					Statement 1					NULL		NULL	NULL	NULL	NULL	gw60_science_294_5548_1895_s_152	11729309	( A) In vitro binding of transportin 2 (Trn2)  to HuR is mediated by HNS.	bind
51786	3	500	6	10	NULL	0	NULL	Trn2	NULL		is	NULL				transportin 2	NULL				NULL		0	NULL	NULL	NULL	gw60_science_294_5548_1895_s_152	11729309	( A) In vitro binding of transportin 2 (Trn2)  to HuR is mediated by HNS.	bind
58037	1	503	5	NULL	NULL	0	NULL	GRIP1	GP		bind			NID		TRbeta	GP		LBD		NULL		0	NULL	NULL	NULL	gw60_genesdev_12_21_3343_s_139	9808622	( a) Individual leucine residues of the LxxLL motif are crucial for binding of GRIP1 NID to TRbeta LBD.	bind
58038	2	503	5	NULL	NULL	0	NULL				is crucial for			leucine residues of the LxxLL motif		statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_21_3343_s_139	9808622	( a) Individual leucine residues of the LxxLL motif are crucial for binding of GRIP1 NID to TRbeta LBD.	bind
1622	1	503	6	NULL	NULL	0	NULL	GRIP1	GP		bind			NID		TRbeta	GP		LBD		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_21_3343_s_139	9808622	( a) Individual leucine residues of the LxxLL motif are crucial for binding of GRIP1 NID to TRbeta LBD.	bind
1623	2	503	6	NULL	NULL	0	NULL	 	AminoAcid		are crucial for			leucine residues of the LxxLL motif		Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_21_3343_s_139	9808622	( a) Individual leucine residues of the LxxLL motif are crucial for binding of GRIP1 NID to TRbeta LBD.	bind
58039	1	507	5	NULL	NULL	0	NULL	Mlc	GP		bind					target DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_embo_20_3_491_s_131	11157755	( A) Inhibition of Mlc binding to its target DNA by dephosphorylated EIICBGlc.	bind
58040	2	507	5	NULL	NULL	0	NULL	EIICBGlc	GP	dephosphorylated	inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_embo_20_3_491_s_131	11157755	( A) Inhibition of Mlc binding to its target DNA by dephosphorylated EIICBGlc.	bind
1624	1	507	6	NULL	NULL	0	NULL	Mlc	GP		bind					target DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_491_s_131	11157755	( A) Inhibition of Mlc binding to its target DNA by dephosphorylated EIICBGlc.	bind
1625	2	507	6	NULL	NULL	0	NULL	EIICBGlc	GP	dephosphorylated	inhibits					Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_491_s_131	11157755	( A) Inhibition of Mlc binding to its target DNA by dephosphorylated EIICBGlc.	bind
58041	1	508	5	NULL	NULL	0	NULL	STAT5	GP		bind					DNA	NucleicAcid				NULL	transfected D10 clone	NULL	NULL	NULL	NULL	gw60_science_283_5399_222_s_145	9880255	( A) Inhibition of STAT5-DNA binding by  FLAG STAT5 Y694F in a transfected D10 clone.	bind
58042	2	508	5	NULL	NULL	0	NULL	STAT5	GP	FLAG-tagged	inhibits			Y694F		statement 1	Process				NULL	transfected D10 clone	0	NULL	NULL	NULL	gw60_science_283_5399_222_s_145	9880255	( A) Inhibition of STAT5-DNA binding by  FLAG STAT5 Y694F in a transfected D10 clone.	bind
1626	1	508	6	NULL	NULL	0	NULL	STAT5	GP		bind					DNA	NucleicAcid				NULL	transfected D10 clone	NULL	NULL	NULL	NULL	gw60_science_283_5399_222_s_145	9880255	( A) Inhibition of STAT5-DNA binding by  FLAG STAT5 Y694F in a transfected D10 clone.	bind
1627	2	508	6	NULL	NULL	0	NULL	STAT5	GP		inhibit			y694F		statement1	Process				NULL	transfected D10 clone	NULL	NULL	NULL	NULL	gw60_science_283_5399_222_s_145	9880255	( A) Inhibition of STAT5-DNA binding by  FLAG STAT5 Y694F in a transfected D10 clone.	bind
58043	1	510	5	NULL	NULL	0	NULL	IpaA	GP		bind					vinculin	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5853_s_292	10545097	( A) IpaA binds to vinculin and leads to a conformational change of vinculin (arrow 1).	bind
58044	2	510	5	NULL	NULL	0	NULL	statement 1	Process		changes					vinculin	GP	conformation of			NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5853_s_292	10545097	( A) IpaA binds to vinculin and leads to a conformational change of vinculin (arrow 1).	bind
1628	1	510	6	NULL	NULL	0	NULL	IpaA	GP		bind					vinculin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_5853_s_292	10545097	( A) IpaA binds to vinculin and leads to a conformational change of vinculin (arrow 1).	bind
1629	2	510	6	NULL	NULL	0	NULL	Statement 1	Process		leads to					vinculin	GP	conformational change of			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_5853_s_292	10545097	( A) IpaA binds to vinculin and leads to a conformational change of vinculin (arrow 1).	bind
58045	1	511	5	NULL	NULL	0	NULL				does not bind			K145E ( spt15-640)		Mot1	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_23_6662_s_158	10581240	( A) K145E ( spt15-640) fails to bind Mot1.	bind
1630	1	511	6	NULL	NULL	0	NULL		AminoAcid		fails to bind			K145E ( spt15-640)		Mot1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6662_s_158	10581240	( A) K145E ( spt15-640) fails to bind Mot1.	bind
58046	1	512	5	NULL	NULL	0	NULL	GST-PDZ1	GP		bind					CFTR	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_98_3_1300_s_137	11158634	( A) Kinetic-response data for GST-PDZ1 binding to CFTR.	bind
1631	1	512	6	NULL	NULL	0	NULL	GST-PDZ1	GP		bind					CFTR	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_3_1300_s_137	11158634	( A) Kinetic-response data for GST-PDZ1 binding to CFTR.	bind
58047	1	513	5	NULL	NULL	0	NULL	NCp	GP		bind					T-ODN1	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_19_5754_s_85	14500839	( A) Kinetics of NCp binding to T-ODN1 with no added constituents.	bind
1632	1	513	6	NULL	NULL	0	NULL	NCp	GP		bind					T-ODN1	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_19_5754_s_85	14500839	( A) Kinetics of NCp binding to T-ODN1 with no added constituents.	bind
58048	1	514	5	NULL	NULL	0	NULL	PTH	GP		bind			(1-34)TMR		GFPN-PTHR	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_102_44_16084_s_123	16236727	( A) Kinetics of PTH(1-34)TMR binding to GFPN-PTHR recorded by decreases in the fluorescence emission of the GFP moiety.	bind
1633	1	514	6	NULL	NULL	0	NULL	PTH-TMR	GP		bind			1-34		GFPN-PTHR	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_44_16084_s_123	16236727	( A) Kinetics of PTH(1-34)TMR binding to GFPN-PTHR recorded by decreases in the fluorescence emission of the GFP moiety.	bind
58049	1	515	5	NULL	NULL	0	NULL	Ste5	GP		bind					Ste4	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_13_2564_s_108	15192700	( A) Kss1 activation is dependent on Ste5 binding to Ste4 and Ste11.	bind
58050	2	515	5	NULL	NULL	0	NULL	Ste5	GP		bind					Ste11	GP				NULL		0	NULL	NULL	NULL	gw70_embo_23_13_2564_s_108	15192700	( A) Kss1 activation is dependent on Ste5 binding to Ste4 and Ste11.	bind
58051	3	515	5	NULL	NULL	0	NULL	Kss1	GP	activation of	is dependent on					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_embo_23_13_2564_s_108	15192700	( A) Kss1 activation is dependent on Ste5 binding to Ste4 and Ste11.	bind
58052	4	515	5	NULL	NULL	0	NULL	Kss1	GP	activation of	is dependent on					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_embo_23_13_2564_s_108	15192700	( A) Kss1 activation is dependent on Ste5 binding to Ste4 and Ste11.	bind
1634	1	515	6	NULL	NULL	0	NULL	Ste5	GP		bind					Ste4	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_13_2564_s_108	15192700	( A) Kss1 activation is dependent on Ste5 binding to Ste4 and Ste11.	bind
1635	2	515	6	NULL	NULL	0	NULL	Ste5	GP		bind					Ste11	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_13_2564_s_108	15192700	( A) Kss1 activation is dependent on Ste5 binding to Ste4 and Ste11.	bind
1637	3	515	6	NULL	NULL	0	NULL	Kss1	GP	activation of	is dependent on					Statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_13_2564_s_108	15192700	( A) Kss1 activation is dependent on Ste5 binding to Ste4 and Ste11.	bind
58053	1	517	5	NULL	NULL	0	NULL	Lef-1	GP		bind					siamois	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_genesdev_11_18_2359_s_119	9308964	( A) Lef-1 binding to the  siamois promoter is competed by an oligonucleotide containing a consensus Lef/Tcf-binding site.	bind
58054	2	517	5	NULL	NULL	0	NULL	oligonucleotide	NucleicAcid		contains							consensus		Lef/Tcf-binding site	NULL		0	NULL	NULL	NULL	gw60_genesdev_11_18_2359_s_119	9308964	( A) Lef-1 binding to the  siamois promoter is competed by an oligonucleotide containing a consensus Lef/Tcf-binding site.	bind
58055	3	517	5	NULL	NULL	0	NULL	statement 2	NucleicAcid		bind					siamois	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_genesdev_11_18_2359_s_119	9308964	( A) Lef-1 binding to the  siamois promoter is competed by an oligonucleotide containing a consensus Lef/Tcf-binding site.	bind
58056	4	517	5	NULL	NULL	0	NULL	statement 3	Process		competes with					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_genesdev_11_18_2359_s_119	9308964	( A) Lef-1 binding to the  siamois promoter is competed by an oligonucleotide containing a consensus Lef/Tcf-binding site.	bind
1638	1	517	6	NULL	NULL	0	NULL	Lef-1	GP		bind					Siamois	GP			Promoter	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_18_2359_s_119	9308964	( A) Lef-1 binding to the  siamois promoter is competed by an oligonucleotide containing a consensus Lef/Tcf-binding site.	bind
1639	2	517	6	NULL	NULL	0	NULL	oligonucleotide	NucleicAcid		bind				consensus Lef/Tcf-binding site	Siamois	GP			Promoter	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_18_2359_s_119	9308964	( A) Lef-1 binding to the  siamois promoter is competed by an oligonucleotide containing a consensus Lef/Tcf-binding site.	bind
51787	3	517	6	NULL	NULL	0	NULL	statement 1	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_18_2359_s_119	9308964	( A) Lef-1 binding to the  siamois promoter is competed by an oligonucleotide containing a consensus Lef/Tcf-binding site.	bind
58057	1	520	5	NULL	NULL	0	NULL	LPS	GP		bind					Hsp 90	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_10_5645_s_131	10318938	( A) LPS binds Hsp 90 but not ovalbumin.	bind
58058	2	520	5	NULL	NULL	0	NULL	LPS	GP		does not bind					ovalbumin	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_10_5645_s_131	10318938	( A) LPS binds Hsp 90 but not ovalbumin.	bind
1640	1	520	6	NULL	NULL	0	NULL	LPS	Chemical		bind					Hsp 90	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_10_5645_s_131	10318938	( A) LPS binds Hsp 90 but not ovalbumin.	bind
1641	2	520	6	NULL	NULL	0	NULL	LPS	Chemical		does not bind					ovalbumin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_10_5645_s_131	10318938	( A) LPS binds Hsp 90 but not ovalbumin.	bind
58059	1	523	5	NULL	NULL	0	NULL	mbeta2M	GP	wt	does not bind					ThT	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_29_10584_s_55	15249659	( A) mbeta2M/wt (filled circles) does not bind ThT.	bind
1642	1	523	6	NULL	NULL	0	NULL	mbeta2M	GP	wild type	does not bind					ThT	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_29_10584_s_55	15249659	( A) mbeta2M/wt (filled circles) does not bind ThT.	bind
58060	1	524	5	NULL	NULL	0	NULL	MBP	GP		bind					maltose	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_98_4_1525_s_130	11171984	( A) MBP binds maltose and undergoes a conformational change from an open to a closed conformation, generating a high-affinity sugar-binding site.	bind
58061	2	524	5	NULL	NULL	0	NULL	statement 1	Process		changes					MBP	GP	conformation of			NULL		0	NULL	NULL	NULL	gw60_pnas_98_4_1525_s_130	11171984	( A) MBP binds maltose and undergoes a conformational change from an open to a closed conformation, generating a high-affinity sugar-binding site.	bind
58062	3	524	5	NULL	NULL	0	NULL	statement 2	Process		generates							high-affinity	sugar-binding site		NULL		0	NULL	NULL	NULL	gw60_pnas_98_4_1525_s_130	11171984	( A) MBP binds maltose and undergoes a conformational change from an open to a closed conformation, generating a high-affinity sugar-binding site.	bind
1643	1	524	6	NULL	NULL	0	NULL	MBP	GP		bind					maltose	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_4_1525_s_130	11171984	( A) MBP binds maltose and undergoes a conformational change from an open to a closed conformation, generating a high-affinity sugar-binding site.	bind
1644	2	524	6	NULL	NULL	0	NULL	Statement 1	Process		change					MBP	GP	conformation of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_4_1525_s_130	11171984	( A) MBP binds maltose and undergoes a conformational change from an open to a closed conformation, generating a high-affinity sugar-binding site.	bind
1645	3	524	6	NULL	NULL	0	NULL	Statement 2	Process		generates						GP	high-affinity		sugar-binding site	NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_4_1525_s_130	11171984	( A) MBP binds maltose and undergoes a conformational change from an open to a closed conformation, generating a high-affinity sugar-binding site.	bind
58063	1	525	5	NULL	NULL	0	NULL	MECA-79	GP		bind					CHO-PSGL-1	Cell				NULL		0	NULL	NULL	NULL	gw70_pnas_101_51_17807_s_113	15591109	( A) MECA-79 binds CHO cells expressing 6-sulfo sialyl Lewis X on extended core 1 (CHO-PSGL-1.	bind
58064	2	525	5	NULL	NULL	0	NULL	CHO-PSGL-1	Cell		is					CHO cells expressing 6-sulfo sialyl Lewis X on extended core 1 	Cell				NULL		0	NULL	NULL	NULL	gw70_pnas_101_51_17807_s_113	15591109	( A) MECA-79 binds CHO cells expressing 6-sulfo sialyl Lewis X on extended core 1 (CHO-PSGL-1.	bind
1636	1	525	6	NULL	NULL	0	NULL	MECA-79	GP		bind					PSGL-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_51_17807_s_113	15591109	( A) MECA-79 binds CHO cells expressing 6-sulfo sialyl Lewis X on extended core 1 (CHO-PSGL-1.	bind
2221	2	525	6	NULL	NULL	0	NULL	PSGL-1	GP		is expressed on					CHO cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_51_17807_s_113	15591109	( A) MECA-79 binds CHO cells expressing 6-sulfo sialyl Lewis X on extended core 1 (CHO-PSGL-1.	bind
58065	1	527	5	NULL	NULL	0	NULL	neutrophils	Cell	unstimulated;;human	bind					Fg	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_102_5_1614_s_83	15665082	( A) Micrographs of wells with unstimulated ( Left) or TNF-stimulated ( Center) human neutrophils binding to Fg, or unstimulated neutrophils binding to plasmin-treated  Fg ( Right).	bind
58066	2	527	5	NULL	NULL	0	NULL	neutrophils	Cell	human	is stimulated by					TNF	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_102_5_1614_s_83	15665082	( A) Micrographs of wells with unstimulated ( Left) or TNF-stimulated ( Center) human neutrophils binding to Fg, or unstimulated neutrophils binding to plasmin-treated  Fg ( Right).	bind
58067	3	527	5	NULL	NULL	0	NULL	statement 2	Cell		bind					Fg	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1614_s_83	15665082	( A) Micrographs of wells with unstimulated ( Left) or TNF-stimulated ( Center) human neutrophils binding to Fg, or unstimulated neutrophils binding to plasmin-treated  Fg ( Right).	bind
58068	4	527	5	NULL	NULL	0	NULL	neutrophils	Cell	unstimulated	bind					Fg	GP	plasmin-treated			NULL		0	NULL	NULL	NULL	gw70_pnas_102_5_1614_s_83	15665082	( A) Micrographs of wells with unstimulated ( Left) or TNF-stimulated ( Center) human neutrophils binding to Fg, or unstimulated neutrophils binding to plasmin-treated  Fg ( Right).	bind
1646	1	527	6	NULL	NULL	0	NULL	neutrophils	Cell	human;;unstimulated	bind					Fg	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1614_s_83	15665082	( A) Micrographs of wells with unstimulated ( Left) or TNF-stimulated ( Center) human neutrophils binding to Fg, or unstimulated neutrophils binding to plasmin-treated  Fg ( Right).	bind
1647	3	527	6	NULL	NULL	0	NULL	statement 2	Process		bind					Fg	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1614_s_83	15665082	( A) Micrographs of wells with unstimulated ( Left) or TNF-stimulated ( Center) human neutrophils binding to Fg, or unstimulated neutrophils binding to plasmin-treated  Fg ( Right).	bind
1648	4	527	6	NULL	NULL	0	NULL	neutrophils	Cell	human;;unstimulated	bind					Fg	GP	plasmin-treated			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1614_s_83	15665082	( A) Micrographs of wells with unstimulated ( Left) or TNF-stimulated ( Center) human neutrophils binding to Fg, or unstimulated neutrophils binding to plasmin-treated  Fg ( Right).	bind
51831	2	527	6	NULL	NULL	0	NULL	TNF	GP		stimulate					neutrophils	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1614_s_83	15665082	( A) Micrographs of wells with unstimulated ( Left) or TNF-stimulated ( Center) human neutrophils binding to Fg, or unstimulated neutrophils binding to plasmin-treated  Fg ( Right).	bind
58069	1	528	5	NULL	NULL	0	NULL	MLL-AF4	GP		bind					CDKN1B	GP			promoter	NULL		0	NULL	NULL	NULL	gw70_pnas_102_39_14028_s_221	16169901	( A) MLL-AF4 binds to the  CDKN1B promoter ( Left) but not to the  CDKN1B coding region	bind
58070	2	528	5	NULL	NULL	0	NULL	MLL-AF4	GP		does not bind					CDKN1B	GP			coding region	NULL		0	NULL	NULL	NULL	gw70_pnas_102_39_14028_s_221	16169901	( A) MLL-AF4 binds to the  CDKN1B promoter ( Left) but not to the  CDKN1B coding region	bind
1649	1	528	6	NULL	NULL	0	NULL	MLL-AF4	GP		bind					CDKN1B	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_14028_s_221	16169901	( A) MLL-AF4 binds to the  CDKN1B promoter ( Left) but not to the  CDKN1B coding region	bind
1650	2	528	6	NULL	NULL	0	NULL	MLL-AF4	GP		does not bind					CDKN1B	GP		coding region		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_14028_s_221	16169901	( A) MLL-AF4 binds to the  CDKN1B promoter ( Left) but not to the  CDKN1B coding region	bind
58071	1	531	5	NULL	NULL	0	NULL	ERM proteins	GP		bind					PIP2	GP				NULL	membrane	0	NULL	NULL	NULL	gw70_embo_22_3_502_s_188	12554651	( A) Model of ERM proteins bound to both PIP2 in a membrane and the ICAM-2 cytoplasmic  tail.	bind
58072	2	531	5	NULL	NULL	0	NULL	ERM proteins	GP		bind					ICAM-2	GP		cytoplasmic tail		NULL		0	NULL	NULL	NULL	gw70_embo_22_3_502_s_188	12554651	( A) Model of ERM proteins bound to both PIP2 in a membrane and the ICAM-2 cytoplasmic  tail.	bind
1651	1	531	6	NULL	NULL	0	NULL	ERM protein	GP		bind					PIP2	GP				NULL	membrane	NULL	NULL	NULL	NULL	gw70_embo_22_3_502_s_188	12554651	( A) Model of ERM proteins bound to both PIP2 in a membrane and the ICAM-2 cytoplasmic  tail.	bind
1652	2	531	6	NULL	NULL	0	NULL	ERM protein	GP		bind					ICAM-2	GP		cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw70_embo_22_3_502_s_188	12554651	( A) Model of ERM proteins bound to both PIP2 in a membrane and the ICAM-2 cytoplasmic  tail.	bind
58073	1	534	5	NULL	NULL	0	NULL	LdTOP1	GP	putative	bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_794_s_169	11809893	( A) Model of the inhibitor CPT bound to the covalent complex of putative LdTOP1 and DNA.	bind
58074	2	534	5	NULL	NULL	0	NULL	statement 1	Process		forms					covalent complex					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_794_s_169	11809893	( A) Model of the inhibitor CPT bound to the covalent complex of putative LdTOP1 and DNA.	bind
58075	3	534	5	NULL	NULL	0	NULL	CPT	Chemical		is a type of					inhibitor					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_794_s_169	11809893	( A) Model of the inhibitor CPT bound to the covalent complex of putative LdTOP1 and DNA.	bind
58076	4	534	5	NULL	NULL	0	NULL	CPT	Chemical		bind					statement 1	GP				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_794_s_169	11809893	( A) Model of the inhibitor CPT bound to the covalent complex of putative LdTOP1 and DNA.	bind
1653	1	534	6	NULL	NULL	0	NULL	LdTOP1	GP	putative	bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_794_s_169	11809893	( A) Model of the inhibitor CPT bound to the covalent complex of putative LdTOP1 and DNA.	bind
1654	2	534	6	NULL	NULL	0	NULL	Statement 1	Process		forms a					covalent complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_794_s_169	11809893	( A) Model of the inhibitor CPT bound to the covalent complex of putative LdTOP1 and DNA.	bind
1655	3	534	6	NULL	NULL	0	NULL	CPT	Chemical	inhibitor	bind					Statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_794_s_169	11809893	( A) Model of the inhibitor CPT bound to the covalent complex of putative LdTOP1 and DNA.	bind
58077	1	535	5	NULL	NULL	0	NULL	LFA-1	GP		bind					ICAM-1 dimers	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_98_12_6830_s_43	11391003	( A) Models of LFA-1 binding to ICAM-1 dimers.	bind
1656	1	535	6	NULL	NULL	0	NULL	LFA-1	GP		bind					ICAM-1 dimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_12_6830_s_43	11391003	( A) Models of LFA-1 binding to ICAM-1 dimers.	bind
58078	1	537	5	NULL	NULL	0	NULL	MT	CellComponent		bind					EGFP-NCFC	GP	wild type			NULL		0	NULL	NULL	NULL	gw70_embo_23_7_1506_s_156	15014437	( A) MT binding of EGFP-NCFC (wild type and Y649F) and MCFC-EGFP (wild type and Y649F).	bind
58079	2	537	5	NULL	NULL	0	NULL	MT	CellComponent		bind					EGFP-NCFC	GP		Y649F		NULL		0	NULL	NULL	NULL	gw70_embo_23_7_1506_s_156	15014437	( A) MT binding of EGFP-NCFC (wild type and Y649F) and MCFC-EGFP (wild type and Y649F).	bind
58080	3	537	5	NULL	NULL	0	NULL	MT	CellComponent		bind					MCFC-EGFP	GP	wild type			NULL		0	NULL	NULL	NULL	gw70_embo_23_7_1506_s_156	15014437	( A) MT binding of EGFP-NCFC (wild type and Y649F) and MCFC-EGFP (wild type and Y649F).	bind
58081	4	537	5	NULL	NULL	0	NULL	MT	CellComponent		bind					MCFC-EGFP	GP		Y649F		NULL		0	NULL	NULL	NULL	gw70_embo_23_7_1506_s_156	15014437	( A) MT binding of EGFP-NCFC (wild type and Y649F) and MCFC-EGFP (wild type and Y649F).	bind
1657	1	537	6	NULL	NULL	0	NULL	MT	CellComponent		bind					 EGFP-NCFC	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1506_s_156	15014437	( A) MT binding of EGFP-NCFC (wild type and Y649F) and MCFC-EGFP (wild type and Y649F).	bind
1658	2	537	6	10	NULL	0	NULL	MT	NULL		bind	NULL				MCFC-EGFP	NULL	wild type			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1506_s_156	15014437	( A) MT binding of EGFP-NCFC (wild type and Y649F) and MCFC-EGFP (wild type and Y649F).	bind
51833	3	537	6	10	NULL	0	NULL	MT	NULL		bind	NULL				EGFP-NCFC	NULL		Y649F		NULL		0	NULL	NULL	NULL	gw70_embo_23_7_1506_s_156	15014437	( A) MT binding of EGFP-NCFC (wild type and Y649F) and MCFC-EGFP (wild type and Y649F).	bind
51834	4	537	6	10	NULL	0	NULL	MT	NULL		bind	NULL				MCFC-EGFP	NULL		Y649F		NULL		0	NULL	NULL	NULL	gw70_embo_23_7_1506_s_156	15014437	( A) MT binding of EGFP-NCFC (wild type and Y649F) and MCFC-EGFP (wild type and Y649F).	bind
58082	1	538	5	NULL	NULL	0	NULL	SIP1 polypeptide	GP		bind			NZF		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_191	10487759	( A) Mutations within NZF3, NZF4, CZF2 and CZF3 abolish DNA binding of short SIP1NZF and SIP1CZF polypeptides.	bind
58083	2	538	5	NULL	NULL	0	NULL	SIP1 polypeptide	GP		bind			CZF		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_191	10487759	( A) Mutations within NZF3, NZF4, CZF2 and CZF3 abolish DNA binding of short SIP1NZF and SIP1CZF polypeptides.	bind
58084	3	538	5	NULL	NULL	0	NULL	NZF3	GP	mutant	abolishes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_18_5073_s_191	10487759	( A) Mutations within NZF3, NZF4, CZF2 and CZF3 abolish DNA binding of short SIP1NZF and SIP1CZF polypeptides.	bind
58085	4	538	5	NULL	NULL	0	NULL	NZF3	GP	mutant	abolishes					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_18_5073_s_191	10487759	( A) Mutations within NZF3, NZF4, CZF2 and CZF3 abolish DNA binding of short SIP1NZF and SIP1CZF polypeptides.	bind
58086	5	538	5	NULL	NULL	0	NULL	NZF4	GP	mutant	abolishes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_18_5073_s_191	10487759	( A) Mutations within NZF3, NZF4, CZF2 and CZF3 abolish DNA binding of short SIP1NZF and SIP1CZF polypeptides.	bind
58087	6	538	5	NULL	NULL	0	NULL	NZF4	GP	mutant	abolishes					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_18_5073_s_191	10487759	( A) Mutations within NZF3, NZF4, CZF2 and CZF3 abolish DNA binding of short SIP1NZF and SIP1CZF polypeptides.	bind
58088	7	538	5	NULL	NULL	0	NULL	CZF2	GP	mutant	abolishes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_18_5073_s_191	10487759	( A) Mutations within NZF3, NZF4, CZF2 and CZF3 abolish DNA binding of short SIP1NZF and SIP1CZF polypeptides.	bind
58089	8	538	5	NULL	NULL	0	NULL	CZF2	GP	mutant	abolishes					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_18_5073_s_191	10487759	( A) Mutations within NZF3, NZF4, CZF2 and CZF3 abolish DNA binding of short SIP1NZF and SIP1CZF polypeptides.	bind
58090	9	538	5	NULL	NULL	0	NULL	CZF3	GP	mutant	abolishes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_18_5073_s_191	10487759	( A) Mutations within NZF3, NZF4, CZF2 and CZF3 abolish DNA binding of short SIP1NZF and SIP1CZF polypeptides.	bind
58091	10	538	5	NULL	NULL	0	NULL	CZF3	GP	mutant	abolishes					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_18_5073_s_191	10487759	( A) Mutations within NZF3, NZF4, CZF2 and CZF3 abolish DNA binding of short SIP1NZF and SIP1CZF polypeptides.	bind
1659	1	538	6	NULL	NULL	0	NULL	short SIP1 polypeptide	GP		bind			NZF		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_191	10487759	( A) Mutations within NZF3, NZF4, CZF2 and CZF3 abolish DNA binding of short SIP1NZF and SIP1CZF polypeptides.	bind
1660	2	538	6	NULL	NULL	0	NULL	short SIP1 polypeptide	GP	mutant	abolish 			 NZF3		DNA	NucleicAcid	binding of			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_191	10487759	( A) Mutations within NZF3, NZF4, CZF2 and CZF3 abolish DNA binding of short SIP1NZF and SIP1CZF polypeptides.	bind
1661	3	538	6	NULL	NULL	0	NULL	short SIP1 polypeptide	GP	mutant	abolish 			 NZF4		DNA	NucleicAcid	binding of			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_191	10487759	( A) Mutations within NZF3, NZF4, CZF2 and CZF3 abolish DNA binding of short SIP1NZF and SIP1CZF polypeptides.	bind
1662	4	538	6	NULL	NULL	0	NULL	short SIP1 polypeptide	GP		bind			CZF		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_191	10487759	( A) Mutations within NZF3, NZF4, CZF2 and CZF3 abolish DNA binding of short SIP1NZF and SIP1CZF polypeptides.	bind
1663	5	538	6	NULL	NULL	0	NULL	short SIP1 polypeptide	GP	mutant	abolish 			 CZF2		DNA	NucleicAcid	binding of			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_191	10487759	( A) Mutations within NZF3, NZF4, CZF2 and CZF3 abolish DNA binding of short SIP1NZF and SIP1CZF polypeptides.	bind
1664	6	538	6	NULL	NULL	0	NULL	short SIP1 polypeptide	GP	mutant	abolish 			CZF3		DNA	NucleicAcid	binding of			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_191	10487759	( A) Mutations within NZF3, NZF4, CZF2 and CZF3 abolish DNA binding of short SIP1NZF and SIP1CZF polypeptides.	bind
58092	1	539	5	NULL	NULL	0	NULL	Myozenin	GP		bind					alpha-actinin-2	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_98_4_1595_s_151	11171996	( A) Myozenin binds to both alpha-actinin-2 and -3 but not to itself ( Left), whereas alpha-actinin-2 and -3 both bind to myozenin as well as to themselves ( Center and  Right).	bind
58093	2	539	5	NULL	NULL	0	NULL	Myozenin	GP		bind					alpha-actinin-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_4_1595_s_151	11171996	( A) Myozenin binds to both alpha-actinin-2 and -3 but not to itself ( Left), whereas alpha-actinin-2 and -3 both bind to myozenin as well as to themselves ( Center and  Right).	bind
58094	3	539	5	NULL	NULL	0	NULL	Myozenin	GP		does not bind					Myozenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_4_1595_s_151	11171996	( A) Myozenin binds to both alpha-actinin-2 and -3 but not to itself ( Left), whereas alpha-actinin-2 and -3 both bind to myozenin as well as to themselves ( Center and  Right).	bind
58095	4	539	5	NULL	NULL	0	NULL	alpha-actinin-2	GP		bind					alpha-actinin-2	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_98_4_1595_s_151	11171996	( A) Myozenin binds to both alpha-actinin-2 and -3 but not to itself ( Left), whereas alpha-actinin-2 and -3 both bind to myozenin as well as to themselves ( Center and  Right).	bind
58096	5	539	5	NULL	NULL	0	NULL	alpha-actinin-3	GP		bind					alpha-actinin-3	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_98_4_1595_s_151	11171996	( A) Myozenin binds to both alpha-actinin-2 and -3 but not to itself ( Left), whereas alpha-actinin-2 and -3 both bind to myozenin as well as to themselves ( Center and  Right).	bind
1900	1	539	6	NULL	NULL	0	NULL	Myozenin	GP		bind					alpha-actinin-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_4_1595_s_151	11171996	( A) Myozenin binds to both alpha-actinin-2 and -3 but not to itself ( Left), whereas alpha-actinin-2 and -3 both bind to myozenin as well as to themselves ( Center and  Right).	bind
1901	2	539	6	NULL	NULL	0	NULL	Myozenin	GP		bind					alpha-actinin-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_4_1595_s_151	11171996	( A) Myozenin binds to both alpha-actinin-2 and -3 but not to itself ( Left), whereas alpha-actinin-2 and -3 both bind to myozenin as well as to themselves ( Center and  Right).	bind
1902	3	539	6	NULL	NULL	0	NULL	Myozenin	GP		does not bind					Myozenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_4_1595_s_151	11171996	( A) Myozenin binds to both alpha-actinin-2 and -3 but not to itself ( Left), whereas alpha-actinin-2 and -3 both bind to myozenin as well as to themselves ( Center and  Right).	bind
1903	4	539	6	NULL	NULL	0	NULL	alpha-actinin-2 	GP		bind					alpha-actinin-2 	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_4_1595_s_151	11171996	( A) Myozenin binds to both alpha-actinin-2 and -3 but not to itself ( Left), whereas alpha-actinin-2 and -3 both bind to myozenin as well as to themselves ( Center and  Right).	bind
1904	5	539	6	NULL	NULL	0	NULL	alpha-actinin-3	GP		bind					alpha-actinin-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_4_1595_s_151	11171996	( A) Myozenin binds to both alpha-actinin-2 and -3 but not to itself ( Left), whereas alpha-actinin-2 and -3 both bind to myozenin as well as to themselves ( Center and  Right).	bind
58097	1	541	5	NULL	NULL	0	NULL	Sec1	GP	neuronal	bind					syntaxin	GP		Habc domain;;SNARE motif		NULL		NULL	NULL	NULL	NULL	gw60_embo_21_22_6114_s_230	12426383	( A) Neuronal Sec1 (blue) binds syntaxin (Habc domain grey, SNARE motif red) in a closed conformation ( Misura  et al., 2000).	bind
1665	1	541	6	NULL	NULL	0	NULL	Sec1	GP	neuronal	bind					syntaxin	GP		Habc domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_21_22_6114_s_230	12426383	( A) Neuronal Sec1 (blue) binds syntaxin (Habc domain grey, SNARE motif red) in a closed conformation ( Misura  et al., 2000).	bind
1666	2	541	6	NULL	NULL	0	NULL	Sec1	GP	neuronal	bind					syntaxin	GP			SNARE motif	NULL		NULL	NULL	NULL	NULL	gw60_embo_21_22_6114_s_230	12426383	( A) Neuronal Sec1 (blue) binds syntaxin (Habc domain grey, SNARE motif red) in a closed conformation ( Misura  et al., 2000).	bind
58098	1	542	5	NULL	NULL	0	NULL	NF-kappaB1 p50 homodimers	GP		bind					HIV-1	Organism	latent		promoter	NULL		0	NULL	NULL	NULL	gw70_embo_25_1_139_s_216	16319923	( A) NF-kappaB1 p50 homodimers bound to the latent HIV-1 promoter recruit HDAC1, which deacetylates  regional histones and compacts local histone structure, thereby inhibiting the binding  of RNA Pol II.	bind
58099	2	542	5	NULL	NULL	0	NULL	statement 1	Process		recruit					HDAC1	GP				NULL		0	NULL	NULL	NULL	gw70_embo_25_1_139_s_216	16319923	( A) NF-kappaB1 p50 homodimers bound to the latent HIV-1 promoter recruit HDAC1, which deacetylates  regional histones and compacts local histone structure, thereby inhibiting the binding  of RNA Pol II.	bind
58100	3	542	5	NULL	NULL	0	NULL	HDAC1	GP		deacetylates					histones	GP	regional			NULL		0	NULL	NULL	NULL	gw70_embo_25_1_139_s_216	16319923	( A) NF-kappaB1 p50 homodimers bound to the latent HIV-1 promoter recruit HDAC1, which deacetylates  regional histones and compacts local histone structure, thereby inhibiting the binding  of RNA Pol II.	bind
58101	4	542	5	NULL	NULL	0	NULL	statement 3	Process		compacts					histone	GP	local  structure of			NULL		0	NULL	NULL	NULL	gw70_embo_25_1_139_s_216	16319923	( A) NF-kappaB1 p50 homodimers bound to the latent HIV-1 promoter recruit HDAC1, which deacetylates  regional histones and compacts local histone structure, thereby inhibiting the binding  of RNA Pol II.	bind
58102	5	542	5	NULL	NULL	0	NULL	statement 4	Process		inhibits					RNA Pol II	GP	binding of			NULL		0	NULL	NULL	NULL	gw70_embo_25_1_139_s_216	16319923	( A) NF-kappaB1 p50 homodimers bound to the latent HIV-1 promoter recruit HDAC1, which deacetylates  regional histones and compacts local histone structure, thereby inhibiting the binding  of RNA Pol II.	bind
1667	1	542	6	NULL	NULL	0	NULL	 NF-kappaB1 p50 homodimers	GP		bind					HIV-1	NucleicAcid	latent		Promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_1_139_s_216	16319923	( A) NF-kappaB1 p50 homodimers bound to the latent HIV-1 promoter recruit HDAC1, which deacetylates  regional histones and compacts local histone structure, thereby inhibiting the binding  of RNA Pol II.	bind
1668	2	542	6	NULL	NULL	0	NULL	 NF-kappaB1 p50 homodimers	GP		recruit					HDAC1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_1_139_s_216	16319923	( A) NF-kappaB1 p50 homodimers bound to the latent HIV-1 promoter recruit HDAC1, which deacetylates  regional histones and compacts local histone structure, thereby inhibiting the binding  of RNA Pol II.	bind
1669	3	542	6	NULL	NULL	0	NULL	HDAC1	GP		deacetylates					regional histones	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_1_139_s_216	16319923	( A) NF-kappaB1 p50 homodimers bound to the latent HIV-1 promoter recruit HDAC1, which deacetylates  regional histones and compacts local histone structure, thereby inhibiting the binding  of RNA Pol II.	bind
1670	4	542	6	NULL	NULL	0	NULL	HDAC1	GP		compacts					histone 	GP	local;; structure of			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_1_139_s_216	16319923	( A) NF-kappaB1 p50 homodimers bound to the latent HIV-1 promoter recruit HDAC1, which deacetylates  regional histones and compacts local histone structure, thereby inhibiting the binding  of RNA Pol II.	bind
1671	5	542	6	NULL	NULL	0	NULL	Statement 3	Process		inhibit					RNA Pol II	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_1_139_s_216	16319923	( A) NF-kappaB1 p50 homodimers bound to the latent HIV-1 promoter recruit HDAC1, which deacetylates  regional histones and compacts local histone structure, thereby inhibiting the binding  of RNA Pol II.	bind
1672	6	542	6	NULL	NULL	0	NULL	Statement 4	Process		inhibit					RNA Pol II	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_1_139_s_216	16319923	( A) NF-kappaB1 p50 homodimers bound to the latent HIV-1 promoter recruit HDAC1, which deacetylates  regional histones and compacts local histone structure, thereby inhibiting the binding  of RNA Pol II.	bind
58103	1	543	5	NULL	NULL	0	NULL	Raf-1	GP		bind					Rb	GP				NULL	HAEC cells	0	NULL	NULL	NULL	gw70_jclininvest_116_8_2208_s_80	16862215	( A) Nicotine induces the binding of Raf-1 to Rb in HAEC and A549 cells as seen by IP/Western  blotting.	bind
58104	2	543	5	NULL	NULL	0	NULL	Raf-1	GP		bind					Rb	GP				NULL	A549 cells	0	NULL	NULL	NULL	gw70_jclininvest_116_8_2208_s_80	16862215	( A) Nicotine induces the binding of Raf-1 to Rb in HAEC and A549 cells as seen by IP/Western  blotting.	bind
58105	3	543	5	NULL	NULL	0	NULL	Nicotine	Chemical		induce					statement 1	Process				NULL	HAEC cells	0	NULL	NULL	NULL	gw70_jclininvest_116_8_2208_s_80	16862215	( A) Nicotine induces the binding of Raf-1 to Rb in HAEC and A549 cells as seen by IP/Western  blotting.	bind
58106	4	543	5	NULL	NULL	0	NULL	Nicotine	Chemical		induce					statement 2	Process				NULL	A549 cells	0	NULL	NULL	NULL	gw70_jclininvest_116_8_2208_s_80	16862215	( A) Nicotine induces the binding of Raf-1 to Rb in HAEC and A549 cells as seen by IP/Western  blotting.	bind
1673	1	543	6	NULL	NULL	0	NULL	Raf-1	GP		bind					Rb	GP				NULL	HAEC cells	NULL	NULL	NULL	NULL	gw70_jclininvest_116_8_2208_s_80	16862215	( A) Nicotine induces the binding of Raf-1 to Rb in HAEC and A549 cells as seen by IP/Western  blotting.	bind
1674	2	543	6	NULL	NULL	0	NULL	Nicotine	Chemical		induces					statement1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_8_2208_s_80	16862215	( A) Nicotine induces the binding of Raf-1 to Rb in HAEC and A549 cells as seen by IP/Western  blotting.	bind
1675	3	543	6	NULL	NULL	0	NULL	Raf-1	GP		bind					Rb	GP				NULL	A549 cells	NULL	NULL	NULL	NULL	gw70_jclininvest_116_8_2208_s_80	16862215	( A) Nicotine induces the binding of Raf-1 to Rb in HAEC and A549 cells as seen by IP/Western  blotting.	bind
1676	4	543	6	NULL	NULL	0	NULL	Nicotine	Chemical		induces					Statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_8_2208_s_80	16862215	( A) Nicotine induces the binding of Raf-1 to Rb in HAEC and A549 cells as seen by IP/Western  blotting.	bind
58107	1	545	5	NULL	NULL	0	NULL	Rpp29	GP		bind					M1 RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5120_s_238	16155184	( A) Northwestern blot analysis of binding of Rpp29 to M1 RNA.	bind
1677	1	545	6	NULL	NULL	0	NULL	Rpp29	GP		bind					M1 RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5120_s_238	16155184	( A) Northwestern blot analysis of binding of Rpp29 to M1 RNA.	bind
58108	1	546	5	NULL	NULL	0	NULL	NSF	GP		bind					syntaxin Q226R-containing complexes	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_98_25_14262_s_120	11762430	( a) NSF binds to syntaxin Q226R-containing complexes via alpha-SNAP.	bind
58109	2	546	5	NULL	NULL	0	NULL	statement 1	Process		via					alpha-SNAP	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_98_25_14262_s_120	11762430	( a) NSF binds to syntaxin Q226R-containing complexes via alpha-SNAP.	bind
1678	1	546	6	NULL	NULL	0	NULL	NSF	GP		bind					syntaxin 	GP		Q226R-containing complexes		NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_25_14262_s_120	11762430	( a) NSF binds to syntaxin Q226R-containing complexes via alpha-SNAP.	bind
1679	2	546	6	NULL	NULL	0	NULL	Statement 1	Process		occurs via					alpha-SNAP	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_25_14262_s_120	11762430	( a) NSF binds to syntaxin Q226R-containing complexes via alpha-SNAP.	bind
58110	1	549	5	NULL	NULL	0	NULL	Sp-1	GP		is a type of					nuclear proteins	GP				NULL		0	NULL	NULL	NULL	gw60_jclininvest_102_10_1850_s_151	9819371	( A) Nuclear proteins binding to the Egr/Sp binding site of  the M-CSF promoter are Sp-1 and Sp-3.	bind
58111	2	549	5	NULL	NULL	0	NULL	Sp-3	GP		is a type of					nuclear protein	GP				NULL		0	NULL	NULL	NULL	gw60_jclininvest_102_10_1850_s_151	9819371	( A) Nuclear proteins binding to the Egr/Sp binding site of  the M-CSF promoter are Sp-1 and Sp-3.	bind
58112	3	549	5	NULL	NULL	0	NULL	Sp-1	GP		bind					M-CSF	GP			Egr/Sp binding site of promoter	NULL		0	NULL	NULL	NULL	gw60_jclininvest_102_10_1850_s_151	9819371	( A) Nuclear proteins binding to the Egr/Sp binding site of  the M-CSF promoter are Sp-1 and Sp-3.	bind
58113	4	549	5	NULL	NULL	0	NULL	Sp-3	GP		bind					M-CSF	GP			Egr/Sp binding site of promoter	NULL		0	NULL	NULL	NULL	gw60_jclininvest_102_10_1850_s_151	9819371	( A) Nuclear proteins binding to the Egr/Sp binding site of  the M-CSF promoter are Sp-1 and Sp-3.	bind
1682	1	549	6	NULL	NULL	0	NULL	Sp1	GP		bind					M-CSF	GP			Egr/Sp binding site in the promoter	NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_10_1850_s_151	9819371	( A) Nuclear proteins binding to the Egr/Sp binding site of  the M-CSF promoter are Sp-1 and Sp-3.	bind
1683	2	549	6	NULL	NULL	0	NULL	Sp-3	GP		bind					M-CSF	GP			Egr/Sp binding site in the promoter	NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_10_1850_s_151	9819371	( A) Nuclear proteins binding to the Egr/Sp binding site of  the M-CSF promoter are Sp-1 and Sp-3.	bind
58114	1	553	5	NULL	NULL	0	NULL	MR3.2scTCR 	GP	human	bind					MHC class II molecule	GP	rat			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_33_30961_s_178	12773544	( A) or  human MR3.2scTCR ( B) binding to a rat MHC class II molecule with  covalent Gp-BP-(69 - 89) (RTL201).	bind
1759	1	553	6	NULL	NULL	0	NULL	MR3.2scTCR	GP	human	bind			Gp-BP-(69 - 89) (RTL201)		MHC class II molecule	GP	rat			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_33_30961_s_178	12773544	( A) or  human MR3.2scTCR ( B) binding to a rat MHC class II molecule with  covalent Gp-BP-(69 - 89) (RTL201).	bind
58115	1	569	5	NULL	NULL	0	NULL	CR2	GP		bind					C3d	GP				NULL		0	NULL	NULL	NULL	gw60_science_292_5522_1725_s_34	11387479	( A) Overall view of the structure of CR2 binding to C3d.	bind
1760	1	569	6	NULL	NULL	0	NULL	CR2	GP		bind					C3d	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_292_5522_1725_s_34	11387479	( A) Overall view of the structure of CR2 binding to C3d.	bind
58116	1	573	5	NULL	NULL	0	NULL	p16	GP		bind					pRNA probe	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4264_s_211	11691914	( A) p16 binds the pRNA probe with a  Kd = 1.5 x 10 - 7 (squares) an affinity 10-fold higher than that for the non-specific RNA240,  Kd  10 - 6 (circles).	bind
58117	2	573	5	NULL	NULL	0	NULL	p16	GP		bind					RNA240	NucleicAcid	non-specific			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4264_s_211	11691914	( A) p16 binds the pRNA probe with a  Kd = 1.5 x 10 - 7 (squares) an affinity 10-fold higher than that for the non-specific RNA240,  Kd  10 - 6 (circles).	bind
58118	3	573	5	NULL	NULL	0	NULL	statement 1	Process	affinity of	is higher than					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4264_s_211	11691914	( A) p16 binds the pRNA probe with a  Kd = 1.5 x 10 - 7 (squares) an affinity 10-fold higher than that for the non-specific RNA240,  Kd  10 - 6 (circles).	bind
1761	1	573	6	NULL	NULL	0	NULL	p16	GP		bind		high affinity			pRNA probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4264_s_211	11691914	( A) p16 binds the pRNA probe with a  Kd = 1.5 x 10 - 7 (squares) an affinity 10-fold higher than that for the non-specific RNA240,  Kd  10 - 6 (circles).	bind
1762	2	573	6	NULL	NULL	0	NULL	p16	GP		bind		less affinity			RNA240	NucleicAcid	non-specific			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4264_s_211	11691914	( A) p16 binds the pRNA probe with a  Kd = 1.5 x 10 - 7 (squares) an affinity 10-fold higher than that for the non-specific RNA240,  Kd  10 - 6 (circles).	bind
58119	1	574	5	NULL	NULL	0	NULL	p42	GP		bind					ErbB3 receptor	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_29_10917_s_181	16832058	( A) p42 but not p48 binds ErbB3 receptor.	bind
58120	2	574	5	NULL	NULL	0	NULL	p48	GP		does not bind					ErbB3 receptor	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_29_10917_s_181	16832058	( A) p42 but not p48 binds ErbB3 receptor.	bind
1763	1	574	6	NULL	NULL	0	NULL	p42	GP		bind					ErbB3 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_29_10917_s_181	16832058	( A) p42 but not p48 binds ErbB3 receptor.	bind
1764	2	574	6	NULL	NULL	0	NULL	p48	GP		does not bind					ErbB3 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_29_10917_s_181	16832058	( A) p42 but not p48 binds ErbB3 receptor.	bind
58121	1	575	5	NULL	NULL	0	NULL	p53 core	GP		bind					Hsp90	GP	native			NULL		0	NULL	NULL	NULL	gw60_pnas_99_17_11085_s_177	12163643	( A) p53 core binds Hsp90 in the native state.	bind
1765	1	575	6	NULL	NULL	0	NULL	p53	GP	core	bind					Hsp90	GP	native			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_17_11085_s_177	12163643	( A) p53 core binds Hsp90 in the native state.	bind
58122	1	576	5	NULL	NULL	0	NULL	p53	GP		recognizes					dsDNA oligonucleotides	NucleicAcid	internal gaps in			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_20_4005_s_65	11024181	( A) p53 recognises internal gaps in dsDNA oligonucleotides as short as 1 nt. Aliquots of 1 and 10 ng of unlabelled dsDNA oligonucleotides with internal single-strand gaps efficiently competed for p53 binding to the labelled ssDNA oligonucleotide NGC.	bind
58123	2	576	5	NULL	NULL	0	NULL	p53	GP		bind					ssDNA oligonucleotide NGC	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_20_4005_s_65	11024181	( A) p53 recognises internal gaps in dsDNA oligonucleotides as short as 1 nt. Aliquots of 1 and 10 ng of unlabelled dsDNA oligonucleotides with internal single-strand gaps efficiently competed for p53 binding to the labelled ssDNA oligonucleotide NGC.	bind
58124	3	576	5	NULL	NULL	0	NULL	dsDNA oligonucleotides	NucleicAcid	unlabeled	contains					single-strand gaps	NucleicAcid	internal			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_20_4005_s_65	11024181	( A) p53 recognises internal gaps in dsDNA oligonucleotides as short as 1 nt. Aliquots of 1 and 10 ng of unlabelled dsDNA oligonucleotides with internal single-strand gaps efficiently competed for p53 binding to the labelled ssDNA oligonucleotide NGC.	bind
58125	4	576	5	NULL	NULL	0	NULL	p53	GP		bind					statement 3	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_20_4005_s_65	11024181	( A) p53 recognises internal gaps in dsDNA oligonucleotides as short as 1 nt. Aliquots of 1 and 10 ng of unlabelled dsDNA oligonucleotides with internal single-strand gaps efficiently competed for p53 binding to the labelled ssDNA oligonucleotide NGC.	bind
58126	5	576	5	NULL	NULL	0	NULL	statement 4	Process		competes with		efficiently			statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_20_4005_s_65	11024181	( A) p53 recognises internal gaps in dsDNA oligonucleotides as short as 1 nt. Aliquots of 1 and 10 ng of unlabelled dsDNA oligonucleotides with internal single-strand gaps efficiently competed for p53 binding to the labelled ssDNA oligonucleotide NGC.	bind
1907	1	576	6	NULL	NULL	0	NULL	p53	GP		bind					ssDNA oligonucleotide NGC	NucleicAcid	labelled			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_20_4005_s_65	11024181	( A) p53 recognises internal gaps in dsDNA oligonucleotides as short as 1 nt. Aliquots of 1 and 10 ng of unlabelled dsDNA oligonucleotides with internal single-strand gaps efficiently competed for p53 binding to the labelled ssDNA oligonucleotide NGC.	bind
1908	2	576	6	NULL	NULL	0	NULL	p53	GP		bind					dsDNA oligonucleotides	NucleicAcid	unlabelled		internal single-strand gaps	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_20_4005_s_65	11024181	( A) p53 recognises internal gaps in dsDNA oligonucleotides as short as 1 nt. Aliquots of 1 and 10 ng of unlabelled dsDNA oligonucleotides with internal single-strand gaps efficiently competed for p53 binding to the labelled ssDNA oligonucleotide NGC.	bind
1909	3	576	6	NULL	NULL	0	NULL	p53	GP		recognizes					dsDNA oligonucleotide	NucleicAcid	internal gaps			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_20_4005_s_65	11024181	( A) p53 recognises internal gaps in dsDNA oligonucleotides as short as 1 nt. Aliquots of 1 and 10 ng of unlabelled dsDNA oligonucleotides with internal single-strand gaps efficiently competed for p53 binding to the labelled ssDNA oligonucleotide NGC.	bind
51835	4	576	6	NULL	NULL	0	NULL	statement 1	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_20_4005_s_65	11024181	( A) p53 recognises internal gaps in dsDNA oligonucleotides as short as 1 nt. Aliquots of 1 and 10 ng of unlabelled dsDNA oligonucleotides with internal single-strand gaps efficiently competed for p53 binding to the labelled ssDNA oligonucleotide NGC.	bind
58127	1	577	5	NULL	NULL	0	NULL	PABP	GP		does not bind			M161A		eIF4G	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_1_104_s_93	15630022	( A) PABP M161A cannot bind to eIF4G.	bind
1766	1	577	6	NULL	NULL	0	NULL	PABP	GP		does not bind			M161A		eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_1_104_s_93	15630022	( A) PABP M161A cannot bind to eIF4G.	bind
58128	1	579	5	NULL	NULL	0	NULL	PAX6	GP		does not bind					hGC 1BLs1 homologues	GP			B1 repetitive elements	NULL		NULL	NULL	NULL	NULL	gw60_gene_245_2_319_s_156	10717483	( A) PAX6 did not bind the hGC 1BLs1 homologues in the consensus B1 repetitive elements (lanes 3-5).	bind
1767	1	579	6	NULL	NULL	0	NULL	PAX6	GP		does not bind					hGC 1BLs1 homologue	GP			B1 repetitive element	NULL		NULL	NULL	NULL	NULL	gw60_gene_245_2_319_s_156	10717483	( A) PAX6 did not bind the hGC 1BLs1 homologues in the consensus B1 repetitive elements (lanes 3-5).	bind
58129	1	581	5	NULL	NULL	0	NULL	PCNA	GP		bind					GST-Cdt1	GP				NULL		0	NULL	NULL	NULL	gw70_embo_25_5_1126_s_196	16482215	( A) PCNA binds to GST-Cdt1, but not to GST.	bind
58130	2	581	5	NULL	NULL	0	NULL	PCNA	GP		does not bind					GST	Chemical				NULL		0	NULL	NULL	NULL	gw70_embo_25_5_1126_s_196	16482215	( A) PCNA binds to GST-Cdt1, but not to GST.	bind
1768	1	581	6	NULL	NULL	0	NULL	PCNA	GP		bind					GST-Cdt1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_5_1126_s_196	16482215	( A) PCNA binds to GST-Cdt1, but not to GST.	bind
58131	1	583	5	NULL	NULL	0	NULL	Socs-1	GP	phosphorylated	does not bind					Elongin BC	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_99_4_2175_s_184	11854514	( A) Phosphorylated Socs-1 does not bind Elongin BC as well as unphosphorylated Socs-1 in coimmunoprecipitation experiments.	bind
58132	2	583	5	NULL	NULL	0	NULL	Socs-1	GP	phosphorylated	does not bind					Socs-1	GP	unphosphorylated			NULL		0	NULL	NULL	NULL	gw60_pnas_99_4_2175_s_184	11854514	( A) Phosphorylated Socs-1 does not bind Elongin BC as well as unphosphorylated Socs-1 in coimmunoprecipitation experiments.	bind
1770	1	583	6	NULL	NULL	0	NULL	Socs-1	GP	phosphorylated	does not bind					Elongin BC	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_4_2175_s_184	11854514	( A) Phosphorylated Socs-1 does not bind Elongin BC as well as unphosphorylated Socs-1 in coimmunoprecipitation experiments.	bind
1772	2	583	6	NULL	NULL	0	NULL	Socs-1	GP	phosphorylated	does not bind					Socs-1	GP	unphosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_4_2175_s_184	11854514	( A) Phosphorylated Socs-1 does not bind Elongin BC as well as unphosphorylated Socs-1 in coimmunoprecipitation experiments.	bind
58133	1	584	5	NULL	NULL	0	NULL	Pho4	GP		bind					Pse1	GP				NULL	extract	0	NULL	NULL	NULL	gw60_genesdev_12_17_2673_s_174	9732266	( A) Phosphorylation affects binding of Pho4 to Pse1 in an extract.	bind
58134	2	584	5	NULL	NULL	0	NULL	phosphorylation	Process		affects					statement 1	Process				NULL	extract	0	NULL	NULL	NULL	gw60_genesdev_12_17_2673_s_174	9732266	( A) Phosphorylation affects binding of Pho4 to Pse1 in an extract.	bind
1773	1	584	6	NULL	NULL	0	NULL	Pho4	GP		bind					Pse1	GP				NULL	extract	NULL	NULL	NULL	NULL	gw60_genesdev_12_17_2673_s_174	9732266	( A) Phosphorylation affects binding of Pho4 to Pse1 in an extract.	bind
1774	2	584	6	NULL	NULL	0	NULL	phosphorylation			affects					Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_17_2673_s_174	9732266	( A) Phosphorylation affects binding of Pho4 to Pse1 in an extract.	bind
58135	1	585	5	NULL	NULL	0	NULL	PACS-1	GP		bind			MR		PACS-1	GP		FBR		NULL		0	NULL	NULL	NULL	gw70_embo_22_23_6234_s_87	14633983	( A) Phosphorylation of PACS-1 Ser278 inhibits PACS-1 MR binding to the PACS-1 FBR.	bind
58136	2	585	5	NULL	NULL	0	NULL	PACS-1	GP	phosphorylation of	inhibits			Ser278		statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_embo_22_23_6234_s_87	14633983	( A) Phosphorylation of PACS-1 Ser278 inhibits PACS-1 MR binding to the PACS-1 FBR.	bind
1775	1	585	6	NULL	NULL	0	NULL	PACS-1	GP		bind			MR		PACS-1	GP		FBR		NULL		NULL	NULL	NULL	NULL	gw70_embo_22_23_6234_s_87	14633983	( A) Phosphorylation of PACS-1 Ser278 inhibits PACS-1 MR binding to the PACS-1 FBR.	bind
1776	2	585	6	NULL	NULL	0	NULL	PACS-1	GP	phosphorylation	inhibit			Ser278		Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_22_23_6234_s_87	14633983	( A) Phosphorylation of PACS-1 Ser278 inhibits PACS-1 MR binding to the PACS-1 FBR.	bind
58137	1	586	5	NULL	NULL	0	NULL	SRE	GP		mediates					gene expression	Process				NULL		0	NULL	NULL	NULL	gw60_embo_19_18_4955_s_67	10990459	( A) PI3K inhibitors decreased NGF-stimulated SRE-mediated gene expression.	bind
58138	2	586	5	NULL	NULL	0	NULL	NGF	GP		stimulates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_embo_19_18_4955_s_67	10990459	( A) PI3K inhibitors decreased NGF-stimulated SRE-mediated gene expression.	bind
58139	3	586	5	NULL	NULL	0	NULL	PI3K inhibitors	GP		decreases					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_embo_19_18_4955_s_67	10990459	( A) PI3K inhibitors decreased NGF-stimulated SRE-mediated gene expression.	bind
58140	1	587	5	NULL	NULL	0	NULL	PIMT	GP		bind					AdoMet	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_98_18_10380_s_156	11517327	( A) PIMT binds AdoMet.	bind
1777	1	587	6	NULL	NULL	0	NULL	PIMT	GP		bind					AdoMet	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_18_10380_s_156	11517327	( A) PIMT binds AdoMet.	bind
58141	1	588	5	NULL	NULL	0	NULL	PIPK Igamma	GP		bind			mu2-subunit		AP-2	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_32_11934_s_90	16880396	( A) PIPK Igamma binds to AP-2 via its mu2-subunit.	bind
1778	1	588	6	NULL	NULL	0	NULL	PIPK Igamma	GP		bind			mu2-subunit		AP-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_32_11934_s_90	16880396	( A) PIPK Igamma binds to AP-2 via its mu2-subunit.	bind
58142	1	589	5	NULL	NULL	0	NULL	PML-RAR	GP		bind					RARbeta2	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_science_295_5557_1079_s_31	11834837	( A) PML-RAR binds to the RARbeta2 promoter.	bind
1779	1	589	6	NULL	NULL	0	NULL	PML-RAR	GP		bind					RARbeta2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_science_295_5557_1079_s_31	11834837	( A) PML-RAR binds to the RARbeta2 promoter.	bind
58143	1	590	5	NULL	NULL	0	NULL	POT1b	GP		bind		efficiently			ss telomeric DNA	NucleicAcid			GGTTAGGGTTAG	NULL		0	NULL	NULL	NULL	gw70_embo_25_21_5180_s_66	17053789	( A) POT1b efficiently binds to a 12 base ss telomeric DNA sequence GGTTAGGGTTAG.	bind
1780	1	590	6	NULL	NULL	0	NULL	POT1b	GP		bind		efficiently			ss telomeric DNA sequence	NucleicAcid			GGTTAGGGTTAG	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_21_5180_s_66	17053789	( A) POT1b efficiently binds to a 12 base ss telomeric DNA sequence GGTTAGGGTTAG.	bind
58144	1	591	5	NULL	NULL	0	NULL	PP1C	GP		bind					PTG	GP				NULL	in vivo	0	NULL	NULL	NULL	gw60_science_275_5305_1475_s_49	9045612	( A) PP1C binds PTG in vivo.	bind
1781	1	591	6	NULL	NULL	0	NULL	PP1C	GP		bind					PTG	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_science_275_5305_1475_s_49	9045612	( A) PP1C binds PTG in vivo.	bind
58145	1	592	5	NULL	NULL	0	NULL				bind				PRE				PHO		NULL		0	NULL	NULL	NULL	gw70_genesdev_19_15_1755_s_68	16077005	( A) PRE binding of PHO, deltaPBD and PCC was studied by bandshift assays.	bind
58146	2	592	5	NULL	NULL	0	NULL				bind				PRE				deltaPBD		NULL		0	NULL	NULL	NULL	gw70_genesdev_19_15_1755_s_68	16077005	( A) PRE binding of PHO, deltaPBD and PCC was studied by bandshift assays.	bind
58147	3	592	5	NULL	NULL	0	NULL				bind				PRE				PCC		NULL		0	NULL	NULL	NULL	gw70_genesdev_19_15_1755_s_68	16077005	( A) PRE binding of PHO, deltaPBD and PCC was studied by bandshift assays.	bind
1782	1	592	6	NULL	NULL	0	NULL		AminoAcid		bind			PHO			GP			PRE	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_15_1755_s_68	16077005	( A) PRE binding of PHO, deltaPBD and PCC was studied by bandshift assays.	bind
1783	2	592	6	NULL	NULL	0	NULL		AminoAcid		bind			deltaPBD			GP			PRE	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_15_1755_s_68	16077005	( A) PRE binding of PHO, deltaPBD and PCC was studied by bandshift assays.	bind
1784	3	592	6	NULL	NULL	0	NULL		AminoAcid		bind			PCC			GP			PRE	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_15_1755_s_68	16077005	( A) PRE binding of PHO, deltaPBD and PCC was studied by bandshift assays.	bind
58148	1	593	5	NULL	NULL	0	NULL	FN	GP		is					fibronectin	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_46_16210_s_148	15520390	( A) Primary rat and human VSMC adhered to Netrin-1 and fibronectin (FN), whereas HAEC  and HMVEC did not adhere to the Netrin-1, but bound tightly to FN.	bind
58149	2	593	5	NULL	NULL	0	NULL	primary VSMC	Cell	rat	adhere to					Netrin-1	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_46_16210_s_148	15520390	( A) Primary rat and human VSMC adhered to Netrin-1 and fibronectin (FN), whereas HAEC  and HMVEC did not adhere to the Netrin-1, but bound tightly to FN.	bind
58150	3	593	5	NULL	NULL	0	NULL	primary VSMC	Cell	human	adhere to					Netrin-1	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_46_16210_s_148	15520390	( A) Primary rat and human VSMC adhered to Netrin-1 and fibronectin (FN), whereas HAEC  and HMVEC did not adhere to the Netrin-1, but bound tightly to FN.	bind
58151	4	593	5	NULL	NULL	0	NULL	primary VSMC	Cell	rat	adhere to					FN	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_46_16210_s_148	15520390	( A) Primary rat and human VSMC adhered to Netrin-1 and fibronectin (FN), whereas HAEC  and HMVEC did not adhere to the Netrin-1, but bound tightly to FN.	bind
58152	5	593	5	NULL	NULL	0	NULL	primary VSMC	Cell	human	adhere to					FN	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_46_16210_s_148	15520390	( A) Primary rat and human VSMC adhered to Netrin-1 and fibronectin (FN), whereas HAEC  and HMVEC did not adhere to the Netrin-1, but bound tightly to FN.	bind
58153	6	593	5	NULL	NULL	0	NULL	HAEC	Cell		does not adhere to					Netrin-1	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_46_16210_s_148	15520390	( A) Primary rat and human VSMC adhered to Netrin-1 and fibronectin (FN), whereas HAEC  and HMVEC did not adhere to the Netrin-1, but bound tightly to FN.	bind
58154	7	593	5	NULL	NULL	0	NULL	HMVEC	Cell		does not adhere to					Netrin-1	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_46_16210_s_148	15520390	( A) Primary rat and human VSMC adhered to Netrin-1 and fibronectin (FN), whereas HAEC  and HMVEC did not adhere to the Netrin-1, but bound tightly to FN.	bind
58155	8	593	5	NULL	NULL	0	NULL	HAEC	Cell		bind		tightly			FN	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_46_16210_s_148	15520390	( A) Primary rat and human VSMC adhered to Netrin-1 and fibronectin (FN), whereas HAEC  and HMVEC did not adhere to the Netrin-1, but bound tightly to FN.	bind
58156	9	593	5	NULL	NULL	0	NULL	HMVEC	Cell		bind		tightly			FN	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_46_16210_s_148	15520390	( A) Primary rat and human VSMC adhered to Netrin-1 and fibronectin (FN), whereas HAEC  and HMVEC did not adhere to the Netrin-1, but bound tightly to FN.	bind
1785	1	593	6	NULL	NULL	0	NULL	primary VSMC	Cell	rat	adhere					Netrin-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_46_16210_s_148	15520390	( A) Primary rat and human VSMC adhered to Netrin-1 and fibronectin (FN), whereas HAEC  and HMVEC did not adhere to the Netrin-1, but bound tightly to FN.	bind
1786	2	593	6	NULL	NULL	0	NULL	primary VSMC	Cell	human	adhere					fibronectin 	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_46_16210_s_148	15520390	( A) Primary rat and human VSMC adhered to Netrin-1 and fibronectin (FN), whereas HAEC  and HMVEC did not adhere to the Netrin-1, but bound tightly to FN.	bind
1787	3	593	6	NULL	NULL	0	NULL	primary VSMC	Cell	rat	adhere					fibronectin 	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_46_16210_s_148	15520390	( A) Primary rat and human VSMC adhered to Netrin-1 and fibronectin (FN), whereas HAEC  and HMVEC did not adhere to the Netrin-1, but bound tightly to FN.	bind
1788	4	593	6	NULL	NULL	0	NULL	primary VSMC	Cell	human	adhere					Netrin-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_46_16210_s_148	15520390	( A) Primary rat and human VSMC adhered to Netrin-1 and fibronectin (FN), whereas HAEC  and HMVEC did not adhere to the Netrin-1, but bound tightly to FN.	bind
1789	5	593	6	NULL	NULL	0	NULL	HAEC	Cell		did not adhere					Netrin1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_46_16210_s_148	15520390	( A) Primary rat and human VSMC adhered to Netrin-1 and fibronectin (FN), whereas HAEC  and HMVEC did not adhere to the Netrin-1, but bound tightly to FN.	bind
1790	6	593	6	NULL	NULL	0	NULL	HMVEC	Cell		did not adhere					Netrin-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_46_16210_s_148	15520390	( A) Primary rat and human VSMC adhered to Netrin-1 and fibronectin (FN), whereas HAEC  and HMVEC did not adhere to the Netrin-1, but bound tightly to FN.	bind
1791	7	593	6	NULL	NULL	0	NULL	HAEC	Cell		bind		tightly			FN	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_46_16210_s_148	15520390	( A) Primary rat and human VSMC adhered to Netrin-1 and fibronectin (FN), whereas HAEC  and HMVEC did not adhere to the Netrin-1, but bound tightly to FN.	bind
1792	8	593	6	NULL	NULL	0	NULL	HMVEC	Cell		bind		tightly			FN	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_46_16210_s_148	15520390	( A) Primary rat and human VSMC adhered to Netrin-1 and fibronectin (FN), whereas HAEC  and HMVEC did not adhere to the Netrin-1, but bound tightly to FN.	bind
58157	1	594	5	NULL	NULL	0	NULL	Prolyl-sulfamoyl-adenylate	Chemical		bind					ProRS	GP	M. thermautotrophicus	active site		NULL		0	NULL	NULL	NULL	gw60_pnas_100_4_1673_s_125	12578991	( a) Prolyl-sulfamoyl-adenylate bound to the active site of  M. thermautotrophicus ProRS.	bind
1793	1	594	6	NULL	NULL	0	NULL		AminoAcid		bind			Prolyl-sulfamoyl-adenylate		ProRS	GP	M. thermautotrophicus	active site		NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_4_1673_s_125	12578991	( a) Prolyl-sulfamoyl-adenylate bound to the active site of  M. thermautotrophicus ProRS.	bind
58158	1	595	5	NULL	NULL	0	NULL	Protein G	GP		bind					IgG Fc fragment	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_99_22_14116_s_118	12381794	( a) Protein G bound to an IgG Fc fragment (1fcc).	bind
58159	2	595	5	NULL	NULL	0	NULL	IgG Fc fragment	GP		is					1fcc	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_99_22_14116_s_118	12381794	( a) Protein G bound to an IgG Fc fragment (1fcc).	bind
1794	1	595	6	NULL	NULL	0	NULL	Protein G	GP		bind					IgG 	GP		Fc fragment		NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_22_14116_s_118	12381794	( a) Protein G bound to an IgG Fc fragment (1fcc).	bind
58160	1	596	5	NULL	NULL	0	NULL	Protein sigma1	GP		bind					NALT M cells	Cell				NULL		0	NULL	NULL	NULL	gw60_pnas_98_16_9318_s_94	11459939	( A) Protein sigma1 (yellow arrows) and UEA-1 (white arrows) binding to NALT M cells at x180.	bind
58161	2	596	5	NULL	NULL	0	NULL	UEA-1	GP		bind					NALT M cells	Cell				NULL		0	NULL	NULL	NULL	gw60_pnas_98_16_9318_s_94	11459939	( A) Protein sigma1 (yellow arrows) and UEA-1 (white arrows) binding to NALT M cells at x180.	bind
1795	1	596	6	NULL	NULL	0	NULL	Protein sigma1	GP		bind					NALT M cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_16_9318_s_94	11459939	( A) Protein sigma1 (yellow arrows) and UEA-1 (white arrows) binding to NALT M cells at x180.	bind
1796	2	596	6	NULL	NULL	0	NULL	UEA-1	GP		bind					NALT M cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_16_9318_s_94	11459939	( A) Protein sigma1 (yellow arrows) and UEA-1 (white arrows) binding to NALT M cells at x180.	bind
58162	1	598	5	NULL	NULL	0	NULL	pTP	GP		bind								TD(30 - 50)		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_12_3274_s_134	12799455	( A) pTP binding to TD(30 - 50) was studied using EMSA.	bind
1797	1	598	6	NULL	NULL	0	NULL	pTP	GP		bind						AminoAcid		TD (30-50)		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_12_3274_s_134	12799455	( A) pTP binding to TD(30 - 50) was studied using EMSA.	bind
58163	1	601	5	NULL	NULL	0	NULL	myosin	GP	purified	bind					P210 BCR-ABL	GP	expressed in;;purified from Sf9 cells			NULL		0	NULL	NULL	NULL	gw60_pnas_96_1_203_s_103	9874796	( a) Purified myosin (0.2 mug) (lane 1) and GST-C32 bound to P210 BCR-ABL (lane 2) expressed in and purified from Sf9 cells were stained by silver nitrate.	bind
58164	2	601	5	NULL	NULL	0	NULL	GST-C32	GP		bind					P210 BCR-ABL	GP	expressed in;;purified from Sf9 cells			NULL		0	NULL	NULL	NULL	gw60_pnas_96_1_203_s_103	9874796	( a) Purified myosin (0.2 mug) (lane 1) and GST-C32 bound to P210 BCR-ABL (lane 2) expressed in and purified from Sf9 cells were stained by silver nitrate.	bind
1905	1	601	6	NULL	NULL	0	NULL	myosin	GP	purified	bind					P210 BCR-ABL	GP				NULL	Sf9 cells	NULL	NULL	NULL	NULL	gw60_pnas_96_1_203_s_103	9874796	( a) Purified myosin (0.2 mug) (lane 1) and GST-C32 bound to P210 BCR-ABL (lane 2) expressed in and purified from Sf9 cells were stained by silver nitrate.	bind
1906	2	601	6	NULL	NULL	0	NULL	GST-C32	GP		bind					P210 BCR-ABL	GP				NULL	Sf9 cells	NULL	NULL	NULL	NULL	gw60_pnas_96_1_203_s_103	9874796	( a) Purified myosin (0.2 mug) (lane 1) and GST-C32 bound to P210 BCR-ABL (lane 2) expressed in and purified from Sf9 cells were stained by silver nitrate.	bind
58165	1	602	5	NULL	NULL	0	NULL	Pyr	GP		bind					PvDHFR	GP	WT			NULL		0	NULL	NULL	NULL	gw70_pnas_102_37_13046_s_97	16135570	( A) Pyr binding with the WT PvDHFR.	bind
2082	1	602	6	NULL	NULL	0	NULL	Pyr	GP		bind					PvDHFR	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_37_13046_s_97	16135570	( A) Pyr binding with the WT PvDHFR.	bind
57	1	602	9	10	NULL	0	NULL	Pyr	NULL		bind	NULL				 PvDHFR	NULL	WT			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_37_13046_s_97	16135570	( A) Pyr binding with the WT PvDHFR.	bind
58166	1	603	5	NULL	NULL	0	NULL	FGF2	GP		bind					heparin	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_14_4833_s_168	15051888	( A) QSulf1 does not affect the binding of FGF2 to heparin.	bind
58167	2	603	5	NULL	NULL	0	NULL	QSulf1	GP		does not affect					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_14_4833_s_168	15051888	( A) QSulf1 does not affect the binding of FGF2 to heparin.	bind
2083	1	603	6	NULL	NULL	0	NULL	FGF2	GP		bind					heparin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_14_4833_s_168	15051888	( A) QSulf1 does not affect the binding of FGF2 to heparin.	bind
2084	2	603	6	NULL	NULL	0	NULL	Qsulf1	GP		does not affect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_14_4833_s_168	15051888	( A) QSulf1 does not affect the binding of FGF2 to heparin.	bind
58	1	603	9	NULL	NULL	0	NULL	FGF2	NULL		bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_14_4833_s_168	15051888	( A) QSulf1 does not affect the binding of FGF2 to heparin.	bind
59	2	603	9	NULL	NULL	0	NULL	QSulf1	NULL		does not affect	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_14_4833_s_168	15051888	( A) QSulf1 does not affect the binding of FGF2 to heparin.	bind
58168	1	605	5	NULL	NULL	0	NULL	Fz proteins	GP		activates					Rac	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_17_2_295_s_51	12533515	( A) Rac activation by specific Fz proteins.	bind
2085	1	605	6	NULL	NULL	0	NULL	Fz proteins	GP	specific	activates					Rac	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_2_295_s_51	12533515	( A) Rac activation by specific Fz proteins.	bind
60	1	605	9	10	NULL	0	NULL	Fz proteins	NULL		activates	NULL				Rac	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_2_295_s_51	12533515	( A) Rac activation by specific Fz proteins.	bind
61	1	606	9	NULL	NULL	0	NULL	SRP54	NULL	Radiolabeled 	bind	NULL				RNC-pPL86	NULL				NULL		0	NULL	NULL	NULL	gw60_science_297_5585_1345_s_55	12193787	( A) Radiolabeled SRP54 was bound to RNC-pPL86 and then treated with DSS.	bind
58169	1	608	5	NULL	NULL	0	NULL	RASSF1	GP		bind					Daxx	GP				NULL	COS7 cells	0	NULL	NULL	NULL	gw70_embo_25_14_3286_s_83	16810318	( A) RASSF1 binds Daxx in COS7 cells.	bind
1798	1	608	6	NULL	NULL	0	NULL	RASSF1	GP		bind					Daxx	GP				NULL	Cos7 cells	NULL	NULL	NULL	NULL	gw70_embo_25_14_3286_s_83	16810318	( A) RASSF1 binds Daxx in COS7 cells.	bind
58170	1	609	5	NULL	NULL	0	NULL	GABAAR beta3	GP	rat	bind					BTX	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_52	16549768	( a) Rat (r) GABAAR beta3 binds BTX, but rat GABAAR beta1, beta2, alpha2, and gamma2 do not.	bind
58171	2	609	5	NULL	NULL	0	NULL	GABAAR beta1	GP	rat	does not bind					BTX	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_52	16549768	( a) Rat (r) GABAAR beta3 binds BTX, but rat GABAAR beta1, beta2, alpha2, and gamma2 do not.	bind
58172	3	609	5	NULL	NULL	0	NULL	GABAAR beta2	GP	rat	does not bind					BTX	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_52	16549768	( a) Rat (r) GABAAR beta3 binds BTX, but rat GABAAR beta1, beta2, alpha2, and gamma2 do not.	bind
58173	4	609	5	NULL	NULL	0	NULL	GABAAR alpha2	GP	rat	does not bind					BTX	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_52	16549768	( a) Rat (r) GABAAR beta3 binds BTX, but rat GABAAR beta1, beta2, alpha2, and gamma2 do not.	bind
58174	5	609	5	NULL	NULL	0	NULL	GABAAR gamma2	GP	rat	does not bind					BTX	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_52	16549768	( a) Rat (r) GABAAR beta3 binds BTX, but rat GABAAR beta1, beta2, alpha2, and gamma2 do not.	bind
1799	1	609	6	NULL	NULL	0	NULL	GABAAR beta3	GP	rat	bind					BTX	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_52	16549768	( a) Rat (r) GABAAR beta3 binds BTX, but rat GABAAR beta1, beta2, alpha2, and gamma2 do not.	bind
1800	2	609	6	NULL	NULL	0	NULL	GABAAR beta1	GP	rat	does not bind					BTX	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_52	16549768	( a) Rat (r) GABAAR beta3 binds BTX, but rat GABAAR beta1, beta2, alpha2, and gamma2 do not.	bind
1801	3	609	6	NULL	NULL	0	NULL	GABAAR beta2	GP	rat	does not bind					BTX	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_52	16549768	( a) Rat (r) GABAAR beta3 binds BTX, but rat GABAAR beta1, beta2, alpha2, and gamma2 do not.	bind
1802	4	609	6	NULL	NULL	0	NULL	GABAAR alpha2	GP	rat	does not bind					BTX	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_52	16549768	( a) Rat (r) GABAAR beta3 binds BTX, but rat GABAAR beta1, beta2, alpha2, and gamma2 do not.	bind
1803	5	609	6	NULL	NULL	0	NULL	GABAAR gamma2	GP	rat	does not bind					BTX	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_52	16549768	( a) Rat (r) GABAAR beta3 binds BTX, but rat GABAAR beta1, beta2, alpha2, and gamma2 do not.	bind
58175	1	611	5	NULL	NULL	0	NULL	Rbx1	GP		bind					Cdc34	GP				NULL	insect cells	0	NULL	NULL	NULL	gw60_science_284_5414_662_s_87	10213692	( A) Rbx1 binds Cdc34 and stimulates association of Cdc53 with Cdc34 in insect cells.	bind
58176	2	611	5	NULL	NULL	0	NULL	Cdc53	GP		associate with					Cdc34	GP				NULL	insect cells	0	NULL	NULL	NULL	gw60_science_284_5414_662_s_87	10213692	( A) Rbx1 binds Cdc34 and stimulates association of Cdc53 with Cdc34 in insect cells.	bind
58177	3	611	5	NULL	NULL	0	NULL	statement 1	Process		stimulates					statement 2	Process				NULL	insect cells	0	NULL	NULL	NULL	gw60_science_284_5414_662_s_87	10213692	( A) Rbx1 binds Cdc34 and stimulates association of Cdc53 with Cdc34 in insect cells.	bind
1827	1	611	6	NULL	NULL	0	NULL	Rbx1	GP		bind					Cdc34	GP				NULL	insect cells	NULL	NULL	NULL	NULL	gw60_science_284_5414_662_s_87	10213692	( A) Rbx1 binds Cdc34 and stimulates association of Cdc53 with Cdc34 in insect cells.	bind
1828	2	611	6	NULL	NULL	0	NULL	Cdc53	GP		bind					Cdc34	GP				NULL	insect cells	NULL	NULL	NULL	NULL	gw60_science_284_5414_662_s_87	10213692	( A) Rbx1 binds Cdc34 and stimulates association of Cdc53 with Cdc34 in insect cells.	bind
1829	3	611	6	NULL	NULL	0	NULL	Statement 1	Process		stimulate					Statement 2	Process				NULL	insect cells	NULL	NULL	NULL	NULL	gw60_science_284_5414_662_s_87	10213692	( A) Rbx1 binds Cdc34 and stimulates association of Cdc53 with Cdc34 in insect cells.	bind
58178	1	612	5	NULL	NULL	0	NULL	Sp-1	GP	endogenous	bind					M-CSF	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_jclininvest_102_10_1850_s_203	9819371	( A) Recombinant Egr-1 decreases the binding of endogenous Sp-1 and Sp-3 from the M-CSF promoter.	bind
58179	2	612	5	NULL	NULL	0	NULL	Sp-3	GP	endogenous	bind					M-CSF	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_jclininvest_102_10_1850_s_203	9819371	( A) Recombinant Egr-1 decreases the binding of endogenous Sp-1 and Sp-3 from the M-CSF promoter.	bind
58180	3	612	5	NULL	NULL	0	NULL	Egr-1	GP	recombinant	decreases					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jclininvest_102_10_1850_s_203	9819371	( A) Recombinant Egr-1 decreases the binding of endogenous Sp-1 and Sp-3 from the M-CSF promoter.	bind
58181	4	612	5	NULL	NULL	0	NULL	Egr-1	GP	recombinant	decreases					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jclininvest_102_10_1850_s_203	9819371	( A) Recombinant Egr-1 decreases the binding of endogenous Sp-1 and Sp-3 from the M-CSF promoter.	bind
1830	1	612	6	NULL	NULL	0	NULL	Sp1	GP	endogenous	bind					M-CSF 	GP			Promoter	NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_10_1850_s_203	9819371	( A) Recombinant Egr-1 decreases the binding of endogenous Sp-1 and Sp-3 from the M-CSF promoter.	bind
1831	2	612	6	NULL	NULL	0	NULL	Sp3	GP	endogenous	bind					M-CSF 	GP			Promoter	NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_10_1850_s_203	9819371	( A) Recombinant Egr-1 decreases the binding of endogenous Sp-1 and Sp-3 from the M-CSF promoter.	bind
1832	3	612	6	NULL	NULL	0	NULL	Egr-1	GP	recombinant	decreases					Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_10_1850_s_203	9819371	( A) Recombinant Egr-1 decreases the binding of endogenous Sp-1 and Sp-3 from the M-CSF promoter.	bind
1833	4	612	6	NULL	NULL	0	NULL	Egr-1	GP	recombinant	decreases					Statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_10_1850_s_203	9819371	( A) Recombinant Egr-1 decreases the binding of endogenous Sp-1 and Sp-3 from the M-CSF promoter.	bind
58182	1	616	5	NULL	NULL	0	NULL	RelA	GP		bind					p300	GP		amino acid residues (1-610)		NULL		0	NULL	NULL	NULL	gw60_embo_17_11_3124_s_36	9606194	( A) RelA binds p300 between amino acid residues 1 and 610.	bind
1834	1	616	6	NULL	NULL	0	NULL	RelA	GP		bind					p300	GP		 amino acid residues 1 and 610		NULL		NULL	NULL	NULL	NULL	gw60_embo_17_11_3124_s_36	9606194	( A) RelA binds p300 between amino acid residues 1 and 610.	bind
58183	1	620	5	NULL	NULL	0	NULL	RFC	GP		forms complex with					Asf1	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1365_s_210	15901673	( A) RFC and Rfc2-5 coprecipitate with Asf1.	bind
58184	2	620	5	NULL	NULL	0	NULL	Rfc2	GP		forms complex with					Asf1	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1365_s_210	15901673	( A) RFC and Rfc2-5 coprecipitate with Asf1.	bind
58185	3	620	5	NULL	NULL	0	NULL	Rfc3	GP		forms complex with					Asf1	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1365_s_210	15901673	( A) RFC and Rfc2-5 coprecipitate with Asf1.	bind
58186	4	620	5	NULL	NULL	0	NULL	Rfc4	GP		forms complex with					Asf1	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1365_s_210	15901673	( A) RFC and Rfc2-5 coprecipitate with Asf1.	bind
58187	5	620	5	NULL	NULL	0	NULL	Rfc5	GP		forms complex with					Asf1	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1365_s_210	15901673	( A) RFC and Rfc2-5 coprecipitate with Asf1.	bind
1835	1	620	6	NULL	NULL	0	NULL	RFC	GP		bind					Asf1	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1365_s_210	15901673	( A) RFC and Rfc2-5 coprecipitate with Asf1.	bind
1836	2	620	6	NULL	NULL	0	NULL	Rfc2-5	GP		bind					Asf1	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1365_s_210	15901673	( A) RFC and Rfc2-5 coprecipitate with Asf1.	bind
58188	1	622	5	NULL	NULL	0	NULL	RAR	GP		bind					all- trans retinoic acid	Chemical				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_68_0_559_s_136	10872460	( a) Ribbon diagram of RAR bound to   all- trans retinoic acid ( red).	bind
1837	1	622	6	NULL	NULL	0	NULL	RAR	GP		bind					 all- trans retinoic acid	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_68_0_559_s_136	10872460	( a) Ribbon diagram of RAR bound to   all- trans retinoic acid ( red).	bind
58189	1	623	5	NULL	NULL	0	NULL	14-3-3c protein dimer	GP	 tobacco	bind					peptide Gln-Ser-Tyr-pThr-Val	AminoAcid				NULL		0	NULL	NULL	NULL	gw70_embo_22_5_987_s_34	12606564	( A) Ribbon plot of two different orientations of the dimeric tobacco 14-3-3c protein  (green) bound to the peptide Gln-Ser-Tyr-pThr-Val (yellow), which constitutes the  C-terminal end of PMA2, a H+-ATPase isoform from  Nicotiana plumbaginifolia.	bind
58190	2	623	5	NULL	NULL	0	NULL	peptide Gln-Ser-Tyr-pThr-Val	AminoAcid		constitutes					PMA2	GP		C-terminal end		NULL		0	NULL	NULL	NULL	gw70_embo_22_5_987_s_34	12606564	( A) Ribbon plot of two different orientations of the dimeric tobacco 14-3-3c protein  (green) bound to the peptide Gln-Ser-Tyr-pThr-Val (yellow), which constitutes the  C-terminal end of PMA2, a H+-ATPase isoform from  Nicotiana plumbaginifolia.	bind
58191	3	623	5	NULL	NULL	0	NULL	PMA2	GP		is an isoform of					H+-ATPase	GP	Nicotiana plumbaginifolia			NULL		0	NULL	NULL	NULL	gw70_embo_22_5_987_s_34	12606564	( A) Ribbon plot of two different orientations of the dimeric tobacco 14-3-3c protein  (green) bound to the peptide Gln-Ser-Tyr-pThr-Val (yellow), which constitutes the  C-terminal end of PMA2, a H+-ATPase isoform from  Nicotiana plumbaginifolia.	bind
58192	1	625	5	NULL	NULL	0	NULL	3G ARNO	GP		bind			PH domain		Ins(1,4,5)P3	Chemical				NULL		0	NULL	NULL	NULL	gw70_embo_23_19_3711_s_40	15359279	( A) Ribbon representation of the 3G ARNO PH domain bound to Ins(1,4,5)P3.	bind
1838	1	625	6	3	NULL	0	NULL	3G ARNO	GP		bind			 PH domain		Ins(1,4,5)P3	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_19_3711_s_40	15359279	( A) Ribbon representation of the 3G ARNO PH domain bound to Ins(1,4,5)P3.	bind
58193	1	626	5	NULL	NULL	0	NULL	RLF	GP		is activated during					metaphase-anaphase transition	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_1_13_s_155	9314525	( a) RLF becomes active at  metaphase-anaphase transition;  Drosophila MCMs binding to chromosomes follows metaphase-anaphase transition.	bind
58194	2	626	5	NULL	NULL	0	NULL	MCMs	GP	Drosophila	bind					chromosomes	Chromosome				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_1_13_s_155	9314525	( a) RLF becomes active at  metaphase-anaphase transition;  Drosophila MCMs binding to chromosomes follows metaphase-anaphase transition.	bind
58195	3	626	5	NULL	NULL	0	NULL	statement 2	Process		follows					metaphase-anaphase transition	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_1_13_s_155	9314525	( a) RLF becomes active at  metaphase-anaphase transition;  Drosophila MCMs binding to chromosomes follows metaphase-anaphase transition.	bind
1839	1	626	6	NULL	NULL	0	NULL	MCMs	GP	Drosophila	bind					chromosomes	Chromosome				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_139_1_13_s_155	9314525	( a) RLF becomes active at  metaphase-anaphase transition;  Drosophila MCMs binding to chromosomes follows metaphase-anaphase transition.	bind
1840	2	626	6	NULL	NULL	0	NULL	Statement 1	Process		follows					metaphase-anaphase 	Process	transition of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_139_1_13_s_155	9314525	( a) RLF becomes active at  metaphase-anaphase transition;  Drosophila MCMs binding to chromosomes follows metaphase-anaphase transition.	bind
1841	3	626	6	NULL	NULL	0	NULL	RLF	GP		is active at					metaphase-anaphase 	Process	transition of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_139_1_13_s_155	9314525	( a) RLF becomes active at  metaphase-anaphase transition;  Drosophila MCMs binding to chromosomes follows metaphase-anaphase transition.	bind
58196	1	628	5	NULL	NULL	0	NULL	Salp	GP		bind					p85	GP		SH3 domain		NULL		0	NULL	NULL	NULL	gw60_gene_240_1_133_s_248	10564820	( A) Salp  binds the p85 SH3 domain.	bind
1842	1	628	6	NULL	NULL	0	NULL	Salp	GP		bind					p85	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_gene_240_1_133_s_248	10564820	( A) Salp  binds the p85 SH3 domain.	bind
58197	1	630	5	NULL	NULL	0	NULL	PDK1	GP		bind					PtdIns(3,4,5)P3	Chemical	biotinylated			NULL		0	NULL	NULL	NULL	gw70_embo_23_20_3918_s_171	15457207	( A) Saturation-binding isotherms of the indicated forms of PDK1 binding to biotinylated-PtdIns(3,4,5)P3 (bPIP3).	bind
58198	2	630	5	NULL	NULL	0	NULL	biotinylated-PtdIns(3,4,5)P3	Chemical		is					bPIP3	Chemical				NULL		0	NULL	NULL	NULL	gw70_embo_23_20_3918_s_171	15457207	( A) Saturation-binding isotherms of the indicated forms of PDK1 binding to biotinylated-PtdIns(3,4,5)P3 (bPIP3).	bind
1865	1	630	6	NULL	NULL	0	NULL	PDK1	GP		bind					PtdIns(3,4,5)P3 (bPIP3)	GP	biotinylated			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_20_3918_s_171	15457207	( A) Saturation-binding isotherms of the indicated forms of PDK1 binding to biotinylated-PtdIns(3,4,5)P3 (bPIP3).	bind
58199	1	631	5	NULL	NULL	0	NULL	NT-3	GP	iodinated	bind					Ltrk	Cell				NULL		0	NULL	NULL	NULL	gw60_embo_17_9_2534_s_134	9564036	( A) Scatchard analyses of saturation curves for iodinated NT-3 binding to the Ltrk fibroblast cell line.	bind
58200	2	631	5	NULL	NULL	0	NULL	Ltrk	Cell		is a type of					fibroblast cell line	Cell				NULL		0	NULL	NULL	NULL	gw60_embo_17_9_2534_s_134	9564036	( A) Scatchard analyses of saturation curves for iodinated NT-3 binding to the Ltrk fibroblast cell line.	bind
1871	1	631	6	NULL	NULL	0	NULL	NT-3	GP	iodinated	bind					Ltrk	Cell				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_9_2534_s_134	9564036	( A) Scatchard analyses of saturation curves for iodinated NT-3 binding to the Ltrk fibroblast cell line.	bind
51837	2	631	6	NULL	NULL	0	NULL	 Ltrk	Cell		is a type of					fibroblast cell line	Cell				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_9_2534_s_134	9564036	( A) Scatchard analyses of saturation curves for iodinated NT-3 binding to the Ltrk fibroblast cell line.	bind
58201	1	632	5	NULL	NULL	0	NULL	EGF	GP		bind					MDCK-EGFR cells	Cell				NULL		0	NULL	NULL	NULL	gw70_embo_23_8_1739_s_83	15057284	( A) Scatchard analysis of EGF binding to MDCK-EGFR cells.	bind
1872	1	632	6	NULL	NULL	0	NULL	EGF 	GP		bind					MDCK-EGFR cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_8_1739_s_83	15057284	( A) Scatchard analysis of EGF binding to MDCK-EGFR cells.	bind
58202	1	641	5	NULL	NULL	0	NULL	MBP-CTD	GP		bind					TBP	GP				NULL	in vitro	0	NULL	NULL	NULL	gw70_pnas_100_17_10108_s_181	12900506	( A) SDS/PAGE analysis of  in vitro protein interactions shows  that MBP-CTD binds TBP, but not VirD2, whereas VirD2  recruits TBP.	bind
58203	2	641	5	NULL	NULL	0	NULL	MBP-CTD	GP		does not bind					VirD2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_100_17_10108_s_181	12900506	( A) SDS/PAGE analysis of  in vitro protein interactions shows  that MBP-CTD binds TBP, but not VirD2, whereas VirD2  recruits TBP.	bind
58204	3	641	5	NULL	NULL	0	NULL	VirD2	GP		recruit					TBP	GP				NULL	in vitro	0	NULL	NULL	NULL	gw70_pnas_100_17_10108_s_181	12900506	( A) SDS/PAGE analysis of  in vitro protein interactions shows  that MBP-CTD binds TBP, but not VirD2, whereas VirD2  recruits TBP.	bind
1873	1	641	6	NULL	NULL	0	NULL	MBP	GP		bind			CTD		TBP	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_100_17_10108_s_181	12900506	( A) SDS/PAGE analysis of  in vitro protein interactions shows  that MBP-CTD binds TBP, but not VirD2, whereas VirD2  recruits TBP.	bind
1874	2	641	6	NULL	NULL	0	NULL	MBP	GP		does not bind			CTD		VirD2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_100_17_10108_s_181	12900506	( A) SDS/PAGE analysis of  in vitro protein interactions shows  that MBP-CTD binds TBP, but not VirD2, whereas VirD2  recruits TBP.	bind
1875	3	641	6	NULL	NULL	0	NULL	VirD2	GP		recruits					TBP	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_100_17_10108_s_181	12900506	( A) SDS/PAGE analysis of  in vitro protein interactions shows  that MBP-CTD binds TBP, but not VirD2, whereas VirD2  recruits TBP.	bind
58205	1	642	5	NULL	NULL	0	NULL	WCE	GP	yeast	bind					ScOrc4p	GP	His6-tagged			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_9_4938_s_178	11296251	( a) SDS/PAGE of proteins from yeast WCE bound to Ni2+-Sepharose saturated with His6-tagged ScOrc4p or RepA (major bands).	bind
58206	2	642	5	NULL	NULL	0	NULL	WCE	GP	yeast	bind					RepA	GP	His6-tagged			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_9_4938_s_178	11296251	( a) SDS/PAGE of proteins from yeast WCE bound to Ni2+-Sepharose saturated with His6-tagged ScOrc4p or RepA (major bands).	bind
58207	3	642	5	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_9_4938_s_178	11296251	( a) SDS/PAGE of proteins from yeast WCE bound to Ni2+-Sepharose saturated with His6-tagged ScOrc4p or RepA (major bands).	bind
1876	1	642	6	NULL	NULL	0	NULL	WCE	GP	yeast	bind					ScOrc4p 	GP	His6-tagged			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_9_4938_s_178	11296251	( a) SDS/PAGE of proteins from yeast WCE bound to Ni2+-Sepharose saturated with His6-tagged ScOrc4p or RepA (major bands).	bind
58208	1	643	5	NULL	NULL	0	NULL	Sec23-24p	GP		bind					Bet1p	GP		COOH-terminal (membrane-proximal) 79 amino acids of the cytosolic domain		NULL		0	NULL	NULL	NULL	gw60_science_281_5377_698_s_77	9685263	( A) Sec23-24p binding is localized to the COOH-terminal (membrane-proximal) 79 amino acids of the cytosolic domain of Bet1p, whereas Sar1p can bind to the 41 COOH-terminal amino acids of the cytosolic domain.	bind
58209	2	643	5	NULL	NULL	0	NULL	Sar1p	GP		bind					Bet1p	GP		COOH-terminal amino acids of cytosolic domain		NULL		0	NULL	NULL	NULL	gw60_science_281_5377_698_s_77	9685263	( A) Sec23-24p binding is localized to the COOH-terminal (membrane-proximal) 79 amino acids of the cytosolic domain of Bet1p, whereas Sar1p can bind to the 41 COOH-terminal amino acids of the cytosolic domain.	bind
1877	1	643	6	NULL	NULL	0	NULL	Sec23-24p	GP		bind					Bet1p	GP		COOH-terminal (membrane-proximal) 79 amino acids of the cytosolic domain		NULL		NULL	NULL	NULL	NULL	gw60_science_281_5377_698_s_77	9685263	( A) Sec23-24p binding is localized to the COOH-terminal (membrane-proximal) 79 amino acids of the cytosolic domain of Bet1p, whereas Sar1p can bind to the 41 COOH-terminal amino acids of the cytosolic domain.	bind
1878	2	643	6	NULL	NULL	0	NULL	Sar1p	GP		bind					Bet1p	GP		41 COOH-terminal amino acids of the cytosolic domain		NULL		NULL	NULL	NULL	NULL	gw60_science_281_5377_698_s_77	9685263	( A) Sec23-24p binding is localized to the COOH-terminal (membrane-proximal) 79 amino acids of the cytosolic domain of Bet1p, whereas Sar1p can bind to the 41 COOH-terminal amino acids of the cytosolic domain.	bind
58210	1	644	5	NULL	NULL	0	NULL	trans-acting delta ribozyme	GP	engineered	bind					HBV target	Organism				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_21_4682_s_27	12409459	( A) Secondary structure of the engineered  trans-acting  delta ribozyme bound to the HBV target.	bind
58211	1	646	5	NULL	NULL	0	NULL	anti-RAS scFv	GP		bind					HRASG12V-GppNp antigen	GP				NULL		0	NULL	NULL	NULL	gw70_embo_22_5_1025_s_139	12606568	( A) Sensograms showing the binding of anti-RAS scFv with HRASG12V-GppNp antigen (immobilized  1500 RU).	bind
1879	1	646	6	NULL	NULL	0	NULL	anti-RAS scFv	GP		bind					HRASG12V-GppNp antigen	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_22_5_1025_s_139	12606568	( A) Sensograms showing the binding of anti-RAS scFv with HRASG12V-GppNp antigen (immobilized  1500 RU).	bind
58212	1	647	5	NULL	NULL	0	NULL	IGFBP-5	GP		bind					IGF-I	GP	biotinylated			NULL		0	NULL	NULL	NULL	gw60_embo_17_22_6558_s_62	9822601	( A) Sensograms showing the binding of IGFBP-5 to a sensor chip SA coated with 5 nM biotinylated IGF-I and IGF-II.	bind
58213	2	647	5	NULL	NULL	0	NULL	IGFBP-5	GP		bind					IGF-II	GP	biotinylated			NULL		0	NULL	NULL	NULL	gw60_embo_17_22_6558_s_62	9822601	( A) Sensograms showing the binding of IGFBP-5 to a sensor chip SA coated with 5 nM biotinylated IGF-I and IGF-II.	bind
1880	1	647	6	NULL	NULL	0	NULL	IGFBP-5 	GP		bind					IGF-I	GP	biotinylated			NULL		NULL	NULL	NULL	NULL	gw60_embo_17_22_6558_s_62	9822601	( A) Sensograms showing the binding of IGFBP-5 to a sensor chip SA coated with 5 nM biotinylated IGF-I and IGF-II.	bind
1881	2	647	6	NULL	NULL	0	NULL	IGFBP-5 	GP		bind					IGF-II	GP	biotinylated			NULL		NULL	NULL	NULL	NULL	gw60_embo_17_22_6558_s_62	9822601	( A) Sensograms showing the binding of IGFBP-5 to a sensor chip SA coated with 5 nM biotinylated IGF-I and IGF-II.	bind
58214	1	652	5	NULL	NULL	0	NULL	hairpin ribozyme	GP		bind					target RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_pnas_98_1_130_s_92	11136250	( A) Sequence and secondary structure of the hairpin ribozyme (capital letters), bound to its target RNA (lowercase letters).	bind
1882	1	652	6	NULL	NULL	0	NULL	hairpin ribozyme	NucleicAcid		bind					target RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_1_130_s_92	11136250	( A) Sequence and secondary structure of the hairpin ribozyme (capital letters), bound to its target RNA (lowercase letters).	bind
58215	1	658	5	NULL	NULL	0	NULL	SIP1	GP		bind			FS		alpha4-integrin	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_137	10487759	( A) SIP1FS and SIP1CZF bind to the alpha4-integrin (alpha4I) promoter.	bind
58216	2	658	5	NULL	NULL	0	NULL	SIP1	GP		bind			CZF		alpha4-integrin	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_137	10487759	( A) SIP1FS and SIP1CZF bind to the alpha4-integrin (alpha4I) promoter.	bind
58217	3	658	5	NULL	NULL	0	NULL	alpha4-integrin	GP		is					alpha4I	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_18_5073_s_137	10487759	( A) SIP1FS and SIP1CZF bind to the alpha4-integrin (alpha4I) promoter.	bind
1883	1	658	6	NULL	NULL	0	NULL	SIP1	GP		bind			FS		alpha4-integrin 	GP			Promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_137	10487759	( A) SIP1FS and SIP1CZF bind to the alpha4-integrin (alpha4I) promoter.	bind
1884	2	658	6	NULL	NULL	0	NULL	SIP1	GP		bind			CZF		alpha4-integrin 	GP			Promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_137	10487759	( A) SIP1FS and SIP1CZF bind to the alpha4-integrin (alpha4I) promoter.	bind
51839	3	658	6	NULL	NULL	0	NULL	alpha4I	GP		is					alpha4-integrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_137	10487759	( A) SIP1FS and SIP1CZF bind to the alpha4-integrin (alpha4I) promoter.	bind
58218	1	659	5	NULL	NULL	0	NULL	SipA	GP		does not bind		directly			T-plastin	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_18_10176_s_119	10468582	( A) SipA does not bind to T-plastin directly.	bind
1885	1	659	6	NULL	NULL	0	NULL	SipA	GP		does not bind		directly			T-plastin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_18_10176_s_119	10468582	( A) SipA does not bind to T-plastin directly.	bind
58219	1	660	5	NULL	NULL	0	NULL	SKAP55	GP		bind			SH3 domain		FYB	GP				NULL	COS cells	0	NULL	NULL	NULL	gw60_pnas_95_15_8779_s_139	9671755	( A) SKAP55 and SKAP55R SH3 domains bind to FYB in COS cells.	bind
58220	2	660	5	NULL	NULL	0	NULL	SKAP55R	GP		bind			SH3 domain		FYB	GP				NULL	COS cells	NULL	NULL	NULL	NULL	gw60_pnas_95_15_8779_s_139	9671755	( A) SKAP55 and SKAP55R SH3 domains bind to FYB in COS cells.	bind
1886	1	660	6	NULL	NULL	0	NULL	SKAP55	GP		bind			SH3 domains		FYB	GP				NULL	COS cells	NULL	NULL	NULL	NULL	gw60_pnas_95_15_8779_s_139	9671755	( A) SKAP55 and SKAP55R SH3 domains bind to FYB in COS cells.	bind
1887	2	660	6	NULL	NULL	0	NULL	SKAP55R 	GP		bind			SH3 domains		FYB	GP				NULL	COS cells	NULL	NULL	NULL	NULL	gw60_pnas_95_15_8779_s_139	9671755	( A) SKAP55 and SKAP55R SH3 domains bind to FYB in COS cells.	bind
58221	1	661	5	NULL	NULL	0	NULL	Smad3	GP		bind			MH1 domain		HEF1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6759_s_115	11118211	( A) Smad3 binds to HEF1 via both Smad3N (MH1) and Smad3C (MH2) domains, but only the N-terminal domain induces the degradation of HEF1.	bind
58222	2	661	5	NULL	NULL	0	NULL	Smad3	GP		bind			MH2 domain		HEF1	GP				NULL		0	NULL	NULL	NULL	gw60_embo_19_24_6759_s_115	11118211	( A) Smad3 binds to HEF1 via both Smad3N (MH1) and Smad3C (MH2) domains, but only the N-terminal domain induces the degradation of HEF1.	bind
58223	3	661	5	NULL	NULL	0	NULL	statement 1	Process		induces					HEF1	GP	degradation of			NULL		0	NULL	NULL	NULL	gw60_embo_19_24_6759_s_115	11118211	( A) Smad3 binds to HEF1 via both Smad3N (MH1) and Smad3C (MH2) domains, but only the N-terminal domain induces the degradation of HEF1.	bind
58224	4	661	5	NULL	NULL	0	NULL	MH1 domain			is					Smad3N					NULL		0	NULL	NULL	NULL	gw60_embo_19_24_6759_s_115	11118211	( A) Smad3 binds to HEF1 via both Smad3N (MH1) and Smad3C (MH2) domains, but only the N-terminal domain induces the degradation of HEF1.	bind
58225	5	661	5	NULL	NULL	0	NULL	MH2 domain			is					Smad3C					NULL		0	NULL	NULL	NULL	gw60_embo_19_24_6759_s_115	11118211	( A) Smad3 binds to HEF1 via both Smad3N (MH1) and Smad3C (MH2) domains, but only the N-terminal domain induces the degradation of HEF1.	bind
1888	1	661	6	NULL	NULL	0	NULL	Smad3	GP		bind			Smad3N		HEF1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6759_s_115	11118211	( A) Smad3 binds to HEF1 via both Smad3N (MH1) and Smad3C (MH2) domains, but only the N-terminal domain induces the degradation of HEF1.	bind
1889	2	661	6	NULL	NULL	0	NULL	Smad3	GP		bind			Smad3C domain		HEF1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6759_s_115	11118211	( A) Smad3 binds to HEF1 via both Smad3N (MH1) and Smad3C (MH2) domains, but only the N-terminal domain induces the degradation of HEF1.	bind
1890	3	661	6	NULL	NULL	0	NULL	Smad3	GP		induces			N-terminal domain		HEF1	GP	degradation of 			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6759_s_115	11118211	( A) Smad3 binds to HEF1 via both Smad3N (MH1) and Smad3C (MH2) domains, but only the N-terminal domain induces the degradation of HEF1.	bind
51937	4	661	6	NULL	NULL	0	NULL	Smad3N	GP		is					MH1 domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6759_s_115	11118211	( A) Smad3 binds to HEF1 via both Smad3N (MH1) and Smad3C (MH2) domains, but only the N-terminal domain induces the degradation of HEF1.	bind
51938	5	661	6	NULL	NULL	0	NULL	 Smad3C	GP		is					MH2 domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6759_s_115	11118211	( A) Smad3 binds to HEF1 via both Smad3N (MH1) and Smad3C (MH2) domains, but only the N-terminal domain induces the degradation of HEF1.	bind
58226	1	662	5	NULL	NULL	0	NULL	SnoN	GP		interacts with					Smad4	GP				NULL		0	NULL	NULL	NULL	gw60_science_286_5440_771_s_55	10531062	( A) SnoN binds to the SBE through interaction with Smad4.	bind
58227	2	662	5	NULL	NULL	0	NULL	statement 1	Process		bind									SBE	NULL		0	NULL	NULL	NULL	gw60_science_286_5440_771_s_55	10531062	( A) SnoN binds to the SBE through interaction with Smad4.	bind
1891	1	662	6	NULL	NULL	0	NULL	SnoN	GP		interacts 					Smad4	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5440_771_s_55	10531062	( A) SnoN binds to the SBE through interaction with Smad4.	bind
1892	2	662	6	NULL	NULL	0	NULL	Statement 1	Process		bind						NucleicAcid			SBE	NULL		NULL	NULL	NULL	NULL	gw60_science_286_5440_771_s_55	10531062	( A) SnoN binds to the SBE through interaction with Smad4.	bind
58228	1	663	5	NULL	NULL	0	NULL	SOCS2	GP		bind					elongin C	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_20_7637_s_54	16675548	( A) SOCS2 binds elongin C (electrostatic surface shown) in a hydrophobic interface of   2,200  Ang 2 (for clarity, elongin B is not shown).	bind
1893	1	663	6	NULL	NULL	0	NULL	SOCS2	GP		bind					elongin C	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_20_7637_s_54	16675548	( A) SOCS2 binds elongin C (electrostatic surface shown) in a hydrophobic interface of   2,200  Ang 2 (for clarity, elongin B is not shown).	bind
58229	1	665	5	NULL	NULL	0	NULL	HKa	GP		bind		specifically			tropomyosin	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_19_12224_s_154	12196635	( A) Specific binding of HKa to purified tropomyosin.	bind
1894	1	665	6	NULL	NULL	0	NULL	HKa	GP		bind		specifically			tropomyosin	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_19_12224_s_154	12196635	( A) Specific binding of HKa to purified tropomyosin.	bind
58230	1	666	5	NULL	NULL	0	NULL	CTCF	GP		bind									Meg1 repeat	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_127	12595547	( A) Specific competition for CTCF binding to the  Meg1 repeat was seen for the canonical CTCF- binding sequence of the chicken beta -globin FII (as shown in F), but not for the transcription factor recognition sequences of SP1 and AP1 (as shown in S and A) and vice versa.	bind
58231	2	666	5	NULL	NULL	0	NULL	CTCF	GP		bind					beta -globin FII	GP	chicken	CTCF- binding sequence		NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_127	12595547	( A) Specific competition for CTCF binding to the  Meg1 repeat was seen for the canonical CTCF- binding sequence of the chicken beta -globin FII (as shown in F), but not for the transcription factor recognition sequences of SP1 and AP1 (as shown in S and A) and vice versa.	bind
58232	3	666	5	NULL	NULL	0	NULL	statement 1	Process		competes with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_127	12595547	( A) Specific competition for CTCF binding to the  Meg1 repeat was seen for the canonical CTCF- binding sequence of the chicken beta -globin FII (as shown in F), but not for the transcription factor recognition sequences of SP1 and AP1 (as shown in S and A) and vice versa.	bind
58234	4	666	5	NULL	NULL	0	NULL	SP1	GP		does not compete with					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_127	12595547	( A) Specific competition for CTCF binding to the  Meg1 repeat was seen for the canonical CTCF- binding sequence of the chicken beta -globin FII (as shown in F), but not for the transcription factor recognition sequences of SP1 and AP1 (as shown in S and A) and vice versa.	bind
58235	5	666	5	NULL	NULL	0	NULL	AP1	GP		does not compete with					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_127	12595547	( A) Specific competition for CTCF binding to the  Meg1 repeat was seen for the canonical CTCF- binding sequence of the chicken beta -globin FII (as shown in F), but not for the transcription factor recognition sequences of SP1 and AP1 (as shown in S and A) and vice versa.	bind
2158	1	666	6	NULL	NULL	0	NULL	beta -globin FII	GP	chicken	bind				CTCF- binding sequence	CTCF 	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_127	12595547	( A) Specific competition for CTCF binding to the  Meg1 repeat was seen for the canonical CTCF- binding sequence of the chicken beta -globin FII (as shown in F), but not for the transcription factor recognition sequences of SP1 and AP1 (as shown in S and A) and vice versa.	bind
2159	2	666	6	NULL	NULL	0	NULL	CTCF	GP		bind						NucleicAcid			Meg1 repeat	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_127	12595547	( A) Specific competition for CTCF binding to the  Meg1 repeat was seen for the canonical CTCF- binding sequence of the chicken beta -globin FII (as shown in F), but not for the transcription factor recognition sequences of SP1 and AP1 (as shown in S and A) and vice versa.	bind
2160	3	666	6	NULL	NULL	0	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_127	12595547	( A) Specific competition for CTCF binding to the  Meg1 repeat was seen for the canonical CTCF- binding sequence of the chicken beta -globin FII (as shown in F), but not for the transcription factor recognition sequences of SP1 and AP1 (as shown in S and A) and vice versa.	bind
2192	4	666	6	NULL	NULL	0	NULL	Sp1	GP		does not compete					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_127	12595547	( A) Specific competition for CTCF binding to the  Meg1 repeat was seen for the canonical CTCF- binding sequence of the chicken beta -globin FII (as shown in F), but not for the transcription factor recognition sequences of SP1 and AP1 (as shown in S and A) and vice versa.	bind
2193	5	666	6	NULL	NULL	0	NULL	Ap1	GP		does not compete					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_127	12595547	( A) Specific competition for CTCF binding to the  Meg1 repeat was seen for the canonical CTCF- binding sequence of the chicken beta -globin FII (as shown in F), but not for the transcription factor recognition sequences of SP1 and AP1 (as shown in S and A) and vice versa.	bind
58236	1	667	5	NULL	NULL	0	NULL	sperm	Cell		release					MSP	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_17_2_187_s_257	12533508	( a) Sperm release MSP, which binds to VAB-1 and another receptor(s) on oocytes and sheath cells.	bind
58237	2	667	5	NULL	NULL	0	NULL	MSP	GP		bind					VAB-1	GP				NULL	oocytes	0	NULL	NULL	NULL	gw60_genesdev_17_2_187_s_257	12533508	( a) Sperm release MSP, which binds to VAB-1 and another receptor(s) on oocytes and sheath cells.	bind
58238	3	667	5	NULL	NULL	0	NULL	MSP	GP		bind					VAB-1	GP				NULL	sheath cells	0	NULL	NULL	NULL	gw60_genesdev_17_2_187_s_257	12533508	( a) Sperm release MSP, which binds to VAB-1 and another receptor(s) on oocytes and sheath cells.	bind
1914	1	667	6	NULL	NULL	0	NULL	sperm	Cell		release					MSP	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_2_187_s_257	12533508	( a) Sperm release MSP, which binds to VAB-1 and another receptor(s) on oocytes and sheath cells.	bind
1915	2	667	6	NULL	NULL	0	NULL	MSP	GP		bind					VAB-1	GP				NULL	oocytes	NULL	NULL	NULL	NULL	gw60_genesdev_17_2_187_s_257	12533508	( a) Sperm release MSP, which binds to VAB-1 and another receptor(s) on oocytes and sheath cells.	bind
1916	3	667	6	NULL	NULL	0	NULL	MSP	GP		bind					receptor	GP				NULL	oocytes 	NULL	NULL	NULL	NULL	gw60_genesdev_17_2_187_s_257	12533508	( a) Sperm release MSP, which binds to VAB-1 and another receptor(s) on oocytes and sheath cells.	bind
51967	4	667	6	NULL	NULL	0	NULL	MSP	GP		bind					VAB-1	GP				NULL	sheath cells	NULL	NULL	NULL	NULL	gw60_genesdev_17_2_187_s_257	12533508	( a) Sperm release MSP, which binds to VAB-1 and another receptor(s) on oocytes and sheath cells.	bind
51968	6	667	6	NULL	NULL	0	NULL	MSP	GP		bind					receptor	GP				NULL	sheath cells	NULL	NULL	NULL	NULL	gw60_genesdev_17_2_187_s_257	12533508	( a) Sperm release MSP, which binds to VAB-1 and another receptor(s) on oocytes and sheath cells.	bind
58239	1	669	5	NULL	NULL	0	NULL	lipid layers	Chemical		contains					PIP2	Chemical				NULL		0	NULL	NULL	NULL	gw70_embo_24_14_2556_s_150	15961997	( A) SPR sensograms showing the binding of the individual PDZ domains of syntenin-2 to  10% PIP2-containing lipid layers.	bind
58240	2	669	5	NULL	NULL	0	NULL	syntenin-2	GP		bind			PDZ domain		statement 1	Chemical				NULL		0	NULL	NULL	NULL	gw70_embo_24_14_2556_s_150	15961997	( A) SPR sensograms showing the binding of the individual PDZ domains of syntenin-2 to  10% PIP2-containing lipid layers.	bind
1917	2	669	6	NULL	NULL	0	NULL	syntenin-2	GP		bind			individual PDZ domains		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_14_2556_s_150	15961997	( A) SPR sensograms showing the binding of the individual PDZ domains of syntenin-2 to  10% PIP2-containing lipid layers.	bind
51969	1	669	6	NULL	NULL	0	NULL	lipid layers	CellComponent		contain					PIP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_14_2556_s_150	15961997	( A) SPR sensograms showing the binding of the individual PDZ domains of syntenin-2 to  10% PIP2-containing lipid layers.	bind
58241	1	672	5	NULL	NULL	0	NULL	uPA	GP		bind			beta-hairpin in GFD		uPAR	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_9_1655_s_132	15861141	( A) Stereo views of the key residues by which AE147 (blue) and the beta-hairpin in GFD of uPA (red) bind to uPAR in our crystal structure and in a GFD uPAR  model, respectively.	bind
1918	1	672	6	NULL	NULL	0	NULL	uPA	GP		bind			AE147		uPAR	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_9_1655_s_132	15861141	( A) Stereo views of the key residues by which AE147 (blue) and the beta-hairpin in GFD of uPA (red) bind to uPAR in our crystal structure and in a GFD uPAR  model, respectively.	bind
1919	2	672	6	NULL	NULL	0	NULL	uPA	GP		bind			beta-hairpin in GFD		uPAR	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_9_1655_s_132	15861141	( A) Stereo views of the key residues by which AE147 (blue) and the beta-hairpin in GFD of uPA (red) bind to uPAR in our crystal structure and in a GFD uPAR  model, respectively.	bind
58242	1	673	5	NULL	NULL	0	NULL	Npl4	GP		bind			NZF		Ub	GP				NULL		0	NULL	NULL	NULL	gw70_embo_23_7_1411_s_55	15029239	( A) Stereoview of Npl4 NZF (ribbon) bound to Ub (surface).	bind
1920	1	673	6	NULL	NULL	0	NULL	Npl4	GP		bind			NZF		Ub	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1411_s_55	15029239	( A) Stereoview of Npl4 NZF (ribbon) bound to Ub (surface).	bind
58243	1	678	5	NULL	NULL	0	NULL	Sos peptide (PPPVPPRRR)	AminoAcid	wild-type	bind					Crk	GP		SH3 domain		NULL		0	NULL	NULL	NULL	gw60_science_282_5396_2088_s_106	9851931	( A) Structure of wild-type Sos peptide (PPPVPPRRR) bound to Crk SH3 domain ( 20).	bind
1921	1	678	6	NULL	NULL	0	NULL	Sos peptide	GP	wild type	bind			PPPVPPRRR		Crk	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_science_282_5396_2088_s_106	9851931	( A) Structure of wild-type Sos peptide (PPPVPPRRR) bound to Crk SH3 domain ( 20).	bind
58244	1	680	5	NULL	NULL	0	NULL	Sum1	GP		bind					HML-E	GP				NULL	in vitro	0	NULL	NULL	NULL	gw70_genesdev_19_15_1811_s_149	16077008	( A) Sum1 bound in vitro to  HML-E, but not the  INO1 promoter region.	bind
58245	2	680	5	NULL	NULL	0	NULL	Sum1	GP		does not bind					INO1	GP			promoter	NULL		0	NULL	NULL	NULL	gw70_genesdev_19_15_1811_s_149	16077008	( A) Sum1 bound in vitro to  HML-E, but not the  INO1 promoter region.	bind
1922	1	680	6	NULL	NULL	0	NULL	Sum1	GP		bind					HML-E	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_genesdev_19_15_1811_s_149	16077008	( A) Sum1 bound in vitro to  HML-E, but not the  INO1 promoter region.	bind
1923	2	680	6	NULL	NULL	0	NULL	Sum1	GP		does not bind					INO1	GP			Promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_15_1811_s_149	16077008	( A) Sum1 bound in vitro to  HML-E, but not the  INO1 promoter region.	bind
58246	1	690	5	NULL	NULL	0	NULL	SWI/SNF	GP		bind		efficiently			H2ABbd nucleosomes	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_19_3815_s_94	15372075	( A) SWI/SNF efficiently binds H2ABbd nucleosomes.	bind
1965	1	690	6	NULL	NULL	0	NULL	SWI/SNF	GP		bind		efficiently			H2ABbd nucleosomes	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_19_3815_s_94	15372075	( A) SWI/SNF efficiently binds H2ABbd nucleosomes.	bind
58247	1	691	5	NULL	NULL	0	NULL	TFIIB	GP		bind					GAPDH	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_4_717_s_157	16332727	( A) TFIIB binding to GAPDH.	bind
1966	1	691	6	NULL	NULL	0	NULL	TFIIB	GP		bind					GAPDH	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_4_717_s_157	16332727	( A) TFIIB binding to GAPDH.	bind
58248	1	693	5	NULL	NULL	0	NULL	TGF-beta1	GP		bind					ALK1	GP				NULL	HUVEC	0	NULL	NULL	NULL	gw60_pnas_97_6_2626_s_172	10716993	( A) TGF-beta1 binds to ALK1 as well as ALK5 (TbetaR-I) in HUVEC.	bind
58249	2	693	5	NULL	NULL	0	NULL	TGF-beta1	GP		bind					ALK5	GP				NULL	HUVEC	0	NULL	NULL	NULL	gw60_pnas_97_6_2626_s_172	10716993	( A) TGF-beta1 binds to ALK1 as well as ALK5 (TbetaR-I) in HUVEC.	bind
58250	3	693	5	NULL	NULL	0	NULL	ALK5	GP		is					TbetaR-I	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_6_2626_s_172	10716993	( A) TGF-beta1 binds to ALK1 as well as ALK5 (TbetaR-I) in HUVEC.	bind
1967	1	693	6	NULL	NULL	0	NULL	TGF-beta1	GP		bind					ALK1	GP				NULL	HUVEC	NULL	NULL	NULL	NULL	gw60_pnas_97_6_2626_s_172	10716993	( A) TGF-beta1 binds to ALK1 as well as ALK5 (TbetaR-I) in HUVEC.	bind
1968	2	693	6	NULL	NULL	0	NULL	TGF-beta1	GP		bind					ALK5	GP				NULL	HUVEC	NULL	NULL	NULL	NULL	gw60_pnas_97_6_2626_s_172	10716993	( A) TGF-beta1 binds to ALK1 as well as ALK5 (TbetaR-I) in HUVEC.	bind
58251	1	695	5	NULL	NULL	0	NULL	GST-eIF5	GP		bind					eIF2	GP	native;;purified			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_18_6_1673_s_100	10075937	( A) The 7A mutation in GST-eIF5 impairs its binding to purified native eIF2 and eIF3  in vitro.	bind
58252	2	695	5	NULL	NULL	0	NULL	GST-eIF5	GP	mutant	impairs					statement 1	Process				NULL	in vitro	0	NULL	NULL	NULL	gw60_embo_18_6_1673_s_100	10075937	( A) The 7A mutation in GST-eIF5 impairs its binding to purified native eIF2 and eIF3  in vitro.	bind
58253	3	695	5	NULL	NULL	0	NULL	GST-eIF5	GP		bind					eIF3	GP	native;;purified			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_18_6_1673_s_100	10075937	( A) The 7A mutation in GST-eIF5 impairs its binding to purified native eIF2 and eIF3  in vitro.	bind
58254	4	695	5	NULL	NULL	0	NULL	GST-eIF5	GP	mutant	impairs					statement 3	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_18_6_1673_s_100	10075937	( A) The 7A mutation in GST-eIF5 impairs its binding to purified native eIF2 and eIF3  in vitro.	bind
1969	1	695	6	NULL	NULL	0	NULL	GST-eIF5	GP		bind					eIF2	GP	purified			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_18_6_1673_s_100	10075937	( A) The 7A mutation in GST-eIF5 impairs its binding to purified native eIF2 and eIF3  in vitro.	bind
1970	2	695	6	NULL	NULL	0	NULL	GST-eIF5	GP		bind					eIF3	GP	purified			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_18_6_1673_s_100	10075937	( A) The 7A mutation in GST-eIF5 impairs its binding to purified native eIF2 and eIF3  in vitro.	bind
1971	3	695	6	NULL	NULL	0	NULL	GST-eIF5	GP		impairs			mutant 7A		Statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_6_1673_s_100	10075937	( A) The 7A mutation in GST-eIF5 impairs its binding to purified native eIF2 and eIF3  in vitro.	bind
1972	4	695	6	NULL	NULL	0	NULL	GST-eIF5	GP		impairs			mutant 7A		Statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_6_1673_s_100	10075937	( A) The 7A mutation in GST-eIF5 impairs its binding to purified native eIF2 and eIF3  in vitro.	bind
58255	1	696	5	NULL	NULL	0	NULL	ADP-ribose molecule	Chemical		bind					Af1521	GP		macro domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_11_1911_s_111	15902274	( A) The ADP-ribose molecule binds the Af1521  macro domain in an L-shaped cleft.	bind
1973	1	696	6	NULL	NULL	0	NULL	ADP-ribose molecule	Chemical		bind					Af1521	GP		macro domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_11_1911_s_111	15902274	( A) The ADP-ribose molecule binds the Af1521  macro domain in an L-shaped cleft.	bind
58256	1	698	5	NULL	NULL	0	NULL	synaptosome	CellComponent		contains					AMPA receptor	GP		GluR2/3 subunit		NULL		0	NULL	NULL	NULL	gw70_embo_22_3_558_s_164	12554656	( A) The AMPA receptor subunits GluR2/3 and GluR1, the GluR2/3 binding partner GRIP,  the NMDA receptor subunit NR1, the plasma membrane marker Na+/K+ ATPase and the synaptic vesicle protein synaptophysin are all clearly detectable  in the crude synaptosome fraction (P2).	bind
58257	2	698	5	NULL	NULL	0	NULL	synaptosome	CellComponent		contains					AMPA receptor	GP		GluR1 subunit		NULL		0	NULL	NULL	NULL	gw70_embo_22_3_558_s_164	12554656	( A) The AMPA receptor subunits GluR2/3 and GluR1, the GluR2/3 binding partner GRIP,  the NMDA receptor subunit NR1, the plasma membrane marker Na+/K+ ATPase and the synaptic vesicle protein synaptophysin are all clearly detectable  in the crude synaptosome fraction (P2).	bind
58258	3	698	5	NULL	NULL	0	NULL	GRIP	GP		bind					GluR2/3	GP				NULL		0	NULL	NULL	NULL	gw70_embo_22_3_558_s_164	12554656	( A) The AMPA receptor subunits GluR2/3 and GluR1, the GluR2/3 binding partner GRIP,  the NMDA receptor subunit NR1, the plasma membrane marker Na+/K+ ATPase and the synaptic vesicle protein synaptophysin are all clearly detectable  in the crude synaptosome fraction (P2).	bind
58259	4	698	5	NULL	NULL	0	NULL	synaptosome	CellComponent		contains					GRIP	GP				NULL		0	NULL	NULL	NULL	gw70_embo_22_3_558_s_164	12554656	( A) The AMPA receptor subunits GluR2/3 and GluR1, the GluR2/3 binding partner GRIP,  the NMDA receptor subunit NR1, the plasma membrane marker Na+/K+ ATPase and the synaptic vesicle protein synaptophysin are all clearly detectable  in the crude synaptosome fraction (P2).	bind
58260	5	698	5	NULL	NULL	0	NULL	synaptosome	CellComponent		contains					NMDA receptor	GP		NR1 subunit		NULL		0	NULL	NULL	NULL	gw70_embo_22_3_558_s_164	12554656	( A) The AMPA receptor subunits GluR2/3 and GluR1, the GluR2/3 binding partner GRIP,  the NMDA receptor subunit NR1, the plasma membrane marker Na+/K+ ATPase and the synaptic vesicle protein synaptophysin are all clearly detectable  in the crude synaptosome fraction (P2).	bind
58261	6	698	5	NULL	NULL	0	NULL	synaptosome	CellComponent		contains					Na+/K+ ATPase	GP				NULL		0	NULL	NULL	NULL	gw70_embo_22_3_558_s_164	12554656	( A) The AMPA receptor subunits GluR2/3 and GluR1, the GluR2/3 binding partner GRIP,  the NMDA receptor subunit NR1, the plasma membrane marker Na+/K+ ATPase and the synaptic vesicle protein synaptophysin are all clearly detectable  in the crude synaptosome fraction (P2).	bind
58262	7	698	5	NULL	NULL	0	NULL	synaptosome	CellComponent		contains					synaptophysin	GP				NULL		0	NULL	NULL	NULL	gw70_embo_22_3_558_s_164	12554656	( A) The AMPA receptor subunits GluR2/3 and GluR1, the GluR2/3 binding partner GRIP,  the NMDA receptor subunit NR1, the plasma membrane marker Na+/K+ ATPase and the synaptic vesicle protein synaptophysin are all clearly detectable  in the crude synaptosome fraction (P2).	bind
58263	8	698	5	NULL	NULL	0	NULL	synaptophysin	GP		is a type of					synaptic vesicle protein 	GP				NULL		0	NULL	NULL	NULL	gw70_embo_22_3_558_s_164	12554656	( A) The AMPA receptor subunits GluR2/3 and GluR1, the GluR2/3 binding partner GRIP,  the NMDA receptor subunit NR1, the plasma membrane marker Na+/K+ ATPase and the synaptic vesicle protein synaptophysin are all clearly detectable  in the crude synaptosome fraction (P2).	bind
58264	9	698	5	NULL	NULL	0	NULL	Na+/K+ ATPase	GP		is a type of					plasma membrane marker	GP				NULL		0	NULL	NULL	NULL	gw70_embo_22_3_558_s_164	12554656	( A) The AMPA receptor subunits GluR2/3 and GluR1, the GluR2/3 binding partner GRIP,  the NMDA receptor subunit NR1, the plasma membrane marker Na+/K+ ATPase and the synaptic vesicle protein synaptophysin are all clearly detectable  in the crude synaptosome fraction (P2).	bind
58265	1	702	5	NULL	NULL	0	NULL	holo-Tf	GP		bind					Tf	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_142	16103367	( A) The binding of holo-Tf to TfR has no effect on GA-induced apoptosis.	bind
58266	2	702	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					GA	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_142	16103367	( A) The binding of holo-Tf to TfR has no effect on GA-induced apoptosis.	bind
58267	3	702	5	NULL	NULL	0	NULL	statement 1	Process		does not effect					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_142	16103367	( A) The binding of holo-Tf to TfR has no effect on GA-induced apoptosis.	bind
1974	1	702	6	NULL	NULL	0	NULL	holo-Tf	GP		bind					TfR	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_142	16103367	( A) The binding of holo-Tf to TfR has no effect on GA-induced apoptosis.	bind
1975	3	702	6	NULL	NULL	0	NULL	Statement 1	Process		has no effect on					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_142	16103367	( A) The binding of holo-Tf to TfR has no effect on GA-induced apoptosis.	bind
51970	2	702	6	NULL	NULL	0	NULL	GA	Chemical		induce					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_142	16103367	( A) The binding of holo-Tf to TfR has no effect on GA-induced apoptosis.	bind
58268	1	703	5	NULL	NULL	0	NULL	JIP-1	GP		bind					HPK1	GP				NULL		0	NULL	NULL	NULL	gw60_science_281_5383_1671_s_77	9733513	( A) The binding of JIP-1 to HPK1, MLK3, DLK, and MKK7 is independent of JNK.	bind
58269	2	703	5	NULL	NULL	0	NULL	statement 1	Process		is independent of					JNK	GP				NULL		0	NULL	NULL	NULL	gw60_science_281_5383_1671_s_77	9733513	( A) The binding of JIP-1 to HPK1, MLK3, DLK, and MKK7 is independent of JNK.	bind
58270	3	703	5	NULL	NULL	0	NULL	JIP-1	GP		bind					MLK3	GP				NULL		0	NULL	NULL	NULL	gw60_science_281_5383_1671_s_77	9733513	( A) The binding of JIP-1 to HPK1, MLK3, DLK, and MKK7 is independent of JNK.	bind
58271	4	703	5	NULL	NULL	0	NULL	statement 3	Process		is independent of					JNK	GP				NULL		0	NULL	NULL	NULL	gw60_science_281_5383_1671_s_77	9733513	( A) The binding of JIP-1 to HPK1, MLK3, DLK, and MKK7 is independent of JNK.	bind
58272	5	703	5	NULL	NULL	0	NULL	JIP-1	GP		bind					DLK	GP				NULL		0	NULL	NULL	NULL	gw60_science_281_5383_1671_s_77	9733513	( A) The binding of JIP-1 to HPK1, MLK3, DLK, and MKK7 is independent of JNK.	bind
58273	6	703	5	NULL	NULL	0	NULL	statement 5	Process		is independent of					JNK	GP				NULL		0	NULL	NULL	NULL	gw60_science_281_5383_1671_s_77	9733513	( A) The binding of JIP-1 to HPK1, MLK3, DLK, and MKK7 is independent of JNK.	bind
58274	7	703	5	NULL	NULL	0	NULL	JIP-1	GP		bind					MKK7	GP				NULL		0	NULL	NULL	NULL	gw60_science_281_5383_1671_s_77	9733513	( A) The binding of JIP-1 to HPK1, MLK3, DLK, and MKK7 is independent of JNK.	bind
58275	8	703	5	NULL	NULL	0	NULL	statement 7	Process		is independent of					JNK	GP				NULL		0	NULL	NULL	NULL	gw60_science_281_5383_1671_s_77	9733513	( A) The binding of JIP-1 to HPK1, MLK3, DLK, and MKK7 is independent of JNK.	bind
1976	1	703	6	NULL	NULL	0	NULL	JIP-1	GP		bind					HPK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_77	9733513	( A) The binding of JIP-1 to HPK1, MLK3, DLK, and MKK7 is independent of JNK.	bind
1977	2	703	6	NULL	NULL	0	NULL	JIP-1	GP		bind					MLK3	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_77	9733513	( A) The binding of JIP-1 to HPK1, MLK3, DLK, and MKK7 is independent of JNK.	bind
1978	3	703	6	NULL	NULL	0	NULL	JIP-1	GP		bind					DLK	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_77	9733513	( A) The binding of JIP-1 to HPK1, MLK3, DLK, and MKK7 is independent of JNK.	bind
1979	4	703	6	NULL	NULL	0	NULL	JIP-1	GP		bind					MKK7	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_77	9733513	( A) The binding of JIP-1 to HPK1, MLK3, DLK, and MKK7 is independent of JNK.	bind
2229	5	703	6	NULL	NULL	0	NULL	statement 1	Process		is independent of					JNK	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_77	9733513	( A) The binding of JIP-1 to HPK1, MLK3, DLK, and MKK7 is independent of JNK.	bind
2230	6	703	6	NULL	NULL	0	NULL	statement 2	Process		is independent of					JNK	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_77	9733513	( A) The binding of JIP-1 to HPK1, MLK3, DLK, and MKK7 is independent of JNK.	bind
2231	7	703	6	NULL	NULL	0	NULL	statement 3	Process		is independent of					JNK	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_77	9733513	( A) The binding of JIP-1 to HPK1, MLK3, DLK, and MKK7 is independent of JNK.	bind
2232	8	703	6	NULL	NULL	0	NULL	statement 4	Process		is independent of					JNK	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_77	9733513	( A) The binding of JIP-1 to HPK1, MLK3, DLK, and MKK7 is independent of JNK.	bind
58276	1	704	5	NULL	NULL	0	NULL	p38	GP	mutant	bind					MKP-5	GP				NULL		0	NULL	NULL	NULL	gw60_embo_20_3_466_s_316	11157753	( A) The binding of the mutant forms of p38 and ERK2 to MKP-5.	bind
58277	2	704	5	NULL	NULL	0	NULL	ERK2	GP	mutant	bind					MKP-5	GP				NULL		0	NULL	NULL	NULL	gw60_embo_20_3_466_s_316	11157753	( A) The binding of the mutant forms of p38 and ERK2 to MKP-5.	bind
1980	1	704	6	NULL	NULL	0	NULL	p38	GP	mutant	bind					MKP-5	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_316	11157753	( A) The binding of the mutant forms of p38 and ERK2 to MKP-5.	bind
1981	2	704	6	NULL	NULL	0	NULL	ERK2	GP	mutant	bind					MKP-5	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_316	11157753	( A) The binding of the mutant forms of p38 and ERK2 to MKP-5.	bind
58278	1	705	5	NULL	NULL	0	NULL	p38	GP	mutant	bind					RSK2	GP				NULL		0	NULL	NULL	NULL	gw60_embo_20_3_466_s_253	11157753	( A) The binding of the mutant forms of p38 and ERK2 to RSK2.	bind
58279	2	705	5	NULL	NULL	0	NULL	ERK2	GP	mutant	bind					RSK2	GP				NULL		0	NULL	NULL	NULL	gw60_embo_20_3_466_s_253	11157753	( A) The binding of the mutant forms of p38 and ERK2 to RSK2.	bind
1982	1	705	6	NULL	NULL	0	NULL	p38	GP	mutant	bind					RSK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_253	11157753	( A) The binding of the mutant forms of p38 and ERK2 to RSK2.	bind
1983	2	705	6	NULL	NULL	0	NULL	ERK2	GP	mutant	bind					RSK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_253	11157753	( A) The binding of the mutant forms of p38 and ERK2 to RSK2.	bind
58280	1	706	5	NULL	NULL	0	NULL	p38	GP	mutant	bind					MSK1	GP				NULL		0	NULL	NULL	NULL	gw60_embo_20_3_466_s_273	11157753	( A) The binding of the mutant forms of p38 to MSK1.	bind
1984	1	706	6	NULL	NULL	0	NULL	p38	GP	mutant	bind					MSK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_273	11157753	( A) The binding of the mutant forms of p38 to MSK1.	bind
58281	1	707	5	NULL	NULL	0	NULL	p38	GP	mutant	bind					MSK2	GP				NULL		0	NULL	NULL	NULL	gw60_embo_20_3_466_s_223	11157753	( A) The binding of the mutant forms of p38 to MSK2.	bind
1985	1	707	6	NULL	NULL	0	NULL	p38	GP	mutant	bind					MSK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_223	11157753	( A) The binding of the mutant forms of p38 to MSK2.	bind
58282	1	710	5	NULL	NULL	0	NULL	DlEC fragment	AminoAcid		bind		specifically			N-S2 cells	Cell				NULL		0	NULL	NULL	NULL	gw60_science_283_5398_91_s_91	9872749	( A) The DlEC fragment specifically binds to N-expressing S2 (N-S2) cells and does not bind to S2 cells alone.	bind
58283	2	710	5	NULL	NULL	0	NULL	DlEC fragment	AminoAcid		does not bind					S2 cells	Cell				NULL		0	NULL	NULL	NULL	gw60_science_283_5398_91_s_91	9872749	( A) The DlEC fragment specifically binds to N-expressing S2 (N-S2) cells and does not bind to S2 cells alone.	bind
58284	3	710	5	NULL	NULL	0	NULL	N-S2 cells	Cell		is					N-expressing S2 cells	Cell				NULL		0	NULL	NULL	NULL	gw60_science_283_5398_91_s_91	9872749	( A) The DlEC fragment specifically binds to N-expressing S2 (N-S2) cells and does not bind to S2 cells alone.	bind
1986	1	710	6	NULL	NULL	0	NULL		NucleicAcid		bind		specifically	DlEC fragment 		S2 (N-S2) cells	Cell	N-expressing			NULL		NULL	NULL	NULL	NULL	gw60_science_283_5398_91_s_91	9872749	( A) The DlEC fragment specifically binds to N-expressing S2 (N-S2) cells and does not bind to S2 cells alone.	bind
1987	2	710	6	NULL	NULL	0	NULL		NucleicAcid		does not bind			DlEC fragment 		S2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_science_283_5398_91_s_91	9872749	( A) The DlEC fragment specifically binds to N-expressing S2 (N-S2) cells and does not bind to S2 cells alone.	bind
58285	1	712	5	NULL	NULL	0	NULL	eIF4E - eIF4G	GP		is					eIF4F core complex	GP				NULL		0	NULL	NULL	NULL	gw60_embo_19_16_4372_s_231	10944120	( A) The eIF4F core complex, eIF4E - eIF4G, binds tightly to capped mRNA. Dcp1 can bind eIF4G, but has no access to the cap.	bind
58286	2	712	5	NULL	NULL	0	NULL	eIF4E - eIF4G	GP		bind		tightly			mRNA	NucleicAcid	capped			NULL		0	NULL	NULL	NULL	gw60_embo_19_16_4372_s_231	10944120	( A) The eIF4F core complex, eIF4E - eIF4G, binds tightly to capped mRNA. Dcp1 can bind eIF4G, but has no access to the cap.	bind
58287	3	712	5	NULL	NULL	0	NULL	Dcp1	GP		bind					eIF4G	GP				NULL		0	NULL	NULL	NULL	gw60_embo_19_16_4372_s_231	10944120	( A) The eIF4F core complex, eIF4E - eIF4G, binds tightly to capped mRNA. Dcp1 can bind eIF4G, but has no access to the cap.	bind
58288	4	712	5	NULL	NULL	0	NULL	Dcp1	GP		does not bind					mRNA	NucleicAcid	capped			NULL		0	NULL	NULL	NULL	gw60_embo_19_16_4372_s_231	10944120	( A) The eIF4F core complex, eIF4E - eIF4G, binds tightly to capped mRNA. Dcp1 can bind eIF4G, but has no access to the cap.	bind
1988	1	712	6	NULL	NULL	0	NULL	eIF4F core complex	GP		constitute					eIF4E - eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_231	10944120	( A) The eIF4F core complex, eIF4E - eIF4G, binds tightly to capped mRNA. Dcp1 can bind eIF4G, but has no access to the cap.	bind
1989	2	712	6	NULL	NULL	0	NULL	 eIF4F core complex	GP		bind		tightly			mRNA	NucleicAcid	capped			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_231	10944120	( A) The eIF4F core complex, eIF4E - eIF4G, binds tightly to capped mRNA. Dcp1 can bind eIF4G, but has no access to the cap.	bind
1990	3	712	6	NULL	NULL	0	NULL	Dcp1	GP		bind					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_231	10944120	( A) The eIF4F core complex, eIF4E - eIF4G, binds tightly to capped mRNA. Dcp1 can bind eIF4G, but has no access to the cap.	bind
1991	4	712	6	NULL	NULL	0	NULL	Dcp1	GP		does not access					cap					NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_231	10944120	( A) The eIF4F core complex, eIF4E - eIF4G, binds tightly to capped mRNA. Dcp1 can bind eIF4G, but has no access to the cap.	bind
58289	1	713	5	NULL	NULL	0	NULL	NHERF	GP		bind			PDZ domain		beta2 receptor	GP		tail		NULL		0	NULL	NULL	NULL	gw60_pnas_95_15_8496_s_107	9671706	( A) The first PDZ domain of NHERF binds well to the beta2 receptor tail, moderately to the P2Y1 receptor tail, and poorly to the P2Y2 receptor tail.	bind
58290	2	713	5	NULL	NULL	0	NULL	NHERF	GP		bind		moderately	PDZ domain		P2Y1 receptor	GP		tail		NULL		0	NULL	NULL	NULL	gw60_pnas_95_15_8496_s_107	9671706	( A) The first PDZ domain of NHERF binds well to the beta2 receptor tail, moderately to the P2Y1 receptor tail, and poorly to the P2Y2 receptor tail.	bind
58291	3	713	5	NULL	NULL	0	NULL	NHERF	GP		bind		poorly	PDZ domain		P2Y2 receptor	GP		tail		NULL		0	NULL	NULL	NULL	gw60_pnas_95_15_8496_s_107	9671706	( A) The first PDZ domain of NHERF binds well to the beta2 receptor tail, moderately to the P2Y1 receptor tail, and poorly to the P2Y2 receptor tail.	bind
1992	1	713	6	NULL	NULL	0	NULL	NHERF	GP		bind			first PDZ domain		beta2 receptor 	GP		tail		NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_15_8496_s_107	9671706	( A) The first PDZ domain of NHERF binds well to the beta2 receptor tail, moderately to the P2Y1 receptor tail, and poorly to the P2Y2 receptor tail.	bind
1993	2	713	6	NULL	NULL	0	NULL	NHERF	GP		bind		moderately	first PDZ domain		P2Y1 receptor	GP		tail		NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_15_8496_s_107	9671706	( A) The first PDZ domain of NHERF binds well to the beta2 receptor tail, moderately to the P2Y1 receptor tail, and poorly to the P2Y2 receptor tail.	bind
1994	3	713	6	NULL	NULL	0	NULL	NHERF	GP		bind		poorly	first PDZ domain		P2Y2 receptor 	GP		tail		NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_15_8496_s_107	9671706	( A) The first PDZ domain of NHERF binds well to the beta2 receptor tail, moderately to the P2Y1 receptor tail, and poorly to the P2Y2 receptor tail.	bind
58292	1	714	5	NULL	NULL	0	NULL	Loco	GP		interacts with			GoLoco motif		Galphai	GP	wild type			NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1341_s_64	15937221	( A) The GoLoco motif of Loco interacts with wild-type Galphai but not GalphaiQ205L, the GTP-bound form of Galphai, in yeast two-hybrid assays.	bind
58293	2	714	5	NULL	NULL	0	NULL	Loco	GP		does not interact with			GoLoco motif		Galphai	GP		Q205L		NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1341_s_64	15937221	( A) The GoLoco motif of Loco interacts with wild-type Galphai but not GalphaiQ205L, the GTP-bound form of Galphai, in yeast two-hybrid assays.	bind
1995	1	714	6	NULL	NULL	0	NULL	Loco	GP		interacts with			GoLoco motif		Galphai	GP	wild-type			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1341_s_64	15937221	( A) The GoLoco motif of Loco interacts with wild-type Galphai but not GalphaiQ205L, the GTP-bound form of Galphai, in yeast two-hybrid assays.	bind
1996	2	714	6	NULL	NULL	0	NULL	Loco	GP		does not bind			GoLoco motif		Galphai	GP		Q205L		NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1341_s_64	15937221	( A) The GoLoco motif of Loco interacts with wild-type Galphai but not GalphaiQ205L, the GTP-bound form of Galphai, in yeast two-hybrid assays.	bind
51971	3	714	6	NULL	NULL	0	NULL	GTP	Chemical		bind					Galphai	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1341_s_64	15937221	( A) The GoLoco motif of Loco interacts with wild-type Galphai but not GalphaiQ205L, the GTP-bound form of Galphai, in yeast two-hybrid assays.	bind
58294	1	715	5	NULL	NULL	0	NULL	PACS-1	GP	HIS-tagged	bind			furin-binding region (115-255)		polycystin-2	GP		carboxy-terminal (741-871)		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_4_705_s_56	15692563	( A) The HIS-tagged furin-binding region of PACS-1 (amino acids 115 255) binds the carboxy-terminal  amino acids 741 871 of polycystin-2 fused to the MBP.	bind
58295	2	715	5	NULL	NULL	0	NULL	polycystin-2	GP		is a type of					MBP-fusion protein	GP				NULL		0	NULL	NULL	NULL	gw70_embo_24_4_705_s_56	15692563	( A) The HIS-tagged furin-binding region of PACS-1 (amino acids 115 255) binds the carboxy-terminal  amino acids 741 871 of polycystin-2 fused to the MBP.	bind
1997	1	715	6	NULL	NULL	0	NULL	PACS-1	GP	HIS-tagged 	bind			amino acids 115 255;;furin-binding region 		polycystin-2	GP		carboxy-terminal amino acids;; 741 871		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_4_705_s_56	15692563	( A) The HIS-tagged furin-binding region of PACS-1 (amino acids 115 255) binds the carboxy-terminal  amino acids 741 871 of polycystin-2 fused to the MBP.	bind
51973	2	715	6	NULL	NULL	0	NULL	polycystin-2	GP		is a type of					MBP fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_4_705_s_56	15692563	( A) The HIS-tagged furin-binding region of PACS-1 (amino acids 115 255) binds the carboxy-terminal  amino acids 741 871 of polycystin-2 fused to the MBP.	bind
58296	1	719	5	NULL	NULL	0	NULL	FITC cholera toxin	GP		bind					GM1	GP				NULL	surface of a stage 3 neuron	0	NULL	NULL	NULL	gw60_embo_18_7_1761_s_45	10202140	( A) The labeling corresponding to the FITC cholera toxin bound to GM1 in the surface of a stage 3 neuron is shown on the left panel (GM1).	bind
1998	1	719	6	NULL	NULL	0	NULL	cholera toxin	Chemical		bind					GM1	GP				NULL	surface of a stage 3 neuron	NULL	NULL	NULL	NULL	gw60_embo_18_7_1761_s_45	10202140	( A) The labeling corresponding to the FITC cholera toxin bound to GM1 in the surface of a stage 3 neuron is shown on the left panel (GM1).	bind
58297	1	722	5	NULL	NULL	0	NULL	pheromone	GP		is a type of					mating factor	GP				NULL		0	NULL	NULL	NULL	gw70_annurevphysiol_64_0_129_s_31	11826266	( A) The mating factor pheromone binds to a cell surface receptor Ste2 (or Ste3), which  promotes GTP binding to the G protein   subunit (Gpa1).	bind
58298	2	722	5	NULL	NULL	0	NULL	Ste2	GP		is a type of					cell surface receptor	GP				NULL		0	NULL	NULL	NULL	gw70_annurevphysiol_64_0_129_s_31	11826266	( A) The mating factor pheromone binds to a cell surface receptor Ste2 (or Ste3), which  promotes GTP binding to the G protein   subunit (Gpa1).	bind
58299	3	722	5	NULL	NULL	0	NULL	Ste3	GP		is a type of					cell surface receptor	GP				NULL		0	NULL	NULL	NULL	gw70_annurevphysiol_64_0_129_s_31	11826266	( A) The mating factor pheromone binds to a cell surface receptor Ste2 (or Ste3), which  promotes GTP binding to the G protein   subunit (Gpa1).	bind
58300	4	722	5	NULL	NULL	0	NULL	Gpa1	GP		is					G protein subunit	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_64_0_129_s_31	11826266	( A) The mating factor pheromone binds to a cell surface receptor Ste2 (or Ste3), which  promotes GTP binding to the G protein   subunit (Gpa1).	bind
58301	5	722	5	NULL	NULL	0	NULL	pheromone	GP		bind					Ste2	GP				NULL		0	NULL	NULL	NULL	gw70_annurevphysiol_64_0_129_s_31	11826266	( A) The mating factor pheromone binds to a cell surface receptor Ste2 (or Ste3), which  promotes GTP binding to the G protein   subunit (Gpa1).	bind
58302	6	722	5	NULL	NULL	0	NULL	pheromone	GP		bind					Ste3	GP				NULL		0	NULL	NULL	NULL	gw70_annurevphysiol_64_0_129_s_31	11826266	( A) The mating factor pheromone binds to a cell surface receptor Ste2 (or Ste3), which  promotes GTP binding to the G protein   subunit (Gpa1).	bind
58303	7	722	5	NULL	NULL	0	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		0	NULL	NULL	NULL	gw70_annurevphysiol_64_0_129_s_31	11826266	( A) The mating factor pheromone binds to a cell surface receptor Ste2 (or Ste3), which  promotes GTP binding to the G protein   subunit (Gpa1).	bind
58304	8	722	5	NULL	NULL	0	NULL	GTP	Chemical		bind					Gpa1	GP				NULL		0	NULL	NULL	NULL	gw70_annurevphysiol_64_0_129_s_31	11826266	( A) The mating factor pheromone binds to a cell surface receptor Ste2 (or Ste3), which  promotes GTP binding to the G protein   subunit (Gpa1).	bind
58305	9	722	5	NULL	NULL	0	NULL	statement 5	Process		promotes					statement 8	Process				NULL		0	NULL	NULL	NULL	gw70_annurevphysiol_64_0_129_s_31	11826266	( A) The mating factor pheromone binds to a cell surface receptor Ste2 (or Ste3), which  promotes GTP binding to the G protein   subunit (Gpa1).	bind
58306	10	722	5	NULL	NULL	0	NULL	statement 6	Process		promotes					statement 8	Process				NULL		0	NULL	NULL	NULL	gw70_annurevphysiol_64_0_129_s_31	11826266	( A) The mating factor pheromone binds to a cell surface receptor Ste2 (or Ste3), which  promotes GTP binding to the G protein   subunit (Gpa1).	bind
1999	1	722	6	NULL	NULL	0	NULL	pheromone	Chemical		bind					Ste2	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_64_0_129_s_31	11826266	( A) The mating factor pheromone binds to a cell surface receptor Ste2 (or Ste3), which  promotes GTP binding to the G protein   subunit (Gpa1).	bind
2000	2	722	6	NULL	NULL	0	NULL	GTP	Chemical		bind					Gpa1	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_64_0_129_s_31	11826266	( A) The mating factor pheromone binds to a cell surface receptor Ste2 (or Ste3), which  promotes GTP binding to the G protein   subunit (Gpa1).	bind
2001	3	722	6	NULL	NULL	0	NULL	Statement 1	Process		promotes					Statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_64_0_129_s_31	11826266	( A) The mating factor pheromone binds to a cell surface receptor Ste2 (or Ste3), which  promotes GTP binding to the G protein   subunit (Gpa1).	bind
51974	4	722	6	NULL	NULL	0	NULL	pheromone	Chemical		bind					Ste3	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_64_0_129_s_31	11826266	( A) The mating factor pheromone binds to a cell surface receptor Ste2 (or Ste3), which  promotes GTP binding to the G protein   subunit (Gpa1).	bind
51975	5	722	6	NULL	NULL	0	NULL	statement 4	Process		promotes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_64_0_129_s_31	11826266	( A) The mating factor pheromone binds to a cell surface receptor Ste2 (or Ste3), which  promotes GTP binding to the G protein   subunit (Gpa1).	bind
51976	6	722	6	NULL	NULL	0	NULL	pheromone	Chemical		is a type of					mating factor	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_64_0_129_s_31	11826266	( A) The mating factor pheromone binds to a cell surface receptor Ste2 (or Ste3), which  promotes GTP binding to the G protein   subunit (Gpa1).	bind
51977	7	722	6	NULL	NULL	0	NULL	Ste2	GP		is a type of					cell surface receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_64_0_129_s_31	11826266	( A) The mating factor pheromone binds to a cell surface receptor Ste2 (or Ste3), which  promotes GTP binding to the G protein   subunit (Gpa1).	bind
51978	8	722	6	NULL	NULL	0	NULL	Ste3	GP		is a type of					cell surface receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_64_0_129_s_31	11826266	( A) The mating factor pheromone binds to a cell surface receptor Ste2 (or Ste3), which  promotes GTP binding to the G protein   subunit (Gpa1).	bind
51979	9	722	6	NULL	NULL	0	NULL	Gpa1	GP		is a type of					G protein subunit	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_64_0_129_s_31	11826266	( A) The mating factor pheromone binds to a cell surface receptor Ste2 (or Ste3), which  promotes GTP binding to the G protein   subunit (Gpa1).	bind
58307	1	724	5	NULL	NULL	0	NULL	Cul1	GP	affinity-purified	bind					GST - CAND1	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_31_11515_s_114	16861300	( A) The neddylation of affinity-purified Cul1 bound to GST - CAND1 is stimulated by  Skp2 in the absence of substrate, and the requirement for substrate is restored by  the fraction not adsorbed to GST - CAND1.	bind
58308	2	724	5	NULL	NULL	0	NULL	Skp2 	GP		stimulates					statement 1	GP	neddylation of			NULL		0	NULL	NULL	NULL	gw70_pnas_103_31_11515_s_114	16861300	( A) The neddylation of affinity-purified Cul1 bound to GST - CAND1 is stimulated by  Skp2 in the absence of substrate, and the requirement for substrate is restored by  the fraction not adsorbed to GST - CAND1.	bind
2002	1	724	6	NULL	NULL	0	NULL	Cul1	GP	purified	bind					GST-CAND1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_31_11515_s_114	16861300	( A) The neddylation of affinity-purified Cul1 bound to GST - CAND1 is stimulated by  Skp2 in the absence of substrate, and the requirement for substrate is restored by  the fraction not adsorbed to GST - CAND1.	bind
2003	2	724	6	NULL	NULL	0	NULL	Skp2	GP		stimulates					Statement 1	Process	neddylation			NULL	in the absence of substrate	NULL	NULL	NULL	NULL	gw70_pnas_103_31_11515_s_114	16861300	( A) The neddylation of affinity-purified Cul1 bound to GST - CAND1 is stimulated by  Skp2 in the absence of substrate, and the requirement for substrate is restored by  the fraction not adsorbed to GST - CAND1.	bind
58309	1	725	5	NULL	NULL	0	NULL	NF-kappaB complex	GP		bind					Bcl-x	GP			putative NF-kappaB-binding sites in promoter	NULL		0	NULL	NULL	NULL	gw60_pnas_96_16_9136_s_133	10430908	( A) The NF-kappaB complex binding to the putative NF-kappaB-binding sites within the Bcl-x promoter consists predominantly of p50, p65, and c-Rel.	bind
58310	2	725	5	NULL	NULL	0	NULL	NF-kappaB complex	GP		consists of					p50	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_16_9136_s_133	10430908	( A) The NF-kappaB complex binding to the putative NF-kappaB-binding sites within the Bcl-x promoter consists predominantly of p50, p65, and c-Rel.	bind
58311	3	725	5	NULL	NULL	0	NULL	NF-kappaB complex	GP		consists of					p65	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_16_9136_s_133	10430908	( A) The NF-kappaB complex binding to the putative NF-kappaB-binding sites within the Bcl-x promoter consists predominantly of p50, p65, and c-Rel.	bind
58312	4	725	5	NULL	NULL	0	NULL	NF-kappaB complex	GP		consists of					c-Rel	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_16_9136_s_133	10430908	( A) The NF-kappaB complex binding to the putative NF-kappaB-binding sites within the Bcl-x promoter consists predominantly of p50, p65, and c-Rel.	bind
2004	1	725	6	NULL	NULL	0	NULL	p50	GP		bind					BCL-x	GP			NF-kappaB-binding sites of promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_16_9136_s_133	10430908	( A) The NF-kappaB complex binding to the putative NF-kappaB-binding sites within the Bcl-x promoter consists predominantly of p50, p65, and c-Rel.	bind
2005	2	725	6	NULL	NULL	0	NULL	p65	GP		bind					BCL-x	GP			NF-kappaB-binding sites of promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_16_9136_s_133	10430908	( A) The NF-kappaB complex binding to the putative NF-kappaB-binding sites within the Bcl-x promoter consists predominantly of p50, p65, and c-Rel.	bind
2006	3	725	6	NULL	NULL	0	NULL	c-rel	GP		bind					BCL-x	GP			NF-kappaB-binding sites of promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_16_9136_s_133	10430908	( A) The NF-kappaB complex binding to the putative NF-kappaB-binding sites within the Bcl-x promoter consists predominantly of p50, p65, and c-Rel.	bind
58313	1	726	5	NULL	NULL	0	NULL	Hsp72	GP		bind					JNK1	GP				NULL	in vitro	0	NULL	NULL	NULL	gw60_embo_20_3_446_s_129	11157751	( A) The peptide binding domain is essential for Hsp72 binding to JNK1  in vitro.	bind
2007	1	726	6	NULL	NULL	0	NULL	Hsp72	GP		bind					JNK1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_20_3_446_s_129	11157751	( A) The peptide binding domain is essential for Hsp72 binding to JNK1  in vitro.	bind
2008	2	726	6	NULL	NULL	0	NULL		GP		is essential for			peptide binding domain		Statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_20_3_446_s_129	11157751	( A) The peptide binding domain is essential for Hsp72 binding to JNK1  in vitro.	bind
58314	1	728	5	NULL	NULL	0	NULL	PIASy	GP		bind			SAP domain		MAR DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_genesdev_15_23_3088_s_238	11731474	( A) The PIASy SAP domain binds to MAR DNA.	bind
2009	1	728	6	NULL	NULL	0	NULL	PIASy	GP		bind			SAP domain		MAR DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_23_3088_s_238	11731474	( A) The PIASy SAP domain binds to MAR DNA.	bind
58315	1	729	5	NULL	NULL	0	NULL	Pit-1 homodimer	GP		bind			POU domain					prolactin Prl-1P site		NULL		0	NULL	NULL	NULL	gw60_science_290_5494_1127_s_52	11073444	( A) The Pit-1 POU domain homodimer is  bound to the prolactin Prl-1P (left) and the growth hormone GH-1  (right) sites.	bind
58316	2	729	5	NULL	NULL	0	NULL	Pit-1 homodimer	GP		bind			POU domain					GH-1 site		NULL		0	NULL	NULL	NULL	gw60_science_290_5494_1127_s_52	11073444	( A) The Pit-1 POU domain homodimer is  bound to the prolactin Prl-1P (left) and the growth hormone GH-1  (right) sites.	bind
58317	3	729	5	NULL	NULL	0	NULL	GH-1	GP		is a type of					growth hormone	GP				NULL		0	NULL	NULL	NULL	gw60_science_290_5494_1127_s_52	11073444	( A) The Pit-1 POU domain homodimer is  bound to the prolactin Prl-1P (left) and the growth hormone GH-1  (right) sites.	bind
2010	1	729	6	NULL	NULL	0	NULL	Pit-1 homodimer	GP		bind			POU domain		Prl-1P	GP			sites	NULL		NULL	NULL	NULL	NULL	gw60_science_290_5494_1127_s_52	11073444	( A) The Pit-1 POU domain homodimer is  bound to the prolactin Prl-1P (left) and the growth hormone GH-1  (right) sites.	bind
2011	2	729	6	NULL	NULL	0	NULL	Pit-1 homodimer	GP		bind			POU domain		GH-1	GP			sites	NULL		NULL	NULL	NULL	NULL	gw60_science_290_5494_1127_s_52	11073444	( A) The Pit-1 POU domain homodimer is  bound to the prolactin Prl-1P (left) and the growth hormone GH-1  (right) sites.	bind
51980	3	729	6	NULL	NULL	0	NULL	Prl-1P	GP		is					prolactin	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_290_5494_1127_s_52	11073444	( A) The Pit-1 POU domain homodimer is  bound to the prolactin Prl-1P (left) and the growth hormone GH-1  (right) sites.	bind
51981	4	729	6	NULL	NULL	0	NULL	GH-1	GP		is					growth hormone	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_290_5494_1127_s_52	11073444	( A) The Pit-1 POU domain homodimer is  bound to the prolactin Prl-1P (left) and the growth hormone GH-1  (right) sites.	bind
58318	1	731	5	NULL	NULL	0	NULL	RdRp	GP		bind					RdRp	NucleicAcid			promoter	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2824_s_171	12771209	( A) The RdRp can bind to both the vRNA and cRNA promoters.	bind
58319	2	731	5	NULL	NULL	0	NULL	RdRp	GP		bind					cRNA	NucleicAcid			promoter	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2824_s_171	12771209	( A) The RdRp can bind to both the vRNA and cRNA promoters.	bind
2012	1	731	6	NULL	NULL	0	NULL	RdRp	GP		bind					vRNA	GP			Promoter	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2824_s_171	12771209	( A) The RdRp can bind to both the vRNA and cRNA promoters.	bind
2013	2	731	6	NULL	NULL	0	NULL	RdRp	GP		bind					cRNA	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2824_s_171	12771209	( A) The RdRp can bind to both the vRNA and cRNA promoters.	bind
58320	1	732	5	NULL	NULL	0	NULL	RepE monomer	GP		bind					ori2 iterons	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_embo_18_13_3856_s_19	10393200	( A) The RepE monomer binds to the four  ori2 iterons [direct repeats (DR)].	bind
2014	1	732	6	NULL	NULL	0	NULL	RepE	GP	monomer	bind					four ori2 iterons				DR	NULL		NULL	NULL	NULL	NULL	gw60_embo_18_13_3856_s_19	10393200	( A) The RepE monomer binds to the four  ori2 iterons [direct repeats (DR)].	bind
51982	2	732	6	10	NULL	0	NULL	DR	NULL		is	NULL				direct repeat	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_18_13_3856_s_19	10393200	( A) The RepE monomer binds to the four  ori2 iterons [direct repeats (DR)].	bind
58321	1	734	5	NULL	NULL	0	NULL	Pax6deltaHD	GP	wild-type	bind					GST-HD	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_8_2661_s_205	15886395	( A) The single mutants of Pax6deltaHD, E112A, E120A and E128A bind to GST-HD with the same affinity as the wild type.	bind
58322	2	734	5	NULL	NULL	0	NULL	Pax6deltaHD	GP	mutant	bind			E112A		GST-HD	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_8_2661_s_205	15886395	( A) The single mutants of Pax6deltaHD, E112A, E120A and E128A bind to GST-HD with the same affinity as the wild type.	bind
58323	3	734	5	NULL	NULL	0	NULL	Pax6deltaHD	GP	mutant	bind			E120A		GST-HD	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_8_2661_s_205	15886395	( A) The single mutants of Pax6deltaHD, E112A, E120A and E128A bind to GST-HD with the same affinity as the wild type.	bind
58324	4	734	5	NULL	NULL	0	NULL	Pax6deltaHD	GP	mutant	bind			E128A		GST-HD	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_8_2661_s_205	15886395	( A) The single mutants of Pax6deltaHD, E112A, E120A and E128A bind to GST-HD with the same affinity as the wild type.	bind
58325	5	734	5	NULL	NULL	0	NULL	statement 2	Process		same affinity as					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_8_2661_s_205	15886395	( A) The single mutants of Pax6deltaHD, E112A, E120A and E128A bind to GST-HD with the same affinity as the wild type.	bind
58326	6	734	5	NULL	NULL	0	NULL	statement 3	Process		same affinity as					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_8_2661_s_205	15886395	( A) The single mutants of Pax6deltaHD, E112A, E120A and E128A bind to GST-HD with the same affinity as the wild type.	bind
58327	7	734	5	NULL	NULL	0	NULL	statement 4	Process		same affinity as					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_8_2661_s_205	15886395	( A) The single mutants of Pax6deltaHD, E112A, E120A and E128A bind to GST-HD with the same affinity as the wild type.	bind
2015	1	734	6	NULL	NULL	0	NULL	Pax6delta	GP		bind			mutant HD		GST-HD	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_8_2661_s_205	15886395	( A) The single mutants of Pax6deltaHD, E112A, E120A and E128A bind to GST-HD with the same affinity as the wild type.	bind
2016	2	734	6	NULL	NULL	0	NULL	Pax6delta	GP		bind			mutant E112A		GST-HD	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_8_2661_s_205	15886395	( A) The single mutants of Pax6deltaHD, E112A, E120A and E128A bind to GST-HD with the same affinity as the wild type.	bind
2017	3	734	6	NULL	NULL	0	NULL	Pax6delta	GP		bind			mutant E120A		GST-HD	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_8_2661_s_205	15886395	( A) The single mutants of Pax6deltaHD, E112A, E120A and E128A bind to GST-HD with the same affinity as the wild type.	bind
2018	4	734	6	NULL	NULL	0	NULL	Pax6delta	GP		bind			mutant E128A		GST-HD	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_8_2661_s_205	15886395	( A) The single mutants of Pax6deltaHD, E112A, E120A and E128A bind to GST-HD with the same affinity as the wild type.	bind
54098	5	734	6	NULL	NULL	0	NULL	Pax6delta	GP	wild type	bind					GST-HD	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_8_2661_s_205	15886395	( A) The single mutants of Pax6deltaHD, E112A, E120A and E128A bind to GST-HD with the same affinity as the wild type.	bind
58328	1	735	5	NULL	NULL	0	NULL	REST/NRSF	GP		is a type of					transcriptional repressor	GP				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3403_s_46	10954611	( A) The transcriptional repressor REST/NRSF contains a DNA-binding domain (Zn-DBD), consisting of eight zinc finger motifs, that bind to the consensus RE1 (or NRSE) sequence.	bind
58329	2	735	5	NULL	NULL	0	NULL	REST/NRSF	GP		bind			Zn-DBD		RE1 sequence	NucleicAcid	consensus			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3403_s_46	10954611	( A) The transcriptional repressor REST/NRSF contains a DNA-binding domain (Zn-DBD), consisting of eight zinc finger motifs, that bind to the consensus RE1 (or NRSE) sequence.	bind
58330	3	735	5	NULL	NULL	0	NULL	REST/NRSF	GP		bind			Zn-DBD		NRSE sequence	NucleicAcid	consensus			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3403_s_46	10954611	( A) The transcriptional repressor REST/NRSF contains a DNA-binding domain (Zn-DBD), consisting of eight zinc finger motifs, that bind to the consensus RE1 (or NRSE) sequence.	bind
58331	4	735	5	NULL	NULL	0	NULL	Zn-DBD	AminoAcid		is					DNA-binding domain	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3403_s_46	10954611	( A) The transcriptional repressor REST/NRSF contains a DNA-binding domain (Zn-DBD), consisting of eight zinc finger motifs, that bind to the consensus RE1 (or NRSE) sequence.	bind
2019	1	735	6	NULL	NULL	0	NULL	REST/NRSF	GP		bind			Zn-DBD			NucleicAcid			consensus RE1 sequence	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3403_s_46	10954611	( A) The transcriptional repressor REST/NRSF contains a DNA-binding domain (Zn-DBD), consisting of eight zinc finger motifs, that bind to the consensus RE1 (or NRSE) sequence.	bind
2020	2	735	6	NULL	NULL	0	NULL		GP		consist of 			Zn-DBD		eight zinc finger motifs	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3403_s_46	10954611	( A) The transcriptional repressor REST/NRSF contains a DNA-binding domain (Zn-DBD), consisting of eight zinc finger motifs, that bind to the consensus RE1 (or NRSE) sequence.	bind
51983	3	735	6	NULL	NULL	0	NULL	REST/NRSF	GP		bind			Zn-DBD			NucleicAcid			consensus NRSE sequence	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3403_s_46	10954611	( A) The transcriptional repressor REST/NRSF contains a DNA-binding domain (Zn-DBD), consisting of eight zinc finger motifs, that bind to the consensus RE1 (or NRSE) sequence.	bind
51984	4	735	6	NULL	NULL	0	NULL	REST/NRSF	GP		is a type of					transcriptional repressor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3403_s_46	10954611	( A) The transcriptional repressor REST/NRSF contains a DNA-binding domain (Zn-DBD), consisting of eight zinc finger motifs, that bind to the consensus RE1 (or NRSE) sequence.	bind
51985	5	735	6	NULL	NULL	0	NULL	Zn-DBD	GP		is					DNA-binding domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3403_s_46	10954611	( A) The transcriptional repressor REST/NRSF contains a DNA-binding domain (Zn-DBD), consisting of eight zinc finger motifs, that bind to the consensus RE1 (or NRSE) sequence.	bind
58332	1	736	5	NULL	NULL	0	NULL	stathmin/OP18	GP	truncated	bind					alpha-tubulin	GP				NULL		0	NULL	NULL	NULL	gw60_embo_19_2_213_s_191	10637225	( A) The truncated forms of stathmin/OP18 bind only to one alpha-tubulin of the heterodimer.	bind
2021	1	736	6	NULL	NULL	0	NULL	stathmin/OP18	GP	truncated	bind					alpha-tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_2_213_s_191	10637225	( A) The truncated forms of stathmin/OP18 bind only to one alpha-tubulin of the heterodimer.	bind
58333	1	739	5	NULL	NULL	0	NULL	U1C	GP		bind					U1 RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_179	15465910	( A) There is little U1C binding to U1 RNA at low temperature, because of a favored RNA  - RNA interaction, depicted as an intramolecular base-pairing interaction between  a putative ps5'' and the 5'ss.	bind
2022	1	739	6	NULL	NULL	0	NULL	U1C	GP		bind		low			U1RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_179	15465910	( A) There is little U1C binding to U1 RNA at low temperature, because of a favored RNA  - RNA interaction, depicted as an intramolecular base-pairing interaction between  a putative ps5'' and the 5'ss.	bind
2023	2	739	6	NULL	NULL	0	NULL	ps5	NucleicAcid	putative	base pairs with					5'ss	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_179	15465910	( A) There is little U1C binding to U1 RNA at low temperature, because of a favored RNA  - RNA interaction, depicted as an intramolecular base-pairing interaction between  a putative ps5'' and the 5'ss.	bind
51986	3	739	6	NULL	NULL	0	NULL	RNA	NucleicAcid		interacts with					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_179	15465910	( A) There is little U1C binding to U1 RNA at low temperature, because of a favored RNA  - RNA interaction, depicted as an intramolecular base-pairing interaction between  a putative ps5'' and the 5'ss.	bind
51987	4	739	6	NULL	NULL	0	NULL	statement 1	Process		because of					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_179	15465910	( A) There is little U1C binding to U1 RNA at low temperature, because of a favored RNA  - RNA interaction, depicted as an intramolecular base-pairing interaction between  a putative ps5'' and the 5'ss.	bind
51988	5	739	6	NULL	NULL	0	NULL	statement 3	Process		depicted as					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_179	15465910	( A) There is little U1C binding to U1 RNA at low temperature, because of a favored RNA  - RNA interaction, depicted as an intramolecular base-pairing interaction between  a putative ps5'' and the 5'ss.	bind
58334	1	740	5	NULL	NULL	0	NULL	Bak	GP		bind		tightly	BH3		Mcl-1	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_101	15901672	( A) Tight binding of Bak BH3 to Mcl-1 and Bcl-xL.	bind
58335	2	740	5	NULL	NULL	0	NULL	Bak	GP		bind		tightly	BH3		Bcl-xL	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_101	15901672	( A) Tight binding of Bak BH3 to Mcl-1 and Bcl-xL.	bind
2024	1	740	6	NULL	NULL	0	NULL	Bak	GP		bind		tightly	BH3		Mcl-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_101	15901672	( A) Tight binding of Bak BH3 to Mcl-1 and Bcl-xL.	bind
2025	2	740	6	NULL	NULL	0	NULL	Bak	GP		bind		tightly	BH3		Bcl-xL	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_101	15901672	( A) Tight binding of Bak BH3 to Mcl-1 and Bcl-xL.	bind
58336	1	742	5	NULL	NULL	0	NULL	TIP47	GP		bind					CI-MPR	GP				NULL		0	NULL	NULL	NULL	gw60_science_292_5520_1373_s_62	11359012	( A) TIP47 binds both CI-MPR and Rab9 in a ternary complex.	bind
58337	2	742	5	NULL	NULL	0	NULL	TIP47	GP		bind					Rab9	GP				NULL		0	NULL	NULL	NULL	gw60_science_292_5520_1373_s_62	11359012	( A) TIP47 binds both CI-MPR and Rab9 in a ternary complex.	bind
2026	1	742	6	NULL	NULL	0	NULL	TIP47	GP		bind					CI-MPR	GP				NULL	ternary complex	NULL	NULL	NULL	NULL	gw60_science_292_5520_1373_s_62	11359012	( A) TIP47 binds both CI-MPR and Rab9 in a ternary complex.	bind
2027	2	742	6	NULL	NULL	0	NULL	TIP47	GP		bind					Rab9	GP				NULL	ternary complex	NULL	NULL	NULL	NULL	gw60_science_292_5520_1373_s_62	11359012	( A) TIP47 binds both CI-MPR and Rab9 in a ternary complex.	bind
58338	1	743	5	NULL	NULL	0	NULL	TMEFF1	GP		bind					Cripto	GP				NULL	CHO cells	0	NULL	NULL	NULL	gw70_genesdev_17_21_2624_s_129	14563676	( A) TMEFF1 binds to Cripto in CHO cells.	bind
2028	1	743	6	NULL	NULL	0	NULL	TMEFF1	GP		bind					Cripto	GP				NULL	CHO cells	NULL	NULL	NULL	NULL	gw70_genesdev_17_21_2624_s_129	14563676	( A) TMEFF1 binds to Cripto in CHO cells.	bind
58339	1	744	5	NULL	NULL	0	NULL	IKK	GP		triggers					IkappaB	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	gw70_embo_24_3_510_s_165	15660126	( A) TNFalpha signals to IKK to trigger IkappaB phosphorylation and degradation, thereby eliciting NF-kappaB nuclear translocation, DNA binding and transcriptional repression of EAAT2.	bind
58340	2	744	5	NULL	NULL	0	NULL	statement 1	Process		leads to					IkappaB	GP	degradation of			NULL		0	NULL	NULL	NULL	gw70_embo_24_3_510_s_165	15660126	( A) TNFalpha signals to IKK to trigger IkappaB phosphorylation and degradation, thereby eliciting NF-kappaB nuclear translocation, DNA binding and transcriptional repression of EAAT2.	bind
58341	3	744	5	NULL	NULL	0	NULL	TNFalpha	GP		signals					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_embo_24_3_510_s_165	15660126	( A) TNFalpha signals to IKK to trigger IkappaB phosphorylation and degradation, thereby eliciting NF-kappaB nuclear translocation, DNA binding and transcriptional repression of EAAT2.	bind
58342	4	744	5	NULL	NULL	0	NULL	NF-kappaB	GP		is translocated to					nucleus	CellComponent				NULL		0	NULL	NULL	NULL	gw70_embo_24_3_510_s_165	15660126	( A) TNFalpha signals to IKK to trigger IkappaB phosphorylation and degradation, thereby eliciting NF-kappaB nuclear translocation, DNA binding and transcriptional repression of EAAT2.	bind
58343	5	744	5	NULL	NULL	0	NULL	statement 2	Process		elicits					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_embo_24_3_510_s_165	15660126	( A) TNFalpha signals to IKK to trigger IkappaB phosphorylation and degradation, thereby eliciting NF-kappaB nuclear translocation, DNA binding and transcriptional repression of EAAT2.	bind
58344	6	744	5	NULL	NULL	0	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_embo_24_3_510_s_165	15660126	( A) TNFalpha signals to IKK to trigger IkappaB phosphorylation and degradation, thereby eliciting NF-kappaB nuclear translocation, DNA binding and transcriptional repression of EAAT2.	bind
58345	7	744	5	NULL	NULL	0	NULL	statement 2	Process		elicits					statement 6	Process				NULL		0	NULL	NULL	NULL	gw70_embo_24_3_510_s_165	15660126	( A) TNFalpha signals to IKK to trigger IkappaB phosphorylation and degradation, thereby eliciting NF-kappaB nuclear translocation, DNA binding and transcriptional repression of EAAT2.	bind
58346	8	744	5	NULL	NULL	0	NULL	statement 2	Process		repress					EAAT2	GP	transcription of			NULL		0	NULL	NULL	NULL	gw70_embo_24_3_510_s_165	15660126	( A) TNFalpha signals to IKK to trigger IkappaB phosphorylation and degradation, thereby eliciting NF-kappaB nuclear translocation, DNA binding and transcriptional repression of EAAT2.	bind
2167	2	744	6	NULL	NULL	0	NULL	statement 1	Process		trigger					IkappaB	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw70_embo_24_3_510_s_165	15660126	( A) TNFalpha signals to IKK to trigger IkappaB phosphorylation and degradation, thereby eliciting NF-kappaB nuclear translocation, DNA binding and transcriptional repression of EAAT2.	bind
2168	3	744	6	NULL	NULL	0	NULL	statement 1	Process		trigger					IkappaB	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw70_embo_24_3_510_s_165	15660126	( A) TNFalpha signals to IKK to trigger IkappaB phosphorylation and degradation, thereby eliciting NF-kappaB nuclear translocation, DNA binding and transcriptional repression of EAAT2.	bind
2169	1	744	6	NULL	NULL	0	NULL	TNFalpha	GP		signals					 IKK	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_3_510_s_165	15660126	( A) TNFalpha signals to IKK to trigger IkappaB phosphorylation and degradation, thereby eliciting NF-kappaB nuclear translocation, DNA binding and transcriptional repression of EAAT2.	bind
2194	4	744	6	NULL	NULL	0	NULL	NF-kappaB	GP		is translocated to					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_3_510_s_165	15660126	( A) TNFalpha signals to IKK to trigger IkappaB phosphorylation and degradation, thereby eliciting NF-kappaB nuclear translocation, DNA binding and transcriptional repression of EAAT2.	bind
2195	5	744	6	NULL	NULL	0	NULL	NF-kappaB	GP		bind					EAAT2	GP			DNA	NULL		NULL	NULL	NULL	NULL	gw70_embo_24_3_510_s_165	15660126	( A) TNFalpha signals to IKK to trigger IkappaB phosphorylation and degradation, thereby eliciting NF-kappaB nuclear translocation, DNA binding and transcriptional repression of EAAT2.	bind
2196	6	744	6	NULL	NULL	0	NULL	NF-kappaB	GP		represses					EAAT2	GP	transcription of 			NULL		NULL	NULL	NULL	NULL	gw70_embo_24_3_510_s_165	15660126	( A) TNFalpha signals to IKK to trigger IkappaB phosphorylation and degradation, thereby eliciting NF-kappaB nuclear translocation, DNA binding and transcriptional repression of EAAT2.	bind
2197	7	744	6	NULL	NULL	0	NULL	statement 2	Process		occur along with					Statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_3_510_s_165	15660126	( A) TNFalpha signals to IKK to trigger IkappaB phosphorylation and degradation, thereby eliciting NF-kappaB nuclear translocation, DNA binding and transcriptional repression of EAAT2.	bind
2198	8	744	6	NULL	NULL	0	NULL	statement 7	Process		elicits					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_3_510_s_165	15660126	( A) TNFalpha signals to IKK to trigger IkappaB phosphorylation and degradation, thereby eliciting NF-kappaB nuclear translocation, DNA binding and transcriptional repression of EAAT2.	bind
2199	9	744	6	NULL	NULL	0	NULL	statement 7	Process		elicits					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_3_510_s_165	15660126	( A) TNFalpha signals to IKK to trigger IkappaB phosphorylation and degradation, thereby eliciting NF-kappaB nuclear translocation, DNA binding and transcriptional repression of EAAT2.	bind
51989	10	744	6	NULL	NULL	0	NULL	statement 7	Process		elicits					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_3_510_s_165	15660126	( A) TNFalpha signals to IKK to trigger IkappaB phosphorylation and degradation, thereby eliciting NF-kappaB nuclear translocation, DNA binding and transcriptional repression of EAAT2.	bind
58347	1	749	5	NULL	NULL	0	NULL	tPA	GP		bind					PDGF-CC	GP	latent	CUB domain;;growth factor domain		NULL		0	NULL	NULL	NULL	gw70_embo_23_19_3793_s_188	15372073	( A) tPA binds to both the CUB domain and the growth factor domain of latent PDGF-CC.	bind
2029	1	749	6	NULL	NULL	0	NULL	tPA	GP		bind					PDGF-CC	GP	latent	CUB domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_19_3793_s_188	15372073	( A) tPA binds to both the CUB domain and the growth factor domain of latent PDGF-CC.	bind
2030	2	749	6	NULL	NULL	0	NULL	tPA	GP		bind					PDGF-CC	GP	latent	growth factor domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_19_3793_s_188	15372073	( A) tPA binds to both the CUB domain and the growth factor domain of latent PDGF-CC.	bind
58348	1	750	5	NULL	NULL	0	NULL	TPP1	GP		bind		directly			TIN2	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_32_11874_s_107	16880378	( a) TPP1 directly binds TIN2 but not TRF2.	bind
58349	2	750	5	NULL	NULL	0	NULL	TPP1	GP		does not bind					TRF2	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_32_11874_s_107	16880378	( a) TPP1 directly binds TIN2 but not TRF2.	bind
2031	1	750	6	NULL	NULL	0	NULL	TPP1	GP		bind		directly			TIN2	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_32_11874_s_107	16880378	( a) TPP1 directly binds TIN2 but not TRF2.	bind
2032	2	750	6	NULL	NULL	0	NULL	TPP1	GP		does not bind		directly			TRF2	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_32_11874_s_107	16880378	( a) TPP1 directly binds TIN2 but not TRF2.	bind
2035	1	751	6	NULL	NULL	0	NULL	TRAF6	GP		bind					Cyt-N	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_4_1234_s_93	9990007	( A) TRAF6 binding with cyt-N was abolished by the QE234-5AA mutation.	bind
2036	2	751	6	NULL	NULL	0	NULL	TRAF6	GP		abolishes			QE234-5AA mutant		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_4_1234_s_93	9990007	( A) TRAF6 binding with cyt-N was abolished by the QE234-5AA mutation.	bind
58351	1	753	5	NULL	NULL	0	NULL	Rab	GP		bind					GDI/REP	GP				NULL		0	NULL	NULL	NULL	gw70_embo_25_1_13_s_181	16395334	( A) Two-step binding of Rab to GDI/REP.	bind
2034	1	753	6	NULL	NULL	0	NULL	Rab	GP		bind					GDI/REP	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_1_13_s_181	16395334	( A) Two-step binding of Rab to GDI/REP.	bind
58352	1	754	5	NULL	NULL	0	NULL	U1 snRNP	GP		bind					dsx pre-mRNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
58353	2	754	5	NULL	NULL	0	NULL	statement 1	Process		is independent of					ESE	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
58354	3	754	5	NULL	NULL	0	NULL	U2	GP		assemble on					dsx pre-mRNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
58355	4	754	5	NULL	NULL	0	NULL	U4/U6	GP		assemble on					dsx pre-mRNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
58356	5	754	5	NULL	NULL	0	NULL	U5 snRNPs	GP		assemble on					dsx pre-mRNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
58357	6	754	5	NULL	NULL	0	NULL	ESE	NucleicAcid		is required for					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
58358	7	754	5	NULL	NULL	0	NULL	ESE	NucleicAcid		is required for					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
58359	8	754	5	NULL	NULL	0	NULL	ESE	NucleicAcid		is required for					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
58360	9	754	5	NULL	NULL	0	NULL	U1 snRNP	GP		is required for					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
58361	10	754	5	NULL	NULL	0	NULL	U1 snRNP	GP		is required for					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
58362	11	754	5	NULL	NULL	0	NULL	U1 snRNP	GP		is required for					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
2173	1	754	6	NULL	NULL	0	NULL	U1 snRNP	GP		bind					dsx pre-mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
2174	2	754	6	NULL	NULL	0	NULL	statement 1	Process		independent of					ESE	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
2175	3	754	6	NULL	NULL	0	NULL	U2 snRNP	GP		assembles on					dsx pre-mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
2178	4	754	6	NULL	NULL	0	NULL	U4/U6 snRNP	GP		assembles on					dsx pre-mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
51990	5	754	6	NULL	NULL	0	NULL	U5 snRNP	GP		assembles on					dsx pre-mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
51991	6	754	6	NULL	NULL	0	NULL	ESE	GP		is required for 					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
51992	7	754	6	NULL	NULL	0	NULL	ESE	GP		is required for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
51993	8	754	6	NULL	NULL	0	NULL	ESE	GP		is required for					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
51994	9	754	6	NULL	NULL	0	NULL	U1 snRNP	GP		is required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
51995	10	754	6	NULL	NULL	0	NULL	U1 snRNP	GP		is required for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
51996	11	754	6	NULL	NULL	0	NULL	U1 snRNP	GP		is required for					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_11_6125_s_111	10339552	( A) U1 snRNP binds to the  dsx pre-mRNA independently of the ESE, whereas the ESE and U1 snRNP are required for the assembly of U2, U4/U6, and U5 snRNPs on the  dsx pre-mRNA.	bind
58363	1	755	5	NULL	NULL	0	NULL	GST - Grb2	GP	WT;;unphosphorylated	bind			C-SH3		Sos peptide	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_23_6793_s_121	11726515	( A) Unphosphorylated GST - Grb2-C-SH3 WT or mutant fusion proteins bind Sos peptide beads.	bind
58364	2	755	5	NULL	NULL	0	NULL	GST - Grb2	GP	mutant;;unphosphorylated	bind			C-SH3		Sos peptide	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_embo_20_23_6793_s_121	11726515	( A) Unphosphorylated GST - Grb2-C-SH3 WT or mutant fusion proteins bind Sos peptide beads.	bind
58365	1	756	5	NULL	NULL	0	NULL	Kss1	GP	unphosphorylated	bind		directly			Ste12	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_18_2887_s_193	9744865	( A) Unphosphorylated Kss1 binds directly to Ste12, and to Dig1 and Dig2, thereby stabilizing Dig1/2-Ste12 complexes and potentiating Dig-mediated repression of Ste12.	bind
58366	2	756	5	NULL	NULL	0	NULL	Kss1	GP	unphosphorylated	bind		directly			Dig1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_18_2887_s_193	9744865	( A) Unphosphorylated Kss1 binds directly to Ste12, and to Dig1 and Dig2, thereby stabilizing Dig1/2-Ste12 complexes and potentiating Dig-mediated repression of Ste12.	bind
58367	3	756	5	NULL	NULL	0	NULL	Kss1	GP	unphosphorylated	bind		directly			Dig2	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_18_2887_s_193	9744865	( A) Unphosphorylated Kss1 binds directly to Ste12, and to Dig1 and Dig2, thereby stabilizing Dig1/2-Ste12 complexes and potentiating Dig-mediated repression of Ste12.	bind
58368	4	756	5	NULL	NULL	0	NULL	statement 1	Process		stabilize					Dig1/2-Ste12 complexes	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_18_2887_s_193	9744865	( A) Unphosphorylated Kss1 binds directly to Ste12, and to Dig1 and Dig2, thereby stabilizing Dig1/2-Ste12 complexes and potentiating Dig-mediated repression of Ste12.	bind
58369	5	756	5	NULL	NULL	0	NULL	statement 2	Process		stabilize					Dig1/2-Ste12 complexes	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_18_2887_s_193	9744865	( A) Unphosphorylated Kss1 binds directly to Ste12, and to Dig1 and Dig2, thereby stabilizing Dig1/2-Ste12 complexes and potentiating Dig-mediated repression of Ste12.	bind
58370	6	756	5	NULL	NULL	0	NULL	statement 3	Process		stabilize					Dig1/2-Ste12 complexes	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_18_2887_s_193	9744865	( A) Unphosphorylated Kss1 binds directly to Ste12, and to Dig1 and Dig2, thereby stabilizing Dig1/2-Ste12 complexes and potentiating Dig-mediated repression of Ste12.	bind
58371	7	756	5	NULL	NULL	0	NULL	Dig	GP		repress					Ste12	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_18_2887_s_193	9744865	( A) Unphosphorylated Kss1 binds directly to Ste12, and to Dig1 and Dig2, thereby stabilizing Dig1/2-Ste12 complexes and potentiating Dig-mediated repression of Ste12.	bind
58372	8	756	5	NULL	NULL	0	NULL	statement 4	Process		potentiate					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_18_2887_s_193	9744865	( A) Unphosphorylated Kss1 binds directly to Ste12, and to Dig1 and Dig2, thereby stabilizing Dig1/2-Ste12 complexes and potentiating Dig-mediated repression of Ste12.	bind
58373	9	756	5	NULL	NULL	0	NULL	statement 5	Process		potentiate					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_18_2887_s_193	9744865	( A) Unphosphorylated Kss1 binds directly to Ste12, and to Dig1 and Dig2, thereby stabilizing Dig1/2-Ste12 complexes and potentiating Dig-mediated repression of Ste12.	bind
58374	10	756	5	NULL	NULL	0	NULL	statement 6	Process		potentiate					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_18_2887_s_193	9744865	( A) Unphosphorylated Kss1 binds directly to Ste12, and to Dig1 and Dig2, thereby stabilizing Dig1/2-Ste12 complexes and potentiating Dig-mediated repression of Ste12.	bind
2039	1	756	6	NULL	NULL	0	NULL	Kss1	GP	unphosphorylated	bind		directly			Ste12	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_18_2887_s_193	9744865	( A) Unphosphorylated Kss1 binds directly to Ste12, and to Dig1 and Dig2, thereby stabilizing Dig1/2-Ste12 complexes and potentiating Dig-mediated repression of Ste12.	bind
2040	2	756	6	NULL	NULL	0	NULL	Kss1	GP	unphosphorylated	bind		directly			Dig1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_18_2887_s_193	9744865	( A) Unphosphorylated Kss1 binds directly to Ste12, and to Dig1 and Dig2, thereby stabilizing Dig1/2-Ste12 complexes and potentiating Dig-mediated repression of Ste12.	bind
2041	3	756	6	NULL	NULL	0	NULL	Kss1	GP	unphosphorylated	bind		directly			Dig2	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_18_2887_s_193	9744865	( A) Unphosphorylated Kss1 binds directly to Ste12, and to Dig1 and Dig2, thereby stabilizing Dig1/2-Ste12 complexes and potentiating Dig-mediated repression of Ste12.	bind
2042	4	756	6	NULL	NULL	0	NULL	Dig	GP		mediates					Ste12	GP	repression of			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_18_2887_s_193	9744865	( A) Unphosphorylated Kss1 binds directly to Ste12, and to Dig1 and Dig2, thereby stabilizing Dig1/2-Ste12 complexes and potentiating Dig-mediated repression of Ste12.	bind
2043	5	756	6	NULL	NULL	0	NULL	Kss1	GP		potentiates					Statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_18_2887_s_193	9744865	( A) Unphosphorylated Kss1 binds directly to Ste12, and to Dig1 and Dig2, thereby stabilizing Dig1/2-Ste12 complexes and potentiating Dig-mediated repression of Ste12.	bind
2044	6	756	6	NULL	NULL	0	NULL	Kss1	GP		stabilizes					Dig1/2-Ste12 complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_18_2887_s_193	9744865	( A) Unphosphorylated Kss1 binds directly to Ste12, and to Dig1 and Dig2, thereby stabilizing Dig1/2-Ste12 complexes and potentiating Dig-mediated repression of Ste12.	bind
58375	1	757	5	NULL	NULL	0	NULL	RNAP	GP	host	bind					A2b	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_embo_20_21_6060_s_213	11689446	( A) Upon phage infection, the host RNAP binds to promoters A2b and A2c, giving rise to transcription of genes 6 to 1 (see Figure 1), while binding to promoter A3 requires synthesis of protein p4.	bind
58376	2	757	5	NULL	NULL	0	NULL	RNAP	GP	host	bind					A2c	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_embo_20_21_6060_s_213	11689446	( A) Upon phage infection, the host RNAP binds to promoters A2b and A2c, giving rise to transcription of genes 6 to 1 (see Figure 1), while binding to promoter A3 requires synthesis of protein p4.	bind
58377	3	757	5	NULL	NULL	0	NULL	statement 1	Process		occurs upon					phage infection	Process				NULL		0	NULL	NULL	NULL	gw60_embo_20_21_6060_s_213	11689446	( A) Upon phage infection, the host RNAP binds to promoters A2b and A2c, giving rise to transcription of genes 6 to 1 (see Figure 1), while binding to promoter A3 requires synthesis of protein p4.	bind
58378	4	757	5	NULL	NULL	0	NULL	statement 2	Process		occurs upon					phage infection	Process				NULL		0	NULL	NULL	NULL	gw60_embo_20_21_6060_s_213	11689446	( A) Upon phage infection, the host RNAP binds to promoters A2b and A2c, giving rise to transcription of genes 6 to 1 (see Figure 1), while binding to promoter A3 requires synthesis of protein p4.	bind
58379	5	757	5	NULL	NULL	0	NULL	RNAP	GP	host	bind					A3	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_embo_20_21_6060_s_213	11689446	( A) Upon phage infection, the host RNAP binds to promoters A2b and A2c, giving rise to transcription of genes 6 to 1 (see Figure 1), while binding to promoter A3 requires synthesis of protein p4.	bind
58380	6	757	5	NULL	NULL	0	NULL	statement 5	Process		requires					protein p4	GP	synthesis of			NULL		0	NULL	NULL	NULL	gw60_embo_20_21_6060_s_213	11689446	( A) Upon phage infection, the host RNAP binds to promoters A2b and A2c, giving rise to transcription of genes 6 to 1 (see Figure 1), while binding to promoter A3 requires synthesis of protein p4.	bind
2045	1	757	6	NULL	NULL	0	NULL	RNAP	GP		bind					A2b	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_6060_s_213	11689446	( A) Upon phage infection, the host RNAP binds to promoters A2b and A2c, giving rise to transcription of genes 6 to 1 (see Figure 1), while binding to promoter A3 requires synthesis of protein p4.	bind
2046	2	757	6	NULL	NULL	0	NULL	RNAP	GP		bind					A2c	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_6060_s_213	11689446	( A) Upon phage infection, the host RNAP binds to promoters A2b and A2c, giving rise to transcription of genes 6 to 1 (see Figure 1), while binding to promoter A3 requires synthesis of protein p4.	bind
2186	3	757	6	NULL	NULL	0	NULL	RNAP	GP		bind					A3	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_6060_s_213	11689446	( A) Upon phage infection, the host RNAP binds to promoters A2b and A2c, giving rise to transcription of genes 6 to 1 (see Figure 1), while binding to promoter A3 requires synthesis of protein p4.	bind
2187	4	757	6	NULL	NULL	0	NULL	statement 3	GP		requires					protein p4	GP	synthesis of			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_6060_s_213	11689446	( A) Upon phage infection, the host RNAP binds to promoters A2b and A2c, giving rise to transcription of genes 6 to 1 (see Figure 1), while binding to promoter A3 requires synthesis of protein p4.	bind
2188	5	757	6	NULL	NULL	0	NULL	statement 1	Process		results in					genes 6 to 1	GP	transcription of 			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_6060_s_213	11689446	( A) Upon phage infection, the host RNAP binds to promoters A2b and A2c, giving rise to transcription of genes 6 to 1 (see Figure 1), while binding to promoter A3 requires synthesis of protein p4.	bind
2189	6	757	6	NULL	NULL	0	NULL	statement 2	Process		results in					genes 6 to 1	GP	transcription of 			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_6060_s_213	11689446	( A) Upon phage infection, the host RNAP binds to promoters A2b and A2c, giving rise to transcription of genes 6 to 1 (see Figure 1), while binding to promoter A3 requires synthesis of protein p4.	bind
58381	1	759	5	NULL	NULL	0	NULL	Asf1	GP		bind					histone H3/H4 complex	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_102_17_5975_s_131	15840725	( a) V94R, D54R, and R108E are involved in the binding of Asf1 to the histone H3/H4 complex.	bind
2047	1	759	6	NULL	NULL	0	NULL	Asf1	GP		bind					histone H3/H4 complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_17_5975_s_131	15840725	( a) V94R, D54R, and R108E are involved in the binding of Asf1 to the histone H3/H4 complex.	bind
2048	2	759	6	NULL	NULL	0	NULL		AminoAcid		is involved in			V94R		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_17_5975_s_131	15840725	( a) V94R, D54R, and R108E are involved in the binding of Asf1 to the histone H3/H4 complex.	bind
2049	3	759	6	NULL	NULL	0	NULL		AminoAcid		is involved in			D54R		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_17_5975_s_131	15840725	( a) V94R, D54R, and R108E are involved in the binding of Asf1 to the histone H3/H4 complex.	bind
52124	4	759	6	NULL	NULL	0	NULL		AminoAcid		is involved in			R108E		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_17_5975_s_131	15840725	( a) V94R, D54R, and R108E are involved in the binding of Asf1 to the histone H3/H4 complex.	bind
58382	1	761	5	NULL	NULL	0	NULL	Vancomycin	GP		bind					peptidoglycan	CellComponent	growing	D-Ala-D-Ala moiety		NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_20_11028_s_18	10500118	( A) Vancomycin binds the D-Ala-D-Ala moiety of the growing peptidoglycan and sterically occludes the transglycosylation and transpeptidation steps of cell-wall assembly.	bind
58383	2	761	5	NULL	NULL	0	NULL	statement 1	Process		occlude		sterically			cell-wall assembly	Process	transglycosylation step of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_20_11028_s_18	10500118	( A) Vancomycin binds the D-Ala-D-Ala moiety of the growing peptidoglycan and sterically occludes the transglycosylation and transpeptidation steps of cell-wall assembly.	bind
58384	3	761	5	NULL	NULL	0	NULL	statement 1	Process		occlude		sterically			cell-wall assembly	Process	transpeptidation step of			NULL		0	NULL	NULL	NULL	gw60_pnas_96_20_11028_s_18	10500118	( A) Vancomycin binds the D-Ala-D-Ala moiety of the growing peptidoglycan and sterically occludes the transglycosylation and transpeptidation steps of cell-wall assembly.	bind
2050	1	761	6	NULL	NULL	0	NULL	Vancomycin	GP		bind					peptidoglycan	CellComponent		D-Ala-D-Ala moiety 		NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_20_11028_s_18	10500118	( A) Vancomycin binds the D-Ala-D-Ala moiety of the growing peptidoglycan and sterically occludes the transglycosylation and transpeptidation steps of cell-wall assembly.	bind
52125	2	761	6	NULL	NULL	0	NULL	statement 1	Process		occludes		sterically			cell-wall 	CellComponent	transglycosylation of;;assembly of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_20_11028_s_18	10500118	( A) Vancomycin binds the D-Ala-D-Ala moiety of the growing peptidoglycan and sterically occludes the transglycosylation and transpeptidation steps of cell-wall assembly.	bind
52126	3	761	6	NULL	NULL	0	NULL	statement 1	Process		occludes		sterically			cell-wall 	CellComponent	transpeptidation of;;assembly of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_20_11028_s_18	10500118	( A) Vancomycin binds the D-Ala-D-Ala moiety of the growing peptidoglycan and sterically occludes the transglycosylation and transpeptidation steps of cell-wall assembly.	bind
58385	1	763	5	NULL	NULL	0	NULL	VEGF-D	GP		bind					VEGFR-3	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_32_11658_s_160	15289610	( A) VEGFR-3 neutralizing antibody treatment, which blocks VEGF-D binding to VEGFR-3,  specifically suppressed lymphangiogenesis, whereas angiogenesis was unaffected.	bind
58386	2	763	5	NULL	NULL	0	NULL	VEGFR-3 neutralizing antibody	GP		blocks					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_32_11658_s_160	15289610	( A) VEGFR-3 neutralizing antibody treatment, which blocks VEGF-D binding to VEGFR-3,  specifically suppressed lymphangiogenesis, whereas angiogenesis was unaffected.	bind
58387	3	763	5	NULL	NULL	0	NULL	statement 2	Process		suppress		specifically			lymphangiogenesis	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_32_11658_s_160	15289610	( A) VEGFR-3 neutralizing antibody treatment, which blocks VEGF-D binding to VEGFR-3,  specifically suppressed lymphangiogenesis, whereas angiogenesis was unaffected.	bind
58388	4	763	5	NULL	NULL	0	NULL	statement 2	Process		does not affect					angiogenesis	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_32_11658_s_160	15289610	( A) VEGFR-3 neutralizing antibody treatment, which blocks VEGF-D binding to VEGFR-3,  specifically suppressed lymphangiogenesis, whereas angiogenesis was unaffected.	bind
2051	1	763	6	NULL	NULL	0	NULL	VEGF-D	GP		bind					VEGFR-3	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_32_11658_s_160	15289610	( A) VEGFR-3 neutralizing antibody treatment, which blocks VEGF-D binding to VEGFR-3,  specifically suppressed lymphangiogenesis, whereas angiogenesis was unaffected.	bind
2052	2	763	6	NULL	NULL	0	NULL	VEGFR-3	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_32_11658_s_160	15289610	( A) VEGFR-3 neutralizing antibody treatment, which blocks VEGF-D binding to VEGFR-3,  specifically suppressed lymphangiogenesis, whereas angiogenesis was unaffected.	bind
2053	3	763	6	NULL	NULL	0	NULL	VEGFR-3	GP		suppressed		specifically			lymphangiogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_32_11658_s_160	15289610	( A) VEGFR-3 neutralizing antibody treatment, which blocks VEGF-D binding to VEGFR-3,  specifically suppressed lymphangiogenesis, whereas angiogenesis was unaffected.	bind
2054	4	763	6	NULL	NULL	0	NULL	VEGFR-3	GP		has no effect					angiogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_32_11658_s_160	15289610	( A) VEGFR-3 neutralizing antibody treatment, which blocks VEGF-D binding to VEGFR-3,  specifically suppressed lymphangiogenesis, whereas angiogenesis was unaffected.	bind
58389	1	764	5	NULL	NULL	0	NULL	radixin			bind			FERM domain		ICAM-2 peptide	GP				NULL		0	NULL	NULL	NULL	gw60_embo_22_3_502_s_46	12554651	( A) Views of the radixin FERM domain bound to the ICAM-2 peptide by ribbon representations.	bind
2055	1	764	6	NULL	NULL	0	NULL	radixin	GP		bind			FERM domain		ICAM-2 peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_3_502_s_46	12554651	( A) Views of the radixin FERM domain bound to the ICAM-2 peptide by ribbon representations.	bind
58390	1	765	5	NULL	NULL	0	NULL	Vinculin	GP		bind					F-actin	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5853_s_167	10545097	( A) Vinculin binds to F-actin in the presence of IpaA in a co-sedimentation assay.	bind
58391	2	765	5	NULL	NULL	0	NULL	statement 1	Process		in the presence of					IpaA	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5853_s_167	10545097	( A) Vinculin binds to F-actin in the presence of IpaA in a co-sedimentation assay.	bind
2056	1	765	6	NULL	NULL	0	NULL	vinculin	GP		bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_5853_s_167	10545097	( A) Vinculin binds to F-actin in the presence of IpaA in a co-sedimentation assay.	bind
2057	2	765	6	NULL	NULL	0	NULL	statement 1	Process		occurs in presence of 					IpaA	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_5853_s_167	10545097	( A) Vinculin binds to F-actin in the presence of IpaA in a co-sedimentation assay.	bind
58392	1	773	5	NULL	NULL	0	NULL	Gcn5	GP	yeast	bind					AcCoA	GP				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_70_0_81_s_223	11395403	( A) yeast Gcn5 ( 138) and ( B) yeast HAT1 bound to acetyl-CoA (AcCoA) ( 78).	bind
58393	2	773	5	NULL	NULL	0	NULL	HAT1	GP	yeast	bind					AcCoA	GP				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_70_0_81_s_223	11395403	( A) yeast Gcn5 ( 138) and ( B) yeast HAT1 bound to acetyl-CoA (AcCoA) ( 78).	bind
58394	3	773	5	NULL	NULL	0	NULL	AcCoA	GP		is					acetyl-CoA	GP				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_70_0_81_s_223	11395403	( A) yeast Gcn5 ( 138) and ( B) yeast HAT1 bound to acetyl-CoA (AcCoA) ( 78).	bind
2058	1	773	6	NULL	NULL	0	NULL	Gcn5	GP	yeast	bind					acetyl-CoA 	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_70_0_81_s_223	11395403	( A) yeast Gcn5 ( 138) and ( B) yeast HAT1 bound to acetyl-CoA (AcCoA) ( 78).	bind
2059	2	773	6	NULL	NULL	0	NULL	HAT1	GP	Yeast	bind					acetyl-CoA 	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_70_0_81_s_223	11395403	( A) yeast Gcn5 ( 138) and ( B) yeast HAT1 bound to acetyl-CoA (AcCoA) ( 78).	bind
52127	3	773	6	NULL	NULL	0	NULL	AcCoA	Chemical		is					acetyl-CoA	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_70_0_81_s_223	11395403	( A) yeast Gcn5 ( 138) and ( B) yeast HAT1 bound to acetyl-CoA (AcCoA) ( 78).	bind
58395	1	774	5	NULL	NULL	0	NULL	guanylyltransferase	GP	yeast	bind					CTD	AminoAcid	phosphorylated			NULL		0	NULL	NULL	NULL	gw60_genesdev_11_24_3306_s_226	9407024	( A) Yeast guanylyltransferase, Ceg-1, methyltransferase, and Abd-1 bind to the phosphorylated CTD.	bind
58396	2	774	5	NULL	NULL	0	NULL	Ceg-1	GP	yeast	bind					CTD	AminoAcid	phosphorylated			NULL		0	NULL	NULL	NULL	gw60_genesdev_11_24_3306_s_226	9407024	( A) Yeast guanylyltransferase, Ceg-1, methyltransferase, and Abd-1 bind to the phosphorylated CTD.	bind
58397	3	774	5	NULL	NULL	0	NULL	methyltransferase	GP	yeast	bind					CTD	AminoAcid	phosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_24_3306_s_226	9407024	( A) Yeast guanylyltransferase, Ceg-1, methyltransferase, and Abd-1 bind to the phosphorylated CTD.	bind
2060	1	774	6	NULL	NULL	0	NULL	guanylyltransferase	GP	Yeast	bind						AminoAcid	phosphorylated	CTD		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_24_3306_s_226	9407024	( A) Yeast guanylyltransferase, Ceg-1, methyltransferase, and Abd-1 bind to the phosphorylated CTD.	bind
2061	2	774	6	NULL	NULL	0	NULL	Ceg-1	GP	Yeast	bind						AminoAcid	phosphorylated	CTD		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_24_3306_s_226	9407024	( A) Yeast guanylyltransferase, Ceg-1, methyltransferase, and Abd-1 bind to the phosphorylated CTD.	bind
2062	3	774	6	NULL	NULL	0	NULL	methyltransferase	GP	Yeast	bind						AminoAcid	phosphorylated	CTD		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_24_3306_s_226	9407024	( A) Yeast guanylyltransferase, Ceg-1, methyltransferase, and Abd-1 bind to the phosphorylated CTD.	bind
2063	4	774	6	NULL	NULL	0	NULL	Abd-1	GP	Yeast	bind						AminoAcid	phosphorylated	CTD		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_24_3306_s_226	9407024	( A) Yeast guanylyltransferase, Ceg-1, methyltransferase, and Abd-1 bind to the phosphorylated CTD.	bind
58398	1	776	5	NULL	NULL	0	NULL	AP-2	GP		bind					synaptotagmin I	GP		C2B domain		NULL		0	NULL	NULL	NULL	gw60_science_285_5431_1268_s_33	10455054	( A) YXX  peptides stimulate AP-2 binding to the C2B domain of synaptotagmin I.	bind
58399	2	776	5	NULL	NULL	0	NULL	YXX peptides	AminoAcid		stimulates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_science_285_5431_1268_s_33	10455054	( A) YXX  peptides stimulate AP-2 binding to the C2B domain of synaptotagmin I.	bind
2064	1	776	6	NULL	NULL	0	NULL	AP2	GP		bind					synaptotagmin I	GP		C2B domain		NULL		NULL	NULL	NULL	NULL	gw60_science_285_5431_1268_s_33	10455054	( A) YXX  peptides stimulate AP-2 binding to the C2B domain of synaptotagmin I.	bind
2065	2	776	6	NULL	NULL	0	NULL	YXX peptides	GP		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5431_1268_s_33	10455054	( A) YXX  peptides stimulate AP-2 binding to the C2B domain of synaptotagmin I.	bind
58400	1	777	5	NULL	NULL	0	NULL	YY1	GP		bind					CFTR	GP			CArG elements	NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5271_s_375	16170155	( A) YY1 binding to CFTR-CArG elements.	bind
2066	1	777	6	NULL	NULL	0	NULL	YY1	GP		bind					CFTR	GP			CArG element	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5271_s_375	16170155	( A) YY1 binding to CFTR-CArG elements.	bind
58401	1	778	5	NULL	NULL	0	NULL	Z-DNA	NucleicAcid		bind					yabZalphaE3L	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_40_14367_s_103	15448208	( A) Z-DNA binding of yabZalphaE3L as measured by CD.	bind
2067	1	778	6	NULL	NULL	0	NULL	Z-DNA	NucleicAcid		bind						AminoAcid		yabZalphaE3L		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_40_14367_s_103	15448208	( A) Z-DNA binding of yabZalphaE3L as measured by CD.	bind
58402	1	779	5	NULL	NULL	0	NULL	ZO-3	GP		bind					ZO-1	GP				NULL	MDCK cell extracts	0	NULL	NULL	NULL	gw60_cellbiol_141_1_199_s_135	9531559	( a) ZO-3 binds  ZO-1 and ZO-2 from MDCK  cell extracts.	bind
58403	2	779	5	NULL	NULL	0	NULL	ZO-3	GP		bind					ZO-2	GP				NULL	MDCK cell extracts	NULL	NULL	NULL	NULL	gw60_cellbiol_141_1_199_s_135	9531559	( a) ZO-3 binds  ZO-1 and ZO-2 from MDCK  cell extracts.	bind
2068	1	779	6	NULL	NULL	0	NULL	ZO-3	GP		bind					ZO-1	GP				NULL	MDCK cell extracts	NULL	NULL	NULL	NULL	gw60_cellbiol_141_1_199_s_135	9531559	( a) ZO-3 binds  ZO-1 and ZO-2 from MDCK  cell extracts.	bind
2069	2	779	6	NULL	NULL	0	NULL	ZO-3	GP		bind					ZO-2	GP				NULL	MDCK cell extracts	NULL	NULL	NULL	NULL	gw60_cellbiol_141_1_199_s_135	9531559	( a) ZO-3 binds  ZO-1 and ZO-2 from MDCK  cell extracts.	bind
58404	1	780	5	NULL	NULL	0	NULL	[gamma-32]GTP-V14RhoA	GP		bind		specifically			RhoGAP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_103_11_1561_s_231	10359565	( a) [gamma-32]GTP-V14RhoA specifically binds RhoGAP (positive control) and GST-IL-1Rcd, but not the negative controls GST and BSA.	bind
58405	2	780	5	NULL	NULL	0	NULL	[gamma-32]GTP-V14RhoA	GP		bind		specifically			GST-IL-1Rcd	GP				NULL		0	NULL	NULL	NULL	gw60_jclininvest_103_11_1561_s_231	10359565	( a) [gamma-32]GTP-V14RhoA specifically binds RhoGAP (positive control) and GST-IL-1Rcd, but not the negative controls GST and BSA.	bind
58406	3	780	5	NULL	NULL	0	NULL	[gamma-32]GTP-V14RhoA	GP		does not bind					GST	Chemical				NULL		0	NULL	NULL	NULL	gw60_jclininvest_103_11_1561_s_231	10359565	( a) [gamma-32]GTP-V14RhoA specifically binds RhoGAP (positive control) and GST-IL-1Rcd, but not the negative controls GST and BSA.	bind
58407	4	780	5	NULL	NULL	0	NULL	[gamma-32]GTP-V14RhoA	GP		does not bind					BSA	Chemical				NULL		0	NULL	NULL	NULL	gw60_jclininvest_103_11_1561_s_231	10359565	( a) [gamma-32]GTP-V14RhoA specifically binds RhoGAP (positive control) and GST-IL-1Rcd, but not the negative controls GST and BSA.	bind
2070	1	780	6	NULL	NULL	0	NULL	GTP-V14RhoA	GP		bind		specifically			RhoGAP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_103_11_1561_s_231	10359565	( a) [gamma-32]GTP-V14RhoA specifically binds RhoGAP (positive control) and GST-IL-1Rcd, but not the negative controls GST and BSA.	bind
2071	2	780	6	NULL	NULL	0	NULL	GTP-V14RhoA	GP		bind		specifically			GST-IL-1Rcd	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_103_11_1561_s_231	10359565	( a) [gamma-32]GTP-V14RhoA specifically binds RhoGAP (positive control) and GST-IL-1Rcd, but not the negative controls GST and BSA.	bind
58408	1	781	5	NULL	NULL	0	NULL	cTnC	GP		bind					cTnI	GP		(1-80)DD		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_24_16681_s_86	10358006	( A),  cTnC  bound to cTnI-(1-80)DD ( B), and free  cTnC  ( C).	bind
2074	1	781	6	NULL	NULL	0	NULL	cTnC	GP		bind					cTnI	GP		(1-80)DD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_24_16681_s_86	10358006	( A),  cTnC  bound to cTnI-(1-80)DD ( B), and free  cTnC  ( C).	bind
2075	2	781	6	NULL	NULL	0	NULL	cTnC	GP		bind					cTnC	GP	free			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_24_16681_s_86	10358006	( A),  cTnC  bound to cTnI-(1-80)DD ( B), and free  cTnC  ( C).	bind
58409	1	796	5	NULL	NULL	0	NULL	SCS	GP	pig	is specific to					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_16_11058_s_185	16481318	( A), GDP bound to pig GTP-specific SCS ( gray) ( B), and ATP bound to glycinamide ribonucleotide transformylase ( gray) (PDB identifier 1kj8) (  ) ( C).	bind
58410	2	796	5	NULL	NULL	0	NULL	GDP	Chemical		bind					statement 1	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_16_11058_s_185	16481318	( A), GDP bound to pig GTP-specific SCS ( gray) ( B), and ATP bound to glycinamide ribonucleotide transformylase ( gray) (PDB identifier 1kj8) (  ) ( C).	bind
58411	3	796	5	NULL	NULL	0	NULL	ATP	Chemical		bind					glycinamide ribonucleotide transformylase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_16_11058_s_185	16481318	( A), GDP bound to pig GTP-specific SCS ( gray) ( B), and ATP bound to glycinamide ribonucleotide transformylase ( gray) (PDB identifier 1kj8) (  ) ( C).	bind
2076	1	796	6	NULL	NULL	0	NULL	GDP	Chemical		bind					SCS	GP	pig;; GTP-specific			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_16_11058_s_185	16481318	( A), GDP bound to pig GTP-specific SCS ( gray) ( B), and ATP bound to glycinamide ribonucleotide transformylase ( gray) (PDB identifier 1kj8) (  ) ( C).	bind
2077	2	796	6	NULL	NULL	0	NULL	ATP	Chemical		bind					glycinamide ribonucleotide transformylase	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_16_11058_s_185	16481318	( A), GDP bound to pig GTP-specific SCS ( gray) ( B), and ATP bound to glycinamide ribonucleotide transformylase ( gray) (PDB identifier 1kj8) (  ) ( C).	bind
63	1	801	6	NULL	NULL	0	NULL	N4BP2	NULL		bind	NULL				GST-Nedd4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
64	2	801	6	NULL	NULL	0	NULL	N4BP2	NULL		bind	NULL				GST-Nedd4:N	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
65	3	801	6	NULL	NULL	0	NULL	N4BP3	NULL		bind	NULL				GST-Nedd4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
66	4	801	6	NULL	NULL	0	NULL	N4BP3	NULL		bind	NULL				GST-Nedd4:N	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
67	5	801	6	NULL	NULL	0	NULL	KIAA0341	NULL		bind	NULL				GST-Nedd4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
68	6	801	6	NULL	NULL	0	NULL	KIAA0341	NULL		bind	NULL				GST-Nedd4:N	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
69	7	801	6	NULL	NULL	0	NULL	N4BP2	NULL		bind	NULL	minimal			GST-Nedd4:C	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
70	8	801	6	NULL	NULL	0	NULL	N4BP2	NULL		bind	NULL	minimal			GST-E6AP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
71	9	801	6	NULL	NULL	0	NULL	N4BP3	NULL		bind	NULL	minimal			GST-Nedd4:C	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
72	10	801	6	NULL	NULL	0	NULL	N4BP3	NULL		bind	NULL	minimal			GST-E6AP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
73	11	801	6	NULL	NULL	0	NULL	KIAA0341	NULL		bind	NULL	minimal			GST-Nedd4:C	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
74	12	801	6	NULL	NULL	0	NULL	KIAA0341	NULL		bind	NULL	minimal			GST-E6AP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
75	13	801	6	NULL	NULL	0	NULL	N4BP2	NULL		does not bind	NULL				GST	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
76	14	801	6	NULL	NULL	0	NULL	N4BP3	NULL		does not bind	NULL				GST	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
77	15	801	6	NULL	NULL	0	NULL	KIAA0341	NULL		does not bind	NULL				GST	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
48147	1	801	7	NULL	NULL	0	NULL	N4BP2	GP		bind					GST-Nedd4	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
48148	2	801	7	NULL	NULL	0	NULL	 N4BP2	GP		bind					GST-Nedd4:N	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
48149	3	801	7	NULL	NULL	0	NULL	N4BP2	GP		bind		minimally			GST-Nedd4:C	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
48150	4	801	7	NULL	NULL	0	NULL	N4BP2	GP		bind		minimally			GST-E6AP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
48151	5	801	7	NULL	NULL	0	NULL	N4BP2 	GP		does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
48152	6	801	7	NULL	NULL	0	NULL	N4BP3	GP		bind					GST-Nedd4	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
48153	7	801	7	NULL	NULL	0	NULL	N4BP3 	GP		bind					GST-Nedd4:N	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
48154	8	801	7	NULL	NULL	0	NULL	N4BP3	GP		bind		minimally			GST-Nedd4:C	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
48155	9	801	7	NULL	NULL	0	NULL	N4BP3	GP		bind		minimally			GST-E6AP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
48156	10	801	7	NULL	NULL	0	NULL	N4BP3	GP		does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
48157	11	801	7	NULL	NULL	0	NULL	KIAA0341	Chemical		bind					GST-Nedd4	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
48158	12	801	7	NULL	NULL	0	NULL	KIAA0341	Chemical		bind					GST-Nedd4:N	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
48159	13	801	7	NULL	NULL	0	NULL	KIAA0341	Chemical		bind		minimally			GST-Nedd4:C	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
48160	14	801	7	NULL	NULL	0	NULL	KIAA0341	Chemical		bind		minimally			GST-E6AP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
48161	15	801	7	NULL	NULL	0	NULL	KIAA0341	Chemical		does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2897_s_133	11717310	( A), N4BP2 ( B), and N4BP3 and KIAA0341 ( C) each bind to GST-Nedd4 ( lane 2 in each panel) and GST-Nedd4:N ( lane 3 in each panel) equally well, but show minimal binding to GST-Nedd4:C ( lane 4 in each panel) and GST-E6AP ( lane 6 in each panel) and no binding to GST ( lane 5 in each panel).	bind
78	1	805	6	10	NULL	0	NULL	P2 Glu	NULL		bind	NULL					NULL	variant of	S554A		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_48786_s_181	14514675	( A), P2 Glu ( B), and P4 Glu ( C) are bound to the S554A variant.	bind
79	2	805	6	10	NULL	0	NULL	P4 Glu	NULL		bind	NULL					NULL	variant of	S554A		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_48786_s_181	14514675	( A), P2 Glu ( B), and P4 Glu ( C) are bound to the S554A variant.	bind
48162	1	805	7	NULL	NULL	0	NULL	P2 Glu	GP		bind							variant of	S554A		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_48786_s_181	14514675	( A), P2 Glu ( B), and P4 Glu ( C) are bound to the S554A variant.	bind
48163	2	805	7	NULL	NULL	0	NULL	P4 Glu	GP		bind							variant of	S554A		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_48786_s_181	14514675	( A), P2 Glu ( B), and P4 Glu ( C) are bound to the S554A variant.	bind
80	1	806	6	NULL	NULL	0	NULL	p21	NULL		bind	NULL				p53	NULL				NULL	wild type MEFs	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_42_41028_s_176	12909629	( A), p21 ( B), and Perp ( C) bound by p53 in wild type ( Wt) and p53S18A MEFs 18 h after UV radiation.	bind
81	2	806	6	NULL	NULL	0	NULL	p21	NULL		bind	NULL				p53	NULL				NULL	p53S18A MEFs	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_42_41028_s_176	12909629	( A), p21 ( B), and Perp ( C) bound by p53 in wild type ( Wt) and p53S18A MEFs 18 h after UV radiation.	bind
168	3	806	6	NULL	NULL	0	NULL	Perp	NULL		bind	NULL				p53	NULL				NULL	wild type MEFs	0	NULL	NULL	NULL	gw70_jbiolchem_278_42_41028_s_176	12909629	( A), p21 ( B), and Perp ( C) bound by p53 in wild type ( Wt) and p53S18A MEFs 18 h after UV radiation.	bind
169	4	806	6	NULL	NULL	0	NULL	Perp	NULL		bind	NULL				p53	NULL				NULL	p53S18A MEFs	0	NULL	NULL	NULL	gw70_jbiolchem_278_42_41028_s_176	12909629	( A), p21 ( B), and Perp ( C) bound by p53 in wild type ( Wt) and p53S18A MEFs 18 h after UV radiation.	bind
48164	1	806	7	NULL	NULL	0	NULL	p53	GP		bind					p21	GP				NULL	wild type MEFs	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_42_41028_s_176	12909629	( A), p21 ( B), and Perp ( C) bound by p53 in wild type ( Wt) and p53S18A MEFs 18 h after UV radiation.	bind
48165	2	806	7	NULL	NULL	0	NULL	p53	GP		bind					p21	GP				NULL	 p53S18A MEFs	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_42_41028_s_176	12909629	( A), p21 ( B), and Perp ( C) bound by p53 in wild type ( Wt) and p53S18A MEFs 18 h after UV radiation.	bind
48166	3	806	7	NULL	NULL	0	NULL	p53	GP		bind					Perp	GP				NULL	wild type MEFs	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_42_41028_s_176	12909629	( A), p21 ( B), and Perp ( C) bound by p53 in wild type ( Wt) and p53S18A MEFs 18 h after UV radiation.	bind
48167	4	806	7	NULL	NULL	0	NULL	p53	GP		bind					Perp	GP				NULL	 p53S18A MEFs	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_42_41028_s_176	12909629	( A), p21 ( B), and Perp ( C) bound by p53 in wild type ( Wt) and p53S18A MEFs 18 h after UV radiation.	bind
171	2	807	6	NULL	NULL	0	NULL	RFC	NULL		bind	NULL				PCNA-WCad	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_8_2546_s_147	16476998	( A), RFC-PCNA-WCad complex formed in the presence of ATP versus DNA bound with streptavidin ( B), RFC versus PCNA-WCad in the presence of ATPgammaS ( C), and RFC-PCNA-WCad complex formed in the presence of ATPgammaS versus DNA - streptavidin ( D).	bind
172	3	807	6	NULL	NULL	0	NULL	statement 2	NULL		forms a 	NULL				complex	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_8_2546_s_147	16476998	( A), RFC-PCNA-WCad complex formed in the presence of ATP versus DNA bound with streptavidin ( B), RFC versus PCNA-WCad in the presence of ATPgammaS ( C), and RFC-PCNA-WCad complex formed in the presence of ATPgammaS versus DNA - streptavidin ( D).	bind
173	4	807	6	NULL	NULL	0	NULL	statement 2	NULL		occurs in presence of	NULL				ATPgammaS	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_8_2546_s_147	16476998	( A), RFC-PCNA-WCad complex formed in the presence of ATP versus DNA bound with streptavidin ( B), RFC versus PCNA-WCad in the presence of ATPgammaS ( C), and RFC-PCNA-WCad complex formed in the presence of ATPgammaS versus DNA - streptavidin ( D).	bind
48170	1	807	7	NULL	NULL	0	NULL	RFC-PCNA	GP		forms complex with					WCad	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_8_2546_s_147	16476998	( A), RFC-PCNA-WCad complex formed in the presence of ATP versus DNA bound with streptavidin ( B), RFC versus PCNA-WCad in the presence of ATPgammaS ( C), and RFC-PCNA-WCad complex formed in the presence of ATPgammaS versus DNA - streptavidin ( D).	bind
48171	2	807	7	NULL	NULL	0	NULL	statement 1	Process		in presence of					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_8_2546_s_147	16476998	( A), RFC-PCNA-WCad complex formed in the presence of ATP versus DNA bound with streptavidin ( B), RFC versus PCNA-WCad in the presence of ATPgammaS ( C), and RFC-PCNA-WCad complex formed in the presence of ATPgammaS versus DNA - streptavidin ( D).	bind
48173	4	807	7	NULL	NULL	0	NULL	statement 1	Process		in presence of					ATPgammaS	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_8_2546_s_147	16476998	( A), RFC-PCNA-WCad complex formed in the presence of ATP versus DNA bound with streptavidin ( B), RFC versus PCNA-WCad in the presence of ATPgammaS ( C), and RFC-PCNA-WCad complex formed in the presence of ATPgammaS versus DNA - streptavidin ( D).	bind
57975	5	807	7	NULL	NULL	0	NULL	streptavidin 	Chemical		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_8_2546_s_147	16476998	( A), RFC-PCNA-WCad complex formed in the presence of ATP versus DNA bound with streptavidin ( B), RFC versus PCNA-WCad in the presence of ATPgammaS ( C), and RFC-PCNA-WCad complex formed in the presence of ATPgammaS versus DNA - streptavidin ( D).	bind
57976	3	807	7	NULL	NULL	0	NULL	PCNA	GP		complex with					WCad	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_8_2546_s_147	16476998	( A), RFC-PCNA-WCad complex formed in the presence of ATP versus DNA bound with streptavidin ( B), RFC versus PCNA-WCad in the presence of ATPgammaS ( C), and RFC-PCNA-WCad complex formed in the presence of ATPgammaS versus DNA - streptavidin ( D).	bind
57977	6	807	7	NULL	NULL	0	NULL	statement 3	Process		in the presence of					ATPgammaS	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_8_2546_s_147	16476998	( A), RFC-PCNA-WCad complex formed in the presence of ATP versus DNA bound with streptavidin ( B), RFC versus PCNA-WCad in the presence of ATPgammaS ( C), and RFC-PCNA-WCad complex formed in the presence of ATPgammaS versus DNA - streptavidin ( D).	bind
82	1	810	6	NULL	NULL	0	NULL	HMM	NULL		bind	NULL				F-actin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_15_10989_s_123	10753900	( A); however, the addition of 0.2 muM CaD enhanced the binding of HMM to F-actin ( B).	bind
83	2	810	6	NULL	NULL	0	NULL	CaD	NULL		enhance	NULL				Statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_15_10989_s_123	10753900	( A); however, the addition of 0.2 muM CaD enhanced the binding of HMM to F-actin ( B).	bind
48174	1	810	7	NULL	NULL	0	NULL	HMM	GP		bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_15_10989_s_123	10753900	( A); however, the addition of 0.2 muM CaD enhanced the binding of HMM to F-actin ( B).	bind
48175	2	810	7	NULL	NULL	0	NULL	CaD	Chemical		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_15_10989_s_123	10753900	( A); however, the addition of 0.2 muM CaD enhanced the binding of HMM to F-actin ( B).	bind
166	1	811	6	NULL	NULL	0	NULL	NPG	NULL		bind	NULL				RSO vesicles	NULL	mutant			NULL		0	NULL	NULL	NULL	gw60_pnas_96_20_11178_s_75	10500150	( A*-E*) Flow dialysis profiles comparing binding of NPG to RSO vesicles containing mutants G115A	bind
50312	2	811	6	10	NULL	0	NULL	RSO vesicles	NULL		contains	NULL					NULL	mutants	G115A		NULL		0	NULL	NULL	NULL	gw60_pnas_96_20_11178_s_75	10500150	( A*-E*) Flow dialysis profiles comparing binding of NPG to RSO vesicles containing mutants G115A	bind
48176	1	811	7	NULL	NULL	0	NULL	NPG	Chemical		bind					RSO vesicles	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_20_11178_s_75	10500150	( A*-E*) Flow dialysis profiles comparing binding of NPG to RSO vesicles containing mutants G115A	bind
50313	2	811	7	NULL	NULL	0	NULL	RSO vesicles	Chemical		contains						AminoAcid	mutants	G115A		NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_20_11178_s_75	10500150	( A*-E*) Flow dialysis profiles comparing binding of NPG to RSO vesicles containing mutants G115A	bind
84	1	813	6	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				JNK1	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_23_11_2185_s_156	15141161	( A, B) The binding affinities of ATP to JNK1 were measured by ITC when pepJIP1 was unbound	bind
48177	1	813	7	NULL	NULL	0	NULL	 ATP	Chemical		bind					JNK1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_11_2185_s_156	15141161	( A, B) The binding affinities of ATP to JNK1 were measured by ITC when pepJIP1 was unbound	bind
86	1	815	6	10	NULL	0	NULL	PIAS1	NULL		interacts with	NULL				SATB2	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3048_s_148	14701874	( A,B) PIAS1 interacts with SATB2 in vivo.	bind
48178	1	815	7	NULL	NULL	0	NULL	PIAS1	GP		interacts with					SATB2	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3048_s_148	14701874	( A,B) PIAS1 interacts with SATB2 in vivo.	bind
87	1	816	6	NULL	NULL	0	NULL	Ephrin-B2	NULL		bind	NULL				EphB-rtk8	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_19_3096_s_130	9765210	( A,C), but only ephrin-B2 can bind to EphB-rtk8 ( B,D).	bind
48179	1	816	7	NULL	NULL	0	NULL	ephrin-B2	GP		bind					 EphB-rtk8	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_19_3096_s_130	9765210	( A,C), but only ephrin-B2 can bind to EphB-rtk8 ( B,D).	bind
88	1	818	6	NULL	NULL	0	NULL	TFIIA	NULL		bind	NULL				TRF2	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_9_4791_s_147	10220372	( a- d) Western blot analysis of TFIIA and TFIIB binding to TRF2.	bind
89	2	818	6	NULL	NULL	0	NULL	TFIIB	NULL		bind	NULL				TRF2	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_9_4791_s_147	10220372	( a- d) Western blot analysis of TFIIA and TFIIB binding to TRF2.	bind
48180	1	818	7	NULL	NULL	0	NULL	TFIIA 	GP		bind					TRF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_9_4791_s_147	10220372	( a- d) Western blot analysis of TFIIA and TFIIB binding to TRF2.	bind
48181	2	818	7	NULL	NULL	0	NULL	TFIIB	GP		bind					TRF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_9_4791_s_147	10220372	( a- d) Western blot analysis of TFIIA and TFIIB binding to TRF2.	bind
90	1	819	6	10	NULL	0	NULL	NF-kappaB	NULL		bind	NULL				DNA	NULL			PRD11 site	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_67	10485885	( a-c) DSP1 helps NF-kappaB ( a) and p50/p50 ( b), but not p65/p65 ( c), bind to DNA bearing PRD11 sites, and an NRE has no effect on that cooperativity.	bind
91	2	819	6	10	NULL	0	NULL	p50/p50	NULL		bind	NULL				DNA	NULL			PRD11 site	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_67	10485885	( a-c) DSP1 helps NF-kappaB ( a) and p50/p50 ( b), but not p65/p65 ( c), bind to DNA bearing PRD11 sites, and an NRE has no effect on that cooperativity.	bind
92	3	819	6	10	NULL	0	NULL	p65/p65	NULL		bind	NULL				DNA	NULL			PRD11	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_67	10485885	( a-c) DSP1 helps NF-kappaB ( a) and p50/p50 ( b), but not p65/p65 ( c), bind to DNA bearing PRD11 sites, and an NRE has no effect on that cooperativity.	bind
93	4	819	6	NULL	NULL	0	NULL	DSP1	NULL		helps	NULL				Statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_67	10485885	( a-c) DSP1 helps NF-kappaB ( a) and p50/p50 ( b), but not p65/p65 ( c), bind to DNA bearing PRD11 sites, and an NRE has no effect on that cooperativity.	bind
94	5	819	6	NULL	NULL	0	NULL	DSP1	NULL		helps	NULL				Statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_67	10485885	( a-c) DSP1 helps NF-kappaB ( a) and p50/p50 ( b), but not p65/p65 ( c), bind to DNA bearing PRD11 sites, and an NRE has no effect on that cooperativity.	bind
95	6	819	6	10	NULL	0	NULL		NULL		has no effect on	NULL			NRE	Statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_67	10485885	( a-c) DSP1 helps NF-kappaB ( a) and p50/p50 ( b), but not p65/p65 ( c), bind to DNA bearing PRD11 sites, and an NRE has no effect on that cooperativity.	bind
96	7	819	6	10	NULL	0	NULL		NULL		has no effect on	NULL			NRE	Statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_67	10485885	( a-c) DSP1 helps NF-kappaB ( a) and p50/p50 ( b), but not p65/p65 ( c), bind to DNA bearing PRD11 sites, and an NRE has no effect on that cooperativity.	bind
50314	8	819	6	10	NULL	0	NULL	DSP1	NULL		does not help	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_67	10485885	( a-c) DSP1 helps NF-kappaB ( a) and p50/p50 ( b), but not p65/p65 ( c), bind to DNA bearing PRD11 sites, and an NRE has no effect on that cooperativity.	bind
48182	1	819	7	NULL	NULL	0	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid			PRD11 site	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_67	10485885	( a-c) DSP1 helps NF-kappaB ( a) and p50/p50 ( b), but not p65/p65 ( c), bind to DNA bearing PRD11 sites, and an NRE has no effect on that cooperativity.	bind
48183	2	819	7	NULL	NULL	0	NULL	p50/p50	GP		bind					DNA	NucleicAcid			PRD11 site	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_67	10485885	( a-c) DSP1 helps NF-kappaB ( a) and p50/p50 ( b), but not p65/p65 ( c), bind to DNA bearing PRD11 sites, and an NRE has no effect on that cooperativity.	bind
48184	3	819	7	NULL	NULL	0	NULL	p65/p65	GP		bind					DNA	NucleicAcid			PRD11 site	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_67	10485885	( a-c) DSP1 helps NF-kappaB ( a) and p50/p50 ( b), but not p65/p65 ( c), bind to DNA bearing PRD11 sites, and an NRE has no effect on that cooperativity.	bind
48185	4	819	7	NULL	NULL	0	NULL	DSP1	GP		helps in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_67	10485885	( a-c) DSP1 helps NF-kappaB ( a) and p50/p50 ( b), but not p65/p65 ( c), bind to DNA bearing PRD11 sites, and an NRE has no effect on that cooperativity.	bind
48186	5	819	7	NULL	NULL	0	NULL	DSP1	GP		helps in					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_67	10485885	( a-c) DSP1 helps NF-kappaB ( a) and p50/p50 ( b), but not p65/p65 ( c), bind to DNA bearing PRD11 sites, and an NRE has no effect on that cooperativity.	bind
48187	6	819	7	NULL	NULL	0	NULL	DSP1	GP		does not help					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_67	10485885	( a-c) DSP1 helps NF-kappaB ( a) and p50/p50 ( b), but not p65/p65 ( c), bind to DNA bearing PRD11 sites, and an NRE has no effect on that cooperativity.	bind
48188	7	819	7	NULL	NULL	0	NULL		GP		has no effect on				NRE	statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_67	10485885	( a-c) DSP1 helps NF-kappaB ( a) and p50/p50 ( b), but not p65/p65 ( c), bind to DNA bearing PRD11 sites, and an NRE has no effect on that cooperativity.	bind
48189	8	819	7	NULL	NULL	0	NULL		GP		has no effect on				NRE	statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_67	10485885	( a-c) DSP1 helps NF-kappaB ( a) and p50/p50 ( b), but not p65/p65 ( c), bind to DNA bearing PRD11 sites, and an NRE has no effect on that cooperativity.	bind
97	1	820	6	10	NULL	0	NULL	FGF7	NULL		bind	NULL				FGFR2c 	NULL		S252W		NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_26_14536_s_146	11121055	( A-C) FGF7 binding to FGFR2c (S252W), FGFR2c (P253R), and FGFR2b, respectively.	bind
98	2	820	6	10	NULL	0	NULL	FGF7	NULL		bind	NULL				FGFR2c	NULL		P253R		NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_26_14536_s_146	11121055	( A-C) FGF7 binding to FGFR2c (S252W), FGFR2c (P253R), and FGFR2b, respectively.	bind
99	3	820	6	NULL	NULL	0	NULL	FGF7	NULL		bind	NULL				FGFR2b	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_26_14536_s_146	11121055	( A-C) FGF7 binding to FGFR2c (S252W), FGFR2c (P253R), and FGFR2b, respectively.	bind
48191	1	820	7	NULL	NULL	0	NULL	FGF7	GP		bind					FGFR2c	GP		S252W		NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_26_14536_s_146	11121055	( A-C) FGF7 binding to FGFR2c (S252W), FGFR2c (P253R), and FGFR2b, respectively.	bind
48192	2	820	7	NULL	NULL	0	NULL	FGF7	GP		bind					FGFR2c	GP		P253R		NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_26_14536_s_146	11121055	( A-C) FGF7 binding to FGFR2c (S252W), FGFR2c (P253R), and FGFR2b, respectively.	bind
48193	3	820	7	NULL	NULL	0	NULL	FGF7	GP		bind					FGFR2b	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_26_14536_s_146	11121055	( A-C) FGF7 binding to FGFR2c (S252W), FGFR2c (P253R), and FGFR2b, respectively.	bind
100	1	825	6	10	NULL	0	NULL	MeCP2	NULL		bind	NULL		MBD		DNA	NULL	methylated			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_20_6603_s_80	16314321	( B -  D) Binding of the MBD of MeCP2 to methylated DNA and four-way junction DNA in the presence  of competitor.	bind
101	2	825	6	NULL	NULL	0	NULL	MeCP2	NULL		bind	NULL		MBD		four-way junction DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_20_6603_s_80	16314321	( B -  D) Binding of the MBD of MeCP2 to methylated DNA and four-way junction DNA in the presence  of competitor.	bind
48194	1	825	7	NULL	NULL	0	NULL	MeCP2	GP		bind			MBD		 DNA	NucleicAcid	 methylated			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_20_6603_s_80	16314321	( B -  D) Binding of the MBD of MeCP2 to methylated DNA and four-way junction DNA in the presence  of competitor.	bind
48195	2	825	7	NULL	NULL	0	NULL	MeCP2	GP		bind			MBD		four-way junction DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_20_6603_s_80	16314321	( B -  D) Binding of the MBD of MeCP2 to methylated DNA and four-way junction DNA in the presence  of competitor.	bind
102	1	828	6	NULL	NULL	0	NULL	PSF	NULL		bind	NULL				GAGE6	NULL			promoter fragments	NULL		0	NULL	NULL	NULL	gw70_pnas_102_34_12189_s_93	16079199	( B and  C) Binding of PSF to  GAGE6 promoter fragments.	bind
103	1	830	6	10	NULL	0	NULL	sera	NULL	mouse	bind	NULL				M21 cells	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_9_5396_s_97	12702756	( B and  C) Flow cytometry histogram showing the binding of mouse sera to human melanoma M21  cells.	bind
50315	2	830	6	10	NULL	0	NULL	M21 cells	NULL		is a type of	NULL				human melanoma cells	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_100_9_5396_s_97	12702756	( B and  C) Flow cytometry histogram showing the binding of mouse sera to human melanoma M21  cells.	bind
48198	1	830	7	NULL	NULL	0	NULL	sera	CellComponent	mouse	bind					M21 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_9_5396_s_97	12702756	( B and  C) Flow cytometry histogram showing the binding of mouse sera to human melanoma M21  cells.	bind
50316	2	830	7	NULL	NULL	0	NULL	M21 cells	Cell		is a type of					human melanoma cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_9_5396_s_97	12702756	( B and  C) Flow cytometry histogram showing the binding of mouse sera to human melanoma M21  cells.	bind
106	1	833	6	10	NULL	0	NULL	Fibrinogen	NULL	Soluble	bind	NULL				293T cell transfectants	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_10_3679_s_94	15738420	( B and  C) Soluble fibrinogen and PAC-1 IgM binding to 293T cell transfectants in the presence  of Ca2+ (white bars), Mn2+ (gray bars), PT25-2 (hatched bars), or Mn/PT25-2 (black bars).	bind
107	2	833	6	10	NULL	0	NULL	PAC-1 IgM	NULL		bind	NULL				293T cell transfectants	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_10_3679_s_94	15738420	( B and  C) Soluble fibrinogen and PAC-1 IgM binding to 293T cell transfectants in the presence  of Ca2+ (white bars), Mn2+ (gray bars), PT25-2 (hatched bars), or Mn/PT25-2 (black bars).	bind
48201	1	833	7	NULL	NULL	0	NULL	 fibrinogen	GP	soluble	bind					 293T cell transfectants	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_10_3679_s_94	15738420	( B and  C) Soluble fibrinogen and PAC-1 IgM binding to 293T cell transfectants in the presence  of Ca2+ (white bars), Mn2+ (gray bars), PT25-2 (hatched bars), or Mn/PT25-2 (black bars).	bind
48202	2	833	7	NULL	NULL	0	NULL	PAC-1 IgM	GP		bind					293T cell transfectants	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_10_3679_s_94	15738420	( B and  C) Soluble fibrinogen and PAC-1 IgM binding to 293T cell transfectants in the presence  of Ca2+ (white bars), Mn2+ (gray bars), PT25-2 (hatched bars), or Mn/PT25-2 (black bars).	bind
48203	3	833	7	NULL	NULL	0	NULL	statement 1	Process		in the presence of					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_10_3679_s_94	15738420	( B and  C) Soluble fibrinogen and PAC-1 IgM binding to 293T cell transfectants in the presence  of Ca2+ (white bars), Mn2+ (gray bars), PT25-2 (hatched bars), or Mn/PT25-2 (black bars).	bind
48204	4	833	7	NULL	NULL	0	NULL	statement 1	Process		in the presence of					Mn2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_10_3679_s_94	15738420	( B and  C) Soluble fibrinogen and PAC-1 IgM binding to 293T cell transfectants in the presence  of Ca2+ (white bars), Mn2+ (gray bars), PT25-2 (hatched bars), or Mn/PT25-2 (black bars).	bind
48205	5	833	7	NULL	NULL	0	NULL	statement 1	Process		in the presence of					PT25-2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_10_3679_s_94	15738420	( B and  C) Soluble fibrinogen and PAC-1 IgM binding to 293T cell transfectants in the presence  of Ca2+ (white bars), Mn2+ (gray bars), PT25-2 (hatched bars), or Mn/PT25-2 (black bars).	bind
48206	6	833	7	NULL	NULL	0	NULL	statement 1	Process		in the presence of					Mn/PT25-2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_10_3679_s_94	15738420	( B and  C) Soluble fibrinogen and PAC-1 IgM binding to 293T cell transfectants in the presence  of Ca2+ (white bars), Mn2+ (gray bars), PT25-2 (hatched bars), or Mn/PT25-2 (black bars).	bind
48207	7	833	7	NULL	NULL	0	NULL	statement 2	Process		in the presence of					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_10_3679_s_94	15738420	( B and  C) Soluble fibrinogen and PAC-1 IgM binding to 293T cell transfectants in the presence  of Ca2+ (white bars), Mn2+ (gray bars), PT25-2 (hatched bars), or Mn/PT25-2 (black bars).	bind
48208	8	833	7	NULL	NULL	0	NULL	statement 2	Process		in the presence of					Mn2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_10_3679_s_94	15738420	( B and  C) Soluble fibrinogen and PAC-1 IgM binding to 293T cell transfectants in the presence  of Ca2+ (white bars), Mn2+ (gray bars), PT25-2 (hatched bars), or Mn/PT25-2 (black bars).	bind
48209	9	833	7	NULL	NULL	0	NULL	statement 2	Process		in the presence of					 PT25-2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_10_3679_s_94	15738420	( B and  C) Soluble fibrinogen and PAC-1 IgM binding to 293T cell transfectants in the presence  of Ca2+ (white bars), Mn2+ (gray bars), PT25-2 (hatched bars), or Mn/PT25-2 (black bars).	bind
48210	10	833	7	NULL	NULL	0	NULL	statement 2	Process		in the presence of					Mn/PT25-2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_10_3679_s_94	15738420	( B and  C) Soluble fibrinogen and PAC-1 IgM binding to 293T cell transfectants in the presence  of Ca2+ (white bars), Mn2+ (gray bars), PT25-2 (hatched bars), or Mn/PT25-2 (black bars).	bind
108	1	834	6	NULL	NULL	0	NULL	PABP	NULL		bind	NULL				ARS	NULL				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_210	16356927	( B and  C) UV crosslinking assays of binding of PABP to ARS and poly	bind
109	2	834	6	NULL	NULL	0	NULL	PABP	NULL		bind	NULL				poly	NULL				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_210	16356927	( B and  C) UV crosslinking assays of binding of PABP to ARS and poly	bind
48211	1	834	7	NULL	NULL	0	NULL	PABP	GP		bind					ARS	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_210	16356927	( B and  C) UV crosslinking assays of binding of PABP to ARS and poly	bind
58233	1	836	7	NULL	NULL	0	NULL	Thrombin	GP	biotinylated	cleaves					RACK1	GP	free			NULL		0	NULL	NULL	NULL	gw70_pnas_101_8_2328_s_57	14983009	( B Left)  In vitro Coomassie stain of GST-fusion protein binding of purified RACK1 to glutathione Sepharose  and free RACK1 that has been cleaved from GST by using biotinylated thrombin followed  by clearing with streptavidin beads.	bind
113	1	837	6	10	NULL	0	NULL	MutS	NULL	 E. coli	bind	NULL				G/T mismatch	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_25_14822_s_48	14634210	( b Middle and  Bottom) AFM surface plots of  E. coli MutS bound to a G/T mismatch and  Taq MutS bound to a 1T-bulge, respectively.	bind
114	2	837	6	10	NULL	0	NULL	MutS	NULL	Taq	bind	NULL				1T-bulge	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_25_14822_s_48	14634210	( b Middle and  Bottom) AFM surface plots of  E. coli MutS bound to a G/T mismatch and  Taq MutS bound to a 1T-bulge, respectively.	bind
48212	1	837	7	NULL	NULL	0	NULL	MutS	GP	E.coli	bind					G/T mismatch	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_25_14822_s_48	14634210	( b Middle and  Bottom) AFM surface plots of  E. coli MutS bound to a G/T mismatch and  Taq MutS bound to a 1T-bulge, respectively.	bind
48213	2	837	7	NULL	NULL	0	NULL	MutS	GP	Taq	bind					1T-bulge	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_25_14822_s_48	14634210	( b Middle and  Bottom) AFM surface plots of  E. coli MutS bound to a G/T mismatch and  Taq MutS bound to a 1T-bulge, respectively.	bind
115	1	838	6	NULL	NULL	0	NULL	Hh	NULL		bind	NULL				receptor Ptc	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
116	2	838	6	NULL	NULL	0	NULL	PKA	NULL		phosphorylates	NULL				Smo	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
117	3	838	6	NULL	NULL	0	NULL	CKIalpha	NULL		phosphorylates	NULL				Smo	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
118	4	838	6	NULL	NULL	0	NULL	Statement 1	NULL		causes	NULL				Statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
119	5	838	6	NULL	NULL	0	NULL	Statement 1	NULL		causes	NULL				Statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
120	6	838	6	10	NULL	0	NULL	Statement 2	NULL		increases	NULL				Smo	NULL	 levels of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
121	7	838	6	10	NULL	0	NULL	Statement 3	NULL		increases	NULL				Smo	NULL	levels of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
50317	8	838	6	10	NULL	0	NULL	Smo	NULL		accumulates on	NULL				cell surface	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
50318	9	838	6	10	NULL	0	NULL	statement 6	NULL		leads to	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
50319	10	838	6	10	NULL	0	NULL	statement 7	NULL		leads to	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
48214	1	838	7	NULL	NULL	0	NULL	Hh 	GP		bind					Ptc receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
48215	2	838	7	NULL	NULL	0	NULL	PKA	GP		phosphorylate					Smo	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
48216	3	838	7	NULL	NULL	0	NULL	CKIalpha	GP		phosphorylate					Smo	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
48217	4	838	7	NULL	NULL	0	NULL	statement 2	Process		occurs after					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
48218	5	838	7	NULL	NULL	0	NULL	statement 3	Process		occurs after					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
48219	6	838	7	NULL	NULL	0	NULL	statement 2	Process		increase					Smo	GP	levels of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
48220	7	838	7	NULL	NULL	0	NULL	statement 3	Process		increase					Smo	GP	levels of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
48221	8	838	7	NULL	NULL	0	NULL	Smo	GP		accumulates on					cell surface	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
48222	9	838	7	NULL	NULL	0	NULL	statement 6	Process		leads to					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
48223	10	838	7	NULL	NULL	0	NULL	statement 7	Process		leads to					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_4_399_s_43	16481469	( B'') When Hh binds to its receptor Ptc, Smo becomes phosphorylated by PKA and CKIalpha, Smo levels increase, and it accumulates on the cell surface.	bind
123	1	839	6	NULL	NULL	0	NULL	A30	NULL		bind	NULL				HER3	NULL	cellular			NULL		0	NULL	NULL	NULL	gw70_pnas_100_16_9226_s_152	12874383	( B)  Binding of A30 to cellular HER3 also shows an increase in binding sites on  addition  of hrg ( ), although less pronounced than in solution.	bind
124	2	839	6	10	NULL	0	NULL	Hrg	NULL		increases	NULL				HER3	NULL	binding sites of;;cellular			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_16_9226_s_152	12874383	( B)  Binding of A30 to cellular HER3 also shows an increase in binding sites on  addition  of hrg ( ), although less pronounced than in solution.	bind
125	3	839	6	NULL	NULL	0	NULL	Statement 1	NULL		causes	NULL				Statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_100_16_9226_s_152	12874383	( B)  Binding of A30 to cellular HER3 also shows an increase in binding sites on  addition  of hrg ( ), although less pronounced than in solution.	bind
48224	1	839	7	NULL	NULL	0	NULL	A30	GP		bind					HER3	GP	cellular			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_16_9226_s_152	12874383	( B)  Binding of A30 to cellular HER3 also shows an increase in binding sites on  addition  of hrg ( ), although less pronounced than in solution.	bind
48225	2	839	7	NULL	NULL	0	NULL	hrg	GP		increase					HER3	GP	binding sites of;;cellular			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_16_9226_s_152	12874383	( B)  Binding of A30 to cellular HER3 also shows an increase in binding sites on  addition  of hrg ( ), although less pronounced than in solution.	bind
50320	3	839	7	NULL	NULL	0	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_16_9226_s_152	12874383	( B)  Binding of A30 to cellular HER3 also shows an increase in binding sites on  addition  of hrg ( ), although less pronounced than in solution.	bind
122	1	842	6	10	NULL	0	NULL	iC3b	NULL		bind	NULL				COS cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_6_1523_s_193	9852148	( B)  Histograms (mean  plus-or-minus  SEM,   n = 3) showing the relative  binding of iC3b to COS cells  expressing CR3 mutants.	bind
50321	2	842	6	10	NULL	0	NULL	COS cells	NULL		express	NULL				CR3	NULL	mutants			NULL		0	NULL	NULL	NULL	gw60_cellbiol_143_6_1523_s_193	9852148	( B)  Histograms (mean  plus-or-minus  SEM,   n = 3) showing the relative  binding of iC3b to COS cells  expressing CR3 mutants.	bind
48226	1	842	7	NULL	NULL	0	NULL	 iC3b	GP		bind					COS cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_6_1523_s_193	9852148	( B)  Histograms (mean  plus-or-minus  SEM,   n = 3) showing the relative  binding of iC3b to COS cells  expressing CR3 mutants.	bind
48227	2	842	7	NULL	NULL	0	NULL	COS cells	Cell		express					CR3	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_6_1523_s_193	9852148	( B)  Histograms (mean  plus-or-minus  SEM,   n = 3) showing the relative  binding of iC3b to COS cells  expressing CR3 mutants.	bind
126	1	843	6	10	NULL	0	NULL	HMGI-C protein	NULL		bind	NULL				IL-15 oligonucleotide	NULL				NULL	In vitro	NULL	NULL	NULL	NULL	gw60_pnas_98_14_7970_s_159	11427729	( B)  In vitro binding of HMGI-C protein to the IL-15 oligonucleotide competed with 30 ng of HMGI/C recombinant protein alone (lane 2) or in presence of two unrelated oligonucleotides (lanes 3 and 4).	bind
127	2	843	6	10	NULL	0	NULL	HMGI/C	NULL	recombinant	bind	NULL				IL-15 oligonucleotide	NULL				NULL	In vitro	NULL	NULL	NULL	NULL	gw60_pnas_98_14_7970_s_159	11427729	( B)  In vitro binding of HMGI-C protein to the IL-15 oligonucleotide competed with 30 ng of HMGI/C recombinant protein alone (lane 2) or in presence of two unrelated oligonucleotides (lanes 3 and 4).	bind
50322	3	843	6	10	NULL	0	NULL	statement 1	NULL		compete with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_98_14_7970_s_159	11427729	( B)  In vitro binding of HMGI-C protein to the IL-15 oligonucleotide competed with 30 ng of HMGI/C recombinant protein alone (lane 2) or in presence of two unrelated oligonucleotides (lanes 3 and 4).	bind
48228	1	843	7	NULL	NULL	0	NULL	HMGI-C protein	GP		bind					IL-15 oligonucleotide	NucleicAcid				NULL	In vitro	NULL	NULL	NULL	NULL	gw60_pnas_98_14_7970_s_159	11427729	( B)  In vitro binding of HMGI-C protein to the IL-15 oligonucleotide competed with 30 ng of HMGI/C recombinant protein alone (lane 2) or in presence of two unrelated oligonucleotides (lanes 3 and 4).	bind
48229	2	843	7	NULL	NULL	0	NULL	HMGI-C protein	GP	recombinant	bind					 IL-15 oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_14_7970_s_159	11427729	( B)  In vitro binding of HMGI-C protein to the IL-15 oligonucleotide competed with 30 ng of HMGI/C recombinant protein alone (lane 2) or in presence of two unrelated oligonucleotides (lanes 3 and 4).	bind
48230	3	843	7	NULL	NULL	0	NULL	statement 1	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_14_7970_s_159	11427729	( B)  In vitro binding of HMGI-C protein to the IL-15 oligonucleotide competed with 30 ng of HMGI/C recombinant protein alone (lane 2) or in presence of two unrelated oligonucleotides (lanes 3 and 4).	bind
128	1	844	6	NULL	NULL	0	NULL	p14ARF	NULL		bind	NULL				MDM2	NULL				NULL	In vitro	0	NULL	NULL	NULL	gw60_embo_17_17_5001_s_121	9724636	( B)  In vitro binding of p14ARF and MDM2.	bind
48231	1	844	7	NULL	NULL	0	NULL	p14ARF	GP		bind					MDM2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_17_17_5001_s_121	9724636	( B)  In vitro binding of p14ARF and MDM2.	bind
129	1	845	6	NULL	NULL	0	NULL	CDC25C	NULL		bind	NULL			5' UTR	Dazl	NULL				NULL	In vitro	0	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2479_s_58	11410654	( B)  In vitro binding of the CDC25C 5' UTR to Dazl.	bind
48232	1	845	7	NULL	NULL	0	NULL	CDC25C	GP		bind				5' UTR	Dazl	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2479_s_58	11410654	( B)  In vitro binding of the CDC25C 5' UTR to Dazl.	bind
130	1	848	6	10	NULL	0	NULL	ALEX	NULL	in vitro translated	bind	NULL	specifically			GST - XL	NULL		XL-domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_14_3849_s_181	11447126	( B)  In vitro translated ALEX binds specifically to the XL-domain of a GST - XL fusion protein.	bind
50323	2	848	6	10	NULL	0	NULL	GST - XL	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_14_3849_s_181	11447126	( B)  In vitro translated ALEX binds specifically to the XL-domain of a GST - XL fusion protein.	bind
48233	1	848	7	NULL	NULL	0	NULL	ALEX	GP	In vitro translated	bind		specifically			GST - XL	GP		XL-domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_14_3849_s_181	11447126	( B)  In vitro translated ALEX binds specifically to the XL-domain of a GST - XL fusion protein.	bind
48234	2	848	7	NULL	NULL	0	NULL	GST-XL	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_14_3849_s_181	11447126	( B)  In vitro translated ALEX binds specifically to the XL-domain of a GST - XL fusion protein.	bind
131	1	849	6	NULL	NULL	0	NULL	DRIP130	NULL	 In vitro translated	bind	NULL				ESX	NULL		activation domain		NULL		0	NULL	NULL	NULL	gw60_pnas_99_20_12747_s_68	12242338	( B)  In vitro translated DRIP130 binds the ESX activation domain but not its activation-deficient mutant.	bind
132	2	849	6	NULL	NULL	0	NULL	DRIP130	NULL	in vitro translated	does not bind	NULL				ESX	NULL	mutant			NULL		0	NULL	NULL	NULL	gw60_pnas_99_20_12747_s_68	12242338	( B)  In vitro translated DRIP130 binds the ESX activation domain but not its activation-deficient mutant.	bind
48235	1	849	7	NULL	NULL	0	NULL	DRIP130	GP	In vitro translated	bind					ESX	GP		activation domain		NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12747_s_68	12242338	( B)  In vitro translated DRIP130 binds the ESX activation domain but not its activation-deficient mutant.	bind
48236	2	849	7	NULL	NULL	0	NULL	DRIP130	GP	In vitro translated	does not bind					ESX	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12747_s_68	12242338	( B)  In vitro translated DRIP130 binds the ESX activation domain but not its activation-deficient mutant.	bind
133	1	850	6	NULL	NULL	0	NULL	MDM2	NULL	in vitro translated	bind	NULL				GST-Sp1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_98_5_2211_s_102	11226218	( B)  In vitro-translated MDM2 binds to GST-Sp1.	bind
48237	1	850	7	NULL	NULL	0	NULL	MDM2	GP	In vitro-translated	bind					GST-Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_5_2211_s_102	11226218	( B)  In vitro-translated MDM2 binds to GST-Sp1.	bind
134	1	851	6	NULL	NULL	0	NULL	K562 cells	NULL	PMA-treated	inhibits	NULL				CS-A	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_5_1024_s_199	9727071	( B)  Inhibition of CS-A binding  by PMA-treated K562  cells in the presence of  mAb Hermes-1 (8 mug/ml).	bind
167	2	851	6	NULL	NULL	0	NULL	Statement 1	NULL		occurs in presence of	NULL				mAb Hermes-1	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_102_5_1024_s_199	9727071	( B)  Inhibition of CS-A binding  by PMA-treated K562  cells in the presence of  mAb Hermes-1 (8 mug/ml).	bind
48238	1	851	7	NULL	NULL	0	NULL	K562 cells	Cells	PMA-treated	inhibit					 CS-A	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_5_1024_s_199	9727071	( B)  Inhibition of CS-A binding  by PMA-treated K562  cells in the presence of  mAb Hermes-1 (8 mug/ml).	bind
48239	2	851	7	NULL	NULL	0	NULL	statement 1	Process		in the presence of					mAb Hermes-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_5_1024_s_199	9727071	( B)  Inhibition of CS-A binding  by PMA-treated K562  cells in the presence of  mAb Hermes-1 (8 mug/ml).	bind
135	1	852	6	NULL	NULL	0	NULL	gp5/trx	NULL		bind	NULL				gp4E	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_14_5096_s_136	15795374	( B)  KD determination of the binding of gp5/trx to gp4E.	bind
48240	1	852	7	NULL	NULL	0	NULL	gp5/trx 	GP		bind					gp4E	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_14_5096_s_136	15795374	( B)  KD determination of the binding of gp5/trx to gp4E.	bind
136	1	853	6	10	NULL	0	NULL	Cdc42.GTPgammaS	NULL		bind	NULL					NULL		B-GBD		NULL		NULL	NULL	NULL	NULL	gw60_science_290_5492_801_s_105	11052943	( B)  PIP2 vesicle binding assays ( 29) show that  Cdc42.GTPgammaS and PIP2 can simultaneously bind the  control region (B-GBD).	bind
137	2	853	6	10	NULL	0	NULL	PIP2	NULL		bind	NULL					NULL		B-GBD		NULL		NULL	NULL	NULL	NULL	gw60_science_290_5492_801_s_105	11052943	( B)  PIP2 vesicle binding assays ( 29) show that  Cdc42.GTPgammaS and PIP2 can simultaneously bind the  control region (B-GBD).	bind
138	3	853	6	10	NULL	0	NULL	Statement 1	NULL		occur simultaneously with	NULL				Statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_290_5492_801_s_105	11052943	( B)  PIP2 vesicle binding assays ( 29) show that  Cdc42.GTPgammaS and PIP2 can simultaneously bind the  control region (B-GBD).	bind
50324	4	853	6	10	NULL	0	NULL	B-GBD	NULL		is a type of	NULL				control region	NULL				NULL		0	NULL	NULL	NULL	gw60_science_290_5492_801_s_105	11052943	( B)  PIP2 vesicle binding assays ( 29) show that  Cdc42.GTPgammaS and PIP2 can simultaneously bind the  control region (B-GBD).	bind
48241	1	853	7	NULL	NULL	0	NULL	Cdc42.GTPgammaS	GP		bind								B-GBD		NULL		NULL	NULL	NULL	NULL	gw60_science_290_5492_801_s_105	11052943	( B)  PIP2 vesicle binding assays ( 29) show that  Cdc42.GTPgammaS and PIP2 can simultaneously bind the  control region (B-GBD).	bind
48242	2	853	7	NULL	NULL	0	NULL	PIP2	GP		bind								B-GBD		NULL		NULL	NULL	NULL	NULL	gw60_science_290_5492_801_s_105	11052943	( B)  PIP2 vesicle binding assays ( 29) show that  Cdc42.GTPgammaS and PIP2 can simultaneously bind the  control region (B-GBD).	bind
48243	3	853	7	NULL	NULL	0	NULL	statement 1	Process		occur simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_290_5492_801_s_105	11052943	( B)  PIP2 vesicle binding assays ( 29) show that  Cdc42.GTPgammaS and PIP2 can simultaneously bind the  control region (B-GBD).	bind
48244	4	853	7	NULL	NULL	0	NULL	B-GBD	GP		is a type of					control region	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_290_5492_801_s_105	11052943	( B)  PIP2 vesicle binding assays ( 29) show that  Cdc42.GTPgammaS and PIP2 can simultaneously bind the  control region (B-GBD).	bind
140	1	854	6	NULL	NULL	0	NULL	R-etodolac	NULL		bind	NULL	directly			RXRalpha	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_7_2525_s_146	15699354	( b)  R-etodolac binds directly to RXRalpha.	bind
48245	1	854	7	NULL	NULL	0	NULL	R-etodolac	Chemical		bind		directly			RXRalpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_7_2525_s_146	15699354	( b)  R-etodolac binds directly to RXRalpha.	bind
139	1	855	6	NULL	NULL	0	NULL	ZO-3	NULL		bind	NULL	directly			ZO-1	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_141_1_199_s_138	9531559	( b)  ZO-3 binds ZO-1 directly.	bind
48246	1	855	7	NULL	NULL	0	NULL	ZO-3 	GP		bind		directly			ZO-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_1_199_s_138	9531559	( b)  ZO-3 binds ZO-1 directly.	bind
141	1	856	6	10	NULL	0	NULL	gp120 IIIB	NULL	125I	bind	NULL				HeLa-CD4 cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_14_8005_s_133	9653130	( B) 125I-gp120 IIIB binding to HeLa-CD4 (clone H1-J) and to control HeLa cells.	bind
142	2	856	6	10	NULL	0	NULL	gp120 IIIB	NULL	125I	bind	NULL				HeLa cells	NULL	control			NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_14_8005_s_133	9653130	( B) 125I-gp120 IIIB binding to HeLa-CD4 (clone H1-J) and to control HeLa cells.	bind
48247	1	856	7	NULL	NULL	0	NULL	gp120 IIIB	GP	125I	bind					HeLa-CD4 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_14_8005_s_133	9653130	( B) 125I-gp120 IIIB binding to HeLa-CD4 (clone H1-J) and to control HeLa cells.	bind
48248	2	856	7	NULL	NULL	0	NULL	gp120 IIIB	GP	125I	bind					HeLa cells	Cell	control			NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_14_8005_s_133	9653130	( B) 125I-gp120 IIIB binding to HeLa-CD4 (clone H1-J) and to control HeLa cells.	bind
143	1	859	6	10	NULL	0	NULL	Sly1 	NULL	15N,13C-labeled	bind	NULL		N-terminal domain		syntaxin 5 peptide	NULL	unlabeled			NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_1_32_s_159	12506202	( B) 2D 13C-filtered, 13C-edited NOESY spectrum of 15N,13C-labeled Sly1 N-terminal domain bound to unlabeled syntaxin 5 peptide.	bind
48249	1	859	7	NULL	NULL	0	NULL	Sly1	GP	 15N,13C-labeled	bind			N-terminal domain		syntaxin 5 peptide	GP	unlabeled			NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_1_32_s_159	12506202	( B) 2D 13C-filtered, 13C-edited NOESY spectrum of 15N,13C-labeled Sly1 N-terminal domain bound to unlabeled syntaxin 5 peptide.	bind
144	1	861	6	NULL	NULL	0	NULL	40S pre-mRNP proteins	NULL		bind	NULL				DNase I 	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_8_1725_s_139	11937625	( B) 40S pre-mRNP proteins bound to DNase I - Sepharose and subsequently analyzed as in	bind
48250	1	861	7	NULL	NULL	0	NULL	40S pre-mRNP proteins	GP		bind					DNase I - Sepharose	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_8_1725_s_139	11937625	( B) 40S pre-mRNP proteins bound to DNase I - Sepharose and subsequently analyzed as in	bind
145	1	864	6	10	NULL	0	NULL	80R scFv	NULL		bind	NULL				S1-Ig	NULL		261 - 672		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_8_2536_s_157	14983044	( B) 80R scFv bound to S1 (261 - 672)-Ig but did not bind to S1 (327)-Ig.	bind
146	2	864	6	10	NULL	0	NULL	80R scFv	NULL		does not bind	NULL				S1-Ig	NULL		327		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_8_2536_s_157	14983044	( B) 80R scFv bound to S1 (261 - 672)-Ig but did not bind to S1 (327)-Ig.	bind
48251	1	864	7	NULL	NULL	0	NULL	 80R scFv	GP		bind					S1-Ig	GP		261 - 672		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_8_2536_s_157	14983044	( B) 80R scFv bound to S1 (261 - 672)-Ig but did not bind to S1 (327)-Ig.	bind
48252	2	864	7	NULL	NULL	0	NULL	 80R scFv	GP		does not bind					S1-Ig	GP		327		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_8_2536_s_157	14983044	( B) 80R scFv bound to S1 (261 - 672)-Ig but did not bind to S1 (327)-Ig.	bind
147	1	867	6	10	NULL	0	NULL	antibodies	NULL	tagged	bind	NULL				IgGs	NULL	chicken			NULL		NULL	NULL	NULL	NULL	gw60_science_276_5313_779_s_59	9115199	( B) A fluorescence micrograph shows light from tagged antibodies to chicken IgG that bound chicken IgGs patterned using a muFN as depicted in Fig.  1B.	bind
48253	1	867	7	NULL	NULL	0	NULL	antibodies	GP	tagged 	bind					IgG	GP	chicken			NULL		NULL	NULL	NULL	NULL	gw60_science_276_5313_779_s_59	9115199	( B) A fluorescence micrograph shows light from tagged antibodies to chicken IgG that bound chicken IgGs patterned using a muFN as depicted in Fig.  1B.	bind
148	1	868	6	NULL	NULL	0	NULL	clathrin	NULL		bind	NULL				GST - GGA2-hinge + GAE	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_22_1_78_s_173	12505986	( B) A mutant His6-Rabaptin-5 (5 - 476) fragment containing three alanine substitutions in codons 438 - 440 (5 - 476*) does not affect the binding of clathrin to GST - GGA2-hinge + GAE.	bind
149	2	868	6	10	NULL	0	NULL	His6-Rabaptin-5 fragment	NULL	mutant	contains	NULL				alanine substitutions	NULL		codons 438 - 440		NULL		NULL	NULL	NULL	NULL	gw60_embo_22_1_78_s_173	12505986	( B) A mutant His6-Rabaptin-5 (5 - 476) fragment containing three alanine substitutions in codons 438 - 440 (5 - 476*) does not affect the binding of clathrin to GST - GGA2-hinge + GAE.	bind
50325	3	868	6	10	NULL	0	NULL	Statement 2	NULL		does not affect	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_22_1_78_s_173	12505986	( B) A mutant His6-Rabaptin-5 (5 - 476) fragment containing three alanine substitutions in codons 438 - 440 (5 - 476*) does not affect the binding of clathrin to GST - GGA2-hinge + GAE.	bind
48254	1	868	7	NULL	NULL	0	NULL	clathrin	GP		bind					GST - GGA2-hinge + GAE	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_1_78_s_173	12505986	( B) A mutant His6-Rabaptin-5 (5 - 476) fragment containing three alanine substitutions in codons 438 - 440 (5 - 476*) does not affect the binding of clathrin to GST - GGA2-hinge + GAE.	bind
48255	2	868	7	NULL	NULL	0	NULL	His6-Rabaptin-5 fragment	GP	mutant	contains					alanine substitutions	AminoAcid		codons 438 - 440		NULL		NULL	NULL	NULL	NULL	gw60_embo_22_1_78_s_173	12505986	( B) A mutant His6-Rabaptin-5 (5 - 476) fragment containing three alanine substitutions in codons 438 - 440 (5 - 476*) does not affect the binding of clathrin to GST - GGA2-hinge + GAE.	bind
48256	3	868	7	NULL	NULL	0	NULL	statement 2	Process		does not affect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_1_78_s_173	12505986	( B) A mutant His6-Rabaptin-5 (5 - 476) fragment containing three alanine substitutions in codons 438 - 440 (5 - 476*) does not affect the binding of clathrin to GST - GGA2-hinge + GAE.	bind
150	1	870	6	10	NULL	0	NULL	TNF ligands	NULL	Flag-tagged 	bind	NULL				BAFF-R:Fc	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5537_2108_s_70	11509692	( B) A panel of Flag-tagged TNF ligands was bound to BAFF-R:Fc, BCMA:Fc, or TACI:Fc coated plates and detected with the use of the HRP-M2 (Sigma).	bind
151	2	870	6	10	NULL	0	NULL	TNF ligands	NULL	Flag-tagged	bind	NULL				BCMA:Fc	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5537_2108_s_70	11509692	( B) A panel of Flag-tagged TNF ligands was bound to BAFF-R:Fc, BCMA:Fc, or TACI:Fc coated plates and detected with the use of the HRP-M2 (Sigma).	bind
152	3	870	6	10	NULL	0	NULL	TNF ligands	NULL	Flag-tagged	bind	NULL				TACI:Fc	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5537_2108_s_70	11509692	( B) A panel of Flag-tagged TNF ligands was bound to BAFF-R:Fc, BCMA:Fc, or TACI:Fc coated plates and detected with the use of the HRP-M2 (Sigma).	bind
48257	1	870	7	NULL	NULL	0	NULL	TNF ligands	GP	Flag-tagged	bind					 BAFF-R:Fc	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5537_2108_s_70	11509692	( B) A panel of Flag-tagged TNF ligands was bound to BAFF-R:Fc, BCMA:Fc, or TACI:Fc coated plates and detected with the use of the HRP-M2 (Sigma).	bind
48258	2	870	7	NULL	NULL	0	NULL	 TNF ligands	GP	Flag-tagged	bind					BCMA:Fc	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5537_2108_s_70	11509692	( B) A panel of Flag-tagged TNF ligands was bound to BAFF-R:Fc, BCMA:Fc, or TACI:Fc coated plates and detected with the use of the HRP-M2 (Sigma).	bind
48259	3	870	7	NULL	NULL	0	NULL	TNF ligands	GP	Flag-tagged	bind					TACI:Fc	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5537_2108_s_70	11509692	( B) A panel of Flag-tagged TNF ligands was bound to BAFF-R:Fc, BCMA:Fc, or TACI:Fc coated plates and detected with the use of the HRP-M2 (Sigma).	bind
153	1	872	6	NULL	NULL	0	NULL	Cdc11 septin	NULL		bind	NULL				Gin4	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_143_3_709_s_104	9813092	( B) A Western blot confirming that the Cdc11 septin binds to the Gin4 affinity column.	bind
48260	1	872	7	NULL	NULL	0	NULL	Cdc11 septin	GP		bind					Gin4	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_3_709_s_104	9813092	( B) A Western blot confirming that the Cdc11 septin binds to the Gin4 affinity column.	bind
154	1	874	6	10	NULL	0	NULL	Smad 3	NULL	activated	bind	NULL				c-jun probe	NULL	32P labeled			NULL	nuclear extracts	NULL	NULL	NULL	NULL	gw60_genesdev_14_20_2610_s_183	11040215	( B) Activated Smad3/4 binding to a 32P labeled c-jun probe was examined in nuclear extracts by EMSA.	bind
48261	1	874	7	NULL	NULL	0	NULL	Smad3/4	GP	activated	bind					c-jun probe	GP	32P labeled			NULL	nuclear extracts	NULL	NULL	NULL	NULL	gw60_genesdev_14_20_2610_s_183	11040215	( B) Activated Smad3/4 binding to a 32P labeled c-jun probe was examined in nuclear extracts by EMSA.	bind
155	1	875	6	NULL	NULL	0	NULL	PICK1	NULL		bind	NULL				GluR2	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_18_3266_s_317	16138078	( B) Activation of NMDARs localised in close proximity to AMPARs results in a Ca2+ flux that raises the local [Ca2+] to around 15 muM and therefore enhances binding of PICK1 to GluR2.	bind
156	2	875	6	NULL	NULL	0	NULL	NMDARs	NULL		localised in close proximity to	NULL				AMPARs	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_18_3266_s_317	16138078	( B) Activation of NMDARs localised in close proximity to AMPARs results in a Ca2+ flux that raises the local [Ca2+] to around 15 muM and therefore enhances binding of PICK1 to GluR2.	bind
157	3	875	6	NULL	NULL	0	NULL	NMDARs	NULL	activated	results in	NULL				Ca2+ flux	NULL				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_18_3266_s_317	16138078	( B) Activation of NMDARs localised in close proximity to AMPARs results in a Ca2+ flux that raises the local [Ca2+] to around 15 muM and therefore enhances binding of PICK1 to GluR2.	bind
158	4	875	6	NULL	NULL	0	NULL	Statement 3	NULL		enhances	NULL				Statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_18_3266_s_317	16138078	( B) Activation of NMDARs localised in close proximity to AMPARs results in a Ca2+ flux that raises the local [Ca2+] to around 15 muM and therefore enhances binding of PICK1 to GluR2.	bind
48262	1	875	7	NULL	NULL	0	NULL	NMDARs	GP		is in close proximity to					AMPARs	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_18_3266_s_317	16138078	( B) Activation of NMDARs localised in close proximity to AMPARs results in a Ca2+ flux that raises the local [Ca2+] to around 15 muM and therefore enhances binding of PICK1 to GluR2.	bind
48263	2	875	7	NULL	NULL	0	NULL	statement 1	Process	activation of	result in					Ca2+ flux	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_18_3266_s_317	16138078	( B) Activation of NMDARs localised in close proximity to AMPARs results in a Ca2+ flux that raises the local [Ca2+] to around 15 muM and therefore enhances binding of PICK1 to GluR2.	bind
48264	3	875	7	NULL	NULL	0	NULL	statement 2	Process		leads to					Ca2+	Chemical	increase in			NULL		NULL	NULL	NULL	NULL	gw70_embo_24_18_3266_s_317	16138078	( B) Activation of NMDARs localised in close proximity to AMPARs results in a Ca2+ flux that raises the local [Ca2+] to around 15 muM and therefore enhances binding of PICK1 to GluR2.	bind
48265	4	875	7	NULL	NULL	0	NULL	PICK1	GP		bind					GluR2	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_18_3266_s_317	16138078	( B) Activation of NMDARs localised in close proximity to AMPARs results in a Ca2+ flux that raises the local [Ca2+] to around 15 muM and therefore enhances binding of PICK1 to GluR2.	bind
48266	5	875	7	NULL	NULL	0	NULL	statement 3	Process		enhance					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_18_3266_s_317	16138078	( B) Activation of NMDARs localised in close proximity to AMPARs results in a Ca2+ flux that raises the local [Ca2+] to around 15 muM and therefore enhances binding of PICK1 to GluR2.	bind
159	1	876	6	NULL	NULL	0	NULL	CN5	NULL		bind	NULL				F-actin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_5_3089_s_243	12446728	( B) addition of TnI to the Tm.TnT binary complex slightly increased the inhibitory effect  on CN5 binding to F-actin.	bind
160	2	876	6	10	NULL	0	NULL	TnI	NULL		added to	NULL				Tm.TnT binary complex	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_5_3089_s_243	12446728	( B) addition of TnI to the Tm.TnT binary complex slightly increased the inhibitory effect  on CN5 binding to F-actin.	bind
161	3	876	6	10	NULL	0	NULL	Statement 2	NULL		increases	NULL				statement 1                                                                                                                                                                                                                                                  	NULL	inhibitory effect of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_5_3089_s_243	12446728	( B) addition of TnI to the Tm.TnT binary complex slightly increased the inhibitory effect  on CN5 binding to F-actin.	bind
48267	1	876	7	NULL	NULL	0	NULL	CN5	GP		bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_5_3089_s_243	12446728	( B) addition of TnI to the Tm.TnT binary complex slightly increased the inhibitory effect  on CN5 binding to F-actin.	bind
48268	2	876	7	NULL	NULL	0	NULL	TnI	GP		added to					Tm.TnT binary complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_5_3089_s_243	12446728	( B) addition of TnI to the Tm.TnT binary complex slightly increased the inhibitory effect  on CN5 binding to F-actin.	bind
48269	3	876	7	NULL	NULL	0	NULL	statement 2	Process		increase					statement 1	Process	inhibitory effect of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_5_3089_s_243	12446728	( B) addition of TnI to the Tm.TnT binary complex slightly increased the inhibitory effect  on CN5 binding to F-actin.	bind
162	1	878	6	NULL	NULL	0	NULL	ADP	NULL		bind	NULL				GroEL	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_67_0_581_s_207	9759498	( B) ADP bound to GroEL in the   GroEL-GroES-(ADP)7 structure.	bind
48270	1	878	7	NULL	NULL	0	NULL	ADP	Chemical		bind					 GroEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_581_s_207	9759498	( B) ADP bound to GroEL in the   GroEL-GroES-(ADP)7 structure.	bind
164	1	880	6	NULL	NULL	0	NULL	Six3	NULL		bind	NULL				Crygf	NULL			promoter sequences	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_2_515_s_238	11139622	( b) Affinity binding of Six3 to  Crygf promoter sequences.	bind
48272	1	880	7	NULL	NULL	0	NULL	 Six3	GP		bind					 Crygf	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_2_515_s_238	11139622	( b) Affinity binding of Six3 to  Crygf promoter sequences.	bind
163	1	882	6	NULL	NULL	0	NULL	IP3	NULL		bind	NULL				IP3R	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_437_s_220	15189149	( B) After agonist stimulus, IP3 binds to the IP3R, causing a conformational change in the channel.	bind
50326	2	882	6	10	NULL	0	NULL	statement 1	NULL		occurs after	NULL				agonist	NULL	stimulus of			NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_437_s_220	15189149	( B) After agonist stimulus, IP3 binds to the IP3R, causing a conformational change in the channel.	bind
50327	3	882	6	10	NULL	0	NULL	statement 1	NULL		causes	NULL				channel	NULL	conformational change of			NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_437_s_220	15189149	( B) After agonist stimulus, IP3 binds to the IP3R, causing a conformational change in the channel.	bind
48273	1	882	7	NULL	NULL	0	NULL	IP3	Chemical		bind					IP3R	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_73_0_437_s_220	15189149	( B) After agonist stimulus, IP3 binds to the IP3R, causing a conformational change in the channel.	bind
48274	2	882	7	NULL	NULL	0	NULL	statement 1	Process		occurs after					agonist	Chemical	stimulus by			NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_73_0_437_s_220	15189149	( B) After agonist stimulus, IP3 binds to the IP3R, causing a conformational change in the channel.	bind
48275	3	882	7	NULL	NULL	0	NULL	statement 1	Process		cause					channel	CellComponent	conformational change of			NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_73_0_437_s_220	15189149	( B) After agonist stimulus, IP3 binds to the IP3R, causing a conformational change in the channel.	bind
174	1	883	6	NULL	NULL	0	NULL	GroES	NULL		bind	NULL				GroEL	NULL		First ring		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_32925_s_27	9407071	( b) After GroES binding to one GroEL ring to form an asymmetric complex, the second ring seems to bind a second GroES molecule to form a symmetric complex with lower affinity ( 14).	bind
175	2	883	6	NULL	NULL	0	NULL	Statement 1	NULL		forms an	NULL				asymmetric complex	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_32925_s_27	9407071	( b) After GroES binding to one GroEL ring to form an asymmetric complex, the second ring seems to bind a second GroES molecule to form a symmetric complex with lower affinity ( 14).	bind
176	3	883	6	NULL	NULL	0	NULL	GroES	NULL		bind	NULL				GroEL 	NULL		second ring		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_32925_s_27	9407071	( b) After GroES binding to one GroEL ring to form an asymmetric complex, the second ring seems to bind a second GroES molecule to form a symmetric complex with lower affinity ( 14).	bind
177	4	883	6	NULL	NULL	0	NULL	Statement 3	NULL		forms a	NULL				symmetric complex	NULL	lower affinity			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_32925_s_27	9407071	( b) After GroES binding to one GroEL ring to form an asymmetric complex, the second ring seems to bind a second GroES molecule to form a symmetric complex with lower affinity ( 14).	bind
50329	5	883	6	10	NULL	0	NULL	statement 3	NULL		occurs after	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_32925_s_27	9407071	( b) After GroES binding to one GroEL ring to form an asymmetric complex, the second ring seems to bind a second GroES molecule to form a symmetric complex with lower affinity ( 14).	bind
48276	1	883	7	NULL	NULL	0	NULL	GroES	GP		bind					GroEL 	GP		first ring		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_32925_s_27	9407071	( b) After GroES binding to one GroEL ring to form an asymmetric complex, the second ring seems to bind a second GroES molecule to form a symmetric complex with lower affinity ( 14).	bind
48277	2	883	7	NULL	NULL	0	NULL	statement 1	Process		forms					asymmetric complex					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_32925_s_27	9407071	( b) After GroES binding to one GroEL ring to form an asymmetric complex, the second ring seems to bind a second GroES molecule to form a symmetric complex with lower affinity ( 14).	bind
48278	3	883	7	NULL	NULL	0	NULL	GroES	GP		bind					GroEL	GP		second ring		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_32925_s_27	9407071	( b) After GroES binding to one GroEL ring to form an asymmetric complex, the second ring seems to bind a second GroES molecule to form a symmetric complex with lower affinity ( 14).	bind
48279	4	883	7	NULL	NULL	0	NULL	statement 3	Process		forms		low affinity			symmetric complex					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_32925_s_27	9407071	( b) After GroES binding to one GroEL ring to form an asymmetric complex, the second ring seems to bind a second GroES molecule to form a symmetric complex with lower affinity ( 14).	bind
48280	5	883	7	NULL	NULL	0	NULL	statement 3	Process		occurs after					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_32925_s_27	9407071	( b) After GroES binding to one GroEL ring to form an asymmetric complex, the second ring seems to bind a second GroES molecule to form a symmetric complex with lower affinity ( 14).	bind
165	1	887	6	10	NULL	0	NULL	DEBP	NULL		bind	NULL				goosecoid DE	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_4_435_s_54	10691736	( B) An activin-inducible protein (DEBP) binds the  goosecoid DE.	bind
50330	2	887	6	10	NULL	0	NULL	DEBP	NULL		is a type of	NULL				activin-inducible protein	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_14_4_435_s_54	10691736	( B) An activin-inducible protein (DEBP) binds the  goosecoid DE.	bind
48281	1	887	7	NULL	NULL	0	NULL	DEBP	GP		bind					 goosecoid 	GP			DE	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_4_435_s_54	10691736	( B) An activin-inducible protein (DEBP) binds the  goosecoid DE.	bind
48282	2	887	7	NULL	NULL	0	NULL	DEBP	GP		is a type of					activin-inducible protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_4_435_s_54	10691736	( B) An activin-inducible protein (DEBP) binds the  goosecoid DE.	bind
178	1	888	6	10	NULL	0	NULL	p53	NULL	bacterially purified	bind	NULL	sequence-specific 			XPC-p53	NULL			 response element	NULL	In vitro	NULL	NULL	NULL	NULL	gw60_pnas_99_20_12985_s_163	12242345	( B) An electrophoretic mobility-shift assay demonstrates sequence-specific DNA binding of bacterially purified p53 to the identified  XPC-p53 response element  in vitro.	bind
48283	1	888	7	NULL	NULL	0	NULL	p53	GP	bacterially purified	bind		sequence-specific			XPC-p53 	GP			response element	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_99_20_12985_s_163	12242345	( B) An electrophoretic mobility-shift assay demonstrates sequence-specific DNA binding of bacterially purified p53 to the identified  XPC-p53 response element  in vitro.	bind
179	1	889	6	10	NULL	0	NULL	C3d mAb	NULL	Alexa Fluor 647 labelled	bind	NULL				IAM	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_115_5_1241_s_140	15849610	( B) An mAb to C3d labeled with Alexa Fluor 647 binds to the IAM.	bind
48284	1	889	7	NULL	NULL	0	NULL	 C3d mAb	GP	 Alexa Fluor 647 labeled	bind					IAM	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_115_5_1241_s_140	15849610	( B) An mAb to C3d labeled with Alexa Fluor 647 binds to the IAM.	bind
180	1	891	6	NULL	NULL	0	NULL	MxiD	NULL		bind	NULL				MxiM	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_6_1111_s_176	15775974	( B) Analysis of MxiD binding to MxiM incubated with the lipid 2-dioctanoylsnnglycero-3-phosphate.	bind
48286	1	891	7	NULL	NULL	0	NULL	MxiD 	GP		bind					MxiM	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_6_1111_s_176	15775974	( B) Analysis of MxiD binding to MxiM incubated with the lipid 2-dioctanoylsnnglycero-3-phosphate.	bind
181	1	892	6	NULL	NULL	0	NULL	Nap1p	NULL		binds to	NULL				GST - histone	NULL		N-terminal tails		NULL		0	NULL	NULL	NULL	gw60_embo_21_23_6527_s_101	12456659	( B) Analysis of Nap1p binding to GST - histone N-terminal tails (1 muM of each) as in	bind
48287	1	892	7	NULL	NULL	0	NULL	Nap1p	GP		bind					 GST - histone	GP		N-terminal tails		NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6527_s_101	12456659	( B) Analysis of Nap1p binding to GST - histone N-terminal tails (1 muM of each) as in	bind
182	1	894	6	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				DNA	NULL			GC box	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_15_4523_s_134	12888513	( B) Analysis of the effect of pH and ZnCl2 on Sp1 binding to GC box DNA in the DNA binding assay.	bind
48288	1	894	7	NULL	NULL	0	NULL	Sp1	GP		bind					DNA	NucleicAcid			GC box	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_15_4523_s_134	12888513	( B) Analysis of the effect of pH and ZnCl2 on Sp1 binding to GC box DNA in the DNA binding assay.	bind
183	1	895	6	NULL	NULL	0	NULL	UL28 protein	NULL		bind	NULL				Ub DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_98_6_3086_s_112	11248036	( B) Analysis of UL28 protein binding to Ub DNA.	bind
48289	1	895	7	NULL	NULL	0	NULL	UL28 protein	GP		bind					Ub DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_6_3086_s_112	11248036	( B) Analysis of UL28 protein binding to Ub DNA.	bind
185	1	896	6	10	NULL	0	NULL	NIP1-N	NULL		binds to	NULL				eIF1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_19_2534_s_57	11018020	( B) and ( C) The amino-terminal segment of eIF3-NIP1 (NIP1-N) binds to eIF1 and eIF5.	bind
186	2	896	6	10	NULL	0	NULL	NIP1-N	NULL		bind	NULL				eIF5	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_19_2534_s_57	11018020	( B) and ( C) The amino-terminal segment of eIF3-NIP1 (NIP1-N) binds to eIF1 and eIF5.	bind
50331	3	896	6	10	NULL	0	NULL	NIP1-N	NULL		is	NULL				amino-terminal segment of eIF3-NIP1	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_14_19_2534_s_57	11018020	( B) and ( C) The amino-terminal segment of eIF3-NIP1 (NIP1-N) binds to eIF1 and eIF5.	bind
48290	1	896	7	NULL	NULL	0	NULL	NIP1-N	GP		bind					eIF1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_19_2534_s_57	11018020	( B) and ( C) The amino-terminal segment of eIF3-NIP1 (NIP1-N) binds to eIF1 and eIF5.	bind
48291	2	896	7	NULL	NULL	0	NULL	NIP1-N	GP		bind					eIF5	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_19_2534_s_57	11018020	( B) and ( C) The amino-terminal segment of eIF3-NIP1 (NIP1-N) binds to eIF1 and eIF5.	bind
48292	3	896	7	NULL	NULL	0	NULL	NIP1-N	GP		is					amino-terminal segment of eIF3-NIP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_19_2534_s_57	11018020	( B) and ( C) The amino-terminal segment of eIF3-NIP1 (NIP1-N) binds to eIF1 and eIF5.	bind
187	1	897	6	NULL	NULL	0	NULL	LGL	NULL	leukemic	bind	NULL				PBMCs	NULL	normal			NULL		0	NULL	NULL	NULL	gw60_jclininvest_107_3_351_s_147	11160159	( b) Annexin-V-FITC binding of leukemic LGL and normal PBMCs in response to DMSO (0) and AG-490 (25, 50, and 100 muM for 48 hours).	bind
48293	1	897	7	NULL	NULL	0	NULL	 Annexin-V-FITC	GP		bind					leukemic LGL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_107_3_351_s_147	11160159	( b) Annexin-V-FITC binding of leukemic LGL and normal PBMCs in response to DMSO (0) and AG-490 (25, 50, and 100 muM for 48 hours).	bind
48294	2	897	7	NULL	NULL	0	NULL	Annexin-V-FITC	GP		bind					PBMCs	Cell	normal			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_107_3_351_s_147	11160159	( b) Annexin-V-FITC binding of leukemic LGL and normal PBMCs in response to DMSO (0) and AG-490 (25, 50, and 100 muM for 48 hours).	bind
48295	3	897	7	NULL	NULL	0	NULL	statement 1	Process		in response to					DMSO	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_107_3_351_s_147	11160159	( b) Annexin-V-FITC binding of leukemic LGL and normal PBMCs in response to DMSO (0) and AG-490 (25, 50, and 100 muM for 48 hours).	bind
48296	4	897	7	NULL	NULL	0	NULL	statement 1	Process		in response to					AG-490	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_107_3_351_s_147	11160159	( b) Annexin-V-FITC binding of leukemic LGL and normal PBMCs in response to DMSO (0) and AG-490 (25, 50, and 100 muM for 48 hours).	bind
48297	5	897	7	NULL	NULL	0	NULL	statement 2	Process		in response to					DMSO	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_107_3_351_s_147	11160159	( b) Annexin-V-FITC binding of leukemic LGL and normal PBMCs in response to DMSO (0) and AG-490 (25, 50, and 100 muM for 48 hours).	bind
48298	6	897	7	NULL	NULL	0	NULL	statement 2	Process		in response to					AG-490	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_107_3_351_s_147	11160159	( b) Annexin-V-FITC binding of leukemic LGL and normal PBMCs in response to DMSO (0) and AG-490 (25, 50, and 100 muM for 48 hours).	bind
188	1	899	6	10	NULL	0	NULL	p65	NULL		bind	NULL				NF-kappaB	NULL			response element	NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_43_s_223	16000401	( B) Antibodies against p65, p50 and c-Rel supershift the nuclear protein binding to  the NF-kappaB response elements.	bind
189	2	899	6	10	NULL	0	NULL	p50	NULL		bind	NULL				NF-kappaB	NULL			response element	NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_43_s_223	16000401	( B) Antibodies against p65, p50 and c-Rel supershift the nuclear protein binding to  the NF-kappaB response elements.	bind
190	3	899	6	10	NULL	0	NULL	c-Rel	NULL		bind	NULL				NF-kappaB	NULL			response element	NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_43_s_223	16000401	( B) Antibodies against p65, p50 and c-Rel supershift the nuclear protein binding to  the NF-kappaB response elements.	bind
51429	4	899	6	10	NULL	0	NULL	p65	NULL		is a type of	NULL				nuclear protein	NULL				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_1_43_s_223	16000401	( B) Antibodies against p65, p50 and c-Rel supershift the nuclear protein binding to  the NF-kappaB response elements.	bind
51430	5	899	6	10	NULL	0	NULL	p50	NULL		is a type of	NULL				nuclear protein	NULL				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_1_43_s_223	16000401	( B) Antibodies against p65, p50 and c-Rel supershift the nuclear protein binding to  the NF-kappaB response elements.	bind
51431	6	899	6	10	NULL	0	NULL	c-Rel	NULL		is a type of	NULL				nuclear protein	NULL				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_1_43_s_223	16000401	( B) Antibodies against p65, p50 and c-Rel supershift the nuclear protein binding to  the NF-kappaB response elements.	bind
48299	1	899	7	NULL	NULL	0	NULL	 p65	GP		bind					NF-kappaB	GP			response element	NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_43_s_223	16000401	( B) Antibodies against p65, p50 and c-Rel supershift the nuclear protein binding to  the NF-kappaB response elements.	bind
48300	2	899	7	NULL	NULL	0	NULL	p50	GP		bind					NF-kappaB	GP			response element	NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_43_s_223	16000401	( B) Antibodies against p65, p50 and c-Rel supershift the nuclear protein binding to  the NF-kappaB response elements.	bind
48301	3	899	7	NULL	NULL	0	NULL	c-Rel	GP		bind					NF-kappaB	GP			response element	NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_43_s_223	16000401	( B) Antibodies against p65, p50 and c-Rel supershift the nuclear protein binding to  the NF-kappaB response elements.	bind
48302	4	899	7	NULL	NULL	0	NULL	p65	GP		is a type of					nuclear protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_43_s_223	16000401	( B) Antibodies against p65, p50 and c-Rel supershift the nuclear protein binding to  the NF-kappaB response elements.	bind
48303	5	899	7	NULL	NULL	0	NULL	p50	GP		is a type of					nuclear protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_43_s_223	16000401	( B) Antibodies against p65, p50 and c-Rel supershift the nuclear protein binding to  the NF-kappaB response elements.	bind
48304	6	899	7	NULL	NULL	0	NULL	c-Rel	GP		is a type of					nuclear protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_43_s_223	16000401	( B) Antibodies against p65, p50 and c-Rel supershift the nuclear protein binding to  the NF-kappaB response elements.	bind
191	1	900	6	10	NULL	0	NULL	SIVmac239 gp120	NULL	125I-labeled	binds to	NULL				CCR5	NULL	rhesus			NULL		NULL	NULL	NULL	NULL	gw60_science_278_5342_1470_s_69	9367961	( B) Antibody inhibition of 125I-labeled SIVmac239 gp120 binding to rhesus CCR5 in the presence (solid bars) or absence (open bars) of 100 nM sCD4.	bind
48305	1	900	7	NULL	NULL	0	NULL	SIVmac239 gp120	GP	125I-labeled 	bind					CCR5	GP	rhesus			NULL		NULL	NULL	NULL	NULL	gw60_science_278_5342_1470_s_69	9367961	( B) Antibody inhibition of 125I-labeled SIVmac239 gp120 binding to rhesus CCR5 in the presence (solid bars) or absence (open bars) of 100 nM sCD4.	bind
193	1	903	6	10	NULL	0	NULL	regulatory proteins	NULL		bind	NULL		ChrD		Lys-9	NULL	methylated			NULL		NULL	NULL	NULL	NULL	gw60_science_292_5514_64_s_46	11294220	( B) As a result of these modifications, the chromodomain (ChrD) of regulatory proteins binds to methylated Lys-9 during gene silencing, and the bromodomain (BrD) of regulatory proteins binds to acetylated Lys-14 during gene activation.	bind
194	2	903	6	NULL	NULL	0	NULL	Statement 1	NULL		occurs during	NULL				gene silencing	NULL				NULL		0	NULL	NULL	NULL	gw60_science_292_5514_64_s_46	11294220	( B) As a result of these modifications, the chromodomain (ChrD) of regulatory proteins binds to methylated Lys-9 during gene silencing, and the bromodomain (BrD) of regulatory proteins binds to acetylated Lys-14 during gene activation.	bind
195	3	903	6	10	NULL	0	NULL	regulatory proteins	NULL		bind	NULL		BrD		Lys-14	NULL	acetylated			NULL		NULL	NULL	NULL	NULL	gw60_science_292_5514_64_s_46	11294220	( B) As a result of these modifications, the chromodomain (ChrD) of regulatory proteins binds to methylated Lys-9 during gene silencing, and the bromodomain (BrD) of regulatory proteins binds to acetylated Lys-14 during gene activation.	bind
196	4	903	6	NULL	NULL	0	NULL	Statement 3	NULL		occurs during	NULL				gene activation	NULL				NULL		0	NULL	NULL	NULL	gw60_science_292_5514_64_s_46	11294220	( B) As a result of these modifications, the chromodomain (ChrD) of regulatory proteins binds to methylated Lys-9 during gene silencing, and the bromodomain (BrD) of regulatory proteins binds to acetylated Lys-14 during gene activation.	bind
51432	5	903	6	10	NULL	0	NULL	ChrD	NULL		is	NULL				chromodomain	NULL				NULL		0	NULL	NULL	NULL	gw60_science_292_5514_64_s_46	11294220	( B) As a result of these modifications, the chromodomain (ChrD) of regulatory proteins binds to methylated Lys-9 during gene silencing, and the bromodomain (BrD) of regulatory proteins binds to acetylated Lys-14 during gene activation.	bind
51433	6	903	6	10	NULL	0	NULL	BrD	NULL		is	NULL				bromodomain	NULL				NULL		0	NULL	NULL	NULL	gw60_science_292_5514_64_s_46	11294220	( B) As a result of these modifications, the chromodomain (ChrD) of regulatory proteins binds to methylated Lys-9 during gene silencing, and the bromodomain (BrD) of regulatory proteins binds to acetylated Lys-14 during gene activation.	bind
48306	1	903	7	NULL	NULL	0	NULL	regulatory protein	GP		bind			ChrD				methylated	Lys-9		NULL		NULL	NULL	NULL	NULL	gw60_science_292_5514_64_s_46	11294220	( B) As a result of these modifications, the chromodomain (ChrD) of regulatory proteins binds to methylated Lys-9 during gene silencing, and the bromodomain (BrD) of regulatory proteins binds to acetylated Lys-14 during gene activation.	bind
48307	2	903	7	NULL	NULL	0	NULL	statement 1	Process		occurs during					gene silencing	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_292_5514_64_s_46	11294220	( B) As a result of these modifications, the chromodomain (ChrD) of regulatory proteins binds to methylated Lys-9 during gene silencing, and the bromodomain (BrD) of regulatory proteins binds to acetylated Lys-14 during gene activation.	bind
48308	3	903	7	NULL	NULL	0	NULL	regulatory protein	GP		bind			BrD				acetylated	Lys-14		NULL		NULL	NULL	NULL	NULL	gw60_science_292_5514_64_s_46	11294220	( B) As a result of these modifications, the chromodomain (ChrD) of regulatory proteins binds to methylated Lys-9 during gene silencing, and the bromodomain (BrD) of regulatory proteins binds to acetylated Lys-14 during gene activation.	bind
48309	4	903	7	NULL	NULL	0	NULL	statement 3	Process		occurs during					gene activation	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_292_5514_64_s_46	11294220	( B) As a result of these modifications, the chromodomain (ChrD) of regulatory proteins binds to methylated Lys-9 during gene silencing, and the bromodomain (BrD) of regulatory proteins binds to acetylated Lys-14 during gene activation.	bind
48310	5	903	7	NULL	NULL	0	NULL				is			ChrD		chromodomain	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_292_5514_64_s_46	11294220	( B) As a result of these modifications, the chromodomain (ChrD) of regulatory proteins binds to methylated Lys-9 during gene silencing, and the bromodomain (BrD) of regulatory proteins binds to acetylated Lys-14 during gene activation.	bind
48311	6	903	7	NULL	NULL	0	NULL				is			BrD		Bromodomain	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_292_5514_64_s_46	11294220	( B) As a result of these modifications, the chromodomain (ChrD) of regulatory proteins binds to methylated Lys-9 during gene silencing, and the bromodomain (BrD) of regulatory proteins binds to acetylated Lys-14 during gene activation.	bind
197	1	904	6	NULL	NULL	0	NULL	calpain	NULL		cleave	NULL				BM-V	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_29_17561_s_191	8663447	( b) Assessment of the actin binding properties of the calpain cleavage products of BM-V indicates that the 80-kDa tail fragment does not bind F-actin.	bind
198	2	904	6	10	NULL	0	NULL	BM-V	NULL		does not bind	NULL		80-kDa tail fragment		F-actin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_29_17561_s_191	8663447	( b) Assessment of the actin binding properties of the calpain cleavage products of BM-V indicates that the 80-kDa tail fragment does not bind F-actin.	bind
48312	1	904	7	NULL	NULL	0	NULL	BM-V	GP		does not bind			80-kDa tail fragment		F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_29_17561_s_191	8663447	( b) Assessment of the actin binding properties of the calpain cleavage products of BM-V indicates that the 80-kDa tail fragment does not bind F-actin.	bind
48313	2	904	7	NULL	NULL	0	NULL	calpain	GP		cleaves					BM-V	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_29_17561_s_191	8663447	( b) Assessment of the actin binding properties of the calpain cleavage products of BM-V indicates that the 80-kDa tail fragment does not bind F-actin.	bind
199	1	905	6	NULL	NULL	0	NULL	U1C	NULL		bind	NULL				ps5	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_181	15465910	( B) At higher temperatures (indicated by kt), there is a conformational change (indicated  by a double arrow in  A) that includes U1C binding to the ps5''.	bind
48314	1	905	7	NULL	NULL	0	NULL	U1C	GP		bind					ps5''	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_181	15465910	( B) At higher temperatures (indicated by kt), there is a conformational change (indicated  by a double arrow in  A) that includes U1C binding to the ps5''.	bind
200	1	906	6	10	NULL	0	NULL	p53c	NULL		bind	NULL				HIF-1alpha peptide	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_16_10305_s_31	12124396	( b) Average of three immunoblot experiments of p53c bound to HIF-1alpha peptide array.	bind
48315	1	906	7	NULL	NULL	0	NULL	p53c	GP		bind					 HIF-1alpha peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_16_10305_s_31	12124396	( b) Average of three immunoblot experiments of p53c bound to HIF-1alpha peptide array.	bind
201	1	907	6	NULL	NULL	0	NULL	QK	NULL		bind	NULL				Flt-1D2	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_40_14215_s_122	16186493	( b) Backbone superposition of the QK representative structure (yellow) and VEGF helix  (red) bound to Flt-1D2.	bind
202	2	907	6	NULL	NULL	0	NULL	VEGF helix	NULL		bind	NULL				Flt-1D2	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_40_14215_s_122	16186493	( b) Backbone superposition of the QK representative structure (yellow) and VEGF helix  (red) bound to Flt-1D2.	bind
48316	1	907	7	NULL	NULL	0	NULL	VEGF helix	GP		bind					Flt-1D2	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_40_14215_s_122	16186493	( b) Backbone superposition of the QK representative structure (yellow) and VEGF helix  (red) bound to Flt-1D2.	bind
51434	2	907	7	NULL	NULL	0	NULL	QK	GP		bind					Flt-1D2	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_40_14215_s_122	16186493	( b) Backbone superposition of the QK representative structure (yellow) and VEGF helix  (red) bound to Flt-1D2.	bind
204	1	911	6	10	NULL	0	NULL	BMP-2 variants	NULL		bind	NULL				BMPR-II	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_13_3314_s_121	10880444	( B) Binding affinity of BMP-2 variants for type II receptors BMPR-II or ActR-II.	bind
205	2	911	6	10	NULL	0	NULL	BMP-2 variants	NULL		bind	NULL				ActR-II	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_13_3314_s_121	10880444	( B) Binding affinity of BMP-2 variants for type II receptors BMPR-II or ActR-II.	bind
51435	3	911	6	10	NULL	0	NULL	BMPR-II	NULL		is a type of	NULL				type II receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_19_13_3314_s_121	10880444	( B) Binding affinity of BMP-2 variants for type II receptors BMPR-II or ActR-II.	bind
51436	4	911	6	10	NULL	0	NULL	ActR-II	NULL		is a type of	NULL				type II receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_19_13_3314_s_121	10880444	( B) Binding affinity of BMP-2 variants for type II receptors BMPR-II or ActR-II.	bind
48317	1	911	7	NULL	NULL	0	NULL	BMP-2 variants	GP		bind					BMPR-II	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_13_3314_s_121	10880444	( B) Binding affinity of BMP-2 variants for type II receptors BMPR-II or ActR-II.	bind
48318	2	911	7	NULL	NULL	0	NULL	BMP-2 variants	GP		bind					ActR-II	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_13_3314_s_121	10880444	( B) Binding affinity of BMP-2 variants for type II receptors BMPR-II or ActR-II.	bind
48319	3	911	7	NULL	NULL	0	NULL	BMPR-II	GP		is a type of					type II receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_13_3314_s_121	10880444	( B) Binding affinity of BMP-2 variants for type II receptors BMPR-II or ActR-II.	bind
48320	4	911	7	NULL	NULL	0	NULL	ActR-II	GP		is a type of					type II receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_13_3314_s_121	10880444	( B) Binding affinity of BMP-2 variants for type II receptors BMPR-II or ActR-II.	bind
206	1	912	6	NULL	NULL	0	NULL	Cry11Aa	NULL		bind	NULL				Cyt1Aa	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_51_18303_s_112	16339907	( B) Binding analysis of Cry11Aa or Cry1Ab to Cyt1Aa by ELISA.	bind
207	2	912	6	NULL	NULL	0	NULL	Cry1Ab	NULL		bind	NULL				Cyt1Aa	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_51_18303_s_112	16339907	( B) Binding analysis of Cry11Aa or Cry1Ab to Cyt1Aa by ELISA.	bind
51437	3	912	6	10	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_51_18303_s_112	16339907	( B) Binding analysis of Cry11Aa or Cry1Ab to Cyt1Aa by ELISA.	bind
48321	1	912	7	NULL	NULL	0	NULL	Cry11Aa	GP		bind					Cyt1Aa	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_51_18303_s_112	16339907	( B) Binding analysis of Cry11Aa or Cry1Ab to Cyt1Aa by ELISA.	bind
48322	2	912	7	NULL	NULL	0	NULL	Cry1Ab	GP		bind					Cyt1Aa	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_51_18303_s_112	16339907	( B) Binding analysis of Cry11Aa or Cry1Ab to Cyt1Aa by ELISA.	bind
48323	3	912	7	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_51_18303_s_112	16339907	( B) Binding analysis of Cry11Aa or Cry1Ab to Cyt1Aa by ELISA.	bind
213	1	913	6	10	NULL	0	NULL	Chk1	NULL		bind	NULL				Pds1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5442_1166_s_90	10550056	( B) Binding and phosphorylation of Pds1 by Chk1.	bind
214	2	913	6	10	NULL	0	NULL	statement 1	NULL		phosphorylates	NULL				Pds1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5442_1166_s_90	10550056	( B) Binding and phosphorylation of Pds1 by Chk1.	bind
48324	1	913	7	NULL	NULL	0	NULL	Chk1	GP		bind					Pds1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5442_1166_s_90	10550056	( B) Binding and phosphorylation of Pds1 by Chk1.	bind
48325	2	913	7	NULL	NULL	0	NULL	statement 1	Process		phosphorylate					Pds1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5442_1166_s_90	10550056	( B) Binding and phosphorylation of Pds1 by Chk1.	bind
215	1	914	6	10	NULL	0	NULL	S1	NULL	His6-tagged	bind	NULL				PK1L SsrA variant	NULL	32P-labeled			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_6_3040_s_132	11248028	( B) Binding curve generated from data in  A. ( C) Binding of His6-tagged ribosomal protein S1 to 100 pM 32P-labeled PK1L and PK3L SsrA variants.	bind
216	2	914	6	10	NULL	0	NULL	S1	NULL	His6-tagged	bind	NULL				PK3L SsrA variant	NULL	32P-labeled			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_6_3040_s_132	11248028	( B) Binding curve generated from data in  A. ( C) Binding of His6-tagged ribosomal protein S1 to 100 pM 32P-labeled PK1L and PK3L SsrA variants.	bind
51438	3	914	6	10	NULL	0	NULL	S1	NULL		is a type of	NULL				ribosomal protein	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_98_6_3040_s_132	11248028	( B) Binding curve generated from data in  A. ( C) Binding of His6-tagged ribosomal protein S1 to 100 pM 32P-labeled PK1L and PK3L SsrA variants.	bind
48326	1	914	7	NULL	NULL	0	NULL	S1 	GP	His6-tagged	bind					PK1L SsrA variant	GP	32P-labeled			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_6_3040_s_132	11248028	( B) Binding curve generated from data in  A. ( C) Binding of His6-tagged ribosomal protein S1 to 100 pM 32P-labeled PK1L and PK3L SsrA variants.	bind
48327	2	914	7	NULL	NULL	0	NULL	S1	GP	His6-tagged 	bind					PK3L SsrA variant	GP	32P-labeled			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_6_3040_s_132	11248028	( B) Binding curve generated from data in  A. ( C) Binding of His6-tagged ribosomal protein S1 to 100 pM 32P-labeled PK1L and PK3L SsrA variants.	bind
48328	3	914	7	NULL	NULL	0	NULL	S1	GP		is a type of					ribosomal protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_6_3040_s_132	11248028	( B) Binding curve generated from data in  A. ( C) Binding of His6-tagged ribosomal protein S1 to 100 pM 32P-labeled PK1L and PK3L SsrA variants.	bind
218	1	915	6	10	NULL	0	NULL	SPP	NULL		bind	NULL				HEK293 EDG-1 cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5356_1552_s_93	9488656	( B) Binding isotherm of [32]SPP to HEK293 EDG-1 cells.	bind
48329	1	915	7	NULL	NULL	0	NULL	SPP	GP		bind					HEK293 EDG-1 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5356_1552_s_93	9488656	( B) Binding isotherm of [32]SPP to HEK293 EDG-1 cells.	bind
219	1	916	6	10	NULL	0	NULL	Ets proteins	NULL	C.elegans	bind	NULL				EBS probe	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_20_4154_s_263	11600704	( B) Binding of  C.elegans Ets proteins to the EBS probe.	bind
48330	1	916	7	NULL	NULL	0	NULL	Ets protein	GP	C.elegans	bind					EBS probe	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_20_4154_s_263	11600704	( B) Binding of  C.elegans Ets proteins to the EBS probe.	bind
220	1	917	6	NULL	NULL	0	NULL	A1	NULL		bind	NULL				CE4	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_18_7_1939_s_184	10202157	( B) Binding of A1 to CE4 or CE4m.	bind
221	2	917	6	NULL	NULL	0	NULL	A1	NULL		bind	NULL				CE4m	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_18_7_1939_s_184	10202157	( B) Binding of A1 to CE4 or CE4m.	bind
48331	1	917	7	NULL	NULL	0	NULL	 A1	GP		bind					CE4	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_7_1939_s_184	10202157	( B) Binding of A1 to CE4 or CE4m.	bind
48332	2	917	7	NULL	NULL	0	NULL	A1	GP		bind					CE4m	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_7_1939_s_184	10202157	( B) Binding of A1 to CE4 or CE4m.	bind
223	1	918	6	10	NULL	0	NULL	APE1	NULL		bind	NULL				AP-dsDNA	NULL				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_5_1552_s_208	16540594	( B) Binding of APE1 and its mutant proteins to the dsDNA containing an AP site (AP-dsDNA).	bind
225	2	918	6	10	NULL	0	NULL	APE1	NULL	mutant	bind	NULL				AP-dsDNA	NULL				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_5_1552_s_208	16540594	( B) Binding of APE1 and its mutant proteins to the dsDNA containing an AP site (AP-dsDNA).	bind
51439	3	918	6	10	NULL	0	NULL	AP-dsDNA	NULL		is	NULL				dsDNA containing an AP site	NULL				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_34_5_1552_s_208	16540594	( B) Binding of APE1 and its mutant proteins to the dsDNA containing an AP site (AP-dsDNA).	bind
48333	1	918	7	NULL	NULL	0	NULL	APE1 	GP		bind					AP-dsDNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_5_1552_s_208	16540594	( B) Binding of APE1 and its mutant proteins to the dsDNA containing an AP site (AP-dsDNA).	bind
48334	2	918	7	NULL	NULL	0	NULL	APE1 	GP	mutant	bind					AP-dsDNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_5_1552_s_208	16540594	( B) Binding of APE1 and its mutant proteins to the dsDNA containing an AP site (AP-dsDNA).	bind
48335	3	918	7	NULL	NULL	0	NULL	AP-dsDNA	NucleicAcid		is					dsDNA	NucleicAcid			AP site containing	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_5_1552_s_208	16540594	( B) Binding of APE1 and its mutant proteins to the dsDNA containing an AP site (AP-dsDNA).	bind
228	1	919	6	NULL	NULL	0	NULL	Bcl-w	NULL		bind	NULL				BimLdeltaC27	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_22_7_1497_s_135	12660157	( B) Binding of Bcl-w to BimLdeltaC27 fits a 1:1 model.	bind
48336	1	919	7	NULL	NULL	0	NULL	Bcl-w	GP		bind					BimLdeltaC27	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_22_7_1497_s_135	12660157	( B) Binding of Bcl-w to BimLdeltaC27 fits a 1:1 model.	bind
229	1	920	6	10	NULL	0	NULL	c-Rel	NULL		bind	NULL				Il12b	NULL	endogenous		Promoter	NULL	bone marrow-derived macrophages stimulated with LPS + IFN-gamma	NULL	NULL	NULL	NULL	gw70_genesdev_19_18_2138_s_223	16166378	( B) Binding of c-Rel and p65 to the endogenous  Il12b promoter in bone marrow-derived macrophages stimulated with LPS + IFN-gamma was monitored by ChIP.	bind
233	2	920	6	10	NULL	0	NULL	p65	NULL		bind	NULL				Il12b	NULL	endogenous		Promoter	NULL	bone marrow-derived macrophages stimulated with LPS + IFN-gamma	NULL	NULL	NULL	NULL	gw70_genesdev_19_18_2138_s_223	16166378	( B) Binding of c-Rel and p65 to the endogenous  Il12b promoter in bone marrow-derived macrophages stimulated with LPS + IFN-gamma was monitored by ChIP.	bind
48340	1	920	7	NULL	NULL	0	NULL	 c-Rel	GP		bind					Il12b	GP	endogenous		promoter	NULL	bone marrow-derived macrophages stimulated with LPS + IFN-gamma	NULL	NULL	NULL	NULL	gw70_genesdev_19_18_2138_s_223	16166378	( B) Binding of c-Rel and p65 to the endogenous  Il12b promoter in bone marrow-derived macrophages stimulated with LPS + IFN-gamma was monitored by ChIP.	bind
48341	2	920	7	NULL	NULL	0	NULL	p65	GP		bind					Il12b	GP	endogenous		promoter	NULL	bone marrow-derived macrophages stimulated with LPS + IFN-gamma	NULL	NULL	NULL	NULL	gw70_genesdev_19_18_2138_s_223	16166378	( B) Binding of c-Rel and p65 to the endogenous  Il12b promoter in bone marrow-derived macrophages stimulated with LPS + IFN-gamma was monitored by ChIP.	bind
234	1	921	6	10	NULL	0	NULL	CBP	NULL		bind	NULL				SRC1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_1_232_s_180	9427757	( B) Binding of CBP to GST fusions of SRC1.	bind
51440	2	921	6	10	NULL	0	NULL	SRC1	NULL		is a type of	NULL				GST fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_17_1_232_s_180	9427757	( B) Binding of CBP to GST fusions of SRC1.	bind
48342	1	921	7	NULL	NULL	0	NULL	CBP	GP		bind					SRC1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_1_232_s_180	9427757	( B) Binding of CBP to GST fusions of SRC1.	bind
48343	2	921	7	NULL	NULL	0	NULL	SRC1	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_1_232_s_180	9427757	( B) Binding of CBP to GST fusions of SRC1.	bind
235	1	922	6	NULL	NULL	0	NULL	cdc45p	NULL		bind	NULL				Mcm2p	NULL				NULL	chromatin	0	NULL	NULL	NULL	gw60_science_280_5363_593_s_99	9554851	( B) Binding of Cdc45p to Mcm2p on chromatin.	bind
48344	1	922	7	NULL	NULL	0	NULL	Cdc45p	GP		bind					Mcm2p	GP				NULL	chromatin	NULL	NULL	NULL	NULL	gw60_science_280_5363_593_s_99	9554851	( B) Binding of Cdc45p to Mcm2p on chromatin.	bind
236	1	923	6	10	NULL	0	NULL	Cdc6	NULL		bind	NULL				ORC	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3293_s_78	11432816	( B) Binding of Cdc6 and RLF-B/Cdt1 onto ORC.	bind
51441	2	923	6	10	NULL	0	NULL	RLF-B/Cdt1	NULL		bind	NULL				ORC	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_13_3293_s_78	11432816	( B) Binding of Cdc6 and RLF-B/Cdt1 onto ORC.	bind
48345	1	923	7	NULL	NULL	0	NULL	Cdc6 	GP		bind					ORC	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3293_s_78	11432816	( B) Binding of Cdc6 and RLF-B/Cdt1 onto ORC.	bind
48346	2	923	7	NULL	NULL	0	NULL	RLF-B/Cdt1 	GP		bind					ORC	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3293_s_78	11432816	( B) Binding of Cdc6 and RLF-B/Cdt1 onto ORC.	bind
237	1	924	6	NULL	NULL	0	NULL	cFos	NULL		bind	NULL				collagenase-1 gene	NULL			colA element	NULL		0	NULL	NULL	NULL	gw60_embo_20_21_6071_s_82	11689447	( B) Binding of cFos to the colA element of the collagenase-1 gene.	bind
48347	1	924	7	NULL	NULL	0	NULL	cFos	GP		bind					collagenase-1 gene	GP			colA element	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_6071_s_82	11689447	( B) Binding of cFos to the colA element of the collagenase-1 gene.	bind
238	1	925	6	10	NULL	0	NULL	IgA	NULL	control	bind	NULL				R2 cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_105_12_1731_s_172	10862788	( b) Binding of control IgA and T15 to R2 cells.	bind
239	2	925	6	NULL	NULL	0	NULL	T15	NULL		bind	NULL				R2 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_105_12_1731_s_172	10862788	( b) Binding of control IgA and T15 to R2 cells.	bind
48348	1	925	7	NULL	NULL	0	NULL	IgA 	GP	control	bind					R2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_105_12_1731_s_172	10862788	( b) Binding of control IgA and T15 to R2 cells.	bind
48349	2	925	7	NULL	NULL	0	NULL	T15	GP		bind					R2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_105_12_1731_s_172	10862788	( b) Binding of control IgA and T15 to R2 cells.	bind
240	1	927	6	NULL	NULL	0	NULL	CYP2E1 	NULL		bind	NULL				FANCG	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_23_1_67_s_110	11756225	( B) Binding of CYP2E1 to FANCG.	bind
48350	1	927	7	NULL	NULL	0	NULL	CYP2E1	GP		bind					FANCG	GP				NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_23_1_67_s_110	11756225	( B) Binding of CYP2E1 to FANCG.	bind
241	1	928	6	NULL	NULL	0	NULL	Dsg1	NULL		bind	NULL				ETA Cmu	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_110_1_53_s_177	12093888	( b) Binding of Dsg1 with ETA Cmu and ETA Amu.	bind
242	2	928	6	NULL	NULL	0	NULL	Dsg1	NULL		bind	NULL				ETA Amu	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_110_1_53_s_177	12093888	( b) Binding of Dsg1 with ETA Cmu and ETA Amu.	bind
48351	1	928	7	NULL	NULL	0	NULL	Dsg1	GP		bind					ETA Cmu 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_110_1_53_s_177	12093888	( b) Binding of Dsg1 with ETA Cmu and ETA Amu.	bind
48352	2	928	7	NULL	NULL	0	NULL	Dsg1	GP		bind					ETA Amu	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_110_1_53_s_177	12093888	( b) Binding of Dsg1 with ETA Cmu and ETA Amu.	bind
243	1	929	6	NULL	NULL	0	NULL	E12	NULL		bind	NULL				p300	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_6_820_s_82	9512516	( B) Binding of E12 to p300.	bind
48353	1	929	7	NULL	NULL	0	NULL	E12 	GP		bind					p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_6_820_s_82	9512516	( B) Binding of E12 to p300.	bind
244	1	930	6	10	NULL	0	NULL	PKCI-r RNA fragment	NULL		bind	NULL				ASF/SF2	NULL	purified;;baculovirus-expressed			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_5_594_s_225	11877379	( B) Binding of each of the five  PKCI-r RNA fragments to ASF/SF2 was then assessed using increasing amounts (0, 17, 50, and 150 ng) of purified baculovirus-expressed ASF/SF2 in gel shift assays.	bind
48354	1	930	7	NULL	NULL	0	NULL	PKCI-r RNA fragments	NucleicAcid		bind					ASF/SF2	GP	purified;;baculovirus-expressed			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_5_594_s_225	11877379	( B) Binding of each of the five  PKCI-r RNA fragments to ASF/SF2 was then assessed using increasing amounts (0, 17, 50, and 150 ng) of purified baculovirus-expressed ASF/SF2 in gel shift assays.	bind
245	1	931	6	10	NULL	0	NULL	Eps15	NULL		bind	NULL				NPF-containing peptides	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_17_2239_s_104	9303539	( B) Binding of Eps15 to GST fusions encompassing NPF-containing peptides.	bind
51442	2	931	6	10	NULL	0	NULL	NPF-containing peptides	NULL		is a type of	NULL				GST fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_11_17_2239_s_104	9303539	( B) Binding of Eps15 to GST fusions encompassing NPF-containing peptides.	bind
48355	1	931	7	NULL	NULL	0	NULL	 Eps15 	GP		bind					NPF-containing peptides	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_17_2239_s_104	9303539	( B) Binding of Eps15 to GST fusions encompassing NPF-containing peptides.	bind
48356	2	931	7	NULL	NULL	0	NULL	NPF-containing peptides	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_17_2239_s_104	9303539	( B) Binding of Eps15 to GST fusions encompassing NPF-containing peptides.	bind
246	1	933	6	NULL	NULL	0	NULL	bacteria	NULL	FimH-expressing	bind	NULL				CHO cells	NULL	CD48-expressing			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_14_8110_s_140	10393956	( B) Binding of FimH-expressing bacteria to CD48-expressing CHO cells and control CHO cells.	bind
51444	2	933	6	10	NULL	0	NULL	bacteria	NULL	FimH-expressing	bind	NULL				CHO cells	NULL	control			NULL		0	NULL	NULL	NULL	gw60_pnas_96_14_8110_s_140	10393956	( B) Binding of FimH-expressing bacteria to CD48-expressing CHO cells and control CHO cells.	bind
48357	1	933	7	NULL	NULL	0	NULL	bacteria	Organism		express					FimH	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_14_8110_s_140	10393956	( B) Binding of FimH-expressing bacteria to CD48-expressing CHO cells and control CHO cells.	bind
48358	2	933	7	NULL	NULL	0	NULL	CHO cells	Cell		express					CD48	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_14_8110_s_140	10393956	( B) Binding of FimH-expressing bacteria to CD48-expressing CHO cells and control CHO cells.	bind
48359	3	933	7	NULL	NULL	0	NULL	statement 1	Process		bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_14_8110_s_140	10393956	( B) Binding of FimH-expressing bacteria to CD48-expressing CHO cells and control CHO cells.	bind
51443	4	933	7	NULL	NULL	0	NULL	statement 1	Process		bind					CHO cells	Cell	control			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_14_8110_s_140	10393956	( B) Binding of FimH-expressing bacteria to CD48-expressing CHO cells and control CHO cells.	bind
247	1	934	6	NULL	NULL	0	NULL	gp5/trx	NULL		bind	NULL				gp4	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_14_5096_s_100	15795374	( B) Binding of gp5/trx to gp4 or gp4-Cdelta17.	bind
248	2	934	6	NULL	NULL	0	NULL	gp5/trx	NULL		bind	NULL				gp4-Cdelta17	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_14_5096_s_100	15795374	( B) Binding of gp5/trx to gp4 or gp4-Cdelta17.	bind
51445	3	934	6	10	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_14_5096_s_100	15795374	( B) Binding of gp5/trx to gp4 or gp4-Cdelta17.	bind
48361	1	934	7	NULL	NULL	0	NULL	gp5/trx	GP		bind					gp4	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_14_5096_s_100	15795374	( B) Binding of gp5/trx to gp4 or gp4-Cdelta17.	bind
48362	2	934	7	NULL	NULL	0	NULL	gp5/trx	GP		bind					gp4-Cdelta17	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_14_5096_s_100	15795374	( B) Binding of gp5/trx to gp4 or gp4-Cdelta17.	bind
48363	3	934	7	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_14_5096_s_100	15795374	( B) Binding of gp5/trx to gp4 or gp4-Cdelta17.	bind
249	1	935	6	NULL	NULL	0	NULL	Griseofulvin	NULL		bind	NULL				Tubulin	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_28_9878_s_150	15985553	( B) Binding of griseofulvin to tubulin.	bind
48364	1	935	7	NULL	NULL	0	NULL	 griseofulvin	GP		bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_28_9878_s_150	15985553	( B) Binding of griseofulvin to tubulin.	bind
250	1	936	6	10	NULL	0	NULL	GST	NULL		bind	NULL				homopolynucleotides	NULL	radiolabeled			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_21_6795_s_201	16396833	( B) Binding of GST and GST - MPP6 fusion proteins to radiolabelled homopolynucleotides  was analysed as described above and the bound RNAs were quantified in a scintillation  counter.	bind
251	2	936	6	10	NULL	0	NULL	GST - MPP6	NULL		bind	NULL				homopolynucleotides	NULL	radiolabeled			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_21_6795_s_201	16396833	( B) Binding of GST and GST - MPP6 fusion proteins to radiolabelled homopolynucleotides  was analysed as described above and the bound RNAs were quantified in a scintillation  counter.	bind
51446	3	936	6	10	NULL	0	NULL	GST - MPP6	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_21_6795_s_201	16396833	( B) Binding of GST and GST - MPP6 fusion proteins to radiolabelled homopolynucleotides  was analysed as described above and the bound RNAs were quantified in a scintillation  counter.	bind
48365	1	936	7	NULL	NULL	0	NULL	GST	Chemical		bind					 homopolynucleotides	NucleicAcid	 radiolabelled 			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_21_6795_s_201	16396833	( B) Binding of GST and GST - MPP6 fusion proteins to radiolabelled homopolynucleotides  was analysed as described above and the bound RNAs were quantified in a scintillation  counter.	bind
48366	2	936	7	NULL	NULL	0	NULL	GST - MPP6	GP		bind					homopolynucleotides	NucleicAcid	radiolabelled			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_21_6795_s_201	16396833	( B) Binding of GST and GST - MPP6 fusion proteins to radiolabelled homopolynucleotides  was analysed as described above and the bound RNAs were quantified in a scintillation  counter.	bind
48367	3	936	7	NULL	NULL	0	NULL	GST - MPP6	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_21_6795_s_201	16396833	( B) Binding of GST and GST - MPP6 fusion proteins to radiolabelled homopolynucleotides  was analysed as described above and the bound RNAs were quantified in a scintillation  counter.	bind
252	1	937	6	NULL	NULL	0	NULL	GST-Dsk2p	NULL		bind	NULL				Ub	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_2_745_s_102	11805328	( B) Binding of GST-Dsk2p to Ub.	bind
48368	1	937	7	NULL	NULL	0	NULL	GST-Dsk2p 	GP		bind					Ub	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_745_s_102	11805328	( B) Binding of GST-Dsk2p to Ub.	bind
253	1	938	6	NULL	NULL	0	NULL	GST-Rup1	NULL		 bind	NULL				Rsp5 proteins	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_13_2414_s_122	15933713	( B) Binding of GST-Rup1 to Rsp5 proteins.	bind
48369	1	938	7	NULL	NULL	0	NULL	GST-Rup1	GP		bind					Rsp5 protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_13_2414_s_122	15933713	( B) Binding of GST-Rup1 to Rsp5 proteins.	bind
254	1	939	6	NULL	NULL	0	NULL	GST-Rup1	NULL		bind	NULL				Ubp2 proteins	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_13_2414_s_133	15933713	( B) Binding of GST-Rup1 to Ubp2 proteins.	bind
48370	1	939	7	NULL	NULL	0	NULL	GST-Rup1	GP		bind					Ubp2 protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_13_2414_s_133	15933713	( B) Binding of GST-Rup1 to Ubp2 proteins.	bind
255	1	940	6	10	NULL	0	NULL	Hop1	NULL		bind	NULL				48 bp duplex DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_8_2378_s_77	15115800	( B) Binding of Hop1 to 48 bp duplex DNA containing a mismatched G/G region.	bind
51447	2	940	6	10	NULL	0	NULL	48 bp duplex DNA	NULL		contains	NULL					NULL			mismatched G/G region	NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_8_2378_s_77	15115800	( B) Binding of Hop1 to 48 bp duplex DNA containing a mismatched G/G region.	bind
48371	1	940	7	NULL	NULL	0	NULL	Hop1	GP		bind					duplex DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_8_2378_s_77	15115800	( B) Binding of Hop1 to 48 bp duplex DNA containing a mismatched G/G region.	bind
51448	2	940	7	NULL	NULL	0	NULL	48 bp duplex DNA	NucleicAcid		contains									mismatched G/G region	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_8_2378_s_77	15115800	( B) Binding of Hop1 to 48 bp duplex DNA containing a mismatched G/G region.	bind
256	1	941	6	NULL	NULL	0	NULL	IAPP	NULL		bind	NULL				IAPP-GI	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_7_2046_s_128	16467158	( B) Binding of IAPP to IAPP-GI as assessed by fluorescence spectroscopy:	bind
48372	1	941	7	NULL	NULL	0	NULL	IAPP	GP		bind					IAPP-GI	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_7_2046_s_128	16467158	( B) Binding of IAPP to IAPP-GI as assessed by fluorescence spectroscopy:	bind
257	1	942	6	NULL	NULL	0	NULL	IMP1	NULL		bind	NULL				ARS RNA	NULL				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_226	16356927	( B) Binding of IMP1 to the ARS RNA. [35]methionine labeled 6x His-tagged IMP1, PABP, UNR and beta-galactosidase were expressed in  E. coliand purified by Ni-NTA agarose as described in Materials and Methods.	bind
48373	1	942	7	NULL	NULL	0	NULL	IMP1	GP		bind					ARS RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_226	16356927	( B) Binding of IMP1 to the ARS RNA. [35]methionine labeled 6x His-tagged IMP1, PABP, UNR and beta-galactosidase were expressed in  E. coliand purified by Ni-NTA agarose as described in Materials and Methods.	bind
258	1	943	6	NULL	NULL	0	NULL	JNK	NULL		bind	NULL				NFAT4	NULL		NH2-terminal region		NULL		0	NULL	NULL	NULL	gw60_science_278_5343_1638_s_42	9374467	( B) Binding of JNK to the NH2-terminal region of NFAT4.	bind
48374	1	943	7	NULL	NULL	0	NULL	JNK	GP		bind					NFAT4	GP		NH2-terminal region		NULL		NULL	NULL	NULL	NULL	gw60_science_278_5343_1638_s_42	9374467	( B) Binding of JNK to the NH2-terminal region of NFAT4.	bind
259	1	944	6	NULL	NULL	0	NULL	JNK1	NULL		bind	NULL				GST	NULL				NULL		0	NULL	NULL	NULL	gw60_science_277_5326_693_s_77	9235893	( B) Binding of JNK1 to GST and GST-JIP-1 (residues 127 to 281) was examined in the absence and presence of synthetic peptides (64 mug/ml).	bind
260	2	944	6	10	NULL	0	NULL	JNK1	NULL		bind	NULL				GST-JIP-1	NULL		residues 127 to 281		NULL		NULL	NULL	NULL	NULL	gw60_science_277_5326_693_s_77	9235893	( B) Binding of JNK1 to GST and GST-JIP-1 (residues 127 to 281) was examined in the absence and presence of synthetic peptides (64 mug/ml).	bind
48375	1	944	7	NULL	NULL	0	NULL	 JNK1	GP		bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_277_5326_693_s_77	9235893	( B) Binding of JNK1 to GST and GST-JIP-1 (residues 127 to 281) was examined in the absence and presence of synthetic peptides (64 mug/ml).	bind
48376	2	944	7	NULL	NULL	0	NULL	 JNK1	GP		bind					GST-JIP-1	GP		residues 127 to 281		NULL		NULL	NULL	NULL	NULL	gw60_science_277_5326_693_s_77	9235893	( B) Binding of JNK1 to GST and GST-JIP-1 (residues 127 to 281) was examined in the absence and presence of synthetic peptides (64 mug/ml).	bind
262	1	946	6	NULL	NULL	0	NULL	MafK	NULL		bind	NULL				ho-1 E2	NULL			enhancer	NULL		0	NULL	NULL	NULL	gw70_embo_23_13_2544_s_231	15175654	( B) Binding of MafK or Nrf2 to the  ho-1 E2 enhancer was examined as in	bind
263	2	946	6	NULL	NULL	0	NULL	Nrf2	NULL		bind	NULL				ho-1 E2	NULL			enhancer	NULL		0	NULL	NULL	NULL	gw70_embo_23_13_2544_s_231	15175654	( B) Binding of MafK or Nrf2 to the  ho-1 E2 enhancer was examined as in	bind
48378	1	946	7	NULL	NULL	0	NULL	MafK	GP		bind					ho-1 E2	GP			enhancer	NULL		NULL	NULL	NULL	NULL	gw70_embo_23_13_2544_s_231	15175654	( B) Binding of MafK or Nrf2 to the  ho-1 E2 enhancer was examined as in	bind
48379	2	946	7	NULL	NULL	0	NULL	Nrf2	GP		bind					ho-1 E2 	GP			enhancer	NULL		NULL	NULL	NULL	NULL	gw70_embo_23_13_2544_s_231	15175654	( B) Binding of MafK or Nrf2 to the  ho-1 E2 enhancer was examined as in	bind
264	1	947	6	NULL	NULL	0	NULL	MAp18	NULL		bind	NULL				TIP47	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_40_14947_s_79	17003132	( B) Binding of MAp18 to TIP47 in a cell lysate-binding assay.	bind
48380	1	947	7	NULL	NULL	0	NULL	MAp18	GP		bind					TIP47	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_40_14947_s_79	17003132	( B) Binding of MAp18 to TIP47 in a cell lysate-binding assay.	bind
265	1	948	6	NULL	NULL	0	NULL	mSIN3A	NULL		bind	NULL				CTCF	NULL				NULL	In vitro	0	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1707_s_133	10734189	( B) Binding of mSIN3A deletions to CTCF  in vitro.	bind
48381	1	948	7	NULL	NULL	0	NULL	mSIN3A	GP	deletion	bind					CTCF	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1707_s_133	10734189	( B) Binding of mSIN3A deletions to CTCF  in vitro.	bind
266	1	949	6	NULL	NULL	0	NULL	mtHsp70	NULL		bind	NULL				peptide substrate	NULL				NULL		0	NULL	NULL	NULL	gw60_science_300_5616_139_s_39	12677068	( B) Binding of mtHsp70 to peptide substrate.	bind
48382	1	949	7	NULL	NULL	0	NULL	mtHsp70	GP		bind					peptide substrate	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5616_139_s_39	12677068	( B) Binding of mtHsp70 to peptide substrate.	bind
267	1	950	6	NULL	NULL	0	NULL	MyoD	NULL		bind	NULL				DNA	NULL			E-box	NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_9_2887_s_247	15908587	( B) Binding of MyoD to E-box DNA.	bind
48383	1	950	7	NULL	NULL	0	NULL	MyoD	GP		bind					DNA	NucleicAcid			E-box	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_9_2887_s_247	15908587	( B) Binding of MyoD to E-box DNA.	bind
268	1	951	6	NULL	NULL	0	NULL	myostatin	NULL		bind	NULL				lectin	NULL	lentil			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_16_9306_s_54	11459935	( b) Binding of myostatin to lentil lectin.	bind
48384	1	951	7	NULL	NULL	0	NULL	myostatin	GP		bind					 lectin	GP	lentil			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_16_9306_s_54	11459935	( b) Binding of myostatin to lentil lectin.	bind
269	1	952	6	NULL	NULL	0	NULL	NS1	NULL		bind	NULL				p85beta	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_38_14194_s_129	16963558	( b) Binding of NS1 to p85beta requires Y89 and M93.	bind
270	2	952	6	NULL	NULL	0	NULL	Statement 1	NULL		requires	NULL				Y89	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_38_14194_s_129	16963558	( b) Binding of NS1 to p85beta requires Y89 and M93.	bind
271	3	952	6	NULL	NULL	0	NULL	Statement 1	NULL		requires	NULL				M93	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_38_14194_s_129	16963558	( b) Binding of NS1 to p85beta requires Y89 and M93.	bind
48385	1	952	7	NULL	NULL	0	NULL	NS1	GP		bind					p85beta	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_38_14194_s_129	16963558	( b) Binding of NS1 to p85beta requires Y89 and M93.	bind
48386	2	952	7	NULL	NULL	0	NULL	statement 1	Process		requires					Y89	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_38_14194_s_129	16963558	( b) Binding of NS1 to p85beta requires Y89 and M93.	bind
48387	3	952	7	NULL	NULL	0	NULL	statement 1	Process		requires					M93	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_38_14194_s_129	16963558	( b) Binding of NS1 to p85beta requires Y89 and M93.	bind
331	1	953	6	10	NULL	0	NULL	OGG1 enzymes	NULL		bind	NULL				substrate	NULL		abasic site		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_5_1620_s_169	16549874	( B) Binding of OGG1 enzymes to an abasic site substrate after adding APE1 was measured  by EMSA.	bind
48388	1	953	7	NULL	NULL	0	NULL	OGG1 enzyme	GP		bind					substrate	GP		abasic site 		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_5_1620_s_169	16549874	( B) Binding of OGG1 enzymes to an abasic site substrate after adding APE1 was measured  by EMSA.	bind
332	1	954	6	NULL	NULL	0	NULL	PCNA	NULL	binding of 	require	NULL				ATP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_14_3811_s_166	10899134	( B) Binding of PCNA requires ATP (lanes 2 and 3) and binding of FEN1 requires PCNA (lanes 1 and 4).	bind
333	2	954	6	NULL	NULL	0	NULL	FEN1	NULL	binding of 	require	NULL				PCNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_14_3811_s_166	10899134	( B) Binding of PCNA requires ATP (lanes 2 and 3) and binding of FEN1 requires PCNA (lanes 1 and 4).	bind
48389	1	954	7	NULL	NULL	0	NULL	PCNA	GP	binding of	requires					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_14_3811_s_166	10899134	( B) Binding of PCNA requires ATP (lanes 2 and 3) and binding of FEN1 requires PCNA (lanes 1 and 4).	bind
48390	2	954	7	NULL	NULL	0	NULL	FEN1	GP	binding of	requires					PCNA	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_14_3811_s_166	10899134	( B) Binding of PCNA requires ATP (lanes 2 and 3) and binding of FEN1 requires PCNA (lanes 1 and 4).	bind
334	1	955	6	10	NULL	0	NULL	PI4,5P2	NULL		bind	NULL					NULL		ABD		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_23_6331_s_223	11101506	( B) Binding of PI4,5P2 to the ABD induces a conformational change that switches on titin binding by making the EF3/4 region available for binding to Z-repeats (ZR7).	bind
336	2	955	6	10	NULL	0	NULL	Statement 1	NULL		induce	NULL					NULL	conformation change of 	ABD		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_23_6331_s_223	11101506	( B) Binding of PI4,5P2 to the ABD induces a conformational change that switches on titin binding by making the EF3/4 region available for binding to Z-repeats (ZR7).	bind
340	3	955	6	NULL	NULL	0	NULL	Statement 2	NULL		makes available	NULL				EF3/4 region	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_23_6331_s_223	11101506	( B) Binding of PI4,5P2 to the ABD induces a conformational change that switches on titin binding by making the EF3/4 region available for binding to Z-repeats (ZR7).	bind
609	4	955	6	NULL	NULL	0	NULL		NULL		bind	NULL		EF3/4 region		titin	NULL	Z-repeats			NULL		0	NULL	NULL	NULL	gw60_embo_19_23_6331_s_223	11101506	( B) Binding of PI4,5P2 to the ABD induces a conformational change that switches on titin binding by making the EF3/4 region available for binding to Z-repeats (ZR7).	bind
610	5	955	6	NULL	NULL	0	NULL	Statement 3	NULL		allows	NULL				Statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_19_23_6331_s_223	11101506	( B) Binding of PI4,5P2 to the ABD induces a conformational change that switches on titin binding by making the EF3/4 region available for binding to Z-repeats (ZR7).	bind
611	6	955	6	NULL	NULL	0	NULL	statement 5 	NULL		turns on	NULL				titin	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_embo_19_23_6331_s_223	11101506	( B) Binding of PI4,5P2 to the ABD induces a conformational change that switches on titin binding by making the EF3/4 region available for binding to Z-repeats (ZR7).	bind
612	7	955	6	NULL	NULL	0	NULL	ZR7	NULL		is	NULL				Z repeats	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_19_23_6331_s_223	11101506	( B) Binding of PI4,5P2 to the ABD induces a conformational change that switches on titin binding by making the EF3/4 region available for binding to Z-repeats (ZR7).	bind
48391	1	955	7	NULL	NULL	0	NULL	PI4,5P2	Chemical		bind								ABD		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_23_6331_s_223	11101506	( B) Binding of PI4,5P2 to the ABD induces a conformational change that switches on titin binding by making the EF3/4 region available for binding to Z-repeats (ZR7).	bind
48392	2	955	7	NULL	NULL	0	NULL	titin	GP		bind			EF3/4 region		ZR7	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_23_6331_s_223	11101506	( B) Binding of PI4,5P2 to the ABD induces a conformational change that switches on titin binding by making the EF3/4 region available for binding to Z-repeats (ZR7).	bind
48393	3	955	7	NULL	NULL	0	NULL	statement 1	Process		induce					conformational change	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_23_6331_s_223	11101506	( B) Binding of PI4,5P2 to the ABD induces a conformational change that switches on titin binding by making the EF3/4 region available for binding to Z-repeats (ZR7).	bind
48394	4	955	7	NULL	NULL	0	NULL	statement 3	Process		switches on					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_23_6331_s_223	11101506	( B) Binding of PI4,5P2 to the ABD induces a conformational change that switches on titin binding by making the EF3/4 region available for binding to Z-repeats (ZR7).	bind
48395	5	955	7	NULL	NULL	0	NULL	ZR7	GP		is a type of					Z-repeat	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_23_6331_s_223	11101506	( B) Binding of PI4,5P2 to the ABD induces a conformational change that switches on titin binding by making the EF3/4 region available for binding to Z-repeats (ZR7).	bind
341	1	956	6	10	NULL	0	NULL	EGSs	NULL		bind	NULL				PR mRNA substrate	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_26_14831_s_111	11742095	( B) Binding of PR mRNA substrate by EGSs.	bind
48396	1	956	7	NULL	NULL	0	NULL	EGSs	GP		bind					PR mRNA substrate	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_26_14831_s_111	11742095	( B) Binding of PR mRNA substrate by EGSs.	bind
342	1	957	6	10	NULL	0	NULL	Ras	NULL		bind	NULL		A59G		Raf kinase	NULL		RBD		NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_19_12138_s_133	12213964	( B) Binding of RasA59G to the Ras-binding domain (RBD) of the Raf kinase.	bind
51449	2	957	6	10	NULL	0	NULL	RBD	NULL		is	NULL				Ras-binding domain	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_19_12138_s_133	12213964	( B) Binding of RasA59G to the Ras-binding domain (RBD) of the Raf kinase.	bind
48397	1	957	7	NULL	NULL	0	NULL	Ras	GP		bind			A59G		Raf kinase	GP		RBD		NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_19_12138_s_133	12213964	( B) Binding of RasA59G to the Ras-binding domain (RBD) of the Raf kinase.	bind
48398	2	957	7	NULL	NULL	0	NULL	RBD	GP		is					Ras-binding domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_19_12138_s_133	12213964	( B) Binding of RasA59G to the Ras-binding domain (RBD) of the Raf kinase.	bind
344	1	958	6	NULL	NULL	0	NULL	RPA-A	NULL		bind	NULL				CPD/AA-10 duplex	NULL				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_16_4747_s_128	12907715	( B) Binding of RPA-A to the CPD/AA-10 duplex as a function of DNA concentration in the  absence (upper) and presence (lower) of equimolar XPA-MBD.	bind
48399	1	958	7	NULL	NULL	0	NULL	RPA-A	GP		bind					CPD/AA-10 duplex	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_16_4747_s_128	12907715	( B) Binding of RPA-A to the CPD/AA-10 duplex as a function of DNA concentration in the  absence (upper) and presence (lower) of equimolar XPA-MBD.	bind
346	1	959	6	NULL	NULL	0	NULL	RPA-A 	NULL		bind	NULL				CPD/AA-10 duplex	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_16_4747_s_128	12907715	( B) Binding of RPA-A to the CPD/AA-10 duplex as a function of DNA concentration in the absence (upper) and presence (lower) of equimolar XPA-MBD.	bind
348	1	960	6	NULL	NULL	0	NULL	Salp	NULL		bind	NULL				p85	NULL		SH3 domain		NULL		0	NULL	NULL	NULL	gw60_gene_240_1_133_s_253	10564820	( B) Binding of Salp  to the p85 SH3 domain.	bind
48400	1	960	7	NULL	NULL	0	NULL	 Salp	GP		bind					p85	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_gene_240_1_133_s_253	10564820	( B) Binding of Salp  to the p85 SH3 domain.	bind
349	1	961	6	NULL	NULL	0	NULL	Sec17p	NULL		bind	NULL				vacuole	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_140_1_61_s_216	9425154	( B) Binding of Sec17p and Sec18p to the vacuole is independent of the Nyv1p and Vam3p.	bind
351	2	961	6	NULL	NULL	0	NULL	Sec18p	NULL		bind	NULL				vacuole	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_140_1_61_s_216	9425154	( B) Binding of Sec17p and Sec18p to the vacuole is independent of the Nyv1p and Vam3p.	bind
352	3	961	6	NULL	NULL	0	NULL	Statement 1	NULL		is independent of	NULL				Nyv1p	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_140_1_61_s_216	9425154	( B) Binding of Sec17p and Sec18p to the vacuole is independent of the Nyv1p and Vam3p.	bind
353	4	961	6	NULL	NULL	0	NULL	statement 2	NULL		is independent of	NULL				Nyv1p	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_140_1_61_s_216	9425154	( B) Binding of Sec17p and Sec18p to the vacuole is independent of the Nyv1p and Vam3p.	bind
354	5	961	6	NULL	NULL	0	NULL	Statement 1	NULL		is independent of	NULL				Vam3p	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_140_1_61_s_216	9425154	( B) Binding of Sec17p and Sec18p to the vacuole is independent of the Nyv1p and Vam3p.	bind
355	6	961	6	NULL	NULL	0	NULL	statement 2	NULL		is independent of	NULL				Vam3p	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_140_1_61_s_216	9425154	( B) Binding of Sec17p and Sec18p to the vacuole is independent of the Nyv1p and Vam3p.	bind
48401	1	961	7	NULL	NULL	0	NULL	Sec17p	GP		bind 					vacuole	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_140_1_61_s_216	9425154	( B) Binding of Sec17p and Sec18p to the vacuole is independent of the Nyv1p and Vam3p.	bind
48402	2	961	7	NULL	NULL	0	NULL	Sec18p	GP		bind					vacuole	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_140_1_61_s_216	9425154	( B) Binding of Sec17p and Sec18p to the vacuole is independent of the Nyv1p and Vam3p.	bind
48403	3	961	7	NULL	NULL	0	NULL	statement 1	Process		is independent of					Nyv1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_140_1_61_s_216	9425154	( B) Binding of Sec17p and Sec18p to the vacuole is independent of the Nyv1p and Vam3p.	bind
48404	4	961	7	NULL	NULL	0	NULL	statement 1	Process		is independent of					 Vam3p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_140_1_61_s_216	9425154	( B) Binding of Sec17p and Sec18p to the vacuole is independent of the Nyv1p and Vam3p.	bind
48405	5	961	7	NULL	NULL	0	NULL	statement 2	Process		is independent of					Nyv1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_140_1_61_s_216	9425154	( B) Binding of Sec17p and Sec18p to the vacuole is independent of the Nyv1p and Vam3p.	bind
48406	6	961	7	NULL	NULL	0	NULL	statement 2	Process		is independent of					Vam3p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_140_1_61_s_216	9425154	( B) Binding of Sec17p and Sec18p to the vacuole is independent of the Nyv1p and Vam3p.	bind
356	1	962	6	NULL	NULL	0	NULL	Ssk2	NULL		bind	NULL				Pbs2	NULL		RSD-I		NULL		0	NULL	NULL	NULL	gw60_embo_22_14_3624_s_120	12853477	( B) Binding of Ssk2 to Pbs2 RSD-I.	bind
48410	1	962	7	NULL	NULL	0	NULL	Ssk2	GP		bind					Pbs2	GP		RSD-I		NULL		NULL	NULL	NULL	NULL	gw60_embo_22_14_3624_s_120	12853477	( B) Binding of Ssk2 to Pbs2 RSD-I.	bind
357	1	963	6	NULL	NULL	0	NULL	sum1	NULL		bind	NULL				HML-E	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_15_1811_s_156	16077008	( B) Binding of Sum1 to  HML-E required the D element.	bind
358	2	963	6	10	NULL	0	NULL	Statement 1	NULL		requires	NULL					NULL			D element	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_15_1811_s_156	16077008	( B) Binding of Sum1 to  HML-E required the D element.	bind
48411	1	963	7	NULL	NULL	0	NULL	Sum1	GP		bind					HML-E	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_15_1811_s_156	16077008	( B) Binding of Sum1 to  HML-E required the D element.	bind
48412	2	963	7	NULL	NULL	0	NULL	statement 1	Process		requires									D element	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_15_1811_s_156	16077008	( B) Binding of Sum1 to  HML-E required the D element.	bind
359	1	964	6	10	NULL	0	NULL	Env	NULL	HIV	bind	NULL				CXCR4	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_8_2078_s_15	16886053	( B) Binding of the HIV envelope glycoprotein (Env) to CXCR4 activates cellular autophagy,  which then leads to both apoptotic and autophagic cell death.	bind
51450	2	964	6	10	NULL	0	NULL	Env	NULL		is	NULL				envelope glycoprotein	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_116_8_2078_s_15	16886053	( B) Binding of the HIV envelope glycoprotein (Env) to CXCR4 activates cellular autophagy,  which then leads to both apoptotic and autophagic cell death.	bind
51451	3	964	6	10	NULL	0	NULL	statement 1	NULL		activates	NULL				cellular autophagy	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_116_8_2078_s_15	16886053	( B) Binding of the HIV envelope glycoprotein (Env) to CXCR4 activates cellular autophagy,  which then leads to both apoptotic and autophagic cell death.	bind
51452	4	964	6	10	NULL	0	NULL	statement 3	NULL		leads to	NULL				apoptotic cell death	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_116_8_2078_s_15	16886053	( B) Binding of the HIV envelope glycoprotein (Env) to CXCR4 activates cellular autophagy,  which then leads to both apoptotic and autophagic cell death.	bind
51453	5	964	6	10	NULL	0	NULL	statement 3	NULL		leads to	NULL				autophagic cell death	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_116_8_2078_s_15	16886053	( B) Binding of the HIV envelope glycoprotein (Env) to CXCR4 activates cellular autophagy,  which then leads to both apoptotic and autophagic cell death.	bind
48413	1	964	7	NULL	NULL	0	NULL	Env	GP	HIV	bind					CXCR4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_8_2078_s_15	16886053	( B) Binding of the HIV envelope glycoprotein (Env) to CXCR4 activates cellular autophagy,  which then leads to both apoptotic and autophagic cell death.	bind
48414	2	964	7	NULL	NULL	0	NULL	statement 1	Process		activates					cellular autophagy	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_8_2078_s_15	16886053	( B) Binding of the HIV envelope glycoprotein (Env) to CXCR4 activates cellular autophagy,  which then leads to both apoptotic and autophagic cell death.	bind
48415	3	964	7	NULL	NULL	0	NULL	statement 2	Process		leads to					apoptotic cell death	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_8_2078_s_15	16886053	( B) Binding of the HIV envelope glycoprotein (Env) to CXCR4 activates cellular autophagy,  which then leads to both apoptotic and autophagic cell death.	bind
48416	4	964	7	NULL	NULL	0	NULL	statement 2	Process		leads to					autophagic cell death	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_8_2078_s_15	16886053	( B) Binding of the HIV envelope glycoprotein (Env) to CXCR4 activates cellular autophagy,  which then leads to both apoptotic and autophagic cell death.	bind
48417	5	964	7	NULL	NULL	0	NULL	Env	GP		is					envelope glycoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_8_2078_s_15	16886053	( B) Binding of the HIV envelope glycoprotein (Env) to CXCR4 activates cellular autophagy,  which then leads to both apoptotic and autophagic cell death.	bind
360	1	966	6	NULL	NULL	0	NULL	Rad9	NULL		bind	NULL		PCNA-like domain		Rad17	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_100_4_1633_s_146	12578958	( B) Binding of the PCNA-like domain of Rad9 to Rad17.	bind
48418	1	966	7	NULL	NULL	0	NULL	Rad9	GP		bind			PCNA-like domain		Rad17	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_4_1633_s_146	12578958	( B) Binding of the PCNA-like domain of Rad9 to Rad17.	bind
361	1	967	6	NULL	NULL	0	NULL	TM7C	NULL		bind	NULL				Meta II	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_22_12854_s_149	9789004	( B) Binding of TM7C to Meta II as shown by immunoblotting.	bind
48419	1	967	7	NULL	NULL	0	NULL	TM7C	GP		bind					Meta II	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_22_12854_s_149	9789004	( B) Binding of TM7C to Meta II as shown by immunoblotting.	bind
363	1	968	6	NULL	NULL	0	NULL	trastuzumab 	NULL		bind	NULL		Fc variant		FcgammaRIIIa	NULL	human	V158		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_11_4005_s_46	16537476	( B) Binding of trastuzumab Fc variants to human V158 ( Left) and F158 ( Right) FcgammaRIIIa ( n = 2).	bind
364	2	968	6	NULL	NULL	0	NULL	trastuzumab 	NULL		bind	NULL		Fc variant		FcgammaRIIIa	NULL	human	F158		NULL		0	NULL	NULL	NULL	gw70_pnas_103_11_4005_s_46	16537476	( B) Binding of trastuzumab Fc variants to human V158 ( Left) and F158 ( Right) FcgammaRIIIa ( n = 2).	bind
48420	1	968	7	NULL	NULL	0	NULL	trastuzumab	GP		bind			Fc variants		FcgammaRIIIa	GP	human	V158		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_11_4005_s_46	16537476	( B) Binding of trastuzumab Fc variants to human V158 ( Left) and F158 ( Right) FcgammaRIIIa ( n = 2).	bind
48421	2	968	7	NULL	NULL	0	NULL	trastuzumab 	GP		bind			Fc variants		FcgammaRIIIa	GP	human	F158		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_11_4005_s_46	16537476	( B) Binding of trastuzumab Fc variants to human V158 ( Left) and F158 ( Right) FcgammaRIIIa ( n = 2).	bind
366	1	969	6	10	NULL	0	NULL	tRNAfMet	NULL		binds to	NULL					NULL			P site in AUG initiator codon	NULL		NULL	NULL	NULL	NULL	gw60_science_278_5340_1093_s_37	9353184	( B) Binding of tRNAfMet to the AUG initiator codon in the P (and E) site directs binding of ASLs to the UUU codon in the A site.	bind
367	2	969	6	10	NULL	0	NULL	ASLs	NULL		binds to	NULL					NULL			A site in UUU codon	NULL		NULL	NULL	NULL	NULL	gw60_science_278_5340_1093_s_37	9353184	( B) Binding of tRNAfMet to the AUG initiator codon in the P (and E) site directs binding of ASLs to the UUU codon in the A site.	bind
368	3	969	6	NULL	NULL	0	NULL	Statement 1	NULL		directs	NULL				Statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_science_278_5340_1093_s_37	9353184	( B) Binding of tRNAfMet to the AUG initiator codon in the P (and E) site directs binding of ASLs to the UUU codon in the A site.	bind
51454	4	969	6	10	NULL	0	NULL	tRNAfMet	NULL		bind	NULL					NULL			E site in AUG initiator codon	NULL		0	NULL	NULL	NULL	gw60_science_278_5340_1093_s_37	9353184	( B) Binding of tRNAfMet to the AUG initiator codon in the P (and E) site directs binding of ASLs to the UUU codon in the A site.	bind
51455	5	969	6	10	NULL	0	NULL	statement 4	NULL		directs	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_science_278_5340_1093_s_37	9353184	( B) Binding of tRNAfMet to the AUG initiator codon in the P (and E) site directs binding of ASLs to the UUU codon in the A site.	bind
48422	1	969	7	NULL	NULL	0	NULL	tRNAfMet	GP		bind									P site in AUG initiator codon	NULL		NULL	NULL	NULL	NULL	gw60_science_278_5340_1093_s_37	9353184	( B) Binding of tRNAfMet to the AUG initiator codon in the P (and E) site directs binding of ASLs to the UUU codon in the A site.	bind
48423	2	969	7	NULL	NULL	0	NULL	ASLs	GP		bind									A site in UUU codon	NULL		NULL	NULL	NULL	NULL	gw60_science_278_5340_1093_s_37	9353184	( B) Binding of tRNAfMet to the AUG initiator codon in the P (and E) site directs binding of ASLs to the UUU codon in the A site.	bind
48424	3	969	7	NULL	NULL	0	NULL	statement 1	Process		directs					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_278_5340_1093_s_37	9353184	( B) Binding of tRNAfMet to the AUG initiator codon in the P (and E) site directs binding of ASLs to the UUU codon in the A site.	bind
51456	4	969	7	NULL	NULL	0	NULL	tRNAfMet	GP		bind									E site in AUG initiator codon	NULL		NULL	NULL	NULL	NULL	gw60_science_278_5340_1093_s_37	9353184	( B) Binding of tRNAfMet to the AUG initiator codon in the P (and E) site directs binding of ASLs to the UUU codon in the A site.	bind
51457	5	969	7	NULL	NULL	0	NULL	statement 4	Process		directs					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_278_5340_1093_s_37	9353184	( B) Binding of tRNAfMet to the AUG initiator codon in the P (and E) site directs binding of ASLs to the UUU codon in the A site.	bind
371	1	970	6	10	NULL	0	NULL	vezatin	NULL		bind	NULL				myosin VIIA	NULL		tail		NULL	co-transfected HEK293 cells	NULL	NULL	NULL	NULL	gw60_embo_19_22_6020_s_63	11080149	( B) Binding of vezatin to the myosin VIIA tail in co-transfected HEK293 cells.	bind
48425	1	970	7	NULL	NULL	0	NULL	vezatin 	GP		bind					myosin VIIA 	GP		tail		NULL	co-transfected HEK293 cells	NULL	NULL	NULL	NULL	gw60_embo_19_22_6020_s_63	11080149	( B) Binding of vezatin to the myosin VIIA tail in co-transfected HEK293 cells.	bind
372	1	971	6	10	NULL	0	NULL	XIAP 	NULL		bind	NULL		H467A		MURR1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_1_244_s_177	14685266	( B) Binding of XIAP H467A to MURR1 and the effects of proteasome inhibition: 293 cells  were transfected as indicated and 1 day later half of the cultures were treated with  lactacystin (10 muM) for an additional 6 h.	bind
48439	1	971	7	NULL	NULL	0	NULL	XIAP	GP		bind			H467A		MURR1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_1_244_s_177	14685266	( B) Binding of XIAP H467A to MURR1 and the effects of proteasome inhibition: 293 cells  were transfected as indicated and 1 day later half of the cultures were treated with  lactacystin (10 muM) for an additional 6 h.	bind
373	1	972	6	NULL	NULL	0	NULL	YopN	NULL		bind	NULL				TyeA	NULL				NULL	Y.enterocolitica	0	NULL	NULL	NULL	gw60_embo_17_7_1907_s_172	9524114	( B) Binding of YopN with TyeA in  Y.enterocolitica.	bind
48440	1	972	7	NULL	NULL	0	NULL	YopN	GP		bind					TyeA	GP				NULL	Y.enterocolitica	NULL	NULL	NULL	NULL	gw60_embo_17_7_1907_s_172	9524114	( B) Binding of YopN with TyeA in  Y.enterocolitica.	bind
374	1	973	6	NULL	NULL	0	NULL	PIR-B peptides	NULL	phosphorylated	bind	NULL				GST-SHP1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_5_2446_s_142	9482905	( B) Binding potential of phosphorylated PIR-B peptides to the GST-SHP 1.	bind
48441	1	973	7	NULL	NULL	0	NULL	PIR-B peptides	GP	phosphorylated	bind					GST-SHP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_5_2446_s_142	9482905	( B) Binding potential of phosphorylated PIR-B peptides to the GST-SHP 1.	bind
455	1	975	6	10	NULL	0	NULL	VPS4A protein	NULL	wild type	bind	NULL		1 - 84		GST-CHMP1B	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13813_s_161	16174732	( B) Biosensor binding isotherms showing wild-type (WT) and L64A mutant VPS4A1 - 84 proteins binding GST-CHMP1B and GST-CHMP1B65 - 196.	bind
456	2	975	6	10	NULL	0	NULL	VPS4A protein	NULL	mutant	bind	NULL		L64A;;1 - 84		GST-CHMP1B	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13813_s_161	16174732	( B) Biosensor binding isotherms showing wild-type (WT) and L64A mutant VPS4A1 - 84 proteins binding GST-CHMP1B and GST-CHMP1B65 - 196.	bind
457	3	975	6	10	NULL	0	NULL	VPS4A protein	NULL	wild type	bind	NULL		1 - 84		GST-CHMP1B	NULL		65 - 196		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13813_s_161	16174732	( B) Biosensor binding isotherms showing wild-type (WT) and L64A mutant VPS4A1 - 84 proteins binding GST-CHMP1B and GST-CHMP1B65 - 196.	bind
458	4	975	6	10	NULL	0	NULL	VPS4A protein	NULL	mutant	bind	NULL		L64A;;1 - 84		GST-CHMP1B	NULL		65 - 196		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13813_s_161	16174732	( B) Biosensor binding isotherms showing wild-type (WT) and L64A mutant VPS4A1 - 84 proteins binding GST-CHMP1B and GST-CHMP1B65 - 196.	bind
48442	1	975	7	NULL	NULL	0	NULL	VPS4A protein	GP	wild-type	bind			1-84		GST-CHMP1B	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13813_s_161	16174732	( B) Biosensor binding isotherms showing wild-type (WT) and L64A mutant VPS4A1 - 84 proteins binding GST-CHMP1B and GST-CHMP1B65 - 196.	bind
48443	2	975	7	NULL	NULL	0	NULL	VPS4A protein	GP	mutant	bind			L64A;;1 - 84		GST-CHMP1B	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13813_s_161	16174732	( B) Biosensor binding isotherms showing wild-type (WT) and L64A mutant VPS4A1 - 84 proteins binding GST-CHMP1B and GST-CHMP1B65 - 196.	bind
48444	3	975	7	NULL	NULL	0	NULL	VPS4A protein	GP	wild-type	bind			1-84		GST-CHMP1B	GP		65 - 196		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13813_s_161	16174732	( B) Biosensor binding isotherms showing wild-type (WT) and L64A mutant VPS4A1 - 84 proteins binding GST-CHMP1B and GST-CHMP1B65 - 196.	bind
48445	4	975	7	NULL	NULL	0	NULL	VPS4A protein	GP	mutant	bind			L64A;;1 - 84		GST-CHMP1B	GP		65 - 196		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13813_s_161	16174732	( B) Biosensor binding isotherms showing wild-type (WT) and L64A mutant VPS4A1 - 84 proteins binding GST-CHMP1B and GST-CHMP1B65 - 196.	bind
48446	5	975	7	NULL	NULL	0	NULL	WT	Organism		is					wild-type	Organism				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13813_s_161	16174732	( B) Biosensor binding isotherms showing wild-type (WT) and L64A mutant VPS4A1 - 84 proteins binding GST-CHMP1B and GST-CHMP1B65 - 196.	bind
503	1	976	6	NULL	NULL	0	NULL	protein	NULL	lamprey	bind	NULL				GST-amphSH3 	NULL				NULL		0	NULL	NULL	NULL	gw60_science_276_5310_259_s_75	9092476	( B) Blots with dynamin antiserum DG1 on lamprey proteins bound to GST-amphSH3 (lane 1), GST-amphSH3mut (lane 2) (lanes 1 and 2 run in parallel), GST-amphSH3 (lane 3), and GST-amphSH3 in the presence of 300 muM of dynamin peptide (lane 4) (lanes 3 and 4 run in parallel) ( 24).	bind
504	2	976	6	NULL	NULL	0	NULL	protein	NULL	lamprey	bind	NULL				GST-amphSH3mut	NULL				NULL		0	NULL	NULL	NULL	gw60_science_276_5310_259_s_75	9092476	( B) Blots with dynamin antiserum DG1 on lamprey proteins bound to GST-amphSH3 (lane 1), GST-amphSH3mut (lane 2) (lanes 1 and 2 run in parallel), GST-amphSH3 (lane 3), and GST-amphSH3 in the presence of 300 muM of dynamin peptide (lane 4) (lanes 3 and 4 run in parallel) ( 24).	bind
613	3	976	6	NULL	NULL	0	NULL	Statement 1	NULL		in presence of	NULL				dynamin peptide	NULL				NULL		0	NULL	NULL	NULL	gw60_science_276_5310_259_s_75	9092476	( B) Blots with dynamin antiserum DG1 on lamprey proteins bound to GST-amphSH3 (lane 1), GST-amphSH3mut (lane 2) (lanes 1 and 2 run in parallel), GST-amphSH3 (lane 3), and GST-amphSH3 in the presence of 300 muM of dynamin peptide (lane 4) (lanes 3 and 4 run in parallel) ( 24).	bind
614	4	976	6	NULL	NULL	0	NULL	Statement 2	NULL		in presence of	NULL				dynamin peptide	NULL				NULL		0	NULL	NULL	NULL	gw60_science_276_5310_259_s_75	9092476	( B) Blots with dynamin antiserum DG1 on lamprey proteins bound to GST-amphSH3 (lane 1), GST-amphSH3mut (lane 2) (lanes 1 and 2 run in parallel), GST-amphSH3 (lane 3), and GST-amphSH3 in the presence of 300 muM of dynamin peptide (lane 4) (lanes 3 and 4 run in parallel) ( 24).	bind
48447	1	976	7	NULL	NULL	0	NULL	proteins	GP	lamprey	bind					 GST-amphSH3	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_276_5310_259_s_75	9092476	( B) Blots with dynamin antiserum DG1 on lamprey proteins bound to GST-amphSH3 (lane 1), GST-amphSH3mut (lane 2) (lanes 1 and 2 run in parallel), GST-amphSH3 (lane 3), and GST-amphSH3 in the presence of 300 muM of dynamin peptide (lane 4) (lanes 3 and 4 run in parallel) ( 24).	bind
48448	2	976	7	NULL	NULL	0	NULL	proteins	GP	lamprey	bind					 GST-amphSH3mut 	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_276_5310_259_s_75	9092476	( B) Blots with dynamin antiserum DG1 on lamprey proteins bound to GST-amphSH3 (lane 1), GST-amphSH3mut (lane 2) (lanes 1 and 2 run in parallel), GST-amphSH3 (lane 3), and GST-amphSH3 in the presence of 300 muM of dynamin peptide (lane 4) (lanes 3 and 4 run in parallel) ( 24).	bind
48449	3	976	7	NULL	NULL	0	NULL	statement 1	Process		in presence of					dynamin peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_276_5310_259_s_75	9092476	( B) Blots with dynamin antiserum DG1 on lamprey proteins bound to GST-amphSH3 (lane 1), GST-amphSH3mut (lane 2) (lanes 1 and 2 run in parallel), GST-amphSH3 (lane 3), and GST-amphSH3 in the presence of 300 muM of dynamin peptide (lane 4) (lanes 3 and 4 run in parallel) ( 24).	bind
48450	4	976	7	NULL	NULL	0	NULL	statement 2	Process		in presence of					dynamin peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_276_5310_259_s_75	9092476	( B) Blots with dynamin antiserum DG1 on lamprey proteins bound to GST-amphSH3 (lane 1), GST-amphSH3mut (lane 2) (lanes 1 and 2 run in parallel), GST-amphSH3 (lane 3), and GST-amphSH3 in the presence of 300 muM of dynamin peptide (lane 4) (lanes 3 and 4 run in parallel) ( 24).	bind
459	1	977	6	NULL	NULL	0	NULL	BLyS	NULL		bind	NULL				U-937 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_science_285_5425_260_s_63	10398604	( B) BLyS binding to U-937 and the myeloma line IM-9.	bind
460	2	977	6	10	NULL	0	NULL	BLyS	NULL		bind	NULL				IM-9	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5425_260_s_63	10398604	( B) BLyS binding to U-937 and the myeloma line IM-9.	bind
51458	3	977	6	10	NULL	0	NULL	IM-9	NULL		is a type of	NULL				myeloma line	NULL				NULL		0	NULL	NULL	NULL	gw60_science_285_5425_260_s_63	10398604	( B) BLyS binding to U-937 and the myeloma line IM-9.	bind
48451	1	977	7	NULL	NULL	0	NULL	BLyS	GP		bind					U-937	Cell				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5425_260_s_63	10398604	( B) BLyS binding to U-937 and the myeloma line IM-9.	bind
48452	2	977	7	NULL	NULL	0	NULL	BLyS	GP		bind					IM-9	Cell				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5425_260_s_63	10398604	( B) BLyS binding to U-937 and the myeloma line IM-9.	bind
48453	3	977	7	NULL	NULL	0	NULL	IM-9	Cell		is a type of					myeloma line	Cell				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5425_260_s_63	10398604	( B) BLyS binding to U-937 and the myeloma line IM-9.	bind
461	1	978	6	NULL	NULL	0	NULL	BMP-6	NULL		bind	NULL				sclerostin	NULL	human			NULL		0	NULL	NULL	NULL	gw70_embo_22_23_6267_s_34	14633986	( B) BMP-6 binding to human sclerostin (circles) or a BSA-blocked plate (triangles) in  an ELISA-based association assay.	bind
48454	1	978	7	NULL	NULL	0	NULL	 BMP-6	GP		bind					sclerostin	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_embo_22_23_6267_s_34	14633986	( B) BMP-6 binding to human sclerostin (circles) or a BSA-blocked plate (triangles) in  an ELISA-based association assay.	bind
463	1	979	6	NULL	NULL	0	NULL	bis-ANS	NULL		bind	NULL				PAI-2	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_22_8_1753_s_136	12682008	( B) Calculated rate of  bis-ANS binding to PAI-2 (mean value of three experiments).	bind
48455	1	979	7	NULL	NULL	0	NULL	bis-ANS	Chemical		bind					PAI-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_8_1753_s_136	12682008	( B) Calculated rate of  bis-ANS binding to PAI-2 (mean value of three experiments).	bind
464	1	980	6	NULL	NULL	0	NULL	CARM1	NULL		bind	NULL	directly			p65	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_1_85_s_98	15616592	( B) CARM1 directly binds to p65.	bind
48456	1	980	7	NULL	NULL	0	NULL	 CARM1	GP		bind		directly			p65	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_1_85_s_98	15616592	( B) CARM1 directly binds to p65.	bind
465	1	981	6	NULL	NULL	0	NULL	Cd+2	NULL		bind	NULL				double cysteine channel	NULL	mutant			NULL	closed state	0	NULL	NULL	NULL	gw70_embo_23_24_4717_s_81	15565171	( B) Cd2+ binds R362C A419C double cysteine mutant channel in the closed state.	bind
48457	1	981	7	10	NULL	0	NULL	Cd2+	Chemical		bind					channel	CellComponent	double cysteine mutant	 R362C;; A419C		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_24_4717_s_81	15565171	( B) Cd2+ binds R362C A419C double cysteine mutant channel in the closed state.	bind
48458	2	981	7	NULL	NULL	0	NULL	statement 1	Process		occur in the 					channel	CellComponent	closed state of			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_24_4717_s_81	15565171	( B) Cd2+ binds R362C A419C double cysteine mutant channel in the closed state.	bind
466	1	982	6	NULL	NULL	0	NULL	CENP-B proteins	NULL		bind	NULL					NULL		CENP-B-box motifs		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_2_309_s_220	9548711	( b) CENP-B  proteins ( red circles) bind to  CENP-B-box motifs and undergo dimerization to cross-link the array into a more stable higher order configuration.	bind
51468	2	982	6	10	NULL	0	NULL	statement 1	NULL		undergo	NULL				dimerization	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_141_2_309_s_220	9548711	( b) CENP-B  proteins ( red circles) bind to  CENP-B-box motifs and undergo dimerization to cross-link the array into a more stable higher order configuration.	bind
51469	3	982	6	10	NULL	0	NULL	statement 2	NULL		crosslink	NULL				array	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_141_2_309_s_220	9548711	( b) CENP-B  proteins ( red circles) bind to  CENP-B-box motifs and undergo dimerization to cross-link the array into a more stable higher order configuration.	bind
51470	4	982	6	10	NULL	0	NULL	statement 3	NULL		leads to	NULL				configuration	NULL	stable;;higher order			NULL		0	NULL	NULL	NULL	gw60_cellbiol_141_2_309_s_220	9548711	( b) CENP-B  proteins ( red circles) bind to  CENP-B-box motifs and undergo dimerization to cross-link the array into a more stable higher order configuration.	bind
48459	1	982	7	NULL	NULL	0	NULL	CENP-B proteins	GP		bind								CENP-B-box motifs		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_2_309_s_220	9548711	( b) CENP-B  proteins ( red circles) bind to  CENP-B-box motifs and undergo dimerization to cross-link the array into a more stable higher order configuration.	bind
48460	2	982	7	NULL	NULL	0	NULL	statement 1	Process		undergo					dimerization	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_2_309_s_220	9548711	( b) CENP-B  proteins ( red circles) bind to  CENP-B-box motifs and undergo dimerization to cross-link the array into a more stable higher order configuration.	bind
48461	3	982	7	NULL	NULL	0	NULL	statement 2	Process		crosslink					array	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_2_309_s_220	9548711	( b) CENP-B  proteins ( red circles) bind to  CENP-B-box motifs and undergo dimerization to cross-link the array into a more stable higher order configuration.	bind
48462	4	982	7	NULL	NULL	0	NULL	statement 3	Process		leads to					configuration	Process	stable;;higher order			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_2_309_s_220	9548711	( b) CENP-B  proteins ( red circles) bind to  CENP-B-box motifs and undergo dimerization to cross-link the array into a more stable higher order configuration.	bind
51471	1	983	6	10	NULL	0	NULL	RalGDS	NULL	WT	bind	NULL		RBD		Ras	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_25_9223_s_186	15197281	( b) Changes in free enthalpy (deltadeltaH degrees ) plotted versus changes in entropy (TdeltadeltaS degrees )of binding between WT and mutant RalGDS-RBD/Ras.	bind
51472	2	983	6	10	NULL	0	NULL	RalGDS	NULL	mutant	bind	NULL		RBD		Ras	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_25_9223_s_186	15197281	( b) Changes in free enthalpy (deltadeltaH degrees ) plotted versus changes in entropy (TdeltadeltaS degrees )of binding between WT and mutant RalGDS-RBD/Ras.	bind
48463	1	983	7	NULL	NULL	0	NULL	RalGDS	GP	WT	bind			RBD		Ras	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_25_9223_s_186	15197281	( b) Changes in free enthalpy (deltadeltaH degrees ) plotted versus changes in entropy (TdeltadeltaS degrees )of binding between WT and mutant RalGDS-RBD/Ras.	bind
48464	2	983	7	NULL	NULL	0	NULL	RalGDS	GP	mutant	bind			RBD		Ras	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_25_9223_s_186	15197281	( b) Changes in free enthalpy (deltadeltaH degrees ) plotted versus changes in entropy (TdeltadeltaS degrees )of binding between WT and mutant RalGDS-RBD/Ras.	bind
468	1	985	6	NULL	NULL	0	NULL	E2F1	NULL		bind	NULL				E2F8	NULL			Promoter	NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_17_5458_s_190	16179649	( B) ChIP analysis of E2F1, E2F4 and E2F7 binding to the  E2F8 promoter.	bind
469	2	985	6	NULL	NULL	0	NULL	E2F4	NULL		bind	NULL				E2F8	NULL			Promoter	NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_17_5458_s_190	16179649	( B) ChIP analysis of E2F1, E2F4 and E2F7 binding to the  E2F8 promoter.	bind
470	3	985	6	NULL	NULL	0	NULL	E2f7	NULL		bind	NULL				E2f8	NULL			Promoter	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_17_5458_s_190	16179649	( B) ChIP analysis of E2F1, E2F4 and E2F7 binding to the  E2F8 promoter.	bind
48465	1	985	7	NULL	NULL	0	NULL	E2F1	GP		bind					E2F8	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_17_5458_s_190	16179649	( B) ChIP analysis of E2F1, E2F4 and E2F7 binding to the  E2F8 promoter.	bind
48466	2	985	7	NULL	NULL	0	NULL	 E2F4	GP		bind					E2F8	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_17_5458_s_190	16179649	( B) ChIP analysis of E2F1, E2F4 and E2F7 binding to the  E2F8 promoter.	bind
48467	3	985	7	NULL	NULL	0	NULL	 E2F7	GP		bind					 E2F8	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_17_5458_s_190	16179649	( B) ChIP analysis of E2F1, E2F4 and E2F7 binding to the  E2F8 promoter.	bind
471	1	986	6	NULL	NULL	0	NULL	Ino2-myc	NULL		bind	NULL				INO1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_embo_24_9_1717_s_91	15861138	( B) ChIP analysis of Ino2-myc or Ino4-myc binding to the  INO1 promoter or the  HSP26 promoter (which served as a negative control).	bind
472	2	986	6	NULL	NULL	0	NULL	Ino4-myc	NULL		bind	NULL				INO1	NULL			Promoter	NULL		0	NULL	NULL	NULL	gw70_embo_24_9_1717_s_91	15861138	( B) ChIP analysis of Ino2-myc or Ino4-myc binding to the  INO1 promoter or the  HSP26 promoter (which served as a negative control).	bind
48468	1	986	7	NULL	NULL	0	NULL	Ino2-myc	GP		bind					INO1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_91	15861138	( B) ChIP analysis of Ino2-myc or Ino4-myc binding to the  INO1 promoter or the  HSP26 promoter (which served as a negative control).	bind
48469	2	986	7	NULL	NULL	0	NULL	Ino4-myc	GP		bind					 INO1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_91	15861138	( B) ChIP analysis of Ino2-myc or Ino4-myc binding to the  INO1 promoter or the  HSP26 promoter (which served as a negative control).	bind
48470	3	986	7	NULL	NULL	0	NULL	Ino2-myc	GP		bind					HSP26 	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_91	15861138	( B) ChIP analysis of Ino2-myc or Ino4-myc binding to the  INO1 promoter or the  HSP26 promoter (which served as a negative control).	bind
48471	4	986	7	NULL	NULL	0	NULL	Ino4-myc	GP		bind					HSP26	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_91	15861138	( B) ChIP analysis of Ino2-myc or Ino4-myc binding to the  INO1 promoter or the  HSP26 promoter (which served as a negative control).	bind
473	1	987	6	NULL	NULL	0	NULL	TFIIB	NULL		bind	NULL				Xist	NULL			P1 promoter	NULL	Ma1L and Ma2L	NULL	NULL	NULL	NULL	gw70_genesdev_19_12_1474_s_159	15964997	( B) ChIP analysis of TFIIB binding to the  Xist P1 and P2 promoters and the  Tsix promoter in Ma1L and Ma2L.	bind
474	2	987	6	NULL	NULL	0	NULL	TFIIB	NULL		bind	NULL				Xist	NULL			P2 promoter	NULL	Ma1L and Ma2L	NULL	NULL	NULL	NULL	gw70_genesdev_19_12_1474_s_159	15964997	( B) ChIP analysis of TFIIB binding to the  Xist P1 and P2 promoters and the  Tsix promoter in Ma1L and Ma2L.	bind
475	3	987	6	NULL	NULL	0	NULL	TFIIB	NULL		bind	NULL				Tsix	NULL			Promoter	NULL	Ma1L and Ma2L	0	NULL	NULL	NULL	gw70_genesdev_19_12_1474_s_159	15964997	( B) ChIP analysis of TFIIB binding to the  Xist P1 and P2 promoters and the  Tsix promoter in Ma1L and Ma2L.	bind
48472	1	987	7	NULL	NULL	0	NULL	TFIIB	GP		bind					 Xist	GP			P1 promoter	NULL	Ma1L and Ma2L	NULL	NULL	NULL	NULL	gw70_genesdev_19_12_1474_s_159	15964997	( B) ChIP analysis of TFIIB binding to the  Xist P1 and P2 promoters and the  Tsix promoter in Ma1L and Ma2L.	bind
48473	2	987	7	NULL	NULL	0	NULL	TFIIB	GP		bind					Xist	GP			P2 promoter	NULL	Ma1L and Ma2L	NULL	NULL	NULL	NULL	gw70_genesdev_19_12_1474_s_159	15964997	( B) ChIP analysis of TFIIB binding to the  Xist P1 and P2 promoters and the  Tsix promoter in Ma1L and Ma2L.	bind
48474	3	987	7	NULL	NULL	0	NULL	TFIIB	GP		bind					Tsix	GP			promoter	NULL	Ma1L and Ma2L	NULL	NULL	NULL	NULL	gw70_genesdev_19_12_1474_s_159	15964997	( B) ChIP analysis of TFIIB binding to the  Xist P1 and P2 promoters and the  Tsix promoter in Ma1L and Ma2L.	bind
476	1	988	6	NULL	NULL	0	NULL	Swi/nf	NULL		bind	NULL				GAL1	NULL			Promoter	NULL		0	NULL	NULL	NULL	gw70_embo_23_20_4040_s_72	15385957	( B) ChIP analysis of the binding of Swi/nf to the  GAL1 and  GAL7 promoters.	bind
477	2	988	6	NULL	NULL	0	NULL	Swi/nf	NULL		bind	NULL				GAL7	NULL			Promoter	NULL		0	NULL	NULL	NULL	gw70_embo_23_20_4040_s_72	15385957	( B) ChIP analysis of the binding of Swi/nf to the  GAL1 and  GAL7 promoters.	bind
48476	1	988	7	NULL	NULL	0	NULL	Swi/nf	GP		bind					GAL1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_23_20_4040_s_72	15385957	( B) ChIP analysis of the binding of Swi/nf to the  GAL1 and  GAL7 promoters.	bind
48477	2	988	7	NULL	NULL	0	NULL	Swi/nf 	GP		bind					GAL7	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_23_20_4040_s_72	15385957	( B) ChIP analysis of the binding of Swi/nf to the  GAL1 and  GAL7 promoters.	bind
478	1	989	6	10	NULL	0	NULL	Swi/nf	NULL		bind	NULL				GAL1 UASG 	NULL				NULL	yeast cells expressing Gal4-Gal11	NULL	NULL	NULL	NULL	gw70_embo_23_20_4040_s_148	15385957	( B) ChIP analysis of the binding of Swi/nf to the  GAL1 UASG in yeast cells expressing Gal4-Gal11.	bind
48478	1	989	7	NULL	NULL	0	NULL	Swi/nf	GP		bind					GAL1 UASG	GP				NULL	yeast cells expressing Gal4-Gal11	NULL	NULL	NULL	NULL	gw70_embo_23_20_4040_s_148	15385957	( B) ChIP analysis of the binding of Swi/nf to the  GAL1 UASG in yeast cells expressing Gal4-Gal11.	bind
479	1	991	6	NULL	NULL	0	NULL	MYC	NULL		bind	NULL				WRN	NULL			Promoter elements	NULL	in vivo	0	NULL	NULL	NULL	gw60_genesdev_17_13_1569_s_57	12842909	( B) ChIP detects  MYC binding to  WRN promoter elements in vivo.	bind
48479	1	991	7	NULL	NULL	0	NULL	MYC	GP		bind					WRN	GP			promoter elements	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_genesdev_17_13_1569_s_57	12842909	( B) ChIP detects  MYC binding to  WRN promoter elements in vivo.	bind
480	1	993	6	10	NULL	0	NULL	TBP	NULL		bind	NULL				INO1	NULL			Promoter	NULL	WT cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_113	15861138	( B) ChIP was performed to determine the level of TBP bound to the  INO1 promoter in wild-type (WT) or  mot1-42 cells.	bind
481	2	993	6	NULL	NULL	0	NULL	TBP	NULL		bind	NULL				INO1	NULL			Promoter	NULL	mot1-42 cells	0	NULL	NULL	NULL	gw70_embo_24_9_1717_s_113	15861138	( B) ChIP was performed to determine the level of TBP bound to the  INO1 promoter in wild-type (WT) or  mot1-42 cells.	bind
51473	3	993	6	10	NULL	0	NULL	WT	NULL		is	NULL				wild-type	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_9_1717_s_113	15861138	( B) ChIP was performed to determine the level of TBP bound to the  INO1 promoter in wild-type (WT) or  mot1-42 cells.	bind
48480	1	993	7	NULL	NULL	0	NULL	TBP	GP		bind					INO1	GP			promoter	NULL	WT cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_113	15861138	( B) ChIP was performed to determine the level of TBP bound to the  INO1 promoter in wild-type (WT) or  mot1-42 cells.	bind
48481	2	993	7	NULL	NULL	0	NULL	TBP	GP		bind					INO1	GP			promoter	NULL	mot1-42 cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_113	15861138	( B) ChIP was performed to determine the level of TBP bound to the  INO1 promoter in wild-type (WT) or  mot1-42 cells.	bind
48482	3	993	7	NULL	NULL	0	NULL	WT	Organism		is					wild-type	Organism				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_113	15861138	( B) ChIP was performed to determine the level of TBP bound to the  INO1 promoter in wild-type (WT) or  mot1-42 cells.	bind
482	1	994	6	10	NULL	0	NULL	Mll	NULL		bind	NULL				p27Kip1	NULL			coding region	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_158	15640349	( B) ChIP with anti-MLLC antibody quantitated with Real-Time PCR shows that Mll binding to the  p27Kip1 coding region is much higher in cells expressing menin.	bind
483	2	994	6	10	NULL	0	NULL	Statement 1	NULL		is higher in	NULL				cells expressing menin 	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_158	15640349	( B) ChIP with anti-MLLC antibody quantitated with Real-Time PCR shows that Mll binding to the  p27Kip1 coding region is much higher in cells expressing menin.	bind
48483	1	994	7	NULL	NULL	0	NULL	Mll	GP		bind					p27Kip1	GP			coding region	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_158	15640349	( B) ChIP with anti-MLLC antibody quantitated with Real-Time PCR shows that Mll binding to the  p27Kip1 coding region is much higher in cells expressing menin.	bind
48484	3	994	7	10	NULL	0	NULL	statement 1	Process		is higher in					cells expressing menin	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_158	15640349	( B) ChIP with anti-MLLC antibody quantitated with Real-Time PCR shows that Mll binding to the  p27Kip1 coding region is much higher in cells expressing menin.	bind
484	1	995	6	NULL	NULL	0	NULL	Cholesterol	NULL		bind	NULL				Nef	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_100_14_8460_s_239	12824470	( b) Cholesterol  binding to Nef increases HIV infectivity.	bind
485	2	995	6	10	NULL	0	NULL	Statement 1	NULL		increases	NULL				HIV	NULL	infectivity of 			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_14_8460_s_239	12824470	( b) Cholesterol  binding to Nef increases HIV infectivity.	bind
48485	1	995	7	NULL	NULL	0	NULL	Cholesterol	Chemical		bind					Nef	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_14_8460_s_239	12824470	( b) Cholesterol  binding to Nef increases HIV infectivity.	bind
48486	2	995	7	NULL	NULL	0	NULL	statement 1	Process		increases					HIV	Organism	infectivity of 			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_14_8460_s_239	12824470	( b) Cholesterol  binding to Nef increases HIV infectivity.	bind
486	1	996	6	10	NULL	0	NULL	Gal4p-myc	NULL		bind	NULL				MTH1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_48_17302_s_158	16301536	( B) Chromatin IP showing galactose-specific binding of Gal4p-myc to  MTH1,  CIN5, and  GAL10 ( Left) and of Mth1p-myc to  HXT7	bind
487	2	996	6	10	NULL	0	NULL	Gal4p-myc	NULL		bind	NULL				CIN5	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_48_17302_s_158	16301536	( B) Chromatin IP showing galactose-specific binding of Gal4p-myc to  MTH1,  CIN5, and  GAL10 ( Left) and of Mth1p-myc to  HXT7	bind
488	3	996	6	10	NULL	0	NULL	Gal4p-myc	NULL		bind	NULL				GAL10	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_48_17302_s_158	16301536	( B) Chromatin IP showing galactose-specific binding of Gal4p-myc to  MTH1,  CIN5, and  GAL10 ( Left) and of Mth1p-myc to  HXT7	bind
489	4	996	6	NULL	NULL	0	NULL	Mth1p-myc	NULL		bind	NULL				HXT7	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_48_17302_s_158	16301536	( B) Chromatin IP showing galactose-specific binding of Gal4p-myc to  MTH1,  CIN5, and  GAL10 ( Left) and of Mth1p-myc to  HXT7	bind
51474	5	996	6	10	NULL	0	NULL	statement 1	NULL		is specific to	NULL				galactose	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_48_17302_s_158	16301536	( B) Chromatin IP showing galactose-specific binding of Gal4p-myc to  MTH1,  CIN5, and  GAL10 ( Left) and of Mth1p-myc to  HXT7	bind
51475	6	996	6	10	NULL	0	NULL	statement 2	NULL		is specific to	NULL				galactose	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_48_17302_s_158	16301536	( B) Chromatin IP showing galactose-specific binding of Gal4p-myc to  MTH1,  CIN5, and  GAL10 ( Left) and of Mth1p-myc to  HXT7	bind
51476	7	996	6	10	NULL	0	NULL	statement 3	NULL		is specific to	NULL				galactose	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_48_17302_s_158	16301536	( B) Chromatin IP showing galactose-specific binding of Gal4p-myc to  MTH1,  CIN5, and  GAL10 ( Left) and of Mth1p-myc to  HXT7	bind
48487	1	996	7	NULL	NULL	0	NULL	Gal4p-myc	GP		bind					MTH1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_48_17302_s_158	16301536	( B) Chromatin IP showing galactose-specific binding of Gal4p-myc to  MTH1,  CIN5, and  GAL10 ( Left) and of Mth1p-myc to  HXT7	bind
48488	2	996	7	NULL	NULL	0	NULL	Gal4p-myc	GP		 bind					CIN5	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_48_17302_s_158	16301536	( B) Chromatin IP showing galactose-specific binding of Gal4p-myc to  MTH1,  CIN5, and  GAL10 ( Left) and of Mth1p-myc to  HXT7	bind
48489	3	996	7	NULL	NULL	0	NULL	Gal4p-myc	GP		bind					GAL10	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_48_17302_s_158	16301536	( B) Chromatin IP showing galactose-specific binding of Gal4p-myc to  MTH1,  CIN5, and  GAL10 ( Left) and of Mth1p-myc to  HXT7	bind
48490	4	996	7	NULL	NULL	0	NULL	 Mth1p-myc	GP		bind					HXT7	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_48_17302_s_158	16301536	( B) Chromatin IP showing galactose-specific binding of Gal4p-myc to  MTH1,  CIN5, and  GAL10 ( Left) and of Mth1p-myc to  HXT7	bind
48491	5	996	7	NULL	NULL	0	NULL	statement 1	Process		is specific to					galactose	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_48_17302_s_158	16301536	( B) Chromatin IP showing galactose-specific binding of Gal4p-myc to  MTH1,  CIN5, and  GAL10 ( Left) and of Mth1p-myc to  HXT7	bind
48492	6	996	7	NULL	NULL	0	NULL	statement 2	Process		is specific to					galactose	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_48_17302_s_158	16301536	( B) Chromatin IP showing galactose-specific binding of Gal4p-myc to  MTH1,  CIN5, and  GAL10 ( Left) and of Mth1p-myc to  HXT7	bind
48493	7	996	7	NULL	NULL	0	NULL	statement 3	Process		is specific to					galactose	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_48_17302_s_158	16301536	( B) Chromatin IP showing galactose-specific binding of Gal4p-myc to  MTH1,  CIN5, and  GAL10 ( Left) and of Mth1p-myc to  HXT7	bind
490	1	997	6	NULL	NULL	0	NULL	DLX2	NULL		bind	NULL				Dlx5/6	NULL			intergenic enhancer	NULL	neonatal retina in situ	0	NULL	NULL	NULL	gw70_nucleicacidsres_32_3_884_s_161	14769946	( b) Chromatin IP: DLX2 but not DLX1 binds to the  Dlx5/6 intergenic enhancer in neonatal retina  in situ. ChIP was performed using P0 retina and specific DLX1 or DLX2 antibodies.	bind
491	2	997	6	NULL	NULL	0	NULL	Dlx1	NULL		does not bind	NULL				Dlx5/6	NULL			intergenic enhancer	NULL	neonatal retina in situ	0	NULL	NULL	NULL	gw70_nucleicacidsres_32_3_884_s_161	14769946	( b) Chromatin IP: DLX2 but not DLX1 binds to the  Dlx5/6 intergenic enhancer in neonatal retina  in situ. ChIP was performed using P0 retina and specific DLX1 or DLX2 antibodies.	bind
48494	1	997	7	NULL	NULL	0	NULL	DLX2	GP		bind					Dlx5/6	GP	 		intergenic enhancer	NULL	neonatal retina in situ	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_3_884_s_161	14769946	( b) Chromatin IP: DLX2 but not DLX1 binds to the  Dlx5/6 intergenic enhancer in neonatal retina  in situ. ChIP was performed using P0 retina and specific DLX1 or DLX2 antibodies.	bind
48495	2	997	7	NULL	NULL	0	NULL	DLX1	GP		does not bind					Dlx5/6 	GP	 		intergenic enhancer	NULL	neonatal retina in situ	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_3_884_s_161	14769946	( b) Chromatin IP: DLX2 but not DLX1 binds to the  Dlx5/6 intergenic enhancer in neonatal retina  in situ. ChIP was performed using P0 retina and specific DLX1 or DLX2 antibodies.	bind
492	1	998	6	NULL	NULL	0	NULL	Chs5p	NULL		bind	NULL				Arf1p	NULL	activated			NULL		0	NULL	NULL	NULL	gw70_embo_25_5_943_s_128	16498409	( B) Chs5p binds to activated Arf1p.	bind
48496	1	998	7	NULL	NULL	0	NULL	Chs5p	GP		bind					Arf1p	GP	activated			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_5_943_s_128	16498409	( B) Chs5p binds to activated Arf1p.	bind
493	1	999	6	NULL	NULL	0	NULL	CIITA	NULL		bind	NULL				GTP	NULL				NULL		0	NULL	NULL	NULL	gw60_science_285_5432_1402_s_50	10464099	( B) CIITA binds GTP.	bind
48497	1	999	7	NULL	NULL	0	NULL	CIITA	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5432_1402_s_50	10464099	( B) CIITA binds GTP.	bind
494	1	1002	6	NULL	NULL	0	NULL	TRAF2	NULL		bind	NULL				CD40 fragment	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_19_10395_s_92	10984535	( B) Close-up view of the CD40 fragment bound to TRAF2 and TRAF3.	bind
495	2	1002	6	NULL	NULL	0	NULL	traf3	NULL		bind	NULL				CD40 fragment	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_19_10395_s_92	10984535	( B) Close-up view of the CD40 fragment bound to TRAF2 and TRAF3.	bind
48498	1	1002	7	NULL	NULL	0	NULL	CD40 fragment 	GP		bind					TRAF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_19_10395_s_92	10984535	( B) Close-up view of the CD40 fragment bound to TRAF2 and TRAF3.	bind
48499	2	1002	7	NULL	NULL	0	NULL	CD40 fragment 	GP		bind					TRAF3	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_19_10395_s_92	10984535	( B) Close-up view of the CD40 fragment bound to TRAF2 and TRAF3.	bind
496	2	1005	6	10	NULL	0	NULL	CHO cells	NULL		express	NULL				alphaIIbbeta3	NULL	WT;;human			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_39	12730600	( B) Comparison of constitutive and DTT-induced fibrinogen binding to CHO cells expressing wild-type (WT) human alphaIIbbeta3 or G708N beta3 mutant.	bind
497	3	1005	6	10	NULL	0	NULL	CHO cells	NULL		express	NULL				beta3	NULL	mutant	G708N		NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_39	12730600	( B) Comparison of constitutive and DTT-induced fibrinogen binding to CHO cells expressing wild-type (WT) human alphaIIbbeta3 or G708N beta3 mutant.	bind
51477	1	1005	6	10	NULL	0	NULL	fibrinogen	NULL		is induced by	NULL				DTT	NULL				NULL		0	NULL	NULL	NULL	gw60_science_300_5620_795_s_39	12730600	( B) Comparison of constitutive and DTT-induced fibrinogen binding to CHO cells expressing wild-type (WT) human alphaIIbbeta3 or G708N beta3 mutant.	bind
51478	4	1005	6	10	NULL	0	NULL	fibrinogen	NULL	constitutive	bind	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_science_300_5620_795_s_39	12730600	( B) Comparison of constitutive and DTT-induced fibrinogen binding to CHO cells expressing wild-type (WT) human alphaIIbbeta3 or G708N beta3 mutant.	bind
51479	5	1005	6	10	NULL	0	NULL	fibrinogen	NULL	constitutive	bind	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_science_300_5620_795_s_39	12730600	( B) Comparison of constitutive and DTT-induced fibrinogen binding to CHO cells expressing wild-type (WT) human alphaIIbbeta3 or G708N beta3 mutant.	bind
51480	6	1005	6	10	NULL	0	NULL	statement 4	NULL		is an alternative to	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_science_300_5620_795_s_39	12730600	( B) Comparison of constitutive and DTT-induced fibrinogen binding to CHO cells expressing wild-type (WT) human alphaIIbbeta3 or G708N beta3 mutant.	bind
51481	7	1005	6	10	NULL	0	NULL	statement 1	NULL		bind	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_science_300_5620_795_s_39	12730600	( B) Comparison of constitutive and DTT-induced fibrinogen binding to CHO cells expressing wild-type (WT) human alphaIIbbeta3 or G708N beta3 mutant.	bind
51482	8	1005	6	10	NULL	0	NULL	statement 1	NULL		bind	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_science_300_5620_795_s_39	12730600	( B) Comparison of constitutive and DTT-induced fibrinogen binding to CHO cells expressing wild-type (WT) human alphaIIbbeta3 or G708N beta3 mutant.	bind
51483	9	1005	6	10	NULL	0	NULL	statement 7	NULL		is an alternative to	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw60_science_300_5620_795_s_39	12730600	( B) Comparison of constitutive and DTT-induced fibrinogen binding to CHO cells expressing wild-type (WT) human alphaIIbbeta3 or G708N beta3 mutant.	bind
48500	1	1005	7	NULL	NULL	0	NULL	CHO cells	Cell		express					 alphaIIbbeta3	GP	WT;; human			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_39	12730600	( B) Comparison of constitutive and DTT-induced fibrinogen binding to CHO cells expressing wild-type (WT) human alphaIIbbeta3 or G708N beta3 mutant.	bind
48501	2	1005	7	NULL	NULL	0	NULL	CHO cells	Cell		express					 beta3	GP	mutant	G708N		NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_39	12730600	( B) Comparison of constitutive and DTT-induced fibrinogen binding to CHO cells expressing wild-type (WT) human alphaIIbbeta3 or G708N beta3 mutant.	bind
48502	3	1005	7	NULL	NULL	0	NULL	fibrinogen	GP	Constitutive	bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_39	12730600	( B) Comparison of constitutive and DTT-induced fibrinogen binding to CHO cells expressing wild-type (WT) human alphaIIbbeta3 or G708N beta3 mutant.	bind
48503	4	1005	7	NULL	NULL	0	NULL	fibrinogen	GP	Constitutive	bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_39	12730600	( B) Comparison of constitutive and DTT-induced fibrinogen binding to CHO cells expressing wild-type (WT) human alphaIIbbeta3 or G708N beta3 mutant.	bind
48504	5	1005	7	NULL	NULL	0	NULL	DTT	Chemical		induce					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_39	12730600	( B) Comparison of constitutive and DTT-induced fibrinogen binding to CHO cells expressing wild-type (WT) human alphaIIbbeta3 or G708N beta3 mutant.	bind
48505	6	1005	7	NULL	NULL	0	NULL	statement 5	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_39	12730600	( B) Comparison of constitutive and DTT-induced fibrinogen binding to CHO cells expressing wild-type (WT) human alphaIIbbeta3 or G708N beta3 mutant.	bind
48506	7	1005	7	NULL	NULL	0	NULL	statement 5	GP		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_39	12730600	( B) Comparison of constitutive and DTT-induced fibrinogen binding to CHO cells expressing wild-type (WT) human alphaIIbbeta3 or G708N beta3 mutant.	bind
51484	8	1005	7	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_39	12730600	( B) Comparison of constitutive and DTT-induced fibrinogen binding to CHO cells expressing wild-type (WT) human alphaIIbbeta3 or G708N beta3 mutant.	bind
51485	9	1005	7	NULL	NULL	0	NULL	statement 6	Process		is an alternative to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_39	12730600	( B) Comparison of constitutive and DTT-induced fibrinogen binding to CHO cells expressing wild-type (WT) human alphaIIbbeta3 or G708N beta3 mutant.	bind
498	1	1006	6	NULL	NULL	0	NULL	RecA	NULL		bind	NULL				lambda-EMBL3	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_21_12295_s_155	9770480	( B) Comparison of RecA binding kinetics to lambda-EMBL3, lambda-EMBL3 dimer, and 156Gmac for a constant externally applied force of 45 pN.	bind
499	2	1006	6	NULL	NULL	0	NULL	RecA	NULL		bind	NULL				lambda-EMBL3 dimer	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_21_12295_s_155	9770480	( B) Comparison of RecA binding kinetics to lambda-EMBL3, lambda-EMBL3 dimer, and 156Gmac for a constant externally applied force of 45 pN.	bind
500	3	1006	6	NULL	NULL	0	NULL	RecA	NULL		bind	NULL				156Gmac	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_21_12295_s_155	9770480	( B) Comparison of RecA binding kinetics to lambda-EMBL3, lambda-EMBL3 dimer, and 156Gmac for a constant externally applied force of 45 pN.	bind
48507	1	1006	7	NULL	NULL	0	NULL	RecA	GP		bind					lambda-EMBL3	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12295_s_155	9770480	( B) Comparison of RecA binding kinetics to lambda-EMBL3, lambda-EMBL3 dimer, and 156Gmac for a constant externally applied force of 45 pN.	bind
48508	2	1006	7	NULL	NULL	0	NULL	RecA	GP		bind					lambda-EMBL3 dimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12295_s_155	9770480	( B) Comparison of RecA binding kinetics to lambda-EMBL3, lambda-EMBL3 dimer, and 156Gmac for a constant externally applied force of 45 pN.	bind
48509	3	1006	7	NULL	NULL	0	NULL	RecA	GP		bind					156Gmac	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12295_s_155	9770480	( B) Comparison of RecA binding kinetics to lambda-EMBL3, lambda-EMBL3 dimer, and 156Gmac for a constant externally applied force of 45 pN.	bind
501	1	1007	6	10	NULL	0	NULL	CBF-A	NULL		bind	NULL					NULL	rat		HRE	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_19_3762_s_203	11000268	( B) Comparison of the binding affinity of CBF-A to the rat HRE and CArG box.	bind
502	2	1007	6	10	NULL	0	NULL	CBF-A	NULL		bind	NULL					NULL	rat		CArG box	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_19_3762_s_203	11000268	( B) Comparison of the binding affinity of CBF-A to the rat HRE and CArG box.	bind
48510	1	1007	7	NULL	NULL	0	NULL	CBF-A	GP		bind							rat		HRE	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_19_3762_s_203	11000268	( B) Comparison of the binding affinity of CBF-A to the rat HRE and CArG box.	bind
48511	2	1007	7	NULL	NULL	0	NULL	CBF-A	GP		bind							rat		CArG box	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_19_3762_s_203	11000268	( B) Comparison of the binding affinity of CBF-A to the rat HRE and CArG box.	bind
615	1	1013	6	NULL	NULL	0	NULL	ORF80	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4973_s_225	11812827	( B) Competition experiments with 250 nM ORF80 bound to 5 nM DNA.	bind
48512	1	1013	7	NULL	NULL	0	NULL	ORF80	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4973_s_225	11812827	( B) Competition experiments with 250 nM ORF80 bound to 5 nM DNA.	bind
653	1	1014	6	10	NULL	0	NULL	SRC1	NULL		bind	NULL				cyclin D1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_22_3488_s_145	9832502	( B) Competition of cyclin D1-SRC1 binding by SRC1 peptides.	bind
654	2	1014	6	10	NULL	0	NULL	SRC1 peptide	NULL		bind	NULL				cyclin D1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_22_3488_s_145	9832502	( B) Competition of cyclin D1-SRC1 binding by SRC1 peptides.	bind
51486	3	1014	6	10	NULL	0	NULL	statement 2	NULL		competes with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_22_3488_s_145	9832502	( B) Competition of cyclin D1-SRC1 binding by SRC1 peptides.	bind
48513	1	1014	7	NULL	NULL	0	NULL	SRC1	GP		bind					cyclin D1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_22_3488_s_145	9832502	( B) Competition of cyclin D1-SRC1 binding by SRC1 peptides.	bind
48514	2	1014	7	NULL	NULL	0	NULL	SRC1 peptides	GP		bind					cyclin D1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_22_3488_s_145	9832502	( B) Competition of cyclin D1-SRC1 binding by SRC1 peptides.	bind
48515	3	1014	7	NULL	NULL	0	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_22_3488_s_145	9832502	( B) Competition of cyclin D1-SRC1 binding by SRC1 peptides.	bind
655	1	1015	6	10	NULL	0	NULL	Prz	NULL		bind	NULL				E-HRP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
656	2	1015	6	10	NULL	0	NULL	Prz	NULL		is	NULL				prazosin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
657	3	1015	6	10	NULL	0	NULL	Yh	NULL		bind	NULL				E-HRP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
658	4	1015	6	10	NULL	0	NULL	Yh	NULL		is	NULL				yohimbine	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
659	5	1015	6	10	NULL	0	NULL	Cln	NULL		bind	NULL				E-HRP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
660	6	1015	6	10	NULL	0	NULL	Cln	NULL		is 	NULL				clonidine	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
661	7	1015	6	NULL	NULL	0	NULL	beta-adrenergic ligand propranolol	NULL		bind	NULL				E-HRP	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
662	8	1015	6	NULL	NULL	0	NULL	Pro	NULL		is	NULL				beta-adrenergic ligand propranolol	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
663	9	1015	6	NULL	NULL	0	NULL	dopamine D2 receptor ligand quinpirole	NULL		bind	NULL				E-HRP	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
664	10	1015	6	NULL	NULL	0	NULL	Quin	NULL		is	NULL				dopamine D2 receptor ligand quinpirole	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
48516	1	1015	7	NULL	NULL	0	NULL	Prz	Chemical		bind					E-HRP	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
48517	2	1015	7	NULL	NULL	0	NULL	Yh	Chemical		bind					E-HRP	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
48518	3	1015	7	NULL	NULL	0	NULL	Cln	Chemical		bind					E-HRP	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
48519	4	1015	7	NULL	NULL	0	NULL	Pro	Chemical		bind					E-HRP	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
48520	5	1015	7	NULL	NULL	0	NULL	Quin	Chemical		bind					E-HRP	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
48521	6	1015	7	NULL	NULL	0	NULL	Prz	Chemical		is					prazosin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
48522	7	1015	7	NULL	NULL	0	NULL	Prz	Chemical		is a type of					alpha1-adrenergic ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
48523	8	1015	7	NULL	NULL	0	NULL	Yh	Chemical		is					 yohimbine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
48524	9	1015	7	NULL	NULL	0	NULL	Yh	Chemical		is a type of					alpha2-adrenergic ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
48525	10	1015	7	NULL	NULL	0	NULL	Cln	Chemical		is					clonidine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
48526	11	1015	7	NULL	NULL	0	NULL	Cln	Chemical		is a type of					alpha2-adrenergic ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
48527	12	1015	7	NULL	NULL	0	NULL	Pro	Chemical		is					propranolol	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
48528	13	1015	7	NULL	NULL	0	NULL	Pro	Chemical		is a type of					beta-adrenergic ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
48529	14	1015	7	NULL	NULL	0	NULL	Quin	Chemical		is					quinpirole	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
48530	15	1015	7	NULL	NULL	0	NULL	Quin	Chemical		is a type of					dopamine D2 receptor ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11603_s_158	11027358	( B) Competition of E-HRP binding by the alpha1-adrenergic ligand prazosin (Prz), alpha2-adrenergic ligands yohimbine (Yh) and clonidine (Cln), beta-adrenergic ligand propranolol (Pro), and the dopamine D2 receptor ligand quinpirole (Quin).	bind
665	1	1016	6	10	NULL	0	NULL	GST MBNL1	NULL		bind	NULL				cTNT MSE1 4 RNA	NULL	labeled;;chicken			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_15_3103_s_135	15257297	( B) Competition of GST MBNL1 binding to labeled chicken cTNT MSE1 4 RNA by nonlabeled  MSE RNAs.	bind
666	2	1016	6	10	NULL	0	NULL	GST MBNL1	NULL		bind	NULL				MSE RNAs	NULL	nonlabeled			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_15_3103_s_135	15257297	( B) Competition of GST MBNL1 binding to labeled chicken cTNT MSE1 4 RNA by nonlabeled  MSE RNAs.	bind
51487	3	1016	6	10	NULL	0	NULL	statement 2	NULL		competes with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_23_15_3103_s_135	15257297	( B) Competition of GST MBNL1 binding to labeled chicken cTNT MSE1 4 RNA by nonlabeled  MSE RNAs.	bind
48531	1	1016	7	NULL	NULL	0	NULL	GST MBNL1	GP		bind					cTNT MSE1 4 RNA	GP	labeled;;chicken			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_15_3103_s_135	15257297	( B) Competition of GST MBNL1 binding to labeled chicken cTNT MSE1 4 RNA by nonlabeled  MSE RNAs.	bind
48532	2	1016	7	NULL	NULL	0	NULL	GST MBNL1	GP		bind					MSE RNA	GP	nonlabeled			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_15_3103_s_135	15257297	( B) Competition of GST MBNL1 binding to labeled chicken cTNT MSE1 4 RNA by nonlabeled  MSE RNAs.	bind
48533	3	1016	7	NULL	NULL	0	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_15_3103_s_135	15257297	( B) Competition of GST MBNL1 binding to labeled chicken cTNT MSE1 4 RNA by nonlabeled  MSE RNAs.	bind
667	1	1017	6	NULL	NULL	0	NULL	PIF3 	NULL		bind	NULL				G-wt	NULL				NULL		0	NULL	NULL	NULL	gw60_science_288_5467_859_s_96	10797009	( B) Competition of PIF3 binding to G-wt by the different G-box sequences from the four light-regulated genes.	bind
669	2	1017	6	10	NULL	0	NULL	PIF3	NULL		bind	NULL				light regulated genes	NULL			G-box sequences	NULL		NULL	NULL	NULL	NULL	gw60_science_288_5467_859_s_96	10797009	( B) Competition of PIF3 binding to G-wt by the different G-box sequences from the four light-regulated genes.	bind
51488	3	1017	6	10	NULL	0	NULL	statement 2	NULL		competes with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_science_288_5467_859_s_96	10797009	( B) Competition of PIF3 binding to G-wt by the different G-box sequences from the four light-regulated genes.	bind
48534	1	1017	7	NULL	NULL	0	NULL	PIF3	GP		bind					 G-wt	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_288_5467_859_s_96	10797009	( B) Competition of PIF3 binding to G-wt by the different G-box sequences from the four light-regulated genes.	bind
48535	2	1017	7	NULL	NULL	0	NULL	PIF3	GP		bind					light-regulated gene	GP			G-box sequences	NULL		NULL	NULL	NULL	NULL	gw60_science_288_5467_859_s_96	10797009	( B) Competition of PIF3 binding to G-wt by the different G-box sequences from the four light-regulated genes.	bind
48536	3	1017	7	NULL	NULL	0	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_288_5467_859_s_96	10797009	( B) Competition of PIF3 binding to G-wt by the different G-box sequences from the four light-regulated genes.	bind
671	1	1018	6	NULL	NULL	0	NULL	HSV gD	NULL		bind	NULL				sV(HIgR)-Fc	NULL				NULL	In vitro	NULL	NULL	NULL	NULL	gw60_pnas_95_26_15700_s_174	9861033	( B) Competition of the  in vitro binding of HSV gD to sV(HIgR)-Fc by mAb R1.302 to PRR1 (R1.302,  ), mAb to gD HD1 (HD1,  ), or purified mouse IgGs (IgG, x).	bind
673	2	1018	6	NULL	NULL	0	NULL	Prr1	NULL		competes	NULL				Statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_26_15700_s_174	9861033	( B) Competition of the  in vitro binding of HSV gD to sV(HIgR)-Fc by mAb R1.302 to PRR1 (R1.302,  ), mAb to gD HD1 (HD1,  ), or purified mouse IgGs (IgG, x).	bind
674	3	1018	6	NULL	NULL	0	NULL	gD HD1	NULL		competes	NULL				Statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_26_15700_s_174	9861033	( B) Competition of the  in vitro binding of HSV gD to sV(HIgR)-Fc by mAb R1.302 to PRR1 (R1.302,  ), mAb to gD HD1 (HD1,  ), or purified mouse IgGs (IgG, x).	bind
675	4	1018	6	NULL	NULL	0	NULL	IgGs	NULL	purified mouse	competes	NULL				Statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_26_15700_s_174	9861033	( B) Competition of the  in vitro binding of HSV gD to sV(HIgR)-Fc by mAb R1.302 to PRR1 (R1.302,  ), mAb to gD HD1 (HD1,  ), or purified mouse IgGs (IgG, x).	bind
48537	1	1018	7	NULL	NULL	0	NULL	 HSV gD	GP		bind					sV(HIgR)-Fc	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_95_26_15700_s_174	9861033	( B) Competition of the  in vitro binding of HSV gD to sV(HIgR)-Fc by mAb R1.302 to PRR1 (R1.302,  ), mAb to gD HD1 (HD1,  ), or purified mouse IgGs (IgG, x).	bind
48538	2	1018	7	NULL	NULL	0	NULL	HSV gD	GP		bind					mAb R1.302	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_26_15700_s_174	9861033	( B) Competition of the  in vitro binding of HSV gD to sV(HIgR)-Fc by mAb R1.302 to PRR1 (R1.302,  ), mAb to gD HD1 (HD1,  ), or purified mouse IgGs (IgG, x).	bind
48539	3	1018	7	NULL	NULL	0	NULL	HSV gD 	GP		bind					PRR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_26_15700_s_174	9861033	( B) Competition of the  in vitro binding of HSV gD to sV(HIgR)-Fc by mAb R1.302 to PRR1 (R1.302,  ), mAb to gD HD1 (HD1,  ), or purified mouse IgGs (IgG, x).	bind
48540	4	1018	7	NULL	NULL	0	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_26_15700_s_174	9861033	( B) Competition of the  in vitro binding of HSV gD to sV(HIgR)-Fc by mAb R1.302 to PRR1 (R1.302,  ), mAb to gD HD1 (HD1,  ), or purified mouse IgGs (IgG, x).	bind
48541	5	1018	7	NULL	NULL	0	NULL	statement 3	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_26_15700_s_174	9861033	( B) Competition of the  in vitro binding of HSV gD to sV(HIgR)-Fc by mAb R1.302 to PRR1 (R1.302,  ), mAb to gD HD1 (HD1,  ), or purified mouse IgGs (IgG, x).	bind
48652	6	1018	7	NULL	NULL	0	NULL	HSV gD	GP		bind					gD HD1 mAb	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_26_15700_s_174	9861033	( B) Competition of the  in vitro binding of HSV gD to sV(HIgR)-Fc by mAb R1.302 to PRR1 (R1.302,  ), mAb to gD HD1 (HD1,  ), or purified mouse IgGs (IgG, x).	bind
48653	7	1018	7	NULL	NULL	0	NULL	HSV gD	GP		bind					IgG	GP	purified mouse			NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_26_15700_s_174	9861033	( B) Competition of the  in vitro binding of HSV gD to sV(HIgR)-Fc by mAb R1.302 to PRR1 (R1.302,  ), mAb to gD HD1 (HD1,  ), or purified mouse IgGs (IgG, x).	bind
48654	8	1018	7	NULL	NULL	0	NULL	statement 6	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_26_15700_s_174	9861033	( B) Competition of the  in vitro binding of HSV gD to sV(HIgR)-Fc by mAb R1.302 to PRR1 (R1.302,  ), mAb to gD HD1 (HD1,  ), or purified mouse IgGs (IgG, x).	bind
48655	9	1018	7	NULL	NULL	0	NULL	statement 7	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_26_15700_s_174	9861033	( B) Competition of the  in vitro binding of HSV gD to sV(HIgR)-Fc by mAb R1.302 to PRR1 (R1.302,  ), mAb to gD HD1 (HD1,  ), or purified mouse IgGs (IgG, x).	bind
676	1	1019	6	NULL	NULL	0	NULL	IAA	NULL		binds	NULL				Insulin	NULL	human	Tyr14A		NULL		0	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
677	2	1019	6	NULL	NULL	0	NULL	Insulin	NULL	human	competes	NULL				Statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
678	3	1019	6	NULL	NULL	0	NULL	Insulin	NULL	human	competes	NULL		B28lysB29pro		Statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
679	4	1019	6	NULL	NULL	0	NULL	Insulin	NULL	human	competes	NULL		A13trpB28lysB29pro		Statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
680	5	1019	6	NULL	NULL	0	NULL	Insulin	NULL	porcine	competes	NULL				Statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
681	6	1019	6	NULL	NULL	0	NULL	Insulin	NULL	sheep	competes	NULL		A8his		Statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
683	7	1019	6	NULL	NULL	0	NULL	Insulin	NULL	fish	competes	NULL				Statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
48542	1	1019	7	NULL	NULL	0	NULL	IAA 	Chemical		bind					 insulin	GP	human	 Tyr14A		NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
48543	2	1019	7	NULL	NULL	0	NULL	IAA	Chemical		bind					insulin	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
48544	3	1019	7	NULL	NULL	0	NULL	IAA	Chemical		bind					proinsulin	GP	human	B28lysB29		NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
48545	4	1019	7	NULL	NULL	0	NULL	IAA	Chemical		bind					pro insulin	GP	human	A13trpB28lysB29		NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
48546	5	1019	7	NULL	NULL	0	NULL	IAA	Chemical		bind					insulin	GP	porcine			NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
48547	6	1019	7	NULL	NULL	0	NULL	IAA	Chemical		bind					insulin	GP	sheep	 A8his		NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
48548	7	1019	7	NULL	NULL	0	NULL	IAA	Chemical		bind					insulin	GP	fish			NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
48575	8	1019	7	NULL	NULL	0	NULL	statement 2	Process		inhibit		competitively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
48576	9	1019	7	NULL	NULL	0	NULL	statement 3	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
48577	10	1019	7	NULL	NULL	0	NULL	statement 4	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
48578	11	1019	7	NULL	NULL	0	NULL	statement 5	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
48579	12	1019	7	NULL	NULL	0	NULL	statement 6	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
48580	13	1019	7	NULL	NULL	0	NULL	statement 7	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_128	15314696	( B) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human insulin (open circles), human B28lysB29pro insulin (open  triangles), human A13trpB28lysB29pro insulin (shaded squares), porcine insulin (shaded  circles), sheep A8his insulin (filled diamonds), and fish insulin (crosses).	bind
684	2	1020	6	10	NULL	0	NULL	calstabin2	NULL	WT	bind	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_129	16481613	( B) Concentration curve of WT calstabin2 vs. calstabin2 - D37V binding to PKA-phosphorylated  RyR2 showed that, at physiologic levels of calstabin2, calstabin2 - D37V exhibited  increased binding to PKA-phosphorylated RyR2 compared with WT calstabin2.	bind
685	3	1020	6	10	NULL	0	NULL	calstabin2 	NULL		bind	NULL		D37V		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_129	16481613	( B) Concentration curve of WT calstabin2 vs. calstabin2 - D37V binding to PKA-phosphorylated  RyR2 showed that, at physiologic levels of calstabin2, calstabin2 - D37V exhibited  increased binding to PKA-phosphorylated RyR2 compared with WT calstabin2.	bind
51491	1	1020	6	10	NULL	0	NULL	RyR2	NULL		is phosphorylated by	NULL				PKA	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_129	16481613	( B) Concentration curve of WT calstabin2 vs. calstabin2 - D37V binding to PKA-phosphorylated  RyR2 showed that, at physiologic levels of calstabin2, calstabin2 - D37V exhibited  increased binding to PKA-phosphorylated RyR2 compared with WT calstabin2.	bind
51492	4	1020	6	10	NULL	0	NULL	statement 3	NULL	affinity of	is higher than	NULL				statement 2	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_129	16481613	( B) Concentration curve of WT calstabin2 vs. calstabin2 - D37V binding to PKA-phosphorylated  RyR2 showed that, at physiologic levels of calstabin2, calstabin2 - D37V exhibited  increased binding to PKA-phosphorylated RyR2 compared with WT calstabin2.	bind
48581	1	1020	7	NULL	NULL	0	NULL	RyR2	GP		is phosphorylated by					PKA	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_129	16481613	( B) Concentration curve of WT calstabin2 vs. calstabin2 - D37V binding to PKA-phosphorylated  RyR2 showed that, at physiologic levels of calstabin2, calstabin2 - D37V exhibited  increased binding to PKA-phosphorylated RyR2 compared with WT calstabin2.	bind
48582	2	1020	7	NULL	NULL	0	NULL	calstabin2	Chemical		bind			D37V		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_129	16481613	( B) Concentration curve of WT calstabin2 vs. calstabin2 - D37V binding to PKA-phosphorylated  RyR2 showed that, at physiologic levels of calstabin2, calstabin2 - D37V exhibited  increased binding to PKA-phosphorylated RyR2 compared with WT calstabin2.	bind
48583	3	1020	7	NULL	NULL	0	NULL	calstabin2	Chemical	WT	bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_129	16481613	( B) Concentration curve of WT calstabin2 vs. calstabin2 - D37V binding to PKA-phosphorylated  RyR2 showed that, at physiologic levels of calstabin2, calstabin2 - D37V exhibited  increased binding to PKA-phosphorylated RyR2 compared with WT calstabin2.	bind
48584	4	1020	7	NULL	NULL	0	NULL	statement 2	Process	affinity of	is higher than					statement 3	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_9_3456_s_129	16481613	( B) Concentration curve of WT calstabin2 vs. calstabin2 - D37V binding to PKA-phosphorylated  RyR2 showed that, at physiologic levels of calstabin2, calstabin2 - D37V exhibited  increased binding to PKA-phosphorylated RyR2 compared with WT calstabin2.	bind
686	1	1023	6	NULL	NULL	0	NULL	CPO	NULL		bind	NULL				CPO-BP	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_17_6195_s_134	15840715	( B) Correlation plot for inhibition of [3]CPO binding to CPO-BP and FP-rhodamine labeling of KIAA1363.	bind
48585	1	1023	7	NULL	NULL	0	NULL	CPO	Chemical		bind					CPO-BP	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_17_6195_s_134	15840715	( B) Correlation plot for inhibition of [3]CPO binding to CPO-BP and FP-rhodamine labeling of KIAA1363.	bind
688	1	1024	6	NULL	NULL	0	NULL	CRSP	NULL		bind	NULL				Ni2+-NTA-agarose resin	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_13_7137_s_80	10377381	( b) CRSP binds to Ni2+-NTA-agarose resin in the presence of competing imidazole.	bind
689	2	1024	6	NULL	NULL	0	NULL	Statement 1	NULL		occurs in presence of	NULL				imidazole	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_13_7137_s_80	10377381	( b) CRSP binds to Ni2+-NTA-agarose resin in the presence of competing imidazole.	bind
48586	1	1024	7	NULL	NULL	0	NULL	CRSP	GP		bind					Ni2+-NTA-agarose resin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_13_7137_s_80	10377381	( b) CRSP binds to Ni2+-NTA-agarose resin in the presence of competing imidazole.	bind
48587	2	1024	7	NULL	NULL	0	NULL	statement 1	Process		in presence of					imidazole	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_13_7137_s_80	10377381	( b) CRSP binds to Ni2+-NTA-agarose resin in the presence of competing imidazole.	bind
690	1	1025	6	10	NULL	0	NULL	Ctf18-Myc	NULL		does not bind	NULL	specifically			telomere VIR	NULL				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_7_1505_s_171	16525505	( B) Ctf18-Myc does not bind specifically to telomere VIR.	bind
48588	1	1025	7	NULL	NULL	0	NULL	Ctf18-Myc	GP		does not bind		specifically			telomere VIR	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_7_1505_s_171	16525505	( B) Ctf18-Myc does not bind specifically to telomere VIR.	bind
691	1	1026	6	NULL	NULL	0	NULL	Cubilin	NULL		bind	NULL				megalin	NULL				NULL	In vitro	NULL	NULL	NULL	NULL	gw70_annurevnutr_21_0_407_s_122	11375443	( b) Cubilin binds in vitro to megalin ( 59).	bind
48589	1	1026	7	NULL	NULL	0	NULL	Cubilin	GP		bind					megalin	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_annurevnutr_21_0_407_s_122	11375443	( b) Cubilin binds in vitro to megalin ( 59).	bind
692	1	1028	6	NULL	NULL	0	NULL	Cdc45	NULL		bind	NULL				chromatin	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_17_9_1141_s_145	12730133	( B) Cut5-dependent binding of Cdc45 and Sld5 to chromatin.	bind
693	2	1028	6	NULL	NULL	0	NULL	Sld5	NULL		bind	NULL				chromatin	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_17_9_1141_s_145	12730133	( B) Cut5-dependent binding of Cdc45 and Sld5 to chromatin.	bind
694	3	1028	6	NULL	NULL	0	NULL	Statement 1	NULL		is dependent on	NULL				Cut5	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_17_9_1141_s_145	12730133	( B) Cut5-dependent binding of Cdc45 and Sld5 to chromatin.	bind
695	4	1028	6	NULL	NULL	0	NULL	statement 2	NULL		is dependent on	NULL				Cut5	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_17_9_1141_s_145	12730133	( B) Cut5-dependent binding of Cdc45 and Sld5 to chromatin.	bind
48590	1	1028	7	NULL	NULL	0	NULL	Cdc45	GP		bind					chromatin	Chromosome				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_9_1141_s_145	12730133	( B) Cut5-dependent binding of Cdc45 and Sld5 to chromatin.	bind
48591	2	1028	7	NULL	NULL	0	NULL	Sld5	GP		bind					chromatin	Chromosome				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_9_1141_s_145	12730133	( B) Cut5-dependent binding of Cdc45 and Sld5 to chromatin.	bind
48592	3	1028	7	NULL	NULL	0	NULL	statement 1	Process		is dependent on					Cut5	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_9_1141_s_145	12730133	( B) Cut5-dependent binding of Cdc45 and Sld5 to chromatin.	bind
48593	4	1028	7	NULL	NULL	0	NULL	statement 2	Process		is dependent on					Cut5	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_9_1141_s_145	12730133	( B) Cut5-dependent binding of Cdc45 and Sld5 to chromatin.	bind
696	1	1029	6	10	NULL	0	NULL	GST-Cdc20p	NULL		bind	NULL				MBP-Hsl1p	NULL		667-872		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_18_2381_s_147	11562348	( B) D box-dependent binding of GST-Cdc20p to MBP-Hsl1p667-872.	bind
697	2	1029	6	NULL	NULL	0	NULL	Statement 1	NULL		is dependent on	NULL					NULL		D box		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_18_2381_s_147	11562348	( B) D box-dependent binding of GST-Cdc20p to MBP-Hsl1p667-872.	bind
48594	1	1029	7	NULL	NULL	0	NULL	GST-Cdc20p	GP		bind					MBP-Hsl1p	GP		667-872		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_18_2381_s_147	11562348	( B) D box-dependent binding of GST-Cdc20p to MBP-Hsl1p667-872.	bind
48595	2	1029	7	NULL	NULL	0	NULL	statement 1	Process		is dependent on									D-box	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_18_2381_s_147	11562348	( B) D box-dependent binding of GST-Cdc20p to MBP-Hsl1p667-872.	bind
698	1	1030	6	10	NULL	0	NULL	d4T triphosphate	NULL		bind	NULL					NULL	 variant	H122G		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_14_3520_s_55	10899107	( B) d4T triphosphate bound to the H122G variant.	bind
48596	1	1030	7	NULL	NULL	0	NULL	d4T triphosphate	Chemical		bind							variant	H122G		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_14_3520_s_55	10899107	( B) d4T triphosphate bound to the H122G variant.	bind
871	1	1032	6	NULL	NULL	0	NULL	Dectin-1	NULL		bind	NULL				S. cerevisiae	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_6_1277_s_70	15729357	( B) Dectin-1 binds  S. cerevisiae and  C. albicans equivalently.	bind
872	2	1032	6	NULL	NULL	0	NULL	Dectin-1	NULL		bind	NULL				C.albicans	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_6_1277_s_70	15729357	( B) Dectin-1 binds  S. cerevisiae and  C. albicans equivalently.	bind
51493	3	1032	6	10	NULL	0	NULL	statement 1	NULL	affinity of	is equivalent to	NULL				statement 2	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw70_embo_24_6_1277_s_70	15729357	( B) Dectin-1 binds  S. cerevisiae and  C. albicans equivalently.	bind
48597	1	1032	7	NULL	NULL	0	NULL	Dectin-1	GP		bind					S. cerevisiae	Organism				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_6_1277_s_70	15729357	( B) Dectin-1 binds  S. cerevisiae and  C. albicans equivalently.	bind
48598	2	1032	7	NULL	NULL	0	NULL	Dectin-1	GP		bind					C. albicans	Organism				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_6_1277_s_70	15729357	( B) Dectin-1 binds  S. cerevisiae and  C. albicans equivalently.	bind
48599	3	1032	7	NULL	NULL	0	NULL	statement 1	Process	affinity of	is equivalent to					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw70_embo_24_6_1277_s_70	15729357	( B) Dectin-1 binds  S. cerevisiae and  C. albicans equivalently.	bind
699	1	1033	6	NULL	NULL	0	NULL	JIP-1	NULL		bind	NULL				JNK1	NULL				NULL		0	NULL	NULL	NULL	gw60_science_281_5383_1671_s_80	9733513	( B) Deletion analysis of the binding of JIP-1 to JNK1, MKK7, MLK3, and DLK.	bind
700	2	1033	6	NULL	NULL	0	NULL	JIP-1	NULL		bind	NULL				MKK7	NULL				NULL		0	NULL	NULL	NULL	gw60_science_281_5383_1671_s_80	9733513	( B) Deletion analysis of the binding of JIP-1 to JNK1, MKK7, MLK3, and DLK.	bind
701	3	1033	6	NULL	NULL	0	NULL	JIP-1	NULL		bind	NULL				MLK3	NULL				NULL		0	NULL	NULL	NULL	gw60_science_281_5383_1671_s_80	9733513	( B) Deletion analysis of the binding of JIP-1 to JNK1, MKK7, MLK3, and DLK.	bind
702	4	1033	6	NULL	NULL	0	NULL	JIP-1	NULL		bind	NULL				DLK	NULL				NULL		0	NULL	NULL	NULL	gw60_science_281_5383_1671_s_80	9733513	( B) Deletion analysis of the binding of JIP-1 to JNK1, MKK7, MLK3, and DLK.	bind
48600	1	1033	7	NULL	NULL	0	NULL	JIP-1	GP		bind					JNK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_80	9733513	( B) Deletion analysis of the binding of JIP-1 to JNK1, MKK7, MLK3, and DLK.	bind
48601	2	1033	7	NULL	NULL	0	NULL	JIP-1	GP		bind					MKK7	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_80	9733513	( B) Deletion analysis of the binding of JIP-1 to JNK1, MKK7, MLK3, and DLK.	bind
48602	3	1033	7	NULL	NULL	0	NULL	JIP-1	GP		bind					MLK3	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_80	9733513	( B) Deletion analysis of the binding of JIP-1 to JNK1, MKK7, MLK3, and DLK.	bind
48603	4	1033	7	NULL	NULL	0	NULL	JIP-1	GP		bind					DLK	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_80	9733513	( B) Deletion analysis of the binding of JIP-1 to JNK1, MKK7, MLK3, and DLK.	bind
704	2	1034	6	10	NULL	0	NULL	CFTR	NULL		bind	NULL	efficiently	deltaF508 		GST-syn1AdeltaC	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_18_10972_s_157	9724814	( B) deltaF508 CFTR binds efficiently to GST-syn1AdeltaC when this mutant is processed at reduced temperature (see text for details).	bind
48604	1	1034	7	NULL	NULL	0	NULL	CFTR	GP		bind		efficiently	deltaF508		GST-syn1AdeltaC	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_18_10972_s_157	9724814	( B) deltaF508 CFTR binds efficiently to GST-syn1AdeltaC when this mutant is processed at reduced temperature (see text for details).	bind
705	1	1035	6	10	NULL	0	NULL	PICK1	NULL		bind	NULL		deltaNT 		GluR2	NULL		C-terminus		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_18_3266_s_81	16138078	( B) deltaNT PICK1 binds GluR2 C-terminus at maximal level in all [Ca2+]free tested.	bind
48606	1	1035	7	NULL	NULL	0	NULL	PICK1	GP		bind			deltaNT		 GluR2 	GP		C-terminus 		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_18_3266_s_81	16138078	( B) deltaNT PICK1 binds GluR2 C-terminus at maximal level in all [Ca2+]free tested.	bind
706	1	1036	6	NULL	NULL	0	NULL	GAPDH	NULL		bind	NULL				Siah1	NULL				NULL	MPTP treated mouse striatum	NULL	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_67	16505364	( b) Deprenyl (DEP) inhibits the binding of GAPDH and Siah1 in MPTP treated mouse striatum.	bind
707	2	1036	6	10	NULL	0	NULL	DEP	NULL		inhibits	NULL				Statement 1	NULL				NULL	MPTP treated mouse striatum	NULL	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_67	16505364	( b) Deprenyl (DEP) inhibits the binding of GAPDH and Siah1 in MPTP treated mouse striatum.	bind
51494	3	1036	6	10	NULL	0	NULL	DEP	NULL		is	NULL				Deprenyl 	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_67	16505364	( b) Deprenyl (DEP) inhibits the binding of GAPDH and Siah1 in MPTP treated mouse striatum.	bind
48607	1	1036	7	3	NULL	0	NULL	GAPDH	GP		bind					Siah1	GP				NULL	MPTP treated mouse striatum	NULL	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_67	16505364	( b) Deprenyl (DEP) inhibits the binding of GAPDH and Siah1 in MPTP treated mouse striatum.	bind
48608	2	1036	7	NULL	NULL	0	NULL	DEP	Chemical		inhibit					statement 1	GP				NULL	MPTP treated mouse striatum	NULL	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_67	16505364	( b) Deprenyl (DEP) inhibits the binding of GAPDH and Siah1 in MPTP treated mouse striatum.	bind
48609	3	1036	7	NULL	NULL	0	NULL	DEP	Chemical		is					Deprenyl	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_67	16505364	( b) Deprenyl (DEP) inhibits the binding of GAPDH and Siah1 in MPTP treated mouse striatum.	bind
708	1	1037	6	NULL	NULL	0	NULL	GAPDH	NULL		bind	NULL				Siah1	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_39	16505364	( b) Deprenyl inhibits the binding of GAPDH and Siah1.	bind
709	2	1037	6	NULL	NULL	0	NULL	Deprenyl	NULL		inhibits	NULL				Statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_39	16505364	( b) Deprenyl inhibits the binding of GAPDH and Siah1.	bind
48610	1	1037	7	NULL	NULL	0	NULL	GAPDH	GP		bind					Siah1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_39	16505364	( b) Deprenyl inhibits the binding of GAPDH and Siah1.	bind
48611	2	1037	7	NULL	NULL	0	NULL	Deprenyl	Chemical		inhibit					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_39	16505364	( b) Deprenyl inhibits the binding of GAPDH and Siah1.	bind
710	1	1039	6	NULL	NULL	0	NULL	BRCA1	NULL	purified	bind	NULL				STAT1alpha	NULL		C-terminus		NULL		0	NULL	NULL	NULL	gw60_pnas_97_10_5208_s_167	10792030	( B) Detection of binding of purified BRCA1 to STAT1alpha C terminus.	bind
48612	1	1039	7	NULL	NULL	0	NULL	BRCA1	GP	purified	bind					STAT1alpha	GP		C terminus		NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_10_5208_s_167	10792030	( B) Detection of binding of purified BRCA1 to STAT1alpha C terminus.	bind
711	1	1042	6	NULL	NULL	0	NULL	NHERF 	NULL		bind	NULL				beta2 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_15_8496_s_110	9671706	( B) Determination of the binding affinity of NHERF for the beta2 receptor and P2Y1 receptor tails.	bind
712	2	1042	6	10	NULL	0	NULL	NHERF 	NULL		bind	NULL				P2Y1 receptor	NULL		 tails		NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_15_8496_s_110	9671706	( B) Determination of the binding affinity of NHERF for the beta2 receptor and P2Y1 receptor tails.	bind
48613	1	1042	7	NULL	NULL	0	NULL	NHERF	GP		bind					beta2 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_15_8496_s_110	9671706	( B) Determination of the binding affinity of NHERF for the beta2 receptor and P2Y1 receptor tails.	bind
48614	2	1042	7	NULL	NULL	0	NULL	NHERF	GP		bind					P2Y1 receptor	GP		tails		NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_15_8496_s_110	9671706	( B) Determination of the binding affinity of NHERF for the beta2 receptor and P2Y1 receptor tails.	bind
713	1	1043	6	NULL	NULL	0	NULL	UL28 protein	NULL		bind	NULL				pac1* DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_98_6_3086_s_155	11248036	( B) Determination of the binding affinity of UL28 protein for  pac1* DNA.	bind
48615	1	1043	7	NULL	NULL	0	NULL	UL28 protein	GP		bind					pac1* DNA	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_6_3086_s_155	11248036	( B) Determination of the binding affinity of UL28 protein for  pac1* DNA.	bind
714	1	1044	6	NULL	NULL	0	NULL	GGA3	NULL		bind	NULL		VHS (Vps27, Hrs, Stam) domain		cargo proteins	NULL				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_19_4423_s_26	16977309	( B) Diagram of GGA3 showing the VHS (Vps27, Hrs, Stam) domain, which binds to cargo  proteins, the GAT (GGA and TOM) domain, which binds to ARF1, the hinge segment, which  contains the autoregulatory acidic-dileucine motif and Ser388, and the GAE (gamma-adaptin ear) domain (Bonifacino, 2004) and GGA3 cargo.	bind
716	2	1044	6	NULL	NULL	0	NULL	GGA3	NULL		 bind	NULL		GAT (GGA and TOM) domain		ARF1	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_25_19_4423_s_26	16977309	( B) Diagram of GGA3 showing the VHS (Vps27, Hrs, Stam) domain, which binds to cargo  proteins, the GAT (GGA and TOM) domain, which binds to ARF1, the hinge segment, which  contains the autoregulatory acidic-dileucine motif and Ser388, and the GAE (gamma-adaptin ear) domain (Bonifacino, 2004) and GGA3 cargo.	bind
48618	1	1044	7	NULL	NULL	0	NULL	 GGA3	GP		bind			VHS domain		cargo proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_19_4423_s_26	16977309	( B) Diagram of GGA3 showing the VHS (Vps27, Hrs, Stam) domain, which binds to cargo  proteins, the GAT (GGA and TOM) domain, which binds to ARF1, the hinge segment, which  contains the autoregulatory acidic-dileucine motif and Ser388, and the GAE (gamma-adaptin ear) domain (Bonifacino, 2004) and GGA3 cargo.	bind
48619	2	1044	7	NULL	NULL	0	NULL	GGA3	GP		bind			GAT domain		ARF1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_19_4423_s_26	16977309	( B) Diagram of GGA3 showing the VHS (Vps27, Hrs, Stam) domain, which binds to cargo  proteins, the GAT (GGA and TOM) domain, which binds to ARF1, the hinge segment, which  contains the autoregulatory acidic-dileucine motif and Ser388, and the GAE (gamma-adaptin ear) domain (Bonifacino, 2004) and GGA3 cargo.	bind
48620	3	1044	7	NULL	NULL	0	NULL	GGA3	GP		contains			hinge segment				autoregulatory	acidic-dileucine motif 		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_19_4423_s_26	16977309	( B) Diagram of GGA3 showing the VHS (Vps27, Hrs, Stam) domain, which binds to cargo  proteins, the GAT (GGA and TOM) domain, which binds to ARF1, the hinge segment, which  contains the autoregulatory acidic-dileucine motif and Ser388, and the GAE (gamma-adaptin ear) domain (Bonifacino, 2004) and GGA3 cargo.	bind
48621	4	1044	7	NULL	NULL	0	NULL	GGA3	GP		bind			hinge segment					Ser388		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_19_4423_s_26	16977309	( B) Diagram of GGA3 showing the VHS (Vps27, Hrs, Stam) domain, which binds to cargo  proteins, the GAT (GGA and TOM) domain, which binds to ARF1, the hinge segment, which  contains the autoregulatory acidic-dileucine motif and Ser388, and the GAE (gamma-adaptin ear) domain (Bonifacino, 2004) and GGA3 cargo.	bind
48622	5	1044	7	NULL	NULL	0	NULL	GGA3	GP		contains			hinge segment						GAE domain	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_19_4423_s_26	16977309	( B) Diagram of GGA3 showing the VHS (Vps27, Hrs, Stam) domain, which binds to cargo  proteins, the GAT (GGA and TOM) domain, which binds to ARF1, the hinge segment, which  contains the autoregulatory acidic-dileucine motif and Ser388, and the GAE (gamma-adaptin ear) domain (Bonifacino, 2004) and GGA3 cargo.	bind
48623	6	1044	7	NULL	NULL	0	NULL	GGA3	GP		bind			hinge segment		GGA3 cargo	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_19_4423_s_26	16977309	( B) Diagram of GGA3 showing the VHS (Vps27, Hrs, Stam) domain, which binds to cargo  proteins, the GAT (GGA and TOM) domain, which binds to ARF1, the hinge segment, which  contains the autoregulatory acidic-dileucine motif and Ser388, and the GAE (gamma-adaptin ear) domain (Bonifacino, 2004) and GGA3 cargo.	bind
48624	7	1044	7	NULL	NULL	0	NULL	GAE domain	GP		is					gamma-adaptin ear domain	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_19_4423_s_26	16977309	( B) Diagram of GGA3 showing the VHS (Vps27, Hrs, Stam) domain, which binds to cargo  proteins, the GAT (GGA and TOM) domain, which binds to ARF1, the hinge segment, which  contains the autoregulatory acidic-dileucine motif and Ser388, and the GAE (gamma-adaptin ear) domain (Bonifacino, 2004) and GGA3 cargo.	bind
718	1	1045	6	NULL	NULL	0	NULL	FtsZ peptide	NULL		bind	NULL				ZipA/M185	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_19_13_3179_s_297	10880432	( B) Difference electron density in the region of the FtsZ peptide bound to ZipA/M185.	bind
48616	1	1045	7	NULL	NULL	0	NULL	FtsZ peptide	GP		bind					 ZipA/M185	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_13_3179_s_297	10880432	( B) Difference electron density in the region of the FtsZ peptide bound to ZipA/M185.	bind
48617	1	1046	7	NULL	NULL	0	NULL	H3	GP	Dimethylation of	diminishes			 lysine 9		TRX 	GP	binding of	SET		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_17_2197_s_106	11544176	( B) Dimethylation of histone H3 on lysine 9 diminishes TRX SET binding.	bind
51495	2	1046	7	NULL	NULL	0	NULL	H3	GP		is a type of					histone	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_17_2197_s_106	11544176	( B) Dimethylation of histone H3 on lysine 9 diminishes TRX SET binding.	bind
812	1	1047	6	NULL	NULL	0	NULL	DinI	NULL		bind	NULL				RecA	NULL	activated			NULL		0	NULL	NULL	NULL	gw60_embo_20_5_1192_s_77	11230142	( B) DinI binds to activated RecA.	bind
48625	1	1047	7	NULL	NULL	0	NULL	DinI	GP		bind					RecA	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_5_1192_s_77	11230142	( B) DinI binds to activated RecA.	bind
875	2	1048	6	10	NULL	0	NULL	p50	NULL		bind	NULL					NULL			p50-specific DNA half site	NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_16_9268_s_158	12886018	( b) Direct  base-specific hydrogen-bonding contacts between p50 and p50-specific [[ DNA  half  site ]] observed in the x-ray structure of p50 homodimer bound to MHC-kappaB  DNA. ( c) Stacking interactions between residues in the linker (P243  and K241) and RNA bases  (G8 and G22) shown by van der  Waals surface model.	bind
877	1	1048	6	10	NULL	0	NULL	p50 homodimer	NULL		bind	NULL				MHC-kappaB DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_16_9268_s_158	12886018	( b) Direct  base-specific hydrogen-bonding contacts between p50 and p50-specific [[ DNA  half  site ]] observed in the x-ray structure of p50 homodimer bound to MHC-kappaB  DNA. ( c) Stacking interactions between residues in the linker (P243  and K241) and RNA bases  (G8 and G22) shown by van der  Waals surface model.	bind
879	3	1048	6	10	NULL	0	NULL		NULL		interact	NULL		l	inker residues (P243 and K241)		NULL			\tRNA bases (G8 and G22)	NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_16_9268_s_158	12886018	( b) Direct  base-specific hydrogen-bonding contacts between p50 and p50-specific [[ DNA  half  site ]] observed in the x-ray structure of p50 homodimer bound to MHC-kappaB  DNA. ( c) Stacking interactions between residues in the linker (P243  and K241) and RNA bases  (G8 and G22) shown by van der  Waals surface model.	bind
48626	1	1048	7	NULL	NULL	0	NULL	p50 homodimer	GP		bind					MHC-kappaB DNA	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_16_9268_s_158	12886018	( b) Direct  base-specific hydrogen-bonding contacts between p50 and p50-specific [[ DNA  half  site ]] observed in the x-ray structure of p50 homodimer bound to MHC-kappaB  DNA. ( c) Stacking interactions between residues in the linker (P243  and K241) and RNA bases  (G8 and G22) shown by van der  Waals surface model.	bind
48627	2	1048	7	NULL	NULL	0	NULL	p50	GP		bind									p50-specific DNA half site	NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_16_9268_s_158	12886018	( b) Direct  base-specific hydrogen-bonding contacts between p50 and p50-specific [[ DNA  half  site ]] observed in the x-ray structure of p50 homodimer bound to MHC-kappaB  DNA. ( c) Stacking interactions between residues in the linker (P243  and K241) and RNA bases  (G8 and G22) shown by van der  Waals surface model.	bind
48628	3	1048	7	10	NULL	0	NULL		NULL		interacts with	NULL			\tlinker residues (P243 and K241)		NULL			\tRNA bases (G8 and G22)	NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_16_9268_s_158	12886018	( b) Direct  base-specific hydrogen-bonding contacts between p50 and p50-specific [[ DNA  half  site ]] observed in the x-ray structure of p50 homodimer bound to MHC-kappaB  DNA. ( c) Stacking interactions between residues in the linker (P243  and K241) and RNA bases  (G8 and G22) shown by van der  Waals surface model.	bind
813	1	1049	6	NULL	NULL	0	NULL	Arp2/3	NULL		bind	NULL				GST-control	NULL		region fragments		NULL		0	NULL	NULL	NULL	gw60_science_290_5492_801_s_76	11052943	( B) Direct binding of Arp2/3 to GST fusions of  control region fragments ( 27).	bind
48629	1	1049	7	NULL	NULL	0	NULL	Arp2/3	GP		bind		directly						control region fragments		NULL		NULL	NULL	NULL	NULL	gw60_science_290_5492_801_s_76	11052943	( B) Direct binding of Arp2/3 to GST fusions of  control region fragments ( 27).	bind
814	1	1050	6	10	NULL	0	NULL	Pbs2	NULL		bind	NULL	directly	RSD-1		Ssk2	NULL		kinase domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_22_14_3624_s_142	12853477	( B) Direct binding of Pbs2 RSD-I to the Ssk2 kinase domain.	bind
48630	1	1050	7	NULL	NULL	0	NULL	Pbs2 	GP		bind		directly	RSD-I		 Ssk2	GP		kinase domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_22_14_3624_s_142	12853477	( B) Direct binding of Pbs2 RSD-I to the Ssk2 kinase domain.	bind
815	1	1051	6	10	NULL	0	NULL	GST-Lyn 	NULL	purified	bind	NULL	directly	SH3		integrin beta proteins	NULL		cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_23_13298_s_182	14593208	( B) Direct binding of purified GST-Lyn SH3 to integrin beta cytoplasmic tail proteins, assessed by ELISA: beta1A ( ), beta2( ), beta3( ), rbeta1A ( ), and rbeta3( ).	bind
48631	1	1051	7	NULL	NULL	0	NULL	GST-Lyn 	GP	purified	bind		directly	SH3		integrin beta proteins	GP		 cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_23_13298_s_182	14593208	( B) Direct binding of purified GST-Lyn SH3 to integrin beta cytoplasmic tail proteins, assessed by ELISA: beta1A ( ), beta2( ), beta3( ), rbeta1A ( ), and rbeta3( ).	bind
816	1	1052	6	NULL	NULL	0	NULL	DM	NULL		bind	NULL				DR	NULL				NULL	cell surface	0	NULL	NULL	NULL	gw60_embo_19_6_1241_s_61	10716924	( B) DM is bound to DR on the cell surface.	bind
48632	1	1052	7	NULL	NULL	0	NULL	DM	GP		bind					DR	GP				NULL	cell surface	NULL	NULL	NULL	NULL	gw60_embo_19_6_1241_s_61	10716924	( B) DM is bound to DR on the cell surface.	bind
817	1	1053	6	10	NULL	0	NULL	DN-14-3-3	NULL		bind	NULL				14-3-3zeta	NULL	native;;WT			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_3_349_s_48	10654934	( B) DN-14-3-3  binds to native WT-14-3-3zeta.	bind
48633	1	1053	7	NULL	NULL	0	NULL	DN-14-3-3	GP		bind					14-3-3zeta	GP	native;;WT			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_3_349_s_48	10654934	( B) DN-14-3-3  binds to native WT-14-3-3zeta.	bind
818	1	1054	6	NULL	NULL	0	NULL	RNAP components	NULL		bind	NULL				psbA2 DNA	NULL			upstream region	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_21_4658_s_153	12409456	( B) DNA binding of RNAP components to the  psbA2 upstream region.	bind
48634	1	1054	7	NULL	NULL	0	NULL	RNAP components	GP		bind					psbA2 DNA	GP			upstream region	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_21_4658_s_153	12409456	( B) DNA binding of RNAP components to the  psbA2 upstream region.	bind
819	1	1058	6	NULL	NULL	0	NULL	OhrR	NULL		bind	NULL				ohrA	NULL			Promoter	NULL		0	NULL	NULL	NULL	gw60_pnas_99_10_6690_s_115	11983871	( B) DNase I footprinting analysis of OhrR binding to the  ohrA (lanes 1-9) and  ohrA* (lanes 10-18) promoters.	bind
48635	1	1058	7	NULL	NULL	0	NULL	OhrR	GP		bind					ohrA	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_10_6690_s_115	11983871	( B) DNase I footprinting analysis of OhrR binding to the  ohrA (lanes 1-9) and  ohrA* (lanes 10-18) promoters.	bind
821	1	1059	6	NULL	NULL	0	NULL	TFIID	NULL		bind	NULL				joc	NULL			Promoter	NULL		0	NULL	NULL	NULL	gw60_genesdev_11_22_3020_s_53	9367984	( B) DNase I footprinting analysis of the binding of TFIID to the  joc promoter.	bind
48636	1	1059	7	NULL	NULL	0	NULL	TFIID 	GP		bind					joc	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_22_3020_s_53	9367984	( B) DNase I footprinting analysis of the binding of TFIID to the  joc promoter.	bind
822	1	1060	6	NULL	NULL	0	NULL	Dnmt3a	NULL		bind	NULL		PDH-like motif		H3 methylase	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_9_2305_s_85	12711675	( B) Dnmt3a binds H3 methylase activity through its conserved PDH-like motif.	bind
48637	1	1060	7	NULL	NULL	0	NULL	Dnmt3a	GP		bind			conserved PDH-like motif		H3 methylase	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_9_2305_s_85	12711675	( B) Dnmt3a binds H3 methylase activity through its conserved PDH-like motif.	bind
823	1	1061	6	10	NULL	0	NULL	Dnmt3L	NULL		bind	NULL				HDAC1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_17_3831_s_39	12202768	( B) Dnmt3L binds the histone deacetylase HDAC1 in GST pull-down experiments.	bind
51498	2	1061	6	10	NULL	0	NULL	HDAC1	NULL		is a type of	NULL				histone deacetylase	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_17_3831_s_39	12202768	( B) Dnmt3L binds the histone deacetylase HDAC1 in GST pull-down experiments.	bind
48638	1	1061	7	NULL	NULL	0	NULL	Dnmt3L	GP		bind					HDAC1 	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_17_3831_s_39	12202768	( B) Dnmt3L binds the histone deacetylase HDAC1 in GST pull-down experiments.	bind
48639	2	1061	7	NULL	NULL	0	NULL	HDAC1	GP		is a type of					histone deacetylase	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_17_3831_s_39	12202768	( B) Dnmt3L binds the histone deacetylase HDAC1 in GST pull-down experiments.	bind
824	1	1062	6	NULL	NULL	0	NULL	CDCA	NULL		bind	NULL				FXR	NULL				NULL		0	NULL	NULL	NULL	gw60_science_284_5418_1365_s_66	10334993	( B) Dose response analysis of CDCA binding to FXR.	bind
48640	1	1062	7	NULL	NULL	0	NULL	CDCA	GP		bind					FXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5418_1365_s_66	10334993	( B) Dose response analysis of CDCA binding to FXR.	bind
825	1	1063	6	10	NULL	0	NULL	CD1d	NULL		bind	NULL	dose dependently			PI	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_29_10685_s_88	15243159	( b) Dose-dependency of CD1d binding to PI.	bind
48641	1	1063	7	NULL	NULL	0	NULL	CD1d	GP		bind		dose-dependently			PI	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_29_10685_s_88	15243159	( b) Dose-dependency of CD1d binding to PI.	bind
826	1	1064	6	10	NULL	0	NULL	mAb 146B7	NULL	biotinylated	bind	NULL	dose dependently			statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_112_10_1571_s_135	14617758	( b) Dose-dependent binding of biotinylated mAb 146B7 (filled squares) to IL-15 bound  to Raji lymphoma cells expressing IL-15Ralpha was shown by flow cytometry.	bind
827	2	1064	6	NULL	NULL	0	NULL	Raji lymphoma cells	NULL		express	NULL				IL-15Ralpha	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_112_10_1571_s_135	14617758	( b) Dose-dependent binding of biotinylated mAb 146B7 (filled squares) to IL-15 bound  to Raji lymphoma cells expressing IL-15Ralpha was shown by flow cytometry.	bind
51499	3	1064	6	10	NULL	0	NULL	IL-15	NULL		bind	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_112_10_1571_s_135	14617758	( b) Dose-dependent binding of biotinylated mAb 146B7 (filled squares) to IL-15 bound  to Raji lymphoma cells expressing IL-15Ralpha was shown by flow cytometry.	bind
48642	3	1064	7	NULL	NULL	0	NULL	mAb 146B7	GP	biotinylated 	bind		dose-dependently			statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_112_10_1571_s_135	14617758	( b) Dose-dependent binding of biotinylated mAb 146B7 (filled squares) to IL-15 bound  to Raji lymphoma cells expressing IL-15Ralpha was shown by flow cytometry.	bind
48643	1	1064	7	NULL	NULL	0	NULL	Raji lymphoma cells	Cell		express					IL-15Ralpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_112_10_1571_s_135	14617758	( b) Dose-dependent binding of biotinylated mAb 146B7 (filled squares) to IL-15 bound  to Raji lymphoma cells expressing IL-15Ralpha was shown by flow cytometry.	bind
48644	2	1064	7	NULL	NULL	0	NULL	IL-15	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_112_10_1571_s_135	14617758	( b) Dose-dependent binding of biotinylated mAb 146B7 (filled squares) to IL-15 bound  to Raji lymphoma cells expressing IL-15Ralpha was shown by flow cytometry.	bind
828	1	1065	6	10	NULL	0	NULL	CFTR	NULL	recombinant;;wild-type	bind	NULL	dose dependently			GST-syn1AH3	NULL	isolated	H3 domain		NULL	COS 7 cell lysates	NULL	NULL	NULL	NULL	gw60_pnas_95_18_10972_s_131	9724814	( B) Dose-dependent binding of CFTR to isolated H3 domain (GST-syn1AH3) in pull-down assay performed on COS 7 cell lysates expressing recombinant wild-type CFTR.	bind
48645	1	1065	7	NULL	NULL	0	NULL	CFTR	GP	recombinant;;wild-type	bind		dose dependently			GST-syn1AH3	GP	isolated	H3 domain		NULL	COS 7 cell lysates	NULL	NULL	NULL	NULL	gw60_pnas_95_18_10972_s_131	9724814	( B) Dose-dependent binding of CFTR to isolated H3 domain (GST-syn1AH3) in pull-down assay performed on COS 7 cell lysates expressing recombinant wild-type CFTR.	bind
829	1	1066	6	NULL	NULL	0	NULL	IP3	NULL		bind	NULL					NULL		PH domain		NULL		0	NULL	NULL	NULL	gw60_science_284_5419_1527_s_34	10348740	( B) Dose-dependent inhibition ( ) of PIP2 binding of the PH domain (2 muM) and estimated IP3 binding to the PH domain ( ) ( n = 3).	bind
830	2	1066	6	NULL	NULL	0	NULL	PIP2	NULL		bind	NULL					NULL		PH domain		NULL		0	NULL	NULL	NULL	gw60_science_284_5419_1527_s_34	10348740	( B) Dose-dependent inhibition ( ) of PIP2 binding of the PH domain (2 muM) and estimated IP3 binding to the PH domain ( ) ( n = 3).	bind
48646	1	1066	7	NULL	NULL	0	NULL	PIP2	GP		bind								PH domain		NULL		NULL	NULL	NULL	NULL	gw60_science_284_5419_1527_s_34	10348740	( B) Dose-dependent inhibition ( ) of PIP2 binding of the PH domain (2 muM) and estimated IP3 binding to the PH domain ( ) ( n = 3).	bind
48647	2	1066	7	NULL	NULL	0	NULL	IP3	Chemical		bind								PH domain		NULL		NULL	NULL	NULL	NULL	gw60_science_284_5419_1527_s_34	10348740	( B) Dose-dependent inhibition ( ) of PIP2 binding of the PH domain (2 muM) and estimated IP3 binding to the PH domain ( ) ( n = 3).	bind
832	1	1067	6	NULL	NULL	0	NULL	Pfu polymerase	NULL		bind	NULL				ssU	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_16_9045_s_127	10430892	( b) Dose-response curve for binding of  Pfu polymerase to ssU.	bind
48648	1	1067	7	NULL	NULL	0	NULL	Pfu polymerase	GP		bind					ssU	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_16_9045_s_127	10430892	( b) Dose-response curve for binding of  Pfu polymerase to ssU.	bind
837	1	1068	6	NULL	NULL	0	NULL	OspA-N40	NULL	FITC-labeled	bind	NULL				TGE	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_106_4_561_s_62	10953031	( b) Dose-response curves are presented for FITC-labeled OspA-N40, OspC, and BSA binding to TGE.	bind
838	2	1068	6	NULL	NULL	0	NULL	OspC	NULL	FITC-labeled	bind	NULL				TGE	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_106_4_561_s_62	10953031	( b) Dose-response curves are presented for FITC-labeled OspA-N40, OspC, and BSA binding to TGE.	bind
839	3	1068	6	NULL	NULL	0	NULL	BSA	NULL	FITC-labeled	bind	NULL				TGE	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_106_4_561_s_62	10953031	( b) Dose-response curves are presented for FITC-labeled OspA-N40, OspC, and BSA binding to TGE.	bind
48649	1	1068	7	NULL	NULL	0	NULL	OspA-N40	GP	FITC-labeled 	bind									TGE	NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_106_4_561_s_62	10953031	( b) Dose-response curves are presented for FITC-labeled OspA-N40, OspC, and BSA binding to TGE.	bind
48650	2	1068	7	NULL	NULL	0	NULL	OspC	GP	FITC-labeled 	bind									TGE	NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_106_4_561_s_62	10953031	( b) Dose-response curves are presented for FITC-labeled OspA-N40, OspC, and BSA binding to TGE.	bind
48651	3	1068	7	NULL	NULL	0	NULL	BSA	GP	FITC-labeled	bind									TGE	NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_106_4_561_s_62	10953031	( b) Dose-response curves are presented for FITC-labeled OspA-N40, OspC, and BSA binding to TGE.	bind
843	3	1069	6	10	NULL	0	NULL	Fibrinogen	NULL		bind	NULL				alphaIIb	NULL	mutant	G972N		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_135	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing the disruptive alphaIIb TM domain mutants G972N, G976L, and G976A and the permissive mutation L983A.	bind
844	7	1069	6	10	NULL	0	NULL	SSA6	NULL		bind	NULL				alphaIIb	NULL	mutant	G976A		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_135	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing the disruptive alphaIIb TM domain mutants G972N, G976L, and G976A and the permissive mutation L983A.	bind
1255	4	1069	6	10	NULL	0	NULL	Fibrinogen	NULL		bind	NULL				alphaIIb	NULL	mutant	G976L		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_135	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing the disruptive alphaIIb TM domain mutants G972N, G976L, and G976A and the permissive mutation L983A.	bind
1256	5	1069	6	10	NULL	0	NULL	Fibrinogen	NULL		bind	NULL				alphaIIb	NULL	mutant	G976A		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_135	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing the disruptive alphaIIb TM domain mutants G972N, G976L, and G976A and the permissive mutation L983A.	bind
1257	6	1069	6	10	NULL	0	NULL	Fibrinogen	NULL		bind	NULL				alphaIIb	NULL	mutant	L983A		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_135	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing the disruptive alphaIIb TM domain mutants G972N, G976L, and G976A and the permissive mutation L983A.	bind
1258	8	1069	6	NULL	NULL	0	NULL	SSA6	NULL	mouse mAb	bind	NULL				alphaIIb	NULL		TM domain mutant L983A		NULL		0	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_135	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing the disruptive alphaIIb TM domain mutants G972N, G976L, and G976A and the permissive mutation L983A.	bind
1259	9	1069	6	NULL	NULL	0	NULL	SSA6	NULL	mouse mAb	bind	NULL				alphaIIb	NULL		TM domain mutant G976L		NULL		0	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_135	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing the disruptive alphaIIb TM domain mutants G972N, G976L, and G976A and the permissive mutation L983A.	bind
1260	10	1069	6	NULL	NULL	0	NULL	SSA6	NULL	mouse mAb	bind	NULL				alphaIIb	NULL		TM domain mutant G972N		NULL		0	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_135	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing the disruptive alphaIIb TM domain mutants G972N, G976L, and G976A and the permissive mutation L983A.	bind
48656	1	1069	7	NULL	NULL	0	NULL	fibrinogen	GP		bind					alphaIIb 	GP	mutant	G972N		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_135	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing the disruptive alphaIIb TM domain mutants G972N, G976L, and G976A and the permissive mutation L983A.	bind
48657	2	1069	7	NULL	NULL	0	NULL	fibrinogen	GP		bind					alphaIIb	GP	mutant	G976L		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_135	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing the disruptive alphaIIb TM domain mutants G972N, G976L, and G976A and the permissive mutation L983A.	bind
48658	3	1069	7	NULL	NULL	0	NULL	fibrinogen	GP		bind					alphaIIb	GP	mutant	G976A		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_135	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing the disruptive alphaIIb TM domain mutants G972N, G976L, and G976A and the permissive mutation L983A.	bind
48659	4	1069	7	NULL	NULL	0	NULL	fibrinogen	GP		bind					alphaIIb	GP	mutant	L983A		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_135	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing the disruptive alphaIIb TM domain mutants G972N, G976L, and G976A and the permissive mutation L983A.	bind
48660	5	1069	7	NULL	NULL	0	NULL	anti-beta3 mouse mAb SSA6 	GP		bind					alphaIIb	GP	mutant	TM domain G972N		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_135	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing the disruptive alphaIIb TM domain mutants G972N, G976L, and G976A and the permissive mutation L983A.	bind
48661	6	1069	7	NULL	NULL	0	NULL	anti-beta3 mouse mAb SSA6	GP		bind					alphaIIb	GP	mutant	TM domain G976L		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_135	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing the disruptive alphaIIb TM domain mutants G972N, G976L, and G976A and the permissive mutation L983A.	bind
48662	7	1069	7	NULL	NULL	0	NULL	anti-beta3 mouse mAb SSA6	GP		bind					alphaIIb	GP	mutant	TM domain G976A		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_135	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing the disruptive alphaIIb TM domain mutants G972N, G976L, and G976A and the permissive mutation L983A.	bind
48663	8	1069	7	NULL	NULL	0	NULL	anti-beta3 mouse mAb SSA6	GP		bind					alphaIIb	GP	mutant	L983A		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_135	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing the disruptive alphaIIb TM domain mutants G972N, G976L, and G976A and the permissive mutation L983A.	bind
845	1	1070	6	NULL	NULL	0	NULL	Fibrinogen	NULL		bind	NULL				alphaIIbbeta3	NULL	human wild type			NULL		0	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_101	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing WT human alphaIIbbeta3 and the alphaIIb mutant G972N.	bind
846	2	1070	6	NULL	NULL	0	NULL	SSA6	NULL	mouse mAb	bind	NULL				alphaIIbbeta3	NULL	human wild type			NULL		0	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_101	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing WT human alphaIIbbeta3 and the alphaIIb mutant G972N.	bind
847	3	1070	6	NULL	NULL	0	NULL	Fibrinogen	NULL		bind	NULL				alphaIIb	NULL	human	TM domain mutant G972N		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_101	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing WT human alphaIIbbeta3 and the alphaIIb mutant G972N.	bind
848	4	1070	6	NULL	NULL	0	NULL	SSA6	NULL	mouse mAb	bind	NULL				alphaIIb	NULL	human	TM domain mutant G972N		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_101	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing WT human alphaIIbbeta3 and the alphaIIb mutant G972N.	bind
48664	1	1070	7	NULL	NULL	0	NULL	cells	Cell		express					alphaIIbbeta3	GP	WT;; human			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_101	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing WT human alphaIIbbeta3 and the alphaIIb mutant G972N.	bind
48665	2	1070	7	NULL	NULL	0	NULL	cells	Cell		express					alphaIIb	GP	mutant	G972N		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_101	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing WT human alphaIIbbeta3 and the alphaIIb mutant G972N.	bind
48666	3	1070	7	NULL	NULL	0	NULL	fibrinogen	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_101	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing WT human alphaIIbbeta3 and the alphaIIb mutant G972N.	bind
48667	4	1070	7	NULL	NULL	0	NULL	fibrinogen	GP		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_101	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing WT human alphaIIbbeta3 and the alphaIIb mutant G972N.	bind
48668	5	1070	7	NULL	NULL	0	NULL	anti-beta3 mouse mAb SSA6	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_101	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing WT human alphaIIbbeta3 and the alphaIIb mutant G972N.	bind
48669	6	1070	7	NULL	NULL	0	NULL	anti-beta3 mouse mAb SSA6	GP		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1424_s_101	15671157	( B) Dot plots of fibrinogen and anti-beta3 mouse mAb SSA6 binding to cells expressing WT human alphaIIbbeta3 and the alphaIIb mutant G972N.	bind
849	1	1071	6	NULL	NULL	0	NULL	HSF	NULL		bind	NULL				H3	NULL	acetylated		heat shock promoter elements	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_23_3003_s_168	11114889	( B) During heat shock, the heat shock transcription factor (HSF) binds to acetylated H3 and H4 residues at the heat shock promoter elements.	bind
851	2	1071	6	NULL	NULL	0	NULL	HSF	NULL		bind	NULL				H4	NULL	acetylated		heat shock promoter elements	NULL		0	NULL	NULL	NULL	gw60_genesdev_14_23_3003_s_168	11114889	( B) During heat shock, the heat shock transcription factor (HSF) binds to acetylated H3 and H4 residues at the heat shock promoter elements.	bind
852	3	1071	6	NULL	NULL	0	NULL	HSF	NULL		is	NULL				heat shock transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_14_23_3003_s_168	11114889	( B) During heat shock, the heat shock transcription factor (HSF) binds to acetylated H3 and H4 residues at the heat shock promoter elements.	bind
48670	1	1071	7	NULL	NULL	0	NULL	HSF	GP		bind					H3 residues	GP	 acetylated		 heat shock promoter element	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_23_3003_s_168	11114889	( B) During heat shock, the heat shock transcription factor (HSF) binds to acetylated H3 and H4 residues at the heat shock promoter elements.	bind
48671	2	1071	7	NULL	NULL	0	NULL	HSF	GP		bind					H4 residues	GP	acetylated		 heat shock promoter element	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_23_3003_s_168	11114889	( B) During heat shock, the heat shock transcription factor (HSF) binds to acetylated H3 and H4 residues at the heat shock promoter elements.	bind
48672	3	1071	7	NULL	NULL	0	NULL	HSF	GP		is					heat shock transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_23_3003_s_168	11114889	( B) During heat shock, the heat shock transcription factor (HSF) binds to acetylated H3 and H4 residues at the heat shock promoter elements.	bind
855	1	1072	6	NULL	NULL	0	NULL	PDGF	NULL		bind	NULL				PDGF-R	NULL				NULL		0	NULL	NULL	NULL	gw60_science_297_5583_948_s_26	12169717	( B) During switch activation, the binding of PDGF to its receptor (PDGF-R) leads to the activation of Ras.	bind
857	2	1072	6	10	NULL	0	NULL	Statement 1	NULL		leads to	NULL				Ras	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw60_science_297_5583_948_s_26	12169717	( B) During switch activation, the binding of PDGF to its receptor (PDGF-R) leads to the activation of Ras.	bind
858	3	1072	6	NULL	NULL	0	NULL	Statement 1	NULL		occurs during	NULL				switch activation	NULL				NULL		0	NULL	NULL	NULL	gw60_science_297_5583_948_s_26	12169717	( B) During switch activation, the binding of PDGF to its receptor (PDGF-R) leads to the activation of Ras.	bind
860	4	1072	6	NULL	NULL	0	NULL	statement 2	NULL		occurs during	NULL				switch activation	NULL				NULL		0	NULL	NULL	NULL	gw60_science_297_5583_948_s_26	12169717	( B) During switch activation, the binding of PDGF to its receptor (PDGF-R) leads to the activation of Ras.	bind
48673	1	1072	7	NULL	NULL	0	NULL	PDGF	GP		bind					PDGF-R	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_297_5583_948_s_26	12169717	( B) During switch activation, the binding of PDGF to its receptor (PDGF-R) leads to the activation of Ras.	bind
48674	2	1072	7	NULL	NULL	0	NULL	statement 1	Process		leads to					Ras	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_science_297_5583_948_s_26	12169717	( B) During switch activation, the binding of PDGF to its receptor (PDGF-R) leads to the activation of Ras.	bind
48675	3	1072	7	NULL	NULL	0	NULL	statement 1	Process		occurs during					switch activation	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_297_5583_948_s_26	12169717	( B) During switch activation, the binding of PDGF to its receptor (PDGF-R) leads to the activation of Ras.	bind
48676	4	1072	7	NULL	NULL	0	NULL	PDGF-R	GP		is					PDGF receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_297_5583_948_s_26	12169717	( B) During switch activation, the binding of PDGF to its receptor (PDGF-R) leads to the activation of Ras.	bind
972	1	1073	6	NULL	NULL	0	NULL	c-Jun	NULL		bind	NULL				TNF	NULL			TRE site	NULL	RAW 264.7 cells	0	NULL	NULL	NULL	gw60_jclininvest_104_4_503_s_214	10449442	( b) E2 treatment of RAW 264.7 cells decreases the binding of c-Jun and JunD to a probe containing an exact copy of the TRE site found in the TNF promoter.	bind
973	2	1073	6	NULL	NULL	0	NULL	JunD	NULL		bind	NULL				TNF	NULL			TRE site	NULL	RAW 264.7 cells	NULL	NULL	NULL	NULL	gw60_jclininvest_104_4_503_s_214	10449442	( b) E2 treatment of RAW 264.7 cells decreases the binding of c-Jun and JunD to a probe containing an exact copy of the TRE site found in the TNF promoter.	bind
1106	3	1073	6	NULL	NULL	0	NULL	E2 	NULL		decreases 	NULL				Statement 1	NULL				NULL	RAW 264.7 cells	NULL	NULL	NULL	NULL	gw60_jclininvest_104_4_503_s_214	10449442	( b) E2 treatment of RAW 264.7 cells decreases the binding of c-Jun and JunD to a probe containing an exact copy of the TRE site found in the TNF promoter.	bind
1107	4	1073	6	NULL	NULL	0	NULL	E2	NULL		decreases 	NULL				Statement 2	NULL				NULL	RAW 264.7 cells	NULL	NULL	NULL	NULL	gw60_jclininvest_104_4_503_s_214	10449442	( b) E2 treatment of RAW 264.7 cells decreases the binding of c-Jun and JunD to a probe containing an exact copy of the TRE site found in the TNF promoter.	bind
48677	1	1073	7	NULL	NULL	0	NULL	c-Jun	GP		bind					TNF	GP			TRE site in promoter	NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_4_503_s_214	10449442	( b) E2 treatment of RAW 264.7 cells decreases the binding of c-Jun and JunD to a probe containing an exact copy of the TRE site found in the TNF promoter.	bind
48678	2	1073	7	NULL	NULL	0	NULL	JunD	GP		bind					TNF	GP			TRE site in promoter	NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_4_503_s_214	10449442	( b) E2 treatment of RAW 264.7 cells decreases the binding of c-Jun and JunD to a probe containing an exact copy of the TRE site found in the TNF promoter.	bind
48679	3	1073	7	NULL	NULL	0	NULL	RAW 264.7 cells	Cell		treated with					E2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_4_503_s_214	10449442	( b) E2 treatment of RAW 264.7 cells decreases the binding of c-Jun and JunD to a probe containing an exact copy of the TRE site found in the TNF promoter.	bind
48680	4	1073	7	NULL	NULL	0	NULL	statement 3	Process		decrease					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_4_503_s_214	10449442	( b) E2 treatment of RAW 264.7 cells decreases the binding of c-Jun and JunD to a probe containing an exact copy of the TRE site found in the TNF promoter.	bind
48681	5	1073	7	NULL	NULL	0	NULL	statement 3	Process		decrease					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_4_503_s_214	10449442	( b) E2 treatment of RAW 264.7 cells decreases the binding of c-Jun and JunD to a probe containing an exact copy of the TRE site found in the TNF promoter.	bind
1003	1	1074	6	NULL	NULL	0	NULL	CRP	NULL		bind	NULL				PAPC	NULL	oxidized			NULL		0	NULL	NULL	NULL	gw60_pnas_99_20_13043_s_108	12244213	( B) Effect of calcium on the binding of CRP to oxidized PAPC.	bind
48682	1	1074	7	NULL	NULL	0	NULL	CRP	GP		bind					PAPC	Chemical	oxidized			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_13043_s_108	12244213	( B) Effect of calcium on the binding of CRP to oxidized PAPC.	bind
1004	1	1075	6	NULL	NULL	0	NULL	OspA	NULL	labeled	bind	NULL				TGE	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_106_4_561_s_71	10953031	( b) Effect of excess unlabeled OspA on the binding of labeled OspA to TGE.	bind
48683	1	1075	7	NULL	NULL	0	NULL	 OspA 	GP	labeled	bind					TGE					NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_106_4_561_s_71	10953031	( b) Effect of excess unlabeled OspA on the binding of labeled OspA to TGE.	bind
1011	1	1076	6	NULL	NULL	0	NULL	nuclear protein	NULL		bind	NULL				oligonucleotide	NULL			GC-box	NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_2_252_s_168	16150893	( B) Effect of mithramycin A on the binding of nuclear proteins to the GC-box oligonucleotide.	bind
48684	1	1076	7	NULL	NULL	0	NULL	nuclear proteins	GP		bind					oligonucleotide	NucleicAcid			GC-box	NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_2_252_s_168	16150893	( B) Effect of mithramycin A on the binding of nuclear proteins to the GC-box oligonucleotide.	bind
1012	1	1078	6	NULL	NULL	0	NULL	GDP	NULL		bind	NULL				Rac1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_9_4826_s_116	10220378	( B) Effect of the DH domain mutant Ras-GRF1(DH(-)) on GDP binding to Rac1.	bind
48685	1	1078	7	NULL	NULL	0	NULL	GDP	Chemical		bind					Rac1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_9_4826_s_116	10220378	( B) Effect of the DH domain mutant Ras-GRF1(DH(-)) on GDP binding to Rac1.	bind
1013	1	1079	6	NULL	NULL	0	NULL	OspA	NULL		bind	NULL				TGE	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_106_4_561_s_214	10953031	( b) Effect of trypsin treatment on OspA binding to TGE.	bind
48686	1	1079	7	NULL	NULL	0	NULL	OspA	GP		bind					TGE	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_106_4_561_s_214	10953031	( b) Effect of trypsin treatment on OspA binding to TGE.	bind
1867	2	1080	6	10	NULL	0	NULL	cabin1	NULL		associate with	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_12_2104_s_184	15902271	( B) Effects of calcium and CaMKIV on association of Cabin1 with MEF2 bound to the endogenous  IL-2 promoter.	bind
1868	1	1080	6	10	NULL	0	NULL	MEF2	NULL		bind	NULL				IL-2	NULL	endogenous		promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_24_12_2104_s_184	15902271	( B) Effects of calcium and CaMKIV on association of Cabin1 with MEF2 bound to the endogenous  IL-2 promoter.	bind
48687	1	1080	7	NULL	NULL	0	NULL	MEF2	GP		bind					IL-2	GP	endogenous		promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_24_12_2104_s_184	15902271	( B) Effects of calcium and CaMKIV on association of Cabin1 with MEF2 bound to the endogenous  IL-2 promoter.	bind
48688	2	1080	7	NULL	NULL	0	NULL	Cabin1	GP		associate with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_12_2104_s_184	15902271	( B) Effects of calcium and CaMKIV on association of Cabin1 with MEF2 bound to the endogenous  IL-2 promoter.	bind
1041	1	1081	6	NULL	NULL	0	NULL	PCNA	NULL		bind	NULL				GST-pol	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_23_19_3886_s_215	15359278	( B) Effects of different salt concentrations on the binding of PCNA to GST-pol  (left) and on PCNA elution from GST-pol  (right).	bind
48689	1	1081	7	NULL	NULL	0	NULL	 PCNA	GP		bind					GST-pol	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_19_3886_s_215	15359278	( B) Effects of different salt concentrations on the binding of PCNA to GST-pol  (left) and on PCNA elution from GST-pol  (right).	bind
58423	1	1082	7	NULL	NULL	0	NULL	forskolin	GP		induce					CREB	GP	activation dependent on			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_7_3652_s_118	10097092	( B) Effects of p/CIP holoprotein and p/CIP ligand binding interaction domain on forskolin-induced CREB-dependent activation as described ( 3).	bind
1042	1	1083	6	NULL	NULL	0	NULL	Dsk2p	NULL		bind	NULL				polyubiquitin	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_2_745_s_137	11805328	( B) Effects of Ub lysine mutants on binding between Dsk2p and polyubiquitin.	bind
48691	1	1083	7	NULL	NULL	0	NULL	Dsk2p	GP		bind					polyubiquitin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_745_s_137	11805328	( B) Effects of Ub lysine mutants on binding between Dsk2p and polyubiquitin.	bind
1043	1	1084	6	NULL	NULL	0	NULL	TVA-EGF	NULL		bind	NULL				M5 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_12_7063_s_90	9618539	( B) EGF competes for TVA-EGF binding to M5 cells.	bind
1044	2	1084	6	10	NULL	0	NULL	EGF	NULL		bind	NULL				M5 cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_12_7063_s_90	9618539	( B) EGF competes for TVA-EGF binding to M5 cells.	bind
51518	3	1084	6	10	NULL	0	NULL	statement 2	NULL		competes with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_12_7063_s_90	9618539	( B) EGF competes for TVA-EGF binding to M5 cells.	bind
48692	1	1084	7	NULL	NULL	0	NULL	TVA-EGF	GP		bind					M5 cells	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_12_7063_s_90	9618539	( B) EGF competes for TVA-EGF binding to M5 cells.	bind
48693	2	1084	7	NULL	NULL	0	NULL	EGF 	GP		bind					M5 cells	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_12_7063_s_90	9618539	( B) EGF competes for TVA-EGF binding to M5 cells.	bind
48694	3	1084	7	NULL	NULL	0	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_12_7063_s_90	9618539	( B) EGF competes for TVA-EGF binding to M5 cells.	bind
1045	1	1088	6	10	NULL	0	NULL	Desrt	NULL	recombinant	bind	NULL		ARID domain		(TTA)9 oligonucleotide	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genomeres_11_8_1327_s_38	11483573	( B) Electrophoretic mobility shift assay (EMSA) of recombinant Desrt-ARID domain binding to a (TTA)9 oligonucleotide (lane  3).	bind
48695	1	1088	7	NULL	NULL	0	NULL	Desrt	GP	recombinant	bind			ARID domain 		(TTA)9 oligonucleotide	GP				NULL		NULL	NULL	NULL	NULL	gw60_genomeres_11_8_1327_s_38	11483573	( B) Electrophoretic mobility shift assay (EMSA) of recombinant Desrt-ARID domain binding to a (TTA)9 oligonucleotide (lane  3).	bind
1046	1	1090	6	10	NULL	0	NULL	CBFA1	NULL		bind	NULL				OSE2 oligonucleotide	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_9_2254_s_260	11331591	( B) Electrophoretic mobility shift assays show CBFA1 binding to an OSE2 oligonucleotide, both in the absence or presence of Smad3 and Smad4.	bind
48696	1	1090	7	NULL	NULL	0	NULL	CBFA1	GP		bind					OSE2 oligonucleotide	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_9_2254_s_260	11331591	( B) Electrophoretic mobility shift assays show CBFA1 binding to an OSE2 oligonucleotide, both in the absence or presence of Smad3 and Smad4.	bind
1077	1	1091	6	10	NULL	0	NULL	MEF2C	NULL		bind	NULL				PGC-1 alpha	NULL	putative		MEF2 sites in proximal promotor of	NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_4_1711_s_155	12578979	( B) Electrophoretic mobility-shift assay for binding of MEF2C to the putative MEF2 sites  of the 3.1-kb proximal  PGC-1alpha promoter.	bind
48697	1	1091	7	NULL	NULL	0	NULL	MEF2C	GP		bind					PGC-1alpha	GP	putative		MEF2 sites in proximal promotor of	NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_4_1711_s_155	12578979	( B) Electrophoretic mobility-shift assay for binding of MEF2C to the putative MEF2 sites  of the 3.1-kb proximal  PGC-1alpha promoter.	bind
831	1	1092	5	10	NULL	0	NULL	MEF2C	GP		bind					PGC-1alpha	GP			putative MEF2 sites of proximal promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_4_1711_s_155	12578979	( B) Electrophoretic mobility-shift assay for binding of MEF2C to the putative MEF2 sites of the 3.1-kb proximal  PGC-1alpha promoter.	bind
217	1	1092	7	10	NULL	0	NULL	MEF2C	GP		bind					PGC-1alpha 	GP			putative MEF2 sites of proximal promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_4_1711_s_155	12578979	( B) Electrophoretic mobility-shift assay for binding of MEF2C to the putative MEF2 sites of the 3.1-kb proximal  PGC-1alpha promoter.	bind
833	1	1093	5	10	NULL	0	NULL	Ab	GP		bind					BDNF	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_25_14702_s_48	11724927	( B) ELISA demonstrating the reduced binding of the Ab to BDNF after modification with the caging group and its successful reactivation by UV light.	bind
48715	2	1093	5	10	NULL	0	NULL	statement 1	Process		occurs after					caging group	Process	modification with			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_25_14702_s_48	11724927	( B) ELISA demonstrating the reduced binding of the Ab to BDNF after modification with the caging group and its successful reactivation by UV light.	bind
48716	3	1093	5	10	NULL	0	NULL	UV light			reactivates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_25_14702_s_48	11724927	( B) ELISA demonstrating the reduced binding of the Ab to BDNF after modification with the caging group and its successful reactivation by UV light.	bind
230	1	1093	7	10	NULL	0	NULL	Ab 	GP		bind					BDNF	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_25_14702_s_48	11724927	( B) ELISA demonstrating the reduced binding of the Ab to BDNF after modification with the caging group and its successful reactivation by UV light.	bind
231	2	1093	7	10	NULL	0	NULL	statement 1	Process		occurs after					caging group 	Process	modification with			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_25_14702_s_48	11724927	( B) ELISA demonstrating the reduced binding of the Ab to BDNF after modification with the caging group and its successful reactivation by UV light.	bind
232	3	1093	7	10	NULL	0	NULL	UV light			reactivates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_25_14702_s_48	11724927	( B) ELISA demonstrating the reduced binding of the Ab to BDNF after modification with the caging group and its successful reactivation by UV light.	bind
834	1	1094	5	10	NULL	0	NULL	RBP	GP		bind					TTR	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_17_4633_s_278	10469643	( B) Elution profile observed for mRBP in wild-type serum: essentially all RBP is bound to TTR.	bind
311	1	1094	7	10	NULL	0	NULL	RBP	GP		bind					TTR	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_17_4633_s_278	10469643	( B) Elution profile observed for mRBP in wild-type serum: essentially all RBP is bound to TTR.	bind
835	1	1095	5	10	NULL	0	NULL	Cdc20	GP		bind					APC	Cell				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_15_24_3278_s_101	11751633	( B) Emi1 does not prevent Cdc20 binding to the APC in vitro.	bind
836	2	1095	5	10	NULL	0	NULL	Emi1	GP		does not prevent					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_24_3278_s_101	11751633	( B) Emi1 does not prevent Cdc20 binding to the APC in vitro.	bind
312	1	1095	7	10	NULL	0	NULL	Cdc20	GP		bind					APC	Cell				NULL	 in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_15_24_3278_s_101	11751633	( B) Emi1 does not prevent Cdc20 binding to the APC in vitro.	bind
313	2	1095	7	10	NULL	0	NULL	Emi1	GP		does not prevent 					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_24_3278_s_101	11751633	( B) Emi1 does not prevent Cdc20 binding to the APC in vitro.	bind
840	1	1096	5	10	NULL	0	NULL	CaMKII	GP		phosphorylate					Emi2	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_3_608_s_65	16407128	( B) Emi2 binds the PBD of Plk1 after phosphorylation by CaMKII.	bind
841	2	1096	5	10	NULL	0	NULL	Emi2	GP		bind					Plk1	GP		PBD		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_3_608_s_65	16407128	( B) Emi2 binds the PBD of Plk1 after phosphorylation by CaMKII.	bind
842	3	1096	5	10	NULL	0	NULL	statement 2	Process		occurs after					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_3_608_s_65	16407128	( B) Emi2 binds the PBD of Plk1 after phosphorylation by CaMKII.	bind
314	1	1096	7	10	NULL	0	NULL	Emi2	GP		bind					Plk1	GP		PBD		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_3_608_s_65	16407128	( B) Emi2 binds the PBD of Plk1 after phosphorylation by CaMKII.	bind
315	2	1096	7	10	NULL	0	NULL	CaMKII	GP		phosphorylate					Emi2	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_3_608_s_65	16407128	( B) Emi2 binds the PBD of Plk1 after phosphorylation by CaMKII.	bind
48698	3	1096	7	10	NULL	0	NULL	statement 1	Process		occurs after					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_3_608_s_65	16407128	( B) Emi2 binds the PBD of Plk1 after phosphorylation by CaMKII.	bind
850	1	1097	5	10	NULL	0	NULL	nuclear protein	GP		bind					COX-2	GP			NF-IL-6 region of promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_4_1788_s_188	9465095	( B) EMSA of binding of nuclear protein to the NF-IL-6 region of the COX-2 promoter.	bind
317	1	1097	7	10	NULL	0	NULL	nuclear protein 	GP		binds to					COX-2	GP			NF-IL-6 promoter 	NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_4_1788_s_188	9465095	( B) EMSA of binding of nuclear protein to the NF-IL-6 region of the COX-2 promoter.	bind
853	1	1098	5	10	NULL	0	NULL	DLX1	GP		bind					Dlx5/ Dlx6	GP	specific		homeodomain binding motifs of intergenic enhancer	NULL	embryonic striatum in situ	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_3_884_s_178	14769946	( b) EMSA of embryonic striatum demonstrates DLX1 and DLX2 binding to specific homeodomain  binding motifs within the  Dlx5/ Dlx6 intergenic enhancer  in situ.	bind
854	2	1098	5	10	NULL	0	NULL	DLX2	GP		bind					Dlx5/ Dlx6	GP	specific		homeodomain binding motifs of intergenic enhancer	NULL	embryonic striatum in situ	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_3_884_s_178	14769946	( b) EMSA of embryonic striatum demonstrates DLX1 and DLX2 binding to specific homeodomain  binding motifs within the  Dlx5/ Dlx6 intergenic enhancer  in situ.	bind
335	1	1098	7	10	NULL	0	NULL	DLX1	GP		binds to 					Dlx5/Dlx6	GP	specific 		homeodomain binding motifs  within intergenic enhancer 	NULL	embryonic striatum in situ	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_3_884_s_178	14769946	( b) EMSA of embryonic striatum demonstrates DLX1 and DLX2 binding to specific homeodomain  binding motifs within the  Dlx5/ Dlx6 intergenic enhancer  in situ.	bind
338	2	1098	7	10	NULL	0	NULL	DLX2	GP		binds to					Dlx5/Dlx6 	GP	specific 		homeodomain binding motifs within intergenic enhancer	NULL	embryonic striatum in situ	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_3_884_s_178	14769946	( b) EMSA of embryonic striatum demonstrates DLX1 and DLX2 binding to specific homeodomain  binding motifs within the  Dlx5/ Dlx6 intergenic enhancer  in situ.	bind
856	1	1099	5	10	NULL	0	NULL	Akt	GP	endogenous	bind					acinus-S	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_20_3543_s_214	16177823	( B) Endogenous Akt binds to acinus-S.	bind
343	1	1099	7	10	NULL	0	NULL	Akt	GP	Endogenous	binds to					acinus-S	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_20_3543_s_214	16177823	( B) Endogenous Akt binds to acinus-S.	bind
859	1	1100	5	10	NULL	0	NULL	E2F	GP	endogenous	bind					BMI1	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_6_1745_s_149	16582100	( B) Endogenous E2F proteins bind to the  BMI1 promoter  in vivo.	bind
345	1	1100	7	10	NULL	0	NULL	E2F proteins 	GP	endogenous	binds to 					BMI1	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_6_1745_s_149	16582100	( B) Endogenous E2F proteins bind to the  BMI1 promoter  in vivo.	bind
861	1	1101	5	10	NULL	0	NULL	FoxO3a	GP	endogenous	bind					cyclin D2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_23_14_2830_s_161	15241468	( B) Endogenous FoxO3a binds to the  cyclin D2 promoter upon inhibition of PI3-kinase.	bind
862	2	1101	5	10	NULL	0	NULL	statement 1	Process		occurs upon					PI3-kinase	GP	inhibiton of			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_14_2830_s_161	15241468	( B) Endogenous FoxO3a binds to the  cyclin D2 promoter upon inhibition of PI3-kinase.	bind
347	1	1101	7	10	NULL	0	NULL	FoxO3a	GP	endogenous 	binds to					cyclin D2 	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_23_14_2830_s_161	15241468	( B) Endogenous FoxO3a binds to the  cyclin D2 promoter upon inhibition of PI3-kinase.	bind
350	2	1101	7	10	NULL	0	NULL	statement 1	Process		occurs upon 					PI3-kinase	GP	inhibition of			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_14_2830_s_161	15241468	( B) Endogenous FoxO3a binds to the  cyclin D2 promoter upon inhibition of PI3-kinase.	bind
863	1	1102	5	10	NULL	0	NULL	MLL	GP	endogenous	bind					CDKN1B	GP			promoter	NULL	MV4 - 11 cells	NULL	NULL	NULL	NULL	gw70_pnas_102_39_14028_s_223	16169901	( B) Endogenous MLL/MLL-AF4 binds to the  CDKN1B promoter in MV4 - 11 and RS4;11 cells.	bind
47877	2	1102	5	10	NULL	0	NULL	MLL-AF4	GP	endogenous	bind					CDKN1B	GP			promoter	NULL	MV4 - 11 cells	NULL	NULL	NULL	NULL	gw70_pnas_102_39_14028_s_223	16169901	( B) Endogenous MLL/MLL-AF4 binds to the  CDKN1B promoter in MV4 - 11 and RS4;11 cells.	bind
47878	3	1102	5	10	NULL	0	NULL	MLL	GP	endogenous	bind					CDKN1B	GP			promoter	NULL	RS4;11 cells	NULL	NULL	NULL	NULL	gw70_pnas_102_39_14028_s_223	16169901	( B) Endogenous MLL/MLL-AF4 binds to the  CDKN1B promoter in MV4 - 11 and RS4;11 cells.	bind
47879	4	1102	5	10	NULL	0	NULL	MLL-AF4	GP	endogenous	bind					CDKN1B	GP			promoter	NULL	RS4;11 cells	NULL	NULL	NULL	NULL	gw70_pnas_102_39_14028_s_223	16169901	( B) Endogenous MLL/MLL-AF4 binds to the  CDKN1B promoter in MV4 - 11 and RS4;11 cells.	bind
362	1	1102	7	10	NULL	0	NULL	MLL	GP	endogenous	bind					CDKN1B	GP			promoter	NULL	MV4 - 11 cells	NULL	NULL	NULL	NULL	gw70_pnas_102_39_14028_s_223	16169901	( B) Endogenous MLL/MLL-AF4 binds to the  CDKN1B promoter in MV4 - 11 and RS4;11 cells.	bind
365	2	1102	7	10	NULL	0	NULL	MLL-AF4 	GP	endogenous	bind					CDKN1B	GP			promoter	NULL	MV4 - 11 cells	NULL	NULL	NULL	NULL	gw70_pnas_102_39_14028_s_223	16169901	( B) Endogenous MLL/MLL-AF4 binds to the  CDKN1B promoter in MV4 - 11 and RS4;11 cells.	bind
369	3	1102	7	10	NULL	0	NULL	MLL	GP	endogenous	bind					CDKN1B	GP			promoter	NULL	RS4;11 cells	NULL	NULL	NULL	NULL	gw70_pnas_102_39_14028_s_223	16169901	( B) Endogenous MLL/MLL-AF4 binds to the  CDKN1B promoter in MV4 - 11 and RS4;11 cells.	bind
370	4	1102	7	10	NULL	0	NULL	MLL-AF4 	GP	endogenous	bind					CDKN1B	GP			promoter	NULL	RS4;11 cells	NULL	NULL	NULL	NULL	gw70_pnas_102_39_14028_s_223	16169901	( B) Endogenous MLL/MLL-AF4 binds to the  CDKN1B promoter in MV4 - 11 and RS4;11 cells.	bind
864	1	1103	5	10	NULL	0	NULL	p53beta	GP	endogenous	bind		differentially							p53-responsive promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_18_2122_s_284	16131611	( B) Endogenous p53beta binds differentially to the p53-responsive promoter.	bind
375	1	1103	7	10	NULL	0	NULL	 p53beta 	GP	endogenous\t	bind		 differentially			 				p53-responsive promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_18_2122_s_284	16131611	( B) Endogenous p53beta binds differentially to the p53-responsive promoter.	bind
865	1	1104	5	10	NULL	0	NULL	RASSF1C	GP	endogenous	bind					Daxx	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_14_3286_s_86	16810318	( B) Endogenous RASSF1C binds endogenous Daxx.	bind
376	1	1104	7	10	NULL	0	NULL	RASSF1C	GP	endogenous	bind					Daxx	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_14_3286_s_86	16810318	( B) Endogenous RASSF1C binds endogenous Daxx.	bind
866	1	1107	5	10	NULL	0	NULL	Yeast	Organism		express					ETR1	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw60_science_283_5404_996_s_72	9974395	( B) Ethylene binding by yeast expressing wild-type and mutant forms of ETR1.	bind
867	2	1107	5	10	NULL	0	NULL	statement 1	Process		bind					Ethylene	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_283_5404_996_s_72	9974395	( B) Ethylene binding by yeast expressing wild-type and mutant forms of ETR1.	bind
48717	3	1107	5	10	NULL	0	NULL	Yeast	Organism		expresses					ETR1	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_science_283_5404_996_s_72	9974395	( B) Ethylene binding by yeast expressing wild-type and mutant forms of ETR1.	bind
48718	4	1107	5	10	NULL	0	NULL	statement 3	Process		bind					Ethylene	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_283_5404_996_s_72	9974395	( B) Ethylene binding by yeast expressing wild-type and mutant forms of ETR1.	bind
377	1	1107	7	10	NULL	0	NULL	Yeast	Organism		expresses					ETR1	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw60_science_283_5404_996_s_72	9974395	( B) Ethylene binding by yeast expressing wild-type and mutant forms of ETR1.	bind
378	2	1107	7	10	NULL	0	NULL	statement 1	Process		bind					Ethylene 	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_283_5404_996_s_72	9974395	( B) Ethylene binding by yeast expressing wild-type and mutant forms of ETR1.	bind
48719	3	1107	7	10	NULL	0	NULL	Yeast	Organism		expresses					ETR1	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_science_283_5404_996_s_72	9974395	( B) Ethylene binding by yeast expressing wild-type and mutant forms of ETR1.	bind
48720	4	1107	7	10	NULL	0	NULL	statement 3	Process		bind					Ethylene	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_283_5404_996_s_72	9974395	( B) Ethylene binding by yeast expressing wild-type and mutant forms of ETR1.	bind
868	1	1110	5	10	NULL	0	NULL	Sema4D	GP		bind					plexin-B1	GP				NULL	HEK293 cells	NULL	NULL	NULL	NULL	gw60_genesdev_16_7_836_s_74	11937491	( B) Expression of RacL61 enhances the binding of Sema4D to plexin-B1 in HEK293 cells.	bind
869	2	1110	5	10	NULL	0	NULL	RacL61	GP		enhances					statement 1	Process				NULL	HEK293 cells	NULL	NULL	NULL	NULL	gw60_genesdev_16_7_836_s_74	11937491	( B) Expression of RacL61 enhances the binding of Sema4D to plexin-B1 in HEK293 cells.	bind
380	1	1110	7	10	NULL	0	NULL	Sema4D	GP		bind					plexin-B1 	GP				NULL	HEK293 cells	NULL	NULL	NULL	NULL	gw60_genesdev_16_7_836_s_74	11937491	( B) Expression of RacL61 enhances the binding of Sema4D to plexin-B1 in HEK293 cells.	bind
382	2	1110	7	10	NULL	0	NULL	RacL61	GP		enhances 					statement 1	Process				NULL	HEK293 cells	NULL	NULL	NULL	NULL	gw60_genesdev_16_7_836_s_74	11937491	( B) Expression of RacL61 enhances the binding of Sema4D to plexin-B1 in HEK293 cells.	bind
870	1	1112	5	10	NULL	0	NULL	YY1	GP		bind		female-specific			Xist cluster	GP				NULL		NULL	NULL	NULL	NULL	gw70_genomeres_16_7_901_s_122	16760423	( B) Female-specific binding of YY1 to the  Xist cluster.	bind
399	1	1112	7	10	NULL	0	NULL	YY1 	GP	 	bind		Female-specific			Xist cluster	GP				NULL		NULL	NULL	NULL	NULL	gw70_genomeres_16_7_901_s_122	16760423	( B) Female-specific binding of YY1 to the  Xist cluster.	bind
873	1	1113	5	10	NULL	0	NULL	SARS-CoV S1180 protein	GP	soluble	bind					CHO cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_44_15748_s_121	15496474	( B) Flow cytometric analysis of soluble SARS-CoV S1180 protein binding to CHO ( Upper) and clone 2.27 ( Lower) cells.	bind
2435	2	1113	5	10	NULL	0	NULL	SARS-CoV S1180 protein	GP	soluble	bind					clone 2.27 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_44_15748_s_121	15496474	( B) Flow cytometric analysis of soluble SARS-CoV S1180 protein binding to CHO ( Upper) and clone 2.27 ( Lower) cells.	bind
404	1	1113	7	10	NULL	0	NULL	SARS-CoV S1180 protein 	GP	soluble	bind					CHO cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_44_15748_s_121	15496474	( B) Flow cytometric analysis of soluble SARS-CoV S1180 protein binding to CHO ( Upper) and clone 2.27 ( Lower) cells.	bind
407	2	1113	7	10	NULL	0	NULL	SARS-CoV S1180 protein 	GP	soluble	bind					clone 2.27 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_44_15748_s_121	15496474	( B) Flow cytometric analysis of soluble SARS-CoV S1180 protein binding to CHO ( Upper) and clone 2.27 ( Lower) cells.	bind
874	1	1114	5	10	NULL	0	NULL	DM	Chemical		bind					apoRfBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_21_11873_s_156	11592998	( B) Fluorescence decays (610 nm) of DM (50 mum) bound to the apoRfBP (400 muM) with a series of concentrations of Gdn.HCl, from 0 M to [[ 2 M.                    To ]] further characterize these "`free"' DM molecules, we measured the time-resolved anisotropy, as shown in Fig.  6 A Inset.	bind
449	1	1114	7	10	NULL	0	NULL	DM	Chemical		binds					 apoRfBP 	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_21_11873_s_156	11592998	( B) Fluorescence decays (610 nm) of DM (50 mum) bound to the apoRfBP (400 muM) with a series of concentrations of Gdn.HCl, from 0 M to [[ 2 M.                    To ]] further characterize these "`free"' DM molecules, we measured the time-resolved anisotropy, as shown in Fig.  6 A Inset.	bind
2436	1	1115	5	10	NULL	0	NULL	four nucleotide	NucleicAcid	substitution of	reduce		significantly			MBNL1	GP	binding of;; recombinant			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_15_3103_s_109	15257297	( B) Four nucleotide substitutions significantly reduce binding of recombinant MBNL1  detected by UV crosslinking.	bind
451	1	1115	7	10	NULL	0	NULL	Four nucleotide	NucleicAcid	substitution of	reduce 		significantly			MBNL1	GP	binding of;; recombinant			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_15_3103_s_109	15257297	( B) Four nucleotide substitutions significantly reduce binding of recombinant MBNL1  detected by UV crosslinking.	bind
878	2	1116	5	10	NULL	0	NULL	Rev14	GP		bind		specifically			RRE IIB RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_8_4247_s_131	9539722	( B) Fourteen arginines (Arg14) or a 14-amino acid Rev peptide (Rev14 corresponds to residues 34-47 of Rev, with Trp-45 Arg and Glu-47 Arg substitutions, and specifically binds RRE IIB RNA; ref.  24) were fused to the HIV Tat activation domain (residues 1-49) in the context of surrounding alanines as shown.	bind
61090	1	1116	5	10	NULL	0	NULL	Arg14	AminoAcid		bind		specifically			RRE IIB RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_8_4247_s_131	9539722	( B) Fourteen arginines (Arg14) or a 14-amino acid Rev peptide (Rev14 corresponds to residues 34-47 of Rev, with Trp-45 Arg and Glu-47 Arg substitutions, and specifically binds RRE IIB RNA; ref.  24) were fused to the HIV Tat activation domain (residues 1-49) in the context of surrounding alanines as shown.	bind
61091	3	1116	5	10	NULL	0	NULL	Arg14	AminoAcid		is					Fourteen arginines	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_pnas_95_8_4247_s_131	9539722	( B) Fourteen arginines (Arg14) or a 14-amino acid Rev peptide (Rev14 corresponds to residues 34-47 of Rev, with Trp-45 Arg and Glu-47 Arg substitutions, and specifically binds RRE IIB RNA; ref.  24) were fused to the HIV Tat activation domain (residues 1-49) in the context of surrounding alanines as shown.	bind
61092	4	1116	5	10	NULL	0	NULL	Rev14	GP		is					14-amino acid Rev peptide	GP		residues 34-47, with Trp-45 Arg and Glu-47 Arg substitutions		NULL		0	NULL	NULL	NULL	gw60_pnas_95_8_4247_s_131	9539722	( B) Fourteen arginines (Arg14) or a 14-amino acid Rev peptide (Rev14 corresponds to residues 34-47 of Rev, with Trp-45 Arg and Glu-47 Arg substitutions, and specifically binds RRE IIB RNA; ref.  24) were fused to the HIV Tat activation domain (residues 1-49) in the context of surrounding alanines as shown.	bind
454	1	1116	7	10	NULL	0	NULL	Arg14	AminoAcid		bind		specifically			RRE IIB RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_8_4247_s_131	9539722	( B) Fourteen arginines (Arg14) or a 14-amino acid Rev peptide (Rev14 corresponds to residues 34-47 of Rev, with Trp-45 Arg and Glu-47 Arg substitutions, and specifically binds RRE IIB RNA; ref.  24) were fused to the HIV Tat activation domain (residues 1-49) in the context of surrounding alanines as shown.	bind
534	2	1116	7	10	NULL	0	NULL	 Rev14	GP		bind		specifically			RRE IIB RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_8_4247_s_131	9539722	( B) Fourteen arginines (Arg14) or a 14-amino acid Rev peptide (Rev14 corresponds to residues 34-47 of Rev, with Trp-45 Arg and Glu-47 Arg substitutions, and specifically binds RRE IIB RNA; ref.  24) were fused to the HIV Tat activation domain (residues 1-49) in the context of surrounding alanines as shown.	bind
536	3	1116	7	10	NULL	0	NULL	Arg14	AminoAcid		is					Fourteen arginines	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_8_4247_s_131	9539722	( B) Fourteen arginines (Arg14) or a 14-amino acid Rev peptide (Rev14 corresponds to residues 34-47 of Rev, with Trp-45 Arg and Glu-47 Arg substitutions, and specifically binds RRE IIB RNA; ref.  24) were fused to the HIV Tat activation domain (residues 1-49) in the context of surrounding alanines as shown.	bind
537	4	1116	7	10	NULL	0	NULL	Rev14	GP		is					14-amino acid Rev peptide	GP		residues 34-47, with Trp-45 Arg and Glu-47 Arg substitutions		NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_8_4247_s_131	9539722	( B) Fourteen arginines (Arg14) or a 14-amino acid Rev peptide (Rev14 corresponds to residues 34-47 of Rev, with Trp-45 Arg and Glu-47 Arg substitutions, and specifically binds RRE IIB RNA; ref.  24) were fused to the HIV Tat activation domain (residues 1-49) in the context of surrounding alanines as shown.	bind
880	1	1117	5	10	NULL	0	NULL	Sug1/Rpt6 protein	GP		bind					GAL1-10	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_science_296_5567_548_s_35	11964484	( B) Gal4 dependence of Sug1/Rpt6 protein binding to the  GAL1-10 promoter.	bind
881	2	1117	5	10	NULL	0	NULL	statement 1	Process		is dependent on					Gal4	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_296_5567_548_s_35	11964484	( B) Gal4 dependence of Sug1/Rpt6 protein binding to the  GAL1-10 promoter.	bind
541	1	1117	7	10	NULL	0	NULL	Sug1/Rpt6 protein	GP		bind					GAL1-10 	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_science_296_5567_548_s_35	11964484	( B) Gal4 dependence of Sug1/Rpt6 protein binding to the  GAL1-10 promoter.	bind
543	2	1117	7	10	NULL	0	NULL	statement 1	Process		is dependent on					Gal4	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_296_5567_548_s_35	11964484	( B) Gal4 dependence of Sug1/Rpt6 protein binding to the  GAL1-10 promoter.	bind
882	1	1118	5	10	NULL	0	NULL	GATA	GP		bind					PPARgamma2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_science_290_5489_134_s_71	11021798	( B) GATA binding to PPARgamma2 promoter determined by DNase I footprinting analysis.	bind
545	1	1118	7	10	NULL	0	NULL	GATA 	GP		bind					PPARgamma2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_science_290_5489_134_s_71	11021798	( B) GATA binding to PPARgamma2 promoter determined by DNase I footprinting analysis.	bind
883	1	1119	5	10	NULL	0	NULL	GDP-Gpa2	GP		bind					adenylate cyclase	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_17_6108_s_197	15831585	( B) GDP-Gpa2 binding to adenylate cyclase facilitates binding of the activated GTP-Gpa2  to both the N-terminal domain and to a site within the catalytic domain that stimulates  adenylate cyclase activity.	bind
884	2	1119	5	10	NULL	0	NULL	GTP-Gpa2	GP	activated	bind					adenylate cyclase	GP		N-terminal domain		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_17_6108_s_197	15831585	( B) GDP-Gpa2 binding to adenylate cyclase facilitates binding of the activated GTP-Gpa2  to both the N-terminal domain and to a site within the catalytic domain that stimulates  adenylate cyclase activity.	bind
885	3	1119	5	10	NULL	0	NULL	GTP-Gpa2	GP	activated	bind					adenylate cyclase	GP		a site within catalytic domain		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_17_6108_s_197	15831585	( B) GDP-Gpa2 binding to adenylate cyclase facilitates binding of the activated GTP-Gpa2  to both the N-terminal domain and to a site within the catalytic domain that stimulates  adenylate cyclase activity.	bind
886	4	1119	5	10	NULL	0	NULL	statement 1	Process		facilitate					statement 2 	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_17_6108_s_197	15831585	( B) GDP-Gpa2 binding to adenylate cyclase facilitates binding of the activated GTP-Gpa2  to both the N-terminal domain and to a site within the catalytic domain that stimulates  adenylate cyclase activity.	bind
47880	5	1119	5	10	NULL	0	NULL	statement 1	Process		facilitate					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_17_6108_s_197	15831585	( B) GDP-Gpa2 binding to adenylate cyclase facilitates binding of the activated GTP-Gpa2  to both the N-terminal domain and to a site within the catalytic domain that stimulates  adenylate cyclase activity.	bind
547	1	1119	7	10	NULL	0	NULL	GDP-Gpa2	GP		bind					adenylate cyclase 	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_17_6108_s_197	15831585	( B) GDP-Gpa2 binding to adenylate cyclase facilitates binding of the activated GTP-Gpa2  to both the N-terminal domain and to a site within the catalytic domain that stimulates  adenylate cyclase activity.	bind
549	2	1119	7	10	NULL	0	NULL	GTP-Gpa2	GP	activated	bind					adenylate cyclase	GP		N-terminal domain 		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_17_6108_s_197	15831585	( B) GDP-Gpa2 binding to adenylate cyclase facilitates binding of the activated GTP-Gpa2  to both the N-terminal domain and to a site within the catalytic domain that stimulates  adenylate cyclase activity.	bind
550	3	1119	7	10	NULL	0	NULL	GTP-Gpa2	GP	activated	binds to					adenylate cyclase	GP		 site within the catalytic domain		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_17_6108_s_197	15831585	( B) GDP-Gpa2 binding to adenylate cyclase facilitates binding of the activated GTP-Gpa2  to both the N-terminal domain and to a site within the catalytic domain that stimulates  adenylate cyclase activity.	bind
1168	4	1119	7	10	NULL	0	NULL	statement 1	Process		facilitate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_17_6108_s_197	15831585	( B) GDP-Gpa2 binding to adenylate cyclase facilitates binding of the activated GTP-Gpa2  to both the N-terminal domain and to a site within the catalytic domain that stimulates  adenylate cyclase activity.	bind
1171	5	1119	7	10	NULL	0	NULL	statement 1	Process		facilitate					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_17_6108_s_197	15831585	( B) GDP-Gpa2 binding to adenylate cyclase facilitates binding of the activated GTP-Gpa2  to both the N-terminal domain and to a site within the catalytic domain that stimulates  adenylate cyclase activity.	bind
887	1	1120	5	10	NULL	0	NULL	AEF-1 protein	GP		bind					Adh	GP			proximal promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_17_4_1076_s_53	9463385	( B) Gel mobility shift assay showing the binding of AEF-1 protein to the  Adh proximal promoter but not to the distal promoter.	bind
888	2	1120	5	10	NULL	0	NULL	AEF-1 protein	GP		does not bind					Adh	GP			distal promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_17_4_1076_s_53	9463385	( B) Gel mobility shift assay showing the binding of AEF-1 protein to the  Adh proximal promoter but not to the distal promoter.	bind
551	1	1120	7	10	NULL	0	NULL	AEF-1protein	GP		binds to					 Adh 	GP			proximal promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_17_4_1076_s_53	9463385	( B) Gel mobility shift assay showing the binding of AEF-1 protein to the  Adh proximal promoter but not to the distal promoter.	bind
552	2	1120	7	10	NULL	0	NULL	AEF-1 protein 	GP		does not bind					Adh	GP			distal promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_17_4_1076_s_53	9463385	( B) Gel mobility shift assay showing the binding of AEF-1 protein to the  Adh proximal promoter but not to the distal promoter.	bind
889	1	1121	5	10	NULL	0	NULL	MEF2A proteins	GP	 in vitro translated	bind									N10 site	NULL		NULL	NULL	NULL	NULL	gw60_embo_19_11_2615_s_117	10835359	( B) Gel retardation analysis of equimolar concentrations of  in vitro translated MEF2A proteins bound to the N10 site (central motif CTATTTATAG; Sharrocks  et al., 1993a).	bind
47881	2	1121	5	10	NULL	0	NULL	N10 site	GP		is									central motif CTATTTATAG	NULL		NULL	NULL	NULL	NULL	gw60_embo_19_11_2615_s_117	10835359	( B) Gel retardation analysis of equimolar concentrations of  in vitro translated MEF2A proteins bound to the N10 site (central motif CTATTTATAG; Sharrocks  et al., 1993a).	bind
553	1	1121	7	10	NULL	0	NULL	MEF2A proteins 	GP	in vitro translated 	bind to									N10 site 	NULL		NULL	NULL	NULL	NULL	gw60_embo_19_11_2615_s_117	10835359	( B) Gel retardation analysis of equimolar concentrations of  in vitro translated MEF2A proteins bound to the N10 site (central motif CTATTTATAG; Sharrocks  et al., 1993a).	bind
47882	2	1121	7	10	NULL	0	NULL	N10 site	GP		is									central motif CTATTTATAG	NULL		NULL	NULL	NULL	NULL	gw60_embo_19_11_2615_s_117	10835359	( B) Gel retardation analysis of equimolar concentrations of  in vitro translated MEF2A proteins bound to the N10 site (central motif CTATTTATAG; Sharrocks  et al., 1993a).	bind
890	1	1122	5	10	NULL	0	NULL	Taz1p	GP	in vitro translated	bind									140 bp telomeric fragment	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_2_527_s_46	10606652	( B) Gel retardation assay showing  in vitro translated (IVT) Taz1p binding to the 140 bp telomeric fragment.	bind
554	1	1122	7	10	NULL	0	NULL	Taz1p	GP	 in vitro translated 	bind									140 bp telomeric fragment	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_2_527_s_46	10606652	( B) Gel retardation assay showing  in vitro translated (IVT) Taz1p binding to the 140 bp telomeric fragment.	bind
891	1	1123	5	10	NULL	0	NULL	R2 protein	GP	full-length	bind					DNA substrates	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_20_6461_s_53	16284201	( B) Gel shifts of the full-length R2 protein bound to mutant DNA substrates at low (36  fmol) and high (360 fmol) protein concentrations in the absence of dNTPs.	bind
555	1	1123	7	10	NULL	0	NULL	 R2 protein 	GP	full-length 	bind					DNA substrates 	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_20_6461_s_53	16284201	( B) Gel shifts of the full-length R2 protein bound to mutant DNA substrates at low (36  fmol) and high (360 fmol) protein concentrations in the absence of dNTPs.	bind
892	1	1124	5	10	NULL	0	NULL	ChREBP	GP		bind to					lipogenic gene	GP			ChRE in promoter of	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_44_15597_s_132	15496471	( B) Gel-shift analysis of ChREBP bound to the ChREs of lipogenic gene promoters after  immunoreaction with ChREBP antibodies.	bind
557	1	1124	7	10	NULL	0	NULL	ChREBP	GP		bind to					lipogenic gene	GP			ChRE of promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_44_15597_s_132	15496471	( B) Gel-shift analysis of ChREBP bound to the ChREs of lipogenic gene promoters after  immunoreaction with ChREBP antibodies.	bind
893	1	1125	5	10	NULL	0	NULL	E-cadherin	GP	glycosylated	bind					beta-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_5999_s_219	11689440	( B) Glycosylated E-cadherin binds beta- and gamma-catenin but not p120-catenin.	bind
894	2	1125	5	10	NULL	0	NULL	E-cadherin	GP	glycosylated	bind					gamma-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_5999_s_219	11689440	( B) Glycosylated E-cadherin binds beta- and gamma-catenin but not p120-catenin.	bind
895	3	1125	5	10	NULL	0	NULL	E-cadherin	GP	glycosylated	does not bind					p120-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_5999_s_219	11689440	( B) Glycosylated E-cadherin binds beta- and gamma-catenin but not p120-catenin.	bind
559	1	1125	7	10	NULL	0	NULL	E-cadherin 	GP	Glycosylated	bind					beta-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_5999_s_219	11689440	( B) Glycosylated E-cadherin binds beta- and gamma-catenin but not p120-catenin.	bind
560	2	1125	7	10	NULL	0	NULL	E-cadherin 	GP	Glycosylated	bind					gamma-catenin 	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_5999_s_219	11689440	( B) Glycosylated E-cadherin binds beta- and gamma-catenin but not p120-catenin.	bind
561	3	1125	7	10	NULL	0	NULL	E-cadherin 	GP	Glycosylated	does not bind					p120-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_5999_s_219	11689440	( B) Glycosylated E-cadherin binds beta- and gamma-catenin but not p120-catenin.	bind
901	1	1127	5	10	NULL	0	NULL	ScMre11p	GP		bind					G4 DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_15_4692_s_146	16116037	( B) Graph showing binding of ScMre11p to G4 DNA.	bind
597	1	1127	7	10	NULL	0	NULL	ScMre11p	GP		bind					G4 DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_15_4692_s_146	16116037	( B) Graph showing binding of ScMre11p to G4 DNA.	bind
902	1	1128	5	10	NULL	0	NULL	RNase III	GP		bind					R1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_9_2381_s_306	12711683	( B) Graphic presentation of the effect of the db17 mutation on RNase III binding to  R1.	bind
47890	2	1128	5	10	NULL	0	NULL	db17	NucleicAcid	mutant	effects					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_9_2381_s_306	12711683	( B) Graphic presentation of the effect of the db17 mutation on RNase III binding to  R1.	bind
598	1	1128	7	10	NULL	0	NULL	RNase III 	GP		bind					R1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_9_2381_s_306	12711683	( B) Graphic presentation of the effect of the db17 mutation on RNase III binding to  R1.	bind
599	2	1128	7	10	NULL	0	NULL	db17 	NucleicAcid	mutant	effects					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_9_2381_s_306	12711683	( B) Graphic presentation of the effect of the db17 mutation on RNase III binding to  R1.	bind
903	1	1132	5	10	NULL	0	NULL	GST-AKIP	GP		bind		directly							C subunit	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_2_349_s_158	15630084	( B) GST pull down showed direct binding of the C subunit with GST-AKIP* as analyzed by SDS/PAGE.	bind
600	1	1132	7	10	NULL	0	NULL				bind		directly	C subunit 		GST-AKIP	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_2_349_s_158	15630084	( B) GST pull down showed direct binding of the C subunit with GST-AKIP* as analyzed by SDS/PAGE.	bind
904	1	1133	5	10	NULL	0	NULL	BRCA2	GP		bind					RAD51	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_95_9_5287_s_121	9560268	( B) GST pull-down assay for the   in vitro binding of BRCA2 to RAD51.	bind
601	1	1133	7	10	NULL	0	NULL	BRCA2	GP		bind					RAD51	GP				NULL	 in vitro 	NULL	NULL	NULL	NULL	gw60_pnas_95_9_5287_s_121	9560268	( B) GST pull-down assay for the   in vitro binding of BRCA2 to RAD51.	bind
905	1	1134	5	10	NULL	0	NULL	Elk	GP		bind			1-93		Elk-1	GP	non-phosphorylated;; GST fusion protein	C-terminal domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_20_5666_s_140	10523309	( B) GST pull-down assay of binding of Elk1-93 and Elk1-168 to GST fusion proteins containing the non-phosphorylated and phosphorylated C-terminal domain of Elk-1.	bind
906	2	1134	5	10	NULL	0	NULL	Elk	GP		bind			1-93		Elk-1	GP	phosphorylated;; GST fusion protein	C-terminal domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_20_5666_s_140	10523309	( B) GST pull-down assay of binding of Elk1-93 and Elk1-168 to GST fusion proteins containing the non-phosphorylated and phosphorylated C-terminal domain of Elk-1.	bind
907	3	1134	5	10	NULL	0	NULL	Elk	GP		bind			1-168		Elk-1	GP	non-phosphorylated;; GST fusion protein	C-terminal domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_20_5666_s_140	10523309	( B) GST pull-down assay of binding of Elk1-93 and Elk1-168 to GST fusion proteins containing the non-phosphorylated and phosphorylated C-terminal domain of Elk-1.	bind
908	4	1134	5	10	NULL	0	NULL	Elk	GP		bind			1-168		Elk-1	GP	phosphorylated;; GST fusion protein	C-terminal domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_20_5666_s_140	10523309	( B) GST pull-down assay of binding of Elk1-93 and Elk1-168 to GST fusion proteins containing the non-phosphorylated and phosphorylated C-terminal domain of Elk-1.	bind
602	1	1134	7	10	NULL	0	NULL	Elk	GP		bind			1-93 		Elk-1	GP	GST fusion proteins;; non-phosphorylated	C-terminal domain 		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_20_5666_s_140	10523309	( B) GST pull-down assay of binding of Elk1-93 and Elk1-168 to GST fusion proteins containing the non-phosphorylated and phosphorylated C-terminal domain of Elk-1.	bind
603	2	1134	7	10	NULL	0	NULL	Elk	GP		bind			1-93		Elk-1	GP	GST fusion proteins;; phosphorylated	C-terminal domain 		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_20_5666_s_140	10523309	( B) GST pull-down assay of binding of Elk1-93 and Elk1-168 to GST fusion proteins containing the non-phosphorylated and phosphorylated C-terminal domain of Elk-1.	bind
604	3	1134	7	10	NULL	0	NULL	Elk	GP		bind			1-168 		Elk-1	GP	GST fusion proteins;; non-phosphorylated	C-terminal domain 		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_20_5666_s_140	10523309	( B) GST pull-down assay of binding of Elk1-93 and Elk1-168 to GST fusion proteins containing the non-phosphorylated and phosphorylated C-terminal domain of Elk-1.	bind
605	4	1134	7	10	NULL	0	NULL	Elk	GP		bind			1-168 		Elk-1	GP	GST fusion protein;; phosphorylated 	C-terminal domain 		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_20_5666_s_140	10523309	( B) GST pull-down assay of binding of Elk1-93 and Elk1-168 to GST fusion proteins containing the non-phosphorylated and phosphorylated C-terminal domain of Elk-1.	bind
909	1	1135	5	10	NULL	0	NULL	PC	GP		bind					GST-C127/203	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2873_s_169	12771214	( B) GST pull-down experiments: binding of PC, PH and SCM to GST, GST-C127/203 and GST-Corto.	bind
910	2	1135	5	10	NULL	0	NULL	PH	GP		bind					GST-C127/203	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2873_s_169	12771214	( B) GST pull-down experiments: binding of PC, PH and SCM to GST, GST-C127/203 and GST-Corto.	bind
911	3	1135	5	10	NULL	0	NULL	SCM	GP		bind					GST-C127/203	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2873_s_169	12771214	( B) GST pull-down experiments: binding of PC, PH and SCM to GST, GST-C127/203 and GST-Corto.	bind
912	4	1135	5	10	NULL	0	NULL	PC	GP		bind					GST-Corto	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2873_s_169	12771214	( B) GST pull-down experiments: binding of PC, PH and SCM to GST, GST-C127/203 and GST-Corto.	bind
913	5	1135	5	10	NULL	0	NULL	PH	GP		bind					GST-Corto	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2873_s_169	12771214	( B) GST pull-down experiments: binding of PC, PH and SCM to GST, GST-C127/203 and GST-Corto.	bind
914	6	1135	5	10	NULL	0	NULL	SCM	GP		bind					GST-Corto	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2873_s_169	12771214	( B) GST pull-down experiments: binding of PC, PH and SCM to GST, GST-C127/203 and GST-Corto.	bind
48843	7	1135	5	10	NULL	0	NULL	PC	GP		bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2873_s_169	12771214	( B) GST pull-down experiments: binding of PC, PH and SCM to GST, GST-C127/203 and GST-Corto.	bind
48844	8	1135	5	10	NULL	0	NULL	PH	GP		bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2873_s_169	12771214	( B) GST pull-down experiments: binding of PC, PH and SCM to GST, GST-C127/203 and GST-Corto.	bind
48845	9	1135	5	10	NULL	0	NULL	SCM	GP		bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2873_s_169	12771214	( B) GST pull-down experiments: binding of PC, PH and SCM to GST, GST-C127/203 and GST-Corto.	bind
606	1	1135	7	10	NULL	0	NULL	PC	GP		bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2873_s_169	12771214	( B) GST pull-down experiments: binding of PC, PH and SCM to GST, GST-C127/203 and GST-Corto.	bind
607	2	1135	7	10	NULL	0	NULL	PC	GP		bind					GST-C127/203	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2873_s_169	12771214	( B) GST pull-down experiments: binding of PC, PH and SCM to GST, GST-C127/203 and GST-Corto.	bind
608	3	1135	7	10	NULL	0	NULL	PC	GP		bind					GST-Corto	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2873_s_169	12771214	( B) GST pull-down experiments: binding of PC, PH and SCM to GST, GST-C127/203 and GST-Corto.	bind
640	4	1135	7	10	NULL	0	NULL	PH 	GP		bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2873_s_169	12771214	( B) GST pull-down experiments: binding of PC, PH and SCM to GST, GST-C127/203 and GST-Corto.	bind
641	5	1135	7	10	NULL	0	NULL	PH	GP		bind					GST-C127/203	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2873_s_169	12771214	( B) GST pull-down experiments: binding of PC, PH and SCM to GST, GST-C127/203 and GST-Corto.	bind
642	6	1135	7	10	NULL	0	NULL	PH	GP		bind					GST-Corto	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2873_s_169	12771214	( B) GST pull-down experiments: binding of PC, PH and SCM to GST, GST-C127/203 and GST-Corto.	bind
643	7	1135	7	10	NULL	0	NULL	SCM	GP		bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2873_s_169	12771214	( B) GST pull-down experiments: binding of PC, PH and SCM to GST, GST-C127/203 and GST-Corto.	bind
644	8	1135	7	10	NULL	0	NULL	SCM	GP		bind					GST-C127/203	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2873_s_169	12771214	( B) GST pull-down experiments: binding of PC, PH and SCM to GST, GST-C127/203 and GST-Corto.	bind
645	9	1135	7	10	NULL	0	NULL	SCM	GP		bind					GST-Corto	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2873_s_169	12771214	( B) GST pull-down experiments: binding of PC, PH and SCM to GST, GST-C127/203 and GST-Corto.	bind
915	1	1136	5	10	NULL	0	NULL	Molt-4 protein	GP		bind					TdT constructs	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_19_10746_s_86	12960389	( B) GST pull-down of Molt-4 and Nalm-6 proteins binding to TdT constructs.	bind
916	2	1136	5	10	NULL	0	NULL	Nalm-6 protein	GP		bind					TdT constructs	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_19_10746_s_86	12960389	( B) GST pull-down of Molt-4 and Nalm-6 proteins binding to TdT constructs.	bind
646	1	1136	7	10	NULL	0	NULL	Molt-4 protein	GP		bind					TdT constructs	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_19_10746_s_86	12960389	( B) GST pull-down of Molt-4 and Nalm-6 proteins binding to TdT constructs.	bind
647	2	1136	7	10	NULL	0	NULL	Nalm-6 protein	GP		bind					TdT constructs	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_19_10746_s_86	12960389	( B) GST pull-down of Molt-4 and Nalm-6 proteins binding to TdT constructs.	bind
917	1	1138	5	10	NULL	0	NULL	GST-(CTLA-4)3	GP	fusion protein	bind					TCRzeta	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_282_5397_2263_s_71	9856951	( B) GST-(CTLA-4)3 fusion protein binds TCRzeta.	bind
648	1	1138	7	10	NULL	0	NULL	GST-(CTLA-4)3	GP	fusion protein	binds					TCRzeta	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_282_5397_2263_s_71	9856951	( B) GST-(CTLA-4)3 fusion protein binds TCRzeta.	bind
918	1	1139	5	10	NULL	0	NULL	GST-Rtt106p	GP		bind					CAF-1 complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_38_13410_s_138	16157874	( B) GST-Rtt106p bound to the CAF-1 complex.	bind
649	1	1139	7	10	NULL	0	NULL	GST-Rtt106p	GP		bind					CAF-1 complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_38_13410_s_138	16157874	( B) GST-Rtt106p bound to the CAF-1 complex.	bind
919	1	1141	5	10	NULL	0	NULL	H-Ras	GP		bind					PLCepsilon	GP		RA domains		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_4_743_s_93	11179219	( B) H-Ras binding to RA domains of PLCepsilon and the RBD of Raf-1.	bind
920	2	1141	5	10	NULL	0	NULL	H-Ras	GP		bind					Raf-1	GP		RBD		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_4_743_s_93	11179219	( B) H-Ras binding to RA domains of PLCepsilon and the RBD of Raf-1.	bind
650	1	1141	7	10	NULL	0	NULL	H-Ras	GP		bind					PLCepsilon	GP		RA domains		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_4_743_s_93	11179219	( B) H-Ras binding to RA domains of PLCepsilon and the RBD of Raf-1.	bind
651	2	1141	7	10	NULL	0	NULL	H-Ras	GP		bind					Raf-1	GP		RBD		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_4_743_s_93	11179219	( B) H-Ras binding to RA domains of PLCepsilon and the RBD of Raf-1.	bind
921	1	1144	5	10	NULL	0	NULL	HetR	GP		bind					hetR 	GP			F hetR-2 of promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_14_4848_s_152	15051891	( B) HetR binding to the fragment F hetR-2 from the  hetR promoter.	bind
652	1	1144	7	10	NULL	0	NULL	HetR	GP		bind					hetR	GP			F hetR-2 of promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_14_4848_s_152	15051891	( B) HetR binding to the fragment F hetR-2 from the  hetR promoter.	bind
922	1	1145	5	10	NULL	0	NULL				bind			F302W		iC3b	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_6_1523_s_260	9852148	( B) Histograms (mean  plus-or-minus  SEM,  n = 5) showing a selective gain of  binding of F302W to iC3b but  not to NIF, and a selective loss  of binding of T209A to iC3b  but not to NIF.	bind
923	2	1145	5	10	NULL	0	NULL				bind			F302W		NIF	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_6_1523_s_260	9852148	( B) Histograms (mean  plus-or-minus  SEM,  n = 5) showing a selective gain of  binding of F302W to iC3b but  not to NIF, and a selective loss  of binding of T209A to iC3b  but not to NIF.	bind
924	3	1145	5	10	NULL	0	NULL				bind			T209A		iC3b	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_6_1523_s_260	9852148	( B) Histograms (mean  plus-or-minus  SEM,  n = 5) showing a selective gain of  binding of F302W to iC3b but  not to NIF, and a selective loss  of binding of T209A to iC3b  but not to NIF.	bind
925	4	1145	5	10	NULL	0	NULL				bind			T209A		NIF	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_6_1523_s_260	9852148	( B) Histograms (mean  plus-or-minus  SEM,  n = 5) showing a selective gain of  binding of F302W to iC3b but  not to NIF, and a selective loss  of binding of T209A to iC3b  but not to NIF.	bind
668	1	1145	7	10	NULL	0	NULL				bind			F302W		iC3b	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_6_1523_s_260	9852148	( B) Histograms (mean  plus-or-minus  SEM,  n = 5) showing a selective gain of  binding of F302W to iC3b but  not to NIF, and a selective loss  of binding of T209A to iC3b  but not to NIF.	bind
670	2	1145	7	10	NULL	0	NULL				bind			F302W		NIF	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_6_1523_s_260	9852148	( B) Histograms (mean  plus-or-minus  SEM,  n = 5) showing a selective gain of  binding of F302W to iC3b but  not to NIF, and a selective loss  of binding of T209A to iC3b  but not to NIF.	bind
682	3	1145	7	10	NULL	0	NULL				bind			T209A		iC3b	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_6_1523_s_260	9852148	( B) Histograms (mean  plus-or-minus  SEM,  n = 5) showing a selective gain of  binding of F302W to iC3b but  not to NIF, and a selective loss  of binding of T209A to iC3b  but not to NIF.	bind
719	4	1145	7	10	NULL	0	NULL				bind			T209A		NIF	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_6_1523_s_260	9852148	( B) Histograms (mean  plus-or-minus  SEM,  n = 5) showing a selective gain of  binding of F302W to iC3b but  not to NIF, and a selective loss  of binding of T209A to iC3b  but not to NIF.	bind
926	1	1146	5	10	NULL	0	NULL	Hog1	GP		bind					STL1	GP			promoter	NULL	cells overexpressing Hot1	NULL	NULL	NULL	NULL	gw60_embo_22_10_2433_s_121	12743037	( B) Hog1 binds to  STL1 promoter upon stress in cells overexpressing Hot1.	bind
2437	2	1146	5	10	NULL	0	NULL	statement 1	Process		occurs upon					 stress	Process				NULL	cells overexpressing Hot1	NULL	NULL	NULL	NULL	gw60_embo_22_10_2433_s_121	12743037	( B) Hog1 binds to  STL1 promoter upon stress in cells overexpressing Hot1.	bind
720	1	1146	7	10	NULL	0	NULL	Hog1	GP		bind					STL1	GP			promoter	NULL	cells overexpressing Hot1	NULL	NULL	NULL	NULL	gw60_embo_22_10_2433_s_121	12743037	( B) Hog1 binds to  STL1 promoter upon stress in cells overexpressing Hot1.	bind
721	2	1146	7	10	NULL	0	NULL	statement 1	Process		occurs upon					 stress	Process				NULL	cells overexpressing Hot1	NULL	NULL	NULL	NULL	gw60_embo_22_10_2433_s_121	12743037	( B) Hog1 binds to  STL1 promoter upon stress in cells overexpressing Hot1.	bind
927	1	1147	5	10	NULL	0	NULL	HCR1	GP		bind			homologous domains		PRT1	GP		RRM		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_20_4_891_s_167	11179233	( B) Homologous domains in HCR1 and TIF32 bind to the PRT1 RRM  in vitro.	bind
928	2	1147	5	10	NULL	0	NULL	TIF32	GP		bind			homologous domains		PRT1	GP		RRM		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_20_4_891_s_167	11179233	( B) Homologous domains in HCR1 and TIF32 bind to the PRT1 RRM  in vitro.	bind
722	1	1147	7	10	NULL	0	NULL	HCR1	GP		bind to			Homologous domain		PRT1	GP		RRM		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_20_4_891_s_167	11179233	( B) Homologous domains in HCR1 and TIF32 bind to the PRT1 RRM  in vitro.	bind
723	2	1147	7	10	NULL	0	NULL	TIF32	GP		bind to			Homologous domain		PRT1	GP		RRM		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_20_4_891_s_167	11179233	( B) Homologous domains in HCR1 and TIF32 bind to the PRT1 RRM  in vitro.	bind
929	1	1148	5	10	NULL	0	NULL	HOS1	GP		bind					ICE1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_103_21_8281_s_96	16702557	( B) HOS1 binds to ICE1  in vitro.	bind
724	1	1148	7	10	NULL	0	NULL	HOS1	GP		bind					ICE1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_103_21_8281_s_96	16702557	( B) HOS1 binds to ICE1  in vitro.	bind
930	2	1149	5	10	NULL	0	NULL	HP1	GP		bind					chromosome 2	Chromosome			rl locus in pericentric region	NULL		NULL	NULL	NULL	NULL	gw70_genomeres_15_9_1265_s_82	16109969	( B) HP1 binding to the  rl locus in the pericentric region of chromosome 2.	bind
725	1	1149	7	10	NULL	0	NULL	HP1	GP		bind					chromosome 2	Chromosome			rl locus in the pericentric region	NULL		NULL	NULL	NULL	NULL	gw70_genomeres_15_9_1265_s_82	16109969	( B) HP1 binding to the  rl locus in the pericentric region of chromosome 2.	bind
931	2	1150	5	10	NULL	0	NULL	HP1beta	GP		bind		directly			Dnmt3a	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_9_2305_s_171	12711675	( B) HP1beta binds directly to Dnmt3a.	bind
726	1	1150	7	10	NULL	0	NULL	HP1beta	GP		bind		direct			Dnmt3a	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_9_2305_s_171	12711675	( B) HP1beta binds directly to Dnmt3a.	bind
932	1	1151	5	10	NULL	0	NULL	GABAAR beta3	GP	human	bind					BTX	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_53	16549768	( b) Human (h) GABAAR beta3 binds BTX, but human GABAAR beta1 does not.	bind
933	2	1151	5	10	NULL	0	NULL	GABAAR beta1	GP	human	does not bind					BTX	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_53	16549768	( b) Human (h) GABAAR beta3 binds BTX, but human GABAAR beta1 does not.	bind
727	1	1151	7	10	NULL	0	NULL	GABAAR beta3	GP	Human	bind					BTX	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_53	16549768	( b) Human (h) GABAAR beta3 binds BTX, but human GABAAR beta1 does not.	bind
728	2	1151	7	10	NULL	0	NULL	GABAAR beta1	GP	Human	does not bind					BTX	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_53	16549768	( b) Human (h) GABAAR beta3 binds BTX, but human GABAAR beta1 does not.	bind
935	1	1152	5	10	NULL	0	NULL	GTP	Chemical		bind					Galpha13	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_280_5372_2109_s_59	9641915	( B) Hydrolysis of GTP bound to Galpha13 ( ) or Galpha12 ( ) was measured at 4 degrees C in the presence of the indicated concentrations of p115 RhoGEF.	bind
936	2	1152	5	10	NULL	0	NULL	GTP	Chemical		bind					Galpha12	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_280_5372_2109_s_59	9641915	( B) Hydrolysis of GTP bound to Galpha13 ( ) or Galpha12 ( ) was measured at 4 degrees C in the presence of the indicated concentrations of p115 RhoGEF.	bind
937	3	1152	5	10	NULL	0	NULL	statement 1	Process		 hydrolyze					p115 RhoGEF	GP	in the presence of			NULL		NULL	NULL	NULL	NULL	gw60_science_280_5372_2109_s_59	9641915	( B) Hydrolysis of GTP bound to Galpha13 ( ) or Galpha12 ( ) was measured at 4 degrees C in the presence of the indicated concentrations of p115 RhoGEF.	bind
938	4	1152	5	10	NULL	0	NULL	statement 2	Process		 hydrolyze					p115 RhoGEF	GP	in the presence of			NULL		NULL	NULL	NULL	NULL	gw60_science_280_5372_2109_s_59	9641915	( B) Hydrolysis of GTP bound to Galpha13 ( ) or Galpha12 ( ) was measured at 4 degrees C in the presence of the indicated concentrations of p115 RhoGEF.	bind
729	1	1152	7	10	NULL	0	NULL	GTP 	Chemical		bind					Galpha13	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_280_5372_2109_s_59	9641915	( B) Hydrolysis of GTP bound to Galpha13 ( ) or Galpha12 ( ) was measured at 4 degrees C in the presence of the indicated concentrations of p115 RhoGEF.	bind
733	3	1152	7	10	NULL	0	NULL	statement 1	Process		 hydrolyze					p115 RhoGEF	GP	in the presence of			NULL		NULL	NULL	NULL	NULL	gw60_science_280_5372_2109_s_59	9641915	( B) Hydrolysis of GTP bound to Galpha13 ( ) or Galpha12 ( ) was measured at 4 degrees C in the presence of the indicated concentrations of p115 RhoGEF.	bind
736	4	1152	7	10	NULL	0	NULL	statement 2	Process		undergoes hydrolysis					p115 RhoGEF	GP	in the presence of			NULL		NULL	NULL	NULL	NULL	gw60_science_280_5372_2109_s_59	9641915	( B) Hydrolysis of GTP bound to Galpha13 ( ) or Galpha12 ( ) was measured at 4 degrees C in the presence of the indicated concentrations of p115 RhoGEF.	bind
48846	2	1152	7	10	NULL	0	NULL	GTP	Chemical		bind					Galpha12	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_280_5372_2109_s_59	9641915	( B) Hydrolysis of GTP bound to Galpha13 ( ) or Galpha12 ( ) was measured at 4 degrees C in the presence of the indicated concentrations of p115 RhoGEF.	bind
942	1	1154	5	10	NULL	0	NULL	Stat1	GP		bind					DNA	NucleicAcid				NULL	WT MEFs	NULL	NULL	NULL	NULL	gw60_science_288_5475_2357_s_39	10875919	( B) IFN-gamma-induced  DNA-binding activities of Stat1 and ISGF3 in WT and  AR1 /  MEFs.	bind
943	2	1154	5	10	NULL	0	NULL	ISGF3	GP		bind					DNA	NucleicAcid				NULL	WT MEFs	NULL	NULL	NULL	NULL	gw60_science_288_5475_2357_s_39	10875919	( B) IFN-gamma-induced  DNA-binding activities of Stat1 and ISGF3 in WT and  AR1 /  MEFs.	bind
945	3	1154	5	10	NULL	0	NULL	IFN-gamma	GP		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_288_5475_2357_s_39	10875919	( B) IFN-gamma-induced  DNA-binding activities of Stat1 and ISGF3 in WT and  AR1 /  MEFs.	bind
946	4	1154	5	10	NULL	0	NULL	IFN-gamma	GP		induce					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_288_5475_2357_s_39	10875919	( B) IFN-gamma-induced  DNA-binding activities of Stat1 and ISGF3 in WT and  AR1 /  MEFs.	bind
48847	5	1154	5	10	NULL	0	NULL	Stat1	GP		bind					DNA	NucleicAcid				NULL	AR1 MEFs	NULL	NULL	NULL	NULL	gw60_science_288_5475_2357_s_39	10875919	( B) IFN-gamma-induced  DNA-binding activities of Stat1 and ISGF3 in WT and  AR1 /  MEFs.	bind
48848	6	1154	5	10	NULL	0	NULL	ISGF3	GP		bind					DNA	NucleicAcid				NULL	AR1 MEFs	NULL	NULL	NULL	NULL	gw60_science_288_5475_2357_s_39	10875919	( B) IFN-gamma-induced  DNA-binding activities of Stat1 and ISGF3 in WT and  AR1 /  MEFs.	bind
48849	7	1154	5	10	NULL	0	NULL	IFN-gamma	GP		induces					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_288_5475_2357_s_39	10875919	( B) IFN-gamma-induced  DNA-binding activities of Stat1 and ISGF3 in WT and  AR1 /  MEFs.	bind
48850	8	1154	5	10	NULL	0	NULL	IFN-gamma	GP		induces					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_288_5475_2357_s_39	10875919	( B) IFN-gamma-induced  DNA-binding activities of Stat1 and ISGF3 in WT and  AR1 /  MEFs.	bind
747	1	1154	7	10	NULL	0	NULL	Stat1	GP		bind 					DNA	NucleicAcid				NULL	WT MEFs	NULL	NULL	NULL	NULL	gw60_science_288_5475_2357_s_39	10875919	( B) IFN-gamma-induced  DNA-binding activities of Stat1 and ISGF3 in WT and  AR1 /  MEFs.	bind
749	2	1154	7	10	NULL	0	NULL	Stat1	GP		bind					DNA	NucleicAcid				NULL	AR1 MEFs	NULL	NULL	NULL	NULL	gw60_science_288_5475_2357_s_39	10875919	( B) IFN-gamma-induced  DNA-binding activities of Stat1 and ISGF3 in WT and  AR1 /  MEFs.	bind
754	3	1154	7	10	NULL	0	NULL	ISGF3	GP		bind					DNA	NucleicAcid				NULL	WT MEFs	NULL	NULL	NULL	NULL	gw60_science_288_5475_2357_s_39	10875919	( B) IFN-gamma-induced  DNA-binding activities of Stat1 and ISGF3 in WT and  AR1 /  MEFs.	bind
755	4	1154	7	10	NULL	0	NULL	ISGF3	GP		bind					DNA	NucleicAcid				NULL	AR1 MEFs	NULL	NULL	NULL	NULL	gw60_science_288_5475_2357_s_39	10875919	( B) IFN-gamma-induced  DNA-binding activities of Stat1 and ISGF3 in WT and  AR1 /  MEFs.	bind
758	5	1154	7	10	NULL	0	NULL	IFN-gamma	GP		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_288_5475_2357_s_39	10875919	( B) IFN-gamma-induced  DNA-binding activities of Stat1 and ISGF3 in WT and  AR1 /  MEFs.	bind
760	6	1154	7	10	NULL	0	NULL	IFN-gamma	GP		induces					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_288_5475_2357_s_39	10875919	( B) IFN-gamma-induced  DNA-binding activities of Stat1 and ISGF3 in WT and  AR1 /  MEFs.	bind
761	8	1154	7	10	NULL	0	NULL	 IFN-gamma	GP		induces					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_288_5475_2357_s_39	10875919	( B) IFN-gamma-induced  DNA-binding activities of Stat1 and ISGF3 in WT and  AR1 /  MEFs.	bind
763	7	1154	7	10	NULL	0	NULL	 IFN-gamma	GP		induces					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_288_5475_2357_s_39	10875919	( B) IFN-gamma-induced  DNA-binding activities of Stat1 and ISGF3 in WT and  AR1 /  MEFs.	bind
947	1	1156	5	10	NULL	0	NULL	His6-Skn7p	GP	immobilized	bind					calcineurin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3473_s_167	11432834	( B) Immobilized His6-Skn7p binds calcineurin and Crz1p, but not GST.	bind
948	2	1156	5	10	NULL	0	NULL	His6-Skn7p	GP	immobilized	bind					Crz1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3473_s_167	11432834	( B) Immobilized His6-Skn7p binds calcineurin and Crz1p, but not GST.	bind
769	1	1156	7	10	NULL	0	NULL	His6-Skn7p	GP	immobilized	bind					calcineurin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3473_s_167	11432834	( B) Immobilized His6-Skn7p binds calcineurin and Crz1p, but not GST.	bind
771	2	1156	7	10	NULL	0	NULL	His6-Skn7p	GP	immobilized 	bind					Crz1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3473_s_167	11432834	( B) Immobilized His6-Skn7p binds calcineurin and Crz1p, but not GST.	bind
974	3	1158	5	NULL	NULL	0	NULL	mtHsp70	NULL		bind	NULL				Tim44	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevcelldevbiol_13_0_25_s_209	9442867	( b) Import motor (pulling); mtHsp70 bound to Tim44 interacts with the precursor polypeptide  ( Horst et al 1996).	bind
975	4	1158	5	NULL	NULL	0	NULL	mtHsp70	NULL	bound to Tim44	interact	NULL				precursor polypeptide	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevcelldevbiol_13_0_25_s_209	9442867	( b) Import motor (pulling); mtHsp70 bound to Tim44 interacts with the precursor polypeptide  ( Horst et al 1996).	bind
775	1	1158	7	NULL	NULL	0	NULL	mtHsp70	NULL		bind	NULL				 Tim44	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevcelldevbiol_13_0_25_s_209	9442867	( b) Import motor (pulling); mtHsp70 bound to Tim44 interacts with the precursor polypeptide  ( Horst et al 1996).	bind
776	5	1158	7	NULL	NULL	0	NULL	mtHsp70	NULL	Tim44 bound	interacts with	NULL				precursor polypeptide	NULL				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_13_0_25_s_209	9442867	( b) Import motor (pulling); mtHsp70 bound to Tim44 interacts with the precursor polypeptide  ( Horst et al 1996).	bind
979	1	1160	5	10	NULL	0	NULL	Scr/xd heterodimers	GP		bind									Hox/Exd-binding sites	NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_16_0_243_s_313	11031237	( B) In the activity regulation model, multiple Hox/Exd heterodimers (in this example,  Scr/xd and Antp/xd) bind to the same Hox/Exd-binding sites.	bind
980	2	1160	5	10	NULL	0	NULL	Antp/xd heterodimers	GP		bind									Hox/Exd-binding sites	NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_16_0_243_s_313	11031237	( B) In the activity regulation model, multiple Hox/Exd heterodimers (in this example,  Scr/xd and Antp/xd) bind to the same Hox/Exd-binding sites.	bind
778	1	1160	7	10	NULL	0	NULL	Scr/xd heterodimers	GP		bind									Hox/Exd-binding sites	NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_16_0_243_s_313	11031237	( B) In the activity regulation model, multiple Hox/Exd heterodimers (in this example,  Scr/xd and Antp/xd) bind to the same Hox/Exd-binding sites.	bind
779	2	1160	7	10	NULL	0	NULL	Antp/xd heterodimers 	GP		bind									Hox/Exd-binding sites	NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_16_0_243_s_313	11031237	( B) In the activity regulation model, multiple Hox/Exd heterodimers (in this example,  Scr/xd and Antp/xd) bind to the same Hox/Exd-binding sites.	bind
981	1	1162	5	10	NULL	0	NULL	p4	GP		bind					p6	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_22_6185_s_247	12426390	( B) In the presence of p6 and low concentrations of p4, a p4 - p6 complex is formed, but RNAP can still bind to the A2c promoter as a closed complex, although open complexes are not formed ( Camacho and Salas, 2001b).	bind
982	2	1162	5	10	NULL	0	NULL	RNAP	GP		bind					A2c	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_21_22_6185_s_247	12426390	( B) In the presence of p6 and low concentrations of p4, a p4 - p6 complex is formed, but RNAP can still bind to the A2c promoter as a closed complex, although open complexes are not formed ( Camacho and Salas, 2001b).	bind
47955	3	1162	5	10	NULL	0	NULL	statement 2	Process		occurs as a 					closed complex	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_22_6185_s_247	12426390	( B) In the presence of p6 and low concentrations of p4, a p4 - p6 complex is formed, but RNAP can still bind to the A2c promoter as a closed complex, although open complexes are not formed ( Camacho and Salas, 2001b).	bind
781	1	1162	7	10	NULL	0	NULL	p4	GP		bind					p6	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_22_6185_s_247	12426390	( B) In the presence of p6 and low concentrations of p4, a p4 - p6 complex is formed, but RNAP can still bind to the A2c promoter as a closed complex, although open complexes are not formed ( Camacho and Salas, 2001b).	bind
783	2	1162	7	10	NULL	0	NULL	RNAP	GP		bind					 A2c	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_21_22_6185_s_247	12426390	( B) In the presence of p6 and low concentrations of p4, a p4 - p6 complex is formed, but RNAP can still bind to the A2c promoter as a closed complex, although open complexes are not formed ( Camacho and Salas, 2001b).	bind
784	3	1162	7	10	NULL	0	NULL	statement 2	Process		occurs as a					closed complex	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_22_6185_s_247	12426390	( B) In the presence of p6 and low concentrations of p4, a p4 - p6 complex is formed, but RNAP can still bind to the A2c promoter as a closed complex, although open complexes are not formed ( Camacho and Salas, 2001b).	bind
983	1	1163	5	10	NULL	0	NULL	SacY	GP		bind					mRNA	NucleicAcid	nascent		RAT site	NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_22_12538_s_59	11606741	( B) In the presence of SacY, SacY binds to the RAT site in the nascent mRNA, causing antitermination so that transcription proceeds through the SacB'-'LacZ coding sequence and beta-galactosidase is formed.	bind
786	1	1163	7	10	NULL	0	NULL	SacY 	GP		bind 					mRNA	NucleicAcid	nascent		 RAT site	NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_22_12538_s_59	11606741	( B) In the presence of SacY, SacY binds to the RAT site in the nascent mRNA, causing antitermination so that transcription proceeds through the SacB'-'LacZ coding sequence and beta-galactosidase is formed.	bind
984	1	1164	5	10	NULL	0	NULL	HFR1	GP		bind					PIF3	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_14_18_2377_s_197	10995393	( B) In vitro binding of HFR1 to PIF3.	bind
790	1	1164	7	10	NULL	0	NULL	HFR1	GP		bind					PIF3	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_14_18_2377_s_197	10995393	( B) In vitro binding of HFR1 to PIF3.	bind
985	1	1165	5	10	NULL	0	NULL	CD11c+	GP	pulmonary APC	bind					pA:pU	Chemical	tagged			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jclininvest_110_8_1175_s_206	12393853	( b) In vivo binding of pulmonary CD11c+ and CD11b+ APCs by tagged pA:pU.	bind
986	2	1165	5	10	NULL	0	NULL	CD11b+	GP	pulmonary APC	bind					pA:pU	Chemical	tagged			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jclininvest_110_8_1175_s_206	12393853	( b) In vivo binding of pulmonary CD11c+ and CD11b+ APCs by tagged pA:pU.	bind
791	1	1165	7	10	NULL	0	NULL	CD11c+ 	GP	pulmonary APC	bind					pA:pU	Chemical	tagged			NULL	In vivo	NULL	NULL	NULL	NULL	gw60_jclininvest_110_8_1175_s_206	12393853	( b) In vivo binding of pulmonary CD11c+ and CD11b+ APCs by tagged pA:pU.	bind
792	2	1165	7	10	NULL	0	NULL	CD11b+ 	GP	pulmonary APC	bind					pA:pU	Chemical	tagged			NULL	In vivo	NULL	NULL	NULL	NULL	gw60_jclininvest_110_8_1175_s_206	12393853	( b) In vivo binding of pulmonary CD11c+ and CD11b+ APCs by tagged pA:pU.	bind
987	1	1170	5	10	NULL	0	NULL	Virus	Organism	radiolabelled	bind					BHK cells	Cell	live			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_3_543_s_53	9927414	( B) Inhibition of binding of radiolabelled virus to live BHK cells by heparin in the presence (dotted line) and absence (solid line) of a 100-fold excess of unlabelled virus.	bind
939	1	1170	7	10	NULL	0	NULL	Virus	Organism	radiolabelled 	bind					BHK cells	Cell	live			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_3_543_s_53	9927414	( B) Inhibition of binding of radiolabelled virus to live BHK cells by heparin in the presence (dotted line) and absence (solid line) of a 100-fold excess of unlabelled virus.	bind
992	1	1171	5	10	NULL	0	NULL	FasL	GP		bind					Fas receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_17_6599_s_93	15084739	( B) Inhibition of FasL binding to the Fas receptor by exocyclic peptidemimetics in a  binding assay.	bind
993	2	1171	5	10	NULL	0	NULL	peptidemimetics	Chemical	exocyclic	inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_17_6599_s_93	15084739	( B) Inhibition of FasL binding to the Fas receptor by exocyclic peptidemimetics in a  binding assay.	bind
944	1	1171	7	10	NULL	0	NULL	FasL	GP		bind					Fas receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_17_6599_s_93	15084739	( B) Inhibition of FasL binding to the Fas receptor by exocyclic peptidemimetics in a  binding assay.	bind
949	2	1171	7	10	NULL	0	NULL	peptidemimetics	Chemical	exocyclic 	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_17_6599_s_93	15084739	( B) Inhibition of FasL binding to the Fas receptor by exocyclic peptidemimetics in a  binding assay.	bind
994	1	1172	5	10	NULL	0	NULL	importin-beta	GP		bind					NuMA	GP		tail II		NULL		NULL	NULL	NULL	NULL	gw60_science_291_5504_653_s_93	11229403	( B) Inhibition of importin-beta binding to NuMA tail II in extracts treated with RanL43E.	bind
995	2	1172	5	10	NULL	0	NULL	RanL43E	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_291_5504_653_s_93	11229403	( B) Inhibition of importin-beta binding to NuMA tail II in extracts treated with RanL43E.	bind
950	1	1172	7	10	NULL	0	NULL	importin-beta	GP		bind					NuMA 	GP		tail II		NULL		NULL	NULL	NULL	NULL	gw60_science_291_5504_653_s_93	11229403	( B) Inhibition of importin-beta binding to NuMA tail II in extracts treated with RanL43E.	bind
951	2	1172	7	10	NULL	0	NULL	RanL43E	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_291_5504_653_s_93	11229403	( B) Inhibition of importin-beta binding to NuMA tail II in extracts treated with RanL43E.	bind
996	1	1173	5	10	NULL	0	NULL	OspA peptide	GP	labeled	bind					TGE	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_106_4_561_s_98	10953031	( b) Inhibition of labeled OspA peptide binding to TGE by unlabeled OspA.	bind
997	2	1173	5	10	NULL	0	NULL	OspA	GP	unlabeled	inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_106_4_561_s_98	10953031	( b) Inhibition of labeled OspA peptide binding to TGE by unlabeled OspA.	bind
952	1	1173	7	10	NULL	0	NULL	OspA peptide	GP	labeled	bind					TGE	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_106_4_561_s_98	10953031	( b) Inhibition of labeled OspA peptide binding to TGE by unlabeled OspA.	bind
953	2	1173	7	10	NULL	0	NULL	OspA	GP	unlabeled	inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_106_4_561_s_98	10953031	( b) Inhibition of labeled OspA peptide binding to TGE by unlabeled OspA.	bind
998	1	1174	5	10	NULL	0	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_9_4844_s_183	10781090	( B) Inhibition of NF-kappaB DNA binding by cyclopentenone.	bind
999	2	1174	5	10	NULL	0	NULL	cyclopentenone	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_9_4844_s_183	10781090	( B) Inhibition of NF-kappaB DNA binding by cyclopentenone.	bind
954	1	1174	7	10	NULL	0	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_9_4844_s_183	10781090	( B) Inhibition of NF-kappaB DNA binding by cyclopentenone.	bind
955	2	1174	7	10	NULL	0	NULL	cyclopentenone	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_9_4844_s_183	10781090	( B) Inhibition of NF-kappaB DNA binding by cyclopentenone.	bind
1000	1	1175	5	10	NULL	0	NULL	biotin-HKa	GP		bind					tropomyosin	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_19_12224_s_157	12196635	( B) Inhibition of the binding of 20 nM biotin-HKa to purified tropomyosin by mAb TM-311.	bind
1001	2	1175	5	10	NULL	0	NULL	mAb TM-311	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_19_12224_s_157	12196635	( B) Inhibition of the binding of 20 nM biotin-HKa to purified tropomyosin by mAb TM-311.	bind
956	1	1175	7	10	NULL	0	NULL	biotin-HKa	GP		bind					tropomyosin	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_19_12224_s_157	12196635	( B) Inhibition of the binding of 20 nM biotin-HKa to purified tropomyosin by mAb TM-311.	bind
957	2	1175	7	10	NULL	0	NULL	mAb TM-311	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_19_12224_s_157	12196635	( B) Inhibition of the binding of 20 nM biotin-HKa to purified tropomyosin by mAb TM-311.	bind
1002	1	1176	5	10	NULL	0	NULL	A-p50	GP		bind					NF-kappaB p50 protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_12_3577_s_137	16855294	( B) Intracellular binding of A-p50 to NF-kappaB p50 protein.	bind
958	1	1176	7	10	NULL	0	NULL	 A-p50	GP		bind 					NF-kappaB p50 protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_12_3577_s_137	16855294	( B) Intracellular binding of A-p50 to NF-kappaB p50 protein.	bind
1005	1	1177	5	10	NULL	0	NULL	Ub	GP		bind								NZF		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1411_s_112	15029239	( B) Isotherms for Ub binding to wt and mutant NZF domains from Vps36p: wt Vps36-1 NZF  (black), Vps36-1 (T13G) NZF mutant (red), Vps36-1 (13TF14 to 13GS14) NZF mutant (blue), and wt Vps36-2 NZF (green).	bind
1006	2	1177	5	10	NULL	0	NULL	Ub	GP		bind								T13G;; NZF		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1411_s_112	15029239	( B) Isotherms for Ub binding to wt and mutant NZF domains from Vps36p: wt Vps36-1 NZF  (black), Vps36-1 (T13G) NZF mutant (red), Vps36-1 (13TF14 to 13GS14) NZF mutant (blue), and wt Vps36-2 NZF (green).	bind
1007	3	1177	5	10	NULL	0	NULL	Ub	GP		bind								13TF14 to 13GS14;; NZF		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1411_s_112	15029239	( B) Isotherms for Ub binding to wt and mutant NZF domains from Vps36p: wt Vps36-1 NZF  (black), Vps36-1 (T13G) NZF mutant (red), Vps36-1 (13TF14 to 13GS14) NZF mutant (blue), and wt Vps36-2 NZF (green).	bind
1008	4	1177	5	10	NULL	0	NULL	Ub	GP		bind								NZF		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1411_s_112	15029239	( B) Isotherms for Ub binding to wt and mutant NZF domains from Vps36p: wt Vps36-1 NZF  (black), Vps36-1 (T13G) NZF mutant (red), Vps36-1 (13TF14 to 13GS14) NZF mutant (blue), and wt Vps36-2 NZF (green).	bind
61093	5	1177	5	10	NULL	0	NULL	statement 1	Process		derived from			NZF		Vps36-1	GP	wt			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1411_s_112	15029239	( B) Isotherms for Ub binding to wt and mutant NZF domains from Vps36p: wt Vps36-1 NZF  (black), Vps36-1 (T13G) NZF mutant (red), Vps36-1 (13TF14 to 13GS14) NZF mutant (blue), and wt Vps36-2 NZF (green).	bind
61094	6	1177	5	10	NULL	0	NULL	statement 2	Process		derived from			NZF		Vps36-1	GP	mutant	T13G		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1411_s_112	15029239	( B) Isotherms for Ub binding to wt and mutant NZF domains from Vps36p: wt Vps36-1 NZF  (black), Vps36-1 (T13G) NZF mutant (red), Vps36-1 (13TF14 to 13GS14) NZF mutant (blue), and wt Vps36-2 NZF (green).	bind
61095	7	1177	5	10	NULL	0	NULL	statement 3	Process		derived from			NZF		Vps36-1	GP	mutant	13TF14 to 13GS14		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1411_s_112	15029239	( B) Isotherms for Ub binding to wt and mutant NZF domains from Vps36p: wt Vps36-1 NZF  (black), Vps36-1 (T13G) NZF mutant (red), Vps36-1 (13TF14 to 13GS14) NZF mutant (blue), and wt Vps36-2 NZF (green).	bind
61096	8	1177	5	10	NULL	0	NULL	statement 4	Process		derived from			NZF		Vps36-2	GP	wt			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1411_s_112	15029239	( B) Isotherms for Ub binding to wt and mutant NZF domains from Vps36p: wt Vps36-1 NZF  (black), Vps36-1 (T13G) NZF mutant (red), Vps36-1 (13TF14 to 13GS14) NZF mutant (blue), and wt Vps36-2 NZF (green).	bind
959	3	1177	7	10	NULL	0	NULL	Ub	GP		bind								NZF		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1411_s_112	15029239	( B) Isotherms for Ub binding to wt and mutant NZF domains from Vps36p: wt Vps36-1 NZF  (black), Vps36-1 (T13G) NZF mutant (red), Vps36-1 (13TF14 to 13GS14) NZF mutant (blue), and wt Vps36-2 NZF (green).	bind
960	1	1177	7	10	NULL	0	NULL	Ub	GP		bind								T13G;;NZF 		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1411_s_112	15029239	( B) Isotherms for Ub binding to wt and mutant NZF domains from Vps36p: wt Vps36-1 NZF  (black), Vps36-1 (T13G) NZF mutant (red), Vps36-1 (13TF14 to 13GS14) NZF mutant (blue), and wt Vps36-2 NZF (green).	bind
961	2	1177	7	10	NULL	0	NULL	Ub	GP		bind								13TF14 to 13GS14;;NZF		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1411_s_112	15029239	( B) Isotherms for Ub binding to wt and mutant NZF domains from Vps36p: wt Vps36-1 NZF  (black), Vps36-1 (T13G) NZF mutant (red), Vps36-1 (13TF14 to 13GS14) NZF mutant (blue), and wt Vps36-2 NZF (green).	bind
962	4	1177	7	10	NULL	0	NULL	Ub	GP		bind 								 NZF		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1411_s_112	15029239	( B) Isotherms for Ub binding to wt and mutant NZF domains from Vps36p: wt Vps36-1 NZF  (black), Vps36-1 (T13G) NZF mutant (red), Vps36-1 (13TF14 to 13GS14) NZF mutant (blue), and wt Vps36-2 NZF (green).	bind
61097	5	1177	7	10	NULL	0	NULL	statement 1	Process		derived from			NZF		Vps36-1	GP	wt			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1411_s_112	15029239	( B) Isotherms for Ub binding to wt and mutant NZF domains from Vps36p: wt Vps36-1 NZF  (black), Vps36-1 (T13G) NZF mutant (red), Vps36-1 (13TF14 to 13GS14) NZF mutant (blue), and wt Vps36-2 NZF (green).	bind
61098	6	1177	7	10	NULL	0	NULL	statement 2	Process		derived from			NZF		Vps36-1	GP	mutant	T13G		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1411_s_112	15029239	( B) Isotherms for Ub binding to wt and mutant NZF domains from Vps36p: wt Vps36-1 NZF  (black), Vps36-1 (T13G) NZF mutant (red), Vps36-1 (13TF14 to 13GS14) NZF mutant (blue), and wt Vps36-2 NZF (green).	bind
61099	7	1177	7	10	NULL	0	NULL	statement 3	Process		derived from			NZF		Vps36-1	GP	mutant	13TF14 to 13GS14		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1411_s_112	15029239	( B) Isotherms for Ub binding to wt and mutant NZF domains from Vps36p: wt Vps36-1 NZF  (black), Vps36-1 (T13G) NZF mutant (red), Vps36-1 (13TF14 to 13GS14) NZF mutant (blue), and wt Vps36-2 NZF (green).	bind
61100	8	1177	7	10	NULL	0	NULL	statement 4	Process		derived from			NZF		Vps36-2	GP	wt			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1411_s_112	15029239	( B) Isotherms for Ub binding to wt and mutant NZF domains from Vps36p: wt Vps36-1 NZF  (black), Vps36-1 (T13G) NZF mutant (red), Vps36-1 (13TF14 to 13GS14) NZF mutant (blue), and wt Vps36-2 NZF (green).	bind
1009	1	1178	5	10	NULL	0	NULL	ISWI	GP		bind					H2A nucleosomes	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_19_3815_s_98	15372075	( B) ISWI binding to the H2A and H2ABbd nucleosomes.	bind
1010	2	1178	5	10	NULL	0	NULL	ISWI	GP		bind					H2ABbd nucleosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_19_3815_s_98	15372075	( B) ISWI binding to the H2A and H2ABbd nucleosomes.	bind
963	1	1178	7	10	NULL	0	NULL	 ISWI	GP		bind					H2A nucleosomes	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_19_3815_s_98	15372075	( B) ISWI binding to the H2A and H2ABbd nucleosomes.	bind
964	2	1178	7	10	NULL	0	NULL	ISWI	GP		bind					H2ABbd nucleosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_19_3815_s_98	15372075	( B) ISWI binding to the H2A and H2ABbd nucleosomes.	bind
1014	1	1179	5	10	NULL	0	NULL	CypA	GP		bind					Itk	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_4_1899_s_156	11830645	( b) Itk phosphorylation following TCR stimulation of Jurkat cells in the presence and absence of CsA. ( c) CypA binding to Itk was monitored by detection of Itk immunoprecipitates with an anti-CypA antibody.	bind
1015	2	1179	5	10	NULL	0	NULL	TCR	GP		stimulate					Itk	GP	phosphorylation of			NULL	Jurkat cells	NULL	NULL	NULL	NULL	gw60_pnas_99_4_1899_s_156	11830645	( b) Itk phosphorylation following TCR stimulation of Jurkat cells in the presence and absence of CsA. ( c) CypA binding to Itk was monitored by detection of Itk immunoprecipitates with an anti-CypA antibody.	bind
965	1	1179	7	10	NULL	0	NULL	TCR	GP		stimulate					Itk	GP	phosphorylation of			NULL	Jurkat cells	NULL	NULL	NULL	NULL	gw60_pnas_99_4_1899_s_156	11830645	( b) Itk phosphorylation following TCR stimulation of Jurkat cells in the presence and absence of CsA. ( c) CypA binding to Itk was monitored by detection of Itk immunoprecipitates with an anti-CypA antibody.	bind
969	2	1179	7	10	NULL	0	NULL	CypA	GP		bind					Itk	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_4_1899_s_156	11830645	( b) Itk phosphorylation following TCR stimulation of Jurkat cells in the presence and absence of CsA. ( c) CypA binding to Itk was monitored by detection of Itk immunoprecipitates with an anti-CypA antibody.	bind
1016	1	1180	5	10	NULL	0	NULL	JNK	GP		bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_17_2658_s_30	9732264	( b) JNK binding to p53 is inhibited by p7.	bind
1017	2	1180	5	10	NULL	0	NULL	p7	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_17_2658_s_30	9732264	( b) JNK binding to p53 is inhibited by p7.	bind
970	1	1180	7	10	NULL	0	NULL	JNK	GP		bind					 p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_17_2658_s_30	9732264	( b) JNK binding to p53 is inhibited by p7.	bind
971	2	1180	7	10	NULL	0	NULL	p7	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_17_2658_s_30	9732264	( b) JNK binding to p53 is inhibited by p7.	bind
1051	1	1181	5	10	NULL	0	NULL	spt	GP		does not bind			K145E ( spt15-640)		TFIIA	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6662_s_162	10581240	( B) K145E ( spt15-640) fails to bind TFIIA.	bind
976	1	1181	7	10	NULL	0	NULL	spt	GP		does not bind			K145E ( spt15-640)		TFIIA	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6662_s_162	10581240	( B) K145E ( spt15-640) fails to bind TFIIA.	bind
1052	1	1182	5	10	NULL	0	NULL	kappaB-DNA	GP		bind		preferentially			p50 homodimer	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_16_9268_s_26	12886018	( b) kappaB-DNA  sequences that preferentially bind the p50 homodimer ( Upper) and  p50/p65 heterodimer ( Lower) are shown.	bind
1053	2	1182	5	10	NULL	0	NULL	kappaB-DNA	GP		bind		preferentially			p50/p65 heterodimer	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_16_9268_s_26	12886018	( b) kappaB-DNA  sequences that preferentially bind the p50 homodimer ( Upper) and  p50/p65 heterodimer ( Lower) are shown.	bind
977	1	1182	7	10	NULL	0	NULL	kappaB-DNA	GP		bind		preferentially			p50 homodimer	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_16_9268_s_26	12886018	( b) kappaB-DNA  sequences that preferentially bind the p50 homodimer ( Upper) and  p50/p65 heterodimer ( Lower) are shown.	bind
978	2	1182	7	10	NULL	0	NULL	kappaB-DNA	GP		bind		preferentially 			p50/p65 heterodimer	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_16_9268_s_26	12886018	( b) kappaB-DNA  sequences that preferentially bind the p50 homodimer ( Upper) and  p50/p65 heterodimer ( Lower) are shown.	bind
1054	1	1183	5	10	NULL	0	NULL	gp120	GP	core	bind					CD4 surface	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_16_9026_s_148	10922058	( B) Kinetic data set collected for core gp120 binding to a CD4 surface.	bind
1018	1	1183	7	10	NULL	0	NULL	gp120	GP	core	bind					CD4 surface	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_16_9026_s_148	10922058	( B) Kinetic data set collected for core gp120 binding to a CD4 surface.	bind
1055	1	1185	5	10	NULL	0	NULL	FGF-2	GP		associate					Namalwa	Cell	transfectants			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1211_s_152	12697740	( b) Kinetics of FGFR-1 binding to FGF-2 - associated Namalwa transfectants.	bind
1056	2	1185	5	10	NULL	0	NULL	FGFR-1	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1211_s_152	12697740	( b) Kinetics of FGFR-1 binding to FGF-2 - associated Namalwa transfectants.	bind
1021	1	1185	7	10	NULL	0	NULL	FGF2	GP		associate					Namalwa	Cell	transfectants			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1211_s_152	12697740	( b) Kinetics of FGFR-1 binding to FGF-2 - associated Namalwa transfectants.	bind
1262	2	1185	7	10	NULL	0	NULL	FGFR-1	GP		bind 					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1211_s_152	12697740	( b) Kinetics of FGFR-1 binding to FGF-2 - associated Namalwa transfectants.	bind
47956	1	1186	5	10	NULL	0	NULL	PNA I	GP		bind					pSD1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_9_5953_s_59	11972051	( b) Kinetics of PNA I binding to pSD1 target as monitored by gel-shift assay.	bind
1022	1	1186	7	10	NULL	0	NULL	PNA I	GP		bind					pSD1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_9_5953_s_59	11972051	( b) Kinetics of PNA I binding to pSD1 target as monitored by gel-shift assay.	bind
1057	1	1187	5	10	NULL	0	NULL	GST-PDZ2	GP		bind					CFTR	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_3_1300_s_138	11158634	( B) Kinetics-response data for GST-PDZ2 binding to CFTR.	bind
1023	1	1187	7	10	NULL	0	NULL	GST-PDZ2	GP		bind					CFTR	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_3_1300_s_138	11158634	( B) Kinetics-response data for GST-PDZ2 binding to CFTR.	bind
1058	1	1188	5	10	NULL	0	NULL	Ku	GP		bind					IP6	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_19_5501_s_176	14500812	( b) Ku binding to IP6.	bind
1024	1	1188	7	10	NULL	0	NULL	Ku	GP		bind					IP6	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_19_5501_s_176	14500812	( b) Ku binding to IP6.	bind
1059	1	1189	5	10	NULL	0	NULL	L525P-Axin 	GP		does not bind					GSK-3beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_9_1066_s_100	12000790	( b) L525P-Axin does not bind GSK-3beta.	bind
1025	1	1189	7	10	NULL	0	NULL	L525P-Axin	GP		does not bind					GSK-3beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_9_1066_s_100	12000790	( b) L525P-Axin does not bind GSK-3beta.	bind
1060	1	1190	5	10	NULL	0	NULL	LARG	GP		bind		directly	PDZ		plexin-B1	GP		C terminus		NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_19_12085_s_192	12196628	( B) LARG-PDZ directly binds the C terminus of plexin-B1.	bind
1026	1	1190	7	10	NULL	0	NULL	LARG	GP		bind 		directly	PDZ		plexin-B1	GP		C terminus		NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_19_12085_s_192	12196628	( B) LARG-PDZ directly binds the C terminus of plexin-B1.	bind
1061	1	1191	5	10	NULL	0	NULL	Lectin	GP		bind					Reelin	GP				NULL	CSF samples	NULL	NULL	NULL	NULL	gw70_pnas_103_14_5573_s_114	16567613	( B) Lectin binding of 180-kDa Reelin in gender- and age-matched CSF samples for 9 NDC  and 11 AD subjects.	bind
1027	1	1191	7	10	NULL	0	NULL	Lectin	GP		bind					Reelin	GP				NULL	CSF samples	NULL	NULL	NULL	NULL	gw70_pnas_103_14_5573_s_114	16567613	( B) Lectin binding of 180-kDa Reelin in gender- and age-matched CSF samples for 9 NDC  and 11 AD subjects.	bind
1062	1	1193	5	10	NULL	0	NULL	PI(3,4,5)P3	Chemical		bind					GST-PLCgamma1	GP		PH		NULL		NULL	NULL	NULL	NULL	gw60_embo_17_2_414_s_52	9430633	( B) Ligand displacement of [32]gPI(3,4,5)P3 binding to GST-PLCgamma1-PH by Ins(1,3,4,5)P4.	bind
1063	2	1193	5	10	NULL	0	NULL	Ins(1,3,4,5)P4	Chemical		bind					GST-PLCgamma1	GP		PH		NULL		NULL	NULL	NULL	NULL	gw60_embo_17_2_414_s_52	9430633	( B) Ligand displacement of [32]gPI(3,4,5)P3 binding to GST-PLCgamma1-PH by Ins(1,3,4,5)P4.	bind
1028	1	1193	7	10	NULL	0	NULL	PI(3,4,5)P3	Chemical		bind					GST-PLCgamma1	GP		PH		NULL		NULL	NULL	NULL	NULL	gw60_embo_17_2_414_s_52	9430633	( B) Ligand displacement of [32]gPI(3,4,5)P3 binding to GST-PLCgamma1-PH by Ins(1,3,4,5)P4.	bind
1029	2	1193	7	10	NULL	0	NULL	Ins(1,3,4,5)P4	Chemical		bind					GST-PLCgamma1	GP		PH		NULL		NULL	NULL	NULL	NULL	gw60_embo_17_2_414_s_52	9430633	( B) Ligand displacement of [32]gPI(3,4,5)P3 binding to GST-PLCgamma1-PH by Ins(1,3,4,5)P4.	bind
1064	1	1194	5	10	NULL	0	NULL	LC13 TcR	GP		bind					FLR - HLA-B8 complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_17_6641_s_99	16617112	( B) Ligated conformation of the LC13 TcR bound to the FLR - HLA-B8 complex (purple).	bind
1030	1	1194	7	10	NULL	0	NULL	LC13 TcR	GP		bind					FLR - HLA-B8 complex 	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_17_6641_s_99	16617112	( B) Ligated conformation of the LC13 TcR bound to the FLR - HLA-B8 complex (purple).	bind
1066	1	1197	5	10	NULL	0	NULL	LSm protein	GP		bind					U6	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_20_5789_s_255	10523320	( B) LSm protein binding of the U6 mutants.	bind
1032	1	1197	7	10	NULL	0	NULL	LSm protein	GP		bind					U6 	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_20_5789_s_255	10523320	( B) LSm protein binding of the U6 mutants.	bind
1067	1	1198	5	10	NULL	0	NULL	cell wall	Cell	maize	bind					EXPB1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_40_14664_s_140	16984999	( B) Maize cell walls bind EXPB1.	bind
1033	1	1198	7	10	NULL	0	NULL	cell wall	Cell	Maize 	bind 					EXPB1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_40_14664_s_140	16984999	( B) Maize cell walls bind EXPB1.	bind
1068	1	1199	5	10	NULL	0	NULL	VEGF	GP		bind					VEGFR2	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_22_12485_s_211	11606713	( B) Mammary tumor sections from TgN-neu (a-c), neu-hTSP1 (d-f), neu- tbsp1  /  (g-i) mice were evaluated for expression of VEGF by using two antibodies: GV39 M, which recognizes VEGF bound to VEGFR2 (b, e, h) and a polyclonal anti-mouse VEGF, which recognizes the receptor-free form (c, f, i).	bind
1034	1	1199	7	10	NULL	0	NULL	VEGF 	GP		bind					VEGFR2	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_22_12485_s_211	11606713	( B) Mammary tumor sections from TgN-neu (a-c), neu-hTSP1 (d-f), neu- tbsp1  /  (g-i) mice were evaluated for expression of VEGF by using two antibodies: GV39 M, which recognizes VEGF bound to VEGFR2 (b, e, h) and a polyclonal anti-mouse VEGF, which recognizes the receptor-free form (c, f, i).	bind
1087	1	1231	6	NULL	NULL	0	NULL	p21	NULL		bind	NULL				PCNA	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_4_1392_s_124	9465025	( B) p21 and p57 bind to PCNA via similar sequences.	bind
1088	2	1231	6	NULL	NULL	0	NULL	p57	NULL		bind	NULL				PCNA	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_4_1392_s_124	9465025	( B) p21 and p57 bind to PCNA via similar sequences.	bind
1092	1	1245	6	NULL	NULL	0	NULL	PGC-1	NULL		bind	NULL				SRC-1	NULL				NULL	cells	NULL	NULL	NULL	NULL	gw60_science_286_5443_1368_s_109	10558993	( B) PPARgamma and NRF-1 increase the binding of PGC-1 to SRC-1 and p300 in cells.	bind
1093	2	1245	6	NULL	NULL	0	NULL	PGC-1	NULL		bind	NULL				p300	NULL				NULL	cells	NULL	NULL	NULL	NULL	gw60_science_286_5443_1368_s_109	10558993	( B) PPARgamma and NRF-1 increase the binding of PGC-1 to SRC-1 and p300 in cells.	bind
1094	3	1245	6	NULL	NULL	0	NULL	PPARgamma	NULL		increases	NULL				Statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_science_286_5443_1368_s_109	10558993	( B) PPARgamma and NRF-1 increase the binding of PGC-1 to SRC-1 and p300 in cells.	bind
1095	4	1245	6	NULL	NULL	0	NULL	PPARgamma	NULL		increases	NULL				Statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_science_286_5443_1368_s_109	10558993	( B) PPARgamma and NRF-1 increase the binding of PGC-1 to SRC-1 and p300 in cells.	bind
1096	5	1245	6	NULL	NULL	0	NULL	NRF-1	NULL		increases	NULL				Statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_science_286_5443_1368_s_109	10558993	( B) PPARgamma and NRF-1 increase the binding of PGC-1 to SRC-1 and p300 in cells.	bind
1097	6	1245	6	NULL	NULL	0	NULL	NRF-1	NULL		increases	NULL				Statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_science_286_5443_1368_s_109	10558993	( B) PPARgamma and NRF-1 increase the binding of PGC-1 to SRC-1 and p300 in cells.	bind
1142	5	1401	5	NULL	NULL	0	NULL	Yan monomer	NULL	phosphorylation	favor	NULL				Crm1	NULL	binding			NULL		0	NULL	NULL	NULL	gw70_genesdev_19_15_1767_s_120	16027171	( B) Upon RTK activation, phosphorylation of the Yan monomer favors Crm1 binding, leading  to the export of the Yan monomer.	bind
1143	6	1401	5	NULL	NULL	0	NULL	RTK	NULL	activation	required for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_15_1767_s_120	16027171	( B) Upon RTK activation, phosphorylation of the Yan monomer favors Crm1 binding, leading  to the export of the Yan monomer.	bind
1144	7	1401	5	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				Yan monomer	NULL	export			NULL		0	NULL	NULL	NULL	gw70_genesdev_19_15_1767_s_120	16027171	( B) Upon RTK activation, phosphorylation of the Yan monomer favors Crm1 binding, leading  to the export of the Yan monomer.	bind
1035	12	1401	7	NULL	NULL	0	NULL	Yan monomer	NULL	 phosphorylated 	bind	NULL				Crm1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_15_1767_s_120	16027171	( B) Upon RTK activation, phosphorylation of the Yan monomer favors Crm1 binding, leading  to the export of the Yan monomer.	bind
1038	13	1401	7	NULL	NULL	0	NULL	statement 12	NULL		leads to 	NULL				Yan monomer	NULL	the export of 			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_15_1767_s_120	16027171	( B) Upon RTK activation, phosphorylation of the Yan monomer favors Crm1 binding, leading  to the export of the Yan monomer.	bind
1583	14	1401	7	NULL	NULL	0	NULL	RTK	NULL	activation of 	required for	NULL				statement 12	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_15_1767_s_120	16027171	( B) Upon RTK activation, phosphorylation of the Yan monomer favors Crm1 binding, leading  to the export of the Yan monomer.	bind
1145	1	1402	5	10	NULL	0	NULL	ATP	Chemical		bind					Hsp104	GP		Y819W		NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_5_2732_s_190	11867765	( B) Urea denaturation of  Hsp104549-908 R826M monitored by CD at 225 nm. ATP ( C) and ADP ( D) binding to Hsp104Y819W R826M fit to a single-site Hill equation.	bind
1146	2	1402	5	10	NULL	0	NULL	ADP	Chemical		bind					Hsp104	GP		Y819W		NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_5_2732_s_190	11867765	( B) Urea denaturation of  Hsp104549-908 R826M monitored by CD at 225 nm. ATP ( C) and ADP ( D) binding to Hsp104Y819W R826M fit to a single-site Hill equation.	bind
1197	1	1402	7	10	NULL	0	NULL	ATP	Chemical		bind					Hsp104	GP		Y819W		NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_5_2732_s_190	11867765	( B) Urea denaturation of  Hsp104549-908 R826M monitored by CD at 225 nm. ATP ( C) and ADP ( D) binding to Hsp104Y819W R826M fit to a single-site Hill equation.	bind
1198	2	1402	7	10	NULL	0	NULL	ADP	Chemical		bind					Hsp104	GP		Y819W		NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_5_2732_s_190	11867765	( B) Urea denaturation of  Hsp104549-908 R826M monitored by CD at 225 nm. ATP ( C) and ADP ( D) binding to Hsp104Y819W R826M fit to a single-site Hill equation.	bind
1147	1	1403	5	10	NULL	0	NULL	ATP	Chemical		bind					TAP1	GP	single chain			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_387_s_155	11157746	( B) US6 does not inhibit ATP binding by single chain TAP1.	bind
1148	2	1403	5	10	NULL	0	NULL	US6	GP		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_387_s_155	11157746	( B) US6 does not inhibit ATP binding by single chain TAP1.	bind
1199	1	1403	7	10	NULL	0	NULL	ATP	Chemical		bind					TAP1	GP	single chain			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_387_s_155	11157746	( B) US6 does not inhibit ATP binding by single chain TAP1.	bind
1200	2	1403	7	10	NULL	0	NULL	US6	GP		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_387_s_155	11157746	( B) US6 does not inhibit ATP binding by single chain TAP1.	bind
1149	1	1404	5	NULL	NULL	0	NULL	USF-1	NULL		bind	NULL				lama3	NULL			promoter	NULL	in vivo	0	NULL	NULL	NULL	gw60_nucleicacidsres_30_8_1789_s_134	11937633	( B) USF-1 binds the  lama3 promoter  in vivo.	bind
1201	3	1404	7	NULL	NULL	0	NULL	USF-1	NULL		bind	NULL				lama3 	NULL			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_8_1789_s_134	11937633	( B) USF-1 binds the  lama3 promoter  in vivo.	bind
1151	1	1406	5	10	NULL	0	NULL	VDR-RXR heterodimers	GP		bind					CYP3A 	GP			VDRE	NULL		NULL	NULL	NULL	NULL	gw60_science_296_5571_1313_s_90	12016314	( B) VDR-RXR heterodimers bind to CYP3A VDREs.	bind
1202	2	1406	7	10	NULL	0	NULL	VDR-RXR heterodimers	GP		bind					CYP3A 	GP			VDRE	NULL		NULL	NULL	NULL	NULL	gw60_science_296_5571_1313_s_90	12016314	( B) VDR-RXR heterodimers bind to CYP3A VDREs.	bind
1152	1	1407	5	10	NULL	0	NULL	Vinculin	GP		bind					IpaA	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_5853_s_77	10545097	( B) Vinculin binding to IpaA is inhibited by MBPV1-265.	bind
1153	2	1407	5	10	NULL	0	NULL	MBPV1-265	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_5853_s_77	10545097	( B) Vinculin binding to IpaA is inhibited by MBPV1-265.	bind
1203	1	1407	7	10	NULL	0	NULL	Vinculin	GP		bind					IpaA	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_5853_s_77	10545097	( B) Vinculin binding to IpaA is inhibited by MBPV1-265.	bind
1204	2	1407	7	10	NULL	0	NULL	MBPV1-265	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_5853_s_77	10545097	( B) Vinculin binding to IpaA is inhibited by MBPV1-265.	bind
1154	1	1409	5	10	NULL	0	NULL	reelin	GP		bind					SNSs	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_9_5479_s_164	12707415	( B) Western immunoblot of reelin bound to SNSs after incubation with or without reelin in the presence or absence of different doses of rapamycin.	bind
1205	1	1409	7	10	NULL	0	NULL	reelin	GP		bind to					SNSs	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_9_5479_s_164	12707415	( B) Western immunoblot of reelin bound to SNSs after incubation with or without reelin in the presence or absence of different doses of rapamycin.	bind
1155	1	1410	5	10	NULL	0	NULL	Hh	GP		bind					Ptc	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3505_s_42	9649421	( B) When Hh binds to Ptc, the inhibitory effect on Smo is suppressed.	bind
1156	2	1410	5	10	NULL	0	NULL	statement 1	Process		suppresses					Smo	GP	inhibitory effect on			NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3505_s_42	9649421	( B) When Hh binds to Ptc, the inhibitory effect on Smo is suppressed.	bind
1281	1	1410	7	10	NULL	0	NULL	Hh	GP		bind 					 Ptc	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3505_s_42	9649421	( B) When Hh binds to Ptc, the inhibitory effect on Smo is suppressed.	bind
1284	2	1410	7	10	NULL	0	NULL	statement 1	Process		suppresses					Smo	GP	inhibitory effect on 			NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3505_s_42	9649421	( B) When Hh binds to Ptc, the inhibitory effect on Smo is suppressed.	bind
1157	1	1411	5	10	NULL	0	NULL	MTs	CellComponent		bind					kinetochore	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_18_0_193_s_328	12142285	( B) When MTs bind a kinetochore, they prevent future CP activation either by competing  for kinetochore-binding sites or by some mechanism for active removal ( straight arrows), perhaps by removing them from the kinetochore with minus end-directed motors.	bind
1158	2	1411	5	10	NULL	0	NULL	statement 1	Process		prevent					CP	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_18_0_193_s_328	12142285	( B) When MTs bind a kinetochore, they prevent future CP activation either by competing  for kinetochore-binding sites or by some mechanism for active removal ( straight arrows), perhaps by removing them from the kinetochore with minus end-directed motors.	bind
1287	1	1411	7	10	NULL	0	NULL	MTs	CellComponent		bind 					kinetochore	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_18_0_193_s_328	12142285	( B) When MTs bind a kinetochore, they prevent future CP activation either by competing  for kinetochore-binding sites or by some mechanism for active removal ( straight arrows), perhaps by removing them from the kinetochore with minus end-directed motors.	bind
1288	2	1411	7	10	NULL	0	NULL	statement 1	Process		prevent					CP	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_18_0_193_s_328	12142285	( B) When MTs bind a kinetochore, they prevent future CP activation either by competing  for kinetochore-binding sites or by some mechanism for active removal ( straight arrows), perhaps by removing them from the kinetochore with minus end-directed motors.	bind
1159	1	1412	5	10	NULL	0	NULL	TBP	GP		bind					BNA1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_174	15861138	( B) Wild-type ( TAF1) and  taf1 cells were grown and heat-shocked as in panel A. TBP binding to the  BNA1 and  URA1 promoters was then determined by ChIP.	bind
1160	2	1412	5	10	NULL	0	NULL	TBP	GP		bind					 URA1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_174	15861138	( B) Wild-type ( TAF1) and  taf1 cells were grown and heat-shocked as in panel A. TBP binding to the  BNA1 and  URA1 promoters was then determined by ChIP.	bind
1388	3	1412	7	10	NULL	0	NULL	TBP	GP		bind					BNA1	GP			 promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_174	15861138	( B) Wild-type ( TAF1) and  taf1 cells were grown and heat-shocked as in panel A. TBP binding to the  BNA1 and  URA1 promoters was then determined by ChIP.	bind
1389	4	1412	7	10	NULL	0	NULL	TBP	GP		bind					URA1 	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_174	15861138	( B) Wild-type ( TAF1) and  taf1 cells were grown and heat-shocked as in panel A. TBP binding to the  BNA1 and  URA1 promoters was then determined by ChIP.	bind
1161	1	1413	5	10	NULL	0	NULL	WT1	GP		bind					GST-U2AF65	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_20_3217_s_84	9784496	( B) WT1 binding to GST-U2AF65 compared to GST alone under different salt concentrations.	bind
1398	1	1413	7	10	NULL	0	NULL	WT1	GP		bind					GST-U2AF65	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_20_3217_s_84	9784496	( B) WT1 binding to GST-U2AF65 compared to GST alone under different salt concentrations.	bind
1162	1	1414	5	10	NULL	0	NULL	dCLOCK-dBMAL1 heterodimer	GP		bind					per	GP			E-box site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_science_280_5369_1599_s_146	9616122	( B) Yeast one-hybrid assay showing binding of the dCLOCK-dBMAL1 heterodimer to the  per E-box site.	bind
1399	1	1414	7	10	NULL	0	NULL	dCLOCK-dBMAL1 heterodimer	GP		bind					per	GP			E-box site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_science_280_5369_1599_s_146	9616122	( B) Yeast one-hybrid assay showing binding of the dCLOCK-dBMAL1 heterodimer to the  per E-box site.	bind
1163	1	1415	5	NULL	NULL	0	NULL	GRIP	NULL		bind	NULL	selectively	PDZ domain 6		SR	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_6_2105_s_116	15684087	( B) Yeast two-hybrid analysis establishes selective binding of GRIP's PDZ domain  6 to SR. ( C and  D) Yeast two-hybrid analysis was used to determine which region of SR interacts with  GRIP.	bind
1401	3	1415	7	NULL	NULL	0	NULL	GRIP	NULL		bind to	NULL	selectively	PDZ domain 6		SR	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_6_2105_s_116	15684087	( B) Yeast two-hybrid analysis establishes selective binding of GRIP's PDZ domain  6 to SR. ( C and  D) Yeast two-hybrid analysis was used to determine which region of SR interacts with  GRIP.	bind
1164	1	1416	5	10	NULL	0	NULL	YopJ	GP		bind		specifically			GST-MKK1	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_science_285_5435_1920_s_35	10489373	( B) YopJ specifically bound recombinant GST-MKK1, GST-MKK3, GST-MKK4/SEK1, and GST-MKK5 but not GST. 35S-methionine-labeled pcDNA3-YopJ was incubated with bacterially expressed recombinant GST (lane 2), GST-MKK1 (lane 3), GST-MKK3 (lane 4), GST-MKK4/SEK1 (lane 5), or GST-MKK5 (lane 6) bound to glutathione-agarose and analyzed as previously described ( 29,  30).	bind
1165	2	1416	5	10	NULL	0	NULL	YopJ	GP		bind		specifically			GST-MKK3	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_science_285_5435_1920_s_35	10489373	( B) YopJ specifically bound recombinant GST-MKK1, GST-MKK3, GST-MKK4/SEK1, and GST-MKK5 but not GST. 35S-methionine-labeled pcDNA3-YopJ was incubated with bacterially expressed recombinant GST (lane 2), GST-MKK1 (lane 3), GST-MKK3 (lane 4), GST-MKK4/SEK1 (lane 5), or GST-MKK5 (lane 6) bound to glutathione-agarose and analyzed as previously described ( 29,  30).	bind
1166	3	1416	5	10	NULL	0	NULL	YopJ	GP		bind		specifically			GST-MKK4/SEK1	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_science_285_5435_1920_s_35	10489373	( B) YopJ specifically bound recombinant GST-MKK1, GST-MKK3, GST-MKK4/SEK1, and GST-MKK5 but not GST. 35S-methionine-labeled pcDNA3-YopJ was incubated with bacterially expressed recombinant GST (lane 2), GST-MKK1 (lane 3), GST-MKK3 (lane 4), GST-MKK4/SEK1 (lane 5), or GST-MKK5 (lane 6) bound to glutathione-agarose and analyzed as previously described ( 29,  30).	bind
1167	4	1416	5	10	NULL	0	NULL	YopJ	GP		bind		specifically			GST-MKK5	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_science_285_5435_1920_s_35	10489373	( B) YopJ specifically bound recombinant GST-MKK1, GST-MKK3, GST-MKK4/SEK1, and GST-MKK5 but not GST. 35S-methionine-labeled pcDNA3-YopJ was incubated with bacterially expressed recombinant GST (lane 2), GST-MKK1 (lane 3), GST-MKK3 (lane 4), GST-MKK4/SEK1 (lane 5), or GST-MKK5 (lane 6) bound to glutathione-agarose and analyzed as previously described ( 29,  30).	bind
1169	5	1416	5	10	NULL	0	NULL	YopJ	GP		does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5435_1920_s_35	10489373	( B) YopJ specifically bound recombinant GST-MKK1, GST-MKK3, GST-MKK4/SEK1, and GST-MKK5 but not GST. 35S-methionine-labeled pcDNA3-YopJ was incubated with bacterially expressed recombinant GST (lane 2), GST-MKK1 (lane 3), GST-MKK3 (lane 4), GST-MKK4/SEK1 (lane 5), or GST-MKK5 (lane 6) bound to glutathione-agarose and analyzed as previously described ( 29,  30).	bind
1431	1	1416	7	10	NULL	0	NULL	YopJ 	GP		bind		specifically			GST-MKK1	GP	recombinant 			NULL		NULL	NULL	NULL	NULL	gw60_science_285_5435_1920_s_35	10489373	( B) YopJ specifically bound recombinant GST-MKK1, GST-MKK3, GST-MKK4/SEK1, and GST-MKK5 but not GST. 35S-methionine-labeled pcDNA3-YopJ was incubated with bacterially expressed recombinant GST (lane 2), GST-MKK1 (lane 3), GST-MKK3 (lane 4), GST-MKK4/SEK1 (lane 5), or GST-MKK5 (lane 6) bound to glutathione-agarose and analyzed as previously described ( 29,  30).	bind
1432	2	1416	7	10	NULL	0	NULL	YopJ	GP		bind 		specifically			GST-MKK3	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_science_285_5435_1920_s_35	10489373	( B) YopJ specifically bound recombinant GST-MKK1, GST-MKK3, GST-MKK4/SEK1, and GST-MKK5 but not GST. 35S-methionine-labeled pcDNA3-YopJ was incubated with bacterially expressed recombinant GST (lane 2), GST-MKK1 (lane 3), GST-MKK3 (lane 4), GST-MKK4/SEK1 (lane 5), or GST-MKK5 (lane 6) bound to glutathione-agarose and analyzed as previously described ( 29,  30).	bind
1433	3	1416	7	10	NULL	0	NULL	YopJ	GP		bind		specifically			GST-MKK4/SEK1	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_science_285_5435_1920_s_35	10489373	( B) YopJ specifically bound recombinant GST-MKK1, GST-MKK3, GST-MKK4/SEK1, and GST-MKK5 but not GST. 35S-methionine-labeled pcDNA3-YopJ was incubated with bacterially expressed recombinant GST (lane 2), GST-MKK1 (lane 3), GST-MKK3 (lane 4), GST-MKK4/SEK1 (lane 5), or GST-MKK5 (lane 6) bound to glutathione-agarose and analyzed as previously described ( 29,  30).	bind
1434	4	1416	7	10	NULL	0	NULL	YopJ	GP		bind		specifically			GST-MKK5	GP	recombinant 			NULL		NULL	NULL	NULL	NULL	gw60_science_285_5435_1920_s_35	10489373	( B) YopJ specifically bound recombinant GST-MKK1, GST-MKK3, GST-MKK4/SEK1, and GST-MKK5 but not GST. 35S-methionine-labeled pcDNA3-YopJ was incubated with bacterially expressed recombinant GST (lane 2), GST-MKK1 (lane 3), GST-MKK3 (lane 4), GST-MKK4/SEK1 (lane 5), or GST-MKK5 (lane 6) bound to glutathione-agarose and analyzed as previously described ( 29,  30).	bind
1435	5	1416	7	10	NULL	0	NULL	YopJ	GP		does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5435_1920_s_35	10489373	( B) YopJ specifically bound recombinant GST-MKK1, GST-MKK3, GST-MKK4/SEK1, and GST-MKK5 but not GST. 35S-methionine-labeled pcDNA3-YopJ was incubated with bacterially expressed recombinant GST (lane 2), GST-MKK1 (lane 3), GST-MKK3 (lane 4), GST-MKK4/SEK1 (lane 5), or GST-MKK5 (lane 6) bound to glutathione-agarose and analyzed as previously described ( 29,  30).	bind
1170	1	1417	5	10	NULL	0	NULL	ZapA	GP		bind					FtsZ	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_19_2544_s_191	12368265	( B) ZapA binds to FtsZ.	bind
1436	1	1417	7	10	NULL	0	NULL	ZapA	GP		bind					FtsZ	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_19_2544_s_191	12368265	( B) ZapA binds to FtsZ.	bind
1172	1	1418	5	NULL	NULL	0	NULL	[gamma-32]GTP-RhoV14	NULL		bind	NULL				GST	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_103_11_1561_s_232	10359565	( b) [gamma-32]GTP-RhoV14 bound to GST, GST-RhoGAP, and GST-IL-1Rcd was quantified by scintillation counting, and cpm bound to GST fusion proteins are normalized to those bound to GST in each of 7 independent experiments.	bind
1173	2	1418	5	NULL	NULL	0	NULL	[gamma-32]GTP-RhoV14	NULL		bind	NULL				GST-RhoGAP	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_103_11_1561_s_232	10359565	( b) [gamma-32]GTP-RhoV14 bound to GST, GST-RhoGAP, and GST-IL-1Rcd was quantified by scintillation counting, and cpm bound to GST fusion proteins are normalized to those bound to GST in each of 7 independent experiments.	bind
1174	3	1418	5	NULL	NULL	0	NULL	[gamma-32]GTP-RhoV14	NULL		bind	NULL				GST-IL-1Rcd	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_103_11_1561_s_232	10359565	( b) [gamma-32]GTP-RhoV14 bound to GST, GST-RhoGAP, and GST-IL-1Rcd was quantified by scintillation counting, and cpm bound to GST fusion proteins are normalized to those bound to GST in each of 7 independent experiments.	bind
1175	4	1418	5	NULL	NULL	0	NULL	cpm	NULL		bind	NULL				GST fusion proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_103_11_1561_s_232	10359565	( b) [gamma-32]GTP-RhoV14 bound to GST, GST-RhoGAP, and GST-IL-1Rcd was quantified by scintillation counting, and cpm bound to GST fusion proteins are normalized to those bound to GST in each of 7 independent experiments.	bind
1437	5	1418	7	NULL	NULL	0	NULL	[gamma-32]GTP-RhoV14	NULL		bind to	NULL				GST	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_103_11_1561_s_232	10359565	( b) [gamma-32]GTP-RhoV14 bound to GST, GST-RhoGAP, and GST-IL-1Rcd was quantified by scintillation counting, and cpm bound to GST fusion proteins are normalized to those bound to GST in each of 7 independent experiments.	bind
1438	6	1418	7	NULL	NULL	0	NULL	 [gamma-32]GTP-RhoV14	NULL		bind to	NULL				GST-RhoGAP	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_103_11_1561_s_232	10359565	( b) [gamma-32]GTP-RhoV14 bound to GST, GST-RhoGAP, and GST-IL-1Rcd was quantified by scintillation counting, and cpm bound to GST fusion proteins are normalized to those bound to GST in each of 7 independent experiments.	bind
1439	7	1418	7	NULL	NULL	0	NULL	[gamma-32]GTP-RhoV14 	NULL		bind to	NULL				GST-IL-1Rcd	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_103_11_1561_s_232	10359565	( b) [gamma-32]GTP-RhoV14 bound to GST, GST-RhoGAP, and GST-IL-1Rcd was quantified by scintillation counting, and cpm bound to GST fusion proteins are normalized to those bound to GST in each of 7 independent experiments.	bind
1588	8	1418	7	NULL	NULL	0	NULL	cpm	NULL		bind	NULL				GST fusion proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_103_11_1561_s_232	10359565	( b) [gamma-32]GTP-RhoV14 bound to GST, GST-RhoGAP, and GST-IL-1Rcd was quantified by scintillation counting, and cpm bound to GST fusion proteins are normalized to those bound to GST in each of 7 independent experiments.	bind
1177	1	1419	5	10	NULL	0	NULL	40S hnRNP proteins	GP		bind					DNase I	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_8_1725_s_167	11937625	( b,  e and  h) Western blot analyses of 40S hnRNP proteins bound to DNase I - Sepharose.	bind
1440	1	1419	7	10	NULL	0	NULL	40S-hnRNP proteins 	GP		bind					DNase I	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_8_1725_s_167	11937625	( b,  e and  h) Western blot analyses of 40S hnRNP proteins bound to DNase I - Sepharose.	bind
1178	1	1420	5	NULL	NULL	0	NULL	importin-GFP	NULL		bind	NULL				Pho4	NULL	WT	zz		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_17_2673_s_132	9732266	( B, C) (Lanes  1,5) About 3% of the importin-GFP loaded; (lanes  2,6) importin-GFP bound to Pho4WT-zz; (lanes  3,7) importin-GFP bound to Pho4delta157-164-zz; (lanes  4,8) importin-GFP bound to the IgG-Sepharose control.	bind
1179	8	1420	5	NULL	NULL	0	NULL	importin-GFP	NULL		bind	NULL				Pho4	NULL		delta157-164-zz		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_17_2673_s_132	9732266	( B, C) (Lanes  1,5) About 3% of the importin-GFP loaded; (lanes  2,6) importin-GFP bound to Pho4WT-zz; (lanes  3,7) importin-GFP bound to Pho4delta157-164-zz; (lanes  4,8) importin-GFP bound to the IgG-Sepharose control.	bind
1180	3	1420	5	NULL	NULL	0	NULL	importin-GFP	NULL		bind	NULL				IgG-Sepharose	NULL	control			NULL		0	NULL	NULL	NULL	gw60_genesdev_12_17_2673_s_132	9732266	( B, C) (Lanes  1,5) About 3% of the importin-GFP loaded; (lanes  2,6) importin-GFP bound to Pho4WT-zz; (lanes  3,7) importin-GFP bound to Pho4delta157-164-zz; (lanes  4,8) importin-GFP bound to the IgG-Sepharose control.	bind
1441	9	1420	7	NULL	NULL	0	NULL	 importin-GFP	NULL		bind to	NULL				Pho4	NULL	WT	zz		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_17_2673_s_132	9732266	( B, C) (Lanes  1,5) About 3% of the importin-GFP loaded; (lanes  2,6) importin-GFP bound to Pho4WT-zz; (lanes  3,7) importin-GFP bound to Pho4delta157-164-zz; (lanes  4,8) importin-GFP bound to the IgG-Sepharose control.	bind
1442	6	1420	7	NULL	NULL	0	NULL	importin-GFP	NULL		bind to	NULL				Pho4	NULL		delta157-164-zz		NULL		0	NULL	NULL	NULL	gw60_genesdev_12_17_2673_s_132	9732266	( B, C) (Lanes  1,5) About 3% of the importin-GFP loaded; (lanes  2,6) importin-GFP bound to Pho4WT-zz; (lanes  3,7) importin-GFP bound to Pho4delta157-164-zz; (lanes  4,8) importin-GFP bound to the IgG-Sepharose control.	bind
1443	7	1420	7	NULL	NULL	0	NULL	importin-GFP	NULL		bind to	NULL				IgG-Sepharose	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_17_2673_s_132	9732266	( B, C) (Lanes  1,5) About 3% of the importin-GFP loaded; (lanes  2,6) importin-GFP bound to Pho4WT-zz; (lanes  3,7) importin-GFP bound to Pho4delta157-164-zz; (lanes  4,8) importin-GFP bound to the IgG-Sepharose control.	bind
1181	1	1422	5	10	NULL	0	NULL	p130	GP	endogenous	bind					HDAC1	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_6_719_s_184	15769944	( B,C) Apoptotic stimuli lead to loss of cellular association between endogenous p130 and  HDAC1 ( B) or Suv39H1 ( C).	bind
1182	2	1422	5	10	NULL	0	NULL	p130	GP	endogenous	bind		alternately			Suv39H1	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_6_719_s_184	15769944	( B,C) Apoptotic stimuli lead to loss of cellular association between endogenous p130 and  HDAC1 ( B) or Suv39H1 ( C).	bind
1183	3	1422	5	10	NULL	0	NULL	apoptotic stimuli 	Process		leads to					statement 1	Process	loss of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_6_719_s_184	15769944	( B,C) Apoptotic stimuli lead to loss of cellular association between endogenous p130 and  HDAC1 ( B) or Suv39H1 ( C).	bind
1184	4	1422	5	10	NULL	0	NULL	apoptotic stimuli	Process		leads to					statement 2	Process	loss of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_6_719_s_184	15769944	( B,C) Apoptotic stimuli lead to loss of cellular association between endogenous p130 and  HDAC1 ( B) or Suv39H1 ( C).	bind
1444	1	1422	7	10	NULL	0	NULL	p130	GP	endogenous	associate					HDAC1	GP	cellular			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_6_719_s_184	15769944	( B,C) Apoptotic stimuli lead to loss of cellular association between endogenous p130 and  HDAC1 ( B) or Suv39H1 ( C).	bind
1445	2	1422	7	10	NULL	0	NULL	p130	GP	endogenous	associate					Suv39H1	GP	cellular			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_6_719_s_184	15769944	( B,C) Apoptotic stimuli lead to loss of cellular association between endogenous p130 and  HDAC1 ( B) or Suv39H1 ( C).	bind
1446	3	1422	7	10	NULL	0	NULL	Apoptotic stimuli	Process		lead to					statement 1	Process	loss of 			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_6_719_s_184	15769944	( B,C) Apoptotic stimuli lead to loss of cellular association between endogenous p130 and  HDAC1 ( B) or Suv39H1 ( C).	bind
1447	4	1422	7	10	NULL	0	NULL	Apoptotic stimuli	Process		lead to					statement 1	Process	loss of 			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_6_719_s_184	15769944	( B,C) Apoptotic stimuli lead to loss of cellular association between endogenous p130 and  HDAC1 ( B) or Suv39H1 ( C).	bind
1185	8	1424	5	NULL	NULL	0	NULL	TLE1	NULL	groucho family protein	bind	NULL				PRDI-BF1	NULL		repression domain		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_13_1_125_s_175	9887105	( B,D) Groucho family proteins TLE1 and TLE2 bind to the repression domain of PRDI-BF1 in vitro.	bind
1186	9	1424	5	NULL	NULL	0	NULL	TLE2	NULL	groucho family protein	bind	NULL				PRDI-BF1	NULL		repression domain		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_13_1_125_s_175	9887105	( B,D) Groucho family proteins TLE1 and TLE2 bind to the repression domain of PRDI-BF1 in vitro.	bind
1448	6	1424	7	NULL	NULL	0	NULL	TLE1	NULL	Groucho family proteins	bind to	NULL		 		PRDI-BF1	NULL		repression domain 		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_13_1_125_s_175	9887105	( B,D) Groucho family proteins TLE1 and TLE2 bind to the repression domain of PRDI-BF1 in vitro.	bind
1449	7	1424	7	NULL	NULL	0	NULL	TLE2	NULL	Groucho family proteins	bind to	NULL				PRDI-BF1	NULL		repression domain 		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_13_1_125_s_175	9887105	( B,D) Groucho family proteins TLE1 and TLE2 bind to the repression domain of PRDI-BF1 in vitro.	bind
1187	1	1425	5	10	NULL	0	NULL	Pcn1	GP	recombinant	bind					GST-Cdc27 proteins	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_19_5_1108_s_52	10698951	( B- D)  In vitro binding of recombinant Pcn1 to GST-Cdc27 proteins.	bind
1450	1	1425	7	10	NULL	0	NULL	Pcn1 	GP	recombinant	bind					GST-Cdc27 proteins	GP				NULL	In vitro	NULL	NULL	NULL	NULL	gw60_embo_19_5_1108_s_52	10698951	( B- D)  In vitro binding of recombinant Pcn1 to GST-Cdc27 proteins.	bind
1190	1	1426	5	NULL	NULL	0	NULL	PL	NULL	from CNC	quenched by	NULL				DNP-BS	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_1_49_s_38	11756675	( Ba) PL from CNC is quenched by DNP-BS  and recovered on the specific binding between DNP-BS  and anti-DNP antibody.	bind
1191	2	1426	5	NULL	NULL	0	NULL	DNP-BS	NULL		bind	NULL	specifically			anti-DNP antibody	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_1_49_s_38	11756675	( Ba) PL from CNC is quenched by DNP-BS  and recovered on the specific binding between DNP-BS  and anti-DNP antibody.	bind
1451	3	1426	7	NULL	NULL	0	NULL	DNP-BS 	NULL		bind	NULL	specific			anti-DNP antibody	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_1_49_s_38	11756675	( Ba) PL from CNC is quenched by DNP-BS  and recovered on the specific binding between DNP-BS  and anti-DNP antibody.	bind
1592	4	1426	7	NULL	NULL	0	NULL	PL	NULL	from CNC	quenched by	NULL				DNP-BS	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_1_49_s_38	11756675	( Ba) PL from CNC is quenched by DNP-BS  and recovered on the specific binding between DNP-BS  and anti-DNP antibody.	bind
1188	1	1427	5	10	NULL	0	NULL	Cbl-b protein	GP		bind					EGFR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_27677_s_154	11375397	( Bind  EGFR) shows the EGF-induced binding of each Cbl-b protein to the EGFR as determined by co-immunoprecipitation.	bind
1189	2	1427	5	10	NULL	0	NULL	EGF	GP		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_27677_s_154	11375397	( Bind  EGFR) shows the EGF-induced binding of each Cbl-b protein to the EGFR as determined by co-immunoprecipitation.	bind
1452	1	1427	7	10	NULL	0	NULL	Cbl-b protein	GP		bind					EGFR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_27677_s_154	11375397	( Bind  EGFR) shows the EGF-induced binding of each Cbl-b protein to the EGFR as determined by co-immunoprecipitation.	bind
1453	2	1427	7	10	NULL	0	NULL	EGF	GP		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_27677_s_154	11375397	( Bind  EGFR) shows the EGF-induced binding of each Cbl-b protein to the EGFR as determined by co-immunoprecipitation.	bind
1192	1	1428	5	10	NULL	0	NULL	Tfp	GP		bind					corneal epithelial cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_26_15276_s_107	11752467	( Bottom) Binding of Tfp to human corneal epithelial cells assesed by indirect immunofluorescence.	bind
1454	1	1428	7	10	NULL	0	NULL	Tfp	GP		bind 					corneal epithelial cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_26_15276_s_107	11752467	( Bottom) Binding of Tfp to human corneal epithelial cells assesed by indirect immunofluorescence.	bind
1193	1	1429	5	10	NULL	0	NULL	myosin	GP		bind		strongly			actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_47_16990_s_134	16287977	( Bottom) However, once a myosin binds strongly to actin, neighboring Tn - Tm regulatory units,  spanning three units, are activated, allowing myosins to bind at an accelerated rate  [ kwsx ( acc/ reg)].	bind
1194	2	1429	5	10	NULL	0	NULL	statement 1	Process		leads to					Tn - Tm regulatory units	GP	activation			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_47_16990_s_134	16287977	( Bottom) However, once a myosin binds strongly to actin, neighboring Tn - Tm regulatory units,  spanning three units, are activated, allowing myosins to bind at an accelerated rate  [ kwsx ( acc/ reg)].	bind
1195	3	1429	5	10	NULL	0	NULL	statement 2	Process		allows					myosin	GP	accelerated binding of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_47_16990_s_134	16287977	( Bottom) However, once a myosin binds strongly to actin, neighboring Tn - Tm regulatory units,  spanning three units, are activated, allowing myosins to bind at an accelerated rate  [ kwsx ( acc/ reg)].	bind
1455	1	1429	7	10	NULL	0	NULL	myosin	GP		bind		strongly			actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_47_16990_s_134	16287977	( Bottom) However, once a myosin binds strongly to actin, neighboring Tn - Tm regulatory units,  spanning three units, are activated, allowing myosins to bind at an accelerated rate  [ kwsx ( acc/ reg)].	bind
1456	2	1429	7	10	NULL	0	NULL	statement 1	Process		leads to					Tn - Tm regulatory units	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_47_16990_s_134	16287977	( Bottom) However, once a myosin binds strongly to actin, neighboring Tn - Tm regulatory units,  spanning three units, are activated, allowing myosins to bind at an accelerated rate  [ kwsx ( acc/ reg)].	bind
47957	3	1429	7	10	NULL	0	NULL	statement 2	Process		allows					myosin	GP	accelerated binding of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_47_16990_s_134	16287977	( Bottom) However, once a myosin binds strongly to actin, neighboring Tn - Tm regulatory units,  spanning three units, are activated, allowing myosins to bind at an accelerated rate  [ kwsx ( acc/ reg)].	bind
1196	1	1430	5	NULL	NULL	0	NULL	X2BP	NULL		bind	NULL	low affinity			NF-Y	NULL				NULL	RFX-deficient BLS cells	0	NULL	NULL	NULL	gw70_annurevimmunol_19_0_331_s_403	11244040	( Bottom) In RFX-deficient BLS cells, cooperative binding is lost, and the residual low binding  affinity of X2BP and NF-Y are not sufficient for stable promoter occupation in vivo.	bind
1549	2	1430	5	NULL	NULL	0	NULL	statement 1	NULL		is not sufficient for	NULL					NULL	stable occupation of		promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_annurevimmunol_19_0_331_s_403	11244040	( Bottom) In RFX-deficient BLS cells, cooperative binding is lost, and the residual low binding  affinity of X2BP and NF-Y are not sufficient for stable promoter occupation in vivo.	bind
1459	6	1430	7	NULL	NULL	0	NULL	X2BP	NULL		bind to	NULL	low affinity			NF-Y	NULL				NULL	in vivo in RFX-deficient BLS cells	NULL	NULL	NULL	NULL	gw70_annurevimmunol_19_0_331_s_403	11244040	( Bottom) In RFX-deficient BLS cells, cooperative binding is lost, and the residual low binding  affinity of X2BP and NF-Y are not sufficient for stable promoter occupation in vivo.	bind
1460	10	1430	7	NULL	NULL	0	NULL	statement 6	NULL		is not sufficient for	NULL					NULL	stable occupation of 		promoter	NULL	in vivo in RFX-deficient BLS cells	NULL	NULL	NULL	NULL	gw70_annurevimmunol_19_0_331_s_403	11244040	( Bottom) In RFX-deficient BLS cells, cooperative binding is lost, and the residual low binding  affinity of X2BP and NF-Y are not sufficient for stable promoter occupation in vivo.	bind
1241	1	1431	5	NULL	NULL	0	NULL	S3LC(2P)	NULL		bind	NULL				Ski	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_16_15_1950_s_190	12154125	( Bottom) S3LC(2P) binds Ski betterR than the unphosphorylated S3LC after extensive washing.	bind
1242	2	1431	5	NULL	NULL	0	NULL	S3LC	NULL	unphosphorylated	bind	NULL				Ski	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_16_15_1950_s_190	12154125	( Bottom) S3LC(2P) binds Ski betterR than the unphosphorylated S3LC after extensive washing.	bind
1243	3	1431	5	NULL	NULL	0	NULL	statement 1	NULL		better than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_16_15_1950_s_190	12154125	( Bottom) S3LC(2P) binds Ski betterR than the unphosphorylated S3LC after extensive washing.	bind
1461	4	1431	7	NULL	NULL	0	NULL	S3LC(2P) 	NULL		binds	NULL				Ski 	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_16_15_1950_s_190	12154125	( Bottom) S3LC(2P) binds Ski betterR than the unphosphorylated S3LC after extensive washing.	bind
1462	5	1431	7	NULL	NULL	0	NULL	S3LC	NULL		binds 	NULL				 Ski	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_16_15_1950_s_190	12154125	( Bottom) S3LC(2P) binds Ski betterR than the unphosphorylated S3LC after extensive washing.	bind
1463	7	1431	7	NULL	NULL	0	NULL	statement 4	NULL		is better than 	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_15_1950_s_190	12154125	( Bottom) S3LC(2P) binds Ski betterR than the unphosphorylated S3LC after extensive washing.	bind
1244	1	1434	5	10	NULL	0	NULL	CHC	GP		bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_9_1087_s_180	16618797	( Bottom) The intensity of relative CHC binding to p53 was quantified by PhosphorImager.	bind
1464	1	1434	7	10	NULL	0	NULL	CHC	GP		bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_9_1087_s_180	16618797	( Bottom) The intensity of relative CHC binding to p53 was quantified by PhosphorImager.	bind
1245	3	1435	5	NULL	NULL	0	NULL	tubby	NULL	putative transcription factor	bind	NULL	directly			PI(4,5)P2 phospholipid	NULL				NULL	in plasma membrane	NULL	NULL	NULL	NULL	gw60_science_292_5524_2019_s_25	11408644	( Bottom) The putative transcription factor tubby is directly bound to PI(4,5)P2, a phospholipid in the plasma membrane.	bind
1465	4	1435	7	NULL	NULL	0	NULL	tubby	NULL	putative transcription factor	bind to	NULL	directly			PI(4,5)P2 phospholipid	NULL				NULL	 in plasma membrane	NULL	NULL	NULL	NULL	gw60_science_292_5524_2019_s_25	11408644	( Bottom) The putative transcription factor tubby is directly bound to PI(4,5)P2, a phospholipid in the plasma membrane.	bind
1246	2	1436	5	NULL	NULL	0	NULL	Noxa	NULL	wild-type	bind	NULL				Mcl-1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_172	15901672	( Bottom) Wild-type, but not mutant, Noxa bound Mcl-1 (fifth panel), disrupting the complex  between Mcl-1 and Bak.	bind
1247	3	1436	5	NULL	NULL	0	NULL	Noxa	NULL	mutant	does not bind	NULL				Mcl-1	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_172	15901672	( Bottom) Wild-type, but not mutant, Noxa bound Mcl-1 (fifth panel), disrupting the complex  between Mcl-1 and Bak.	bind
1248	4	1436	5	NULL	NULL	0	NULL	Mcl-1	NULL		bind	NULL				Bak	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_172	15901672	( Bottom) Wild-type, but not mutant, Noxa bound Mcl-1 (fifth panel), disrupting the complex  between Mcl-1 and Bak.	bind
1249	5	1436	5	NULL	NULL	0	NULL	statement 1	NULL		disrupt	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_172	15901672	( Bottom) Wild-type, but not mutant, Noxa bound Mcl-1 (fifth panel), disrupting the complex  between Mcl-1 and Bak.	bind
1466	6	1436	7	NULL	NULL	0	NULL	Noxa	NULL	Wild-type	bind to	NULL				Mcl-1	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_172	15901672	( Bottom) Wild-type, but not mutant, Noxa bound Mcl-1 (fifth panel), disrupting the complex  between Mcl-1 and Bak.	bind
1467	7	1436	7	NULL	NULL	0	NULL	Noxa	NULL	mutant	does not bind	NULL				Mcl-1	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_172	15901672	( Bottom) Wild-type, but not mutant, Noxa bound Mcl-1 (fifth panel), disrupting the complex  between Mcl-1 and Bak.	bind
1468	10	1436	7	NULL	NULL	0	NULL	Mcl-1	NULL		forms complex with	NULL				Bak	NULL				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_172	15901672	( Bottom) Wild-type, but not mutant, Noxa bound Mcl-1 (fifth panel), disrupting the complex  between Mcl-1 and Bak.	bind
1469	11	1436	7	NULL	NULL	0	NULL	statement 6	NULL		disrupts	NULL				statement 10	NULL				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1294_s_172	15901672	( Bottom) Wild-type, but not mutant, Noxa bound Mcl-1 (fifth panel), disrupting the complex  between Mcl-1 and Bak.	bind
49173	1	1439	5	10	NULL	0	NULL	GST - CBS1-4	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
49174	2	1439	5	10	NULL	0	NULL	GST - CBS1-4	GP		is obtained from					gamma1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
49175	3	1439	5	10	NULL	0	NULL	GST - CBS1-4	GP		is obtained from					gamma2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
49176	4	1439	5	10	NULL	0	NULL	GST - CBS1-4	GP		is obtained from					gamma3	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
49177	5	1439	5	10	NULL	0	NULL	AMP	Chemical		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
49178	6	1439	5	10	NULL	0	NULL	AMP	Chemical		bind					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
49179	7	1439	5	10	NULL	0	NULL	AMP	Chemical		bind					statement 4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
49180	8	1439	5	10	NULL	0	NULL	ATP	Chemical		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
49181	9	1439	5	10	NULL	0	NULL	ATP	Chemical		bind					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
49182	10	1439	5	10	NULL	0	NULL	ATP	Chemical		bind					statement 4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
1471	1	1439	7	10	NULL	0	NULL	GST - CBS1-4	GP		is obtained from					gamma1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
1472	2	1439	7	10	NULL	0	NULL	GST - CBS1-4	GP		is obtained from					gamma2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
1473	3	1439	7	10	NULL	0	NULL	GST - CBS1-4	GP		is obtained from					gamma3	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
1474	4	1439	7	10	NULL	0	NULL	GST - CBS1-4	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
48964	5	1439	7	10	NULL	0	NULL	AMP	Chemical		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
48965	6	1439	7	10	NULL	0	NULL	AMP	Chemical		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
48966	7	1439	7	10	NULL	0	NULL	AMP	Chemical		bind					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
48967	8	1439	7	10	NULL	0	NULL	ATP	Chemical		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
48968	9	1439	7	10	NULL	0	NULL	ATP	Chemical		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
48969	10	1439	7	10	NULL	0	NULL	ATP	Chemical		bind					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_105	14722619	( c and  d) Binding of AMP ( c) and ATP ( d) by the GST - CBS1-4 fusion proteins from gamma1, gamma2, and gamma3.	bind
1250	1	1442	5	10	NULL	0	NULL	Cy3-cAMP	Chemical		bind					Dictyostelium cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_science_294_5543_864_s_35	11679673	( C and  D) Fluorescence  images of Cy3-cAMP bound to  Dictyostelium cells.	bind
1476	2	1442	7	10	NULL	0	NULL	Cy3-cAMP	Chemical		bind					Dictyostelium cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_science_294_5543_864_s_35	11679673	( C and  D) Fluorescence  images of Cy3-cAMP bound to  Dictyostelium cells.	bind
1251	1	1443	5	10	NULL	0	NULL	pG3zf	GP		bind					BcrAbl probe	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4865_s_107	11121477	( c and  d) Gel retardation assays of pG3zf and pG4zf binding the  BcrAbl probe in the presence of the  NonSp competitor.	bind
1252	2	1443	5	10	NULL	0	NULL	pG4zf	GP		bind					BcrAbl probe	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4865_s_107	11121477	( c and  d) Gel retardation assays of pG3zf and pG4zf binding the  BcrAbl probe in the presence of the  NonSp competitor.	bind
1477	1	1443	7	10	NULL	0	NULL	pG3zf	GP		bind					BcrAbl probe	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4865_s_107	11121477	( c and  d) Gel retardation assays of pG3zf and pG4zf binding the  BcrAbl probe in the presence of the  NonSp competitor.	bind
1478	2	1443	7	10	NULL	0	NULL	pG4zf	GP		bind					BcrAbl probe	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4865_s_107	11121477	( c and  d) Gel retardation assays of pG3zf and pG4zf binding the  BcrAbl probe in the presence of the  NonSp competitor.	bind
1253	1	1445	5	10	NULL	0	NULL	GAPDH	GP		bind					Siah1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_42	16505364	( c and  d) RAW264.7 cells were treated the same as in  b. ( c) TCH346 inhibits the binding of GAPDH and Siah1.	bind
1254	2	1445	5	10	NULL	0	NULL	TCH346	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_42	16505364	( c and  d) RAW264.7 cells were treated the same as in  b. ( c) TCH346 inhibits the binding of GAPDH and Siah1.	bind
1479	1	1445	7	10	NULL	0	NULL	GAPDH	GP		bind 					Siah1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_42	16505364	( c and  d) RAW264.7 cells were treated the same as in  b. ( c) TCH346 inhibits the binding of GAPDH and Siah1.	bind
1480	2	1445	7	10	NULL	0	NULL	TCH346	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_10_3887_s_42	16505364	( c and  d) RAW264.7 cells were treated the same as in  b. ( c) TCH346 inhibits the binding of GAPDH and Siah1.	bind
1261	1	1446	5	NULL	NULL	0	NULL	LPC	NULL	isotherms of	bind	NULL				HEK293 G2A.GFP cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5530_702_s_60	11474113	( C and  D) Saturation isotherms of  [3]LPC and [3]SPC binding to HEK293  G2A.GFP cells.	bind
1263	2	1446	5	NULL	NULL	0	NULL	SPC	NULL	isotherms of	bind	NULL				HEK293 G2A.GFP cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5530_702_s_60	11474113	( C and  D) Saturation isotherms of  [3]LPC and [3]SPC binding to HEK293  G2A.GFP cells.	bind
1481	5	1446	7	NULL	NULL	0	NULL	[3]LPC	NULL	isotherms of 	bind to	NULL				HEK293 G2A.GFP cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5530_702_s_60	11474113	( C and  D) Saturation isotherms of  [3]LPC and [3]SPC binding to HEK293  G2A.GFP cells.	bind
1482	6	1446	7	NULL	NULL	0	NULL	[3]SPC	NULL	isotherms of	bind to	NULL				HEK293 G2A.GFP cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5530_702_s_60	11474113	( C and  D) Saturation isotherms of  [3]LPC and [3]SPC binding to HEK293  G2A.GFP cells.	bind
1264	1	1447	5	10	NULL	0	NULL	FGFR3c	GP		bind					heparin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_4_935_s_205	14732692	( C and  D) Sensorgrams of the two-versus three-Ig form of FGFR3c binding to heparin.	bind
48904	1	1447	7	10	NULL	0	NULL	FGFR3c	GP		bind					heparin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_4_935_s_205	14732692	( C and  D) Sensorgrams of the two-versus three-Ig form of FGFR3c binding to heparin.	bind
1265	1	1448	5	10	NULL	0	NULL	IP3R	GP	Purified;; full-length;; WT	bind					GAPDH	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_5_1357_s_55	15677321	( C Left) Purified full-length WT IP3R and GAPDH  in vitro binding demonstrated by Western analysis.	bind
1483	1	1448	7	10	NULL	0	NULL	IP3R	GP	Purified;; full-length;; WT	bind					GAPDH	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_5_1357_s_55	15677321	( C Left) Purified full-length WT IP3R and GAPDH  in vitro binding demonstrated by Western analysis.	bind
1266	1	1450	5	10	NULL	0	NULL	dCBP	GP		bind					Modulo	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_99_5_2895_s_99	11854460	( C)  In vitro binding between dCBP and Modulo.	bind
1484	1	1450	7	10	NULL	0	NULL	dCBP	GP		bind					Modulo	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_99_5_2895_s_99	11854460	( C)  In vitro binding between dCBP and Modulo.	bind
1267	1	1451	5	10	NULL	0	NULL	BRG1	GP		bind					HP1s	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_64	12411497	( C)  In vitro binding of BRG1 to HP1s.	bind
1485	1	1451	7	10	NULL	0	NULL	BRG1	GP		bind					HP1s	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_64	12411497	( C)  In vitro binding of BRG1 to HP1s.	bind
1268	1	1452	5	10	NULL	0	NULL	EF1gamma	GP		bind					Fez1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_98_18_10374_s_138	11504921	( C)  In vitro binding of EF1gamma to Fez1.	bind
1486	1	1452	7	10	NULL	0	NULL	EF1gamma	GP		bind					Fez1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_98_18_10374_s_138	11504921	( C)  In vitro binding of EF1gamma to Fez1.	bind
1269	1	1453	5	10	NULL	0	NULL	Mex67p	GP		bind					Yra1p	GP	GST-tagged			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_19_3_410_s_129	10722314	( C)  In vitro binding of Mex67p to GST-tagged Yra1p.	bind
1487	1	1453	7	10	NULL	0	NULL	Mex67p	GP		bind					Yra1p	GP	GST-tagged			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_19_3_410_s_129	10722314	( C)  In vitro binding of Mex67p to GST-tagged Yra1p.	bind
1270	1	1454	5	10	NULL	0	NULL	PalF	GP		bind					PalH	GP		cytoplasmic tail		NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_34_12141_s_94	16099830	( C)  In vitro binding of PalF to the PalH cytoplasmic tail.	bind
1488	1	1454	7	10	NULL	0	NULL	PalF 	GP		bind					PalH 	GP		cytoplasmic tail		NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_34_12141_s_94	16099830	( C)  In vitro binding of PalF to the PalH cytoplasmic tail.	bind
1271	1	1455	5	10	NULL	0	NULL	Rb	GP		bind					NS5B	GP	wt			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_50_18159_s_136	16332962	( C)  In vitro binding of Rb to wt and mutated NS5B.	bind
1272	2	1455	5	10	NULL	0	NULL	Rb	GP		bind					NS5B	GP	mutant			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_50_18159_s_136	16332962	( C)  In vitro binding of Rb to wt and mutated NS5B.	bind
1489	1	1455	7	10	NULL	0	NULL	Rb	GP		bind					NS5B	GP	wt			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_50_18159_s_136	16332962	( C)  In vitro binding of Rb to wt and mutated NS5B.	bind
1490	2	1455	7	10	NULL	0	NULL	Rb	GP		bind					NS5B	GP	mutant			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_50_18159_s_136	16332962	( C)  In vitro binding of Rb to wt and mutated NS5B.	bind
1273	1	1456	5	10	NULL	0	NULL	She2p	GP		bind					E2Bmin	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_50_18005_s_135	16326802	( c)  In vitro binding of She2p and She3p to E2Bmin.	bind
1274	2	1456	5	10	NULL	0	NULL	She3p	GP		bind					E2Bmin	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_50_18005_s_135	16326802	( c)  In vitro binding of She2p and She3p to E2Bmin.	bind
1491	1	1456	7	10	NULL	0	NULL	 She2p	GP		bind					 E2Bmin	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_50_18005_s_135	16326802	( c)  In vitro binding of She2p and She3p to E2Bmin.	bind
1492	2	1456	7	10	NULL	0	NULL	She3p	GP		bind 					E2Bmin	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_50_18005_s_135	16326802	( c)  In vitro binding of She2p and She3p to E2Bmin.	bind
1275	1	1457	5	10	NULL	0	NULL	MDM2	GP	in vitro-translated	bind					GST-RB	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_5_2211_s_127	11226218	( C)  In vitro-translated MDM2 binds to GST-RB and GST-Sp1.	bind
1276	2	1457	5	10	NULL	0	NULL	MDM2	GP	in vitro-translated	bind					GST-Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_5_2211_s_127	11226218	( C)  In vitro-translated MDM2 binds to GST-RB and GST-Sp1.	bind
1493	1	1457	7	10	NULL	0	NULL	MDM2	GP	In vitro-translated	bind					GST-RB	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_5_2211_s_127	11226218	( C)  In vitro-translated MDM2 binds to GST-RB and GST-Sp1.	bind
1494	2	1457	7	10	NULL	0	NULL	MDM2	GP	In vitro-translated	bind 					GST-Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_5_2211_s_127	11226218	( C)  In vitro-translated MDM2 binds to GST-RB and GST-Sp1.	bind
1277	1	1459	5	10	NULL	0	NULL	Pbs2	GP		bind					Ste11	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_embo_22_14_3624_s_145	12853477	( C)  In vivo binding of Pbs2 to Ste11.	bind
1495	1	1459	7	10	NULL	0	NULL	Pbs2	GP		bind					Ste11	GP				NULL	In vivo	NULL	NULL	NULL	NULL	gw60_embo_22_14_3624_s_145	12853477	( C)  In vivo binding of Pbs2 to Ste11.	bind
1278	1	1460	5	NULL	NULL	0	NULL	NF1	NULL	lipid-inhibited	bind	NULL				Ras GTP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_3_1566_s_230	8576154	( c)  Lipid-inhibited NF1 binds to Ras GTP propagating a signal through  NF1.	bind
2461	2	1460	5	NULL	NULL	0	NULL	signal	NULL		propagate through	NULL				NF1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_3_1566_s_230	8576154	( c)  Lipid-inhibited NF1 binds to Ras GTP propagating a signal through  NF1.	bind
2462	3	1460	5	NULL	NULL	0	NULL	statement 1	NULL		cause	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_3_1566_s_230	8576154	( c)  Lipid-inhibited NF1 binds to Ras GTP propagating a signal through  NF1.	bind
1604	2	1460	7	NULL	NULL	0	NULL	NF1	NULL	Lipid-inhibited	bind	NULL				Ras GTP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1566_s_230	8576154	( c)  Lipid-inhibited NF1 binds to Ras GTP propagating a signal through  NF1.	bind
1605	3	1460	7	NULL	NULL	0	NULL	signal	NULL		propagate through	NULL				NF1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1566_s_230	8576154	( c)  Lipid-inhibited NF1 binds to Ras GTP propagating a signal through  NF1.	bind
1924	4	1460	7	NULL	NULL	0	NULL	statement 2	NULL		cause	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_3_1566_s_230	8576154	( c)  Lipid-inhibited NF1 binds to Ras GTP propagating a signal through  NF1.	bind
1292	1	1464	5	10	NULL	0	NULL	RNase III	GP	S. aureus	bind		specifically			RNAIII	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_4_824_s_184	15678100	( C)  S. aureus RNase III binds specifically to RNAIII.	bind
1607	1	1464	7	10	NULL	0	NULL	RNase III	GP	S. aureus	bind		specifically			RNAIII	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_4_824_s_184	15678100	( C)  S. aureus RNase III binds specifically to RNAIII.	bind
1298	1	1465	5	10	NULL	0	NULL	actin	GP		bind					G6	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5446_1939_s_36	10583954	( C) (Left) Structure of the nonactivated G6 ( 4); (right) actin-bound form of G6 in a similar orientation.	bind
1758	1	1465	7	10	NULL	0	NULL	actin	GP		bind					G6	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5446_1939_s_36	10583954	( C) (Left) Structure of the nonactivated G6 ( 4); (right) actin-bound form of G6 in a similar orientation.	bind
1301	1	1468	5	10	NULL	0	NULL	9- Cis-4-oxo-RA	Chemical		bind					RARbeta-RXRalpha heterodimer	GP		 subunit		NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_26_15424_s_166	9860984	( C) 9- Cis-4-oxo-RA binds both subunits of RARbeta-RXRalpha heterodimers.	bind
1619	1	1468	7	10	NULL	0	NULL	9- Cis-4-oxo-RA	Chemical		bind					RARbeta-RXRalpha heterodimer	GP		 subunit		NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_26_15424_s_166	9860984	( C) 9- Cis-4-oxo-RA binds both subunits of RARbeta-RXRalpha heterodimers.	bind
1304	1	1469	5	NULL	NULL	0	NULL	GABAAR beta1 subunit	NULL	mutant	does not bind	NULL				BTX	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_54	16549768	( c) A GABAAR beta1 subunit that had been mutated to enhance its ability to form pentamers (beta1*) failed to bind BTX.	bind
2463	2	1469	5	NULL	NULL	0	NULL	GABAAR beta1	NULL	mutated	is enhanced for	NULL				pentamer beta1	NULL	formation of			NULL		0	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_54	16549768	( c) A GABAAR beta1 subunit that had been mutated to enhance its ability to form pentamers (beta1*) failed to bind BTX.	bind
1680	4	1469	7	NULL	NULL	0	NULL	GABAAR beta1	NULL	mutated	does not bind	NULL				BTX	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_54	16549768	( c) A GABAAR beta1 subunit that had been mutated to enhance its ability to form pentamers (beta1*) failed to bind BTX.	bind
1681	5	1469	7	NULL	NULL	0	NULL	GABAAR beta1	NULL	mutated	is enhanced for	NULL				pentamers beta1	NULL	formation of 			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_54	16549768	( c) A GABAAR beta1 subunit that had been mutated to enhance its ability to form pentamers (beta1*) failed to bind BTX.	bind
1305	1	1470	5	10	NULL	0	NULL	CRK3	GP		bind					p13 suc1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10153_s_233	9553063	( c) A putative inhibitor protein binds to the CRK3 kinase in metacyclic cells and interferes with the binding interaction between CRK3 and p13 suc1.	bind
1307	2	1470	5	10	NULL	0	NULL	inhibitor protein	GP	putative 	bind					CRK3 kinase	GP				NULL	metacyclic cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10153_s_233	9553063	( c) A putative inhibitor protein binds to the CRK3 kinase in metacyclic cells and interferes with the binding interaction between CRK3 and p13 suc1.	bind
1309	3	1470	5	10	NULL	0	NULL	statement 2	Process		interferes with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10153_s_233	9553063	( c) A putative inhibitor protein binds to the CRK3 kinase in metacyclic cells and interferes with the binding interaction between CRK3 and p13 suc1.	bind
1684	1	1470	7	10	NULL	0	NULL	inhibitor protein	GP	putative	bind					CRK3 kinase	GP				NULL	in metacyclic cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10153_s_233	9553063	( c) A putative inhibitor protein binds to the CRK3 kinase in metacyclic cells and interferes with the binding interaction between CRK3 and p13 suc1.	bind
1685	2	1470	7	10	NULL	0	NULL	CRK3	GP		bind					p13 suc1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10153_s_233	9553063	( c) A putative inhibitor protein binds to the CRK3 kinase in metacyclic cells and interferes with the binding interaction between CRK3 and p13 suc1.	bind
1686	3	1470	7	10	NULL	0	NULL	statement 1	Process		interferes with					statement 2 	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10153_s_233	9553063	( c) A putative inhibitor protein binds to the CRK3 kinase in metacyclic cells and interferes with the binding interaction between CRK3 and p13 suc1.	bind
1311	1	1471	5	10	NULL	0	NULL			specific	bind			BRC repeat		RAD51	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_9_5287_s_130	9560268	( C) A specific BRC repeat binds to RAD51.	bind
1687	1	1471	7	10	NULL	0	NULL			specific	bind			BRC repeat		RAD51	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_9_5287_s_130	9560268	( C) A specific BRC repeat binds to RAD51.	bind
1312	1	1472	5	10	NULL	0	NULL	H22	GP		bind					S15	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_2_629_s_239	12527771	( C) A stereo view of the binding of H22 to S15.	bind
1688	1	1472	7	10	NULL	0	NULL	H22	GP		bind					S15	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_2_629_s_239	12527771	( C) A stereo view of the binding of H22 to S15.	bind
1313	1	1475	5	10	NULL	0	NULL	Ab	GP		bind					Abeta aggregates	GP		1-40		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_20_7115_s_99	15883377	( c) Ab binding to Abeta(1-40) aggregates.	bind
1689	1	1475	7	10	NULL	0	NULL	Ab	GP		bind					Abeta aggregates	GP		1-40		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_20_7115_s_99	15883377	( c) Ab binding to Abeta(1-40) aggregates.	bind
1314	1	1476	5	10	NULL	0	NULL	Cabin1	GP		bind					MEF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5440_790_s_99	10531067	( C) Activated CaM competes for Cabin1 binding with MEF2.	bind
1315	2	1476	5	10	NULL	0	NULL	CaM	GP	activated	bind					MEF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5440_790_s_99	10531067	( C) Activated CaM competes for Cabin1 binding with MEF2.	bind
2723	3	1476	5	10	NULL	0	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5440_790_s_99	10531067	( C) Activated CaM competes for Cabin1 binding with MEF2.	bind
1690	1	1476	7	10	NULL	0	NULL	Cabin1	GP		bind					MEF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5440_790_s_99	10531067	( C) Activated CaM competes for Cabin1 binding with MEF2.	bind
1691	2	1476	7	10	NULL	0	NULL	CaM	GP	Activated	bind					MEF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5440_790_s_99	10531067	( C) Activated CaM competes for Cabin1 binding with MEF2.	bind
1925	3	1476	7	10	NULL	0	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5440_790_s_99	10531067	( C) Activated CaM competes for Cabin1 binding with MEF2.	bind
1316	1	1477	5	10	NULL	0	NULL	Adipophilin	GP		does not bind					Rab9	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_11_7450_s_142	12032303	( C) Adipophilin does not bind Rab9.	bind
1692	1	1477	7	10	NULL	0	NULL	Adipophilin 	GP		does not bind					Rab9	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_11_7450_s_142	12032303	( C) Adipophilin does not bind Rab9.	bind
1317	1	1478	5	10	NULL	0	NULL	spORC	GP		bind					ars1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_52_17952_s_168	15598736	( C) AFM images of spORC and spOrc4p bound to  ars1.	bind
1318	2	1478	5	10	NULL	0	NULL	spOrc4p	GP		bind					ars1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_52_17952_s_168	15598736	( C) AFM images of spORC and spOrc4p bound to  ars1.	bind
1693	1	1478	7	10	NULL	0	NULL	spORC	GP		bind					ars1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_52_17952_s_168	15598736	( C) AFM images of spORC and spOrc4p bound to  ars1.	bind
1694	2	1478	7	10	NULL	0	NULL	spOrc4p	GP		bind					ars1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_52_17952_s_168	15598736	( C) AFM images of spORC and spOrc4p bound to  ars1.	bind
1319	1	1481	5	NULL	NULL	0	NULL	HrcQB	NULL		bind	NULL				His-10-HrcQA protein	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_1_70_s_136	14694203	( C) An autoradiogram that shows the binding of HrcQB to His-10-HrcQA protein and to the C-terminal truncated version.	bind
1320	2	1481	5	NULL	NULL	0	NULL	HrcQB	NULL		bind	NULL				His-10-HrcQA protein	NULL		C-terminal truncated version		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_1_70_s_136	14694203	( C) An autoradiogram that shows the binding of HrcQB to His-10-HrcQA protein and to the C-terminal truncated version.	bind
1695	3	1481	7	NULL	NULL	0	NULL	HrcQB	NULL		bind to	NULL				His-10-HrcQA	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_1_70_s_136	14694203	( C) An autoradiogram that shows the binding of HrcQB to His-10-HrcQA protein and to the C-terminal truncated version.	bind
1696	4	1481	7	NULL	NULL	0	NULL	HrcQB	NULL		bind to	NULL				His-10-HrcQA	NULL		C-terminal truncated version		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_1_70_s_136	14694203	( C) An autoradiogram that shows the binding of HrcQB to His-10-HrcQA protein and to the C-terminal truncated version.	bind
1321	1	1482	5	10	NULL	0	NULL	Cry11Aa toxin	GP		bind					Cyt1Aa	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_51_18303_s_216	16339907	( C) Analysis of binding of Cry11Aa toxin to Cyt1Aa by ELISA in the presence or absence  of 10 - 100 M excess of synthetic peptides corresponding to the loops and exposed  regions of Cry11Aa-domain II.	bind
1697	1	1482	7	10	NULL	0	NULL	Cry11Aa toxin	GP		bind					Cyt1Aa	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_51_18303_s_216	16339907	( C) Analysis of binding of Cry11Aa toxin to Cyt1Aa by ELISA in the presence or absence  of 10 - 100 M excess of synthetic peptides corresponding to the loops and exposed  regions of Cry11Aa-domain II.	bind
1322	1	1483	5	10	NULL	0	NULL	Tat	GP	HIV-1	bind					TAR RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_22_3512_s_187	9832504	( C) Analysis of the ability of murine CycT1 to enhance the binding of HIV-1 Tat to TAR RNA.	bind
1323	2	1483	5	10	NULL	0	NULL	CycT1	GP	murine	enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_22_3512_s_187	9832504	( C) Analysis of the ability of murine CycT1 to enhance the binding of HIV-1 Tat to TAR RNA.	bind
1699	1	1483	7	10	NULL	0	NULL	 Tat 	GP	HIV-1	bind					TAR RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_22_3512_s_187	9832504	( C) Analysis of the ability of murine CycT1 to enhance the binding of HIV-1 Tat to TAR RNA.	bind
1700	2	1483	7	10	NULL	0	NULL	CycT1 	GP	murine	enhance					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_22_3512_s_187	9832504	( C) Analysis of the ability of murine CycT1 to enhance the binding of HIV-1 Tat to TAR RNA.	bind
1324	1	1484	5	10	NULL	0	NULL	APA1/1 antibody	GP		bind					TCR	GP				NULL	in the cortex of the thymus	NULL	NULL	NULL	NULL	gw70_pnas_103_25_9625_s_57	16766661	( C) APA1/1 antibody binds to the TCR in the cortex of the thymus but not in the medulla.	bind
46523	2	1484	5	10	NULL	0	NULL	APA1/1 antibody	GP		does not bind					TCR	GP				NULL	medulla of thymus	NULL	NULL	NULL	NULL	gw70_pnas_103_25_9625_s_57	16766661	( C) APA1/1 antibody binds to the TCR in the cortex of the thymus but not in the medulla.	bind
1701	1	1484	7	10	NULL	0	NULL	APA1/1 antibody	GP		bind					TCR	GP				NULL	in the cortex of the thymus	NULL	NULL	NULL	NULL	gw70_pnas_103_25_9625_s_57	16766661	( C) APA1/1 antibody binds to the TCR in the cortex of the thymus but not in the medulla.	bind
1702	2	1484	7	10	NULL	0	NULL	APA1/1 antibody	GP		does not bind 					TCR	GP				NULL	medulla of thymus	NULL	NULL	NULL	NULL	gw70_pnas_103_25_9625_s_57	16766661	( C) APA1/1 antibody binds to the TCR in the cortex of the thymus but not in the medulla.	bind
1325	1	1485	5	10	NULL	0	NULL	tubulin	GP	bovine	bind					GST-Aut2p glutathione-Sepharose 4B	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3597_s_134	9649430	( C) As described in (B), bovine tubulin binds to GST-Aut2p glutathione-Sepharose 4B (lane 12), but not to GST glutathione-Sepharose 4B (lane 9).	bind
1326	2	1485	5	10	NULL	0	NULL	tubulin	GP	bovine	does not bind					GST glutathione-Sepharose 4B	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3597_s_134	9649430	( C) As described in (B), bovine tubulin binds to GST-Aut2p glutathione-Sepharose 4B (lane 12), but not to GST glutathione-Sepharose 4B (lane 9).	bind
1703	1	1485	7	10	NULL	0	NULL	tubulin 	GP	bovine	bind					GST-Aut2p glutathione-Sepharose 4B	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3597_s_134	9649430	( C) As described in (B), bovine tubulin binds to GST-Aut2p glutathione-Sepharose 4B (lane 12), but not to GST glutathione-Sepharose 4B (lane 9).	bind
1704	2	1485	7	10	NULL	0	NULL	tubulin 	GP	bovine	does not bind					GST glutathione-Sepharose 4B 	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3597_s_134	9649430	( C) As described in (B), bovine tubulin binds to GST-Aut2p glutathione-Sepharose 4B (lane 12), but not to GST glutathione-Sepharose 4B (lane 9).	bind
1334	1	1486	5	10	NULL	0	NULL	Par6	GP		bind					Cdc42	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_22_5_1125_s_83	12606577	( C) Asp38 is not required for binding of Par6 to Cdc42.	bind
1335	2	1486	5	10	NULL	0	NULL				is not required for			Asp38		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_22_5_1125_s_83	12606577	( C) Asp38 is not required for binding of Par6 to Cdc42.	bind
1705	1	1486	7	10	NULL	0	NULL	Par6 	GP		bind 					Cdc42	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_22_5_1125_s_83	12606577	( C) Asp38 is not required for binding of Par6 to Cdc42.	bind
1706	2	1486	7	10	NULL	0	NULL				is not required for			Asp38		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_22_5_1125_s_83	12606577	( C) Asp38 is not required for binding of Par6 to Cdc42.	bind
1344	1	1488	5	10	NULL	0	NULL	1alpha,25(OH)2D3	Chemical		bind					VDR	GP		LBD		NULL		NULL	NULL	NULL	NULL	gw60_embo_21_22_5960_s_80	12426368	( C) Atomic model of 1alpha,25(OH)2D3 bound to the VDR LBD ( Rochel  et al., 2000; PDB code 1DB1).	bind
1708	1	1488	7	10	NULL	0	NULL	1alpha,25(OH)2D3	Chemical		bind 					VDR	GP		LBD		NULL		NULL	NULL	NULL	NULL	gw60_embo_21_22_5960_s_80	12426368	( C) Atomic model of 1alpha,25(OH)2D3 bound to the VDR LBD ( Rochel  et al., 2000; PDB code 1DB1).	bind
1350	1	1489	5	10	NULL	0	NULL	DnaB	GP	32P-labeled	bind					Tus-GST	GP	wt			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_17_9569_s_141	11493686	( C) Autoradiogram showing the binding of 32P-labeled DnaB to wt and mutant form of Tus-GST affinity matrices and the lack of binding of labeled DnaG to the wt Tus-GST matrix.	bind
1352	2	1489	5	10	NULL	0	NULL	DnaB	GP	32P-labeled	bind					Tus-GST	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_17_9569_s_141	11493686	( C) Autoradiogram showing the binding of 32P-labeled DnaB to wt and mutant form of Tus-GST affinity matrices and the lack of binding of labeled DnaG to the wt Tus-GST matrix.	bind
1353	3	1489	5	10	NULL	0	NULL	DnaG	GP	labeled	does not bind					Tus-GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_17_9569_s_141	11493686	( C) Autoradiogram showing the binding of 32P-labeled DnaB to wt and mutant form of Tus-GST affinity matrices and the lack of binding of labeled DnaG to the wt Tus-GST matrix.	bind
1709	1	1489	7	10	NULL	0	NULL	 DnaB	GP	32P-labeled	bind 					Tus-GST	GP	wt 			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_17_9569_s_141	11493686	( C) Autoradiogram showing the binding of 32P-labeled DnaB to wt and mutant form of Tus-GST affinity matrices and the lack of binding of labeled DnaG to the wt Tus-GST matrix.	bind
1710	2	1489	7	10	NULL	0	NULL	DnaB	GP	32P-labeled 	bind					Tus-GST	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_17_9569_s_141	11493686	( C) Autoradiogram showing the binding of 32P-labeled DnaB to wt and mutant form of Tus-GST affinity matrices and the lack of binding of labeled DnaG to the wt Tus-GST matrix.	bind
1711	3	1489	7	10	NULL	0	NULL	 DnaG	GP	labeled	does not bind					Tus-GST 	GP	wt			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_17_9569_s_141	11493686	( C) Autoradiogram showing the binding of 32P-labeled DnaB to wt and mutant form of Tus-GST affinity matrices and the lack of binding of labeled DnaG to the wt Tus-GST matrix.	bind
1358	1	1490	5	10	NULL	0	NULL	BC1/BC200	GP		bind					PABP	GP		adenine-rich region		NULL		NULL	NULL	NULL	NULL	gw70_annurevneurosci_29_0_77_s_310	16776580	( C) BC1/BC200 bind to PABP through an adenine-rich region, titrating PABP and possibly  other initiation factors away from mRNAs and thus inhibiting translation.	bind
1712	1	1490	7	10	NULL	0	NULL	BC1/BC200	GP		bind					PABP 	GP		adenine-rich region		NULL		NULL	NULL	NULL	NULL	gw70_annurevneurosci_29_0_77_s_310	16776580	( C) BC1/BC200 bind to PABP through an adenine-rich region, titrating PABP and possibly  other initiation factors away from mRNAs and thus inhibiting translation.	bind
1360	1	1491	5	10	NULL	0	NULL	beta-NAD+	Chemical		bind					TRPM2 fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_1804_s_82	16601673	( C) beta-NAD+ binding to the TRPM2 fusion proteins in the presence (+) or absence (-) of cADPR.	bind
1715	1	1491	7	10	NULL	0	NULL	 beta-NAD+	Chemical		bind 					TRPM2 fusion proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_1804_s_82	16601673	( C) beta-NAD+ binding to the TRPM2 fusion proteins in the presence (+) or absence (-) of cADPR.	bind
1361	1	1492	5	10	NULL	0	NULL	 B. pertussis	Organism		bind					mucin-coated plates	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_25_13847_s_160	11087813	( c) Binding of  B. pertussis to mucin-coated plates.	bind
1713	2	1492	7	10	NULL	0	NULL	B. pertussis	Organism		bind 					mucin-coated plates	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_25_13847_s_160	11087813	( c) Binding of  B. pertussis to mucin-coated plates.	bind
1363	1	1493	5	10	NULL	0	NULL	Af-SRP19	GP		bind					SRP RNAs	NucleicAcid	various			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_6_1365_s_159	10684931	( C) Binding of Af-SRP19 and Af-SRP54 to various SRP RNAs.	bind
1364	2	1493	5	10	NULL	0	NULL	Af-SRP54	GP		bind					SRP RNAs	NucleicAcid	various			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_6_1365_s_159	10684931	( C) Binding of Af-SRP19 and Af-SRP54 to various SRP RNAs.	bind
1716	1	1493	7	10	NULL	0	NULL	Af-SRP19	GP		bind					SRP RNAs	NucleicAcid	various			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_6_1365_s_159	10684931	( C) Binding of Af-SRP19 and Af-SRP54 to various SRP RNAs.	bind
1717	5	1493	7	10	NULL	0	NULL	Af-SRP54	GP		bind					SRP RNAs	NucleicAcid	various			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_6_1365_s_159	10684931	( C) Binding of Af-SRP19 and Af-SRP54 to various SRP RNAs.	bind
1365	1	1495	5	NULL	NULL	0	NULL	anti-C1q autoantibodies	NULL		bind	NULL				C1q	NULL				NULL	present on the immune complexes	NULL	NULL	NULL	NULL	gw70_jclininvest_114_5_679_s_223	15343386	( C) Binding of anti-C1q autoantibodies to C1q present on the immune complexes.	bind
1718	2	1495	7	NULL	NULL	0	NULL	anti-C1q autoantibodies	NULL		bind to	NULL				C1q 	NULL				NULL	present on the immune complexes	0	NULL	NULL	NULL	gw70_jclininvest_114_5_679_s_223	15343386	( C) Binding of anti-C1q autoantibodies to C1q present on the immune complexes.	bind
1366	1	1496	5	10	NULL	0	NULL	B cells	Cell		bind					PtC liposomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_23_13459_s_142	14595020	( C) Binding of B cells to PtC liposomes.	bind
1719	1	1496	7	10	NULL	0	NULL	B cells	Cell		bind					PtC liposomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_23_13459_s_142	14595020	( C) Binding of B cells to PtC liposomes.	bind
1367	1	1497	5	NULL	NULL	0	NULL	CBFA1	NULL		bind	NULL				OSE2 oligonucleotide	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_9_2254_s_265	11331591	( C) Binding of CBFA1 to an OSE2 oligonucleotide, in the absence or presence of equimolar levels of Smad3 and Smad4.	bind
1720	3	1497	7	NULL	NULL	0	NULL	CBFA1	NULL		bind to	NULL				OSE2 oligonucleotide	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_9_2254_s_265	11331591	( C) Binding of CBFA1 to an OSE2 oligonucleotide, in the absence or presence of equimolar levels of Smad3 and Smad4.	bind
1368	1	1498	5	10	NULL	0	NULL	IgA	GP		bind					R1 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_105_12_1731_s_173	10862788	( c) Binding of control IgA and T15 to R1 cells.	bind
1369	2	1498	5	10	NULL	0	NULL	T15	GP		bind					R1 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_105_12_1731_s_173	10862788	( c) Binding of control IgA and T15 to R1 cells.	bind
1724	1	1498	7	10	NULL	0	NULL	IgA	GP		bind					R1 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_105_12_1731_s_173	10862788	( c) Binding of control IgA and T15 to R1 cells.	bind
1725	2	1498	7	10	NULL	0	NULL	T15	GP		bind 					R1 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_105_12_1731_s_173	10862788	( c) Binding of control IgA and T15 to R1 cells.	bind
1370	1	1499	5	10	NULL	0	NULL	Crb2	GP		bind					Cut5	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_11_24_3387_s_85	9407031	( C) Binding of Crb2 and Crb3 with Cut5 in vitro.	bind
1371	2	1499	5	10	NULL	0	NULL	Crb3	GP		bind					Cut5	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_11_24_3387_s_85	9407031	( C) Binding of Crb2 and Crb3 with Cut5 in vitro.	bind
1726	1	1499	7	10	NULL	0	NULL	Crb2	GP		bind					Cut5	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_11_24_3387_s_85	9407031	( C) Binding of Crb2 and Crb3 with Cut5 in vitro.	bind
1727	2	1499	7	10	NULL	0	NULL	Crb3	GP		bind					Cut5	GP				NULL	 in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_11_24_3387_s_85	9407031	( C) Binding of Crb2 and Crb3 with Cut5 in vitro.	bind
1372	1	1500	5	NULL	NULL	0	NULL	DHE	NULL		bind	NULL				NPC2	NULL				NULL	at pH 5 and 7	0	NULL	NULL	NULL	gw60_pnas_100_5_2512_s_88	12591954	( C) Binding of DHE to NPC2 at pH 5 and 7.	bind
1728	2	1500	7	NULL	NULL	0	NULL	DHE	NULL		bind to	NULL				NPC2	NULL				NULL	at pH 5	0	NULL	NULL	NULL	gw60_pnas_100_5_2512_s_88	12591954	( C) Binding of DHE to NPC2 at pH 5 and 7.	bind
1729	3	1500	7	NULL	NULL	0	NULL	DHE	NULL		bind to	NULL				NPC2	NULL				NULL	at pH 7	0	NULL	NULL	NULL	gw60_pnas_100_5_2512_s_88	12591954	( C) Binding of DHE to NPC2 at pH 5 and 7.	bind
1373	1	1501	5	NULL	NULL	0	NULL	EIL proteins	NULL		bind	NULL				ERF1	NULL			EIN3 target site in promoter	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_23_3703_s_84	9851977	( C) Binding of EIL proteins to the EIN3 target site in the  ERF1 promoter.	bind
1730	2	1501	7	NULL	NULL	0	NULL	EIL proteins	NULL		bind to	NULL				ERF1	NULL			EIN3 target site in the promoter of 	NULL		0	NULL	NULL	NULL	gw60_genesdev_12_23_3703_s_84	9851977	( C) Binding of EIL proteins to the EIN3 target site in the  ERF1 promoter.	bind
1374	1	1502	5	NULL	NULL	0	NULL	GluR2/3	NULL	endogenous	bind	NULL				GRIP1aHA	NULL	overexpressed			NULL		0	NULL	NULL	NULL	gw70_embo_24_18_3266_s_188	16138078	( C) Binding of endogenous GluR2/3 to overexpressed GRIP1aHA is not Ca2+-sensitive.	bind
1375	2	1502	5	NULL	NULL	0	NULL	statement 1	NULL		is not sensitive to	NULL				Ca2+	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_18_3266_s_188	16138078	( C) Binding of endogenous GluR2/3 to overexpressed GRIP1aHA is not Ca2+-sensitive.	bind
1731	3	1502	7	NULL	NULL	0	NULL	GluR2/3	NULL	endogenous	bind to	NULL				GRIP1aHA	NULL	overexpressed			NULL		0	NULL	NULL	NULL	gw70_embo_24_18_3266_s_188	16138078	( C) Binding of endogenous GluR2/3 to overexpressed GRIP1aHA is not Ca2+-sensitive.	bind
1732	4	1502	7	NULL	NULL	0	NULL	statement 3	NULL		is not sensitive to	NULL				Ca2+	NULL				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_18_3266_s_188	16138078	( C) Binding of endogenous GluR2/3 to overexpressed GRIP1aHA is not Ca2+-sensitive.	bind
1376	1	1503	5	NULL	NULL	0	NULL	gp4	NULL		bind	NULL				flow cells	NULL				NULL	containing gp5/trx - primer/template	NULL	NULL	NULL	NULL	gw70_pnas_102_14_5096_s_183	15795374	( C) Binding of gp4 and gp4-Cdelta17 to flow cells containing the gp5/trx - primer/template in the two orientations  shown in  A.	bind
1377	2	1503	5	NULL	NULL	0	NULL	gp4-Cdelta17	NULL		bind	NULL				flow cells	NULL				NULL	containing gp5/trx - primer/template	NULL	NULL	NULL	NULL	gw70_pnas_102_14_5096_s_183	15795374	( C) Binding of gp4 and gp4-Cdelta17 to flow cells containing the gp5/trx - primer/template in the two orientations  shown in  A.	bind
1733	4	1503	7	NULL	NULL	0	NULL	gp4	NULL		bind to	NULL				flow cells	NULL				NULL	containing the gp5/trx - primer/template	NULL	NULL	NULL	NULL	gw70_pnas_102_14_5096_s_183	15795374	( C) Binding of gp4 and gp4-Cdelta17 to flow cells containing the gp5/trx - primer/template in the two orientations  shown in  A.	bind
1735	6	1503	7	NULL	NULL	0	NULL	gp4-Cdelta17	NULL		bind to	NULL				flow cells	NULL				NULL	containing the gp5/trx - primer/template	NULL	NULL	NULL	NULL	gw70_pnas_102_14_5096_s_183	15795374	( C) Binding of gp4 and gp4-Cdelta17 to flow cells containing the gp5/trx - primer/template in the two orientations  shown in  A.	bind
1378	1	1504	5	10	NULL	0	NULL	GST-Rsp5 proteins	GP		bind					Ubp2	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_13_2414_s_125	15933713	( C) Binding of GST-Rsp5 proteins to Ubp2.	bind
1737	1	1504	7	10	NULL	0	NULL	GST-Rsp5 proteins	GP		bind					Ubp2	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_13_2414_s_125	15933713	( C) Binding of GST-Rsp5 proteins to Ubp2.	bind
1379	1	1505	5	NULL	NULL	0	NULL	GST-Rsp5	NULL		bind	NULL				Ubp2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_13_2414_s_137	15933713	( C) Binding of GST-Rsp5 to Ubp2, in the presence of Rup1.	bind
1550	2	1505	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				Rup1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_13_2414_s_137	15933713	( C) Binding of GST-Rsp5 to Ubp2, in the presence of Rup1.	bind
1738	3	1505	7	NULL	NULL	0	NULL	GST-Rsp5	NULL		bind to	NULL				Ubp2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_13_2414_s_137	15933713	( C) Binding of GST-Rsp5 to Ubp2, in the presence of Rup1.	bind
2206	4	1505	7	NULL	NULL	0	NULL	statement 3	NULL		in the presence of 	NULL				Rup1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_13_2414_s_137	15933713	( C) Binding of GST-Rsp5 to Ubp2, in the presence of Rup1.	bind
1380	1	1506	5	10	NULL	0	NULL	HCV	GP		bind					CD81	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_282_5390_938_s_77	9794763	( C) Binding of HCV to CD81.	bind
1739	1	1506	7	10	NULL	0	NULL	HCV	GP		bind 					CD81	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_282_5390_938_s_77	9794763	( C) Binding of HCV to CD81.	bind
1381	1	1507	5	10	NULL	0	NULL	histone H4	GP		bind					UBC9	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_23_13225_s_101	14578449	( C) Binding of histone H4 to UBC9.	bind
1740	1	1507	7	10	NULL	0	NULL	histone H4	GP		bind					UBC9	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_23_13225_s_101	14578449	( C) Binding of histone H4 to UBC9.	bind
1383	1	1508	5	10	NULL	0	NULL	mad2 gene product	GP	in vitro-translated;;35S labeled	bind					GST-Slp1 fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5353_1045_s_37	9461438	( C) Binding of in vitro-translated  mad2 gene product labeled by 35S (lane 1) to GST protein or a fusion protein, GST-Slp1, which were bound to glutathione-Sepharose 4B beads.	bind
1743	1	1508	7	10	NULL	0	NULL	mad2 gene product	GP	in vitro-translated;;35S labeled	bind					GST-Slp1 fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5353_1045_s_37	9461438	( C) Binding of in vitro-translated  mad2 gene product labeled by 35S (lane 1) to GST protein or a fusion protein, GST-Slp1, which were bound to glutathione-Sepharose 4B beads.	bind
1384	1	1509	5	10	NULL	0	NULL				bind			catalytic IDH2 site		isocitrate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_12864_s_270	12562755	( C) Binding of isocitrate by the catalytic IDH2 site, but not by the regulatory IDH1 site, requires Mg2+.	bind
1385	2	1509	5	10	NULL	0	NULL	statement 1	Process		require					Mg2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_12864_s_270	12562755	( C) Binding of isocitrate by the catalytic IDH2 site, but not by the regulatory IDH1 site, requires Mg2+.	bind
1386	3	1509	5	10	NULL	0	NULL				does not bind			regulatory IDH1 site		isocitrate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_12864_s_270	12562755	( C) Binding of isocitrate by the catalytic IDH2 site, but not by the regulatory IDH1 site, requires Mg2+.	bind
1744	1	1509	7	10	NULL	0	NULL	isocitrate	Chemical		bind to 								catalytic IDH2 site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_12864_s_270	12562755	( C) Binding of isocitrate by the catalytic IDH2 site, but not by the regulatory IDH1 site, requires Mg2+.	bind
1745	2	1509	7	10	NULL	0	NULL	isocitrate	Chemical		does not bind								regulatory IDH1 site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_12864_s_270	12562755	( C) Binding of isocitrate by the catalytic IDH2 site, but not by the regulatory IDH1 site, requires Mg2+.	bind
1746	3	1509	7	10	NULL	0	NULL	statement 1	Process		requires					Mg2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_12864_s_270	12562755	( C) Binding of isocitrate by the catalytic IDH2 site, but not by the regulatory IDH1 site, requires Mg2+.	bind
1387	1	1510	5	10	NULL	0	NULL	mAb 9C7	GP		bind					Hc proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_112_8_1164_s_299	14561701	( c) Binding of mAb 9C7 to  Hc proteins after serial treatment and reactivity of the  Hc-binding mAb s to recombinant protein (second through fourth lanes).	bind
2464	2	1510	5	10	NULL	0	NULL	Hc-binding mAbs	GP		reacts with					recombinant protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_112_8_1164_s_299	14561701	( c) Binding of mAb 9C7 to  Hc proteins after serial treatment and reactivity of the  Hc-binding mAb s to recombinant protein (second through fourth lanes).	bind
2465	3	1510	5	10	NULL	0	NULL	statement 1	Process		occurs after					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_112_8_1164_s_299	14561701	( c) Binding of mAb 9C7 to  Hc proteins after serial treatment and reactivity of the  Hc-binding mAb s to recombinant protein (second through fourth lanes).	bind
1747	1	1510	7	10	NULL	0	NULL	mAb 9C7	GP		bind					Hc proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_112_8_1164_s_299	14561701	( c) Binding of mAb 9C7 to  Hc proteins after serial treatment and reactivity of the  Hc-binding mAb s to recombinant protein (second through fourth lanes).	bind
1748	2	1510	7	10	NULL	0	NULL	Hc-binding mAbs	GP		reacts with					recombinant protein 	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_112_8_1164_s_299	14561701	( c) Binding of mAb 9C7 to  Hc proteins after serial treatment and reactivity of the  Hc-binding mAb s to recombinant protein (second through fourth lanes).	bind
1749	3	1510	7	10	NULL	0	NULL	statement 1	Process		occurs after					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_112_8_1164_s_299	14561701	( c) Binding of mAb 9C7 to  Hc proteins after serial treatment and reactivity of the  Hc-binding mAb s to recombinant protein (second through fourth lanes).	bind
1390	1	1511	5	10	NULL	0	NULL	NC	GP		bind					(TG)4	NucleicAcid			156.6 RU surface	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_472_s_114	16434700	( C) Binding of NC to a 156.6 RU surface of (TG)4.	bind
1750	1	1511	7	10	NULL	0	NULL	NC	GP		bind					(TG)4	NucleicAcid			156.6 RU surface of 	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_472_s_114	16434700	( C) Binding of NC to a 156.6 RU surface of (TG)4.	bind
1391	1	1512	5	10	NULL	0	NULL	ORCA1	GP		bind					Str	GP			RV fragment of the promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_18_16_4455_s_150	10449411	( C) Binding of ORCA1 to the RV fragment of the  Str promoter.	bind
1751	1	1512	7	10	NULL	0	NULL	ORCA1 	GP		bind					Str	GP			RV fragment in the promoter of 	NULL		NULL	NULL	NULL	NULL	gw60_embo_18_16_4455_s_150	10449411	( C) Binding of ORCA1 to the RV fragment of the  Str promoter.	bind
1392	1	1513	5	10	NULL	0	NULL	OspA	GP		bind					OspA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_106_4_561_s_75	10953031	( c) Binding of OspA with OspA.	bind
1752	1	1513	7	10	NULL	0	NULL	OspA	GP		bind					OspA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_106_4_561_s_75	10953031	( c) Binding of OspA with OspA.	bind
1393	1	1514	5	NULL	NULL	0	NULL	phyB	NULL		bind	NULL				PIF3	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_24_13419_s_88	11069292	( c) Binding of phyB and phyA to PIF3 as a function of phy input level.	bind
1394	2	1514	5	NULL	NULL	0	NULL	phyA	NULL		bind	NULL				PIF3	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_24_13419_s_88	11069292	( c) Binding of phyB and phyA to PIF3 as a function of phy input level.	bind
2467	3	1514	5	NULL	NULL	0	NULL	statement 1	NULL		is a function of	NULL				phy input level	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_24_13419_s_88	11069292	( c) Binding of phyB and phyA to PIF3 as a function of phy input level.	bind
2470	4	1514	5	NULL	NULL	0	NULL	statement 2	NULL		is a function of	NULL				phy input level	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_24_13419_s_88	11069292	( c) Binding of phyB and phyA to PIF3 as a function of phy input level.	bind
1753	3	1514	7	NULL	NULL	0	NULL	phyB	NULL		bind to	NULL				PIF3	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_24_13419_s_88	11069292	( c) Binding of phyB and phyA to PIF3 as a function of phy input level.	bind
1754	4	1514	7	NULL	NULL	0	NULL	phyA	NULL		bind to	NULL				PIF3	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_24_13419_s_88	11069292	( c) Binding of phyB and phyA to PIF3 as a function of phy input level.	bind
1755	5	1514	7	NULL	NULL	0	NULL	statement 3	NULL		is a function of 	NULL				phy input level	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_24_13419_s_88	11069292	( c) Binding of phyB and phyA to PIF3 as a function of phy input level.	bind
1756	6	1514	7	NULL	NULL	0	NULL	statement 4	NULL		is a function of 	NULL				phy input level	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_24_13419_s_88	11069292	( c) Binding of phyB and phyA to PIF3 as a function of phy input level.	bind
1395	1	1515	5	10	NULL	0	NULL	PriA Bs	GP		bind					ssiA strands	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_7_1593_s_164	11917020	( C) Binding of PriA Bs to  ssiA strands covered by SSB Bs.	bind
61155	2	1515	5	10	NULL	0	NULL	ssiA strands	NucleicAcid		covered by					SSB Bs	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_7_1593_s_164	11917020	( C) Binding of PriA Bs to  ssiA strands covered by SSB Bs.	bind
1757	1	1515	7	10	NULL	0	NULL	PriA Bs 	GP		bind					ssiA strands	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_7_1593_s_164	11917020	( C) Binding of PriA Bs to  ssiA strands covered by SSB Bs.	bind
61156	2	1515	7	10	NULL	0	NULL	ssiA strands	NucleicAcid		covered by					SSB Bs	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_7_1593_s_164	11917020	( C) Binding of PriA Bs to  ssiA strands covered by SSB Bs.	bind
1396	1	1516	5	10	NULL	0	NULL	CtBP	GP	recombinant	bind					GST-E1ACter	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_295_5561_1895_s_22	11847309	( C) Binding of recombinant CtBP to GST-E1A at various concentrations of NAD+ and NADH. Glutathione beads were coated with GST-E1ACter (COOH-terminal 67 amino acids of E1A), and bound CtBP was quantified by Western blotting.	bind
2729	2	1516	5	10	NULL	0	NULL	GST E1ACter	GP		is					COOH-terminal 67 amino acids of E1A	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_295_5561_1895_s_22	11847309	( C) Binding of recombinant CtBP to GST-E1A at various concentrations of NAD+ and NADH. Glutathione beads were coated with GST-E1ACter (COOH-terminal 67 amino acids of E1A), and bound CtBP was quantified by Western blotting.	bind
1805	2	1516	7	10	NULL	0	NULL	CtBP	GP	recombinant	bind					GST-E1ACter	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_295_5561_1895_s_22	11847309	( C) Binding of recombinant CtBP to GST-E1A at various concentrations of NAD+ and NADH. Glutathione beads were coated with GST-E1ACter (COOH-terminal 67 amino acids of E1A), and bound CtBP was quantified by Western blotting.	bind
3200	1	1516	7	10	NULL	0	NULL	GST-E1ACter	GP		is					COOH-terminal 67 amino acids of E1A	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_295_5561_1895_s_22	11847309	( C) Binding of recombinant CtBP to GST-E1A at various concentrations of NAD+ and NADH. Glutathione beads were coated with GST-E1ACter (COOH-terminal 67 amino acids of E1A), and bound CtBP was quantified by Western blotting.	bind
1397	1	1517	5	10	NULL	0	NULL	ezrin	GP	recombinant	bind					SS phagosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_2_199_s_273	10637224	( C) Binding of recombinant ezrin to SS phagosomes.	bind
1807	2	1517	7	10	NULL	0	NULL	ezrin	GP	recombinant	bind					SS phagosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_2_199_s_273	10637224	( C) Binding of recombinant ezrin to SS phagosomes.	bind
1400	1	1518	5	NULL	NULL	0	NULL	RPA-AB	NULL		bind	NULL				CPD/AA-10 duplex	NULL				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_16_4747_s_130	12907715	( C) Binding of RPA-AB to the CPD/AA-10 duplex as a function of DNA concentration in  the absence (upper) and presence (lower) of equimolar XPA-MBD.	bind
2475	2	1518	5	NULL	NULL	0	NULL	statement 1	NULL		is a function of	NULL				DNA concentration	NULL				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_16_4747_s_130	12907715	( C) Binding of RPA-AB to the CPD/AA-10 duplex as a function of DNA concentration in  the absence (upper) and presence (lower) of equimolar XPA-MBD.	bind
1808	3	1518	7	NULL	NULL	0	NULL	RPA-AB	NULL		bind to	NULL				 CPD/AA-10 duplex 	NULL				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_16_4747_s_130	12907715	( C) Binding of RPA-AB to the CPD/AA-10 duplex as a function of DNA concentration in  the absence (upper) and presence (lower) of equimolar XPA-MBD.	bind
1810	5	1518	7	NULL	NULL	0	NULL	statement 3	NULL		is a function of 	NULL				DNA concentration	NULL				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_16_4747_s_130	12907715	( C) Binding of RPA-AB to the CPD/AA-10 duplex as a function of DNA concentration in  the absence (upper) and presence (lower) of equimolar XPA-MBD.	bind
1402	1	1519	5	10	NULL	0	NULL	RPA-AB	GP		bind					CPD/AA-10 duplex	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_16_4747_s_130	12907715	( C) Binding of RPA-AB to the CPD/AA-10 duplex as a function of DNA concentration in the absence (upper) and presence (lower) of equimolar XPA-MBD.	bind
49374	2	1519	7	10	NULL	0	NULL	RPA-AB	GP		bind					CPD/AA-10 duplex	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_16_4747_s_130	12907715	( C) Binding of RPA-AB to the CPD/AA-10 duplex as a function of DNA concentration in the absence (upper) and presence (lower) of equimolar XPA-MBD.	bind
1403	1	1520	5	10	NULL	0	NULL	C2A-C2B	GP	soluble	bind					C2A-C2B	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_4_2082_s_100	12578982	( C) Binding of soluble C2A-C2B from syt I (3 muM) to immobilized C2A-C2B from syt II  was assayed as described in  B.	bind
1812	2	1520	7	10	NULL	0	NULL	C2A-C2B	GP	soluble	bind					C2A-C2B	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_4_2082_s_100	12578982	( C) Binding of soluble C2A-C2B from syt I (3 muM) to immobilized C2A-C2B from syt II  was assayed as described in  B.	bind
1404	1	1521	5	10	NULL	0	NULL	FGF-7	GP	soluble	bind					perlecan	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1599_s_182	9788974	( C) Binding of soluble FGF-7 to immobilized perlecan or type I collagen as  detected by protein overlay assay and immunoblotting.	bind
1405	2	1521	5	10	NULL	0	NULL	FGF-7	GP	soluble	bind					type I collagen	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1599_s_182	9788974	( C) Binding of soluble FGF-7 to immobilized perlecan or type I collagen as  detected by protein overlay assay and immunoblotting.	bind
1813	1	1521	7	10	NULL	0	NULL	FGF-7	GP	soluble	bind 					perlecan	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1599_s_182	9788974	( C) Binding of soluble FGF-7 to immobilized perlecan or type I collagen as  detected by protein overlay assay and immunoblotting.	bind
1814	2	1521	7	10	NULL	0	NULL	FGF-7	GP	soluble	bind					type I collagen	GP	 immobilized 			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1599_s_182	9788974	( C) Binding of soluble FGF-7 to immobilized perlecan or type I collagen as  detected by protein overlay assay and immunoblotting.	bind
1406	1	1522	5	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				Sp1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_science_296_5576_2238_s_80	11988536	( C) Binding of Sp1 to the D2 promoter is inhibited in the caudate of the human HD postmortem brain.	bind
1407	2	1522	5	NULL	NULL	0	NULL	statement 1	NULL		inhibited in	NULL				human HD postmortem brain	NULL	caudate			NULL		NULL	NULL	NULL	NULL	gw60_science_296_5576_2238_s_80	11988536	( C) Binding of Sp1 to the D2 promoter is inhibited in the caudate of the human HD postmortem brain.	bind
1815	3	1522	7	NULL	NULL	0	NULL	Sp1	NULL		bind to	NULL				D2	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_science_296_5576_2238_s_80	11988536	( C) Binding of Sp1 to the D2 promoter is inhibited in the caudate of the human HD postmortem brain.	bind
1816	4	1522	7	NULL	NULL	0	NULL	statement 3	NULL		is inhibited 	NULL				human HD postmortem brain	NULL	in the caudate of  			NULL		NULL	NULL	NULL	NULL	gw60_science_296_5576_2238_s_80	11988536	( C) Binding of Sp1 to the D2 promoter is inhibited in the caudate of the human HD postmortem brain.	bind
1408	1	1523	5	10	NULL	0	NULL	Spc29p	GP		bind					Bbp1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_3_421_s_44	10654940	( C) Binding of Spc29p to Bbp1p.	bind
1817	1	1523	7	10	NULL	0	NULL	Spc29p	GP		bind					Bbp1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_3_421_s_44	10654940	( C) Binding of Spc29p to Bbp1p.	bind
1409	1	1524	5	NULL	NULL	0	NULL		NULL		bind	NULL		R domain fragments			NULL		GST-N-Tail		NULL		NULL	NULL	NULL	NULL	gw60_science_286_5439_544_s_101	10521352	( C) Binding of the indicated R domain fragments to GST-N-Tail (2.85 muM).	bind
1818	1	1524	7	10	NULL	0	NULL		NULL	 	bind	NULL		R domain fragments			NULL		GST-N-Tail		NULL		NULL	NULL	NULL	NULL	gw60_science_286_5439_544_s_101	10521352	( C) Binding of the indicated R domain fragments to GST-N-Tail (2.85 muM).	bind
1410	1	1525	5	10	NULL	0	NULL	Plk1	GP		bind			PBD		Cdc25C	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_science_299_5610_1228_s_89	12595692	( C) Binding of the Plk1 PBD to Cdc25C in vivo.	bind
1819	1	1525	7	10	NULL	0	NULL	Plk1 	GP		bind 			PBD		Cdc25C	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_science_299_5610_1228_s_89	12595692	( C) Binding of the Plk1 PBD to Cdc25C in vivo.	bind
1411	1	1526	5	10	NULL	0	NULL	SnoN fragments	GP		bind					Smad2	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5440_771_s_36	10531062	( C) Binding of the SnoN fragments to Smad2 and Smad4.	bind
1412	2	1526	5	10	NULL	0	NULL	SnoN fragments	GP		bind					Smad4	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5440_771_s_36	10531062	( C) Binding of the SnoN fragments to Smad2 and Smad4.	bind
1820	1	1526	7	10	NULL	0	NULL	SnoN fragments	GP		bind					Smad2	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5440_771_s_36	10531062	( C) Binding of the SnoN fragments to Smad2 and Smad4.	bind
1821	2	1526	7	10	NULL	0	NULL	SnoN fragments	GP		bind					Smad4	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5440_771_s_36	10531062	( C) Binding of the SnoN fragments to Smad2 and Smad4.	bind
1413	1	1527	5	10	NULL	0	NULL	TIF32	GP		bind					GST - HCR1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_20_4_891_s_59	11179233	( C) Binding of TIF32 and PRT1 to GST - HCR1  in vitro.	bind
1414	2	1527	5	10	NULL	0	NULL	PRT1	GP		bind					GST - HCR1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_20_4_891_s_59	11179233	( C) Binding of TIF32 and PRT1 to GST - HCR1  in vitro.	bind
1822	1	1527	7	10	NULL	0	NULL	TIF32	GP		bind					GST - HCR1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_20_4_891_s_59	11179233	( C) Binding of TIF32 and PRT1 to GST - HCR1  in vitro.	bind
1823	2	1527	7	10	NULL	0	NULL	PRT1	GP		bind					GST - HCR1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_20_4_891_s_59	11179233	( C) Binding of TIF32 and PRT1 to GST - HCR1  in vitro.	bind
1415	1	1528	5	10	NULL	0	NULL	p100	GP	transfected	bind					IKKalpha	GP	endogenous			NULL	Tax-expressing cells	NULL	NULL	NULL	NULL	gw60_embo_20_23_6805_s_190	11726516	( C) Binding of transfected p100 to endogenous IKKalpha in Tax-expressing cells.	bind
1824	1	1528	7	10	NULL	0	NULL	p100	GP	transfected 	bind 					IKKalpha	GP	endogenous			NULL	Tax-expressing cells	NULL	NULL	NULL	NULL	gw60_embo_20_23_6805_s_190	11726516	( C) Binding of transfected p100 to endogenous IKKalpha in Tax-expressing cells.	bind
1416	1	1529	5	10	NULL	0	NULL	trastuzumab Fc variants	GP		bind					FcgammaRIIb	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_11_4005_s_47	16537476	( C) Binding of trastuzumab Fc variants to human FcgammaRIIb ( n = 2).	bind
1825	1	1529	7	10	NULL	0	NULL	trastuzumab Fc variants	GP		bind					FcgammaRIIb	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_11_4005_s_47	16537476	( C) Binding of trastuzumab Fc variants to human FcgammaRIIb ( n = 2).	bind
1417	1	1530	5	10	NULL	0	NULL	Ub	GP		bind					Dsk2p	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_745_s_106	11805328	( C) Binding of Ub to Dsk2p.	bind
1826	1	1530	7	10	NULL	0	NULL	Ub	GP		bind					Dsk2p	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_745_s_106	11805328	( C) Binding of Ub to Dsk2p.	bind
1418	1	1531	5	NULL	NULL	0	NULL	Lt rREL1	NULL	unlabeled purified	bind	NULL				L-complex	NULL	REL1-depleted			NULL		0	NULL	NULL	NULL	gw70_pnas_102_13_4712_s_156	15781861	( C) Binding of unlabeled purified Lt rREL1 to REL1-depleted L-complex.	bind
1843	2	1531	7	NULL	NULL	0	NULL	Lt rREL1	NULL	unlabeled purified	bind to	NULL				 L-complex	NULL	REL1-depleted			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_13_4712_s_156	15781861	( C) Binding of unlabeled purified Lt rREL1 to REL1-depleted L-complex.	bind
1419	1	1532	5	10	NULL	0	NULL	UNR	GP		bind					ARS RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_236	16356927	( C) Binding of UNR to the ARS RNA.	bind
1844	1	1532	7	10	NULL	0	NULL	UNR	GP		bind					 ARS RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_236	16356927	( C) Binding of UNR to the ARS RNA.	bind
1420	1	1533	5	10	NULL	0	NULL	vezatin	GP		bind					myosin VIIA	GP		C-terminal FERM domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_22_6020_s_66	11080149	( C) Binding of vezatin to the myosin VIIA C-terminal FERM domain.	bind
1845	1	1533	7	10	NULL	0	NULL	vezatin	GP		bind					myosin VIIA	GP		C-terminal FERM domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_22_6020_s_66	11080149	( C) Binding of vezatin to the myosin VIIA C-terminal FERM domain.	bind
1421	1	1534	5	10	NULL	0	NULL	Penelope EN	GP	WT	bind					ps1 target	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14719_s_148	15465912	( C) Binding of WT  Penelope EN to the ps1 target at different concentrations of poly(dI).	bind
1846	1	1534	7	10	NULL	0	NULL	Penelope EN	GP	WT	bind					ps1 target	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14719_s_148	15465912	( C) Binding of WT  Penelope EN to the ps1 target at different concentrations of poly(dI).	bind
1422	1	1535	5	10	NULL	0	NULL	XDRP1	GP		bind					A-type cyclins	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5009_s_99	10487753	( C) Binding of XDRP1 to other A-type cyclins.	bind
1847	1	1535	7	10	NULL	0	NULL	XDRP1	GP		bind					A-type cyclins	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5009_s_99	10487753	( C) Binding of XDRP1 to other A-type cyclins.	bind
1423	1	1536	5	NULL	NULL	0	NULL	ZO-2	NULL		bind	NULL				Ad9	NULL			 E4-ORF1	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_20_5578_s_70	11598001	( C) Binding of ZO-2 to Ad9 E4-ORF1 but not to Ad5 and Ad12 E4-ORF1 in GST pulldown assays.	bind
1424	2	1536	5	NULL	NULL	0	NULL	ZO-2	NULL		does not bind	NULL				Ad5	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_20_5578_s_70	11598001	( C) Binding of ZO-2 to Ad9 E4-ORF1 but not to Ad5 and Ad12 E4-ORF1 in GST pulldown assays.	bind
1425	3	1536	5	NULL	NULL	0	NULL	ZO-2	NULL		bind	NULL				Ad12	NULL			 E4-ORF1	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_20_5578_s_70	11598001	( C) Binding of ZO-2 to Ad9 E4-ORF1 but not to Ad5 and Ad12 E4-ORF1 in GST pulldown assays.	bind
1848	4	1536	7	NULL	NULL	0	NULL	ZO-2	NULL		bind to	NULL				Ad9 	NULL			E4-ORF1	NULL		0	NULL	NULL	NULL	gw60_embo_20_20_5578_s_70	11598001	( C) Binding of ZO-2 to Ad9 E4-ORF1 but not to Ad5 and Ad12 E4-ORF1 in GST pulldown assays.	bind
1849	5	1536	7	NULL	NULL	0	NULL	ZO-2	NULL		does not bind	NULL				Ad5	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_20_5578_s_70	11598001	( C) Binding of ZO-2 to Ad9 E4-ORF1 but not to Ad5 and Ad12 E4-ORF1 in GST pulldown assays.	bind
1850	6	1536	7	NULL	NULL	0	NULL	ZO-2	NULL		does not bind	NULL				Ad12 	NULL			E4-ORF1	NULL		0	NULL	NULL	NULL	gw60_embo_20_20_5578_s_70	11598001	( C) Binding of ZO-2 to Ad9 E4-ORF1 but not to Ad5 and Ad12 E4-ORF1 in GST pulldown assays.	bind
1426	1	1537	5	10	NULL	0	NULL	TGF-beta2	GP		bind					TGF-beta receptors	GP				NULL	cell surface of Mv1Lu cells	NULL	NULL	NULL	NULL	gw60_embo_20_3_480_s_93	11157754	( C) Binding of [125]TGF-beta2 to TGF-beta receptors at the cell surface of Mv1Lu and R1b/L17 cells.	bind
49523	2	1537	5	10	NULL	0	NULL	TGF-beta2	GP		bind					TGF-beta receptor	GP				NULL	cell surface of R1b/L17 cells	NULL	NULL	NULL	NULL	gw60_embo_20_3_480_s_93	11157754	( C) Binding of [125]TGF-beta2 to TGF-beta receptors at the cell surface of Mv1Lu and R1b/L17 cells.	bind
1851	1	1537	7	10	NULL	0	NULL	TGF-beta2	GP		bind					TGF-beta receptors	GP				NULL	cell surface of Mv1Lu cells	NULL	NULL	NULL	NULL	gw60_embo_20_3_480_s_93	11157754	( C) Binding of [125]TGF-beta2 to TGF-beta receptors at the cell surface of Mv1Lu and R1b/L17 cells.	bind
49524	2	1537	7	10	NULL	0	NULL	TGF-beta2	GP		bind					TGF-beta receptor	GP				NULL	cell surface of R1b/L17 cells	NULL	NULL	NULL	NULL	gw60_embo_20_3_480_s_93	11157754	( C) Binding of [125]TGF-beta2 to TGF-beta receptors at the cell surface of Mv1Lu and R1b/L17 cells.	bind
1427	1	1538	5	NULL	NULL	0	NULL	platelet P-selectin	NULL		bind	NULL				PSGL-1	NULL	microparticle			NULL		0	NULL	NULL	NULL	gw70_jclininvest_115_12_3355_s_172	16322780	( C) Blood-borne tissue factor associated with microparticles accumulates on the platelet  thrombus through the binding of platelet P-selectin and microparticle PSGL-1.	bind
1428	2	1538	5	NULL	NULL	0	NULL	blood-borne tissue factor	NULL		associate with	NULL				microparticles	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_115_12_3355_s_172	16322780	( C) Blood-borne tissue factor associated with microparticles accumulates on the platelet  thrombus through the binding of platelet P-selectin and microparticle PSGL-1.	bind
2478	3	1538	5	NULL	NULL	0	NULL	statement 2	NULL		accumulates on	NULL				platelet thrombus	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_115_12_3355_s_172	16322780	( C) Blood-borne tissue factor associated with microparticles accumulates on the platelet  thrombus through the binding of platelet P-selectin and microparticle PSGL-1.	bind
2479	4	1538	5	NULL	NULL	0	NULL	statement 3	NULL		occurs through	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_115_12_3355_s_172	16322780	( C) Blood-borne tissue factor associated with microparticles accumulates on the platelet  thrombus through the binding of platelet P-selectin and microparticle PSGL-1.	bind
1855	3	1538	7	NULL	NULL	0	NULL	P-selectin	NULL	platelet	bind to	NULL				PSGL-1	NULL	microparticle			NULL		0	NULL	NULL	NULL	gw70_jclininvest_115_12_3355_s_172	16322780	( C) Blood-borne tissue factor associated with microparticles accumulates on the platelet  thrombus through the binding of platelet P-selectin and microparticle PSGL-1.	bind
1856	4	1538	7	NULL	NULL	0	NULL	Blood-borne tissue factor	NULL		associate with	NULL				microparticles	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_115_12_3355_s_172	16322780	( C) Blood-borne tissue factor associated with microparticles accumulates on the platelet  thrombus through the binding of platelet P-selectin and microparticle PSGL-1.	bind
1857	5	1538	7	NULL	NULL	0	NULL	statement 4	NULL		accumulates on	NULL				platelet thrombus	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_115_12_3355_s_172	16322780	( C) Blood-borne tissue factor associated with microparticles accumulates on the platelet  thrombus through the binding of platelet P-selectin and microparticle PSGL-1.	bind
1858	6	1538	7	NULL	NULL	0	NULL	statement 5	NULL		occurs through	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_115_12_3355_s_172	16322780	( C) Blood-borne tissue factor associated with microparticles accumulates on the platelet  thrombus through the binding of platelet P-selectin and microparticle PSGL-1.	bind
1429	1	1539	5	10	NULL	0	NULL	Asf1	GP	full-length	interact with					RFC	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1365_s_217	15901673	( C) Both full-length and the N terminus of Asf1 interact with RFC.	bind
1430	2	1539	5	10	NULL	0	NULL	Asf1	GP		interact with			N terminus		RFC	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1365_s_217	15901673	( C) Both full-length and the N terminus of Asf1 interact with RFC.	bind
1853	1	1539	7	10	NULL	0	NULL	Asf1	GP	full-length	interact with					RFC	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1365_s_217	15901673	( C) Both full-length and the N terminus of Asf1 interact with RFC.	bind
1854	2	1539	7	10	NULL	0	NULL	Asf1	GP		interact with			N terminus		RFC	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1365_s_217	15901673	( C) Both full-length and the N terminus of Asf1 interact with RFC.	bind
506	1	1540	5	NULL	NULL	0	NULL	LIF	NULL		bind	NULL				gp130 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11563_s_181	11016970	( c) Both LIF and IL-6 bind to the gp130 receptor and initiate signal transduction through Janus kinase-signal transducers and activators of transcription (STAT) pathways.	bind
507	2	1540	5	NULL	NULL	0	NULL	IL-6	NULL		bind	NULL				gp130 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11563_s_181	11016970	( c) Both LIF and IL-6 bind to the gp130 receptor and initiate signal transduction through Janus kinase-signal transducers and activators of transcription (STAT) pathways.	bind
508	3	1540	5	NULL	NULL	0	NULL	statement 1	NULL		initiate	NULL				signal transduction	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11563_s_181	11016970	( c) Both LIF and IL-6 bind to the gp130 receptor and initiate signal transduction through Janus kinase-signal transducers and activators of transcription (STAT) pathways.	bind
509	4	1540	5	NULL	NULL	0	NULL	statement 2	NULL		initiate	NULL				signal transduction	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11563_s_181	11016970	( c) Both LIF and IL-6 bind to the gp130 receptor and initiate signal transduction through Janus kinase-signal transducers and activators of transcription (STAT) pathways.	bind
510	5	1540	5	NULL	NULL	0	NULL	statement 1	NULL		occurs through	NULL				Janus kinase-STAT pathway	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11563_s_181	11016970	( c) Both LIF and IL-6 bind to the gp130 receptor and initiate signal transduction through Janus kinase-signal transducers and activators of transcription (STAT) pathways.	bind
2491	6	1540	5	NULL	NULL	0	NULL	statement 2	NULL		occurs through	NULL				Janus kinase-STAT pathway	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11563_s_181	11016970	( c) Both LIF and IL-6 bind to the gp130 receptor and initiate signal transduction through Janus kinase-signal transducers and activators of transcription (STAT) pathways.	bind
2494	7	1540	5	NULL	NULL	0	NULL	Janus kinase-STAT	NULL		is	NULL				Janus kinase-signal transducers and activators of transcription	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11563_s_181	11016970	( c) Both LIF and IL-6 bind to the gp130 receptor and initiate signal transduction through Janus kinase-signal transducers and activators of transcription (STAT) pathways.	bind
1859	6	1540	7	NULL	NULL	0	NULL	LIF	NULL		bind to	NULL				gp130 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11563_s_181	11016970	( c) Both LIF and IL-6 bind to the gp130 receptor and initiate signal transduction through Janus kinase-signal transducers and activators of transcription (STAT) pathways.	bind
1860	7	1540	7	NULL	NULL	0	NULL	IL-6	NULL		bind to	NULL				gp130 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11563_s_181	11016970	( c) Both LIF and IL-6 bind to the gp130 receptor and initiate signal transduction through Janus kinase-signal transducers and activators of transcription (STAT) pathways.	bind
1861	8	1540	7	NULL	NULL	0	NULL	statement 6	NULL		initiate	NULL				signal transduction	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11563_s_181	11016970	( c) Both LIF and IL-6 bind to the gp130 receptor and initiate signal transduction through Janus kinase-signal transducers and activators of transcription (STAT) pathways.	bind
1862	9	1540	7	NULL	NULL	0	NULL	statement 7	NULL		initiate	NULL				 signal transduction 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11563_s_181	11016970	( c) Both LIF and IL-6 bind to the gp130 receptor and initiate signal transduction through Janus kinase-signal transducers and activators of transcription (STAT) pathways.	bind
1863	10	1540	7	NULL	NULL	0	NULL	statement 8	NULL		occurs through	NULL				Janus kinase-STAT pathway	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11563_s_181	11016970	( c) Both LIF and IL-6 bind to the gp130 receptor and initiate signal transduction through Janus kinase-signal transducers and activators of transcription (STAT) pathways.	bind
1864	11	1540	7	NULL	NULL	0	NULL	statement 9	NULL		occurs through	NULL				Janus kinase-STAT pathway	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11563_s_181	11016970	( c) Both LIF and IL-6 bind to the gp130 receptor and initiate signal transduction through Janus kinase-signal transducers and activators of transcription (STAT) pathways.	bind
2209	12	1540	7	NULL	NULL	0	NULL	Janus kinase-STAT	NULL		is	NULL				Janus kinase-signal transducers and activators of transcription	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11563_s_181	11016970	( c) Both LIF and IL-6 bind to the gp130 receptor and initiate signal transduction through Janus kinase-signal transducers and activators of transcription (STAT) pathways.	bind
2078	1	1541	6	10	NULL	0	NULL	noggin	GP		bind					BMP4	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_274_5290_1115_s_46	8895454	( C) Both noggin and chordin bind to BMP4.	bind
2079	2	1541	6	10	NULL	0	NULL	chordin	GP		bind					BMP4	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_274_5290_1115_s_46	8895454	( C) Both noggin and chordin bind to BMP4.	bind
2080	1	1542	6	10	NULL	0	NULL	C-Mad2	GP		bind					Mad1	GP			Mad2-binding site	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_6_1273_s_51	16525508	( C) C-Mad2 bound to the Mad2-binding site of Mad1 (green, PDB ID 1GO4).	bind
2081	1	1543	6	10	NULL	0	NULL	CCT	GP		bind					Gbeta	GP	deletion mutants			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_22_8360_s_93	16717193	( C) CCT binding to Gbeta deletion mutants.	bind
2088	1	1545	6	10	NULL	0	NULL	CDC20	GP	mutant	bind		less			Mad2	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5353_1041_s_93	9461437	( C) Checkpoint-resistant  CDC20 mutants have diminished binding of Mad2 and Mad3.	bind
2089	2	1545	6	10	NULL	0	NULL	CDC20	GP	mutant	bind		less			Mad3	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5353_1041_s_93	9461437	( C) Checkpoint-resistant  CDC20 mutants have diminished binding of Mad2 and Mad3.	bind
2090	1	1547	6	10	NULL	0	NULL	PPARgamma	GP		associate with					GyK gene	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_4_453_s_76	15681609	( C) ChIP analysis of PPARgamma association with GyK and aP2 genes.	bind
2091	2	1547	6	10	NULL	0	NULL	PPARgamma	GP		associate with					aP2 gene	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_4_453_s_76	15681609	( C) ChIP analysis of PPARgamma association with GyK and aP2 genes.	bind
2092	1	1548	6	10	NULL	0	NULL	Myc proteins	GP		bind					hTERT	GP	exogenous		promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_14_8211_s_176	12821782	( C) CHIP assay  detects Myc and high-risk E6 proteins bound to an exogenous hTERT promoter.	bind
2093	2	1548	6	10	NULL	0	NULL	E6 proteins	GP	high-risk	bind					hTERT	GP	exogenous		promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_14_8211_s_176	12821782	( C) CHIP assay  detects Myc and high-risk E6 proteins bound to an exogenous hTERT promoter.	bind
2094	1	1549	6	10	NULL	0	NULL	HDAC1	GP		bind					HMG-CoA synthase	GP	endogenous;;mitochondrial		promoter	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_6_1693_s_144	12626711	( C) ChIP assay of HDAC1 bound to endogenous mitochondrial HMG-CoA synthase promoter.	bind
2095	1	1550	6	10	NULL	0	NULL	Nkx6.1	GP		bind					glucagon	GP	endogenous		promoter	NULL	class 3 cell line (832/3)	NULL	NULL	NULL	NULL	gw70_pnas_102_20_7297_s_150	15883383	( C) ChIP assay of Nkx6.1 binding to the endogenous glucagon promoter in a class 3 cell  line (832/3).	bind
2096	1	1551	6	10	NULL	0	NULL	RUNX1	GP		bind		specifically			MIP-1alpha	GP	endogenous		promoter	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2735_s_129	12771199	( C) ChIP assays demonstrating specific binding of RUNX1 to the endogenous MIP-1alpha promoter.	bind
2097	1	1552	6	10	NULL	0	NULL	Dnmt3a	GP		does not bind					ODC	GP				NULL	c-myc+/+ cells	NULL	NULL	NULL	NULL	gw70_embo_24_2_336_s_134	15616584	( C) ChIPs performed in  c-myc+/+ cells show that Dnmt3a does not bind the Myc-activated E-box genes  ODC and  NM23-H2.	bind
2098	2	1552	6	10	NULL	0	NULL	Dnmt3a	GP		does not bind					NM23-H2	GP				NULL	c-myc+/+ cells	NULL	NULL	NULL	NULL	gw70_embo_24_2_336_s_134	15616584	( C) ChIPs performed in  c-myc+/+ cells show that Dnmt3a does not bind the Myc-activated E-box genes  ODC and  NM23-H2.	bind
46172	3	1552	6	10	NULL	0	NULL	Myc	GP		activates					E-box genes	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_336_s_134	15616584	( C) ChIPs performed in  c-myc+/+ cells show that Dnmt3a does not bind the Myc-activated E-box genes  ODC and  NM23-H2.	bind
46173	4	1552	6	10	NULL	0	NULL	ODC	GP		is a type of					E-box genes	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_336_s_134	15616584	( C) ChIPs performed in  c-myc+/+ cells show that Dnmt3a does not bind the Myc-activated E-box genes  ODC and  NM23-H2.	bind
46174	5	1552	6	10	NULL	0	NULL	NM23-H2	GP		is a type of					E-box genes	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_336_s_134	15616584	( C) ChIPs performed in  c-myc+/+ cells show that Dnmt3a does not bind the Myc-activated E-box genes  ODC and  NM23-H2.	bind
2099	1	1553	6	10	NULL	0	NULL	HMG-D	GP		bind					66 bp DNA circles	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_11_2852_s_193	12771212	( C) Circularization curves for L9, A36, V32 and T33 series of mutants and Spec. ( D) EMSA of HMG-D bound to the 66 bp DNA circles (lanes 1 - 8) and 77 bp circles (lanes  9 - 16).	bind
2100	2	1553	6	10	NULL	0	NULL	HMG-D	GP		bind					77 bp DNA circles	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_11_2852_s_193	12771212	( C) Circularization curves for L9, A36, V32 and T33 series of mutants and Spec. ( D) EMSA of HMG-D bound to the 66 bp DNA circles (lanes 1 - 8) and 77 bp circles (lanes  9 - 16).	bind
2190	1	1556	6	10	NULL	0	NULL	HEXIM1	GP		oligomerizes in					cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7000_s_155	16377779	( C) Combined disruptions of the CR and the 7SK snRNA binding site abolish completely  HEXIM1 oligomerization in cells.	bind
2191	2	1556	6	10	NULL	0	NULL			disruption of	abolish		completely	 CR 		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7000_s_155	16377779	( C) Combined disruptions of the CR and the 7SK snRNA binding site abolish completely  HEXIM1 oligomerization in cells.	bind
52600	3	1556	6	10	NULL	0	NULL			disruption of	abolish		completely	7SK snRNA binding site		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7000_s_155	16377779	( C) Combined disruptions of the CR and the 7SK snRNA binding site abolish completely  HEXIM1 oligomerization in cells.	bind
2101	1	1557	6	10	NULL	0	NULL	TFIIB	GP		bind					Xist P1	GP			promoter	NULL	female TS cells	NULL	NULL	NULL	NULL	gw70_genesdev_19_12_1474_s_139	15964997	( C) Comparative analysis of the  Xist/Tsix transcripts ratio (black bars) with the ratio of TFIIB binding to  Xist P1 promoter versus  Tsix promoter (gray bars) in female TS cells, ES cells, and MEFs.	bind
2102	2	1557	6	10	NULL	0	NULL	TFIIB	GP		bind					Tsix 	GP			promoter	NULL	female TS cells	NULL	NULL	NULL	NULL	gw70_genesdev_19_12_1474_s_139	15964997	( C) Comparative analysis of the  Xist/Tsix transcripts ratio (black bars) with the ratio of TFIIB binding to  Xist P1 promoter versus  Tsix promoter (gray bars) in female TS cells, ES cells, and MEFs.	bind
2103	3	1557	6	10	NULL	0	NULL	TFIIB	GP		bind					Xist P1	GP			promoter	NULL	ES cells	NULL	NULL	NULL	NULL	gw70_genesdev_19_12_1474_s_139	15964997	( C) Comparative analysis of the  Xist/Tsix transcripts ratio (black bars) with the ratio of TFIIB binding to  Xist P1 promoter versus  Tsix promoter (gray bars) in female TS cells, ES cells, and MEFs.	bind
2104	4	1557	6	10	NULL	0	NULL	TFIIB	GP		bind					Tsix 	GP			promoter	NULL	ES cells	NULL	NULL	NULL	NULL	gw70_genesdev_19_12_1474_s_139	15964997	( C) Comparative analysis of the  Xist/Tsix transcripts ratio (black bars) with the ratio of TFIIB binding to  Xist P1 promoter versus  Tsix promoter (gray bars) in female TS cells, ES cells, and MEFs.	bind
2105	5	1557	6	10	NULL	0	NULL	TFIIB	GP		bind					Xist P1	GP			promoter	NULL	MEFs	NULL	NULL	NULL	NULL	gw70_genesdev_19_12_1474_s_139	15964997	( C) Comparative analysis of the  Xist/Tsix transcripts ratio (black bars) with the ratio of TFIIB binding to  Xist P1 promoter versus  Tsix promoter (gray bars) in female TS cells, ES cells, and MEFs.	bind
2106	6	1557	6	10	NULL	0	NULL	TFIIB	GP		bind					Tsix 	GP			promoter	NULL	MEFs	NULL	NULL	NULL	NULL	gw70_genesdev_19_12_1474_s_139	15964997	( C) Comparative analysis of the  Xist/Tsix transcripts ratio (black bars) with the ratio of TFIIB binding to  Xist P1 promoter versus  Tsix promoter (gray bars) in female TS cells, ES cells, and MEFs.	bind
2107	1	1558	6	10	NULL	0	NULL	SRF	GP		bind					CFTR	GP			CArG box	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5271_s_409	16170155	( C) Comparative binding of SRF to  CFTR CArG boxes.	bind
2108	1	1559	6	10	NULL	0	NULL	KaiA	GP	wild type	bind					KaiC	GP	His-tagged			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_8_1688_s_168	15071498	( C) Comparison of binding profiles of mutant and wild-type KaiA and KaiB proteins to  6x-His-tagged KaiC bound to Ni beads.	bind
2109	2	1559	6	10	NULL	0	NULL	KaiA	GP	mutant	bind					KaiC	GP	His-tagged			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_8_1688_s_168	15071498	( C) Comparison of binding profiles of mutant and wild-type KaiA and KaiB proteins to  6x-His-tagged KaiC bound to Ni beads.	bind
2110	3	1559	6	10	NULL	0	NULL	KaiB	GP	wild type	bind					KaiC	GP	His-tagged			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_8_1688_s_168	15071498	( C) Comparison of binding profiles of mutant and wild-type KaiA and KaiB proteins to  6x-His-tagged KaiC bound to Ni beads.	bind
2111	4	1559	6	10	NULL	0	NULL	KaiB	GP	mutant	bind					KaiC	GP	His-tagged			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_8_1688_s_168	15071498	( C) Comparison of binding profiles of mutant and wild-type KaiA and KaiB proteins to  6x-His-tagged KaiC bound to Ni beads.	bind
2112	1	1560	6	10	NULL	0	NULL	CFTR	GP		bind					GST-alpha1-AMPK 	GP		NH2-terminal		NULL	CHO-BQ2 cells	NULL	NULL	NULL	NULL	gw60_jclininvest_105_12_1711_s_149	10862786	( c) Comparison of binding strengths of CFTR with NH2-terminal and COOH-terminal GST-alpha1-AMPK fusion proteins in CHO-BQ2 cells.	bind
2113	2	1560	6	10	NULL	0	NULL	CFTR	GP		bind					GST-alpha1-AMPK 	GP		COOH-terminal		NULL	CHO-BQ2 cells	NULL	NULL	NULL	NULL	gw60_jclininvest_105_12_1711_s_149	10862786	( c) Comparison of binding strengths of CFTR with NH2-terminal and COOH-terminal GST-alpha1-AMPK fusion proteins in CHO-BQ2 cells.	bind
52601	3	1560	6	10	NULL	0	NULL	GST-alpha1-AMPK 	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_105_12_1711_s_149	10862786	( c) Comparison of binding strengths of CFTR with NH2-terminal and COOH-terminal GST-alpha1-AMPK fusion proteins in CHO-BQ2 cells.	bind
2114	1	1561	6	10	NULL	0	NULL	ICAM-2 peptide	GP		bind					radixin	GP		FERM domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_22_3_502_s_213	12554651	( C) Comparison of the 310 helix in the ICAM-2 peptide bound to the radixin FERM domain with the beta-turn of the NPxY motif in the IR peptide bound to the IRS-1 PTB domain.	bind
2115	2	1561	6	10	NULL	0	NULL	IR peptide	GP		bind			beta-turn of the NPxY motif		IRS-1	GP		PTB domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_22_3_502_s_213	12554651	( C) Comparison of the 310 helix in the ICAM-2 peptide bound to the radixin FERM domain with the beta-turn of the NPxY motif in the IR peptide bound to the IRS-1 PTB domain.	bind
2116	1	1562	6	10	NULL	0	NULL	m7G	Chemical		bind					CBP20	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_20_5548_s_115	12374755	( C) Comparison of the mode of m7G binding to CBP20, VP39 and eIF4E.	bind
2117	2	1562	6	10	NULL	0	NULL	m7G	Chemical		bind					VP39	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_20_5548_s_115	12374755	( C) Comparison of the mode of m7G binding to CBP20, VP39 and eIF4E.	bind
2118	3	1562	6	10	NULL	0	NULL	m7G	Chemical		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_20_5548_s_115	12374755	( C) Comparison of the mode of m7G binding to CBP20, VP39 and eIF4E.	bind
2119	1	1563	6	10	NULL	0	NULL	QacR	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_5_1210_s_70	11867549	( C) Comparison of two TetR family members bound to DNA: QacR and TetR ( Orth  et al., 2000).	bind
2120	2	1563	6	10	NULL	0	NULL	TetR	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_5_1210_s_70	11867549	( C) Comparison of two TetR family members bound to DNA: QacR and TetR ( Orth  et al., 2000).	bind
2121	1	1564	6	10	NULL	0	NULL	SmpB	GP		bind					SsrA	GP	32P -labeled			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_13_3793_s_104	10393194	( C) Competition for binding of SmpB to 100 pM 32P -labeled SsrA by unlabeled SsrA RNA or total yeast tRNA.	bind
2122	2	1564	6	10	NULL	0	NULL	SmpB 	GP		bind					SsrA RNA	NucleicAcid	unlabeled			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_13_3793_s_104	10393194	( C) Competition for binding of SmpB to 100 pM 32P -labeled SsrA by unlabeled SsrA RNA or total yeast tRNA.	bind
2466	3	1564	6	10	NULL	0	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_13_3793_s_104	10393194	( C) Competition for binding of SmpB to 100 pM 32P -labeled SsrA by unlabeled SsrA RNA or total yeast tRNA.	bind
2468	4	1564	6	10	NULL	0	NULL	total yeast tRNA	NucleicAcid	unlabeled	bind					SsrA	NucleicAcid	32P-labeled			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_13_3793_s_104	10393194	( C) Competition for binding of SmpB to 100 pM 32P -labeled SsrA by unlabeled SsrA RNA or total yeast tRNA.	bind
2469	5	1564	6	10	NULL	0	NULL	statement 4	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_13_3793_s_104	10393194	( C) Competition for binding of SmpB to 100 pM 32P -labeled SsrA by unlabeled SsrA RNA or total yeast tRNA.	bind
2124	1	1565	6	10	NULL	0	NULL	Ets1	GP		bind					28 bp oligonucleotide	GP			Ets-binding site 	NULL		NULL	NULL	NULL	NULL	gw60_embo_21_3_365_s_144	11823429	( C) Competition gel mobility shift assay for Ets1 binding to a 28 bp oligonucleotide (see Materials and methods) carrying an Ets-binding site.	bind
2125	1	1566	6	10	NULL	0	NULL	CRP	GP		bind					PC-KLH	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_13043_s_110	12244213	( C) Competition immunoassays for binding of CRP to PC-KLH.	bind
2126	1	1568	6	10	NULL	0	NULL	Stat2	GP		bind					p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_11_3124_s_45	9606194	( C) Competitive binding of Stat2 and RelA to p300 (CH1).	bind
2127	2	1568	6	10	NULL	0	NULL	RelA	GP		bind					p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_11_3124_s_45	9606194	( C) Competitive binding of Stat2 and RelA to p300 (CH1).	bind
2413	3	1568	6	10	NULL	0	NULL	statement 1	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_11_3124_s_45	9606194	( C) Competitive binding of Stat2 and RelA to p300 (CH1).	bind
2128	1	1569	6	10	NULL	0	NULL	IAA	Chemical		bind					insulin	GP	human	Tyr14A		NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_135	15314696	( C) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human proinsulin (filled circles) for each of the sera shown  in  B.	bind
2129	2	1569	6	10	NULL	0	NULL	proinsulin	GP	human	bind					IAA	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_135	15314696	( C) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human proinsulin (filled circles) for each of the sera shown  in  B.	bind
46175	3	1569	6	10	NULL	0	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_589_s_135	15314696	( C) Competitive inhibition of IAA binding to Tyr14A [125] human insulin using human proinsulin (filled circles) for each of the sera shown  in  B.	bind
2130	1	1571	6	10	NULL	0	NULL	malonyl-CoA	Chemical		bind					CPT1c	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_19_7282_s_55	16651524	( C) Concentration dependence of malonyl-CoA binding to CPT1c.	bind
2131	1	1573	6	10	NULL	0	NULL	spastin	GP		bind					atlastin	GP		C-tail		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_28_10666_s_46	16815977	( C) Coomassie blue-stained gel showing that spastin binds to the atlastin C-tail.	bind
2132	1	1574	6	10	NULL	0	NULL	DSX	GP		bind			DM domain		DNA	NucleicAcid			palindromic site 5''-ACTACA ATTGTTGCA-3''	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_14_1750_s_149	10898790	( C) Cooperative low-affinity binding of the DSX DM domain to a palindromic (sym) DNA site (5''-ACTACA ATTGTTGCA-3''; central base pair in boldface type) using fluorescein (at 5' of top strand) as probe.	bind
2133	1	1575	6	10	NULL	0	NULL	C3G	GP		bind					Trk	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_12_2358_s_164	15167895	( C) CrkL increases the binding of C3G and Trk upon NGF treatment.	bind
2134	3	1575	6	10	NULL	0	NULL	CrkL	GP		increases					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_12_2358_s_164	15167895	( C) CrkL increases the binding of C3G and Trk upon NGF treatment.	bind
2205	2	1575	6	10	NULL	0	NULL	NGF	GP		is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_12_2358_s_164	15167895	( C) CrkL increases the binding of C3G and Trk upon NGF treatment.	bind
2135	1	1576	6	10	NULL	0	NULL	eIF4E	GP	human	bind					m7GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_21_5138_s_113	17036047	( C) Crystal structure of human eIF4E bound to m7GDP (PDB 1EJ1).	bind
2136	1	1577	6	10	NULL	0	NULL	CID derivatives	GP		bind								CTD		NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_13_1572_s_138	15998810	( C) CTD pull-down analysis for binding between CID derivatives and the CTD.	bind
2137	1	1578	6	10	NULL	0	NULL	D-Axin	GP		bind					Arm	GP		Armadillo repeat domain		NULL		NULL	NULL	NULL	NULL	gw60_science_283_5408_1739_s_43	10073940	( C) D-Axin binds to the Armadillo repeat domain of Arm.	bind
2138	1	1580	6	10	NULL	0	NULL	LPS	Chemical		induces					IkappaBalpha	GP	degradation of 			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_7_873_s_61	12654725	( C) Degradation of IkappaBalpha induced by lipopolysaccharide (LPS) and interleukin-1beta (IL-1beta).	bind
2139	2	1580	6	10	NULL	0	NULL	IL-1beta	GP		induces					IkappaBalpha	GP	degradation of 			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_7_873_s_61	12654725	( C) Degradation of IkappaBalpha induced by lipopolysaccharide (LPS) and interleukin-1beta (IL-1beta).	bind
45914	3	1580	6	10	NULL	0	NULL	LPS	Chemical		is					lipopolysaccharide 	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_7_873_s_61	12654725	( C) Degradation of IkappaBalpha induced by lipopolysaccharide (LPS) and interleukin-1beta (IL-1beta).	bind
45916	4	1580	6	10	NULL	0	NULL	IL-1beta	GP		is					 interleukin-1beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_7_873_s_61	12654725	( C) Degradation of IkappaBalpha induced by lipopolysaccharide (LPS) and interleukin-1beta (IL-1beta).	bind
2140	1	1581	6	10	NULL	0	NULL	bradykinin	GP		bind					OppA	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_23_12487_s_79	11050157	( C) Determination of the dissociation constant ( Kd) for bradykinin binding to OppA.	bind
2141	1	1582	6	10	NULL	0	NULL	dFOXO	GP		bind		specifically			d4EBP	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_genesdev_17_16_2006_s_182	12893776	( C) dFOXO  binds specifically to d4EBP and dInR promoters in vivo.	bind
2142	2	1582	6	10	NULL	0	NULL	dFOXO	GP		bind		specifically			dInR	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_genesdev_17_16_2006_s_182	12893776	( C) dFOXO  binds specifically to d4EBP and dInR promoters in vivo.	bind
2143	1	1583	6	10	NULL	0	NULL	dFOXO	GP		bind					dInR	GP			promoter	NULL	S2 cells	NULL	NULL	NULL	NULL	gw70_genesdev_19_20_2435_s_71	16230533	( C) dFOXO binds to the dInR promoter in S2 cells upon starvation.	bind
52602	2	1583	6	10	NULL	0	NULL	statement 1	Process		occurs upon					starvation	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_20_2435_s_71	16230533	( C) dFOXO binds to the dInR promoter in S2 cells upon starvation.	bind
2144	1	1584	6	10	NULL	0	NULL	Rad18	GP		bind		directly			pol	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_19_3886_s_174	15359278	( C) Direct binding of Rad18 with pol .	bind
2145	1	1585	6	10	NULL	0	NULL				bind		directly	alphaX I domain					Glu		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1614_s_175	15665082	( C) Direct binding of the alphaX I domain to Glu.	bind
2146	1	1586	6	10	NULL	0	NULL	MBD1	GP		bind		directly	TRD		MPG	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_100_22_12859_s_73	14555760	( C) Direct binding of the TRD of MBD1 to MPG  in vitro.	bind
2147	1	1587	6	10	NULL	0	NULL	fibrillin	GP		bind					ABI2	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_15_6061_s_58	16571665	( C) Discriminative binding of fibrillin to ABI2 and mutant abi2 analyzed by pulldown  assay.	bind
2148	2	1587	6	10	NULL	0	NULL	fibrillin	GP		bind					abi2	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_15_6061_s_58	16571665	( C) Discriminative binding of fibrillin to ABI2 and mutant abi2 analyzed by pulldown  assay.	bind
2149	1	1589	6	10	NULL	0	NULL	DM	GP		counteracts					MBP peptides	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_6_1241_s_32	10716924	( C) DM counteracts binding of MBP peptides.	bind
2150	1	1590	6	10	NULL	0	NULL	R2 proteins	GP		bind					28S rRNA gene	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_20_6461_s_89	16284201	( C) DNA sequence of the 28S rRNA gene region bound by R2 proteins.	bind
2151	1	1591	6	10	NULL	0	NULL	NFAT5	GP		bind		competitively			ATF-2/c-jun	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_12_3845_s_154	16027109	( C) DNase I footprinting assay of competitive binding of NFAT5 and ATF-2/c-jun.	bind
203	1	1592	5	10	NULL	0	NULL	LEF1	GP	recombinant	bind							predicted		LEF/TCF site 	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_9_6064_s_142	11983900	( C) DNase I footprinting revealing binding of recombinant LEF1 protein to the predicted LEF/TCF site (shown in bold).	bind
2152	1	1592	6	10	NULL	0	NULL	LEF1 protein	GP	recombinant	bind									LEF/TCF site	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_9_6064_s_142	11983900	( C) DNase I footprinting revealing binding of recombinant LEF1 protein to the predicted LEF/TCF site (shown in bold).	bind
208	1	1593	5	10	NULL	0	NULL	Dnmt3L	GP		bind					HDAC1	GP	specific regions			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_17_3831_s_45	12202768	( C) Dnmt3L binds specific regions of HDAC1  in vitro.	bind
2153	1	1593	6	10	NULL	0	NULL	Dnmt3L	GP		bind					HDAC1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_17_3831_s_45	12202768	( C) Dnmt3L binds specific regions of HDAC1  in vitro.	bind
209	1	1594	5	10	NULL	0	NULL	griseofulvin	GP		bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_28_9878_s_154	15985553	( C) Double-reciprocal plot for the binding of griseofulvin to tubulin.	bind
2154	2	1594	6	10	NULL	0	NULL	griseofulvin	GP		bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_28_9878_s_154	15985553	( C) Double-reciprocal plot for the binding of griseofulvin to tubulin.	bind
210	1	1595	5	10	NULL	0	NULL	DRIP130	GP		bind		specifically			ESX	GP		activation domain		NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12747_s_70	12242338	( C) DRIP130 binds specifically to the ESX activation domain.	bind
2155	1	1595	6	10	NULL	0	NULL	DRIP130	GP		bind		specifically			ESX	GP		activation domain		NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12747_s_70	12242338	( C) DRIP130 binds specifically to the ESX activation domain.	bind
211	1	1596	5	10	NULL	0	NULL	c-Fos	GP		bind					TNF 	GP	probe		TRE site in promoter	NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_4_503_s_217	10449442	( c) E2 decreases the binding of c-Fos to a probe containing an exact copy of the TRE site in the TNF promoter.	bind
212	2	1596	5	10	NULL	0	NULL	E2	GP		decreases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_4_503_s_217	10449442	( c) E2 decreases the binding of c-Fos to a probe containing an exact copy of the TRE site in the TNF promoter.	bind
2156	3	1596	6	10	NULL	0	NULL	c-fos	GP		bind					TNF	GP			TRE site in promoter	NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_4_503_s_217	10449442	( c) E2 decreases the binding of c-Fos to a probe containing an exact copy of the TRE site in the TNF promoter.	bind
2157	4	1596	6	10	NULL	0	NULL	E2	GP		decreases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_4_503_s_217	10449442	( c) E2 decreases the binding of c-Fos to a probe containing an exact copy of the TRE site in the TNF promoter.	bind
222	1	1597	5	10	NULL	0	NULL	p35srj	GP		bind					p300	GP		CH1		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_13_1_64_s_104	9887100	( C) Effect of p35srj 224-255 peptide on in vitro binding of p35srj to p300-CH1.	bind
2233	1	1597	6	10	NULL	0	NULL	p35srj	GP		bind					p300	GP		CH1		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_13_1_64_s_104	9887100	( C) Effect of p35srj 224-255 peptide on in vitro binding of p35srj to p300-CH1.	bind
224	1	1598	5	10	NULL	0	NULL	La protein	GP		bind					BiP	GP			IRES	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_5009_s_130	11812831	( C) Effect of the initiator AUG on binding of La protein to the BiP IRES.	bind
2234	1	1598	6	10	NULL	0	NULL	La protein	GP		bind					BiP	GP			IRES	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_5009_s_130	11812831	( C) Effect of the initiator AUG on binding of La protein to the BiP IRES.	bind
226	1	1599	5	10	NULL	0	NULL	PSF protein	GP		bind					GAGE6	GP			promoter DNA	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12189_s_105	16079199	( C) Effect of VL30 RNA on binding of PSF protein and DBD to  GAGE6 promoter DNA.	bind
227	2	1599	5	10	NULL	0	NULL				bind			DBD		GAGE6	GP			promoter DNA	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12189_s_105	16079199	( C) Effect of VL30 RNA on binding of PSF protein and DBD to  GAGE6 promoter DNA.	bind
2235	1	1599	6	10	NULL	0	NULL	PSF protein	GP		bind					GAGE6	GP			promoter DNA	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12189_s_105	16079199	( C) Effect of VL30 RNA on binding of PSF protein and DBD to  GAGE6 promoter DNA.	bind
2236	2	1599	6	10	NULL	0	NULL				bind			DBD		GAGE6	GP			promoter DNA	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12189_s_105	16079199	( C) Effect of VL30 RNA on binding of PSF protein and DBD to  GAGE6 promoter DNA.	bind
272	1	1600	5	10	NULL	0	NULL	eIF4E	GP		bind					4E-T	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_12_3142_s_71	10856257	( C) eIF4E binds to 4E-T and eIF4G through a shared sequence.	bind
273	2	1600	5	10	NULL	0	NULL	eIF4E	GP		bind					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_12_3142_s_71	10856257	( C) eIF4E binds to 4E-T and eIF4G through a shared sequence.	bind
2237	1	1600	6	10	NULL	0	NULL	eIF4E	GP		bind					4E-T	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_12_3142_s_71	10856257	( C) eIF4E binds to 4E-T and eIF4G through a shared sequence.	bind
2238	2	1600	6	10	NULL	0	NULL	eIF4E	GP		bind					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_12_3142_s_71	10856257	( C) eIF4E binds to 4E-T and eIF4G through a shared sequence.	bind
274	1	1601	5	10	NULL	0	NULL	IgA	GP	intestinal secretory	bind					Xa-CAT 	GP	purified			NULL	wild-type E. coli expressing Xa-CAT  in the intestine in vivo	NULL	NULL	NULL	NULL	gw60_science_288_5474_2222_s_78	10864873	( C) ELISA of intestinal  secretory IgA or serum IgA binding to purified Xa-CAT chimeric protein  35 days after colonization with wild-type  E. coli expressing  this protein in the intestine in vivo.	bind
275	2	1601	5	10	NULL	0	NULL	IgA	GP	serum	bind					Xa-CAT	GP	purified			NULL	wild-type E. coli expressing Xa-CAT  in the intestine in vivo	NULL	NULL	NULL	NULL	gw60_science_288_5474_2222_s_78	10864873	( C) ELISA of intestinal  secretory IgA or serum IgA binding to purified Xa-CAT chimeric protein  35 days after colonization with wild-type  E. coli expressing  this protein in the intestine in vivo.	bind
46153	3	1601	5	10	NULL	0	NULL	Xa-CAT	GP		is a type of					chimeric protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_288_5474_2222_s_78	10864873	( C) ELISA of intestinal  secretory IgA or serum IgA binding to purified Xa-CAT chimeric protein  35 days after colonization with wild-type  E. coli expressing  this protein in the intestine in vivo.	bind
2239	1	1601	6	10	NULL	0	NULL	IgA	GP	intestinal secretory	bind					Xa-CAT 	GP	purified			NULL	wild-type E. coli expressing  Xa-CAT in the intestine in vivo	NULL	NULL	NULL	NULL	gw60_science_288_5474_2222_s_78	10864873	( C) ELISA of intestinal  secretory IgA or serum IgA binding to purified Xa-CAT chimeric protein  35 days after colonization with wild-type  E. coli expressing  this protein in the intestine in vivo.	bind
2240	2	1601	6	10	NULL	0	NULL	IgA	GP	serum	bind					Xa-CAT	GP	purified			NULL	wild-type E. coli expressing Xa-CAT in the intestine in vivo	NULL	NULL	NULL	NULL	gw60_science_288_5474_2222_s_78	10864873	( C) ELISA of intestinal  secretory IgA or serum IgA binding to purified Xa-CAT chimeric protein  35 days after colonization with wild-type  E. coli expressing  this protein in the intestine in vivo.	bind
46176	3	1601	6	10	NULL	0	NULL	Xa-CAT	GP		is a type of					chimeric protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_288_5474_2222_s_78	10864873	( C) ELISA of intestinal  secretory IgA or serum IgA binding to purified Xa-CAT chimeric protein  35 days after colonization with wild-type  E. coli expressing  this protein in the intestine in vivo.	bind
276	1	1602	5	10	NULL	0	NULL	p19ARF	GP	endogenous	bind					E2F1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_8_4455_s_151	11274364	( C) Endogenous p19ARF binds to E2F1.	bind
2241	1	1602	6	10	NULL	0	NULL	p19ARF	GP	endogenous	bind					E2F1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_8_4455_s_151	11274364	( C) Endogenous p19ARF binds to E2F1.	bind
277	1	1603	5	10	NULL	0	NULL	PU.1	GP	endogenously expressed	bind					Dab2	GP			regulatory sequence	NULL		NULL	NULL	NULL	NULL	gw60_embo_21_3_211_s_63	11823414	( C) Endogenously expressed PU.1 binds to the Dab2 regulatory sequence.	bind
2242	1	1603	6	10	NULL	0	NULL	PU.1	GP	endogenously expressed	bind					Dab2	GP			regulatory sequence	NULL		NULL	NULL	NULL	NULL	gw60_embo_21_3_211_s_63	11823414	( C) Endogenously expressed PU.1 binds to the Dab2 regulatory sequence.	bind
278	1	1606	5	10	NULL	0	NULL	FGF-2	GP		bind					Namalwa-CD44vRA	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1211_s_130	12697740	( c) Excess soluble heparin blocks the binding of FGF-2 to Namalwa-CD44vRA.	bind
2734	2	1606	5	10	NULL	0	NULL	heparin	GP	excess soluble	blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1211_s_130	12697740	( c) Excess soluble heparin blocks the binding of FGF-2 to Namalwa-CD44vRA.	bind
2243	1	1606	6	10	NULL	0	NULL	FGF2	GP		bind					Namalwa-CD44vRA	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1211_s_130	12697740	( c) Excess soluble heparin blocks the binding of FGF-2 to Namalwa-CD44vRA.	bind
2244	2	1606	6	10	NULL	0	NULL	heparin	GP	excess soluble	blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1211_s_130	12697740	( c) Excess soluble heparin blocks the binding of FGF-2 to Namalwa-CD44vRA.	bind
280	1	1609	5	10	NULL	0	NULL	Ferritin	GP		bind				IRE	ACN	GP	purified	C517A		NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_18_10412_s_109	10468622	( C) Ferritin IRE binding activity of purified ACNC517A.	bind
2245	1	1609	6	10	NULL	0	NULL	Ferritin	GP		bind				IRE	ACN	GP	purified	C517A		NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_18_10412_s_109	10468622	( C) Ferritin IRE binding activity of purified ACNC517A.	bind
281	1	1610	5	10	NULL	0	NULL	FGF-2	GP		bind					Namalwa-CD44vRA	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_111_8_1211_s_156	12697740	( c) FGF-2 bound to Namalwa-CD44vRA induces enhanced proliferation of BaF-32 cells expressing  FGFR-1.	bind
282	2	1610	5	10	NULL	0	NULL	statement 1	Process		induce					BaF-32 cells	Cell	enhanced proliferation of			NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_111_8_1211_s_156	12697740	( c) FGF-2 bound to Namalwa-CD44vRA induces enhanced proliferation of BaF-32 cells expressing  FGFR-1.	bind
2735	3	1610	5	10	NULL	0	NULL	BaF-32 cells	Cell		express					FGFR-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_111_8_1211_s_156	12697740	( c) FGF-2 bound to Namalwa-CD44vRA induces enhanced proliferation of BaF-32 cells expressing  FGFR-1.	bind
2246	1	1610	6	10	NULL	0	NULL	FGF-2	GP		bind					Namalwa-CD44vRA	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_111_8_1211_s_156	12697740	( c) FGF-2 bound to Namalwa-CD44vRA induces enhanced proliferation of BaF-32 cells expressing  FGFR-1.	bind
2247	2	1610	6	10	NULL	0	NULL	BaF-32 cells	Cell		express					FGFR-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_111_8_1211_s_156	12697740	( c) FGF-2 bound to Namalwa-CD44vRA induces enhanced proliferation of BaF-32 cells expressing  FGFR-1.	bind
2248	3	1610	6	10	NULL	0	NULL	statement1	Process		induces					BaF-32 cells	Cell	enhanced proliferation of			NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_111_8_1211_s_156	12697740	( c) FGF-2 bound to Namalwa-CD44vRA induces enhanced proliferation of BaF-32 cells expressing  FGFR-1.	bind
283	1	1614	5	10	NULL	0	NULL	Five phenylalanine molecules	Chemical		bind					stimulatory complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_3_1212_s_104	11818540	( C) Five phenylalanine molecules bound to the stimulatory complex are depicted on the molecular surfaces of the GFRP pentamer with one GFRP monomer as a ribbon model (magenta).	bind
2249	1	1614	6	10	NULL	0	NULL	Five phenylalanine molecules	Chemical		bind					stimulatory complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_3_1212_s_104	11818540	( C) Five phenylalanine molecules bound to the stimulatory complex are depicted on the molecular surfaces of the GFRP pentamer with one GFRP monomer as a ribbon model (magenta).	bind
284	1	1615	5	10	NULL	0	NULL	p300	GP		bind					Smad3	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_10_2453_s_97	12743039	( C) Formation of a p300 - Smad3 - ZEB-1/deltaEF1 complex requires the binding of p300 to Smad3.	bind
285	2	1615	5	10	NULL	0	NULL	p300 - Smad3 - ZEB-1/deltaEF1	GP		forms					complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_10_2453_s_97	12743039	( C) Formation of a p300 - Smad3 - ZEB-1/deltaEF1 complex requires the binding of p300 to Smad3.	bind
286	3	1615	5	10	NULL	0	NULL	statement 2	Process		require					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_10_2453_s_97	12743039	( C) Formation of a p300 - Smad3 - ZEB-1/deltaEF1 complex requires the binding of p300 to Smad3.	bind
2300	1	1615	6	10	NULL	0	NULL	p300	GP		bind					Smad3	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_10_2453_s_97	12743039	( C) Formation of a p300 - Smad3 - ZEB-1/deltaEF1 complex requires the binding of p300 to Smad3.	bind
2301	2	1615	6	10	NULL	0	NULL	p300 - Smad3 - ZEB-1/deltaEF1	GP		forms 					complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_10_2453_s_97	12743039	( C) Formation of a p300 - Smad3 - ZEB-1/deltaEF1 complex requires the binding of p300 to Smad3.	bind
2302	3	1615	6	10	NULL	0	NULL	statement 2	Process		require					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_10_2453_s_97	12743039	( C) Formation of a p300 - Smad3 - ZEB-1/deltaEF1 complex requires the binding of p300 to Smad3.	bind
287	1	1616	5	10	NULL	0	NULL	hnRNP proteins	GP		bind					HIV	Organism			tat exon 2 ESS	NULL		NULL	NULL	NULL	NULL	gw60_embo_18_14_4060_s_54	10406810	( C) Further identification of hnRNP proteins that bind to the HIV  tat exon 2 ESS.	bind
2303	1	1616	6	10	NULL	0	NULL	hnRNP proteins	GP		bind					HIV	Organism			tat exon 2 ESS	NULL		NULL	NULL	NULL	NULL	gw60_embo_18_14_4060_s_54	10406810	( C) Further identification of hnRNP proteins that bind to the HIV  tat exon 2 ESS.	bind
2304	1	1617	6	10	NULL	0	NULL	GA	Chemical		bind					cell surface protein	GP	biotinylated			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_103	16103367	( C) GA binds to a biotinylated cell surface protein.	bind
288	1	1618	5	10	NULL	0	NULL	GA	Chemical		bind					TfR	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_132	16103367	( C) GA bound to TfR  in vitro can be displaced by active GA derivatives.	bind
289	2	1618	5	10	NULL	0	NULL	GA derivatives	Chemical		displaces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_132	16103367	( C) GA bound to TfR  in vitro can be displaced by active GA derivatives.	bind
2305	1	1618	6	10	NULL	0	NULL	GA	Chemical		bind					TfR	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_132	16103367	( C) GA bound to TfR  in vitro can be displaced by active GA derivatives.	bind
2306	2	1618	6	10	NULL	0	NULL	GA derivatives	Chemical	active	displaces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_132	16103367	( C) GA bound to TfR  in vitro can be displaced by active GA derivatives.	bind
290	1	1619	5	10	NULL	0	NULL	Gab1	GP		bind			MBD		Grb2	GP		C-terminal SH3 domain		NULL	293 cells	NULL	NULL	NULL	NULL	gw60_pnas_98_11_6074_s_57	11353842	( C) Gab1 binds to the C-terminal SH3 domain of Grb2 through the MBD. 293 cells were transfected with the expression vector for Flag-tagged MBD of Gab1.	bind
2307	1	1619	6	10	NULL	0	NULL	Gab1	GP		bind			MBD		Grb2	GP		C-terminal SH3 domain		NULL	293 cells	NULL	NULL	NULL	NULL	gw60_pnas_98_11_6074_s_57	11353842	( C) Gab1 binds to the C-terminal SH3 domain of Grb2 through the MBD. 293 cells were transfected with the expression vector for Flag-tagged MBD of Gab1.	bind
291	1	1620	5	10	NULL	0	NULL	Ets-1	GP		bind					beta6 	GP			putative Ets sites in promoter	NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_115_2_339_s_72	15668738	( C) Gel mobility shift assay for Ets-1 binding to putative Ets sites in the beta6 promoter.	bind
2308	1	1620	6	10	NULL	0	NULL	Ets-1	GP		bind					beta6	GP			putative Ets sites of promoter	NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_115_2_339_s_72	15668738	( C) Gel mobility shift assay for Ets-1 binding to putative Ets sites in the beta6 promoter.	bind
292	1	1621	5	10	NULL	0	NULL	Rpp29	GP		bind					M1 RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5120_s_243	16155184	( C) Gel shift analysis of binding of Rpp29 to M1 RNA.	bind
2309	1	1621	6	10	NULL	0	NULL	Rpp29	GP		bind					M1 RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5120_s_243	16155184	( C) Gel shift analysis of binding of Rpp29 to M1 RNA.	bind
293	1	1622	5	10	NULL	0	NULL	GGA1	GP		bind			GAT domain		Arf1-GTP	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_20_0_153_s_248	15473838	( c) GGA1 GAT domain hook bound to Arf1-GTP (PDB ID 1J2J).	bind
2310	1	1622	6	10	NULL	0	NULL	GGA1	GP		bind			GAT domain		Arf1-GTP	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_20_0_153_s_248	15473838	( c) GGA1 GAT domain hook bound to Arf1-GTP (PDB ID 1J2J).	bind
2311	1	1623	6	10	NULL	0	NULL	nuclear proteins	GP		bind									dfd-1 element	NULL	body axis	NULL	NULL	NULL	NULL	gw60_pnas_96_4_1445_s_147	9990043	( C) Gradient of nuclear proteins binding to the dfd-1 element along the body axis with sharp decrease of DNA-protein interactions in TFZ and head tissue.	bind
2312	2	1623	6	10	NULL	0	NULL	DNA	NucleicAcid		interacts with					protein	GP				NULL	TFZ 	NULL	NULL	NULL	NULL	gw60_pnas_96_4_1445_s_147	9990043	( C) Gradient of nuclear proteins binding to the dfd-1 element along the body axis with sharp decrease of DNA-protein interactions in TFZ and head tissue.	bind
52614	3	1623	6	10	NULL	0	NULL	DNA	NucleicAcid		interacts with					protein	GP				NULL	head tissue	NULL	NULL	NULL	NULL	gw60_pnas_96_4_1445_s_147	9990043	( C) Gradient of nuclear proteins binding to the dfd-1 element along the body axis with sharp decrease of DNA-protein interactions in TFZ and head tissue.	bind
52615	4	1623	6	10	NULL	0	NULL	statement 1	Process		decrease					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_4_1445_s_147	9990043	( C) Gradient of nuclear proteins binding to the dfd-1 element along the body axis with sharp decrease of DNA-protein interactions in TFZ and head tissue.	bind
52616	5	1623	6	10	NULL	0	NULL	statement 1	Process		decrease					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_4_1445_s_147	9990043	( C) Gradient of nuclear proteins binding to the dfd-1 element along the body axis with sharp decrease of DNA-protein interactions in TFZ and head tissue.	bind
3112	1	1624	5	10	NULL	0	NULL	Elk	GP		bind			1-93		Elk-1	GP		B-box		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_20_5666_s_142	10523309	( C) GST pull-down assay of binding of Elk1-93 to GST fusion proteins containing the Elk-1 B-box or D-domain in the absence (lanes 1 and 3) or presence (lanes 2 and 4) of B-box competitor peptide (7 muM).	bind
3114	2	1624	5	10	NULL	0	NULL	Elk	GP		bind			1-93		Elk-1	GP		D-domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_20_5666_s_142	10523309	( C) GST pull-down assay of binding of Elk1-93 to GST fusion proteins containing the Elk-1 B-box or D-domain in the absence (lanes 1 and 3) or presence (lanes 2 and 4) of B-box competitor peptide (7 muM).	bind
2313	1	1624	6	10	NULL	0	NULL	Elk	GP		bind			1-93		ELk-1	GP		B-box		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_20_5666_s_142	10523309	( C) GST pull-down assay of binding of Elk1-93 to GST fusion proteins containing the Elk-1 B-box or D-domain in the absence (lanes 1 and 3) or presence (lanes 2 and 4) of B-box competitor peptide (7 muM).	bind
2314	2	1624	6	10	NULL	0	NULL	Elk	GP		bind			1-93		ELk-1	GP		D-domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_20_5666_s_142	10523309	( C) GST pull-down assay of binding of Elk1-93 to GST fusion proteins containing the Elk-1 B-box or D-domain in the absence (lanes 1 and 3) or presence (lanes 2 and 4) of B-box competitor peptide (7 muM).	bind
295	1	1625	5	10	NULL	0	NULL	GST-cyclin E-Cdk2	GP		bind					Fbw7	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_294_5540_173_s_48	11533444	( C) GST-cyclin E-Cdk2 binds Fbw7.	bind
2315	1	1625	6	10	NULL	0	NULL	GST-cyclin E-Cdk2	GP		bind					Fbw7	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_294_5540_173_s_48	11533444	( C) GST-cyclin E-Cdk2 binds Fbw7.	bind
296	1	1626	5	10	NULL	0	NULL	GST-DSCR1/calcineurin	GP		bind					FK506/FKBP12	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_13_1595_s_76	10887154	( C) GST-DSCR1/calcineurin bound to FK506/FKBP12 in the presence of calmodulin and 2 mM CaCl2.	bind
3147	2	1626	5	10	NULL	0	NULL	statement 1	Process		in the presence of					calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_13_1595_s_76	10887154	( C) GST-DSCR1/calcineurin bound to FK506/FKBP12 in the presence of calmodulin and 2 mM CaCl2.	bind
3148	3	1626	5	10	NULL	0	NULL	statement 1	Process		in the presence of					CaCl2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_13_1595_s_76	10887154	( C) GST-DSCR1/calcineurin bound to FK506/FKBP12 in the presence of calmodulin and 2 mM CaCl2.	bind
2316	1	1626	6	10	NULL	0	NULL	GST-DSCR1/calcineurin	GP		bind					FK506/FKBP12	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_13_1595_s_76	10887154	( C) GST-DSCR1/calcineurin bound to FK506/FKBP12 in the presence of calmodulin and 2 mM CaCl2.	bind
2317	2	1626	6	10	NULL	0	NULL	statement 1	Process		in presence of 					calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_13_1595_s_76	10887154	( C) GST-DSCR1/calcineurin bound to FK506/FKBP12 in the presence of calmodulin and 2 mM CaCl2.	bind
2318	3	1626	6	10	NULL	0	NULL	statement 1	Process		in presence of 					CaCl2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_13_1595_s_76	10887154	( C) GST-DSCR1/calcineurin bound to FK506/FKBP12 in the presence of calmodulin and 2 mM CaCl2.	bind
297	1	1628	5	10	NULL	0	NULL	Gst-IsdC	GP		bind		 dose-dependently			heme-agarose beads	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_science_299_5608_906_s_56	12574635	( C) Gst-IsdC binds heme-agarose beads in a dose-dependent manner and incubation with  heme-iron abolishes this binding.	bind
298	2	1628	5	10	NULL	0	NULL	heme-iron 	Chemical		abolish					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_science_299_5608_906_s_56	12574635	( C) Gst-IsdC binds heme-agarose beads in a dose-dependent manner and incubation with  heme-iron abolishes this binding.	bind
2320	1	1628	6	10	NULL	0	NULL	Gst-IsdC	GP		bind		dose-dependently			heme-agarose beads	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_science_299_5608_906_s_56	12574635	( C) Gst-IsdC binds heme-agarose beads in a dose-dependent manner and incubation with  heme-iron abolishes this binding.	bind
2321	2	1628	6	10	NULL	0	NULL	heme-iron	Chemical		abolishes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_science_299_5608_906_s_56	12574635	( C) Gst-IsdC binds heme-agarose beads in a dose-dependent manner and incubation with  heme-iron abolishes this binding.	bind
299	1	1630	5	10	NULL	0	NULL	GTP	Chemical		bind		specifically			CIITA	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5432_1402_s_53	10464099	( C) GTP binding by CIITA is specific.	bind
2322	1	1630	6	10	NULL	0	NULL	GTP	Chemical		bind		specifically			CIITA	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5432_1402_s_53	10464099	( C) GTP binding by CIITA is specific.	bind
300	1	1631	5	10	NULL	0	NULL	MukF	GP	His-tagged	bind			302-440		MukE	GP		1-209		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_11_1921_s_139	15902272	( C) His-tagged MukF(302 440) binds MukE(1 209).	bind
2323	1	1631	6	10	NULL	0	NULL	MukF	GP	His-tagged	bind			302-440		MukE	GP		1-209		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_11_1921_s_139	15902272	( C) His-tagged MukF(302 440) binds MukE(1 209).	bind
896	1	1633	5	10	NULL	0	NULL				bind			F302W		mAb 7E3	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_6_1523_s_261	9852148	( C) Histograms (mean  plus-or-minus  SEM,  n = 4)  showing a gain of F302W  binding to mAb 7E3 and a loss  of T209A binding to this mAb.	bind
897	2	1633	5	10	NULL	0	NULL				bind			T209A		mAb 7E3	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_6_1523_s_261	9852148	( C) Histograms (mean  plus-or-minus  SEM,  n = 4)  showing a gain of F302W  binding to mAb 7E3 and a loss  of T209A binding to this mAb.	bind
2324	1	1633	6	10	NULL	0	NULL				bind			F302W		mAb 7E3	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_6_1523_s_261	9852148	( C) Histograms (mean  plus-or-minus  SEM,  n = 4)  showing a gain of F302W  binding to mAb 7E3 and a loss  of T209A binding to this mAb.	bind
2325	2	1633	6	10	NULL	0	NULL				bind			T209A		mAb 7E3	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_6_1523_s_261	9852148	( C) Histograms (mean  plus-or-minus  SEM,  n = 4)  showing a gain of F302W  binding to mAb 7E3 and a loss  of T209A binding to this mAb.	bind
301	1	1634	5	10	NULL	0	NULL	hRAP74cc	GP		bind					GST-hFCP1pep	GP		941-961		NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_5_2296_s_26	12591941	( c) hRAP74cc binding to GST-hFCP1pep (941-961).	bind
2326	1	1634	6	10	NULL	0	NULL	RAP74cc	GP	human	bind					GST-FCP1pep	GP	human	941-961		NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_5_2296_s_26	12591941	( c) hRAP74cc binding to GST-hFCP1pep (941-961).	bind
302	1	1635	5	10	NULL	0	NULL	Hrr25p	GP		phosphorylate					Crz1p	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_genesdev_17_21_2698_s_52	14597664	( C) Hrr25p phosphorylates and binds to Crz1p in vivo.	bind
303	2	1635	5	10	NULL	0	NULL	Hrr25p	GP		bind					Crz1p	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_genesdev_17_21_2698_s_52	14597664	( C) Hrr25p phosphorylates and binds to Crz1p in vivo.	bind
2327	1	1635	6	10	NULL	0	NULL	Hrr25p	GP		phosphorylates					Crz1p	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_genesdev_17_21_2698_s_52	14597664	( C) Hrr25p phosphorylates and binds to Crz1p in vivo.	bind
2328	2	1635	6	10	NULL	0	NULL	Hrr25p	GP		bind					Crz1p	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_genesdev_17_21_2698_s_52	14597664	( C) Hrr25p phosphorylates and binds to Crz1p in vivo.	bind
304	1	1636	5	10	NULL	0	NULL	HuR protein	GP		bind					p27 	GP			5'UTR	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_23_3087_s_135	12464637	( C) HuR protein binds to the p27 5'UTR.	bind
2329	1	1636	6	10	NULL	0	NULL	HuR protein	GP		bind					p27	GP			5' UTR	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_23_3087_s_135	12464637	( C) HuR protein binds to the p27 5'UTR.	bind
305	1	1637	5	10	NULL	0	NULL	ICE1	GP		bind		strongly			MYC-2 DNA fragment	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_8_1043_s_168	12672693	( C) ICE1 binds to the MYC-2 DNA fragment more strongly than to the other DNA fragments.	bind
2343	1	1637	6	10	NULL	0	NULL	ICE1	GP		bind		strongly			MYC-2 DNA fragment	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_8_1043_s_168	12672693	( C) ICE1 binds to the MYC-2 DNA fragment more strongly than to the other DNA fragments.	bind
306	1	1638	5	10	NULL	0	NULL	ICSBP	GP		bind					Dab2	GP			promoter	NULL	myeloid progenitor cells	NULL	NULL	NULL	NULL	gw60_embo_21_3_211_s_100	11823414	( C) ICSBP and PU.1 bind to the Dab2 promoter in myeloid progenitor cells.	bind
3149	2	1638	5	10	NULL	0	NULL	PU.1	GP		bind					Dab2	GP			promoter	NULL	myeloid progenitor cells	NULL	NULL	NULL	NULL	gw60_embo_21_3_211_s_100	11823414	( C) ICSBP and PU.1 bind to the Dab2 promoter in myeloid progenitor cells.	bind
2358	1	1638	6	10	NULL	0	NULL	ICSBP	GP		bind					Dab2	GP			promoter	NULL	myeloid progenitor cells	NULL	NULL	NULL	NULL	gw60_embo_21_3_211_s_100	11823414	( C) ICSBP and PU.1 bind to the Dab2 promoter in myeloid progenitor cells.	bind
2359	2	1638	6	10	NULL	0	NULL	PU.1	GP		bind					Dab2	GP			promoter	NULL	myeloid progenitor cells	NULL	NULL	NULL	NULL	gw60_embo_21_3_211_s_100	11823414	( C) ICSBP and PU.1 bind to the Dab2 promoter in myeloid progenitor cells.	bind
307	1	1640	5	10	NULL	0	NULL	ICSBP	GP		bind					Dab2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_21_3_211_s_116	11823414	( C) IFN-gamma induces ICSBP binding to the Dab2 promoter.	bind
308	2	1640	5	10	NULL	0	NULL	IFN-gamma	GP		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_3_211_s_116	11823414	( C) IFN-gamma induces ICSBP binding to the Dab2 promoter.	bind
2360	1	1640	6	10	NULL	0	NULL	ICSBP	GP		bind					Dab2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_21_3_211_s_116	11823414	( C) IFN-gamma induces ICSBP binding to the Dab2 promoter.	bind
2361	2	1640	6	10	NULL	0	NULL	IFN-gamma	GP		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_3_211_s_116	11823414	( C) IFN-gamma induces ICSBP binding to the Dab2 promoter.	bind
309	1	1641	5	10	NULL	0	NULL	Ikaros	GP		bind					lambda5 	GP			Ik-2 site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_11_2812_s_62	11387214	( C) Ikaros and Aiolos bind to the Ik-2 site of the lambda5 promoter.	bind
310	2	1641	5	10	NULL	0	NULL	Aiolos	GP		bind					lambda5	GP			Ik-2 site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_11_2812_s_62	11387214	( C) Ikaros and Aiolos bind to the Ik-2 site of the lambda5 promoter.	bind
2362	1	1641	6	10	NULL	0	NULL	Ikaros	GP		bind					lambda5	GP			Ik-2 site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_11_2812_s_62	11387214	( C) Ikaros and Aiolos bind to the Ik-2 site of the lambda5 promoter.	bind
2363	2	1641	6	10	NULL	0	NULL	Aiolos	GP		bind					lambda5	GP			Ik-2 site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_11_2812_s_62	11387214	( C) Ikaros and Aiolos bind to the Ik-2 site of the lambda5 promoter.	bind
318	1	1642	5	10	NULL	0	NULL	Gbeta1	Chemical		bind					GIRK-GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_17_9771_s_114	10944236	( C) Immunoblots from GST pull down assays with Gbetacommon (betac) and gamma2 antisera demonstrate binding of beta1 ( 1), beta3 ( 3), and beta4 ( 4), as well as gamma2, to each of the GIRK-GST fusion proteins; Gbetagamma subunits did not bind to GST alone.	bind
319	2	1642	5	10	NULL	0	NULL	Gbeta3	Chemical		bind					GIRK-GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_17_9771_s_114	10944236	( C) Immunoblots from GST pull down assays with Gbetacommon (betac) and gamma2 antisera demonstrate binding of beta1 ( 1), beta3 ( 3), and beta4 ( 4), as well as gamma2, to each of the GIRK-GST fusion proteins; Gbetagamma subunits did not bind to GST alone.	bind
320	3	1642	5	10	NULL	0	NULL	Gbeta4	Chemical		bind					GIRK-GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_17_9771_s_114	10944236	( C) Immunoblots from GST pull down assays with Gbetacommon (betac) and gamma2 antisera demonstrate binding of beta1 ( 1), beta3 ( 3), and beta4 ( 4), as well as gamma2, to each of the GIRK-GST fusion proteins; Gbetagamma subunits did not bind to GST alone.	bind
321	4	1642	5	10	NULL	0	NULL	Ggamma2	Chemical		bind					GIRK-GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_17_9771_s_114	10944236	( C) Immunoblots from GST pull down assays with Gbetacommon (betac) and gamma2 antisera demonstrate binding of beta1 ( 1), beta3 ( 3), and beta4 ( 4), as well as gamma2, to each of the GIRK-GST fusion proteins; Gbetagamma subunits did not bind to GST alone.	bind
3322	5	1642	5	10	NULL	0	NULL	Gbeta1	Chemical		does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_17_9771_s_114	10944236	( C) Immunoblots from GST pull down assays with Gbetacommon (betac) and gamma2 antisera demonstrate binding of beta1 ( 1), beta3 ( 3), and beta4 ( 4), as well as gamma2, to each of the GIRK-GST fusion proteins; Gbetagamma subunits did not bind to GST alone.	bind
3323	6	1642	5	10	NULL	0	NULL	Gbeta3	Chemical		does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_17_9771_s_114	10944236	( C) Immunoblots from GST pull down assays with Gbetacommon (betac) and gamma2 antisera demonstrate binding of beta1 ( 1), beta3 ( 3), and beta4 ( 4), as well as gamma2, to each of the GIRK-GST fusion proteins; Gbetagamma subunits did not bind to GST alone.	bind
3324	7	1642	5	10	NULL	0	NULL	Gbeta4	Chemical		does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_17_9771_s_114	10944236	( C) Immunoblots from GST pull down assays with Gbetacommon (betac) and gamma2 antisera demonstrate binding of beta1 ( 1), beta3 ( 3), and beta4 ( 4), as well as gamma2, to each of the GIRK-GST fusion proteins; Gbetagamma subunits did not bind to GST alone.	bind
3325	8	1642	5	10	NULL	0	NULL	Ggamma2	Chemical		does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_17_9771_s_114	10944236	( C) Immunoblots from GST pull down assays with Gbetacommon (betac) and gamma2 antisera demonstrate binding of beta1 ( 1), beta3 ( 3), and beta4 ( 4), as well as gamma2, to each of the GIRK-GST fusion proteins; Gbetagamma subunits did not bind to GST alone.	bind
46156	9	1642	5	10	NULL	0	NULL	GIRK-GST	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_17_9771_s_114	10944236	( C) Immunoblots from GST pull down assays with Gbetacommon (betac) and gamma2 antisera demonstrate binding of beta1 ( 1), beta3 ( 3), and beta4 ( 4), as well as gamma2, to each of the GIRK-GST fusion proteins; Gbetagamma subunits did not bind to GST alone.	bind
2364	1	1642	6	10	NULL	0	NULL	GIRK-GST	GP		bind					Gbeta1	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_17_9771_s_114	10944236	( C) Immunoblots from GST pull down assays with Gbetacommon (betac) and gamma2 antisera demonstrate binding of beta1 ( 1), beta3 ( 3), and beta4 ( 4), as well as gamma2, to each of the GIRK-GST fusion proteins; Gbetagamma subunits did not bind to GST alone.	bind
2365	2	1642	6	10	NULL	0	NULL	GIRK-GST	GP		bind					Gbeta3	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_17_9771_s_114	10944236	( C) Immunoblots from GST pull down assays with Gbetacommon (betac) and gamma2 antisera demonstrate binding of beta1 ( 1), beta3 ( 3), and beta4 ( 4), as well as gamma2, to each of the GIRK-GST fusion proteins; Gbetagamma subunits did not bind to GST alone.	bind
2366	3	1642	6	10	NULL	0	NULL	GIRK-GST	GP		bind					Gbeta4	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_17_9771_s_114	10944236	( C) Immunoblots from GST pull down assays with Gbetacommon (betac) and gamma2 antisera demonstrate binding of beta1 ( 1), beta3 ( 3), and beta4 ( 4), as well as gamma2, to each of the GIRK-GST fusion proteins; Gbetagamma subunits did not bind to GST alone.	bind
2367	4	1642	6	10	NULL	0	NULL	GIRK-GST	GP		bind					Ggamma2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_17_9771_s_114	10944236	( C) Immunoblots from GST pull down assays with Gbetacommon (betac) and gamma2 antisera demonstrate binding of beta1 ( 1), beta3 ( 3), and beta4 ( 4), as well as gamma2, to each of the GIRK-GST fusion proteins; Gbetagamma subunits did not bind to GST alone.	bind
2368	5	1642	6	10	NULL	0	NULL	Gbeta1	Chemical		does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_17_9771_s_114	10944236	( C) Immunoblots from GST pull down assays with Gbetacommon (betac) and gamma2 antisera demonstrate binding of beta1 ( 1), beta3 ( 3), and beta4 ( 4), as well as gamma2, to each of the GIRK-GST fusion proteins; Gbetagamma subunits did not bind to GST alone.	bind
2369	6	1642	6	10	NULL	0	NULL	Gbeta3	Chemical		does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_17_9771_s_114	10944236	( C) Immunoblots from GST pull down assays with Gbetacommon (betac) and gamma2 antisera demonstrate binding of beta1 ( 1), beta3 ( 3), and beta4 ( 4), as well as gamma2, to each of the GIRK-GST fusion proteins; Gbetagamma subunits did not bind to GST alone.	bind
2370	7	1642	6	10	NULL	0	NULL	Gbeta4	Chemical		does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_17_9771_s_114	10944236	( C) Immunoblots from GST pull down assays with Gbetacommon (betac) and gamma2 antisera demonstrate binding of beta1 ( 1), beta3 ( 3), and beta4 ( 4), as well as gamma2, to each of the GIRK-GST fusion proteins; Gbetagamma subunits did not bind to GST alone.	bind
2371	8	1642	6	10	NULL	0	NULL	Ggamma2	Chemical		does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_17_9771_s_114	10944236	( C) Immunoblots from GST pull down assays with Gbetacommon (betac) and gamma2 antisera demonstrate binding of beta1 ( 1), beta3 ( 3), and beta4 ( 4), as well as gamma2, to each of the GIRK-GST fusion proteins; Gbetagamma subunits did not bind to GST alone.	bind
46177	9	1642	6	10	NULL	0	NULL	GST-GIRK	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_17_9771_s_114	10944236	( C) Immunoblots from GST pull down assays with Gbetacommon (betac) and gamma2 antisera demonstrate binding of beta1 ( 1), beta3 ( 3), and beta4 ( 4), as well as gamma2, to each of the GIRK-GST fusion proteins; Gbetagamma subunits did not bind to GST alone.	bind
322	1	1643	5	10	NULL	0	NULL	MAGI-2	GP		bind					GST - nephrin	GP		tail		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_28_9814_s_97	15994232	( C) Immunoblotting with anti-MAGI-2/S-SCAM IgG and anti-MAGI-2 IgG showed that MAGI-2  binds to GST - nephrin tail (lane 1) but not to GST alone (lane 2).	bind
3152	2	1643	5	10	NULL	0	NULL	MAGI-2	GP		does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_28_9814_s_97	15994232	( C) Immunoblotting with anti-MAGI-2/S-SCAM IgG and anti-MAGI-2 IgG showed that MAGI-2  binds to GST - nephrin tail (lane 1) but not to GST alone (lane 2).	bind
2372	1	1643	6	10	NULL	0	NULL	MAGI-2	GP		bind					GST-nephrin	GP		tail		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_28_9814_s_97	15994232	( C) Immunoblotting with anti-MAGI-2/S-SCAM IgG and anti-MAGI-2 IgG showed that MAGI-2  binds to GST - nephrin tail (lane 1) but not to GST alone (lane 2).	bind
2373	2	1643	6	10	NULL	0	NULL	MAGI-2	GP		does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_28_9814_s_97	15994232	( C) Immunoblotting with anti-MAGI-2/S-SCAM IgG and anti-MAGI-2 IgG showed that MAGI-2  binds to GST - nephrin tail (lane 1) but not to GST alone (lane 2).	bind
323	1	1644	5	10	NULL	0	NULL	Pho4	GP	unphosphorylated	bind					Pse1	GP				NULL		NULL	NULL	NULL	NULL	gw60_annurevcelldevbiol_15_0_291_s_104	10611964	( c) In   low-phosphate conditions unphosphorylated Pho4 binds to   its import receptor, Pse1, and is translocated   into the nucleus.	bind
324	2	1644	5	10	NULL	0	NULL	statement 1	Process		translocated to					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_annurevcelldevbiol_15_0_291_s_104	10611964	( c) In   low-phosphate conditions unphosphorylated Pho4 binds to   its import receptor, Pse1, and is translocated   into the nucleus.	bind
2883	3	1644	5	10	NULL	0	NULL	statement 1	Process		occurs in					low-phosphate conditions	Process				NULL		NULL	NULL	NULL	NULL	gw60_annurevcelldevbiol_15_0_291_s_104	10611964	( c) In   low-phosphate conditions unphosphorylated Pho4 binds to   its import receptor, Pse1, and is translocated   into the nucleus.	bind
46157	4	1644	5	10	NULL	0	NULL	Pse1	GP		is a type of					import receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_annurevcelldevbiol_15_0_291_s_104	10611964	( c) In   low-phosphate conditions unphosphorylated Pho4 binds to   its import receptor, Pse1, and is translocated   into the nucleus.	bind
52622	5	1644	5	10	NULL	0	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_annurevcelldevbiol_15_0_291_s_104	10611964	( c) In   low-phosphate conditions unphosphorylated Pho4 binds to   its import receptor, Pse1, and is translocated   into the nucleus.	bind
2374	1	1644	6	10	NULL	0	NULL	Pho4	GP	unphosphorylated	bind					Pse1	GP				NULL		NULL	NULL	NULL	NULL	gw60_annurevcelldevbiol_15_0_291_s_104	10611964	( c) In   low-phosphate conditions unphosphorylated Pho4 binds to   its import receptor, Pse1, and is translocated   into the nucleus.	bind
2375	2	1644	6	10	NULL	0	NULL	statement 1	Process		occurs in					low-phosphate conditions	Process				NULL		NULL	NULL	NULL	NULL	gw60_annurevcelldevbiol_15_0_291_s_104	10611964	( c) In   low-phosphate conditions unphosphorylated Pho4 binds to   its import receptor, Pse1, and is translocated   into the nucleus.	bind
2376	3	1644	6	10	NULL	0	NULL	Pho4	GP	unphosphorylated	translocated to					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_annurevcelldevbiol_15_0_291_s_104	10611964	( c) In   low-phosphate conditions unphosphorylated Pho4 binds to   its import receptor, Pse1, and is translocated   into the nucleus.	bind
2377	4	1644	6	10	NULL	0	NULL	statement 1	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_annurevcelldevbiol_15_0_291_s_104	10611964	( c) In   low-phosphate conditions unphosphorylated Pho4 binds to   its import receptor, Pse1, and is translocated   into the nucleus.	bind
46179	5	1644	6	10	NULL	0	NULL	Pse1	GP		is a type of					import receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_annurevcelldevbiol_15_0_291_s_104	10611964	( c) In   low-phosphate conditions unphosphorylated Pho4 binds to   its import receptor, Pse1, and is translocated   into the nucleus.	bind
325	1	1645	5	10	NULL	0	NULL	T cells	Cell	activated	decrease					Bcl-2	GP	levels of			NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_22_0_765_s_231	15032596	( C) In activated T cells levels of Bcl-2 fall, and consequently less of the Bim protein  is bound to Bcl-2.	bind
326	2	1645	5	10	NULL	0	NULL	Bim protein	GP		bind					Bcl-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_22_0_765_s_231	15032596	( C) In activated T cells levels of Bcl-2 fall, and consequently less of the Bim protein  is bound to Bcl-2.	bind
327	3	1645	5	10	NULL	0	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_22_0_765_s_231	15032596	( C) In activated T cells levels of Bcl-2 fall, and consequently less of the Bim protein  is bound to Bcl-2.	bind
2378	1	1645	6	10	NULL	0	NULL	Bim protein	GP		bind					Bcl-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_22_0_765_s_231	15032596	( C) In activated T cells levels of Bcl-2 fall, and consequently less of the Bim protein  is bound to Bcl-2.	bind
2379	2	1645	6	10	NULL	0	NULL	T cells	Cell	activated	decreases					Bcl-2	GP	levels of 			NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_22_0_765_s_231	15032596	( C) In activated T cells levels of Bcl-2 fall, and consequently less of the Bim protein  is bound to Bcl-2.	bind
2380	3	1645	6	10	NULL	0	NULL	statement 2	Process		leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_22_0_765_s_231	15032596	( C) In activated T cells levels of Bcl-2 fall, and consequently less of the Bim protein  is bound to Bcl-2.	bind
328	1	1646	5	10	NULL	0	NULL	Cdc42p	GP		bind					Gic2p	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_18_5360_s_183	9736614	( C) In contrast to Gic2p-N1-208,  cdc4-1 cells overexpressing Gic2p-crib- from the  GAL promoter at 30 degrees C were viable, confirming that binding of Cdc42p to Gic2p is required for its function (Brown  et al., 1997  ).	bind
3153	2	1646	5	10	NULL	0	NULL	cdc4-1 cells	Cell		overexpress					Gic2p-crib-	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_18_5360_s_183	9736614	( C) In contrast to Gic2p-N1-208,  cdc4-1 cells overexpressing Gic2p-crib- from the  GAL promoter at 30 degrees C were viable, confirming that binding of Cdc42p to Gic2p is required for its function (Brown  et al., 1997  ).	bind
3157	3	1646	5	10	NULL	0	NULL	statement 1	Process		is required for					Gic2p	GP	function of			NULL		NULL	NULL	NULL	NULL	gw60_embo_17_18_5360_s_183	9736614	( C) In contrast to Gic2p-N1-208,  cdc4-1 cells overexpressing Gic2p-crib- from the  GAL promoter at 30 degrees C were viable, confirming that binding of Cdc42p to Gic2p is required for its function (Brown  et al., 1997  ).	bind
3159	4	1646	5	10	NULL	0	NULL	statement 1	Process		is required for					cdc4-1 cells	Cell	function of			NULL		NULL	NULL	NULL	NULL	gw60_embo_17_18_5360_s_183	9736614	( C) In contrast to Gic2p-N1-208,  cdc4-1 cells overexpressing Gic2p-crib- from the  GAL promoter at 30 degrees C were viable, confirming that binding of Cdc42p to Gic2p is required for its function (Brown  et al., 1997  ).	bind
2381	1	1646	6	10	NULL	0	NULL	Cdc42p	GP		bind					Gic2p	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_18_5360_s_183	9736614	( C) In contrast to Gic2p-N1-208,  cdc4-1 cells overexpressing Gic2p-crib- from the  GAL promoter at 30 degrees C were viable, confirming that binding of Cdc42p to Gic2p is required for its function (Brown  et al., 1997  ).	bind
2382	2	1646	6	10	NULL	0	NULL	cdc4-1 cells	Cell		overexpress					Gic2p-crib-	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_18_5360_s_183	9736614	( C) In contrast to Gic2p-N1-208,  cdc4-1 cells overexpressing Gic2p-crib- from the  GAL promoter at 30 degrees C were viable, confirming that binding of Cdc42p to Gic2p is required for its function (Brown  et al., 1997  ).	bind
2476	3	1646	6	10	NULL	0	NULL	statement 1	Process		is required for					Gic2p	GP	function of 			NULL		NULL	NULL	NULL	NULL	gw60_embo_17_18_5360_s_183	9736614	( C) In contrast to Gic2p-N1-208,  cdc4-1 cells overexpressing Gic2p-crib- from the  GAL promoter at 30 degrees C were viable, confirming that binding of Cdc42p to Gic2p is required for its function (Brown  et al., 1997  ).	bind
2477	4	1646	6	10	NULL	0	NULL	statement 1	Process		is required for					cdc4-1 cells	Cell	function of			NULL		NULL	NULL	NULL	NULL	gw60_embo_17_18_5360_s_183	9736614	( C) In contrast to Gic2p-N1-208,  cdc4-1 cells overexpressing Gic2p-crib- from the  GAL promoter at 30 degrees C were viable, confirming that binding of Cdc42p to Gic2p is required for its function (Brown  et al., 1997  ).	bind
329	1	1647	5	10	NULL	0	NULL	PDK1	GP		bind					PKB	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_16_4380_s_254	11500365	( C) In contrast, the PIF-binding pocket of PDK1 is not involved in the binding of PDK1 to PKB.	bind
330	2	1647	5	10	NULL	0	NULL	PDK1	GP		not involved in			PIF-binding pocket		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_16_4380_s_254	11500365	( C) In contrast, the PIF-binding pocket of PDK1 is not involved in the binding of PDK1 to PKB.	bind
2383	1	1647	6	10	NULL	0	NULL	PDK1	GP		bind					PKB	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_16_4380_s_254	11500365	( C) In contrast, the PIF-binding pocket of PDK1 is not involved in the binding of PDK1 to PKB.	bind
2384	2	1647	6	10	NULL	0	NULL	PDK1	GP		is not involved in			PIF-binding pocket		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_16_4380_s_254	11500365	( C) In contrast, the PIF-binding pocket of PDK1 is not involved in the binding of PDK1 to PKB.	bind
379	1	1648	5	10	NULL	0	NULL	PrPC	GP	mutant	bind					protein X	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_793_s_95	9759504	( C) In inherited disease and perhaps   with spontaneous disease in the presence of a somatic cell mutation,   mutant PrPC can bind protein X and form the PrP*/X/PrP*/X   encounter complex, which can then form PrPSc/ut in the absence of a PrPSc template.	bind
381	2	1648	5	10	NULL	0	NULL	statement 1	Process		forms					PrP*/X/PrP*/X encounter complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_793_s_95	9759504	( C) In inherited disease and perhaps   with spontaneous disease in the presence of a somatic cell mutation,   mutant PrPC can bind protein X and form the PrP*/X/PrP*/X   encounter complex, which can then form PrPSc/ut in the absence of a PrPSc template.	bind
383	3	1648	5	10	NULL	0	NULL	statement 2	Process		forms					PrPSc/ut	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_793_s_95	9759504	( C) In inherited disease and perhaps   with spontaneous disease in the presence of a somatic cell mutation,   mutant PrPC can bind protein X and form the PrP*/X/PrP*/X   encounter complex, which can then form PrPSc/ut in the absence of a PrPSc template.	bind
45935	4	1648	5	10	NULL	0	NULL	statement 3	Process		in the absence of					PrPSc template	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_793_s_95	9759504	( C) In inherited disease and perhaps   with spontaneous disease in the presence of a somatic cell mutation,   mutant PrPC can bind protein X and form the PrP*/X/PrP*/X   encounter complex, which can then form PrPSc/ut in the absence of a PrPSc template.	bind
2471	1	1648	6	10	NULL	0	NULL	PrPC	GP	mutant	bind					protein X	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_793_s_95	9759504	( C) In inherited disease and perhaps   with spontaneous disease in the presence of a somatic cell mutation,   mutant PrPC can bind protein X and form the PrP*/X/PrP*/X   encounter complex, which can then form PrPSc/ut in the absence of a PrPSc template.	bind
2472	2	1648	6	10	NULL	0	NULL	statement 1	Process		forms					PrP*/X/PrP*/X encounter complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_793_s_95	9759504	( C) In inherited disease and perhaps   with spontaneous disease in the presence of a somatic cell mutation,   mutant PrPC can bind protein X and form the PrP*/X/PrP*/X   encounter complex, which can then form PrPSc/ut in the absence of a PrPSc template.	bind
2473	3	1648	6	10	NULL	0	NULL	PrP*/X/PrP*/X encounter complex	GP		forms					PrPSc/ut 	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_793_s_95	9759504	( C) In inherited disease and perhaps   with spontaneous disease in the presence of a somatic cell mutation,   mutant PrPC can bind protein X and form the PrP*/X/PrP*/X   encounter complex, which can then form PrPSc/ut in the absence of a PrPSc template.	bind
2474	4	1648	6	10	NULL	0	NULL	statement 3	Process		 in absence of 					PrPSc template	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_793_s_95	9759504	( C) In inherited disease and perhaps   with spontaneous disease in the presence of a somatic cell mutation,   mutant PrPC can bind protein X and form the PrP*/X/PrP*/X   encounter complex, which can then form PrPSc/ut in the absence of a PrPSc template.	bind
384	1	1649	5	10	NULL	0	NULL	Pho4	GP	unphosphorylated	bind					Pse1	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_291_s_120	10611964	( c) In low-phosphate conditions unphosphorylated Pho4 binds to its import receptor,  Pse1, and is translocated into the nucleus.	bind
385	2	1649	5	10	NULL	0	NULL	statement 1	Process		translocated to					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_291_s_120	10611964	( c) In low-phosphate conditions unphosphorylated Pho4 binds to its import receptor,  Pse1, and is translocated into the nucleus.	bind
2885	3	1649	5	10	NULL	0	NULL	statement 1	Process		occurs in					low-phosphate conditions	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_291_s_120	10611964	( c) In low-phosphate conditions unphosphorylated Pho4 binds to its import receptor,  Pse1, and is translocated into the nucleus.	bind
52623	4	1649	5	10	NULL	0	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_291_s_120	10611964	( c) In low-phosphate conditions unphosphorylated Pho4 binds to its import receptor,  Pse1, and is translocated into the nucleus.	bind
52624	5	1649	5	10	NULL	0	NULL	Pse1	GP		is a type of					import receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_291_s_120	10611964	( c) In low-phosphate conditions unphosphorylated Pho4 binds to its import receptor,  Pse1, and is translocated into the nucleus.	bind
2385	1	1649	6	10	NULL	0	NULL	Pho4	GP	unphosphorylated	bind					Pse1	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_291_s_120	10611964	( c) In low-phosphate conditions unphosphorylated Pho4 binds to its import receptor,  Pse1, and is translocated into the nucleus.	bind
2386	2	1649	6	10	NULL	0	NULL	statement 1	Process		occurs in					low-phosphate conditions	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_291_s_120	10611964	( c) In low-phosphate conditions unphosphorylated Pho4 binds to its import receptor,  Pse1, and is translocated into the nucleus.	bind
2387	3	1649	6	10	NULL	0	NULL	Pho4	GP	unphosphorylated	is translocated to					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_291_s_120	10611964	( c) In low-phosphate conditions unphosphorylated Pho4 binds to its import receptor,  Pse1, and is translocated into the nucleus.	bind
2388	4	1649	6	10	NULL	0	NULL	statement 1	Process		leads to					Statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_291_s_120	10611964	( c) In low-phosphate conditions unphosphorylated Pho4 binds to its import receptor,  Pse1, and is translocated into the nucleus.	bind
52625	5	1649	6	10	NULL	0	NULL	Pse1	GP		is a type of					import receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_291_s_120	10611964	( c) In low-phosphate conditions unphosphorylated Pho4 binds to its import receptor,  Pse1, and is translocated into the nucleus.	bind
386	1	1650	5	10	NULL	0	NULL	RecBCD	GP		bind					DNA	NucleicAcid			double-strand tail	NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8181_s_132	11459951	( C) In recombination proficient strains, RecBCD binds to the double-strand tail ( C1); degradation takes place until the first recognized CHI site (CHI is an octameric sequence that switches RecBCD from an exonuclease to a recombinase enzyme) and is followed by a genetic exchange mediated by RecA ( C2); RuvC resolves the first Holliday junction bound by RuvAB ( C3).	bind
387	2	1650	5	10	NULL	0	NULL	RuvAB	GP		bind					Holliday junction	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8181_s_132	11459951	( C) In recombination proficient strains, RecBCD binds to the double-strand tail ( C1); degradation takes place until the first recognized CHI site (CHI is an octameric sequence that switches RecBCD from an exonuclease to a recombinase enzyme) and is followed by a genetic exchange mediated by RecA ( C2); RuvC resolves the first Holliday junction bound by RuvAB ( C3).	bind
388	3	1650	5	10	NULL	0	NULL	RuvC	GP		resolves					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8181_s_132	11459951	( C) In recombination proficient strains, RecBCD binds to the double-strand tail ( C1); degradation takes place until the first recognized CHI site (CHI is an octameric sequence that switches RecBCD from an exonuclease to a recombinase enzyme) and is followed by a genetic exchange mediated by RecA ( C2); RuvC resolves the first Holliday junction bound by RuvAB ( C3).	bind
46159	4	1650	5	10	NULL	0	NULL	RecA	GP		mediate					genetic exchange	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8181_s_132	11459951	( C) In recombination proficient strains, RecBCD binds to the double-strand tail ( C1); degradation takes place until the first recognized CHI site (CHI is an octameric sequence that switches RecBCD from an exonuclease to a recombinase enzyme) and is followed by a genetic exchange mediated by RecA ( C2); RuvC resolves the first Holliday junction bound by RuvAB ( C3).	bind
46161	5	1650	5	10	NULL	0	NULL	RecBCD exonuclease	GP		switches to					RecBCD recombinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8181_s_132	11459951	( C) In recombination proficient strains, RecBCD binds to the double-strand tail ( C1); degradation takes place until the first recognized CHI site (CHI is an octameric sequence that switches RecBCD from an exonuclease to a recombinase enzyme) and is followed by a genetic exchange mediated by RecA ( C2); RuvC resolves the first Holliday junction bound by RuvAB ( C3).	bind
46163	6	1650	5	10	NULL	0	NULL				leads to				CHI site	statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8181_s_132	11459951	( C) In recombination proficient strains, RecBCD binds to the double-strand tail ( C1); degradation takes place until the first recognized CHI site (CHI is an octameric sequence that switches RecBCD from an exonuclease to a recombinase enzyme) and is followed by a genetic exchange mediated by RecA ( C2); RuvC resolves the first Holliday junction bound by RuvAB ( C3).	bind
2480	1	1650	6	10	NULL	0	NULL	RecBCD	GP		bind to					DNA	NucleicAcid			double-strand tail	NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8181_s_132	11459951	( C) In recombination proficient strains, RecBCD binds to the double-strand tail ( C1); degradation takes place until the first recognized CHI site (CHI is an octameric sequence that switches RecBCD from an exonuclease to a recombinase enzyme) and is followed by a genetic exchange mediated by RecA ( C2); RuvC resolves the first Holliday junction bound by RuvAB ( C3).	bind
2481	2	1650	6	10	NULL	0	NULL	RecA	GP		mediates					genetic exchange	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8181_s_132	11459951	( C) In recombination proficient strains, RecBCD binds to the double-strand tail ( C1); degradation takes place until the first recognized CHI site (CHI is an octameric sequence that switches RecBCD from an exonuclease to a recombinase enzyme) and is followed by a genetic exchange mediated by RecA ( C2); RuvC resolves the first Holliday junction bound by RuvAB ( C3).	bind
2482	3	1650	6	10	NULL	0	NULL	RuvAB	GP		bind					Holliday junction	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8181_s_132	11459951	( C) In recombination proficient strains, RecBCD binds to the double-strand tail ( C1); degradation takes place until the first recognized CHI site (CHI is an octameric sequence that switches RecBCD from an exonuclease to a recombinase enzyme) and is followed by a genetic exchange mediated by RecA ( C2); RuvC resolves the first Holliday junction bound by RuvAB ( C3).	bind
2483	4	1650	6	10	NULL	0	NULL	RuvC	GP		resolves					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8181_s_132	11459951	( C) In recombination proficient strains, RecBCD binds to the double-strand tail ( C1); degradation takes place until the first recognized CHI site (CHI is an octameric sequence that switches RecBCD from an exonuclease to a recombinase enzyme) and is followed by a genetic exchange mediated by RecA ( C2); RuvC resolves the first Holliday junction bound by RuvAB ( C3).	bind
2484	5	1650	6	10	NULL	0	NULL	RecBCD exonuclease	GP		switches to 					RecBCD recombinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8181_s_132	11459951	( C) In recombination proficient strains, RecBCD binds to the double-strand tail ( C1); degradation takes place until the first recognized CHI site (CHI is an octameric sequence that switches RecBCD from an exonuclease to a recombinase enzyme) and is followed by a genetic exchange mediated by RecA ( C2); RuvC resolves the first Holliday junction bound by RuvAB ( C3).	bind
2485	6	1650	6	10	NULL	0	NULL				leads to				CH1 site	statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8181_s_132	11459951	( C) In recombination proficient strains, RecBCD binds to the double-strand tail ( C1); degradation takes place until the first recognized CHI site (CHI is an octameric sequence that switches RecBCD from an exonuclease to a recombinase enzyme) and is followed by a genetic exchange mediated by RecA ( C2); RuvC resolves the first Holliday junction bound by RuvAB ( C3).	bind
389	1	1651	5	10	NULL	0	NULL	WASP	GP		bind					proteins	GP		SH3 domain		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jclininvest_111_9_1389_s_184	12727931	( c) In vitro binding of WASP to SH3 domain-containing proteins.	bind
2389	1	1651	6	10	NULL	0	NULL	WASP	GP		bind					protein	GP		SH3 domain containing		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jclininvest_111_9_1389_s_184	12727931	( c) In vitro binding of WASP to SH3 domain-containing proteins.	bind
390	1	1652	5	10	NULL	0	NULL			mutant	does not bind			PH domain		PI(4,5)P2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_24_13964_s_163	14612561	( C) Incorporation of GFP-actin by Triton cytoskeletons from cells transfected with a  mutant PH domain that does not bind PI(4,5)P2 ( Upper) or by cytoskeletons from cells transfected with PH-GFP, which does bind PI(4,5)P2  ( Lower).	bind
391	2	1652	5	10	NULL	0	NULL				bind			PH-GFP		PI(4,5)P2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_24_13964_s_163	14612561	( C) Incorporation of GFP-actin by Triton cytoskeletons from cells transfected with a  mutant PH domain that does not bind PI(4,5)P2 ( Upper) or by cytoskeletons from cells transfected with PH-GFP, which does bind PI(4,5)P2  ( Lower).	bind
2486	1	1652	6	10	NULL	0	NULL				bind			PH-GFP		PI(4,5)P2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_24_13964_s_163	14612561	( C) Incorporation of GFP-actin by Triton cytoskeletons from cells transfected with a  mutant PH domain that does not bind PI(4,5)P2 ( Upper) or by cytoskeletons from cells transfected with PH-GFP, which does bind PI(4,5)P2  ( Lower).	bind
2487	2	1652	6	10	NULL	0	NULL			mutant	does not bind			PH domain		PI(4,5)P2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_24_13964_s_163	14612561	( C) Incorporation of GFP-actin by Triton cytoskeletons from cells transfected with a  mutant PH domain that does not bind PI(4,5)P2 ( Upper) or by cytoskeletons from cells transfected with PH-GFP, which does bind PI(4,5)P2  ( Lower).	bind
392	1	1653	5	10	NULL	0	NULL	DNA	NucleicAcid		bind					HSF3	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_277_5323_246_s_77	9211854	( C) Induction of HSF3 DNA binding activity by c-Myb.	bind
3163	2	1653	5	10	NULL	0	NULL	statement 1	Process		induce					c-Myb	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_277_5323_246_s_77	9211854	( C) Induction of HSF3 DNA binding activity by c-Myb.	bind
2390	1	1653	6	10	NULL	0	NULL	HSF3	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_science_277_5323_246_s_77	9211854	( C) Induction of HSF3 DNA binding activity by c-Myb.	bind
2391	2	1653	6	10	NULL	0	NULL	c-Myb	GP		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_277_5323_246_s_77	9211854	( C) Induction of HSF3 DNA binding activity by c-Myb.	bind
393	1	1654	5	10	NULL	0	NULL	importin-beta	GP		bind					NuMA	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw60_science_291_5504_653_s_96	11229403	( C) Inhibition of binding of importin-beta to endogenous NuMA by RanL43E.	bind
395	2	1654	5	10	NULL	0	NULL	Ran	GP		inhibit			L43E		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_291_5504_653_s_96	11229403	( C) Inhibition of binding of importin-beta to endogenous NuMA by RanL43E.	bind
2392	1	1654	6	10	NULL	0	NULL	importin-beta	GP		bind					NuMA	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw60_science_291_5504_653_s_96	11229403	( C) Inhibition of binding of importin-beta to endogenous NuMA by RanL43E.	bind
2393	2	1654	6	10	NULL	0	NULL	Ran	GP		inhibits			L43E		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_291_5504_653_s_96	11229403	( C) Inhibition of binding of importin-beta to endogenous NuMA by RanL43E.	bind
396	1	1655	5	10	NULL	0	NULL	PIP2	Chemical		bind					GFP-PHD	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5419_1527_s_35	10348740	( C) Inhibition of PIP2 binding of 2 muM GFP-PHD by 2 muM IP3 (InsP3), inositol 1,3,4-trisphosphate [Ins(1,3,4)P3], and inositol 1,3,4,5-tetrakisphosphate (InsP4).	bind
397	2	1655	5	10	NULL	0	NULL	InsP3	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5419_1527_s_35	10348740	( C) Inhibition of PIP2 binding of 2 muM GFP-PHD by 2 muM IP3 (InsP3), inositol 1,3,4-trisphosphate [Ins(1,3,4)P3], and inositol 1,3,4,5-tetrakisphosphate (InsP4).	bind
398	3	1655	5	10	NULL	0	NULL	InsP3	Chemical		is					IP3	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5419_1527_s_35	10348740	( C) Inhibition of PIP2 binding of 2 muM GFP-PHD by 2 muM IP3 (InsP3), inositol 1,3,4-trisphosphate [Ins(1,3,4)P3], and inositol 1,3,4,5-tetrakisphosphate (InsP4).	bind
400	4	1655	5	10	NULL	0	NULL	Ins(1,3,4)P3	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5419_1527_s_35	10348740	( C) Inhibition of PIP2 binding of 2 muM GFP-PHD by 2 muM IP3 (InsP3), inositol 1,3,4-trisphosphate [Ins(1,3,4)P3], and inositol 1,3,4,5-tetrakisphosphate (InsP4).	bind
401	5	1655	5	10	NULL	0	NULL	Ins(1,3,4)P3	Chemical		is					inositol 1,3,4-trisphosphate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5419_1527_s_35	10348740	( C) Inhibition of PIP2 binding of 2 muM GFP-PHD by 2 muM IP3 (InsP3), inositol 1,3,4-trisphosphate [Ins(1,3,4)P3], and inositol 1,3,4,5-tetrakisphosphate (InsP4).	bind
402	6	1655	5	10	NULL	0	NULL	InsP4	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5419_1527_s_35	10348740	( C) Inhibition of PIP2 binding of 2 muM GFP-PHD by 2 muM IP3 (InsP3), inositol 1,3,4-trisphosphate [Ins(1,3,4)P3], and inositol 1,3,4,5-tetrakisphosphate (InsP4).	bind
403	7	1655	5	10	NULL	0	NULL	InsP4	Chemical		is					inositol 1,3,4,5-tetrakisphosphate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5419_1527_s_35	10348740	( C) Inhibition of PIP2 binding of 2 muM GFP-PHD by 2 muM IP3 (InsP3), inositol 1,3,4-trisphosphate [Ins(1,3,4)P3], and inositol 1,3,4,5-tetrakisphosphate (InsP4).	bind
2394	1	1655	6	10	NULL	0	NULL	PIP2	Chemical		bind					GFP-PHD	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5419_1527_s_35	10348740	( C) Inhibition of PIP2 binding of 2 muM GFP-PHD by 2 muM IP3 (InsP3), inositol 1,3,4-trisphosphate [Ins(1,3,4)P3], and inositol 1,3,4,5-tetrakisphosphate (InsP4).	bind
2395	2	1655	6	10	NULL	0	NULL	IP3	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5419_1527_s_35	10348740	( C) Inhibition of PIP2 binding of 2 muM GFP-PHD by 2 muM IP3 (InsP3), inositol 1,3,4-trisphosphate [Ins(1,3,4)P3], and inositol 1,3,4,5-tetrakisphosphate (InsP4).	bind
2396	3	1655	6	10	NULL	0	NULL	Ins(1,3,4)P3	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5419_1527_s_35	10348740	( C) Inhibition of PIP2 binding of 2 muM GFP-PHD by 2 muM IP3 (InsP3), inositol 1,3,4-trisphosphate [Ins(1,3,4)P3], and inositol 1,3,4,5-tetrakisphosphate (InsP4).	bind
2397	4	1655	6	10	NULL	0	NULL	Ins(1,3,4)P3	Chemical		is					inositol 1,3,4-trisphosphate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5419_1527_s_35	10348740	( C) Inhibition of PIP2 binding of 2 muM GFP-PHD by 2 muM IP3 (InsP3), inositol 1,3,4-trisphosphate [Ins(1,3,4)P3], and inositol 1,3,4,5-tetrakisphosphate (InsP4).	bind
2398	5	1655	6	10	NULL	0	NULL	InsP4	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5419_1527_s_35	10348740	( C) Inhibition of PIP2 binding of 2 muM GFP-PHD by 2 muM IP3 (InsP3), inositol 1,3,4-trisphosphate [Ins(1,3,4)P3], and inositol 1,3,4,5-tetrakisphosphate (InsP4).	bind
2399	6	1655	6	10	NULL	0	NULL	InsP4	Chemical		is					inositol 1,3,4,5-tetrakisphosphate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5419_1527_s_35	10348740	( C) Inhibition of PIP2 binding of 2 muM GFP-PHD by 2 muM IP3 (InsP3), inositol 1,3,4-trisphosphate [Ins(1,3,4)P3], and inositol 1,3,4,5-tetrakisphosphate (InsP4).	bind
3077	7	1655	6	10	NULL	0	NULL	IP3	Chemical		is					InsP3	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5419_1527_s_35	10348740	( C) Inhibition of PIP2 binding of 2 muM GFP-PHD by 2 muM IP3 (InsP3), inositol 1,3,4-trisphosphate [Ins(1,3,4)P3], and inositol 1,3,4,5-tetrakisphosphate (InsP4).	bind
405	1	1656	5	10	NULL	0	NULL	biotin-HKa	GP		bind					tropomyosin	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_19_12224_s_158	12196635	( C) Inhibition of the binding of biotin-HKa (10 nM) to purified tropomyosin by HKa D5.	bind
406	2	1656	5	10	NULL	0	NULL	HKa D5	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_19_12224_s_158	12196635	( C) Inhibition of the binding of biotin-HKa (10 nM) to purified tropomyosin by HKa D5.	bind
2400	1	1656	6	10	NULL	0	NULL	biotin-HKa	GP		bind					tropomyosin	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_19_12224_s_158	12196635	( C) Inhibition of the binding of biotin-HKa (10 nM) to purified tropomyosin by HKa D5.	bind
2401	2	1656	6	10	NULL	0	NULL	HKaD5	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_19_12224_s_158	12196635	( C) Inhibition of the binding of biotin-HKa (10 nM) to purified tropomyosin by HKa D5.	bind
899	2	1657	5	10	NULL	0	NULL	HoxD9	GP	2H,15N-labeled 	bind			 homeodomain		Nhb nonspecific DNA duplexes 	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_41_15062_s_44	17008406	( c) Intermolecular 1HN-gamma2 PREs arising from the dT-EDTA-Mn2+ measured on uniformly 2H,15N-labeled HoxD9 homeodomain bound to the Nhb nonspecific ( Left) and Shb-specific ( Right) DNA duplexes at 20 mM NaCl.	bind
900	3	1657	5	10	NULL	0	NULL	HoxD9	GP	2H,15N-labeled 	bind			 homeodomain		Shb-specific DNA duplexes 	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_41_15062_s_44	17008406	( c) Intermolecular 1HN-gamma2 PREs arising from the dT-EDTA-Mn2+ measured on uniformly 2H,15N-labeled HoxD9 homeodomain bound to the Nhb nonspecific ( Left) and Shb-specific ( Right) DNA duplexes at 20 mM NaCl.	bind
2488	1	1657	6	10	NULL	0	NULL	HoxD9	GP	2H,15N-labeled	bind			homeodomain		Nhb nonspecific DNA duplexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_41_15062_s_44	17008406	( c) Intermolecular 1HN-gamma2 PREs arising from the dT-EDTA-Mn2+ measured on uniformly 2H,15N-labeled HoxD9 homeodomain bound to the Nhb nonspecific ( Left) and Shb-specific ( Right) DNA duplexes at 20 mM NaCl.	bind
2489	2	1657	6	10	NULL	0	NULL	HoxD9	GP	2H,15N-labeled	bind			homeodomain		Shb-specific DNA duplexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_41_15062_s_44	17008406	( c) Intermolecular 1HN-gamma2 PREs arising from the dT-EDTA-Mn2+ measured on uniformly 2H,15N-labeled HoxD9 homeodomain bound to the Nhb nonspecific ( Left) and Shb-specific ( Right) DNA duplexes at 20 mM NaCl.	bind
408	1	1659	5	10	NULL	0	NULL	vinculin 	GP		bind					F-actin	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_5853_s_179	10545097	( C) IpaA induces vinculin binding to immobilized F-actin.	bind
409	2	1659	5	10	NULL	0	NULL	IpaA	GP		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_5853_s_179	10545097	( C) IpaA induces vinculin binding to immobilized F-actin.	bind
2492	1	1659	6	10	NULL	0	NULL	vinculin	GP		bind					F-actin	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_5853_s_179	10545097	( C) IpaA induces vinculin binding to immobilized F-actin.	bind
2493	2	1659	6	10	NULL	0	NULL	IpaA	GP		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_5853_s_179	10545097	( C) IpaA induces vinculin binding to immobilized F-actin.	bind
410	1	1660	5	10	NULL	0	NULL	talin	GP		bind					vinculin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_5853_s_85	10545097	( C) IpaA inhibits talin binding to vinculin.	bind
411	2	1660	5	10	NULL	0	NULL	IpaA	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_5853_s_85	10545097	( C) IpaA inhibits talin binding to vinculin.	bind
2495	1	1660	6	10	NULL	0	NULL	talin	GP		bind					vinculin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_5853_s_85	10545097	( C) IpaA inhibits talin binding to vinculin.	bind
2496	2	1660	6	10	NULL	0	NULL	IpaA	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_5853_s_85	10545097	( C) IpaA inhibits talin binding to vinculin.	bind
412	1	1661	5	10	NULL	0	NULL	p31comet	GP		bind					N2-Mad2	GP		R133A		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_15_3133_s_137	15257285	( C) ITC analysis of the binding between p31comet and N2-Mad2R133A.	bind
2497	1	1661	6	10	NULL	0	NULL	p31comet	GP		bind					N2-Mad2	GP		R133A		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_15_3133_s_137	15257285	( C) ITC analysis of the binding between p31comet and N2-Mad2R133A.	bind
413	1	1662	5	10	NULL	0	NULL	JNKK1	GP		bind					JNK1	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_21_3369_s_201	9808624	( C) JNKK1 binds endogenous JNK1.	bind
2498	1	1662	6	10	NULL	0	NULL	JNKK1	GP		bind					JNK1	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_21_3369_s_201	9808624	( C) JNKK1 binds endogenous JNK1.	bind
414	1	1663	5	10	NULL	0	NULL	P15 INK4b	GP		bind					Cdk4	GP				NULL	MEFs treated with TGF-beta	NULL	NULL	NULL	NULL	gw60_embo_19_13_3496_s_120	10880462	( C) Levels of P15 INK4b, P16 INK4a, P21 Cip1 and P27 Kip1 proteins bound to Cdk4 in MEFs treated with TGF-beta for the times indicated.	bind
415	2	1663	5	10	NULL	0	NULL	P16 INK4a	GP		bind					Cdk4	GP				NULL	MEFs treated with TGF-beta	NULL	NULL	NULL	NULL	gw60_embo_19_13_3496_s_120	10880462	( C) Levels of P15 INK4b, P16 INK4a, P21 Cip1 and P27 Kip1 proteins bound to Cdk4 in MEFs treated with TGF-beta for the times indicated.	bind
416	3	1663	5	10	NULL	0	NULL	P21 Cip1	GP		bind					Cdk4	GP				NULL	MEFs treated with TGF-beta	NULL	NULL	NULL	NULL	gw60_embo_19_13_3496_s_120	10880462	( C) Levels of P15 INK4b, P16 INK4a, P21 Cip1 and P27 Kip1 proteins bound to Cdk4 in MEFs treated with TGF-beta for the times indicated.	bind
417	4	1663	5	10	NULL	0	NULL	P27 Kip1	GP		bind					Cdk4	GP				NULL	MEFs treated with TGF-beta	NULL	NULL	NULL	NULL	gw60_embo_19_13_3496_s_120	10880462	( C) Levels of P15 INK4b, P16 INK4a, P21 Cip1 and P27 Kip1 proteins bound to Cdk4 in MEFs treated with TGF-beta for the times indicated.	bind
2499	1	1663	6	10	NULL	0	NULL	P15 INK4b	GP		bind					Cdk4	GP				NULL	MEFs treated with TGF-beta	NULL	NULL	NULL	NULL	gw60_embo_19_13_3496_s_120	10880462	( C) Levels of P15 INK4b, P16 INK4a, P21 Cip1 and P27 Kip1 proteins bound to Cdk4 in MEFs treated with TGF-beta for the times indicated.	bind
2500	2	1663	6	10	NULL	0	NULL	P16 INK4a	GP		bind					Cdk4	GP				NULL	MEFs treated with TGF-beta	NULL	NULL	NULL	NULL	gw60_embo_19_13_3496_s_120	10880462	( C) Levels of P15 INK4b, P16 INK4a, P21 Cip1 and P27 Kip1 proteins bound to Cdk4 in MEFs treated with TGF-beta for the times indicated.	bind
2501	3	1663	6	10	NULL	0	NULL	P21 Cip1	GP		bind					Cdk4	GP				NULL	MEFs treated with TGF-beta	NULL	NULL	NULL	NULL	gw60_embo_19_13_3496_s_120	10880462	( C) Levels of P15 INK4b, P16 INK4a, P21 Cip1 and P27 Kip1 proteins bound to Cdk4 in MEFs treated with TGF-beta for the times indicated.	bind
2502	4	1663	6	10	NULL	0	NULL	P27 Kip1	GP		bind					Cdk4	GP				NULL	MEFs treated with TGF-beta	NULL	NULL	NULL	NULL	gw60_embo_19_13_3496_s_120	10880462	( C) Levels of P15 INK4b, P16 INK4a, P21 Cip1 and P27 Kip1 proteins bound to Cdk4 in MEFs treated with TGF-beta for the times indicated.	bind
2539	1	1664	6	10	NULL	0	NULL	HP1beta	GP	GFP full length	bind 					 histone H3	GP	methylated	W42L;;Lys-9		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_489_s_156	14765118	( C) Localisation of GFP full-length HP1beta with point mutations that cripple binding to Lys-9-methylated histone H3 (W42L),  Lys-9-methylated histone H3 and PXVXL proteins (W42L, W170), dimerisation and binding  to PXVXL proteins (I161E), and dimerisation and binding to PXVXL proteins and binding  to Lys-9-methylated histone H3 (W42L, I161E).	bind
2540	2	1664	6	10	NULL	0	NULL	HP1beta	GP	mutant;;GFP full length	cripple					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_489_s_156	14765118	( C) Localisation of GFP full-length HP1beta with point mutations that cripple binding to Lys-9-methylated histone H3 (W42L),  Lys-9-methylated histone H3 and PXVXL proteins (W42L, W170), dimerisation and binding  to PXVXL proteins (I161E), and dimerisation and binding to PXVXL proteins and binding  to Lys-9-methylated histone H3 (W42L, I161E).	bind
2541	3	1664	6	10	NULL	0	NULL	HP1beta	GP	GFP full length	bind					PXVXL proteins	GP		W42L;;W170		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_489_s_156	14765118	( C) Localisation of GFP full-length HP1beta with point mutations that cripple binding to Lys-9-methylated histone H3 (W42L),  Lys-9-methylated histone H3 and PXVXL proteins (W42L, W170), dimerisation and binding  to PXVXL proteins (I161E), and dimerisation and binding to PXVXL proteins and binding  to Lys-9-methylated histone H3 (W42L, I161E).	bind
2542	4	1664	6	10	NULL	0	NULL	HP1beta	GP	mutant;;GFP full length	cripple					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_489_s_156	14765118	( C) Localisation of GFP full-length HP1beta with point mutations that cripple binding to Lys-9-methylated histone H3 (W42L),  Lys-9-methylated histone H3 and PXVXL proteins (W42L, W170), dimerisation and binding  to PXVXL proteins (I161E), and dimerisation and binding to PXVXL proteins and binding  to Lys-9-methylated histone H3 (W42L, I161E).	bind
3080	5	1664	6	10	NULL	0	NULL	HP1 beta	GP	GFP full length	bind					PXVXL protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_489_s_156	14765118	( C) Localisation of GFP full-length HP1beta with point mutations that cripple binding to Lys-9-methylated histone H3 (W42L),  Lys-9-methylated histone H3 and PXVXL proteins (W42L, W170), dimerisation and binding  to PXVXL proteins (I161E), and dimerisation and binding to PXVXL proteins and binding  to Lys-9-methylated histone H3 (W42L, I161E).	bind
4025	6	1664	6	10	NULL	0	NULL	HP1 beta	GP	mutant;;GFP full length	cripple					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_489_s_156	14765118	( C) Localisation of GFP full-length HP1beta with point mutations that cripple binding to Lys-9-methylated histone H3 (W42L),  Lys-9-methylated histone H3 and PXVXL proteins (W42L, W170), dimerisation and binding  to PXVXL proteins (I161E), and dimerisation and binding to PXVXL proteins and binding  to Lys-9-methylated histone H3 (W42L, I161E).	bind
4026	7	1664	6	10	NULL	0	NULL	HP1 beta	GP	GFP full length	bind					PXVXL protein	GP		I161E		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_489_s_156	14765118	( C) Localisation of GFP full-length HP1beta with point mutations that cripple binding to Lys-9-methylated histone H3 (W42L),  Lys-9-methylated histone H3 and PXVXL proteins (W42L, W170), dimerisation and binding  to PXVXL proteins (I161E), and dimerisation and binding to PXVXL proteins and binding  to Lys-9-methylated histone H3 (W42L, I161E).	bind
4027	8	1664	6	10	NULL	0	NULL	HP1 beta	GP	mutant;;GFP full length	cripple					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_489_s_156	14765118	( C) Localisation of GFP full-length HP1beta with point mutations that cripple binding to Lys-9-methylated histone H3 (W42L),  Lys-9-methylated histone H3 and PXVXL proteins (W42L, W170), dimerisation and binding  to PXVXL proteins (I161E), and dimerisation and binding to PXVXL proteins and binding  to Lys-9-methylated histone H3 (W42L, I161E).	bind
4028	9	1664	6	10	NULL	0	NULL	HP1 beta	GP	mutant;;GFP full length	cripple					PXVXL protein	GP	dimerisation of	I161E		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_489_s_156	14765118	( C) Localisation of GFP full-length HP1beta with point mutations that cripple binding to Lys-9-methylated histone H3 (W42L),  Lys-9-methylated histone H3 and PXVXL proteins (W42L, W170), dimerisation and binding  to PXVXL proteins (I161E), and dimerisation and binding to PXVXL proteins and binding  to Lys-9-methylated histone H3 (W42L, I161E).	bind
52805	10	1664	6	10	NULL	0	NULL	HP1beta	GP	GFP full length	bind					histone H3	GP	methylated	Lys-9		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_489_s_156	14765118	( C) Localisation of GFP full-length HP1beta with point mutations that cripple binding to Lys-9-methylated histone H3 (W42L),  Lys-9-methylated histone H3 and PXVXL proteins (W42L, W170), dimerisation and binding  to PXVXL proteins (I161E), and dimerisation and binding to PXVXL proteins and binding  to Lys-9-methylated histone H3 (W42L, I161E).	bind
52806	11	1664	6	10	NULL	0	NULL	HP1beta	GP	mutant;;GFP full length	cripple					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_489_s_156	14765118	( C) Localisation of GFP full-length HP1beta with point mutations that cripple binding to Lys-9-methylated histone H3 (W42L),  Lys-9-methylated histone H3 and PXVXL proteins (W42L, W170), dimerisation and binding  to PXVXL proteins (I161E), and dimerisation and binding to PXVXL proteins and binding  to Lys-9-methylated histone H3 (W42L, I161E).	bind
52808	12	1664	6	10	NULL	0	NULL	HP1beta	GP	mutant;;GFP full length	cripple					PXVXL proteins	GP	dimerisation of			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_489_s_156	14765118	( C) Localisation of GFP full-length HP1beta with point mutations that cripple binding to Lys-9-methylated histone H3 (W42L),  Lys-9-methylated histone H3 and PXVXL proteins (W42L, W170), dimerisation and binding  to PXVXL proteins (I161E), and dimerisation and binding to PXVXL proteins and binding  to Lys-9-methylated histone H3 (W42L, I161E).	bind
52809	13	1664	6	10	NULL	0	NULL	HP1beta	GP	GFP full length	bind					histone H3	GP	methylated	W42L;; I161E;;Lys-9		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_489_s_156	14765118	( C) Localisation of GFP full-length HP1beta with point mutations that cripple binding to Lys-9-methylated histone H3 (W42L),  Lys-9-methylated histone H3 and PXVXL proteins (W42L, W170), dimerisation and binding  to PXVXL proteins (I161E), and dimerisation and binding to PXVXL proteins and binding  to Lys-9-methylated histone H3 (W42L, I161E).	bind
52810	14	1664	6	10	NULL	0	NULL	HP1beta	GP	mutant;;GFP full length	cripple					statement 13	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_489_s_156	14765118	( C) Localisation of GFP full-length HP1beta with point mutations that cripple binding to Lys-9-methylated histone H3 (W42L),  Lys-9-methylated histone H3 and PXVXL proteins (W42L, W170), dimerisation and binding  to PXVXL proteins (I161E), and dimerisation and binding to PXVXL proteins and binding  to Lys-9-methylated histone H3 (W42L, I161E).	bind
418	1	1665	5	10	NULL	0	NULL	mAb LM-142	GP		bind					protein A/G resin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_4_1163_s_92	15657120	( C) mAb LM-142 was bound to protein A/G resin and coated with secreted purified alphavbeta3 (500 ng).	bind
419	2	1665	5	10	NULL	0	NULL	mAb LM-142	GP		coated with					alphavbeta3	GP	secreted;; purified 			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_4_1163_s_92	15657120	( C) mAb LM-142 was bound to protein A/G resin and coated with secreted purified alphavbeta3 (500 ng).	bind
2503	1	1665	6	10	NULL	0	NULL	mAb LM-142	GP		bind					A/G resin protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_4_1163_s_92	15657120	( C) mAb LM-142 was bound to protein A/G resin and coated with secreted purified alphavbeta3 (500 ng).	bind
2504	2	1665	6	10	NULL	0	NULL	mAb LM-142	GP		coated with					alphavbeta3	GP	secreted;;purified			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_4_1163_s_92	15657120	( C) mAb LM-142 was bound to protein A/G resin and coated with secreted purified alphavbeta3 (500 ng).	bind
420	1	1666	5	10	NULL	0	NULL	calmodulin	GP		bind					MLCK	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_5_1159_s_108	16432210	( C) Main-chain ribbon diagrams of calmodulin (yellow) bound to the target proteins myosin  light chain kinase (MLCK), SK channel, GAD, and EF (red).	bind
421	2	1666	5	10	NULL	0	NULL	MLCK	GP		is					myosin light chain kinase	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_5_1159_s_108	16432210	( C) Main-chain ribbon diagrams of calmodulin (yellow) bound to the target proteins myosin  light chain kinase (MLCK), SK channel, GAD, and EF (red).	bind
422	3	1666	5	10	NULL	0	NULL	calmodulin	GP		bind					SK channel	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_5_1159_s_108	16432210	( C) Main-chain ribbon diagrams of calmodulin (yellow) bound to the target proteins myosin  light chain kinase (MLCK), SK channel, GAD, and EF (red).	bind
423	4	1666	5	10	NULL	0	NULL	calmodulin	GP		bind					GAD	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_5_1159_s_108	16432210	( C) Main-chain ribbon diagrams of calmodulin (yellow) bound to the target proteins myosin  light chain kinase (MLCK), SK channel, GAD, and EF (red).	bind
424	5	1666	5	10	NULL	0	NULL	calmodulin	GP		bind					EF	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_5_1159_s_108	16432210	( C) Main-chain ribbon diagrams of calmodulin (yellow) bound to the target proteins myosin  light chain kinase (MLCK), SK channel, GAD, and EF (red).	bind
2505	1	1666	6	10	NULL	0	NULL	calmodulin	GP		bind to					MLCK	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_5_1159_s_108	16432210	( C) Main-chain ribbon diagrams of calmodulin (yellow) bound to the target proteins myosin  light chain kinase (MLCK), SK channel, GAD, and EF (red).	bind
2506	2	1666	6	10	NULL	0	NULL	calmodulin	GP		bind to					SK channel	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_5_1159_s_108	16432210	( C) Main-chain ribbon diagrams of calmodulin (yellow) bound to the target proteins myosin  light chain kinase (MLCK), SK channel, GAD, and EF (red).	bind
2507	3	1666	6	10	NULL	0	NULL	calmodulin	GP		bind to					GAD	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_5_1159_s_108	16432210	( C) Main-chain ribbon diagrams of calmodulin (yellow) bound to the target proteins myosin  light chain kinase (MLCK), SK channel, GAD, and EF (red).	bind
2508	4	1666	6	10	NULL	0	NULL	calmodulin	GP		bind to					EF	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_5_1159_s_108	16432210	( C) Main-chain ribbon diagrams of calmodulin (yellow) bound to the target proteins myosin  light chain kinase (MLCK), SK channel, GAD, and EF (red).	bind
45936	5	1666	6	10	NULL	0	NULL	MLCK	GP		is					myosin light chain kinase	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_5_1159_s_108	16432210	( C) Main-chain ribbon diagrams of calmodulin (yellow) bound to the target proteins myosin  light chain kinase (MLCK), SK channel, GAD, and EF (red).	bind
505	1	1667	5	10	NULL	0	NULL	Mant-GTP	GP		bind					Rac1A	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_7_1620_s_179	11285226	( C) Mant-GTP binding to Rac1A results in an increase in fluorescence.	bind
2509	1	1667	6	10	NULL	0	NULL	Mant-GTP	GP		bind to					Rac1A	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_7_1620_s_179	11285226	( C) Mant-GTP binding to Rac1A results in an increase in fluorescence.	bind
425	1	1668	5	10	NULL	0	NULL	AKIN10	GP		bind					AKIN11	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_9_5322_s_38	10220464	( C) Mapping of PRL1 domain involved in binding of AKIN10 and AKIN11.	bind
426	2	1668	5	10	NULL	0	NULL				involved in			PRL1 domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_9_5322_s_38	10220464	( C) Mapping of PRL1 domain involved in binding of AKIN10 and AKIN11.	bind
2510	1	1668	6	10	NULL	0	NULL	AKIN11	GP		bind					AKIN10	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_9_5322_s_38	10220464	( C) Mapping of PRL1 domain involved in binding of AKIN10 and AKIN11.	bind
2511	2	1668	6	10	NULL	0	NULL				is involved in			PRL1 domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_9_5322_s_38	10220464	( C) Mapping of PRL1 domain involved in binding of AKIN10 and AKIN11.	bind
427	1	1669	5	10	NULL	0	NULL	MBP - Kap114p	GP		bind					GST - histones	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6527_s_103	12456659	( C) MBP - Kap114p (200 nM) binding to GST - histones as in	bind
2512	1	1669	6	10	NULL	0	NULL	MBP - Kap114p	GP		bind					GST - histones	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6527_s_103	12456659	( C) MBP - Kap114p (200 nM) binding to GST - histones as in	bind
428	1	1670	5	10	NULL	0	NULL	P2	GP		bind					CHO cell line	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_105_6_793_s_218	10727448	( c) Mean fluorescence intensity of P2 binding to the 3 CHO cell lines.	bind
2513	1	1670	6	10	NULL	0	NULL	P2	GP		bind					CHO cell lines	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_105_6_793_s_218	10727448	( c) Mean fluorescence intensity of P2 binding to the 3 CHO cell lines.	bind
429	1	1671	5	10	NULL	0	NULL	MED-1	GP		bind					tbx-35	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_development_133_16_3097_s_106	16831832	( C) MED-1 binds the  tbx-35 promoter.	bind
2514	1	1671	6	10	NULL	0	NULL	MED-1	GP		bind					tbx-35	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_development_133_16_3097_s_106	16831832	( C) MED-1 binds the  tbx-35 promoter.	bind
430	1	1672	5	10	NULL	0	NULL	MEF2C 	GP		bind					PGC-1alpha	GP			MEF-binding site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_12_7111_s_112	12764228	( C) MEF2C binds to the MEF-binding site in the  PGC-1alpha promoter.	bind
2515	1	1672	6	10	NULL	0	NULL	MEF2C	GP		bind					PGC-1alpha	GP			MEF binding site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_12_7111_s_112	12764228	( C) MEF2C binds to the MEF-binding site in the  PGC-1alpha promoter.	bind
431	1	1673	5	10	NULL	0	NULL	PS1	GP		bind		preferentially			Nct	GP	mature			NULL	membrane fractions of HEK 293 cells	NULL	NULL	NULL	NULL	gw60_pnas_99_13_8666_s_87	12048259	( C) Membrane fractions of HEK 293 cells stably coexpressing swAPP and Nct were solubilized with CHAPS and analyzed for PS/Nct interactions as in  B. Note that PS1 preferentially binds to mature Nct. ( D) HEK 293 cells stably coexpressing swAPP, wild-type PS1, and wild-type Nct were treated with cycloheximide (100 mug/ml) for the indicated time points.	bind
2516	1	1673	6	10	NULL	0	NULL	PS1	GP		bind		preferentially			Nct	GP	mature			NULL	HEK293 cells treated with cycloheximide	NULL	NULL	NULL	NULL	gw60_pnas_99_13_8666_s_87	12048259	( C) Membrane fractions of HEK 293 cells stably coexpressing swAPP and Nct were solubilized with CHAPS and analyzed for PS/Nct interactions as in  B. Note that PS1 preferentially binds to mature Nct. ( D) HEK 293 cells stably coexpressing swAPP, wild-type PS1, and wild-type Nct were treated with cycloheximide (100 mug/ml) for the indicated time points.	bind
432	1	1674	5	10	NULL	0	NULL	trimeric MBP subunits	GP	dimer of	bind					MASP2	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_10_2348_s_220	12743029	( C) Model of a dimer of trimeric MBP subunits bound to the MASP2 model shown in	bind
2517	1	1674	6	10	NULL	0	NULL	trimeric MBP subunits	GP	dimer of	bind					MASP2	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_10_2348_s_220	12743029	( C) Model of a dimer of trimeric MBP subunits bound to the MASP2 model shown in	bind
433	1	1675	5	10	NULL	0	NULL	TF1-v1	GP		bind					theophylline	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1631_s_150	11266567	( C) Model of TF1-v1 bound to theophylline (encircled T).	bind
2518	1	1675	6	10	NULL	0	NULL	TF1-v1	GP		bind					theophylline	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1631_s_150	11266567	( C) Model of TF1-v1 bound to theophylline (encircled T).	bind
434	1	1676	5	10	NULL	0	NULL	SUMO1	GP		modify					SATB2	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3048_s_117	14701874	( C) Modification of SATB2 by SUMO1 and SUMO3.	bind
435	2	1676	5	10	NULL	0	NULL	SUMO3	GP		modify					SATB2	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3048_s_117	14701874	( C) Modification of SATB2 by SUMO1 and SUMO3.	bind
2519	1	1676	6	10	NULL	0	NULL	SUMO1	GP		modify					SATB2	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3048_s_117	14701874	( C) Modification of SATB2 by SUMO1 and SUMO3.	bind
2520	2	1676	6	10	NULL	0	NULL	SUMO3	GP		modify					SATB2	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3048_s_117	14701874	( C) Modification of SATB2 by SUMO1 and SUMO3.	bind
436	1	1677	5	10	NULL	0	NULL	GST-Src	GP		bind			 SH2		PSD-95 peptides	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_20_4971_s_206	16990796	( C) Modified ELISAs to measure binding of GST-Src SH2 to each of the PSD-95 peptides.	bind
2521	1	1677	6	10	NULL	0	NULL	GST-Src	GP		bind			SH2		PSD-95 peptides	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_20_4971_s_206	16990796	( C) Modified ELISAs to measure binding of GST-Src SH2 to each of the PSD-95 peptides.	bind
437	1	1678	5	10	NULL	0	NULL	Mre11p	GP		bind					telomere	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_19_10854_s_161	12963812	( c) Mre11p and Xrs2p binding to telomeres.	bind
438	2	1678	5	10	NULL	0	NULL	Xrs2p	GP		bind					telomere	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_19_10854_s_161	12963812	( c) Mre11p and Xrs2p binding to telomeres.	bind
2522	1	1678	6	10	NULL	0	NULL	Mre11p	GP		bind					telomere	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_19_10854_s_161	12963812	( c) Mre11p and Xrs2p binding to telomeres.	bind
2523	2	1678	6	10	NULL	0	NULL	Xrs2p	GP		bind					telomere	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_19_10854_s_161	12963812	( c) Mre11p and Xrs2p binding to telomeres.	bind
439	1	1679	5	10	NULL	0	NULL	MT	CellComponent		bind					KIF1A	GP	deletion variants			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1506_s_72	15014437	( C) MT binding of the KIF1A deletion variants.	bind
2524	1	1679	6	10	NULL	0	NULL	KIF1A	GP	deletion variants	bind					MT	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1506_s_72	15014437	( C) MT binding of the KIF1A deletion variants.	bind
440	1	1680	5	10	NULL	0	NULL	MT	CellComponent		bind					KIF1A	GP	deletions			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1506_s_42	15014437	( C) MT-binding properties of the KIF1A deletions.	bind
2525	1	1680	6	10	NULL	0	NULL	KIF1A	GP	deletions	bind					MT	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1506_s_42	15014437	( C) MT-binding properties of the KIF1A deletions.	bind
441	1	1681	5	10	NULL	0	NULL	PpPex7p	GP	mutated	does not bind					ScFox3p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_140_4_807_s_375	9472033	( C) Mutated PpPex7p fails to bind to ScFox3p  in a two-hybrid analysis.	bind
2526	1	1681	6	10	NULL	0	NULL	PpPex7p	GP	mutant	does not bind					ScFox3p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_140_4_807_s_375	9472033	( C) Mutated PpPex7p fails to bind to ScFox3p  in a two-hybrid analysis.	bind
442	1	1683	5	10	NULL	0	NULL	ZF5	GP		bind									RRS	NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_26_14991_s_141	11734633	( C) Mutations in zinc fingers 3 and 4 disrupt binding of ZF5 to the RRS.	bind
443	2	1683	5	10	NULL	0	NULL	ZF5	GP		disrupt			mutant zinc finger 3		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_26_14991_s_141	11734633	( C) Mutations in zinc fingers 3 and 4 disrupt binding of ZF5 to the RRS.	bind
444	3	1683	5	10	NULL	0	NULL	ZF5	GP		disrupt			mutant zinc finger 4		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_26_14991_s_141	11734633	( C) Mutations in zinc fingers 3 and 4 disrupt binding of ZF5 to the RRS.	bind
2527	1	1683	6	10	NULL	0	NULL	ZF5	GP		bind									RRS	NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_26_14991_s_141	11734633	( C) Mutations in zinc fingers 3 and 4 disrupt binding of ZF5 to the RRS.	bind
2528	2	1683	6	10	NULL	0	NULL	ZF5	GP		disrupt			mutant zinc finger 3		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_26_14991_s_141	11734633	( C) Mutations in zinc fingers 3 and 4 disrupt binding of ZF5 to the RRS.	bind
2529	3	1683	6	10	NULL	0	NULL	ZF5	GP		disrupt			mutant zinc finger 4		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_26_14991_s_141	11734633	( C) Mutations in zinc fingers 3 and 4 disrupt binding of ZF5 to the RRS.	bind
445	1	1684	5	10	NULL	0	NULL	SIP1	GP		bind			FS		alpha4I	GP	WT			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_199	10487759	( C) Mutations within NZF3, NZF4, CZF2 or CZF3 abolish the binding of SIP1FS to alpha4IWT.	bind
446	2	1684	5	10	NULL	0	NULL			mutant	abolish			NZF3		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_199	10487759	( C) Mutations within NZF3, NZF4, CZF2 or CZF3 abolish the binding of SIP1FS to alpha4IWT.	bind
447	3	1684	5	10	NULL	0	NULL			mutant	abolish			NZF4		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_199	10487759	( C) Mutations within NZF3, NZF4, CZF2 or CZF3 abolish the binding of SIP1FS to alpha4IWT.	bind
448	4	1684	5	10	NULL	0	NULL			mutant	abolish			CZF2		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_199	10487759	( C) Mutations within NZF3, NZF4, CZF2 or CZF3 abolish the binding of SIP1FS to alpha4IWT.	bind
450	5	1684	5	10	NULL	0	NULL			mutant	abolish			CZF3		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_199	10487759	( C) Mutations within NZF3, NZF4, CZF2 or CZF3 abolish the binding of SIP1FS to alpha4IWT.	bind
2530	1	1684	6	10	NULL	0	NULL	SIP1	GP		bind			FS		alpha4I	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_199	10487759	( C) Mutations within NZF3, NZF4, CZF2 or CZF3 abolish the binding of SIP1FS to alpha4IWT.	bind
2531	2	1684	6	10	NULL	0	NULL			mutant	abolish			NZF3		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_199	10487759	( C) Mutations within NZF3, NZF4, CZF2 or CZF3 abolish the binding of SIP1FS to alpha4IWT.	bind
2532	3	1684	6	10	NULL	0	NULL			mutant	abolish			NZF4		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_199	10487759	( C) Mutations within NZF3, NZF4, CZF2 or CZF3 abolish the binding of SIP1FS to alpha4IWT.	bind
2533	4	1684	6	10	NULL	0	NULL			mutant	abolish			CZF2		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_199	10487759	( C) Mutations within NZF3, NZF4, CZF2 or CZF3 abolish the binding of SIP1FS to alpha4IWT.	bind
2534	5	1684	6	10	NULL	0	NULL			mutant	abolish			CZF3		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5073_s_199	10487759	( C) Mutations within NZF3, NZF4, CZF2 or CZF3 abolish the binding of SIP1FS to alpha4IWT.	bind
452	1	1685	5	10	NULL	0	NULL	Siglec	GP		bind					gangliosides 	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_41527_s_256	11553646	( c) Myelin-associated glycoprotein is a Siglec (sialic acid-specific lectin) that binds to complex gangliosides, an interaction essential for maintaining normal myelin structure ( 49,  50).	bind
453	2	1685	5	10	NULL	0	NULL	Siglec	GP		is					sialic acid-specific lectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_41527_s_256	11553646	( c) Myelin-associated glycoprotein is a Siglec (sialic acid-specific lectin) that binds to complex gangliosides, an interaction essential for maintaining normal myelin structure ( 49,  50).	bind
3304	3	1685	5	10	NULL	0	NULL	statement 1	Process		maintain					myelin structure	GP	normal			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_41527_s_256	11553646	( c) Myelin-associated glycoprotein is a Siglec (sialic acid-specific lectin) that binds to complex gangliosides, an interaction essential for maintaining normal myelin structure ( 49,  50).	bind
46150	4	1685	5	10	NULL	0	NULL	Siglec	GP		is a type of					myelin-associated glycoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_41527_s_256	11553646	( c) Myelin-associated glycoprotein is a Siglec (sialic acid-specific lectin) that binds to complex gangliosides, an interaction essential for maintaining normal myelin structure ( 49,  50).	bind
2535	1	1685	6	10	NULL	0	NULL	Siglec	GP		is a type of					Myelin-associated glycoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_41527_s_256	11553646	( c) Myelin-associated glycoprotein is a Siglec (sialic acid-specific lectin) that binds to complex gangliosides, an interaction essential for maintaining normal myelin structure ( 49,  50).	bind
2536	2	1685	6	10	NULL	0	NULL	Siglec	GP		is					sialic acid-specific lectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_41527_s_256	11553646	( c) Myelin-associated glycoprotein is a Siglec (sialic acid-specific lectin) that binds to complex gangliosides, an interaction essential for maintaining normal myelin structure ( 49,  50).	bind
2537	3	1685	6	10	NULL	0	NULL	statement 1	Process		bind to					complex gangliosides	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_41527_s_256	11553646	( c) Myelin-associated glycoprotein is a Siglec (sialic acid-specific lectin) that binds to complex gangliosides, an interaction essential for maintaining normal myelin structure ( 49,  50).	bind
2538	4	1685	6	10	NULL	0	NULL	statement 3	Process		maintains					mylein structure	GP	normal			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_41527_s_256	11553646	( c) Myelin-associated glycoprotein is a Siglec (sialic acid-specific lectin) that binds to complex gangliosides, an interaction essential for maintaining normal myelin structure ( 49,  50).	bind
511	1	1687	5	10	NULL	0	NULL	Smad1	GP		bind		direct			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_541_s_107	14739937	( C) N1ICD potentiates transcriptional activity of Smad1 independent of direct binding  of Smad1 to DNA. HepG2 cells were transfected with combinations of N1ICD, Gal4, Gal4-Smad1  and Gal4-M1-Luc.	bind
512	2	1687	5	10	NULL	0	NULL	N1ICD	GP		potentiate					Smad1	GP	transcriptional activity of			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_541_s_107	14739937	( C) N1ICD potentiates transcriptional activity of Smad1 independent of direct binding  of Smad1 to DNA. HepG2 cells were transfected with combinations of N1ICD, Gal4, Gal4-Smad1  and Gal4-M1-Luc.	bind
513	3	1687	5	10	NULL	0	NULL	statement 2	Process		independent of					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_541_s_107	14739937	( C) N1ICD potentiates transcriptional activity of Smad1 independent of direct binding  of Smad1 to DNA. HepG2 cells were transfected with combinations of N1ICD, Gal4, Gal4-Smad1  and Gal4-M1-Luc.	bind
2543	1	1687	6	10	NULL	0	NULL	Smad1	GP		bind		directly			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_541_s_107	14739937	( C) N1ICD potentiates transcriptional activity of Smad1 independent of direct binding  of Smad1 to DNA. HepG2 cells were transfected with combinations of N1ICD, Gal4, Gal4-Smad1  and Gal4-M1-Luc.	bind
2544	2	1687	6	10	NULL	0	NULL	N1ICD	GP		potentiates					Smad1	GP	transcriptional activity of			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_541_s_107	14739937	( C) N1ICD potentiates transcriptional activity of Smad1 independent of direct binding  of Smad1 to DNA. HepG2 cells were transfected with combinations of N1ICD, Gal4, Gal4-Smad1  and Gal4-M1-Luc.	bind
2545	3	1687	6	10	NULL	0	NULL	statement 2	Process		is independent of					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_541_s_107	14739937	( C) N1ICD potentiates transcriptional activity of Smad1 independent of direct binding  of Smad1 to DNA. HepG2 cells were transfected with combinations of N1ICD, Gal4, Gal4-Smad1  and Gal4-M1-Luc.	bind
514	1	1688	5	10	NULL	0	NULL	Nef	GP		bind					cholesterol	Chemical				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_100_14_8460_s_206	12824470	( c) Nef binds cholesterol  in vitro.	bind
2546	1	1688	6	10	NULL	0	NULL	Nef	GP		bind					cholesterol	Chemical				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_100_14_8460_s_206	12824470	( c) Nef binds cholesterol  in vitro.	bind
515	1	1689	5	10	NULL	0	NULL	2G12 IgG1	GP		bind					SOS gp 140	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5628_2065_s_82	12829775	( C) Negative -stain electron microscopy of unbound b12 IgG1 (top row), unbound 2G12 IgG1 (middle row), and 2G12 IgG1 bound to SOS gp 140 [bottom row (  34)] shows that the 2G12 IgG1 (bound and unbound) adopts an unusual linear shape as opposed to a classic Y shape such as that of b12.	bind
3305	2	1689	5	10	NULL	0	NULL	2G12 IgG1	GP	unbound	adopt					linear shape		unusual			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5628_2065_s_82	12829775	( C) Negative -stain electron microscopy of unbound b12 IgG1 (top row), unbound 2G12 IgG1 (middle row), and 2G12 IgG1 bound to SOS gp 140 [bottom row (  34)] shows that the 2G12 IgG1 (bound and unbound) adopts an unusual linear shape as opposed to a classic Y shape such as that of b12.	bind
3306	3	1689	5	10	NULL	0	NULL	2G12 IgG1	GP	bound	adopt					linear shape		unusual			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5628_2065_s_82	12829775	( C) Negative -stain electron microscopy of unbound b12 IgG1 (top row), unbound 2G12 IgG1 (middle row), and 2G12 IgG1 bound to SOS gp 140 [bottom row (  34)] shows that the 2G12 IgG1 (bound and unbound) adopts an unusual linear shape as opposed to a classic Y shape such as that of b12.	bind
3307	4	1689	5	10	NULL	0	NULL	b12	GP		adopt					Y shape		classic			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5628_2065_s_82	12829775	( C) Negative -stain electron microscopy of unbound b12 IgG1 (top row), unbound 2G12 IgG1 (middle row), and 2G12 IgG1 bound to SOS gp 140 [bottom row (  34)] shows that the 2G12 IgG1 (bound and unbound) adopts an unusual linear shape as opposed to a classic Y shape such as that of b12.	bind
2549	1	1689	6	10	NULL	0	NULL	2G12 IgG1	GP		bind					SOS gp 140	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5628_2065_s_82	12829775	( C) Negative -stain electron microscopy of unbound b12 IgG1 (top row), unbound 2G12 IgG1 (middle row), and 2G12 IgG1 bound to SOS gp 140 [bottom row (  34)] shows that the 2G12 IgG1 (bound and unbound) adopts an unusual linear shape as opposed to a classic Y shape such as that of b12.	bind
2550	2	1689	6	10	NULL	0	NULL	2G12 IgG1	GP	unbound	adopts					linear shape		unusual			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5628_2065_s_82	12829775	( C) Negative -stain electron microscopy of unbound b12 IgG1 (top row), unbound 2G12 IgG1 (middle row), and 2G12 IgG1 bound to SOS gp 140 [bottom row (  34)] shows that the 2G12 IgG1 (bound and unbound) adopts an unusual linear shape as opposed to a classic Y shape such as that of b12.	bind
2551	3	1689	6	10	NULL	0	NULL	2G12 IgG1	GP	bound	adopts					linear shape		unusual			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5628_2065_s_82	12829775	( C) Negative -stain electron microscopy of unbound b12 IgG1 (top row), unbound 2G12 IgG1 (middle row), and 2G12 IgG1 bound to SOS gp 140 [bottom row (  34)] shows that the 2G12 IgG1 (bound and unbound) adopts an unusual linear shape as opposed to a classic Y shape such as that of b12.	bind
2552	4	1689	6	10	NULL	0	NULL	b12	GP		adopts					Y shape		classic			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5628_2065_s_82	12829775	( C) Negative -stain electron microscopy of unbound b12 IgG1 (top row), unbound 2G12 IgG1 (middle row), and 2G12 IgG1 bound to SOS gp 140 [bottom row (  34)] shows that the 2G12 IgG1 (bound and unbound) adopts an unusual linear shape as opposed to a classic Y shape such as that of b12.	bind
516	1	1690	5	10	NULL	0	NULL	p300	GP		bind					Nur77	GP	minimal		MEF2-responsive element in promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4323_s_94	10944115	( C) NFATp enhances p300 binding to the minimal MEF2-responsive element on the Nur77 promoter.	bind
517	2	1690	5	10	NULL	0	NULL	NFATp	GP		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4323_s_94	10944115	( C) NFATp enhances p300 binding to the minimal MEF2-responsive element on the Nur77 promoter.	bind
2553	1	1690	6	10	NULL	0	NULL	p300	GP		bind					Nur77	GP	minimal		MEF2-responsive element of the promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4323_s_94	10944115	( C) NFATp enhances p300 binding to the minimal MEF2-responsive element on the Nur77 promoter.	bind
2554	2	1690	6	10	NULL	0	NULL	NFATp	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4323_s_94	10944115	( C) NFATp enhances p300 binding to the minimal MEF2-responsive element on the Nur77 promoter.	bind
518	1	1691	5	10	NULL	0	NULL				does not bind			AP-2 subunits		GST - synaptobrevin/VAMP	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_22_6011_s_43	11080148	( C) None of the AP-2 subunits can bind to GST - synaptobrevin/VAMP.	bind
2555	1	1691	6	10	NULL	0	NULL				does not bind			AP-2 subunits		GST - synaptobrevin/VAMP	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_22_6011_s_43	11080148	( C) None of the AP-2 subunits can bind to GST - synaptobrevin/VAMP.	bind
519	1	1692	5	10	NULL	0	NULL	SMX	Chemical		bind		direct			MHC-peptide complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1591_s_201	9788973	( C) Nonreactive drugs such as SMX or  lidocaine bind directly to the MHC-peptide complex (noncovalent, processing-independent pathway).	bind
520	2	1692	5	10	NULL	0	NULL	lidocaine	Chemical		bind		direct			MHC-peptide complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1591_s_201	9788973	( C) Nonreactive drugs such as SMX or  lidocaine bind directly to the MHC-peptide complex (noncovalent, processing-independent pathway).	bind
46151	3	1692	5	10	NULL	0	NULL	SMX	Chemical		is a type of					nonreactive drug	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1591_s_201	9788973	( C) Nonreactive drugs such as SMX or  lidocaine bind directly to the MHC-peptide complex (noncovalent, processing-independent pathway).	bind
46152	4	1692	5	10	NULL	0	NULL	lidocaine	Chemical		is a type of					nonreactive drug	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1591_s_201	9788973	( C) Nonreactive drugs such as SMX or  lidocaine bind directly to the MHC-peptide complex (noncovalent, processing-independent pathway).	bind
2556	1	1692	6	10	NULL	0	NULL	SMX	Chemical		bind		directly			MHC-peptide complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1591_s_201	9788973	( C) Nonreactive drugs such as SMX or  lidocaine bind directly to the MHC-peptide complex (noncovalent, processing-independent pathway).	bind
2557	2	1692	6	10	NULL	0	NULL	lidocaine	Chemical		bind		directly			MHC-peptide complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1591_s_201	9788973	( C) Nonreactive drugs such as SMX or  lidocaine bind directly to the MHC-peptide complex (noncovalent, processing-independent pathway).	bind
46169	3	1692	6	10	NULL	0	NULL	SMX	Chemical		is a type of					nonreactive drug	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1591_s_201	9788973	( C) Nonreactive drugs such as SMX or  lidocaine bind directly to the MHC-peptide complex (noncovalent, processing-independent pathway).	bind
46170	4	1692	6	10	NULL	0	NULL	lidocaine	Chemical		is a type of					nonreactive drug	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1591_s_201	9788973	( C) Nonreactive drugs such as SMX or  lidocaine bind directly to the MHC-peptide complex (noncovalent, processing-independent pathway).	bind
521	1	1693	5	10	NULL	0	NULL	Akt	GP	nuclear	bind		selectively			Ebp1	GP				NULL	PC12 cells	NULL	NULL	NULL	NULL	gw70_embo_25_10_2083_s_257	16642037	( C) Nuclear but not plasma membrane Akt selectively binds to Ebp1 wild type and S360D  mutant in PC12 cells.	bind
522	2	1693	5	10	NULL	0	NULL	Akt	GP	plasma membrane	does not bind		selectively			Ebp1	GP	wild type			NULL	PC12 cells	NULL	NULL	NULL	NULL	gw70_embo_25_10_2083_s_257	16642037	( C) Nuclear but not plasma membrane Akt selectively binds to Ebp1 wild type and S360D  mutant in PC12 cells.	bind
523	3	1693	5	10	NULL	0	NULL	Akt	GP	nuclear	bind		selectively			Ebp1	GP	mutant		S360D	NULL	PC12 cells	NULL	NULL	NULL	NULL	gw70_embo_25_10_2083_s_257	16642037	( C) Nuclear but not plasma membrane Akt selectively binds to Ebp1 wild type and S360D  mutant in PC12 cells.	bind
524	4	1693	5	10	NULL	0	NULL	Akt	GP	plasma membrane	does not bind		selectively			Ebp1	GP	mutant		S360D	NULL	PC12 cells	NULL	NULL	NULL	NULL	gw70_embo_25_10_2083_s_257	16642037	( C) Nuclear but not plasma membrane Akt selectively binds to Ebp1 wild type and S360D  mutant in PC12 cells.	bind
2558	1	1693	6	10	NULL	0	NULL	Akt	GP	nuclear	bind		selectively			Ebp1	GP	wild type			NULL	PC12 cells	NULL	NULL	NULL	NULL	gw70_embo_25_10_2083_s_257	16642037	( C) Nuclear but not plasma membrane Akt selectively binds to Ebp1 wild type and S360D  mutant in PC12 cells.	bind
2559	2	1693	6	10	NULL	0	NULL	Akt	GP	nuclear	bind		selectively			Ebp1	GP		S360D mutant		NULL	PC12 cells	NULL	NULL	NULL	NULL	gw70_embo_25_10_2083_s_257	16642037	( C) Nuclear but not plasma membrane Akt selectively binds to Ebp1 wild type and S360D  mutant in PC12 cells.	bind
2560	3	1693	6	10	NULL	0	NULL	Akt	GP	plasma membrane	does not bind					Ebp1	GP	wild type			NULL	PC12 cells	NULL	NULL	NULL	NULL	gw70_embo_25_10_2083_s_257	16642037	( C) Nuclear but not plasma membrane Akt selectively binds to Ebp1 wild type and S360D  mutant in PC12 cells.	bind
3229	4	1693	6	10	NULL	0	NULL	Akt	GP	plasma membrane	does not bind					Ebp1	GP		mutant S360D		NULL	PC12 cells	NULL	NULL	NULL	NULL	gw70_embo_25_10_2083_s_257	16642037	( C) Nuclear but not plasma membrane Akt selectively binds to Ebp1 wild type and S360D  mutant in PC12 cells.	bind
525	1	1695	5	10	NULL	0	NULL	Oct-2	GP		bind		specifically			CD36 octamer	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_8_1767_s_136	11937630	( C) Oct-2 specifically binds to the CD36 octamer.	bind
2562	1	1695	6	10	NULL	0	NULL	Oct-2	GP		bind		specifically			CD36 octamer	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_8_1767_s_136	11937630	( C) Oct-2 specifically binds to the CD36 octamer.	bind
526	1	1696	5	10	NULL	0	NULL	Olig2	GP		bind					 oligonucleotide	NucleicAcid			M100A	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_2_282_s_179	15655114	( C) Olig2 binds to the M100A oligonucleotide, whereas the Olig2 DNA-binding mutant Olig2-AQ  lacks this activity.	bind
527	2	1696	5	10	NULL	0	NULL	Olig2-AQ	GP	 mutant	does not bind					 oligonucleotide	NucleicAcid			M100A	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_2_282_s_179	15655114	( C) Olig2 binds to the M100A oligonucleotide, whereas the Olig2 DNA-binding mutant Olig2-AQ  lacks this activity.	bind
46269	3	1696	5	10	NULL	0	NULL	Olig2-AQ	GP		is a type of					Olig2 DNA-binding mutant 	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_2_282_s_179	15655114	( C) Olig2 binds to the M100A oligonucleotide, whereas the Olig2 DNA-binding mutant Olig2-AQ  lacks this activity.	bind
2563	1	1696	6	10	NULL	0	NULL	Olig2	GP		bind					 oligonucleotide	NucleicAcid			M100A	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_2_282_s_179	15655114	( C) Olig2 binds to the M100A oligonucleotide, whereas the Olig2 DNA-binding mutant Olig2-AQ  lacks this activity.	bind
2564	2	1696	6	10	NULL	0	NULL	Olig2-AQ	GP	mutant	does not bind					 oligonucleotide	NucleicAcid			M100A	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_2_282_s_179	15655114	( C) Olig2 binds to the M100A oligonucleotide, whereas the Olig2 DNA-binding mutant Olig2-AQ  lacks this activity.	bind
46268	3	1696	6	10	NULL	0	NULL	Olig2-AQ	GP		is a type of					Olig2 DNA binding mutant	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_2_282_s_179	15655114	( C) Olig2 binds to the M100A oligonucleotide, whereas the Olig2 DNA-binding mutant Olig2-AQ  lacks this activity.	bind
528	1	1697	5	10	NULL	0	NULL	ZONAB	GP		bind			CSD		RalA	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_1_54_s_52	15592429	( C) Only the ZONAB CSD binds RalA in a GTP-dependent manner.	bind
562	2	1697	5	10	NULL	0	NULL	statement 1	Process		dependent on					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_1_54_s_52	15592429	( C) Only the ZONAB CSD binds RalA in a GTP-dependent manner.	bind
2565	1	1697	6	10	NULL	0	NULL	ZONAB	GP		bind			CSD		RalA	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_1_54_s_52	15592429	( C) Only the ZONAB CSD binds RalA in a GTP-dependent manner.	bind
2566	2	1697	6	10	NULL	0	NULL	statement 1	Process		dependent on					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_1_54_s_52	15592429	( C) Only the ZONAB CSD binds RalA in a GTP-dependent manner.	bind
529	1	1698	5	10	NULL	0	NULL	Ins(1,4,5)P3	Chemical		bind					3G ARNO	GP		PH domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_19_3711_s_135	15359279	( C) Overlay of Ins(1,4,5)P3 bound to the 3G ARNO PH domain with the electron density corresponding to inorganic  sulfate ions from the unliganded 3G Grp1 PH domain following superposition of Calpha atoms.	bind
2567	1	1698	6	10	NULL	0	NULL	Ins(1,4,5)P3	Chemical		bind					3G ARNO	GP		PH domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_19_3711_s_135	15359279	( C) Overlay of Ins(1,4,5)P3 bound to the 3G ARNO PH domain with the electron density corresponding to inorganic  sulfate ions from the unliganded 3G Grp1 PH domain following superposition of Calpha atoms.	bind
530	1	1699	5	10	NULL	0	NULL	G-switch RNA	NucleicAcid	15N-labeled	bind					guanine	Chemical	unlabeled			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1372_s_34	15665103	( C) Overlay of the imino regions of 1H, 15N-HSQC spectra of the uniformly 15N-labeled G-switch RNA in its free form (black) and bound to unlabeled guanine (red)  at 283 K. ( D) Imino region of an 1H, 15N-HSQC spectrum of 15N-labeled guanine bound to only cytidine-13C, 15N-labeled G-switch RNA.	bind
531	2	1699	5	10	NULL	0	NULL	guanine	Chemical	15N-labeled	bind					cytidine-13C	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1372_s_34	15665103	( C) Overlay of the imino regions of 1H, 15N-HSQC spectra of the uniformly 15N-labeled G-switch RNA in its free form (black) and bound to unlabeled guanine (red)  at 283 K. ( D) Imino region of an 1H, 15N-HSQC spectrum of 15N-labeled guanine bound to only cytidine-13C, 15N-labeled G-switch RNA.	bind
46271	3	1699	5	10	NULL	0	NULL	guanine	Chemical	15N-labeled	bind					G-switch RNA	NucleicAcid	15N-labeled			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1372_s_34	15665103	( C) Overlay of the imino regions of 1H, 15N-HSQC spectra of the uniformly 15N-labeled G-switch RNA in its free form (black) and bound to unlabeled guanine (red)  at 283 K. ( D) Imino region of an 1H, 15N-HSQC spectrum of 15N-labeled guanine bound to only cytidine-13C, 15N-labeled G-switch RNA.	bind
3003	1	1699	6	10	NULL	0	NULL	G-switch RNA	NucleicAcid	15N-labeled	bind					guanine	Chemical	unlabeled			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1372_s_34	15665103	( C) Overlay of the imino regions of 1H, 15N-HSQC spectra of the uniformly 15N-labeled G-switch RNA in its free form (black) and bound to unlabeled guanine (red)  at 283 K. ( D) Imino region of an 1H, 15N-HSQC spectrum of 15N-labeled guanine bound to only cytidine-13C, 15N-labeled G-switch RNA.	bind
3004	2	1699	6	10	NULL	0	NULL	guanine 	Chemical	15N-labeled	bind					cytidine-13C	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1372_s_34	15665103	( C) Overlay of the imino regions of 1H, 15N-HSQC spectra of the uniformly 15N-labeled G-switch RNA in its free form (black) and bound to unlabeled guanine (red)  at 283 K. ( D) Imino region of an 1H, 15N-HSQC spectrum of 15N-labeled guanine bound to only cytidine-13C, 15N-labeled G-switch RNA.	bind
46270	3	1699	6	10	NULL	0	NULL	guanine	Chemical	15N-labeled	bind					G-switch RNA	NucleicAcid	15N-labeled			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_5_1372_s_34	15665103	( C) Overlay of the imino regions of 1H, 15N-HSQC spectra of the uniformly 15N-labeled G-switch RNA in its free form (black) and bound to unlabeled guanine (red)  at 283 K. ( D) Imino region of an 1H, 15N-HSQC spectrum of 15N-labeled guanine bound to only cytidine-13C, 15N-labeled G-switch RNA.	bind
532	1	1700	5	10	NULL	0	NULL	p185	GP		bind					SKP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_17_9855_s_151	12904573	( C) p185 binds to SKP1  in an FBW6-dependent manner.	bind
533	2	1700	5	10	NULL	0	NULL	statement 1	Process		dependent on					FBW6	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_17_9855_s_151	12904573	( C) p185 binds to SKP1  in an FBW6-dependent manner.	bind
2632	1	1700	6	10	NULL	0	NULL	p185	GP		bind					SKP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_17_9855_s_151	12904573	( C) p185 binds to SKP1  in an FBW6-dependent manner.	bind
2633	2	1700	6	10	NULL	0	NULL	statement 1	Process		is dependent on					FBW6	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_17_9855_s_151	12904573	( C) p185 binds to SKP1  in an FBW6-dependent manner.	bind
563	1	1701	5	10	NULL	0	NULL	p53	GP		bind					DNA	NucleicAcid				NULL	chimeric embryo brain extracts	NULL	NULL	NULL	NULL	gw60_embo_20_13_3402_s_156	11432828	( C) p53 gel shift analysis on chimeric embryo brain extracts demonstrates that p53 DNA binding activity correlates with the degree of  Rb - / -  chimerism.	bind
564	2	1701	5	10	NULL	0	NULL	statement 1	Process		correlates with					Rb - / - chimerism	Process	degree of			NULL	chimeric embryo brain extracts	NULL	NULL	NULL	NULL	gw60_embo_20_13_3402_s_156	11432828	( C) p53 gel shift analysis on chimeric embryo brain extracts demonstrates that p53 DNA binding activity correlates with the degree of  Rb - / -  chimerism.	bind
2634	1	1701	6	10	NULL	0	NULL	p53	GP		bind					DNA	NucleicAcid			site	NULL	chimeric embryo brain extracts	NULL	NULL	NULL	NULL	gw60_embo_20_13_3402_s_156	11432828	( C) p53 gel shift analysis on chimeric embryo brain extracts demonstrates that p53 DNA binding activity correlates with the degree of  Rb - / -  chimerism.	bind
2635	2	1701	6	10	NULL	0	NULL	statement 1	Process		correlates with 					Rb - / - chimerism	Process	degree of			NULL	chimeric embryo brain extracts	NULL	NULL	NULL	NULL	gw60_embo_20_13_3402_s_156	11432828	( C) p53 gel shift analysis on chimeric embryo brain extracts demonstrates that p53 DNA binding activity correlates with the degree of  Rb - / -  chimerism.	bind
565	1	1702	5	10	NULL	0	NULL	T3 	GP		bind					TRbeta	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5197_s_40	16549781	( C) Percentage increase in KCNH2 current in the presence of 3 muM 1-850, an antagonist  of T3 binding to TRbeta, or after overnight transfection with mutant TRbeta receptors.	bind
2636	1	1702	6	10	NULL	0	NULL	T3	GP		bind					TRbeta	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5197_s_40	16549781	( C) Percentage increase in KCNH2 current in the presence of 3 muM 1-850, an antagonist  of T3 binding to TRbeta, or after overnight transfection with mutant TRbeta receptors.	bind
566	1	1703	5	10	NULL	0	NULL	SUMO	GP		conjugate					SATB2	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3048_s_155	14701874	( C) PIAS1 stimulates SUMO conjugation to SATB2 in vivo.	bind
567	2	1703	5	10	NULL	0	NULL	PIAS1	GP		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3048_s_155	14701874	( C) PIAS1 stimulates SUMO conjugation to SATB2 in vivo.	bind
2637	1	1703	6	10	NULL	0	NULL	SUMO	GP		conjugates					SATB2	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3048_s_155	14701874	( C) PIAS1 stimulates SUMO conjugation to SATB2 in vivo.	bind
2638	2	1703	6	10	NULL	0	NULL	PIAS1	GP		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3048_s_155	14701874	( C) PIAS1 stimulates SUMO conjugation to SATB2 in vivo.	bind
568	1	1704	5	10	NULL	0	NULL	PIF3	GP		bind					G-wt probe	GP	labeled 			NULL		NULL	NULL	NULL	NULL	gw60_science_288_5467_859_s_98	10797009	( C) PIF3 binding to labeled G-wt probe is competed only by the LRE that contains a G-box ( 47).	bind
569	2	1704	5	10	NULL	0	NULL				bind				LRE G-box	G-wt probe	GP	labeled 			NULL		NULL	NULL	NULL	NULL	gw60_science_288_5467_859_s_98	10797009	( C) PIF3 binding to labeled G-wt probe is competed only by the LRE that contains a G-box ( 47).	bind
3308	3	1704	5	10	NULL	0	NULL	statement 1	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_288_5467_859_s_98	10797009	( C) PIF3 binding to labeled G-wt probe is competed only by the LRE that contains a G-box ( 47).	bind
2639	1	1704	6	10	NULL	0	NULL	PIF3	GP		bind					G-wt probe	GP	labeled			NULL		NULL	NULL	NULL	NULL	gw60_science_288_5467_859_s_98	10797009	( C) PIF3 binding to labeled G-wt probe is competed only by the LRE that contains a G-box ( 47).	bind
2640	2	1704	6	10	NULL	0	NULL				bind				LRE G-box	G-wt probe	GP	labeled			NULL		NULL	NULL	NULL	NULL	gw60_science_288_5467_859_s_98	10797009	( C) PIF3 binding to labeled G-wt probe is competed only by the LRE that contains a G-box ( 47).	bind
3236	3	1704	6	10	NULL	0	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_288_5467_859_s_98	10797009	( C) PIF3 binding to labeled G-wt probe is competed only by the LRE that contains a G-box ( 47).	bind
570	1	1705	5	10	NULL	0	NULL	PIP2	GP		bind					BAF complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_5_2824_s_90	11880634	( C) PIP2 binding by the BAF complex requires Brg, actin, and BAF53.	bind
571	2	1705	5	10	NULL	0	NULL	statement 1	Process		require					Brg	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_5_2824_s_90	11880634	( C) PIP2 binding by the BAF complex requires Brg, actin, and BAF53.	bind
572	3	1705	5	10	NULL	0	NULL	statement 1	Process		require					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_5_2824_s_90	11880634	( C) PIP2 binding by the BAF complex requires Brg, actin, and BAF53.	bind
573	4	1705	5	10	NULL	0	NULL	statement 1	Process		require					BAF53	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_5_2824_s_90	11880634	( C) PIP2 binding by the BAF complex requires Brg, actin, and BAF53.	bind
2641	1	1705	6	10	NULL	0	NULL	PIP2	GP		bind					BAF complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_5_2824_s_90	11880634	( C) PIP2 binding by the BAF complex requires Brg, actin, and BAF53.	bind
2642	2	1705	6	10	NULL	0	NULL	statement 1	Process		requires					Brg	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_5_2824_s_90	11880634	( C) PIP2 binding by the BAF complex requires Brg, actin, and BAF53.	bind
2643	3	1705	6	10	NULL	0	NULL	statement 1	Process		requires					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_5_2824_s_90	11880634	( C) PIP2 binding by the BAF complex requires Brg, actin, and BAF53.	bind
2644	4	1705	6	10	NULL	0	NULL	statement 1	Process		requires					BAF53	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_5_2824_s_90	11880634	( C) PIP2 binding by the BAF complex requires Brg, actin, and BAF53.	bind
574	1	1707	5	10	NULL	0	NULL	hTAFII130	GP		bind					HP1gamma	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_9_5919_s_125	11959914	( C) Point mutations in the HP1 box compromised hTAFII130 binding to HP1gamma.	bind
575	2	1707	5	10	NULL	0	NULL			point mutations	compromise			HP1 box		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_9_5919_s_125	11959914	( C) Point mutations in the HP1 box compromised hTAFII130 binding to HP1gamma.	bind
2645	1	1707	6	10	NULL	0	NULL	hTAFII130	GP		bind					HP1gamma	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_9_5919_s_125	11959914	( C) Point mutations in the HP1 box compromised hTAFII130 binding to HP1gamma.	bind
2646	2	1707	6	10	NULL	0	NULL			mutant	compromise			HP1 box		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_9_5919_s_125	11959914	( C) Point mutations in the HP1 box compromised hTAFII130 binding to HP1gamma.	bind
576	1	1708	5	10	NULL	0	NULL	PPAR	GP		bind									PPREs	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_embo_23_10_2083_s_115	15103326	( C) PPAR and RXR binding to PPREs  in vivo.	bind
577	2	1708	5	10	NULL	0	NULL	RXR	GP		bind									PPREs	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_embo_23_10_2083_s_115	15103326	( C) PPAR and RXR binding to PPREs  in vivo.	bind
2647	1	1708	6	10	NULL	0	NULL	PPAR	GP		bind									PPRE	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_embo_23_10_2083_s_115	15103326	( C) PPAR and RXR binding to PPREs  in vivo.	bind
2648	2	1708	6	10	NULL	0	NULL	RXR	GP		bind									PPRE	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_embo_23_10_2083_s_115	15103326	( C) PPAR and RXR binding to PPREs  in vivo.	bind
578	1	1709	5	10	NULL	0	NULL	pol	GP		bind		preferentially			PCNA	GP	monoubiquitinated			NULL	living cells	NULL	NULL	NULL	NULL	gw70_embo_23_19_3886_s_219	15359278	( C) Preferential binding of pol  to monoubiquitinated PCNA in living cells.	bind
2649	1	1709	6	10	NULL	0	NULL	Pol	GP		bind		preferentially			PCNA	GP	monoubiquitinated			NULL	living cells	NULL	NULL	NULL	NULL	gw70_embo_23_19_3886_s_219	15359278	( C) Preferential binding of pol  to monoubiquitinated PCNA in living cells.	bind
579	1	1710	5	10	NULL	0	NULL	protamine	Chemical		bind		preferentially							SAR	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_20_6111_s_136	15562002	( C) Preferential binding of protamine to the SAR.	bind
2650	1	1710	6	10	NULL	0	NULL	protamine	Chemical		bind		preferentially							SAR	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_20_6111_s_136	15562002	( C) Preferential binding of protamine to the SAR.	bind
580	1	1711	5	10	NULL	0	NULL	C4bp	GP	primate	bind					MS11	GP	Por1B strain			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_47_17142_s_174	16275906	( C) Primate C4bp binding to Por1B strains MS11 and FA1090.	bind
581	2	1711	5	10	NULL	0	NULL	C4bp	GP	primate	bind					FA1090	GP	Por1B strain			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_47_17142_s_174	16275906	( C) Primate C4bp binding to Por1B strains MS11 and FA1090.	bind
2651	2	1711	6	10	NULL	0	NULL	C4bp	GP	primate	bind					MS11	GP	Por1B strain			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_47_17142_s_174	16275906	( C) Primate C4bp binding to Por1B strains MS11 and FA1090.	bind
2652	1	1711	6	10	NULL	0	NULL	C4bp	GP	primate	bind					FA1090	GP	Por1B strain			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_47_17142_s_174	16275906	( C) Primate C4bp binding to Por1B strains MS11 and FA1090.	bind
582	1	1712	5	10	NULL	0	NULL	T-Taxol	Chemical		bind					beta-TB	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_9_5312_s_69	11309480	( c) Proposed T-Taxol conformation bound to beta-TB.	bind
2653	1	1712	6	10	NULL	0	NULL	T-Taxol	Chemical		bind					beta-TB	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_9_5312_s_69	11309480	( c) Proposed T-Taxol conformation bound to beta-TB.	bind
583	1	1713	5	10	NULL	0	NULL	ADP-ribose	Chemical		bind							yeast	macro domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_11_1911_s_173	15902274	( C) Pulldown assays for the binding of ADP-ribose to yeast and human  macro domains.	bind
584	2	1713	5	10	NULL	0	NULL	ADP-ribose	Chemical		bind							human	macro domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_11_1911_s_173	15902274	( C) Pulldown assays for the binding of ADP-ribose to yeast and human  macro domains.	bind
2654	1	1713	6	10	NULL	0	NULL	ADP-ribose	Chemical		bind							yeast	macro domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_11_1911_s_173	15902274	( C) Pulldown assays for the binding of ADP-ribose to yeast and human  macro domains.	bind
2655	2	1713	6	10	NULL	0	NULL	ADP-ribose	Chemical		bind							human	macro domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_11_1911_s_173	15902274	( C) Pulldown assays for the binding of ADP-ribose to yeast and human  macro domains.	bind
585	1	1714	5	10	NULL	0	NULL	NF-kappaB protein	GP	purified;; recombinant	bind					NF-kappaB oligo	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8638_s_160	11438703	( C) Purified recombinant NF-kappaB protein binds to a consensus NF-kappaB oligo, but not to the  5.2 kb or to a consensus Stat 1 (hSIE) element.	bind
586	2	1714	5	10	NULL	0	NULL	NF-kappaB protein	GP	purified;; recombinant	does not bind									hSIE	NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8638_s_160	11438703	( C) Purified recombinant NF-kappaB protein binds to a consensus NF-kappaB oligo, but not to the  5.2 kb or to a consensus Stat 1 (hSIE) element.	bind
587	3	1714	5	10	NULL	0	NULL	hSIE	GP		is					Stat 1 element	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8638_s_160	11438703	( C) Purified recombinant NF-kappaB protein binds to a consensus NF-kappaB oligo, but not to the  5.2 kb or to a consensus Stat 1 (hSIE) element.	bind
2656	1	1714	6	10	NULL	0	NULL	NF-kappaB	GP	purified;;recombinant	bind					NF-kappaB oligo	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8638_s_160	11438703	( C) Purified recombinant NF-kappaB protein binds to a consensus NF-kappaB oligo, but not to the  5.2 kb or to a consensus Stat 1 (hSIE) element.	bind
2657	2	1714	6	10	NULL	0	NULL	NF-kappaB	GP	purified;;recombinant	does not bind									consensus hSIE element	NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8638_s_160	11438703	( C) Purified recombinant NF-kappaB protein binds to a consensus NF-kappaB oligo, but not to the  5.2 kb or to a consensus Stat 1 (hSIE) element.	bind
46097	3	1714	6	10	NULL	0	NULL	hSIE	GP		is					Stat 1 element	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8638_s_160	11438703	( C) Purified recombinant NF-kappaB protein binds to a consensus NF-kappaB oligo, but not to the  5.2 kb or to a consensus Stat 1 (hSIE) element.	bind
588	1	1715	5	10	NULL	0	NULL	SRP54	GP	purified;; radiolabeled	bind					RNC-pPL86	GP	wheat germ			NULL		NULL	NULL	NULL	NULL	gw60_science_297_5585_1345_s_46	12193787	( C) Purified, radiolabeled SRP54 bound to wheat germ RNC-pPL86 or RNC-pPL86-mut was cross-linked with DSS and the reactions were analyzed by SDS-PAGE and phosphorimaging.	bind
589	2	1715	5	10	NULL	0	NULL	SRP54	GP	purified;; radiolabeled	bind					RNC-pPL86	GP	mut			NULL		NULL	NULL	NULL	NULL	gw60_science_297_5585_1345_s_46	12193787	( C) Purified, radiolabeled SRP54 bound to wheat germ RNC-pPL86 or RNC-pPL86-mut was cross-linked with DSS and the reactions were analyzed by SDS-PAGE and phosphorimaging.	bind
46099	3	1715	5	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_297_5585_1345_s_46	12193787	( C) Purified, radiolabeled SRP54 bound to wheat germ RNC-pPL86 or RNC-pPL86-mut was cross-linked with DSS and the reactions were analyzed by SDS-PAGE and phosphorimaging.	bind
2658	1	1715	6	10	NULL	0	NULL	SRP54	GP	purified;; radiolabeled	bind					RNC-pPL86	GP	wheat germ			NULL		NULL	NULL	NULL	NULL	gw60_science_297_5585_1345_s_46	12193787	( C) Purified, radiolabeled SRP54 bound to wheat germ RNC-pPL86 or RNC-pPL86-mut was cross-linked with DSS and the reactions were analyzed by SDS-PAGE and phosphorimaging.	bind
2659	2	1715	6	10	NULL	0	NULL	SRP54	GP	purified;; radiolabeled	bind					RNC-pPL86	GP	mutant 			NULL		NULL	NULL	NULL	NULL	gw60_science_297_5585_1345_s_46	12193787	( C) Purified, radiolabeled SRP54 bound to wheat germ RNC-pPL86 or RNC-pPL86-mut was cross-linked with DSS and the reactions were analyzed by SDS-PAGE and phosphorimaging.	bind
46101	3	1715	6	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_297_5585_1345_s_46	12193787	( C) Purified, radiolabeled SRP54 bound to wheat germ RNC-pPL86 or RNC-pPL86-mut was cross-linked with DSS and the reactions were analyzed by SDS-PAGE and phosphorimaging.	bind
590	1	1717	5	10	NULL	0	NULL	FGF2	GP		bind					FGFR1c-AP 	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_14_4833_s_175	15051888	( C) Quantification of FGF2 bound to FGFR1c-AP in the presence of QSulf1- or QSulf1(C-A)-treated  heparin.	bind
3117	2	1717	5	10	NULL	0	NULL	heparin	Chemical		treated with					QSulf1	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_14_4833_s_175	15051888	( C) Quantification of FGF2 bound to FGFR1c-AP in the presence of QSulf1- or QSulf1(C-A)-treated  heparin.	bind
3118	3	1717	5	10	NULL	0	NULL	heparin	Chemical		treated with					QSulf1(C-A)	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_14_4833_s_175	15051888	( C) Quantification of FGF2 bound to FGFR1c-AP in the presence of QSulf1- or QSulf1(C-A)-treated  heparin.	bind
46102	6	1717	5	10	NULL	0	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_14_4833_s_175	15051888	( C) Quantification of FGF2 bound to FGFR1c-AP in the presence of QSulf1- or QSulf1(C-A)-treated  heparin.	bind
52891	4	1717	5	10	NULL	0	NULL	statement 1	Process		in presence of					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_14_4833_s_175	15051888	( C) Quantification of FGF2 bound to FGFR1c-AP in the presence of QSulf1- or QSulf1(C-A)-treated  heparin.	bind
52892	5	1717	5	10	NULL	0	NULL	statement 1	Process		in presence of					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_14_4833_s_175	15051888	( C) Quantification of FGF2 bound to FGFR1c-AP in the presence of QSulf1- or QSulf1(C-A)-treated  heparin.	bind
2662	1	1717	6	10	NULL	0	NULL	FGF2	GP		bind					FGFR1c-AP	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_14_4833_s_175	15051888	( C) Quantification of FGF2 bound to FGFR1c-AP in the presence of QSulf1- or QSulf1(C-A)-treated  heparin.	bind
2663	2	1717	6	10	NULL	0	NULL	heparin	Chemical		treated with					QSulf1	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_14_4833_s_175	15051888	( C) Quantification of FGF2 bound to FGFR1c-AP in the presence of QSulf1- or QSulf1(C-A)-treated  heparin.	bind
3238	3	1717	6	10	NULL	0	NULL	heparin	Chemical		treated with					QSulf1(C-A)	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_14_4833_s_175	15051888	( C) Quantification of FGF2 bound to FGFR1c-AP in the presence of QSulf1- or QSulf1(C-A)-treated  heparin.	bind
46103	6	1717	6	10	NULL	0	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_14_4833_s_175	15051888	( C) Quantification of FGF2 bound to FGFR1c-AP in the presence of QSulf1- or QSulf1(C-A)-treated  heparin.	bind
52893	4	1717	6	10	NULL	0	NULL	statement 1	Process		in presence of					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_14_4833_s_175	15051888	( C) Quantification of FGF2 bound to FGFR1c-AP in the presence of QSulf1- or QSulf1(C-A)-treated  heparin.	bind
52894	5	1717	6	10	NULL	0	NULL	statement 1	Process		in presence of					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_14_4833_s_175	15051888	( C) Quantification of FGF2 bound to FGFR1c-AP in the presence of QSulf1- or QSulf1(C-A)-treated  heparin.	bind
592	1	1719	5	10	NULL	0	NULL	tau	GP		bind					AD P-tau	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_23_8864_s_50	16735465	( C) Quantitations of the tau bound to AD P-tau ( ) and to PHF ( ).	bind
593	2	1719	5	10	NULL	0	NULL	tau	GP		bind					PHF	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_23_8864_s_50	16735465	( C) Quantitations of the tau bound to AD P-tau ( ) and to PHF ( ).	bind
2665	1	1719	6	10	NULL	0	NULL	tau	GP		bind					ADP-tau	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_23_8864_s_50	16735465	( C) Quantitations of the tau bound to AD P-tau ( ) and to PHF ( ).	bind
2666	2	1719	6	10	NULL	0	NULL	tau	GP		bind					PHF	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_23_8864_s_50	16735465	( C) Quantitations of the tau bound to AD P-tau ( ) and to PHF ( ).	bind
594	1	1720	5	10	NULL	0	NULL	Rapamycin	Chemical		inhibit					Tor proteins	GP				NULL	cells replete with amino acids	NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_214	16153175	( c) Rapamycin activates Gcn2p by inhibiting the Tor proteins and, at least in part,  by dephosphorylation of Ser-577, increasing the affinity for uncharged tRNA and permitting  tRNA binding and kinase activation by basal levels of uncharged tRNAs in cells replete  with amino acids.	bind
623	2	1720	5	10	NULL	0	NULL	Rapamycin	Chemical		activate					Gcn2p	GP				NULL	cells replete with amino acids	NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_214	16153175	( c) Rapamycin activates Gcn2p by inhibiting the Tor proteins and, at least in part,  by dephosphorylation of Ser-577, increasing the affinity for uncharged tRNA and permitting  tRNA binding and kinase activation by basal levels of uncharged tRNAs in cells replete  with amino acids.	bind
624	6	1720	5	10	NULL	NULL	NULL	statement 2	Process		increase					tRNA	NucleicAcid	affinity of;;uncharged			NULL	cells replete with amino acids	NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_214	16153175	( c) Rapamycin activates Gcn2p by inhibiting the Tor proteins and, at least in part,  by dephosphorylation of Ser-577, increasing the affinity for uncharged tRNA and permitting  tRNA binding and kinase activation by basal levels of uncharged tRNAs in cells replete  with amino acids.	bind
625	7	1720	5	10	NULL	NULL	NULL	statement 2	Process		permit					tRNA	NucleicAcid	binding of			NULL	cells replete with amino acids	NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_214	16153175	( c) Rapamycin activates Gcn2p by inhibiting the Tor proteins and, at least in part,  by dephosphorylation of Ser-577, increasing the affinity for uncharged tRNA and permitting  tRNA binding and kinase activation by basal levels of uncharged tRNAs in cells replete  with amino acids.	bind
626	8	1720	5	10	NULL	0	NULL	statement 2	Process		permit					kinase	GP	activation of			NULL	cells replete with amino acids	NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_214	16153175	( c) Rapamycin activates Gcn2p by inhibiting the Tor proteins and, at least in part,  by dephosphorylation of Ser-577, increasing the affinity for uncharged tRNA and permitting  tRNA binding and kinase activation by basal levels of uncharged tRNAs in cells replete  with amino acids.	bind
3234	3	1720	5	10	NULL	0	NULL	Rapamycin	Chemical		dephosphorylate								Ser-577		NULL	cells replete with amino acids	NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_214	16153175	( c) Rapamycin activates Gcn2p by inhibiting the Tor proteins and, at least in part,  by dephosphorylation of Ser-577, increasing the affinity for uncharged tRNA and permitting  tRNA binding and kinase activation by basal levels of uncharged tRNAs in cells replete  with amino acids.	bind
52895	4	1720	5	10	NULL	0	NULL	statement 2	Process		depends on		partly			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_214	16153175	( c) Rapamycin activates Gcn2p by inhibiting the Tor proteins and, at least in part,  by dephosphorylation of Ser-577, increasing the affinity for uncharged tRNA and permitting  tRNA binding and kinase activation by basal levels of uncharged tRNAs in cells replete  with amino acids.	bind
52896	5	1720	5	10	NULL	0	NULL	statement 2	Process		depends on					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_214	16153175	( c) Rapamycin activates Gcn2p by inhibiting the Tor proteins and, at least in part,  by dephosphorylation of Ser-577, increasing the affinity for uncharged tRNA and permitting  tRNA binding and kinase activation by basal levels of uncharged tRNAs in cells replete  with amino acids.	bind
2667	1	1720	6	10	NULL	0	NULL	Rapamycin	Chemical		activates					Gcn2p	GP				NULL	cells replete with amino acids	NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_214	16153175	( c) Rapamycin activates Gcn2p by inhibiting the Tor proteins and, at least in part,  by dephosphorylation of Ser-577, increasing the affinity for uncharged tRNA and permitting  tRNA binding and kinase activation by basal levels of uncharged tRNAs in cells replete  with amino acids.	bind
2668	2	1720	6	10	NULL	0	NULL	Rapamycin	Chemical		inhibits					Tor proteins	GP				NULL	cells replete with amino acids	NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_214	16153175	( c) Rapamycin activates Gcn2p by inhibiting the Tor proteins and, at least in part,  by dephosphorylation of Ser-577, increasing the affinity for uncharged tRNA and permitting  tRNA binding and kinase activation by basal levels of uncharged tRNAs in cells replete  with amino acids.	bind
2669	3	1720	6	10	NULL	0	NULL	statement 1	Process		is dependent on					statement 2	Process				NULL	cells replete with amino acids	NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_214	16153175	( c) Rapamycin activates Gcn2p by inhibiting the Tor proteins and, at least in part,  by dephosphorylation of Ser-577, increasing the affinity for uncharged tRNA and permitting  tRNA binding and kinase activation by basal levels of uncharged tRNAs in cells replete  with amino acids.	bind
2670	4	1720	6	10	NULL	0	NULL	Rapamycin	Chemical		dephosphorylates								Ser-577		NULL	cells replete with amino acids	NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_214	16153175	( c) Rapamycin activates Gcn2p by inhibiting the Tor proteins and, at least in part,  by dephosphorylation of Ser-577, increasing the affinity for uncharged tRNA and permitting  tRNA binding and kinase activation by basal levels of uncharged tRNAs in cells replete  with amino acids.	bind
2671	5	1720	6	10	NULL	0	NULL	statement 1	Process		dependent on		partly			Statement 4	Process				NULL	cells replete with amino acids	NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_214	16153175	( c) Rapamycin activates Gcn2p by inhibiting the Tor proteins and, at least in part,  by dephosphorylation of Ser-577, increasing the affinity for uncharged tRNA and permitting  tRNA binding and kinase activation by basal levels of uncharged tRNAs in cells replete  with amino acids.	bind
2672	6	1720	6	10	NULL	NULL	NULL	statement 1	Process		increases					tRNA	NucleicAcid	affinity of;;uncharged			NULL	cells replete with amino acids	NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_214	16153175	( c) Rapamycin activates Gcn2p by inhibiting the Tor proteins and, at least in part,  by dephosphorylation of Ser-577, increasing the affinity for uncharged tRNA and permitting  tRNA binding and kinase activation by basal levels of uncharged tRNAs in cells replete  with amino acids.	bind
2673	7	1720	6	10	NULL	NULL	NULL	statement 1	Process		permits					tRNA	NucleicAcid	binding of			NULL	cells replete with amino acids	NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_214	16153175	( c) Rapamycin activates Gcn2p by inhibiting the Tor proteins and, at least in part,  by dephosphorylation of Ser-577, increasing the affinity for uncharged tRNA and permitting  tRNA binding and kinase activation by basal levels of uncharged tRNAs in cells replete  with amino acids.	bind
2674	8	1720	6	10	NULL	0	NULL	statement 1	Process		permits					kinase	GP	activation			NULL	cells replete with amino acids	NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_214	16153175	( c) Rapamycin activates Gcn2p by inhibiting the Tor proteins and, at least in part,  by dephosphorylation of Ser-577, increasing the affinity for uncharged tRNA and permitting  tRNA binding and kinase activation by basal levels of uncharged tRNAs in cells replete  with amino acids.	bind
627	1	1721	5	10	NULL	0	NULL	GATA-1	GP		bind					beta major	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_18_11760_s_201	12193659	( C) Real-time PCR ChIP analysis of binding of GATA-1, p45/NF-E2, and pol II to the beta major promoter.	bind
628	2	1721	5	10	NULL	0	NULL	p45/NF-E2	GP		bind					beta major	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_18_11760_s_201	12193659	( C) Real-time PCR ChIP analysis of binding of GATA-1, p45/NF-E2, and pol II to the beta major promoter.	bind
629	3	1721	5	10	NULL	0	NULL	pol II	GP		bind					beta major	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_18_11760_s_201	12193659	( C) Real-time PCR ChIP analysis of binding of GATA-1, p45/NF-E2, and pol II to the beta major promoter.	bind
2677	1	1721	6	10	NULL	0	NULL	GATA-1	GP		bind					beta major	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_18_11760_s_201	12193659	( C) Real-time PCR ChIP analysis of binding of GATA-1, p45/NF-E2, and pol II to the beta major promoter.	bind
2678	2	1721	6	10	NULL	0	NULL	p45/NF-E2	GP		bind					beta major	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_18_11760_s_201	12193659	( C) Real-time PCR ChIP analysis of binding of GATA-1, p45/NF-E2, and pol II to the beta major promoter.	bind
2679	3	1721	6	10	NULL	0	NULL	pol II	GP		bind					beta major	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_18_11760_s_201	12193659	( C) Real-time PCR ChIP analysis of binding of GATA-1, p45/NF-E2, and pol II to the beta major promoter.	bind
630	1	1722	5	10	NULL	0	NULL	MDM2	GP		bind					ARF	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_18_3279_s_201	16107876	( C) Relative binding affinity of MDM2 to ARF and KAP1.	bind
631	2	1722	5	10	NULL	0	NULL	MDM2	GP		bind					KAP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_18_3279_s_201	16107876	( C) Relative binding affinity of MDM2 to ARF and KAP1.	bind
2675	1	1722	6	10	NULL	0	NULL	MDM2	GP		bind					ARF	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_18_3279_s_201	16107876	( C) Relative binding affinity of MDM2 to ARF and KAP1.	bind
2676	2	1722	6	10	NULL	0	NULL	MDM2	GP		bind					KAP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_18_3279_s_201	16107876	( C) Relative binding affinity of MDM2 to ARF and KAP1.	bind
632	1	1723	5	10	NULL	0	NULL	JNK	GP		bind					IB1	GP	wt			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_179	16456539	( C) Relative binding of JNK, MKK7 and MLK3 to wt or mutant IB1.	bind
633	2	1723	5	10	NULL	0	NULL	JNK	GP		bind					IB1	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_179	16456539	( C) Relative binding of JNK, MKK7 and MLK3 to wt or mutant IB1.	bind
634	3	1723	5	10	NULL	0	NULL	MKK7	GP		bind					IB1	GP	wt			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_179	16456539	( C) Relative binding of JNK, MKK7 and MLK3 to wt or mutant IB1.	bind
635	4	1723	5	10	NULL	0	NULL	MKK7	GP		bind					IB1	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_179	16456539	( C) Relative binding of JNK, MKK7 and MLK3 to wt or mutant IB1.	bind
636	5	1723	5	10	NULL	0	NULL	MLK3	GP		bind					IB1	GP	wt			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_179	16456539	( C) Relative binding of JNK, MKK7 and MLK3 to wt or mutant IB1.	bind
637	6	1723	5	10	NULL	0	NULL	MLK3	GP		bind					IB1	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_179	16456539	( C) Relative binding of JNK, MKK7 and MLK3 to wt or mutant IB1.	bind
46109	7	1723	5	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_179	16456539	( C) Relative binding of JNK, MKK7 and MLK3 to wt or mutant IB1.	bind
46110	8	1723	5	10	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_179	16456539	( C) Relative binding of JNK, MKK7 and MLK3 to wt or mutant IB1.	bind
46111	9	1723	5	10	NULL	0	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_179	16456539	( C) Relative binding of JNK, MKK7 and MLK3 to wt or mutant IB1.	bind
2680	1	1723	6	10	NULL	0	NULL	JNK	GP		bind					IB1	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_179	16456539	( C) Relative binding of JNK, MKK7 and MLK3 to wt or mutant IB1.	bind
2681	2	1723	6	10	NULL	0	NULL	JNK	GP		bind					IB1	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_179	16456539	( C) Relative binding of JNK, MKK7 and MLK3 to wt or mutant IB1.	bind
2682	3	1723	6	10	NULL	0	NULL	MKK7	GP		bind					IB1	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_179	16456539	( C) Relative binding of JNK, MKK7 and MLK3 to wt or mutant IB1.	bind
2683	4	1723	6	10	NULL	0	NULL	MKK7	GP		bind					IB1	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_179	16456539	( C) Relative binding of JNK, MKK7 and MLK3 to wt or mutant IB1.	bind
2684	5	1723	6	10	NULL	0	NULL	MLK3	GP		bind					IB1	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_179	16456539	( C) Relative binding of JNK, MKK7 and MLK3 to wt or mutant IB1.	bind
2685	6	1723	6	10	NULL	0	NULL	MLK3	GP		bind					IB1	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_179	16456539	( C) Relative binding of JNK, MKK7 and MLK3 to wt or mutant IB1.	bind
46112	7	1723	6	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_179	16456539	( C) Relative binding of JNK, MKK7 and MLK3 to wt or mutant IB1.	bind
46113	8	1723	6	10	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_179	16456539	( C) Relative binding of JNK, MKK7 and MLK3 to wt or mutant IB1.	bind
46114	9	1723	6	10	NULL	0	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_179	16456539	( C) Relative binding of JNK, MKK7 and MLK3 to wt or mutant IB1.	bind
638	1	1724	5	10	NULL	0	NULL	RelB	GP		bind					 Bcl-xL	GP			promoter	NULL	RelA-deficient MEFs	NULL	NULL	NULL	NULL	gw70_pnas_102_41_14635_s_169	16192349	( C) RelB is bound to the  Bcl-xL promoter after TNF-alpha stimulation in RelA-deficient MEFs.	bind
639	2	1724	5	10	NULL	0	NULL	TNF-alpha	GP		stimulate					statement 1	Process				NULL	RelA-deficient MEFs	NULL	NULL	NULL	NULL	gw70_pnas_102_41_14635_s_169	16192349	( C) RelB is bound to the  Bcl-xL promoter after TNF-alpha stimulation in RelA-deficient MEFs.	bind
3122	3	1724	5	10	NULL	0	NULL	statement 2	Process		is necessary for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_41_14635_s_169	16192349	( C) RelB is bound to the  Bcl-xL promoter after TNF-alpha stimulation in RelA-deficient MEFs.	bind
2686	1	1724	6	10	NULL	0	NULL	RelB	GP		bind					Bcl-xL	GP			promoter	NULL	RelA-deficient MEFs	NULL	NULL	NULL	NULL	gw70_pnas_102_41_14635_s_169	16192349	( C) RelB is bound to the  Bcl-xL promoter after TNF-alpha stimulation in RelA-deficient MEFs.	bind
2687	2	1724	6	10	NULL	0	NULL	TNF-alpha	GP		stimulates					statement 1	Process				NULL	RelA-deficient MEFs	NULL	NULL	NULL	NULL	gw70_pnas_102_41_14635_s_169	16192349	( C) RelB is bound to the  Bcl-xL promoter after TNF-alpha stimulation in RelA-deficient MEFs.	bind
3239	3	1724	6	10	NULL	0	NULL	statement 2	Process		is necessary for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_41_14635_s_169	16192349	( C) RelB is bound to the  Bcl-xL promoter after TNF-alpha stimulation in RelA-deficient MEFs.	bind
731	1	1725	5	10	NULL	0	NULL	Bc-12	GP		bind					MDA-MB-435 cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_96	15563590	( C) Requirement of integrin alphavbeta3 activation for Bc-12 and Bc-15 binding to human breast cancer cells: MDA-MB-435  (beta3 - ) cells lack alphavbeta3 or express alphavbeta3 either in a nonactivated (beta3WT and ParentCo) or activated functional form (beta3D723R, Bone, and Lung), and BMS cells that were isolated from breast cancer patient blood.	bind
732	2	1725	5	10	NULL	0	NULL	Bc-15	GP		bind					MDA-MB-435 cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_96	15563590	( C) Requirement of integrin alphavbeta3 activation for Bc-12 and Bc-15 binding to human breast cancer cells: MDA-MB-435  (beta3 - ) cells lack alphavbeta3 or express alphavbeta3 either in a nonactivated (beta3WT and ParentCo) or activated functional form (beta3D723R, Bone, and Lung), and BMS cells that were isolated from breast cancer patient blood.	bind
734	5	1725	5	10	NULL	0	NULL	integrin alphavbeta3	GP	activation	is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_96	15563590	( C) Requirement of integrin alphavbeta3 activation for Bc-12 and Bc-15 binding to human breast cancer cells: MDA-MB-435  (beta3 - ) cells lack alphavbeta3 or express alphavbeta3 either in a nonactivated (beta3WT and ParentCo) or activated functional form (beta3D723R, Bone, and Lung), and BMS cells that were isolated from breast cancer patient blood.	bind
735	6	1725	5	10	NULL	0	NULL	integrin alphavbeta3	GP	activation	is required for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_96	15563590	( C) Requirement of integrin alphavbeta3 activation for Bc-12 and Bc-15 binding to human breast cancer cells: MDA-MB-435  (beta3 - ) cells lack alphavbeta3 or express alphavbeta3 either in a nonactivated (beta3WT and ParentCo) or activated functional form (beta3D723R, Bone, and Lung), and BMS cells that were isolated from breast cancer patient blood.	bind
3125	3	1725	5	10	NULL	0	NULL	Bc-12	GP		bind					BMS cells	Cell				NULL	from breast cancer patient blood	NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_96	15563590	( C) Requirement of integrin alphavbeta3 activation for Bc-12 and Bc-15 binding to human breast cancer cells: MDA-MB-435  (beta3 - ) cells lack alphavbeta3 or express alphavbeta3 either in a nonactivated (beta3WT and ParentCo) or activated functional form (beta3D723R, Bone, and Lung), and BMS cells that were isolated from breast cancer patient blood.	bind
3126	4	1725	5	10	NULL	0	NULL	Bc-15	GP		bind					BMS cells	Cell				NULL	from breast cancer patient blood	NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_96	15563590	( C) Requirement of integrin alphavbeta3 activation for Bc-12 and Bc-15 binding to human breast cancer cells: MDA-MB-435  (beta3 - ) cells lack alphavbeta3 or express alphavbeta3 either in a nonactivated (beta3WT and ParentCo) or activated functional form (beta3D723R, Bone, and Lung), and BMS cells that were isolated from breast cancer patient blood.	bind
3128	7	1725	5	10	NULL	0	NULL	integrin alphavbeta3	GP	activation	is required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_96	15563590	( C) Requirement of integrin alphavbeta3 activation for Bc-12 and Bc-15 binding to human breast cancer cells: MDA-MB-435  (beta3 - ) cells lack alphavbeta3 or express alphavbeta3 either in a nonactivated (beta3WT and ParentCo) or activated functional form (beta3D723R, Bone, and Lung), and BMS cells that were isolated from breast cancer patient blood.	bind
3129	8	1725	5	10	NULL	0	NULL	integrin alphavbeta3	GP	activation	is required for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_96	15563590	( C) Requirement of integrin alphavbeta3 activation for Bc-12 and Bc-15 binding to human breast cancer cells: MDA-MB-435  (beta3 - ) cells lack alphavbeta3 or express alphavbeta3 either in a nonactivated (beta3WT and ParentCo) or activated functional form (beta3D723R, Bone, and Lung), and BMS cells that were isolated from breast cancer patient blood.	bind
46116	9	1725	5	10	NULL	0	NULL	MDA-MB-435 cells	Cell		is a type of					breast cancer cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_96	15563590	( C) Requirement of integrin alphavbeta3 activation for Bc-12 and Bc-15 binding to human breast cancer cells: MDA-MB-435  (beta3 - ) cells lack alphavbeta3 or express alphavbeta3 either in a nonactivated (beta3WT and ParentCo) or activated functional form (beta3D723R, Bone, and Lung), and BMS cells that were isolated from breast cancer patient blood.	bind
3005	1	1725	6	10	NULL	0	NULL	Bc-12	GP		bind					MDA-MB-435 (beta3 - ) cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_96	15563590	( C) Requirement of integrin alphavbeta3 activation for Bc-12 and Bc-15 binding to human breast cancer cells: MDA-MB-435  (beta3 - ) cells lack alphavbeta3 or express alphavbeta3 either in a nonactivated (beta3WT and ParentCo) or activated functional form (beta3D723R, Bone, and Lung), and BMS cells that were isolated from breast cancer patient blood.	bind
3006	2	1725	6	10	NULL	0	NULL	MDA-MB-435 (beta3 - ) cells	Cell		is a type of					breast cancer cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_96	15563590	( C) Requirement of integrin alphavbeta3 activation for Bc-12 and Bc-15 binding to human breast cancer cells: MDA-MB-435  (beta3 - ) cells lack alphavbeta3 or express alphavbeta3 either in a nonactivated (beta3WT and ParentCo) or activated functional form (beta3D723R, Bone, and Lung), and BMS cells that were isolated from breast cancer patient blood.	bind
3007	3	1725	6	10	NULL	0	NULL	Bc-15	Cell		bind					MDA-MB-435 (beta3 - ) cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_96	15563590	( C) Requirement of integrin alphavbeta3 activation for Bc-12 and Bc-15 binding to human breast cancer cells: MDA-MB-435  (beta3 - ) cells lack alphavbeta3 or express alphavbeta3 either in a nonactivated (beta3WT and ParentCo) or activated functional form (beta3D723R, Bone, and Lung), and BMS cells that were isolated from breast cancer patient blood.	bind
3024	4	1725	6	10	NULL	0	NULL	integrin alphavbeta3	GP	activation of	is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_96	15563590	( C) Requirement of integrin alphavbeta3 activation for Bc-12 and Bc-15 binding to human breast cancer cells: MDA-MB-435  (beta3 - ) cells lack alphavbeta3 or express alphavbeta3 either in a nonactivated (beta3WT and ParentCo) or activated functional form (beta3D723R, Bone, and Lung), and BMS cells that were isolated from breast cancer patient blood.	bind
3025	5	1725	6	10	NULL	0	NULL	integrin alphavbeta3	GP	activation of	is required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_96	15563590	( C) Requirement of integrin alphavbeta3 activation for Bc-12 and Bc-15 binding to human breast cancer cells: MDA-MB-435  (beta3 - ) cells lack alphavbeta3 or express alphavbeta3 either in a nonactivated (beta3WT and ParentCo) or activated functional form (beta3D723R, Bone, and Lung), and BMS cells that were isolated from breast cancer patient blood.	bind
46165	6	1725	6	10	NULL	0	NULL	Bc-12	GP		bind					BMS cells	Cell				NULL	breast cancer patient blood	NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_96	15563590	( C) Requirement of integrin alphavbeta3 activation for Bc-12 and Bc-15 binding to human breast cancer cells: MDA-MB-435  (beta3 - ) cells lack alphavbeta3 or express alphavbeta3 either in a nonactivated (beta3WT and ParentCo) or activated functional form (beta3D723R, Bone, and Lung), and BMS cells that were isolated from breast cancer patient blood.	bind
46166	7	1725	6	10	NULL	0	NULL	Bc-15	GP		bind					BMS cells	Cell				NULL	breast cancer patient blood	NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_96	15563590	( C) Requirement of integrin alphavbeta3 activation for Bc-12 and Bc-15 binding to human breast cancer cells: MDA-MB-435  (beta3 - ) cells lack alphavbeta3 or express alphavbeta3 either in a nonactivated (beta3WT and ParentCo) or activated functional form (beta3D723R, Bone, and Lung), and BMS cells that were isolated from breast cancer patient blood.	bind
52897	8	1725	6	10	NULL	0	NULL	integrin alphavbeta3	GP	activation of	is required for					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_96	15563590	( C) Requirement of integrin alphavbeta3 activation for Bc-12 and Bc-15 binding to human breast cancer cells: MDA-MB-435  (beta3 - ) cells lack alphavbeta3 or express alphavbeta3 either in a nonactivated (beta3WT and ParentCo) or activated functional form (beta3D723R, Bone, and Lung), and BMS cells that were isolated from breast cancer patient blood.	bind
52898	9	1725	6	10	NULL	0	NULL	integrin alphavbeta3	GP	activation of	is required for					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_49_17210_s_96	15563590	( C) Requirement of integrin alphavbeta3 activation for Bc-12 and Bc-15 binding to human breast cancer cells: MDA-MB-435  (beta3 - ) cells lack alphavbeta3 or express alphavbeta3 either in a nonactivated (beta3WT and ParentCo) or activated functional form (beta3D723R, Bone, and Lung), and BMS cells that were isolated from breast cancer patient blood.	bind
737	1	1727	5	10	NULL	0	NULL	Rtt106p	GP		bind					H3	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_pnas_102_38_13410_s_195	16157874	( C) Rtt106p binds to H3 and H4  in vivo.	bind
738	2	1727	5	10	NULL	0	NULL	Rtt106p	GP		bind					H4	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_pnas_102_38_13410_s_195	16157874	( C) Rtt106p binds to H3 and H4  in vivo.	bind
2688	1	1727	6	10	NULL	0	NULL	Rtt106p	GP		bind					H3	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_pnas_102_38_13410_s_195	16157874	( C) Rtt106p binds to H3 and H4  in vivo.	bind
2689	2	1727	6	10	NULL	0	NULL	Rtt106p	GP		bind					H4	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_pnas_102_38_13410_s_195	16157874	( C) Rtt106p binds to H3 and H4  in vivo.	bind
739	1	1728	5	10	NULL	0	NULL	ADP-ribose	Chemical		bind								macro domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_11_1911_s_132	15902274	( C) Schematic representation for the binding of ADP-ribose to the  macro domain.	bind
2690	1	1728	6	10	NULL	0	NULL	ADP-ribose	Chemical		bind								macro domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_11_1911_s_132	15902274	( C) Schematic representation for the binding of ADP-ribose to the  macro domain.	bind
744	1	1729	5	10	NULL	0	NULL	YY1	GP	allele-specific	bind							unmethylated		Xist cluster	NULL	Xi of female	NULL	NULL	NULL	NULL	gw70_genomeres_16_7_901_s_127	16760423	( C) Schematic representation of allele-specific YY1 binding to the  Xist locus based on the results of  B. YY1 binds to the  Xist cluster located in the Xi of female, which is unmethylated.	bind
2691	1	1729	6	10	NULL	0	NULL	YY1	GP	allele-specific	bind							unmethylated		Xist cluster 	NULL	Xi of female	NULL	NULL	NULL	NULL	gw70_genomeres_16_7_901_s_127	16760423	( C) Schematic representation of allele-specific YY1 binding to the  Xist locus based on the results of  B. YY1 binds to the  Xist cluster located in the Xi of female, which is unmethylated.	bind
745	1	1730	5	10	NULL	0	NULL	ataxin-3	GP	derivatives	bind					VCP	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_embo_23_3_659_s_137	14749733	( C) Schematic representation of the ataxin-3 deletion mutants and summary of the data  obtained from the  in vitro assay of the binding of ataxin-3 derivatives to VCP.	bind
2692	1	1730	6	10	NULL	0	NULL	ataxin-3	GP	derivatives	bind					VCP	GP				NULL	in vitro assay	NULL	NULL	NULL	NULL	gw70_embo_23_3_659_s_137	14749733	( C) Schematic representation of the ataxin-3 deletion mutants and summary of the data  obtained from the  in vitro assay of the binding of ataxin-3 derivatives to VCP.	bind
746	1	1732	5	10	NULL	0	NULL	hSNF5	GP		regulate 					E2F targets	GP	selection of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_6_665_s_119	15769941	( C) Selection of E2F targets and mitotic controllers, regulated by hSNF5 identified  by whole-genome expression profiling.	bind
748	2	1732	5	10	NULL	0	NULL	hSNF5	GP		regulate					mitotic controllers	GP	selection of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_6_665_s_119	15769941	( C) Selection of E2F targets and mitotic controllers, regulated by hSNF5 identified  by whole-genome expression profiling.	bind
2693	1	1732	6	10	NULL	0	NULL	hSNF5	GP		regulates					E2F targets	GP	selection of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_6_665_s_119	15769941	( C) Selection of E2F targets and mitotic controllers, regulated by hSNF5 identified  by whole-genome expression profiling.	bind
2694	2	1732	6	10	NULL	0	NULL	hSNF5	GP		regulates					mitotic controllers	GP	selection of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_6_665_s_119	15769941	( C) Selection of E2F targets and mitotic controllers, regulated by hSNF5 identified  by whole-genome expression profiling.	bind
750	1	1733	5	10	NULL	0	NULL	Sema-2a-AP	GP		bind					PlexB	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_133_11_2125_s_238	16672342	( C) Sema-2a-AP binds to PlexB in the presence of 1 mM and 10 mM (inset) EDTA.	bind
3131	2	1733	5	10	NULL	0	NULL	statement 1	Process		in the presence of					EDTA	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_development_133_11_2125_s_238	16672342	( C) Sema-2a-AP binds to PlexB in the presence of 1 mM and 10 mM (inset) EDTA.	bind
2695	1	1733	6	10	NULL	0	NULL	Sema-2a-AP 	GP		bind					PlexB	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_133_11_2125_s_238	16672342	( C) Sema-2a-AP binds to PlexB in the presence of 1 mM and 10 mM (inset) EDTA.	bind
2696	2	1733	6	10	NULL	0	NULL	statement 1	Process		in presence of 					EDTA	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_development_133_11_2125_s_238	16672342	( C) Sema-2a-AP binds to PlexB in the presence of 1 mM and 10 mM (inset) EDTA.	bind
752	1	1734	5	10	NULL	0	NULL	Sens	GP		bind			Zn-finger domains		Sc	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_133_10_1979_s_232	16624856	( C) Sens binds to Sc through its Zn-finger domains.	bind
2697	1	1734	6	10	NULL	0	NULL	Sens	GP		bind			Zn-finger domain		Sc	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_133_10_1979_s_232	16624856	( C) Sens binds to Sc through its Zn-finger domains.	bind
753	1	1737	5	10	NULL	0	NULL	Src	GP		bind			SH3 domain		TRPV1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_24_4211_s_125	16319926	( C) SH3 domain of Src binds to TRPV1.	bind
2698	1	1737	6	10	NULL	0	NULL	Src	GP		bind			SH3 domain		TRPV1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_24_4211_s_125	16319926	( C) SH3 domain of Src binds to TRPV1.	bind
756	1	1738	5	10	NULL	0	NULL	Elk-1	GP	activated	recruit					mSin3A	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_22_2_281_s_251	12514134	( C) Shortly after fully fledged activation, Elk-1 recruits the co-repressor mSin3A which  binds to its DNA-binding domain (N-terminus) and attenuates histone acetylation (Yang   et al.	bind
757	2	1738	5	10	NULL	0	NULL	mSin3A	GP		bind					Elk-1	GP		DNA-binding domain (N-terminus)		NULL		NULL	NULL	NULL	NULL	gw70_embo_22_2_281_s_251	12514134	( C) Shortly after fully fledged activation, Elk-1 recruits the co-repressor mSin3A which  binds to its DNA-binding domain (N-terminus) and attenuates histone acetylation (Yang   et al.	bind
759	3	1738	5	10	NULL	0	NULL	statement 2	Process		attenuate					histone 	GP	acetylation			NULL		NULL	NULL	NULL	NULL	gw70_embo_22_2_281_s_251	12514134	( C) Shortly after fully fledged activation, Elk-1 recruits the co-repressor mSin3A which  binds to its DNA-binding domain (N-terminus) and attenuates histone acetylation (Yang   et al.	bind
46123	4	1738	5	10	NULL	0	NULL	mSin3A	GP		is a type of					co-repressor	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_22_2_281_s_251	12514134	( C) Shortly after fully fledged activation, Elk-1 recruits the co-repressor mSin3A which  binds to its DNA-binding domain (N-terminus) and attenuates histone acetylation (Yang   et al.	bind
2699	1	1738	6	10	NULL	0	NULL	mSin3A	GP		is a type of					corepressor	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_22_2_281_s_251	12514134	( C) Shortly after fully fledged activation, Elk-1 recruits the co-repressor mSin3A which  binds to its DNA-binding domain (N-terminus) and attenuates histone acetylation (Yang   et al.	bind
2700	2	1738	6	10	NULL	0	NULL	Elk1	GP	activated	recruits					mSin3A	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_22_2_281_s_251	12514134	( C) Shortly after fully fledged activation, Elk-1 recruits the co-repressor mSin3A which  binds to its DNA-binding domain (N-terminus) and attenuates histone acetylation (Yang   et al.	bind
46167	3	1738	6	10	NULL	0	NULL	mSin3A	GP		bind					Elk-1	GP		DNA-binding domain (N-terminus)		NULL		NULL	NULL	NULL	NULL	gw70_embo_22_2_281_s_251	12514134	( C) Shortly after fully fledged activation, Elk-1 recruits the co-repressor mSin3A which  binds to its DNA-binding domain (N-terminus) and attenuates histone acetylation (Yang   et al.	bind
46168	4	1738	6	10	NULL	0	NULL	statement 3	Process		attenuates					histone	GP	acetylation of			NULL		NULL	NULL	NULL	NULL	gw70_embo_22_2_281_s_251	12514134	( C) Shortly after fully fledged activation, Elk-1 recruits the co-repressor mSin3A which  binds to its DNA-binding domain (N-terminus) and attenuates histone acetylation (Yang   et al.	bind
762	1	1739	5	10	NULL	0	NULL	SKN-1	GP		bind		specifically			GST - GSK-3 	GP	C. elegans			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_45_16275_s_116	16251270	( C) SKN-1 binds specifically to a  C. elegans GST - GSK-3 fusion protein  in vitro.	bind
46124	2	1739	5	10	NULL	0	NULL	GSK-3	GP		is a type of					GST-fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_45_16275_s_116	16251270	( C) SKN-1 binds specifically to a  C. elegans GST - GSK-3 fusion protein  in vitro.	bind
2702	1	1739	6	10	NULL	0	NULL	SKN-1	GP		bind		specifically			GST-GSK3	GP	C. elegans  			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_45_16275_s_116	16251270	( C) SKN-1 binds specifically to a  C. elegans GST - GSK-3 fusion protein  in vitro.	bind
46125	2	1739	6	10	NULL	0	NULL	GSK-3	GP		is a type of					GST-fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_45_16275_s_116	16251270	( C) SKN-1 binds specifically to a  C. elegans GST - GSK-3 fusion protein  in vitro.	bind
766	1	1740	5	10	NULL	0	NULL	Smad1	GP		bind		directly							GCAT motif	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_14_3107_s_61	12136093	( C) Smad1 binds directly to the GCAT motif (and Smad4 binds weakly).	bind
768	2	1740	5	10	NULL	0	NULL	Smad4	GP		bind		weakly							GCAT motif	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_14_3107_s_61	12136093	( C) Smad1 binds directly to the GCAT motif (and Smad4 binds weakly).	bind
2703	1	1740	6	10	NULL	0	NULL	Smad1	GP		bind		directly							GCAT motif	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_14_3107_s_61	12136093	( C) Smad1 binds directly to the GCAT motif (and Smad4 binds weakly).	bind
2704	2	1740	6	10	NULL	0	NULL	Smad4	GP		bind		weakly							GCAT motif	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_14_3107_s_61	12136093	( C) Smad1 binds directly to the GCAT motif (and Smad4 binds weakly).	bind
770	1	1741	5	10	NULL	0	NULL	Smad1	GP		bind		directly							SBE III	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_14_3107_s_50	12136093	( C) Smad1, Smad3 and Smad4 bind directly to SBE III.	bind
772	2	1741	5	10	NULL	0	NULL	Smad3	GP		bind		directly							SBE III	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_14_3107_s_50	12136093	( C) Smad1, Smad3 and Smad4 bind directly to SBE III.	bind
773	3	1741	5	10	NULL	0	NULL	Smad4	GP		bind		directly							SBE III	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_14_3107_s_50	12136093	( C) Smad1, Smad3 and Smad4 bind directly to SBE III.	bind
2705	1	1741	6	10	NULL	0	NULL	Smad1	GP		bind		directly							SBE III	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_14_3107_s_50	12136093	( C) Smad1, Smad3 and Smad4 bind directly to SBE III.	bind
2706	2	1741	6	10	NULL	0	NULL	Smad3	GP		bind		directly							SBE III	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_14_3107_s_50	12136093	( C) Smad1, Smad3 and Smad4 bind directly to SBE III.	bind
2707	3	1741	6	10	NULL	0	NULL	Smad4	GP		bind		directly							SBE III	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_14_3107_s_50	12136093	( C) Smad1, Smad3 and Smad4 bind directly to SBE III.	bind
793	1	1742	5	10	NULL	0	NULL	TGF-beta	GP		induce 					p15 Ink4B	GP	transcription from		promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_19_19_5178_s_95	11013220	( C) Smad3 is required for TGF-beta-induced transcription from the p15 Ink4B promoter.	bind
794	2	1742	5	10	NULL	0	NULL	Smad3	GP		is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_19_5178_s_95	11013220	( C) Smad3 is required for TGF-beta-induced transcription from the p15 Ink4B promoter.	bind
2708	1	1742	6	10	NULL	0	NULL	TGF-beta	GP		induce					p15 Ink4B	GP	transcription from		promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_19_19_5178_s_95	11013220	( C) Smad3 is required for TGF-beta-induced transcription from the p15 Ink4B promoter.	bind
3390	2	1742	6	10	NULL	0	NULL	Smad3	GP		is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_19_5178_s_95	11013220	( C) Smad3 is required for TGF-beta-induced transcription from the p15 Ink4B promoter.	bind
795	1	1743	5	10	NULL	0	NULL	p21	GP		bind		specifically			Wnt4 gene	GP			TATA box-proximal region	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_12_1485_s_153	15964998	( C) Specific binding of p21 to the TATA box-proximal region of the  Wnt4 gene.	bind
2709	1	1743	6	10	NULL	0	NULL	p21	GP		bind		specifically			Wnt4 gene	GP			TATA box-proximal region	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_12_1485_s_153	15964998	( C) Specific binding of p21 to the TATA box-proximal region of the  Wnt4 gene.	bind
796	1	1744	5	10	NULL	0	NULL	CD1d	GP		bind					PI	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_29_10685_s_90	15243159	( c) Specificity of CD1d binding to PI and inhibition of CD1d - PI interaction by preloading  of CD1d with free PI.	bind
3132	2	1744	5	10	NULL	0	NULL	PI	Chemical	free	inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_29_10685_s_90	15243159	( c) Specificity of CD1d binding to PI and inhibition of CD1d - PI interaction by preloading  of CD1d with free PI.	bind
2710	1	1744	6	10	NULL	0	NULL	CD1d	GP		bind					PI	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_29_10685_s_90	15243159	( c) Specificity of CD1d binding to PI and inhibition of CD1d - PI interaction by preloading  of CD1d with free PI.	bind
2711	2	1744	6	10	NULL	0	NULL	PI	Chemical	free	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_29_10685_s_90	15243159	( c) Specificity of CD1d binding to PI and inhibition of CD1d - PI interaction by preloading  of CD1d with free PI.	bind
797	1	1745	5	10	NULL	0	NULL	ss telomeric DNA	NucleicAcid		bind					POT1a N	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_21_5180_s_72	17053789	( C) Specificity of ss telomeric DNA binding to POT1a N and ( D) POT1b N.	bind
798	2	1745	5	10	NULL	0	NULL	ss telomeric DNA	NucleicAcid		bind					POT1b N	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_21_5180_s_72	17053789	( C) Specificity of ss telomeric DNA binding to POT1a N and ( D) POT1b N.	bind
2712	1	1745	6	10	NULL	0	NULL	ss telomeric DNA	NucleicAcid		bind					POT1a N	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_21_5180_s_72	17053789	( C) Specificity of ss telomeric DNA binding to POT1a N and ( D) POT1b N.	bind
2713	2	1745	6	10	NULL	0	NULL	ss telomeric DNA	NucleicAcid		bind					POT1b N	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_21_5180_s_72	17053789	( C) Specificity of ss telomeric DNA binding to POT1a N and ( D) POT1b N.	bind
802	1	1746	5	10	NULL	0	NULL	syntenin-2	GP		bind					PIP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_14_2556_s_44	15961997	( C) SPR sensogram showing that the binding of syntenin-2 to PIP2 increases as the PIP2 concentration in the lipid layers increases.	bind
803	2	1746	5	10	NULL	0	NULL	PIP2	GP	increase in	increases					statement 1	Process				NULL	lipid layers	NULL	NULL	NULL	NULL	gw70_embo_24_14_2556_s_44	15961997	( C) SPR sensogram showing that the binding of syntenin-2 to PIP2 increases as the PIP2 concentration in the lipid layers increases.	bind
2714	1	1746	6	10	NULL	0	NULL	syntenin-2	GP		bind					PIP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_14_2556_s_44	15961997	( C) SPR sensogram showing that the binding of syntenin-2 to PIP2 increases as the PIP2 concentration in the lipid layers increases.	bind
2715	2	1746	6	10	NULL	0	NULL	PIP2	GP	increased	increases					statement 1	Process				NULL	lipid layers	NULL	NULL	NULL	NULL	gw70_embo_24_14_2556_s_44	15961997	( C) SPR sensogram showing that the binding of syntenin-2 to PIP2 increases as the PIP2 concentration in the lipid layers increases.	bind
799	1	1747	5	10	NULL	0	NULL	p53RE	GP		bind					p63gamma	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_20_5487_s_199	12374749	( C) SSRP1 directly binds to the p53RE-bound p63gamma.	bind
800	2	1747	5	10	NULL	0	NULL	SSRP1	GP		bind		directly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_20_5487_s_199	12374749	( C) SSRP1 directly binds to the p53RE-bound p63gamma.	bind
2716	1	1747	6	10	NULL	0	NULL	p53RE	GP		bind					p63gamma	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_20_5487_s_199	12374749	( C) SSRP1 directly binds to the p53RE-bound p63gamma.	bind
3391	2	1747	6	10	NULL	0	NULL	SSRP1	GP		bind		directly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_20_5487_s_199	12374749	( C) SSRP1 directly binds to the p53RE-bound p63gamma.	bind
801	1	1748	5	10	NULL	0	NULL	RIS	GP		bind					FPPS	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_20_7829_s_50	16684881	( C) Stereoview detail of RIS binding to FPPS (blue).	bind
2717	1	1748	6	10	NULL	0	NULL	RIS	GP		bind					FPPS	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_20_7829_s_50	16684881	( C) Stereoview detail of RIS binding to FPPS (blue).	bind
804	1	1749	5	10	NULL	0	NULL	glucocorticoid receptor	GP		bind							MMTV		LTR	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10788_s_224	10485904	( C) Steroid-dependent glucocorticoid receptor binding to the MMTV LTR disrupts nucleosome activating recombination but not transcription.	bind
805	2	1749	5	10	NULL	0	NULL	statement 1	Process		disrupt					recombination	Process	nucleosome activating			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10788_s_224	10485904	( C) Steroid-dependent glucocorticoid receptor binding to the MMTV LTR disrupts nucleosome activating recombination but not transcription.	bind
806	3	1749	5	10	NULL	0	NULL	statement 1	Process		does not disrupt					transcription	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10788_s_224	10485904	( C) Steroid-dependent glucocorticoid receptor binding to the MMTV LTR disrupts nucleosome activating recombination but not transcription.	bind
46126	4	1749	5	10	NULL	0	NULL	statement 1	Process		depends on					steroid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10788_s_224	10485904	( C) Steroid-dependent glucocorticoid receptor binding to the MMTV LTR disrupts nucleosome activating recombination but not transcription.	bind
2718	1	1749	6	10	NULL	0	NULL	glucocorticoid receptor	GP		bind							MMTV		LTR	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10788_s_224	10485904	( C) Steroid-dependent glucocorticoid receptor binding to the MMTV LTR disrupts nucleosome activating recombination but not transcription.	bind
2719	2	1749	6	10	NULL	0	NULL	statement 1	Process		depends on					Steroid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10788_s_224	10485904	( C) Steroid-dependent glucocorticoid receptor binding to the MMTV LTR disrupts nucleosome activating recombination but not transcription.	bind
2720	3	1749	6	10	NULL	0	NULL	statement 1	Process		disrupt					recombination	Process	nucleosome activating			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10788_s_224	10485904	( C) Steroid-dependent glucocorticoid receptor binding to the MMTV LTR disrupts nucleosome activating recombination but not transcription.	bind
2721	4	1749	6	10	NULL	0	NULL	statement 1	Process		does not disrupt					transcription	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10788_s_224	10485904	( C) Steroid-dependent glucocorticoid receptor binding to the MMTV LTR disrupts nucleosome activating recombination but not transcription.	bind
807	1	1750	5	10	NULL	0	NULL	Mj TyrRS	GP	WT	bind					Tyr	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_17_6483_s_52	16618920	( C) Structure of the WT  Mj TyrRS ( ) bound to Tyr.	bind
2722	1	1750	6	10	NULL	0	NULL	Mj TyrRS	GP	wild type	bind					Tyr	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_17_6483_s_52	16618920	( C) Structure of the WT  Mj TyrRS ( ) bound to Tyr.	bind
808	1	1751	5	10	NULL	0	NULL	TyrRS	GP	WT	bind					Tyr	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_17_6483_s_92	16618920	( C) Structure of the WT TyrRS bound to Tyr ( ).	bind
2724	1	1751	6	10	NULL	0	NULL	TyrRS	GP	wild type	bind					Tyr	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_17_6483_s_92	16618920	( C) Structure of the WT TyrRS bound to Tyr ( ).	bind
809	1	1752	5	10	NULL	0	NULL	helicase	GP		bind					G4 DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_18_3954_s_106	12235379	( C) Summary of binding affinity, comparing  kD for each helicase binding to G4 DNA and HJ, and showing relative affinities of binding to G4 DNA and HJ.	bind
810	2	1752	5	10	NULL	0	NULL	helicase	GP		bind					HJ	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_18_3954_s_106	12235379	( C) Summary of binding affinity, comparing  kD for each helicase binding to G4 DNA and HJ, and showing relative affinities of binding to G4 DNA and HJ.	bind
2725	1	1752	6	10	NULL	0	NULL	helicase	GP		bind					G4 DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_18_3954_s_106	12235379	( C) Summary of binding affinity, comparing  kD for each helicase binding to G4 DNA and HJ, and showing relative affinities of binding to G4 DNA and HJ.	bind
2726	2	1752	6	10	NULL	0	NULL	helicase	GP		bind					HJ	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_18_3954_s_106	12235379	( C) Summary of binding affinity, comparing  kD for each helicase binding to G4 DNA and HJ, and showing relative affinities of binding to G4 DNA and HJ.	bind
811	1	1754	5	10	NULL	0	NULL	Rae-1 	GP		bind		specifically	epsilon-CD4		NKG2d	GP		CD4		NULL		NULL	NULL	NULL	NULL	gw60_science_294_5542_605_s_81	11567106	( C) Surface plasmon resonance  indicates specific binding of Rae-1 epsilon-CD4 to  NKG2d-CD4.	bind
2727	1	1754	6	10	NULL	0	NULL	Rae-1	GP		bind		specifically	epsilon-CD4		NKG2d	GP		CD4		NULL		NULL	NULL	NULL	NULL	gw60_science_294_5542_605_s_81	11567106	( C) Surface plasmon resonance  indicates specific binding of Rae-1 epsilon-CD4 to  NKG2d-CD4.	bind
1554	1	1756	5	10	NULL	0	NULL	syn1AdeltaC	GP		bind					GST-N-CFTR	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_18_10972_s_84	9724814	( C) syn1AdeltaC binds to GST-N-CFTR with an approximately 1:1 stoichiometry.	bind
2434	1	1756	7	10	NULL	0	NULL	 syn1AdeltaC	GP		bind					GST-N-CFTR	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_18_10972_s_84	9724814	( C) syn1AdeltaC binds to GST-N-CFTR with an approximately 1:1 stoichiometry.	bind
1555	1	1757	5	10	NULL	0	NULL	proteins	GP	E. coli	bind					RNA	NucleicAcid	E. coli			NULL		NULL	NULL	NULL	NULL	gw70_embo_24_19_3360_s_84	16163391	( C) Sypro ruby stain of the same gel shown in (B) indicates that both  E. coli and  B. subtilis proteins are bound to the  E. coli RNA in this assay.	bind
1556	2	1757	5	10	NULL	0	NULL	proteins	GP	B. subtilis	bind					RNA	NucleicAcid	E. coli			NULL		NULL	NULL	NULL	NULL	gw70_embo_24_19_3360_s_84	16163391	( C) Sypro ruby stain of the same gel shown in (B) indicates that both  E. coli and  B. subtilis proteins are bound to the  E. coli RNA in this assay.	bind
2438	1	1757	7	10	NULL	0	NULL	proteins	GP	E. coli 	bind					RNA	NucleicAcid	E. coli 			NULL		NULL	NULL	NULL	NULL	gw70_embo_24_19_3360_s_84	16163391	( C) Sypro ruby stain of the same gel shown in (B) indicates that both  E. coli and  B. subtilis proteins are bound to the  E. coli RNA in this assay.	bind
2439	2	1757	7	10	NULL	0	NULL	proteins	GP	B. subtilis 	bind 					RNA	NucleicAcid	E. coli 			NULL		NULL	NULL	NULL	NULL	gw70_embo_24_19_3360_s_84	16163391	( C) Sypro ruby stain of the same gel shown in (B) indicates that both  E. coli and  B. subtilis proteins are bound to the  E. coli RNA in this assay.	bind
1557	3	1758	5	10	NULL	0	NULL	TBP	GP		bind					BNA	GP			promoter	NULL	in vivo, chromatin from wild-type (WT) or mot1-42 mutant cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_151	15861138	( C) TBP binding to  BNA and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
1558	2	1758	5	10	NULL	0	NULL	TBP	GP		bind					URA1	GP			promoter	NULL	in vivo, chromatin from wild-type (WT) or mot1-42 mutant cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_151	15861138	( C) TBP binding to  BNA and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
2440	4	1758	7	10	NULL	0	NULL	 TBP 	GP		 bind					BNA	GP			promoter	NULL	  chromatin in vivo from wild-type (WT) cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_151	15861138	( C) TBP binding to  BNA and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
2441	5	1758	7	10	NULL	0	NULL	TBP 	GP		bind					BNA	GP			promoter	NULL	chromatin in vivo from mot1-42 mutant cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_151	15861138	( C) TBP binding to  BNA and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
2442	6	1758	7	10	NULL	0	NULL	TBP	GP		bind					URA1	GP			promoter	NULL	chromatin in vivo from wild-type (WT) cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_151	15861138	( C) TBP binding to  BNA and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
2443	7	1758	7	10	NULL	0	NULL	TBP	GP		bind 					URA1 	GP			promoter	NULL	chromatin in vivo from mot1-42 mutant cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_151	15861138	( C) TBP binding to  BNA and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
1559	1	1759	5	10	NULL	0	NULL	m7G	Chemical		bind					VP39 	GP	mutant	D182A		NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_13_7149_s_70	10377383	( c) The 1.83- Ang  difference electron density (2.5sigma level) of m7G bound to VP39 mutant D182A (Table  1).	bind
2445	2	1759	7	10	NULL	0	NULL	m7G	Chemical		bind					VP39	GP	mutant 	D182A		NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_13_7149_s_70	10377383	( c) The 1.83- Ang  difference electron density (2.5sigma level) of m7G bound to VP39 mutant D182A (Table  1).	bind
2446	1	1760	7	10	NULL	0	NULL	cdk2	GP		bind					p27	GP	 wild type			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_21_5159_s_176	17053782	( C) The amount of cdk2 and cdk4 bound to p27 wild type or p27T198A was measured by Western  blot analysis after immunoprecipitation against p27.	bind
2447	2	1760	7	10	NULL	0	NULL	cdk2	GP		bind					p27	GP		T198A		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_21_5159_s_176	17053782	( C) The amount of cdk2 and cdk4 bound to p27 wild type or p27T198A was measured by Western  blot analysis after immunoprecipitation against p27.	bind
2448	3	1760	7	10	NULL	0	NULL	cdk4	GP		bind					p27	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_21_5159_s_176	17053782	( C) The amount of cdk2 and cdk4 bound to p27 wild type or p27T198A was measured by Western  blot analysis after immunoprecipitation against p27.	bind
2449	4	1760	7	10	NULL	0	NULL	cdk4	GP		bind					p27	GP		T198A		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_21_5159_s_176	17053782	( C) The amount of cdk2 and cdk4 bound to p27 wild type or p27T198A was measured by Western  blot analysis after immunoprecipitation against p27.	bind
1564	1	1761	5	10	NULL	0	NULL	DLT	GP		bind					RA1-HSF	GP	radiolabeled			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_13_3755_s_140	16893958	( C) The binding activity of DLm, and DLd, Lm and Ld, and D alone are tested by a competition  assay using an excess of each of these protein constructs to compete the binding  of DLT to radiolabeled RA1-HSF.	bind
2450	1	1761	7	10	NULL	0	NULL	DLT	GP		bind					RA1-HSF	GP	radiolabeled			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_13_3755_s_140	16893958	( C) The binding activity of DLm, and DLd, Lm and Ld, and D alone are tested by a competition  assay using an excess of each of these protein constructs to compete the binding  of DLT to radiolabeled RA1-HSF.	bind
1565	1	1762	5	10	NULL	0	NULL	ERK2	GP		bind			CDm		MSK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_284	11157753	( C) The binding of ERK2 CDm to MSK1 was examined as in	bind
2456	1	1762	7	10	NULL	0	NULL	ERK2 	GP		bind			CDm		MSK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_284	11157753	( C) The binding of ERK2 CDm to MSK1 was examined as in	bind
1566	1	1763	5	10	NULL	0	NULL	sCD26	GP	labeled	bind					p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8439_s_88	10900005	( C) The binding of labeled sCD26 to p300 was inhibited by an excess amount of nonlabeled sCD26.	bind
1567	2	1763	5	10	NULL	0	NULL	sCD26	GP	nonlabeled	inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8439_s_88	10900005	( C) The binding of labeled sCD26 to p300 was inhibited by an excess amount of nonlabeled sCD26.	bind
2459	1	1763	7	10	NULL	0	NULL	sCD26	GP	labeled	bind					p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8439_s_88	10900005	( C) The binding of labeled sCD26 to p300 was inhibited by an excess amount of nonlabeled sCD26.	bind
2460	2	1763	7	10	NULL	0	NULL	sCD26	GP	nonlabeled	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8439_s_88	10900005	( C) The binding of labeled sCD26 to p300 was inhibited by an excess amount of nonlabeled sCD26.	bind
1569	1	1765	5	10	NULL	0	NULL	BRG1	GP		bind					HP1beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_120	12411497	( C) The C-terminal chromoshadow domain of HP1alpha is sufficient to promote BRG1 binding to HP1beta and HP1gamma.	bind
1570	2	1765	5	10	NULL	0	NULL	BRG1	GP		bind					HP1gamma	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_120	12411497	( C) The C-terminal chromoshadow domain of HP1alpha is sufficient to promote BRG1 binding to HP1beta and HP1gamma.	bind
1571	3	1765	5	10	NULL	0	NULL	HP1alpha	GP		promote		is sufficient to	C-terminal chromoshadow domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_120	12411497	( C) The C-terminal chromoshadow domain of HP1alpha is sufficient to promote BRG1 binding to HP1beta and HP1gamma.	bind
1572	4	1765	5	10	NULL	0	NULL	HP1alpha	GP		promote		is sufficient to	C-terminal chromoshadow domain		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_120	12411497	( C) The C-terminal chromoshadow domain of HP1alpha is sufficient to promote BRG1 binding to HP1beta and HP1gamma.	bind
2568	1	1765	7	10	NULL	0	NULL	BRG1	GP		bind					HP1beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_120	12411497	( C) The C-terminal chromoshadow domain of HP1alpha is sufficient to promote BRG1 binding to HP1beta and HP1gamma.	bind
2569	2	1765	7	10	NULL	0	NULL	BRG1	GP		bind					HP1gamma	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_120	12411497	( C) The C-terminal chromoshadow domain of HP1alpha is sufficient to promote BRG1 binding to HP1beta and HP1gamma.	bind
2570	3	1765	7	10	NULL	0	NULL	HP1alpha	GP		promotes			 C-terminal chromoshadow domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_120	12411497	( C) The C-terminal chromoshadow domain of HP1alpha is sufficient to promote BRG1 binding to HP1beta and HP1gamma.	bind
2571	4	1765	7	10	NULL	0	NULL	HP1alpha	GP		promotes			C-terminal chromoshadow domain		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_120	12411497	( C) The C-terminal chromoshadow domain of HP1alpha is sufficient to promote BRG1 binding to HP1beta and HP1gamma.	bind
1573	1	1766	5	10	NULL	0	NULL	C1	GP		bind			carboxy-terminal cytoplasmic domain		TRAF proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_3_1224_s_105	11158621	( C) The C1 carboxy-terminal cytoplasmic domain can bind to TRAF proteins.	bind
2573	2	1766	7	10	NULL	0	NULL	C1 	GP		bind 			carboxy-terminal cytoplasmic domain 		TRAF proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_3_1224_s_105	11158621	( C) The C1 carboxy-terminal cytoplasmic domain can bind to TRAF proteins.	bind
1574	1	1767	5	10	NULL	0	NULL	GTP	Chemical		bind					Ypt7p	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_19_5216_s_159	10508155	( C) The catalytically active fragments with the lowest specific activity were used to follow time kinetics of hydrolysis of GTP bound to Ypt7p.	bind
2572	1	1767	7	10	NULL	0	NULL	GTP	Chemical		bind					Ypt7p	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_19_5216_s_159	10508155	( C) The catalytically active fragments with the lowest specific activity were used to follow time kinetics of hydrolysis of GTP bound to Ypt7p.	bind
1575	1	1768	5	10	NULL	0	NULL	CARM1	GP		bind			central domain		p65	GP		RHD domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_1_85_s_102	15616592	( C) The central domain of CARM1 binds to the RHD domain of p65.	bind
2576	1	1768	7	10	NULL	0	NULL	CARM1	GP		bind			central domain 		 p65	GP		RHD domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_1_85_s_102	15616592	( C) The central domain of CARM1 binds to the RHD domain of p65.	bind
2577	1	1770	7	10	NULL	0	NULL	CREM factor	GP		bind					Oxct2b	GP			promoter ( - 40/ - 20)	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3401_s_211	15951513	( C) The CREM factor binds to the Oxct2b promoter ( - 40/ - 20)  in vitro.	bind
1577	1	1772	5	10	NULL	0	NULL			distal	bind				G/C element	Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw60_gene_242_1_209_s_227	10721714	( C) The distal G/C element binds Sp1 in EMSA. 32P-labelled -72; -48 probe was incubated with NIH3T3 nuclear extracts, in the presence of a 100-fold molar excess of cold competitor.	bind
2578	1	1772	7	10	NULL	0	NULL			distal	bind				G/C element	Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw60_gene_242_1_209_s_227	10721714	( C) The distal G/C element binds Sp1 in EMSA. 32P-labelled -72; -48 probe was incubated with NIH3T3 nuclear extracts, in the presence of a 100-fold molar excess of cold competitor.	bind
1578	1	1774	5	10	NULL	0	NULL	HOPS complex	GP		bind		directly			Vam7p	GP		PX domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_8_1579_s_191	16601699	( C) The HOPS complex binds directly to the Vam7p PX domain.	bind
2579	1	1774	7	10	NULL	0	NULL	HOPS complex	GP		binds		directly			Vam7p	GP		PX domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_8_1579_s_191	16601699	( C) The HOPS complex binds directly to the Vam7p PX domain.	bind
1579	1	1775	5	10	NULL	0	NULL	L-valine molecule	AminoAcid		bind					IleRS	GP		aminoacylation site		NULL		NULL	NULL	NULL	NULL	gw60_science_280_5363_578_s_80	9554847	( C) The L-valine molecule bound to the aminoacylation site of IleRS.	bind
2580	1	1775	7	10	NULL	0	NULL	 L-valine	AminoAcid		bind					IleRS	GP		 aminoacylation site		NULL		NULL	NULL	NULL	NULL	gw60_science_280_5363_578_s_80	9554847	( C) The L-valine molecule bound to the aminoacylation site of IleRS.	bind
1580	1	1776	5	10	NULL	0	NULL	L13	AminoAcid	mutation of 	change					U1C	GP	conformation of 			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_183	15465910	( C) The L13 mutation causes a U1C conformational change (blue square rather than blue  oval), which binds poorly to RNA. U1 RNA therefore has a tendency to adopt the low-temperature  conformation as in  A, which allows the ps5'' to interact with the 5' end of U1 (double arrow)  and compete with pre-mRNA base-pairing.	bind
1581	2	1776	5	10	NULL	0	NULL	statement 1	Process		bind		poorly			RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_183	15465910	( C) The L13 mutation causes a U1C conformational change (blue square rather than blue  oval), which binds poorly to RNA. U1 RNA therefore has a tendency to adopt the low-temperature  conformation as in  A, which allows the ps5'' to interact with the 5' end of U1 (double arrow)  and compete with pre-mRNA base-pairing.	bind
1584	3	1776	5	10	NULL	0	NULL	U1 RNA	NucleicAcid		adopt		tendency to			low-temperature conformation	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_183	15465910	( C) The L13 mutation causes a U1C conformational change (blue square rather than blue  oval), which binds poorly to RNA. U1 RNA therefore has a tendency to adopt the low-temperature  conformation as in  A, which allows the ps5'' to interact with the 5' end of U1 (double arrow)  and compete with pre-mRNA base-pairing.	bind
1585	4	1776	5	10	NULL	0	NULL	ps5''	GP		interact with					U1	NucleicAcid		5' end		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_183	15465910	( C) The L13 mutation causes a U1C conformational change (blue square rather than blue  oval), which binds poorly to RNA. U1 RNA therefore has a tendency to adopt the low-temperature  conformation as in  A, which allows the ps5'' to interact with the 5' end of U1 (double arrow)  and compete with pre-mRNA base-pairing.	bind
1587	5	1776	5	10	NULL	0	NULL	statement 3	Process		allows					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_183	15465910	( C) The L13 mutation causes a U1C conformational change (blue square rather than blue  oval), which binds poorly to RNA. U1 RNA therefore has a tendency to adopt the low-temperature  conformation as in  A, which allows the ps5'' to interact with the 5' end of U1 (double arrow)  and compete with pre-mRNA base-pairing.	bind
1590	6	1776	5	10	NULL	0	NULL	ps5''	GP		compete with					pre-mRNA base-pairing	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_183	15465910	( C) The L13 mutation causes a U1C conformational change (blue square rather than blue  oval), which binds poorly to RNA. U1 RNA therefore has a tendency to adopt the low-temperature  conformation as in  A, which allows the ps5'' to interact with the 5' end of U1 (double arrow)  and compete with pre-mRNA base-pairing.	bind
1591	7	1776	5	10	NULL	0	NULL	statement 3	Process		allows					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_183	15465910	( C) The L13 mutation causes a U1C conformational change (blue square rather than blue  oval), which binds poorly to RNA. U1 RNA therefore has a tendency to adopt the low-temperature  conformation as in  A, which allows the ps5'' to interact with the 5' end of U1 (double arrow)  and compete with pre-mRNA base-pairing.	bind
2581	2	1776	7	10	NULL	0	NULL	statement 1	Process		bind		poorly			RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_183	15465910	( C) The L13 mutation causes a U1C conformational change (blue square rather than blue  oval), which binds poorly to RNA. U1 RNA therefore has a tendency to adopt the low-temperature  conformation as in  A, which allows the ps5'' to interact with the 5' end of U1 (double arrow)  and compete with pre-mRNA base-pairing.	bind
2582	3	1776	7	10	NULL	0	NULL	ps5''	GP		bind					U1	NucleicAcid			5' end	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_183	15465910	( C) The L13 mutation causes a U1C conformational change (blue square rather than blue  oval), which binds poorly to RNA. U1 RNA therefore has a tendency to adopt the low-temperature  conformation as in  A, which allows the ps5'' to interact with the 5' end of U1 (double arrow)  and compete with pre-mRNA base-pairing.	bind
2583	1	1776	7	10	NULL	0	NULL	L13 	AminoAcid	mutation of	change					U1C 	GP	conformation of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_183	15465910	( C) The L13 mutation causes a U1C conformational change (blue square rather than blue  oval), which binds poorly to RNA. U1 RNA therefore has a tendency to adopt the low-temperature  conformation as in  A, which allows the ps5'' to interact with the 5' end of U1 (double arrow)  and compete with pre-mRNA base-pairing.	bind
2584	4	1776	7	10	NULL	0	NULL	U1 RNA	NucleicAcid		adopts					low-temperature conformation	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_183	15465910	( C) The L13 mutation causes a U1C conformational change (blue square rather than blue  oval), which binds poorly to RNA. U1 RNA therefore has a tendency to adopt the low-temperature  conformation as in  A, which allows the ps5'' to interact with the 5' end of U1 (double arrow)  and compete with pre-mRNA base-pairing.	bind
2585	5	1776	7	10	NULL	0	NULL	statement 4	Process		allows					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_183	15465910	( C) The L13 mutation causes a U1C conformational change (blue square rather than blue  oval), which binds poorly to RNA. U1 RNA therefore has a tendency to adopt the low-temperature  conformation as in  A, which allows the ps5'' to interact with the 5' end of U1 (double arrow)  and compete with pre-mRNA base-pairing.	bind
2586	6	1776	7	10	NULL	0	NULL	 ps5''	GP		compete with					pre-mRNA base-pairing	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_183	15465910	( C) The L13 mutation causes a U1C conformational change (blue square rather than blue  oval), which binds poorly to RNA. U1 RNA therefore has a tendency to adopt the low-temperature  conformation as in  A, which allows the ps5'' to interact with the 5' end of U1 (double arrow)  and compete with pre-mRNA base-pairing.	bind
61570	7	1776	7	10	NULL	0	NULL	statement 4	Process		allows					statement 6	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_41_14841_s_183	15465910	( C) The L13 mutation causes a U1C conformational change (blue square rather than blue  oval), which binds poorly to RNA. U1 RNA therefore has a tendency to adopt the low-temperature  conformation as in  A, which allows the ps5'' to interact with the 5' end of U1 (double arrow)  and compete with pre-mRNA base-pairing.	bind
1595	1	1777	5	10	NULL	0	NULL	Nbp2	GP		bind			N-terminal domain (residues 1 115)		Ptc1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_2_302_s_164	14685261	( C) The Nbp2 N-terminal domain (residues 1 115) binds Ptc1.	bind
2587	2	1777	7	10	NULL	0	NULL	Nbp2	GP		binds			N-terminal domain (residues 1 115) 		Ptc1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_2_302_s_164	14685261	( C) The Nbp2 N-terminal domain (residues 1 115) binds Ptc1.	bind
1597	1	1778	5	10	NULL	0	NULL	NCT	GP		bind			TM		PSCT	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_24_4738_s_79	15549135	( C) The NCT TM binds PSCT also in the context of VSVG-EGFP, another type I protein.	bind
2588	1	1778	7	10	NULL	0	NULL	NCT	GP		bind			 TM		PSCT	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_24_4738_s_79	15549135	( C) The NCT TM binds PSCT also in the context of VSVG-EGFP, another type I protein.	bind
1598	1	1780	5	10	NULL	0	NULL	VAP-1	GP	oligosaccahride modifications	bind					lectin-like molecule	GP	unknown			NULL	lymphocytes	NULL	NULL	NULL	NULL	gw60_embo_20_15_3893_s_117	11483492	( C) The oligosaccahride modifications of VAP-1 (purple extensions) can bind to an unknown lectin-like molecule (yellow) on lymphocytes.	bind
2591	1	1780	7	10	NULL	0	NULL	VAP-1 	GP	oligosaccahride modifications	bind					lectin-like molecule	GP	unknown			NULL	lymphocytes	NULL	NULL	NULL	NULL	gw60_embo_20_15_3893_s_117	11483492	( C) The oligosaccahride modifications of VAP-1 (purple extensions) can bind to an unknown lectin-like molecule (yellow) on lymphocytes.	bind
2593	1	1781	7	10	NULL	0	NULL	Dlg1	GP		bind					E4-ORF1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_6_1406_s_98	16511562	( C) The PDZ1+2 conformational unit is necessary and sufficient to mediate binding of  Dlg1 to E4-ORF1.	bind
2595	2	1781	7	10	NULL	0	NULL	PDZ1+2	GP		is necessary for			conformational unit		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_6_1406_s_98	16511562	( C) The PDZ1+2 conformational unit is necessary and sufficient to mediate binding of  Dlg1 to E4-ORF1.	bind
1602	1	1782	5	10	NULL	0	NULL	PACS-1	GP	recombinant HIS-tagged	bind			furin-binding region (115 255)		polycystin-2 fragment	GP	recombinant GST-tagged	741 871 		NULL	in vitro	NULL	NULL	NULL	NULL	gw70_embo_24_4_705_s_42	15692563	( C) The recombinant HIS-tagged furin-binding region of PACS-1 (HIS.PACS-1115 255) binds a recombinant GST-tagged polycystin-2 fragment containing amino acids 741  871 (GST. PKD2741 871)  in vitro (upper panel).	bind
2601	1	1782	7	10	NULL	0	NULL	PACS-1	GP	recombinant HIS-tagged	bind			furin-binding region HIS.PACS-1115 255		polycystin-2 fragment	GP	recombinant GST-tagged 	amino acids 741 to 871		NULL	in vitro	NULL	NULL	NULL	NULL	gw70_embo_24_4_705_s_42	15692563	( C) The recombinant HIS-tagged furin-binding region of PACS-1 (HIS.PACS-1115 255) binds a recombinant GST-tagged polycystin-2 fragment containing amino acids 741  871 (GST. PKD2741 871)  in vitro (upper panel).	bind
2603	1	1783	7	10	NULL	0	NULL	mTAb1	GP		bind					mTOR	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_13_7772_s_120	9636226	( C) The relative amounts of mTAb1 bound to mTOR were determined by laser densitometry.	bind
1608	1	1784	5	10	NULL	0	NULL	PIAS3	GP	mutant	does not bind			RING domain		p300	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_1_99_s_147	14691252	( C) The RING domain mutant PIAS3 cannot bind to p300.	bind
2605	1	1784	7	10	NULL	0	NULL	PIAS3 	GP	mutant	does not bind			RING domain 		p300	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_1_99_s_147	14691252	( C) The RING domain mutant PIAS3 cannot bind to p300.	bind
1609	1	1785	5	10	NULL	0	NULL	fibronectin	GP		bind					beta1 integrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_2_692_s_77	10639141	( c) The same experiment as  a in the presence of 2 mg/ml RGD peptide, which inhibits fibronectin binding to the beta1 integrin ( 19,  20).	bind
1610	2	1785	5	10	NULL	0	NULL	RGD peptide	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_2_692_s_77	10639141	( c) The same experiment as  a in the presence of 2 mg/ml RGD peptide, which inhibits fibronectin binding to the beta1 integrin ( 19,  20).	bind
2607	1	1785	7	10	NULL	0	NULL	fibronectin	GP		bind					beta1 integrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_2_692_s_77	10639141	( c) The same experiment as  a in the presence of 2 mg/ml RGD peptide, which inhibits fibronectin binding to the beta1 integrin ( 19,  20).	bind
2609	2	1785	7	10	NULL	0	NULL	RGD peptide	GP		inhibits					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_2_692_s_77	10639141	( c) The same experiment as  a in the presence of 2 mg/ml RGD peptide, which inhibits fibronectin binding to the beta1 integrin ( 19,  20).	bind
1612	1	1786	5	10	NULL	0	NULL	FGFR	GP		bind			D2		FGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_750_s_20	12730587	( C) The second (D2) and third (D3) Ig-like extracellular domains of FGFR bind to FGF; the cofactor heparin binds to a positively charged region in D2.	bind
1613	2	1786	5	10	NULL	0	NULL	D2	GP		is					second Ig-like extracellular domains	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_750_s_20	12730587	( C) The second (D2) and third (D3) Ig-like extracellular domains of FGFR bind to FGF; the cofactor heparin binds to a positively charged region in D2.	bind
1614	3	1786	5	10	NULL	0	NULL	FGFR	GP		bind			D3		FGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_750_s_20	12730587	( C) The second (D2) and third (D3) Ig-like extracellular domains of FGFR bind to FGF; the cofactor heparin binds to a positively charged region in D2.	bind
1616	4	1786	5	10	NULL	0	NULL	D3	GP		is					third Ig-like extracellular domains	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_750_s_20	12730587	( C) The second (D2) and third (D3) Ig-like extracellular domains of FGFR bind to FGF; the cofactor heparin binds to a positively charged region in D2.	bind
1618	5	1786	5	10	NULL	0	NULL	heparin	GP	cofactor	bind					D2	GP		positively charged region		NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_750_s_20	12730587	( C) The second (D2) and third (D3) Ig-like extracellular domains of FGFR bind to FGF; the cofactor heparin binds to a positively charged region in D2.	bind
2610	1	1786	7	10	NULL	0	NULL	FGFR	GP		bind			D2 domain		FGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_750_s_20	12730587	( C) The second (D2) and third (D3) Ig-like extracellular domains of FGFR bind to FGF; the cofactor heparin binds to a positively charged region in D2.	bind
2611	2	1786	7	10	NULL	0	NULL	Heparin	GP	cofactor	bind					D2	GP		positively charged region 		NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_750_s_20	12730587	( C) The second (D2) and third (D3) Ig-like extracellular domains of FGFR bind to FGF; the cofactor heparin binds to a positively charged region in D2.	bind
50332	3	1786	7	10	NULL	0	NULL	FGFR	GP		bind			D3 domain		FGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_750_s_20	12730587	( C) The second (D2) and third (D3) Ig-like extracellular domains of FGFR bind to FGF; the cofactor heparin binds to a positively charged region in D2.	bind
50333	4	1786	7	10	NULL	0	NULL	D2	GP		is					second Ig-like extracellular domains 	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_750_s_20	12730587	( C) The second (D2) and third (D3) Ig-like extracellular domains of FGFR bind to FGF; the cofactor heparin binds to a positively charged region in D2.	bind
50334	5	1786	7	10	NULL	0	NULL	D3	GP		is					third Ig-like extracellular domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_750_s_20	12730587	( C) The second (D2) and third (D3) Ig-like extracellular domains of FGFR bind to FGF; the cofactor heparin binds to a positively charged region in D2.	bind
1611	1	1788	5	10	NULL	0	NULL	SMN complex	GP		bind					U1 snRNA	NucleicAcid		SL1		NULL		NULL	NULL	NULL	NULL	gw60_embo_21_5_1188_s_100	11867547	( C) The SMN complex binding to the SL1 of U1 snRNA is sequence specific.	bind
2574	2	1788	5	10	NULL	0	NULL	statement 1	Process		occurs in					sequence specific manner	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_5_1188_s_100	11867547	( C) The SMN complex binding to the SL1 of U1 snRNA is sequence specific.	bind
2612	1	1788	7	10	NULL	0	NULL	SMN complex	GP		bind					U1 snRNA	NucleicAcid		SL1 		NULL		NULL	NULL	NULL	NULL	gw60_embo_21_5_1188_s_100	11867547	( C) The SMN complex binding to the SL1 of U1 snRNA is sequence specific.	bind
2613	2	1788	7	10	NULL	0	NULL	statement 1	Process		occur in 					sequence specific manner	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_5_1188_s_100	11867547	( C) The SMN complex binding to the SL1 of U1 snRNA is sequence specific.	bind
2736	1	1789	5	10	NULL	0	NULL	SMN complex	GP		bind					U1 snRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_5_1188_s_71	11867547	( C) The SMN complex binding to U1 snRNA is independent of Sm core assembly.	bind
2737	2	1789	5	10	NULL	0	NULL	statement 1	Process		independent of					Sm core assembly	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_5_1188_s_71	11867547	( C) The SMN complex binding to U1 snRNA is independent of Sm core assembly.	bind
2614	1	1789	7	10	NULL	0	NULL	SMN complex	GP		bind					 U1 snRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_5_1188_s_71	11867547	( C) The SMN complex binding to U1 snRNA is independent of Sm core assembly.	bind
2615	2	1789	7	10	NULL	0	NULL	statement 1	Process		is independent of					Sm core assembly	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_5_1188_s_71	11867547	( C) The SMN complex binding to U1 snRNA is independent of Sm core assembly.	bind
2746	1	1790	5	10	NULL	0	NULL	ssDNA	NucleicAcid		bind					hRad54	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_6_1346_s_143	11884632	( C) The ssDNA binding of hRad54 and hRad54B.	bind
2747	2	1790	5	10	NULL	0	NULL	ssDNA	NucleicAcid		bind					hRad54B	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_6_1346_s_143	11884632	( C) The ssDNA binding of hRad54 and hRad54B.	bind
2616	1	1790	7	10	NULL	0	NULL	ssDNA	NucleicAcid		bind					hRad54	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_6_1346_s_143	11884632	( C) The ssDNA binding of hRad54 and hRad54B.	bind
2617	2	1790	7	10	NULL	0	NULL	ssDNA	NucleicAcid		bind					hRad54B	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_6_1346_s_143	11884632	( C) The ssDNA binding of hRad54 and hRad54B.	bind
2749	1	1791	5	10	NULL	0	NULL	TIF32	GP		bind			CTD		18S rRNA	NucleicAcid	biotinylated			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_6_786_s_192	12651896	( C) The TIF32-CTD binds to biotinylated 18S rRNA in Northwestern assays.	bind
2618	1	1791	7	10	NULL	0	NULL	TIF32	GP		bind			CTD		18S rRNA	NucleicAcid	biotinylated			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_6_786_s_192	12651896	( C) The TIF32-CTD binds to biotinylated 18S rRNA in Northwestern assays.	bind
2619	1	1792	7	10	NULL	0	NULL	Ku 	GP		bind					TRF1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_22_2807_s_123	11090128	( C) The TRF1 homodimer bound to internal telomeric tracts with Ku bound to TRF1.	bind
2620	2	1792	7	10	NULL	0	NULL	TRF1 homodimer	GP		binds to							internal 	telomeric tracts		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_22_2807_s_123	11090128	( C) The TRF1 homodimer bound to internal telomeric tracts with Ku bound to TRF1.	bind
2762	1	1793	5	10	NULL	0	NULL	TRX	GP		bind			SET domain		histone	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_17_2197_s_20	11544176	( C) The TRX SET domain binds to a histone-affinity matrix.	bind
2621	1	1793	7	10	NULL	0	NULL	 TRX	GP		bind			SET domain		histone	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_17_2197_s_20	11544176	( C) The TRX SET domain binds to a histone-affinity matrix.	bind
2764	1	1794	5	10	NULL	0	NULL	FANCG	GP		bind					CYP2E1	GP				NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_23_1_67_s_114	11756225	( C) The upper panel shows the binding of FANCG to CYP2E1.	bind
2622	1	1794	7	10	NULL	0	NULL	FANCG	GP		bind					 CYP2E1	GP				NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_23_1_67_s_114	11756225	( C) The upper panel shows the binding of FANCG to CYP2E1.	bind
2767	1	1795	5	10	NULL	0	NULL	holo-TFIID	GP		bind					TBP antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5447_2153_s_94	10591646	( C) The yellow mesh shows the density difference between the holo-TFIID and TFIID that is bound to the TBP antibody.	bind
2768	2	1795	5	10	NULL	0	NULL	TFIID	GP		bind					TBP antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5447_2153_s_94	10591646	( C) The yellow mesh shows the density difference between the holo-TFIID and TFIID that is bound to the TBP antibody.	bind
2623	1	1795	7	10	NULL	0	NULL	holo-TFIID	GP		bind					TBP antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5447_2153_s_94	10591646	( C) The yellow mesh shows the density difference between the holo-TFIID and TFIID that is bound to the TBP antibody.	bind
2624	2	1795	7	10	NULL	0	NULL	TFIID	GP		bind					TBP antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5447_2153_s_94	10591646	( C) The yellow mesh shows the density difference between the holo-TFIID and TFIID that is bound to the TBP antibody.	bind
2776	1	1796	5	10	NULL	0	NULL	PIC	GP		bind									Ad origin of DNA replication	NULL		NULL	NULL	NULL	NULL	gw60_gene_236_1_1_s_193	10433960	( C) This PIC binds the Ad origin of DNA replication (the 5' attached TP was omitted for simplification), most likely in a irregular, bent DNA structure.	bind
2778	2	1796	5	10	NULL	0	NULL	statement 1	Process		occurs					DNA structure	NucleicAcid	irregular bent			NULL		NULL	NULL	NULL	NULL	gw60_gene_236_1_1_s_193	10433960	( C) This PIC binds the Ad origin of DNA replication (the 5' attached TP was omitted for simplification), most likely in a irregular, bent DNA structure.	bind
2625	1	1796	7	10	NULL	0	NULL	PIC	GP		bind									Ad origin of DNA replication	NULL		NULL	NULL	NULL	NULL	gw60_gene_236_1_1_s_193	10433960	( C) This PIC binds the Ad origin of DNA replication (the 5' attached TP was omitted for simplification), most likely in a irregular, bent DNA structure.	bind
2626	2	1796	7	10	NULL	0	NULL	statement 1	Process		occurs					 DNA structure	NucleicAcid	 irregular bent			NULL		NULL	NULL	NULL	NULL	gw60_gene_236_1_1_s_193	10433960	( C) This PIC binds the Ad origin of DNA replication (the 5' attached TP was omitted for simplification), most likely in a irregular, bent DNA structure.	bind
2780	1	1797	5	10	NULL	0	NULL	THP-1 	GP		bind					MCP-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_289_5482_1202_s_105	10947989	( C) THP-1 cell receptor binding of MCP-3 and  MCP-3(5-76).	bind
2781	2	1797	5	10	NULL	0	NULL	THP-1	GP		bind					MCP-3	GP		5-76		NULL		NULL	NULL	NULL	NULL	gw60_science_289_5482_1202_s_105	10947989	( C) THP-1 cell receptor binding of MCP-3 and  MCP-3(5-76).	bind
50335	3	1797	5	10	NULL	0	NULL	THP-1	GP		is a type of					cell receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_289_5482_1202_s_105	10947989	( C) THP-1 cell receptor binding of MCP-3 and  MCP-3(5-76).	bind
2627	1	1797	7	10	NULL	0	NULL	THP-1	GP		bind					MCP-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_289_5482_1202_s_105	10947989	( C) THP-1 cell receptor binding of MCP-3 and  MCP-3(5-76).	bind
2628	2	1797	7	10	NULL	0	NULL	THP-1	GP		bind					MCP-3	GP		5-76		NULL		NULL	NULL	NULL	NULL	gw60_science_289_5482_1202_s_105	10947989	( C) THP-1 cell receptor binding of MCP-3 and  MCP-3(5-76).	bind
50337	3	1797	7	10	NULL	0	NULL	THP-1	GP		is a type of					cell receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_289_5482_1202_s_105	10947989	( C) THP-1 cell receptor binding of MCP-3 and  MCP-3(5-76).	bind
2783	1	1799	5	10	NULL	0	NULL	Tpr	GP		does not bind					importin alpha/beta-NLS complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_1_31_s_419	9531546	( C) Tpr does not bind to importin  alpha/beta-NLS complexes.	bind
2629	1	1799	7	10	NULL	0	NULL	Tpr	GP		does not bind					importin alpha/beta-NLS complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_1_31_s_419	9531546	( C) Tpr does not bind to importin  alpha/beta-NLS complexes.	bind
2787	1	1800	5	10	NULL	0	NULL	translesion polymerase	GP		bind					recA	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_37_0_31_s_295	14616055	( c) Translesion polymerase binds to recA and related proteins.	bind
2788	2	1800	5	10	NULL	0	NULL	translesion polymerase	GP		bind					related proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_37_0_31_s_295	14616055	( c) Translesion polymerase binds to recA and related proteins.	bind
2630	1	1800	7	10	NULL	0	NULL	Translesion polymerase	GP		bind					recA	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_37_0_31_s_295	14616055	( c) Translesion polymerase binds to recA and related proteins.	bind
2631	2	1800	7	10	NULL	0	NULL	Translesion polymerase	GP	 	bind					recA related proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_37_0_31_s_295	14616055	( c) Translesion polymerase binds to recA and related proteins.	bind
2789	1	1801	5	10	NULL	0	NULL	Tre1	GP		bind					Bsd2	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_embo_25_4_662_s_141	16456538	( C) Tre1 binds Bsd2  in vivo.	bind
1926	1	1801	7	10	NULL	0	NULL	 Tre1	GP		bind					Bsd2	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_embo_25_4_662_s_141	16456538	( C) Tre1 binds Bsd2  in vivo.	bind
2790	1	1802	5	10	NULL	0	NULL	tRNA	NucleicAcid		bind		directly			Exp5	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_22_6216_s_177	12426393	( C) tRNA can bind directly to Exp5.	bind
1927	1	1802	7	10	NULL	0	NULL	tRNA	NucleicAcid		bind		directly			Exp5	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_22_6216_s_177	12426393	( C) tRNA can bind directly to Exp5.	bind
2791	1	1803	5	10	NULL	0	NULL	p65	GP	unphosphorylated	bind					HDAC1	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_10_1991_s_285	15192014	( C) Unphosphorylated p65 but not phosphorylated (S536) p65 binds to HDAC1 and 3.	bind
2792	2	1803	5	10	NULL	0	NULL	p65	GP	unphosphorylated	bind					HDAC3	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_10_1991_s_285	15192014	( C) Unphosphorylated p65 but not phosphorylated (S536) p65 binds to HDAC1 and 3.	bind
2793	3	1803	5	10	NULL	0	NULL	p65	GP	phosphorylated	does not bind			S536		HDAC1	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_10_1991_s_285	15192014	( C) Unphosphorylated p65 but not phosphorylated (S536) p65 binds to HDAC1 and 3.	bind
2794	4	1803	5	10	NULL	0	NULL	p65	GP	phosphorylated	does not bind			S536		HDAC3	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_10_1991_s_285	15192014	( C) Unphosphorylated p65 but not phosphorylated (S536) p65 binds to HDAC1 and 3.	bind
1928	1	1803	7	10	NULL	0	NULL	p65	GP	unphosphorylated	bind					 HDAC1	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_10_1991_s_285	15192014	( C) Unphosphorylated p65 but not phosphorylated (S536) p65 binds to HDAC1 and 3.	bind
1929	2	1803	7	10	NULL	0	NULL	p65	GP	unphosphorylated	binds to					HDAC3	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_10_1991_s_285	15192014	( C) Unphosphorylated p65 but not phosphorylated (S536) p65 binds to HDAC1 and 3.	bind
1930	3	1803	7	10	NULL	0	NULL	p65	GP	phosphorylated 	does not bind			S536		HDAC1	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_10_1991_s_285	15192014	( C) Unphosphorylated p65 but not phosphorylated (S536) p65 binds to HDAC1 and 3.	bind
1931	4	1803	7	10	NULL	0	NULL	p65	GP	phosphorylated 	does not bind			S536		HDAC3	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_10_1991_s_285	15192014	( C) Unphosphorylated p65 but not phosphorylated (S536) p65 binds to HDAC1 and 3.	bind
2820	1	1806	5	10	NULL	0	NULL	eIF4E	GP		bind					m7G-Sepharose	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_52_18105_s_57	15601771	( c) Western blot of eIF4E remaining bound to m7G-Sepharose upon competition with various concentrations of m7GTP or RTP.	bind
2821	2	1806	5	10	NULL	0	NULL	eIF4E	GP		bind					m7GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_52_18105_s_57	15601771	( c) Western blot of eIF4E remaining bound to m7G-Sepharose upon competition with various concentrations of m7GTP or RTP.	bind
2822	3	1806	5	10	NULL	0	NULL	eIF4E	GP		bind					RTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_52_18105_s_57	15601771	( c) Western blot of eIF4E remaining bound to m7G-Sepharose upon competition with various concentrations of m7GTP or RTP.	bind
2823	4	1806	5	10	NULL	0	NULL	statement 2	Process		compete					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_52_18105_s_57	15601771	( c) Western blot of eIF4E remaining bound to m7G-Sepharose upon competition with various concentrations of m7GTP or RTP.	bind
3201	5	1806	5	10	NULL	0	NULL	statement 3	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_52_18105_s_57	15601771	( c) Western blot of eIF4E remaining bound to m7G-Sepharose upon competition with various concentrations of m7GTP or RTP.	bind
1932	1	1806	7	10	NULL	0	NULL	eIF4E	GP		bind to					m7G-Sepharose	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_52_18105_s_57	15601771	( c) Western blot of eIF4E remaining bound to m7G-Sepharose upon competition with various concentrations of m7GTP or RTP.	bind
1933	2	1806	7	10	NULL	0	NULL	eIF4E	GP		bind to					m7GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_52_18105_s_57	15601771	( c) Western blot of eIF4E remaining bound to m7G-Sepharose upon competition with various concentrations of m7GTP or RTP.	bind
1934	3	1806	7	10	NULL	0	NULL	eIF4E	GP		bind to					RTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_52_18105_s_57	15601771	( c) Western blot of eIF4E remaining bound to m7G-Sepharose upon competition with various concentrations of m7GTP or RTP.	bind
2207	4	1806	7	10	NULL	0	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_52_18105_s_57	15601771	( c) Western blot of eIF4E remaining bound to m7G-Sepharose upon competition with various concentrations of m7GTP or RTP.	bind
2208	5	1806	7	10	NULL	0	NULL	statement 3	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_52_18105_s_57	15601771	( c) Western blot of eIF4E remaining bound to m7G-Sepharose upon competition with various concentrations of m7GTP or RTP.	bind
1935	1	1809	7	10	NULL	0	NULL	GST. PRIC285	GP		bind					GST-PPARalpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_18_11836_s_138	12189208	( C) [35]Methionine-labeled full-length PRIC285 generated by  in vitro translation was incubated with GSH-Sepharose beads bound with purified  E. coli-expressed GST-PPARalpha or GST. PRIC285 bound to PPARalpha in the absence of ligand, and the addition of ligand increased the binding  2-fold.	bind
1936	2	1809	7	10	NULL	0	NULL	statement 1	Process		occurs in absence of 					ligand	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_18_11836_s_138	12189208	( C) [35]Methionine-labeled full-length PRIC285 generated by  in vitro translation was incubated with GSH-Sepharose beads bound with purified  E. coli-expressed GST-PPARalpha or GST. PRIC285 bound to PPARalpha in the absence of ligand, and the addition of ligand increased the binding  2-fold.	bind
1937	3	1809	7	10	NULL	0	NULL	ligand	GP	presence of 	increase					statement 1	Process	 			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_18_11836_s_138	12189208	( C) [35]Methionine-labeled full-length PRIC285 generated by  in vitro translation was incubated with GSH-Sepharose beads bound with purified  E. coli-expressed GST-PPARalpha or GST. PRIC285 bound to PPARalpha in the absence of ligand, and the addition of ligand increased the binding  2-fold.	bind
2824	1	1810	5	10	NULL	0	NULL	Galphai	GP		does not bind		directly			ERalpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_49_17126_s_172	15569929	( C)Galphai does not bind directly to ERalpha.	bind
1938	1	1810	7	10	NULL	0	NULL	Galphai	GP		does not bind		directly			ERalpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_49_17126_s_172	15569929	( C)Galphai does not bind directly to ERalpha.	bind
2825	1	1812	5	10	NULL	0	NULL	Swi/nf	GP		bind					GAL1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_23_20_4040_s_74	15385957	( C, D) Binding of Swi/nf to the  GAL1 and  GAL7 promoters, respectively.	bind
2826	2	1812	5	10	NULL	0	NULL	Swi/nf	GP		bind					GAL7	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_23_20_4040_s_74	15385957	( C, D) Binding of Swi/nf to the  GAL1 and  GAL7 promoters, respectively.	bind
1939	1	1812	7	10	NULL	0	NULL	 Swi/nf	GP		bind					 GAL1 	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_23_20_4040_s_74	15385957	( C, D) Binding of Swi/nf to the  GAL1 and  GAL7 promoters, respectively.	bind
1940	2	1812	7	10	NULL	0	NULL	Swi/nf	GP		bind					GAL7 	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_23_20_4040_s_74	15385957	( C, D) Binding of Swi/nf to the  GAL1 and  GAL7 promoters, respectively.	bind
2827	1	1813	5	10	NULL	0	NULL	TNF-alpha	GP		degrade					IkappaB-alpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_22_2668_s_130	16260493	( C,D) IkappaB-alpha degradation and JNK phosphorylation by TNF-alpha ( C) or IL-1 ( D) were analyzed by immunoblotting with antibodies specific for IkappaB-alpha and phospho-JNK, respectively.	bind
2828	2	1813	5	10	NULL	0	NULL	IL-1	GP		degrade					IkappaB-alpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_22_2668_s_130	16260493	( C,D) IkappaB-alpha degradation and JNK phosphorylation by TNF-alpha ( C) or IL-1 ( D) were analyzed by immunoblotting with antibodies specific for IkappaB-alpha and phospho-JNK, respectively.	bind
2829	3	1813	5	10	NULL	0	NULL	TNF-alpha	GP		phosphorylate					JNK	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_22_2668_s_130	16260493	( C,D) IkappaB-alpha degradation and JNK phosphorylation by TNF-alpha ( C) or IL-1 ( D) were analyzed by immunoblotting with antibodies specific for IkappaB-alpha and phospho-JNK, respectively.	bind
2830	4	1813	5	10	NULL	0	NULL	IL-1	GP		phosphorylate					JNK	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_22_2668_s_130	16260493	( C,D) IkappaB-alpha degradation and JNK phosphorylation by TNF-alpha ( C) or IL-1 ( D) were analyzed by immunoblotting with antibodies specific for IkappaB-alpha and phospho-JNK, respectively.	bind
1941	1	1813	7	10	NULL	0	NULL	JNK 	GP		phosphorylated by					TNF-alpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_22_2668_s_130	16260493	( C,D) IkappaB-alpha degradation and JNK phosphorylation by TNF-alpha ( C) or IL-1 ( D) were analyzed by immunoblotting with antibodies specific for IkappaB-alpha and phospho-JNK, respectively.	bind
1942	2	1813	7	10	NULL	0	NULL	JNK	GP		phosphorylated by					 IL-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_22_2668_s_130	16260493	( C,D) IkappaB-alpha degradation and JNK phosphorylation by TNF-alpha ( C) or IL-1 ( D) were analyzed by immunoblotting with antibodies specific for IkappaB-alpha and phospho-JNK, respectively.	bind
50340	3	1813	7	10	NULL	0	NULL	TNF-alpha	GP		degrade					IkappaB-alpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_22_2668_s_130	16260493	( C,D) IkappaB-alpha degradation and JNK phosphorylation by TNF-alpha ( C) or IL-1 ( D) were analyzed by immunoblotting with antibodies specific for IkappaB-alpha and phospho-JNK, respectively.	bind
50341	4	1813	7	10	NULL	0	NULL	IL-1	GP		degrade					IkappaB-alpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_22_2668_s_130	16260493	( C,D) IkappaB-alpha degradation and JNK phosphorylation by TNF-alpha ( C) or IL-1 ( D) were analyzed by immunoblotting with antibodies specific for IkappaB-alpha and phospho-JNK, respectively.	bind
2831	1	1815	5	10	NULL	0	NULL	R anti-CD21 antibody	GP		bind					CD21	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_16_10641_s_190	12122212	( Center) Flow cytometry showing binding of R anti-CD21 antibody to CD21 and CD21mut (dark lines) but not to L cells transfected with vector alone.	bind
2832	2	1815	5	10	NULL	0	NULL	R anti-CD21 antibody	GP		bind					CD21mut	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_16_10641_s_190	12122212	( Center) Flow cytometry showing binding of R anti-CD21 antibody to CD21 and CD21mut (dark lines) but not to L cells transfected with vector alone.	bind
2833	3	1815	5	10	NULL	0	NULL	R anti-CD21 antibody	GP		does not bind					L cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_16_10641_s_190	12122212	( Center) Flow cytometry showing binding of R anti-CD21 antibody to CD21 and CD21mut (dark lines) but not to L cells transfected with vector alone.	bind
1943	1	1815	7	10	NULL	0	NULL	R anti-CD21 antibody	GP		bind 					CD21	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_16_10641_s_190	12122212	( Center) Flow cytometry showing binding of R anti-CD21 antibody to CD21 and CD21mut (dark lines) but not to L cells transfected with vector alone.	bind
1944	2	1815	7	10	NULL	0	NULL	R anti-CD21 antibody	GP		bind 					CD21mut	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_16_10641_s_190	12122212	( Center) Flow cytometry showing binding of R anti-CD21 antibody to CD21 and CD21mut (dark lines) but not to L cells transfected with vector alone.	bind
1945	3	1815	7	10	NULL	0	NULL	R anti-CD21 antibody	GP		does not bind					L cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_16_10641_s_190	12122212	( Center) Flow cytometry showing binding of R anti-CD21 antibody to CD21 and CD21mut (dark lines) but not to L cells transfected with vector alone.	bind
2834	1	1817	5	10	NULL	0	NULL	HeLa cells	Cell		transfected with					pCR3-uniTM-huPrP	GP		1 - 253		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_5863_s_72	11689427	( D - F) Binding of GST::huPrP23 - 230 by HeLa cells transfected with pCR3-uniTM-huPrP1 - 253.	bind
2835	2	1817	5	10	NULL	0	NULL	statement 1	Process		bind					GST::huPrP	GP		23 - 230		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_5863_s_72	11689427	( D - F) Binding of GST::huPrP23 - 230 by HeLa cells transfected with pCR3-uniTM-huPrP1 - 253.	bind
1946	1	1817	7	10	NULL	0	NULL	 HeLa cells	Cell		transfected with					pCR3-uniTM-huPrP	GP		1 - 253		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_5863_s_72	11689427	( D - F) Binding of GST::huPrP23 - 230 by HeLa cells transfected with pCR3-uniTM-huPrP1 - 253.	bind
46218	2	1817	7	10	NULL	0	NULL	GST::huPrP	GP		bind			23 - 230 		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_5863_s_72	11689427	( D - F) Binding of GST::huPrP23 - 230 by HeLa cells transfected with pCR3-uniTM-huPrP1 - 253.	bind
2837	1	1822	5	10	NULL	0	NULL	CI-MPRs	GP	mutant	bind					GST-GGA2	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_292_5522_1716_s_47	11387476	( D to  G) Binding of mutant CI-MPRs to GST-GGA2.	bind
1954	1	1822	7	10	NULL	0	NULL	CI-MPRs	GP	mutant	bind					GST-GGA2	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_292_5522_1716_s_47	11387476	( D to  G) Binding of mutant CI-MPRs to GST-GGA2.	bind
2838	1	1824	5	10	NULL	0	NULL	palF58 protein	GP		bind			S86P		PalH	GP		C-terminal region		NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_34_12141_s_133	16099830	( D)  In vitro binding of  palF58 (S86P) and  palF60 (I331K) proteins to the C-terminal region of PalH.	bind
2839	2	1824	5	10	NULL	0	NULL	palF60 protein	GP		bind			I331K		PalH	GP		C-terminal region		NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_34_12141_s_133	16099830	( D)  In vitro binding of  palF58 (S86P) and  palF60 (I331K) proteins to the C-terminal region of PalH.	bind
1955	1	1824	7	10	NULL	0	NULL	palF58 proteins	GP		bind			S86P		PalH	GP		C-terminal region of		NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_34_12141_s_133	16099830	( D)  In vitro binding of  palF58 (S86P) and  palF60 (I331K) proteins to the C-terminal region of PalH.	bind
1956	2	1824	7	10	NULL	0	NULL	palF60 proteins	GP		bind			I331K		PalH	GP		C-terminal region of		NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_34_12141_s_133	16099830	( D)  In vitro binding of  palF58 (S86P) and  palF60 (I331K) proteins to the C-terminal region of PalH.	bind
2840	1	1825	5	10	NULL	0	NULL	Fez1 proteins	GP		bind					EF1gamma protein	GP		N-terminal		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_98_18_10374_s_144	11504921	( D)  In vitro binding of Fez1 proteins to N-terminal EF1gamma protein.	bind
1957	1	1825	7	10	NULL	0	NULL	Fez1 proteins	GP		bind					EF1gamma protein	GP		N-terminal		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_98_18_10374_s_144	11504921	( D)  In vitro binding of Fez1 proteins to N-terminal EF1gamma protein.	bind
2841	1	1826	5	10	NULL	0	NULL	U1 snRNA	NucleicAcid		bind					U1 snRNP proteins	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_8_2493_s_202	15863726	( D)  In vitro U1 snRNA binding of U1 snRNP proteins.	bind
1958	1	1826	7	10	NULL	0	NULL	U1 snRNA	NucleicAcid		binds to					U1 snRNP proteins	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_8_2493_s_202	15863726	( D)  In vitro U1 snRNA binding of U1 snRNP proteins.	bind
2842	1	1828	5	10	NULL	0	NULL	5'' vRNA	NucleicAcid		bind					polymerase	GP		PB1 sequence		NULL		NULL	NULL	NULL	NULL	gw70_embo_22_5_1188_s_73	12606583	( D) 5'' vRNA and 5' cRNA bind to the same PB1 sequence in the polymerase.	bind
2843	2	1828	5	10	NULL	0	NULL	5' cRNA	NucleicAcid		bind					polymerase	GP		PB1 sequence		NULL		NULL	NULL	NULL	NULL	gw70_embo_22_5_1188_s_73	12606583	( D) 5'' vRNA and 5' cRNA bind to the same PB1 sequence in the polymerase.	bind
1959	1	1828	7	10	NULL	0	NULL	5'' vRNA	NucleicAcid		bind					polymerase	GP		PB1 sequence		NULL		NULL	NULL	NULL	NULL	gw70_embo_22_5_1188_s_73	12606583	( D) 5'' vRNA and 5' cRNA bind to the same PB1 sequence in the polymerase.	bind
1960	2	1828	7	10	NULL	0	NULL	5' cRNA	NucleicAcid		bind					polymerase	GP		PB1 sequence		NULL		NULL	NULL	NULL	NULL	gw70_embo_22_5_1188_s_73	12606583	( D) 5'' vRNA and 5' cRNA bind to the same PB1 sequence in the polymerase.	bind
2844	1	1829	5	10	NULL	0	NULL	STAT5A	GP		bind					beta-casein	GP			promoter containing a GAS element	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_12_8253_s_124	12048235	( D) A gel-shift assay demonstrating the DNA-binding activity of the STAT5A with the beta-casein promoter, which contained a GAS element.	bind
1961	1	1829	7	10	NULL	0	NULL	STAT5A	GP		bind					 beta-casein	GP			promoter containing a GAS element	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_12_8253_s_124	12048235	( D) A gel-shift assay demonstrating the DNA-binding activity of the STAT5A with the beta-casein promoter, which contained a GAS element.	bind
2845	1	1830	5	10	NULL	0	NULL	PACS-1 protein	GP	recombinant	contains			amino acids 85-280		MBP	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_4_705_s_44	15692563	( D) A recombinant PACS-1 protein (amino acids 85 280) containing the maltose-binding  protein (MBP) (MBP.PACS-185 280) immobilizes polycystin-2 from mouse kidney lysates, demonstrating that native polycystin-2  recognizes and binds PACS-1.	bind
2846	2	1830	5	10	NULL	0	NULL	MBP 	GP		is					maltose-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_4_705_s_44	15692563	( D) A recombinant PACS-1 protein (amino acids 85 280) containing the maltose-binding  protein (MBP) (MBP.PACS-185 280) immobilizes polycystin-2 from mouse kidney lysates, demonstrating that native polycystin-2  recognizes and binds PACS-1.	bind
2847	3	1830	5	10	NULL	0	NULL	statement 1	Process		immobilizes					polycystin-2	GP				NULL	mouse kidney lysates	NULL	NULL	NULL	NULL	gw70_embo_24_4_705_s_44	15692563	( D) A recombinant PACS-1 protein (amino acids 85 280) containing the maltose-binding  protein (MBP) (MBP.PACS-185 280) immobilizes polycystin-2 from mouse kidney lysates, demonstrating that native polycystin-2  recognizes and binds PACS-1.	bind
2848	4	1830	5	10	NULL	0	NULL	polycystin-2	GP	native	recognizes					PACS-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_4_705_s_44	15692563	( D) A recombinant PACS-1 protein (amino acids 85 280) containing the maltose-binding  protein (MBP) (MBP.PACS-185 280) immobilizes polycystin-2 from mouse kidney lysates, demonstrating that native polycystin-2  recognizes and binds PACS-1.	bind
2849	5	1830	5	10	NULL	0	NULL	polycystin-2	GP	native	bind					PACS-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_4_705_s_44	15692563	( D) A recombinant PACS-1 protein (amino acids 85 280) containing the maltose-binding  protein (MBP) (MBP.PACS-185 280) immobilizes polycystin-2 from mouse kidney lysates, demonstrating that native polycystin-2  recognizes and binds PACS-1.	bind
1962	1	1830	7	10	NULL	0	NULL	PACS-1 protein	GP	recombinant	contains			amino acids 85 - 280		MBP	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_4_705_s_44	15692563	( D) A recombinant PACS-1 protein (amino acids 85 280) containing the maltose-binding  protein (MBP) (MBP.PACS-185 280) immobilizes polycystin-2 from mouse kidney lysates, demonstrating that native polycystin-2  recognizes and binds PACS-1.	bind
1963	2	1830	7	10	NULL	0	NULL	MBP	GP		is					maltose-binding protein 	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_4_705_s_44	15692563	( D) A recombinant PACS-1 protein (amino acids 85 280) containing the maltose-binding  protein (MBP) (MBP.PACS-185 280) immobilizes polycystin-2 from mouse kidney lysates, demonstrating that native polycystin-2  recognizes and binds PACS-1.	bind
1964	3	1830	7	10	NULL	0	NULL	statement 1	Process		immobilizes					polycystin-2	GP				NULL	mouse kidney lysates	NULL	NULL	NULL	NULL	gw70_embo_24_4_705_s_44	15692563	( D) A recombinant PACS-1 protein (amino acids 85 280) containing the maltose-binding  protein (MBP) (MBP.PACS-185 280) immobilizes polycystin-2 from mouse kidney lysates, demonstrating that native polycystin-2  recognizes and binds PACS-1.	bind
46276	4	1830	7	10	NULL	0	NULL	polycystin-2	GP	native	recognize					PACS-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_4_705_s_44	15692563	( D) A recombinant PACS-1 protein (amino acids 85 280) containing the maltose-binding  protein (MBP) (MBP.PACS-185 280) immobilizes polycystin-2 from mouse kidney lysates, demonstrating that native polycystin-2  recognizes and binds PACS-1.	bind
46277	5	1830	7	10	NULL	0	NULL	polycystin-2	GP	native	bind					PACS-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_4_705_s_44	15692563	( D) A recombinant PACS-1 protein (amino acids 85 280) containing the maltose-binding  protein (MBP) (MBP.PACS-185 280) immobilizes polycystin-2 from mouse kidney lysates, demonstrating that native polycystin-2  recognizes and binds PACS-1.	bind
2850	1	1831	5	10	NULL	0	NULL	c-Rel homodimer	GP		bind			RHR		IL-2	GP			promoter containing CD28 response element	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_18_2138_s_128	16166378	( D) A structural model of the c-Rel RHR homodimer bound to the CD28 response element  from the IL-2 promoter is shown (Huang et al. 2001 ).	bind
2210	1	1831	7	10	NULL	0	NULL	c-Rel homodimer	GP		bind			RHR		IL-2	GP			CD28 response element in the promoter of 	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_18_2138_s_128	16166378	( D) A structural model of the c-Rel RHR homodimer bound to the CD28 response element  from the IL-2 promoter is shown (Huang et al. 2001 ).	bind
2851	1	1832	5	10	NULL	0	NULL	phosphatase	GP		activate					E2F	GP	binding of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_99_22_14200_s_77	12379745	( D) Activation of E2F binding by phosphatase treatment in vitro.	bind
2211	1	1832	7	10	NULL	0	NULL	phosphatase	GP		activates					E2F	GP	binding of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_99_22_14200_s_77	12379745	( D) Activation of E2F binding by phosphatase treatment in vitro.	bind
2852	1	1833	5	10	NULL	0	NULL	Akt	GP	active	bind					Ebp1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_10_2083_s_144	16642037	( D) Active Akt binds Ebp1.	bind
2212	1	1833	7	10	NULL	0	NULL	Akt	GP	active	bind					Ebp1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_10_2083_s_144	16642037	( D) Active Akt binds Ebp1.	bind
2853	1	1834	5	10	NULL	0	NULL	Rabkinesin-6	GP		bind			motor domain		MT	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5350_580_s_45	9438855	( D) Adenosine triphosphate-dependent MT-binding activity of Rabkinesin-6 motor domain.	bind
2854	2	1834	5	10	NULL	0	NULL	statement 1	Process		is dependent on					Adenosine triphosphate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5350_580_s_45	9438855	( D) Adenosine triphosphate-dependent MT-binding activity of Rabkinesin-6 motor domain.	bind
2213	1	1834	7	10	NULL	0	NULL	Rabkinesin-6 	GP		binds			motor domain		MT	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5350_580_s_45	9438855	( D) Adenosine triphosphate-dependent MT-binding activity of Rabkinesin-6 motor domain.	bind
2214	2	1834	7	10	NULL	0	NULL	statement 1	Process		is dependent on					adenosine triphosphate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5350_580_s_45	9438855	( D) Adenosine triphosphate-dependent MT-binding activity of Rabkinesin-6 motor domain.	bind
2855	1	1835	5	10	NULL	0	NULL	CD26	GP		bind					caveolin-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_39_14186_s_90	15353589	( D) Amino acids 201 - 211 and DPPIV of CD26 were required for binding of CD26 to caveolin-1.	bind
2856	2	1835	5	10	NULL	0	NULL	CD26	GP		is required for			amino acids 201 - 211		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_39_14186_s_90	15353589	( D) Amino acids 201 - 211 and DPPIV of CD26 were required for binding of CD26 to caveolin-1.	bind
2857	3	1835	5	10	NULL	0	NULL	CD26	GP		is required for			DPPIV		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_39_14186_s_90	15353589	( D) Amino acids 201 - 211 and DPPIV of CD26 were required for binding of CD26 to caveolin-1.	bind
2215	1	1835	7	10	NULL	0	NULL	CD26	GP		bind					caveolin-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_39_14186_s_90	15353589	( D) Amino acids 201 - 211 and DPPIV of CD26 were required for binding of CD26 to caveolin-1.	bind
2216	2	1835	7	10	NULL	0	NULL	CD26	GP		is required for			 Amino acids 201 - 211 		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_39_14186_s_90	15353589	( D) Amino acids 201 - 211 and DPPIV of CD26 were required for binding of CD26 to caveolin-1.	bind
2217	3	1835	7	10	NULL	0	NULL	CD26	GP		is required for			DPPIV 		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_39_14186_s_90	15353589	( D) Amino acids 201 - 211 and DPPIV of CD26 were required for binding of CD26 to caveolin-1.	bind
2858	1	1836	5	10	NULL	0	NULL	Mot1	GP		bind					TBPc-DNA complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_7_1492_s_70	16541100	( D) An isotherm calculated from (C) for the binding of Mot1 to the TBPc-DNA complex.	bind
2218	1	1836	7	10	NULL	0	NULL	Mot1	GP		bind					TBPc-DNA complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_7_1492_s_70	16541100	( D) An isotherm calculated from (C) for the binding of Mot1 to the TBPc-DNA complex.	bind
2859	1	1838	5	10	NULL	0	NULL	HCV	Organism		bind					CD81	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_science_282_5390_938_s_83	9794763	( D) Antibodies that neutralize HCV infection in vivo inhibit binding of HCV to CD81 in vitro.	bind
2860	2	1838	5	10	NULL	0	NULL	antibodies	GP		neutralize					HCV infection	Organism				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_science_282_5390_938_s_83	9794763	( D) Antibodies that neutralize HCV infection in vivo inhibit binding of HCV to CD81 in vitro.	bind
2861	3	1838	5	10	NULL	0	NULL	statement 2	Process		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_282_5390_938_s_83	9794763	( D) Antibodies that neutralize HCV infection in vivo inhibit binding of HCV to CD81 in vitro.	bind
2219	1	1838	7	10	NULL	0	NULL	HCV	Organism		bind					CD81	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_science_282_5390_938_s_83	9794763	( D) Antibodies that neutralize HCV infection in vivo inhibit binding of HCV to CD81 in vitro.	bind
2220	2	1838	7	10	NULL	0	NULL	Antibodies	GP		neutralize					HCV	Organism				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_science_282_5390_938_s_83	9794763	( D) Antibodies that neutralize HCV infection in vivo inhibit binding of HCV to CD81 in vitro.	bind
2222	3	1838	7	10	NULL	0	NULL	statement 2	Process		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_282_5390_938_s_83	9794763	( D) Antibodies that neutralize HCV infection in vivo inhibit binding of HCV to CD81 in vitro.	bind
2862	1	1840	5	10	NULL	0	NULL	ATP	Chemical		bind					BVR	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_20_7109_s_165	15870194	( d) ATP binding to BVR is necessary for it to phosphorylate IRS-1.	bind
2863	2	1840	5	10	NULL	0	NULL	BVR	GP		phosphorylate					IRS-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_20_7109_s_165	15870194	( d) ATP binding to BVR is necessary for it to phosphorylate IRS-1.	bind
2864	3	1840	5	10	NULL	0	NULL	statement 1	Process		is necessary for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_20_7109_s_165	15870194	( d) ATP binding to BVR is necessary for it to phosphorylate IRS-1.	bind
2223	1	1840	7	10	NULL	0	NULL	ATP	Chemical		bind					BVR	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_20_7109_s_165	15870194	( d) ATP binding to BVR is necessary for it to phosphorylate IRS-1.	bind
2224	2	1840	7	10	NULL	0	NULL	BVR 	GP		phosphorylate					IRS-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_20_7109_s_165	15870194	( d) ATP binding to BVR is necessary for it to phosphorylate IRS-1.	bind
2225	3	1840	7	10	NULL	0	NULL	statement 1	Process		is required for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_20_7109_s_165	15870194	( d) ATP binding to BVR is necessary for it to phosphorylate IRS-1.	bind
2865	1	1841	5	10	NULL	0	NULL	ATP-agarose	Chemical		bind					TAP1	GP				NULL	HeLa-M cell transfectants	NULL	NULL	NULL	NULL	gw60_embo_20_3_387_s_214	11157746	( D) ATP-agarose binding of TAP1 in the HeLa-M cell transfectants.	bind
2226	1	1841	7	10	NULL	0	NULL	ATP-agarose	Chemical		bind					TAP1	GP				NULL	in HeLa-M cell transfectants	NULL	NULL	NULL	NULL	gw60_embo_20_3_387_s_214	11157746	( D) ATP-agarose binding of TAP1 in the HeLa-M cell transfectants.	bind
2867	1	1843	5	10	NULL	0	NULL	3H-PIP2	GP		bind					GST-RKC	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_10_5820_s_76	10318968	( D) Binding of 3H-PIP2 to GST-RKC (100 nM) in the absence of antibody (control,  ), in the presence of 1 muM ( ) or 10 muM ( ) antibody (labeled Ab).	bind
2228	1	1843	7	10	NULL	0	NULL	3H-PIP2	GP		bind					GST-RKC	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_10_5820_s_76	10318968	( D) Binding of 3H-PIP2 to GST-RKC (100 nM) in the absence of antibody (control,  ), in the presence of 1 muM ( ) or 10 muM ( ) antibody (labeled Ab).	bind
2868	1	1844	5	10	NULL	0	NULL	3R-tau	GP		bind					tubulin	GP	normal			NULL		NULL	NULL	NULL	NULL	gw70_embo_22_1_70_s_72	12505985	( D) Binding of 3R-tau to normal tubulin in the absence or presence of kinesin motor  domains (K).	bind
2251	1	1844	7	10	NULL	0	NULL	3R-tau	GP		bind					tubulin	GP	normal			NULL		NULL	NULL	NULL	NULL	gw70_embo_22_1_70_s_72	12505985	( D) Binding of 3R-tau to normal tubulin in the absence or presence of kinesin motor  domains (K).	bind
2871	1	1846	5	10	NULL	0	NULL	ABI1	GP		bind					PA	GP				NULL	in vesicles	NULL	NULL	NULL	NULL	gw70_pnas_101_25_9508_s_175	15197253	( D) Binding of ABI1 and mutant proteins to PA in vesicles.	bind
2872	2	1846	5	10	NULL	0	NULL	mutant proteins	GP		bind					PA	GP				NULL	in vesicles	NULL	NULL	NULL	NULL	gw70_pnas_101_25_9508_s_175	15197253	( D) Binding of ABI1 and mutant proteins to PA in vesicles.	bind
2252	1	1846	7	10	NULL	0	NULL	ABI1	GP		bind					PA 	GP				NULL	in vesicles	NULL	NULL	NULL	NULL	gw70_pnas_101_25_9508_s_175	15197253	( D) Binding of ABI1 and mutant proteins to PA in vesicles.	bind
2253	2	1846	7	10	NULL	0	NULL	mutant proteins	GP		bind					 PA	GP				NULL	in vesicles	NULL	NULL	NULL	NULL	gw70_pnas_101_25_9508_s_175	15197253	( D) Binding of ABI1 and mutant proteins to PA in vesicles.	bind
2873	1	1847	5	10	NULL	0	NULL	biotin-GA	GP		bind					TfR	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_134	16103367	( D) Binding of biotin-GA and tritium-GA to TfR is not inhibited by either apo-transferrin  or holo-transferrin.	bind
2874	2	1847	5	10	NULL	0	NULL	tritium-GA	GP		bind					TfR	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_134	16103367	( D) Binding of biotin-GA and tritium-GA to TfR is not inhibited by either apo-transferrin  or holo-transferrin.	bind
2875	3	1847	5	10	NULL	0	NULL	statement 1	Process		is not inhibited by					apo-transferrin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_134	16103367	( D) Binding of biotin-GA and tritium-GA to TfR is not inhibited by either apo-transferrin  or holo-transferrin.	bind
2876	4	1847	5	10	NULL	0	NULL	statement 2	Process		is not inhibited by					apo-transferrin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_134	16103367	( D) Binding of biotin-GA and tritium-GA to TfR is not inhibited by either apo-transferrin  or holo-transferrin.	bind
2877	5	1847	5	10	NULL	0	NULL	statement 1	Process		is not inhibited by					holo-transferrin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_134	16103367	( D) Binding of biotin-GA and tritium-GA to TfR is not inhibited by either apo-transferrin  or holo-transferrin.	bind
2878	6	1847	5	10	NULL	0	NULL	statement 2	Process		is not inhibited by					holo-transferrin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_134	16103367	( D) Binding of biotin-GA and tritium-GA to TfR is not inhibited by either apo-transferrin  or holo-transferrin.	bind
2254	1	1847	7	10	NULL	0	NULL	biotin-GA	GP		bind					TfR	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_134	16103367	( D) Binding of biotin-GA and tritium-GA to TfR is not inhibited by either apo-transferrin  or holo-transferrin.	bind
2255	2	1847	7	10	NULL	0	NULL	tritium-GA	GP		bind					TfR	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_134	16103367	( D) Binding of biotin-GA and tritium-GA to TfR is not inhibited by either apo-transferrin  or holo-transferrin.	bind
2256	3	1847	7	10	NULL	0	NULL	statement 1	Process		is not inhibited by					apo-transferrin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_134	16103367	( D) Binding of biotin-GA and tritium-GA to TfR is not inhibited by either apo-transferrin  or holo-transferrin.	bind
2257	4	1847	7	10	NULL	0	NULL	statement 1	Process		is not inhibited by					holo-transferrin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_134	16103367	( D) Binding of biotin-GA and tritium-GA to TfR is not inhibited by either apo-transferrin  or holo-transferrin.	bind
2258	5	1847	7	10	NULL	0	NULL	statement 2	Process		is not inhibited by					apo-transferrin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_134	16103367	( D) Binding of biotin-GA and tritium-GA to TfR is not inhibited by either apo-transferrin  or holo-transferrin.	bind
2259	6	1847	7	10	NULL	0	NULL	statement 2	Process		is not inhibited by					holo-transferrin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_134	16103367	( D) Binding of biotin-GA and tritium-GA to TfR is not inhibited by either apo-transferrin  or holo-transferrin.	bind
2879	1	1848	5	10	NULL	0	NULL	BRCA1	GP		bind					CBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_3_1020_s_161	10655477	( D) Binding of BRCA1 to CBP is not affected by phosphorylation.	bind
2880	2	1848	5	10	NULL	0	NULL	statement 1	Process		is not affected by					phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_3_1020_s_161	10655477	( D) Binding of BRCA1 to CBP is not affected by phosphorylation.	bind
2260	1	1848	7	10	NULL	0	NULL	BRCA1	GP		bind					CBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_3_1020_s_161	10655477	( D) Binding of BRCA1 to CBP is not affected by phosphorylation.	bind
2261	2	1848	7	10	NULL	0	NULL	statement 1	Process		is not affected by 					phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_3_1020_s_161	10655477	( D) Binding of BRCA1 to CBP is not affected by phosphorylation.	bind
2881	1	1849	5	10	NULL	0	NULL				bind			CBD		collagen	GP	insoluble			NULL		NULL	NULL	NULL	NULL	gw60_embo_22_8_1743_s_140	12682007	( D) Binding of CBD to insoluble collagen.	bind
2262	1	1849	7	10	NULL	0	NULL				bind			CBD		collagen	GP	insoluble			NULL		NULL	NULL	NULL	NULL	gw60_embo_22_8_1743_s_140	12682007	( D) Binding of CBD to insoluble collagen.	bind
2882	1	1850	5	10	NULL	0	NULL	Chordin	GP		bind					Bmp2	GP	Cvl2-N saturated;; immobilized			NULL		NULL	NULL	NULL	NULL	gw70_development_133_5_801_s_203	16439480	( D) Binding of Chordin to Cvl2-N saturated immobilized Bmp2.	bind
2263	1	1850	7	10	NULL	0	NULL	Chordin	GP		bind					Bmp2	GP	Cvl2-N saturated;; immobilized			NULL		NULL	NULL	NULL	NULL	gw70_development_133_5_801_s_203	16439480	( D) Binding of Chordin to Cvl2-N saturated immobilized Bmp2.	bind
2901	1	1851	5	10	NULL	0	NULL	CNTF	GP		activate					STAT1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_278_5337_477_s_168	9334309	( D) Binding of CNTF-activated STAT1 and STAT3 to a specific site within the GFAP promoter ( 47).	bind
2902	2	1851	5	10	NULL	0	NULL	CNTF	GP		activate					STAT3	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_278_5337_477_s_168	9334309	( D) Binding of CNTF-activated STAT1 and STAT3 to a specific site within the GFAP promoter ( 47).	bind
2903	3	1851	5	10	NULL	0	NULL	statement 1	Process		bind					GFAP	GP			a specific site within promoter	NULL		NULL	NULL	NULL	NULL	gw60_science_278_5337_477_s_168	9334309	( D) Binding of CNTF-activated STAT1 and STAT3 to a specific site within the GFAP promoter ( 47).	bind
2904	4	1851	5	10	NULL	0	NULL	statement 2	Process		bind					GFAP	GP			a specific site within promoter	NULL		NULL	NULL	NULL	NULL	gw60_science_278_5337_477_s_168	9334309	( D) Binding of CNTF-activated STAT1 and STAT3 to a specific site within the GFAP promoter ( 47).	bind
2264	1	1851	7	10	NULL	0	NULL	CNTF	GP		activate					STAT1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_278_5337_477_s_168	9334309	( D) Binding of CNTF-activated STAT1 and STAT3 to a specific site within the GFAP promoter ( 47).	bind
2265	2	1851	7	10	NULL	0	NULL	CNTF	GP		activate					STAT3	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_278_5337_477_s_168	9334309	( D) Binding of CNTF-activated STAT1 and STAT3 to a specific site within the GFAP promoter ( 47).	bind
3446	3	1851	7	10	NULL	0	NULL	statement 1	Process		bind					GFAP	GP			specific site within the promoter of 	NULL		NULL	NULL	NULL	NULL	gw60_science_278_5337_477_s_168	9334309	( D) Binding of CNTF-activated STAT1 and STAT3 to a specific site within the GFAP promoter ( 47).	bind
3447	4	1851	7	10	NULL	0	NULL	statement 2	GP		bind					GFAP	GP			specific site within the promoter of 	NULL		NULL	NULL	NULL	NULL	gw60_science_278_5337_477_s_168	9334309	( D) Binding of CNTF-activated STAT1 and STAT3 to a specific site within the GFAP promoter ( 47).	bind
2905	1	1852	5	10	NULL	0	NULL	His6-C-mu2	GP		bind					PIPK Igamma kinase	GP		core domain		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_32_11934_s_99	16880396	( D) Binding of His6-C-mu2 to the PIPK Igamma kinase core domain determined by surface plasmon resonance.	bind
2266	1	1852	7	10	NULL	0	NULL	His6-C-mu2	GP		binds to					PIPK Igamma kinase 	GP		core domain		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_32_11934_s_99	16880396	( D) Binding of His6-C-mu2 to the PIPK Igamma kinase core domain determined by surface plasmon resonance.	bind
2906	1	1853	5	10	NULL	0	NULL	JNK	GP		bind					NFAT4	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_278_5343_1638_s_52	9374467	( D) Binding of JNK and calcineurin to different sites on NFAT4.	bind
2907	2	1853	5	10	NULL	0	NULL	calcineurin	GP		bind					NFAT4	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_278_5343_1638_s_52	9374467	( D) Binding of JNK and calcineurin to different sites on NFAT4.	bind
2267	1	1853	7	10	NULL	0	NULL	JNK	GP		bind					NFAT4	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_278_5343_1638_s_52	9374467	( D) Binding of JNK and calcineurin to different sites on NFAT4.	bind
2268	2	1853	7	10	NULL	0	NULL	calcineurin	GP		bind					NFAT4	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_278_5343_1638_s_52	9374467	( D) Binding of JNK and calcineurin to different sites on NFAT4.	bind
3071	1	1854	5	10	NULL	0	NULL	JNK1	GP		bind					JIP-1	GP	deletion mutant	residues between127-202		NULL		NULL	NULL	NULL	NULL	gw60_science_277_5326_693_s_42	9235893	( D) Binding of JNK1 and JNK2 to GST and GST fusion proteins corresponding to JIP-1 with small deletions between residues 127 and 202.	bind
3072	2	1854	5	10	NULL	0	NULL	JNK2	GP		bind					JIP-1	GP	deletion mutant	residues between 127-202		NULL		NULL	NULL	NULL	NULL	gw60_science_277_5326_693_s_42	9235893	( D) Binding of JNK1 and JNK2 to GST and GST fusion proteins corresponding to JIP-1 with small deletions between residues 127 and 202.	bind
2270	1	1854	7	10	NULL	0	NULL	JNK1 	GP		bind					JIP-1	GP	deletion mutant	between residues 127 and 202		NULL		NULL	NULL	NULL	NULL	gw60_science_277_5326_693_s_42	9235893	( D) Binding of JNK1 and JNK2 to GST and GST fusion proteins corresponding to JIP-1 with small deletions between residues 127 and 202.	bind
2272	2	1854	7	10	NULL	0	NULL	JNK2	GP		bind					JIP-1	GP	deletion mutant	between residues 127 and 202		NULL		NULL	NULL	NULL	NULL	gw60_science_277_5326_693_s_42	9235893	( D) Binding of JNK1 and JNK2 to GST and GST fusion proteins corresponding to JIP-1 with small deletions between residues 127 and 202.	bind
2908	1	1855	5	10	NULL	0	NULL	myostatin	GP 		bind					ActRIIB	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_16_9306_s_63	11459935	( d) Binding of myostatin to ActRIIB.	bind
2273	1	1855	7	10	NULL	0	NULL	myostatin	GP		bind					ActRIIB	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_16_9306_s_63	11459935	( d) Binding of myostatin to ActRIIB.	bind
2928	1	1856	5	10	NULL	0	NULL	NC	GP		bind									(TG)4	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_472_s_118	16434700	( D) Binding of NC to (TG)4 in buffer containing 250 mM rather than 150 mM NaCl.	bind
2274	1	1856	7	10	NULL	0	NULL	NC	GP		bind									(TG)4	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_472_s_118	16434700	( D) Binding of NC to (TG)4 in buffer containing 250 mM rather than 150 mM NaCl.	bind
2912	1	1857	5	10	NULL	0	NULL	NFAT family members	GP		bind					Sp1	GP				NULL	NHK cells exposed to high Ca2+	NULL	NULL	NULL	NULL	gw70_pnas_102_39_13921_s_48	16172401	( d) Binding of NFAT family members to Sp1 on exposure of NHK cells to high Ca2+.	bind
2275	1	1857	7	10	NULL	0	NULL	NFAT family	GP		bind					Sp1	GP				NULL	in NHK cells exposed to high Ca2+	NULL	NULL	NULL	NULL	gw70_pnas_102_39_13921_s_48	16172401	( d) Binding of NFAT family members to Sp1 on exposure of NHK cells to high Ca2+.	bind
2919	1	1859	5	10	NULL	0	NULL	Sho1	GP		bind					Ste50	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_13_3033_s_48	16778768	( D) Binding of Sho1 to Ste50 and Ste11.	bind
2920	2	1859	5	10	NULL	0	NULL	Sho1	GP		bind					Ste11	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_13_3033_s_48	16778768	( D) Binding of Sho1 to Ste50 and Ste11.	bind
2277	1	1859	7	10	NULL	0	NULL	Sho1	GP		bind					Ste50	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_13_3033_s_48	16778768	( D) Binding of Sho1 to Ste50 and Ste11.	bind
2278	2	1859	7	10	NULL	0	NULL	Sho1	GP		bind					Ste11	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_13_3033_s_48	16778768	( D) Binding of Sho1 to Ste50 and Ste11.	bind
2921	1	1860	5	10	NULL	0	NULL	FGF-7	GP	soluble	bind					perlecan	Chemical	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1599_s_187	9788974	( D) Binding of soluble FGF-7 to  immobilized perlecan (4 mug) in the presence of increasing concentrations of heparan sulfate as indicated.	bind
2923	2	1860	5	10	NULL	0	NULL	statement 1	Process		in the presence of					heparan sulfate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1599_s_187	9788974	( D) Binding of soluble FGF-7 to  immobilized perlecan (4 mug) in the presence of increasing concentrations of heparan sulfate as indicated.	bind
2279	1	1860	7	10	NULL	0	NULL	FGF-7	GP	soluble	bind					perlecan	Chemical	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1599_s_187	9788974	( D) Binding of soluble FGF-7 to  immobilized perlecan (4 mug) in the presence of increasing concentrations of heparan sulfate as indicated.	bind
46207	2	1860	7	10	NULL	0	NULL	statement 1	Process		in presence of					heparan sulfate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1599_s_187	9788974	( D) Binding of soluble FGF-7 to  immobilized perlecan (4 mug) in the presence of increasing concentrations of heparan sulfate as indicated.	bind
2933	1	1861	5	10	NULL	0	NULL	RBP-Jkappa protein	GP		bind					p21	GP	endogenous		promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3427_s_139	11432830	( D) Binding of the RBP-Jkappa protein to the endogenous p21 promoter as assessed by chromatin immunoprecipitation.	bind
2280	1	1861	7	10	NULL	0	NULL	RBP-Jkappa protein	GP		bind					p21	GP	endogenous		promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3427_s_139	11432830	( D) Binding of the RBP-Jkappa protein to the endogenous p21 promoter as assessed by chromatin immunoprecipitation.	bind
2937	1	1862	5	10	NULL	0	NULL	ubiquitin chains	GP		bind					Vps9	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_6_1273_s_116	12628920	( D) Binding of ubiquitin chains to Vps9 and Cue1 CUE domains.	bind
2939	2	1862	5	10	NULL	0	NULL	ubiquitin chains	GP		bind					Cue1	GP		CUE domains		NULL		NULL	NULL	NULL	NULL	gw60_embo_22_6_1273_s_116	12628920	( D) Binding of ubiquitin chains to Vps9 and Cue1 CUE domains.	bind
2281	1	1862	7	10	NULL	0	NULL	ubiquitin chains	GP		bind					Vps9	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_6_1273_s_116	12628920	( D) Binding of ubiquitin chains to Vps9 and Cue1 CUE domains.	bind
2282	2	1862	7	10	NULL	0	NULL	ubiquitin chains	GP		bind					Cue1	GP		CUE		NULL		NULL	NULL	NULL	NULL	gw60_embo_22_6_1273_s_116	12628920	( D) Binding of ubiquitin chains to Vps9 and Cue1 CUE domains.	bind
2943	1	1863	5	10	NULL	0	NULL	GST-KAPP fusion protein	GP	truncated	bind					MBP fusions	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_14_7821_s_119	10393905	( D) Binding results between truncated GST-KAPP fusion proteins and MBP fusions.	bind
2283	1	1863	7	10	NULL	0	NULL	GST-KAPP fusion proteins	GP	truncated	bind					MBP fusions	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_14_7821_s_119	10393905	( D) Binding results between truncated GST-KAPP fusion proteins and MBP fusions.	bind
2947	1	1864	5	10	NULL	0	NULL	BRG1	GP		associate with					chromatin	Chromosome	downstream			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_11_1392_s_138	12782657	( D) BRG1 association with downstream  chromatin following heat shock depends on polymerase movement.	bind
2948	2	1864	5	10	NULL	0	NULL	statement 1	Process		occurs following					heat shock	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_11_1392_s_138	12782657	( D) BRG1 association with downstream  chromatin following heat shock depends on polymerase movement.	bind
2950	3	1864	5	10	NULL	0	NULL	statement 1	Process		depends on					polymerase	GP	movement of			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_11_1392_s_138	12782657	( D) BRG1 association with downstream  chromatin following heat shock depends on polymerase movement.	bind
2284	1	1864	7	10	NULL	0	NULL	BRG1	GP		bind					chromatin	Chromosome	downstream			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_11_1392_s_138	12782657	( D) BRG1 association with downstream  chromatin following heat shock depends on polymerase movement.	bind
2285	2	1864	7	10	NULL	0	NULL	statement 1	Process		occurs upon					heat shock 	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_11_1392_s_138	12782657	( D) BRG1 association with downstream  chromatin following heat shock depends on polymerase movement.	bind
2286	3	1864	7	10	NULL	0	NULL	statement 1	Process		depends on					polymerase	GP	movement of			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_11_1392_s_138	12782657	( D) BRG1 association with downstream  chromatin following heat shock depends on polymerase movement.	bind
2951	1	1865	5	10	NULL	0	NULL	C-Maf	GP		bind					IL-4	GP			promoter DNA	NULL		NULL	NULL	NULL	NULL	gw60_embo_18_2_420_s_189	9889198	( D) C-Maf binding to IL-4 promoter DNA is facilitated by phosphorylated JunB.	bind
2953	2	1865	5	10	NULL	0	NULL	statement 1	Process		is facilitated by					JunB	GP	phosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_2_420_s_189	9889198	( D) C-Maf binding to IL-4 promoter DNA is facilitated by phosphorylated JunB.	bind
2287	1	1865	7	10	NULL	0	NULL	C-Maf	GP		bind					IL-4	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_18_2_420_s_189	9889198	( D) C-Maf binding to IL-4 promoter DNA is facilitated by phosphorylated JunB.	bind
2288	2	1865	7	10	NULL	0	NULL	statement 1	Process		is facilitated by 					JunB	GP	phosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_2_420_s_189	9889198	( D) C-Maf binding to IL-4 promoter DNA is facilitated by phosphorylated JunB.	bind
2954	1	1866	5	10	NULL	0	NULL	c-Myc	GP		bind		directly			bmi-1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_10_3645_s_67	16537449	( D) c-Myc binds directly to the  bmi-1 promoter.	bind
2289	1	1866	7	10	NULL	0	NULL	c-Myc	GP		bind		directly			bmi-1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_10_3645_s_67	16537449	( D) c-Myc binds directly to the  bmi-1 promoter.	bind
2955	1	1867	5	10	NULL	0	NULL	TR	GP		bind					E1A	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6267_s_84	15849266	( D) CBM peptide blocks TR binding to E1A and N-CoR.	bind
2956	2	1867	5	10	NULL	0	NULL	TR	GP		bind					N-CoR	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6267_s_84	15849266	( D) CBM peptide blocks TR binding to E1A and N-CoR.	bind
2957	3	1867	5	10	NULL	0	NULL	CBM peptide	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6267_s_84	15849266	( D) CBM peptide blocks TR binding to E1A and N-CoR.	bind
2958	4	1867	5	10	NULL	0	NULL	CBM peptide	GP		blocks					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6267_s_84	15849266	( D) CBM peptide blocks TR binding to E1A and N-CoR.	bind
2290	1	1867	7	10	NULL	0	NULL	TR	GP		bind					E1A	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6267_s_84	15849266	( D) CBM peptide blocks TR binding to E1A and N-CoR.	bind
2291	2	1867	7	10	NULL	0	NULL	TR	GP		bind					N-CoR	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6267_s_84	15849266	( D) CBM peptide blocks TR binding to E1A and N-CoR.	bind
2292	3	1867	7	10	NULL	0	NULL	CBM peptide	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6267_s_84	15849266	( D) CBM peptide blocks TR binding to E1A and N-CoR.	bind
2293	4	1867	7	10	NULL	0	NULL	CBM peptide	GP		blocks					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6267_s_84	15849266	( D) CBM peptide blocks TR binding to E1A and N-CoR.	bind
2959	1	1868	5	10	NULL	0	NULL	CCT	GP		bind					Gbeta	GP		WD40 repeats		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_22_8360_s_95	16717193	( D) CCT binding to individual WD40 repeats of Gbeta ( n = 3).	bind
2294	1	1868	7	10	NULL	0	NULL	CCT	GP		bind					Gbeta	GP		WD40 repeats		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_22_8360_s_95	16717193	( D) CCT binding to individual WD40 repeats of Gbeta ( n = 3).	bind
2960	1	1869	5	10	NULL	0	NULL	p27	GP		bind					Cdk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_7_865_s_111	10510327	( d) Cdk2 immunoprecipitates: p27 bound to Cdk2, Cdk2 level, and Cdk2 activity in total (left column) or fractionated extracts (remaining columns).	bind
2295	1	1869	7	10	NULL	0	NULL	 p27 	GP		bind					Cdk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_7_865_s_111	10510327	( d) Cdk2 immunoprecipitates: p27 bound to Cdk2, Cdk2 level, and Cdk2 activity in total (left column) or fractionated extracts (remaining columns).	bind
2965	1	1872	5	10	NULL	0	NULL	SRF	GP		bind							endogenous		CArG regions	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5271_s_415	16170155	( D) ChIP analysis of SRF binding to the endogenous CArG regions.	bind
2296	1	1872	7	10	NULL	0	NULL	SRF	GP		bind							endogenous		CArG regions	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5271_s_415	16170155	( D) ChIP analysis of SRF binding to the endogenous CArG regions.	bind
2966	1	1873	5	10	NULL	0	NULL	E6	GP		bind					hTERT	GP	endogenous		promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_14_8211_s_185	12821782	( D) CHIP assay detects E6 and Myc proteins  bound to the endogenous hTERT promoter.	bind
2967	2	1873	5	10	NULL	0	NULL	Myc proteins	GP		bind					hTERT	GP	endogenous		promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_14_8211_s_185	12821782	( D) CHIP assay detects E6 and Myc proteins  bound to the endogenous hTERT promoter.	bind
2297	1	1873	7	10	NULL	0	NULL	E6	GP		bind					hTERT	GP	endogenous		promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_14_8211_s_185	12821782	( D) CHIP assay detects E6 and Myc proteins  bound to the endogenous hTERT promoter.	bind
2298	2	1873	7	10	NULL	0	NULL	Myc	GP		bind					hTERT	GP	endogenous		promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_14_8211_s_185	12821782	( D) CHIP assay detects E6 and Myc proteins  bound to the endogenous hTERT promoter.	bind
3284	1	1874	7	10	NULL	0	NULL	Nfatc3	NULL		binds	NULL				Sftpb	NULL			 5''-regulatory region	NULL	MLE-15 cells 	NULL	NULL	NULL	NULL	gw70_jclininvest_116_10_2597_s_128	16998587	( D) ChIP assays on 5''-regulatory regions of  Sftpb and  Abca3 gene (black boxes, GGAAA; white boxes, AGAAA) in MLE-15 cells, which express high  levels of Nfatc3 identified direct binding of Nfatc3 in the chromatin.	bind
3285	2	1874	7	NULL	NULL	0	NULL	Nfatc3	NULL		binds	NULL				Abca3	NULL			5''-regulatory region	NULL	MLE-15 cells	NULL	NULL	NULL	NULL	gw70_jclininvest_116_10_2597_s_128	16998587	( D) ChIP assays on 5''-regulatory regions of  Sftpb and  Abca3 gene (black boxes, GGAAA; white boxes, AGAAA) in MLE-15 cells, which express high  levels of Nfatc3 identified direct binding of Nfatc3 in the chromatin.	bind
3445	3	1874	7	NULL	NULL	0	NULL	MLE-15 cells	NULL		express	NULL				Nfatc3 	NULL	high levels of 			NULL		0	NULL	NULL	NULL	gw70_jclininvest_116_10_2597_s_128	16998587	( D) ChIP assays on 5''-regulatory regions of  Sftpb and  Abca3 gene (black boxes, GGAAA; white boxes, AGAAA) in MLE-15 cells, which express high  levels of Nfatc3 identified direct binding of Nfatc3 in the chromatin.	bind
2970	1	1875	5	10	NULL	0	NULL	Chk1	GP		bind					PPM1D	GP	mutant forms			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1162_s_86	15870257	( D) Chk1 binds to mutant forms of PPM1D except for one mutant missing part of the phosphatase  domain.	bind
2971	2	1875	5	10	NULL	0	NULL	Chk1	GP		does not bind					PPM1D	GP	mutant missing part of	phosphatase domain		NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1162_s_86	15870257	( D) Chk1 binds to mutant forms of PPM1D except for one mutant missing part of the phosphatase  domain.	bind
2330	1	1875	7	10	NULL	0	NULL	Chk1	GP		bind					PPM1D	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1162_s_86	15870257	( D) Chk1 binds to mutant forms of PPM1D except for one mutant missing part of the phosphatase  domain.	bind
2331	2	1875	7	10	NULL	0	NULL	Chk1	GP		does not bind					PPM1D	GP	mutant missing part of  	phosphatase domain		NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1162_s_86	15870257	( D) Chk1 binds to mutant forms of PPM1D except for one mutant missing part of the phosphatase  domain.	bind
2972	1	1876	5	10	NULL	0	NULL	EWS - WT1(+KTS)	GP		bind									HC63	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_genesdev_17_17_2094_s_90	12923058	( D) Chromatin immunoprecipitation (ChIP) analysis to demonstrate in  vivo binding of  EWS - WT1(+KTS) to HC63.	bind
2332	1	1876	7	10	NULL	0	NULL	EWS - WT1(+KTS)	GP		bind									HC63	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_genesdev_17_17_2094_s_90	12923058	( D) Chromatin immunoprecipitation (ChIP) analysis to demonstrate in  vivo binding of  EWS - WT1(+KTS) to HC63.	bind
2973	1	1877	5	10	NULL	0	NULL	Gdf11	GP		bind					IIA	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_21_2749_s_117	12414726	( D) Coimmunoprecipitation analyses showing that Gdf11 binds to IIA and IIB to different degrees.	bind
2974	2	1877	5	10	NULL	0	NULL	Gdf11	GP		bind					IIB	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_21_2749_s_117	12414726	( D) Coimmunoprecipitation analyses showing that Gdf11 binds to IIA and IIB to different degrees.	bind
2333	1	1877	7	10	NULL	0	NULL	Gdf11	GP		bind					IIA	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_21_2749_s_117	12414726	( D) Coimmunoprecipitation analyses showing that Gdf11 binds to IIA and IIB to different degrees.	bind
2334	2	1877	7	10	NULL	0	NULL	Gdf11	GP		bind					IIB	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_21_2749_s_117	12414726	( D) Coimmunoprecipitation analyses showing that Gdf11 binds to IIA and IIB to different degrees.	bind
2975	1	1878	5	10	NULL	0	NULL	kinesin	GP		bind					CPEB-myc13	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_5_638_s_131	12629046	( D) Coimmunoprecipitation of kinesin and dynein with CPEB-myc13.	bind
2976	2	1878	5	10	NULL	0	NULL	dynein	GP		bind					CPEB-myc13	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_5_638_s_131	12629046	( D) Coimmunoprecipitation of kinesin and dynein with CPEB-myc13.	bind
2335	1	1878	7	10	NULL	NULL	NULL	kinesin	GP		 bind					CPEB-myc13	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_5_638_s_131	12629046	( D) Coimmunoprecipitation of kinesin and dynein with CPEB-myc13.	bind
2336	2	1878	7	10	NULL	NULL	NULL	dynein 	GP		bind					CPEB-myc13	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_5_638_s_131	12629046	( D) Coimmunoprecipitation of kinesin and dynein with CPEB-myc13.	bind
2977	1	1879	5	10	NULL	NULL	NULL	c-Myb	GP		bind					GST-histone H3	GP		tail		NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_20_2447_s_63	16195416	( D) Comparison of c-Myb binding to various GST-histone H3 tail constructs.	bind
2337	1	1879	7	10	NULL	NULL	NULL	c-Myb	GP		bind					GST-histone H3	GP		tail		NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_20_2447_s_63	16195416	( D) Comparison of c-Myb binding to various GST-histone H3 tail constructs.	bind
2978	1	1880	5	10	NULL	NULL	NULL	CD-40-p1	GP		bind					TRAF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_15_8408_s_151	10411888	( D) Comparison of CD-40-p1 (orange) and TNF-R2 (light blue) bound to TRAF2 (CD40-p1 complex, gray; TNF-R2 complex, blue).	bind
2979	2	1880	5	10	NULL	NULL	NULL	TNF-R2	GP		bind					TRAF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_15_8408_s_151	10411888	( D) Comparison of CD-40-p1 (orange) and TNF-R2 (light blue) bound to TRAF2 (CD40-p1 complex, gray; TNF-R2 complex, blue).	bind
2338	1	1880	7	10	NULL	NULL	NULL	CD-40-p1	GP		bind					TRAF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_15_8408_s_151	10411888	( D) Comparison of CD-40-p1 (orange) and TNF-R2 (light blue) bound to TRAF2 (CD40-p1 complex, gray; TNF-R2 complex, blue).	bind
2339	2	1880	7	10	NULL	NULL	NULL	TNF-R2	GP		bind					TRAF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_15_8408_s_151	10411888	( D) Comparison of CD-40-p1 (orange) and TNF-R2 (light blue) bound to TRAF2 (CD40-p1 complex, gray; TNF-R2 complex, blue).	bind
2980	1	1881	5	10	NULL	NULL	NULL	malonyl-CoA	Chemical		bind					CPT1a	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_19_7282_s_56	16651524	( D) Comparison of malonyl-CoA binding to CPT1a and CPT1c.	bind
2981	2	1881	5	10	NULL	NULL	NULL	malonyl-CoA	Chemical		bind					CPT1c	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_19_7282_s_56	16651524	( D) Comparison of malonyl-CoA binding to CPT1a and CPT1c.	bind
2340	1	1881	7	10	NULL	NULL	NULL	malonyl-CoA	Chemical		bind					CPT1a	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_19_7282_s_56	16651524	( D) Comparison of malonyl-CoA binding to CPT1a and CPT1c.	bind
2341	2	1881	7	10	NULL	NULL	NULL	malonyl-CoA	Chemical		bind					CPT1c	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_19_7282_s_56	16651524	( D) Comparison of malonyl-CoA binding to CPT1a and CPT1c.	bind
2982	1	1882	5	10	NULL	NULL	NULL	RBD12	GP	nucleolin 	bind					b2	GP			NRE	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_22_6461_s_73	14602904	( D) Competition experiments of nucleolin RBD12 binding to b2NRE.	bind
2342	1	1882	7	10	NULL	NULL	NULL	RBD12	GP	nucleolin	bind					b2	GP			NRE	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_22_6461_s_73	14602904	( D) Competition experiments of nucleolin RBD12 binding to b2NRE.	bind
2983	1	1883	5	10	NULL	NULL	NULL	TNP-ATP	Chemical		bind					Kir6.2 proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_7_1318_s_37	15775962	( D) Competition of 10 muM TNP-ATP binding to Kir6.2 proteins by PIP2.	bind
2984	2	1883	5	10	NULL	NULL	NULL	PIP2	Chemical		bind					Kir6.2 proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_7_1318_s_37	15775962	( D) Competition of 10 muM TNP-ATP binding to Kir6.2 proteins by PIP2.	bind
3282	3	1883	5	10	NULL	NULL	NULL	statement 1	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_7_1318_s_37	15775962	( D) Competition of 10 muM TNP-ATP binding to Kir6.2 proteins by PIP2.	bind
2344	1	1883	7	10	NULL	NULL	NULL	TNP-ATP	Chemical		bind					Kir6.2	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_7_1318_s_37	15775962	( D) Competition of 10 muM TNP-ATP binding to Kir6.2 proteins by PIP2.	bind
2345	2	1883	7	10	NULL	NULL	NULL	PIP2	Chemical		bind					Kir6.2	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_7_1318_s_37	15775962	( D) Competition of 10 muM TNP-ATP binding to Kir6.2 proteins by PIP2.	bind
4224	3	1883	7	10	NULL	NULL	NULL	statement 1	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_7_1318_s_37	15775962	( D) Competition of 10 muM TNP-ATP binding to Kir6.2 proteins by PIP2.	bind
2985	1	1884	5	10	NULL	NULL	NULL	Fab 2F1	GP		bind					G9-280-HLA-A2 complexes	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_14_9421_s_87	12093904	( D) Competition of MHC-peptide complexes for binding of Fab 2F1 to immobolized G9-280-HLA-A2 complexes; W/O, without competitior.	bind
2986	2	1884	5	10	NULL	NULL	NULL	MHC-peptide complexes	GP		bind					G9-280-HLA-A2 complexes	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_14_9421_s_87	12093904	( D) Competition of MHC-peptide complexes for binding of Fab 2F1 to immobolized G9-280-HLA-A2 complexes; W/O, without competitior.	bind
2346	1	1884	7	10	NULL	NULL	NULL	Fab 2F1	GP		bind					G9-280-HLA-A2 complexes	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_14_9421_s_87	12093904	( D) Competition of MHC-peptide complexes for binding of Fab 2F1 to immobolized G9-280-HLA-A2 complexes; W/O, without competitior.	bind
2347	2	1884	7	10	NULL	NULL	NULL	MHC-peptide complexes	GP		bind					G9-280-HLA-A2 complexes	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_14_9421_s_87	12093904	( D) Competition of MHC-peptide complexes for binding of Fab 2F1 to immobolized G9-280-HLA-A2 complexes; W/O, without competitior.	bind
2987	1	1885	5	10	NULL	NULL	NULL	actin	GP		bind					ABD/1-24	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_21_3442_s_117	9808630	( D) Concentration-dependent binding of actin to ABD/1-24.	bind
2348	1	1885	7	10	NULL	NULL	NULL	actin	GP		bind					ABD/1-24	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_21_3442_s_117	9808630	( D) Concentration-dependent binding of actin to ABD/1-24.	bind
3008	1	1886	5	10	NULL	NULL	NULL	CHO cells	Cell		express					alphaIIbbeta3	GP	WT			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_42	12730600	( D) Constitutive fibrinogen binding to CHO cells expressing WT alphaIIbbeta3 and the G702N and G708N beta3 mutants as a function of fibrinogen concentration.	bind
3009	2	1886	5	10	NULL	NULL	NULL	CHO cells	Cell		express					beta3	GP	mutant	G702N		NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_42	12730600	( D) Constitutive fibrinogen binding to CHO cells expressing WT alphaIIbbeta3 and the G702N and G708N beta3 mutants as a function of fibrinogen concentration.	bind
3010	3	1886	5	10	NULL	NULL	NULL	CHO cells	Cell		express					beta3	GP	mutant	G708N		NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_42	12730600	( D) Constitutive fibrinogen binding to CHO cells expressing WT alphaIIbbeta3 and the G702N and G708N beta3 mutants as a function of fibrinogen concentration.	bind
3011	4	1886	5	10	NULL	NULL	NULL	fibrinogen	GP		bind		constitutively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_42	12730600	( D) Constitutive fibrinogen binding to CHO cells expressing WT alphaIIbbeta3 and the G702N and G708N beta3 mutants as a function of fibrinogen concentration.	bind
3012	5	1886	5	10	NULL	NULL	NULL	fibrinogen	GP		bind		constitutively			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_42	12730600	( D) Constitutive fibrinogen binding to CHO cells expressing WT alphaIIbbeta3 and the G702N and G708N beta3 mutants as a function of fibrinogen concentration.	bind
3013	6	1886	5	10	NULL	NULL	NULL	fibrinogen	GP		bind		constitutively			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_42	12730600	( D) Constitutive fibrinogen binding to CHO cells expressing WT alphaIIbbeta3 and the G702N and G708N beta3 mutants as a function of fibrinogen concentration.	bind
2349	1	1886	7	10	NULL	NULL	NULL	CHO cells 	Cell		express					alphaIIbbeta3	GP	WT			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_42	12730600	( D) Constitutive fibrinogen binding to CHO cells expressing WT alphaIIbbeta3 and the G702N and G708N beta3 mutants as a function of fibrinogen concentration.	bind
46213	2	1886	7	10	NULL	NULL	NULL	CHO cells	Cell		express					beta3	GP	mutant	G702N		NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_42	12730600	( D) Constitutive fibrinogen binding to CHO cells expressing WT alphaIIbbeta3 and the G702N and G708N beta3 mutants as a function of fibrinogen concentration.	bind
46214	3	1886	7	10	NULL	NULL	NULL	CHO cells	Cell		express					beta3	GP	mutant	G708N		NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_42	12730600	( D) Constitutive fibrinogen binding to CHO cells expressing WT alphaIIbbeta3 and the G702N and G708N beta3 mutants as a function of fibrinogen concentration.	bind
46215	4	1886	7	10	NULL	NULL	NULL	fibrinogen	GP		bind		constitutively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_42	12730600	( D) Constitutive fibrinogen binding to CHO cells expressing WT alphaIIbbeta3 and the G702N and G708N beta3 mutants as a function of fibrinogen concentration.	bind
46216	5	1886	7	10	NULL	NULL	NULL	fibrinogen	GP		bind		constitutively			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_42	12730600	( D) Constitutive fibrinogen binding to CHO cells expressing WT alphaIIbbeta3 and the G702N and G708N beta3 mutants as a function of fibrinogen concentration.	bind
46217	6	1886	7	10	NULL	NULL	NULL	fibrinogen	GP		bind		constitutively			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_42	12730600	( D) Constitutive fibrinogen binding to CHO cells expressing WT alphaIIbbeta3 and the G702N and G708N beta3 mutants as a function of fibrinogen concentration.	bind
2989	1	1887	5	10	NULL	NULL	NULL	CREB	GP		bind					nNOS	GP			CREs	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8617_s_165	10900019	( D) CREB and ATF-2 bind to the nNOS CREs.	bind
2990	2	1887	5	10	NULL	NULL	NULL	ATF-2	GP		bind					nNOS	GP			CREs	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8617_s_165	10900019	( D) CREB and ATF-2 bind to the nNOS CREs.	bind
2351	1	1887	7	10	NULL	NULL	NULL	CREB	GP		bind					nNOS 	GP			CRE	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8617_s_165	10900019	( D) CREB and ATF-2 bind to the nNOS CREs.	bind
2352	2	1887	7	10	NULL	NULL	NULL	ATF-2	GP		bind					 nNOS	GP			CRE	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8617_s_165	10900019	( D) CREB and ATF-2 bind to the nNOS CREs.	bind
3017	1	1888	5	10	NULL	NULL	NULL	Sp1	GP		bind					p21WAF1/CIP1	GP			promoter	NULL	in high Ca2+-treated NHK cells	NULL	NULL	NULL	NULL	gw70_pnas_102_39_13921_s_149	16172401	( d) Cyclosporin A (CsA) abrogated the binding of Sp1 and NFAT1 to the p21WAF1/CIP1 promoter in high Ca2+-treated NHK cells, restoring the binding of KLF16, as assayed by a chromatin immunoprecipitation  assay.	bind
3018	2	1888	5	10	NULL	NULL	NULL	NFAT1	GP		bind					p21WAF1/CIP1	GP			promoter	NULL	in high Ca2+-treated NHK cells	NULL	NULL	NULL	NULL	gw70_pnas_102_39_13921_s_149	16172401	( d) Cyclosporin A (CsA) abrogated the binding of Sp1 and NFAT1 to the p21WAF1/CIP1 promoter in high Ca2+-treated NHK cells, restoring the binding of KLF16, as assayed by a chromatin immunoprecipitation  assay.	bind
3019	3	1888	5	10	NULL	NULL	NULL	CsA	Chemical		abrogate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13921_s_149	16172401	( d) Cyclosporin A (CsA) abrogated the binding of Sp1 and NFAT1 to the p21WAF1/CIP1 promoter in high Ca2+-treated NHK cells, restoring the binding of KLF16, as assayed by a chromatin immunoprecipitation  assay.	bind
3020	4	1888	5	10	NULL	NULL	NULL	CsA	Chemical		is					Cyclosporin A	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13921_s_149	16172401	( d) Cyclosporin A (CsA) abrogated the binding of Sp1 and NFAT1 to the p21WAF1/CIP1 promoter in high Ca2+-treated NHK cells, restoring the binding of KLF16, as assayed by a chromatin immunoprecipitation  assay.	bind
3021	5	1888	5	10	NULL	NULL	NULL	CsA	Chemical		abrogate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13921_s_149	16172401	( d) Cyclosporin A (CsA) abrogated the binding of Sp1 and NFAT1 to the p21WAF1/CIP1 promoter in high Ca2+-treated NHK cells, restoring the binding of KLF16, as assayed by a chromatin immunoprecipitation  assay.	bind
3022	6	1888	5	10	NULL	NULL	NULL	statement 3	Process		restore					KLF16	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13921_s_149	16172401	( d) Cyclosporin A (CsA) abrogated the binding of Sp1 and NFAT1 to the p21WAF1/CIP1 promoter in high Ca2+-treated NHK cells, restoring the binding of KLF16, as assayed by a chromatin immunoprecipitation  assay.	bind
3023	7	1888	5	10	NULL	NULL	NULL	statement 5	Process		restore					KLF16	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13921_s_149	16172401	( d) Cyclosporin A (CsA) abrogated the binding of Sp1 and NFAT1 to the p21WAF1/CIP1 promoter in high Ca2+-treated NHK cells, restoring the binding of KLF16, as assayed by a chromatin immunoprecipitation  assay.	bind
2353	1	1888	7	10	NULL	NULL	NULL	Sp1	GP		bind					p21WAF1/CIP1	GP			promoter	NULL	in high Ca2+-treated NHK cells	NULL	NULL	NULL	NULL	gw70_pnas_102_39_13921_s_149	16172401	( d) Cyclosporin A (CsA) abrogated the binding of Sp1 and NFAT1 to the p21WAF1/CIP1 promoter in high Ca2+-treated NHK cells, restoring the binding of KLF16, as assayed by a chromatin immunoprecipitation  assay.	bind
2354	2	1888	7	10	NULL	NULL	NULL	NFAT1	GP		bind					p21WAF1/CIP1	GP			promoter	NULL	in high Ca2+-treated NHK cells	NULL	NULL	NULL	NULL	gw70_pnas_102_39_13921_s_149	16172401	( d) Cyclosporin A (CsA) abrogated the binding of Sp1 and NFAT1 to the p21WAF1/CIP1 promoter in high Ca2+-treated NHK cells, restoring the binding of KLF16, as assayed by a chromatin immunoprecipitation  assay.	bind
2356	3	1888	7	10	NULL	NULL	NULL	CsA	Chemical		abrogates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13921_s_149	16172401	( d) Cyclosporin A (CsA) abrogated the binding of Sp1 and NFAT1 to the p21WAF1/CIP1 promoter in high Ca2+-treated NHK cells, restoring the binding of KLF16, as assayed by a chromatin immunoprecipitation  assay.	bind
2357	4	1888	7	10	NULL	NULL	NULL	CsA	Chemical		abrogates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13921_s_149	16172401	( d) Cyclosporin A (CsA) abrogated the binding of Sp1 and NFAT1 to the p21WAF1/CIP1 promoter in high Ca2+-treated NHK cells, restoring the binding of KLF16, as assayed by a chromatin immunoprecipitation  assay.	bind
51217	5	1888	7	10	NULL	NULL	NULL	CsA	Chemical		is					Cyclosporin A	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13921_s_149	16172401	( d) Cyclosporin A (CsA) abrogated the binding of Sp1 and NFAT1 to the p21WAF1/CIP1 promoter in high Ca2+-treated NHK cells, restoring the binding of KLF16, as assayed by a chromatin immunoprecipitation  assay.	bind
51218	6	1888	7	10	NULL	NULL	NULL	statement 3	Process		restore					KLF16	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13921_s_149	16172401	( d) Cyclosporin A (CsA) abrogated the binding of Sp1 and NFAT1 to the p21WAF1/CIP1 promoter in high Ca2+-treated NHK cells, restoring the binding of KLF16, as assayed by a chromatin immunoprecipitation  assay.	bind
51219	7	1888	7	10	NULL	NULL	NULL	statement 4	Process		restore					KLF16	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_39_13921_s_149	16172401	( d) Cyclosporin A (CsA) abrogated the binding of Sp1 and NFAT1 to the p21WAF1/CIP1 promoter in high Ca2+-treated NHK cells, restoring the binding of KLF16, as assayed by a chromatin immunoprecipitation  assay.	bind
3076	1	1889	5	10	NULL	NULL	NULL	HuR	GP	cellular	bind					IGF-IR	GP			5''-UTR	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_9_2962_s_167	15914670	( D) Demonstration of binding of cellular HuR to the IGF-IR 5''-UTR by altered mobility  on immunoblot (western-shift assay).	bind
2402	1	1889	7	10	NULL	NULL	NULL	HuR	GP	cellular	bind					IGF-IR	GP			5''-UTR	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_9_2962_s_167	15914670	( D) Demonstration of binding of cellular HuR to the IGF-IR 5''-UTR by altered mobility  on immunoblot (western-shift assay).	bind
3040	1	1890	5	10	NULL	NULL	NULL	pol	GP		bind		directly			PCNA	GP	monoubiquitinated			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_19_3886_s_225	15359278	( D) Direct binding of pol  to monoubiquitinated PCNA.	bind
2403	1	1890	7	10	NULL	NULL	NULL	pol	GP		binds to		directly			PCNA	GP	monoubiquitinated 			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_19_3886_s_225	15359278	( D) Direct binding of pol  to monoubiquitinated PCNA.	bind
3041	1	1891	5	10	NULL	NULL	NULL	PTEN	GP		bind		directly			NHERFs	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_910_s_60	16456542	( D) Direct binding of PTEN and PDGFR to NHERFs.	bind
3042	2	1891	5	10	NULL	NULL	NULL	PDGFR	GP		bind		directly			NHERFs	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_910_s_60	16456542	( D) Direct binding of PTEN and PDGFR to NHERFs.	bind
2404	1	1891	7	10	NULL	NULL	NULL	PTEN	GP		bind		directly			NHERFs	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_910_s_60	16456542	( D) Direct binding of PTEN and PDGFR to NHERFs.	bind
2405	2	1891	7	10	NULL	NULL	NULL	PDGFR	GP		bind		directly			NHERFs	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_910_s_60	16456542	( D) Direct binding of PTEN and PDGFR to NHERFs.	bind
3043	1	1892	5	10	NULL	NULL	NULL	GST-c-Src	GP	purified	bind		directly	SH3		integrin beta proteins	GP		cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_23_13298_s_112	14593208	( D) Direct binding of purified GST-c-Src SH3 to integrin beta cytoplasmic tail proteins, assessed by ELISA: beta3 ( ), rbeta3 ( ), beta3(delta758) ( ), beta1A ( ), and beta2 ( ).	bind
2406	1	1892	7	10	NULL	NULL	NULL	GST-c-Src	GP	purified	bind		directly	SH3		integrin beta proteins	GP		cytoplasmic tail 		NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_23_13298_s_112	14593208	( D) Direct binding of purified GST-c-Src SH3 to integrin beta cytoplasmic tail proteins, assessed by ELISA: beta3 ( ), rbeta3 ( ), beta3(delta758) ( ), beta1A ( ), and beta2 ( ).	bind
3044	1	1894	5	10	NULL	NULL	NULL	RNAP	GP		bind					A37	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_15_4245_s_126	16920742	( D) DNase I protection assay using RNAP bound to the  A37 promoter.	bind
2411	1	1894	7	10	NULL	NULL	NULL	RNAP	GP		bind					 A37	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_15_4245_s_126	16920742	( D) DNase I protection assay using RNAP bound to the  A37 promoter.	bind
3045	1	1895	5	10	NULL	NULL	NULL	Dsk2p	GP		bind					polyubiquitin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_745_s_110	11805328	( D) Dsk2p binds to polyubiquitin.	bind
2412	1	1895	7	10	NULL	NULL	NULL	Dsk2p	GP		bind					polyubiquitin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_745_s_110	11805328	( D) Dsk2p binds to polyubiquitin.	bind
3046	1	1896	5	10	NULL	NULL	NULL	E2F3	GP		bind					Cdc6	GP			promoter	NULL	at G1/S	NULL	NULL	NULL	NULL	gw60_embo_21_21_5775_s_161	12411495	( D) E2F3 but not E2F1 binds to the Cdc6 and RR1 promoter at G1/S.	bind
3047	2	1896	5	10	NULL	NULL	NULL	E2F3	GP		bind					RR1	GP			promoter	NULL	at G1/S	NULL	NULL	NULL	NULL	gw60_embo_21_21_5775_s_161	12411495	( D) E2F3 but not E2F1 binds to the Cdc6 and RR1 promoter at G1/S.	bind
3048	3	1896	5	10	NULL	NULL	NULL	E2F1	GP		does not bind					Cdc6	GP			promoter	NULL	at G1/S	NULL	NULL	NULL	NULL	gw60_embo_21_21_5775_s_161	12411495	( D) E2F3 but not E2F1 binds to the Cdc6 and RR1 promoter at G1/S.	bind
3049	4	1896	5	10	NULL	NULL	NULL	E2F1	GP		does not bind					RR1	GP			promoter	NULL	at G1/S	NULL	NULL	NULL	NULL	gw60_embo_21_21_5775_s_161	12411495	( D) E2F3 but not E2F1 binds to the Cdc6 and RR1 promoter at G1/S.	bind
2414	1	1896	7	10	NULL	NULL	NULL	E2F3	GP		bind					Cdc6	GP			promoter	NULL	at G1/S	NULL	NULL	NULL	NULL	gw60_embo_21_21_5775_s_161	12411495	( D) E2F3 but not E2F1 binds to the Cdc6 and RR1 promoter at G1/S.	bind
2415	2	1896	7	10	NULL	NULL	NULL	E2F3	GP		bind					RR1	GP			promoter	NULL	at G1/S	NULL	NULL	NULL	NULL	gw60_embo_21_21_5775_s_161	12411495	( D) E2F3 but not E2F1 binds to the Cdc6 and RR1 promoter at G1/S.	bind
2416	3	1896	7	10	NULL	NULL	NULL	E2F1	GP		does not bind					Cdc6	GP			promoter	NULL	at G1/S	NULL	NULL	NULL	NULL	gw60_embo_21_21_5775_s_161	12411495	( D) E2F3 but not E2F1 binds to the Cdc6 and RR1 promoter at G1/S.	bind
2417	4	1896	7	10	NULL	NULL	NULL	E2F1	GP		does not bind					RR1	GP			promoter	NULL	at G1/S	NULL	NULL	NULL	NULL	gw60_embo_21_21_5775_s_161	12411495	( D) E2F3 but not E2F1 binds to the Cdc6 and RR1 promoter at G1/S.	bind
3078	1	1897	5	10	NULL	NULL	NULL	EGF	GP		bind					EGFR/LckF505	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17896_s_167	8663450	( d) EGF binding to EGFR/LckF505 may allow the phosphorylation of the chimera by transphosphorylation of the EGFR/Lck dimer or phosphorylation by another PTK ( 60,  61) at Lck autophosphorylation site, Tyr-394, or possibly at the recently reported site within the Lck SH2 domain, Tyr-192 ( 62,  63).	bind
3079	2	1897	5	10	NULL	NULL	NULL	statement 1	Process		phosphorylate		may 			EGFR/LckF505	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17896_s_167	8663450	( d) EGF binding to EGFR/LckF505 may allow the phosphorylation of the chimera by transphosphorylation of the EGFR/Lck dimer or phosphorylation by another PTK ( 60,  61) at Lck autophosphorylation site, Tyr-394, or possibly at the recently reported site within the Lck SH2 domain, Tyr-192 ( 62,  63).	bind
3081	3	1897	5	10	NULL	NULL	NULL	statement 2	Process		occurs by					EGFR/Lck dimer	GP	transphosphorylation			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17896_s_167	8663450	( d) EGF binding to EGFR/LckF505 may allow the phosphorylation of the chimera by transphosphorylation of the EGFR/Lck dimer or phosphorylation by another PTK ( 60,  61) at Lck autophosphorylation site, Tyr-394, or possibly at the recently reported site within the Lck SH2 domain, Tyr-192 ( 62,  63).	bind
3082	4	1897	5	10	NULL	NULL	NULL	PTK	GP		phosphorylate					EGFR/Lck dimer	GP		Lck autophosphorylation site Tyr-394		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17896_s_167	8663450	( d) EGF binding to EGFR/LckF505 may allow the phosphorylation of the chimera by transphosphorylation of the EGFR/Lck dimer or phosphorylation by another PTK ( 60,  61) at Lck autophosphorylation site, Tyr-394, or possibly at the recently reported site within the Lck SH2 domain, Tyr-192 ( 62,  63).	bind
3083	5	1897	5	10	NULL	NULL	NULL	PTK	GP		phosphorylate					EGFR/Lck dimer	GP		Lck SH2 domain, Tyr-192		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17896_s_167	8663450	( d) EGF binding to EGFR/LckF505 may allow the phosphorylation of the chimera by transphosphorylation of the EGFR/Lck dimer or phosphorylation by another PTK ( 60,  61) at Lck autophosphorylation site, Tyr-394, or possibly at the recently reported site within the Lck SH2 domain, Tyr-192 ( 62,  63).	bind
3104	6	1897	5	10	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17896_s_167	8663450	( d) EGF binding to EGFR/LckF505 may allow the phosphorylation of the chimera by transphosphorylation of the EGFR/Lck dimer or phosphorylation by another PTK ( 60,  61) at Lck autophosphorylation site, Tyr-394, or possibly at the recently reported site within the Lck SH2 domain, Tyr-192 ( 62,  63).	bind
2419	1	1897	7	10	NULL	NULL	NULL	EGF	GP		bind					EGFR/LckF505 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17896_s_167	8663450	( d) EGF binding to EGFR/LckF505 may allow the phosphorylation of the chimera by transphosphorylation of the EGFR/Lck dimer or phosphorylation by another PTK ( 60,  61) at Lck autophosphorylation site, Tyr-394, or possibly at the recently reported site within the Lck SH2 domain, Tyr-192 ( 62,  63).	bind
2420	2	1897	7	10	NULL	NULL	NULL	statement 1	Process		phosphorylate		may			EGFR/LckF505	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17896_s_167	8663450	( d) EGF binding to EGFR/LckF505 may allow the phosphorylation of the chimera by transphosphorylation of the EGFR/Lck dimer or phosphorylation by another PTK ( 60,  61) at Lck autophosphorylation site, Tyr-394, or possibly at the recently reported site within the Lck SH2 domain, Tyr-192 ( 62,  63).	bind
2421	3	1897	7	10	NULL	NULL	NULL	statement 2	Process		occurs through					EGFR/Lck dimer	GP	transphosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17896_s_167	8663450	( d) EGF binding to EGFR/LckF505 may allow the phosphorylation of the chimera by transphosphorylation of the EGFR/Lck dimer or phosphorylation by another PTK ( 60,  61) at Lck autophosphorylation site, Tyr-394, or possibly at the recently reported site within the Lck SH2 domain, Tyr-192 ( 62,  63).	bind
2422	4	1897	7	10	NULL	NULL	NULL	PTK	GP		phosphorylate					EGFR/LckF505	GP		Lck autophosphorylation site, Tyr-394		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17896_s_167	8663450	( d) EGF binding to EGFR/LckF505 may allow the phosphorylation of the chimera by transphosphorylation of the EGFR/Lck dimer or phosphorylation by another PTK ( 60,  61) at Lck autophosphorylation site, Tyr-394, or possibly at the recently reported site within the Lck SH2 domain, Tyr-192 ( 62,  63).	bind
2423	5	1897	7	10	NULL	NULL	NULL	PTK	GP		phosphorylate					EGFR/LckF505	GP		Lck SH2 domain, Tyr-192		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17896_s_167	8663450	( d) EGF binding to EGFR/LckF505 may allow the phosphorylation of the chimera by transphosphorylation of the EGFR/Lck dimer or phosphorylation by another PTK ( 60,  61) at Lck autophosphorylation site, Tyr-394, or possibly at the recently reported site within the Lck SH2 domain, Tyr-192 ( 62,  63).	bind
2424	6	1897	7	10	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17896_s_167	8663450	( d) EGF binding to EGFR/LckF505 may allow the phosphorylation of the chimera by transphosphorylation of the EGFR/Lck dimer or phosphorylation by another PTK ( 60,  61) at Lck autophosphorylation site, Tyr-394, or possibly at the recently reported site within the Lck SH2 domain, Tyr-192 ( 62,  63).	bind
3050	1	1898	5	10	NULL	NULL	NULL	EGL-17	GP		bind					Ce-LRP-2	GP		YWTD region		NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_22_2798_s_205	14630941	( D) EGL-17 binds to Ce-LRP-2 YWTD region.	bind
2418	1	1898	7	10	NULL	NULL	NULL	EGL-17	GP		bind					Ce-LRP-2	GP		YWTD		NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_22_2798_s_205	14630941	( D) EGL-17 binds to Ce-LRP-2 YWTD region.	bind
3051	1	1899	5	10	NULL	NULL	NULL	AEBP1	GP		bind		specifically			hPPARgamma1	GP			AE-1 homologous sequences in the promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_7_2346_s_64	16461908	( D) EMSA shows that AEBP1 specifically binds to AE-1 homologous sequences in the promoter  regions of hPPARgamma1 and mLXRalpha but not to the mutated sequences (hPPARgamma1-M and mLXRalpha-M).	bind
3052	2	1899	5	10	NULL	NULL	NULL	AEBP1	GP		bind		specifically			mLXRalpha	GP			AE-1 homologous sequences in the promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_7_2346_s_64	16461908	( D) EMSA shows that AEBP1 specifically binds to AE-1 homologous sequences in the promoter  regions of hPPARgamma1 and mLXRalpha but not to the mutated sequences (hPPARgamma1-M and mLXRalpha-M).	bind
3053	3	1899	5	10	NULL	NULL	NULL	AEBP1	GP		does not bind					hPPARgamma1-M	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_7_2346_s_64	16461908	( D) EMSA shows that AEBP1 specifically binds to AE-1 homologous sequences in the promoter  regions of hPPARgamma1 and mLXRalpha but not to the mutated sequences (hPPARgamma1-M and mLXRalpha-M).	bind
3054	4	1899	5	10	NULL	NULL	NULL	AEBP1	GP		does not bind					mLXRalpha-M	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_7_2346_s_64	16461908	( D) EMSA shows that AEBP1 specifically binds to AE-1 homologous sequences in the promoter  regions of hPPARgamma1 and mLXRalpha but not to the mutated sequences (hPPARgamma1-M and mLXRalpha-M).	bind
2425	1	1899	7	10	NULL	NULL	NULL	AEBP1	GP		binds to		specifically			hPPARgamma1	GP			 AE-1 homologous sequences in the promoter of 	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_7_2346_s_64	16461908	( D) EMSA shows that AEBP1 specifically binds to AE-1 homologous sequences in the promoter  regions of hPPARgamma1 and mLXRalpha but not to the mutated sequences (hPPARgamma1-M and mLXRalpha-M).	bind
2426	2	1899	7	10	NULL	NULL	NULL	AEBP1	GP		binds to		specifically			mLXRalpha	GP			AE-1 homologous sequences in the promoter of	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_7_2346_s_64	16461908	( D) EMSA shows that AEBP1 specifically binds to AE-1 homologous sequences in the promoter  regions of hPPARgamma1 and mLXRalpha but not to the mutated sequences (hPPARgamma1-M and mLXRalpha-M).	bind
2427	3	1899	7	10	NULL	NULL	NULL	AEBP1	GP		does not bind					hPPARgamma1-M	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_7_2346_s_64	16461908	( D) EMSA shows that AEBP1 specifically binds to AE-1 homologous sequences in the promoter  regions of hPPARgamma1 and mLXRalpha but not to the mutated sequences (hPPARgamma1-M and mLXRalpha-M).	bind
2428	4	1899	7	10	NULL	NULL	NULL	AEBP1	GP		does not bind					mLXRalpha-M	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_7_2346_s_64	16461908	( D) EMSA shows that AEBP1 specifically binds to AE-1 homologous sequences in the promoter  regions of hPPARgamma1 and mLXRalpha but not to the mutated sequences (hPPARgamma1-M and mLXRalpha-M).	bind
3055	1	1900	5	10	NULL	NULL	NULL	SLP-76	GP		bind					PLCgamma1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_12_1762_s_231	15599401	( D) EphB6 augmented binding of SLP-76 with PLCgamma1 after TCR activation.	bind
3056	2	1900	5	10	NULL	NULL	NULL	statement 1	Process		occurs following					TCR	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_12_1762_s_231	15599401	( D) EphB6 augmented binding of SLP-76 with PLCgamma1 after TCR activation.	bind
3057	3	1900	5	10	NULL	NULL	NULL	EphB6	GP		augment					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_12_1762_s_231	15599401	( D) EphB6 augmented binding of SLP-76 with PLCgamma1 after TCR activation.	bind
2431	1	1900	7	10	NULL	NULL	NULL	SLP-76	GP		bind					PLCgamma1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_12_1762_s_231	15599401	( D) EphB6 augmented binding of SLP-76 with PLCgamma1 after TCR activation.	bind
2432	2	1900	7	10	NULL	NULL	NULL	 EphB6	GP		augment					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_12_1762_s_231	15599401	( D) EphB6 augmented binding of SLP-76 with PLCgamma1 after TCR activation.	bind
2433	3	1900	7	10	NULL	NULL	NULL	statement 2	Process		occurs after					TCR	GP	activation of 			NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_12_1762_s_231	15599401	( D) EphB6 augmented binding of SLP-76 with PLCgamma1 after TCR activation.	bind
3058	1	1901	5	10	NULL	NULL	NULL	ERs	GP		does not bind					TNF	GP			RE	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_26_15161_s_99	10611355	( D) ERs do not bind to the TNF-RE.	bind
3202	1	1901	7	10	NULL	NULL	NULL	ERs	GP		does not bind					TNF	GP			RE	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_26_15161_s_99	10611355	( D) ERs do not bind to the TNF-RE.	bind
3059	1	1902	5	10	NULL	NULL	NULL	PB1	GP		bind					vRNA oligonucleotide	NucleicAcid	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_429_s_189	11788704	( D) Estimation of the quantity of PB1 bound to the immobilised vRNA oligonucleotide.	bind
3204	1	1902	7	10	NULL	NULL	NULL	PB1	GP		bind					vRNA oligonucleotide	NucleicAcid	immobilised			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_429_s_189	11788704	( D) Estimation of the quantity of PB1 bound to the immobilised vRNA oligonucleotide.	bind
3060	1	1904	5	10	NULL	NULL	NULL	Fbw7	GP		bind		preferentially			cyclin E-Cdk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_294_5540_173_s_53	11533444	( D) Fbw7 preferentially binds cyclin E-Cdk2.	bind
3206	1	1904	7	10	NULL	NULL	NULL	Fbw7	GP		bind		preferentially			cyclin E-Cdk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_294_5540_173_s_53	11533444	( D) Fbw7 preferentially binds cyclin E-Cdk2.	bind
3061	1	1905	5	10	NULL	NULL	NULL	Fhl1	GP		bind		specifically			 RP	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_18_20_2491_s_279	15466158	( D) Fhl1 and Ifh1 bind specifically to  RP promoters.	bind
3062	2	1905	5	10	NULL	NULL	NULL	Ifh1	GP		bind		specifically			RP	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_18_20_2491_s_279	15466158	( D) Fhl1 and Ifh1 bind specifically to  RP promoters.	bind
3207	1	1905	7	10	NULL	NULL	NULL	Fhl1	GP		bind		specifically			RP	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_18_20_2491_s_279	15466158	( D) Fhl1 and Ifh1 bind specifically to  RP promoters.	bind
3208	2	1905	7	10	NULL	NULL	NULL	 Ifh1	GP		bind		specifically			RP	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_18_20_2491_s_279	15466158	( D) Fhl1 and Ifh1 bind specifically to  RP promoters.	bind
3063	1	1906	5	10	NULL	NULL	NULL	mAb 1D11	GP		bind					Jurkat-NKG2D	Cell	transfectants			NULL		NULL	NULL	NULL	NULL	gw60_science_285_5428_727_s_71	10426993	( D) Flow cytometry showed binding of mAb 1D11 to the Jurkat-NKG2D transfectants but not to the untransfected cells.	bind
3064	2	1906	5	10	NULL	NULL	NULL	mAb 1D11	GP		does not bind					untransfected cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5428_727_s_71	10426993	( D) Flow cytometry showed binding of mAb 1D11 to the Jurkat-NKG2D transfectants but not to the untransfected cells.	bind
3217	1	1906	7	10	NULL	NULL	NULL	mAb 1D11	GP		bind					 Jurkat-NKG2D 	Cell	transfectants			NULL		NULL	NULL	NULL	NULL	gw60_science_285_5428_727_s_71	10426993	( D) Flow cytometry showed binding of mAb 1D11 to the Jurkat-NKG2D transfectants but not to the untransfected cells.	bind
3218	2	1906	7	10	NULL	NULL	NULL	mAb 1D11	GP		does not bind					untransfected cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5428_727_s_71	10426993	( D) Flow cytometry showed binding of mAb 1D11 to the Jurkat-NKG2D transfectants but not to the untransfected cells.	bind
3065	1	1907	5	10	NULL	NULL	NULL	GA	GP		bind					TfR	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_105	16103367	( D) GA binds to TfR.	bind
3219	1	1907	7	10	NULL	NULL	NULL	GA	GP		bind					 TfR	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_34_12095_s_105	16103367	( D) GA binds to TfR.	bind
3066	1	1909	5	10	NULL	NULL	NULL	GST-Aly	GP		bind					ORF57	GP	WT			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_41_15190_s_124	17005724	( d) GST pull-down assays were repeated to compare the binding affinity of GST-Aly with  WT ORF57 and ORF57NLS1M.	bind
3067	2	1909	5	10	NULL	NULL	NULL	GST-Aly	GP		bind					ORF57	GP		NLS1M		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_41_15190_s_124	17005724	( d) GST pull-down assays were repeated to compare the binding affinity of GST-Aly with  WT ORF57 and ORF57NLS1M.	bind
3220	1	1909	7	10	NULL	NULL	NULL	GST-Aly	GP		bind					 ORF57	GP	WT 			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_41_15190_s_124	17005724	( d) GST pull-down assays were repeated to compare the binding affinity of GST-Aly with  WT ORF57 and ORF57NLS1M.	bind
3221	2	1909	7	10	NULL	NULL	NULL	GST-Aly	GP		bind					ORF57	GP		NLS1M		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_41_15190_s_124	17005724	( d) GST pull-down assays were repeated to compare the binding affinity of GST-Aly with  WT ORF57 and ORF57NLS1M.	bind
3068	1	1910	5	10	NULL	NULL	NULL	HBP1	GP		does not bind									LEF/TCF DNA binding site	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_16_4500_s_160	11500377	( D) HBP1 does not bind the TOPFLASH LEF/TCF DNA binding site.	bind
3222	1	1910	7	10	NULL	NULL	NULL	HBP1	GP		does not bind									 LEF/TCF DNA binding site	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_16_4500_s_160	11500377	( D) HBP1 does not bind the TOPFLASH LEF/TCF DNA binding site.	bind
3327	1	1911	5	10	NULL	NULL	NULL	FGF-2	GP		bind					Namalwa-CD44vRA	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1211_s_135	12697740	( d) Heparinase treatment reduces FGF-2 binding to Namalwa-CD44vRA.	bind
3328	2	1911	5	10	NULL	NULL	NULL	Heparinase	GP		reduce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1211_s_135	12697740	( d) Heparinase treatment reduces FGF-2 binding to Namalwa-CD44vRA.	bind
3223	1	1911	7	10	NULL	NULL	NULL	FGF-2	GP		bind					Namalwa CD44vRA	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1211_s_135	12697740	( d) Heparinase treatment reduces FGF-2 binding to Namalwa-CD44vRA.	bind
3224	2	1911	7	10	NULL	NULL	NULL	Heparinase	GP		reduces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1211_s_135	12697740	( d) Heparinase treatment reduces FGF-2 binding to Namalwa-CD44vRA.	bind
3329	1	1912	5	10	NULL	NULL	NULL	HsdR	GP		bind					MTase	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_23_4188_s_102	16292342	( D) HsdR binding rate to the MTase at different HsdR concentrations obtained from fitting  the triplex displacement curves.	bind
3225	1	1912	7	10	NULL	NULL	NULL	HsdR	GP		binds to					MTase	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_23_4188_s_102	16292342	( D) HsdR binding rate to the MTase at different HsdR concentrations obtained from fitting  the triplex displacement curves.	bind
3331	1	1913	5	10	NULL	NULL	NULL	hTAFII130	GP		bind					HP1alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_9_5919_s_128	11959914	( D) hTAFII130 bound to HP1alpha and HP1gamma but not to HP1beta.	bind
3332	2	1913	5	10	NULL	NULL	NULL	hTAFII130	GP		bind					HP1gamma	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_9_5919_s_128	11959914	( D) hTAFII130 bound to HP1alpha and HP1gamma but not to HP1beta.	bind
3333	3	1913	5	10	NULL	NULL	NULL	hTAFII130	GP		does not bind					HP1beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_9_5919_s_128	11959914	( D) hTAFII130 bound to HP1alpha and HP1gamma but not to HP1beta.	bind
3226	1	1913	7	10	NULL	NULL	NULL	hTAFII130	GP		bind					HP1alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_9_5919_s_128	11959914	( D) hTAFII130 bound to HP1alpha and HP1gamma but not to HP1beta.	bind
3227	2	1913	7	10	NULL	NULL	NULL	hTAFII130	GP		bind					HP1gamma 	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_9_5919_s_128	11959914	( D) hTAFII130 bound to HP1alpha and HP1gamma but not to HP1beta.	bind
3228	3	1913	7	10	NULL	NULL	NULL	 hTAFII130	GP		does not bind					HP1beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_9_5919_s_128	11959914	( D) hTAFII130 bound to HP1alpha and HP1gamma but not to HP1beta.	bind
3334	1	1915	5	10	NULL	NULL	NULL	ICSBP	GP		bind					Dab2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_21_3_211_s_65	11823414	( D) ICSBP and PU.1 bind to the Dab2 promoter.	bind
3335	2	1915	5	10	NULL	NULL	NULL	PU.1	GP		bind					Dab2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_21_3_211_s_65	11823414	( D) ICSBP and PU.1 bind to the Dab2 promoter.	bind
3230	1	1915	7	10	NULL	NULL	NULL	ICSBP	GP		bind					Dab2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_21_3_211_s_65	11823414	( D) ICSBP and PU.1 bind to the Dab2 promoter.	bind
3231	2	1915	7	10	NULL	NULL	NULL	PU.1	GP		bind					Dab2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_21_3_211_s_65	11823414	( D) ICSBP and PU.1 bind to the Dab2 promoter.	bind
3336	1	1916	5	10	NULL	NULL	NULL	poliota	GP		bind					Ub	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_12_2847_s_49	16763556	( D) In addition to poliota, pol  also binds to Ub.	bind
3337	2	1916	5	10	NULL	NULL	NULL	pol	GP		bind					Ub	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_12_2847_s_49	16763556	( D) In addition to poliota, pol  also binds to Ub.	bind
3232	1	1916	7	10	NULL	NULL	NULL	poliota	GP		bind					Ub	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_12_2847_s_49	16763556	( D) In addition to poliota, pol  also binds to Ub.	bind
3233	2	1916	7	10	NULL	NULL	NULL	pol	GP		bind					Ub	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_12_2847_s_49	16763556	( D) In addition to poliota, pol  also binds to Ub.	bind
3442	1	1917	5	10	NULL	NULL	NULL	annexin-V biotin	GP		bind					K5/rTA DT	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_16_9139_s_139	11481479	( D) Increased annexin-V biotin binding of K5/rTA DT but not control keratinocytes 48 h after addition of doxycycline.	bind
3443	2	1917	5	10	NULL	NULL	NULL	doxycycline	Chemical	addition	increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_16_9139_s_139	11481479	( D) Increased annexin-V biotin binding of K5/rTA DT but not control keratinocytes 48 h after addition of doxycycline.	bind
3444	3	1917	5	10	NULL	NULL	NULL	annexin-V biotin	GP		does not bind					keratinocytes	Cell	control			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_16_9139_s_139	11481479	( D) Increased annexin-V biotin binding of K5/rTA DT but not control keratinocytes 48 h after addition of doxycycline.	bind
3235	1	1917	7	10	NULL	NULL	NULL	annexin-V biotin	GP		bind					K5/rTA DT	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_16_9139_s_139	11481479	( D) Increased annexin-V biotin binding of K5/rTA DT but not control keratinocytes 48 h after addition of doxycycline.	bind
3237	2	1917	7	10	NULL	NULL	NULL	annexin-V biotin	GP		does not bind					 keratinocytes	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_16_9139_s_139	11481479	( D) Increased annexin-V biotin binding of K5/rTA DT but not control keratinocytes 48 h after addition of doxycycline.	bind
4596	3	1917	7	10	NULL	NULL	NULL	doxycycline	Chemical	addition	increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_16_9139_s_139	11481479	( D) Increased annexin-V biotin binding of K5/rTA DT but not control keratinocytes 48 h after addition of doxycycline.	bind
3490	1	1918	5	10	NULL	NULL	NULL	calmodulin	GP	rat brain;; cytosolic	bind					mGluR 7	GP		tail regions		NULL		NULL	NULL	NULL	NULL	gw60_science_286_5442_1180_s_38	10550060	( D) Incubating rat brain cytosolic proteins with GST, GST-7A, or GST-7B in the presence of CaCl2 (1 mM) or EGTA (5 mM) revealed that the binding of calmodulin to the mGluR 7 tail regions is Ca2+- dependent.	bind
3491	2	1918	5	10	NULL	NULL	NULL	statement 1	Process		is dependent on					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5442_1180_s_38	10550060	( D) Incubating rat brain cytosolic proteins with GST, GST-7A, or GST-7B in the presence of CaCl2 (1 mM) or EGTA (5 mM) revealed that the binding of calmodulin to the mGluR 7 tail regions is Ca2+- dependent.	bind
3240	1	1918	7	10	NULL	NULL	NULL	calmodulin	GP	rat brain;; cytosolic	bind					mGluR 7	GP		tail region		NULL		NULL	NULL	NULL	NULL	gw60_science_286_5442_1180_s_38	10550060	( D) Incubating rat brain cytosolic proteins with GST, GST-7A, or GST-7B in the presence of CaCl2 (1 mM) or EGTA (5 mM) revealed that the binding of calmodulin to the mGluR 7 tail regions is Ca2+- dependent.	bind
3241	2	1918	7	10	NULL	NULL	NULL	statement 1	Process		is dependent on					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5442_1180_s_38	10550060	( D) Incubating rat brain cytosolic proteins with GST, GST-7A, or GST-7B in the presence of CaCl2 (1 mM) or EGTA (5 mM) revealed that the binding of calmodulin to the mGluR 7 tail regions is Ca2+- dependent.	bind
3495	2	1919	5	10	NULL	NULL	NULL	rGL-7	GP		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_13_7454_s_142	12802014	( D) Induction of  NAD+ glycohydrolase activity by rGL-7.	bind
46204	1	1919	5	10	NULL	NULL	NULL	NAD+	Chemical		activates					glycohydrolase 	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_13_7454_s_142	12802014	( D) Induction of  NAD+ glycohydrolase activity by rGL-7.	bind
46208	1	1919	7	10	NULL	NULL	NULL	NAD+	Chemical		activates					glycohydrolase 	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_13_7454_s_142	12802014	( D) Induction of  NAD+ glycohydrolase activity by rGL-7.	bind
46209	2	1919	7	10	NULL	NULL	NULL	 rGL-7	GP		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_13_7454_s_142	12802014	( D) Induction of  NAD+ glycohydrolase activity by rGL-7.	bind
3496	1	1920	5	10	NULL	NULL	NULL	IpaA	GP		does not bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_5853_s_185	10545097	( D) IpaA does not bind to F-actin.	bind
3243	1	1920	7	10	NULL	NULL	NULL	IpaA	GP		does not bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_5853_s_185	10545097	( D) IpaA does not bind to F-actin.	bind
3497	1	1921	5	10	NULL	NULL	NULL	ubiquitin	GP		bind					HDAC6	GP		ZnF-UBP		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_14_3357_s_40	16810319	( D) ITC profile for the binding of ubiquitin to HDAC6 ZnF-UBP.	bind
3244	1	1921	7	10	NULL	NULL	NULL	ubiquitin	GP		bind					HDAC6	GP		 ZnF-UBP		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_14_3357_s_40	16810319	( D) ITC profile for the binding of ubiquitin to HDAC6 ZnF-UBP.	bind
3498	1	1922	5	10	NULL	NULL	NULL	JunB	GP		does not bind					PPARbeta	GP			AP-1 site of promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_23_21_4211_s_107	15470497	( D) JunB is not binding to the AP-1 site of the PPARbeta promoter.	bind
3245	1	1922	7	10	NULL	NULL	NULL	JunB	GP		does not bind					PPARbeta	GP			AP-1 site promoter of	NULL		NULL	NULL	NULL	NULL	gw70_embo_23_21_4211_s_107	15470497	( D) JunB is not binding to the AP-1 site of the PPARbeta promoter.	bind
3795	1	1923	5	10	NULL	NULL	NULL	L-Sox5	GP		bind									48 bp probe	NULL		NULL	NULL	NULL	NULL	gw60_embo_17_19_5718_s_91	9755172	( D) L-Sox5, Sox6 and SOX9 bound to the 48 bp probe.	bind
3796	2	1923	5	10	NULL	NULL	NULL	Sox6	GP		bind									48 bp probe	NULL		NULL	NULL	NULL	NULL	gw60_embo_17_19_5718_s_91	9755172	( D) L-Sox5, Sox6 and SOX9 bound to the 48 bp probe.	bind
3797	3	1923	5	10	NULL	NULL	NULL	SOX9	GP		bind									48 bp probe	NULL		NULL	NULL	NULL	NULL	gw60_embo_17_19_5718_s_91	9755172	( D) L-Sox5, Sox6 and SOX9 bound to the 48 bp probe.	bind
3246	1	1923	7	10	NULL	NULL	NULL	L-Sox5	GP		 bind									48 bp probe	NULL		NULL	NULL	NULL	NULL	gw60_embo_17_19_5718_s_91	9755172	( D) L-Sox5, Sox6 and SOX9 bound to the 48 bp probe.	bind
3247	2	1923	7	10	NULL	NULL	NULL	Sox6	GP		bind									48 bp probe	NULL		NULL	NULL	NULL	NULL	gw60_embo_17_19_5718_s_91	9755172	( D) L-Sox5, Sox6 and SOX9 bound to the 48 bp probe.	bind
3248	3	1923	7	10	NULL	NULL	NULL	SOX9 	GP		bind									48 bp probe	NULL		NULL	NULL	NULL	NULL	gw60_embo_17_19_5718_s_91	9755172	( D) L-Sox5, Sox6 and SOX9 bound to the 48 bp probe.	bind
3501	1	1924	5	10	NULL	NULL	NULL	STAT3	GP		bind					Nanog	GP	putative		STAT-binding site in regulatory region	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_27_10294_s_46	16801560	( D) LIF-dependent binding of STAT3 to the putative STAT-binding site in the  Nanog regulatory region.	bind
3502	2	1924	5	10	NULL	NULL	NULL	statement 1	Process		is dependent on					LIF	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_27_10294_s_46	16801560	( D) LIF-dependent binding of STAT3 to the putative STAT-binding site in the  Nanog regulatory region.	bind
3249	1	1924	7	10	NULL	NULL	NULL	STAT3	GP		bind					Nanog	GP	putative		STAT-binding site regulatory region	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_27_10294_s_46	16801560	( D) LIF-dependent binding of STAT3 to the putative STAT-binding site in the  Nanog regulatory region.	bind
3250	2	1924	7	10	NULL	NULL	NULL	statement 1	Process		is dependent  on					LIF	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_27_10294_s_46	16801560	( D) LIF-dependent binding of STAT3 to the putative STAT-binding site in the  Nanog regulatory region.	bind
3504	1	1925	5	10	NULL	NULL	NULL	SB203580	Chemical		is a type of					MAP kinase inhibitor	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1162_s_211	15870257	( D) MAP kinase inhibitor SB203580 completely abrogates p38 MAP kinase activity.	bind
3505	2	1925	5	10	NULL	NULL	NULL	SB203580	Chemical		abrogate		completely			p38 MAP kinase	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1162_s_211	15870257	( D) MAP kinase inhibitor SB203580 completely abrogates p38 MAP kinase activity.	bind
3267	1	1925	7	10	NULL	NULL	NULL	SB203580	Chemical		abrogates		completely			p38 MAP kinase 	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1162_s_211	15870257	( D) MAP kinase inhibitor SB203580 completely abrogates p38 MAP kinase activity.	bind
4597	2	1925	7	10	NULL	NULL	NULL	SB203580 	Chemical		is a type of					MAP kinase inhibitor	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1162_s_211	15870257	( D) MAP kinase inhibitor SB203580 completely abrogates p38 MAP kinase activity.	bind
3508	1	1927	5	10	NULL	NULL	NULL	MBP - Kap114p	GP		bind					GST - histone	GP		N-terminal tail		NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6527_s_106	12456659	( D) MBP - Kap114p (200 nM) binding to GST - histone N-terminal tails as in (B).	bind
3268	1	1927	7	10	NULL	NULL	NULL	MBP - Kap114p	GP		bind					GST - histone	GP		N-terminal tails		NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6527_s_106	12456659	( D) MBP - Kap114p (200 nM) binding to GST - histone N-terminal tails as in (B).	bind
3509	1	1930	5	10	NULL	NULL	NULL	TF1-v1	GP		bind					theophylline	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1631_s_153	11266567	( D) Model of TF1-v1 bound to theophylline and FMN (encircled F).	bind
3510	2	1930	5	10	NULL	NULL	NULL	TF1-v1	GP		bind					FMN	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1631_s_153	11266567	( D) Model of TF1-v1 bound to theophylline and FMN (encircled F).	bind
3269	1	1930	7	10	NULL	NULL	NULL	TF1-v1	GP		bind					theophylline	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1631_s_153	11266567	( D) Model of TF1-v1 bound to theophylline and FMN (encircled F).	bind
3270	2	1930	7	10	NULL	NULL	NULL	TF1-v1	GP		bind					FMN	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1631_s_153	11266567	( D) Model of TF1-v1 bound to theophylline and FMN (encircled F).	bind
3512	1	1931	5	10	NULL	NULL	NULL	MTA-1	GP		bind					GST-FOG-1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_embo_24_13_2367_s_140	15920470	( D) MTA-1, MTA-2 and RbAP48 bind GST-FOG-1(45)  in vitro.	bind
3513	2	1931	5	10	NULL	NULL	NULL	MTA-2	GP		bind					GST-FOG-1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_embo_24_13_2367_s_140	15920470	( D) MTA-1, MTA-2 and RbAP48 bind GST-FOG-1(45)  in vitro.	bind
3514	3	1931	5	10	NULL	NULL	NULL	RbAP48	GP		bind					GST-FOG-1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_embo_24_13_2367_s_140	15920470	( D) MTA-1, MTA-2 and RbAP48 bind GST-FOG-1(45)  in vitro.	bind
3271	1	1931	7	10	NULL	NULL	NULL	MTA-1	GP		bind					GST-FOG-1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_embo_24_13_2367_s_140	15920470	( D) MTA-1, MTA-2 and RbAP48 bind GST-FOG-1(45)  in vitro.	bind
3272	2	1931	7	10	NULL	NULL	NULL	MTA-2	GP		bind					GST-FOG-1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_embo_24_13_2367_s_140	15920470	( D) MTA-1, MTA-2 and RbAP48 bind GST-FOG-1(45)  in vitro.	bind
3273	3	1931	7	10	NULL	NULL	NULL	RbAP48	GP		bind					GST-FOG-1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_embo_24_13_2367_s_140	15920470	( D) MTA-1, MTA-2 and RbAP48 bind GST-FOG-1(45)  in vitro.	bind
3515	1	1932	5	10	NULL	NULL	NULL	GST-N-CFTR	GP		bind					syn1AdeltaC	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_18_10972_s_86	9724814	( D) Munc-18a blocks the binding of GST-N-CFTR to syn1AdeltaC.	bind
3516	2	1932	5	10	NULL	NULL	NULL	Munc-18a	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_18_10972_s_86	9724814	( D) Munc-18a blocks the binding of GST-N-CFTR to syn1AdeltaC.	bind
3274	1	1932	7	10	NULL	NULL	NULL	GST-N-CFTR	GP		bind					syn1AdeltaC	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_18_10972_s_86	9724814	( D) Munc-18a blocks the binding of GST-N-CFTR to syn1AdeltaC.	bind
3275	2	1932	7	10	NULL	NULL	NULL	Munc-18a	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_18_10972_s_86	9724814	( D) Munc-18a blocks the binding of GST-N-CFTR to syn1AdeltaC.	bind
3523	1	1933	5	10	NULL	NULL	NULL	importin-alpha	GP		is					Kap60p	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_21_3681_s_121	16222336	( D) Mutants in the Nup2p residues analogous to those identified in the two importin-alpha-binding regions of Nup50 do not displace the monopartite or bipartite NLSs from yeast  importin-alpha (Kap60p).	bind
3528	2	1933	5	10	NULL	NULL	NULL	Nup2p	GP	mutant	analogus to					Nup50	GP		 importin-alpha-binding regions		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_21_3681_s_121	16222336	( D) Mutants in the Nup2p residues analogous to those identified in the two importin-alpha-binding regions of Nup50 do not displace the monopartite or bipartite NLSs from yeast  importin-alpha (Kap60p).	bind
3530	3	1933	5	10	NULL	NULL	NULL	statement 2	Process		does not displace					 importin-alpha	GP	yeast	monopartite NLS		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_21_3681_s_121	16222336	( D) Mutants in the Nup2p residues analogous to those identified in the two importin-alpha-binding regions of Nup50 do not displace the monopartite or bipartite NLSs from yeast  importin-alpha (Kap60p).	bind
3531	4	1933	5	10	NULL	NULL	NULL	statement 2	Process		does not displace					importin-alpha	GP	yeast	bipartite NLS		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_21_3681_s_121	16222336	( D) Mutants in the Nup2p residues analogous to those identified in the two importin-alpha-binding regions of Nup50 do not displace the monopartite or bipartite NLSs from yeast  importin-alpha (Kap60p).	bind
3276	1	1933	7	10	NULL	NULL	NULL	Nup2p	GP	mutant	does not displace					importin-alpha	GP	yeast	monopartite NLSs		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_21_3681_s_121	16222336	( D) Mutants in the Nup2p residues analogous to those identified in the two importin-alpha-binding regions of Nup50 do not displace the monopartite or bipartite NLSs from yeast  importin-alpha (Kap60p).	bind
3277	2	1933	7	10	NULL	NULL	NULL	Nup2p	GP	mutant	does not displace					importin-alpha 	GP	yeast	bipartite NLSs		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_21_3681_s_121	16222336	( D) Mutants in the Nup2p residues analogous to those identified in the two importin-alpha-binding regions of Nup50 do not displace the monopartite or bipartite NLSs from yeast  importin-alpha (Kap60p).	bind
3278	3	1933	7	10	NULL	NULL	NULL	Nup2p 	GP	Mutant	is analogous 			residues		Nup50	GP		two importin-alpha-binding regions		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_21_3681_s_121	16222336	( D) Mutants in the Nup2p residues analogous to those identified in the two importin-alpha-binding regions of Nup50 do not displace the monopartite or bipartite NLSs from yeast  importin-alpha (Kap60p).	bind
3279	4	1933	7	10	NULL	NULL	NULL	importin-alpha	GP		is					Kap60p	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_21_3681_s_121	16222336	( D) Mutants in the Nup2p residues analogous to those identified in the two importin-alpha-binding regions of Nup50 do not displace the monopartite or bipartite NLSs from yeast  importin-alpha (Kap60p).	bind
3520	1	1934	5	10	NULL	NULL	NULL	Myc	GP		bind		directly			Dnmt3a	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_336_s_161	15616584	( D) Myc binds directly to Dnmt3a, whereas Miz-1 only weakly binds directly to Dnmt3a.	bind
3522	2	1934	5	10	NULL	NULL	NULL	Miz-1	GP		bind		weakly			Dnmt3a	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_336_s_161	15616584	( D) Myc binds directly to Dnmt3a, whereas Miz-1 only weakly binds directly to Dnmt3a.	bind
3280	1	1934	7	10	NULL	NULL	NULL	Myc	GP		binds		directly			Dnmt3a	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_336_s_161	15616584	( D) Myc binds directly to Dnmt3a, whereas Miz-1 only weakly binds directly to Dnmt3a.	bind
3281	2	1934	7	10	NULL	NULL	NULL	Miz-1	GP		binds		weakly			Dnmt3a	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_336_s_161	15616584	( D) Myc binds directly to Dnmt3a, whereas Miz-1 only weakly binds directly to Dnmt3a.	bind
3518	1	1935	5	10	NULL	NULL	NULL	Naphthalene cis-dihydrodiol	Chemical		bind					NDO	GP		active site		NULL		NULL	NULL	NULL	NULL	gw70_science_299_5609_1039_s_38	12586937	( D) Naphthalene  cis-dihydrodiol bound to the active site of NDO.	bind
3283	1	1935	7	10	NULL	NULL	NULL	Naphthalene cis-dihydrodiol	Chemical		bind					NDO	GP		active site of		NULL		NULL	NULL	NULL	NULL	gw70_science_299_5609_1039_s_38	12586937	( D) Naphthalene  cis-dihydrodiol bound to the active site of NDO.	bind
3653	1	1936	5	10	NULL	NULL	NULL	NAPQI-MIF	GP		bind					microvascular endothelial cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_1_144_s_167	11773615	( D) NAPQI-MIF shows decreased cell surface binding to human microvascular endothelial cells.	bind
3326	1	1936	7	10	NULL	NULL	NULL	NAPQI-MIF	GP		binds to					microvascular endothelial cell surface	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_1_144_s_167	11773615	( D) NAPQI-MIF shows decreased cell surface binding to human microvascular endothelial cells.	bind
3548	1	1937	5	10	NULL	NULL	NULL	Nef	GP		bind					cholesterol	Chemical				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_pnas_100_14_8460_s_210	12824470	( d) Nef binds  cholesterol  in vivo.	bind
3339	1	1937	7	10	NULL	NULL	NULL	Nef 	GP		bind					cholesterol	Chemical				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_pnas_100_14_8460_s_210	12824470	( d) Nef binds  cholesterol  in vivo.	bind
3554	1	1938	5	10	NULL	NULL	NULL	NF-IL6beta	GP		bind									C/EBP element	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_1_217_s_204	16397300	( D) NF-IL6beta binds to the C/EBP and CRE elements in DNA affinity precipitation assay.	bind
3555	2	1938	5	10	NULL	NULL	NULL	NF-IL6beta	GP		bind									CRE elements	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_1_217_s_204	16397300	( D) NF-IL6beta binds to the C/EBP and CRE elements in DNA affinity precipitation assay.	bind
3340	1	1938	7	10	NULL	NULL	NULL	NF-IL6beta 	GP		bind									C/EBP element	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_1_217_s_204	16397300	( D) NF-IL6beta binds to the C/EBP and CRE elements in DNA affinity precipitation assay.	bind
3341	2	1938	7	10	NULL	NULL	NULL	NF-IL6beta 	GP		bind									CRE element	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_1_217_s_204	16397300	( D) NF-IL6beta binds to the C/EBP and CRE elements in DNA affinity precipitation assay.	bind
5209	1	1939	5	10	NULL	NULL	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid			single consensus Rel-binding site	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_71	10485885	( d) NF-kappaB binds cooperatively with DSP1 to DNA bearing solely a single consensus Rel-binding site.	bind
5212	2	1939	5	10	NULL	NULL	NULL	DSP1	GP		bind					DNA	NucleicAcid			single consensus Rel-binding site	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_71	10485885	( d) NF-kappaB binds cooperatively with DSP1 to DNA bearing solely a single consensus Rel-binding site.	bind
5213	3	1939	5	10	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_71	10485885	( d) NF-kappaB binds cooperatively with DSP1 to DNA bearing solely a single consensus Rel-binding site.	bind
3344	1	1939	7	10	NULL	NULL	NULL	NF-kappaB 	GP		bind					DNA	NucleicAcid			single consensus Rel-binding site	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_71	10485885	( d) NF-kappaB binds cooperatively with DSP1 to DNA bearing solely a single consensus Rel-binding site.	bind
3345	2	1939	7	10	NULL	NULL	NULL	DSP1	GP		bind					DNA	NucleicAcid			single consensus Rel-binding site	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_71	10485885	( d) NF-kappaB binds cooperatively with DSP1 to DNA bearing solely a single consensus Rel-binding site.	bind
4598	3	1939	7	10	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10679_s_71	10485885	( d) NF-kappaB binds cooperatively with DSP1 to DNA bearing solely a single consensus Rel-binding site.	bind
3655	1	1940	5	10	NULL	NULL	NULL	Ure2p	GP		bind					Gln3p	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_73_0_617_s_90	15189155	( D) Normally Ure2p binds the transcription factor Gln3p, preventing the upregulation  of genes, such as  DAL5, required for uptake of poor nitrogen sources.	bind
3656	2	1940	5	10	NULL	NULL	NULL	statement 1	Process		prevent					DAL5 gene	GP	upregulation of			NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_73_0_617_s_90	15189155	( D) Normally Ure2p binds the transcription factor Gln3p, preventing the upregulation  of genes, such as  DAL5, required for uptake of poor nitrogen sources.	bind
3657	3	1940	5	10	NULL	NULL	NULL	DAL5 gene	GP		is required for					poor nitrogen sources	Process	uptake of			NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_73_0_617_s_90	15189155	( D) Normally Ure2p binds the transcription factor Gln3p, preventing the upregulation  of genes, such as  DAL5, required for uptake of poor nitrogen sources.	bind
45663	4	1940	5	10	NULL	NULL	NULL	Gln3p	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_73_0_617_s_90	15189155	( D) Normally Ure2p binds the transcription factor Gln3p, preventing the upregulation  of genes, such as  DAL5, required for uptake of poor nitrogen sources.	bind
3346	1	1940	7	10	NULL	NULL	NULL	Ure2p	GP		bind					Gln3p	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_73_0_617_s_90	15189155	( D) Normally Ure2p binds the transcription factor Gln3p, preventing the upregulation  of genes, such as  DAL5, required for uptake of poor nitrogen sources.	bind
3347	2	1940	7	10	NULL	NULL	NULL	statement 1	Process		prevent					DAL5	GP	upregulation			NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_73_0_617_s_90	15189155	( D) Normally Ure2p binds the transcription factor Gln3p, preventing the upregulation  of genes, such as  DAL5, required for uptake of poor nitrogen sources.	bind
3348	3	1940	7	10	NULL	NULL	NULL	DAL5	GP		is required for					 poor nitrogen sources	Process	uptake of			NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_73_0_617_s_90	15189155	( D) Normally Ure2p binds the transcription factor Gln3p, preventing the upregulation  of genes, such as  DAL5, required for uptake of poor nitrogen sources.	bind
45665	4	1940	7	10	NULL	NULL	NULL	Gln3p	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_73_0_617_s_90	15189155	( D) Normally Ure2p binds the transcription factor Gln3p, preventing the upregulation  of genes, such as  DAL5, required for uptake of poor nitrogen sources.	bind
3658	1	1943	5	10	NULL	NULL	NULL	p25	GP		bind					STAT3	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_101_17_6728_s_100	15096606	( D) p25 binds STAT3  in vitro.	bind
3349	1	1943	7	10	NULL	NULL	NULL	 p25 	GP		binds					STAT3	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_101_17_6728_s_100	15096606	( D) p25 binds STAT3  in vitro.	bind
3659	1	1944	5	10	NULL	NULL	NULL	p52	GP		bind					Cyclin D1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_20_4820_s_58	16990795	( D) p52 binds the Cyclin D1 promoter.	bind
3350	1	1944	7	10	NULL	NULL	NULL	p52	GP		bind					Cyclin D1 	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_20_4820_s_58	16990795	( D) p52 binds the Cyclin D1 promoter.	bind
3660	1	1945	5	10	NULL	NULL	NULL	p53	GP		bind					MLH1	GP			p53RE	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_13_4813_s_132	15781865	( D) p53 binds to the MLH1 p53RE  in vitro.	bind
3351	1	1945	7	10	NULL	NULL	NULL	p53	GP		bind					MLH1	GP			p53RE	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_13_4813_s_132	15781865	( D) p53 binds to the MLH1 p53RE  in vitro.	bind
3661	1	1946	5	10	NULL	NULL	NULL	p65	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_10_1991_s_259	15192014	( D) p65 and H3 deacetylation is accompanied by inhibition of p65 binding to DNA. JB6  P+ cells were transfected with HDAC1 expression vector.	bind
3662	2	1946	5	10	NULL	NULL	NULL	p65	GP		undergoes					deacetylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_10_1991_s_259	15192014	( D) p65 and H3 deacetylation is accompanied by inhibition of p65 binding to DNA. JB6  P+ cells were transfected with HDAC1 expression vector.	bind
3663	3	1946	5	10	NULL	NULL	NULL	H3	GP		undergoes					deacetylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_10_1991_s_259	15192014	( D) p65 and H3 deacetylation is accompanied by inhibition of p65 binding to DNA. JB6  P+ cells were transfected with HDAC1 expression vector.	bind
50364	4	1946	5	10	NULL	NULL	NULL	statement 2	Process		is accompanied with					statement 1	Process	inhibition of 			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_10_1991_s_259	15192014	( D) p65 and H3 deacetylation is accompanied by inhibition of p65 binding to DNA. JB6  P+ cells were transfected with HDAC1 expression vector.	bind
50365	5	1946	5	10	NULL	NULL	NULL	statement 3	Process		is accompanied with					statement 1	Process	inhibition of			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_10_1991_s_259	15192014	( D) p65 and H3 deacetylation is accompanied by inhibition of p65 binding to DNA. JB6  P+ cells were transfected with HDAC1 expression vector.	bind
3352	1	1946	7	10	NULL	NULL	NULL	 p65 	GP		undergoes					deacetylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_10_1991_s_259	15192014	( D) p65 and H3 deacetylation is accompanied by inhibition of p65 binding to DNA. JB6  P+ cells were transfected with HDAC1 expression vector.	bind
3353	2	1946	7	10	NULL	NULL	NULL	H3 	GP		undergoes					deacetylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_10_1991_s_259	15192014	( D) p65 and H3 deacetylation is accompanied by inhibition of p65 binding to DNA. JB6  P+ cells were transfected with HDAC1 expression vector.	bind
3354	3	1946	7	10	NULL	NULL	NULL	p65	GP		binds					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_10_1991_s_259	15192014	( D) p65 and H3 deacetylation is accompanied by inhibition of p65 binding to DNA. JB6  P+ cells were transfected with HDAC1 expression vector.	bind
3355	4	1946	7	10	NULL	NULL	NULL	statement 1	Process		is accompanied with					statement 3	Process	inhibition of			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_10_1991_s_259	15192014	( D) p65 and H3 deacetylation is accompanied by inhibition of p65 binding to DNA. JB6  P+ cells were transfected with HDAC1 expression vector.	bind
3356	5	1946	7	10	NULL	NULL	NULL	statement 2	Process		is accompanied with					statement 3	Process	inhibition of			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_10_1991_s_259	15192014	( D) p65 and H3 deacetylation is accompanied by inhibition of p65 binding to DNA. JB6  P+ cells were transfected with HDAC1 expression vector.	bind
3664	1	1947	5	10	NULL	NULL	NULL	Mixer SIM peptide	GP		bind					Smad2	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_1_145_s_224	11782434	( D) Peptides corresponding to the Mixer SIM or to the SARA SBD peptide bind both Smad2 and phosphorylated Smad2, but only the SIM can bind a heteromeric complex of Smad2 and Smad4.	bind
3665	2	1947	5	10	NULL	NULL	NULL	Mixer SIM peptide	GP		bind					Smad2	GP	phosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_embo_21_1_145_s_224	11782434	( D) Peptides corresponding to the Mixer SIM or to the SARA SBD peptide bind both Smad2 and phosphorylated Smad2, but only the SIM can bind a heteromeric complex of Smad2 and Smad4.	bind
3666	3	1947	5	10	NULL	NULL	NULL	SARA SBD peptide	GP		bind					Smad2	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_1_145_s_224	11782434	( D) Peptides corresponding to the Mixer SIM or to the SARA SBD peptide bind both Smad2 and phosphorylated Smad2, but only the SIM can bind a heteromeric complex of Smad2 and Smad4.	bind
3667	4	1947	5	10	NULL	NULL	NULL	SARA SBD peptide	GP		bind					Smad2	GP	phosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_embo_21_1_145_s_224	11782434	( D) Peptides corresponding to the Mixer SIM or to the SARA SBD peptide bind both Smad2 and phosphorylated Smad2, but only the SIM can bind a heteromeric complex of Smad2 and Smad4.	bind
3668	5	1947	5	10	NULL	NULL	NULL	Smad2	GP		forms complex with					Smad4	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_1_145_s_224	11782434	( D) Peptides corresponding to the Mixer SIM or to the SARA SBD peptide bind both Smad2 and phosphorylated Smad2, but only the SIM can bind a heteromeric complex of Smad2 and Smad4.	bind
5214	6	1947	5	10	NULL	NULL	NULL	SIM	GP		bind					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_1_145_s_224	11782434	( D) Peptides corresponding to the Mixer SIM or to the SARA SBD peptide bind both Smad2 and phosphorylated Smad2, but only the SIM can bind a heteromeric complex of Smad2 and Smad4.	bind
3357	1	1947	7	10	NULL	NULL	NULL	Mixer SIM 	GP		bind					Smad2 	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_1_145_s_224	11782434	( D) Peptides corresponding to the Mixer SIM or to the SARA SBD peptide bind both Smad2 and phosphorylated Smad2, but only the SIM can bind a heteromeric complex of Smad2 and Smad4.	bind
3358	2	1947	7	10	NULL	NULL	NULL	Mixer SIM 	GP		bind					Smad2	GP	phosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_embo_21_1_145_s_224	11782434	( D) Peptides corresponding to the Mixer SIM or to the SARA SBD peptide bind both Smad2 and phosphorylated Smad2, but only the SIM can bind a heteromeric complex of Smad2 and Smad4.	bind
3359	3	1947	7	10	NULL	NULL	NULL	SARA SBD peptide 	GP		bind					Smad2	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_1_145_s_224	11782434	( D) Peptides corresponding to the Mixer SIM or to the SARA SBD peptide bind both Smad2 and phosphorylated Smad2, but only the SIM can bind a heteromeric complex of Smad2 and Smad4.	bind
3360	4	1947	7	10	NULL	NULL	NULL	SARA SBD peptide 	GP		bind					Smad2	GP	phosphorylated 			NULL		NULL	NULL	NULL	NULL	gw60_embo_21_1_145_s_224	11782434	( D) Peptides corresponding to the Mixer SIM or to the SARA SBD peptide bind both Smad2 and phosphorylated Smad2, but only the SIM can bind a heteromeric complex of Smad2 and Smad4.	bind
3361	5	1947	7	10	NULL	NULL	NULL	Smad2	GP		forms complex with					Smad4	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_1_145_s_224	11782434	( D) Peptides corresponding to the Mixer SIM or to the SARA SBD peptide bind both Smad2 and phosphorylated Smad2, but only the SIM can bind a heteromeric complex of Smad2 and Smad4.	bind
3455	6	1947	7	10	NULL	NULL	NULL	SIM 	GP		bind					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_1_145_s_224	11782434	( D) Peptides corresponding to the Mixer SIM or to the SARA SBD peptide bind both Smad2 and phosphorylated Smad2, but only the SIM can bind a heteromeric complex of Smad2 and Smad4.	bind
3669	1	1948	5	10	NULL	NULL	NULL	PIP2	GP		bind					syntenin-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_14_2556_s_45	15961997	( D) PIP2 binding of syntenin-2 in overlay assay.	bind
3362	1	1948	7	10	NULL	NULL	NULL	PIP2	GP		bind					syntenin-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_14_2556_s_45	15961997	( D) PIP2 binding of syntenin-2 in overlay assay.	bind
3670	1	1949	5	10	NULL	NULL	NULL	PKNOX1	GP		bind		specifically							Pbx/POU target site	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_11_2769_s_175	12771203	( D) PKNOX1 binds specifically to the Pbx/POU target site and this binding is abolished  by the anti-PKNOX1 antibody.	bind
3671	2	1949	5	10	NULL	NULL	NULL	anti-PKNOX1 antibody	GP		abolish					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_11_2769_s_175	12771203	( D) PKNOX1 binds specifically to the Pbx/POU target site and this binding is abolished  by the anti-PKNOX1 antibody.	bind
3363	1	1949	7	10	NULL	NULL	NULL	PKNOX1	GP		binds		specifically							Pbx/POU target site 	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_11_2769_s_175	12771203	( D) PKNOX1 binds specifically to the Pbx/POU target site and this binding is abolished  by the anti-PKNOX1 antibody.	bind
3364	2	1949	7	10	NULL	NULL	NULL	statement 1	Process		is inhibited by					anti-PKNOX1 antibody	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_11_2769_s_175	12771203	( D) PKNOX1 binds specifically to the Pbx/POU target site and this binding is abolished  by the anti-PKNOX1 antibody.	bind
3672	1	1951	5	10	NULL	NULL	NULL	PTG	GP		bind					glycogen synthase	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_275_5305_1475_s_56	9045612	( D) PTG binds glycogen synthase.	bind
3365	1	1951	7	10	NULL	NULL	NULL	PTG 	GP		bind					glycogen synthase	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_275_5305_1475_s_56	9045612	( D) PTG binds glycogen synthase.	bind
3673	1	1952	5	10	NULL	NULL	NULL	MT	CellComponent		bind					KIF1A	GP	deletions			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1506_s_44	15014437	( D) Quantitative analysis of the MT binding (mean s.d.) of KIF1A deletions.	bind
4599	1	1952	7	10	NULL	NULL	NULL	MT	CellComponent		bind					KIF1A	GP	deletions of			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1506_s_44	15014437	( D) Quantitative analysis of the MT binding (mean s.d.) of KIF1A deletions.	bind
4032	1	1954	5	10	NULL	NULL	NULL	GATA-1	GP		bind					GATA- 2	GP			- 2.8 kb region of locus	NULL	untreated FOG-1 - / - cells	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_102	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  - 2.8 kb region  of  GATA- 2 locus in untreated and tamoxifen-treated (1muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM, five independent experiments).	bind
4033	2	1954	5	10	NULL	NULL	NULL	GATA-2	GP		bind					GATA- 2	GP			- 2.8 kb region of locus	NULL	untreated FOG-1 - / - cells	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_102	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  - 2.8 kb region  of  GATA- 2 locus in untreated and tamoxifen-treated (1muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM, five independent experiments).	bind
4034	3	1954	5	10	NULL	NULL	NULL	GATA-1	GP		bind					GATA- 2	GP			- 2.8 kb region of locus	NULL	tamoxifen-treated FOG-1 - / - cells	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_102	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  - 2.8 kb region  of  GATA- 2 locus in untreated and tamoxifen-treated (1muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM, five independent experiments).	bind
4035	4	1954	5	10	NULL	NULL	NULL	GATA-2	GP		bind					GATA- 2	GP			- 2.8 kb region of locus	NULL	tamoxifen-treated FOG-1 - / - cells	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_102	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  - 2.8 kb region  of  GATA- 2 locus in untreated and tamoxifen-treated (1muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM, five independent experiments).	bind
4253	5	1954	5	10	NULL	NULL	NULL	GATA-1	GP		bind					GATA- 2	GP			- 2.8 kb region of locus	NULL	untreated FOG-1 - / - -ER - GATA-1 cells	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_102	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  - 2.8 kb region  of  GATA- 2 locus in untreated and tamoxifen-treated (1muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM, five independent experiments).	bind
4254	6	1954	5	10	NULL	NULL	NULL	GATA-2	GP		bind					GATA- 2	GP			- 2.8 kb region of locus	NULL	untreated FOG-1 - / - -ER - GATA-1 cells	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_102	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  - 2.8 kb region  of  GATA- 2 locus in untreated and tamoxifen-treated (1muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM, five independent experiments).	bind
4255	7	1954	5	10	NULL	NULL	NULL	GATA-1	GP		bind					GATA- 2	GP			- 2.8 kb region of locus	NULL	tamoxifen-treated FOG-1 - / - -ER - GATA-1 cells	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_102	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  - 2.8 kb region  of  GATA- 2 locus in untreated and tamoxifen-treated (1muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM, five independent experiments).	bind
4256	8	1954	5	10	NULL	NULL	NULL	GATA-2	GP		bind					GATA- 2	GP			- 2.8 kb region of locus	NULL	tamoxifen-treated FOG-1 - / - -ER - GATA-1 cells	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_102	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  - 2.8 kb region  of  GATA- 2 locus in untreated and tamoxifen-treated (1muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM, five independent experiments).	bind
3366	1	1954	7	10	NULL	NULL	NULL	GATA-1	GP		binds to					GATA- 2 	GP	 		2.8 kb locus 	NULL	untreated FOG-1 - / - cells	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_102	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  - 2.8 kb region  of  GATA- 2 locus in untreated and tamoxifen-treated (1muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM, five independent experiments).	bind
3367	5	1954	7	10	NULL	NULL	NULL	GATA-2	GP		bind					GATA- 2	GP	 		2.8 kb  locus 	NULL	 untreated FOG-1 - / - cells	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_102	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  - 2.8 kb region  of  GATA- 2 locus in untreated and tamoxifen-treated (1muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM, five independent experiments).	bind
4602	2	1954	7	10	NULL	NULL	NULL	GATA-1	GP		bind					GATA- 2	GP	  		2.8 kb  locus	NULL	tamoxifen-treated FOG-1 - / - -ER - GATA-1 cells	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_102	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  - 2.8 kb region  of  GATA- 2 locus in untreated and tamoxifen-treated (1muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM, five independent experiments).	bind
4604	7	1954	7	10	NULL	NULL	NULL	GATA-2	GP		bind					GATA- 2 	GP	 		2.8 kb locus	NULL	tamoxifen-treated FOG-1 - / - -ER - GATA-1 cells	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_102	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  - 2.8 kb region  of  GATA- 2 locus in untreated and tamoxifen-treated (1muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM, five independent experiments).	bind
4607	3	1954	7	10	NULL	NULL	NULL	GATA-1	GP		bind					GATA- 2	GP			2.8 kb  locus	NULL	untreated FOG-1 - / - -ER - GATA-1 cells	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_102	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  - 2.8 kb region  of  GATA- 2 locus in untreated and tamoxifen-treated (1muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM, five independent experiments).	bind
4608	4	1954	7	10	NULL	NULL	NULL	GATA-1	GP		bind					GATA- 2	GP			2.8 kb  locus	NULL	tamoxifen-treated FOG-1 - / - cells	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_102	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  - 2.8 kb region  of  GATA- 2 locus in untreated and tamoxifen-treated (1muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM, five independent experiments).	bind
4609	6	1954	7	10	NULL	NULL	NULL	GATA-2 	GP		bind					GATA- 2 	GP			2.8 kb locus	NULL	untreated FOG-1 - / - -ER - GATA-1 cells 	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_102	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  - 2.8 kb region  of  GATA- 2 locus in untreated and tamoxifen-treated (1muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM, five independent experiments).	bind
4611	8	1954	7	10	NULL	NULL	NULL	GATA-2	GP		bind					 GATA- 2 	GP			2.8 kb locus	NULL	tamoxifen-treated FOG-1 - / - cells	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_102	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  - 2.8 kb region  of  GATA- 2 locus in untreated and tamoxifen-treated (1muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM, five independent experiments).	bind
4036	1	1955	5	10	NULL	NULL	NULL	GATA-1	GP		bind									GATA- 2 locus	NULL	FOG-1 - / - cells infected with empty vector	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_142	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  GATA- 2 locus in FOG-1 - / -  cells infected with empty or FOG-1-expressing retrovirus (mean  plus-or-minus  SEM  of five independent experiments).	bind
4037	2	1955	5	10	NULL	NULL	NULL	GATA-2	GP		bind									GATA- 2 locus	NULL	FOG-1 - / - cells infected with empty vector	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_142	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  GATA- 2 locus in FOG-1 - / -  cells infected with empty or FOG-1-expressing retrovirus (mean  plus-or-minus  SEM  of five independent experiments).	bind
4257	3	1955	5	10	NULL	NULL	NULL	GATA-1	GP		bind									GATA- 2 locus	NULL	FOG-1 - / - cells infected with FOG-1-expressing retrovirus	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_142	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  GATA- 2 locus in FOG-1 - / -  cells infected with empty or FOG-1-expressing retrovirus (mean  plus-or-minus  SEM  of five independent experiments).	bind
4258	4	1955	5	10	NULL	NULL	NULL	GATA-2	GP		bind									GATA- 2 locus	NULL	FOG-1 - / - cells infected with FOG-1-expressing retrovirus	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_142	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  GATA- 2 locus in FOG-1 - / -  cells infected with empty or FOG-1-expressing retrovirus (mean  plus-or-minus  SEM  of five independent experiments).	bind
3368	1	1955	7	10	NULL	NULL	NULL	GATA-1 	GP		bind									GATA- 2 locus 	NULL	 FOG-1 - / - cells infected with empty vector	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_142	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  GATA- 2 locus in FOG-1 - / -  cells infected with empty or FOG-1-expressing retrovirus (mean  plus-or-minus  SEM  of five independent experiments).	bind
3369	2	1955	7	10	NULL	NULL	NULL	GATA-2	GP		bind									GATA- 2 locus 	NULL	FOG-1 - / - cells infected with empty vector	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_142	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  GATA- 2 locus in FOG-1 - / -  cells infected with empty or FOG-1-expressing retrovirus (mean  plus-or-minus  SEM  of five independent experiments).	bind
46211	3	1955	7	10	NULL	NULL	NULL	 GATA-1	GP		bind									GATA- 2 locus	NULL	FOG-1 - / - cells infected with FOG-1-expressing retrovirus	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_142	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  GATA- 2 locus in FOG-1 - / -  cells infected with empty or FOG-1-expressing retrovirus (mean  plus-or-minus  SEM  of five independent experiments).	bind
46212	4	1955	7	10	NULL	NULL	NULL	GATA-2 	GP		bind									GATA- 2 locus	NULL	FOG-1 - / - cells infected with FOG-1-expressing retrovirus	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_142	14715908	( D) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to the  GATA- 2 locus in FOG-1 - / -  cells infected with empty or FOG-1-expressing retrovirus (mean  plus-or-minus  SEM  of five independent experiments).	bind
4038	1	1956	5	10	NULL	NULL	NULL	GATA-2	GP		bind									GATA- 2 locus	NULL	G1E cells	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_73	14715908	( D) Quantitative ChIP analysis of GATA-2 binding to the  GATA- 2 locus in G1E and FOG-1 - / -  cells (mean  plus-or-minus  SEM of three independent experiments).	bind
4259	2	1956	5	10	NULL	NULL	NULL	GATA-2	GP		bind									GATA- 2 locus	NULL	FOG-1 - / - cells	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_73	14715908	( D) Quantitative ChIP analysis of GATA-2 binding to the  GATA- 2 locus in G1E and FOG-1 - / -  cells (mean  plus-or-minus  SEM of three independent experiments).	bind
3370	1	1956	7	10	NULL	NULL	NULL	GATA-2 	GP		bind					 				GATA- 2 locus	NULL	G1E cells 	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_73	14715908	( D) Quantitative ChIP analysis of GATA-2 binding to the  GATA- 2 locus in G1E and FOG-1 - / -  cells (mean  plus-or-minus  SEM of three independent experiments).	bind
4620	2	1956	7	10	NULL	NULL	NULL	GATA-2	GP		bind									GATA- 2 locus	NULL	FOG-1 - / - cells	NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_73	14715908	( D) Quantitative ChIP analysis of GATA-2 binding to the  GATA- 2 locus in G1E and FOG-1 - / -  cells (mean  plus-or-minus  SEM of three independent experiments).	bind
3675	1	1957	5	10	NULL	NULL	NULL	Oct-1	GP		bind					 hIL2	GP			ARRE2 region in the promotor of	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_5_1081_s_68	16498406	( D) Quantitative ChIP analysis was performed to determine the binding of Oct-1 and NFAT  and the modification of histone in the ARRE2 region of the  hIL2 promoter using real-time PCR.	bind
3676	2	1957	5	10	NULL	NULL	NULL	NFAT	GP		bind					hIL2	GP			ARRE2 region in the promotor of	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_5_1081_s_68	16498406	( D) Quantitative ChIP analysis was performed to determine the binding of Oct-1 and NFAT  and the modification of histone in the ARRE2 region of the  hIL2 promoter using real-time PCR.	bind
5217	3	1957	5	10	NULL	NULL	NULL	histone	GP		is modified in					hIL2	GP			ARRE2 region in the promotor of	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_5_1081_s_68	16498406	( D) Quantitative ChIP analysis was performed to determine the binding of Oct-1 and NFAT  and the modification of histone in the ARRE2 region of the  hIL2 promoter using real-time PCR.	bind
3371	1	1957	7	10	NULL	NULL	NULL	Oct-1	GP		bind					hIL2	GP			ARRE2 region in the promoter of	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_5_1081_s_68	16498406	( D) Quantitative ChIP analysis was performed to determine the binding of Oct-1 and NFAT  and the modification of histone in the ARRE2 region of the  hIL2 promoter using real-time PCR.	bind
3372	2	1957	7	10	NULL	NULL	NULL	NFAT	GP		bind					hIL2 	GP			 ARRE2 region in the promoter of	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_5_1081_s_68	16498406	( D) Quantitative ChIP analysis was performed to determine the binding of Oct-1 and NFAT  and the modification of histone in the ARRE2 region of the  hIL2 promoter using real-time PCR.	bind
4662	3	1957	7	10	NULL	NULL	NULL	histone	GP		is modified in					hIL2	GP			ARRE2 region in the promoter of	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_5_1081_s_68	16498406	( D) Quantitative ChIP analysis was performed to determine the binding of Oct-1 and NFAT  and the modification of histone in the ARRE2 region of the  hIL2 promoter using real-time PCR.	bind
3677	1	1958	5	NULL	NULL	0	NULL	MDM2	NULL		bind	NULL				MDMX	NULL	different forms of			NULL	Saos2-MDMX cells	0	NULL	NULL	NULL	gw70_embo_24_19_3411_s_86	16163388	( D) Saos2-MDMX cells were tested for binding efficiencies of MDM2 to different forms  of MDMX by MDM2 IP and MDMX Western blot after irradiation in the presence of MG132.	bind
3678	2	1958	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				MG132	NULL				NULL	Saos2-MDMX cells	NULL	NULL	NULL	NULL	gw70_embo_24_19_3411_s_86	16163388	( D) Saos2-MDMX cells were tested for binding efficiencies of MDM2 to different forms  of MDMX by MDM2 IP and MDMX Western blot after irradiation in the presence of MG132.	bind
3679	1	1959	5	10	NULL	NULL	NULL	Sema-2a-AP	GP		bind					S2R+ cells	Cell	PlexB-expressing			NULL		NULL	NULL	NULL	NULL	gw70_development_133_11_2125_s_239	16672342	( D) Scatchard analysis of Sema-2a-AP binding to PlexB-expressing S2R+ cells.	bind
3373	1	1959	7	10	NULL	NULL	NULL	Sema-2a-AP 	GP		bind					S2R+ cells	Cell	PlexB-expressing 			NULL		NULL	NULL	NULL	NULL	gw70_development_133_11_2125_s_239	16672342	( D) Scatchard analysis of Sema-2a-AP binding to PlexB-expressing S2R+ cells.	bind
3680	1	1960	5	10	NULL	NULL	NULL	AP-DCD	GP		bind					21NT breast cancer cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_19_10931_s_150	12953101	( D) Scatchard transformation of binding analysis of AP-DCD to 21NT breast cancer cells.	bind
3374	1	1960	7	10	NULL	NULL	NULL	AP-DCD 	GP		bind					21NT breast cancer cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_19_10931_s_150	12953101	( D) Scatchard transformation of binding analysis of AP-DCD to 21NT breast cancer cells.	bind
3681	1	1962	5	10	NULL	NULL	NULL	GST-PDZ1-2 fusion proteins	GP		bind					CFTR	GP		C terminus		NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_3_1300_s_140	11158634	( D) Sensorgram overlays for various GST-PDZ1-2 fusion proteins binding to CFTR C terminus at a concentration of 50 nM.	bind
3375	1	1962	7	10	NULL	NULL	NULL	GST-PDZ1-2 fusion proteins 	GP		bind					CFTR	GP		C terminus 		NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_3_1300_s_140	11158634	( D) Sensorgram overlays for various GST-PDZ1-2 fusion proteins binding to CFTR C terminus at a concentration of 50 nM.	bind
3682	1	1963	5	10	NULL	NULL	NULL	c-Jun	GP		bind					CSN5/Jab1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_7_1630_s_129	11285227	( D) Sequence alignment of the regions of c-Jun ( Claret  et al., 1996) and p27 Kip1 ( Tomoda  et al., 1999) that bind to CSN5/Jab1 with deltap53(1 - 154).	bind
3683	2	1963	5	10	NULL	NULL	NULL	p27 Kip1	GP		bind					 CSN5/Jab1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_7_1630_s_129	11285227	( D) Sequence alignment of the regions of c-Jun ( Claret  et al., 1996) and p27 Kip1 ( Tomoda  et al., 1999) that bind to CSN5/Jab1 with deltap53(1 - 154).	bind
3376	1	1963	7	10	NULL	NULL	NULL	c-Jun 	GP		bind					CSN5/Jab1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_7_1630_s_129	11285227	( D) Sequence alignment of the regions of c-Jun ( Claret  et al., 1996) and p27 Kip1 ( Tomoda  et al., 1999) that bind to CSN5/Jab1 with deltap53(1 - 154).	bind
3377	2	1963	7	10	NULL	NULL	NULL	p27 Kip1 	GP		bind					CSN5/Jab1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_7_1630_s_129	11285227	( D) Sequence alignment of the regions of c-Jun ( Claret  et al., 1996) and p27 Kip1 ( Tomoda  et al., 1999) that bind to CSN5/Jab1 with deltap53(1 - 154).	bind
3685	1	1964	5	10	NULL	NULL	NULL	Sid4p-myc	GP		bind		directly			Sid4deltaNp-HA	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_10_5249_s_192	10805785	( D) Sid4p-myc binds directly to Sid4deltaNp-HA.	bind
3379	1	1964	7	10	NULL	NULL	NULL	Sid4p-myc 	GP		binds		directly			Sid4deltaNp-HA	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_10_5249_s_192	10805785	( D) Sid4p-myc binds directly to Sid4deltaNp-HA.	bind
3686	1	1965	5	10	NULL	NULL	NULL	tubulin	GP	bovine	does not bind					GST-Aut7p glutathione-Sepharose 4B	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3597_s_137	9649430	( D) Similar to (C), bovine tubulin does not bind to GST-Aut7p glutathione-Sepharose 4B (lane 12) and to GST glutathione-Sepharose 4B (lane 9).	bind
3687	2	1965	5	10	NULL	NULL	NULL	tubulin	GP	bovine	does not bind					GST glutathione-Sepharose 4B	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3597_s_137	9649430	( D) Similar to (C), bovine tubulin does not bind to GST-Aut7p glutathione-Sepharose 4B (lane 12) and to GST glutathione-Sepharose 4B (lane 9).	bind
3380	1	1965	7	10	NULL	NULL	NULL	tubulin	GP	bovine	does not bind					GST-Aut7p glutathione-Sepharose 4B 	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3597_s_137	9649430	( D) Similar to (C), bovine tubulin does not bind to GST-Aut7p glutathione-Sepharose 4B (lane 12) and to GST glutathione-Sepharose 4B (lane 9).	bind
3381	2	1965	7	10	NULL	NULL	NULL	tubulin	GP	bovine	does not bind					GST glutathione-Sepharose 4B 	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3597_s_137	9649430	( D) Similar to (C), bovine tubulin does not bind to GST-Aut7p glutathione-Sepharose 4B (lane 12) and to GST glutathione-Sepharose 4B (lane 9).	bind
3688	1	1966	5	10	NULL	NULL	NULL	Sir1	GP		colocalize with					Ndc10	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_19_2356_s_50	12975325	( D) Sir1 colocalizes with centromere protein Ndc10.	bind
45677	2	1966	5	10	NULL	NULL	NULL	Ndc10	GP		is a type of					centromeric protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_19_2356_s_50	12975325	( D) Sir1 colocalizes with centromere protein Ndc10.	bind
3382	1	1966	7	10	NULL	NULL	NULL	Sir1	GP		colocalizes with					Ndc10 	GP		 		NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_19_2356_s_50	12975325	( D) Sir1 colocalizes with centromere protein Ndc10.	bind
45679	2	1966	7	10	NULL	NULL	NULL	Ndc10	GP		is a type of					centromeric protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_19_2356_s_50	12975325	( D) Sir1 colocalizes with centromere protein Ndc10.	bind
3689	1	1967	5	10	NULL	NULL	NULL	U1 snRNA	NucleicAcid		bind					SMN complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_5_1188_s_73	11867547	( D) SL1 domain of U1 snRNA is necessary for U1 snRNA binding of the SMN complex.	bind
3690	2	1967	5	10	NULL	NULL	NULL	U1 snRNA	NucleicAcid		is necessary for			SL1 domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_5_1188_s_73	11867547	( D) SL1 domain of U1 snRNA is necessary for U1 snRNA binding of the SMN complex.	bind
3383	1	1967	7	10	NULL	NULL	NULL	U1 snRNA 	NucleicAcid		binds to					 SMN complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_5_1188_s_73	11867547	( D) SL1 domain of U1 snRNA is necessary for U1 snRNA binding of the SMN complex.	bind
3384	2	1967	7	10	NULL	NULL	NULL	U1 snRNA 	NucleicAcid		is required for			SL1 domain 		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_5_1188_s_73	11867547	( D) SL1 domain of U1 snRNA is necessary for U1 snRNA binding of the SMN complex.	bind
3691	1	1968	5	10	NULL	NULL	NULL	Src	GP		bind					TRPV1	GP		proline-rich domain in the N-terminal region		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_24_4211_s_128	16319926	( D) Src binds to a proline-rich domain in the N-terminal region of TRPV1.	bind
3385	1	1968	7	10	NULL	NULL	NULL	 Src 	GP		bind					TRPV1	GP		proline-rich domain in the N-terminal region 		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_24_4211_s_128	16319926	( D) Src binds to a proline-rich domain in the N-terminal region of TRPV1.	bind
3692	1	1969	5	10	NULL	NULL	NULL	G1-Tbeta4	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_18_3599_s_88	15329672	( D) Stereo view of the structural overlap within the LKKTET-related motif between the  actin-bound forms of G1-Tbeta4 and ciboulot.	bind
3693	2	1969	5	10	NULL	NULL	NULL	ciboulot	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_18_3599_s_88	15329672	( D) Stereo view of the structural overlap within the LKKTET-related motif between the  actin-bound forms of G1-Tbeta4 and ciboulot.	bind
3386	1	1969	7	10	NULL	NULL	NULL	actin 	GP		bind					G1-Tbeta4 	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_18_3599_s_88	15329672	( D) Stereo view of the structural overlap within the LKKTET-related motif between the  actin-bound forms of G1-Tbeta4 and ciboulot.	bind
3387	2	1969	7	10	NULL	NULL	NULL	actin	GP		bind					ciboulot	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_18_3599_s_88	15329672	( D) Stereo view of the structural overlap within the LKKTET-related motif between the  actin-bound forms of G1-Tbeta4 and ciboulot.	bind
3694	1	1970	5	10	NULL	NULL	NULL	ThKaiCII peptide	GP		bind					ThKaiA	GP		C-terminal domains		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_2017_s_76	16628225	( D) Structural comparison between the NMR  ThKaiCII peptide bound to  ThKaiA C-terminal domains and the crystallographic model of the C-terminal end of the   SeKaiC A-chain: r.m.s. deviation 2.1  Ang .	bind
3389	1	1970	7	10	NULL	NULL	NULL	ThKaiCII peptide 	GP		bind					ThKaiA 	GP		C-terminal domains 		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_2017_s_76	16628225	( D) Structural comparison between the NMR  ThKaiCII peptide bound to  ThKaiA C-terminal domains and the crystallographic model of the C-terminal end of the   SeKaiC A-chain: r.m.s. deviation 2.1  Ang .	bind
3695	2	1971	5	10	NULL	NULL	NULL	Bcl-xL	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_35_s_131	16212486	( d) Structure of Bcl-xL bound to a BH3 peptide from Bad ( purple).	bind
46205	1	1971	5	10	NULL	NULL	NULL	BH3 peptide	GP		is derived from					Bad	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_35_s_131	16212486	( d) Structure of Bcl-xL bound to a BH3 peptide from Bad ( purple).	bind
3462	2	1971	7	10	NULL	NULL	NULL	Bcl-xL	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_35_s_131	16212486	( d) Structure of Bcl-xL bound to a BH3 peptide from Bad ( purple).	bind
46210	1	1971	7	10	NULL	NULL	NULL	BH3 peptide	GP		derived from					Bad	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_35_s_131	16212486	( d) Structure of Bcl-xL bound to a BH3 peptide from Bad ( purple).	bind
3696	1	1974	5	10	NULL	NULL	NULL	GST-eIF5	GP		bind					eIF2beta	GP		N		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_45_16164_s_115	16254050	( D) Summary of effects of eIF5 mutations, indicated to the right, on GST-eIF5 binding  to eIF2beta-N ( a), eIF3c-N ( b), and eIF1 ( c).	bind
3697	2	1974	5	10	NULL	NULL	NULL	GST-eIF5	GP		bind					eIF3c	GP		N		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_45_16164_s_115	16254050	( D) Summary of effects of eIF5 mutations, indicated to the right, on GST-eIF5 binding  to eIF2beta-N ( a), eIF3c-N ( b), and eIF1 ( c).	bind
3698	3	1974	5	10	NULL	NULL	NULL	GST-eIF5	GP		bind					eIF1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_45_16164_s_115	16254050	( D) Summary of effects of eIF5 mutations, indicated to the right, on GST-eIF5 binding  to eIF2beta-N ( a), eIF3c-N ( b), and eIF1 ( c).	bind
3481	1	1974	7	10	NULL	NULL	NULL	GST-eIF5	GP		bind					eIF2 beta	GP		N		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_45_16164_s_115	16254050	( D) Summary of effects of eIF5 mutations, indicated to the right, on GST-eIF5 binding  to eIF2beta-N ( a), eIF3c-N ( b), and eIF1 ( c).	bind
3482	2	1974	7	10	NULL	NULL	NULL	GST-eIF5	GP		bind					 eIF3c	GP		N		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_45_16164_s_115	16254050	( D) Summary of effects of eIF5 mutations, indicated to the right, on GST-eIF5 binding  to eIF2beta-N ( a), eIF3c-N ( b), and eIF1 ( c).	bind
3483	3	1974	7	10	NULL	NULL	NULL	GST-eIF5	GP		bind					eIF1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_45_16164_s_115	16254050	( D) Summary of effects of eIF5 mutations, indicated to the right, on GST-eIF5 binding  to eIF2beta-N ( a), eIF3c-N ( b), and eIF1 ( c).	bind
3699	1	1975	5	10	NULL	NULL	NULL	mt molecule	GP	nematode	bind					mt protein	GP	nematode			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_24_5444_s_177	12490713	( D) Summary of the binding specificities of nematode mt and bacterial EF-Tu molecules to nematode mt and bacterial EF-Ts proteins.	bind
3700	2	1975	5	10	NULL	NULL	NULL	mt molecule	GP	nematode	bind					EF-Ts protein	GP	bacterial			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_24_5444_s_177	12490713	( D) Summary of the binding specificities of nematode mt and bacterial EF-Tu molecules to nematode mt and bacterial EF-Ts proteins.	bind
3701	3	1975	5	10	NULL	NULL	NULL	EF-Tu molecule	GP	bacterial	bind					mt protein	GP	nematode			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_24_5444_s_177	12490713	( D) Summary of the binding specificities of nematode mt and bacterial EF-Tu molecules to nematode mt and bacterial EF-Ts proteins.	bind
3702	4	1975	5	10	NULL	NULL	NULL	EF-Tu molecule	GP	bacterial	bind					EF-Ts protein	GP	bacterial			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_24_5444_s_177	12490713	( D) Summary of the binding specificities of nematode mt and bacterial EF-Tu molecules to nematode mt and bacterial EF-Ts proteins.	bind
3484	1	1975	7	10	NULL	NULL	NULL	 mt  molecules	GP	nematode	bind					mt proteins	GP	nematode			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_24_5444_s_177	12490713	( D) Summary of the binding specificities of nematode mt and bacterial EF-Tu molecules to nematode mt and bacterial EF-Ts proteins.	bind
3485	2	1975	7	10	NULL	NULL	NULL	EF-Tu molecule	GP	bacterial	bind					EF-Ts proteins	GP	bacterial			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_24_5444_s_177	12490713	( D) Summary of the binding specificities of nematode mt and bacterial EF-Tu molecules to nematode mt and bacterial EF-Ts proteins.	bind
4227	3	1975	7	10	NULL	NULL	NULL	mt molecule	GP	nematode	bind					EF-Ts proteins	GP	bacterial			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_24_5444_s_177	12490713	( D) Summary of the binding specificities of nematode mt and bacterial EF-Tu molecules to nematode mt and bacterial EF-Ts proteins.	bind
4230	4	1975	7	10	NULL	NULL	NULL	EF-Tu molecule	GP	bacterial	bind					mt proteins	GP	nematode			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_24_5444_s_177	12490713	( D) Summary of the binding specificities of nematode mt and bacterial EF-Tu molecules to nematode mt and bacterial EF-Ts proteins.	bind
3703	1	1976	5	10	NULL	NULL	NULL	LEF1	GP	SUMO-modified	bind					beta-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_23_3088_s_190	11731474	( D) SUMO-modified LEF1 binds to beta-catenin.	bind
3486	1	1976	7	10	NULL	NULL	NULL	SUMO	GP		modifies					LEF1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_23_3088_s_190	11731474	( D) SUMO-modified LEF1 binds to beta-catenin.	bind
3487	2	1976	7	10	NULL	NULL	NULL	statement 1	Process		bind					beta-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_23_3088_s_190	11731474	( D) SUMO-modified LEF1 binds to beta-catenin.	bind
3704	1	1977	5	10	NULL	NULL	NULL	pTP	GP		bind					Oct-1	GP	mutant	POUhd		NULL		NULL	NULL	NULL	NULL	gw60_embo_21_4_725_s_101	11847120	( D) Surface map of pTP binding by all identified Oct-1 POUhd mutants.	bind
3488	1	1977	7	10	NULL	NULL	NULL	pTP	GP		bind					Oct-1 	GP	mutants	POUhd		NULL		NULL	NULL	NULL	NULL	gw60_embo_21_4_725_s_101	11847120	( D) Surface map of pTP binding by all identified Oct-1 POUhd mutants.	bind
3705	1	1979	5	10	NULL	NULL	NULL	LIF	GP		induce					SOCS-3	GP	protein synthesis of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_9_1277_s_224	10545526	( d) Sustained deactivation of LIF signaling also occurs through LIF-induced SOCS-3 protein synthesis and binding to JAK2, which appears maximally between 40 and 60 minutes of LIF stimulation.	bind
3706	2	1979	5	10	NULL	NULL	NULL	SOCS-3	GP		bind					JAK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_9_1277_s_224	10545526	( d) Sustained deactivation of LIF signaling also occurs through LIF-induced SOCS-3 protein synthesis and binding to JAK2, which appears maximally between 40 and 60 minutes of LIF stimulation.	bind
3707	3	1979	5	10	NULL	NULL	NULL	LIF	GP		induce					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_9_1277_s_224	10545526	( d) Sustained deactivation of LIF signaling also occurs through LIF-induced SOCS-3 protein synthesis and binding to JAK2, which appears maximally between 40 and 60 minutes of LIF stimulation.	bind
3708	4	1979	5	10	NULL	NULL	NULL	LIF signaling	Process	deactivation of	occurs through					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_9_1277_s_224	10545526	( d) Sustained deactivation of LIF signaling also occurs through LIF-induced SOCS-3 protein synthesis and binding to JAK2, which appears maximally between 40 and 60 minutes of LIF stimulation.	bind
3709	5	1979	5	10	NULL	NULL	NULL	LIF signaling	Process	deactivation of	occurs through					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_9_1277_s_224	10545526	( d) Sustained deactivation of LIF signaling also occurs through LIF-induced SOCS-3 protein synthesis and binding to JAK2, which appears maximally between 40 and 60 minutes of LIF stimulation.	bind
3552	1	1979	7	10	NULL	NULL	NULL	LIF	GP		induce					SOCS-3	GP	protein synthesis of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_9_1277_s_224	10545526	( d) Sustained deactivation of LIF signaling also occurs through LIF-induced SOCS-3 protein synthesis and binding to JAK2, which appears maximally between 40 and 60 minutes of LIF stimulation.	bind
3553	2	1979	7	10	NULL	NULL	NULL	SOCS-3	GP		binds to					JAK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_9_1277_s_224	10545526	( d) Sustained deactivation of LIF signaling also occurs through LIF-induced SOCS-3 protein synthesis and binding to JAK2, which appears maximally between 40 and 60 minutes of LIF stimulation.	bind
3556	3	1979	7	10	NULL	NULL	NULL	statement 1	Process		cause					LIF signaling 	Process	 deactivation of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_9_1277_s_224	10545526	( d) Sustained deactivation of LIF signaling also occurs through LIF-induced SOCS-3 protein synthesis and binding to JAK2, which appears maximally between 40 and 60 minutes of LIF stimulation.	bind
3940	4	1979	7	10	NULL	NULL	NULL	LIF	GP		induce					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_9_1277_s_224	10545526	( d) Sustained deactivation of LIF signaling also occurs through LIF-induced SOCS-3 protein synthesis and binding to JAK2, which appears maximally between 40 and 60 minutes of LIF stimulation.	bind
3941	5	1979	7	10	NULL	NULL	NULL	statement 4	Process		cause					LIF signaling 	Process	deactivation of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_9_1277_s_224	10545526	( d) Sustained deactivation of LIF signaling also occurs through LIF-induced SOCS-3 protein synthesis and binding to JAK2, which appears maximally between 40 and 60 minutes of LIF stimulation.	bind
3739	1	1980	5	10	NULL	NULL	NULL	SXR:RXR heterodimers	GP		bind									IR-6 elements	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_20_3195_s_127	9784494	( D) SXR:RXR heterodimers bind to IR-6 elements.	bind
3489	1	1980	7	10	NULL	NULL	NULL	SXR:RXR	GP		binds to									IR-6	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_20_3195_s_127	9784494	( D) SXR:RXR heterodimers bind to IR-6 elements.	bind
3742	1	1981	5	10	NULL	NULL	NULL	synaptotagmin	GP		bind								mu2		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_22_6011_s_46	11080148	( D) Synaptotagmin binds the mu2 and alpha subunits of disassembled AP-2.	bind
3808	2	1981	5	10	NULL	NULL	NULL	mu2	GP		is a subunit of					AP-2	GP	disassembled			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_22_6011_s_46	11080148	( D) Synaptotagmin binds the mu2 and alpha subunits of disassembled AP-2.	bind
3809	3	1981	5	10	NULL	NULL	NULL	synaptotagmin	GP		bind								alpha		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_22_6011_s_46	11080148	( D) Synaptotagmin binds the mu2 and alpha subunits of disassembled AP-2.	bind
3810	4	1981	5	10	NULL	NULL	NULL	alpha	GP		is a subunit of					AP-2	GP	disassembled			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_22_6011_s_46	11080148	( D) Synaptotagmin binds the mu2 and alpha subunits of disassembled AP-2.	bind
3492	1	1981	7	10	NULL	NULL	NULL	Synaptotagmin 	GP		bind								mu2		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_22_6011_s_46	11080148	( D) Synaptotagmin binds the mu2 and alpha subunits of disassembled AP-2.	bind
3493	2	1981	7	10	NULL	NULL	NULL	mu2	GP		is a subunit of					AP-2	GP	disassembled			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_22_6011_s_46	11080148	( D) Synaptotagmin binds the mu2 and alpha subunits of disassembled AP-2.	bind
3935	3	1981	7	10	NULL	NULL	NULL	Synaptotagmin	GP		bind								alpha		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_22_6011_s_46	11080148	( D) Synaptotagmin binds the mu2 and alpha subunits of disassembled AP-2.	bind
3936	4	1981	7	10	NULL	NULL	NULL	alpha	GP		is a subunit of					AP-2	GP	disassembled			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_22_6011_s_46	11080148	( D) Synaptotagmin binds the mu2 and alpha subunits of disassembled AP-2.	bind
3744	1	1982	5	10	NULL	NULL	NULL	TFIIB	GP		bind					BNA1	GP			promoter	NULL	in vivo from WT mot1-42 cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_153	15861138	( D) TFIIB binding to  BNA1 and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
3745	3	1982	5	10	NULL	NULL	NULL	TFIIB	GP		bind					URA1	GP			promoter	NULL	in vivo from WT mot1-42 cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_153	15861138	( D) TFIIB binding to  BNA1 and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
46310	2	1982	5	10	NULL	NULL	NULL	TFIIB	GP		bind					BNA1	GP			promoter	NULL	in vivo from mot1-42 mutant cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_153	15861138	( D) TFIIB binding to  BNA1 and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
46311	4	1982	5	10	NULL	NULL	NULL	TFIIB	GP		bind					URA1	GP			promoter	NULL	in vivo from mot1-42 mutant cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_153	15861138	( D) TFIIB binding to  BNA1 and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
46312	5	1982	5	10	NULL	NULL	NULL	WT	Organism		is					wild-type	Organism				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_153	15861138	( D) TFIIB binding to  BNA1 and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
3494	1	1982	7	10	NULL	NULL	NULL	TFIIB 	GP		bind					BNA1 	GP			promoter	NULL	in vivo from WT mot1-42  cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_153	15861138	( D) TFIIB binding to  BNA1 and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
3499	2	1982	7	10	NULL	NULL	NULL	TFIIB	GP		bind					BNA1	GP			promoter	NULL	in vivo from mot1-42 mutant cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_153	15861138	( D) TFIIB binding to  BNA1 and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
3500	3	1982	7	10	NULL	NULL	NULL	TFIIB	GP		bind					URA1	GP			promoter	NULL	in vivo from WT mot1-42  cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_153	15861138	( D) TFIIB binding to  BNA1 and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
46278	4	1982	7	10	NULL	NULL	NULL	TFIIB	GP		bind					URA1	GP			promoter	NULL	in vivo from mot1-42 mutant cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_153	15861138	( D) TFIIB binding to  BNA1 and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
46279	5	1982	7	10	NULL	NULL	NULL	WT	Organism		is					wild-type	Organism				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_153	15861138	( D) TFIIB binding to  BNA1 and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
3746	1	1983	5	10	NULL	NULL	NULL	AKAP protein Yotiao	GP		bind					NMDA receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_9_1027_s_276	10809663	( D) The AKAP protein Yotiao binds to the NMDA receptor, PKA in the inactive form, and PP1 in the active form.	bind
3747	2	1983	5	10	NULL	NULL	NULL	AKAP protein Yotiao	GP		bind					PKA	GP	in inactive form			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_9_1027_s_276	10809663	( D) The AKAP protein Yotiao binds to the NMDA receptor, PKA in the inactive form, and PP1 in the active form.	bind
3748	3	1983	5	10	NULL	NULL	NULL	AKAP protein Yotiao	GP		bind					PP1	GP	in active form			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_9_1027_s_276	10809663	( D) The AKAP protein Yotiao binds to the NMDA receptor, PKA in the inactive form, and PP1 in the active form.	bind
3503	1	1983	7	10	NULL	NULL	NULL	AKAP protein Yotiao	GP		bind					NMDA receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_9_1027_s_276	10809663	( D) The AKAP protein Yotiao binds to the NMDA receptor, PKA in the inactive form, and PP1 in the active form.	bind
3506	2	1983	7	10	NULL	NULL	NULL	AKAP protein Yotiao	GP		binds to					PKA	GP	inactive form of 			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_9_1027_s_276	10809663	( D) The AKAP protein Yotiao binds to the NMDA receptor, PKA in the inactive form, and PP1 in the active form.	bind
3507	3	1983	7	10	NULL	NULL	NULL	AKAP protein Yotiao	GP		binds to					PP1	GP	active form of			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_9_1027_s_276	10809663	( D) The AKAP protein Yotiao binds to the NMDA receptor, PKA in the inactive form, and PP1 in the active form.	bind
3749	2	1984	5	10	NULL	NULL	NULL	Rad5p	GP		is not required for			ATP-binding motif		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_18_5878_s_41	16224103	( D) The ATP-binding motif of Rad5p is not required for polyubiquitylation of PCNA.	bind
46206	1	1984	5	10	NULL	NULL	NULL	PCNA	GP		undergoes					polyubiquitylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_18_5878_s_41	16224103	( D) The ATP-binding motif of Rad5p is not required for polyubiquitylation of PCNA.	bind
3511	1	1984	7	10	NULL	NULL	NULL	PCNA	GP		undergoes					polyubiquitylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_18_5878_s_41	16224103	( D) The ATP-binding motif of Rad5p is not required for polyubiquitylation of PCNA.	bind
3517	2	1984	7	10	NULL	NULL	NULL	Rad5p	GP		is not required for			ATP-binding motif		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_18_5878_s_41	16224103	( D) The ATP-binding motif of Rad5p is not required for polyubiquitylation of PCNA.	bind
3750	1	1985	5	10	NULL	NULL	NULL	ERK2	GP	mutant	bind					3pk	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_59	11157753	( D) The binding of the mutant forms of ERK2 to 3pk.	bind
3519	1	1985	7	10	NULL	NULL	NULL	ERK2	GP	mutant	bind					3pk	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_59	11157753	( D) The binding of the mutant forms of ERK2 to 3pk.	bind
3751	1	1986	5	10	NULL	NULL	NULL	ERK2	GP	mutant	bind					MSK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_287	11157753	( D) The binding of the mutant forms of ERK2 to MSK1 was examined as in	bind
3521	1	1986	7	10	NULL	NULL	NULL	ERK2	GP	mutant	bind					MSK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_287	11157753	( D) The binding of the mutant forms of ERK2 to MSK1 was examined as in	bind
3752	1	1987	5	10	NULL	NULL	NULL	p38	GP	mutant	bind					PRAK	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_237	11157753	( D) The binding of the mutant forms of p38 and ERK2 to PRAK was examined as in	bind
3753	2	1987	5	10	NULL	NULL	NULL	ERK2	GP	mutant	bind					PRAK	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_237	11157753	( D) The binding of the mutant forms of p38 and ERK2 to PRAK was examined as in	bind
3524	1	1987	7	10	NULL	NULL	NULL	p38	GP	mutant	bind 					PRAK	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_237	11157753	( D) The binding of the mutant forms of p38 and ERK2 to PRAK was examined as in	bind
3525	2	1987	7	10	NULL	NULL	NULL	ERK2	GP	mutant	bind					PRAK	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_237	11157753	( D) The binding of the mutant forms of p38 and ERK2 to PRAK was examined as in	bind
3754	1	1989	5	10	NULL	NULL	NULL	CREM factor	GP		bind					Oxct2b	GP			promoter	NULL	germ cell nuclei	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3401_s_213	15951513	( D) The CREM factor binds to the Oxct2b promoter in germ cell nuclei.	bind
3526	1	1989	7	10	NULL	NULL	NULL	CREM factor	GP		bind					Oxct2b	GP			promoter	NULL	in germ cell nuclei	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3401_s_213	15951513	( D) The CREM factor binds to the Oxct2b promoter in germ cell nuclei.	bind
3755	1	1991	5	10	NULL	NULL	NULL	dsDNA	NucleicAcid		bind					hRad54	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_6_1346_s_147	11884632	( D) The dsDNA binding of hRad54 and hRad54B.	bind
3756	2	1991	5	10	NULL	NULL	NULL	dsDNA	NucleicAcid		bind					hRad54B	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_6_1346_s_147	11884632	( D) The dsDNA binding of hRad54 and hRad54B.	bind
3527	1	1991	7	10	NULL	NULL	NULL	hRad54	GP		binds					dsDNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_6_1346_s_147	11884632	( D) The dsDNA binding of hRad54 and hRad54B.	bind
3529	2	1991	7	10	NULL	NULL	NULL	hRad54B	GP		binds					dsDNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_6_1346_s_147	11884632	( D) The dsDNA binding of hRad54 and hRad54B.	bind
4103	1	1992	5	10	NULL	NULL	NULL	kinase	GP		bind					E2F-1	GP		AD		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_15_4280_s_126	10428966	( D) The E2F-1 (AD)-bound kinase phosphorylates four substrates of TFIIH and the bound proteins comprise p62, p89 and cdk7.	bind
5223	2	1992	5	10	NULL	NULL	NULL	statement 1	Process		phosphorylate					four substrates of TFIIH	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_15_4280_s_126	10428966	( D) The E2F-1 (AD)-bound kinase phosphorylates four substrates of TFIIH and the bound proteins comprise p62, p89 and cdk7.	bind
3532	1	1992	7	10	NULL	NULL	NULL	kinase	GP		bind					E2F-1	GP		AD		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_15_4280_s_126	10428966	( D) The E2F-1 (AD)-bound kinase phosphorylates four substrates of TFIIH and the bound proteins comprise p62, p89 and cdk7.	bind
4664	2	1992	7	10	NULL	NULL	NULL	statement 1	Process		phosphorylates					four substrates of TFIIH 	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_15_4280_s_126	10428966	( D) The E2F-1 (AD)-bound kinase phosphorylates four substrates of TFIIH and the bound proteins comprise p62, p89 and cdk7.	bind
2602	1	1993	5	10	NULL	NULL	NULL	8-azido-[gamma-32]ATP	Chemical		bind					Kir6.2 proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_7_1318_s_55	15775962	( D) The IC50 values for Na-ATP competition of 8-azido-[gamma-32]ATP binding to Kir6.2 proteins confirms the synergistic effect of N- and C-terminal  interactions on nucleotide binding.	bind
2604	2	1993	5	10	NULL	NULL	NULL	Na-ATP	Chemical		bind					Kir6.2 proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_7_1318_s_55	15775962	( D) The IC50 values for Na-ATP competition of 8-azido-[gamma-32]ATP binding to Kir6.2 proteins confirms the synergistic effect of N- and C-terminal  interactions on nucleotide binding.	bind
3286	3	1993	5	10	NULL	NULL	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_7_1318_s_55	15775962	( D) The IC50 values for Na-ATP competition of 8-azido-[gamma-32]ATP binding to Kir6.2 proteins confirms the synergistic effect of N- and C-terminal  interactions on nucleotide binding.	bind
3287	4	1993	5	10	NULL	NULL	NULL	N- and C-terminal interactions	Process		has synergistic effect on					nucleotide binding	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_7_1318_s_55	15775962	( D) The IC50 values for Na-ATP competition of 8-azido-[gamma-32]ATP binding to Kir6.2 proteins confirms the synergistic effect of N- and C-terminal  interactions on nucleotide binding.	bind
3288	5	1993	5	10	NULL	NULL	NULL	statement 3	Process		confirms					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_7_1318_s_55	15775962	( D) The IC50 values for Na-ATP competition of 8-azido-[gamma-32]ATP binding to Kir6.2 proteins confirms the synergistic effect of N- and C-terminal  interactions on nucleotide binding.	bind
3536	1	1993	7	10	NULL	NULL	NULL	8-azido-[gamma-32]ATP	Chemical		bind					Kir6.2 proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_7_1318_s_55	15775962	( D) The IC50 values for Na-ATP competition of 8-azido-[gamma-32]ATP binding to Kir6.2 proteins confirms the synergistic effect of N- and C-terminal  interactions on nucleotide binding.	bind
3537	2	1993	7	10	NULL	NULL	NULL	Na-ATP	Chemical		bind					Kir6.2 proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_7_1318_s_55	15775962	( D) The IC50 values for Na-ATP competition of 8-azido-[gamma-32]ATP binding to Kir6.2 proteins confirms the synergistic effect of N- and C-terminal  interactions on nucleotide binding.	bind
3539	4	1993	7	10	NULL	NULL	NULL	statement 1	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_7_1318_s_55	15775962	( D) The IC50 values for Na-ATP competition of 8-azido-[gamma-32]ATP binding to Kir6.2 proteins confirms the synergistic effect of N- and C-terminal  interactions on nucleotide binding.	bind
4231	5	1993	7	10	NULL	NULL	NULL	N- and C-terminal interactions 	Process		has synergistic effect on					nucleotide binding	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_7_1318_s_55	15775962	( D) The IC50 values for Na-ATP competition of 8-azido-[gamma-32]ATP binding to Kir6.2 proteins confirms the synergistic effect of N- and C-terminal  interactions on nucleotide binding.	bind
4232	6	1993	7	10	NULL	NULL	NULL	statement 4	Process		confirms					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_7_1318_s_55	15775962	( D) The IC50 values for Na-ATP competition of 8-azido-[gamma-32]ATP binding to Kir6.2 proteins confirms the synergistic effect of N- and C-terminal  interactions on nucleotide binding.	bind
2599	1	1995	5	10	NULL	NULL	NULL	MBS	GP		bind					moesin	GP		NH2-terminal domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_2_409_s_204	9548719	( D) The kinetic study of the MBS binding to the NH2-terminal domain  of moesin and the full-length moesin.	bind
2600	2	1995	5	10	NULL	NULL	NULL	MBS	GP		bind					moesin	GP	full-length			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_2_409_s_204	9548719	( D) The kinetic study of the MBS binding to the NH2-terminal domain  of moesin and the full-length moesin.	bind
3540	1	1995	7	10	NULL	NULL	NULL	MBS	GP		bind					moesin	GP		NH2-terminal domain 		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_2_409_s_204	9548719	( D) The kinetic study of the MBS binding to the NH2-terminal domain  of moesin and the full-length moesin.	bind
3541	2	1995	7	10	NULL	NULL	NULL	MBS	GP		bind					moesin	GP	full-length			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_2_409_s_204	9548719	( D) The kinetic study of the MBS binding to the NH2-terminal domain  of moesin and the full-length moesin.	bind
2594	1	1996	5	10	NULL	NULL	NULL	Ubc4(C/A)	GP		bind					pIkappaBalpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_4003_s_160	11483504	( D) The NEDD8 system does not support the binding of Ubc4(C/A) and Ubc4(C/S) to pIkappaBalpha.	bind
2596	2	1996	5	10	NULL	NULL	NULL	Ubc4(C/S)	GP		bind					pIkappaBalpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_4003_s_160	11483504	( D) The NEDD8 system does not support the binding of Ubc4(C/A) and Ubc4(C/S) to pIkappaBalpha.	bind
2597	3	1996	5	10	NULL	NULL	NULL	NEDD8 system	GP		does not support					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_4003_s_160	11483504	( D) The NEDD8 system does not support the binding of Ubc4(C/A) and Ubc4(C/S) to pIkappaBalpha.	bind
2598	4	1996	5	10	NULL	NULL	NULL	NEDD8 system	GP		does not support					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_4003_s_160	11483504	( D) The NEDD8 system does not support the binding of Ubc4(C/A) and Ubc4(C/S) to pIkappaBalpha.	bind
3542	1	1996	7	10	NULL	NULL	NULL	Ubc4(C/A)	GP		bind					pIkappaBalpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_4003_s_160	11483504	( D) The NEDD8 system does not support the binding of Ubc4(C/A) and Ubc4(C/S) to pIkappaBalpha.	bind
3543	2	1996	7	10	NULL	NULL	NULL	Ubc4(C/S)	GP		bind					pIkappaBalpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_4003_s_160	11483504	( D) The NEDD8 system does not support the binding of Ubc4(C/A) and Ubc4(C/S) to pIkappaBalpha.	bind
3544	3	1996	7	10	NULL	NULL	NULL	NEDD8 system	GP		does not support					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_4003_s_160	11483504	( D) The NEDD8 system does not support the binding of Ubc4(C/A) and Ubc4(C/S) to pIkappaBalpha.	bind
3545	4	1996	7	10	NULL	NULL	NULL	NEDD8 system	GP		does not support					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_4003_s_160	11483504	( D) The NEDD8 system does not support the binding of Ubc4(C/A) and Ubc4(C/S) to pIkappaBalpha.	bind
2590	1	1999	5	10	NULL	NULL	NULL	Cas	GP		bind					c-Crk	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_26_15394_s_91	9860979	( D) The substrate domain of Cas is required for Cas binding to c-Crk.	bind
2592	2	1999	5	10	NULL	NULL	NULL	Cas	GP		is required for			substrate domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_26_15394_s_91	9860979	( D) The substrate domain of Cas is required for Cas binding to c-Crk.	bind
3546	1	1999	7	10	NULL	NULL	NULL	 Cas	GP		bind					c-Crk	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_26_15394_s_91	9860979	( D) The substrate domain of Cas is required for Cas binding to c-Crk.	bind
3547	2	1999	7	10	NULL	NULL	NULL	Cas	GP		is required for			substrate domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_26_15394_s_91	9860979	( D) The substrate domain of Cas is required for Cas binding to c-Crk.	bind
2589	1	2000	5	10	NULL	0	NULL	serine	AminoAcid		bind					aMb-SerRS	GP		active site		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2498_s_116	16675947	( D) The superposition of Ser-AMS, ATP and serine bound to the active site of aMb-SerRS.	bind
3289	2	2000	5	10	NULL	0	NULL	ATP	Chemical		bind					aMb-SerRS	GP		active site		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2498_s_116	16675947	( D) The superposition of Ser-AMS, ATP and serine bound to the active site of aMb-SerRS.	bind
3290	3	2000	5	10	NULL	0	NULL	Ser-AMS	Chemical		bind					aMb-SerRS	GP		active site		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2498_s_116	16675947	( D) The superposition of Ser-AMS, ATP and serine bound to the active site of aMb-SerRS.	bind
3549	1	2000	7	10	NULL	0	NULL	Ser-AMS	Chemical		binds to					aMb-SerRS	GP		active site of		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2498_s_116	16675947	( D) The superposition of Ser-AMS, ATP and serine bound to the active site of aMb-SerRS.	bind
3550	2	2000	7	10	NULL	0	NULL	ATP	Chemical		binds to					aMb-SerRS	GP		active site of		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2498_s_116	16675947	( D) The superposition of Ser-AMS, ATP and serine bound to the active site of aMb-SerRS.	bind
3551	3	2000	7	10	NULL	0	NULL	serine	AminoAcid		binds to					aMb-SerRS	GP		active site of		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2498_s_116	16675947	( D) The superposition of Ser-AMS, ATP and serine bound to the active site of aMb-SerRS.	bind
2731	1	2001	6	10	NULL	0	NULL	TAK1	GP		bind					DR1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_14_4194_s_234	15302918	( D) TIP27 does not inhibit binding of TAK1 to DR1.	bind
2732	2	2001	6	10	NULL	0	NULL	TIP27	GP		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_14_4194_s_234	15302918	( D) TIP27 does not inhibit binding of TAK1 to DR1.	bind
3557	1	2001	7	10	NULL	0	NULL	TAK1	GP		binds to					DR1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_14_4194_s_234	15302918	( D) TIP27 does not inhibit binding of TAK1 to DR1.	bind
3558	2	2001	7	10	NULL	0	NULL	TIP27 	GP		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_14_4194_s_234	15302918	( D) TIP27 does not inhibit binding of TAK1 to DR1.	bind
2733	1	2002	6	10	NULL	0	NULL	TMEFF1	GP		bind		directly			Cripto coreceptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_21_2624_s_56	14563676	( D) TMEFF1 binds directly to the Cripto coreceptor.	bind
3559	1	2002	7	10	NULL	0	NULL	 TMEFF1	GP		binds		directly			Cripto coreceptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_21_2624_s_56	14563676	( D) TMEFF1 binds directly to the Cripto coreceptor.	bind
2738	1	2003	6	10	NULL	0	NULL	RA sera	CellComponent		bind					B7-H1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_111_3_363_s_94	12569162	( d) To examine specificity of RA sera binding to B7-H1, diluted sera were preincubated  with PBS, 2 mug/ml of soluble B7-H1Ig or control Ig (mIgG2a).	bind
3560	1	2003	7	10	NULL	0	NULL	RA sera	CellComponent		binds					B7-H1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_111_3_363_s_94	12569162	( d) To examine specificity of RA sera binding to B7-H1, diluted sera were preincubated  with PBS, 2 mug/ml of soluble B7-H1Ig or control Ig (mIgG2a).	bind
2739	1	2005	6	10	NULL	0	NULL	TRBP	GP		bind					TR	GP	liganded			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_97_11_6212_s_74	10823961	( D) TRBP binds to liganded TR and retinoic acid receptor (RAR)  in vitro.	bind
2740	2	2005	6	10	NULL	0	NULL	TRBP	GP		bind					RAR	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_97_11_6212_s_74	10823961	( D) TRBP binds to liganded TR and retinoic acid receptor (RAR)  in vitro.	bind
45776	3	2005	6	10	NULL	0	NULL	RAR	GP		is					retinoic acid receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_11_6212_s_74	10823961	( D) TRBP binds to liganded TR and retinoic acid receptor (RAR)  in vitro.	bind
3561	1	2005	7	10	NULL	0	NULL	TRBP	GP		binds to					TR	GP	liganded			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_97_11_6212_s_74	10823961	( D) TRBP binds to liganded TR and retinoic acid receptor (RAR)  in vitro.	bind
3562	2	2005	7	10	NULL	0	NULL	TRBP	GP		binds to					retinoic acid receptor 	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_97_11_6212_s_74	10823961	( D) TRBP binds to liganded TR and retinoic acid receptor (RAR)  in vitro.	bind
3563	3	2005	7	10	NULL	0	NULL	retinoic acid receptor	GP		is 					RAR	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_11_6212_s_74	10823961	( D) TRBP binds to liganded TR and retinoic acid receptor (RAR)  in vitro.	bind
2741	1	2006	6	10	NULL	0	NULL	COS-7 cells	Cell	live	express					VAB-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_2_187_s_86	12533508	( d) Two-hundred nanomolar MSP binds to the surface of live COS-7 cells (arrow) expressing VAB-1 ( upper panel), but not n-Src ( lower panel).	bind
2742	2	2006	6	10	NULL	0	NULL	MSP	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_2_187_s_86	12533508	( d) Two-hundred nanomolar MSP binds to the surface of live COS-7 cells (arrow) expressing VAB-1 ( upper panel), but not n-Src ( lower panel).	bind
2743	3	2006	6	10	NULL	0	NULL	COS-7 cells	Cell	live	express					n-Src	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_2_187_s_86	12533508	( d) Two-hundred nanomolar MSP binds to the surface of live COS-7 cells (arrow) expressing VAB-1 ( upper panel), but not n-Src ( lower panel).	bind
51547	4	2006	6	10	NULL	0	NULL	MSP	GP		does not bind					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_2_187_s_86	12533508	( d) Two-hundred nanomolar MSP binds to the surface of live COS-7 cells (arrow) expressing VAB-1 ( upper panel), but not n-Src ( lower panel).	bind
3564	1	2006	7	10	NULL	0	NULL	COS-7 cells	Cell	live	express					VAB-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_2_187_s_86	12533508	( d) Two-hundred nanomolar MSP binds to the surface of live COS-7 cells (arrow) expressing VAB-1 ( upper panel), but not n-Src ( lower panel).	bind
3565	2	2006	7	10	NULL	0	NULL	MSP	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_2_187_s_86	12533508	( d) Two-hundred nanomolar MSP binds to the surface of live COS-7 cells (arrow) expressing VAB-1 ( upper panel), but not n-Src ( lower panel).	bind
46265	3	2006	7	10	NULL	0	NULL	COS-7 cells	Cell	live	express					n-Src	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_2_187_s_86	12533508	( d) Two-hundred nanomolar MSP binds to the surface of live COS-7 cells (arrow) expressing VAB-1 ( upper panel), but not n-Src ( lower panel).	bind
46266	4	2006	7	10	NULL	0	NULL	MSP	GP		does not bind					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_2_187_s_86	12533508	( d) Two-hundred nanomolar MSP binds to the surface of live COS-7 cells (arrow) expressing VAB-1 ( upper panel), but not n-Src ( lower panel).	bind
2744	1	2007	6	10	NULL	0	NULL	c-Myc	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_86	12808131	( D) Venn diagram comparing the DNA  binding of c-Myc and Max.	bind
2745	2	2007	6	10	NULL	0	NULL	Max	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_86	12808131	( D) Venn diagram comparing the DNA  binding of c-Myc and Max.	bind
3566	1	2007	7	10	NULL	0	NULL	c-Myc	GP		binds					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_86	12808131	( D) Venn diagram comparing the DNA  binding of c-Myc and Max.	bind
3567	2	2007	7	10	NULL	0	NULL	Max	GP		binds 					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_86	12808131	( D) Venn diagram comparing the DNA  binding of c-Myc and Max.	bind
2748	1	2008	6	10	NULL	0	NULL	BCD	GP		bind					eIF4E	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_19_2576_s_37	12368268	( d) Western blots showing that BCD bound to m7GTP-sepharose coupled recombinant eIF4E (lanes  1,4) can be competed for with 100 nM (lane  2) and 1 mM (lanes  3,5) of a peptide containing the YDRKFL motif of human BP1, whereas 1 mM of a mutated human BP1 peptide (mutated motif is ADRKFR) did not interfere with the binding of BCD to eIF4E (lane  6).	bind
2750	2	2008	6	10	NULL	0	NULL	BP1	GP	human	bind			YDRKFL motif		e1F4E	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_19_2576_s_37	12368268	( d) Western blots showing that BCD bound to m7GTP-sepharose coupled recombinant eIF4E (lanes  1,4) can be competed for with 100 nM (lane  2) and 1 mM (lanes  3,5) of a peptide containing the YDRKFL motif of human BP1, whereas 1 mM of a mutated human BP1 peptide (mutated motif is ADRKFR) did not interfere with the binding of BCD to eIF4E (lane  6).	bind
2753	3	2008	6	10	NULL	0	NULL	BP1 peptide	GP	human;;mutant	does not interfere with			ADRKFR		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_19_2576_s_37	12368268	( d) Western blots showing that BCD bound to m7GTP-sepharose coupled recombinant eIF4E (lanes  1,4) can be competed for with 100 nM (lane  2) and 1 mM (lanes  3,5) of a peptide containing the YDRKFL motif of human BP1, whereas 1 mM of a mutated human BP1 peptide (mutated motif is ADRKFR) did not interfere with the binding of BCD to eIF4E (lane  6).	bind
5531	4	2008	6	10	NULL	0	NULL	statement 1	Process		competes with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_19_2576_s_37	12368268	( d) Western blots showing that BCD bound to m7GTP-sepharose coupled recombinant eIF4E (lanes  1,4) can be competed for with 100 nM (lane  2) and 1 mM (lanes  3,5) of a peptide containing the YDRKFL motif of human BP1, whereas 1 mM of a mutated human BP1 peptide (mutated motif is ADRKFR) did not interfere with the binding of BCD to eIF4E (lane  6).	bind
3572	1	2008	7	10	NULL	0	NULL	BCD	GP		binds to					eIF4E	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_19_2576_s_37	12368268	( d) Western blots showing that BCD bound to m7GTP-sepharose coupled recombinant eIF4E (lanes  1,4) can be competed for with 100 nM (lane  2) and 1 mM (lanes  3,5) of a peptide containing the YDRKFL motif of human BP1, whereas 1 mM of a mutated human BP1 peptide (mutated motif is ADRKFR) did not interfere with the binding of BCD to eIF4E (lane  6).	bind
3573	2	2008	7	10	NULL	0	NULL	 BP1	GP	human	binds to			YDRKFL motif		  eIF4E	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_19_2576_s_37	12368268	( d) Western blots showing that BCD bound to m7GTP-sepharose coupled recombinant eIF4E (lanes  1,4) can be competed for with 100 nM (lane  2) and 1 mM (lanes  3,5) of a peptide containing the YDRKFL motif of human BP1, whereas 1 mM of a mutated human BP1 peptide (mutated motif is ADRKFR) did not interfere with the binding of BCD to eIF4E (lane  6).	bind
3574	3	2008	7	10	NULL	0	NULL	BP1 peptide	GP	mutant;;human 	does not interfere with			ADRKFR motif		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_19_2576_s_37	12368268	( d) Western blots showing that BCD bound to m7GTP-sepharose coupled recombinant eIF4E (lanes  1,4) can be competed for with 100 nM (lane  2) and 1 mM (lanes  3,5) of a peptide containing the YDRKFL motif of human BP1, whereas 1 mM of a mutated human BP1 peptide (mutated motif is ADRKFR) did not interfere with the binding of BCD to eIF4E (lane  6).	bind
4233	4	2008	7	10	NULL	0	NULL	statement 1	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_19_2576_s_37	12368268	( d) Western blots showing that BCD bound to m7GTP-sepharose coupled recombinant eIF4E (lanes  1,4) can be competed for with 100 nM (lane  2) and 1 mM (lanes  3,5) of a peptide containing the YDRKFL motif of human BP1, whereas 1 mM of a mutated human BP1 peptide (mutated motif is ADRKFR) did not interfere with the binding of BCD to eIF4E (lane  6).	bind
2754	1	2009	6	10	NULL	0	NULL	Gal4 protein	GP	wild type	does not bind					Ubx	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_18_21_2596_s_40	15520279	( D) Wild-type GAL4 protein does not bind to the  Ubx promoter region.	bind
3568	1	2009	7	10	NULL	0	NULL	GAL4 protein	GP	Wild-type	does not bind					Ubx	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_18_21_2596_s_40	15520279	( D) Wild-type GAL4 protein does not bind to the  Ubx promoter region.	bind
2755	2	2010	6	10	NULL	0	NULL	XCdc6	GP		bind					statement 1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_2_472_s_243	10606645	( D) XCdc6 binds to the XORC-containing DNA.	bind
51548	1	2010	6	10	NULL	0	NULL	DNA	NucleicAcid		contains					XORC	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_2_472_s_243	10606645	( D) XCdc6 binds to the XORC-containing DNA.	bind
3569	2	2010	7	10	NULL	0	NULL	XCdc6	GP		bind					statement 1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_2_472_s_243	10606645	( D) XCdc6 binds to the XORC-containing DNA.	bind
46267	1	2010	7	10	NULL	0	NULL	DNA	NucleicAcid		contains					XORC	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_2_472_s_243	10606645	( D) XCdc6 binds to the XORC-containing DNA.	bind
2756	1	2011	6	10	NULL	0	NULL	synaptotagmin I 	GP		bind					AP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5431_1268_s_44	10455054	( D) YXX  peptides do not stimulate binding of synaptotagmin I to AP-1.	bind
3392	2	2011	6	10	NULL	0	NULL	YXX peptides	AminoAcid		does not stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5431_1268_s_44	10455054	( D) YXX  peptides do not stimulate binding of synaptotagmin I to AP-1.	bind
3937	1	2011	7	10	NULL	0	NULL	synaptotagmin I	GP		bind to					AP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5431_1268_s_44	10455054	( D) YXX  peptides do not stimulate binding of synaptotagmin I to AP-1.	bind
3938	2	2011	7	10	NULL	0	NULL	YXX peptides	AminoAcid		do not stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5431_1268_s_44	10455054	( D) YXX  peptides do not stimulate binding of synaptotagmin I to AP-1.	bind
2757	1	2012	6	10	NULL	0	NULL	ZF5	GP		bind		specifically						RRS motif		NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_26_14991_s_143	11734633	( D) ZF5 binds specifically to the RRS motif.	bind
3939	1	2012	7	10	NULL	0	NULL	ZF5	GP		binds		specifically						RRS motif		NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_26_14991_s_143	11734633	( D) ZF5 binds specifically to the RRS motif.	bind
2758	1	2013	6	10	NULL	0	NULL	Zip1	GP		bind					Pof1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_3_599_s_178	15660136	( D, E) Binding between Zip1 and Pof1.	bind
3942	1	2013	7	10	NULL	0	NULL	Zip1	GP		binds to					Pof1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_3_599_s_178	15660136	( D, E) Binding between Zip1 and Pof1.	bind
2759	1	2014	6	10	NULL	0	NULL	Robo2	GP	FLAG-tagged	bind			D1 5		Slit fragments	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_22_4406_s_75	15496984	( D, E) Binding of FLAG-tagged Robo2 D1 5 (D) and Robo3 D1 5 (E) to immobilised Slit fragments.	bind
2760	2	2014	6	10	NULL	0	NULL	Robo3	GP	FLAG-tagged	bind			D1 5		Slit fragments	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_22_4406_s_75	15496984	( D, E) Binding of FLAG-tagged Robo2 D1 5 (D) and Robo3 D1 5 (E) to immobilised Slit fragments.	bind
3943	1	2014	7	10	NULL	0	NULL	Robo2 	GP	FLAG-tagged	binds to			D1 5		Slit fragments	GP	immobilised			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_22_4406_s_75	15496984	( D, E) Binding of FLAG-tagged Robo2 D1 5 (D) and Robo3 D1 5 (E) to immobilised Slit fragments.	bind
3944	2	2014	7	10	NULL	0	NULL	Robo3 	GP	FLAG-tagged	binds to			D1 5		Slit fragments	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_22_4406_s_75	15496984	( D, E) Binding of FLAG-tagged Robo2 D1 5 (D) and Robo3 D1 5 (E) to immobilised Slit fragments.	bind
2996	1	2015	6	10	NULL	0	NULL	TIF32	GP		interacts with			NTD		RPS0A	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_6_786_s_302	12651896	( D,E) Hypothetical location of the eIF3 complex on the 3D model of the 40S subunit based  on the results of this study, including the requirements for the N- and C-terminal  domains in both NIP1 and TIF32 for 40S binding, interaction between the TIF32-NTD  and RPS0A, binding of the TIF32-CTD to helices 16-18 of 18S rRNA, and binding of  NIP1 to RPS0A and 18S rRNA.	bind
2997	2	2015	6	10	NULL	0	NULL	TIF32	GP		bind			CTD		18S rRNA	NucleicAcid			helices 16-18	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_6_786_s_302	12651896	( D,E) Hypothetical location of the eIF3 complex on the 3D model of the 40S subunit based  on the results of this study, including the requirements for the N- and C-terminal  domains in both NIP1 and TIF32 for 40S binding, interaction between the TIF32-NTD  and RPS0A, binding of the TIF32-CTD to helices 16-18 of 18S rRNA, and binding of  NIP1 to RPS0A and 18S rRNA.	bind
2998	3	2015	6	10	NULL	0	NULL	NIP1	GP		bind					RPS0A	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_6_786_s_302	12651896	( D,E) Hypothetical location of the eIF3 complex on the 3D model of the 40S subunit based  on the results of this study, including the requirements for the N- and C-terminal  domains in both NIP1 and TIF32 for 40S binding, interaction between the TIF32-NTD  and RPS0A, binding of the TIF32-CTD to helices 16-18 of 18S rRNA, and binding of  NIP1 to RPS0A and 18S rRNA.	bind
2999	4	2015	6	10	NULL	0	NULL	NIP1	GP		bind					18S rRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_6_786_s_302	12651896	( D,E) Hypothetical location of the eIF3 complex on the 3D model of the 40S subunit based  on the results of this study, including the requirements for the N- and C-terminal  domains in both NIP1 and TIF32 for 40S binding, interaction between the TIF32-NTD  and RPS0A, binding of the TIF32-CTD to helices 16-18 of 18S rRNA, and binding of  NIP1 to RPS0A and 18S rRNA.	bind
3000	5	2015	6	10	NULL	0	NULL	NIP1	GP		bind			N-terminal domain;;C-terminal domain		40S rRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_6_786_s_302	12651896	( D,E) Hypothetical location of the eIF3 complex on the 3D model of the 40S subunit based  on the results of this study, including the requirements for the N- and C-terminal  domains in both NIP1 and TIF32 for 40S binding, interaction between the TIF32-NTD  and RPS0A, binding of the TIF32-CTD to helices 16-18 of 18S rRNA, and binding of  NIP1 to RPS0A and 18S rRNA.	bind
3001	6	2015	6	10	NULL	0	NULL	TIF32	GP		bind			N-terminal domain;;C-terminal domain		40S rRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_6_786_s_302	12651896	( D,E) Hypothetical location of the eIF3 complex on the 3D model of the 40S subunit based  on the results of this study, including the requirements for the N- and C-terminal  domains in both NIP1 and TIF32 for 40S binding, interaction between the TIF32-NTD  and RPS0A, binding of the TIF32-CTD to helices 16-18 of 18S rRNA, and binding of  NIP1 to RPS0A and 18S rRNA.	bind
3945	1	2015	7	10	NULL	0	NULL	NIP1	GP		bind			N-terminal domain;;C-terminal domain		40S rRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_6_786_s_302	12651896	( D,E) Hypothetical location of the eIF3 complex on the 3D model of the 40S subunit based  on the results of this study, including the requirements for the N- and C-terminal  domains in both NIP1 and TIF32 for 40S binding, interaction between the TIF32-NTD  and RPS0A, binding of the TIF32-CTD to helices 16-18 of 18S rRNA, and binding of  NIP1 to RPS0A and 18S rRNA.	bind
3946	2	2015	7	10	NULL	0	NULL	TIF32	GP		bind			N-terminal domain;;C-terminal domain		40S rRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_6_786_s_302	12651896	( D,E) Hypothetical location of the eIF3 complex on the 3D model of the 40S subunit based  on the results of this study, including the requirements for the N- and C-terminal  domains in both NIP1 and TIF32 for 40S binding, interaction between the TIF32-NTD  and RPS0A, binding of the TIF32-CTD to helices 16-18 of 18S rRNA, and binding of  NIP1 to RPS0A and 18S rRNA.	bind
3947	3	2015	7	10	NULL	0	NULL	TIF32	GP		interacts with			NTD		RPS0A	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_6_786_s_302	12651896	( D,E) Hypothetical location of the eIF3 complex on the 3D model of the 40S subunit based  on the results of this study, including the requirements for the N- and C-terminal  domains in both NIP1 and TIF32 for 40S binding, interaction between the TIF32-NTD  and RPS0A, binding of the TIF32-CTD to helices 16-18 of 18S rRNA, and binding of  NIP1 to RPS0A and 18S rRNA.	bind
3948	4	2015	7	10	NULL	0	NULL	TIF32	GP		bind			CTD		18S rRNA	NucleicAcid			helices 16-18 of	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_6_786_s_302	12651896	( D,E) Hypothetical location of the eIF3 complex on the 3D model of the 40S subunit based  on the results of this study, including the requirements for the N- and C-terminal  domains in both NIP1 and TIF32 for 40S binding, interaction between the TIF32-NTD  and RPS0A, binding of the TIF32-CTD to helices 16-18 of 18S rRNA, and binding of  NIP1 to RPS0A and 18S rRNA.	bind
3949	5	2015	7	10	NULL	0	NULL	NIP1	GP		bind					RPS0A 	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_6_786_s_302	12651896	( D,E) Hypothetical location of the eIF3 complex on the 3D model of the 40S subunit based  on the results of this study, including the requirements for the N- and C-terminal  domains in both NIP1 and TIF32 for 40S binding, interaction between the TIF32-NTD  and RPS0A, binding of the TIF32-CTD to helices 16-18 of 18S rRNA, and binding of  NIP1 to RPS0A and 18S rRNA.	bind
3950	6	2015	7	10	NULL	0	NULL	NIP1	GP		bind					18S rRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_6_786_s_302	12651896	( D,E) Hypothetical location of the eIF3 complex on the 3D model of the 40S subunit based  on the results of this study, including the requirements for the N- and C-terminal  domains in both NIP1 and TIF32 for 40S binding, interaction between the TIF32-NTD  and RPS0A, binding of the TIF32-CTD to helices 16-18 of 18S rRNA, and binding of  NIP1 to RPS0A and 18S rRNA.	bind
2761	1	2017	6	10	NULL	0	NULL	Frat1	GP		bind					Dvl	GP				NULL	COS-7 cells	NULL	NULL	NULL	NULL	gw60_embo_18_15_4233_s_132	10428961	( D- F) Frat1 binds to Dvl in COS-7 cells.	bind
3951	1	2017	7	10	NULL	0	NULL	Frat1	GP		binds to					Dvl	GP				NULL	COS-7 cells	NULL	NULL	NULL	NULL	gw60_embo_18_15_4233_s_132	10428961	( D- F) Frat1 binds to Dvl in COS-7 cells.	bind
2763	1	2018	6	10	NULL	0	NULL	FGF2	GP		bind					FGFR2c	GP		S252W		NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_26_14536_s_147	11121055	( D-F) FGF2 binding to FGFR2c (S252W), FGFR2c (P253R), and FGFR2c, respectively.	bind
2765	2	2018	6	10	NULL	0	NULL	FGF2	GP		bind					FGFR2c	GP		P253R		NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_26_14536_s_147	11121055	( D-F) FGF2 binding to FGFR2c (S252W), FGFR2c (P253R), and FGFR2c, respectively.	bind
2766	3	2018	6	10	NULL	0	NULL	FGF2	GP		bind					FGFR2c	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_26_14536_s_147	11121055	( D-F) FGF2 binding to FGFR2c (S252W), FGFR2c (P253R), and FGFR2c, respectively.	bind
3952	1	2018	7	10	NULL	0	NULL	FGF2	GP		binds to					FGFR2c	GP		S252W		NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_26_14536_s_147	11121055	( D-F) FGF2 binding to FGFR2c (S252W), FGFR2c (P253R), and FGFR2c, respectively.	bind
3953	2	2018	7	10	NULL	0	NULL	FGF2	GP		binds to					FGFR2c	GP		P253R		NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_26_14536_s_147	11121055	( D-F) FGF2 binding to FGFR2c (S252W), FGFR2c (P253R), and FGFR2c, respectively.	bind
3954	3	2018	7	10	NULL	0	NULL	FGF2	GP		binds to					FGFR2c	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_26_14536_s_147	11121055	( D-F) FGF2 binding to FGFR2c (S252W), FGFR2c (P253R), and FGFR2c, respectively.	bind
2769	1	2019	6	10	NULL	0	NULL	AP-1	GP		bind					TGN	GP				NULL	mu1A-deficient cells	NULL	NULL	NULL	NULL	gw60_embo_19_10_2193_s_108	10811610	( E -  H) Binding of AP-1 to the TGN of control (E and H) and mu1A-deficient cells (F and G) permeabilized with digitonin.	bind
4234	1	2019	7	10	NULL	0	NULL	AP-1	GP		bind					TGN	GP				NULL	mu1A-deficient cells	NULL	NULL	NULL	NULL	gw60_embo_19_10_2193_s_108	10811610	( E -  H) Binding of AP-1 to the TGN of control (E and H) and mu1A-deficient cells (F and G) permeabilized with digitonin.	bind
2773	1	2021	6	10	NULL	0	NULL	F3 qdots	Chemical		bind					MDA-MB-435	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12617_s_77	12235356	( e and  f) F3 qdots bind to MDA-MB-435 breast carcinoma cells ( e); free F3 peptide (500 muM) inhibits the binding ( f).	bind
2774	2	2021	6	10	NULL	0	NULL	MDA-MB-435	Cell		is a type of					breast carcinoma cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12617_s_77	12235356	( e and  f) F3 qdots bind to MDA-MB-435 breast carcinoma cells ( e); free F3 peptide (500 muM) inhibits the binding ( f).	bind
2775	3	2021	6	10	NULL	0	NULL	F3 peptide	GP	free	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12617_s_77	12235356	( e and  f) F3 qdots bind to MDA-MB-435 breast carcinoma cells ( e); free F3 peptide (500 muM) inhibits the binding ( f).	bind
4235	1	2021	7	10	NULL	0	NULL	F3 qdots	Chemical		binds to					MDA-MB-435	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12617_s_77	12235356	( e and  f) F3 qdots bind to MDA-MB-435 breast carcinoma cells ( e); free F3 peptide (500 muM) inhibits the binding ( f).	bind
4236	2	2021	7	10	NULL	0	NULL	 F3 peptide	GP	free	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12617_s_77	12235356	( e and  f) F3 qdots bind to MDA-MB-435 breast carcinoma cells ( e); free F3 peptide (500 muM) inhibits the binding ( f).	bind
45793	3	2021	7	10	NULL	0	NULL	MDA-MB-435	Cell		is a type of					breast carcinoma cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12617_s_77	12235356	( e and  f) F3 qdots bind to MDA-MB-435 breast carcinoma cells ( e); free F3 peptide (500 muM) inhibits the binding ( f).	bind
2777	1	2022	6	10	NULL	0	NULL	LPC	Chemical		bind					G2A	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5530_702_s_63	11474113	( E and  F) Structural specificity of  [3]-16:0 LPC and [3]SPC  binding to G2A.	bind
2779	2	2022	6	10	NULL	0	NULL	SPC	Chemical		bind					G2A	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5530_702_s_63	11474113	( E and  F) Structural specificity of  [3]-16:0 LPC and [3]SPC  binding to G2A.	bind
4237	1	2022	7	10	NULL	0	NULL	LPC	Chemical		binds to					G2A	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5530_702_s_63	11474113	( E and  F) Structural specificity of  [3]-16:0 LPC and [3]SPC  binding to G2A.	bind
4238	2	2022	7	10	NULL	0	NULL	SPC	Chemical		binds to					G2A	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5530_702_s_63	11474113	( E and  F) Structural specificity of  [3]-16:0 LPC and [3]SPC  binding to G2A.	bind
2782	1	2023	6	10	NULL	0	NULL	MDMX	GP	in vitro translated	bind					GST-RB	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_5_2211_s_130	11226218	( E)  In vitro-translated MDMX binds to GST-RB and to GST-Sp1.	bind
2784	2	2023	6	10	NULL	0	NULL	MDMX	GP	in vitro translated	bind					GST-Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_5_2211_s_130	11226218	( E)  In vitro-translated MDMX binds to GST-RB and to GST-Sp1.	bind
4239	1	2023	7	10	NULL	0	NULL	MDMX	GP	in vitro-translated	binds to					GST-RB	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_5_2211_s_130	11226218	( E)  In vitro-translated MDMX binds to GST-RB and to GST-Sp1.	bind
4240	2	2023	7	10	NULL	0	NULL	MDMX	GP	in vitro-translated	binds to					GST-Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_5_2211_s_130	11226218	( E)  In vitro-translated MDMX binds to GST-RB and to GST-Sp1.	bind
2785	1	2024	6	10	NULL	0	NULL			hu6k array	bind				fraction of promotor or coding region	C-Myc	GP				NULL	Daudi cells	NULL	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_90	12808131	( E) A comparison of the fraction of promoter  or coding regions represented on the hu6K  array that are bound by c-Myc, Max,  or both in Daudi cells.	bind
2786	2	2024	6	10	NULL	0	NULL			hu6k array	bind				fraction of promotor or coding region	Max	GP				NULL	Daudi cells	NULL	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_90	12808131	( E) A comparison of the fraction of promoter  or coding regions represented on the hu6K  array that are bound by c-Myc, Max,  or both in Daudi cells.	bind
5787	3	2024	6	10	NULL	0	NULL	statement 1	Process		occur in conjunction with		may			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_90	12808131	( E) A comparison of the fraction of promoter  or coding regions represented on the hu6K  array that are bound by c-Myc, Max,  or both in Daudi cells.	bind
4241	1	2024	7	10	NULL	0	NULL			hu6K array	bind				fraction of promoter or coding regions 	 c-Myc	GP				NULL	in Daudi cells	NULL	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_90	12808131	( E) A comparison of the fraction of promoter  or coding regions represented on the hu6K  array that are bound by c-Myc, Max,  or both in Daudi cells.	bind
4242	2	2024	7	10	NULL	0	NULL			hu6K array	bind				fraction of promoter or coding regions 	Max	GP				NULL	in Daudi cells	NULL	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_90	12808131	( E) A comparison of the fraction of promoter  or coding regions represented on the hu6K  array that are bound by c-Myc, Max,  or both in Daudi cells.	bind
4665	3	2024	7	10	NULL	0	NULL	statement 1	Process		occur in conjunction with		may			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_90	12808131	( E) A comparison of the fraction of promoter  or coding regions represented on the hu6K  array that are bound by c-Myc, Max,  or both in Daudi cells.	bind
2795	1	2026	6	10	NULL	0	NULL	GFP-beta-CaMKII	GP	mutant	does not dissociate			A303R		F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5411_162_s_143	10102820	( E) A GFP-beta-CaMKII mutant deficient in calmodulin binding (A303R) fails to dissociate from F-actin after ionomycin addition.	bind
2796	2	2026	6	10	NULL	0	NULL	statement 1	Process		occurs after					ionomycin	Chemical	addition of			NULL		NULL	NULL	NULL	NULL	gw60_science_284_5411_162_s_143	10102820	( E) A GFP-beta-CaMKII mutant deficient in calmodulin binding (A303R) fails to dissociate from F-actin after ionomycin addition.	bind
5529	3	2026	6	10	NULL	0	NULL	CaMKII	GP	mutant	is deficient in			A303R		calmodulin	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_science_284_5411_162_s_143	10102820	( E) A GFP-beta-CaMKII mutant deficient in calmodulin binding (A303R) fails to dissociate from F-actin after ionomycin addition.	bind
4243	1	2026	7	10	NULL	0	NULL	GFP-beta-CaMKII 	GP	mutant	does not dissociate			A303R		F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5411_162_s_143	10102820	( E) A GFP-beta-CaMKII mutant deficient in calmodulin binding (A303R) fails to dissociate from F-actin after ionomycin addition.	bind
4244	2	2026	7	10	NULL	0	NULL	GFP-beta-CaMKII	GP	mutant	is deficient in			A303R		calmodulin 	GP	 binding of			NULL		NULL	NULL	NULL	NULL	gw60_science_284_5411_162_s_143	10102820	( E) A GFP-beta-CaMKII mutant deficient in calmodulin binding (A303R) fails to dissociate from F-actin after ionomycin addition.	bind
4245	3	2026	7	10	NULL	0	NULL	statement 1	Process		occurs after					ionomycin 	Chemical	addition of			NULL		NULL	NULL	NULL	NULL	gw60_science_284_5411_162_s_143	10102820	( E) A GFP-beta-CaMKII mutant deficient in calmodulin binding (A303R) fails to dissociate from F-actin after ionomycin addition.	bind
2797	1	2027	6	10	NULL	0	NULL	isocitrate	Chemical		bind					IDH1	GP		regulatory binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_12864_s_275	12562755	( E) A prerequisite for binding of AMP is binding of isocitrate by the IDH1 regulatory binding site.	bind
2798	2	2027	6	10	NULL	0	NULL	statement 1	Process		is prerequisite for					AMP	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_12864_s_275	12562755	( E) A prerequisite for binding of AMP is binding of isocitrate by the IDH1 regulatory binding site.	bind
4246	1	2027	7	10	NULL	0	NULL	IDH1 	GP		bind			regulatory binding site		isocitrate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_12864_s_275	12562755	( E) A prerequisite for binding of AMP is binding of isocitrate by the IDH1 regulatory binding site.	bind
4247	2	2027	7	10	NULL	0	NULL	statement 1	Process		is prerequisite					AMP	GP	for binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_12864_s_275	12562755	( E) A prerequisite for binding of AMP is binding of isocitrate by the IDH1 regulatory binding site.	bind
2799	1	2028	6	10	NULL	0	NULL	forskolin/TCDD-induced complex	GP		bind									DRE	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_26_9218_s_69	15972329	( E) AHR and ARNT proteins are present in the forskolin/TCDD-induced complex bound to  DRE.	bind
2800	2	2028	6	10	NULL	0	NULL	AHR protein	GP		present in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_26_9218_s_69	15972329	( E) AHR and ARNT proteins are present in the forskolin/TCDD-induced complex bound to  DRE.	bind
2801	3	2028	6	10	NULL	0	NULL	ARNT protein	GP		present in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_26_9218_s_69	15972329	( E) AHR and ARNT proteins are present in the forskolin/TCDD-induced complex bound to  DRE.	bind
4297	1	2028	7	10	NULL	0	NULL	forskolin/TCDD-induced complex	GP		bind									DRE	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_26_9218_s_69	15972329	( E) AHR and ARNT proteins are present in the forskolin/TCDD-induced complex bound to  DRE.	bind
4298	2	2028	7	10	NULL	0	NULL	AHR proteins	GP		 present in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_26_9218_s_69	15972329	( E) AHR and ARNT proteins are present in the forskolin/TCDD-induced complex bound to  DRE.	bind
4299	3	2028	7	10	NULL	0	NULL	ARNT proteins	GP		 present in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_26_9218_s_69	15972329	( E) AHR and ARNT proteins are present in the forskolin/TCDD-induced complex bound to  DRE.	bind
2802	1	2030	6	10	NULL	0	NULL	ASK1	GP		bind					AIP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_111_12_1933_s_289	12813029	( e) ASK1 binding and the GAP activity of AIP1 are required for AIP1-enhanced ASK1 activation.	bind
2803	2	2030	6	10	NULL	0	NULL	AIP1	GP		activates					GAP	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_111_12_1933_s_289	12813029	( e) ASK1 binding and the GAP activity of AIP1 are required for AIP1-enhanced ASK1 activation.	bind
2804	4	2030	6	10	NULL	0	NULL	statement 1	Process		is required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_111_12_1933_s_289	12813029	( e) ASK1 binding and the GAP activity of AIP1 are required for AIP1-enhanced ASK1 activation.	bind
2805	5	2030	6	10	NULL	0	NULL	statement 2	Process		is required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_111_12_1933_s_289	12813029	( e) ASK1 binding and the GAP activity of AIP1 are required for AIP1-enhanced ASK1 activation.	bind
45805	3	2030	6	10	NULL	0	NULL	AIP1	GP		enhance					ASK1	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_111_12_1933_s_289	12813029	( e) ASK1 binding and the GAP activity of AIP1 are required for AIP1-enhanced ASK1 activation.	bind
4248	1	2030	7	10	NULL	0	NULL	ASK1	GP		bind					AIP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_111_12_1933_s_289	12813029	( e) ASK1 binding and the GAP activity of AIP1 are required for AIP1-enhanced ASK1 activation.	bind
4249	2	2030	7	10	NULL	0	NULL	AIP1	Chemical		activates					GAP	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_111_12_1933_s_289	12813029	( e) ASK1 binding and the GAP activity of AIP1 are required for AIP1-enhanced ASK1 activation.	bind
4250	3	2030	7	10	NULL	0	NULL	AIP1	GP		enhance					ASK1	GP	activation of 			NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_111_12_1933_s_289	12813029	( e) ASK1 binding and the GAP activity of AIP1 are required for AIP1-enhanced ASK1 activation.	bind
4251	4	2030	7	10	NULL	0	NULL	statement 1	Process		is required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_111_12_1933_s_289	12813029	( e) ASK1 binding and the GAP activity of AIP1 are required for AIP1-enhanced ASK1 activation.	bind
4252	5	2030	7	10	NULL	0	NULL	statement 2	Process		is required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_111_12_1933_s_289	12813029	( e) ASK1 binding and the GAP activity of AIP1 are required for AIP1-enhanced ASK1 activation.	bind
2806	1	2031	6	10	NULL	0	NULL	Stat1	GP		associates 					Runx2	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_16_1979_s_184	12923053	( E) Association of Stat1 and Stat1CYF with Runx2 and the effect of  IFN-gamma on their phosphorylation and interaction.	bind
2807	2	2031	6	10	NULL	0	NULL	Stat1CYF	GP		associates 					Runx2	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_16_1979_s_184	12923053	( E) Association of Stat1 and Stat1CYF with Runx2 and the effect of  IFN-gamma on their phosphorylation and interaction.	bind
4300	1	2031	7	10	NULL	0	NULL	Stat1	GP		associate with					Runx2	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_16_1979_s_184	12923053	( E) Association of Stat1 and Stat1CYF with Runx2 and the effect of  IFN-gamma on their phosphorylation and interaction.	bind
4301	2	2031	7	10	NULL	0	NULL	Stat1CYF 	GP		associates with					Runx2	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_16_1979_s_184	12923053	( E) Association of Stat1 and Stat1CYF with Runx2 and the effect of  IFN-gamma on their phosphorylation and interaction.	bind
2808	1	2033	6	10	NULL	0	NULL	plasminogen	GP	125I-labeled	bind					ATP synthase	GP	human	alpha subunit		NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_6_2811_s_201	10077593	( E) Binding of 0.5 muM 125I-labeled plasminogen to the alpha-subunit of human ATP synthase.	bind
4306	1	2033	7	10	NULL	0	NULL	plasminogen	GP	125I-labeled	bind					ATP synthase	GP	human	alpha-subunit		NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_6_2811_s_201	10077593	( E) Binding of 0.5 muM 125I-labeled plasminogen to the alpha-subunit of human ATP synthase.	bind
2809	1	2034	6	10	NULL	0	NULL	EZI	GP	endogenous	bind					STAT3	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw60_embo_21_22_6174_s_120	12426389	( E) Binding of endogenous EZI and STAT3.	bind
4307	1	2034	7	10	NULL	0	NULL	 EZI	GP	endogenous	bind					STAT3	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw60_embo_21_22_6174_s_120	12426389	( E) Binding of endogenous EZI and STAT3.	bind
2810	1	2035	6	10	NULL	0	NULL	GST-beta1	GP		bind					mu2 constructs	GP		core domain (residues 283-394)		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_41_14871_s_111	16192353	( e) Binding of GST beta1 and beta3 to all constructs containing the core domain (residues 283-394) of mu2, whereas  GST-EGFR ( f), which contains a tyrosine type motif, binds to full length mu2	bind
2811	2	2035	6	10	NULL	0	NULL	GST-beta3	GP		bind					mu2 constructs	GP		core domain (residues 283-394)		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_41_14871_s_111	16192353	( e) Binding of GST beta1 and beta3 to all constructs containing the core domain (residues 283-394) of mu2, whereas  GST-EGFR ( f), which contains a tyrosine type motif, binds to full length mu2	bind
2812	3	2035	6	10	NULL	0	NULL	 GST-EGFR	GP		bind					mu2	GP	full length			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_41_14871_s_111	16192353	( e) Binding of GST beta1 and beta3 to all constructs containing the core domain (residues 283-394) of mu2, whereas  GST-EGFR ( f), which contains a tyrosine type motif, binds to full length mu2	bind
51549	3	2035	6	10	NULL	0	NULL	GST-EGFR	GP		contains								tyrosine type motif		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_41_14871_s_111	16192353	( e) Binding of GST beta1 and beta3 to all constructs containing the core domain (residues 283-394) of mu2, whereas  GST-EGFR ( f), which contains a tyrosine type motif, binds to full length mu2	bind
4308	1	2035	7	10	NULL	0	NULL	GST beta1	GP		bind					mu2 constructs	GP		core domain (residues 283-394)		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_41_14871_s_111	16192353	( e) Binding of GST beta1 and beta3 to all constructs containing the core domain (residues 283-394) of mu2, whereas  GST-EGFR ( f), which contains a tyrosine type motif, binds to full length mu2	bind
4309	2	2035	7	10	NULL	0	NULL	GST-beta3 	GP		bind					mu2 constructs	GP		core domain (residues 283-394)		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_41_14871_s_111	16192353	( e) Binding of GST beta1 and beta3 to all constructs containing the core domain (residues 283-394) of mu2, whereas  GST-EGFR ( f), which contains a tyrosine type motif, binds to full length mu2	bind
4310	3	2035	7	10	NULL	0	NULL	GST-EGFR	GP		bind					mu2	GP	full length 			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_41_14871_s_111	16192353	( e) Binding of GST beta1 and beta3 to all constructs containing the core domain (residues 283-394) of mu2, whereas  GST-EGFR ( f), which contains a tyrosine type motif, binds to full length mu2	bind
51550	4	2035	7	10	NULL	0	NULL	GST-EGFR	GP		contains								tyrosine type motif		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_41_14871_s_111	16192353	( e) Binding of GST beta1 and beta3 to all constructs containing the core domain (residues 283-394) of mu2, whereas  GST-EGFR ( f), which contains a tyrosine type motif, binds to full length mu2	bind
2813	1	2036	6	10	NULL	0	NULL	SF	GP	iodinated;;uncleavable	bind					A549	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_10_1418_s_61	15545993	( E) Binding of iodinated uncleavable SF to A549 human lung carcinoma cells.	bind
2814	2	2036	6	10	NULL	0	NULL	A549	Cell		is 					human lung carcinoma cells.	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_10_1418_s_61	15545993	( E) Binding of iodinated uncleavable SF to A549 human lung carcinoma cells.	bind
4311	1	2036	7	10	NULL	0	NULL	SF	GP	iodinated;;uncleavable	bind					A549	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_10_1418_s_61	15545993	( E) Binding of iodinated uncleavable SF to A549 human lung carcinoma cells.	bind
45806	2	2036	7	10	NULL	0	NULL	A549	Cell		is					human lung carcinoma cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_10_1418_s_61	15545993	( E) Binding of iodinated uncleavable SF to A549 human lung carcinoma cells.	bind
2815	1	2037	6	10	NULL	0	NULL	ORCA2	GP		bind					Str 	GP			RV fragment of promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_18_16_4455_s_152	10449411	( E) Binding of ORCA2 to the RV fragment of the  Str promoter.	bind
4312	1	2037	7	10	NULL	0	NULL	ORCA2	GP		bind					Str	GP			RV fragment of promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_18_16_4455_s_152	10449411	( E) Binding of ORCA2 to the RV fragment of the  Str promoter.	bind
2816	1	2038	6	10	NULL	0	NULL	p53	GP		bind					p38 kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6845_s_97	10581258	( E) Binding of p53 and p38 kinase.	bind
4313	1	2038	7	10	NULL	0	NULL	p53	GP		bind					p38 kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6845_s_97	10581258	( E) Binding of p53 and p38 kinase.	bind
2817	1	2039	6	10	NULL	0	NULL	PARP	GP		bind									cis-element	NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_1_48_s_177	11134536	( E) Binding of PARP to the  cis-element in GMSA.	bind
4314	1	2039	7	10	NULL	0	NULL	PARP	GP		bind									cis-element	NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_1_48_s_177	11134536	( E) Binding of PARP to the  cis-element in GMSA.	bind
2818	1	2040	6	10	NULL	0	NULL	CtBP	GP	recombinant	bind					GST-ZEB	GP		595-720		NULL		NULL	NULL	NULL	NULL	gw60_science_295_5561_1895_s_24	11847309	( E) Binding of recombinant CtBP to GST-ZEB595-720 at various concentrations of NAD+ and NADH.       [View Larger Version of this Image (76K GIF file)]	bind
4315	1	2040	7	10	NULL	0	NULL	CtBP	GP	recombinant	bind					GST-ZEB	GP		595-720		NULL		NULL	NULL	NULL	NULL	gw60_science_295_5561_1895_s_24	11847309	( E) Binding of recombinant CtBP to GST-ZEB595-720 at various concentrations of NAD+ and NADH.       [View Larger Version of this Image (76K GIF file)]	bind
2819	1	2041	6	10	NULL	0	NULL	IMP1	GP	recombinant	bind					CD44 mRNA	NucleicAcid			3'UTR 	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_7_1456_s_227	16541107	( E) Binding of recombinant IMP1 to the 3'UTR of  CD44 mRNA.	bind
4316	1	2041	7	10	NULL	0	NULL	IMP1	GP	recombinant	bind					CD44 mRNA	NucleicAcid			 3'UTR 	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_7_1456_s_227	16541107	( E) Binding of recombinant IMP1 to the 3'UTR of  CD44 mRNA.	bind
2886	1	2042	6	10	NULL	0	NULL	VDR	GP	recombinant	bind					DR3 oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2269_s_90	15849313	( E) Binding of recombinant VDR and RXR (100 ng) alone and in combination with the DR3  and DRE oligonucleotides.	bind
2887	2	2042	6	10	NULL	0	NULL	VDR	GP	recombinant	bind					DRE oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2269_s_90	15849313	( E) Binding of recombinant VDR and RXR (100 ng) alone and in combination with the DR3  and DRE oligonucleotides.	bind
2888	3	2042	6	10	NULL	0	NULL	RXR	GP	recombinant	bind					DR3 oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2269_s_90	15849313	( E) Binding of recombinant VDR and RXR (100 ng) alone and in combination with the DR3  and DRE oligonucleotides.	bind
2889	4	2042	6	10	NULL	0	NULL	RXR	GP	recombinant	bind					DRE oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2269_s_90	15849313	( E) Binding of recombinant VDR and RXR (100 ng) alone and in combination with the DR3  and DRE oligonucleotides.	bind
46180	5	2042	6	10	NULL	0	NULL	VDR-RXR	GP	recombinant	bind					DR3 oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2269_s_90	15849313	( E) Binding of recombinant VDR and RXR (100 ng) alone and in combination with the DR3  and DRE oligonucleotides.	bind
46181	6	2042	6	10	NULL	0	NULL	VDR-RXR	GP	recombinant	bind					DRE oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2269_s_90	15849313	( E) Binding of recombinant VDR and RXR (100 ng) alone and in combination with the DR3  and DRE oligonucleotides.	bind
4318	2	2042	7	10	NULL	0	NULL	VDR	GP	recombinant	binds					DR3 oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2269_s_90	15849313	( E) Binding of recombinant VDR and RXR (100 ng) alone and in combination with the DR3  and DRE oligonucleotides.	bind
4319	3	2042	7	10	NULL	0	NULL	VDR	GP	recombinant	binds					DRE oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2269_s_90	15849313	( E) Binding of recombinant VDR and RXR (100 ng) alone and in combination with the DR3  and DRE oligonucleotides.	bind
4666	4	2042	7	10	NULL	0	NULL	RXR	GP	recombinant	binds					DR3 oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2269_s_90	15849313	( E) Binding of recombinant VDR and RXR (100 ng) alone and in combination with the DR3  and DRE oligonucleotides.	bind
4667	5	2042	7	10	NULL	0	NULL	RXR	GP	recombinant	binds					DRE oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2269_s_90	15849313	( E) Binding of recombinant VDR and RXR (100 ng) alone and in combination with the DR3  and DRE oligonucleotides.	bind
46280	6	2042	7	10	NULL	0	NULL	VDR-RXR	GP	recombinant	bind					DR3 oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2269_s_90	15849313	( E) Binding of recombinant VDR and RXR (100 ng) alone and in combination with the DR3  and DRE oligonucleotides.	bind
46281	1	2042	7	10	NULL	0	NULL	VDR-RXR	GP	recombinant	bind					DRE oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2269_s_90	15849313	( E) Binding of recombinant VDR and RXR (100 ng) alone and in combination with the DR3  and DRE oligonucleotides.	bind
2890	1	2043	6	10	NULL	0	NULL	rML-LBP21	GP		bind					laminin alpha2 chain	GP		rG domain		NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_17_9857_s_189	10449784	( E) Binding of rML-LBP21 to the rG domain of laminin alpha2 chain in ELISA.	bind
4320	1	2043	7	10	NULL	0	NULL	rML-LBP21	GP		bind					laminin alpha2 chain	GP		 rG domain		NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_17_9857_s_189	10449784	( E) Binding of rML-LBP21 to the rG domain of laminin alpha2 chain in ELISA.	bind
2892	1	2045	6	10	NULL	0	NULL	FGF-7	GP	soluble	bind					perlecan	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1599_s_189	9788974	( E) Binding of soluble FGF-7 to immobilized perlecan before and after heparitinase ( HSase) treatment.	bind
45807	2	2045	6	10	NULL	0	NULL	heparitinase \t	GP		is					HSase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1599_s_189	9788974	( E) Binding of soluble FGF-7 to immobilized perlecan before and after heparitinase ( HSase) treatment.	bind
4323	1	2045	7	10	NULL	0	NULL	FGF-7	GP	soluble	bind					perlecan	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1599_s_189	9788974	( E) Binding of soluble FGF-7 to immobilized perlecan before and after heparitinase ( HSase) treatment.	bind
4324	2	2045	7	10	NULL	0	NULL	heparitinase	GP		is					HSase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_8_1599_s_189	9788974	( E) Binding of soluble FGF-7 to immobilized perlecan before and after heparitinase ( HSase) treatment.	bind
2894	1	2046	6	10	NULL	0	NULL	sperm proteins	GP		bind					ZP	CellComponent	biotinylated			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_50_18028_s_154	16330764	( E) Binding of sperm proteins to biotinylated ZP.	bind
4325	1	2046	7	10	NULL	0	NULL	sperm proteins	GP		bind					ZP	CellComponent	biotinylated			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_50_18028_s_154	16330764	( E) Binding of sperm proteins to biotinylated ZP.	bind
2895	1	2047	6	10	NULL	0	NULL	TMEFF1	GP		bind					Cripto	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_21_2624_s_57	14563676	( E) Binding of TMEFF1 to Cripto reduces the association of ALK4 with Cripto.	bind
2896	2	2047	6	10	NULL	0	NULL	ALK4	GP		bind					Cripto	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_21_2624_s_57	14563676	( E) Binding of TMEFF1 to Cripto reduces the association of ALK4 with Cripto.	bind
2897	3	2047	6	10	NULL	0	NULL	statement 1	Process		reduces					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_21_2624_s_57	14563676	( E) Binding of TMEFF1 to Cripto reduces the association of ALK4 with Cripto.	bind
4326	1	2047	7	10	NULL	0	NULL	TMEFF1	GP		bind					Cripto	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_21_2624_s_57	14563676	( E) Binding of TMEFF1 to Cripto reduces the association of ALK4 with Cripto.	bind
4327	2	2047	7	10	NULL	0	NULL	 ALK4	GP		bind					Cripto	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_21_2624_s_57	14563676	( E) Binding of TMEFF1 to Cripto reduces the association of ALK4 with Cripto.	bind
4328	3	2047	7	10	NULL	0	NULL	statement 1	Process		reduce  					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_21_2624_s_57	14563676	( E) Binding of TMEFF1 to Cripto reduces the association of ALK4 with Cripto.	bind
2898	1	2049	6	10	NULL	0	NULL	rML-LBP21	GP		bind					alpha2-laminins	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_17_9857_s_51	10449784	( E) Characterization of rML-LBP21 binding to alpha2-laminins.	bind
4329	1	2049	7	10	NULL	0	NULL	rML-LBP21	GP		binds to					alpha2-laminins	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_17_9857_s_51	10449784	( E) Characterization of rML-LBP21 binding to alpha2-laminins.	bind
2909	1	2050	6	10	NULL	0	NULL	Pol II	GP		bind			delta5		c-myc 	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5139_s_63	16157863	( E) ChIP analysis revealed similar binding of Pol II delta5 and Pol II wt to the c- myc promoter (lanes 3 and 11, respectively), while binding was not detectable in the  Mock cell line (lane 7), or ( F) to a non-transcribed region in the insulin gene.	bind
2910	2	2050	6	10	NULL	0	NULL	Pol II	GP	wt	bind					c-myc 	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5139_s_63	16157863	( E) ChIP analysis revealed similar binding of Pol II delta5 and Pol II wt to the c- myc promoter (lanes 3 and 11, respectively), while binding was not detectable in the  Mock cell line (lane 7), or ( F) to a non-transcribed region in the insulin gene.	bind
2913	3	2050	6	10	NULL	0	NULL	statement 1	Process		is not detected in					Mock cell line	Cell				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5139_s_63	16157863	( E) ChIP analysis revealed similar binding of Pol II delta5 and Pol II wt to the c- myc promoter (lanes 3 and 11, respectively), while binding was not detectable in the  Mock cell line (lane 7), or ( F) to a non-transcribed region in the insulin gene.	bind
2914	4	2050	6	10	NULL	0	NULL	statement 2	Process		is not detected in					Mock cell line	Cell				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5139_s_63	16157863	( E) ChIP analysis revealed similar binding of Pol II delta5 and Pol II wt to the c- myc promoter (lanes 3 and 11, respectively), while binding was not detectable in the  Mock cell line (lane 7), or ( F) to a non-transcribed region in the insulin gene.	bind
2916	5	2050	6	10	NULL	0	NULL	statement 1	Process		is not detected in					insulin gene	GP			non transcribed region	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5139_s_63	16157863	( E) ChIP analysis revealed similar binding of Pol II delta5 and Pol II wt to the c- myc promoter (lanes 3 and 11, respectively), while binding was not detectable in the  Mock cell line (lane 7), or ( F) to a non-transcribed region in the insulin gene.	bind
2917	6	2050	6	10	NULL	0	NULL	statement 2	Process		is not detected in					insulin gene	GP			non transcribed region	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5139_s_63	16157863	( E) ChIP analysis revealed similar binding of Pol II delta5 and Pol II wt to the c- myc promoter (lanes 3 and 11, respectively), while binding was not detectable in the  Mock cell line (lane 7), or ( F) to a non-transcribed region in the insulin gene.	bind
4330	1	2050	7	10	NULL	0	NULL	Pol II 	GP		bind			delta5		c- myc	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5139_s_63	16157863	( E) ChIP analysis revealed similar binding of Pol II delta5 and Pol II wt to the c- myc promoter (lanes 3 and 11, respectively), while binding was not detectable in the  Mock cell line (lane 7), or ( F) to a non-transcribed region in the insulin gene.	bind
4331	2	2050	7	10	NULL	0	NULL	Pol II	GP	wt	bind					c- myc	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5139_s_63	16157863	( E) ChIP analysis revealed similar binding of Pol II delta5 and Pol II wt to the c- myc promoter (lanes 3 and 11, respectively), while binding was not detectable in the  Mock cell line (lane 7), or ( F) to a non-transcribed region in the insulin gene.	bind
4332	3	2050	7	10	NULL	0	NULL	statement 1	Process		not detected in					Mock cell line	Cell				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5139_s_63	16157863	( E) ChIP analysis revealed similar binding of Pol II delta5 and Pol II wt to the c- myc promoter (lanes 3 and 11, respectively), while binding was not detectable in the  Mock cell line (lane 7), or ( F) to a non-transcribed region in the insulin gene.	bind
4333	4	2050	7	10	NULL	0	NULL	statement 2	Process		not detected in					Mock cell line	Cell				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5139_s_63	16157863	( E) ChIP analysis revealed similar binding of Pol II delta5 and Pol II wt to the c- myc promoter (lanes 3 and 11, respectively), while binding was not detectable in the  Mock cell line (lane 7), or ( F) to a non-transcribed region in the insulin gene.	bind
4334	5	2050	7	10	NULL	0	NULL	statement 1	Process		not detected in					insulin gene	GP			non-transcribed region in	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5139_s_63	16157863	( E) ChIP analysis revealed similar binding of Pol II delta5 and Pol II wt to the c- myc promoter (lanes 3 and 11, respectively), while binding was not detectable in the  Mock cell line (lane 7), or ( F) to a non-transcribed region in the insulin gene.	bind
4335	6	2050	7	10	NULL	0	NULL	statement 2	Process		not detected in					insulin gene	GP			non-transcribed region in	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5139_s_63	16157863	( E) ChIP analysis revealed similar binding of Pol II delta5 and Pol II wt to the c- myc promoter (lanes 3 and 11, respectively), while binding was not detectable in the  Mock cell line (lane 7), or ( F) to a non-transcribed region in the insulin gene.	bind
2922	1	2051	6	10	NULL	0	NULL	CIITA	GP		bind					GTP	Chemical				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_science_285_5432_1402_s_62	10464099	( E) CIITA binds GTP in vivo.	bind
4336	1	2051	7	10	NULL	0	NULL	CIITA	GP		bind					GTP	Chemical				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_science_285_5432_1402_s_62	10464099	( E) CIITA binds GTP in vivo.	bind
2924	1	2052	6	10	NULL	0	NULL	Topotecan	GP		bind					enzyme-substrate complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_24_15387_s_71	12426403	( E) Comparison of the 22-mer duplex oligonucleotides of the drug-bound (blue) and nondrug-bound (yellow) complexes reveals that Topotecan (CPK) binds to the enzyme-substrate complex by intercalating in the DNA and shifting the downstream bases by  3.6  Ang , equivalent to the rise of one base pair.	bind
45808	2	2052	6	10	NULL	0	NULL	Topotecan	GP		is					CPK	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_24_15387_s_71	12426403	( E) Comparison of the 22-mer duplex oligonucleotides of the drug-bound (blue) and nondrug-bound (yellow) complexes reveals that Topotecan (CPK) binds to the enzyme-substrate complex by intercalating in the DNA and shifting the downstream bases by  3.6  Ang , equivalent to the rise of one base pair.	bind
4339	4	2052	7	10	NULL	0	NULL	Topotecan	GP		binds to					enzyme-substrate complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_24_15387_s_71	12426403	( E) Comparison of the 22-mer duplex oligonucleotides of the drug-bound (blue) and nondrug-bound (yellow) complexes reveals that Topotecan (CPK) binds to the enzyme-substrate complex by intercalating in the DNA and shifting the downstream bases by  3.6  Ang , equivalent to the rise of one base pair.	bind
4347	10	2052	7	10	NULL	0	NULL	Topotecan	GP		is					CPK	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_24_15387_s_71	12426403	( E) Comparison of the 22-mer duplex oligonucleotides of the drug-bound (blue) and nondrug-bound (yellow) complexes reveals that Topotecan (CPK) binds to the enzyme-substrate complex by intercalating in the DNA and shifting the downstream bases by  3.6  Ang , equivalent to the rise of one base pair.	bind
2925	1	2053	6	10	NULL	0	NULL	antihormones	Chemical	synthetic	bind					mPRgamma protein	GP	recombinant;;human			NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_5_2237_s_152	12601167	( e) Competition curves of binding of synthetic antihormones to the recombinant human mPRgamma protein.	bind
4348	1	2053	7	10	NULL	0	NULL	antihormones	Chemical	synthetic	binds to					mPRgamma protein	GP	recombinant;;human			NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_5_2237_s_152	12601167	( e) Competition curves of binding of synthetic antihormones to the recombinant human mPRgamma protein.	bind
2926	1	2054	6	10	NULL	0	NULL	GTP	Chemical		bind					Rac1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1133_s_315	12697733	( e) Competition of GTP binding to Rac1 or Ras by 6-Thio-GTP.	bind
2927	2	2054	6	10	NULL	0	NULL	GTP	Chemical		bind					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1133_s_315	12697733	( e) Competition of GTP binding to Rac1 or Ras by 6-Thio-GTP.	bind
2929	3	2054	6	10	NULL	0	NULL	6-Thio-GTP	Chemical		bind					Rac1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1133_s_315	12697733	( e) Competition of GTP binding to Rac1 or Ras by 6-Thio-GTP.	bind
2930	4	2054	6	10	NULL	0	NULL	6-Thio-GTP	Chemical		bind					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1133_s_315	12697733	( e) Competition of GTP binding to Rac1 or Ras by 6-Thio-GTP.	bind
3393	5	2054	6	10	NULL	0	NULL	statement 3	Process		competes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1133_s_315	12697733	( e) Competition of GTP binding to Rac1 or Ras by 6-Thio-GTP.	bind
46329	6	2054	6	10	NULL	0	NULL	statement 4	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1133_s_315	12697733	( e) Competition of GTP binding to Rac1 or Ras by 6-Thio-GTP.	bind
4349	1	2054	7	10	NULL	0	NULL	GTP	Chemical		binds to					Rac1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1133_s_315	12697733	( e) Competition of GTP binding to Rac1 or Ras by 6-Thio-GTP.	bind
4350	2	2054	7	10	NULL	0	NULL	GTP	Chemical		binds to					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1133_s_315	12697733	( e) Competition of GTP binding to Rac1 or Ras by 6-Thio-GTP.	bind
4351	3	2054	7	10	NULL	0	NULL	6-Thio-GTP	Chemical		binds to					Rac1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1133_s_315	12697733	( e) Competition of GTP binding to Rac1 or Ras by 6-Thio-GTP.	bind
4352	4	2054	7	10	NULL	0	NULL	6-Thio-GTP	Chemical		binds to					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1133_s_315	12697733	( e) Competition of GTP binding to Rac1 or Ras by 6-Thio-GTP.	bind
4353	5	2054	7	10	NULL	0	NULL	statement 3	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1133_s_315	12697733	( e) Competition of GTP binding to Rac1 or Ras by 6-Thio-GTP.	bind
4354	6	2054	7	10	NULL	0	NULL	statement 4	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_111_8_1133_s_315	12697733	( e) Competition of GTP binding to Rac1 or Ras by 6-Thio-GTP.	bind
2931	1	2055	6	10	NULL	0	NULL				bind			F-actin-binding domains		F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_26_14865_s_159	11752434	( E) Competitive binding of F-actin-binding domains to F-actin.	bind
4355	1	2055	7	10	NULL	0	NULL				binds to			F-actin-binding domains		F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_26_14865_s_159	11752434	( E) Competitive binding of F-actin-binding domains to F-actin.	bind
2932	1	2057	6	10	NULL	0	NULL	CHO cells	Cell		express					beta3	GP	WT			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_43	12730600	( E) Constitutive fibrinogen binding to CHO cells expressing WT beta3 and the indicated beta3 mutants.	bind
2934	2	2057	6	10	NULL	0	NULL	CHO cells	Cell		express					beta3 	GP	mutants			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_43	12730600	( E) Constitutive fibrinogen binding to CHO cells expressing WT beta3 and the indicated beta3 mutants.	bind
2935	3	2057	6	10	NULL	0	NULL	fibrinogen	GP		bind		constitutively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_43	12730600	( E) Constitutive fibrinogen binding to CHO cells expressing WT beta3 and the indicated beta3 mutants.	bind
2936	4	2057	6	10	NULL	0	NULL	fibrinogen	GP		bind		constitutively			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_43	12730600	( E) Constitutive fibrinogen binding to CHO cells expressing WT beta3 and the indicated beta3 mutants.	bind
4668	1	2057	7	10	NULL	0	NULL	CHO cells 	Cell		express					 beta3	GP	WT			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_43	12730600	( E) Constitutive fibrinogen binding to CHO cells expressing WT beta3 and the indicated beta3 mutants.	bind
4669	2	2057	7	10	NULL	0	NULL	CHO cells	Cell		bind					beta3 	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_43	12730600	( E) Constitutive fibrinogen binding to CHO cells expressing WT beta3 and the indicated beta3 mutants.	bind
4670	3	2057	7	10	NULL	0	NULL	fibrinogen	GP		binds to		constitutively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_43	12730600	( E) Constitutive fibrinogen binding to CHO cells expressing WT beta3 and the indicated beta3 mutants.	bind
4671	4	2057	7	10	NULL	0	NULL	fibrinogen	GP		binds to		constitutively			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_43	12730600	( E) Constitutive fibrinogen binding to CHO cells expressing WT beta3 and the indicated beta3 mutants.	bind
2938	1	2058	6	10	NULL	0	NULL	CREB	GP		bind					nNOS	GP			CRE	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8617_s_170	10900019	( E) CREB and ATF-2 bind to nNOS CRE.	bind
2940	2	2058	6	10	NULL	0	NULL	ATF-2	GP		bind					nNOS	GP			CRE	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8617_s_170	10900019	( E) CREB and ATF-2 bind to nNOS CRE.	bind
4672	1	2058	7	10	NULL	0	NULL	CREB	GP		bind					nNOS	GP			CRE	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8617_s_170	10900019	( E) CREB and ATF-2 bind to nNOS CRE.	bind
4673	2	2058	7	10	NULL	0	NULL	ATF-2 	GP		bind					nNOS	GP			CRE	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8617_s_170	10900019	( E) CREB and ATF-2 bind to nNOS CRE.	bind
2941	1	2059	6	10	NULL	0	NULL	CTCF	GP		bind					Tsix	GP				NULL	in vivo female fibroblasts	NULL	NULL	NULL	NULL	gw60_science_295_5553_345_s_77	11743158	( E) CTCF binds  Tsix in vivo (female fibroblasts) using ChIP analysis as described ( 28).	bind
4674	1	2059	7	10	NULL	0	NULL	CTCF	GP		bind					 Tsix	GP				NULL	in vivo female fibroblasts	NULL	NULL	NULL	NULL	gw60_science_295_5553_345_s_77	11743158	( E) CTCF binds  Tsix in vivo (female fibroblasts) using ChIP analysis as described ( 28).	bind
2942	1	2060	6	10	NULL	0	NULL	DCX	GP		favors					13pf MTs	CellComponent	polymerization of			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_19_4448_s_61	16957770	( E) DCX favours polymerisation of 13pf MTs independent of the guanine nucleotide bound  to beta-tubulin.	bind
2944	2	2060	6	10	NULL	0	NULL	guanine nucleotide	NucleicAcid		bind					beta-tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_19_4448_s_61	16957770	( E) DCX favours polymerisation of 13pf MTs independent of the guanine nucleotide bound  to beta-tubulin.	bind
2945	3	2060	6	10	NULL	0	NULL	statement 1	Process		is independent of					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_19_4448_s_61	16957770	( E) DCX favours polymerisation of 13pf MTs independent of the guanine nucleotide bound  to beta-tubulin.	bind
4675	1	2060	7	10	NULL	0	NULL	DCX	GP		favours					13pf MTs	CellComponent	polymerisation of			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_19_4448_s_61	16957770	( E) DCX favours polymerisation of 13pf MTs independent of the guanine nucleotide bound  to beta-tubulin.	bind
4676	2	2060	7	10	NULL	0	NULL	guanine nucleotide	NucleicAcid		bind					beta-tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_19_4448_s_61	16957770	( E) DCX favours polymerisation of 13pf MTs independent of the guanine nucleotide bound  to beta-tubulin.	bind
4677	3	2060	7	10	NULL	0	NULL	statement 1	Process		is independent of					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_19_4448_s_61	16957770	( E) DCX favours polymerisation of 13pf MTs independent of the guanine nucleotide bound  to beta-tubulin.	bind
2946	1	2061	6	10	NULL	0	NULL	CREB	GP		bind					D-loop DNA	NucleicAcid	mitochondrial			NULL	in vivo in mouse primary cultures	NULL	NULL	NULL	NULL	gw70_pnas_102_39_13915_s_191	16169904	( E) DFO modulates  in vivo CREB binding to the mitochondrial D-loop DNA in mouse primary cultures.	bind
2949	2	2061	6	10	NULL	0	NULL	DFO	Chemical		modulates					statement 1	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_pnas_102_39_13915_s_191	16169904	( E) DFO modulates  in vivo CREB binding to the mitochondrial D-loop DNA in mouse primary cultures.	bind
4679	1	2061	7	10	NULL	0	NULL	CREB	GP		binds to					D-loop DNA	NucleicAcid	mitochondrial			NULL	in vivo in mouse primary cultures	NULL	NULL	NULL	NULL	gw70_pnas_102_39_13915_s_191	16169904	( E) DFO modulates  in vivo CREB binding to the mitochondrial D-loop DNA in mouse primary cultures.	bind
4680	2	2061	7	10	NULL	0	NULL	DFO	Chemical		modulates					statement 1	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_pnas_102_39_13915_s_191	16169904	( E) DFO modulates  in vivo CREB binding to the mitochondrial D-loop DNA in mouse primary cultures.	bind
2952	1	2062	6	10	NULL	0	NULL	TLX	GP		bind		directly			Plce1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_10_1308_s_217	16702404	( E) Direct binding of TLX to the  Plce1 promoter was determined by gel shift assays as described in Figure  6F.	bind
4681	1	2062	7	10	NULL	0	NULL	TLX	GP		binds		directly			Plce1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_10_1308_s_217	16702404	( E) Direct binding of TLX to the  Plce1 promoter was determined by gel shift assays as described in Figure  6F.	bind
2961	1	2063	6	10	NULL	0	NULL	fusion proteins	GP		bind			GST-PDZ domain		synaptojanin 2A 	GP		C-terminal peptide		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_11_2991_s_80	10357812	( E) Dose-response curves of binding of GST-PDZ domain fusion proteins to the synaptojanin 2A C-terminal peptide in an ELISA assay.	bind
4682	1	2063	7	10	NULL	0	NULL	fusion proteins	GP		binds			GST-PDZ domain		synaptojanin 2A	GP		C-terminal peptide		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_11_2991_s_80	10357812	( E) Dose-response curves of binding of GST-PDZ domain fusion proteins to the synaptojanin 2A C-terminal peptide in an ELISA assay.	bind
2962	1	2064	6	10	NULL	0	NULL	Ecsit 2	GP		bind					Tlx2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_23_2933_s_249	14633973	( E) Ecsit 2, Smad1, and Smad4 bind to the  Tlx2 promoter.	bind
2963	2	2064	6	10	NULL	0	NULL	Smad1	GP		bind					Tlx2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_23_2933_s_249	14633973	( E) Ecsit 2, Smad1, and Smad4 bind to the  Tlx2 promoter.	bind
2964	3	2064	6	10	NULL	0	NULL	Smad4	GP		bind					Tlx2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_23_2933_s_249	14633973	( E) Ecsit 2, Smad1, and Smad4 bind to the  Tlx2 promoter.	bind
4685	1	2064	7	10	NULL	0	NULL	Ecsit 2	GP		binds					Tlx2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_23_2933_s_249	14633973	( E) Ecsit 2, Smad1, and Smad4 bind to the  Tlx2 promoter.	bind
4687	2	2064	7	10	NULL	0	NULL	Smad1	GP		binds					Tlx2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_23_2933_s_249	14633973	( E) Ecsit 2, Smad1, and Smad4 bind to the  Tlx2 promoter.	bind
4688	3	2064	7	10	NULL	0	NULL	Smad4	GP		binds					Tlx2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_23_2933_s_249	14633973	( E) Ecsit 2, Smad1, and Smad4 bind to the  Tlx2 promoter.	bind
2991	1	2065	6	10	NULL	0	NULL	AP-1	GP		bind									CRE	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_29_10194_s_61	16000406	( E) Effect of CHX on AP-1 and CRE binding.	bind
4690	1	2065	7	10	NULL	0	NULL	AP-1	GP		binds									CRE	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_29_10194_s_61	16000406	( E) Effect of CHX on AP-1 and CRE binding.	bind
2992	1	2066	6	10	NULL	0	NULL	E2F4	GP		bind					c-myc 	GP			promoter	NULL	C2C12 cells	NULL	NULL	NULL	NULL	gw60_pnas_100_6_3245_s_124	12629224	( E) Effects of lithium stimulation on binding of E2F4, p130, and HDAC1 to the c- Myc promoter in C2C12 cells.	bind
2993	2	2066	6	10	NULL	0	NULL	p130	GP		bind					c-myc 	GP			promoter	NULL	C2C12 cells	NULL	NULL	NULL	NULL	gw60_pnas_100_6_3245_s_124	12629224	( E) Effects of lithium stimulation on binding of E2F4, p130, and HDAC1 to the c- Myc promoter in C2C12 cells.	bind
2994	3	2066	6	10	NULL	0	NULL	HDAC1	GP		bind					c-myc 	GP			promoter	NULL	C2C12 cells	NULL	NULL	NULL	NULL	gw60_pnas_100_6_3245_s_124	12629224	( E) Effects of lithium stimulation on binding of E2F4, p130, and HDAC1 to the c- Myc promoter in C2C12 cells.	bind
4695	1	2066	7	10	NULL	0	NULL	E2F4	GP		binds					 c- Myc	GP			promoter	NULL	in C2C12 cells	NULL	NULL	NULL	NULL	gw60_pnas_100_6_3245_s_124	12629224	( E) Effects of lithium stimulation on binding of E2F4, p130, and HDAC1 to the c- Myc promoter in C2C12 cells.	bind
4696	2	2066	7	10	NULL	0	NULL	p130	GP		binds					 c- Myc	GP			promoter	NULL	in C2C12 cells	NULL	NULL	NULL	NULL	gw60_pnas_100_6_3245_s_124	12629224	( E) Effects of lithium stimulation on binding of E2F4, p130, and HDAC1 to the c- Myc promoter in C2C12 cells.	bind
4697	3	2066	7	10	NULL	0	NULL	HDAC1	GP		binds					c- myc	GP			promoter	NULL	in C2C12 cells	NULL	NULL	NULL	NULL	gw60_pnas_100_6_3245_s_124	12629224	( E) Effects of lithium stimulation on binding of E2F4, p130, and HDAC1 to the c- Myc promoter in C2C12 cells.	bind
2995	1	2067	6	10	NULL	0	NULL	Emi1	GP		bind					Cdc20	GP		SBR		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_24_3278_s_110	11751633	( E) Emi1 binds the substrate-binding region (SBR) of Cdc20.	bind
3394	2	2067	6	10	NULL	0	NULL	SBR	AminoAcid		is					substrate-binding region	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_24_3278_s_110	11751633	( E) Emi1 binds the substrate-binding region (SBR) of Cdc20.	bind
4699	1	2067	7	10	NULL	0	NULL	Emi1	GP		binds					Cdc20	GP		SBR		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_24_3278_s_110	11751633	( E) Emi1 binds the substrate-binding region (SBR) of Cdc20.	bind
4700	2	2067	7	10	NULL	0	NULL	SBR	AminoAcid		is 					substrate-binding region	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_24_3278_s_110	11751633	( E) Emi1 binds the substrate-binding region (SBR) of Cdc20.	bind
3028	1	2068	6	10	NULL	0	NULL	Nup98-Hoxa9 	GP		bind					Hoxa9 	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_7_1469_s_119	16525506	( E) EMSA. Smad4 dose-dependently inhibits the DNA-binding ability of Nup98-Hoxa9 to   Hoxa9 promoter probe, whether in the absence or in the presence of PBX1a, at molar ratios  of 0.2, 0.4 and 1 of Smad4 compared to Nup98-Hoxa9.	bind
3029	2	2068	6	10	NULL	0	NULL	Smad4	GP		inhibits		dose dependently			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_7_1469_s_119	16525506	( E) EMSA. Smad4 dose-dependently inhibits the DNA-binding ability of Nup98-Hoxa9 to   Hoxa9 promoter probe, whether in the absence or in the presence of PBX1a, at molar ratios  of 0.2, 0.4 and 1 of Smad4 compared to Nup98-Hoxa9.	bind
4701	1	2068	7	10	NULL	0	NULL	Nup98-Hoxa9	GP		binds					Hoxa9	GP			promoter 	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_7_1469_s_119	16525506	( E) EMSA. Smad4 dose-dependently inhibits the DNA-binding ability of Nup98-Hoxa9 to   Hoxa9 promoter probe, whether in the absence or in the presence of PBX1a, at molar ratios  of 0.2, 0.4 and 1 of Smad4 compared to Nup98-Hoxa9.	bind
4702	2	2068	7	10	NULL	0	NULL	Smad4	GP		inhibits		dose-dependently			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_7_1469_s_119	16525506	( E) EMSA. Smad4 dose-dependently inhibits the DNA-binding ability of Nup98-Hoxa9 to   Hoxa9 promoter probe, whether in the absence or in the presence of PBX1a, at molar ratios  of 0.2, 0.4 and 1 of Smad4 compared to Nup98-Hoxa9.	bind
3030	1	2069	6	10	NULL	0	NULL	GATA-1	GP		bind					EKLF	GP			enhancer	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_14_3264_s_260	16858405	( E) GATA-1 binding to the EKLF enhancer is increased when MAPK signalling is inhibited.	bind
3031	2	2069	6	10	NULL	0	NULL	MAPK signalling	Process	inhibition of	increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_14_3264_s_260	16858405	( E) GATA-1 binding to the EKLF enhancer is increased when MAPK signalling is inhibited.	bind
4708	1	2069	7	10	NULL	0	NULL	GATA-1	GP		binds					EKLF 	GP			enhancer	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_14_3264_s_260	16858405	( E) GATA-1 binding to the EKLF enhancer is increased when MAPK signalling is inhibited.	bind
4710	2	2069	7	10	NULL	0	NULL	MAPK signalling	Process	inhibition of	increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_14_3264_s_260	16858405	( E) GATA-1 binding to the EKLF enhancer is increased when MAPK signalling is inhibited.	bind
3032	1	2070	6	10	NULL	0	NULL	Ggamma5	GP		interacts		directly			AEBP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_14_4004_s_142	10406805	( E) Ggamma5 directly interacts with AEBP1 and prevents binding of AEBP1 to AE-1 oligonucleotides.	bind
3033	2	2070	6	10	NULL	0	NULL	AEBP1	GP		bind					AE-1 oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_14_4004_s_142	10406805	( E) Ggamma5 directly interacts with AEBP1 and prevents binding of AEBP1 to AE-1 oligonucleotides.	bind
3034	3	2070	6	10	NULL	0	NULL	statement 1	Process		prevents					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_14_4004_s_142	10406805	( E) Ggamma5 directly interacts with AEBP1 and prevents binding of AEBP1 to AE-1 oligonucleotides.	bind
4713	1	2070	7	10	NULL	0	NULL	Ggamma5	GP		interacts with		directly			AEBP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_14_4004_s_142	10406805	( E) Ggamma5 directly interacts with AEBP1 and prevents binding of AEBP1 to AE-1 oligonucleotides.	bind
4714	2	2070	7	10	NULL	0	NULL	AEBP1	GP		binds					AE-1 oligonucleotides	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_14_4004_s_142	10406805	( E) Ggamma5 directly interacts with AEBP1 and prevents binding of AEBP1 to AE-1 oligonucleotides.	bind
4715	3	2070	7	10	NULL	0	NULL	statement 1	Process		prevents					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_14_4004_s_142	10406805	( E) Ggamma5 directly interacts with AEBP1 and prevents binding of AEBP1 to AE-1 oligonucleotides.	bind
3035	1	2072	6	10	NULL	0	NULL	NE	GP		bind					QseC	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_27_10420_s_71	16803956	( E) Graphical representation of the amount of [3]NE bound to QseC after incubation with 5 and 10 muM [3]NE alone or in the presence of 50 muM PE.	bind
4716	1	2072	7	10	NULL	0	NULL	NE	GP		binds					QseC	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_27_10420_s_71	16803956	( E) Graphical representation of the amount of [3]NE bound to QseC after incubation with 5 and 10 muM [3]NE alone or in the presence of 50 muM PE.	bind
3036	1	2073	6	10	NULL	0	NULL	GroEL	GP		bind					Gbeta	GP		WD40 repeats		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_22_8360_s_96	16717193	( E) GroEL binding to individual WD40 repeats of Gbeta.	bind
4719	1	2073	7	10	NULL	0	NULL	GroEL	GP		binds					Gbeta	GP		WD40 repeats		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_22_8360_s_96	16717193	( E) GroEL binding to individual WD40 repeats of Gbeta.	bind
3037	1	2074	6	10	NULL	0	NULL	Smad3	GP		bind					CBP	GP				NULL	293T cells	NULL	NULL	NULL	NULL	gw70_embo_24_14_2543_s_136	15990875	( E) HDAC5 decreases the binding of Smad3 to CBP. 293T cells expressing the indicated  proteins were subject to immunoprecipitation with anti-Flag antibodies.	bind
3038	2	2074	6	10	NULL	0	NULL	HDAC5	GP		decreases					statement 1	Process				NULL	293T cells	NULL	NULL	NULL	NULL	gw70_embo_24_14_2543_s_136	15990875	( E) HDAC5 decreases the binding of Smad3 to CBP. 293T cells expressing the indicated  proteins were subject to immunoprecipitation with anti-Flag antibodies.	bind
4720	1	2074	7	10	NULL	0	NULL	Smad3	GP		binds					CBP	GP				NULL	293T cells	NULL	NULL	NULL	NULL	gw70_embo_24_14_2543_s_136	15990875	( E) HDAC5 decreases the binding of Smad3 to CBP. 293T cells expressing the indicated  proteins were subject to immunoprecipitation with anti-Flag antibodies.	bind
4721	2	2074	7	10	NULL	0	NULL	HDAC5	GP		decreases					statement 1	Process				NULL	293T cells	NULL	NULL	NULL	NULL	gw70_embo_24_14_2543_s_136	15990875	( E) HDAC5 decreases the binding of Smad3 to CBP. 293T cells expressing the indicated  proteins were subject to immunoprecipitation with anti-Flag antibodies.	bind
3039	1	2075	6	10	NULL	0	NULL	ice1	GP	mutant	bind					MYC-2 DNA fragment	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_8_1043_s_170	12672693	( E) ice1 mutant protein also binds to the MYC-2 DNA fragment.	bind
4722	1	2075	7	10	NULL	0	NULL	ice1	GP	mutant	binds					MYC-2 DNA fragment	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_8_1043_s_170	12672693	( E) ice1 mutant protein also binds to the MYC-2 DNA fragment.	bind
3084	1	2076	6	10	NULL	0	NULL	IgG	GP		bind					B3 protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_115_5_1352_s_52	15841210	( E) IEF immunoblot with CSF (C) and serum (S) from 3 MS patients (adjusted to 10 mg  IgG/l) was performed to compare IgG binding patterns to proteins B3, C5, and G4.	bind
3085	2	2076	6	10	NULL	0	NULL	IgG	GP		bind					C5 protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_115_5_1352_s_52	15841210	( E) IEF immunoblot with CSF (C) and serum (S) from 3 MS patients (adjusted to 10 mg  IgG/l) was performed to compare IgG binding patterns to proteins B3, C5, and G4.	bind
3086	3	2076	6	10	NULL	0	NULL	IgG	GP		bind					G4 protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_115_5_1352_s_52	15841210	( E) IEF immunoblot with CSF (C) and serum (S) from 3 MS patients (adjusted to 10 mg  IgG/l) was performed to compare IgG binding patterns to proteins B3, C5, and G4.	bind
4723	1	2076	7	10	NULL	0	NULL	IgG	GP		binds					B3 proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_115_5_1352_s_52	15841210	( E) IEF immunoblot with CSF (C) and serum (S) from 3 MS patients (adjusted to 10 mg  IgG/l) was performed to compare IgG binding patterns to proteins B3, C5, and G4.	bind
4724	2	2076	7	10	NULL	0	NULL	IgG	GP		binds					C5 proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_115_5_1352_s_52	15841210	( E) IEF immunoblot with CSF (C) and serum (S) from 3 MS patients (adjusted to 10 mg  IgG/l) was performed to compare IgG binding patterns to proteins B3, C5, and G4.	bind
4725	3	2076	7	10	NULL	0	NULL	IgG	GP		binds					G4 proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_115_5_1352_s_52	15841210	( E) IEF immunoblot with CSF (C) and serum (S) from 3 MS patients (adjusted to 10 mg  IgG/l) was performed to compare IgG binding patterns to proteins B3, C5, and G4.	bind
3087	1	2077	6	10	NULL	0	NULL	IgG1	GP		bind					MDA-LDL 	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_3_427_s_169	15286809	( E) IgG1 binding to MDA-LDL ( F), IgM binding to OxLDL, and ( G) T15/EO6 antibodies of individual plasmas at 1:250 dilution before and after immunization.	bind
3088	2	2077	6	10	NULL	0	NULL	IgM	GP		bind					OxLDL	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_3_427_s_169	15286809	( E) IgG1 binding to MDA-LDL ( F), IgM binding to OxLDL, and ( G) T15/EO6 antibodies of individual plasmas at 1:250 dilution before and after immunization.	bind
3089	3	2077	6	10	NULL	0	NULL	IgM	GP		bind					T15/EO6 antibodies	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_3_427_s_169	15286809	( E) IgG1 binding to MDA-LDL ( F), IgM binding to OxLDL, and ( G) T15/EO6 antibodies of individual plasmas at 1:250 dilution before and after immunization.	bind
4726	1	2077	7	10	NULL	0	NULL	IgG1	GP		binds to					 MDA-LDL	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_3_427_s_169	15286809	( E) IgG1 binding to MDA-LDL ( F), IgM binding to OxLDL, and ( G) T15/EO6 antibodies of individual plasmas at 1:250 dilution before and after immunization.	bind
4727	2	2077	7	10	NULL	0	NULL	IgM	GP		binds					OxLDL	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_3_427_s_169	15286809	( E) IgG1 binding to MDA-LDL ( F), IgM binding to OxLDL, and ( G) T15/EO6 antibodies of individual plasmas at 1:250 dilution before and after immunization.	bind
46282	3	2077	7	10	NULL	0	NULL	IgM	GP		bind					T15/EO6 antibodies	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_3_427_s_169	15286809	( E) IgG1 binding to MDA-LDL ( F), IgM binding to OxLDL, and ( G) T15/EO6 antibodies of individual plasmas at 1:250 dilution before and after immunization.	bind
3090	1	2078	6	10	NULL	0	NULL	p53	GP		bind					CHC	GP				NULL	H1299 cells	NULL	NULL	NULL	NULL	gw70_genesdev_20_9_1087_s_188	16618797	( E) Inhibition of the association of p53 with CHC by CLCb in H1299 cells through direct  binding of CLCb to CHC.	bind
3091	2	2078	6	10	NULL	0	NULL	CLCb	GP		bind		directly			CHC	GP				NULL	H1299 cells	NULL	NULL	NULL	NULL	gw70_genesdev_20_9_1087_s_188	16618797	( E) Inhibition of the association of p53 with CHC by CLCb in H1299 cells through direct  binding of CLCb to CHC.	bind
3092	3	2078	6	10	NULL	0	NULL	statement 2	Process		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_9_1087_s_188	16618797	( E) Inhibition of the association of p53 with CHC by CLCb in H1299 cells through direct  binding of CLCb to CHC.	bind
4728	1	2078	7	10	NULL	0	NULL	p53	GP		binds					CHC	GP				NULL	H1299 cells	NULL	NULL	NULL	NULL	gw70_genesdev_20_9_1087_s_188	16618797	( E) Inhibition of the association of p53 with CHC by CLCb in H1299 cells through direct  binding of CLCb to CHC.	bind
4729	2	2078	7	10	NULL	0	NULL	CLCb	GP		binds		directly			CHC	GP				NULL	H1299 cells	NULL	NULL	NULL	NULL	gw70_genesdev_20_9_1087_s_188	16618797	( E) Inhibition of the association of p53 with CHC by CLCb in H1299 cells through direct  binding of CLCb to CHC.	bind
4730	3	2078	7	10	NULL	0	NULL	statement 2	Process		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_9_1087_s_188	16618797	( E) Inhibition of the association of p53 with CHC by CLCb in H1299 cells through direct  binding of CLCb to CHC.	bind
3093	1	2079	6	10	NULL	0	NULL	KLF4	GP		bind		directly			Cx26	GP	proximal		promoter	NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_5_1243_s_87	16628254	( E) KLF4 binds directly to the proximal Cx26 promoter.	bind
4731	1	2079	7	10	NULL	0	NULL	KLF4	GP		binds		directly			Cx26	GP	proximal		promoter	NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_5_1243_s_87	16628254	( E) KLF4 binds directly to the proximal Cx26 promoter.	bind
3094	1	2080	6	10	NULL	0	NULL	VP16-ERalpha	GP	wild type	bind					peptides	AminoAcid	GAL4-DBD-tagged;;wild type			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_10_3593_s_168	15728727	( E) Mammalian two-hybrid receptor binding assay of GAL4-DBD-tagged wild type and mutant  peptides to VP16-ERalpha wild type.	bind
3095	2	2080	6	10	NULL	0	NULL	VP16-ERalpha	GP	wild type	bind					peptides	AminoAcid	GAL4-DBD-tagged;;mutant type			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_10_3593_s_168	15728727	( E) Mammalian two-hybrid receptor binding assay of GAL4-DBD-tagged wild type and mutant  peptides to VP16-ERalpha wild type.	bind
4732	1	2080	7	10	NULL	0	NULL	peptide	AminoAcid	wild type;;GAL4-DBD-tagged	bind					VP16-ERalpha 	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_10_3593_s_168	15728727	( E) Mammalian two-hybrid receptor binding assay of GAL4-DBD-tagged wild type and mutant  peptides to VP16-ERalpha wild type.	bind
4733	2	2080	7	10	NULL	0	NULL	peptide	AminoAcid	mutant;;GAL4-DBD-tagged 	bind					VP16-ERalpha	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_10_3593_s_168	15728727	( E) Mammalian two-hybrid receptor binding assay of GAL4-DBD-tagged wild type and mutant  peptides to VP16-ERalpha wild type.	bind
3096	1	2081	6	10	NULL	0	NULL	Mant-GTP	Chemical		bind					RacC	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_7_1620_s_184	11285226	( E) Mant-GTP binding to RacC or ( F) mant-GDP dissociation from RacE in the presence or absence of 8 muM 2D.	bind
3097	2	2081	6	10	NULL	0	NULL	Mant-GDP	Chemical		dissociates from					RacE	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_7_1620_s_184	11285226	( E) Mant-GTP binding to RacC or ( F) mant-GDP dissociation from RacE in the presence or absence of 8 muM 2D.	bind
4734	1	2081	7	10	NULL	0	NULL	Mant-GTP	Chemical		binds					RacC	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_7_1620_s_184	11285226	( E) Mant-GTP binding to RacC or ( F) mant-GDP dissociation from RacE in the presence or absence of 8 muM 2D.	bind
4735	2	2081	7	10	NULL	0	NULL	mant-GDP 	Chemical		dissociates from					RacE	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_7_1620_s_184	11285226	( E) Mant-GTP binding to RacC or ( F) mant-GDP dissociation from RacE in the presence or absence of 8 muM 2D.	bind
3098	1	2082	6	10	NULL	0	NULL	Nurr1	GP		bind					DAT	GP			promoter sequences	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_8_2874_s_108	16477036	( E) Nurr1 and Pitx3 bind cooperatively to DAT promoter sequences.	bind
3099	2	2082	6	10	NULL	0	NULL	Pitx3	GP		bind					DAT	GP			promoter sequences	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_8_2874_s_108	16477036	( E) Nurr1 and Pitx3 bind cooperatively to DAT promoter sequences.	bind
3100	3	2082	6	10	NULL	0	NULL	statement 1	Process		cooperates with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_8_2874_s_108	16477036	( E) Nurr1 and Pitx3 bind cooperatively to DAT promoter sequences.	bind
4736	1	2082	7	10	NULL	0	NULL	Nurr1	GP		binds					DAT	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_8_2874_s_108	16477036	( E) Nurr1 and Pitx3 bind cooperatively to DAT promoter sequences.	bind
4737	2	2082	7	10	NULL	0	NULL	Pitx3	GP		bind					DAT	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_8_2874_s_108	16477036	( E) Nurr1 and Pitx3 bind cooperatively to DAT promoter sequences.	bind
4738	3	2082	7	10	NULL	0	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_8_2874_s_108	16477036	( E) Nurr1 and Pitx3 bind cooperatively to DAT promoter sequences.	bind
3101	1	2083	6	10	NULL	0	NULL	FOXO1	GP		bind					InR 	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_20_2435_s_227	16230533	( E) Phosphorylation by Akt prevents binding of FOXO1 to the InR promoter probe.	bind
3102	2	2083	6	10	NULL	0	NULL	Akt	GP		phosphorylate					FOXO1	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_20_2435_s_227	16230533	( E) Phosphorylation by Akt prevents binding of FOXO1 to the InR promoter probe.	bind
4029	3	2083	6	10	NULL	0	NULL	statement 2	Process		prevents					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_20_2435_s_227	16230533	( E) Phosphorylation by Akt prevents binding of FOXO1 to the InR promoter probe.	bind
4739	1	2083	7	10	NULL	0	NULL	FOXO1	GP		binds					 InR 	GP			promoter 	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_20_2435_s_227	16230533	( E) Phosphorylation by Akt prevents binding of FOXO1 to the InR promoter probe.	bind
4740	2	2083	7	10	NULL	0	NULL	Akt	GP		phosphorylates					FOXO1	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_20_2435_s_227	16230533	( E) Phosphorylation by Akt prevents binding of FOXO1 to the InR promoter probe.	bind
4741	3	2083	7	10	NULL	0	NULL	statement 2	Process		prevents					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_20_2435_s_227	16230533	( E) Phosphorylation by Akt prevents binding of FOXO1 to the InR promoter probe.	bind
3103	1	2084	6	10	NULL	0	NULL	Pin-1	GP		bind					cyclin D1	GP	phosphorylated	Thr-286		NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_3_1335_s_170	11805292	( E) Pin1 binds cyclin D1 phosphorylated on Thr-286.	bind
4742	1	2084	7	10	NULL	0	NULL	Pin1	GP		binds					cyclin D1	GP	phosphorylated	 Thr-286 		NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_3_1335_s_170	11805292	( E) Pin1 binds cyclin D1 phosphorylated on Thr-286.	bind
3105	1	2085	6	10	NULL	0	NULL	Pmo25	GP		bind					Nak1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_embo_24_17_3012_s_102	16096637	( E) Pmo25 binds to Nak1  in vitro.	bind
4743	1	2085	7	10	NULL	0	NULL	Pmo25	GP		binds					Nak1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_embo_24_17_3012_s_102	16096637	( E) Pmo25 binds to Nak1  in vitro.	bind
3107	1	2086	6	10	NULL	0	NULL	120 kD protein	GP	purified	bind					SRE-containing probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_19_2482_s_78	9334314	( E) Purifed 120 kD protein binds to an SRE-containing probe.	bind
4744	1	2086	7	10	NULL	0	NULL	120 kD protein	GP	purified	binds to					SRE-containing probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_19_2482_s_78	9334314	( E) Purifed 120 kD protein binds to an SRE-containing probe.	bind
3108	1	2087	6	10	NULL	0	NULL	p53	GP		bind					p21	GP			promoter	NULL	IMR90 	NULL	NULL	NULL	NULL	gw70_genesdev_19_2_196_s_126	15655109	( E) Quantitative analysis of p53 binding to the  p21 promoter in control IMR90 and IMR90 depleted of p400.	bind
3109	2	2087	6	10	NULL	0	NULL	p53	GP		bind					p21	GP			promoter	NULL	IMR90 depleted of p400	NULL	NULL	NULL	NULL	gw70_genesdev_19_2_196_s_126	15655109	( E) Quantitative analysis of p53 binding to the  p21 promoter in control IMR90 and IMR90 depleted of p400.	bind
4745	1	2087	7	10	NULL	0	NULL	p53	GP		binds to					 p21	GP			promoter	NULL	in IMR90	NULL	NULL	NULL	NULL	gw70_genesdev_19_2_196_s_126	15655109	( E) Quantitative analysis of p53 binding to the  p21 promoter in control IMR90 and IMR90 depleted of p400.	bind
4746	2	2087	7	10	NULL	0	NULL	p53	GP		binds					p21	GP			promoter	NULL	in IMR90 depleted of p400	NULL	NULL	NULL	NULL	gw70_genesdev_19_2_196_s_126	15655109	( E) Quantitative analysis of p53 binding to the  p21 promoter in control IMR90 and IMR90 depleted of p400.	bind
3111	1	2088	6	10	NULL	0	NULL	GATA-1	GP		bind					GATA-1	GP			HS1	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_103	14715908	( E) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to  GATA- 1 HS1, alpha-globin HS-26, and  ALAS- 2 intron 8 in untreated and tamoxifen-treated (1 muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM of three independent experiments).	bind
3186	2	2088	6	10	NULL	0	NULL	GATA-1	GP		bind					alpha-globin	GP			HS-26	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_103	14715908	( E) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to  GATA- 1 HS1, alpha-globin HS-26, and  ALAS- 2 intron 8 in untreated and tamoxifen-treated (1 muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM of three independent experiments).	bind
3187	3	2088	6	10	NULL	0	NULL	GATA-1	GP		bind					ALAS-2	GP			intron 8	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_103	14715908	( E) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to  GATA- 1 HS1, alpha-globin HS-26, and  ALAS- 2 intron 8 in untreated and tamoxifen-treated (1 muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM of three independent experiments).	bind
3188	4	2088	6	10	NULL	0	NULL	GATA-2	GP		bind					GATA-1	GP			HS1	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_103	14715908	( E) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to  GATA- 1 HS1, alpha-globin HS-26, and  ALAS- 2 intron 8 in untreated and tamoxifen-treated (1 muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM of three independent experiments).	bind
3189	5	2088	6	10	NULL	0	NULL	GATA-2	GP		bind					alpha-globin	GP			HS-26	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_103	14715908	( E) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to  GATA- 1 HS1, alpha-globin HS-26, and  ALAS- 2 intron 8 in untreated and tamoxifen-treated (1 muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM of three independent experiments).	bind
3190	6	2088	6	10	NULL	0	NULL	GATA-2	GP		bind					ALAS-2	GP			intron 8	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_103	14715908	( E) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to  GATA- 1 HS1, alpha-globin HS-26, and  ALAS- 2 intron 8 in untreated and tamoxifen-treated (1 muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM of three independent experiments).	bind
4747	1	2088	7	10	NULL	0	NULL	GATA-1	GP		binds					GATA- 1 	GP			HS1	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_103	14715908	( E) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to  GATA- 1 HS1, alpha-globin HS-26, and  ALAS- 2 intron 8 in untreated and tamoxifen-treated (1 muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM of three independent experiments).	bind
4748	2	2088	7	10	NULL	0	NULL	GATA-1	GP		binds					alpha-globin 	GP			HS-26	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_103	14715908	( E) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to  GATA- 1 HS1, alpha-globin HS-26, and  ALAS- 2 intron 8 in untreated and tamoxifen-treated (1 muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM of three independent experiments).	bind
4749	3	2088	7	10	NULL	0	NULL	GATA-1	GP		binds					ALAS- 2 	GP			intron 8	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_103	14715908	( E) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to  GATA- 1 HS1, alpha-globin HS-26, and  ALAS- 2 intron 8 in untreated and tamoxifen-treated (1 muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM of three independent experiments).	bind
4750	4	2088	7	10	NULL	0	NULL	GATA-2	GP		binds					GATA- 1 	GP			HS1	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_103	14715908	( E) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to  GATA- 1 HS1, alpha-globin HS-26, and  ALAS- 2 intron 8 in untreated and tamoxifen-treated (1 muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM of three independent experiments).	bind
4751	5	2088	7	10	NULL	0	NULL	GATA-2	GP		binds					alpha-globin 	GP			HS-26	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_103	14715908	( E) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to  GATA- 1 HS1, alpha-globin HS-26, and  ALAS- 2 intron 8 in untreated and tamoxifen-treated (1 muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM of three independent experiments).	bind
4752	6	2088	7	10	NULL	0	NULL	GATA-2 	GP		binds					ALAS- 2 	GP			intron 8	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_4_980_s_103	14715908	( E) Quantitative ChIP analysis of GATA-1 and GATA-2 binding to  GATA- 1 HS1, alpha-globin HS-26, and  ALAS- 2 intron 8 in untreated and tamoxifen-treated (1 muM, 24 h) FOG-1 - / -  and FOG-1 - / - -ER - GATA-1 cells (mean  plus-or-minus  SEM of three independent experiments).	bind
3113	1	2089	6	10	NULL	0	NULL	palmitate	Chemical		bind					paralemmin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_3_795_s_249	9813098	( E) Release of paralemmin-bound [3]palmitate by hydrolysis with hydroxylamine.	bind
46183	2	2089	6	10	NULL	0	NULL	statement 1	GP		is hydrolysed with					hydroxylamine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_3_795_s_249	9813098	( E) Release of paralemmin-bound [3]palmitate by hydrolysis with hydroxylamine.	bind
46184	3	2089	6	10	NULL	0	NULL	statement 2	Process		release					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_3_795_s_249	9813098	( E) Release of paralemmin-bound [3]palmitate by hydrolysis with hydroxylamine.	bind
4759	1	2089	7	10	NULL	0	NULL	paralemmin	GP		binds					palmitate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_3_795_s_249	9813098	( E) Release of paralemmin-bound [3]palmitate by hydrolysis with hydroxylamine.	bind
4760	2	2089	7	10	NULL	0	NULL	statement 1	GP		is hydrolysed with					hydroxylamine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_3_795_s_249	9813098	( E) Release of paralemmin-bound [3]palmitate by hydrolysis with hydroxylamine.	bind
4761	3	2089	7	10	NULL	0	NULL	statement 2	Process		release					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_3_795_s_249	9813098	( E) Release of paralemmin-bound [3]palmitate by hydrolysis with hydroxylamine.	bind
3115	1	2090	6	10	NULL	0	NULL	RNA Pol II	GP		bind					BNA1	GP			promoter	NULL	in vivo in wild type cells 	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_155	15861138	( E) RNA Pol II binding to  BNA1 and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
3116	2	2090	6	10	NULL	0	NULL	RNA Pol II	GP		bind					URA1	GP			promoter	NULL	in vivo in wild type cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_155	15861138	( E) RNA Pol II binding to  BNA1 and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
3119	3	2090	6	10	NULL	0	NULL	RNA Pol II	GP		bind					BNA1	GP			promoter	NULL	in vivo in mot1-42 mutant cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_155	15861138	( E) RNA Pol II binding to  BNA1 and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
3120	4	2090	6	10	NULL	0	NULL	RNA Pol II	GP		bind					URA1	GP			promoter	NULL	in vivo in mot1-42 mutant cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_155	15861138	( E) RNA Pol II binding to  BNA1 and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
4762	1	2090	7	10	NULL	0	NULL	RNA Pol II	GP		binds to					BNA1	GP			promoter	NULL	in vivo from wild-type (WT) cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_155	15861138	( E) RNA Pol II binding to  BNA1 and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
4763	2	2090	7	10	NULL	0	NULL	RNA Pol II	GP		binds to					URA1	GP			promoter	NULL	in vivo from wild-type (WT) cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_155	15861138	( E) RNA Pol II binding to  BNA1 and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
4764	3	2090	7	10	NULL	0	NULL	RNA Pol II	GP		binds to					BNA1	GP			promoter	NULL	in vivo from mot1-42 mutant cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_155	15861138	( E) RNA Pol II binding to  BNA1 and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
4765	4	2090	7	10	NULL	0	NULL	RNA Pol II	GP		binds to					URA1	GP			promoter	NULL	in vivo from mot1-42 mutant cells	NULL	NULL	NULL	NULL	gw70_embo_24_9_1717_s_155	15861138	( E) RNA Pol II binding to  BNA1 and  URA1 promoters  in vivo was determined by ChIP using chromatin from wild-type (WT) or  mot1-42 mutant cells.	bind
3121	1	2091	6	10	NULL	0	NULL	myostatin	GP		bind					ActRIIB	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_16_9306_s_65	11459935	( e) Scatchard analysis of the data shown in  d. ( f) Inhibition of myostatin binding to ActRIIB by follistatin (diamonds) and the propeptide (circles).	bind
3123	2	2091	6	10	NULL	0	NULL	follistatin	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_16_9306_s_65	11459935	( e) Scatchard analysis of the data shown in  d. ( f) Inhibition of myostatin binding to ActRIIB by follistatin (diamonds) and the propeptide (circles).	bind
3124	3	2091	6	10	NULL	0	NULL	propeptide	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_16_9306_s_65	11459935	( e) Scatchard analysis of the data shown in  d. ( f) Inhibition of myostatin binding to ActRIIB by follistatin (diamonds) and the propeptide (circles).	bind
4766	1	2091	7	10	NULL	0	NULL	myostatin	GP		binds to					ActRIIB	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_16_9306_s_65	11459935	( e) Scatchard analysis of the data shown in  d. ( f) Inhibition of myostatin binding to ActRIIB by follistatin (diamonds) and the propeptide (circles).	bind
4767	2	2091	7	10	NULL	0	NULL	follistatin	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_16_9306_s_65	11459935	( e) Scatchard analysis of the data shown in  d. ( f) Inhibition of myostatin binding to ActRIIB by follistatin (diamonds) and the propeptide (circles).	bind
4768	3	2091	7	10	NULL	0	NULL	propeptide	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_16_9306_s_65	11459935	( e) Scatchard analysis of the data shown in  d. ( f) Inhibition of myostatin binding to ActRIIB by follistatin (diamonds) and the propeptide (circles).	bind
3127	1	2092	6	10	NULL	0	NULL	calcineurin A	GP	residues	bind					atrogin-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_8_1058_s_89	15489953	( E) Schematic representations of calcineurin A residues that bind to atrogin-1.	bind
4769	1	2092	7	10	NULL	0	NULL	calcineurin A	GP	residues of	binds					atrogin-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_8_1058_s_89	15489953	( E) Schematic representations of calcineurin A residues that bind to atrogin-1.	bind
3130	1	2093	6	10	NULL	0	NULL	ERalpha	GP		bind					Rsk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3484_s_109	11432835	( E) Schematic showing homology between the region in ERalpha that binds to Rsk2 and the analogous region of ERbeta.	bind
46185	2	2093	6	10	NULL	0	NULL	ERalpha	GP	binding region of	is homologous to					ERbeta	GP	binding region of 			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3484_s_109	11432835	( E) Schematic showing homology between the region in ERalpha that binds to Rsk2 and the analogous region of ERbeta.	bind
4770	1	2093	7	10	NULL	0	NULL	ERalpha	GP		binds to					Rsk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3484_s_109	11432835	( E) Schematic showing homology between the region in ERalpha that binds to Rsk2 and the analogous region of ERbeta.	bind
4771	2	2093	7	10	NULL	0	NULL	 ERalpha	GP	binding region	is homologous to					ERbeta	GP	binding region			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3484_s_109	11432835	( E) Schematic showing homology between the region in ERalpha that binds to Rsk2 and the analogous region of ERbeta.	bind
3133	1	2095	6	10	NULL	0	NULL	Smads	GP		bind					Xtwn	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8358_s_138	10890911	( E) Smads and LEF1 expressed in mammalian cells bind to the Xtwn promoter.	bind
3134	2	2095	6	10	NULL	0	NULL	LEF1	GP		bind					Xtwn	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8358_s_138	10890911	( E) Smads and LEF1 expressed in mammalian cells bind to the Xtwn promoter.	bind
46186	3	2095	6	10	NULL	0	NULL	Smads	GP		is expressed in					mammalian cell	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8358_s_138	10890911	( E) Smads and LEF1 expressed in mammalian cells bind to the Xtwn promoter.	bind
46187	4	2095	6	10	NULL	0	NULL	LEF1	GP		is expressed in					mammalian cell	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8358_s_138	10890911	( E) Smads and LEF1 expressed in mammalian cells bind to the Xtwn promoter.	bind
4772	1	2095	7	10	NULL	0	NULL	Smads 	GP		bind					Xtwn	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8358_s_138	10890911	( E) Smads and LEF1 expressed in mammalian cells bind to the Xtwn promoter.	bind
4773	2	2095	7	10	NULL	0	NULL	LEF1	GP		bind					Xtwn	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8358_s_138	10890911	( E) Smads and LEF1 expressed in mammalian cells bind to the Xtwn promoter.	bind
4774	3	2095	7	10	NULL	0	NULL	Smads	GP		expressed in					mammalian cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8358_s_138	10890911	( E) Smads and LEF1 expressed in mammalian cells bind to the Xtwn promoter.	bind
4775	4	2095	7	10	NULL	0	NULL	LEF1	GP		expressed in					mammalian cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_15_8358_s_138	10890911	( E) Smads and LEF1 expressed in mammalian cells bind to the Xtwn promoter.	bind
3135	1	2096	6	10	NULL	0	NULL	Sf-H2	GP	recombinant;;iodinated	bind		species specific			bindin particles	GP	purified			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_20_2502_s_62	14561772	( E) Species-specific binding of recombinant iodinated  Sf-H2 to purified bindin particles.	bind
4776	1	2096	7	10	NULL	0	NULL	Sf-H2	GP	recombinant;;iodinated	binds		species specific			bindin particles	GP	purified			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_20_2502_s_62	14561772	( E) Species-specific binding of recombinant iodinated  Sf-H2 to purified bindin particles.	bind
3136	1	2097	6	10	NULL	0	NULL	kappaB-Ras	GP		bind		specifically			GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_287_5454_869_s_40	10657303	( E) Specific binding of kappaB-Ras to GTP.	bind
4778	1	2097	7	10	NULL	0	NULL	 kappaB-Ras	GP		binds		specifically			GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_287_5454_869_s_40	10657303	( E) Specific binding of kappaB-Ras to GTP.	bind
3141	2	2098	6	10	NULL	0	NULL	SRC1	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_10_2083_s_124	15103326	( E) SRC1 binds to DNA-bound RXR, in a 9 -cis RA-dependent manner.	bind
3142	3	2098	6	10	NULL	0	NULL	statement 2	Process		is dependent on					9 -cis RA	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_10_2083_s_124	15103326	( E) SRC1 binds to DNA-bound RXR, in a 9 -cis RA-dependent manner.	bind
60879	1	2098	6	10	NULL	0	NULL	RXR	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_embo_23_10_2083_s_124	15103326	( E) SRC1 binds to DNA-bound RXR, in a 9 -cis RA-dependent manner.	bind
4779	2	2098	7	10	NULL	0	NULL	SRC1	GP		binds to					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_10_2083_s_124	15103326	( E) SRC1 binds to DNA-bound RXR, in a 9 -cis RA-dependent manner.	bind
4780	3	2098	7	10	NULL	0	NULL	statement 2	Process		is dependent on					9 -cis RA	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_10_2083_s_124	15103326	( E) SRC1 binds to DNA-bound RXR, in a 9 -cis RA-dependent manner.	bind
60880	1	2098	7	10	NULL	0	NULL	RXR	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_embo_23_10_2083_s_124	15103326	( E) SRC1 binds to DNA-bound RXR, in a 9 -cis RA-dependent manner.	bind
3143	1	2099	6	10	NULL	0	NULL	EAT-2	GP	mouse	bind					CD150 peptide	GP		pTyr281		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_5840_s_59	11689425	( E) Superimposition of the mouse EAT-2 and human SH2D1A structures bound to the CD150 pTyr281 peptide.	bind
3144	2	2099	6	10	NULL	0	NULL	SH2D1A	GP	human	bind					CD150 peptide	GP		pTyr281		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_5840_s_59	11689425	( E) Superimposition of the mouse EAT-2 and human SH2D1A structures bound to the CD150 pTyr281 peptide.	bind
4783	1	2099	7	10	NULL	0	NULL	EAT-2	GP	mouse	binds to					CD150  peptide	GP		pTyr281		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_5840_s_59	11689425	( E) Superimposition of the mouse EAT-2 and human SH2D1A structures bound to the CD150 pTyr281 peptide.	bind
4784	2	2099	7	10	NULL	0	NULL	SH2D1A	GP	human	binds to					CD150  peptide	GP		pTyr281		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_5840_s_59	11689425	( E) Superimposition of the mouse EAT-2 and human SH2D1A structures bound to the CD150 pTyr281 peptide.	bind
3145	1	2101	6	10	NULL	0	NULL	p38	GP	mutant	bind					MNK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_291	11157753	( E) The binding of the mutant forms of p38 and ERK2 to MNK1.	bind
3146	2	2101	6	10	NULL	0	NULL	ERK2	GP	mutant	bind					MNK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_291	11157753	( E) The binding of the mutant forms of p38 and ERK2 to MNK1.	bind
4856	1	2101	7	10	NULL	0	NULL	p38 	GP	mutant	binds					MNK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_291	11157753	( E) The binding of the mutant forms of p38 and ERK2 to MNK1.	bind
4857	2	2101	7	10	NULL	0	NULL	ERK2	GP	Mutant	binds					MNK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_466_s_291	11157753	( E) The binding of the mutant forms of p38 and ERK2 to MNK1.	bind
3150	1	2102	6	10	NULL	0	NULL	axin	GP		bind					GSK-3beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_11_6371_s_121	10339594	( E) The coiled-coil RGS protein axin binds GSK-3beta, but does not interact with polycystin.	bind
3151	2	2102	6	10	NULL	0	NULL	axin	GP		does not bind					polycystin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_11_6371_s_121	10339594	( E) The coiled-coil RGS protein axin binds GSK-3beta, but does not interact with polycystin.	bind
45873	3	2102	6	10	NULL	0	NULL	axin	GP		is a type of					coiled-coil RGS protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_11_6371_s_121	10339594	( E) The coiled-coil RGS protein axin binds GSK-3beta, but does not interact with polycystin.	bind
4858	1	2102	7	10	NULL	0	NULL	axin	GP		binds					GSK-3beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_11_6371_s_121	10339594	( E) The coiled-coil RGS protein axin binds GSK-3beta, but does not interact with polycystin.	bind
4859	2	2102	7	10	NULL	0	NULL	axin	GP		does not bind					polycystin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_11_6371_s_121	10339594	( E) The coiled-coil RGS protein axin binds GSK-3beta, but does not interact with polycystin.	bind
45874	3	2102	7	10	NULL	0	NULL	axin	GP		is a type of					coiled-coil RGS protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_11_6371_s_121	10339594	( E) The coiled-coil RGS protein axin binds GSK-3beta, but does not interact with polycystin.	bind
3154	1	2103	6	10	NULL	0	NULL	mAb 196	GP		bind					Abeta	GP		N-terminus		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_21_7718_s_206	15894613	( E) The levels of salphaAPP released to the cells' media were analyzed after 24 and 48 h by Western blot  using mAb 196, which binds Abeta in the N terminus.	bind
4884	1	2103	7	10	NULL	0	NULL	mAb 196	GP		binds					Abeta	GP		N terminus		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_21_7718_s_206	15894613	( E) The levels of salphaAPP released to the cells' media were analyzed after 24 and 48 h by Western blot  using mAb 196, which binds Abeta in the N terminus.	bind
3156	1	2104	6	10	NULL	0	NULL	VEGF-C	GP		bind					VEGFR3	GP				NULL	corneal epithelium	NULL	NULL	NULL	NULL	gw70_pnas_103_30_11405_s_45	16849433	( E) VEGF-C binds to corneal epithelial VEGFR3 and leads to VEGFR3 activation.	bind
3158	2	2104	6	10	NULL	0	NULL	statement 1	Process		leads to					VEGFR3	GP	activation of			NULL	corneal epithelium	NULL	NULL	NULL	NULL	gw70_pnas_103_30_11405_s_45	16849433	( E) VEGF-C binds to corneal epithelial VEGFR3 and leads to VEGFR3 activation.	bind
4882	1	2104	7	10	NULL	0	NULL	VEGF-C 	GP		binds					VEGFR3	GP				NULL	corneal epithelium	NULL	NULL	NULL	NULL	gw70_pnas_103_30_11405_s_45	16849433	( E) VEGF-C binds to corneal epithelial VEGFR3 and leads to VEGFR3 activation.	bind
4883	2	2104	7	10	NULL	0	NULL	statement 1	Process		leads to					VEGFR3	GP	activation of			NULL	corneal epithelium	NULL	NULL	NULL	NULL	gw70_pnas_103_30_11405_s_45	16849433	( E) VEGF-C binds to corneal epithelial VEGFR3 and leads to VEGFR3 activation.	bind
3160	1	2105	6	10	NULL	0	NULL	ZO-3	GP		does not bind					ZO-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_1_199_s_151	9531559	( e) ZO-3  does not bind to ZO-2.	bind
4885	1	2105	7	10	NULL	0	NULL	ZO-3	GP		does not bind					ZO-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_1_199_s_151	9531559	( e) ZO-3  does not bind to ZO-2.	bind
3161	1	2106	6	10	NULL	0	NULL	synaptotagmin 2	GP	WT	bind					SNARE complexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_10_2039_s_66	16642042	( E, F) Binding of WT and I337N-mutant synaptotagmin 2 to SNARE complexes analyzed by immunoprecipitations.	bind
3162	2	2106	6	10	NULL	0	NULL	synaptotagmin 2	GP	mutant	bind			I337N		SNARE complexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_10_2039_s_66	16642042	( E, F) Binding of WT and I337N-mutant synaptotagmin 2 to SNARE complexes analyzed by immunoprecipitations.	bind
4887	1	2106	7	10	NULL	0	NULL	synaptotagmin 2	GP	WT	binds					SNARE complexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_10_2039_s_66	16642042	( E, F) Binding of WT and I337N-mutant synaptotagmin 2 to SNARE complexes analyzed by immunoprecipitations.	bind
4891	2	2106	7	10	NULL	0	NULL	synaptotagmin 2	GP	mutant	binds			I337N		SNARE complexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_10_2039_s_66	16642042	( E, F) Binding of WT and I337N-mutant synaptotagmin 2 to SNARE complexes analyzed by immunoprecipitations.	bind
3164	1	2107	6	10	NULL	0	NULL	TCF	GP		bind					nkd	GP			control region	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_12_2735_s_163	16710294	( E, F) ChIP analysis shows overlapping binding of TCF (E) and CtBP (F) to the  nkd control region.	bind
3165	2	2107	6	10	NULL	0	NULL	CtBP	GP		bind					nkd	GP			control region	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_12_2735_s_163	16710294	( E, F) ChIP analysis shows overlapping binding of TCF (E) and CtBP (F) to the  nkd control region.	bind
51551	3	2107	6	10	NULL	0	NULL	statement 1	Process		overlaps					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_12_2735_s_163	16710294	( E, F) ChIP analysis shows overlapping binding of TCF (E) and CtBP (F) to the  nkd control region.	bind
4894	1	2107	7	10	NULL	0	NULL	TCF	GP		binds					nkd	GP			control region	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_12_2735_s_163	16710294	( E, F) ChIP analysis shows overlapping binding of TCF (E) and CtBP (F) to the  nkd control region.	bind
4896	2	2107	7	10	NULL	0	NULL	CtBP	GP		binds					nkd	GP			control region	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_12_2735_s_163	16710294	( E, F) ChIP analysis shows overlapping binding of TCF (E) and CtBP (F) to the  nkd control region.	bind
4900	3	2107	7	10	NULL	0	NULL	statement 1	Process		overlaps					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_12_2735_s_163	16710294	( E, F) ChIP analysis shows overlapping binding of TCF (E) and CtBP (F) to the  nkd control region.	bind
3166	1	2108	6	10	NULL	0	NULL	PPARgamma/RXR	GP		bind					FXR 	GP			DR-1 element in promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_18_2_157_s_108	14729567	( E,F) PPARgamma/RXR binds to the DR-1 elements in both FXR promoters.	bind
4898	1	2108	7	10	NULL	0	NULL	PPARgamma/RXR	GP		binds					FXR	GP			DR-1 elements in the promoter of	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_18_2_157_s_108	14729567	( E,F) PPARgamma/RXR binds to the DR-1 elements in both FXR promoters.	bind
3167	1	2109	6	10	NULL	0	NULL				bind			DSX domain		DNA probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_14_1750_s_155	10898790	( E,right gel) Major groove base modifications do not perturb binding of DSX domain to 15 base-pair DNA probe (5''-CACTACAATGTTGCA-3'' and complement): (lanes  e- g) single nebularine substitutions at positions 5, 7, and 8 of upper strand and (lanes  h- j) single 5-methylcytosine or uridine substituitions at positions 6, 9, and 11 of upper strand.	bind
3168	2	2109	6	10	NULL	0	NULL	major groove 		base modifications of	have no effect on					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_14_1750_s_155	10898790	( E,right gel) Major groove base modifications do not perturb binding of DSX domain to 15 base-pair DNA probe (5''-CACTACAATGTTGCA-3'' and complement): (lanes  e- g) single nebularine substitutions at positions 5, 7, and 8 of upper strand and (lanes  h- j) single 5-methylcytosine or uridine substituitions at positions 6, 9, and 11 of upper strand.	bind
4901	1	2109	7	10	NULL	0	NULL				binds			DSX domain 		DNA probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_14_1750_s_155	10898790	( E,right gel) Major groove base modifications do not perturb binding of DSX domain to 15 base-pair DNA probe (5''-CACTACAATGTTGCA-3'' and complement): (lanes  e- g) single nebularine substitutions at positions 5, 7, and 8 of upper strand and (lanes  h- j) single 5-methylcytosine or uridine substituitions at positions 6, 9, and 11 of upper strand.	bind
4903	2	2109	7	10	NULL	0	NULL	major groove		base modifications of	do not perturb					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_14_1750_s_155	10898790	( E,right gel) Major groove base modifications do not perturb binding of DSX domain to 15 base-pair DNA probe (5''-CACTACAATGTTGCA-3'' and complement): (lanes  e- g) single nebularine substitutions at positions 5, 7, and 8 of upper strand and (lanes  h- j) single 5-methylcytosine or uridine substituitions at positions 6, 9, and 11 of upper strand.	bind
3169	1	2110	6	10	NULL	0	NULL	GFP-alpha-CaMKII	GP		bind					calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5411_162_s_107	10102820	( F) A GFP-alpha-CaMKII mutant deficient in calmodulin binding (A302R) fails to translocate to PSDs [same protocol as in (D)].	bind
3170	2	2110	6	10	NULL	0	NULL	GFP-alpha-CaMKII	GP		translocate to					PSDs	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5411_162_s_107	10102820	( F) A GFP-alpha-CaMKII mutant deficient in calmodulin binding (A302R) fails to translocate to PSDs [same protocol as in (D)].	bind
3171	3	2110	6	10	NULL	0	NULL	GFP-alpha-CaMKII	GP	mutant	does not bind			A302R		calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5411_162_s_107	10102820	( F) A GFP-alpha-CaMKII mutant deficient in calmodulin binding (A302R) fails to translocate to PSDs [same protocol as in (D)].	bind
46297	4	2110	6	10	NULL	0	NULL	GFP-alpha-CaMKII	GP	mutant	inhibits			A302R		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5411_162_s_107	10102820	( F) A GFP-alpha-CaMKII mutant deficient in calmodulin binding (A302R) fails to translocate to PSDs [same protocol as in (D)].	bind
4910	1	2110	7	10	NULL	0	NULL	GFP-alpha-CaMKII	GP	mutant	does not bind			A302R		calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5411_162_s_107	10102820	( F) A GFP-alpha-CaMKII mutant deficient in calmodulin binding (A302R) fails to translocate to PSDs [same protocol as in (D)].	bind
4912	2	2110	7	10	NULL	0	NULL	GFP-alpha-CaMKII	GP		translocate to					PSDs	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5411_162_s_107	10102820	( F) A GFP-alpha-CaMKII mutant deficient in calmodulin binding (A302R) fails to translocate to PSDs [same protocol as in (D)].	bind
46298	3	2110	7	10	NULL	0	NULL	GFP-alpha-CaMKII	GP	mutant	inhibit			A302R		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5411_162_s_107	10102820	( F) A GFP-alpha-CaMKII mutant deficient in calmodulin binding (A302R) fails to translocate to PSDs [same protocol as in (D)].	bind
3172	1	2111	6	10	NULL	0	NULL	EDA-A1	GP		bind					EDAR	GP				NULL	MCF7 cells	NULL	NULL	NULL	NULL	gw60_science_290_5491_523_s_98	11039935	( F) Binding of  EDA-A1 to EDAR results in activation of NF-kappaB in MCF7 cells.	bind
3173	2	2111	6	10	NULL	0	NULL	statement 1	Process		activates					NF-kappaB	GP				NULL	MCF7 cells	NULL	NULL	NULL	NULL	gw60_science_290_5491_523_s_98	11039935	( F) Binding of  EDA-A1 to EDAR results in activation of NF-kappaB in MCF7 cells.	bind
4916	1	2111	7	10	NULL	0	NULL	EDA-A1	GP		binds					EDAR	GP				NULL	in MCF7 cells	NULL	NULL	NULL	NULL	gw60_science_290_5491_523_s_98	11039935	( F) Binding of  EDA-A1 to EDAR results in activation of NF-kappaB in MCF7 cells.	bind
4917	2	2111	7	10	NULL	0	NULL	statement 1	Process		activates					NF-kappaB	GP				NULL	in MCF7 cells	NULL	NULL	NULL	NULL	gw60_science_290_5491_523_s_98	11039935	( F) Binding of  EDA-A1 to EDAR results in activation of NF-kappaB in MCF7 cells.	bind
3174	1	2112	6	10	NULL	0	NULL	ARF	GP		bind					Mix.2	GP	Xenopus		activin-response element of the promoter	NULL		NULL	NULL	NULL	NULL	gw60_science_298_5600_1996_s_100	12471260	( F) Binding of a FoxH1-Smad2-Smad4 transcription factor complex (ARF) to the activin-response element from the Xenopus  Mix.2 promoter ( 25) is inhibited by addition of DRAP1 in an electrophoretic mobility shift assay, whereas Dr1 has little or no effect; addition of antibodies to Smad2 (fig. S3) or to Smad4 supershifts the FoxH1-Smad2-Smad4 complex.	bind
3175	2	2112	6	10	NULL	0	NULL	ARF	GP		is					FoxH1-Smad2-Smad4 transcription factor complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_298_5600_1996_s_100	12471260	( F) Binding of a FoxH1-Smad2-Smad4 transcription factor complex (ARF) to the activin-response element from the Xenopus  Mix.2 promoter ( 25) is inhibited by addition of DRAP1 in an electrophoretic mobility shift assay, whereas Dr1 has little or no effect; addition of antibodies to Smad2 (fig. S3) or to Smad4 supershifts the FoxH1-Smad2-Smad4 complex.	bind
3176	3	2112	6	10	NULL	0	NULL	DRAP1	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_298_5600_1996_s_100	12471260	( F) Binding of a FoxH1-Smad2-Smad4 transcription factor complex (ARF) to the activin-response element from the Xenopus  Mix.2 promoter ( 25) is inhibited by addition of DRAP1 in an electrophoretic mobility shift assay, whereas Dr1 has little or no effect; addition of antibodies to Smad2 (fig. S3) or to Smad4 supershifts the FoxH1-Smad2-Smad4 complex.	bind
3177	4	2112	6	10	NULL	0	NULL	Dr1	GP		effect		may			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_298_5600_1996_s_100	12471260	( F) Binding of a FoxH1-Smad2-Smad4 transcription factor complex (ARF) to the activin-response element from the Xenopus  Mix.2 promoter ( 25) is inhibited by addition of DRAP1 in an electrophoretic mobility shift assay, whereas Dr1 has little or no effect; addition of antibodies to Smad2 (fig. S3) or to Smad4 supershifts the FoxH1-Smad2-Smad4 complex.	bind
4918	1	2112	7	10	NULL	0	NULL	FoxH1-Smad2-Smad4 transcription factor complex 	GP		binds					Mix.2	GP	Xenopus		activin-response element promoter of	NULL		NULL	NULL	NULL	NULL	gw60_science_298_5600_1996_s_100	12471260	( F) Binding of a FoxH1-Smad2-Smad4 transcription factor complex (ARF) to the activin-response element from the Xenopus  Mix.2 promoter ( 25) is inhibited by addition of DRAP1 in an electrophoretic mobility shift assay, whereas Dr1 has little or no effect; addition of antibodies to Smad2 (fig. S3) or to Smad4 supershifts the FoxH1-Smad2-Smad4 complex.	bind
4919	2	2112	7	10	NULL	0	NULL	DRAP1	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_298_5600_1996_s_100	12471260	( F) Binding of a FoxH1-Smad2-Smad4 transcription factor complex (ARF) to the activin-response element from the Xenopus  Mix.2 promoter ( 25) is inhibited by addition of DRAP1 in an electrophoretic mobility shift assay, whereas Dr1 has little or no effect; addition of antibodies to Smad2 (fig. S3) or to Smad4 supershifts the FoxH1-Smad2-Smad4 complex.	bind
4920	3	2112	7	10	NULL	0	NULL	Dr1	GP		effect		may			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_298_5600_1996_s_100	12471260	( F) Binding of a FoxH1-Smad2-Smad4 transcription factor complex (ARF) to the activin-response element from the Xenopus  Mix.2 promoter ( 25) is inhibited by addition of DRAP1 in an electrophoretic mobility shift assay, whereas Dr1 has little or no effect; addition of antibodies to Smad2 (fig. S3) or to Smad4 supershifts the FoxH1-Smad2-Smad4 complex.	bind
4922	4	2112	7	10	NULL	0	NULL	FoxH1-Smad2-Smad4 transcription factor complex	GP		is					ARF	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_298_5600_1996_s_100	12471260	( F) Binding of a FoxH1-Smad2-Smad4 transcription factor complex (ARF) to the activin-response element from the Xenopus  Mix.2 promoter ( 25) is inhibited by addition of DRAP1 in an electrophoretic mobility shift assay, whereas Dr1 has little or no effect; addition of antibodies to Smad2 (fig. S3) or to Smad4 supershifts the FoxH1-Smad2-Smad4 complex.	bind
3178	1	2113	6	10	NULL	0	NULL	NFAT1	GP		bind					TRAP gene	GP			NFAT binding element in promoter	NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_475_s_154	15314684	( F) Binding of NFAT1 to NFAT-binding element present in TRAP gene promoter ( - 523 to   - 507).	bind
46272	2	2113	6	10	NULL	0	NULL				is present in				NFAT-binding element	TRAP gene	GP			- 523 to - 507 of promoter	NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_475_s_154	15314684	( F) Binding of NFAT1 to NFAT-binding element present in TRAP gene promoter ( - 523 to   - 507).	bind
4923	1	2113	7	10	NULL	0	NULL	NFAT1	GP		binds					TRAP gene	GP			 NFAT-binding element in promoter	NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_475_s_154	15314684	( F) Binding of NFAT1 to NFAT-binding element present in TRAP gene promoter ( - 523 to   - 507).	bind
4924	2	2113	7	10	NULL	0	NULL				is present in				 NFAT-binding element 	TRAP gene	GP			 - 523 to - 507 promoter	NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_114_4_475_s_154	15314684	( F) Binding of NFAT1 to NFAT-binding element present in TRAP gene promoter ( - 523 to   - 507).	bind
3199	1	2114	6	10	NULL	0	NULL	menin	GP	wild type	bind									p27Kip1 locus	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
3212	2	2114	6	10	NULL	0	NULL	menin	GP	mutant	bind			L22R						p27Kip1 locus	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
3213	3	2114	6	10	NULL	0	NULL	statement 2	Process		is reduced than					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
3214	5	2114	6	10	NULL	0	NULL	menin	GP	wild type	bind									p18Ink4c loci	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
3645	4	2114	6	10	NULL	0	NULL	menin	GP	mutant	bind			A242V						p27Kip1 locus	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
3646	6	2114	6	10	NULL	0	NULL	statement 4	Process		is reduced than					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
3647	7	2114	6	10	NULL	0	NULL	menin	GP	mutant	bind			A242V						p18Ink4c loci	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
3648	8	2114	6	10	NULL	0	NULL	statement 7	Process		is reduced than					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
3649	9	2114	6	10	NULL	0	NULL	menin	GP	mutant	bind			L22R						p18Ink4c loci	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
3650	10	2114	6	10	NULL	0	NULL	statement 9	Process		is reduced than					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
4935	1	2114	7	10	NULL	0	NULL	menin	GP	Wild-type	binds									p27Kip1 locus	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
4936	2	2114	7	10	NULL	0	NULL	menin	GP	Wild-type	binds									p18Ink4c locus	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
4937	3	2114	7	10	NULL	0	NULL	menin	GP	mutant	binds			L22R						p27Kip1 locus	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
4942	4	2114	7	10	NULL	0	NULL	menin	GP	mutant	binds			L22R						p18Ink4c locus	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
4946	5	2114	7	10	NULL	0	NULL	menin	GP	mutant	binds			A242V						p27Kip1 locus	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
4947	6	2114	7	10	NULL	0	NULL	menin	GP	mutant	binds			A242V						p18Ink4c locus	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
4957	7	2114	7	10	NULL	0	NULL	statement 3	Process		is reduced than					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
6239	8	2114	7	10	NULL	0	NULL	statement 4	Process		is reduced than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
6241	9	2114	7	10	NULL	0	NULL	statement 5	Process		is reduced than					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
6243	10	2114	7	10	NULL	0	NULL	statement 6	Process		is reduced than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_3_749_s_142	15640349	( F) Binding of the menin mutants L22R (gray) and A242V (red) are reduced at the  p27Kip1 and  p18Ink4c loci compared with wild-type menin ( Men1-/- with reexpressed menin, green).	bind
3179	1	2116	6	10	NULL	0	NULL	Ebp1	GP		bind			N-terminus		Akt	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_10_2083_s_153	16642037	( F) Both N- and C-termini of Ebp1 bind to Akt.	bind
3180	2	2116	6	10	NULL	0	NULL	Ebp1	GP		bind			C-terminus		Akt	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_10_2083_s_153	16642037	( F) Both N- and C-termini of Ebp1 bind to Akt.	bind
4958	1	2116	7	10	NULL	0	NULL	Ebp1 	GP		binds			N terminus		Akt	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_10_2083_s_153	16642037	( F) Both N- and C-termini of Ebp1 bind to Akt.	bind
4959	2	2116	7	10	NULL	0	NULL	Ebp1 	GP		binds			C terminus		Akt	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_10_2083_s_153	16642037	( F) Both N- and C-termini of Ebp1 bind to Akt.	bind
3181	1	2117	6	10	NULL	0	NULL	p27	GP		bind					Cdk2	GP				NULL	Bosc23 cells	NULL	NULL	NULL	NULL	gw60_jclininvest_104_7_865_s_195	10510327	( f) Cdk2 immunoprecipitates in Bosc23 cells: p27 bound to Cdk2, Cdk2 level, and Cdk2 activity in total or fractionated extracts.	bind
4960	1	2117	7	10	NULL	0	NULL	p27	GP		binds					Cdk2	GP				NULL	Bosc23 cells	NULL	NULL	NULL	NULL	gw60_jclininvest_104_7_865_s_195	10510327	( f) Cdk2 immunoprecipitates in Bosc23 cells: p27 bound to Cdk2, Cdk2 level, and Cdk2 activity in total or fractionated extracts.	bind
3209	1	2119	6	10	NULL	0	NULL	Srb4-Myc	GP		bind					GAL1	GP			UASG	NULL	yeast cells	NULL	NULL	NULL	NULL	gw70_embo_23_20_4040_s_153	15385957	( F) ChIP analysis of the binding of Srb4-Myc and Rpb1 to the  GAL1 UASG in yeast cells expressing a Gal4-Gal11 fusion (KLY091 and KLY092).	bind
3210	2	2119	6	10	NULL	0	NULL	Rbp1	GP		bind					GAL1	GP			UASG	NULL	yeast cells	NULL	NULL	NULL	NULL	gw70_embo_23_20_4040_s_153	15385957	( F) ChIP analysis of the binding of Srb4-Myc and Rpb1 to the  GAL1 UASG in yeast cells expressing a Gal4-Gal11 fusion (KLY091 and KLY092).	bind
3211	3	2119	6	10	NULL	0	NULL	yeast cells 	Cell		express					Gal4-Gal11	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_20_4040_s_153	15385957	( F) ChIP analysis of the binding of Srb4-Myc and Rpb1 to the  GAL1 UASG in yeast cells expressing a Gal4-Gal11 fusion (KLY091 and KLY092).	bind
46138	4	2119	6	10	NULL	0	NULL	Gal4-Gal11	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_20_4040_s_153	15385957	( F) ChIP analysis of the binding of Srb4-Myc and Rpb1 to the  GAL1 UASG in yeast cells expressing a Gal4-Gal11 fusion (KLY091 and KLY092).	bind
4961	1	2119	7	10	NULL	0	NULL	Srb4-Myc	GP		bind					GAL1	GP			UASG	NULL	yeast cells	NULL	NULL	NULL	NULL	gw70_embo_23_20_4040_s_153	15385957	( F) ChIP analysis of the binding of Srb4-Myc and Rpb1 to the  GAL1 UASG in yeast cells expressing a Gal4-Gal11 fusion (KLY091 and KLY092).	bind
4962	2	2119	7	10	NULL	0	NULL	Rpb1	GP		bind					GAL1 	GP			UASG	NULL	yeast cells	NULL	NULL	NULL	NULL	gw70_embo_23_20_4040_s_153	15385957	( F) ChIP analysis of the binding of Srb4-Myc and Rpb1 to the  GAL1 UASG in yeast cells expressing a Gal4-Gal11 fusion (KLY091 and KLY092).	bind
46139	4	2119	7	10	NULL	0	NULL	Gal4-Gal11	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_20_4040_s_153	15385957	( F) ChIP analysis of the binding of Srb4-Myc and Rpb1 to the  GAL1 UASG in yeast cells expressing a Gal4-Gal11 fusion (KLY091 and KLY092).	bind
46283	3	2119	7	10	NULL	0	NULL	yeast cells	Cell		express					Gal4-Gal11	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_20_4040_s_153	15385957	( F) ChIP analysis of the binding of Srb4-Myc and Rpb1 to the  GAL1 UASG in yeast cells expressing a Gal4-Gal11 fusion (KLY091 and KLY092).	bind
3182	1	2121	6	10	NULL	0	NULL	NFAT	GP		bind					ARRE2	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_5_1081_s_108	16498406	( F) CpG site 1 methylation inhibits NFAT and Oct-1 binding to ARRE2.	bind
3183	2	2121	6	10	NULL	0	NULL	Oct-1	GP		bind					ARRE2	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_5_1081_s_108	16498406	( F) CpG site 1 methylation inhibits NFAT and Oct-1 binding to ARRE2.	bind
3184	3	2121	6	10	NULL	0	NULL	CpG	GP	methylation	inhibits				site 1	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_5_1081_s_108	16498406	( F) CpG site 1 methylation inhibits NFAT and Oct-1 binding to ARRE2.	bind
3185	4	2121	6	10	NULL	0	NULL	CpG	GP	methylation	inhibits				site 1	statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_5_1081_s_108	16498406	( F) CpG site 1 methylation inhibits NFAT and Oct-1 binding to ARRE2.	bind
4965	1	2121	7	10	NULL	0	NULL	NFAT	GP		binds					ARRE2	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_5_1081_s_108	16498406	( F) CpG site 1 methylation inhibits NFAT and Oct-1 binding to ARRE2.	bind
4966	2	2121	7	10	NULL	0	NULL	Oct-1	GP		binds					ARRE2	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_5_1081_s_108	16498406	( F) CpG site 1 methylation inhibits NFAT and Oct-1 binding to ARRE2.	bind
4967	3	2121	7	10	NULL	0	NULL	CpG 	GP	methylation 	inhibits				site 1	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_5_1081_s_108	16498406	( F) CpG site 1 methylation inhibits NFAT and Oct-1 binding to ARRE2.	bind
4968	4	2121	7	10	NULL	0	NULL	CpG 	GP	methylation	inhibits				site 1	statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_5_1081_s_108	16498406	( F) CpG site 1 methylation inhibits NFAT and Oct-1 binding to ARRE2.	bind
3251	1	2122	6	10	NULL	0	NULL	Myc	GP	endogenous	bind		directly							hGCN5 locus	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_embo_25_12_2723_s_98	16724113	( F) Direct binding of endogenous Myc to the hGCN5 locus  in vivo.	bind
4969	1	2122	7	10	NULL	0	NULL	Myc	GP	endogenous	binds to		directly							hGCN5 locus	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_embo_25_12_2723_s_98	16724113	( F) Direct binding of endogenous Myc to the hGCN5 locus  in vivo.	bind
3252	1	2123	6	10	NULL	0	NULL	TLX	GP		bind		directly			Pten	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_10_1308_s_161	16702404	( F) Direct binding of TLX to the  Pten promoter region in gel shift assays.	bind
4970	1	2123	7	10	NULL	0	NULL	TLX 	GP		binds to		directly			Pten	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_10_1308_s_161	16702404	( F) Direct binding of TLX to the  Pten promoter region in gel shift assays.	bind
3253	1	2125	6	10	NULL	0	NULL	Spn-F	GP		bind					GST-Ddlc	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_133_8_1477_s_222	16540510	( F) In vitro binding of Spn-F to GST-Ddlc.	bind
4972	1	2125	7	10	NULL	0	NULL	Spn-F	GP		binds					GST-Ddlc	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_133_8_1477_s_222	16540510	( F) In vitro binding of Spn-F to GST-Ddlc.	bind
3254	1	2126	6	10	NULL	0	NULL	Prp 	GP		does not bind			27-30		HDL particles	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_30_11312_s_67	16849426	( F) Incubation of PrP 27 - 30 with HDL shows that virtually no HDL particles bind to  the prion rods.	bind
4973	1	2126	7	10	NULL	0	NULL	HDL	Chemical		does not bind					PrP	GP		27 - 30		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_30_11312_s_67	16849426	( F) Incubation of PrP 27 - 30 with HDL shows that virtually no HDL particles bind to  the prion rods.	bind
3255	1	2128	6	10	NULL	0	NULL	Imp4 	GP		bind		weakly			U3 MINI	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_43_15301_s_127	15489263	( F) Nondenaturing PAGE shows that the Imp4 core protein binds weakly to U3 MINI but  does not promote formation of the U3 - ETS duplex.	bind
3256	2	2128	6	10	NULL	0	NULL	Imp4	GP		does not promote 					U3 - ETS duplex	NucleicAcid	formation of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_43_15301_s_127	15489263	( F) Nondenaturing PAGE shows that the Imp4 core protein binds weakly to U3 MINI but  does not promote formation of the U3 - ETS duplex.	bind
46300	3	2128	6	10	NULL	0	NULL	Imp4	GP		is a type of					core protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_43_15301_s_127	15489263	( F) Nondenaturing PAGE shows that the Imp4 core protein binds weakly to U3 MINI but  does not promote formation of the U3 - ETS duplex.	bind
4974	1	2128	7	10	NULL	0	NULL	Imp4	GP		binds		weakly			U3 MINI	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_43_15301_s_127	15489263	( F) Nondenaturing PAGE shows that the Imp4 core protein binds weakly to U3 MINI but  does not promote formation of the U3 - ETS duplex.	bind
4975	2	2128	7	10	NULL	0	NULL	Imp4	GP		does not promote					U3 - ETS duplex	NucleicAcid	formation of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_43_15301_s_127	15489263	( F) Nondenaturing PAGE shows that the Imp4 core protein binds weakly to U3 MINI but  does not promote formation of the U3 - ETS duplex.	bind
46299	3	2128	7	10	NULL	0	NULL	Imp4	GP		is a type of					core protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_43_15301_s_127	15489263	( F) Nondenaturing PAGE shows that the Imp4 core protein binds weakly to U3 MINI but  does not promote formation of the U3 - ETS duplex.	bind
3257	1	2129	6	10	NULL	0	NULL	p97	GP		bind					eIF2beta	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_embo_25_17_4008_s_72	16932749	( F) p97 binds eIF2beta in vivo.	bind
4976	1	2129	7	10	NULL	0	NULL	 p97	GP		binds					eIF2beta	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_embo_25_17_4008_s_72	16932749	( F) p97 binds eIF2beta in vivo.	bind
3258	1	2130	6	10	NULL	0	NULL	PTG	GP		bind					phosphorylase kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_275_5305_1475_s_62	9045612	( F) PTG binds phosphorylase kinase.	bind
4977	1	2130	7	10	NULL	0	NULL	PTG	GP		binds					phosphorylase kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_275_5305_1475_s_62	9045612	( F) PTG binds phosphorylase kinase.	bind
3259	1	2131	6	10	NULL	0	NULL	AQP1-specific antibody	GP		bind					AQP1	GP		carboxyl domain 		NULL	ZG membrane intragranular side	NULL	NULL	NULL	NULL	gw60_pnas_99_7_4720_s_161	11917120	( F) Schematic diagram of ZG membrane depicting AQP1-specific antibody binding to the carboxyl domain of AQP1 at the intragranular side to block water gating.	bind
46192	2	2131	6	10	NULL	0	NULL	statement 1	Process		blocks					water gating	Process				NULL	ZG membrane intragranular side	NULL	NULL	NULL	NULL	gw60_pnas_99_7_4720_s_161	11917120	( F) Schematic diagram of ZG membrane depicting AQP1-specific antibody binding to the carboxyl domain of AQP1 at the intragranular side to block water gating.	bind
4978	1	2131	7	10	NULL	0	NULL	AQP1-specific antibody	GP		binds to 					AQP1	GP		 carboxyl domain		NULL	ZG membrane intragranular side	NULL	NULL	NULL	NULL	gw60_pnas_99_7_4720_s_161	11917120	( F) Schematic diagram of ZG membrane depicting AQP1-specific antibody binding to the carboxyl domain of AQP1 at the intragranular side to block water gating.	bind
4980	3	2131	7	10	NULL	0	NULL	statement 1	Process		blocks					water gating	Process				NULL	ZG membrane intragranular side	NULL	NULL	NULL	NULL	gw60_pnas_99_7_4720_s_161	11917120	( F) Schematic diagram of ZG membrane depicting AQP1-specific antibody binding to the carboxyl domain of AQP1 at the intragranular side to block water gating.	bind
3260	1	2133	6	10	NULL	0	NULL	HVEM-Fc	GP		bind					BTLA-Fc	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_4_1116_s_135	15647361	( F) Sensorgrams of HVEM-Fc (10 nM) binding to immobilized BTLA-Fc in the presence of  increasing amounts of gD (delta290 - 299).	bind
3261	2	2133	6	10	NULL	0	NULL	statement 1	Process		in presence of 					gD	GP	increasing amounts of	delta290 - 299		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_4_1116_s_135	15647361	( F) Sensorgrams of HVEM-Fc (10 nM) binding to immobilized BTLA-Fc in the presence of  increasing amounts of gD (delta290 - 299).	bind
4981	1	2133	7	10	NULL	0	NULL	HVEM-Fc	GP		binds to					BTLA-Fc 	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_4_1116_s_135	15647361	( F) Sensorgrams of HVEM-Fc (10 nM) binding to immobilized BTLA-Fc in the presence of  increasing amounts of gD (delta290 - 299).	bind
4982	2	2133	7	10	NULL	0	NULL	statement 1	Process		occurs in the presence					 gD	GP	increasing amounts of	delta290 - 299		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_4_1116_s_135	15647361	( F) Sensorgrams of HVEM-Fc (10 nM) binding to immobilized BTLA-Fc in the presence of  increasing amounts of gD (delta290 - 299).	bind
3262	1	2134	6	10	NULL	0	NULL	MukF	GP	tagged	bind			331-440		MukB	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_11_1921_s_142	15902272	( F) Tagged MukF(331 440) binds MukB.	bind
4984	1	2134	7	10	NULL	0	NULL	MukF	GP	Tagged	binds			331-440		MukB	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_11_1921_s_142	15902272	( F) Tagged MukF(331 440) binds MukB.	bind
3263	1	2135	6	10	NULL	0	NULL	c-Src	GP		bind					nAchRs	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_8_2208_s_129	16862215	( F) The binding between c-Src and nAChRs was inhibited by the Src inhibitor PP2.	bind
3264	2	2135	6	10	NULL	0	NULL	PP2	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_8_2208_s_129	16862215	( F) The binding between c-Src and nAChRs was inhibited by the Src inhibitor PP2.	bind
45892	3	2135	6	10	NULL	0	NULL	PP2	GP		is a type of					Src inhibitor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_8_2208_s_129	16862215	( F) The binding between c-Src and nAChRs was inhibited by the Src inhibitor PP2.	bind
4985	1	2135	7	10	NULL	0	NULL	c-Src	GP		binds					nAChRs	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_8_2208_s_129	16862215	( F) The binding between c-Src and nAChRs was inhibited by the Src inhibitor PP2.	bind
4986	2	2135	7	10	NULL	0	NULL	statement 1	Process		is inhibited by					PP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_8_2208_s_129	16862215	( F) The binding between c-Src and nAChRs was inhibited by the Src inhibitor PP2.	bind
45893	3	2135	7	10	NULL	0	NULL	PP2	GP		is a type of					Src inhibitor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_8_2208_s_129	16862215	( F) The binding between c-Src and nAChRs was inhibited by the Src inhibitor PP2.	bind
3265	1	2136	6	10	NULL	0	NULL	IE2	GP	mutant	bind					p53/p300 complex	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_11_2269_s_192	15141169	( F) The HAT inhibition mutant of IE2 binds to the endogenous p53/p300 complex on the   p21 promoter.	bind
3266	2	2136	6	10	NULL	0	NULL	IE2	GP	mutant	inhibits					HAT	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_11_2269_s_192	15141169	( F) The HAT inhibition mutant of IE2 binds to the endogenous p53/p300 complex on the   p21 promoter.	bind
45897	3	2136	6	10	NULL	0	NULL	statement 1	Process		occurs in					p21	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_23_11_2269_s_192	15141169	( F) The HAT inhibition mutant of IE2 binds to the endogenous p53/p300 complex on the   p21 promoter.	bind
5104	1	2136	7	10	NULL	0	NULL	IE2	GP	mutant	binds to					 p53/p300 complex	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_11_2269_s_192	15141169	( F) The HAT inhibition mutant of IE2 binds to the endogenous p53/p300 complex on the   p21 promoter.	bind
5106	2	2136	7	10	NULL	0	NULL	statement 1	Process		occurs in 					p21	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_23_11_2269_s_192	15141169	( F) The HAT inhibition mutant of IE2 binds to the endogenous p53/p300 complex on the   p21 promoter.	bind
45896	3	2136	7	10	NULL	0	NULL	IE2	GP	mutant	inhibit					HAT	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_11_2269_s_192	15141169	( F) The HAT inhibition mutant of IE2 binds to the endogenous p53/p300 complex on the   p21 promoter.	bind
3291	1	2137	6	10	NULL	0	NULL	TMEFF1	GP	mutant	bind			follistatin modules		Cripto	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_21_2624_s_134	14563676	( F) The TMEFF1 deletion mutants that lack either the follistatin modules or the EGF  motif still bind to Cripto.	bind
3292	2	2137	6	10	NULL	0	NULL	TMEFF1	GP	mutant	bind			EGF motif		Cripto	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_21_2624_s_134	14563676	( F) The TMEFF1 deletion mutants that lack either the follistatin modules or the EGF  motif still bind to Cripto.	bind
5107	1	2137	7	10	NULL	0	NULL	 TMEFF1 	GP	mutant	binds			follistatin modules		Cripto	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_21_2624_s_134	14563676	( F) The TMEFF1 deletion mutants that lack either the follistatin modules or the EGF  motif still bind to Cripto.	bind
5108	2	2137	7	10	NULL	0	NULL	TMEFF1	GP	mutant	binds			EGF motif		Cripto	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_21_2624_s_134	14563676	( F) The TMEFF1 deletion mutants that lack either the follistatin modules or the EGF  motif still bind to Cripto.	bind
3293	1	2138	6	10	NULL	0	NULL	progesterone	GP		bind		specifically			mPRgamma	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_5_2237_s_156	12601167	( f) Time course of association and dissociation of specific progesterone binding to  human mPRgamma.	bind
5109	1	2138	7	10	NULL	0	NULL	progesterone	GP		binds to		specifically			mPRgamma	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_5_2237_s_156	12601167	( f) Time course of association and dissociation of specific progesterone binding to  human mPRgamma.	bind
3294	1	2140	6	10	NULL	0	NULL				bind			V3IIIB		Fv	GP		residues T303		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_38_13950_s_92	16966601	( F) V3IIIB bound to 0.5beta Fv; residues T303 and K322, not included in the NMR structure, were modeled.	bind
3295	2	2140	6	10	NULL	0	NULL				bind			V3IIIB		Fv	GP		residues K322		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_38_13950_s_92	16966601	( F) V3IIIB bound to 0.5beta Fv; residues T303 and K322, not included in the NMR structure, were modeled.	bind
5110	1	2140	7	10	NULL	0	NULL				bind			V3IIIB		 Fv	GP		residues T303		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_38_13950_s_92	16966601	( F) V3IIIB bound to 0.5beta Fv; residues T303 and K322, not included in the NMR structure, were modeled.	bind
46293	2	2140	7	10	NULL	0	NULL				bind			V3IIIB 		Fv	GP		residues K322		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_38_13950_s_92	16966601	( F) V3IIIB bound to 0.5beta Fv; residues T303 and K322, not included in the NMR structure, were modeled.	bind
3296	1	2141	6	10	NULL	0	NULL	Oct-1	GP		bind					SV40	GP			octamer element of enhancer	NULL	HeLa nuclear extracts	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_9_4575_s_239	7876228	( Fig. 6  B) Thus the predominant  complexes formed in HeLa nuclear extracts with this region of the SV40  enhancer contain Oct-1 bound to the octamer element and HIP116 bound  specifically to the SPH repeats.	bind
3297	2	2141	6	10	NULL	0	NULL	HIP116	GP		bind		specifically			SV40	GP			SPH repeats of enhancer	NULL	HeLa nuclear extracts	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_9_4575_s_239	7876228	( Fig. 6  B) Thus the predominant  complexes formed in HeLa nuclear extracts with this region of the SV40  enhancer contain Oct-1 bound to the octamer element and HIP116 bound  specifically to the SPH repeats.	bind
5111	1	2141	7	10	NULL	0	NULL	Oct-1	GP		binds					SV40	GP			octamer element of enhancer	NULL	HeLa nuclear extracts	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_9_4575_s_239	7876228	( Fig. 6  B) Thus the predominant  complexes formed in HeLa nuclear extracts with this region of the SV40  enhancer contain Oct-1 bound to the octamer element and HIP116 bound  specifically to the SPH repeats.	bind
5112	2	2141	7	10	NULL	0	NULL	HIP116	GP		binds		specifically			SV40	GP			SPH repeats of enhancer	NULL	HeLa nuclear extracts	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_9_4575_s_239	7876228	( Fig. 6  B) Thus the predominant  complexes formed in HeLa nuclear extracts with this region of the SV40  enhancer contain Oct-1 bound to the octamer element and HIP116 bound  specifically to the SPH repeats.	bind
3298	1	2142	6	10	NULL	0	NULL	TBL1	GP		bind					H2B	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_66_0_315_s_230	14977406	( Figures 3 and 5) ( 177, 180, 184, 189); TBL1 and TBLR1 also bind to histones H2B and H4 ( 189) and may help in chromatin substrate recognition.	bind
3299	2	2142	6	10	NULL	0	NULL	TBL1	GP		bind					H4	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_66_0_315_s_230	14977406	( Figures 3 and 5) ( 177, 180, 184, 189); TBL1 and TBLR1 also bind to histones H2B and H4 ( 189) and may help in chromatin substrate recognition.	bind
3300	3	2142	6	10	NULL	0	NULL	TBLR1	GP		bind					H2B	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_66_0_315_s_230	14977406	( Figures 3 and 5) ( 177, 180, 184, 189); TBL1 and TBLR1 also bind to histones H2B and H4 ( 189) and may help in chromatin substrate recognition.	bind
3301	4	2142	6	10	NULL	0	NULL	TBLR1	GP		bind					H4	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_66_0_315_s_230	14977406	( Figures 3 and 5) ( 177, 180, 184, 189); TBL1 and TBLR1 also bind to histones H2B and H4 ( 189) and may help in chromatin substrate recognition.	bind
3302	5	2142	6	10	NULL	0	NULL	TBL1	GP		help in		may			chromatin substrate	GP	recognition of			NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_66_0_315_s_230	14977406	( Figures 3 and 5) ( 177, 180, 184, 189); TBL1 and TBLR1 also bind to histones H2B and H4 ( 189) and may help in chromatin substrate recognition.	bind
3303	6	2142	6	10	NULL	0	NULL	TBLR1	GP		help in		may			chromatin substrate	GP	recognition of			NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_66_0_315_s_230	14977406	( Figures 3 and 5) ( 177, 180, 184, 189); TBL1 and TBLR1 also bind to histones H2B and H4 ( 189) and may help in chromatin substrate recognition.	bind
45902	7	2142	6	10	NULL	0	NULL	H2B	GP		is a type of					histone	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_66_0_315_s_230	14977406	( Figures 3 and 5) ( 177, 180, 184, 189); TBL1 and TBLR1 also bind to histones H2B and H4 ( 189) and may help in chromatin substrate recognition.	bind
45903	8	2142	6	10	NULL	0	NULL	H4	GP		is a type of					histone	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_66_0_315_s_230	14977406	( Figures 3 and 5) ( 177, 180, 184, 189); TBL1 and TBLR1 also bind to histones H2B and H4 ( 189) and may help in chromatin substrate recognition.	bind
5116	1	2142	7	10	NULL	0	NULL	TBL1	GP		binds					H2B	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_66_0_315_s_230	14977406	( Figures 3 and 5) ( 177, 180, 184, 189); TBL1 and TBLR1 also bind to histones H2B and H4 ( 189) and may help in chromatin substrate recognition.	bind
5117	2	2142	7	10	NULL	0	NULL	TBL1	GP		binds					H4	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_66_0_315_s_230	14977406	( Figures 3 and 5) ( 177, 180, 184, 189); TBL1 and TBLR1 also bind to histones H2B and H4 ( 189) and may help in chromatin substrate recognition.	bind
5118	3	2142	7	10	NULL	0	NULL	TBLR1	GP		binds					H2B	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_66_0_315_s_230	14977406	( Figures 3 and 5) ( 177, 180, 184, 189); TBL1 and TBLR1 also bind to histones H2B and H4 ( 189) and may help in chromatin substrate recognition.	bind
5119	4	2142	7	10	NULL	0	NULL	TBLR1	GP		binds					H4	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_66_0_315_s_230	14977406	( Figures 3 and 5) ( 177, 180, 184, 189); TBL1 and TBLR1 also bind to histones H2B and H4 ( 189) and may help in chromatin substrate recognition.	bind
5120	5	2142	7	10	NULL	0	NULL	statement 1	Process		helps in					chromatin substrate	GP	recognizing			NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_66_0_315_s_230	14977406	( Figures 3 and 5) ( 177, 180, 184, 189); TBL1 and TBLR1 also bind to histones H2B and H4 ( 189) and may help in chromatin substrate recognition.	bind
5121	6	2142	7	10	NULL	0	NULL	statement 2	Process		helps in					chromatin substrate	GP	recognizing			NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_66_0_315_s_230	14977406	( Figures 3 and 5) ( 177, 180, 184, 189); TBL1 and TBLR1 also bind to histones H2B and H4 ( 189) and may help in chromatin substrate recognition.	bind
5122	7	2142	7	10	NULL	0	NULL	statement 3	Process		helps in					chromatin substrate	GP	recognizing			NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_66_0_315_s_230	14977406	( Figures 3 and 5) ( 177, 180, 184, 189); TBL1 and TBLR1 also bind to histones H2B and H4 ( 189) and may help in chromatin substrate recognition.	bind
5123	8	2142	7	10	NULL	0	NULL	statement 4	Process		helps in					chromatin substrate	GP	recognizing			NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_66_0_315_s_230	14977406	( Figures 3 and 5) ( 177, 180, 184, 189); TBL1 and TBLR1 also bind to histones H2B and H4 ( 189) and may help in chromatin substrate recognition.	bind
45904	9	2142	7	10	NULL	0	NULL	H2B	GP		is a type of					histone	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_66_0_315_s_230	14977406	( Figures 3 and 5) ( 177, 180, 184, 189); TBL1 and TBLR1 also bind to histones H2B and H4 ( 189) and may help in chromatin substrate recognition.	bind
45905	10	2142	7	10	NULL	0	NULL	H4 \t	GP		is a type of					histone	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_66_0_315_s_230	14977406	( Figures 3 and 5) ( 177, 180, 184, 189); TBL1 and TBLR1 also bind to histones H2B and H4 ( 189) and may help in chromatin substrate recognition.	bind
3395	1	2143	6	10	NULL	0	NULL	p53	GP		bind					DNA	NucleicAcid				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_embo_23_11_2269_s_240	15141169	( Figures 3,  5, and  7), and that IE2 deletion mutants (aa 136 579 and 169 579) lacking the minimal N-terminal  HAT inhibitory domain failed to repress the  in vivo DNA binding of p53 and local histone acetylation ( Figures 1C,  5,  7E, F,  8, and  9).	bind
3396	2	2143	6	10	NULL	0	NULL	IE2	GP	deletion mutant	fail to repress			aa 136 579;;169 579		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_11_2269_s_240	15141169	( Figures 3,  5, and  7), and that IE2 deletion mutants (aa 136 579 and 169 579) lacking the minimal N-terminal  HAT inhibitory domain failed to repress the  in vivo DNA binding of p53 and local histone acetylation ( Figures 1C,  5,  7E, F,  8, and  9).	bind
3798	3	2143	6	10	NULL	0	NULL	IE2	GP	deletion mutant	lacks			aa 136 579;;169 579					minimal N-terminal HAT inhibitory domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_11_2269_s_240	15141169	( Figures 3,  5, and  7), and that IE2 deletion mutants (aa 136 579 and 169 579) lacking the minimal N-terminal  HAT inhibitory domain failed to repress the  in vivo DNA binding of p53 and local histone acetylation ( Figures 1C,  5,  7E, F,  8, and  9).	bind
3799	4	2143	6	10	NULL	0	NULL	IE2	GP	deletion mutant	fail to repress			aa 136 579;;169 579		histone	GP	acetylation of			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_11_2269_s_240	15141169	( Figures 3,  5, and  7), and that IE2 deletion mutants (aa 136 579 and 169 579) lacking the minimal N-terminal  HAT inhibitory domain failed to repress the  in vivo DNA binding of p53 and local histone acetylation ( Figures 1C,  5,  7E, F,  8, and  9).	bind
5124	1	2143	7	10	NULL	0	NULL	p53	GP		binds					DNA	NucleicAcid				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_embo_23_11_2269_s_240	15141169	( Figures 3,  5, and  7), and that IE2 deletion mutants (aa 136 579 and 169 579) lacking the minimal N-terminal  HAT inhibitory domain failed to repress the  in vivo DNA binding of p53 and local histone acetylation ( Figures 1C,  5,  7E, F,  8, and  9).	bind
5125	2	2143	7	10	NULL	0	NULL	Histone	GP		undergoes					acetylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_11_2269_s_240	15141169	( Figures 3,  5, and  7), and that IE2 deletion mutants (aa 136 579 and 169 579) lacking the minimal N-terminal  HAT inhibitory domain failed to repress the  in vivo DNA binding of p53 and local histone acetylation ( Figures 1C,  5,  7E, F,  8, and  9).	bind
5126	3	2143	7	10	NULL	0	NULL	IE2	GP	deletion mutants 	lacks			aa 136 579;;169 579					N-terminal HAT inhibitory domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_11_2269_s_240	15141169	( Figures 3,  5, and  7), and that IE2 deletion mutants (aa 136 579 and 169 579) lacking the minimal N-terminal  HAT inhibitory domain failed to repress the  in vivo DNA binding of p53 and local histone acetylation ( Figures 1C,  5,  7E, F,  8, and  9).	bind
5127	4	2143	7	10	NULL	0	NULL	statement 3	Process		does not repress					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_11_2269_s_240	15141169	( Figures 3,  5, and  7), and that IE2 deletion mutants (aa 136 579 and 169 579) lacking the minimal N-terminal  HAT inhibitory domain failed to repress the  in vivo DNA binding of p53 and local histone acetylation ( Figures 1C,  5,  7E, F,  8, and  9).	bind
5128	5	2143	7	10	NULL	0	NULL	statement 3	Process		does not repress					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_11_2269_s_240	15141169	( Figures 3,  5, and  7), and that IE2 deletion mutants (aa 136 579 and 169 579) lacking the minimal N-terminal  HAT inhibitory domain failed to repress the  in vivo DNA binding of p53 and local histone acetylation ( Figures 1C,  5,  7E, F,  8, and  9).	bind
3397	1	2144	6	10	NULL	0	NULL	KIF1A	GP		bind			N-terminal motor domain		MT	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1506_s_234	15014437	( Figures 4 and  5) and that disruption of this interaction enhances MT binding of KIF1A mainly through  the N-terminal motor domain ( Figure 6).	bind
5129	1	2144	7	10	NULL	0	NULL	MT 	CellComponent		binds					KIF1A	GP		N-terminal motor domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1506_s_234	15014437	( Figures 4 and  5) and that disruption of this interaction enhances MT binding of KIF1A mainly through  the N-terminal motor domain ( Figure 6).	bind
3398	1	2145	6	10	NULL	0	NULL	CREB	GP		bind					Egr-1	GP			CRE motif in promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
3399	2	2145	6	10	NULL	0	NULL	CREB	GP		bind					Egr-1	GP			SRE motif in promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
3400	3	2145	6	10	NULL	0	NULL	LPA	Chemical		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
3401	4	2145	6	10	NULL	0	NULL	LPA	Chemical		induces					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
3402	5	2145	6	10	NULL	0	NULL	SRF	GP		bind					Egr-1	GP			CRE motif in promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
3403	6	2145	6	10	NULL	0	NULL	SRF	GP		bind					Egr-1	GP			SRE motif in promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
3404	7	2145	6	10	NULL	0	NULL	LPA	Chemical		induces					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
3405	8	2145	6	10	NULL	0	NULL	LPA	Chemical		induces					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
3406	9	2145	6	10	NULL	0	NULL	LPA	Chemical		activates					Egr-1	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
3407	10	2145	6	10	NULL	0	NULL	Egr-1	GP		contribute		possibly		CRE motif of promoter	statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
3408	11	2145	6	10	NULL	0	NULL	Egr-1	GP		contribute		possibly		SRE motif of promoter	statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
5130	1	2145	7	10	NULL	0	NULL	CREB	GP		binds					Egr-1	GP			CRE motifs in the promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
5131	2	2145	7	10	NULL	0	NULL	SRF	GP		binds to					Egr-1	GP			proximal SRE motifs in the promoter of	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
5132	3	2145	7	10	NULL	0	NULL	LPA	Chemical		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
5133	4	2145	7	10	NULL	0	NULL	LPA	Chemical		induces					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
5134	5	2145	7	10	NULL	0	NULL	LPA	Chemical		activates					Egr-1	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
5135	6	2145	7	10	NULL	0	NULL	Egr-1	GP		contributes		possibly		CRE motifs in the promoter of	statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
5136	7	2145	7	10	NULL	0	NULL	Egr-1	GP		contributes		possibly		proximal SRE motifs in the promoter of	statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
46284	8	2145	7	10	NULL	0	NULL	CREB	GP		bind					Egr-1	GP			proximal SRE motifs in the promoter of	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
46285	9	2145	7	10	NULL	0	NULL	SRF	GP		bind					Egr-1	GP			CRE motifs in the promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
46286	10	2145	7	10	NULL	0	NULL	LPA	Chemical		induce					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
46287	11	2145	7	10	NULL	0	NULL	LPA	Chemical		induce					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1029_s_174	16497989	( Figures 4 and 5  ) indicate that LPA induces binding activities of CREB and SRF to the CRE and SRE motifs in the Egr-1 promoter, suggesting that CRE and the proximal SRE motifs of the Egr-1 promoter possibly contribute to LPA activation of Egr-1 transcription.	bind
3409	1	2146	6	10	NULL	0	NULL	Ca+2	Chemical		bind					myofilaments	CellComponent		TnT-I79N		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_4_428_s_223	12600890	( Figures 6 and 8) with no change in L-type Ca2+ current ( Figure 5B) and SR Ca2+ content ( Figure 8F) suggests that initially more Ca2+ is bound to TnT-I79N containing myofilaments, but later on, as the muscle starts to relax, the additional Ca2+ that comes off the myofilaments produces the slower decay of Ca2+ transients.	bind
5137	1	2146	7	10	NULL	0	NULL	Ca2+	Chemical		binds					myofilaments	CellComponent		TnT-I79N		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_4_428_s_223	12600890	( Figures 6 and 8) with no change in L-type Ca2+ current ( Figure 5B) and SR Ca2+ content ( Figure 8F) suggests that initially more Ca2+ is bound to TnT-I79N containing myofilaments, but later on, as the muscle starts to relax, the additional Ca2+ that comes off the myofilaments produces the slower decay of Ca2+ transients.	bind
3651	1	2148	6	10	NULL	0	NULL	IgG	GP		bind					anchoring fibrils	CellComponent				NULL	lamina densa of the dermoepidermal junction	NULL	NULL	NULL	NULL	gw70_jclininvest_116_5_1159_s_30	16670756	( G -  I) Epidermolysis bullosa acquisita is associated with IgG (and sometimes IgA) binding  to the anchoring fibrils underneath the lamina densa of the dermoepidermal junction  ( G), resulting in a subepidermal loss of adhesion ( H) and tense blisters with a tendency toward scarring and milia formation	bind
3652	2	2148	6	10	NULL	0	NULL	statement 1	Process		leads to 					adhesion	Process	subepidermal loss of			NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_5_1159_s_30	16670756	( G -  I) Epidermolysis bullosa acquisita is associated with IgG (and sometimes IgA) binding  to the anchoring fibrils underneath the lamina densa of the dermoepidermal junction  ( G), resulting in a subepidermal loss of adhesion ( H) and tense blisters with a tendency toward scarring and milia formation	bind
3800	3	2148	6	10	NULL	0	NULL	IgA	GP		bind		sometimes			anchoring fibrils	CellComponent				NULL	lamina densa of the dermoepidermal junction	NULL	NULL	NULL	NULL	gw70_jclininvest_116_5_1159_s_30	16670756	( G -  I) Epidermolysis bullosa acquisita is associated with IgG (and sometimes IgA) binding  to the anchoring fibrils underneath the lamina densa of the dermoepidermal junction  ( G), resulting in a subepidermal loss of adhesion ( H) and tense blisters with a tendency toward scarring and milia formation	bind
3801	4	2148	6	10	NULL	0	NULL	Epidermolysis bullosa acquisita			is associated with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_5_1159_s_30	16670756	( G -  I) Epidermolysis bullosa acquisita is associated with IgG (and sometimes IgA) binding  to the anchoring fibrils underneath the lamina densa of the dermoepidermal junction  ( G), resulting in a subepidermal loss of adhesion ( H) and tense blisters with a tendency toward scarring and milia formation	bind
3802	5	2148	6	10	NULL	0	NULL	Epidermolysis bullosa acquisita			is associated with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_5_1159_s_30	16670756	( G -  I) Epidermolysis bullosa acquisita is associated with IgG (and sometimes IgA) binding  to the anchoring fibrils underneath the lamina densa of the dermoepidermal junction  ( G), resulting in a subepidermal loss of adhesion ( H) and tense blisters with a tendency toward scarring and milia formation	bind
5138	1	2148	7	10	NULL	0	NULL	 IgG 	GP		binds					anchoring fibrils	CellComponent				NULL	underneath the lamina densa of the dermoepidermal junction	NULL	NULL	NULL	NULL	gw70_jclininvest_116_5_1159_s_30	16670756	( G -  I) Epidermolysis bullosa acquisita is associated with IgG (and sometimes IgA) binding  to the anchoring fibrils underneath the lamina densa of the dermoepidermal junction  ( G), resulting in a subepidermal loss of adhesion ( H) and tense blisters with a tendency toward scarring and milia formation	bind
5139	2	2148	7	10	NULL	0	NULL	IgA	GP		binds					anchoring fibrils	CellComponent				NULL	underneath the lamina densa of the dermoepidermal junction	NULL	NULL	NULL	NULL	gw70_jclininvest_116_5_1159_s_30	16670756	( G -  I) Epidermolysis bullosa acquisita is associated with IgG (and sometimes IgA) binding  to the anchoring fibrils underneath the lamina densa of the dermoepidermal junction  ( G), resulting in a subepidermal loss of adhesion ( H) and tense blisters with a tendency toward scarring and milia formation	bind
5140	3	2148	7	10	NULL	0	NULL	Epidermolysis bullosa acquisita			is associated with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_5_1159_s_30	16670756	( G -  I) Epidermolysis bullosa acquisita is associated with IgG (and sometimes IgA) binding  to the anchoring fibrils underneath the lamina densa of the dermoepidermal junction  ( G), resulting in a subepidermal loss of adhesion ( H) and tense blisters with a tendency toward scarring and milia formation	bind
5141	4	2148	7	10	NULL	0	NULL	Epidermolysis bullosa acquisita			is associated with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_5_1159_s_30	16670756	( G -  I) Epidermolysis bullosa acquisita is associated with IgG (and sometimes IgA) binding  to the anchoring fibrils underneath the lamina densa of the dermoepidermal junction  ( G), resulting in a subepidermal loss of adhesion ( H) and tense blisters with a tendency toward scarring and milia formation	bind
5142	5	2148	7	10	NULL	0	NULL	statement 1	Process		results in					adhesion	Process	 subepidermal loss of			NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_5_1159_s_30	16670756	( G -  I) Epidermolysis bullosa acquisita is associated with IgG (and sometimes IgA) binding  to the anchoring fibrils underneath the lamina densa of the dermoepidermal junction  ( G), resulting in a subepidermal loss of adhesion ( H) and tense blisters with a tendency toward scarring and milia formation	bind
5143	6	2148	7	10	NULL	0	NULL	statement 2	Process		results in					adhesion	Process	subepidermal loss of			NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_5_1159_s_30	16670756	( G -  I) Epidermolysis bullosa acquisita is associated with IgG (and sometimes IgA) binding  to the anchoring fibrils underneath the lamina densa of the dermoepidermal junction  ( G), resulting in a subepidermal loss of adhesion ( H) and tense blisters with a tendency toward scarring and milia formation	bind
6251	7	2148	7	10	NULL	0	NULL	statement 1	Process		results in					tense blisters	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_5_1159_s_30	16670756	( G -  I) Epidermolysis bullosa acquisita is associated with IgG (and sometimes IgA) binding  to the anchoring fibrils underneath the lamina densa of the dermoepidermal junction  ( G), resulting in a subepidermal loss of adhesion ( H) and tense blisters with a tendency toward scarring and milia formation	bind
6252	9	2148	7	10	NULL	0	NULL	tense blisters			has tendency toward					scarring	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_5_1159_s_30	16670756	( G -  I) Epidermolysis bullosa acquisita is associated with IgG (and sometimes IgA) binding  to the anchoring fibrils underneath the lamina densa of the dermoepidermal junction  ( G), resulting in a subepidermal loss of adhesion ( H) and tense blisters with a tendency toward scarring and milia formation	bind
46288	10	2148	7	10	NULL	0	NULL	tense blisters			has tendency toward					milia formation	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_5_1159_s_30	16670756	( G -  I) Epidermolysis bullosa acquisita is associated with IgG (and sometimes IgA) binding  to the anchoring fibrils underneath the lamina densa of the dermoepidermal junction  ( G), resulting in a subepidermal loss of adhesion ( H) and tense blisters with a tendency toward scarring and milia formation	bind
46289	8	2148	7	10	NULL	0	NULL	statement 2	Process		results in					tense blisters	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_5_1159_s_30	16670756	( G -  I) Epidermolysis bullosa acquisita is associated with IgG (and sometimes IgA) binding  to the anchoring fibrils underneath the lamina densa of the dermoepidermal junction  ( G), resulting in a subepidermal loss of adhesion ( H) and tense blisters with a tendency toward scarring and milia formation	bind
3410	1	2149	6	10	NULL	0	NULL	Akt	GP		bind					Ebp1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_10_2083_s_157	16642037	( G) Akt binds Ebp1 in an NGF-dependent manner.	bind
3411	2	2149	6	10	NULL	0	NULL	statement 1	Process		dependent on					NGF	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_10_2083_s_157	16642037	( G) Akt binds Ebp1 in an NGF-dependent manner.	bind
5144	1	2149	7	10	NULL	0	NULL	Akt	GP		binds					Ebp1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_10_2083_s_157	16642037	( G) Akt binds Ebp1 in an NGF-dependent manner.	bind
5145	2	2149	7	10	NULL	0	NULL	statement 1	Process		is dependent on					NGF	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_10_2083_s_157	16642037	( G) Akt binds Ebp1 in an NGF-dependent manner.	bind
3412	1	2150	6	10	NULL	0	NULL	AP-Nogo-66	GP		bind					Fc-MAG	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_297_5584_1190_s_50	12089450	( G) AP-Nogo-66 or AP-NgR bound to Fc-MAG.	bind
3413	2	2150	6	10	NULL	0	NULL	AP-NgR	GP		bind					Fc-MAG	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_297_5584_1190_s_50	12089450	( G) AP-Nogo-66 or AP-NgR bound to Fc-MAG.	bind
4397	3	2150	6	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_297_5584_1190_s_50	12089450	( G) AP-Nogo-66 or AP-NgR bound to Fc-MAG.	bind
5146	1	2150	7	10	NULL	0	NULL	 AP-Nogo-66	GP		binds					Fc-MAG	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_297_5584_1190_s_50	12089450	( G) AP-Nogo-66 or AP-NgR bound to Fc-MAG.	bind
5147	2	2150	7	10	NULL	0	NULL	AP-NgR	GP		binds					Fc-MAG	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_297_5584_1190_s_50	12089450	( G) AP-Nogo-66 or AP-NgR bound to Fc-MAG.	bind
51552	3	2150	7	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_297_5584_1190_s_50	12089450	( G) AP-Nogo-66 or AP-NgR bound to Fc-MAG.	bind
3414	1	2151	6	10	NULL	0	NULL	PAIRED DNA	NucleicAcid		bind									100 bp so probe	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_4_802_s_187	11179224	( G) Bacterially synthesized ANTP HD inhibits PAIRED DNA binding to the 100 bp  so probe ( Niimi  et al., 1999).	bind
3415	2	2151	6	10	NULL	0	NULL	ANTP	GP	bacterially synthesized	inhibits			HD		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_4_802_s_187	11179224	( G) Bacterially synthesized ANTP HD inhibits PAIRED DNA binding to the 100 bp  so probe ( Niimi  et al., 1999).	bind
5148	1	2151	7	10	NULL	0	NULL	PAIRED DNA	NucleicAcid		binds									100 bp	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_4_802_s_187	11179224	( G) Bacterially synthesized ANTP HD inhibits PAIRED DNA binding to the 100 bp  so probe ( Niimi  et al., 1999).	bind
5149	2	2151	7	10	NULL	0	NULL	ANTP	GP	Bacterially synthesized	inhibits			HD		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_4_802_s_187	11179224	( G) Bacterially synthesized ANTP HD inhibits PAIRED DNA binding to the 100 bp  so probe ( Niimi  et al., 1999).	bind
3416	1	2152	6	10	NULL	0	NULL	LyP-1	GP		bind					MDA-MB-435 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12617_s_78	12235356	( g) Binding of LyP-1 qdots to MDA-MB-435 cells.	bind
5150	1	2152	7	10	NULL	0	NULL	LyP-1	GP		binds to					MDA-MB-435 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12617_s_78	12235356	( g) Binding of LyP-1 qdots to MDA-MB-435 cells.	bind
3417	1	2153	6	10	NULL	0	NULL	Myc	GP		bind					Miz-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_336_s_169	15616584	( G) Corepression of  p21Cip1 by Myc and Dnmt3a requires binding of Myc to Miz-1.	bind
3418	2	2153	6	10	NULL	0	NULL	Myc	GP		corepresses					p21Cip1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_336_s_169	15616584	( G) Corepression of  p21Cip1 by Myc and Dnmt3a requires binding of Myc to Miz-1.	bind
3419	3	2153	6	10	NULL	0	NULL	Dnmt3a	GP		corepresses					p21Cip1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_336_s_169	15616584	( G) Corepression of  p21Cip1 by Myc and Dnmt3a requires binding of Myc to Miz-1.	bind
3420	4	2153	6	10	NULL	0	NULL	statement 2	Process		requires					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_336_s_169	15616584	( G) Corepression of  p21Cip1 by Myc and Dnmt3a requires binding of Myc to Miz-1.	bind
3421	5	2153	6	10	NULL	0	NULL	statement 3	Process		requires					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_336_s_169	15616584	( G) Corepression of  p21Cip1 by Myc and Dnmt3a requires binding of Myc to Miz-1.	bind
5151	1	2153	7	10	NULL	0	NULL	Myc	GP		binds					Miz-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_336_s_169	15616584	( G) Corepression of  p21Cip1 by Myc and Dnmt3a requires binding of Myc to Miz-1.	bind
5152	2	2153	7	10	NULL	0	NULL	Myc	GP		corepress					p21Cip1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_336_s_169	15616584	( G) Corepression of  p21Cip1 by Myc and Dnmt3a requires binding of Myc to Miz-1.	bind
5153	3	2153	7	10	NULL	0	NULL	Dnmt3a	GP		corepress					p21Cip1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_336_s_169	15616584	( G) Corepression of  p21Cip1 by Myc and Dnmt3a requires binding of Myc to Miz-1.	bind
5154	4	2153	7	10	NULL	0	NULL	statement 2	Process		requires					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_336_s_169	15616584	( G) Corepression of  p21Cip1 by Myc and Dnmt3a requires binding of Myc to Miz-1.	bind
5155	5	2153	7	10	NULL	0	NULL	statement 3	Process		requires					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_336_s_169	15616584	( G) Corepression of  p21Cip1 by Myc and Dnmt3a requires binding of Myc to Miz-1.	bind
3422	1	2155	6	10	NULL	0	NULL	RAD50	GP	human	bind			NH2-terminus		BRCA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5428_747_s_40	10426999	( G) NH2-terminus of hRad50 binds BRCA1 in a yeast two-hybrid assay.	bind
5156	1	2155	7	10	NULL	0	NULL	hRad50	GP		binds			NH2-terminus		BRCA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5428_747_s_40	10426999	( G) NH2-terminus of hRad50 binds BRCA1 in a yeast two-hybrid assay.	bind
3423	1	2156	6	10	NULL	0	NULL	CaBP1	GP		bind					Ins P3R-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_11_7711_s_163	12032348	( G) Quantitative analysis of competition for CaBP1 binding to Ins P3R-3 by s-CaBP1 with data normalized to binding in the absence of added s-CaBP1.	bind
3424	2	2156	6	10	NULL	0	NULL	s-CaBP1	GP		bind					Ins P3R-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_11_7711_s_163	12032348	( G) Quantitative analysis of competition for CaBP1 binding to Ins P3R-3 by s-CaBP1 with data normalized to binding in the absence of added s-CaBP1.	bind
3425	3	2156	6	10	NULL	0	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_11_7711_s_163	12032348	( G) Quantitative analysis of competition for CaBP1 binding to Ins P3R-3 by s-CaBP1 with data normalized to binding in the absence of added s-CaBP1.	bind
5157	1	2156	7	10	NULL	0	NULL	CaBP1	GP		binds					Ins P3R-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_11_7711_s_163	12032348	( G) Quantitative analysis of competition for CaBP1 binding to Ins P3R-3 by s-CaBP1 with data normalized to binding in the absence of added s-CaBP1.	bind
5158	2	2156	7	10	NULL	0	NULL	 s-CaBP1	GP		binds					Ins P3R-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_11_7711_s_163	12032348	( G) Quantitative analysis of competition for CaBP1 binding to Ins P3R-3 by s-CaBP1 with data normalized to binding in the absence of added s-CaBP1.	bind
5159	3	2156	7	10	NULL	0	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_11_7711_s_163	12032348	( G) Quantitative analysis of competition for CaBP1 binding to Ins P3R-3 by s-CaBP1 with data normalized to binding in the absence of added s-CaBP1.	bind
3426	1	2157	6	10	NULL	0	NULL	MukF	GP	tagged	bind			331 440		MukB	GP		ATPase domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_11_1921_s_143	15902272	( G) Tagged MukF(331 440) binds the ATPase domain of MukB.	bind
5160	1	2157	7	10	NULL	0	NULL	MukF	GP	Tagged	binds			331 440		MukB	GP		ATPase domain of		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_11_1921_s_143	15902272	( G) Tagged MukF(331 440) binds the ATPase domain of MukB.	bind
3427	1	2158	6	10	NULL	0	NULL	Triol	GP		bind		directly			PXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_3_833_s_78	12569201	( g) Triol binds directly to PXR.	bind
5161	1	2158	7	10	NULL	0	NULL	Triol 	GP		binds		directly			PXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_3_833_s_78	12569201	( g) Triol binds directly to PXR.	bind
3428	1	2159	6	10	NULL	0	NULL	GST-Six3	GP	bacteria expressed	bind		strongly			Wnt1	GP			element I of promoter	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_3_368_s_140	12569128	( G``) A magnification of the electroporated embryo shown in  G. ( H) EMSA assay shows that bacteria-expressed GST-Six3 fusion protein binds to the  Wnt1 promoter elements I and II (lanes  3,8) strongly, very weakly to element III (lane  13), and not at all to element IV (data not shown).	bind
3429	2	2159	6	10	NULL	0	NULL	GST-Six3	GP	bacteria expressed	bind		strongly			Wnt1	GP			element II of promoter	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_3_368_s_140	12569128	( G``) A magnification of the electroporated embryo shown in  G. ( H) EMSA assay shows that bacteria-expressed GST-Six3 fusion protein binds to the  Wnt1 promoter elements I and II (lanes  3,8) strongly, very weakly to element III (lane  13), and not at all to element IV (data not shown).	bind
3430	3	2159	6	10	NULL	0	NULL	GST-Six3	GP	bacteria expressed	bind		weakly			Wnt1	GP			element III of promoter	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_3_368_s_140	12569128	( G``) A magnification of the electroporated embryo shown in  G. ( H) EMSA assay shows that bacteria-expressed GST-Six3 fusion protein binds to the  Wnt1 promoter elements I and II (lanes  3,8) strongly, very weakly to element III (lane  13), and not at all to element IV (data not shown).	bind
3431	4	2159	6	10	NULL	0	NULL	GST-Six3	GP		does not bind					Wnt1	GP			element IV of promoter	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_3_368_s_140	12569128	( G``) A magnification of the electroporated embryo shown in  G. ( H) EMSA assay shows that bacteria-expressed GST-Six3 fusion protein binds to the  Wnt1 promoter elements I and II (lanes  3,8) strongly, very weakly to element III (lane  13), and not at all to element IV (data not shown).	bind
45957	5	2159	6	10	NULL	0	NULL	GST-Six3	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_3_368_s_140	12569128	( G``) A magnification of the electroporated embryo shown in  G. ( H) EMSA assay shows that bacteria-expressed GST-Six3 fusion protein binds to the  Wnt1 promoter elements I and II (lanes  3,8) strongly, very weakly to element III (lane  13), and not at all to element IV (data not shown).	bind
5162	1	2159	7	10	NULL	0	NULL	GST-Six3	GP	bacteria-expressed	binds to		strongly			Wnt1	GP			promoter elements I	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_3_368_s_140	12569128	( G``) A magnification of the electroporated embryo shown in  G. ( H) EMSA assay shows that bacteria-expressed GST-Six3 fusion protein binds to the  Wnt1 promoter elements I and II (lanes  3,8) strongly, very weakly to element III (lane  13), and not at all to element IV (data not shown).	bind
5163	2	2159	7	10	NULL	0	NULL	GST-Six3	GP	bacteria-expressed	binds to		strongly			Wnt1	GP			promoter elements II	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_3_368_s_140	12569128	( G``) A magnification of the electroporated embryo shown in  G. ( H) EMSA assay shows that bacteria-expressed GST-Six3 fusion protein binds to the  Wnt1 promoter elements I and II (lanes  3,8) strongly, very weakly to element III (lane  13), and not at all to element IV (data not shown).	bind
5164	3	2159	7	10	NULL	0	NULL	GST-Six3	GP	bacteria-expressed	binds to		very weakly			Wnt1	GP			promoter elements III	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_3_368_s_140	12569128	( G``) A magnification of the electroporated embryo shown in  G. ( H) EMSA assay shows that bacteria-expressed GST-Six3 fusion protein binds to the  Wnt1 promoter elements I and II (lanes  3,8) strongly, very weakly to element III (lane  13), and not at all to element IV (data not shown).	bind
5165	4	2159	7	10	NULL	0	NULL	GST-Six3	GP	bacteria-expressed	does not bind					Wnt1	GP			promoter elements IV	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_3_368_s_140	12569128	( G``) A magnification of the electroporated embryo shown in  G. ( H) EMSA assay shows that bacteria-expressed GST-Six3 fusion protein binds to the  Wnt1 promoter elements I and II (lanes  3,8) strongly, very weakly to element III (lane  13), and not at all to element IV (data not shown).	bind
45956	5	2159	7	10	NULL	0	NULL	GST-Six3	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_3_368_s_140	12569128	( G``) A magnification of the electroporated embryo shown in  G. ( H) EMSA assay shows that bacteria-expressed GST-Six3 fusion protein binds to the  Wnt1 promoter elements I and II (lanes  3,8) strongly, very weakly to element III (lane  13), and not at all to element IV (data not shown).	bind
3432	1	2160	6	10	NULL	0	NULL	ATX1	GP	cellular	bind					PI5P	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_15_6049_s_132	16585509	( H and  I) Cellular ATX1 binds PI5P.	bind
5166	1	2160	7	10	NULL	0	NULL	ATX1	GP	cellular	binds					PI5P	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_15_6049_s_132	16585509	( H and  I) Cellular ATX1 binds PI5P.	bind
3433	1	2161	6	10	NULL	0	NULL	LyP-1	GP		does not bind					LE cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12617_s_79	12235356	( h and  i) GFE qdots do not recognize the MDA-MB-435 cells ( h) and LyP-1 qdots do not bind to the LE cells ( i).	bind
3434	2	2161	6	10	NULL	0	NULL	GFE	GP		does not recognize					MDA-MB-435 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12617_s_79	12235356	( h and  i) GFE qdots do not recognize the MDA-MB-435 cells ( h) and LyP-1 qdots do not bind to the LE cells ( i).	bind
5167	1	2161	7	10	NULL	0	NULL	GFE 	GP		do not recognize					MDA-MB-435 cells 	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12617_s_79	12235356	( h and  i) GFE qdots do not recognize the MDA-MB-435 cells ( h) and LyP-1 qdots do not bind to the LE cells ( i).	bind
5168	2	2161	7	10	NULL	0	NULL	 LyP-1	GP		does not bind					LE cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12617_s_79	12235356	( h and  i) GFE qdots do not recognize the MDA-MB-435 cells ( h) and LyP-1 qdots do not bind to the LE cells ( i).	bind
3435	1	2162	6	10	NULL	0	NULL	M1 RNA	NucleicAcid		bind					Rpp29	GP		KH		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5120_s_282	16155184	( H) Binding of M1 RNA by the indicated concentrations of Rpp29KH (lanes 2 - 4) or Rpp29K179N  (lanes 5 - 7).	bind
3436	2	2162	6	10	NULL	0	NULL	M1 RNA	NucleicAcid		bind					Rpp29	GP		K179N		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5120_s_282	16155184	( H) Binding of M1 RNA by the indicated concentrations of Rpp29KH (lanes 2 - 4) or Rpp29K179N  (lanes 5 - 7).	bind
5169	1	2162	7	10	NULL	0	NULL	Rpp29	GP		binds			KH		M1RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5120_s_282	16155184	( H) Binding of M1 RNA by the indicated concentrations of Rpp29KH (lanes 2 - 4) or Rpp29K179N  (lanes 5 - 7).	bind
5170	2	2162	7	10	NULL	0	NULL	Rpp29	GP		binds			K179N		M1RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_16_5120_s_282	16155184	( H) Binding of M1 RNA by the indicated concentrations of Rpp29KH (lanes 2 - 4) or Rpp29K179N  (lanes 5 - 7).	bind
3437	1	2163	6	10	NULL	0	NULL	E2F	GP		bind					hTERT	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_31_11328_s_137	15263087	( H) Changes in the binding of E2F and pocket proteins to the hTERT promoter during the  cell cycle.	bind
3438	2	2163	6	10	NULL	0	NULL	pocket proteins	GP		bind					hTERT	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_31_11328_s_137	15263087	( H) Changes in the binding of E2F and pocket proteins to the hTERT promoter during the  cell cycle.	bind
5171	1	2163	7	10	NULL	0	NULL	E2F	GP		binds					hTERT	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_31_11328_s_137	15263087	( H) Changes in the binding of E2F and pocket proteins to the hTERT promoter during the  cell cycle.	bind
5172	2	2163	7	10	NULL	0	NULL	pocket proteins	GP		binds					hTERT	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_31_11328_s_137	15263087	( H) Changes in the binding of E2F and pocket proteins to the hTERT promoter during the  cell cycle.	bind
3439	1	2164	6	10	NULL	0	NULL	CFTR	GP		bind					EBP50	GP				NULL	calu-3 cells 	NULL	NULL	NULL	NULL	gw70_pnas_100_1_342_s_185	12502786	( H) Coimmunoprecipitation of CFTR and EBP50 from calu-3 cells treated with or without  cpt-cAMP mixture for 10 min at 37 degrees C. cpt-cAMP treatment diminishes EBP50  binding during coimmunoprecipitation.	bind
3441	2	2164	6	10	NULL	0	NULL	cpt-cAMP	Chemical	treatment of	diminishes					statement 1	Process				NULL	calu-3 cells 	NULL	NULL	NULL	NULL	gw70_pnas_100_1_342_s_185	12502786	( H) Coimmunoprecipitation of CFTR and EBP50 from calu-3 cells treated with or without  cpt-cAMP mixture for 10 min at 37 degrees C. cpt-cAMP treatment diminishes EBP50  binding during coimmunoprecipitation.	bind
6253	1	2164	7	10	NULL	0	NULL	CFTR	GP		binds					EBP50	GP				NULL	calu-3 cells	NULL	NULL	NULL	NULL	gw70_pnas_100_1_342_s_185	12502786	( H) Coimmunoprecipitation of CFTR and EBP50 from calu-3 cells treated with or without  cpt-cAMP mixture for 10 min at 37 degrees C. cpt-cAMP treatment diminishes EBP50  binding during coimmunoprecipitation.	bind
6254	2	2164	7	10	NULL	0	NULL	cpt-cAMP	Chemical	treatment	diminishes					statement 1	Process				NULL	calu-3 cells 	NULL	NULL	NULL	NULL	gw70_pnas_100_1_342_s_185	12502786	( H) Coimmunoprecipitation of CFTR and EBP50 from calu-3 cells treated with or without  cpt-cAMP mixture for 10 min at 37 degrees C. cpt-cAMP treatment diminishes EBP50  binding during coimmunoprecipitation.	bind
3448	1	2168	6	10	NULL	0	NULL	Basonuclin	GP		bind									dyad sequence within BBS1	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_17_9628_s_203	10449744	( i) Basonuclin binds to two dyad sequences, one completely within BBS1 and the other divided between BBS1 and BBS2.	bind
3449	2	2168	6	10	NULL	0	NULL	Basonuclin	GP		bind									dyad sequence between BBS1 and BBS2	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_17_9628_s_203	10449744	( i) Basonuclin binds to two dyad sequences, one completely within BBS1 and the other divided between BBS1 and BBS2.	bind
5173	1	2168	7	10	NULL	0	NULL	Basonuclin	GP		binds									dyad sequence within BBS1	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_17_9628_s_203	10449744	( i) Basonuclin binds to two dyad sequences, one completely within BBS1 and the other divided between BBS1 and BBS2.	bind
5174	2	2168	7	10	NULL	0	NULL	Basonuclin	GP		binds									dyad sequence between BBS1 and BBS2	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_17_9628_s_203	10449744	( i) Basonuclin binds to two dyad sequences, one completely within BBS1 and the other divided between BBS1 and BBS2.	bind
3450	1	2170	6	10	NULL	0	NULL	NPC1	GP		bind		low affinity			cholesterol	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_34_12473_s_231	15314240	( i) NPC1 binds to cholesterol as its substrate and transports it at the late endosomal membrane; this possibility would be consistent with the current finding that NPC1 binds to cholesterol with low affinity.	bind
3452	2	2170	6	10	NULL	0	NULL	cholesterol	Chemical		is transported to					late endosomal membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_34_12473_s_231	15314240	( i) NPC1 binds to cholesterol as its substrate and transports it at the late endosomal membrane; this possibility would be consistent with the current finding that NPC1 binds to cholesterol with low affinity.	bind
3453	3	2170	6	10	NULL	0	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_34_12473_s_231	15314240	( i) NPC1 binds to cholesterol as its substrate and transports it at the late endosomal membrane; this possibility would be consistent with the current finding that NPC1 binds to cholesterol with low affinity.	bind
5175	1	2170	7	10	NULL	0	NULL	NPC1	GP		binds to		low affinity			cholesterol	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_34_12473_s_231	15314240	( i) NPC1 binds to cholesterol as its substrate and transports it at the late endosomal membrane; this possibility would be consistent with the current finding that NPC1 binds to cholesterol with low affinity.	bind
5176	2	2170	7	10	NULL	0	NULL	cholesterol	Chemical		is transported to					late endosomal membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_34_12473_s_231	15314240	( i) NPC1 binds to cholesterol as its substrate and transports it at the late endosomal membrane; this possibility would be consistent with the current finding that NPC1 binds to cholesterol with low affinity.	bind
5177	3	2170	7	10	NULL	0	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_34_12473_s_231	15314240	( i) NPC1 binds to cholesterol as its substrate and transports it at the late endosomal membrane; this possibility would be consistent with the current finding that NPC1 binds to cholesterol with low affinity.	bind
3454	1	2171	6	10	NULL	0	NULL	ORC	NucleicAcid		bind					ACS	NucleicAcid	essential			NULL	ARS309 in vitro 	NULL	NULL	NULL	NULL	gw60_pnas_94_20_10786_s_134	9380711	( i) Our  in vitro analysis of  ARS309 indicates that ORC binds to the essential ACS.	bind
5178	1	2171	7	10	NULL	0	NULL	ORC	NucleicAcid		binds					ACS	NucleicAcid	essential			NULL	ARS309 in vitro 	NULL	NULL	NULL	NULL	gw60_pnas_94_20_10786_s_134	9380711	( i) Our  in vitro analysis of  ARS309 indicates that ORC binds to the essential ACS.	bind
3456	1	2172	6	10	NULL	0	NULL	S1	GP		bind					actin	GP	oriented			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_9_6011_s_201	11972024	( i) Spectroscopic studies of the orientation of the LC domain, measured by using paramagnetic ( 19) or fluorescent ( 15) probes, have found that the orientation of the LC domains were similar when S1 or HMM were bound to oriented actin, and both were similar to rigor fibers.	bind
3457	2	2172	6	10	NULL	0	NULL	HMM	GP		bind					actin	GP	oriented			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_9_6011_s_201	11972024	( i) Spectroscopic studies of the orientation of the LC domain, measured by using paramagnetic ( 19) or fluorescent ( 15) probes, have found that the orientation of the LC domains were similar when S1 or HMM were bound to oriented actin, and both were similar to rigor fibers.	bind
5180	1	2172	7	10	NULL	0	NULL	S1	GP		binds					actin	GP	oriented			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_9_6011_s_201	11972024	( i) Spectroscopic studies of the orientation of the LC domain, measured by using paramagnetic ( 19) or fluorescent ( 15) probes, have found that the orientation of the LC domains were similar when S1 or HMM were bound to oriented actin, and both were similar to rigor fibers.	bind
5181	2	2172	7	10	NULL	0	NULL	HMM	GP		binds					actin	GP	oriented			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_9_6011_s_201	11972024	( i) Spectroscopic studies of the orientation of the LC domain, measured by using paramagnetic ( 19) or fluorescent ( 15) probes, have found that the orientation of the LC domains were similar when S1 or HMM were bound to oriented actin, and both were similar to rigor fibers.	bind
3458	1	2173	6	10	NULL	0	NULL	icon	GP		bind					vascular endothelium	Cell	human tumor			NULL	SCID mice	NULL	NULL	NULL	NULL	gw60_pnas_98_21_12180_s_248	11593034	( i) The icon binds to the vascular endothelium of a human tumor in SCID mice, but does not bind to the mouse liver or kidney, and probably not to other normal tissues.	bind
3459	2	2173	6	10	NULL	0	NULL	icon	GP		does not bind					liver	OrganismPart	mouse			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_21_12180_s_248	11593034	( i) The icon binds to the vascular endothelium of a human tumor in SCID mice, but does not bind to the mouse liver or kidney, and probably not to other normal tissues.	bind
3460	3	2173	6	10	NULL	0	NULL	icon	GP		does not bind					kidney	OrganismPart	mouse			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_21_12180_s_248	11593034	( i) The icon binds to the vascular endothelium of a human tumor in SCID mice, but does not bind to the mouse liver or kidney, and probably not to other normal tissues.	bind
3461	4	2173	6	10	NULL	0	NULL	icon	GP		does not bind		probably			tissues	OrganismPart	normal			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_21_12180_s_248	11593034	( i) The icon binds to the vascular endothelium of a human tumor in SCID mice, but does not bind to the mouse liver or kidney, and probably not to other normal tissues.	bind
5182	1	2173	7	10	NULL	0	NULL	 icon	GP		binds to					vascular endothelium	OrganismPart	human tumor			NULL	SCID mice	NULL	NULL	NULL	NULL	gw60_pnas_98_21_12180_s_248	11593034	( i) The icon binds to the vascular endothelium of a human tumor in SCID mice, but does not bind to the mouse liver or kidney, and probably not to other normal tissues.	bind
5183	2	2173	7	10	NULL	0	NULL	icon	GP		does not bind					liver	OrganismPart	mouse			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_21_12180_s_248	11593034	( i) The icon binds to the vascular endothelium of a human tumor in SCID mice, but does not bind to the mouse liver or kidney, and probably not to other normal tissues.	bind
5184	3	2173	7	10	NULL	0	NULL	icon	GP		does not bind					kidney	OrganismPart	mouse			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_21_12180_s_248	11593034	( i) The icon binds to the vascular endothelium of a human tumor in SCID mice, but does not bind to the mouse liver or kidney, and probably not to other normal tissues.	bind
5185	4	2173	7	10	NULL	0	NULL	icon	GP		does not bind		probably			tissues	OrganismPart	normal			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_21_12180_s_248	11593034	( i) The icon binds to the vascular endothelium of a human tumor in SCID mice, but does not bind to the mouse liver or kidney, and probably not to other normal tissues.	bind
3463	1	2174	6	10	NULL	0	NULL	TSG101	GP		bind					p6	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_955_s_172	11805336	( i) The reported ability of TSG101 and other E2-like proteins to inhibit or modify the target specificity of ubiquitination ( 29,  45) raises the possibility that binding of TSG101 by p6 could alter the extent to which Gag becomes ubiquitinated.	bind
3464	2	2174	6	10	NULL	0	NULL	statement 1	Process		alters					Gag	GP	ubiquitination of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_955_s_172	11805336	( i) The reported ability of TSG101 and other E2-like proteins to inhibit or modify the target specificity of ubiquitination ( 29,  45) raises the possibility that binding of TSG101 by p6 could alter the extent to which Gag becomes ubiquitinated.	bind
46195	3	2174	6	10	NULL	0	NULL	TSG101	GP		inhibit					ubiquitination	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_955_s_172	11805336	( i) The reported ability of TSG101 and other E2-like proteins to inhibit or modify the target specificity of ubiquitination ( 29,  45) raises the possibility that binding of TSG101 by p6 could alter the extent to which Gag becomes ubiquitinated.	bind
46197	4	2174	6	10	NULL	0	NULL	TSG101	GP		modify					ubiquitination	Process	target specificity of 			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_955_s_172	11805336	( i) The reported ability of TSG101 and other E2-like proteins to inhibit or modify the target specificity of ubiquitination ( 29,  45) raises the possibility that binding of TSG101 by p6 could alter the extent to which Gag becomes ubiquitinated.	bind
46198	5	2174	6	10	NULL	0	NULL	E2-like proteins	GP		inhibit					ubiquitination	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_955_s_172	11805336	( i) The reported ability of TSG101 and other E2-like proteins to inhibit or modify the target specificity of ubiquitination ( 29,  45) raises the possibility that binding of TSG101 by p6 could alter the extent to which Gag becomes ubiquitinated.	bind
46199	6	2174	6	10	NULL	0	NULL	E2-like proteins	GP		modify					ubiquitination	Process	target specificity of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_955_s_172	11805336	( i) The reported ability of TSG101 and other E2-like proteins to inhibit or modify the target specificity of ubiquitination ( 29,  45) raises the possibility that binding of TSG101 by p6 could alter the extent to which Gag becomes ubiquitinated.	bind
51553	7	2174	6	10	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_955_s_172	11805336	( i) The reported ability of TSG101 and other E2-like proteins to inhibit or modify the target specificity of ubiquitination ( 29,  45) raises the possibility that binding of TSG101 by p6 could alter the extent to which Gag becomes ubiquitinated.	bind
51554	8	2174	6	10	NULL	0	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_955_s_172	11805336	( i) The reported ability of TSG101 and other E2-like proteins to inhibit or modify the target specificity of ubiquitination ( 29,  45) raises the possibility that binding of TSG101 by p6 could alter the extent to which Gag becomes ubiquitinated.	bind
5186	1	2174	7	10	NULL	0	NULL	 p6	GP		binds					TSG101	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_955_s_172	11805336	( i) The reported ability of TSG101 and other E2-like proteins to inhibit or modify the target specificity of ubiquitination ( 29,  45) raises the possibility that binding of TSG101 by p6 could alter the extent to which Gag becomes ubiquitinated.	bind
5188	3	2174	7	10	NULL	0	NULL	statement 1	Process		alters					Gag	GP	ubiquitination of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_955_s_172	11805336	( i) The reported ability of TSG101 and other E2-like proteins to inhibit or modify the target specificity of ubiquitination ( 29,  45) raises the possibility that binding of TSG101 by p6 could alter the extent to which Gag becomes ubiquitinated.	bind
5189	4	2174	7	10	NULL	0	NULL	TSG101	GP		inhibits					ubiquitination 	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_955_s_172	11805336	( i) The reported ability of TSG101 and other E2-like proteins to inhibit or modify the target specificity of ubiquitination ( 29,  45) raises the possibility that binding of TSG101 by p6 could alter the extent to which Gag becomes ubiquitinated.	bind
5190	5	2174	7	10	NULL	0	NULL	TSG101	GP		modify					ubiquitination	Process	target specificity of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_955_s_172	11805336	( i) The reported ability of TSG101 and other E2-like proteins to inhibit or modify the target specificity of ubiquitination ( 29,  45) raises the possibility that binding of TSG101 by p6 could alter the extent to which Gag becomes ubiquitinated.	bind
5191	6	2174	7	10	NULL	0	NULL	E2-like proteins	GP		inhibits					ubiquitination	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_955_s_172	11805336	( i) The reported ability of TSG101 and other E2-like proteins to inhibit or modify the target specificity of ubiquitination ( 29,  45) raises the possibility that binding of TSG101 by p6 could alter the extent to which Gag becomes ubiquitinated.	bind
5192	7	2174	7	10	NULL	0	NULL	E2-like proteins	GP		modify					ubiquitination	Process	target specificity of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_955_s_172	11805336	( i) The reported ability of TSG101 and other E2-like proteins to inhibit or modify the target specificity of ubiquitination ( 29,  45) raises the possibility that binding of TSG101 by p6 could alter the extent to which Gag becomes ubiquitinated.	bind
46290	8	2174	7	10	NULL	0	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_955_s_172	11805336	( i) The reported ability of TSG101 and other E2-like proteins to inhibit or modify the target specificity of ubiquitination ( 29,  45) raises the possibility that binding of TSG101 by p6 could alter the extent to which Gag becomes ubiquitinated.	bind
46291	9	2174	7	10	NULL	0	NULL	statement 6	Process		is an alternative to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_955_s_172	11805336	( i) The reported ability of TSG101 and other E2-like proteins to inhibit or modify the target specificity of ubiquitination ( 29,  45) raises the possibility that binding of TSG101 by p6 could alter the extent to which Gag becomes ubiquitinated.	bind
3465	1	2175	6	10	NULL	0	NULL	tRNAIle	NucleicAcid		bind					IleRS/Val-AMP complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_585_s_215	11782529	( i) tRNAIle binds to the IleRS/Val-AMP complex.	bind
5193	1	2175	7	10	NULL	0	NULL	tRNAIle	NucleicAcid		binds to					IleRS/Val-AMP complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_585_s_215	11782529	( i) tRNAIle binds to the IleRS/Val-AMP complex.	bind
3466	1	2176	6	10	NULL	0	NULL	IP3	GP		bind					type 2 receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_20_17571_s_204	11875073	( I) whether or not they have IP3 bound, whereas IP3 binding protects type 2 receptors from Ca2+ inhibition.	bind
3467	2	2176	6	10	NULL	0	NULL	Ca2+	Chemical		inhibits					type 2 receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_20_17571_s_204	11875073	( I) whether or not they have IP3 bound, whereas IP3 binding protects type 2 receptors from Ca2+ inhibition.	bind
46200	3	2176	6	10	NULL	0	NULL	statement 1	Process		protects					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_20_17571_s_204	11875073	( I) whether or not they have IP3 bound, whereas IP3 binding protects type 2 receptors from Ca2+ inhibition.	bind
5194	1	2176	7	10	NULL	0	NULL	 IP3	GP		binds					type 2 receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_20_17571_s_204	11875073	( I) whether or not they have IP3 bound, whereas IP3 binding protects type 2 receptors from Ca2+ inhibition.	bind
5195	2	2176	7	10	NULL	0	NULL	Ca2+	Chemical		inhibits					type 2 receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_20_17571_s_204	11875073	( I) whether or not they have IP3 bound, whereas IP3 binding protects type 2 receptors from Ca2+ inhibition.	bind
5196	3	2176	7	10	NULL	0	NULL	statement 1	Process		protects					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_20_17571_s_204	11875073	( I) whether or not they have IP3 bound, whereas IP3 binding protects type 2 receptors from Ca2+ inhibition.	bind
3468	1	2178	6	10	NULL	0	NULL	N-3	Chemical		bind					SW Mb	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1594_2_341_s_147	11904230	( I=800 mM) using decreasing concentrations of divalent SO2-4 with both Mbs, or monovalent Cl- only with HH Mb due to the effect that this anion has on N-3 binding to SW Mb (see  Fig. 2).	bind
5370	1	2178	7	10	NULL	0	NULL	N-3	Chemical		binds					SW Mb	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1594_2_341_s_147	11904230	( I=800 mM) using decreasing concentrations of divalent SO2-4 with both Mbs, or monovalent Cl- only with HH Mb due to the effect that this anion has on N-3 binding to SW Mb (see  Fig. 2).	bind
3469	1	2179	6	10	NULL	0	NULL	GalCer	Chemical		bind					P1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25649_s_178	11940580	( If) as a function of P1 concentration exhibits a sharp transition between P1 concentration of 25 and 50 muM in both raft lipids and PBS environment, indicating that the GalCer* binding affinity to the P1 depends strongly on P1 concentration and, therefore, on P1 secondary structure (see Fig.  2).	bind
3470	2	2179	6	10	NULL	0	NULL	statement 1	Process		depends 		strongly			P1	GP	concentration of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25649_s_178	11940580	( If) as a function of P1 concentration exhibits a sharp transition between P1 concentration of 25 and 50 muM in both raft lipids and PBS environment, indicating that the GalCer* binding affinity to the P1 depends strongly on P1 concentration and, therefore, on P1 secondary structure (see Fig.  2).	bind
3471	3	2179	6	10	NULL	0	NULL	statement 1	Process		depends 					P1	GP	secondary structure of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25649_s_178	11940580	( If) as a function of P1 concentration exhibits a sharp transition between P1 concentration of 25 and 50 muM in both raft lipids and PBS environment, indicating that the GalCer* binding affinity to the P1 depends strongly on P1 concentration and, therefore, on P1 secondary structure (see Fig.  2).	bind
5372	1	2179	7	10	NULL	0	NULL	GalCer	Process		binds					P1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25649_s_178	11940580	( If) as a function of P1 concentration exhibits a sharp transition between P1 concentration of 25 and 50 muM in both raft lipids and PBS environment, indicating that the GalCer* binding affinity to the P1 depends strongly on P1 concentration and, therefore, on P1 secondary structure (see Fig.  2).	bind
5374	2	2179	7	10	NULL	0	NULL	statement 1	Process		is dependent on 		strongly			P1	GP	concentration of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25649_s_178	11940580	( If) as a function of P1 concentration exhibits a sharp transition between P1 concentration of 25 and 50 muM in both raft lipids and PBS environment, indicating that the GalCer* binding affinity to the P1 depends strongly on P1 concentration and, therefore, on P1 secondary structure (see Fig.  2).	bind
5377	3	2179	7	10	NULL	0	NULL	statement 1	Process		is dependent on					P1	GP	secondary structure of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25649_s_178	11940580	( If) as a function of P1 concentration exhibits a sharp transition between P1 concentration of 25 and 50 muM in both raft lipids and PBS environment, indicating that the GalCer* binding affinity to the P1 depends strongly on P1 concentration and, therefore, on P1 secondary structure (see Fig.  2).	bind
3472	1	2180	6	10	NULL	0	NULL	TVA-EGF	GP		bind					M5 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_12_7063_s_137	9618539	( ii) A recombinant human EGF protein specifically blocked TVA-EGF binding to M5 cells and TVA-EGF mediated viral entry.	bind
3473	2	2180	6	10	NULL	0	NULL	EGF protein	GP	recombinant;;human	blocks		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_12_7063_s_137	9618539	( ii) A recombinant human EGF protein specifically blocked TVA-EGF binding to M5 cells and TVA-EGF mediated viral entry.	bind
3474	3	2180	6	10	NULL	0	NULL	TVA-EGF	GP		mediates					viral entry	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_12_7063_s_137	9618539	( ii) A recombinant human EGF protein specifically blocked TVA-EGF binding to M5 cells and TVA-EGF mediated viral entry.	bind
3475	4	2180	6	10	NULL	0	NULL	EGF protein	GP	recombinant;;human	blocks		specifically			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_12_7063_s_137	9618539	( ii) A recombinant human EGF protein specifically blocked TVA-EGF binding to M5 cells and TVA-EGF mediated viral entry.	bind
5378	1	2180	7	10	NULL	0	NULL	TVA-EGF	GP		binds					M5 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_12_7063_s_137	9618539	( ii) A recombinant human EGF protein specifically blocked TVA-EGF binding to M5 cells and TVA-EGF mediated viral entry.	bind
5379	2	2180	7	10	NULL	0	NULL	EGF protein 	GP	human;;recombinant	blocks		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_12_7063_s_137	9618539	( ii) A recombinant human EGF protein specifically blocked TVA-EGF binding to M5 cells and TVA-EGF mediated viral entry.	bind
5380	3	2180	7	10	NULL	0	NULL	TVA-EGF	GP		mediates					viral entry	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_12_7063_s_137	9618539	( ii) A recombinant human EGF protein specifically blocked TVA-EGF binding to M5 cells and TVA-EGF mediated viral entry.	bind
5381	4	2180	7	10	NULL	0	NULL	EGF protelin 	GP	human;;recombinant	blocks		specifically			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_12_7063_s_137	9618539	( ii) A recombinant human EGF protein specifically blocked TVA-EGF binding to M5 cells and TVA-EGF mediated viral entry.	bind
3476	1	2181	6	10	NULL	0	NULL	gp33	GP		bind					gp55 holoenzyme	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_50_17365_s_137	15574501	( ii) Binding of gp33 to gp55 holoenzyme was comparable with binding to core at low gp33 concentrations but reached saturation at higher gp33 concentrations ( Fig. 3 B).	bind
5382	1	2181	7	10	NULL	0	NULL	gp33 	GP		binds					gp55 holoenzyme	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_50_17365_s_137	15574501	( ii) Binding of gp33 to gp55 holoenzyme was comparable with binding to core at low gp33 concentrations but reached saturation at higher gp33 concentrations ( Fig. 3 B).	bind
3477	1	2182	6	10	NULL	0	NULL	eIF4F	GP		recognizes			eIF4E subunit		mRNA 	NucleicAcid			m7G cap at 5''-terminus	NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_13_7029_s_16	11416183	( ii) Binding of the 43S complex to mRNA, which in most instances occurs by a mechanism that involves initial recognition of the m7G cap at the mRNA 5''-terminus by the eIF4E (cap-binding) subunit of eIF4F.	bind
3478	2	2182	6	10	NULL	0	NULL	43S complex	GP		bind					mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_13_7029_s_16	11416183	( ii) Binding of the 43S complex to mRNA, which in most instances occurs by a mechanism that involves initial recognition of the m7G cap at the mRNA 5''-terminus by the eIF4E (cap-binding) subunit of eIF4F.	bind
3479	3	2182	6	10	NULL	0	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_13_7029_s_16	11416183	( ii) Binding of the 43S complex to mRNA, which in most instances occurs by a mechanism that involves initial recognition of the m7G cap at the mRNA 5''-terminus by the eIF4E (cap-binding) subunit of eIF4F.	bind
46035	4	2182	6	10	NULL	0	NULL	eIF4F	GP		is a type of			eIF4E subunit		cap-binding subunit	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_13_7029_s_16	11416183	( ii) Binding of the 43S complex to mRNA, which in most instances occurs by a mechanism that involves initial recognition of the m7G cap at the mRNA 5''-terminus by the eIF4E (cap-binding) subunit of eIF4F.	bind
5384	1	2182	7	10	NULL	0	NULL	43S complex	GP		binds					mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_13_7029_s_16	11416183	( ii) Binding of the 43S complex to mRNA, which in most instances occurs by a mechanism that involves initial recognition of the m7G cap at the mRNA 5''-terminus by the eIF4E (cap-binding) subunit of eIF4F.	bind
5385	2	2182	7	10	NULL	0	NULL	eIF4F	GP		recognizes			eIF4E subunit		mRNA	NucleicAcid			m7G cap at 5'' terminus	NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_13_7029_s_16	11416183	( ii) Binding of the 43S complex to mRNA, which in most instances occurs by a mechanism that involves initial recognition of the m7G cap at the mRNA 5''-terminus by the eIF4E (cap-binding) subunit of eIF4F.	bind
5386	3	2182	7	10	NULL	0	NULL	statement 1	Process		occurs by					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_13_7029_s_16	11416183	( ii) Binding of the 43S complex to mRNA, which in most instances occurs by a mechanism that involves initial recognition of the m7G cap at the mRNA 5''-terminus by the eIF4E (cap-binding) subunit of eIF4F.	bind
5387	4	2182	7	10	NULL	0	NULL	eIF4F	GP		is a type of			eIF4E subunit		cap-binding subunit	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_13_7029_s_16	11416183	( ii) Binding of the 43S complex to mRNA, which in most instances occurs by a mechanism that involves initial recognition of the m7G cap at the mRNA 5''-terminus by the eIF4E (cap-binding) subunit of eIF4F.	bind
3480	1	2183	6	10	NULL	0	NULL	AC	Chemical		bind					NPC1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_34_12473_s_163	15314240	( ii) Does the binding of [3]AC to NPC1 require the presence of NPC2?	bind
4398	2	2183	6	10	NULL	0	NULL	statement 1	Process		requires		possibly			NPC2	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_34_12473_s_163	15314240	( ii) Does the binding of [3]AC to NPC1 require the presence of NPC2?	bind
5388	1	2183	7	10	NULL	0	NULL	AC	Chemical		binds					NPC1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_34_12473_s_163	15314240	( ii) Does the binding of [3]AC to NPC1 require the presence of NPC2?	bind
46036	2	2183	7	10	NULL	0	NULL	statement 1	Process		requires		possibly			NPC2	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_34_12473_s_163	15314240	( ii) Does the binding of [3]AC to NPC1 require the presence of NPC2?	bind
3640	1	2185	6	10	NULL	0	NULL	Sp1	GP		does not bind					MYCN	GP			promoter	NULL	SH-EP cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5110_s_265	14645238	( ii) Even prolonged treatment of 1A3 cells with 5-aC before induction with 4-OHT did not result in binding of E2F-1-ER or activation of endogenous  MYCN.( iii) In SH-EP cells, there was also no binding of Sp1 and Sp3 to the  MYCN promoter, although binding of Sp1 is not affected by methylation of DNA ( ).	bind
3641	2	2185	6	10	NULL	0	NULL	Sp3	GP		does not bind					MYCN	GP			promoter	NULL	SH-EP cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5110_s_265	14645238	( ii) Even prolonged treatment of 1A3 cells with 5-aC before induction with 4-OHT did not result in binding of E2F-1-ER or activation of endogenous  MYCN.( iii) In SH-EP cells, there was also no binding of Sp1 and Sp3 to the  MYCN promoter, although binding of Sp1 is not affected by methylation of DNA ( ).	bind
3642	3	2185	6	10	NULL	0	NULL	DNA	NucleicAcid	methylation	does not affect					statement 1	Process				NULL	SH-EP cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5110_s_265	14645238	( ii) Even prolonged treatment of 1A3 cells with 5-aC before induction with 4-OHT did not result in binding of E2F-1-ER or activation of endogenous  MYCN.( iii) In SH-EP cells, there was also no binding of Sp1 and Sp3 to the  MYCN promoter, although binding of Sp1 is not affected by methylation of DNA ( ).	bind
5399	1	2185	7	10	NULL	0	NULL	Sp1	GP		does not bind					MYCN	GP			promoter	NULL	in SH-EP cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5110_s_265	14645238	( ii) Even prolonged treatment of 1A3 cells with 5-aC before induction with 4-OHT did not result in binding of E2F-1-ER or activation of endogenous  MYCN.( iii) In SH-EP cells, there was also no binding of Sp1 and Sp3 to the  MYCN promoter, although binding of Sp1 is not affected by methylation of DNA ( ).	bind
5400	2	2185	7	10	NULL	0	NULL	Sp3	GP		does not bind					MYCN	GP			promoter	NULL	in SH-EP cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5110_s_265	14645238	( ii) Even prolonged treatment of 1A3 cells with 5-aC before induction with 4-OHT did not result in binding of E2F-1-ER or activation of endogenous  MYCN.( iii) In SH-EP cells, there was also no binding of Sp1 and Sp3 to the  MYCN promoter, although binding of Sp1 is not affected by methylation of DNA ( ).	bind
5401	3	2185	7	10	NULL	0	NULL	statement 1	Process		is not affected by					DNA	NucleicAcid	methylation of			NULL	in SH-EP cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5110_s_265	14645238	( ii) Even prolonged treatment of 1A3 cells with 5-aC before induction with 4-OHT did not result in binding of E2F-1-ER or activation of endogenous  MYCN.( iii) In SH-EP cells, there was also no binding of Sp1 and Sp3 to the  MYCN promoter, although binding of Sp1 is not affected by methylation of DNA ( ).	bind
3570	1	2186	6	10	NULL	0	NULL	GroES	GP		bind					GroEL-polypeptide complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12163_s_22	9770457	( ii) GroES binds to the GroEL-polypeptide complex, forming a  cis ternary complex in which the polypeptide is encapsulated within the GroEL-GroES structure ( 8-10).	bind
3571	2	2186	6	10	NULL	0	NULL	statement 1	Process		forms a					cis ternary complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12163_s_22	9770457	( ii) GroES binds to the GroEL-polypeptide complex, forming a  cis ternary complex in which the polypeptide is encapsulated within the GroEL-GroES structure ( 8-10).	bind
51555	3	2186	6	10	NULL	0	NULL	polypeptide	GP		is  encapsulated within					GroEL-GroES	GP	structure of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12163_s_22	9770457	( ii) GroES binds to the GroEL-polypeptide complex, forming a  cis ternary complex in which the polypeptide is encapsulated within the GroEL-GroES structure ( 8-10).	bind
51556	5	2186	6	10	NULL	0	NULL	statement 4	Process		is present in					cis ternary complex \t	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12163_s_22	9770457	( ii) GroES binds to the GroEL-polypeptide complex, forming a  cis ternary complex in which the polypeptide is encapsulated within the GroEL-GroES structure ( 8-10).	bind
5402	1	2186	7	10	NULL	0	NULL	GroES	GP		binds to					GroEL-polypeptide complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12163_s_22	9770457	( ii) GroES binds to the GroEL-polypeptide complex, forming a  cis ternary complex in which the polypeptide is encapsulated within the GroEL-GroES structure ( 8-10).	bind
5403	2	2186	7	10	NULL	0	NULL	statement 1	Process		forms					cis ternary complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12163_s_22	9770457	( ii) GroES binds to the GroEL-polypeptide complex, forming a  cis ternary complex in which the polypeptide is encapsulated within the GroEL-GroES structure ( 8-10).	bind
5404	3	2186	7	10	NULL	0	NULL	polypeptide	GP		is  encapsulated within					GroEL-GroES	GP	structure of 			NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12163_s_22	9770457	( ii) GroES binds to the GroEL-polypeptide complex, forming a  cis ternary complex in which the polypeptide is encapsulated within the GroEL-GroES structure ( 8-10).	bind
46037	4	2186	7	10	NULL	0	NULL	statement 4	Process		is present in					cis ternary complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12163_s_22	9770457	( ii) GroES binds to the GroEL-polypeptide complex, forming a  cis ternary complex in which the polypeptide is encapsulated within the GroEL-GroES structure ( 8-10).	bind
3576	1	2187	6	10	NULL	0	NULL	ICP0	GP		bind			RING finger domain		cdc34	GP				NULL	in vitro substrate-independent ubiquitination system	NULL	NULL	NULL	NULL	gw60_pnas_98_15_8815_s_6	11447293	( ii) In an  in vitro substrate-independent ubiquitination system, the RING finger domain encoded by exon 2 of ICP0 binds cdc34, whereas the carboxyl-terminal domain of ICP0 functions as an E3 ligase independent of the RING finger domain.	bind
3577	2	2187	6	10	NULL	0	NULL	ICP0	GP		functions as			carboxyl-terminal domain		E3 ligase	GP				NULL	in vitro substrate-independent ubiquitination system	NULL	NULL	NULL	NULL	gw60_pnas_98_15_8815_s_6	11447293	( ii) In an  in vitro substrate-independent ubiquitination system, the RING finger domain encoded by exon 2 of ICP0 binds cdc34, whereas the carboxyl-terminal domain of ICP0 functions as an E3 ligase independent of the RING finger domain.	bind
3578	3	2187	6	10	NULL	0	NULL	statement 2	Process		independent of					ICP0	GP		RING finger domain		NULL	in vitro substrate-independent ubiquitination system	NULL	NULL	NULL	NULL	gw60_pnas_98_15_8815_s_6	11447293	( ii) In an  in vitro substrate-independent ubiquitination system, the RING finger domain encoded by exon 2 of ICP0 binds cdc34, whereas the carboxyl-terminal domain of ICP0 functions as an E3 ligase independent of the RING finger domain.	bind
3579	4	2187	6	10	NULL	0	NULL	ICP0	GP		encodes				exon 2	ICP0	GP		RING finger domain		NULL	in vitro substrate-independent ubiquitination system	NULL	NULL	NULL	NULL	gw60_pnas_98_15_8815_s_6	11447293	( ii) In an  in vitro substrate-independent ubiquitination system, the RING finger domain encoded by exon 2 of ICP0 binds cdc34, whereas the carboxyl-terminal domain of ICP0 functions as an E3 ligase independent of the RING finger domain.	bind
5405	1	2187	7	10	NULL	0	NULL	ICP0	GP		binds			RING finger domain		cdc34	GP				NULL	in vitro substrate-independent ubiquitination system	NULL	NULL	NULL	NULL	gw60_pnas_98_15_8815_s_6	11447293	( ii) In an  in vitro substrate-independent ubiquitination system, the RING finger domain encoded by exon 2 of ICP0 binds cdc34, whereas the carboxyl-terminal domain of ICP0 functions as an E3 ligase independent of the RING finger domain.	bind
5406	2	2187	7	10	NULL	0	NULL	ICP0	GP		functions as 			carboxyl-terminal domain 		E3 ligase	GP				NULL	in vitro substrate-independent ubiquitination system	NULL	NULL	NULL	NULL	gw60_pnas_98_15_8815_s_6	11447293	( ii) In an  in vitro substrate-independent ubiquitination system, the RING finger domain encoded by exon 2 of ICP0 binds cdc34, whereas the carboxyl-terminal domain of ICP0 functions as an E3 ligase independent of the RING finger domain.	bind
5407	3	2187	7	10	NULL	0	NULL	statement 2	Process		is independent of					ICP0	GP		RING finger domain		NULL	in vitro substrate-independent ubiquitination system	NULL	NULL	NULL	NULL	gw60_pnas_98_15_8815_s_6	11447293	( ii) In an  in vitro substrate-independent ubiquitination system, the RING finger domain encoded by exon 2 of ICP0 binds cdc34, whereas the carboxyl-terminal domain of ICP0 functions as an E3 ligase independent of the RING finger domain.	bind
5408	4	2187	7	10	NULL	0	NULL	ICP0	GP		is encoded by			RING finger domain		ICP0	GP			exon 2	NULL	in vitro substrate-independent ubiquitination system	NULL	NULL	NULL	NULL	gw60_pnas_98_15_8815_s_6	11447293	( ii) In an  in vitro substrate-independent ubiquitination system, the RING finger domain encoded by exon 2 of ICP0 binds cdc34, whereas the carboxyl-terminal domain of ICP0 functions as an E3 ligase independent of the RING finger domain.	bind
3580	1	2188	6	10	NULL	0	NULL	CCR5	GP		bind					MIP-1alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_10_5740_s_32	9576954	( ii) It was reported that a complex of gp120 and soluble CD4 could inhibit binding between CCR5 and MIP-1alpha or MIP-1beta.	bind
3581	2	2188	6	10	NULL	0	NULL	CCR5	GP		bind					MIP-1beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_10_5740_s_32	9576954	( ii) It was reported that a complex of gp120 and soluble CD4 could inhibit binding between CCR5 and MIP-1alpha or MIP-1beta.	bind
3583	3	2188	6	10	NULL	0	NULL	gp120	GP		forms complex with					CD4	GP	soluble			NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_10_5740_s_32	9576954	( ii) It was reported that a complex of gp120 and soluble CD4 could inhibit binding between CCR5 and MIP-1alpha or MIP-1beta.	bind
3584	4	2188	6	10	NULL	0	NULL	statement 3	Process		inhibit		probably			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_10_5740_s_32	9576954	( ii) It was reported that a complex of gp120 and soluble CD4 could inhibit binding between CCR5 and MIP-1alpha or MIP-1beta.	bind
3585	5	2188	6	10	NULL	0	NULL	statement 3	Process		inhibit		probably			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_10_5740_s_32	9576954	( ii) It was reported that a complex of gp120 and soluble CD4 could inhibit binding between CCR5 and MIP-1alpha or MIP-1beta.	bind
5411	1	2188	7	10	NULL	0	NULL	CCR5	GP		binds					MIP-1alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_10_5740_s_32	9576954	( ii) It was reported that a complex of gp120 and soluble CD4 could inhibit binding between CCR5 and MIP-1alpha or MIP-1beta.	bind
5412	2	2188	7	10	NULL	0	NULL	CCR5	GP		binds					MIP-1beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_10_5740_s_32	9576954	( ii) It was reported that a complex of gp120 and soluble CD4 could inhibit binding between CCR5 and MIP-1alpha or MIP-1beta.	bind
5413	3	2188	7	10	NULL	0	NULL	 gp120	GP		forms complex with					CD4	GP	soluble			NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_10_5740_s_32	9576954	( ii) It was reported that a complex of gp120 and soluble CD4 could inhibit binding between CCR5 and MIP-1alpha or MIP-1beta.	bind
5414	4	2188	7	10	NULL	0	NULL	statement 3	Process		inhibit		may			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_10_5740_s_32	9576954	( ii) It was reported that a complex of gp120 and soluble CD4 could inhibit binding between CCR5 and MIP-1alpha or MIP-1beta.	bind
5415	5	2188	7	10	NULL	0	NULL	statement 3	Process		inhibit		may			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_10_5740_s_32	9576954	( ii) It was reported that a complex of gp120 and soluble CD4 could inhibit binding between CCR5 and MIP-1alpha or MIP-1beta.	bind
3586	1	2189	6	10	NULL	0	NULL	nucleosomes	Chromosome		bind		may	H3.1		nucleosomes	Chromosome		H3.1		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_17_6428_s_114	16571659	( ii) Nucleosomes that contain H3.1 might bind to other H3.1-containing nucleosomes through internucleosomal disulfide bonds between cysteines 96.	bind
3587	2	2189	6	10	NULL	0	NULL	statement 1	Process		occurs through					disulfide bonds		internucleosomal	cysteines 96		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_17_6428_s_114	16571659	( ii) Nucleosomes that contain H3.1 might bind to other H3.1-containing nucleosomes through internucleosomal disulfide bonds between cysteines 96.	bind
5417	1	2189	7	10	NULL	0	NULL	nucleosomes	Chromosome		bind		may	H3.1		nucleosomes	Chromosome		H3.1		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_17_6428_s_114	16571659	( ii) Nucleosomes that contain H3.1 might bind to other H3.1-containing nucleosomes through internucleosomal disulfide bonds between cysteines 96.	bind
46342	2	2189	7	10	NULL	0	NULL	statement 1	Process		occurs through					disulfide bonds		internucleosomal	cysteines 96		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_17_6428_s_114	16571659	( ii) Nucleosomes that contain H3.1 might bind to other H3.1-containing nucleosomes through internucleosomal disulfide bonds between cysteines 96.	bind
3588	1	2190	6	10	NULL	0	NULL	MHC peptide complex	GP		are present on					B cells	Cell				NULL	B cells and APCs	NULL	NULL	NULL	NULL	gw70_pnas_102_18_6245_s_74	15843460	( ii) T cells recognize and bind to the MHC peptide complex on B cells and APCs. ( iii) B cells are stimulated, either directly by T cell binding or indirectly through  the bystander effect.	bind
3589	2	2190	6	10	NULL	0	NULL	MHC peptide complex	GP		is present at					APC	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6245_s_74	15843460	( ii) T cells recognize and bind to the MHC peptide complex on B cells and APCs. ( iii) B cells are stimulated, either directly by T cell binding or indirectly through  the bystander effect.	bind
3590	3	2190	6	10	NULL	0	NULL	T cells	Cell	binding of	stimulate		directly			B cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6245_s_74	15843460	( ii) T cells recognize and bind to the MHC peptide complex on B cells and APCs. ( iii) B cells are stimulated, either directly by T cell binding or indirectly through  the bystander effect.	bind
3591	4	2190	6	10	NULL	0	NULL	bystander effect	Process		stimulate		indirectly			B cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6245_s_74	15843460	( ii) T cells recognize and bind to the MHC peptide complex on B cells and APCs. ( iii) B cells are stimulated, either directly by T cell binding or indirectly through  the bystander effect.	bind
46301	5	2190	6	10	NULL	0	NULL	T cells	Cell		recognize					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6245_s_74	15843460	( ii) T cells recognize and bind to the MHC peptide complex on B cells and APCs. ( iii) B cells are stimulated, either directly by T cell binding or indirectly through  the bystander effect.	bind
46302	6	2190	6	10	NULL	0	NULL	T cell	Cell		recognize					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6245_s_74	15843460	( ii) T cells recognize and bind to the MHC peptide complex on B cells and APCs. ( iii) B cells are stimulated, either directly by T cell binding or indirectly through  the bystander effect.	bind
46303	7	2190	6	10	NULL	0	NULL	T cells	Cell		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6245_s_74	15843460	( ii) T cells recognize and bind to the MHC peptide complex on B cells and APCs. ( iii) B cells are stimulated, either directly by T cell binding or indirectly through  the bystander effect.	bind
46304	8	2190	6	10	NULL	0	NULL	T cells	Cell		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6245_s_74	15843460	( ii) T cells recognize and bind to the MHC peptide complex on B cells and APCs. ( iii) B cells are stimulated, either directly by T cell binding or indirectly through  the bystander effect.	bind
5419	1	2190	7	10	NULL	0	NULL	MHC peptide complex	GP		is present at					B cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6245_s_74	15843460	( ii) T cells recognize and bind to the MHC peptide complex on B cells and APCs. ( iii) B cells are stimulated, either directly by T cell binding or indirectly through  the bystander effect.	bind
5420	2	2190	7	10	NULL	0	NULL	MHC peptide complex	GP		is present at					APCs	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6245_s_74	15843460	( ii) T cells recognize and bind to the MHC peptide complex on B cells and APCs. ( iii) B cells are stimulated, either directly by T cell binding or indirectly through  the bystander effect.	bind
5421	3	2190	7	10	NULL	0	NULL	T cells	Cell		recognize					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6245_s_74	15843460	( ii) T cells recognize and bind to the MHC peptide complex on B cells and APCs. ( iii) B cells are stimulated, either directly by T cell binding or indirectly through  the bystander effect.	bind
5422	4	2190	7	10	NULL	0	NULL	T cells 	Cell		recognize					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6245_s_74	15843460	( ii) T cells recognize and bind to the MHC peptide complex on B cells and APCs. ( iii) B cells are stimulated, either directly by T cell binding or indirectly through  the bystander effect.	bind
46343	5	2190	7	10	NULL	0	NULL	T cells	Cell		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6245_s_74	15843460	( ii) T cells recognize and bind to the MHC peptide complex on B cells and APCs. ( iii) B cells are stimulated, either directly by T cell binding or indirectly through  the bystander effect.	bind
46344	6	2190	7	10	NULL	0	NULL	T cells	Cell		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6245_s_74	15843460	( ii) T cells recognize and bind to the MHC peptide complex on B cells and APCs. ( iii) B cells are stimulated, either directly by T cell binding or indirectly through  the bystander effect.	bind
46345	7	2190	7	10	NULL	0	NULL	T cells	Cell	binding of	stimulate		directly			B cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6245_s_74	15843460	( ii) T cells recognize and bind to the MHC peptide complex on B cells and APCs. ( iii) B cells are stimulated, either directly by T cell binding or indirectly through  the bystander effect.	bind
46346	8	2190	7	10	NULL	0	NULL	bystander effect	Process		stimulate		indirectly			B cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_18_6245_s_74	15843460	( ii) T cells recognize and bind to the MHC peptide complex on B cells and APCs. ( iii) B cells are stimulated, either directly by T cell binding or indirectly through  the bystander effect.	bind
3592	1	2192	6	10	NULL	0	NULL	PP1	GP	purified	does not bind			C subunit		GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_20_10624_s_104	9380685	( ii) The purified C subunit of PP1 did not show binding to either GST or GST-alpha4 (Fig.  1 c).	bind
3593	2	2192	6	10	NULL	0	NULL	PP1	GP	purified	does not bind			C subunit		GST-alpha4	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_20_10624_s_104	9380685	( ii) The purified C subunit of PP1 did not show binding to either GST or GST-alpha4 (Fig.  1 c).	bind
5423	1	2192	7	10	NULL	0	NULL	PP1	GP	purified	does not bind			C subunit 		GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_20_10624_s_104	9380685	( ii) The purified C subunit of PP1 did not show binding to either GST or GST-alpha4 (Fig.  1 c).	bind
5424	2	2192	7	10	NULL	0	NULL	PP1	GP	purified	does not bind			C subunit 		GST-alpha4	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_20_10624_s_104	9380685	( ii) The purified C subunit of PP1 did not show binding to either GST or GST-alpha4 (Fig.  1 c).	bind
3594	1	2193	6	10	NULL	0	NULL	X5	GP		bind					gp120	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_10_6913_s_176	11997472	( ii) X5 binding to gp120 was enhanced by the A32 mAb, which binds a CD4-inducible epitope; in turn X5 binding enhanced the exposure of the A32 epitope (data not shown).	bind
3595	2	2193	6	10	NULL	0	NULL	statement 1	Process		enhanced by					A32 mAb	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_10_6913_s_176	11997472	( ii) X5 binding to gp120 was enhanced by the A32 mAb, which binds a CD4-inducible epitope; in turn X5 binding enhanced the exposure of the A32 epitope (data not shown).	bind
3596	3	2193	6	10	NULL	0	NULL	A32 mAb	GP		bind					CD4-inducible epitope					NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_10_6913_s_176	11997472	( ii) X5 binding to gp120 was enhanced by the A32 mAb, which binds a CD4-inducible epitope; in turn X5 binding enhanced the exposure of the A32 epitope (data not shown).	bind
3597	4	2193	6	10	NULL	0	NULL	statement 1	Process		enhance					A32 epitope		exposure of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_10_6913_s_176	11997472	( ii) X5 binding to gp120 was enhanced by the A32 mAb, which binds a CD4-inducible epitope; in turn X5 binding enhanced the exposure of the A32 epitope (data not shown).	bind
5425	1	2193	7	10	NULL	0	NULL	X5	GP		binds to					gp120	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_10_6913_s_176	11997472	( ii) X5 binding to gp120 was enhanced by the A32 mAb, which binds a CD4-inducible epitope; in turn X5 binding enhanced the exposure of the A32 epitope (data not shown).	bind
5426	2	2193	7	10	NULL	0	NULL	statement 1	Process		is enhanced by					A32 mAb	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_10_6913_s_176	11997472	( ii) X5 binding to gp120 was enhanced by the A32 mAb, which binds a CD4-inducible epitope; in turn X5 binding enhanced the exposure of the A32 epitope (data not shown).	bind
5427	3	2193	7	10	NULL	0	NULL	A32 mAb	GP		binds					CD4-inducible epitope					NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_10_6913_s_176	11997472	( ii) X5 binding to gp120 was enhanced by the A32 mAb, which binds a CD4-inducible epitope; in turn X5 binding enhanced the exposure of the A32 epitope (data not shown).	bind
5428	4	2193	7	10	NULL	0	NULL	statement 1	Process		enhanced 					A32 epitope		exposure of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_10_6913_s_176	11997472	( ii) X5 binding to gp120 was enhanced by the A32 mAb, which binds a CD4-inducible epitope; in turn X5 binding enhanced the exposure of the A32 epitope (data not shown).	bind
3598	1	2195	6	10	NULL	0	NULL	NPC2	GP		bind		may			membranes	CellComponent	cholesterol rich			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_5_2518_s_318	12591949	( iii) NPC2 could bind to cholesterol-rich membranes and, through protein-protein interactions, could influence the localization of other proteins, such as NPC1, that mobilize lipids.	bind
3599	2	2195	6	10	NULL	0	NULL	statement 1	Process		influence 		may			NPC1	GP	localization of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_5_2518_s_318	12591949	( iii) NPC2 could bind to cholesterol-rich membranes and, through protein-protein interactions, could influence the localization of other proteins, such as NPC1, that mobilize lipids.	bind
3600	3	2195	6	10	NULL	0	NULL	NPC1	GP		mobilize					lipids	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_5_2518_s_318	12591949	( iii) NPC2 could bind to cholesterol-rich membranes and, through protein-protein interactions, could influence the localization of other proteins, such as NPC1, that mobilize lipids.	bind
5429	1	2195	7	10	NULL	0	NULL	NPC2	GP		bind to		could			membranes	CellComponent	cholesterol-rich 			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_5_2518_s_318	12591949	( iii) NPC2 could bind to cholesterol-rich membranes and, through protein-protein interactions, could influence the localization of other proteins, such as NPC1, that mobilize lipids.	bind
5431	2	2195	7	10	NULL	0	NULL	statement 1	Process		influence		could			NPC1	GP	localization of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_5_2518_s_318	12591949	( iii) NPC2 could bind to cholesterol-rich membranes and, through protein-protein interactions, could influence the localization of other proteins, such as NPC1, that mobilize lipids.	bind
5434	3	2195	7	10	NULL	0	NULL	NPC1	GP		mobilize					lipids	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_5_2518_s_318	12591949	( iii) NPC2 could bind to cholesterol-rich membranes and, through protein-protein interactions, could influence the localization of other proteins, such as NPC1, that mobilize lipids.	bind
3601	1	2196	6	10	NULL	0	NULL	GTP[gamma35] 	Chemical		bind					platelet membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_16_8750_s_167	9238049	( iii) The binding of GTP[gamma35] to patient platelet membranes in response to thrombin stimulation was markedly diminished.	bind
3602	2	2196	6	10	NULL	0	NULL	statement 1	Process		in response to					thrombin	GP	stimulation			NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_16_8750_s_167	9238049	( iii) The binding of GTP[gamma35] to patient platelet membranes in response to thrombin stimulation was markedly diminished.	bind
5436	1	2196	7	10	NULL	0	NULL	GTP[gamma35]	Chemical		binds to					platelet membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_16_8750_s_167	9238049	( iii) The binding of GTP[gamma35] to patient platelet membranes in response to thrombin stimulation was markedly diminished.	bind
5437	2	2196	7	10	NULL	0	NULL	Thrombin	GP	stimulation of	leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_16_8750_s_167	9238049	( iii) The binding of GTP[gamma35] to patient platelet membranes in response to thrombin stimulation was markedly diminished.	bind
3604	2	2197	6	10	NULL	0	NULL	anti-8-nitroguanosine antibody	GP		bind					8-nitroguanosine-BSA conjugate	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_2_685_s_81	12522148	( Inset) Binding of anti-8-nitroguanosine antibody to BSA or 8-nitroguanosine-BSA conjugate  fixed on microtiter plates.	bind
46294	1	2197	6	10	NULL	0	NULL	anti-8-nitroguanosine antibody	GP		bind					BSA	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_2_685_s_81	12522148	( Inset) Binding of anti-8-nitroguanosine antibody to BSA or 8-nitroguanosine-BSA conjugate  fixed on microtiter plates.	bind
5440	1	2197	7	10	NULL	0	NULL	anti-8-nitroguanosine antibody	GP		bind					BSA	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_2_685_s_81	12522148	( Inset) Binding of anti-8-nitroguanosine antibody to BSA or 8-nitroguanosine-BSA conjugate  fixed on microtiter plates.	bind
46295	2	2197	7	10	NULL	0	NULL	 anti-8-nitroguanosine antibody 	GP		bind					 8-nitroguanosine-BSA	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_2_685_s_81	12522148	( Inset) Binding of anti-8-nitroguanosine antibody to BSA or 8-nitroguanosine-BSA conjugate  fixed on microtiter plates.	bind
3643	1	2199	6	10	NULL	0	NULL	bicuculline	Chemical		blocks					BTX	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
3644	2	2199	6	10	NULL	0	NULL	Bic	Chemical		is					bicuculline	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
46062	3	2199	6	10	NULL	0	NULL	bicuculline	Chemical		is an antagonist of					GABAAR	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
46305	4	2199	6	10	NULL	0	NULL	MLA	Chemical		is					methyllycaconitine	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
46306	5	2199	6	10	NULL	0	NULL	Nic	Chemical		is					nicotine	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
46307	6	2199	6	10	NULL	0	NULL	Hexa	Chemical		is					hexamethonium	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
46308	7	2199	6	10	NULL	0	NULL	PB	Chemical		is					pentobarbital	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
46309	8	2199	6	10	NULL	0	NULL	pentobarbital	Chemical		is a type of					GABAAR modulator 	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
51557	9	2199	6	10	NULL	0	NULL	MLA	Chemical		is a type of					nAChR blocker	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
51558	10	2199	6	10	NULL	0	NULL	Nic	Chemical		is a type of					nAChR blocker	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
51559	11	2199	6	10	NULL	0	NULL	Hexa	Chemical		is a type of					nAChR blocker	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
6320	2	2199	7	10	NULL	0	NULL	MLA	Chemical		is					methyllycaconitine	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
6321	3	2199	7	10	NULL	0	NULL	Nic	Chemical		is					nicotine	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
6322	4	2199	7	10	NULL	0	NULL	hexa	Chemical		is					hexamethonium	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
6323	5	2199	7	10	NULL	0	NULL	PB	Chemical		is					pentobarbital	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
6324	6	2199	7	10	NULL	0	NULL	pentobarbital	Chemical		is a type of					GABAAR modulator	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
6325	7	2199	7	10	NULL	0	NULL	Bic	Chemical		is					bicuculline	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
6326	8	2199	7	10	NULL	0	NULL	bicuculline	Chemical		is antagonist of					GABAAR	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
6327	9	2199	7	10	NULL	0	NULL	MLA	Chemical		is a type of					nAChR blocker	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
6328	10	2199	7	10	NULL	0	NULL	Nic	Chemical		is a type of					nAChR blocker	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
6329	11	2199	7	10	NULL	0	NULL	hexa	Chemical		is a type of					nAChR blocker	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
46347	1	2199	7	10	NULL	0	NULL	Bic	Chemical		blocks					BTX	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_13_5149_s_41	16549768	( Inset) Double-reciprocal plot shows that  Kd  50 nM. ( b) BTX binding to this cell line was insensitive to preincubation with blockers of  nAChRs containing alpha1 or alpha7 subunits [methyllycaconitine (MLA), nicotine (Nic), and hexamethonium (Hexa)] or  the GABAAR modulator pentobarbital (PB) but was blocked by the GABAAR antagonist bicuculline (Bic).	bind
3605	1	2200	6	10	NULL	0	NULL	RecA	GP	wild type	bind					p/t DNA	NucleicAcid			15-nt oh	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_17_11061_s_117	12177433	( Inset) The data depict wild-type RecA binding to p/t DNA with a 15-nt oh; RecA protein binding to p/t DNA with a 12-nt oh; RecA 1730 protein binding to p/t with a 15-nt oh; RecA1730 protein binding to p/t with a 12-nt oh.	bind
3606	2	2200	6	10	NULL	0	NULL	RecA protein	GP		bind					p/t DNA	NucleicAcid			12-nt oh	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_17_11061_s_117	12177433	( Inset) The data depict wild-type RecA binding to p/t DNA with a 15-nt oh; RecA protein binding to p/t DNA with a 12-nt oh; RecA 1730 protein binding to p/t with a 15-nt oh; RecA1730 protein binding to p/t with a 12-nt oh.	bind
3607	3	2200	6	10	NULL	0	NULL	RecA 1730 protein	GP		bind					p/t DNA	NucleicAcid			15-nt oh	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_17_11061_s_117	12177433	( Inset) The data depict wild-type RecA binding to p/t DNA with a 15-nt oh; RecA protein binding to p/t DNA with a 12-nt oh; RecA 1730 protein binding to p/t with a 15-nt oh; RecA1730 protein binding to p/t with a 12-nt oh.	bind
3608	4	2200	6	10	NULL	0	NULL	RecA 1730 protein	GP		bind					p/t DNA	NucleicAcid			12-nt oh	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_17_11061_s_117	12177433	( Inset) The data depict wild-type RecA binding to p/t DNA with a 15-nt oh; RecA protein binding to p/t DNA with a 12-nt oh; RecA 1730 protein binding to p/t with a 15-nt oh; RecA1730 protein binding to p/t with a 12-nt oh.	bind
5464	1	2200	7	10	NULL	0	NULL	RecA	GP	Wild-type	binds to					p/t DNA	NucleicAcid			15-nt oh	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_17_11061_s_117	12177433	( Inset) The data depict wild-type RecA binding to p/t DNA with a 15-nt oh; RecA protein binding to p/t DNA with a 12-nt oh; RecA 1730 protein binding to p/t with a 15-nt oh; RecA1730 protein binding to p/t with a 12-nt oh.	bind
5466	2	2200	7	10	NULL	0	NULL	RecA protein	GP		binds to					p/t DNA	NucleicAcid			12-nt oh	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_17_11061_s_117	12177433	( Inset) The data depict wild-type RecA binding to p/t DNA with a 15-nt oh; RecA protein binding to p/t DNA with a 12-nt oh; RecA 1730 protein binding to p/t with a 15-nt oh; RecA1730 protein binding to p/t with a 12-nt oh.	bind
5468	3	2200	7	10	NULL	0	NULL	RecA 1730 protein	GP		binds to					p/t DNA	NucleicAcid			15-nt oh	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_17_11061_s_117	12177433	( Inset) The data depict wild-type RecA binding to p/t DNA with a 15-nt oh; RecA protein binding to p/t DNA with a 12-nt oh; RecA 1730 protein binding to p/t with a 15-nt oh; RecA1730 protein binding to p/t with a 12-nt oh.	bind
5471	4	2200	7	10	NULL	0	NULL	RecA1730 protein	GP		binds to					p/t DNA	NucleicAcid			12-nt oh	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_17_11061_s_117	12177433	( Inset) The data depict wild-type RecA binding to p/t DNA with a 15-nt oh; RecA protein binding to p/t DNA with a 12-nt oh; RecA 1730 protein binding to p/t with a 15-nt oh; RecA1730 protein binding to p/t with a 12-nt oh.	bind
3766	1	2202	5	10	NULL	0	NULL	IRp antibody	GP		bind					IR	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11692_s_142	9326672	( iv) An antibody to IRp binds to IR (but not to a deletion mutant of IR or to IGF-1R), inhibits insulin-induced internalization of IR, enhances insulin-stimulated glucose uptake, and competes with IRp for binding.	bind
3767	2	2202	5	10	NULL	0	NULL	IRp antibody	GP		does not bind					IR	GP	deletion mutant			NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11692_s_142	9326672	( iv) An antibody to IRp binds to IR (but not to a deletion mutant of IR or to IGF-1R), inhibits insulin-induced internalization of IR, enhances insulin-stimulated glucose uptake, and competes with IRp for binding.	bind
3768	3	2202	5	10	NULL	0	NULL	IRp antibody	GP		does not bind					IGF-1R	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11692_s_142	9326672	( iv) An antibody to IRp binds to IR (but not to a deletion mutant of IR or to IGF-1R), inhibits insulin-induced internalization of IR, enhances insulin-stimulated glucose uptake, and competes with IRp for binding.	bind
3769	4	2202	5	10	NULL	0	NULL	insulin	GP		induce					IR	GP	internalization of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11692_s_142	9326672	( iv) An antibody to IRp binds to IR (but not to a deletion mutant of IR or to IGF-1R), inhibits insulin-induced internalization of IR, enhances insulin-stimulated glucose uptake, and competes with IRp for binding.	bind
3770	5	2202	5	10	NULL	0	NULL	IRp antibody	GP		inhibit					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11692_s_142	9326672	( iv) An antibody to IRp binds to IR (but not to a deletion mutant of IR or to IGF-1R), inhibits insulin-induced internalization of IR, enhances insulin-stimulated glucose uptake, and competes with IRp for binding.	bind
3771	6	2202	5	10	NULL	0	NULL	insulin	GP		stimulate					glucose uptake	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11692_s_142	9326672	( iv) An antibody to IRp binds to IR (but not to a deletion mutant of IR or to IGF-1R), inhibits insulin-induced internalization of IR, enhances insulin-stimulated glucose uptake, and competes with IRp for binding.	bind
3772	7	2202	5	10	NULL	0	NULL	IRp antibody	GP		enhance					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11692_s_142	9326672	( iv) An antibody to IRp binds to IR (but not to a deletion mutant of IR or to IGF-1R), inhibits insulin-induced internalization of IR, enhances insulin-stimulated glucose uptake, and competes with IRp for binding.	bind
3773	8	2202	5	10	NULL	0	NULL	IRp	GP		bind					IR	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11692_s_142	9326672	( iv) An antibody to IRp binds to IR (but not to a deletion mutant of IR or to IGF-1R), inhibits insulin-induced internalization of IR, enhances insulin-stimulated glucose uptake, and competes with IRp for binding.	bind
3774	9	2202	5	10	NULL	0	NULL	statement 1	Process		compete with					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11692_s_142	9326672	( iv) An antibody to IRp binds to IR (but not to a deletion mutant of IR or to IGF-1R), inhibits insulin-induced internalization of IR, enhances insulin-stimulated glucose uptake, and competes with IRp for binding.	bind
3609	1	2202	6	10	NULL	0	NULL	IRp antibody	GP		bind					IR	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11692_s_142	9326672	( iv) An antibody to IRp binds to IR (but not to a deletion mutant of IR or to IGF-1R), inhibits insulin-induced internalization of IR, enhances insulin-stimulated glucose uptake, and competes with IRp for binding.	bind
3610	2	2202	6	10	NULL	0	NULL	IRp antibody	GP		does not bind					IR	GP	deletion mutant			NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11692_s_142	9326672	( iv) An antibody to IRp binds to IR (but not to a deletion mutant of IR or to IGF-1R), inhibits insulin-induced internalization of IR, enhances insulin-stimulated glucose uptake, and competes with IRp for binding.	bind
3611	3	2202	6	10	NULL	0	NULL	IRp antibody	GP		does not bind					IGF-1R	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11692_s_142	9326672	( iv) An antibody to IRp binds to IR (but not to a deletion mutant of IR or to IGF-1R), inhibits insulin-induced internalization of IR, enhances insulin-stimulated glucose uptake, and competes with IRp for binding.	bind
3612	4	2202	6	10	NULL	0	NULL	insulin	GP		induces					IR	GP	internalization of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11692_s_142	9326672	( iv) An antibody to IRp binds to IR (but not to a deletion mutant of IR or to IGF-1R), inhibits insulin-induced internalization of IR, enhances insulin-stimulated glucose uptake, and competes with IRp for binding.	bind
3613	5	2202	6	10	NULL	0	NULL	IRp antibody	GP		inhibits					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11692_s_142	9326672	( iv) An antibody to IRp binds to IR (but not to a deletion mutant of IR or to IGF-1R), inhibits insulin-induced internalization of IR, enhances insulin-stimulated glucose uptake, and competes with IRp for binding.	bind
3614	6	2202	6	10	NULL	0	NULL	insulin	GP		stimulates					glucose uptake	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11692_s_142	9326672	( iv) An antibody to IRp binds to IR (but not to a deletion mutant of IR or to IGF-1R), inhibits insulin-induced internalization of IR, enhances insulin-stimulated glucose uptake, and competes with IRp for binding.	bind
3615	7	2202	6	10	NULL	0	NULL	IRp antibody	GP		enhances					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11692_s_142	9326672	( iv) An antibody to IRp binds to IR (but not to a deletion mutant of IR or to IGF-1R), inhibits insulin-induced internalization of IR, enhances insulin-stimulated glucose uptake, and competes with IRp for binding.	bind
3616	8	2202	6	10	NULL	0	NULL	IRp	GP		bind					IR	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11692_s_142	9326672	( iv) An antibody to IRp binds to IR (but not to a deletion mutant of IR or to IGF-1R), inhibits insulin-induced internalization of IR, enhances insulin-stimulated glucose uptake, and competes with IRp for binding.	bind
3617	9	2202	6	10	NULL	0	NULL	statement 1	Process		competes					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11692_s_142	9326672	( iv) An antibody to IRp binds to IR (but not to a deletion mutant of IR or to IGF-1R), inhibits insulin-induced internalization of IR, enhances insulin-stimulated glucose uptake, and competes with IRp for binding.	bind
3775	1	2203	5	10	NULL	0	NULL	nuclear proteins	GP		bind					ks1	GP			cis regulatory elements	NULL	mutant reg-16	NULL	NULL	NULL	NULL	gw60_pnas_96_4_1445_s_197	9990043	( iv) In mutant reg-16, a high level of nuclear proteins binds to  ks1 cis regulatory elements (Fig.  6 B).	bind
3618	1	2203	6	10	NULL	0	NULL	nuclear proteins	GP		bind					ks1	GP			cis regulatory elements	NULL	mutant reg-16	NULL	NULL	NULL	NULL	gw60_pnas_96_4_1445_s_197	9990043	( iv) In mutant reg-16, a high level of nuclear proteins binds to  ks1 cis regulatory elements (Fig.  6 B).	bind
3776	1	2204	5	10	NULL	0	NULL	p300 histone acetyltransferase	GP		acetylate					core histones	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_genesdev_19_23_2912_s_122	16322561	( Left panel) Bacterially expressed NIR INHAT regions prevent acetylation of all core histones  by the p300 histone acetyltransferase in vitro.	bind
3777	2	2204	5	10	NULL	0	NULL	NIR INHAT	GP	bacterially expressed regions of	prevent					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_genesdev_19_23_2912_s_122	16322561	( Left panel) Bacterially expressed NIR INHAT regions prevent acetylation of all core histones  by the p300 histone acetyltransferase in vitro.	bind
3619	1	2204	6	10	NULL	0	NULL	histone acetyltransferase p300	GP		acetylates					core histones	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_genesdev_19_23_2912_s_122	16322561	( Left panel) Bacterially expressed NIR INHAT regions prevent acetylation of all core histones  by the p300 histone acetyltransferase in vitro.	bind
3620	2	2204	6	10	NULL	0	NULL	NIR INHAT	GP	Bacterially expressed regions of	prevents					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_genesdev_19_23_2912_s_122	16322561	( Left panel) Bacterially expressed NIR INHAT regions prevent acetylation of all core histones  by the p300 histone acetyltransferase in vitro.	bind
3778	1	2207	5	10	NULL	0	NULL	Nrp-1 receptors	GP		associate with		functionally			Plexin-signaling receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_9_1013_s_76	15879551	( Left) Functional association of Nrp-1 and Nrp-2 receptors with Plexin-signaling receptors  transduce Sema3 signals.	bind
3779	2	2207	5	10	NULL	0	NULL	Nrp-2 receptors	GP		associate with		functionally			Plexin-signaling receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_9_1013_s_76	15879551	( Left) Functional association of Nrp-1 and Nrp-2 receptors with Plexin-signaling receptors  transduce Sema3 signals.	bind
3780	3	2207	5	10	NULL	0	NULL	statement 1	Process		transduce					Sema3 signals	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_9_1013_s_76	15879551	( Left) Functional association of Nrp-1 and Nrp-2 receptors with Plexin-signaling receptors  transduce Sema3 signals.	bind
3781	4	2207	5	10	NULL	0	NULL	statement 2	Process		transduce					Sema3 signals	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_9_1013_s_76	15879551	( Left) Functional association of Nrp-1 and Nrp-2 receptors with Plexin-signaling receptors  transduce Sema3 signals.	bind
3621	1	2207	6	10	NULL	0	NULL	Nrp-1 receptor	GP		associate		functionaly			plexin-signaling receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_9_1013_s_76	15879551	( Left) Functional association of Nrp-1 and Nrp-2 receptors with Plexin-signaling receptors  transduce Sema3 signals.	bind
3622	2	2207	6	10	NULL	0	NULL	Nrp-2 receptor	GP		associate		functionaly			plexin-signaling receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_9_1013_s_76	15879551	( Left) Functional association of Nrp-1 and Nrp-2 receptors with Plexin-signaling receptors  transduce Sema3 signals.	bind
3623	3	2207	6	10	NULL	0	NULL	statement 1	Process		transduce					Sema3 signals	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_9_1013_s_76	15879551	( Left) Functional association of Nrp-1 and Nrp-2 receptors with Plexin-signaling receptors  transduce Sema3 signals.	bind
3624	4	2207	6	10	NULL	0	NULL	statement 2	Process		transduce					Sema3 signals	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_9_1013_s_76	15879551	( Left) Functional association of Nrp-1 and Nrp-2 receptors with Plexin-signaling receptors  transduce Sema3 signals.	bind
3782	1	2208	5	10	NULL	0	NULL	cGMP	Chemical		bind					monomeric PKG	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_5_2380_s_143	12591946	( Left) Model of cGMP binding to monomeric PKG that is used to generate binding curves.	bind
3625	1	2208	6	10	NULL	0	NULL	cGMP	Chemical		bind					monomeric PKG	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_5_2380_s_143	12591946	( Left) Model of cGMP binding to monomeric PKG that is used to generate binding curves.	bind
3783	1	2209	5	10	NULL	0	NULL	Cbl	GP		bind					IF	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_19_0_173_s_217	10448521	( Left) The transcytosis of Cbl following the apical internalization of Cbl bound to intrinsic  factor (IF).	bind
3784	2	2209	5	10	NULL	0	NULL	IF	GP		is					intrinsic factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_19_0_173_s_217	10448521	( Left) The transcytosis of Cbl following the apical internalization of Cbl bound to intrinsic  factor (IF).	bind
3785	3	2209	5	10	NULL	0	NULL	statement 1	Process		undergoes					apical internalization	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_19_0_173_s_217	10448521	( Left) The transcytosis of Cbl following the apical internalization of Cbl bound to intrinsic  factor (IF).	bind
3786	4	2209	5	10	NULL	0	NULL	statement 3	Process		leads to					Cbl	GP	transcytosis of			NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_19_0_173_s_217	10448521	( Left) The transcytosis of Cbl following the apical internalization of Cbl bound to intrinsic  factor (IF).	bind
3626	1	2209	6	10	NULL	0	NULL	Cbl	GP		bind					IF	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_19_0_173_s_217	10448521	( Left) The transcytosis of Cbl following the apical internalization of Cbl bound to intrinsic  factor (IF).	bind
3627	2	2209	6	10	NULL	0	NULL	IF	GP		is					intrinsic factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_19_0_173_s_217	10448521	( Left) The transcytosis of Cbl following the apical internalization of Cbl bound to intrinsic  factor (IF).	bind
46349	3	2209	6	10	NULL	0	NULL	statement 1	Process		undergoes					apical internalization	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_19_0_173_s_217	10448521	( Left) The transcytosis of Cbl following the apical internalization of Cbl bound to intrinsic  factor (IF).	bind
46351	4	2209	6	10	NULL	0	NULL	statement 3	Process		leads to					Cbl	GP	transcytosis of			NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_19_0_173_s_217	10448521	( Left) The transcytosis of Cbl following the apical internalization of Cbl bound to intrinsic  factor (IF).	bind
3788	1	2211	5	10	NULL	0	NULL	SRY	GP	wt	bind					DNA	NucleicAcid			SRY DNA-binding consesus site AACAAT	NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_12_7045_s_129	12764225	( Lower) A typical single EMSA experiment demonstrating SRYwt,  SRYR62G, and SRYR133W (860  pg) binding to the SRY DNA-binding consensus site  AACAAT.	bind
3789	2	2211	5	10	NULL	0	NULL	SRY	GP		bind			R62G		DNA	NucleicAcid			SRY DNA-binding consesus site AACAAT	NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_12_7045_s_129	12764225	( Lower) A typical single EMSA experiment demonstrating SRYwt,  SRYR62G, and SRYR133W (860  pg) binding to the SRY DNA-binding consensus site  AACAAT.	bind
3790	3	2211	5	10	NULL	0	NULL	SRY	GP		bind			R133W		DNA	NucleicAcid			SRY DNA-binding consesus site AACAAT	NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_12_7045_s_129	12764225	( Lower) A typical single EMSA experiment demonstrating SRYwt,  SRYR62G, and SRYR133W (860  pg) binding to the SRY DNA-binding consensus site  AACAAT.	bind
3628	1	2211	6	10	NULL	0	NULL	SRY	GP	wt	bind					DNA	NucleicAcid			SRY DNA-binding consensus site AACAAT	NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_12_7045_s_129	12764225	( Lower) A typical single EMSA experiment demonstrating SRYwt,  SRYR62G, and SRYR133W (860  pg) binding to the SRY DNA-binding consensus site  AACAAT.	bind
3629	2	2211	6	10	NULL	0	NULL	SRY	GP		bind			R62G		DNA	NucleicAcid			SRY DNA-binding consensus site AACAAT	NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_12_7045_s_129	12764225	( Lower) A typical single EMSA experiment demonstrating SRYwt,  SRYR62G, and SRYR133W (860  pg) binding to the SRY DNA-binding consensus site  AACAAT.	bind
3630	3	2211	6	10	NULL	0	NULL	SRY	GP		bind			R133W		DNA	NucleicAcid			SRY DNA-binding consensus site AACAAT	NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_12_7045_s_129	12764225	( Lower) A typical single EMSA experiment demonstrating SRYwt,  SRYR62G, and SRYR133W (860  pg) binding to the SRY DNA-binding consensus site  AACAAT.	bind
3791	1	2213	5	10	NULL	0	NULL	Go-GDP	GP		bind					MBP-Pins	GP	purified			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_17_6524_s_108	16617104	( Lower) Go-GDP binds purified MBP-Pins; Go-GTP binds much less.	bind
3792	2	2213	5	10	NULL	0	NULL	Go-GTP	GP		bind		lesser			MBP-Pins	GP	purified			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_17_6524_s_108	16617104	( Lower) Go-GDP binds purified MBP-Pins; Go-GTP binds much less.	bind
3631	1	2213	6	10	NULL	0	NULL	Go-GDP	GP		bind					MBP-Pins	GP	purified			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_17_6524_s_108	16617104	( Lower) Go-GDP binds purified MBP-Pins; Go-GTP binds much less.	bind
3632	2	2213	6	10	NULL	0	NULL	Go-GTP	GP		bind		less			MBP-Pins	GP	purified			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_17_6524_s_108	16617104	( Lower) Go-GDP binds purified MBP-Pins; Go-GTP binds much less.	bind
3793	1	2216	5	10	NULL	0	NULL	vitellogenin mRNA	NucleicAcid		contains				3''-UTR					two APyrUGA elements	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_23_12498_s_73	11050168	( Lower) The sequence of the vitellogenin B1 3''-UTR bound by vigilin containing the only two APyrUGA elements present in the 3''-UTR of vitellogenin mRNA ( 18).	bind
3794	2	2216	5	10	NULL	0	NULL	vitellogenin B1	NucleicAcid		bind				3''-UTR	vigilin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_23_12498_s_73	11050168	( Lower) The sequence of the vitellogenin B1 3''-UTR bound by vigilin containing the only two APyrUGA elements present in the 3''-UTR of vitellogenin mRNA ( 18).	bind
3633	1	2216	6	10	NULL	0	NULL	vitellogenin B1	NucleicAcid		bind				3''-UTR	vigilin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_23_12498_s_73	11050168	( Lower) The sequence of the vitellogenin B1 3''-UTR bound by vigilin containing the only two APyrUGA elements present in the 3''-UTR of vitellogenin mRNA ( 18).	bind
3634	2	2216	6	10	NULL	0	NULL	vitellogenin mRNA	NucleicAcid		contains				3''-UTR					two APyrUGA elements	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_23_12498_s_73	11050168	( Lower) The sequence of the vitellogenin B1 3''-UTR bound by vigilin containing the only two APyrUGA elements present in the 3''-UTR of vitellogenin mRNA ( 18).	bind
3811	1	2217	5	10	NULL	0	NULL				superimpose with			1-850		T3	GP	crystal structure			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_12_7354_s_130	12777627	( Lower)1-850 superimposes with the crystal structure of T3  (green), bound to active TR  and clashes with the active conformation of helix  H12 (cyan).	bind
3812	2	2217	5	10	NULL	0	NULL				bind			1-850		TR	GP	active			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_12_7354_s_130	12777627	( Lower)1-850 superimposes with the crystal structure of T3  (green), bound to active TR  and clashes with the active conformation of helix  H12 (cyan).	bind
3813	3	2217	5	10	NULL	0	NULL				clashes with			1-850		helix H12 	GP	active conformation of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_12_7354_s_130	12777627	( Lower)1-850 superimposes with the crystal structure of T3  (green), bound to active TR  and clashes with the active conformation of helix  H12 (cyan).	bind
4399	1	2217	6	10	NULL	0	NULL				superimpose with			1-850		T3	GP	crystal structure			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_12_7354_s_130	12777627	( Lower)1-850 superimposes with the crystal structure of T3  (green), bound to active TR  and clashes with the active conformation of helix  H12 (cyan).	bind
4401	2	2217	6	10	NULL	0	NULL				bind			1-850		TR	GP	active			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_12_7354_s_130	12777627	( Lower)1-850 superimposes with the crystal structure of T3  (green), bound to active TR  and clashes with the active conformation of helix  H12 (cyan).	bind
4404	3	2217	6	10	NULL	0	NULL				clashes with 			1-850		helix H12	GP	active conformation of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_12_7354_s_130	12777627	( Lower)1-850 superimposes with the crystal structure of T3  (green), bound to active TR  and clashes with the active conformation of helix  H12 (cyan).	bind
3814	1	2219	5	10	NULL	0	NULL	Shh	GP		induce					Gli1	GP	expression			NULL	dermal fibroblasts isolated from wild-type skin	NULL	NULL	NULL	NULL	gw60_genesdev_17_2_282_s_115	12533516	( M) Shh induces  Gli1 and  Ptc1 expression in dermal fibroblasts isolated from wild-type skin, as revealed by RT-PCR analysis.	bind
3815	2	2219	5	10	NULL	0	NULL	Shh	GP		induce					Ptc1	GP	expression			NULL	dermal fibroblasts isolated from wild-type skin	NULL	NULL	NULL	NULL	gw60_genesdev_17_2_282_s_115	12533516	( M) Shh induces  Gli1 and  Ptc1 expression in dermal fibroblasts isolated from wild-type skin, as revealed by RT-PCR analysis.	bind
3635	1	2219	6	10	NULL	0	NULL	Shh	GP		induces					Gli1	GP	expression of 			NULL	dermal fibroblasts isolated from wild-type skin	NULL	NULL	NULL	NULL	gw60_genesdev_17_2_282_s_115	12533516	( M) Shh induces  Gli1 and  Ptc1 expression in dermal fibroblasts isolated from wild-type skin, as revealed by RT-PCR analysis.	bind
3636	2	2219	6	10	NULL	0	NULL	Shh	GP		induces					Ptc1	GP	expression of 			NULL	dermal fibroblasts isolated from wild-type skin	NULL	NULL	NULL	NULL	gw60_genesdev_17_2_282_s_115	12533516	( M) Shh induces  Gli1 and  Ptc1 expression in dermal fibroblasts isolated from wild-type skin, as revealed by RT-PCR analysis.	bind
3816	1	2220	5	10	NULL	0	NULL	Hh	GP		bind					Ptc	GP				NULL	A-compartment cells near the A/P boundary (B cell) 	NULL	NULL	NULL	NULL	gw60_genesdev_16_18_2315_s_94	12231619	( Middle) In A-compartment cells near the A/P boundary (B cell) or cells near the MF (M cell), Hh binds Ptc, alleviating its repression on Smo.	bind
3817	2	2220	5	10	NULL	0	NULL	statement 1	Process		alleviate					Smo	GP	repression on			NULL	A-compartment cells near the A/P boundary (B cell)	NULL	NULL	NULL	NULL	gw60_genesdev_16_18_2315_s_94	12231619	( Middle) In A-compartment cells near the A/P boundary (B cell) or cells near the MF (M cell), Hh binds Ptc, alleviating its repression on Smo.	bind
52943	3	2220	5	10	NULL	0	NULL	Hh	GP		bind					Ptc	GP				NULL	cells near the MF (M cell)	NULL	NULL	NULL	NULL	gw60_genesdev_16_18_2315_s_94	12231619	( Middle) In A-compartment cells near the A/P boundary (B cell) or cells near the MF (M cell), Hh binds Ptc, alleviating its repression on Smo.	bind
52945	4	2220	5	10	NULL	0	NULL	statement 3	Process		alleviate					Smo	GP	repression on			NULL	cells near the MF (M cell)	NULL	NULL	NULL	NULL	gw60_genesdev_16_18_2315_s_94	12231619	( Middle) In A-compartment cells near the A/P boundary (B cell) or cells near the MF (M cell), Hh binds Ptc, alleviating its repression on Smo.	bind
3637	1	2220	6	10	NULL	0	NULL	Hh	GP		bind					Ptc	GP				NULL	In A-compartment cells near the A/P boundary (B cell) 	NULL	NULL	NULL	NULL	gw60_genesdev_16_18_2315_s_94	12231619	( Middle) In A-compartment cells near the A/P boundary (B cell) or cells near the MF (M cell), Hh binds Ptc, alleviating its repression on Smo.	bind
3638	2	2220	6	10	NULL	0	NULL	statement 1	Process		alleviate					Smo	GP	repression on			NULL	In A-compartment cells near the A/P boundary (B cell) 	NULL	NULL	NULL	NULL	gw60_genesdev_16_18_2315_s_94	12231619	( Middle) In A-compartment cells near the A/P boundary (B cell) or cells near the MF (M cell), Hh binds Ptc, alleviating its repression on Smo.	bind
52946	3	2220	6	10	NULL	0	NULL	Hh	GP		bind					Ptc	GP				NULL	cells near the MF (M cell)	NULL	NULL	NULL	NULL	gw60_genesdev_16_18_2315_s_94	12231619	( Middle) In A-compartment cells near the A/P boundary (B cell) or cells near the MF (M cell), Hh binds Ptc, alleviating its repression on Smo.	bind
52947	4	2220	6	10	NULL	0	NULL	statement 3	Process		alleviate					Smo	GP	repression on			NULL	cells near the MF (M cell)	NULL	NULL	NULL	NULL	gw60_genesdev_16_18_2315_s_94	12231619	( Middle) In A-compartment cells near the A/P boundary (B cell) or cells near the MF (M cell), Hh binds Ptc, alleviating its repression on Smo.	bind
3818	1	2221	5	10	NULL	0	NULL	III-31-C	Chemical		bind					PS1 NTF/CTF heterodimer	GP		active site		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_9_3230_s_160	15722417	( Middle) Transition-state analogue III-31-C binds to PS1 NTF/CTF heterodimer at the active  site, located internally and containing two aspartates (denoted as "`D"`).	bind
3819	2	2221	5	10	NULL	0	NULL	PS1 NTF/CTF heterodimer	GP		is located			active site		internally					NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_9_3230_s_160	15722417	( Middle) Transition-state analogue III-31-C binds to PS1 NTF/CTF heterodimer at the active  site, located internally and containing two aspartates (denoted as "`D"`).	bind
3820	3	2221	5	10	NULL	0	NULL	PS1 NTF/CTF heterodimer	GP		contains			active site		aspartate	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_9_3230_s_160	15722417	( Middle) Transition-state analogue III-31-C binds to PS1 NTF/CTF heterodimer at the active  site, located internally and containing two aspartates (denoted as "`D"`).	bind
46352	4	2221	5	10	NULL	0	NULL	III-31-C	Chemical		is a type of					Transition-state analogue	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_9_3230_s_160	15722417	( Middle) Transition-state analogue III-31-C binds to PS1 NTF/CTF heterodimer at the active  site, located internally and containing two aspartates (denoted as "`D"`).	bind
3710	1	2221	6	10	NULL	0	NULL	 III-31-C	Chemical		bind					PS1 NTF/CTF heterodimer	GP		active site		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_9_3230_s_160	15722417	( Middle) Transition-state analogue III-31-C binds to PS1 NTF/CTF heterodimer at the active  site, located internally and containing two aspartates (denoted as "`D"`).	bind
46353	2	2221	6	10	NULL	0	NULL	PS1 NTF/CTF heterodimer	GP		contains			active site		aspartate	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_9_3230_s_160	15722417	( Middle) Transition-state analogue III-31-C binds to PS1 NTF/CTF heterodimer at the active  site, located internally and containing two aspartates (denoted as "`D"`).	bind
46398	3	2221	6	10	NULL	0	NULL	III-31-C	Chemical		is a type of					Transition-state analogue	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_9_3230_s_160	15722417	( Middle) Transition-state analogue III-31-C binds to PS1 NTF/CTF heterodimer at the active  site, located internally and containing two aspartates (denoted as "`D"`).	bind
52948	4	2221	6	10	NULL	0	NULL	PS1 NTF/CTF heterodimer	Chemical		is located			active site		internally					NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_9_3230_s_160	15722417	( Middle) Transition-state analogue III-31-C binds to PS1 NTF/CTF heterodimer at the active  site, located internally and containing two aspartates (denoted as "`D"`).	bind
3821	1	2222	5	10	NULL	0	NULL	Lhx5	GP		bind					sfrp1a	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_development_133_16_3191_s_293	16854974	( O) Lhx5 binds to the  sfrp1a promoter.	bind
3711	1	2222	6	10	NULL	0	NULL	Lhx5	GP		bind					Sfrp1a	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_development_133_16_3191_s_293	16854974	( O) Lhx5 binds to the  sfrp1a promoter.	bind
3822	1	2223	5	10	NULL	0	NULL	lactoferrin	GP		bind					OVR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_31_18219_s_223	7543099	( Panel B), for lactoferrin binding to OVR ( Panel  C), and for binding of an unrelated single chain antibody to the  LDL receptor	bind
3823	2	2223	5	10	NULL	0	NULL	single chain antibody	GP	unrelated 	bind					 LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_31_18219_s_223	7543099	( Panel B), for lactoferrin binding to OVR ( Panel  C), and for binding of an unrelated single chain antibody to the  LDL receptor	bind
3712	1	2223	6	10	NULL	0	NULL	lactoferrin	GP		bind					OVR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_31_18219_s_223	7543099	( Panel B), for lactoferrin binding to OVR ( Panel  C), and for binding of an unrelated single chain antibody to the  LDL receptor	bind
3713	2	2223	6	10	NULL	0	NULL	single chain antibody	GP	unrelated	bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_31_18219_s_223	7543099	( Panel B), for lactoferrin binding to OVR ( Panel  C), and for binding of an unrelated single chain antibody to the  LDL receptor	bind
3824	1	2224	5	10	NULL	0	NULL	EGFR mAb 3A	GP		bind					Protein A	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_8335_s_107	10075741	( Panels A and  B) or EGFR mAbs 3A/4A bound to Protein A ( Panels C and  D), as described under	bind
5224	2	2224	5	10	NULL	0	NULL	EGFR mAb 4A	GP		bind					Protein A	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_8335_s_107	10075741	( Panels A and  B) or EGFR mAbs 3A/4A bound to Protein A ( Panels C and  D), as described under	bind
3714	1	2224	6	10	NULL	0	NULL	EGFR mAb 3A	GP		bind					Protein A	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_8335_s_107	10075741	( Panels A and  B) or EGFR mAbs 3A/4A bound to Protein A ( Panels C and  D), as described under	bind
3715	2	2224	6	10	NULL	0	NULL	EGFR mAb 4A	GP		bind					Protein A	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_8335_s_107	10075741	( Panels A and  B) or EGFR mAbs 3A/4A bound to Protein A ( Panels C and  D), as described under	bind
5251	1	2225	5	10	NULL	0	NULL	Epibatidine	Chemical		is a type of					nAChR agonist	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_287_3_847_s_2	9864263	( plus-or-minus )-Epibatidine (EPIB) and A-85380 are nicotinic acetylcholine receptor (nAChR) agonists that bind to the agonist ([3]cytisine) binding site with 40 to 50 pM affinity but have different affinities in nAChR subtype selective functional receptor assays.	bind
5252	2	2225	5	10	NULL	0	NULL	nAChR	GP		is					nicotinic acetylcholine receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_287_3_847_s_2	9864263	( plus-or-minus )-Epibatidine (EPIB) and A-85380 are nicotinic acetylcholine receptor (nAChR) agonists that bind to the agonist ([3]cytisine) binding site with 40 to 50 pM affinity but have different affinities in nAChR subtype selective functional receptor assays.	bind
5253	3	2225	5	10	NULL	0	NULL	Epibatidine	Chemical		bind					nAChR	GP		agonist (cytisine) binding site		NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_287_3_847_s_2	9864263	( plus-or-minus )-Epibatidine (EPIB) and A-85380 are nicotinic acetylcholine receptor (nAChR) agonists that bind to the agonist ([3]cytisine) binding site with 40 to 50 pM affinity but have different affinities in nAChR subtype selective functional receptor assays.	bind
5254	4	2225	5	10	NULL	0	NULL	A-85380	Chemical		is a type of					nAChR agonist	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_287_3_847_s_2	9864263	( plus-or-minus )-Epibatidine (EPIB) and A-85380 are nicotinic acetylcholine receptor (nAChR) agonists that bind to the agonist ([3]cytisine) binding site with 40 to 50 pM affinity but have different affinities in nAChR subtype selective functional receptor assays.	bind
5255	5	2225	5	10	NULL	0	NULL	A-85380	Chemical		bind					nAChR	GP		agonist (cytisine) binding site		NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_287_3_847_s_2	9864263	( plus-or-minus )-Epibatidine (EPIB) and A-85380 are nicotinic acetylcholine receptor (nAChR) agonists that bind to the agonist ([3]cytisine) binding site with 40 to 50 pM affinity but have different affinities in nAChR subtype selective functional receptor assays.	bind
46399	6	2225	5	10	NULL	0	NULL	EPIB	Chemical		is					Epibatidine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_287_3_847_s_2	9864263	( plus-or-minus )-Epibatidine (EPIB) and A-85380 are nicotinic acetylcholine receptor (nAChR) agonists that bind to the agonist ([3]cytisine) binding site with 40 to 50 pM affinity but have different affinities in nAChR subtype selective functional receptor assays.	bind
3925	1	2225	6	10	NULL	0	NULL	Epibatidine 	Chemical		is a type of					nAChR agonist	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_287_3_847_s_2	9864263	( plus-or-minus )-Epibatidine (EPIB) and A-85380 are nicotinic acetylcholine receptor (nAChR) agonists that bind to the agonist ([3]cytisine) binding site with 40 to 50 pM affinity but have different affinities in nAChR subtype selective functional receptor assays.	bind
3926	2	2225	6	10	NULL	0	NULL	A-85380	Chemical		is a type of					nAChR agonist	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_287_3_847_s_2	9864263	( plus-or-minus )-Epibatidine (EPIB) and A-85380 are nicotinic acetylcholine receptor (nAChR) agonists that bind to the agonist ([3]cytisine) binding site with 40 to 50 pM affinity but have different affinities in nAChR subtype selective functional receptor assays.	bind
3927	3	2225	6	10	NULL	0	NULL	nAChR	GP		is					nicotinic acetylcholine receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_287_3_847_s_2	9864263	( plus-or-minus )-Epibatidine (EPIB) and A-85380 are nicotinic acetylcholine receptor (nAChR) agonists that bind to the agonist ([3]cytisine) binding site with 40 to 50 pM affinity but have different affinities in nAChR subtype selective functional receptor assays.	bind
3928	4	2225	6	10	NULL	0	NULL	statement 1	Process		bind					nAChR	GP		agonist (cytisine) binding site		NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_287_3_847_s_2	9864263	( plus-or-minus )-Epibatidine (EPIB) and A-85380 are nicotinic acetylcholine receptor (nAChR) agonists that bind to the agonist ([3]cytisine) binding site with 40 to 50 pM affinity but have different affinities in nAChR subtype selective functional receptor assays.	bind
3929	5	2225	6	10	NULL	0	NULL	statement 2	Process		bind					nAChR	GP		agonist (cytisine) binding site		NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_287_3_847_s_2	9864263	( plus-or-minus )-Epibatidine (EPIB) and A-85380 are nicotinic acetylcholine receptor (nAChR) agonists that bind to the agonist ([3]cytisine) binding site with 40 to 50 pM affinity but have different affinities in nAChR subtype selective functional receptor assays.	bind
46400	6	2225	6	10	NULL	0	NULL	EPIB	Chemical		is					Epibatidine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_287_3_847_s_2	9864263	( plus-or-minus )-Epibatidine (EPIB) and A-85380 are nicotinic acetylcholine receptor (nAChR) agonists that bind to the agonist ([3]cytisine) binding site with 40 to 50 pM affinity but have different affinities in nAChR subtype selective functional receptor assays.	bind
3825	1	2226	5	10	NULL	0	NULL	tRNAs	NucleicAcid		bind					Arc1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_8_6000_s_111	11069915	( Pool A) contain tRNAs bound to Arc1p, whereas fractions 20-23	bind
3716	1	2226	6	10	NULL	0	NULL	tRNA	NucleicAcid		bind					Arc1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_8_6000_s_111	11069915	( Pool A) contain tRNAs bound to Arc1p, whereas fractions 20-23	bind
3826	1	2227	5	10	NULL	0	NULL	receptor for Activated- C Kinase 1	GP		bind		specifically			PKC	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_24_22073_s_36	11934885	( Receptor for  Activated- C  Kinase 1), specifically binds to activated PKC ( 24,  25).	bind
3717	1	2227	6	10	NULL	0	NULL	Receptor for Activated- C Kinase 1	GP		bind		specifically			PKC	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_24_22073_s_36	11934885	( Receptor for  Activated- C  Kinase 1), specifically binds to activated PKC ( 24,  25).	bind
3827	1	2228	5	10	NULL	0	NULL	Lz-AT	GP		is					Lz-binding site and adjacent AT sequences	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_7_838_s_108	12670867	( Right panel) A probe containing a Lz-binding site and adjacent AT sequences from the  dpn enhancer [Lz-AT(d1); Table  1] can bind Lz (black arrowhead, lane  9) and Cut (white arrowhead, lane  10).	bind
3828	2	2228	5	10	NULL	0	NULL	dpn	GP		bind				Lz-AT	Lz	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_7_838_s_108	12670867	( Right panel) A probe containing a Lz-binding site and adjacent AT sequences from the  dpn enhancer [Lz-AT(d1); Table  1] can bind Lz (black arrowhead, lane  9) and Cut (white arrowhead, lane  10).	bind
3829	3	2228	5	10	NULL	0	NULL	dpn	GP		bind				Lz-AT	Cut	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_7_838_s_108	12670867	( Right panel) A probe containing a Lz-binding site and adjacent AT sequences from the  dpn enhancer [Lz-AT(d1); Table  1] can bind Lz (black arrowhead, lane  9) and Cut (white arrowhead, lane  10).	bind
3718	1	2228	6	10	NULL	0	NULL	dpn	GP		bind				Lz-AT	Lz	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_7_838_s_108	12670867	( Right panel) A probe containing a Lz-binding site and adjacent AT sequences from the  dpn enhancer [Lz-AT(d1); Table  1] can bind Lz (black arrowhead, lane  9) and Cut (white arrowhead, lane  10).	bind
3930	2	2228	6	10	NULL	0	NULL	dpn	GP		bind				Lz-AT	Cut	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_7_838_s_108	12670867	( Right panel) A probe containing a Lz-binding site and adjacent AT sequences from the  dpn enhancer [Lz-AT(d1); Table  1] can bind Lz (black arrowhead, lane  9) and Cut (white arrowhead, lane  10).	bind
3960	3	2228	6	10	NULL	0	NULL	Lz-AT	GP		is					Lz-binding site and adjacent AT sequences	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_7_838_s_108	12670867	( Right panel) A probe containing a Lz-binding site and adjacent AT sequences from the  dpn enhancer [Lz-AT(d1); Table  1] can bind Lz (black arrowhead, lane  9) and Cut (white arrowhead, lane  10).	bind
3830	1	2229	5	10	NULL	0	NULL	immune complexes	GP		contains					G9a	GP				NULL	wild-type cells	NULL	NULL	NULL	NULL	gw70_genesdev_19_7_815_s_193	15774718	( Right panels) Similarly, immune complexes from wild-type cells obtained with anti-GLP antibody  also contain G9a.	bind
3719	1	2229	6	10	NULL	0	NULL	immune complex	GP		contain					G9a	GP				NULL	wild type cells	NULL	NULL	NULL	NULL	gw70_genesdev_19_7_815_s_193	15774718	( Right panels) Similarly, immune complexes from wild-type cells obtained with anti-GLP antibody  also contain G9a.	bind
3831	1	2230	5	10	NULL	0	NULL	Pax6	GP		is absent in				alpha enhancer	Vax1 DNA fragments	NucleicAcid				NULL	Vax double knock-outs	NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1249_s_179	15905411	( Right panels) The Pax6 alpha-enhancer was not detected in Vax1 or Vax2 ChIP DNA fragments from  Vax double knock-outs, and Vax1 and Vax2 binding to the alpha-enhancer could not be detected in ChIPs performed from  Vax1 and  Vax2 mutants, respectively.	bind
3832	2	2230	5	10	NULL	0	NULL	Pax6	GP		is absent in				alpha enhancer	Vax2 DNA fragments	NucleicAcid				NULL	Vax double knock-outs	NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1249_s_179	15905411	( Right panels) The Pax6 alpha-enhancer was not detected in Vax1 or Vax2 ChIP DNA fragments from  Vax double knock-outs, and Vax1 and Vax2 binding to the alpha-enhancer could not be detected in ChIPs performed from  Vax1 and  Vax2 mutants, respectively.	bind
3833	3	2230	5	10	NULL	0	NULL	Vax1	GP	mutant	does not bind					Pax6	GP			alpha enhancer	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1249_s_179	15905411	( Right panels) The Pax6 alpha-enhancer was not detected in Vax1 or Vax2 ChIP DNA fragments from  Vax double knock-outs, and Vax1 and Vax2 binding to the alpha-enhancer could not be detected in ChIPs performed from  Vax1 and  Vax2 mutants, respectively.	bind
3834	4	2230	5	10	NULL	0	NULL	Vax2	GP	mutant	does not bind					Pax6	GP			alpha enhancer	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1249_s_179	15905411	( Right panels) The Pax6 alpha-enhancer was not detected in Vax1 or Vax2 ChIP DNA fragments from  Vax double knock-outs, and Vax1 and Vax2 binding to the alpha-enhancer could not be detected in ChIPs performed from  Vax1 and  Vax2 mutants, respectively.	bind
3722	1	2230	6	10	NULL	0	NULL	Vax1	GP	mutant	does not bind					Pax6	GP			alpha-enhancer	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1249_s_179	15905411	( Right panels) The Pax6 alpha-enhancer was not detected in Vax1 or Vax2 ChIP DNA fragments from  Vax double knock-outs, and Vax1 and Vax2 binding to the alpha-enhancer could not be detected in ChIPs performed from  Vax1 and  Vax2 mutants, respectively.	bind
3723	2	2230	6	10	NULL	0	NULL	Vax2	GP	mutant	does not bind					Pax6	GP			alpha-enhancer	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1249_s_179	15905411	( Right panels) The Pax6 alpha-enhancer was not detected in Vax1 or Vax2 ChIP DNA fragments from  Vax double knock-outs, and Vax1 and Vax2 binding to the alpha-enhancer could not be detected in ChIPs performed from  Vax1 and  Vax2 mutants, respectively.	bind
5409	3	2230	6	10	NULL	0	NULL	Pax6	GP		is absent in				alpha enhancer	Vax 1 DNA fragments	NucleicAcid				NULL	Vax double knock-outs	NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1249_s_179	15905411	( Right panels) The Pax6 alpha-enhancer was not detected in Vax1 or Vax2 ChIP DNA fragments from  Vax double knock-outs, and Vax1 and Vax2 binding to the alpha-enhancer could not be detected in ChIPs performed from  Vax1 and  Vax2 mutants, respectively.	bind
5410	4	2230	6	10	NULL	0	NULL	Pax6	GP		is absent in				alpha enhancer	Vax 2 DNA fragments	NucleicAcid				NULL	Vax double knock-outs	NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1249_s_179	15905411	( Right panels) The Pax6 alpha-enhancer was not detected in Vax1 or Vax2 ChIP DNA fragments from  Vax double knock-outs, and Vax1 and Vax2 binding to the alpha-enhancer could not be detected in ChIPs performed from  Vax1 and  Vax2 mutants, respectively.	bind
4265	1	2232	5	10	NULL	0	NULL	E2F1	GP		bind					Bim	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_44_16090_s_153	16243973	( Right) E2F1 binding to the Bim promoter was analyzed by ChIP.	bind
3724	1	2232	6	10	NULL	0	NULL	E2F1	GP		bind					Bim	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_44_16090_s_153	16243973	( Right) E2F1 binding to the Bim promoter was analyzed by ChIP.	bind
3835	1	2233	5	10	NULL	0	NULL	SHBG	GP		bind					Te con	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_17_6740_s_79	15090645	( Right) Estimated free ( Upper) and SHBG-bound ( Lower) Te con.	bind
3725	1	2233	6	10	NULL	0	NULL	SHBG	GP		bind					Te con	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_17_6740_s_79	15090645	( Right) Estimated free ( Upper) and SHBG-bound ( Lower) Te con.	bind
4266	1	2234	5	10	NULL	0	NULL	alphaGMRx	GP		generate					H2O2	Chemical				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_14_5044_s_125	15795385	( Right) GM-dependent (100 nM) H2O2 generation  in vitro by alphaGMRx or mutant (C136Sx) bound to Ni+-nitrilotriacetic acid plates, as quantified by fluorescence spectroscopy.	bind
4267	2	2234	5	10	NULL	0	NULL			mutant	bind			C136Sx		Ni+-nitrilotriacetic acid plates	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_14_5044_s_125	15795385	( Right) GM-dependent (100 nM) H2O2 generation  in vitro by alphaGMRx or mutant (C136Sx) bound to Ni+-nitrilotriacetic acid plates, as quantified by fluorescence spectroscopy.	bind
46403	3	2234	5	10	NULL	0	NULL	statement 1	Process		is dependent on					GM	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_14_5044_s_125	15795385	( Right) GM-dependent (100 nM) H2O2 generation  in vitro by alphaGMRx or mutant (C136Sx) bound to Ni+-nitrilotriacetic acid plates, as quantified by fluorescence spectroscopy.	bind
3726	1	2234	6	10	NULL	0	NULL	alphaGMRx	GP		generates					H2O2	Chemical				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_14_5044_s_125	15795385	( Right) GM-dependent (100 nM) H2O2 generation  in vitro by alphaGMRx or mutant (C136Sx) bound to Ni+-nitrilotriacetic acid plates, as quantified by fluorescence spectroscopy.	bind
3727	2	2234	6	10	NULL	0	NULL	statement 1	Process		is dependent on					GM	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_14_5044_s_125	15795385	( Right) GM-dependent (100 nM) H2O2 generation  in vitro by alphaGMRx or mutant (C136Sx) bound to Ni+-nitrilotriacetic acid plates, as quantified by fluorescence spectroscopy.	bind
3728	3	2234	6	10	NULL	0	NULL			mutant	bind			C136Sx		Ni+-nitrilotriacetic acid plates	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_14_5044_s_125	15795385	( Right) GM-dependent (100 nM) H2O2 generation  in vitro by alphaGMRx or mutant (C136Sx) bound to Ni+-nitrilotriacetic acid plates, as quantified by fluorescence spectroscopy.	bind
3836	1	2235	5	10	NULL	0	NULL	Pg	GP		bind					mPR	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5619_594_s_18	12714732	( Right) In contrast, binding of Pg to mPR leads to inhibition of adenylyl cyclase through activation of Galphai or inhibition of Galphas.	bind
3837	2	2235	5	10	NULL	0	NULL	statement 1	Process		leads to					adenylyl cyclase	GP	inhibition of			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5619_594_s_18	12714732	( Right) In contrast, binding of Pg to mPR leads to inhibition of adenylyl cyclase through activation of Galphai or inhibition of Galphas.	bind
3838	3	2235	5	10	NULL	0	NULL	statement 2	Process		occurs through					Galphai	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5619_594_s_18	12714732	( Right) In contrast, binding of Pg to mPR leads to inhibition of adenylyl cyclase through activation of Galphai or inhibition of Galphas.	bind
3839	4	2235	5	10	NULL	0	NULL	statement 2	Process		occurs through					Galphas	GP	inhibition of			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5619_594_s_18	12714732	( Right) In contrast, binding of Pg to mPR leads to inhibition of adenylyl cyclase through activation of Galphai or inhibition of Galphas.	bind
5225	5	2235	5	10	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5619_594_s_18	12714732	( Right) In contrast, binding of Pg to mPR leads to inhibition of adenylyl cyclase through activation of Galphai or inhibition of Galphas.	bind
3729	1	2235	6	10	NULL	0	NULL	Pg	GP		bind					mPR	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5619_594_s_18	12714732	( Right) In contrast, binding of Pg to mPR leads to inhibition of adenylyl cyclase through activation of Galphai or inhibition of Galphas.	bind
3730	2	2235	6	10	NULL	0	NULL	statement 1	Process		leads to					adenylyl cyclase	GP	inhibition of			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5619_594_s_18	12714732	( Right) In contrast, binding of Pg to mPR leads to inhibition of adenylyl cyclase through activation of Galphai or inhibition of Galphas.	bind
3731	3	2235	6	10	NULL	0	NULL	statement 1	Process		leads to					Galphai	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5619_594_s_18	12714732	( Right) In contrast, binding of Pg to mPR leads to inhibition of adenylyl cyclase through activation of Galphai or inhibition of Galphas.	bind
3732	4	2235	6	10	NULL	0	NULL	statement 1	Process		leads to					Galphas	GP	inhibition of			NULL		NULL	NULL	NULL	NULL	gw60_science_300_5619_594_s_18	12714732	( Right) In contrast, binding of Pg to mPR leads to inhibition of adenylyl cyclase through activation of Galphai or inhibition of Galphas.	bind
4861	5	2235	6	10	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5619_594_s_18	12714732	( Right) In contrast, binding of Pg to mPR leads to inhibition of adenylyl cyclase through activation of Galphai or inhibition of Galphas.	bind
3857	1	2236	5	10	NULL	0	NULL	VCB	GP		bind			 pVHL		Elongin B/C complex	GP		Socs box		NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_70_0_503_s_430	11395416	( Right) In VCB, the substrate-recognizing subunit pVHL binds to the Elongin B/C complex  through a motif known as the Socs box, which is present in other proteins that may  be the substrate-recognizing subunits of distinct VCB-like E3s ( 31,  139).	bind
3858	2	2236	5	10	NULL	0	NULL				is present in			Socs box		VCB-like E3s	GP		substrate-recognizing subunits of 		NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_70_0_503_s_430	11395416	( Right) In VCB, the substrate-recognizing subunit pVHL binds to the Elongin B/C complex  through a motif known as the Socs box, which is present in other proteins that may  be the substrate-recognizing subunits of distinct VCB-like E3s ( 31,  139).	bind
46405	3	2236	5	10	NULL	0	NULL	pVHL	GP		is a type of					substrate-recognizing subunit	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_70_0_503_s_430	11395416	( Right) In VCB, the substrate-recognizing subunit pVHL binds to the Elongin B/C complex  through a motif known as the Socs box, which is present in other proteins that may  be the substrate-recognizing subunits of distinct VCB-like E3s ( 31,  139).	bind
3733	1	2236	6	10	NULL	0	NULL	VCB	GP		bind			pVHL		Elongin B/C complex	GP		Socs box		NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_70_0_503_s_430	11395416	( Right) In VCB, the substrate-recognizing subunit pVHL binds to the Elongin B/C complex  through a motif known as the Socs box, which is present in other proteins that may  be the substrate-recognizing subunits of distinct VCB-like E3s ( 31,  139).	bind
4862	2	2236	6	10	NULL	0	NULL				is present in			Socs box		VCB-like E3s	GP		substrate-recognizing subunits of		NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_70_0_503_s_430	11395416	( Right) In VCB, the substrate-recognizing subunit pVHL binds to the Elongin B/C complex  through a motif known as the Socs box, which is present in other proteins that may  be the substrate-recognizing subunits of distinct VCB-like E3s ( 31,  139).	bind
46406	3	2236	6	10	NULL	0	NULL	pVHL	GP		is a type of					substrate-recognizing subunit	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_70_0_503_s_430	11395416	( Right) In VCB, the substrate-recognizing subunit pVHL binds to the Elongin B/C complex  through a motif known as the Socs box, which is present in other proteins that may  be the substrate-recognizing subunits of distinct VCB-like E3s ( 31,  139).	bind
3859	1	2237	5	10	NULL	0	NULL	EAC3d	GP		bind					CD21	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_16_10641_s_192	12122212	( Right) Photomicrographs (magnification x137) showing EAC3d binding to CD21 and CD21mut, but not to L cells transfected with vector alone.	bind
3860	2	2237	5	10	NULL	0	NULL	EAC3d	GP		bind					CD21	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_16_10641_s_192	12122212	( Right) Photomicrographs (magnification x137) showing EAC3d binding to CD21 and CD21mut, but not to L cells transfected with vector alone.	bind
3861	3	2237	5	10	NULL	0	NULL	EAC3d	GP		does not bind					L cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_16_10641_s_192	12122212	( Right) Photomicrographs (magnification x137) showing EAC3d binding to CD21 and CD21mut, but not to L cells transfected with vector alone.	bind
3734	1	2237	6	10	NULL	0	NULL	EAC3d	GP		bind					CD21	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_16_10641_s_192	12122212	( Right) Photomicrographs (magnification x137) showing EAC3d binding to CD21 and CD21mut, but not to L cells transfected with vector alone.	bind
3735	2	2237	6	10	NULL	0	NULL	EAC3d	GP		bind					CD21	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_16_10641_s_192	12122212	( Right) Photomicrographs (magnification x137) showing EAC3d binding to CD21 and CD21mut, but not to L cells transfected with vector alone.	bind
3736	3	2237	6	10	NULL	0	NULL	EAC3d	GP		does not bind					L cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_16_10641_s_192	12122212	( Right) Photomicrographs (magnification x137) showing EAC3d binding to CD21 and CD21mut, but not to L cells transfected with vector alone.	bind
3862	1	2238	5	10	NULL	0	NULL	fMTX	Chemical		bind		high-affinity			DHFR	GP	reconstituted			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_10_5394_s_91	10318894	( Right) The fluorescence assay is based on high-affinity binding of the specific DHFR inhibitor fMTX to reconstituted DHFR.	bind
46407	2	2238	5	10	NULL	0	NULL	fMTX	Chemical		is a type of					DHFR inhibitor	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_10_5394_s_91	10318894	( Right) The fluorescence assay is based on high-affinity binding of the specific DHFR inhibitor fMTX to reconstituted DHFR.	bind
3803	1	2238	6	10	NULL	0	NULL	fMTX	Chemical		bind		high affinity			DHFR	GP	reconstituted			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_10_5394_s_91	10318894	( Right) The fluorescence assay is based on high-affinity binding of the specific DHFR inhibitor fMTX to reconstituted DHFR.	bind
46408	2	2238	6	10	NULL	0	NULL	fMTX	Chemical		is a type of					DHFR inhibitor	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_10_5394_s_91	10318894	( Right) The fluorescence assay is based on high-affinity binding of the specific DHFR inhibitor fMTX to reconstituted DHFR.	bind
3864	1	2239	5	10	NULL	0	NULL	HsUbc2b	GP		bind					Uba1	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26823_s_210	12740388	( Table  II) is in the range of the  K m values  of 123  plus-or-minus  19 and 102  plus-or-minus  13 nM found for HsUbc2b binding  to human and rabbit Uba1 orthologs, respectively  ( ).	bind
3866	2	2239	5	10	NULL	0	NULL	HsUbc2b	GP		bind					Uba1	GP	rabbit			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26823_s_210	12740388	( Table  II) is in the range of the  K m values  of 123  plus-or-minus  19 and 102  plus-or-minus  13 nM found for HsUbc2b binding  to human and rabbit Uba1 orthologs, respectively  ( ).	bind
3805	1	2239	6	10	NULL	0	NULL	HsUbc2b	GP		bind					Uba1	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26823_s_210	12740388	( Table  II) is in the range of the  K m values  of 123  plus-or-minus  19 and 102  plus-or-minus  13 nM found for HsUbc2b binding  to human and rabbit Uba1 orthologs, respectively  ( ).	bind
3806	2	2239	6	10	NULL	0	NULL	HsUbc2b	GP		bind					Uba1	GP	rabbit			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26823_s_210	12740388	( Table  II) is in the range of the  K m values  of 123  plus-or-minus  19 and 102  plus-or-minus  13 nM found for HsUbc2b binding  to human and rabbit Uba1 orthologs, respectively  ( ).	bind
3869	1	2240	5	10	NULL	0	NULL	ATP	Chemical		bind					Uba1	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26823_s_208	12740388	( Table  II) was considerably higher than the   K m of 7.0  plus-or-minus  1.1 muM recently  reported for ATP binding to human Uba1  ( ); however, Nedd8  activation must remain saturating with respect to the normal cellular ATP  concentration of about 5 mM.	bind
3807	1	2240	6	10	NULL	0	NULL	ATP	Chemical		bind					Uba1	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26823_s_208	12740388	( Table  II) was considerably higher than the   K m of 7.0  plus-or-minus  1.1 muM recently  reported for ATP binding to human Uba1  ( ); however, Nedd8  activation must remain saturating with respect to the normal cellular ATP  concentration of about 5 mM.	bind
3873	1	2242	5	10	NULL	0	NULL	Nedd4	GP		bind					ENaC	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20019_s_217	12654927	( Table  II), suggesting that the inhibitory role of intracellular  Na+ is not mediated by directly affecting the binding of Nedd4 to  ENaC.	bind
3874	2	2242	5	10	NULL	0	NULL	Na+	Chemical	inhibitory role of;;intracellular	is not mediated by					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20019_s_217	12654927	( Table  II), suggesting that the inhibitory role of intracellular  Na+ is not mediated by directly affecting the binding of Nedd4 to  ENaC.	bind
3840	1	2242	6	10	NULL	0	NULL	Nedd4	GP		bind					ENaC	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20019_s_217	12654927	( Table  II), suggesting that the inhibitory role of intracellular  Na+ is not mediated by directly affecting the binding of Nedd4 to  ENaC.	bind
3841	2	2242	6	10	NULL	0	NULL	Na+	Chemical	inhibitory role of;; intracellular	is not mediated by					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20019_s_217	12654927	( Table  II), suggesting that the inhibitory role of intracellular  Na+ is not mediated by directly affecting the binding of Nedd4 to  ENaC.	bind
3875	1	2243	5	10	NULL	0	NULL	ATP	Chemical		bind					NBD1	GP	mutant	C682A		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_33_30764_s_184	12783859	( Table  II, 9.0  versus 8.5), further supporting our conclusion  that the  K d value was mainly attributed to ATP  binding to the C682A-mutated NBD1.	bind
3842	1	2243	6	10	NULL	0	NULL	ATP	Chemical		bind					NBD1	GP	mutant	 C682A		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_33_30764_s_184	12783859	( Table  II, 9.0  versus 8.5), further supporting our conclusion  that the  K d value was mainly attributed to ATP  binding to the C682A-mutated NBD1.	bind
3877	1	2244	5	10	NULL	0	NULL	sgk1	GP		does not bind					Nedd4-2	GP		WW domains		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20019_s_223	12654927	( Table  III), suggesting that sgk1 does not bind (or binds very poorly) to  the WW domains of Nedd4-2.	bind
3878	2	2244	5	10	NULL	0	NULL	sgk1	GP		bind		very poorly			Nedd4-2	GP		WW domains		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20019_s_223	12654927	( Table  III), suggesting that sgk1 does not bind (or binds very poorly) to  the WW domains of Nedd4-2.	bind
46409	3	2244	5	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20019_s_223	12654927	( Table  III), suggesting that sgk1 does not bind (or binds very poorly) to  the WW domains of Nedd4-2.	bind
3843	1	2244	6	10	NULL	0	NULL	sgk1	GP		does not bind					Nedd4-2	GP		WW domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20019_s_223	12654927	( Table  III), suggesting that sgk1 does not bind (or binds very poorly) to  the WW domains of Nedd4-2.	bind
3844	2	2244	6	10	NULL	0	NULL	sgk1	GP		bind		very poorly			Nedd4-2	GP		WW domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20019_s_223	12654927	( Table  III), suggesting that sgk1 does not bind (or binds very poorly) to  the WW domains of Nedd4-2.	bind
46410	3	2244	6	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20019_s_223	12654927	( Table  III), suggesting that sgk1 does not bind (or binds very poorly) to  the WW domains of Nedd4-2.	bind
3879	1	2245	5	10	NULL	0	NULL	PAI-1	GP		bind		low affinity			LRP	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_21_22595_s_318	15001579	( Table I) and others ( - ) have shown that these forms of PAI-1 only bind to LRP with low affinity.	bind
3845	1	2245	6	10	NULL	0	NULL	PAI-1	GP		bind		low affinity			LRP	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_21_22595_s_318	15001579	( Table I) and others ( - ) have shown that these forms of PAI-1 only bind to LRP with low affinity.	bind
3880	1	2246	5	10	NULL	0	NULL	Rabaptin-5	GP		does not bind		directly			ubiquitin	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_30_31409_s_258	15143060	( Table I), it is likely to derive from the presence in the cytosol of Rabaptin-5-associated proteins that also bind ubiquitin or undergo ubiquitin-dependent modification (Rabaptin-5 does not bind ubiquitin directly; results not shown).	bind
3881	2	2246	5	10	NULL	0	NULL	Rabaptin-5-associated proteins	GP		bind					ubiquitin	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_30_31409_s_258	15143060	( Table I), it is likely to derive from the presence in the cytosol of Rabaptin-5-associated proteins that also bind ubiquitin or undergo ubiquitin-dependent modification (Rabaptin-5 does not bind ubiquitin directly; results not shown).	bind
3882	3	2246	5	10	NULL	0	NULL	Rabaptin-5-associated proteins	GP		undergoes					ubiquitin-dependent modification	Process				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_30_31409_s_258	15143060	( Table I), it is likely to derive from the presence in the cytosol of Rabaptin-5-associated proteins that also bind ubiquitin or undergo ubiquitin-dependent modification (Rabaptin-5 does not bind ubiquitin directly; results not shown).	bind
3846	1	2246	6	10	NULL	0	NULL	Rabaptin-5-associated proteins	GP		bind					ubiquitin	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_30_31409_s_258	15143060	( Table I), it is likely to derive from the presence in the cytosol of Rabaptin-5-associated proteins that also bind ubiquitin or undergo ubiquitin-dependent modification (Rabaptin-5 does not bind ubiquitin directly; results not shown).	bind
3847	2	2246	6	10	NULL	0	NULL	Rabaptin-5-associated proteins	GP		undergoes					ubiquitin-dependent modification	Process				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_30_31409_s_258	15143060	( Table I), it is likely to derive from the presence in the cytosol of Rabaptin-5-associated proteins that also bind ubiquitin or undergo ubiquitin-dependent modification (Rabaptin-5 does not bind ubiquitin directly; results not shown).	bind
3848	3	2246	6	10	NULL	0	NULL	Rabaptin-5	GP		does not bind		directly			ubiquitin	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_30_31409_s_258	15143060	( Table I), it is likely to derive from the presence in the cytosol of Rabaptin-5-associated proteins that also bind ubiquitin or undergo ubiquitin-dependent modification (Rabaptin-5 does not bind ubiquitin directly; results not shown).	bind
3883	1	2247	5	10	NULL	0	NULL	Sti1	GP		bind		weakly			Ssa1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_28_25970_s_144	12716905	( Table I), Sti1 binding to Ssa1  is about 2 orders of magnitude weakerR.	bind
3849	1	2247	6	10	NULL	0	NULL	Sti1	GP		bind		weakly			Ssa1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_28_25970_s_144	12716905	( Table I), Sti1 binding to Ssa1  is about 2 orders of magnitude weakerR.	bind
3931	1	2248	5	10	NULL	0	NULL	dGTP	Chemical		is incorporated into					primer strand	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_17_2957_s_84	16107880	( Table I), we found that dGTP was incorporated into the primer strand and that the product  PPi remains bound to Dpo4 and occupies the same space as the triphosphate moiety  of dNTP ( Figure 1D).	bind
3932	2	2248	5	10	NULL	0	NULL	PPi	Chemical		bind					Dpo4	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_17_2957_s_84	16107880	( Table I), we found that dGTP was incorporated into the primer strand and that the product  PPi remains bound to Dpo4 and occupies the same space as the triphosphate moiety  of dNTP ( Figure 1D).	bind
3850	1	2248	6	10	NULL	0	NULL	PPi	Chemical		bind					Dpo4	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_17_2957_s_84	16107880	( Table I), we found that dGTP was incorporated into the primer strand and that the product  PPi remains bound to Dpo4 and occupies the same space as the triphosphate moiety  of dNTP ( Figure 1D).	bind
3851	2	2248	6	10	NULL	0	NULL	dGTP	Chemical		incorporates					primer strand	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_17_2957_s_84	16107880	( Table I), we found that dGTP was incorporated into the primer strand and that the product  PPi remains bound to Dpo4 and occupies the same space as the triphosphate moiety  of dNTP ( Figure 1D).	bind
3934	1	2251	5	10	NULL	0	NULL	apoA-I	GP	WT	bind					ABCA1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_49931_s_242	15383537	( Table II) and the  Kd value for binding of WT apoA-I to ABCA1 is 2 mug/ml ( ).	bind
3852	1	2251	6	10	NULL	0	NULL	apoA-I	GP	wild type	bind					ABCA1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_49931_s_242	15383537	( Table II) and the  Kd value for binding of WT apoA-I to ABCA1 is 2 mug/ml ( ).	bind
3977	1	2252	5	10	NULL	0	NULL				does not bind		stoichiometrically	R281A		oriC	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51156_s_217	15371441	( Table II) revealed that R281A fails to bind stoichiometrically to  oriC, in contrast to gel mobility shift assays in which the mutant DnaA was comparable with wild-type DnaA in binding to the DnaA boxes of  oriC ( Fig. 3).	bind
3978	2	2252	5	10	NULL	0	NULL	DnaA	GP	wild-type	bind					oriC	NucleicAcid			DnaA boxes	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51156_s_217	15371441	( Table II) revealed that R281A fails to bind stoichiometrically to  oriC, in contrast to gel mobility shift assays in which the mutant DnaA was comparable with wild-type DnaA in binding to the DnaA boxes of  oriC ( Fig. 3).	bind
4260	3	2252	5	10	NULL	0	NULL	DnaA	GP	mutant	bind					oriC	NucleicAcid			DnaA boxes	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51156_s_217	15371441	( Table II) revealed that R281A fails to bind stoichiometrically to  oriC, in contrast to gel mobility shift assays in which the mutant DnaA was comparable with wild-type DnaA in binding to the DnaA boxes of  oriC ( Fig. 3).	bind
3853	1	2252	6	10	NULL	0	NULL	DnaA	GP	wild type	bind					oriC	NucleicAcid			DnaA boxes	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51156_s_217	15371441	( Table II) revealed that R281A fails to bind stoichiometrically to  oriC, in contrast to gel mobility shift assays in which the mutant DnaA was comparable with wild-type DnaA in binding to the DnaA boxes of  oriC ( Fig. 3).	bind
3854	2	2252	6	10	NULL	0	NULL	DnaA	GP	mutant	bind					oriC	NucleicAcid			DnaA boxes	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51156_s_217	15371441	( Table II) revealed that R281A fails to bind stoichiometrically to  oriC, in contrast to gel mobility shift assays in which the mutant DnaA was comparable with wild-type DnaA in binding to the DnaA boxes of  oriC ( Fig. 3).	bind
3855	3	2252	6	10	NULL	0	NULL				does not bind		stoichiometrically	 R281A		oriC	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51156_s_217	15371441	( Table II) revealed that R281A fails to bind stoichiometrically to  oriC, in contrast to gel mobility shift assays in which the mutant DnaA was comparable with wild-type DnaA in binding to the DnaA boxes of  oriC ( Fig. 3).	bind
3980	1	2253	5	10	NULL	0	NULL	Runx2	GP		bind					osteocalcin	GP			cis-acting elements in promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_19_20307_s_159	15007057	( Table II) was not sufficient to normalize  Runx2 binding to  cis-acting elements in the osteocalcin promoter ( Fig. 5 C).	bind
3856	1	2253	6	10	NULL	0	NULL	Runx2 	GP		bind					osteocalcin	GP			cis-acting element of promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_19_20307_s_159	15007057	( Table II) was not sufficient to normalize  Runx2 binding to  cis-acting elements in the osteocalcin promoter ( Fig. 5 C).	bind
3981	1	2254	5	10	NULL	0	NULL				bind			L2 loop		BlaR1	GP		sensor domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_47278_s_265	15322076	( Table II), perhaps because either tag interferes with the binding of the L2 loop to the BlaR1 sensor domain.	bind
3863	1	2254	6	10	NULL	0	NULL				bind			L2 loop		BlaR1	GP		sensor domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_47278_s_265	15322076	( Table II), perhaps because either tag interferes with the binding of the L2 loop to the BlaR1 sensor domain.	bind
3983	1	2255	5	10	NULL	0	NULL	LT	GP		bind					bacteria	Organism	Re mutant			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8070_s_82	14660669	( Table II), purified Re LPS would be able to block the binding of LT to Re mutant bacteria.	bind
3984	2	2255	5	10	NULL	0	NULL	Re LPS	Chemical	purified	block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8070_s_82	14660669	( Table II), purified Re LPS would be able to block the binding of LT to Re mutant bacteria.	bind
3865	1	2255	6	10	NULL	0	NULL	LT	GP		bind					bacteria	Organism	Re mutant			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8070_s_82	14660669	( Table II), purified Re LPS would be able to block the binding of LT to Re mutant bacteria.	bind
3867	2	2255	6	10	NULL	0	NULL	Re LPS	Chemical	purified	blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8070_s_82	14660669	( Table II), purified Re LPS would be able to block the binding of LT to Re mutant bacteria.	bind
3985	1	2256	5	10	NULL	0	NULL	galectin-4	GP		bind					glycosphingolipids	Chemical	sulfated			NULL	gastrointestinal tract	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_6_4730_s_220	15546874	( Table II), the binding between galectin-4 and sulfated glycosphingolipids may function for the cell adhesion of epithelial cells in the gastrointestinal tract.	bind
3986	2	2256	5	10	NULL	0	NULL	statement 1	Process		function for		may			epithelial cells	Cell	cell adhesion of			NULL	gastrointestinal tract	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_6_4730_s_220	15546874	( Table II), the binding between galectin-4 and sulfated glycosphingolipids may function for the cell adhesion of epithelial cells in the gastrointestinal tract.	bind
3868	1	2256	6	10	NULL	0	NULL	galectin-4	GP		bind					glycosphingolipids	Chemical	sulfated			NULL	gastrointestinal tract	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_6_4730_s_220	15546874	( Table II), the binding between galectin-4 and sulfated glycosphingolipids may function for the cell adhesion of epithelial cells in the gastrointestinal tract.	bind
3870	2	2256	6	10	NULL	0	NULL	statement 1	Process		may act in					epithelial cells	Cell	cell adhesion of			NULL	gastrointestinal tract	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_6_4730_s_220	15546874	( Table II), the binding between galectin-4 and sulfated glycosphingolipids may function for the cell adhesion of epithelial cells in the gastrointestinal tract.	bind
3987	1	2257	5	10	NULL	0	NULL	cGMP	Chemical		bind					PDE2A GAF-AB	GP		GAF-B domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_36_37928_s_188	15210692	( Table II), which is consistent with the crystal structure that showed cGMP bound to only the GAF-B domain of PDE2A GAF-AB ( ).	bind
3871	1	2257	6	10	NULL	0	NULL	cGMP	Chemical		bind					PDE2A  GAF-AB	GP		GAF-B domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_36_37928_s_188	15210692	( Table II), which is consistent with the crystal structure that showed cGMP bound to only the GAF-B domain of PDE2A GAF-AB ( ).	bind
3988	1	2261	5	10	NULL	0	NULL	Sp1	GP		bind					DNA	NucleicAcid			GC boxes in cellular promoters	NULL		NULL	NULL	NULL	NULL	gw60_science_296_5576_2149_s_19	12077389	( Top) The transcription factor Sp1 binds to DNA elements called GC boxes in cellular promoters.	bind
52989	2	2261	5	10	NULL	0	NULL	Sp1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_296_5576_2149_s_19	12077389	( Top) The transcription factor Sp1 binds to DNA elements called GC boxes in cellular promoters.	bind
3884	1	2261	6	10	NULL	0	NULL	Sp1	GP		bind					DNA	NucleicAcid			GC box in cellular promoter	NULL		NULL	NULL	NULL	NULL	gw60_science_296_5576_2149_s_19	12077389	( Top) The transcription factor Sp1 binds to DNA elements called GC boxes in cellular promoters.	bind
52990	2	2261	6	10	NULL	0	NULL	Sp1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_296_5576_2149_s_19	12077389	( Top) The transcription factor Sp1 binds to DNA elements called GC boxes in cellular promoters.	bind
3989	1	2264	5	10	NULL	0	NULL	mSin3a	GP		bind					KLF11	GP	Flag-tagged;; WT			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_13_4807_s_117	15774581	( Upper) A representative Western blot of coimmunoprecipitation experiments ( n = 2) showing mSin3a binding of Flag-tagged KLF11 (WT and variants) or empty vector  (control).	bind
3990	2	2264	5	10	NULL	0	NULL	mSin3a	GP		bind					KLF11	GP	Flag-tagged ;;variants			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_13_4807_s_117	15774581	( Upper) A representative Western blot of coimmunoprecipitation experiments ( n = 2) showing mSin3a binding of Flag-tagged KLF11 (WT and variants) or empty vector  (control).	bind
3885	1	2264	6	10	NULL	0	NULL	mSin3a	GP		bind					KLF11	GP	 Flag-tagged ;; wild type			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_13_4807_s_117	15774581	( Upper) A representative Western blot of coimmunoprecipitation experiments ( n = 2) showing mSin3a binding of Flag-tagged KLF11 (WT and variants) or empty vector  (control).	bind
3886	2	2264	6	10	NULL	0	NULL	mSin3a	GP		bind					KLF11	GP	 Flag-tagged;; variant			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_13_4807_s_117	15774581	( Upper) A representative Western blot of coimmunoprecipitation experiments ( n = 2) showing mSin3a binding of Flag-tagged KLF11 (WT and variants) or empty vector  (control).	bind
3992	1	2266	5	10	NULL	0	NULL	 GAS1 expressing cells	Cell		does not bind					IgG	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_20_11347_s_85	11572986	( Upper) Cells expressing GAS1 (red, detected by anti-GAS1 and Cy3-2 degrees  Abs) do not bind human IgG (Ig, green, detected by FITC-anti-Fc).	bind
3888	1	2266	6	10	NULL	0	NULL	GAS1 expressing cells	Cell		does not bind					IgG	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_20_11347_s_85	11572986	( Upper) Cells expressing GAS1 (red, detected by anti-GAS1 and Cy3-2 degrees  Abs) do not bind human IgG (Ig, green, detected by FITC-anti-Fc).	bind
3993	1	2267	5	10	NULL	0	NULL	Crk	GP		bind			SH2 domain		Crk phosphopeptide	GP		residues 221-224		NULL	in the ternary complex	NULL	NULL	NULL	NULL	gw60_pnas_99_22_14053_s_136	12384576	( Upper) Detail of the Crk SH2 domain bound to the Crk phosphopeptide (residues 221-224) in the ternary complex.	bind
3889	1	2267	6	10	NULL	0	NULL	Crk	GP		bind			SH2 domain		Crk phosphopeptide 	GP		residues 221-224		NULL	ternary complex	NULL	NULL	NULL	NULL	gw60_pnas_99_22_14053_s_136	12384576	( Upper) Detail of the Crk SH2 domain bound to the Crk phosphopeptide (residues 221-224) in the ternary complex.	bind
3994	1	2268	5	10	NULL	0	NULL	epsins	GP	yeast	bind					Cdc24	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_11_4116_s_211	16537494	( vii) Other authors  and our unpublished data show that the yeast epsins bind Cdc24, the Cdc42 guanine nucleotide exchange factor.	bind
3995	2	2268	5	10	NULL	0	NULL	Cdc24	GP		is					Cdc42 guanine nucleotide exchange factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_11_4116_s_211	16537494	( vii) Other authors  and our unpublished data show that the yeast epsins bind Cdc24, the Cdc42 guanine nucleotide exchange factor.	bind
3890	1	2268	6	10	NULL	0	NULL	epsins	GP	yeast	bind					Cdc24	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_11_4116_s_211	16537494	( vii) Other authors  and our unpublished data show that the yeast epsins bind Cdc24, the Cdc42 guanine nucleotide exchange factor.	bind
3891	2	2268	6	10	NULL	0	NULL	Cdc24	GP		is 					Cdc42 guanine nucleotide exchange factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_11_4116_s_211	16537494	( vii) Other authors  and our unpublished data show that the yeast epsins bind Cdc24, the Cdc42 guanine nucleotide exchange factor.	bind
3996	1	2270	5	10	NULL	0	NULL	Pax5 protein	GP	partially degraded	bind					CD19	GP			 site	NULL		NULL	NULL	NULL	NULL	gw70_genetics_171_3_1125_s_270	16079238	(*) indicates partially degraded Pax5  protein that still binds to the CD19 site.	bind
3892	1	2270	6	10	NULL	0	NULL	Pax5 protein	GP	partially degraded	bind					CD19	GP			site	NULL		NULL	NULL	NULL	NULL	gw70_genetics_171_3_1125_s_270	16079238	(*) indicates partially degraded Pax5  protein that still binds to the CD19 site.	bind
3997	1	2271	5	10	NULL	0	NULL	SREBP	GP		bind					LDLR	GP			SRE	NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_46_5_862_s_214	15716578	(+) Indicates the positive control reaction, in which SREBP is  bound with labeled LDL receptor (LDLR) SRE.	bind
3998	2	2271	5	10	NULL	0	NULL	LDLR	GP		is					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_46_5_862_s_214	15716578	(+) Indicates the positive control reaction, in which SREBP is  bound with labeled LDL receptor (LDLR) SRE.	bind
3893	1	2271	6	10	NULL	0	NULL	SREBP	GP		bind					LDL receptor	GP			SRE	NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_46_5_862_s_214	15716578	(+) Indicates the positive control reaction, in which SREBP is  bound with labeled LDL receptor (LDLR) SRE.	bind
4863	2	2271	6	10	NULL	0	NULL	LDLR	GP		is					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_46_5_862_s_214	15716578	(+) Indicates the positive control reaction, in which SREBP is  bound with labeled LDL receptor (LDLR) SRE.	bind
3999	1	2272	5	10	NULL	0	NULL	(+)-BPDE	Chemical		bind		covalently			guanine	Chemical				NULL	DNA	NULL	NULL	NULL	NULL	gw60_carcinogenesis_20_12_2279_s_13	10590220	(+)-BPDE covalently binds predominantly to guanine in DNA (10,11 and references therein) whereas ( - )-B[ c]PhDE binds preferentially to adenine in DNA ( 12, 13).	bind
4000	2	2272	5	10	NULL	0	NULL	( - )-BPhDE	Chemical		bind		preferentially			adenine	Chemical				NULL	DNA	NULL	NULL	NULL	NULL	gw60_carcinogenesis_20_12_2279_s_13	10590220	(+)-BPDE covalently binds predominantly to guanine in DNA (10,11 and references therein) whereas ( - )-B[ c]PhDE binds preferentially to adenine in DNA ( 12, 13).	bind
3894	1	2272	6	10	NULL	0	NULL	(+)-BPDE	Chemical		bind		covalently			guanine	Chemical				NULL	DNA	NULL	NULL	NULL	NULL	gw60_carcinogenesis_20_12_2279_s_13	10590220	(+)-BPDE covalently binds predominantly to guanine in DNA (10,11 and references therein) whereas ( - )-B[ c]PhDE binds preferentially to adenine in DNA ( 12, 13).	bind
3895	2	2272	6	10	NULL	0	NULL	( - )-BPhDE 	Chemical		bind		preferentially			adenine	Chemical				NULL	DNA	NULL	NULL	NULL	NULL	gw60_carcinogenesis_20_12_2279_s_13	10590220	(+)-BPDE covalently binds predominantly to guanine in DNA (10,11 and references therein) whereas ( - )-B[ c]PhDE binds preferentially to adenine in DNA ( 12, 13).	bind
4001	1	2273	5	10	NULL	0	NULL	MK-801	Chemical		non-competitive antagonist of					NMDA receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_423_3_376_s_3	9515743	(+)-MK-801 ((+)-5-methyl-10,11-dihydro-5 H-dibenzo[ a, d]cyclohepten-5,10-imine maleate) is a non-competitive  N-methyl- -aspartate (NMDA) receptor antagonist binding the phencyclidine (PCP) binding site of the receptors  [ 1.	bind
4002	2	2273	5	10	NULL	0	NULL	MK-801	Chemical		is					(+)-5-methyl-10,11-dihydro-5 H-dibenzo[ a, d]cyclohepten-5,10-imine maleate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_423_3_376_s_3	9515743	(+)-MK-801 ((+)-5-methyl-10,11-dihydro-5 H-dibenzo[ a, d]cyclohepten-5,10-imine maleate) is a non-competitive  N-methyl- -aspartate (NMDA) receptor antagonist binding the phencyclidine (PCP) binding site of the receptors  [ 1.	bind
4003	3	2273	5	10	NULL	0	NULL	NMDA	Chemical		is					N-methyl- -aspartate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_423_3_376_s_3	9515743	(+)-MK-801 ((+)-5-methyl-10,11-dihydro-5 H-dibenzo[ a, d]cyclohepten-5,10-imine maleate) is a non-competitive  N-methyl- -aspartate (NMDA) receptor antagonist binding the phencyclidine (PCP) binding site of the receptors  [ 1.	bind
4004	4	2273	5	10	NULL	0	NULL	statement 1	Process		bind					receptors	GP			PCP binding site	NULL		NULL	NULL	NULL	NULL	gw60_febslett_423_3_376_s_3	9515743	(+)-MK-801 ((+)-5-methyl-10,11-dihydro-5 H-dibenzo[ a, d]cyclohepten-5,10-imine maleate) is a non-competitive  N-methyl- -aspartate (NMDA) receptor antagonist binding the phencyclidine (PCP) binding site of the receptors  [ 1.	bind
4005	5	2273	5	10	NULL	0	NULL	PCP	Chemical		is					phencyclidine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_423_3_376_s_3	9515743	(+)-MK-801 ((+)-5-methyl-10,11-dihydro-5 H-dibenzo[ a, d]cyclohepten-5,10-imine maleate) is a non-competitive  N-methyl- -aspartate (NMDA) receptor antagonist binding the phencyclidine (PCP) binding site of the receptors  [ 1.	bind
3896	1	2273	6	10	NULL	0	NULL	(+)-5-methyl-10,11-dihydro-5 H-dibenzo cyclohepten-5,10-imine maleate	Chemical		non-competitive antagonist of 					NMDA receptor 	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_423_3_376_s_3	9515743	(+)-MK-801 ((+)-5-methyl-10,11-dihydro-5 H-dibenzo[ a, d]cyclohepten-5,10-imine maleate) is a non-competitive  N-methyl- -aspartate (NMDA) receptor antagonist binding the phencyclidine (PCP) binding site of the receptors  [ 1.	bind
3897	2	2273	6	10	NULL	0	NULL	NMDA	Chemical		is					N-methyl- -aspartate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_423_3_376_s_3	9515743	(+)-MK-801 ((+)-5-methyl-10,11-dihydro-5 H-dibenzo[ a, d]cyclohepten-5,10-imine maleate) is a non-competitive  N-methyl- -aspartate (NMDA) receptor antagonist binding the phencyclidine (PCP) binding site of the receptors  [ 1.	bind
3898	3	2273	6	10	NULL	0	NULL	statement 1	Process		bind					receptor 	GP			PCP binding site	NULL		NULL	NULL	NULL	NULL	gw60_febslett_423_3_376_s_3	9515743	(+)-MK-801 ((+)-5-methyl-10,11-dihydro-5 H-dibenzo[ a, d]cyclohepten-5,10-imine maleate) is a non-competitive  N-methyl- -aspartate (NMDA) receptor antagonist binding the phencyclidine (PCP) binding site of the receptors  [ 1.	bind
3899	4	2273	6	10	NULL	0	NULL	PCP	Chemical		is					phencyclidine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_423_3_376_s_3	9515743	(+)-MK-801 ((+)-5-methyl-10,11-dihydro-5 H-dibenzo[ a, d]cyclohepten-5,10-imine maleate) is a non-competitive  N-methyl- -aspartate (NMDA) receptor antagonist binding the phencyclidine (PCP) binding site of the receptors  [ 1.	bind
54263	5	2273	6	10	NULL	0	NULL	MK-801	Chemical		is					5-methyl-10,11-dihydro-5 H-dibenzo[ a, d]cyclohepten-5,10-imine maleate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_423_3_376_s_3	9515743	(+)-MK-801 ((+)-5-methyl-10,11-dihydro-5 H-dibenzo[ a, d]cyclohepten-5,10-imine maleate) is a non-competitive  N-methyl- -aspartate (NMDA) receptor antagonist binding the phencyclidine (PCP) binding site of the receptors  [ 1.	bind
4006	1	2274	5	10	NULL	0	NULL	amnesiac	GroupOfPeople		is deficient in					neuropeptide gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_3_445_s_421	9539121	(1)  amnesiac is deficient in a gene for a neuropeptide that binds to a G protein-coupled receptor that stimulates adenylyl cyclase (Feaney and Quinn, 1995).	bind
4007	2	2274	5	10	NULL	0	NULL	neuropeptide gene	GP		bind					G protein-coupled receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_3_445_s_421	9539121	(1)  amnesiac is deficient in a gene for a neuropeptide that binds to a G protein-coupled receptor that stimulates adenylyl cyclase (Feaney and Quinn, 1995).	bind
4008	3	2274	5	10	NULL	0	NULL	statement 2	Process		stimulate					adenylyl cyclase	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_3_445_s_421	9539121	(1)  amnesiac is deficient in a gene for a neuropeptide that binds to a G protein-coupled receptor that stimulates adenylyl cyclase (Feaney and Quinn, 1995).	bind
3900	1	2274	6	10	NULL	0	NULL	G protein-coupled receptor	GP		stimulates					adenylyl cyclase	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_3_445_s_421	9539121	(1)  amnesiac is deficient in a gene for a neuropeptide that binds to a G protein-coupled receptor that stimulates adenylyl cyclase (Feaney and Quinn, 1995).	bind
3901	2	2274	6	10	NULL	0	NULL	neuropeptide gene	GP		bind					G protein-coupled receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_3_445_s_421	9539121	(1)  amnesiac is deficient in a gene for a neuropeptide that binds to a G protein-coupled receptor that stimulates adenylyl cyclase (Feaney and Quinn, 1995).	bind
3902	3	2274	6	10	NULL	0	NULL	amnesiac	GroupOfPeople		is associated with					neuropeptide gene	GP	deficiency of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_3_445_s_421	9539121	(1)  amnesiac is deficient in a gene for a neuropeptide that binds to a G protein-coupled receptor that stimulates adenylyl cyclase (Feaney and Quinn, 1995).	bind
4009	1	2275	5	10	NULL	0	NULL	PsbP	GP	chlamydomonas	bind		directly			PS II	GP	chlamydomonas			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_3	16049780	(1)  Chlamydomonas PsbP and PsbQ directly bound to Chlamydomonas PS II independent  of the other extrinsic proteins but not to spinach PS II.	bind
4010	2	2275	5	10	NULL	0	NULL	statement 1	Process		is independent of					extrinsic proteins	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_3	16049780	(1)  Chlamydomonas PsbP and PsbQ directly bound to Chlamydomonas PS II independent  of the other extrinsic proteins but not to spinach PS II.	bind
4011	3	2275	5	10	NULL	0	NULL	PsbQ	GP	chlamydomonas	bind		directly			PS II	GP	chlamydomonas			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_3	16049780	(1)  Chlamydomonas PsbP and PsbQ directly bound to Chlamydomonas PS II independent  of the other extrinsic proteins but not to spinach PS II.	bind
4012	4	2275	5	10	NULL	0	NULL	statement 3	Process		is independent of					extrinsic proteins	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_3	16049780	(1)  Chlamydomonas PsbP and PsbQ directly bound to Chlamydomonas PS II independent  of the other extrinsic proteins but not to spinach PS II.	bind
4013	5	2275	5	10	NULL	0	NULL	PsbP	GP	chlamydomonas	does not bind		directly			PS II	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_3	16049780	(1)  Chlamydomonas PsbP and PsbQ directly bound to Chlamydomonas PS II independent  of the other extrinsic proteins but not to spinach PS II.	bind
4014	6	2275	5	10	NULL	0	NULL	PsbQ	GP	chlamydomonas	does not bind		directly			PS II	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_3	16049780	(1)  Chlamydomonas PsbP and PsbQ directly bound to Chlamydomonas PS II independent  of the other extrinsic proteins but not to spinach PS II.	bind
3903	1	2275	6	10	NULL	0	NULL	PsbP	GP	Chlamydomonas	bind		directly			PSII	GP	Chlamydomonas			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_3	16049780	(1)  Chlamydomonas PsbP and PsbQ directly bound to Chlamydomonas PS II independent  of the other extrinsic proteins but not to spinach PS II.	bind
3904	2	2275	6	10	NULL	0	NULL	PsbQ	GP	Chlamydomonas	bind		directly			PS II	GP	Chlamydomonas			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_3	16049780	(1)  Chlamydomonas PsbP and PsbQ directly bound to Chlamydomonas PS II independent  of the other extrinsic proteins but not to spinach PS II.	bind
3905	3	2275	6	10	NULL	0	NULL	statement 1	Process		is independent of					extrinsic proteins	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_3	16049780	(1)  Chlamydomonas PsbP and PsbQ directly bound to Chlamydomonas PS II independent  of the other extrinsic proteins but not to spinach PS II.	bind
3906	4	2275	6	10	NULL	0	NULL	statement 2	GP		is independent of					extrinsic proteins	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_3	16049780	(1)  Chlamydomonas PsbP and PsbQ directly bound to Chlamydomonas PS II independent  of the other extrinsic proteins but not to spinach PS II.	bind
3907	5	2275	6	10	NULL	0	NULL	PsbP	GP	Chlamydomonas	does not bind					PS II	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_3	16049780	(1)  Chlamydomonas PsbP and PsbQ directly bound to Chlamydomonas PS II independent  of the other extrinsic proteins but not to spinach PS II.	bind
3908	6	2275	6	10	NULL	0	NULL	PsbQ	GP	Chlamydomonas	does not bind					PS II	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_3	16049780	(1)  Chlamydomonas PsbP and PsbQ directly bound to Chlamydomonas PS II independent  of the other extrinsic proteins but not to spinach PS II.	bind
4015	1	2276	5	10	NULL	0	NULL	US11	GP		bind			lumenal domain		MHCI 	GP		heavy chain substrate		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_9_3690_s_222	12972557	(1) After insertion into the ER, the lumenal  domain of US11 binds to the MHCI heavy chain substrate, possibly in a complex with  beta2m (recognition).	bind
4016	2	2276	5	10	NULL	0	NULL	statement 1	Process		is in complex with		possibly			 beta2m	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_9_3690_s_222	12972557	(1) After insertion into the ER, the lumenal  domain of US11 binds to the MHCI heavy chain substrate, possibly in a complex with  beta2m (recognition).	bind
4017	4	2276	5	10	NULL	0	NULL	statement 1	Process		occurs after					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_9_3690_s_222	12972557	(1) After insertion into the ER, the lumenal  domain of US11 binds to the MHCI heavy chain substrate, possibly in a complex with  beta2m (recognition).	bind
5247	3	2276	5	10	NULL	0	NULL				insert into			Lumenal domain		ER	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_9_3690_s_222	12972557	(1) After insertion into the ER, the lumenal  domain of US11 binds to the MHCI heavy chain substrate, possibly in a complex with  beta2m (recognition).	bind
3909	1	2276	6	10	NULL	0	NULL	US11	NULL		bind	NULL		lumenal domain		MHCI	NULL		heavy chain substrate		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_9_3690_s_222	12972557	(1) After insertion into the ER, the lumenal  domain of US11 binds to the MHCI heavy chain substrate, possibly in a complex with  beta2m (recognition).	bind
3910	2	2276	6	10	NULL	0	NULL	US11	GP		forms complex with		possibly			beta2m	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_9_3690_s_222	12972557	(1) After insertion into the ER, the lumenal  domain of US11 binds to the MHCI heavy chain substrate, possibly in a complex with  beta2m (recognition).	bind
4864	3	2276	6	10	NULL	0	NULL				insert into			lumenal domain		ER	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_9_3690_s_222	12972557	(1) After insertion into the ER, the lumenal  domain of US11 binds to the MHCI heavy chain substrate, possibly in a complex with  beta2m (recognition).	bind
4865	4	2276	6	10	NULL	0	NULL	statement 1	Process		occurs after					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_9_3690_s_222	12972557	(1) After insertion into the ER, the lumenal  domain of US11 binds to the MHCI heavy chain substrate, possibly in a complex with  beta2m (recognition).	bind
4018	1	2277	5	10	NULL	0	NULL	Nef	GP		bind			acidic cluster 62EEEE65		PACS-1/AP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_6_853_s_286	12526811	(1) Binding of Nef acidic cluster 62EEEE65 to PACS-1/AP-1 targets Nef to the TGN.	bind
4019	2	2277	5	10	NULL	0	NULL	Nef	GP		is targeted to					TGN	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_6_853_s_286	12526811	(1) Binding of Nef acidic cluster 62EEEE65 to PACS-1/AP-1 targets Nef to the TGN.	bind
4020	3	2277	5	10	NULL	0	NULL	statement 1	Process		is necessary for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_6_853_s_286	12526811	(1) Binding of Nef acidic cluster 62EEEE65 to PACS-1/AP-1 targets Nef to the TGN.	bind
3911	1	2277	6	10	NULL	0	NULL	Nef	GP		bind			acidic cluster 62EEEE65		PACS-1/AP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_6_853_s_286	12526811	(1) Binding of Nef acidic cluster 62EEEE65 to PACS-1/AP-1 targets Nef to the TGN.	bind
3913	2	2277	6	10	NULL	0	NULL	Nef	GP		targeted to					TGN	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_6_853_s_286	12526811	(1) Binding of Nef acidic cluster 62EEEE65 to PACS-1/AP-1 targets Nef to the TGN.	bind
3914	3	2277	6	10	NULL	0	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_6_853_s_286	12526811	(1) Binding of Nef acidic cluster 62EEEE65 to PACS-1/AP-1 targets Nef to the TGN.	bind
4021	1	2278	5	10	NULL	0	NULL	Cdc42	GP		bind								GBD		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_7_534_s_215	12676083	(1) Cdc42 binding to the GBD disrupts the autoregulatory interaction with DAD  [13]  , and (2) the GTPase-Drf3 complex becomes recruited to the cell cortex.	bind
4022	2	2278	5	10	NULL	0	NULL	statement 1	Process		disrupt							autoregulatory interaction with	DAD		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_7_534_s_215	12676083	(1) Cdc42 binding to the GBD disrupts the autoregulatory interaction with DAD  [13]  , and (2) the GTPase-Drf3 complex becomes recruited to the cell cortex.	bind
4023	3	2278	5	10	NULL	0	NULL	GTPase-Drf3 complex	GP		is recruited to					cell cortex	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_7_534_s_215	12676083	(1) Cdc42 binding to the GBD disrupts the autoregulatory interaction with DAD  [13]  , and (2) the GTPase-Drf3 complex becomes recruited to the cell cortex.	bind
46422	4	2278	5	10	NULL	0	NULL	statement 1	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_7_534_s_215	12676083	(1) Cdc42 binding to the GBD disrupts the autoregulatory interaction with DAD  [13]  , and (2) the GTPase-Drf3 complex becomes recruited to the cell cortex.	bind
3916	1	2278	6	10	NULL	0	NULL	Cdc42	GP		bind								GBD		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_7_534_s_215	12676083	(1) Cdc42 binding to the GBD disrupts the autoregulatory interaction with DAD  [13]  , and (2) the GTPase-Drf3 complex becomes recruited to the cell cortex.	bind
3917	2	2278	6	10	NULL	0	NULL	statement 1	Process		disrupts							autoregulatory interaction with	DAD		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_7_534_s_215	12676083	(1) Cdc42 binding to the GBD disrupts the autoregulatory interaction with DAD  [13]  , and (2) the GTPase-Drf3 complex becomes recruited to the cell cortex.	bind
3918	3	2278	6	10	NULL	0	NULL	GTPase-Drf3 complex	GP	complex	is recruited					cell cortex	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_7_534_s_215	12676083	(1) Cdc42 binding to the GBD disrupts the autoregulatory interaction with DAD  [13]  , and (2) the GTPase-Drf3 complex becomes recruited to the cell cortex.	bind
3919	4	2278	6	10	NULL	0	NULL	statement 1	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_7_534_s_215	12676083	(1) Cdc42 binding to the GBD disrupts the autoregulatory interaction with DAD  [13]  , and (2) the GTPase-Drf3 complex becomes recruited to the cell cortex.	bind
4269	1	2279	5	10	NULL	0	NULL	cholera toxin	GP		bind		selectively	B subunit		excitatory opioid receptors	GP	putative;; allosteric	GM1 regulatory site		NULL	mice	NULL	NULL	NULL	NULL	gw60_brainres_888_1_75_s_132	11146054	(1) Cotreatment of mice with low doses of cholera toxin-B subunit (ca. 10  g/kg, i.p.), which binds selectively to a putative allosteric GM1 regulatory site on excitatory opioid receptors [ 12,   30,  31 and   37], blocks opioid-induced hyperalgesia and unmasks potent opioid analgesia (Shen and Crain, in preparation), comparable to the effects of ultra-low-dose NTX.	bind
4270	2	2279	5	10	NULL	0	NULL	opioid	Chemical		induce					hyperalgesia	MedicalFinding				NULL	mice	NULL	NULL	NULL	NULL	gw60_brainres_888_1_75_s_132	11146054	(1) Cotreatment of mice with low doses of cholera toxin-B subunit (ca. 10  g/kg, i.p.), which binds selectively to a putative allosteric GM1 regulatory site on excitatory opioid receptors [ 12,   30,  31 and   37], blocks opioid-induced hyperalgesia and unmasks potent opioid analgesia (Shen and Crain, in preparation), comparable to the effects of ultra-low-dose NTX.	bind
4271	3	2279	5	10	NULL	0	NULL	statement 1	Process		blocks					statement 2	Process				NULL	mice	NULL	NULL	NULL	NULL	gw60_brainres_888_1_75_s_132	11146054	(1) Cotreatment of mice with low doses of cholera toxin-B subunit (ca. 10  g/kg, i.p.), which binds selectively to a putative allosteric GM1 regulatory site on excitatory opioid receptors [ 12,   30,  31 and   37], blocks opioid-induced hyperalgesia and unmasks potent opioid analgesia (Shen and Crain, in preparation), comparable to the effects of ultra-low-dose NTX.	bind
46423	4	2279	5	10	NULL	0	NULL	statement 1	Process		unmasks					opioid analgesia	MedicalFinding	potent			NULL	mice	NULL	NULL	NULL	NULL	gw60_brainres_888_1_75_s_132	11146054	(1) Cotreatment of mice with low doses of cholera toxin-B subunit (ca. 10  g/kg, i.p.), which binds selectively to a putative allosteric GM1 regulatory site on excitatory opioid receptors [ 12,   30,  31 and   37], blocks opioid-induced hyperalgesia and unmasks potent opioid analgesia (Shen and Crain, in preparation), comparable to the effects of ultra-low-dose NTX.	bind
3920	1	2279	6	10	NULL	0	NULL	cholera toxin	GP		bind		selectively	B subunit		excitatory opioid receptors	GP	putative;; allosteric	GM1 regulatory site		NULL	mice	NULL	NULL	NULL	NULL	gw60_brainres_888_1_75_s_132	11146054	(1) Cotreatment of mice with low doses of cholera toxin-B subunit (ca. 10  g/kg, i.p.), which binds selectively to a putative allosteric GM1 regulatory site on excitatory opioid receptors [ 12,   30,  31 and   37], blocks opioid-induced hyperalgesia and unmasks potent opioid analgesia (Shen and Crain, in preparation), comparable to the effects of ultra-low-dose NTX.	bind
3921	3	2279	6	10	NULL	0	NULL	statement 1	Process		blocks					statement 2	Process				NULL	mice	NULL	NULL	NULL	NULL	gw60_brainres_888_1_75_s_132	11146054	(1) Cotreatment of mice with low doses of cholera toxin-B subunit (ca. 10  g/kg, i.p.), which binds selectively to a putative allosteric GM1 regulatory site on excitatory opioid receptors [ 12,   30,  31 and   37], blocks opioid-induced hyperalgesia and unmasks potent opioid analgesia (Shen and Crain, in preparation), comparable to the effects of ultra-low-dose NTX.	bind
3922	4	2279	6	10	NULL	0	NULL	statement 1	Process		unmasks					opioid analgesia	MedicalFinding	potent			NULL	mice	NULL	NULL	NULL	NULL	gw60_brainres_888_1_75_s_132	11146054	(1) Cotreatment of mice with low doses of cholera toxin-B subunit (ca. 10  g/kg, i.p.), which binds selectively to a putative allosteric GM1 regulatory site on excitatory opioid receptors [ 12,   30,  31 and   37], blocks opioid-induced hyperalgesia and unmasks potent opioid analgesia (Shen and Crain, in preparation), comparable to the effects of ultra-low-dose NTX.	bind
46424	2	2279	6	10	NULL	0	NULL	opiod	Chemical		induce					hyperalgesia	MedicalFinding				NULL	mice	NULL	NULL	NULL	NULL	gw60_brainres_888_1_75_s_132	11146054	(1) Cotreatment of mice with low doses of cholera toxin-B subunit (ca. 10  g/kg, i.p.), which binds selectively to a putative allosteric GM1 regulatory site on excitatory opioid receptors [ 12,   30,  31 and   37], blocks opioid-induced hyperalgesia and unmasks potent opioid analgesia (Shen and Crain, in preparation), comparable to the effects of ultra-low-dose NTX.	bind
4024	1	2280	5	10	NULL	0	NULL	Cyclin D	GP		bind					Cdk4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_8_2703_s_120	10436023	(1) Cyclin D binds Cdk4; the filled circle (node) on the line represents the CycD:Cdk4 complex itself.	bind
46425	2	2280	5	10	NULL	0	NULL	statement 1	Process		forms					CycD:Cdk4 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_8_2703_s_120	10436023	(1) Cyclin D binds Cdk4; the filled circle (node) on the line represents the CycD:Cdk4 complex itself.	bind
3923	1	2280	6	10	NULL	0	NULL	Cyclin D	GP		bind					Cdk4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_8_2703_s_120	10436023	(1) Cyclin D binds Cdk4; the filled circle (node) on the line represents the CycD:Cdk4 complex itself.	bind
3924	2	2280	6	10	NULL	0	NULL	statement 1	Process		forms 					CycD:Cdk4 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_8_2703_s_120	10436023	(1) Cyclin D binds Cdk4; the filled circle (node) on the line represents the CycD:Cdk4 complex itself.	bind
4039	1	2281	5	10	NULL	0	NULL	cortisol	Chemical		bind					Type I (mineralocorticoid) receptor	GP	human			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
4040	2	2281	5	10	NULL	0	NULL	11 beta-OHSD	GP	decreased activity	permit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
4042	3	2281	5	10	NULL	0	NULL	AME	MedicalFinding		is					 apparent mineralocorticoid excess	MedicalFinding				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
5248	8	2281	5	10	NULL	0	NULL	AME	MedicalFinding		is associated with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
5249	9	2281	5	10	NULL	0	NULL	AME	MedicalFinding		is associated with					statement 5	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
5250	10	2281	5	10	NULL	0	NULL	AME	MedicalFinding		is associated with					statement 6	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
46692	4	2281	5	10	NULL	0	NULL	Na+ retention	Process		is inhibited by					spironolactone	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
46693	5	2281	5	10	NULL	0	NULL	statement 2	Process		produce					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
46694	6	2281	5	10	NULL	0	NULL	statement 2	Process		produce					hypokalemia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
46695	7	2281	5	10	NULL	0	NULL	statement 2	Process		produce					hypertension	MedicalFinding				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
3955	1	2281	6	10	NULL	0	NULL	cortisol	Chemical		bind					Type I mineralocorticoid receptor	GP	human			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
3956	2	2281	6	10	NULL	0	NULL	11 beta-OHSD 	GP	decreased activity of	permits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
3957	3	2281	6	10	NULL	0	NULL	Na+ retention	Process		is inhibited by					spironolactone	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
3958	4	2281	6	10	NULL	0	NULL	statement 2	Process		produce					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
3959	5	2281	6	10	NULL	0	NULL	statement 2	Process		produce					hypokalemia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
4603	7	2281	6	10	NULL	0	NULL	AME	MedicalFinding		is					apparent mineralocorticoid excess	MedicalFinding				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
4605	8	2281	6	10	NULL	0	NULL	AME	MedicalFinding		is associated with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
4606	10	2281	6	10	NULL	0	NULL	AME	MedicalFinding		is associated with					statement 6	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
4610	9	2281	6	10	NULL	0	NULL	AME	MedicalFinding		is associated with					statement 5	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
46696	6	2281	6	10	NULL	0	NULL	statement 2	Process		produce					hypertension	MedicalFinding				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_kidney-int_42_6_1474763_s_2	1474763	(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the  Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable  Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid  excess (AME).	bind
4043	1	2282	5	10	NULL	0	NULL	Arp2/3	GP		bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_26_5_1579_s_145	16452681	(1) Ena/VASP inhibits Arp2/3 binding to F-actin, thereby decreasing F-actin branching and lamellipodia formation (Krause et al., 2003 ).	bind
4044	2	2282	5	10	NULL	0	NULL	Ena/VASP	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_26_5_1579_s_145	16452681	(1) Ena/VASP inhibits Arp2/3 binding to F-actin, thereby decreasing F-actin branching and lamellipodia formation (Krause et al., 2003 ).	bind
4045	3	2282	5	10	NULL	0	NULL	statement 2	Process		decrease					F-actin	GP	branching of			NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_26_5_1579_s_145	16452681	(1) Ena/VASP inhibits Arp2/3 binding to F-actin, thereby decreasing F-actin branching and lamellipodia formation (Krause et al., 2003 ).	bind
4046	4	2282	5	10	NULL	0	NULL	statement 2	Process		decrease					lamellipodia	CellComponent	formation of			NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_26_5_1579_s_145	16452681	(1) Ena/VASP inhibits Arp2/3 binding to F-actin, thereby decreasing F-actin branching and lamellipodia formation (Krause et al., 2003 ).	bind
3961	1	2282	6	10	NULL	0	NULL	Arp2/3	GP		bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_26_5_1579_s_145	16452681	(1) Ena/VASP inhibits Arp2/3 binding to F-actin, thereby decreasing F-actin branching and lamellipodia formation (Krause et al., 2003 ).	bind
3962	2	2282	6	10	NULL	0	NULL	Ena/VASP	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_26_5_1579_s_145	16452681	(1) Ena/VASP inhibits Arp2/3 binding to F-actin, thereby decreasing F-actin branching and lamellipodia formation (Krause et al., 2003 ).	bind
3963	3	2282	6	10	NULL	0	NULL	statement 2	Process		decreases					F-actin	GP	branching of 			NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_26_5_1579_s_145	16452681	(1) Ena/VASP inhibits Arp2/3 binding to F-actin, thereby decreasing F-actin branching and lamellipodia formation (Krause et al., 2003 ).	bind
3964	4	2282	6	10	NULL	0	NULL	statement 2	Process		decreases					lamellipodia 	CellComponent	formation of			NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_26_5_1579_s_145	16452681	(1) Ena/VASP inhibits Arp2/3 binding to F-actin, thereby decreasing F-actin branching and lamellipodia formation (Krause et al., 2003 ).	bind
4047	1	2283	5	10	NULL	0	NULL	THDOC	Chemical		inhibit					TBPS	Chemical	 binding of			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_1_330_s_225	11150350	(1) It decreased the fraction of [35]TBPS binding inhibited by THDOC (Fig.  1), suggesting a decrease in sensitivity to THDOC, and (2) it enhanced the potentiation of [35]TBPS binding by GABA in stratum oriens and attenuated the inhibition of [35]TBPS binding by GABA in stratum radiatum (Fig.  3).	bind
4048	2	2283	5	10	NULL	0	NULL	statement 1	Process		decrease					THDOC	Chemical	sensitivity to			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_1_330_s_225	11150350	(1) It decreased the fraction of [35]TBPS binding inhibited by THDOC (Fig.  1), suggesting a decrease in sensitivity to THDOC, and (2) it enhanced the potentiation of [35]TBPS binding by GABA in stratum oriens and attenuated the inhibition of [35]TBPS binding by GABA in stratum radiatum (Fig.  3).	bind
5256	3	2283	5	10	NULL	0	NULL	GABA	Chemical		bind					TBPS	Chemical				NULL	stratium oriens	NULL	NULL	NULL	NULL	gw60_jneurosci_21_1_330_s_225	11150350	(1) It decreased the fraction of [35]TBPS binding inhibited by THDOC (Fig.  1), suggesting a decrease in sensitivity to THDOC, and (2) it enhanced the potentiation of [35]TBPS binding by GABA in stratum oriens and attenuated the inhibition of [35]TBPS binding by GABA in stratum radiatum (Fig.  3).	bind
5257	4	2283	5	10	NULL	0	NULL	GABA	Chemical		bind					TBPS	Chemical				NULL	stratum radiatum	NULL	NULL	NULL	NULL	gw60_jneurosci_21_1_330_s_225	11150350	(1) It decreased the fraction of [35]TBPS binding inhibited by THDOC (Fig.  1), suggesting a decrease in sensitivity to THDOC, and (2) it enhanced the potentiation of [35]TBPS binding by GABA in stratum oriens and attenuated the inhibition of [35]TBPS binding by GABA in stratum radiatum (Fig.  3).	bind
4612	1	2283	6	10	NULL	0	NULL	THDOC	Chemical		inhibits					TBPS	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_1_330_s_225	11150350	(1) It decreased the fraction of [35]TBPS binding inhibited by THDOC (Fig.  1), suggesting a decrease in sensitivity to THDOC, and (2) it enhanced the potentiation of [35]TBPS binding by GABA in stratum oriens and attenuated the inhibition of [35]TBPS binding by GABA in stratum radiatum (Fig.  3).	bind
4613	2	2283	6	10	NULL	0	NULL	GABA	Chemical		bind					TBPS	Chemical				NULL	stratum oriens	NULL	NULL	NULL	NULL	gw60_jneurosci_21_1_330_s_225	11150350	(1) It decreased the fraction of [35]TBPS binding inhibited by THDOC (Fig.  1), suggesting a decrease in sensitivity to THDOC, and (2) it enhanced the potentiation of [35]TBPS binding by GABA in stratum oriens and attenuated the inhibition of [35]TBPS binding by GABA in stratum radiatum (Fig.  3).	bind
4614	3	2283	6	10	NULL	0	NULL	GABA	Chemical		bind					TBPS	Chemical				NULL	stratum radiatum	NULL	NULL	NULL	NULL	gw60_jneurosci_21_1_330_s_225	11150350	(1) It decreased the fraction of [35]TBPS binding inhibited by THDOC (Fig.  1), suggesting a decrease in sensitivity to THDOC, and (2) it enhanced the potentiation of [35]TBPS binding by GABA in stratum oriens and attenuated the inhibition of [35]TBPS binding by GABA in stratum radiatum (Fig.  3).	bind
4866	4	2283	6	10	NULL	0	NULL	statement 1	Process		decrease					THDOC	Chemical	sensitivity to			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_1_330_s_225	11150350	(1) It decreased the fraction of [35]TBPS binding inhibited by THDOC (Fig.  1), suggesting a decrease in sensitivity to THDOC, and (2) it enhanced the potentiation of [35]TBPS binding by GABA in stratum oriens and attenuated the inhibition of [35]TBPS binding by GABA in stratum radiatum (Fig.  3).	bind
4050	1	2284	5	10	NULL	0	NULL	CbbR	GP		does not bind									cbbR-cbbL intergenic region	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1245_s_235	12562794	(1) No CbbR bound to the  cbbR-cbbL intergenic region.	bind
3965	1	2284	6	10	NULL	0	NULL	CbbR	GP		does not bind									cbbR-cbbL intergenic region	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1245_s_235	12562794	(1) No CbbR bound to the  cbbR-cbbL intergenic region.	bind
4106	1	2285	5	10	NULL	0	NULL	CGS 21680	Chemical		bind		poorly			A1 receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_112_2_319_s_171	12044450	(1) Numerous studies have shown that CGS 21680 binds poorly to A1 receptors with a  Ki close to 1  M.	bind
3966	1	2285	6	10	NULL	0	NULL	CGS 21680	Chemical		bind		poorly			A1 receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_112_2_319_s_171	12044450	(1) Numerous studies have shown that CGS 21680 binds poorly to A1 receptors with a  Ki close to 1  M.	bind
4107	1	2286	5	10	NULL	0	NULL	nucleotide	NucleicAcid		bind								cleft 1		NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
4108	2	2286	5	10	NULL	0	NULL	NEDD8	GP		bind								cleft 2		NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
4109	3	2286	5	10	NULL	0	NULL	adenylation reaction	Process		involves					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
4110	4	2286	5	10	NULL	0	NULL	adenylation reaction	Process		involves					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
4112	5	2286	5	10	NULL	0	NULL	cysteine	AminoAcid	catalytic	forms					NEDD8	GP	thioester with			NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
4113	6	2286	5	10	NULL	0	NULL	NEDD8	GP		undergoes					adenylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
4114	7	2286	5	10	NULL	0	NULL	E2	GP		bind								cleft 1		NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
4115	8	2286	5	10	NULL	0	NULL	nucleotide-binding pocket	NucleicAcid	occupation of	facilitate					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
4116	9	2286	5	10	NULL	0	NULL	Ublp	GP	E1 thioester-linked	is transferred to					E2	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
4117	10	2286	5	10	NULL	0	NULL	statement 8	Process		promote					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
3967	1	2286	6	10	NULL	0	NULL	nucleotide	NucleicAcid		bind								cleft 1		NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
3968	2	2286	6	10	NULL	0	NULL	NEDD8	GP		bind								cleft 2		NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
4615	3	2286	6	10	NULL	0	NULL	adenylation reaction	Process		involves					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
4616	4	2286	6	10	NULL	0	NULL	adenylation reaction	Process		involves					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
4617	5	2286	6	10	NULL	0	NULL	cysteine	AminoAcid	catalytic 	forms 					NEDD8	GP	thioester with			NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
4618	6	2286	6	10	NULL	0	NULL	E2	GP		bind								cleft 1		NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
4619	7	2286	6	10	NULL	0	NULL	NEDD8	GP		undergoes					adenylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
4621	10	2286	6	10	NULL	0	NULL	statement 8	Process		promote					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
46879	8	2286	6	10	NULL	0	NULL	nucleotide-binding pocket	NucleicAcid	occupation of 	faciliate					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
46880	9	2286	6	10	NULL	0	NULL	Ublp	GP	E1 thioester-linked	is transfered to					E2	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_330_s_139	12646924	(1) The adenylation reaction involves nucleotide binding  to cleft 1 and NEDD8 binding to cleft 2; (2) the catalytic cysteine, facing NEDD8,  forms a thioester with NEDD8; (3) a second molecule of NEDD8 is adenylated; (4) occupation  of the nucleotide-binding pocket facilitates binding of E2 in cleft 1, promoting  transfer of the E1 thioester-linked Ublp to E2.	bind
4118	2	2287	5	10	NULL	0	NULL	LRH-1	GP		differ from			coactivator binding surface 		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_1_1_s_35	12852843	(1) The coactivator binding surface in LRH-1 differs in its details from that found in prototypic agonist-bound nuclear receptors; as a result, coactivators may bind to LRH-1 by utilizing nontraditional receptor surfaces, or LRH-1 may use novel coactivators in place of the usual suspects.	bind
4119	3	2287	5	10	NULL	0	NULL	coactivators	GP		bind		may			LRH-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_1_1_s_35	12852843	(1) The coactivator binding surface in LRH-1 differs in its details from that found in prototypic agonist-bound nuclear receptors; as a result, coactivators may bind to LRH-1 by utilizing nontraditional receptor surfaces, or LRH-1 may use novel coactivators in place of the usual suspects.	bind
4120	4	2287	5	10	NULL	0	NULL	statement 2	Process		utilize					receptor surfaces	GP	nontraditional			NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_1_1_s_35	12852843	(1) The coactivator binding surface in LRH-1 differs in its details from that found in prototypic agonist-bound nuclear receptors; as a result, coactivators may bind to LRH-1 by utilizing nontraditional receptor surfaces, or LRH-1 may use novel coactivators in place of the usual suspects.	bind
4121	5	2287	5	10	NULL	0	NULL	LRH-1	GP		use		may			coactivators	GP	novel			NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_1_1_s_35	12852843	(1) The coactivator binding surface in LRH-1 differs in its details from that found in prototypic agonist-bound nuclear receptors; as a result, coactivators may bind to LRH-1 by utilizing nontraditional receptor surfaces, or LRH-1 may use novel coactivators in place of the usual suspects.	bind
4122	6	2287	5	10	NULL	0	NULL	statement 2	NULL		results in	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_1_1_s_35	12852843	(1) The coactivator binding surface in LRH-1 differs in its details from that found in prototypic agonist-bound nuclear receptors; as a result, coactivators may bind to LRH-1 by utilizing nontraditional receptor surfaces, or LRH-1 may use novel coactivators in place of the usual suspects.	bind
4123	7	2287	5	10	NULL	0	NULL	statement 2	NULL		results in	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_1_1_s_35	12852843	(1) The coactivator binding surface in LRH-1 differs in its details from that found in prototypic agonist-bound nuclear receptors; as a result, coactivators may bind to LRH-1 by utilizing nontraditional receptor surfaces, or LRH-1 may use novel coactivators in place of the usual suspects.	bind
5258	8	2287	5	10	NULL	0	NULL	statement 6	NULL		is an alternative to	NULL				statement 7	NULL				NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_1_1_s_35	12852843	(1) The coactivator binding surface in LRH-1 differs in its details from that found in prototypic agonist-bound nuclear receptors; as a result, coactivators may bind to LRH-1 by utilizing nontraditional receptor surfaces, or LRH-1 may use novel coactivators in place of the usual suspects.	bind
46426	1	2287	5	10	NULL	0	NULL	prototypic agonist	Chemical		bind					nuclear receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_1_1_s_35	12852843	(1) The coactivator binding surface in LRH-1 differs in its details from that found in prototypic agonist-bound nuclear receptors; as a result, coactivators may bind to LRH-1 by utilizing nontraditional receptor surfaces, or LRH-1 may use novel coactivators in place of the usual suspects.	bind
4622	1	2287	6	10	NULL	0	NULL	coactivator	GP		bind		may			LRH-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_1_1_s_35	12852843	(1) The coactivator binding surface in LRH-1 differs in its details from that found in prototypic agonist-bound nuclear receptors; as a result, coactivators may bind to LRH-1 by utilizing nontraditional receptor surfaces, or LRH-1 may use novel coactivators in place of the usual suspects.	bind
4623	2	2287	6	10	NULL	0	NULL	statement 1	Process		utilize					receptor surface	GP	nontraditional			NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_1_1_s_35	12852843	(1) The coactivator binding surface in LRH-1 differs in its details from that found in prototypic agonist-bound nuclear receptors; as a result, coactivators may bind to LRH-1 by utilizing nontraditional receptor surfaces, or LRH-1 may use novel coactivators in place of the usual suspects.	bind
4989	4	2287	6	10	NULL	0	NULL	LRH-1	GP		differ from			coactivator binding surface 		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_1_1_s_35	12852843	(1) The coactivator binding surface in LRH-1 differs in its details from that found in prototypic agonist-bound nuclear receptors; as a result, coactivators may bind to LRH-1 by utilizing nontraditional receptor surfaces, or LRH-1 may use novel coactivators in place of the usual suspects.	bind
4990	5	2287	6	10	NULL	0	NULL	LRH-1	GP		use		may			coactivators	GP	novel			NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_1_1_s_35	12852843	(1) The coactivator binding surface in LRH-1 differs in its details from that found in prototypic agonist-bound nuclear receptors; as a result, coactivators may bind to LRH-1 by utilizing nontraditional receptor surfaces, or LRH-1 may use novel coactivators in place of the usual suspects.	bind
4991	6	2287	6	10	NULL	0	NULL	statement 4	Process		results in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_1_1_s_35	12852843	(1) The coactivator binding surface in LRH-1 differs in its details from that found in prototypic agonist-bound nuclear receptors; as a result, coactivators may bind to LRH-1 by utilizing nontraditional receptor surfaces, or LRH-1 may use novel coactivators in place of the usual suspects.	bind
4992	7	2287	6	10	NULL	0	NULL	statement 4	Process		results in					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_1_1_s_35	12852843	(1) The coactivator binding surface in LRH-1 differs in its details from that found in prototypic agonist-bound nuclear receptors; as a result, coactivators may bind to LRH-1 by utilizing nontraditional receptor surfaces, or LRH-1 may use novel coactivators in place of the usual suspects.	bind
4993	8	2287	6	10	NULL	0	NULL	statement 6	Process		is an alternative to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_1_1_s_35	12852843	(1) The coactivator binding surface in LRH-1 differs in its details from that found in prototypic agonist-bound nuclear receptors; as a result, coactivators may bind to LRH-1 by utilizing nontraditional receptor surfaces, or LRH-1 may use novel coactivators in place of the usual suspects.	bind
46427	3	2287	6	10	NULL	0	NULL	prototypic agonist	Chemical		bind					nuclear receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_1_1_s_35	12852843	(1) The coactivator binding surface in LRH-1 differs in its details from that found in prototypic agonist-bound nuclear receptors; as a result, coactivators may bind to LRH-1 by utilizing nontraditional receptor surfaces, or LRH-1 may use novel coactivators in place of the usual suspects.	bind
4124	1	2288	5	10	NULL	0	NULL	import substrate	GP		bind					importin-alpha/beta heterodimer	GP		NLS binding site		NULL		NULL	NULL	NULL	NULL	gw60_embo_17_10_2721_s_59	9582265	(1) The initial, cytoplasmic event in NLS-dependent import is the binding of the import substrate to the importin-alpha/beta heterodimer, where the importin-alpha subunit provides the NLS binding site.	bind
4125	2	2288	5	10	NULL	0	NULL	importin-alpha subunit	GP		provide								NLS binding site		NULL		NULL	NULL	NULL	NULL	gw60_embo_17_10_2721_s_59	9582265	(1) The initial, cytoplasmic event in NLS-dependent import is the binding of the import substrate to the importin-alpha/beta heterodimer, where the importin-alpha subunit provides the NLS binding site.	bind
4126	3	2288	5	10	NULL	0	NULL	NLS-dependent import	Process	initial, cytoplasmic event in	involves					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_10_2721_s_59	9582265	(1) The initial, cytoplasmic event in NLS-dependent import is the binding of the import substrate to the importin-alpha/beta heterodimer, where the importin-alpha subunit provides the NLS binding site.	bind
3969	1	2288	6	10	NULL	0	NULL	import substrate	GP		bind					 importin-alpha/beta heterodimer	GP		NLS binding site		NULL		NULL	NULL	NULL	NULL	gw60_embo_17_10_2721_s_59	9582265	(1) The initial, cytoplasmic event in NLS-dependent import is the binding of the import substrate to the importin-alpha/beta heterodimer, where the importin-alpha subunit provides the NLS binding site.	bind
3970	2	2288	6	10	NULL	0	NULL	importin-alpha subunit	GP		provides								NLS binding site		NULL		NULL	NULL	NULL	NULL	gw60_embo_17_10_2721_s_59	9582265	(1) The initial, cytoplasmic event in NLS-dependent import is the binding of the import substrate to the importin-alpha/beta heterodimer, where the importin-alpha subunit provides the NLS binding site.	bind
52991	3	2288	6	10	NULL	0	NULL	NLS-dependent import	Process	initial, cytoplasmic event in	involves					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_10_2721_s_59	9582265	(1) The initial, cytoplasmic event in NLS-dependent import is the binding of the import substrate to the importin-alpha/beta heterodimer, where the importin-alpha subunit provides the NLS binding site.	bind
4127	1	2289	5	10	NULL	0	NULL	MS2 peptide	GP		bind								fourth Ig-like domain		NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_9_3460_s_150	9547253	(1) The peptide MS2, which binds to the fourth Ig-like domain, reduced the magnitude of LTP by a constant amount, from the beginning to the end of the recording period after TBS, but only if it was present during TBS.	bind
4128	2	2289	5	10	NULL	0	NULL	statement 1	Process		reduced					LTP	Process	magnitude of			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_9_3460_s_150	9547253	(1) The peptide MS2, which binds to the fourth Ig-like domain, reduced the magnitude of LTP by a constant amount, from the beginning to the end of the recording period after TBS, but only if it was present during TBS.	bind
3971	1	2289	6	10	NULL	0	NULL	MS2 peptide	GP		bind								fourth Ig-like domain		NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_9_3460_s_150	9547253	(1) The peptide MS2, which binds to the fourth Ig-like domain, reduced the magnitude of LTP by a constant amount, from the beginning to the end of the recording period after TBS, but only if it was present during TBS.	bind
3972	2	2289	6	10	NULL	0	NULL	MS2 peptide	GP		reduces					LTP	Process	magnitude of			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_9_3460_s_150	9547253	(1) The peptide MS2, which binds to the fourth Ig-like domain, reduced the magnitude of LTP by a constant amount, from the beginning to the end of the recording period after TBS, but only if it was present during TBS.	bind
4129	1	2291	5	10	NULL	0	NULL	synuclein	GP		bind					BAD	GP				NULL	cytoplasm	NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4131	2	2291	5	10	NULL	0	NULL	BAD	GP		translocated to					mitochondria	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4132	3	2291	5	10	NULL	0	NULL	statement 1	Process		prevent					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4133	5	2291	5	10	NULL	0	NULL	BAD	GP		induce					cytochrome c	GP	release			NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4134	6	2291	5	10	NULL	0	NULL	MPP+	Chemical	exposure	inhibit					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4135	7	2291	5	10	NULL	0	NULL	cytochrome c	GP		mediate					caspase-3	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4136	8	2291	5	10	NULL	0	NULL	MPP+	Chemical	exposure of	block		subsequently			statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4137	9	2291	5	10	NULL	0	NULL	caspase-3	GP		mediate					PKC	GP	 proteolytic cleavage			NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4138	10	2291	5	10	NULL	0	NULL	MPP+	Chemical	exposure	attenuate					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4139	11	2291	5	10	NULL	0	NULL	synuclein	GP		bind					PKC	GP				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4140	12	2291	5	10	NULL	0	NULL	statement 11	Process		prevent					PKC	GP	proteolytic cleavage of			NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4141	13	2291	5	10	NULL	0	NULL	statement 12	Process		attenuate		significantly			DNA fragmentation	Process				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4142	14	2291	5	10	NULL	0	NULL	statement 12	Process		attenuate		significantly			cellular apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
46428	4	2291	5	10	NULL	0	NULL	statement 1	Process		occurs upon					MPP+	Chemical	exposure to			NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
46429	15	2291	5	10	NULL	0	NULL	BAD	GP		is a type of					 pro-apoptotic factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
46430	16	2291	5	10	NULL	0	NULL	PKC	GP		is a type of					pro-apoptotic kinase	GP				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4624	1	2291	6	10	NULL	0	NULL	synuclein	GP		bind					BAD	GP				NULL	cytoplasm	NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4994	2	2291	6	10	NULL	0	NULL	statement 1	Process		occurs upon 					MPP+	Chemical	exposure of			NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4995	3	2291	6	10	NULL	0	NULL	BAD	GP		induces					cytochrome c	GP	release of			NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4996	4	2291	6	10	NULL	0	NULL	MPP+	Chemical	exposure to	inhibits					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4997	5	2291	6	10	NULL	0	NULL	cytochrome c	GP		mediates					caspase-3	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4998	6	2291	6	10	NULL	0	NULL	MPP+	Chemical	exposure to	blocks					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4999	7	2291	6	10	NULL	0	NULL	caspase-3	GP		mediates					PKC	GP	proteolytic cleavage of			NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
5000	8	2291	6	10	NULL	0	NULL	MPP+	Chemical	exposure to	attenuates					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
5001	9	2291	6	10	NULL	0	NULL	synuclein	GP		bind					PKC	GP				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
5002	10	2291	6	10	NULL	0	NULL	statement 9	Process		prevents					PKC	GP	proteolytic cleavage of			NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
5003	11	2291	6	10	NULL	0	NULL	statement 10	Process		attenuates		significantly			DNA fragmentation	Process				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
5004	12	2291	6	10	NULL	0	NULL	statement 10	Process		attenuates		significantly			cellular apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
46433	13	2291	6	10	NULL	0	NULL	BAD	GP		translocates to					mitochondria	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
46434	14	2291	6	10	NULL	0	NULL	statement 1	Process		prevents					statement 13	Process				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
46436	15	2291	6	10	NULL	0	NULL	BAD	GP		is a type of					pro-apoptotic factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
46437	16	2291	6	10	NULL	0	NULL	PKC	GP		is a type of					pro-apoptotic kinase	GP				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_139_1_137_s_367	15978696	(1) Upon exposure to MPP+,  -synuclein binds to the pro-apoptotic factor BAD in the cytoplasm and prevents  its translocation to the mitochondria; (2) BAD-induced cytochrome  c release is inhibited; (3) cytochrome  c-mediated activation of caspase-3 is subsequently blocked; (4) caspase-3-mediated  proteolytic cleavage of PKC  is attenuated; (5)  -synuclein also binds to the pro-apoptotic  kinase PKC  and (6) prevents proteolytic cleavage of PKC  which significantly attenuates  (7) DNA fragmentation and cellular apoptosis.	bind
4144	1	2293	5	10	NULL	0	NULL	protein b1	GP		bind					protein bn	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_18_5945_s_81	16237128	(1) where  P( b1| bn) is the probability of finding a protein bound right next to another one that is already bound to DNA ( ).  b1| bn denotes the protein  b1 binding to the protein  bn:	bind
4275	2	2293	5	10	NULL	0	NULL	b1| bn	GP		denotes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_18_5945_s_81	16237128	(1) where  P( b1| bn) is the probability of finding a protein bound right next to another one that is already bound to DNA ( ).  b1| bn denotes the protein  b1 binding to the protein  bn:	bind
3975	1	2293	6	10	NULL	0	NULL	protein b1	GP		bind					protein bn	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_18_5945_s_81	16237128	(1) where  P( b1| bn) is the probability of finding a protein bound right next to another one that is already bound to DNA ( ).  b1| bn denotes the protein  b1 binding to the protein  bn:	bind
3976	2	2293	6	10	NULL	0	NULL	statement 1	Process		denotes					 b1| bn	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_18_5945_s_81	16237128	(1) where  P( b1| bn) is the probability of finding a protein bound right next to another one that is already bound to DNA ( ).  b1| bn denotes the protein  b1 binding to the protein  bn:	bind
4145	1	2294	5	10	NULL	0	NULL	cAMP	NucleicAcid		bind					PKA	GP				NULL	lateral region of the caudate-putamen and the parietal cortex	NULL	NULL	NULL	NULL	gw60_neuroscience_94_2_361_s_218	10579200	(1) Within 3 h of MCA occlusion, there was a significant reduction in cAMP binding to PKA in the lateral region of the caudate-putamen and the parietal cortex.	bind
4146	2	2294	5	10	NULL	0	NULL	MCA 	OrganismPart	occlusion of	reduce		significantly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_94_2_361_s_218	10579200	(1) Within 3 h of MCA occlusion, there was a significant reduction in cAMP binding to PKA in the lateral region of the caudate-putamen and the parietal cortex.	bind
4030	1	2294	6	10	NULL	0	NULL	cAMP	NucleicAcid		bind					PKA	GP				NULL	lateral region of the caudate-putamen and the parietal cortex	NULL	NULL	NULL	NULL	gw60_neuroscience_94_2_361_s_218	10579200	(1) Within 3 h of MCA occlusion, there was a significant reduction in cAMP binding to PKA in the lateral region of the caudate-putamen and the parietal cortex.	bind
4031	2	2294	6	10	NULL	0	NULL	MCA	OrganismPart	occlusion of	reduce		significantly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_94_2_361_s_218	10579200	(1) Within 3 h of MCA occlusion, there was a significant reduction in cAMP binding to PKA in the lateral region of the caudate-putamen and the parietal cortex.	bind
4175	1	2295	5	10	NULL	0	NULL	ATP-actin	GP		bind					profilin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_453_s_88	12600310	(10) Profilin catalyzes the exchange of ADP for ATP (turning the subunits white), returning subunits to (11) the pool of ATP-actin bound to profilin, ready to elongate barbed ends as they become available.	bind
4176	2	2295	5	10	NULL	0	NULL	ADP	Chemical		exchange for					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_453_s_88	12600310	(10) Profilin catalyzes the exchange of ADP for ATP (turning the subunits white), returning subunits to (11) the pool of ATP-actin bound to profilin, ready to elongate barbed ends as they become available.	bind
4177	3	2295	5	10	NULL	0	NULL	profilin	GP		catalyze					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_453_s_88	12600310	(10) Profilin catalyzes the exchange of ADP for ATP (turning the subunits white), returning subunits to (11) the pool of ATP-actin bound to profilin, ready to elongate barbed ends as they become available.	bind
4051	1	2295	6	10	NULL	0	NULL	ATP-actin	GP		bind					profilin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_453_s_88	12600310	(10) Profilin catalyzes the exchange of ADP for ATP (turning the subunits white), returning subunits to (11) the pool of ATP-actin bound to profilin, ready to elongate barbed ends as they become available.	bind
4630	2	2295	6	10	NULL	0	NULL	ADP	Chemical		exchange for					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_453_s_88	12600310	(10) Profilin catalyzes the exchange of ADP for ATP (turning the subunits white), returning subunits to (11) the pool of ATP-actin bound to profilin, ready to elongate barbed ends as they become available.	bind
4631	3	2295	6	10	NULL	0	NULL	profilin	GP		catalyzes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_453_s_88	12600310	(10) Profilin catalyzes the exchange of ADP for ATP (turning the subunits white), returning subunits to (11) the pool of ATP-actin bound to profilin, ready to elongate barbed ends as they become available.	bind
4179	1	2296	5	10	NULL	0	NULL	(125)I-C5	GP		bind		reversibly			C6	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_274_45_10542204_s_7	10542204	(125)I-C5 binds reversibly  to C6 in an ionic strength-dependent fashion, but (125)I-C5 binds only  weakly to C6des-FIMs and not at all to C6des-CCP/FIMs.	bind
4180	2	2296	5	10	NULL	0	NULL	statement 1	Process		is dependent on					ionic strength	QuantityOrMeasure				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_274_45_10542204_s_7	10542204	(125)I-C5 binds reversibly  to C6 in an ionic strength-dependent fashion, but (125)I-C5 binds only  weakly to C6des-FIMs and not at all to C6des-CCP/FIMs.	bind
4181	3	2296	5	10	NULL	0	NULL	(125)I-C5	GP		bind		weakly			C6	GP		des-FIMs		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_274_45_10542204_s_7	10542204	(125)I-C5 binds reversibly  to C6 in an ionic strength-dependent fashion, but (125)I-C5 binds only  weakly to C6des-FIMs and not at all to C6des-CCP/FIMs.	bind
4182	4	2296	5	10	NULL	0	NULL	(125)I-C5	GP		does not bind					C6	GP		des-CCP/FIMs		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_274_45_10542204_s_7	10542204	(125)I-C5 binds reversibly  to C6 in an ionic strength-dependent fashion, but (125)I-C5 binds only  weakly to C6des-FIMs and not at all to C6des-CCP/FIMs.	bind
4052	1	2296	6	10	NULL	0	NULL	I-C5	GP		bind		reversibly			C6	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_274_45_10542204_s_7	10542204	(125)I-C5 binds reversibly  to C6 in an ionic strength-dependent fashion, but (125)I-C5 binds only  weakly to C6des-FIMs and not at all to C6des-CCP/FIMs.	bind
4053	2	2296	6	10	NULL	0	NULL	statement 1	Process		is dependent on					ionic strength	QuantityOrMeasure				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_274_45_10542204_s_7	10542204	(125)I-C5 binds reversibly  to C6 in an ionic strength-dependent fashion, but (125)I-C5 binds only  weakly to C6des-FIMs and not at all to C6des-CCP/FIMs.	bind
4054	3	2296	6	10	NULL	0	NULL	I-C5	GP		bind		weakly			C6	GP		des-FIMs		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_274_45_10542204_s_7	10542204	(125)I-C5 binds reversibly  to C6 in an ionic strength-dependent fashion, but (125)I-C5 binds only  weakly to C6des-FIMs and not at all to C6des-CCP/FIMs.	bind
4055	4	2296	6	10	NULL	0	NULL	I-C5	GP		does not bind					C6	GP		des-CCP/FIMs		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_274_45_10542204_s_7	10542204	(125)I-C5 binds reversibly  to C6 in an ionic strength-dependent fashion, but (125)I-C5 binds only  weakly to C6des-FIMs and not at all to C6des-CCP/FIMs.	bind
4183	1	2297	5	10	NULL	0	NULL	Cry1Ac	GP	(125)I-labeled	bind		specifically			brush border membrane vesicles	CellComponent	E. insulana			NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_appl-environ-microbiol_72_1_16391075_s_12	16391075	(125)I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
4184	2	2297	5	10	NULL	0	NULL	Cry1Ab	GP	(125)I-labeled	bind		specifically			brush border membrane vesicles	CellComponent	E. insulana			NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_appl-environ-microbiol_72_1_16391075_s_12	16391075	(125)I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
4185	3	2297	5	10	NULL	0	NULL	Cry1Ba	GP	biotinylated	bind		specifically			brush border membrane vesicles	CellComponent	E. insulana			NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_appl-environ-microbiol_72_1_16391075_s_12	16391075	(125)I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
4186	4	2297	5	10	NULL	0	NULL	Cry1Ia	GP	biotinylated	bind		specifically			brush border membrane vesicles	CellComponent	E. insulana			NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_appl-environ-microbiol_72_1_16391075_s_12	16391075	(125)I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
4187	5	2297	5	10	NULL	0	NULL	Cry9Ca	GP	biotinylated	bind		specifically			brush border membrane vesicles	CellComponent	E. insulana			NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_appl-environ-microbiol_72_1_16391075_s_12	16391075	(125)I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
4056	1	2297	6	10	NULL	0	NULL	Cry1Ac	GP	(125)I-labeled	bind		specifically			brush border membrane vesicles	CellComponent	E. insulana  			NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_appl-environ-microbiol_72_1_16391075_s_12	16391075	(125)I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
4057	2	2297	6	10	NULL	0	NULL	Cry1Ab	GP	(125)I-labeled	bind		specifically			brush border membrane vesicles	CellComponent	E. insulana			NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_appl-environ-microbiol_72_1_16391075_s_12	16391075	(125)I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
4058	3	2297	6	10	NULL	0	NULL	Cry1Ba	GP	biotinylated	bind		specifically			brush border membrane vesicles	CellComponent	E. insulana			NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_appl-environ-microbiol_72_1_16391075_s_12	16391075	(125)I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
4059	4	2297	6	10	NULL	0	NULL	Cry1Ia	GP	biotinylated	bind		specifically			brush border membrane vesicles	CellComponent	E. insulana  			NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_appl-environ-microbiol_72_1_16391075_s_12	16391075	(125)I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
4060	5	2297	6	10	NULL	0	NULL	Cry9Ca	GP	biotinylated	bind		specifically			brush border membrane vesicles	CellComponent	E. insulana			NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_appl-environ-microbiol_72_1_16391075_s_12	16391075	(125)I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
4188	1	2298	5	10	NULL	0	NULL	dopamine	Chemical		bind					striatal D-2 site	OrganismPart	rat			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_128_4_881_s_263	10556922	(1982) [3]-dopamine binding to rat striatal D-2 and D-3 sites: enhancement by magnesium and inhibition by guanine nucleotides and sodium.	bind
4189	2	2298	5	10	NULL	0	NULL	dopamine	Chemical		bind					striatal D-3 site	OrganismPart	rat			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_128_4_881_s_263	10556922	(1982) [3]-dopamine binding to rat striatal D-2 and D-3 sites: enhancement by magnesium and inhibition by guanine nucleotides and sodium.	bind
5259	3	2298	5	10	NULL	0	NULL	magnesium	Chemical		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_128_4_881_s_263	10556922	(1982) [3]-dopamine binding to rat striatal D-2 and D-3 sites: enhancement by magnesium and inhibition by guanine nucleotides and sodium.	bind
5260	4	2298	5	10	NULL	0	NULL	magnesium	Chemical		enhance					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_128_4_881_s_263	10556922	(1982) [3]-dopamine binding to rat striatal D-2 and D-3 sites: enhancement by magnesium and inhibition by guanine nucleotides and sodium.	bind
5261	5	2298	5	10	NULL	0	NULL	guanine nucleotides	NucleicAcid		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_128_4_881_s_263	10556922	(1982) [3]-dopamine binding to rat striatal D-2 and D-3 sites: enhancement by magnesium and inhibition by guanine nucleotides and sodium.	bind
5262	6	2298	5	10	NULL	0	NULL	guanine nucleotides	NucleicAcid		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_128_4_881_s_263	10556922	(1982) [3]-dopamine binding to rat striatal D-2 and D-3 sites: enhancement by magnesium and inhibition by guanine nucleotides and sodium.	bind
5263	7	2298	5	10	NULL	0	NULL	sodium	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_128_4_881_s_263	10556922	(1982) [3]-dopamine binding to rat striatal D-2 and D-3 sites: enhancement by magnesium and inhibition by guanine nucleotides and sodium.	bind
5264	8	2298	5	10	NULL	0	NULL	sodium	Chemical		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_128_4_881_s_263	10556922	(1982) [3]-dopamine binding to rat striatal D-2 and D-3 sites: enhancement by magnesium and inhibition by guanine nucleotides and sodium.	bind
4061	1	2298	6	10	NULL	0	NULL	dopamine	Chemical		bind					striatal D-2 site	OrganismPart	rat			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_128_4_881_s_263	10556922	(1982) [3]-dopamine binding to rat striatal D-2 and D-3 sites: enhancement by magnesium and inhibition by guanine nucleotides and sodium.	bind
4062	2	2298	6	10	NULL	0	NULL	dopamine	Chemical		bind					striatal D-3 site	OrganismPart	rat			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_128_4_881_s_263	10556922	(1982) [3]-dopamine binding to rat striatal D-2 and D-3 sites: enhancement by magnesium and inhibition by guanine nucleotides and sodium.	bind
4063	3	2298	6	10	NULL	0	NULL	magnesium	Chemical		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_128_4_881_s_263	10556922	(1982) [3]-dopamine binding to rat striatal D-2 and D-3 sites: enhancement by magnesium and inhibition by guanine nucleotides and sodium.	bind
4064	4	2298	6	10	NULL	0	NULL	magnesium	Chemical		enhances					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_128_4_881_s_263	10556922	(1982) [3]-dopamine binding to rat striatal D-2 and D-3 sites: enhancement by magnesium and inhibition by guanine nucleotides and sodium.	bind
4065	5	2298	6	10	NULL	0	NULL	guanine nucleotides	NucleicAcid		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_128_4_881_s_263	10556922	(1982) [3]-dopamine binding to rat striatal D-2 and D-3 sites: enhancement by magnesium and inhibition by guanine nucleotides and sodium.	bind
4066	6	2298	6	10	NULL	0	NULL	guanine nucleotides	NucleicAcid		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_128_4_881_s_263	10556922	(1982) [3]-dopamine binding to rat striatal D-2 and D-3 sites: enhancement by magnesium and inhibition by guanine nucleotides and sodium.	bind
4067	7	2298	6	10	NULL	0	NULL	sodium	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_128_4_881_s_263	10556922	(1982) [3]-dopamine binding to rat striatal D-2 and D-3 sites: enhancement by magnesium and inhibition by guanine nucleotides and sodium.	bind
4068	8	2298	6	10	NULL	0	NULL	sodium	Chemical		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_128_4_881_s_263	10556922	(1982) [3]-dopamine binding to rat striatal D-2 and D-3 sites: enhancement by magnesium and inhibition by guanine nucleotides and sodium.	bind
4190	1	2299	5	10	NULL	0	NULL	Acyl-CoA	GP		bind					FadR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33652_s_358	9837950	(1991)  J. Biol. Chem.  266, 23824-23828 [Abstract]         aman, N.    (1996)   tudies on Acyl-CoA Binding to the Transcription Factor FadR, Ph.D. dissertation, University of Tennessee, Memphis	bind
52992	2	2299	5	10	NULL	0	NULL	FadR	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33652_s_358	9837950	(1991)  J. Biol. Chem.  266, 23824-23828 [Abstract]         aman, N.    (1996)   tudies on Acyl-CoA Binding to the Transcription Factor FadR, Ph.D. dissertation, University of Tennessee, Memphis	bind
4069	1	2299	6	10	NULL	0	NULL	Acyl-CoA	GP		bind					FadR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33652_s_358	9837950	(1991)  J. Biol. Chem.  266, 23824-23828 [Abstract]         aman, N.    (1996)   tudies on Acyl-CoA Binding to the Transcription Factor FadR, Ph.D. dissertation, University of Tennessee, Memphis	bind
52993	2	2299	6	10	NULL	0	NULL	FadR	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33652_s_358	9837950	(1991)  J. Biol. Chem.  266, 23824-23828 [Abstract]         aman, N.    (1996)   tudies on Acyl-CoA Binding to the Transcription Factor FadR, Ph.D. dissertation, University of Tennessee, Memphis	bind
4191	1	2300	5	10	NULL	0	NULL	P-glycoprotein	GP		contains								azidopine binding site		NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiolrev_21_1_55_s_961	9299702	(1992) Characterization of the azidopine and vinblastine binding site of P-glycoprotein.	bind
4192	2	2300	5	10	NULL	0	NULL	P-glycoprotein	GP		contains								vinblastine binding site		NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiolrev_21_1_55_s_961	9299702	(1992) Characterization of the azidopine and vinblastine binding site of P-glycoprotein.	bind
4632	1	2300	6	10	NULL	0	NULL	P-glycoprotein	GP		contains								azidopine binding site		NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiolrev_21_1_55_s_961	9299702	(1992) Characterization of the azidopine and vinblastine binding site of P-glycoprotein.	bind
4633	2	2300	6	10	NULL	0	NULL	P-glycoprotein	GP		contains								 vinblastine binding site		NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiolrev_21_1_55_s_961	9299702	(1992) Characterization of the azidopine and vinblastine binding site of P-glycoprotein.	bind
4193	1	2301	5	10	NULL	0	NULL	casein kinase II	GP		phosphorylate					mUBF	GP		C-terminal hyperacidic tail		NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3692_s_462	9649439	(1992) The nucleolar transcription factor mUBF is phosphorylated by casein kinase II in the C-terminal hyperacidic tail which is essential for transactivation.	bind
4194	2	2301	5	10	NULL	0	NULL	mUBF	GP		is essential for			C-terminal hyperacidic tail		transactivation	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3692_s_462	9649439	(1992) The nucleolar transcription factor mUBF is phosphorylated by casein kinase II in the C-terminal hyperacidic tail which is essential for transactivation.	bind
46457	3	2301	5	10	NULL	0	NULL	mUBF	GP		is a type of					nucleolar transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3692_s_462	9649439	(1992) The nucleolar transcription factor mUBF is phosphorylated by casein kinase II in the C-terminal hyperacidic tail which is essential for transactivation.	bind
4070	1	2301	6	10	NULL	0	NULL	casein kinase II	GP		phosphorylates					mUBF	GP		C-terminal hyperacidic tail		NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3692_s_462	9649439	(1992) The nucleolar transcription factor mUBF is phosphorylated by casein kinase II in the C-terminal hyperacidic tail which is essential for transactivation.	bind
4071	2	2301	6	10	NULL	0	NULL	mUBF	GP		is essential for			C-terminal hyperacidic tail		transactivation	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3692_s_462	9649439	(1992) The nucleolar transcription factor mUBF is phosphorylated by casein kinase II in the C-terminal hyperacidic tail which is essential for transactivation.	bind
46458	3	2301	6	10	NULL	0	NULL	mUBF	GP		is a type of					nucleolar transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3692_s_462	9649439	(1992) The nucleolar transcription factor mUBF is phosphorylated by casein kinase II in the C-terminal hyperacidic tail which is essential for transactivation.	bind
4195	1	2302	5	10	NULL	0	NULL	collagen	GP		bind					NG7C	Organism				NULL		NULL	NULL	NULL	NULL	gw60_femsimmunolmedmic_19_3_247_s_213	9453395	(1993) Collagen binding to  Escherichia coli strain NG7C.	bind
61101	2	2302	5	10	NULL	0	NULL	NG7C	Organism		is a strain of					Escherichia coli	Organism				NULL		NULL	NULL	NULL	NULL	gw60_femsimmunolmedmic_19_3_247_s_213	9453395	(1993) Collagen binding to  Escherichia coli strain NG7C.	bind
4073	1	2302	6	10	NULL	0	NULL	Collagen	GP		bind					 NG7C	Organism				NULL		NULL	NULL	NULL	NULL	gw60_femsimmunolmedmic_19_3_247_s_213	9453395	(1993) Collagen binding to  Escherichia coli strain NG7C.	bind
61102	2	2302	6	10	NULL	0	NULL	NG7C	Organism		is a strain of					Escherichia coli	Organism				NULL		0	NULL	NULL	NULL	gw60_femsimmunolmedmic_19_3_247_s_213	9453395	(1993) Collagen binding to  Escherichia coli strain NG7C.	bind
4196	1	2303	5	10	NULL	0	NULL	tissue plasminogen activator	GP		bind					endothelial cell membrane receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_1_146_s_233	8550827	(1993) Homocysteine-induced modulation of tissue plasminogen activator binding to its endothelial cell membrane receptor.	bind
4197	2	2303	5	10	NULL	0	NULL	homocysteine	AminoAcid		induce					statement 1	Process	modulation of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_1_146_s_233	8550827	(1993) Homocysteine-induced modulation of tissue plasminogen activator binding to its endothelial cell membrane receptor.	bind
4074	1	2303	6	10	NULL	0	NULL	tissue plasminogen activator	GP		bind					endothelial cell membrane receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_1_146_s_233	8550827	(1993) Homocysteine-induced modulation of tissue plasminogen activator binding to its endothelial cell membrane receptor.	bind
4075	2	2303	6	10	NULL	0	NULL	Homocysteine	AminoAcid		induce					statement 1	Process	modulation  of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_1_146_s_233	8550827	(1993) Homocysteine-induced modulation of tissue plasminogen activator binding to its endothelial cell membrane receptor.	bind
4198	1	2304	5	10	NULL	0	NULL	NAD+	Chemical		bind					TrkA	GP	Escherichia coli 			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_13_3491_s_184	9642210	(1993) NAD+ binding to the  Escherichia coli K+-uptake protein TrkA and sequence similarity between TrkA and domains of a family of dehydrogenases suggest a role of NAD+ in bacterial transport.	bind
4199	2	2304	5	10	NULL	0	NULL	TrkA	GP	sequence 	is similar to					dehydrogenases	GP	a family of 	domains of		NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_13_3491_s_184	9642210	(1993) NAD+ binding to the  Escherichia coli K+-uptake protein TrkA and sequence similarity between TrkA and domains of a family of dehydrogenases suggest a role of NAD+ in bacterial transport.	bind
4200	3	2304	5	10	NULL	0	NULL	NAD+	Chemical		is required for					bacterial transport	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_13_3491_s_184	9642210	(1993) NAD+ binding to the  Escherichia coli K+-uptake protein TrkA and sequence similarity between TrkA and domains of a family of dehydrogenases suggest a role of NAD+ in bacterial transport.	bind
4201	4	2304	5	10	NULL	0	NULL	statement 1	Process		suggest					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_13_3491_s_184	9642210	(1993) NAD+ binding to the  Escherichia coli K+-uptake protein TrkA and sequence similarity between TrkA and domains of a family of dehydrogenases suggest a role of NAD+ in bacterial transport.	bind
4202	5	2304	5	10	NULL	0	NULL	statement 2	Process		suggest					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_13_3491_s_184	9642210	(1993) NAD+ binding to the  Escherichia coli K+-uptake protein TrkA and sequence similarity between TrkA and domains of a family of dehydrogenases suggest a role of NAD+ in bacterial transport.	bind
46459	6	2304	5	10	NULL	0	NULL	TrkA	GP	Escherichia coli	is a type of					K+-uptake protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_13_3491_s_184	9642210	(1993) NAD+ binding to the  Escherichia coli K+-uptake protein TrkA and sequence similarity between TrkA and domains of a family of dehydrogenases suggest a role of NAD+ in bacterial transport.	bind
4076	1	2304	6	10	NULL	0	NULL	NAD+	Chemical		bind					TrkA	GP	Escherichia coli			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_13_3491_s_184	9642210	(1993) NAD+ binding to the  Escherichia coli K+-uptake protein TrkA and sequence similarity between TrkA and domains of a family of dehydrogenases suggest a role of NAD+ in bacterial transport.	bind
4077	2	2304	6	10	NULL	0	NULL	TrkA	GP	Escherichia coli	is a type of					K+-uptake protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_13_3491_s_184	9642210	(1993) NAD+ binding to the  Escherichia coli K+-uptake protein TrkA and sequence similarity between TrkA and domains of a family of dehydrogenases suggest a role of NAD+ in bacterial transport.	bind
4078	3	2304	6	10	NULL	0	NULL	NAD+	Chemical		plays a role in					bacterial transport	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_13_3491_s_184	9642210	(1993) NAD+ binding to the  Escherichia coli K+-uptake protein TrkA and sequence similarity between TrkA and domains of a family of dehydrogenases suggest a role of NAD+ in bacterial transport.	bind
46460	4	2304	6	10	NULL	0	NULL	TrkA	GP	sequence	is similar to					dehydrogenases	GP	 family of 	domains of		NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_13_3491_s_184	9642210	(1993) NAD+ binding to the  Escherichia coli K+-uptake protein TrkA and sequence similarity between TrkA and domains of a family of dehydrogenases suggest a role of NAD+ in bacterial transport.	bind
46462	5	2304	6	10	NULL	0	NULL	statement 1	Process		suggest					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_13_3491_s_184	9642210	(1993) NAD+ binding to the  Escherichia coli K+-uptake protein TrkA and sequence similarity between TrkA and domains of a family of dehydrogenases suggest a role of NAD+ in bacterial transport.	bind
46464	6	2304	6	10	NULL	0	NULL	statement 4	Process		suggest					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_13_3491_s_184	9642210	(1993) NAD+ binding to the  Escherichia coli K+-uptake protein TrkA and sequence similarity between TrkA and domains of a family of dehydrogenases suggest a role of NAD+ in bacterial transport.	bind
4203	1	2305	5	10	NULL	0	NULL	NADPH oxidase	GP	phagocyte	bind			Src homology 3 domain		NADPH oxidase	GP	phagocyte	proline-rich targets		NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6312_s_366	12456638	(1994) Assembly of the phagocyte NADPH oxidase: binding of Src homology 3 domains to proline-rich targets.	bind
4079	1	2305	6	10	NULL	0	NULL	NADPH oxidase	GP	phagocyte	bind			Src homology 3 domains		NADPH oxidase	GP	phagocyte	proline-rich targets		NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6312_s_366	12456638	(1994) Assembly of the phagocyte NADPH oxidase: binding of Src homology 3 domains to proline-rich targets.	bind
4204	1	2306	5	10	NULL	0	NULL	semaphorin	GP		bind									C-SRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39647_s_345	10993894	(1997) A novel transmembrane semaphorin can bind C-SRE  Mol.	bind
46465	2	2306	5	10	NULL	0	NULL	semaphorin	GP		is a type of					transmembrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39647_s_345	10993894	(1997) A novel transmembrane semaphorin can bind C-SRE  Mol.	bind
4080	1	2306	6	10	NULL	0	NULL	semaphorin	GP		bind									C-SRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39647_s_345	10993894	(1997) A novel transmembrane semaphorin can bind C-SRE  Mol.	bind
46466	2	2306	6	10	NULL	0	NULL	semaphorin	GP		is a type of					transmembrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39647_s_345	10993894	(1997) A novel transmembrane semaphorin can bind C-SRE  Mol.	bind
4205	1	2307	5	10	NULL	0	NULL	kininogen	GP		bind					endothelial cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1521_s_352	10636838	(1997) Binding of high molecular weight kininogen to human endothelial cells is mediated via a site within domains 2 and 3 of the urokinase receptor.	bind
4206	2	2307	5	10	NULL	0	NULL	urokinase receptor	GP		mediate			site with domain 2		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1521_s_352	10636838	(1997) Binding of high molecular weight kininogen to human endothelial cells is mediated via a site within domains 2 and 3 of the urokinase receptor.	bind
5265	3	2307	5	10	NULL	0	NULL	urokinase receptor	GP		mediate			site with domain 3		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1521_s_352	10636838	(1997) Binding of high molecular weight kininogen to human endothelial cells is mediated via a site within domains 2 and 3 of the urokinase receptor.	bind
4081	1	2307	6	10	NULL	0	NULL	kininogen	GP		bind					endothelial cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1521_s_352	10636838	(1997) Binding of high molecular weight kininogen to human endothelial cells is mediated via a site within domains 2 and 3 of the urokinase receptor.	bind
4082	2	2307	6	10	NULL	0	NULL	urokinase receptor	GP		mediates			site within domain 2		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1521_s_352	10636838	(1997) Binding of high molecular weight kininogen to human endothelial cells is mediated via a site within domains 2 and 3 of the urokinase receptor.	bind
4083	3	2307	6	10	NULL	0	NULL	urokinase receptor	GP		mediates			site within domain 3		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1521_s_352	10636838	(1997) Binding of high molecular weight kininogen to human endothelial cells is mediated via a site within domains 2 and 3 of the urokinase receptor.	bind
4207	1	2308	5	10	NULL	0	NULL	FtsZ	GP		bind		directly			ZipA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_13_3486_s_156	9642209	(1997) Direct binding of FtsZ to ZipA, an essential component of the septal ring structure that mediates cell division in  E. coli.	bind
4208	2	2308	5	10	NULL	0	NULL	ZipA	GP		is a component of					septal ring structure	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_13_3486_s_156	9642209	(1997) Direct binding of FtsZ to ZipA, an essential component of the septal ring structure that mediates cell division in  E. coli.	bind
5266	3	2308	5	10	NULL	0	NULL	septal ring structure	GP		mediate					cell division	Process				NULL	E.coli	NULL	NULL	NULL	NULL	gw60_jbacteriol_180_13_3486_s_156	9642209	(1997) Direct binding of FtsZ to ZipA, an essential component of the septal ring structure that mediates cell division in  E. coli.	bind
4084	1	2308	6	10	NULL	0	NULL	FtsZ	GP		bind		directly			ZipA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_13_3486_s_156	9642209	(1997) Direct binding of FtsZ to ZipA, an essential component of the septal ring structure that mediates cell division in  E. coli.	bind
4085	2	2308	6	10	NULL	0	NULL	ZipA	GP		is a component of					septal ring structure	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_13_3486_s_156	9642209	(1997) Direct binding of FtsZ to ZipA, an essential component of the septal ring structure that mediates cell division in  E. coli.	bind
4086	3	2308	6	10	NULL	0	NULL	septal ring structure	GP		mediates					cell division	Process				NULL	E.coli	NULL	NULL	NULL	NULL	gw60_jbacteriol_180_13_3486_s_156	9642209	(1997) Direct binding of FtsZ to ZipA, an essential component of the septal ring structure that mediates cell division in  E. coli.	bind
4209	1	2309	5	10	NULL	0	NULL	fibroblast growth factor	GP	basic	bind					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1521_s_271	10636838	(1998) Binding of basic fibroblast growth factor to fibrinogen and fibrin.	bind
4210	2	2309	5	10	NULL	0	NULL	fibroblast growth factor	GP	basic	bind					fibrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1521_s_271	10636838	(1998) Binding of basic fibroblast growth factor to fibrinogen and fibrin.	bind
4087	1	2309	6	10	NULL	0	NULL	fibroblast growth factor	GP	basic	bind					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1521_s_271	10636838	(1998) Binding of basic fibroblast growth factor to fibrinogen and fibrin.	bind
4088	2	2309	6	10	NULL	0	NULL	fibroblast growth factor	GP	basic	bind					fibrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1521_s_271	10636838	(1998) Binding of basic fibroblast growth factor to fibrinogen and fibrin.	bind
4211	1	2310	5	10	NULL	0	NULL	CcpA	GP		bind					xyn	GP	Bacillus subtilis		cre	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_3917_s_383	11483495	(1999) Phosphoryl ation of either crh or HPr mediates binding of CcpA to the  Bacillus subtilis xyn cre and catabolite repression of the  xyn operon.	bind
4212	2	2310	5	10	NULL	0	NULL	crh	GP	phosphorylation of	mediate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_3917_s_383	11483495	(1999) Phosphoryl ation of either crh or HPr mediates binding of CcpA to the  Bacillus subtilis xyn cre and catabolite repression of the  xyn operon.	bind
4213	3	2310	5	10	NULL	0	NULL	HPr	GP	phosphorylation of	mediate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_3917_s_383	11483495	(1999) Phosphoryl ation of either crh or HPr mediates binding of CcpA to the  Bacillus subtilis xyn cre and catabolite repression of the  xyn operon.	bind
4214	4	2310	5	10	NULL	0	NULL	crh	GP	phosphorylation of	mediate					xyn operon	NucleicAcid	catabolite repression of			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_3917_s_383	11483495	(1999) Phosphoryl ation of either crh or HPr mediates binding of CcpA to the  Bacillus subtilis xyn cre and catabolite repression of the  xyn operon.	bind
4215	5	2310	5	10	NULL	0	NULL	HPr	GP	phosphorylation of	mediate					xyn operon	NucleicAcid	catabolite repression of			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_3917_s_383	11483495	(1999) Phosphoryl ation of either crh or HPr mediates binding of CcpA to the  Bacillus subtilis xyn cre and catabolite repression of the  xyn operon.	bind
5267	6	2310	5	10	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_3917_s_383	11483495	(1999) Phosphoryl ation of either crh or HPr mediates binding of CcpA to the  Bacillus subtilis xyn cre and catabolite repression of the  xyn operon.	bind
5268	7	2310	5	10	NULL	0	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_3917_s_383	11483495	(1999) Phosphoryl ation of either crh or HPr mediates binding of CcpA to the  Bacillus subtilis xyn cre and catabolite repression of the  xyn operon.	bind
4089	1	2310	6	10	NULL	0	NULL	CcpA	GP		bind					xyn	GP	Bacillus subtilis 		CRE	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_3917_s_383	11483495	(1999) Phosphoryl ation of either crh or HPr mediates binding of CcpA to the  Bacillus subtilis xyn cre and catabolite repression of the  xyn operon.	bind
4090	2	2310	6	10	NULL	0	NULL	crh	GP	phosphorylation of	mediates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_3917_s_383	11483495	(1999) Phosphoryl ation of either crh or HPr mediates binding of CcpA to the  Bacillus subtilis xyn cre and catabolite repression of the  xyn operon.	bind
4091	3	2310	6	10	NULL	0	NULL	Hpr	GP	phosphorylation of	mediates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_3917_s_383	11483495	(1999) Phosphoryl ation of either crh or HPr mediates binding of CcpA to the  Bacillus subtilis xyn cre and catabolite repression of the  xyn operon.	bind
4092	4	2310	6	10	NULL	0	NULL	crh	GP	phosphorylation of	mediates					Xyn operon	NucleicAcid	catabolite repression of			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_3917_s_383	11483495	(1999) Phosphoryl ation of either crh or HPr mediates binding of CcpA to the  Bacillus subtilis xyn cre and catabolite repression of the  xyn operon.	bind
4093	5	2310	6	10	NULL	0	NULL	Hpr	GP	phosphorylation of	mediates					Xyn operon	NucleicAcid	catabolite repression of			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_3917_s_383	11483495	(1999) Phosphoryl ation of either crh or HPr mediates binding of CcpA to the  Bacillus subtilis xyn cre and catabolite repression of the  xyn operon.	bind
4987	6	2310	6	10	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_3917_s_383	11483495	(1999) Phosphoryl ation of either crh or HPr mediates binding of CcpA to the  Bacillus subtilis xyn cre and catabolite repression of the  xyn operon.	bind
4988	7	2310	6	10	NULL	0	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_15_3917_s_383	11483495	(1999) Phosphoryl ation of either crh or HPr mediates binding of CcpA to the  Bacillus subtilis xyn cre and catabolite repression of the  xyn operon.	bind
4216	1	2311	5	10	NULL	0	NULL	actin	GP		bind					profilin	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_86	11294914	(2)   Three reactions contributed to the observed dissociation rate constant,  kobs: dissociation from free actin (Af), actin bound to wild-type profilin (Awt), and actin bound to Y79R profilin (Amu).	bind
4217	2	2311	5	10	NULL	0	NULL	actin	GP		bind					profilin	GP		Y79R		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_86	11294914	(2)   Three reactions contributed to the observed dissociation rate constant,  kobs: dissociation from free actin (Af), actin bound to wild-type profilin (Awt), and actin bound to Y79R profilin (Amu).	bind
4094	1	2311	6	10	NULL	0	NULL	actin	GP		bind					profilin	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_86	11294914	(2)   Three reactions contributed to the observed dissociation rate constant,  kobs: dissociation from free actin (Af), actin bound to wild-type profilin (Awt), and actin bound to Y79R profilin (Amu).	bind
4095	2	2311	6	10	NULL	0	NULL	actin	GP		bind					profilin	GP		Y79R		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_86	11294914	(2)   Three reactions contributed to the observed dissociation rate constant,  kobs: dissociation from free actin (Af), actin bound to wild-type profilin (Awt), and actin bound to Y79R profilin (Amu).	bind
4220	1	2312	5	10	NULL	0	NULL	p53	GP	total cytoplasmic	bind					Parc	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_1_1_s_33	12526785	(2) A large fraction of total cytoplasmic p53 is bound to Parc.	bind
4096	1	2312	6	10	NULL	0	NULL	p53	GP	total cytoplasmic	bind					Parc	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_1_1_s_33	12526785	(2) A large fraction of total cytoplasmic p53 is bound to Parc.	bind
4221	1	2313	5	10	NULL	0	NULL	Mdv1p	GP		bind					Fis1p	GP		TPR-like binding pocket		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_2_291_s_272	16247028	(2) Assembly begins when Mdv1p binds the Fis1p TPR-like binding pocket.	bind
4097	1	2313	6	10	NULL	0	NULL	Mdv1p	GP		bind					Fis1p	GP		TPR-like binding pocket		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_2_291_s_272	16247028	(2) Assembly begins when Mdv1p binds the Fis1p TPR-like binding pocket.	bind
4222	1	2314	5	10	NULL	0	NULL	AP-1	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-leukoc-biol_67_2_10670587_s_6	10670587	(2) At high (50 microM) concentration  it prevents translocation of PKCalpha, and subsequently inhibits ERK1/ERK2  phosphorylation, DNA binding activities of AP-1 and nuclear factor-KB  transcription factors, and the production of both tested cytokines.	bind
46467	2	2314	5	10	NULL	0	NULL	AP-1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-leukoc-biol_67_2_10670587_s_6	10670587	(2) At high (50 microM) concentration  it prevents translocation of PKCalpha, and subsequently inhibits ERK1/ERK2  phosphorylation, DNA binding activities of AP-1 and nuclear factor-KB  transcription factors, and the production of both tested cytokines.	bind
46468	3	2314	5	10	NULL	0	NULL	nuclear factor-KB 	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-leukoc-biol_67_2_10670587_s_6	10670587	(2) At high (50 microM) concentration  it prevents translocation of PKCalpha, and subsequently inhibits ERK1/ERK2  phosphorylation, DNA binding activities of AP-1 and nuclear factor-KB  transcription factors, and the production of both tested cytokines.	bind
46469	4	2314	5	10	NULL	0	NULL	nuclear factor-KB 	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-leukoc-biol_67_2_10670587_s_6	10670587	(2) At high (50 microM) concentration  it prevents translocation of PKCalpha, and subsequently inhibits ERK1/ERK2  phosphorylation, DNA binding activities of AP-1 and nuclear factor-KB  transcription factors, and the production of both tested cytokines.	bind
4098	1	2314	6	10	NULL	0	NULL	AP-1	GP		bind					DNA	NucleicAcid			site	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-leukoc-biol_67_2_10670587_s_6	10670587	(2) At high (50 microM) concentration  it prevents translocation of PKCalpha, and subsequently inhibits ERK1/ERK2  phosphorylation, DNA binding activities of AP-1 and nuclear factor-KB  transcription factors, and the production of both tested cytokines.	bind
4099	2	2314	6	10	NULL	0	NULL	nuclear factor-KB	GP		bind					DNA	NucleicAcid			site	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-leukoc-biol_67_2_10670587_s_6	10670587	(2) At high (50 microM) concentration  it prevents translocation of PKCalpha, and subsequently inhibits ERK1/ERK2  phosphorylation, DNA binding activities of AP-1 and nuclear factor-KB  transcription factors, and the production of both tested cytokines.	bind
46470	3	2314	6	10	NULL	0	NULL	AP-1 	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-leukoc-biol_67_2_10670587_s_6	10670587	(2) At high (50 microM) concentration  it prevents translocation of PKCalpha, and subsequently inhibits ERK1/ERK2  phosphorylation, DNA binding activities of AP-1 and nuclear factor-KB  transcription factors, and the production of both tested cytokines.	bind
46471	4	2314	6	10	NULL	0	NULL	nuclear factor-KB 	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-leukoc-biol_67_2_10670587_s_6	10670587	(2) At high (50 microM) concentration  it prevents translocation of PKCalpha, and subsequently inhibits ERK1/ERK2  phosphorylation, DNA binding activities of AP-1 and nuclear factor-KB  transcription factors, and the production of both tested cytokines.	bind
4223	1	2315	5	10	NULL	0	NULL	InsP3R	GP		bind					PIP2	GP				NULL	lipid rafts	NULL	NULL	NULL	NULL	gw60_neuron_34_2_173_s_34	11970857	(2) Binding between the InsP3R and PIP2 found in lipid rafts can facilitate rapid signaling.	bind
4225	2	2315	5	10	NULL	0	NULL	statement 1	GP		facilitate					rapid signaling	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_2_173_s_34	11970857	(2) Binding between the InsP3R and PIP2 found in lipid rafts can facilitate rapid signaling.	bind
4100	1	2315	6	10	NULL	0	NULL	InsP3R	GP		bind					PIP2	GP				NULL	lipid rafts	NULL	NULL	NULL	NULL	gw60_neuron_34_2_173_s_34	11970857	(2) Binding between the InsP3R and PIP2 found in lipid rafts can facilitate rapid signaling.	bind
4101	2	2315	6	10	NULL	0	NULL	statement 1	Process		facilitate					rapid signaling	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_2_173_s_34	11970857	(2) Binding between the InsP3R and PIP2 found in lipid rafts can facilitate rapid signaling.	bind
4226	1	2317	5	10	NULL	0	NULL	PSA	GP		bind					phage-displayed peptides	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_zhejiang-da-xue-xue-bao-yi-xue-ban_34_5_16216051_s_6	16216051	(2) Dot blot  was used to analyze the influence of the alpha-Met-D-mannoside on binding  between PSA and phage-displayed peptides.	bind
4102	1	2317	6	10	NULL	0	NULL	PSA	GP		bind					phage-displayed peptides	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_zhejiang-da-xue-xue-bao-yi-xue-ban_34_5_16216051_s_6	16216051	(2) Dot blot  was used to analyze the influence of the alpha-Met-D-mannoside on binding  between PSA and phage-displayed peptides.	bind
4228	1	2318	5	10	NULL	0	NULL	EHD3	GP		bind					Rab11-FIP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
4229	2	2318	5	10	NULL	0	NULL	statement 1	Process		occurs via					EH - NPF 	GP	interactions			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
4867	3	2318	5	10	NULL	0	NULL	vesicles	CellComponent		carry					Rab11-FIP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
4868	4	2318	5	10	NULL	0	NULL	vesicles	CellComponent		carry		possibly			Rab11	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
4869	6	2318	5	10	NULL	0	NULL	statement 3	Process		transported to					ERC	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
4870	7	2318	5	10	NULL	0	NULL	statement 4	Process		transported from					early endosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
4871	8	2318	5	10	NULL	0	NULL	statement 4	Process		transported to					ERC	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
4872	11	2318	5	10	NULL	0	NULL	statement 9	Process		function in					EHD1	GP	 concert with			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
52994	5	2318	5	10	NULL	0	NULL	statement 3	Process		transported from					early endosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
52999	9	2318	5	10	NULL	0	NULL	statement 6	Process		occur after					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
53000	10	2318	5	10	NULL	0	NULL	statement 8	Process		occur after					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
53001	12	2318	5	10	NULL	0	NULL	statement 10	Process		function in					EHD1	GP	concert with			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
4634	1	2318	6	10	NULL	0	NULL	EHD3	GP		bind					Rab11-FIP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
4635	2	2318	6	10	NULL	0	NULL	statement 1	Process		via					EH - NPF interactions	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
4636	3	2318	6	10	NULL	0	NULL	vesicles	CellComponent		carry					Rab11-FIP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
4637	4	2318	6	10	NULL	0	NULL	vesicles	CellComponent		carry		possibly			Rab11	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
4638	5	2318	6	10	NULL	0	NULL	statement 3	Process		transported from					early endosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
4639	6	2318	6	10	NULL	0	NULL	statement 3	Process		transported to					ERC	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
4640	7	2318	6	10	NULL	0	NULL	statement 4	Process		transported from					early endosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
53002	8	2318	6	10	NULL	0	NULL	statement 4	Process		transported to					ERC	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
53003	9	2318	6	10	NULL	0	NULL	statement 6	Process		occur after					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
53004	10	2318	6	10	NULL	0	NULL	statement 8	Process		occur after					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
53005	11	2318	6	10	NULL	0	NULL	statement 9	Process		function in					EHD1	GP	concert with			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
53006	12	2318	6	10	NULL	0	NULL	statement 10	Process		function in					EHD1	GP	concert with			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_163_s_338	16251358	(2) EHD3 also binds to Rab11-FIP2  via EH - NPF interactions and may play an additional role in transport of vesicles  carrying Rab11-FIP2 (and possibly Rab11) from the early endosome to the ERC, where  they function in concert with EHD1 to control recycling from the ERC to the PM.	bind
4147	1	2319	6	10	NULL	0	NULL	gene regulatory protein	GP	unidentified	bind		hypothetically			RNR3	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_4_502_s_292	12600943	(2) Even if an unidentified gene regulatory protein binds to the  RNR3 promoter, it is insufficient to maintain the presence of SWI/SNF and PIC components at the promoter.	bind
4277	1	2320	5	10	NULL	0	NULL	IQ peptides	GP	free	bind					calmodulin	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_22_7_2487_s_252	11923413	(2) High concentrations of free IQ peptides, which should bind to endogenous calmodulin, had no effect on Myo1c binding.	bind
4278	2	2320	5	10	NULL	0	NULL	statement 1	Process		does not effect					Myo1c	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_22_7_2487_s_252	11923413	(2) High concentrations of free IQ peptides, which should bind to endogenous calmodulin, had no effect on Myo1c binding.	bind
4148	1	2320	6	10	NULL	0	NULL	IQ peptides	GP	free	bind					calmodulin	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_22_7_2487_s_252	11923413	(2) High concentrations of free IQ peptides, which should bind to endogenous calmodulin, had no effect on Myo1c binding.	bind
4149	2	2320	6	10	NULL	0	NULL	statement 1	Process		has no effect on					Myo1c	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_22_7_2487_s_252	11923413	(2) High concentrations of free IQ peptides, which should bind to endogenous calmodulin, had no effect on Myo1c binding.	bind
4279	1	2321	5	10	NULL	0	NULL	anti-CRP antibody	GP	labeled	bind					FcgammaRIIa receptors	GP				NULL	in antibody solution	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2372_s_172	15486314	(2) In contrast, binding of labeled anti-CRP antibody alone to FcgammaRIIa receptors can only be observed as long as the antibody is present in solution.	bind
4150	1	2321	6	10	NULL	0	NULL	anti-CRP antibody	GP	labeled	bind					FcgammaRIIa receptors	GP				NULL	in antibody solution	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2372_s_172	15486314	(2) In contrast, binding of labeled anti-CRP antibody alone to FcgammaRIIa receptors can only be observed as long as the antibody is present in solution.	bind
4281	1	2322	5	10	NULL	0	NULL	CCR4-NOT protein	GP		bind		directly			TBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_3_1045_s_226	10880468	(2) It is possible that the CCR4-NOT proteins bind directly to TBP and prevent the interaction of TBP with other stabilizing factors like TFIIA and SPT3.	bind
4282	2	2322	5	10	NULL	0	NULL	TBP	GP		interact					TFIIA	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_3_1045_s_226	10880468	(2) It is possible that the CCR4-NOT proteins bind directly to TBP and prevent the interaction of TBP with other stabilizing factors like TFIIA and SPT3.	bind
4283	3	2322	5	10	NULL	0	NULL	TBP	GP		interact					SPT3	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_3_1045_s_226	10880468	(2) It is possible that the CCR4-NOT proteins bind directly to TBP and prevent the interaction of TBP with other stabilizing factors like TFIIA and SPT3.	bind
4284	4	2322	5	10	NULL	0	NULL	statement 1	Process		prevent					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_3_1045_s_226	10880468	(2) It is possible that the CCR4-NOT proteins bind directly to TBP and prevent the interaction of TBP with other stabilizing factors like TFIIA and SPT3.	bind
4285	5	2322	5	10	NULL	0	NULL	statement 1	Process		prevent					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_3_1045_s_226	10880468	(2) It is possible that the CCR4-NOT proteins bind directly to TBP and prevent the interaction of TBP with other stabilizing factors like TFIIA and SPT3.	bind
46472	6	2322	5	10	NULL	0	NULL	TFIIA	GP		is a type of					stabilizing factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_3_1045_s_226	10880468	(2) It is possible that the CCR4-NOT proteins bind directly to TBP and prevent the interaction of TBP with other stabilizing factors like TFIIA and SPT3.	bind
46473	7	2322	5	10	NULL	0	NULL	SPT3	GP		is a type of					stabilizing factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_3_1045_s_226	10880468	(2) It is possible that the CCR4-NOT proteins bind directly to TBP and prevent the interaction of TBP with other stabilizing factors like TFIIA and SPT3.	bind
4151	1	2322	6	10	NULL	0	NULL	CCR4-NOT protein	GP		bind		directly			TBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_3_1045_s_226	10880468	(2) It is possible that the CCR4-NOT proteins bind directly to TBP and prevent the interaction of TBP with other stabilizing factors like TFIIA and SPT3.	bind
4152	2	2322	6	10	NULL	0	NULL	TBP	GP		interact with					TFIIA	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_3_1045_s_226	10880468	(2) It is possible that the CCR4-NOT proteins bind directly to TBP and prevent the interaction of TBP with other stabilizing factors like TFIIA and SPT3.	bind
4153	3	2322	6	10	NULL	0	NULL	TBP	GP		interact with					SPT3	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_3_1045_s_226	10880468	(2) It is possible that the CCR4-NOT proteins bind directly to TBP and prevent the interaction of TBP with other stabilizing factors like TFIIA and SPT3.	bind
4154	4	2322	6	10	NULL	0	NULL	statement 1	Process		prevents					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_3_1045_s_226	10880468	(2) It is possible that the CCR4-NOT proteins bind directly to TBP and prevent the interaction of TBP with other stabilizing factors like TFIIA and SPT3.	bind
4155	5	2322	6	10	NULL	0	NULL	statement 1	Process		prevents					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_3_1045_s_226	10880468	(2) It is possible that the CCR4-NOT proteins bind directly to TBP and prevent the interaction of TBP with other stabilizing factors like TFIIA and SPT3.	bind
46474	6	2322	6	10	NULL	0	NULL	TFIIA	GP		is a type of					stabilizing factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_3_1045_s_226	10880468	(2) It is possible that the CCR4-NOT proteins bind directly to TBP and prevent the interaction of TBP with other stabilizing factors like TFIIA and SPT3.	bind
46475	7	2322	6	10	NULL	0	NULL	SPT3	GP		is a type of					stabilizing factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_3_1045_s_226	10880468	(2) It is possible that the CCR4-NOT proteins bind directly to TBP and prevent the interaction of TBP with other stabilizing factors like TFIIA and SPT3.	bind
4286	1	2323	5	10	NULL	0	NULL	SRF	GP		bind									CArG B	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_81_4_600_s_253	9314842	(2) MHox enhanced SRF binding to CArG B (Fig 6  ).	bind
4287	2	2323	5	10	NULL	0	NULL	MHox	GP		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_81_4_600_s_253	9314842	(2) MHox enhanced SRF binding to CArG B (Fig 6  ).	bind
4156	1	2323	6	10	NULL	0	NULL	SRF	GP		bind									CArG B	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_81_4_600_s_253	9314842	(2) MHox enhanced SRF binding to CArG B (Fig 6  ).	bind
4157	2	2323	6	10	NULL	0	NULL	MHox	GP		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_81_4_600_s_253	9314842	(2) MHox enhanced SRF binding to CArG B (Fig 6  ).	bind
4288	1	2324	5	10	NULL	0	NULL	 CbbR dimer	GP		bind					IR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1245_s_237	12562794	(2) One CbbR dimer bound to IR1.	bind
4158	1	2324	6	10	NULL	0	NULL	CbbR dimer	GP		bind					IR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1245_s_237	12562794	(2) One CbbR dimer bound to IR1.	bind
4289	1	2325	5	10	NULL	0	NULL	CSP	GP		bind					Hsc70	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_31_6_987_s_308	11580898	(2) Simultaneous binding of CSP and SGT to Hsc70 maximally stimulates the ATPase activity of Hsc70 to a level 19-fold higherR than that of Hsc70 alone.	bind
4290	2	2325	5	10	NULL	0	NULL	SGT	GP		bind					Hsc70	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_31_6_987_s_308	11580898	(2) Simultaneous binding of CSP and SGT to Hsc70 maximally stimulates the ATPase activity of Hsc70 to a level 19-fold higherR than that of Hsc70 alone.	bind
4291	3	2325	5	10	NULL	0	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_31_6_987_s_308	11580898	(2) Simultaneous binding of CSP and SGT to Hsc70 maximally stimulates the ATPase activity of Hsc70 to a level 19-fold higherR than that of Hsc70 alone.	bind
4292	5	2325	5	10	NULL	0	NULL	statement 3	Process		stimulate					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_31_6_987_s_308	11580898	(2) Simultaneous binding of CSP and SGT to Hsc70 maximally stimulates the ATPase activity of Hsc70 to a level 19-fold higherR than that of Hsc70 alone.	bind
53007	4	2325	5	10	NULL	0	NULL	Hsc70	GP		activates					ATPase	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_31_6_987_s_308	11580898	(2) Simultaneous binding of CSP and SGT to Hsc70 maximally stimulates the ATPase activity of Hsc70 to a level 19-fold higherR than that of Hsc70 alone.	bind
4159	1	2325	6	10	NULL	0	NULL	CSP	GP		bind					Hsc70	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_31_6_987_s_308	11580898	(2) Simultaneous binding of CSP and SGT to Hsc70 maximally stimulates the ATPase activity of Hsc70 to a level 19-fold higherR than that of Hsc70 alone.	bind
4160	2	2325	6	10	NULL	0	NULL	SGT	GP		bind					Hsc70	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_31_6_987_s_308	11580898	(2) Simultaneous binding of CSP and SGT to Hsc70 maximally stimulates the ATPase activity of Hsc70 to a level 19-fold higherR than that of Hsc70 alone.	bind
4161	3	2325	6	10	NULL	0	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_31_6_987_s_308	11580898	(2) Simultaneous binding of CSP and SGT to Hsc70 maximally stimulates the ATPase activity of Hsc70 to a level 19-fold higherR than that of Hsc70 alone.	bind
4162	5	2325	6	10	NULL	0	NULL	statement 3	Process		stimulates					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_31_6_987_s_308	11580898	(2) Simultaneous binding of CSP and SGT to Hsc70 maximally stimulates the ATPase activity of Hsc70 to a level 19-fold higherR than that of Hsc70 alone.	bind
53008	4	2325	6	10	NULL	0	NULL	Hsc70	GP		activates					ATPase	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_31_6_987_s_308	11580898	(2) Simultaneous binding of CSP and SGT to Hsc70 maximally stimulates the ATPase activity of Hsc70 to a level 19-fold higherR than that of Hsc70 alone.	bind
4293	1	2328	5	10	NULL	0	NULL	signal receptor	GP	soluble	bind					cognate membrane receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_491_s_43	12600313	(2) The ribosome nascent chain complex (RNC) is targeted to the membrane by the binding of the soluble signal receptor to a cognate membrane receptor.	bind
4294	2	2328	5	10	NULL	0	NULL	RNC	GP		is targeted to					membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_491_s_43	12600313	(2) The ribosome nascent chain complex (RNC) is targeted to the membrane by the binding of the soluble signal receptor to a cognate membrane receptor.	bind
4295	3	2328	5	10	NULL	0	NULL	RNC 	GP		is					ribosome nascent chain complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_491_s_43	12600313	(2) The ribosome nascent chain complex (RNC) is targeted to the membrane by the binding of the soluble signal receptor to a cognate membrane receptor.	bind
4296	4	2328	5	10	NULL	0	NULL	statement 2	Process		is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_491_s_43	12600313	(2) The ribosome nascent chain complex (RNC) is targeted to the membrane by the binding of the soluble signal receptor to a cognate membrane receptor.	bind
4163	1	2328	6	10	NULL	0	NULL	signal receptor	GP	soluble	bind					cognate membrane receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_491_s_43	12600313	(2) The ribosome nascent chain complex (RNC) is targeted to the membrane by the binding of the soluble signal receptor to a cognate membrane receptor.	bind
4164	2	2328	6	10	NULL	0	NULL	RNC	GP		targeted to					membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_491_s_43	12600313	(2) The ribosome nascent chain complex (RNC) is targeted to the membrane by the binding of the soluble signal receptor to a cognate membrane receptor.	bind
4165	3	2328	6	10	NULL	0	NULL	RNC  	GP		is					ribosome nascent chain complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_491_s_43	12600313	(2) The ribosome nascent chain complex (RNC) is targeted to the membrane by the binding of the soluble signal receptor to a cognate membrane receptor.	bind
4166	4	2328	6	10	NULL	0	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_491_s_43	12600313	(2) The ribosome nascent chain complex (RNC) is targeted to the membrane by the binding of the soluble signal receptor to a cognate membrane receptor.	bind
4357	1	2329	5	10	NULL	0	NULL	AK	GP	one native form of	bind					AMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_528_1_161_s_40	12297297	(2) There are two native forms of AK existing in solution, of which one binds with substrates AMP, MgATP, as well as ANS and AP5A, whereas the other binds with ADP and MgADP but not with ANS and AP5A.	bind
4358	2	2329	5	10	NULL	0	NULL	AK	GP	one native form of	bind					MgATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_528_1_161_s_40	12297297	(2) There are two native forms of AK existing in solution, of which one binds with substrates AMP, MgATP, as well as ANS and AP5A, whereas the other binds with ADP and MgADP but not with ANS and AP5A.	bind
4359	4	2329	5	10	NULL	0	NULL	AK	GP	one native form of	bind					ANS	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_528_1_161_s_40	12297297	(2) There are two native forms of AK existing in solution, of which one binds with substrates AMP, MgATP, as well as ANS and AP5A, whereas the other binds with ADP and MgADP but not with ANS and AP5A.	bind
4360	3	2329	5	10	NULL	0	NULL	AK	GP	one native form of	bind					AP5A	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_528_1_161_s_40	12297297	(2) There are two native forms of AK existing in solution, of which one binds with substrates AMP, MgATP, as well as ANS and AP5A, whereas the other binds with ADP and MgADP but not with ANS and AP5A.	bind
4361	6	2329	5	10	NULL	0	NULL	AK	GP	other native form of	bind					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_528_1_161_s_40	12297297	(2) There are two native forms of AK existing in solution, of which one binds with substrates AMP, MgATP, as well as ANS and AP5A, whereas the other binds with ADP and MgADP but not with ANS and AP5A.	bind
4362	7	2329	5	10	NULL	0	NULL	AK	GP	other native form of	bind					MgADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_528_1_161_s_40	12297297	(2) There are two native forms of AK existing in solution, of which one binds with substrates AMP, MgATP, as well as ANS and AP5A, whereas the other binds with ADP and MgADP but not with ANS and AP5A.	bind
4363	8	2329	5	10	NULL	0	NULL	AK	GP	other native form of	does not bind					ANS	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_528_1_161_s_40	12297297	(2) There are two native forms of AK existing in solution, of which one binds with substrates AMP, MgATP, as well as ANS and AP5A, whereas the other binds with ADP and MgADP but not with ANS and AP5A.	bind
4364	5	2329	5	10	NULL	0	NULL	AK	GP	other native form of	does not bind					AP5A	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_528_1_161_s_40	12297297	(2) There are two native forms of AK existing in solution, of which one binds with substrates AMP, MgATP, as well as ANS and AP5A, whereas the other binds with ADP and MgADP but not with ANS and AP5A.	bind
4167	1	2329	6	10	NULL	0	NULL	AK 	GP	one native form of	bind					AMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_528_1_161_s_40	12297297	(2) There are two native forms of AK existing in solution, of which one binds with substrates AMP, MgATP, as well as ANS and AP5A, whereas the other binds with ADP and MgADP but not with ANS and AP5A.	bind
4168	2	2329	6	10	NULL	0	NULL	AK	GP	one native form of	bind					MgATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_528_1_161_s_40	12297297	(2) There are two native forms of AK existing in solution, of which one binds with substrates AMP, MgATP, as well as ANS and AP5A, whereas the other binds with ADP and MgADP but not with ANS and AP5A.	bind
4169	3	2329	6	10	NULL	0	NULL	AK 	GP	one native form of	bind					ANS	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_528_1_161_s_40	12297297	(2) There are two native forms of AK existing in solution, of which one binds with substrates AMP, MgATP, as well as ANS and AP5A, whereas the other binds with ADP and MgADP but not with ANS and AP5A.	bind
4170	4	2329	6	10	NULL	0	NULL	AK	GP	one native form of	bind					AP5A	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_528_1_161_s_40	12297297	(2) There are two native forms of AK existing in solution, of which one binds with substrates AMP, MgATP, as well as ANS and AP5A, whereas the other binds with ADP and MgADP but not with ANS and AP5A.	bind
4171	5	2329	6	10	NULL	0	NULL	AK 	GP	other native form of	bind					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_528_1_161_s_40	12297297	(2) There are two native forms of AK existing in solution, of which one binds with substrates AMP, MgATP, as well as ANS and AP5A, whereas the other binds with ADP and MgADP but not with ANS and AP5A.	bind
4172	6	2329	6	10	NULL	0	NULL	AK 	GP	other native form of	bind					MgADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_528_1_161_s_40	12297297	(2) There are two native forms of AK existing in solution, of which one binds with substrates AMP, MgATP, as well as ANS and AP5A, whereas the other binds with ADP and MgADP but not with ANS and AP5A.	bind
4173	7	2329	6	10	NULL	0	NULL	AK 	GP	other native form of	does not bind					ANS	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_528_1_161_s_40	12297297	(2) There are two native forms of AK existing in solution, of which one binds with substrates AMP, MgATP, as well as ANS and AP5A, whereas the other binds with ADP and MgADP but not with ANS and AP5A.	bind
4174	8	2329	6	10	NULL	0	NULL	AK 	GP	other native form of	does not bind					AP5A	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_528_1_161_s_40	12297297	(2) There are two native forms of AK existing in solution, of which one binds with substrates AMP, MgATP, as well as ANS and AP5A, whereas the other binds with ADP and MgADP but not with ANS and AP5A.	bind
4369	1	2330	5	10	NULL	0	NULL	cellular membrane	CellComponent		is linked to					actin cytoskeleton	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
4370	2	2330	5	10	NULL	0	NULL	ezrin	GP		is necessary for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
4371	3	2330	5	10	NULL	0	NULL	moesin	GP		is necessary for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
4372	4	2330	5	10	NULL	0	NULL	pili- dependent adhesion	Process		induce					ezrin	GP	recruitment of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
4373	5	2330	5	10	NULL	0	NULL	statement 4	Process		occurs through					Rho GTPase-independent pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
4374	6	2330	5	10	NULL	0	NULL	pili- dependent adhesion	Process		induce					moesin	GP	recruitment of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
4375	7	2330	5	10	NULL	0	NULL	statement 6	Process		occurs through					Rho GTPase-independent pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
4376	8	2330	5	10	NULL	0	NULL	CD44	GP		bind					ezrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
4377	9	2330	5	10	NULL	0	NULL	ICAM-1	GP		bind					ezrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
4378	10	2330	5	10	NULL	0	NULL	ErbB2	GP		cluster					statement 8	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
4379	11	2330	5	10	NULL	0	NULL	ErbB2	GP		cluster					statement 9	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
4380	12	2330	5	10	NULL	0	NULL	pili- dependent adhesion	Process		induce					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
4381	13	2330	5	10	NULL	0	NULL	pili- dependent adhesion	Process		induce					statement 11	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
4382	14	2330	5	10	NULL	0	NULL	statement 12	Process		occurs through					Rho GTPase-independent pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
4383	15	2330	5	10	NULL	0	NULL	statement 13	Process		occurs through					Rho GTPase-independent pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
4643	1	2330	6	10	NULL	0	NULL	cellular membrane	CellComponent		linked to					actin cytoskeleton	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
4644	4	2330	6	10	NULL	0	NULL	pili- dependent adhesion	Process		induce					ezrin	GP	recruitment of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
4645	5	2330	6	10	NULL	0	NULL	statement 4	Process		occurs through					Rho GTPase-independent pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
5775	2	2330	6	10	NULL	0	NULL	ezrin	GP		is necessary for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
5776	3	2330	6	10	NULL	0	NULL	moesin	GP		is necessary for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
5777	6	2330	6	10	NULL	0	NULL	pili- dependent adhesion	Process		induce					moesin	GP	recruitment of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
5778	7	2330	6	10	NULL	0	NULL	statement 6	Process		occurs through					Rho GTPase-independent pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
5779	8	2330	6	10	NULL	0	NULL	CD44	GP		bind					ezrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
5780	9	2330	6	10	NULL	0	NULL	ICAM-1	GP		bind					ezrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
5781	10	2330	6	10	NULL	0	NULL	ErbB2	GP		forms cluster with					statement 8	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
5782	11	2330	6	10	NULL	0	NULL	ErbB2	GP		forms cluster with					statement 9	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
5783	12	2330	6	10	NULL	0	NULL	pili- dependent adhesion	Process		induce					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
5784	13	2330	6	10	NULL	0	NULL	pili- dependent adhesion	Process		induce					statement 11	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
5785	14	2330	6	10	NULL	0	NULL	statement 12	Process		occurs through					Rho GTPase-independent pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
5786	15	2330	6	10	NULL	0	NULL	statement 13	Process		occurs through					Rho GTPase-independent pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_133_s_248	11581290	(2) This pili- dependent adhesion induces, through a Rho GTPase-independent pathway, the recruitment of ezrin and moesin, two proteins that link the cellular membrane to the actin cytoskeleton, and the clustering of several transmembrane proteins: ErbB2 and the ezrin binding proteins CD44 and ICAM-1.	bind
4365	1	2331	5	10	NULL	0	NULL	VAF	GP		bind					IRF7	GP			ISRE	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12262_s_214	15664995	(2) VAF upon virus infection also binds to IRF7 ISRE and IRFE and activates IRF7 transcription.	bind
4366	2	2331	5	10	NULL	0	NULL	VAF	GP		bind					IRF7	GP			IRFE	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12262_s_214	15664995	(2) VAF upon virus infection also binds to IRF7 ISRE and IRFE and activates IRF7 transcription.	bind
4367	3	2331	5	10	NULL	0	NULL	statement 1	Process		activate					IRF7 	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12262_s_214	15664995	(2) VAF upon virus infection also binds to IRF7 ISRE and IRFE and activates IRF7 transcription.	bind
4368	4	2331	5	10	NULL	0	NULL	statement 2	Process		activate					IRF7 	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12262_s_214	15664995	(2) VAF upon virus infection also binds to IRF7 ISRE and IRFE and activates IRF7 transcription.	bind
53013	5	2331	5	10	NULL	0	NULL	statement 1	Process		occur upon					virus	Organism	infection of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12262_s_214	15664995	(2) VAF upon virus infection also binds to IRF7 ISRE and IRFE and activates IRF7 transcription.	bind
53014	6	2331	5	10	NULL	0	NULL	statement 2	Process		occur upon					virus	Organism	infection of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12262_s_214	15664995	(2) VAF upon virus infection also binds to IRF7 ISRE and IRFE and activates IRF7 transcription.	bind
53015	7	2331	5	10	NULL	0	NULL	statement 3	Process		occur upon					virus	Organism	infection of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12262_s_214	15664995	(2) VAF upon virus infection also binds to IRF7 ISRE and IRFE and activates IRF7 transcription.	bind
53016	8	2331	5	10	NULL	0	NULL	statement 4	Process		occur upon					virus	Organism	infection of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12262_s_214	15664995	(2) VAF upon virus infection also binds to IRF7 ISRE and IRFE and activates IRF7 transcription.	bind
4414	1	2331	6	10	NULL	0	NULL	VAF	GP		bind					IRF7	GP			ISRE	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12262_s_214	15664995	(2) VAF upon virus infection also binds to IRF7 ISRE and IRFE and activates IRF7 transcription.	bind
4416	2	2331	6	10	NULL	0	NULL	statement 1	Process		occurs upon					virus	Organism	infection of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12262_s_214	15664995	(2) VAF upon virus infection also binds to IRF7 ISRE and IRFE and activates IRF7 transcription.	bind
4417	3	2331	6	10	NULL	0	NULL	VAF	GP		bind					IRF7	GP			IRFE	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12262_s_214	15664995	(2) VAF upon virus infection also binds to IRF7 ISRE and IRFE and activates IRF7 transcription.	bind
4418	4	2331	6	10	NULL	0	NULL	statement 3	Process		occurs upon					virus	Organism	infection of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12262_s_214	15664995	(2) VAF upon virus infection also binds to IRF7 ISRE and IRFE and activates IRF7 transcription.	bind
4420	5	2331	6	10	NULL	0	NULL	VAF	GP		activates					IRF7	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12262_s_214	15664995	(2) VAF upon virus infection also binds to IRF7 ISRE and IRFE and activates IRF7 transcription.	bind
4422	6	2331	6	10	NULL	0	NULL	statement 5	Process		occurs upon					virus	Organism	infection of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12262_s_214	15664995	(2) VAF upon virus infection also binds to IRF7 ISRE and IRFE and activates IRF7 transcription.	bind
4384	1	2332	5	10	NULL	0	NULL	ATP	Chemical		bind					KinI	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1422_s_250	15029249	(2) When  ATP binds to KinI, it induces a conformational change in the catalytic core that  pulls the tubulins at the L2 and 'neck'' attachments and pushes in at the  intradimer interface, curving the dimer.	bind
4385	2	2332	5	10	NULL	0	NULL	statement 1	Process		induce							conformational change of	catalytic core		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1422_s_250	15029249	(2) When  ATP binds to KinI, it induces a conformational change in the catalytic core that  pulls the tubulins at the L2 and 'neck'' attachments and pushes in at the  intradimer interface, curving the dimer.	bind
4425	1	2332	6	10	NULL	0	NULL	ATP	Chemical		bind					KinI	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1422_s_250	15029249	(2) When  ATP binds to KinI, it induces a conformational change in the catalytic core that  pulls the tubulins at the L2 and 'neck'' attachments and pushes in at the  intradimer interface, curving the dimer.	bind
4647	2	2332	6	10	NULL	0	NULL	statement 1	Process		induces							conformational change of	catalytic core		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1422_s_250	15029249	(2) When  ATP binds to KinI, it induces a conformational change in the catalytic core that  pulls the tubulins at the L2 and 'neck'' attachments and pushes in at the  intradimer interface, curving the dimer.	bind
4390	1	2333	5	10	NULL	0	NULL	Thiamine derivatives	Chemical		bind		directly			messenger RNAs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_13_10859_s_824	12556463	(2002) Thiamine derivatives bind messenger RNAs directly to regulate bacterial gene expression.	bind
4391	2	2333	5	10	NULL	0	NULL	statement 1	Process		regulate					gene expression	Process	bacterial			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_13_10859_s_824	12556463	(2002) Thiamine derivatives bind messenger RNAs directly to regulate bacterial gene expression.	bind
53018	3	2333	5	10	NULL	0	NULL	statement 1	Process		lead to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_13_10859_s_824	12556463	(2002) Thiamine derivatives bind messenger RNAs directly to regulate bacterial gene expression.	bind
4524	1	2333	6	10	NULL	0	NULL	Thiamine derivatives	Chemical		bind		directly			mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_13_10859_s_824	12556463	(2002) Thiamine derivatives bind messenger RNAs directly to regulate bacterial gene expression.	bind
4525	2	2333	6	10	NULL	0	NULL	Thiamine derivatives	Chemical		regulates					gene expression	Process	bacterial 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_13_10859_s_824	12556463	(2002) Thiamine derivatives bind messenger RNAs directly to regulate bacterial gene expression.	bind
4526	3	2333	6	10	NULL	0	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_13_10859_s_824	12556463	(2002) Thiamine derivatives bind messenger RNAs directly to regulate bacterial gene expression.	bind
4392	1	2335	5	10	NULL	0	NULL	epsilonATP	Chemical		dissociate from					free actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_87	11294914	(3)   where  kf,  kwt, and  kmu are rate constants for epsilonATP dissociation from free actin, actin bound to wild-type profilin and actin bound to Y79R.	bind
4393	2	2335	5	10	NULL	0	NULL	actin	GP		bind					profilin	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_87	11294914	(3)   where  kf,  kwt, and  kmu are rate constants for epsilonATP dissociation from free actin, actin bound to wild-type profilin and actin bound to Y79R.	bind
4394	3	2335	5	10	NULL	0	NULL	epsilonATP	Chemical		dissociate from					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_87	11294914	(3)   where  kf,  kwt, and  kmu are rate constants for epsilonATP dissociation from free actin, actin bound to wild-type profilin and actin bound to Y79R.	bind
4395	4	2335	5	10	NULL	0	NULL	actin	GP		bind								Y79R		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_87	11294914	(3)   where  kf,  kwt, and  kmu are rate constants for epsilonATP dissociation from free actin, actin bound to wild-type profilin and actin bound to Y79R.	bind
4396	5	2335	5	10	NULL	0	NULL	epsilonATP	Chemical		dissociate from					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_87	11294914	(3)   where  kf,  kwt, and  kmu are rate constants for epsilonATP dissociation from free actin, actin bound to wild-type profilin and actin bound to Y79R.	bind
4527	1	2335	6	10	NULL	0	NULL	actin	GP		bind					profilin	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_87	11294914	(3)   where  kf,  kwt, and  kmu are rate constants for epsilonATP dissociation from free actin, actin bound to wild-type profilin and actin bound to Y79R.	bind
4528	2	2335	6	10	NULL	0	NULL	actin	GP		bind								Y79R		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_87	11294914	(3)   where  kf,  kwt, and  kmu are rate constants for epsilonATP dissociation from free actin, actin bound to wild-type profilin and actin bound to Y79R.	bind
53020	3	2335	6	10	NULL	0	NULL	epsilonATP	Chemical		dissociate from					free actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_87	11294914	(3)   where  kf,  kwt, and  kmu are rate constants for epsilonATP dissociation from free actin, actin bound to wild-type profilin and actin bound to Y79R.	bind
53021	5	2335	6	10	NULL	0	NULL	epsilonATP	Chemical		dissociate from					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_87	11294914	(3)   where  kf,  kwt, and  kmu are rate constants for epsilonATP dissociation from free actin, actin bound to wild-type profilin and actin bound to Y79R.	bind
53025	4	2335	6	10	NULL	0	NULL	epsilonATP	Chemical		dissociate from					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_87	11294914	(3)   where  kf,  kwt, and  kmu are rate constants for epsilonATP dissociation from free actin, actin bound to wild-type profilin and actin bound to Y79R.	bind
4400	1	2336	5	10	NULL	0	NULL	CcpA	GP		bind		specifically			gnt gene	GP	B. subtilis		CRE	NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_19_3_187_s_129	9050218	(3)  Using gel-retardation analysis, it was demonstrated that specific binding of CcpA  to CRE of the  B. subtilis gnt gene is triggered by HPr(Ser-P) but not by free HPr.	bind
4402	2	2336	5	10	NULL	0	NULL	statement 1	Process		is triggered by					HPr	GP		Ser-P		NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_19_3_187_s_129	9050218	(3)  Using gel-retardation analysis, it was demonstrated that specific binding of CcpA  to CRE of the  B. subtilis gnt gene is triggered by HPr(Ser-P) but not by free HPr.	bind
4403	3	2336	5	10	NULL	0	NULL	statement 1	Process		is not triggered by					HPr	GP	free			NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_19_3_187_s_129	9050218	(3)  Using gel-retardation analysis, it was demonstrated that specific binding of CcpA  to CRE of the  B. subtilis gnt gene is triggered by HPr(Ser-P) but not by free HPr.	bind
4529	1	2336	6	10	NULL	0	NULL	CcpA	GP		bind		specifically			gnt gene	GP	B. subtilis		CRE	NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_19_3_187_s_129	9050218	(3)  Using gel-retardation analysis, it was demonstrated that specific binding of CcpA  to CRE of the  B. subtilis gnt gene is triggered by HPr(Ser-P) but not by free HPr.	bind
4530	2	2336	6	10	NULL	0	NULL	Hpr	GP		triggers			Ser-P		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_19_3_187_s_129	9050218	(3)  Using gel-retardation analysis, it was demonstrated that specific binding of CcpA  to CRE of the  B. subtilis gnt gene is triggered by HPr(Ser-P) but not by free HPr.	bind
4531	3	2336	6	10	NULL	0	NULL	Hpr	GP	free	does not trigger					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_19_3_187_s_129	9050218	(3)  Using gel-retardation analysis, it was demonstrated that specific binding of CcpA  to CRE of the  B. subtilis gnt gene is triggered by HPr(Ser-P) but not by free HPr.	bind
4405	1	2337	5	10	NULL	0	NULL	Apo A-1	GP		bind		possibly;;directly			caveola	GP		FC-rich ;;exofacial face of 		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1529_1_210_s_171	11111090	(3) Apo A-1 (or pre- -HDL) could bind directly to the FC-rich exofacial face of the caveola to facilitate FC desorption [  93].	bind
4406	2	2337	5	10	NULL	0	NULL	pre- -HDL	Chemical		bind		possibly;;directly			caveola	GP		FC-rich;;exofacial face of		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1529_1_210_s_171	11111090	(3) Apo A-1 (or pre- -HDL) could bind directly to the FC-rich exofacial face of the caveola to facilitate FC desorption [  93].	bind
4407	3	2337	5	10	NULL	0	NULL	statement 1	Process		facilitate					FC desorption	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1529_1_210_s_171	11111090	(3) Apo A-1 (or pre- -HDL) could bind directly to the FC-rich exofacial face of the caveola to facilitate FC desorption [  93].	bind
4408	4	2337	5	10	NULL	0	NULL	statement 2	Process		facilitate					FC desorption	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1529_1_210_s_171	11111090	(3) Apo A-1 (or pre- -HDL) could bind directly to the FC-rich exofacial face of the caveola to facilitate FC desorption [  93].	bind
5931	5	2337	5	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1529_1_210_s_171	11111090	(3) Apo A-1 (or pre- -HDL) could bind directly to the FC-rich exofacial face of the caveola to facilitate FC desorption [  93].	bind
4532	1	2337	6	10	NULL	0	NULL	Apo A-1	GP		bind		possibly ;;directly			 caveola	GP		FC-rich;; exofacial face of		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1529_1_210_s_171	11111090	(3) Apo A-1 (or pre- -HDL) could bind directly to the FC-rich exofacial face of the caveola to facilitate FC desorption [  93].	bind
4533	2	2337	6	10	NULL	0	NULL	pre- -HDL	Chemical		bind		possibly;;directly			caveola	GP		FC-rich;; exofacial face of		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1529_1_210_s_171	11111090	(3) Apo A-1 (or pre- -HDL) could bind directly to the FC-rich exofacial face of the caveola to facilitate FC desorption [  93].	bind
4534	3	2337	6	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1529_1_210_s_171	11111090	(3) Apo A-1 (or pre- -HDL) could bind directly to the FC-rich exofacial face of the caveola to facilitate FC desorption [  93].	bind
4535	4	2337	6	10	NULL	0	NULL	Apo A-1	GP		facilitate					FC desorption	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1529_1_210_s_171	11111090	(3) Apo A-1 (or pre- -HDL) could bind directly to the FC-rich exofacial face of the caveola to facilitate FC desorption [  93].	bind
4536	5	2337	6	10	NULL	0	NULL	statement 1	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1529_1_210_s_171	11111090	(3) Apo A-1 (or pre- -HDL) could bind directly to the FC-rich exofacial face of the caveola to facilitate FC desorption [  93].	bind
4875	1	2338	5	10	NULL	0	NULL	bicarbonate	Chemical		increase					Mn2+ 	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
4876	3	2338	5	10	NULL	0	NULL	Mn cluster	Chemical		is capable of					water oxidation	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
4877	4	2338	5	10	NULL	0	NULL	bicarbonate	Chemical		stabilize		indirectly			WOC	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
5556	2	2338	5	10	NULL	0	NULL	bicarbonate	Chemical		increase					Mn cluster	Chemical	formation of 			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
5557	5	2338	5	10	NULL	0	NULL	Bicarbonate	Chemical		bind					PSII components	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
5558	6	2338	5	10	NULL	0	NULL	statement 5	Process		is required for					whole PSII complex	GP	structural/functional organization of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
5559	7	2338	5	10	NULL	0	NULL	statement 5	Process		is required for					Mn	Chemical	functional binding of 			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
5560	8	2338	5	10	NULL	0	NULL	bicarbonate	Chemical		bind					acceptor side	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
5561	9	2338	5	10	NULL	0	NULL	statement 8	Process		is required for					PSII	GP	activity of donor sides			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
5930	10	2338	5	10	NULL	0	NULL	statement 8	Process		is required for					PS II	GP	activity of acceptor sides			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
53031	11	2338	5	10	NULL	0	NULL	statement 4	Process		occur through					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
4648	1	2338	6	10	NULL	0	NULL	Bicarbonate	Chemical		increases					Mn+2	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
4649	2	2338	6	10	NULL	0	NULL	Mn cluster	Chemical		oxidizes					water	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
4650	3	2338	6	10	NULL	0	NULL	Bicarbonate	Chemical		increases					Mn cluster	Chemical	formation of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
4651	4	2338	6	10	NULL	0	NULL	Bicarbonate	Chemical		stabilizes		indirectly			WOC	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
4652	5	2338	6	10	NULL	0	NULL	Bicarbonate	Chemical		bind					PSII components	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
4653	6	2338	6	NULL	NULL	0	NULL	Bicarbonate	NULL		bind	NULL					NULL		acceptor side		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
4654	7	2338	6	NULL	NULL	0	NULL	statement 6	NULL		is required for	NULL				PSII 	NULL	activity of 	acceptor side		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
5743	8	2338	6	NULL	NULL	0	NULL	statement 6	NULL		is required for	NULL				PS II	NULL	activity of	donor side		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
53032	9	2338	6	10	NULL	0	NULL	statement 4	NULL		occur through	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
53033	10	2338	6	10	NULL	0	NULL	statement 5	NULL		is required for	NULL				 whole PSII complex	NULL	structural/functional organization of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
53034	11	2338	6	10	NULL	0	NULL	statement 5	NULL		is required for	NULL				Mn	NULL	functional binding of 			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_1_187_s_154	11115633	(3) Bicarbonate increases the Mn2+ binding [ 15], the formation of the Mn cluster capable of water oxidation [ 18 and  22] and stabilizes the WOC [ 19] indirectly, through its binding to other PSII components that is important for structural/functional organization of the whole PSII complex and, in particular, for functional binding of Mn. Govindjee and co-workers [  40] suggested that bicarbonate bound to the acceptor side is required for PSII activity both on the acceptor and the donor sides.	bind
4409	1	2339	5	10	NULL	0	NULL	GR	GP		bind					glucocorticoid	GP			responsive elements	NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_126_3_537_s_181	10188959	(3) Binding of GR to glucocorticoid responsive elements modulates TF-induced transactivation.	bind
4410	2	2339	5	10	NULL	0	NULL	TF	GP		induce					transactivation	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_126_3_537_s_181	10188959	(3) Binding of GR to glucocorticoid responsive elements modulates TF-induced transactivation.	bind
46477	3	2339	5	10	NULL	0	NULL	statement 1	Process		modulate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_126_3_537_s_181	10188959	(3) Binding of GR to glucocorticoid responsive elements modulates TF-induced transactivation.	bind
4537	1	2339	6	10	NULL	0	NULL	GR	GP		bind					glucocorticoid	GP			 responsive element	NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_126_3_537_s_181	10188959	(3) Binding of GR to glucocorticoid responsive elements modulates TF-induced transactivation.	bind
4538	2	2339	6	10	NULL	0	NULL	TF	GP		induce					transactivation	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_126_3_537_s_181	10188959	(3) Binding of GR to glucocorticoid responsive elements modulates TF-induced transactivation.	bind
46478	3	2339	6	10	NULL	0	NULL	statement 1	Process		modulate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_126_3_537_s_181	10188959	(3) Binding of GR to glucocorticoid responsive elements modulates TF-induced transactivation.	bind
4411	1	2340	5	10	NULL	0	NULL	VLA-4	Cell		bind					VCAM-1	GP	endothelial			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_353_s_130	10669630	(3) Binding of monocyte VLA-4 by endothelial VCAM-1 is needed for the induction of IL-1beta in monocytes.	bind
4412	2	2340	5	10	NULL	0	NULL	statement 1	Process		induce					IL-1beta	GP				NULL	monocytes	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_353_s_130	10669630	(3) Binding of monocyte VLA-4 by endothelial VCAM-1 is needed for the induction of IL-1beta in monocytes.	bind
53035	3	2340	5	10	NULL	0	NULL	VLA-4	Cell		is a type of					monocyte	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_353_s_130	10669630	(3) Binding of monocyte VLA-4 by endothelial VCAM-1 is needed for the induction of IL-1beta in monocytes.	bind
4539	1	2340	6	10	NULL	0	NULL	VLA-4	GP		bind					VCAM-1	GP	endothelial			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_353_s_130	10669630	(3) Binding of monocyte VLA-4 by endothelial VCAM-1 is needed for the induction of IL-1beta in monocytes.	bind
4540	2	2340	6	10	NULL	0	NULL	statement 1	Process		induces					IL-1beta	GP				NULL	monocytes	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_353_s_130	10669630	(3) Binding of monocyte VLA-4 by endothelial VCAM-1 is needed for the induction of IL-1beta in monocytes.	bind
53036	3	2340	6	10	NULL	0	NULL	VLA-4	Cell		is a type of					monocyte	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_353_s_130	10669630	(3) Binding of monocyte VLA-4 by endothelial VCAM-1 is needed for the induction of IL-1beta in monocytes.	bind
4413	1	2341	5	10	NULL	0	NULL	PsbP	GP	chlamydomonas	bind		functionally			PS II	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_5	16049780	(3) Both Chlamydomonas  PsbP and spinach PsbP functionally bound to spinach PS II in the presence  of spinach PsbO.	bind
4415	2	2341	5	10	NULL	0	NULL	statement 1	Process		in the presence of					PsbO	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_5	16049780	(3) Both Chlamydomonas  PsbP and spinach PsbP functionally bound to spinach PS II in the presence  of spinach PsbO.	bind
4419	3	2341	5	10	NULL	0	NULL	PsbP	GP	spinach	bind		functionally			PS II	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_5	16049780	(3) Both Chlamydomonas  PsbP and spinach PsbP functionally bound to spinach PS II in the presence  of spinach PsbO.	bind
4421	4	2341	5	10	NULL	0	NULL	statement 3	Process		in the presence of					PsbO	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_5	16049780	(3) Both Chlamydomonas  PsbP and spinach PsbP functionally bound to spinach PS II in the presence  of spinach PsbO.	bind
4541	1	2341	6	10	NULL	0	NULL	PsbP	GP	Chlamydomonas	bind		functionaly			PS II	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_5	16049780	(3) Both Chlamydomonas  PsbP and spinach PsbP functionally bound to spinach PS II in the presence  of spinach PsbO.	bind
4542	2	2341	6	10	NULL	0	NULL	PsbP	GP	spinach	bind		functionaly			PS II	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_5	16049780	(3) Both Chlamydomonas  PsbP and spinach PsbP functionally bound to spinach PS II in the presence  of spinach PsbO.	bind
4543	3	2341	6	10	NULL	0	NULL	statement 1	Process		occurs in presence of					PsbO	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_5	16049780	(3) Both Chlamydomonas  PsbP and spinach PsbP functionally bound to spinach PS II in the presence  of spinach PsbO.	bind
4544	4	2341	6	10	NULL	0	NULL	statement 2	Process		occurs in presence of					PsbO	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_5	16049780	(3) Both Chlamydomonas  PsbP and spinach PsbP functionally bound to spinach PS II in the presence  of spinach PsbO.	bind
4423	1	2342	5	10	NULL	0	NULL	p19ARF	GP		bind			amino-terminal domain		Mdm2	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_18_2358_s_102	10995391	(3) Conversely, the amino-terminal domain of p19ARF, which binds to Mdm2, also appears to be important in ensuring the interaction of ARF with another target required for S phase entry.	bind
4424	2	2342	5	10	NULL	0	NULL	ARF	GP		interact with					target required for S phase entry					NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_18_2358_s_102	10995391	(3) Conversely, the amino-terminal domain of p19ARF, which binds to Mdm2, also appears to be important in ensuring the interaction of ARF with another target required for S phase entry.	bind
4426	3	2342	5	10	NULL	0	NULL	p19ARF	GP		ensures			amino-terminal domain		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_18_2358_s_102	10995391	(3) Conversely, the amino-terminal domain of p19ARF, which binds to Mdm2, also appears to be important in ensuring the interaction of ARF with another target required for S phase entry.	bind
4545	1	2342	6	10	NULL	0	NULL	p19ARF	GP		bind			amino-terminal domain		Mdm2	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_18_2358_s_102	10995391	(3) Conversely, the amino-terminal domain of p19ARF, which binds to Mdm2, also appears to be important in ensuring the interaction of ARF with another target required for S phase entry.	bind
4546	2	2342	6	10	NULL	0	NULL	ARF	GP		interacts					target required for S phase entry					NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_18_2358_s_102	10995391	(3) Conversely, the amino-terminal domain of p19ARF, which binds to Mdm2, also appears to be important in ensuring the interaction of ARF with another target required for S phase entry.	bind
4547	3	2342	6	10	NULL	0	NULL	p19ARF	GP		ensures			amino-terminal domain		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_18_2358_s_102	10995391	(3) Conversely, the amino-terminal domain of p19ARF, which binds to Mdm2, also appears to be important in ensuring the interaction of ARF with another target required for S phase entry.	bind
4427	1	2343	5	10	NULL	0	NULL	E2F1	GP		bind					TopBP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_18_6_673_s_284	15075294	(3) E2F1 binding to TopBP1 is induced by ATM-dependent phosphorylation of E2F1; E2F binding to pRb is inhibited by phosphorylation of pRb.	bind
4428	2	2343	5	10	NULL	0	NULL	E2F1	GP	phosphorylation	dependent on					ATM	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_18_6_673_s_284	15075294	(3) E2F1 binding to TopBP1 is induced by ATM-dependent phosphorylation of E2F1; E2F binding to pRb is inhibited by phosphorylation of pRb.	bind
4429	3	2343	5	10	NULL	0	NULL	statement 2	Process		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_18_6_673_s_284	15075294	(3) E2F1 binding to TopBP1 is induced by ATM-dependent phosphorylation of E2F1; E2F binding to pRb is inhibited by phosphorylation of pRb.	bind
4430	4	2343	5	10	NULL	0	NULL	E2F	GP		bind					pRb	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_18_6_673_s_284	15075294	(3) E2F1 binding to TopBP1 is induced by ATM-dependent phosphorylation of E2F1; E2F binding to pRb is inhibited by phosphorylation of pRb.	bind
4431	5	2343	5	10	NULL	0	NULL	pRb	GP	phosphorylation	inhibit					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_18_6_673_s_284	15075294	(3) E2F1 binding to TopBP1 is induced by ATM-dependent phosphorylation of E2F1; E2F binding to pRb is inhibited by phosphorylation of pRb.	bind
4548	1	2343	6	10	NULL	0	NULL	E2F1	GP		bind					TopBP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_18_6_673_s_284	15075294	(3) E2F1 binding to TopBP1 is induced by ATM-dependent phosphorylation of E2F1; E2F binding to pRb is inhibited by phosphorylation of pRb.	bind
4549	2	2343	6	10	NULL	0	NULL	E2F1	GP	phosphorylation of	is dependent on					ATM	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_18_6_673_s_284	15075294	(3) E2F1 binding to TopBP1 is induced by ATM-dependent phosphorylation of E2F1; E2F binding to pRb is inhibited by phosphorylation of pRb.	bind
4550	3	2343	6	10	NULL	0	NULL	statement 2	Process		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_18_6_673_s_284	15075294	(3) E2F1 binding to TopBP1 is induced by ATM-dependent phosphorylation of E2F1; E2F binding to pRb is inhibited by phosphorylation of pRb.	bind
4551	4	2343	6	10	NULL	0	NULL	E2F	GP		bind					pRb	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_18_6_673_s_284	15075294	(3) E2F1 binding to TopBP1 is induced by ATM-dependent phosphorylation of E2F1; E2F binding to pRb is inhibited by phosphorylation of pRb.	bind
4552	5	2343	6	10	NULL	0	NULL	statement 4	Process		is inhibited by					pRb	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_18_6_673_s_284	15075294	(3) E2F1 binding to TopBP1 is induced by ATM-dependent phosphorylation of E2F1; E2F binding to pRb is inhibited by phosphorylation of pRb.	bind
4432	1	2344	5	10	NULL	0	NULL	fatty acids	Chemical		released from					triglyceride stores	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1504_1_70_s_183	11239486	(3) Fatty acids are released from the triglyceride stores and serve two functions: (3a) they are activated to acyl-CoA, then converted to acyl-carnitine and transported into the mitochondrial matrix where they will substrate for oxidation and (3b) free fatty acids bind to UCP1 to increase its proton conductance.	bind
4433	2	2344	5	10	NULL	0	NULL	fatty acids	Chemical		are activated to					acyl-CoA	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1504_1_70_s_183	11239486	(3) Fatty acids are released from the triglyceride stores and serve two functions: (3a) they are activated to acyl-CoA, then converted to acyl-carnitine and transported into the mitochondrial matrix where they will substrate for oxidation and (3b) free fatty acids bind to UCP1 to increase its proton conductance.	bind
4434	3	2344	5	10	NULL	0	NULL	statement 2	Process		converted to					acyl-carnitine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1504_1_70_s_183	11239486	(3) Fatty acids are released from the triglyceride stores and serve two functions: (3a) they are activated to acyl-CoA, then converted to acyl-carnitine and transported into the mitochondrial matrix where they will substrate for oxidation and (3b) free fatty acids bind to UCP1 to increase its proton conductance.	bind
4435	4	2344	5	10	NULL	0	NULL	statement 3	Process		transported to					mitochondrial matrix	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1504_1_70_s_183	11239486	(3) Fatty acids are released from the triglyceride stores and serve two functions: (3a) they are activated to acyl-CoA, then converted to acyl-carnitine and transported into the mitochondrial matrix where they will substrate for oxidation and (3b) free fatty acids bind to UCP1 to increase its proton conductance.	bind
4436	5	2344	5	10	NULL	0	NULL	statement 4	Process		substrate for					oxidation	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1504_1_70_s_183	11239486	(3) Fatty acids are released from the triglyceride stores and serve two functions: (3a) they are activated to acyl-CoA, then converted to acyl-carnitine and transported into the mitochondrial matrix where they will substrate for oxidation and (3b) free fatty acids bind to UCP1 to increase its proton conductance.	bind
4437	6	2344	5	10	NULL	0	NULL	fatty acids	Chemical	free	bind					UCP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1504_1_70_s_183	11239486	(3) Fatty acids are released from the triglyceride stores and serve two functions: (3a) they are activated to acyl-CoA, then converted to acyl-carnitine and transported into the mitochondrial matrix where they will substrate for oxidation and (3b) free fatty acids bind to UCP1 to increase its proton conductance.	bind
4438	7	2344	5	10	NULL	0	NULL	statement 6	Process		increase					proton conductance	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1504_1_70_s_183	11239486	(3) Fatty acids are released from the triglyceride stores and serve two functions: (3a) they are activated to acyl-CoA, then converted to acyl-carnitine and transported into the mitochondrial matrix where they will substrate for oxidation and (3b) free fatty acids bind to UCP1 to increase its proton conductance.	bind
4553	1	2344	6	10	NULL	0	NULL	fatty acids	Chemical		released from					triglyceride stores	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1504_1_70_s_183	11239486	(3) Fatty acids are released from the triglyceride stores and serve two functions: (3a) they are activated to acyl-CoA, then converted to acyl-carnitine and transported into the mitochondrial matrix where they will substrate for oxidation and (3b) free fatty acids bind to UCP1 to increase its proton conductance.	bind
4589	2	2344	6	10	NULL	0	NULL	fatty acids	Chemical		are activated to					acyl-CoA	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1504_1_70_s_183	11239486	(3) Fatty acids are released from the triglyceride stores and serve two functions: (3a) they are activated to acyl-CoA, then converted to acyl-carnitine and transported into the mitochondrial matrix where they will substrate for oxidation and (3b) free fatty acids bind to UCP1 to increase its proton conductance.	bind
4590	3	2344	6	10	NULL	0	NULL	Acyl-CoA	GP		is converted to					acyl-carnitine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1504_1_70_s_183	11239486	(3) Fatty acids are released from the triglyceride stores and serve two functions: (3a) they are activated to acyl-CoA, then converted to acyl-carnitine and transported into the mitochondrial matrix where they will substrate for oxidation and (3b) free fatty acids bind to UCP1 to increase its proton conductance.	bind
4591	4	2344	6	10	NULL	0	NULL	fatty acids	Chemical		transported to					mitochondrial matrix	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1504_1_70_s_183	11239486	(3) Fatty acids are released from the triglyceride stores and serve two functions: (3a) they are activated to acyl-CoA, then converted to acyl-carnitine and transported into the mitochondrial matrix where they will substrate for oxidation and (3b) free fatty acids bind to UCP1 to increase its proton conductance.	bind
4592	5	2344	6	10	NULL	0	NULL	statement 3	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1504_1_70_s_183	11239486	(3) Fatty acids are released from the triglyceride stores and serve two functions: (3a) they are activated to acyl-CoA, then converted to acyl-carnitine and transported into the mitochondrial matrix where they will substrate for oxidation and (3b) free fatty acids bind to UCP1 to increase its proton conductance.	bind
4593	6	2344	6	10	NULL	0	NULL	fatty acids	Chemical	free	bind					UCP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1504_1_70_s_183	11239486	(3) Fatty acids are released from the triglyceride stores and serve two functions: (3a) they are activated to acyl-CoA, then converted to acyl-carnitine and transported into the mitochondrial matrix where they will substrate for oxidation and (3b) free fatty acids bind to UCP1 to increase its proton conductance.	bind
4594	7	2344	6	10	NULL	0	NULL	UCP1	GP		conducts					protons	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1504_1_70_s_183	11239486	(3) Fatty acids are released from the triglyceride stores and serve two functions: (3a) they are activated to acyl-CoA, then converted to acyl-carnitine and transported into the mitochondrial matrix where they will substrate for oxidation and (3b) free fatty acids bind to UCP1 to increase its proton conductance.	bind
4655	8	2344	6	10	NULL	0	NULL	statement 6	Process		increases					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1504_1_70_s_183	11239486	(3) Fatty acids are released from the triglyceride stores and serve two functions: (3a) they are activated to acyl-CoA, then converted to acyl-carnitine and transported into the mitochondrial matrix where they will substrate for oxidation and (3b) free fatty acids bind to UCP1 to increase its proton conductance.	bind
4439	1	2345	5	10	NULL	0	NULL	GalR	GP		bind					gal DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_17_2273_s_23	11544184	(3) Finally, there is a tripartite cooperativity between GalR and HU in binding to  gal DNA; binding of HU to  hbs is absolutely dependent on binding of GalR dimers to both operators and HU binding, in turn, results in increasing the strength of GalR binding.	bind
4440	2	2345	5	10	NULL	0	NULL	HU	GP		bind					gal DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_17_2273_s_23	11544184	(3) Finally, there is a tripartite cooperativity between GalR and HU in binding to  gal DNA; binding of HU to  hbs is absolutely dependent on binding of GalR dimers to both operators and HU binding, in turn, results in increasing the strength of GalR binding.	bind
4441	3	2345	5	10	NULL	0	NULL	HU	GP		bind					hbs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_17_2273_s_23	11544184	(3) Finally, there is a tripartite cooperativity between GalR and HU in binding to  gal DNA; binding of HU to  hbs is absolutely dependent on binding of GalR dimers to both operators and HU binding, in turn, results in increasing the strength of GalR binding.	bind
4442	4	2345	5	10	NULL	0	NULL	GalR dimers	GP		bind									operators	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_17_2273_s_23	11544184	(3) Finally, there is a tripartite cooperativity between GalR and HU in binding to  gal DNA; binding of HU to  hbs is absolutely dependent on binding of GalR dimers to both operators and HU binding, in turn, results in increasing the strength of GalR binding.	bind
4443	5	2345	5	10	NULL	0	NULL	statement 3	Process		dependent on					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_17_2273_s_23	11544184	(3) Finally, there is a tripartite cooperativity between GalR and HU in binding to  gal DNA; binding of HU to  hbs is absolutely dependent on binding of GalR dimers to both operators and HU binding, in turn, results in increasing the strength of GalR binding.	bind
4444	6	2345	5	10	NULL	0	NULL	statement 3	Process		increases					GalR	GP	strength of;;binding of			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_17_2273_s_23	11544184	(3) Finally, there is a tripartite cooperativity between GalR and HU in binding to  gal DNA; binding of HU to  hbs is absolutely dependent on binding of GalR dimers to both operators and HU binding, in turn, results in increasing the strength of GalR binding.	bind
5929	7	2345	5	10	NULL	0	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_17_2273_s_23	11544184	(3) Finally, there is a tripartite cooperativity between GalR and HU in binding to  gal DNA; binding of HU to  hbs is absolutely dependent on binding of GalR dimers to both operators and HU binding, in turn, results in increasing the strength of GalR binding.	bind
4656	1	2345	6	10	NULL	0	NULL	GalR	GP		bind					gal DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_17_2273_s_23	11544184	(3) Finally, there is a tripartite cooperativity between GalR and HU in binding to  gal DNA; binding of HU to  hbs is absolutely dependent on binding of GalR dimers to both operators and HU binding, in turn, results in increasing the strength of GalR binding.	bind
4657	2	2345	6	10	NULL	0	NULL	HU	GP		bind					gal DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_17_2273_s_23	11544184	(3) Finally, there is a tripartite cooperativity between GalR and HU in binding to  gal DNA; binding of HU to  hbs is absolutely dependent on binding of GalR dimers to both operators and HU binding, in turn, results in increasing the strength of GalR binding.	bind
4658	3	2345	6	10	NULL	0	NULL	GalR dimer	GP		bind									operators	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_17_2273_s_23	11544184	(3) Finally, there is a tripartite cooperativity between GalR and HU in binding to  gal DNA; binding of HU to  hbs is absolutely dependent on binding of GalR dimers to both operators and HU binding, in turn, results in increasing the strength of GalR binding.	bind
4659	4	2345	6	10	NULL	0	NULL	HU	GP		bind					hbs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_17_2273_s_23	11544184	(3) Finally, there is a tripartite cooperativity between GalR and HU in binding to  gal DNA; binding of HU to  hbs is absolutely dependent on binding of GalR dimers to both operators and HU binding, in turn, results in increasing the strength of GalR binding.	bind
4660	5	2345	6	10	NULL	0	NULL	statement 4	Process		is dependent on					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_17_2273_s_23	11544184	(3) Finally, there is a tripartite cooperativity between GalR and HU in binding to  gal DNA; binding of HU to  hbs is absolutely dependent on binding of GalR dimers to both operators and HU binding, in turn, results in increasing the strength of GalR binding.	bind
4661	6	2345	6	10	NULL	0	NULL	statement 4	Process		increases					GalR	GP	strength of ;;binding of			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_17_2273_s_23	11544184	(3) Finally, there is a tripartite cooperativity between GalR and HU in binding to  gal DNA; binding of HU to  hbs is absolutely dependent on binding of GalR dimers to both operators and HU binding, in turn, results in increasing the strength of GalR binding.	bind
5746	7	2345	6	10	NULL	0	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_17_2273_s_23	11544184	(3) Finally, there is a tripartite cooperativity between GalR and HU in binding to  gal DNA; binding of HU to  hbs is absolutely dependent on binding of GalR dimers to both operators and HU binding, in turn, results in increasing the strength of GalR binding.	bind
4445	1	2346	5	10	NULL	0	NULL	Importin alpha	GP		bind								NLSs		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_169_3_415_s_292	15883195	(3) Importin alpha binds to the NLSs and mediates the nuclear import of myopodin (4).	bind
4446	3	2346	5	10	NULL	0	NULL	Importin alpha	GP		mediate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_169_3_415_s_292	15883195	(3) Importin alpha binds to the NLSs and mediates the nuclear import of myopodin (4).	bind
46479	2	2346	5	10	NULL	0	NULL	myopodin	GP		imported to					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_169_3_415_s_292	15883195	(3) Importin alpha binds to the NLSs and mediates the nuclear import of myopodin (4).	bind
4595	1	2346	6	10	NULL	0	NULL	Importin alpha	GP		bind								NLS		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_169_3_415_s_292	15883195	(3) Importin alpha binds to the NLSs and mediates the nuclear import of myopodin (4).	bind
4600	2	2346	6	10	NULL	0	NULL	myopodin	GP		imported					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_169_3_415_s_292	15883195	(3) Importin alpha binds to the NLSs and mediates the nuclear import of myopodin (4).	bind
4601	3	2346	6	10	NULL	0	NULL	Importin alpha	GP		mediates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_169_3_415_s_292	15883195	(3) Importin alpha binds to the NLSs and mediates the nuclear import of myopodin (4).	bind
4447	1	2347	5	10	NULL	0	NULL	19S RP	GP		bind		directly			Sec61 channel	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_435_s_42	16212502	(3) In a third scenario, the 19S RP binds directly to the Sec61 channel  and extracts misfolded proteins from the ER.	bind
4448	3	2347	5	10	NULL	0	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_435_s_42	16212502	(3) In a third scenario, the 19S RP binds directly to the Sec61 channel  and extracts misfolded proteins from the ER.	bind
46480	2	2347	5	10	NULL	0	NULL	 misfolded proteins	GP		extracted from					ER	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_435_s_42	16212502	(3) In a third scenario, the 19S RP binds directly to the Sec61 channel  and extracts misfolded proteins from the ER.	bind
4703	1	2347	6	10	NULL	0	NULL	19S RP	GP		bind		directly			Sec61 channel	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_435_s_42	16212502	(3) In a third scenario, the 19S RP binds directly to the Sec61 channel  and extracts misfolded proteins from the ER.	bind
4704	2	2347	6	10	NULL	0	NULL	misfolded proteins	GP		are extracted from					ER	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_435_s_42	16212502	(3) In a third scenario, the 19S RP binds directly to the Sec61 channel  and extracts misfolded proteins from the ER.	bind
4705	3	2347	6	10	NULL	0	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_435_s_42	16212502	(3) In a third scenario, the 19S RP binds directly to the Sec61 channel  and extracts misfolded proteins from the ER.	bind
4449	1	2348	5	10	NULL	0	NULL	neuropilin-1	GP		bind					SEMA-3A	GP		semaphorin portion		NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_18_7870_s_238	10479689	(3) In contrast, neither the A nor the B domains of neuropilin-1 appear to be required for the binding of the semaphorin portion of SEMA-3A.	bind
4450	2	2348	5	10	NULL	0	NULL	neuropilin-1	GP		is not required for			A domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_18_7870_s_238	10479689	(3) In contrast, neither the A nor the B domains of neuropilin-1 appear to be required for the binding of the semaphorin portion of SEMA-3A.	bind
4451	3	2348	5	10	NULL	0	NULL	neuropilin-1	GP		is not required for			B domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_18_7870_s_238	10479689	(3) In contrast, neither the A nor the B domains of neuropilin-1 appear to be required for the binding of the semaphorin portion of SEMA-3A.	bind
4706	2	2348	6	10	NULL	0	NULL	neuropilin-1	GP		is not required for 			A domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_18_7870_s_238	10479689	(3) In contrast, neither the A nor the B domains of neuropilin-1 appear to be required for the binding of the semaphorin portion of SEMA-3A.	bind
4781	3	2348	6	10	NULL	0	NULL	neuropilin-1	GP		are not required for 			B domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_18_7870_s_238	10479689	(3) In contrast, neither the A nor the B domains of neuropilin-1 appear to be required for the binding of the semaphorin portion of SEMA-3A.	bind
53037	1	2348	6	10	NULL	0	NULL	neuropilin-1	GP		bind					SEMA-3A	GP		semaphorin portion		NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_18_7870_s_238	10479689	(3) In contrast, neither the A nor the B domains of neuropilin-1 appear to be required for the binding of the semaphorin portion of SEMA-3A.	bind
4452	1	2349	5	10	NULL	0	NULL	Kar9p	GP		bind					Myo2p	GP		globular tail		NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_20_0_559_s_241	15473852	(3) Kar9p also binds the globular tail of Myo2p (myosin-V).	bind
4453	2	2349	5	10	NULL	0	NULL	Myo2p	GP		is					myosin-V	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_20_0_559_s_241	15473852	(3) Kar9p also binds the globular tail of Myo2p (myosin-V).	bind
4782	1	2349	6	10	NULL	0	NULL	Kar9p	GP		bind					Myo2p	GP		globular tail 		NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_20_0_559_s_241	15473852	(3) Kar9p also binds the globular tail of Myo2p (myosin-V).	bind
46481	2	2349	6	10	NULL	0	NULL	Myo2p	GP		is					myosin-V	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_20_0_559_s_241	15473852	(3) Kar9p also binds the globular tail of Myo2p (myosin-V).	bind
4454	2	2350	5	10	NULL	0	NULL	GST-Nck	GP	purified	bind		directly	SH2		statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_oncogene_15_15_9362449_s_11	9362449	(3) Purified GST-Nck-SH2 binds directly to  the GAP-associated p62.	bind
46482	1	2350	5	10	NULL	0	NULL	GAP	GP		associate with					p62	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_oncogene_15_15_9362449_s_11	9362449	(3) Purified GST-Nck-SH2 binds directly to  the GAP-associated p62.	bind
4785	2	2350	6	10	NULL	0	NULL	GST-Nck	GP	purified	bind		directly	SH2 domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_oncogene_15_15_9362449_s_11	9362449	(3) Purified GST-Nck-SH2 binds directly to  the GAP-associated p62.	bind
46483	1	2350	6	10	NULL	0	NULL	GAP	GP		associate with					p62	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_oncogene_15_15_9362449_s_11	9362449	(3) Purified GST-Nck-SH2 binds directly to  the GAP-associated p62.	bind
4455	1	2351	5	10	NULL	0	NULL	band 3 dimers	GP	stabilized	bind		effectively			GAPDH	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1559_1_43_s_256	11825587	(3) Stabilized band 3 dimers can also effectively bind GAPDH.	bind
4786	1	2351	6	10	NULL	0	NULL	band 3 dimers	GP	stabilized	bind		effectively			GAPDH	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1559_1_43_s_256	11825587	(3) Stabilized band 3 dimers can also effectively bind GAPDH.	bind
4456	1	2352	5	10	NULL	0	NULL	p53	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_4_462_s_211	9472015	(3) Stimulation of p53 DNA binding by HMG-1 was two to threefold greater when p53 half sites were separated by 10, 15, or 30 bp than when they were adjacent (data not shown).	bind
4457	2	2352	5	10	NULL	0	NULL	HMG-1	GP		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_4_462_s_211	9472015	(3) Stimulation of p53 DNA binding by HMG-1 was two to threefold greater when p53 half sites were separated by 10, 15, or 30 bp than when they were adjacent (data not shown).	bind
4788	1	2352	6	10	NULL	0	NULL	p53	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_4_462_s_211	9472015	(3) Stimulation of p53 DNA binding by HMG-1 was two to threefold greater when p53 half sites were separated by 10, 15, or 30 bp than when they were adjacent (data not shown).	bind
4789	2	2352	6	10	NULL	0	NULL	HMG-1	GP		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_4_462_s_211	9472015	(3) Stimulation of p53 DNA binding by HMG-1 was two to threefold greater when p53 half sites were separated by 10, 15, or 30 bp than when they were adjacent (data not shown).	bind
4458	1	2353	5	10	NULL	0	NULL	PD98059	Chemical		supress					ERK-AP-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_545_s_143	15020252	(3) Suppression  of ERK-AP-1 by PD98059 or dominant-negative mutants of ERK did not affect the apoptosis-promoting  effect of MG132.	bind
4459	2	2353	5	10	NULL	0	NULL	ERK	GP	dominant-negative mutants	supress					ERK-AP-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_545_s_143	15020252	(3) Suppression  of ERK-AP-1 by PD98059 or dominant-negative mutants of ERK did not affect the apoptosis-promoting  effect of MG132.	bind
4460	4	2353	5	10	NULL	0	NULL	statement 1	Process		does not affect					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_545_s_143	15020252	(3) Suppression  of ERK-AP-1 by PD98059 or dominant-negative mutants of ERK did not affect the apoptosis-promoting  effect of MG132.	bind
4461	5	2353	5	10	NULL	0	NULL	statement 2	Process		does not affect					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_545_s_143	15020252	(3) Suppression  of ERK-AP-1 by PD98059 or dominant-negative mutants of ERK did not affect the apoptosis-promoting  effect of MG132.	bind
46484	3	2353	5	10	NULL	0	NULL	MG132	Chemical		promotes					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_545_s_143	15020252	(3) Suppression  of ERK-AP-1 by PD98059 or dominant-negative mutants of ERK did not affect the apoptosis-promoting  effect of MG132.	bind
4792	1	2353	6	10	NULL	0	NULL	PD98059	Chemical		suppresses					ERK-AP-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_545_s_143	15020252	(3) Suppression  of ERK-AP-1 by PD98059 or dominant-negative mutants of ERK did not affect the apoptosis-promoting  effect of MG132.	bind
4793	2	2353	6	10	NULL	0	NULL	MG132	Chemical		promotes					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_545_s_143	15020252	(3) Suppression  of ERK-AP-1 by PD98059 or dominant-negative mutants of ERK did not affect the apoptosis-promoting  effect of MG132.	bind
46881	3	2353	6	10	NULL	0	NULL	ERK	GP	dominant-negative mutant	suppress					 ERK-AP-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_545_s_143	15020252	(3) Suppression  of ERK-AP-1 by PD98059 or dominant-negative mutants of ERK did not affect the apoptosis-promoting  effect of MG132.	bind
46882	4	2353	6	10	NULL	0	NULL	statement 1	Process		does not affect					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_545_s_143	15020252	(3) Suppression  of ERK-AP-1 by PD98059 or dominant-negative mutants of ERK did not affect the apoptosis-promoting  effect of MG132.	bind
53038	5	2353	6	10	NULL	0	NULL	statement 3	Process		does not affect					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_545_s_143	15020252	(3) Suppression  of ERK-AP-1 by PD98059 or dominant-negative mutants of ERK did not affect the apoptosis-promoting  effect of MG132.	bind
4463	1	2354	5	10	NULL	0	NULL	Mre11 protein	GP	mutant	bind					Rad50	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_5_705_s_74	9845372	(3) The  mre11-58 mutation inhibits  the complex formation by preventing binding of the mutant Mre11 protein to  Rad50 and Xrs2.	bind
4464	2	2354	5	10	NULL	0	NULL	Mre11 protein	GP	mutant	bind					Xrs2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_5_705_s_74	9845372	(3) The  mre11-58 mutation inhibits  the complex formation by preventing binding of the mutant Mre11 protein to  Rad50 and Xrs2.	bind
4465	3	2354	5	10	NULL	0	NULL	Mre11 protein	GP	mutation	prevent			mre11-58		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_5_705_s_74	9845372	(3) The  mre11-58 mutation inhibits  the complex formation by preventing binding of the mutant Mre11 protein to  Rad50 and Xrs2.	bind
4466	4	2354	5	10	NULL	0	NULL	Mre11 protein	GP	mutation	prevent			mre11-58		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_5_705_s_74	9845372	(3) The  mre11-58 mutation inhibits  the complex formation by preventing binding of the mutant Mre11 protein to  Rad50 and Xrs2.	bind
4467	5	2354	5	10	NULL	0	NULL	Mre11 protein	GP	mutation	inhibit			mre11-58		complex formation	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_5_705_s_74	9845372	(3) The  mre11-58 mutation inhibits  the complex formation by preventing binding of the mutant Mre11 protein to  Rad50 and Xrs2.	bind
4468	6	2354	5	10	NULL	0	NULL	statement 5	Process		occurs by					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_5_705_s_74	9845372	(3) The  mre11-58 mutation inhibits  the complex formation by preventing binding of the mutant Mre11 protein to  Rad50 and Xrs2.	bind
4469	7	2354	5	10	NULL	0	NULL	statement 5	Process		occurs by					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_5_705_s_74	9845372	(3) The  mre11-58 mutation inhibits  the complex formation by preventing binding of the mutant Mre11 protein to  Rad50 and Xrs2.	bind
4794	1	2354	6	10	NULL	0	NULL	Mre11 protein	GP		bind					Rad50	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_5_705_s_74	9845372	(3) The  mre11-58 mutation inhibits  the complex formation by preventing binding of the mutant Mre11 protein to  Rad50 and Xrs2.	bind
4795	2	2354	6	10	NULL	0	NULL	Mre11 protein	GP		bind					Xrs2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_5_705_s_74	9845372	(3) The  mre11-58 mutation inhibits  the complex formation by preventing binding of the mutant Mre11 protein to  Rad50 and Xrs2.	bind
4796	3	2354	6	10	NULL	0	NULL	Mre11 protein	GP	mutant	prevents			 mre11-58		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_5_705_s_74	9845372	(3) The  mre11-58 mutation inhibits  the complex formation by preventing binding of the mutant Mre11 protein to  Rad50 and Xrs2.	bind
4797	4	2354	6	10	NULL	0	NULL	Mre11 protein	GP	mutant	prevents			 mre11-58		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_5_705_s_74	9845372	(3) The  mre11-58 mutation inhibits  the complex formation by preventing binding of the mutant Mre11 protein to  Rad50 and Xrs2.	bind
4798	5	2354	6	10	NULL	0	NULL	Mre11 protein	GP	mutant	inhibits			 mre11-58		complex formation	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_5_705_s_74	9845372	(3) The  mre11-58 mutation inhibits  the complex formation by preventing binding of the mutant Mre11 protein to  Rad50 and Xrs2.	bind
53039	6	2354	6	10	NULL	0	NULL	statement 5	Process		occur by					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_5_705_s_74	9845372	(3) The  mre11-58 mutation inhibits  the complex formation by preventing binding of the mutant Mre11 protein to  Rad50 and Xrs2.	bind
53040	7	2354	6	10	NULL	0	NULL	statement 5	Process		occur by					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_5_705_s_74	9845372	(3) The  mre11-58 mutation inhibits  the complex formation by preventing binding of the mutant Mre11 protein to  Rad50 and Xrs2.	bind
4470	1	2356	5	10	NULL	0	NULL	RMP: RecO/Rad52/UvsY	GP		bind					SSB-ssDNA complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_24_15327_s_224	12438681	(3) The recombination mediator protein (RMP: RecO/Rad52/UvsY) binds to the SSB-ssDNA complex.	bind
4471	2	2356	5	10	NULL	0	NULL	RMP: RecO/Rad52/UvsY	GP		is					recombination mediator protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_24_15327_s_224	12438681	(3) The recombination mediator protein (RMP: RecO/Rad52/UvsY) binds to the SSB-ssDNA complex.	bind
4799	1	2356	6	10	NULL	0	NULL	RMP: RecO/Rad52/UvsY	GP		bind					SSB-ssDNA complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_24_15327_s_224	12438681	(3) The recombination mediator protein (RMP: RecO/Rad52/UvsY) binds to the SSB-ssDNA complex.	bind
4800	2	2356	6	10	NULL	0	NULL	RMP: RecO/Rad52/UvsY	GP		is					recombination mediator protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_24_15327_s_224	12438681	(3) The recombination mediator protein (RMP: RecO/Rad52/UvsY) binds to the SSB-ssDNA complex.	bind
4472	1	2357	5	10	NULL	0	NULL	PSA	GP		bind					HRP	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_zhejiang-da-xue-xue-bao-yi-xue-ban_34_5_16216051_s_7	16216051	(3) Three peptides (RMWSF, RYDYSY,  LRLRQL) were selectively synthesized, and different concentrations were  used to inhibit PSA and ConA binding to the HRP.	bind
4473	2	2357	5	10	NULL	0	NULL	ConA	GP		bind					HRP	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_zhejiang-da-xue-xue-bao-yi-xue-ban_34_5_16216051_s_7	16216051	(3) Three peptides (RMWSF, RYDYSY,  LRLRQL) were selectively synthesized, and different concentrations were  used to inhibit PSA and ConA binding to the HRP.	bind
4474	3	2357	5	10	NULL	0	NULL	RMWSF peptide	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_zhejiang-da-xue-xue-bao-yi-xue-ban_34_5_16216051_s_7	16216051	(3) Three peptides (RMWSF, RYDYSY,  LRLRQL) were selectively synthesized, and different concentrations were  used to inhibit PSA and ConA binding to the HRP.	bind
4475	4	2357	5	10	NULL	0	NULL	RMWSF peptide	GP		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_zhejiang-da-xue-xue-bao-yi-xue-ban_34_5_16216051_s_7	16216051	(3) Three peptides (RMWSF, RYDYSY,  LRLRQL) were selectively synthesized, and different concentrations were  used to inhibit PSA and ConA binding to the HRP.	bind
4476	5	2357	5	10	NULL	0	NULL	RYDYSY peptide	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_zhejiang-da-xue-xue-bao-yi-xue-ban_34_5_16216051_s_7	16216051	(3) Three peptides (RMWSF, RYDYSY,  LRLRQL) were selectively synthesized, and different concentrations were  used to inhibit PSA and ConA binding to the HRP.	bind
4477	6	2357	5	10	NULL	0	NULL	RYDYSY peptide	GP		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_zhejiang-da-xue-xue-bao-yi-xue-ban_34_5_16216051_s_7	16216051	(3) Three peptides (RMWSF, RYDYSY,  LRLRQL) were selectively synthesized, and different concentrations were  used to inhibit PSA and ConA binding to the HRP.	bind
4478	7	2357	5	10	NULL	0	NULL	LRLRQL peptide	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_zhejiang-da-xue-xue-bao-yi-xue-ban_34_5_16216051_s_7	16216051	(3) Three peptides (RMWSF, RYDYSY,  LRLRQL) were selectively synthesized, and different concentrations were  used to inhibit PSA and ConA binding to the HRP.	bind
4479	8	2357	5	10	NULL	0	NULL	LRLRQL peptide	GP		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_zhejiang-da-xue-xue-bao-yi-xue-ban_34_5_16216051_s_7	16216051	(3) Three peptides (RMWSF, RYDYSY,  LRLRQL) were selectively synthesized, and different concentrations were  used to inhibit PSA and ConA binding to the HRP.	bind
4801	1	2357	6	10	NULL	0	NULL	PSA	GP		bind					HRP	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_zhejiang-da-xue-xue-bao-yi-xue-ban_34_5_16216051_s_7	16216051	(3) Three peptides (RMWSF, RYDYSY,  LRLRQL) were selectively synthesized, and different concentrations were  used to inhibit PSA and ConA binding to the HRP.	bind
4802	2	2357	6	10	NULL	0	NULL	ConA	GP		bind					HRP	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_zhejiang-da-xue-xue-bao-yi-xue-ban_34_5_16216051_s_7	16216051	(3) Three peptides (RMWSF, RYDYSY,  LRLRQL) were selectively synthesized, and different concentrations were  used to inhibit PSA and ConA binding to the HRP.	bind
6458	3	2357	6	10	NULL	0	NULL	RMWSF peptide	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_zhejiang-da-xue-xue-bao-yi-xue-ban_34_5_16216051_s_7	16216051	(3) Three peptides (RMWSF, RYDYSY,  LRLRQL) were selectively synthesized, and different concentrations were  used to inhibit PSA and ConA binding to the HRP.	bind
6459	4	2357	6	10	NULL	0	NULL	RMWSF peptide	GP		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_zhejiang-da-xue-xue-bao-yi-xue-ban_34_5_16216051_s_7	16216051	(3) Three peptides (RMWSF, RYDYSY,  LRLRQL) were selectively synthesized, and different concentrations were  used to inhibit PSA and ConA binding to the HRP.	bind
6460	5	2357	6	10	NULL	0	NULL	RYDYSY peptide	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_zhejiang-da-xue-xue-bao-yi-xue-ban_34_5_16216051_s_7	16216051	(3) Three peptides (RMWSF, RYDYSY,  LRLRQL) were selectively synthesized, and different concentrations were  used to inhibit PSA and ConA binding to the HRP.	bind
6461	6	2357	6	10	NULL	0	NULL	RYDYSY peptide	GP		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_zhejiang-da-xue-xue-bao-yi-xue-ban_34_5_16216051_s_7	16216051	(3) Three peptides (RMWSF, RYDYSY,  LRLRQL) were selectively synthesized, and different concentrations were  used to inhibit PSA and ConA binding to the HRP.	bind
6462	7	2357	6	10	NULL	0	NULL	 LRLRQL peptide	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_zhejiang-da-xue-xue-bao-yi-xue-ban_34_5_16216051_s_7	16216051	(3) Three peptides (RMWSF, RYDYSY,  LRLRQL) were selectively synthesized, and different concentrations were  used to inhibit PSA and ConA binding to the HRP.	bind
6463	8	2357	6	10	NULL	0	NULL	 LRLRQL peptide	GP		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_zhejiang-da-xue-xue-bao-yi-xue-ban_34_5_16216051_s_7	16216051	(3) Three peptides (RMWSF, RYDYSY,  LRLRQL) were selectively synthesized, and different concentrations were  used to inhibit PSA and ConA binding to the HRP.	bind
4480	1	2358	5	10	NULL	0	NULL	 CbbR dimers	GP		bind					IR1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to IR1 and IR3, resulting in the bending of DNA at an angle of 64 degrees .	bind
4481	2	2358	5	10	NULL	0	NULL	 CbbR dimers	GP		bind					IR3	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to IR1 and IR3, resulting in the bending of DNA at an angle of 64 degrees .	bind
4482	3	2358	5	10	NULL	0	NULL	statement 1	Process		results in					DNA 	NucleicAcid	 bending of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to IR1 and IR3, resulting in the bending of DNA at an angle of 64 degrees .	bind
4483	4	2358	5	10	NULL	0	NULL	statement 2	Process		results in					DNA	NucleicAcid	 bending of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to IR1 and IR3, resulting in the bending of DNA at an angle of 64 degrees .	bind
4803	1	2358	6	10	NULL	0	NULL	CbbR dimer	GP		bind					IR1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to IR1 and IR3, resulting in the bending of DNA at an angle of 64 degrees .	bind
4804	2	2358	6	10	NULL	0	NULL	CbbR dimer	GP		bind					IR3	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to IR1 and IR3, resulting in the bending of DNA at an angle of 64 degrees .	bind
4805	3	2358	6	10	NULL	0	NULL	statement 1	Process		results in					DNA	NucleicAcid	bending of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to IR1 and IR3, resulting in the bending of DNA at an angle of 64 degrees .	bind
4806	4	2358	6	10	NULL	0	NULL	statement 2	Process		results in					DNA	NucleicAcid	bending of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to IR1 and IR3, resulting in the bending of DNA at an angle of 64 degrees .	bind
4484	1	2359	5	10	NULL	0	NULL	CbbR dimers	GP		bind					DNA	NucleicAcid			IR1 site	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to sites IR1 and IR2, relaxing the DNA bend by 9 degrees  to 55 degrees  in the presence of the CbbR inducer  NADPH.	bind
4485	2	2359	5	10	NULL	0	NULL	 CbbR dimers	GP		bind					DNA	NucleicAcid			IR2 site	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to sites IR1 and IR2, relaxing the DNA bend by 9 degrees  to 55 degrees  in the presence of the CbbR inducer  NADPH.	bind
4486	3	2359	5	10	NULL	0	NULL	statement 1	Process		relax					DNA bend	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to sites IR1 and IR2, relaxing the DNA bend by 9 degrees  to 55 degrees  in the presence of the CbbR inducer  NADPH.	bind
4487	4	2359	5	10	NULL	0	NULL	statement 2	Process		relax					DNA bend	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to sites IR1 and IR2, relaxing the DNA bend by 9 degrees  to 55 degrees  in the presence of the CbbR inducer  NADPH.	bind
4488	5	2359	5	10	NULL	0	NULL	statement 3	Process		in the presence of					NADPH	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to sites IR1 and IR2, relaxing the DNA bend by 9 degrees  to 55 degrees  in the presence of the CbbR inducer  NADPH.	bind
4489	6	2359	5	10	NULL	0	NULL	statement 4	Process		in the presence of					NADPH	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to sites IR1 and IR2, relaxing the DNA bend by 9 degrees  to 55 degrees  in the presence of the CbbR inducer  NADPH.	bind
46485	7	2359	5	10	NULL	0	NULL	NADPH	Chemical		is a type of					CbbR inducer	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to sites IR1 and IR2, relaxing the DNA bend by 9 degrees  to 55 degrees  in the presence of the CbbR inducer  NADPH.	bind
5005	1	2359	6	10	NULL	0	NULL	CbbR dimer	GP		bind					DNA	NucleicAcid			site IR1	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to sites IR1 and IR2, relaxing the DNA bend by 9 degrees  to 55 degrees  in the presence of the CbbR inducer  NADPH.	bind
5006	2	2359	6	10	NULL	0	NULL	CbbR dimer	GP		bind					DNA	NucleicAcid			site IR2	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to sites IR1 and IR2, relaxing the DNA bend by 9 degrees  to 55 degrees  in the presence of the CbbR inducer  NADPH.	bind
5007	3	2359	6	10	NULL	0	NULL	statement 1	Process		relaxes					DNA bend	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to sites IR1 and IR2, relaxing the DNA bend by 9 degrees  to 55 degrees  in the presence of the CbbR inducer  NADPH.	bind
5008	4	2359	6	10	NULL	0	NULL	statement 2	Process		relaxes					DNA bend	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to sites IR1 and IR2, relaxing the DNA bend by 9 degrees  to 55 degrees  in the presence of the CbbR inducer  NADPH.	bind
5009	5	2359	6	10	NULL	0	NULL	statement 3	Process		occurs in presence of					NADPH	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to sites IR1 and IR2, relaxing the DNA bend by 9 degrees  to 55 degrees  in the presence of the CbbR inducer  NADPH.	bind
5010	6	2359	6	10	NULL	0	NULL	statement 4	Process		occurs in presence of					NADPH	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to sites IR1 and IR2, relaxing the DNA bend by 9 degrees  to 55 degrees  in the presence of the CbbR inducer  NADPH.	bind
46486	7	2359	6	10	NULL	0	NULL	NADPH	Process		is a type of					CbbR inducer	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_4_1245_s_238	12562794	(3) Two CbbR dimers bound to sites IR1 and IR2, relaxing the DNA bend by 9 degrees  to 55 degrees  in the presence of the CbbR inducer  NADPH.	bind
4490	1	2360	5	10	NULL	0	NULL	CcpA	GP		bind		specifically			gnt gene	GP	B. subtilis		CRE	NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiolrev_19_3_187_s_129	9050218	(3) Using gel-retardation analysis, it was demonstrated that specific binding of CcpA to CRE of the  B. subtilis gnt gene is triggered by HPr(Ser-P) but not by free HPr.	bind
4491	2	2360	5	10	NULL	0	NULL	statement 1	Process		is triggered by					HPr	GP		Ser-P		NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiolrev_19_3_187_s_129	9050218	(3) Using gel-retardation analysis, it was demonstrated that specific binding of CcpA to CRE of the  B. subtilis gnt gene is triggered by HPr(Ser-P) but not by free HPr.	bind
4492	3	2360	5	10	NULL	0	NULL	statement 1	Process		is not triggered by					HPr	GP	free			NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiolrev_19_3_187_s_129	9050218	(3) Using gel-retardation analysis, it was demonstrated that specific binding of CcpA to CRE of the  B. subtilis gnt gene is triggered by HPr(Ser-P) but not by free HPr.	bind
5011	1	2360	6	10	NULL	0	NULL	CcpA	GP		bind		specifically			gnt gene	GP	B. subtilis		CRE	NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiolrev_19_3_187_s_129	9050218	(3) Using gel-retardation analysis, it was demonstrated that specific binding of CcpA to CRE of the  B. subtilis gnt gene is triggered by HPr(Ser-P) but not by free HPr.	bind
5012	2	2360	6	10	NULL	0	NULL	HPr	GP		triggers			Ser-P		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiolrev_19_3_187_s_129	9050218	(3) Using gel-retardation analysis, it was demonstrated that specific binding of CcpA to CRE of the  B. subtilis gnt gene is triggered by HPr(Ser-P) but not by free HPr.	bind
5013	3	2360	6	10	NULL	0	NULL	HPr	GP	free	does not trigger					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiolrev_19_3_187_s_129	9050218	(3) Using gel-retardation analysis, it was demonstrated that specific binding of CcpA to CRE of the  B. subtilis gnt gene is triggered by HPr(Ser-P) but not by free HPr.	bind
4493	1	2361	5	10	NULL	0	NULL	 permease	GP		bind			D55C		sugar co-substrate	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-biophys-res-commun_178_3_1872836_s_4	1872836	(3H) p-nitrophenyl-alpha-D-galactoside  (NPG) binding studies demonstrated that D55C permease binds the sugar  co-substrate but Na+ (or Li+) ions do no longer enhance the affinity of  D55C permease for the co-transported sugar.	bind
4494	2	2361	5	10	NULL	0	NULL	Na+ ions	Chemical		does not enhance					statement 1	Process	affinity of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-biophys-res-commun_178_3_1872836_s_4	1872836	(3H) p-nitrophenyl-alpha-D-galactoside  (NPG) binding studies demonstrated that D55C permease binds the sugar  co-substrate but Na+ (or Li+) ions do no longer enhance the affinity of  D55C permease for the co-transported sugar.	bind
4495	3	2361	5	10	NULL	0	NULL	Li+ ions	Chemical		does not enhance					statement 1	Process	affinity of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-biophys-res-commun_178_3_1872836_s_4	1872836	(3H) p-nitrophenyl-alpha-D-galactoside  (NPG) binding studies demonstrated that D55C permease binds the sugar  co-substrate but Na+ (or Li+) ions do no longer enhance the affinity of  D55C permease for the co-transported sugar.	bind
46487	4	2361	5	10	NULL	0	NULL	NPG	Chemical		is					p-nitrophenyl-alpha-D-galactoside	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-biophys-res-commun_178_3_1872836_s_4	1872836	(3H) p-nitrophenyl-alpha-D-galactoside  (NPG) binding studies demonstrated that D55C permease binds the sugar  co-substrate but Na+ (or Li+) ions do no longer enhance the affinity of  D55C permease for the co-transported sugar.	bind
46488	5	2361	5	10	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-biophys-res-commun_178_3_1872836_s_4	1872836	(3H) p-nitrophenyl-alpha-D-galactoside  (NPG) binding studies demonstrated that D55C permease binds the sugar  co-substrate but Na+ (or Li+) ions do no longer enhance the affinity of  D55C permease for the co-transported sugar.	bind
5014	1	2361	6	10	NULL	0	NULL	permease	GP		bind			D55C		sugar co-substrate	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-biophys-res-commun_178_3_1872836_s_4	1872836	(3H) p-nitrophenyl-alpha-D-galactoside  (NPG) binding studies demonstrated that D55C permease binds the sugar  co-substrate but Na+ (or Li+) ions do no longer enhance the affinity of  D55C permease for the co-transported sugar.	bind
5015	2	2361	6	10	NULL	0	NULL	NPG 	Chemical		is					p-nitrophenyl-alpha-D-galactoside	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-biophys-res-commun_178_3_1872836_s_4	1872836	(3H) p-nitrophenyl-alpha-D-galactoside  (NPG) binding studies demonstrated that D55C permease binds the sugar  co-substrate but Na+ (or Li+) ions do no longer enhance the affinity of  D55C permease for the co-transported sugar.	bind
5016	3	2361	6	10	NULL	0	NULL	Na+ ion	Chemical		do not enhance					statement 1	Process	affinity of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-biophys-res-commun_178_3_1872836_s_4	1872836	(3H) p-nitrophenyl-alpha-D-galactoside  (NPG) binding studies demonstrated that D55C permease binds the sugar  co-substrate but Na+ (or Li+) ions do no longer enhance the affinity of  D55C permease for the co-transported sugar.	bind
5017	4	2361	6	10	NULL	0	NULL	Li+ ion	Chemical		do not enhance					statement 1	Process	affinity of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-biophys-res-commun_178_3_1872836_s_4	1872836	(3H) p-nitrophenyl-alpha-D-galactoside  (NPG) binding studies demonstrated that D55C permease binds the sugar  co-substrate but Na+ (or Li+) ions do no longer enhance the affinity of  D55C permease for the co-transported sugar.	bind
5018	5	2361	6	10	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-biophys-res-commun_178_3_1872836_s_4	1872836	(3H) p-nitrophenyl-alpha-D-galactoside  (NPG) binding studies demonstrated that D55C permease binds the sugar  co-substrate but Na+ (or Li+) ions do no longer enhance the affinity of  D55C permease for the co-transported sugar.	bind
4496	1	2363	5	10	NULL	0	NULL	Src	GP	activated	bind					hDia2C	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_3_287_s_34	12636908	(4) Activated Src binds to hDia2C.	bind
5019	1	2363	6	10	NULL	0	NULL	Src	GP	activated	bind					hDia2C	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_3_287_s_34	12636908	(4) Activated Src binds to hDia2C.	bind
4497	1	2364	5	10	NULL	0	NULL	ATP	Chemical		bind					myosin	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_546_2_209_s_134	12832041	(4) ATP binding to the myosin causes the myosin to detach from the actin and change its structure (swinging back of the lever).	bind
4498	2	2364	5	10	NULL	0	NULL	myosin	GP		detaches from					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_546_2_209_s_134	12832041	(4) ATP binding to the myosin causes the myosin to detach from the actin and change its structure (swinging back of the lever).	bind
4499	3	2364	5	10	NULL	0	NULL	statement 1	Process		causes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_546_2_209_s_134	12832041	(4) ATP binding to the myosin causes the myosin to detach from the actin and change its structure (swinging back of the lever).	bind
4500	4	2364	5	10	NULL	0	NULL	statement 1	Process		causes					myosin	GP	structural change of			NULL		NULL	NULL	NULL	NULL	gw60_febslett_546_2_209_s_134	12832041	(4) ATP binding to the myosin causes the myosin to detach from the actin and change its structure (swinging back of the lever).	bind
5020	1	2364	6	10	NULL	0	NULL	ATP	Chemical		bind					myosin	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_546_2_209_s_134	12832041	(4) ATP binding to the myosin causes the myosin to detach from the actin and change its structure (swinging back of the lever).	bind
5021	2	2364	6	10	NULL	0	NULL	myosin	GP		detach from					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_546_2_209_s_134	12832041	(4) ATP binding to the myosin causes the myosin to detach from the actin and change its structure (swinging back of the lever).	bind
5022	3	2364	6	10	NULL	0	NULL	statement 1	Process		causes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_546_2_209_s_134	12832041	(4) ATP binding to the myosin causes the myosin to detach from the actin and change its structure (swinging back of the lever).	bind
5023	4	2364	6	10	NULL	0	NULL	statement 1	Process		causes					myosin	GP	structural change of			NULL		NULL	NULL	NULL	NULL	gw60_febslett_546_2_209_s_134	12832041	(4) ATP binding to the myosin causes the myosin to detach from the actin and change its structure (swinging back of the lever).	bind
4501	2	2365	5	10	NULL	0	NULL	statement 1	Process		downregulates during					adipogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_2_147_s_219	12705864	(4) Levels of active, GTP bound Rho are normally downregulated during the course of adipogenesis.	bind
46489	1	2365	5	10	NULL	0	NULL	GTP	Chemical		bind					Rho	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_2_147_s_219	12705864	(4) Levels of active, GTP bound Rho are normally downregulated during the course of adipogenesis.	bind
5025	1	2365	6	10	NULL	0	NULL	GTP	Chemical		bind					Rho	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_2_147_s_219	12705864	(4) Levels of active, GTP bound Rho are normally downregulated during the course of adipogenesis.	bind
5026	2	2365	6	10	NULL	0	NULL	statement 1	Process		downregulates during					adipogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_2_147_s_219	12705864	(4) Levels of active, GTP bound Rho are normally downregulated during the course of adipogenesis.	bind
4502	1	2367	5	10	NULL	0	NULL	PsbP	GP	chlamydomonas	bind		functionally			PS II	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_6	16049780	(4) While Chlamydomonas PsbP functionally bound to spinach  PS II in the presence of Chlamydomonas PsbO, spinach PsbP bound loosely  to spinach PS II in the presence of Chlamydomonas PsbO with no concomitant  restoration of oxygen evolution.	bind
4503	2	2367	5	10	NULL	0	NULL	statement 1	Process		in the presence of					PsbO	GP	chlamydomonas			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_6	16049780	(4) While Chlamydomonas PsbP functionally bound to spinach  PS II in the presence of Chlamydomonas PsbO, spinach PsbP bound loosely  to spinach PS II in the presence of Chlamydomonas PsbO with no concomitant  restoration of oxygen evolution.	bind
4504	3	2367	5	10	NULL	0	NULL	PsbP	GP	spinach	bind		loosely			PS II	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_6	16049780	(4) While Chlamydomonas PsbP functionally bound to spinach  PS II in the presence of Chlamydomonas PsbO, spinach PsbP bound loosely  to spinach PS II in the presence of Chlamydomonas PsbO with no concomitant  restoration of oxygen evolution.	bind
4505	4	2367	5	10	NULL	0	NULL	statement 3	Process		in the presence of					PsbO	GP	chlamydomonas			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_6	16049780	(4) While Chlamydomonas PsbP functionally bound to spinach  PS II in the presence of Chlamydomonas PsbO, spinach PsbP bound loosely  to spinach PS II in the presence of Chlamydomonas PsbO with no concomitant  restoration of oxygen evolution.	bind
5027	1	2367	6	10	NULL	0	NULL	PsbP	GP	Chlamydomonas	bind					PS II	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_6	16049780	(4) While Chlamydomonas PsbP functionally bound to spinach  PS II in the presence of Chlamydomonas PsbO, spinach PsbP bound loosely  to spinach PS II in the presence of Chlamydomonas PsbO with no concomitant  restoration of oxygen evolution.	bind
5028	2	2367	6	10	NULL	0	NULL	statement 1	Process		 in presence of					PsbO	GP	Chlamydomonas			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_6	16049780	(4) While Chlamydomonas PsbP functionally bound to spinach  PS II in the presence of Chlamydomonas PsbO, spinach PsbP bound loosely  to spinach PS II in the presence of Chlamydomonas PsbO with no concomitant  restoration of oxygen evolution.	bind
5029	3	2367	6	10	NULL	0	NULL	Psbp	GP	spinach	bind		loosely			PS II	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_6	16049780	(4) While Chlamydomonas PsbP functionally bound to spinach  PS II in the presence of Chlamydomonas PsbO, spinach PsbP bound loosely  to spinach PS II in the presence of Chlamydomonas PsbO with no concomitant  restoration of oxygen evolution.	bind
5030	4	2367	6	10	NULL	0	NULL	statement 3	Process		 in presence of					PsbO	GP	Chlamydomonas			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_6	16049780	(4) While Chlamydomonas PsbP functionally bound to spinach  PS II in the presence of Chlamydomonas PsbO, spinach PsbP bound loosely  to spinach PS II in the presence of Chlamydomonas PsbO with no concomitant  restoration of oxygen evolution.	bind
4506	1	2369	5	10	NULL	0	NULL	PsbQ	GP	chlamydomonas	bind					PS II	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
4507	2	2369	5	10	NULL	0	NULL	statement 1	Process		in the presence of					PsbP	GP	chlamydomonas			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
4508	3	2369	5	10	NULL	0	NULL	statement 1	Process		in the presence of					PsbO	GP	chlamydomonas			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
4509	4	2369	5	10	NULL	0	NULL	statement 1	Process		in the presence of					PsbO	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
4510	5	2369	5	10	NULL	0	NULL	PsbQ	GP	chlamydomonas	does not bind					PS II	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
4511	6	2369	5	10	NULL	0	NULL	statement 5	Process		in the presence of					PsbP	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
4512	7	2369	5	10	NULL	0	NULL	statement 5	Process		in the presence of					PsbO	GP	chlamydomonas			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
4513	8	2369	5	10	NULL	0	NULL	statement 5	Process		in the presence of					PsbO	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
53041	9	2369	5	10	NULL	0	NULL	statement 4	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
53042	10	2369	5	10	NULL	0	NULL	statement 8	Process		is an alternative to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
5031	1	2369	6	10	NULL	0	NULL	PsbQ	GP	Chlamydomonas	bind					PS II	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
5032	2	2369	6	10	NULL	0	NULL	statement 1	Process		occurs in presence of					PsbP	GP	Chlamydomonas			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
5033	3	2369	6	10	NULL	0	NULL	statement 1	Process		occurs in presence of					PsbO	GP	Chlamydomonas			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
5034	4	2369	6	10	NULL	0	NULL	statement 1	Process		occurs in presence of					PsbO	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
5035	5	2369	6	10	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
5036	6	2369	6	10	NULL	0	NULL	PsbQ	GP	Chlamydomonas	does not bind					PS II	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
5037	7	2369	6	10	NULL	0	NULL	statement 6	Process		occurs in presence of					PsbP	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
5038	8	2369	6	10	NULL	0	NULL	statement 6	Process		occurs in presence of					PsbO	GP	Chlamydomonas			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
5039	9	2369	6	10	NULL	0	NULL	statement 6	Process		occurs in presence of					PsbO	GP	spinach			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
5040	10	2369	6	10	NULL	0	NULL	statement 8	Process		is an alternative to					statement 9	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_photosynth-res_84_1-3_16049780_s_7	16049780	(5) Chlamydomonas PsbQ bound to spinach  PS II in the presence of Chlamydomonas PsbP and PsbO or spinach PsbO but  not to spinach PS II in the presence of spinach PsbP and Chlamydomonas  PsbO or spinach PsbO.	bind
4878	1	2371	5	10	NULL	0	NULL	HGF variant	GP		bind					HGF-NK1 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
4879	2	2371	5	10	NULL	0	NULL	HGF variant	GP		bind					HGF-NK2 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
4880	3	2371	5	10	NULL	0	NULL	HGF variant	GP		bind					pro-HGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
4881	4	2371	5	10	NULL	0	NULL	HGF variant	GP		bind					MSP chain	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
46699	5	2371	5	10	NULL	0	NULL	MSP variant	GP		bind					HGF-NK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
46700	9	2371	5	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
46701	6	2371	5	10	NULL	0	NULL	MSP variant	GP		bind					HGF-NK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
46702	10	2371	5	10	NULL	0	NULL	statement 2	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
46703	7	2371	5	10	NULL	0	NULL	MSP variant	GP		bind					pro-HGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
46704	8	2371	5	10	NULL	0	NULL	MSP variant	GP		bind					MSP chain	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
46705	11	2371	5	10	NULL	0	NULL	statement 3	Process		is an alternative to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
46706	12	2371	5	10	NULL	0	NULL	statement 4	Process		is an alternative to					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
5042	1	2371	6	10	NULL	0	NULL	HGF variant	GP		bind					HGF-NK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
5043	2	2371	6	10	NULL	0	NULL	HGF variant	GP		bind					HGF-NK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
5044	3	2371	6	10	NULL	0	NULL	HGF variant	GP		bind					pro-HGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
5045	4	2371	6	10	NULL	0	NULL	HGF variant	GP		bind					MSP chain	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
5046	5	2371	6	10	NULL	0	NULL	MSP variant	GP		bind					HGF-NK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
5047	6	2371	6	10	NULL	0	NULL	MSP variant	GP		bind					HGF-NK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
5048	7	2371	6	10	NULL	0	NULL	MSP variant	GP		bind					pro-HGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
5049	8	2371	6	10	NULL	0	NULL	MSP variant	GP		bind					MSP chain	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
5050	9	2371	6	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
5051	10	2371	6	10	NULL	0	NULL	statement 2	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
5052	11	2371	6	10	NULL	0	NULL	statement 3	Process		is an alternative to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
5053	12	2371	6	10	NULL	0	NULL	statement 4	Process		is an alternative to					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_1_1_s_79	9657372	(5) The  Kd values of HGF or MSP variants that bind to receptor (HGF-NK1, HGF-NK2, pro-HGF, MSP   chain) are 2-10-fold higher than the  Kds of the mature intact ligands.	bind
4514	1	2372	5	10	NULL	0	NULL	eIF4GII	GP		bind			Leu					Trp-73		NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_6_707_s_153	10394359	(6) ( Leu in eIF4GII and  Met in 4E-BP1) binds to Trp-73, Leu-131, and Leu-135.	bind
4515	2	2372	5	10	NULL	0	NULL	eIF4GII	GP		bind			Leu					Leu-131		NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_6_707_s_153	10394359	(6) ( Leu in eIF4GII and  Met in 4E-BP1) binds to Trp-73, Leu-131, and Leu-135.	bind
4516	3	2372	5	10	NULL	0	NULL	eIF4GII	GP		bind			Leu					Leu-135		NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_6_707_s_153	10394359	(6) ( Leu in eIF4GII and  Met in 4E-BP1) binds to Trp-73, Leu-131, and Leu-135.	bind
4517	4	2372	5	10	NULL	0	NULL	4E-BP1	GP		bind			Met					Trp-73		NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_6_707_s_153	10394359	(6) ( Leu in eIF4GII and  Met in 4E-BP1) binds to Trp-73, Leu-131, and Leu-135.	bind
4518	5	2372	5	10	NULL	0	NULL	4E-BP1	GP		bind			Met					Leu-131		NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_6_707_s_153	10394359	(6) ( Leu in eIF4GII and  Met in 4E-BP1) binds to Trp-73, Leu-131, and Leu-135.	bind
4519	6	2372	5	10	NULL	0	NULL	4E-BP1	GP		bind			Met					Leu-135		NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_6_707_s_153	10394359	(6) ( Leu in eIF4GII and  Met in 4E-BP1) binds to Trp-73, Leu-131, and Leu-135.	bind
5054	1	2372	6	10	NULL	0	NULL	eIF4GII	GP		bind			Leu					Trp-73		NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_6_707_s_153	10394359	(6) ( Leu in eIF4GII and  Met in 4E-BP1) binds to Trp-73, Leu-131, and Leu-135.	bind
5055	2	2372	6	10	NULL	0	NULL	eIF4GII	GP		bind			Leu					Leu-131		NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_6_707_s_153	10394359	(6) ( Leu in eIF4GII and  Met in 4E-BP1) binds to Trp-73, Leu-131, and Leu-135.	bind
5056	3	2372	6	10	NULL	0	NULL	eIF4GII	GP		bind			Leu					Leu-135		NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_6_707_s_153	10394359	(6) ( Leu in eIF4GII and  Met in 4E-BP1) binds to Trp-73, Leu-131, and Leu-135.	bind
5057	4	2372	6	10	NULL	0	NULL	4E-BP1	GP		bind			Met					Trp-73		NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_6_707_s_153	10394359	(6) ( Leu in eIF4GII and  Met in 4E-BP1) binds to Trp-73, Leu-131, and Leu-135.	bind
5058	5	2372	6	10	NULL	0	NULL	4E-BP1	GP		bind			Met					Leu-131		NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_6_707_s_153	10394359	(6) ( Leu in eIF4GII and  Met in 4E-BP1) binds to Trp-73, Leu-131, and Leu-135.	bind
5059	6	2372	6	10	NULL	0	NULL	4E-BP1	GP		bind			Met					Leu-135		NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_6_707_s_153	10394359	(6) ( Leu in eIF4GII and  Met in 4E-BP1) binds to Trp-73, Leu-131, and Leu-135.	bind
4520	1	2375	5	10	NULL	0	NULL	E2F1	GP		bind					DP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_8_2703_s_126	10436023	(7) E2F1 binds DP1.	bind
5060	1	2375	6	10	NULL	0	NULL	E2F1	GP		bind					DP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_8_2703_s_126	10436023	(7) E2F1 binds DP1.	bind
4521	1	2376	5	10	NULL	0	NULL	ATP	Chemical		bind					actin	GP		subunit		NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_453_s_86	12600310	(8) Filaments age by hydrolysis of ATP bound to each actin subunit (white subunits turn yellow) followed by dissociation of the   phosphate (subunits turn red).	bind
4522	2	2376	5	10	NULL	0	NULL	filaments	CellComponent		age by					statement 1	Process	hydrolysis of			NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_453_s_86	12600310	(8) Filaments age by hydrolysis of ATP bound to each actin subunit (white subunits turn yellow) followed by dissociation of the   phosphate (subunits turn red).	bind
4523	3	2376	5	10	NULL	0	NULL	statement 2	Process		occurs following					phosphate	Chemical	dissociation of			NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_453_s_86	12600310	(8) Filaments age by hydrolysis of ATP bound to each actin subunit (white subunits turn yellow) followed by dissociation of the   phosphate (subunits turn red).	bind
5061	1	2376	6	10	NULL	0	NULL	ATP	Chemical		bind					actin subunit	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_453_s_86	12600310	(8) Filaments age by hydrolysis of ATP bound to each actin subunit (white subunits turn yellow) followed by dissociation of the   phosphate (subunits turn red).	bind
6568	2	2376	6	10	NULL	0	NULL	filaments 	CellComponent		age by					statement 1	Process	hydrolysis of			NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_453_s_86	12600310	(8) Filaments age by hydrolysis of ATP bound to each actin subunit (white subunits turn yellow) followed by dissociation of the   phosphate (subunits turn red).	bind
6569	3	2376	6	10	NULL	0	NULL	statement 2	Process		occurs following					phosphate	Chemical	dissociation of			NULL		NULL	NULL	NULL	NULL	gw60_cell_112_4_453_s_86	12600310	(8) Filaments age by hydrolysis of ATP bound to each actin subunit (white subunits turn yellow) followed by dissociation of the   phosphate (subunits turn red).	bind
4893	1	2377	5	10	NULL	0	NULL	H43 peptide	GP		does not bind		apparently			DnaK	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25668_s_118	11970958	(9-mers were derived from the overlap windows of DnaK-binding ( i.e. peptides H10, H18, H32, M18, and M39) or homologous ( i.e. peptides M10 and H39) regions; peptides H43 and H44 did not show apparent binding of DnaK, but were theoretically predicted to contain a DnaK-binding site (see Fig.  6).)	bind
4895	2	2377	5	10	NULL	0	NULL	H44 peptide	GP		does not bind		apparently			DnaK	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25668_s_118	11970958	(9-mers were derived from the overlap windows of DnaK-binding ( i.e. peptides H10, H18, H32, M18, and M39) or homologous ( i.e. peptides M10 and H39) regions; peptides H43 and H44 did not show apparent binding of DnaK, but were theoretically predicted to contain a DnaK-binding site (see Fig.  6).)	bind
4897	3	2377	5	10	NULL	0	NULL	H43 peptide	GP		contain		may						DnaK-binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25668_s_118	11970958	(9-mers were derived from the overlap windows of DnaK-binding ( i.e. peptides H10, H18, H32, M18, and M39) or homologous ( i.e. peptides M10 and H39) regions; peptides H43 and H44 did not show apparent binding of DnaK, but were theoretically predicted to contain a DnaK-binding site (see Fig.  6).)	bind
4899	4	2377	5	10	NULL	0	NULL	H44 peptide	GP		contain		may						DnaK-binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25668_s_118	11970958	(9-mers were derived from the overlap windows of DnaK-binding ( i.e. peptides H10, H18, H32, M18, and M39) or homologous ( i.e. peptides M10 and H39) regions; peptides H43 and H44 did not show apparent binding of DnaK, but were theoretically predicted to contain a DnaK-binding site (see Fig.  6).)	bind
5226	1	2377	6	10	NULL	0	NULL	peptide H43	GP		does not bind					DnaK	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25668_s_118	11970958	(9-mers were derived from the overlap windows of DnaK-binding ( i.e. peptides H10, H18, H32, M18, and M39) or homologous ( i.e. peptides M10 and H39) regions; peptides H43 and H44 did not show apparent binding of DnaK, but were theoretically predicted to contain a DnaK-binding site (see Fig.  6).)	bind
5227	2	2377	6	10	NULL	0	NULL	peptide H44	GP		does not bind					DnaK	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25668_s_118	11970958	(9-mers were derived from the overlap windows of DnaK-binding ( i.e. peptides H10, H18, H32, M18, and M39) or homologous ( i.e. peptides M10 and H39) regions; peptides H43 and H44 did not show apparent binding of DnaK, but were theoretically predicted to contain a DnaK-binding site (see Fig.  6).)	bind
5228	3	2377	6	10	NULL	0	NULL	peptide H43	GP		contain		may						DnaK-binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25668_s_118	11970958	(9-mers were derived from the overlap windows of DnaK-binding ( i.e. peptides H10, H18, H32, M18, and M39) or homologous ( i.e. peptides M10 and H39) regions; peptides H43 and H44 did not show apparent binding of DnaK, but were theoretically predicted to contain a DnaK-binding site (see Fig.  6).)	bind
5229	4	2377	6	10	NULL	0	NULL	peptide H44	GP		 contain		may						DnaK-binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25668_s_118	11970958	(9-mers were derived from the overlap windows of DnaK-binding ( i.e. peptides H10, H18, H32, M18, and M39) or homologous ( i.e. peptides M10 and H39) regions; peptides H43 and H44 did not show apparent binding of DnaK, but were theoretically predicted to contain a DnaK-binding site (see Fig.  6).)	bind
4904	1	2379	5	10	NULL	0	NULL	DNA	NucleicAcid		bind					ORC	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
4905	2	2379	5	10	NULL	0	NULL	statement 1	Process		in the presence of					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
4906	3	2379	5	10	NULL	0	NULL	DNA	NucleicAcid	wild-type	bind					ORC-1A	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
4907	4	2379	5	10	NULL	0	NULL	statement 2	Process		in the presence of					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
4908	5	2379	5	10	NULL	0	NULL	DNA	NucleicAcid	mutant	bind					ORC-1A	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
4909	6	2379	5	10	NULL	0	NULL	statement 5	Process		in the presence of					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
4911	7	2379	5	10	NULL	0	NULL	DNA	NucleicAcid	wild-type	bind					ORC-5A	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
4913	8	2379	5	10	NULL	0	NULL	statement 7	Process		in the presence of					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
4914	9	2379	5	10	NULL	0	NULL	DNA	NucleicAcid	mutant	bind					ORC-5A	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
4915	10	2379	5	10	NULL	0	NULL	statement 9	Process		in the presence of					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
5230	1	2379	6	10	NULL	0	NULL	DNA	NucleicAcid		bind					ORC	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
5231	2	2379	6	10	NULL	0	NULL	statement 1	Process		occurs in presence of					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
5232	3	2379	6	10	NULL	0	NULL	DNA	NucleicAcid	wild type	bind					ORC-1A	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
5233	4	2379	6	10	NULL	0	NULL	statement 3	Process		occurs in presence of					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
5234	5	2379	6	10	NULL	0	NULL	DNA	NucleicAcid	mutant	bind					ORC-1A	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
5235	6	2379	6	10	NULL	0	NULL	statement 5	Process		occurs in presence of					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
5236	7	2379	6	10	NULL	0	NULL	DNA	NucleicAcid	wild type	bind					ORC-5A	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
5237	8	2379	6	10	NULL	0	NULL	statement 7	Process		occurs in presence of					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
5238	9	2379	6	10	NULL	0	NULL	DNA	NucleicAcid	mutant	bind					ORC-5A	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
5239	10	2379	6	10	NULL	0	NULL	statement 9	Process		occurs in presence of					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_166	12966094	(A - B1 - ) DNA bound to wild-type ORC in 5 mM or 5 muM ATP, respectively; 29 or 14 fmol of wild-type DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively, and 16 or 15 fmol of mutant DNA bound to ORC-1A in 5 mM or 5 muM ATP, respectively; 55 or 54 fmol of wild-type DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively, and 46 or 40 fmol of mutant DNA bound to ORC-5A in 5 mM or 5 muM ATP, respectively.	bind
4925	1	2381	5	10	NULL	0	NULL	ADP	Chemical		dissociate from					acto-myosin complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_6_1263_s_184	12628919	(A - M) to weak binding (A + M - ATP) of acto-myosin follows ADP dissociation from acto-myosin complex and subsequent binding of ATP to myosin.	bind
4926	2	2381	5	10	NULL	0	NULL	ATP	Chemical		bind					myosin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_6_1263_s_184	12628919	(A - M) to weak binding (A + M - ATP) of acto-myosin follows ADP dissociation from acto-myosin complex and subsequent binding of ATP to myosin.	bind
4927	3	2381	5	10	NULL	0	NULL	statement 2	Process		occurs following					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_6_1263_s_184	12628919	(A - M) to weak binding (A + M - ATP) of acto-myosin follows ADP dissociation from acto-myosin complex and subsequent binding of ATP to myosin.	bind
4928	4	2381	5	10	NULL	0	NULL	acto-myosin	GP	weak binding of	follows					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_6_1263_s_184	12628919	(A - M) to weak binding (A + M - ATP) of acto-myosin follows ADP dissociation from acto-myosin complex and subsequent binding of ATP to myosin.	bind
6564	1	2381	6	10	NULL	0	NULL	ADP	Chemical		dissociates from					acto-myosin complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_6_1263_s_184	12628919	(A - M) to weak binding (A + M - ATP) of acto-myosin follows ADP dissociation from acto-myosin complex and subsequent binding of ATP to myosin.	bind
6565	2	2381	6	10	NULL	0	NULL	ATP	Chemical		bind					myosin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_6_1263_s_184	12628919	(A - M) to weak binding (A + M - ATP) of acto-myosin follows ADP dissociation from acto-myosin complex and subsequent binding of ATP to myosin.	bind
6566	3	2381	6	10	NULL	0	NULL	statement 2	Process		occurs following					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_6_1263_s_184	12628919	(A - M) to weak binding (A + M - ATP) of acto-myosin follows ADP dissociation from acto-myosin complex and subsequent binding of ATP to myosin.	bind
6567	4	2381	6	10	NULL	0	NULL	acto-myosin	GP	weak binding of	follows					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_6_1263_s_184	12628919	(A - M) to weak binding (A + M - ATP) of acto-myosin follows ADP dissociation from acto-myosin complex and subsequent binding of ATP to myosin.	bind
4929	1	2382	5	10	NULL	0	NULL	2 -NH3+ group	Chemical		deprotonates in					aqueous solution	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_7_2_85_s_75	10662698	(A 2 -NH3+ group deprotonates with a pKa of  6.2 in aqueous solution  [20]  ; the pKa of this group is even lower with rSN bound to the ribozyme, as described below.)	bind
4930	2	2382	5	10	NULL	0	NULL	rSN	NucleicAcid		bind					ribozyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_7_2_85_s_75	10662698	(A 2 -NH3+ group deprotonates with a pKa of  6.2 in aqueous solution  [20]  ; the pKa of this group is even lower with rSN bound to the ribozyme, as described below.)	bind
5063	1	2382	6	10	NULL	0	NULL	rSN	NucleicAcid		bind					ribozyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_7_2_85_s_75	10662698	(A 2 -NH3+ group deprotonates with a pKa of  6.2 in aqueous solution  [20]  ; the pKa of this group is even lower with rSN bound to the ribozyme, as described below.)	bind
53043	2	2382	6	10	NULL	0	NULL	2 -NH3+ group	Chemical		deprotonates in					aqueous solution	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_7_2_85_s_75	10662698	(A 2 -NH3+ group deprotonates with a pKa of  6.2 in aqueous solution  [20]  ; the pKa of this group is even lower with rSN bound to the ribozyme, as described below.)	bind
4554	1	2383	5	10	NULL	0	NULL	HDMEC	Cell		bind					TSP-1	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-invest-dermatol_106_2_8601718_s_10	8601718	(A 4.1 and C 6.1) failed to block HDMEC binding to TSP-1, but  both MoAbs inhibited G361 human melanoma cell binding to TSP-1 by 60%.	bind
4555	2	2383	5	10	NULL	0	NULL	A 4.1	GP		failed to block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-invest-dermatol_106_2_8601718_s_10	8601718	(A 4.1 and C 6.1) failed to block HDMEC binding to TSP-1, but  both MoAbs inhibited G361 human melanoma cell binding to TSP-1 by 60%.	bind
4556	3	2383	5	10	NULL	0	NULL	C 6.1	GP		failed to block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-invest-dermatol_106_2_8601718_s_10	8601718	(A 4.1 and C 6.1) failed to block HDMEC binding to TSP-1, but  both MoAbs inhibited G361 human melanoma cell binding to TSP-1 by 60%.	bind
4557	4	2383	5	10	NULL	0	NULL	G361	Cell		bind					TSP-1	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-invest-dermatol_106_2_8601718_s_10	8601718	(A 4.1 and C 6.1) failed to block HDMEC binding to TSP-1, but  both MoAbs inhibited G361 human melanoma cell binding to TSP-1 by 60%.	bind
4558	5	2383	5	10	NULL	0	NULL	A 4.1	GP		inhibit					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-invest-dermatol_106_2_8601718_s_10	8601718	(A 4.1 and C 6.1) failed to block HDMEC binding to TSP-1, but  both MoAbs inhibited G361 human melanoma cell binding to TSP-1 by 60%.	bind
46697	6	2383	5	10	NULL	0	NULL	G361	Cell		is a type of					human melanoma cell	Cell				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-invest-dermatol_106_2_8601718_s_10	8601718	(A 4.1 and C 6.1) failed to block HDMEC binding to TSP-1, but  both MoAbs inhibited G361 human melanoma cell binding to TSP-1 by 60%.	bind
53044	7	2383	5	10	NULL	0	NULL	 C 6.1	GP		inhibit					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-invest-dermatol_106_2_8601718_s_10	8601718	(A 4.1 and C 6.1) failed to block HDMEC binding to TSP-1, but  both MoAbs inhibited G361 human melanoma cell binding to TSP-1 by 60%.	bind
53045	8	2383	5	10	NULL	0	NULL	A 4.1	GP		is a type of					MoAbs	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-invest-dermatol_106_2_8601718_s_10	8601718	(A 4.1 and C 6.1) failed to block HDMEC binding to TSP-1, but  both MoAbs inhibited G361 human melanoma cell binding to TSP-1 by 60%.	bind
53046	9	2383	5	10	NULL	0	NULL	C 6.1	GP		is a type of					MoAbs	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-invest-dermatol_106_2_8601718_s_10	8601718	(A 4.1 and C 6.1) failed to block HDMEC binding to TSP-1, but  both MoAbs inhibited G361 human melanoma cell binding to TSP-1 by 60%.	bind
5064	1	2383	6	10	NULL	0	NULL	HDMEC	Cell		bind					TSP-1	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-invest-dermatol_106_2_8601718_s_10	8601718	(A 4.1 and C 6.1) failed to block HDMEC binding to TSP-1, but  both MoAbs inhibited G361 human melanoma cell binding to TSP-1 by 60%.	bind
5065	2	2383	6	10	NULL	0	NULL	A 4.1	GP		failed to block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-invest-dermatol_106_2_8601718_s_10	8601718	(A 4.1 and C 6.1) failed to block HDMEC binding to TSP-1, but  both MoAbs inhibited G361 human melanoma cell binding to TSP-1 by 60%.	bind
5066	3	2383	6	10	NULL	0	NULL	C 6.1	GP		failed to block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-invest-dermatol_106_2_8601718_s_10	8601718	(A 4.1 and C 6.1) failed to block HDMEC binding to TSP-1, but  both MoAbs inhibited G361 human melanoma cell binding to TSP-1 by 60%.	bind
5067	4	2383	6	10	NULL	0	NULL	G361 	Cell		bind					TSP-1	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-invest-dermatol_106_2_8601718_s_10	8601718	(A 4.1 and C 6.1) failed to block HDMEC binding to TSP-1, but  both MoAbs inhibited G361 human melanoma cell binding to TSP-1 by 60%.	bind
5068	5	2383	6	10	NULL	0	NULL	A 4.1	GP		inhibits					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-invest-dermatol_106_2_8601718_s_10	8601718	(A 4.1 and C 6.1) failed to block HDMEC binding to TSP-1, but  both MoAbs inhibited G361 human melanoma cell binding to TSP-1 by 60%.	bind
5069	6	2383	6	10	NULL	0	NULL	C 6.1	GP		inhibits					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-invest-dermatol_106_2_8601718_s_10	8601718	(A 4.1 and C 6.1) failed to block HDMEC binding to TSP-1, but  both MoAbs inhibited G361 human melanoma cell binding to TSP-1 by 60%.	bind
46698	7	2383	6	10	NULL	0	NULL	G361	Cell		is a type of					human melanoma cell	Cell				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-invest-dermatol_106_2_8601718_s_10	8601718	(A 4.1 and C 6.1) failed to block HDMEC binding to TSP-1, but  both MoAbs inhibited G361 human melanoma cell binding to TSP-1 by 60%.	bind
53047	8	2383	6	10	NULL	0	NULL	A 4.1	GP		is a type of					MoAbs	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-invest-dermatol_106_2_8601718_s_10	8601718	(A 4.1 and C 6.1) failed to block HDMEC binding to TSP-1, but  both MoAbs inhibited G361 human melanoma cell binding to TSP-1 by 60%.	bind
53048	9	2383	6	10	NULL	0	NULL	C 6.1	GP		is a type of					MoAbs	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-invest-dermatol_106_2_8601718_s_10	8601718	(A 4.1 and C 6.1) failed to block HDMEC binding to TSP-1, but  both MoAbs inhibited G361 human melanoma cell binding to TSP-1 by 60%.	bind
4559	1	2384	5	10	NULL	0	NULL	EspF	GP		bind		specifically			MBP-SNX9214	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_8_3110_s_65	16585770	(A and  B), but EspF bound specifically to MBP-SNX9214 and GST-SNX9FL (C).	bind
4560	2	2384	5	10	NULL	0	NULL	EspF	GP		bind		specifically			GST-SNX9FL	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_8_3110_s_65	16585770	(A and  B), but EspF bound specifically to MBP-SNX9214 and GST-SNX9FL (C).	bind
5070	1	2384	6	10	NULL	0	NULL	EspF	GP		bind		specifically			MBP-SNX9214	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_8_3110_s_65	16585770	(A and  B), but EspF bound specifically to MBP-SNX9214 and GST-SNX9FL (C).	bind
5071	2	2384	6	10	NULL	0	NULL	EspF	GP		bind		specifically			GST-SNX9FL	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_8_3110_s_65	16585770	(A and  B), but EspF bound specifically to MBP-SNX9214 and GST-SNX9FL (C).	bind
4561	1	2385	5	10	NULL	0	NULL	Wnt-5a	GP		activate					NLK	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_1_131_s_192	12482967	(A and B) Activation of NLK by Wnt-5a  is dependent on CaMKII and TAK1.	bind
4562	2	2385	5	10	NULL	0	NULL	statement 1	Process		is dependent on					CaMKII	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_1_131_s_192	12482967	(A and B) Activation of NLK by Wnt-5a  is dependent on CaMKII and TAK1.	bind
4563	3	2385	5	10	NULL	0	NULL	statement 1	Process		is dependent on					TAK1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_1_131_s_192	12482967	(A and B) Activation of NLK by Wnt-5a  is dependent on CaMKII and TAK1.	bind
5072	1	2385	6	10	NULL	0	NULL	Wnt-5a	GP		activates					NLK	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_1_131_s_192	12482967	(A and B) Activation of NLK by Wnt-5a  is dependent on CaMKII and TAK1.	bind
5073	2	2385	6	10	NULL	0	NULL	statement 1	Process		is dependent on					CaMKII	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_1_131_s_192	12482967	(A and B) Activation of NLK by Wnt-5a  is dependent on CaMKII and TAK1.	bind
5074	3	2385	6	10	NULL	0	NULL	statement 1	Process		is dependent on					TAK1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_1_131_s_192	12482967	(A and B) Activation of NLK by Wnt-5a  is dependent on CaMKII and TAK1.	bind
4564	1	2386	5	10	NULL	0	NULL	hOGG1	GP	wild-type	bind					DNA fragment	NucleicAcid	native		1234 bp	NULL		NULL	NULL	NULL	NULL	gw60_chembiol_9_3_345_s_84	11927259	(A and B) AFM images of wild-type hOGG1 bound to a 1234 bp native DNA fragment (no oxoG specifically introduced).	bind
5075	1	2386	6	10	NULL	0	NULL	hOGG1	GP	wild type	bind					DNA fragment	NucleicAcid	native		1234 bp 	NULL		NULL	NULL	NULL	NULL	gw60_chembiol_9_3_345_s_84	11927259	(A and B) AFM images of wild-type hOGG1 bound to a 1234 bp native DNA fragment (no oxoG specifically introduced).	bind
4565	1	2387	5	10	NULL	0	NULL	D1	GP		bind			ATP binding regions		ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_1_203_s_115	10790395	(A and B) Aligned sequences representing the ATP-binding regions of the D1	bind
5077	1	2387	6	10	NULL	0	NULL	D1	GP		bind			ATP binding regions		ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_1_203_s_115	10790395	(A and B) Aligned sequences representing the ATP-binding regions of the D1	bind
4566	1	2388	5	10	NULL	0	NULL	lactoferrin	GP	human	bind					D39	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_5_3372_s_220	11292760	(A and B) Binding of human and bovine lactoferrin and human transferrin to  S. pneumoniae D39 and EF3296.	bind
4567	2	2388	5	10	NULL	0	NULL	lactoferrin	GP	bovine	bind					D39	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_5_3372_s_220	11292760	(A and B) Binding of human and bovine lactoferrin and human transferrin to  S. pneumoniae D39 and EF3296.	bind
4568	3	2388	5	10	NULL	0	NULL	lactoferrin	GP	human	bind					EF3296	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_5_3372_s_220	11292760	(A and B) Binding of human and bovine lactoferrin and human transferrin to  S. pneumoniae D39 and EF3296.	bind
4569	4	2388	5	10	NULL	0	NULL	lactoferrin	GP	bovine	bind					EF3296	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_5_3372_s_220	11292760	(A and B) Binding of human and bovine lactoferrin and human transferrin to  S. pneumoniae D39 and EF3296.	bind
4570	5	2388	5	10	NULL	0	NULL	transferrin	GP	human	bind					D39	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_5_3372_s_220	11292760	(A and B) Binding of human and bovine lactoferrin and human transferrin to  S. pneumoniae D39 and EF3296.	bind
4571	6	2388	5	10	NULL	0	NULL	transferrin	GP	human	bind					EF3296	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_5_3372_s_220	11292760	(A and B) Binding of human and bovine lactoferrin and human transferrin to  S. pneumoniae D39 and EF3296.	bind
61103	7	2388	5	10	NULL	0	NULL	D39	Organism		is a strain of					S. pneumoniae	Organism				NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_5_3372_s_220	11292760	(A and B) Binding of human and bovine lactoferrin and human transferrin to  S. pneumoniae D39 and EF3296.	bind
61104	8	2388	5	10	NULL	0	NULL	EF3296	Organism		is a strain of					S. pneumoniae	Organism				NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_5_3372_s_220	11292760	(A and B) Binding of human and bovine lactoferrin and human transferrin to  S. pneumoniae D39 and EF3296.	bind
5078	1	2388	6	10	NULL	0	NULL	lactoferrin	GP	human	bind					D39	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_5_3372_s_220	11292760	(A and B) Binding of human and bovine lactoferrin and human transferrin to  S. pneumoniae D39 and EF3296.	bind
5079	2	2388	6	10	NULL	0	NULL	lactoferrin	GP	human	bind					EF3296	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_5_3372_s_220	11292760	(A and B) Binding of human and bovine lactoferrin and human transferrin to  S. pneumoniae D39 and EF3296.	bind
5080	3	2388	6	10	NULL	0	NULL	lactoferrin	GP	bovine	bind					D39	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_5_3372_s_220	11292760	(A and B) Binding of human and bovine lactoferrin and human transferrin to  S. pneumoniae D39 and EF3296.	bind
5081	4	2388	6	10	NULL	0	NULL	lactoferrin	GP	bovine	bind					EF3296	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_5_3372_s_220	11292760	(A and B) Binding of human and bovine lactoferrin and human transferrin to  S. pneumoniae D39 and EF3296.	bind
5082	5	2388	6	10	NULL	0	NULL	transferrin	GP	human	bind					D39	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_5_3372_s_220	11292760	(A and B) Binding of human and bovine lactoferrin and human transferrin to  S. pneumoniae D39 and EF3296.	bind
5083	6	2388	6	10	NULL	0	NULL	transferrin	GP	human	bind					EF3296	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_5_3372_s_220	11292760	(A and B) Binding of human and bovine lactoferrin and human transferrin to  S. pneumoniae D39 and EF3296.	bind
61105	8	2388	6	10	NULL	0	NULL	EF3296	Organism		is a strain of					S. pneumoniae	Organism				NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_5_3372_s_220	11292760	(A and B) Binding of human and bovine lactoferrin and human transferrin to  S. pneumoniae D39 and EF3296.	bind
61106	7	2388	6	10	NULL	0	NULL	D39	Organism		is a strain of					S. pneumoniae	Organism				NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_5_3372_s_220	11292760	(A and B) Binding of human and bovine lactoferrin and human transferrin to  S. pneumoniae D39 and EF3296.	bind
4931	1	2389	5	10	NULL	0	NULL	C3	GP		bind					bacteria	Organism				NULL	BALB/cByJ serum	NULL	NULL	NULL	NULL	gw70_infectimmun_71_1_218_s_236	12496169	(A and B) C3  bound to bacteria after opsonization in BALB/cByJ serum, detected by ELISA, as described  in Materials and Methods.	bind
5084	1	2389	6	10	NULL	0	NULL	C3	GP		bind					bacteria	Organism				NULL	BALB/cByJ serum	NULL	NULL	NULL	NULL	gw70_infectimmun_71_1_218_s_236	12496169	(A and B) C3  bound to bacteria after opsonization in BALB/cByJ serum, detected by ELISA, as described  in Materials and Methods.	bind
4933	1	2390	5	10	NULL	0	NULL	C3	GP		bind					bacteria	Organism				NULL	BALB/cByJ serum	NULL	NULL	NULL	NULL	gw60_infectimmun_71_1_218_s_236	12496169	(A and B) C3 bound to bacteria after opsonization in BALB/cByJ serum, detected by ELISA, as described in Materials and Methods.	bind
5086	1	2390	6	10	NULL	0	NULL	C3	GP		bind					bacteria	Organism				NULL	BALB/cByJ serum	NULL	NULL	NULL	NULL	gw60_infectimmun_71_1_218_s_236	12496169	(A and B) C3 bound to bacteria after opsonization in BALB/cByJ serum, detected by ELISA, as described in Materials and Methods.	bind
4938	1	2394	5	10	NULL	0	NULL	3E5 IgG1 MAb	GP		bind					GXM antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_3_1057_s_80	9488395	(A and B) ELISAs of 3E5 IgG (IgG1, IgG2a, IgG2b, and IgG3) and of 4H3 IgG (IgG1, IgG2b, and IgG3) MAb binding to GXM antigen, respectively; (C and D) competition assays.	bind
4939	2	2394	5	10	NULL	0	NULL	3E5 IgG2a MAb	GP		bind					GXM antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_3_1057_s_80	9488395	(A and B) ELISAs of 3E5 IgG (IgG1, IgG2a, IgG2b, and IgG3) and of 4H3 IgG (IgG1, IgG2b, and IgG3) MAb binding to GXM antigen, respectively; (C and D) competition assays.	bind
4940	3	2394	5	10	NULL	0	NULL	3E5 IgG2b MAb	GP		bind					GXM antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_3_1057_s_80	9488395	(A and B) ELISAs of 3E5 IgG (IgG1, IgG2a, IgG2b, and IgG3) and of 4H3 IgG (IgG1, IgG2b, and IgG3) MAb binding to GXM antigen, respectively; (C and D) competition assays.	bind
4941	4	2394	5	10	NULL	0	NULL	3E5 IgG3 MAb	GP		bind					GXM antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_3_1057_s_80	9488395	(A and B) ELISAs of 3E5 IgG (IgG1, IgG2a, IgG2b, and IgG3) and of 4H3 IgG (IgG1, IgG2b, and IgG3) MAb binding to GXM antigen, respectively; (C and D) competition assays.	bind
4943	5	2394	5	10	NULL	0	NULL	4H3 IgG1 MAb	GP		bind					GXM antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_3_1057_s_80	9488395	(A and B) ELISAs of 3E5 IgG (IgG1, IgG2a, IgG2b, and IgG3) and of 4H3 IgG (IgG1, IgG2b, and IgG3) MAb binding to GXM antigen, respectively; (C and D) competition assays.	bind
4944	6	2394	5	10	NULL	0	NULL	4H3 IgG2b MAb	GP		bind					GXM antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_3_1057_s_80	9488395	(A and B) ELISAs of 3E5 IgG (IgG1, IgG2a, IgG2b, and IgG3) and of 4H3 IgG (IgG1, IgG2b, and IgG3) MAb binding to GXM antigen, respectively; (C and D) competition assays.	bind
4945	7	2394	5	10	NULL	0	NULL	4H3 IgG3 MAb	GP		bind					GXM antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_3_1057_s_80	9488395	(A and B) ELISAs of 3E5 IgG (IgG1, IgG2a, IgG2b, and IgG3) and of 4H3 IgG (IgG1, IgG2b, and IgG3) MAb binding to GXM antigen, respectively; (C and D) competition assays.	bind
5088	1	2394	6	10	NULL	0	NULL	3E5 IgG1 MAb	GP		bind					GXM antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_3_1057_s_80	9488395	(A and B) ELISAs of 3E5 IgG (IgG1, IgG2a, IgG2b, and IgG3) and of 4H3 IgG (IgG1, IgG2b, and IgG3) MAb binding to GXM antigen, respectively; (C and D) competition assays.	bind
5089	2	2394	6	10	NULL	0	NULL	3E5 IgG2a MAb	GP		bind					GXM antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_3_1057_s_80	9488395	(A and B) ELISAs of 3E5 IgG (IgG1, IgG2a, IgG2b, and IgG3) and of 4H3 IgG (IgG1, IgG2b, and IgG3) MAb binding to GXM antigen, respectively; (C and D) competition assays.	bind
5090	3	2394	6	10	NULL	0	NULL	3E5 IgG2b MAb	GP		bind					GXM antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_3_1057_s_80	9488395	(A and B) ELISAs of 3E5 IgG (IgG1, IgG2a, IgG2b, and IgG3) and of 4H3 IgG (IgG1, IgG2b, and IgG3) MAb binding to GXM antigen, respectively; (C and D) competition assays.	bind
5091	4	2394	6	10	NULL	0	NULL	3E5 IgG3 MAb	GP		bind					GXM antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_3_1057_s_80	9488395	(A and B) ELISAs of 3E5 IgG (IgG1, IgG2a, IgG2b, and IgG3) and of 4H3 IgG (IgG1, IgG2b, and IgG3) MAb binding to GXM antigen, respectively; (C and D) competition assays.	bind
5092	5	2394	6	10	NULL	0	NULL	4H3 IgG1 MAb	GP		bind					GXM antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_3_1057_s_80	9488395	(A and B) ELISAs of 3E5 IgG (IgG1, IgG2a, IgG2b, and IgG3) and of 4H3 IgG (IgG1, IgG2b, and IgG3) MAb binding to GXM antigen, respectively; (C and D) competition assays.	bind
5093	6	2394	6	10	NULL	0	NULL	4H3 IgG2b MAb	GP		bind					GXM antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_3_1057_s_80	9488395	(A and B) ELISAs of 3E5 IgG (IgG1, IgG2a, IgG2b, and IgG3) and of 4H3 IgG (IgG1, IgG2b, and IgG3) MAb binding to GXM antigen, respectively; (C and D) competition assays.	bind
5094	7	2394	6	10	NULL	0	NULL	4H3 IgG3 MAb	GP		bind					GXM antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_3_1057_s_80	9488395	(A and B) ELISAs of 3E5 IgG (IgG1, IgG2a, IgG2b, and IgG3) and of 4H3 IgG (IgG1, IgG2b, and IgG3) MAb binding to GXM antigen, respectively; (C and D) competition assays.	bind
4572	1	2397	5	10	NULL	0	NULL	Gab2	GP		is recruited to					phagocytic cups	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_161_6_1151_s_172	12821647	(A and B) Gab2 recruitment to the phagocytic cups correlates with PIP3 binding to Gab2 PH domain.	bind
4573	2	2397	5	10	NULL	0	NULL	PIP3	GP		bind					Gab2	GP		PH domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_161_6_1151_s_172	12821647	(A and B) Gab2 recruitment to the phagocytic cups correlates with PIP3 binding to Gab2 PH domain.	bind
4574	3	2397	5	10	NULL	0	NULL	statement 1	Process		correlates with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_161_6_1151_s_172	12821647	(A and B) Gab2 recruitment to the phagocytic cups correlates with PIP3 binding to Gab2 PH domain.	bind
5095	1	2397	6	10	NULL	0	NULL	PIP3	GP		bind					Gab2	GP		PH domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_161_6_1151_s_172	12821647	(A and B) Gab2 recruitment to the phagocytic cups correlates with PIP3 binding to Gab2 PH domain.	bind
5096	2	2397	6	10	NULL	0	NULL	Gab2	GP		recruited					phagocytic cups	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_161_6_1151_s_172	12821647	(A and B) Gab2 recruitment to the phagocytic cups correlates with PIP3 binding to Gab2 PH domain.	bind
5097	3	2397	6	10	NULL	0	NULL	statement 2	Process		correlates with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_161_6_1151_s_172	12821647	(A and B) Gab2 recruitment to the phagocytic cups correlates with PIP3 binding to Gab2 PH domain.	bind
4575	1	2400	5	10	NULL	0	NULL	E2F	GP		bind					PIN1	GP			promoter	NULL	 breast cell lines	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_15_5281_s_170	12101225	(A and B) Levels of E2F binding to the  PIN1 promoter in different breast cell lines.	bind
5098	1	2400	6	10	NULL	0	NULL	E2F	GP		bind					PIN1	GP			promoter	NULL	breast cell line	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_15_5281_s_170	12101225	(A and B) Levels of E2F binding to the  PIN1 promoter in different breast cell lines.	bind
5099	2	2401	6	10	NULL	0	NULL	LXR/RXR heterodimer	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_6_2182_s_191	12612088	(A and B) LXR/RXR heterodimers bind to DR4 from the human PLTP promoter region.	bind
46250	1	2401	6	10	NULL	0	NULL				is present in				DR4	PLTP	GP	human		promoter region	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_6_2182_s_191	12612088	(A and B) LXR/RXR heterodimers bind to DR4 from the human PLTP promoter region.	bind
5606	2	2401	7	10	NULL	0	NULL	LXR/RXR heterodimers	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_6_2182_s_191	12612088	(A and B) LXR/RXR heterodimers bind to DR4 from the human PLTP promoter region.	bind
46249	1	2401	7	10	NULL	0	NULL				is present in				DR4	PLTP	GP	human		promoter region	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_6_2182_s_191	12612088	(A and B) LXR/RXR heterodimers bind to DR4 from the human PLTP promoter region.	bind
5100	1	2404	6	10	NULL	0	NULL	Akt1	GP	phosphorylated	bind			Thr-308		JIP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_1_61_s_85	15998799	(A and B) shows that Akt1 phosphorylated on Thr-308 and that Ser-473 binds to JIP1.	bind
5101	2	2404	6	10	NULL	0	NULL	Akt1	GP	phosphorylated	bind			Ser-473		JIP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_1_61_s_85	15998799	(A and B) shows that Akt1 phosphorylated on Thr-308 and that Ser-473 binds to JIP1.	bind
5607	1	2404	7	10	NULL	0	NULL	Akt1	GP	phosphorylated	bind			Thr-308		JIP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_1_61_s_85	15998799	(A and B) shows that Akt1 phosphorylated on Thr-308 and that Ser-473 binds to JIP1.	bind
46251	2	2404	7	10	NULL	0	NULL	Akt1	GP	phosphorylated	bind			Ser-473		JIP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_1_61_s_85	15998799	(A and B) shows that Akt1 phosphorylated on Thr-308 and that Ser-473 binds to JIP1.	bind
5102	1	2405	6	10	NULL	0	NULL	Akt1	GP		bind					SEK1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_1_61_s_217	15998799	(A and B) shows that binding of Akt1 to SEK1 gradually increased as a function of time during glucose deprivation without changes in the intracellular level of Akt1.	bind
5103	2	2405	6	10	NULL	0	NULL	glucose	Chemical	deprivation of	increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_1_61_s_217	15998799	(A and B) shows that binding of Akt1 to SEK1 gradually increased as a function of time during glucose deprivation without changes in the intracellular level of Akt1.	bind
5105	3	2405	6	10	NULL	0	NULL	statement 2	Process		does not change					Akt1	GP	intracellular level of 			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_1_61_s_217	15998799	(A and B) shows that binding of Akt1 to SEK1 gradually increased as a function of time during glucose deprivation without changes in the intracellular level of Akt1.	bind
5608	1	2405	7	10	NULL	0	NULL	Akt1	GP		binds					SEK1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_1_61_s_217	15998799	(A and B) shows that binding of Akt1 to SEK1 gradually increased as a function of time during glucose deprivation without changes in the intracellular level of Akt1.	bind
5609	2	2405	7	10	NULL	0	NULL	statement 1	Process		increased during					glucose	Chemical	deprivation of			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_1_61_s_217	15998799	(A and B) shows that binding of Akt1 to SEK1 gradually increased as a function of time during glucose deprivation without changes in the intracellular level of Akt1.	bind
5610	3	2405	7	10	NULL	0	NULL	statement 2	Process		does not change					Akt1	GP	intracellular level of			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_1_61_s_217	15998799	(A and B) shows that binding of Akt1 to SEK1 gradually increased as a function of time during glucose deprivation without changes in the intracellular level of Akt1.	bind
5197	1	2406	6	10	NULL	0	NULL	SHP2	GP		bind					p97	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_6_729_s_219	9885561	(A and B) SHP2 binding to p97 is dispensable for IL-3-induced MAPK activation.	bind
5198	2	2406	6	10	NULL	0	NULL	IL-3	GP		induces					MAPK	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_6_729_s_219	9885561	(A and B) SHP2 binding to p97 is dispensable for IL-3-induced MAPK activation.	bind
5199	3	2406	6	10	NULL	0	NULL	statement 1	Process		is dispensable for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_6_729_s_219	9885561	(A and B) SHP2 binding to p97 is dispensable for IL-3-induced MAPK activation.	bind
5611	1	2406	7	10	NULL	0	NULL	SHP2	GP		bind					 p97	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_6_729_s_219	9885561	(A and B) SHP2 binding to p97 is dispensable for IL-3-induced MAPK activation.	bind
5612	2	2406	7	10	NULL	0	NULL	IL-3	GP		induce					MAPK	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_6_729_s_219	9885561	(A and B) SHP2 binding to p97 is dispensable for IL-3-induced MAPK activation.	bind
5613	3	2406	7	10	NULL	0	NULL	statement 1	Process		is dispensable for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_6_729_s_219	9885561	(A and B) SHP2 binding to p97 is dispensable for IL-3-induced MAPK activation.	bind
5200	1	2407	6	10	NULL	0	NULL	Snf2p	GP	myc-tagged	bind					ARG1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8829_s_77	14612422	(A and B) The  gcn4delta SNF2-myc (SY127) and  gcn4delta SNF5-myc (SY166) strains described in the legend to Fig.  1 were transformed with single-copy (s.c) plasmid p2382 or pSY285, harboring  GCN4-HA or  gcn4-14Ala-HA, respectively, or high-copy-number (h.c.) plasmid pHQ1303 or pHQ1304, harboring  GCN4 or  gcn4-14Ala, respectively, and subjected to ChIP analysis as described in the legend to Fig.   1 to measure binding of myc-tagged Snf2p or Snf5p to  ARG1	bind
5201	2	2407	6	10	NULL	0	NULL	Snf5p	GP	myc-tagged	bind					ARG1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8829_s_77	14612422	(A and B) The  gcn4delta SNF2-myc (SY127) and  gcn4delta SNF5-myc (SY166) strains described in the legend to Fig.  1 were transformed with single-copy (s.c) plasmid p2382 or pSY285, harboring  GCN4-HA or  gcn4-14Ala-HA, respectively, or high-copy-number (h.c.) plasmid pHQ1303 or pHQ1304, harboring  GCN4 or  gcn4-14Ala, respectively, and subjected to ChIP analysis as described in the legend to Fig.   1 to measure binding of myc-tagged Snf2p or Snf5p to  ARG1	bind
5202	3	2407	6	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8829_s_77	14612422	(A and B) The  gcn4delta SNF2-myc (SY127) and  gcn4delta SNF5-myc (SY166) strains described in the legend to Fig.  1 were transformed with single-copy (s.c) plasmid p2382 or pSY285, harboring  GCN4-HA or  gcn4-14Ala-HA, respectively, or high-copy-number (h.c.) plasmid pHQ1303 or pHQ1304, harboring  GCN4 or  gcn4-14Ala, respectively, and subjected to ChIP analysis as described in the legend to Fig.   1 to measure binding of myc-tagged Snf2p or Snf5p to  ARG1	bind
5614	1	2407	7	10	NULL	0	NULL	Snf2p	GP	myc-tagged	binds					ARG1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8829_s_77	14612422	(A and B) The  gcn4delta SNF2-myc (SY127) and  gcn4delta SNF5-myc (SY166) strains described in the legend to Fig.  1 were transformed with single-copy (s.c) plasmid p2382 or pSY285, harboring  GCN4-HA or  gcn4-14Ala-HA, respectively, or high-copy-number (h.c.) plasmid pHQ1303 or pHQ1304, harboring  GCN4 or  gcn4-14Ala, respectively, and subjected to ChIP analysis as described in the legend to Fig.   1 to measure binding of myc-tagged Snf2p or Snf5p to  ARG1	bind
5615	2	2407	7	10	NULL	0	NULL	Snf5p	GP	myc-tagged	binds					ARG1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8829_s_77	14612422	(A and B) The  gcn4delta SNF2-myc (SY127) and  gcn4delta SNF5-myc (SY166) strains described in the legend to Fig.  1 were transformed with single-copy (s.c) plasmid p2382 or pSY285, harboring  GCN4-HA or  gcn4-14Ala-HA, respectively, or high-copy-number (h.c.) plasmid pHQ1303 or pHQ1304, harboring  GCN4 or  gcn4-14Ala, respectively, and subjected to ChIP analysis as described in the legend to Fig.   1 to measure binding of myc-tagged Snf2p or Snf5p to  ARG1	bind
46252	3	2407	7	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8829_s_77	14612422	(A and B) The  gcn4delta SNF2-myc (SY127) and  gcn4delta SNF5-myc (SY166) strains described in the legend to Fig.  1 were transformed with single-copy (s.c) plasmid p2382 or pSY285, harboring  GCN4-HA or  gcn4-14Ala-HA, respectively, or high-copy-number (h.c.) plasmid pHQ1303 or pHQ1304, harboring  GCN4 or  gcn4-14Ala, respectively, and subjected to ChIP analysis as described in the legend to Fig.   1 to measure binding of myc-tagged Snf2p or Snf5p to  ARG1	bind
5203	2	2408	6	10	NULL	0	NULL	MeCP2	GP		bind					statement 1	Process				NULL	E11.5 cells	NULL	NULL	NULL	NULL	gw70_febslett_572_1_184_s_129	15304345	(A and B) The abundant binding of MeCP2 to the methylated   318 CpG site within the S100  gene promoter region in E11.5 cells.	bind
46253	1	2408	6	10	NULL	0	NULL			methylated	is present within				318 CpG site	S100 gene	GP			promoter region	NULL	E11.5 cells	NULL	NULL	NULL	NULL	gw70_febslett_572_1_184_s_129	15304345	(A and B) The abundant binding of MeCP2 to the methylated   318 CpG site within the S100  gene promoter region in E11.5 cells.	bind
5616	2	2408	7	10	NULL	0	NULL	MeCP2	GP		bind					statement 1	Process				NULL	E11.5 cells	NULL	NULL	NULL	NULL	gw70_febslett_572_1_184_s_129	15304345	(A and B) The abundant binding of MeCP2 to the methylated   318 CpG site within the S100  gene promoter region in E11.5 cells.	bind
46256	1	2408	7	10	NULL	0	NULL			methylated	is present within				318 CpG site	S100 gene	GP			promoter region	NULL	E11.5 cells	NULL	NULL	NULL	NULL	gw70_febslett_572_1_184_s_129	15304345	(A and B) The abundant binding of MeCP2 to the methylated   318 CpG site within the S100  gene promoter region in E11.5 cells.	bind
5204	1	2409	6	10	NULL	0	NULL	GFP-ssrA	GP	denatured	bind					GroEL trap	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_4_639_s_37	10882100	(A and B) The ClpX6 concentration was 0.3  M, the concentration of modified or unmodified ClpP14 was 1  M, and the concentration of GroEL14 trap was 10  M. Gel filtration experiments confirmed that denaturated GFP-ssrA was bound to the GroEL trap when the latter molecule was present (data not shown).	bind
5666	1	2409	7	10	NULL	0	NULL	GFP-ssrA	GP	denatured	binds					GroEL trap	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_4_639_s_37	10882100	(A and B) The ClpX6 concentration was 0.3  M, the concentration of modified or unmodified ClpP14 was 1  M, and the concentration of GroEL14 trap was 10  M. Gel filtration experiments confirmed that denaturated GFP-ssrA was bound to the GroEL trap when the latter molecule was present (data not shown).	bind
5205	1	2411	6	10	NULL	0	NULL	PDGF alpha receptor	GP		bind					PDGF chain	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_131_8_1546_s_21	11139430	(A and B), and two receptors for PDGF (alpha and beta) bind these two PDGF chains with different affinities (Claesson-Welsh, 1994  ).	bind
5206	2	2411	6	10	NULL	0	NULL	PDGF beta receptor	GP		bind					PDGF chain	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_131_8_1546_s_21	11139430	(A and B), and two receptors for PDGF (alpha and beta) bind these two PDGF chains with different affinities (Claesson-Welsh, 1994  ).	bind
5667	1	2411	7	10	NULL	0	NULL	PDGF alpha receptor	GP		bind					PDGF chain	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_131_8_1546_s_21	11139430	(A and B), and two receptors for PDGF (alpha and beta) bind these two PDGF chains with different affinities (Claesson-Welsh, 1994  ).	bind
5668	2	2411	7	10	NULL	0	NULL	PDGF beta receptor	GP		bind					PDGF chain	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_131_8_1546_s_21	11139430	(A and B), and two receptors for PDGF (alpha and beta) bind these two PDGF chains with different affinities (Claesson-Welsh, 1994  ).	bind
5671	3	2411	7	10	NULL	0	NULL	statement 1	Process	 affinity of	is different from					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_131_8_1546_s_21	11139430	(A and B), and two receptors for PDGF (alpha and beta) bind these two PDGF chains with different affinities (Claesson-Welsh, 1994  ).	bind
5210	1	2413	6	10	NULL	0	NULL	MT	CellComponent		bind			G-NM domain		MT	CellComponent	rhodamine labeled			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_1_46_s_245	13679510	(A and B, E and F) Micrographs of reconstituted Ran regulation of the MT binding  of the G-NM domain to rhodamine-labeled MTs. (C and D) Micrographs of NLS-2 MT binding  in the absence and presence of importin alpha/beta.	bind
5211	2	2413	6	10	NULL	0	NULL	Ran	GP		regulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_1_46_s_245	13679510	(A and B, E and F) Micrographs of reconstituted Ran regulation of the MT binding  of the G-NM domain to rhodamine-labeled MTs. (C and D) Micrographs of NLS-2 MT binding  in the absence and presence of importin alpha/beta.	bind
5673	1	2413	7	10	NULL	0	NULL	MT	GP		binds			G-NM domain		MTs	GP	rhodamine-labeled			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_1_46_s_245	13679510	(A and B, E and F) Micrographs of reconstituted Ran regulation of the MT binding  of the G-NM domain to rhodamine-labeled MTs. (C and D) Micrographs of NLS-2 MT binding  in the absence and presence of importin alpha/beta.	bind
5674	2	2413	7	10	NULL	0	NULL	Ran	GP		regulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_1_46_s_245	13679510	(A and B, E and F) Micrographs of reconstituted Ran regulation of the MT binding  of the G-NM domain to rhodamine-labeled MTs. (C and D) Micrographs of NLS-2 MT binding  in the absence and presence of importin alpha/beta.	bind
5215	1	2414	6	10	NULL	0	NULL	CLIC5	GP		bind		strongly			GST-ezrin	GP		475-586		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_5_1509_s_266	10793131	(A and B, lanes 4), we observed strong binding of CLIC5 and relatively low levels of CLIC4 binding to GST-ezrin 475-586.	bind
5216	2	2414	6	10	NULL	0	NULL	CLIC4	GP		bind		low 			GST-ezrin	GP		475-586		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_5_1509_s_266	10793131	(A and B, lanes 4), we observed strong binding of CLIC5 and relatively low levels of CLIC4 binding to GST-ezrin 475-586.	bind
5675	1	2414	7	10	NULL	0	NULL	CLIC5	GP		binds		strongly			GST-ezrin	GP		475-586		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_5_1509_s_266	10793131	(A and B, lanes 4), we observed strong binding of CLIC5 and relatively low levels of CLIC4 binding to GST-ezrin 475-586.	bind
5676	2	2414	7	10	NULL	0	NULL	CLIC4 	GP		binds		low level			GST-ezrin	GP		475-586		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_5_1509_s_266	10793131	(A and B, lanes 4), we observed strong binding of CLIC5 and relatively low levels of CLIC4 binding to GST-ezrin 475-586.	bind
5218	1	2416	6	10	NULL	0	NULL	ERalpha	GP		bind					pS2	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3358_s_308	11971969	(A and C) The in vivo binding of ERalpha, AIB1, and ERAP140 to the pS2 promoter was examined by the ChIP assay.	bind
5219	2	2416	6	10	NULL	0	NULL	AIB1	GP		bind					pS2	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3358_s_308	11971969	(A and C) The in vivo binding of ERalpha, AIB1, and ERAP140 to the pS2 promoter was examined by the ChIP assay.	bind
5220	3	2416	6	10	NULL	0	NULL	ERAP140	GP		bind					pS2	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3358_s_308	11971969	(A and C) The in vivo binding of ERalpha, AIB1, and ERAP140 to the pS2 promoter was examined by the ChIP assay.	bind
5677	1	2416	7	10	NULL	0	NULL	ERalpha	GP		bind					pS2	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3358_s_308	11971969	(A and C) The in vivo binding of ERalpha, AIB1, and ERAP140 to the pS2 promoter was examined by the ChIP assay.	bind
5678	2	2416	7	10	NULL	0	NULL	AIB1	GP		bind					pS2	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3358_s_308	11971969	(A and C) The in vivo binding of ERalpha, AIB1, and ERAP140 to the pS2 promoter was examined by the ChIP assay.	bind
5679	3	2416	7	10	NULL	0	NULL	ERAP140	GP		bind					pS2	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3358_s_308	11971969	(A and C) The in vivo binding of ERalpha, AIB1, and ERAP140 to the pS2 promoter was examined by the ChIP assay.	bind
5221	1	2417	6	10	NULL	0	NULL	membrin	GP		bind		efficiently			Arf-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_7_1039_s_121	15781476	(A and C), membrin efficiently bound to Arf-1 in the presence of the cross-linker.	bind
5222	2	2417	6	10	NULL	0	NULL	statement 1	Process		occurs in presence of					cross-linker					NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_7_1039_s_121	15781476	(A and C), membrin efficiently bound to Arf-1 in the presence of the cross-linker.	bind
5680	1	2417	7	10	NULL	0	NULL	membrin	GP		bind		efficiently			Arf-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_7_1039_s_121	15781476	(A and C), membrin efficiently bound to Arf-1 in the presence of the cross-linker.	bind
5681	2	2417	7	10	NULL	0	NULL	statement 1	Process		in the presence of					cross-linker					NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_7_1039_s_121	15781476	(A and C), membrin efficiently bound to Arf-1 in the presence of the cross-linker.	bind
5240	1	2418	6	10	NULL	0	NULL	bacteria	Organism		bind					rabbit anti- Shigella LPS antiserum					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_11_6449_s_148	11035758	(A and E) Bacteria binding rabbit anti- Shigella LPS antiserum or goat anti-rabbit IgG conjugated with Texas red.	bind
5241	2	2418	6	10	NULL	0	NULL	bacteria	Organism		bind					goat anti-rabbit IgG	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_11_6449_s_148	11035758	(A and E) Bacteria binding rabbit anti- Shigella LPS antiserum or goat anti-rabbit IgG conjugated with Texas red.	bind
5682	1	2418	7	10	NULL	0	NULL	Bacteria	Organism		binds					rabbit anti- Shigella LPS antiserum					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_11_6449_s_148	11035758	(A and E) Bacteria binding rabbit anti- Shigella LPS antiserum or goat anti-rabbit IgG conjugated with Texas red.	bind
5683	2	2418	7	10	NULL	0	NULL	Bacteria	Organism		bind					goat anti-rabbit IgG	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_11_6449_s_148	11035758	(A and E) Bacteria binding rabbit anti- Shigella LPS antiserum or goat anti-rabbit IgG conjugated with Texas red.	bind
5242	1	2419	6	10	NULL	0	NULL	TFIIIB	GP		bind		sequentially			RNA polymerase III	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_5_749_s_9	9660958	(A box and B box) are recognized directly by TFIIIC, which in turn directs sequential binding of TFIIIB and RNA polymerase III.	bind
5243	2	2419	6	10	NULL	0	NULL				is recognized by		directly		A box	TFIIIC	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_5_749_s_9	9660958	(A box and B box) are recognized directly by TFIIIC, which in turn directs sequential binding of TFIIIB and RNA polymerase III.	bind
5244	3	2419	6	10	NULL	0	NULL				is recognized by		directly		B box	TFIIIC	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_5_749_s_9	9660958	(A box and B box) are recognized directly by TFIIIC, which in turn directs sequential binding of TFIIIB and RNA polymerase III.	bind
5245	4	2419	6	10	NULL	0	NULL	statement 2	Process		directs					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_5_749_s_9	9660958	(A box and B box) are recognized directly by TFIIIC, which in turn directs sequential binding of TFIIIB and RNA polymerase III.	bind
5246	5	2419	6	10	NULL	0	NULL	statement 3	Process		directs					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_5_749_s_9	9660958	(A box and B box) are recognized directly by TFIIIC, which in turn directs sequential binding of TFIIIB and RNA polymerase III.	bind
5685	1	2419	7	10	NULL	0	NULL	TFIIIB	GP		bind		sequentially			RNA polymerase III	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_5_749_s_9	9660958	(A box and B box) are recognized directly by TFIIIC, which in turn directs sequential binding of TFIIIB and RNA polymerase III.	bind
5389	1	2420	6	10	NULL	0	NULL	ORF	NucleicAcid		bind				consensus sequence	ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_8_1995_s_152	9555878	(A consensus sequence or P loop), suggesting that the protein product of this ORF binds ATP or GTP ( 49,  58).	bind
5390	2	2420	6	10	NULL	0	NULL	ORF	NucleicAcid		bind				P loop	ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_8_1995_s_152	9555878	(A consensus sequence or P loop), suggesting that the protein product of this ORF binds ATP or GTP ( 49,  58).	bind
5391	3	2420	6	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_8_1995_s_152	9555878	(A consensus sequence or P loop), suggesting that the protein product of this ORF binds ATP or GTP ( 49,  58).	bind
5392	4	2420	6	10	NULL	0	NULL	ORF	NucleicAcid		bind				consensus sequence	GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_8_1995_s_152	9555878	(A consensus sequence or P loop), suggesting that the protein product of this ORF binds ATP or GTP ( 49,  58).	bind
5393	5	2420	6	10	NULL	0	NULL	ORF	NucleicAcid		bind				P loop	GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_8_1995_s_152	9555878	(A consensus sequence or P loop), suggesting that the protein product of this ORF binds ATP or GTP ( 49,  58).	bind
5394	6	2420	6	10	NULL	0	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_8_1995_s_152	9555878	(A consensus sequence or P loop), suggesting that the protein product of this ORF binds ATP or GTP ( 49,  58).	bind
5686	1	2420	7	10	NULL	0	NULL	ORF	NucleicAcid		binds				P loop	ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_8_1995_s_152	9555878	(A consensus sequence or P loop), suggesting that the protein product of this ORF binds ATP or GTP ( 49,  58).	bind
5687	2	2420	7	10	NULL	0	NULL	ORF	NucleicAcid		binds				P loop	GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_8_1995_s_152	9555878	(A consensus sequence or P loop), suggesting that the protein product of this ORF binds ATP or GTP ( 49,  58).	bind
5395	1	2421	6	10	NULL	0	NULL	GCP1	GP		bind					germ cell nuclear factors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5056_s_146	9030569	(A instead of C), are required for maximal binding of GCP1 to germ cell nuclear factors.	bind
5688	1	2421	7	10	NULL	0	NULL	GCP1	GP		binds to					germ cell nuclear factors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5056_s_146	9030569	(A instead of C), are required for maximal binding of GCP1 to germ cell nuclear factors.	bind
5396	1	2422	6	10	NULL	0	NULL	kinase anchor protein 79	GP		bind					PKC	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_23_3_788_s_270	12574407	(A kinase anchor protein 79) that binds both PKC and phosphatase 2B (Klauck et al., 1996  ) may be involved in the local regulation of phosphorylation cascades.	bind
5397	2	2422	6	10	NULL	0	NULL	kinase anchor protein 79	GP		bind					phosphatase 2B	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_23_3_788_s_270	12574407	(A kinase anchor protein 79) that binds both PKC and phosphatase 2B (Klauck et al., 1996  ) may be involved in the local regulation of phosphorylation cascades.	bind
5398	3	2422	6	10	NULL	0	NULL	kinase anchor protein 79	GP		regulate		may			phosphorylation cascade	Process				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_23_3_788_s_270	12574407	(A kinase anchor protein 79) that binds both PKC and phosphatase 2B (Klauck et al., 1996  ) may be involved in the local regulation of phosphorylation cascades.	bind
5689	1	2422	7	10	NULL	0	NULL	A kinase anchor protein 79	GP		binds to					PKC	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_23_3_788_s_270	12574407	(A kinase anchor protein 79) that binds both PKC and phosphatase 2B (Klauck et al., 1996  ) may be involved in the local regulation of phosphorylation cascades.	bind
5690	2	2422	7	10	NULL	0	NULL	A kinase anchor protein 79	GP		binds to					phosphatase 2B	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_23_3_788_s_270	12574407	(A kinase anchor protein 79) that binds both PKC and phosphatase 2B (Klauck et al., 1996  ) may be involved in the local regulation of phosphorylation cascades.	bind
5691	3	2422	7	10	NULL	0	NULL	A kinase anchor protein 79	GP		regulate		may			phosphorylation cascades	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_23_3_788_s_270	12574407	(A kinase anchor protein 79) that binds both PKC and phosphatase 2B (Klauck et al., 1996  ) may be involved in the local regulation of phosphorylation cascades.	bind
5430	1	2423	6	10	NULL	0	NULL	neutrophil specific decoy receptor	GP		is					Fc RIIIB	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_19_0_275_s_40	11244038	(A neutrophil specific decoy receptor, Fc RIIIB, is additionally found in humans  that binds IgG immune complexes without triggering activation.)	bind
5433	2	2423	6	10	NULL	0	NULL	Fc RIIIB	GP		bind					IgG immune complexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_19_0_275_s_40	11244038	(A neutrophil specific decoy receptor, Fc RIIIB, is additionally found in humans  that binds IgG immune complexes without triggering activation.)	bind
5435	3	2423	6	10	NULL	0	NULL	statement 2	Process		does not trigger					activation	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_19_0_275_s_40	11244038	(A neutrophil specific decoy receptor, Fc RIIIB, is additionally found in humans  that binds IgG immune complexes without triggering activation.)	bind
5692	1	2423	7	10	NULL	0	NULL	Fc RIIIB	GP	human	binds					IgG immune complexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_19_0_275_s_40	11244038	(A neutrophil specific decoy receptor, Fc RIIIB, is additionally found in humans  that binds IgG immune complexes without triggering activation.)	bind
5693	2	2423	7	10	NULL	0	NULL	Fc RIIIB	GP		is					neutrophil specific decoy receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_19_0_275_s_40	11244038	(A neutrophil specific decoy receptor, Fc RIIIB, is additionally found in humans  that binds IgG immune complexes without triggering activation.)	bind
5694	3	2423	7	10	NULL	0	NULL	statement 1	Process		does not trigger					activation	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_19_0_275_s_40	11244038	(A neutrophil specific decoy receptor, Fc RIIIB, is additionally found in humans  that binds IgG immune complexes without triggering activation.)	bind
5438	1	2425	6	10	NULL	0	NULL	PP2Ac	GP		bind		alternatively						alpha-4 subunit		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_37_15252037_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4,  a subunit related to yeast Tap42 protein, which also associates with phosphatases  PP4 or PP6.	bind
5439	2	2425	6	10	NULL	0	NULL	alpha-4 subunit	GP		is related to					Tap42 protein	GP	yeast			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_37_15252037_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4,  a subunit related to yeast Tap42 protein, which also associates with phosphatases  PP4 or PP6.	bind
5441	3	2425	6	10	NULL	0	NULL	Tap42 protein	GP	yeast	associate					PP4	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_37_15252037_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4,  a subunit related to yeast Tap42 protein, which also associates with phosphatases  PP4 or PP6.	bind
5442	4	2425	6	10	NULL	0	NULL	Tap42 protein	GP	yeast	associate					PP6	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_37_15252037_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4,  a subunit related to yeast Tap42 protein, which also associates with phosphatases  PP4 or PP6.	bind
5443	5	2425	6	10	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_37_15252037_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4,  a subunit related to yeast Tap42 protein, which also associates with phosphatases  PP4 or PP6.	bind
46258	6	2425	6	10	NULL	0	NULL	PP4	GP		is a type of					phosphatases	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_37_15252037_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4,  a subunit related to yeast Tap42 protein, which also associates with phosphatases  PP4 or PP6.	bind
46259	7	2425	6	10	NULL	0	NULL	PP6	GP		is a type of					phosphatases	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_37_15252037_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4,  a subunit related to yeast Tap42 protein, which also associates with phosphatases  PP4 or PP6.	bind
5695	1	2425	7	10	NULL	0	NULL	PP2Ac	GP		binds		alternatively						alpha-4 subunit		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_37_15252037_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4,  a subunit related to yeast Tap42 protein, which also associates with phosphatases  PP4 or PP6.	bind
5696	2	2425	7	10	NULL	0	NULL	alpha-4 subunit	GP		is related to					Tap42 protein	GP	yeast			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_37_15252037_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4,  a subunit related to yeast Tap42 protein, which also associates with phosphatases  PP4 or PP6.	bind
5697	3	2425	7	10	NULL	0	NULL	PP4	GP		binds								alpha-4 subunit		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_37_15252037_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4,  a subunit related to yeast Tap42 protein, which also associates with phosphatases  PP4 or PP6.	bind
5698	4	2425	7	10	NULL	0	NULL	PP6	GP		binds								alpha-4 subunit		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_37_15252037_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4,  a subunit related to yeast Tap42 protein, which also associates with phosphatases  PP4 or PP6.	bind
46262	5	2425	7	10	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_37_15252037_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4,  a subunit related to yeast Tap42 protein, which also associates with phosphatases  PP4 or PP6.	bind
46263	6	2425	7	10	NULL	0	NULL	PP4	GP		is a type of					phosphatases	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_37_15252037_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4,  a subunit related to yeast Tap42 protein, which also associates with phosphatases  PP4 or PP6.	bind
46264	7	2425	7	10	NULL	0	NULL	PP6	GP		is a type of					phosphatases	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_37_15252037_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4,  a subunit related to yeast Tap42 protein, which also associates with phosphatases  PP4 or PP6.	bind
5444	1	2426	6	10	NULL	0	NULL	PP2Ac	GP		bind		alternatively			alpha-4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_37_38912_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4, a subunit related to yeast Tap42 protein, which also associates with phosphatases PP4 or PP6.	bind
5445	2	2426	6	10	NULL	0	NULL	alpha-4 subunit	GP		is related to					Tap42 protein	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_37_38912_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4, a subunit related to yeast Tap42 protein, which also associates with phosphatases PP4 or PP6.	bind
5446	3	2426	6	10	NULL	0	NULL	Tap42 protein	GP	yeast	associate					PP4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_37_38912_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4, a subunit related to yeast Tap42 protein, which also associates with phosphatases PP4 or PP6.	bind
5447	4	2426	6	10	NULL	0	NULL	Tap42 protein	GP	yeast	associate					PP6	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_37_38912_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4, a subunit related to yeast Tap42 protein, which also associates with phosphatases PP4 or PP6.	bind
5448	5	2426	6	10	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_37_38912_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4, a subunit related to yeast Tap42 protein, which also associates with phosphatases PP4 or PP6.	bind
61107	6	2426	6	10	NULL	0	NULL	PP4	GP		is a type of					phosphatase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_37_38912_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4, a subunit related to yeast Tap42 protein, which also associates with phosphatases PP4 or PP6.	bind
61108	7	2426	6	10	NULL	0	NULL	PP6	GP		is a type of					phosphatase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_37_38912_s_4	15252037	(A subunit or PR65); however, PP2Ac alternatively binds to alpha-4, a subunit related to yeast Tap42 protein, which also associates with phosphatases PP4 or PP6.	bind
5449	1	2427	6	10	NULL	0	NULL	MEF2 isoforms	GP		bind					Cabin1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5440_790_s_31	10531067	(A through D), we suspected that all isoforms of MEF2 could bind to Cabin1, as was subsequently confirmed ( 15).	bind
5699	1	2427	7	10	NULL	0	NULL	MEF2 isoforms	GP		bind					Cabin1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5440_790_s_31	10531067	(A through D), we suspected that all isoforms of MEF2 could bind to Cabin1, as was subsequently confirmed ( 15).	bind
5601	1	2428	6	10	NULL	0	NULL	ATP	Chemical		is formed from					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_1_88_s_145	7788886	(A through D, top) showing formation of ATP from ADP and phosphoenolpyruvate (PEP) by sarcoplasmic reticulum (SR) - bound pyruvate kinase (PK), detected by high-performance liquid chromatography of supernatant (bottom).	bind
5602	3	2428	6	10	NULL	0	NULL	PEP	GP		is					phosphoenolpyruvate	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_1_88_s_145	7788886	(A through D, top) showing formation of ATP from ADP and phosphoenolpyruvate (PEP) by sarcoplasmic reticulum (SR) - bound pyruvate kinase (PK), detected by high-performance liquid chromatography of supernatant (bottom).	bind
5603	5	2428	6	10	NULL	0	NULL	statement 1	Process		is formed by					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_1_88_s_145	7788886	(A through D, top) showing formation of ATP from ADP and phosphoenolpyruvate (PEP) by sarcoplasmic reticulum (SR) - bound pyruvate kinase (PK), detected by high-performance liquid chromatography of supernatant (bottom).	bind
5604	7	2428	6	10	NULL	0	NULL	SR	CellComponent		is					sarcoplasmic reticulum	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_1_88_s_145	7788886	(A through D, top) showing formation of ATP from ADP and phosphoenolpyruvate (PEP) by sarcoplasmic reticulum (SR) - bound pyruvate kinase (PK), detected by high-performance liquid chromatography of supernatant (bottom).	bind
5605	8	2428	6	10	NULL	0	NULL	PK	GP		is					Pyruvate kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_1_88_s_145	7788886	(A through D, top) showing formation of ATP from ADP and phosphoenolpyruvate (PEP) by sarcoplasmic reticulum (SR) - bound pyruvate kinase (PK), detected by high-performance liquid chromatography of supernatant (bottom).	bind
46314	4	2428	6	10	NULL	0	NULL	PK	GP		bind					SR	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_1_88_s_145	7788886	(A through D, top) showing formation of ATP from ADP and phosphoenolpyruvate (PEP) by sarcoplasmic reticulum (SR) - bound pyruvate kinase (PK), detected by high-performance liquid chromatography of supernatant (bottom).	bind
61109	2	2428	6	10	NULL	0	NULL	ATP	Chemical		is formed from					PEP	GP				NULL		0	NULL	NULL	NULL	gw60_circulationres_77_1_88_s_145	7788886	(A through D, top) showing formation of ATP from ADP and phosphoenolpyruvate (PEP) by sarcoplasmic reticulum (SR) - bound pyruvate kinase (PK), detected by high-performance liquid chromatography of supernatant (bottom).	bind
61110	6	2428	6	10	NULL	0	NULL	statement 2	Process		is formed by					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_circulationres_77_1_88_s_145	7788886	(A through D, top) showing formation of ATP from ADP and phosphoenolpyruvate (PEP) by sarcoplasmic reticulum (SR) - bound pyruvate kinase (PK), detected by high-performance liquid chromatography of supernatant (bottom).	bind
61112	9	2428	6	10	NULL	0	NULL	statement 1	Process		occurs along with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_circulationres_77_1_88_s_145	7788886	(A through D, top) showing formation of ATP from ADP and phosphoenolpyruvate (PEP) by sarcoplasmic reticulum (SR) - bound pyruvate kinase (PK), detected by high-performance liquid chromatography of supernatant (bottom).	bind
5700	1	2428	7	10	NULL	0	NULL	ATP	Chemical		is formed from					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_1_88_s_145	7788886	(A through D, top) showing formation of ATP from ADP and phosphoenolpyruvate (PEP) by sarcoplasmic reticulum (SR) - bound pyruvate kinase (PK), detected by high-performance liquid chromatography of supernatant (bottom).	bind
5701	2	2428	7	10	NULL	0	NULL	ATP	Chemical		is formed from					PEP	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_1_88_s_145	7788886	(A through D, top) showing formation of ATP from ADP and phosphoenolpyruvate (PEP) by sarcoplasmic reticulum (SR) - bound pyruvate kinase (PK), detected by high-performance liquid chromatography of supernatant (bottom).	bind
5702	4	2428	7	10	NULL	0	NULL	statement 1	Process		is formed by					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_1_88_s_145	7788886	(A through D, top) showing formation of ATP from ADP and phosphoenolpyruvate (PEP) by sarcoplasmic reticulum (SR) - bound pyruvate kinase (PK), detected by high-performance liquid chromatography of supernatant (bottom).	bind
5703	5	2428	7	10	NULL	0	NULL	PEP	GP		is					phosphoenolpyruvate	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_1_88_s_145	7788886	(A through D, top) showing formation of ATP from ADP and phosphoenolpyruvate (PEP) by sarcoplasmic reticulum (SR) - bound pyruvate kinase (PK), detected by high-performance liquid chromatography of supernatant (bottom).	bind
5704	6	2428	7	10	NULL	0	NULL	SR	CellComponent		is					sarcoplasmic reticulum	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_1_88_s_145	7788886	(A through D, top) showing formation of ATP from ADP and phosphoenolpyruvate (PEP) by sarcoplasmic reticulum (SR) - bound pyruvate kinase (PK), detected by high-performance liquid chromatography of supernatant (bottom).	bind
5705	7	2428	7	10	NULL	0	NULL	PK	GP		is					pyruvate kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_1_88_s_145	7788886	(A through D, top) showing formation of ATP from ADP and phosphoenolpyruvate (PEP) by sarcoplasmic reticulum (SR) - bound pyruvate kinase (PK), detected by high-performance liquid chromatography of supernatant (bottom).	bind
46313	3	2428	7	10	NULL	0	NULL	PK	GP		bind					SR	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_1_88_s_145	7788886	(A through D, top) showing formation of ATP from ADP and phosphoenolpyruvate (PEP) by sarcoplasmic reticulum (SR) - bound pyruvate kinase (PK), detected by high-performance liquid chromatography of supernatant (bottom).	bind
61111	8	2428	7	10	NULL	0	NULL	statement 2	Process		is formed by					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_circulationres_77_1_88_s_145	7788886	(A through D, top) showing formation of ATP from ADP and phosphoenolpyruvate (PEP) by sarcoplasmic reticulum (SR) - bound pyruvate kinase (PK), detected by high-performance liquid chromatography of supernatant (bottom).	bind
61113	9	2428	7	10	NULL	0	NULL	statement 1	Process		occurs along with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_circulationres_77_1_88_s_145	7788886	(A through D, top) showing formation of ATP from ADP and phosphoenolpyruvate (PEP) by sarcoplasmic reticulum (SR) - bound pyruvate kinase (PK), detected by high-performance liquid chromatography of supernatant (bottom).	bind
5455	1	2429	6	10	NULL	0	NULL	FecI	GP		bind					beta''	GP		1-313		NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_6_1796_s_149	12618442	(A to C) Binding of FecI to beta''1-313	bind
5706	1	2429	7	10	NULL	0	NULL	FecI	GP		binds					beta''	GP		1-313		NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_6_1796_s_149	12618442	(A to C) Binding of FecI to beta''1-313	bind
5457	1	2431	6	10	NULL	0	NULL	p107	GP		bind					GST-cyclin A-cdk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_316	9710622	(A to C) Western blot analysis carried out after GST precipitation of GST-cyclin A-cdk2 shows the capacity of peptides p107S and p107N, but not p107N-mut, to compete the binding of p107 to cyclin A-cdk2.	bind
5459	2	2431	6	10	NULL	0	NULL	peptide p107S	GP		bind					GST-cyclin A-cdk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_316	9710622	(A to C) Western blot analysis carried out after GST precipitation of GST-cyclin A-cdk2 shows the capacity of peptides p107S and p107N, but not p107N-mut, to compete the binding of p107 to cyclin A-cdk2.	bind
5460	3	2431	6	10	NULL	0	NULL	statement 2	Process		competes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_316	9710622	(A to C) Western blot analysis carried out after GST precipitation of GST-cyclin A-cdk2 shows the capacity of peptides p107S and p107N, but not p107N-mut, to compete the binding of p107 to cyclin A-cdk2.	bind
5461	4	2431	6	10	NULL	0	NULL	peptide p107N	GP		bind					GST-cyclin A-cdk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_316	9710622	(A to C) Western blot analysis carried out after GST precipitation of GST-cyclin A-cdk2 shows the capacity of peptides p107S and p107N, but not p107N-mut, to compete the binding of p107 to cyclin A-cdk2.	bind
5462	5	2431	6	10	NULL	0	NULL	statement 4	Process		competes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_316	9710622	(A to C) Western blot analysis carried out after GST precipitation of GST-cyclin A-cdk2 shows the capacity of peptides p107S and p107N, but not p107N-mut, to compete the binding of p107 to cyclin A-cdk2.	bind
5463	6	2431	6	10	NULL	0	NULL	p107N-mut	GP		does not bind					GST-cyclin A-cdk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_316	9710622	(A to C) Western blot analysis carried out after GST precipitation of GST-cyclin A-cdk2 shows the capacity of peptides p107S and p107N, but not p107N-mut, to compete the binding of p107 to cyclin A-cdk2.	bind
5707	1	2431	7	10	NULL	0	NULL	p107 peptide	GP		binds to					GST-cyclin A-cdk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_316	9710622	(A to C) Western blot analysis carried out after GST precipitation of GST-cyclin A-cdk2 shows the capacity of peptides p107S and p107N, but not p107N-mut, to compete the binding of p107 to cyclin A-cdk2.	bind
5708	2	2431	7	10	NULL	0	NULL	p107S peptide	GP		binds to					GST-cyclin A-cdk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_316	9710622	(A to C) Western blot analysis carried out after GST precipitation of GST-cyclin A-cdk2 shows the capacity of peptides p107S and p107N, but not p107N-mut, to compete the binding of p107 to cyclin A-cdk2.	bind
5709	3	2431	7	10	NULL	0	NULL	p107N peptide	GP		binds to					GST-cyclin A-cdk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_316	9710622	(A to C) Western blot analysis carried out after GST precipitation of GST-cyclin A-cdk2 shows the capacity of peptides p107S and p107N, but not p107N-mut, to compete the binding of p107 to cyclin A-cdk2.	bind
5710	4	2431	7	10	NULL	0	NULL	p107N-mut peptide	GP		does not bind					GST-cyclin A-cdk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_316	9710622	(A to C) Western blot analysis carried out after GST precipitation of GST-cyclin A-cdk2 shows the capacity of peptides p107S and p107N, but not p107N-mut, to compete the binding of p107 to cyclin A-cdk2.	bind
5711	5	2431	7	10	NULL	0	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_316	9710622	(A to C) Western blot analysis carried out after GST precipitation of GST-cyclin A-cdk2 shows the capacity of peptides p107S and p107N, but not p107N-mut, to compete the binding of p107 to cyclin A-cdk2.	bind
5712	6	2431	7	10	NULL	0	NULL	statement 3	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_316	9710622	(A to C) Western blot analysis carried out after GST precipitation of GST-cyclin A-cdk2 shows the capacity of peptides p107S and p107N, but not p107N-mut, to compete the binding of p107 to cyclin A-cdk2.	bind
5477	1	2432	6	10	NULL	0	NULL	MEF2	GP		bind					GLUT4	GP			MEF2 element	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5143_s_340	12861002	(A to C), whereas MEF2 comprises the binding complex formed  at the GLUT4 and MCK MEF2 elements, and this binding decreases when using MOV-P nuclear  extract (D and E).	bind
5478	2	2432	6	10	NULL	0	NULL	MEF2	GP		bind					MCK 	GP			MEF2 element	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5143_s_340	12861002	(A to C), whereas MEF2 comprises the binding complex formed  at the GLUT4 and MCK MEF2 elements, and this binding decreases when using MOV-P nuclear  extract (D and E).	bind
5480	3	2432	6	10	NULL	0	NULL	MOV-P nuclear extract			decreases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5143_s_340	12861002	(A to C), whereas MEF2 comprises the binding complex formed  at the GLUT4 and MCK MEF2 elements, and this binding decreases when using MOV-P nuclear  extract (D and E).	bind
5481	4	2432	6	10	NULL	0	NULL	MOV-P nuclear extract			decreases					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5143_s_340	12861002	(A to C), whereas MEF2 comprises the binding complex formed  at the GLUT4 and MCK MEF2 elements, and this binding decreases when using MOV-P nuclear  extract (D and E).	bind
6266	1	2432	7	10	NULL	0	NULL	MEF2	GP		binds					GLUT4	GP			MEF2 elements	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5143_s_340	12861002	(A to C), whereas MEF2 comprises the binding complex formed  at the GLUT4 and MCK MEF2 elements, and this binding decreases when using MOV-P nuclear  extract (D and E).	bind
6268	2	2432	7	10	NULL	0	NULL	MEF2	GP		binds					MCK	GP			MEF2 elements	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5143_s_340	12861002	(A to C), whereas MEF2 comprises the binding complex formed  at the GLUT4 and MCK MEF2 elements, and this binding decreases when using MOV-P nuclear  extract (D and E).	bind
6309	3	2432	7	10	NULL	0	NULL	MOV-P nuclear extract			decreases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5143_s_340	12861002	(A to C), whereas MEF2 comprises the binding complex formed  at the GLUT4 and MCK MEF2 elements, and this binding decreases when using MOV-P nuclear  extract (D and E).	bind
6310	4	2432	7	10	NULL	0	NULL	MOV-P nuclear extract			decreases					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5143_s_340	12861002	(A to C), whereas MEF2 comprises the binding complex formed  at the GLUT4 and MCK MEF2 elements, and this binding decreases when using MOV-P nuclear  extract (D and E).	bind
5482	1	2434	6	10	NULL	0	NULL	PCL	GP		bind					Ubx	GP			PRE	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_9_3352_s_235	12697833	(A to F) Binding of PCL, SU(Z)12, and RPD3 to the  Ubx PRE in vivo.	bind
5483	2	2434	6	10	NULL	0	NULL	SU(Z)12	GP		bind					Ubx	GP			PRE	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_9_3352_s_235	12697833	(A to F) Binding of PCL, SU(Z)12, and RPD3 to the  Ubx PRE in vivo.	bind
5485	3	2434	6	10	NULL	0	NULL	RPD3	GP		bind					Ubx	GP			PRE	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_9_3352_s_235	12697833	(A to F) Binding of PCL, SU(Z)12, and RPD3 to the  Ubx PRE in vivo.	bind
5713	1	2434	7	10	NULL	0	NULL	PCL	GP		binds					Ubx	GP			PRE	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_9_3352_s_235	12697833	(A to F) Binding of PCL, SU(Z)12, and RPD3 to the  Ubx PRE in vivo.	bind
5714	2	2434	7	10	NULL	0	NULL	SU(Z)12	GP		binds					Ubx	GP			PRE	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_9_3352_s_235	12697833	(A to F) Binding of PCL, SU(Z)12, and RPD3 to the  Ubx PRE in vivo.	bind
5715	3	2434	7	10	NULL	0	NULL	RPD3	GP		binds					Ubx	GP			PRE	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_9_3352_s_235	12697833	(A to F) Binding of PCL, SU(Z)12, and RPD3 to the  Ubx PRE in vivo.	bind
5487	1	2436	6	10	NULL	0	NULL	Pax6	GP		bind					glucagon	GP	mouse		G1 element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4702_s_210	12052878	(A to T in the human sequence) was chosen because it had been shown to specifically reduce Pax6 binding to the mouse glucagon G1 element ( 2).	bind
5489	2	2436	6	10	NULL	0	NULL	A to T sequence	Chemical	human	reduces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4702_s_210	12052878	(A to T in the human sequence) was chosen because it had been shown to specifically reduce Pax6 binding to the mouse glucagon G1 element ( 2).	bind
5716	1	2436	7	10	NULL	0	NULL	Pax6	GP		binds to					glucagon	GP	mouse		G1 element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4702_s_210	12052878	(A to T in the human sequence) was chosen because it had been shown to specifically reduce Pax6 binding to the mouse glucagon G1 element ( 2).	bind
46315	2	2436	7	10	NULL	0	NULL	A to T sequence	Chemical	human	reduces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4702_s_210	12052878	(A to T in the human sequence) was chosen because it had been shown to specifically reduce Pax6 binding to the mouse glucagon G1 element ( 2).	bind
5490	1	2438	6	10	NULL	0	NULL	Ac transposase	GP		bind					chromatid	Chromosome			fAc 3''-end	NULL		NULL	NULL	NULL	NULL	gw70_genetics_171_1_333_s_283	15965263	(A)  Ac transposase binds to a  fAc 3''-end and an  Ac 5''-end in the same chromatid.	bind
5491	2	2438	6	10	NULL	0	NULL	Ac transposase	GP		bind					chromatid	Chromosome			Ac 5''-end	NULL		NULL	NULL	NULL	NULL	gw70_genetics_171_1_333_s_283	15965263	(A)  Ac transposase binds to a  fAc 3''-end and an  Ac 5''-end in the same chromatid.	bind
5717	1	2438	7	10	NULL	0	NULL	Ac transposase	GP		binds					chromatid	Chromosome			fAc 3''-end	NULL		NULL	NULL	NULL	NULL	gw70_genetics_171_1_333_s_283	15965263	(A)  Ac transposase binds to a  fAc 3''-end and an  Ac 5''-end in the same chromatid.	bind
5718	2	2438	7	10	NULL	0	NULL	Ac transposase	GP		binds					chromatid	Chromosome			Ac 5''-end	NULL		NULL	NULL	NULL	NULL	gw70_genetics_171_1_333_s_283	15965263	(A)  Ac transposase binds to a  fAc 3''-end and an  Ac 5''-end in the same chromatid.	bind
5492	1	2440	6	10	NULL	0	NULL	Keap1	GP		bind					Neh2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_8_2887_s_268	16581765	(A)  Binding model of Keap1 and Neh2.	bind
6257	1	2440	7	10	NULL	0	NULL	Keap1	GP		binds					Neh2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_8_2887_s_268	16581765	(A)  Binding model of Keap1 and Neh2.	bind
5495	1	2441	6	10	NULL	0	NULL	PTF1 complexes	GP	reconstituted;;authentic	bind					Ela1	GP	wild type		PTF1 binding site	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_118	16354684	(A)  Binding of reconstituted and authentic PTF1 complexes to wild-type and mutant  Ela1 PTF1 binding sites; (B) reconstituted and authentic PTF1 bind to PTF1 binding sites  from the promoter regions of several digestive enzyme genes.	bind
5496	2	2441	6	10	NULL	0	NULL	PTF1 complexes	GP	reconstituted;;authentic	bind					Ela1	GP	mutant		PTF1 binding site	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_118	16354684	(A)  Binding of reconstituted and authentic PTF1 complexes to wild-type and mutant  Ela1 PTF1 binding sites; (B) reconstituted and authentic PTF1 bind to PTF1 binding sites  from the promoter regions of several digestive enzyme genes.	bind
5504	3	2441	6	10	NULL	0	NULL	PTF1	GP	reconstituted;;authentic	bind					digestive enzyme genes	GP			PTF1 binding site of promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_118	16354684	(A)  Binding of reconstituted and authentic PTF1 complexes to wild-type and mutant  Ela1 PTF1 binding sites; (B) reconstituted and authentic PTF1 bind to PTF1 binding sites  from the promoter regions of several digestive enzyme genes.	bind
5719	1	2441	7	10	NULL	0	NULL	PTF1 complex	GP	reconstituted;;authentic	bind					Ela1	GP	wild-type		PTF1 binding sites	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_118	16354684	(A)  Binding of reconstituted and authentic PTF1 complexes to wild-type and mutant  Ela1 PTF1 binding sites; (B) reconstituted and authentic PTF1 bind to PTF1 binding sites  from the promoter regions of several digestive enzyme genes.	bind
5720	2	2441	7	10	NULL	0	NULL	PTF1 complex	GP	reconstituted;;authentic	binds to					Ela1	GP	mutant		PTF1 binding sites	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_118	16354684	(A)  Binding of reconstituted and authentic PTF1 complexes to wild-type and mutant  Ela1 PTF1 binding sites; (B) reconstituted and authentic PTF1 bind to PTF1 binding sites  from the promoter regions of several digestive enzyme genes.	bind
5721	3	2441	7	10	NULL	0	NULL	PTF1	GP	reconstituted;;authentic	binds to					digestive enzyme	GP			PTF1 binding sites in the promoter of	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_118	16354684	(A)  Binding of reconstituted and authentic PTF1 complexes to wild-type and mutant  Ela1 PTF1 binding sites; (B) reconstituted and authentic PTF1 bind to PTF1 binding sites  from the promoter regions of several digestive enzyme genes.	bind
5506	1	2442	6	10	NULL	0	NULL			purified;;recombinant	bind			TRAP A-domain		HepG2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_9_5883_s_157	16113307	(A)  Binding of various concentrations of the purified recombinant TRAP A-domain and GST  (as a control) to 1 x 106 HepG2 cells.	bind
5507	2	2442	6	10	NULL	0	NULL	GST	Chemical		bind					HepG2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_9_5883_s_157	16113307	(A)  Binding of various concentrations of the purified recombinant TRAP A-domain and GST  (as a control) to 1 x 106 HepG2 cells.	bind
5722	1	2442	7	10	NULL	0	NULL			purified;;recombinant	binds to			TRAP A-domain		HepG2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_9_5883_s_157	16113307	(A)  Binding of various concentrations of the purified recombinant TRAP A-domain and GST  (as a control) to 1 x 106 HepG2 cells.	bind
5723	2	2442	7	10	NULL	0	NULL	GST	Chemical		binds to					HepG2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_9_5883_s_157	16113307	(A)  Binding of various concentrations of the purified recombinant TRAP A-domain and GST  (as a control) to 1 x 106 HepG2 cells.	bind
5516	1	2449	6	10	NULL	0	NULL	Importin 13	GP		bind		specifically			zz-NF-YBGST-NF-YC complex	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5339_s_275	15964792	(A)  Importin 13 was bound specifically to the immobilized zz-NF-YBGST-NF-YC complex,  and this binding was abolished by a 10-fold molar excess of NF-YA.	bind
5518	2	2449	6	10	NULL	0	NULL	NF-YA	GP	excess of	abolishes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5339_s_275	15964792	(A)  Importin 13 was bound specifically to the immobilized zz-NF-YBGST-NF-YC complex,  and this binding was abolished by a 10-fold molar excess of NF-YA.	bind
5727	1	2449	7	10	NULL	0	NULL	Importin 13	GP		binds to		specifically			 zz-NF-YBGST-NF-YC complex	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5339_s_275	15964792	(A)  Importin 13 was bound specifically to the immobilized zz-NF-YBGST-NF-YC complex,  and this binding was abolished by a 10-fold molar excess of NF-YA.	bind
5728	2	2449	7	10	NULL	0	NULL	statement 1	Process		is abolished by					NF-YA	GP	excess of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5339_s_275	15964792	(A)  Importin 13 was bound specifically to the immobilized zz-NF-YBGST-NF-YC complex,  and this binding was abolished by a 10-fold molar excess of NF-YA.	bind
5520	1	2450	6	10	NULL	0	NULL	2-MeS-ADP	Chemical		bind					platelets	Cell	human			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_brjpharmacol_132_1_47_s_139	11156560	(A)  In vitro effect of R-99224 (10 muM) combined with ARL-66096 (0.3 muM) on [3]-2-MeS-ADP binding to washed human platelets; (B)  In vitro effects of A3P5PS (300 muM) combined with R-99224 (10 muM) or ARL-66096 (0.3 muM) on [3]-2-MeS-ADP binding to washed human platelets.	bind
5733	1	2450	7	10	NULL	0	NULL	2-MeS-ADP	Chemical		bind					platelets	Cell	human			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_brjpharmacol_132_1_47_s_139	11156560	(A)  In vitro effect of R-99224 (10 muM) combined with ARL-66096 (0.3 muM) on [3]-2-MeS-ADP binding to washed human platelets; (B)  In vitro effects of A3P5PS (300 muM) combined with R-99224 (10 muM) or ARL-66096 (0.3 muM) on [3]-2-MeS-ADP binding to washed human platelets.	bind
5523	1	2451	6	10	NULL	0	NULL	MKP5	GP		bind					JNK	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8619_s_246	16166642	(a)  JAMP outcompetes MKP5 binding to JNK in vivo.	bind
5525	2	2451	6	10	NULL	0	NULL	JAMP	GP		bind					JNK	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8619_s_246	16166642	(a)  JAMP outcompetes MKP5 binding to JNK in vivo.	bind
5526	3	2451	6	10	NULL	0	NULL	statement 1	Process		outcompetes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8619_s_246	16166642	(a)  JAMP outcompetes MKP5 binding to JNK in vivo.	bind
5872	1	2451	7	10	NULL	0	NULL	MKP5	GP		binds to					JNK	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8619_s_246	16166642	(a)  JAMP outcompetes MKP5 binding to JNK in vivo.	bind
5873	2	2451	7	10	NULL	0	NULL	 JAMP	GP		bind					JNK	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8619_s_246	16166642	(a)  JAMP outcompetes MKP5 binding to JNK in vivo.	bind
7882	3	2451	7	10	NULL	0	NULL	statement 2	Process		outcompetes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8619_s_246	16166642	(a)  JAMP outcompetes MKP5 binding to JNK in vivo.	bind
5536	1	2452	6	10	NULL	0	NULL	AnaO23A5	GP		bind					A. marginale protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_12_7257_s_120	15557651	(A)  Phase-contrast microscopy was used to locate intraerythrocytic  A. marginale and the associated inclusion appendage; (B) rhodamine-phalloidin was used to label  F-actin; and (C) goat-anti-mouse IgG conjugated to Alexa 488 was used to detect MAb  AnaO23A5 bound to the  A. marginale protein.	bind
46316	2	2452	6	10	NULL	0	NULL	AnaO23A5	GP		is a type of					MAb	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_12_7257_s_120	15557651	(A)  Phase-contrast microscopy was used to locate intraerythrocytic  A. marginale and the associated inclusion appendage; (B) rhodamine-phalloidin was used to label  F-actin; and (C) goat-anti-mouse IgG conjugated to Alexa 488 was used to detect MAb  AnaO23A5 bound to the  A. marginale protein.	bind
5874	1	2452	7	10	NULL	0	NULL	AnaO23A5	GP		binds to					 A. marginale protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_12_7257_s_120	15557651	(A)  Phase-contrast microscopy was used to locate intraerythrocytic  A. marginale and the associated inclusion appendage; (B) rhodamine-phalloidin was used to label  F-actin; and (C) goat-anti-mouse IgG conjugated to Alexa 488 was used to detect MAb  AnaO23A5 bound to the  A. marginale protein.	bind
46317	2	2452	7	10	NULL	0	NULL	AnaO23A5	GP		is a type of					MAb	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_12_7257_s_120	15557651	(A)  Phase-contrast microscopy was used to locate intraerythrocytic  A. marginale and the associated inclusion appendage; (B) rhodamine-phalloidin was used to label  F-actin; and (C) goat-anti-mouse IgG conjugated to Alexa 488 was used to detect MAb  AnaO23A5 bound to the  A. marginale protein.	bind
5538	1	2453	6	10	NULL	0	NULL	Bim	GP		bind					Bcl-w	GP				NULL	epilepsy brain samples	NULL	NULL	NULL	NULL	gw70_jclininvest_113_7_1059_s_266	15057313	(A)  Representative Western blot (WB) showing Bim binding to Bcl-w immunoprecipitates  in epilepsy but not control brain samples.	bind
5539	2	2453	6	10	NULL	0	NULL	Bim	GP		does not bind					Bcl-w	GP				NULL	control brain samples	NULL	NULL	NULL	NULL	gw70_jclininvest_113_7_1059_s_266	15057313	(A)  Representative Western blot (WB) showing Bim binding to Bcl-w immunoprecipitates  in epilepsy but not control brain samples.	bind
5875	1	2453	7	10	NULL	0	NULL	Bim	GP		binds to					Bcl-w	GP				NULL	epilepsy brain sample	NULL	NULL	NULL	NULL	gw70_jclininvest_113_7_1059_s_266	15057313	(A)  Representative Western blot (WB) showing Bim binding to Bcl-w immunoprecipitates  in epilepsy but not control brain samples.	bind
61114	2	2453	7	10	NULL	0	NULL	Bim	GP		does not bind					Bcl-w	GP				NULL	control brain samples	0	NULL	NULL	NULL	gw70_jclininvest_113_7_1059_s_266	15057313	(A)  Representative Western blot (WB) showing Bim binding to Bcl-w immunoprecipitates  in epilepsy but not control brain samples.	bind
5549	1	2454	6	10	NULL	0	NULL	nuclear protein	GP		bind									C1 region	NULL	human endometrial cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_10_5795_s_219	8621448	(A)  RNA of the RL95-2 cells with a concatenated FP1 sequence in order to  isolate the nuclear protein that binds to the C1 region in human  endometrial cells.	bind
5876	1	2454	7	10	NULL	0	NULL	nuclear protein	GP		binds									C1 region	NULL	human endometrial cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_10_5795_s_219	8621448	(A)  RNA of the RL95-2 cells with a concatenated FP1 sequence in order to  isolate the nuclear protein that binds to the C1 region in human  endometrial cells.	bind
5550	1	2455	6	10	NULL	0	NULL	MSL	GP		bind		weakly			X chromosome	Chromosome				NULL	roX1 roX2 double mutant male nucleus	NULL	NULL	NULL	NULL	gw60_molcell_11_4_977_s_199	12718883	(A)  roX1 roX2 double mutant male nucleus showing weak MSL binding to the X chromosome and ectopic binding to autosomal sites and heterochromatin (arrowhead).	bind
5551	2	2455	6	10	NULL	0	NULL	MSL	GP		bind		ectopicaly			autosomal sites	Chromosome				NULL	roX1 roX2 double mutant male nucleus	NULL	NULL	NULL	NULL	gw60_molcell_11_4_977_s_199	12718883	(A)  roX1 roX2 double mutant male nucleus showing weak MSL binding to the X chromosome and ectopic binding to autosomal sites and heterochromatin (arrowhead).	bind
5552	3	2455	6	10	NULL	0	NULL	MSL	GP		bind		ectopicaly			heterochromatin	Chromosome				NULL	roX1 roX2 double mutant male nucleus	NULL	NULL	NULL	NULL	gw60_molcell_11_4_977_s_199	12718883	(A)  roX1 roX2 double mutant male nucleus showing weak MSL binding to the X chromosome and ectopic binding to autosomal sites and heterochromatin (arrowhead).	bind
5877	1	2455	7	10	NULL	0	NULL	MSL	GP		binds		weakly			X chromosome	Chromosome				NULL	roX1 roX2 double mutant male nucleus	NULL	NULL	NULL	NULL	gw60_molcell_11_4_977_s_199	12718883	(A)  roX1 roX2 double mutant male nucleus showing weak MSL binding to the X chromosome and ectopic binding to autosomal sites and heterochromatin (arrowhead).	bind
5878	2	2455	7	10	NULL	0	NULL	MSL	GP		binds		ectopically			autosomal sites	Chromosome				NULL	roX1 roX2 double mutant male nucleus	NULL	NULL	NULL	NULL	gw60_molcell_11_4_977_s_199	12718883	(A)  roX1 roX2 double mutant male nucleus showing weak MSL binding to the X chromosome and ectopic binding to autosomal sites and heterochromatin (arrowhead).	bind
5879	3	2455	7	10	NULL	0	NULL	MSL	GP		binds		ectopically			heterochromatin	Chromosome				NULL	roX1 roX2 double mutant male nucleus	NULL	NULL	NULL	NULL	gw60_molcell_11_4_977_s_199	12718883	(A)  roX1 roX2 double mutant male nucleus showing weak MSL binding to the X chromosome and ectopic binding to autosomal sites and heterochromatin (arrowhead).	bind
5554	1	2457	6	10	NULL	0	NULL	MeCP2	GP		bind					Uqcrc1	GP			promoter	NULL	wild type mouse brain	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_13_5033_s_193	16782889	(a)  Uqcrc1 promoter map showing CpG frequency, methylation status, and the region used for PCR  amplification of immunoprecipitated DNA. (b) Chromatin immunoprecipitation reveals  MeCP2 bound to the  Uqcrc1 promoter in wt mouse brain but not in  Mecp2-null mouse brain.	bind
5555	2	2457	6	10	NULL	0	NULL	MeCP2	GP		does not bind					Uqcrc1	GP			promoter	NULL	Mecp2-null mouse brain	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_13_5033_s_193	16782889	(a)  Uqcrc1 promoter map showing CpG frequency, methylation status, and the region used for PCR  amplification of immunoprecipitated DNA. (b) Chromatin immunoprecipitation reveals  MeCP2 bound to the  Uqcrc1 promoter in wt mouse brain but not in  Mecp2-null mouse brain.	bind
5880	1	2457	7	10	NULL	0	NULL	MeCP2	GP		binds					Uqcrc1	GP			promoter	NULL	wt mouse brain	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_13_5033_s_193	16782889	(a)  Uqcrc1 promoter map showing CpG frequency, methylation status, and the region used for PCR  amplification of immunoprecipitated DNA. (b) Chromatin immunoprecipitation reveals  MeCP2 bound to the  Uqcrc1 promoter in wt mouse brain but not in  Mecp2-null mouse brain.	bind
5881	2	2457	7	10	NULL	0	NULL	MeCP2	GP		does not bind					Uqcrc1	GP			promoter	NULL	Mecp2-null mouse brain	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_13_5033_s_193	16782889	(a)  Uqcrc1 promoter map showing CpG frequency, methylation status, and the region used for PCR  amplification of immunoprecipitated DNA. (b) Chromatin immunoprecipitation reveals  MeCP2 bound to the  Uqcrc1 promoter in wt mouse brain but not in  Mecp2-null mouse brain.	bind
5562	1	2459	6	10	NULL	0	NULL	PAX6	GP		bind			PD		hGC 	GP			1BL sequence	NULL		NULL	NULL	NULL	NULL	gw60_gene_245_2_319_s_88	10717483	(A) ( Epstein et al., 1994), but not by the Pax-6 HD binding sequence P3 (   Czerny et al., 1997) (  Fig. 2A), suggesting that PAX6 bound the hGC 1BL sequence through its PD.	bind
5885	1	2459	7	10	NULL	0	NULL	PAX6 	GP		binds			 PD		hGC	GP			1BL sequence	NULL		NULL	NULL	NULL	NULL	gw60_gene_245_2_319_s_88	10717483	(A) ( Epstein et al., 1994), but not by the Pax-6 HD binding sequence P3 (   Czerny et al., 1997) (  Fig. 2A), suggesting that PAX6 bound the hGC 1BL sequence through its PD.	bind
5563	1	2460	6	10	NULL	0	NULL	melittin	GP		bind					POPC vesicles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_1_26_s_204	15533303	(A) (a) Kinetics of the helix formation upon melittin binding to POPC vesicles  (Ri=90; [POPC]=3 mM; [melittin]=35  M).	bind
5886	1	2460	7	10	NULL	0	NULL	melittin	GP		binds					POPC vesicles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_1_26_s_204	15533303	(A) (a) Kinetics of the helix formation upon melittin binding to POPC vesicles  (Ri=90; [POPC]=3 mM; [melittin]=35  M).	bind
5564	1	2462	6	10	NULL	0	NULL	THC	GP		bind					SMC	GP				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_120_2_91_s_161	14741398	(A) (lane 4) and poly (U) (lane 6) displaced THC  binding to the SMC, while poly (C) displaced neither SMC nor FMC.	bind
5566	3	2462	6	10	NULL	0	NULL	statement 2	Process		displaces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_120_2_91_s_161	14741398	(A) (lane 4) and poly (U) (lane 6) displaced THC  binding to the SMC, while poly (C) displaced neither SMC nor FMC.	bind
5569	4	2462	6	10	NULL	0	NULL	poly (C)	Chemical		does not displace					SMC	GP				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_120_2_91_s_161	14741398	(A) (lane 4) and poly (U) (lane 6) displaced THC  binding to the SMC, while poly (C) displaced neither SMC nor FMC.	bind
5571	5	2462	6	10	NULL	0	NULL	poly (C)	Chemical		does not displace					FMC	GP				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_120_2_91_s_161	14741398	(A) (lane 4) and poly (U) (lane 6) displaced THC  binding to the SMC, while poly (C) displaced neither SMC nor FMC.	bind
46318	2	2462	6	10	NULL	0	NULL	poly (U) 	Chemical		bind					SMC	GP				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_120_2_91_s_161	14741398	(A) (lane 4) and poly (U) (lane 6) displaced THC  binding to the SMC, while poly (C) displaced neither SMC nor FMC.	bind
5887	1	2462	7	10	NULL	0	NULL	THC	GP		binds					SMC	GP				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_120_2_91_s_161	14741398	(A) (lane 4) and poly (U) (lane 6) displaced THC  binding to the SMC, while poly (C) displaced neither SMC nor FMC.	bind
5888	2	2462	7	10	NULL	0	NULL	poly (U)	Chemical		binds					SMC	GP				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_120_2_91_s_161	14741398	(A) (lane 4) and poly (U) (lane 6) displaced THC  binding to the SMC, while poly (C) displaced neither SMC nor FMC.	bind
5889	3	2462	7	10	NULL	0	NULL	poly (U)	Chemical		displaces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_120_2_91_s_161	14741398	(A) (lane 4) and poly (U) (lane 6) displaced THC  binding to the SMC, while poly (C) displaced neither SMC nor FMC.	bind
5890	4	2462	7	10	NULL	0	NULL	poly (C)	Chemical		does not displace					SMC	GP				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_120_2_91_s_161	14741398	(A) (lane 4) and poly (U) (lane 6) displaced THC  binding to the SMC, while poly (C) displaced neither SMC nor FMC.	bind
5891	5	2462	7	10	NULL	0	NULL	poly (C)	Chemical		does not displace					FMC	GP				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_120_2_91_s_161	14741398	(A) (lane 4) and poly (U) (lane 6) displaced THC  binding to the SMC, while poly (C) displaced neither SMC nor FMC.	bind
5572	1	2465	6	10	NULL	0	NULL	RIM1	GP		bind					Munc13	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_30_1_183_s_112	11343654	(A) (Left) RIM1 binding to Munc13 GST fusion proteins in cosedimentation assays.	bind
46319	2	2465	6	10	NULL	0	NULL	Munc13	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_30_1_183_s_112	11343654	(A) (Left) RIM1 binding to Munc13 GST fusion proteins in cosedimentation assays.	bind
5892	1	2465	7	10	NULL	0	NULL	RIM1	GP		binds					Munc13	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_30_1_183_s_112	11343654	(A) (Left) RIM1 binding to Munc13 GST fusion proteins in cosedimentation assays.	bind
46320	2	2465	7	10	NULL	0	NULL	Munc13	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_30_1_183_s_112	11343654	(A) (Left) RIM1 binding to Munc13 GST fusion proteins in cosedimentation assays.	bind
5573	1	2467	6	NULL	NULL	0	NULL	PP2A A subunit protein	NULL		bind	NULL				Hsc-70	NULL				NULL	bovine liver cytosol	0	NULL	NULL	NULL	gw60_cellbiol_160_5_699_s_151	12604586	(A) 100 mug of GST or GST fusion peptide corresponding to the PP2A A subunit protein was bound to glutathione-Sepharose beads and used to pull down Hsc-70 from 2 mg of bovine liver cytosol.	bind
46321	2	2467	6	10	NULL	0	NULL	PP2A A subunit protein	NULL		is a type of	NULL				GST fusion peptide	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_160_5_699_s_151	12604586	(A) 100 mug of GST or GST fusion peptide corresponding to the PP2A A subunit protein was bound to glutathione-Sepharose beads and used to pull down Hsc-70 from 2 mg of bovine liver cytosol.	bind
5973	1	2467	7	10	NULL	0	NULL	PP2A A subunit protein 	NULL		binds	NULL				Hsc-70	NULL				NULL	bovine liver cytosol	NULL	NULL	NULL	NULL	gw60_cellbiol_160_5_699_s_151	12604586	(A) 100 mug of GST or GST fusion peptide corresponding to the PP2A A subunit protein was bound to glutathione-Sepharose beads and used to pull down Hsc-70 from 2 mg of bovine liver cytosol.	bind
46322	2	2467	7	10	NULL	0	NULL	PP2A A subunit protein	NULL		is a type of	NULL				GST fusion peptide	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_160_5_699_s_151	12604586	(A) 100 mug of GST or GST fusion peptide corresponding to the PP2A A subunit protein was bound to glutathione-Sepharose beads and used to pull down Hsc-70 from 2 mg of bovine liver cytosol.	bind
5574	1	2468	6	10	NULL	0	NULL	lactoferrin	GP	125I-labeled;;recombinant;;human	bind		specifically			Kupffer cells	Cell	mouse			NULL		NULL	NULL	NULL	NULL	gw60_clindiagnlabimmun_8_6_1234_s_134	11687469	(a) 125I-labeled recombinant human lactoferrin specifically bound to mouse Kupffer cells.	bind
5893	1	2468	7	10	NULL	0	NULL	 lactoferrin	GP	125I-labeled;;recombinant;;human	binds		specifically			Kupffer cells	Cell	mouse			NULL		NULL	NULL	NULL	NULL	gw60_clindiagnlabimmun_8_6_1234_s_134	11687469	(a) 125I-labeled recombinant human lactoferrin specifically bound to mouse Kupffer cells.	bind
5575	1	2469	6	10	NULL	0	NULL	293T cells	Cell		express		transiently			Hck499F	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6984_s_112	10958693	(A) 293T cells transiently expressing Hck499F or  tsHck499F were incubated at the indicated temperature for 48 h and then lysed with NP-40 lysis buffer.	bind
5576	2	2469	6	10	NULL	0	NULL	293T cells	Cell		express		transiently			tsHck499F	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6984_s_112	10958693	(A) 293T cells transiently expressing Hck499F or  tsHck499F were incubated at the indicated temperature for 48 h and then lysed with NP-40 lysis buffer.	bind
6557	1	2469	7	10	NULL	0	NULL	 293T cells	Cell		express		transiently			Hck499F	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6984_s_112	10958693	(A) 293T cells transiently expressing Hck499F or  tsHck499F were incubated at the indicated temperature for 48 h and then lysed with NP-40 lysis buffer.	bind
6558	2	2469	7	10	NULL	0	NULL	293T cells	Cell		express		transiently			tsHck499F	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6984_s_112	10958693	(A) 293T cells transiently expressing Hck499F or  tsHck499F were incubated at the indicated temperature for 48 h and then lysed with NP-40 lysis buffer.	bind
5577	1	2471	6	10	NULL	0	NULL	HIRA	GP	35S-labeled	bind					GST-H2B	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5546_s_187	9710638	(A) 35S-labeled HIRA binds GST-H2B and GST-HIRIP3 but not GST immobilized on glutathione beads.	bind
5578	2	2471	6	10	NULL	0	NULL	HIRA	GP	35S-labeled	bind					GST-HIRIP3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5546_s_187	9710638	(A) 35S-labeled HIRA binds GST-H2B and GST-HIRIP3 but not GST immobilized on glutathione beads.	bind
5579	3	2471	6	10	NULL	0	NULL	HIRA	GP	35S-labeled	does not bind					GST	Chemical	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5546_s_187	9710638	(A) 35S-labeled HIRA binds GST-H2B and GST-HIRIP3 but not GST immobilized on glutathione beads.	bind
5895	1	2471	7	10	NULL	0	NULL	HIRA	GP	35S-labeled	binds					GST-H2B	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5546_s_187	9710638	(A) 35S-labeled HIRA binds GST-H2B and GST-HIRIP3 but not GST immobilized on glutathione beads.	bind
5896	2	2471	7	10	NULL	0	NULL	HIRA	GP	35S-labeled	binds					GST-HIRIP3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5546_s_187	9710638	(A) 35S-labeled HIRA binds GST-H2B and GST-HIRIP3 but not GST immobilized on glutathione beads.	bind
5897	3	2471	7	10	NULL	0	NULL	HIRA	GP	35S-labeled	does not bind					GST	Chemical	immobilized 			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5546_s_187	9710638	(A) 35S-labeled HIRA binds GST-H2B and GST-HIRIP3 but not GST immobilized on glutathione beads.	bind
5580	1	2473	6	10	NULL	0	NULL	prohibitin	GP	35S-labeled	bind					GST-Phb	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_2_459_s_92	14637159	(A) 35S-labeled prohibitin binds to GST-Phb but not control GST beads in vitro.	bind
5581	2	2473	6	10	NULL	0	NULL	prohibitin	GP	35S-labeled	does not bind					GST	Chemical	control			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_2_459_s_92	14637159	(A) 35S-labeled prohibitin binds to GST-Phb but not control GST beads in vitro.	bind
5898	1	2473	7	10	NULL	0	NULL	prohibitin	GP	35S-labeled	binds					GST-Phb	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_2_459_s_92	14637159	(A) 35S-labeled prohibitin binds to GST-Phb but not control GST beads in vitro.	bind
5899	2	2473	7	10	NULL	0	NULL	prohibitin	GP	35S-labeled	does not bind					GST	Chemical	control			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_2_459_s_92	14637159	(A) 35S-labeled prohibitin binds to GST-Phb but not control GST beads in vitro.	bind
5582	1	2474	6	10	NULL	0	NULL	SGP1	GP		bind					c-erbB-3	GP		extracellular epitope		NULL	untreated MCF-7 fractions	NULL	NULL	NULL	NULL	gw60_cellbiol_157_6_929_s_87	12045181	(A) 400 mug protein from untreated (-) or LMB-treated (+) C or N MCF-7 fractions were immunoprecipitated (IP) with SGP1, which detects an extracellular epitope of c-erbB-3, or with mIgG1 and blotted (IB) with C17, which binds to the cytoplasmic part of c-erbB-3.	bind
5583	2	2474	6	10	NULL	0	NULL	SGP1	GP		bind					c-erbB-3	GP		extracellular epitope		NULL	LMB-treated (+) MCF-7 fractions	NULL	NULL	NULL	NULL	gw60_cellbiol_157_6_929_s_87	12045181	(A) 400 mug protein from untreated (-) or LMB-treated (+) C or N MCF-7 fractions were immunoprecipitated (IP) with SGP1, which detects an extracellular epitope of c-erbB-3, or with mIgG1 and blotted (IB) with C17, which binds to the cytoplasmic part of c-erbB-3.	bind
5584	3	2474	6	10	NULL	0	NULL	C17	GP		bind					c-erbB-3	GP		cytoplasmic part		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_6_929_s_87	12045181	(A) 400 mug protein from untreated (-) or LMB-treated (+) C or N MCF-7 fractions were immunoprecipitated (IP) with SGP1, which detects an extracellular epitope of c-erbB-3, or with mIgG1 and blotted (IB) with C17, which binds to the cytoplasmic part of c-erbB-3.	bind
6330	1	2474	7	10	NULL	0	NULL	SGP1	GP		binds					c-erbB-3 \t	GP		extracellular epitope		NULL	untreated MCF-7 fractions	NULL	NULL	NULL	NULL	gw60_cellbiol_157_6_929_s_87	12045181	(A) 400 mug protein from untreated (-) or LMB-treated (+) C or N MCF-7 fractions were immunoprecipitated (IP) with SGP1, which detects an extracellular epitope of c-erbB-3, or with mIgG1 and blotted (IB) with C17, which binds to the cytoplasmic part of c-erbB-3.	bind
6331	2	2474	7	10	NULL	0	NULL	SGP1	GP		bind					c-erbB-3	GP		extracellular epitope		NULL	LMB-treated (+) MCF-7 fractions	NULL	NULL	NULL	NULL	gw60_cellbiol_157_6_929_s_87	12045181	(A) 400 mug protein from untreated (-) or LMB-treated (+) C or N MCF-7 fractions were immunoprecipitated (IP) with SGP1, which detects an extracellular epitope of c-erbB-3, or with mIgG1 and blotted (IB) with C17, which binds to the cytoplasmic part of c-erbB-3.	bind
6334	3	2474	7	10	NULL	0	NULL	C17	GP		binds					c-erbB-3	GP		cytoplasmic part		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_6_929_s_87	12045181	(A) 400 mug protein from untreated (-) or LMB-treated (+) C or N MCF-7 fractions were immunoprecipitated (IP) with SGP1, which detects an extracellular epitope of c-erbB-3, or with mIgG1 and blotted (IB) with C17, which binds to the cytoplasmic part of c-erbB-3.	bind
5585	1	2475	6	10	NULL	0	NULL	GTP S	Chemical		bind					5-ht5A/HEK293 membranes	CellComponent	guinea pig			NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_207	16846620	(A) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of SB-699551-A (0.1, 0.3, 1 and 3   M).	bind
5586	2	2475	6	10	NULL	0	NULL	5-HT	Chemical		induced					statement 1	Process	stimulation of			NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_207	16846620	(A) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of SB-699551-A (0.1, 0.3, 1 and 3   M).	bind
5906	1	2475	7	10	NULL	0	NULL	GTP S	Chemical		binds					5-ht5A/HEK293 membranes	CellComponent	guinea pig			NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_207	16846620	(A) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of SB-699551-A (0.1, 0.3, 1 and 3   M).	bind
5907	2	2475	7	10	NULL	0	NULL	5-HT	Chemical		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_207	16846620	(A) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of SB-699551-A (0.1, 0.3, 1 and 3   M).	bind
5587	1	2477	6	10	NULL	0	NULL	9G8	GP		bind					Flag-TAP	GP				NULL	transfected cells	NULL	NULL	NULL	NULL	gw60_molcell_11_3_837_s_31	12667464	(A) 9G8 binds Flag-TAP in transfected cells.	bind
6335	1	2477	7	10	NULL	0	NULL	9G8	GP		binds					Flag-TAP	GP				NULL	transfected cells	NULL	NULL	NULL	NULL	gw60_molcell_11_3_837_s_31	12667464	(A) 9G8 binds Flag-TAP in transfected cells.	bind
7631	1	2478	6	10	NULL	0	NULL	cis-acting elements	NucleicAcid		involved in					fbp1	GP	regulation of transcription			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6426_s_103	10938120	(A) A deletion series was constructed within the  fbp1 promoter of the  fbp1-lacZ reporter to identify  cis-acting elements involved in the regulation of  fbp1 transcription.	bind
6336	1	2478	7	10	NULL	0	NULL	cis-acting elements	NucleicAcid		involved in 					fbp1	GP	regulation of transcription of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6426_s_103	10938120	(A) A deletion series was constructed within the  fbp1 promoter of the  fbp1-lacZ reporter to identify  cis-acting elements involved in the regulation of  fbp1 transcription.	bind
5588	1	2481	6	10	NULL	0	NULL	repressosome	GP		bind									I* element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4219_s_433	10330162	(A) A multiprotein complex (repressosome) binds to the I* element.	bind
46323	2	2481	6	10	NULL	0	NULL	repressosome	GP		is a type of					multiprotein complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4219_s_433	10330162	(A) A multiprotein complex (repressosome) binds to the I* element.	bind
6337	1	2481	7	10	NULL	0	NULL	repressosome	GP		binds									I* element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4219_s_433	10330162	(A) A multiprotein complex (repressosome) binds to the I* element.	bind
46324	2	2481	7	10	NULL	0	NULL	repressosome	GP		is a type of					multiprotein complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4219_s_433	10330162	(A) A multiprotein complex (repressosome) binds to the I* element.	bind
5589	1	2483	6	10	NULL	0	NULL	PKN	GP		bind			effector domain		RhoA	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_5_793_s_53	10619026	(A) A ribbon representation of the PKN effector domain (blue) bound to RhoA (brown).	bind
6339	1	2483	7	10	NULL	0	NULL	 PKN	GP		binds			effector domain		RhoA	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_5_793_s_53	10619026	(A) A ribbon representation of the PKN effector domain (blue) bound to RhoA (brown).	bind
5590	1	2484	6	10	NULL	0	NULL	eIF4A	GP		bind					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_1_26_s_365	12482958	(A) A sandwich model of eIF4A binding to eIF4G is shown ( 32).	bind
6340	1	2484	7	10	NULL	0	NULL	eIF4A	GP		binds					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_1_26_s_365	12482958	(A) A sandwich model of eIF4A binding to eIF4G is shown ( 32).	bind
5591	1	2485	6	10	NULL	0	NULL	single P. aeruginosa bacterium	Organism		bind					PM 	CellComponent				NULL	CFTE cell	NULL	NULL	NULL	NULL	gw60_febslett_405_2_200_s_113	9089291	(A) A single  P. aeruginosa bacterium bound to the plasma membrane of a CFTE cell (magnification=14800x); (B) a single bacterium bound to the plasma membrane (PM) of a CFTE cell and encircled by microvilli (magnification=23040x); (C) two bacteria entrapped inside a CFTE cell within a vacuole (V) (magnification=6320x); (D) a single bacterium in contact with a mitochondrion inside a CFTE cell (magnification=6122x); (E,F) bacteria penetrating HTE cells (normal cells) forming deep invaginations (magnifications=26730x and 25740x, respectively).	bind
5592	2	2485	6	10	NULL	0	NULL	PM	CellComponent		is					plasma membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_febslett_405_2_200_s_113	9089291	(A) A single  P. aeruginosa bacterium bound to the plasma membrane of a CFTE cell (magnification=14800x); (B) a single bacterium bound to the plasma membrane (PM) of a CFTE cell and encircled by microvilli (magnification=23040x); (C) two bacteria entrapped inside a CFTE cell within a vacuole (V) (magnification=6320x); (D) a single bacterium in contact with a mitochondrion inside a CFTE cell (magnification=6122x); (E,F) bacteria penetrating HTE cells (normal cells) forming deep invaginations (magnifications=26730x and 25740x, respectively).	bind
5593	3	2485	6	10	NULL	0	NULL	statement 1	Process		encircled by					microvilli	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_febslett_405_2_200_s_113	9089291	(A) A single  P. aeruginosa bacterium bound to the plasma membrane of a CFTE cell (magnification=14800x); (B) a single bacterium bound to the plasma membrane (PM) of a CFTE cell and encircled by microvilli (magnification=23040x); (C) two bacteria entrapped inside a CFTE cell within a vacuole (V) (magnification=6320x); (D) a single bacterium in contact with a mitochondrion inside a CFTE cell (magnification=6122x); (E,F) bacteria penetrating HTE cells (normal cells) forming deep invaginations (magnifications=26730x and 25740x, respectively).	bind
5594	4	2485	6	10	NULL	0	NULL	P. aeruginosa bacteria	Organism		entrapped inside					vacuole	CellComponent				NULL	CFTE cell	NULL	NULL	NULL	NULL	gw60_febslett_405_2_200_s_113	9089291	(A) A single  P. aeruginosa bacterium bound to the plasma membrane of a CFTE cell (magnification=14800x); (B) a single bacterium bound to the plasma membrane (PM) of a CFTE cell and encircled by microvilli (magnification=23040x); (C) two bacteria entrapped inside a CFTE cell within a vacuole (V) (magnification=6320x); (D) a single bacterium in contact with a mitochondrion inside a CFTE cell (magnification=6122x); (E,F) bacteria penetrating HTE cells (normal cells) forming deep invaginations (magnifications=26730x and 25740x, respectively).	bind
5595	5	2485	6	10	NULL	0	NULL	P. aeruginosa bacteria	Organism		is in contact with					mitochondria	CellComponent				NULL	CFTE cell	NULL	NULL	NULL	NULL	gw60_febslett_405_2_200_s_113	9089291	(A) A single  P. aeruginosa bacterium bound to the plasma membrane of a CFTE cell (magnification=14800x); (B) a single bacterium bound to the plasma membrane (PM) of a CFTE cell and encircled by microvilli (magnification=23040x); (C) two bacteria entrapped inside a CFTE cell within a vacuole (V) (magnification=6320x); (D) a single bacterium in contact with a mitochondrion inside a CFTE cell (magnification=6122x); (E,F) bacteria penetrating HTE cells (normal cells) forming deep invaginations (magnifications=26730x and 25740x, respectively).	bind
5596	6	2485	6	10	NULL	0	NULL	P. aeruginosa bacteria	Organism		penetrate					HTE cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_febslett_405_2_200_s_113	9089291	(A) A single  P. aeruginosa bacterium bound to the plasma membrane of a CFTE cell (magnification=14800x); (B) a single bacterium bound to the plasma membrane (PM) of a CFTE cell and encircled by microvilli (magnification=23040x); (C) two bacteria entrapped inside a CFTE cell within a vacuole (V) (magnification=6320x); (D) a single bacterium in contact with a mitochondrion inside a CFTE cell (magnification=6122x); (E,F) bacteria penetrating HTE cells (normal cells) forming deep invaginations (magnifications=26730x and 25740x, respectively).	bind
5597	7	2485	6	10	NULL	0	NULL	statement 6	Process		form					invaginations	Process	deep			NULL		NULL	NULL	NULL	NULL	gw60_febslett_405_2_200_s_113	9089291	(A) A single  P. aeruginosa bacterium bound to the plasma membrane of a CFTE cell (magnification=14800x); (B) a single bacterium bound to the plasma membrane (PM) of a CFTE cell and encircled by microvilli (magnification=23040x); (C) two bacteria entrapped inside a CFTE cell within a vacuole (V) (magnification=6320x); (D) a single bacterium in contact with a mitochondrion inside a CFTE cell (magnification=6122x); (E,F) bacteria penetrating HTE cells (normal cells) forming deep invaginations (magnifications=26730x and 25740x, respectively).	bind
6341	1	2485	7	10	NULL	0	NULL	P. aeruginosa bacterium	Organism		binds to					plasma membrane	CellComponent				NULL	CFTE cell	NULL	NULL	NULL	NULL	gw60_febslett_405_2_200_s_113	9089291	(A) A single  P. aeruginosa bacterium bound to the plasma membrane of a CFTE cell (magnification=14800x); (B) a single bacterium bound to the plasma membrane (PM) of a CFTE cell and encircled by microvilli (magnification=23040x); (C) two bacteria entrapped inside a CFTE cell within a vacuole (V) (magnification=6320x); (D) a single bacterium in contact with a mitochondrion inside a CFTE cell (magnification=6122x); (E,F) bacteria penetrating HTE cells (normal cells) forming deep invaginations (magnifications=26730x and 25740x, respectively).	bind
6342	2	2485	7	10	NULL	0	NULL	statement 1	Process		is encircled by					microvilli	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_febslett_405_2_200_s_113	9089291	(A) A single  P. aeruginosa bacterium bound to the plasma membrane of a CFTE cell (magnification=14800x); (B) a single bacterium bound to the plasma membrane (PM) of a CFTE cell and encircled by microvilli (magnification=23040x); (C) two bacteria entrapped inside a CFTE cell within a vacuole (V) (magnification=6320x); (D) a single bacterium in contact with a mitochondrion inside a CFTE cell (magnification=6122x); (E,F) bacteria penetrating HTE cells (normal cells) forming deep invaginations (magnifications=26730x and 25740x, respectively).	bind
6343	3	2485	7	10	NULL	0	NULL	bacteria	Organism		trapped inside					vacuole	CellComponent				NULL	CFTE cell	NULL	NULL	NULL	NULL	gw60_febslett_405_2_200_s_113	9089291	(A) A single  P. aeruginosa bacterium bound to the plasma membrane of a CFTE cell (magnification=14800x); (B) a single bacterium bound to the plasma membrane (PM) of a CFTE cell and encircled by microvilli (magnification=23040x); (C) two bacteria entrapped inside a CFTE cell within a vacuole (V) (magnification=6320x); (D) a single bacterium in contact with a mitochondrion inside a CFTE cell (magnification=6122x); (E,F) bacteria penetrating HTE cells (normal cells) forming deep invaginations (magnifications=26730x and 25740x, respectively).	bind
6344	4	2485	7	10	NULL	0	NULL	bacterium	Organism		is in contact with					mitochondria	CellComponent				NULL	CFTE cell	NULL	NULL	NULL	NULL	gw60_febslett_405_2_200_s_113	9089291	(A) A single  P. aeruginosa bacterium bound to the plasma membrane of a CFTE cell (magnification=14800x); (B) a single bacterium bound to the plasma membrane (PM) of a CFTE cell and encircled by microvilli (magnification=23040x); (C) two bacteria entrapped inside a CFTE cell within a vacuole (V) (magnification=6320x); (D) a single bacterium in contact with a mitochondrion inside a CFTE cell (magnification=6122x); (E,F) bacteria penetrating HTE cells (normal cells) forming deep invaginations (magnifications=26730x and 25740x, respectively).	bind
6345	5	2485	7	10	NULL	0	NULL	bacteria	Organism		penetrates					HTE cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_febslett_405_2_200_s_113	9089291	(A) A single  P. aeruginosa bacterium bound to the plasma membrane of a CFTE cell (magnification=14800x); (B) a single bacterium bound to the plasma membrane (PM) of a CFTE cell and encircled by microvilli (magnification=23040x); (C) two bacteria entrapped inside a CFTE cell within a vacuole (V) (magnification=6320x); (D) a single bacterium in contact with a mitochondrion inside a CFTE cell (magnification=6122x); (E,F) bacteria penetrating HTE cells (normal cells) forming deep invaginations (magnifications=26730x and 25740x, respectively).	bind
6346	6	2485	7	10	NULL	0	NULL	statement 5	Process		forms					invaginations	Process	deep			NULL		NULL	NULL	NULL	NULL	gw60_febslett_405_2_200_s_113	9089291	(A) A single  P. aeruginosa bacterium bound to the plasma membrane of a CFTE cell (magnification=14800x); (B) a single bacterium bound to the plasma membrane (PM) of a CFTE cell and encircled by microvilli (magnification=23040x); (C) two bacteria entrapped inside a CFTE cell within a vacuole (V) (magnification=6320x); (D) a single bacterium in contact with a mitochondrion inside a CFTE cell (magnification=6122x); (E,F) bacteria penetrating HTE cells (normal cells) forming deep invaginations (magnifications=26730x and 25740x, respectively).	bind
6347	7	2485	7	10	NULL	0	NULL	PM	CellComponent		is					plasma membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_febslett_405_2_200_s_113	9089291	(A) A single  P. aeruginosa bacterium bound to the plasma membrane of a CFTE cell (magnification=14800x); (B) a single bacterium bound to the plasma membrane (PM) of a CFTE cell and encircled by microvilli (magnification=23040x); (C) two bacteria entrapped inside a CFTE cell within a vacuole (V) (magnification=6320x); (D) a single bacterium in contact with a mitochondrion inside a CFTE cell (magnification=6122x); (E,F) bacteria penetrating HTE cells (normal cells) forming deep invaginations (magnifications=26730x and 25740x, respectively).	bind
6348	8	2485	7	10	NULL	0	NULL	V	CellComponent		is					Vacuole	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_febslett_405_2_200_s_113	9089291	(A) A single  P. aeruginosa bacterium bound to the plasma membrane of a CFTE cell (magnification=14800x); (B) a single bacterium bound to the plasma membrane (PM) of a CFTE cell and encircled by microvilli (magnification=23040x); (C) two bacteria entrapped inside a CFTE cell within a vacuole (V) (magnification=6320x); (D) a single bacterium in contact with a mitochondrion inside a CFTE cell (magnification=6122x); (E,F) bacteria penetrating HTE cells (normal cells) forming deep invaginations (magnifications=26730x and 25740x, respectively).	bind
5598	1	2486	6	10	NULL	0	NULL	HRP-2	GP		bind					heme	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_9_8_881_s_98	12204687	(A) a strong inhibitor, compound  24, and (B) a weak inhibitor,  10, on heme binding by HRP-2 using the microtiterplate assay described under Experimental Procedures.	bind
5599	2	2486	6	10	NULL	0	NULL	compound 24	Chemical		inhibits		strongly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_9_8_881_s_98	12204687	(A) a strong inhibitor, compound  24, and (B) a weak inhibitor,  10, on heme binding by HRP-2 using the microtiterplate assay described under Experimental Procedures.	bind
5600	3	2486	6	10	NULL	0	NULL	compound 10	Chemical		inhibits		weakly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_9_8_881_s_98	12204687	(A) a strong inhibitor, compound  24, and (B) a weak inhibitor,  10, on heme binding by HRP-2 using the microtiterplate assay described under Experimental Procedures.	bind
6349	1	2486	7	10	NULL	0	NULL	heme	Chemical		binds					HRP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_9_8_881_s_98	12204687	(A) a strong inhibitor, compound  24, and (B) a weak inhibitor,  10, on heme binding by HRP-2 using the microtiterplate assay described under Experimental Procedures.	bind
6350	2	2486	7	10	NULL	0	NULL	compound 24	Chemical		inhibit		strongly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_9_8_881_s_98	12204687	(A) a strong inhibitor, compound  24, and (B) a weak inhibitor,  10, on heme binding by HRP-2 using the microtiterplate assay described under Experimental Procedures.	bind
6351	3	2486	7	10	NULL	0	NULL	compound 10	Chemical		inhibit		weakly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_9_8_881_s_98	12204687	(A) a strong inhibitor, compound  24, and (B) a weak inhibitor,  10, on heme binding by HRP-2 using the microtiterplate assay described under Experimental Procedures.	bind
5617	1	2487	6	10	NULL	0	NULL	CREB	GP		bind			DNA binding domain 		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_967_s_155	9447994	(A) A-CREB, but not A-VBP or A-Fos, inhibits the DNA binding activity of the DNA binding domain of CREB.	bind
5618	2	2487	6	10	NULL	0	NULL	A-CREB	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_967_s_155	9447994	(A) A-CREB, but not A-VBP or A-Fos, inhibits the DNA binding activity of the DNA binding domain of CREB.	bind
5619	3	2487	6	10	NULL	0	NULL	A-VBP	GP		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_967_s_155	9447994	(A) A-CREB, but not A-VBP or A-Fos, inhibits the DNA binding activity of the DNA binding domain of CREB.	bind
5622	4	2487	6	10	NULL	0	NULL	A-Fos	GP		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_967_s_155	9447994	(A) A-CREB, but not A-VBP or A-Fos, inhibits the DNA binding activity of the DNA binding domain of CREB.	bind
5624	5	2487	6	10	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_967_s_155	9447994	(A) A-CREB, but not A-VBP or A-Fos, inhibits the DNA binding activity of the DNA binding domain of CREB.	bind
6352	1	2487	7	10	NULL	0	NULL	CREB	GP		binds			DNA binding domain		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_967_s_155	9447994	(A) A-CREB, but not A-VBP or A-Fos, inhibits the DNA binding activity of the DNA binding domain of CREB.	bind
6353	2	2487	7	10	NULL	0	NULL	A-CREB	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_967_s_155	9447994	(A) A-CREB, but not A-VBP or A-Fos, inhibits the DNA binding activity of the DNA binding domain of CREB.	bind
6354	3	2487	7	10	NULL	0	NULL	A-VBP	GP		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_967_s_155	9447994	(A) A-CREB, but not A-VBP or A-Fos, inhibits the DNA binding activity of the DNA binding domain of CREB.	bind
6355	4	2487	7	10	NULL	0	NULL	A-Fos	GP		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_967_s_155	9447994	(A) A-CREB, but not A-VBP or A-Fos, inhibits the DNA binding activity of the DNA binding domain of CREB.	bind
61116	5	2487	7	10	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_2_967_s_155	9447994	(A) A-CREB, but not A-VBP or A-Fos, inhibits the DNA binding activity of the DNA binding domain of CREB.	bind
5628	1	2488	6	10	NULL	0	NULL	A190	GP		bind		stably			Net1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_1_45_s_126	11511359	(A) A190 but not Nop1 binds stably to Net1.	bind
5629	2	2488	6	10	NULL	0	NULL	Nop1	GP		does not bind					Net1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_1_45_s_126	11511359	(A) A190 but not Nop1 binds stably to Net1.	bind
6356	1	2488	7	10	NULL	0	NULL	A190	GP		binds 		stably			Net1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_1_45_s_126	11511359	(A) A190 but not Nop1 binds stably to Net1.	bind
6357	2	2488	7	10	NULL	0	NULL	Nop1	GP		does not bind					Net1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_1_45_s_126	11511359	(A) A190 but not Nop1 binds stably to Net1.	bind
5633	1	2490	6	10	NULL	0	NULL	GTP	Chemical		bind					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_7_386_s_50	9545198	(a) Accumulation of the GTP-bound form of Ras (Ras-GTP) as a function of time.	bind
6361	1	2490	7	10	NULL	0	NULL	GTP	Chemical		binds					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_7_386_s_50	9545198	(a) Accumulation of the GTP-bound form of Ras (Ras-GTP) as a function of time.	bind
5634	1	2491	6	10	NULL	0	NULL	CBP	GP		acetylates					GCMa 	GP		TAD		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8401_s_332	16166624	(A) Acetylation of GCMa TAD by CBP increases  its transcriptional activity and protein stability.	bind
5635	2	2491	6	10	NULL	0	NULL	statement 1	Process		increases					GCMa	GP	transcriptional activity of	TAD		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8401_s_332	16166624	(A) Acetylation of GCMa TAD by CBP increases  its transcriptional activity and protein stability.	bind
5636	3	2491	6	10	NULL	0	NULL	statement 1	Process		increases					GCMa	GP	protein stability of	TAD		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8401_s_332	16166624	(A) Acetylation of GCMa TAD by CBP increases  its transcriptional activity and protein stability.	bind
6362	1	2491	7	10	NULL	0	NULL	CBP	GP		acetylates					GCMa 	GP		TAD		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8401_s_332	16166624	(A) Acetylation of GCMa TAD by CBP increases  its transcriptional activity and protein stability.	bind
6363	2	2491	7	10	NULL	0	NULL	statement 1	Process		increases					GCMa	GP	transcriptional activity of	TAD		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8401_s_332	16166624	(A) Acetylation of GCMa TAD by CBP increases  its transcriptional activity and protein stability.	bind
6364	3	2491	7	10	NULL	0	NULL	statement 1	Process		increases					GCMa	GP	protein stability of	TAD		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8401_s_332	16166624	(A) Acetylation of GCMa TAD by CBP increases  its transcriptional activity and protein stability.	bind
5637	1	2493	6	10	NULL	0	NULL	ARF1	GP	activated	bind		selectively			SNARE	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_34	15657398	(A) Activated ARF1 binds selectively to SNARE cargo proteins.	bind
46325	2	2493	6	10	NULL	0	NULL	SNARE	GP		is a type of					cargo proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_34	15657398	(A) Activated ARF1 binds selectively to SNARE cargo proteins.	bind
6365	1	2493	7	10	NULL	0	NULL	ARF1	GP	activated	binds to		selectively			SNARE	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_34	15657398	(A) Activated ARF1 binds selectively to SNARE cargo proteins.	bind
46326	2	2493	7	10	NULL	0	NULL	SNARE	GP		is a type of					cargo proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_34	15657398	(A) Activated ARF1 binds selectively to SNARE cargo proteins.	bind
5729	1	2494	6	10	NULL	0	NULL	Ly49H NK cell receptor	GP		bind					MCMV m157 gene product	GP				NULL	C57BL/6 mouse strain	NULL	NULL	NULL	NULL	gw70_microbesinfect_5_13_1263_s_119	14623023	(A) Activation of NK cells in C57BL/6 mouse strain is a consequence of binding  of the Ly49H NK cell receptor to the MCMV  m157 gene product, leading to efficacious virus control in vivo, which can be compromised  by depletion of NK cells.	bind
5730	2	2494	6	10	NULL	0	NULL	NK cells	Cell	activation of	is a consequence of 					statement 1	Process				NULL	C57BL/6 mouse strain	NULL	NULL	NULL	NULL	gw70_microbesinfect_5_13_1263_s_119	14623023	(A) Activation of NK cells in C57BL/6 mouse strain is a consequence of binding  of the Ly49H NK cell receptor to the MCMV  m157 gene product, leading to efficacious virus control in vivo, which can be compromised  by depletion of NK cells.	bind
5731	3	2494	6	10	NULL	0	NULL	statement 1	Process		leads to					virus control	Process	efficacious			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_microbesinfect_5_13_1263_s_119	14623023	(A) Activation of NK cells in C57BL/6 mouse strain is a consequence of binding  of the Ly49H NK cell receptor to the MCMV  m157 gene product, leading to efficacious virus control in vivo, which can be compromised  by depletion of NK cells.	bind
5732	4	2494	6	10	NULL	0	NULL	NK cells	Cell	depletion of 	compromises					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_microbesinfect_5_13_1263_s_119	14623023	(A) Activation of NK cells in C57BL/6 mouse strain is a consequence of binding  of the Ly49H NK cell receptor to the MCMV  m157 gene product, leading to efficacious virus control in vivo, which can be compromised  by depletion of NK cells.	bind
6366	1	2494	7	10	NULL	0	NULL	Ly49H NK cell receptor	GP		binds to					MCMV m157 gene product	GP				NULL	C57BL/6 mouse strain	NULL	NULL	NULL	NULL	gw70_microbesinfect_5_13_1263_s_119	14623023	(A) Activation of NK cells in C57BL/6 mouse strain is a consequence of binding  of the Ly49H NK cell receptor to the MCMV  m157 gene product, leading to efficacious virus control in vivo, which can be compromised  by depletion of NK cells.	bind
6367	2	2494	7	10	NULL	0	NULL	NK cells 	Cell	 activation of	is a consequence of					statement 1	Process				NULL	C57BL/6 mouse strain	NULL	NULL	NULL	NULL	gw70_microbesinfect_5_13_1263_s_119	14623023	(A) Activation of NK cells in C57BL/6 mouse strain is a consequence of binding  of the Ly49H NK cell receptor to the MCMV  m157 gene product, leading to efficacious virus control in vivo, which can be compromised  by depletion of NK cells.	bind
6368	3	2494	7	10	NULL	0	NULL	statement 1	Process		leads to					 virus control	Process	efficacious			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_microbesinfect_5_13_1263_s_119	14623023	(A) Activation of NK cells in C57BL/6 mouse strain is a consequence of binding  of the Ly49H NK cell receptor to the MCMV  m157 gene product, leading to efficacious virus control in vivo, which can be compromised  by depletion of NK cells.	bind
6369	4	2494	7	10	NULL	0	NULL	statement 1	Cell		is compromised by					NK cells	Cell	depletion of			NULL		NULL	NULL	NULL	NULL	gw70_microbesinfect_5_13_1263_s_119	14623023	(A) Activation of NK cells in C57BL/6 mouse strain is a consequence of binding  of the Ly49H NK cell receptor to the MCMV  m157 gene product, leading to efficacious virus control in vivo, which can be compromised  by depletion of NK cells.	bind
5883	1	2495	6	10	NULL	0	NULL	tTA	GP		bind									TRE	NULL	293 Tet-Off cells	NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1393_s_127	11359930	(A) Activation of the transactivator tTA, a fusion protein consisting of the tet-repressor and the VP16 activation domain, by removal of doxycycline (Dox) from the culture medium results in the binding of tTA to the tet-responsive element TRE and transcription of Flag-tagged HD exon 1 fragments with 20, 51, and 83 CAG repeats in 293 Tet-Off cells.	bind
5884	2	2495	6	10	NULL	0	NULL	TRE	NucleicAcid		is					tet-responsive element	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1393_s_127	11359930	(A) Activation of the transactivator tTA, a fusion protein consisting of the tet-repressor and the VP16 activation domain, by removal of doxycycline (Dox) from the culture medium results in the binding of tTA to the tet-responsive element TRE and transcription of Flag-tagged HD exon 1 fragments with 20, 51, and 83 CAG repeats in 293 Tet-Off cells.	bind
6204	3	2495	6	10	NULL	0	NULL	tTA	GP		consists of					tet repressor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1393_s_127	11359930	(A) Activation of the transactivator tTA, a fusion protein consisting of the tet-repressor and the VP16 activation domain, by removal of doxycycline (Dox) from the culture medium results in the binding of tTA to the tet-responsive element TRE and transcription of Flag-tagged HD exon 1 fragments with 20, 51, and 83 CAG repeats in 293 Tet-Off cells.	bind
6205	4	2495	6	10	NULL	0	NULL	tTA 	GP		is a type of					transactivator	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1393_s_127	11359930	(A) Activation of the transactivator tTA, a fusion protein consisting of the tet-repressor and the VP16 activation domain, by removal of doxycycline (Dox) from the culture medium results in the binding of tTA to the tet-responsive element TRE and transcription of Flag-tagged HD exon 1 fragments with 20, 51, and 83 CAG repeats in 293 Tet-Off cells.	bind
6206	5	2495	6	10	NULL	0	NULL	tTA	GP		consists of								VP16 activation domain		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1393_s_127	11359930	(A) Activation of the transactivator tTA, a fusion protein consisting of the tet-repressor and the VP16 activation domain, by removal of doxycycline (Dox) from the culture medium results in the binding of tTA to the tet-responsive element TRE and transcription of Flag-tagged HD exon 1 fragments with 20, 51, and 83 CAG repeats in 293 Tet-Off cells.	bind
6207	6	2495	6	10	NULL	0	NULL	doxycycline	Chemical		is removed from					culture medium	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1393_s_127	11359930	(A) Activation of the transactivator tTA, a fusion protein consisting of the tet-repressor and the VP16 activation domain, by removal of doxycycline (Dox) from the culture medium results in the binding of tTA to the tet-responsive element TRE and transcription of Flag-tagged HD exon 1 fragments with 20, 51, and 83 CAG repeats in 293 Tet-Off cells.	bind
6208	7	2495	6	10	NULL	0	NULL	statement 6	Process		results in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1393_s_127	11359930	(A) Activation of the transactivator tTA, a fusion protein consisting of the tet-repressor and the VP16 activation domain, by removal of doxycycline (Dox) from the culture medium results in the binding of tTA to the tet-responsive element TRE and transcription of Flag-tagged HD exon 1 fragments with 20, 51, and 83 CAG repeats in 293 Tet-Off cells.	bind
6209	8	2495	6	10	NULL	0	NULL	statement 6	Process		results in					HD exon1	GP	transcription of		CAG repeats	NULL	293 Tet-Off cells	NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1393_s_127	11359930	(A) Activation of the transactivator tTA, a fusion protein consisting of the tet-repressor and the VP16 activation domain, by removal of doxycycline (Dox) from the culture medium results in the binding of tTA to the tet-responsive element TRE and transcription of Flag-tagged HD exon 1 fragments with 20, 51, and 83 CAG repeats in 293 Tet-Off cells.	bind
46327	9	2495	6	10	NULL	0	NULL	tTA	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1393_s_127	11359930	(A) Activation of the transactivator tTA, a fusion protein consisting of the tet-repressor and the VP16 activation domain, by removal of doxycycline (Dox) from the culture medium results in the binding of tTA to the tet-responsive element TRE and transcription of Flag-tagged HD exon 1 fragments with 20, 51, and 83 CAG repeats in 293 Tet-Off cells.	bind
6370	1	2495	7	10	NULL	0	NULL	tTA	GP		binds to									TRE	NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1393_s_127	11359930	(A) Activation of the transactivator tTA, a fusion protein consisting of the tet-repressor and the VP16 activation domain, by removal of doxycycline (Dox) from the culture medium results in the binding of tTA to the tet-responsive element TRE and transcription of Flag-tagged HD exon 1 fragments with 20, 51, and 83 CAG repeats in 293 Tet-Off cells.	bind
6371	2	2495	7	10	NULL	0	NULL	 tTA	GP		consist of					tet-repressor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1393_s_127	11359930	(A) Activation of the transactivator tTA, a fusion protein consisting of the tet-repressor and the VP16 activation domain, by removal of doxycycline (Dox) from the culture medium results in the binding of tTA to the tet-responsive element TRE and transcription of Flag-tagged HD exon 1 fragments with 20, 51, and 83 CAG repeats in 293 Tet-Off cells.	bind
6372	3	2495	7	10	NULL	0	NULL	tTA	GP		consist of								VP16 activation domain		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1393_s_127	11359930	(A) Activation of the transactivator tTA, a fusion protein consisting of the tet-repressor and the VP16 activation domain, by removal of doxycycline (Dox) from the culture medium results in the binding of tTA to the tet-responsive element TRE and transcription of Flag-tagged HD exon 1 fragments with 20, 51, and 83 CAG repeats in 293 Tet-Off cells.	bind
6373	4	2495	7	10	NULL	0	NULL	tTA	GP		is a type of					transactivator	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1393_s_127	11359930	(A) Activation of the transactivator tTA, a fusion protein consisting of the tet-repressor and the VP16 activation domain, by removal of doxycycline (Dox) from the culture medium results in the binding of tTA to the tet-responsive element TRE and transcription of Flag-tagged HD exon 1 fragments with 20, 51, and 83 CAG repeats in 293 Tet-Off cells.	bind
6374	5	2495	7	10	NULL	0	NULL	tTA	GP	activation of	results in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1393_s_127	11359930	(A) Activation of the transactivator tTA, a fusion protein consisting of the tet-repressor and the VP16 activation domain, by removal of doxycycline (Dox) from the culture medium results in the binding of tTA to the tet-responsive element TRE and transcription of Flag-tagged HD exon 1 fragments with 20, 51, and 83 CAG repeats in 293 Tet-Off cells.	bind
6375	6	2495	7	10	NULL	0	NULL	doxycycline	Chemical	 	removed from					culture medium	Chemical			CAG repeats	NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1393_s_127	11359930	(A) Activation of the transactivator tTA, a fusion protein consisting of the tet-repressor and the VP16 activation domain, by removal of doxycycline (Dox) from the culture medium results in the binding of tTA to the tet-responsive element TRE and transcription of Flag-tagged HD exon 1 fragments with 20, 51, and 83 CAG repeats in 293 Tet-Off cells.	bind
6376	7	2495	7	10	NULL	0	NULL	tTA	GP	activation of	results in					HD exon1	GP	transcription of		CAG repeats \t	NULL	293 Tet-Off cells	NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1393_s_127	11359930	(A) Activation of the transactivator tTA, a fusion protein consisting of the tet-repressor and the VP16 activation domain, by removal of doxycycline (Dox) from the culture medium results in the binding of tTA to the tet-responsive element TRE and transcription of Flag-tagged HD exon 1 fragments with 20, 51, and 83 CAG repeats in 293 Tet-Off cells.	bind
6377	8	2495	7	10	NULL	0	NULL	statement 1	Process		occurs after					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1393_s_127	11359930	(A) Activation of the transactivator tTA, a fusion protein consisting of the tet-repressor and the VP16 activation domain, by removal of doxycycline (Dox) from the culture medium results in the binding of tTA to the tet-responsive element TRE and transcription of Flag-tagged HD exon 1 fragments with 20, 51, and 83 CAG repeats in 293 Tet-Off cells.	bind
6379	10	2495	7	10	NULL	0	NULL	Dox	Chemical		is					doxycycline	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1393_s_127	11359930	(A) Activation of the transactivator tTA, a fusion protein consisting of the tet-repressor and the VP16 activation domain, by removal of doxycycline (Dox) from the culture medium results in the binding of tTA to the tet-responsive element TRE and transcription of Flag-tagged HD exon 1 fragments with 20, 51, and 83 CAG repeats in 293 Tet-Off cells.	bind
46328	9	2495	7	10	NULL	0	NULL	TRE	NucleicAcid		is					tet-responsive element	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1393_s_127	11359930	(A) Activation of the transactivator tTA, a fusion protein consisting of the tet-repressor and the VP16 activation domain, by removal of doxycycline (Dox) from the culture medium results in the binding of tTA to the tet-responsive element TRE and transcription of Flag-tagged HD exon 1 fragments with 20, 51, and 83 CAG repeats in 293 Tet-Off cells.	bind
5900	1	2497	6	10	NULL	0	NULL	uPA	GP	active	bind					uPAR	GP				NULL	PM	NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1467_s_296	11359936	(A) Active uPA binds to uPAR on the PM.	bind
6380	1	2497	7	10	NULL	0	NULL	uPA	GP	active	binds to					uPAR	GP				NULL	PM	NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1467_s_296	11359936	(A) Active uPA binds to uPAR on the PM.	bind
5901	1	2498	6	10	NULL	0	NULL	Activin	GP		bind					ActRIIB receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_93_4_557_s_198	9604931	(A) Activin  binds to ActRIIB receptors in a concentration-dependent manner.	bind
5902	2	2498	6	10	NULL	0	NULL	statement 1	GP		is dependent on					concentration	QuantityOrMeasure				NULL		NULL	NULL	NULL	NULL	gw60_cell_93_4_557_s_198	9604931	(A) Activin  binds to ActRIIB receptors in a concentration-dependent manner.	bind
6381	1	2498	7	10	NULL	0	NULL	Activin	GP		binds to					ActRIIB receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_93_4_557_s_198	9604931	(A) Activin  binds to ActRIIB receptors in a concentration-dependent manner.	bind
6382	2	2498	7	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				concentration	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_93_4_557_s_198	9604931	(A) Activin  binds to ActRIIB receptors in a concentration-dependent manner.	bind
5903	1	2499	6	10	NULL	0	NULL	Ad12 E1B protein	GP		bind		directly			PCAF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_294	10891493	(A) Ad12 E1B 55-kDa protein binds directly to PCAF.	bind
6383	1	2499	7	10	NULL	0	NULL	Ad12 E1B protein	GP		binds		directly			PCAF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_294	10891493	(A) Ad12 E1B 55-kDa protein binds directly to PCAF.	bind
5904	1	2500	6	10	NULL	0	NULL	CPSF	GP		bind					class I RNA	NucleicAcid			RNA element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_52_33654_s_197	8969235	(A) addition data, the binding of CPSF to the class I RNA containing both RNA elements was greater than to the RNAs containing either element alone (Fig.  3 C, 8.1,  lane 3).	bind
6384	1	2500	7	10	NULL	0	NULL	CPSF	GP		binds					class I RNA	NucleicAcid			RNA element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_52_33654_s_197	8969235	(A) addition data, the binding of CPSF to the class I RNA containing both RNA elements was greater than to the RNAs containing either element alone (Fig.  3 C, 8.1,  lane 3).	bind
5905	1	2502	6	10	NULL	0	NULL	V-ATPase	GP		bind			V1 domain on E subunit		H6.1 MAb	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_2_575_s_227	15632060	(a) After cell  stimulation, V-ATPase was immunoprecipitated from the lysates with H6.1 MAb, which  binds the V1 domain on its E subunit.	bind
5908	2	2502	6	10	NULL	0	NULL	statement 1	Process		occurs after					cell stimulation	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_2_575_s_227	15632060	(a) After cell  stimulation, V-ATPase was immunoprecipitated from the lysates with H6.1 MAb, which  binds the V1 domain on its E subunit.	bind
6386	1	2502	7	10	NULL	0	NULL	V-ATPase	GP		binds					H6.1 MAb	GP		V1 domain E subunit		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_2_575_s_227	15632060	(a) After cell  stimulation, V-ATPase was immunoprecipitated from the lysates with H6.1 MAb, which  binds the V1 domain on its E subunit.	bind
6387	2	2502	7	10	NULL	0	NULL	statement 1	Process		occurs after					cell stimulation	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_2_575_s_227	15632060	(a) After cell  stimulation, V-ATPase was immunoprecipitated from the lysates with H6.1 MAb, which  binds the V1 domain on its E subunit.	bind
5909	1	2503	6	10	NULL	0	NULL	Akt	GP		phosphorylate					p300	GP		Ser-1834		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6592_s_272	16024795	(A) Akt phosphorylation of p300 at Ser-1834 binds p/CAF in vitro.	bind
5910	2	2503	6	10	NULL	0	NULL	statement 1	Process		bind					p/CAF	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6592_s_272	16024795	(A) Akt phosphorylation of p300 at Ser-1834 binds p/CAF in vitro.	bind
6388	2	2503	7	10	NULL	0	NULL	statement 1	Process		binds					p/CAF	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6592_s_272	16024795	(A) Akt phosphorylation of p300 at Ser-1834 binds p/CAF in vitro.	bind
6389	1	2503	7	10	NULL	0	NULL	Akt	GP		phosphorylates					p300	GP		Ser-1834		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6592_s_272	16024795	(A) Akt phosphorylation of p300 at Ser-1834 binds p/CAF in vitro.	bind
5911	1	2505	6	10	NULL	0	NULL	transcription factor	GP	drosophila	bind			eh-1 like sequences		Gro	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_24_10711_s_80	16314497	(A) Alignment of eh1-like sequences found in  Drosophila transcription factors that bind Gro in vitro (C).	bind
6391	1	2505	7	10	NULL	0	NULL	transcription factors	GP	Drosophila	binds			eh1-like sequences		Gro	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_24_10711_s_80	16314497	(A) Alignment of eh1-like sequences found in  Drosophila transcription factors that bind Gro in vitro (C).	bind
5912	2	2507	6	10	NULL	0	NULL	statement 1	Process		bind					MAb	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_10_5529_s_82	16988228	(A) Alignment of the  P. yoelii YM AMA1 protein sequence with the deduced 7-mer sequences from phage clones that  bound to the MAb.	bind
46330	1	2507	6	10	NULL	0	NULL	phage clones			contains					7-mer sequences	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_10_5529_s_82	16988228	(A) Alignment of the  P. yoelii YM AMA1 protein sequence with the deduced 7-mer sequences from phage clones that  bound to the MAb.	bind
6464	2	2507	7	10	NULL	0	NULL	statement 1	Process		bind					MAb	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_10_5529_s_82	16988228	(A) Alignment of the  P. yoelii YM AMA1 protein sequence with the deduced 7-mer sequences from phage clones that  bound to the MAb.	bind
46331	1	2507	7	10	NULL	0	NULL	phage clones			contains					7-mer sequences	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_10_5529_s_82	16988228	(A) Alignment of the  P. yoelii YM AMA1 protein sequence with the deduced 7-mer sequences from phage clones that  bound to the MAb.	bind
5913	1	2511	6	10	NULL	0	NULL	Met4-myc	GP	endogenous	bind					MET25	GP	biotinylated		promoter	NULL	extracts prepared from cells 	NULL	NULL	NULL	NULL	gw60_cell_102_3_303_s_239	10975521	(A) All forms  of Met4 bind to the  MET25 promoter: Extracts prepared from cells expressing endogenous  Met4-myc and Cbf1-HA (PY752) were incubated with biotinylated  MET25 promotor fragments or a  biotinylated control DNA.	bind
5914	2	2511	6	10	NULL	0	NULL	Cbf1-HA	GP	endogenous	bind			PY752		MET25	GP	biotinylated		promoter	NULL	extracts prepared from cells 	NULL	NULL	NULL	NULL	gw60_cell_102_3_303_s_239	10975521	(A) All forms  of Met4 bind to the  MET25 promoter: Extracts prepared from cells expressing endogenous  Met4-myc and Cbf1-HA (PY752) were incubated with biotinylated  MET25 promotor fragments or a  biotinylated control DNA.	bind
6465	1	2511	7	10	NULL	0	NULL	Met4-myc	GP	endogenous	binds					MET25	GP	biotinylated		promoter	NULL	extracts prepared from cells 	NULL	NULL	NULL	NULL	gw60_cell_102_3_303_s_239	10975521	(A) All forms  of Met4 bind to the  MET25 promoter: Extracts prepared from cells expressing endogenous  Met4-myc and Cbf1-HA (PY752) were incubated with biotinylated  MET25 promotor fragments or a  biotinylated control DNA.	bind
46332	2	2511	7	10	NULL	0	NULL	Cbf1-HA	GP	endogenous	bind			PY752		MET25	GP	biotinylated		promoter	NULL	extracts prepared from cells 	NULL	NULL	NULL	NULL	gw60_cell_102_3_303_s_239	10975521	(A) All forms  of Met4 bind to the  MET25 promoter: Extracts prepared from cells expressing endogenous  Met4-myc and Cbf1-HA (PY752) were incubated with biotinylated  MET25 promotor fragments or a  biotinylated control DNA.	bind
5915	1	2514	6	10	NULL	0	NULL	CD14-IgG	GP		bind					cortical neurons	Cell	primary			NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_50_2_229_s_147	16289250	(A) Amounts of a CD14-IgG chimera that  bound to primary cortical neurons pre-treated with 10 ng/ml prostaglandins as shown.	bind
5916	2	2514	6	10	NULL	0	NULL	cortical neurons	Cell	primary	pre-treated with					prostaglandins	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_50_2_229_s_147	16289250	(A) Amounts of a CD14-IgG chimera that  bound to primary cortical neurons pre-treated with 10 ng/ml prostaglandins as shown.	bind
46333	3	2514	6	10	NULL	0	NULL	CD14-IgG	GP		is a type of					chimera	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_50_2_229_s_147	16289250	(A) Amounts of a CD14-IgG chimera that  bound to primary cortical neurons pre-treated with 10 ng/ml prostaglandins as shown.	bind
6466	1	2514	7	10	NULL	0	NULL	CD14-IgG	GP		binds to					cortical neurons	Cell	primary			NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_50_2_229_s_147	16289250	(A) Amounts of a CD14-IgG chimera that  bound to primary cortical neurons pre-treated with 10 ng/ml prostaglandins as shown.	bind
6467	2	2514	7	10	NULL	0	NULL	cortical neurons	Cell	primary	is pretreated with					prostaglandins	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_50_2_229_s_147	16289250	(A) Amounts of a CD14-IgG chimera that  bound to primary cortical neurons pre-treated with 10 ng/ml prostaglandins as shown.	bind
46335	3	2514	7	10	NULL	0	NULL	CD14-IgG	GP		is a type of					chimera	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_50_2_229_s_147	16289250	(A) Amounts of a CD14-IgG chimera that  bound to primary cortical neurons pre-treated with 10 ng/ml prostaglandins as shown.	bind
5917	1	2515	6	10	NULL	0	NULL	xpt RNAs	NucleicAcid	in vitro-transcribed	bind					guanine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_5_577_s_148	12787499	(A) An equilibrium dialysis strategy was used to confirm that in vitro-transcribed 93  xpt RNAs bind to guanine and can discriminate against various analogs.	bind
6468	1	2515	7	10	NULL	0	NULL	xpt RNA	NucleicAcid	in vitro-transcribed 	binds					guanine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_5_577_s_148	12787499	(A) An equilibrium dialysis strategy was used to confirm that in vitro-transcribed 93  xpt RNAs bind to guanine and can discriminate against various analogs.	bind
5919	1	2516	6	10	NULL	0	NULL	MAP2	GP		bind					microtubule	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_305_1_72_s_60	12732198	(A) An SDS-PAGE showing the  binding of MAP2 to microtubules at pH 6.9.	bind
6469	1	2516	7	10	NULL	0	NULL	MAP2	GP		binds					microtubules	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_305_1_72_s_60	12732198	(A) An SDS-PAGE showing the  binding of MAP2 to microtubules at pH 6.9.	bind
5921	1	2518	6	10	NULL	0	NULL	p150-Spir	GP		bind			four WH2 domains		actin monomer	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_6_345_s_22	10744979	(a) An unique array of structural motifs in p150-Spir: an acidic region, four WH2 domains, which bind monomeric actin, a modified FYVE Zn-Finger structure and a JNK-binding domain at the carboxyl terminus containing a DEJL motif.	bind
6470	1	2518	7	10	NULL	0	NULL	p150-Spir	GP		binds			four WH2 domains		actin monomer	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_6_345_s_22	10744979	(a) An unique array of structural motifs in p150-Spir: an acidic region, four WH2 domains, which bind monomeric actin, a modified FYVE Zn-Finger structure and a JNK-binding domain at the carboxyl terminus containing a DEJL motif.	bind
5925	1	2519	6	10	NULL	0	NULL	TAF6 protein derivatives	GP	purified	bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_206_s_132	15601843	(A) Analysis  of the DNA binding of purified TAF6 and TAF9 protein derivatives either alone or  as a complex by EMSA.	bind
5926	2	2519	6	10	NULL	0	NULL	TAF9 protein derivatives	GP	purified	bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_206_s_132	15601843	(A) Analysis  of the DNA binding of purified TAF6 and TAF9 protein derivatives either alone or  as a complex by EMSA.	bind
5927	3	2519	6	10	NULL	0	NULL	TAF6 protein derivatives	GP	purified	forms a complex with					TAF9 protein derivatives	GP	purified			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_206_s_132	15601843	(A) Analysis  of the DNA binding of purified TAF6 and TAF9 protein derivatives either alone or  as a complex by EMSA.	bind
7859	4	2519	6	10	NULL	0	NULL	statement 3	Process		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_206_s_132	15601843	(A) Analysis  of the DNA binding of purified TAF6 and TAF9 protein derivatives either alone or  as a complex by EMSA.	bind
6487	1	2519	7	10	NULL	0	NULL	TAF6 protein derivatives	GP	purified	bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_206_s_132	15601843	(A) Analysis  of the DNA binding of purified TAF6 and TAF9 protein derivatives either alone or  as a complex by EMSA.	bind
6490	2	2519	7	10	NULL	0	NULL	TAF9 protein derivatives	GP	purified	bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_206_s_132	15601843	(A) Analysis  of the DNA binding of purified TAF6 and TAF9 protein derivatives either alone or  as a complex by EMSA.	bind
6491	3	2519	7	10	NULL	0	NULL	TAF6 protein derivatives	GP	purified	forms a complex with					TAF9 protein derivatives	GP	purified			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_206_s_132	15601843	(A) Analysis  of the DNA binding of purified TAF6 and TAF9 protein derivatives either alone or  as a complex by EMSA.	bind
6496	4	2519	7	10	NULL	0	NULL	statement 3	Process		binds					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_206_s_132	15601843	(A) Analysis  of the DNA binding of purified TAF6 and TAF9 protein derivatives either alone or  as a complex by EMSA.	bind
5933	2	2520	6	10	NULL	0	NULL	MMP-8	GP	latent	bind					collagen	GP				NULL	GCF	NULL	NULL	NULL	NULL	gw60_infectimmun_67_5_2319_s_228	10225890	(A) Analysis of active and latent forms of MMP-8 from GCF that bind to collagen.	bind
5934	1	2520	6	10	NULL	0	NULL	MMP-8	GP	active	bind					collagen	GP				NULL	GCF	NULL	NULL	NULL	NULL	gw60_infectimmun_67_5_2319_s_228	10225890	(A) Analysis of active and latent forms of MMP-8 from GCF that bind to collagen.	bind
6497	1	2520	7	10	NULL	0	NULL	MMP-8	GP	active	binds					collagen	GP				NULL	GCF	NULL	NULL	NULL	NULL	gw60_infectimmun_67_5_2319_s_228	10225890	(A) Analysis of active and latent forms of MMP-8 from GCF that bind to collagen.	bind
6498	2	2520	7	10	NULL	0	NULL	MMP-8	GP	latent	binds					collagen	GP				NULL	GCF	NULL	NULL	NULL	NULL	gw60_infectimmun_67_5_2319_s_228	10225890	(A) Analysis of active and latent forms of MMP-8 from GCF that bind to collagen.	bind
5936	1	2521	6	10	NULL	0	NULL	AlgZ	GP		bind					algD	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_24_7297_s_38	14645293	(A) Analysis of AlgZ binding to  algD by electrophoretic mobility shift assay.	bind
6503	1	2521	7	10	NULL	0	NULL	AlgZ	GP		binds	GP				algD	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_24_7297_s_38	14645293	(A) Analysis of AlgZ binding to  algD by electrophoretic mobility shift assay.	bind
5937	1	2523	6	10	NULL	0	NULL	P. multocida 232	Organism		pre incubated with					anti-PmOmpA	GP	mouse			NULL		NULL	NULL	NULL	NULL	gw70_microbpathogenesis_35_4_147_s_154	12946327	(A) and (B) Binding of Fn to  P. multocida 232 pre-incubated with mouse anti-PmOmpA (lanes 2 and 4), in the presence or absence  of Hp (lanes 1, and 3, respectively).	bind
5938	2	2523	6	10	NULL	0	NULL	Fn	GP		bind					statement 1	Organism				NULL		NULL	NULL	NULL	NULL	gw70_microbpathogenesis_35_4_147_s_154	12946327	(A) and (B) Binding of Fn to  P. multocida 232 pre-incubated with mouse anti-PmOmpA (lanes 2 and 4), in the presence or absence  of Hp (lanes 1, and 3, respectively).	bind
6505	1	2523	7	10	NULL	0	NULL	Fn	GP		binds					 P. multocida 232	Organism				NULL		NULL	NULL	NULL	NULL	gw70_microbpathogenesis_35_4_147_s_154	12946327	(A) and (B) Binding of Fn to  P. multocida 232 pre-incubated with mouse anti-PmOmpA (lanes 2 and 4), in the presence or absence  of Hp (lanes 1, and 3, respectively).	bind
6507	2	2523	7	10	NULL	0	NULL	 P. multocida 232	Organism		is pre-incubated with					anti-PmOmpA	GP	mouse			NULL		NULL	NULL	NULL	NULL	gw70_microbpathogenesis_35_4_147_s_154	12946327	(A) and (B) Binding of Fn to  P. multocida 232 pre-incubated with mouse anti-PmOmpA (lanes 2 and 4), in the presence or absence  of Hp (lanes 1, and 3, respectively).	bind
5939	1	2525	6	10	NULL	0	NULL	HOCl	Chemical		oxidizes					LDL	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1902_s_113	11742862	(A) and analysis of HOCl-oxidized LDL released and remaining bound to heparin-Sepharose (B and C).	bind
5940	2	2525	6	10	NULL	0	NULL	LDL	Chemical	unoxidized	bind					heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1902_s_113	11742862	(A) and analysis of HOCl-oxidized LDL released and remaining bound to heparin-Sepharose (B and C).	bind
6511	1	2525	7	10	NULL	0	NULL	LDL	Chemical		binds to					heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1902_s_113	11742862	(A) and analysis of HOCl-oxidized LDL released and remaining bound to heparin-Sepharose (B and C).	bind
6512	2	2525	7	10	NULL	0	NULL	HOCl	Chemical		oxidizes					LDL	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1902_s_113	11742862	(A) and analysis of HOCl-oxidized LDL released and remaining bound to heparin-Sepharose (B and C).	bind
5941	1	2528	6	10	NULL	0	NULL	[15N, 2]cTnC	GP	Ca2+ saturated	bind					cTnI	GP		1-80		NULL		NULL	NULL	NULL	NULL	gw60_febslett_469_2_168_s_143	10713265	(A) and Ca2+ saturated [15N, 2]cTnC bound to cTnI(1-80) and cTnIp at a ratio of 1:1:1.4 (B) and Ca2+ saturated [15N, 2]cTnC bound to cTnI(1-80) and cTnIp at a stoichiometry of 1:1:2.6 (C).	bind
5942	2	2528	6	10	NULL	0	NULL	[15N, 2]cTnC	GP	Ca2+ saturated	bind					cTnIp	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_469_2_168_s_143	10713265	(A) and Ca2+ saturated [15N, 2]cTnC bound to cTnI(1-80) and cTnIp at a ratio of 1:1:1.4 (B) and Ca2+ saturated [15N, 2]cTnC bound to cTnI(1-80) and cTnIp at a stoichiometry of 1:1:2.6 (C).	bind
6519	1	2528	7	10	NULL	0	NULL	[15N, 2]cTnC	GP	Ca2+ saturated	binds					cTnI	GP		1-80		NULL		NULL	NULL	NULL	NULL	gw60_febslett_469_2_168_s_143	10713265	(A) and Ca2+ saturated [15N, 2]cTnC bound to cTnI(1-80) and cTnIp at a ratio of 1:1:1.4 (B) and Ca2+ saturated [15N, 2]cTnC bound to cTnI(1-80) and cTnIp at a stoichiometry of 1:1:2.6 (C).	bind
6520	2	2528	7	10	NULL	0	NULL	[15N, 2]cTnC	GP	Ca2+ saturated	bind					cTnIp	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_469_2_168_s_143	10713265	(A) and Ca2+ saturated [15N, 2]cTnC bound to cTnI(1-80) and cTnIp at a ratio of 1:1:1.4 (B) and Ca2+ saturated [15N, 2]cTnC bound to cTnI(1-80) and cTnIp at a stoichiometry of 1:1:2.6 (C).	bind
5943	1	2529	6	10	NULL	0	NULL	CDK2	GP		bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_6_1321_s_47	11430833	(A) and CDK2 (B) bound to ATP are shown.	bind
6521	1	2529	7	10	NULL	0	NULL	CDK2	GP		binds to					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_6_1321_s_47	11430833	(A) and CDK2 (B) bound to ATP are shown.	bind
5944	1	2530	6	10	NULL	0	NULL	Cyclin E	GP		bind					p107	GP	full length			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_291	9710622	(A) and cyclin E (B) bind delta10N and N385, albeit less efficiently than full-length p107, but do not bind the mutant delta10N-AAA.	bind
5945	2	2530	6	10	NULL	0	NULL	Cyclin E	GP		bind		less efficiently			p107	GP	mutant	delta10N		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_291	9710622	(A) and cyclin E (B) bind delta10N and N385, albeit less efficiently than full-length p107, but do not bind the mutant delta10N-AAA.	bind
5946	3	2530	6	10	NULL	0	NULL	Cyclin E	GP		bind		less efficiently			p107	GP	mutant	N385		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_291	9710622	(A) and cyclin E (B) bind delta10N and N385, albeit less efficiently than full-length p107, but do not bind the mutant delta10N-AAA.	bind
5947	4	2530	6	10	NULL	0	NULL	Cyclin E	GP		does not bind					p107	GP	mutant	delta10N-AAA		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_291	9710622	(A) and cyclin E (B) bind delta10N and N385, albeit less efficiently than full-length p107, but do not bind the mutant delta10N-AAA.	bind
6522	1	2530	7	10	NULL	0	NULL	cyclin E	GP		bind					p107	GP		delta10N		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_291	9710622	(A) and cyclin E (B) bind delta10N and N385, albeit less efficiently than full-length p107, but do not bind the mutant delta10N-AAA.	bind
6523	2	2530	7	10	NULL	0	NULL	cyclin E	GP		bind					p107	GP		N385		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_291	9710622	(A) and cyclin E (B) bind delta10N and N385, albeit less efficiently than full-length p107, but do not bind the mutant delta10N-AAA.	bind
6524	3	2530	7	10	NULL	0	NULL	cyclin E	GP		bind					p107	GP	full-length			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_291	9710622	(A) and cyclin E (B) bind delta10N and N385, albeit less efficiently than full-length p107, but do not bind the mutant delta10N-AAA.	bind
6525	4	2530	7	10	NULL	0	NULL	cyclin E	GP		does not bind					p107	GP	mutant	delta10N-AAA		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_291	9710622	(A) and cyclin E (B) bind delta10N and N385, albeit less efficiently than full-length p107, but do not bind the mutant delta10N-AAA.	bind
6526	5	2530	7	10	NULL	0	NULL	statement 1	GP		is less efficient than					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_291	9710622	(A) and cyclin E (B) bind delta10N and N385, albeit less efficiently than full-length p107, but do not bind the mutant delta10N-AAA.	bind
6527	6	2530	7	10	NULL	0	NULL	statement 2	GP		is less efficient than					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_291	9710622	(A) and cyclin E (B) bind delta10N and N385, albeit less efficiently than full-length p107, but do not bind the mutant delta10N-AAA.	bind
5948	1	2532	6	10	NULL	0	NULL	APPA	Chemical		bind					GABAB receptors	GP	native			NULL	rat cortical membranes	NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_307_1_322_s_165	12954816	(A) and dissociation (B) of [3]APPA binding to native GABAB receptors in rat cortical membranes.	bind
6528	1	2532	7	10	NULL	0	NULL	[3]APPA	Chemical		binds to					GABAB receptors	GP	native			NULL	rat cortical membranes	NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_307_1_322_s_165	12954816	(A) and dissociation (B) of [3]APPA binding to native GABAB receptors in rat cortical membranes.	bind
5949	1	2533	6	10	NULL	0	NULL	NahR	GP		bind					PsaI	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1725_2_247_s_210	15978733	(A) and dissociation (B) phases of NahR binding  to  Psal.	bind
6529	1	2533	7	10	NULL	0	NULL	NahR	GP		binds					Psal	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1725_2_247_s_210	15978733	(A) and dissociation (B) phases of NahR binding  to  Psal.	bind
5950	1	2534	6	10	NULL	0	NULL	XylS	GP	wild type	bind		specifically	N-terminal		Om	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_4_1118_s_179	10648539	(A) and DNase I footprinting (B) showing that wt N-XylS and XylS CTD bind specifically to  Om.	bind
5951	2	2534	6	10	NULL	0	NULL	XylS	GP		bind		specifically	CTD		Om	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_4_1118_s_179	10648539	(A) and DNase I footprinting (B) showing that wt N-XylS and XylS CTD bind specifically to  Om.	bind
6530	1	2534	7	10	NULL	0	NULL	XylS 	GP	wt	bind		specifically	N-terminal		Om	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_4_1118_s_179	10648539	(A) and DNase I footprinting (B) showing that wt N-XylS and XylS CTD bind specifically to  Om.	bind
6531	2	2534	7	10	NULL	0	NULL	XylS	GP		bind		specifically	CTD		Om	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_4_1118_s_179	10648539	(A) and DNase I footprinting (B) showing that wt N-XylS and XylS CTD bind specifically to  Om.	bind
5952	1	2535	6	10	NULL	0	NULL	FbsA	GP		bind					fibrinogen	GP	native			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_6_3495_s_210	15155657	(A) and dot blot experiments to detect binding of the FbsA and FbsB  fusion proteins to native fibrinogen (B).	bind
5953	2	2535	6	10	NULL	0	NULL	FbsB	GP		bind					fibrinogen	GP	native			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_6_3495_s_210	15155657	(A) and dot blot experiments to detect binding of the FbsA and FbsB  fusion proteins to native fibrinogen (B).	bind
46336	3	2535	6	10	NULL	0	NULL	FbsA	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_6_3495_s_210	15155657	(A) and dot blot experiments to detect binding of the FbsA and FbsB  fusion proteins to native fibrinogen (B).	bind
46337	4	2535	6	10	NULL	0	NULL	FbsB	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_6_3495_s_210	15155657	(A) and dot blot experiments to detect binding of the FbsA and FbsB  fusion proteins to native fibrinogen (B).	bind
6532	1	2535	7	10	NULL	0	NULL	FbsA	GP		bind					fibrinogen	GP	native			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_6_3495_s_210	15155657	(A) and dot blot experiments to detect binding of the FbsA and FbsB  fusion proteins to native fibrinogen (B).	bind
6533	2	2535	7	10	NULL	0	NULL	FbsB	GP		bind					fibrinogen	GP	native			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_6_3495_s_210	15155657	(A) and dot blot experiments to detect binding of the FbsA and FbsB  fusion proteins to native fibrinogen (B).	bind
46338	3	2535	7	10	NULL	0	NULL	FbsA	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_6_3495_s_210	15155657	(A) and dot blot experiments to detect binding of the FbsA and FbsB  fusion proteins to native fibrinogen (B).	bind
46339	4	2535	7	10	NULL	0	NULL	FbsB	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_6_3495_s_210	15155657	(A) and dot blot experiments to detect binding of the FbsA and FbsB  fusion proteins to native fibrinogen (B).	bind
5954	1	2537	6	10	NULL	0	NULL	endothelin-1	GP		bind					endothelin receptor 	GP	atypical			NULL	primary rat astrocytes	NULL	NULL	NULL	NULL	gw60_neuroscience_91_3_1067_s_305	10391484	(A) and ET(B) specific ligands synergistically antagonize endothelin-1 binding to an atypical endothelin receptor in primary rat astrocytes.	bind
5955	2	2537	6	10	NULL	0	NULL	ET specific ligands	Chemical		antagonize		synergistically			statement 1	Process				NULL	primary rat astrocytes	NULL	NULL	NULL	NULL	gw60_neuroscience_91_3_1067_s_305	10391484	(A) and ET(B) specific ligands synergistically antagonize endothelin-1 binding to an atypical endothelin receptor in primary rat astrocytes.	bind
6534	1	2537	7	10	NULL	0	NULL	endothelin-1	GP		bind					endothelin receptor	GP	atypical			NULL	primary rat astrocytes	NULL	NULL	NULL	NULL	gw60_neuroscience_91_3_1067_s_305	10391484	(A) and ET(B) specific ligands synergistically antagonize endothelin-1 binding to an atypical endothelin receptor in primary rat astrocytes.	bind
6535	2	2537	7	10	NULL	0	NULL	ET specific ligands	Chemical		antagonize		synergistically			statement 1	Process				NULL	primary rat astrocytes	NULL	NULL	NULL	NULL	gw60_neuroscience_91_3_1067_s_305	10391484	(A) and ET(B) specific ligands synergistically antagonize endothelin-1 binding to an atypical endothelin receptor in primary rat astrocytes.	bind
7861	1	2538	6	10	NULL	0	NULL	Fn	GP		bind					lactobacillus	Organism				NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_206_1_31_s_129	11786253	(A) and Fn (B) binding by  Lactobacillus.	bind
6536	1	2538	7	10	NULL	0	NULL	Fn 	GP		binds to					Lactobacillus	Organism				NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_206_1_31_s_129	11786253	(A) and Fn (B) binding by  Lactobacillus.	bind
5956	1	2541	6	10	NULL	0	NULL	SREBP-1	GP		bind					malic enzyme gene	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_43_8_1220_s_84	12177166	(A) and gel mobility shift assay for binding of SREBP-1 to the malic enzyme gene promoter (B).	bind
6537	1	2541	7	10	NULL	0	NULL	SREBP-1	GP		binds to					malic enzyme gene 	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_43_8_1220_s_84	12177166	(A) and gel mobility shift assay for binding of SREBP-1 to the malic enzyme gene promoter (B).	bind
5958	1	2543	6	10	NULL	0	NULL	Gpp(NH)p	GP		bind					ARF1	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_487_2_252_s_132	11150519	(A) and Gpp(NH)p (B) bound conformations of ARF1.	bind
6539	1	2543	7	10	NULL	0	NULL	Gpp(NH)p	GP		bind					ARF1	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_487_2_252_s_132	11150519	(A) and Gpp(NH)p (B) bound conformations of ARF1.	bind
5959	1	2544	6	10	NULL	0	NULL	progesterone	GP		inhibits					pentazocine	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_289_1_251_s_274	10087012	(A) and inhibition of [3]-(+)-pentazocine binding by progesterone (B).	bind
6540	1	2544	7	10	NULL	0	NULL	progesterone	GP		inhibits					pentazocine	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_289_1_251_s_274	10087012	(A) and inhibition of [3]-(+)-pentazocine binding by progesterone (B).	bind
5960	1	2545	6	10	NULL	0	NULL	actininn2	GP		bind		non-specifically			Protein A	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_473_2_188_s_229	10812072	(A) and lane 1 in (B) and (C) exclude non-specific binding of  actininn2 and Kv1.5 to the protein A-Sepharose.	bind
5961	2	2545	6	10	NULL	0	NULL	Kv1.5	GP		bind		non-specifically			Protein A	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_473_2_188_s_229	10812072	(A) and lane 1 in (B) and (C) exclude non-specific binding of  actininn2 and Kv1.5 to the protein A-Sepharose.	bind
6541	1	2545	7	10	NULL	0	NULL	actininn2	GP		bind		non-specifically			protein A	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_473_2_188_s_229	10812072	(A) and lane 1 in (B) and (C) exclude non-specific binding of  actininn2 and Kv1.5 to the protein A-Sepharose.	bind
6542	2	2545	7	10	NULL	0	NULL	Kv1.5	GP		bind		non-specifically			protein A	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_473_2_188_s_229	10812072	(A) and lane 1 in (B) and (C) exclude non-specific binding of  actininn2 and Kv1.5 to the protein A-Sepharose.	bind
5962	1	2546	6	10	NULL	0	NULL	mt-CMT1	GP		bind					GST-SAHH	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1590_1_93_s_155	12063172	(A) and mt-CMT1 (B) were bound by the GST-SAHH fusion protein but not by GST alone, indicating that binding of xCMT1 to xSAHH was independent of the tag sequence used.	bind
5963	2	2546	6	10	NULL	0	NULL	mt-CMT1	GP		does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1590_1_93_s_155	12063172	(A) and mt-CMT1 (B) were bound by the GST-SAHH fusion protein but not by GST alone, indicating that binding of xCMT1 to xSAHH was independent of the tag sequence used.	bind
5964	3	2546	6	10	NULL	0	NULL	statement 1	Process		is independent of					tag sequence	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1590_1_93_s_155	12063172	(A) and mt-CMT1 (B) were bound by the GST-SAHH fusion protein but not by GST alone, indicating that binding of xCMT1 to xSAHH was independent of the tag sequence used.	bind
46359	4	2546	6	10	NULL	0	NULL	GST-SAHH	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1590_1_93_s_155	12063172	(A) and mt-CMT1 (B) were bound by the GST-SAHH fusion protein but not by GST alone, indicating that binding of xCMT1 to xSAHH was independent of the tag sequence used.	bind
6543	1	2546	7	10	NULL	0	NULL	mt-CMT1	GP		binds					GST-SAHH	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1590_1_93_s_155	12063172	(A) and mt-CMT1 (B) were bound by the GST-SAHH fusion protein but not by GST alone, indicating that binding of xCMT1 to xSAHH was independent of the tag sequence used.	bind
6544	2	2546	7	10	NULL	0	NULL	 mt-CMT1	GP		does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1590_1_93_s_155	12063172	(A) and mt-CMT1 (B) were bound by the GST-SAHH fusion protein but not by GST alone, indicating that binding of xCMT1 to xSAHH was independent of the tag sequence used.	bind
6545	3	2546	7	10	NULL	0	NULL	statement 1	Process		is independent of					tag sequence	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1590_1_93_s_155	12063172	(A) and mt-CMT1 (B) were bound by the GST-SAHH fusion protein but not by GST alone, indicating that binding of xCMT1 to xSAHH was independent of the tag sequence used.	bind
46360	4	2546	7	10	NULL	0	NULL	GST-SAHH	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1590_1_93_s_155	12063172	(A) and mt-CMT1 (B) were bound by the GST-SAHH fusion protein but not by GST alone, indicating that binding of xCMT1 to xSAHH was independent of the tag sequence used.	bind
5965	1	2547	6	10	NULL	0	NULL	E1A protein	GP	mutant	bind		selectively			p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_510_1_50_s_167	11755530	(A) and neurite outgrowth (B) are inhibited by an E1A mutant protein that selectively binds p300.	bind
5966	2	2547	6	10	NULL	0	NULL	E1A protein	GP	mutant	inhibits					neurite outgrowth	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_510_1_50_s_167	11755530	(A) and neurite outgrowth (B) are inhibited by an E1A mutant protein that selectively binds p300.	bind
6546	1	2547	7	10	NULL	0	NULL	E1A protein	GP	mutant	binds to 		selectively			p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_510_1_50_s_167	11755530	(A) and neurite outgrowth (B) are inhibited by an E1A mutant protein that selectively binds p300.	bind
6547	2	2547	7	10	NULL	0	NULL	neurite outgrowth	Process		is inhibited by					E1A protein	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_febslett_510_1_50_s_167	11755530	(A) and neurite outgrowth (B) are inhibited by an E1A mutant protein that selectively binds p300.	bind
5967	1	2549	6	10	NULL	0	NULL	eIF4G2	GP		bind					eIF1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5431_s_120	12861028	(A) and point mutations (B) on eIF4G2 binding to eIF1  and eIF5.	bind
5968	2	2549	6	10	NULL	0	NULL	eIF4G2	GP		bind					eIF5	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5431_s_120	12861028	(A) and point mutations (B) on eIF4G2 binding to eIF1  and eIF5.	bind
6548	1	2549	7	10	NULL	0	NULL	eIF4G2	GP		binds to					eIF1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5431_s_120	12861028	(A) and point mutations (B) on eIF4G2 binding to eIF1  and eIF5.	bind
6549	2	2549	7	10	NULL	0	NULL	eIF4G2	GP		binds to					eIF5	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5431_s_120	12861028	(A) and point mutations (B) on eIF4G2 binding to eIF1  and eIF5.	bind
5969	1	2550	6	10	NULL	0	NULL	eIF4G2	GP		bind					eIF1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_15_5431_s_120	12861028	(A) and point mutations (B) on eIF4G2 binding to eIF1 and eIF5.	bind
5970	2	2550	6	10	NULL	0	NULL	eIF4G2	GP		bind					eIF5	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_15_5431_s_120	12861028	(A) and point mutations (B) on eIF4G2 binding to eIF1 and eIF5.	bind
7862	1	2551	6	10	NULL	0	NULL	Poly(g) sequences	NucleicAcid		inserted into					coding sequences	NucleicAcid	yeast;;upstream of			NULL		NULL	NULL	NULL	NULL	gw60_genetics_152_1_101_s_331	10224246	(A) and poly(G) sequences inserted upstream of the coding sequences stimulate transcription in yeast in the absence of the binding of known transcription factors.	bind
7863	2	2551	6	10	NULL	0	NULL	statement 1	Process		stimulate					transcription	Process	yeast			NULL		NULL	NULL	NULL	NULL	gw60_genetics_152_1_101_s_331	10224246	(A) and poly(G) sequences inserted upstream of the coding sequences stimulate transcription in yeast in the absence of the binding of known transcription factors.	bind
7864	3	2551	6	10	NULL	0	NULL	statement 2	Process		occurs in absence of					transcription factors	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_genetics_152_1_101_s_331	10224246	(A) and poly(G) sequences inserted upstream of the coding sequences stimulate transcription in yeast in the absence of the binding of known transcription factors.	bind
6550	1	2551	7	10	NULL	0	NULL	poly(G) sequences	NucleicAcid		is inserted into					coding sequences	NucleicAcid	yeast;;upstream of			NULL		NULL	NULL	NULL	NULL	gw60_genetics_152_1_101_s_331	10224246	(A) and poly(G) sequences inserted upstream of the coding sequences stimulate transcription in yeast in the absence of the binding of known transcription factors.	bind
6551	2	2551	7	10	NULL	0	NULL	statement 1	Process		stimulate					transcription 	Process	yeast			NULL		NULL	NULL	NULL	NULL	gw60_genetics_152_1_101_s_331	10224246	(A) and poly(G) sequences inserted upstream of the coding sequences stimulate transcription in yeast in the absence of the binding of known transcription factors.	bind
6552	3	2551	7	10	NULL	0	NULL	statement 2	Process		occurs in the absence of 					transcription factors	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_genetics_152_1_101_s_331	10224246	(A) and poly(G) sequences inserted upstream of the coding sequences stimulate transcription in yeast in the absence of the binding of known transcription factors.	bind
5971	1	2553	6	10	NULL	0	NULL	125I-[Tyr3]MP	GP		bind					HSR	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_57_6_1235_s_191	10825395	(A) and Scatchard (B) plots of 125I-[Tyr3]MP binding to HSR.	bind
6553	1	2553	7	10	NULL	0	NULL	125I-[Tyr3]MP	GP		binds					HSR	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_57_6_1235_s_191	10825395	(A) and Scatchard (B) plots of 125I-[Tyr3]MP binding to HSR.	bind
61567	1	2554	6	10	NULL	0	NULL	CFT	Chemical		bind					DAT	GP	WT			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_56_2_434_s_146	10419565	(A) and Scatchard analysis of [3]CFT binding activity (B) with the WT DAT (top) and two representative DAT mutants 3F155A (middle) and 7F361A (bottom).	bind
61568	2	2554	6	10	NULL	0	NULL	CFT	Chemical		bind					DAT	GP	mutant	3F155A		NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_2_434_s_146	10419565	(A) and Scatchard analysis of [3]CFT binding activity (B) with the WT DAT (top) and two representative DAT mutants 3F155A (middle) and 7F361A (bottom).	bind
61569	3	2554	6	10	NULL	0	NULL	CFT	Chemical		bind					DAT	GP	mutant	7F361A		NULL		0	NULL	NULL	NULL	gw60_molpharmacol_56_2_434_s_146	10419565	(A) and Scatchard analysis of [3]CFT binding activity (B) with the WT DAT (top) and two representative DAT mutants 3F155A (middle) and 7F361A (bottom).	bind
6554	1	2554	7	10	NULL	0	NULL	[3]CFT	Chemical		binds					DAT	GP	WT			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_2_434_s_146	10419565	(A) and Scatchard analysis of [3]CFT binding activity (B) with the WT DAT (top) and two representative DAT mutants 3F155A (middle) and 7F361A (bottom).	bind
6555	2	2554	7	10	NULL	0	NULL	[3]CFT	Chemical		binds					DAT	GP	mutant	3F155A		NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_2_434_s_146	10419565	(A) and Scatchard analysis of [3]CFT binding activity (B) with the WT DAT (top) and two representative DAT mutants 3F155A (middle) and 7F361A (bottom).	bind
6556	3	2554	7	10	NULL	0	NULL	[3]CFT	Chemical		binds					DAT	GP	mutant	 7F361A		NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_2_434_s_146	10419565	(A) and Scatchard analysis of [3]CFT binding activity (B) with the WT DAT (top) and two representative DAT mutants 3F155A (middle) and 7F361A (bottom).	bind
5972	1	2557	6	10	NULL	0	NULL	SLM-2	GP		bind					poly(G) homopolymeric RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_52_54398_s_177	15471878	(A) and SLM-2 bound poly(G) homopolymeric RNA when cotransfections were performed with the empty expression vector.	bind
6815	1	2557	7	10	NULL	0	NULL	SLM-2	GP		bind					poly(G) homopolymeric RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_52_54398_s_177	15471878	(A) and SLM-2 bound poly(G) homopolymeric RNA when cotransfections were performed with the empty expression vector.	bind
5974	1	2558	6	10	NULL	0	NULL	puroA	GP		bind					POPG SUV	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_16_4938_s_176	12897014	(A) and Stern-Volmer plots (B) for 2 muM puroA bound to POPG SUVs (lines a) and to POPC SUVs (lines b) and in buffer (lines c).	bind
5975	2	2558	6	10	NULL	0	NULL	puroA	GP		bind					POPC SUV	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_16_4938_s_176	12897014	(A) and Stern-Volmer plots (B) for 2 muM puroA bound to POPG SUVs (lines a) and to POPC SUVs (lines b) and in buffer (lines c).	bind
6816	1	2558	7	10	NULL	0	NULL	puroA	GP		binds					POPG SUVs	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_16_4938_s_176	12897014	(A) and Stern-Volmer plots (B) for 2 muM puroA bound to POPG SUVs (lines a) and to POPC SUVs (lines b) and in buffer (lines c).	bind
6818	2	2558	7	10	NULL	0	NULL	puroA	GP		binds					POPC SUVs	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_16_4938_s_176	12897014	(A) and Stern-Volmer plots (B) for 2 muM puroA bound to POPG SUVs (lines a) and to POPC SUVs (lines b) and in buffer (lines c).	bind
7865	1	2560	6	10	NULL	0	NULL	Cn-I	GP		bind					CRL 639	GP	L. acidophilus			NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_206_1_31_s_141	11786253	(A) and temperature (B) on binding of Cn-I ( ) and Fn ( ) by  L. acidophilus CRL 639.	bind
7866	2	2560	6	10	NULL	0	NULL	Fn	GP		bind					CRL 639	GP	L. acidophilus			NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_206_1_31_s_141	11786253	(A) and temperature (B) on binding of Cn-I ( ) and Fn ( ) by  L. acidophilus CRL 639.	bind
6823	1	2560	7	10	NULL	0	NULL	Cn-I	GP		binds					CRL 639	GP	L. acidophilus 			NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_206_1_31_s_141	11786253	(A) and temperature (B) on binding of Cn-I ( ) and Fn ( ) by  L. acidophilus CRL 639.	bind
6824	2	2560	7	10	NULL	0	NULL	Fn	GP		binds					CRL 639	GP	L. acidophilus 			NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_206_1_31_s_141	11786253	(A) and temperature (B) on binding of Cn-I ( ) and Fn ( ) by  L. acidophilus CRL 639.	bind
5976	1	2562	6	10	NULL	0	NULL				bind			TM helices		Chl molecules	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44542_s_5	12923171	(A) and the third (C) transmembrane (TM) helices that binds 6 Chl molecules and two carotenoids is conserved structurally, whereas the interface between the first and the second TM helices and the outer surface of the second TM helix differ significantly among the LHCI and LHCII polypeptides.	bind
5977	2	2562	6	10	NULL	0	NULL				bind			transmembrane helices		carotenoids	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44542_s_5	12923171	(A) and the third (C) transmembrane (TM) helices that binds 6 Chl molecules and two carotenoids is conserved structurally, whereas the interface between the first and the second TM helices and the outer surface of the second TM helix differ significantly among the LHCI and LHCII polypeptides.	bind
5978	3	2562	6	10	NULL	0	NULL	TM helics	AminoAcid		is					transmembrane helics	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44542_s_5	12923171	(A) and the third (C) transmembrane (TM) helices that binds 6 Chl molecules and two carotenoids is conserved structurally, whereas the interface between the first and the second TM helices and the outer surface of the second TM helix differ significantly among the LHCI and LHCII polypeptides.	bind
7867	4	2562	6	10	NULL	0	NULL	LHCI polypeptide	GP		differ		significantly	first TM helices		LHCII polypeptide	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44542_s_5	12923171	(A) and the third (C) transmembrane (TM) helices that binds 6 Chl molecules and two carotenoids is conserved structurally, whereas the interface between the first and the second TM helices and the outer surface of the second TM helix differ significantly among the LHCI and LHCII polypeptides.	bind
7868	5	2562	6	10	NULL	0	NULL	LHCI polypeptide	GP		differ		significantly	second TM helices		LHCII polypeptide	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44542_s_5	12923171	(A) and the third (C) transmembrane (TM) helices that binds 6 Chl molecules and two carotenoids is conserved structurally, whereas the interface between the first and the second TM helices and the outer surface of the second TM helix differ significantly among the LHCI and LHCII polypeptides.	bind
7869	6	2562	6	10	NULL	0	NULL	LHCI polypeptide	GP		differ		significantly	outer surface of the second TM helix		LHCII polypeptide	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44542_s_5	12923171	(A) and the third (C) transmembrane (TM) helices that binds 6 Chl molecules and two carotenoids is conserved structurally, whereas the interface between the first and the second TM helices and the outer surface of the second TM helix differ significantly among the LHCI and LHCII polypeptides.	bind
6826	1	2562	7	10	NULL	0	NULL	 			binds			transmembrane helices		Chl molecules	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44542_s_5	12923171	(A) and the third (C) transmembrane (TM) helices that binds 6 Chl molecules and two carotenoids is conserved structurally, whereas the interface between the first and the second TM helices and the outer surface of the second TM helix differ significantly among the LHCI and LHCII polypeptides.	bind
6827	2	2562	7	10	NULL	0	NULL				binds			transmembrane helices		carotenoids	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44542_s_5	12923171	(A) and the third (C) transmembrane (TM) helices that binds 6 Chl molecules and two carotenoids is conserved structurally, whereas the interface between the first and the second TM helices and the outer surface of the second TM helix differ significantly among the LHCI and LHCII polypeptides.	bind
6904	3	2562	7	10	NULL	0	NULL	TM helics	AminoAcid		is					transmembrane helics	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44542_s_5	12923171	(A) and the third (C) transmembrane (TM) helices that binds 6 Chl molecules and two carotenoids is conserved structurally, whereas the interface between the first and the second TM helices and the outer surface of the second TM helix differ significantly among the LHCI and LHCII polypeptides.	bind
7194	5	2562	7	10	NULL	0	NULL	LHCI polypeptides	GP	Interface of 	differ		significantly	first TM helix		LHCII polypeptides	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44542_s_5	12923171	(A) and the third (C) transmembrane (TM) helices that binds 6 Chl molecules and two carotenoids is conserved structurally, whereas the interface between the first and the second TM helices and the outer surface of the second TM helix differ significantly among the LHCI and LHCII polypeptides.	bind
7196	6	2562	7	10	NULL	0	NULL	LHCI polypeptides	GP	Interface of	differ		significantly	second TM helix		LHCII polypeptides	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44542_s_5	12923171	(A) and the third (C) transmembrane (TM) helices that binds 6 Chl molecules and two carotenoids is conserved structurally, whereas the interface between the first and the second TM helices and the outer surface of the second TM helix differ significantly among the LHCI and LHCII polypeptides.	bind
7271	4	2562	7	10	NULL	0	NULL	LHCI polypeptides	GP		differ		significantly	outer surface of second TM helix		LHCII polypeptides	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44542_s_5	12923171	(A) and the third (C) transmembrane (TM) helices that binds 6 Chl molecules and two carotenoids is conserved structurally, whereas the interface between the first and the second TM helices and the outer surface of the second TM helix differ significantly among the LHCI and LHCII polypeptides.	bind
5979	1	2563	6	10	NULL	0	NULL	transferrin	GP		bind					rTbpB proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_9_4183_s_218	9712766	(A) and transferrin binding of rTbpB proteins (B).	bind
6833	1	2563	7	10	NULL	0	NULL	transferrin	GP		binds					rTbpB proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_9_4183_s_218	9712766	(A) and transferrin binding of rTbpB proteins (B).	bind
5980	1	2564	6	10	NULL	0	NULL	TTF-1	GP		bind					CaSR-C	GP			TTF-1 element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7410_s_263	9819427	(A) and TTF-1 binding to the CaSR-C TTF-1 element (B) are decreased by the ATP- or A23187-increased the internal Ca2+ signal, and kinase C activation can synergistically increase the Ca2+ signal effect.	bind
5981	2	2564	6	10	NULL	0	NULL	ATP	Chemical		decreases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7410_s_263	9819427	(A) and TTF-1 binding to the CaSR-C TTF-1 element (B) are decreased by the ATP- or A23187-increased the internal Ca2+ signal, and kinase C activation can synergistically increase the Ca2+ signal effect.	bind
5982	3	2564	6	10	NULL	0	NULL	A23187	Chemical		increased					Ca+2 signal	Process	internal			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7410_s_263	9819427	(A) and TTF-1 binding to the CaSR-C TTF-1 element (B) are decreased by the ATP- or A23187-increased the internal Ca2+ signal, and kinase C activation can synergistically increase the Ca2+ signal effect.	bind
5983	4	2564	6	10	NULL	0	NULL	A23187	Chemical		increased					kinase C	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7410_s_263	9819427	(A) and TTF-1 binding to the CaSR-C TTF-1 element (B) are decreased by the ATP- or A23187-increased the internal Ca2+ signal, and kinase C activation can synergistically increase the Ca2+ signal effect.	bind
6212	5	2564	6	10	NULL	0	NULL	statement 3	Process		act synergistically with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7410_s_263	9819427	(A) and TTF-1 binding to the CaSR-C TTF-1 element (B) are decreased by the ATP- or A23187-increased the internal Ca2+ signal, and kinase C activation can synergistically increase the Ca2+ signal effect.	bind
6213	6	2564	6	10	NULL	0	NULL	statement 5	Process		increase					Ca+2 signal effect	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7410_s_263	9819427	(A) and TTF-1 binding to the CaSR-C TTF-1 element (B) are decreased by the ATP- or A23187-increased the internal Ca2+ signal, and kinase C activation can synergistically increase the Ca2+ signal effect.	bind
6834	1	2564	7	10	NULL	0	NULL	TTF-1	GP		bind					CaSR-C	GP			TTF-1 element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7410_s_263	9819427	(A) and TTF-1 binding to the CaSR-C TTF-1 element (B) are decreased by the ATP- or A23187-increased the internal Ca2+ signal, and kinase C activation can synergistically increase the Ca2+ signal effect.	bind
6835	2	2564	7	10	NULL	0	NULL	statement 1	Process		is decreased by					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7410_s_263	9819427	(A) and TTF-1 binding to the CaSR-C TTF-1 element (B) are decreased by the ATP- or A23187-increased the internal Ca2+ signal, and kinase C activation can synergistically increase the Ca2+ signal effect.	bind
6836	3	2564	7	10	NULL	0	NULL	A23187	Chemical		increased					Ca2+ signal	Process	internal 			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7410_s_263	9819427	(A) and TTF-1 binding to the CaSR-C TTF-1 element (B) are decreased by the ATP- or A23187-increased the internal Ca2+ signal, and kinase C activation can synergistically increase the Ca2+ signal effect.	bind
7902	5	2564	7	10	NULL	0	NULL	A23187	Chemical		increased					Kinase C	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7410_s_263	9819427	(A) and TTF-1 binding to the CaSR-C TTF-1 element (B) are decreased by the ATP- or A23187-increased the internal Ca2+ signal, and kinase C activation can synergistically increase the Ca2+ signal effect.	bind
7909	6	2564	7	10	NULL	0	NULL	statement 5	Process		act synergistically with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7410_s_263	9819427	(A) and TTF-1 binding to the CaSR-C TTF-1 element (B) are decreased by the ATP- or A23187-increased the internal Ca2+ signal, and kinase C activation can synergistically increase the Ca2+ signal effect.	bind
5984	1	2565	6	10	NULL	0	NULL	VLDL	Chemical		bind					Sf9-CLA-1 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2341_s_172	9409200	(A) and VLDL (B) binding to Sf9-CLA-1 cells.	bind
6838	1	2565	7	10	NULL	0	NULL	VLDL 	Chemical		binds					Sf9-CLA-1 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2341_s_172	9409200	(A) and VLDL (B) binding to Sf9-CLA-1 cells.	bind
5985	1	2566	6	10	NULL	0	NULL	PlyA	GP	recombinant	bind		specifically			sphingomyelin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1679_1_65_s_161	15245918	(A) and Western immunoblotting (B) for recombinant PlyA, and sphingomyelin-specific  binding of recombinant PlyA (C).	bind
6839	1	2566	7	10	NULL	0	NULL	sphingomyelin	Chemical		binds		specifically			PlyA	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1679_1_65_s_161	15245918	(A) and Western immunoblotting (B) for recombinant PlyA, and sphingomyelin-specific  binding of recombinant PlyA (C).	bind
5986	1	2567	6	10	NULL	0	NULL	hSNF5/INI1	GP	FLAG-tagged	bind					protein	GP	myc-tagged			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_7050_s_258	10490642	(A) Anti-FLAG Western blot of anti-myc immunoprecipitates showing the amount of coimmunoprecipitated FLAG-tagged hSNF5/INI1 (lanes 1 to 7) and FLAG-tagged hSNF5/INI1 and GADD34 (lane 8) proteins bound to the myc-tagged proteins expressed in the transfections described below.	bind
5987	2	2567	6	10	NULL	0	NULL	GADD34	GP	FLAG-tagged	bind					protein	GP	myc-tagged			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_7050_s_258	10490642	(A) Anti-FLAG Western blot of anti-myc immunoprecipitates showing the amount of coimmunoprecipitated FLAG-tagged hSNF5/INI1 (lanes 1 to 7) and FLAG-tagged hSNF5/INI1 and GADD34 (lane 8) proteins bound to the myc-tagged proteins expressed in the transfections described below.	bind
6840	1	2567	7	10	NULL	0	NULL	hSNF5/INI1	GP	FLAG-tagged	binds					protein	GP	myc-tagged			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_7050_s_258	10490642	(A) Anti-FLAG Western blot of anti-myc immunoprecipitates showing the amount of coimmunoprecipitated FLAG-tagged hSNF5/INI1 (lanes 1 to 7) and FLAG-tagged hSNF5/INI1 and GADD34 (lane 8) proteins bound to the myc-tagged proteins expressed in the transfections described below.	bind
7912	2	2567	7	10	NULL	0	NULL	GADD34	GP	FLAG-tagged	bind					protein	GP	myc-tagged			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_7050_s_258	10490642	(A) Anti-FLAG Western blot of anti-myc immunoprecipitates showing the amount of coimmunoprecipitated FLAG-tagged hSNF5/INI1 (lanes 1 to 7) and FLAG-tagged hSNF5/INI1 and GADD34 (lane 8) proteins bound to the myc-tagged proteins expressed in the transfections described below.	bind
6841	1	2568	7	NULL	NULL	0	NULL	IRS	NULL		is	NULL				anti-TX0016 immune serum	NULL				NULL		0	NULL	NULL	NULL	gw60_femsimmunolmedmic_28_4_291_s_181	10891652	(A) anti-TX0016 immune serum (IRS), pre-immune serum (PRS), or immune serum adsorbed with either TX0016 or a phagocytosis-susceptible strain of  E. faecium (RLA-3), or (B) IRS alone or with purified carbohydrate or a surface protein Zwittergent extract from TX0016, and exposed to PMNs as in  Fig. 1, and data are presented as the number of bacteria bound per PMN (mean+S.E.M.,  n=3-7).	bind
6842	2	2568	7	NULL	NULL	0	NULL	PRS	NULL		is	NULL				pre-immune serum 	NULL				NULL		0	NULL	NULL	NULL	gw60_femsimmunolmedmic_28_4_291_s_181	10891652	(A) anti-TX0016 immune serum (IRS), pre-immune serum (PRS), or immune serum adsorbed with either TX0016 or a phagocytosis-susceptible strain of  E. faecium (RLA-3), or (B) IRS alone or with purified carbohydrate or a surface protein Zwittergent extract from TX0016, and exposed to PMNs as in  Fig. 1, and data are presented as the number of bacteria bound per PMN (mean+S.E.M.,  n=3-7).	bind
5988	1	2569	6	10	NULL	0	NULL	AP1 protein	GP		bind									AP1 response element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4522_s_207	12052862	(A) AP1 protein binding to the AP1 response element.	bind
6843	1	2569	7	10	NULL	0	NULL	AP1 protein	GP		binds									AP1 response element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4522_s_207	12052862	(A) AP1 protein binding to the AP1 response element.	bind
5989	1	2570	6	10	NULL	0	NULL	Apg-2	GP		bind					ZO-1	GP		SH3 domain		NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molbiolcell_17_3_1322_s_106	16407410	(A) Apg-2 binds to the SH3 domain  of ZO-1 in vitro.	bind
6844	1	2570	7	10	NULL	0	NULL	Apg-2 	GP		binds					ZO-1	GP		SH3 domain		NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molbiolcell_17_3_1322_s_106	16407410	(A) Apg-2 binds to the SH3 domain  of ZO-1 in vitro.	bind
5990	1	2571	6	10	NULL	0	NULL	PABP	GP		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_479_s_32	10882133	(A) appears to stimulate cap-dependent translation through a mechanism involving protein-protein interactions between PABP, eIF4G, and thecap binding protein eIF4E (  Tarun and Sachs 1997  ; Imataka et al. 1998  ).	bind
5991	2	2571	6	10	NULL	0	NULL	eIF4G	GP		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_479_s_32	10882133	(A) appears to stimulate cap-dependent translation through a mechanism involving protein-protein interactions between PABP, eIF4G, and thecap binding protein eIF4E (  Tarun and Sachs 1997  ; Imataka et al. 1998  ).	bind
5992	3	2571	6	10	NULL	0	NULL	statement 1	Process		stimulate					cap-dependent translation	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_479_s_32	10882133	(A) appears to stimulate cap-dependent translation through a mechanism involving protein-protein interactions between PABP, eIF4G, and thecap binding protein eIF4E (  Tarun and Sachs 1997  ; Imataka et al. 1998  ).	bind
7870	4	2571	6	10	NULL	0	NULL	statement 2	Process		stimulate					cap-dependent translation	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_479_s_32	10882133	(A) appears to stimulate cap-dependent translation through a mechanism involving protein-protein interactions between PABP, eIF4G, and thecap binding protein eIF4E (  Tarun and Sachs 1997  ; Imataka et al. 1998  ).	bind
46361	5	2571	6	10	NULL	0	NULL	eIF4E	GP		is a type of					cap binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_479_s_32	10882133	(A) appears to stimulate cap-dependent translation through a mechanism involving protein-protein interactions between PABP, eIF4G, and thecap binding protein eIF4E (  Tarun and Sachs 1997  ; Imataka et al. 1998  ).	bind
6845	1	2571	7	10	NULL	0	NULL	PABP	GP		binds					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_479_s_32	10882133	(A) appears to stimulate cap-dependent translation through a mechanism involving protein-protein interactions between PABP, eIF4G, and thecap binding protein eIF4E (  Tarun and Sachs 1997  ; Imataka et al. 1998  ).	bind
6846	2	2571	7	10	NULL	0	NULL	PABP	GP		binds					eIF4E 	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_479_s_32	10882133	(A) appears to stimulate cap-dependent translation through a mechanism involving protein-protein interactions between PABP, eIF4G, and thecap binding protein eIF4E (  Tarun and Sachs 1997  ; Imataka et al. 1998  ).	bind
6847	3	2571	7	10	NULL	0	NULL	 eIF4G	GP		binds					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_479_s_32	10882133	(A) appears to stimulate cap-dependent translation through a mechanism involving protein-protein interactions between PABP, eIF4G, and thecap binding protein eIF4E (  Tarun and Sachs 1997  ; Imataka et al. 1998  ).	bind
6848	4	2571	7	10	NULL	0	NULL	statement 1	Process		stimulate					cap-dependent translation 	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_479_s_32	10882133	(A) appears to stimulate cap-dependent translation through a mechanism involving protein-protein interactions between PABP, eIF4G, and thecap binding protein eIF4E (  Tarun and Sachs 1997  ; Imataka et al. 1998  ).	bind
6849	5	2571	7	10	NULL	0	NULL	statement 2	Process		stimulate					cap-dependent translation 	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_479_s_32	10882133	(A) appears to stimulate cap-dependent translation through a mechanism involving protein-protein interactions between PABP, eIF4G, and thecap binding protein eIF4E (  Tarun and Sachs 1997  ; Imataka et al. 1998  ).	bind
6850	6	2571	7	10	NULL	0	NULL	statement 3	Process		stimulate					cap-dependent translation 	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_479_s_32	10882133	(A) appears to stimulate cap-dependent translation through a mechanism involving protein-protein interactions between PABP, eIF4G, and thecap binding protein eIF4E (  Tarun and Sachs 1997  ; Imataka et al. 1998  ).	bind
46362	7	2571	7	10	NULL	0	NULL	eIF4E	GP		is a type of					cap binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_479_s_32	10882133	(A) appears to stimulate cap-dependent translation through a mechanism involving protein-protein interactions between PABP, eIF4G, and thecap binding protein eIF4E (  Tarun and Sachs 1997  ; Imataka et al. 1998  ).	bind
5993	1	2573	6	10	NULL	0	NULL	Arp8	GP		bind		preferentially			H3	GP				NULL	in solution	NULL	NULL	NULL	NULL	gw60_molcell_12_1_147_s_188	12887900	(A) Arp8 preferentially binds to H3 and H4 in solution.	bind
5994	2	2573	6	10	NULL	0	NULL	Arp8	GP		bind		preferentially			H4	GP				NULL	in solution	NULL	NULL	NULL	NULL	gw60_molcell_12_1_147_s_188	12887900	(A) Arp8 preferentially binds to H3 and H4 in solution.	bind
6851	1	2573	7	10	NULL	0	NULL	Arp8	GP		binds		preferentially			H3	GP				NULL	in solution	NULL	NULL	NULL	NULL	gw60_molcell_12_1_147_s_188	12887900	(A) Arp8 preferentially binds to H3 and H4 in solution.	bind
6852	2	2573	7	10	NULL	0	NULL	Arp8	GP		binds		preferentially			H4	GP				NULL	in solution	NULL	NULL	NULL	NULL	gw60_molcell_12_1_147_s_188	12887900	(A) Arp8 preferentially binds to H3 and H4 in solution.	bind
5995	1	2574	6	10	NULL	0	NULL	G	GP	purified	bind					Csk	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_6_733_s_197	12062086	(A) As shown by anti-Csk Western blot, purified G   bound to Ni-NTA beads pulled down purified Csk, but not boiled Csk. (B) Coimmunoprecipitation experiments with NG108 cell extract showed that anti-Csk antibody precipitated G   bound to Csk after stimulation of mAChR with carbachol.	bind
5996	2	2574	6	10	NULL	0	NULL	G	GP	purified	does not bind					Csk	GP	boiled			NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_6_733_s_197	12062086	(A) As shown by anti-Csk Western blot, purified G   bound to Ni-NTA beads pulled down purified Csk, but not boiled Csk. (B) Coimmunoprecipitation experiments with NG108 cell extract showed that anti-Csk antibody precipitated G   bound to Csk after stimulation of mAChR with carbachol.	bind
5997	3	2574	6	10	NULL	0	NULL	G	GP		bind					Csk	GP				NULL	NG108 cell extract	NULL	NULL	NULL	NULL	gw60_devcell_2_6_733_s_197	12062086	(A) As shown by anti-Csk Western blot, purified G   bound to Ni-NTA beads pulled down purified Csk, but not boiled Csk. (B) Coimmunoprecipitation experiments with NG108 cell extract showed that anti-Csk antibody precipitated G   bound to Csk after stimulation of mAChR with carbachol.	bind
5998	4	2574	6	10	NULL	0	NULL	carbachol	Chemical		stimulates					mAChR	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_6_733_s_197	12062086	(A) As shown by anti-Csk Western blot, purified G   bound to Ni-NTA beads pulled down purified Csk, but not boiled Csk. (B) Coimmunoprecipitation experiments with NG108 cell extract showed that anti-Csk antibody precipitated G   bound to Csk after stimulation of mAChR with carbachol.	bind
5999	5	2574	6	10	NULL	0	NULL	statement 3	Process		occurs after					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_6_733_s_197	12062086	(A) As shown by anti-Csk Western blot, purified G   bound to Ni-NTA beads pulled down purified Csk, but not boiled Csk. (B) Coimmunoprecipitation experiments with NG108 cell extract showed that anti-Csk antibody precipitated G   bound to Csk after stimulation of mAChR with carbachol.	bind
6853	1	2574	7	10	NULL	0	NULL	G	GP	purified	binds					Csk	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_6_733_s_197	12062086	(A) As shown by anti-Csk Western blot, purified G   bound to Ni-NTA beads pulled down purified Csk, but not boiled Csk. (B) Coimmunoprecipitation experiments with NG108 cell extract showed that anti-Csk antibody precipitated G   bound to Csk after stimulation of mAChR with carbachol.	bind
6854	2	2574	7	10	NULL	0	NULL	G	GP	purified	does not bind					Csk	GP	boiled			NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_6_733_s_197	12062086	(A) As shown by anti-Csk Western blot, purified G   bound to Ni-NTA beads pulled down purified Csk, but not boiled Csk. (B) Coimmunoprecipitation experiments with NG108 cell extract showed that anti-Csk antibody precipitated G   bound to Csk after stimulation of mAChR with carbachol.	bind
6855	3	2574	7	10	NULL	0	NULL	G	GP		binds					Csk	GP				NULL	NG108 cell extract 	NULL	NULL	NULL	NULL	gw60_devcell_2_6_733_s_197	12062086	(A) As shown by anti-Csk Western blot, purified G   bound to Ni-NTA beads pulled down purified Csk, but not boiled Csk. (B) Coimmunoprecipitation experiments with NG108 cell extract showed that anti-Csk antibody precipitated G   bound to Csk after stimulation of mAChR with carbachol.	bind
6856	4	2574	7	10	NULL	0	NULL	carbachol 	Chemical		stimulate					mAChR	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_6_733_s_197	12062086	(A) As shown by anti-Csk Western blot, purified G   bound to Ni-NTA beads pulled down purified Csk, but not boiled Csk. (B) Coimmunoprecipitation experiments with NG108 cell extract showed that anti-Csk antibody precipitated G   bound to Csk after stimulation of mAChR with carbachol.	bind
6857	5	2574	7	10	NULL	0	NULL	statement 3	Process		occurs after					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_6_733_s_197	12062086	(A) As shown by anti-Csk Western blot, purified G   bound to Ni-NTA beads pulled down purified Csk, but not boiled Csk. (B) Coimmunoprecipitation experiments with NG108 cell extract showed that anti-Csk antibody precipitated G   bound to Csk after stimulation of mAChR with carbachol.	bind
6000	1	2575	6	10	NULL	0	NULL	SBP	GP		bind					glycolipid	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_43_42050_s_70	12917406	(a) Assay for Binding Activity of the SBP Binding of the SBP to Glycolipids --	bind
6861	1	2575	7	10	NULL	0	NULL	SBP	GP		binds to					Glycolipids	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_43_42050_s_70	12917406	(a) Assay for Binding Activity of the SBP Binding of the SBP to Glycolipids --	bind
6001	1	2576	6	10	NULL	0	NULL	GST-MyoD 	GP		bind					MEF-1 oligodeoxynucleotide	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_1074_s_273	9448005	(A) Assays involving the binding of GST-MyoD fusion protein to the MEF-1 oligodeoxynucleotide.	bind
46363	2	2576	6	10	NULL	0	NULL	GST-MyoD	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_1074_s_273	9448005	(A) Assays involving the binding of GST-MyoD fusion protein to the MEF-1 oligodeoxynucleotide.	bind
6862	1	2576	7	10	NULL	0	NULL	GST-MyoD	GP		binds					MEF-1oligodeoxynucleotide	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_1074_s_273	9448005	(A) Assays involving the binding of GST-MyoD fusion protein to the MEF-1 oligodeoxynucleotide.	bind
46364	2	2576	7	10	NULL	0	NULL	GST-MyoD	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_1074_s_273	9448005	(A) Assays involving the binding of GST-MyoD fusion protein to the MEF-1 oligodeoxynucleotide.	bind
6002	1	2577	6	10	NULL	0	NULL	GAPDH	GP		associate					lysosomes	CellComponent	intact 			NULL	untreated fed rats, 48-h starved rats (Strv) or fed rats treated with paraquat (PQ)	NULL	NULL	NULL	NULL	gw70_molbiolcell_15_11_4829_s_197	15331765	(A) Association and binding of GAPDH  and RNase A to intact lysosomes from untreated fed rats, 48-h starved rats (Strv)  or fed rats treated with paraquat (PQ).	bind
6003	2	2577	6	10	NULL	0	NULL	GAPDH	GP		bind					lysosomes	CellComponent	intact 			NULL	untreated fed rats, 48-h starved rats (Strv) or fed rats treated with paraquat (PQ)	NULL	NULL	NULL	NULL	gw70_molbiolcell_15_11_4829_s_197	15331765	(A) Association and binding of GAPDH  and RNase A to intact lysosomes from untreated fed rats, 48-h starved rats (Strv)  or fed rats treated with paraquat (PQ).	bind
6004	3	2577	6	10	NULL	0	NULL	RNase A	GP		bind					 lysosomes	CellComponent	intact			NULL	untreated fed rats, 48-h starved rats (Strv) or fed rats treated with paraquat (PQ)	NULL	NULL	NULL	NULL	gw70_molbiolcell_15_11_4829_s_197	15331765	(A) Association and binding of GAPDH  and RNase A to intact lysosomes from untreated fed rats, 48-h starved rats (Strv)  or fed rats treated with paraquat (PQ).	bind
6005	4	2577	6	10	NULL	0	NULL	RNase A	GP		associate					lysosomes	CellComponent	intact			NULL	untreated fed rats, 48-h starved rats (Strv) or fed rats treated with paraquat (PQ)	NULL	NULL	NULL	NULL	gw70_molbiolcell_15_11_4829_s_197	15331765	(A) Association and binding of GAPDH  and RNase A to intact lysosomes from untreated fed rats, 48-h starved rats (Strv)  or fed rats treated with paraquat (PQ).	bind
6863	1	2577	7	10	NULL	0	NULL	RNaseA	GP		binds					lysosomes	CellComponent	intact;;rat			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_11_4829_s_197	15331765	(A) Association and binding of GAPDH  and RNase A to intact lysosomes from untreated fed rats, 48-h starved rats (Strv)  or fed rats treated with paraquat (PQ).	bind
6864	2	2577	7	10	NULL	0	NULL	GAPDH	GP		binds					lysosomes	CellComponent	intact;;rat			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_11_4829_s_197	15331765	(A) Association and binding of GAPDH  and RNase A to intact lysosomes from untreated fed rats, 48-h starved rats (Strv)  or fed rats treated with paraquat (PQ).	bind
6006	1	2578	6	10	NULL	0	NULL	Ast*	GP		bind					CRF-R1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_729_s_60	9918582	(A) Ast* or (B) Ucn* bound to CRF-R1 by astressin ( ), r/hCRF ( ) and Ucn ( ).	bind
6007	2	2578	6	10	NULL	0	NULL	Ucn*	GP		bind					CRF-R1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_729_s_60	9918582	(A) Ast* or (B) Ucn* bound to CRF-R1 by astressin ( ), r/hCRF ( ) and Ucn ( ).	bind
6008	3	2578	6	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_729_s_60	9918582	(A) Ast* or (B) Ucn* bound to CRF-R1 by astressin ( ), r/hCRF ( ) and Ucn ( ).	bind
6865	1	2578	7	10	NULL	0	NULL	Ast*	GP		binds					CRF-R1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_729_s_60	9918582	(A) Ast* or (B) Ucn* bound to CRF-R1 by astressin ( ), r/hCRF ( ) and Ucn ( ).	bind
6866	2	2578	7	10	NULL	0	NULL	Ucn*	GP		binds					CRF-R1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_729_s_60	9918582	(A) Ast* or (B) Ucn* bound to CRF-R1 by astressin ( ), r/hCRF ( ) and Ucn ( ).	bind
6867	3	2578	7	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_729_s_60	9918582	(A) Ast* or (B) Ucn* bound to CRF-R1 by astressin ( ), r/hCRF ( ) and Ucn ( ).	bind
6009	1	2579	6	10	NULL	0	NULL	ATM	GP		phosphorylates					p53	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_360	16267266	(a) ATM phosphorylates  p53; this phosphorylation blocks the binding of p53 to Mdm2, thereby preventing rapid  MdM2-induced p53 degradation.	bind
6010	2	2579	6	10	NULL	0	NULL	p53	GP		bind					Mdm2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_360	16267266	(a) ATM phosphorylates  p53; this phosphorylation blocks the binding of p53 to Mdm2, thereby preventing rapid  MdM2-induced p53 degradation.	bind
6011	3	2579	6	10	NULL	0	NULL	statement 1	Process		blocks					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_360	16267266	(a) ATM phosphorylates  p53; this phosphorylation blocks the binding of p53 to Mdm2, thereby preventing rapid  MdM2-induced p53 degradation.	bind
6012	4	2579	6	10	NULL	0	NULL	MdM2	GP		induces					p53	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_360	16267266	(a) ATM phosphorylates  p53; this phosphorylation blocks the binding of p53 to Mdm2, thereby preventing rapid  MdM2-induced p53 degradation.	bind
6013	5	2579	6	10	NULL	0	NULL	statement 3	Process		prevents					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_360	16267266	(a) ATM phosphorylates  p53; this phosphorylation blocks the binding of p53 to Mdm2, thereby preventing rapid  MdM2-induced p53 degradation.	bind
6868	1	2579	7	10	NULL	0	NULL	ATM	GP		phosphorylates					p53	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_360	16267266	(a) ATM phosphorylates  p53; this phosphorylation blocks the binding of p53 to Mdm2, thereby preventing rapid  MdM2-induced p53 degradation.	bind
6869	2	2579	7	10	NULL	0	NULL	p53	GP		binds					Mdm2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_360	16267266	(a) ATM phosphorylates  p53; this phosphorylation blocks the binding of p53 to Mdm2, thereby preventing rapid  MdM2-induced p53 degradation.	bind
6870	3	2579	7	10	NULL	0	NULL	statement 1	Process		blocks					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_360	16267266	(a) ATM phosphorylates  p53; this phosphorylation blocks the binding of p53 to Mdm2, thereby preventing rapid  MdM2-induced p53 degradation.	bind
6871	4	2579	7	10	NULL	0	NULL	MdM2	GP		induce					p53	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_360	16267266	(a) ATM phosphorylates  p53; this phosphorylation blocks the binding of p53 to Mdm2, thereby preventing rapid  MdM2-induced p53 degradation.	bind
7913	5	2579	7	10	NULL	0	NULL	statement 3	Process		prevents					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_360	16267266	(a) ATM phosphorylates  p53; this phosphorylation blocks the binding of p53 to Mdm2, thereby preventing rapid  MdM2-induced p53 degradation.	bind
6014	1	2581	6	10	NULL	0	NULL	ATP	Chemical		bind					erbB2	GP		active site		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_307_2_267_s_51	12859950	(A) ATP bound to the active site of erbB2.	bind
6872	1	2581	7	10	NULL	0	NULL	ATP	Chemical		bind					erbB2	GP		active site		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_307_2_267_s_51	12859950	(A) ATP bound to the active site of erbB2.	bind
6015	1	2582	6	10	NULL	0	NULL	PKA	GP		phosphorylates					RyR1	GP				NULL	skeletal muscle of sham-operated (control) and HF rats	NULL	NULL	NULL	NULL	gw70_cellbiol_160_6_919_s_164	12629052	(A) Autoradiogram showing PKA back phosphorylation of RyR1 from skeletal muscle of  sham-operated (control) and HF rats, bar graph shows relative PKA phosphorylation  of RyR1 (expressed as inverse of back phosphorylation as previously described [ ]).	bind
6873	1	2582	7	10	NULL	0	NULL	PKA	GP		phosphorylate					RyR1	GP				NULL	from skeletal muscle of sham-operated and HF rats	NULL	NULL	NULL	NULL	gw70_cellbiol_160_6_919_s_164	12629052	(A) Autoradiogram showing PKA back phosphorylation of RyR1 from skeletal muscle of  sham-operated (control) and HF rats, bar graph shows relative PKA phosphorylation  of RyR1 (expressed as inverse of back phosphorylation as previously described [ ]).	bind
6016	1	2586	6	10	NULL	0	NULL	Bax	GP		bind			BH3 domain		Bcl-2 family members	GP	pro-apoptotic factor			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_currbiol_7_12_913_s_95	9382837	(a) BH3 domains from Bax and Bak can bind to pro-apoptotic and anti-apoptotic Bcl-2 family members  in vitro.	bind
6017	2	2586	6	10	NULL	0	NULL	bak	GP		bind			BH3 domain		Bcl-2 family members	GP	pro-apoptotic factor			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_currbiol_7_12_913_s_95	9382837	(a) BH3 domains from Bax and Bak can bind to pro-apoptotic and anti-apoptotic Bcl-2 family members  in vitro.	bind
7871	3	2586	6	10	NULL	0	NULL	Bax	GP		bind			BH3 domain		Bcl-2 family members	GP	anti-apoptotic			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_currbiol_7_12_913_s_95	9382837	(a) BH3 domains from Bax and Bak can bind to pro-apoptotic and anti-apoptotic Bcl-2 family members  in vitro.	bind
7872	4	2586	6	10	NULL	0	NULL	Bak	GP		bind			BH3 domain		Bcl-2 family members	GP	anti-apoptotic			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_currbiol_7_12_913_s_95	9382837	(a) BH3 domains from Bax and Bak can bind to pro-apoptotic and anti-apoptotic Bcl-2 family members  in vitro.	bind
6886	1	2586	7	10	NULL	0	NULL	Bax	GP		bind			BH3 domain		Bcl-2 family members	GP	pro-apoptotic			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_currbiol_7_12_913_s_95	9382837	(a) BH3 domains from Bax and Bak can bind to pro-apoptotic and anti-apoptotic Bcl-2 family members  in vitro.	bind
6887	2	2586	7	10	NULL	0	NULL	Bak	GP		bind			BH3 domain		Bcl-2 family members	GP	pro-apoptotic			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_currbiol_7_12_913_s_95	9382837	(a) BH3 domains from Bax and Bak can bind to pro-apoptotic and anti-apoptotic Bcl-2 family members  in vitro.	bind
6888	3	2586	7	10	NULL	0	NULL	Bax	GP		bind			BH3 domain		Bcl-2 family members	GP	anti-apoptotic			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_currbiol_7_12_913_s_95	9382837	(a) BH3 domains from Bax and Bak can bind to pro-apoptotic and anti-apoptotic Bcl-2 family members  in vitro.	bind
6889	4	2586	7	10	NULL	0	NULL	Bak	GP		bind			BH3 domain		Bcl-2 family members	GP	anti-apoptotic			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_currbiol_7_12_913_s_95	9382837	(a) BH3 domains from Bax and Bak can bind to pro-apoptotic and anti-apoptotic Bcl-2 family members  in vitro.	bind
6018	1	2588	6	10	NULL	0	NULL	GCK	GP	endogenous	bind					TRAF6	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_9165_s_282	15456887	(A) Binding  of endogenous GCK to TRAF6.	bind
6890	1	2588	7	10	NULL	0	NULL	GCK	GP	endogenous	binds					TRAF6	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_9165_s_282	15456887	(A) Binding  of endogenous GCK to TRAF6.	bind
6019	1	2589	6	10	NULL	0	NULL	Tac1p-GST	GP		bind									GRE	NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_3_6_1639_s_122	15590837	(A) Binding  saturation of the DRE by Tac1p-GST.	bind
6891	1	2589	7	10	NULL	0	NULL	Tac1p-GST	GP		binds									DRE	NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_3_6_1639_s_122	15590837	(A) Binding  saturation of the DRE by Tac1p-GST.	bind
7873	1	2590	6	10	NULL	0	NULL	Paip1	GP		bind					PABP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3769_s_403	11997512	(A) binding activity of PABP ( 6,  24) and Paip1 interacts strongly with this region, additional experiments will be necessary to determine whether Paip1 binding to PABP affects the poly	bind
6892	1	2590	7	10	NULL	0	NULL	Paip1	GP		binds					PABP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3769_s_403	11997512	(A) binding activity of PABP ( 6,  24) and Paip1 interacts strongly with this region, additional experiments will be necessary to determine whether Paip1 binding to PABP affects the poly	bind
6020	1	2593	6	10	NULL	0	NULL	eIF4F	GP		bind					m7G cap	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_23_17740_s_17	10748132	(A) binding affinity of PABP and the m7G-cap binding affinity of eIF4F and eIF-iso4F ( 5,  6).	bind
6021	2	2593	6	10	NULL	0	NULL	eIF-iso4F	GP		bind					m7G cap	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_23_17740_s_17	10748132	(A) binding affinity of PABP and the m7G-cap binding affinity of eIF4F and eIF-iso4F ( 5,  6).	bind
6895	3	2593	7	10	NULL	0	NULL	m7G-cap	NucleicAcid		binds					eIF4F	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_23_17740_s_17	10748132	(A) binding affinity of PABP and the m7G-cap binding affinity of eIF4F and eIF-iso4F ( 5,  6).	bind
6896	4	2593	7	10	NULL	0	NULL	m7G-cap	NucleicAcid		binds					eIF-iso4F	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_23_17740_s_17	10748132	(A) binding affinity of PABP and the m7G-cap binding affinity of eIF4F and eIF-iso4F ( 5,  6).	bind
6022	1	2595	6	10	NULL	0	NULL	peptide	GP	synthetic	bind					MAb 15F3-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclinmicrobiol_39_3_977_s_108	11230414	(A) Binding assay of synthetic peptide with MAb 15F3-1.	bind
6897	1	2595	7	10	NULL	0	NULL	peptide	GP	synthetic	binds					MAb 15F3-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclinmicrobiol_39_3_977_s_108	11230414	(A) Binding assay of synthetic peptide with MAb 15F3-1.	bind
6023	1	2596	6	10	NULL	0	NULL	C5	GP	free	bind					p16	GP	S-tagged			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_3_421_s_176	9660926	(A) Binding between free C5 and S-tagged p16.	bind
6898	1	2596	7	10	NULL	0	NULL	C5	GP	free	binds					p16	GP	S-tagged			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_3_421_s_176	9660926	(A) Binding between free C5 and S-tagged p16.	bind
6024	1	2597	6	10	NULL	0	NULL	Nef	GP		bind					V1H	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_13_6_2045_s_156	12058068	(A) Binding between Nef and V1H, beta1, and beta2 using the yeast two hybrid liquid assay.	bind
6025	2	2597	6	10	NULL	0	NULL	Nef	GP		bind								beta2		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_13_6_2045_s_156	12058068	(A) Binding between Nef and V1H, beta1, and beta2 using the yeast two hybrid liquid assay.	bind
7874	3	2597	6	10	NULL	0	NULL	Nef	GP		bind								beta 1		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_13_6_2045_s_156	12058068	(A) Binding between Nef and V1H, beta1, and beta2 using the yeast two hybrid liquid assay.	bind
6899	1	2597	7	10	NULL	0	NULL	Nef	GP		binds					V1H	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_13_6_2045_s_156	12058068	(A) Binding between Nef and V1H, beta1, and beta2 using the yeast two hybrid liquid assay.	bind
6900	2	2597	7	10	NULL	0	NULL	Nef	GP		binds								beta1		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_13_6_2045_s_156	12058068	(A) Binding between Nef and V1H, beta1, and beta2 using the yeast two hybrid liquid assay.	bind
7936	3	2597	7	10	NULL	0	NULL	Nef 	GP		binds								beta2		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_13_6_2045_s_156	12058068	(A) Binding between Nef and V1H, beta1, and beta2 using the yeast two hybrid liquid assay.	bind
6026	1	2599	6	10	NULL	0	NULL	BAZF	GP		bind			148-319d27		Bcl6	GP		1-520		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_303_2_600_s_115	12659862	(A) Binding of  BAZF(148-319d27) deleted with the 27 aa including the conserved 17 aa to Bcl6(1-520)  by the mammalian two-hybrid assay.	bind
6901	1	2599	7	10	NULL	0	NULL	BAZF	GP		binds			148-319d27		Bcl6	GP		1-520		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_303_2_600_s_115	12659862	(A) Binding of  BAZF(148-319d27) deleted with the 27 aa including the conserved 17 aa to Bcl6(1-520)  by the mammalian two-hybrid assay.	bind
6027	1	2600	6	10	NULL	0	NULL	plectin	GP		bind			ABD		plectin 1C	GP		ABD		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
6028	2	2600	6	10	NULL	0	NULL	plectin	GP		bind			ABD					beta4		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
6029	3	2600	6	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
6030	4	2600	6	10	NULL	0	NULL	dystonin	GP		bind			ABD		plectin 1C	GP		ABD		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
6031	5	2600	6	10	NULL	0	NULL	dystonin	GP		bind			ABD					beta4		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
6032	6	2600	6	10	NULL	0	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
6033	7	2600	6	10	NULL	0	NULL	dystrophin	GP		bind			ABD		plectin 1C	GP		ABD		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
6034	8	2600	6	10	NULL	0	NULL	dystrophin	GP		bind			ABD					beta4		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
6035	9	2600	6	10	NULL	0	NULL	statement 7	Process		is an alternative to					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
6036	10	2600	6	10	NULL	0	NULL	alpha-actinin	GP		bind			ABD		plectin 1C	GP		ABD		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
6037	11	2600	6	10	NULL	0	NULL	alpha-actinin	GP		bind			ABD					beta4		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
6038	12	2600	6	10	NULL	0	NULL	statement 10	Process		is an alternative to					statement 11	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
6039	13	2600	6	10	NULL	0	NULL	utrophin	GP		bind			ABD		plectin 1C	GP		ABD		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
6040	14	2600	6	10	NULL	0	NULL	utrophin	GP		bind			ABD					beta4		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
6041	15	2600	6	10	NULL	0	NULL	statement 13	Process		is an alternative to					statement 14	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
6042	16	2600	6	10	NULL	0	NULL	filamin	GP		bind			ABD		plectin 1C	GP		ABD		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
6043	17	2600	6	10	NULL	0	NULL	filamin	GP		bind			ABD					beta4		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
6044	18	2600	6	10	NULL	0	NULL	statement 16	Process		is an alternative to					statement 17	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
7067	1	2600	7	10	NULL	0	NULL	plectin	GP		binds			ABD					beta4		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
7068	2	2600	7	10	NULL	0	NULL	plectin	GP		binds			ABD		plectin-1C	GP		ABD		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
7069	3	2600	7	10	NULL	0	NULL	dystonin	GP		binds			ABD					beta4		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
7070	4	2600	7	10	NULL	0	NULL	dystonin	GP		binds			ABD		plectin-1C	GP		ABD		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
7071	5	2600	7	10	NULL	0	NULL	dystrophin	GP		binds			ABD					beta4		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
7072	6	2600	7	10	NULL	0	NULL	dystrophin	GP		binds			ABD		plectin-1C	GP		ABD		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
7073	7	2600	7	10	NULL	0	NULL	alpha-actinin	GP		binds			ABD					beta4		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
7074	8	2600	7	10	NULL	0	NULL	alpha-actinin	GP		binds			ABD		plectin-1C	GP		ABD		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
7075	9	2600	7	10	NULL	0	NULL	utrophin	GP		binds			ABD					beta4		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
7076	10	2600	7	10	NULL	0	NULL	utrophin	GP		binds			ABD		plectin-1C	GP		ABD		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
7077	11	2600	7	10	NULL	0	NULL	filamin	GP		binds			ABD					beta4		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
7078	12	2600	7	10	NULL	0	NULL	filamin	GP		binds			ABD		plectin-1C	GP		ABD		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
46591	13	2600	7	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
46592	14	2600	7	10	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
46593	15	2600	7	10	NULL	0	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
46594	16	2600	7	10	NULL	0	NULL	statement 7	Process		is an alternative to					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
46595	17	2600	7	10	NULL	0	NULL	statement 9	Process		is an alternative to					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
46596	18	2600	7	10	NULL	0	NULL	statement 11	Process		is an alternative to					statement 12	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_10_4039_s_68	14517317	(A) Binding of ABDs of plectin, dystonin, dystrophin,  alpha-actinin, utrophin and filamin to either beta4 or the plectin-1C ABD.	bind
4576	1	2601	5	10	NULL	0	NULL	ActA peptide	GP		bind			DFPPPPTDEEL		Mena	GP		EVH1 domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_97_4_471_s_61	10338211	(A) Binding of ActA peptide (DFPPPPTDEEL) to the Mena EVH1 domain, measured using  a fluorescence perturbation assay.	bind
7079	1	2601	7	10	NULL	0	NULL	ActA peptide	GP		binds			DFPPPPTDEEL		Mena	GP		EVH1		NULL		NULL	NULL	NULL	NULL	gw60_cell_97_4_471_s_61	10338211	(A) Binding of ActA peptide (DFPPPPTDEEL) to the Mena EVH1 domain, measured using  a fluorescence perturbation assay.	bind
4578	1	2602	5	10	NULL	0	NULL	AIM2	GP		bind					GST-p202	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_474_1_38_s_145	10828447	(a) Binding of AIM2 to GST-p202.	bind
7080	1	2602	7	10	NULL	0	NULL	 AIM2	GP		binds					GST-p202	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_474_1_38_s_145	10828447	(a) Binding of AIM2 to GST-p202.	bind
4579	1	2603	5	10	NULL	0	NULL	AP-1	GP		bind					GST-Nef	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_22_1235_s_70	9811606	(a) Binding of AP-1 to GST-Nef fusion proteins.	bind
7081	1	2603	7	10	NULL	0	NULL	AP-1	GP		binds					GST-Nef	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_22_1235_s_70	9811606	(a) Binding of AP-1 to GST-Nef fusion proteins.	bind
4581	1	2605	5	10	NULL	0	NULL	B-cell nuclear extract proteins	GP		bind					mb-1	GP			distal region	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_24_8539_s_236	12446773	(A) Binding of B-cell nuclear extract proteins to the  mb-1 distal region is specifically inhibited by wild type, but not mutated  mb-1 promoter sequences.	bind
4582	2	2605	5	10	NULL	0	NULL	mb-1	GP	wild-type	inhibit		specifically		promoter	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_24_8539_s_236	12446773	(A) Binding of B-cell nuclear extract proteins to the  mb-1 distal region is specifically inhibited by wild type, but not mutated  mb-1 promoter sequences.	bind
4583	3	2605	5	10	NULL	0	NULL	mb-1	GP	mutant	does not inhibit				promoter sequences	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_24_8539_s_236	12446773	(A) Binding of B-cell nuclear extract proteins to the  mb-1 distal region is specifically inhibited by wild type, but not mutated  mb-1 promoter sequences.	bind
7083	1	2605	7	10	NULL	0	NULL	B-cell nuclear extract proteins	GP		binds 					 mb-1	GP			distal region	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_24_8539_s_236	12446773	(A) Binding of B-cell nuclear extract proteins to the  mb-1 distal region is specifically inhibited by wild type, but not mutated  mb-1 promoter sequences.	bind
7084	2	2605	7	10	NULL	0	NULL	statement 1	Process		 inhibited by		specifically			mb-1	GP	wild type		promoter sequences	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_24_8539_s_236	12446773	(A) Binding of B-cell nuclear extract proteins to the  mb-1 distal region is specifically inhibited by wild type, but not mutated  mb-1 promoter sequences.	bind
7085	3	2605	7	10	NULL	0	NULL	statement 1	Process		is not inhibited by					mb-1	GP	mutated		promoter sequences	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_24_8539_s_236	12446773	(A) Binding of B-cell nuclear extract proteins to the  mb-1 distal region is specifically inhibited by wild type, but not mutated  mb-1 promoter sequences.	bind
4584	1	2606	5	10	NULL	0	NULL	c-Src	GP		bind					mDia1	GP	active			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_18_6844_s_87	16943426	(A) Binding of c-Src by active mDia1.	bind
7086	1	2606	7	10	NULL	0	NULL	c-Src	GP		binds					mDia1	GP	active			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_18_6844_s_87	16943426	(A) Binding of c-Src by active mDia1.	bind
4585	1	2607	5	10	NULL	0	NULL	C/EBP	GP		bind									C/EBP-binding element	NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_3_907_s_102	12051744	(A) Binding of C/EBP  and C/EBP  to a C/EBP-binding element is increased after treatment with glucocorticoids.	bind
4586	2	2607	5	10	NULL	0	NULL	glucocorticoids	Chemical	treatment	increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_3_907_s_102	12051744	(A) Binding of C/EBP  and C/EBP  to a C/EBP-binding element is increased after treatment with glucocorticoids.	bind
7087	1	2607	7	10	NULL	0	NULL	C/EBP 	GP		binds to									C/EBP-binding element	NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_3_907_s_102	12051744	(A) Binding of C/EBP  and C/EBP  to a C/EBP-binding element is increased after treatment with glucocorticoids.	bind
7088	2	2607	7	10	NULL	0	NULL	glucocorticoids	Chemical	treatment with	increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_3_907_s_102	12051744	(A) Binding of C/EBP  and C/EBP  to a C/EBP-binding element is increased after treatment with glucocorticoids.	bind
4587	1	2608	5	10	NULL	0	NULL	c95A0 	GP		bind			c21		dystroglycan	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_4_755_s_158	8607994	(A) Binding of c95A0 c21 and c95A4 c21 to  -dystroglycan.	bind
4588	2	2608	5	10	NULL	0	NULL	c95A4 	GP		bind			c21		dystroglycan	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_4_755_s_158	8607994	(A) Binding of c95A0 c21 and c95A4 c21 to  -dystroglycan.	bind
7089	1	2608	7	10	NULL	0	NULL	c95A0	GP		binds			c21		dystroglycan	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_4_755_s_158	8607994	(A) Binding of c95A0 c21 and c95A4 c21 to  -dystroglycan.	bind
7090	2	2608	7	10	NULL	0	NULL	 c95A4 	GP		binds 			c21		dystroglycan	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_4_755_s_158	8607994	(A) Binding of c95A0 c21 and c95A4 c21 to  -dystroglycan.	bind
4678	1	2609	5	10	NULL	0	NULL	c95A0	GP		lack			c21					C-terminal 21 kDa		NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_4_755_s_193	8607994	(A) Binding of c95A0 c21 and c95A4 c21, lacking the most C-terminal 21 kDa, to chick muscle cells.	bind
4683	2	2609	5	10	NULL	0	NULL	statement 1	GP		bind					muscle cells	Cell	chick			NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_4_755_s_193	8607994	(A) Binding of c95A0 c21 and c95A4 c21, lacking the most C-terminal 21 kDa, to chick muscle cells.	bind
4684	3	2609	5	10	NULL	0	NULL	c95A4	GP		lack			c21					C-terminal 21 kDa		NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_4_755_s_193	8607994	(A) Binding of c95A0 c21 and c95A4 c21, lacking the most C-terminal 21 kDa, to chick muscle cells.	bind
4686	4	2609	5	10	NULL	0	NULL	statement 1	GP		bind					muscle cells	Cell	chick			NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_4_755_s_193	8607994	(A) Binding of c95A0 c21 and c95A4 c21, lacking the most C-terminal 21 kDa, to chick muscle cells.	bind
7091	1	2609	7	10	NULL	0	NULL	c95A0	GP		binds			c21		muscle cells	Cell	chick			NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_4_755_s_193	8607994	(A) Binding of c95A0 c21 and c95A4 c21, lacking the most C-terminal 21 kDa, to chick muscle cells.	bind
7092	2	2609	7	10	NULL	0	NULL	c95A4	GP		binds			c21		muscle cells	Cell	chick			NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_4_755_s_193	8607994	(A) Binding of c95A0 c21 and c95A4 c21, lacking the most C-terminal 21 kDa, to chick muscle cells.	bind
7093	3	2609	7	10	NULL	0	NULL	c95A0	GP		lacks								C-terminal 21 kDa		NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_4_755_s_193	8607994	(A) Binding of c95A0 c21 and c95A4 c21, lacking the most C-terminal 21 kDa, to chick muscle cells.	bind
7094	4	2609	7	10	NULL	0	NULL	c95A4	GP		lacks								C-terminal 21 kDa		NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_4_755_s_193	8607994	(A) Binding of c95A0 c21 and c95A4 c21, lacking the most C-terminal 21 kDa, to chick muscle cells.	bind
4689	1	2610	5	10	NULL	0	NULL	CCR1 antisera			bind					CCR1 receptor	GP	transfectants			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_2_112_s_49	9024623	(a) Binding of CCR1 antisera to CCR1 receptor transfectants.	bind
7095	1	2610	7	10	NULL	0	NULL	CCR1 antisera			binds					CCR1 receptor	GP	transfectant			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_2_112_s_49	9024623	(a) Binding of CCR1 antisera to CCR1 receptor transfectants.	bind
4692	1	2611	5	10	NULL	0	NULL	HCP	GP	cellular	bind					p58	GP	phosphotyrosyl peptides			NULL		NULL	NULL	NULL	NULL	gw60_immunity_4_1_77_s_138	8574854	(A) Binding of cellular HCP to p58 phosphotyrosyl peptides.	bind
7096	1	2611	7	10	NULL	0	NULL	HCP	GP	cellular	binds					p58	GP	phosphotyrosyl peptides			NULL		NULL	NULL	NULL	NULL	gw60_immunity_4_1_77_s_138	8574854	(A) Binding of cellular HCP to p58 phosphotyrosyl peptides.	bind
4693	1	2612	5	10	NULL	0	NULL	CIDR1alpha	GP		bind					Igs fragments	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_9_5412_s_162	15322039	(A) Binding of CIDR1alpha to human Igs and Ig fragments.	bind
4694	2	2612	5	10	NULL	0	NULL	CIDR1alpha	GP		bind					Ig fragments	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_9_5412_s_162	15322039	(A) Binding of CIDR1alpha to human Igs and Ig fragments.	bind
7097	1	2612	7	10	NULL	0	NULL	CIDR1alpha	GP		binds					Igs	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_9_5412_s_162	15322039	(A) Binding of CIDR1alpha to human Igs and Ig fragments.	bind
7098	2	2612	7	10	NULL	0	NULL	CIDR1alpha	GP		binds					Ig fragments	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_9_5412_s_162	15322039	(A) Binding of CIDR1alpha to human Igs and Ig fragments.	bind
4698	1	2613	5	10	NULL	0	NULL	CMV gB	GP		bind					DC-SIGN	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_5_653_s_177	12433371	(A) Binding of CMV gB to DC-SIGN.	bind
7099	1	2613	7	10	NULL	0	NULL	CMV gB	GP		binds					DC-SIGN	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_5_653_s_177	12433371	(A) Binding of CMV gB to DC-SIGN.	bind
4948	1	2614	5	10	NULL	0	NULL	EF-G	GP		bind					RC	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_87	12859902	(A) Binding of EF-G and GDP to RC Before and After Release of Peptide from the P-site tRNA with and without fus.	bind
4949	2	2614	5	10	NULL	0	NULL	peptide	AminoAcid		released from					tRNA	NucleicAcid		P-site		NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_87	12859902	(A) Binding of EF-G and GDP to RC Before and After Release of Peptide from the P-site tRNA with and without fus.	bind
4950	3	2614	5	10	NULL	0	NULL	statement 2	Process		occurs with					fus	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_87	12859902	(A) Binding of EF-G and GDP to RC Before and After Release of Peptide from the P-site tRNA with and without fus.	bind
4951	4	2614	5	10	NULL	0	NULL	statement 2	Process		occurs without					fus	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_87	12859902	(A) Binding of EF-G and GDP to RC Before and After Release of Peptide from the P-site tRNA with and without fus.	bind
4952	5	2614	5	10	NULL	0	NULL	statement 1	Process		occurs before					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_87	12859902	(A) Binding of EF-G and GDP to RC Before and After Release of Peptide from the P-site tRNA with and without fus.	bind
4953	6	2614	5	10	NULL	0	NULL	statement 1	Process		occurs after					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_87	12859902	(A) Binding of EF-G and GDP to RC Before and After Release of Peptide from the P-site tRNA with and without fus.	bind
4954	7	2614	5	10	NULL	0	NULL	GDP	Chemical		bind					RC	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_87	12859902	(A) Binding of EF-G and GDP to RC Before and After Release of Peptide from the P-site tRNA with and without fus.	bind
4955	8	2614	5	10	NULL	0	NULL	statement 7	NULL		occurs before	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_87	12859902	(A) Binding of EF-G and GDP to RC Before and After Release of Peptide from the P-site tRNA with and without fus.	bind
4956	9	2614	5	10	NULL	0	NULL	statement 7	NULL		occurs after	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_87	12859902	(A) Binding of EF-G and GDP to RC Before and After Release of Peptide from the P-site tRNA with and without fus.	bind
7100	1	2614	7	10	NULL	0	NULL	EF-G	GP		binds					RC	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_87	12859902	(A) Binding of EF-G and GDP to RC Before and After Release of Peptide from the P-site tRNA with and without fus.	bind
7101	2	2614	7	10	NULL	0	NULL	GDP	Chemical		binds					RC	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_87	12859902	(A) Binding of EF-G and GDP to RC Before and After Release of Peptide from the P-site tRNA with and without fus.	bind
7102	3	2614	7	10	NULL	0	NULL	statement 1	Process		occurs before					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_87	12859902	(A) Binding of EF-G and GDP to RC Before and After Release of Peptide from the P-site tRNA with and without fus.	bind
7103	4	2614	7	10	NULL	0	NULL	statement 1	Process		occurs after					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_87	12859902	(A) Binding of EF-G and GDP to RC Before and After Release of Peptide from the P-site tRNA with and without fus.	bind
7110	5	2614	7	10	NULL	0	NULL	peptide	AminoAcid		release from					tRNA	NucleicAcid		P-site 		NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_87	12859902	(A) Binding of EF-G and GDP to RC Before and After Release of Peptide from the P-site tRNA with and without fus.	bind
7112	6	2614	7	10	NULL	0	NULL	statement 2	Process		occurs before					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_87	12859902	(A) Binding of EF-G and GDP to RC Before and After Release of Peptide from the P-site tRNA with and without fus.	bind
7115	7	2614	7	10	NULL	0	NULL	statement 2	Process		occurs after					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_87	12859902	(A) Binding of EF-G and GDP to RC Before and After Release of Peptide from the P-site tRNA with and without fus.	bind
4707	1	2615	5	10	NULL	0	NULL	M-280 protein A Dynabeads			coated with					2D VCAM-1 - Fc	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_6_1073_s_130	16365170	(A) Binding of either wt or Y991A alpha4beta1-expressing cells to M-280 protein A Dynabeads coated with 2D VCAM-1 - Fc. Relative  bead binding was determined by side scattering analysis.	bind
4709	2	2615	5	10	NULL	0	NULL	alpha4beta1-expressing cells	Cell	wt	bind					statement 1					NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_6_1073_s_130	16365170	(A) Binding of either wt or Y991A alpha4beta1-expressing cells to M-280 protein A Dynabeads coated with 2D VCAM-1 - Fc. Relative  bead binding was determined by side scattering analysis.	bind
4711	3	2615	5	10	NULL	0	NULL	alpha4beta1-expressing cells	Cell		bind			Y991A		statement 1					NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_6_1073_s_130	16365170	(A) Binding of either wt or Y991A alpha4beta1-expressing cells to M-280 protein A Dynabeads coated with 2D VCAM-1 - Fc. Relative  bead binding was determined by side scattering analysis.	bind
4712	4	2615	5	10	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_6_1073_s_130	16365170	(A) Binding of either wt or Y991A alpha4beta1-expressing cells to M-280 protein A Dynabeads coated with 2D VCAM-1 - Fc. Relative  bead binding was determined by side scattering analysis.	bind
7122	1	2615	7	10	NULL	0	NULL	alpha4beta1-expressing cells	Cell	wt	binds					M-280 protein A dynabeads					NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_6_1073_s_130	16365170	(A) Binding of either wt or Y991A alpha4beta1-expressing cells to M-280 protein A Dynabeads coated with 2D VCAM-1 - Fc. Relative  bead binding was determined by side scattering analysis.	bind
7124	2	2615	7	10	NULL	0	NULL	M-280 protein A Dynabeads			is coated with					2D VCAM-1 - Fc	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_6_1073_s_130	16365170	(A) Binding of either wt or Y991A alpha4beta1-expressing cells to M-280 protein A Dynabeads coated with 2D VCAM-1 - Fc. Relative  bead binding was determined by side scattering analysis.	bind
7125	3	2615	7	10	NULL	0	NULL	alpha4beta1-expressing cells	Cell		binds			 Y991A		M-280 protein A dynabeads					NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_6_1073_s_130	16365170	(A) Binding of either wt or Y991A alpha4beta1-expressing cells to M-280 protein A Dynabeads coated with 2D VCAM-1 - Fc. Relative  bead binding was determined by side scattering analysis.	bind
4790	1	2616	5	10	NULL	0	NULL	En2deltaSP	GP		bind									HF1 site	NULL		NULL	NULL	NULL	NULL	gw60_development_130_9_1867_s_84	12642491	(A) Binding of En2deltaSP and Foxa2 to the HF1 site.	bind
4791	2	2616	5	10	NULL	0	NULL	Foxa2	GP		bind									HF1 site	NULL		NULL	NULL	NULL	NULL	gw60_development_130_9_1867_s_84	12642491	(A) Binding of En2deltaSP and Foxa2 to the HF1 site.	bind
7126	1	2616	7	10	NULL	0	NULL	En2deltaSP	GP		binds to									HF1 site	NULL		NULL	NULL	NULL	NULL	gw60_development_130_9_1867_s_84	12642491	(A) Binding of En2deltaSP and Foxa2 to the HF1 site.	bind
7127	2	2616	7	10	NULL	0	NULL	Foxa2	GP		binds to									HF1 site	NULL		NULL	NULL	NULL	NULL	gw60_development_130_9_1867_s_84	12642491	(A) Binding of En2deltaSP and Foxa2 to the HF1 site.	bind
4807	1	2617	5	10	NULL	0	NULL	FGF10	GP		bind					HSPG	GP				NULL	lung epithelial cells	NULL	NULL	NULL	NULL	gw70_devbiol_258_1_185_s_123	12781692	(A) Binding of FGF10 to HSPG is increased when compared with FGF7 in confluent  20-3 lung epithelial cells; however, binding to FGFR2 is similar for both FGFs (see  Materials and methods).	bind
4808	2	2617	5	10	NULL	0	NULL	FGF7	GP		bind					HSPG	GP				NULL	lung epithelial cells	NULL	NULL	NULL	NULL	gw70_devbiol_258_1_185_s_123	12781692	(A) Binding of FGF10 to HSPG is increased when compared with FGF7 in confluent  20-3 lung epithelial cells; however, binding to FGFR2 is similar for both FGFs (see  Materials and methods).	bind
4810	3	2617	5	10	NULL	0	NULL	FGF10	GP		bind					FGFR2	GP				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_258_1_185_s_123	12781692	(A) Binding of FGF10 to HSPG is increased when compared with FGF7 in confluent  20-3 lung epithelial cells; however, binding to FGFR2 is similar for both FGFs (see  Materials and methods).	bind
4811	4	2617	5	10	NULL	0	NULL	FGF7	GP		bind					FGFR2	GP				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_258_1_185_s_123	12781692	(A) Binding of FGF10 to HSPG is increased when compared with FGF7 in confluent  20-3 lung epithelial cells; however, binding to FGFR2 is similar for both FGFs (see  Materials and methods).	bind
54107	5	2617	5	10	NULL	0	NULL	statement 3	Process		is similar to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_258_1_185_s_123	12781692	(A) Binding of FGF10 to HSPG is increased when compared with FGF7 in confluent  20-3 lung epithelial cells; however, binding to FGFR2 is similar for both FGFs (see  Materials and methods).	bind
7151	1	2617	7	10	NULL	0	NULL	FGF10	GP		binds					 HSPG	GP				NULL	confluent 20-3 lung epithelial cells	NULL	NULL	NULL	NULL	gw70_devbiol_258_1_185_s_123	12781692	(A) Binding of FGF10 to HSPG is increased when compared with FGF7 in confluent  20-3 lung epithelial cells; however, binding to FGFR2 is similar for both FGFs (see  Materials and methods).	bind
7152	2	2617	7	10	NULL	0	NULL	FGF7	GP		binds					HSPG	GP				NULL	confluent 20-3 lung epithelial cells	NULL	NULL	NULL	NULL	gw70_devbiol_258_1_185_s_123	12781692	(A) Binding of FGF10 to HSPG is increased when compared with FGF7 in confluent  20-3 lung epithelial cells; however, binding to FGFR2 is similar for both FGFs (see  Materials and methods).	bind
7154	3	2617	7	10	NULL	0	NULL	FGF10	GP		binds to					FGFR2	GP				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_258_1_185_s_123	12781692	(A) Binding of FGF10 to HSPG is increased when compared with FGF7 in confluent  20-3 lung epithelial cells; however, binding to FGFR2 is similar for both FGFs (see  Materials and methods).	bind
7155	4	2617	7	10	NULL	0	NULL	FGF7	GP		binds to					FGFR2	GP				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_258_1_185_s_123	12781692	(A) Binding of FGF10 to HSPG is increased when compared with FGF7 in confluent  20-3 lung epithelial cells; however, binding to FGFR2 is similar for both FGFs (see  Materials and methods).	bind
54108	5	2617	7	10	NULL	0	NULL	statement 3	Process		is similar to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_258_1_185_s_123	12781692	(A) Binding of FGF10 to HSPG is increased when compared with FGF7 in confluent  20-3 lung epithelial cells; however, binding to FGFR2 is similar for both FGFs (see  Materials and methods).	bind
4819	1	2619	5	10	NULL	0	NULL	GAGA protein	GP		bind					iab-7	GP			PRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1311_s_159	11158316	(A) Binding of GAGA protein to the  iab-7 PRE.	bind
7156	1	2619	7	10	NULL	0	NULL	GAGA protein	GP		binds					iab-7	GP			PRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1311_s_159	11158316	(A) Binding of GAGA protein to the  iab-7 PRE.	bind
4820	1	2620	5	10	NULL	0	NULL	Rab9	GP	GST	bind					EEA1	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
4821	2	2620	5	10	NULL	0	NULL	Rab9	GP	GST	bind					rabaptin-5	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
4822	3	2620	5	10	NULL	0	NULL	Rab5	GP	GST	bind					EEA1	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
4823	4	2620	5	10	NULL	0	NULL	Rab5	GP	GST	bind					rabaptin-5	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
4824	5	2620	5	10	NULL	0	NULL	Rab9/5	GP	GST	bind					EEA1	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
4825	6	2620	5	10	NULL	0	NULL	Rab9/5	GP	GST 	bind					rabaptin-5	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
4826	7	2620	5	10	NULL	0	NULL	Rab5/9	GP	GST	bind					EEA1	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
4827	8	2620	5	10	NULL	0	NULL	Rab5/9	GP	GST	bind					rabaptin-5	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
46242	9	2620	5	10	NULL	0	NULL	EEA1	GP		is a type of					Rab5 effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
46243	10	2620	5	10	NULL	0	NULL	rabaptin-5	GP		is a type of					Rab5 effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
7157	1	2620	7	10	NULL	0	NULL	Rab9	GP	GST	binds					EEA1 	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
7158	2	2620	7	10	NULL	0	NULL	Rab9	GP	GST	binds					rabaptin-5	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
7159	3	2620	7	10	NULL	0	NULL	Rab5	GP	GST	binds					EEA1 	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
7160	4	2620	7	10	NULL	0	NULL	Rab5	GP	GST	binds					rabaptin-5	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
7161	5	2620	7	10	NULL	0	NULL	Rab9/5	GP	GST	binds					EEA1 	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
7162	6	2620	7	10	NULL	0	NULL	Rab9/5	GP	GST	binds					rabaptin-5	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
7163	7	2620	7	10	NULL	0	NULL	Rab5/9	GP	GST	binds					EEA1 	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
7164	8	2620	7	10	NULL	0	NULL	Rab5/9	GP	GST	binds					rabaptin-5	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
46244	9	2620	7	10	NULL	0	NULL	EEA1	GP		is a type of					Rab5 effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
46245	10	2620	7	10	NULL	0	NULL	rabaptin-5	GP		is a type of					Rab5 effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_77	16769818	(A) Binding of GST versions of Rab9, Rab5, Rab9/5, and Rab5/9 to Rab5 effectors EEA1  and rabaptin-5 from cytosol.	bind
4828	1	2621	5	10	NULL	0	NULL	GTP	Chemical		bind					Rac	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_5_1571_s_121	12054696	(A) Binding of GST-PAK2-RBD to the GTP-bound form of Rac.	bind
46246	2	2621	5	10	NULL	0	NULL	GST-PAK2	GP		bind			RBD		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_5_1571_s_121	12054696	(A) Binding of GST-PAK2-RBD to the GTP-bound form of Rac.	bind
7167	1	2621	7	10	NULL	0	NULL	GTP	Chemical		bind					Rac	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_5_1571_s_121	12054696	(A) Binding of GST-PAK2-RBD to the GTP-bound form of Rac.	bind
46248	2	2621	7	10	NULL	0	NULL	GST-PAK2	GP		bind			RBD		statement1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_5_1571_s_121	12054696	(A) Binding of GST-PAK2-RBD to the GTP-bound form of Rac.	bind
4829	1	2622	5	10	NULL	0	NULL	GST-s-synaphin	GP		bind					r-syntaxin	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_cell_104_3_421_s_54	11239399	(A) Binding of GST-s-synaphin to recombinant r-syntaxin in the presence or absence of r-SNAP-25 (1 muM) and/or r-synaptobrevin 2 (2 muM), or both.	bind
7168	1	2622	7	10	NULL	0	NULL	GST-s-synaphin	GP		binds					r-syntaxin	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_cell_104_3_421_s_54	11239399	(A) Binding of GST-s-synaphin to recombinant r-syntaxin in the presence or absence of r-SNAP-25 (1 muM) and/or r-synaptobrevin 2 (2 muM), or both.	bind
4839	1	2623	5	10	NULL	0	NULL	hMutS	GP		bind					substrates	GP	containing two-nucleotide loops			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_9_1181_s_51	8805365	(a) Binding of hMutS  and hMutS  to substrates containing two-nucleotide loops.	bind
7170	1	2623	7	10	NULL	0	NULL	hMutS	GP		binds to					substrates	GP	containing two-nucleotide loops			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_9_1181_s_51	8805365	(a) Binding of hMutS  and hMutS  to substrates containing two-nucleotide loops.	bind
4841	1	2624	5	10	NULL	0	NULL	IL-15 IgG 2b	GP		bind					PMN	Cell				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_6_2640_s_109	9596728	(A) Binding of IL-15 IgG 2b fusion protein to PMN.	bind
46254	2	2624	5	10	NULL	0	NULL	IL-15 IgG 2b	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_6_2640_s_109	9596728	(A) Binding of IL-15 IgG 2b fusion protein to PMN.	bind
7171	1	2624	7	10	NULL	0	NULL	IL-15 IgG 2b	GP		binds					PMN	Cell				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_6_2640_s_109	9596728	(A) Binding of IL-15 IgG 2b fusion protein to PMN.	bind
46255	2	2624	7	10	NULL	0	NULL	IL-15 IgG 2b	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_6_2640_s_109	9596728	(A) Binding of IL-15 IgG 2b fusion protein to PMN.	bind
4842	1	2626	5	NULL	NULL	0	NULL		NULL	isolated	bind	NULL		PDZ domains		PIP2 micelles	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_9_6_1215_s_133	12086619	(A) Binding of isolated PDZ domains to PIP2 micelles.	bind
7172	1	2626	7	NULL	NULL	0	NULL		NULL	isolated	binds	NULL		PDZ domains		PIP2 micelles	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_9_6_1215_s_133	12086619	(A) Binding of isolated PDZ domains to PIP2 micelles.	bind
4843	1	2627	5	10	NULL	0	NULL	JSAP1	GP		bind					MAPKKKs	GP	mammalian			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7539_s_285	10523642	(A) Binding of JSAP1 to mammalian MAPKKKs.	bind
7173	1	2627	7	10	NULL	0	NULL	JSAP1	GP		binds to					MAPKKK	GP	mammalian			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7539_s_285	10523642	(A) Binding of JSAP1 to mammalian MAPKKKs.	bind
4846	1	2630	5	10	NULL	0	NULL	lens cell extracts	Cell		bind					zeta ZPE	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2067_s_150	9528779	(a) Binding of lens cell extracts and recombinant Pax6 proteins to the zeta ZPE.	bind
4847	2	2630	5	10	NULL	0	NULL	Pax6 protein	GP	recombinant	bind					zeta ZPE	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2067_s_150	9528779	(a) Binding of lens cell extracts and recombinant Pax6 proteins to the zeta ZPE.	bind
7186	1	2630	7	10	NULL	0	NULL	lens cell extracts	Cell		binds					 zeta ZPE	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2067_s_150	9528779	(a) Binding of lens cell extracts and recombinant Pax6 proteins to the zeta ZPE.	bind
7187	2	2630	7	10	NULL	0	NULL	Pax6	GP	recombinant	binds					zeta ZPE	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2067_s_150	9528779	(a) Binding of lens cell extracts and recombinant Pax6 proteins to the zeta ZPE.	bind
4848	1	2631	5	10	NULL	0	NULL	Mbt	GP		bind					Rho-type GTPases	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_130_3_427_s_171	12490550	(A) Binding of Mbt to Rho-type GTPases.	bind
7188	1	2631	7	10	NULL	0	NULL	Mbt	GP		binds					Rho-type GTPases	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_130_3_427_s_171	12490550	(A) Binding of Mbt to Rho-type GTPases.	bind
4849	1	2632	5	10	NULL	0	NULL	LGN	GP	mouse	bind					heterotrimeric G-proteins	GP	Galpha subunits of			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3144_s_251	12925752	(A) Binding of mouse LGN to Galpha subunits of  heterotrimeric G-proteins.	bind
7189	1	2632	7	10	NULL	0	NULL	LGN	GP	mouse	binds					heterotrimeric G-proteins	GP	Galpha subunits of 			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3144_s_251	12925752	(A) Binding of mouse LGN to Galpha subunits of  heterotrimeric G-proteins.	bind
4850	1	2633	5	10	NULL	0	NULL	myosin-VIIa	GP		bind			tail		GST	Chemical	purified			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_163_3_559_s_122	14610058	(A) Binding of myosin-VIIa tail (left) or myosin-Va (middle) to purified GST or GST  - MyRIP constructs immobilized on glutathione - Sepharose beads.	bind
4851	2	2633	5	10	NULL	0	NULL	myosin-Va	GP		bind					GST	Chemical	purified			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_163_3_559_s_122	14610058	(A) Binding of myosin-VIIa tail (left) or myosin-Va (middle) to purified GST or GST  - MyRIP constructs immobilized on glutathione - Sepharose beads.	bind
4852	3	2633	5	10	NULL	0	NULL	myosin-VIIa	GP		bind			tail		GST - MyRIP	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_163_3_559_s_122	14610058	(A) Binding of myosin-VIIa tail (left) or myosin-Va (middle) to purified GST or GST  - MyRIP constructs immobilized on glutathione - Sepharose beads.	bind
4853	4	2633	5	10	NULL	0	NULL	myosin-Va	GP		bind					GST - MyRIP	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_163_3_559_s_122	14610058	(A) Binding of myosin-VIIa tail (left) or myosin-Va (middle) to purified GST or GST  - MyRIP constructs immobilized on glutathione - Sepharose beads.	bind
7281	1	2633	7	10	NULL	0	NULL	myosin-VIIa	GP		binds			tail		GST	Chemical	purified			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_163_3_559_s_122	14610058	(A) Binding of myosin-VIIa tail (left) or myosin-Va (middle) to purified GST or GST  - MyRIP constructs immobilized on glutathione - Sepharose beads.	bind
7282	2	2633	7	10	NULL	0	NULL	myosin-VIIa	GP		binds			tail		GST - MyRIP	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_163_3_559_s_122	14610058	(A) Binding of myosin-VIIa tail (left) or myosin-Va (middle) to purified GST or GST  - MyRIP constructs immobilized on glutathione - Sepharose beads.	bind
7283	3	2633	7	10	NULL	0	NULL	myosin-Va	GP		binds					GST	Chemical	purified			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_163_3_559_s_122	14610058	(A) Binding of myosin-VIIa tail (left) or myosin-Va (middle) to purified GST or GST  - MyRIP constructs immobilized on glutathione - Sepharose beads.	bind
7284	4	2633	7	10	NULL	0	NULL	myosin-Va	GP		binds					GST - MyRIP	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_163_3_559_s_122	14610058	(A) Binding of myosin-VIIa tail (left) or myosin-Va (middle) to purified GST or GST  - MyRIP constructs immobilized on glutathione - Sepharose beads.	bind
4854	1	2634	5	10	NULL	0	NULL	n-sec1	GP		bind					syntaxin 1a	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_6_1229_s_88	8663999	(A) Binding of n-sec1 to syntaxin 1a in the absence of NO.	bind
4855	2	2634	5	10	NULL	0	NULL	statement 1	GP		in the absence of					NO	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_6_1229_s_88	8663999	(A) Binding of n-sec1 to syntaxin 1a in the absence of NO.	bind
7285	1	2634	7	10	NULL	0	NULL	 n-sec1	GP		binds to					syntaxin 1a	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_6_1229_s_88	8663999	(A) Binding of n-sec1 to syntaxin 1a in the absence of NO.	bind
7286	2	2634	7	10	NULL	0	NULL	statement 1	Process		occurs in the absence of					NO	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_6_1229_s_88	8663999	(A) Binding of n-sec1 to syntaxin 1a in the absence of NO.	bind
5565	1	2635	5	10	NULL	0	NULL	NusA	GP		bind					N. NusA	GP	deletion mutants of	amino-terminal		NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_133	9659923	(A) Binding of NusA and RNAP to amino-terminal deletion mutants of N. NusA (lane 2) or RNAP (lane 10) was loaded onto 0.5 mg/ml GST, GST-N73-107, GST-N58-107, GST-N48-107, GST-N34-107, GST-N23-107, and GST-N columns (as indicated).	bind
5567	2	2635	5	10	NULL	0	NULL	NusA	GP		bind					RNAP	GP	deletion mutants of	amino-terminal		NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_133	9659923	(A) Binding of NusA and RNAP to amino-terminal deletion mutants of N. NusA (lane 2) or RNAP (lane 10) was loaded onto 0.5 mg/ml GST, GST-N73-107, GST-N58-107, GST-N48-107, GST-N34-107, GST-N23-107, and GST-N columns (as indicated).	bind
5568	3	2635	5	10	NULL	0	NULL	RNAP	GP		bind					N. NusA	GP	deletion mutants of	amino-terminal 		NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_133	9659923	(A) Binding of NusA and RNAP to amino-terminal deletion mutants of N. NusA (lane 2) or RNAP (lane 10) was loaded onto 0.5 mg/ml GST, GST-N73-107, GST-N58-107, GST-N48-107, GST-N34-107, GST-N23-107, and GST-N columns (as indicated).	bind
5570	4	2635	5	10	NULL	0	NULL	RNAP	GP		bind					RNAP	GP	deletion mutants of	amino-terminal 		NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_133	9659923	(A) Binding of NusA and RNAP to amino-terminal deletion mutants of N. NusA (lane 2) or RNAP (lane 10) was loaded onto 0.5 mg/ml GST, GST-N73-107, GST-N58-107, GST-N48-107, GST-N34-107, GST-N23-107, and GST-N columns (as indicated).	bind
7287	1	2635	7	10	NULL	0	NULL	NusA	GP		binds					N. NusA	GP	deletion mutants of	amino-terminal 		NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_133	9659923	(A) Binding of NusA and RNAP to amino-terminal deletion mutants of N. NusA (lane 2) or RNAP (lane 10) was loaded onto 0.5 mg/ml GST, GST-N73-107, GST-N58-107, GST-N48-107, GST-N34-107, GST-N23-107, and GST-N columns (as indicated).	bind
7288	2	2635	7	10	NULL	0	NULL	RNAP	GP		binds					N. NusA	GP	deletion mutants of	amino-terminal 		NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_133	9659923	(A) Binding of NusA and RNAP to amino-terminal deletion mutants of N. NusA (lane 2) or RNAP (lane 10) was loaded onto 0.5 mg/ml GST, GST-N73-107, GST-N58-107, GST-N48-107, GST-N34-107, GST-N23-107, and GST-N columns (as indicated).	bind
7289	3	2635	7	10	NULL	0	NULL	NusA	GP		binds					RNAP	GP	deletion mutants of	amino-terminal 		NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_133	9659923	(A) Binding of NusA and RNAP to amino-terminal deletion mutants of N. NusA (lane 2) or RNAP (lane 10) was loaded onto 0.5 mg/ml GST, GST-N73-107, GST-N58-107, GST-N48-107, GST-N34-107, GST-N23-107, and GST-N columns (as indicated).	bind
7290	4	2635	7	10	NULL	0	NULL	RNAP	GP		binds					RNAP	GP	deletion mutants of	amino-terminal		NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_133	9659923	(A) Binding of NusA and RNAP to amino-terminal deletion mutants of N. NusA (lane 2) or RNAP (lane 10) was loaded onto 0.5 mg/ml GST, GST-N73-107, GST-N58-107, GST-N48-107, GST-N34-107, GST-N23-107, and GST-N columns (as indicated).	bind
5269	1	2636	5	10	NULL	0	NULL	p34 cdc2	GP		bind					CksHs2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_3659_s_214	9632748	(A) Binding of p34 cdc2 and cyclin B to CksHs2-Sepharose beads.	bind
5270	2	2636	5	10	NULL	0	NULL	cyclin B	GP		bind					CksHs2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_3659_s_214	9632748	(A) Binding of p34 cdc2 and cyclin B to CksHs2-Sepharose beads.	bind
7291	1	2636	7	10	NULL	0	NULL	p34 cdc2	GP		binds					CksHs2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_3659_s_214	9632748	(A) Binding of p34 cdc2 and cyclin B to CksHs2-Sepharose beads.	bind
7292	2	2636	7	10	NULL	0	NULL	cyclin B	GP		binds					CksHs2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_3659_s_214	9632748	(A) Binding of p34 cdc2 and cyclin B to CksHs2-Sepharose beads.	bind
5271	1	2637	5	10	NULL	0	NULL	pb2-DHFR	GP		bind					mitochondria	CellComponent	mutant			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1509_1_86_s_128	11118520	(A) Binding of pb2-DHFR with mutant mitochondria (MITO) and mitoplasts (MTP) in the absence of the inner membrane potential (-   ).	bind
5272	2	2637	5	10	NULL	0	NULL	statement 1	Process		in the absence of					inner membrane potential					NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1509_1_86_s_128	11118520	(A) Binding of pb2-DHFR with mutant mitochondria (MITO) and mitoplasts (MTP) in the absence of the inner membrane potential (-   ).	bind
5273	3	2637	5	10	NULL	0	NULL	pb2-DHFR	GP		bind					mitoplasts	CellComponent	mutant			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1509_1_86_s_128	11118520	(A) Binding of pb2-DHFR with mutant mitochondria (MITO) and mitoplasts (MTP) in the absence of the inner membrane potential (-   ).	bind
5274	4	2637	5	10	NULL	0	NULL	statement 3	Process		in the absence of					inner membrane potential					NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1509_1_86_s_128	11118520	(A) Binding of pb2-DHFR with mutant mitochondria (MITO) and mitoplasts (MTP) in the absence of the inner membrane potential (-   ).	bind
54130	5	2637	5	10	NULL	0	NULL	MITO	CellComponent		is					mitochondria	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1509_1_86_s_128	11118520	(A) Binding of pb2-DHFR with mutant mitochondria (MITO) and mitoplasts (MTP) in the absence of the inner membrane potential (-   ).	bind
54131	6	2637	5	10	NULL	0	NULL	MTP	CellComponent		is					mitoplast	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1509_1_86_s_128	11118520	(A) Binding of pb2-DHFR with mutant mitochondria (MITO) and mitoplasts (MTP) in the absence of the inner membrane potential (-   ).	bind
7293	1	2637	7	10	NULL	0	NULL	pb2-DHFR	GP		binds					mitochondria	CellComponent	mutant			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1509_1_86_s_128	11118520	(A) Binding of pb2-DHFR with mutant mitochondria (MITO) and mitoplasts (MTP) in the absence of the inner membrane potential (-   ).	bind
7294	2	2637	7	10	NULL	0	NULL	pb2-DHFR	GP		binds					mitoplasts	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1509_1_86_s_128	11118520	(A) Binding of pb2-DHFR with mutant mitochondria (MITO) and mitoplasts (MTP) in the absence of the inner membrane potential (-   ).	bind
7295	3	2637	7	10	NULL	0	NULL	MITO	CellComponent		is					mitochondria	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1509_1_86_s_128	11118520	(A) Binding of pb2-DHFR with mutant mitochondria (MITO) and mitoplasts (MTP) in the absence of the inner membrane potential (-   ).	bind
7296	4	2637	7	10	NULL	0	NULL	MTP	CellComponent		is					mitoplasts	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1509_1_86_s_128	11118520	(A) Binding of pb2-DHFR with mutant mitochondria (MITO) and mitoplasts (MTP) in the absence of the inner membrane potential (-   ).	bind
54132	5	2637	7	10	NULL	0	NULL	statement 1	Process		occurs in the absence of					inner membrane potential					NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1509_1_86_s_128	11118520	(A) Binding of pb2-DHFR with mutant mitochondria (MITO) and mitoplasts (MTP) in the absence of the inner membrane potential (-   ).	bind
54133	6	2637	7	10	NULL	0	NULL	statement 2	Process		occurs in the absence of					inner membrane potential					NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1509_1_86_s_128	11118520	(A) Binding of pb2-DHFR with mutant mitochondria (MITO) and mitoplasts (MTP) in the absence of the inner membrane potential (-   ).	bind
5275	1	2638	5	10	NULL	0	NULL	PP1	GP		bind					AKAP149	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_6_1251_s_163	10995432	(A) Binding of PP1 to AKAP149.	bind
7297	1	2638	7	10	NULL	0	NULL	PP1	GP		binds					AKAP149	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_6_1251_s_163	10995432	(A) Binding of PP1 to AKAP149.	bind
5276	1	2639	5	10	NULL	0	NULL	pRb	GP		bind					GST-CBFA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_303_s_205	11545733	(A) Binding of pRb and tumor-derived mutants expressed in Cos cells to GST-CBFA1 or GST.	bind
5277	2	2639	5	10	NULL	0	NULL	pRb	GP		bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_303_s_205	11545733	(A) Binding of pRb and tumor-derived mutants expressed in Cos cells to GST-CBFA1 or GST.	bind
5278	3	2639	5	10	NULL	0	NULL	tumor-derived mutants	GP	expressed in Cos cells	bind					GST-CBFA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_303_s_205	11545733	(A) Binding of pRb and tumor-derived mutants expressed in Cos cells to GST-CBFA1 or GST.	bind
5279	4	2639	5	10	NULL	0	NULL	tumor-derived mutants	GP	expressed in Cos cells	bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_303_s_205	11545733	(A) Binding of pRb and tumor-derived mutants expressed in Cos cells to GST-CBFA1 or GST.	bind
7298	1	2639	7	10	NULL	0	NULL	pRb	GP		binds					GST-CBFA1 	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_303_s_205	11545733	(A) Binding of pRb and tumor-derived mutants expressed in Cos cells to GST-CBFA1 or GST.	bind
7299	2	2639	7	10	NULL	0	NULL	pRb	GP		binds					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_303_s_205	11545733	(A) Binding of pRb and tumor-derived mutants expressed in Cos cells to GST-CBFA1 or GST.	bind
7300	3	2639	7	10	NULL	0	NULL	tumor-derived mutants	GP	expressed in cos cells	binds to					GST-CBFA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_303_s_205	11545733	(A) Binding of pRb and tumor-derived mutants expressed in Cos cells to GST-CBFA1 or GST.	bind
7301	4	2639	7	10	NULL	0	NULL	tumor-derived mutants	GP	expressed in cos cells	binds					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_303_s_205	11545733	(A) Binding of pRb and tumor-derived mutants expressed in Cos cells to GST-CBFA1 or GST.	bind
5280	2	2640	5	10	NULL	0	NULL	olfactory epithelial nuclear proteins	GP	rat	bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_72_1_65_s_104	10521600	(A) Binding of rat olfactory epithelial nuclear proteins with putative NFI-binding sites from genes expressed abundantly within the olfactory epithelium.	bind
5281	1	2640	5	10	NULL	0	NULL	genes	GP		is expressed		abundantly		NFI-binding sites	olfactory epithelium	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_72_1_65_s_104	10521600	(A) Binding of rat olfactory epithelial nuclear proteins with putative NFI-binding sites from genes expressed abundantly within the olfactory epithelium.	bind
7302	1	2640	7	10	NULL	0	NULL	olfactory epithelial nuclear proteins	GP	rat	binds							putative		NFI-binding sites	NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_72_1_65_s_104	10521600	(A) Binding of rat olfactory epithelial nuclear proteins with putative NFI-binding sites from genes expressed abundantly within the olfactory epithelium.	bind
7303	2	2640	7	10	NULL	0	NULL	genes	GP		is expressed in		abundantly		NFI-binding sites	olfactory epithelium	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_72_1_65_s_104	10521600	(A) Binding of rat olfactory epithelial nuclear proteins with putative NFI-binding sites from genes expressed abundantly within the olfactory epithelium.	bind
5282	1	2641	5	10	NULL	0	NULL	RIN1	GP		bind					GST-RAS	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_3_916_s_136	11784866	(A) Binding of RIN1 to GST-RAS.	bind
7304	1	2641	7	10	NULL	0	NULL	RIN1	GP		binds					GST-RAS	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_3_916_s_136	11784866	(A) Binding of RIN1 to GST-RAS.	bind
5283	1	2642	5	10	NULL	0	NULL	RNCs	GP		bind					TX-PK-RM	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_1_53_s_182	10893256	(A) Binding of RNCs to TX-PK-RM was assayed by adjusting samples to 2.1 M sucrose and applying them as the bottom layer of a three-step discontinuous sucrose gradient (see Materials and Methods).	bind
7305	1	2642	7	10	NULL	0	NULL	RNCs	GP		binds to					TX-PK-RM	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_1_53_s_182	10893256	(A) Binding of RNCs to TX-PK-RM was assayed by adjusting samples to 2.1 M sucrose and applying them as the bottom layer of a three-step discontinuous sucrose gradient (see Materials and Methods).	bind
5284	1	2643	5	10	NULL	0	NULL	syncollin	GP		bind					GST-syntaxin fragments	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_2_325_s_68	9244306	(A) Binding of syncollin to various  GST-syntaxin fragments.	bind
7306	1	2643	7	10	NULL	0	NULL	syncollin	GP		binds to					GST-syntaxin fragments	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_2_325_s_68	9244306	(A) Binding of syncollin to various  GST-syntaxin fragments.	bind
5285	1	2644	5	10	NULL	0	NULL	syntaxin-1a	GP		bind					tomosyn	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_5_905_s_136	9620695	(A) Binding of syntaxin-1a to tomosyn.	bind
7307	1	2644	7	10	NULL	0	NULL	syntaxin-1a	GP		binds					tomosyn	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_5_905_s_136	9620695	(A) Binding of syntaxin-1a to tomosyn.	bind
5286	1	2645	5	10	NULL	0	NULL	TFs	GP		bind					c-fos	GP	human		SRE	NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1574_1_100_s_51	11955618	(A) Binding of TFs to the human c-fos SRE.	bind
7308	1	2645	7	10	NULL	0	NULL	TF	GP		binds					c-fos	GP	human		SRE	NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1574_1_100_s_51	11955618	(A) Binding of TFs to the human c-fos SRE.	bind
5287	1	2646	5	10	NULL	0	NULL	eEF1 complex	GP		bind					G-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1527_3_130_s_236	11479029	(A) Binding of the eEF1   complex to G-actin.	bind
7309	1	2646	7	10	NULL	0	NULL	eEF1 complex	GP		binds to					G-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1527_3_130_s_236	11479029	(A) Binding of the eEF1   complex to G-actin.	bind
7176	1	2648	5	10	NULL	0	NULL				bind			Skn domain		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_3039_s_105	10082571	(A) Binding of the Skn domain and the delta1-9 Skn domain mutant ( 2) to DNA, assayed by EMSA at room temperature (RT).	bind
54137	2	2648	5	10	NULL	0	NULL			mutant	bind			delta1-9 Skn domain		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_3039_s_105	10082571	(A) Binding of the Skn domain and the delta1-9 Skn domain mutant ( 2) to DNA, assayed by EMSA at room temperature (RT).	bind
7326	1	2648	7	10	NULL	0	NULL				binds			Skn domain		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_3039_s_105	10082571	(A) Binding of the Skn domain and the delta1-9 Skn domain mutant ( 2) to DNA, assayed by EMSA at room temperature (RT).	bind
7327	2	2648	7	10	NULL	0	NULL			mutant	binds			delta1-9 Skn domain		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_3039_s_105	10082571	(A) Binding of the Skn domain and the delta1-9 Skn domain mutant ( 2) to DNA, assayed by EMSA at room temperature (RT).	bind
5288	1	2649	5	10	NULL	0	NULL	thyroglobulin	GP		bind					SpeB extracts	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_2_784_s_141	12540558	(A) Binding of thyroglobulin to SpeB extracts of the  rgg mutant strain NZ131 rgg.	bind
46257	2	2649	5	10	NULL	0	NULL	SpeB extracts	GP		are derived from					NZ131 rgg strain	Organism	mutant			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_2_784_s_141	12540558	(A) Binding of thyroglobulin to SpeB extracts of the  rgg mutant strain NZ131 rgg.	bind
7328	1	2649	7	10	NULL	0	NULL	thyroglobulin	GP		binds to					SpeB extracts	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_2_784_s_141	12540558	(A) Binding of thyroglobulin to SpeB extracts of the  rgg mutant strain NZ131 rgg.	bind
7329	2	2649	7	10	NULL	0	NULL	SpeB extracts	GP		is derived from	Organism				NZ131 rgg strain	Organism	mutant			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_2_784_s_141	12540558	(A) Binding of thyroglobulin to SpeB extracts of the  rgg mutant strain NZ131 rgg.	bind
5289	1	2650	5	10	NULL	0	NULL	Vav-3	GP		bind			delta1-144		Rho family proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7870_s_267	10523675	(A) Binding of Vav-3 (delta1-144) to Rho family proteins.	bind
7330	1	2650	7	10	NULL	0	NULL	Vav-3	GP		binds to			delta1-144		Rho family proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7870_s_267	10523675	(A) Binding of Vav-3 (delta1-144) to Rho family proteins.	bind
5290	1	2651	5	10	NULL	0	NULL	VEGF-E	GP		bind					VEGFR - IgG	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_161_6_1163_s_247	12810700	(a) Binding of VEGF-E to VEGFR - IgG fusion proteins.	bind
46260	2	2651	5	10	NULL	0	NULL	VEGFR- IgG	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_161_6_1163_s_247	12810700	(a) Binding of VEGF-E to VEGFR - IgG fusion proteins.	bind
7332	1	2651	7	10	NULL	0	NULL	VEGF-E	GP		binds to					VEGFR - IgG 	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_161_6_1163_s_247	12810700	(a) Binding of VEGF-E to VEGFR - IgG fusion proteins.	bind
46261	2	2651	7	10	NULL	0	NULL	VEGFR- IgG	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_161_6_1163_s_247	12810700	(a) Binding of VEGF-E to VEGFR - IgG fusion proteins.	bind
5291	1	2652	5	10	NULL	0	NULL	vitronectin	GP		bind					UspA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_9_4374_s_274	9712790	(A) Binding of vitronectin to UspA1 and UspA2.	bind
5292	2	2652	5	10	NULL	0	NULL	vitronectin	GP		bind					UspA2	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_9_4374_s_274	9712790	(A) Binding of vitronectin to UspA1 and UspA2.	bind
7333	1	2652	7	10	NULL	0	NULL	vitronectin	GP		binds to					UspA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_9_4374_s_274	9712790	(A) Binding of vitronectin to UspA1 and UspA2.	bind
7334	2	2652	7	10	NULL	0	NULL	vitronectin	GP		binds to					UspA2	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_9_4374_s_274	9712790	(A) Binding of vitronectin to UspA1 and UspA2.	bind
5293	1	2653	5	10	NULL	0	NULL	HGFSF	GP	wt	bind					Met-Fc	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_3_125_s_128	9443912	(a) Binding of wt-HGFSF and HP1 to Met-Fc.	bind
5294	2	2653	5	10	NULL	0	NULL	HP1	GP		bind					Met-Fc	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_3_125_s_128	9443912	(a) Binding of wt-HGFSF and HP1 to Met-Fc.	bind
7335	1	2653	7	10	NULL	0	NULL	HGFSF	GP	wt	binds to					Met-Fc	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_3_125_s_128	9443912	(a) Binding of wt-HGFSF and HP1 to Met-Fc.	bind
7336	2	2653	7	10	NULL	0	NULL	HP1	GP		binds to					Met-Fc	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_3_125_s_128	9443912	(a) Binding of wt-HGFSF and HP1 to Met-Fc.	bind
5295	1	2654	5	10	NULL	0	NULL	tpm3	GP	Wt	bind					F actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_2_300_s_99	12163017	(A) Binding of Wt-tpm3 to F actin and troponin.	bind
5296	2	2654	5	10	NULL	0	NULL	tpm3	GP	Wt	bind					troponin	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_2_300_s_99	12163017	(A) Binding of Wt-tpm3 to F actin and troponin.	bind
7337	1	2654	7	10	NULL	0	NULL	tpm3	GP	Wt	binds					F actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_2_300_s_99	12163017	(A) Binding of Wt-tpm3 to F actin and troponin.	bind
7338	2	2654	7	10	NULL	0	NULL	tpm3	GP	Wt	binds					troponin	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_2_300_s_99	12163017	(A) Binding of Wt-tpm3 to F actin and troponin.	bind
5297	1	2655	5	10	NULL	0	NULL	XIP-I	GP		bind					polysaccharides	Chemical	water-insoluble			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_136_s_195	12922177	(A) Binding of XIP-I or BASI to water-insoluble polysaccharides was measured as described in  Materials and methods.	bind
5298	2	2655	5	10	NULL	0	NULL	BASI	GP		bind					polysaccharides	Chemical	water-insoluble			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_136_s_195	12922177	(A) Binding of XIP-I or BASI to water-insoluble polysaccharides was measured as described in  Materials and methods.	bind
7339	1	2655	7	10	NULL	0	NULL	XIP-I	GP		binds					 polysaccharides	Chemical	water-insoluble			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_136_s_195	12922177	(A) Binding of XIP-I or BASI to water-insoluble polysaccharides was measured as described in  Materials and methods.	bind
7340	2	2655	7	10	NULL	0	NULL	BASI	GP		binds					polysaccharides	Chemical	water-insoluble			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_136_s_195	12922177	(A) Binding of XIP-I or BASI to water-insoluble polysaccharides was measured as described in  Materials and methods.	bind
5299	1	2656	5	10	NULL	0	NULL	XPC	GP		bind					nucleosomal DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9173_s_167	11094069	(A) Binding of XPC to nucleosomal DNA.	bind
7341	1	2656	7	10	NULL	0	NULL	XPC	GP		binds to					nucleosomal DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9173_s_167	11094069	(A) Binding of XPC to nucleosomal DNA.	bind
5300	1	2657	5	10	NULL	0	NULL	yeast cells	Cell		bind					BSA	Chemical	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_1_140_s_75	9423850	(A) Binding of yeast cells to BSA (BSA), effects of preincubation with BSA on binding of yeast cells to immobilized BSA (BSA/BSA) and following washout of free BSA [BSA(wash)/BSA], and effects of preincubation with gelatin on the binding of yeast cells to immobilized BSA (PreGel-BSA).	bind
7342	1	2657	7	10	NULL	0	NULL	yeast cells	Cell		binds					BSA	Chemical	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_1_140_s_75	9423850	(A) Binding of yeast cells to BSA (BSA), effects of preincubation with BSA on binding of yeast cells to immobilized BSA (BSA/BSA) and following washout of free BSA [BSA(wash)/BSA], and effects of preincubation with gelatin on the binding of yeast cells to immobilized BSA (PreGel-BSA).	bind
5301	1	2658	5	10	NULL	0	NULL	YopN	GP		bind					TyeA	GP				NULL	E.coli	NULL	NULL	NULL	NULL	gw60_embo_17_7_1907_s_166	9524114	(A) Binding of YopN to TyeA in  E.coli.	bind
7345	1	2658	7	10	NULL	0	NULL	YopN	GP		binds					TyeA	GP				NULL	E.coli	NULL	NULL	NULL	NULL	gw60_embo_17_7_1907_s_166	9524114	(A) Binding of YopN to TyeA in  E.coli.	bind
5302	1	2659	5	10	NULL	0	NULL	[3]SSO	Chemical		bind					DRMs	CellComponent				NULL	live cells	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_1_24_s_147	15496455	(A) Binding of [3]SSO to DRMs of live cells.	bind
7346	1	2659	7	10	NULL	0	NULL	[3]SSO	Chemical		binds					DRMs	CellComponent				NULL	live cells	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_1_24_s_147	15496455	(A) Binding of [3]SSO to DRMs of live cells.	bind
5303	1	2660	5	10	NULL	0	NULL	NAC	GP		bind					apoE	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_44_1_105_s_63	9030704	(A) Binding of []NAC to apoE in VLDL.	bind
5304	2	2660	5	10	NULL	0	NULL	statement 1	Process		occurs in					VLDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_44_1_105_s_63	9030704	(A) Binding of []NAC to apoE in VLDL.	bind
7347	1	2660	7	10	NULL	0	NULL	NAC	GP		binds					apoE	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_44_1_105_s_63	9030704	(A) Binding of []NAC to apoE in VLDL.	bind
8074	2	2660	7	10	NULL	0	NULL	statement 1	Process		occurs in					VLDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_44_1_105_s_63	9030704	(A) Binding of []NAC to apoE in VLDL.	bind
5870	1	2661	5	10	NULL	0	NULL	4F	GP		bind					cap analogue	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_1026	15157733	(A) binding protein  enhances the binding affinity of eukaryotic initiation factor 4F and (iso)4F for  cap analogues.	bind
5871	2	2661	5	10	NULL	0	NULL	(iso)4F	GP		bind					cap analogue	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_1026	15157733	(A) binding protein  enhances the binding affinity of eukaryotic initiation factor 4F and (iso)4F for  cap analogues.	bind
8179	3	2661	5	10	NULL	0	NULL	4F	GP		is a type of					eukaryotic initiation factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_1026	15157733	(A) binding protein  enhances the binding affinity of eukaryotic initiation factor 4F and (iso)4F for  cap analogues.	bind
8180	4	2661	5	10	NULL	0	NULL	(iso)4F	GP		is a type of					eukaryotic initiation factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_1026	15157733	(A) binding protein  enhances the binding affinity of eukaryotic initiation factor 4F and (iso)4F for  cap analogues.	bind
7348	1	2661	7	10	NULL	0	NULL	4F	GP		binds					cap analogues	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_1026	15157733	(A) binding protein  enhances the binding affinity of eukaryotic initiation factor 4F and (iso)4F for  cap analogues.	bind
7349	2	2661	7	10	NULL	0	NULL	(iso)4F	GP		binds					cap analogues	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_1026	15157733	(A) binding protein  enhances the binding affinity of eukaryotic initiation factor 4F and (iso)4F for  cap analogues.	bind
7350	3	2661	7	10	NULL	0	NULL	4F	GP		is a type of					eukaryotic initiation factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_1026	15157733	(A) binding protein  enhances the binding affinity of eukaryotic initiation factor 4F and (iso)4F for  cap analogues.	bind
7351	4	2661	7	10	NULL	0	NULL	(iso)4F	GP		is a type of					eukaryotic initiation factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_1026	15157733	(A) binding protein  enhances the binding affinity of eukaryotic initiation factor 4F and (iso)4F for  cap analogues.	bind
5305	1	2662	5	10	NULL	0	NULL	PABP	GP		bind					PCBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_6_1439_s_161	11250909	(A) binding protein (PABP) and poly(rC) binding protein (PCBP) interact with each other and the ends of the viral RNA to form a circular RNP complex.	bind
5306	2	2662	5	10	NULL	0	NULL	PCBP	GP		is					poly(rC) binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_6_1439_s_161	11250909	(A) binding protein (PABP) and poly(rC) binding protein (PCBP) interact with each other and the ends of the viral RNA to form a circular RNP complex.	bind
5307	3	2662	5	10	NULL	0	NULL	PABP	GP		bind					viral RNA	NucleicAcid		ends of		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_6_1439_s_161	11250909	(A) binding protein (PABP) and poly(rC) binding protein (PCBP) interact with each other and the ends of the viral RNA to form a circular RNP complex.	bind
5308	4	2662	5	10	NULL	0	NULL	PCBP	GP		bind					viral RNA	NucleicAcid		ends of		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_6_1439_s_161	11250909	(A) binding protein (PABP) and poly(rC) binding protein (PCBP) interact with each other and the ends of the viral RNA to form a circular RNP complex.	bind
5309	5	2662	5	10	NULL	0	NULL	statement 1	Process		forms					RNP complex	GP	circular			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_6_1439_s_161	11250909	(A) binding protein (PABP) and poly(rC) binding protein (PCBP) interact with each other and the ends of the viral RNA to form a circular RNP complex.	bind
5310	6	2662	5	10	NULL	0	NULL	statement 3	Process		forms					RNP complex	GP	circular 			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_6_1439_s_161	11250909	(A) binding protein (PABP) and poly(rC) binding protein (PCBP) interact with each other and the ends of the viral RNA to form a circular RNP complex.	bind
5311	7	2662	5	10	NULL	0	NULL	statement 4	Process		forms					RNP complex	GP	circular 			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_6_1439_s_161	11250909	(A) binding protein (PABP) and poly(rC) binding protein (PCBP) interact with each other and the ends of the viral RNA to form a circular RNP complex.	bind
5320	8	2662	5	10	NULL	0	NULL	PABP	GP		is					poly (A) binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_6_1439_s_161	11250909	(A) binding protein (PABP) and poly(rC) binding protein (PCBP) interact with each other and the ends of the viral RNA to form a circular RNP complex.	bind
7352	1	2662	7	10	NULL	0	NULL	PABP	GP		binds					PCBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_6_1439_s_161	11250909	(A) binding protein (PABP) and poly(rC) binding protein (PCBP) interact with each other and the ends of the viral RNA to form a circular RNP complex.	bind
7353	2	2662	7	10	NULL	0	NULL	PABP	GP		is					poly (A) binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_6_1439_s_161	11250909	(A) binding protein (PABP) and poly(rC) binding protein (PCBP) interact with each other and the ends of the viral RNA to form a circular RNP complex.	bind
7354	3	2662	7	10	NULL	0	NULL	PCBP	GP		is					poly(rC) binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_6_1439_s_161	11250909	(A) binding protein (PABP) and poly(rC) binding protein (PCBP) interact with each other and the ends of the viral RNA to form a circular RNP complex.	bind
7355	4	2662	7	10	NULL	0	NULL	PABP	GP		binds					Viral RNA	NucleicAcid		ends of		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_6_1439_s_161	11250909	(A) binding protein (PABP) and poly(rC) binding protein (PCBP) interact with each other and the ends of the viral RNA to form a circular RNP complex.	bind
7356	5	2662	7	10	NULL	0	NULL	PCBP	GP		binds					Viral RNA	NucleicAcid		ends of		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_6_1439_s_161	11250909	(A) binding protein (PABP) and poly(rC) binding protein (PCBP) interact with each other and the ends of the viral RNA to form a circular RNP complex.	bind
7357	6	2662	7	10	NULL	0	NULL	statement 1	Process		forms					RNP complex	GP	circular			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_6_1439_s_161	11250909	(A) binding protein (PABP) and poly(rC) binding protein (PCBP) interact with each other and the ends of the viral RNA to form a circular RNP complex.	bind
7358	7	2662	7	10	NULL	0	NULL	statement 4	Process		forms					RNP complex	GP	circular			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_6_1439_s_161	11250909	(A) binding protein (PABP) and poly(rC) binding protein (PCBP) interact with each other and the ends of the viral RNA to form a circular RNP complex.	bind
7359	8	2662	7	10	NULL	0	NULL	statement 5	Process		forms					RNP complex	GP	circular			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_6_1439_s_161	11250909	(A) binding protein (PABP) and poly(rC) binding protein (PCBP) interact with each other and the ends of the viral RNA to form a circular RNP complex.	bind
5312	1	2663	5	10	NULL	0	NULL	PABP	GP		bind					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4277_s_31	16705177	(A) binding protein (PABP); PABP also binds eIF4G.	bind
5321	2	2663	5	10	NULL	0	NULL	PABP	GP		is					poly (A) binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4277_s_31	16705177	(A) binding protein (PABP); PABP also binds eIF4G.	bind
7360	1	2663	7	10	NULL	0	NULL	PABP	GP		binds					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4277_s_31	16705177	(A) binding protein (PABP); PABP also binds eIF4G.	bind
7361	2	2663	7	10	NULL	0	NULL	PABP	GP		is					poly (A) binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4277_s_31	16705177	(A) binding protein (PABP); PABP also binds eIF4G.	bind
5313	1	2664	5	10	NULL	0	NULL	protein C1	GP		bind					pre-mRNA	NucleicAcid	nuclear			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_mol-cell-biol_26_8_16581783_s_1	16581783	(A) binding protein C1 binds nuclear pre-mRNA poly	bind
7876	1	2664	7	10	NULL	0	NULL	Protein C1	GP		binds					pre-mRNA	NucleicAcid	nuclear			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_mol-cell-biol_26_8_16581783_s_1	16581783	(A) binding protein C1 binds nuclear pre-mRNA poly	bind
5314	1	2668	5	10	NULL	0	NULL	Pab1	GP		bind					Dcp1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_42	10944120	(A) binding protein Pab1 bind to Dcp1, either independently, or when these proteins are in the 5'' - 3' translation complex involving eIF4F and Pab1.	bind
5315	2	2668	5	10	NULL	0	NULL	statement 1	Process		occur					independently					NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_42	10944120	(A) binding protein Pab1 bind to Dcp1, either independently, or when these proteins are in the 5'' - 3' translation complex involving eIF4F and Pab1.	bind
5316	3	2668	5	10	NULL	0	NULL	statement 1	Process		occurs in complex with					eIF4F	GP	5'' - 3' translation complex			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_42	10944120	(A) binding protein Pab1 bind to Dcp1, either independently, or when these proteins are in the 5'' - 3' translation complex involving eIF4F and Pab1.	bind
5317	4	2668	5	10	NULL	0	NULL	statement 1	Process		occurs in complex with					Pab1	GP	5'' - 3' translation complex			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_42	10944120	(A) binding protein Pab1 bind to Dcp1, either independently, or when these proteins are in the 5'' - 3' translation complex involving eIF4F and Pab1.	bind
5318	5	2668	5	10	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_42	10944120	(A) binding protein Pab1 bind to Dcp1, either independently, or when these proteins are in the 5'' - 3' translation complex involving eIF4F and Pab1.	bind
5319	6	2668	5	10	NULL	0	NULL	statement 2	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_42	10944120	(A) binding protein Pab1 bind to Dcp1, either independently, or when these proteins are in the 5'' - 3' translation complex involving eIF4F and Pab1.	bind
7362	1	2668	7	10	NULL	0	NULL	Pab1	GP		binds					Dcp1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_42	10944120	(A) binding protein Pab1 bind to Dcp1, either independently, or when these proteins are in the 5'' - 3' translation complex involving eIF4F and Pab1.	bind
7363	2	2668	7	10	NULL	0	NULL	statement 1	Process		occurs					independently					NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_42	10944120	(A) binding protein Pab1 bind to Dcp1, either independently, or when these proteins are in the 5'' - 3' translation complex involving eIF4F and Pab1.	bind
7364	3	2668	7	10	NULL	0	NULL	statement 1	Process		occurs in complex with					eIF4F	GP	5'' - 3' translation complex			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_42	10944120	(A) binding protein Pab1 bind to Dcp1, either independently, or when these proteins are in the 5'' - 3' translation complex involving eIF4F and Pab1.	bind
7365	4	2668	7	10	NULL	0	NULL	statement 1	Process		occurs in complex with					Pab1	GP	5'' - 3' translation complex			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_42	10944120	(A) binding protein Pab1 bind to Dcp1, either independently, or when these proteins are in the 5'' - 3' translation complex involving eIF4F and Pab1.	bind
8075	5	2668	7	10	NULL	0	NULL	statement 3	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_42	10944120	(A) binding protein Pab1 bind to Dcp1, either independently, or when these proteins are in the 5'' - 3' translation complex involving eIF4F and Pab1.	bind
8076	6	2668	7	10	NULL	0	NULL	statement 4	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_42	10944120	(A) binding protein Pab1 bind to Dcp1, either independently, or when these proteins are in the 5'' - 3' translation complex involving eIF4F and Pab1.	bind
5322	1	2669	5	10	NULL	0	NULL	RCC1	GP	endogenous	bind					mitotic chromosomes	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_5_635_s_155	12604592	(A) Both RanGDP and RanT24N strongly stimulate the binding of the endogenous RCC1  in the egg extract to the mitotic chromosomes assembled from the sperm chromatin.	bind
5323	2	2669	5	10	NULL	0	NULL	RanGDP	GP		stimulate		strongly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_5_635_s_155	12604592	(A) Both RanGDP and RanT24N strongly stimulate the binding of the endogenous RCC1  in the egg extract to the mitotic chromosomes assembled from the sperm chromatin.	bind
5324	3	2669	5	10	NULL	0	NULL	RanT24N	GP		stimulate		strongly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_5_635_s_155	12604592	(A) Both RanGDP and RanT24N strongly stimulate the binding of the endogenous RCC1  in the egg extract to the mitotic chromosomes assembled from the sperm chromatin.	bind
54140	4	2669	5	10	NULL	0	NULL	RCC1	GP		is from					egg extract	Cell				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_5_635_s_155	12604592	(A) Both RanGDP and RanT24N strongly stimulate the binding of the endogenous RCC1  in the egg extract to the mitotic chromosomes assembled from the sperm chromatin.	bind
54141	5	2669	5	10	NULL	0	NULL	mitotic chromosomes	Chromosome		are assembled from					sperm chromatin	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_5_635_s_155	12604592	(A) Both RanGDP and RanT24N strongly stimulate the binding of the endogenous RCC1  in the egg extract to the mitotic chromosomes assembled from the sperm chromatin.	bind
7366	1	2669	7	10	NULL	0	NULL	RCC1	GP	 endogenous	binds					mitotic chromosomes	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_5_635_s_155	12604592	(A) Both RanGDP and RanT24N strongly stimulate the binding of the endogenous RCC1  in the egg extract to the mitotic chromosomes assembled from the sperm chromatin.	bind
7367	2	2669	7	10	NULL	0	NULL	RCC1	GP		is from					egg extract	Cell				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_5_635_s_155	12604592	(A) Both RanGDP and RanT24N strongly stimulate the binding of the endogenous RCC1  in the egg extract to the mitotic chromosomes assembled from the sperm chromatin.	bind
7368	3	2669	7	10	NULL	0	NULL	mitotic chromosomes	Chromosome		are assembled from					sperm chromatin	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_5_635_s_155	12604592	(A) Both RanGDP and RanT24N strongly stimulate the binding of the endogenous RCC1  in the egg extract to the mitotic chromosomes assembled from the sperm chromatin.	bind
7369	4	2669	7	10	NULL	0	NULL	RanGDP	GP		stimulate		strongly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_5_635_s_155	12604592	(A) Both RanGDP and RanT24N strongly stimulate the binding of the endogenous RCC1  in the egg extract to the mitotic chromosomes assembled from the sperm chromatin.	bind
7370	5	2669	7	10	NULL	0	NULL	RanT24N	GP		stimulate		strongly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_5_635_s_155	12604592	(A) Both RanGDP and RanT24N strongly stimulate the binding of the endogenous RCC1  in the egg extract to the mitotic chromosomes assembled from the sperm chromatin.	bind
5325	1	2670	5	10	NULL	0	NULL	APP	GP		bind		directly	C terminus		KLC	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_2_449_s_126	11144355	(A) C terminus of APP directly binds KLC.	bind
7371	1	2670	7	10	NULL	0	NULL	APP	GP		binds		directly	C terminus		KLC	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_2_449_s_126	11144355	(A) C terminus of APP directly binds KLC.	bind
5326	1	2671	5	10	NULL	0	NULL	C1 bacteriophage	Organism		bind					cell wall	CellComponent	group C streptococcus			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_11_3325_s_84	12754230	(A) C1 bacteriophage binding to the cell wall of a group C streptococcus.	bind
7372	1	2671	7	10	NULL	0	NULL	C1 bacteriophage	Organism		binds to					cell wall	CellComponent	group C streptococcus			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_11_3325_s_84	12754230	(A) C1 bacteriophage binding to the cell wall of a group C streptococcus.	bind
5327	1	2672	5	NULL	NULL	0	NULL		NULL		bind	NULL		C644G			NULL			GRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8146_s_301	10567540	(A) C644G can bind to a GRE by EMSA.	bind
7373	1	2672	7	NULL	NULL	0	NULL		NULL		bind	NULL		C644G			NULL			GRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8146_s_301	10567540	(A) C644G can bind to a GRE by EMSA.	bind
5328	1	2673	5	10	NULL	0	NULL	syntaxin	GP		bind					synaptotagmin	GP		C2A domain		NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_86_1_39_s_129	9692742	(A) Ca2+-dependent syntaxin binding to synaptotagmin C2A domain.	bind
46340	2	2673	5	10	NULL	0	NULL	statement 1	GP		is dependent on					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_86_1_39_s_129	9692742	(A) Ca2+-dependent syntaxin binding to synaptotagmin C2A domain.	bind
7374	1	2673	7	10	NULL	0	NULL	syntaxin	GP		binds to					synaptotagmin	GP		C2A domain		NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_86_1_39_s_129	9692742	(A) Ca2+-dependent syntaxin binding to synaptotagmin C2A domain.	bind
46341	2	2673	7	10	NULL	0	NULL	statement 1	GP		is dependent on					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_86_1_39_s_129	9692742	(A) Ca2+-dependent syntaxin binding to synaptotagmin C2A domain.	bind
5330	1	2674	5	10	NULL	0	NULL	CAT	GP		bind					SHP2	GP				NULL	A549 cells	NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_89	15556604	(A) CAT binds SHP2 in A549 cells after FBS-stimulation.	bind
5331	2	2674	5	10	NULL	0	NULL	statement 1	GP		occurs after					FBS	Chemical	stimulation			NULL	A549 cells \t	NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_89	15556604	(A) CAT binds SHP2 in A549 cells after FBS-stimulation.	bind
7375	1	2674	7	10	NULL	0	NULL	 CAT	GP		binds					SHP2	GP				NULL	A549 cells	NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_89	15556604	(A) CAT binds SHP2 in A549 cells after FBS-stimulation.	bind
7376	2	2674	7	10	NULL	0	NULL	statement 1	Process		occurs after					FBS	Chemical	stimulation by			NULL	A549 cells \t	NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_89	15556604	(A) CAT binds SHP2 in A549 cells after FBS-stimulation.	bind
5332	1	2675	5	10	NULL	0	NULL	CAT	GP		bind					SHP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_102	15556604	(A) CAT binds SHP2 upon stimulation of HeLa cells with FBS or fibrinogen,  while herbimycin-A and peptides comprising fibronectin functional sequence suppress  the biding.	bind
5333	2	2675	5	10	NULL	0	NULL	HeLa cells	Cell		is stimulated with					FBS	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_102	15556604	(A) CAT binds SHP2 upon stimulation of HeLa cells with FBS or fibrinogen,  while herbimycin-A and peptides comprising fibronectin functional sequence suppress  the biding.	bind
5334	3	2675	5	10	NULL	0	NULL	HeLa cells	Cell		is stimulated with					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_102	15556604	(A) CAT binds SHP2 upon stimulation of HeLa cells with FBS or fibrinogen,  while herbimycin-A and peptides comprising fibronectin functional sequence suppress  the biding.	bind
5335	4	2675	5	10	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_102	15556604	(A) CAT binds SHP2 upon stimulation of HeLa cells with FBS or fibrinogen,  while herbimycin-A and peptides comprising fibronectin functional sequence suppress  the biding.	bind
5336	5	2675	5	10	NULL	0	NULL	statement 2	Process		is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_102	15556604	(A) CAT binds SHP2 upon stimulation of HeLa cells with FBS or fibrinogen,  while herbimycin-A and peptides comprising fibronectin functional sequence suppress  the biding.	bind
5337	6	2675	5	10	NULL	0	NULL	statement 3	Process		is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_102	15556604	(A) CAT binds SHP2 upon stimulation of HeLa cells with FBS or fibrinogen,  while herbimycin-A and peptides comprising fibronectin functional sequence suppress  the biding.	bind
5338	7	2675	5	10	NULL	0	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_102	15556604	(A) CAT binds SHP2 upon stimulation of HeLa cells with FBS or fibrinogen,  while herbimycin-A and peptides comprising fibronectin functional sequence suppress  the biding.	bind
5339	8	2675	5	10	NULL	0	NULL	herbimycin-A	Chemical		supress					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_102	15556604	(A) CAT binds SHP2 upon stimulation of HeLa cells with FBS or fibrinogen,  while herbimycin-A and peptides comprising fibronectin functional sequence suppress  the biding.	bind
5340	9	2675	5	10	NULL	0	NULL	statement 10	Process		supress					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_102	15556604	(A) CAT binds SHP2 upon stimulation of HeLa cells with FBS or fibrinogen,  while herbimycin-A and peptides comprising fibronectin functional sequence suppress  the biding.	bind
54236	10	2675	5	10	NULL	0	NULL	peptides	AminoAcid		comprise					fibronectin	GP	functional sequence			NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_102	15556604	(A) CAT binds SHP2 upon stimulation of HeLa cells with FBS or fibrinogen,  while herbimycin-A and peptides comprising fibronectin functional sequence suppress  the biding.	bind
7377	1	2675	7	10	NULL	0	NULL	CAT	GP		binds					SHP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_102	15556604	(A) CAT binds SHP2 upon stimulation of HeLa cells with FBS or fibrinogen,  while herbimycin-A and peptides comprising fibronectin functional sequence suppress  the biding.	bind
7378	2	2675	7	10	NULL	0	NULL	HeLa cells	Cell		stimulated with					FBS	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_102	15556604	(A) CAT binds SHP2 upon stimulation of HeLa cells with FBS or fibrinogen,  while herbimycin-A and peptides comprising fibronectin functional sequence suppress  the biding.	bind
7379	3	2675	7	10	NULL	0	NULL	HeLa cells	Cell		stimulated with					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_102	15556604	(A) CAT binds SHP2 upon stimulation of HeLa cells with FBS or fibrinogen,  while herbimycin-A and peptides comprising fibronectin functional sequence suppress  the biding.	bind
7380	4	2675	7	10	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_102	15556604	(A) CAT binds SHP2 upon stimulation of HeLa cells with FBS or fibrinogen,  while herbimycin-A and peptides comprising fibronectin functional sequence suppress  the biding.	bind
7381	5	2675	7	10	NULL	0	NULL	statement 1	Process		occurs upon					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_102	15556604	(A) CAT binds SHP2 upon stimulation of HeLa cells with FBS or fibrinogen,  while herbimycin-A and peptides comprising fibronectin functional sequence suppress  the biding.	bind
54241	6	2675	7	10	NULL	0	NULL	herbimycin-A	Chemical		suppress					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_102	15556604	(A) CAT binds SHP2 upon stimulation of HeLa cells with FBS or fibrinogen,  while herbimycin-A and peptides comprising fibronectin functional sequence suppress  the biding.	bind
54242	7	2675	7	10	NULL	0	NULL	peptides	AminoAcid		comprise					fibronectin	GP	functional sequence			NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_102	15556604	(A) CAT binds SHP2 upon stimulation of HeLa cells with FBS or fibrinogen,  while herbimycin-A and peptides comprising fibronectin functional sequence suppress  the biding.	bind
54243	8	2675	7	10	NULL	0	NULL	statement 7	Process		suppress					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_102	15556604	(A) CAT binds SHP2 upon stimulation of HeLa cells with FBS or fibrinogen,  while herbimycin-A and peptides comprising fibronectin functional sequence suppress  the biding.	bind
5341	1	2677	5	10	NULL	0	NULL	ICP-1	GP	CBD-tagged	does not bind					CSC-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_229_s_131	12707312	(A) CBD-tagged ICP-1  does not bind to CSC-1 and binds weakly to BIR-1.	bind
5342	2	2677	5	10	NULL	0	NULL	ICP-1	GP	CBD-tagged	bind		weakly			BIR-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_229_s_131	12707312	(A) CBD-tagged ICP-1  does not bind to CSC-1 and binds weakly to BIR-1.	bind
7388	1	2677	7	10	NULL	0	NULL	ICP-1	GP	CBD-tagged	does not bind					CSC-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_229_s_131	12707312	(A) CBD-tagged ICP-1  does not bind to CSC-1 and binds weakly to BIR-1.	bind
7389	2	2677	7	10	NULL	0	NULL	ICP-1	GP	CBD-tagged	binds		weakly			BIR-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_229_s_131	12707312	(A) CBD-tagged ICP-1  does not bind to CSC-1 and binds weakly to BIR-1.	bind
5343	1	2679	5	10	NULL	0	NULL	Cdc24p	GP		bind					Gbeta	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_6_1187_s_265	10087263	(A) Cdc24p binds Gbeta in the presence of  MBPFar1.	bind
5344	2	2679	5	10	NULL	0	NULL	statement 1	Process		in the presence of					MBPFar1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_6_1187_s_265	10087263	(A) Cdc24p binds Gbeta in the presence of  MBPFar1.	bind
7390	1	2679	7	10	NULL	0	NULL	Cdc24p	GP		binds					Gbeta	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_6_1187_s_265	10087263	(A) Cdc24p binds Gbeta in the presence of  MBPFar1.	bind
7391	2	2679	7	10	NULL	0	NULL	statement 1	Process		occurs in the presence of					MBPFar1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_6_1187_s_265	10087263	(A) Cdc24p binds Gbeta in the presence of  MBPFar1.	bind
5345	1	2680	5	10	NULL	0	NULL	Cdc28	GP		bind					Cln2-deltaN-Sic1 fusions	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4463_s_266	12052857	(A) Cdc28 binds to Cln2-deltaN-Sic1 fusions.	bind
7392	1	2680	7	10	NULL	0	NULL	Cdc28	GP		binds					Cln2-deltaN-Sic1 fusions	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4463_s_266	12052857	(A) Cdc28 binds to Cln2-deltaN-Sic1 fusions.	bind
5346	1	2681	5	10	NULL	0	NULL	Cdc42Hs	GP		bind		spontaneously	F28L		GTP- -35S	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_10_794_s_18	9368762	(a) Cdc42Hs(F28L) spontaneously binds GTP-  -35S.	bind
7393	1	2681	7	10	NULL	0	NULL	Cdc42Hs	GP		binds		spontaneously	F28L		GTP- -35S	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_10_794_s_18	9368762	(a) Cdc42Hs(F28L) spontaneously binds GTP-  -35S.	bind
5347	1	2682	5	10	NULL	0	NULL	CDP/Cux	GP		bind					DNA pol alpha gene	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_3013_s_296	12665598	(A) CDP/Cux  binds to the DNA pol alpha gene promoter in vivo.	bind
7394	1	2682	7	10	NULL	0	NULL	CDP/Cux	GP		binds to					DNA pol alpha	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_3013_s_296	12665598	(A) CDP/Cux  binds to the DNA pol alpha gene promoter in vivo.	bind
5349	1	2686	5	10	NULL	0	NULL	CtIP	GP	cell-free;; synthesized	bind		specifically			GST-CtBP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10379_s_214	16287852	(A) Cell-free synthesized  CtIP binds specifically to GST-CtBP1 (lane 2) and GST-SHARP-RD (lane 3) but not to  GST-RBP-2N (lane 1).	bind
5350	2	2686	5	10	NULL	0	NULL	CtIP	GP	cell-free;; synthesized	bind		specifically			GST-SHARP	GP		RD		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10379_s_214	16287852	(A) Cell-free synthesized  CtIP binds specifically to GST-CtBP1 (lane 2) and GST-SHARP-RD (lane 3) but not to  GST-RBP-2N (lane 1).	bind
5351	3	2686	5	10	NULL	0	NULL	CtIP	GP	cell-free;; synthesized	does not bind					GST-RBP	GP		2N		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10379_s_214	16287852	(A) Cell-free synthesized  CtIP binds specifically to GST-CtBP1 (lane 2) and GST-SHARP-RD (lane 3) but not to  GST-RBP-2N (lane 1).	bind
7395	1	2686	7	10	NULL	0	NULL	CtIP	GP	Cell-free;; synthesized	binds		specifically			GST-CtBP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10379_s_214	16287852	(A) Cell-free synthesized  CtIP binds specifically to GST-CtBP1 (lane 2) and GST-SHARP-RD (lane 3) but not to  GST-RBP-2N (lane 1).	bind
7396	2	2686	7	10	NULL	0	NULL	CtIP	GP	Cell-free;; synthesized	binds		specifically			GST-SHARP	GP		RD		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10379_s_214	16287852	(A) Cell-free synthesized  CtIP binds specifically to GST-CtBP1 (lane 2) and GST-SHARP-RD (lane 3) but not to  GST-RBP-2N (lane 1).	bind
7397	3	2686	7	10	NULL	0	NULL	CtIP	GP	Cell-free;; synthesized	does not bind					GST-RBP	GP		2N		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10379_s_214	16287852	(A) Cell-free synthesized  CtIP binds specifically to GST-CtBP1 (lane 2) and GST-SHARP-RD (lane 3) but not to  GST-RBP-2N (lane 1).	bind
5861	1	2687	5	10	NULL	0	NULL	GTP	Chemical		bind					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_2807_s_227	12429740	(A) cells    ells were cultured for 24 h in the absence or presence of 1 muM dexamethasone; cell extracts were subjected to immunoprecipitation using the pan-Ras antibody   Y13259, and GTP and GTP + GDP bound to Ras were determined as described under	bind
5862	2	2687	5	10	NULL	0	NULL	GTP + GDP	Chemical		bind					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_2807_s_227	12429740	(A) cells    ells were cultured for 24 h in the absence or presence of 1 muM dexamethasone; cell extracts were subjected to immunoprecipitation using the pan-Ras antibody   Y13259, and GTP and GTP + GDP bound to Ras were determined as described under	bind
7398	1	2687	7	10	NULL	0	NULL	GTP	Chemical		binds to					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_2807_s_227	12429740	(A) cells    ells were cultured for 24 h in the absence or presence of 1 muM dexamethasone; cell extracts were subjected to immunoprecipitation using the pan-Ras antibody   Y13259, and GTP and GTP + GDP bound to Ras were determined as described under	bind
7399	2	2687	7	10	NULL	0	NULL	GTP + GDP	Chemical		binds to					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_2807_s_227	12429740	(A) cells    ells were cultured for 24 h in the absence or presence of 1 muM dexamethasone; cell extracts were subjected to immunoprecipitation using the pan-Ras antibody   Y13259, and GTP and GTP + GDP bound to Ras were determined as described under	bind
7240	1	2688	5	10	NULL	0	NULL	Ras 	GP	signaling of	activate		directly			Rho	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_2807_s_185	12429740	(A) Cells and NIH 3T3 Cells Transiently Transfected with Wild Type and Activated Ras-- Rho proteins are required for Ras-induced transformation, but there are conflicting data concerning whether Ras signaling directly causes Rho activation or whether some changes in Rho activity occur only during the selection of Ras-transformed cells  ( 5,  8,  16,  18,  23).	bind
7241	2	2688	5	10	NULL	0	NULL	Rho activity	Process	changes in	occur during					Ras-transformed cells	Cell	selection of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_2807_s_185	12429740	(A) Cells and NIH 3T3 Cells Transiently Transfected with Wild Type and Activated Ras-- Rho proteins are required for Ras-induced transformation, but there are conflicting data concerning whether Ras signaling directly causes Rho activation or whether some changes in Rho activity occur only during the selection of Ras-transformed cells  ( 5,  8,  16,  18,  23).	bind
7242	3	2688	5	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_2807_s_185	12429740	(A) Cells and NIH 3T3 Cells Transiently Transfected with Wild Type and Activated Ras-- Rho proteins are required for Ras-induced transformation, but there are conflicting data concerning whether Ras signaling directly causes Rho activation or whether some changes in Rho activity occur only during the selection of Ras-transformed cells  ( 5,  8,  16,  18,  23).	bind
7403	1	2688	7	10	NULL	0	NULL	Ras 	GP	signaling of	activate		directly			Rho	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_2807_s_185	12429740	(A) Cells and NIH 3T3 Cells Transiently Transfected with Wild Type and Activated Ras-- Rho proteins are required for Ras-induced transformation, but there are conflicting data concerning whether Ras signaling directly causes Rho activation or whether some changes in Rho activity occur only during the selection of Ras-transformed cells  ( 5,  8,  16,  18,  23).	bind
7404	2	2688	7	10	NULL	0	NULL	Rho activity	Process	changes in	occur during					Ras-transformed cells 	Cell	selection of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_2807_s_185	12429740	(A) Cells and NIH 3T3 Cells Transiently Transfected with Wild Type and Activated Ras-- Rho proteins are required for Ras-induced transformation, but there are conflicting data concerning whether Ras signaling directly causes Rho activation or whether some changes in Rho activity occur only during the selection of Ras-transformed cells  ( 5,  8,  16,  18,  23).	bind
7877	3	2688	7	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_2807_s_185	12429740	(A) Cells and NIH 3T3 Cells Transiently Transfected with Wild Type and Activated Ras-- Rho proteins are required for Ras-induced transformation, but there are conflicting data concerning whether Ras signaling directly causes Rho activation or whether some changes in Rho activity occur only during the selection of Ras-transformed cells  ( 5,  8,  16,  18,  23).	bind
5352	1	2691	5	10	NULL	0	NULL	Ssb1/2p	GP		bind					HSF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_5_1739_s_268	10793148	(A) Cells were grown in 5% glucose to prevent the binding of Ssb1/2p to HSF under normal growth conditions.	bind
7405	1	2691	7	10	NULL	0	NULL	Ssb1/2p	GP		binds					HSF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_5_1739_s_268	10793148	(A) Cells were grown in 5% glucose to prevent the binding of Ssb1/2p to HSF under normal growth conditions.	bind
5355	1	2692	5	10	NULL	0	NULL	nuclear proteins	GP		bind					IL-8 gene	GP			NF-kappaB binding site	NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_8_3872_s_167	10417151	(A) Characterization of nuclear proteins bound to the NF-kappaB binding site of the IL-8 gene.	bind
7407	1	2692	7	10	NULL	0	NULL	nuclear proteins	GP		binds to					IL-8 gene	GP			NF-kappaB binding site	NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_8_3872_s_167	10417151	(A) Characterization of nuclear proteins bound to the NF-kappaB binding site of the IL-8 gene.	bind
5356	1	2693	5	10	NULL	0	NULL	Smad1	GP		bind									I-BRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6646_s_335	12944489	(A) ChIP of Smad1 bound to I-BRE and BRE-1.	bind
5357	2	2693	5	10	NULL	0	NULL	Smad1	GP		bind									BRE-1	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6646_s_335	12944489	(A) ChIP of Smad1 bound to I-BRE and BRE-1.	bind
7408	1	2693	7	10	NULL	0	NULL	Smad1	GP		binds									I-BRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6646_s_335	12944489	(A) ChIP of Smad1 bound to I-BRE and BRE-1.	bind
7409	2	2693	7	10	NULL	0	NULL	Smad1	GP		binds									BRE-1	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6646_s_335	12944489	(A) ChIP of Smad1 bound to I-BRE and BRE-1.	bind
5358	1	2694	5	10	NULL	0	NULL	Smad1	GP		bind									I-BRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6646_s_224	12944489	(A) ChIP of Smad1 bound to I-BRE.	bind
7410	1	2694	7	10	NULL	0	NULL	Smad1	GP		binds to									I-BRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6646_s_224	12944489	(A) ChIP of Smad1 bound to I-BRE.	bind
5359	1	2695	5	10	NULL	0	NULL	HBP1	GP		bind					p47phox gene	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_7_3011_s_247	15024088	(A) ChIPs were used to test the binding of HBP1 to the endogenous p47phox gene.	bind
7411	1	2695	7	10	NULL	0	NULL	HBP1	GP		binds					p47phox gene	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_7_3011_s_247	15024088	(A) ChIPs were used to test the binding of HBP1 to the endogenous p47phox gene.	bind
5360	1	2697	5	10	NULL	0	NULL	E2F1	GP		bind					PPAR 1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_39_s_105	12110166	(A) Chromatin immunoprecipitation (ChIP) assays demonstrating binding of E2F1 and E2F4 to the  PPAR 1 promoter.	bind
5361	2	2697	5	10	NULL	0	NULL	E2F4	GP		bind					PPAR 1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_39_s_105	12110166	(A) Chromatin immunoprecipitation (ChIP) assays demonstrating binding of E2F1 and E2F4 to the  PPAR 1 promoter.	bind
7412	1	2697	7	10	NULL	0	NULL	E2F1	GP		binds					PPAR 1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_39_s_105	12110166	(A) Chromatin immunoprecipitation (ChIP) assays demonstrating binding of E2F1 and E2F4 to the  PPAR 1 promoter.	bind
7413	2	2697	7	10	NULL	0	NULL	E2F4	GP		binds					PPAR 1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_39_s_105	12110166	(A) Chromatin immunoprecipitation (ChIP) assays demonstrating binding of E2F1 and E2F4 to the  PPAR 1 promoter.	bind
5362	1	2698	5	10	NULL	0	NULL	NF-Y	GP		bind					ODF gene	GP	mouse			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_512_s_124	15601870	(A) Chromatin immunoprecipitation analysis of NF-Y binding to the  mouse ODF gene in vivo.	bind
7414	1	2698	7	10	NULL	0	NULL	NF-Y	GP		binds					ODF gene	GP	mouse			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_512_s_124	15601870	(A) Chromatin immunoprecipitation analysis of NF-Y binding to the  mouse ODF gene in vivo.	bind
5363	1	2699	5	10	NULL	0	NULL	Bet1	GP		bind			LxxLE sequence 		Sec23/24 complex	GP		B site		NULL		NULL	NULL	NULL	NULL	gw60_cell_114_4_483_s_60	12941276	(A) Close-up view of the Bet1 LxxLE sequence bound to the B site of the Sec23/24 complex.	bind
7415	1	2699	7	10	NULL	0	NULL	Bet1	GP		binds to			LxxLE sequence		Sec23/24 complex	GP		B site of 		NULL		NULL	NULL	NULL	NULL	gw60_cell_114_4_483_s_60	12941276	(A) Close-up view of the Bet1 LxxLE sequence bound to the B site of the Sec23/24 complex.	bind
5364	1	2700	5	10	NULL	0	NULL	EDA isoforms	GP		bind					EDAR receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_gene_371_1_42_s_107	16423472	(A) Co-immunoprecipitation analysis  for binding of EDA isoforms to EDAR, XEDAR, or TROY receptors.	bind
5365	2	2700	5	10	NULL	0	NULL	EDA isoforms	GP		bind					XEDAR receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_gene_371_1_42_s_107	16423472	(A) Co-immunoprecipitation analysis  for binding of EDA isoforms to EDAR, XEDAR, or TROY receptors.	bind
5366	3	2700	5	10	NULL	0	NULL	EDA isoforms	GP		bind					TROY receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_gene_371_1_42_s_107	16423472	(A) Co-immunoprecipitation analysis  for binding of EDA isoforms to EDAR, XEDAR, or TROY receptors.	bind
5367	4	2700	5	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_gene_371_1_42_s_107	16423472	(A) Co-immunoprecipitation analysis  for binding of EDA isoforms to EDAR, XEDAR, or TROY receptors.	bind
5368	5	2700	5	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_gene_371_1_42_s_107	16423472	(A) Co-immunoprecipitation analysis  for binding of EDA isoforms to EDAR, XEDAR, or TROY receptors.	bind
5369	6	2700	5	10	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_gene_371_1_42_s_107	16423472	(A) Co-immunoprecipitation analysis  for binding of EDA isoforms to EDAR, XEDAR, or TROY receptors.	bind
7944	1	2700	7	10	NULL	0	NULL	EDA isoforms	GP		bind					EDAR receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_gene_371_1_42_s_107	16423472	(A) Co-immunoprecipitation analysis  for binding of EDA isoforms to EDAR, XEDAR, or TROY receptors.	bind
7945	2	2700	7	10	NULL	0	NULL	EDA isoforms	GP		bind					XEDAR receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_gene_371_1_42_s_107	16423472	(A) Co-immunoprecipitation analysis  for binding of EDA isoforms to EDAR, XEDAR, or TROY receptors.	bind
7946	3	2700	7	10	NULL	0	NULL	EDA isoforms	GP		bind					TROY receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_gene_371_1_42_s_107	16423472	(A) Co-immunoprecipitation analysis  for binding of EDA isoforms to EDAR, XEDAR, or TROY receptors.	bind
54143	4	2700	7	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_gene_371_1_42_s_107	16423472	(A) Co-immunoprecipitation analysis  for binding of EDA isoforms to EDAR, XEDAR, or TROY receptors.	bind
54144	5	2700	7	10	NULL	0	NULL	statement 1	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_gene_371_1_42_s_107	16423472	(A) Co-immunoprecipitation analysis  for binding of EDA isoforms to EDAR, XEDAR, or TROY receptors.	bind
54145	6	2700	7	10	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_gene_371_1_42_s_107	16423472	(A) Co-immunoprecipitation analysis  for binding of EDA isoforms to EDAR, XEDAR, or TROY receptors.	bind
5371	1	2701	5	10	NULL	0	NULL	Vav	GP		bind					SLP-76	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_155_s_88	9047237	(A) Coexpression of ZAP-70 induces binding between Vav and SLP-76.	bind
5373	2	2701	5	10	NULL	0	NULL	ZAP-70	GP	coexpression of	induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_155_s_88	9047237	(A) Coexpression of ZAP-70 induces binding between Vav and SLP-76.	bind
7947	1	2701	7	10	NULL	0	NULL	Vav	GP		bind					SLP-76	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_155_s_88	9047237	(A) Coexpression of ZAP-70 induces binding between Vav and SLP-76.	bind
7948	2	2701	7	10	NULL	0	NULL	ZAP-70	GP	coexpression of 	induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_155_s_88	9047237	(A) Coexpression of ZAP-70 induces binding between Vav and SLP-76.	bind
5375	1	2702	5	10	NULL	0	NULL	Rad24	GP		bind					Rfc5	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5485_s_252	9710632	(A) Coimmunoprecipitation of Rad24 and Rfc2 with Rfc5.	bind
5376	2	2702	5	10	NULL	0	NULL	Rfc2	GP		bind					Rfc5	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5485_s_252	9710632	(A) Coimmunoprecipitation of Rad24 and Rfc2 with Rfc5.	bind
7949	1	2702	7	10	NULL	0	NULL	Rad24	GP		bind					Rfc5	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5485_s_252	9710632	(A) Coimmunoprecipitation of Rad24 and Rfc2 with Rfc5.	bind
7950	2	2702	7	10	NULL	0	NULL	Rfc2	GP		bind					Rfc5	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5485_s_252	9710632	(A) Coimmunoprecipitation of Rad24 and Rfc2 with Rfc5.	bind
7243	1	2703	5	10	NULL	0	NULL	C3d	GP		bind		covalently			CD19 & Ag-IgM	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_107_s_218	9047233	(A) Coligation of CD19 and the Ag-receptor complex (IgM) by C3d covalently bound to Ag amplifies B cell responses.	bind
7244	2	2703	5	10	NULL	0	NULL	Ag-IgM	GP		is					Ag-receptor complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_107_s_218	9047233	(A) Coligation of CD19 and the Ag-receptor complex (IgM) by C3d covalently bound to Ag amplifies B cell responses.	bind
7245	3	2703	5	10	NULL	0	NULL	C3d	GP		coligates					CD19 & Ag-IgM	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_107_s_218	9047233	(A) Coligation of CD19 and the Ag-receptor complex (IgM) by C3d covalently bound to Ag amplifies B cell responses.	bind
7246	4	2703	5	10	NULL	0	NULL	statement 3	Process		amplifies					B cell responses	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_107_s_218	9047233	(A) Coligation of CD19 and the Ag-receptor complex (IgM) by C3d covalently bound to Ag amplifies B cell responses.	bind
7951	1	2703	7	10	NULL	0	NULL	C3d 	GP		bind		covalently			Ag	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_107_s_218	9047233	(A) Coligation of CD19 and the Ag-receptor complex (IgM) by C3d covalently bound to Ag amplifies B cell responses.	bind
7952	2	2703	7	10	NULL	0	NULL	statement 1	Process		coligates					CD19 & Ag-IgM	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_107_s_218	9047233	(A) Coligation of CD19 and the Ag-receptor complex (IgM) by C3d covalently bound to Ag amplifies B cell responses.	bind
7953	3	2703	7	10	NULL	0	NULL	Ag-IgM	GP		is					Ag-receptor complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_107_s_218	9047233	(A) Coligation of CD19 and the Ag-receptor complex (IgM) by C3d covalently bound to Ag amplifies B cell responses.	bind
7954	4	2703	7	10	NULL	0	NULL	statement 2	Process		amplifies					B cell responses	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_107_s_218	9047233	(A) Coligation of CD19 and the Ag-receptor complex (IgM) by C3d covalently bound to Ag amplifies B cell responses.	bind
5451	1	2707	5	10	NULL	0	NULL	histidine	AminoAcid		bind					hemes	Chemical				NULL	R. gelatinosus	NULL	NULL	NULL	NULL	gw60_jbacteriol_184_14_3815_s_153	12081951	(A) Comparison of the helix IV sequences showing the two histidines that bind the hemes (shaded) and the extra residue (boldface and underlined) in the  R. gelatinosus sequence.	bind
5452	2	2707	5	10	NULL	0	NULL	histidine	AminoAcid		bind					extra residue					NULL	R. gelatinosus	NULL	NULL	NULL	NULL	gw60_jbacteriol_184_14_3815_s_153	12081951	(A) Comparison of the helix IV sequences showing the two histidines that bind the hemes (shaded) and the extra residue (boldface and underlined) in the  R. gelatinosus sequence.	bind
7956	1	2707	7	10	NULL	0	NULL	histidine	AminoAcid		bind					hemes	Chemical				NULL	in R. gelatinosus	NULL	NULL	NULL	NULL	gw60_jbacteriol_184_14_3815_s_153	12081951	(A) Comparison of the helix IV sequences showing the two histidines that bind the hemes (shaded) and the extra residue (boldface and underlined) in the  R. gelatinosus sequence.	bind
7957	2	2707	7	10	NULL	0	NULL	histidines	AminoAcid		bind					extra residue					NULL	in R. gelatinosus	NULL	NULL	NULL	NULL	gw60_jbacteriol_184_14_3815_s_153	12081951	(A) Comparison of the helix IV sequences showing the two histidines that bind the hemes (shaded) and the extra residue (boldface and underlined) in the  R. gelatinosus sequence.	bind
5465	1	2709	5	10	NULL	0	NULL	GTP S	Chemical		bind					membranes	CellComponent	limbic forebrain			NULL	control mice	NULL	NULL	NULL	NULL	gw60_neuroscience_117_3_639_s_104	12617968	(A) Comparison of the stimulation of [35]GTP S binding by dopamine to membranes of the limbic forebrain obtained from control (B0: square) and BPA-treated (B2: triangle) mice.	bind
5467	2	2709	5	10	NULL	0	NULL	GTP S	Chemical		bind					membranes	CellComponent	limbic forebrain			NULL	BPA-treated mice	NULL	NULL	NULL	NULL	gw60_neuroscience_117_3_639_s_104	12617968	(A) Comparison of the stimulation of [35]GTP S binding by dopamine to membranes of the limbic forebrain obtained from control (B0: square) and BPA-treated (B2: triangle) mice.	bind
5469	3	2709	5	10	NULL	0	NULL	dopamine	Chemical		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_117_3_639_s_104	12617968	(A) Comparison of the stimulation of [35]GTP S binding by dopamine to membranes of the limbic forebrain obtained from control (B0: square) and BPA-treated (B2: triangle) mice.	bind
5470	4	2709	5	10	NULL	0	NULL	dopamine	Chemical		stimulate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_117_3_639_s_104	12617968	(A) Comparison of the stimulation of [35]GTP S binding by dopamine to membranes of the limbic forebrain obtained from control (B0: square) and BPA-treated (B2: triangle) mice.	bind
7958	1	2709	7	10	NULL	0	NULL	GTP S	Chemical		bind					membranes	CellComponent	limbic forebrain			NULL	in control mice	NULL	NULL	NULL	NULL	gw60_neuroscience_117_3_639_s_104	12617968	(A) Comparison of the stimulation of [35]GTP S binding by dopamine to membranes of the limbic forebrain obtained from control (B0: square) and BPA-treated (B2: triangle) mice.	bind
7959	2	2709	7	10	NULL	0	NULL	GTP S	Chemical		bind					 membranes	CellComponent	limbic forebrain			NULL	in BPA-treated mice	NULL	NULL	NULL	NULL	gw60_neuroscience_117_3_639_s_104	12617968	(A) Comparison of the stimulation of [35]GTP S binding by dopamine to membranes of the limbic forebrain obtained from control (B0: square) and BPA-treated (B2: triangle) mice.	bind
8851	3	2709	7	10	NULL	0	NULL	dopamine	Chemical		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_117_3_639_s_104	12617968	(A) Comparison of the stimulation of [35]GTP S binding by dopamine to membranes of the limbic forebrain obtained from control (B0: square) and BPA-treated (B2: triangle) mice.	bind
8852	4	2709	7	10	NULL	0	NULL	dopamine	Chemical		stimulate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_117_3_639_s_104	12617968	(A) Comparison of the stimulation of [35]GTP S binding by dopamine to membranes of the limbic forebrain obtained from control (B0: square) and BPA-treated (B2: triangle) mice.	bind
5472	1	2710	5	10	NULL	0	NULL	AP-1	GP		bind					AP-1 probe	NucleicAcid	unlabeled			NULL		NULL	NULL	NULL	NULL	gw60_brainres_872_1_282_s_78	10924710	(A) Competition of AP-1 binding with unlabeled AP-1 probe.	bind
7960	1	2710	7	10	NULL	0	NULL	AP-1	GP		bind					AP-1 probe	NucleicAcid	unlabeled			NULL		NULL	NULL	NULL	NULL	gw60_brainres_872_1_282_s_78	10924710	(A) Competition of AP-1 binding with unlabeled AP-1 probe.	bind
5473	1	2711	5	10	NULL	0	NULL	complex			bind					(eIF)-4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4723_s_36	10970864	(A) complex binds to the translation factor eukaryotic initiation factor (eIF)-4G, which in turn interacts with eIF-4E bound to the cap ( Tarun and Sachs, 1996).	bind
5474	2	2711	5	10	NULL	0	NULL	(eIF)-4G	GP		is					translation factor eukaryotic initiation factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4723_s_36	10970864	(A) complex binds to the translation factor eukaryotic initiation factor (eIF)-4G, which in turn interacts with eIF-4E bound to the cap ( Tarun and Sachs, 1996).	bind
5475	3	2711	5	10	NULL	0	NULL	eIF-4E	GP		bind					cap	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4723_s_36	10970864	(A) complex binds to the translation factor eukaryotic initiation factor (eIF)-4G, which in turn interacts with eIF-4E bound to the cap ( Tarun and Sachs, 1996).	bind
5476	4	2711	5	10	NULL	0	NULL	statement 1	Process		interact with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4723_s_36	10970864	(A) complex binds to the translation factor eukaryotic initiation factor (eIF)-4G, which in turn interacts with eIF-4E bound to the cap ( Tarun and Sachs, 1996).	bind
7961	1	2711	7	10	NULL	0	NULL	complex			binds					 eIF-4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4723_s_36	10970864	(A) complex binds to the translation factor eukaryotic initiation factor (eIF)-4G, which in turn interacts with eIF-4E bound to the cap ( Tarun and Sachs, 1996).	bind
7962	3	2711	7	10	NULL	0	NULL	statement 1	Process		bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4723_s_36	10970864	(A) complex binds to the translation factor eukaryotic initiation factor (eIF)-4G, which in turn interacts with eIF-4E bound to the cap ( Tarun and Sachs, 1996).	bind
7963	2	2711	7	10	NULL	0	NULL	eIF-4E	GP		bind					cap	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4723_s_36	10970864	(A) complex binds to the translation factor eukaryotic initiation factor (eIF)-4G, which in turn interacts with eIF-4E bound to the cap ( Tarun and Sachs, 1996).	bind
8853	4	2711	7	10	NULL	0	NULL	(eIF)-4G	GP		is					eukaryotic initiation factor 	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4723_s_36	10970864	(A) complex binds to the translation factor eukaryotic initiation factor (eIF)-4G, which in turn interacts with eIF-4E bound to the cap ( Tarun and Sachs, 1996).	bind
5479	1	2712	5	10	NULL	0	NULL	Kap121p	GP	recombinant	bind					GST-Ste12p	GP		aa494-688		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2544_s_269	11909949	(A) Complexes containing recombinant Kap121p bound to GST-Ste12p (aa494-688) and immobilized on GT-Sepharose were incubated with Ran-GTP ( 120 ng), Ran-GDP ( 120 ng), or GTP-loading buffer, as indicated, for 30 min at room temperature.	bind
8069	1	2712	7	10	NULL	0	NULL	Kap121p	GP	recombinant	bind					GST-Ste12p	GP		aa 494-688		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2544_s_269	11909949	(A) Complexes containing recombinant Kap121p bound to GST-Ste12p (aa494-688) and immobilized on GT-Sepharose were incubated with Ran-GTP ( 120 ng), Ran-GDP ( 120 ng), or GTP-loading buffer, as indicated, for 30 min at room temperature.	bind
5484	1	2714	5	10	NULL	0	NULL	HSV-1 capsids	CellComponent	isolated	bind					liver nuclei	CellComponent	purified;; rat			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4922_s_203	10848617	(A) Confocal immunofluorescence microscopy of isolated HSV-1 capsids bound to purified rat liver nuclei in the presence of rat liver cytosol (control panel).	bind
5486	2	2714	5	10	NULL	0	NULL	statement 1	Process		in the presence of					liver cytosol 	CellComponent	rat			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4922_s_203	10848617	(A) Confocal immunofluorescence microscopy of isolated HSV-1 capsids bound to purified rat liver nuclei in the presence of rat liver cytosol (control panel).	bind
8070	1	2714	7	10	NULL	0	NULL	HSV-1 capsids	CellComponent	isolated	bind					liver nuclei	CellComponent	purified;; rat 			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4922_s_203	10848617	(A) Confocal immunofluorescence microscopy of isolated HSV-1 capsids bound to purified rat liver nuclei in the presence of rat liver cytosol (control panel).	bind
46396	2	2714	7	10	NULL	0	NULL	statement 1	Process		occurs in presence of					liver cytosol	CellComponent	rat			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4922_s_203	10848617	(A) Confocal immunofluorescence microscopy of isolated HSV-1 capsids bound to purified rat liver nuclei in the presence of rat liver cytosol (control panel).	bind
5488	1	2716	5	10	NULL	0	NULL	GFP-Ras isoforms	GP	constitutively;; active	bind		preferentially			GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_5_865_s_55	12021258	(A) Constitutively active GFP-Ras isoforms preferentially bind GTP.	bind
8071	1	2716	7	10	NULL	0	NULL	GFP-Ras isoforms	GP	Constitutively;; active	bind		preferentially			GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_5_865_s_55	12021258	(A) Constitutively active GFP-Ras isoforms preferentially bind GTP.	bind
5497	1	2722	5	10	NULL	0	NULL	Yrb1	GP		bind					GST-Gsp1GTP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4295_s_216	10825193	(A) Cooperative binding of Yrb1 and Xpo1 to GST-Gsp1GTP.	bind
5498	2	2722	5	10	NULL	0	NULL	Xpo1	GP		bind					GST-Gsp1GTP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4295_s_216	10825193	(A) Cooperative binding of Yrb1 and Xpo1 to GST-Gsp1GTP.	bind
5499	3	2722	5	10	NULL	0	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4295_s_216	10825193	(A) Cooperative binding of Yrb1 and Xpo1 to GST-Gsp1GTP.	bind
8072	1	2722	7	10	NULL	0	NULL	Yrb1	GP		bind					GST-Gsp1GTP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4295_s_216	10825193	(A) Cooperative binding of Yrb1 and Xpo1 to GST-Gsp1GTP.	bind
8073	2	2722	7	10	NULL	0	NULL	Xpo1	GP		bind					GST-Gsp1GTP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4295_s_216	10825193	(A) Cooperative binding of Yrb1 and Xpo1 to GST-Gsp1GTP.	bind
8096	3	2722	7	10	NULL	0	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4295_s_216	10825193	(A) Cooperative binding of Yrb1 and Xpo1 to GST-Gsp1GTP.	bind
5500	1	2723	5	10	NULL	0	NULL	Oct-1	GP		bind			POU domain		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_14_4700_s_242	11416146	(A) Cooperative VP16 binding to the Oct-1 POU domain-DNA complex.	bind
5501	2	2723	5	10	NULL	0	NULL	VP16	GP		bind		cooperative			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_14_4700_s_242	11416146	(A) Cooperative VP16 binding to the Oct-1 POU domain-DNA complex.	bind
8097	1	2723	7	10	NULL	0	NULL	VP16 	GP		bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_14_4700_s_242	11416146	(A) Cooperative VP16 binding to the Oct-1 POU domain-DNA complex.	bind
8854	2	2723	7	10	NULL	0	NULL	Oct-1	GP		bind			POU		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_14_4700_s_242	11416146	(A) Cooperative VP16 binding to the Oct-1 POU domain-DNA complex.	bind
5508	1	2725	5	10	NULL	0	NULL	CR2	GP		bind					Tax	GP	putative	transactivation domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_16_5520_s_222	11463834	(A) CR2 binds to the putative transactivation domain of Tax.	bind
8100	1	2725	7	10	NULL	0	NULL	 CR2	GP		bind					Tax	GP	putative 	transactivation domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_16_5520_s_222	11463834	(A) CR2 binds to the putative transactivation domain of Tax.	bind
5512	1	2726	5	10	NULL	0	NULL	OspB	GP		bind					CR3	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_9_6138_s_94	16113335	(A) CR3 clustering (red); (B) OspB binding superimposed  on CR3 (green).	bind
54148	1	2726	7	10	NULL	0	NULL	OspB	GP		bind					CR3	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_9_6138_s_94	16113335	(A) CR3 clustering (red); (B) OspB binding superimposed  on CR3 (green).	bind
5513	1	2727	5	10	NULL	0	NULL	p53	GP		bind					CBP	GP		KIX domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4849_s_87	10848610	(A) CREB enhances p53 binding to the KIX domain of CBP.	bind
5514	2	2727	5	10	NULL	0	NULL	CREB	GP		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4849_s_87	10848610	(A) CREB enhances p53 binding to the KIX domain of CBP.	bind
8147	1	2727	7	10	NULL	0	NULL	p53	GP		binds					CBP	GP		KIX		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4849_s_87	10848610	(A) CREB enhances p53 binding to the KIX domain of CBP.	bind
8148	2	2727	7	10	NULL	0	NULL	CREB	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4849_s_87	10848610	(A) CREB enhances p53 binding to the KIX domain of CBP.	bind
5515	1	2728	5	10	NULL	0	NULL	CRF	GP		bind					CRF receptor 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_30_4_513_s_140	16198122	(A) CRF binds to CRF receptor 1 to evoke protein kinase C-mediated signaling pathways  and cause a fine tuning state A of the common CRF and UCN signaling machinery (Sig  A).	bind
5517	2	2728	5	10	NULL	0	NULL	statement 1	Process		evoke					protein kinase C-mediated signaling pathways	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_30_4_513_s_140	16198122	(A) CRF binds to CRF receptor 1 to evoke protein kinase C-mediated signaling pathways  and cause a fine tuning state A of the common CRF and UCN signaling machinery (Sig  A).	bind
5519	3	2728	5	10	NULL	0	NULL	statement 1	Process		causes					common CRF signaling machinery	Process	fine tuning state A of 			NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_30_4_513_s_140	16198122	(A) CRF binds to CRF receptor 1 to evoke protein kinase C-mediated signaling pathways  and cause a fine tuning state A of the common CRF and UCN signaling machinery (Sig  A).	bind
9047	4	2728	5	10	NULL	0	NULL	statement 1	Process		causes					common UCN signaling machinery	Process	fine tuning state A of			NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_30_4_513_s_140	16198122	(A) CRF binds to CRF receptor 1 to evoke protein kinase C-mediated signaling pathways  and cause a fine tuning state A of the common CRF and UCN signaling machinery (Sig  A).	bind
8149	1	2728	7	10	NULL	0	NULL	CRF	GP		binds					CRF receptor 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_30_4_513_s_140	16198122	(A) CRF binds to CRF receptor 1 to evoke protein kinase C-mediated signaling pathways  and cause a fine tuning state A of the common CRF and UCN signaling machinery (Sig  A).	bind
8150	2	2728	7	10	NULL	0	NULL	statement 1	Process		evoke					protein kinase C-mediated signaling pathways	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_30_4_513_s_140	16198122	(A) CRF binds to CRF receptor 1 to evoke protein kinase C-mediated signaling pathways  and cause a fine tuning state A of the common CRF and UCN signaling machinery (Sig  A).	bind
8151	3	2728	7	10	NULL	0	NULL	statement 1	Process		cause					common CRF signaling machinery	Process	fine tuning state A of			NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_30_4_513_s_140	16198122	(A) CRF binds to CRF receptor 1 to evoke protein kinase C-mediated signaling pathways  and cause a fine tuning state A of the common CRF and UCN signaling machinery (Sig  A).	bind
8152	4	2728	7	10	NULL	0	NULL	statement 1	Process		cause					UCN signaling machinery 	Process	fine tuning state A of			NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_30_4_513_s_140	16198122	(A) CRF binds to CRF receptor 1 to evoke protein kinase C-mediated signaling pathways  and cause a fine tuning state A of the common CRF and UCN signaling machinery (Sig  A).	bind
5521	1	2729	5	10	NULL	0	NULL	CRP	GP		bind					Ppac	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_7_2215_s_89	15028709	(A) CRP binding to the  Ppac promoter.	bind
8163	1	2729	7	10	NULL	0	NULL	CRP	GP		binds					Ppac	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_7_2215_s_89	15028709	(A) CRP binding to the  Ppac promoter.	bind
5522	1	2730	5	10	NULL	0	NULL	CRT	GP		bind					NES	AminoAcid	WT			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_1_127_s_231	11149926	(A) CRT binding to the WT NES requires the presence of RanGTP.	bind
5524	2	2730	5	10	NULL	0	NULL	statement 1	Process		occurs in presence of					RanGTP	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_1_127_s_231	11149926	(A) CRT binding to the WT NES requires the presence of RanGTP.	bind
8280	1	2730	7	10	NULL	0	NULL	CRT	GP		binds					NES	AminoAcid	WT			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_1_127_s_231	11149926	(A) CRT binding to the WT NES requires the presence of RanGTP.	bind
8281	2	2730	7	10	NULL	0	NULL	statement 1	Process		occurs in the presence of					RanGTP	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_1_127_s_231	11149926	(A) CRT binding to the WT NES requires the presence of RanGTP.	bind
5527	1	2731	5	10	NULL	0	NULL	CtsR	GP		bind		specifically			clpB	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_4_1165_s_171	14762012	(A) CtsR binds specifically to the  clpB promoter region.	bind
8282	1	2731	7	10	NULL	0	NULL	CtsR	GP		bind		specifically			clpB	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_4_1165_s_171	14762012	(A) CtsR binds specifically to the  clpB promoter region.	bind
5528	1	2732	5	10	NULL	0	NULL	CtsR	GP		bind		specifically			clpP	GP	S. salivarius		promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_2_683_s_51	12511518	(A) CtsR binds specifically to the  S. salivarius clpP promoter region.	bind
8283	1	2732	7	10	NULL	0	NULL	CtsR	GP		bind		specifically			clpP	GP	S. salivarius		promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_2_683_s_51	12511518	(A) CtsR binds specifically to the  S. salivarius clpP promoter region.	bind
5530	1	2733	5	10	NULL	0	NULL	AgrA	GP		bind							isolated		P2 repeats	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_22_7549_s_149	15516566	(A) Curves showing binding of AgrA to isolated P2 and P3 repeats and to P3  mutant fragments.	bind
5532	2	2733	5	10	NULL	0	NULL	AgrA	GP		bind							isolated		P3 repeats	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_22_7549_s_149	15516566	(A) Curves showing binding of AgrA to isolated P2 and P3 repeats and to P3  mutant fragments.	bind
5533	3	2733	5	10	NULL	0	NULL	AgrA	GP		bind					P3 fragments	AminoAcid	mutant 			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_22_7549_s_149	15516566	(A) Curves showing binding of AgrA to isolated P2 and P3 repeats and to P3  mutant fragments.	bind
8284	1	2733	7	10	NULL	0	NULL	AgrA	GP		binds							isolated		P2 repeats	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_22_7549_s_149	15516566	(A) Curves showing binding of AgrA to isolated P2 and P3 repeats and to P3  mutant fragments.	bind
8285	2	2733	7	10	NULL	0	NULL	AgrA	GP		bind							isolated		P3 repeats	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_22_7549_s_149	15516566	(A) Curves showing binding of AgrA to isolated P2 and P3 repeats and to P3  mutant fragments.	bind
8286	3	2733	7	10	NULL	0	NULL	AgrA	GP		bind					P3 fragment	AminoAcid	mutant			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_22_7549_s_149	15516566	(A) Curves showing binding of AgrA to isolated P2 and P3 repeats and to P3  mutant fragments.	bind
5534	1	2735	5	10	NULL	0	NULL	Daam1	GP		bind					Dvl2	GP		PDZ domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_843_s_98	11779461	(A) Daam1  and C-Daam1 bind to the Dvl2 PDZ  and DEP domains, but not to the DIX  domain.	bind
5535	2	2735	5	10	NULL	0	NULL	Daam1	GP		bind					Dvl2	GP		DEP domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_843_s_98	11779461	(A) Daam1  and C-Daam1 bind to the Dvl2 PDZ  and DEP domains, but not to the DIX  domain.	bind
5537	3	2735	5	10	NULL	0	NULL	Daam1	GP		does not bind					Dvl2	GP		DIX domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_843_s_98	11779461	(A) Daam1  and C-Daam1 bind to the Dvl2 PDZ  and DEP domains, but not to the DIX  domain.	bind
5540	4	2735	5	10	NULL	0	NULL	C-Daam1	GP		bind					Dvl2	GP		PDZ domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_843_s_98	11779461	(A) Daam1  and C-Daam1 bind to the Dvl2 PDZ  and DEP domains, but not to the DIX  domain.	bind
5541	5	2735	5	10	NULL	0	NULL	C-Daam1	GP		bind					Dvl2	GP		DEP domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_843_s_98	11779461	(A) Daam1  and C-Daam1 bind to the Dvl2 PDZ  and DEP domains, but not to the DIX  domain.	bind
5542	6	2735	5	10	NULL	0	NULL	C-Daam1	GP		does not bind					Dvl2	GP		DIX domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_843_s_98	11779461	(A) Daam1  and C-Daam1 bind to the Dvl2 PDZ  and DEP domains, but not to the DIX  domain.	bind
8287	1	2735	7	10	NULL	0	NULL	Daam1	GP		bind					Dvl2	GP		PDZ		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_843_s_98	11779461	(A) Daam1  and C-Daam1 bind to the Dvl2 PDZ  and DEP domains, but not to the DIX  domain.	bind
8288	2	2735	7	10	NULL	0	NULL	Daam1	GP		bind					Dvl2	GP		DEP		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_843_s_98	11779461	(A) Daam1  and C-Daam1 bind to the Dvl2 PDZ  and DEP domains, but not to the DIX  domain.	bind
8289	3	2735	7	10	NULL	0	NULL	Daam1	GP		does not bind					Dvl2	GP		DIX		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_843_s_98	11779461	(A) Daam1  and C-Daam1 bind to the Dvl2 PDZ  and DEP domains, but not to the DIX  domain.	bind
8290	4	2735	7	10	NULL	0	NULL	C-Daam1	GP		bind					Dvl2	GP		PDZ		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_843_s_98	11779461	(A) Daam1  and C-Daam1 bind to the Dvl2 PDZ  and DEP domains, but not to the DIX  domain.	bind
8291	5	2735	7	10	NULL	0	NULL	C-Daam1	GP		bind					Dvl2	GP		DEP		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_843_s_98	11779461	(A) Daam1  and C-Daam1 bind to the Dvl2 PDZ  and DEP domains, but not to the DIX  domain.	bind
8292	6	2735	7	10	NULL	0	NULL	C-Daam1	GP		does not bind					Dvl2	GP		DIX		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_843_s_98	11779461	(A) Daam1  and C-Daam1 bind to the Dvl2 PDZ  and DEP domains, but not to the DIX  domain.	bind
5543	1	2736	5	10	NULL	0	NULL	SLP-76	GP		bind			SH2 domain		CD6P	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_17_6727_s_176	16914752	(A) Data for two concentrations (muM) of the  SLP-76 SH2 domain show binding to CD6P, weaker binding to 662F, and no binding to  CD6, where only the bulk effect of the high-protein concentration is seen.	bind
5544	2	2736	5	10	NULL	0	NULL	SLP-76	GP		bind		weakly	SH2 domain					662F		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_17_6727_s_176	16914752	(A) Data for two concentrations (muM) of the  SLP-76 SH2 domain show binding to CD6P, weaker binding to 662F, and no binding to  CD6, where only the bulk effect of the high-protein concentration is seen.	bind
5545	3	2736	5	10	NULL	0	NULL	SLP-76	GP		does not bind			SH2 domain		CD6	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_17_6727_s_176	16914752	(A) Data for two concentrations (muM) of the  SLP-76 SH2 domain show binding to CD6P, weaker binding to 662F, and no binding to  CD6, where only the bulk effect of the high-protein concentration is seen.	bind
8293	1	2736	7	10	NULL	0	NULL	SLP-76	GP		bind			SH2 domain		CD6P	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_17_6727_s_176	16914752	(A) Data for two concentrations (muM) of the  SLP-76 SH2 domain show binding to CD6P, weaker binding to 662F, and no binding to  CD6, where only the bulk effect of the high-protein concentration is seen.	bind
8294	2	2736	7	10	NULL	0	NULL	SLP-76	GP		bind		weakly	SH2 domain					662F		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_17_6727_s_176	16914752	(A) Data for two concentrations (muM) of the  SLP-76 SH2 domain show binding to CD6P, weaker binding to 662F, and no binding to  CD6, where only the bulk effect of the high-protein concentration is seen.	bind
8295	3	2736	7	10	NULL	0	NULL	SLP-76	GP		does not bind			SH2 domain		CD6	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_17_6727_s_176	16914752	(A) Data for two concentrations (muM) of the  SLP-76 SH2 domain show binding to CD6P, weaker binding to 662F, and no binding to  CD6, where only the bulk effect of the high-protein concentration is seen.	bind
5852	1	2737	5	10	NULL	0	NULL	DDR	GP		bind					collagens	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_129	9659900	(A) DDR binding to different types of commercially-derived collagens; note weaker binding of both DDR1 and DDR2 to network-forming collagen type IV as compared to rest of collagens, which are all examples of fibril-forming collagens (K, kangaroo tail; B, bovine nasal septum; C, calf skin; H, human placenta; R, rat tail; roman numerals represent biochemical types of collagen).	bind
5853	2	2737	5	10	NULL	0	NULL	DDR1	GP		bind					collagen type IV	GP	network-forming			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_129	9659900	(A) DDR binding to different types of commercially-derived collagens; note weaker binding of both DDR1 and DDR2 to network-forming collagen type IV as compared to rest of collagens, which are all examples of fibril-forming collagens (K, kangaroo tail; B, bovine nasal septum; C, calf skin; H, human placenta; R, rat tail; roman numerals represent biochemical types of collagen).	bind
5854	3	2737	5	10	NULL	0	NULL	DDR2	GP		bind					collagen type IV	GP	network-forming			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_129	9659900	(A) DDR binding to different types of commercially-derived collagens; note weaker binding of both DDR1 and DDR2 to network-forming collagen type IV as compared to rest of collagens, which are all examples of fibril-forming collagens (K, kangaroo tail; B, bovine nasal septum; C, calf skin; H, human placenta; R, rat tail; roman numerals represent biochemical types of collagen).	bind
5855	4	2737	5	10	NULL	0	NULL	DDR1	GP		bind					collagens	GP	fibril-forming			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_129	9659900	(A) DDR binding to different types of commercially-derived collagens; note weaker binding of both DDR1 and DDR2 to network-forming collagen type IV as compared to rest of collagens, which are all examples of fibril-forming collagens (K, kangaroo tail; B, bovine nasal septum; C, calf skin; H, human placenta; R, rat tail; roman numerals represent biochemical types of collagen).	bind
5856	5	2737	5	10	NULL	0	NULL	DDR2	GP		bind					collagens	GP	fibril-forming			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_129	9659900	(A) DDR binding to different types of commercially-derived collagens; note weaker binding of both DDR1 and DDR2 to network-forming collagen type IV as compared to rest of collagens, which are all examples of fibril-forming collagens (K, kangaroo tail; B, bovine nasal septum; C, calf skin; H, human placenta; R, rat tail; roman numerals represent biochemical types of collagen).	bind
5857	6	2737	5	10	NULL	0	NULL	statement 2	Process		weaker than					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_129	9659900	(A) DDR binding to different types of commercially-derived collagens; note weaker binding of both DDR1 and DDR2 to network-forming collagen type IV as compared to rest of collagens, which are all examples of fibril-forming collagens (K, kangaroo tail; B, bovine nasal septum; C, calf skin; H, human placenta; R, rat tail; roman numerals represent biochemical types of collagen).	bind
5858	7	2737	5	10	NULL	0	NULL	statement 2	Process		weaker than					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_129	9659900	(A) DDR binding to different types of commercially-derived collagens; note weaker binding of both DDR1 and DDR2 to network-forming collagen type IV as compared to rest of collagens, which are all examples of fibril-forming collagens (K, kangaroo tail; B, bovine nasal septum; C, calf skin; H, human placenta; R, rat tail; roman numerals represent biochemical types of collagen).	bind
5859	8	2737	5	10	NULL	0	NULL	statement 3	Process		weaker than					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_129	9659900	(A) DDR binding to different types of commercially-derived collagens; note weaker binding of both DDR1 and DDR2 to network-forming collagen type IV as compared to rest of collagens, which are all examples of fibril-forming collagens (K, kangaroo tail; B, bovine nasal septum; C, calf skin; H, human placenta; R, rat tail; roman numerals represent biochemical types of collagen).	bind
5860	9	2737	5	10	NULL	0	NULL	statement 3	Process		weaker than					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_129	9659900	(A) DDR binding to different types of commercially-derived collagens; note weaker binding of both DDR1 and DDR2 to network-forming collagen type IV as compared to rest of collagens, which are all examples of fibril-forming collagens (K, kangaroo tail; B, bovine nasal septum; C, calf skin; H, human placenta; R, rat tail; roman numerals represent biochemical types of collagen).	bind
8296	1	2737	7	10	NULL	0	NULL	DDR	GP		bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_129	9659900	(A) DDR binding to different types of commercially-derived collagens; note weaker binding of both DDR1 and DDR2 to network-forming collagen type IV as compared to rest of collagens, which are all examples of fibril-forming collagens (K, kangaroo tail; B, bovine nasal septum; C, calf skin; H, human placenta; R, rat tail; roman numerals represent biochemical types of collagen).	bind
8297	2	2737	7	10	NULL	0	NULL	DDR1	GP		bind		weakly			collagen type IV	GP	network forming			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_129	9659900	(A) DDR binding to different types of commercially-derived collagens; note weaker binding of both DDR1 and DDR2 to network-forming collagen type IV as compared to rest of collagens, which are all examples of fibril-forming collagens (K, kangaroo tail; B, bovine nasal septum; C, calf skin; H, human placenta; R, rat tail; roman numerals represent biochemical types of collagen).	bind
8298	3	2737	7	10	NULL	0	NULL	DDR2	GP		bind		weakly			collagen type IV	GP	network forming			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_129	9659900	(A) DDR binding to different types of commercially-derived collagens; note weaker binding of both DDR1 and DDR2 to network-forming collagen type IV as compared to rest of collagens, which are all examples of fibril-forming collagens (K, kangaroo tail; B, bovine nasal septum; C, calf skin; H, human placenta; R, rat tail; roman numerals represent biochemical types of collagen).	bind
9107	4	2737	7	10	NULL	0	NULL	DDR1	GP		bind					collagen	GP	fibril-forming			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_129	9659900	(A) DDR binding to different types of commercially-derived collagens; note weaker binding of both DDR1 and DDR2 to network-forming collagen type IV as compared to rest of collagens, which are all examples of fibril-forming collagens (K, kangaroo tail; B, bovine nasal septum; C, calf skin; H, human placenta; R, rat tail; roman numerals represent biochemical types of collagen).	bind
9108	5	2737	7	10	NULL	0	NULL	DDR2	GP		bind					collagen	GP	fibril-forming			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_129	9659900	(A) DDR binding to different types of commercially-derived collagens; note weaker binding of both DDR1 and DDR2 to network-forming collagen type IV as compared to rest of collagens, which are all examples of fibril-forming collagens (K, kangaroo tail; B, bovine nasal septum; C, calf skin; H, human placenta; R, rat tail; roman numerals represent biochemical types of collagen).	bind
9109	6	2737	7	10	NULL	0	NULL	statement 2	Process		is weaker than					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_129	9659900	(A) DDR binding to different types of commercially-derived collagens; note weaker binding of both DDR1 and DDR2 to network-forming collagen type IV as compared to rest of collagens, which are all examples of fibril-forming collagens (K, kangaroo tail; B, bovine nasal septum; C, calf skin; H, human placenta; R, rat tail; roman numerals represent biochemical types of collagen).	bind
9110	7	2737	7	10	NULL	0	NULL	statement 3	Process		is weaker than					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_129	9659900	(A) DDR binding to different types of commercially-derived collagens; note weaker binding of both DDR1 and DDR2 to network-forming collagen type IV as compared to rest of collagens, which are all examples of fibril-forming collagens (K, kangaroo tail; B, bovine nasal septum; C, calf skin; H, human placenta; R, rat tail; roman numerals represent biochemical types of collagen).	bind
5546	1	2739	5	10	NULL	0	NULL	Rac	GP		bind					GST-PAK-1	GP		CRIB domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_481_s_166	11980921	(A) Detection of Rac bound to the GST-PAK-1 CRIB domain after fibronectin adhesion for the given times.	bind
5547	2	2739	5	10	NULL	0	NULL	fibronectin adhesion	Process		is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_481_s_166	11980921	(A) Detection of Rac bound to the GST-PAK-1 CRIB domain after fibronectin adhesion for the given times.	bind
8299	1	2739	7	10	NULL	0	NULL	Rac	GP		bind					GST-PAK-1	GP		CRIB		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_481_s_166	11980921	(A) Detection of Rac bound to the GST-PAK-1 CRIB domain after fibronectin adhesion for the given times.	bind
8300	2	2739	7	10	NULL	0	NULL	statement 1	Process		occurs after					fibronectin adhesion	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_481_s_166	11980921	(A) Detection of Rac bound to the GST-PAK-1 CRIB domain after fibronectin adhesion for the given times.	bind
5548	1	2740	5	10	NULL	0	NULL	T10-TM	GP	in vitro-translated	bind		selectively			Enigma	GP		PDZ domain		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_6_1973_s_131	10359609	(A) Detergent extracts of skeletal beta-TM fusion protein (35S-T10-TM) generated by in vitro translation were probed with glutathione-agarose-coupled GST or GST-PDZ domains of Enigma, Dlg (PDZs 1 and 2), LIM kinase, and ENH. T10-TM binds selectively to the PDZ domain of Enigma.	bind
8313	1	2740	7	10	NULL	0	NULL	T10-TM 	GP	In vitro-translated	bind		selectively			Enigma	GP		PDZ		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_6_1973_s_131	10359609	(A) Detergent extracts of skeletal beta-TM fusion protein (35S-T10-TM) generated by in vitro translation were probed with glutathione-agarose-coupled GST or GST-PDZ domains of Enigma, Dlg (PDZs 1 and 2), LIM kinase, and ENH. T10-TM binds selectively to the PDZ domain of Enigma.	bind
5648	1	2742	5	10	NULL	0	NULL	HSF	GP		activate					hsp70	GP	Drosophila		promoter	NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_5_511_s_25	8805267	(a) Diagram of  Drosophila hsp70  preset  promoter before (top) and after (bottom) activation by heat-shock factor (HSF), which binds to the heat-shock elements (HSEs).	bind
5649	2	2742	5	10	NULL	0	NULL	HSF	GP		is					heat-shock factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_5_511_s_25	8805267	(a) Diagram of  Drosophila hsp70  preset  promoter before (top) and after (bottom) activation by heat-shock factor (HSF), which binds to the heat-shock elements (HSEs).	bind
5650	3	2742	5	10	NULL	0	NULL	hsp70	GP	Drosophila	bind				promoter	HSEs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_5_511_s_25	8805267	(a) Diagram of  Drosophila hsp70  preset  promoter before (top) and after (bottom) activation by heat-shock factor (HSF), which binds to the heat-shock elements (HSEs).	bind
5651	4	2742	5	10	NULL	0	NULL	HSEs	NucleicAcid		is					heat-shock elements	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_5_511_s_25	8805267	(a) Diagram of  Drosophila hsp70  preset  promoter before (top) and after (bottom) activation by heat-shock factor (HSF), which binds to the heat-shock elements (HSEs).	bind
5652	5	2742	5	10	NULL	0	NULL	statement 3	Process		occurs before					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_5_511_s_25	8805267	(a) Diagram of  Drosophila hsp70  preset  promoter before (top) and after (bottom) activation by heat-shock factor (HSF), which binds to the heat-shock elements (HSEs).	bind
5653	6	2742	5	10	NULL	0	NULL	statement 3	Process		occurs after					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_5_511_s_25	8805267	(a) Diagram of  Drosophila hsp70  preset  promoter before (top) and after (bottom) activation by heat-shock factor (HSF), which binds to the heat-shock elements (HSEs).	bind
8314	1	2742	7	10	NULL	0	NULL	hsp70	GP	Drosophila	bind				preset promoter	HSEs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_5_511_s_25	8805267	(a) Diagram of  Drosophila hsp70  preset  promoter before (top) and after (bottom) activation by heat-shock factor (HSF), which binds to the heat-shock elements (HSEs).	bind
8315	2	2742	7	10	NULL	0	NULL	HSEs	NucleicAcid		is					 heat-shock elements	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_5_511_s_25	8805267	(a) Diagram of  Drosophila hsp70  preset  promoter before (top) and after (bottom) activation by heat-shock factor (HSF), which binds to the heat-shock elements (HSEs).	bind
8316	3	2742	7	10	NULL	0	NULL	statement 1	Process		occurs before					HSF	GP	activation by			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_5_511_s_25	8805267	(a) Diagram of  Drosophila hsp70  preset  promoter before (top) and after (bottom) activation by heat-shock factor (HSF), which binds to the heat-shock elements (HSEs).	bind
8318	4	2742	7	10	NULL	0	NULL	statement 1	Process		occurs after					HSF	GP	activation by			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_5_511_s_25	8805267	(a) Diagram of  Drosophila hsp70  preset  promoter before (top) and after (bottom) activation by heat-shock factor (HSF), which binds to the heat-shock elements (HSEs).	bind
8320	5	2742	7	10	NULL	0	NULL	HSF	GP		is					heat-shock factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_5_511_s_25	8805267	(a) Diagram of  Drosophila hsp70  preset  promoter before (top) and after (bottom) activation by heat-shock factor (HSF), which binds to the heat-shock elements (HSEs).	bind
54149	6	2742	7	10	NULL	0	NULL	HSF	GP		activate					hsp70	GP	Drosophila		promoter	NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_5_511_s_25	8805267	(a) Diagram of  Drosophila hsp70  preset  promoter before (top) and after (bottom) activation by heat-shock factor (HSF), which binds to the heat-shock elements (HSEs).	bind
5654	1	2743	5	10	NULL	0	NULL	DIAP1	GP		bind					DCP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_98_4_453_s_119	10481910	(A) DIAP1 binds DCP-1 and HID, and the first 37 residues of  HID are required for this interaction.	bind
5655	2	2743	5	10	NULL	0	NULL	DIAP1	GP		bind					HID	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_98_4_453_s_119	10481910	(A) DIAP1 binds DCP-1 and HID, and the first 37 residues of  HID are required for this interaction.	bind
5656	3	2743	5	10	NULL	0	NULL	HID	GP		is required for			first 37 residues		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_98_4_453_s_119	10481910	(A) DIAP1 binds DCP-1 and HID, and the first 37 residues of  HID are required for this interaction.	bind
8323	1	2743	7	10	NULL	0	NULL	DIAP1	GP		binds					DCP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_98_4_453_s_119	10481910	(A) DIAP1 binds DCP-1 and HID, and the first 37 residues of  HID are required for this interaction.	bind
8325	2	2743	7	10	NULL	0	NULL	DIAP1 	GP		binds					HID	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_98_4_453_s_119	10481910	(A) DIAP1 binds DCP-1 and HID, and the first 37 residues of  HID are required for this interaction.	bind
8328	3	2743	7	10	NULL	0	NULL	statement 2	Process		requires					HID	GP		first 37 residues		NULL		NULL	NULL	NULL	NULL	gw60_cell_98_4_453_s_119	10481910	(A) DIAP1 binds DCP-1 and HID, and the first 37 residues of  HID are required for this interaction.	bind
5657	1	2744	5	10	NULL	0	NULL	C hnRNP protein	GP		bind					U2 snRNP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_40_24922_s_50	8798770	(A) did not compete for the binding of C hnRNP protein to U2 snRNP (Fig.  2,  lane 4).	bind
8332	1	2744	7	10	NULL	0	NULL	C hnRNP	GP		bind					U2 snRNP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_40_24922_s_50	8798770	(A) did not compete for the binding of C hnRNP protein to U2 snRNP (Fig.  2,  lane 4).	bind
5658	1	2745	5	10	NULL	0	NULL	C3G peptide	AminoAcid		bind					c-Crk	GP		SH3-N		NULL		NULL	NULL	NULL	NULL	gw60_structure_3_2_215_s_67	7735837	(a) Difference electron-density map for the C3G peptide bound to c-Crk SH3-N.	bind
8333	1	2745	7	10	NULL	0	NULL	C3G peptide	AminoAcid		bind					c-Crk	GP		SH3-N		NULL		NULL	NULL	NULL	NULL	gw60_structure_3_2_215_s_67	7735837	(a) Difference electron-density map for the C3G peptide bound to c-Crk SH3-N.	bind
5659	1	2746	5	10	NULL	0	NULL	laminin-2	GP	biotinylated	bind		directly			PGL-1	Chemical	native;; M. leprae			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_511_s_102	11081637	(A) Direct binding of biotinylated  laminin-2 to native  M. leprae PGL-1 and its derivatives.	bind
5660	2	2746	5	10	NULL	0	NULL	laminin-2	GP	biotinylated	bind		directly			PGL-1 derivatives	Chemical	native;; M. leprae			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_511_s_102	11081637	(A) Direct binding of biotinylated  laminin-2 to native  M. leprae PGL-1 and its derivatives.	bind
8335	1	2746	7	10	NULL	0	NULL	laminin-2	GP	biotinylated 	bind		directly			PGL-1	Chemical	native;; M. leprae			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_511_s_102	11081637	(A) Direct binding of biotinylated  laminin-2 to native  M. leprae PGL-1 and its derivatives.	bind
8336	2	2746	7	10	NULL	0	NULL	laminin-2	GP	biotinylated 	bind		directly			PGL-1 derivatives	Chemical	native;; M. leprae			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_511_s_102	11081637	(A) Direct binding of biotinylated  laminin-2 to native  M. leprae PGL-1 and its derivatives.	bind
5661	1	2747	5	10	NULL	0	NULL	125I- -bungarotoxin	Chemical		bind					SH-SY5Y-h 7 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_126	11044725	(A) displacement of 125I- -bungarotoxin ( -BTx) binding to SH-SY5Y-h 7 cells by diltiazem.	bind
5662	2	2747	5	10	NULL	0	NULL	diltiazem	Chemical		bind					SH-SY5Y-h 7 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_126	11044725	(A) displacement of 125I- -bungarotoxin ( -BTx) binding to SH-SY5Y-h 7 cells by diltiazem.	bind
5663	3	2747	5	10	NULL	0	NULL	statement 1	Process		is displaced by					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_126	11044725	(A) displacement of 125I- -bungarotoxin ( -BTx) binding to SH-SY5Y-h 7 cells by diltiazem.	bind
46397	4	2747	5	10	NULL	0	NULL	BTx	Chemical		is					bungarotoxin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_126	11044725	(A) displacement of 125I- -bungarotoxin ( -BTx) binding to SH-SY5Y-h 7 cells by diltiazem.	bind
8337	1	2747	7	10	NULL	0	NULL	125I- -bungarotoxin	Chemical		bind					SH-SY5Y-h 7 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_126	11044725	(A) displacement of 125I- -bungarotoxin ( -BTx) binding to SH-SY5Y-h 7 cells by diltiazem.	bind
8338	2	2747	7	10	NULL	0	NULL	BTx	Chemical		is					bungarotoxin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_126	11044725	(A) displacement of 125I- -bungarotoxin ( -BTx) binding to SH-SY5Y-h 7 cells by diltiazem.	bind
8340	3	2747	7	10	NULL	0	NULL	diltiazem	Chemical		bind					SH-SY5Y-h 7 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_126	11044725	(A) displacement of 125I- -bungarotoxin ( -BTx) binding to SH-SY5Y-h 7 cells by diltiazem.	bind
8341	4	2747	7	10	NULL	0	NULL	diltiazem	Chemical		displaces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_126	11044725	(A) displacement of 125I- -bungarotoxin ( -BTx) binding to SH-SY5Y-h 7 cells by diltiazem.	bind
5664	1	2748	5	10	NULL	0	NULL	RNAP	GP		bind					RNA:DNA hybrid	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_1_55_s_84	9702191	(A) Dissociation of the   subunit after binding of RNAP to the RNA:DNA hybrid.	bind
8343	1	2748	7	10	NULL	0	NULL	RNAP	GP		bind					RNA:DNA hybrid	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_1_55_s_84	9702191	(A) Dissociation of the   subunit after binding of RNAP to the RNA:DNA hybrid.	bind
5734	1	2749	5	10	NULL	0	NULL	p53	GP		bind					DNA	NucleicAcid			PG13	NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_92	11463392	(A) DNA binding activity of p53 to oligonucleotides containing two consensus p53 binding sites (PG13), PUMA binding site 1 (PUMA BS1), PUMA binding site 2 (PUMA BS2), and mutant PUMA binding site 2 (mt PUMA BS2).	bind
5736	2	2749	5	10	NULL	0	NULL	p53	GP		bind					oligonucleotides	NucleicAcid			PUMA BS1	NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_92	11463392	(A) DNA binding activity of p53 to oligonucleotides containing two consensus p53 binding sites (PG13), PUMA binding site 1 (PUMA BS1), PUMA binding site 2 (PUMA BS2), and mutant PUMA binding site 2 (mt PUMA BS2).	bind
5737	3	2749	5	10	NULL	0	NULL	PUMA BS1	NucleicAcid		is					PUMA binding site 1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_92	11463392	(A) DNA binding activity of p53 to oligonucleotides containing two consensus p53 binding sites (PG13), PUMA binding site 1 (PUMA BS1), PUMA binding site 2 (PUMA BS2), and mutant PUMA binding site 2 (mt PUMA BS2).	bind
5738	4	2749	5	10	NULL	0	NULL	p53	GP		bind					oligonucleotides	NucleicAcid			PUMA BS2	NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_92	11463392	(A) DNA binding activity of p53 to oligonucleotides containing two consensus p53 binding sites (PG13), PUMA binding site 1 (PUMA BS1), PUMA binding site 2 (PUMA BS2), and mutant PUMA binding site 2 (mt PUMA BS2).	bind
5739	5	2749	5	10	NULL	0	NULL	PUMA BS2	NucleicAcid		is					PUMA binding site 2	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_92	11463392	(A) DNA binding activity of p53 to oligonucleotides containing two consensus p53 binding sites (PG13), PUMA binding site 1 (PUMA BS1), PUMA binding site 2 (PUMA BS2), and mutant PUMA binding site 2 (mt PUMA BS2).	bind
5740	6	2749	5	10	NULL	0	NULL	p53	GP		bind					oligonucleotides	NucleicAcid			mt PUMA BS2	NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_92	11463392	(A) DNA binding activity of p53 to oligonucleotides containing two consensus p53 binding sites (PG13), PUMA binding site 1 (PUMA BS1), PUMA binding site 2 (PUMA BS2), and mutant PUMA binding site 2 (mt PUMA BS2).	bind
5741	7	2749	5	10	NULL	0	NULL	mt PUMA BS2	NucleicAcid		is					mutant PUMA binding site 2	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_92	11463392	(A) DNA binding activity of p53 to oligonucleotides containing two consensus p53 binding sites (PG13), PUMA binding site 1 (PUMA BS1), PUMA binding site 2 (PUMA BS2), and mutant PUMA binding site 2 (mt PUMA BS2).	bind
8365	1	2749	7	10	NULL	0	NULL	p53	GP		bind					DNA	NucleicAcid			PG13	NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_92	11463392	(A) DNA binding activity of p53 to oligonucleotides containing two consensus p53 binding sites (PG13), PUMA binding site 1 (PUMA BS1), PUMA binding site 2 (PUMA BS2), and mutant PUMA binding site 2 (mt PUMA BS2).	bind
8369	2	2749	7	10	NULL	0	NULL	p53	GP		bind					oligonucleotide	NucleicAcid			PUMA BS1	NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_92	11463392	(A) DNA binding activity of p53 to oligonucleotides containing two consensus p53 binding sites (PG13), PUMA binding site 1 (PUMA BS1), PUMA binding site 2 (PUMA BS2), and mutant PUMA binding site 2 (mt PUMA BS2).	bind
8372	3	2749	7	10	NULL	0	NULL	p53	GP		bind					oligonucleotide	NucleicAcid			PUMA BS2	NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_92	11463392	(A) DNA binding activity of p53 to oligonucleotides containing two consensus p53 binding sites (PG13), PUMA binding site 1 (PUMA BS1), PUMA binding site 2 (PUMA BS2), and mutant PUMA binding site 2 (mt PUMA BS2).	bind
8373	4	2749	7	10	NULL	0	NULL	p53	GP		bind					oligonucleotide	NucleicAcid			mt PUMA BS2	NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_92	11463392	(A) DNA binding activity of p53 to oligonucleotides containing two consensus p53 binding sites (PG13), PUMA binding site 1 (PUMA BS1), PUMA binding site 2 (PUMA BS2), and mutant PUMA binding site 2 (mt PUMA BS2).	bind
8374	5	2749	7	10	NULL	0	NULL	PG13	NucleicAcid		is					 p53 binding site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_92	11463392	(A) DNA binding activity of p53 to oligonucleotides containing two consensus p53 binding sites (PG13), PUMA binding site 1 (PUMA BS1), PUMA binding site 2 (PUMA BS2), and mutant PUMA binding site 2 (mt PUMA BS2).	bind
8375	6	2749	7	10	NULL	0	NULL	PUMA BS1	NucleicAcid		is					PUMA binding site 1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_92	11463392	(A) DNA binding activity of p53 to oligonucleotides containing two consensus p53 binding sites (PG13), PUMA binding site 1 (PUMA BS1), PUMA binding site 2 (PUMA BS2), and mutant PUMA binding site 2 (mt PUMA BS2).	bind
8376	7	2749	7	10	NULL	0	NULL	PUMA BS2	NucleicAcid		is					PUMA binding site 2	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_92	11463392	(A) DNA binding activity of p53 to oligonucleotides containing two consensus p53 binding sites (PG13), PUMA binding site 1 (PUMA BS1), PUMA binding site 2 (PUMA BS2), and mutant PUMA binding site 2 (mt PUMA BS2).	bind
8377	8	2749	7	10	NULL	0	NULL	mt PUMA BS2	NucleicAcid		is					mutant PUMA binding site 2	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_92	11463392	(A) DNA binding activity of p53 to oligonucleotides containing two consensus p53 binding sites (PG13), PUMA binding site 1 (PUMA BS1), PUMA binding site 2 (PUMA BS2), and mutant PUMA binding site 2 (mt PUMA BS2).	bind
5742	1	2751	5	10	NULL	NULL	NULL	255 bp fragment	NucleicAcid		include					Race	GP	proximal region of		533 bp enhancer (349-533)	NULL		NULL	NULL	NULL	NULL	gw70_development_132_7_1637_s_164	15728670	(A) DNAse I footprinting analysis of Mad and Zen GST fusion proteins  bound to a 255 bp fragment that includes the proximal region of the  Race 533 bp enhancer (349-533) and 70 nucleotides from the Bluescript vector.	bind
5744	2	2751	5	10	NULL	NULL	NULL	255 bp fragment	NucleicAcid		include					70 nucleotides	NucleicAcid	from Bluescript vector			NULL		NULL	NULL	NULL	NULL	gw70_development_132_7_1637_s_164	15728670	(A) DNAse I footprinting analysis of Mad and Zen GST fusion proteins  bound to a 255 bp fragment that includes the proximal region of the  Race 533 bp enhancer (349-533) and 70 nucleotides from the Bluescript vector.	bind
5745	3	2751	5	10	NULL	NULL	NULL	Mad	GP		bind					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_132_7_1637_s_164	15728670	(A) DNAse I footprinting analysis of Mad and Zen GST fusion proteins  bound to a 255 bp fragment that includes the proximal region of the  Race 533 bp enhancer (349-533) and 70 nucleotides from the Bluescript vector.	bind
5747	4	2751	5	10	NULL	NULL	NULL	Zen	GP		bind					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_132_7_1637_s_164	15728670	(A) DNAse I footprinting analysis of Mad and Zen GST fusion proteins  bound to a 255 bp fragment that includes the proximal region of the  Race 533 bp enhancer (349-533) and 70 nucleotides from the Bluescript vector.	bind
54237	5	2751	5	10	NULL	NULL	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_132_7_1637_s_164	15728670	(A) DNAse I footprinting analysis of Mad and Zen GST fusion proteins  bound to a 255 bp fragment that includes the proximal region of the  Race 533 bp enhancer (349-533) and 70 nucleotides from the Bluescript vector.	bind
54238	6	2751	5	10	NULL	NULL	NULL	Mad	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_132_7_1637_s_164	15728670	(A) DNAse I footprinting analysis of Mad and Zen GST fusion proteins  bound to a 255 bp fragment that includes the proximal region of the  Race 533 bp enhancer (349-533) and 70 nucleotides from the Bluescript vector.	bind
54239	7	2751	5	10	NULL	NULL	NULL	Zen	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_132_7_1637_s_164	15728670	(A) DNAse I footprinting analysis of Mad and Zen GST fusion proteins  bound to a 255 bp fragment that includes the proximal region of the  Race 533 bp enhancer (349-533) and 70 nucleotides from the Bluescript vector.	bind
8836	1	2751	7	10	NULL	NULL	NULL	255 bp fragment	NucleicAcid		contains					Race	GP			proximal region of  533 bp enhancer (349-533)	NULL		NULL	NULL	NULL	NULL	gw70_development_132_7_1637_s_164	15728670	(A) DNAse I footprinting analysis of Mad and Zen GST fusion proteins  bound to a 255 bp fragment that includes the proximal region of the  Race 533 bp enhancer (349-533) and 70 nucleotides from the Bluescript vector.	bind
8837	4	2751	7	10	NULL	NULL	NULL	Mad	GP		bind					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_132_7_1637_s_164	15728670	(A) DNAse I footprinting analysis of Mad and Zen GST fusion proteins  bound to a 255 bp fragment that includes the proximal region of the  Race 533 bp enhancer (349-533) and 70 nucleotides from the Bluescript vector.	bind
8838	3	2751	7	10	NULL	NULL	NULL	statement 1	Process		occur simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_132_7_1637_s_164	15728670	(A) DNAse I footprinting analysis of Mad and Zen GST fusion proteins  bound to a 255 bp fragment that includes the proximal region of the  Race 533 bp enhancer (349-533) and 70 nucleotides from the Bluescript vector.	bind
8839	2	2751	7	10	NULL	NULL	NULL	255 bp fragment	NucleicAcid		contains					70 nucleotides 	NucleicAcid	  Bluescript vector			NULL		NULL	NULL	NULL	NULL	gw70_development_132_7_1637_s_164	15728670	(A) DNAse I footprinting analysis of Mad and Zen GST fusion proteins  bound to a 255 bp fragment that includes the proximal region of the  Race 533 bp enhancer (349-533) and 70 nucleotides from the Bluescript vector.	bind
54244	5	2751	7	10	NULL	NULL	NULL	Zen	GP		bind					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_132_7_1637_s_164	15728670	(A) DNAse I footprinting analysis of Mad and Zen GST fusion proteins  bound to a 255 bp fragment that includes the proximal region of the  Race 533 bp enhancer (349-533) and 70 nucleotides from the Bluescript vector.	bind
54245	6	2751	7	10	NULL	NULL	NULL	Mad	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_132_7_1637_s_164	15728670	(A) DNAse I footprinting analysis of Mad and Zen GST fusion proteins  bound to a 255 bp fragment that includes the proximal region of the  Race 533 bp enhancer (349-533) and 70 nucleotides from the Bluescript vector.	bind
54246	7	2751	7	10	NULL	NULL	NULL	Zen	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_132_7_1637_s_164	15728670	(A) DNAse I footprinting analysis of Mad and Zen GST fusion proteins  bound to a 255 bp fragment that includes the proximal region of the  Race 533 bp enhancer (349-533) and 70 nucleotides from the Bluescript vector.	bind
5748	1	2752	5	10	NULL	NULL	NULL	XylRdeltaA protein	GP		bind					Pu	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_86_2_331_s_58	8706137	(A) DNase I footprints  caused by increasing amounts of XylRdeltaA protein (0, 0.1, 0.2, 0.4, 0.6, 0.8, and 1.0 muM) bound to the  Pu promoter in the presence or absence of 5 mM ATP.	bind
8840	1	2752	7	10	NULL	NULL	NULL	XylRdeltaA protein	GP		bind					Pu	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_86_2_331_s_58	8706137	(A) DNase I footprints  caused by increasing amounts of XylRdeltaA protein (0, 0.1, 0.2, 0.4, 0.6, 0.8, and 1.0 muM) bound to the  Pu promoter in the presence or absence of 5 mM ATP.	bind
5752	1	2753	5	10	NULL	NULL	NULL	PtxS	GP		bind					ptxS	GP			upstream region	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_16_4890_s_190	10438759	(A) DNase I protection analysis of PtxS binding to the  ptxS upstream region.	bind
8841	1	2753	7	10	NULL	NULL	NULL	PtxS	GP		bind					ptxS	GP			 upstream region	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_16_4890_s_190	10438759	(A) DNase I protection analysis of PtxS binding to the  ptxS upstream region.	bind
5753	1	2754	5	10	NULL	NULL	NULL	DOKL	GP		bind					v-Abl	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8314_s_269	10567556	(A) DOKL binding to v-Abl requires Abl kinase activity and the DOKL PTB domain.	bind
5754	2	2754	5	10	NULL	NULL	NULL	Abl kinase 	GP	activity of	is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8314_s_269	10567556	(A) DOKL binding to v-Abl requires Abl kinase activity and the DOKL PTB domain.	bind
5755	3	2754	5	10	NULL	NULL	NULL	DOKL	GP		is required for			PTB domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8314_s_269	10567556	(A) DOKL binding to v-Abl requires Abl kinase activity and the DOKL PTB domain.	bind
8842	1	2754	7	10	NULL	NULL	NULL	DOKL	GP		bind					v-Abl	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8314_s_269	10567556	(A) DOKL binding to v-Abl requires Abl kinase activity and the DOKL PTB domain.	bind
8843	2	2754	7	10	NULL	NULL	NULL	statement 1	Process		requires					Abl kinase	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8314_s_269	10567556	(A) DOKL binding to v-Abl requires Abl kinase activity and the DOKL PTB domain.	bind
8844	3	2754	7	10	NULL	NULL	NULL	statement 1	Process		requires					DOKL 	GP		PTB		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8314_s_269	10567556	(A) DOKL binding to v-Abl requires Abl kinase activity and the DOKL PTB domain.	bind
5756	1	2755	5	10	NULL	NULL	NULL	Domain III proteins	GP		bind					E1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_1_111_s_189	16216925	(A) Domain III proteins bind to E1 during fusion.	bind
5757	2	2755	5	10	NULL	NULL	NULL	statement 1	Process		occurs during					fusion	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_1_111_s_189	16216925	(A) Domain III proteins bind to E1 during fusion.	bind
8845	1	2755	7	10	NULL	NULL	NULL	Domain III protein	GP		bind					E1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_1_111_s_189	16216925	(A) Domain III proteins bind to E1 during fusion.	bind
8846	2	2755	7	10	NULL	NULL	NULL	statement 1	Process		occurs during					fusion	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_1_111_s_189	16216925	(A) Domain III proteins bind to E1 during fusion.	bind
5758	1	2758	5	10	NULL	NULL	NULL	CSL	GP		bind		non specific;;dose-dependently			Caco-2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_10_5282_s_234	10496907	(A) Dose-dependent binding of CSL to Caco-2 cells, corrected for nonspecific binding.	bind
8847	1	2758	7	10	NULL	NULL	NULL	CSL	GP		bind		non specific;;dose-dependently			Caco-2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_10_5282_s_234	10496907	(A) Dose-dependent binding of CSL to Caco-2 cells, corrected for nonspecific binding.	bind
5760	1	2759	5	10	NULL	NULL	NULL	dTAFII110	GP		bind					NFATp	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3503_s_171	11313476	(A) dTAFII110 binds to NFATp.	bind
8848	1	2759	7	10	NULL	NULL	NULL	dTAFII110	GP		bind					NFATp	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3503_s_171	11313476	(A) dTAFII110 binds to NFATp.	bind
5761	1	2760	5	10	NULL	NULL	NULL	DtxR	GP		bind					IRP6	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_17_4846_s_140	12169610	(A) DtxR binding of IRP6 requires a divalent transitional metal ion, such as Co2+.	bind
5762	2	2760	5	10	NULL	NULL	NULL	statement 1	Process		require					Co2+	Chemical	divalent transitional metal ion			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_17_4846_s_140	12169610	(A) DtxR binding of IRP6 requires a divalent transitional metal ion, such as Co2+.	bind
8849	1	2760	7	10	NULL	NULL	NULL	DtxR	GP		bind					IRP6	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_17_4846_s_140	12169610	(A) DtxR binding of IRP6 requires a divalent transitional metal ion, such as Co2+.	bind
8850	2	2760	7	10	NULL	NULL	NULL	statement 1	Process		requires					Co2+	Chemical	divalent transitional metal ion			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_17_4846_s_140	12169610	(A) DtxR binding of IRP6 requires a divalent transitional metal ion, such as Co2+.	bind
5763	1	2761	5	10	NULL	NULL	NULL	Comm	GP		serves as					adaptor protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_36_1_5_s_54	12367500	(A) During a growth cone's approach to the midline, Comm serves as an adaptor protein binding to Robo as well as to Nedd4.	bind
5764	2	2761	5	10	NULL	NULL	NULL	Comm	GP		bind					Robo	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_36_1_5_s_54	12367500	(A) During a growth cone's approach to the midline, Comm serves as an adaptor protein binding to Robo as well as to Nedd4.	bind
5765	3	2761	5	10	NULL	NULL	NULL	Comm	GP		bind					Nedd4	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_36_1_5_s_54	12367500	(A) During a growth cone's approach to the midline, Comm serves as an adaptor protein binding to Robo as well as to Nedd4.	bind
5766	4	2761	5	10	NULL	NULL	NULL	statement 2	Process		occurs during					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_36_1_5_s_54	12367500	(A) During a growth cone's approach to the midline, Comm serves as an adaptor protein binding to Robo as well as to Nedd4.	bind
5767	5	2761	5	10	NULL	NULL	NULL	statement 3	Process		occurs during					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_36_1_5_s_54	12367500	(A) During a growth cone's approach to the midline, Comm serves as an adaptor protein binding to Robo as well as to Nedd4.	bind
46401	6	2761	5	10	NULL	NULL	NULL	growth cone	CellComponent		approach to					midline	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_neuron_36_1_5_s_54	12367500	(A) During a growth cone's approach to the midline, Comm serves as an adaptor protein binding to Robo as well as to Nedd4.	bind
8855	1	2761	7	10	NULL	NULL	NULL	Comm	GP		bind					Robo	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_36_1_5_s_54	12367500	(A) During a growth cone's approach to the midline, Comm serves as an adaptor protein binding to Robo as well as to Nedd4.	bind
8856	2	2761	7	10	NULL	NULL	NULL	Comm	GP		bind					Nedd4	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_36_1_5_s_54	12367500	(A) During a growth cone's approach to the midline, Comm serves as an adaptor protein binding to Robo as well as to Nedd4.	bind
8857	3	2761	7	10	NULL	NULL	NULL	Comm	GP		serves as an					adaptor protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_36_1_5_s_54	12367500	(A) During a growth cone's approach to the midline, Comm serves as an adaptor protein binding to Robo as well as to Nedd4.	bind
11754	4	2761	7	10	NULL	NULL	NULL	statement 1	Process		occur during					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_36_1_5_s_54	12367500	(A) During a growth cone's approach to the midline, Comm serves as an adaptor protein binding to Robo as well as to Nedd4.	bind
11755	5	2761	7	10	NULL	NULL	NULL	statement 3	Process		occur during					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_36_1_5_s_54	12367500	(A) During a growth cone's approach to the midline, Comm serves as an adaptor protein binding to Robo as well as to Nedd4.	bind
46402	6	2761	7	10	NULL	NULL	NULL	growth cone	CellComponent		approach to					midline	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_neuron_36_1_5_s_54	12367500	(A) During a growth cone's approach to the midline, Comm serves as an adaptor protein binding to Robo as well as to Nedd4.	bind
5768	2	2762	5	10	NULL	NULL	NULL	INS	GP	unidentified	bind					DAF-2 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_1_9_s_65	11782310	(A) During favorable growth conditions,  unc-64 and  unc-31 function to promote an as yet unidentified insulin-like ligand (INS) that binds to the DAF-2 receptor.	bind
5769	3	2762	5	10	NULL	NULL	NULL	unc-64	GP		promote					INS	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_1_9_s_65	11782310	(A) During favorable growth conditions,  unc-64 and  unc-31 function to promote an as yet unidentified insulin-like ligand (INS) that binds to the DAF-2 receptor.	bind
5770	4	2762	5	10	NULL	NULL	NULL	unc-31	GP		promote					INS	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_1_9_s_65	11782310	(A) During favorable growth conditions,  unc-64 and  unc-31 function to promote an as yet unidentified insulin-like ligand (INS) that binds to the DAF-2 receptor.	bind
5771	5	2762	5	10	NULL	NULL	NULL	statement 3	Process		occurs during					favorable growth conditions	Process				NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_1_9_s_65	11782310	(A) During favorable growth conditions,  unc-64 and  unc-31 function to promote an as yet unidentified insulin-like ligand (INS) that binds to the DAF-2 receptor.	bind
5772	6	2762	5	10	NULL	NULL	NULL	statement 4	Process		occurs during					favorable growth conditions	Process				NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_1_9_s_65	11782310	(A) During favorable growth conditions,  unc-64 and  unc-31 function to promote an as yet unidentified insulin-like ligand (INS) that binds to the DAF-2 receptor.	bind
11930	1	2762	5	10	NULL	NULL	NULL	insulin-like ligand	GP		is					INS	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_1_9_s_65	11782310	(A) During favorable growth conditions,  unc-64 and  unc-31 function to promote an as yet unidentified insulin-like ligand (INS) that binds to the DAF-2 receptor.	bind
8858	1	2762	7	10	NULL	NULL	NULL	insulin-like ligand	GP		bind					DAF-2 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_1_9_s_65	11782310	(A) During favorable growth conditions,  unc-64 and  unc-31 function to promote an as yet unidentified insulin-like ligand (INS) that binds to the DAF-2 receptor.	bind
8859	2	2762	7	10	NULL	NULL	NULL	insulin-like ligand	GP		is					INS	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_1_9_s_65	11782310	(A) During favorable growth conditions,  unc-64 and  unc-31 function to promote an as yet unidentified insulin-like ligand (INS) that binds to the DAF-2 receptor.	bind
8860	3	2762	7	10	NULL	NULL	NULL	 unc-64	GP		promote					INS	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_1_9_s_65	11782310	(A) During favorable growth conditions,  unc-64 and  unc-31 function to promote an as yet unidentified insulin-like ligand (INS) that binds to the DAF-2 receptor.	bind
8861	4	2762	7	10	NULL	NULL	NULL	unc-31	GP		promote					INS	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_1_9_s_65	11782310	(A) During favorable growth conditions,  unc-64 and  unc-31 function to promote an as yet unidentified insulin-like ligand (INS) that binds to the DAF-2 receptor.	bind
11756	5	2762	7	10	NULL	NULL	NULL	statement 3	Process		occur during					growth favourable condition	Process				NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_1_9_s_65	11782310	(A) During favorable growth conditions,  unc-64 and  unc-31 function to promote an as yet unidentified insulin-like ligand (INS) that binds to the DAF-2 receptor.	bind
11757	6	2762	7	10	NULL	NULL	NULL	statement 4	Process		occur during					growth favourable condition	Process				NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_1_9_s_65	11782310	(A) During favorable growth conditions,  unc-64 and  unc-31 function to promote an as yet unidentified insulin-like ligand (INS) that binds to the DAF-2 receptor.	bind
5773	1	2764	5	10	NULL	NULL	NULL	E2F	GP		bind					MCM4	GP			promoter	NULL	in serum-stimulated T98G cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_84	15121871	(A) E2F binding  to the MCM4 promoter in serum-stimulated T98G cells as determined by ChIP (% total)  overlapped with the percentage of cells in S phase as determined by BrdU incorporation  and fluorescence-activated cell sorting.	bind
8862	1	2764	7	10	NULL	NULL	NULL	E2F	GP		bind					MCM4	GP			promoter	NULL	serum-stimulated T98G cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_84	15121871	(A) E2F binding  to the MCM4 promoter in serum-stimulated T98G cells as determined by ChIP (% total)  overlapped with the percentage of cells in S phase as determined by BrdU incorporation  and fluorescence-activated cell sorting.	bind
5774	1	2765	5	10	NULL	NULL	NULL	AFP	GP	native	bind					MDM	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_3_507_s_101	12176010	(A) Effect of anti-AFP antibodies (anti-AFP) or its isotype on the binding of native [125]AFP to MDM.	bind
8863	1	2765	7	10	NULL	NULL	NULL	[125]AFP	GP	native	bind					MDM	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_3_507_s_101	12176010	(A) Effect of anti-AFP antibodies (anti-AFP) or its isotype on the binding of native [125]AFP to MDM.	bind
5788	1	2766	5	10	NULL	NULL	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_206_s_136	9864217	(A) Effect of CHX on induction of the DNA binding of NF-kappaB by LPS with or without pretreatment with IFN-gamma.	bind
5789	2	2766	5	10	NULL	NULL	NULL	LPS	Chemical		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_206_s_136	9864217	(A) Effect of CHX on induction of the DNA binding of NF-kappaB by LPS with or without pretreatment with IFN-gamma.	bind
8864	1	2766	7	10	NULL	NULL	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_206_s_136	9864217	(A) Effect of CHX on induction of the DNA binding of NF-kappaB by LPS with or without pretreatment with IFN-gamma.	bind
9483	2	2766	7	10	NULL	NULL	NULL	LPS	Chemical		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_206_s_136	9864217	(A) Effect of CHX on induction of the DNA binding of NF-kappaB by LPS with or without pretreatment with IFN-gamma.	bind
5793	1	2767	5	10	NULL	NULL	NULL	HEK 293 cells	Cell		express		stably			AT1R - YFP	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_178	12721105	(a) Effect of PMA on [3]AII binding to HEK 293 cells stably expressing AT1R - YFP. Results are expressed as percent of the maximal specific binding recorded in the control curve (8 nM of radioligand).	bind
5794	2	2767	5	10	NULL	NULL	NULL	AII	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_178	12721105	(a) Effect of PMA on [3]AII binding to HEK 293 cells stably expressing AT1R - YFP. Results are expressed as percent of the maximal specific binding recorded in the control curve (8 nM of radioligand).	bind
8874	1	2767	7	10	NULL	NULL	NULL	HEK 293 cells	Cell		express					AT1R - YFP	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_178	12721105	(a) Effect of PMA on [3]AII binding to HEK 293 cells stably expressing AT1R - YFP. Results are expressed as percent of the maximal specific binding recorded in the control curve (8 nM of radioligand).	bind
46404	2	2767	7	10	NULL	NULL	NULL	AII	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_178	12721105	(a) Effect of PMA on [3]AII binding to HEK 293 cells stably expressing AT1R - YFP. Results are expressed as percent of the maximal specific binding recorded in the control curve (8 nM of radioligand).	bind
5795	1	2768	5	10	NULL	NULL	NULL	p97	GP		bind					RanBP2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2379_s_190	9398662	(A) Effect of Ran on the binding of p97 to RanBP2.	bind
8875	1	2768	7	10	NULL	NULL	NULL	p97	GP		bind					RanBP2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2379_s_190	9398662	(A) Effect of Ran on the binding of p97 to RanBP2.	bind
5796	1	2769	5	10	NULL	NULL	NULL	Bas1p	GP		bind					ADE5,7	GP			promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_23_7901_s_326	11689683	(A) Effect of SAICAR and AICAR on cooperative in vitro binding of Bas1p and Bas2p to the  ADE5,7 promoter.	bind
5797	2	2769	5	10	NULL	NULL	NULL	Bas2p	GP		bind					ADE5,7	GP			promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_23_7901_s_326	11689683	(A) Effect of SAICAR and AICAR on cooperative in vitro binding of Bas1p and Bas2p to the  ADE5,7 promoter.	bind
5798	3	2769	5	10	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_23_7901_s_326	11689683	(A) Effect of SAICAR and AICAR on cooperative in vitro binding of Bas1p and Bas2p to the  ADE5,7 promoter.	bind
8876	1	2769	7	10	NULL	NULL	NULL	Bas1p	GP		bind					ADE5,7	GP			promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_23_7901_s_326	11689683	(A) Effect of SAICAR and AICAR on cooperative in vitro binding of Bas1p and Bas2p to the  ADE5,7 promoter.	bind
8877	2	2769	7	10	NULL	NULL	NULL	Bas2p	GP		bind					ADE5,7	GP			promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_23_7901_s_326	11689683	(A) Effect of SAICAR and AICAR on cooperative in vitro binding of Bas1p and Bas2p to the  ADE5,7 promoter.	bind
8894	3	2769	7	10	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_23_7901_s_326	11689683	(A) Effect of SAICAR and AICAR on cooperative in vitro binding of Bas1p and Bas2p to the  ADE5,7 promoter.	bind
5799	1	2770	5	10	NULL	NULL	NULL	SIL	CellComponent		bind					KG-1a	Cell				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1509_1_299_s_218	11118541	(A) Effect of the lipid concentration on the degree of SIL binding to KG-1a.	bind
8900	1	2770	7	10	NULL	NULL	NULL	SIL	CellComponent		bind					KG-1a	Cell				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1509_1_299_s_218	11118541	(A) Effect of the lipid concentration on the degree of SIL binding to KG-1a.	bind
5801	1	2773	5	10	NULL	NULL	NULL	arsenite	Chemical		induce					ERK	GP	activation			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5178_s_226	9710602	(A) Effects of suramin and tyrphostin AG1478 on arsenite-induced ERK activation.	bind
8981	1	2773	7	10	NULL	NULL	NULL	arsenite	Chemical		induce					ERK	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5178_s_226	9710602	(A) Effects of suramin and tyrphostin AG1478 on arsenite-induced ERK activation.	bind
5802	1	2774	5	10	NULL	NULL	NULL	HEXIM1	GP	isolated	bind			NLS		7SK	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_12_5094_s_146	15169877	(A) Efficient in vivo binding of the isolated NLS of HEXIM1  to 7SK but not P-TEFb.	bind
5803	2	2774	5	10	NULL	NULL	NULL	HEXIM1	GP	isolated	does not bind			NLS		P-TEFb	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_12_5094_s_146	15169877	(A) Efficient in vivo binding of the isolated NLS of HEXIM1  to 7SK but not P-TEFb.	bind
8982	1	2774	7	10	NULL	NULL	NULL	HEXIM1	GP	isolated	bind			NLS		7SK	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_12_5094_s_146	15169877	(A) Efficient in vivo binding of the isolated NLS of HEXIM1  to 7SK but not P-TEFb.	bind
8983	2	2774	7	10	NULL	NULL	NULL	HEXIM1	GP	isolated	does not bind			NLS		P-TEFb	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_12_5094_s_146	15169877	(A) Efficient in vivo binding of the isolated NLS of HEXIM1  to 7SK but not P-TEFb.	bind
5804	1	2775	5	10	NULL	NULL	NULL	EKLF	GP		bind					beta gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_102_s_238	9418858	(A) EKLF bound to the beta gene recruits a subcomplex of the transcriptional machinery and enables formation of a transcription initiation complex (IC) of the beta gene together with TFIID containing TATA box-binding protein (TBP), RNA polymerase II (pol II) holoenzyme, and probably other subcomplexes recruited by other transcriptional activators.	bind
5805	2	2775	5	10	NULL	NULL	NULL	statement 1	Process		recruit					transcriptional machinery	GP	a subcomplex of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_102_s_238	9418858	(A) EKLF bound to the beta gene recruits a subcomplex of the transcriptional machinery and enables formation of a transcription initiation complex (IC) of the beta gene together with TFIID containing TATA box-binding protein (TBP), RNA polymerase II (pol II) holoenzyme, and probably other subcomplexes recruited by other transcriptional activators.	bind
5806	3	2775	5	10	NULL	NULL	NULL	statement 1	Process		enables					IC of beta gene	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_102_s_238	9418858	(A) EKLF bound to the beta gene recruits a subcomplex of the transcriptional machinery and enables formation of a transcription initiation complex (IC) of the beta gene together with TFIID containing TATA box-binding protein (TBP), RNA polymerase II (pol II) holoenzyme, and probably other subcomplexes recruited by other transcriptional activators.	bind
5807	4	2775	5	10	NULL	NULL	NULL	IC	GP		is					transcription initiation complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_102_s_238	9418858	(A) EKLF bound to the beta gene recruits a subcomplex of the transcriptional machinery and enables formation of a transcription initiation complex (IC) of the beta gene together with TFIID containing TATA box-binding protein (TBP), RNA polymerase II (pol II) holoenzyme, and probably other subcomplexes recruited by other transcriptional activators.	bind
5808	5	2775	5	10	NULL	NULL	NULL	statement 3	Process		occurs along with					TBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_102_s_238	9418858	(A) EKLF bound to the beta gene recruits a subcomplex of the transcriptional machinery and enables formation of a transcription initiation complex (IC) of the beta gene together with TFIID containing TATA box-binding protein (TBP), RNA polymerase II (pol II) holoenzyme, and probably other subcomplexes recruited by other transcriptional activators.	bind
5809	6	2775	5	10	NULL	NULL	NULL	TBP	GP		is					TATA box-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_102_s_238	9418858	(A) EKLF bound to the beta gene recruits a subcomplex of the transcriptional machinery and enables formation of a transcription initiation complex (IC) of the beta gene together with TFIID containing TATA box-binding protein (TBP), RNA polymerase II (pol II) holoenzyme, and probably other subcomplexes recruited by other transcriptional activators.	bind
5810	7	2775	5	10	NULL	NULL	NULL	statement 3	Process		occurs along with					pol II	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_102_s_238	9418858	(A) EKLF bound to the beta gene recruits a subcomplex of the transcriptional machinery and enables formation of a transcription initiation complex (IC) of the beta gene together with TFIID containing TATA box-binding protein (TBP), RNA polymerase II (pol II) holoenzyme, and probably other subcomplexes recruited by other transcriptional activators.	bind
5811	8	2775	5	10	NULL	NULL	NULL	pol II	GP		is					RNA polymerase II holoenzyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_102_s_238	9418858	(A) EKLF bound to the beta gene recruits a subcomplex of the transcriptional machinery and enables formation of a transcription initiation complex (IC) of the beta gene together with TFIID containing TATA box-binding protein (TBP), RNA polymerase II (pol II) holoenzyme, and probably other subcomplexes recruited by other transcriptional activators.	bind
5812	9	2775	5	10	NULL	NULL	NULL	transcriptional activators	GP		recruit					subcomplexes	GP	other			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_102_s_238	9418858	(A) EKLF bound to the beta gene recruits a subcomplex of the transcriptional machinery and enables formation of a transcription initiation complex (IC) of the beta gene together with TFIID containing TATA box-binding protein (TBP), RNA polymerase II (pol II) holoenzyme, and probably other subcomplexes recruited by other transcriptional activators.	bind
5813	10	2775	5	10	NULL	NULL	NULL	statement 3	Process		occurs along with		probably			statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_102_s_238	9418858	(A) EKLF bound to the beta gene recruits a subcomplex of the transcriptional machinery and enables formation of a transcription initiation complex (IC) of the beta gene together with TFIID containing TATA box-binding protein (TBP), RNA polymerase II (pol II) holoenzyme, and probably other subcomplexes recruited by other transcriptional activators.	bind
8984	1	2775	7	10	NULL	NULL	NULL	EKLF	GP		bind					beta gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_102_s_238	9418858	(A) EKLF bound to the beta gene recruits a subcomplex of the transcriptional machinery and enables formation of a transcription initiation complex (IC) of the beta gene together with TFIID containing TATA box-binding protein (TBP), RNA polymerase II (pol II) holoenzyme, and probably other subcomplexes recruited by other transcriptional activators.	bind
8985	2	2775	7	10	NULL	NULL	NULL	statement 1	Process		recruits					transcriptional machinery	GP	subcomplex of the			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_102_s_238	9418858	(A) EKLF bound to the beta gene recruits a subcomplex of the transcriptional machinery and enables formation of a transcription initiation complex (IC) of the beta gene together with TFIID containing TATA box-binding protein (TBP), RNA polymerase II (pol II) holoenzyme, and probably other subcomplexes recruited by other transcriptional activators.	bind
8986	3	2775	7	10	NULL	NULL	NULL	statement 2	Process		enables 					IC of beta gene	GP	formation of 			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_102_s_238	9418858	(A) EKLF bound to the beta gene recruits a subcomplex of the transcriptional machinery and enables formation of a transcription initiation complex (IC) of the beta gene together with TFIID containing TATA box-binding protein (TBP), RNA polymerase II (pol II) holoenzyme, and probably other subcomplexes recruited by other transcriptional activators.	bind
8990	4	2775	7	10	NULL	NULL	NULL	transcription initiation complex	GP		consist of					TFIID containing TATA box-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_102_s_238	9418858	(A) EKLF bound to the beta gene recruits a subcomplex of the transcriptional machinery and enables formation of a transcription initiation complex (IC) of the beta gene together with TFIID containing TATA box-binding protein (TBP), RNA polymerase II (pol II) holoenzyme, and probably other subcomplexes recruited by other transcriptional activators.	bind
8991	5	2775	7	10	NULL	NULL	NULL	transcription initiation complex	GP		consist of					RNA polymerase II holoenzyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_102_s_238	9418858	(A) EKLF bound to the beta gene recruits a subcomplex of the transcriptional machinery and enables formation of a transcription initiation complex (IC) of the beta gene together with TFIID containing TATA box-binding protein (TBP), RNA polymerase II (pol II) holoenzyme, and probably other subcomplexes recruited by other transcriptional activators.	bind
8992	6	2775	7	10	NULL	NULL	NULL	transcription initiation complex	GP		consist of					 transcriptional activators	GP	subcomplexes recruited by other			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_102_s_238	9418858	(A) EKLF bound to the beta gene recruits a subcomplex of the transcriptional machinery and enables formation of a transcription initiation complex (IC) of the beta gene together with TFIID containing TATA box-binding protein (TBP), RNA polymerase II (pol II) holoenzyme, and probably other subcomplexes recruited by other transcriptional activators.	bind
8993	7	2775	7	10	NULL	NULL	NULL	IC	GP		is					transcription initiation complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_102_s_238	9418858	(A) EKLF bound to the beta gene recruits a subcomplex of the transcriptional machinery and enables formation of a transcription initiation complex (IC) of the beta gene together with TFIID containing TATA box-binding protein (TBP), RNA polymerase II (pol II) holoenzyme, and probably other subcomplexes recruited by other transcriptional activators.	bind
8994	8	2775	7	10	NULL	NULL	NULL	TBP	GP		is					TATA box-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_102_s_238	9418858	(A) EKLF bound to the beta gene recruits a subcomplex of the transcriptional machinery and enables formation of a transcription initiation complex (IC) of the beta gene together with TFIID containing TATA box-binding protein (TBP), RNA polymerase II (pol II) holoenzyme, and probably other subcomplexes recruited by other transcriptional activators.	bind
8995	9	2775	7	10	NULL	NULL	NULL	pol II	GP		is					RNA polymerase II holoenzyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_102_s_238	9418858	(A) EKLF bound to the beta gene recruits a subcomplex of the transcriptional machinery and enables formation of a transcription initiation complex (IC) of the beta gene together with TFIID containing TATA box-binding protein (TBP), RNA polymerase II (pol II) holoenzyme, and probably other subcomplexes recruited by other transcriptional activators.	bind
5814	1	2776	5	10	NULL	NULL	NULL	Isw2 complex	GP		bind					NCPs	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9165_s_172	16227570	(A) Electromobility  shift assay measuring binding of Isw2 complex to wild-type or mutant NCPs. NCPs bound  by Isw2 complex and unbound NCPs are indicated by white and black arrows, respectively.	bind
5815	2	2776	5	10	NULL	NULL	NULL	Isw2 complex	GP		bind					NCPs	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9165_s_172	16227570	(A) Electromobility  shift assay measuring binding of Isw2 complex to wild-type or mutant NCPs. NCPs bound  by Isw2 complex and unbound NCPs are indicated by white and black arrows, respectively.	bind
8987	1	2776	7	10	NULL	NULL	NULL	Isw2 complex	GP		bind					NCPs	GP	wild-type			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9165_s_172	16227570	(A) Electromobility  shift assay measuring binding of Isw2 complex to wild-type or mutant NCPs. NCPs bound  by Isw2 complex and unbound NCPs are indicated by white and black arrows, respectively.	bind
8988	2	2776	7	10	NULL	NULL	NULL	Isw2 complex	GP		bind					NCPs	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9165_s_172	16227570	(A) Electromobility  shift assay measuring binding of Isw2 complex to wild-type or mutant NCPs. NCPs bound  by Isw2 complex and unbound NCPs are indicated by white and black arrows, respectively.	bind
5816	1	2777	5	10	NULL	NULL	NULL	TBP molecules	GP	full-length;;wild-type	bind					U6	GP	human		promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_108_5_615_s_28	11893333	(A) Electrophoretic mobility retardation analysis of full-length wild-type and mutant TBP molecules binding to the human U6 promoter.	bind
5817	2	2777	5	10	NULL	NULL	NULL	TBP molecules	GP	mutant	bind					U6	GP	human		promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_108_5_615_s_28	11893333	(A) Electrophoretic mobility retardation analysis of full-length wild-type and mutant TBP molecules binding to the human U6 promoter.	bind
8865	1	2777	7	10	NULL	NULL	NULL	TBP	GP	 full-length;;wild-type	bind					U6	GP	human		promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_108_5_615_s_28	11893333	(A) Electrophoretic mobility retardation analysis of full-length wild-type and mutant TBP molecules binding to the human U6 promoter.	bind
8866	2	2777	7	10	NULL	NULL	NULL	TBP	GP	mutant	bind					U6	GP	human		promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_108_5_615_s_28	11893333	(A) Electrophoretic mobility retardation analysis of full-length wild-type and mutant TBP molecules binding to the human U6 promoter.	bind
5818	1	2780	5	10	NULL	NULL	NULL	IgM antibodies	GP		bind					LDL	GP	oxidized			NULL	sera of apoE-deficient mice	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_734_s_176	10073981	(A) ELISA assay showing the binding of IgM and IgG antibodies to oxidized LDL in the sera of apoE-deficient mice.	bind
5819	2	2780	5	10	NULL	NULL	NULL	IgG antibodies	GP		bind					LDL	GP	oxidized			NULL	sera of apoE-deficient mice	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_734_s_176	10073981	(A) ELISA assay showing the binding of IgM and IgG antibodies to oxidized LDL in the sera of apoE-deficient mice.	bind
8867	1	2780	7	10	NULL	NULL	NULL	IgM antibodies	GP		bind					LDL	GP	oxidized			NULL	in the sera of apoE-deficient mice	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_734_s_176	10073981	(A) ELISA assay showing the binding of IgM and IgG antibodies to oxidized LDL in the sera of apoE-deficient mice.	bind
8868	2	2780	7	10	NULL	NULL	NULL	IgG antibodies	GP		bind					LDL	GP	oxidized			NULL	in the sera of apoE-deficient mice	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_734_s_176	10073981	(A) ELISA assay showing the binding of IgM and IgG antibodies to oxidized LDL in the sera of apoE-deficient mice.	bind
5820	1	2781	5	10	NULL	NULL	NULL	ELMO1-GFP	GP		bind					Dock180	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_1_27_s_230	11595183	(A) ELMO1-GFP binds Dock180.	bind
8869	1	2781	7	10	NULL	NULL	NULL	ELMO1-GFP	GP		bind					Dock180	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_1_27_s_230	11595183	(A) ELMO1-GFP binds Dock180.	bind
5822	1	2784	5	10	NULL	NULL	NULL	YY1	GP		bind					b4C	GP	wt			NULL		NULL	NULL	NULL	NULL	gw60_development_129_16_3887_s_220	12135926	(A) EMSA competition experiments showing the ability of specific mutations to interfere with the binding of YY1 and NF-Y to b4Cwt.	bind
5823	2	2784	5	10	NULL	NULL	NULL	NF-Y	GP		bind					b4C	GP	wt			NULL		NULL	NULL	NULL	NULL	gw60_development_129_16_3887_s_220	12135926	(A) EMSA competition experiments showing the ability of specific mutations to interfere with the binding of YY1 and NF-Y to b4Cwt.	bind
8870	1	2784	7	10	NULL	NULL	NULL	YY1	GP		bind					b4C	GP	wt			NULL		NULL	NULL	NULL	NULL	gw60_development_129_16_3887_s_220	12135926	(A) EMSA competition experiments showing the ability of specific mutations to interfere with the binding of YY1 and NF-Y to b4Cwt.	bind
8871	2	2784	7	10	NULL	NULL	NULL	NF-Y	GP		bind					b4C	GP	wt			NULL		NULL	NULL	NULL	NULL	gw60_development_129_16_3887_s_220	12135926	(A) EMSA competition experiments showing the ability of specific mutations to interfere with the binding of YY1 and NF-Y to b4Cwt.	bind
5826	1	2785	5	10	NULL	NULL	NULL	GST-CP2b	GP	recombinant	bind		weakly			probe DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6005_s_250	15988015	(A) EMSA demonstrated that recombinant GST-CP2b bound very weakly to the probe DNA,  while other isoforms showed strong DNA binding activities (a).	bind
8873	1	2785	7	10	NULL	NULL	NULL	GST-CP2b	GP	recombinant	bind		very weakly			probe DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6005_s_250	15988015	(A) EMSA demonstrated that recombinant GST-CP2b bound very weakly to the probe DNA,  while other isoforms showed strong DNA binding activities (a).	bind
5828	1	2786	5	10	NULL	NULL	NULL	AP-1	GP		bind					fra-1 oligonucleotide	NucleicAcid			TRE	NULL	FRTL-5MEK	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4401_s_250	12773579	(A) EMSA of AP-1 binding to the  fra-1 TRE oligonucleotide in the FRTL-5-derived cell clones expressing the constitutively  active form of MEK and/or Rac (FRTL-5MEK, FRTL-5Rac, and FRTL-5MEK/Rac).	bind
5829	2	2786	5	10	NULL	NULL	NULL	FRTL-5-derived cell clones	Cell		express					MEK	GP	constitutively active form of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4401_s_250	12773579	(A) EMSA of AP-1 binding to the  fra-1 TRE oligonucleotide in the FRTL-5-derived cell clones expressing the constitutively  active form of MEK and/or Rac (FRTL-5MEK, FRTL-5Rac, and FRTL-5MEK/Rac).	bind
5830	3	2786	5	10	NULL	NULL	NULL	FRTL-5MEK	Cell		is					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4401_s_250	12773579	(A) EMSA of AP-1 binding to the  fra-1 TRE oligonucleotide in the FRTL-5-derived cell clones expressing the constitutively  active form of MEK and/or Rac (FRTL-5MEK, FRTL-5Rac, and FRTL-5MEK/Rac).	bind
5831	4	2786	5	10	NULL	NULL	NULL	FRTL-5-derived cell clones	Cell		express					Rac	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4401_s_250	12773579	(A) EMSA of AP-1 binding to the  fra-1 TRE oligonucleotide in the FRTL-5-derived cell clones expressing the constitutively  active form of MEK and/or Rac (FRTL-5MEK, FRTL-5Rac, and FRTL-5MEK/Rac).	bind
5832	5	2786	5	10	NULL	NULL	NULL	FRTL-5Rac	Cell		is					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4401_s_250	12773579	(A) EMSA of AP-1 binding to the  fra-1 TRE oligonucleotide in the FRTL-5-derived cell clones expressing the constitutively  active form of MEK and/or Rac (FRTL-5MEK, FRTL-5Rac, and FRTL-5MEK/Rac).	bind
5833	6	2786	5	10	NULL	NULL	NULL	statement 2	Process		occurs simultaneously with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4401_s_250	12773579	(A) EMSA of AP-1 binding to the  fra-1 TRE oligonucleotide in the FRTL-5-derived cell clones expressing the constitutively  active form of MEK and/or Rac (FRTL-5MEK, FRTL-5Rac, and FRTL-5MEK/Rac).	bind
5834	7	2786	5	10	NULL	NULL	NULL	statement 6	Process		is					FRTL-5MEK/Rac	Cell				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4401_s_250	12773579	(A) EMSA of AP-1 binding to the  fra-1 TRE oligonucleotide in the FRTL-5-derived cell clones expressing the constitutively  active form of MEK and/or Rac (FRTL-5MEK, FRTL-5Rac, and FRTL-5MEK/Rac).	bind
5835	8	2786	5	10	NULL	NULL	NULL	AP-1	GP		bind					fra-1 TRE oligonucleotide	NucleicAcid				NULL	FRTL-5Rac	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4401_s_250	12773579	(A) EMSA of AP-1 binding to the  fra-1 TRE oligonucleotide in the FRTL-5-derived cell clones expressing the constitutively  active form of MEK and/or Rac (FRTL-5MEK, FRTL-5Rac, and FRTL-5MEK/Rac).	bind
5836	9	2786	5	10	NULL	NULL	NULL	AP-1	GP		bind					fra-1 TRE oligonucleotide	NucleicAcid				NULL	FRTL-5MEK/Rac	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4401_s_250	12773579	(A) EMSA of AP-1 binding to the  fra-1 TRE oligonucleotide in the FRTL-5-derived cell clones expressing the constitutively  active form of MEK and/or Rac (FRTL-5MEK, FRTL-5Rac, and FRTL-5MEK/Rac).	bind
8996	1	2786	7	10	NULL	0	NULL	 AP-1			bind					 fra-1oligonucleotide				TRE 	NULL	FRTL-5MEK	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4401_s_250	12773579	(A) EMSA of AP-1 binding to the  fra-1 TRE oligonucleotide in the FRTL-5-derived cell clones expressing the constitutively  active form of MEK and/or Rac (FRTL-5MEK, FRTL-5Rac, and FRTL-5MEK/Rac).	bind
8997	2	2786	7	10	NULL	NULL	NULL	FRTL-5-derived cell	Cell		express					MEK	GP	constitutively active form of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4401_s_250	12773579	(A) EMSA of AP-1 binding to the  fra-1 TRE oligonucleotide in the FRTL-5-derived cell clones expressing the constitutively  active form of MEK and/or Rac (FRTL-5MEK, FRTL-5Rac, and FRTL-5MEK/Rac).	bind
8998	3	2786	7	10	NULL	NULL	NULL	FRTL-5-derived cell	Cell		express					Rac	GP	constitutively active form of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4401_s_250	12773579	(A) EMSA of AP-1 binding to the  fra-1 TRE oligonucleotide in the FRTL-5-derived cell clones expressing the constitutively  active form of MEK and/or Rac (FRTL-5MEK, FRTL-5Rac, and FRTL-5MEK/Rac).	bind
8999	4	2786	7	10	NULL	NULL	NULL	statement 2	Process		is					FRTL-5MEK	Cell				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4401_s_250	12773579	(A) EMSA of AP-1 binding to the  fra-1 TRE oligonucleotide in the FRTL-5-derived cell clones expressing the constitutively  active form of MEK and/or Rac (FRTL-5MEK, FRTL-5Rac, and FRTL-5MEK/Rac).	bind
9000	5	2786	7	10	NULL	NULL	NULL	statement 3	Process		is					FRTL-5Rac	Cell				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4401_s_250	12773579	(A) EMSA of AP-1 binding to the  fra-1 TRE oligonucleotide in the FRTL-5-derived cell clones expressing the constitutively  active form of MEK and/or Rac (FRTL-5MEK, FRTL-5Rac, and FRTL-5MEK/Rac).	bind
9001	6	2786	7	10	NULL	NULL	NULL	FRTL-5-derived cell	Cell		express					MEK/Rac	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4401_s_250	12773579	(A) EMSA of AP-1 binding to the  fra-1 TRE oligonucleotide in the FRTL-5-derived cell clones expressing the constitutively  active form of MEK and/or Rac (FRTL-5MEK, FRTL-5Rac, and FRTL-5MEK/Rac).	bind
11760	7	2786	7	10	NULL	NULL	NULL	statement 2 	Process		occur simultaneously with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4401_s_250	12773579	(A) EMSA of AP-1 binding to the  fra-1 TRE oligonucleotide in the FRTL-5-derived cell clones expressing the constitutively  active form of MEK and/or Rac (FRTL-5MEK, FRTL-5Rac, and FRTL-5MEK/Rac).	bind
5837	1	2790	5	10	NULL	NULL	NULL	RBP-Jkappa proteins	GP	endogenous	bind		strongly			GST-SHARP	GP	immobilized	2002-3664		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10379_s_194	16287852	(A) Endogenous RBP-Jkappa proteins bind strongly to GST-SHARP(2002-3664) immobilized on glutathione Sepharose  beads.	bind
9002	1	2790	7	10	NULL	NULL	NULL	RBP-Jkappa proteins	GP	endogenous	bind		strongly			GST-SHARP	GP	immobilized	2002-3664		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10379_s_194	16287852	(A) Endogenous RBP-Jkappa proteins bind strongly to GST-SHARP(2002-3664) immobilized on glutathione Sepharose  beads.	bind
5838	1	2791	5	10	NULL	NULL	NULL	TRF2	GP	endogenous	bind					POT1	GP				NULL	IMR90 fibroblasts	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_3_1070_s_211	15657433	(A) Endogenous TRF2 bound to POT1 in IMR90 fibroblasts  by coimmunoprecipitation.	bind
9003	1	2791	7	10	NULL	NULL	NULL	TRF2	GP	endogenous	bind					 POT1	GP				NULL	IMR90 fibroblasts	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_3_1070_s_211	15657433	(A) Endogenous TRF2 bound to POT1 in IMR90 fibroblasts  by coimmunoprecipitation.	bind
5839	1	2792	5	10	NULL	NULL	NULL	Ent3p	GP		bind					clathrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_3_499_s_196	12967568	(A) Ent3p binds clathrin.	bind
9004	1	2792	7	10	NULL	NULL	NULL	Ent3p 	GP		bind					clathrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_3_499_s_196	12967568	(A) Ent3p binds clathrin.	bind
5840	1	2795	5	10	NULL	NULL	NULL	ERKs	GP		does not bind					Mxi2	GP	deletion mutant form lacking	C terminus		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_9_3079_s_293	12697810	(A) ERKs cannot bind  to a deletion mutant form of Mxi2 lacking the C terminus.	bind
9005	1	2795	7	10	NULL	NULL	NULL	ERKs	GP		does not bind					Mxi2 	GP	deletion mutant form lacking	C terminus		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_9_3079_s_293	12697810	(A) ERKs cannot bind  to a deletion mutant form of Mxi2 lacking the C terminus.	bind
5841	1	2797	5	10	NULL	NULL	NULL	ETO	GP		bind					HDAC-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_167	11533236	(A) ETO binds HDAC-1, HDAC-2, and HDAC-3.	bind
5842	2	2797	5	10	NULL	NULL	NULL	ETO	GP		bind					HDAC-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_167	11533236	(A) ETO binds HDAC-1, HDAC-2, and HDAC-3.	bind
5843	3	2797	5	10	NULL	NULL	NULL	ETO	GP		bind					HDAC-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_167	11533236	(A) ETO binds HDAC-1, HDAC-2, and HDAC-3.	bind
9006	1	2797	7	10	NULL	NULL	NULL	ETO	GP		binds					HDAC-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_167	11533236	(A) ETO binds HDAC-1, HDAC-2, and HDAC-3.	bind
9007	2	2797	7	10	NULL	NULL	NULL	ETO	GP		bind					HDAC-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_167	11533236	(A) ETO binds HDAC-1, HDAC-2, and HDAC-3.	bind
9008	3	2797	7	10	NULL	NULL	NULL	ETO	GP		bind					HDAC-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_167	11533236	(A) ETO binds HDAC-1, HDAC-2, and HDAC-3.	bind
5844	1	2798	5	10	NULL	NULL	NULL	peptide	AminoAcid		bind					deltaSET7/9 	GP		E-330 A		NULL		NULL	NULL	NULL	NULL	gw60_cell_111_1_105_s_216	12372304	(A) Example of ITC trace (upper) and fitted binding curve (lower) of peptide binding to deltaSET7/9 E-330 A.  (B) Summary of dissociation constants for peptide and AdoMet binding to SET7/9 constructs monitored by ITC and fluorescence spectroscopy.	bind
5845	2	2798	5	10	NULL	NULL	NULL	AdoMet	GP		bind					SET7/9 constructs	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_1_105_s_216	12372304	(A) Example of ITC trace (upper) and fitted binding curve (lower) of peptide binding to deltaSET7/9 E-330 A.  (B) Summary of dissociation constants for peptide and AdoMet binding to SET7/9 constructs monitored by ITC and fluorescence spectroscopy.	bind
9009	1	2798	7	10	NULL	NULL	NULL	peptide	AminoAcid		bind					deltaSET7/9	GP		E-330 A		NULL		NULL	NULL	NULL	NULL	gw60_cell_111_1_105_s_216	12372304	(A) Example of ITC trace (upper) and fitted binding curve (lower) of peptide binding to deltaSET7/9 E-330 A.  (B) Summary of dissociation constants for peptide and AdoMet binding to SET7/9 constructs monitored by ITC and fluorescence spectroscopy.	bind
9010	2	2798	7	10	NULL	NULL	NULL	AdoMet	GP		bind					SET7/9 constructs	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_1_105_s_216	12372304	(A) Example of ITC trace (upper) and fitted binding curve (lower) of peptide binding to deltaSET7/9 E-330 A.  (B) Summary of dissociation constants for peptide and AdoMet binding to SET7/9 constructs monitored by ITC and fluorescence spectroscopy.	bind
5847	1	2799	5	10	NULL	NULL	NULL	IBB	AminoAcid		is					importin beta binding fragment of importin	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_104_1_83_s_82	11163242	(A) Excess of NLS peptide  and of the importin beta binding fragment of importin   (IBB) promotes microtubule  assembly in  Xenopus M phase extracts.	bind
5848	2	2799	5	10	NULL	NULL	NULL	NLS peptide	AminoAcid	excess	promote					microtubule assembly	Process				NULL	in Xenopus M phase extracts	NULL	NULL	NULL	NULL	gw60_cell_104_1_83_s_82	11163242	(A) Excess of NLS peptide  and of the importin beta binding fragment of importin   (IBB) promotes microtubule  assembly in  Xenopus M phase extracts.	bind
5849	3	2799	5	10	NULL	NULL	NULL	IBB	GP	excess of 	promote					microtubule assembly	Process				NULL	in Xenopus M phase extracts	NULL	NULL	NULL	NULL	gw60_cell_104_1_83_s_82	11163242	(A) Excess of NLS peptide  and of the importin beta binding fragment of importin   (IBB) promotes microtubule  assembly in  Xenopus M phase extracts.	bind
9011	1	2799	7	10	NULL	NULL	NULL	NLS peptide	AminoAcid	excess of	promotes					microtubule assembly	Process				NULL	Xenopus M phase extracts	NULL	NULL	NULL	NULL	gw60_cell_104_1_83_s_82	11163242	(A) Excess of NLS peptide  and of the importin beta binding fragment of importin   (IBB) promotes microtubule  assembly in  Xenopus M phase extracts.	bind
9012	2	2799	7	10	NULL	NULL	NULL	IBB	AminoAcid	excess	promotes					microtubule assembly	Process				NULL	Xenopus M phase extracts	NULL	NULL	NULL	NULL	gw60_cell_104_1_83_s_82	11163242	(A) Excess of NLS peptide  and of the importin beta binding fragment of importin   (IBB) promotes microtubule  assembly in  Xenopus M phase extracts.	bind
9013	3	2799	7	10	NULL	NULL	NULL	IBB	AminoAcid		is					importin beta binding fragment of importin	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_104_1_83_s_82	11163242	(A) Excess of NLS peptide  and of the importin beta binding fragment of importin   (IBB) promotes microtubule  assembly in  Xenopus M phase extracts.	bind
5850	1	2800	5	10	NULL	NULL	NULL	SKP1	GP		bind					CUL1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_168	12504026	(A) Expression of CAND1 prevents SKP1 binding to CUL1.	bind
5851	2	2800	5	10	NULL	NULL	NULL	CAND1	GP	expression	prevent					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_168	12504026	(A) Expression of CAND1 prevents SKP1 binding to CUL1.	bind
9014	1	2800	7	10	NULL	NULL	NULL	SKP1	GP		bind					CUL1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_168	12504026	(A) Expression of CAND1 prevents SKP1 binding to CUL1.	bind
9015	2	2800	7	10	NULL	NULL	NULL	CAND1	GP	expression of	prevents					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_168	12504026	(A) Expression of CAND1 prevents SKP1 binding to CUL1.	bind
6062	2	2802	5	10	NULL	NULL	NULL	13C4 mAb	GP		inhibit			Fab-fragment		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_8_2453_s_150	11514628	(A) Fab-fragment of 13C4 mAb inhibits STxB binding to Gb3.	bind
6063	1	2802	5	10	NULL	NULL	NULL	STxB	GP		bind					Gb3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_8_2453_s_150	11514628	(A) Fab-fragment of 13C4 mAb inhibits STxB binding to Gb3.	bind
6045	1	2802	6	10	NULL	NULL	NULL	STxB 	GP		bind					Gb3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_8_2453_s_150	11514628	(A) Fab-fragment of 13C4 mAb inhibits STxB binding to Gb3.	bind
6046	2	2802	6	10	NULL	NULL	NULL	13C4 mAb	GP		inhibits			Fab-fragment		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_8_2453_s_150	11514628	(A) Fab-fragment of 13C4 mAb inhibits STxB binding to Gb3.	bind
6064	1	2803	5	10	NULL	NULL	NULL	CPSF	GP		bind					GST-TFIIS	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6154_s_174	10454562	(A) factors CPSF and CstF bound to GST-TFIIS ( 41) but not to GST-VP16.	bind
6065	2	2803	5	10	NULL	NULL	NULL	CstF	GP		bind					GST-TFIIS	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6154_s_174	10454562	(A) factors CPSF and CstF bound to GST-TFIIS ( 41) but not to GST-VP16.	bind
6066	3	2803	5	10	NULL	NULL	NULL	CPSF	GP		does not bind					GST-VP16	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6154_s_174	10454562	(A) factors CPSF and CstF bound to GST-TFIIS ( 41) but not to GST-VP16.	bind
6067	4	2803	5	10	NULL	NULL	NULL	CstF	GP		does not bind					GST-VP16	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6154_s_174	10454562	(A) factors CPSF and CstF bound to GST-TFIIS ( 41) but not to GST-VP16.	bind
6047	1	2803	6	10	NULL	NULL	NULL	CPSF	GP		bind					GST-TFIIS	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6154_s_174	10454562	(A) factors CPSF and CstF bound to GST-TFIIS ( 41) but not to GST-VP16.	bind
6048	2	2803	6	10	NULL	NULL	NULL	CstF	GP		bind					GST-TFIIS	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6154_s_174	10454562	(A) factors CPSF and CstF bound to GST-TFIIS ( 41) but not to GST-VP16.	bind
6049	3	2803	6	10	NULL	NULL	NULL	CPSF	GP		does not bind					GST-VP16	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6154_s_174	10454562	(A) factors CPSF and CstF bound to GST-TFIIS ( 41) but not to GST-VP16.	bind
6050	4	2803	6	10	NULL	NULL	NULL	CstF	GP		does not bind					GST-VP16	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6154_s_174	10454562	(A) factors CPSF and CstF bound to GST-TFIIS ( 41) but not to GST-VP16.	bind
6068	1	2804	5	10	NULL	NULL	NULL	Fibulin-1	GP		bind					BPV-1 E6	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_4_962_s_112	12200142	(A) Fibulin-1 binds to BPV-1 E6 and HPV-16 E6.	bind
6069	2	2804	5	10	NULL	NULL	NULL	Fibulin-1	GP		bind					HPV-16 E6	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_4_962_s_112	12200142	(A) Fibulin-1 binds to BPV-1 E6 and HPV-16 E6.	bind
6051	1	2804	6	10	NULL	NULL	NULL	Fibulin-1	GP		bind					BPV-1 E6	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_4_962_s_112	12200142	(A) Fibulin-1 binds to BPV-1 E6 and HPV-16 E6.	bind
6052	2	2804	6	10	NULL	NULL	NULL	Fibulin-1	GP		bind					HPV-16 E6	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_4_962_s_112	12200142	(A) Fibulin-1 binds to BPV-1 E6 and HPV-16 E6.	bind
6070	1	2805	5	10	NULL	NULL	NULL	PSC	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_3_545_s_136	11583617	(A) Filter binding assay for binding of PSC (top panel) and PCC (bottom panel) to DNA.	bind
6071	2	2805	5	10	NULL	NULL	NULL	PCC	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_3_545_s_136	11583617	(A) Filter binding assay for binding of PSC (top panel) and PCC (bottom panel) to DNA.	bind
6053	1	2805	6	10	NULL	NULL	NULL	PSC	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_3_545_s_136	11583617	(A) Filter binding assay for binding of PSC (top panel) and PCC (bottom panel) to DNA.	bind
6054	2	2805	6	10	NULL	NULL	NULL	PCC	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_3_545_s_136	11583617	(A) Filter binding assay for binding of PSC (top panel) and PCC (bottom panel) to DNA.	bind
6072	1	2808	5	10	NULL	NULL	NULL	diazepam	Chemical		bind					HSA	GP	native			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1750_1_93_s_168	15890566	(A) Fluorescence quench titration results of diazepam binding to native HSA  ( ) and HSA denatured with 1.0 M ( ) 1.8 M ( ) and 6.0 M ( ) GnHCl concentration.	bind
6073	2	2808	5	10	NULL	NULL	NULL	diazepam	Chemical		bind					HSA	GP	denatured			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1750_1_93_s_168	15890566	(A) Fluorescence quench titration results of diazepam binding to native HSA  ( ) and HSA denatured with 1.0 M ( ) 1.8 M ( ) and 6.0 M ( ) GnHCl concentration.	bind
53054	3	2808	5	10	NULL	NULL	NULL	GnHCl	Chemical		denatures					HSA	GP	native			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1750_1_93_s_168	15890566	(A) Fluorescence quench titration results of diazepam binding to native HSA  ( ) and HSA denatured with 1.0 M ( ) 1.8 M ( ) and 6.0 M ( ) GnHCl concentration.	bind
6055	1	2808	6	10	NULL	NULL	NULL	diazepam	Chemical		bind					HSA	GP	native			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1750_1_93_s_168	15890566	(A) Fluorescence quench titration results of diazepam binding to native HSA  ( ) and HSA denatured with 1.0 M ( ) 1.8 M ( ) and 6.0 M ( ) GnHCl concentration.	bind
6056	2	2808	6	10	NULL	NULL	NULL	diazepam	Chemical		bind					HSA	GP	denatured			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1750_1_93_s_168	15890566	(A) Fluorescence quench titration results of diazepam binding to native HSA  ( ) and HSA denatured with 1.0 M ( ) 1.8 M ( ) and 6.0 M ( ) GnHCl concentration.	bind
6057	3	2808	6	10	NULL	NULL	NULL	GnHCl	Chemical		denatures					HSA	GP	native			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1750_1_93_s_168	15890566	(A) Fluorescence quench titration results of diazepam binding to native HSA  ( ) and HSA denatured with 1.0 M ( ) 1.8 M ( ) and 6.0 M ( ) GnHCl concentration.	bind
6074	1	2809	5	10	NULL	NULL	NULL	SarA	GP		bind					sarV	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_16_5267_s_186	15292128	(A) Footprint analysis of SarA binding to the  sarV promoter region.	bind
6058	1	2809	6	10	NULL	NULL	NULL	SarA	GP		bind					sarV	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_16_5267_s_186	15292128	(A) Footprint analysis of SarA binding to the  sarV promoter region.	bind
6075	1	2811	5	NULL	NULL	0	NULL		NULL	free	bind	NULL		N1-22			NULL		N1-22		NULL		0	NULL	NULL	NULL	gw60_molcell_1_2_265_s_45	9659923	(A) free N1-22, (B) free  boxB RNA, and  boxB RNA bound to (C) N1-22, (D) N1-47, and (E) the full-length N protein.	bind
6076	2	2811	5	NULL	NULL	0	NULL		NULL	free	bind	NULL		N1-22			NULL		N1-47		NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_45	9659923	(A) free N1-22, (B) free  boxB RNA, and  boxB RNA bound to (C) N1-22, (D) N1-47, and (E) the full-length N protein.	bind
6077	3	2811	5	10	NULL	NULL	NULL			free	bind			N1-22		N protein	GP	full-length			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_45	9659923	(A) free N1-22, (B) free  boxB RNA, and  boxB RNA bound to (C) N1-22, (D) N1-47, and (E) the full-length N protein.	bind
6078	4	2811	5	10	NULL	NULL	NULL	RNA	NucleicAcid	free	bind				boxB				N1-22		NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_45	9659923	(A) free N1-22, (B) free  boxB RNA, and  boxB RNA bound to (C) N1-22, (D) N1-47, and (E) the full-length N protein.	bind
6079	5	2811	5	10	NULL	NULL	NULL	RNA	NucleicAcid	free	bind				boxB				N1-47		NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_45	9659923	(A) free N1-22, (B) free  boxB RNA, and  boxB RNA bound to (C) N1-22, (D) N1-47, and (E) the full-length N protein.	bind
6080	6	2811	5	10	NULL	NULL	NULL	RNA	NucleicAcid	free	bind				boxB	N protein	GP	full-length			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_45	9659923	(A) free N1-22, (B) free  boxB RNA, and  boxB RNA bound to (C) N1-22, (D) N1-47, and (E) the full-length N protein.	bind
6081	7	2811	5	10	NULL	NULL	NULL	RNA	NucleicAcid		bind				boxB				N1-22		NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_45	9659923	(A) free N1-22, (B) free  boxB RNA, and  boxB RNA bound to (C) N1-22, (D) N1-47, and (E) the full-length N protein.	bind
6082	8	2811	5	10	NULL	NULL	NULL	RNA	NucleicAcid		bind				boxB				N1-47		NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_45	9659923	(A) free N1-22, (B) free  boxB RNA, and  boxB RNA bound to (C) N1-22, (D) N1-47, and (E) the full-length N protein.	bind
6083	9	2811	5	10	NULL	NULL	NULL	RNA	NucleicAcid		bind				boxB	N protein	GP	full-length			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_45	9659923	(A) free N1-22, (B) free  boxB RNA, and  boxB RNA bound to (C) N1-22, (D) N1-47, and (E) the full-length N protein.	bind
6225	1	2811	6	10	NULL	NULL	NULL	RNA	NucleicAcid		bind				boxB				N1-22		NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_45	9659923	(A) free N1-22, (B) free  boxB RNA, and  boxB RNA bound to (C) N1-22, (D) N1-47, and (E) the full-length N protein.	bind
6226	2	2811	6	10	NULL	NULL	NULL	RNA	NucleicAcid		bind				boxB				N1-47		NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_45	9659923	(A) free N1-22, (B) free  boxB RNA, and  boxB RNA bound to (C) N1-22, (D) N1-47, and (E) the full-length N protein.	bind
6227	3	2811	6	10	NULL	NULL	NULL	RNA	NucleicAcid		bind				boxB	N protein	GP	full length			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_45	9659923	(A) free N1-22, (B) free  boxB RNA, and  boxB RNA bound to (C) N1-22, (D) N1-47, and (E) the full-length N protein.	bind
7272	4	2811	6	NULL	NULL	0	NULL		NULL	free	bind	NULL		N1-22			NULL		N1-22		NULL		0	NULL	NULL	NULL	gw60_molcell_1_2_265_s_45	9659923	(A) free N1-22, (B) free  boxB RNA, and  boxB RNA bound to (C) N1-22, (D) N1-47, and (E) the full-length N protein.	bind
7273	5	2811	6	NULL	NULL	0	NULL		NULL	free	bind	NULL		N1-22			NULL		N1-47		NULL		0	NULL	NULL	NULL	gw60_molcell_1_2_265_s_45	9659923	(A) free N1-22, (B) free  boxB RNA, and  boxB RNA bound to (C) N1-22, (D) N1-47, and (E) the full-length N protein.	bind
7274	6	2811	6	10	NULL	NULL	NULL			free	bind			N1-22		N protein	GP	full length			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_45	9659923	(A) free N1-22, (B) free  boxB RNA, and  boxB RNA bound to (C) N1-22, (D) N1-47, and (E) the full-length N protein.	bind
7275	7	2811	6	10	NULL	NULL	NULL	RNA	NucleicAcid	free	bind				boxB				N1-22		NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_45	9659923	(A) free N1-22, (B) free  boxB RNA, and  boxB RNA bound to (C) N1-22, (D) N1-47, and (E) the full-length N protein.	bind
7276	8	2811	6	10	NULL	NULL	NULL	RNA	NucleicAcid	free	bind				boxB				N1-47		NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_45	9659923	(A) free N1-22, (B) free  boxB RNA, and  boxB RNA bound to (C) N1-22, (D) N1-47, and (E) the full-length N protein.	bind
53055	9	2811	6	10	NULL	NULL	NULL	 RNA	NucleicAcid	free	bind				boxB	N protein	GP	full-length			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_45	9659923	(A) free N1-22, (B) free  boxB RNA, and  boxB RNA bound to (C) N1-22, (D) N1-47, and (E) the full-length N protein.	bind
6084	1	2814	5	10	NULL	NULL	NULL	GATA3	GP		bind					RALDH2-T	GP			GATA site in the promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6939_s_225	9819382	(A) GATA3 binds to the GATA site in the RALDH2-T promoter.	bind
6059	1	2814	6	10	NULL	NULL	NULL	GATA3	GP		bind					RALDH2-T	GP			GATA site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6939_s_225	9819382	(A) GATA3 binds to the GATA site in the RALDH2-T promoter.	bind
6085	1	2815	5	10	NULL	NULL	NULL	Gcn4	GP		bind									GCREs	NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1309_s_131	11163205	(A) Gcn4 binds GCREs independently of Gcn5.	bind
6086	2	2815	5	10	NULL	NULL	NULL	statement 1	Process		is independent of					Gcn5	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1309_s_131	11163205	(A) Gcn4 binds GCREs independently of Gcn5.	bind
6060	1	2815	6	10	NULL	NULL	NULL	Gcn4	GP		bind									GCRE	NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1309_s_131	11163205	(A) Gcn4 binds GCREs independently of Gcn5.	bind
6061	2	2815	6	10	NULL	NULL	NULL	statement 1	Process		is independent of					Gcn5	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1309_s_131	11163205	(A) Gcn4 binds GCREs independently of Gcn5.	bind
6087	1	2816	5	10	NULL	NULL	NULL	NFATp	GP	purified;;recombinant	bind					IL-3	GP			NFAT-like elements in enhancer	NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_175_s_145	9047239	(A) Gel electrophoretic mobility shift assays of purified recombinant NFATp and AP-1 binding to NFAT-like elements in the IL-3 enhancer.	bind
6088	2	2816	5	10	NULL	NULL	NULL	AP-1	GP	purified;;recombinant	bind					IL-3	GP			NFAT-like elements in enhancer	NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_175_s_145	9047239	(A) Gel electrophoretic mobility shift assays of purified recombinant NFATp and AP-1 binding to NFAT-like elements in the IL-3 enhancer.	bind
6228	1	2816	6	10	NULL	NULL	NULL	NFATp	GP	purified;;recombinant	bind					IL-3	GP			NFAT-like elements in enhancer	NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_175_s_145	9047239	(A) Gel electrophoretic mobility shift assays of purified recombinant NFATp and AP-1 binding to NFAT-like elements in the IL-3 enhancer.	bind
6229	2	2816	6	10	NULL	NULL	NULL	AP-1	GP	purified;;recombinant	bind					IL-3	GP			NFAT-like elements in enhancer	NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_175_s_145	9047239	(A) Gel electrophoretic mobility shift assays of purified recombinant NFATp and AP-1 binding to NFAT-like elements in the IL-3 enhancer.	bind
6089	1	2817	5	10	NULL	NULL	NULL	Tead2	GP		bind									CE	NULL		NULL	NULL	NULL	NULL	gw70_development_132_21_4719_s_169	16207754	(A) Gel mobility shift assay  showing that Tead2 and Tead4 bind to the CE.	bind
6090	2	2817	5	10	NULL	NULL	NULL	Tead4	GP		bind									CE	NULL		NULL	NULL	NULL	NULL	gw70_development_132_21_4719_s_169	16207754	(A) Gel mobility shift assay  showing that Tead2 and Tead4 bind to the CE.	bind
6230	1	2817	6	10	NULL	NULL	NULL	Tead2	GP		bind									CE	NULL		NULL	NULL	NULL	NULL	gw70_development_132_21_4719_s_169	16207754	(A) Gel mobility shift assay  showing that Tead2 and Tead4 bind to the CE.	bind
6231	2	2817	6	10	NULL	NULL	NULL	Tead4	GP		bind									CE	NULL		NULL	NULL	NULL	NULL	gw70_development_132_21_4719_s_169	16207754	(A) Gel mobility shift assay  showing that Tead2 and Tead4 bind to the CE.	bind
6091	1	2821	5	10	NULL	NULL	NULL	factors			bind					NF- B	GP				NULL	in nuclear extracts from pro-B cells	NULL	NULL	NULL	NULL	gw60_immunity_6_2_131_s_137	9047235	(A) Gel shift analysis of factors in nuclear extracts from pro- and pre-B cells that bind to NF- B or octamer probes.	bind
6092	2	2821	5	10	NULL	NULL	NULL	factors			bind					octamer probes	NucleicAcid				NULL	in nuclear extracts from pro-B cells	NULL	NULL	NULL	NULL	gw60_immunity_6_2_131_s_137	9047235	(A) Gel shift analysis of factors in nuclear extracts from pro- and pre-B cells that bind to NF- B or octamer probes.	bind
6093	3	2821	5	10	NULL	NULL	NULL	factors			bind					NF- B	GP				NULL	in nuclear extracts from pre-B cells	NULL	NULL	NULL	NULL	gw60_immunity_6_2_131_s_137	9047235	(A) Gel shift analysis of factors in nuclear extracts from pro- and pre-B cells that bind to NF- B or octamer probes.	bind
6094	4	2821	5	10	NULL	NULL	NULL	factors			bind					octamer probes	NucleicAcid				NULL	in nuclear extracts from pre-B cells	NULL	NULL	NULL	NULL	gw60_immunity_6_2_131_s_137	9047235	(A) Gel shift analysis of factors in nuclear extracts from pro- and pre-B cells that bind to NF- B or octamer probes.	bind
46516	5	2821	5	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_131_s_137	9047235	(A) Gel shift analysis of factors in nuclear extracts from pro- and pre-B cells that bind to NF- B or octamer probes.	bind
46517	6	2821	5	10	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_131_s_137	9047235	(A) Gel shift analysis of factors in nuclear extracts from pro- and pre-B cells that bind to NF- B or octamer probes.	bind
6232	1	2821	6	10	NULL	NULL	NULL	factor			bind					NF-B 	GP			site	NULL	nuclear extracts from pro-B cells	NULL	NULL	NULL	NULL	gw60_immunity_6_2_131_s_137	9047235	(A) Gel shift analysis of factors in nuclear extracts from pro- and pre-B cells that bind to NF- B or octamer probes.	bind
6233	2	2821	6	10	NULL	NULL	NULL	factor			bind					octamer probe	NucleicAcid			site	NULL	nuclear extracts from pro-B cells	NULL	NULL	NULL	NULL	gw60_immunity_6_2_131_s_137	9047235	(A) Gel shift analysis of factors in nuclear extracts from pro- and pre-B cells that bind to NF- B or octamer probes.	bind
6234	3	2821	6	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_131_s_137	9047235	(A) Gel shift analysis of factors in nuclear extracts from pro- and pre-B cells that bind to NF- B or octamer probes.	bind
46513	4	2821	6	10	NULL	NULL	NULL	factors			bind					NF-B 	GP				NULL	 in nuclear extracts from pre-B cells	NULL	NULL	NULL	NULL	gw60_immunity_6_2_131_s_137	9047235	(A) Gel shift analysis of factors in nuclear extracts from pro- and pre-B cells that bind to NF- B or octamer probes.	bind
46514	5	2821	6	10	NULL	NULL	NULL	factors			bind					octamer probes	NucleicAcid				NULL	in nuclear extracts from pre-B cells	NULL	NULL	NULL	NULL	gw60_immunity_6_2_131_s_137	9047235	(A) Gel shift analysis of factors in nuclear extracts from pro- and pre-B cells that bind to NF- B or octamer probes.	bind
46515	6	2821	6	10	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_131_s_137	9047235	(A) Gel shift analysis of factors in nuclear extracts from pro- and pre-B cells that bind to NF- B or octamer probes.	bind
6095	1	2822	5	NULL	NULL	0	NULL		NULL	complete	contain	NULL			127-nt enhancer		NULL	wild-type		pyrimidine tract	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6096	2	2822	5	NULL	NULL	0	NULL		NULL	complete	contain	NULL			127-nt enhancer		NULL	mutant		purine	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6097	3	2822	5	10	NULL	NULL	NULL			complete	contain				127-nt enhancer	U2AF	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6098	4	2822	5	10	NULL	NULL	NULL	PTB	GP		bind					statement 1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6099	5	2822	5	10	NULL	NULL	NULL	PTB	GP		bind					statement 2	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6100	6	2822	5	10	NULL	NULL	NULL	PTB	GP		bind					statement 3	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6101	7	2822	5	10	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6102	8	2822	5	10	NULL	NULL	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6103	9	2822	5	10	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6104	10	2822	5	10	NULL	NULL	NULL	U2AF	GP		bind					statement 1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6105	11	2822	5	10	NULL	NULL	NULL	U2AF	GP		bind					statement 2	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6106	12	2822	5	10	NULL	NULL	NULL	U2AF	GP		bind					statement 3	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6107	13	2822	5	10	NULL	NULL	NULL	statement 10	Process		is an alternative to					statement 11	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6108	14	2822	5	10	NULL	NULL	NULL	statement 10	Process		is an alternative to					statement 12	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6109	15	2822	5	10	NULL	NULL	NULL	statement 11	Process		is an alternative to					statement 12	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6235	1	2822	6	10	NULL	NULL	NULL			complete	contains				 127-nt enhancer 	pyrimidine tract	NucleicAcid	wild type			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6236	2	2822	6	10	NULL	NULL	NULL			complete	contains				127-nt enhancer	purine	NucleicAcid	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6237	3	2822	6	10	NULL	NULL	NULL			complete	contains				127-nt enhancer	U2AF	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6238	4	2822	6	10	NULL	NULL	NULL	U2AF	GP		bind					statement 1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6905	5	2822	6	10	NULL	NULL	NULL	U2AF	GP		bind					statement 2	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6906	6	2822	6	10	NULL	NULL	NULL	U2AF	GP		bind					statement 3	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6907	7	2822	6	10	NULL	NULL	NULL	PTB	GP		bind					statement 1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
46886	8	2822	6	10	NULL	NULL	NULL	PTB	GP		bind					statement 2	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
46887	9	2822	6	10	NULL	NULL	NULL	PTB	GP		bind					statement 3	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
53065	10	2822	6	10	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
53066	11	2822	6	10	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
53067	12	2822	6	10	NULL	NULL	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
53068	13	2822	6	10	NULL	NULL	NULL	statement 7	Process		is an alternative to					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
53069	14	2822	6	10	NULL	NULL	NULL	statement 7	Process		is an alternative to					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
53070	15	2822	6	10	NULL	NULL	NULL	statement 8	Process		is an alternative to					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_78_s_203	9858533	(A) Gel shift analysis of the binding of PTB (top) and U2AF (bottom) to the 127-nt complete enhancer containing the wild-type pyrimidine tract (wild type), purine mutation (purine), or U2AF mutation (U2AF).	bind
6110	1	2823	5	10	NULL	NULL	NULL	CcpA	GP		is in complex with					HPr	GP		Ser-P		NULL		NULL	NULL	NULL	NULL	gw70_applenvironmicrob_70_9_5244_s_188	15345406	(A) Gel shift assay showing the binding of the complex consisting of CcpA  and HPr-[Ser-P] to the  cre site.	bind
6111	2	2823	5	10	NULL	NULL	NULL	statement 1	Process		bind									cre site	NULL		NULL	NULL	NULL	NULL	gw70_applenvironmicrob_70_9_5244_s_188	15345406	(A) Gel shift assay showing the binding of the complex consisting of CcpA  and HPr-[Ser-P] to the  cre site.	bind
6240	1	2823	6	10	NULL	NULL	NULL	CcpA	GP		forms a complex with					HPr	GP		Ser-P		NULL		NULL	NULL	NULL	NULL	gw70_applenvironmicrob_70_9_5244_s_188	15345406	(A) Gel shift assay showing the binding of the complex consisting of CcpA  and HPr-[Ser-P] to the  cre site.	bind
6242	2	2823	6	10	NULL	NULL	NULL	statement 1	Process		bind									cre site	NULL		NULL	NULL	NULL	NULL	gw70_applenvironmicrob_70_9_5244_s_188	15345406	(A) Gel shift assay showing the binding of the complex consisting of CcpA  and HPr-[Ser-P] to the  cre site.	bind
6112	1	2824	5	10	NULL	NULL	NULL	TR	GP		bind					PGDS	GP			T3RE	NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_55_2_321_s_133	9582446	(A) Gel-shift assay showing the binding properties of TR to the PGDS-T3RE.	bind
6244	1	2824	6	10	NULL	NULL	NULL	TR	GP		bind					PGDS	GP			T3RE	NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_55_2_321_s_133	9582446	(A) Gel-shift assay showing the binding properties of TR to the PGDS-T3RE.	bind
6113	1	2825	5	10	NULL	NULL	NULL	Tem1	GP		bind					Bub2	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_172	14734533	(A) Gic1 disrupts the binding between Tem1 and Bub2.	bind
6115	2	2825	5	10	NULL	NULL	NULL	Gic1	GP		disrupt					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_172	14734533	(A) Gic1 disrupts the binding between Tem1 and Bub2.	bind
6245	1	2825	6	10	NULL	NULL	NULL	Tem1	GP		bind					Bub2	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_172	14734533	(A) Gic1 disrupts the binding between Tem1 and Bub2.	bind
6246	2	2825	6	10	NULL	NULL	NULL	Gic1	GP		disrupts					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_172	14734533	(A) Gic1 disrupts the binding between Tem1 and Bub2.	bind
6116	1	2826	5	10	NULL	NULL	NULL	GrB-OG	GP		bind					CI-MPR+ cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_491_s_84	11081635	(A) GrB-OG  binding to CI-MPR+ cells in the presence or absence of M6P or  D-mannose at different concentrations, or with 50 mM D-glucose or D-glucose-6 phosphate.	bind
6247	1	2826	6	10	NULL	NULL	NULL	GrB-OG	GP		bind					CI-MPR+ cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_491_s_84	11081635	(A) GrB-OG  binding to CI-MPR+ cells in the presence or absence of M6P or  D-mannose at different concentrations, or with 50 mM D-glucose or D-glucose-6 phosphate.	bind
6129	1	2828	5	10	NULL	NULL	NULL	ankyrin B	GP		bind					L1-CAM	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_6_2696_s_232	16597699	(A) Growth-factor inhibition of ankyrin B binding to L1-CAM is dependent  on activation of the MAPK pathway.	bind
6130	2	2828	5	10	NULL	NULL	NULL	growth-factor	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_6_2696_s_232	16597699	(A) Growth-factor inhibition of ankyrin B binding to L1-CAM is dependent  on activation of the MAPK pathway.	bind
6131	3	2828	5	10	NULL	NULL	NULL	statement 2	Process		is dependent on					MAPK pathway	Process	activation of 			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_6_2696_s_232	16597699	(A) Growth-factor inhibition of ankyrin B binding to L1-CAM is dependent  on activation of the MAPK pathway.	bind
6250	1	2828	6	10	NULL	NULL	NULL	ankyrin B	GP		bind					L1-CAM	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_6_2696_s_232	16597699	(A) Growth-factor inhibition of ankyrin B binding to L1-CAM is dependent  on activation of the MAPK pathway.	bind
6255	2	2828	6	10	NULL	NULL	NULL	growth factor	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_6_2696_s_232	16597699	(A) Growth-factor inhibition of ankyrin B binding to L1-CAM is dependent  on activation of the MAPK pathway.	bind
6256	3	2828	6	10	NULL	NULL	NULL	statement 2	Process		is dependent on					MAPK pathway	Process	activation of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_6_2696_s_232	16597699	(A) Growth-factor inhibition of ankyrin B binding to L1-CAM is dependent  on activation of the MAPK pathway.	bind
6134	1	2848	5	10	NULL	NULL	NULL	GST-p300	GP		bind					Cdk2	GP	from nuclear extracts			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_157	10330164	(A) GST-p300 binds Cdk2 from nuclear extracts.	bind
6258	1	2848	6	10	NULL	NULL	NULL	GST-p300	GP		bind					Cdk2	GP	nuclear extracts			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_157	10330164	(A) GST-p300 binds Cdk2 from nuclear extracts.	bind
6135	1	2851	5	10	NULL	NULL	NULL	ARF1t	GP	human	bind					coatomer	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_96_6_893_s_44	10102276	(A) GTP-dependent binding  of human ARF1t to coatomer.	bind
6136	2	2851	5	10	NULL	NULL	NULL	statement 1	Process		is dependent on					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_96_6_893_s_44	10102276	(A) GTP-dependent binding  of human ARF1t to coatomer.	bind
6259	1	2851	6	10	NULL	NULL	NULL	ARF1t	GP	human	bind					coatomer	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_96_6_893_s_44	10102276	(A) GTP-dependent binding  of human ARF1t to coatomer.	bind
6260	2	2851	6	10	NULL	NULL	NULL	statement 1	Process		is dependent on					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_96_6_893_s_44	10102276	(A) GTP-dependent binding  of human ARF1t to coatomer.	bind
6137	1	2852	5	10	NULL	NULL	NULL	DRIP205	GP		bind					PPARgamma-RXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_21_8008_s_134	11027271	(A) GW1929 titration of DRIP205 binding to PPARgamma-RXR.	bind
6261	1	2852	6	10	NULL	NULL	NULL	DRIP205	GP		bind					PPARgamma-RXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_21_8008_s_134	11027271	(A) GW1929 titration of DRIP205 binding to PPARgamma-RXR.	bind
6138	1	2853	5	10	NULL	NULL	NULL	H1	AminoAcid		bind					GDP-like (Taxol) microtubules	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5373_s_161	16120651	(A) H1 binds GDP-like (Taxol)  microtubules with a 0.67  plus-or-minus  0.08 muM affinity; (B) H1 binds GTP-like  (GMPCPP) microtubules with a 0.40  plus-or-minus  0.05 muM affinity; (C) H1 binds  GTP tubulin with a 0.26  plus-or-minus  0.04 muM affinity; (D) binding kinetics were  studied by adding tubulin (1 muM, blue); 2 muM, red; or 4 muM green) to labeled H1.	bind
6139	2	2853	5	10	NULL	NULL	NULL	H1	AminoAcid		bind					GTP-like (GMPCPP) microtubules	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5373_s_161	16120651	(A) H1 binds GDP-like (Taxol)  microtubules with a 0.67  plus-or-minus  0.08 muM affinity; (B) H1 binds GTP-like  (GMPCPP) microtubules with a 0.40  plus-or-minus  0.05 muM affinity; (C) H1 binds  GTP tubulin with a 0.26  plus-or-minus  0.04 muM affinity; (D) binding kinetics were  studied by adding tubulin (1 muM, blue); 2 muM, red; or 4 muM green) to labeled H1.	bind
6140	3	2853	5	10	NULL	NULL	NULL	H1	AminoAcid		bind					GTP tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5373_s_161	16120651	(A) H1 binds GDP-like (Taxol)  microtubules with a 0.67  plus-or-minus  0.08 muM affinity; (B) H1 binds GTP-like  (GMPCPP) microtubules with a 0.40  plus-or-minus  0.05 muM affinity; (C) H1 binds  GTP tubulin with a 0.26  plus-or-minus  0.04 muM affinity; (D) binding kinetics were  studied by adding tubulin (1 muM, blue); 2 muM, red; or 4 muM green) to labeled H1.	bind
6262	1	2853	6	10	NULL	NULL	NULL	H1	AminoAcid		bind					GDP-like (Taxol) microtubules	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5373_s_161	16120651	(A) H1 binds GDP-like (Taxol)  microtubules with a 0.67  plus-or-minus  0.08 muM affinity; (B) H1 binds GTP-like  (GMPCPP) microtubules with a 0.40  plus-or-minus  0.05 muM affinity; (C) H1 binds  GTP tubulin with a 0.26  plus-or-minus  0.04 muM affinity; (D) binding kinetics were  studied by adding tubulin (1 muM, blue); 2 muM, red; or 4 muM green) to labeled H1.	bind
6263	2	2853	6	10	NULL	NULL	NULL	H1	AminoAcid		bind					GTP-like (GMPCPP) microtubules	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5373_s_161	16120651	(A) H1 binds GDP-like (Taxol)  microtubules with a 0.67  plus-or-minus  0.08 muM affinity; (B) H1 binds GTP-like  (GMPCPP) microtubules with a 0.40  plus-or-minus  0.05 muM affinity; (C) H1 binds  GTP tubulin with a 0.26  plus-or-minus  0.04 muM affinity; (D) binding kinetics were  studied by adding tubulin (1 muM, blue); 2 muM, red; or 4 muM green) to labeled H1.	bind
6264	3	2853	6	10	NULL	NULL	NULL	H1	AminoAcid		bind					GTP tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5373_s_161	16120651	(A) H1 binds GDP-like (Taxol)  microtubules with a 0.67  plus-or-minus  0.08 muM affinity; (B) H1 binds GTP-like  (GMPCPP) microtubules with a 0.40  plus-or-minus  0.05 muM affinity; (C) H1 binds  GTP tubulin with a 0.26  plus-or-minus  0.04 muM affinity; (D) binding kinetics were  studied by adding tubulin (1 muM, blue); 2 muM, red; or 4 muM green) to labeled H1.	bind
6141	1	2855	5	10	NULL	NULL	NULL	Nup53	GP		bind					FG-nups	GP	subset of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2382_s_157	15703211	(A) HeLa cells were processed for immunofluorescence  microscopy and probed with affinity-purified rabbit antibodies directed against a  putative vertebrate counterpart of Nup53 and a mouse mAb (mAb414) that binds a subset  of FG-nups.	bind
6142	2	2855	5	10	NULL	NULL	NULL	mAb414	GP	mouse	bind					FG-nups	GP	subset of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2382_s_157	15703211	(A) HeLa cells were processed for immunofluorescence  microscopy and probed with affinity-purified rabbit antibodies directed against a  putative vertebrate counterpart of Nup53 and a mouse mAb (mAb414) that binds a subset  of FG-nups.	bind
6265	1	2855	6	10	NULL	NULL	NULL	mAb414	GP	mouse	bind					FG-nups	GP	subset of 			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2382_s_157	15703211	(A) HeLa cells were processed for immunofluorescence  microscopy and probed with affinity-purified rabbit antibodies directed against a  putative vertebrate counterpart of Nup53 and a mouse mAb (mAb414) that binds a subset  of FG-nups.	bind
46521	2	2855	6	10	NULL	NULL	NULL	Nup53	GP		bind					FG-nups	GP	subset of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2382_s_157	15703211	(A) HeLa cells were processed for immunofluorescence  microscopy and probed with affinity-purified rabbit antibodies directed against a  putative vertebrate counterpart of Nup53 and a mouse mAb (mAb414) that binds a subset  of FG-nups.	bind
6143	1	2858	5	10	NULL	NULL	NULL	CBP	GP		bind		high affinity			p65	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_277_s_139	9659924	(A) High-affinity binding of CBP with p65 requires the synergism-specific domain.	bind
6144	2	2858	5	10	NULL	NULL	NULL	statement 1	Process		require								synergism-specific domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_277_s_139	9659924	(A) High-affinity binding of CBP with p65 requires the synergism-specific domain.	bind
6291	1	2858	6	10	NULL	NULL	NULL	CBP	GP		bind					p65	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_277_s_139	9659924	(A) High-affinity binding of CBP with p65 requires the synergism-specific domain.	bind
7277	2	2858	6	10	NULL	NULL	NULL	statement 1	Process		require								synergism-specific domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_277_s_139	9659924	(A) High-affinity binding of CBP with p65 requires the synergism-specific domain.	bind
6145	1	2859	5	10	NULL	NULL	NULL	His6NSF	GP		bind					GST-GluR2	GP		C terminus		NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_51	11931741	(A) His6NSF binding to GST-GluR2 C terminus (R2C) is sensitive to ATP hydrolysis.	bind
6146	2	2859	5	10	NULL	NULL	NULL	statement 1	Process		is sensitive to					ATP 	Chemical	hydrolysis of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_51	11931741	(A) His6NSF binding to GST-GluR2 C terminus (R2C) is sensitive to ATP hydrolysis.	bind
46522	3	2859	5	10	NULL	NULL	NULL	R2C	GP		is					GST-GluR2	GP		C terminus		NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_51	11931741	(A) His6NSF binding to GST-GluR2 C terminus (R2C) is sensitive to ATP hydrolysis.	bind
6300	1	2859	6	10	NULL	NULL	NULL	His6NSF	GP		bind					GST-GluR2	GP		 C terminus		NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_51	11931741	(A) His6NSF binding to GST-GluR2 C terminus (R2C) is sensitive to ATP hydrolysis.	bind
6302	2	2859	6	10	NULL	NULL	NULL	statement 1	Process		is sensitive to 					ATP	Chemical	hydrolysis of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_51	11931741	(A) His6NSF binding to GST-GluR2 C terminus (R2C) is sensitive to ATP hydrolysis.	bind
46524	3	2859	6	10	NULL	NULL	NULL	R2C	GP		is					GST-GluR2	GP		C terminus		NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_51	11931741	(A) His6NSF binding to GST-GluR2 C terminus (R2C) is sensitive to ATP hydrolysis.	bind
6147	1	2860	5	10	NULL	NULL	NULL	FW	Chemical		bind					AMPA receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_133_7_1055_s_105	11487516	(A) Histogram showing the concentration curve for AChE enhancement of [3]-FW binding to AMPA receptors solubilized with 1% octylglucopyranoside There was a significant increase ( P<0.01, non paired Student's  t-test) in binding to AChE-treated solubilized compared to solubilized control samples.	bind
6148	2	2860	5	10	NULL	NULL	NULL	AChE	GP		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_133_7_1055_s_105	11487516	(A) Histogram showing the concentration curve for AChE enhancement of [3]-FW binding to AMPA receptors solubilized with 1% octylglucopyranoside There was a significant increase ( P<0.01, non paired Student's  t-test) in binding to AChE-treated solubilized compared to solubilized control samples.	bind
6303	1	2860	6	10	NULL	NULL	NULL	FW	Chemical		bind					AMPA receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_133_7_1055_s_105	11487516	(A) Histogram showing the concentration curve for AChE enhancement of [3]-FW binding to AMPA receptors solubilized with 1% octylglucopyranoside There was a significant increase ( P<0.01, non paired Student's  t-test) in binding to AChE-treated solubilized compared to solubilized control samples.	bind
6304	2	2860	6	10	NULL	NULL	NULL	AChE	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_133_7_1055_s_105	11487516	(A) Histogram showing the concentration curve for AChE enhancement of [3]-FW binding to AMPA receptors solubilized with 1% octylglucopyranoside There was a significant increase ( P<0.01, non paired Student's  t-test) in binding to AChE-treated solubilized compared to solubilized control samples.	bind
6149	1	2861	5	10	NULL	NULL	NULL	Gpa2p	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6110_s_284	10454558	(A) Histone H1 phosphorylation was assayed with GST-Ime2p purified from  E. coli and [gamma-32]ATP in the presence of BSA (lane 2), Gpa2p bound to GDP (lane 3), or Gpa2p bound to GTPgammaS (lane 4), washed free of unbound guanine nucleotides.	bind
6150	2	2861	5	10	NULL	NULL	NULL	Gpa2p	GP		bind					GTPgammaS	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6110_s_284	10454558	(A) Histone H1 phosphorylation was assayed with GST-Ime2p purified from  E. coli and [gamma-32]ATP in the presence of BSA (lane 2), Gpa2p bound to GDP (lane 3), or Gpa2p bound to GTPgammaS (lane 4), washed free of unbound guanine nucleotides.	bind
6312	1	2861	6	10	NULL	NULL	NULL	Gpa2p	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6110_s_284	10454558	(A) Histone H1 phosphorylation was assayed with GST-Ime2p purified from  E. coli and [gamma-32]ATP in the presence of BSA (lane 2), Gpa2p bound to GDP (lane 3), or Gpa2p bound to GTPgammaS (lane 4), washed free of unbound guanine nucleotides.	bind
6314	2	2861	6	10	NULL	NULL	NULL	Gpa2p	GP		bind					GTPgammaS	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6110_s_284	10454558	(A) Histone H1 phosphorylation was assayed with GST-Ime2p purified from  E. coli and [gamma-32]ATP in the presence of BSA (lane 2), Gpa2p bound to GDP (lane 3), or Gpa2p bound to GTPgammaS (lane 4), washed free of unbound guanine nucleotides.	bind
6151	1	2862	5	10	NULL	NULL	NULL	HMG-1	GP		bind					Z-3	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_186	10825199	(A) HMG-1 and ZEBRA bind cooperatively to Z-3 and Z-4.	bind
6152	2	2862	5	10	NULL	NULL	NULL	ZEBRA	GP		bind					Z-3	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_186	10825199	(A) HMG-1 and ZEBRA bind cooperatively to Z-3 and Z-4.	bind
6153	3	2862	5	10	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_186	10825199	(A) HMG-1 and ZEBRA bind cooperatively to Z-3 and Z-4.	bind
6154	4	2862	5	10	NULL	NULL	NULL	HMG-1	GP		bind					Z-4	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_186	10825199	(A) HMG-1 and ZEBRA bind cooperatively to Z-3 and Z-4.	bind
6155	5	2862	5	10	NULL	NULL	NULL	ZEBRA	GP		bind					Z-4	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_186	10825199	(A) HMG-1 and ZEBRA bind cooperatively to Z-3 and Z-4.	bind
6156	6	2862	5	10	NULL	NULL	NULL	statement 4	Process		occurs in cooperation with					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_186	10825199	(A) HMG-1 and ZEBRA bind cooperatively to Z-3 and Z-4.	bind
6417	1	2862	6	10	NULL	NULL	NULL	HMG-1	GP		bind					Z-3	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_186	10825199	(A) HMG-1 and ZEBRA bind cooperatively to Z-3 and Z-4.	bind
6418	2	2862	6	10	NULL	NULL	NULL	HMG-1	GP		bind					Z-4	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_186	10825199	(A) HMG-1 and ZEBRA bind cooperatively to Z-3 and Z-4.	bind
6419	3	2862	6	10	NULL	NULL	NULL	ZEBRA	GP		bind					Z-3	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_186	10825199	(A) HMG-1 and ZEBRA bind cooperatively to Z-3 and Z-4.	bind
6420	4	2862	6	10	NULL	NULL	NULL	ZEBRA	GP		bind					Z-4	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_186	10825199	(A) HMG-1 and ZEBRA bind cooperatively to Z-3 and Z-4.	bind
46525	5	2862	6	10	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_186	10825199	(A) HMG-1 and ZEBRA bind cooperatively to Z-3 and Z-4.	bind
46526	6	2862	6	10	NULL	NULL	NULL	statement 2	Process		occurs in cooperation with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_186	10825199	(A) HMG-1 and ZEBRA bind cooperatively to Z-3 and Z-4.	bind
6157	2	2863	5	10	NULL	NULL	NULL	HSF	GP		bind					statement 1	Process				NULL	polytene chromosomes of wild-type larvae	NULL	NULL	NULL	NULL	gw70_cellbiol_161_4_707_s_127	12756231	(A) HSF and (B) POLII binding heat shock -  induced puffs in polytene chromosomes  of wild-type larvae.	bind
6158	3	2863	5	10	NULL	NULL	NULL	POLII	GP		bind					statement 1	Process				NULL	polytene chromosomes of wild-type larvae	NULL	NULL	NULL	NULL	gw70_cellbiol_161_4_707_s_127	12756231	(A) HSF and (B) POLII binding heat shock -  induced puffs in polytene chromosomes  of wild-type larvae.	bind
46527	1	2863	5	10	NULL	NULL	NULL	heat shock			induce					puffs	Chromosome				NULL	 polytene chromosomes of wild-type larvae	NULL	NULL	NULL	NULL	gw70_cellbiol_161_4_707_s_127	12756231	(A) HSF and (B) POLII binding heat shock -  induced puffs in polytene chromosomes  of wild-type larvae.	bind
6421	1	2863	6	10	NULL	NULL	NULL	heat shock			induces					puffs	Chromosome				NULL	in polytene chromosomes of wild-type larvae	NULL	NULL	NULL	NULL	gw70_cellbiol_161_4_707_s_127	12756231	(A) HSF and (B) POLII binding heat shock -  induced puffs in polytene chromosomes  of wild-type larvae.	bind
6422	2	2863	6	10	NULL	NULL	NULL	HSF	GP		bind					statement 1	Process				NULL	in polytene chromosomes of wild-type larvae	NULL	NULL	NULL	NULL	gw70_cellbiol_161_4_707_s_127	12756231	(A) HSF and (B) POLII binding heat shock -  induced puffs in polytene chromosomes  of wild-type larvae.	bind
6423	3	2863	6	10	NULL	NULL	NULL	POLII	GP		bind					statement 1	Process				NULL	in polytene chromosomes of wild-type larvae	NULL	NULL	NULL	NULL	gw70_cellbiol_161_4_707_s_127	12756231	(A) HSF and (B) POLII binding heat shock -  induced puffs in polytene chromosomes  of wild-type larvae.	bind
6159	1	2864	5	10	NULL	NULL	NULL	Hsp70	GP		bind					DC	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_3_353_s_33	12354387	(A) Hsp70 binds to human DC by a mechanism with the characteristics of a saturable receptor system.	bind
6160	2	2864	5	10	NULL	NULL	NULL	statement 1	Process		involves					saturable receptor system	GP	mechanism of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_3_353_s_33	12354387	(A) Hsp70 binds to human DC by a mechanism with the characteristics of a saturable receptor system.	bind
6424	1	2864	6	10	NULL	NULL	NULL	Hsp70	GP		bind					DC	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_3_353_s_33	12354387	(A) Hsp70 binds to human DC by a mechanism with the characteristics of a saturable receptor system.	bind
53071	2	2864	6	10	NULL	NULL	NULL	statement 1	Process		involves					 saturable receptor system	GP	mechanism of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_3_353_s_33	12354387	(A) Hsp70 binds to human DC by a mechanism with the characteristics of a saturable receptor system.	bind
6161	1	2865	5	10	NULL	NULL	NULL	hTR	GP		bind					hTERT	GP	mutant	E-region		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6234_s_200	12167716	(A) hTR binding to hTERT E-region mutants.	bind
6425	1	2865	6	10	NULL	NULL	NULL	hTR	GP		bind					hTERT	GP	mutant	E-region		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6234_s_200	12167716	(A) hTR binding to hTERT E-region mutants.	bind
6173	1	2869	5	10	NULL	NULL	NULL	MyoD	GP		bind		sequence specific			MEF-1 oligodeoxynucleotide	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_307	11940648	(A) Id2, Id1, and Id3 inhibit the sequence-specific binding of MyoD to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition, as determined by EMSA.	bind
6174	2	2869	5	10	NULL	NULL	NULL	Id2	GP		inhibit					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_307	11940648	(A) Id2, Id1, and Id3 inhibit the sequence-specific binding of MyoD to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition, as determined by EMSA.	bind
6175	3	2869	5	10	NULL	NULL	NULL	Id1	GP		inhibit					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_307	11940648	(A) Id2, Id1, and Id3 inhibit the sequence-specific binding of MyoD to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition, as determined by EMSA.	bind
6176	4	2869	5	10	NULL	NULL	NULL	Id3	GP		inhibit					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_307	11940648	(A) Id2, Id1, and Id3 inhibit the sequence-specific binding of MyoD to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition, as determined by EMSA.	bind
6177	5	2869	5	10	NULL	NULL	NULL	p204	GP		overcomes					statement 2	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_307	11940648	(A) Id2, Id1, and Id3 inhibit the sequence-specific binding of MyoD to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition, as determined by EMSA.	bind
6178	6	2869	5	10	NULL	NULL	NULL	p204	GP		overcomes					statement 3	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_307	11940648	(A) Id2, Id1, and Id3 inhibit the sequence-specific binding of MyoD to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition, as determined by EMSA.	bind
6179	7	2869	5	10	NULL	NULL	NULL	p204	GP		overcomes					statement 4	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_307	11940648	(A) Id2, Id1, and Id3 inhibit the sequence-specific binding of MyoD to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition, as determined by EMSA.	bind
6432	1	2869	6	10	NULL	NULL	NULL	MyoD	GP		bind					MEF-1 oligodeoxynucleotide	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_307	11940648	(A) Id2, Id1, and Id3 inhibit the sequence-specific binding of MyoD to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition, as determined by EMSA.	bind
6433	2	2869	6	10	NULL	NULL	NULL	Id1	GP		inhibit					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_307	11940648	(A) Id2, Id1, and Id3 inhibit the sequence-specific binding of MyoD to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition, as determined by EMSA.	bind
6434	3	2869	6	10	NULL	NULL	NULL	Id2	GP		inhibit					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_307	11940648	(A) Id2, Id1, and Id3 inhibit the sequence-specific binding of MyoD to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition, as determined by EMSA.	bind
6435	4	2869	6	10	NULL	NULL	NULL	Id3	GP		inhibit					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_307	11940648	(A) Id2, Id1, and Id3 inhibit the sequence-specific binding of MyoD to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition, as determined by EMSA.	bind
6436	5	2869	6	10	NULL	NULL	NULL	p204	GP		overcomes					statement 2	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_307	11940648	(A) Id2, Id1, and Id3 inhibit the sequence-specific binding of MyoD to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition, as determined by EMSA.	bind
6437	6	2869	6	10	NULL	NULL	NULL	p204	GP		overcomes					statement 3	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_307	11940648	(A) Id2, Id1, and Id3 inhibit the sequence-specific binding of MyoD to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition, as determined by EMSA.	bind
6438	7	2869	6	10	NULL	NULL	NULL	p204	GP		overcomes					statement 4	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_307	11940648	(A) Id2, Id1, and Id3 inhibit the sequence-specific binding of MyoD to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition, as determined by EMSA.	bind
6180	1	2870	5	10	NULL	NULL	NULL	IE2 protein	GP		does not bind					il1b	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_6803_s_328	10490619	(a) IE2 protein does not bind to the  il1b promoter.	bind
6439	1	2870	6	10	NULL	NULL	NULL	IE2 protein	GP		does not bind					il1b	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_6803_s_328	10490619	(a) IE2 protein does not bind to the  il1b promoter.	bind
6181	1	2872	5	10	NULL	NULL	NULL	preS2 peptide	AminoAcid		bind			120-132		r-HBsAg	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_febslett_441_3_407_s_144	9891981	(A) IgG and (B) scFv to r-HBsAg binding by preS2 peptides 120-132, 120-145 and 148-174.	bind
6182	2	2872	5	10	NULL	NULL	NULL	preS2 peptide	AminoAcid		bind			120-145		r-HBsAg	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_febslett_441_3_407_s_144	9891981	(A) IgG and (B) scFv to r-HBsAg binding by preS2 peptides 120-132, 120-145 and 148-174.	bind
6183	3	2872	5	10	NULL	NULL	NULL	preS2 peptide	AminoAcid		bind			148-174		r-HBsAg	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_febslett_441_3_407_s_144	9891981	(A) IgG and (B) scFv to r-HBsAg binding by preS2 peptides 120-132, 120-145 and 148-174.	bind
6962	1	2872	6	10	NULL	NULL	NULL	preS2 peptides	AminoAcid		bind			120-132		 r-HBsAg	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_febslett_441_3_407_s_144	9891981	(A) IgG and (B) scFv to r-HBsAg binding by preS2 peptides 120-132, 120-145 and 148-174.	bind
6963	2	2872	6	10	NULL	NULL	NULL	preS2 peptides 	AminoAcid		bind			120-145		 r-HBsAg	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_febslett_441_3_407_s_144	9891981	(A) IgG and (B) scFv to r-HBsAg binding by preS2 peptides 120-132, 120-145 and 148-174.	bind
46707	3	2872	6	10	NULL	NULL	NULL	preS2 peptides	AminoAcid		bind			148-174		r-HBsAg	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_febslett_441_3_407_s_144	9891981	(A) IgG and (B) scFv to r-HBsAg binding by preS2 peptides 120-132, 120-145 and 148-174.	bind
6184	1	2873	5	10	NULL	NULL	NULL	MT	CellComponent		bind					His6-CLASP2	GP	bacterially expressed	340 - 1084		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_169_6_929_s_184	15955847	(A) Immunoblot of a MT sedimentation assay of bacterially expressed His6-CLASP2(340  - 1084) at constant concentration incubated with increasing concentrations of MTs.  Note the slightly smaller degradation product ( 70 kD), which does not bind to MTs. (B) Comparison of MT binding of His6-CLASP2(340  - 1084) and His6-CLASP2(340 - 875).	bind
6185	2	2873	5	10	NULL	NULL	NULL	MT	CellComponent		bind					His6-CLASP2	GP	bacterially expressed	340 - 875		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_169_6_929_s_184	15955847	(A) Immunoblot of a MT sedimentation assay of bacterially expressed His6-CLASP2(340  - 1084) at constant concentration incubated with increasing concentrations of MTs.  Note the slightly smaller degradation product ( 70 kD), which does not bind to MTs. (B) Comparison of MT binding of His6-CLASP2(340  - 1084) and His6-CLASP2(340 - 875).	bind
6186	3	2873	5	10	NULL	NULL	NULL	70 kD degradation product	GP		does not bind					MT	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_169_6_929_s_184	15955847	(A) Immunoblot of a MT sedimentation assay of bacterially expressed His6-CLASP2(340  - 1084) at constant concentration incubated with increasing concentrations of MTs.  Note the slightly smaller degradation product ( 70 kD), which does not bind to MTs. (B) Comparison of MT binding of His6-CLASP2(340  - 1084) and His6-CLASP2(340 - 875).	bind
6440	1	2873	6	10	NULL	NULL	NULL	His6-CLASP2	GP	bacterially expressed	bind			340-1084		MT	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_169_6_929_s_184	15955847	(A) Immunoblot of a MT sedimentation assay of bacterially expressed His6-CLASP2(340  - 1084) at constant concentration incubated with increasing concentrations of MTs.  Note the slightly smaller degradation product ( 70 kD), which does not bind to MTs. (B) Comparison of MT binding of His6-CLASP2(340  - 1084) and His6-CLASP2(340 - 875).	bind
6441	2	2873	6	10	NULL	NULL	NULL	His6-CLASP2	GP	bacterially expressed	bind			340-875		MT	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_169_6_929_s_184	15955847	(A) Immunoblot of a MT sedimentation assay of bacterially expressed His6-CLASP2(340  - 1084) at constant concentration incubated with increasing concentrations of MTs.  Note the slightly smaller degradation product ( 70 kD), which does not bind to MTs. (B) Comparison of MT binding of His6-CLASP2(340  - 1084) and His6-CLASP2(340 - 875).	bind
46528	3	2873	6	10	NULL	NULL	NULL	70 kD degradation product	GP		does not bind					MT	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_169_6_929_s_184	15955847	(A) Immunoblot of a MT sedimentation assay of bacterially expressed His6-CLASP2(340  - 1084) at constant concentration incubated with increasing concentrations of MTs.  Note the slightly smaller degradation product ( 70 kD), which does not bind to MTs. (B) Comparison of MT binding of His6-CLASP2(340  - 1084) and His6-CLASP2(340 - 875).	bind
6187	1	2874	5	10	NULL	NULL	NULL	proteins	GP	rat brain deoxycholate extracts 	bind					microcystin-LR	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4690_s_234	12052877	(A) Immunoblots of proteins from rat brain deoxycholate extracts (input) bound to microcystin-LR-Sepharose.	bind
6442	1	2874	6	10	NULL	NULL	NULL	 protein	GP	rat brain deoxycholate extracts	bind					microcystin-LR	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4690_s_234	12052877	(A) Immunoblots of proteins from rat brain deoxycholate extracts (input) bound to microcystin-LR-Sepharose.	bind
6188	1	2875	5	10	NULL	NULL	NULL	Smad2	GP		bind					tubulin	GP				NULL	wild type Mv1Lu cells	NULL	NULL	NULL	NULL	gw60_molcell_5_1_27_s_51	10678166	(A) Immunoprecipitation of Mv1Lu cell lysates by an anti-tubulin antibody followed by Western blotting with a polyclonal anti-Smad2 antibody confirms the binding of Smad2 to tubulin in wild type and mutant Mv1Lu cells.	bind
6189	2	2875	5	10	NULL	NULL	NULL	Smad2	GP		bind					tubulin	GP				NULL	mutant Mv1Lu cells	NULL	NULL	NULL	NULL	gw60_molcell_5_1_27_s_51	10678166	(A) Immunoprecipitation of Mv1Lu cell lysates by an anti-tubulin antibody followed by Western blotting with a polyclonal anti-Smad2 antibody confirms the binding of Smad2 to tubulin in wild type and mutant Mv1Lu cells.	bind
6573	1	2875	6	10	NULL	NULL	NULL	Smad2	GP		bind					tubulin	GP				NULL	wild type Mv1Lu cells	NULL	NULL	NULL	NULL	gw60_molcell_5_1_27_s_51	10678166	(A) Immunoprecipitation of Mv1Lu cell lysates by an anti-tubulin antibody followed by Western blotting with a polyclonal anti-Smad2 antibody confirms the binding of Smad2 to tubulin in wild type and mutant Mv1Lu cells.	bind
6574	2	2875	6	10	NULL	NULL	NULL	Smad2	GP		bind					tubulin	GP				NULL	mutant Mv1Lu cells	NULL	NULL	NULL	NULL	gw60_molcell_5_1_27_s_51	10678166	(A) Immunoprecipitation of Mv1Lu cell lysates by an anti-tubulin antibody followed by Western blotting with a polyclonal anti-Smad2 antibody confirms the binding of Smad2 to tubulin in wild type and mutant Mv1Lu cells.	bind
6190	1	2878	5	10	NULL	NULL	NULL	Bcr	GP	constitutively active	phosphorylate					AF-6	GP				NULL	quiescent cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4663_s_318	12808105	(A) In quiescent cells the constitutively active Bcr phosphorylates  AF-6 (step 1), which leads to the interaction of the PDZ domain of AF-6 with the  PDZ-binding motif of Bcr (step 2).	bind
6191	2	2878	5	10	NULL	NULL	NULL	AF-6	GP		bind			PDZ domain		Bcr	GP		PDZ-binding motif		NULL	quiescent cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4663_s_318	12808105	(A) In quiescent cells the constitutively active Bcr phosphorylates  AF-6 (step 1), which leads to the interaction of the PDZ domain of AF-6 with the  PDZ-binding motif of Bcr (step 2).	bind
6192	3	2878	5	10	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4663_s_318	12808105	(A) In quiescent cells the constitutively active Bcr phosphorylates  AF-6 (step 1), which leads to the interaction of the PDZ domain of AF-6 with the  PDZ-binding motif of Bcr (step 2).	bind
6577	1	2878	6	10	NULL	NULL	NULL	Bcr	GP	constitutively active	phosphorylates					AF-6	GP				NULL	quiescent cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4663_s_318	12808105	(A) In quiescent cells the constitutively active Bcr phosphorylates  AF-6 (step 1), which leads to the interaction of the PDZ domain of AF-6 with the  PDZ-binding motif of Bcr (step 2).	bind
6580	2	2878	6	10	NULL	NULL	NULL	AF-6	GP		bind			PDZ domain		Bcr	GP		PDZ binding motif		NULL	quiescent cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4663_s_318	12808105	(A) In quiescent cells the constitutively active Bcr phosphorylates  AF-6 (step 1), which leads to the interaction of the PDZ domain of AF-6 with the  PDZ-binding motif of Bcr (step 2).	bind
6581	3	2878	6	10	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4663_s_318	12808105	(A) In quiescent cells the constitutively active Bcr phosphorylates  AF-6 (step 1), which leads to the interaction of the PDZ domain of AF-6 with the  PDZ-binding motif of Bcr (step 2).	bind
6193	1	2880	5	10	NULL	NULL	NULL	ephexin	GP		bind		stably			EphA receptors	GP				NULL	membrane	NULL	NULL	NULL	NULL	gw60_cell_105_2_233_s_270	11336673	(A) In regions of the growth cone  not in contact with ephrin-A, ephexin is stably  bound to EphA receptors at the membrane, where  ephexin contributes to the activation of RhoA, Cdc42, and  Rac1.	bind
6194	2	2880	5	10	NULL	NULL	NULL	ephexin	GP		contribute to					RhoA	GP	activation of			NULL	membrane	NULL	NULL	NULL	NULL	gw60_cell_105_2_233_s_270	11336673	(A) In regions of the growth cone  not in contact with ephrin-A, ephexin is stably  bound to EphA receptors at the membrane, where  ephexin contributes to the activation of RhoA, Cdc42, and  Rac1.	bind
6195	3	2880	5	10	NULL	NULL	NULL	ephexin	GP		contribute to					Cdc42	GP	activation of			NULL	membrane	NULL	NULL	NULL	NULL	gw60_cell_105_2_233_s_270	11336673	(A) In regions of the growth cone  not in contact with ephrin-A, ephexin is stably  bound to EphA receptors at the membrane, where  ephexin contributes to the activation of RhoA, Cdc42, and  Rac1.	bind
6196	4	2880	5	10	NULL	NULL	NULL	ephexin	GP		contribute to					Rac1	GP	activation of			NULL	membrane	NULL	NULL	NULL	NULL	gw60_cell_105_2_233_s_270	11336673	(A) In regions of the growth cone  not in contact with ephrin-A, ephexin is stably  bound to EphA receptors at the membrane, where  ephexin contributes to the activation of RhoA, Cdc42, and  Rac1.	bind
6583	1	2880	6	10	NULL	NULL	NULL	ephexin	GP		bind		stably			EphA receptors	GP				NULL	membrane	NULL	NULL	NULL	NULL	gw60_cell_105_2_233_s_270	11336673	(A) In regions of the growth cone  not in contact with ephrin-A, ephexin is stably  bound to EphA receptors at the membrane, where  ephexin contributes to the activation of RhoA, Cdc42, and  Rac1.	bind
6584	2	2880	6	10	NULL	NULL	NULL	ephexin	GP		contributes to					RhoA	GP	activation of			NULL	membrane	NULL	NULL	NULL	NULL	gw60_cell_105_2_233_s_270	11336673	(A) In regions of the growth cone  not in contact with ephrin-A, ephexin is stably  bound to EphA receptors at the membrane, where  ephexin contributes to the activation of RhoA, Cdc42, and  Rac1.	bind
6585	3	2880	6	10	NULL	NULL	NULL	ephexin	GP		contributes to					Cdc42	GP	activation of			NULL	membrane	NULL	NULL	NULL	NULL	gw60_cell_105_2_233_s_270	11336673	(A) In regions of the growth cone  not in contact with ephrin-A, ephexin is stably  bound to EphA receptors at the membrane, where  ephexin contributes to the activation of RhoA, Cdc42, and  Rac1.	bind
6588	4	2880	6	10	NULL	NULL	NULL	ephexin	GP		contributes to					Rac1	GP	activation of			NULL	membrane	NULL	NULL	NULL	NULL	gw60_cell_105_2_233_s_270	11336673	(A) In regions of the growth cone  not in contact with ephrin-A, ephexin is stably  bound to EphA receptors at the membrane, where  ephexin contributes to the activation of RhoA, Cdc42, and  Rac1.	bind
53072	1	2881	5	10	NULL	NULL	NULL				bind			Galpha subunit 		GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_3_495_s_33	15755912	(A) In the absence of an extracellular  ligand, the G protein is present as an inactive heterotrimer (Galpha is in green, Gbeta is in blue, and Ggamma is in red), with the Galpha subunit bound to GDP.	bind
53073	2	2881	5	10	NULL	NULL	NULL	G protein	GP		present as					heterotrimer		inactive			NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_3_495_s_33	15755912	(A) In the absence of an extracellular  ligand, the G protein is present as an inactive heterotrimer (Galpha is in green, Gbeta is in blue, and Ggamma is in red), with the Galpha subunit bound to GDP.	bind
53074	3	2881	5	10	NULL	NULL	NULL	statement 2	Process		in absence of					extracellular ligand	GP				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_3_495_s_33	15755912	(A) In the absence of an extracellular  ligand, the G protein is present as an inactive heterotrimer (Galpha is in green, Gbeta is in blue, and Ggamma is in red), with the Galpha subunit bound to GDP.	bind
6590	1	2881	6	10	NULL	NULL	NULL				bind			Galpha subunit		GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_3_495_s_33	15755912	(A) In the absence of an extracellular  ligand, the G protein is present as an inactive heterotrimer (Galpha is in green, Gbeta is in blue, and Ggamma is in red), with the Galpha subunit bound to GDP.	bind
6593	2	2881	6	10	NULL	NULL	NULL	G protein	GP		present as an					heterotrimer		inactive			NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_3_495_s_33	15755912	(A) In the absence of an extracellular  ligand, the G protein is present as an inactive heterotrimer (Galpha is in green, Gbeta is in blue, and Ggamma is in red), with the Galpha subunit bound to GDP.	bind
6594	3	2881	6	10	NULL	NULL	NULL	statement 2	Process		occurs in absence of					extracellular ligand	GP				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_3_495_s_33	15755912	(A) In the absence of an extracellular  ligand, the G protein is present as an inactive heterotrimer (Galpha is in green, Gbeta is in blue, and Ggamma is in red), with the Galpha subunit bound to GDP.	bind
6197	1	2882	5	10	NULL	NULL	NULL	CBP	GP		bind					CIITA	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_941_s_235	9858618	(A) In the absence of dexamethasone, CBP binds to CIITA.	bind
6198	2	2882	5	10	NULL	NULL	NULL	statement 1	Process		in the absence of					dexamethasone	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_941_s_235	9858618	(A) In the absence of dexamethasone, CBP binds to CIITA.	bind
6595	1	2882	6	10	NULL	NULL	NULL	CBP	GP		bind					CIITA	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_941_s_235	9858618	(A) In the absence of dexamethasone, CBP binds to CIITA.	bind
6596	2	2882	6	10	NULL	NULL	NULL	statement 1	Process		occurs in absence of					dexamethasone	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_941_s_235	9858618	(A) In the absence of dexamethasone, CBP binds to CIITA.	bind
6201	1	2883	5	10	NULL	NULL	NULL	Akt1	GP		bind					JIP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_35_4_697_s_278	12194869	(A) In the basal state, Akt1 binds JIP1, preventing formation of JIP1-mediated, proapoptotic JNK complexes.	bind
6202	2	2883	5	10	NULL	NULL	NULL	JIP1	GP		mediate					proapoptotic JNK complexes	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_35_4_697_s_278	12194869	(A) In the basal state, Akt1 binds JIP1, preventing formation of JIP1-mediated, proapoptotic JNK complexes.	bind
6203	3	2883	5	10	NULL	NULL	NULL	statement 1	Process		prevent					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_35_4_697_s_278	12194869	(A) In the basal state, Akt1 binds JIP1, preventing formation of JIP1-mediated, proapoptotic JNK complexes.	bind
46529	4	2883	5	10	NULL	NULL	NULL	statement 1	Process		occurs in					basal state					NULL		NULL	NULL	NULL	NULL	gw60_neuron_35_4_697_s_278	12194869	(A) In the basal state, Akt1 binds JIP1, preventing formation of JIP1-mediated, proapoptotic JNK complexes.	bind
6598	1	2883	6	10	NULL	NULL	NULL	Akt1	GP		bind					JIP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_35_4_697_s_278	12194869	(A) In the basal state, Akt1 binds JIP1, preventing formation of JIP1-mediated, proapoptotic JNK complexes.	bind
6600	2	2883	6	10	NULL	NULL	NULL	statement 1	Process		occurs in the 					basal state					NULL		NULL	NULL	NULL	NULL	gw60_neuron_35_4_697_s_278	12194869	(A) In the basal state, Akt1 binds JIP1, preventing formation of JIP1-mediated, proapoptotic JNK complexes.	bind
6603	3	2883	6	10	NULL	NULL	NULL	JIP1	GP		mediates					proapoptotic JNK complexes	GP	formation of 			NULL		NULL	NULL	NULL	NULL	gw60_neuron_35_4_697_s_278	12194869	(A) In the basal state, Akt1 binds JIP1, preventing formation of JIP1-mediated, proapoptotic JNK complexes.	bind
6604	4	2883	6	10	NULL	NULL	NULL	statement 1	Process		prevents					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_35_4_697_s_278	12194869	(A) In the basal state, Akt1 binds JIP1, preventing formation of JIP1-mediated, proapoptotic JNK complexes.	bind
6199	1	2884	5	10	NULL	NULL	NULL	CPE	NucleicAcid		bind					CPEB	GP				NULL	oocyte cytoplasm	NULL	NULL	NULL	NULL	gw60_molcell_6_5_1253_s_137	11106762	(A) In the oocyte cytoplasm, the CPE is bound by CPEB even in unstimulated oocytes.	bind
6200	2	2884	5	10	NULL	NULL	NULL	CPE	NucleicAcid		bind					CPEB	GP				NULL	unstimulated oocytes	NULL	NULL	NULL	NULL	gw60_molcell_6_5_1253_s_137	11106762	(A) In the oocyte cytoplasm, the CPE is bound by CPEB even in unstimulated oocytes.	bind
6605	1	2884	6	10	NULL	NULL	NULL	CPE	NucleicAcid		bind					CPEB	GP				NULL	oocyte cytoplasm	NULL	NULL	NULL	NULL	gw60_molcell_6_5_1253_s_137	11106762	(A) In the oocyte cytoplasm, the CPE is bound by CPEB even in unstimulated oocytes.	bind
7278	2	2884	6	10	NULL	NULL	NULL	CPE	NucleicAcid		bind					CPEB	GP				NULL	unstimulated oocytes	NULL	NULL	NULL	NULL	gw60_molcell_6_5_1253_s_137	11106762	(A) In the oocyte cytoplasm, the CPE is bound by CPEB even in unstimulated oocytes.	bind
6267	1	2886	5	10	NULL	NULL	NULL	BLM	GP		bind					Top3alpha	GP				NULL	in PML nuclear bodies of unstressed cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_20_8925_s_310	16199871	(A) In unstressed cells, BLM is bound to Top3alpha in the PML nuclear bodies ( ) (bindings between two molecular species are shown as double-headed arrows.	bind
6611	1	2886	6	10	NULL	NULL	NULL	BLM	GP		bind					Top3alpha	GP				NULL	PML nuclear bodies in unstressed cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_20_8925_s_310	16199871	(A) In unstressed cells, BLM is bound to Top3alpha in the PML nuclear bodies ( ) (bindings between two molecular species are shown as double-headed arrows.	bind
53075	1	2887	5	10	NULL	NULL	NULL	pp F 	GP	In vitro - synthesized;;radiolabeled	bind					SecC	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_97_5_553_s_90	10367885	(A) In vitro - synthesized, radiolabeled pp F was bound to Sec complex (SecC) reconstituted into proteoliposomes  or incubated with liposomes lacking protein.	bind
53076	2	2887	5	10	NULL	NULL	NULL	SecC	GP		is					Sec complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_97_5_553_s_90	10367885	(A) In vitro - synthesized, radiolabeled pp F was bound to Sec complex (SecC) reconstituted into proteoliposomes  or incubated with liposomes lacking protein.	bind
53077	3	2887	5	10	NULL	NULL	NULL	SecC	GP		reconsituted into					proteoliposomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_97_5_553_s_90	10367885	(A) In vitro - synthesized, radiolabeled pp F was bound to Sec complex (SecC) reconstituted into proteoliposomes  or incubated with liposomes lacking protein.	bind
6612	1	2887	6	10	NULL	NULL	NULL	pp F	GP	In vitro - synthesized;;radiolabeled	bind					SecC	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_97_5_553_s_90	10367885	(A) In vitro - synthesized, radiolabeled pp F was bound to Sec complex (SecC) reconstituted into proteoliposomes  or incubated with liposomes lacking protein.	bind
6613	2	2887	6	10	NULL	NULL	NULL	SecC	GP		is					Sec complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_97_5_553_s_90	10367885	(A) In vitro - synthesized, radiolabeled pp F was bound to Sec complex (SecC) reconstituted into proteoliposomes  or incubated with liposomes lacking protein.	bind
6615	3	2887	6	10	NULL	NULL	NULL	SecC	GP		reconstituted into					proteoliposomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_97_5_553_s_90	10367885	(A) In vitro - synthesized, radiolabeled pp F was bound to Sec complex (SecC) reconstituted into proteoliposomes  or incubated with liposomes lacking protein.	bind
6269	1	2888	5	10	NULL	NULL	NULL	hADA3	GP		bind					p53	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_16_5801_s_205	12138191	(A) In vitro binding between hADA3 and p53.	bind
6621	1	2888	6	10	NULL	NULL	NULL	hADA3	GP		bind					p53	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_16_5801_s_205	12138191	(A) In vitro binding between hADA3 and p53.	bind
6270	1	2889	5	10	NULL	NULL	NULL	junD	GP		bind									A-TRE	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5073_s_107	9710591	(A) In vitro binding of  junD to the A-TRE is greatly enhanced in the presence of c- fos protein.	bind
6271	2	2889	5	10	NULL	NULL	NULL	statement 1	Process		enhance					c- fos protein	GP	in the presence of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5073_s_107	9710591	(A) In vitro binding of  junD to the A-TRE is greatly enhanced in the presence of c- fos protein.	bind
6622	1	2889	6	10	NULL	NULL	NULL	junD	GP		bind									A-TRE	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5073_s_107	9710591	(A) In vitro binding of  junD to the A-TRE is greatly enhanced in the presence of c- fos protein.	bind
6623	2	2889	6	10	NULL	NULL	NULL	statement 1	Process		enhanced					c-fos protein	GP	 in presence of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5073_s_107	9710591	(A) In vitro binding of  junD to the A-TRE is greatly enhanced in the presence of c- fos protein.	bind
6272	1	2890	5	10	NULL	NULL	NULL	CRM1s	GP		bind					RanBP3	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8751_s_251	14612415	(A) In vitro binding of CRM1s to RanBP3.	bind
6624	1	2890	6	10	NULL	NULL	NULL	CRM1s	GP		bind					RanBP3	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8751_s_251	14612415	(A) In vitro binding of CRM1s to RanBP3.	bind
6273	1	2891	5	10	NULL	NULL	NULL	GST-RhoA	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2650_s_240	11909959	(A) In vitro binding of Nir2 to GDP-bound GST-RhoA.	bind
6274	2	2891	5	10	NULL	NULL	NULL	Nir2	GP		bind					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2650_s_240	11909959	(A) In vitro binding of Nir2 to GDP-bound GST-RhoA.	bind
6715	1	2891	6	10	NULL	NULL	NULL	GDP	Chemical		bind					GST-RhoA	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2650_s_240	11909959	(A) In vitro binding of Nir2 to GDP-bound GST-RhoA.	bind
6716	2	2891	6	10	NULL	NULL	NULL	Nir2	GP		bind					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2650_s_240	11909959	(A) In vitro binding of Nir2 to GDP-bound GST-RhoA.	bind
6275	1	2892	5	10	NULL	NULL	NULL	RB	GP		bind					GST-E2F-1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4032_s_186	9632788	(A) In vitro binding of RB to GST-E2F-1.	bind
6717	1	2892	6	10	NULL	NULL	NULL	RB	GP		bind					GST-E2F-1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4032_s_186	9632788	(A) In vitro binding of RB to GST-E2F-1.	bind
6718	1	2893	6	10	NULL	NULL	NULL	TBP	GP		bind					SNR6	GP			promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6429_s_258	11533232	(A) In vitro binding of TBP to  SNR6 promoters.	bind
6277	1	2894	5	10	NULL	NULL	NULL	E2F1	GP		bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_1_78_s_253	11739724	(A) In vitro competition assay using baculovirus-expressed cyclin A (2, 5, or 10 mug) to compete out the binding of E2F1 to p53.	bind
6278	2	2894	5	10	NULL	NULL	NULL	cyclin A	GP	baculovirus-expressed	bind					p53	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_1_78_s_253	11739724	(A) In vitro competition assay using baculovirus-expressed cyclin A (2, 5, or 10 mug) to compete out the binding of E2F1 to p53.	bind
6279	3	2894	5	10	NULL	NULL	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_1_78_s_253	11739724	(A) In vitro competition assay using baculovirus-expressed cyclin A (2, 5, or 10 mug) to compete out the binding of E2F1 to p53.	bind
6719	1	2894	6	10	NULL	NULL	NULL	E2F1	GP		bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_1_78_s_253	11739724	(A) In vitro competition assay using baculovirus-expressed cyclin A (2, 5, or 10 mug) to compete out the binding of E2F1 to p53.	bind
6720	2	2894	6	10	NULL	NULL	NULL	cyclin A	GP	baculovirus-expressed	bind					p53	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_1_78_s_253	11739724	(A) In vitro competition assay using baculovirus-expressed cyclin A (2, 5, or 10 mug) to compete out the binding of E2F1 to p53.	bind
6721	3	2894	6	10	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_1_78_s_253	11739724	(A) In vitro competition assay using baculovirus-expressed cyclin A (2, 5, or 10 mug) to compete out the binding of E2F1 to p53.	bind
6280	1	2895	5	10	NULL	NULL	NULL	Stat1-ER chimera	GP		bind					DNA	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_2913_s_151	10082558	(A) In vitro DNA binding of the Stat1-ER chimera.	bind
6722	1	2895	6	10	NULL	NULL	NULL	DNA	NucleicAcid		bind					Stat1-ER chimera	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_2913_s_151	10082558	(A) In vitro DNA binding of the Stat1-ER chimera.	bind
7104	1	2900	5	10	NULL	NULL	NULL	MEF2 protein	GP	in vitro-translated	bind					Act57B	GP			MEF2 site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_mechdev_110_1_39_s_153	11744367	(A) In vitro translated MEF2 protein bound to the MEF2 site (complex b), is competed with a wild type MEF2 oligonucleotide sequence (wtMEF2), and is competed only weakly by a mutant MEF2 oligonucleotide sequence (mMEF2), demonstrating specificity for MEF2 binding within the context of the  Act57B promoter.	bind
7105	2	2900	5	10	NULL	NULL	NULL	wtMEF2	NucleicAcid		bind					Act57B	GP			MEF2 site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_mechdev_110_1_39_s_153	11744367	(A) In vitro translated MEF2 protein bound to the MEF2 site (complex b), is competed with a wild type MEF2 oligonucleotide sequence (wtMEF2), and is competed only weakly by a mutant MEF2 oligonucleotide sequence (mMEF2), demonstrating specificity for MEF2 binding within the context of the  Act57B promoter.	bind
7106	4	2900	5	10	NULL	NULL	NULL	statement 1	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_110_1_39_s_153	11744367	(A) In vitro translated MEF2 protein bound to the MEF2 site (complex b), is competed with a wild type MEF2 oligonucleotide sequence (wtMEF2), and is competed only weakly by a mutant MEF2 oligonucleotide sequence (mMEF2), demonstrating specificity for MEF2 binding within the context of the  Act57B promoter.	bind
7107	5	2900	5	10	NULL	NULL	NULL	mMEF2	NucleicAcid		bind		weakly			Act57B	GP			MEF2 site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_mechdev_110_1_39_s_153	11744367	(A) In vitro translated MEF2 protein bound to the MEF2 site (complex b), is competed with a wild type MEF2 oligonucleotide sequence (wtMEF2), and is competed only weakly by a mutant MEF2 oligonucleotide sequence (mMEF2), demonstrating specificity for MEF2 binding within the context of the  Act57B promoter.	bind
7108	6	2900	5	10	NULL	NULL	NULL	mMEF2	NucleicAcid		is					mutant MEF2 oligonucleotide sequence 	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_110_1_39_s_153	11744367	(A) In vitro translated MEF2 protein bound to the MEF2 site (complex b), is competed with a wild type MEF2 oligonucleotide sequence (wtMEF2), and is competed only weakly by a mutant MEF2 oligonucleotide sequence (mMEF2), demonstrating specificity for MEF2 binding within the context of the  Act57B promoter.	bind
7109	3	2900	5	10	NULL	NULL	NULL	wtMEF2	NucleicAcid		is					wild type MEF2 oligonucleotide sequence 	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_110_1_39_s_153	11744367	(A) In vitro translated MEF2 protein bound to the MEF2 site (complex b), is competed with a wild type MEF2 oligonucleotide sequence (wtMEF2), and is competed only weakly by a mutant MEF2 oligonucleotide sequence (mMEF2), demonstrating specificity for MEF2 binding within the context of the  Act57B promoter.	bind
7111	7	2900	5	10	NULL	NULL	NULL	statement 1	Process		compete with		weakly			statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_110_1_39_s_153	11744367	(A) In vitro translated MEF2 protein bound to the MEF2 site (complex b), is competed with a wild type MEF2 oligonucleotide sequence (wtMEF2), and is competed only weakly by a mutant MEF2 oligonucleotide sequence (mMEF2), demonstrating specificity for MEF2 binding within the context of the  Act57B promoter.	bind
6723	1	2900	6	10	NULL	NULL	NULL	MEF2 protein	GP	in vitro-translated	bind					Act57B 	GP			MEF2 site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_mechdev_110_1_39_s_153	11744367	(A) In vitro translated MEF2 protein bound to the MEF2 site (complex b), is competed with a wild type MEF2 oligonucleotide sequence (wtMEF2), and is competed only weakly by a mutant MEF2 oligonucleotide sequence (mMEF2), demonstrating specificity for MEF2 binding within the context of the  Act57B promoter.	bind
6724	2	2900	6	10	NULL	NULL	NULL	MEF2 oligoucleotide	NucleicAcid	wild type	bind					Act57B 	GP			MEF2 site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_mechdev_110_1_39_s_153	11744367	(A) In vitro translated MEF2 protein bound to the MEF2 site (complex b), is competed with a wild type MEF2 oligonucleotide sequence (wtMEF2), and is competed only weakly by a mutant MEF2 oligonucleotide sequence (mMEF2), demonstrating specificity for MEF2 binding within the context of the  Act57B promoter.	bind
6725	3	2900	6	10	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_110_1_39_s_153	11744367	(A) In vitro translated MEF2 protein bound to the MEF2 site (complex b), is competed with a wild type MEF2 oligonucleotide sequence (wtMEF2), and is competed only weakly by a mutant MEF2 oligonucleotide sequence (mMEF2), demonstrating specificity for MEF2 binding within the context of the  Act57B promoter.	bind
6726	4	2900	6	10	NULL	NULL	NULL	MEF2 oligoucleotide	NucleicAcid	mutant	bind		weakly			Act57B 	GP			MEF2 site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_mechdev_110_1_39_s_153	11744367	(A) In vitro translated MEF2 protein bound to the MEF2 site (complex b), is competed with a wild type MEF2 oligonucleotide sequence (wtMEF2), and is competed only weakly by a mutant MEF2 oligonucleotide sequence (mMEF2), demonstrating specificity for MEF2 binding within the context of the  Act57B promoter.	bind
6727	5	2900	6	10	NULL	NULL	NULL	statement 1	Process		competes		weakly			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_110_1_39_s_153	11744367	(A) In vitro translated MEF2 protein bound to the MEF2 site (complex b), is competed with a wild type MEF2 oligonucleotide sequence (wtMEF2), and is competed only weakly by a mutant MEF2 oligonucleotide sequence (mMEF2), demonstrating specificity for MEF2 binding within the context of the  Act57B promoter.	bind
53078	6	2900	6	10	NULL	NULL	NULL	wtMEF2	NucleicAcid		is					wild type MEF2 oligonucleotide sequence 	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_110_1_39_s_153	11744367	(A) In vitro translated MEF2 protein bound to the MEF2 site (complex b), is competed with a wild type MEF2 oligonucleotide sequence (wtMEF2), and is competed only weakly by a mutant MEF2 oligonucleotide sequence (mMEF2), demonstrating specificity for MEF2 binding within the context of the  Act57B promoter.	bind
53079	7	2900	6	10	NULL	NULL	NULL	mMEF2	NucleicAcid		is					mutant MEF2 oligonucleotide sequence 	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_110_1_39_s_153	11744367	(A) In vitro translated MEF2 protein bound to the MEF2 site (complex b), is competed with a wild type MEF2 oligonucleotide sequence (wtMEF2), and is competed only weakly by a mutant MEF2 oligonucleotide sequence (mMEF2), demonstrating specificity for MEF2 binding within the context of the  Act57B promoter.	bind
6285	1	2901	5	10	NULL	NULL	NULL	Hrs	GP	in vitro translated;;35S-labeled	bind					GST-RGS-PX1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5538_s_140	15469987	(A) In vitro translated, 35S-labeled Hrs binds to GST-RGS-PX1(PXC) but not to GST alone.	bind
6286	2	2901	5	10	NULL	NULL	NULL	Hrs	GP	in vitro-translated;;35S labeled	does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5538_s_140	15469987	(A) In vitro translated, 35S-labeled Hrs binds to GST-RGS-PX1(PXC) but not to GST alone.	bind
6728	1	2901	6	10	NULL	NULL	NULL	Hrs	GP	in vitro-translated;;35S labeled	bind					GST-RGS-PX1	GP			PXC	NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5538_s_140	15469987	(A) In vitro translated, 35S-labeled Hrs binds to GST-RGS-PX1(PXC) but not to GST alone.	bind
6729	2	2901	6	10	NULL	NULL	NULL	Hrs	GP	in vitro-translated;;35S labeled	does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5538_s_140	15469987	(A) In vitro translated, 35S-labeled Hrs binds to GST-RGS-PX1(PXC) but not to GST alone.	bind
6287	1	2902	5	10	NULL	NULL	NULL	Ada	GP		is					Adaptin	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_2_221_s_158	12194853	(A) In vitro-translated  -Adaptin (Ada) protein binds GST-Numb, but not GST.	bind
6288	2	2902	5	10	NULL	NULL	NULL	Ada protein	GP	in vitro-translated	bind					GST-Numb	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_2_221_s_158	12194853	(A) In vitro-translated  -Adaptin (Ada) protein binds GST-Numb, but not GST.	bind
6289	3	2902	5	10	NULL	NULL	NULL	Ada protein	GP	in vitro translated	does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_2_221_s_158	12194853	(A) In vitro-translated  -Adaptin (Ada) protein binds GST-Numb, but not GST.	bind
6730	1	2902	6	10	NULL	NULL	NULL	Adaptin	GP	in vitro-translated	bind					GST-Numb	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_2_221_s_158	12194853	(A) In vitro-translated  -Adaptin (Ada) protein binds GST-Numb, but not GST.	bind
6731	2	2902	6	10	NULL	NULL	NULL	Adaptin	GP	in vitro-translated	does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_2_221_s_158	12194853	(A) In vitro-translated  -Adaptin (Ada) protein binds GST-Numb, but not GST.	bind
6732	3	2902	6	10	NULL	NULL	NULL	Adaptin	GP		is					Ada	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_2_221_s_158	12194853	(A) In vitro-translated  -Adaptin (Ada) protein binds GST-Numb, but not GST.	bind
6290	1	2903	5	10	NULL	0	NULL	ARVCF	NULL	in vitro-translated	bind	NULL				ZO-1	NULL		PDZ domains		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5503_s_103	15456900	(A) In vitro-translated ARVCF binds to a GST fusion protein  containing the PDZ domains of ZO-1.	bind
46547	2	2903	5	10	NULL	0	NULL	ZO-1	NULL		is a type of	NULL		PDZ domain		 GST fusion protein 	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_12_5503_s_103	15456900	(A) In vitro-translated ARVCF binds to a GST fusion protein  containing the PDZ domains of ZO-1.	bind
6733	1	2903	6	10	NULL	0	NULL	ARVCF	NULL	in vitro-translated	bind	NULL				ZO-1	NULL		PDZ domain		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5503_s_103	15456900	(A) In vitro-translated ARVCF binds to a GST fusion protein  containing the PDZ domains of ZO-1.	bind
46548	2	2903	6	10	NULL	0	NULL	ZO-1	NULL		is a type of	NULL		PDZ domain		GST fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_12_5503_s_103	15456900	(A) In vitro-translated ARVCF binds to a GST fusion protein  containing the PDZ domains of ZO-1.	bind
6292	1	2904	5	10	NULL	NULL	NULL	p150Glued	GP	in vitro-translated;; full length	bind					GST-EB1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1405_s_122	12686597	(A) In vitro-translated full-length p150Glued was retained on a GST-EB1 column, but amino-terminal p150Glued deletion constructs p135MMRQ, pMT7-1, and pMT1-1 did not bind significantly to GST-EB1.	bind
6293	2	2904	5	10	NULL	NULL	NULL	p135MMRQ	AminoAcid		is a type of					p150Glued 	GP	deletion construct	amino-terminal 		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1405_s_122	12686597	(A) In vitro-translated full-length p150Glued was retained on a GST-EB1 column, but amino-terminal p150Glued deletion constructs p135MMRQ, pMT7-1, and pMT1-1 did not bind significantly to GST-EB1.	bind
6294	3	2904	5	10	NULL	NULL	NULL	pMT7-1	AminoAcid		is a type of					p150Glued 	GP	deletion construct	amino-terminal		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1405_s_122	12686597	(A) In vitro-translated full-length p150Glued was retained on a GST-EB1 column, but amino-terminal p150Glued deletion constructs p135MMRQ, pMT7-1, and pMT1-1 did not bind significantly to GST-EB1.	bind
6295	4	2904	5	10	NULL	NULL	NULL	pMT1-1	AminoAcid		is a type of					p150Glued 	GP	deletion construct	amino-terminal		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1405_s_122	12686597	(A) In vitro-translated full-length p150Glued was retained on a GST-EB1 column, but amino-terminal p150Glued deletion constructs p135MMRQ, pMT7-1, and pMT1-1 did not bind significantly to GST-EB1.	bind
6296	5	2904	5	10	NULL	NULL	NULL	statement 2	AminoAcid		does not bind		significantly			GST-EB1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1405_s_122	12686597	(A) In vitro-translated full-length p150Glued was retained on a GST-EB1 column, but amino-terminal p150Glued deletion constructs p135MMRQ, pMT7-1, and pMT1-1 did not bind significantly to GST-EB1.	bind
6297	6	2904	5	10	NULL	NULL	NULL	statement 3	AminoAcid		does not bind		significantly			GST-EB1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1405_s_122	12686597	(A) In vitro-translated full-length p150Glued was retained on a GST-EB1 column, but amino-terminal p150Glued deletion constructs p135MMRQ, pMT7-1, and pMT1-1 did not bind significantly to GST-EB1.	bind
6298	7	2904	5	10	NULL	NULL	NULL	statement 4	AminoAcid		does not bind		significantly			GST-EB1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1405_s_122	12686597	(A) In vitro-translated full-length p150Glued was retained on a GST-EB1 column, but amino-terminal p150Glued deletion constructs p135MMRQ, pMT7-1, and pMT1-1 did not bind significantly to GST-EB1.	bind
6734	1	2904	6	10	NULL	NULL	NULL	p150Glued	GP	in vitro-translated;;full length	bind					GST-EB1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1405_s_122	12686597	(A) In vitro-translated full-length p150Glued was retained on a GST-EB1 column, but amino-terminal p150Glued deletion constructs p135MMRQ, pMT7-1, and pMT1-1 did not bind significantly to GST-EB1.	bind
6735	2	2904	6	10	NULL	NULL	NULL	p135MMRQ	AminoAcid		is a type of					 p150Glued	GP	deletion construct	amino-terminal		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1405_s_122	12686597	(A) In vitro-translated full-length p150Glued was retained on a GST-EB1 column, but amino-terminal p150Glued deletion constructs p135MMRQ, pMT7-1, and pMT1-1 did not bind significantly to GST-EB1.	bind
6736	3	2904	6	10	NULL	NULL	NULL	pMT7-1	AminoAcid		is a type of					p150Glued	GP	deletion construct	amino-terminal		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1405_s_122	12686597	(A) In vitro-translated full-length p150Glued was retained on a GST-EB1 column, but amino-terminal p150Glued deletion constructs p135MMRQ, pMT7-1, and pMT1-1 did not bind significantly to GST-EB1.	bind
6737	4	2904	6	10	NULL	NULL	NULL	pMT1-1	AminoAcid		is a type of					p150Glued	GP	deletion construct	amino-terminal		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1405_s_122	12686597	(A) In vitro-translated full-length p150Glued was retained on a GST-EB1 column, but amino-terminal p150Glued deletion constructs p135MMRQ, pMT7-1, and pMT1-1 did not bind significantly to GST-EB1.	bind
53110	5	2904	6	10	NULL	NULL	NULL	statement 2	AminoAcid		does not bind		significantly			GST-EB1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1405_s_122	12686597	(A) In vitro-translated full-length p150Glued was retained on a GST-EB1 column, but amino-terminal p150Glued deletion constructs p135MMRQ, pMT7-1, and pMT1-1 did not bind significantly to GST-EB1.	bind
53111	6	2904	6	10	NULL	NULL	NULL	statement 3	AminoAcid		does not bind		significantly			GST-EB1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1405_s_122	12686597	(A) In vitro-translated full-length p150Glued was retained on a GST-EB1 column, but amino-terminal p150Glued deletion constructs p135MMRQ, pMT7-1, and pMT1-1 did not bind significantly to GST-EB1.	bind
53112	7	2904	6	10	NULL	NULL	NULL	statement 4	AminoAcid		does not bind		significantly			GST-EB1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1405_s_122	12686597	(A) In vitro-translated full-length p150Glued was retained on a GST-EB1 column, but amino-terminal p150Glued deletion constructs p135MMRQ, pMT7-1, and pMT1-1 did not bind significantly to GST-EB1.	bind
6299	1	2905	5	10	NULL	NULL	NULL	Galphas	GP	in vitro translated;;35S-labeled	bind					GST-Hrs	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5538_s_156	15469987	(A) In vitro-translated, 35S-labeled Galphas binds to GST-Hrs but not to GST alone.	bind
6301	2	2905	5	10	NULL	NULL	NULL	Galphas	GP	in vitro translated;;35S-labeled	does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5538_s_156	15469987	(A) In vitro-translated, 35S-labeled Galphas binds to GST-Hrs but not to GST alone.	bind
6738	1	2905	6	10	NULL	NULL	NULL	Galphas	GP	in vitro-translated;;35S labeled	bind					GST-Hrs	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5538_s_156	15469987	(A) In vitro-translated, 35S-labeled Galphas binds to GST-Hrs but not to GST alone.	bind
6739	2	2905	6	10	NULL	NULL	NULL	Galphas	GP	in vitro-translated;;35S labeled	does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5538_s_156	15469987	(A) In vitro-translated, 35S-labeled Galphas binds to GST-Hrs but not to GST alone.	bind
6305	1	2906	5	10	NULL	NULL	NULL	IRF-5	GP		bind					IFNA	GP	endogenous		promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_390	12138184	(A) In vivo binding of IRF-5 and IRF-3 to the endogenous IFNA promoter as analyzed by the chromatin immunoprecipitation assay.	bind
6306	2	2906	5	10	NULL	NULL	NULL	IRF-3	GP		bind					IFNA	GP	endogenous		promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_390	12138184	(A) In vivo binding of IRF-5 and IRF-3 to the endogenous IFNA promoter as analyzed by the chromatin immunoprecipitation assay.	bind
6740	1	2906	6	10	NULL	NULL	NULL	IRF-5	GP		bind					IFNA	GP	endogenous		promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_390	12138184	(A) In vivo binding of IRF-5 and IRF-3 to the endogenous IFNA promoter as analyzed by the chromatin immunoprecipitation assay.	bind
6741	2	2906	6	10	NULL	NULL	NULL	IRF-3	GP		bind					IFNA	GP	endogenous		promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_390	12138184	(A) In vivo binding of IRF-5 and IRF-3 to the endogenous IFNA promoter as analyzed by the chromatin immunoprecipitation assay.	bind
7116	1	2907	5	10	NULL	NULL	NULL	PI(4)P shuttle	GP		bind					AP-1	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_cell_114_3_299_s_164	12914695	(A) In vivo rescue of  -adaptin (AP-1) binding by shuttle PI(4)P. PI4KII  RNAi cells were incubated with polyamine shuttle carriers in the presence or absence of 20  M diC16-PI(4)P or diC16-PIP2 for 30 min at 37 degrees C.	bind
7117	2	2907	5	10	NULL	NULL	NULL	AP-1	GP		is					adaptin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_3_299_s_164	12914695	(A) In vivo rescue of  -adaptin (AP-1) binding by shuttle PI(4)P. PI4KII  RNAi cells were incubated with polyamine shuttle carriers in the presence or absence of 20  M diC16-PI(4)P or diC16-PIP2 for 30 min at 37 degrees C.	bind
6742	1	2907	6	10	NULL	NULL	NULL	adaptin	GP		bind					shuttle PI(4)P	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_cell_114_3_299_s_164	12914695	(A) In vivo rescue of  -adaptin (AP-1) binding by shuttle PI(4)P. PI4KII  RNAi cells were incubated with polyamine shuttle carriers in the presence or absence of 20  M diC16-PI(4)P or diC16-PIP2 for 30 min at 37 degrees C.	bind
46549	2	2907	6	10	NULL	NULL	NULL	AP-1	GP		is					adaptin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_3_299_s_164	12914695	(A) In vivo rescue of  -adaptin (AP-1) binding by shuttle PI(4)P. PI4KII  RNAi cells were incubated with polyamine shuttle carriers in the presence or absence of 20  M diC16-PI(4)P or diC16-PIP2 for 30 min at 37 degrees C.	bind
6307	1	2908	5	10	NULL	NULL	NULL	Sir3	GP		bind					Sir4	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_385	15899856	(A) In wild-type cells, the nucleation  and spreading of silent chromatin require both the binding of Sir3 to Sir4 and the  deacetylation of nucleosomes by Sir2.	bind
6308	2	2908	5	10	NULL	NULL	NULL	Sir2	GP		deacetylate					nucleosomes	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_385	15899856	(A) In wild-type cells, the nucleation  and spreading of silent chromatin require both the binding of Sir3 to Sir4 and the  deacetylation of nucleosomes by Sir2.	bind
6392	3	2908	5	10	NULL	NULL	NULL	silent chromatin	Chromosome	nucleation of 	require					statement 1	Process				NULL	wild-type cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_385	15899856	(A) In wild-type cells, the nucleation  and spreading of silent chromatin require both the binding of Sir3 to Sir4 and the  deacetylation of nucleosomes by Sir2.	bind
6393	4	2908	5	10	NULL	NULL	NULL	silent chromatin	Chromosome	nucleation of	require					statement 2	Process				NULL	wild-type cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_385	15899856	(A) In wild-type cells, the nucleation  and spreading of silent chromatin require both the binding of Sir3 to Sir4 and the  deacetylation of nucleosomes by Sir2.	bind
6394	5	2908	5	10	NULL	0	NULL	silent chromatin	NULL	spreading of 	require	NULL				statement 1	NULL				NULL	wild-type cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_385	15899856	(A) In wild-type cells, the nucleation  and spreading of silent chromatin require both the binding of Sir3 to Sir4 and the  deacetylation of nucleosomes by Sir2.	bind
6395	6	2908	5	10	NULL	NULL	NULL	silent chromatin	Chromosome	spreading of	require					statement 2	Process				NULL	wild-type cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_385	15899856	(A) In wild-type cells, the nucleation  and spreading of silent chromatin require both the binding of Sir3 to Sir4 and the  deacetylation of nucleosomes by Sir2.	bind
6743	1	2908	6	10	NULL	NULL	NULL	Sir3	GP		bind					Sir4	GP				NULL	wild type cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_385	15899856	(A) In wild-type cells, the nucleation  and spreading of silent chromatin require both the binding of Sir3 to Sir4 and the  deacetylation of nucleosomes by Sir2.	bind
6744	2	2908	6	10	NULL	NULL	NULL	Sir2	GP		deacetylates					nucleosomes	Chromosome				NULL	wild type cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_385	15899856	(A) In wild-type cells, the nucleation  and spreading of silent chromatin require both the binding of Sir3 to Sir4 and the  deacetylation of nucleosomes by Sir2.	bind
6745	3	2908	6	10	NULL	NULL	NULL	silent chromatin	Chromosome	nucleation  of	require					statement 1	Process				NULL	wild type cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_385	15899856	(A) In wild-type cells, the nucleation  and spreading of silent chromatin require both the binding of Sir3 to Sir4 and the  deacetylation of nucleosomes by Sir2.	bind
6746	4	2908	6	10	NULL	NULL	NULL	silent chromatin	Chromosome	nucleation of	require					statement 2	Process				NULL	wild type cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_385	15899856	(A) In wild-type cells, the nucleation  and spreading of silent chromatin require both the binding of Sir3 to Sir4 and the  deacetylation of nucleosomes by Sir2.	bind
46556	5	2908	6	10	NULL	NULL	NULL	silent chromatin	Chromosome	spreading of	require					statement 1	Process				NULL	wild-type cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_385	15899856	(A) In wild-type cells, the nucleation  and spreading of silent chromatin require both the binding of Sir3 to Sir4 and the  deacetylation of nucleosomes by Sir2.	bind
46557	6	2908	6	10	NULL	NULL	NULL	silent chromatin	Chromosome	spreading of	require					statement 2	Process				NULL	wild-type cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_385	15899856	(A) In wild-type cells, the nucleation  and spreading of silent chromatin require both the binding of Sir3 to Sir4 and the  deacetylation of nucleosomes by Sir2.	bind
6396	1	2909	5	10	NULL	NULL	NULL	NEM	Chemical		inactivate					UBE	NucleicAcid	binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_72_1_65_s_129	10521600	(A) Inactivation of the UBE binding activity by NEM.	bind
6747	1	2909	6	10	NULL	NULL	NULL	NEM	Chemical		inactivates					UBE	NucleicAcid	binding activity of 			NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_72_1_65_s_129	10521600	(A) Inactivation of the UBE binding activity by NEM.	bind
6397	1	2911	5	10	NULL	NULL	NULL	Pex14p ligand	GP		bind					Pex13p	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_5_1007_s_106	12453410	(A) Independent binding of the Pex14p and Pex5p ligands to the Pex13p SH3 domain.	bind
6398	2	2911	5	10	NULL	NULL	NULL	Pex5p ligand	GP		bind					Pex13p	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_5_1007_s_106	12453410	(A) Independent binding of the Pex14p and Pex5p ligands to the Pex13p SH3 domain.	bind
6399	3	2911	5	10	NULL	NULL	NULL	statement 1	Process		is independent of					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_5_1007_s_106	12453410	(A) Independent binding of the Pex14p and Pex5p ligands to the Pex13p SH3 domain.	bind
6798	1	2911	6	10	NULL	NULL	NULL	Pex14p	GP		bind					Pex13p	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_5_1007_s_106	12453410	(A) Independent binding of the Pex14p and Pex5p ligands to the Pex13p SH3 domain.	bind
6799	2	2911	6	10	NULL	NULL	NULL	Pex5p	GP		bind					Pex13p	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_5_1007_s_106	12453410	(A) Independent binding of the Pex14p and Pex5p ligands to the Pex13p SH3 domain.	bind
7875	3	2911	6	10	NULL	NULL	NULL	statement 1	Process		is independent of					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_5_1007_s_106	12453410	(A) Independent binding of the Pex14p and Pex5p ligands to the Pex13p SH3 domain.	bind
6400	1	2912	5	10	NULL	NULL	NULL	Sp1	GP		bind					DNA	NucleicAcid				NULL	Hep3B cells	NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_4_1005_s_110	12200149	(A) Induction of the DNA-binding activity of Sp1 by TSA treatment in Hep3B cells.	bind
6401	2	2912	5	10	NULL	NULL	NULL	TSA	Chemical		induce					statement 1	Process				NULL	Hep3B cells	NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_4_1005_s_110	12200149	(A) Induction of the DNA-binding activity of Sp1 by TSA treatment in Hep3B cells.	bind
6800	1	2912	6	10	NULL	NULL	NULL	Sp1	GP		bind					DNA	NucleicAcid				NULL	Hep3B cells	NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_4_1005_s_110	12200149	(A) Induction of the DNA-binding activity of Sp1 by TSA treatment in Hep3B cells.	bind
6801	2	2912	6	10	NULL	NULL	NULL	TSA	Chemical		induces					statement 1	Process				NULL	Hep3B cells	NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_4_1005_s_110	12200149	(A) Induction of the DNA-binding activity of Sp1 by TSA treatment in Hep3B cells.	bind
6402	1	2913	5	10	NULL	NULL	NULL	ALDO	GP		bind					MR	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1589_1_31_s_140	11909639	(A) Inhibition of ALDO binding to MR by PLP is concentration- and time-dependent.	bind
6403	2	2913	5	10	NULL	NULL	NULL	PLP	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1589_1_31_s_140	11909639	(A) Inhibition of ALDO binding to MR by PLP is concentration- and time-dependent.	bind
6404	3	2913	5	10	NULL	NULL	NULL	statement 2	Process		is dependent on					concentration	QuantityOrMeasure				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1589_1_31_s_140	11909639	(A) Inhibition of ALDO binding to MR by PLP is concentration- and time-dependent.	bind
6405	4	2913	5	10	NULL	NULL	NULL	statement 2	Process		is dependent on					time	Time				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1589_1_31_s_140	11909639	(A) Inhibition of ALDO binding to MR by PLP is concentration- and time-dependent.	bind
6802	1	2913	6	10	NULL	NULL	NULL	ALDO	GP		bind					MR	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1589_1_31_s_140	11909639	(A) Inhibition of ALDO binding to MR by PLP is concentration- and time-dependent.	bind
6803	2	2913	6	10	NULL	NULL	NULL	PLP	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1589_1_31_s_140	11909639	(A) Inhibition of ALDO binding to MR by PLP is concentration- and time-dependent.	bind
6804	3	2913	6	10	NULL	NULL	NULL	statement 2	Process		is dependent on					concentration	QuantityOrMeasure				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1589_1_31_s_140	11909639	(A) Inhibition of ALDO binding to MR by PLP is concentration- and time-dependent.	bind
6805	4	2913	6	10	NULL	NULL	NULL	statement 2	Process		is dependent on					time	Time				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1589_1_31_s_140	11909639	(A) Inhibition of ALDO binding to MR by PLP is concentration- and time-dependent.	bind
6406	1	2914	5	10	NULL	NULL	NULL	BMP-7	GP		bind					ROS 17/2	Cell				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_4_858_s_192	12927798	(A) Inhibition of BMP-7 binding to ROS 17/2.	bind
6810	1	2914	6	10	NULL	NULL	NULL	BMP-7	GP		bind					ROS 17/2	Cell				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_4_858_s_192	12927798	(A) Inhibition of BMP-7 binding to ROS 17/2.	bind
7118	1	2915	5	10	NULL	NULL	NULL	TCP	Chemical		bind					NMDA receptors	GP		NR2B subunit		NULL	rat brain membranes	NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_296_1_150_s_123	11123375	(A) inhibition of NR1a/2B receptors expressed in  Xenopus oocytes or (B) inhibition of [3]TCP binding to NR2B subunit containing NMDA receptors in rat brain membranes or (C) inhibition of [3]DTG binding to sigma sites in rat brain membranes.	bind
7119	2	2915	5	10	NULL	NULL	NULL	DTG	Chemical		bind								sigma sites		NULL	rat brain membrane	NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_296_1_150_s_123	11123375	(A) inhibition of NR1a/2B receptors expressed in  Xenopus oocytes or (B) inhibition of [3]TCP binding to NR2B subunit containing NMDA receptors in rat brain membranes or (C) inhibition of [3]DTG binding to sigma sites in rat brain membranes.	bind
46558	3	2915	5	10	NULL	NULL	NULL	NR1a/2B receptors	GP		is expressed in					 oocytes	Cell	Xenopus			NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_296_1_150_s_123	11123375	(A) inhibition of NR1a/2B receptors expressed in  Xenopus oocytes or (B) inhibition of [3]TCP binding to NR2B subunit containing NMDA receptors in rat brain membranes or (C) inhibition of [3]DTG binding to sigma sites in rat brain membranes.	bind
6811	1	2915	6	10	NULL	NULL	NULL	NR1a/2B receptors	GP		expressed in					oocytes	Cell	Xenopus			NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_296_1_150_s_123	11123375	(A) inhibition of NR1a/2B receptors expressed in  Xenopus oocytes or (B) inhibition of [3]TCP binding to NR2B subunit containing NMDA receptors in rat brain membranes or (C) inhibition of [3]DTG binding to sigma sites in rat brain membranes.	bind
6813	3	2915	6	10	NULL	NULL	NULL	TCP	Chemical		bind					NMDA receptors	GP		NR2B subunit		NULL	rat brain membranes	NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_296_1_150_s_123	11123375	(A) inhibition of NR1a/2B receptors expressed in  Xenopus oocytes or (B) inhibition of [3]TCP binding to NR2B subunit containing NMDA receptors in rat brain membranes or (C) inhibition of [3]DTG binding to sigma sites in rat brain membranes.	bind
6814	2	2915	6	10	NULL	NULL	NULL	DTG	Chemical		bind								sigma sites 		NULL	rat brain membranes	NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_296_1_150_s_123	11123375	(A) inhibition of NR1a/2B receptors expressed in  Xenopus oocytes or (B) inhibition of [3]TCP binding to NR2B subunit containing NMDA receptors in rat brain membranes or (C) inhibition of [3]DTG binding to sigma sites in rat brain membranes.	bind
6413	1	2916	5	10	NULL	NULL	NULL	peptide V	AminoAcid		mediate					LDL	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_286	10191300	(A) Inhibition of peptide V-mediated binding of LDL by LDL, HDL, and AcLDL.	bind
6414	2	2916	5	10	NULL	NULL	NULL	LDL	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_286	10191300	(A) Inhibition of peptide V-mediated binding of LDL by LDL, HDL, and AcLDL.	bind
6415	3	2916	5	10	NULL	NULL	NULL	HDL	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_286	10191300	(A) Inhibition of peptide V-mediated binding of LDL by LDL, HDL, and AcLDL.	bind
6416	4	2916	5	10	NULL	NULL	NULL	AcLDL	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_286	10191300	(A) Inhibition of peptide V-mediated binding of LDL by LDL, HDL, and AcLDL.	bind
6817	1	2916	6	10	NULL	NULL	NULL	peptide V	AminoAcid		mediates					LDL	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_286	10191300	(A) Inhibition of peptide V-mediated binding of LDL by LDL, HDL, and AcLDL.	bind
6819	2	2916	6	10	NULL	NULL	NULL	LDL	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_286	10191300	(A) Inhibition of peptide V-mediated binding of LDL by LDL, HDL, and AcLDL.	bind
6820	3	2916	6	10	NULL	NULL	NULL	HDL	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_286	10191300	(A) Inhibition of peptide V-mediated binding of LDL by LDL, HDL, and AcLDL.	bind
6825	4	2916	6	10	NULL	NULL	NULL	AcLDL	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_286	10191300	(A) Inhibition of peptide V-mediated binding of LDL by LDL, HDL, and AcLDL.	bind
7120	1	2917	5	10	NULL	NULL	NULL	K2-3f	GP		bind			scFv		Ab1 mAb K2-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1638_3_257_s_276	12878327	(A) Inhibition of scFv K2-3f binding to Ab1 mAb K2-3 by cocaine.	bind
7121	2	2917	5	10	NULL	NULL	NULL	cocaine	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1638_3_257_s_276	12878327	(A) Inhibition of scFv K2-3f binding to Ab1 mAb K2-3 by cocaine.	bind
6918	1	2917	6	10	NULL	NULL	NULL	K2-3f	GP		bind			scFv		Ab1 mAb K2-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1638_3_257_s_276	12878327	(A) Inhibition of scFv K2-3f binding to Ab1 mAb K2-3 by cocaine.	bind
6919	2	2917	6	10	NULL	NULL	NULL	cocaine	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1638_3_257_s_276	12878327	(A) Inhibition of scFv K2-3f binding to Ab1 mAb K2-3 by cocaine.	bind
6443	1	2918	5	10	NULL	NULL	NULL	mAb	GP		bind					TcP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_4_819_s_65	12589786	(A) Inhibition of the  binding of mAb to TcP2  by scFv. TcP2 -coated plates were incubated with different  concentrations of scFv alone, scFv plus R13, or scFv plus TMVP.	bind
6444	2	2918	5	10	NULL	NULL	NULL	scFv	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_4_819_s_65	12589786	(A) Inhibition of the  binding of mAb to TcP2  by scFv. TcP2 -coated plates were incubated with different  concentrations of scFv alone, scFv plus R13, or scFv plus TMVP.	bind
6920	1	2918	6	10	NULL	NULL	NULL	mAb	GP		bind					TcP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_4_819_s_65	12589786	(A) Inhibition of the  binding of mAb to TcP2  by scFv. TcP2 -coated plates were incubated with different  concentrations of scFv alone, scFv plus R13, or scFv plus TMVP.	bind
6921	2	2918	6	10	NULL	NULL	NULL	scFv	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_4_819_s_65	12589786	(A) Inhibition of the  binding of mAb to TcP2  by scFv. TcP2 -coated plates were incubated with different  concentrations of scFv alone, scFv plus R13, or scFv plus TMVP.	bind
6445	1	2919	5	10	NULL	NULL	NULL	mAb	GP		bind					TcP2	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_301_4_819_s_65	12589786	(A) Inhibition of the binding of mAb to TcP2  by scFv. TcP2 -coated plates were incubated with different concentrations of scFv alone, scFv plus R13, or scFv plus TMVP.	bind
6446	2	2919	5	10	NULL	NULL	NULL	scFv	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_301_4_819_s_65	12589786	(A) Inhibition of the binding of mAb to TcP2  by scFv. TcP2 -coated plates were incubated with different concentrations of scFv alone, scFv plus R13, or scFv plus TMVP.	bind
6922	1	2919	6	10	NULL	NULL	NULL	mAb	GP		bind					TcP2	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_301_4_819_s_65	12589786	(A) Inhibition of the binding of mAb to TcP2  by scFv. TcP2 -coated plates were incubated with different concentrations of scFv alone, scFv plus R13, or scFv plus TMVP.	bind
6923	2	2919	6	10	NULL	NULL	NULL	scFv	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_301_4_819_s_65	12589786	(A) Inhibition of the binding of mAb to TcP2  by scFv. TcP2 -coated plates were incubated with different concentrations of scFv alone, scFv plus R13, or scFv plus TMVP.	bind
6447	1	2920	5	10	NULL	NULL	NULL	SOCS-1	GP		bind					IR	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_12_5434_s_147	15169905	(a) Insulin-dependent binding of SOCS-1  and SOCS-3 to the IR in vivo.	bind
6448	2	2920	5	10	NULL	NULL	NULL	statement 1	Process		is dependent on					insulin	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_12_5434_s_147	15169905	(a) Insulin-dependent binding of SOCS-1  and SOCS-3 to the IR in vivo.	bind
6449	3	2920	5	10	NULL	NULL	NULL	SOCS-3	GP		bind					IR	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_12_5434_s_147	15169905	(a) Insulin-dependent binding of SOCS-1  and SOCS-3 to the IR in vivo.	bind
6450	4	2920	5	10	NULL	NULL	NULL	statement 3	Process		is dependent on					insulin	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_12_5434_s_147	15169905	(a) Insulin-dependent binding of SOCS-1  and SOCS-3 to the IR in vivo.	bind
6924	1	2920	6	10	NULL	NULL	NULL	SOCS-1	GP		bind					IR	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_12_5434_s_147	15169905	(a) Insulin-dependent binding of SOCS-1  and SOCS-3 to the IR in vivo.	bind
6925	2	2920	6	10	NULL	NULL	NULL	SOCS-3	GP		bind					IR	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_12_5434_s_147	15169905	(a) Insulin-dependent binding of SOCS-1  and SOCS-3 to the IR in vivo.	bind
6926	3	2920	6	10	NULL	NULL	NULL	statement 1	Process		is dependent on					insulin	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_12_5434_s_147	15169905	(a) Insulin-dependent binding of SOCS-1  and SOCS-3 to the IR in vivo.	bind
6927	4	2920	6	10	NULL	NULL	NULL	statement 2	Process		is dependent on					insulin	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_12_5434_s_147	15169905	(a) Insulin-dependent binding of SOCS-1  and SOCS-3 to the IR in vivo.	bind
6451	1	2921	5	10	NULL	NULL	NULL	Val-tRNAIle	NucleicAcid		interact with					IleRS	GP		editing domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_103_5_793_s_170	11114335	(A) Interactions  of the Val-tRNAIle with the IleRS editing domain at the posttransfer editing  step.	bind
6452	2	2921	5	10	NULL	NULL	NULL	statement 1	Process		occurs at					posttransfer editing step	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_5_793_s_170	11114335	(A) Interactions  of the Val-tRNAIle with the IleRS editing domain at the posttransfer editing  step.	bind
6928	1	2921	6	10	NULL	NULL	NULL	Val-tRNAIle	NucleicAcid		interact with					IleRS	GP		editing domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_103_5_793_s_170	11114335	(A) Interactions  of the Val-tRNAIle with the IleRS editing domain at the posttransfer editing  step.	bind
6929	2	2921	6	10	NULL	NULL	NULL	statement 1	Process		occurs at					posttransfer editing step	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_5_793_s_170	11114335	(A) Interactions  of the Val-tRNAIle with the IleRS editing domain at the posttransfer editing  step.	bind
6453	1	2922	5	10	NULL	NULL	NULL	BTX BR36	GP		interacts with					AChR	GP		ACh binding pocket		NULL		NULL	NULL	NULL	NULL	gw60_neuron_35_2_319_s_171	12160749	(A) Interactions of  -BTX BR36 (blue) in the ACh binding pocket of AChR at the interface between the  1 and   subunits and (B) at the interface between the  1 and   subunits.	bind
7123	2	2922	5	10	NULL	NULL	NULL	statement 1	Process		occurs at								interface between 1 and subunits		NULL		NULL	NULL	NULL	NULL	gw60_neuron_35_2_319_s_171	12160749	(A) Interactions of  -BTX BR36 (blue) in the ACh binding pocket of AChR at the interface between the  1 and   subunits and (B) at the interface between the  1 and   subunits.	bind
7020	1	2922	6	10	NULL	NULL	NULL	BTX Br36	GP		interacts with					AChR	GP		ACh binding pocket		NULL		NULL	NULL	NULL	NULL	gw60_neuron_35_2_319_s_171	12160749	(A) Interactions of  -BTX BR36 (blue) in the ACh binding pocket of AChR at the interface between the  1 and   subunits and (B) at the interface between the  1 and   subunits.	bind
7021	2	2922	6	10	NULL	NULL	NULL	statement 1	Process		occurs at								interface between the 1 and subunits		NULL		NULL	NULL	NULL	NULL	gw60_neuron_35_2_319_s_171	12160749	(A) Interactions of  -BTX BR36 (blue) in the ACh binding pocket of AChR at the interface between the  1 and   subunits and (B) at the interface between the  1 and   subunits.	bind
6454	1	2923	5	10	NULL	NULL	NULL	Iqg1p	GP		bind					Sec3p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_4_601_s_130	12446742	(A) Iqg1p binds Sec3p.	bind
6935	1	2923	6	10	NULL	NULL	NULL	Iqg1p	GP		bind					Sec3p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_4_601_s_130	12446742	(A) Iqg1p binds Sec3p.	bind
6455	1	2924	5	10	NULL	NULL	NULL	SR	GP		bind			 SRX domain		GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_6_793_s_208	12654246	(A) Isothermal calorimetric titration of SR  bound to GTP (cyan diamonds) or GDP (magenta diamonds) with the SRX domain of SR .	bind
6456	2	2924	5	10	NULL	NULL	NULL	SR	GP		bind			 SRX domain		GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_6_793_s_208	12654246	(A) Isothermal calorimetric titration of SR  bound to GTP (cyan diamonds) or GDP (magenta diamonds) with the SRX domain of SR .	bind
46559	3	2924	5	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_6_793_s_208	12654246	(A) Isothermal calorimetric titration of SR  bound to GTP (cyan diamonds) or GDP (magenta diamonds) with the SRX domain of SR .	bind
6939	1	2924	6	10	NULL	NULL	NULL	SR	GP		bind			SRX domain		GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_6_793_s_208	12654246	(A) Isothermal calorimetric titration of SR  bound to GTP (cyan diamonds) or GDP (magenta diamonds) with the SRX domain of SR .	bind
6940	2	2924	6	10	NULL	NULL	NULL	SR	GP		bind			SRX domain		GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_6_793_s_208	12654246	(A) Isothermal calorimetric titration of SR  bound to GTP (cyan diamonds) or GDP (magenta diamonds) with the SRX domain of SR .	bind
46560	3	2924	6	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_6_793_s_208	12654246	(A) Isothermal calorimetric titration of SR  bound to GTP (cyan diamonds) or GDP (magenta diamonds) with the SRX domain of SR .	bind
6457	1	2925	5	10	NULL	NULL	NULL	Abl	GP	purified	bind			kinase domain		c-Abl 1b peptide	AminoAcid	myristoylated	Myr-GQQPGKVLGDQRRPSL		NULL		NULL	NULL	NULL	NULL	gw60_cell_112_6_845_s_67	12654250	(A) Isothermal titration calorimetry measuring binding of the purified Abl kinase domain to a myristoylated c-Abl 1b peptide (Myr-GQQPGKVLGDQRRPSL).	bind
6945	1	2925	6	10	NULL	NULL	NULL	Abl 	GP	purified	bind			kinase domain		c-Abl 1b peptide	AminoAcid	myristoylated	Myr-GQQPGKVLGDQRRPSL		NULL		NULL	NULL	NULL	NULL	gw60_cell_112_6_845_s_67	12654250	(A) Isothermal titration calorimetry measuring binding of the purified Abl kinase domain to a myristoylated c-Abl 1b peptide (Myr-GQQPGKVLGDQRRPSL).	bind
6474	1	2926	5	10	NULL	NULL	NULL	paxillin	GP		bind					alpha4	GP		tail		NULL	JB4 cells	NULL	NULL	NULL	NULL	gw70_cellbiol_171_6_1073_s_75	16365170	(A) JB4 cells expressing either wt alpha4 or alpha4(Y991A) were pretreated for 15 min with A7B7C7, a cell-permeable inhibitor of paxillin  binding to the alpha4 tail, or with the control compound A6B6C6, both present at 5 muM.	bind
6475	2	2926	5	10	NULL	NULL	NULL	A7B7C7	Chemical		inhibit					statement 1	Process				NULL	JB4 cells	NULL	NULL	NULL	NULL	gw70_cellbiol_171_6_1073_s_75	16365170	(A) JB4 cells expressing either wt alpha4 or alpha4(Y991A) were pretreated for 15 min with A7B7C7, a cell-permeable inhibitor of paxillin  binding to the alpha4 tail, or with the control compound A6B6C6, both present at 5 muM.	bind
46799	3	2926	5	10	NULL	NULL	NULL	A7B7C7	Chemical		is a type of					cell-permeable inhibitor	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_6_1073_s_75	16365170	(A) JB4 cells expressing either wt alpha4 or alpha4(Y991A) were pretreated for 15 min with A7B7C7, a cell-permeable inhibitor of paxillin  binding to the alpha4 tail, or with the control compound A6B6C6, both present at 5 muM.	bind
7024	1	2926	6	10	NULL	NULL	NULL	paxillin	GP		bind					alpha-4	GP		tail		NULL	JB4 cells	NULL	NULL	NULL	NULL	gw70_cellbiol_171_6_1073_s_75	16365170	(A) JB4 cells expressing either wt alpha4 or alpha4(Y991A) were pretreated for 15 min with A7B7C7, a cell-permeable inhibitor of paxillin  binding to the alpha4 tail, or with the control compound A6B6C6, both present at 5 muM.	bind
7025	2	2926	6	10	NULL	NULL	NULL	A7B7C7	Chemical		inhibits					statement 1	Process				NULL	JB4 cells	NULL	NULL	NULL	NULL	gw70_cellbiol_171_6_1073_s_75	16365170	(A) JB4 cells expressing either wt alpha4 or alpha4(Y991A) were pretreated for 15 min with A7B7C7, a cell-permeable inhibitor of paxillin  binding to the alpha4 tail, or with the control compound A6B6C6, both present at 5 muM.	bind
46800	3	2926	6	10	NULL	NULL	NULL	A7B7C7	Chemical		is a type of 					cell-permeable inhibitor	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_6_1073_s_75	16365170	(A) JB4 cells expressing either wt alpha4 or alpha4(Y991A) were pretreated for 15 min with A7B7C7, a cell-permeable inhibitor of paxillin  binding to the alpha4 tail, or with the control compound A6B6C6, both present at 5 muM.	bind
6476	1	2927	5	10	NULL	NULL	NULL	JDP2	GP		bind					ATF-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4815_s_86	12052888	(A) JDP2 binds to DRE as a heterodimer with ATF-2.	bind
6477	2	2927	5	10	NULL	NULL	NULL	statement 1	Process		bind									DRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4815_s_86	12052888	(A) JDP2 binds to DRE as a heterodimer with ATF-2.	bind
6950	1	2927	6	10	NULL	NULL	NULL	JDP2	GP		bind					ATF-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4815_s_86	12052888	(A) JDP2 binds to DRE as a heterodimer with ATF-2.	bind
6951	2	2927	6	10	NULL	NULL	NULL	statement 1	Process		forms a 					heterodimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4815_s_86	12052888	(A) JDP2 binds to DRE as a heterodimer with ATF-2.	bind
6954	3	2927	6	10	NULL	NULL	NULL	statement 2	Process		bind									DRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4815_s_86	12052888	(A) JDP2 binds to DRE as a heterodimer with ATF-2.	bind
6478	1	2929	5	10	NULL	NULL	NULL	Kalirin	GP		bind					PAM-CD/GST	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_3_629_s_129	11251076	(A) Kalirin binding to mutant PAM-CD/GST fusion proteins: CHO cells stably expressing  myc.	bind
46561	2	2929	5	10	NULL	NULL	NULL	CHO cells	Cell		express		stably			myc	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_3_629_s_129	11251076	(A) Kalirin binding to mutant PAM-CD/GST fusion proteins: CHO cells stably expressing  myc.	bind
67056	3	2929	5	10	NULL	0	NULL	PAM-CD/GST	GP		is a type of					fusion protein	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_3_629_s_129	11251076	(A) Kalirin binding to mutant PAM-CD/GST fusion proteins: CHO cells stably expressing  myc.	bind
6959	1	2929	6	10	NULL	NULL	NULL	Kalirin	GP		bind					PAM-CD/GST	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_3_629_s_129	11251076	(A) Kalirin binding to mutant PAM-CD/GST fusion proteins: CHO cells stably expressing  myc.	bind
6960	2	2929	6	10	NULL	NULL	NULL	CHO cells	Cell		express		stably			myc	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_3_629_s_129	11251076	(A) Kalirin binding to mutant PAM-CD/GST fusion proteins: CHO cells stably expressing  myc.	bind
67057	3	2929	6	10	NULL	0	NULL	PAM-CD/GST	GP		is a type of					fusion protein	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_3_629_s_129	11251076	(A) Kalirin binding to mutant PAM-CD/GST fusion proteins: CHO cells stably expressing  myc.	bind
6479	1	2930	5	10	NULL	NULL	NULL	KdgR	GP		bind					eda	GP			P2 promoter 	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_3_991_s_202	15659677	(A) KdgR binding to the  eda P2 promoter region.	bind
6961	1	2930	6	10	NULL	NULL	NULL	KdgR	GP		bind					eda	GP			P2 promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_3_991_s_202	15659677	(A) KdgR binding to the  eda P2 promoter region.	bind
6480	1	2931	5	10	NULL	NULL	NULL	P6EtG/HLA-A2	GP		bind					A6	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_4_475_s_106	11070166	(A) Kinetic data for P6EtG/HLA-A2 binding to A6.	bind
6964	1	2931	6	10	NULL	NULL	NULL	P6EtG/HLA-A2	GP		bind					A6	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_4_475_s_106	11070166	(A) Kinetic data for P6EtG/HLA-A2 binding to A6.	bind
6483	1	2933	5	10	NULL	NULL	NULL	12aa(+PO4) peptide	AminoAcid		bind					Nck	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_3_407_s_172	14757753	(A) Latex beads were coated with 12aa(+PO4), a peptide that binds human Nck; 12aa, a nonphosphorylated peptide that lacks Nck-binding  activity; or 7aa(+PO4), a peptide that binds Nck poorly ( ).	bind
6484	2	2933	5	10	NULL	NULL	NULL	12aa peptide	AminoAcid	nonphosphorylated	lacks					Nck	GP	human;;binding activity of			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_3_407_s_172	14757753	(A) Latex beads were coated with 12aa(+PO4), a peptide that binds human Nck; 12aa, a nonphosphorylated peptide that lacks Nck-binding  activity; or 7aa(+PO4), a peptide that binds Nck poorly ( ).	bind
6485	3	2933	5	10	NULL	NULL	NULL	7aa(+PO4) peptide	AminoAcid		bind		poorly			Nck	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_3_407_s_172	14757753	(A) Latex beads were coated with 12aa(+PO4), a peptide that binds human Nck; 12aa, a nonphosphorylated peptide that lacks Nck-binding  activity; or 7aa(+PO4), a peptide that binds Nck poorly ( ).	bind
6965	1	2933	6	10	NULL	NULL	NULL	 12aa(+PO4) peptide	AminoAcid		bind					Nck	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_3_407_s_172	14757753	(A) Latex beads were coated with 12aa(+PO4), a peptide that binds human Nck; 12aa, a nonphosphorylated peptide that lacks Nck-binding  activity; or 7aa(+PO4), a peptide that binds Nck poorly ( ).	bind
6966	2	2933	6	10	NULL	NULL	NULL	12aa peptide	AminoAcid	nonphosphorylated	lacks					Nck	GP	human;;binding activity of			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_3_407_s_172	14757753	(A) Latex beads were coated with 12aa(+PO4), a peptide that binds human Nck; 12aa, a nonphosphorylated peptide that lacks Nck-binding  activity; or 7aa(+PO4), a peptide that binds Nck poorly ( ).	bind
6967	3	2933	6	10	NULL	NULL	NULL	7aa(+PO4) peptide	AminoAcid		bind		poorly			Nck	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_3_407_s_172	14757753	(A) Latex beads were coated with 12aa(+PO4), a peptide that binds human Nck; 12aa, a nonphosphorylated peptide that lacks Nck-binding  activity; or 7aa(+PO4), a peptide that binds Nck poorly ( ).	bind
6481	1	2937	5	10	NULL	NULL	NULL	Ras	GP		bind					Raf-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_8_1353_s_88	12807734	(A) Levels of Ras bound  to Raf-1.	bind
6968	1	2937	6	10	NULL	NULL	NULL	Ras	GP		bind					Raf-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_8_1353_s_88	12807734	(A) Levels of Ras bound  to Raf-1.	bind
6482	1	2938	5	10	NULL	NULL	NULL	Ras	GP		bind					Raf-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_24_8_1353_s_88	12807734	(A) Levels of Ras bound to Raf-1.	bind
6969	1	2938	6	10	NULL	NULL	NULL	Ras	GP		bind					Raf-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_24_8_1353_s_88	12807734	(A) Levels of Ras bound to Raf-1.	bind
6486	1	2940	5	10	NULL	NULL	NULL	LIN-1	GP		bind					LIN-31	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_cell_93_4_569_s_101	9604932	(A) LIN-1 binds  to LIN-31 in vivo.	bind
6970	1	2940	6	10	NULL	NULL	NULL	LIN-1	GP		bind					LIN-31	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_cell_93_4_569_s_101	9604932	(A) LIN-1 binds  to LIN-31 in vivo.	bind
6488	1	2941	5	10	NULL	NULL	NULL	pAFS60 plasmid	NucleicAcid	2mum-based	carry									lac operator repeats	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4218_s_186	12024034	(A) Localization of 2mum-based plasmid pAFS60, which carries  lac operator repeats that bind GFP-Lacr fusion protein.	bind
6489	2	2941	5	10	NULL	NULL	NULL	statement 1	Process		bind					GFP-Lacr	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4218_s_186	12024034	(A) Localization of 2mum-based plasmid pAFS60, which carries  lac operator repeats that bind GFP-Lacr fusion protein.	bind
67058	3	2941	5	10	NULL	0	NULL	GFP-Lacr	GP		is a type of					fusion protein	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_12_4218_s_186	12024034	(A) Localization of 2mum-based plasmid pAFS60, which carries  lac operator repeats that bind GFP-Lacr fusion protein.	bind
6971	1	2941	6	10	NULL	NULL	NULL	plasmid pAFS60	NucleicAcid		carry									lac operator repeats	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4218_s_186	12024034	(A) Localization of 2mum-based plasmid pAFS60, which carries  lac operator repeats that bind GFP-Lacr fusion protein.	bind
6972	2	2941	6	10	NULL	NULL	NULL	statement 1	Process		bind					GFP-Lacr	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4218_s_186	12024034	(A) Localization of 2mum-based plasmid pAFS60, which carries  lac operator repeats that bind GFP-Lacr fusion protein.	bind
67059	3	2941	6	10	NULL	0	NULL	GFP-Lacr	GP		is a type of					fusion protein	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_12_4218_s_186	12024034	(A) Localization of 2mum-based plasmid pAFS60, which carries  lac operator repeats that bind GFP-Lacr fusion protein.	bind
6492	1	2942	5	10	NULL	NULL	NULL	Pan3p	GP		bind					Pab1p	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_12_5521_s_216	15169912	(A) Location in the primary  structure of Pab1p of point mutants that alter Pan3p binding to Pab1p.	bind
6493	2	2942	5	10	NULL	NULL	NULL	Pab1p	GP	point mutants	alter					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_12_5521_s_216	15169912	(A) Location in the primary  structure of Pab1p of point mutants that alter Pan3p binding to Pab1p.	bind
6973	1	2942	6	10	NULL	NULL	NULL	Pan3p	GP		bind					Pab1p	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_12_5521_s_216	15169912	(A) Location in the primary  structure of Pab1p of point mutants that alter Pan3p binding to Pab1p.	bind
6974	2	2942	6	10	NULL	NULL	NULL	Pab1p	GP	point mutant	alters					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_12_5521_s_216	15169912	(A) Location in the primary  structure of Pab1p of point mutants that alter Pan3p binding to Pab1p.	bind
7128	1	2944	5	10	NULL	NULL	NULL	IRES	GP	wild type	bind			loop between J and K domains		eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_29_18599_s_99	9660832	(A) loop between J and K domains that is bound by eIF4G in the wild type IRES is intact in this mutant (Fig.  3 A).	bind
6975	1	2944	6	10	NULL	NULL	NULL	eIF4G	GP		bind					IRES	GP	wild type	loop betweeJ and K domains		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_29_18599_s_99	9660832	(A) loop between J and K domains that is bound by eIF4G in the wild type IRES is intact in this mutant (Fig.  3 A).	bind
7129	1	2945	5	10	NULL	NULL	NULL	basal transcription	Process	low level of	in the absence of					AfaF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_227	12618452	(A) Low level of basal transcription in the absence of AfaF and alanine; GATCdist is methylated, whereas Lrp is bound to GATCprox; ClpB is bound near to the promoter region.	bind
7130	2	2945	5	10	NULL	NULL	NULL	basal transcription	Process	low level of	in the absence of								alanine		NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_227	12618452	(A) Low level of basal transcription in the absence of AfaF and alanine; GATCdist is methylated, whereas Lrp is bound to GATCprox; ClpB is bound near to the promoter region.	bind
7131	3	2945	5	10	NULL	NULL	NULL				undergoes				GATCdist	methylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_227	12618452	(A) Low level of basal transcription in the absence of AfaF and alanine; GATCdist is methylated, whereas Lrp is bound to GATCprox; ClpB is bound near to the promoter region.	bind
7132	4	2945	5	10	NULL	NULL	NULL	Lrp	GP		bind									GATCprox	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_227	12618452	(A) Low level of basal transcription in the absence of AfaF and alanine; GATCdist is methylated, whereas Lrp is bound to GATCprox; ClpB is bound near to the promoter region.	bind
7133	5	2945	5	10	NULL	NULL	NULL	ClpB	GP		bind									near to promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_227	12618452	(A) Low level of basal transcription in the absence of AfaF and alanine; GATCdist is methylated, whereas Lrp is bound to GATCprox; ClpB is bound near to the promoter region.	bind
6976	1	2945	6	10	NULL	NULL	NULL	Lrp	GP		bind									GATCprox	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_227	12618452	(A) Low level of basal transcription in the absence of AfaF and alanine; GATCdist is methylated, whereas Lrp is bound to GATCprox; ClpB is bound near to the promoter region.	bind
6977	2	2945	6	10	NULL	NULL	NULL				undergoes				GATCdist	methylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_227	12618452	(A) Low level of basal transcription in the absence of AfaF and alanine; GATCdist is methylated, whereas Lrp is bound to GATCprox; ClpB is bound near to the promoter region.	bind
6978	3	2945	6	10	NULL	NULL	NULL	ClpB	GP		bind									near to the promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_227	12618452	(A) Low level of basal transcription in the absence of AfaF and alanine; GATCdist is methylated, whereas Lrp is bound to GATCprox; ClpB is bound near to the promoter region.	bind
46562	4	2945	6	10	NULL	NULL	NULL	basal transcription	Process	low level of 	in the absence of					AfaF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_227	12618452	(A) Low level of basal transcription in the absence of AfaF and alanine; GATCdist is methylated, whereas Lrp is bound to GATCprox; ClpB is bound near to the promoter region.	bind
46563	5	2945	6	10	NULL	NULL	NULL	basal transcription	Process	low level of	in the absence of								alanine		NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_227	12618452	(A) Low level of basal transcription in the absence of AfaF and alanine; GATCdist is methylated, whereas Lrp is bound to GATCprox; ClpB is bound near to the promoter region.	bind
6494	1	2946	5	10	NULL	NULL	NULL	Fli-I	GP		bind			LRR domain		GRIP1	GP		N-terminal region		NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_5_2103_s_268	14966289	(A) LRR domain of Fli-I binds to GRIP1 N-terminal region in vitro.	bind
6979	1	2946	6	10	NULL	NULL	NULL	Fli-I	GP		bind			LRR domain		GRIP1	GP		N-terminal region		NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_5_2103_s_268	14966289	(A) LRR domain of Fli-I binds to GRIP1 N-terminal region in vitro.	bind
6495	1	2947	5	10	NULL	0	NULL		NULL		bind	NULL		Ly49C		Kb molecules	NULL				NULL	lymphoblasts	NULL	NULL	NULL	NULL	gw60_immunity_11_1_67_s_110	10435580	(A) Ly49C and Ly49I bind to Kb molecules on lymphoblasts but not appreciably to Db molecules.	bind
6499	2	2947	5	NULL	NULL	0	NULL		NULL		bind	NULL	not appreciable	Ly49C		Db molecules	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_11_1_67_s_110	10435580	(A) Ly49C and Ly49I bind to Kb molecules on lymphoblasts but not appreciably to Db molecules.	bind
6501	3	2947	5	10	NULL	0	NULL		NULL		bind	NULL		Ly49I		Kb molecules	NULL				NULL	lymphoblasts	NULL	NULL	NULL	NULL	gw60_immunity_11_1_67_s_110	10435580	(A) Ly49C and Ly49I bind to Kb molecules on lymphoblasts but not appreciably to Db molecules.	bind
6502	4	2947	5	NULL	NULL	0	NULL		NULL		bind	NULL	not appreciable	Ly49I		Db molecules	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_11_1_67_s_110	10435580	(A) Ly49C and Ly49I bind to Kb molecules on lymphoblasts but not appreciably to Db molecules.	bind
6980	1	2947	6	NULL	NULL	0	NULL		NULL		bind	NULL		Ly49C		Kb molecules	NULL				NULL	lymphoblasts	0	NULL	NULL	NULL	gw60_immunity_11_1_67_s_110	10435580	(A) Ly49C and Ly49I bind to Kb molecules on lymphoblasts but not appreciably to Db molecules.	bind
6981	2	2947	6	NULL	NULL	0	NULL		NULL		bind	NULL		Ly49I		Kb molecules	NULL				NULL	lymphoblasts	0	NULL	NULL	NULL	gw60_immunity_11_1_67_s_110	10435580	(A) Ly49C and Ly49I bind to Kb molecules on lymphoblasts but not appreciably to Db molecules.	bind
6982	3	2947	6	NULL	NULL	0	NULL		NULL		bind	NULL	not appreciably	Ly49C		Db molecules	NULL				NULL	lymphoblasts	NULL	NULL	NULL	NULL	gw60_immunity_11_1_67_s_110	10435580	(A) Ly49C and Ly49I bind to Kb molecules on lymphoblasts but not appreciably to Db molecules.	bind
6983	4	2947	6	NULL	NULL	0	NULL		NULL		bind	NULL	not appreciably	Ly49I		Db molecules	NULL				NULL	lymphoblasts	NULL	NULL	NULL	NULL	gw60_immunity_11_1_67_s_110	10435580	(A) Ly49C and Ly49I bind to Kb molecules on lymphoblasts but not appreciably to Db molecules.	bind
6506	1	2949	5	10	NULL	NULL	NULL	Mad2	GP		bind					Mad1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_2_153_s_71	16636141	(A) Mad2 binds to Mad1 and adopts the N2'' conformation.	bind
6508	2	2949	5	10	NULL	NULL	NULL	statement 1	Process		adopt					N2'' conformation					NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_2_153_s_71	16636141	(A) Mad2 binds to Mad1 and adopts the N2'' conformation.	bind
53113	3	2949	5	10	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_2_153_s_71	16636141	(A) Mad2 binds to Mad1 and adopts the N2'' conformation.	bind
6984	1	2949	6	10	NULL	NULL	NULL	Mad2	GP		bind					Mad1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_2_153_s_71	16636141	(A) Mad2 binds to Mad1 and adopts the N2'' conformation.	bind
6985	2	2949	6	10	NULL	NULL	NULL	Mad2	GP		adopts					N2'' conformation					NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_2_153_s_71	16636141	(A) Mad2 binds to Mad1 and adopts the N2'' conformation.	bind
6986	3	2949	6	10	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_2_153_s_71	16636141	(A) Mad2 binds to Mad1 and adopts the N2'' conformation.	bind
6570	1	2950	5	10	NULL	NULL	NULL	MBP	GP		bind					maltose	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_5_1225_s_19	11844750	(A) MBP binds maltose, undergoing a change from an open conformation to a closed conformation, generating a high-affinity sugar-binding site.	bind
6571	2	2950	5	10	NULL	NULL	NULL	statement 1	Process	open conformation of	changes to					statement 1	Process	closed conformation of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_5_1225_s_19	11844750	(A) MBP binds maltose, undergoing a change from an open conformation to a closed conformation, generating a high-affinity sugar-binding site.	bind
6572	3	2950	5	10	NULL	NULL	NULL	statement 2	Process		generate							high-affinity	sugar-binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_5_1225_s_19	11844750	(A) MBP binds maltose, undergoing a change from an open conformation to a closed conformation, generating a high-affinity sugar-binding site.	bind
6987	1	2950	6	10	NULL	NULL	NULL	MBP	GP		bind					maltose	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_5_1225_s_19	11844750	(A) MBP binds maltose, undergoing a change from an open conformation to a closed conformation, generating a high-affinity sugar-binding site.	bind
7026	2	2950	6	10	NULL	NULL	NULL	statement 1	Process	open conformation of	changes to					statement 1	Process	closed conformation of 			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_5_1225_s_19	11844750	(A) MBP binds maltose, undergoing a change from an open conformation to a closed conformation, generating a high-affinity sugar-binding site.	bind
7027	3	2950	6	10	NULL	NULL	NULL	statement 2	Process		generates							high-affinity	sugar binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_5_1225_s_19	11844750	(A) MBP binds maltose, undergoing a change from an open conformation to a closed conformation, generating a high-affinity sugar-binding site.	bind
6575	1	2955	5	10	NULL	NULL	NULL	MEF2	GP		bind		specifically			HRC	GP			MEF2 site	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_9_3757_s_210	15082771	(A) MEF2 binds specifically  to the HRC MEF2 site in vitro.	bind
6988	1	2955	6	10	NULL	NULL	NULL	MEF2	GP		bind		specifically			HRC	GP			MEF2 site 	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_9_3757_s_210	15082771	(A) MEF2 binds specifically  to the HRC MEF2 site in vitro.	bind
6576	1	2956	5	10	NULL	NULL	NULL	p24-32 peptide	AminoAcid		bind					H2-Dd	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_7_3829_s_152	15213124	(A) MHC class I stabilization assay indicated that the p24-32 peptide binds to H2-Dd.	bind
6989	1	2956	6	10	NULL	NULL	NULL	p24-32 peptide	AminoAcid		bind					H2-Dd	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_7_3829_s_152	15213124	(A) MHC class I stabilization assay indicated that the p24-32 peptide binds to H2-Dd.	bind
6578	1	2957	5	10	NULL	NULL	NULL	Mig6	GP		bind					Grb2	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_2_337_s_226	16247031	(A) Mig6 binds Grb2.	bind
6990	1	2957	6	10	NULL	NULL	NULL	Mig6	GP		bind					Grb2	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_2_337_s_226	16247031	(A) Mig6 binds Grb2.	bind
6579	1	2958	5	10	NULL	NULL	NULL	GRB2	GP	cotransfected	bind					p27	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_11_3735_s_179	12748278	(A) Mitogen stimulation enhances binding of cotransfected GRB2  and p27.	bind
6582	2	2958	5	10	NULL	NULL	NULL	mitogen	Chemical	stimulation	enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_11_3735_s_179	12748278	(A) Mitogen stimulation enhances binding of cotransfected GRB2  and p27.	bind
6991	1	2958	6	10	NULL	NULL	NULL	Grb2	GP		bind					p27	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_11_3735_s_179	12748278	(A) Mitogen stimulation enhances binding of cotransfected GRB2  and p27.	bind
6992	2	2958	6	10	NULL	NULL	NULL	mitogen	Chemical	stimulation of	enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_11_3735_s_179	12748278	(A) Mitogen stimulation enhances binding of cotransfected GRB2  and p27.	bind
6586	1	2960	5	10	NULL	NULL	NULL	Mlc1p	GP		bind					Myo1p	GP		IQ1		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_165_6_843_s_126	15210731	(A) Mlc1p binds to Myo1p through IQ1.	bind
6993	1	2960	6	10	NULL	NULL	NULL	Mlc1p	GP		bind					Myo1p	GP		IQ1		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_165_6_843_s_126	15210731	(A) Mlc1p binds to Myo1p through IQ1.	bind
6589	1	2961	5	10	NULL	NULL	NULL	MoB34	GP	purified from mouse ascites fluid	bind		dose dependently			NMGB bacteria	Organism				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6399_s_209	16177311	(A) MoB34 purified from mouse ascites fluid bound to NMGB bacteria in dose-dependent  manner.	bind
6994	1	2961	6	10	NULL	NULL	NULL	MoB34	GP	purified from mouse ascites	bind		dose dependently			NMGB bacteria	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6399_s_209	16177311	(A) MoB34 purified from mouse ascites fluid bound to NMGB bacteria in dose-dependent  manner.	bind
6592	1	2962	5	10	NULL	NULL	NULL	CRP	GP	E. coli	bind			recognition helix		DNA	NucleicAcid			half-side consensus sequence	NULL		NULL	NULL	NULL	NULL	gw70_febslett_571_1_154_s_175	15280034	(A) Mode  of binding between the recognition helix of  E. coli CRP and the half-side consensus DNA sequence.	bind
6996	1	2962	6	10	NULL	NULL	NULL	CRP	GP	E.coli	bind			recognition helix		DNA	NucleicAcid			half side consensus	NULL		NULL	NULL	NULL	NULL	gw70_febslett_571_1_154_s_175	15280034	(A) Mode  of binding between the recognition helix of  E. coli CRP and the half-side consensus DNA sequence.	bind
6597	1	2963	5	10	NULL	NULL	NULL	phosphoserine-proline dipeptide	AminoAcid		bind					Pin1	GP		active site		NULL		NULL	NULL	NULL	NULL	gw60_cell_89_6_875_s_168	9200606	(A) Model for a phosphoserine-proline dipeptide bound to Pin1's active site.	bind
6997	1	2963	6	10	NULL	NULL	NULL	phosphoserine-proline dipeptide	AminoAcid		bind					Pin1	GP		active site		NULL		NULL	NULL	NULL	NULL	gw60_cell_89_6_875_s_168	9200606	(A) Model for a phosphoserine-proline dipeptide bound to Pin1's active site.	bind
6599	1	2965	5	10	NULL	NULL	NULL	 9G11	GP		bind					CD31	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_5_316_s_124	9115397	(a) Monoclonal antibody 9G11 binding to CD31;  (b) rabbit polyclonal antibodies binding to P-selectin;  (c) monoclonal antibody 15.2 binding to ICAM-1.	bind
6601	2	2965	5	10	NULL	NULL	NULL	polyclonal antibodies	GP	rabbit	bind					P-selectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_5_316_s_124	9115397	(a) Monoclonal antibody 9G11 binding to CD31;  (b) rabbit polyclonal antibodies binding to P-selectin;  (c) monoclonal antibody 15.2 binding to ICAM-1.	bind
6602	3	2965	5	10	NULL	NULL	NULL	monoclonal antibody 15.2	GP		bind					ICAM-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_5_316_s_124	9115397	(a) Monoclonal antibody 9G11 binding to CD31;  (b) rabbit polyclonal antibodies binding to P-selectin;  (c) monoclonal antibody 15.2 binding to ICAM-1.	bind
53114	4	2965	5	10	NULL	NULL	NULL	9G11	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_5_316_s_124	9115397	(a) Monoclonal antibody 9G11 binding to CD31;  (b) rabbit polyclonal antibodies binding to P-selectin;  (c) monoclonal antibody 15.2 binding to ICAM-1.	bind
6998	1	2965	6	10	NULL	NULL	NULL	 9G11	GP		bind					CD31	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_5_316_s_124	9115397	(a) Monoclonal antibody 9G11 binding to CD31;  (b) rabbit polyclonal antibodies binding to P-selectin;  (c) monoclonal antibody 15.2 binding to ICAM-1.	bind
6999	2	2965	6	10	NULL	NULL	NULL	polyclonal antibodies	GP	rabbit	bind					P-selectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_5_316_s_124	9115397	(a) Monoclonal antibody 9G11 binding to CD31;  (b) rabbit polyclonal antibodies binding to P-selectin;  (c) monoclonal antibody 15.2 binding to ICAM-1.	bind
7000	3	2965	6	10	NULL	NULL	NULL	monoclonal antibody 15.2	GP		bind					ICAM-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_5_316_s_124	9115397	(a) Monoclonal antibody 9G11 binding to CD31;  (b) rabbit polyclonal antibodies binding to P-selectin;  (c) monoclonal antibody 15.2 binding to ICAM-1.	bind
53115	4	2965	6	10	NULL	NULL	NULL	9G11	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_5_316_s_124	9115397	(a) Monoclonal antibody 9G11 binding to CD31;  (b) rabbit polyclonal antibodies binding to P-selectin;  (c) monoclonal antibody 15.2 binding to ICAM-1.	bind
6606	1	2966	5	10	NULL	NULL	NULL	chromomycin A3	Chemical		bind		preferentially					viral		CRE flanking sequences	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_721_s_224	9447968	(A) MPE:Fe footprinting shows that chromomycin A3 binds preferentially to the viral CRE flanking sequences.	bind
7001	1	2966	6	10	NULL	NULL	NULL	chromomycin A3	Chemical		bind		preferentially					viral		CRE flanking sequences	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_721_s_224	9447968	(A) MPE:Fe footprinting shows that chromomycin A3 binds preferentially to the viral CRE flanking sequences.	bind
6607	1	2967	5	10	NULL	NULL	NULL	Munc13-1	GP		bind					RIM1	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_30_1_183_s_140	11343654	(A) Munc13-1 and Rab3A binding to RIM1 is mutually exclusive.	bind
6608	2	2967	5	10	NULL	NULL	NULL	Rab3A	GP		bind					RIM1	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_30_1_183_s_140	11343654	(A) Munc13-1 and Rab3A binding to RIM1 is mutually exclusive.	bind
6609	3	2967	5	10	NULL	NULL	NULL	statement 1	Process		mutually exclusive to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_30_1_183_s_140	11343654	(A) Munc13-1 and Rab3A binding to RIM1 is mutually exclusive.	bind
7002	1	2967	6	10	NULL	NULL	NULL	Munc13-1	GP		bind					RIM1	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_30_1_183_s_140	11343654	(A) Munc13-1 and Rab3A binding to RIM1 is mutually exclusive.	bind
7003	2	2967	6	10	NULL	NULL	NULL	Rab3A	GP		bind					RIM1	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_30_1_183_s_140	11343654	(A) Munc13-1 and Rab3A binding to RIM1 is mutually exclusive.	bind
7004	3	2967	6	10	NULL	NULL	NULL	statement 1	Process		is independent of					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_30_1_183_s_140	11343654	(A) Munc13-1 and Rab3A binding to RIM1 is mutually exclusive.	bind
6610	1	2968	5	10	NULL	NULL	NULL	poly-L-proline	AminoAcid		bind							mutant	Y5A		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
6614	2	2968	5	10	NULL	NULL	NULL	poly-L-proline	AminoAcid		bind							mutant	Y5D		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
6616	3	2968	5	10	NULL	NULL	NULL	poly-L-proline	AminoAcid		bind							mutant	Y120D		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
6619	4	2968	5	10	NULL	NULL	NULL	poly-L-proline	AminoAcid		bind							mutant	Y120A		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
6620	5	2968	5	10	NULL	NULL	NULL	poly-L-proline	AminoAcid		bind							mutant	Y126D		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
6625	6	2968	5	10	NULL	NULL	NULL	actin	GP		bind							mutant	Y79R		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
6626	7	2968	5	10	NULL	NULL	NULL	actin	GP		bind							mutant	K81E		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
6627	8	2968	5	10	NULL	NULL	NULL	actin	GP		bind							mutant	K81Y		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
6628	9	2968	5	10	NULL	NULL	NULL	actin	GP		bind							mutant	P107Y		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
6629	10	2968	5	10	NULL	NULL	NULL	actin	GP		bind							mutant	A111E		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
7005	1	2968	6	10	NULL	NULL	NULL	poly-L-proline	AminoAcid		bind							mutant	Y5A		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
7006	2	2968	6	10	NULL	NULL	NULL	poly-L-proline	AminoAcid		bind							mutant	Y5D		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
7007	3	2968	6	10	NULL	NULL	NULL	poly-L-proline	AminoAcid		bind							mutant	Y120A		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
7008	4	2968	6	10	NULL	NULL	NULL	poly-L-proline	AminoAcid		bind							mutant	Y126D		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
7009	5	2968	6	10	NULL	NULL	NULL	actin	GP		bind							mutant	Y79R		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
7010	6	2968	6	10	NULL	NULL	NULL	actin	GP		bind							mutant	K81E		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
7011	7	2968	6	10	NULL	NULL	NULL	actin	GP		bind							mutant	K81Y		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
7012	8	2968	6	10	NULL	NULL	NULL	actin	GP		bind							mutant	P107Y (+)		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
7013	9	2968	6	10	NULL	NULL	NULL	actin	GP		bind							mutant	A111E		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
46577	10	2968	6	10	NULL	NULL	NULL	 poly-L-proline	AminoAcid		bind							mutant	Y120D		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_198	11294914	(A) Mutants that are equal to or more stable than C89S ( ) were considered as stable, including poly-L-proline binding mutants Y5A ( ), Y5D ( ), Y120D ( ), Y120A ( ), Y126D ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107Y (+), A111E ( ), and wild-type profilin ( ).	bind
6630	1	2970	5	10	NULL	NULL	NULL	PICK1	GP		bind					GluR2	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_80	11931741	(A) Mutations in the  NSF binding region  reduce PICK1 binding to GluR2.	bind
6631	2	2970	5	10	NULL	NULL	NULL			mutation in	reduce			NSF binding region		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_80	11931741	(A) Mutations in the  NSF binding region  reduce PICK1 binding to GluR2.	bind
7014	1	2970	6	10	NULL	NULL	NULL	PICK1	GP		bind					GluR2	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_80	11931741	(A) Mutations in the  NSF binding region  reduce PICK1 binding to GluR2.	bind
7015	2	2970	6	10	NULL	NULL	NULL			mutant	reduce			NSF binding region		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_80	11931741	(A) Mutations in the  NSF binding region  reduce PICK1 binding to GluR2.	bind
6632	1	2972	5	10	NULL	NULL	NULL	MutS/MutL	GP		bind					Sb-G/C-bS	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_233_s_146	12887908	(A) MutS/MutL binding to biotin-streptavidin double blocked-end G/C control DNA (Sb-G/C-bS).	bind
6633	2	2972	5	10	NULL	NULL	NULL	Sb-G/C-bS	NucleicAcid		is					biotin-streptavidin double blocked-end G/C control DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_233_s_146	12887908	(A) MutS/MutL binding to biotin-streptavidin double blocked-end G/C control DNA (Sb-G/C-bS).	bind
7016	1	2972	6	10	NULL	NULL	NULL	MutS/MutL	GP		bind					Sb-G/C-bS	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_233_s_146	12887908	(A) MutS/MutL binding to biotin-streptavidin double blocked-end G/C control DNA (Sb-G/C-bS).	bind
46578	2	2972	6	10	NULL	NULL	NULL	Sb-G/C-bS	NucleicAcid		is					 biotin-streptavidin double blocked-end G/C control DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_233_s_146	12887908	(A) MutS/MutL binding to biotin-streptavidin double blocked-end G/C control DNA (Sb-G/C-bS).	bind
6634	1	2973	5	10	NULL	NULL	NULL	NFATp	GP		bind					TNF-alpha	GP			shared sites in promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2620_s_119	11909956	(A) Mutually exclusive binding of NFATp and Sp1 to shared sites in the TNF-alpha promoter.	bind
6635	2	2973	5	10	NULL	NULL	NULL	Sp1	GP		bind					TNF-alpha	GP			shared sites in promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2620_s_119	11909956	(A) Mutually exclusive binding of NFATp and Sp1 to shared sites in the TNF-alpha promoter.	bind
6636	3	2973	5	10	NULL	NULL	NULL	statement 1	Process		mutually exclusive to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2620_s_119	11909956	(A) Mutually exclusive binding of NFATp and Sp1 to shared sites in the TNF-alpha promoter.	bind
7017	1	2973	6	10	NULL	NULL	NULL	NFATp	GP		bind					TNF-alpha	GP			shared site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2620_s_119	11909956	(A) Mutually exclusive binding of NFATp and Sp1 to shared sites in the TNF-alpha promoter.	bind
7018	2	2973	6	10	NULL	NULL	NULL	Sp1	GP		bind					TNF-alpha	GP			shared site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2620_s_119	11909956	(A) Mutually exclusive binding of NFATp and Sp1 to shared sites in the TNF-alpha promoter.	bind
7019	3	2973	6	10	NULL	NULL	NULL	statement 1	Process		is mutually exclusive to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2620_s_119	11909956	(A) Mutually exclusive binding of NFATp and Sp1 to shared sites in the TNF-alpha promoter.	bind
6637	1	2974	5	10	NULL	NULL	NULL	VDR	GP		bind					GM550	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4191_s_138	10330159	(A) Mutually exclusive binding of VDR and NFATXS to GM550.	bind
6638	2	2974	5	10	NULL	NULL	NULL	NFATXS	GP		bind					GM550	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4191_s_138	10330159	(A) Mutually exclusive binding of VDR and NFATXS to GM550.	bind
6639	3	2974	5	10	NULL	NULL	NULL	statement 1	Process		mutually exclusive to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4191_s_138	10330159	(A) Mutually exclusive binding of VDR and NFATXS to GM550.	bind
7028	1	2974	6	10	NULL	NULL	NULL	VDR	GP		bind					GM550	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4191_s_138	10330159	(A) Mutually exclusive binding of VDR and NFATXS to GM550.	bind
7029	2	2974	6	10	NULL	NULL	NULL	NFATXS	GP		bind					GM550	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4191_s_138	10330159	(A) Mutually exclusive binding of VDR and NFATXS to GM550.	bind
7030	3	2974	6	10	NULL	NULL	NULL	statement 1	Process		is mutually exclusive to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4191_s_138	10330159	(A) Mutually exclusive binding of VDR and NFATXS to GM550.	bind
6640	1	2975	5	10	NULL	NULL	NULL				bind			 N1-47		NusA	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_114	9659923	(A) N1-47 binds NusA.	bind
7031	1	2975	6	10	NULL	NULL	NULL				bind			N1-47		NusA	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_265_s_114	9659923	(A) N1-47 binds NusA.	bind
6641	1	2976	5	10	NULL	NULL	NULL	N2N	GP		bind		directly			NE	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_1_58_s_196	14673143	(A) N2N directly binds  to NE in GST pull-down assays.	bind
7032	1	2976	6	10	NULL	NULL	NULL	N2N	GP		bind		directly			NE	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_1_58_s_196	14673143	(A) N2N directly binds  to NE in GST pull-down assays.	bind
6642	1	2977	5	10	NULL	NULL	NULL	NC2alpha	GP		bind					DNA	NucleicAcid			B-TFIID	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_22_10072_s_225	15509807	(A) NC2alpha binds to both B-TFIID and TBP on DNA.	bind
6643	2	2977	5	10	NULL	NULL	NULL	NC2alpha	GP		bind					DNA	NucleicAcid			TBP	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_22_10072_s_225	15509807	(A) NC2alpha binds to both B-TFIID and TBP on DNA.	bind
7033	1	2977	6	10	NULL	NULL	NULL	NC2alpha	GP		bind					DNA	NucleicAcid			B-TFIID site	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_22_10072_s_225	15509807	(A) NC2alpha binds to both B-TFIID and TBP on DNA.	bind
7034	2	2977	6	10	NULL	NULL	NULL	NC2alpha	GP		bind					DNA	NucleicAcid			TBP site	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_22_10072_s_225	15509807	(A) NC2alpha binds to both B-TFIID and TBP on DNA.	bind
6644	1	2978	5	10	NULL	NULL	NULL	Nck	GP		bind					CD3	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_41	12110186	(A) Nck binds to CD3  but not to other CD3 subunits.	bind
6645	2	2978	5	10	NULL	NULL	NULL	Nck	GP		does not bind					CD3	GP		other subunits of		NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_41	12110186	(A) Nck binds to CD3  but not to other CD3 subunits.	bind
7035	1	2978	6	10	NULL	NULL	NULL	Nck	GP		bind					CD3	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_41	12110186	(A) Nck binds to CD3  but not to other CD3 subunits.	bind
7036	2	2978	6	10	NULL	NULL	NULL	Nck	GP		does not bind					CD3 	GP		subunits		NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_41	12110186	(A) Nck binds to CD3  but not to other CD3 subunits.	bind
6646	1	2979	5	10	NULL	NULL	NULL	NE proteins	GP		bind					A3 RNA	NucleicAcid	biotinylated			NULL		NULL	NULL	NULL	NULL	gw60_cell_93_1_139_s_84	9546399	(A) NE proteins  bound to biotinylated A3 or S3 RNA were analyzed by Western blot  with anti-Tra2 antibodies (lanes 1 - 4) or mAb104 (lanes 5 - 8) before (-) or after (+) treatment with  CIP.	bind
6647	2	2979	5	10	NULL	NULL	NULL	NE proteins	GP		bind					S3 RNA	NucleicAcid	biotinylated			NULL		NULL	NULL	NULL	NULL	gw60_cell_93_1_139_s_84	9546399	(A) NE proteins  bound to biotinylated A3 or S3 RNA were analyzed by Western blot  with anti-Tra2 antibodies (lanes 1 - 4) or mAb104 (lanes 5 - 8) before (-) or after (+) treatment with  CIP.	bind
46580	3	2979	5	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_93_1_139_s_84	9546399	(A) NE proteins  bound to biotinylated A3 or S3 RNA were analyzed by Western blot  with anti-Tra2 antibodies (lanes 1 - 4) or mAb104 (lanes 5 - 8) before (-) or after (+) treatment with  CIP.	bind
7037	1	2979	6	10	NULL	NULL	NULL	NE proteins	GP		bind					A3 RNA	NucleicAcid	biotinylated			NULL		NULL	NULL	NULL	NULL	gw60_cell_93_1_139_s_84	9546399	(A) NE proteins  bound to biotinylated A3 or S3 RNA were analyzed by Western blot  with anti-Tra2 antibodies (lanes 1 - 4) or mAb104 (lanes 5 - 8) before (-) or after (+) treatment with  CIP.	bind
7038	2	2979	6	10	NULL	NULL	NULL	NE proteins	GP		bind					S3 RNA	NucleicAcid	biotinylated			NULL		NULL	NULL	NULL	NULL	gw60_cell_93_1_139_s_84	9546399	(A) NE proteins  bound to biotinylated A3 or S3 RNA were analyzed by Western blot  with anti-Tra2 antibodies (lanes 1 - 4) or mAb104 (lanes 5 - 8) before (-) or after (+) treatment with  CIP.	bind
7039	3	2979	6	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_93_1_139_s_84	9546399	(A) NE proteins  bound to biotinylated A3 or S3 RNA were analyzed by Western blot  with anti-Tra2 antibodies (lanes 1 - 4) or mAb104 (lanes 5 - 8) before (-) or after (+) treatment with  CIP.	bind
6648	1	2980	5	10	NULL	NULL	NULL	Nef	GP		bind					MHC-I	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_2_548_s_178	16760313	(A) Nef binds to MHC-I  early in the secretory pathway.	bind
6649	2	2980	5	10	NULL	NULL	NULL	statement 1	Process		occur					secretory pathway	Process	early in 			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_2_548_s_178	16760313	(A) Nef binds to MHC-I  early in the secretory pathway.	bind
7040	1	2980	6	10	NULL	NULL	NULL	Nef	GP		bind					MHC-I	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_2_548_s_178	16760313	(A) Nef binds to MHC-I  early in the secretory pathway.	bind
7041	2	2980	6	10	NULL	NULL	NULL	statement 1	Process		occurs 					secretory pathway	Process	early in			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_2_548_s_178	16760313	(A) Nef binds to MHC-I  early in the secretory pathway.	bind
6650	1	2981	5	10	NULL	NULL	NULL	Smc2p	GP		bind					chromosome VI	Chromosome			replication origins	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7216_s_120	16055730	(A) Negative  correlation between Smc2p and ORC complex binding at chromosome (Chr.) VI replication  origins.	bind
6651	2	2981	5	10	NULL	NULL	NULL	ORC complex	GP		bind					chromosome  VI	Chromosome			replication origins	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7216_s_120	16055730	(A) Negative  correlation between Smc2p and ORC complex binding at chromosome (Chr.) VI replication  origins.	bind
7042	1	2981	6	10	NULL	NULL	NULL	Smc2p	GP		bind					chromosome VI 	Chromosome			replication origins	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7216_s_120	16055730	(A) Negative  correlation between Smc2p and ORC complex binding at chromosome (Chr.) VI replication  origins.	bind
7043	2	2981	6	10	NULL	NULL	NULL	ORC complex	GP		bind					chromosome VI 	Chromosome			replication origins	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7216_s_120	16055730	(A) Negative  correlation between Smc2p and ORC complex binding at chromosome (Chr.) VI replication  origins.	bind
6652	1	2982	5	10	NULL	NULL	NULL	LDL	Chemical		bind		specifically			mSR-AI	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_105	10191300	(A) Net specific binding activity of LDL to mSR-AI mediated by peptide V.	bind
6653	2	2982	5	10	NULL	NULL	NULL	statement 1	Process		is mediated by					peptide V	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_105	10191300	(A) Net specific binding activity of LDL to mSR-AI mediated by peptide V.	bind
7044	1	2982	6	10	NULL	NULL	NULL	LDL	Chemical		bind		specifically			mSR-AI	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_105	10191300	(A) Net specific binding activity of LDL to mSR-AI mediated by peptide V.	bind
7045	2	2982	6	10	NULL	NULL	NULL	statement 1	Process		is mediated by					peptide V	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_105	10191300	(A) Net specific binding activity of LDL to mSR-AI mediated by peptide V.	bind
7135	1	2983	5	10	NULL	NULL	NULL	CTX	GP		bind		specifically			GM1	Chemical				NULL	Neuro2a cells	NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_157_s_161	12370242	(A) Neuro2a cells transfected with a GFRalpha1 construct were Triton-extracted and fixed with 4% PFA before staining with an antibody to GFRalpha1 and cholera toxin (CTX), which specifically binds to the lipid raft ganglioside GM1.	bind
7136	2	2983	5	10	NULL	NULL	NULL	CTX	GP		is					cholera toxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_157_s_161	12370242	(A) Neuro2a cells transfected with a GFRalpha1 construct were Triton-extracted and fixed with 4% PFA before staining with an antibody to GFRalpha1 and cholera toxin (CTX), which specifically binds to the lipid raft ganglioside GM1.	bind
7137	3	2983	5	10	NULL	NULL	NULL	GFRalpha1	GP		bind		specifically			GM1	Chemical				NULL	Neuro2a cells	NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_157_s_161	12370242	(A) Neuro2a cells transfected with a GFRalpha1 construct were Triton-extracted and fixed with 4% PFA before staining with an antibody to GFRalpha1 and cholera toxin (CTX), which specifically binds to the lipid raft ganglioside GM1.	bind
46584	4	2983	5	10	NULL	NULL	NULL	GM1	Chemical		is a type of					lipid raft ganglioside	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_157_s_161	12370242	(A) Neuro2a cells transfected with a GFRalpha1 construct were Triton-extracted and fixed with 4% PFA before staining with an antibody to GFRalpha1 and cholera toxin (CTX), which specifically binds to the lipid raft ganglioside GM1.	bind
7046	1	2983	6	10	NULL	NULL	NULL	GM1	Chemical		is a type of					lipid raft ganglioside	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_157_s_161	12370242	(A) Neuro2a cells transfected with a GFRalpha1 construct were Triton-extracted and fixed with 4% PFA before staining with an antibody to GFRalpha1 and cholera toxin (CTX), which specifically binds to the lipid raft ganglioside GM1.	bind
7047	2	2983	6	10	NULL	NULL	NULL	GFRalpha1	GP		bind		specifically			GM1	Chemical				NULL	Neuro2a cells	NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_157_s_161	12370242	(A) Neuro2a cells transfected with a GFRalpha1 construct were Triton-extracted and fixed with 4% PFA before staining with an antibody to GFRalpha1 and cholera toxin (CTX), which specifically binds to the lipid raft ganglioside GM1.	bind
7048	3	2983	6	10	NULL	NULL	NULL	Cholera toxin	GP		bind		specifically			GM1	Chemical				NULL	Neuro2a cells	NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_157_s_161	12370242	(A) Neuro2a cells transfected with a GFRalpha1 construct were Triton-extracted and fixed with 4% PFA before staining with an antibody to GFRalpha1 and cholera toxin (CTX), which specifically binds to the lipid raft ganglioside GM1.	bind
7049	4	2983	6	10	NULL	NULL	NULL	CTX	GP		is					cholera toxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_157_s_161	12370242	(A) Neuro2a cells transfected with a GFRalpha1 construct were Triton-extracted and fixed with 4% PFA before staining with an antibody to GFRalpha1 and cholera toxin (CTX), which specifically binds to the lipid raft ganglioside GM1.	bind
6654	1	2986	5	10	NULL	NULL	NULL	NG2	GP		bind					EC surface	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_8_3580_s_128	15181153	(A) NG2 binding to the EC surface.	bind
7050	1	2986	6	10	NULL	NULL	NULL	NG2	GP		bind					EC surface	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_8_3580_s_128	15181153	(A) NG2 binding to the EC surface.	bind
6655	1	2987	5	10	NULL	NULL	NULL	VCAM-1	GP	soluble	bind					T cells	Cell	activated			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_509_s_107	11980922	(A) NH2-terminal regions of TSP1 and TSP2 inhibit binding of soluble VCAM-1 to activated T cells.	bind
6656	2	2987	5	10	NULL	NULL	NULL	TSP1	GP		inhibit			NH2-terminal region		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_509_s_107	11980922	(A) NH2-terminal regions of TSP1 and TSP2 inhibit binding of soluble VCAM-1 to activated T cells.	bind
6657	3	2987	5	10	NULL	NULL	NULL	TSP2	GP		inhibit			NH2-terminal region		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_509_s_107	11980922	(A) NH2-terminal regions of TSP1 and TSP2 inhibit binding of soluble VCAM-1 to activated T cells.	bind
7051	1	2987	6	10	NULL	NULL	NULL	VCAM-1	GP	soluble	bind					T cells	Cell	activated			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_509_s_107	11980922	(A) NH2-terminal regions of TSP1 and TSP2 inhibit binding of soluble VCAM-1 to activated T cells.	bind
7052	2	2987	6	10	NULL	NULL	NULL	TSP1	GP		inhibit			NH2-terminus		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_509_s_107	11980922	(A) NH2-terminal regions of TSP1 and TSP2 inhibit binding of soluble VCAM-1 to activated T cells.	bind
7053	3	2987	6	10	NULL	NULL	NULL	TSP2	GP		inhibit			NH2-terminus		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_509_s_107	11980922	(A) NH2-terminal regions of TSP1 and TSP2 inhibit binding of soluble VCAM-1 to activated T cells.	bind
6658	1	2989	5	10	NULL	NULL	NULL	LdTOP1L	GP		bind					LdTOP1S	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_565_1_81_s_184	15135057	(A) Ni2+-NTA agarose co-immobilization binding between LdTOP1L and LdTOP1S.	bind
7054	1	2989	6	10	NULL	NULL	NULL	LdTOP1L	GP		bind					LdTOP1S	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_565_1_81_s_184	15135057	(A) Ni2+-NTA agarose co-immobilization binding between LdTOP1L and LdTOP1S.	bind
7138	1	2991	5	10	NULL	NULL	NULL				mediate			NLS		NRK cells	Cell	import in			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_2_411_s_119	11266456	(A) NLS-mediated import in NRK cells; (B) the solubilization of Nup358 and Nup153 (left) and the association of importin beta with these Nups (right); and (C) the binding of importin beta to GST-Nup62.	bind
7141	4	2991	5	10	NULL	NULL	NULL	importin beta	GP		associate with					Nup358	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_2_411_s_119	11266456	(A) NLS-mediated import in NRK cells; (B) the solubilization of Nup358 and Nup153 (left) and the association of importin beta with these Nups (right); and (C) the binding of importin beta to GST-Nup62.	bind
7142	5	2991	5	10	NULL	NULL	NULL	importin beta	GP		associate with					Nup153	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_2_411_s_119	11266456	(A) NLS-mediated import in NRK cells; (B) the solubilization of Nup358 and Nup153 (left) and the association of importin beta with these Nups (right); and (C) the binding of importin beta to GST-Nup62.	bind
7143	6	2991	5	10	NULL	NULL	NULL	importin beta	GP		bind					GST-Nup62	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_2_411_s_119	11266456	(A) NLS-mediated import in NRK cells; (B) the solubilization of Nup358 and Nup153 (left) and the association of importin beta with these Nups (right); and (C) the binding of importin beta to GST-Nup62.	bind
7251	1	2991	6	10	NULL	NULL	NULL				mediates			NLS		NRK cells	Cell	import in			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_2_411_s_119	11266456	(A) NLS-mediated import in NRK cells; (B) the solubilization of Nup358 and Nup153 (left) and the association of importin beta with these Nups (right); and (C) the binding of importin beta to GST-Nup62.	bind
7252	2	2991	6	10	NULL	NULL	NULL	importin beta	GP		associates					Nup358	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_2_411_s_119	11266456	(A) NLS-mediated import in NRK cells; (B) the solubilization of Nup358 and Nup153 (left) and the association of importin beta with these Nups (right); and (C) the binding of importin beta to GST-Nup62.	bind
7253	3	2991	6	10	NULL	NULL	NULL	importin beta	GP		associates					Nup153	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_2_411_s_119	11266456	(A) NLS-mediated import in NRK cells; (B) the solubilization of Nup358 and Nup153 (left) and the association of importin beta with these Nups (right); and (C) the binding of importin beta to GST-Nup62.	bind
7254	4	2991	6	10	NULL	NULL	NULL	importin beta	GP		bind					GST-Nup62	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_2_411_s_119	11266456	(A) NLS-mediated import in NRK cells; (B) the solubilization of Nup358 and Nup153 (left) and the association of importin beta with these Nups (right); and (C) the binding of importin beta to GST-Nup62.	bind
6659	2	2992	5	10	NULL	NULL	NULL	Nmd3p	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3405_s_187	11313466	(A) Nmd3p binds to GST-tagged Rpl10p when expressed in  E. coli.	bind
53116	1	2992	5	10	NULL	NULL	NULL	Rpl10p	GP	GST-tagged	is expressed in					E.coli	Cell				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3405_s_187	11313466	(A) Nmd3p binds to GST-tagged Rpl10p when expressed in  E. coli.	bind
7055	1	2992	6	10	NULL	NULL	NULL	Rpl10p	GP	GST-tagged	expressed in					E.coli	Cell				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3405_s_187	11313466	(A) Nmd3p binds to GST-tagged Rpl10p when expressed in  E. coli.	bind
7056	2	2992	6	10	NULL	NULL	NULL	Nmd3p	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3405_s_187	11313466	(A) Nmd3p binds to GST-tagged Rpl10p when expressed in  E. coli.	bind
6660	1	2993	5	10	NULL	NULL	NULL	Nmd5p	GP		bind					GST - Crz1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_951_s_108	11535618	(A) Nmd5p binding to Crz1p is disrupted by Gsp1p - GTP. 5 mug GST - Crz1p was bound to glutathione resin and incubated with 5 mug thrombin-cleaved Nmd5p.	bind
6661	2	2993	5	10	NULL	NULL	NULL	Gsp1p - GTP	GP		disrupt					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_951_s_108	11535618	(A) Nmd5p binding to Crz1p is disrupted by Gsp1p - GTP. 5 mug GST - Crz1p was bound to glutathione resin and incubated with 5 mug thrombin-cleaved Nmd5p.	bind
7057	1	2993	6	10	NULL	NULL	NULL	Nmd5p	GP		bind					GST - Crz1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_951_s_108	11535618	(A) Nmd5p binding to Crz1p is disrupted by Gsp1p - GTP. 5 mug GST - Crz1p was bound to glutathione resin and incubated with 5 mug thrombin-cleaved Nmd5p.	bind
7058	2	2993	6	10	NULL	NULL	NULL	Gsp1p - GTP	GP		disrupts					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_951_s_108	11535618	(A) Nmd5p binding to Crz1p is disrupted by Gsp1p - GTP. 5 mug GST - Crz1p was bound to glutathione resin and incubated with 5 mug thrombin-cleaved Nmd5p.	bind
6663	1	2994	5	10	NULL	NULL	NULL	Nocodazole	Chemical		does not depolymerize					CPP MTs	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_349_s_160	12719474	(A) Nocodazole does not depolymerize CPP MTs in our assay.	bind
7059	1	2994	6	10	NULL	NULL	NULL	Nocodazole	Chemical		does not depolymerize					CPP MTs	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_349_s_160	12719474	(A) Nocodazole does not depolymerize CPP MTs in our assay.	bind
7144	1	2995	5	10	NULL	NULL	NULL	M21 cell extracts 		normoxic	bind					HSR probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_2_469_s_219	9450968	(A) Normoxic (N) and hypoxic (H) M21 cell extracts bound to the 3  HSR probe were subjected to UV-cross-linking/Nase treatment and analyzed by reducing SDS-PAGE.	bind
7145	2	2995	5	10	NULL	NULL	NULL	M21 cell extracts		hypoxic	bind					HSR probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_2_469_s_219	9450968	(A) Normoxic (N) and hypoxic (H) M21 cell extracts bound to the 3  HSR probe were subjected to UV-cross-linking/Nase treatment and analyzed by reducing SDS-PAGE.	bind
7060	1	2995	6	10	NULL	NULL	NULL	M21 cell extracts		Normoxic	bind					HSR probe	NucleicAcid			site	NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_2_469_s_219	9450968	(A) Normoxic (N) and hypoxic (H) M21 cell extracts bound to the 3  HSR probe were subjected to UV-cross-linking/Nase treatment and analyzed by reducing SDS-PAGE.	bind
7061	2	2995	6	10	NULL	NULL	NULL	M21 cell extracts		hypoxic	bind					HSR probe	NucleicAcid			site	NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_2_469_s_219	9450968	(A) Normoxic (N) and hypoxic (H) M21 cell extracts bound to the 3  HSR probe were subjected to UV-cross-linking/Nase treatment and analyzed by reducing SDS-PAGE.	bind
6665	1	2996	5	10	NULL	NULL	NULL	[35]GTP S 	Chemical		bind					MBP-T43NTR-G 	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_100	11287004	(A) NT-induced [35]GTP S binding to  E. coli membrane-inserted MBP-T43NTR-G  fusion proteins or to homogenates of transfected CHO-NTR cells expressing the rat NTR.	bind
6666	2	2996	5	10	NULL	NULL	NULL	NT	GP		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_100	11287004	(A) NT-induced [35]GTP S binding to  E. coli membrane-inserted MBP-T43NTR-G  fusion proteins or to homogenates of transfected CHO-NTR cells expressing the rat NTR.	bind
6667	3	2996	5	10	NULL	NULL	NULL	CHO-NTR cells	Cell	homogenates of transfected	express					NTR	GP	rat			NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_100	11287004	(A) NT-induced [35]GTP S binding to  E. coli membrane-inserted MBP-T43NTR-G  fusion proteins or to homogenates of transfected CHO-NTR cells expressing the rat NTR.	bind
6668	4	2996	5	10	NULL	NULL	NULL	[35]GTP S	Chemical		bind					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_100	11287004	(A) NT-induced [35]GTP S binding to  E. coli membrane-inserted MBP-T43NTR-G  fusion proteins or to homogenates of transfected CHO-NTR cells expressing the rat NTR.	bind
6669	5	2996	5	10	NULL	NULL	NULL	NT	GP		induce					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_100	11287004	(A) NT-induced [35]GTP S binding to  E. coli membrane-inserted MBP-T43NTR-G  fusion proteins or to homogenates of transfected CHO-NTR cells expressing the rat NTR.	bind
53125	6	2996	5	10	NULL	NULL	NULL	MBP-T43NTR-G	GP		is a type of					fusion protein	GP	E. coli membrane-inserted			NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_100	11287004	(A) NT-induced [35]GTP S binding to  E. coli membrane-inserted MBP-T43NTR-G  fusion proteins or to homogenates of transfected CHO-NTR cells expressing the rat NTR.	bind
7255	1	2996	6	10	NULL	NULL	NULL	[35]GTP S	Chemical		bind					MBP-T43NTR-G 	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_100	11287004	(A) NT-induced [35]GTP S binding to  E. coli membrane-inserted MBP-T43NTR-G  fusion proteins or to homogenates of transfected CHO-NTR cells expressing the rat NTR.	bind
7256	2	2996	6	10	NULL	NULL	NULL	NT	GP		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_100	11287004	(A) NT-induced [35]GTP S binding to  E. coli membrane-inserted MBP-T43NTR-G  fusion proteins or to homogenates of transfected CHO-NTR cells expressing the rat NTR.	bind
7279	3	2996	6	10	NULL	NULL	NULL	CHO-NTR cells 	Cell		express					NTR	GP	rat			NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_100	11287004	(A) NT-induced [35]GTP S binding to  E. coli membrane-inserted MBP-T43NTR-G  fusion proteins or to homogenates of transfected CHO-NTR cells expressing the rat NTR.	bind
7280	4	2996	6	10	NULL	NULL	NULL	GTP S	Chemical		bind					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_100	11287004	(A) NT-induced [35]GTP S binding to  E. coli membrane-inserted MBP-T43NTR-G  fusion proteins or to homogenates of transfected CHO-NTR cells expressing the rat NTR.	bind
46585	5	2996	6	10	NULL	NULL	NULL	NT	GP		induce					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_100	11287004	(A) NT-induced [35]GTP S binding to  E. coli membrane-inserted MBP-T43NTR-G  fusion proteins or to homogenates of transfected CHO-NTR cells expressing the rat NTR.	bind
53126	6	2996	6	10	NULL	NULL	NULL	MBP-T43NTR-G	GP		is a type of					fusion protein	GP	E. coli membrane-inserted			NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_100	11287004	(A) NT-induced [35]GTP S binding to  E. coli membrane-inserted MBP-T43NTR-G  fusion proteins or to homogenates of transfected CHO-NTR cells expressing the rat NTR.	bind
6664	1	3001	5	10	NULL	NULL	NULL	Nup60p	GP		bind					Gsp1p - GTP	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_937_s_176	11535617	(A) Nup60p binds Gsp1p - GTP.	bind
7062	1	3001	6	10	NULL	NULL	NULL	Nup60p	GP		bind					Gsp1p - GTP	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_937_s_176	11535617	(A) Nup60p binds Gsp1p - GTP.	bind
6670	1	3002	5	10	NULL	NULL	NULL	Nup60p	GP		bind					Kap95p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_937_s_65	11535617	(A) Nup60p binds Kap95p, but only in the absence of Gsp1p - GTP.	bind
6671	2	3002	5	10	NULL	NULL	NULL	statement 1	Process		occurs in absence of		only			Gsp1p - GTP	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_937_s_65	11535617	(A) Nup60p binds Kap95p, but only in the absence of Gsp1p - GTP.	bind
7063	1	3002	6	10	NULL	NULL	NULL	Nup60p	GP		bind					Kap95p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_937_s_65	11535617	(A) Nup60p binds Kap95p, but only in the absence of Gsp1p - GTP.	bind
7064	2	3002	6	10	NULL	NULL	NULL	statement 1	Process		occurs in absence of		only			Gsp1p - GTP	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_937_s_65	11535617	(A) Nup60p binds Kap95p, but only in the absence of Gsp1p - GTP.	bind
6672	1	3003	5	10	NULL	NULL	NULL	NURF	GP		bind					HSF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_3_531_s_194	11583616	(A) NURF binds to HSF and VP16.	bind
6673	2	3003	5	10	NULL	NULL	NULL	NURF	GP		bind					VP16	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_3_531_s_194	11583616	(A) NURF binds to HSF and VP16.	bind
7065	1	3003	6	10	NULL	NULL	NULL	NURF	GP		bind					HSF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_3_531_s_194	11583616	(A) NURF binds to HSF and VP16.	bind
7066	2	3003	6	10	NULL	NULL	NULL	NURF	GP		bind					VP16	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_3_531_s_194	11583616	(A) NURF binds to HSF and VP16.	bind
6674	1	3004	5	10	NULL	NULL	NULL	Oct-1 	GP		bind					HLA-DRA 	GP			octamer element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6495_s_283	11533238	(A) Oct-1 binding to the HLA-DRA octamer element is disrupted by HDAC inhibitors.	bind
6675	2	3004	5	10	NULL	NULL	NULL	HDAC inhibitors	Chemical		disrupt					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6495_s_283	11533238	(A) Oct-1 binding to the HLA-DRA octamer element is disrupted by HDAC inhibitors.	bind
7174	1	3004	6	10	NULL	NULL	NULL	Oct-1	GP		bind					HLA-DRA	GP			octamer element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6495_s_283	11533238	(A) Oct-1 binding to the HLA-DRA octamer element is disrupted by HDAC inhibitors.	bind
7175	2	3004	6	10	NULL	NULL	NULL	HDAC inhibitors	Chemical		disrupts					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6495_s_283	11533238	(A) Oct-1 binding to the HLA-DRA octamer element is disrupted by HDAC inhibitors.	bind
6676	1	3005	5	10	NULL	NULL	NULL	Bcd	GP		bind					TAF60	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_128_12_2281_s_223	11493547	(A) of Bcd binds TAF60, this type of domain is also frequently implicated in transcriptional repression in vivo ( Hanna-Rose and Hansen, 1996).	bind
7177	1	3005	6	10	NULL	NULL	NULL	Bcd	GP		bind					TAF60	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_128_12_2281_s_223	11493547	(A) of Bcd binds TAF60, this type of domain is also frequently implicated in transcriptional repression in vivo ( Hanna-Rose and Hansen, 1996).	bind
6677	1	3006	5	10	NULL	NULL	NULL				bind			tail		PAB	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4723_s_259	10970864	(A) on the reporter mRNAs in yeast cells; the tails could bind endogenous PAB and minimize MS2 - yPAB s effects.	bind
6678	2	3006	5	10	NULL	NULL	NULL	statement 1	Process		minimize					MS2 - yPAB s effects	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4723_s_259	10970864	(A) on the reporter mRNAs in yeast cells; the tails could bind endogenous PAB and minimize MS2 - yPAB s effects.	bind
7178	1	3006	6	10	NULL	NULL	NULL				bind			tails		PAB	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4723_s_259	10970864	(A) on the reporter mRNAs in yeast cells; the tails could bind endogenous PAB and minimize MS2 - yPAB s effects.	bind
7179	2	3006	6	10	NULL	NULL	NULL	statement 1	Process		minimize					MS2 - yPAB s effects	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4723_s_259	10970864	(A) on the reporter mRNAs in yeast cells; the tails could bind endogenous PAB and minimize MS2 - yPAB s effects.	bind
6679	1	3007	5	10	NULL	NULL	NULL	E2BD	AminoAcid		bind					E3 dimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_structure_4_3_277_s_109	8805537	(a) One E2BD (blue) is shown bound to one E3 dimer, as observed in the crystal structure.	bind
7180	1	3007	6	10	NULL	NULL	NULL	E2BD	AminoAcid		bind					E3 dimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_structure_4_3_277_s_109	8805537	(a) One E2BD (blue) is shown bound to one E3 dimer, as observed in the crystal structure.	bind
6681	1	3016	5	10	NULL	NULL	NULL	Pc	GP	oxidized	bind					EYL:DOTAP+	Chemical				NULL	large unilamellar vesicles	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1463_2_429_s_69	10675519	(A) Original infrared spectra corresponding to oxidized Pc bound to EYL:DOTAP+ (1:4 molar ratio) large unilamellar vesicles (----), and to the same liposome suspension in the absence of protein (- - -).	bind
7182	1	3016	6	10	NULL	NULL	NULL	Pc	GP	oxidized	bind					EYL:DOTAP+	Chemical				NULL	large unilamellar vesicles	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1463_2_429_s_69	10675519	(A) Original infrared spectra corresponding to oxidized Pc bound to EYL:DOTAP+ (1:4 molar ratio) large unilamellar vesicles (----), and to the same liposome suspension in the absence of protein (- - -).	bind
6682	1	3017	5	10	NULL	NULL	NULL	Munc18c	GP	overexpression of	occludes								syntaxin 4 binding sites		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_1_379_s_266	10594040	(A) Overexpression of Munc18c occludes all the syntaxin 4 binding sites, thereby preventing the association of the GSV with the plasma membrane and hence translocation.	bind
6683	2	3017	5	10	NULL	NULL	NULL	GSV	CellComponent		associate with					plasma membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_1_379_s_266	10594040	(A) Overexpression of Munc18c occludes all the syntaxin 4 binding sites, thereby preventing the association of the GSV with the plasma membrane and hence translocation.	bind
6684	3	3017	5	10	NULL	NULL	NULL	statement 1	Process		prevent					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_1_379_s_266	10594040	(A) Overexpression of Munc18c occludes all the syntaxin 4 binding sites, thereby preventing the association of the GSV with the plasma membrane and hence translocation.	bind
6685	4	3017	5	10	NULL	NULL	NULL	statement 1	Process		prevents					GSV	CellComponent	translocation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_1_379_s_266	10594040	(A) Overexpression of Munc18c occludes all the syntaxin 4 binding sites, thereby preventing the association of the GSV with the plasma membrane and hence translocation.	bind
7257	1	3017	6	10	NULL	NULL	NULL	GSV	CellComponent		associates					plasma membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_1_379_s_266	10594040	(A) Overexpression of Munc18c occludes all the syntaxin 4 binding sites, thereby preventing the association of the GSV with the plasma membrane and hence translocation.	bind
7258	2	3017	6	10	NULL	NULL	NULL	Munc18c	GP	overexpression	occludes								syntaxin 4 binding site		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_1_379_s_266	10594040	(A) Overexpression of Munc18c occludes all the syntaxin 4 binding sites, thereby preventing the association of the GSV with the plasma membrane and hence translocation.	bind
7259	3	3017	6	10	NULL	NULL	NULL	statement 2	Process		prevents					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_1_379_s_266	10594040	(A) Overexpression of Munc18c occludes all the syntaxin 4 binding sites, thereby preventing the association of the GSV with the plasma membrane and hence translocation.	bind
7260	4	3017	6	10	NULL	NULL	NULL	statement 2	Process		prevents					GSV	CellComponent	translocation of 			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_1_379_s_266	10594040	(A) Overexpression of Munc18c occludes all the syntaxin 4 binding sites, thereby preventing the association of the GSV with the plasma membrane and hence translocation.	bind
6686	1	3018	5	10	NULL	NULL	NULL	p35	GP		bind					GST-hAATYKs-p35BPN169	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_2_398_s_95	14521924	(A) p35 or Cdk5 bound  to GST-hAATYKs-p35BPN169 (lanes 1-3) was detected by immunoblotting with anti-p35 (p35) or anti-Cdk5 (Cdk5).	bind
6687	2	3018	5	10	NULL	NULL	NULL	Cdk5	GP		bind					GST-hAATYKs-p35BPN169	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_2_398_s_95	14521924	(A) p35 or Cdk5 bound  to GST-hAATYKs-p35BPN169 (lanes 1-3) was detected by immunoblotting with anti-p35 (p35) or anti-Cdk5 (Cdk5).	bind
53128	3	3018	5	10	NULL	NULL	NULL	statement 1	GP		is an alternative to					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_2_398_s_95	14521924	(A) p35 or Cdk5 bound  to GST-hAATYKs-p35BPN169 (lanes 1-3) was detected by immunoblotting with anti-p35 (p35) or anti-Cdk5 (Cdk5).	bind
7183	1	3018	6	10	NULL	NULL	NULL	p35	GP		bind					GST-hAATYKs-p35BPN169	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_2_398_s_95	14521924	(A) p35 or Cdk5 bound  to GST-hAATYKs-p35BPN169 (lanes 1-3) was detected by immunoblotting with anti-p35 (p35) or anti-Cdk5 (Cdk5).	bind
7184	2	3018	6	10	NULL	NULL	NULL	Cdk5	GP		bind					GST-hAATYKs-p35BPN169	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_2_398_s_95	14521924	(A) p35 or Cdk5 bound  to GST-hAATYKs-p35BPN169 (lanes 1-3) was detected by immunoblotting with anti-p35 (p35) or anti-Cdk5 (Cdk5).	bind
7185	3	3018	6	10	NULL	NULL	NULL	statement 1	GP		is an alternative to					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_2_398_s_95	14521924	(A) p35 or Cdk5 bound  to GST-hAATYKs-p35BPN169 (lanes 1-3) was detected by immunoblotting with anti-p35 (p35) or anti-Cdk5 (Cdk5).	bind
6688	1	3019	5	10	NULL	NULL	NULL	p53	GP		bind					Mix.2 gene	GP	putative		p53-binding sites	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_130_17_3929_s_224	12874116	(A) p53 binds to the putative p53-binding sites from  Mix.2 gene in vitro.	bind
7191	1	3019	6	10	NULL	NULL	NULL	p53	GP		bind					Mix.2 gene	GP	putative		p53-binding site	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_130_17_3929_s_224	12874116	(A) p53 binds to the putative p53-binding sites from  Mix.2 gene in vitro.	bind
6689	1	3020	5	10	NULL	NULL	NULL	p55	GP		bind					 ARP53D	GP			E gene promoter 	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_9124_s_237	15456884	(A) p55 binds to the E gene promoter   ARP53D.	bind
7192	1	3020	6	10	NULL	NULL	NULL	p55	GP		bind					ARP53D	GP			E gene promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_9124_s_237	15456884	(A) p55 binds to the E gene promoter   ARP53D.	bind
6690	1	3021	5	10	NULL	NULL	NULL	p63	GP		bind					p73	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_8_3536_s_341	15060172	(A) p63 binds to p73 but not to p53.	bind
6691	2	3021	5	10	NULL	NULL	NULL	p63	GP		does not bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_8_3536_s_341	15060172	(A) p63 binds to p73 but not to p53.	bind
7193	1	3021	6	10	NULL	NULL	NULL	p63	GP		bind					p73	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_8_3536_s_341	15060172	(A) p63 binds to p73 but not to p53.	bind
7195	2	3021	6	10	NULL	NULL	NULL	p63	GP		does not bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_8_3536_s_341	15060172	(A) p63 binds to p73 but not to p53.	bind
6692	1	3022	5	10	NULL	NULL	NULL	p70 MGR	GP		bind					PCNA	GP	Drosophila		promoter	NULL		NULL	NULL	NULL	NULL	gw60_mechdev_114_1_37_s_150	12175488	(A) p70 MGR binds to the  Drosophila PCNA promoter.	bind
7197	1	3022	6	10	NULL	NULL	NULL	p70 MGR	GP		bind					PCNA	GP	drosophila		promoter	NULL		NULL	NULL	NULL	NULL	gw60_mechdev_114_1_37_s_150	12175488	(A) p70 MGR binds to the  Drosophila PCNA promoter.	bind
6693	1	3023	5	10	NULL	NULL	NULL	p97	GP		bind					c-Raf-1	GP	baculovirus			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_6_2235_s_200	11238956	(A) p97 binds c-Raf-1 from baculovirus.	bind
7198	1	3023	6	10	NULL	NULL	NULL	p97	GP		bind					c-Raf-1	GP	baculovirus			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_6_2235_s_200	11238956	(A) p97 binds c-Raf-1 from baculovirus.	bind
6694	1	3024	5	10	NULL	NULL	NULL	p97	GP		does not bind					MEK	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_6_2235_s_232	11238956	(A) p97 does not bind to MEK and is not activated by MEK.	bind
6695	2	3024	5	10	NULL	NULL	NULL	p97	GP		is not activated by					MEK	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_6_2235_s_232	11238956	(A) p97 does not bind to MEK and is not activated by MEK.	bind
7199	1	3024	6	10	NULL	NULL	NULL	p97	GP		does not bind					MEK	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_6_2235_s_232	11238956	(A) p97 does not bind to MEK and is not activated by MEK.	bind
7200	2	3024	6	10	NULL	NULL	NULL	p97	GP		is not activated by					MEK	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_6_2235_s_232	11238956	(A) p97 does not bind to MEK and is not activated by MEK.	bind
6696	1	3025	5	10	NULL	NULL	NULL	Par3L	GP		does not bind		detectably			PKC	GP				NULL		NULL	NULL	NULL	NULL	gw60_gene_294_1_99_s_195	12234671	(A) Par3L does not bind detectably to PKC .	bind
7201	1	3025	6	10	NULL	NULL	NULL	Par3L	GP		does not bind		detectably			PKC	GP				NULL		NULL	NULL	NULL	NULL	gw60_gene_294_1_99_s_195	12234671	(A) Par3L does not bind detectably to PKC .	bind
6697	1	3026	5	10	NULL	NULL	NULL	PARC	GP		bind					p53	GP				NULL	MEFs	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5579_s_219	15964813	(A) PARC binds p53 in MEFs.	bind
7202	1	3026	6	10	NULL	NULL	NULL	PARC	GP		bind					p53	GP				NULL	MEFs	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5579_s_219	15964813	(A) PARC binds p53 in MEFs.	bind
6698	1	3029	5	10	NULL	NULL	NULL	R1 peptide	AminoAcid		bind					AMA1	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6981_s_161	16177378	(A) Phage  displaying the R1 peptide binding to immobilized AMA1 derived from a number of parasite  lines.	bind
67194	2	3029	5	10	NULL	NULL	NULL	AMA1	GP	immobilized	is derived from					parasite lines	Organism				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6981_s_161	16177378	(A) Phage  displaying the R1 peptide binding to immobilized AMA1 derived from a number of parasite  lines.	bind
7203	1	3029	6	10	NULL	NULL	NULL	R1 peptide	AminoAcid		bind					AMA1	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6981_s_161	16177378	(A) Phage  displaying the R1 peptide binding to immobilized AMA1 derived from a number of parasite  lines.	bind
7204	2	3029	6	10	NULL	NULL	NULL	AMA1	GP	immobilized	is derived from					parasite lines	Organism				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6981_s_161	16177378	(A) Phage  displaying the R1 peptide binding to immobilized AMA1 derived from a number of parasite  lines.	bind
6699	1	3030	5	10	NULL	NULL	NULL	p47	GP	phosphorylated	bind					p97	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_161_6_1067_s_141	12810701	(A) Phosphorylated p47 binds to p97.	bind
7205	1	3030	6	10	NULL	NULL	NULL	p47	GP	phosphorylated	bind					p97	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_161_6_1067_s_141	12810701	(A) Phosphorylated p47 binds to p97.	bind
6700	1	3031	5	10	NULL	NULL	NULL	Ste11	GP		bind					Rad24	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_1_3_389_s_204	11702950	(A) Phosphorylation-dependent binding between Ste11 and Rad24.	bind
6701	2	3031	5	10	NULL	NULL	NULL	statement 1	Process		is dependent on					phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_devcell_1_3_389_s_204	11702950	(A) Phosphorylation-dependent binding between Ste11 and Rad24.	bind
7206	1	3031	6	10	NULL	NULL	NULL	Ste11	GP		bind					Rad24	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_1_3_389_s_204	11702950	(A) Phosphorylation-dependent binding between Ste11 and Rad24.	bind
7207	2	3031	6	10	NULL	NULL	NULL	statement 1	Process		is dependent on					phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_devcell_1_3_389_s_204	11702950	(A) Phosphorylation-dependent binding between Ste11 and Rad24.	bind
6702	1	3033	5	10	NULL	NULL	NULL	BAD	GP		bind					BCL-XL	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_1_41_s_211	10949026	(A) PKA and 14-3-3 cooperate to induce phosphorylation of BAD Ser-155 when BAD is bound to BCL-XL.	bind
6703	2	3033	5	10	NULL	NULL	NULL	PKA	GP		induce					BAD	GP	phosphorylation of	Ser-155		NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_1_41_s_211	10949026	(A) PKA and 14-3-3 cooperate to induce phosphorylation of BAD Ser-155 when BAD is bound to BCL-XL.	bind
6704	3	3033	5	10	NULL	NULL	NULL	14-3-3	GP		induce					BAD	GP	phosphorylation of	Ser-155		NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_1_41_s_211	10949026	(A) PKA and 14-3-3 cooperate to induce phosphorylation of BAD Ser-155 when BAD is bound to BCL-XL.	bind
6705	4	3033	5	10	NULL	NULL	NULL	statement 2	Process		occurs in cooperation with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_1_41_s_211	10949026	(A) PKA and 14-3-3 cooperate to induce phosphorylation of BAD Ser-155 when BAD is bound to BCL-XL.	bind
6706	5	3033	5	10	NULL	NULL	NULL	statement 4	Process		occurs following					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_1_41_s_211	10949026	(A) PKA and 14-3-3 cooperate to induce phosphorylation of BAD Ser-155 when BAD is bound to BCL-XL.	bind
7208	1	3033	6	10	NULL	NULL	NULL	PKA	GP		induce					BAD	GP	phosphorylation of	Ser-155		NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_1_41_s_211	10949026	(A) PKA and 14-3-3 cooperate to induce phosphorylation of BAD Ser-155 when BAD is bound to BCL-XL.	bind
7209	2	3033	6	10	NULL	NULL	NULL	14-3-3	GP		induce					BAD	GP	phosphorylation of	Ser-155		NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_1_41_s_211	10949026	(A) PKA and 14-3-3 cooperate to induce phosphorylation of BAD Ser-155 when BAD is bound to BCL-XL.	bind
7210	3	3033	6	10	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_1_41_s_211	10949026	(A) PKA and 14-3-3 cooperate to induce phosphorylation of BAD Ser-155 when BAD is bound to BCL-XL.	bind
7211	4	3033	6	10	NULL	NULL	NULL	BAD	GP		bind					BCL-XL	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_1_41_s_211	10949026	(A) PKA and 14-3-3 cooperate to induce phosphorylation of BAD Ser-155 when BAD is bound to BCL-XL.	bind
7212	5	3033	6	10	NULL	NULL	NULL	statement 4	Process		leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_1_41_s_211	10949026	(A) PKA and 14-3-3 cooperate to induce phosphorylation of BAD Ser-155 when BAD is bound to BCL-XL.	bind
7213	6	3033	6	10	NULL	NULL	NULL	statement 4	Process		leads to 					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_1_41_s_211	10949026	(A) PKA and 14-3-3 cooperate to induce phosphorylation of BAD Ser-155 when BAD is bound to BCL-XL.	bind
6707	1	3034	5	10	NULL	NULL	NULL	PKC	GP		bind					RACK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1487_2_163_s_243	11018469	(A) PKC  binding to RACK1 and peptide inhibited binding.	bind
8183	2	3034	5	10	NULL	NULL	NULL	peptide	AminoAcid		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1487_2_163_s_243	11018469	(A) PKC  binding to RACK1 and peptide inhibited binding.	bind
7214	1	3034	6	10	NULL	NULL	NULL	PKC	GP		bind					RACK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1487_2_163_s_243	11018469	(A) PKC  binding to RACK1 and peptide inhibited binding.	bind
7215	2	3034	6	10	NULL	NULL	NULL	peptide	AminoAcid		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1487_2_163_s_243	11018469	(A) PKC  binding to RACK1 and peptide inhibited binding.	bind
6708	3	3035	5	10	NULL	NULL	NULL	PKC	GP		bind		 	alpha C2 domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_56_s_161	16236797	(A) PKCalphaC2 domain and (B) cPLA2alphaC2 domain binding to phospholipid vesicles containing 3:1 PC:	bind
6709	2	3035	5	10	NULL	NULL	NULL	cPLA2	GP		bind			alpha C2 domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_56_s_161	16236797	(A) PKCalphaC2 domain and (B) cPLA2alphaC2 domain binding to phospholipid vesicles containing 3:1 PC:	bind
67195	1	3035	5	10	NULL	NULL	NULL	phospholipid vesicles \t	CellComponent		contains					PC	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_56_s_161	16236797	(A) PKCalphaC2 domain and (B) cPLA2alphaC2 domain binding to phospholipid vesicles containing 3:1 PC:	bind
7216	1	3035	6	10	NULL	NULL	NULL	phospholipid vesicles	CellComponent		contain					PC	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_56_s_161	16236797	(A) PKCalphaC2 domain and (B) cPLA2alphaC2 domain binding to phospholipid vesicles containing 3:1 PC:	bind
7217	2	3035	6	10	NULL	NULL	NULL	PKC	GP		bind			alpha C2 domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_56_s_161	16236797	(A) PKCalphaC2 domain and (B) cPLA2alphaC2 domain binding to phospholipid vesicles containing 3:1 PC:	bind
7218	3	3035	6	10	NULL	NULL	NULL	cPLA2	GP		bind			alpha C2 domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_56_s_161	16236797	(A) PKCalphaC2 domain and (B) cPLA2alphaC2 domain binding to phospholipid vesicles containing 3:1 PC:	bind
6710	1	3036	5	10	NULL	NULL	NULL	nuclear proteins	GP		bind									AP-1/TRE DNA-binding site	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3423_s_124	10207066	(A) PKD2 induces binding of nuclear proteins to the AP-1/TRE DNA-binding site.	bind
6711	2	3036	5	10	NULL	NULL	NULL	PKD2	GP		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3423_s_124	10207066	(A) PKD2 induces binding of nuclear proteins to the AP-1/TRE DNA-binding site.	bind
7219	1	3036	6	10	NULL	NULL	NULL	nuclear proteins	GP		bind									AP-1/TRE DNA-binding site	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3423_s_124	10207066	(A) PKD2 induces binding of nuclear proteins to the AP-1/TRE DNA-binding site.	bind
7220	2	3036	6	10	NULL	NULL	NULL	PKD2	GP		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3423_s_124	10207066	(A) PKD2 induces binding of nuclear proteins to the AP-1/TRE DNA-binding site.	bind
6712	1	3038	5	10	NULL	NULL	NULL	anti-K18 peptide	GP		bind					SAg protein	GP				NULL	in solution	NULL	NULL	NULL	NULL	gw60_immunity_15_4_591_s_230	11672541	(A) Polyclonal anti-K18 peptide Abs bind the SAg protein in solution.	bind
53129	2	3038	5	10	NULL	NULL	NULL	anti-K18 peptide	GP		is a type of					polyclonal Ab	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_4_591_s_230	11672541	(A) Polyclonal anti-K18 peptide Abs bind the SAg protein in solution.	bind
7221	1	3038	6	10	NULL	NULL	NULL	anti-K18 peptide 	GP		bind					SAg protein	GP				NULL	in solution	NULL	NULL	NULL	NULL	gw60_immunity_15_4_591_s_230	11672541	(A) Polyclonal anti-K18 peptide Abs bind the SAg protein in solution.	bind
40685	2	3038	6	10	NULL	NULL	NULL	anti-K18 peptide	GP		is a type of					polyclonal Abs	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_4_591_s_230	11672541	(A) Polyclonal anti-K18 peptide Abs bind the SAg protein in solution.	bind
6713	1	3039	5	10	NULL	NULL	NULL	CF I 	GP		bind					pre-mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_11_6107_s_12	8626397	(A) polymerase (PAP) had no detectable effect on the binding of CF  I   to pre-mRNA.	bind
6714	2	3039	5	10	NULL	NULL	NULL	PAP	GP		does not effect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_11_6107_s_12	8626397	(A) polymerase (PAP) had no detectable effect on the binding of CF  I   to pre-mRNA.	bind
53130	3	3039	5	10	NULL	NULL	NULL	PAP	GP		is a type of					polymerase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_11_6107_s_12	8626397	(A) polymerase (PAP) had no detectable effect on the binding of CF  I   to pre-mRNA.	bind
7222	1	3039	6	10	NULL	NULL	NULL	CF I	GP		bind					pre-mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_11_6107_s_12	8626397	(A) polymerase (PAP) had no detectable effect on the binding of CF  I   to pre-mRNA.	bind
7223	2	3039	6	10	NULL	NULL	NULL	PAP	GP		had no effect on					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_11_6107_s_12	8626397	(A) polymerase (PAP) had no detectable effect on the binding of CF  I   to pre-mRNA.	bind
53131	3	3039	6	10	NULL	NULL	NULL	PAP	GP		is a type of					polymerase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_11_6107_s_12	8626397	(A) polymerase (PAP) had no detectable effect on the binding of CF  I   to pre-mRNA.	bind
7146	1	3040	5	10	NULL	NULL	NULL	PAP	GP		is present					blastomeres	Cell	throughout			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_435_s_107	11081630	(A) polymerase (PAP), and  the 100 kDa subunit of CPSF (the AAUAAA binding complex) were all detected  throughout the blastomeres, although there was a slight concentration of these proteins at  the centrosomes.	bind
7147	2	3040	5	10	NULL	NULL	NULL	CPSF	GP		is present			100 kDa subunit		blastomeres	Cell	throughout			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_435_s_107	11081630	(A) polymerase (PAP), and  the 100 kDa subunit of CPSF (the AAUAAA binding complex) were all detected  throughout the blastomeres, although there was a slight concentration of these proteins at  the centrosomes.	bind
7148	3	3040	5	10	NULL	NULL	NULL	CPSF	GP		is			100 kDa subunit		AAUAAA binding complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_435_s_107	11081630	(A) polymerase (PAP), and  the 100 kDa subunit of CPSF (the AAUAAA binding complex) were all detected  throughout the blastomeres, although there was a slight concentration of these proteins at  the centrosomes.	bind
7149	4	3040	5	10	NULL	NULL	NULL	PAP	GP		is present in					centrosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_435_s_107	11081630	(A) polymerase (PAP), and  the 100 kDa subunit of CPSF (the AAUAAA binding complex) were all detected  throughout the blastomeres, although there was a slight concentration of these proteins at  the centrosomes.	bind
7150	5	3040	5	10	NULL	NULL	NULL	CPSF	GP		is present in			100 kDa subunit		centrosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_435_s_107	11081630	(A) polymerase (PAP), and  the 100 kDa subunit of CPSF (the AAUAAA binding complex) were all detected  throughout the blastomeres, although there was a slight concentration of these proteins at  the centrosomes.	bind
7224	1	3041	6	10	NULL	NULL	NULL	polymerase	GP		bind					pre-mRNA 	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_7_991_s_138	9651582	(A) polymerase or CstF binding to the pre-mRNA substrate (data not shown), the binding of CPSF to the L3 pre-mRNA precursor was prevented by the NS1 protein (  Figure 4).	bind
7225	2	3041	6	10	NULL	NULL	NULL	CstF	GP		bind					pre-mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_7_991_s_138	9651582	(A) polymerase or CstF binding to the pre-mRNA substrate (data not shown), the binding of CPSF to the L3 pre-mRNA precursor was prevented by the NS1 protein (  Figure 4).	bind
7226	3	3041	6	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_7_991_s_138	9651582	(A) polymerase or CstF binding to the pre-mRNA substrate (data not shown), the binding of CPSF to the L3 pre-mRNA precursor was prevented by the NS1 protein (  Figure 4).	bind
7227	4	3041	6	10	NULL	NULL	NULL	CPSF	GP		bind					L3 pre-mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_7_991_s_138	9651582	(A) polymerase or CstF binding to the pre-mRNA substrate (data not shown), the binding of CPSF to the L3 pre-mRNA precursor was prevented by the NS1 protein (  Figure 4).	bind
7228	5	3041	6	10	NULL	NULL	NULL	NS1 protein	GP		prevents					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_7_991_s_138	9651582	(A) polymerase or CstF binding to the pre-mRNA substrate (data not shown), the binding of CPSF to the L3 pre-mRNA precursor was prevented by the NS1 protein (  Figure 4).	bind
6748	1	3043	5	10	NULL	NULL	NULL	PP2A	GP	catalytically active 	bind					AR	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_197	15684382	(A) PP2A bound to AR is catalytically  active.	bind
7229	1	3043	6	10	NULL	NULL	NULL	PP2A	GP	catalytically active	bind					AR	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_197	15684382	(A) PP2A bound to AR is catalytically  active.	bind
6750	1	3044	5	10	NULL	NULL	NULL	Rac1	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6872_s_231	10958683	(A) Precipitation of FRL by the GTPgammaS- or GDP-bound form of Rac1.	bind
6751	2	3044	5	10	NULL	NULL	NULL	Rac1	GP		bind					GTPgammaS	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6872_s_231	10958683	(A) Precipitation of FRL by the GTPgammaS- or GDP-bound form of Rac1.	bind
6752	3	3044	5	10	NULL	NULL	NULL	FRL	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6872_s_231	10958683	(A) Precipitation of FRL by the GTPgammaS- or GDP-bound form of Rac1.	bind
6753	4	3044	5	10	NULL	NULL	NULL	FRL	GP		bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6872_s_231	10958683	(A) Precipitation of FRL by the GTPgammaS- or GDP-bound form of Rac1.	bind
53135	5	3044	5	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6872_s_231	10958683	(A) Precipitation of FRL by the GTPgammaS- or GDP-bound form of Rac1.	bind
7230	1	3044	6	10	NULL	NULL	NULL	Rac1	GP		bind					GTPgammaS	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6872_s_231	10958683	(A) Precipitation of FRL by the GTPgammaS- or GDP-bound form of Rac1.	bind
7231	2	3044	6	10	NULL	NULL	NULL	 Rac1	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6872_s_231	10958683	(A) Precipitation of FRL by the GTPgammaS- or GDP-bound form of Rac1.	bind
7232	3	3044	6	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6872_s_231	10958683	(A) Precipitation of FRL by the GTPgammaS- or GDP-bound form of Rac1.	bind
53132	4	3044	6	10	NULL	NULL	NULL	FRL	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6872_s_231	10958683	(A) Precipitation of FRL by the GTPgammaS- or GDP-bound form of Rac1.	bind
53134	5	3044	6	10	NULL	NULL	NULL	FRL	GP		bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6872_s_231	10958683	(A) Precipitation of FRL by the GTPgammaS- or GDP-bound form of Rac1.	bind
6754	1	3045	5	10	NULL	NULL	NULL	BCS1 precursor	GP		lacks								first 82 amino acid residues		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_7_2239_s_269	12640110	(A) Precursor lacking the first 82 amino acid residues of BCS1 can bind to OMV in a receptor-dependent manner.	bind
6755	2	3045	5	10	NULL	NULL	NULL	statement 1	Process		bind					OMV	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_7_2239_s_269	12640110	(A) Precursor lacking the first 82 amino acid residues of BCS1 can bind to OMV in a receptor-dependent manner.	bind
6756	3	3045	5	10	NULL	NULL	NULL	statement 2	Process		is dependent on					receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_7_2239_s_269	12640110	(A) Precursor lacking the first 82 amino acid residues of BCS1 can bind to OMV in a receptor-dependent manner.	bind
7233	1	3045	6	10	NULL	NULL	NULL	BCS1 precursor	GP		lacks								82 amino acid residues		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_7_2239_s_269	12640110	(A) Precursor lacking the first 82 amino acid residues of BCS1 can bind to OMV in a receptor-dependent manner.	bind
7234	2	3045	6	10	NULL	NULL	NULL	statement 1	Process		bind					OMV	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_7_2239_s_269	12640110	(A) Precursor lacking the first 82 amino acid residues of BCS1 can bind to OMV in a receptor-dependent manner.	bind
7235	3	3045	6	10	NULL	NULL	NULL	statement 2	Process		is dependent on					receptor 	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_7_2239_s_269	12640110	(A) Precursor lacking the first 82 amino acid residues of BCS1 can bind to OMV in a receptor-dependent manner.	bind
6757	1	3049	5	10	NULL	NULL	NULL	Arp2	GP		bind					nucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_315_s_245	15657399	(A) Proposed relative contributions of Arp2 and Arp3 nucleotide binding to actin  filament nucleation and a yet to be determined structural activity.	bind
6758	2	3049	5	10	NULL	NULL	NULL	Arp3	GP		bind					nucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_315_s_245	15657399	(A) Proposed relative contributions of Arp2 and Arp3 nucleotide binding to actin  filament nucleation and a yet to be determined structural activity.	bind
8184	3	3049	5	10	NULL	NULL	NULL	statement 1	Process		contribute to		may			actin filament	CellComponent	nucleation of			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_315_s_245	15657399	(A) Proposed relative contributions of Arp2 and Arp3 nucleotide binding to actin  filament nucleation and a yet to be determined structural activity.	bind
8185	4	3049	5	10	NULL	NULL	NULL	statement 2	Process		contribute to		may			actin filament	CellComponent	nucleation of			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_315_s_245	15657399	(A) Proposed relative contributions of Arp2 and Arp3 nucleotide binding to actin  filament nucleation and a yet to be determined structural activity.	bind
7236	1	3049	6	10	NULL	NULL	NULL	Arp2	GP		bind					nucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_315_s_245	15657399	(A) Proposed relative contributions of Arp2 and Arp3 nucleotide binding to actin  filament nucleation and a yet to be determined structural activity.	bind
7237	2	3049	6	10	NULL	NULL	NULL	Arp3	GP		bind					nucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_315_s_245	15657399	(A) Proposed relative contributions of Arp2 and Arp3 nucleotide binding to actin  filament nucleation and a yet to be determined structural activity.	bind
7238	3	3049	6	10	NULL	NULL	NULL	statement 1	Process		contribute in		may			actin filament	CellComponent	nucleation of 			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_315_s_245	15657399	(A) Proposed relative contributions of Arp2 and Arp3 nucleotide binding to actin  filament nucleation and a yet to be determined structural activity.	bind
7239	4	3049	6	10	NULL	NULL	NULL	statement 2	Process		contribute in		may			actin filament	CellComponent	nucleation of 			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_315_s_245	15657399	(A) Proposed relative contributions of Arp2 and Arp3 nucleotide binding to actin  filament nucleation and a yet to be determined structural activity.	bind
6759	1	3050	5	10	NULL	NULL	NULL	XARP	GP		associate with					Xdsh	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2228_s_219	10688669	(A) Protein complexes containing XARP in association with Xdsh did not significantly bind GSK3, whereas the pool of XARP that is not bound to Xdsh retained GSK3.	bind
6760	3	3050	5	10	NULL	NULL	NULL	statement 2	Process		does not bind		significantly			GSK3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2228_s_219	10688669	(A) Protein complexes containing XARP in association with Xdsh did not significantly bind GSK3, whereas the pool of XARP that is not bound to Xdsh retained GSK3.	bind
6761	4	3050	5	10	NULL	NULL	NULL	XARP	GP		bind					GSK3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2228_s_219	10688669	(A) Protein complexes containing XARP in association with Xdsh did not significantly bind GSK3, whereas the pool of XARP that is not bound to Xdsh retained GSK3.	bind
44734	2	3050	5	10	NULL	NULL	NULL	statement 1	Process		forms a 					complex					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2228_s_219	10688669	(A) Protein complexes containing XARP in association with Xdsh did not significantly bind GSK3, whereas the pool of XARP that is not bound to Xdsh retained GSK3.	bind
7247	1	3050	6	10	NULL	NULL	NULL	XARP	GP		associates					Xdsh	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2228_s_219	10688669	(A) Protein complexes containing XARP in association with Xdsh did not significantly bind GSK3, whereas the pool of XARP that is not bound to Xdsh retained GSK3.	bind
7248	2	3050	6	10	NULL	NULL	NULL	statement 1	Process		forms a 					complex					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2228_s_219	10688669	(A) Protein complexes containing XARP in association with Xdsh did not significantly bind GSK3, whereas the pool of XARP that is not bound to Xdsh retained GSK3.	bind
7249	3	3050	6	10	NULL	NULL	NULL	statement 2	Process		did not bind		significantly			GSK3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2228_s_219	10688669	(A) Protein complexes containing XARP in association with Xdsh did not significantly bind GSK3, whereas the pool of XARP that is not bound to Xdsh retained GSK3.	bind
7250	4	3050	6	10	NULL	NULL	NULL	XARP	GP		bind					GSK3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2228_s_219	10688669	(A) Protein complexes containing XARP in association with Xdsh did not significantly bind GSK3, whereas the pool of XARP that is not bound to Xdsh retained GSK3.	bind
6762	1	3051	5	10	NULL	NULL	NULL	rat brain subfraction protein	GP		bind					sAPP695T	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1571_3_225_s_186	12090937	(A) Proteins from rat brain subfractions that binds sAPP695T.	bind
7416	1	3051	6	10	NULL	NULL	NULL	rat brain subfraction protein	GP		bind					sAPP695T	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1571_3_225_s_186	12090937	(A) Proteins from rat brain subfractions that binds sAPP695T.	bind
6763	1	3052	5	10	NULL	NULL	NULL	nuclear extract protein	GP	HeLa cells	bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9419_s_122	16227592	(a) Proteins in nuclear extracts  of HeLa cells that bound to GST (lane 3), GST-FGF-2 (lane 5), or GST-FGF-2 in the  presence of a 10-fold excess of hrFGF-2 (lane 6) were separated on a SDS-PAGE gel  and stained with Coomassie blue.	bind
6764	2	3052	5	10	NULL	NULL	NULL	nuclear extract protein	GP	HeLa cells	bind					GST-FGF-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9419_s_122	16227592	(a) Proteins in nuclear extracts  of HeLa cells that bound to GST (lane 3), GST-FGF-2 (lane 5), or GST-FGF-2 in the  presence of a 10-fold excess of hrFGF-2 (lane 6) were separated on a SDS-PAGE gel  and stained with Coomassie blue.	bind
6765	3	3052	5	10	NULL	NULL	NULL	nuclear extract protein	GP	HeLa cells	bind					GST-FGF-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9419_s_122	16227592	(a) Proteins in nuclear extracts  of HeLa cells that bound to GST (lane 3), GST-FGF-2 (lane 5), or GST-FGF-2 in the  presence of a 10-fold excess of hrFGF-2 (lane 6) were separated on a SDS-PAGE gel  and stained with Coomassie blue.	bind
44735	4	3052	5	10	NULL	NULL	NULL	statement 3	Process		occurs in presence of					hrFGF-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9419_s_122	16227592	(a) Proteins in nuclear extracts  of HeLa cells that bound to GST (lane 3), GST-FGF-2 (lane 5), or GST-FGF-2 in the  presence of a 10-fold excess of hrFGF-2 (lane 6) were separated on a SDS-PAGE gel  and stained with Coomassie blue.	bind
7417	1	3052	6	10	NULL	NULL	NULL	nuclear extract protein	GP	HeLa cells	bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9419_s_122	16227592	(a) Proteins in nuclear extracts  of HeLa cells that bound to GST (lane 3), GST-FGF-2 (lane 5), or GST-FGF-2 in the  presence of a 10-fold excess of hrFGF-2 (lane 6) were separated on a SDS-PAGE gel  and stained with Coomassie blue.	bind
7418	2	3052	6	10	NULL	NULL	NULL	nuclear extract protein	GP	HeLa cells	bind					GST-FGF-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9419_s_122	16227592	(a) Proteins in nuclear extracts  of HeLa cells that bound to GST (lane 3), GST-FGF-2 (lane 5), or GST-FGF-2 in the  presence of a 10-fold excess of hrFGF-2 (lane 6) were separated on a SDS-PAGE gel  and stained with Coomassie blue.	bind
7419	3	3052	6	10	NULL	NULL	NULL	nuclear extract protein	GP	HeLa cells	bind					GST-FGF-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9419_s_122	16227592	(a) Proteins in nuclear extracts  of HeLa cells that bound to GST (lane 3), GST-FGF-2 (lane 5), or GST-FGF-2 in the  presence of a 10-fold excess of hrFGF-2 (lane 6) were separated on a SDS-PAGE gel  and stained with Coomassie blue.	bind
44736	4	3052	6	10	NULL	NULL	NULL	statement 3	Process		occurs in presence of					hrFGF-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9419_s_122	16227592	(a) Proteins in nuclear extracts  of HeLa cells that bound to GST (lane 3), GST-FGF-2 (lane 5), or GST-FGF-2 in the  presence of a 10-fold excess of hrFGF-2 (lane 6) were separated on a SDS-PAGE gel  and stained with Coomassie blue.	bind
6766	1	3053	5	10	NULL	NULL	NULL	Rac	GP		bind		selectively			PAK	GP		PBD-GST		NULL		NULL	NULL	NULL	NULL	gw60_neuron_33_5_741_s_55	11879651	(A) Pull-down assays showing that Rac is bound selectively by PBD-GST (PAK), RhoA is bound selectively by RBD-GST (Rhotekin), and Cdc42 is bound selectively by WBD-GST (WASP).	bind
6767	2	3053	5	10	NULL	NULL	NULL	RhoA	GP		bind		selectively			Rhotekin	GP		RBD-GST		NULL		NULL	NULL	NULL	NULL	gw60_neuron_33_5_741_s_55	11879651	(A) Pull-down assays showing that Rac is bound selectively by PBD-GST (PAK), RhoA is bound selectively by RBD-GST (Rhotekin), and Cdc42 is bound selectively by WBD-GST (WASP).	bind
6768	3	3053	5	10	NULL	NULL	NULL	Cdc42	GP		bind		selectively			WASP	GP		WBD-GST		NULL		NULL	NULL	NULL	NULL	gw60_neuron_33_5_741_s_55	11879651	(A) Pull-down assays showing that Rac is bound selectively by PBD-GST (PAK), RhoA is bound selectively by RBD-GST (Rhotekin), and Cdc42 is bound selectively by WBD-GST (WASP).	bind
7420	1	3053	6	10	NULL	NULL	NULL	Rac	GP		bind		selectively			PAK	GP		PBD-GST		NULL		NULL	NULL	NULL	NULL	gw60_neuron_33_5_741_s_55	11879651	(A) Pull-down assays showing that Rac is bound selectively by PBD-GST (PAK), RhoA is bound selectively by RBD-GST (Rhotekin), and Cdc42 is bound selectively by WBD-GST (WASP).	bind
7421	2	3053	6	10	NULL	NULL	NULL	RhoA	GP		bind		selectively			Rhotekin	GP		RBD-GST		NULL		NULL	NULL	NULL	NULL	gw60_neuron_33_5_741_s_55	11879651	(A) Pull-down assays showing that Rac is bound selectively by PBD-GST (PAK), RhoA is bound selectively by RBD-GST (Rhotekin), and Cdc42 is bound selectively by WBD-GST (WASP).	bind
7423	3	3053	6	10	NULL	NULL	NULL	Cdc42	GP		bind		selectively			WASP	GP		WBD-GST		NULL		NULL	NULL	NULL	NULL	gw60_neuron_33_5_741_s_55	11879651	(A) Pull-down assays showing that Rac is bound selectively by PBD-GST (PAK), RhoA is bound selectively by RBD-GST (Rhotekin), and Cdc42 is bound selectively by WBD-GST (WASP).	bind
6769	1	3056	5	10	NULL	NULL	NULL	(BV)Ase1p	GP	purified	bind		directly			MTs 	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_160_4_517_s_114	12591913	(A) Purified (BV)Ase1p binds MTs directly.	bind
7424	1	3056	6	10	NULL	NULL	NULL	Ase1p (BV)	GP	purified	bind		directly			MTs	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_160_4_517_s_114	12591913	(A) Purified (BV)Ase1p binds MTs directly.	bind
6770	1	3059	5	10	NULL	NULL	NULL	p53 protein	GP	Purified;; recombinant	bind							overlapping		HNF-3/p53 sites	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1279_s_251	9891062	(A) Purified recombinant p53 protein binds to the overlapping HNF-3/p53 sites.	bind
7425	1	3059	6	10	NULL	NULL	NULL	p53 protein	GP	Purified;; recombinant	bind							overlapping		HNF-3/p53 sites	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1279_s_251	9891062	(A) Purified recombinant p53 protein binds to the overlapping HNF-3/p53 sites.	bind
6771	1	3060	5	10	NULL	NULL	NULL	Sp1	GP		bind					bcl-2	GP			P1 promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_233	15713621	(A) Quantitative ChIP assays of the binding of Sp1, CREB,  and CBP to the  bcl-2 P1 promoter.	bind
6772	2	3060	5	10	NULL	NULL	NULL	CREB	GP		bind					 bcl-2	GP			P1 promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_233	15713621	(A) Quantitative ChIP assays of the binding of Sp1, CREB,  and CBP to the  bcl-2 P1 promoter.	bind
6773	3	3060	5	10	NULL	NULL	NULL	CBP	GP		bind					bcl-2	GP			P1 promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_233	15713621	(A) Quantitative ChIP assays of the binding of Sp1, CREB,  and CBP to the  bcl-2 P1 promoter.	bind
7426	1	3060	6	10	NULL	NULL	NULL	Sp1	GP		bind					bcl-2	GP			P1 promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_233	15713621	(A) Quantitative ChIP assays of the binding of Sp1, CREB,  and CBP to the  bcl-2 P1 promoter.	bind
7427	2	3060	6	10	NULL	NULL	NULL	CREB	GP		bind					bcl-2	GP			P1 promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_233	15713621	(A) Quantitative ChIP assays of the binding of Sp1, CREB,  and CBP to the  bcl-2 P1 promoter.	bind
7428	3	3060	6	10	NULL	NULL	NULL	CBP	GP		bind					bcl-2	GP			P1 promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_233	15713621	(A) Quantitative ChIP assays of the binding of Sp1, CREB,  and CBP to the  bcl-2 P1 promoter.	bind
6774	1	3061	5	10	NULL	NULL	NULL	Sec complex	GP		reconstituted into					proteoliposomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_97_5_553_s_122	10367885	(A) Radiolabeled pp F was bound to Sec complex reconstituted into proteoliposomes.	bind
6775	2	3061	5	10	NULL	NULL	NULL	pp F	GP	radiolabelled	bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_97_5_553_s_122	10367885	(A) Radiolabeled pp F was bound to Sec complex reconstituted into proteoliposomes.	bind
7429	2	3061	6	10	NULL	NULL	NULL	pp F	GP	radiolabeled	bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_97_5_553_s_122	10367885	(A) Radiolabeled pp F was bound to Sec complex reconstituted into proteoliposomes.	bind
7430	1	3061	6	10	NULL	NULL	NULL	Sec complex	GP		reconstituted into					proteoliposomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_97_5_553_s_122	10367885	(A) Radiolabeled pp F was bound to Sec complex reconstituted into proteoliposomes.	bind
6776	1	3062	5	10	NULL	NULL	NULL	SLC	GP		activate					Rap1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_417_s_40	12707305	(A) Rap1 activation by SLC.	bind
7431	1	3062	6	10	NULL	NULL	NULL	SLC	GP		activates					Rap1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_417_s_40	12707305	(A) Rap1 activation by SLC.	bind
10046	1	3063	5	10	NULL	NULL	NULL	Ras-GTP	GP		bind					Raf1	GP	GST tagged	RBD		NULL		NULL	NULL	NULL	NULL	gw70_febslett_579_2_455_s_214	15642358	(a) Ras activity in spreading NIH 3T3 fibroblasts was quantified  at different timepoints after plating on fibronectin as indicated, employing a Ras  activation assay based on Ras-GTP pulldowns using the GST-tagged Ras binding domain  (RBD) of Raf1.	bind
10047	2	3063	5	10	NULL	NULL	NULL	RBD	AminoAcid		is					Ras binding domain	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_febslett_579_2_455_s_214	15642358	(a) Ras activity in spreading NIH 3T3 fibroblasts was quantified  at different timepoints after plating on fibronectin as indicated, employing a Ras  activation assay based on Ras-GTP pulldowns using the GST-tagged Ras binding domain  (RBD) of Raf1.	bind
7749	1	3063	6	10	NULL	NULL	NULL	Ras-GTP	GP		bind					Raf1	GP	GST tagged	RBD		NULL		NULL	NULL	NULL	NULL	gw70_febslett_579_2_455_s_214	15642358	(a) Ras activity in spreading NIH 3T3 fibroblasts was quantified  at different timepoints after plating on fibronectin as indicated, employing a Ras  activation assay based on Ras-GTP pulldowns using the GST-tagged Ras binding domain  (RBD) of Raf1.	bind
7750	2	3063	6	10	NULL	NULL	NULL	RBD	AminoAcid		is					Ras binding domain	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_febslett_579_2_455_s_214	15642358	(a) Ras activity in spreading NIH 3T3 fibroblasts was quantified  at different timepoints after plating on fibronectin as indicated, employing a Ras  activation assay based on Ras-GTP pulldowns using the GST-tagged Ras binding domain  (RBD) of Raf1.	bind
6777	1	3065	5	10	NULL	NULL	NULL	RasG12V	GP		bind					MST1	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_4_253_s_139	11864565	(A) RasG12V binds MST1 through NORE1.	bind
6778	2	3065	5	10	NULL	NULL	NULL	statement 1	Process		occurs through					NORE1	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_4_253_s_139	11864565	(A) RasG12V binds MST1 through NORE1.	bind
7432	1	3065	6	10	NULL	NULL	NULL	RasG12V	GP		bind					MST1	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_4_253_s_139	11864565	(A) RasG12V binds MST1 through NORE1.	bind
8186	2	3065	6	10	NULL	NULL	NULL	statement 1	Process		occurs through					NORE1	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_4_253_s_139	11864565	(A) RasG12V binds MST1 through NORE1.	bind
6779	1	3067	5	10	NULL	NULL	NULL	3H-PREGS	Chemical		bind					GABA receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1619_3_301_s_757	12573490	(A) receptor:  3H-PREGS binding to GABA receptor.	bind
7433	1	3067	6	10	NULL	NULL	NULL	3H-PREGS	Chemical		bind					GABA receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1619_3_301_s_757	12573490	(A) receptor:  3H-PREGS binding to GABA receptor.	bind
6780	1	3068	5	10	NULL	NULL	NULL	IRP1	GP	Manduca;; recombinant	bind		specifically			ferritin	GP	M. sexta		IRE transcripts	NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_85_s_185	11719072	(A) Recombinant  Manduca IRP1 binds specifically  M. sexta ferritin IRE transcripts.	bind
7434	1	3068	6	10	NULL	NULL	NULL	IRP1	GP	Manduca;; recombinant	bind		specifically			ferritin	GP	M.sexta		IRE transcripts	NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_85_s_185	11719072	(A) Recombinant  Manduca IRP1 binds specifically  M. sexta ferritin IRE transcripts.	bind
6781	1	3070	5	10	NULL	NULL	NULL	IBP39	GP	recombinant	bind					ferredoxin	CellComponent	single		Inr element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_22_7872_s_274	11604521	(A) Recombinant IBP39 binds the ferredoxin single Inr element.	bind
7435	1	3070	6	10	NULL	NULL	NULL	IBP39	GP	recombinant	bind					ferredoxin	Chemical	single		Inr element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_22_7872_s_274	11604521	(A) Recombinant IBP39 binds the ferredoxin single Inr element.	bind
6782	1	3071	5	10	NULL	NULL	NULL	hrs	GP	recombinant	bind					actinin-4	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2470_s_342	15772161	(A) Recombinant protein binding experiments suggest that there is an  ordered assembly for the complex: 1) hrs binds to actinin-4; 2) BERP binds to hrs/actinin-4;  and 3) myosin V binds to hrs/actinin-4/BERP.	bind
6783	2	3071	5	10	NULL	NULL	NULL	BERP	GP	recombinant	bind					hrs/actinin-4	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2470_s_342	15772161	(A) Recombinant protein binding experiments suggest that there is an  ordered assembly for the complex: 1) hrs binds to actinin-4; 2) BERP binds to hrs/actinin-4;  and 3) myosin V binds to hrs/actinin-4/BERP.	bind
6784	3	3071	5	10	NULL	NULL	NULL	myosin V	GP	recombinant	bind					hrs/actinin-4/BERP	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2470_s_342	15772161	(A) Recombinant protein binding experiments suggest that there is an  ordered assembly for the complex: 1) hrs binds to actinin-4; 2) BERP binds to hrs/actinin-4;  and 3) myosin V binds to hrs/actinin-4/BERP.	bind
7486	1	3071	6	10	NULL	NULL	NULL	hrs	GP	recombinant	bind					actinin-4	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2470_s_342	15772161	(A) Recombinant protein binding experiments suggest that there is an  ordered assembly for the complex: 1) hrs binds to actinin-4; 2) BERP binds to hrs/actinin-4;  and 3) myosin V binds to hrs/actinin-4/BERP.	bind
7487	2	3071	6	10	NULL	NULL	NULL	BERP	GP	recombinant	bind					hrs/actinin-4	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2470_s_342	15772161	(A) Recombinant protein binding experiments suggest that there is an  ordered assembly for the complex: 1) hrs binds to actinin-4; 2) BERP binds to hrs/actinin-4;  and 3) myosin V binds to hrs/actinin-4/BERP.	bind
7488	3	3071	6	10	NULL	NULL	NULL	myosin V	GP	recombinant	bind					hrs/actinin-4/BERP	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2470_s_342	15772161	(A) Recombinant protein binding experiments suggest that there is an  ordered assembly for the complex: 1) hrs binds to actinin-4; 2) BERP binds to hrs/actinin-4;  and 3) myosin V binds to hrs/actinin-4/BERP.	bind
6785	1	3072	5	10	NULL	NULL	NULL	SWI/SNF	GP	recruitment of	results in					protein A	GP	stabilized binding of			NULL		NULL	NULL	NULL	NULL	gw60_cell_109_3_267_s_122	12015975	(A) recruits a chromatin-remodeling complex (SWI/SNF), which results in stabilized binding of protein A through an ATP-dependent perturbation of nucleosomal structure.	bind
6786	2	3072	5	10	NULL	NULL	NULL	SWI/SNF	GP		is a type of					chromatin-remodeling complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_109_3_267_s_122	12015975	(A) recruits a chromatin-remodeling complex (SWI/SNF), which results in stabilized binding of protein A through an ATP-dependent perturbation of nucleosomal structure.	bind
6787	3	3072	5	10	NULL	NULL	NULL	nucleosomal structure	CellComponent	perturbation of	is dependent on					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_109_3_267_s_122	12015975	(A) recruits a chromatin-remodeling complex (SWI/SNF), which results in stabilized binding of protein A through an ATP-dependent perturbation of nucleosomal structure.	bind
44740	4	3072	5	10	NULL	NULL	NULL	statement 1	Process		occurs through					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_109_3_267_s_122	12015975	(A) recruits a chromatin-remodeling complex (SWI/SNF), which results in stabilized binding of protein A through an ATP-dependent perturbation of nucleosomal structure.	bind
7436	1	3072	6	10	NULL	NULL	NULL	SWI/SNF	GP		is a type of					chromatin-remodeling complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_109_3_267_s_122	12015975	(A) recruits a chromatin-remodeling complex (SWI/SNF), which results in stabilized binding of protein A through an ATP-dependent perturbation of nucleosomal structure.	bind
7437	2	3072	6	10	NULL	NULL	NULL	SWI/SNF	GP	recruitment of	results in					Protein A	GP	stabilized binding of			NULL		NULL	NULL	NULL	NULL	gw60_cell_109_3_267_s_122	12015975	(A) recruits a chromatin-remodeling complex (SWI/SNF), which results in stabilized binding of protein A through an ATP-dependent perturbation of nucleosomal structure.	bind
7438	3	3072	6	10	NULL	NULL	NULL	nucleosomal structure	CellComponent	perturbation of	is dependent on					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_109_3_267_s_122	12015975	(A) recruits a chromatin-remodeling complex (SWI/SNF), which results in stabilized binding of protein A through an ATP-dependent perturbation of nucleosomal structure.	bind
7439	4	3072	6	10	NULL	NULL	NULL	statement 2	Process		occurs through					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_109_3_267_s_122	12015975	(A) recruits a chromatin-remodeling complex (SWI/SNF), which results in stabilized binding of protein A through an ATP-dependent perturbation of nucleosomal structure.	bind
6788	1	3073	5	10	NULL	NULL	NULL	rhodanese	GP		bind					EL229C	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_71	11672529	(A) Refolding  of 0.5 muM rhodanese bound to either  0.5 muM EL229C ( ) or EL229C-B ( ) in the  presence of 1 muM GroES and 5  mM ATP.	bind
6789	2	3073	5	10	NULL	NULL	NULL	statement 1	Process		in the presence of					GroES	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_71	11672529	(A) Refolding  of 0.5 muM rhodanese bound to either  0.5 muM EL229C ( ) or EL229C-B ( ) in the  presence of 1 muM GroES and 5  mM ATP.	bind
6790	3	3073	5	10	NULL	NULL	NULL	statement 1	Process		in the presence of					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_71	11672529	(A) Refolding  of 0.5 muM rhodanese bound to either  0.5 muM EL229C ( ) or EL229C-B ( ) in the  presence of 1 muM GroES and 5  mM ATP.	bind
6791	4	3073	5	10	NULL	NULL	NULL	rhodanese	GP		bind					EL229C-B	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_71	11672529	(A) Refolding  of 0.5 muM rhodanese bound to either  0.5 muM EL229C ( ) or EL229C-B ( ) in the  presence of 1 muM GroES and 5  mM ATP.	bind
6792	5	3073	5	10	NULL	NULL	NULL	statement 4	Process		in the presence of					GroES	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_71	11672529	(A) Refolding  of 0.5 muM rhodanese bound to either  0.5 muM EL229C ( ) or EL229C-B ( ) in the  presence of 1 muM GroES and 5  mM ATP.	bind
6793	6	3073	5	10	NULL	NULL	NULL	statement 4	Process		in the presence of					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_71	11672529	(A) Refolding  of 0.5 muM rhodanese bound to either  0.5 muM EL229C ( ) or EL229C-B ( ) in the  presence of 1 muM GroES and 5  mM ATP.	bind
6794	7	3073	5	10	NULL	NULL	NULL	statement 2	Process		undergoes					refolding	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_71	11672529	(A) Refolding  of 0.5 muM rhodanese bound to either  0.5 muM EL229C ( ) or EL229C-B ( ) in the  presence of 1 muM GroES and 5  mM ATP.	bind
6795	8	3073	5	10	NULL	NULL	NULL	statement 3	Process		undergoes					refolding	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_71	11672529	(A) Refolding  of 0.5 muM rhodanese bound to either  0.5 muM EL229C ( ) or EL229C-B ( ) in the  presence of 1 muM GroES and 5  mM ATP.	bind
6796	9	3073	5	10	NULL	NULL	NULL	statement 6	Process		undergoes					refolding	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_71	11672529	(A) Refolding  of 0.5 muM rhodanese bound to either  0.5 muM EL229C ( ) or EL229C-B ( ) in the  presence of 1 muM GroES and 5  mM ATP.	bind
6797	10	3073	5	10	NULL	NULL	NULL	statement 7	Process		undergoes					refolding	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_71	11672529	(A) Refolding  of 0.5 muM rhodanese bound to either  0.5 muM EL229C ( ) or EL229C-B ( ) in the  presence of 1 muM GroES and 5  mM ATP.	bind
7712	1	3073	6	10	NULL	NULL	NULL	rhodanese	GP		bind					EL229C	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_71	11672529	(A) Refolding  of 0.5 muM rhodanese bound to either  0.5 muM EL229C ( ) or EL229C-B ( ) in the  presence of 1 muM GroES and 5  mM ATP.	bind
7713	2	3073	6	10	NULL	NULL	NULL	rhodanese	GP		bind					EL229C-B	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_71	11672529	(A) Refolding  of 0.5 muM rhodanese bound to either  0.5 muM EL229C ( ) or EL229C-B ( ) in the  presence of 1 muM GroES and 5  mM ATP.	bind
7714	3	3073	6	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_71	11672529	(A) Refolding  of 0.5 muM rhodanese bound to either  0.5 muM EL229C ( ) or EL229C-B ( ) in the  presence of 1 muM GroES and 5  mM ATP.	bind
7715	4	3073	6	10	NULL	NULL	NULL	statement 1	Process		occurs in presence of					GroES	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_71	11672529	(A) Refolding  of 0.5 muM rhodanese bound to either  0.5 muM EL229C ( ) or EL229C-B ( ) in the  presence of 1 muM GroES and 5  mM ATP.	bind
7716	5	3073	6	10	NULL	NULL	NULL	statement 2	Process		occurs in presence of					GroES	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_71	11672529	(A) Refolding  of 0.5 muM rhodanese bound to either  0.5 muM EL229C ( ) or EL229C-B ( ) in the  presence of 1 muM GroES and 5  mM ATP.	bind
7717	6	3073	6	10	NULL	NULL	NULL	statement 1	Process		occurs in presence of					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_71	11672529	(A) Refolding  of 0.5 muM rhodanese bound to either  0.5 muM EL229C ( ) or EL229C-B ( ) in the  presence of 1 muM GroES and 5  mM ATP.	bind
7718	7	3073	6	10	NULL	NULL	NULL	statement 2	Process		occurs in presence of					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_71	11672529	(A) Refolding  of 0.5 muM rhodanese bound to either  0.5 muM EL229C ( ) or EL229C-B ( ) in the  presence of 1 muM GroES and 5  mM ATP.	bind
9692	8	3073	6	10	NULL	NULL	NULL	rhodanese	GP	refolding of	occurs during					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_71	11672529	(A) Refolding  of 0.5 muM rhodanese bound to either  0.5 muM EL229C ( ) or EL229C-B ( ) in the  presence of 1 muM GroES and 5  mM ATP.	bind
9693	9	3073	6	10	NULL	NULL	NULL	rhodanese	GP	refolding of	occurs during					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_71	11672529	(A) Refolding  of 0.5 muM rhodanese bound to either  0.5 muM EL229C ( ) or EL229C-B ( ) in the  presence of 1 muM GroES and 5  mM ATP.	bind
6829	1	3075	5	10	NULL	NULL	NULL	bilirubin	Chemical		bind					HSA	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1750_1_93_s_151	15890566	(A) Relative fluorescence of bilirubin bound to HSA in the presence of 0.0  M ( ), 1.2 M ( ), 2.2 M () and 2.4 M ( ) and 6.0 M ( ) GnHCl.	bind
6830	2	3075	5	10	NULL	NULL	NULL	statement 1	Process		in the presence of					GnHCl	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1750_1_93_s_151	15890566	(A) Relative fluorescence of bilirubin bound to HSA in the presence of 0.0  M ( ), 1.2 M ( ), 2.2 M () and 2.4 M ( ) and 6.0 M ( ) GnHCl.	bind
7489	1	3075	6	10	NULL	NULL	NULL	bilirubin	Chemical		bind					HSA	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1750_1_93_s_151	15890566	(A) Relative fluorescence of bilirubin bound to HSA in the presence of 0.0  M ( ), 1.2 M ( ), 2.2 M () and 2.4 M ( ) and 6.0 M ( ) GnHCl.	bind
7492	2	3075	6	10	NULL	NULL	NULL	statement 1	Process		occurs in presence of					GnHCl	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1750_1_93_s_151	15890566	(A) Relative fluorescence of bilirubin bound to HSA in the presence of 0.0  M ( ), 1.2 M ( ), 2.2 M () and 2.4 M ( ) and 6.0 M ( ) GnHCl.	bind
6831	1	3077	5	10	NULL	NULL	NULL	fraction S	NucleicAcid		bind					anti-Z-DNA antibody	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_14_5382_s_271	16809774	(A) Relaxed minicircles; (B) fraction S minicircles; (C)  fraction S bound to anti-Z-DNA antibody; (D) fraction S bound to SSB.	bind
6832	2	3077	5	10	NULL	NULL	NULL	fraction S	NucleicAcid		bind					SSB	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_14_5382_s_271	16809774	(A) Relaxed minicircles; (B) fraction S minicircles; (C)  fraction S bound to anti-Z-DNA antibody; (D) fraction S bound to SSB.	bind
7493	1	3077	6	10	NULL	NULL	NULL	fraction S	NucleicAcid		bind					anti-Z-DNA antibody	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_14_5382_s_271	16809774	(A) Relaxed minicircles; (B) fraction S minicircles; (C)  fraction S bound to anti-Z-DNA antibody; (D) fraction S bound to SSB.	bind
7494	2	3077	6	10	NULL	NULL	NULL	fraction S	NucleicAcid		bind					SSB	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_14_5382_s_271	16809774	(A) Relaxed minicircles; (B) fraction S minicircles; (C)  fraction S bound to anti-Z-DNA antibody; (D) fraction S bound to SSB.	bind
6858	1	3078	5	10	NULL	NULL	NULL	phage A1-10	Organism		bind					OppA-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_1_51_s_217	14679224	(A) Representative  dose-response graph of peptide inhibition of binding of phage A1-10 to OppA-1.	bind
7496	1	3078	6	10	NULL	NULL	NULL	phage A1-10	Organism		bind					OppA-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_1_51_s_217	14679224	(A) Representative  dose-response graph of peptide inhibition of binding of phage A1-10 to OppA-1.	bind
6859	1	3079	5	10	NULL	NULL	NULL	Hal3p	GP		bind					Ppz1deltaN-GST	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8683_s_203	16166647	(A) Representative  Western blot showing the amount of Hal3p (top) or Ypi1p (bottom) bound by the Ppz1deltaN-GST affinity resin at the pH indicated and the amount of Hal3p or Ypi1p in the starting  extracts (input).	bind
6860	2	3079	5	10	NULL	NULL	NULL	Ypi1p	GP		bind					Ppz1deltaN-GST	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8683_s_203	16166647	(A) Representative  Western blot showing the amount of Hal3p (top) or Ypi1p (bottom) bound by the Ppz1deltaN-GST affinity resin at the pH indicated and the amount of Hal3p or Ypi1p in the starting  extracts (input).	bind
53136	3	3079	5	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8683_s_203	16166647	(A) Representative  Western blot showing the amount of Hal3p (top) or Ypi1p (bottom) bound by the Ppz1deltaN-GST affinity resin at the pH indicated and the amount of Hal3p or Ypi1p in the starting  extracts (input).	bind
7498	1	3079	6	10	NULL	NULL	NULL	Hal3p	GP		bind					Ppz1deltaN-GST	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8683_s_203	16166647	(A) Representative  Western blot showing the amount of Hal3p (top) or Ypi1p (bottom) bound by the Ppz1deltaN-GST affinity resin at the pH indicated and the amount of Hal3p or Ypi1p in the starting  extracts (input).	bind
7499	2	3079	6	10	NULL	NULL	NULL	Ypi1p	GP		bind					Ppz1deltaN-GST	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8683_s_203	16166647	(A) Representative  Western blot showing the amount of Hal3p (top) or Ypi1p (bottom) bound by the Ppz1deltaN-GST affinity resin at the pH indicated and the amount of Hal3p or Ypi1p in the starting  extracts (input).	bind
7500	3	3079	6	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8683_s_203	16166647	(A) Representative  Western blot showing the amount of Hal3p (top) or Ypi1p (bottom) bound by the Ppz1deltaN-GST affinity resin at the pH indicated and the amount of Hal3p or Ypi1p in the starting  extracts (input).	bind
6908	1	3080	5	10	NULL	NULL	NULL	TBPS	Chemical		bind					C57BL/6 brain sections	OrganismPart	mouse 			NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_48_4_469_s_141	15755475	(A) Representative autoradiographic images of [35]TBPS binding to C57BL/6 and  2I77 mouse brain sections in the presence and absence  of 0.5  M GABA and 30  M DMCM. Gr, granule cell layer; Mol, molecular layer; (B)  quantitative results of the regions.	bind
6913	2	3080	5	10	NULL	NULL	NULL	TBPS	Chemical		bind					2I77 brain sections	OrganismPart	mouse 			NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_48_4_469_s_141	15755475	(A) Representative autoradiographic images of [35]TBPS binding to C57BL/6 and  2I77 mouse brain sections in the presence and absence  of 0.5  M GABA and 30  M DMCM. Gr, granule cell layer; Mol, molecular layer; (B)  quantitative results of the regions.	bind
7501	1	3080	6	10	NULL	NULL	NULL	TBPS	Chemical		bind					C57BL/6 brain sections	OrganismPart	mouse 			NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_48_4_469_s_141	15755475	(A) Representative autoradiographic images of [35]TBPS binding to C57BL/6 and  2I77 mouse brain sections in the presence and absence  of 0.5  M GABA and 30  M DMCM. Gr, granule cell layer; Mol, molecular layer; (B)  quantitative results of the regions.	bind
7502	2	3080	6	10	NULL	NULL	NULL	TBPS	Chemical		bind					2I77 brain sections	OrganismPart	mouse			NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_48_4_469_s_141	15755475	(A) Representative autoradiographic images of [35]TBPS binding to C57BL/6 and  2I77 mouse brain sections in the presence and absence  of 0.5  M GABA and 30  M DMCM. Gr, granule cell layer; Mol, molecular layer; (B)  quantitative results of the regions.	bind
6930	1	3082	5	10	NULL	NULL	NULL	Mot1p	GP		bind					HXT genes	GP				NULL	wild-type cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_167	15923605	(A) Representative PCR and PhosphorImager  quantification of Mot1p binding to  HXT genes in wild-type (Wt),  gcn5delta,  spt3delta, and  spt8delta cells.	bind
6931	2	3082	5	10	NULL	NULL	NULL	Mot1p	GP		bind					HXT genes	GP				NULL	gcn5delta cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_167	15923605	(A) Representative PCR and PhosphorImager  quantification of Mot1p binding to  HXT genes in wild-type (Wt),  gcn5delta,  spt3delta, and  spt8delta cells.	bind
6932	3	3082	5	10	NULL	NULL	NULL	Mot1p	GP		bind					HXT genes	GP				NULL	spt3delta cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_167	15923605	(A) Representative PCR and PhosphorImager  quantification of Mot1p binding to  HXT genes in wild-type (Wt),  gcn5delta,  spt3delta, and  spt8delta cells.	bind
6933	4	3082	5	10	NULL	NULL	NULL	Mot1p	GP		bind					HXT genes	GP				NULL	spt8delta cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_167	15923605	(A) Representative PCR and PhosphorImager  quantification of Mot1p binding to  HXT genes in wild-type (Wt),  gcn5delta,  spt3delta, and  spt8delta cells.	bind
7503	1	3082	6	10	NULL	NULL	NULL	Mot1p	GP		bind					HXT genes	GP				NULL	wild type cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_167	15923605	(A) Representative PCR and PhosphorImager  quantification of Mot1p binding to  HXT genes in wild-type (Wt),  gcn5delta,  spt3delta, and  spt8delta cells.	bind
7504	2	3082	6	10	NULL	NULL	NULL	Mot1p	GP		bind					HXT genes	GP				NULL	gcn5delta cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_167	15923605	(A) Representative PCR and PhosphorImager  quantification of Mot1p binding to  HXT genes in wild-type (Wt),  gcn5delta,  spt3delta, and  spt8delta cells.	bind
7505	3	3082	6	10	NULL	NULL	NULL	Mot1p	GP		bind					HXT genes	GP				NULL	spt3delta cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_167	15923605	(A) Representative PCR and PhosphorImager  quantification of Mot1p binding to  HXT genes in wild-type (Wt),  gcn5delta,  spt3delta, and  spt8delta cells.	bind
7506	4	3082	6	10	NULL	NULL	NULL	Mot1p	GP		bind					HXT genes	GP				NULL	spt8delta cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_167	15923605	(A) Representative PCR and PhosphorImager  quantification of Mot1p binding to  HXT genes in wild-type (Wt),  gcn5delta,  spt3delta, and  spt8delta cells.	bind
6934	1	3085	5	10	NULL	NULL	NULL	apoB-100	GP		bind					apo[a]	GP				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_46_4_769_s_159	15654123	(A) resulted in high-levels of Lp[a, with most of  the apoB-100 bound to apo[a (C).	bind
7507	1	3085	6	10	NULL	NULL	NULL	apoB-100	GP		bind					apo[a]	GP				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_46_4_769_s_159	15654123	(A) resulted in high-levels of Lp[a, with most of  the apoB-100 bound to apo[a (C).	bind
6936	1	3086	5	10	NULL	NULL	NULL	CodY	GP		bind					PD-3	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_10_3118_s_196	12730172	(A) Results of  CodY binding to PD-3, the sigmaD-dependent promoter.	bind
44741	2	3086	5	10	NULL	NULL	NULL	PD-3	NucleicAcid		is dependent on					sigmaD	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_10_3118_s_196	12730172	(A) Results of  CodY binding to PD-3, the sigmaD-dependent promoter.	bind
7508	1	3086	6	10	NULL	NULL	NULL	PD-3	NucleicAcid		is dependent on					sigmaD	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_10_3118_s_196	12730172	(A) Results of  CodY binding to PD-3, the sigmaD-dependent promoter.	bind
7509	2	3086	6	10	NULL	NULL	NULL	CodY	GP		bind					PD-3	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_10_3118_s_196	12730172	(A) Results of  CodY binding to PD-3, the sigmaD-dependent promoter.	bind
6938	1	3089	5	10	NULL	NULL	NULL	rIB2	GP		bind					MKK3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4073_s_192	12024021	(A) rIB2 binds to MKK3.	bind
7512	1	3089	6	10	NULL	NULL	NULL	rIB2	GP		bind					MKK3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4073_s_192	12024021	(A) rIB2 binds to MKK3.	bind
6941	1	3090	5	10	NULL	NULL	NULL	RXR	GP		bind			LBD		SRC-1	GP		LxxLL motif		NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_545_s_122	10882139	(a) Ribbon drawings of the RXR  LBD bound to the SRC-1 LxxLL motif (magenta) and 9cRA.	bind
6942	2	3090	5	10	NULL	NULL	NULL	RXR	GP		bind			LBD		9cRA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_545_s_122	10882139	(a) Ribbon drawings of the RXR  LBD bound to the SRC-1 LxxLL motif (magenta) and 9cRA.	bind
7513	1	3090	6	10	NULL	NULL	NULL	RXR	GP		bind			LBD		SRC-1	GP		LxxLL motif		NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_545_s_122	10882139	(a) Ribbon drawings of the RXR  LBD bound to the SRC-1 LxxLL motif (magenta) and 9cRA.	bind
7514	2	3090	6	10	NULL	NULL	NULL	RXR	GP		bind			LBD		9cRA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_545_s_122	10882139	(a) Ribbon drawings of the RXR  LBD bound to the SRC-1 LxxLL motif (magenta) and 9cRA.	bind
6943	1	3092	5	10	NULL	NULL	NULL	HP0525	GP		bind					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_7_1919_s_84	15028675	(A) Ribbon presentation of  HP0525 bound to ADP.	bind
7515	1	3092	6	10	NULL	NULL	NULL	HP0525	GP		bind					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_7_1919_s_84	15028675	(A) Ribbon presentation of  HP0525 bound to ADP.	bind
6946	1	3093	5	10	NULL	NULL	NULL	ARF1t	GP	nucleotide-free;; human	bind					Gea2	GP	yeast	Sec7 domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_237_s_151	9790530	(A) Ribbon representation of nucleotide-free human ARF1t (blue) bound  to the Sec7 domain of yeast Gea2 (pink).	bind
7516	1	3093	6	10	NULL	NULL	NULL	ARF1t	GP	nucleotide-free;; human	bind					Gea2	GP	yeast	Sec7 domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_237_s_151	9790530	(A) Ribbon representation of nucleotide-free human ARF1t (blue) bound  to the Sec7 domain of yeast Gea2 (pink).	bind
6947	1	3095	5	10	NULL	NULL	NULL	Rifampin	Chemical		bind					TL	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1688_2_102_s_101	14990340	(A) Rifampin binding to TL.	bind
7517	1	3095	6	10	NULL	NULL	NULL	Rifampin	Chemical		bind					TL	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1688_2_102_s_101	14990340	(A) Rifampin binding to TL.	bind
6948	1	3096	5	10	NULL	NULL	NULL	Rig protein	GP		bind					DHR3	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_131_1_25_s_202	14645129	(A) Rig protein binds to DHR3, EcR, betaFTZ-F1, USP and SVP in vitro.	bind
6949	2	3096	5	10	NULL	NULL	NULL	Rig protein	GP		bind					EcR	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_131_1_25_s_202	14645129	(A) Rig protein binds to DHR3, EcR, betaFTZ-F1, USP and SVP in vitro.	bind
6952	3	3096	5	10	NULL	NULL	NULL	Rig protein	GP		bind					betaFTZ-F1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_131_1_25_s_202	14645129	(A) Rig protein binds to DHR3, EcR, betaFTZ-F1, USP and SVP in vitro.	bind
6953	4	3096	5	10	NULL	NULL	NULL	Rig protein	GP		bind					USP	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_131_1_25_s_202	14645129	(A) Rig protein binds to DHR3, EcR, betaFTZ-F1, USP and SVP in vitro.	bind
6955	5	3096	5	10	NULL	NULL	NULL	Rig protein	GP		bind					SVP	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_131_1_25_s_202	14645129	(A) Rig protein binds to DHR3, EcR, betaFTZ-F1, USP and SVP in vitro.	bind
7518	1	3096	6	10	NULL	NULL	NULL	Rig protein	GP		bind					DHR3	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_131_1_25_s_202	14645129	(A) Rig protein binds to DHR3, EcR, betaFTZ-F1, USP and SVP in vitro.	bind
7519	2	3096	6	10	NULL	NULL	NULL	Rig protein	GP		bind					EcR	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_131_1_25_s_202	14645129	(A) Rig protein binds to DHR3, EcR, betaFTZ-F1, USP and SVP in vitro.	bind
7520	3	3096	6	10	NULL	NULL	NULL	Rig protein	GP		bind					betaFTZ-F1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_131_1_25_s_202	14645129	(A) Rig protein binds to DHR3, EcR, betaFTZ-F1, USP and SVP in vitro.	bind
7521	4	3096	6	10	NULL	NULL	NULL	Rig protein	GP		bind					USP	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_131_1_25_s_202	14645129	(A) Rig protein binds to DHR3, EcR, betaFTZ-F1, USP and SVP in vitro.	bind
7522	5	3096	6	10	NULL	NULL	NULL	Rig protein	GP		bind					SVP	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_131_1_25_s_202	14645129	(A) Rig protein binds to DHR3, EcR, betaFTZ-F1, USP and SVP in vitro.	bind
6956	1	3097	5	10	NULL	NULL	NULL	RIP2	GP		bind					caspase-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_99_s_173	11051551	(A) RIP2 binds  caspase-1 in an LPS-dependent manner (upper panel, lane 3 versus lane 1).	bind
6957	2	3097	5	10	NULL	NULL	NULL	statement 1	Process		is dependent on					LPS	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_99_s_173	11051551	(A) RIP2 binds  caspase-1 in an LPS-dependent manner (upper panel, lane 3 versus lane 1).	bind
7523	1	3097	6	10	NULL	NULL	NULL	RIP2	GP		bind					caspase-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_99_s_173	11051551	(A) RIP2 binds  caspase-1 in an LPS-dependent manner (upper panel, lane 3 versus lane 1).	bind
7524	2	3097	6	10	NULL	NULL	NULL	statement 1	Process		is dependent on					LPS	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_99_s_173	11051551	(A) RIP2 binds  caspase-1 in an LPS-dependent manner (upper panel, lane 3 versus lane 1).	bind
6958	1	3098	5	10	NULL	NULL	NULL	RIP2	GP		bind					caspase-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_99_s_89	11051551	(A) RIP2 binds caspase-1 (left and right upper panels).	bind
7525	1	3098	6	10	NULL	NULL	NULL	RIP2	GP		bind					caspase-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_99_s_89	11051551	(A) RIP2 binds caspase-1 (left and right upper panels).	bind
79247	1	3100	11	NULL	NULL	0	NULL	RNA	NucleicAcidSubstance		is a part of 					RNase P assay	ResearchActivity				NULL		0	NULL	NULL	NULL	gw60_febslett_511_1_107_s_112	11821058	(A) RNA in the RNase P assay, we sought to provide a competitor RNA that could bind NeoR or R3G through non-specific, electrostatic interactions and thus reduce their availability for similar interactions with the ptRNA substrate.	bind
7312	1	3102	5	11	NULL	0	NULL	RNA polymerase II 	GP		paused at					arrest site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
7313	2	3102	5	11	NULL	0	NULL	statement 1	Process		expose					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
7314	3	3102	5	11	NULL	0	NULL	SLBP	GP		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
7315	4	3102	5	11	NULL	0	NULL	U7 snRNP	NucleicAcid		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
7316	5	3102	5	11	NULL	0	NULL	statement 2	Process		allows					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
7317	6	3102	5	11	NULL	0	NULL	statement 2	Process		allows					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
7318	7	3102	5	11	NULL	0	NULL	statement 2	Process		allows					transcript	NucleicAcid	processing of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
9142	1	3102	7	11	NULL	0	NULL	SLBP	GP		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
9143	2	3102	7	11	NULL	0	NULL	U7 snRNP	NucleicAcid		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
9144	3	3102	7	11	NULL	0	NULL	RNA polymerase II	GP		pause at					arrest site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
9145	4	3102	7	11	NULL	0	NULL	statement 3	Process		allows					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
9146	5	3102	7	11	NULL	0	NULL	statement 3	Process		allows					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
54165	7	3102	7	11	NULL	0	NULL	statement 3	Process		allows					transcript	NucleicAcid	processing of 			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
79248	1	3102	11	NULL	NULL	0	NULL	 RNA polymerase II	GeneOrProtein		paused at the					arrest site	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
79249	2	3102	11	NULL	NULL	0	NULL	SLBP	GeneOrProtein		binds					RNA	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
79250	3	3102	11	NULL	NULL	0	NULL	 U7 snRNP	NucleicAcidSubstance		binds					RNA	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
79251	4	3102	11	NULL	NULL	0	NULL	statement 1	Process		minimize exposure for 					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
79252	5	3102	11	NULL	NULL	0	NULL	statement 2	Process		minimize exposure for 					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
79253	6	3102	11	NULL	NULL	0	NULL	statement 2	Process		occurs along with					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
79254	7	3102	11	NULL	NULL	0	NULL	statement 1	Process		is a part of processing					transcript	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
79255	8	3102	11	NULL	NULL	0	NULL	statement 2	Process		is a part of processing					transcript	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
79256	9	3102	11	NULL	NULL	0	NULL	statement 3	Process		is a part of processing					transcript	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_12_4046_s_279	12773550	(A) RNA polymerase II paused at the arrest site leaves just enough RNA exposed  to allow binding of SLBP and the U7 snRNP and processing of the transcript.	bind
7440	1	3105	5	11	NULL	0	NULL	RNA	NucleicAcid		bind					RRM3	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_98_6_835_s_234	10499800	(A) RNA would favor binding of  RRM3 and then RRM4.	bind
7441	2	3105	5	11	NULL	0	NULL	RNA	NucleicAcid		bind					RRM4	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_98_6_835_s_234	10499800	(A) RNA would favor binding of  RRM3 and then RRM4.	bind
9485	1	3105	7	11	NULL	0	NULL	RRM3	GP		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_98_6_835_s_234	10499800	(A) RNA would favor binding of  RRM3 and then RRM4.	bind
9486	2	3105	7	11	NULL	0	NULL	RRM4	GP		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_98_6_835_s_234	10499800	(A) RNA would favor binding of  RRM3 and then RRM4.	bind
79558	1	3105	11	NULL	NULL	0	NULL	RNA	NucleicAcidSubstance		binds to 					RRM3	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_cell_98_6_835_s_234	10499800	(A) RNA would favor binding of  RRM3 and then RRM4.	bind
79559	2	3105	11	NULL	NULL	0	NULL	RNA	NucleicAcidSubstance		binds to 					RRM4	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_cell_98_6_835_s_234	10499800	(A) RNA would favor binding of  RRM3 and then RRM4.	bind
79560	3	3105	11	NULL	NULL	0	NULL	statement 2	Process		occurs after					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cell_98_6_835_s_234	10499800	(A) RNA would favor binding of  RRM3 and then RRM4.	bind
7443	1	3106	5	11	NULL	0	NULL	Rtn1p	GP		bind					Sec6p 	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_7_3009_s_274	16624861	(A) Rtn1p binds to the Sec6p subunit of the exocyst.	bind
44742	2	3106	5	11	NULL	0	NULL	Sec6p	GP		is a subunit of					exocyst	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_7_3009_s_274	16624861	(A) Rtn1p binds to the Sec6p subunit of the exocyst.	bind
9147	1	3106	7	11	NULL	0	NULL	Rtn1p	GP		bind					Sec6p 	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_7_3009_s_274	16624861	(A) Rtn1p binds to the Sec6p subunit of the exocyst.	bind
44743	2	3106	7	11	NULL	0	NULL	Sec6p	GP		is a subunit of					exocyst	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_7_3009_s_274	16624861	(A) Rtn1p binds to the Sec6p subunit of the exocyst.	bind
79561	1	3106	11	NULL	NULL	0	NULL	Sec6p	GeneOrProtein		is a subunit of					exocyst	CellComponent				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_7_3009_s_274	16624861	(A) Rtn1p binds to the Sec6p subunit of the exocyst.	bind
79562	2	3106	11	NULL	NULL	0	NULL	Rtn1p	GeneOrProtein		binds to 					Sec6p	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_7_3009_s_274	16624861	(A) Rtn1p binds to the Sec6p subunit of the exocyst.	bind
7444	1	3108	5	11	NULL	0	NULL	sAPP695T	GP		bind					HK forms	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1571_3_225_s_245	12090937	(A) sAPP695T binds to HK forms.	bind
9148	1	3108	7	11	NULL	0	NULL	sAPP695T	GP		bind					HK forms	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1571_3_225_s_245	12090937	(A) sAPP695T binds to HK forms.	bind
79563	1	3108	11	NULL	NULL	0	NULL	sAPP695T	GeneOrProtein		binds to 					HK	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1571_3_225_s_245	12090937	(A) sAPP695T binds to HK forms.	bind
7445	1	3109	5	11	NULL	0	NULL	[125]DTX	Chemical		bind					Kv1.2	GP				NULL	transfected COS1 cells	NULL	NULL	NULL	NULL	gw60_neuron_16_4_843_s_150	8608002	(A) Saturable binding of [125]DTX to Kv1.2 in transfected COS1 cells.	bind
9149	1	3109	7	11	NULL	0	NULL	[125]DTX	Chemical		bind					Kv1.2	GP				NULL	transfected COS1 cells	NULL	NULL	NULL	NULL	gw60_neuron_16_4_843_s_150	8608002	(A) Saturable binding of [125]DTX to Kv1.2 in transfected COS1 cells.	bind
79564	1	3109	11	NULL	NULL	0	NULL	[125]DTX	Chemical		Saturably binds to					Kv1.2	GeneOrProtein	in transfected COS1 cells			NULL		0	NULL	NULL	NULL	gw60_neuron_16_4_843_s_150	8608002	(A) Saturable binding of [125]DTX to Kv1.2 in transfected COS1 cells.	bind
7446	1	3110	5	11	NULL	0	NULL	[3]RX 821002	Chemical		bind					2A AR membrane	CellComponent	wt			NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_42_6_855_s_103	12015212	(A) Saturation binding curve of [3]RX 821002 to wt  2A AR membrane preparation (5  g protein) was performed as described in  Materials and methods.	bind
9150	1	3110	7	11	NULL	0	NULL	[3]RX 821002	Chemical		bind					2A AR membrane	CellComponent	wt			NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_42_6_855_s_103	12015212	(A) Saturation binding curve of [3]RX 821002 to wt  2A AR membrane preparation (5  g protein) was performed as described in  Materials and methods.	bind
7447	1	3111	5	11	NULL	0	NULL	[35]GTP S	Chemical		bind					SPM	CellComponent	mouse;; brain			NULL		NULL	NULL	NULL	NULL	gw60_brainres_815_1_89_s_122	9974126	(A) Saturation binding of [35]GTP S binding to SPM from mouse brain.	bind
9151	1	3111	7	11	NULL	0	NULL	[35]GTP S	Chemical		bind					SPM	CellComponent	mouse;; brain			NULL		NULL	NULL	NULL	NULL	gw60_brainres_815_1_89_s_122	9974126	(A) Saturation binding of [35]GTP S binding to SPM from mouse brain.	bind
79833	1	3111	11	NULL	NULL	NULL	NULL	[35]GTP S	NonProteinOrNucleicAcidChemical		bind		Saturation			SPM	CellComponent	mouse;;brain			NULL		NULL	NULL	NULL	NULL	gw60_brainres_815_1_89_s_122	9974126	(A) Saturation binding of [35]GTP S binding to SPM from mouse brain.	bind
7448	1	3112	5	11	NULL	0	NULL	[3]P4	Chemical		bind					DPR	GP		LBD		NULL		NULL	NULL	NULL	NULL	gw60_febslett_465_1_12_s_161	10620698	(a) Scatchard analysis of [3]P4 and [3]17 ,20 -DP binding to the DPR-LBD.	bind
7449	2	3112	5	11	NULL	0	NULL	[3]17 ,20 -D	Chemical		bind					DPR	GP		LBD		NULL		NULL	NULL	NULL	NULL	gw60_febslett_465_1_12_s_161	10620698	(a) Scatchard analysis of [3]P4 and [3]17 ,20 -DP binding to the DPR-LBD.	bind
9152	1	3112	7	11	NULL	0	NULL	[3]P4	Chemical		bind					DPR	GP		LBD		NULL		NULL	NULL	NULL	NULL	gw60_febslett_465_1_12_s_161	10620698	(a) Scatchard analysis of [3]P4 and [3]17 ,20 -DP binding to the DPR-LBD.	bind
9153	2	3112	7	11	NULL	0	NULL	[3]17 ,20 -DP	Chemical		bind					DPR	GP		LBD		NULL		NULL	NULL	NULL	NULL	gw60_febslett_465_1_12_s_161	10620698	(a) Scatchard analysis of [3]P4 and [3]17 ,20 -DP binding to the DPR-LBD.	bind
79834	1	3112	11	NULL	NULL	0	NULL	17 ,20 -DP	NonProteinOrNucleicAcidChemical		binds to 					DPR-LBD	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_febslett_465_1_12_s_161	10620698	(a) Scatchard analysis of [3]P4 and [3]17 ,20 -DP binding to the DPR-LBD.	bind
79835	2	3112	11	NULL	NULL	NULL	NULL	P4	NonProteinOrNucleicAcidChemical		binds to 					DPR-LBD	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	gw60_febslett_465_1_12_s_161	10620698	(a) Scatchard analysis of [3]P4 and [3]17 ,20 -DP binding to the DPR-LBD.	bind
7450	1	3114	5	11	NULL	0	NULL	Mnk2a	GP		bind					MAPK	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_16_5692_s_474	12897141	(A) Schematic  presentation of Mnk2a bound to MAP kinase (MAPK).	bind
7451	2	3114	5	11	NULL	0	NULL	MAPK	GP		is					MAP kinase	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_16_5692_s_474	12897141	(A) Schematic  presentation of Mnk2a bound to MAP kinase (MAPK).	bind
9154	1	3114	7	11	NULL	0	NULL	Mnk2a 	GP		bind					MAP kinase	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_16_5692_s_474	12897141	(A) Schematic  presentation of Mnk2a bound to MAP kinase (MAPK).	bind
9155	2	3114	7	11	NULL	0	NULL	MAP kinase	GP		is					MAPK	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_16_5692_s_474	12897141	(A) Schematic  presentation of Mnk2a bound to MAP kinase (MAPK).	bind
79565	1	3114	11	NULL	NULL	0	NULL	Mnk2a	GeneOrProtein		binds to 					MAP kinase	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_16_5692_s_474	12897141	(A) Schematic  presentation of Mnk2a bound to MAP kinase (MAPK).	bind
7452	1	3116	5	11	NULL	0	NULL	amphiphysin protein	GP		bind			NH2-terminal domain		lipid bilayers	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_45_6_787_s_120	14529717	(A) Schematic cartoon of the amphiphysin primary  protein sequence showing the highly conserved NH2-terminal domain known to bind and  tubulate lipid bilayers, an internal poly-proline rich region just upstream of the  clathrin and AP-2 binding sites, and a COOH-terminal SH3 domain.	bind
7453	2	3116	5	11	NULL	0	NULL	amphiphysin protein	GP		tubulate			NH2-terminal region		lipid bilayers	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_45_6_787_s_120	14529717	(A) Schematic cartoon of the amphiphysin primary  protein sequence showing the highly conserved NH2-terminal domain known to bind and  tubulate lipid bilayers, an internal poly-proline rich region just upstream of the  clathrin and AP-2 binding sites, and a COOH-terminal SH3 domain.	bind
9487	1	3116	7	11	NULL	0	NULL	amphiphysin	GP		bind			conserved NH2-terminal		lipid bilayer	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_45_6_787_s_120	14529717	(A) Schematic cartoon of the amphiphysin primary  protein sequence showing the highly conserved NH2-terminal domain known to bind and  tubulate lipid bilayers, an internal poly-proline rich region just upstream of the  clathrin and AP-2 binding sites, and a COOH-terminal SH3 domain.	bind
9488	2	3116	7	11	NULL	0	NULL	amphiphysin	GP		tubulate			conserved NH2-terminal		lipid bilayer	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_45_6_787_s_120	14529717	(A) Schematic cartoon of the amphiphysin primary  protein sequence showing the highly conserved NH2-terminal domain known to bind and  tubulate lipid bilayers, an internal poly-proline rich region just upstream of the  clathrin and AP-2 binding sites, and a COOH-terminal SH3 domain.	bind
79836	1	3116	11	NULL	NULL	0	NULL	amphiphysin	Protein		has								NH2-terminal domain		NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_6_787_s_120	14529717	(A) Schematic cartoon of the amphiphysin primary  protein sequence showing the highly conserved NH2-terminal domain known to bind and  tubulate lipid bilayers, an internal poly-proline rich region just upstream of the  clathrin and AP-2 binding sites, and a COOH-terminal SH3 domain.	bind
79837	2	3116	11	NULL	NULL	0	NULL	amphiphysin 	Protein		bind			 NH2-terminal domain		lipid bilayers	CellComponent				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_6_787_s_120	14529717	(A) Schematic cartoon of the amphiphysin primary  protein sequence showing the highly conserved NH2-terminal domain known to bind and  tubulate lipid bilayers, an internal poly-proline rich region just upstream of the  clathrin and AP-2 binding sites, and a COOH-terminal SH3 domain.	bind
79838	3	3116	11	NULL	NULL	0	NULL	amphiphysin	Protein		tubulate			 NH2-terminal domain		lipid bilayers	CellComponent				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_6_787_s_120	14529717	(A) Schematic cartoon of the amphiphysin primary  protein sequence showing the highly conserved NH2-terminal domain known to bind and  tubulate lipid bilayers, an internal poly-proline rich region just upstream of the  clathrin and AP-2 binding sites, and a COOH-terminal SH3 domain.	bind
79839	4	3116	11	NULL	NULL	0	NULL	statement 2	Process		occurs along with					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_6_787_s_120	14529717	(A) Schematic cartoon of the amphiphysin primary  protein sequence showing the highly conserved NH2-terminal domain known to bind and  tubulate lipid bilayers, an internal poly-proline rich region just upstream of the  clathrin and AP-2 binding sites, and a COOH-terminal SH3 domain.	bind
79840	5	3116	11	NULL	NULL	0	NULL	amphiphysin	Protein		has								COOH-terminal SH3 domain		NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_6_787_s_120	14529717	(A) Schematic cartoon of the amphiphysin primary  protein sequence showing the highly conserved NH2-terminal domain known to bind and  tubulate lipid bilayers, an internal poly-proline rich region just upstream of the  clathrin and AP-2 binding sites, and a COOH-terminal SH3 domain.	bind
79841	6	3116	11	NULL	NULL	0	NULL	amphiphysin	Protein		has binding site for					clathrin	Protein				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_6_787_s_120	14529717	(A) Schematic cartoon of the amphiphysin primary  protein sequence showing the highly conserved NH2-terminal domain known to bind and  tubulate lipid bilayers, an internal poly-proline rich region just upstream of the  clathrin and AP-2 binding sites, and a COOH-terminal SH3 domain.	bind
79842	7	3116	11	NULL	NULL	0	NULL	amphiphysin	Protein		has binding site for					AP-2	Protein				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_6_787_s_120	14529717	(A) Schematic cartoon of the amphiphysin primary  protein sequence showing the highly conserved NH2-terminal domain known to bind and  tubulate lipid bilayers, an internal poly-proline rich region just upstream of the  clathrin and AP-2 binding sites, and a COOH-terminal SH3 domain.	bind
7454	1	3117	5	NULL	NULL	NULL	NULL	trp	GP		bind				repressor	trp	GP			operator	NULL		NULL	NULL	NULL	NULL	gw60_structure_3_7_635_s_56	8591039	(a) Schematic diagram of the  trp repressor binding to the 20 base-pair  trp operator DNA showing the potential primary and secondary binding modes.	bind
9156	1	3117	7	10	NULL	0	NULL	trp repressor	GP		bind					DNA	NucleicAcid			trp operator	NULL		NULL	NULL	NULL	NULL	gw60_structure_3_7_635_s_56	8591039	(a) Schematic diagram of the  trp repressor binding to the 20 base-pair  trp operator DNA showing the potential primary and secondary binding modes.	bind
79843	1	3117	11	NULL	NULL	NULL	NULL	trp repressor	GeneOrProtein		binds to 					trp operator DNA	NucleicAcidSubstance			20 base-pair	NULL		NULL	NULL	NULL	NULL	gw60_structure_3_7_635_s_56	8591039	(a) Schematic diagram of the  trp repressor binding to the 20 base-pair  trp operator DNA showing the potential primary and secondary binding modes.	bind
7455	1	3119	5	11	NULL	0	NULL	importin	GP	full-length	bind								IBB domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_6_1345_s_117	12504010	(A) Schematic model of full-length importin   bound to both IBB domain and PTHrP-ncNLS.	bind
7456	2	3119	5	11	NULL	0	NULL	importin	GP	full-length	bind					PTHrP	GP		ncNLS		NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_6_1345_s_117	12504010	(A) Schematic model of full-length importin   bound to both IBB domain and PTHrP-ncNLS.	bind
9157	1	3119	7	11	NULL	0	NULL	importin	GP	full-length	bind								IBB domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_6_1345_s_117	12504010	(A) Schematic model of full-length importin   bound to both IBB domain and PTHrP-ncNLS.	bind
9158	2	3119	7	11	NULL	0	NULL	importin	GP	full-length	bind					PTHrP	GP		ncNLS		NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_6_1345_s_117	12504010	(A) Schematic model of full-length importin   bound to both IBB domain and PTHrP-ncNLS.	bind
79844	1	3119	11	NULL	NULL	0	NULL	importin	Protein		binds to 								IBB domain		NULL		0	NULL	NULL	NULL	gw60_molcell_10_6_1345_s_117	12504010	(A) Schematic model of full-length importin   bound to both IBB domain and PTHrP-ncNLS.	bind
79845	2	3119	11	NULL	NULL	0	NULL	importin	Protein		binds to 					PTHrP-ncNLS.	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_10_6_1345_s_117	12504010	(A) Schematic model of full-length importin   bound to both IBB domain and PTHrP-ncNLS.	bind
7459	1	3123	5	11	NULL	0	NULL	Che-1	GP		bind					Tau	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_4_1038_s_84	14697667	(A) Schematic representation  of myc-Che-1 constructs used to identify portions of Che-1 that bind Tau.	bind
9159	1	3123	7	11	NULL	0	NULL	Che-1 	GP		bind					Tau	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_4_1038_s_84	14697667	(A) Schematic representation  of myc-Che-1 constructs used to identify portions of Che-1 that bind Tau.	bind
79846	1	3123	11	NULL	NULL	0	NULL	Che-1	Protein		binds to 					Tau	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellneurosci_24_4_1038_s_84	14697667	(A) Schematic representation  of myc-Che-1 constructs used to identify portions of Che-1 that bind Tau.	bind
7460	1	3124	5	11	NULL	0	NULL	myc-Tau	GP		bind					Che-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_4_1038_s_72	14697667	(A) Schematic representation  of myc-Tau constructs used to identify the portion of Tau that binds Che-1.	bind
9160	1	3124	7	11	NULL	0	NULL	myc-Tau	GP		bind					Che-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_4_1038_s_72	14697667	(A) Schematic representation  of myc-Tau constructs used to identify the portion of Tau that binds Che-1.	bind
79847	1	3124	11	NULL	NULL	0	NULL	Tau	Protein		binds to 					Che-1	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellneurosci_24_4_1038_s_72	14697667	(A) Schematic representation  of myc-Tau constructs used to identify the portion of Tau that binds Che-1.	bind
79757	1	3125	11	NULL	NULL	NULL	NULL	TAP tag	PartOfProtein		composed of 					protein A	Protein				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3519_s_256	15831458	(A) Schematic representation of  CKIP-1 with an amino-terminal TAP tag that is composed of protein A and a calmodulin  binding peptide separated by a TEV cleavage site.	bind
79758	2	3125	11	NULL	NULL	0	NULL	TAP tag	PartOfProtein		composed of 					 calmodulin binding peptide	PartOfProtein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_9_3519_s_256	15831458	(A) Schematic representation of  CKIP-1 with an amino-terminal TAP tag that is composed of protein A and a calmodulin  binding peptide separated by a TEV cleavage site.	bind
79759	3	3125	11	NULL	NULL	NULL	NULL	protein A	Protein		occurs along with					calmodulin binding peptide	PartOfProtein				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3519_s_256	15831458	(A) Schematic representation of  CKIP-1 with an amino-terminal TAP tag that is composed of protein A and a calmodulin  binding peptide separated by a TEV cleavage site.	bind
79849	4	3125	11	NULL	NULL	0	NULL	CKIP-1	Protein		has								 amino-terminal TAP		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_9_3519_s_256	15831458	(A) Schematic representation of  CKIP-1 with an amino-terminal TAP tag that is composed of protein A and a calmodulin  binding peptide separated by a TEV cleavage site.	bind
7461	1	3126	5	11	NULL	0	NULL	Axin	GP		bind			RGS domain		APC	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_3_407_s_142	12636921	(A) Schematic representation of Axin (not to scale) indicating the RGS domain that binds APC, the binding domains for Zw3/Sgg kinase and Armadillo, and the DIX dimerization domain.	bind
9161	1	3126	7	11	NULL	0	NULL	Axin	GP		bind			RGS domain		APC	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_3_407_s_142	12636921	(A) Schematic representation of Axin (not to scale) indicating the RGS domain that binds APC, the binding domains for Zw3/Sgg kinase and Armadillo, and the DIX dimerization domain.	bind
79831	1	3126	11	NULL	NULL	NULL	NULL	Axin	Protein		binds			RGS		APC					NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_3_407_s_142	12636921	(A) Schematic representation of Axin (not to scale) indicating the RGS domain that binds APC, the binding domains for Zw3/Sgg kinase and Armadillo, and the DIX dimerization domain.	bind
79853	3	3126	11	NULL	NULL	0	NULL	Axin	Protein		has binding domain for					Zw3/Sgg kinase	Protein				NULL		0	NULL	NULL	NULL	gw60_devcell_4_3_407_s_142	12636921	(A) Schematic representation of Axin (not to scale) indicating the RGS domain that binds APC, the binding domains for Zw3/Sgg kinase and Armadillo, and the DIX dimerization domain.	bind
79855	4	3126	11	NULL	NULL	0	NULL	Axin	Protein		has binding domain for					Armadillo	Protein				NULL		0	NULL	NULL	NULL	gw60_devcell_4_3_407_s_142	12636921	(A) Schematic representation of Axin (not to scale) indicating the RGS domain that binds APC, the binding domains for Zw3/Sgg kinase and Armadillo, and the DIX dimerization domain.	bind
79856	5	3126	11	NULL	NULL	NULL	NULL	Axin	Protein		has 					DIX			dimerization domain		NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_3_407_s_142	12636921	(A) Schematic representation of Axin (not to scale) indicating the RGS domain that binds APC, the binding domains for Zw3/Sgg kinase and Armadillo, and the DIX dimerization domain.	bind
7465	1	3128	5	11	NULL	0	NULL	Raichu-RalA	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_6_2549_s_54	15034142	(A) Schematic representation of Raichu-RalA bound  to GDP or GTP.	bind
7466	2	3128	5	11	NULL	0	NULL	Raichu-RalA	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_6_2549_s_54	15034142	(A) Schematic representation of Raichu-RalA bound  to GDP or GTP.	bind
7467	3	3128	5	11	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_6_2549_s_54	15034142	(A) Schematic representation of Raichu-RalA bound  to GDP or GTP.	bind
9165	1	3128	7	11	NULL	0	NULL	Raichu-RalA	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_6_2549_s_54	15034142	(A) Schematic representation of Raichu-RalA bound  to GDP or GTP.	bind
9166	2	3128	7	11	NULL	0	NULL	Raichu-RalA	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_6_2549_s_54	15034142	(A) Schematic representation of Raichu-RalA bound  to GDP or GTP.	bind
11922	3	3128	7	11	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_6_2549_s_54	15034142	(A) Schematic representation of Raichu-RalA bound  to GDP or GTP.	bind
79857	1	3128	11	NULL	NULL	NULL	NULL	Raichu-RalA	GeneOrProtein		binds to 					GDP	NonProteinOrNucleicAcidChemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_6_2549_s_54	15034142	(A) Schematic representation of Raichu-RalA bound  to GDP or GTP.	bind
79858	2	3128	11	NULL	NULL	NULL	NULL	Raichu-RalA	GeneOrProtein		binds to 					GTP	NonProteinOrNucleicAcidChemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_6_2549_s_54	15034142	(A) Schematic representation of Raichu-RalA bound  to GDP or GTP.	bind
79760	1	3130	11	NULL	NULL	NULL	NULL	 IMD2 sequence	Gene		contain					 NSE region	NucleicAcidSubstance				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_17_6279_s_79	12917348	(A) Schematic representation of the  IMD2 sequence in the NSE region and comparison with the consensus binding elements of  Gcr1p and Abf1p.	bind
7468	1	3132	5	11	NULL	0	NULL	liver transcription factors	GP		bind					HNF-3	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_mechdev_89_1_185_s_13	10559496	(A) Schematic representation of the liver transcription factors binding to the HNF-3   promoter region.	bind
9167	1	3132	7	11	NULL	0	NULL	liver transcription factors	GP		binds to					HNF-3	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_mechdev_89_1_185_s_13	10559496	(A) Schematic representation of the liver transcription factors binding to the HNF-3   promoter region.	bind
79859	1	3132	11	NULL	NULL	NULL	NULL	liver transcription factor	Protein		binds to 					HNF-3	Gene			promoter region	NULL		NULL	NULL	NULL	NULL	gw60_mechdev_89_1_185_s_13	10559496	(A) Schematic representation of the liver transcription factors binding to the HNF-3   promoter region.	bind
7469	1	3136	5	11	NULL	0	NULL	Raichu-Rac	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6582_s_62	12192056	(A) Schematic representations of Raichu-Rac and Raichu-Cdc42 bound to GDP or GTP.	bind
7470	2	3136	5	11	NULL	0	NULL	Raichu-Rac	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6582_s_62	12192056	(A) Schematic representations of Raichu-Rac and Raichu-Cdc42 bound to GDP or GTP.	bind
7471	3	3136	5	11	NULL	0	NULL	Raichu-Cdc42	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6582_s_62	12192056	(A) Schematic representations of Raichu-Rac and Raichu-Cdc42 bound to GDP or GTP.	bind
7472	4	3136	5	11	NULL	0	NULL	Raichu-Cdc42	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6582_s_62	12192056	(A) Schematic representations of Raichu-Rac and Raichu-Cdc42 bound to GDP or GTP.	bind
7473	5	3136	5	11	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6582_s_62	12192056	(A) Schematic representations of Raichu-Rac and Raichu-Cdc42 bound to GDP or GTP.	bind
7474	6	3136	5	11	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6582_s_62	12192056	(A) Schematic representations of Raichu-Rac and Raichu-Cdc42 bound to GDP or GTP.	bind
9168	1	3136	7	11	NULL	0	NULL	Raichu-Rac	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6582_s_62	12192056	(A) Schematic representations of Raichu-Rac and Raichu-Cdc42 bound to GDP or GTP.	bind
9169	2	3136	7	11	NULL	0	NULL	Raichu-Rac	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6582_s_62	12192056	(A) Schematic representations of Raichu-Rac and Raichu-Cdc42 bound to GDP or GTP.	bind
9170	3	3136	7	11	NULL	0	NULL	Raichu-Cdc42	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6582_s_62	12192056	(A) Schematic representations of Raichu-Rac and Raichu-Cdc42 bound to GDP or GTP.	bind
9171	4	3136	7	11	NULL	0	NULL	Raichu-Cdc42	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6582_s_62	12192056	(A) Schematic representations of Raichu-Rac and Raichu-Cdc42 bound to GDP or GTP.	bind
11923	5	3136	7	11	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6582_s_62	12192056	(A) Schematic representations of Raichu-Rac and Raichu-Cdc42 bound to GDP or GTP.	bind
11924	6	3136	7	11	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6582_s_62	12192056	(A) Schematic representations of Raichu-Rac and Raichu-Cdc42 bound to GDP or GTP.	bind
79863	1	3136	11	NULL	NULL	NULL	NULL	Raichu-Rac	GeneOrProtein		binds to 					GDP	NonProteinOrNucleicAcidChemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6582_s_62	12192056	(A) Schematic representations of Raichu-Rac and Raichu-Cdc42 bound to GDP or GTP.	bind
79864	2	3136	11	NULL	NULL	NULL	NULL	Raichu-Rac	GeneOrProtein		binds to 					GTP	NonProteinOrNucleicAcidChemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6582_s_62	12192056	(A) Schematic representations of Raichu-Rac and Raichu-Cdc42 bound to GDP or GTP.	bind
79865	3	3136	11	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6582_s_62	12192056	(A) Schematic representations of Raichu-Rac and Raichu-Cdc42 bound to GDP or GTP.	bind
79866	4	3136	11	NULL	NULL	NULL	NULL	Raichu-Cdc42	GeneOrProtein		binds to 					GDP	NonProteinOrNucleicAcidChemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6582_s_62	12192056	(A) Schematic representations of Raichu-Rac and Raichu-Cdc42 bound to GDP or GTP.	bind
79867	5	3136	11	NULL	NULL	NULL	NULL	Raichu-Cdc42	GeneOrProtein		binds to 					GTP	NonProteinOrNucleicAcidChemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6582_s_62	12192056	(A) Schematic representations of Raichu-Rac and Raichu-Cdc42 bound to GDP or GTP.	bind
79868	6	3136	11	NULL	NULL	0	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6582_s_62	12192056	(A) Schematic representations of Raichu-Rac and Raichu-Cdc42 bound to GDP or GTP.	bind
7475	1	3137	5	11	NULL	0	NULL	Raichu-RhoA	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_162_2_223_s_43	12860967	(A) Schematic representations of Raichu-RhoA bound to GDP or GTP.	bind
7476	2	3137	5	11	NULL	0	NULL	Raichu-RhoA	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_162_2_223_s_43	12860967	(A) Schematic representations of Raichu-RhoA bound to GDP or GTP.	bind
7477	3	3137	5	11	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_162_2_223_s_43	12860967	(A) Schematic representations of Raichu-RhoA bound to GDP or GTP.	bind
9172	1	3137	7	11	NULL	0	NULL	Raichu-RhoA	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_162_2_223_s_43	12860967	(A) Schematic representations of Raichu-RhoA bound to GDP or GTP.	bind
9173	2	3137	7	11	NULL	0	NULL	Raichu-RhoA	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_162_2_223_s_43	12860967	(A) Schematic representations of Raichu-RhoA bound to GDP or GTP.	bind
61115	3	3137	7	11	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_162_2_223_s_43	12860967	(A) Schematic representations of Raichu-RhoA bound to GDP or GTP.	bind
79869	1	3137	11	NULL	NULL	NULL	NULL	Raichu-RhoA	GeneOrProtein		binds to 					GDP	NonProteinOrNucleicAcidChemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_162_2_223_s_43	12860967	(A) Schematic representations of Raichu-RhoA bound to GDP or GTP.	bind
79870	2	3137	11	NULL	NULL	NULL	NULL	Raichu-RhoA	GeneOrProtein		binds to 					GTP	NonProteinOrNucleicAcidChemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_162_2_223_s_43	12860967	(A) Schematic representations of Raichu-RhoA bound to GDP or GTP.	bind
79871	3	3137	11	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_162_2_223_s_43	12860967	(A) Schematic representations of Raichu-RhoA bound to GDP or GTP.	bind
7478	1	3141	5	11	NULL	0	NULL	NS1 protein	GP		bind					PABII	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_8_2273_s_275	10205180	(A) sequence is blocked by the binding of the NS1 protein to PABII, resulting in the nuclear accumulation of cleaved pre-mRNAs containing short poly	bind
7481	2	3141	5	11	NULL	0	NULL	statement 1	Process		results in					pre-mRNA	NucleicAcid	nuclear accumulation of			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_8_2273_s_275	10205180	(A) sequence is blocked by the binding of the NS1 protein to PABII, resulting in the nuclear accumulation of cleaved pre-mRNAs containing short poly	bind
9278	1	3141	7	11	NULL	0	NULL	NS1	GP		bind					PABII	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_8_2273_s_275	10205180	(A) sequence is blocked by the binding of the NS1 protein to PABII, resulting in the nuclear accumulation of cleaved pre-mRNAs containing short poly	bind
9279	2	3141	7	11	NULL	0	NULL	statement 1	Process		result in					cleaved pre-mRNA	NucleicAcid	nuclear accumulation of			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_8_2273_s_275	10205180	(A) sequence is blocked by the binding of the NS1 protein to PABII, resulting in the nuclear accumulation of cleaved pre-mRNAs containing short poly	bind
79872	1	3141	11	NULL	NULL	NULL	NULL	NS1 protein	Protein		binds to 					PABII	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_8_2273_s_275	10205180	(A) sequence is blocked by the binding of the NS1 protein to PABII, resulting in the nuclear accumulation of cleaved pre-mRNAs containing short poly	bind
79873	2	3141	11	NULL	NULL	NULL	NULL	statement 1	Process		accumulate		nuclear			pre-mRNAs	NucleicAcidSubstance	cleaved			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_8_2273_s_275	10205180	(A) sequence is blocked by the binding of the NS1 protein to PABII, resulting in the nuclear accumulation of cleaved pre-mRNAs containing short poly	bind
79876	1	3142	11	NULL	NULL	0	NULL	tendamistat	Protein		has binding site for					amylase	Protein				NULL		0	NULL	NULL	NULL	gw60_chembiol_10_1_53_s_47	12573698	(A) Sequence of a peptide Ten(15-23) derived from  -amylase binding site of tendamistat  [17]  .	bind
79877	2	3142	11	NULL	NULL	0	NULL	Ten peptide	PartOfProtein		derived from					 tendamistat	Protein		amylase binding site		NULL		0	NULL	NULL	NULL	gw60_chembiol_10_1_53_s_47	12573698	(A) Sequence of a peptide Ten(15-23) derived from  -amylase binding site of tendamistat  [17]  .	bind
79878	1	3144	11	NULL	NULL	NULL	NULL	Phyl	GeneOrProtein		has binding site for					Sina	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_19_6854_s_360	12215542	(A) Sequence of the Sina-binding region of Phyl from residues 109 to 127.	bind
7490	1	3146	5	11	NULL	0	NULL	p53 proteins	GP		bind		sequence specific			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1517_3_392_s_94	11342217	(A) Sequence-specific DNA binding of various p53 proteins.	bind
9280	1	3146	7	11	NULL	0	NULL	p53 protein	GP		bind		sequence-specific			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1517_3_392_s_94	11342217	(A) Sequence-specific DNA binding of various p53 proteins.	bind
79879	1	3146	11	NULL	NULL	0	NULL	p53 protein	Protein		binds to 		Sequence-specific			DNA	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1517_3_392_s_94	11342217	(A) Sequence-specific DNA binding of various p53 proteins.	bind
7491	1	3147	5	11	NULL	0	NULL	enolase	GP	A. hydrophila	bind					plasminogen	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_microbpathogenesis_34_4_195_s_117	12668143	(A) showing  A. hydrophila enolase binding to human plasminogen.	bind
9281	1	3147	7	11	NULL	0	NULL	 enolase	GP	A. hydrophila	bind					plasminogen	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_microbpathogenesis_34_4_195_s_117	12668143	(A) showing  A. hydrophila enolase binding to human plasminogen.	bind
79881	1	3147	11	NULL	NULL	NULL	NULL	enolase	Protein	A. hydrophila	binds to 					plasminogen	Protein	human			NULL		NULL	NULL	NULL	NULL	gw60_microbpathogenesis_34_4_195_s_117	12668143	(A) showing  A. hydrophila enolase binding to human plasminogen.	bind
7495	1	3148	5	11	NULL	0	NULL	SFA	Chemical		bind			cyclic region		cyclophilin	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_555_2_335_s_120	14644438	(A) shows CsA  [ 33] and (B) shows macrolide 16 [ 32], an analogue of SFA s cyclic region that binds to the cyclophilin, bound to the  active site of human cyclophilin A. Images were produced using Protein Explorer [  34] with the contact surface between the protein and ligand predicted and points of  theoretical contact marked by the rings.	bind
7592	2	3148	5	11	NULL	0	NULL	macrolide 16	Chemical		is an analogue of					SFA	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_febslett_555_2_335_s_120	14644438	(A) shows CsA  [ 33] and (B) shows macrolide 16 [ 32], an analogue of SFA s cyclic region that binds to the cyclophilin, bound to the  active site of human cyclophilin A. Images were produced using Protein Explorer [  34] with the contact surface between the protein and ligand predicted and points of  theoretical contact marked by the rings.	bind
7593	3	3148	5	11	NULL	0	NULL	macrolide 16	Chemical		bind					cyclophilin A	GP	human	active site		NULL		NULL	NULL	NULL	NULL	gw70_febslett_555_2_335_s_120	14644438	(A) shows CsA  [ 33] and (B) shows macrolide 16 [ 32], an analogue of SFA s cyclic region that binds to the cyclophilin, bound to the  active site of human cyclophilin A. Images were produced using Protein Explorer [  34] with the contact surface between the protein and ligand predicted and points of  theoretical contact marked by the rings.	bind
7594	4	3148	5	11	NULL	0	NULL	CsA	Chemical		bind					cyclophilin A	GP	human	active site		NULL		NULL	NULL	NULL	NULL	gw70_febslett_555_2_335_s_120	14644438	(A) shows CsA  [ 33] and (B) shows macrolide 16 [ 32], an analogue of SFA s cyclic region that binds to the cyclophilin, bound to the  active site of human cyclophilin A. Images were produced using Protein Explorer [  34] with the contact surface between the protein and ligand predicted and points of  theoretical contact marked by the rings.	bind
9282	1	3148	7	11	NULL	0	NULL	SFA	Chemical		bind			cyclic region		cyclophilinA	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_555_2_335_s_120	14644438	(A) shows CsA  [ 33] and (B) shows macrolide 16 [ 32], an analogue of SFA s cyclic region that binds to the cyclophilin, bound to the  active site of human cyclophilin A. Images were produced using Protein Explorer [  34] with the contact surface between the protein and ligand predicted and points of  theoretical contact marked by the rings.	bind
11926	2	3148	7	11	NULL	0	NULL	CsA	Chemical		bind					cyclophilinA	GP	human	active site 		NULL		NULL	NULL	NULL	NULL	gw70_febslett_555_2_335_s_120	14644438	(A) shows CsA  [ 33] and (B) shows macrolide 16 [ 32], an analogue of SFA s cyclic region that binds to the cyclophilin, bound to the  active site of human cyclophilin A. Images were produced using Protein Explorer [  34] with the contact surface between the protein and ligand predicted and points of  theoretical contact marked by the rings.	bind
11927	3	3148	7	11	NULL	0	NULL	 macrolide 16	Chemical		bind					cyclophilinA	GP	human	active site		NULL		NULL	NULL	NULL	NULL	gw70_febslett_555_2_335_s_120	14644438	(A) shows CsA  [ 33] and (B) shows macrolide 16 [ 32], an analogue of SFA s cyclic region that binds to the cyclophilin, bound to the  active site of human cyclophilin A. Images were produced using Protein Explorer [  34] with the contact surface between the protein and ligand predicted and points of  theoretical contact marked by the rings.	bind
11928	4	3148	7	11	NULL	0	NULL	 macrolide 16	Chemical		is an analogue of					SFA	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_febslett_555_2_335_s_120	14644438	(A) shows CsA  [ 33] and (B) shows macrolide 16 [ 32], an analogue of SFA s cyclic region that binds to the cyclophilin, bound to the  active site of human cyclophilin A. Images were produced using Protein Explorer [  34] with the contact surface between the protein and ligand predicted and points of  theoretical contact marked by the rings.	bind
79882	1	3148	11	NULL	NULL	NULL	NULL	macrolide 16	NonProteinOrNucleicAcidChemical		is an analogue of					SFA	NonProteinOrNucleicAcidChemical	cyclic region			NULL		NULL	NULL	NULL	NULL	gw70_febslett_555_2_335_s_120	14644438	(A) shows CsA  [ 33] and (B) shows macrolide 16 [ 32], an analogue of SFA s cyclic region that binds to the cyclophilin, bound to the  active site of human cyclophilin A. Images were produced using Protein Explorer [  34] with the contact surface between the protein and ligand predicted and points of  theoretical contact marked by the rings.	bind
79883	2	3148	11	NULL	NULL	NULL	NULL	SFA	NonProteinOrNucleicAcidChemical	 cyclic region	binds to 					cyclophilin	Protein				NULL		NULL	NULL	NULL	NULL	gw70_febslett_555_2_335_s_120	14644438	(A) shows CsA  [ 33] and (B) shows macrolide 16 [ 32], an analogue of SFA s cyclic region that binds to the cyclophilin, bound to the  active site of human cyclophilin A. Images were produced using Protein Explorer [  34] with the contact surface between the protein and ligand predicted and points of  theoretical contact marked by the rings.	bind
79884	3	3148	11	NULL	NULL	NULL	NULL	CsA	NonProteinOrNucleicAcidChemical		binds to 					cyclophilin A	Protein	human			NULL		NULL	NULL	NULL	NULL	gw70_febslett_555_2_335_s_120	14644438	(A) shows CsA  [ 33] and (B) shows macrolide 16 [ 32], an analogue of SFA s cyclic region that binds to the cyclophilin, bound to the  active site of human cyclophilin A. Images were produced using Protein Explorer [  34] with the contact surface between the protein and ligand predicted and points of  theoretical contact marked by the rings.	bind
79885	4	3148	11	NULL	NULL	NULL	NULL	macrolide 16	NonProteinOrNucleicAcidChemical		binds to 					cyclophilin A	Protein	human			NULL		NULL	NULL	NULL	NULL	gw70_febslett_555_2_335_s_120	14644438	(A) shows CsA  [ 33] and (B) shows macrolide 16 [ 32], an analogue of SFA s cyclic region that binds to the cyclophilin, bound to the  active site of human cyclophilin A. Images were produced using Protein Explorer [  34] with the contact surface between the protein and ligand predicted and points of  theoretical contact marked by the rings.	bind
7595	1	3151	5	11	NULL	0	NULL	virus	Organism	signal of	bind		effectively			GTFs	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_834_s_44	10629040	(A) signal of the virus binds GTFs effectively in a manner characteristic of a promoter.	bind
7596	2	3151	5	11	NULL	0	NULL	statement 1	Process		occurs in manner							characteristic of		promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_834_s_44	10629040	(A) signal of the virus binds GTFs effectively in a manner characteristic of a promoter.	bind
9283	1	3151	7	11	NULL	0	NULL	virus	Organism	signal of	bind		effectively			GTFs	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_834_s_44	10629040	(A) signal of the virus binds GTFs effectively in a manner characteristic of a promoter.	bind
11929	2	3151	7	11	NULL	0	NULL	statement 1	Process		occurs in a manner					promoter	NucleicAcid	characteristic of 			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_834_s_44	10629040	(A) signal of the virus binds GTFs effectively in a manner characteristic of a promoter.	bind
79886	1	3151	11	NULL	NULL	NULL	NULL	 signal	MolecularProcess	 virus	binds to 					GTFs	Gene			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_834_s_44	10629040	(A) signal of the virus binds GTFs effectively in a manner characteristic of a promoter.	bind
7597	1	3152	5	11	NULL	0	NULL			upstream	interact with				polypyrimidine tract	polypyrimidine tract binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_376_s_282	9858561	(A) signal, there is an upstream polypyrimidine tract which has been shown to interact both with polypyrimidine tract binding protein and with CstF, which binds cooperatively with CPSF ( 19a).	bind
7598	2	3152	5	11	NULL	0	NULL			upstream	bind				polypyrimidine tract	CstF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_376_s_282	9858561	(A) signal, there is an upstream polypyrimidine tract which has been shown to interact both with polypyrimidine tract binding protein and with CstF, which binds cooperatively with CPSF ( 19a).	bind
7599	3	3152	5	11	NULL	0	NULL	CstF	GP		bind					CPSF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_376_s_282	9858561	(A) signal, there is an upstream polypyrimidine tract which has been shown to interact both with polypyrimidine tract binding protein and with CstF, which binds cooperatively with CPSF ( 19a).	bind
7600	4	3152	5	11	NULL	0	NULL	polypyrimidine tract binding protein	GP		bind					CPSF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_376_s_282	9858561	(A) signal, there is an upstream polypyrimidine tract which has been shown to interact both with polypyrimidine tract binding protein and with CstF, which binds cooperatively with CPSF ( 19a).	bind
7601	5	3152	5	11	NULL	0	NULL	statement 3	Process		occurs in cooperation with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_376_s_282	9858561	(A) signal, there is an upstream polypyrimidine tract which has been shown to interact both with polypyrimidine tract binding protein and with CstF, which binds cooperatively with CPSF ( 19a).	bind
9284	1	3152	7	11	NULL	0	NULL			upstream	bind				polypyrimidine tract	polypyrimidine tract binding protein 	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_376_s_282	9858561	(A) signal, there is an upstream polypyrimidine tract which has been shown to interact both with polypyrimidine tract binding protein and with CstF, which binds cooperatively with CPSF ( 19a).	bind
9285	2	3152	7	11	NULL	0	NULL			upstream	bind				polypyrimidine tract	CstF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_376_s_282	9858561	(A) signal, there is an upstream polypyrimidine tract which has been shown to interact both with polypyrimidine tract binding protein and with CstF, which binds cooperatively with CPSF ( 19a).	bind
9286	3	3152	7	11	NULL	0	NULL	polypyrimidine tract binding protein	GP		bind					CPSF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_376_s_282	9858561	(A) signal, there is an upstream polypyrimidine tract which has been shown to interact both with polypyrimidine tract binding protein and with CstF, which binds cooperatively with CPSF ( 19a).	bind
9287	4	3152	7	11	NULL	0	NULL	CstF	GP		bind					CPSF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_376_s_282	9858561	(A) signal, there is an upstream polypyrimidine tract which has been shown to interact both with polypyrimidine tract binding protein and with CstF, which binds cooperatively with CPSF ( 19a).	bind
11931	5	3152	7	11	NULL	0	NULL	statement 3	Process		occurs in cooperation with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_376_s_282	9858561	(A) signal, there is an upstream polypyrimidine tract which has been shown to interact both with polypyrimidine tract binding protein and with CstF, which binds cooperatively with CPSF ( 19a).	bind
79889	1	3152	11	NULL	NULL	0	NULL	polypyrimidine tract	NucleicAcidSubstance		interact with					polypyrimidine tract binding protein	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_376_s_282	9858561	(A) signal, there is an upstream polypyrimidine tract which has been shown to interact both with polypyrimidine tract binding protein and with CstF, which binds cooperatively with CPSF ( 19a).	bind
79890	2	3152	11	NULL	NULL	0	NULL	polypyrimidine tract	NucleicAcidSubstance		interact with					CstF	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_376_s_282	9858561	(A) signal, there is an upstream polypyrimidine tract which has been shown to interact both with polypyrimidine tract binding protein and with CstF, which binds cooperatively with CPSF ( 19a).	bind
79891	3	3152	11	NULL	NULL	0	NULL	statement 1	Process		occurs along with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_376_s_282	9858561	(A) signal, there is an upstream polypyrimidine tract which has been shown to interact both with polypyrimidine tract binding protein and with CstF, which binds cooperatively with CPSF ( 19a).	bind
79892	4	3152	11	NULL	NULL	0	NULL	CstF	Protein		binds to 		cooperatively			CPSF	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_376_s_282	9858561	(A) signal, there is an upstream polypyrimidine tract which has been shown to interact both with polypyrimidine tract binding protein and with CstF, which binds cooperatively with CPSF ( 19a).	bind
7602	1	3153	5	11	NULL	0	NULL	CPSF	GP		bind					RNAs	NucleicAcid	pre-wt			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2660_s_224	10733568	(A) signal, we used electrophoretic mobility shift assays to examine the stability of CPSF binding to the pre-wt and pre-Sp RNAs.	bind
7603	2	3153	5	11	NULL	0	NULL	CPSF	GP		bind					RNAs	NucleicAcid	pre-Sp			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2660_s_224	10733568	(A) signal, we used electrophoretic mobility shift assays to examine the stability of CPSF binding to the pre-wt and pre-Sp RNAs.	bind
9288	1	3153	7	11	NULL	0	NULL	CPSF	GP		bind					RNA	NucleicAcid	pre-wt			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2660_s_224	10733568	(A) signal, we used electrophoretic mobility shift assays to examine the stability of CPSF binding to the pre-wt and pre-Sp RNAs.	bind
9289	2	3153	7	11	NULL	0	NULL	CPSF	GP		bind					RNA	NucleicAcid	pre-Sp			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2660_s_224	10733568	(A) signal, we used electrophoretic mobility shift assays to examine the stability of CPSF binding to the pre-wt and pre-Sp RNAs.	bind
79894	1	3153	11	NULL	NULL	NULL	NULL	CPSF	Protein		binds to 					RNAs	NucleicAcidSubstance	pre-Sp 			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2660_s_224	10733568	(A) signal, we used electrophoretic mobility shift assays to examine the stability of CPSF binding to the pre-wt and pre-Sp RNAs.	bind
79895	2	3153	11	NULL	NULL	NULL	NULL	CPSF	Protein		binds to 					RNAs	NucleicAcidSubstance	pre-wt 			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2660_s_224	10733568	(A) signal, we used electrophoretic mobility shift assays to examine the stability of CPSF binding to the pre-wt and pre-Sp RNAs.	bind
79896	3	3153	11	NULL	NULL	0	NULL	electrophoretic mobility shift assays	ResearchActivity		examine the stability of					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_8_2660_s_224	10733568	(A) signal, we used electrophoretic mobility shift assays to examine the stability of CPSF binding to the pre-wt and pre-Sp RNAs.	bind
79897	4	3153	11	NULL	NULL	0	NULL	electrophoretic mobility shift assays	ResearchActivity		examine the stability of					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_8_2660_s_224	10733568	(A) signal, we used electrophoretic mobility shift assays to examine the stability of CPSF binding to the pre-wt and pre-Sp RNAs.	bind
79950	1	3154	11	NULL	NULL	0	NULL	CPSF	GeneOrProtein		has binding site for					RNA	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_genesdev_17_11_1321_s_114	12782649	(A) signals in the RNA  by the RNA-binding components of CPSF and CstF, and/or by  phosphorylation/dephosphorylation of key components.	bind
79951	2	3154	11	NULL	NULL	0	NULL	CstF	GeneOrProtein		has binding site for					RNA	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_genesdev_17_11_1321_s_114	12782649	(A) signals in the RNA  by the RNA-binding components of CPSF and CstF, and/or by  phosphorylation/dephosphorylation of key components.	bind
7604	1	3155	5	11	NULL	0	NULL	AP-ES	GP		bind					CPAE cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_811_s_109	11336704	(A) Significant reduction of AP-ES binding to CPAE cells is seen after pre-treatment with sodium chlorate and 100 nM of Heparinase I, III, or I+II+III, as compared to untreated cells.	bind
7605	2	3155	5	11	NULL	0	NULL	statement 1	Process		reduced by		significantly			sodium chlorate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_811_s_109	11336704	(A) Significant reduction of AP-ES binding to CPAE cells is seen after pre-treatment with sodium chlorate and 100 nM of Heparinase I, III, or I+II+III, as compared to untreated cells.	bind
7606	3	3155	5	11	NULL	0	NULL	statement 1	Process		reduced by		significantly			Heparinase I	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_811_s_109	11336704	(A) Significant reduction of AP-ES binding to CPAE cells is seen after pre-treatment with sodium chlorate and 100 nM of Heparinase I, III, or I+II+III, as compared to untreated cells.	bind
7607	4	3155	5	11	NULL	0	NULL	statement 1	Process		reduced by		significantly			Heparinase III	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_811_s_109	11336704	(A) Significant reduction of AP-ES binding to CPAE cells is seen after pre-treatment with sodium chlorate and 100 nM of Heparinase I, III, or I+II+III, as compared to untreated cells.	bind
7608	5	3155	5	11	NULL	0	NULL	statement 1	Process		reduced by		significantly			Heparinase I+II+III	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_811_s_109	11336704	(A) Significant reduction of AP-ES binding to CPAE cells is seen after pre-treatment with sodium chlorate and 100 nM of Heparinase I, III, or I+II+III, as compared to untreated cells.	bind
9290	1	3155	7	11	NULL	0	NULL	AP-ES	GP		bind					CPAE cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_811_s_109	11336704	(A) Significant reduction of AP-ES binding to CPAE cells is seen after pre-treatment with sodium chlorate and 100 nM of Heparinase I, III, or I+II+III, as compared to untreated cells.	bind
9291	2	3155	7	11	NULL	0	NULL	statement 1	Process		 reduced by		significantly			sodium chlorate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_811_s_109	11336704	(A) Significant reduction of AP-ES binding to CPAE cells is seen after pre-treatment with sodium chlorate and 100 nM of Heparinase I, III, or I+II+III, as compared to untreated cells.	bind
9292	3	3155	7	11	NULL	0	NULL	statement 1	Process		 reduced by		significantly			Heparinase I	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_811_s_109	11336704	(A) Significant reduction of AP-ES binding to CPAE cells is seen after pre-treatment with sodium chlorate and 100 nM of Heparinase I, III, or I+II+III, as compared to untreated cells.	bind
9293	4	3155	7	11	NULL	0	NULL	statement 1	Process		 reduced by		significantly			Heparinase I+II+III	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_811_s_109	11336704	(A) Significant reduction of AP-ES binding to CPAE cells is seen after pre-treatment with sodium chlorate and 100 nM of Heparinase I, III, or I+II+III, as compared to untreated cells.	bind
9294	5	3155	7	11	NULL	0	NULL	statement 1	Process		reduced by		significantly			Heparinase III	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_811_s_109	11336704	(A) Significant reduction of AP-ES binding to CPAE cells is seen after pre-treatment with sodium chlorate and 100 nM of Heparinase I, III, or I+II+III, as compared to untreated cells.	bind
79952	1	3155	11	NULL	NULL	NULL	NULL	AP-ES	GeneOrProtein		binds to 					CPAE cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_811_s_109	11336704	(A) Significant reduction of AP-ES binding to CPAE cells is seen after pre-treatment with sodium chlorate and 100 nM of Heparinase I, III, or I+II+III, as compared to untreated cells.	bind
79953	2	3155	11	NULL	NULL	NULL	NULL	sodium chlorate	NonProteinOrNucleicAcidChemical	pre-treatment	reduces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_811_s_109	11336704	(A) Significant reduction of AP-ES binding to CPAE cells is seen after pre-treatment with sodium chlorate and 100 nM of Heparinase I, III, or I+II+III, as compared to untreated cells.	bind
79954	3	3155	11	NULL	NULL	0	NULL	Heparinase I	Protein		reduces					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_7_4_811_s_109	11336704	(A) Significant reduction of AP-ES binding to CPAE cells is seen after pre-treatment with sodium chlorate and 100 nM of Heparinase I, III, or I+II+III, as compared to untreated cells.	bind
79955	4	3155	11	NULL	NULL	0	NULL	Heparinase III	Protein		reduces					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_7_4_811_s_109	11336704	(A) Significant reduction of AP-ES binding to CPAE cells is seen after pre-treatment with sodium chlorate and 100 nM of Heparinase I, III, or I+II+III, as compared to untreated cells.	bind
79956	5	3155	11	NULL	NULL	0	NULL	Heparinase II	Protein		reduces					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_7_4_811_s_109	11336704	(A) Significant reduction of AP-ES binding to CPAE cells is seen after pre-treatment with sodium chlorate and 100 nM of Heparinase I, III, or I+II+III, as compared to untreated cells.	bind
79957	6	3155	11	NULL	NULL	0	NULL	statement 3	Process		occurs along with					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_7_4_811_s_109	11336704	(A) Significant reduction of AP-ES binding to CPAE cells is seen after pre-treatment with sodium chlorate and 100 nM of Heparinase I, III, or I+II+III, as compared to untreated cells.	bind
79958	7	3155	11	NULL	NULL	0	NULL	statement 3	Process		occurs along with					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_7_4_811_s_109	11336704	(A) Significant reduction of AP-ES binding to CPAE cells is seen after pre-treatment with sodium chlorate and 100 nM of Heparinase I, III, or I+II+III, as compared to untreated cells.	bind
79959	8	3155	11	NULL	NULL	0	NULL	statement 4	Process		occurs along with					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_7_4_811_s_109	11336704	(A) Significant reduction of AP-ES binding to CPAE cells is seen after pre-treatment with sodium chlorate and 100 nM of Heparinase I, III, or I+II+III, as compared to untreated cells.	bind
7615	1	3156	5	11	NULL	0	NULL	MIWI	GP		bind					oligo(dT)	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_36_13415_s_86	16938833	(A) significantly reduces both MIWI and MSY2 binding in both RNP and polysome fractions, indicating that MIWI binds oligo(dT) through associated poly	bind
9298	1	3156	7	11	NULL	0	NULL	MIWI	GP		bind					oligo(dT)	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_36_13415_s_86	16938833	(A) significantly reduces both MIWI and MSY2 binding in both RNP and polysome fractions, indicating that MIWI binds oligo(dT) through associated poly	bind
79960	1	3156	11	NULL	NULL	0	NULL	MIWI 	Protein		binds to 					oligo(dT)	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_pnas_103_36_13415_s_86	16938833	(A) significantly reduces both MIWI and MSY2 binding in both RNP and polysome fractions, indicating that MIWI binds oligo(dT) through associated poly	bind
79961	1	3157	11	NULL	NULL	NULL	NULL	ZZ-WT Op18	NucleicAcidSubstance		binds to 					IgG Sepharose	Protein				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_1_149_s_107	11285281	(A) Silver-stained gel of MgCl2 elutions of control, ZZ-WT, -AAA, and -EEE Op18 bound to IgG Sepharose retrieved from extracts.	bind
79962	2	3157	11	NULL	NULL	NULL	NULL	ZZ-AAA Op18	NucleicAcidSubstance		binds to 					IgG Sepharose	Protein				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_1_149_s_107	11285281	(A) Silver-stained gel of MgCl2 elutions of control, ZZ-WT, -AAA, and -EEE Op18 bound to IgG Sepharose retrieved from extracts.	bind
79963	3	3157	11	NULL	NULL	NULL	NULL	ZZ-EEE Op18	NucleicAcidSubstance		binds to 					IgG Sepharose	Protein				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_1_149_s_107	11285281	(A) Silver-stained gel of MgCl2 elutions of control, ZZ-WT, -AAA, and -EEE Op18 bound to IgG Sepharose retrieved from extracts.	bind
7616	1	3158	5	11	NULL	0	NULL	CstF	GP		is					cleavage stimulation factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6603_s_31	12456666	(A) site also requires cleavage stimulation factor (CstF) that binds to a GU/U-rich element downstream of the cleavage site and interacts with CPSF.	bind
7617	2	3158	5	11	NULL	0	NULL				lies downstream of				GU/U-rich element	cleavage site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6603_s_31	12456666	(A) site also requires cleavage stimulation factor (CstF) that binds to a GU/U-rich element downstream of the cleavage site and interacts with CPSF.	bind
7618	3	3158	5	11	NULL	0	NULL	CstF	GP		interact with					CPSF	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6603_s_31	12456666	(A) site also requires cleavage stimulation factor (CstF) that binds to a GU/U-rich element downstream of the cleavage site and interacts with CPSF.	bind
44745	4	3158	5	11	NULL	0	NULL	CstF	GP		bind					statement 2	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6603_s_31	12456666	(A) site also requires cleavage stimulation factor (CstF) that binds to a GU/U-rich element downstream of the cleavage site and interacts with CPSF.	bind
9299	1	3158	7	11	NULL	0	NULL				lies downstream of				GU/U-rich element	clevage site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6603_s_31	12456666	(A) site also requires cleavage stimulation factor (CstF) that binds to a GU/U-rich element downstream of the cleavage site and interacts with CPSF.	bind
9300	2	3158	7	11	NULL	0	NULL	statement 1	NucleicAcid		binds					CPSF	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6603_s_31	12456666	(A) site also requires cleavage stimulation factor (CstF) that binds to a GU/U-rich element downstream of the cleavage site and interacts with CPSF.	bind
9301	3	3158	7	11	NULL	0	NULL	cleavage stimulation factor 	GP		is					CstF	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6603_s_31	12456666	(A) site also requires cleavage stimulation factor (CstF) that binds to a GU/U-rich element downstream of the cleavage site and interacts with CPSF.	bind
44746	4	3158	7	11	NULL	0	NULL	CstF	GP		bind					statement 1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6603_s_31	12456666	(A) site also requires cleavage stimulation factor (CstF) that binds to a GU/U-rich element downstream of the cleavage site and interacts with CPSF.	bind
79964	1	3158	11	NULL	NULL	0	NULL	cleavage stimulation factor	Protein		is					CstF	Protein				NULL		0	NULL	NULL	NULL	gw60_embo_21_23_6603_s_31	12456666	(A) site also requires cleavage stimulation factor (CstF) that binds to a GU/U-rich element downstream of the cleavage site and interacts with CPSF.	bind
79965	2	3158	11	NULL	NULL	0	NULL	CstF	Protein		binds to 									GU/U-rich element	NULL		0	NULL	NULL	NULL	gw60_embo_21_23_6603_s_31	12456666	(A) site also requires cleavage stimulation factor (CstF) that binds to a GU/U-rich element downstream of the cleavage site and interacts with CPSF.	bind
79966	3	3158	11	NULL	NULL	NULL	NULL	CstF	Protein		interacts with					CPSF	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6603_s_31	12456666	(A) site also requires cleavage stimulation factor (CstF) that binds to a GU/U-rich element downstream of the cleavage site and interacts with CPSF.	bind
7619	1	3159	5	11	NULL	0	NULL	CPSF	GP		bind					pre-mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_41825_s_295	11551915	(A) site are necessary for the predominant use of the L1 site early in infection ( 39,  44), that splice sites are not involved ( 41), and that binding of CPSF to the pre-mRNA is stabilized by these regulatory sequences ( 53).	bind
7620	2	3159	5	11	NULL	0	NULL				stabilize				regulatory sequences	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_41825_s_295	11551915	(A) site are necessary for the predominant use of the L1 site early in infection ( 39,  44), that splice sites are not involved ( 41), and that binding of CPSF to the pre-mRNA is stabilized by these regulatory sequences ( 53).	bind
9302	1	3159	7	11	NULL	0	NULL	CPSF	GP		bind					pre-mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_41825_s_295	11551915	(A) site are necessary for the predominant use of the L1 site early in infection ( 39,  44), that splice sites are not involved ( 41), and that binding of CPSF to the pre-mRNA is stabilized by these regulatory sequences ( 53).	bind
11932	2	3159	7	11	NULL	0	NULL				stabilize				regulatory sequences	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_41825_s_295	11551915	(A) site are necessary for the predominant use of the L1 site early in infection ( 39,  44), that splice sites are not involved ( 41), and that binding of CPSF to the pre-mRNA is stabilized by these regulatory sequences ( 53).	bind
79967	1	3159	11	NULL	NULL	0	NULL	 CPSF	Protein		binds to 					pre-mRNA	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_41825_s_295	11551915	(A) site are necessary for the predominant use of the L1 site early in infection ( 39,  44), that splice sites are not involved ( 41), and that binding of CPSF to the pre-mRNA is stabilized by these regulatory sequences ( 53).	bind
79968	2	3159	11	NULL	NULL	0	NULL	statement 1	Process		is stabilized by					regulatory sequences	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_41825_s_295	11551915	(A) site are necessary for the predominant use of the L1 site early in infection ( 39,  44), that splice sites are not involved ( 41), and that binding of CPSF to the pre-mRNA is stabilized by these regulatory sequences ( 53).	bind
7621	1	3163	5	11	NULL	0	NULL	CPSF	GP		bind							upstream of cleavage site		A(A/U)UAAA hexamer	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1315_s_5	15937220	(A) site selection appears to rely primarily on the binding of CPSF to an A(A/U)UAAA hexamer upstream of the cleavage site and CstF to a downstream GU-rich element.	bind
7622	2	3163	5	11	NULL	0	NULL	CstF	GP		bind							downstream		GU-rich element	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1315_s_5	15937220	(A) site selection appears to rely primarily on the binding of CPSF to an A(A/U)UAAA hexamer upstream of the cleavage site and CstF to a downstream GU-rich element.	bind
9303	1	3163	7	11	NULL	0	NULL	CPSF	GP		bind							upstream of the cleavage site		A(A/U)UAAA hexamer	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1315_s_5	15937220	(A) site selection appears to rely primarily on the binding of CPSF to an A(A/U)UAAA hexamer upstream of the cleavage site and CstF to a downstream GU-rich element.	bind
9304	2	3163	7	11	NULL	0	NULL	CstF	GP		bind							downstream		 GU-rich element	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1315_s_5	15937220	(A) site selection appears to rely primarily on the binding of CPSF to an A(A/U)UAAA hexamer upstream of the cleavage site and CstF to a downstream GU-rich element.	bind
79969	1	3163	11	NULL	NULL	0	NULL	CPSF	Protein		binds to 									A(A/U)UAAA hexamer	NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1315_s_5	15937220	(A) site selection appears to rely primarily on the binding of CPSF to an A(A/U)UAAA hexamer upstream of the cleavage site and CstF to a downstream GU-rich element.	bind
79970	2	3163	11	NULL	NULL	0	NULL	CstF	Protein		binds to 									GU-rich element	NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1315_s_5	15937220	(A) site selection appears to rely primarily on the binding of CPSF to an A(A/U)UAAA hexamer upstream of the cleavage site and CstF to a downstream GU-rich element.	bind
7623	1	3164	5	11	NULL	0	NULL	CstF-64	GP		bind							downstream		G/U-rich sequence	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_6_1684_s_28	11865048	(A) site, while CstF-64 binds a downstream G/U-rich sequence.	bind
9305	1	3164	7	11	NULL	0	NULL	CstF-64	GP		binds 							downstream		G/U-rich sequence	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_6_1684_s_28	11865048	(A) site, while CstF-64 binds a downstream G/U-rich sequence.	bind
79971	1	3164	11	NULL	NULL	0	NULL	CstF-64	Protein		binds to 									G/U-rich sequence	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_6_1684_s_28	11865048	(A) site, while CstF-64 binds a downstream G/U-rich sequence.	bind
7624	1	3165	5	11	NULL	0	NULL	CPSF	GP		bind					pre-mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1315_s_348	15937220	(A) site-containing RNA, and that CFIm enhanced the binding of CPSF to the pre-mRNA.	bind
7625	2	3165	5	11	NULL	0	NULL	CFIm	GP		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1315_s_348	15937220	(A) site-containing RNA, and that CFIm enhanced the binding of CPSF to the pre-mRNA.	bind
9306	1	3165	7	11	NULL	0	NULL	CPSF	GP		bind					pre-mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1315_s_348	15937220	(A) site-containing RNA, and that CFIm enhanced the binding of CPSF to the pre-mRNA.	bind
9307	2	3165	7	11	NULL	0	NULL	CFIm 	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1315_s_348	15937220	(A) site-containing RNA, and that CFIm enhanced the binding of CPSF to the pre-mRNA.	bind
79972	1	3165	11	NULL	NULL	0	NULL	CPSF	Protein		binds to 					pre-mRNA	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1315_s_348	15937220	(A) site-containing RNA, and that CFIm enhanced the binding of CPSF to the pre-mRNA.	bind
79973	2	3165	11	NULL	NULL	0	NULL	RNA	NucleicAcidSubstance		enhances					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1315_s_348	15937220	(A) site-containing RNA, and that CFIm enhanced the binding of CPSF to the pre-mRNA.	bind
79974	3	3165	11	NULL	NULL	NULL	NULL	CFIm	GeneOrProtein		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_11_1315_s_348	15937220	(A) site-containing RNA, and that CFIm enhanced the binding of CPSF to the pre-mRNA.	bind
7626	1	3167	5	11	NULL	0	NULL	L3	GP		bind					CstF	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_779_s_124	8945502	(A) sites have different strengths so that  L3 binds CstF with higher affinity than L1.	bind
7627	2	3167	5	11	NULL	0	NULL	L3	GP		bind					L1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_779_s_124	8945502	(A) sites have different strengths so that  L3 binds CstF with higher affinity than L1.	bind
7628	3	3167	5	11	NULL	0	NULL	statement 1	Process		has higher affinity than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_779_s_124	8945502	(A) sites have different strengths so that  L3 binds CstF with higher affinity than L1.	bind
9308	1	3167	7	11	NULL	0	NULL	L3	GP		bind					CstF	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_779_s_124	8945502	(A) sites have different strengths so that  L3 binds CstF with higher affinity than L1.	bind
9309	2	3167	7	11	NULL	0	NULL	L1	GP		bind					CstF	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_779_s_124	8945502	(A) sites have different strengths so that  L3 binds CstF with higher affinity than L1.	bind
9310	3	3167	7	11	NULL	0	NULL	statement 1	Process		has higher affinity than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_779_s_124	8945502	(A) sites have different strengths so that  L3 binds CstF with higher affinity than L1.	bind
79975	1	3167	11	NULL	NULL	0	NULL	L3	NucleicAcidSubstance		binds to 					CstF	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_87_5_779_s_124	8945502	(A) sites have different strengths so that  L3 binds CstF with higher affinity than L1.	bind
79976	2	3167	11	NULL	NULL	0	NULL	L1	NucleicAcidSubstance		binds to 					CstF	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_87_5_779_s_124	8945502	(A) sites have different strengths so that  L3 binds CstF with higher affinity than L1.	bind
79977	3	3167	11	NULL	NULL	0	NULL	statement 1	Process		has more affinity than					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_cell_87_5_779_s_124	8945502	(A) sites have different strengths so that  L3 binds CstF with higher affinity than L1.	bind
7629	1	3168	5	11	NULL	0	NULL	Skp2	GP		interact with					Smad4	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_17_7524_s_74	15314162	(A) Skp2 interacts with Smad4 but not other  Smads.	bind
7630	2	3168	5	11	NULL	0	NULL	Skp2	GP		does not bind					Smads	GP	other			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_17_7524_s_74	15314162	(A) Skp2 interacts with Smad4 but not other  Smads.	bind
9311	1	3168	7	11	NULL	0	NULL	Skp2	GP		binds					Smad4	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_17_7524_s_74	15314162	(A) Skp2 interacts with Smad4 but not other  Smads.	bind
9312	2	3168	7	11	NULL	0	NULL	Skp2	GP		does not bind					Smads	GP	other			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_17_7524_s_74	15314162	(A) Skp2 interacts with Smad4 but not other  Smads.	bind
79978	1	3168	11	NULL	NULL	NULL	NULL	Skp2	GeneOrProtein		interacts with					Smad4	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_17_7524_s_74	15314162	(A) Skp2 interacts with Smad4 but not other  Smads.	bind
7645	1	3169	5	11	NULL	0	NULL	Smad3A	GP		does not bind					PKA 	GP		regulatory subunit		NULL	TGFbeta-treated cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_5_2169_s_177	14966294	(A) Smad3A does not bind to the PKA regulatory subunit in TGFbeta-treated  cells.	bind
9313	1	3169	7	11	NULL	0	NULL	Smad3A	GP		does not bind					PKA	GP		regulatory subunit		NULL	TGFbeta-treated cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_5_2169_s_177	14966294	(A) Smad3A does not bind to the PKA regulatory subunit in TGFbeta-treated  cells.	bind
79979	1	3169	11	NULL	NULL	0	NULL	 Smad3A	GeneOrProtein		does not bind to					PKA	GeneOrProtein			regulatory subunit	NULL	TGFbeta-treated cells	0	NULL	NULL	NULL	gw70_molcellbiol_24_5_2169_s_177	14966294	(A) Smad3A does not bind to the PKA regulatory subunit in TGFbeta-treated  cells.	bind
7643	1	3170	5	11	NULL	0	NULL	Smad7	GP		bind					p38	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_529_s_242	12589052	(A) Smad7 binds to p38 in vivo.	bind
9314	1	3170	7	11	NULL	0	NULL	Smad7	GP		bind					p38	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_529_s_242	12589052	(A) Smad7 binds to p38 in vivo.	bind
79980	1	3170	11	NULL	NULL	0	NULL	 Smad7	GeneOrProtein		binds to 					 p38	GeneOrProtein				NULL	in vivo	0	NULL	NULL	NULL	gw60_molbiolcell_14_2_529_s_242	12589052	(A) Smad7 binds to p38 in vivo.	bind
7646	1	3171	5	11	NULL	0	NULL	Smad7	GP		bind			Y211A		TGF receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1365_s_250	11163210	(A) Smad7(Y211A) binds to TGF  receptors but has a reduced ability to recruit Smurf2 to the receptor complex.	bind
7647	2	3171	5	11	NULL	0	NULL	Smurf2	GP		is recruited to					receptor complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1365_s_250	11163210	(A) Smad7(Y211A) binds to TGF  receptors but has a reduced ability to recruit Smurf2 to the receptor complex.	bind
9315	1	3171	7	11	NULL	0	NULL	Smad7	GP		bind			Y211A		TGF receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1365_s_250	11163210	(A) Smad7(Y211A) binds to TGF  receptors but has a reduced ability to recruit Smurf2 to the receptor complex.	bind
9316	2	3171	7	11	NULL	0	NULL	Smurf2	GP		is recruited to					receptor complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1365_s_250	11163210	(A) Smad7(Y211A) binds to TGF  receptors but has a reduced ability to recruit Smurf2 to the receptor complex.	bind
9317	3	3171	7	11	NULL	0	NULL	Smad7	GP		has reduced ability for			Y211A		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1365_s_250	11163210	(A) Smad7(Y211A) binds to TGF  receptors but has a reduced ability to recruit Smurf2 to the receptor complex.	bind
79981	1	3171	11	NULL	NULL	0	NULL	 Smad7	Protein		binds to 			Y211A		TGF receptor	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_6_6_1365_s_250	11163210	(A) Smad7(Y211A) binds to TGF  receptors but has a reduced ability to recruit Smurf2 to the receptor complex.	bind
79982	2	3171	11	NULL	NULL	NULL	NULL	Smad7	Protein		recruit		reduced ability to	Y211A		Smurf2	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1365_s_250	11163210	(A) Smad7(Y211A) binds to TGF  receptors but has a reduced ability to recruit Smurf2 to the receptor complex.	bind
7648	1	3173	5	11	NULL	0	NULL	H3 peptide	GP		contain							trimethylated	K9		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5535_s_125	15964809	(a) Space-filling  representation of H3 peptide containing trimethylated K9 bound to  Drosophila HP1 chromodomain.	bind
7650	2	3173	5	11	NULL	0	NULL	statement 1	GP		bind					HP1	GP	Drosophila	chromodomain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5535_s_125	15964809	(a) Space-filling  representation of H3 peptide containing trimethylated K9 bound to  Drosophila HP1 chromodomain.	bind
9318	1	3173	7	11	NULL	0	NULL	H3 peptide	GP		contain							trimethylated	K9		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5535_s_125	15964809	(a) Space-filling  representation of H3 peptide containing trimethylated K9 bound to  Drosophila HP1 chromodomain.	bind
44747	2	3173	7	11	NULL	0	NULL	statement 1	GP		bind					HP1	GP	Drosophila	chromodomain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5535_s_125	15964809	(a) Space-filling  representation of H3 peptide containing trimethylated K9 bound to  Drosophila HP1 chromodomain.	bind
79983	1	3173	11	NULL	NULL	0	NULL	H3 peptide	PartOfProtein		contains					K9	PartOfProtein	trimethylated			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_13_5535_s_125	15964809	(a) Space-filling  representation of H3 peptide containing trimethylated K9 bound to  Drosophila HP1 chromodomain.	bind
79984	2	3173	11	NULL	NULL	0	NULL	H3 peptide 	PartOfProtein		binds to 			trimethylated K9		HP1 chromodomain	PartOfProtein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_13_5535_s_125	15964809	(a) Space-filling  representation of H3 peptide containing trimethylated K9 bound to  Drosophila HP1 chromodomain.	bind
7654	1	3174	5	11	NULL	0	NULL	SPB	Chromosome		bind					Cdc14p	GP				NULL	cdc15-1 cells	NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_367_s_269	11970961	(A) SPB binding of Cdc14p in  cdc15-1 and  dbf2-2 cells.	bind
7656	2	3174	5	11	NULL	0	NULL	SPB	Chromosome		bind					Cdc14p	GP				NULL	dbf2-2 cells	NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_367_s_269	11970961	(A) SPB binding of Cdc14p in  cdc15-1 and  dbf2-2 cells.	bind
9319	1	3174	7	11	NULL	0	NULL	SPB	Chromosome		bind					Cdc14p	GP				NULL	cdc15-1 cells	NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_367_s_269	11970961	(A) SPB binding of Cdc14p in  cdc15-1 and  dbf2-2 cells.	bind
9320	2	3174	7	11	NULL	0	NULL	SPB	Chromosome		bind					Cdc14p	GP				NULL	dbf2-2 cells	NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_367_s_269	11970961	(A) SPB binding of Cdc14p in  cdc15-1 and  dbf2-2 cells.	bind
79985	1	3174	11	NULL	NULL	0	NULL	Cdc14p	Protein		binds to 					SPB	CellComponent	cdc15-1;;dbf2-2 cells			NULL		0	NULL	NULL	NULL	gw60_cellbiol_157_3_367_s_269	11970961	(A) SPB binding of Cdc14p in  cdc15-1 and  dbf2-2 cells.	bind
7660	1	3176	5	11	NULL	0	NULL	tomosyn	GP		bind		specifically			syntaxin-1a	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_5_905_s_72	9620695	(A) Specific binding of tomosyn to syntaxin-1a.	bind
9321	1	3176	7	11	NULL	0	NULL	tomosyn	GP		bind		specifically			syntaxin-1a	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_5_905_s_72	9620695	(A) Specific binding of tomosyn to syntaxin-1a.	bind
79986	1	3176	11	NULL	NULL	NULL	NULL	tomosyn	GeneOrProtein		binds to 					syntaxin-1a	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_5_905_s_72	9620695	(A) Specific binding of tomosyn to syntaxin-1a.	bind
7668	1	3177	5	11	NULL	0	NULL	VHH	GP		bind		specifically	9C		ISP	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1624_1_21_s_83	14642809	(A) Specific binding of VHH 9C with  P. pastoris-produced ISP as determined with surface plasmon resonance using the anti-ISP VHH  immobilized on flow cell 2 and an anti-lipase VHH on flow cell 1.	bind
9322	1	3177	7	11	NULL	0	NULL	VHH	GP		binds		specifically	 9C		ISP	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1624_1_21_s_83	14642809	(A) Specific binding of VHH 9C with  P. pastoris-produced ISP as determined with surface plasmon resonance using the anti-ISP VHH  immobilized on flow cell 2 and an anti-lipase VHH on flow cell 1.	bind
79987	1	3177	11	NULL	NULL	NULL	NULL	VHH 9C	Protein		binds to 					ISP	Protein	P. pastoris			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1624_1_21_s_83	14642809	(A) Specific binding of VHH 9C with  P. pastoris-produced ISP as determined with surface plasmon resonance using the anti-ISP VHH  immobilized on flow cell 2 and an anti-lipase VHH on flow cell 1.	bind
7675	2	3178	5	11	NULL	0	NULL	[3]AII	GP		bind		specifically			statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_99	12721105	(a) Specific binding of [3]AII to HEK 293 cells stably or transiently expressing AT1R - YFP or to untransfected cells.	bind
7676	4	3178	5	11	NULL	0	NULL	[3]AII	GP		bind		specifically			statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_99	12721105	(a) Specific binding of [3]AII to HEK 293 cells stably or transiently expressing AT1R - YFP or to untransfected cells.	bind
7678	5	3178	5	11	NULL	0	NULL	[3]AII	GP		bind		specifically			HEK 293 cells	Cell	untransfected cells			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_99	12721105	(a) Specific binding of [3]AII to HEK 293 cells stably or transiently expressing AT1R - YFP or to untransfected cells.	bind
7679	6	3178	5	11	NULL	0	NULL	statement 5	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_99	12721105	(a) Specific binding of [3]AII to HEK 293 cells stably or transiently expressing AT1R - YFP or to untransfected cells.	bind
7680	7	3178	5	11	NULL	0	NULL	statement 4	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_99	12721105	(a) Specific binding of [3]AII to HEK 293 cells stably or transiently expressing AT1R - YFP or to untransfected cells.	bind
44759	1	3178	5	11	NULL	0	NULL	HEK 293 cells	Cell		express		stably			AT1R - YFP	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_99	12721105	(a) Specific binding of [3]AII to HEK 293 cells stably or transiently expressing AT1R - YFP or to untransfected cells.	bind
44760	3	3178	5	11	NULL	0	NULL	HEK 293 cells	Cell		express		transiently			AT1R - YFP	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_99	12721105	(a) Specific binding of [3]AII to HEK 293 cells stably or transiently expressing AT1R - YFP or to untransfected cells.	bind
9323	3	3178	7	11	NULL	0	NULL	[3]AII	GP		bind		specifically			statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_99	12721105	(a) Specific binding of [3]AII to HEK 293 cells stably or transiently expressing AT1R - YFP or to untransfected cells.	bind
9324	4	3178	7	11	NULL	0	NULL	[3]AII	GP		bind		specifically			statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_99	12721105	(a) Specific binding of [3]AII to HEK 293 cells stably or transiently expressing AT1R - YFP or to untransfected cells.	bind
9325	5	3178	7	11	NULL	0	NULL	[3]AII	GP		bind		specifically			HEK 293 cells	Cell	untransfected			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_99	12721105	(a) Specific binding of [3]AII to HEK 293 cells stably or transiently expressing AT1R - YFP or to untransfected cells.	bind
11936	6	3178	7	11	NULL	0	NULL	statement 3	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_99	12721105	(a) Specific binding of [3]AII to HEK 293 cells stably or transiently expressing AT1R - YFP or to untransfected cells.	bind
11937	7	3178	7	11	NULL	0	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_99	12721105	(a) Specific binding of [3]AII to HEK 293 cells stably or transiently expressing AT1R - YFP or to untransfected cells.	bind
44726	1	3178	7	11	NULL	0	NULL	HEK293 cells	Cell		express		stably			AT1R - YFP	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_99	12721105	(a) Specific binding of [3]AII to HEK 293 cells stably or transiently expressing AT1R - YFP or to untransfected cells.	bind
44727	2	3178	7	11	NULL	0	NULL	HEK293 cells	Cell		express		transiently			AT1R - YFP	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_99	12721105	(a) Specific binding of [3]AII to HEK 293 cells stably or transiently expressing AT1R - YFP or to untransfected cells.	bind
79989	1	3178	11	NULL	NULL	NULL	NULL	AII	GeneOrProtein		binds to 		Specific			HEK 293 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_99	12721105	(a) Specific binding of [3]AII to HEK 293 cells stably or transiently expressing AT1R - YFP or to untransfected cells.	bind
7684	1	3179	5	11	NULL	0	NULL	PPARalpha/RXRalpha	GP		bind		specifically			PEX11alpha/perilipin	GP			PPRE	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1313_s_236	14729975	(A) Specific PPARalpha/RXRalpha binding to the PEX11alpha/perilipin-PPRE.	bind
9326	1	3179	7	11	NULL	0	NULL	PPARalpha/RXRalpha	GP		bind		specifically			PEX11alpha/perilipin	GP			PPRE	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1313_s_236	14729975	(A) Specific PPARalpha/RXRalpha binding to the PEX11alpha/perilipin-PPRE.	bind
79996	1	3179	11	NULL	NULL	NULL	NULL	PPARalpha	GeneOrProtein		complex with 					RXRalpha	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1313_s_236	14729975	(A) Specific PPARalpha/RXRalpha binding to the PEX11alpha/perilipin-PPRE.	bind
79997	2	3179	11	NULL	NULL	NULL	NULL	PEX11alpha	GeneOrProtein		complex with 					perilipin	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1313_s_236	14729975	(A) Specific PPARalpha/RXRalpha binding to the PEX11alpha/perilipin-PPRE.	bind
79998	3	3179	11	NULL	NULL	NULL	NULL	statement 2	GeneOrProtein		complex with 					PPRE	Gene				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1313_s_236	14729975	(A) Specific PPARalpha/RXRalpha binding to the PEX11alpha/perilipin-PPRE.	bind
79999	4	3179	11	NULL	NULL	NULL	NULL	statement 1	GeneOrProtein		binds to 					statement 3	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1313_s_236	14729975	(A) Specific PPARalpha/RXRalpha binding to the PEX11alpha/perilipin-PPRE.	bind
7773	1	3180	5	11	NULL	0	NULL	transferrin	GP		bind		specifically			L5 fusion	GP		Loop 5		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_2_732_s_217	11796606	(A) Specific transferrin binding to L5 fusion (Loop 5) compared to CBD alone (CBD control).	bind
7774	2	3180	5	11	NULL	0	NULL	transferrin	GP		bind							control	CBD		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_2_732_s_217	11796606	(A) Specific transferrin binding to L5 fusion (Loop 5) compared to CBD alone (CBD control).	bind
9327	1	3180	7	11	NULL	0	NULL	transferrin	GP		bind		specifically			 L5 fusion	GP		Loop 5		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_2_732_s_217	11796606	(A) Specific transferrin binding to L5 fusion (Loop 5) compared to CBD alone (CBD control).	bind
9328	2	3180	7	11	NULL	0	NULL	transferrin	GP		bind								CBD		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_2_732_s_217	11796606	(A) Specific transferrin binding to L5 fusion (Loop 5) compared to CBD alone (CBD control).	bind
80000	1	3180	11	NULL	NULL	0	NULL	 transferrin	Protein		binds to 					 L5 fusion	PartOfProtein		Loop 5		NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_2_732_s_217	11796606	(A) Specific transferrin binding to L5 fusion (Loop 5) compared to CBD alone (CBD control).	bind
80001	2	3180	11	NULL	NULL	0	NULL	transferrin	Protein		binds to 								CBD		NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_2_732_s_217	11796606	(A) Specific transferrin binding to L5 fusion (Loop 5) compared to CBD alone (CBD control).	bind
7772	1	3181	5	11	NULL	0	NULL	SRC-1	GP		bind					UNC-5	GP		cytosolic domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6485_s_48	16024786	(A) SRC-1 binds  the UNC-5 cytosolic domain.	bind
9329	1	3181	7	11	NULL	0	NULL	SRC-1	GP		binds					UNC-5	GP		cytosolic domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6485_s_48	16024786	(A) SRC-1 binds  the UNC-5 cytosolic domain.	bind
80002	1	3181	11	NULL	NULL	NULL	NULL	SRC-1	GeneOrProtein		binds to 					UNC-5	Protein		cytosolic domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6485_s_48	16024786	(A) SRC-1 binds  the UNC-5 cytosolic domain.	bind
7775	1	3182	5	11	NULL	0	NULL	SREBP-1a	GP		bind					LDL receptor	GP	rat		SRE within promoter at 242 to 234 bp	NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1761_4_492_s_167	16647292	(A) SREBP-1a  binding to the SRE identified within the rat LDL receptor promoter at  242 to  234  bp.	bind
9330	1	3182	7	11	NULL	0	NULL	SREBP-1a	GP		binds to					LDL receptor	GP	rat		SRE promoter at 242 to 234 bp	NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1761_4_492_s_167	16647292	(A) SREBP-1a  binding to the SRE identified within the rat LDL receptor promoter at  242 to  234  bp.	bind
80003	1	3182	11	NULL	NULL	NULL	NULL	SREBP-1a	GeneOrProtein		binds to 					 LDL receptor	Gene	rat		promoter	NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1761_4_492_s_167	16647292	(A) SREBP-1a  binding to the SRE identified within the rat LDL receptor promoter at  242 to  234  bp.	bind
80004	2	3182	11	NULL	NULL	NULL	NULL				is a part of				SRE	LDL receptor	Gene			promoter	NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1761_4_492_s_167	16647292	(A) SREBP-1a  binding to the SRE identified within the rat LDL receptor promoter at  242 to  234  bp.	bind
7777	1	3183	5	11	NULL	0	NULL	caspase-7	GP	active	bind					XIAP fragment	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_3_399_s_80	11701129	(A) Stabilization of the catalytic cleft by the  loop-bundle in the active caspase-7 bound with  an XIAP fragment (PDB code 1I51).	bind
7780	2	3183	5	11	NULL	0	NULL	statement 1	Process		stabilize								catalytic cleft		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_3_399_s_80	11701129	(A) Stabilization of the catalytic cleft by the  loop-bundle in the active caspase-7 bound with  an XIAP fragment (PDB code 1I51).	bind
9331	1	3183	7	11	NULL	0	NULL	caspase-7 	GP	active	bind					 XIAP fragment	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_3_399_s_80	11701129	(A) Stabilization of the catalytic cleft by the  loop-bundle in the active caspase-7 bound with  an XIAP fragment (PDB code 1I51).	bind
11939	2	3183	7	11	NULL	0	NULL	statement 1	Process		stabilize								catalytic cleft		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_3_399_s_80	11701129	(A) Stabilization of the catalytic cleft by the  loop-bundle in the active caspase-7 bound with  an XIAP fragment (PDB code 1I51).	bind
80005	1	3183	11	NULL	NULL	NULL	NULL	caspase-7	GeneOrProtein		binds to 					XIAP fragment	PartOfProtein				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_3_399_s_80	11701129	(A) Stabilization of the catalytic cleft by the  loop-bundle in the active caspase-7 bound with  an XIAP fragment (PDB code 1I51).	bind
7784	1	3184	5	11	NULL	0	NULL	Ste12	GP	yeast lysates	bind		specifically			GST-Rst1	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_4_228_s_78	9094309	(a) Ste12 and Fus3 from yeast lysates bind specifically to GST-Rst1 and GST-Rst2 fusion proteins.	bind
7786	2	3184	5	11	NULL	0	NULL	Ste12	GP	yeast lysates	bind		specifically			GST-Rst2	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_4_228_s_78	9094309	(a) Ste12 and Fus3 from yeast lysates bind specifically to GST-Rst1 and GST-Rst2 fusion proteins.	bind
7787	3	3184	5	11	NULL	0	NULL	Fus3	GP	yeast lysates	bind		specifically			GST-Rst1	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_4_228_s_78	9094309	(a) Ste12 and Fus3 from yeast lysates bind specifically to GST-Rst1 and GST-Rst2 fusion proteins.	bind
7788	4	3184	5	11	NULL	0	NULL	Fus3	GP	yeast lysates	bind		specifically			GST-Rst2	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_4_228_s_78	9094309	(a) Ste12 and Fus3 from yeast lysates bind specifically to GST-Rst1 and GST-Rst2 fusion proteins.	bind
9332	1	3184	7	11	NULL	0	NULL	Ste12	GP	 yeast lysates	bind		specifically			GST-Rst1	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_4_228_s_78	9094309	(a) Ste12 and Fus3 from yeast lysates bind specifically to GST-Rst1 and GST-Rst2 fusion proteins.	bind
9333	2	3184	7	11	NULL	0	NULL	Ste12 	GP	yeast lysates	bind		specifically			GST-Rst2	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_4_228_s_78	9094309	(a) Ste12 and Fus3 from yeast lysates bind specifically to GST-Rst1 and GST-Rst2 fusion proteins.	bind
9334	3	3184	7	11	NULL	0	NULL	Fus3	GP	yeast lysates	bind		specifically			GST-Rst1	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_4_228_s_78	9094309	(a) Ste12 and Fus3 from yeast lysates bind specifically to GST-Rst1 and GST-Rst2 fusion proteins.	bind
9335	4	3184	7	11	NULL	0	NULL	Fus3	GP	yeast lysates	bind		specifically			GST-Rst2	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_4_228_s_78	9094309	(a) Ste12 and Fus3 from yeast lysates bind specifically to GST-Rst1 and GST-Rst2 fusion proteins.	bind
80006	1	3184	11	NULL	NULL	NULL	NULL	Ste12	GeneOrProtein	yeast	binds to 		specifically			GST-Rst2 fusion protein	Protein				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_4_228_s_78	9094309	(a) Ste12 and Fus3 from yeast lysates bind specifically to GST-Rst1 and GST-Rst2 fusion proteins.	bind
80007	2	3184	11	NULL	NULL	NULL	NULL	Fus3	GeneOrProtein	yeast	binds to 		specifically			GST-Rst2 fusion protein	Protein				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_4_228_s_78	9094309	(a) Ste12 and Fus3 from yeast lysates bind specifically to GST-Rst1 and GST-Rst2 fusion proteins.	bind
80008	3	3184	11	NULL	NULL	NULL	NULL	Ste12	GeneOrProtein	yeast	binds to 		specifically			GST-Rst1 fusion protein	Protein				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_4_228_s_78	9094309	(a) Ste12 and Fus3 from yeast lysates bind specifically to GST-Rst1 and GST-Rst2 fusion proteins.	bind
80009	4	3184	11	NULL	NULL	NULL	NULL	Fus3	GeneOrProtein	yeast	binds to 		specifically			GST-Rst1 fusion protein	Protein				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_4_228_s_78	9094309	(a) Ste12 and Fus3 from yeast lysates bind specifically to GST-Rst1 and GST-Rst2 fusion proteins.	bind
7789	1	3185	5	11	NULL	0	NULL	STE50	GP		bind		constitutively			STE11	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5788_s_243	9742096	(A) STE50 binds to STE11 in a constitutive manner.	bind
9336	1	3185	7	11	NULL	0	NULL	STE50	GP		binds		constitutively			STE11	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5788_s_243	9742096	(A) STE50 binds to STE11 in a constitutive manner.	bind
80010	1	3185	11	NULL	NULL	NULL	NULL	STE50	GeneOrProtein		binds to 					STE11	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5788_s_243	9742096	(A) STE50 binds to STE11 in a constitutive manner.	bind
9337	1	3187	7	11	NULL	0	NULL	[35]GTP S	Chemical		bind					 5-ht5A/HEK293 membrane	CellComponent	guinea pig			NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_195	16846620	(A) Stimulation by 5-HT, 5-CT, ergotamine, LSD and 8-OH-DPAT of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes; (B) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of LSD, clozapine, SB-269970-A or  WAY-100635.	bind
9338	2	3187	7	11	NULL	0	NULL	5-HT	GP		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_195	16846620	(A) Stimulation by 5-HT, 5-CT, ergotamine, LSD and 8-OH-DPAT of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes; (B) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of LSD, clozapine, SB-269970-A or  WAY-100635.	bind
9339	3	3187	7	11	NULL	0	NULL	5-CT	Chemical		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_195	16846620	(A) Stimulation by 5-HT, 5-CT, ergotamine, LSD and 8-OH-DPAT of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes; (B) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of LSD, clozapine, SB-269970-A or  WAY-100635.	bind
9340	4	3187	7	11	NULL	0	NULL	ergotamine	Chemical		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_195	16846620	(A) Stimulation by 5-HT, 5-CT, ergotamine, LSD and 8-OH-DPAT of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes; (B) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of LSD, clozapine, SB-269970-A or  WAY-100635.	bind
9341	5	3187	7	11	NULL	0	NULL	LSD	Chemical		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_195	16846620	(A) Stimulation by 5-HT, 5-CT, ergotamine, LSD and 8-OH-DPAT of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes; (B) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of LSD, clozapine, SB-269970-A or  WAY-100635.	bind
9342	6	3187	7	11	NULL	0	NULL	8-OH-DPAT	Chemical		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_195	16846620	(A) Stimulation by 5-HT, 5-CT, ergotamine, LSD and 8-OH-DPAT of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes; (B) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of LSD, clozapine, SB-269970-A or  WAY-100635.	bind
80012	1	3187	11	NULL	NULL	NULL	NULL	[35]GTP S	NonProteinOrNucleicAcidChemical		binds to 					5-ht5A	GeneOrProtein	HEK293 membrane;;guinea pig			NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_195	16846620	(A) Stimulation by 5-HT, 5-CT, ergotamine, LSD and 8-OH-DPAT of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes; (B) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of LSD, clozapine, SB-269970-A or  WAY-100635.	bind
80013	2	3187	11	NULL	NULL	NULL	NULL	 5-HT	NonProteinOrNucleicAcidChemical		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_195	16846620	(A) Stimulation by 5-HT, 5-CT, ergotamine, LSD and 8-OH-DPAT of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes; (B) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of LSD, clozapine, SB-269970-A or  WAY-100635.	bind
80014	3	3187	11	NULL	NULL	NULL	NULL	5-CT	NonProteinOrNucleicAcidChemical		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_195	16846620	(A) Stimulation by 5-HT, 5-CT, ergotamine, LSD and 8-OH-DPAT of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes; (B) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of LSD, clozapine, SB-269970-A or  WAY-100635.	bind
80015	4	3187	11	NULL	NULL	NULL	NULL	ergotamine	NonProteinOrNucleicAcidChemical		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_195	16846620	(A) Stimulation by 5-HT, 5-CT, ergotamine, LSD and 8-OH-DPAT of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes; (B) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of LSD, clozapine, SB-269970-A or  WAY-100635.	bind
80016	5	3187	11	NULL	NULL	NULL	NULL	LSD	NonProteinOrNucleicAcidChemical		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_195	16846620	(A) Stimulation by 5-HT, 5-CT, ergotamine, LSD and 8-OH-DPAT of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes; (B) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of LSD, clozapine, SB-269970-A or  WAY-100635.	bind
80017	6	3187	11	NULL	NULL	NULL	NULL	8-OH-DPAT	NonProteinOrNucleicAcidChemical		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_195	16846620	(A) Stimulation by 5-HT, 5-CT, ergotamine, LSD and 8-OH-DPAT of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes; (B) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of LSD, clozapine, SB-269970-A or  WAY-100635.	bind
80018	7	3187	11	NULL	NULL	0	NULL	statement 2	Process		is independent of					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_195	16846620	(A) Stimulation by 5-HT, 5-CT, ergotamine, LSD and 8-OH-DPAT of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes; (B) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of LSD, clozapine, SB-269970-A or  WAY-100635.	bind
80019	8	3187	11	NULL	NULL	NULL	NULL	statement 2	Process		is independent of					clozapine	NonProteinOrNucleicAcidChemical				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_195	16846620	(A) Stimulation by 5-HT, 5-CT, ergotamine, LSD and 8-OH-DPAT of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes; (B) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of LSD, clozapine, SB-269970-A or  WAY-100635.	bind
80020	9	3187	11	NULL	NULL	NULL	NULL	statement 2	Process		is independent of					SB-269970-A	NonProteinOrNucleicAcidChemical				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_195	16846620	(A) Stimulation by 5-HT, 5-CT, ergotamine, LSD and 8-OH-DPAT of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes; (B) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of LSD, clozapine, SB-269970-A or  WAY-100635.	bind
80021	10	3187	11	NULL	NULL	NULL	NULL	statement 2	Process		is independent of					WAY-100635	NonProteinOrNucleicAcidChemical				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_51_3_566_s_195	16846620	(A) Stimulation by 5-HT, 5-CT, ergotamine, LSD and 8-OH-DPAT of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes; (B) 5-HT-induced stimulation of [35]GTP S binding to guinea pig 5-ht5A/HEK293 membranes in the absence, and presence, of LSD, clozapine, SB-269970-A or  WAY-100635.	bind
7790	1	3188	5	11	NULL	0	NULL	Rac	GP		bind					PAK	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_1_205_s_115	10893268	(A) Stimulation of Rac and Cdc42 binding to PAK.	bind
7791	2	3188	5	11	NULL	0	NULL	Cdc42	GP		bind					PAK	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_1_205_s_115	10893268	(A) Stimulation of Rac and Cdc42 binding to PAK.	bind
9343	1	3188	7	11	NULL	0	NULL	Rac	GP		bind					PAK	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_1_205_s_115	10893268	(A) Stimulation of Rac and Cdc42 binding to PAK.	bind
9344	2	3188	7	11	NULL	0	NULL	Cdc42	GP		bind					PAK	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_1_205_s_115	10893268	(A) Stimulation of Rac and Cdc42 binding to PAK.	bind
80022	1	3188	11	NULL	NULL	NULL	NULL	 Rac	GeneOrProtein		binds to 					PAK	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_1_205_s_115	10893268	(A) Stimulation of Rac and Cdc42 binding to PAK.	bind
80023	2	3188	11	NULL	NULL	NULL	NULL	Cdc42	GeneOrProtein		binds to 					PAK	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_1_205_s_115	10893268	(A) Stimulation of Rac and Cdc42 binding to PAK.	bind
7792	1	3189	5	11	NULL	0	NULL	PABP	GP		bind					adenosine residues	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genomeres_12_9_1333_s_240	12213770	(A) stretches in a cooperative manner, in which one molecule of PABP binds ~25 adenosine residues (Smith et al. 1997  ).	bind
9345	1	3189	7	11	NULL	0	NULL	PABP 	GP		bind					adenosine residues	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genomeres_12_9_1333_s_240	12213770	(A) stretches in a cooperative manner, in which one molecule of PABP binds ~25 adenosine residues (Smith et al. 1997  ).	bind
80027	1	3189	11	NULL	NULL	NULL	NULL	PABP	GeneOrProtein		binds to 					adenosine	NucleicAcidSubstance			~25 residues	NULL		NULL	NULL	NULL	NULL	gw60_genomeres_12_9_1333_s_240	12213770	(A) stretches in a cooperative manner, in which one molecule of PABP binds ~25 adenosine residues (Smith et al. 1997  ).	bind
7793	1	3190	5	11	NULL	0	NULL	BC1 RNAs	NucleicAcid		bind					PABP	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_8_2374_s_280	16682445	(A) stretches of the RNA and could be alleviated by the addition of PABP ( ), suggesting that the suppression is mediated through binding of PABP by BC1 and BC200 RNAs.	bind
7794	2	3190	5	11	NULL	0	NULL	BC200 RNAs	NucleicAcid		bind					PABP	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_8_2374_s_280	16682445	(A) stretches of the RNA and could be alleviated by the addition of PABP ( ), suggesting that the suppression is mediated through binding of PABP by BC1 and BC200 RNAs.	bind
9346	1	3190	7	11	NULL	0	NULL	PABP	GP		bind					BC1 RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_8_2374_s_280	16682445	(A) stretches of the RNA and could be alleviated by the addition of PABP ( ), suggesting that the suppression is mediated through binding of PABP by BC1 and BC200 RNAs.	bind
9347	2	3190	7	11	NULL	0	NULL	PABP	GP		bind					BC200 RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_8_2374_s_280	16682445	(A) stretches of the RNA and could be alleviated by the addition of PABP ( ), suggesting that the suppression is mediated through binding of PABP by BC1 and BC200 RNAs.	bind
80028	1	3190	11	NULL	NULL	NULL	NULL	PABP	GeneOrProtein		alleviate 					RNA	NucleicAcidSubstance	stretches			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_8_2374_s_280	16682445	(A) stretches of the RNA and could be alleviated by the addition of PABP ( ), suggesting that the suppression is mediated through binding of PABP by BC1 and BC200 RNAs.	bind
80029	2	3190	11	NULL	NULL	NULL	NULL	PABP	GeneOrProtein		binds to 					BC200 RNA	NucleicAcidSubstance				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_8_2374_s_280	16682445	(A) stretches of the RNA and could be alleviated by the addition of PABP ( ), suggesting that the suppression is mediated through binding of PABP by BC1 and BC200 RNAs.	bind
80030	3	3190	11	NULL	NULL	NULL	NULL	PABP	GeneOrProtein		binds to 					BC1 RNA	NucleicAcidSubstance				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_8_2374_s_280	16682445	(A) stretches of the RNA and could be alleviated by the addition of PABP ( ), suggesting that the suppression is mediated through binding of PABP by BC1 and BC200 RNAs.	bind
7795	1	3191	5	11	NULL	0	NULL	RNAP II	GP	S. cerevisiae	bind					nucleic acids	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_1_12_s_19	16524917	(A) Structure of  S. cerevisiae RNAP II bound to nucleic acids (PDB accession number 1Y1W).	bind
9348	1	3191	7	11	NULL	0	NULL	RNAP II	GP	S. cerevisiae	bind					nucleic acids	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_1_12_s_19	16524917	(A) Structure of  S. cerevisiae RNAP II bound to nucleic acids (PDB accession number 1Y1W).	bind
80031	1	3191	11	NULL	NULL	NULL	NULL	RNAP II	GeneOrProtein	S. cerevisiae	binds to 					nucleic acid	NucleicAcidSubstance				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_1_12_s_19	16524917	(A) Structure of  S. cerevisiae RNAP II bound to nucleic acids (PDB accession number 1Y1W).	bind
7796	1	3194	5	11	NULL	0	NULL				bind			tandem SH3 domains		p22 peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_3_343_s_196	12732142	(A) Structure of the tandem SH3 domains bound to the p22 peptide.	bind
9349	1	3194	7	11	NULL	0	NULL				bind			tandem SH3 domains		p22 peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_3_343_s_196	12732142	(A) Structure of the tandem SH3 domains bound to the p22 peptide.	bind
80032	1	3194	11	NULL	NULL	0	NULL				binds to 			SH3 domains		p22 peptide	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_cell_113_3_343_s_196	12732142	(A) Structure of the tandem SH3 domains bound to the p22 peptide.	bind
7806	1	3196	5	11	NULL	0	NULL	Caf1	GP		bind					chaperone G1	GP	donor strand			NULL		NULL	NULL	NULL	NULL	gw60_cell_113_5_587_s_250	12787500	(A) Superposition of Caf1  (red) bound to the chaperone G1 donor strand (blue) and Caf1  (yellow) bound to the Caf1  Gd donor strand (orange) (stereo view).	bind
7809	2	3196	5	11	NULL	0	NULL	Caf1	GP		bind					Caf1 Gd	GP	donor strand			NULL		NULL	NULL	NULL	NULL	gw60_cell_113_5_587_s_250	12787500	(A) Superposition of Caf1  (red) bound to the chaperone G1 donor strand (blue) and Caf1  (yellow) bound to the Caf1  Gd donor strand (orange) (stereo view).	bind
9350	1	3196	7	11	NULL	0	NULL	Caf1	GP		bind					chaperone G1	GP	donor strand			NULL		NULL	NULL	NULL	NULL	gw60_cell_113_5_587_s_250	12787500	(A) Superposition of Caf1  (red) bound to the chaperone G1 donor strand (blue) and Caf1  (yellow) bound to the Caf1  Gd donor strand (orange) (stereo view).	bind
9351	2	3196	7	11	NULL	0	NULL	Caf1	GP		bind					Caf1 Gd	GP	donor strand			NULL		NULL	NULL	NULL	NULL	gw60_cell_113_5_587_s_250	12787500	(A) Superposition of Caf1  (red) bound to the chaperone G1 donor strand (blue) and Caf1  (yellow) bound to the Caf1  Gd donor strand (orange) (stereo view).	bind
80033	1	3196	11	NULL	NULL	NULL	NULL	Caf1	GeneOrProtein		binds to 					chaperone G1	GeneOrProtein	donor strand			NULL		NULL	NULL	NULL	NULL	gw60_cell_113_5_587_s_250	12787500	(A) Superposition of Caf1  (red) bound to the chaperone G1 donor strand (blue) and Caf1  (yellow) bound to the Caf1  Gd donor strand (orange) (stereo view).	bind
80034	2	3196	11	NULL	NULL	NULL	NULL	Caf1	GeneOrProtein		binds to 					Caf1 Gd	GeneOrProtein	donor strand			NULL		NULL	NULL	NULL	NULL	gw60_cell_113_5_587_s_250	12787500	(A) Superposition of Caf1  (red) bound to the chaperone G1 donor strand (blue) and Caf1  (yellow) bound to the Caf1  Gd donor strand (orange) (stereo view).	bind
8194	1	3197	5	11	NULL	0	NULL	TSL	NucleicAcid		bind					TruB	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_929_s_102	11779468	(A) Superposition of the TSL  bound to TruB (colored as in     Figure 1) with  the corresponding residues from the structure of  tRNAPhe (in green).	bind
9352	1	3197	7	11	NULL	0	NULL	TSL	NucleicAcid		bind					TruB	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_929_s_102	11779468	(A) Superposition of the TSL  bound to TruB (colored as in     Figure 1) with  the corresponding residues from the structure of  tRNAPhe (in green).	bind
80035	1	3197	11	NULL	NULL	0	NULL	TSL	NucleicAcidSubstance		binds to 					 TruB	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_107_7_929_s_102	11779468	(A) Superposition of the TSL  bound to TruB (colored as in     Figure 1) with  the corresponding residues from the structure of  tRNAPhe (in green).	bind
7811	1	3198	5	11	NULL	0	NULL	SWI/SNF	GP		bind					HO	GP			URS1	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_139	16705163	(A) SWI/SNF binding to  HO URS1 and URS2 is restored in a  gcn5 ash1 mutant.	bind
7821	2	3198	5	11	NULL	0	NULL	SWI/SNF	GP		bind					HO	GP			URS2	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_139	16705163	(A) SWI/SNF binding to  HO URS1 and URS2 is restored in a  gcn5 ash1 mutant.	bind
7823	3	3198	5	11	NULL	0	NULL	gcn5 ash1	GP	mutant	restore					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_139	16705163	(A) SWI/SNF binding to  HO URS1 and URS2 is restored in a  gcn5 ash1 mutant.	bind
7824	4	3198	5	11	NULL	0	NULL	gcn5 ash1	GP	mutant	restore					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_139	16705163	(A) SWI/SNF binding to  HO URS1 and URS2 is restored in a  gcn5 ash1 mutant.	bind
9353	1	3198	7	11	NULL	0	NULL	SWI/SNF	GP		bind					HO URS1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_139	16705163	(A) SWI/SNF binding to  HO URS1 and URS2 is restored in a  gcn5 ash1 mutant.	bind
9354	2	3198	7	11	NULL	0	NULL	SWI/SNF	GP		bind					HO URS2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_139	16705163	(A) SWI/SNF binding to  HO URS1 and URS2 is restored in a  gcn5 ash1 mutant.	bind
9355	3	3198	7	11	NULL	0	NULL	statement 1	Process		is restored in					gcn5 ash1 	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_139	16705163	(A) SWI/SNF binding to  HO URS1 and URS2 is restored in a  gcn5 ash1 mutant.	bind
9356	4	3198	7	11	NULL	0	NULL	statement 2	Process		is restored in					gcn5 ash1 	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_139	16705163	(A) SWI/SNF binding to  HO URS1 and URS2 is restored in a  gcn5 ash1 mutant.	bind
80036	1	3198	11	NULL	NULL	NULL	NULL	SWI/SNF	GeneOrProtein		binds to 					HO URS1	GeneOrProtein				NULL	gcn5 ash1 mutant	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_139	16705163	(A) SWI/SNF binding to  HO URS1 and URS2 is restored in a  gcn5 ash1 mutant.	bind
80037	2	3198	11	NULL	NULL	NULL	NULL	SWI/SNF	GeneOrProtein		binds to 					HO URS2	GeneOrProtein				NULL	gcn5 ash1 mutant.	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_139	16705163	(A) SWI/SNF binding to  HO URS1 and URS2 is restored in a  gcn5 ash1 mutant.	bind
7826	1	3201	5	11	NULL	0	NULL	eIF4G	GP		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_251	15157733	(A) tail also affects the activity of maskin, a translational  inhibitor identified in  Xenopus oocytes, which competes with eIF4G binding to eIF4E.	bind
7828	2	3201	5	11	NULL	0	NULL	maskin	GP		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_251	15157733	(A) tail also affects the activity of maskin, a translational  inhibitor identified in  Xenopus oocytes, which competes with eIF4G binding to eIF4E.	bind
7829	4	3201	5	11	NULL	0	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_251	15157733	(A) tail also affects the activity of maskin, a translational  inhibitor identified in  Xenopus oocytes, which competes with eIF4G binding to eIF4E.	bind
7832	3	3201	5	11	NULL	0	NULL	maskin	GP		is a type of					translational inhibitor	GP				NULL	Xenopus oocytes	NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_251	15157733	(A) tail also affects the activity of maskin, a translational  inhibitor identified in  Xenopus oocytes, which competes with eIF4G binding to eIF4E.	bind
9489	1	3201	7	11	NULL	0	NULL	eIF4G	GP		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_251	15157733	(A) tail also affects the activity of maskin, a translational  inhibitor identified in  Xenopus oocytes, which competes with eIF4G binding to eIF4E.	bind
9490	3	3201	7	11	NULL	0	NULL	Maskin	GP		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_251	15157733	(A) tail also affects the activity of maskin, a translational  inhibitor identified in  Xenopus oocytes, which competes with eIF4G binding to eIF4E.	bind
9491	4	3201	7	11	NULL	0	NULL	statement 3	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_251	15157733	(A) tail also affects the activity of maskin, a translational  inhibitor identified in  Xenopus oocytes, which competes with eIF4G binding to eIF4E.	bind
12362	2	3201	7	11	NULL	0	NULL	Maskin	GP		is a type of					translational inhibitor	GP				NULL	Xenopus oocytes	NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_251	15157733	(A) tail also affects the activity of maskin, a translational  inhibitor identified in  Xenopus oocytes, which competes with eIF4G binding to eIF4E.	bind
80038	1	3201	11	NULL	NULL	0	NULL	maskin	Protein		is a type of 					translational inhibitor	Protein				NULL	Xenopus oocytes	0	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_251	15157733	(A) tail also affects the activity of maskin, a translational  inhibitor identified in  Xenopus oocytes, which competes with eIF4G binding to eIF4E.	bind
80039	2	3201	11	NULL	NULL	NULL	NULL	eIF4G	GeneOrProtein		binds to 					eIF4E	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_251	15157733	(A) tail also affects the activity of maskin, a translational  inhibitor identified in  Xenopus oocytes, which competes with eIF4G binding to eIF4E.	bind
80040	3	3201	11	NULL	NULL	NULL	NULL	maskin	GeneOrProtein		binds to 					eIF4E	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_251	15157733	(A) tail also affects the activity of maskin, a translational  inhibitor identified in  Xenopus oocytes, which competes with eIF4G binding to eIF4E.	bind
80041	4	3201	11	NULL	NULL	0	NULL	statement 2	Process		competes with					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_251	15157733	(A) tail also affects the activity of maskin, a translational  inhibitor identified in  Xenopus oocytes, which competes with eIF4G binding to eIF4E.	bind
7838	1	3202	5	11	NULL	0	NULL	eIF4A	GP		bind						NucleicAcid			5' UTR	NULL		NULL	NULL	NULL	NULL	gw60_nature_392_6675_520_s_79	9548260	(A) tail and eIF4A bound to the 5' UTR ( Fig. 4a).	bind
9492	1	3202	7	11	NULL	0	NULL	eIF4A	GP		bind						NucleicAcid			5' UTR	NULL		NULL	NULL	NULL	NULL	gw60_nature_392_6675_520_s_79	9548260	(A) tail and eIF4A bound to the 5' UTR ( Fig. 4a).	bind
80042	1	3202	11	NULL	NULL	0	NULL	(A) tail	NucleicAcidSubstance		binds to 					5' UTR	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_nature_392_6675_520_s_79	9548260	(A) tail and eIF4A bound to the 5' UTR ( Fig. 4a).	bind
80043	2	3202	11	NULL	NULL	NULL	NULL	eIF4A	GeneOrProtein		binds to 					5' UTR	NucleicAcidSubstance				NULL		NULL	NULL	NULL	NULL	gw60_nature_392_6675_520_s_79	9548260	(A) tail and eIF4A bound to the 5' UTR ( Fig. 4a).	bind
7846	1	3203	5	11	NULL	0	NULL	Unr protein	GP		bind					mCRD	NucleicAcid			purine stretches	NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_29_s_290	11051545	(A) tail and the Unr protein binds to the purine stretches in  the mCRD.	bind
9493	1	3203	7	11	NULL	0	NULL	Unr protein	GP		bind					mCRD	NucleicAcid			purine stretches	NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_29_s_290	11051545	(A) tail and the Unr protein binds to the purine stretches in  the mCRD.	bind
80044	1	3203	11	NULL	NULL	0	NULL	(A) tail 	NucleicAcidSubstance		binds to 					mCRD	GeneOrProtein			 purine stretches	NULL		0	NULL	NULL	NULL	gw60_cell_103_1_29_s_290	11051545	(A) tail and the Unr protein binds to the purine stretches in  the mCRD.	bind
80045	2	3203	11	NULL	NULL	0	NULL	Unr protein	Protein		binds to 					mCRD	GeneOrProtein			purine stretches	NULL		0	NULL	NULL	NULL	gw60_cell_103_1_29_s_290	11051545	(A) tail and the Unr protein binds to the purine stretches in  the mCRD.	bind
7879	1	3204	5	11	NULL	0	NULL	eIF4E	GP		bind					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_21_4068_s_19	11058101	(A) tail are recognised, respectively, by the eukaryotic initiation factor (eIF) 4F holoenzyme complex [consisting of the cap-binding protein (eIF4E) and an ATP-dependent RNA helicase (eIF4A) bound to a central scaffold molecule (eIF4G)] (for reviews see  3, 9) and by the poly	bind
7880	2	3204	5	11	NULL	0	NULL	eIF4A	GP		bind					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_21_4068_s_19	11058101	(A) tail are recognised, respectively, by the eukaryotic initiation factor (eIF) 4F holoenzyme complex [consisting of the cap-binding protein (eIF4E) and an ATP-dependent RNA helicase (eIF4A) bound to a central scaffold molecule (eIF4G)] (for reviews see  3, 9) and by the poly	bind
7881	3	3204	5	11	NULL	0	NULL	(eIF) 4F holoenzyme complex	GP		consists of					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_21_4068_s_19	11058101	(A) tail are recognised, respectively, by the eukaryotic initiation factor (eIF) 4F holoenzyme complex [consisting of the cap-binding protein (eIF4E) and an ATP-dependent RNA helicase (eIF4A) bound to a central scaffold molecule (eIF4G)] (for reviews see  3, 9) and by the poly	bind
9494	1	3204	7	11	NULL	0	NULL	eIF4E	GP		bind					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_21_4068_s_19	11058101	(A) tail are recognised, respectively, by the eukaryotic initiation factor (eIF) 4F holoenzyme complex [consisting of the cap-binding protein (eIF4E) and an ATP-dependent RNA helicase (eIF4A) bound to a central scaffold molecule (eIF4G)] (for reviews see  3, 9) and by the poly	bind
9495	2	3204	7	11	NULL	0	NULL	eIF4A	GP		bind					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_21_4068_s_19	11058101	(A) tail are recognised, respectively, by the eukaryotic initiation factor (eIF) 4F holoenzyme complex [consisting of the cap-binding protein (eIF4E) and an ATP-dependent RNA helicase (eIF4A) bound to a central scaffold molecule (eIF4G)] (for reviews see  3, 9) and by the poly	bind
9496	3	3204	7	11	NULL	0	NULL	eukaryotic initiation factor 4F holoenzyme complex	GP		consist of					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_21_4068_s_19	11058101	(A) tail are recognised, respectively, by the eukaryotic initiation factor (eIF) 4F holoenzyme complex [consisting of the cap-binding protein (eIF4E) and an ATP-dependent RNA helicase (eIF4A) bound to a central scaffold molecule (eIF4G)] (for reviews see  3, 9) and by the poly	bind
9497	4	3204	7	11	NULL	0	NULL	eukaryotic initiation factor 4F holoenzyme complex	GP		consist of					eIF4A	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_21_4068_s_19	11058101	(A) tail are recognised, respectively, by the eukaryotic initiation factor (eIF) 4F holoenzyme complex [consisting of the cap-binding protein (eIF4E) and an ATP-dependent RNA helicase (eIF4A) bound to a central scaffold molecule (eIF4G)] (for reviews see  3, 9) and by the poly	bind
9498	5	3204	7	11	NULL	0	NULL	 eukaryotic initiation factor 	GP		is					eIF	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_21_4068_s_19	11058101	(A) tail are recognised, respectively, by the eukaryotic initiation factor (eIF) 4F holoenzyme complex [consisting of the cap-binding protein (eIF4E) and an ATP-dependent RNA helicase (eIF4A) bound to a central scaffold molecule (eIF4G)] (for reviews see  3, 9) and by the poly	bind
9499	6	3204	7	11	NULL	0	NULL	eIF4E	GP		is a type of					cap-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_21_4068_s_19	11058101	(A) tail are recognised, respectively, by the eukaryotic initiation factor (eIF) 4F holoenzyme complex [consisting of the cap-binding protein (eIF4E) and an ATP-dependent RNA helicase (eIF4A) bound to a central scaffold molecule (eIF4G)] (for reviews see  3, 9) and by the poly	bind
9500	7	3204	7	11	NULL	0	NULL	eIF4A	GP		is a type of					ATP-dependent RNA helicase 	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_21_4068_s_19	11058101	(A) tail are recognised, respectively, by the eukaryotic initiation factor (eIF) 4F holoenzyme complex [consisting of the cap-binding protein (eIF4E) and an ATP-dependent RNA helicase (eIF4A) bound to a central scaffold molecule (eIF4G)] (for reviews see  3, 9) and by the poly	bind
9501	8	3204	7	11	NULL	0	NULL	eIF4G	GP		is a type of					central scaffold molecule	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_21_4068_s_19	11058101	(A) tail are recognised, respectively, by the eukaryotic initiation factor (eIF) 4F holoenzyme complex [consisting of the cap-binding protein (eIF4E) and an ATP-dependent RNA helicase (eIF4A) bound to a central scaffold molecule (eIF4G)] (for reviews see  3, 9) and by the poly	bind
80046	1	3204	11	NULL	NULL	NULL	NULL	eukaryotic initiation factor 4F	Protein		is a part of					holoenzyme complex	Protein				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_21_4068_s_19	11058101	(A) tail are recognised, respectively, by the eukaryotic initiation factor (eIF) 4F holoenzyme complex [consisting of the cap-binding protein (eIF4E) and an ATP-dependent RNA helicase (eIF4A) bound to a central scaffold molecule (eIF4G)] (for reviews see  3, 9) and by the poly	bind
80047	2	3204	11	NULL	NULL	NULL	NULL	holoenzyme complex	Protein		consisting of 					cap-binding protein	Protein				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_21_4068_s_19	11058101	(A) tail are recognised, respectively, by the eukaryotic initiation factor (eIF) 4F holoenzyme complex [consisting of the cap-binding protein (eIF4E) and an ATP-dependent RNA helicase (eIF4A) bound to a central scaffold molecule (eIF4G)] (for reviews see  3, 9) and by the poly	bind
80048	3	3204	11	NULL	NULL	0	NULL	eIF4E	Protein		is a type of 					cap-binding protein	Protein				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_21_4068_s_19	11058101	(A) tail are recognised, respectively, by the eukaryotic initiation factor (eIF) 4F holoenzyme complex [consisting of the cap-binding protein (eIF4E) and an ATP-dependent RNA helicase (eIF4A) bound to a central scaffold molecule (eIF4G)] (for reviews see  3, 9) and by the poly	bind
80049	4	3204	11	NULL	NULL	NULL	NULL	holoenzyme complex	Protein		consisting of 					RNA helicase 	Protein	ATP-dependent			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_21_4068_s_19	11058101	(A) tail are recognised, respectively, by the eukaryotic initiation factor (eIF) 4F holoenzyme complex [consisting of the cap-binding protein (eIF4E) and an ATP-dependent RNA helicase (eIF4A) bound to a central scaffold molecule (eIF4G)] (for reviews see  3, 9) and by the poly	bind
80050	5	3204	11	NULL	NULL	0	NULL	eIF4A	Protein		is a type of 					RNA helicase 	Protein	ATP-dependent			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_21_4068_s_19	11058101	(A) tail are recognised, respectively, by the eukaryotic initiation factor (eIF) 4F holoenzyme complex [consisting of the cap-binding protein (eIF4E) and an ATP-dependent RNA helicase (eIF4A) bound to a central scaffold molecule (eIF4G)] (for reviews see  3, 9) and by the poly	bind
80051	6	3204	11	NULL	NULL	0	NULL	holoenzyme complex	Protein		consisting of 					eIF4G	Protein				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_21_4068_s_19	11058101	(A) tail are recognised, respectively, by the eukaryotic initiation factor (eIF) 4F holoenzyme complex [consisting of the cap-binding protein (eIF4E) and an ATP-dependent RNA helicase (eIF4A) bound to a central scaffold molecule (eIF4G)] (for reviews see  3, 9) and by the poly	bind
80052	7	3204	11	NULL	NULL	0	NULL	eIF4E	Protein		binds to 					eIF4G	Protein				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_21_4068_s_19	11058101	(A) tail are recognised, respectively, by the eukaryotic initiation factor (eIF) 4F holoenzyme complex [consisting of the cap-binding protein (eIF4E) and an ATP-dependent RNA helicase (eIF4A) bound to a central scaffold molecule (eIF4G)] (for reviews see  3, 9) and by the poly	bind
80053	8	3204	11	NULL	NULL	0	NULL	eIF4A	Protein		binds to 					eIF4G	Protein				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_21_4068_s_19	11058101	(A) tail are recognised, respectively, by the eukaryotic initiation factor (eIF) 4F holoenzyme complex [consisting of the cap-binding protein (eIF4E) and an ATP-dependent RNA helicase (eIF4A) bound to a central scaffold molecule (eIF4G)] (for reviews see  3, 9) and by the poly	bind
7884	1	3205	5	11	NULL	0	NULL	NSP3	GP	viral 	interact with					eIF4GI	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0760-0779_j-virol_80_18_16940515_s_8	16940515	(A) tail but have instead  a consensus sequence at their 3' ends that is bound by the viral nonstructural  protein NSP3, which also interacts with eIF4GI, using the same region  employed by PABP.	bind
9502	1	3205	7	11	NULL	0	NULL	NSP3	GP	viral 	bind					eIF4GI	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0760-0779_j-virol_80_18_16940515_s_8	16940515	(A) tail but have instead  a consensus sequence at their 3' ends that is bound by the viral nonstructural  protein NSP3, which also interacts with eIF4GI, using the same region  employed by PABP.	bind
80054	1	3205	11	NULL	NULL	0	NULL	(A) tail	NucleicAcidSubstance		has					consensus sequence	NucleicAcidSubstance			 3' ends	NULL		0	NULL	NULL	NULL	abs-batch0760-0779_j-virol_80_18_16940515_s_8	16940515	(A) tail but have instead  a consensus sequence at their 3' ends that is bound by the viral nonstructural  protein NSP3, which also interacts with eIF4GI, using the same region  employed by PABP.	bind
80055	2	3205	11	NULL	NULL	0	NULL	statement 1	NucleicAcidSubstance		binds to 					NSP3	Protein				NULL		0	NULL	NULL	NULL	abs-batch0760-0779_j-virol_80_18_16940515_s_8	16940515	(A) tail but have instead  a consensus sequence at their 3' ends that is bound by the viral nonstructural  protein NSP3, which also interacts with eIF4GI, using the same region  employed by PABP.	bind
80056	3	3205	11	NULL	NULL	0	NULL	NSP3	Protein		is a type of 					nonstructural protein	Protein	viral 			NULL		0	NULL	NULL	NULL	abs-batch0760-0779_j-virol_80_18_16940515_s_8	16940515	(A) tail but have instead  a consensus sequence at their 3' ends that is bound by the viral nonstructural  protein NSP3, which also interacts with eIF4GI, using the same region  employed by PABP.	bind
80057	4	3205	11	NULL	NULL	0	NULL	NSP3	Protein		interact with					eIF4GI	Protein				NULL		0	NULL	NULL	NULL	abs-batch0760-0779_j-virol_80_18_16940515_s_8	16940515	(A) tail but have instead  a consensus sequence at their 3' ends that is bound by the viral nonstructural  protein NSP3, which also interacts with eIF4GI, using the same region  employed by PABP.	bind
8709	1	3206	5	11	NULL	0	NULL	Maskin	GP		is displaced from					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_47_16961_s_239	16287976	(A) tail elongation leading to PABP-binding, recruitment of eIF4G, displacement of Maskin from eIF4E, and activation of translation ( ).	bind
9504	1	3206	7	11	NULL	0	NULL	Maskin	GP		displaced from					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_47_16961_s_239	16287976	(A) tail elongation leading to PABP-binding, recruitment of eIF4G, displacement of Maskin from eIF4E, and activation of translation ( ).	bind
80058	1	3206	11	NULL	NULL	0	NULL	elongation	MolecularProcess	(A) tail	binds to 					PABP	Protein				NULL		0	NULL	NULL	NULL	gw70_pnas_102_47_16961_s_239	16287976	(A) tail elongation leading to PABP-binding, recruitment of eIF4G, displacement of Maskin from eIF4E, and activation of translation ( ).	bind
80059	2	3206	11	NULL	NULL	0	NULL	elongation	MolecularProcess	(A) tail	recruit					eIF4G	Protein				NULL		0	NULL	NULL	NULL	gw70_pnas_102_47_16961_s_239	16287976	(A) tail elongation leading to PABP-binding, recruitment of eIF4G, displacement of Maskin from eIF4E, and activation of translation ( ).	bind
80060	3	3206	11	NULL	NULL	0	NULL	Maskin	Protein		binds to 					eIF4E	Protein				NULL		0	NULL	NULL	NULL	gw70_pnas_102_47_16961_s_239	16287976	(A) tail elongation leading to PABP-binding, recruitment of eIF4G, displacement of Maskin from eIF4E, and activation of translation ( ).	bind
80061	4	3206	11	NULL	NULL	NULL	NULL	elongation	MolecularProcess	(A) tail	displaces					Maskin	Protein	from eIF4E			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_47_16961_s_239	16287976	(A) tail elongation leading to PABP-binding, recruitment of eIF4G, displacement of Maskin from eIF4E, and activation of translation ( ).	bind
80062	5	3206	11	NULL	NULL	NULL	NULL	elongation	MolecularProcess	(A) tail	activates					translation	MolecularProcess				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_47_16961_s_239	16287976	(A) tail elongation leading to PABP-binding, recruitment of eIF4G, displacement of Maskin from eIF4E, and activation of translation ( ).	bind
80063	1	3208	11	NULL	NULL	0	NULL	CPSF	Protein		binds to 					(A) tail	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1315_s_138	15937220	(A) tail length control is dependent upon the binding of both CPSF and PABPN1 (Wahle 1995 ), the extended poly	bind
80064	2	3208	11	NULL	NULL	0	NULL	PABPN1	Protein		binds to 					(A) tail	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1315_s_138	15937220	(A) tail length control is dependent upon the binding of both CPSF and PABPN1 (Wahle 1995 ), the extended poly	bind
80065	3	3208	11	NULL	NULL	0	NULL	statement 1	Process		controls					length	Measurement	(A) tail 			NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1315_s_138	15937220	(A) tail length control is dependent upon the binding of both CPSF and PABPN1 (Wahle 1995 ), the extended poly	bind
80066	4	3208	11	NULL	NULL	0	NULL	statement 2	Process		controls					length	Measurement	(A) tail 			NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1315_s_138	15937220	(A) tail length control is dependent upon the binding of both CPSF and PABPN1 (Wahle 1995 ), the extended poly	bind
80067	5	3208	11	NULL	NULL	0	NULL	statement 3	Process		occurs along with					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_11_1315_s_138	15937220	(A) tail length control is dependent upon the binding of both CPSF and PABPN1 (Wahle 1995 ), the extended poly	bind
7889	1	3209	5	11	NULL	0	NULL	eIF4G	GP		bind					PABP/poly	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_19_2510_s_273	9334316	(A) tail or the binding of eIF4G to the PABP/poly	bind
9505	1	3209	7	11	NULL	0	NULL	eIF4G	GP		bind					PABP/poly	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_19_2510_s_273	9334316	(A) tail or the binding of eIF4G to the PABP/poly	bind
7890	1	3210	5	11	NULL	0	NULL	initiation factor	GP		bind					m7G cap	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_1_104_s_186	15630022	(A) tail stimulates initiation factor binding to the m7G cap.	bind
9506	1	3210	7	11	NULL	0	NULL	initiation factor	GP		bind					m7G cap	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_1_104_s_186	15630022	(A) tail stimulates initiation factor binding to the m7G cap.	bind
80068	1	3210	11	NULL	NULL	0	NULL	initiation factor	Protein		binds to 					m7G cap	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_1_104_s_186	15630022	(A) tail stimulates initiation factor binding to the m7G cap.	bind
80069	2	3210	11	NULL	NULL	0	NULL	(A) tail	NucleicAcidSubstance		stimulates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_1_104_s_186	15630022	(A) tail stimulates initiation factor binding to the m7G cap.	bind
7892	1	3211	5	11	NULL	0	NULL	PABPN1	GP		bind					NS1 protein	GP	influenza virus			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_481	15157733	(A) tail synthesis has been confirmed in vivo: PABPN1  is bound and inactivated by the influenza virus protein NS1, and mRNAs containing  very short oligo	bind
7893	2	3211	5	11	NULL	0	NULL	NS1 protein	GP	influenza virus	inactivate					PABPN1	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_481	15157733	(A) tail synthesis has been confirmed in vivo: PABPN1  is bound and inactivated by the influenza virus protein NS1, and mRNAs containing  very short oligo	bind
9508	1	3211	7	11	NULL	0	NULL	PABPN1	GP		binds					NS1 protein	GP	influenza virus 			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_481	15157733	(A) tail synthesis has been confirmed in vivo: PABPN1  is bound and inactivated by the influenza virus protein NS1, and mRNAs containing  very short oligo	bind
9509	2	3211	7	11	NULL	0	NULL	NS1 protein	GP	influenza virus 	inactivate					PABPN1	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_481	15157733	(A) tail synthesis has been confirmed in vivo: PABPN1  is bound and inactivated by the influenza virus protein NS1, and mRNAs containing  very short oligo	bind
80070	1	3211	11	NULL	NULL	0	NULL	NS1 protein	Protein	influenza virus	binds to 					PABPN1	Protein				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_481	15157733	(A) tail synthesis has been confirmed in vivo: PABPN1  is bound and inactivated by the influenza virus protein NS1, and mRNAs containing  very short oligo	bind
80071	2	3211	11	NULL	NULL	0	NULL	NS1 protein	Protein	influenza virus	inactivates					PABPN1	Protein				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_481	15157733	(A) tail synthesis has been confirmed in vivo: PABPN1  is bound and inactivated by the influenza virus protein NS1, and mRNAs containing  very short oligo	bind
80072	3	3211	11	NULL	NULL	0	NULL	statement 1	Process		occurs along with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_67_s_481	15157733	(A) tail synthesis has been confirmed in vivo: PABPN1  is bound and inactivated by the influenza virus protein NS1, and mRNAs containing  very short oligo	bind
7896	1	3212	5	11	NULL	0	NULL	GST-RNG105	GP		bind					brain RNA	NucleicAcid	rat 			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jneurosci_25_17_4420_s_273	15858068	(A) tails in the  in vitro binding assay showed that the binding of GST-RNG105 to rat brain RNAs was not significantly altered in the presence or absence of poly(dT), suggesting that poly	bind
9510	1	3212	7	11	NULL	0	NULL	GST-RNG105	GP		binds					brain RNA	NucleicAcid	rat			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jneurosci_25_17_4420_s_273	15858068	(A) tails in the  in vitro binding assay showed that the binding of GST-RNG105 to rat brain RNAs was not significantly altered in the presence or absence of poly(dT), suggesting that poly	bind
80073	1	3212	11	NULL	NULL	0	NULL	GST-RNG105	Protein		binds to 					RNAs	NucleicAcidSubstance	 rat brain 			NULL		0	NULL	NULL	NULL	gw70_jneurosci_25_17_4420_s_273	15858068	(A) tails in the  in vitro binding assay showed that the binding of GST-RNG105 to rat brain RNAs was not significantly altered in the presence or absence of poly(dT), suggesting that poly	bind
80074	2	3212	11	NULL	NULL	0	NULL	statement 1	Process		is independent of					poly(dT)	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_jneurosci_25_17_4420_s_273	15858068	(A) tails in the  in vitro binding assay showed that the binding of GST-RNG105 to rat brain RNAs was not significantly altered in the presence or absence of poly(dT), suggesting that poly	bind
7897	1	3213	5	11	NULL	0	NULL	PABPs	GP		bind					DAZL	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_14_2656_s_314	16001084	(A) tails may  benefit the most from the binding of PABPs to DAZL, as seen in  Figures 3 and  7.	bind
9511	1	3213	7	11	NULL	0	NULL	PABPs	GP		bind					DAZL	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_14_2656_s_314	16001084	(A) tails may  benefit the most from the binding of PABPs to DAZL, as seen in  Figures 3 and  7.	bind
80075	1	3213	11	NULL	NULL	0	NULL	PABPs	Protein		binds to 					DAZL	Protein				NULL		0	NULL	NULL	NULL	gw70_embo_24_14_2656_s_314	16001084	(A) tails may  benefit the most from the binding of PABPs to DAZL, as seen in  Figures 3 and  7.	bind
7898	1	3215	5	11	NULL	0	NULL	Tbx5	GP		bind					GST-LIM2/3	GP				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_273_1_106_s_131	15302601	(A) Tbx5 binds to GST-LIM2/3.	bind
9512	1	3215	7	11	NULL	0	NULL	Tbx5	GP		binds					GST-LIM2/3	GP				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_273_1_106_s_131	15302601	(A) Tbx5 binds to GST-LIM2/3.	bind
80076	1	3215	11	NULL	NULL	0	NULL	Tbx5	Protein		binds to 					GST-LIM2/3	Protein				NULL		0	NULL	NULL	NULL	gw70_devbiol_273_1_106_s_131	15302601	(A) Tbx5 binds to GST-LIM2/3.	bind
7899	1	3216	5	11	NULL	0	NULL	TCR-CD3	GP		bind					Nck	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_129	12110186	(A) TCR-CD3 binding to Nck is independent of tyrosine phosphorylation.	bind
7900	2	3216	5	11	NULL	0	NULL	statement 1	Process		is independent of							phosphorylation	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_129	12110186	(A) TCR-CD3 binding to Nck is independent of tyrosine phosphorylation.	bind
9513	1	3216	7	11	NULL	0	NULL	TCR-CD3	GP		binds					Nck	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_129	12110186	(A) TCR-CD3 binding to Nck is independent of tyrosine phosphorylation.	bind
9514	2	3216	7	11	NULL	0	NULL	statement 1	Process		is independent of					 		phosphorylation 	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_129	12110186	(A) TCR-CD3 binding to Nck is independent of tyrosine phosphorylation.	bind
80077	1	3216	11	NULL	NULL	0	NULL	TCR-CD3	Protein		binds to 					Nck	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_109_7_901_s_129	12110186	(A) TCR-CD3 binding to Nck is independent of tyrosine phosphorylation.	bind
80078	2	3216	11	NULL	NULL	0	NULL	statement 1	Process		is independent of					phosphorylation	MolecularProcess	tyrosine			NULL		0	NULL	NULL	NULL	gw60_cell_109_7_901_s_129	12110186	(A) TCR-CD3 binding to Nck is independent of tyrosine phosphorylation.	bind
7901	1	3218	5	11	NULL	0	NULL	Tet(O)	GP		bind					fMet-tRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_5_1037_s_84	11389850	(a) Tet(O) bound to fMet-tRNA.	bind
9515	1	3218	7	11	NULL	0	NULL	Tet(O)	GP		bind					fMet-tRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_5_1037_s_84	11389850	(a) Tet(O) bound to fMet-tRNA.	bind
80079	1	3218	11	NULL	NULL	0	NULL	Tet(O)	Protein		binds to 					fMet-tRNA	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcell_7_5_1037_s_84	11389850	(a) Tet(O) bound to fMet-tRNA.	bind
7903	1	3219	5	11	NULL	0	NULL	p300 fragments	GP		end at			carboxy-terminal 					amino acid 2414		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_71	10330164	(A) TFIIB binds to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1710.	bind
7904	2	3219	5	11	NULL	0	NULL	p300 fragments	GP		end at			carboxy-terminal					amino acid 1906		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_71	10330164	(A) TFIIB binds to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1710.	bind
7905	3	3219	5	11	NULL	0	NULL	p300 fragments	GP		end at			carboxy-terminal					amino acid 1710		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_71	10330164	(A) TFIIB binds to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1710.	bind
7906	4	3219	5	11	NULL	0	NULL	TFIIB	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_71	10330164	(A) TFIIB binds to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1710.	bind
7907	5	3219	5	11	NULL	0	NULL	TFIIB	GP		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_71	10330164	(A) TFIIB binds to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1710.	bind
7908	6	3219	5	11	NULL	0	NULL	TFIIB	GP		bind					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_71	10330164	(A) TFIIB binds to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1710.	bind
9516	1	3219	7	11	NULL	0	NULL	p300 fragments	GP		end at			carboxy-terminal					amino acids 2414		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_71	10330164	(A) TFIIB binds to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1710.	bind
12367	2	3219	7	11	NULL	0	NULL	p300 fragments	GP		end at			carboxy-terminal					amino acids 1906		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_71	10330164	(A) TFIIB binds to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1710.	bind
12369	3	3219	7	11	NULL	0	NULL	p300 fragments	GP		end at			carboxy-terminal					amino acids 1710		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_71	10330164	(A) TFIIB binds to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1710.	bind
12371	4	3219	7	11	NULL	0	NULL	TFIIB	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_71	10330164	(A) TFIIB binds to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1710.	bind
12373	5	3219	7	11	NULL	0	NULL	TFIIB	GP		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_71	10330164	(A) TFIIB binds to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1710.	bind
12374	6	3219	7	11	NULL	0	NULL	TFIIB	GP		bind					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_71	10330164	(A) TFIIB binds to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1710.	bind
80111	1	3219	11	NULL	NULL	0	NULL	TFIIB	Protein		binds to 					p300	Protein	carboxy-terminal	amino acids 2414, 1906, and 1710		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_71	10330164	(A) TFIIB binds to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1710.	bind
7910	1	3221	5	11	NULL	0	NULL	Flo8	GP		bind									UAS1-2	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_214	15485921	(A) The  ste12delta and  tec1delta mutations eliminate Flo8 and Mss11 binding to UAS1-2.	bind
7911	2	3221	5	11	NULL	0	NULL	Mss11	GP		bind									UAS1-2	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_214	15485921	(A) The  ste12delta and  tec1delta mutations eliminate Flo8 and Mss11 binding to UAS1-2.	bind
7914	3	3221	5	11	NULL	0	NULL	 ste12delta	GP	mutant	eliminate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_214	15485921	(A) The  ste12delta and  tec1delta mutations eliminate Flo8 and Mss11 binding to UAS1-2.	bind
7915	4	3221	5	11	NULL	0	NULL	ste12delta	GP	mutant	eliminate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_214	15485921	(A) The  ste12delta and  tec1delta mutations eliminate Flo8 and Mss11 binding to UAS1-2.	bind
7916	5	3221	5	11	NULL	0	NULL	tec1delta	GP	mutant	eliminate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_214	15485921	(A) The  ste12delta and  tec1delta mutations eliminate Flo8 and Mss11 binding to UAS1-2.	bind
7917	6	3221	5	11	NULL	0	NULL	 tec1delta	GP	mutant	eliminate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_214	15485921	(A) The  ste12delta and  tec1delta mutations eliminate Flo8 and Mss11 binding to UAS1-2.	bind
9517	1	3221	7	11	NULL	0	NULL	Flo8	GP		bind									UAS1-2	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_214	15485921	(A) The  ste12delta and  tec1delta mutations eliminate Flo8 and Mss11 binding to UAS1-2.	bind
9518	2	3221	7	11	NULL	0	NULL	Mss11	GP		bind									UAS1-2	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_214	15485921	(A) The  ste12delta and  tec1delta mutations eliminate Flo8 and Mss11 binding to UAS1-2.	bind
9519	3	3221	7	11	NULL	0	NULL	ste12delta	GP	mutant	eliminate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_214	15485921	(A) The  ste12delta and  tec1delta mutations eliminate Flo8 and Mss11 binding to UAS1-2.	bind
9520	4	3221	7	11	NULL	0	NULL	ste12delta	GP	mutant	eliminate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_214	15485921	(A) The  ste12delta and  tec1delta mutations eliminate Flo8 and Mss11 binding to UAS1-2.	bind
9521	5	3221	7	11	NULL	0	NULL	 tec1delta	GP	mutant	eliminate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_214	15485921	(A) The  ste12delta and  tec1delta mutations eliminate Flo8 and Mss11 binding to UAS1-2.	bind
9522	6	3221	7	11	NULL	0	NULL	 tec1delta	GP	mutant	eliminate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_214	15485921	(A) The  ste12delta and  tec1delta mutations eliminate Flo8 and Mss11 binding to UAS1-2.	bind
80112	1	3221	11	NULL	NULL	0	NULL	Mss11	Protein		binds to 					UAS1-2	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_214	15485921	(A) The  ste12delta and  tec1delta mutations eliminate Flo8 and Mss11 binding to UAS1-2.	bind
80113	2	3221	11	NULL	NULL	0	NULL	Flo8	Protein		binds to 					UAS1-2	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_214	15485921	(A) The  ste12delta and  tec1delta mutations eliminate Flo8 and Mss11 binding to UAS1-2.	bind
80114	3	3221	11	NULL	NULL	NULL	NULL	ste12delta	GeneOrProtein	mutation of	eliminate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_214	15485921	(A) The  ste12delta and  tec1delta mutations eliminate Flo8 and Mss11 binding to UAS1-2.	bind
80115	4	3221	11	NULL	NULL	0	NULL	ste12delta	GeneOrProtein	mutation of	eliminate					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_214	15485921	(A) The  ste12delta and  tec1delta mutations eliminate Flo8 and Mss11 binding to UAS1-2.	bind
80116	5	3221	11	NULL	NULL	0	NULL	tec1delta	GeneOrProtein	mutation of	eliminate					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_214	15485921	(A) The  ste12delta and  tec1delta mutations eliminate Flo8 and Mss11 binding to UAS1-2.	bind
80117	6	3221	11	NULL	NULL	0	NULL	tec1delta	GeneOrProtein	mutation of	eliminate					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_214	15485921	(A) The  ste12delta and  tec1delta mutations eliminate Flo8 and Mss11 binding to UAS1-2.	bind
7918	1	3222	5	11	NULL	0	NULL	ste50delta 	GP		effect					cell cycle arrest	Process	pheromone-induced 			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_7_2425_s_189	10397774	(A) The  ste50delta and the deletion of Ste50p binding domain of Ste11p had the same effect on the pheromone-induced cell cycle arrest.	bind
7919	2	3222	5	11	NULL	0	NULL				deleted from			Ste50p binding domain		Ste11p	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_7_2425_s_189	10397774	(A) The  ste50delta and the deletion of Ste50p binding domain of Ste11p had the same effect on the pheromone-induced cell cycle arrest.	bind
7920	3	3222	5	11	NULL	0	NULL	statement 2	Process		effect					cell cycle arrest	Process	pheromone-induced			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_7_2425_s_189	10397774	(A) The  ste50delta and the deletion of Ste50p binding domain of Ste11p had the same effect on the pheromone-induced cell cycle arrest.	bind
7921	4	3222	5	11	NULL	0	NULL	statement 1	Process		same effect as					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_7_2425_s_189	10397774	(A) The  ste50delta and the deletion of Ste50p binding domain of Ste11p had the same effect on the pheromone-induced cell cycle arrest.	bind
9523	1	3222	7	11	NULL	0	NULL	pheromone	Chemical		induce					cell cycle arrest	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_7_2425_s_189	10397774	(A) The  ste50delta and the deletion of Ste50p binding domain of Ste11p had the same effect on the pheromone-induced cell cycle arrest.	bind
9524	2	3222	7	11	NULL	0	NULL	ste50delta	GP		effect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_7_2425_s_189	10397774	(A) The  ste50delta and the deletion of Ste50p binding domain of Ste11p had the same effect on the pheromone-induced cell cycle arrest.	bind
9525	3	3222	7	11	NULL	0	NULL	Ste11p	GP	deletion of	effect			Ste50p binding domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_7_2425_s_189	10397774	(A) The  ste50delta and the deletion of Ste50p binding domain of Ste11p had the same effect on the pheromone-induced cell cycle arrest.	bind
12377	4	3222	7	11	NULL	0	NULL	statement 2	Process		same effect as					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_7_2425_s_189	10397774	(A) The  ste50delta and the deletion of Ste50p binding domain of Ste11p had the same effect on the pheromone-induced cell cycle arrest.	bind
80118	1	3222	11	NULL	NULL	0	NULL	pheromone	Chemical		induced					cell cycle arrest	MolecularProcess				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_7_2425_s_189	10397774	(A) The  ste50delta and the deletion of Ste50p binding domain of Ste11p had the same effect on the pheromone-induced cell cycle arrest.	bind
80119	2	3222	11	NULL	NULL	0	NULL	Ste11p	GeneOrProtein		has binding domain for					Ste50p	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_7_2425_s_189	10397774	(A) The  ste50delta and the deletion of Ste50p binding domain of Ste11p had the same effect on the pheromone-induced cell cycle arrest.	bind
7922	1	3223	5	11	NULL	0	NULL	Upc2p	GP		bind					ERG2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6395_s_287	11533229	(A) The 7-bp sequence TCGTATA was necessary for Upc2p binding to the  ERG2 promoter.	bind
7923	2	3223	5	11	NULL	0	NULL				is necessary for				TCGTATA	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6395_s_287	11533229	(A) The 7-bp sequence TCGTATA was necessary for Upc2p binding to the  ERG2 promoter.	bind
9526	1	3223	7	11	NULL	0	NULL	Upc2p	GP		bind					ERG2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6395_s_287	11533229	(A) The 7-bp sequence TCGTATA was necessary for Upc2p binding to the  ERG2 promoter.	bind
9527	2	3223	7	11	NULL	0	NULL				is necessary for				TCGTATA	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6395_s_287	11533229	(A) The 7-bp sequence TCGTATA was necessary for Upc2p binding to the  ERG2 promoter.	bind
80120	1	3223	11	NULL	NULL	0	NULL	Upc2p	GeneOrProtein		binds to 					ERG2 promoter	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_19_6395_s_287	11533229	(A) The 7-bp sequence TCGTATA was necessary for Upc2p binding to the  ERG2 promoter.	bind
80121	2	3223	11	NULL	NULL	0	NULL	Upc2p	Gene		is  necessary for				TCGTATA	statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_19_6395_s_287	11533229	(A) The 7-bp sequence TCGTATA was necessary for Upc2p binding to the  ERG2 promoter.	bind
7924	1	3227	5	11	NULL	0	NULL	MAPs	GP	addition of	restore					aster 	CellComponent	formation of			NULL	deltaRanBPdeltaAPA extract	NULL	NULL	NULL	NULL	gw60_cell_104_1_95_s_209	11163243	(A) The addition of MAPs or importin beta binding  proteins can restore aster formation in the deltaRanBPdeltaAPA extract.	bind
7925	2	3227	5	11	NULL	0	NULL	importin beta binding protein	GP	addition of	restore					aster 	CellComponent	formation of			NULL	deltaRanBPdeltaAPA extract	NULL	NULL	NULL	NULL	gw60_cell_104_1_95_s_209	11163243	(A) The addition of MAPs or importin beta binding  proteins can restore aster formation in the deltaRanBPdeltaAPA extract.	bind
9529	1	3227	7	11	NULL	0	NULL	MAPs	GP	addition of	restore					aster	CellComponent	formation of			NULL	deltaRanBPdeltaAPA extract	NULL	NULL	NULL	NULL	gw60_cell_104_1_95_s_209	11163243	(A) The addition of MAPs or importin beta binding  proteins can restore aster formation in the deltaRanBPdeltaAPA extract.	bind
9530	2	3227	7	11	NULL	0	NULL	importin beta binding proteins	GP	addition of	restore					aster	CellComponent	formation of			NULL	deltaRanBPdeltaAPA extract	NULL	NULL	NULL	NULL	gw60_cell_104_1_95_s_209	11163243	(A) The addition of MAPs or importin beta binding  proteins can restore aster formation in the deltaRanBPdeltaAPA extract.	bind
80122	1	3227	11	NULL	NULL	0	NULL	deltaRanBPdeltaAPA extract	Thing		can form					aster	CellComponent				NULL		0	NULL	NULL	NULL	gw60_cell_104_1_95_s_209	11163243	(A) The addition of MAPs or importin beta binding  proteins can restore aster formation in the deltaRanBPdeltaAPA extract.	bind
80123	2	3227	11	NULL	NULL	0	NULL	MAPs	Protein		can restore					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cell_104_1_95_s_209	11163243	(A) The addition of MAPs or importin beta binding  proteins can restore aster formation in the deltaRanBPdeltaAPA extract.	bind
80124	3	3227	11	NULL	NULL	0	NULL	importin beta binding proteins	Protein		can restore					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cell_104_1_95_s_209	11163243	(A) The addition of MAPs or importin beta binding  proteins can restore aster formation in the deltaRanBPdeltaAPA extract.	bind
7927	1	3229	5	11	NULL	0	NULL	Galpha	GP		bind			alphaN domain		receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4557_s_45	16030250	(A) The alphaN domain provides one of the binding interfaces between Galpha and Gbeta and the receptor.	bind
7928	2	3229	5	11	NULL	0	NULL	Gbeta	GP		bind			alphaN domain		receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4557_s_45	16030250	(A) The alphaN domain provides one of the binding interfaces between Galpha and Gbeta and the receptor.	bind
9531	1	3229	7	11	NULL	0	NULL	Galpha 	GP		bind			alphaN domain		receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4557_s_45	16030250	(A) The alphaN domain provides one of the binding interfaces between Galpha and Gbeta and the receptor.	bind
9532	2	3229	7	11	NULL	0	NULL	Gbeta	GP		bind			alphaN domain		receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4557_s_45	16030250	(A) The alphaN domain provides one of the binding interfaces between Galpha and Gbeta and the receptor.	bind
80125	1	3229	11	NULL	NULL	NULL	NULL	Galpha	Protein		binds to 			alphaN domain		receptor	Protein				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4557_s_45	16030250	(A) The alphaN domain provides one of the binding interfaces between Galpha and Gbeta and the receptor.	bind
80126	2	3229	11	NULL	NULL	0	NULL	Gbeta	Protein		binds to 					receptor	Protein				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4557_s_45	16030250	(A) The alphaN domain provides one of the binding interfaces between Galpha and Gbeta and the receptor.	bind
7931	1	3232	5	11	NULL	0	NULL	ATM	GP		bind					linear plasmid DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_319	15964794	(A) The anti-C147 antibodies prevent ATM binding to the linear plasmid DNA.	bind
7932	2	3232	5	11	NULL	0	NULL	anti-C147 antibodies	GP		prevent					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_319	15964794	(A) The anti-C147 antibodies prevent ATM binding to the linear plasmid DNA.	bind
9533	1	3232	7	11	NULL	0	NULL	ATM	GP		bind					linear plasmid DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_319	15964794	(A) The anti-C147 antibodies prevent ATM binding to the linear plasmid DNA.	bind
9534	2	3232	7	11	NULL	0	NULL	anti-C147 antibodies	GP		prevent					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_319	15964794	(A) The anti-C147 antibodies prevent ATM binding to the linear plasmid DNA.	bind
80127	1	3232	11	NULL	NULL	0	NULL	ATM	Protein		binds to 					DNA	NucleicAcidSubstance	linear plasmid			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_319	15964794	(A) The anti-C147 antibodies prevent ATM binding to the linear plasmid DNA.	bind
80128	2	3232	11	NULL	NULL	0	NULL	anti-C147 antibodies	PartOfProtein		prevents					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_319	15964794	(A) The anti-C147 antibodies prevent ATM binding to the linear plasmid DNA.	bind
8195	1	3233	5	11	NULL	0	NULL	anti-VapA	GP		reacted with					VapA	GP				NULL	in SRA	NULL	NULL	NULL	NULL	gw70_infectimmun_71_11_6329_s_74	14573652	(A) The anti-VapA monoclonal antibody reacted with  VapA in SRA and the pellet antigen and six protein bands in the CFS antigen.	bind
8196	2	3233	5	11	NULL	0	NULL	anti-VapA	GP		reacted with					pellet antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_11_6329_s_74	14573652	(A) The anti-VapA monoclonal antibody reacted with  VapA in SRA and the pellet antigen and six protein bands in the CFS antigen.	bind
8197	3	3233	5	11	NULL	0	NULL	anti-VapA	GP		reacted with					six protein bands	GP				NULL	in CFS antigen	NULL	NULL	NULL	NULL	gw70_infectimmun_71_11_6329_s_74	14573652	(A) The anti-VapA monoclonal antibody reacted with  VapA in SRA and the pellet antigen and six protein bands in the CFS antigen.	bind
44748	4	3233	5	11	NULL	0	NULL	anti-VapA	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_11_6329_s_74	14573652	(A) The anti-VapA monoclonal antibody reacted with  VapA in SRA and the pellet antigen and six protein bands in the CFS antigen.	bind
9535	1	3233	7	11	NULL	0	NULL	 anti-VapA 	GP		reacts with					VapA	GP				NULL	in SRA	NULL	NULL	NULL	NULL	gw70_infectimmun_71_11_6329_s_74	14573652	(A) The anti-VapA monoclonal antibody reacted with  VapA in SRA and the pellet antigen and six protein bands in the CFS antigen.	bind
9925	2	3233	7	11	NULL	0	NULL	anti-VapA	GP		reacts with					pellet antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_11_6329_s_74	14573652	(A) The anti-VapA monoclonal antibody reacted with  VapA in SRA and the pellet antigen and six protein bands in the CFS antigen.	bind
12378	3	3233	7	11	NULL	0	NULL	anti-VapA	GP		reacts with					six protein bands 	GP				NULL	CFS antigen	NULL	NULL	NULL	NULL	gw70_infectimmun_71_11_6329_s_74	14573652	(A) The anti-VapA monoclonal antibody reacted with  VapA in SRA and the pellet antigen and six protein bands in the CFS antigen.	bind
44749	4	3233	7	11	NULL	0	NULL	anti-VapA	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_11_6329_s_74	14573652	(A) The anti-VapA monoclonal antibody reacted with  VapA in SRA and the pellet antigen and six protein bands in the CFS antigen.	bind
80129	1	3233	11	NULL	NULL	0	NULL	anti-VapA	PartOfProtein	monoclonal antibody	reacted with					VapA	Protein	in SRA			NULL		0	NULL	NULL	NULL	gw70_infectimmun_71_11_6329_s_74	14573652	(A) The anti-VapA monoclonal antibody reacted with  VapA in SRA and the pellet antigen and six protein bands in the CFS antigen.	bind
7933	1	3234	5	11	NULL	0	NULL	LexA-Snf1	GP		bind					lacZ reporter	NucleicAcid			LexA sites 5' to promoter of	NULL		NULL	NULL	NULL	NULL	gw60_genetics_163_2_507_s_147	12618390	(A) The assay for kinase activity entails binding of LexA-Snf1 to LexA sites 5' to the promoter of a  lacZ reporter.	bind
9552	1	3234	7	11	NULL	0	NULL	LexA-Snf1	GP		bind					lacZ reporter	NucleicAcid			LexA sites 5' to the promoter of	NULL		NULL	NULL	NULL	NULL	gw60_genetics_163_2_507_s_147	12618390	(A) The assay for kinase activity entails binding of LexA-Snf1 to LexA sites 5' to the promoter of a  lacZ reporter.	bind
80130	1	3234	11	NULL	NULL	NULL	NULL	LexA-Snf1	Protein		binds to 					LexA	Gene			sites 5'	NULL		NULL	NULL	NULL	NULL	gw60_genetics_163_2_507_s_147	12618390	(A) The assay for kinase activity entails binding of LexA-Snf1 to LexA sites 5' to the promoter of a  lacZ reporter.	bind
80131	2	3234	11	NULL	NULL	0	NULL	statement 1	Protein		binds to 					lacZ reporter	Gene	promoter			NULL		0	NULL	NULL	NULL	gw60_genetics_163_2_507_s_147	12618390	(A) The assay for kinase activity entails binding of LexA-Snf1 to LexA sites 5' to the promoter of a  lacZ reporter.	bind
7934	1	3236	5	11	NULL	0	NULL	BTAF1	GP	ATPase-deficient;; mutant	bind					TBP	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_22_10072_s_122	15509807	(A) The ATPase-deficient mutant of BTAF1 binds to TBP in the presence of NC2alpha.	bind
7935	2	3236	5	11	NULL	0	NULL	statement 1	Process		in the presence of					NC2alpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_22_10072_s_122	15509807	(A) The ATPase-deficient mutant of BTAF1 binds to TBP in the presence of NC2alpha.	bind
9553	1	3236	7	11	NULL	0	NULL	BTAF1	GP	ATPase-deficient;; mutant	bind					TBP	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_22_10072_s_122	15509807	(A) The ATPase-deficient mutant of BTAF1 binds to TBP in the presence of NC2alpha.	bind
9554	2	3236	7	11	NULL	0	NULL	statement 1	Process		occurs in the presence of					NC2alpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_22_10072_s_122	15509807	(A) The ATPase-deficient mutant of BTAF1 binds to TBP in the presence of NC2alpha.	bind
80132	1	3236	11	NULL	NULL	0	NULL	BTAF1	GeneOrProtein	 ATPase-deficient mutant	binds to 					TBP	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_22_10072_s_122	15509807	(A) The ATPase-deficient mutant of BTAF1 binds to TBP in the presence of NC2alpha.	bind
80133	2	3236	11	NULL	NULL	0	NULL	statement 1	Process		occurs in the presence of					NC2alpha	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_22_10072_s_122	15509807	(A) The ATPase-deficient mutant of BTAF1 binds to TBP in the presence of NC2alpha.	bind
7937	1	3238	5	11	NULL	0	NULL	Pho4p	GP		bind			helix-loop-helix domain		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_yeast_19_7_641_s_154	11967834	(A) The basic helix-loop-helix domain  from Pho4p bound to DNA (PDB Accession No. 1A0A).	bind
9555	1	3238	7	11	NULL	0	NULL	Pho4p	GP		bind			basic helix-loop-helix		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_yeast_19_7_641_s_154	11967834	(A) The basic helix-loop-helix domain  from Pho4p bound to DNA (PDB Accession No. 1A0A).	bind
80134	1	3238	11	NULL	NULL	0	NULL	Pho4p	Protein		binds to 			helix-loop-helix domain		DNA	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_yeast_19_7_641_s_154	11967834	(A) The basic helix-loop-helix domain  from Pho4p bound to DNA (PDB Accession No. 1A0A).	bind
7938	1	3239	5	11	NULL	0	NULL	ASK1	GP		bind					TRAF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2198_s_118	10688666	(A) The binding of ASK1 and TRAF2 involves the amino-terminal (aa 1 to 460) and carboxyl-terminal (aa 937 to 1375) noncatalytic domains of ASK1.	bind
7940	2	3239	5	11	NULL	0	NULL	statement 1	Process		involves					ASK1	GP	noncatalytic domain	amino-terminal (aa 1 to 460)		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2198_s_118	10688666	(A) The binding of ASK1 and TRAF2 involves the amino-terminal (aa 1 to 460) and carboxyl-terminal (aa 937 to 1375) noncatalytic domains of ASK1.	bind
7941	3	3239	5	11	NULL	0	NULL	statement 1	Process		involves					ASK1	GP	noncatalytic domain	carboxyl-terminal (aa 937 to 1375)		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2198_s_118	10688666	(A) The binding of ASK1 and TRAF2 involves the amino-terminal (aa 1 to 460) and carboxyl-terminal (aa 937 to 1375) noncatalytic domains of ASK1.	bind
9556	1	3239	7	11	NULL	0	NULL	ASK1	GP		bind					TRAF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2198_s_118	10688666	(A) The binding of ASK1 and TRAF2 involves the amino-terminal (aa 1 to 460) and carboxyl-terminal (aa 937 to 1375) noncatalytic domains of ASK1.	bind
12379	2	3239	7	11	NULL	0	NULL	statement 1	Process		involves					ASK1	GP	noncatalytic	amino-terminal aa 1 to 460		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2198_s_118	10688666	(A) The binding of ASK1 and TRAF2 involves the amino-terminal (aa 1 to 460) and carboxyl-terminal (aa 937 to 1375) noncatalytic domains of ASK1.	bind
12380	3	3239	7	11	NULL	0	NULL	statement 1	Process		involves					ASK1	GP	noncatalytic	carboxyl-terminal aa 937 to 1375		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2198_s_118	10688666	(A) The binding of ASK1 and TRAF2 involves the amino-terminal (aa 1 to 460) and carboxyl-terminal (aa 937 to 1375) noncatalytic domains of ASK1.	bind
80135	1	3239	11	NULL	NULL	0	NULL	ASK1	Protein		binds to 			amino-terminal (aa 1 to 460);;carboxyl-terminal (aa 937 to 1375)		TRAF2	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_6_2198_s_118	10688666	(A) The binding of ASK1 and TRAF2 involves the amino-terminal (aa 1 to 460) and carboxyl-terminal (aa 937 to 1375) noncatalytic domains of ASK1.	bind
8198	1	3241	5	11	NULL	0	NULL	DDP1	GP		bind					oligo 6Rc	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
8199	2	3241	5	11	NULL	0	NULL	DDP1	GP		bind					oligo 9Rc	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
8200	3	3241	5	11	NULL	0	NULL	DDP1	GP		bind					oligo 9R	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
8201	4	3241	5	11	NULL	0	NULL	DDP1	GP		bind					fragment 12R	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
8202	5	3241	5	11	NULL	0	NULL	DDP1	GP		bind					fragment 42R	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
9926	1	3241	7	11	NULL	0	NULL	 DDP1	GP		bind					oligo 6Rc	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
9927	2	3241	7	11	NULL	0	NULL	DDP1	GP		bind					oligo 9Rc	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
9928	3	3241	7	11	NULL	0	NULL	DDP1	GP		bind					oligo 9R	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
9929	4	3241	7	11	NULL	0	NULL	DDP1	GP		bind					fragment 12R	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
9930	5	3241	7	11	NULL	0	NULL	DDP1	GP		bind					fragment 42R	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
80147	1	3241	11	NULL	NULL	0	NULL	DDP1	Protein		binds to 					 oligo 6Rc	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
80148	2	3241	11	NULL	NULL	0	NULL	DDP1	Protein		binds to 					oligo 9Rc	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
80149	3	3241	11	NULL	NULL	0	NULL	DDP1	Protein		binds to 					 oligo 9R	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
80150	4	3241	11	NULL	NULL	0	NULL	 DDP1	Protein		binds to 					fragment 12R	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
80151	5	3241	11	NULL	NULL	0	NULL	DDP1	Protein		binds to 					fragment 42R	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
80152	6	3241	11	NULL	NULL	NULL	NULL	1/2DDP1	Protein		binds to 					oligo 6Rc	NucleicAcidSubstance				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
80153	7	3241	11	NULL	NULL	0	NULL	1/2DDP1	Protein		binds to 					oligo 9Rc 	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
80154	8	3241	11	NULL	NULL	0	NULL	1/2DDP1	Protein		binds to 					oligo 9Rc	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
80155	9	3241	11	NULL	NULL	0	NULL	1/2DDP1	Protein		binds to 					fragment 12R	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
80156	10	3241	11	NULL	NULL	0	NULL	1/2DDP1	Protein		binds to 					fragment 42R	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_11_3860_s_198	10805729	(A) The binding of DDP1 and 1/2DDP1 to oligo 6Rc (panels 6Rc), oligo 9Rc (panels 9Rc), oligo 9R (panels 9R), fragment 12R (panels 12R), and fragment 42R (panels 42R) is presented as a function of increasing protein concentrations: a threefold-higher protein concentration was used in lanes 2 than in lanes 1.	bind
7942	1	3242	5	11	NULL	0	NULL	GST-LSP1 fusion proteins	GP		bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1642_1_17_s_86	12972289	(A) The binding of GST and  the indicated GST-LSP1 fusion proteins to F-actin was determined in a high-speed  co-sedimentation assay.	bind
7943	2	3242	5	11	NULL	0	NULL	GST	GP		bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1642_1_17_s_86	12972289	(A) The binding of GST and  the indicated GST-LSP1 fusion proteins to F-actin was determined in a high-speed  co-sedimentation assay.	bind
9931	1	3242	7	11	NULL	0	NULL	GST	GP		bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1642_1_17_s_86	12972289	(A) The binding of GST and  the indicated GST-LSP1 fusion proteins to F-actin was determined in a high-speed  co-sedimentation assay.	bind
9932	2	3242	7	11	NULL	0	NULL	GST-LSP1	GP		bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1642_1_17_s_86	12972289	(A) The binding of GST and  the indicated GST-LSP1 fusion proteins to F-actin was determined in a high-speed  co-sedimentation assay.	bind
80157	1	3242	11	NULL	NULL	0	NULL	GST	Protein		binds to 					F-actin	Protein				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1642_1_17_s_86	12972289	(A) The binding of GST and  the indicated GST-LSP1 fusion proteins to F-actin was determined in a high-speed  co-sedimentation assay.	bind
80158	2	3242	11	NULL	NULL	0	NULL	GST-LSP1	Protein		binds to 					F-actin	Protein				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1642_1_17_s_86	12972289	(A) The binding of GST and  the indicated GST-LSP1 fusion proteins to F-actin was determined in a high-speed  co-sedimentation assay.	bind
80159	3	3242	11	NULL	NULL	0	NULL	high-speed co-sedimentation assay	ResearchActivity		determines					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1642_1_17_s_86	12972289	(A) The binding of GST and  the indicated GST-LSP1 fusion proteins to F-actin was determined in a high-speed  co-sedimentation assay.	bind
80160	4	3242	11	NULL	NULL	0	NULL	high-speed co-sedimentation assay	ResearchActivity		determines					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1642_1_17_s_86	12972289	(A) The binding of GST and  the indicated GST-LSP1 fusion proteins to F-actin was determined in a high-speed  co-sedimentation assay.	bind
8015	1	3244	5	11	NULL	0	NULL	MutS	GP		bind									ICLs	NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
8016	2	3244	5	11	NULL	0	NULL	PCNA	GP		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
8017	3	3244	5	11	NULL	0	NULL	DNA helicase	GP		creates					open region	NucleicAcid	proximate to 		ICL	NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
8018	4	3244	5	11	NULL	0	NULL	RPA	GP		creates					open region	NucleicAcid	proximate to		ICL	NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
8019	5	3244	5	11	NULL	0	NULL	statement 3	Process		occurs in cooperation with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
9933	1	3244	7	11	NULL	0	NULL	MutS	GP		bind					ICLs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
9934	2	3244	7	11	NULL	0	NULL	statement 1	Process		is stimulated by					PCNA	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
9935	3	3244	7	11	NULL	0	NULL	DNA helicase	GP		creates					open region	NucleicAcid	proximate to		ICL	NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
9936	4	3244	7	11	NULL	0	NULL	RPA	GP		creates					 open region	NucleicAcid	proximate to		ICL	NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
9937	5	3244	7	11	NULL	0	NULL	statement 3	Process		occurs in cooperation with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
80161	1	3244	11	NULL	NULL	0	NULL	MutS	Protein		binds to 					ICLs	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
80162	2	3244	11	NULL	NULL	0	NULL	PCNA	Protein		stimulates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
80163	3	3244	11	NULL	NULL	NULL	NULL	PCNA	Protein		creates					bubble	NucleicAcidSubstance	proximate to the ICL			NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
80164	4	3244	11	NULL	NULL	0	NULL	RPA	Protein		creates					bubble	NucleicAcidSubstance	proximate to the ICL			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
80165	5	3244	11	NULL	NULL	0	NULL	PCNA	Protein		is a type of 					DNA helicase	Protein				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
80166	6	3244	11	NULL	NULL	0	NULL	PCNA	Protein		creates					open region	NucleicAcidSubstance	proximate to the ICL			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
80167	7	3244	11	NULL	NULL	0	NULL	RPA	Protein		creates					open region	NucleicAcidSubstance	proximate to the ICL			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
80168	8	3244	11	NULL	NULL	0	NULL	statement 3	Process		occurs along with					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
80169	9	3244	11	NULL	NULL	0	NULL	statement 6	Process		occurs along with					statement 7	Process				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
80170	10	3244	11	NULL	NULL	0	NULL	Ercc1-Xpf	Protein		forms					incisions					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_1_71_s_144	12943665	(A) The binding of MutS   to ICLs is stimulated by PCNA, (B) a DNA helicase in cooperation with RPA creates  a bubble or open region proximate to the ICL. Ercc1-Xpf is recruited to the site  and forms incisions on either side of the lesion as shown in (C).	bind
8022	1	3246	5	11	NULL	0	NULL	p65	GP		bind					IkappaBalpha	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_3_1113_s_269	15657437	(A) The binding of p65 to the  IkappaBalpha promoter is increased in  Pias1 null cells.	bind
8023	2	3246	5	11	NULL	0	NULL	statement 1	Process		is increased in					Pias1 null cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_3_1113_s_269	15657437	(A) The binding of p65 to the  IkappaBalpha promoter is increased in  Pias1 null cells.	bind
9938	1	3246	7	11	NULL	0	NULL	p65	GP		binds					IkappaBalpha	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_3_1113_s_269	15657437	(A) The binding of p65 to the  IkappaBalpha promoter is increased in  Pias1 null cells.	bind
9939	2	3246	7	11	NULL	0	NULL	statement 1	Process		is increased in					Pias1 null cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_3_1113_s_269	15657437	(A) The binding of p65 to the  IkappaBalpha promoter is increased in  Pias1 null cells.	bind
80171	1	3246	11	NULL	NULL	0	NULL	p65	Protein		binds to 					IkappaBalpha promoter	Gene				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_3_1113_s_269	15657437	(A) The binding of p65 to the  IkappaBalpha promoter is increased in  Pias1 null cells.	bind
80172	2	3246	11	NULL	NULL	0	NULL	statement 1	Process		increased in					Pias1 null cells	Cell				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_3_1113_s_269	15657437	(A) The binding of p65 to the  IkappaBalpha promoter is increased in  Pias1 null cells.	bind
8024	1	3247	5	11	NULL	0	NULL	S-CDK	GP	binding of	restrict					Sic1	GP	ubiquitination of;; number of	lysines		NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_6_1435_s_163	12820958	(A) The binding of S-CDK restricts the number of lysines in Sic1 that can be ubiquitinated.	bind
9941	1	3247	7	11	NULL	0	NULL	S-CDK	GP	binding of	restricts					Sic1	GP	ubiquitination of;; number of	lysine		NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_6_1435_s_163	12820958	(A) The binding of S-CDK restricts the number of lysines in Sic1 that can be ubiquitinated.	bind
80173	1	3247	11	NULL	NULL	0	NULL	S-CDK	Protein		binds to 					Sic1	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_11_6_1435_s_163	12820958	(A) The binding of S-CDK restricts the number of lysines in Sic1 that can be ubiquitinated.	bind
80174	2	3247	11	NULL	NULL	0	NULL	 lysines	AminoAcid	in Sic1	 can be					ubiquitinated	MolecularProcess				NULL		0	NULL	NULL	NULL	gw60_molcell_11_6_1435_s_163	12820958	(A) The binding of S-CDK restricts the number of lysines in Sic1 that can be ubiquitinated.	bind
80175	3	3247	11	NULL	NULL	0	NULL	statement 1	Process		 restricts					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_11_6_1435_s_163	12820958	(A) The binding of S-CDK restricts the number of lysines in Sic1 that can be ubiquitinated.	bind
8025	1	3248	5	11	NULL	0	NULL	SPN	GP		bind					importin-beta	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4660_s_261	16030253	(A) The binding of SPN to importin-beta is increased upon mutation or truncation of the C terminus.	bind
8026	2	3248	5	11	NULL	0	NULL			mutation of	increases			C terminus		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4660_s_261	16030253	(A) The binding of SPN to importin-beta is increased upon mutation or truncation of the C terminus.	bind
8027	3	3248	5	11	NULL	0	NULL			truncation of	increases			C terminus		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4660_s_261	16030253	(A) The binding of SPN to importin-beta is increased upon mutation or truncation of the C terminus.	bind
8028	4	3248	5	11	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4660_s_261	16030253	(A) The binding of SPN to importin-beta is increased upon mutation or truncation of the C terminus.	bind
9976	1	3248	7	11	NULL	0	NULL	SPN	GP		bind					importin-beta	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4660_s_261	16030253	(A) The binding of SPN to importin-beta is increased upon mutation or truncation of the C terminus.	bind
9977	2	3248	7	11	NULL	0	NULL	statement 1	Process		is increased upon					C terminus	GP	mutation of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4660_s_261	16030253	(A) The binding of SPN to importin-beta is increased upon mutation or truncation of the C terminus.	bind
9978	3	3248	7	11	NULL	0	NULL	statement 1	Process		is increased upon					C terminus	GP	truncation of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4660_s_261	16030253	(A) The binding of SPN to importin-beta is increased upon mutation or truncation of the C terminus.	bind
12381	4	3248	7	11	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4660_s_261	16030253	(A) The binding of SPN to importin-beta is increased upon mutation or truncation of the C terminus.	bind
80176	1	3248	11	NULL	NULL	0	NULL	SPN	Protein		binds to 					importin-beta	Protein				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4660_s_261	16030253	(A) The binding of SPN to importin-beta is increased upon mutation or truncation of the C terminus.	bind
80177	2	3248	11	NULL	NULL	0	NULL	statement 1	Process		increased in					mutation	MolecularProcess	of the C terminus			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4660_s_261	16030253	(A) The binding of SPN to importin-beta is increased upon mutation or truncation of the C terminus.	bind
80178	3	3248	11	NULL	NULL	0	NULL	statement 1	Process		increased in					truncation	MolecularProcess	of the C terminus			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4660_s_261	16030253	(A) The binding of SPN to importin-beta is increased upon mutation or truncation of the C terminus.	bind
80179	4	3248	11	NULL	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4660_s_261	16030253	(A) The binding of SPN to importin-beta is increased upon mutation or truncation of the C terminus.	bind
8218	2	3249	5	11	NULL	0	NULL	tRNAIle	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_4_519_s_52	10549284	(a) The binding of tRNAIle to IleRS complexed to a misactivated valine (Val ) first results in the translocation of the misactivated amino acid from the active site to the editing site (for this illustration, no distinction is made between misactivated valine as Val-AMP or as Val-tRNAIle).	bind
8219	1	3249	5	11	NULL	0	NULL	IleRS	GP		is in complex with					valine	AminoAcid	misactivated			NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_4_519_s_52	10549284	(a) The binding of tRNAIle to IleRS complexed to a misactivated valine (Val ) first results in the translocation of the misactivated amino acid from the active site to the editing site (for this illustration, no distinction is made between misactivated valine as Val-AMP or as Val-tRNAIle).	bind
8220	3	3249	5	11	NULL	0	NULL	statement 2	Process		results in					amino acid	AminoAcid	translocation of;; misactivated 			NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_4_519_s_52	10549284	(a) The binding of tRNAIle to IleRS complexed to a misactivated valine (Val ) first results in the translocation of the misactivated amino acid from the active site to the editing site (for this illustration, no distinction is made between misactivated valine as Val-AMP or as Val-tRNAIle).	bind
8221	4	3249	5	11	NULL	0	NULL	misactivated amino acid	AminoAcid		is translocated to					editing site	GP	from active site			NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_4_519_s_52	10549284	(a) The binding of tRNAIle to IleRS complexed to a misactivated valine (Val ) first results in the translocation of the misactivated amino acid from the active site to the editing site (for this illustration, no distinction is made between misactivated valine as Val-AMP or as Val-tRNAIle).	bind
9979	2	3249	7	11	NULL	0	NULL	tRNAIle	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_4_519_s_52	10549284	(a) The binding of tRNAIle to IleRS complexed to a misactivated valine (Val ) first results in the translocation of the misactivated amino acid from the active site to the editing site (for this illustration, no distinction is made between misactivated valine as Val-AMP or as Val-tRNAIle).	bind
9980	1	3249	7	11	NULL	0	NULL	IleRS	GP		is complexed to					valine 	AminoAcid	misactivated 			NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_4_519_s_52	10549284	(a) The binding of tRNAIle to IleRS complexed to a misactivated valine (Val ) first results in the translocation of the misactivated amino acid from the active site to the editing site (for this illustration, no distinction is made between misactivated valine as Val-AMP or as Val-tRNAIle).	bind
9981	3	3249	7	11	NULL	0	NULL	statement 2	Process		results in 					amino acid	AminoAcid	misactivated;; translocation of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_4_519_s_52	10549284	(a) The binding of tRNAIle to IleRS complexed to a misactivated valine (Val ) first results in the translocation of the misactivated amino acid from the active site to the editing site (for this illustration, no distinction is made between misactivated valine as Val-AMP or as Val-tRNAIle).	bind
9982	4	3249	7	11	NULL	0	NULL	statement 3	Process		occurs from					editing site	GP	from the active site to			NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_4_519_s_52	10549284	(a) The binding of tRNAIle to IleRS complexed to a misactivated valine (Val ) first results in the translocation of the misactivated amino acid from the active site to the editing site (for this illustration, no distinction is made between misactivated valine as Val-AMP or as Val-tRNAIle).	bind
9983	5	3249	7	11	NULL	0	NULL	valine	AminoAcid		is					Val	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_4_519_s_52	10549284	(a) The binding of tRNAIle to IleRS complexed to a misactivated valine (Val ) first results in the translocation of the misactivated amino acid from the active site to the editing site (for this illustration, no distinction is made between misactivated valine as Val-AMP or as Val-tRNAIle).	bind
80180	1	3249	11	NULL	NULL	0	NULL	 tRNAIle	NucleicAcidSubstance		binds to 					IleRS	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcell_4_4_519_s_52	10549284	(a) The binding of tRNAIle to IleRS complexed to a misactivated valine (Val ) first results in the translocation of the misactivated amino acid from the active site to the editing site (for this illustration, no distinction is made between misactivated valine as Val-AMP or as Val-tRNAIle).	bind
80181	2	3249	11	NULL	NULL	0	NULL	statement 1	NucleicAcidSubstance		complexed to					valine	AminoAcid	misactivated			NULL		0	NULL	NULL	NULL	gw60_molcell_4_4_519_s_52	10549284	(a) The binding of tRNAIle to IleRS complexed to a misactivated valine (Val ) first results in the translocation of the misactivated amino acid from the active site to the editing site (for this illustration, no distinction is made between misactivated valine as Val-AMP or as Val-tRNAIle).	bind
80182	3	3249	11	NULL	NULL	0	NULL	Val	AminoAcid		is					valine	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_molcell_4_4_519_s_52	10549284	(a) The binding of tRNAIle to IleRS complexed to a misactivated valine (Val ) first results in the translocation of the misactivated amino acid from the active site to the editing site (for this illustration, no distinction is made between misactivated valine as Val-AMP or as Val-tRNAIle).	bind
80183	4	3249	11	NULL	NULL	NULL	NULL	valine	AminoAcid	misactivated;;from the active site	undergoes					translocation	MolecularProcess	to the editing site			NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_4_519_s_52	10549284	(a) The binding of tRNAIle to IleRS complexed to a misactivated valine (Val ) first results in the translocation of the misactivated amino acid from the active site to the editing site (for this illustration, no distinction is made between misactivated valine as Val-AMP or as Val-tRNAIle).	bind
8029	1	3250	5	11	NULL	0	NULL	histone H3	GP	[35]methionine-labeled	bind					RbAP46	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_239	15601853	(A) The binding of [35]methionine-labeled histone H3 to RbAP46 was competed with hypo- or hyperacetylated  core histones.	bind
8030	2	3250	5	11	NULL	0	NULL	core histones	GP	hypoacetylated	bind					RbAP46	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_239	15601853	(A) The binding of [35]methionine-labeled histone H3 to RbAP46 was competed with hypo- or hyperacetylated  core histones.	bind
8031	3	3250	5	11	NULL	0	NULL	core histones	GP	hyperacetylated	bind					RbAP46	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_239	15601853	(A) The binding of [35]methionine-labeled histone H3 to RbAP46 was competed with hypo- or hyperacetylated  core histones.	bind
8032	4	3250	5	11	NULL	0	NULL	statement 2	GP		compete with					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_239	15601853	(A) The binding of [35]methionine-labeled histone H3 to RbAP46 was competed with hypo- or hyperacetylated  core histones.	bind
8033	5	3250	5	11	NULL	0	NULL	statement 3	GP		compete with					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_239	15601853	(A) The binding of [35]methionine-labeled histone H3 to RbAP46 was competed with hypo- or hyperacetylated  core histones.	bind
9984	1	3250	7	11	NULL	0	NULL	 histone H3	GP	[35]methionine-labeled	bind					RbAP46	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_239	15601853	(A) The binding of [35]methionine-labeled histone H3 to RbAP46 was competed with hypo- or hyperacetylated  core histones.	bind
9985	2	3250	7	11	NULL	0	NULL	 core histones	GP	hypoacetylated	bind					RbAP46	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_239	15601853	(A) The binding of [35]methionine-labeled histone H3 to RbAP46 was competed with hypo- or hyperacetylated  core histones.	bind
9986	3	3250	7	11	NULL	0	NULL	core histones	GP	hyperacetylated 	bind					RbAP46	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_239	15601853	(A) The binding of [35]methionine-labeled histone H3 to RbAP46 was competed with hypo- or hyperacetylated  core histones.	bind
9987	4	3250	7	11	NULL	0	NULL	statement 2	GP		compete with					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_239	15601853	(A) The binding of [35]methionine-labeled histone H3 to RbAP46 was competed with hypo- or hyperacetylated  core histones.	bind
9988	5	3250	7	11	NULL	0	NULL	statement 3	GP		compete with					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_239	15601853	(A) The binding of [35]methionine-labeled histone H3 to RbAP46 was competed with hypo- or hyperacetylated  core histones.	bind
80184	1	3250	11	NULL	NULL	0	NULL	histone H3	Protein	[35]methionine-labeled	binds to 					RbAP46	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_239	15601853	(A) The binding of [35]methionine-labeled histone H3 to RbAP46 was competed with hypo- or hyperacetylated  core histones.	bind
80185	2	3250	11	NULL	NULL	0	NULL	histones	Protein	hyperacetylated core	binds to 					RbAP46	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_239	15601853	(A) The binding of [35]methionine-labeled histone H3 to RbAP46 was competed with hypo- or hyperacetylated  core histones.	bind
80186	3	3250	11	NULL	NULL	0	NULL	histones	Protein	hypoacetylated core	binds to 					RbAP46	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_239	15601853	(A) The binding of [35]methionine-labeled histone H3 to RbAP46 was competed with hypo- or hyperacetylated  core histones.	bind
80187	4	3250	11	NULL	NULL	0	NULL	statement 1	Process		competes with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_239	15601853	(A) The binding of [35]methionine-labeled histone H3 to RbAP46 was competed with hypo- or hyperacetylated  core histones.	bind
80188	5	3250	11	NULL	NULL	0	NULL	statement 1	Process		competes with					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_239	15601853	(A) The binding of [35]methionine-labeled histone H3 to RbAP46 was competed with hypo- or hyperacetylated  core histones.	bind
8034	1	3251	5	11	NULL	0	NULL	CycT1	GP		bind			C-terminal region		CTD	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_1_321_s_206	11739744	(A) The C-terminal region of CycT1 binds the CTD in vitro.	bind
9989	1	3251	7	11	NULL	0	NULL	CycT1	GP		bind			C-terminal region		CTD	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_1_321_s_206	11739744	(A) The C-terminal region of CycT1 binds the CTD in vitro.	bind
80189	1	3251	11	NULL	NULL	0	NULL	CycT1	Gene	C-terminal 	binds to 								CTD		NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_22_1_321_s_206	11739744	(A) The C-terminal region of CycT1 binds the CTD in vitro.	bind
8035	1	3252	5	11	NULL	0	NULL	C/EBPbeta	GP		bind				SBE in promoter	Stat1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2108_s_336	9528783	(A) The C/EBPbeta promoter contains an SBE that binds Stat1 and Stat3.	bind
8036	2	3252	5	11	NULL	0	NULL	C/EBPbeta	GP		bind				SBE in promoter	Stat3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2108_s_336	9528783	(A) The C/EBPbeta promoter contains an SBE that binds Stat1 and Stat3.	bind
9990	1	3252	7	11	NULL	0	NULL	Stat1	GP		bind					C/EBPbeta	GP			SBE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2108_s_336	9528783	(A) The C/EBPbeta promoter contains an SBE that binds Stat1 and Stat3.	bind
9991	2	3252	7	11	NULL	0	NULL	Stat3	GP		bind					C/EBPbeta	GP			SBE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2108_s_336	9528783	(A) The C/EBPbeta promoter contains an SBE that binds Stat1 and Stat3.	bind
80190	1	3252	11	NULL	NULL	0	NULL	C/EBPbeta promoter	NucleicAcidSubstance		contains					SBE	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_2108_s_336	9528783	(A) The C/EBPbeta promoter contains an SBE that binds Stat1 and Stat3.	bind
80191	2	3252	11	NULL	NULL	0	NULL	C/EBPbeta promoter	NucleicAcidSubstance		binds to 				SBE	Stat1	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_2108_s_336	9528783	(A) The C/EBPbeta promoter contains an SBE that binds Stat1 and Stat3.	bind
80192	3	3252	11	NULL	NULL	0	NULL	C/EBPbeta promoter	NucleicAcidSubstance		binds to 				SBE	Stat3	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_2108_s_336	9528783	(A) The C/EBPbeta promoter contains an SBE that binds Stat1 and Stat3.	bind
8037	1	3253	5	11	NULL	0	NULL	Adf-1	GP		bind			carboxy terminus		TAFII110	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2252_s_260	9528796	(A) The carboxy terminus of Adf-1 binds TAFII110 and TAFII250.	bind
8038	2	3253	5	11	NULL	0	NULL	Adf-1	GP		bind			carboxy terminus		TAFII250	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2252_s_260	9528796	(A) The carboxy terminus of Adf-1 binds TAFII110 and TAFII250.	bind
9992	1	3253	7	11	NULL	0	NULL	Adf-1	GP		bind			carboxy terminus		TAFII110	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2252_s_260	9528796	(A) The carboxy terminus of Adf-1 binds TAFII110 and TAFII250.	bind
9993	2	3253	7	11	NULL	0	NULL	Adf-1	GP		bind			carboxy terminus		TAFII250	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2252_s_260	9528796	(A) The carboxy terminus of Adf-1 binds TAFII110 and TAFII250.	bind
80193	1	3253	11	NULL	NULL	0	NULL	Adf-1	Protein	carboxy terminus	binds to 					TAFII110	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_2252_s_260	9528796	(A) The carboxy terminus of Adf-1 binds TAFII110 and TAFII250.	bind
80194	2	3253	11	NULL	NULL	0	NULL	Adf-1	Protein	carboxy terminus	binds to 					TAFII250	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_2252_s_260	9528796	(A) The carboxy terminus of Adf-1 binds TAFII110 and TAFII250.	bind
8039	1	3254	5	11	NULL	0	NULL	HDAC4	GP		bind			carboxyl-terminal region		PC4	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2242_s_444	15743821	(A) The carboxyl-terminal  region of HDAC4 binds PC4.	bind
9994	1	3254	7	11	NULL	0	NULL	HDAC4	GP		bind			carboxyl-terminal 		PC4	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2242_s_444	15743821	(A) The carboxyl-terminal  region of HDAC4 binds PC4.	bind
80195	1	3254	11	NULL	NULL	0	NULL	 HDAC4	Protein	carboxyl-terminal	binds to 					PC4	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_6_2242_s_444	15743821	(A) The carboxyl-terminal  region of HDAC4 binds PC4.	bind
8040	1	3255	5	11	NULL	NULL	NULL	CArG-like site	GP		bind		weakly		 - 122/ - 85 promoter fragment	SRF	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_131_3_669_s_76	14711876	(A) The CArG-like  site in  - 122/ - 85 promoter fragment binds SRF only weakly (complex labelled S);  GATA4 protein binds efficiently to the GATA#2 site present in the same probe (labelled  G); simultaneous binding of SRF and GATA4 can be detected (arrow).	bind
8041	2	3255	5	11	NULL	NULL	NULL	GATA4 protein	GP		bind		efficiently			probe	NucleicAcid			GATA#2 site	NULL		NULL	NULL	NULL	NULL	gw70_development_131_3_669_s_76	14711876	(A) The CArG-like  site in  - 122/ - 85 promoter fragment binds SRF only weakly (complex labelled S);  GATA4 protein binds efficiently to the GATA#2 site present in the same probe (labelled  G); simultaneous binding of SRF and GATA4 can be detected (arrow).	bind
8042	3	3255	5	11	NULL	0	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_131_3_669_s_76	14711876	(A) The CArG-like  site in  - 122/ - 85 promoter fragment binds SRF only weakly (complex labelled S);  GATA4 protein binds efficiently to the GATA#2 site present in the same probe (labelled  G); simultaneous binding of SRF and GATA4 can be detected (arrow).	bind
10006	1	3255	7	11	NULL	0	NULL	CArG-like site	GP		bind		weakly		- 122/ - 85 promoter fragment	SRF	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_131_3_669_s_76	14711876	(A) The CArG-like  site in  - 122/ - 85 promoter fragment binds SRF only weakly (complex labelled S);  GATA4 protein binds efficiently to the GATA#2 site present in the same probe (labelled  G); simultaneous binding of SRF and GATA4 can be detected (arrow).	bind
10007	2	3255	7	11	NULL	0	NULL	GATA4	GP		bind		efficiently							GATA#2 site	NULL		NULL	NULL	NULL	NULL	gw70_development_131_3_669_s_76	14711876	(A) The CArG-like  site in  - 122/ - 85 promoter fragment binds SRF only weakly (complex labelled S);  GATA4 protein binds efficiently to the GATA#2 site present in the same probe (labelled  G); simultaneous binding of SRF and GATA4 can be detected (arrow).	bind
10008	3	3255	7	11	NULL	0	NULL	statement 1	Process		occur simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_131_3_669_s_76	14711876	(A) The CArG-like  site in  - 122/ - 85 promoter fragment binds SRF only weakly (complex labelled S);  GATA4 protein binds efficiently to the GATA#2 site present in the same probe (labelled  G); simultaneous binding of SRF and GATA4 can be detected (arrow).	bind
81258	1	3255	11	NULL	NULL	0	NULL	SRF	GeneOrProtein		binds to 		simultaneously			GATA4	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw70_development_131_3_669_s_76	14711876	(A) The CArG-like  site in  - 122/ - 85 promoter fragment binds SRF only weakly (complex labelled S);  GATA4 protein binds efficiently to the GATA#2 site present in the same probe (labelled  G); simultaneous binding of SRF and GATA4 can be detected (arrow).	bind
80196	1	3256	11	NULL	NULL	0	NULL	FOXO	Protein		is a type of 					Forkhead transcription factor	Protein				NULL		0	NULL	NULL	NULL	gw70_cellbiol_162_4_613_s_137	12913110	(A) The consensus binding site for the FOXO subfamily of Forkhead transcription factors  and a known FOXO binding site in the Fas ligand promoter (FasL) are compared with  the conserved bim1 and bim2 sites located close to the  bim promoter.	bind
80197	2	3256	11	NULL	NULL	0	NULL	FasL	Protein		is					Fas ligand promoter	Protein				NULL		0	NULL	NULL	NULL	gw70_cellbiol_162_4_613_s_137	12913110	(A) The consensus binding site for the FOXO subfamily of Forkhead transcription factors  and a known FOXO binding site in the Fas ligand promoter (FasL) are compared with  the conserved bim1 and bim2 sites located close to the  bim promoter.	bind
80198	3	3256	11	NULL	NULL	0	NULL	bim1	NucleicAcidSubstance	conserved sites	located close to					bim promoter	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_cellbiol_162_4_613_s_137	12913110	(A) The consensus binding site for the FOXO subfamily of Forkhead transcription factors  and a known FOXO binding site in the Fas ligand promoter (FasL) are compared with  the conserved bim1 and bim2 sites located close to the  bim promoter.	bind
80199	4	3256	11	NULL	NULL	0	NULL	bim2	NucleicAcidSubstance	conserved sites	located close to					bim promoter	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_cellbiol_162_4_613_s_137	12913110	(A) The consensus binding site for the FOXO subfamily of Forkhead transcription factors  and a known FOXO binding site in the Fas ligand promoter (FasL) are compared with  the conserved bim1 and bim2 sites located close to the  bim promoter.	bind
8043	1	3257	5	11	NULL	0	NULL	[125]GA3	GP		bind					SMMC7721-Tie2	Cell				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_4_1004_s_84	14985112	(A) The counts of [125]GA3 bound to Tie2 positive expressing SMMC7721-Tie2 and Tie2 negative parent cells  SMMC7721 with (GA3*/GA3) or without (GA3*) addition of 100-fold molar excess of cold  GA3.	bind
8044	2	3257	5	11	NULL	0	NULL	[125]GA3	GP		bind					SMMC7721	Cell				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_4_1004_s_84	14985112	(A) The counts of [125]GA3 bound to Tie2 positive expressing SMMC7721-Tie2 and Tie2 negative parent cells  SMMC7721 with (GA3*/GA3) or without (GA3*) addition of 100-fold molar excess of cold  GA3.	bind
44753	3	3257	5	11	NULL	0	NULL	SMMC7721-Tie2	Cell		is a type of					Tie2 positive expressing cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_4_1004_s_84	14985112	(A) The counts of [125]GA3 bound to Tie2 positive expressing SMMC7721-Tie2 and Tie2 negative parent cells  SMMC7721 with (GA3*/GA3) or without (GA3*) addition of 100-fold molar excess of cold  GA3.	bind
44754	4	3257	5	11	NULL	0	NULL	SMMC7721	Cell		is a type of					Tie2 negative parent cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_4_1004_s_84	14985112	(A) The counts of [125]GA3 bound to Tie2 positive expressing SMMC7721-Tie2 and Tie2 negative parent cells  SMMC7721 with (GA3*/GA3) or without (GA3*) addition of 100-fold molar excess of cold  GA3.	bind
10084	1	3257	7	11	NULL	0	NULL	[125]GA3	GP		bind					SMMC7721-Tie2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_4_1004_s_84	14985112	(A) The counts of [125]GA3 bound to Tie2 positive expressing SMMC7721-Tie2 and Tie2 negative parent cells  SMMC7721 with (GA3*/GA3) or without (GA3*) addition of 100-fold molar excess of cold  GA3.	bind
10085	2	3257	7	11	NULL	0	NULL	[125]GA3	GP		bind					SMMC7721 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_4_1004_s_84	14985112	(A) The counts of [125]GA3 bound to Tie2 positive expressing SMMC7721-Tie2 and Tie2 negative parent cells  SMMC7721 with (GA3*/GA3) or without (GA3*) addition of 100-fold molar excess of cold  GA3.	bind
44755	3	3257	7	11	NULL	0	NULL	SMMC7721-Tie2	Cell		is a type of					Tie2 positive expressing cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_4_1004_s_84	14985112	(A) The counts of [125]GA3 bound to Tie2 positive expressing SMMC7721-Tie2 and Tie2 negative parent cells  SMMC7721 with (GA3*/GA3) or without (GA3*) addition of 100-fold molar excess of cold  GA3.	bind
44756	4	3257	7	11	NULL	0	NULL	SMMC7721	Cell		is a type of					Tie2 negative parent cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_4_1004_s_84	14985112	(A) The counts of [125]GA3 bound to Tie2 positive expressing SMMC7721-Tie2 and Tie2 negative parent cells  SMMC7721 with (GA3*/GA3) or without (GA3*) addition of 100-fold molar excess of cold  GA3.	bind
8045	1	3258	5	11	NULL	0	NULL	L11	NucleicAcid		bind								L11BD		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_10_8_769_s_143	12954336	(A) The crystal structure of L11 bound to L11BD  [24]   is overlaid onto the L11BD coordinates.	bind
10009	1	3258	7	11	NULL	0	NULL	L11 	NucleicAcid		bind					 			L11BD		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_10_8_769_s_143	12954336	(A) The crystal structure of L11 bound to L11BD  [24]   is overlaid onto the L11BD coordinates.	bind
80200	1	3258	11	NULL	NULL	0	NULL	L11	Protein		binds to 								L11BD		NULL		0	NULL	NULL	NULL	gw60_chembiol_10_8_769_s_143	12954336	(A) The crystal structure of L11 bound to L11BD  [24]   is overlaid onto the L11BD coordinates.	bind
8046	1	3259	5	11	NULL	0	NULL	pRB	GP		bind					E7 peptide	GP	papillomavirus			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_2_179_s_102	12040123	(A) The crystal structure of pRB  bound to an E7 peptide (from papillomavirus) containing an LXCXE motif (PDB code  1Gux [ ]).	bind
8047	2	3259	5	11	NULL	0	NULL	E7 peptide	GP	papillomavirus	contain								LXCXE motif		NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_2_179_s_102	12040123	(A) The crystal structure of pRB  bound to an E7 peptide (from papillomavirus) containing an LXCXE motif (PDB code  1Gux [ ]).	bind
10010	1	3259	7	11	NULL	0	NULL	 pRB	GP		bind					E7 peptide	GP	papillomavirus			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_2_179_s_102	12040123	(A) The crystal structure of pRB  bound to an E7 peptide (from papillomavirus) containing an LXCXE motif (PDB code  1Gux [ ]).	bind
12386	2	3259	7	11	NULL	0	NULL	E7 peptide	GP		contain								LXCXE motif		NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_2_179_s_102	12040123	(A) The crystal structure of pRB  bound to an E7 peptide (from papillomavirus) containing an LXCXE motif (PDB code  1Gux [ ]).	bind
80201	1	3259	11	NULL	NULL	0	NULL	pRB	Protein	crystal structure	binds to 					E7 peptide	PartOfProtein	papillomavirus	LXCXE motif		NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_2_179_s_102	12040123	(A) The crystal structure of pRB  bound to an E7 peptide (from papillomavirus) containing an LXCXE motif (PDB code  1Gux [ ]).	bind
8048	1	3261	5	11	NULL	0	NULL	cortactin protein	GP		contain								F-actin-binding sites		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_6_2162_s_90	12612086	(a) The diagram depicts different domains of the cortactin protein including the F-actin-binding sites, C-terminal tyrosines that are phosphorylated by Src kinases, and the SH3 domain that binds Dyn2.	bind
8049	2	3261	5	11	NULL	0	NULL	Src kinases	GP		phosphorylate					cortactin protein	GP		C-terminal tyrosines		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_6_2162_s_90	12612086	(a) The diagram depicts different domains of the cortactin protein including the F-actin-binding sites, C-terminal tyrosines that are phosphorylated by Src kinases, and the SH3 domain that binds Dyn2.	bind
8050	3	3261	5	11	NULL	0	NULL	cortactin protein	GP		bind			SH3 domain		Dyn2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_6_2162_s_90	12612086	(a) The diagram depicts different domains of the cortactin protein including the F-actin-binding sites, C-terminal tyrosines that are phosphorylated by Src kinases, and the SH3 domain that binds Dyn2.	bind
10011	1	3261	7	11	NULL	0	NULL	cortactin	GP		bind			SH3		Dyn2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_6_2162_s_90	12612086	(a) The diagram depicts different domains of the cortactin protein including the F-actin-binding sites, C-terminal tyrosines that are phosphorylated by Src kinases, and the SH3 domain that binds Dyn2.	bind
10012	2	3261	7	11	NULL	0	NULL	cortactin	GP		phosphorylated by			C-terminal tyrosines		Src kinases	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_6_2162_s_90	12612086	(a) The diagram depicts different domains of the cortactin protein including the F-actin-binding sites, C-terminal tyrosines that are phosphorylated by Src kinases, and the SH3 domain that binds Dyn2.	bind
10013	3	3261	7	11	NULL	0	NULL	cortactin	GP		has					 F-actin-binding site	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_6_2162_s_90	12612086	(a) The diagram depicts different domains of the cortactin protein including the F-actin-binding sites, C-terminal tyrosines that are phosphorylated by Src kinases, and the SH3 domain that binds Dyn2.	bind
80202	1	3261	11	NULL	NULL	0	NULL	cortactin protein	Protein		binds to 			SH3 domain		Dyn2	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_6_2162_s_90	12612086	(a) The diagram depicts different domains of the cortactin protein including the F-actin-binding sites, C-terminal tyrosines that are phosphorylated by Src kinases, and the SH3 domain that binds Dyn2.	bind
80203	2	3261	11	NULL	NULL	0	NULL	 Src kinase	Protein		phosphorylate					cortactin protein			C-terminal tyrosines		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_6_2162_s_90	12612086	(a) The diagram depicts different domains of the cortactin protein including the F-actin-binding sites, C-terminal tyrosines that are phosphorylated by Src kinases, and the SH3 domain that binds Dyn2.	bind
80204	3	3261	11	NULL	NULL	0	NULL	cortactin protein	Protein		has binding site for					 F-actin					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_6_2162_s_90	12612086	(a) The diagram depicts different domains of the cortactin protein including the F-actin-binding sites, C-terminal tyrosines that are phosphorylated by Src kinases, and the SH3 domain that binds Dyn2.	bind
8053	1	3262	5	11	NULL	0	NULL	FBP17	GP		bind		strongly	EFC domain		PS	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_172_2_269_s_85	16418535	(A) The EFC domain of FBP17 strongly bound to PS and PI(4,5)P2.	bind
8054	2	3262	5	11	NULL	0	NULL	FBP17	GP		bind		strongly	EFC domain		PI(4,5)P2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_172_2_269_s_85	16418535	(A) The EFC domain of FBP17 strongly bound to PS and PI(4,5)P2.	bind
10014	1	3262	7	11	NULL	0	NULL	FBP17 	GP		bind		strongly	EFC		PS	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_172_2_269_s_85	16418535	(A) The EFC domain of FBP17 strongly bound to PS and PI(4,5)P2.	bind
10015	2	3262	7	11	NULL	0	NULL	FBP17	GP		bind		strongly	EFC		PI(4,5)P2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_172_2_269_s_85	16418535	(A) The EFC domain of FBP17 strongly bound to PS and PI(4,5)P2.	bind
80205	1	3262	11	NULL	NULL	0	NULL	FBP17	Protein		binds to 			EFC domain		PS	Protein				NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_2_269_s_85	16418535	(A) The EFC domain of FBP17 strongly bound to PS and PI(4,5)P2.	bind
80206	2	3262	11	NULL	NULL	0	NULL	FBP17	Protein		binds to 			EFC domain		PI(4,5)P2	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_2_269_s_85	16418535	(A) The EFC domain of FBP17 strongly bound to PS and PI(4,5)P2.	bind
8055	1	3264	5	11	NULL	0	NULL	ANS	Chemical		bind		efficiently			EF-Ts	GP	thermally denatured form of			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1764_7_1277_s_35	16781902	(A) The emission spectra of thermally denatured EF-Ts(wt) with ANS (EF-Ts + ANS(T))  and native EF-Ts(wt) with ANS (EF-Ts + ANS) show efficient binding of ANS into thermally  denatured form of EF-Ts.	bind
10016	1	3264	7	11	NULL	0	NULL	EF-Ts	GP	thermally denatured wt	bind		efficiently			ANS	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1764_7_1277_s_35	16781902	(A) The emission spectra of thermally denatured EF-Ts(wt) with ANS (EF-Ts + ANS(T))  and native EF-Ts(wt) with ANS (EF-Ts + ANS) show efficient binding of ANS into thermally  denatured form of EF-Ts.	bind
80207	1	3264	11	NULL	NULL	0	NULL	ANS	Chemical		binds to 					EF-Ts	Protein	thermally denatured 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1764_7_1277_s_35	16781902	(A) The emission spectra of thermally denatured EF-Ts(wt) with ANS (EF-Ts + ANS(T))  and native EF-Ts(wt) with ANS (EF-Ts + ANS) show efficient binding of ANS into thermally  denatured form of EF-Ts.	bind
8056	1	3265	5	11	NULL	0	NULL	MutL proteins	GP	mutant 	bind		equilibrium			ATP S	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_233_s_228	12887908	(A) The equilibrium binding of ATP S by MutL mutant proteins.	bind
10020	1	3265	7	11	NULL	0	NULL	ATP S	Chemical		bind		equilibrium			MutL	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_233_s_228	12887908	(A) The equilibrium binding of ATP S by MutL mutant proteins.	bind
80208	1	3265	11	NULL	NULL	0	NULL	MutL protein	Protein	mutant	binds to 					ATP S	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcell_12_1_233_s_228	12887908	(A) The equilibrium binding of ATP S by MutL mutant proteins.	bind
10042	1	3269	5	11	NULL	0	NULL	Npn-1	GP	deletion mutant	is expressed in					COS7 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_5_1093_s_65	9856464	(A) The indicated deletion mutants of Npn-1 were expressed in COS7 cells, and binding of the full length c-semD (10 nM c-semD-AP), the sema domain ligand (10 nM CAP-4), or the basic-rich carboxyl tail ligand (10 nM basic) was visualized by staining for bound AP.	bind
10043	2	3269	5	11	NULL	0	NULL	statement 1	Cell		bind					c-semD	Chemical	full length			NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_5_1093_s_65	9856464	(A) The indicated deletion mutants of Npn-1 were expressed in COS7 cells, and binding of the full length c-semD (10 nM c-semD-AP), the sema domain ligand (10 nM CAP-4), or the basic-rich carboxyl tail ligand (10 nM basic) was visualized by staining for bound AP.	bind
10044	3	3269	5	11	NULL	0	NULL	statement 1	Cell		bind					CAP-4	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_5_1093_s_65	9856464	(A) The indicated deletion mutants of Npn-1 were expressed in COS7 cells, and binding of the full length c-semD (10 nM c-semD-AP), the sema domain ligand (10 nM CAP-4), or the basic-rich carboxyl tail ligand (10 nM basic) was visualized by staining for bound AP.	bind
10045	4	3269	5	11	NULL	0	NULL	statement 1	Cell		bind					ligand	Chemical	basic-rich	carboxyl tail		NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_5_1093_s_65	9856464	(A) The indicated deletion mutants of Npn-1 were expressed in COS7 cells, and binding of the full length c-semD (10 nM c-semD-AP), the sema domain ligand (10 nM CAP-4), or the basic-rich carboxyl tail ligand (10 nM basic) was visualized by staining for bound AP.	bind
54240	5	3269	5	11	NULL	0	NULL	CAP-4	Chemical		is a type of					sema domain ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_5_1093_s_65	9856464	(A) The indicated deletion mutants of Npn-1 were expressed in COS7 cells, and binding of the full length c-semD (10 nM c-semD-AP), the sema domain ligand (10 nM CAP-4), or the basic-rich carboxyl tail ligand (10 nM basic) was visualized by staining for bound AP.	bind
10021	1	3269	7	11	NULL	0	NULL	c-semD	Chemical		bind					AP					NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_5_1093_s_65	9856464	(A) The indicated deletion mutants of Npn-1 were expressed in COS7 cells, and binding of the full length c-semD (10 nM c-semD-AP), the sema domain ligand (10 nM CAP-4), or the basic-rich carboxyl tail ligand (10 nM basic) was visualized by staining for bound AP.	bind
10022	2	3269	7	11	NULL	0	NULL	sema domain ligand	Chemical		bind					AP					NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_5_1093_s_65	9856464	(A) The indicated deletion mutants of Npn-1 were expressed in COS7 cells, and binding of the full length c-semD (10 nM c-semD-AP), the sema domain ligand (10 nM CAP-4), or the basic-rich carboxyl tail ligand (10 nM basic) was visualized by staining for bound AP.	bind
10023	3	3269	7	11	NULL	0	NULL	basic-rich carboxyl tail ligand	Chemical		bind					AP					NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_5_1093_s_65	9856464	(A) The indicated deletion mutants of Npn-1 were expressed in COS7 cells, and binding of the full length c-semD (10 nM c-semD-AP), the sema domain ligand (10 nM CAP-4), or the basic-rich carboxyl tail ligand (10 nM basic) was visualized by staining for bound AP.	bind
80209	1	3269	11	NULL	NULL	0	NULL	Npn-1	Protein	deletion mutants	were expressed in					COS7 cells	Cell				NULL		0	NULL	NULL	NULL	gw60_neuron_21_5_1093_s_65	9856464	(A) The indicated deletion mutants of Npn-1 were expressed in COS7 cells, and binding of the full length c-semD (10 nM c-semD-AP), the sema domain ligand (10 nM CAP-4), or the basic-rich carboxyl tail ligand (10 nM basic) was visualized by staining for bound AP.	bind
80210	2	3269	11	NULL	NULL	0	NULL	statement 1	Protein		binds to 					c-semD	Protein				NULL		0	NULL	NULL	NULL	gw60_neuron_21_5_1093_s_65	9856464	(A) The indicated deletion mutants of Npn-1 were expressed in COS7 cells, and binding of the full length c-semD (10 nM c-semD-AP), the sema domain ligand (10 nM CAP-4), or the basic-rich carboxyl tail ligand (10 nM basic) was visualized by staining for bound AP.	bind
80211	3	3269	11	NULL	NULL	0	NULL	CAP-4	Protein		is a type of 					sema domain ligand	Protein				NULL		0	NULL	NULL	NULL	gw60_neuron_21_5_1093_s_65	9856464	(A) The indicated deletion mutants of Npn-1 were expressed in COS7 cells, and binding of the full length c-semD (10 nM c-semD-AP), the sema domain ligand (10 nM CAP-4), or the basic-rich carboxyl tail ligand (10 nM basic) was visualized by staining for bound AP.	bind
80212	4	3269	11	NULL	NULL	0	NULL	Npn-1	Protein	deletion mutants	binds to 					sema domain ligand	Protein				NULL		0	NULL	NULL	NULL	gw60_neuron_21_5_1093_s_65	9856464	(A) The indicated deletion mutants of Npn-1 were expressed in COS7 cells, and binding of the full length c-semD (10 nM c-semD-AP), the sema domain ligand (10 nM CAP-4), or the basic-rich carboxyl tail ligand (10 nM basic) was visualized by staining for bound AP.	bind
80213	5	3269	11	NULL	NULL	0	NULL	Npn-1	Protein	deletion mutants	binds to 					basic-rich carboxyl tail ligand	Protein				NULL		0	NULL	NULL	NULL	gw60_neuron_21_5_1093_s_65	9856464	(A) The indicated deletion mutants of Npn-1 were expressed in COS7 cells, and binding of the full length c-semD (10 nM c-semD-AP), the sema domain ligand (10 nM CAP-4), or the basic-rich carboxyl tail ligand (10 nM basic) was visualized by staining for bound AP.	bind
8058	1	3270	5	11	NULL	0	NULL	migfilin	GP		bind					filamin	GP		C-terminal fragment		NULL		NULL	NULL	NULL	NULL	gw60_cell_113_1_37_s_192	12679033	(A) The interaction between migfilin and filamin C-terminal fragments containing different repeats were determined by yeast two-hybrid binding assays as described in the Experimental Procedures.	bind
10026	1	3270	7	11	NULL	0	NULL	migfilin	GP		bind					filamin	GP		C-terminal fragment		NULL		NULL	NULL	NULL	NULL	gw60_cell_113_1_37_s_192	12679033	(A) The interaction between migfilin and filamin C-terminal fragments containing different repeats were determined by yeast two-hybrid binding assays as described in the Experimental Procedures.	bind
80214	1	3270	11	NULL	NULL	0	NULL	migfilin	PartOfProtein	C-terminal fragments	interact with					filamin	PartOfProtein	C-terminal fragments			NULL		0	NULL	NULL	NULL	gw60_cell_113_1_37_s_192	12679033	(A) The interaction between migfilin and filamin C-terminal fragments containing different repeats were determined by yeast two-hybrid binding assays as described in the Experimental Procedures.	bind
80215	2	3270	11	NULL	NULL	0	NULL	statement 1	Process		determined by					yeast two-hybrid binding assays	ResearchActivity				NULL		0	NULL	NULL	NULL	gw60_cell_113_1_37_s_192	12679033	(A) The interaction between migfilin and filamin C-terminal fragments containing different repeats were determined by yeast two-hybrid binding assays as described in the Experimental Procedures.	bind
8059	1	3271	5	11	NULL	0	NULL	CD27	GP	intracellular region of 	does not bind					Ku	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_immunity_11_3_339_s_78	10514012	(A) The intracellular region of CD27 or that of CD30 does not bind to Ku.	bind
8060	2	3271	5	11	NULL	0	NULL	CD30	GP	intracellular region of	does not bind					Ku	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_immunity_11_3_339_s_78	10514012	(A) The intracellular region of CD27 or that of CD30 does not bind to Ku.	bind
10027	1	3271	7	11	NULL	0	NULL	CD27	GP	intracellular region of	does not bind					Ku	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_immunity_11_3_339_s_78	10514012	(A) The intracellular region of CD27 or that of CD30 does not bind to Ku.	bind
10028	2	3271	7	11	NULL	0	NULL	CD30	GP	intracellular region of	does not bind					Ku	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_immunity_11_3_339_s_78	10514012	(A) The intracellular region of CD27 or that of CD30 does not bind to Ku.	bind
80216	1	3271	11	NULL	NULL	0	NULL	CD27	Protein	intracellular region	does not bind to					Ku	Protein				NULL		0	NULL	NULL	NULL	gw60_immunity_11_3_339_s_78	10514012	(A) The intracellular region of CD27 or that of CD30 does not bind to Ku.	bind
80217	2	3271	11	NULL	NULL	0	NULL	CD30	Protein	intracellular region	does not bind to					Ku	Protein				NULL		0	NULL	NULL	NULL	gw60_immunity_11_3_339_s_78	10514012	(A) The intracellular region of CD27 or that of CD30 does not bind to Ku.	bind
8061	1	3272	5	11	NULL	0	NULL	AtMYB2	GP		bind					MBS-1 sequence	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genetics_149_2_479_s_123	9611167	(A) The left panel shows binding of AtMYB2 to both MBS-1 and MBS-2 sequences.	bind
8062	2	3272	5	11	NULL	0	NULL	AtMYB2	GP		bind					MBS-2 sequence	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genetics_149_2_479_s_123	9611167	(A) The left panel shows binding of AtMYB2 to both MBS-1 and MBS-2 sequences.	bind
10033	1	3272	7	11	NULL	0	NULL	AtMYB2	GP		bind					MBS-1 sequence	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genetics_149_2_479_s_123	9611167	(A) The left panel shows binding of AtMYB2 to both MBS-1 and MBS-2 sequences.	bind
10034	2	3272	7	11	NULL	0	NULL	AtMYB2	GP		bind					MBS-2 sequence	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genetics_149_2_479_s_123	9611167	(A) The left panel shows binding of AtMYB2 to both MBS-1 and MBS-2 sequences.	bind
80218	1	3272	11	NULL	NULL	0	NULL	AtMYB2	Protein		binds to 					MBS-1 sequences	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_genetics_149_2_479_s_123	9611167	(A) The left panel shows binding of AtMYB2 to both MBS-1 and MBS-2 sequences.	bind
80219	2	3272	11	NULL	NULL	0	NULL	AtMYB2	Protein		binds to 					MBS-2 sequence	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_genetics_149_2_479_s_123	9611167	(A) The left panel shows binding of AtMYB2 to both MBS-1 and MBS-2 sequences.	bind
80220	1	3274	11	NULL	NULL	0	NULL	FGFR1-IIIc	Protein	ligand binding regions	fused to					immunoglobulin 	Protein	 mouse	Fc fragment		NULL		0	NULL	NULL	NULL	gw70_development_131_14_3333_s_101	15201222	(A) The ligand binding regions of FGFR1-IIIc and FGFR2-IIIb (red) were fused to the  Fc fragment of a mouse immunoglobulin (blue) to generated secreted receptor versions.	bind
80221	2	3274	11	NULL	NULL	0	NULL	FGFR2-IIIb	Protein		fused to					immunoglobulin	Protein	mouse\t	Fc fragment		NULL		0	NULL	NULL	NULL	gw70_development_131_14_3333_s_101	15201222	(A) The ligand binding regions of FGFR1-IIIc and FGFR2-IIIb (red) were fused to the  Fc fragment of a mouse immunoglobulin (blue) to generated secreted receptor versions.	bind
8064	1	3275	5	11	NULL	0	NULL	ATP S	Chemical		bind					MutL	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_233_s_253	12887908	(A) The MutH protein enhanced ATP S binding by MutL.	bind
8065	2	3275	5	11	NULL	0	NULL	MutH protein	GP		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_233_s_253	12887908	(A) The MutH protein enhanced ATP S binding by MutL.	bind
10036	1	3275	7	11	NULL	0	NULL	ATP S	Chemical		bind					MutL	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_233_s_253	12887908	(A) The MutH protein enhanced ATP S binding by MutL.	bind
10037	2	3275	7	11	NULL	0	NULL	MutH	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_233_s_253	12887908	(A) The MutH protein enhanced ATP S binding by MutL.	bind
80222	1	3275	11	NULL	NULL	0	NULL	MutL	Protein		binds to 					ATP S	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcell_12_1_233_s_253	12887908	(A) The MutH protein enhanced ATP S binding by MutL.	bind
80223	2	3275	11	NULL	NULL	0	NULL	MutH protein	Protein		enhances					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_12_1_233_s_253	12887908	(A) The MutH protein enhanced ATP S binding by MutL.	bind
8063	1	3276	5	11	NULL	0	NULL	MutS protein	GP		bind					G/T mismatch DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_233_s_174	12887908	(A) The MutS protein (200 nM) was bound to G/T mismatch DNA in buffer B (marked  MutS ).	bind
10038	1	3276	7	11	NULL	0	NULL	MutS protein	GP		bind					G/T mismatch DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_233_s_174	12887908	(A) The MutS protein (200 nM) was bound to G/T mismatch DNA in buffer B (marked  MutS ).	bind
80224	1	3276	11	NULL	NULL	0	NULL	MutS protein	Protein		binds to 					DNA	NucleicAcidSubstance	in buffer B		G/T mismatch	NULL		0	NULL	NULL	NULL	gw60_molcell_12_1_233_s_174	12887908	(A) The MutS protein (200 nM) was bound to G/T mismatch DNA in buffer B (marked  MutS ).	bind
8066	1	3277	5	11	NULL	0	NULL	CNN	GP		bind			NH2-terminal domain		gamma-tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_5_757_s_60	12939255	(A) The NH2-terminal domain of CNN binds to gamma-tubulin.	bind
10039	1	3277	7	11	NULL	0	NULL	CNN	GP		bind			NH2-terminal domain		gamma-tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_5_757_s_60	12939255	(A) The NH2-terminal domain of CNN binds to gamma-tubulin.	bind
80225	1	3277	11	NULL	NULL	0	NULL	CNN	Protein		binds to 			NH2-terminal domain		gamma-tubulin	Protein				NULL		0	NULL	NULL	NULL	gw70_cellbiol_162_5_757_s_60	12939255	(A) The NH2-terminal domain of CNN binds to gamma-tubulin.	bind
8067	1	3278	5	11	NULL	0	NULL	NXF3 protein	GP		bind		specifically			Crm1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_397_s_109	11545741	(A) The NXF3 protein binds Crm1 specifically in a mammalian two-hybrid assay.	bind
10040	1	3278	7	11	NULL	0	NULL	NXF3	GP		bind		specifically			Crm1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_397_s_109	11545741	(A) The NXF3 protein binds Crm1 specifically in a mammalian two-hybrid assay.	bind
80226	1	3278	11	NULL	NULL	0	NULL	 NXF3 protein	Protein		binds to 					Crm1	Protein				NULL	mammalian two-hybrid assay	0	NULL	NULL	NULL	gw60_molcell_8_2_397_s_109	11545741	(A) The NXF3 protein binds Crm1 specifically in a mammalian two-hybrid assay.	bind
8068	1	3279	5	11	NULL	0	NULL	H5 peptide	GP		bind					SDS micelle	Chemical				NULL	in solution	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1545_1_153_s_117	11342041	(a) The overall structures of the H5 peptide bound to SDS micelle in solution, shown as a superposition of the backbone heavy atoms of the ten lowest energy structures, obtained by distance geometry and simulated annealing calculations.	bind
10041	1	3279	7	11	NULL	0	NULL	H5 peptide	GP		bind					SDS micelle	Chemical				NULL	in solution	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1545_1_153_s_117	11342041	(a) The overall structures of the H5 peptide bound to SDS micelle in solution, shown as a superposition of the backbone heavy atoms of the ten lowest energy structures, obtained by distance geometry and simulated annealing calculations.	bind
80227	1	3279	11	NULL	NULL	0	NULL	H5 peptide	PartOfProtein		binds to 					SDS micelle	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1545_1_153_s_117	11342041	(a) The overall structures of the H5 peptide bound to SDS micelle in solution, shown as a superposition of the backbone heavy atoms of the ten lowest energy structures, obtained by distance geometry and simulated annealing calculations.	bind
80228	1	3280	11	NULL	NULL	0	NULL	PAX3-FKHR chimeric transcription factor	Protein		generated by					t(2;13) translocation	MolecularProcess	 in alveolar rhabdomyosarcoma			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_14_5019_s_31	10866659	(A) The PAX3-FKHR chimeric transcription factor generated by the t(2;13) translocation in alveolar rhabdomyosarcoma (ARMS) retains the PAX3 paired box (PB) and homeodomain (HD) DNA binding motifs, has a disrupted forkhead (FD) DNA binding domain, and acquires a COOH-terminal FKHR-derived activation domain.	bind
80229	2	3280	11	NULL	NULL	0	NULL	alveolar rhabdomyosarcoma	Disease		is					ARMS	Disease				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_14_5019_s_31	10866659	(A) The PAX3-FKHR chimeric transcription factor generated by the t(2;13) translocation in alveolar rhabdomyosarcoma (ARMS) retains the PAX3 paired box (PB) and homeodomain (HD) DNA binding motifs, has a disrupted forkhead (FD) DNA binding domain, and acquires a COOH-terminal FKHR-derived activation domain.	bind
80230	3	3280	11	NULL	NULL	0	NULL	PAX3-FKHR chimeric transcription factor	Protein		retains					PAX3 paired box	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_14_5019_s_31	10866659	(A) The PAX3-FKHR chimeric transcription factor generated by the t(2;13) translocation in alveolar rhabdomyosarcoma (ARMS) retains the PAX3 paired box (PB) and homeodomain (HD) DNA binding motifs, has a disrupted forkhead (FD) DNA binding domain, and acquires a COOH-terminal FKHR-derived activation domain.	bind
80231	4	3280	11	NULL	NULL	0	NULL	PAX3-FKHR chimeric transcription factor	Protein		retains								homeodomain		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_14_5019_s_31	10866659	(A) The PAX3-FKHR chimeric transcription factor generated by the t(2;13) translocation in alveolar rhabdomyosarcoma (ARMS) retains the PAX3 paired box (PB) and homeodomain (HD) DNA binding motifs, has a disrupted forkhead (FD) DNA binding domain, and acquires a COOH-terminal FKHR-derived activation domain.	bind
80232	5	3280	11	NULL	NULL	0	NULL	PAX3 paired box	Protein		is					PB	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_14_5019_s_31	10866659	(A) The PAX3-FKHR chimeric transcription factor generated by the t(2;13) translocation in alveolar rhabdomyosarcoma (ARMS) retains the PAX3 paired box (PB) and homeodomain (HD) DNA binding motifs, has a disrupted forkhead (FD) DNA binding domain, and acquires a COOH-terminal FKHR-derived activation domain.	bind
80233	6	3280	11	NULL	NULL	0	NULL	homeodomain	PartOfProtein		is					HD	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_14_5019_s_31	10866659	(A) The PAX3-FKHR chimeric transcription factor generated by the t(2;13) translocation in alveolar rhabdomyosarcoma (ARMS) retains the PAX3 paired box (PB) and homeodomain (HD) DNA binding motifs, has a disrupted forkhead (FD) DNA binding domain, and acquires a COOH-terminal FKHR-derived activation domain.	bind
80234	7	3280	11	NULL	NULL	0	NULL	PAX3 paired box	PartOfProtein		is a type of 					DNA binding motif	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_14_5019_s_31	10866659	(A) The PAX3-FKHR chimeric transcription factor generated by the t(2;13) translocation in alveolar rhabdomyosarcoma (ARMS) retains the PAX3 paired box (PB) and homeodomain (HD) DNA binding motifs, has a disrupted forkhead (FD) DNA binding domain, and acquires a COOH-terminal FKHR-derived activation domain.	bind
80235	8	3280	11	NULL	NULL	0	NULL	homeodomain	PartOfProtein		is a type of 					DNA binding motif	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_14_5019_s_31	10866659	(A) The PAX3-FKHR chimeric transcription factor generated by the t(2;13) translocation in alveolar rhabdomyosarcoma (ARMS) retains the PAX3 paired box (PB) and homeodomain (HD) DNA binding motifs, has a disrupted forkhead (FD) DNA binding domain, and acquires a COOH-terminal FKHR-derived activation domain.	bind
80236	9	3280	11	NULL	NULL	0	NULL	PAX3-FKHR chimeric transcription factor	Protein		has 					forkhead DNA binding domain	PartOfProtein	disrupted			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_14_5019_s_31	10866659	(A) The PAX3-FKHR chimeric transcription factor generated by the t(2;13) translocation in alveolar rhabdomyosarcoma (ARMS) retains the PAX3 paired box (PB) and homeodomain (HD) DNA binding motifs, has a disrupted forkhead (FD) DNA binding domain, and acquires a COOH-terminal FKHR-derived activation domain.	bind
80237	10	3280	11	NULL	NULL	0	NULL	PAX3-FKHR chimeric transcription factor	Protein		acquires					FKHR-derived activation domain			COOH-terminal		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_14_5019_s_31	10866659	(A) The PAX3-FKHR chimeric transcription factor generated by the t(2;13) translocation in alveolar rhabdomyosarcoma (ARMS) retains the PAX3 paired box (PB) and homeodomain (HD) DNA binding motifs, has a disrupted forkhead (FD) DNA binding domain, and acquires a COOH-terminal FKHR-derived activation domain.	bind
8222	1	3281	5	11	NULL	0	NULL	peptide analogous to KCNK9	GP	wild-type	bind			N terminus		beta-COP	GP	rat;; brain			NULL		NULL	NULL	NULL	NULL	gw60_cell_111_4_577_s_170	12437930	(A) The peptide analogous to the wild-type N terminus of KCNK9 (and KCNK3) binds beta-COP from rat brain, while peptides with the NQ mutation do not (left).	bind
8223	2	3281	5	11	NULL	0	NULL	peptide analogous to KCNK3	GP	wild-type	bind			N terminus		beta-COP	GP	rat;; brain			NULL		NULL	NULL	NULL	NULL	gw60_cell_111_4_577_s_170	12437930	(A) The peptide analogous to the wild-type N terminus of KCNK9 (and KCNK3) binds beta-COP from rat brain, while peptides with the NQ mutation do not (left).	bind
8224	3	3281	5	11	NULL	0	NULL	peptide	GP	mutant	does not bind			NQ		beta-COP	GP	rat;; brain			NULL		NULL	NULL	NULL	NULL	gw60_cell_111_4_577_s_170	12437930	(A) The peptide analogous to the wild-type N terminus of KCNK9 (and KCNK3) binds beta-COP from rat brain, while peptides with the NQ mutation do not (left).	bind
10057	1	3281	7	11	NULL	0	NULL	peptide analogous to KCNK9	GP	wild-type	binds			N terminus		beta-COP	GP	rat;; brain			NULL		NULL	NULL	NULL	NULL	gw60_cell_111_4_577_s_170	12437930	(A) The peptide analogous to the wild-type N terminus of KCNK9 (and KCNK3) binds beta-COP from rat brain, while peptides with the NQ mutation do not (left).	bind
10058	2	3281	7	11	NULL	0	NULL	peptide analogous to KCNK3	GP	wild-type	bind			N terminus		beta-COP	GP	rat;; brain			NULL		NULL	NULL	NULL	NULL	gw60_cell_111_4_577_s_170	12437930	(A) The peptide analogous to the wild-type N terminus of KCNK9 (and KCNK3) binds beta-COP from rat brain, while peptides with the NQ mutation do not (left).	bind
10059	3	3281	7	11	NULL	0	NULL	peptides	GP	mutant	does not bind			NQ		beta-COP	GP	rat;; brain			NULL		NULL	NULL	NULL	NULL	gw60_cell_111_4_577_s_170	12437930	(A) The peptide analogous to the wild-type N terminus of KCNK9 (and KCNK3) binds beta-COP from rat brain, while peptides with the NQ mutation do not (left).	bind
80238	1	3281	11	NULL	NULL	0	NULL	 peptide analog 	PartOfProtein	wild-type KCNK9	binds to 			N terminus		beta-COP	Protein	rat brain			NULL		0	NULL	NULL	NULL	gw60_cell_111_4_577_s_170	12437930	(A) The peptide analogous to the wild-type N terminus of KCNK9 (and KCNK3) binds beta-COP from rat brain, while peptides with the NQ mutation do not (left).	bind
80239	2	3281	11	NULL	NULL	0	NULL	peptide analog	PartOfProtein	wild-type KCNK3	binds to 			N terminus		beta-COP	Protein	rat brain			NULL		0	NULL	NULL	NULL	gw60_cell_111_4_577_s_170	12437930	(A) The peptide analogous to the wild-type N terminus of KCNK9 (and KCNK3) binds beta-COP from rat brain, while peptides with the NQ mutation do not (left).	bind
80240	3	3281	11	NULL	NULL	0	NULL	peptides	PartOfProtein	NQ mutation	does not bind to					beta-COP	Protein	rat brain			NULL		0	NULL	NULL	NULL	gw60_cell_111_4_577_s_170	12437930	(A) The peptide analogous to the wild-type N terminus of KCNK9 (and KCNK3) binds beta-COP from rat brain, while peptides with the NQ mutation do not (left).	bind
80241	1	3283	11	NULL	NULL	0	NULL	GAL4 DNA binding site	PartOfProtein		is upstream of					SNRPN promoter	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_14_5107_s_224	10866667	(A) The reporter construct contains five copies of the GAL4 DNA binding site (5 x GAL) upstream of the  SNRPN promoter.	bind
8226	1	3288	5	11	NULL	0	NULL	p65	GP		bind		specifically			IkappaBalpha	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_3_1038_s_210	16428456	(A) The specificity of binding of p65 to IkappaBalpha and Bcl-X promoters.	bind
8227	2	3288	5	11	NULL	0	NULL	p65	GP		bind		specifically			Bcl-X	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_3_1038_s_210	16428456	(A) The specificity of binding of p65 to IkappaBalpha and Bcl-X promoters.	bind
10060	1	3288	7	11	NULL	0	NULL	p65 	GP		binds		specifically			IkappaBalpha	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_3_1038_s_210	16428456	(A) The specificity of binding of p65 to IkappaBalpha and Bcl-X promoters.	bind
10061	2	3288	7	11	NULL	0	NULL	p65	GP		binds		specifically			 Bcl-X 	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_3_1038_s_210	16428456	(A) The specificity of binding of p65 to IkappaBalpha and Bcl-X promoters.	bind
80242	1	3288	11	NULL	NULL	NULL	NULL	p65	Protein		binds to 					IkappaBalpha promoter	NucleicAcidSubstance				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_3_1038_s_210	16428456	(A) The specificity of binding of p65 to IkappaBalpha and Bcl-X promoters.	bind
80243	2	3288	11	NULL	NULL	0	NULL	p65	Protein		binds to 					Bcl-X promoter	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_3_1038_s_210	16428456	(A) The specificity of binding of p65 to IkappaBalpha and Bcl-X promoters.	bind
80244	1	3289	11	NULL	NULL	NULL	NULL	Pol II	Protein		binds to 					GAL10 promoter	NucleicAcidSubstance	induced			NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1301_s_133	12769853	(A) The strain was deleted for  spt20, and the binding of Pol II and of the Mediator were measured at the  GAL10 (Gal1p13i; see Experimental Procedures) promoter following induction.	bind
8378	1	3290	5	11	NULL	0	NULL	betaPIX	GP		bind			N-terminal SH3 domain		PAK	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6354_s_160	10938112	(A) The structural domains of betaPIX include its N-terminal SH3 domain, which binds PAK, a catalytic Dbl homology (DH) region promoting nucleotide exchange on Rac1, and a C-terminal region (bar) which was used to bind GIT1 (B) by overlay.	bind
8379	2	3290	5	11	NULL	0	NULL	betaPIX	GP	catalytic	promote			DH		Rac1	GP	nucleotide exchange on			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6354_s_160	10938112	(A) The structural domains of betaPIX include its N-terminal SH3 domain, which binds PAK, a catalytic Dbl homology (DH) region promoting nucleotide exchange on Rac1, and a C-terminal region (bar) which was used to bind GIT1 (B) by overlay.	bind
8380	3	3290	5	11	NULL	0	NULL	DH	GP		is					Dbl homology region	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6354_s_160	10938112	(A) The structural domains of betaPIX include its N-terminal SH3 domain, which binds PAK, a catalytic Dbl homology (DH) region promoting nucleotide exchange on Rac1, and a C-terminal region (bar) which was used to bind GIT1 (B) by overlay.	bind
8381	4	3290	5	11	NULL	0	NULL	betaPIX	GP		bind			C-terminal region		GIT1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6354_s_160	10938112	(A) The structural domains of betaPIX include its N-terminal SH3 domain, which binds PAK, a catalytic Dbl homology (DH) region promoting nucleotide exchange on Rac1, and a C-terminal region (bar) which was used to bind GIT1 (B) by overlay.	bind
10062	1	3290	7	11	NULL	0	NULL	betaPIX	GP		binds			N-terminal SH3 domain		PAK	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6354_s_160	10938112	(A) The structural domains of betaPIX include its N-terminal SH3 domain, which binds PAK, a catalytic Dbl homology (DH) region promoting nucleotide exchange on Rac1, and a C-terminal region (bar) which was used to bind GIT1 (B) by overlay.	bind
10063	2	3290	7	11	NULL	0	NULL	betaPIX	GP		binds			C-terminal region		GIT1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6354_s_160	10938112	(A) The structural domains of betaPIX include its N-terminal SH3 domain, which binds PAK, a catalytic Dbl homology (DH) region promoting nucleotide exchange on Rac1, and a C-terminal region (bar) which was used to bind GIT1 (B) by overlay.	bind
10064	3	3290	7	11	NULL	0	NULL	betaPIX	GP	catalytic	promote			 Dbl homology region		Rac1	GP	nucleotide exchange on			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6354_s_160	10938112	(A) The structural domains of betaPIX include its N-terminal SH3 domain, which binds PAK, a catalytic Dbl homology (DH) region promoting nucleotide exchange on Rac1, and a C-terminal region (bar) which was used to bind GIT1 (B) by overlay.	bind
12394	4	3290	7	11	NULL	0	NULL	Dbl homology region	GP		is					DH	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6354_s_160	10938112	(A) The structural domains of betaPIX include its N-terminal SH3 domain, which binds PAK, a catalytic Dbl homology (DH) region promoting nucleotide exchange on Rac1, and a C-terminal region (bar) which was used to bind GIT1 (B) by overlay.	bind
80245	1	3290	11	NULL	NULL	NULL	NULL	betaPIX	Protein		binds to 			N-terminal SH3 domain		PAK	Protein				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6354_s_160	10938112	(A) The structural domains of betaPIX include its N-terminal SH3 domain, which binds PAK, a catalytic Dbl homology (DH) region promoting nucleotide exchange on Rac1, and a C-terminal region (bar) which was used to bind GIT1 (B) by overlay.	bind
80246	2	3290	11	NULL	NULL	0	NULL	PAK	Protein		exchange		nucleotide	catalytic Dbl homology region		Rac1	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6354_s_160	10938112	(A) The structural domains of betaPIX include its N-terminal SH3 domain, which binds PAK, a catalytic Dbl homology (DH) region promoting nucleotide exchange on Rac1, and a C-terminal region (bar) which was used to bind GIT1 (B) by overlay.	bind
80247	3	3290	11	NULL	NULL	0	NULL	PAK	Protein	 C-terminal 	binds to 					GIT1	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6354_s_160	10938112	(A) The structural domains of betaPIX include its N-terminal SH3 domain, which binds PAK, a catalytic Dbl homology (DH) region promoting nucleotide exchange on Rac1, and a C-terminal region (bar) which was used to bind GIT1 (B) by overlay.	bind
8385	1	3291	5	11	NULL	0	NULL	DIAP1-BIR2	GP		bind					Skl peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_2_125_s_130	11818063	(A) The structure of a DIAP1-BIR2 (cyan) bound to a Skl peptide (green) is superimposed with that complexed with a Hid (pink) or Grim (orange) peptide.	bind
10065	1	3291	7	11	NULL	0	NULL	DIAP1-BIR2	GP		bind					Skl peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_2_125_s_130	11818063	(A) The structure of a DIAP1-BIR2 (cyan) bound to a Skl peptide (green) is superimposed with that complexed with a Hid (pink) or Grim (orange) peptide.	bind
80248	1	3291	11	NULL	NULL	0	NULL	DIAP1-BIR2	Protein		binds to 					Skl peptide	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_currbiol_12_2_125_s_130	11818063	(A) The structure of a DIAP1-BIR2 (cyan) bound to a Skl peptide (green) is superimposed with that complexed with a Hid (pink) or Grim (orange) peptide.	bind
80249	2	3291	11	NULL	NULL	0	NULL	Skl peptide	PartOfProtein		complexed with					Hid peptide	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_currbiol_12_2_125_s_130	11818063	(A) The structure of a DIAP1-BIR2 (cyan) bound to a Skl peptide (green) is superimposed with that complexed with a Hid (pink) or Grim (orange) peptide.	bind
80250	3	3291	11	NULL	NULL	0	NULL	Skl peptide	PartOfProtein		complexed with					Grim peptide	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_currbiol_12_2_125_s_130	11818063	(A) The structure of a DIAP1-BIR2 (cyan) bound to a Skl peptide (green) is superimposed with that complexed with a Hid (pink) or Grim (orange) peptide.	bind
8386	1	3292	5	11	NULL	0	NULL	PI3K	GP		bind					ATP	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_6_931_s_274	11136978	(A) The structure of PI3K  bound to ATP is traced through the C  s  as a black dotted line.	bind
10068	1	3292	7	11	NULL	0	NULL	PI3K 	GP		binds					ATP	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_6_931_s_274	11136978	(A) The structure of PI3K  bound to ATP is traced through the C  s  as a black dotted line.	bind
80251	1	3292	11	NULL	NULL	0	NULL	PI3K	Protein		binds to 					ATP	Chemical				NULL		0	NULL	NULL	NULL	gw60_cell_103_6_931_s_274	11136978	(A) The structure of PI3K  bound to ATP is traced through the C  s  as a black dotted line.	bind
8387	1	3293	5	11	NULL	0	NULL	tRNAVal	NucleicAcid		bind			CCA region					editing domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_103_5_793_s_147	11114335	(A) The tRNAVal CCA region is bound to  the editing domain.	bind
10069	1	3293	7	11	NULL	0	NULL	tRNAVal	NucleicAcid		binds			CCA region					editing domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_103_5_793_s_147	11114335	(A) The tRNAVal CCA region is bound to  the editing domain.	bind
80252	1	3293	11	NULL	NULL	0	NULL	tRNAVal	NucleicAcidSubstance	CCA region	binds to 								editing domain		NULL		0	NULL	NULL	NULL	gw60_cell_103_5_793_s_147	11114335	(A) The tRNAVal CCA region is bound to  the editing domain.	bind
8388	1	3294	5	11	NULL	0	NULL	FGFR2	GP	two-loop form of	bind		marginal affinity			FGF-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_367	10490614	(A) The two-loop form of FGFR2, deltaAD, binds to FGF-1 with marginal affinity and transmits weak downstream signals.	bind
8389	2	3294	5	11	NULL	0	NULL				bind		marginal affinity	deltaAD		FGF-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_367	10490614	(A) The two-loop form of FGFR2, deltaAD, binds to FGF-1 with marginal affinity and transmits weak downstream signals.	bind
10070	1	3294	7	11	NULL	0	NULL	FGFR2	GP	two-loop form of	binds		with marginal affinity	deltaAD		FGF-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_367	10490614	(A) The two-loop form of FGFR2, deltaAD, binds to FGF-1 with marginal affinity and transmits weak downstream signals.	bind
12401	2	3294	7	11	NULL	0	NULL	statement 1	GP		transmits					weak downstream signals					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_367	10490614	(A) The two-loop form of FGFR2, deltaAD, binds to FGF-1 with marginal affinity and transmits weak downstream signals.	bind
80253	1	3294	11	NULL	NULL	0	NULL	FGFR2	Protein	two-loop form	binds to 		marginal affinity			FGF-1	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_367	10490614	(A) The two-loop form of FGFR2, deltaAD, binds to FGF-1 with marginal affinity and transmits weak downstream signals.	bind
80254	2	3294	11	NULL	NULL	0	NULL	deltaAD	PartOfProtein		binds to 		marginal affinity			FGF-1	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_367	10490614	(A) The two-loop form of FGFR2, deltaAD, binds to FGF-1 with marginal affinity and transmits weak downstream signals.	bind
80255	3	3294	11	NULL	NULL	0	NULL	statement 1	Process		transmits					downstream signals	MolecularProcess	weak			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_367	10490614	(A) The two-loop form of FGFR2, deltaAD, binds to FGF-1 with marginal affinity and transmits weak downstream signals.	bind
80256	4	3294	11	NULL	NULL	0	NULL	statement 2	Process		transmits					downstream signals	MolecularProcess	weak			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_367	10490614	(A) The two-loop form of FGFR2, deltaAD, binds to FGF-1 with marginal affinity and transmits weak downstream signals.	bind
8392	1	3295	5	11	NULL	0	NULL	Vg1	GP		bind				LS	similar oocyte factors	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_235	15292452	(A) The Vg1 LS and Xcat2 3'UTR bind  to similar oocyte factors.	bind
8393	2	3295	5	11	NULL	0	NULL	Xcat2	GP		bind				3'UTR	similar oocyte factors	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_235	15292452	(A) The Vg1 LS and Xcat2 3'UTR bind  to similar oocyte factors.	bind
10071	1	3295	7	11	NULL	0	NULL	Vg1 	GP		bind				LS	oocyte factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_235	15292452	(A) The Vg1 LS and Xcat2 3'UTR bind  to similar oocyte factors.	bind
10072	2	3295	7	11	NULL	0	NULL	Xcat2 	GP		bind				3'UTR	oocyte factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_235	15292452	(A) The Vg1 LS and Xcat2 3'UTR bind  to similar oocyte factors.	bind
80257	1	3295	11	NULL	NULL	0	NULL	Vg1 LS	NucleicAcidSubstance		binds to 				3'UTR	oocyte factor	Protein				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_235	15292452	(A) The Vg1 LS and Xcat2 3'UTR bind  to similar oocyte factors.	bind
80258	2	3295	11	NULL	NULL	0	NULL	Xcat2	NucleicAcidSubstance		binds to 				3'UTR	oocyte factor	Protein				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_235	15292452	(A) The Vg1 LS and Xcat2 3'UTR bind  to similar oocyte factors.	bind
8394	1	3296	5	11	NULL	0	NULL	MIM	GP		bind		specifically	WH2 domain		G-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_3_453_s_113	15684034	(A) The WH2 domain of MIM specifically binds G-actin.	bind
10073	1	3296	7	11	NULL	0	NULL	MIM	GP		binds		specifically	WH2 domain		G-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_3_453_s_113	15684034	(A) The WH2 domain of MIM specifically binds G-actin.	bind
80259	1	3296	11	NULL	NULL	0	NULL	MIM	Protein		binds to 		specifically	WH2 domain		G-actin	Protein				NULL		0	NULL	NULL	NULL	gw70_cellbiol_168_3_453_s_113	15684034	(A) The WH2 domain of MIM specifically binds G-actin.	bind
8395	1	3297	5	11	NULL	0	NULL	BP-1	GP		bind					E1B 19K	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4390_s_131	10330179	(A) The yeast two-hybrid assay was used to demonstrate binding between BP-1 and E1B 19K.	bind
10074	1	3297	7	11	NULL	0	NULL	BP-1	GP		binds					E1B 19K	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4390_s_131	10330179	(A) The yeast two-hybrid assay was used to demonstrate binding between BP-1 and E1B 19K.	bind
80267	1	3297	11	NULL	NULL	0	NULL	BP-1	Protein		binds to 					E1B	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4390_s_131	10330179	(A) The yeast two-hybrid assay was used to demonstrate binding between BP-1 and E1B 19K.	bind
8396	1	3298	5	11	NULL	0	NULL	Yop-specific chaperone	GP		bind					cognate Yop protein	GP		translocation domain		NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_2_379_s_730	9618447	(A) The Yop-specific chaperone binds to the translocation domain of its cognate Yop protein.	bind
10075	1	3298	7	11	NULL	0	NULL	Yop-specific chaperone	GP		binds					Yop protein	GP		translocation domain		NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_2_379_s_730	9618447	(A) The Yop-specific chaperone binds to the translocation domain of its cognate Yop protein.	bind
80268	1	3298	11	NULL	NULL	0	NULL	Yop-specific chaperone	Protein		binds to 					cognate Yop protein	Protein		translocation domain		NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_2_379_s_730	9618447	(A) The Yop-specific chaperone binds to the translocation domain of its cognate Yop protein.	bind
8397	1	3299	5	11	NULL	0	NULL	THP-1 cell	Cell		bind					von Willebrand factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_5_905_s_236	11381078	(A) THP-1 cell binding to von Willebrand factor was examined in the presence of antibodies against the beta2 (7E4), alphaVbeta3 (LM609), or alphaIIbbeta3 (P2) integrins.	bind
10076	1	3299	7	11	NULL	0	NULL	THP-1 cell 	Cell		binds					von Willebrand factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_5_905_s_236	11381078	(A) THP-1 cell binding to von Willebrand factor was examined in the presence of antibodies against the beta2 (7E4), alphaVbeta3 (LM609), or alphaIIbbeta3 (P2) integrins.	bind
80269	1	3299	11	NULL	NULL	0	NULL	THP-1 cell	cell		binds to 					von Willebrand factor	Protein				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_5_905_s_236	11381078	(A) THP-1 cell binding to von Willebrand factor was examined in the presence of antibodies against the beta2 (7E4), alphaVbeta3 (LM609), or alphaIIbbeta3 (P2) integrins.	bind
8398	1	3302	5	11	NULL	0	NULL	poly-L-proline	AminoAcid		bind							mutant	Y5D		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_274	11294914	(A) Time course of polymerization of actin alone ( ) and with wild-type profilin ( ), poly-L-proline binding mutant Y5D ( ), and actin binding mutants Y79R ( ), K81F ( ), and P107W ( ).	bind
8399	2	3302	5	11	NULL	0	NULL	actin	GP		bind							mutant	Y79R		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_274	11294914	(A) Time course of polymerization of actin alone ( ) and with wild-type profilin ( ), poly-L-proline binding mutant Y5D ( ), and actin binding mutants Y79R ( ), K81F ( ), and P107W ( ).	bind
8400	3	3302	5	11	NULL	0	NULL	actin	GP		bind							mutant	K81F		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_274	11294914	(A) Time course of polymerization of actin alone ( ) and with wild-type profilin ( ), poly-L-proline binding mutant Y5D ( ), and actin binding mutants Y79R ( ), K81F ( ), and P107W ( ).	bind
8401	4	3302	5	11	NULL	0	NULL	actin	GP		bind							mutant	P107W		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_274	11294914	(A) Time course of polymerization of actin alone ( ) and with wild-type profilin ( ), poly-L-proline binding mutant Y5D ( ), and actin binding mutants Y79R ( ), K81F ( ), and P107W ( ).	bind
11725	1	3302	7	11	NULL	0	NULL	 poly-L-proline	AminoAcid		bind							mutant	Y5D		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_274	11294914	(A) Time course of polymerization of actin alone ( ) and with wild-type profilin ( ), poly-L-proline binding mutant Y5D ( ), and actin binding mutants Y79R ( ), K81F ( ), and P107W ( ).	bind
11726	2	3302	7	11	NULL	0	NULL	actin	GP		bind							mutant	Y79R		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_274	11294914	(A) Time course of polymerization of actin alone ( ) and with wild-type profilin ( ), poly-L-proline binding mutant Y5D ( ), and actin binding mutants Y79R ( ), K81F ( ), and P107W ( ).	bind
11727	3	3302	7	11	NULL	0	NULL	actin	GP		bind							mutant	K81F		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_274	11294914	(A) Time course of polymerization of actin alone ( ) and with wild-type profilin ( ), poly-L-proline binding mutant Y5D ( ), and actin binding mutants Y79R ( ), K81F ( ), and P107W ( ).	bind
11728	4	3302	7	11	NULL	0	NULL	actin	GP		bind							mutant	P107W		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_274	11294914	(A) Time course of polymerization of actin alone ( ) and with wild-type profilin ( ), poly-L-proline binding mutant Y5D ( ), and actin binding mutants Y79R ( ), K81F ( ), and P107W ( ).	bind
80270	1	3302	11	NULL	NULL	0	NULL	poly-L-proline	AminoAcid		binds to 					Y5D	PartOfProtein	 mutant			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_274	11294914	(A) Time course of polymerization of actin alone ( ) and with wild-type profilin ( ), poly-L-proline binding mutant Y5D ( ), and actin binding mutants Y79R ( ), K81F ( ), and P107W ( ).	bind
80271	2	3302	11	NULL	NULL	0	NULL	actin	Protein		binds to 					Y79R	PartOfProtein	mutant			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_274	11294914	(A) Time course of polymerization of actin alone ( ) and with wild-type profilin ( ), poly-L-proline binding mutant Y5D ( ), and actin binding mutants Y79R ( ), K81F ( ), and P107W ( ).	bind
80272	3	3302	11	NULL	NULL	0	NULL	actin	Protein		binds to 					K81F	PartOfProtein	mutant			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_274	11294914	(A) Time course of polymerization of actin alone ( ) and with wild-type profilin ( ), poly-L-proline binding mutant Y5D ( ), and actin binding mutants Y79R ( ), K81F ( ), and P107W ( ).	bind
80273	4	3302	11	NULL	NULL	0	NULL	actin	Protein		binds to 					P107W	PartOfProtein	mutant			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_274	11294914	(A) Time course of polymerization of actin alone ( ) and with wild-type profilin ( ), poly-L-proline binding mutant Y5D ( ), and actin binding mutants Y79R ( ), K81F ( ), and P107W ( ).	bind
8402	1	3303	5	11	NULL	0	NULL	GTP S	Chemical		bind					ARF	GP	bovine			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_6_387_s_43	9197239	(a) Time course of the binding of GTP  S to bovine ARF.	bind
10295	1	3303	7	11	NULL	0	NULL	GTP S 	Chemical		bind					ARF	GP	bovine			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_6_387_s_43	9197239	(a) Time course of the binding of GTP  S to bovine ARF.	bind
80274	1	3303	11	NULL	NULL	0	NULL	ARF	Protein	bovine	binds to 					GTP S	Chemical				NULL		0	NULL	NULL	NULL	gw60_currbiol_7_6_387_s_43	9197239	(a) Time course of the binding of GTP  S to bovine ARF.	bind
10299	1	3304	7	11	NULL	0	NULL	Trx-PreS	GP		bind					HBcAg-coated wells					NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_319_3_959_s_121	15184075	(A) Time-course of Trx-PreS binding to HBcAg-coated wells.	bind
80275	1	3304	11	NULL	NULL	0	NULL	Trx-PreS	Chemical		binds to 					wells	Thing	HBcAg-coated			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_319_3_959_s_121	15184075	(A) Time-course of Trx-PreS binding to HBcAg-coated wells.	bind
8403	1	3305	5	11	NULL	0	NULL	BMP2	GP		activate					p38 kinase	GP				NULL	C3H10T1/2	NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_545_s_174	12589053	(A) Time-dependent activation of p38 kinase by BMP2 in C3H10T1/2.	bind
10302	1	3305	7	11	NULL	0	NULL	BMP2	GP		activate					p38 kinase	GP				NULL	C3H10T1/2	NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_545_s_174	12589053	(A) Time-dependent activation of p38 kinase by BMP2 in C3H10T1/2.	bind
80276	1	3305	11	NULL	NULL	0	NULL	 BMP2	Protein		binds to 					p38 kinase	Protein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_2_545_s_174	12589053	(A) Time-dependent activation of p38 kinase by BMP2 in C3H10T1/2.	bind
8405	1	3306	5	11	NULL	0	NULL	GDP	Chemical		bind					RF3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_4_789_s_175	12419223	(A) Time-dependent exchange of RF3-bound [3]GDP to cold GDP is catalyzed by mutant and wild-type factors bound to the ribosome.	bind
8406	2	3306	5	11	NULL	0	NULL	statement 1	Chemical		is exchanged with					GDP	Chemical	cold 			NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_4_789_s_175	12419223	(A) Time-dependent exchange of RF3-bound [3]GDP to cold GDP is catalyzed by mutant and wild-type factors bound to the ribosome.	bind
8407	3	3306	5	11	NULL	0	NULL	factors	GP	wild-type	bind					ribosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_4_789_s_175	12419223	(A) Time-dependent exchange of RF3-bound [3]GDP to cold GDP is catalyzed by mutant and wild-type factors bound to the ribosome.	bind
8408	4	3306	5	11	NULL	0	NULL	factors	GP	mutant	bind					ribosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_4_789_s_175	12419223	(A) Time-dependent exchange of RF3-bound [3]GDP to cold GDP is catalyzed by mutant and wild-type factors bound to the ribosome.	bind
8409	5	3306	5	11	NULL	0	NULL	statement 3	Process		catalyze					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_4_789_s_175	12419223	(A) Time-dependent exchange of RF3-bound [3]GDP to cold GDP is catalyzed by mutant and wild-type factors bound to the ribosome.	bind
8410	6	3306	5	11	NULL	0	NULL	statement 4	Process		catalyze					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_4_789_s_175	12419223	(A) Time-dependent exchange of RF3-bound [3]GDP to cold GDP is catalyzed by mutant and wild-type factors bound to the ribosome.	bind
10303	1	3306	7	11	NULL	0	NULL	RF3-bound [3]GDP	GP		exchange					GDP	Chemical	cold			NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_4_789_s_175	12419223	(A) Time-dependent exchange of RF3-bound [3]GDP to cold GDP is catalyzed by mutant and wild-type factors bound to the ribosome.	bind
10304	2	3306	7	11	NULL	0	NULL	statement 1	Process		is catalysed by					factors bound to ribosome	CellComponent	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_4_789_s_175	12419223	(A) Time-dependent exchange of RF3-bound [3]GDP to cold GDP is catalyzed by mutant and wild-type factors bound to the ribosome.	bind
10305	3	3306	7	11	NULL	0	NULL	statement 1	Process		is catalysed by					factors bound to ribosome	CellComponent	wild-type			NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_4_789_s_175	12419223	(A) Time-dependent exchange of RF3-bound [3]GDP to cold GDP is catalyzed by mutant and wild-type factors bound to the ribosome.	bind
80281	1	3306	11	NULL	NULL	0	NULL	RF3	Protein		binds to 					GDP	Chemical				NULL		0	NULL	NULL	NULL	gw60_molcell_10_4_789_s_175	12419223	(A) Time-dependent exchange of RF3-bound [3]GDP to cold GDP is catalyzed by mutant and wild-type factors bound to the ribosome.	bind
80282	2	3306	11	NULL	NULL	0	NULL	wild-type factors	Thing		binds to 					ribosome	CellComponent				NULL		0	NULL	NULL	NULL	gw60_molcell_10_4_789_s_175	12419223	(A) Time-dependent exchange of RF3-bound [3]GDP to cold GDP is catalyzed by mutant and wild-type factors bound to the ribosome.	bind
80283	3	3306	11	NULL	NULL	0	NULL	mutant factors	Thing		binds to 					ribosome	CellComponent				NULL		0	NULL	NULL	NULL	gw60_molcell_10_4_789_s_175	12419223	(A) Time-dependent exchange of RF3-bound [3]GDP to cold GDP is catalyzed by mutant and wild-type factors bound to the ribosome.	bind
80284	4	3306	11	NULL	NULL	0	NULL	statement 1	Process		exchange to		Time-dependent			GDP	Chemical	cold			NULL		0	NULL	NULL	NULL	gw60_molcell_10_4_789_s_175	12419223	(A) Time-dependent exchange of RF3-bound [3]GDP to cold GDP is catalyzed by mutant and wild-type factors bound to the ribosome.	bind
80285	5	3306	11	NULL	NULL	0	NULL	statement 2	Thing		catalyzes					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_10_4_789_s_175	12419223	(A) Time-dependent exchange of RF3-bound [3]GDP to cold GDP is catalyzed by mutant and wild-type factors bound to the ribosome.	bind
80286	6	3306	11	NULL	NULL	0	NULL	statement 3	Thing		catalyzes					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_10_4_789_s_175	12419223	(A) Time-dependent exchange of RF3-bound [3]GDP to cold GDP is catalyzed by mutant and wild-type factors bound to the ribosome.	bind
8411	1	3307	5	11	NULL	0	NULL	melittin	GP		bind					POPC membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1665_1_29_s_148	15471568	(a) Time-resolved fluorescence intensity decay of melittin bound to POPC membranes.	bind
10308	1	3307	7	11	NULL	0	NULL	melittin	GP		bind					POPC membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1665_1_29_s_148	15471568	(a) Time-resolved fluorescence intensity decay of melittin bound to POPC membranes.	bind
80287	1	3307	11	NULL	NULL	0	NULL	melittin	Protein		binds to 					membranes	CellComponent	POPC 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1665_1_29_s_148	15471568	(a) Time-resolved fluorescence intensity decay of melittin bound to POPC membranes.	bind
8412	1	3308	5	11	NULL	0	NULL	GDP	Chemical		bind					NDP kinase B	GP	wild type;; human			NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_63_3_538_s_147	12606760	(A) to d4T triphosphate (green) bound  to the same protein in the 1.85  Ang  resolution structure determined by (Meyer et al.,  2000 ) in (B), to GDP bound to wild type human NDP kinase B (Morera et al., 1995 ).	bind
10314	1	3308	7	11	NULL	0	NULL	GDP	Chemical		bind					NDP kinase B 	GP	wild type;; human			NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_63_3_538_s_147	12606760	(A) to d4T triphosphate (green) bound  to the same protein in the 1.85  Ang  resolution structure determined by (Meyer et al.,  2000 ) in (B), to GDP bound to wild type human NDP kinase B (Morera et al., 1995 ).	bind
80288	1	3308	11	NULL	NULL	0	NULL	GDP	Chemical		binds to 					NDP kinase B 	Protein	wild type;;human			NULL		0	NULL	NULL	NULL	gw70_molpharmacol_63_3_538_s_147	12606760	(A) to d4T triphosphate (green) bound  to the same protein in the 1.85  Ang  resolution structure determined by (Meyer et al.,  2000 ) in (B), to GDP bound to wild type human NDP kinase B (Morera et al., 1995 ).	bind
8413	1	3312	5	11	NULL	0	NULL	pp F			bind					Sec complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_94_6_795_s_36	9753326	(A) To probe  the environment of pp F bound to the Sec complex by cross-linking, the indicated  lysine residues (K) were replaced by photoreactive lysine derivatives.	bind
10315	1	3312	7	11	NULL	0	NULL	pp F			bind					Sec complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_94_6_795_s_36	9753326	(A) To probe  the environment of pp F bound to the Sec complex by cross-linking, the indicated  lysine residues (K) were replaced by photoreactive lysine derivatives.	bind
80289	1	3312	11	NULL	NULL	0	NULL	pp&#945;F 	Protein		binds to 		 cross-linking			Sec complex	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_94_6_795_s_36	9753326	(A) To probe  the environment of pp F bound to the Sec complex by cross-linking, the indicated  lysine residues (K) were replaced by photoreactive lysine derivatives.	bind
80290	2	3312	11	NULL	NULL	0	NULL	 lysine residue	AminoAcid		is					K	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_cell_94_6_795_s_36	9753326	(A) To probe  the environment of pp F bound to the Sec complex by cross-linking, the indicated  lysine residues (K) were replaced by photoreactive lysine derivatives.	bind
80291	3	3312	11	NULL	NULL	0	NULL	 lysine residue	AminoAcid		replaced by					lysine derivative	AminoAcid	photoreactive			NULL		0	NULL	NULL	NULL	gw60_cell_94_6_795_s_36	9753326	(A) To probe  the environment of pp F bound to the Sec complex by cross-linking, the indicated  lysine residues (K) were replaced by photoreactive lysine derivatives.	bind
8414	1	3313	5	11	NULL	0	NULL	Tollip	GP		bind					IRAK	GP				NULL	HEK293T cells	NULL	NULL	NULL	NULL	gw70_febslett_575_1_136_s_123	15388348	(A) Tollip binds to IRAK in an immunoprecipitation  assay in HEK293T cells.	bind
10318	1	3313	7	11	NULL	0	NULL	Tollip	GP		binds					 IRAK	GP				NULL	HEK293T cells	NULL	NULL	NULL	NULL	gw70_febslett_575_1_136_s_123	15388348	(A) Tollip binds to IRAK in an immunoprecipitation  assay in HEK293T cells.	bind
80292	1	3313	11	NULL	NULL	0	NULL	Tollip	Protein		binds to 					IRAK	Protein				NULL	HEK293T cells	0	NULL	NULL	NULL	gw70_febslett_575_1_136_s_123	15388348	(A) Tollip binds to IRAK in an immunoprecipitation  assay in HEK293T cells.	bind
80293	2	3313	11	NULL	NULL	0	NULL	statement 1	Process		happens in					immunoprecipitation assay	ResearchActivity				NULL		0	NULL	NULL	NULL	gw70_febslett_575_1_136_s_123	15388348	(A) Tollip binds to IRAK in an immunoprecipitation  assay in HEK293T cells.	bind
8415	1	3314	5	11	NULL	0	NULL	HEK cells	Cell		transfected with					AChR cDNAs	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_17_1_157_s_134	8755487	(A) Total  -bgt binding to intact HEK cells transfected with the indicated AChR cDNAs.	bind
8416	2	3314	5	11	NULL	0	NULL	Total -bgt	Chemical		bind					statement 1	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuron_17_1_157_s_134	8755487	(A) Total  -bgt binding to intact HEK cells transfected with the indicated AChR cDNAs.	bind
10321	2	3314	7	11	NULL	0	NULL	Total -bgt	Chemical		bind					statement 1	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuron_17_1_157_s_134	8755487	(A) Total  -bgt binding to intact HEK cells transfected with the indicated AChR cDNAs.	bind
10323	1	3314	7	11	NULL	0	NULL	HEK cells	Cell		is transfected with					AChR cDNA	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_17_1_157_s_134	8755487	(A) Total  -bgt binding to intact HEK cells transfected with the indicated AChR cDNAs.	bind
80294	1	3314	11	NULL	NULL	0	NULL	HEK cells	cell	intact	transfected with					AChR cDNAs	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_neuron_17_1_157_s_134	8755487	(A) Total  -bgt binding to intact HEK cells transfected with the indicated AChR cDNAs.	bind
80295	2	3314	11	NULL	NULL	0	NULL	bgt	Protein		binds to 					statement 1	Cell				NULL		0	NULL	NULL	NULL	gw60_neuron_17_1_157_s_134	8755487	(A) Total  -bgt binding to intact HEK cells transfected with the indicated AChR cDNAs.	bind
8417	1	3315	5	11	NULL	0	NULL	rhotekin	GP		bind		specifically	Rho-binding domain		Rho	GP	activated			NULL	total cell extracts from mouse primary keratinocytes	NULL	NULL	NULL	NULL	gw60_cellbiol_156_1_137_s_33	11777936	(A) Total cell extracts from mouse primary keratinocytes under low calcium conditions and at various times of calcium exposure were incubated with beads coupled to the Rho-binding domain of rhotekin, which binds specifically to activated Rho.	bind
10344	1	3315	7	11	NULL	0	NULL	 rhotekin	GP		bind		specifically	Rho-binding domain 		Rho	GP	activated			NULL	cell extracts from mouse primary keratinocytes 	NULL	NULL	NULL	NULL	gw60_cellbiol_156_1_137_s_33	11777936	(A) Total cell extracts from mouse primary keratinocytes under low calcium conditions and at various times of calcium exposure were incubated with beads coupled to the Rho-binding domain of rhotekin, which binds specifically to activated Rho.	bind
80296	1	3315	11	NULL	NULL	0	NULL	rhotekin	Protein		has								Rho-binding domain 		NULL		0	NULL	NULL	NULL	gw60_cellbiol_156_1_137_s_33	11777936	(A) Total cell extracts from mouse primary keratinocytes under low calcium conditions and at various times of calcium exposure were incubated with beads coupled to the Rho-binding domain of rhotekin, which binds specifically to activated Rho.	bind
80297	2	3315	11	NULL	NULL	0	NULL	rhotekin	Protein		binds to 		specifically	Rho-binding domain 		Rho	Protein	activated			NULL		0	NULL	NULL	NULL	gw60_cellbiol_156_1_137_s_33	11777936	(A) Total cell extracts from mouse primary keratinocytes under low calcium conditions and at various times of calcium exposure were incubated with beads coupled to the Rho-binding domain of rhotekin, which binds specifically to activated Rho.	bind
8418	1	3316	5	11	NULL	0	NULL	Sfl1	GP		bind					FLO11	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_3981_s_355	12024012	(A) Tpk2 controls binding of Sfl1 and Flo8 to the  FLO11 promoter.	bind
8419	2	3316	5	11	NULL	0	NULL	Flo8	GP		bind					FLO11	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_3981_s_355	12024012	(A) Tpk2 controls binding of Sfl1 and Flo8 to the  FLO11 promoter.	bind
8420	3	3316	5	11	NULL	0	NULL	Tpk2	GP		control					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_3981_s_355	12024012	(A) Tpk2 controls binding of Sfl1 and Flo8 to the  FLO11 promoter.	bind
8421	4	3316	5	11	NULL	0	NULL	Tpk2	GP		control					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_3981_s_355	12024012	(A) Tpk2 controls binding of Sfl1 and Flo8 to the  FLO11 promoter.	bind
10345	1	3316	7	11	NULL	0	NULL	Sfl1	GP		bind					FLO11	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_3981_s_355	12024012	(A) Tpk2 controls binding of Sfl1 and Flo8 to the  FLO11 promoter.	bind
10346	2	3316	7	11	NULL	0	NULL	Flo8	GP		bind					FLO11	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_3981_s_355	12024012	(A) Tpk2 controls binding of Sfl1 and Flo8 to the  FLO11 promoter.	bind
10347	3	3316	7	11	NULL	0	NULL	Tpk2	GP		controls					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_3981_s_355	12024012	(A) Tpk2 controls binding of Sfl1 and Flo8 to the  FLO11 promoter.	bind
10348	4	3316	7	11	NULL	0	NULL	Tpk2	GP		controls					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_3981_s_355	12024012	(A) Tpk2 controls binding of Sfl1 and Flo8 to the  FLO11 promoter.	bind
80298	1	3316	11	NULL	NULL	0	NULL	Sfl1	Protein		binds to 					FLO11 promoter	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_12_3981_s_355	12024012	(A) Tpk2 controls binding of Sfl1 and Flo8 to the  FLO11 promoter.	bind
80299	2	3316	11	NULL	NULL	0	NULL	Flo8	Protein		binds to 					FLO11 promoter	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_12_3981_s_355	12024012	(A) Tpk2 controls binding of Sfl1 and Flo8 to the  FLO11 promoter.	bind
80300	3	3316	11	NULL	NULL	0	NULL	Tpk2	Protein		controls					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_12_3981_s_355	12024012	(A) Tpk2 controls binding of Sfl1 and Flo8 to the  FLO11 promoter.	bind
80301	4	3316	11	NULL	NULL	0	NULL	Tpk2	Protein		controls					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_12_3981_s_355	12024012	(A) Tpk2 controls binding of Sfl1 and Flo8 to the  FLO11 promoter.	bind
80302	1	3317	11	NULL	NULL	0	NULL	TS aceA	Protein		is					Transcriptional start site	NucleicAcidSubstance	aceA			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_7_2554_s_206	16547043	(A) Transcriptional start sites of  aceA and  aceB are designated TS aceA and TS aceB, respectively, and the RamB binding site is designated the 13-bp motif.	bind
80303	2	3317	11	NULL	NULL	0	NULL	TS aceB	NucleicAcidSubstance		is					Transcriptional start sites	NucleicAcidSubstance	aceB			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_7_2554_s_206	16547043	(A) Transcriptional start sites of  aceA and  aceB are designated TS aceA and TS aceB, respectively, and the RamB binding site is designated the 13-bp motif.	bind
80304	3	3317	11	NULL	NULL	0	NULL	RamB	Protein	binding site	is								13-bp motif		NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_7_2554_s_206	16547043	(A) Transcriptional start sites of  aceA and  aceB are designated TS aceA and TS aceB, respectively, and the RamB binding site is designated the 13-bp motif.	bind
8892	2	3318	5	11	NULL	0	NULL	SRP	Chemical		recognizes			10 hydrophobic residues		signal sequence	NucleicAcid	exposed sufficiently			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6704_s_92	11118205	(A) translation of the polypeptide from the emergence of the tag sequence from the ribosome until the signal sequence is exposed sufficiently to be recognized by SRP ( 10 hydrophobic residues); (B) SRP binding to the nascent chain - ribosome complex; (C) targeting of the ternary complex to the ER membrane; and (D) translocation of the N-terminal portion across the membrane.	bind
8896	1	3318	5	11	NULL	0	NULL	polypeptide	AminoAcid	translation of	occurs					from ribosome	Cell	from emergence of the tag sequence			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6704_s_92	11118205	(A) translation of the polypeptide from the emergence of the tag sequence from the ribosome until the signal sequence is exposed sufficiently to be recognized by SRP ( 10 hydrophobic residues); (B) SRP binding to the nascent chain - ribosome complex; (C) targeting of the ternary complex to the ER membrane; and (D) translocation of the N-terminal portion across the membrane.	bind
8898	3	3318	5	11	NULL	0	NULL	statement 1	Process		occurs untill					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6704_s_92	11118205	(A) translation of the polypeptide from the emergence of the tag sequence from the ribosome until the signal sequence is exposed sufficiently to be recognized by SRP ( 10 hydrophobic residues); (B) SRP binding to the nascent chain - ribosome complex; (C) targeting of the ternary complex to the ER membrane; and (D) translocation of the N-terminal portion across the membrane.	bind
8899	4	3318	5	11	NULL	0	NULL	SRP	Chemical		bind					nascent chain - ribosome complex	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6704_s_92	11118205	(A) translation of the polypeptide from the emergence of the tag sequence from the ribosome until the signal sequence is exposed sufficiently to be recognized by SRP ( 10 hydrophobic residues); (B) SRP binding to the nascent chain - ribosome complex; (C) targeting of the ternary complex to the ER membrane; and (D) translocation of the N-terminal portion across the membrane.	bind
8901	5	3318	5	11	NULL	0	NULL	ternary complex	GP		is targeted to					ER membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6704_s_92	11118205	(A) translation of the polypeptide from the emergence of the tag sequence from the ribosome until the signal sequence is exposed sufficiently to be recognized by SRP ( 10 hydrophobic residues); (B) SRP binding to the nascent chain - ribosome complex; (C) targeting of the ternary complex to the ER membrane; and (D) translocation of the N-terminal portion across the membrane.	bind
8902	6	3318	5	11	NULL	0	NULL				is translocated across			N-terminal portion		membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6704_s_92	11118205	(A) translation of the polypeptide from the emergence of the tag sequence from the ribosome until the signal sequence is exposed sufficiently to be recognized by SRP ( 10 hydrophobic residues); (B) SRP binding to the nascent chain - ribosome complex; (C) targeting of the ternary complex to the ER membrane; and (D) translocation of the N-terminal portion across the membrane.	bind
10349	1	3318	7	11	NULL	0	NULL	SRP	Chemical		bind					nascent chain - ribosome complex	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6704_s_92	11118205	(A) translation of the polypeptide from the emergence of the tag sequence from the ribosome until the signal sequence is exposed sufficiently to be recognized by SRP ( 10 hydrophobic residues); (B) SRP binding to the nascent chain - ribosome complex; (C) targeting of the ternary complex to the ER membrane; and (D) translocation of the N-terminal portion across the membrane.	bind
10350	2	3318	7	11	NULL	0	NULL	ternary complex	GP		is targeted to					ER membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6704_s_92	11118205	(A) translation of the polypeptide from the emergence of the tag sequence from the ribosome until the signal sequence is exposed sufficiently to be recognized by SRP ( 10 hydrophobic residues); (B) SRP binding to the nascent chain - ribosome complex; (C) targeting of the ternary complex to the ER membrane; and (D) translocation of the N-terminal portion across the membrane.	bind
10351	3	3318	7	11	NULL	0	NULL				translocates across the			N-terminal portion 		membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6704_s_92	11118205	(A) translation of the polypeptide from the emergence of the tag sequence from the ribosome until the signal sequence is exposed sufficiently to be recognized by SRP ( 10 hydrophobic residues); (B) SRP binding to the nascent chain - ribosome complex; (C) targeting of the ternary complex to the ER membrane; and (D) translocation of the N-terminal portion across the membrane.	bind
14950	4	3318	7	11	NULL	0	NULL	SRP	Chemical		recognizes			10 hydrophobic residues		Signal sequence	NucleicAcid	sufficiently exposed			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6704_s_92	11118205	(A) translation of the polypeptide from the emergence of the tag sequence from the ribosome until the signal sequence is exposed sufficiently to be recognized by SRP ( 10 hydrophobic residues); (B) SRP binding to the nascent chain - ribosome complex; (C) targeting of the ternary complex to the ER membrane; and (D) translocation of the N-terminal portion across the membrane.	bind
80305	1	3318	11	NULL	NULL	0	NULL	SRP	SmallMolecule		binds to 					ribosome complex	CellComponent	nascent chain			NULL		0	NULL	NULL	NULL	gw60_embo_19_24_6704_s_92	11118205	(A) translation of the polypeptide from the emergence of the tag sequence from the ribosome until the signal sequence is exposed sufficiently to be recognized by SRP ( 10 hydrophobic residues); (B) SRP binding to the nascent chain - ribosome complex; (C) targeting of the ternary complex to the ER membrane; and (D) translocation of the N-terminal portion across the membrane.	bind
80306	2	3318	11	NULL	NULL	0	NULL	ternary complex	PartOfProtein		targets to					ER membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw60_embo_19_24_6704_s_92	11118205	(A) translation of the polypeptide from the emergence of the tag sequence from the ribosome until the signal sequence is exposed sufficiently to be recognized by SRP ( 10 hydrophobic residues); (B) SRP binding to the nascent chain - ribosome complex; (C) targeting of the ternary complex to the ER membrane; and (D) translocation of the N-terminal portion across the membrane.	bind
80338	3	3318	11	NULL	NULL	0	NULL	nascent chain	NucleicAcidSubstance		complex with 					ribosome complex	CellComponent				NULL		0	NULL	NULL	NULL	gw60_embo_19_24_6704_s_92	11118205	(A) translation of the polypeptide from the emergence of the tag sequence from the ribosome until the signal sequence is exposed sufficiently to be recognized by SRP ( 10 hydrophobic residues); (B) SRP binding to the nascent chain - ribosome complex; (C) targeting of the ternary complex to the ER membrane; and (D) translocation of the N-terminal portion across the membrane.	bind
80339	4	3318	11	NULL	NULL	0	NULL	SRP	SmallMolecule		binds to 					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_embo_19_24_6704_s_92	11118205	(A) translation of the polypeptide from the emergence of the tag sequence from the ribosome until the signal sequence is exposed sufficiently to be recognized by SRP ( 10 hydrophobic residues); (B) SRP binding to the nascent chain - ribosome complex; (C) targeting of the ternary complex to the ER membrane; and (D) translocation of the N-terminal portion across the membrane.	bind
80340	5	3318	11	NULL	NULL	0	NULL	ternary complex	Protein		targets to					ER membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw60_embo_19_24_6704_s_92	11118205	(A) translation of the polypeptide from the emergence of the tag sequence from the ribosome until the signal sequence is exposed sufficiently to be recognized by SRP ( 10 hydrophobic residues); (B) SRP binding to the nascent chain - ribosome complex; (C) targeting of the ternary complex to the ER membrane; and (D) translocation of the N-terminal portion across the membrane.	bind
8422	1	3322	5	11	NULL	0	NULL	Ufd2	GP		bind					Cdc48	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_3_840_s_40	15240124	(A) Ufd2 binds with Cdc48.	bind
10352	1	3322	7	11	NULL	0	NULL	Ufd2	GP		binds					Cdc48	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_3_840_s_40	15240124	(A) Ufd2 binds with Cdc48.	bind
80341	1	3322	11	NULL	NULL	0	NULL	Ufd2	Protein		binds to 					Cdc48	Protein				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_3_840_s_40	15240124	(A) Ufd2 binds with Cdc48.	bind
8423	1	3323	5	11	NULL	0	NULL	RSK2	GP	unphosphorylated	bind					CBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_7089_s_114	11564891	(A) Unphosphorylated RSK2 binds to CBP. COS-1 cells were cotransfected with wild-type RSK2 and CBP and left untreated, treated with EGF, treated with EGF and PD98059, or cotransfected with PDK1.	bind
10353	1	3323	7	11	NULL	0	NULL	RSK2	GP	Unphosphorylated	binds to					CBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_7089_s_114	11564891	(A) Unphosphorylated RSK2 binds to CBP. COS-1 cells were cotransfected with wild-type RSK2 and CBP and left untreated, treated with EGF, treated with EGF and PD98059, or cotransfected with PDK1.	bind
80342	1	3323	11	NULL	NULL	0	NULL	RSK2	Protein	Unphosphorylated	binds to 					CBP	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_20_7089_s_114	11564891	(A) Unphosphorylated RSK2 binds to CBP. COS-1 cells were cotransfected with wild-type RSK2 and CBP and left untreated, treated with EGF, treated with EGF and PD98059, or cotransfected with PDK1.	bind
80343	2	3323	11	NULL	NULL	0	NULL	COS-1 cells	cell		transfected with					RSK2	Protein	wild-type			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_20_7089_s_114	11564891	(A) Unphosphorylated RSK2 binds to CBP. COS-1 cells were cotransfected with wild-type RSK2 and CBP and left untreated, treated with EGF, treated with EGF and PD98059, or cotransfected with PDK1.	bind
80344	3	3323	11	NULL	NULL	0	NULL	COS-1 cells	cell		transfected with					CBP	Protein	wild-type			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_20_7089_s_114	11564891	(A) Unphosphorylated RSK2 binds to CBP. COS-1 cells were cotransfected with wild-type RSK2 and CBP and left untreated, treated with EGF, treated with EGF and PD98059, or cotransfected with PDK1.	bind
80345	4	3323	11	NULL	NULL	0	NULL	statement 2	Process		occurs along with					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_20_7089_s_114	11564891	(A) Unphosphorylated RSK2 binds to CBP. COS-1 cells were cotransfected with wild-type RSK2 and CBP and left untreated, treated with EGF, treated with EGF and PD98059, or cotransfected with PDK1.	bind
80346	1	3324	11	NULL	NULL	0	NULL	PRE	CellComponent		is					preimmune serum	CellComponent				NULL		0	NULL	NULL	NULL	gw60_molcell_8_1_137_s_68	11511367	(A) Untreated interphase extract (Control), extract incubated with protein A beads bound to preimmune serum (PRE), and extract incubated with protein A beads bound to anti-X-Mre11 antibodies (X-Mre11 Ab) were probed with a polyclonal serum specific for X-Mre11 protein.	bind
80347	2	3324	11	NULL	NULL	0	NULL	extract	AnatomicalPart		incubated with					protein A	Protein	beads			NULL		0	NULL	NULL	NULL	gw60_molcell_8_1_137_s_68	11511367	(A) Untreated interphase extract (Control), extract incubated with protein A beads bound to preimmune serum (PRE), and extract incubated with protein A beads bound to anti-X-Mre11 antibodies (X-Mre11 Ab) were probed with a polyclonal serum specific for X-Mre11 protein.	bind
80348	3	3324	11	NULL	NULL	0	NULL	statement 2	AnatomicalPart		binds to 					preimmune serum	CellComponent				NULL		0	NULL	NULL	NULL	gw60_molcell_8_1_137_s_68	11511367	(A) Untreated interphase extract (Control), extract incubated with protein A beads bound to preimmune serum (PRE), and extract incubated with protein A beads bound to anti-X-Mre11 antibodies (X-Mre11 Ab) were probed with a polyclonal serum specific for X-Mre11 protein.	bind
80349	4	3324	11	NULL	NULL	0	NULL	statement 2	AnatomicalPart		binds to 					anti-X-Mre11 antibodies	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_8_1_137_s_68	11511367	(A) Untreated interphase extract (Control), extract incubated with protein A beads bound to preimmune serum (PRE), and extract incubated with protein A beads bound to anti-X-Mre11 antibodies (X-Mre11 Ab) were probed with a polyclonal serum specific for X-Mre11 protein.	bind
80350	5	3324	11	NULL	NULL	0	NULL	anti-X-Mre11 antibodies	Protein		is					X-Mre11 Ab	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_8_1_137_s_68	11511367	(A) Untreated interphase extract (Control), extract incubated with protein A beads bound to preimmune serum (PRE), and extract incubated with protein A beads bound to anti-X-Mre11 antibodies (X-Mre11 Ab) were probed with a polyclonal serum specific for X-Mre11 protein.	bind
8424	1	3325	5	11	NULL	0	NULL	Upc2p	GP		bind		directly			ERG2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6395_s_267	11533229	(A) Upc2p bound directly to the  ERG2 promoter in a SRE-dependent manner.	bind
8425	2	3325	5	11	NULL	0	NULL	statement 1	Process		is dependent on									SRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6395_s_267	11533229	(A) Upc2p bound directly to the  ERG2 promoter in a SRE-dependent manner.	bind
10354	1	3325	7	11	NULL	0	NULL	Upc2p	GP		bind		directly			ERG2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6395_s_267	11533229	(A) Upc2p bound directly to the  ERG2 promoter in a SRE-dependent manner.	bind
10355	2	3325	7	11	NULL	0	NULL	statement 1	Process		is dependent on					SRE	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6395_s_267	11533229	(A) Upc2p bound directly to the  ERG2 promoter in a SRE-dependent manner.	bind
80351	1	3325	11	NULL	NULL	0	NULL	Upc2p	Protein		binds to 		 directly			ERG2 promoter	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_19_6395_s_267	11533229	(A) Upc2p bound directly to the  ERG2 promoter in a SRE-dependent manner.	bind
80352	2	3325	11	NULL	NULL	0	NULL	statement 1	Process		depends on					SRE	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_19_6395_s_267	11533229	(A) Upc2p bound directly to the  ERG2 promoter in a SRE-dependent manner.	bind
8426	1	3329	5	11	NULL	0	NULL	Vimentin	GP		bind		preferentially			Fyn	GP		SH2 domain		NULL	in pervanadate-treated MC/9 mast cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_1_202_s_80	14511671	(A) Vimentin, pyruvate kinase, and SLP-76 in pervanadate-treated MC/9 mast cells  preferentially bound to the SH2 domain of Fyn.	bind
8427	2	3329	5	11	NULL	0	NULL	pyruvate kinase	GP		bind		preferentially			Fyn	GP		SH2 domain		NULL	in pervanadate-treated MC/9 mast cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_1_202_s_80	14511671	(A) Vimentin, pyruvate kinase, and SLP-76 in pervanadate-treated MC/9 mast cells  preferentially bound to the SH2 domain of Fyn.	bind
8428	3	3329	5	11	NULL	0	NULL	SLP-76	GP		bind		preferentially			Fyn	GP		SH2 domain		NULL	in pervanadate-treated MC/9 mast cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_1_202_s_80	14511671	(A) Vimentin, pyruvate kinase, and SLP-76 in pervanadate-treated MC/9 mast cells  preferentially bound to the SH2 domain of Fyn.	bind
10356	1	3329	7	11	NULL	0	NULL	Vimentin	GP		bind		preferentially			Fyn	GP		SH2 domain		NULL	pervanadate-treated MC/9 mast cells 	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_1_202_s_80	14511671	(A) Vimentin, pyruvate kinase, and SLP-76 in pervanadate-treated MC/9 mast cells  preferentially bound to the SH2 domain of Fyn.	bind
10357	2	3329	7	11	NULL	0	NULL	 pyruvate kinase	GP		bind		preferentially			Fyn	GP		SH2		NULL	pervanadate-treated MC/9 mast cells 	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_1_202_s_80	14511671	(A) Vimentin, pyruvate kinase, and SLP-76 in pervanadate-treated MC/9 mast cells  preferentially bound to the SH2 domain of Fyn.	bind
10358	3	3329	7	11	NULL	0	NULL	SLP-76 	GP		bind		preferentially			Fyn	GP		SH2		NULL	pervanadate-treated MC/9 mast cells 	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_1_202_s_80	14511671	(A) Vimentin, pyruvate kinase, and SLP-76 in pervanadate-treated MC/9 mast cells  preferentially bound to the SH2 domain of Fyn.	bind
80353	1	3329	11	NULL	NULL	0	NULL	Vimentin	Protein		binds to 		preferentially			Fyn	Protein		SH2 domain		NULL	pervanadate-treated MC/9 mast cells	0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_1_202_s_80	14511671	(A) Vimentin, pyruvate kinase, and SLP-76 in pervanadate-treated MC/9 mast cells  preferentially bound to the SH2 domain of Fyn.	bind
80354	2	3329	11	NULL	NULL	0	NULL	pyruvate kinase	Protein		binds to 		preferentially			Fyn	Protein		SH2 domain		NULL	pervanadate-treated MC/9 mast cells	0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_1_202_s_80	14511671	(A) Vimentin, pyruvate kinase, and SLP-76 in pervanadate-treated MC/9 mast cells  preferentially bound to the SH2 domain of Fyn.	bind
80355	3	3329	11	NULL	NULL	0	NULL	SLP-76	Protein		binds to 		preferentially			Fyn	Protein		SH2 domain		NULL	pervanadate-treated MC/9 mast cells	0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_1_202_s_80	14511671	(A) Vimentin, pyruvate kinase, and SLP-76 in pervanadate-treated MC/9 mast cells  preferentially bound to the SH2 domain of Fyn.	bind
8429	1	3330	5	11	NULL	0	NULL	Vps21p	GP		bind					Vac1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_3_159_s_65	10021387	(a) Vps21p binds Vac1p and Vps9p.	bind
8430	2	3330	5	11	NULL	0	NULL	Vps21p	GP		bind					Vps9p	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_3_159_s_65	10021387	(a) Vps21p binds Vac1p and Vps9p.	bind
10359	1	3330	7	11	NULL	0	NULL	Vps21p	GP		binds					Vac1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_3_159_s_65	10021387	(a) Vps21p binds Vac1p and Vps9p.	bind
10360	2	3330	7	11	NULL	0	NULL	Vps21p	GP		binds					Vps9p	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_3_159_s_65	10021387	(a) Vps21p binds Vac1p and Vps9p.	bind
80356	1	3330	11	NULL	NULL	0	NULL	Vps21p	Protein		binds to 					Vac1p	Protein				NULL		0	NULL	NULL	NULL	gw60_currbiol_9_3_159_s_65	10021387	(a) Vps21p binds Vac1p and Vps9p.	bind
80357	2	3330	11	NULL	NULL	0	NULL	Vps21p	Protein		binds to 					Vps9p	Protein				NULL		0	NULL	NULL	NULL	gw60_currbiol_9_3_159_s_65	10021387	(a) Vps21p binds Vac1p and Vps9p.	bind
8431	1	3333	5	11	NULL	0	NULL	cyclin A	GP		bind					p107 derivatives	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_292	9710622	(A) Western blot analysis of cyclin A bound to p107 derivatives.	bind
10361	1	3333	7	11	NULL	0	NULL	cyclin A	GP		bind					p107 derivatives	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_292	9710622	(A) Western blot analysis of cyclin A bound to p107 derivatives.	bind
80358	1	3333	11	NULL	NULL	0	NULL	cyclin A	Protein		binds to 					p107 derivative	Protein 				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_292	9710622	(A) Western blot analysis of cyclin A bound to p107 derivatives.	bind
8432	1	3334	5	11	NULL	0	NULL	tn-R2 antibody	GP		bind					TN-R	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_863_1_42_s_83	10773191	(A) Western blot analysis of tn-R2 and 473 HD antibody binding to TN-R.	bind
8433	2	3334	5	11	NULL	0	NULL	473 HD antibody	GP		bind					TN-R	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_863_1_42_s_83	10773191	(A) Western blot analysis of tn-R2 and 473 HD antibody binding to TN-R.	bind
10362	1	3334	7	11	NULL	0	NULL	tn-R2 	GP		bind					TN-R	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_863_1_42_s_83	10773191	(A) Western blot analysis of tn-R2 and 473 HD antibody binding to TN-R.	bind
10363	2	3334	7	11	NULL	0	NULL	473 HD antibody 	GP		bind					TN-R	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_863_1_42_s_83	10773191	(A) Western blot analysis of tn-R2 and 473 HD antibody binding to TN-R.	bind
80359	1	3334	11	NULL	NULL	NULL	NULL	tn-R2 antibody	PartOfProtein		binds to 					TN-R	Protein				NULL		NULL	NULL	NULL	NULL	gw60_brainres_863_1_42_s_83	10773191	(A) Western blot analysis of tn-R2 and 473 HD antibody binding to TN-R.	bind
80360	2	3334	11	NULL	NULL	0	NULL	473 HD antibody 	PartOfProtein		binds to 					TN-R	Protein				NULL		0	NULL	NULL	NULL	gw60_brainres_863_1_42_s_83	10773191	(A) Western blot analysis of tn-R2 and 473 HD antibody binding to TN-R.	bind
8434	1	3335	5	11	NULL	0	NULL	6His-CD45	GP		bind			C817S		GST proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_40_s_221	12922168	(A) Western blot of 6His-CD45C817S (upper panel) or 6His-Lck SH2 (lower panel) remaining bound to GST proteins.	bind
8435	2	3335	5	11	NULL	0	NULL	6His-Lck	GP		bind			SH2		GST proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_40_s_221	12922168	(A) Western blot of 6His-CD45C817S (upper panel) or 6His-Lck SH2 (lower panel) remaining bound to GST proteins.	bind
10364	1	3335	7	11	NULL	0	NULL	6His-CD45 	GP		bind			C817S		GST protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_40_s_221	12922168	(A) Western blot of 6His-CD45C817S (upper panel) or 6His-Lck SH2 (lower panel) remaining bound to GST proteins.	bind
10365	2	3335	7	11	NULL	0	NULL	6His-Lck 	GP		bind			SH2 		GST protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_40_s_221	12922168	(A) Western blot of 6His-CD45C817S (upper panel) or 6His-Lck SH2 (lower panel) remaining bound to GST proteins.	bind
80361	1	3335	11	NULL	NULL	0	NULL	6His-CD45C817S	PartOfProtein		binds to 					GST proteins	Protein				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_40_s_221	12922168	(A) Western blot of 6His-CD45C817S (upper panel) or 6His-Lck SH2 (lower panel) remaining bound to GST proteins.	bind
80362	2	3335	11	NULL	NULL	0	NULL	6His-Lck SH2	PartOfProtein		binds to 					GST proteins	Protein				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_40_s_221	12922168	(A) Western blot of 6His-CD45C817S (upper panel) or 6His-Lck SH2 (lower panel) remaining bound to GST proteins.	bind
8436	1	3336	5	11	NULL	0	NULL	6His-Lck	GP		bind			SH2		GST proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_40_s_204	12922168	(A) Western blot of 6His-Lck SH2 remaining bound to various GST proteins (indicated above the blot) detected with an anti-6His antibody.	bind
11729	1	3336	7	11	NULL	0	NULL	 6His-Lck	GP		bind			SH2		GST protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_40_s_204	12922168	(A) Western blot of 6His-Lck SH2 remaining bound to various GST proteins (indicated above the blot) detected with an anti-6His antibody.	bind
80363	1	3336	11	NULL	NULL	0	NULL	6His-Lck SH2	PartOfProtein		binds to 					GST proteins	Protein				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_40_s_204	12922168	(A) Western blot of 6His-Lck SH2 remaining bound to various GST proteins (indicated above the blot) detected with an anti-6His antibody.	bind
80364	2	3336	11	NULL	NULL	0	NULL	statement 1	Process		detected with					anti-6His antibody	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_40_s_204	12922168	(A) Western blot of 6His-Lck SH2 remaining bound to various GST proteins (indicated above the blot) detected with an anti-6His antibody.	bind
8437	1	3337	5	11	NULL	0	NULL	JAS	Chemical		alter					actin	GP	distribution of			NULL	in T. gondii	NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
8438	2	3337	5	11	NULL	0	NULL	JAS	Chemical		does not affect					microtubules 	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
8439	3	3337	5	11	NULL	0	NULL	JAS	Chemical		does not affect					reticular network filaments	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
8440	4	3337	5	11	NULL	0	NULL	JAS	Chemical		did not affect					myosin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
54210	5	3337	5	11	NULL	0	NULL	microtubules	CellComponent		is					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
54211	6	3337	5	11	NULL	0	NULL	IMC1	CellComponent		is					reticular network filaments	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
54212	7	3337	5	11	NULL	0	NULL	TgMyoA tail	GP		is					myosin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
10366	1	3337	7	11	NULL	0	NULL	JAS	Chemical		alters					actin	GP	distribution of			NULL	T. gondii 	NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
10367	2	3337	7	11	NULL	0	NULL	JAS	Chemical		does not affect					microtubules	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
10368	3	3337	7	11	NULL	0	NULL	JAS	Chemical		does not affect					 reticular network filaments 	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
10369	4	3337	7	11	NULL	0	NULL	JAS	Chemical		does not affect					myosin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
10370	5	3337	7	11	NULL	0	NULL	microtubule	CellComponent		is					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
10371	6	3337	7	11	NULL	0	NULL	reticular network filaments 	CellComponent		is					IMCI	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
10372	7	3337	7	11	NULL	0	NULL	myosin	GP		is					TgMyoA tail	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
80365	1	3337	11	NULL	NULL	0	NULL	tubulin	CellComponent		is a type of 					microtubules	CellComponent				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
80366	2	3337	11	NULL	NULL	NULL	NULL	IMC1	CellComponent		is a type of 					reticular network filaments	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
80367	3	3337	11	NULL	NULL	0	NULL	TgMyoA	Protein		is a type of 					myosin	Protein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
80368	4	3337	11	NULL	NULL	0	NULL	JAS	Chemical		alters		distribution of			actin	Protein	T. gondii			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
80369	5	3337	11	NULL	NULL	0	NULL	JAS	Chemical		does not affect					microtubules	CellComponent				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
80370	6	3337	11	NULL	NULL	0	NULL	JAS	Chemical		does not affect					reticular network filaments	CellComponent				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
80371	7	3337	11	NULL	NULL	0	NULL	JAS	Chemical		does not affect					myosin	CellComponent				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_2_396_s_144	12589042	(A) Wide-field fluorescence microscopy demonstrates that JAS alters the distribution of actin in  T. gondii but does not affect microtubules (tubulin), reticular network filaments (IMC1), or myosin (TgMyoA tail).	bind
80372	1	3338	11	NULL	NULL	0	NULL	Y79R ( )	PartOfProtein		is a type of 					actin binding mutant	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_211	11294914	(A) Wild-type ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107W ( ), P107Y ( ), A111E ( ), and minimally stable mutant C89S ( ).	bind
80373	2	3338	11	NULL	NULL	0	NULL	K81E ( )	PartOfProtein		is a type of 					actin binding mutant	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_211	11294914	(A) Wild-type ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107W ( ), P107Y ( ), A111E ( ), and minimally stable mutant C89S ( ).	bind
80374	3	3338	11	NULL	NULL	0	NULL	K81Y ( )	PartOfProtein		is a type of 					actin binding mutant	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_211	11294914	(A) Wild-type ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107W ( ), P107Y ( ), A111E ( ), and minimally stable mutant C89S ( ).	bind
80375	4	3338	11	NULL	NULL	0	NULL	P107W ( )	PartOfProtein		is a type of 					actin binding mutants	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_211	11294914	(A) Wild-type ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107W ( ), P107Y ( ), A111E ( ), and minimally stable mutant C89S ( ).	bind
80376	5	3338	11	NULL	NULL	0	NULL	P107Y ( )	PartOfProtein		is a type of 					actin binding mutant	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_211	11294914	(A) Wild-type ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107W ( ), P107Y ( ), A111E ( ), and minimally stable mutant C89S ( ).	bind
80377	6	3338	11	NULL	NULL	0	NULL	A111E ( )	PartOfProtein		is a type of 					actin binding mutant	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_4_1161_s_211	11294914	(A) Wild-type ( ) and actin binding mutants Y79R ( ), K81E ( ), K81Y ( ), P107W ( ), P107Y ( ), A111E ( ), and minimally stable mutant C89S ( ).	bind
8441	1	3339	5	11	NULL	0	NULL	s7betaCD	Chemical		bind					alphaHL	GP	WT			NULL		NULL	NULL	NULL	NULL	gw60_science_291_5504_636_s_32	11158673	(A) wild-type (WT), (B) M113N, and (C) N139Q alphaHL; ( D to  F) binding of s7betaCD to (D) WT, (E) M113N, and (F) N139Q alphaHL.	bind
8442	2	3339	5	11	NULL	0	NULL	s7betaCD	Chemical		bind					alphaHL	GP		M113N		NULL		NULL	NULL	NULL	NULL	gw60_science_291_5504_636_s_32	11158673	(A) wild-type (WT), (B) M113N, and (C) N139Q alphaHL; ( D to  F) binding of s7betaCD to (D) WT, (E) M113N, and (F) N139Q alphaHL.	bind
8443	3	3339	5	11	NULL	0	NULL	s7betaCD	Chemical		bind					alphaHL	GP		N139Q		NULL		NULL	NULL	NULL	NULL	gw60_science_291_5504_636_s_32	11158673	(A) wild-type (WT), (B) M113N, and (C) N139Q alphaHL; ( D to  F) binding of s7betaCD to (D) WT, (E) M113N, and (F) N139Q alphaHL.	bind
10373	1	3339	7	11	NULL	0	NULL	s7betaCD	Chemical		bind					alphaHL	GP	WT			NULL		NULL	NULL	NULL	NULL	gw60_science_291_5504_636_s_32	11158673	(A) wild-type (WT), (B) M113N, and (C) N139Q alphaHL; ( D to  F) binding of s7betaCD to (D) WT, (E) M113N, and (F) N139Q alphaHL.	bind
10374	2	3339	7	11	NULL	0	NULL	s7betaCD	Chemical		bind					alphaHL	GP		N139Q		NULL		NULL	NULL	NULL	NULL	gw60_science_291_5504_636_s_32	11158673	(A) wild-type (WT), (B) M113N, and (C) N139Q alphaHL; ( D to  F) binding of s7betaCD to (D) WT, (E) M113N, and (F) N139Q alphaHL.	bind
10375	3	3339	7	11	NULL	0	NULL	s7betaCD	Chemical		bind					alphaHL	GP		M113N		NULL		NULL	NULL	NULL	NULL	gw60_science_291_5504_636_s_32	11158673	(A) wild-type (WT), (B) M113N, and (C) N139Q alphaHL; ( D to  F) binding of s7betaCD to (D) WT, (E) M113N, and (F) N139Q alphaHL.	bind
8444	1	3342	5	11	NULL	0	NULL	Siah-1 protein	GP	wild-type	bind					DCC	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_724_s_171	9858595	(A) Wild-type and mutant Siah-1 proteins bind to DCC in vitro.	bind
8445	2	3342	5	11	NULL	0	NULL	Siah-1 protein	GP	mutant	bind					DCC	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_724_s_171	9858595	(A) Wild-type and mutant Siah-1 proteins bind to DCC in vitro.	bind
10376	1	3342	7	11	NULL	0	NULL	Siah-1 protein	GP	Wild-type 	bind					DCC	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_724_s_171	9858595	(A) Wild-type and mutant Siah-1 proteins bind to DCC in vitro.	bind
10377	2	3342	7	11	NULL	0	NULL	Siah-1 protein	GP	mutant	bind					DCC	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_724_s_171	9858595	(A) Wild-type and mutant Siah-1 proteins bind to DCC in vitro.	bind
80378	1	3342	11	NULL	NULL	NULL	NULL	Siah-1 protein	Protein	Wild-type	binds to 					DCC	Protein				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_724_s_171	9858595	(A) Wild-type and mutant Siah-1 proteins bind to DCC in vitro.	bind
80379	2	3342	11	NULL	NULL	0	NULL	Siah-1 protein	Protein	mutant	binds to 					DCC	Protein				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_19_1_724_s_171	9858595	(A) Wild-type and mutant Siah-1 proteins bind to DCC in vitro.	bind
8446	1	3343	5	11	NULL	0	NULL	MCAK	GP	wild-type	bind					MT lattice	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_169_3_391_s_108	15883193	(A) Wild-type MCAK binds MT lattice in the absence of ATP (left, lane 1).	bind
8447	2	3343	5	11	NULL	0	NULL	statement 1	Process		in the abscence of					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_169_3_391_s_108	15883193	(A) Wild-type MCAK binds MT lattice in the absence of ATP (left, lane 1).	bind
10378	1	3343	7	11	NULL	0	NULL	MCAK	GP	wild-type	binds					MT lattice	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_169_3_391_s_108	15883193	(A) Wild-type MCAK binds MT lattice in the absence of ATP (left, lane 1).	bind
10379	2	3343	7	11	NULL	0	NULL	statement 1	Process		occurs in the absence of					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_169_3_391_s_108	15883193	(A) Wild-type MCAK binds MT lattice in the absence of ATP (left, lane 1).	bind
80380	1	3343	11	NULL	NULL	0	NULL	MCAK	Protein	Wild-type	binds to 					MT lattice	CellComponent				NULL	in the absence of ATP	0	NULL	NULL	NULL	gw70_cellbiol_169_3_391_s_108	15883193	(A) Wild-type MCAK binds MT lattice in the absence of ATP (left, lane 1).	bind
80381	1	3345	11	NULL	NULL	0	NULL	eIF4G1	Protein	yeast	binds to 					Pab1p	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_51_s_179	9418852	(A) with reasonable affinity, we next investigated their ability to associate with the Pab1p-binding regions of yeast eIF4G1 and eIF4G2.	bind
80382	2	3345	11	NULL	NULL	0	NULL	eIF4G2	Protein	yeast	binds to 					Pab1p	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_51_s_179	9418852	(A) with reasonable affinity, we next investigated their ability to associate with the Pab1p-binding regions of yeast eIF4G1 and eIF4G2.	bind
8448	1	3346	5	11	NULL	0	NULL	PlexB	GP		bind					Rac1	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_1_39_s_86	11604137	(A) Within PlexB 3 region, PlexB binds to Rac1 and Rac2 but not to other Rho family GTPases.	bind
8449	2	3346	5	11	NULL	0	NULL	PlexB	GP		bind					Rac2	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_1_39_s_86	11604137	(A) Within PlexB 3 region, PlexB binds to Rac1 and Rac2 but not to other Rho family GTPases.	bind
8450	3	3346	5	11	NULL	0	NULL	PlexB	GP		does not bind					Rho family GTPases	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_1_39_s_86	11604137	(A) Within PlexB 3 region, PlexB binds to Rac1 and Rac2 but not to other Rho family GTPases.	bind
10380	1	3346	7	11	NULL	0	NULL	PlexB	GP		bind					Rac1	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_1_39_s_86	11604137	(A) Within PlexB 3 region, PlexB binds to Rac1 and Rac2 but not to other Rho family GTPases.	bind
10381	2	3346	7	11	NULL	0	NULL	PlexB	GP		bind					Rac2	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_1_39_s_86	11604137	(A) Within PlexB 3 region, PlexB binds to Rac1 and Rac2 but not to other Rho family GTPases.	bind
10382	3	3346	7	11	NULL	0	NULL	PlexB	GP		does not bind					Rho family GTPases	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_1_39_s_86	11604137	(A) Within PlexB 3 region, PlexB binds to Rac1 and Rac2 but not to other Rho family GTPases.	bind
80383	1	3346	11	NULL	NULL	0	NULL	PlexB	Protein		binds to 					Rac1	Protein				NULL		0	NULL	NULL	NULL	gw60_neuron_32_1_39_s_86	11604137	(A) Within PlexB 3 region, PlexB binds to Rac1 and Rac2 but not to other Rho family GTPases.	bind
80384	2	3346	11	NULL	NULL	0	NULL	PlexB	Protein		binds to 					Rac2	Protein				NULL		0	NULL	NULL	NULL	gw60_neuron_32_1_39_s_86	11604137	(A) Within PlexB 3 region, PlexB binds to Rac1 and Rac2 but not to other Rho family GTPases.	bind
80385	3	3346	11	NULL	NULL	0	NULL	Rac1	Protein		is a type of 					Rho family GTPase	Protein				NULL		0	NULL	NULL	NULL	gw60_neuron_32_1_39_s_86	11604137	(A) Within PlexB 3 region, PlexB binds to Rac1 and Rac2 but not to other Rho family GTPases.	bind
80386	4	3346	11	NULL	NULL	0	NULL	Rac2	Protein		is a type of 					Rho family GTPase	Protein				NULL		0	NULL	NULL	NULL	gw60_neuron_32_1_39_s_86	11604137	(A) Within PlexB 3 region, PlexB binds to Rac1 and Rac2 but not to other Rho family GTPases.	bind
8451	1	3347	5	11	NULL	0	NULL	PC4	Chemical		bind					DNA bubble substrates					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_13_6084_s_207	15199162	(A) XPG protein enhances PC4 binding to DNA bubble substrates.	bind
8452	2	3347	5	11	NULL	0	NULL	XPG protein	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_13_6084_s_207	15199162	(A) XPG protein enhances PC4 binding to DNA bubble substrates.	bind
10383	1	3347	7	11	NULL	0	NULL	PC4	Chemical		bind					DNA bubble substrates					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_13_6084_s_207	15199162	(A) XPG protein enhances PC4 binding to DNA bubble substrates.	bind
10384	2	3347	7	11	NULL	0	NULL	 XPG protein	GP		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_13_6084_s_207	15199162	(A) XPG protein enhances PC4 binding to DNA bubble substrates.	bind
80387	1	3347	11	NULL	NULL	0	NULL	PC4	Protein		binds to 					DNA bubble	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_13_6084_s_207	15199162	(A) XPG protein enhances PC4 binding to DNA bubble substrates.	bind
80388	2	3347	11	NULL	NULL	0	NULL	XPG protein	Protein		enhances					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_13_6084_s_207	15199162	(A) XPG protein enhances PC4 binding to DNA bubble substrates.	bind
8453	1	3348	5	11	NULL	0	NULL	eIF4A	GP	yeast	bind					eIF4G1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5557_s_237	10409745	(A) Yeast eIF4A binds to eIF4G1 and eIF4G2 in vitro.	bind
8454	2	3348	5	11	NULL	0	NULL	eIF4A	GP	yeast	bind					eIF4G2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5557_s_237	10409745	(A) Yeast eIF4A binds to eIF4G1 and eIF4G2 in vitro.	bind
10394	1	3348	7	11	NULL	0	NULL	eIF4A	GP	yeast	bind					eIF4G1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5557_s_237	10409745	(A) Yeast eIF4A binds to eIF4G1 and eIF4G2 in vitro.	bind
10395	2	3348	7	11	NULL	0	NULL	eIF4A	GP	yeast	bind					eIF4G2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5557_s_237	10409745	(A) Yeast eIF4A binds to eIF4G1 and eIF4G2 in vitro.	bind
80389	1	3348	11	NULL	NULL	0	NULL	eIF4A	Protein	yeast	binds to 					eIF4G1	Protein				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5557_s_237	10409745	(A) Yeast eIF4A binds to eIF4G1 and eIF4G2 in vitro.	bind
80390	2	3348	11	NULL	NULL	0	NULL	eIF4A	Protein	yeast	binds to 					eIF4G2	Protein				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5557_s_237	10409745	(A) Yeast eIF4A binds to eIF4G1 and eIF4G2 in vitro.	bind
8455	1	3349	5	11	NULL	0	NULL	PRA1	GP		bind					Piccolo	GP		zinc finger domains		NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_1_203_s_161	10707984	(A) Yeast two-hybrid assay assessing binding of PRA1 and rab3A to the Piccolo (Pic-Zn2) and rabphilin-3A (Rabp-Zn) zinc finger domains.	bind
8456	2	3349	5	11	NULL	0	NULL	rab3A	GP		bind					Piccolo	GP		zinc finger domains		NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_1_203_s_161	10707984	(A) Yeast two-hybrid assay assessing binding of PRA1 and rab3A to the Piccolo (Pic-Zn2) and rabphilin-3A (Rabp-Zn) zinc finger domains.	bind
8457	3	3349	5	11	NULL	0	NULL	rab3A	GP		bind					rabphilin-3A	GP		zinc finger domains		NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_1_203_s_161	10707984	(A) Yeast two-hybrid assay assessing binding of PRA1 and rab3A to the Piccolo (Pic-Zn2) and rabphilin-3A (Rabp-Zn) zinc finger domains.	bind
8458	4	3349	5	11	NULL	0	NULL	PRA1	GP		bind					rabphilin-3A	GP		zinc finger domains		NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_1_203_s_161	10707984	(A) Yeast two-hybrid assay assessing binding of PRA1 and rab3A to the Piccolo (Pic-Zn2) and rabphilin-3A (Rabp-Zn) zinc finger domains.	bind
54213	5	3349	5	11	NULL	0	NULL	Piccolo	GP		is					Pic-Zn2	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_1_203_s_161	10707984	(A) Yeast two-hybrid assay assessing binding of PRA1 and rab3A to the Piccolo (Pic-Zn2) and rabphilin-3A (Rabp-Zn) zinc finger domains.	bind
54214	6	3349	5	11	NULL	0	NULL	Rabp-Zn	GP		is					rabphilin-3A	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_1_203_s_161	10707984	(A) Yeast two-hybrid assay assessing binding of PRA1 and rab3A to the Piccolo (Pic-Zn2) and rabphilin-3A (Rabp-Zn) zinc finger domains.	bind
10396	1	3349	7	11	NULL	0	NULL	PRA1	GP		bind					Piccolo	GP		zinc finger domain		NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_1_203_s_161	10707984	(A) Yeast two-hybrid assay assessing binding of PRA1 and rab3A to the Piccolo (Pic-Zn2) and rabphilin-3A (Rabp-Zn) zinc finger domains.	bind
10397	2	3349	7	11	NULL	0	NULL	PRA1	GP		bind					rabphilin-3A 	GP		zinc finger domain		NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_1_203_s_161	10707984	(A) Yeast two-hybrid assay assessing binding of PRA1 and rab3A to the Piccolo (Pic-Zn2) and rabphilin-3A (Rabp-Zn) zinc finger domains.	bind
10398	3	3349	7	11	NULL	0	NULL	rab3A	GP		bind					Piccolo	GP		zinc finger domain		NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_1_203_s_161	10707984	(A) Yeast two-hybrid assay assessing binding of PRA1 and rab3A to the Piccolo (Pic-Zn2) and rabphilin-3A (Rabp-Zn) zinc finger domains.	bind
10399	4	3349	7	11	NULL	0	NULL	rab3A	GP		bind					rabphilin-3A 	GP		zinc finger domain		NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_1_203_s_161	10707984	(A) Yeast two-hybrid assay assessing binding of PRA1 and rab3A to the Piccolo (Pic-Zn2) and rabphilin-3A (Rabp-Zn) zinc finger domains.	bind
10402	5	3349	7	11	NULL	0	NULL	Piccolo	GP		is					Pic-Zn2	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_1_203_s_161	10707984	(A) Yeast two-hybrid assay assessing binding of PRA1 and rab3A to the Piccolo (Pic-Zn2) and rabphilin-3A (Rabp-Zn) zinc finger domains.	bind
10405	6	3349	7	11	NULL	0	NULL	rabphilin-3A 	GP		is					Rabp-Zn	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_1_203_s_161	10707984	(A) Yeast two-hybrid assay assessing binding of PRA1 and rab3A to the Piccolo (Pic-Zn2) and rabphilin-3A (Rabp-Zn) zinc finger domains.	bind
80391	1	3349	11	NULL	NULL	NULL	NULL	PRA1	Protein		binds to 					Piccolo	Protein		zinc finger domain		NULL	Yeast two-hybrid assay	NULL	NULL	NULL	NULL	gw60_neuron_25_1_203_s_161	10707984	(A) Yeast two-hybrid assay assessing binding of PRA1 and rab3A to the Piccolo (Pic-Zn2) and rabphilin-3A (Rabp-Zn) zinc finger domains.	bind
80392	2	3349	11	NULL	NULL	0	NULL	PRA1	Protein		binds to 					rabphilin-3A	Protein		zinc finger domain		NULL	Yeast two-hybrid assay	0	NULL	NULL	NULL	gw60_neuron_25_1_203_s_161	10707984	(A) Yeast two-hybrid assay assessing binding of PRA1 and rab3A to the Piccolo (Pic-Zn2) and rabphilin-3A (Rabp-Zn) zinc finger domains.	bind
80393	3	3349	11	NULL	NULL	0	NULL	rab3A	Protein		binds to 					Piccolo	Protein		zinc finger domain		NULL	Yeast two-hybrid assay	0	NULL	NULL	NULL	gw60_neuron_25_1_203_s_161	10707984	(A) Yeast two-hybrid assay assessing binding of PRA1 and rab3A to the Piccolo (Pic-Zn2) and rabphilin-3A (Rabp-Zn) zinc finger domains.	bind
80394	4	3349	11	NULL	NULL	0	NULL	rab3A	Protein		binds to 					rabphilin-3A	Protein		zinc finger domain		NULL	Yeast two-hybrid assay	0	NULL	NULL	NULL	gw60_neuron_25_1_203_s_161	10707984	(A) Yeast two-hybrid assay assessing binding of PRA1 and rab3A to the Piccolo (Pic-Zn2) and rabphilin-3A (Rabp-Zn) zinc finger domains.	bind
80395	5	3349	11	NULL	NULL	0	NULL	Pic-Zn2	Protein		is					Piccolo			zinc finger domain		NULL		0	NULL	NULL	NULL	gw60_neuron_25_1_203_s_161	10707984	(A) Yeast two-hybrid assay assessing binding of PRA1 and rab3A to the Piccolo (Pic-Zn2) and rabphilin-3A (Rabp-Zn) zinc finger domains.	bind
80396	6	3349	11	NULL	NULL	0	NULL	Rabp-Zn	Protein		is					 rabphilin-3A	Protein		zinc finger domain		NULL		0	NULL	NULL	NULL	gw60_neuron_25_1_203_s_161	10707984	(A) Yeast two-hybrid assay assessing binding of PRA1 and rab3A to the Piccolo (Pic-Zn2) and rabphilin-3A (Rabp-Zn) zinc finger domains.	bind
8459	1	3352	5	11	NULL	0	NULL	ZPC	GP		bind					ZP receptors	GP	sperm			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1469_3_197_s_876	11063883	(A) ZP proteins (most likely ZPC) bind to sperm ZP receptors, leading to aggregation and tyrosine (Y) phosphorylation.	bind
8460	2	3352	5	11	NULL	0	NULL	statement 1	Process		leads to					aggregation	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1469_3_197_s_876	11063883	(A) ZP proteins (most likely ZPC) bind to sperm ZP receptors, leading to aggregation and tyrosine (Y) phosphorylation.	bind
8461	3	3352	5	11	NULL	0	NULL	statement 1	Process		leads to					tyrosine	AminoAcid	phosphorylation of 			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1469_3_197_s_876	11063883	(A) ZP proteins (most likely ZPC) bind to sperm ZP receptors, leading to aggregation and tyrosine (Y) phosphorylation.	bind
10408	1	3352	7	11	NULL	0	NULL	ZPC	GP		bind					ZP receptors	GP	sperm			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1469_3_197_s_876	11063883	(A) ZP proteins (most likely ZPC) bind to sperm ZP receptors, leading to aggregation and tyrosine (Y) phosphorylation.	bind
10410	2	3352	7	11	NULL	0	NULL	statement 1	Process		leads to					aggregation	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1469_3_197_s_876	11063883	(A) ZP proteins (most likely ZPC) bind to sperm ZP receptors, leading to aggregation and tyrosine (Y) phosphorylation.	bind
10413	3	3352	7	11	NULL	0	NULL	statement 1	Process		leads to					tyrosine 	AminoAcid	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1469_3_197_s_876	11063883	(A) ZP proteins (most likely ZPC) bind to sperm ZP receptors, leading to aggregation and tyrosine (Y) phosphorylation.	bind
80397	1	3352	11	NULL	NULL	0	NULL	ZPC	Protein		is a type of 					ZP protein	Protein				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1469_3_197_s_876	11063883	(A) ZP proteins (most likely ZPC) bind to sperm ZP receptors, leading to aggregation and tyrosine (Y) phosphorylation.	bind
80398	2	3352	11	NULL	NULL	0	NULL	ZP protein	Protein		binds to 					ZP receptor	Protein	sperm			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1469_3_197_s_876	11063883	(A) ZP proteins (most likely ZPC) bind to sperm ZP receptors, leading to aggregation and tyrosine (Y) phosphorylation.	bind
80399	3	3352	11	NULL	NULL	0	NULL	tyrosine	AminoAcid		is					Y	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1469_3_197_s_876	11063883	(A) ZP proteins (most likely ZPC) bind to sperm ZP receptors, leading to aggregation and tyrosine (Y) phosphorylation.	bind
80400	4	3352	11	NULL	NULL	0	NULL	statement 2	Process		leads to					aggregation	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1469_3_197_s_876	11063883	(A) ZP proteins (most likely ZPC) bind to sperm ZP receptors, leading to aggregation and tyrosine (Y) phosphorylation.	bind
80401	5	3352	11	NULL	NULL	0	NULL	statement 2	Process		leads to					phosphorylation	MolecularProcess	tyrosine			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1469_3_197_s_876	11063883	(A) ZP proteins (most likely ZPC) bind to sperm ZP receptors, leading to aggregation and tyrosine (Y) phosphorylation.	bind
8462	1	3353	5	11	NULL	0	NULL	[11,12-3H(N)] all- trans retinol	Chemical		bind					RFABG	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_7_1222_s_162	10393207	(A) [11,12-3H(N)] all- trans retinol (0.2 muM) bound to RFABG or   of a 100-fold excess unlabeled heme.	bind
8463	2	3353	5	11	NULL	0	NULL	[11,12-3H(N)] all- trans retinol	Chemical		bind					heme	Chemical	unlabeled			NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_7_1222_s_162	10393207	(A) [11,12-3H(N)] all- trans retinol (0.2 muM) bound to RFABG or   of a 100-fold excess unlabeled heme.	bind
8465	3	3353	5	11	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_7_1222_s_162	10393207	(A) [11,12-3H(N)] all- trans retinol (0.2 muM) bound to RFABG or   of a 100-fold excess unlabeled heme.	bind
10420	1	3353	7	11	NULL	0	NULL	[11,12-3H(N)] all- trans retinol 	Chemical		bind					heme	Chemical	unlabeled			NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_7_1222_s_162	10393207	(A) [11,12-3H(N)] all- trans retinol (0.2 muM) bound to RFABG or   of a 100-fold excess unlabeled heme.	bind
10421	2	3353	7	11	NULL	0	NULL	[11,12-3H(N)] all- trans retinol 	Chemical		bind					RFABG	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_7_1222_s_162	10393207	(A) [11,12-3H(N)] all- trans retinol (0.2 muM) bound to RFABG or   of a 100-fold excess unlabeled heme.	bind
80402	1	3353	11	NULL	NULL	0	NULL	[11,12-3H(N)] all- trans retinol	Chemical		binds to 					RFABG	Chemical				NULL		0	NULL	NULL	NULL	gw60_jlipidres_40_7_1222_s_162	10393207	(A) [11,12-3H(N)] all- trans retinol (0.2 muM) bound to RFABG or   of a 100-fold excess unlabeled heme.	bind
8464	1	3354	5	11	NULL	0	NULL	CGRP	GP	Human	bind					HEK293EBNA cell membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1539_1_131_s_72	11389975	(A) [125]Human CGRP binding to HEK293EBNA cell membranes was assayed.	bind
10422	1	3354	7	11	NULL	0	NULL	CGRP 	GP	Human	bind					HEK293EBNA cell membranes 	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1539_1_131_s_72	11389975	(A) [125]Human CGRP binding to HEK293EBNA cell membranes was assayed.	bind
80403	1	3354	11	NULL	NULL	0	NULL	CGRP	Protein	Human	binds to 					cell membrane	CellComponent	HEK293EBNA cell			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1539_1_131_s_72	11389975	(A) [125]Human CGRP binding to HEK293EBNA cell membranes was assayed.	bind
8466	1	3357	5	11	NULL	0	NULL	ARD-1	GP		bind					9 S RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_21_13823_s_112	9153239	(A)) in 10-fold excess ( lanes 7 and  8) or tRNA in 50-fold excess ( lane 9) did not prevent binding of ARD-1 to 9 S RNA, both of these RNAs reduced 9 S-specific binding of ARD-1 when added in still greater excess.	bind
10423	1	3357	7	11	NULL	0	NULL	ARD-1	GP		bind					9 S RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_21_13823_s_112	9153239	(A)) in 10-fold excess ( lanes 7 and  8) or tRNA in 50-fold excess ( lane 9) did not prevent binding of ARD-1 to 9 S RNA, both of these RNAs reduced 9 S-specific binding of ARD-1 when added in still greater excess.	bind
80404	1	3357	11	NULL	NULL	0	NULL	ARD-1	GeneOrProtein		binds to 					 9 S RNA	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_21_13823_s_112	9153239	(A)) in 10-fold excess ( lanes 7 and  8) or tRNA in 50-fold excess ( lane 9) did not prevent binding of ARD-1 to 9 S RNA, both of these RNAs reduced 9 S-specific binding of ARD-1 when added in still greater excess.	bind
8469	1	3358	5	11	NULL	0	NULL	TIAR	GP		bind					tumor necrosis factor alpha mRNA	NucleicAcid			AU-rich element	NULL	in macrophages	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6287_s_43	10938105	(A)+ RNA in the cytoplasmic foci known as stress granules ( 28), and it has been reported previously ( 22) that TIAR binds to the translational regulatory AU-rich element of tumor necrosis factor alpha mRNA in macrophages and may be involved in translational repression.	bind
8470	2	3358	5	11	NULL	0	NULL	statement 1	Process		involved in		may be			translational repression	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6287_s_43	10938105	(A)+ RNA in the cytoplasmic foci known as stress granules ( 28), and it has been reported previously ( 22) that TIAR binds to the translational regulatory AU-rich element of tumor necrosis factor alpha mRNA in macrophages and may be involved in translational repression.	bind
10424	1	3358	7	11	NULL	0	NULL	TIAR	GP		bind					tumor necrosis factor alpha mRNA	NucleicAcid			AU-rich element 	NULL	macrophages	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6287_s_43	10938105	(A)+ RNA in the cytoplasmic foci known as stress granules ( 28), and it has been reported previously ( 22) that TIAR binds to the translational regulatory AU-rich element of tumor necrosis factor alpha mRNA in macrophages and may be involved in translational repression.	bind
10425	2	3358	7	11	NULL	0	NULL	statement 1	Process		 involved in		may be			translational repression	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6287_s_43	10938105	(A)+ RNA in the cytoplasmic foci known as stress granules ( 28), and it has been reported previously ( 22) that TIAR binds to the translational regulatory AU-rich element of tumor necrosis factor alpha mRNA in macrophages and may be involved in translational repression.	bind
80405	1	3358	11	NULL	NULL	0	NULL	RNA	NucleicAcidSubstance	cytoplasmic foci	is a type of 					stress granule	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6287_s_43	10938105	(A)+ RNA in the cytoplasmic foci known as stress granules ( 28), and it has been reported previously ( 22) that TIAR binds to the translational regulatory AU-rich element of tumor necrosis factor alpha mRNA in macrophages and may be involved in translational repression.	bind
80406	2	3358	11	NULL	NULL	0	NULL	TIAR	Protein		binds to 					tumor necrosis factor alpha mRNA	NucleicAcidSubstance	 macrophages		translational regulatory AU-rich element	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6287_s_43	10938105	(A)+ RNA in the cytoplasmic foci known as stress granules ( 28), and it has been reported previously ( 22) that TIAR binds to the translational regulatory AU-rich element of tumor necrosis factor alpha mRNA in macrophages and may be involved in translational repression.	bind
80407	3	3358	11	NULL	NULL	0	NULL	statement 2	Process		involved in		may be			translational repression	MolecularProcess				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6287_s_43	10938105	(A)+ RNA in the cytoplasmic foci known as stress granules ( 28), and it has been reported previously ( 22) that TIAR binds to the translational regulatory AU-rich element of tumor necrosis factor alpha mRNA in macrophages and may be involved in translational repression.	bind
10426	1	3360	7	NULL	NULL	0	NULL	 FBF-binding elements 	NULL	predicted	bind	NULL				FBF	NULL				NULL		0	NULL	NULL	NULL	gw70_genetics_168_1_147_s_291	15454534	(A)+ tail; brackets, regions tested for binding; gray boxes, predicted FBF-binding elements  ( e.g., a, FBE-a); only solid boxes bind FBF (see below).	bind
10427	2	3360	7	NULL	NULL	0	NULL	FBF-binding elements 	NULL		is	NULL				FBE	NULL				NULL		0	NULL	NULL	NULL	gw70_genetics_168_1_147_s_291	15454534	(A)+ tail; brackets, regions tested for binding; gray boxes, predicted FBF-binding elements  ( e.g., a, FBE-a); only solid boxes bind FBF (see below).	bind
8471	1	3361	5	11	NULL	0	NULL	Cbl	GP		does not bind					EGFR	GP	inactive			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
8472	2	3361	5	11	NULL	0	NULL	SETA/CIN85	GP		does not bind					EGFR	GP	inactive			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
8473	3	3361	5	11	NULL	0	NULL	EGFR	GP	activation	leads to					EGFR	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
8474	4	3361	5	11	NULL	0	NULL	Cbl	GP		bind					SETA/CIN85	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
8476	5	3361	5	11	NULL	0	NULL	statement 4	Process		results in					SETA/CIN85	GP	ubiquitination of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
8478	6	3361	5	11	NULL	0	NULL	statement 4	Process		results in					Cbl	GP	ubiquitination of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
8480	7	3361	5	11	NULL	0	NULL	statement 4	Process		results in					EGFR	GP	ubiquitination of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
8482	8	3361	5	11	NULL	0	NULL	statement 4	Process		results in					EGFR	GP	internalization of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
10428	1	3361	7	11	NULL	0	NULL	Cbl	GP		does not bind					EGFR	GP	inactive			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
10429	2	3361	7	11	NULL	0	NULL	SETA/CIN85 	GP		does not bind					EGFR	GP	inactive			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
10430	3	3361	7	11	NULL	0	NULL	EGFR	GP	activated	leads to					EGFR	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
10431	4	3361	7	11	NULL	0	NULL	Cbl	GP		bind					SETA/CIN85	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
10432	5	3361	7	11	NULL	0	NULL	statement 4	Process		results in					SETA/CIN85	GP	ubiquitination of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
10433	6	3361	7	11	NULL	0	NULL	statement 4	Process		results in					Cbl	GP	ubiquitination of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
10434	7	3361	7	11	NULL	0	NULL	statement 4	Process		results in					EGFR	GP	ubiquitination of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
10435	8	3361	7	11	NULL	0	NULL	statement 4	Process		results in					EGFR	GP	internalization of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
80408	1	3361	11	NULL	NULL	0	NULL	Cbl	Protein		does not bind to					inactive receptor	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
80409	2	3361	11	NULL	NULL	0	NULL	SETA/CIN85	Protein		does not bind to					inactive receptor	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
80410	3	3361	11	NULL	NULL	0	NULL	EGFR	Protein	active	phosphorylate					EGFR	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
80411	4	3361	11	NULL	NULL	0	NULL	EGFR	Protein	active	binds to 					Cbl	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
80412	5	3361	11	NULL	NULL	0	NULL	EGFR	Protein	active	binds to 					SETA/CIN85	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
80413	6	3361	11	NULL	NULL	0	NULL	statement 3	Process		ubiquitinated					EGFR	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
80414	7	3361	11	NULL	NULL	0	NULL	statement 3	Process		internalize 					EGFR	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
80415	8	3361	11	NULL	NULL	0	NULL	statement 6	Process		occurs along with					statement 7	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
80416	9	3361	11	NULL	NULL	0	NULL	statement 4	Process		ubiquitinated					Cbl	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
80417	10	3361	11	NULL	NULL	0	NULL	statement 5	Process		ubiquitinated					SETA/CIN85	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_20_8981_s_354	15456872	(A),  while previous work has shown that Cbl and SETA/CIN85 do not bind to the inactive  receptor, but that EGFR activation leads to phosphorylation of the EGFR and the binding  of Cbl and SETA/CIN85, which results in SETA/CIN85, Cbl, and EGFR ubiquitination  and EGFR internalization (B).	bind
8484	1	3362	5	11	NULL	0	NULL	PT	Chemical		bind		covalently						alphaL262C		NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_307_1_42_s_247	14500778	(A), after propanethiol (PT) covalent binding to alphaL262C (B), and after PT covalent binding to alphaL263C (C).	bind
8485	2	3362	5	11	NULL	0	NULL	PT	Chemical		is					propanethiol	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_307_1_42_s_247	14500778	(A), after propanethiol (PT) covalent binding to alphaL262C (B), and after PT covalent binding to alphaL263C (C).	bind
8486	3	3362	5	11	NULL	0	NULL	PT	Chemical		bind		covalently						alphaL263C		NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_307_1_42_s_247	14500778	(A), after propanethiol (PT) covalent binding to alphaL262C (B), and after PT covalent binding to alphaL263C (C).	bind
10437	1	3362	7	11	NULL	0	NULL	propanethiol	Chemical		bind		covalently			alphaL262C	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_307_1_42_s_247	14500778	(A), after propanethiol (PT) covalent binding to alphaL262C (B), and after PT covalent binding to alphaL263C (C).	bind
10438	2	3362	7	11	NULL	0	NULL	propanethiol	Chemical		bind		covalently			alphaL263C	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_307_1_42_s_247	14500778	(A), after propanethiol (PT) covalent binding to alphaL262C (B), and after PT covalent binding to alphaL263C (C).	bind
10439	3	3362	7	11	NULL	0	NULL	propanethiol 	Chemical		is					PT	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_307_1_42_s_247	14500778	(A), after propanethiol (PT) covalent binding to alphaL262C (B), and after PT covalent binding to alphaL263C (C).	bind
80418	1	3362	11	NULL	NULL	0	NULL	propanethiol	Chemical		is					PT	Chemical				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_307_1_42_s_247	14500778	(A), after propanethiol (PT) covalent binding to alphaL262C (B), and after PT covalent binding to alphaL263C (C).	bind
80419	2	3362	11	NULL	NULL	0	NULL	propanethiol	Chemical		binds to 		covalent			alphaL262C	AminoAcid				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_307_1_42_s_247	14500778	(A), after propanethiol (PT) covalent binding to alphaL262C (B), and after PT covalent binding to alphaL263C (C).	bind
80420	3	3362	11	NULL	NULL	0	NULL	PT	Chemical		binds to 		covalent			alphaL263C	AminoAcid				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_307_1_42_s_247	14500778	(A), after propanethiol (PT) covalent binding to alphaL262C (B), and after PT covalent binding to alphaL263C (C).	bind
8487	1	3363	5	11	NULL	0	NULL	A2A 	GP		bind					hippocampal nerve terminals	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_301_2_441_s_156	11961042	(A), and A2A (B) adenosine receptors antibody binding to hippocampal nerve terminals.	bind
44757	2	3363	5	11	NULL	0	NULL	A2A	GP		is a type of					adenosine receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_301_2_441_s_156	11961042	(A), and A2A (B) adenosine receptors antibody binding to hippocampal nerve terminals.	bind
10440	1	3363	7	11	NULL	0	NULL	A2A	GP		bind					hippocampal nerve terminals	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_301_2_441_s_156	11961042	(A), and A2A (B) adenosine receptors antibody binding to hippocampal nerve terminals.	bind
44758	2	3363	7	11	NULL	0	NULL	A2A	GP		is a type of					adenosine receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_301_2_441_s_156	11961042	(A), and A2A (B) adenosine receptors antibody binding to hippocampal nerve terminals.	bind
80421	1	3363	11	NULL	NULL	0	NULL	A2A	Protein		is a type of 					adenosine receptor	Protein				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_301_2_441_s_156	11961042	(A), and A2A (B) adenosine receptors antibody binding to hippocampal nerve terminals.	bind
80422	2	3363	11	NULL	NULL	0	NULL	A2A	Protein	antibody	binds to 					nerve terminal	Organism part	hippocampal			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_301_2_441_s_156	11961042	(A), and A2A (B) adenosine receptors antibody binding to hippocampal nerve terminals.	bind
8488	1	3365	5	11	NULL	0	NULL	spectrin	GP	brain	bind					red blood cell membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1611_1_115_s_89	12659952	(A), binding of  the brain spectrin by red blood cell membranes (B), binding of the erythrocyte spectrin  by red blood cell membranes (C), and binding of the erythrocyte spectrin by synaptic  plasma membranes (D).	bind
8489	2	3365	5	11	NULL	0	NULL	spectrin	GP	erythrocyte	bind					red blood cell membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1611_1_115_s_89	12659952	(A), binding of  the brain spectrin by red blood cell membranes (B), binding of the erythrocyte spectrin  by red blood cell membranes (C), and binding of the erythrocyte spectrin by synaptic  plasma membranes (D).	bind
8490	3	3365	5	11	NULL	0	NULL	spectrin	GP	erythrocyte	bind					synaptic plasma membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1611_1_115_s_89	12659952	(A), binding of  the brain spectrin by red blood cell membranes (B), binding of the erythrocyte spectrin  by red blood cell membranes (C), and binding of the erythrocyte spectrin by synaptic  plasma membranes (D).	bind
10441	1	3365	7	11	NULL	0	NULL	spectrin	GP	brain	bind					red blood cell membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1611_1_115_s_89	12659952	(A), binding of  the brain spectrin by red blood cell membranes (B), binding of the erythrocyte spectrin  by red blood cell membranes (C), and binding of the erythrocyte spectrin by synaptic  plasma membranes (D).	bind
10442	2	3365	7	11	NULL	0	NULL	spectrin	GP	erythrocyte	bind					red blood cell membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1611_1_115_s_89	12659952	(A), binding of  the brain spectrin by red blood cell membranes (B), binding of the erythrocyte spectrin  by red blood cell membranes (C), and binding of the erythrocyte spectrin by synaptic  plasma membranes (D).	bind
10443	3	3365	7	11	NULL	0	NULL	spectrin	GP	erythrocyte	bind					synaptic plasma membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1611_1_115_s_89	12659952	(A), binding of  the brain spectrin by red blood cell membranes (B), binding of the erythrocyte spectrin  by red blood cell membranes (C), and binding of the erythrocyte spectrin by synaptic  plasma membranes (D).	bind
80423	1	3365	11	NULL	NULL	0	NULL	spectrin	Protein	brain	binds to 					cell membrane	CellComponent	red blood cell			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1611_1_115_s_89	12659952	(A), binding of  the brain spectrin by red blood cell membranes (B), binding of the erythrocyte spectrin  by red blood cell membranes (C), and binding of the erythrocyte spectrin by synaptic  plasma membranes (D).	bind
80424	2	3365	11	NULL	NULL	0	NULL	spectrin	Protein	erythrocyte	binds to 					cell membrane	CellComponent	red blood cell			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1611_1_115_s_89	12659952	(A), binding of  the brain spectrin by red blood cell membranes (B), binding of the erythrocyte spectrin  by red blood cell membranes (C), and binding of the erythrocyte spectrin by synaptic  plasma membranes (D).	bind
80425	3	3365	11	NULL	NULL	0	NULL	spectrin	Protein	erythrocyte	binds to 					plasma membrane	CellComponent	synaptic 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1611_1_115_s_89	12659952	(A), binding of  the brain spectrin by red blood cell membranes (B), binding of the erythrocyte spectrin  by red blood cell membranes (C), and binding of the erythrocyte spectrin by synaptic  plasma membranes (D).	bind
8491	1	3366	5	11	NULL	0	NULL	spectrin	GP	brain	bind					red blood cell membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1611_1_115_s_89	12659952	(A), binding of the brain spectrin by red blood cell membranes (B), binding of the erythrocyte spectrin by red blood cell membranes (C), and binding of the erythrocyte spectrin by synaptic plasma membranes (D).	bind
8492	2	3366	5	11	NULL	0	NULL	spectrin	GP	erythrocyte	bind					red blood cell membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1611_1_115_s_89	12659952	(A), binding of the brain spectrin by red blood cell membranes (B), binding of the erythrocyte spectrin by red blood cell membranes (C), and binding of the erythrocyte spectrin by synaptic plasma membranes (D).	bind
8493	3	3366	5	11	NULL	0	NULL	spectrin	GP	erythrocyte	bind					synaptic plasma membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1611_1_115_s_89	12659952	(A), binding of the brain spectrin by red blood cell membranes (B), binding of the erythrocyte spectrin by red blood cell membranes (C), and binding of the erythrocyte spectrin by synaptic plasma membranes (D).	bind
8494	1	3367	5	11	NULL	0	NULL	Nef	GP		downregulate					CD4	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_2_548_s_73	16760313	(A), CD4 downregulation by Nef (B), and AP binding mediated by the Nef dileucine  motif (C).	bind
8495	2	3367	5	11	NULL	0	NULL	Nef	GP		mediate			dileucine motif		AP	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_2_548_s_73	16760313	(A), CD4 downregulation by Nef (B), and AP binding mediated by the Nef dileucine  motif (C).	bind
10444	1	3367	7	11	NULL	0	NULL	Nef	GP		downregulates					CD4	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_2_548_s_73	16760313	(A), CD4 downregulation by Nef (B), and AP binding mediated by the Nef dileucine  motif (C).	bind
10445	2	3367	7	11	NULL	0	NULL	Nef	GP		mediates			dileucine motif 		AP	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_2_548_s_73	16760313	(A), CD4 downregulation by Nef (B), and AP binding mediated by the Nef dileucine  motif (C).	bind
80426	1	3367	11	NULL	NULL	NULL	NULL	Nef	Protein		downregulate			dileucine motif		CD4	Protein				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_2_548_s_73	16760313	(A), CD4 downregulation by Nef (B), and AP binding mediated by the Nef dileucine  motif (C).	bind
80431	2	3367	11	NULL	NULL	0	NULL	AP	Protein		binds to 					CD4	Protein				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_2_548_s_73	16760313	(A), CD4 downregulation by Nef (B), and AP binding mediated by the Nef dileucine  motif (C).	bind
80432	3	3367	11	NULL	NULL	0	NULL	statement 2	Process		downregulate					CD4	Protein				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_2_548_s_73	16760313	(A), CD4 downregulation by Nef (B), and AP binding mediated by the Nef dileucine  motif (C).	bind
80434	4	3367	11	NULL	NULL	0	NULL	statement 3	Process		mediated by					Nef	Protein		dileucine motif 		NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_2_548_s_73	16760313	(A), CD4 downregulation by Nef (B), and AP binding mediated by the Nef dileucine  motif (C).	bind
8496	1	3368	5	11	NULL	0	NULL	Swi6p	GP		bind					CLN2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_9_3126_s_274	12697814	(A), cell size (B), expression of the  SCB: lacZ reporter gene (C), and binding of Swi6p to the  CLN2 promoter (D) were analyzed as described previously.	bind
10446	1	3368	7	11	NULL	0	NULL	Swi6p	GP		bind					CLN2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_9_3126_s_274	12697814	(A), cell size (B), expression of the  SCB: lacZ reporter gene (C), and binding of Swi6p to the  CLN2 promoter (D) were analyzed as described previously.	bind
80435	1	3368	11	NULL	NULL	0	NULL	Swi6p	Protein		binds to 					CLN2 promoter	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_9_3126_s_274	12697814	(A), cell size (B), expression of the  SCB: lacZ reporter gene (C), and binding of Swi6p to the  CLN2 promoter (D) were analyzed as described previously.	bind
8497	1	3369	5	11	NULL	0	NULL	delta50HA	GP		bind					X chromosome	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_20_8913_s_166	16199870	(A), delta50HA binds weakly (B), and delta26HA binds more strongly to the X chromosome than delta50HA (C); but staining intensity is consistently less than for MSL1NHA (Fig.  2C and D).	bind
8498	2	3369	5	11	NULL	0	NULL	delta26HA	GP		bind					X chromosome	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_20_8913_s_166	16199870	(A), delta50HA binds weakly (B), and delta26HA binds more strongly to the X chromosome than delta50HA (C); but staining intensity is consistently less than for MSL1NHA (Fig.  2C and D).	bind
8499	3	3369	5	11	NULL	0	NULL	statement 2	Process		is stronger than					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_20_8913_s_166	16199870	(A), delta50HA binds weakly (B), and delta26HA binds more strongly to the X chromosome than delta50HA (C); but staining intensity is consistently less than for MSL1NHA (Fig.  2C and D).	bind
10447	1	3369	7	11	NULL	0	NULL	delta50HA	GP		bind					 X chromosome 	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_20_8913_s_166	16199870	(A), delta50HA binds weakly (B), and delta26HA binds more strongly to the X chromosome than delta50HA (C); but staining intensity is consistently less than for MSL1NHA (Fig.  2C and D).	bind
10448	2	3369	7	11	NULL	0	NULL	delta26HA	GP		bind					X chromosome 	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_20_8913_s_166	16199870	(A), delta50HA binds weakly (B), and delta26HA binds more strongly to the X chromosome than delta50HA (C); but staining intensity is consistently less than for MSL1NHA (Fig.  2C and D).	bind
10449	3	3369	7	11	NULL	0	NULL	statement 1	Process		is weaker than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_20_8913_s_166	16199870	(A), delta50HA binds weakly (B), and delta26HA binds more strongly to the X chromosome than delta50HA (C); but staining intensity is consistently less than for MSL1NHA (Fig.  2C and D).	bind
80439	1	3369	11	NULL	NULL	0	NULL	delta50HA	Protein		binds to 		weakly			X chromosome	Chromosome				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_20_8913_s_166	16199870	(A), delta50HA binds weakly (B), and delta26HA binds more strongly to the X chromosome than delta50HA (C); but staining intensity is consistently less than for MSL1NHA (Fig.  2C and D).	bind
80440	2	3369	11	NULL	NULL	0	NULL	delta26HA	Protein		binds to 		strongly			X chromosome	Chromosome				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_20_8913_s_166	16199870	(A), delta50HA binds weakly (B), and delta26HA binds more strongly to the X chromosome than delta50HA (C); but staining intensity is consistently less than for MSL1NHA (Fig.  2C and D).	bind
8500	1	3370	5	11	NULL	0	NULL	myosin	GP		bind					UNC-45	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_295_5555_669_s_66	11809970	(A), except that  they were incubated at 30 degrees C for 30 min. Myosin bound both UNC-45 and  Hsp90.	bind
8501	2	3370	5	11	NULL	0	NULL	myosin	GP		bind					Hsp90	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_295_5555_669_s_66	11809970	(A), except that  they were incubated at 30 degrees C for 30 min. Myosin bound both UNC-45 and  Hsp90.	bind
10450	1	3370	7	11	NULL	0	NULL	Myosin	GP		bind					UNC-45 	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_295_5555_669_s_66	11809970	(A), except that  they were incubated at 30 degrees C for 30 min. Myosin bound both UNC-45 and  Hsp90.	bind
10451	2	3370	7	11	NULL	0	NULL	Myosin	GP		bind					Hsp90	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_295_5555_669_s_66	11809970	(A), except that  they were incubated at 30 degrees C for 30 min. Myosin bound both UNC-45 and  Hsp90.	bind
80442	1	3370	11	NULL	NULL	0	NULL	Myosin	Protein		binds to 					UNC-45	Protein				NULL		0	NULL	NULL	NULL	gw60_science_295_5555_669_s_66	11809970	(A), except that  they were incubated at 30 degrees C for 30 min. Myosin bound both UNC-45 and  Hsp90.	bind
80443	2	3370	11	NULL	NULL	0	NULL	Myosin	Protein		binds to 					Hsp90	Protein				NULL		0	NULL	NULL	NULL	gw60_science_295_5555_669_s_66	11809970	(A), except that  they were incubated at 30 degrees C for 30 min. Myosin bound both UNC-45 and  Hsp90.	bind
8502	1	3375	5	11	NULL	0	NULL	Ser	AminoAcid		bind					Tsr	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_48_17354_s_65	16293695	(A), in response to two stimuli, Ser and MeAsp, which bind to Tsr and Tar, respectively.	bind
8503	2	3375	5	11	NULL	0	NULL	MeAsp	AminoAcid		bind					Tar	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_48_17354_s_65	16293695	(A), in response to two stimuli, Ser and MeAsp, which bind to Tsr and Tar, respectively.	bind
10569	1	3375	7	11	NULL	0	NULL	Ser	AminoAcid		bind					Tsr	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_48_17354_s_65	16293695	(A), in response to two stimuli, Ser and MeAsp, which bind to Tsr and Tar, respectively.	bind
10570	2	3375	7	11	NULL	0	NULL	MeAsp	AminoAcid		bind					Tar	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_48_17354_s_65	16293695	(A), in response to two stimuli, Ser and MeAsp, which bind to Tsr and Tar, respectively.	bind
80453	1	3375	11	NULL	NULL	0	NULL	Ser	AminoAcid		binds to 					Tsr	Protein				NULL		0	NULL	NULL	NULL	gw70_pnas_102_48_17354_s_65	16293695	(A), in response to two stimuli, Ser and MeAsp, which bind to Tsr and Tar, respectively.	bind
80454	2	3375	11	NULL	NULL	0	NULL	MeAsp	AminoAcid		binds to 					Tar	Protein				NULL		0	NULL	NULL	NULL	gw70_pnas_102_48_17354_s_65	16293695	(A), in response to two stimuli, Ser and MeAsp, which bind to Tsr and Tar, respectively.	bind
8504	1	3376	5	11	NULL	0	NULL	KLC	GP		bind					KHC	GP				NULL	subcortical microtubule array nucleates particles	NULL	NULL	NULL	NULL	gw70_development_130_22_5425_s_301	14507779	(A), KLC bound to KHC on [[ the subcortical microtubule  array nucleates particles ]] that include GBP and its binding partner Dsh.	bind
8505	2	3376	5	11	NULL	0	NULL	GBP	GP		bind					Dsh	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_22_5425_s_301	14507779	(A), KLC bound to KHC on [[ the subcortical microtubule  array nucleates particles ]] that include GBP and its binding partner Dsh.	bind
8507	3	3376	5	11	NULL	0	NULL	statement 1	Process		include					GBP	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_22_5425_s_301	14507779	(A), KLC bound to KHC on [[ the subcortical microtubule  array nucleates particles ]] that include GBP and its binding partner Dsh.	bind
8508	4	3376	5	11	NULL	0	NULL	statement 1	Process		include					Dsh	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_22_5425_s_301	14507779	(A), KLC bound to KHC on [[ the subcortical microtubule  array nucleates particles ]] that include GBP and its binding partner Dsh.	bind
10572	1	3376	7	11	NULL	0	NULL	KLC	GP		bind					KHC	GP				NULL	subcortical microtubule array nucleates particles	NULL	NULL	NULL	NULL	gw70_development_130_22_5425_s_301	14507779	(A), KLC bound to KHC on [[ the subcortical microtubule  array nucleates particles ]] that include GBP and its binding partner Dsh.	bind
10574	2	3376	7	11	NULL	0	NULL	GBP	GP		bind					Dsh	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_22_5425_s_301	14507779	(A), KLC bound to KHC on [[ the subcortical microtubule  array nucleates particles ]] that include GBP and its binding partner Dsh.	bind
10575	3	3376	7	11	NULL	0	NULL	statement 1	Process		include					GBP	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_22_5425_s_301	14507779	(A), KLC bound to KHC on [[ the subcortical microtubule  array nucleates particles ]] that include GBP and its binding partner Dsh.	bind
10576	4	3376	7	11	NULL	0	NULL	statement 1	Process		include					Dsh	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_22_5425_s_301	14507779	(A), KLC bound to KHC on [[ the subcortical microtubule  array nucleates particles ]] that include GBP and its binding partner Dsh.	bind
80481	1	3376	11	NULL	NULL	0	NULL	KLC	PartOfProtein		binds to 					KHC	PartOfProtein				NULL	subcortical microtubule	0	NULL	NULL	NULL	gw70_development_130_22_5425_s_301	14507779	(A), KLC bound to KHC on [[ the subcortical microtubule  array nucleates particles ]] that include GBP and its binding partner Dsh.	bind
80482	2	3376	11	NULL	NULL	0	NULL	statement 1	Process		nucleates					GBP	Protein				NULL		0	NULL	NULL	NULL	gw70_development_130_22_5425_s_301	14507779	(A), KLC bound to KHC on [[ the subcortical microtubule  array nucleates particles ]] that include GBP and its binding partner Dsh.	bind
80483	3	3376	11	NULL	NULL	0	NULL	statement 1	Process		nucleates					GBP	Protein				NULL		0	NULL	NULL	NULL	gw70_development_130_22_5425_s_301	14507779	(A), KLC bound to KHC on [[ the subcortical microtubule  array nucleates particles ]] that include GBP and its binding partner Dsh.	bind
80484	4	3376	11	NULL	NULL	0	NULL	Dsh	Protein		is a binding partner of 					GBP	Protein				NULL		0	NULL	NULL	NULL	gw70_development_130_22_5425_s_301	14507779	(A), KLC bound to KHC on [[ the subcortical microtubule  array nucleates particles ]] that include GBP and its binding partner Dsh.	bind
8509	1	3378	5	11	NULL	0	NULL	SP-B21 cells	Cell	anti-CD3-stimulated	bind					IL-5	GP			RE-II	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_26_16453_s_256	9195954	(A), NF-Y(B), and c-Jun transcription factors were tested for the ability to recognize specific proteins from anti-CD3-stimulated SP-B21 cells bound to IL-5 RE-II in EMSAs.	bind
10578	1	3378	7	11	NULL	0	NULL	 SP-B21 cells	Cell	anti-CD3-stimulated	bind					IL-5 	GP			RE-II	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_26_16453_s_256	9195954	(A), NF-Y(B), and c-Jun transcription factors were tested for the ability to recognize specific proteins from anti-CD3-stimulated SP-B21 cells bound to IL-5 RE-II in EMSAs.	bind
80485	1	3378	11	NULL	NULL	0	NULL	NF-Y	Protein		is a type of 					transcription factor	Protein				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_26_16453_s_256	9195954	(A), NF-Y(B), and c-Jun transcription factors were tested for the ability to recognize specific proteins from anti-CD3-stimulated SP-B21 cells bound to IL-5 RE-II in EMSAs.	bind
80486	2	3378	11	NULL	NULL	0	NULL	c-Jun	Protein		is a type of 					transcription factor	Protein				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_26_16453_s_256	9195954	(A), NF-Y(B), and c-Jun transcription factors were tested for the ability to recognize specific proteins from anti-CD3-stimulated SP-B21 cells bound to IL-5 RE-II in EMSAs.	bind
80487	3	3378	11	NULL	NULL	0	NULL	anti-CD3	PartOfProtein		stimulates					SP-B21 cells	Cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_26_16453_s_256	9195954	(A), NF-Y(B), and c-Jun transcription factors were tested for the ability to recognize specific proteins from anti-CD3-stimulated SP-B21 cells bound to IL-5 RE-II in EMSAs.	bind
80488	4	3378	11	NULL	NULL	0	NULL	SP-B21 cell	cell		binds to 					IL-5 RE-II	PartOfProtein				NULL	in EMSAs	0	NULL	NULL	NULL	gw60_jbiolchem_272_26_16453_s_256	9195954	(A), NF-Y(B), and c-Jun transcription factors were tested for the ability to recognize specific proteins from anti-CD3-stimulated SP-B21 cells bound to IL-5 RE-II in EMSAs.	bind
10582	1	3381	7	11	NULL	0	NULL	P-selectin	GP		bind					fibrinogen	GP				NULL	 circulating platelets	NULL	NULL	NULL	NULL	gw60_circulation_93_2_229_s_112	8548893	(A), P-selectin (B), bound fibrinogen (C), and activated fibrinogen receptor (D) on circulating platelets in AMI patients (n=15) before and after (4, 8, 24, and 48 hours) successful recanalization of the infarct-related vessel ( ).	bind
10583	2	3381	7	11	NULL	0	NULL	statement 1	Process		activates					fibrinogen receptor	GP				NULL	circulating platelets	NULL	NULL	NULL	NULL	gw60_circulation_93_2_229_s_112	8548893	(A), P-selectin (B), bound fibrinogen (C), and activated fibrinogen receptor (D) on circulating platelets in AMI patients (n=15) before and after (4, 8, 24, and 48 hours) successful recanalization of the infarct-related vessel ( ).	bind
80489	1	3381	11	NULL	NULL	0	NULL	P-selectin	Protein		expressed on					circulating platelets	CellComponent				NULL	in AMI patients	0	NULL	NULL	NULL	gw60_circulation_93_2_229_s_112	8548893	(A), P-selectin (B), bound fibrinogen (C), and activated fibrinogen receptor (D) on circulating platelets in AMI patients (n=15) before and after (4, 8, 24, and 48 hours) successful recanalization of the infarct-related vessel ( ).	bind
80490	2	3381	11	NULL	NULL	0	NULL	fibrinogen	Protein	bound	expressed on					circulating platelets	CellComponent				NULL	in AMI patients	0	NULL	NULL	NULL	gw60_circulation_93_2_229_s_112	8548893	(A), P-selectin (B), bound fibrinogen (C), and activated fibrinogen receptor (D) on circulating platelets in AMI patients (n=15) before and after (4, 8, 24, and 48 hours) successful recanalization of the infarct-related vessel ( ).	bind
80491	3	3381	11	NULL	NULL	0	NULL	fibrinogen receptor	Protein	active	expressed on					circulating platelets	CellComponent				NULL	in AMI patients	0	NULL	NULL	NULL	gw60_circulation_93_2_229_s_112	8548893	(A), P-selectin (B), bound fibrinogen (C), and activated fibrinogen receptor (D) on circulating platelets in AMI patients (n=15) before and after (4, 8, 24, and 48 hours) successful recanalization of the infarct-related vessel ( ).	bind
8510	1	3385	5	11	NULL	0	NULL	Stx1	GP		bind					granulocyte cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_11_6680_s_79	15501802	(A), Stx1 (B), and Stx2 (C) binding to cells on granulocyte  smears are shown.	bind
8511	2	3385	5	11	NULL	0	NULL	Stx2	GP		bind					granulocyte cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_11_6680_s_79	15501802	(A), Stx1 (B), and Stx2 (C) binding to cells on granulocyte  smears are shown.	bind
10584	1	3385	7	11	NULL	0	NULL	Stx1	GP		binds					granulocyte cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_11_6680_s_79	15501802	(A), Stx1 (B), and Stx2 (C) binding to cells on granulocyte  smears are shown.	bind
10585	2	3385	7	11	NULL	0	NULL	Stx2	GP		bind					granulocyte cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_11_6680_s_79	15501802	(A), Stx1 (B), and Stx2 (C) binding to cells on granulocyte  smears are shown.	bind
80492	1	3385	11	NULL	NULL	0	NULL	 Stx1	Protein		binds to 					granulocyte	Cell				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_11_6680_s_79	15501802	(A), Stx1 (B), and Stx2 (C) binding to cells on granulocyte  smears are shown.	bind
80493	2	3385	11	NULL	NULL	0	NULL	Stx2	Protein		binds to 					granulocyte	Cell				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_11_6680_s_79	15501802	(A), Stx1 (B), and Stx2 (C) binding to cells on granulocyte  smears are shown.	bind
8512	1	3388	5	11	NULL	0	NULL	MMP-2	GP	active	bind			HP		endostatin	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_febslett_519_1_147_s_113	12023034	(A), the active MMP-2 HP (B), and the GST-fused MMP-2 HP domain (C) binding to the immobilized endostatin (thick line) or TIMP-2 as a control (thin line) were shown.	bind
8513	2	3388	5	11	NULL	0	NULL	MMP-2	GP	active	bind			HP		TIMP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_519_1_147_s_113	12023034	(A), the active MMP-2 HP (B), and the GST-fused MMP-2 HP domain (C) binding to the immobilized endostatin (thick line) or TIMP-2 as a control (thin line) were shown.	bind
8514	3	3388	5	11	NULL	0	NULL	MMP-2	GP	GST-fused	bind			HP domain		endostatin	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_febslett_519_1_147_s_113	12023034	(A), the active MMP-2 HP (B), and the GST-fused MMP-2 HP domain (C) binding to the immobilized endostatin (thick line) or TIMP-2 as a control (thin line) were shown.	bind
8515	4	3388	5	11	NULL	0	NULL	MMP-2	GP	GST-fused	bind			HP domain		TIMP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_519_1_147_s_113	12023034	(A), the active MMP-2 HP (B), and the GST-fused MMP-2 HP domain (C) binding to the immobilized endostatin (thick line) or TIMP-2 as a control (thin line) were shown.	bind
10586	1	3388	7	11	NULL	0	NULL	MMP-2 	GP	active	bind			HP		endostatin 	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_febslett_519_1_147_s_113	12023034	(A), the active MMP-2 HP (B), and the GST-fused MMP-2 HP domain (C) binding to the immobilized endostatin (thick line) or TIMP-2 as a control (thin line) were shown.	bind
10587	2	3388	7	11	NULL	0	NULL	MMP-2	GP	active	bind			HP		TIMP-2 	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_519_1_147_s_113	12023034	(A), the active MMP-2 HP (B), and the GST-fused MMP-2 HP domain (C) binding to the immobilized endostatin (thick line) or TIMP-2 as a control (thin line) were shown.	bind
10588	3	3388	7	11	NULL	0	NULL	MMP-2	GP	GST-fused 	bind			HP		endostatin 	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_febslett_519_1_147_s_113	12023034	(A), the active MMP-2 HP (B), and the GST-fused MMP-2 HP domain (C) binding to the immobilized endostatin (thick line) or TIMP-2 as a control (thin line) were shown.	bind
10589	4	3388	7	11	NULL	0	NULL	MMP-2	GP	GST-fused 	bind			HP		TIMP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_519_1_147_s_113	12023034	(A), the active MMP-2 HP (B), and the GST-fused MMP-2 HP domain (C) binding to the immobilized endostatin (thick line) or TIMP-2 as a control (thin line) were shown.	bind
80494	1	3388	11	NULL	NULL	0	NULL	MMP-2 HP	Protein	active	binds to 					endostatin	Protein	immobilized			NULL		0	NULL	NULL	NULL	gw60_febslett_519_1_147_s_113	12023034	(A), the active MMP-2 HP (B), and the GST-fused MMP-2 HP domain (C) binding to the immobilized endostatin (thick line) or TIMP-2 as a control (thin line) were shown.	bind
80495	2	3388	11	NULL	NULL	0	NULL	GST	Protein		fused to					MMP-2 HP	Protein				NULL		0	NULL	NULL	NULL	gw60_febslett_519_1_147_s_113	12023034	(A), the active MMP-2 HP (B), and the GST-fused MMP-2 HP domain (C) binding to the immobilized endostatin (thick line) or TIMP-2 as a control (thin line) were shown.	bind
80496	3	3388	11	NULL	NULL	0	NULL	statement 2	Protein		binds to 					endostatin	Protein	immobilized			NULL		0	NULL	NULL	NULL	gw60_febslett_519_1_147_s_113	12023034	(A), the active MMP-2 HP (B), and the GST-fused MMP-2 HP domain (C) binding to the immobilized endostatin (thick line) or TIMP-2 as a control (thin line) were shown.	bind
80497	4	3388	11	NULL	NULL	0	NULL	MMP-2 HP	Protein	active	binds to 					TIMP-2	Protein				NULL		0	NULL	NULL	NULL	gw60_febslett_519_1_147_s_113	12023034	(A), the active MMP-2 HP (B), and the GST-fused MMP-2 HP domain (C) binding to the immobilized endostatin (thick line) or TIMP-2 as a control (thin line) were shown.	bind
80498	5	3388	11	NULL	NULL	0	NULL	statement 2	Protein		binds to 					TIMP-2	Protein				NULL		0	NULL	NULL	NULL	gw60_febslett_519_1_147_s_113	12023034	(A), the active MMP-2 HP (B), and the GST-fused MMP-2 HP domain (C) binding to the immobilized endostatin (thick line) or TIMP-2 as a control (thin line) were shown.	bind
80499	1	3389	11	NULL	NULL	0	NULL	TIM-1-578	Protein		binds to 					GST-PER	Protein	beads			NULL		0	NULL	NULL	NULL	gw60_neuron_17_5_911_s_175	8938123	(A), TIM-1-578 (B), TIM-715-1389 (C), TIM-914-1389 (D), and TIM-1-914 (E) that bound to the indicated GST-PER beads were detected by autoradiography.	bind
80500	2	3389	11	NULL	NULL	0	NULL	TIM-715-1389	Protein		binds to 					GST-PER	Protein	beads			NULL		0	NULL	NULL	NULL	gw60_neuron_17_5_911_s_175	8938123	(A), TIM-1-578 (B), TIM-715-1389 (C), TIM-914-1389 (D), and TIM-1-914 (E) that bound to the indicated GST-PER beads were detected by autoradiography.	bind
80501	3	3389	11	NULL	NULL	0	NULL	TIM-914-1389	Protein		binds to 					GST-PER	Protein	beads			NULL		0	NULL	NULL	NULL	gw60_neuron_17_5_911_s_175	8938123	(A), TIM-1-578 (B), TIM-715-1389 (C), TIM-914-1389 (D), and TIM-1-914 (E) that bound to the indicated GST-PER beads were detected by autoradiography.	bind
80502	4	3389	11	NULL	NULL	0	NULL	TIM-1-914	Protein		binds to 					GST-PER	Protein	beads			NULL		0	NULL	NULL	NULL	gw60_neuron_17_5_911_s_175	8938123	(A), TIM-1-578 (B), TIM-715-1389 (C), TIM-914-1389 (D), and TIM-1-914 (E) that bound to the indicated GST-PER beads were detected by autoradiography.	bind
80503	5	3389	11	NULL	NULL	0	NULL	statement 1	Process		detected by					autoradiography	ResearchActivity				NULL		0	NULL	NULL	NULL	gw60_neuron_17_5_911_s_175	8938123	(A), TIM-1-578 (B), TIM-715-1389 (C), TIM-914-1389 (D), and TIM-1-914 (E) that bound to the indicated GST-PER beads were detected by autoradiography.	bind
80504	6	3389	11	NULL	NULL	0	NULL	statement 2	Process		detected by					autoradiography	ResearchActivity				NULL		0	NULL	NULL	NULL	gw60_neuron_17_5_911_s_175	8938123	(A), TIM-1-578 (B), TIM-715-1389 (C), TIM-914-1389 (D), and TIM-1-914 (E) that bound to the indicated GST-PER beads were detected by autoradiography.	bind
80505	7	3389	11	NULL	NULL	0	NULL	statement 3	Process		detected by					autoradiography	ResearchActivity				NULL		0	NULL	NULL	NULL	gw60_neuron_17_5_911_s_175	8938123	(A), TIM-1-578 (B), TIM-715-1389 (C), TIM-914-1389 (D), and TIM-1-914 (E) that bound to the indicated GST-PER beads were detected by autoradiography.	bind
80506	8	3389	11	NULL	NULL	0	NULL	statement 4	Process		detected by					autoradiography	ResearchActivity				NULL		0	NULL	NULL	NULL	gw60_neuron_17_5_911_s_175	8938123	(A), TIM-1-578 (B), TIM-715-1389 (C), TIM-914-1389 (D), and TIM-1-914 (E) that bound to the indicated GST-PER beads were detected by autoradiography.	bind
8516	1	3390	5	11	NULL	0	NULL	VLA-4	GP		bind					VCAM-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_2_153_s_95	10904000	(A), treated with mAb Lia (nonblocking control) (B), mAb HP1/3 (anti-VLA-4, blocking FN binding) (C), vessel treated with mAb MK-2.7 to VCAM-1 (D), ILDV peptide present during perfusion (E), HP1/2 blocking VLA-4 binding to VCAM-1, and FN (F).	bind
8517	2	3390	5	11	NULL	0	NULL	VLA-4	GP		bind					FN	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_2_153_s_95	10904000	(A), treated with mAb Lia (nonblocking control) (B), mAb HP1/3 (anti-VLA-4, blocking FN binding) (C), vessel treated with mAb MK-2.7 to VCAM-1 (D), ILDV peptide present during perfusion (E), HP1/2 blocking VLA-4 binding to VCAM-1, and FN (F).	bind
8518	3	3390	5	11	NULL	0	NULL	HP1/2	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_2_153_s_95	10904000	(A), treated with mAb Lia (nonblocking control) (B), mAb HP1/3 (anti-VLA-4, blocking FN binding) (C), vessel treated with mAb MK-2.7 to VCAM-1 (D), ILDV peptide present during perfusion (E), HP1/2 blocking VLA-4 binding to VCAM-1, and FN (F).	bind
8519	4	3390	5	11	NULL	0	NULL	HP1/2	GP		blocks					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_2_153_s_95	10904000	(A), treated with mAb Lia (nonblocking control) (B), mAb HP1/3 (anti-VLA-4, blocking FN binding) (C), vessel treated with mAb MK-2.7 to VCAM-1 (D), ILDV peptide present during perfusion (E), HP1/2 blocking VLA-4 binding to VCAM-1, and FN (F).	bind
10593	1	3390	7	11	NULL	0	NULL	VLA-4	GP		bind					VCAM-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_2_153_s_95	10904000	(A), treated with mAb Lia (nonblocking control) (B), mAb HP1/3 (anti-VLA-4, blocking FN binding) (C), vessel treated with mAb MK-2.7 to VCAM-1 (D), ILDV peptide present during perfusion (E), HP1/2 blocking VLA-4 binding to VCAM-1, and FN (F).	bind
10594	2	3390	7	11	NULL	0	NULL	VLA-4	GP		bind					FN	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_2_153_s_95	10904000	(A), treated with mAb Lia (nonblocking control) (B), mAb HP1/3 (anti-VLA-4, blocking FN binding) (C), vessel treated with mAb MK-2.7 to VCAM-1 (D), ILDV peptide present during perfusion (E), HP1/2 blocking VLA-4 binding to VCAM-1, and FN (F).	bind
14951	3	3390	7	11	NULL	0	NULL	HP1/2	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_2_153_s_95	10904000	(A), treated with mAb Lia (nonblocking control) (B), mAb HP1/3 (anti-VLA-4, blocking FN binding) (C), vessel treated with mAb MK-2.7 to VCAM-1 (D), ILDV peptide present during perfusion (E), HP1/2 blocking VLA-4 binding to VCAM-1, and FN (F).	bind
14952	4	3390	7	11	NULL	0	NULL	HP1/2	GP		blocks					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_2_153_s_95	10904000	(A), treated with mAb Lia (nonblocking control) (B), mAb HP1/3 (anti-VLA-4, blocking FN binding) (C), vessel treated with mAb MK-2.7 to VCAM-1 (D), ILDV peptide present during perfusion (E), HP1/2 blocking VLA-4 binding to VCAM-1, and FN (F).	bind
80507	1	3390	11	NULL	NULL	0	NULL	VLA-4	Protein		binds to 					VCAM-1	Protein				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_2_153_s_95	10904000	(A), treated with mAb Lia (nonblocking control) (B), mAb HP1/3 (anti-VLA-4, blocking FN binding) (C), vessel treated with mAb MK-2.7 to VCAM-1 (D), ILDV peptide present during perfusion (E), HP1/2 blocking VLA-4 binding to VCAM-1, and FN (F).	bind
80508	2	3390	11	NULL	NULL	0	NULL	VLA-4	Protein		binds to 					FN	Protein				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_2_153_s_95	10904000	(A), treated with mAb Lia (nonblocking control) (B), mAb HP1/3 (anti-VLA-4, blocking FN binding) (C), vessel treated with mAb MK-2.7 to VCAM-1 (D), ILDV peptide present during perfusion (E), HP1/2 blocking VLA-4 binding to VCAM-1, and FN (F).	bind
80509	3	3390	11	NULL	NULL	0	NULL	HP1/2	PartOfProtein		blocks					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_2_153_s_95	10904000	(A), treated with mAb Lia (nonblocking control) (B), mAb HP1/3 (anti-VLA-4, blocking FN binding) (C), vessel treated with mAb MK-2.7 to VCAM-1 (D), ILDV peptide present during perfusion (E), HP1/2 blocking VLA-4 binding to VCAM-1, and FN (F).	bind
80510	4	3390	11	NULL	NULL	0	NULL	HP1/2	PartOfProtein		blocks					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_2_153_s_95	10904000	(A), treated with mAb Lia (nonblocking control) (B), mAb HP1/3 (anti-VLA-4, blocking FN binding) (C), vessel treated with mAb MK-2.7 to VCAM-1 (D), ILDV peptide present during perfusion (E), HP1/2 blocking VLA-4 binding to VCAM-1, and FN (F).	bind
8520	1	3392	5	11	NULL	0	NULL	NXT1	GP		bind		preferentially			GTP-Ran	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8616_s_166	10567585	(A), whereas NXT1 preferentially bound GTP-Ran (B).	bind
10596	1	3392	7	11	NULL	0	NULL	NXT1	GP		bind		preferentially			GTP-Ran	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8616_s_166	10567585	(A), whereas NXT1 preferentially bound GTP-Ran (B).	bind
80511	1	3392	11	NULL	NULL	0	NULL	NXT1	Protein		binds to 					GTP-Ran	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_12_8616_s_166	10567585	(A), whereas NXT1 preferentially bound GTP-Ran (B).	bind
8521	1	3393	5	11	NULL	0	NULL	stem-loop IIIa	NucleicAcid		bind					GAPDH	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_24_14134_s_163	8662893	(A), whereas poly(C) had no apparent effect on stem-loop IIIa binding to GAPDH or p39.	bind
8522	2	3393	5	11	NULL	0	NULL	stem-loop IIIa	NucleicAcid		bind					p39	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_24_14134_s_163	8662893	(A), whereas poly(C) had no apparent effect on stem-loop IIIa binding to GAPDH or p39.	bind
8523	3	3393	5	11	NULL	0	NULL	poly(C)	NucleicAcid		does not effect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_24_14134_s_163	8662893	(A), whereas poly(C) had no apparent effect on stem-loop IIIa binding to GAPDH or p39.	bind
8524	4	3393	5	11	NULL	0	NULL	poly(C)	NucleicAcid		does not effect					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_24_14134_s_163	8662893	(A), whereas poly(C) had no apparent effect on stem-loop IIIa binding to GAPDH or p39.	bind
8525	5	3393	5	11	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_24_14134_s_163	8662893	(A), whereas poly(C) had no apparent effect on stem-loop IIIa binding to GAPDH or p39.	bind
10597	1	3393	7	11	NULL	0	NULL	stem-loop IIIa	NucleicAcid		bind					GAPDH	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_24_14134_s_163	8662893	(A), whereas poly(C) had no apparent effect on stem-loop IIIa binding to GAPDH or p39.	bind
10598	2	3393	7	11	NULL	0	NULL	stem-loop IIIa	NucleicAcid		bind					p39	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_24_14134_s_163	8662893	(A), whereas poly(C) had no apparent effect on stem-loop IIIa binding to GAPDH or p39.	bind
10599	3	3393	7	11	NULL	0	NULL	poly(C)	NucleicAcid		does not effect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_24_14134_s_163	8662893	(A), whereas poly(C) had no apparent effect on stem-loop IIIa binding to GAPDH or p39.	bind
10600	4	3393	7	11	NULL	0	NULL	poly(C)	NucleicAcid		does not effect					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_24_14134_s_163	8662893	(A), whereas poly(C) had no apparent effect on stem-loop IIIa binding to GAPDH or p39.	bind
80512	1	3393	11	NULL	NULL	0	NULL	stem-loop IIIa	NucleicAcidSubstance		binds to 					GAPDH	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_24_14134_s_163	8662893	(A), whereas poly(C) had no apparent effect on stem-loop IIIa binding to GAPDH or p39.	bind
80513	2	3393	11	NULL	NULL	0	NULL	stem-loop IIIa	NucleicAcidSubstance		binds to 					p39	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_24_14134_s_163	8662893	(A), whereas poly(C) had no apparent effect on stem-loop IIIa binding to GAPDH or p39.	bind
8526	1	3396	5	11	NULL	0	NULL	Rab5	GP		bind					GST-GDI	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_2_421_s_55	11239470	(A), with 0-1  M GST-GDI and with or without 100  M ATP S. Rab5 bound to GST-GDI is compared to Rab5 remaining on endosomes after the experiment.	bind
10601	1	3396	7	11	NULL	0	NULL	Rab5	GP		bind					GST-GDI	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_2_421_s_55	11239470	(A), with 0-1  M GST-GDI and with or without 100  M ATP S. Rab5 bound to GST-GDI is compared to Rab5 remaining on endosomes after the experiment.	bind
80514	1	3396	11	NULL	NULL	0	NULL	Rab5	Protein		binds to 					GST-GDI	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_7_2_421_s_55	11239470	(A), with 0-1  M GST-GDI and with or without 100  M ATP S. Rab5 bound to GST-GDI is compared to Rab5 remaining on endosomes after the experiment.	bind
80515	2	3396	11	NULL	NULL	0	NULL	Rab5	Protein		remaining on					endosomes	CellComponent				NULL		0	NULL	NULL	NULL	gw60_molcell_7_2_421_s_55	11239470	(A), with 0-1  M GST-GDI and with or without 100  M ATP S. Rab5 bound to GST-GDI is compared to Rab5 remaining on endosomes after the experiment.	bind
80516	1	3397	11	NULL	NULL	0	NULL	Pab1p	Protein		binds to 					eIF4G1	Protein		115 amino acid		NULL		0	NULL	NULL	NULL	gw60_embo_18_11_3153_s_277	10357826	(A), with 115 amino acid Pab1p-binding fragments of either eIF4G1 or eIF4G2 fused at their N-termini to glutathione  S-transferase (GST) (Tarun and Sachs, 1996  ; Tarun  et al., 1997  ).	bind
80517	2	3397	11	NULL	NULL	0	NULL	Pab1p	Protein		binds to 					eIF4G2	Protein		115 amino acid		NULL		0	NULL	NULL	NULL	gw60_embo_18_11_3153_s_277	10357826	(A), with 115 amino acid Pab1p-binding fragments of either eIF4G1 or eIF4G2 fused at their N-termini to glutathione  S-transferase (GST) (Tarun and Sachs, 1996  ; Tarun  et al., 1997  ).	bind
80518	3	3397	11	NULL	NULL	0	NULL	eIF4G1	Protein		fused to					glutathione S-transferase	Protein		N-termini		NULL		0	NULL	NULL	NULL	gw60_embo_18_11_3153_s_277	10357826	(A), with 115 amino acid Pab1p-binding fragments of either eIF4G1 or eIF4G2 fused at their N-termini to glutathione  S-transferase (GST) (Tarun and Sachs, 1996  ; Tarun  et al., 1997  ).	bind
80519	4	3397	11	NULL	NULL	0	NULL	eIF4G2	Protein		fused to					glutathione S-transferase	Protein		N-termini		NULL		0	NULL	NULL	NULL	gw60_embo_18_11_3153_s_277	10357826	(A), with 115 amino acid Pab1p-binding fragments of either eIF4G1 or eIF4G2 fused at their N-termini to glutathione  S-transferase (GST) (Tarun and Sachs, 1996  ; Tarun  et al., 1997  ).	bind
80520	5	3397	11	NULL	NULL	0	NULL	glutathione S-transferase	Protein		is					GST	Protein				NULL		0	NULL	NULL	NULL	gw60_embo_18_11_3153_s_277	10357826	(A), with 115 amino acid Pab1p-binding fragments of either eIF4G1 or eIF4G2 fused at their N-termini to glutathione  S-transferase (GST) (Tarun and Sachs, 1996  ; Tarun  et al., 1997  ).	bind
80521	1	3399	11	NULL	NULL	0	NULL	PABP	Protein		binds to 					 3' poly	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_annurevphytopathol_43_0_39_s_161	16078876	(A)-binding  protein (PABP) bound to the 3' poly	bind
7533	1	3401	6	11	NULL	0	NULL	hnRNPA1	GP		bind					single-stranded RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_14338_s_204	11278842	(A)-binding protein ( 19); and hnRNPA1 ( 16), which binds single-stranded RNA and the structure of the first two RBD of nucleolin bound to the NRE motif ( 20).	bind
7534	2	3401	6	11	NULL	0	NULL	nucleolin	GP		bind			RBD					NRE motif		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_14338_s_204	11278842	(A)-binding protein ( 19); and hnRNPA1 ( 16), which binds single-stranded RNA and the structure of the first two RBD of nucleolin bound to the NRE motif ( 20).	bind
10602	1	3401	7	11	NULL	0	NULL	hnRNPA1	GP		bind					single-stranded RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_14338_s_204	11278842	(A)-binding protein ( 19); and hnRNPA1 ( 16), which binds single-stranded RNA and the structure of the first two RBD of nucleolin bound to the NRE motif ( 20).	bind
10603	2	3401	7	11	NULL	0	NULL	 nucleolin	GP		bind			RBD					NRE motif		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_14338_s_204	11278842	(A)-binding protein ( 19); and hnRNPA1 ( 16), which binds single-stranded RNA and the structure of the first two RBD of nucleolin bound to the NRE motif ( 20).	bind
80522	1	3401	11	NULL	NULL	0	NULL	hnRNPA1	Protein		binds to 					RNA	NucleicAcidSubstance	single-stranded			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_14338_s_204	11278842	(A)-binding protein ( 19); and hnRNPA1 ( 16), which binds single-stranded RNA and the structure of the first two RBD of nucleolin bound to the NRE motif ( 20).	bind
80523	2	3401	11	NULL	NULL	0	NULL	nucleolin	Protein		binds to 			RBD					NRE motif		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_14338_s_204	11278842	(A)-binding protein ( 19); and hnRNPA1 ( 16), which binds single-stranded RNA and the structure of the first two RBD of nucleolin bound to the NRE motif ( 20).	bind
7536	1	3402	6	11	NULL	0	NULL	nucleolin	GP		bind								RRM		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4765_s_221	10848602	(A)-binding protein ( 7), nucleolin ( 50), SF2 (also known as ASF) ( 8), and U2AF ( 56), binding by a single RRM is much weaker and/or less specific than binding by a combination of two or more RRMs.	bind
7537	2	3402	6	11	NULL	0	NULL	SF2	GP		bind								RRM		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4765_s_221	10848602	(A)-binding protein ( 7), nucleolin ( 50), SF2 (also known as ASF) ( 8), and U2AF ( 56), binding by a single RRM is much weaker and/or less specific than binding by a combination of two or more RRMs.	bind
7538	3	3402	6	11	NULL	0	NULL	SF2	GP		is					ASF	GP	a synonym of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4765_s_221	10848602	(A)-binding protein ( 7), nucleolin ( 50), SF2 (also known as ASF) ( 8), and U2AF ( 56), binding by a single RRM is much weaker and/or less specific than binding by a combination of two or more RRMs.	bind
7539	4	3402	6	11	NULL	0	NULL	U2AF	GP		bind								RRM		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4765_s_221	10848602	(A)-binding protein ( 7), nucleolin ( 50), SF2 (also known as ASF) ( 8), and U2AF ( 56), binding by a single RRM is much weaker and/or less specific than binding by a combination of two or more RRMs.	bind
10604	1	3402	7	11	NULL	0	NULL	nucleolin	GP		bind								RRM		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4765_s_221	10848602	(A)-binding protein ( 7), nucleolin ( 50), SF2 (also known as ASF) ( 8), and U2AF ( 56), binding by a single RRM is much weaker and/or less specific than binding by a combination of two or more RRMs.	bind
10605	2	3402	7	11	NULL	0	NULL	SF2	GP		bind								RRM		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4765_s_221	10848602	(A)-binding protein ( 7), nucleolin ( 50), SF2 (also known as ASF) ( 8), and U2AF ( 56), binding by a single RRM is much weaker and/or less specific than binding by a combination of two or more RRMs.	bind
10606	3	3402	7	11	NULL	0	NULL	U2AF	GP		bind								RRM		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4765_s_221	10848602	(A)-binding protein ( 7), nucleolin ( 50), SF2 (also known as ASF) ( 8), and U2AF ( 56), binding by a single RRM is much weaker and/or less specific than binding by a combination of two or more RRMs.	bind
10608	4	3402	7	11	NULL	0	NULL	SF2	GP		is					ASF	GP	a synonym of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4765_s_221	10848602	(A)-binding protein ( 7), nucleolin ( 50), SF2 (also known as ASF) ( 8), and U2AF ( 56), binding by a single RRM is much weaker and/or less specific than binding by a combination of two or more RRMs.	bind
80524	1	3402	11	NULL	NULL	0	NULL	SF2	Protein		is					ASF	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_13_4765_s_221	10848602	(A)-binding protein ( 7), nucleolin ( 50), SF2 (also known as ASF) ( 8), and U2AF ( 56), binding by a single RRM is much weaker and/or less specific than binding by a combination of two or more RRMs.	bind
80525	2	3402	11	NULL	NULL	0	NULL	nucleolin	Protein		binds to 		weakly;;less specific						single RRM		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_13_4765_s_221	10848602	(A)-binding protein ( 7), nucleolin ( 50), SF2 (also known as ASF) ( 8), and U2AF ( 56), binding by a single RRM is much weaker and/or less specific than binding by a combination of two or more RRMs.	bind
80526	3	3402	11	NULL	NULL	0	NULL	SF2	Protein		binds to 		weakly;;less specific						single RRM		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_13_4765_s_221	10848602	(A)-binding protein ( 7), nucleolin ( 50), SF2 (also known as ASF) ( 8), and U2AF ( 56), binding by a single RRM is much weaker and/or less specific than binding by a combination of two or more RRMs.	bind
80527	4	3402	11	NULL	NULL	0	NULL	U2AF	Protein		binds to 		weakly;;less specific						single RRM		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_13_4765_s_221	10848602	(A)-binding protein ( 7), nucleolin ( 50), SF2 (also known as ASF) ( 8), and U2AF ( 56), binding by a single RRM is much weaker and/or less specific than binding by a combination of two or more RRMs.	bind
7541	2	3404	6	11	NULL	0	NULL	PABP	GP		bind					eIF4A	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_7_4449_s_20	12475969	(A)-binding protein (PABP) and a C-terminal fragment (cpC) that binds eIF4A and eIF3 ( ) (see Fig.  1).	bind
7542	3	3404	6	11	NULL	0	NULL	PABP	GP		bind					eIF3	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_7_4449_s_20	12475969	(A)-binding protein (PABP) and a C-terminal fragment (cpC) that binds eIF4A and eIF3 ( ) (see Fig.  1).	bind
7543	4	3404	6	11	NULL	0	NULL	cpC	AminoAcid		is					C-terminal fragment	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_7_4449_s_20	12475969	(A)-binding protein (PABP) and a C-terminal fragment (cpC) that binds eIF4A and eIF3 ( ) (see Fig.  1).	bind
7544	5	3404	6	11	NULL	0	NULL				bind			cpC		eIF4A	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_7_4449_s_20	12475969	(A)-binding protein (PABP) and a C-terminal fragment (cpC) that binds eIF4A and eIF3 ( ) (see Fig.  1).	bind
7545	6	3404	6	11	NULL	0	NULL				bind			cpC		eIF3	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_7_4449_s_20	12475969	(A)-binding protein (PABP) and a C-terminal fragment (cpC) that binds eIF4A and eIF3 ( ) (see Fig.  1).	bind
10609	1	3404	7	11	NULL	0	NULL	PABP	GP		bind					 eIF4A	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_7_4449_s_20	12475969	(A)-binding protein (PABP) and a C-terminal fragment (cpC) that binds eIF4A and eIF3 ( ) (see Fig.  1).	bind
10610	2	3404	7	11	NULL	0	NULL	PABP	GP		bind					eIF3	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_7_4449_s_20	12475969	(A)-binding protein (PABP) and a C-terminal fragment (cpC) that binds eIF4A and eIF3 ( ) (see Fig.  1).	bind
10611	3	3404	7	11	NULL	0	NULL				bind			C-terminal fragment		eIF4A	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_7_4449_s_20	12475969	(A)-binding protein (PABP) and a C-terminal fragment (cpC) that binds eIF4A and eIF3 ( ) (see Fig.  1).	bind
10612	4	3404	7	11	NULL	0	NULL				bind			C-terminal fragment		eIF3	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_7_4449_s_20	12475969	(A)-binding protein (PABP) and a C-terminal fragment (cpC) that binds eIF4A and eIF3 ( ) (see Fig.  1).	bind
10613	5	3404	7	11	NULL	0	NULL	C-terminal fragment	AminoAcid		is					cpC	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_7_4449_s_20	12475969	(A)-binding protein (PABP) and a C-terminal fragment (cpC) that binds eIF4A and eIF3 ( ) (see Fig.  1).	bind
80528	1	3404	11	NULL	NULL	0	NULL	PABP	Protein		binds to 					eIF4A	Protein				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_4449_s_20	12475969	(A)-binding protein (PABP) and a C-terminal fragment (cpC) that binds eIF4A and eIF3 ( ) (see Fig.  1).	bind
80529	2	3404	11	NULL	NULL	0	NULL	PABP	Protein		binds to 					eIF3	Protein				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_4449_s_20	12475969	(A)-binding protein (PABP) and a C-terminal fragment (cpC) that binds eIF4A and eIF3 ( ) (see Fig.  1).	bind
80530	3	3404	11	NULL	NULL	0	NULL				binds to 			C-terminal fragment		eIF4A	Protein				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_4449_s_20	12475969	(A)-binding protein (PABP) and a C-terminal fragment (cpC) that binds eIF4A and eIF3 ( ) (see Fig.  1).	bind
80531	4	3404	11	NULL	NULL	0	NULL				binds to 			C-terminal fragment		eIF3	Protein				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_4449_s_20	12475969	(A)-binding protein (PABP) and a C-terminal fragment (cpC) that binds eIF4A and eIF3 ( ) (see Fig.  1).	bind
80532	5	3404	11	NULL	NULL	0	NULL	C-terminal fragment	PartOfProtein		is					cpC	PartOfProtein				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_4449_s_20	12475969	(A)-binding protein (PABP) and a C-terminal fragment (cpC) that binds eIF4A and eIF3 ( ) (see Fig.  1).	bind
7547	1	3407	6	11	NULL	0	NULL	PABP	GP		bind					mRNA	NucleicAcid			ARS in 5''-untranslated region	NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_nucleic-acids-res_33_22_16356927_s_4	16356927	(A)-binding protein (PABP) mRNA translation involves  the binding of PABP to the adenine-rich autoregulatory sequence (ARS)  in the 5''-untranslated region of its own mRNA.	bind
7548	2	3407	6	11	NULL	0	NULL	ARS	NucleicAcid		is					adenine-rich autoregulatory sequence	NucleicAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_nucleic-acids-res_33_22_16356927_s_4	16356927	(A)-binding protein (PABP) mRNA translation involves  the binding of PABP to the adenine-rich autoregulatory sequence (ARS)  in the 5''-untranslated region of its own mRNA.	bind
7549	3	3407	6	11	NULL	0	NULL	PABP mRNA	NucleicAcid	translation of	involves					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_nucleic-acids-res_33_22_16356927_s_4	16356927	(A)-binding protein (PABP) mRNA translation involves  the binding of PABP to the adenine-rich autoregulatory sequence (ARS)  in the 5''-untranslated region of its own mRNA.	bind
10614	1	3407	7	11	NULL	0	NULL	PABP	GP		bind					mRNA	NucleicAcid			ARS in 5''-untranslated region	NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_nucleic-acids-res_33_22_16356927_s_4	16356927	(A)-binding protein (PABP) mRNA translation involves  the binding of PABP to the adenine-rich autoregulatory sequence (ARS)  in the 5''-untranslated region of its own mRNA.	bind
10615	2	3407	7	11	NULL	0	NULL	 adenine-rich autoregulatory sequence	NucleicAcid		is					ARS	NucleicAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_nucleic-acids-res_33_22_16356927_s_4	16356927	(A)-binding protein (PABP) mRNA translation involves  the binding of PABP to the adenine-rich autoregulatory sequence (ARS)  in the 5''-untranslated region of its own mRNA.	bind
52799	3	3407	7	11	NULL	0	NULL	PABP mRNA	NucleicAcid	translation of	involves					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_nucleic-acids-res_33_22_16356927_s_4	16356927	(A)-binding protein (PABP) mRNA translation involves  the binding of PABP to the adenine-rich autoregulatory sequence (ARS)  in the 5''-untranslated region of its own mRNA.	bind
80533	1	3407	11	NULL	NULL	0	NULL	PABP 	Protein		binds to 					PABP mRNA	NucleicAcidSubstance	adenine-rich autoregulatory sequence		5''-untranslated region	NULL		0	NULL	NULL	NULL	abs-batch0550-0559_nucleic-acids-res_33_22_16356927_s_4	16356927	(A)-binding protein (PABP) mRNA translation involves  the binding of PABP to the adenine-rich autoregulatory sequence (ARS)  in the 5''-untranslated region of its own mRNA.	bind
80534	2	3407	11	NULL	NULL	0	NULL	statement 1	Process		leads to					translation	MolecularProcess	PABP mRNA			NULL		0	NULL	NULL	NULL	abs-batch0550-0559_nucleic-acids-res_33_22_16356927_s_4	16356927	(A)-binding protein (PABP) mRNA translation involves  the binding of PABP to the adenine-rich autoregulatory sequence (ARS)  in the 5''-untranslated region of its own mRNA.	bind
7550	1	3409	6	11	NULL	0	NULL	p17M1234	NucleicAcid		is a type of					mutated RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2307_s_25	8999938	(A)-binding protein (PABP1) binds specifically to INS-1 within the p17 gag mRNA, but not to mutated RNA (p17M1234).	bind
7551	2	3409	6	11	NULL	0	NULL	PABP1	GP		bind		specifically			p17 gag mRNA	NucleicAcid			INS-1	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2307_s_25	8999938	(A)-binding protein (PABP1) binds specifically to INS-1 within the p17 gag mRNA, but not to mutated RNA (p17M1234).	bind
7552	3	3409	6	11	NULL	0	NULL	PABP1	GP		does not bind					p17M1234	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2307_s_25	8999938	(A)-binding protein (PABP1) binds specifically to INS-1 within the p17 gag mRNA, but not to mutated RNA (p17M1234).	bind
10616	1	3409	7	11	NULL	0	NULL	PABP1	GP		bind		specifically			p17 gag mRNA	NucleicAcid			INS-1	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2307_s_25	8999938	(A)-binding protein (PABP1) binds specifically to INS-1 within the p17 gag mRNA, but not to mutated RNA (p17M1234).	bind
10617	2	3409	7	11	NULL	0	NULL	PABP1	GP		does not bind					p17M1234	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2307_s_25	8999938	(A)-binding protein (PABP1) binds specifically to INS-1 within the p17 gag mRNA, but not to mutated RNA (p17M1234).	bind
10618	3	3409	7	11	NULL	0	NULL	p17M1234	NucleicAcid		is a type of					mutated RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2307_s_25	8999938	(A)-binding protein (PABP1) binds specifically to INS-1 within the p17 gag mRNA, but not to mutated RNA (p17M1234).	bind
80535	1	3409	11	NULL	NULL	NULL	NULL	PABP1	Protein		binds to 		specifically			statement 2	NucleicAcidSubstance				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2307_s_25	8999938	(A)-binding protein (PABP1) binds specifically to INS-1 within the p17 gag mRNA, but not to mutated RNA (p17M1234).	bind
80536	2	3409	11	NULL	NULL	0	NULL	INS-1	NucleicAcidSubstance		is within					p17 gag mRNA	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_4_2307_s_25	8999938	(A)-binding protein (PABP1) binds specifically to INS-1 within the p17 gag mRNA, but not to mutated RNA (p17M1234).	bind
80537	3	3409	11	NULL	NULL	0	NULL	PABP1	Protein		does not bind to					p17 gag mRNA	NucleicAcidSubstance	mutated		p17M1234	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_4_2307_s_25	8999938	(A)-binding protein (PABP1) binds specifically to INS-1 within the p17 gag mRNA, but not to mutated RNA (p17M1234).	bind
7554	2	3410	6	11	NULL	0	NULL	PABP1	GP		bind		preferentially			p17 gag mRNA	NucleicAcid			INS-1	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2307_s_6	8999938	(A)-binding protein 1 (PABP1) binds preferentially to INS-1 within the p17 gag mRNA, but not to a mutated mRNA in which INS-1 function is eliminated.	bind
7555	3	3410	6	11	NULL	0	NULL	p17 gag mRNA	NucleicAcid	mutant	lacks									INS-1	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2307_s_6	8999938	(A)-binding protein 1 (PABP1) binds preferentially to INS-1 within the p17 gag mRNA, but not to a mutated mRNA in which INS-1 function is eliminated.	bind
7556	4	3410	6	11	NULL	0	NULL	PABP1	GP		does not bind					statement 3	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2307_s_6	8999938	(A)-binding protein 1 (PABP1) binds preferentially to INS-1 within the p17 gag mRNA, but not to a mutated mRNA in which INS-1 function is eliminated.	bind
10619	1	3410	7	11	NULL	0	NULL	PABP1	GP		bind		preferentially			p17 gag mRNA	NucleicAcid			INS-1	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2307_s_6	8999938	(A)-binding protein 1 (PABP1) binds preferentially to INS-1 within the p17 gag mRNA, but not to a mutated mRNA in which INS-1 function is eliminated.	bind
10620	2	3410	7	11	NULL	0	NULL	PABP1	GP		does not bind					statement 3	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2307_s_6	8999938	(A)-binding protein 1 (PABP1) binds preferentially to INS-1 within the p17 gag mRNA, but not to a mutated mRNA in which INS-1 function is eliminated.	bind
10621	3	3410	7	11	NULL	0	NULL	p17 gag mRNA	NucleicAcid	mutant	lacks									INS-1	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2307_s_6	8999938	(A)-binding protein 1 (PABP1) binds preferentially to INS-1 within the p17 gag mRNA, but not to a mutated mRNA in which INS-1 function is eliminated.	bind
7557	1	3411	6	11	NULL	0	NULL	poly(U)-binding protein 1	GP		is					Pub1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
7558	2	3411	6	11	NULL	0	NULL	Pub1p	GP		cross link to					RNA	NucleicAcid	polyadenylated			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
7559	3	3411	6	11	NULL	0	NULL	Npl3p	GP		cross link to					RNA	NucleicAcid	polyadenylated			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
7560	4	3411	6	11	NULL	0	NULL	hnRNP-like protein 1	GP		is					Hrp1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
7561	5	3411	6	11	NULL	0	NULL	Hrp1p	GP		cross link to					RNA	NucleicAcid	polyadenylated			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
7562	6	3411	6	11	NULL	0	NULL	nuclear polyadenylated RNA binding 2	GP		is					Nab2p	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
7563	7	3411	6	11	NULL	0	NULL	Nab2p	GP		cross link to					RNA	NucleicAcid	polyadenylated			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
52811	8	3411	6	11	NULL	0	NULL	Npl3p	GP		is					nuclear protein localization 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
10622	1	3411	7	11	NULL	0	NULL	Pub1p	GP		crosslink to					RNA	NucleicAcid	polyadenylated			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
10623	2	3411	7	11	NULL	0	NULL	Npl3p	GP		crosslink to					RNA	NucleicAcid	polyadenylated			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
10624	3	3411	7	11	NULL	0	NULL	Hrp1p	GP		crosslink to					RNA	NucleicAcid	polyadenylated 			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
10625	4	3411	7	11	NULL	0	NULL	Nab2p 	GP		crosslink to					RNA	NucleicAcid	polyadenylated			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
10626	5	3411	7	11	NULL	0	NULL	Pub1p	GP		is					poly(U)-binding protein 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
10629	6	3411	7	11	NULL	0	NULL	Npl3p	GP		is					nuclear protein localization 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
10634	7	3411	7	11	NULL	0	NULL	Hrp1p 	GP		is					hnRNP-like protein 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
10636	8	3411	7	11	NULL	0	NULL	Nab2p	GP		is					nuclear polyadenylated RNA binding 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
80538	1	3411	11	NULL	NULL	0	NULL	Pub1p	Protein		is					poly(U)-binding protein 1	Protein				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
80539	2	3411	11	NULL	NULL	0	NULL	Npl3p	Protein		is					nuclear protein localization 3	Protein				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
80540	3	3411	11	NULL	NULL	0	NULL	Hrp1p	Protein		is					hnRNP-like protein 1	Protein				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
80541	4	3411	11	NULL	NULL	0	NULL	Nab2p	Protein		is					nuclear polyadenylated RNA binding 2	Protein				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
80542	5	3411	11	NULL	NULL	0	NULL	Pub1p	Protein		cross-link to					RNA	NucleicAcidSubstance	polyadenylated			NULL	in vivo	0	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
80543	6	3411	11	NULL	NULL	0	NULL	Npl3p	Protein		cross-link to					RNA	NucleicAcidSubstance	polyadenylated			NULL	in vivo	0	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
80544	7	3411	11	NULL	NULL	0	NULL	Hrp1p	Protein		cross-link to					RNA	NucleicAcidSubstance	polyadenylated			NULL	in vivo	0	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
80545	8	3411	11	NULL	NULL	0	NULL	Nab2p	Protein		cross-link to					RNA	NucleicAcidSubstance	polyadenylated			NULL	in vivo	0	NULL	NULL	NULL	gw60_jbiolchem_277_10_7752_s_48	11779864	(A)-binding protein 1), Pub1p (poly(U)-binding protein 1), Npl3p (nuclear protein localization 3), Hrp1p (hnRNP-like protein 1), and Nab2p (nuclear polyadenylated RNA binding 2), were identified in a screen for proteins that cross-link to polyadenylated RNA  in vivo ( 26,  27).	bind
7564	1	3412	6	11	NULL	0	NULL	poly(A)-binding protein cytoplasmic 1	GP		is					PABPC1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_26_9773_s_137	16785428	(A)-binding protein cytoplasmic 1 (PABPC1) binds and colocalizes with paxillin, and disruption of this interaction inhibited cell migration ( ).	bind
7565	2	3412	6	11	NULL	0	NULL	PABPC1	GP		bind					paxillin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_26_9773_s_137	16785428	(A)-binding protein cytoplasmic 1 (PABPC1) binds and colocalizes with paxillin, and disruption of this interaction inhibited cell migration ( ).	bind
7566	3	3412	6	11	NULL	0	NULL	PABPC1	GP		colocalizes with					paxillin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_26_9773_s_137	16785428	(A)-binding protein cytoplasmic 1 (PABPC1) binds and colocalizes with paxillin, and disruption of this interaction inhibited cell migration ( ).	bind
7567	4	3412	6	11	NULL	0	NULL	statement 2	Process	disruption of	inhibits					cell migration	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_26_9773_s_137	16785428	(A)-binding protein cytoplasmic 1 (PABPC1) binds and colocalizes with paxillin, and disruption of this interaction inhibited cell migration ( ).	bind
10637	1	3412	7	11	NULL	0	NULL	PABPC1	GP		bind					paxillin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_26_9773_s_137	16785428	(A)-binding protein cytoplasmic 1 (PABPC1) binds and colocalizes with paxillin, and disruption of this interaction inhibited cell migration ( ).	bind
10639	2	3412	7	11	NULL	0	NULL	PABPC1	GP		colocalizes with					paxillin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_26_9773_s_137	16785428	(A)-binding protein cytoplasmic 1 (PABPC1) binds and colocalizes with paxillin, and disruption of this interaction inhibited cell migration ( ).	bind
10640	3	3412	7	11	NULL	0	NULL	statement 1	Process	disruption of	inhibits					cell migration	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_26_9773_s_137	16785428	(A)-binding protein cytoplasmic 1 (PABPC1) binds and colocalizes with paxillin, and disruption of this interaction inhibited cell migration ( ).	bind
80546	1	3412	11	NULL	NULL	0	NULL	PABPC1	Protein		binds to 					paxillin	Protein				NULL		0	NULL	NULL	NULL	gw70_pnas_103_26_9773_s_137	16785428	(A)-binding protein cytoplasmic 1 (PABPC1) binds and colocalizes with paxillin, and disruption of this interaction inhibited cell migration ( ).	bind
80547	2	3412	11	NULL	NULL	0	NULL	PABPC1	Protein		colocalizes with					paxillin	Protein				NULL		0	NULL	NULL	NULL	gw70_pnas_103_26_9773_s_137	16785428	(A)-binding protein cytoplasmic 1 (PABPC1) binds and colocalizes with paxillin, and disruption of this interaction inhibited cell migration ( ).	bind
80548	3	3412	11	NULL	NULL	0	NULL	statement 1	Process		occurs along with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_103_26_9773_s_137	16785428	(A)-binding protein cytoplasmic 1 (PABPC1) binds and colocalizes with paxillin, and disruption of this interaction inhibited cell migration ( ).	bind
80549	4	3412	11	NULL	NULL	0	NULL	statement 1	Process	disruption of	inhibit					cell migration	BiologicalProcess				NULL		0	NULL	NULL	NULL	gw70_pnas_103_26_9773_s_137	16785428	(A)-binding protein cytoplasmic 1 (PABPC1) binds and colocalizes with paxillin, and disruption of this interaction inhibited cell migration ( ).	bind
7568	1	3413	6	11	NULL	0	NULL	Pab1p	GP		bind					eIF4F	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_13_4107_s_219	9233819	(A)-binding protein Pab1p which binds eIF4F only in the presence of poly	bind
10641	1	3413	7	11	NULL	0	NULL	Pab1p	GP		bind					eIF4F	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_13_4107_s_219	9233819	(A)-binding protein Pab1p which binds eIF4F only in the presence of poly	bind
80550	1	3413	11	NULL	NULL	0	NULL	 Pab1p	Protein		binds to 					eIF4F	Protein				NULL		0	NULL	NULL	NULL	gw60_embo_16_13_4107_s_219	9233819	(A)-binding protein Pab1p which binds eIF4F only in the presence of poly	bind
7571	1	3414	6	11	NULL	0	NULL	poly(A)-binding protein	GP		is					Pab1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_4_1492_s_252	9841679	(A)-binding protein Pab1p, are also found associated with the eIF4F components of  S. cerevisiae; p20 competes with eIF4G for binding to eIF4E, and Pab1p binds to eIF4F via a site on eIF4G ( 10,  15,  539).	bind
7572	2	3414	6	11	NULL	0	NULL	Pab1p	GP		bind					eIF4F	GP	S. cerevisiae			NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_4_1492_s_252	9841679	(A)-binding protein Pab1p, are also found associated with the eIF4F components of  S. cerevisiae; p20 competes with eIF4G for binding to eIF4E, and Pab1p binds to eIF4F via a site on eIF4G ( 10,  15,  539).	bind
7573	3	3414	6	11	NULL	0	NULL	statement 2	Process		occurs via					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_4_1492_s_252	9841679	(A)-binding protein Pab1p, are also found associated with the eIF4F components of  S. cerevisiae; p20 competes with eIF4G for binding to eIF4E, and Pab1p binds to eIF4F via a site on eIF4G ( 10,  15,  539).	bind
7574	4	3414	6	11	NULL	0	NULL	eIF4E	GP		bind					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_4_1492_s_252	9841679	(A)-binding protein Pab1p, are also found associated with the eIF4F components of  S. cerevisiae; p20 competes with eIF4G for binding to eIF4E, and Pab1p binds to eIF4F via a site on eIF4G ( 10,  15,  539).	bind
7575	5	3414	6	11	NULL	0	NULL	p20	GP		bind					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_4_1492_s_252	9841679	(A)-binding protein Pab1p, are also found associated with the eIF4F components of  S. cerevisiae; p20 competes with eIF4G for binding to eIF4E, and Pab1p binds to eIF4F via a site on eIF4G ( 10,  15,  539).	bind
7576	6	3414	6	11	NULL	0	NULL	statement 4	GP		competes					statement 5	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_4_1492_s_252	9841679	(A)-binding protein Pab1p, are also found associated with the eIF4F components of  S. cerevisiae; p20 competes with eIF4G for binding to eIF4E, and Pab1p binds to eIF4F via a site on eIF4G ( 10,  15,  539).	bind
10645	1	3414	7	11	NULL	0	NULL	p20	GP		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_4_1492_s_252	9841679	(A)-binding protein Pab1p, are also found associated with the eIF4F components of  S. cerevisiae; p20 competes with eIF4G for binding to eIF4E, and Pab1p binds to eIF4F via a site on eIF4G ( 10,  15,  539).	bind
10646	2	3414	7	11	NULL	0	NULL	eIF4G	GP		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_4_1492_s_252	9841679	(A)-binding protein Pab1p, are also found associated with the eIF4F components of  S. cerevisiae; p20 competes with eIF4G for binding to eIF4E, and Pab1p binds to eIF4F via a site on eIF4G ( 10,  15,  539).	bind
10648	3	3414	7	11	NULL	0	NULL	statement 1	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_4_1492_s_252	9841679	(A)-binding protein Pab1p, are also found associated with the eIF4F components of  S. cerevisiae; p20 competes with eIF4G for binding to eIF4E, and Pab1p binds to eIF4F via a site on eIF4G ( 10,  15,  539).	bind
10649	4	3414	7	11	NULL	0	NULL	Pab1p	GP		bind					eIF4F	GP	S. cerevisiae			NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_4_1492_s_252	9841679	(A)-binding protein Pab1p, are also found associated with the eIF4F components of  S. cerevisiae; p20 competes with eIF4G for binding to eIF4E, and Pab1p binds to eIF4F via a site on eIF4G ( 10,  15,  539).	bind
10651	5	3414	7	11	NULL	0	NULL	statement 4	Process		occurs via					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_4_1492_s_252	9841679	(A)-binding protein Pab1p, are also found associated with the eIF4F components of  S. cerevisiae; p20 competes with eIF4G for binding to eIF4E, and Pab1p binds to eIF4F via a site on eIF4G ( 10,  15,  539).	bind
80551	1	3414	11	NULL	NULL	0	NULL	Pab1p	Protein		associated with					eIF4F 	Protein	S. cerevisiae			NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_4_1492_s_252	9841679	(A)-binding protein Pab1p, are also found associated with the eIF4F components of  S. cerevisiae; p20 competes with eIF4G for binding to eIF4E, and Pab1p binds to eIF4F via a site on eIF4G ( 10,  15,  539).	bind
80552	2	3414	11	NULL	NULL	0	NULL	p20	Protein		competes with					eIF4G	Protein				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_4_1492_s_252	9841679	(A)-binding protein Pab1p, are also found associated with the eIF4F components of  S. cerevisiae; p20 competes with eIF4G for binding to eIF4E, and Pab1p binds to eIF4F via a site on eIF4G ( 10,  15,  539).	bind
80553	3	3414	11	NULL	NULL	0	NULL	p20	Protein		binds to 					eIF4E	Protein				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_4_1492_s_252	9841679	(A)-binding protein Pab1p, are also found associated with the eIF4F components of  S. cerevisiae; p20 competes with eIF4G for binding to eIF4E, and Pab1p binds to eIF4F via a site on eIF4G ( 10,  15,  539).	bind
80554	4	3414	11	NULL	NULL	0	NULL	eIF4G	Protein		binds to 					eIF4E	Protein				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_4_1492_s_252	9841679	(A)-binding protein Pab1p, are also found associated with the eIF4F components of  S. cerevisiae; p20 competes with eIF4G for binding to eIF4E, and Pab1p binds to eIF4F via a site on eIF4G ( 10,  15,  539).	bind
80555	5	3414	11	NULL	NULL	0	NULL	statement 1	Process		occurs via					eIF4G	Protein				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_4_1492_s_252	9841679	(A)-binding protein Pab1p, are also found associated with the eIF4F components of  S. cerevisiae; p20 competes with eIF4G for binding to eIF4E, and Pab1p binds to eIF4F via a site on eIF4G ( 10,  15,  539).	bind
7579	1	3415	6	11	NULL	0	NULL	Xenopus-specific protein	GP		bind									AU-rich sequences	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_2060_s_91	15713657	(A)-binding protein was identified as a  Xenopus-specific protein that binds AU-rich sequences ( ).	bind
10652	1	3415	7	11	NULL	0	NULL	Xenopus-specific protein	GP		bind									AU-rich sequences	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_2060_s_91	15713657	(A)-binding protein was identified as a  Xenopus-specific protein that binds AU-rich sequences ( ).	bind
80556	1	3415	11	NULL	NULL	0	NULL	protein	Protein	Xenopus-specific	binds to 					AU-rich sequence	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_5_2060_s_91	15713657	(A)-binding protein was identified as a  Xenopus-specific protein that binds AU-rich sequences ( ).	bind
7581	2	3418	6	11	NULL	0	NULL	eIF4B	GP		does not bind					Hsp27	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_12_1460_s_8	10859165	(A)-binding protein, eIF4B, and eIF3 were not bound by Hsp27 and were not recruited into insoluble complexes.	bind
7582	3	3418	6	11	NULL	0	NULL	eIF3	GP		does not bind					Hsp27	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_12_1460_s_8	10859165	(A)-binding protein, eIF4B, and eIF3 were not bound by Hsp27 and were not recruited into insoluble complexes.	bind
7584	5	3418	6	11	NULL	0	NULL	eIF4B	GP		are not recruited into					insoluble complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_12_1460_s_8	10859165	(A)-binding protein, eIF4B, and eIF3 were not bound by Hsp27 and were not recruited into insoluble complexes.	bind
7585	6	3418	6	11	NULL	0	NULL	eIF3	GP		are not recruited into					insoluble complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_12_1460_s_8	10859165	(A)-binding protein, eIF4B, and eIF3 were not bound by Hsp27 and were not recruited into insoluble complexes.	bind
10654	1	3418	7	11	NULL	0	NULL	eIF4B	GP		does not bind					Hsp27	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_12_1460_s_8	10859165	(A)-binding protein, eIF4B, and eIF3 were not bound by Hsp27 and were not recruited into insoluble complexes.	bind
10655	2	3418	7	11	NULL	0	NULL	 eIF3	GP		does not bind					Hsp27	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_12_1460_s_8	10859165	(A)-binding protein, eIF4B, and eIF3 were not bound by Hsp27 and were not recruited into insoluble complexes.	bind
10657	3	3418	7	11	NULL	0	NULL	 eIF4B	GP		is not recruited into					insoluble complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_12_1460_s_8	10859165	(A)-binding protein, eIF4B, and eIF3 were not bound by Hsp27 and were not recruited into insoluble complexes.	bind
10658	4	3418	7	11	NULL	0	NULL	eIF3	GP		is not recruited into					insoluble complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_12_1460_s_8	10859165	(A)-binding protein, eIF4B, and eIF3 were not bound by Hsp27 and were not recruited into insoluble complexes.	bind
80557	1	3418	11	NULL	NULL	0	NULL	eIF4B	Protein		not bind to					Hsp27	Protein				NULL		0	NULL	NULL	NULL	gw60_genesdev_14_12_1460_s_8	10859165	(A)-binding protein, eIF4B, and eIF3 were not bound by Hsp27 and were not recruited into insoluble complexes.	bind
80558	2	3418	11	NULL	NULL	0	NULL	eIF3	Protein		not bind to 					Hsp27	Protein				NULL		0	NULL	NULL	NULL	gw60_genesdev_14_12_1460_s_8	10859165	(A)-binding protein, eIF4B, and eIF3 were not bound by Hsp27 and were not recruited into insoluble complexes.	bind
7587	2	3421	6	11	NULL	0	NULL	PARN	GP		bind 									EDEN sequence	NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_35_0_365_s_98	11700288	(A)-specific RNase (PARN) ( 100) and EDEN-BP ( 162), which binds to the EDEN sequence.	bind
7588	3	3421	6	11	NULL	0	NULL	EDEN-BP	GP		bind									EDEN sequence	NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_35_0_365_s_98	11700288	(A)-specific RNase (PARN) ( 100) and EDEN-BP ( 162), which binds to the EDEN sequence.	bind
10659	1	3421	7	11	NULL	0	NULL	PARN	GP		bind									EDEN sequence	NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_35_0_365_s_98	11700288	(A)-specific RNase (PARN) ( 100) and EDEN-BP ( 162), which binds to the EDEN sequence.	bind
10660	2	3421	7	11	NULL	0	NULL	EDEN-BP	GP		bind									EDEN sequence	NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_35_0_365_s_98	11700288	(A)-specific RNase (PARN) ( 100) and EDEN-BP ( 162), which binds to the EDEN sequence.	bind
80559	1	3421	11	NULL	NULL	0	NULL	PARN	Protein		binds to 					EDEN sequence	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_annurevgenet_35_0_365_s_98	11700288	(A)-specific RNase (PARN) ( 100) and EDEN-BP ( 162), which binds to the EDEN sequence.	bind
80560	2	3421	11	NULL	NULL	0	NULL	EDEN-BP	Protein		binds to 					EDEN sequence	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_annurevgenet_35_0_365_s_98	11700288	(A)-specific RNase (PARN) ( 100) and EDEN-BP ( 162), which binds to the EDEN sequence.	bind
7589	1	3422	6	11	NULL	0	NULL	poly(A)-tail-induced initiation factor 	GP		bind					m7G cap	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_1_104_s_163	15630022	(A)-tail-induced initiation factor binding to the m7G cap.	bind
10661	1	3422	7	11	NULL	0	NULL	poly(A)-tail-induced initiation factor	GP		bind					m7G cap	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_1_104_s_163	15630022	(A)-tail-induced initiation factor binding to the m7G cap.	bind
80561	1	3422	11	NULL	NULL	0	NULL	initiation factor	Protein		binds to 					m7G cap	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_1_104_s_163	15630022	(A)-tail-induced initiation factor binding to the m7G cap.	bind
7590	1	3423	6	11	NULL	0	NULL	NC	GP		bind									(TG)4	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_472_s_300	16434700	(A)30 (open squares) or (TG)10 (open triangles), was able to completely prevent the binding of NC to (TG)4 on the SPR surface (i.e. the ISmin was 0, as indicated in  Table 3).	bind
7591	2	3423	6	11	NULL	0	NULL				prevents				(TG)10	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_472_s_300	16434700	(A)30 (open squares) or (TG)10 (open triangles), was able to completely prevent the binding of NC to (TG)4 on the SPR surface (i.e. the ISmin was 0, as indicated in  Table 3).	bind
10663	1	3423	7	11	NULL	0	NULL	NC 	GP		bind									(TG)4	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_472_s_300	16434700	(A)30 (open squares) or (TG)10 (open triangles), was able to completely prevent the binding of NC to (TG)4 on the SPR surface (i.e. the ISmin was 0, as indicated in  Table 3).	bind
10664	2	3423	7	11	NULL	0	NULL				prevent				(TG)10	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_472_s_300	16434700	(A)30 (open squares) or (TG)10 (open triangles), was able to completely prevent the binding of NC to (TG)4 on the SPR surface (i.e. the ISmin was 0, as indicated in  Table 3).	bind
80562	1	3423	11	NULL	NULL	0	NULL	NC	Chemical		binds to 					(TG)4	NucleicAcidSubstance	SPR surface			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_472_s_300	16434700	(A)30 (open squares) or (TG)10 (open triangles), was able to completely prevent the binding of NC to (TG)4 on the SPR surface (i.e. the ISmin was 0, as indicated in  Table 3).	bind
7632	1	3424	6	11	NULL	0	NULL	NC	GP		bind									(TG)4	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_472_s_259	16434700	(A)30 completely eliminated binding of NC to (TG)4, as expected.	bind
10666	1	3424	7	11	NULL	0	NULL	NC	GP		bind									(TG)4	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_472_s_259	16434700	(A)30 completely eliminated binding of NC to (TG)4, as expected.	bind
80563	1	3424	11	NULL	NULL	0	NULL	NC 	Chemical		binds to 					(TG)4	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_472_s_259	16434700	(A)30 completely eliminated binding of NC to (TG)4, as expected.	bind
7634	1	3426	6	11	NULL	0	NULL	RNA	NucleicAcid	radioactively labeled	bind				ARS	PABP	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_248	16356927	(A)50 RNA ( Figure 2C, lanes 9 - 14 and legend crosses in  Figure 2D) to attain a similar level of inhibition of the binding of radioactively labeled ARS RNA to PABP.	bind
7635	2	3426	6	11	NULL	0	NULL	50 RNA	NucleicAcid		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_248	16356927	(A)50 RNA ( Figure 2C, lanes 9 - 14 and legend crosses in  Figure 2D) to attain a similar level of inhibition of the binding of radioactively labeled ARS RNA to PABP.	bind
10686	1	3426	7	11	NULL	0	NULL	PABP	GP		bind					RNA	NucleicAcid	radioactively labeled		ARS	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_248	16356927	(A)50 RNA ( Figure 2C, lanes 9 - 14 and legend crosses in  Figure 2D) to attain a similar level of inhibition of the binding of radioactively labeled ARS RNA to PABP.	bind
14953	2	3426	7	11	NULL	0	NULL	50 RNA	NucleicAcid		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_248	16356927	(A)50 RNA ( Figure 2C, lanes 9 - 14 and legend crosses in  Figure 2D) to attain a similar level of inhibition of the binding of radioactively labeled ARS RNA to PABP.	bind
80564	1	3426	11	NULL	NULL	0	NULL	ARS RNA	NucleicAcidSubstance	radioactively labeled	inhibit					PABP	Protein				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_248	16356927	(A)50 RNA ( Figure 2C, lanes 9 - 14 and legend crosses in  Figure 2D) to attain a similar level of inhibition of the binding of radioactively labeled ARS RNA to PABP.	bind
7636	1	3427	6	11	NULL	0	NULL	IMP1	GP		bind					RNA	NucleicAcid	labeled		ARS	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_294	16356927	(A)50 RNA competed with the binding of both 63 (IMP1) and 105 (UNR) kDa polypeptides to the labeled ARS RNA.	bind
7637	2	3427	6	11	NULL	0	NULL	50 RNA	NucleicAcid		bind					RNA	NucleicAcid	labeled		ARS	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_294	16356927	(A)50 RNA competed with the binding of both 63 (IMP1) and 105 (UNR) kDa polypeptides to the labeled ARS RNA.	bind
7638	3	3427	6	11	NULL	0	NULL	statement 1	GP		competes					statement 2	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_294	16356927	(A)50 RNA competed with the binding of both 63 (IMP1) and 105 (UNR) kDa polypeptides to the labeled ARS RNA.	bind
7639	4	3427	6	10	NULL	0	NULL	UNR	NULL		bind	NULL				RNA	NULL	labeled		ARS	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_294	16356927	(A)50 RNA competed with the binding of both 63 (IMP1) and 105 (UNR) kDa polypeptides to the labeled ARS RNA.	bind
7641	5	3427	6	10	NULL	0	NULL	statement 4	NULL		competes	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_294	16356927	(A)50 RNA competed with the binding of both 63 (IMP1) and 105 (UNR) kDa polypeptides to the labeled ARS RNA.	bind
10687	1	3427	7	11	NULL	0	NULL	IMP1 polypeptide	GP		bind					 RNA	NucleicAcid	labeled		ARS	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_294	16356927	(A)50 RNA competed with the binding of both 63 (IMP1) and 105 (UNR) kDa polypeptides to the labeled ARS RNA.	bind
10688	2	3427	7	11	NULL	0	NULL	UNR polypeptide	GP		bind					 RNA	NucleicAcid	labeled		ARS	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_294	16356927	(A)50 RNA competed with the binding of both 63 (IMP1) and 105 (UNR) kDa polypeptides to the labeled ARS RNA.	bind
14958	5	3427	7	11	NULL	0	NULL	50 RNA	NucleicAcid		bind					 RNA	NucleicAcid			ARS	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_294	16356927	(A)50 RNA competed with the binding of both 63 (IMP1) and 105 (UNR) kDa polypeptides to the labeled ARS RNA.	bind
14959	6	3427	7	11	NULL	0	NULL	statement 5	NucleicAcid		compete with					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_294	16356927	(A)50 RNA competed with the binding of both 63 (IMP1) and 105 (UNR) kDa polypeptides to the labeled ARS RNA.	bind
14960	7	3427	7	11	NULL	0	NULL	statement 5	NucleicAcid		compete with					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_294	16356927	(A)50 RNA competed with the binding of both 63 (IMP1) and 105 (UNR) kDa polypeptides to the labeled ARS RNA.	bind
80565	1	3427	11	NULL	NULL	0	NULL	poly(A)50 RNA	NucleicAcidSubstance		competes with					IMP1 polypeptide	PartOfProtein				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_294	16356927	(A)50 RNA competed with the binding of both 63 (IMP1) and 105 (UNR) kDa polypeptides to the labeled ARS RNA.	bind
80566	2	3427	11	NULL	NULL	0	NULL	poly(A)50 RNA	NucleicAcidSubstance		competes with					UNR polypeptide	PartOfProtein				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_294	16356927	(A)50 RNA competed with the binding of both 63 (IMP1) and 105 (UNR) kDa polypeptides to the labeled ARS RNA.	bind
80567	3	3427	11	NULL	NULL	0	NULL	poly(A)50 RNA	NucleicAcidSubstance		binds to 					ARS RNA	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_294	16356927	(A)50 RNA competed with the binding of both 63 (IMP1) and 105 (UNR) kDa polypeptides to the labeled ARS RNA.	bind
80568	4	3427	11	NULL	NULL	0	NULL	IMP1 polypeptide	PartOfProtein		binds to 					ARS RNA	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_294	16356927	(A)50 RNA competed with the binding of both 63 (IMP1) and 105 (UNR) kDa polypeptides to the labeled ARS RNA.	bind
80569	5	3427	11	NULL	NULL	0	NULL	UNR polypeptide	PartOfProtein		binds to 					ARS RNA	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_294	16356927	(A)50 RNA competed with the binding of both 63 (IMP1) and 105 (UNR) kDa polypeptides to the labeled ARS RNA.	bind
80570	1	3428	11	NULL	NULL	0	NULL	NF-IL-6	Protein		contain					 palindrome	NucleicAcidSubstance			CCTTGCTGCAAGG	NULL		0	NULL	NULL	NULL	gw60_gene_237_1_177_s_66	10524248	(A); a palindrome (CCTTGCTGCAAGG) containing NF-IL-6 and GAS-like elements (P); two IRF-1-like sites (I1 and I2); an Ets-1 binding motif (E); and an ISRE.	bind
7642	1	3430	6	11	NULL	0	NULL	GDP	Chemical		bind					Rab11A	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_8_3530_s_149	15181150	(A); with the GDP-bound  form of Rab11A (C); and with the GppNHp-bound form of Rab4B (D).	bind
7644	2	3430	6	11	NULL	0	NULL	GppNHp	Chemical		bind					Rab4B	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_8_3530_s_149	15181150	(A); with the GDP-bound  form of Rab11A (C); and with the GppNHp-bound form of Rab4B (D).	bind
10689	1	3430	7	11	NULL	0	NULL	GDP	Chemical		bind					Rab11A	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_8_3530_s_149	15181150	(A); with the GDP-bound  form of Rab11A (C); and with the GppNHp-bound form of Rab4B (D).	bind
10690	2	3430	7	11	NULL	0	NULL	GppNHp	Chemical		bind					Rab4B	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_8_3530_s_149	15181150	(A); with the GDP-bound  form of Rab11A (C); and with the GppNHp-bound form of Rab4B (D).	bind
80571	1	3430	11	NULL	NULL	0	NULL	Rab11A	Protein		binds to 					 GDP	Chemical				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3530_s_149	15181150	(A); with the GDP-bound  form of Rab11A (C); and with the GppNHp-bound form of Rab4B (D).	bind
80572	2	3430	11	NULL	NULL	0	NULL	Rab4B	Protein		binds to 					GppNHp	Chemical				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3530_s_149	15181150	(A); with the GDP-bound  form of Rab11A (C); and with the GppNHp-bound form of Rab4B (D).	bind
7649	1	3431	6	11	NULL	0	NULL	eukaryotic initiation factor 4F	GP		bind					cap analogues	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_507	10944120	(A)binding protein enhances the binding affinity of eukaryotic initiation factor 4F and (iso)4F for cap analogues.	bind
7651	2	3431	6	11	NULL	0	NULL	eukaryotic initiation factor (iso)4F	GP		bind					cap analogues	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_507	10944120	(A)binding protein enhances the binding affinity of eukaryotic initiation factor 4F and (iso)4F for cap analogues.	bind
10691	1	3431	7	11	NULL	0	NULL	 eukaryotic initiation factor 4F	GP		bind					cap analogues	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_507	10944120	(A)binding protein enhances the binding affinity of eukaryotic initiation factor 4F and (iso)4F for cap analogues.	bind
10694	2	3431	7	11	NULL	0	NULL	eukaryotic initiation factor (iso)4F	GP		bind					cap analogues	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_16_4372_s_507	10944120	(A)binding protein enhances the binding affinity of eukaryotic initiation factor 4F and (iso)4F for cap analogues.	bind
80573	1	3431	11	NULL	NULL	0	NULL	poly(A)binding protein 	Protein		binds to 		enhances			eukaryotic initiation factor 4F	Protein				NULL		0	NULL	NULL	NULL	gw60_embo_19_16_4372_s_507	10944120	(A)binding protein enhances the binding affinity of eukaryotic initiation factor 4F and (iso)4F for cap analogues.	bind
80574	1	3432	11	NULL	NULL	0	NULL	GABAAR &#946;3	Protein	dephosphorylated	binds to 		high affinity			AP2	Protein				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_proc-natl-acad-sci-u-s-a_102_41_16192353_s_10	16192353	(A)R beta3 subunit binds  to AP2 with high affinity only when dephosphorylated.	bind
7657	1	3435	6	11	NULL	0	NULL				bind				S-TATA composite box	GTFs	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_834_s_121	10629040	(A)S-TATA composite box binds GTFs.	bind
10701	1	3435	7	11	NULL	0	NULL				binds				S-TATA composite box	GTFs	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_834_s_121	10629040	(A)S-TATA composite box binds GTFs.	bind
7658	1	3436	6	11	NULL	0	NULL				does not bind		efficiently		S-TATA	TBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_834_s_127	10629040	(A)S-TATA does not bind TBP efficiently (lane 1) but binds the mixture of the three GTF proteins (lane 7).	bind
7659	2	3436	6	11	NULL	0	NULL				bind				S-TATA	GTF proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_834_s_127	10629040	(A)S-TATA does not bind TBP efficiently (lane 1) but binds the mixture of the three GTF proteins (lane 7).	bind
10702	1	3436	7	11	NULL	0	NULL				does not bind		efficiently		S-TATA	TBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_834_s_127	10629040	(A)S-TATA does not bind TBP efficiently (lane 1) but binds the mixture of the three GTF proteins (lane 7).	bind
10703	2	3436	7	11	NULL	0	NULL				bind				S-TATA	GTF proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_834_s_127	10629040	(A)S-TATA does not bind TBP efficiently (lane 1) but binds the mixture of the three GTF proteins (lane 7).	bind
80575	1	3436	11	NULL	NULL	0	NULL	P(A)S-TATA	NucleicAcidSubstance		does not bind to					TBP	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_3_834_s_127	10629040	(A)S-TATA does not bind TBP efficiently (lane 1) but binds the mixture of the three GTF proteins (lane 7).	bind
80576	2	3436	11	NULL	NULL	0	NULL	P(A)S-TATA	NucleicAcidSubstance		binds to 					GTF proteins	Protein	mixture			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_3_834_s_127	10629040	(A)S-TATA does not bind TBP efficiently (lane 1) but binds the mixture of the three GTF proteins (lane 7).	bind
7661	1	3437	6	11	NULL	0	NULL				bind				s-TATA	GTFs	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_834_s_154	10629040	(A)S-TATA sequence binds the GTFs in a manner genuinely characteristic of a promoter.	bind
7662	2	3437	6	11	NULL	0	NULL	statement 1	Process		is characteristic of									promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_834_s_154	10629040	(A)S-TATA sequence binds the GTFs in a manner genuinely characteristic of a promoter.	bind
10704	1	3437	7	11	NULL	0	NULL				binds				S-TATA sequence	GTFs	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_834_s_154	10629040	(A)S-TATA sequence binds the GTFs in a manner genuinely characteristic of a promoter.	bind
14965	2	3437	7	11	NULL	0	NULL	statement 1	Process		is characteristic of									promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_834_s_154	10629040	(A)S-TATA sequence binds the GTFs in a manner genuinely characteristic of a promoter.	bind
7698	1	3439	6	11	NULL	0	NULL	SH-SY5Y-h 7 cells	Cell	transfected	overexpress					7 receptors	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_113	11044725	(A)] and saturation 125I- BTx binding [ Fig. 4(B)] to transfected SH-SY5Y-h 7 neuroblastoma cells overexpressing human  7 receptors also were consistent with a non-competitive mechanism of functional block by diltiazem.	bind
7699	2	3439	6	11	NULL	0	NULL	BTx	Chemical	125I-labeled	bind					statement 1	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_113	11044725	(A)] and saturation 125I- BTx binding [ Fig. 4(B)] to transfected SH-SY5Y-h 7 neuroblastoma cells overexpressing human  7 receptors also were consistent with a non-competitive mechanism of functional block by diltiazem.	bind
52812	3	3439	6	11	NULL	0	NULL	SH-SY5Y-h 7 cells	Cell		is a type of					neuroblastoma cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_113	11044725	(A)] and saturation 125I- BTx binding [ Fig. 4(B)] to transfected SH-SY5Y-h 7 neuroblastoma cells overexpressing human  7 receptors also were consistent with a non-competitive mechanism of functional block by diltiazem.	bind
10730	1	3439	7	11	NULL	0	NULL	BTx	Chemical	125I-labeled	bind					SH-SY5Y-h 7 cells	Cell	transfected			NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_113	11044725	(A)] and saturation 125I- BTx binding [ Fig. 4(B)] to transfected SH-SY5Y-h 7 neuroblastoma cells overexpressing human  7 receptors also were consistent with a non-competitive mechanism of functional block by diltiazem.	bind
11753	2	3439	7	11	NULL	0	NULL	SH-SY5Y-h 7 cells	Cell	transfected	overexpress					7 receptors	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_113	11044725	(A)] and saturation 125I- BTx binding [ Fig. 4(B)] to transfected SH-SY5Y-h 7 neuroblastoma cells overexpressing human  7 receptors also were consistent with a non-competitive mechanism of functional block by diltiazem.	bind
52813	3	3439	7	11	NULL	0	NULL	SH-SY5Y-h 7 cells	Cell		is a type of					neuroblastoma cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_113	11044725	(A)] and saturation 125I- BTx binding [ Fig. 4(B)] to transfected SH-SY5Y-h 7 neuroblastoma cells overexpressing human  7 receptors also were consistent with a non-competitive mechanism of functional block by diltiazem.	bind
7663	1	3441	6	11	NULL	0	NULL	Ang IV	GP	125I-labeled	bind					MDBK cell membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_113	10565848	(A,  n = 4) and dithiothreitol (B,  n = 3) on 125I-Ang IV and 125I-divalinal Ang IV binding to MDBK cell membranes and 125I-Ang II binding to rat liver membranes.	bind
7664	2	3441	6	11	NULL	0	NULL	divalinal Ang IV	GP	125I-labeled	bind					MDBK cell membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_113	10565848	(A,  n = 4) and dithiothreitol (B,  n = 3) on 125I-Ang IV and 125I-divalinal Ang IV binding to MDBK cell membranes and 125I-Ang II binding to rat liver membranes.	bind
7665	3	3441	6	11	NULL	0	NULL	Ang II	GP	125I-labeled	bind					liver membranes	OrganismPart	rat			NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_113	10565848	(A,  n = 4) and dithiothreitol (B,  n = 3) on 125I-Ang IV and 125I-divalinal Ang IV binding to MDBK cell membranes and 125I-Ang II binding to rat liver membranes.	bind
10731	1	3441	7	11	NULL	0	NULL	divalinal Ang IV	GP	125I-labeled	bind					MDBK cell membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_113	10565848	(A,  n = 4) and dithiothreitol (B,  n = 3) on 125I-Ang IV and 125I-divalinal Ang IV binding to MDBK cell membranes and 125I-Ang II binding to rat liver membranes.	bind
10732	2	3441	7	11	NULL	0	NULL	Ang II	GP	125I-labeled	bind					liver membrane	OrganismPart	rat			NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_113	10565848	(A,  n = 4) and dithiothreitol (B,  n = 3) on 125I-Ang IV and 125I-divalinal Ang IV binding to MDBK cell membranes and 125I-Ang II binding to rat liver membranes.	bind
52814	3	3441	7	11	NULL	0	NULL	Ang IV	GP	125I-labeled	bind					MDBK cell membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_113	10565848	(A,  n = 4) and dithiothreitol (B,  n = 3) on 125I-Ang IV and 125I-divalinal Ang IV binding to MDBK cell membranes and 125I-Ang II binding to rat liver membranes.	bind
80577	1	3441	11	NULL	NULL	0	NULL	125I-Ang II	Protein		binds to 					membrane	CellComponent	rat liver			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_113	10565848	(A,  n = 4) and dithiothreitol (B,  n = 3) on 125I-Ang IV and 125I-divalinal Ang IV binding to MDBK cell membranes and 125I-Ang II binding to rat liver membranes.	bind
80578	2	3441	11	NULL	NULL	0	NULL	125I-divalinal Ang IV	Protein		binds to 					cell membrane	CellComponent	MDBK			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_113	10565848	(A,  n = 4) and dithiothreitol (B,  n = 3) on 125I-Ang IV and 125I-divalinal Ang IV binding to MDBK cell membranes and 125I-Ang II binding to rat liver membranes.	bind
80579	3	3441	11	NULL	NULL	0	NULL	125I-Ang IV	Protein		binds to 					cell membrane	CellComponent	MDBK			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_113	10565848	(A,  n = 4) and dithiothreitol (B,  n = 3) on 125I-Ang IV and 125I-divalinal Ang IV binding to MDBK cell membranes and 125I-Ang II binding to rat liver membranes.	bind
80580	1	3445	11	NULL	NULL	0	NULL	GST-fused protein	Protein		binds to 					glutathione-Sepharose 4B	PartOfProtein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_6_2242_s_300	15743821	(A, B, D, and E) The indicated [35]methionine-labeled products in vitro translated in rabbit reticulocyte lysates were  incubated with the different GST-fused proteins bound to glutathione-Sepharose 4B.	bind
7666	1	3447	6	11	NULL	0	NULL	TetR-GFP	GP		bind									TetO repeats	NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_1_55_s_172	15643060	(A, C, and E) and  TetR-GFP bound to  TetO repeats (B, D, and F) were visualized by fluorescence microscopy with UV and fluorescein  isothiocyanate optics, respectively.	bind
10733	1	3447	7	11	NULL	0	NULL	TetR-GFP	GP		bind									TetO repeats	NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_1_55_s_172	15643060	(A, C, and E) and  TetR-GFP bound to  TetO repeats (B, D, and F) were visualized by fluorescence microscopy with UV and fluorescein  isothiocyanate optics, respectively.	bind
80581	1	3447	11	NULL	NULL	0	NULL	TetR-GFP	PartOfProtein		binds to 					TetO repeats	PartOfProtein				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_55_s_172	15643060	(A, C, and E) and  TetR-GFP bound to  TetO repeats (B, D, and F) were visualized by fluorescence microscopy with UV and fluorescein  isothiocyanate optics, respectively.	bind
7667	1	3448	6	11	NULL	0	NULL	MAb 1E5 	GP		bind					PvpA	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_3_1265_s_143	12595441	(A, C, and E), although the corresponding membranes  were immunostained with a rabbit anti-GapA polyclonal antibody (B and D) or with  MAb 1E5 that binds the PvpA surface protein (F). "`+"`	bind
52817	2	3448	6	11	NULL	0	NULL	PvpA	GP		is a type of					surface protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_3_1265_s_143	12595441	(A, C, and E), although the corresponding membranes  were immunostained with a rabbit anti-GapA polyclonal antibody (B and D) or with  MAb 1E5 that binds the PvpA surface protein (F). "`+"`	bind
10734	1	3448	7	11	NULL	0	NULL	MAb 1E5	GP		bind					PvpA	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_3_1265_s_143	12595441	(A, C, and E), although the corresponding membranes  were immunostained with a rabbit anti-GapA polyclonal antibody (B and D) or with  MAb 1E5 that binds the PvpA surface protein (F). "`+"`	bind
52819	2	3448	7	11	NULL	0	NULL	PvpA	GP		is a type of					surface protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_3_1265_s_143	12595441	(A, C, and E), although the corresponding membranes  were immunostained with a rabbit anti-GapA polyclonal antibody (B and D) or with  MAb 1E5 that binds the PvpA surface protein (F). "`+"`	bind
80582	1	3448	11	NULL	NULL	0	NULL	MAb 1E5	Protein		binds to 					PvpA	Gene				NULL		0	NULL	NULL	NULL	gw70_infectimmun_71_3_1265_s_143	12595441	(A, C, and E), although the corresponding membranes  were immunostained with a rabbit anti-GapA polyclonal antibody (B and D) or with  MAb 1E5 that binds the PvpA surface protein (F). "`+"`	bind
7700	1	3452	6	11	NULL	0	NULL	amphiphysin	GP		bind					adaptin	GP		appendage domain		NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
7701	2	3452	6	11	NULL	0	NULL	Eps15	GP		bind					adaptin	GP		appendage domain		NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
7702	3	3452	6	11	NULL	0	NULL	AP180	GP		bind					adaptin	GP		appendage domain		NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
7703	4	3452	6	11	NULL	0	NULL	clathrin	GP		bind					adaptin	GP		appendage domain		NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
7704	5	3452	6	11	NULL	0	NULL	DPW peptides	AminoAcid		inhibit					statement 1	Process				NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
7705	6	3452	6	11	NULL	0	NULL	DPW peptides	AminoAcid		inhibits					statement 2	Process				NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
7706	7	3452	6	11	NULL	0	NULL	DPW peptides	AminoAcid		inhibits					statement 3	Process				NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
7707	8	3452	6	11	NULL	0	NULL	DPW peptides	AminoAcid		inhibits					statement 4	Process				NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
7708	9	3452	6	11	NULL	0	NULL	DPF peptides	AminoAcid		inhibits					statement 1	Process				NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
7709	10	3452	6	11	NULL	0	NULL	DPF peptides	AminoAcid		inhibits					statement 2	Process				NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
7710	11	3452	6	11	NULL	0	NULL	DPF peptides	AminoAcid		inhibits					statement 3	Process				NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
7711	12	3452	6	11	NULL	0	NULL	DPF peptides	AminoAcid		inhibits					statement 4	Process				NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
10735	1	3452	7	11	NULL	0	NULL	amphiphysin	GP		bind					adaptin	GP		appendage domain 		NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
10736	2	3452	7	11	NULL	0	NULL	Eps15	GP		bind					adaptin	GP		appendage domain 		NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
10737	3	3452	7	11	NULL	0	NULL	AP180	GP		bind					adaptin	GP		appendage domain 		NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
10738	4	3452	7	11	NULL	0	NULL	clathrin	GP		bind					adaptin	GP		appendage domain 		NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
10739	5	3452	7	11	NULL	0	NULL	DPW peptide	AminoAcid		inhibit					statement 1	Process				NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
10740	6	3452	7	11	NULL	0	NULL	DPW peptide	AminoAcid		inhibit					statement 2	Process				NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
10741	7	3452	7	11	NULL	0	NULL	DPW peptide	AminoAcid		inhibit					statement 3	Process				NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
10742	8	3452	7	11	NULL	0	NULL	DPW peptide	AminoAcid		inhibit					statement 4	Process				NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
10743	9	3452	7	11	NULL	0	NULL	DPF peptide	AminoAcid		inhibit					statement 1	Process				NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
10744	10	3452	7	11	NULL	0	NULL	DPF peptide	AminoAcid		inhibit					statement 2	Process				NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
10745	11	3452	7	11	NULL	0	NULL	DPF peptide	AminoAcid		inhibit					statement 3	Process				NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
10746	12	3452	7	11	NULL	0	NULL	DPF peptide	AminoAcid		inhibit					statement 4	Process				NULL	total brain cytosol	NULL	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
80583	1	3452	11	NULL	NULL	0	NULL	amphiphysin	Protein		binds to 					GST	Protein		adaptin appendage domain		NULL	from total brain cytosol	0	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
80584	2	3452	11	NULL	NULL	0	NULL	Eps15	Protein		binds to 					GST	Protein		adaptin appendage domain		NULL	from total brain cytosol	0	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
80585	3	3452	11	NULL	NULL	0	NULL	AP180	Protein		binds to 					GST	Protein		adaptin appendage domain		NULL	from total brain cytosol	0	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
80586	4	3452	11	NULL	NULL	0	NULL	clathrin	Protein		binds to 					GST	Protein		adaptin appendage domain		NULL	from total brain cytosol	0	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
80587	5	3452	11	NULL	NULL	0	NULL	DPF peptide	PartOfProtein		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
80588	6	3452	11	NULL	NULL	0	NULL	DPF peptide	PartOfProtein		inhibit					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
80589	7	3452	11	NULL	NULL	0	NULL	DPF peptide	PartOfProtein		inhibit					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
80590	8	3452	11	NULL	NULL	0	NULL	DPW peptide	PartOfProtein		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
80591	9	3452	11	NULL	NULL	0	NULL	DPW peptide	PartOfProtein		inhibit					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
80592	10	3452	11	NULL	NULL	0	NULL	DPW peptide	PartOfProtein		inhibit					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_cell_97_6_805_s_125	10380931	(A, lower panels), and DPW and DPF  peptides at concentrations of 500 muM (B) inhibit binding of amphiphysin, Eps15, AP180, and clathrin to  GST  -adaptin appendage domain in pull-down experiments from total brain cytosol.	bind
7669	1	3453	6	11	NULL	0	NULL	IGF-I	GP		induce					MC3T3-E1 cells	Cell	chemotaxis of			NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_3_636_s_47	14975748	(A,B)  Chemotaxis of MC3T3-E1 cells induced by PDGF, VEGF, and IGF-I.	bind
7670	2	3453	6	11	NULL	0	NULL	VEGF	GP		induce					MC3T3-E1 cells	Cell	chemotaxis of			NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_3_636_s_47	14975748	(A,B)  Chemotaxis of MC3T3-E1 cells induced by PDGF, VEGF, and IGF-I.	bind
7671	3	3453	6	11	NULL	0	NULL	PDGF	GP		induce					MC3T3-E1 cells	Cell	chemotaxis of			NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_3_636_s_47	14975748	(A,B)  Chemotaxis of MC3T3-E1 cells induced by PDGF, VEGF, and IGF-I.	bind
10747	1	3453	7	11	NULL	0	NULL	PDGF	GP		induce					MC3T3-E1 cells	Cell	chemotaxis of			NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_3_636_s_47	14975748	(A,B)  Chemotaxis of MC3T3-E1 cells induced by PDGF, VEGF, and IGF-I.	bind
10748	2	3453	7	11	NULL	0	NULL	VEGF	GP		induce					MC3T3-E1 cells	Cell	chemotaxis of			NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_3_636_s_47	14975748	(A,B)  Chemotaxis of MC3T3-E1 cells induced by PDGF, VEGF, and IGF-I.	bind
10749	3	3453	7	11	NULL	0	NULL	IGF-I	GP		induce					MC3T3-E1 cells	Cell	chemotaxis of			NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_3_636_s_47	14975748	(A,B)  Chemotaxis of MC3T3-E1 cells induced by PDGF, VEGF, and IGF-I.	bind
80593	1	3453	11	NULL	NULL	0	NULL	PDGF	Protein		induce					Chemotaxis	BiologicalProcess	MC3T3-E1 cells			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_3_636_s_47	14975748	(A,B)  Chemotaxis of MC3T3-E1 cells induced by PDGF, VEGF, and IGF-I.	bind
80594	2	3453	11	NULL	NULL	0	NULL	VEGF	Protein		induce					Chemotaxis	BiologicalProcess	MC3T3-E1 cells			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_3_636_s_47	14975748	(A,B)  Chemotaxis of MC3T3-E1 cells induced by PDGF, VEGF, and IGF-I.	bind
80596	3	3453	11	NULL	NULL	0	NULL	IGF-I	Protein		induce					Chemotaxis	BiologicalProcess	MC3T3-E1 cells			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_3_636_s_47	14975748	(A,B)  Chemotaxis of MC3T3-E1 cells induced by PDGF, VEGF, and IGF-I.	bind
7672	1	3456	6	11	NULL	0	NULL	lectin	GP		bind					gastric mucins	GP	purified;; pig			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1674_2_131_s_139	15374617	(A,B) Lectin binding to purified pig gastric mucins.	bind
10750	1	3456	7	11	NULL	0	NULL	Lectin	GP		bind					gastric mucins	GP	purified;; pig 			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1674_2_131_s_139	15374617	(A,B) Lectin binding to purified pig gastric mucins.	bind
80602	1	3456	11	NULL	NULL	0	NULL	Lectin	Protein		binds to 					gastric mucin	Chemical	purified;;pig			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1674_2_131_s_139	15374617	(A,B) Lectin binding to purified pig gastric mucins.	bind
7673	1	3459	6	11	NULL	0	NULL	SPRY2	GP		bind					GRB2	GP				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_96_1_91_s_85	10940627	(A,B) SPRY2 binds GRB2.	bind
10818	1	3459	7	11	NULL	0	NULL	SPRY2	GP		bind					GRB2	GP				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_96_1_91_s_85	10940627	(A,B) SPRY2 binds GRB2.	bind
80603	1	3459	11	NULL	NULL	0	NULL	SPRY2	Protein		binds to 					GRB2	Protein				NULL		0	NULL	NULL	NULL	gw60_mechdev_96_1_91_s_85	10940627	(A,B) SPRY2 binds GRB2.	bind
7719	1	3460	6	11	NULL	0	NULL	prazosin	Chemical		bind			BODIPY FL		alpha-1 adrenoceptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_132_4_851_s_194	11181426	(A,B) the cells were incubated in the presence of BODIPY FL prazosin and unlabelled prazosin 10-6M (which blocks the binding of BODIPY FL prazosin to the alpha-1 adrenoceptors).	bind
7720	2	3460	6	11	NULL	0	NULL	prazosin	Chemical	unlabelled	blocks					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_132_4_851_s_194	11181426	(A,B) the cells were incubated in the presence of BODIPY FL prazosin and unlabelled prazosin 10-6M (which blocks the binding of BODIPY FL prazosin to the alpha-1 adrenoceptors).	bind
10819	1	3460	7	11	NULL	0	NULL	 prazosin	Chemical		bind			BODIPY FL		alpha-1 adrenoceptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_132_4_851_s_194	11181426	(A,B) the cells were incubated in the presence of BODIPY FL prazosin and unlabelled prazosin 10-6M (which blocks the binding of BODIPY FL prazosin to the alpha-1 adrenoceptors).	bind
14982	2	3460	7	11	NULL	0	NULL	prazosin	Chemical	unlabelled 	blocks					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_132_4_851_s_194	11181426	(A,B) the cells were incubated in the presence of BODIPY FL prazosin and unlabelled prazosin 10-6M (which blocks the binding of BODIPY FL prazosin to the alpha-1 adrenoceptors).	bind
80604	1	3460	11	NULL	NULL	0	NULL	BODIPY FL prazosin	Chemical		binds to 					alpha-1 adrenoceptors	Protein				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_132_4_851_s_194	11181426	(A,B) the cells were incubated in the presence of BODIPY FL prazosin and unlabelled prazosin 10-6M (which blocks the binding of BODIPY FL prazosin to the alpha-1 adrenoceptors).	bind
80605	2	3460	11	NULL	NULL	0	NULL	prazosin	Chemical	unlabelled	blocks					statement 1	Chemical				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_132_4_851_s_194	11181426	(A,B) the cells were incubated in the presence of BODIPY FL prazosin and unlabelled prazosin 10-6M (which blocks the binding of BODIPY FL prazosin to the alpha-1 adrenoceptors).	bind
7674	1	3461	6	11	NULL	0	NULL	GPA-16	GP		bind					GST-GPR-1/2	GP		amino acids 374-476		NULL		NULL	NULL	NULL	NULL	gw70_development_132_20_4449_s_203	16162648	(A,B,E) [[ Surface plasmon  resonance ]] was used to analyze the binding of GPA-16 to GST-GPR-1/2 (amino acids 374-476)	bind
10820	1	3461	7	11	NULL	0	NULL	GPA-16	GP		bind					GST-GPR-1/2 	GP		374-476		NULL		NULL	NULL	NULL	NULL	gw70_development_132_20_4449_s_203	16162648	(A,B,E) [[ Surface plasmon  resonance ]] was used to analyze the binding of GPA-16 to GST-GPR-1/2 (amino acids 374-476)	bind
80606	1	3461	11	NULL	NULL	0	NULL	GPA-16	Protein		binds to 					GST-GPR-1/2	Protein		amino acids 374-476		NULL		0	NULL	NULL	NULL	gw70_development_132_20_4449_s_203	16162648	(A,B,E) [[ Surface plasmon  resonance ]] was used to analyze the binding of GPA-16 to GST-GPR-1/2 (amino acids 374-476)	bind
7721	1	3463	6	11	NULL	0	NULL	D-type cyclins	GP		bind					CDK4	GP		cyclin binding sequence		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7041_s_19	11096103	(A- and B-type) bind CDKs that contain the conserved cyclin-binding sequence PSTAIRE, whereas D-type cyclins bind CDK4 and -6, which have the sequence P(I/L)ST(V/I)RE (reviewed in Ref.  13).	bind
7722	2	3463	6	11	NULL	0	NULL	D-type cyclins	GP		bind					CDK6	GP		cyclin binding sequence		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7041_s_19	11096103	(A- and B-type) bind CDKs that contain the conserved cyclin-binding sequence PSTAIRE, whereas D-type cyclins bind CDK4 and -6, which have the sequence P(I/L)ST(V/I)RE (reviewed in Ref.  13).	bind
7751	3	3463	6	11	NULL	0	NULL	P(I/L)ST(V/I)RE	NucleicAcid		is a type of					cyclin binding sequence	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7041_s_19	11096103	(A- and B-type) bind CDKs that contain the conserved cyclin-binding sequence PSTAIRE, whereas D-type cyclins bind CDK4 and -6, which have the sequence P(I/L)ST(V/I)RE (reviewed in Ref.  13).	bind
10823	3	3463	7	11	NULL	0	NULL	D-type cyclins	GP		bind					CDK4	GP		P(I/L)ST(V/I)RE		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7041_s_19	11096103	(A- and B-type) bind CDKs that contain the conserved cyclin-binding sequence PSTAIRE, whereas D-type cyclins bind CDK4 and -6, which have the sequence P(I/L)ST(V/I)RE (reviewed in Ref.  13).	bind
10824	4	3463	7	11	NULL	0	NULL	D-type cyclins	GP		bind					CDK6	GP		P(I/L)ST(V/I)RE		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7041_s_19	11096103	(A- and B-type) bind CDKs that contain the conserved cyclin-binding sequence PSTAIRE, whereas D-type cyclins bind CDK4 and -6, which have the sequence P(I/L)ST(V/I)RE (reviewed in Ref.  13).	bind
52826	5	3463	7	11	NULL	0	NULL	P(I/L)ST(V/I)RE	NucleicAcid		is a type of					cyclin binding sequence	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7041_s_19	11096103	(A- and B-type) bind CDKs that contain the conserved cyclin-binding sequence PSTAIRE, whereas D-type cyclins bind CDK4 and -6, which have the sequence P(I/L)ST(V/I)RE (reviewed in Ref.  13).	bind
80607	1	3463	11	NULL	NULL	0	NULL	PSTAIRE	PartOfProtein		is a part of 					cyclin-binding sequence	PartOfProtein	conserved			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_10_7041_s_19	11096103	(A- and B-type) bind CDKs that contain the conserved cyclin-binding sequence PSTAIRE, whereas D-type cyclins bind CDK4 and -6, which have the sequence P(I/L)ST(V/I)RE (reviewed in Ref.  13).	bind
80608	2	3463	11	NULL	NULL	0	NULL	CDK	Protein		contain					PSTAIRE	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_10_7041_s_19	11096103	(A- and B-type) bind CDKs that contain the conserved cyclin-binding sequence PSTAIRE, whereas D-type cyclins bind CDK4 and -6, which have the sequence P(I/L)ST(V/I)RE (reviewed in Ref.  13).	bind
80609	3	3463	11	NULL	NULL	NULL	NULL	D-type cyclin	Protein		binds to 					CDK4	Protein		P(I/L)ST(V/I)RE		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7041_s_19	11096103	(A- and B-type) bind CDKs that contain the conserved cyclin-binding sequence PSTAIRE, whereas D-type cyclins bind CDK4 and -6, which have the sequence P(I/L)ST(V/I)RE (reviewed in Ref.  13).	bind
80610	4	3463	11	NULL	NULL	NULL	NULL	D-type cyclin	Protein		binds to 					CDK6	Protein		P(I/L)ST(V/I)RE		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7041_s_19	11096103	(A- and B-type) bind CDKs that contain the conserved cyclin-binding sequence PSTAIRE, whereas D-type cyclins bind CDK4 and -6, which have the sequence P(I/L)ST(V/I)RE (reviewed in Ref.  13).	bind
7677	1	3464	6	11	NULL	0	NULL	Sir1p	GP		bind					HMR a	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1955_s_197	16479013	(A-) still requires  SIR1 (Palacios DeBeer and Fox, unpublished), indicating that Sir1p must bind  HMR a in this mutant by some mechanism.	bind
10825	1	3464	7	11	NULL	0	NULL	Sir1p 	GP		bind					HMR a	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1955_s_197	16479013	(A-) still requires  SIR1 (Palacios DeBeer and Fox, unpublished), indicating that Sir1p must bind  HMR a in this mutant by some mechanism.	bind
80611	1	3464	11	NULL	NULL	0	NULL	Sir1p	Protein		binds to 					HMRa	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1955_s_197	16479013	(A-) still requires  SIR1 (Palacios DeBeer and Fox, unpublished), indicating that Sir1p must bind  HMR a in this mutant by some mechanism.	bind
7723	1	3465	6	11	NULL	0	NULL	 IL-3 	GP	murine	bind		directly			beta(IL-3)receptor	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_j-biol-chem_279_25_15060062_s_9	15060062	(A-B loop), Phe(85), and Asn(87) (E-F loop) of  domain 1; Ile(320) of the interdomain loop; and Tyr(348) (B''-C'' loop)  and Tyr(401) (F''-G'' loop) of domain 4 were shown to have critical individual  roles and Arg(84) and Tyr(317) major secondary roles in direct murine  IL-3 binding to the beta(IL-3)receptor.	bind
7752	2	3465	6	11	NULL	0	NULL				plays critical role in			Phe(85);;Asn(87) (E-F loop) of domain 1		statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_j-biol-chem_279_25_15060062_s_9	15060062	(A-B loop), Phe(85), and Asn(87) (E-F loop) of  domain 1; Ile(320) of the interdomain loop; and Tyr(348) (B''-C'' loop)  and Tyr(401) (F''-G'' loop) of domain 4 were shown to have critical individual  roles and Arg(84) and Tyr(317) major secondary roles in direct murine  IL-3 binding to the beta(IL-3)receptor.	bind
7753	3	3465	6	11	NULL	0	NULL				plays critical role in			Ile(320) of the interdomain loop		statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_j-biol-chem_279_25_15060062_s_9	15060062	(A-B loop), Phe(85), and Asn(87) (E-F loop) of  domain 1; Ile(320) of the interdomain loop; and Tyr(348) (B''-C'' loop)  and Tyr(401) (F''-G'' loop) of domain 4 were shown to have critical individual  roles and Arg(84) and Tyr(317) major secondary roles in direct murine  IL-3 binding to the beta(IL-3)receptor.	bind
7754	4	3465	6	11	NULL	0	NULL				plays critical role in			Tyr(348) (B''-C'' loop)		statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_j-biol-chem_279_25_15060062_s_9	15060062	(A-B loop), Phe(85), and Asn(87) (E-F loop) of  domain 1; Ile(320) of the interdomain loop; and Tyr(348) (B''-C'' loop)  and Tyr(401) (F''-G'' loop) of domain 4 were shown to have critical individual  roles and Arg(84) and Tyr(317) major secondary roles in direct murine  IL-3 binding to the beta(IL-3)receptor.	bind
7755	5	3465	6	11	NULL	0	NULL				plays critical role in			Tyr(401) (F''-G'' loop) of domain 4		statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_j-biol-chem_279_25_15060062_s_9	15060062	(A-B loop), Phe(85), and Asn(87) (E-F loop) of  domain 1; Ile(320) of the interdomain loop; and Tyr(348) (B''-C'' loop)  and Tyr(401) (F''-G'' loop) of domain 4 were shown to have critical individual  roles and Arg(84) and Tyr(317) major secondary roles in direct murine  IL-3 binding to the beta(IL-3)receptor.	bind
7756	6	3465	6	11	NULL	0	NULL	Arg(84)			plays major secondary role in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_j-biol-chem_279_25_15060062_s_9	15060062	(A-B loop), Phe(85), and Asn(87) (E-F loop) of  domain 1; Ile(320) of the interdomain loop; and Tyr(348) (B''-C'' loop)  and Tyr(401) (F''-G'' loop) of domain 4 were shown to have critical individual  roles and Arg(84) and Tyr(317) major secondary roles in direct murine  IL-3 binding to the beta(IL-3)receptor.	bind
7757	7	3465	6	11	NULL	0	NULL	Tyr(317)	AminoAcid		plays major secondary role in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_j-biol-chem_279_25_15060062_s_9	15060062	(A-B loop), Phe(85), and Asn(87) (E-F loop) of  domain 1; Ile(320) of the interdomain loop; and Tyr(348) (B''-C'' loop)  and Tyr(401) (F''-G'' loop) of domain 4 were shown to have critical individual  roles and Arg(84) and Tyr(317) major secondary roles in direct murine  IL-3 binding to the beta(IL-3)receptor.	bind
10826	1	3465	7	11	NULL	0	NULL	IL-3	GP	murine	bind		directly			beta(IL-3)receptor	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_j-biol-chem_279_25_15060062_s_9	15060062	(A-B loop), Phe(85), and Asn(87) (E-F loop) of  domain 1; Ile(320) of the interdomain loop; and Tyr(348) (B''-C'' loop)  and Tyr(401) (F''-G'' loop) of domain 4 were shown to have critical individual  roles and Arg(84) and Tyr(317) major secondary roles in direct murine  IL-3 binding to the beta(IL-3)receptor.	bind
10827	2	3465	7	11	NULL	0	NULL				has critical role in			Phe(85);;Asn(87) (E-F loop) of domain 1		statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_j-biol-chem_279_25_15060062_s_9	15060062	(A-B loop), Phe(85), and Asn(87) (E-F loop) of  domain 1; Ile(320) of the interdomain loop; and Tyr(348) (B''-C'' loop)  and Tyr(401) (F''-G'' loop) of domain 4 were shown to have critical individual  roles and Arg(84) and Tyr(317) major secondary roles in direct murine  IL-3 binding to the beta(IL-3)receptor.	bind
10829	4	3465	7	11	NULL	0	NULL				has critical role in			Ile(320) of the interdomain loop		statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_j-biol-chem_279_25_15060062_s_9	15060062	(A-B loop), Phe(85), and Asn(87) (E-F loop) of  domain 1; Ile(320) of the interdomain loop; and Tyr(348) (B''-C'' loop)  and Tyr(401) (F''-G'' loop) of domain 4 were shown to have critical individual  roles and Arg(84) and Tyr(317) major secondary roles in direct murine  IL-3 binding to the beta(IL-3)receptor.	bind
10830	5	3465	7	11	NULL	0	NULL				has critical role in			Tyr(348) (B''-C'' loop) of domain 4		statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_j-biol-chem_279_25_15060062_s_9	15060062	(A-B loop), Phe(85), and Asn(87) (E-F loop) of  domain 1; Ile(320) of the interdomain loop; and Tyr(348) (B''-C'' loop)  and Tyr(401) (F''-G'' loop) of domain 4 were shown to have critical individual  roles and Arg(84) and Tyr(317) major secondary roles in direct murine  IL-3 binding to the beta(IL-3)receptor.	bind
10831	6	3465	7	11	NULL	0	NULL				has critical role in			Tyr(401) (F''-G'' loop) of domain 4		statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_j-biol-chem_279_25_15060062_s_9	15060062	(A-B loop), Phe(85), and Asn(87) (E-F loop) of  domain 1; Ile(320) of the interdomain loop; and Tyr(348) (B''-C'' loop)  and Tyr(401) (F''-G'' loop) of domain 4 were shown to have critical individual  roles and Arg(84) and Tyr(317) major secondary roles in direct murine  IL-3 binding to the beta(IL-3)receptor.	bind
10832	7	3465	7	11	NULL	0	NULL	Arg(84)	AminoAcid		has major secondary role in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_j-biol-chem_279_25_15060062_s_9	15060062	(A-B loop), Phe(85), and Asn(87) (E-F loop) of  domain 1; Ile(320) of the interdomain loop; and Tyr(348) (B''-C'' loop)  and Tyr(401) (F''-G'' loop) of domain 4 were shown to have critical individual  roles and Arg(84) and Tyr(317) major secondary roles in direct murine  IL-3 binding to the beta(IL-3)receptor.	bind
10833	8	3465	7	11	NULL	0	NULL	Tyr(317)	AminoAcid		has major secondary role in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_j-biol-chem_279_25_15060062_s_9	15060062	(A-B loop), Phe(85), and Asn(87) (E-F loop) of  domain 1; Ile(320) of the interdomain loop; and Tyr(348) (B''-C'' loop)  and Tyr(401) (F''-G'' loop) of domain 4 were shown to have critical individual  roles and Arg(84) and Tyr(317) major secondary roles in direct murine  IL-3 binding to the beta(IL-3)receptor.	bind
80612	1	3465	11	NULL	NULL	0	NULL	IL-3	Protein	murine	binds to 		direct			beta(IL-3)receptor	Protein				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-biol-chem_279_25_15060062_s_9	15060062	(A-B loop), Phe(85), and Asn(87) (E-F loop) of  domain 1; Ile(320) of the interdomain loop; and Tyr(348) (B''-C'' loop)  and Tyr(401) (F''-G'' loop) of domain 4 were shown to have critical individual  roles and Arg(84) and Tyr(317) major secondary roles in direct murine  IL-3 binding to the beta(IL-3)receptor.	bind
7681	1	3466	6	11	NULL	0	NULL	3H-CGP 39653	Chemical		bind					spinal cord sections	OrganismPart	mouse			NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_86_1_23_s_117	11165368	(A-B) Autoradiograms showing binding of 3H-CGP 39653 to sections of mouse spinal cord.	bind
10834	1	3466	7	11	NULL	0	NULL	3H-CGP 39653	Chemical		bind					 spinal cord	OrganismPart	mouse			NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_86_1_23_s_117	11165368	(A-B) Autoradiograms showing binding of 3H-CGP 39653 to sections of mouse spinal cord.	bind
80625	1	3466	11	NULL	NULL	0	NULL	3H-CGP 39653	PartOfProtein		binds to 					spinal cord	Organism part	mouse			NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_86_1_23_s_117	11165368	(A-B) Autoradiograms showing binding of 3H-CGP 39653 to sections of mouse spinal cord.	bind
7682	1	3467	6	11	NULL	0	NULL	Bcr	GP		does not bind					Max	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_5_437_s_106	12620195	(A-C) Bcr does not bind Max or the c-Myc Max heterodimer.	bind
7683	2	3467	6	11	NULL	0	NULL	Bcr	GP		does not bind					c-Myc Max heterodimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_5_437_s_106	12620195	(A-C) Bcr does not bind Max or the c-Myc Max heterodimer.	bind
10835	1	3467	7	11	NULL	0	NULL	Bcr 	GP		does not bind					 Max	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_5_437_s_106	12620195	(A-C) Bcr does not bind Max or the c-Myc Max heterodimer.	bind
10836	2	3467	7	11	NULL	0	NULL	Bcr	GP		does not bind					c-Myc Max heterodimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_5_437_s_106	12620195	(A-C) Bcr does not bind Max or the c-Myc Max heterodimer.	bind
80627	1	3467	11	NULL	NULL	0	NULL	 c-Myc	Protein		heterodimerize with					Max	Protein				NULL		0	NULL	NULL	NULL	gw60_currbiol_13_5_437_s_106	12620195	(A-C) Bcr does not bind Max or the c-Myc Max heterodimer.	bind
80629	2	3467	11	NULL	NULL	0	NULL	Bcr	Protein		does not bind to					Max	Protein				NULL		0	NULL	NULL	NULL	gw60_currbiol_13_5_437_s_106	12620195	(A-C) Bcr does not bind Max or the c-Myc Max heterodimer.	bind
80630	3	3467	11	NULL	NULL	0	NULL	Bcr	Protein		does not bind to					statement 1	Protein				NULL		0	NULL	NULL	NULL	gw60_currbiol_13_5_437_s_106	12620195	(A-C) Bcr does not bind Max or the c-Myc Max heterodimer.	bind
7724	1	3468	6	11	NULL	0	NULL	RF3 GDPNP	GP		bind					RC	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7725	2	3468	6	11	NULL	0	NULL	RF3 GDPNP	GP		bind					IC	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7726	3	3468	6	11	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7727	4	3468	6	11	NULL	0	NULL	statement 1	Process		occurs in presence of					deacylated tRNA in the P site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7728	5	3468	6	11	NULL	0	NULL	statement 1	Process		occurs in presence of					peptidyl-tRNA in the P site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7729	6	3468	6	11	NULL	0	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7730	7	3468	6	11	NULL	0	NULL	statement 2	Process		occurs in presence of					deacylated tRNA in the P site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7731	8	3468	6	11	NULL	0	NULL	statement 2	Process		occurs in presence of					peptidyl-tRNA in the P site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7732	9	3468	6	11	NULL	0	NULL	statement 7	Process		is an alternative to					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7758	10	3468	6	11	NULL	0	NULL	EF-G GDPNP	GP		bind					RC	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7759	11	3468	6	11	NULL	0	NULL	EF-G GDPNP	GP		bind					IC	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7760	12	3468	6	11	NULL	0	NULL	statement 10	Process		is an alternative to					statement 11	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7763	13	3468	6	11	NULL	0	NULL	statement 10	Process		occurs in presence of					deacylated tRNA in the P site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7764	14	3468	6	11	NULL	0	NULL	statement 10	Process		occurs in presence of					peptidyl-tRNA in the P site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7765	15	3468	6	11	NULL	0	NULL	statement 13	Process		is an alternative to					statement 14	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7766	16	3468	6	11	NULL	0	NULL	statement 11	Process		occurs in presence of					peptidyl-tRNA in the P site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7767	17	3468	6	11	NULL	0	NULL	statement 11	Process		occurs in presence of					deacetylated-tRNA in the P site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7769	18	3468	6	11	NULL	0	NULL	statement 16	Process		is an alternative to					statement 17	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7770	19	3468	6	11	NULL	0	NULL	IF2 GDPNP	GP		bind					RC	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7771	20	3468	6	11	NULL	0	NULL	IF2 GDPNP	GP		bind					IC	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7776	21	3468	6	11	NULL	0	NULL	statement 19	Process		is an alternative to					statement 20	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7778	22	3468	6	11	NULL	0	NULL	statement 19	Process		occurs in presence of					deacetylated-tRNA in the P site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7779	23	3468	6	11	NULL	0	NULL	statement 19	Process		occurs in presence of					peptidyl-tRNA in the P site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7781	24	3468	6	11	NULL	0	NULL	statement 22	Process		is an alternative to					statement 23	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7782	25	3468	6	11	NULL	0	NULL	statement 20	Process		occurs in presence of					peptidyl-tRNA in the P site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7783	26	3468	6	11	NULL	0	NULL	statement 20	Process		occurs in presence of					deacetylated-tRNA in the P site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7785	27	3468	6	11	NULL	0	NULL	statement 25	Process		is an alternative to					statement 26	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
10844	1	3468	7	11	NULL	0	NULL	RF3 GDPNP	GP		bind					IC	GP			peptidyl-tRNA in the P site 	NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
10845	2	3468	7	11	NULL	0	NULL	RF3 GDPNP	GP		bind					RC	GP			deacylated tRNA in the P site	NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
10846	3	3468	7	11	NULL	0	NULL	RF3 GDPNP	GP		bind					IC	GP			deacylated tRNA in the P site	NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
10847	5	3468	7	11	NULL	0	NULL	EF-G GDPNP	GP		bind					RC	GP			peptidyl-tRNA in the P site 	NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
10848	4	3468	7	11	NULL	0	NULL	 RF3 GDPNP	GP		bind					RC	GP			peptidyl-tRNA in the P site 	NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
10849	7	3468	7	11	NULL	0	NULL	EF-G GDPNP	GP		bind					IC	GP			peptidyl-tRNA in the P site 	NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
10850	8	3468	7	11	NULL	0	NULL	EF-G GDPNP	GP		bind					IC	GP			deacylated tRNA in the P site	NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
10851	9	3468	7	11	NULL	0	NULL	IF2 GDPNP	GP		bind					RC	GP			peptidyl-tRNA in the P site 	NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
10852	10	3468	7	11	NULL	0	NULL	IF2 GDPNP	GP		bind					RC	GP			deacylated tRNA in the P site	NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
10853	11	3468	7	11	NULL	0	NULL	IF2 GDPNP	GP		bind					IC	GP			peptidyl-tRNA in the P site 	NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
10854	6	3468	7	11	NULL	0	NULL	EF-G GDPNP	GP		bind					RC	GP			deacylated tRNA in the P site	NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
10855	12	3468	7	11	NULL	0	NULL	IF2 GDPNP	GP		bind					IC	GP			deacylated tRNA in the P site	NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
80631	1	3468	11	NULL	NULL	NULL	NULL	RF3 GDPNP	Protein		binds to 					RC	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
80632	2	3468	11	NULL	NULL	NULL	NULL	EF-G GDPNP	Protein		binds to 					RC	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
80633	3	3468	11	NULL	NULL	NULL	NULL	IF2 GDPNP	Protein		binds to 					RC	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
80634	4	3468	11	NULL	NULL	0	NULL	RC	CellComponent		has					 peptidyl-tRNA	CellComponent	in the P site			NULL		0	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
80635	5	3468	11	NULL	NULL	0	NULL	RC	CellComponent		has					deacylated tRNA	CellComponent	in the P site			NULL		0	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
80636	6	3468	11	NULL	NULL	0	NULL	 IC	Protein		with					peptidyl-tRNA	CellComponent	in the P site			NULL		0	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
80637	7	3468	11	NULL	NULL	0	NULL	IC	Protein		with					deacylated tRNA	CellComponent	in the P site			NULL		0	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
80650	8	3468	11	NULL	NULL	0	NULL	RF3 GDPNP	Protein		binds to 					IC	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
80662	9	3468	11	NULL	NULL	0	NULL	EF-G GDPNP	Protein		binds to 					IC	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
80664	10	3468	11	NULL	NULL	0	NULL	IF2 GDPNP	Protein		binds to 					IC	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_114_1_113_s_67	12859902	(A-C) Binding of RF3 GDPNP, EF-G GDPNP, and IF2 GDPNP to RC or IC with peptidyl-tRNA or deacylated tRNA in the P site.	bind
7685	1	3469	6	11	NULL	0	NULL	dATP	Chemical		bind					RVLM	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_113_4_809_s_145	12182888	(A-C) Binding of [ 33]dATP can be seen in a number of brainstem regions, including the RVLM, CVLM and IOC.	bind
7686	2	3469	6	11	NULL	0	NULL	dATP	Chemical		bind					CVLM	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_113_4_809_s_145	12182888	(A-C) Binding of [ 33]dATP can be seen in a number of brainstem regions, including the RVLM, CVLM and IOC.	bind
7687	3	3469	6	11	NULL	0	NULL	dATP	Chemical		bind					IOC	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_113_4_809_s_145	12182888	(A-C) Binding of [ 33]dATP can be seen in a number of brainstem regions, including the RVLM, CVLM and IOC.	bind
52843	4	3469	6	11	NULL	0	NULL	RVLM	OrganismPart		is a type of					brainstem region	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_113_4_809_s_145	12182888	(A-C) Binding of [ 33]dATP can be seen in a number of brainstem regions, including the RVLM, CVLM and IOC.	bind
52844	5	3469	6	11	NULL	0	NULL	CVLM 	OrganismPart		is a type of					brainstem region	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_113_4_809_s_145	12182888	(A-C) Binding of [ 33]dATP can be seen in a number of brainstem regions, including the RVLM, CVLM and IOC.	bind
52845	6	3469	6	11	NULL	0	NULL	IOC	OrganismPart		is a type of					brainstem region	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_113_4_809_s_145	12182888	(A-C) Binding of [ 33]dATP can be seen in a number of brainstem regions, including the RVLM, CVLM and IOC.	bind
10856	1	3469	7	11	NULL	0	NULL	dATP	Chemical		bind					RVLM	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_113_4_809_s_145	12182888	(A-C) Binding of [ 33]dATP can be seen in a number of brainstem regions, including the RVLM, CVLM and IOC.	bind
10857	2	3469	7	11	NULL	0	NULL	dATP	Chemical		bind					CVLM	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_113_4_809_s_145	12182888	(A-C) Binding of [ 33]dATP can be seen in a number of brainstem regions, including the RVLM, CVLM and IOC.	bind
10858	3	3469	7	11	NULL	0	NULL	dATP	Chemical		bind					IOC	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_113_4_809_s_145	12182888	(A-C) Binding of [ 33]dATP can be seen in a number of brainstem regions, including the RVLM, CVLM and IOC.	bind
52846	4	3469	7	11	NULL	0	NULL	RVLM	OrganismPart		is a type of					brainstem region	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_113_4_809_s_145	12182888	(A-C) Binding of [ 33]dATP can be seen in a number of brainstem regions, including the RVLM, CVLM and IOC.	bind
52847	5	3469	7	11	NULL	0	NULL	CVLM 	OrganismPart		is a type of					brainstem region	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_113_4_809_s_145	12182888	(A-C) Binding of [ 33]dATP can be seen in a number of brainstem regions, including the RVLM, CVLM and IOC.	bind
52848	6	3469	7	11	NULL	0	NULL	IOC	OrganismPart		is a type of					brainstem region	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_113_4_809_s_145	12182888	(A-C) Binding of [ 33]dATP can be seen in a number of brainstem regions, including the RVLM, CVLM and IOC.	bind
80666	1	3469	11	NULL	NULL	0	NULL	[ 33]dATP	Chemical		binds to 		(A-C)			RVLM	AnatomicalPart	brainstem region			NULL		0	NULL	NULL	NULL	gw60_neuroscience_113_4_809_s_145	12182888	(A-C) Binding of [ 33]dATP can be seen in a number of brainstem regions, including the RVLM, CVLM and IOC.	bind
80667	2	3469	11	NULL	NULL	0	NULL	 [ 33]dATP	Chemical		binds to 		A-C			CVLM	AnatomicalPart	brainstem region			NULL		0	NULL	NULL	NULL	gw60_neuroscience_113_4_809_s_145	12182888	(A-C) Binding of [ 33]dATP can be seen in a number of brainstem regions, including the RVLM, CVLM and IOC.	bind
80668	3	3469	11	NULL	NULL	0	NULL	[ 33]dATP	Chemical		binds to 		(A-C)			IOC	AnatomicalPart	brainstem region			NULL		0	NULL	NULL	NULL	gw60_neuroscience_113_4_809_s_145	12182888	(A-C) Binding of [ 33]dATP can be seen in a number of brainstem regions, including the RVLM, CVLM and IOC.	bind
7688	1	3470	6	11	NULL	0	NULL	 roX1 RNA	NucleicAcid		bind					polytene X chromosome	Chromosome				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_3_136_s_63	10679323	(a-c) RNA fluorescence  in situ hybridization showing the polytene X chromosome binding pattern of (a)  roX1 RNA and (b)  roX2 RNA.	bind
7689	2	3470	6	11	NULL	0	NULL	 roX2 RNA	NucleicAcid		bind					polytene X chromosome	Chromosome				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_3_136_s_63	10679323	(a-c) RNA fluorescence  in situ hybridization showing the polytene X chromosome binding pattern of (a)  roX1 RNA and (b)  roX2 RNA.	bind
10859	1	3470	7	11	NULL	0	NULL	polytene X chromosome	Chromosome		bind					roX1 RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_3_136_s_63	10679323	(a-c) RNA fluorescence  in situ hybridization showing the polytene X chromosome binding pattern of (a)  roX1 RNA and (b)  roX2 RNA.	bind
10860	2	3470	7	11	NULL	0	NULL	polytene X chromosome	Chromosome		bind					roX2 RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_3_136_s_63	10679323	(a-c) RNA fluorescence  in situ hybridization showing the polytene X chromosome binding pattern of (a)  roX1 RNA and (b)  roX2 RNA.	bind
80671	1	3470	11	NULL	NULL	0	NULL	roX1 RNA	NucleicAcidSubstance		binds to 					 polytene X chromosome	Chromosome				NULL	RNA fluorescence in situ hybridization	0	NULL	NULL	NULL	gw60_currbiol_10_3_136_s_63	10679323	(a-c) RNA fluorescence  in situ hybridization showing the polytene X chromosome binding pattern of (a)  roX1 RNA and (b)  roX2 RNA.	bind
80674	2	3470	11	NULL	NULL	0	NULL	roX2 RNA	NucleicAcidSubstance		binds to 					polytene X chromosome	Chromosome				NULL	RNA fluorescence in situ hybridization	0	NULL	NULL	NULL	gw60_currbiol_10_3_136_s_63	10679323	(a-c) RNA fluorescence  in situ hybridization showing the polytene X chromosome binding pattern of (a)  roX1 RNA and (b)  roX2 RNA.	bind
7690	1	3471	6	11	NULL	0	NULL	HNf-4	GP		bind					Smad3	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_3_1279_s_250	12631740	(A-C) Two regions of HNF-4 defined by amino acids 1-49 (domain A/B) and 388-455 (domain  F) mediate binding of HNF-4 to Smad3.	bind
7691	2	3471	6	11	NULL	0	NULL	HNF-4	GP		mediates			domain A/B		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_3_1279_s_250	12631740	(A-C) Two regions of HNF-4 defined by amino acids 1-49 (domain A/B) and 388-455 (domain  F) mediate binding of HNF-4 to Smad3.	bind
7692	3	3471	6	11	NULL	0	NULL	HNF-4	GP		mediates			domain F		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_3_1279_s_250	12631740	(A-C) Two regions of HNF-4 defined by amino acids 1-49 (domain A/B) and 388-455 (domain  F) mediate binding of HNF-4 to Smad3.	bind
7693	4	3471	6	11	NULL	0	NULL	HNF-4	GP		corresponds to			amino acids 1-49		HNF-4	GP		domain A/B		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_3_1279_s_250	12631740	(A-C) Two regions of HNF-4 defined by amino acids 1-49 (domain A/B) and 388-455 (domain  F) mediate binding of HNF-4 to Smad3.	bind
7694	5	3471	6	11	NULL	0	NULL	HNF-4	GP		corresponds to			amino acids 388-455		HNF-4	GP		domain F		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_3_1279_s_250	12631740	(A-C) Two regions of HNF-4 defined by amino acids 1-49 (domain A/B) and 388-455 (domain  F) mediate binding of HNF-4 to Smad3.	bind
10861	1	3471	7	11	NULL	0	NULL	HNF-4	GP		corresponds to			domain A/B		HNF-4	GP		amino acids 1-49		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_3_1279_s_250	12631740	(A-C) Two regions of HNF-4 defined by amino acids 1-49 (domain A/B) and 388-455 (domain  F) mediate binding of HNF-4 to Smad3.	bind
10862	2	3471	7	11	NULL	0	NULL	HNF-4	GP		corresponds to			 domain F		HNF-4	GP		amino acids 388-455		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_3_1279_s_250	12631740	(A-C) Two regions of HNF-4 defined by amino acids 1-49 (domain A/B) and 388-455 (domain  F) mediate binding of HNF-4 to Smad3.	bind
14994	3	3471	7	11	NULL	0	NULL	HNF-4	GP		bind					Smad3	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_3_1279_s_250	12631740	(A-C) Two regions of HNF-4 defined by amino acids 1-49 (domain A/B) and 388-455 (domain  F) mediate binding of HNF-4 to Smad3.	bind
14995	4	3471	7	11	NULL	0	NULL	statement 1	Process		mediate					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_3_1279_s_250	12631740	(A-C) Two regions of HNF-4 defined by amino acids 1-49 (domain A/B) and 388-455 (domain  F) mediate binding of HNF-4 to Smad3.	bind
14996	5	3471	7	11	NULL	0	NULL	statement 2	Process		mediate					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_3_1279_s_250	12631740	(A-C) Two regions of HNF-4 defined by amino acids 1-49 (domain A/B) and 388-455 (domain  F) mediate binding of HNF-4 to Smad3.	bind
80675	1	3471	11	NULL	NULL	0	NULL	HNF-4 	Protein		binds to 					Smad3	Protein				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_3_1279_s_250	12631740	(A-C) Two regions of HNF-4 defined by amino acids 1-49 (domain A/B) and 388-455 (domain  F) mediate binding of HNF-4 to Smad3.	bind
80677	2	3471	11	NULL	NULL	NULL	NULL				is a part of 			domain A/B;;amino acids 1-49		HNF-4	Protein				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_3_1279_s_250	12631740	(A-C) Two regions of HNF-4 defined by amino acids 1-49 (domain A/B) and 388-455 (domain  F) mediate binding of HNF-4 to Smad3.	bind
80678	3	3471	11	NULL	NULL	0	NULL				is a part of 			domain F;;388-455		HNF-4 	Protein				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_3_1279_s_250	12631740	(A-C) Two regions of HNF-4 defined by amino acids 1-49 (domain A/B) and 388-455 (domain  F) mediate binding of HNF-4 to Smad3.	bind
80681	4	3471	11	NULL	NULL	0	NULL	statement 2	Protein		mediates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_3_1279_s_250	12631740	(A-C) Two regions of HNF-4 defined by amino acids 1-49 (domain A/B) and 388-455 (domain  F) mediate binding of HNF-4 to Smad3.	bind
80682	5	3471	11	NULL	NULL	0	NULL	statement 3	Protein		mediates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_3_1279_s_250	12631740	(A-C) Two regions of HNF-4 defined by amino acids 1-49 (domain A/B) and 388-455 (domain  F) mediate binding of HNF-4 to Smad3.	bind
80683	1	3473	11	NULL	NULL	NULL	NULL	[3]CNQX	Chemical		binds to 		two days after lesion			animal	Organism				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_77_2_473_s_97	9472405	(A-C) [3]CNQX binding in an animal two days after lesion; (D-F) [3]MK-801 binding in an animal 30 days after lesion.	bind
80684	2	3473	11	NULL	NULL	0	NULL	[3]MK-801	Chemical		binds to 		30 days after lesion			animal	Organism				NULL		0	NULL	NULL	NULL	gw60_neuroscience_77_2_473_s_97	9472405	(A-C) [3]CNQX binding in an animal two days after lesion; (D-F) [3]MK-801 binding in an animal 30 days after lesion.	bind
7695	1	3474	6	11	NULL	0	NULL	receptor	GP		bind					EGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_3_525_s_180	10069801	(a-d) Receptors bound to EGF-Affi-Gel 15 were phosphorylated with [gamma-32]ATP under autophosphorylation conditions.	bind
7696	2	3474	6	11	NULL	0	NULL	statement 1	GP		undergoes					autophosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_3_525_s_180	10069801	(a-d) Receptors bound to EGF-Affi-Gel 15 were phosphorylated with [gamma-32]ATP under autophosphorylation conditions.	bind
10863	2	3474	7	11	NULL	0	NULL	statement 1	GP		undergoes					autophosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_3_525_s_180	10069801	(a-d) Receptors bound to EGF-Affi-Gel 15 were phosphorylated with [gamma-32]ATP under autophosphorylation conditions.	bind
52920	1	3474	7	11	NULL	0	NULL	receptor	GP		bind					EGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_3_525_s_180	10069801	(a-d) Receptors bound to EGF-Affi-Gel 15 were phosphorylated with [gamma-32]ATP under autophosphorylation conditions.	bind
80685	1	3474	11	NULL	NULL	0	NULL	Receptors	Protein		binds to 					EGF-Affi-Gel 15	Protein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_3_525_s_180	10069801	(a-d) Receptors bound to EGF-Affi-Gel 15 were phosphorylated with [gamma-32]ATP under autophosphorylation conditions.	bind
80686	1	3478	11	NULL	NULL	NULL	NULL	Apo2L fragment	Protein	recombinant soluble 114 - 281	lacks					polyhistidine tag	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_104_2_155_s_44	10411544	(Although it lacks a polyhistidine tag, the recombinant soluble 114 - 281 Apo2L fragment bound to the Ni-NTA column, probably through endogenous histidine residues.)	bind
80687	2	3478	11	NULL	NULL	0	NULL	Apo2L fragment	Protein	recombinant soluble 114 - 281	binds to 			endogenous histidine residue		Ni-NTA column	LaboratoryExperimentalFactor				NULL		0	NULL	NULL	NULL	gw60_jclininvest_104_2_155_s_44	10411544	(Although it lacks a polyhistidine tag, the recombinant soluble 114 - 281 Apo2L fragment bound to the Ni-NTA column, probably through endogenous histidine residues.)	bind
7733	1	3479	6	11	NULL	0	NULL	Asf1	GP		bind		stably			Rad53	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_1_13_s_92	11172707	(Although perhaps counterintuitive, loss of Mec1 function is not expected to decrease the amount of Asf1 stably bound to Rad53).	bind
14200	2	3479	6	11	NULL	0	NULL	Mec1	GP	loss of;;function of	does not decrease					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_1_13_s_92	11172707	(Although perhaps counterintuitive, loss of Mec1 function is not expected to decrease the amount of Asf1 stably bound to Rad53).	bind
10866	1	3479	7	11	NULL	0	NULL	Asf1	GP		bind		stably			Rad53	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_1_13_s_92	11172707	(Although perhaps counterintuitive, loss of Mec1 function is not expected to decrease the amount of Asf1 stably bound to Rad53).	bind
10867	2	3479	7	11	NULL	0	NULL	Mec1	GP	loss of;;function of	does not decrease					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_1_13_s_92	11172707	(Although perhaps counterintuitive, loss of Mec1 function is not expected to decrease the amount of Asf1 stably bound to Rad53).	bind
80688	1	3479	11	NULL	NULL	0	NULL	Asf1	Protein		binds to 		stably			Rad53	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_7_1_13_s_92	11172707	(Although perhaps counterintuitive, loss of Mec1 function is not expected to decrease the amount of Asf1 stably bound to Rad53).	bind
80689	2	3479	11	NULL	NULL	0	NULL	Mec1	Protein	loss of function	is not expected to decrease					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_7_1_13_s_92	11172707	(Although perhaps counterintuitive, loss of Mec1 function is not expected to decrease the amount of Asf1 stably bound to Rad53).	bind
7734	1	3480	6	11	NULL	0	NULL	TFIID	GP		does not bind					GST-Gcn4p	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_15_6871_s_102	15254252	(Although Taf9p and Taf12p are shared by SAGA and TFIID, we showed previously that TFIID does not bind to GST-Gcn4p in these assays ( ).	bind
10868	1	3480	7	11	NULL	0	NULL	TFIID 	GP		does not bind					GST-Gcn4p	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_15_6871_s_102	15254252	(Although Taf9p and Taf12p are shared by SAGA and TFIID, we showed previously that TFIID does not bind to GST-Gcn4p in these assays ( ).	bind
80690	1	3480	11	NULL	NULL	0	NULL	TFIID	Protein		does not bind to					GST-Gcn4p	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_15_6871_s_102	15254252	(Although Taf9p and Taf12p are shared by SAGA and TFIID, we showed previously that TFIID does not bind to GST-Gcn4p in these assays ( ).	bind
80691	2	3480	11	NULL	NULL	0	NULL	Taf9p	Protein		shared by					SAGA	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_15_6871_s_102	15254252	(Although Taf9p and Taf12p are shared by SAGA and TFIID, we showed previously that TFIID does not bind to GST-Gcn4p in these assays ( ).	bind
80692	3	3480	11	NULL	NULL	0	NULL	Taf9p	Protein		shared by					TFIID	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_15_6871_s_102	15254252	(Although Taf9p and Taf12p are shared by SAGA and TFIID, we showed previously that TFIID does not bind to GST-Gcn4p in these assays ( ).	bind
80693	4	3480	11	NULL	NULL	0	NULL	Taf12p	Protein		shared by					SAGA	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_15_6871_s_102	15254252	(Although Taf9p and Taf12p are shared by SAGA and TFIID, we showed previously that TFIID does not bind to GST-Gcn4p in these assays ( ).	bind
80694	5	3480	11	NULL	NULL	0	NULL	Taf12p	Protein		shared by					TFIID	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_15_6871_s_102	15254252	(Although Taf9p and Taf12p are shared by SAGA and TFIID, we showed previously that TFIID does not bind to GST-Gcn4p in these assays ( ).	bind
7735	1	3485	6	11	NULL	0	NULL	Arf-GTPase-activating protein 1	GP		bind		constitutively			CIN85	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_39_28919_s_419	16895919	(Arf-GTPase-activating protein 1) constitutively binds to CIN85 and induces an increase in EGF receptor recycling ( ,  ).	bind
7736	2	3485	6	11	NULL	0	NULL	statement 1	Process		increase					EGF receptor	GP	recycling of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_39_28919_s_419	16895919	(Arf-GTPase-activating protein 1) constitutively binds to CIN85 and induces an increase in EGF receptor recycling ( ,  ).	bind
10869	1	3485	7	11	NULL	0	NULL	Arf-GTPase-activating protein 1	GP		bind		constitutively			CIN85	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_39_28919_s_419	16895919	(Arf-GTPase-activating protein 1) constitutively binds to CIN85 and induces an increase in EGF receptor recycling ( ,  ).	bind
10870	2	3485	7	11	NULL	0	NULL	statement 1	Process		increase					EGF receptor	GP	recycling of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_39_28919_s_419	16895919	(Arf-GTPase-activating protein 1) constitutively binds to CIN85 and induces an increase in EGF receptor recycling ( ,  ).	bind
80695	1	3485	11	NULL	NULL	0	NULL	Arf-GTPase-activating protein 1	Protein		binds to 					CIN85	Protein				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_39_28919_s_419	16895919	(Arf-GTPase-activating protein 1) constitutively binds to CIN85 and induces an increase in EGF receptor recycling ( ,  ).	bind
80696	2	3485	11	NULL	NULL	0	NULL	statement 1	Process		induces					recycling	Process	EGF receptor			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_39_28919_s_419	16895919	(Arf-GTPase-activating protein 1) constitutively binds to CIN85 and induces an increase in EGF receptor recycling ( ,  ).	bind
7737	1	3486	6	11	NULL	0	NULL	Grb2	GP		bind					PTPalpha	GP	endogenous;;WT			NULL	Neo control cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_24_21922_s_181	11923305	(As previously noted, Grb2 bound a larger fraction of endogenous WT PTPalpha ( i.e. in the Neo control cells) than overexpressed WT PTPalpha.	bind
52940	2	3486	6	11	NULL	0	NULL	Grb2	GP		bind					PTPalpha	GP	overexpressed;;WT			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_24_21922_s_181	11923305	(As previously noted, Grb2 bound a larger fraction of endogenous WT PTPalpha ( i.e. in the Neo control cells) than overexpressed WT PTPalpha.	bind
52941	3	3486	6	11	NULL	0	NULL	statement 1	Process		greater than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_24_21922_s_181	11923305	(As previously noted, Grb2 bound a larger fraction of endogenous WT PTPalpha ( i.e. in the Neo control cells) than overexpressed WT PTPalpha.	bind
10871	1	3486	7	11	NULL	0	NULL	Grb2	GP		bind					PTPalpha	GP	endogenous;; WT			NULL	in the Neo control cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_24_21922_s_181	11923305	(As previously noted, Grb2 bound a larger fraction of endogenous WT PTPalpha ( i.e. in the Neo control cells) than overexpressed WT PTPalpha.	bind
10872	2	3486	7	11	NULL	0	NULL	Grb2	GP		bind					PTPalpha	GP	overexpressed;;WT			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_24_21922_s_181	11923305	(As previously noted, Grb2 bound a larger fraction of endogenous WT PTPalpha ( i.e. in the Neo control cells) than overexpressed WT PTPalpha.	bind
10873	3	3486	7	11	NULL	0	NULL	statement 1	Process		greater than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_24_21922_s_181	11923305	(As previously noted, Grb2 bound a larger fraction of endogenous WT PTPalpha ( i.e. in the Neo control cells) than overexpressed WT PTPalpha.	bind
80697	1	3486	11	NULL	NULL	0	NULL	Grb2	Protein		binds to 					WT PTPalpha	Protein	endogenous			NULL	 Neo control cells	0	NULL	NULL	NULL	gw60_jbiolchem_277_24_21922_s_181	11923305	(As previously noted, Grb2 bound a larger fraction of endogenous WT PTPalpha ( i.e. in the Neo control cells) than overexpressed WT PTPalpha.	bind
80698	2	3486	11	NULL	NULL	0	NULL	Grb2	Protein		binds to 					WT PTPalpha	Protein	overexpressed			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_24_21922_s_181	11923305	(As previously noted, Grb2 bound a larger fraction of endogenous WT PTPalpha ( i.e. in the Neo control cells) than overexpressed WT PTPalpha.	bind
7738	1	3487	6	11	NULL	0	NULL	lidocaine	Chemical		bind					IS	Process				NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_66_3_648_s_213	15322257	(As shown in  Fig. 4, the  KD for lidocaine binding to IS is similar to the  KD for lidocaine binding to IM).	bind
7739	2	3487	6	11	NULL	0	NULL	lidocaine	Chemical		bind					IM	Process				NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_66_3_648_s_213	15322257	(As shown in  Fig. 4, the  KD for lidocaine binding to IS is similar to the  KD for lidocaine binding to IM).	bind
10885	1	3487	7	11	NULL	0	NULL	lidocaine	Chemical		bind					IS 	Process				NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_66_3_648_s_213	15322257	(As shown in  Fig. 4, the  KD for lidocaine binding to IS is similar to the  KD for lidocaine binding to IM).	bind
10886	2	3487	7	11	NULL	0	NULL	lidocaine	Chemical		bind					IM	Process				NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_66_3_648_s_213	15322257	(As shown in  Fig. 4, the  KD for lidocaine binding to IS is similar to the  KD for lidocaine binding to IM).	bind
80699	1	3487	11	NULL	NULL	0	NULL	lidocaine	Chemical		binds to 					IS	LaboratoryExperimentalFactor				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_66_3_648_s_213	15322257	(As shown in  Fig. 4, the  KD for lidocaine binding to IS is similar to the  KD for lidocaine binding to IM).	bind
80700	2	3487	11	NULL	NULL	0	NULL	lidocaine	Chemical		binds to 					IM	LaboratoryExperimentalFactor				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_66_3_648_s_213	15322257	(As shown in  Fig. 4, the  KD for lidocaine binding to IS is similar to the  KD for lidocaine binding to IM).	bind
80701	3	3487	11	NULL	NULL	0	NULL	statement 1	Process	KD	is similar to					statement 2	Process	KD			NULL		0	NULL	NULL	NULL	gw70_molpharmacol_66_3_648_s_213	15322257	(As shown in  Fig. 4, the  KD for lidocaine binding to IS is similar to the  KD for lidocaine binding to IM).	bind
7740	1	3489	6	11	NULL	0	NULL	enolase	GP	A. hydrophila	bind					plasminogen	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_microbpathogenesis_34_4_195_s_124	12668143	(B and C)  A. hydrophila enolase binds with human plasminogen based on sandwich Western blot analysis.	bind
10888	1	3489	7	11	NULL	0	NULL	enolase	GP	A. hydrophila	bind					plasminogen	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_microbpathogenesis_34_4_195_s_124	12668143	(B and C)  A. hydrophila enolase binds with human plasminogen based on sandwich Western blot analysis.	bind
80706	1	3489	11	NULL	NULL	0	NULL	enolase	Protein	A. hydrophila	binds to 					plasminogen	Protein	human			NULL	sandwich Western blot analysis	0	NULL	NULL	NULL	gw60_microbpathogenesis_34_4_195_s_124	12668143	(B and C)  A. hydrophila enolase binds with human plasminogen based on sandwich Western blot analysis.	bind
80708	1	3490	11	NULL	NULL	0	NULL	70Z/3 cells	cell		stimulated with					LPS	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_14_6488_s_163	15226448	(B and C) 70Z/3 cells were stimulated with LPS or PMA (B) or UV light (C) for the  times indicated, and whole-cell extracts were analyzed for NF-kappaB and AP-1 DNA binding and JunB, JunD, and p65 expression levels by Western blotting.	bind
80709	2	3490	11	NULL	NULL	0	NULL	70Z/3 cells	cell		stimulated with					PMA	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_14_6488_s_163	15226448	(B and C) 70Z/3 cells were stimulated with LPS or PMA (B) or UV light (C) for the  times indicated, and whole-cell extracts were analyzed for NF-kappaB and AP-1 DNA binding and JunB, JunD, and p65 expression levels by Western blotting.	bind
80710	3	3490	11	NULL	NULL	0	NULL	70Z/3 cells	cell		stimulated with					UV light	LaboratoryExperimentalFactor				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_14_6488_s_163	15226448	(B and C) 70Z/3 cells were stimulated with LPS or PMA (B) or UV light (C) for the  times indicated, and whole-cell extracts were analyzed for NF-kappaB and AP-1 DNA binding and JunB, JunD, and p65 expression levels by Western blotting.	bind
80711	4	3490	11	NULL	NULL	0	NULL	DNA	NucleicAcidSubstance		binds to 					NF-kappaB	Protein				NULL	70Z/3 whole-cell extract	0	NULL	NULL	NULL	gw70_molcellbiol_24_14_6488_s_163	15226448	(B and C) 70Z/3 cells were stimulated with LPS or PMA (B) or UV light (C) for the  times indicated, and whole-cell extracts were analyzed for NF-kappaB and AP-1 DNA binding and JunB, JunD, and p65 expression levels by Western blotting.	bind
80712	5	3490	11	NULL	NULL	0	NULL	DNA	NucleicAcidSubstance		binds to 					AP-1	Protein				NULL	70Z/3 whole-cell extract	0	NULL	NULL	NULL	gw70_molcellbiol_24_14_6488_s_163	15226448	(B and C) 70Z/3 cells were stimulated with LPS or PMA (B) or UV light (C) for the  times indicated, and whole-cell extracts were analyzed for NF-kappaB and AP-1 DNA binding and JunB, JunD, and p65 expression levels by Western blotting.	bind
80713	6	3490	11	NULL	NULL	0	NULL	70Z/3 cells	cell	whole-cell extract	express					JunB	Gene				NULL	Western blotting	0	NULL	NULL	NULL	gw70_molcellbiol_24_14_6488_s_163	15226448	(B and C) 70Z/3 cells were stimulated with LPS or PMA (B) or UV light (C) for the  times indicated, and whole-cell extracts were analyzed for NF-kappaB and AP-1 DNA binding and JunB, JunD, and p65 expression levels by Western blotting.	bind
80714	7	3490	11	NULL	NULL	0	NULL	70Z/3 cells	cell	whole-cell extract	express					JunD	Gene				NULL	Western blotting	0	NULL	NULL	NULL	gw70_molcellbiol_24_14_6488_s_163	15226448	(B and C) 70Z/3 cells were stimulated with LPS or PMA (B) or UV light (C) for the  times indicated, and whole-cell extracts were analyzed for NF-kappaB and AP-1 DNA binding and JunB, JunD, and p65 expression levels by Western blotting.	bind
80715	8	3490	11	NULL	NULL	0	NULL	70Z/3 cells	cell	whole-cell extract	express					p65	Gene				NULL	Western blotting	0	NULL	NULL	NULL	gw70_molcellbiol_24_14_6488_s_163	15226448	(B and C) 70Z/3 cells were stimulated with LPS or PMA (B) or UV light (C) for the  times indicated, and whole-cell extracts were analyzed for NF-kappaB and AP-1 DNA binding and JunB, JunD, and p65 expression levels by Western blotting.	bind
7743	1	3491	6	11	NULL	0	NULL	ATF6alpha	GP		bind									ERSE-CC	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1239_s_185	11158310	(B and C) Binding of ATF6alpha(B) and ATF6beta (C) in the presence of NF-Y to resin carrying ERSE-CC.	bind
7744	2	3491	6	11	NULL	0	NULL	ATF6beta	GP		bind									ERSE-CC	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1239_s_185	11158310	(B and C) Binding of ATF6alpha(B) and ATF6beta (C) in the presence of NF-Y to resin carrying ERSE-CC.	bind
7745	3	3491	6	11	NULL	0	NULL	statement 1	Process		occurs in presence of					NF-Y	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1239_s_185	11158310	(B and C) Binding of ATF6alpha(B) and ATF6beta (C) in the presence of NF-Y to resin carrying ERSE-CC.	bind
7746	4	3491	6	11	NULL	0	NULL	statement 2	Process		occurs in presence of					NF-Y	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1239_s_185	11158310	(B and C) Binding of ATF6alpha(B) and ATF6beta (C) in the presence of NF-Y to resin carrying ERSE-CC.	bind
10894	1	3491	7	11	NULL	0	NULL	ATF6alpha	GP		bind									ERSE-CC	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1239_s_185	11158310	(B and C) Binding of ATF6alpha(B) and ATF6beta (C) in the presence of NF-Y to resin carrying ERSE-CC.	bind
10895	2	3491	7	11	NULL	0	NULL	ATF6beta	GP		bind									ERSE-CC	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1239_s_185	11158310	(B and C) Binding of ATF6alpha(B) and ATF6beta (C) in the presence of NF-Y to resin carrying ERSE-CC.	bind
52942	3	3491	7	11	NULL	0	NULL	statement 1	Process		occurs in presence of					NF-Y	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1239_s_185	11158310	(B and C) Binding of ATF6alpha(B) and ATF6beta (C) in the presence of NF-Y to resin carrying ERSE-CC.	bind
52944	4	3491	7	11	NULL	0	NULL	statement 2	Process		occurs in presence of					NF-Y	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1239_s_185	11158310	(B and C) Binding of ATF6alpha(B) and ATF6beta (C) in the presence of NF-Y to resin carrying ERSE-CC.	bind
80716	1	3491	11	NULL	NULL	0	NULL	ATF6alpha	Protein		binds to 					ERSE-CC	NucleicAcidSubstance	resin carrying			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1239_s_185	11158310	(B and C) Binding of ATF6alpha(B) and ATF6beta (C) in the presence of NF-Y to resin carrying ERSE-CC.	bind
80717	2	3491	11	NULL	NULL	0	NULL	ATF6beta	Protein		binds to 					ERSE-CC	NucleicAcidSubstance	resin carrying			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1239_s_185	11158310	(B and C) Binding of ATF6alpha(B) and ATF6beta (C) in the presence of NF-Y to resin carrying ERSE-CC.	bind
80719	3	3491	11	NULL	NULL	0	NULL	statement 1	Process		occurs in the presence of					NF-Y	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1239_s_185	11158310	(B and C) Binding of ATF6alpha(B) and ATF6beta (C) in the presence of NF-Y to resin carrying ERSE-CC.	bind
80720	4	3491	11	NULL	NULL	0	NULL	statement 2	Process		occurs in the presence of					NF-Y	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1239_s_185	11158310	(B and C) Binding of ATF6alpha(B) and ATF6beta (C) in the presence of NF-Y to resin carrying ERSE-CC.	bind
7747	1	3492	6	11	NULL	0	NULL	NF-Y	GP		bind					HLA-DRA	GP			Y box	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6495_s_290	11533238	(B and C) Binding of NF-Y to the HLA-DRA Y box and YY1 to the +62/+72 HLA-DRA YY1 binding element is not affected by treatment of cells with HDAC inhibitors.	bind
7748	2	3492	6	11	NULL	0	NULL	NF-Y	GP		bind					HLA-DRA	GP			YY1 binding element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6495_s_290	11533238	(B and C) Binding of NF-Y to the HLA-DRA Y box and YY1 to the +62/+72 HLA-DRA YY1 binding element is not affected by treatment of cells with HDAC inhibitors.	bind
7797	3	3492	6	11	NULL	0	NULL	HDAC inhibitors	Chemical		have no effect on					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6495_s_290	11533238	(B and C) Binding of NF-Y to the HLA-DRA Y box and YY1 to the +62/+72 HLA-DRA YY1 binding element is not affected by treatment of cells with HDAC inhibitors.	bind
7798	4	3492	6	11	NULL	0	NULL	HDAC inhibitors	Chemical		have no effect on					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6495_s_290	11533238	(B and C) Binding of NF-Y to the HLA-DRA Y box and YY1 to the +62/+72 HLA-DRA YY1 binding element is not affected by treatment of cells with HDAC inhibitors.	bind
10900	1	3492	7	11	NULL	0	NULL	NF-Y	GP		bind					HLA-DRA	GP			Y box	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6495_s_290	11533238	(B and C) Binding of NF-Y to the HLA-DRA Y box and YY1 to the +62/+72 HLA-DRA YY1 binding element is not affected by treatment of cells with HDAC inhibitors.	bind
10906	2	3492	7	11	NULL	0	NULL	YY1	GP		bind					HLA-DRA	GP			YY1 binding element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6495_s_290	11533238	(B and C) Binding of NF-Y to the HLA-DRA Y box and YY1 to the +62/+72 HLA-DRA YY1 binding element is not affected by treatment of cells with HDAC inhibitors.	bind
10907	3	3492	7	11	NULL	0	NULL	statement 1	Process		is not affected by 					HDAC inhibitors	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6495_s_290	11533238	(B and C) Binding of NF-Y to the HLA-DRA Y box and YY1 to the +62/+72 HLA-DRA YY1 binding element is not affected by treatment of cells with HDAC inhibitors.	bind
10908	4	3492	7	11	NULL	0	NULL	statement 2	Process		is not affected by					HDAC inhibitors	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6495_s_290	11533238	(B and C) Binding of NF-Y to the HLA-DRA Y box and YY1 to the +62/+72 HLA-DRA YY1 binding element is not affected by treatment of cells with HDAC inhibitors.	bind
80721	1	3492	11	NULL	NULL	NULL	NULL	NF-Y	Protein		binds to 					HLA-DRA	Gene	Y box			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6495_s_290	11533238	(B and C) Binding of NF-Y to the HLA-DRA Y box and YY1 to the +62/+72 HLA-DRA YY1 binding element is not affected by treatment of cells with HDAC inhibitors.	bind
80722	2	3492	11	NULL	NULL	0	NULL	YY1	Protein		binds to 					HLA-DRA	Gene				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_19_6495_s_290	11533238	(B and C) Binding of NF-Y to the HLA-DRA Y box and YY1 to the +62/+72 HLA-DRA YY1 binding element is not affected by treatment of cells with HDAC inhibitors.	bind
80723	3	3492	11	NULL	NULL	0	NULL	HLA-DRA	Gene		is not affected by				YY1 binding element	inhibitors	Chemical	HDAC			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_19_6495_s_290	11533238	(B and C) Binding of NF-Y to the HLA-DRA Y box and YY1 to the +62/+72 HLA-DRA YY1 binding element is not affected by treatment of cells with HDAC inhibitors.	bind
7799	1	3493	6	11	NULL	0	NULL	TFIIB	GP	binding of	is dependent on					Swi5	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_6_1213_s_91	11430824	(B and C) Binding of TFIIB and Kin28 depends on Swi5.	bind
7800	2	3493	6	11	NULL	0	NULL	Kin28	GP	binding of	is dependent on					Swi5	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_6_1213_s_91	11430824	(B and C) Binding of TFIIB and Kin28 depends on Swi5.	bind
10910	1	3493	7	11	NULL	0	NULL	TFIIB	GP	binding of	is dependent on					Swi5	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_6_1213_s_91	11430824	(B and C) Binding of TFIIB and Kin28 depends on Swi5.	bind
10912	2	3493	7	11	NULL	0	NULL	Kin28 	GP	binding of	is dependent on					Swi5	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_6_1213_s_91	11430824	(B and C) Binding of TFIIB and Kin28 depends on Swi5.	bind
80724	1	3493	11	NULL	NULL	0	NULL	Binding	MolecularProcess	 TFIIB	depends on					Swi5	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_7_6_1213_s_91	11430824	(B and C) Binding of TFIIB and Kin28 depends on Swi5.	bind
80725	2	3493	11	NULL	NULL	0	NULL	Binding	MolecularProcess	Kin28	depends on					Swi5	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_7_6_1213_s_91	11430824	(B and C) Binding of TFIIB and Kin28 depends on Swi5.	bind
7801	1	3494	6	11	NULL	0	NULL	RXR-TR heterodimer	GP		bind							specific		TRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
7802	2	3494	6	11	NULL	0	NULL	TRAP220	GP		bind			RBD		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
7804	3	3494	6	11	NULL	0	NULL				is necessary for			RBD-1		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
14598	4	3494	6	11	NULL	0	NULL				is necessary for			RBD-2		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
14599	5	3494	6	11	NULL	0	NULL	statement 3	Process		is simultaneous with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
14600	7	3494	6	11	NULL	0	NULL			proper spacing of	is necessary for			RBD-1		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
17772	8	3494	6	11	NULL	0	NULL			proper spacing of	is necessary for			RBD-2		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
17773	9	3494	6	11	NULL	0	NULL	statement 7	Process		is simultaneous with					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
10915	1	3494	7	11	NULL	0	NULL	RXR-TR heterodimer	GP		bind							specific		TRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
10916	2	3494	7	11	NULL	0	NULL	TRAP220 	GP		bind			RBD		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
10917	3	3494	7	11	NULL	0	NULL				is necessary for			RBD-1		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
10918	4	3494	7	11	NULL	0	NULL				is necessary for			RBD-2		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
15014	5	3494	7	11	NULL	0	NULL	statement 3	Process		is simultaneous with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
15015	6	3494	7	11	NULL	0	NULL			proper spacing of	is necessary for			RBD-1		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
15016	7	3494	7	11	NULL	0	NULL			proper spacing of	is necessary for			RBD-2		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
15017	8	3494	7	11	NULL	0	NULL	statement 6	Process		is simultaneous with					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
80726	1	3494	11	NULL	NULL	0	NULL	RXR-TR	Protein		is a type of 					heterodimer	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
80727	2	3494	11	NULL	NULL	NULL	NULL	RXR-TR heterodimer	GeneOrProtein		binds to 					 TRE	NucleicAcidSubstance	specific			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
80728	3	3494	11	NULL	NULL	0	NULL	TRAP220 RBD	Protein		binds to 					statement 2	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
80729	4	3494	11	NULL	NULL	0	NULL	RBD-1	Protein	presence;;proper spacing	necessary for					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
80730	5	3494	11	NULL	NULL	0	NULL	RBD-2 	Protein	presence;;proper spacing	necessary for					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_252	10891484	(B and C) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-TR heterodimer bound to a specific TRE.	bind
7805	1	3495	6	11	NULL	0	NULL	Gsp1p-GTP	GP		bind					Los1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_11_6374_s_306	9774653	(B and C) Cooperative binding of Gsp1p-GTP and tRNA to Los1p.	bind
7807	2	3495	6	11	NULL	0	NULL	tRNA	NucleicAcid		bind					Los1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_11_6374_s_306	9774653	(B and C) Cooperative binding of Gsp1p-GTP and tRNA to Los1p.	bind
7808	3	3495	6	11	NULL	0	NULL	statement 1	Process		acts in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_11_6374_s_306	9774653	(B and C) Cooperative binding of Gsp1p-GTP and tRNA to Los1p.	bind
10919	1	3495	7	11	NULL	0	NULL	Gsp1p-GTP	GP		bind					Los1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_11_6374_s_306	9774653	(B and C) Cooperative binding of Gsp1p-GTP and tRNA to Los1p.	bind
10920	2	3495	7	11	NULL	0	NULL	tRNA	NucleicAcid		bind					Los1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_11_6374_s_306	9774653	(B and C) Cooperative binding of Gsp1p-GTP and tRNA to Los1p.	bind
10921	3	3495	7	11	NULL	0	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_11_6374_s_306	9774653	(B and C) Cooperative binding of Gsp1p-GTP and tRNA to Los1p.	bind
80731	1	3495	11	NULL	NULL	0	NULL	Gsp1p-GTP	Protein		binds to 		cooperatively			Los1p	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_11_6374_s_306	9774653	(B and C) Cooperative binding of Gsp1p-GTP and tRNA to Los1p.	bind
80732	2	3495	11	NULL	NULL	0	NULL	tRNA	NucleicAcidSubstance		binds to 		cooperatively			Los1p	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_11_6374_s_306	9774653	(B and C) Cooperative binding of Gsp1p-GTP and tRNA to Los1p.	bind
7810	1	3496	6	11	NULL	0	NULL	GST-Hairy derivatives	GP		bind					Gro	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2080_s_156	10022895	(B and C) Expression of HairyWRPW (B) and HairyGEH-17 (C) under the control of the  hb promoter causes efficient repression of  Sxl. (D) Binding of GST-Hairy derivatives to Gro in vitro.	bind
7812	2	3496	6	11	NULL	0	NULL	hb	GP		controls				promoter	HairyWRPW	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2080_s_156	10022895	(B and C) Expression of HairyWRPW (B) and HairyGEH-17 (C) under the control of the  hb promoter causes efficient repression of  Sxl. (D) Binding of GST-Hairy derivatives to Gro in vitro.	bind
7813	3	3496	6	11	NULL	0	NULL	hb	GP		controls				promoter	HairyGEH-17	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2080_s_156	10022895	(B and C) Expression of HairyWRPW (B) and HairyGEH-17 (C) under the control of the  hb promoter causes efficient repression of  Sxl. (D) Binding of GST-Hairy derivatives to Gro in vitro.	bind
7814	4	3496	6	11	NULL	0	NULL	HairyWRPW	GP	expression of	repress		efficiently			Sxl	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2080_s_156	10022895	(B and C) Expression of HairyWRPW (B) and HairyGEH-17 (C) under the control of the  hb promoter causes efficient repression of  Sxl. (D) Binding of GST-Hairy derivatives to Gro in vitro.	bind
7815	5	3496	6	11	NULL	0	NULL	HairyGEH-17	GP	expression of	repress		efficiently			Sxl	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2080_s_156	10022895	(B and C) Expression of HairyWRPW (B) and HairyGEH-17 (C) under the control of the  hb promoter causes efficient repression of  Sxl. (D) Binding of GST-Hairy derivatives to Gro in vitro.	bind
10922	1	3496	7	11	NULL	0	NULL	GST-Hairy derivatives	GP		bind					Gro	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2080_s_156	10022895	(B and C) Expression of HairyWRPW (B) and HairyGEH-17 (C) under the control of the  hb promoter causes efficient repression of  Sxl. (D) Binding of GST-Hairy derivatives to Gro in vitro.	bind
10923	2	3496	7	11	NULL	0	NULL	HairyWRPW	GP	expression of	repress		efficiently			Sxl	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2080_s_156	10022895	(B and C) Expression of HairyWRPW (B) and HairyGEH-17 (C) under the control of the  hb promoter causes efficient repression of  Sxl. (D) Binding of GST-Hairy derivatives to Gro in vitro.	bind
10924	3	3496	7	11	NULL	0	NULL	HairyGEH-17	GP	expression of	repress		efficiently			Sxl	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2080_s_156	10022895	(B and C) Expression of HairyWRPW (B) and HairyGEH-17 (C) under the control of the  hb promoter causes efficient repression of  Sxl. (D) Binding of GST-Hairy derivatives to Gro in vitro.	bind
10925	4	3496	7	11	NULL	0	NULL	statement 2	Process		occus under					hb	GP	the control of		promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2080_s_156	10022895	(B and C) Expression of HairyWRPW (B) and HairyGEH-17 (C) under the control of the  hb promoter causes efficient repression of  Sxl. (D) Binding of GST-Hairy derivatives to Gro in vitro.	bind
10926	5	3496	7	11	NULL	0	NULL	statement 3	Process		occurs under 					hb	GP	the control of		promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2080_s_156	10022895	(B and C) Expression of HairyWRPW (B) and HairyGEH-17 (C) under the control of the  hb promoter causes efficient repression of  Sxl. (D) Binding of GST-Hairy derivatives to Gro in vitro.	bind
80733	1	3496	11	NULL	NULL	0	NULL	GST-Hairy	Protein	derivatives	binds to 					Gro	Protein				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2080_s_156	10022895	(B and C) Expression of HairyWRPW (B) and HairyGEH-17 (C) under the control of the  hb promoter causes efficient repression of  Sxl. (D) Binding of GST-Hairy derivatives to Gro in vitro.	bind
80734	2	3496	11	NULL	NULL	0	NULL	hb promoter	NucleicAcidSubstance		controls					Expression	MolecularProcess	HairyWRPW			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2080_s_156	10022895	(B and C) Expression of HairyWRPW (B) and HairyGEH-17 (C) under the control of the  hb promoter causes efficient repression of  Sxl. (D) Binding of GST-Hairy derivatives to Gro in vitro.	bind
80735	3	3496	11	NULL	NULL	0	NULL	statement 2	Process		repress					Sxl	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2080_s_156	10022895	(B and C) Expression of HairyWRPW (B) and HairyGEH-17 (C) under the control of the  hb promoter causes efficient repression of  Sxl. (D) Binding of GST-Hairy derivatives to Gro in vitro.	bind
80736	4	3496	11	NULL	NULL	0	NULL	hb promoter	NucleicAcidSubstance		controls					Expression	MolecularProcess	HairyGEH-17			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2080_s_156	10022895	(B and C) Expression of HairyWRPW (B) and HairyGEH-17 (C) under the control of the  hb promoter causes efficient repression of  Sxl. (D) Binding of GST-Hairy derivatives to Gro in vitro.	bind
80737	5	3496	11	NULL	NULL	0	NULL	statement 4	Process		repress					Sxl	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2080_s_156	10022895	(B and C) Expression of HairyWRPW (B) and HairyGEH-17 (C) under the control of the  hb promoter causes efficient repression of  Sxl. (D) Binding of GST-Hairy derivatives to Gro in vitro.	bind
7816	1	3497	6	11	NULL	0	NULL	Flo8	GP		bind					UAS2-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_194	15485921	(B and C) Flo8 and Mss11  binding to UAS2-1 requires Ste12 and Tec1.	bind
7817	2	3497	6	11	NULL	0	NULL	Mss11	GP		bind					UAS2-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_194	15485921	(B and C) Flo8 and Mss11  binding to UAS2-1 requires Ste12 and Tec1.	bind
7818	3	3497	6	11	NULL	0	NULL	statement 1	Process		requires					Ste12	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_194	15485921	(B and C) Flo8 and Mss11  binding to UAS2-1 requires Ste12 and Tec1.	bind
7819	4	3497	6	11	NULL	0	NULL	statement 1	Process		requires					Tec1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_194	15485921	(B and C) Flo8 and Mss11  binding to UAS2-1 requires Ste12 and Tec1.	bind
7820	5	3497	6	11	NULL	0	NULL	statement 2	Process		requires					Ste12	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_194	15485921	(B and C) Flo8 and Mss11  binding to UAS2-1 requires Ste12 and Tec1.	bind
7822	6	3497	6	11	NULL	0	NULL	statement 2	Process		requires					Tec1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_194	15485921	(B and C) Flo8 and Mss11  binding to UAS2-1 requires Ste12 and Tec1.	bind
10927	1	3497	7	11	NULL	0	NULL	Flo8	GP		bind					UAS2-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_194	15485921	(B and C) Flo8 and Mss11  binding to UAS2-1 requires Ste12 and Tec1.	bind
10928	2	3497	7	11	NULL	0	NULL	Mss11	GP		bind					UAS2-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_194	15485921	(B and C) Flo8 and Mss11  binding to UAS2-1 requires Ste12 and Tec1.	bind
10929	3	3497	7	11	NULL	0	NULL	statement 1	Process		requires					Ste12	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_194	15485921	(B and C) Flo8 and Mss11  binding to UAS2-1 requires Ste12 and Tec1.	bind
10930	4	3497	7	11	NULL	0	NULL	statement 1	Process		requires					Tec1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_194	15485921	(B and C) Flo8 and Mss11  binding to UAS2-1 requires Ste12 and Tec1.	bind
10931	5	3497	7	11	NULL	0	NULL	statement 2	Process		requires					Ste12	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_194	15485921	(B and C) Flo8 and Mss11  binding to UAS2-1 requires Ste12 and Tec1.	bind
10932	6	3497	7	11	NULL	0	NULL	statement 2	Process		requires					Tec1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_194	15485921	(B and C) Flo8 and Mss11  binding to UAS2-1 requires Ste12 and Tec1.	bind
80738	1	3497	11	NULL	NULL	NULL	NULL	Flo8	GeneOrProtein		binds to 					UAS2-1	NucleicAcidSubstance				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_194	15485921	(B and C) Flo8 and Mss11  binding to UAS2-1 requires Ste12 and Tec1.	bind
80739	2	3497	11	NULL	NULL	0	NULL	Mss11	GeneOrProtein		binds to 					UAS2-1	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_194	15485921	(B and C) Flo8 and Mss11  binding to UAS2-1 requires Ste12 and Tec1.	bind
80740	3	3497	11	NULL	NULL	0	NULL	statement 1	Process		requires					Ste12	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_194	15485921	(B and C) Flo8 and Mss11  binding to UAS2-1 requires Ste12 and Tec1.	bind
80741	4	3497	11	NULL	NULL	NULL	NULL	statement 1	Process		requires					Tec1	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_194	15485921	(B and C) Flo8 and Mss11  binding to UAS2-1 requires Ste12 and Tec1.	bind
80742	5	3497	11	NULL	NULL	0	NULL	statement 2	Process		requires					Ste12	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_194	15485921	(B and C) Flo8 and Mss11  binding to UAS2-1 requires Ste12 and Tec1.	bind
80743	6	3497	11	NULL	NULL	0	NULL	statement 2	Process		requires					Tec1	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_194	15485921	(B and C) Flo8 and Mss11  binding to UAS2-1 requires Ste12 and Tec1.	bind
7825	1	3499	6	11	NULL	0	NULL	eIF2B subunits	GP		bind					eIF2alpha	GP	phosphorylated			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3063_s_290	15798194	(B and C) Mutations of eIF2alpha residues near and remote from Ser51 impair binding of eIF2B subunits to phosphorylated  eIF2alpha.	bind
7827	2	3499	6	11	NULL	0	NULL	eIF2alpha	GP	mutation of	impair 			 near Ser51		statement 1	Process	binding of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3063_s_290	15798194	(B and C) Mutations of eIF2alpha residues near and remote from Ser51 impair binding of eIF2B subunits to phosphorylated  eIF2alpha.	bind
14201	3	3499	6	11	NULL	0	NULL	eIF2alpha	GP	mutation of	impair			remote from Ser51		statement 1	Process	binding of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3063_s_290	15798194	(B and C) Mutations of eIF2alpha residues near and remote from Ser51 impair binding of eIF2B subunits to phosphorylated  eIF2alpha.	bind
10933	1	3499	7	11	NULL	0	NULL	eIF2B subunits	GP		bind					eIF2alpha	GP	phosphorylated			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3063_s_290	15798194	(B and C) Mutations of eIF2alpha residues near and remote from Ser51 impair binding of eIF2B subunits to phosphorylated  eIF2alpha.	bind
10934	2	3499	7	11	NULL	0	NULL	eIF2alpha	GP	mutation of 	impair			near Ser51		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3063_s_290	15798194	(B and C) Mutations of eIF2alpha residues near and remote from Ser51 impair binding of eIF2B subunits to phosphorylated  eIF2alpha.	bind
10935	3	3499	7	11	NULL	0	NULL	eIF2alpha	GP	mutations of	impair			remote from Ser51		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3063_s_290	15798194	(B and C) Mutations of eIF2alpha residues near and remote from Ser51 impair binding of eIF2B subunits to phosphorylated  eIF2alpha.	bind
80744	1	3499	11	NULL	NULL	0	NULL	eIF2B	Protein		binds to 					eIF2alpha	Protein	phosphorylated			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3063_s_290	15798194	(B and C) Mutations of eIF2alpha residues near and remote from Ser51 impair binding of eIF2B subunits to phosphorylated  eIF2alpha.	bind
80745	2	3499	11	NULL	NULL	0	NULL	eIF2alpha	Protein	mutation of	impair			near Ser51		statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3063_s_290	15798194	(B and C) Mutations of eIF2alpha residues near and remote from Ser51 impair binding of eIF2B subunits to phosphorylated  eIF2alpha.	bind
80746	3	3499	11	NULL	NULL	0	NULL	eIF2alpha	Protein	mutation of	impair			remote from Ser51		statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3063_s_290	15798194	(B and C) Mutations of eIF2alpha residues near and remote from Ser51 impair binding of eIF2B subunits to phosphorylated  eIF2alpha.	bind
7830	1	3500	6	11	NULL	0	NULL	Abl	GP	Purified;; recombinant;; Drosophila	bind					GST-Dlar	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_neuron_22_2_301_s_85	10069336	(B and C) Purified, recombinant  Drosophila Abl (B) or v-Abl (C) binds to GST-Dlar in vitro, as assessed by a pull down assay in which dAbl protein has been prelabeled with  32P-ATP before mixing with the fusion proteins.	bind
7831	2	3500	6	11	NULL	0	NULL	v-Abl	GP	Purified;; recombinant;; Drosophila	bind					GST-Dlar	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_neuron_22_2_301_s_85	10069336	(B and C) Purified, recombinant  Drosophila Abl (B) or v-Abl (C) binds to GST-Dlar in vitro, as assessed by a pull down assay in which dAbl protein has been prelabeled with  32P-ATP before mixing with the fusion proteins.	bind
10936	1	3500	7	11	NULL	0	NULL	Abl	GP	Purified;; recombinant;; Drosophila	binds					 GST-Dlar	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_neuron_22_2_301_s_85	10069336	(B and C) Purified, recombinant  Drosophila Abl (B) or v-Abl (C) binds to GST-Dlar in vitro, as assessed by a pull down assay in which dAbl protein has been prelabeled with  32P-ATP before mixing with the fusion proteins.	bind
10937	2	3500	7	11	NULL	0	NULL	v-Abl	GP	Purified;; recombinant;; Drosophila	binds					GST-Dlar	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_neuron_22_2_301_s_85	10069336	(B and C) Purified, recombinant  Drosophila Abl (B) or v-Abl (C) binds to GST-Dlar in vitro, as assessed by a pull down assay in which dAbl protein has been prelabeled with  32P-ATP before mixing with the fusion proteins.	bind
80747	1	3500	11	NULL	NULL	0	NULL	Abl	GeneOrProtein	Purified;;recombinant;;Drosophila	binds to 					GST-Dlar	Protein				NULL	in vitro	0	NULL	NULL	NULL	gw60_neuron_22_2_301_s_85	10069336	(B and C) Purified, recombinant  Drosophila Abl (B) or v-Abl (C) binds to GST-Dlar in vitro, as assessed by a pull down assay in which dAbl protein has been prelabeled with  32P-ATP before mixing with the fusion proteins.	bind
80748	2	3500	11	NULL	NULL	0	NULL	v-Abl	Protein		binds to 					GST-Dlar	Protein				NULL	in vitro	0	NULL	NULL	NULL	gw60_neuron_22_2_301_s_85	10069336	(B and C) Purified, recombinant  Drosophila Abl (B) or v-Abl (C) binds to GST-Dlar in vitro, as assessed by a pull down assay in which dAbl protein has been prelabeled with  32P-ATP before mixing with the fusion proteins.	bind
80749	3	3500	11	NULL	NULL	0	NULL	dAbl protein	Protein		prelabeled with					32P-ATP	Chemical				NULL		0	NULL	NULL	NULL	gw60_neuron_22_2_301_s_85	10069336	(B and C) Purified, recombinant  Drosophila Abl (B) or v-Abl (C) binds to GST-Dlar in vitro, as assessed by a pull down assay in which dAbl protein has been prelabeled with  32P-ATP before mixing with the fusion proteins.	bind
7833	1	3501	6	11	NULL	0	NULL	EGaseA	GP	Soybean	bind					GIP1	GP	P. sojae			NULL		NULL	NULL	NULL	NULL	gw70_genetics_169_2_1009_s_173	15545660	(b and c) Soybean EGaseA (solvent accessible surface) bound to  P. sojae GIP1 (ribbon diagram).	bind
10938	1	3501	7	11	NULL	0	NULL	EGaseA	GP	Soybean	bind					GIP1	GP	P. sojae			NULL		NULL	NULL	NULL	NULL	gw70_genetics_169_2_1009_s_173	15545660	(b and c) Soybean EGaseA (solvent accessible surface) bound to  P. sojae GIP1 (ribbon diagram).	bind
80750	1	3501	11	NULL	NULL	0	NULL	EGaseA	Protein	Soybean	binds to 					GIP1	Protein	P. sojae			NULL		0	NULL	NULL	NULL	gw70_genetics_169_2_1009_s_173	15545660	(b and c) Soybean EGaseA (solvent accessible surface) bound to  P. sojae GIP1 (ribbon diagram).	bind
7835	1	3502	6	11	NULL	0	NULL	p97	GP		bind					RanBP2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2379_s_179	9398662	(B and C) Titration of p97 binding to RanBP2 and p62, respectively.	bind
7836	2	3502	6	11	NULL	0	NULL	p97	GP		bind					p62	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2379_s_179	9398662	(B and C) Titration of p97 binding to RanBP2 and p62, respectively.	bind
10939	1	3502	7	11	NULL	0	NULL	p97	GP		bind					RanBP2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2379_s_179	9398662	(B and C) Titration of p97 binding to RanBP2 and p62, respectively.	bind
10940	2	3502	7	11	NULL	0	NULL	p97	GP		bind					p62	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2379_s_179	9398662	(B and C) Titration of p97 binding to RanBP2 and p62, respectively.	bind
80751	1	3502	11	NULL	NULL	NULL	NULL	p97	Protein	Titration	binds to 					RanBP2	Protein				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2379_s_179	9398662	(B and C) Titration of p97 binding to RanBP2 and p62, respectively.	bind
80752	2	3502	11	NULL	NULL	0	NULL	 p97 	Protein	Titration	binds to 					p62	Protein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_8_12_2379_s_179	9398662	(B and C) Titration of p97 binding to RanBP2 and p62, respectively.	bind
7837	1	3503	6	11	NULL	0	NULL	BCP	GP		bind					GPDH	GP	L.mexicana			NULL		NULL	NULL	NULL	NULL	gw60_chembiol_9_11_1189_s_59	12445769	(B and C) Two alternative conformations (conformation A, green; conformation B, red) of BCP bound to  L. mexicana GPDH in a model-unbiased, sigmaA-weighted Fo-Fc map (B) contoured at 3.5   (light brown) and an anomalous difference Fourier map contoured at 4.5   (red) and (C) an anomalous difference Fourier map contoured at 5.5   (red).	bind
11009	1	3503	7	11	NULL	0	NULL	BCP	GP		bind					GPDH	GP	L. mexicana 			NULL		NULL	NULL	NULL	NULL	gw60_chembiol_9_11_1189_s_59	12445769	(B and C) Two alternative conformations (conformation A, green; conformation B, red) of BCP bound to  L. mexicana GPDH in a model-unbiased, sigmaA-weighted Fo-Fc map (B) contoured at 3.5   (light brown) and an anomalous difference Fourier map contoured at 4.5   (red) and (C) an anomalous difference Fourier map contoured at 5.5   (red).	bind
80753	1	3503	11	NULL	NULL	0	NULL	BCP	Chemical		binds to 					GPDH	Protein	L. mexicana			NULL		0	NULL	NULL	NULL	gw60_chembiol_9_11_1189_s_59	12445769	(B and C) Two alternative conformations (conformation A, green; conformation B, red) of BCP bound to  L. mexicana GPDH in a model-unbiased, sigmaA-weighted Fo-Fc map (B) contoured at 3.5   (light brown) and an anomalous difference Fourier map contoured at 4.5   (red) and (C) an anomalous difference Fourier map contoured at 5.5   (red).	bind
7839	1	3505	6	11	NULL	0	NULL	Aft1	GP		bind					MRS4	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_280	16024809	(B and D) In vivo DNA  binding of Aft1 and Aft2 to the  MRS4 promoter.	bind
7841	2	3505	6	11	NULL	0	NULL	Aft2	GP		bind					MRS4	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_280	16024809	(B and D) In vivo DNA  binding of Aft1 and Aft2 to the  MRS4 promoter.	bind
11012	1	3505	7	11	NULL	0	NULL	Aft1	GP		bind					MRS4	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_280	16024809	(B and D) In vivo DNA  binding of Aft1 and Aft2 to the  MRS4 promoter.	bind
11014	2	3505	7	11	NULL	0	NULL	Aft2	GP		bind					MRS4	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_280	16024809	(B and D) In vivo DNA  binding of Aft1 and Aft2 to the  MRS4 promoter.	bind
80754	1	3505	11	NULL	NULL	NULL	NULL	Aft1	Protein		binds to 					MRS4 promoter	NucleicAcidSubstance				NULL	In vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_280	16024809	(B and D) In vivo DNA  binding of Aft1 and Aft2 to the  MRS4 promoter.	bind
80755	2	3505	11	NULL	NULL	0	NULL	Aft2	Protein		binds to 					MRS4 promoter	NucleicAcidSubstance				NULL	in vivo	0	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_280	16024809	(B and D) In vivo DNA  binding of Aft1 and Aft2 to the  MRS4 promoter.	bind
7842	1	3506	6	11	NULL	0	NULL	Aft1	GP		bind					SMF3	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_256	16024809	(B and D) In vivo DNA  binding of Aft1 and Aft2 to the  SMF3 promoter.	bind
7843	2	3506	6	11	NULL	0	NULL	Aft2	GP		bind					SMF3	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_256	16024809	(B and D) In vivo DNA  binding of Aft1 and Aft2 to the  SMF3 promoter.	bind
11028	1	3506	7	11	NULL	0	NULL	Aft1	GP		bind					SMF3	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_256	16024809	(B and D) In vivo DNA  binding of Aft1 and Aft2 to the  SMF3 promoter.	bind
11029	2	3506	7	11	NULL	0	NULL	Aft2	GP		bind					SMF3	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_256	16024809	(B and D) In vivo DNA  binding of Aft1 and Aft2 to the  SMF3 promoter.	bind
80756	1	3506	11	NULL	NULL	0	NULL	Aft1	Protein		binds to 					SMF3 promoter	NucleicAcidSubstance				NULL	in vivo	0	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_256	16024809	(B and D) In vivo DNA  binding of Aft1 and Aft2 to the  SMF3 promoter.	bind
80757	2	3506	11	NULL	NULL	0	NULL	Aft2	Protein		binds to 					SMF3 promoter	NucleicAcidSubstance				NULL	in vivo	0	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_256	16024809	(B and D) In vivo DNA  binding of Aft1 and Aft2 to the  SMF3 promoter.	bind
7844	1	3507	6	11	NULL	0	NULL	Aft1-HA	GP		bind					FET3	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_198	16024809	(B and D) In vivo DNA  binding of Aft1-HA and Aft2-HA to the  FET3 promoter.	bind
7845	2	3507	6	11	NULL	0	NULL	Aft2-HA	GP		bind					FET3	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_198	16024809	(B and D) In vivo DNA  binding of Aft1-HA and Aft2-HA to the  FET3 promoter.	bind
11015	1	3507	7	11	NULL	0	NULL	 Aft1-HA	GP		bind					FET3	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_198	16024809	(B and D) In vivo DNA  binding of Aft1-HA and Aft2-HA to the  FET3 promoter.	bind
11016	2	3507	7	11	NULL	0	NULL	Aft2-HA	GP		bind					FET3	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_198	16024809	(B and D) In vivo DNA  binding of Aft1-HA and Aft2-HA to the  FET3 promoter.	bind
80758	1	3507	11	NULL	NULL	0	NULL	Aft1-HA	Protein		binds to 					FET3 promoter	NucleicAcidSubstance				NULL	in vivo	0	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_198	16024809	(B and D) In vivo DNA  binding of Aft1-HA and Aft2-HA to the  FET3 promoter.	bind
80759	2	3507	11	NULL	NULL	0	NULL	Aft2-HA	Protein		binds to 					FET3 promoter	NucleicAcidSubstance				NULL	in vivo	0	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_198	16024809	(B and D) In vivo DNA  binding of Aft1-HA and Aft2-HA to the  FET3 promoter.	bind
7848	1	3508	6	11	NULL	0	NULL	Aft1-HA	GP		bind					FTR1	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_228	16024809	(B and D) In vivo DNA  binding of Aft1-HA and Aft2-HA to the  FTR1 promoter.	bind
7849	2	3508	6	11	NULL	0	NULL	Aft2-HA	GP		bind					FTR1	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_228	16024809	(B and D) In vivo DNA  binding of Aft1-HA and Aft2-HA to the  FTR1 promoter.	bind
11017	1	3508	7	11	NULL	0	NULL	Aft1-HA	GP		bind					FTR1	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_228	16024809	(B and D) In vivo DNA  binding of Aft1-HA and Aft2-HA to the  FTR1 promoter.	bind
11019	2	3508	7	11	NULL	0	NULL	Aft2-HA	GP		bind					FTR1	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_228	16024809	(B and D) In vivo DNA  binding of Aft1-HA and Aft2-HA to the  FTR1 promoter.	bind
80760	1	3508	11	NULL	NULL	0	NULL	Aft1-HA	Protein		binds to 					FTR1 promoter	NucleicAcidSubstance				NULL	in vivo	0	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_228	16024809	(B and D) In vivo DNA  binding of Aft1-HA and Aft2-HA to the  FTR1 promoter.	bind
80761	2	3508	11	NULL	NULL	0	NULL	Aft2-HA	Protein		binds to 					 FTR1 promoter	NucleicAcidSubstance				NULL	in vivo	0	NULL	NULL	NULL	gw70_molcellbiol_25_15_6760_s_228	16024809	(B and D) In vivo DNA  binding of Aft1-HA and Aft2-HA to the  FTR1 promoter.	bind
7850	1	3509	6	11	NULL	0	NULL	GM1	GP		bind					EtxB	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_3_1527_s_145	12595472	(B to D) Analysis of Trp-fluorescence upon GM1 binding by EtxB, EtxB(G33D), and EtxB(H57S) by fluorescence spectroscopy.	bind
7851	2	3509	6	11	NULL	0	NULL	GM1	GP		bind					EtxB	Chemical		G33D		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_3_1527_s_145	12595472	(B to D) Analysis of Trp-fluorescence upon GM1 binding by EtxB, EtxB(G33D), and EtxB(H57S) by fluorescence spectroscopy.	bind
7852	3	3509	6	11	NULL	0	NULL	GM1	GP		bind					EtxB	Chemical		H57S		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_3_1527_s_145	12595472	(B to D) Analysis of Trp-fluorescence upon GM1 binding by EtxB, EtxB(G33D), and EtxB(H57S) by fluorescence spectroscopy.	bind
11020	1	3509	7	11	NULL	0	NULL	GM1	GP		bind					EtxB	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_3_1527_s_145	12595472	(B to D) Analysis of Trp-fluorescence upon GM1 binding by EtxB, EtxB(G33D), and EtxB(H57S) by fluorescence spectroscopy.	bind
11021	2	3509	7	11	NULL	0	NULL	GM1	GP		bind					EtxB	Chemical		G33D		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_3_1527_s_145	12595472	(B to D) Analysis of Trp-fluorescence upon GM1 binding by EtxB, EtxB(G33D), and EtxB(H57S) by fluorescence spectroscopy.	bind
11022	3	3509	7	11	NULL	0	NULL	GM1	GP		bind					EtxB	Chemical		H57S		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_3_1527_s_145	12595472	(B to D) Analysis of Trp-fluorescence upon GM1 binding by EtxB, EtxB(G33D), and EtxB(H57S) by fluorescence spectroscopy.	bind
80762	1	3509	11	NULL	NULL	NULL	NULL	GM1	Protein		binds to 					EtxB	Protein				NULL	fluorescence spectroscopy	NULL	NULL	NULL	NULL	gw60_infectimmun_71_3_1527_s_145	12595472	(B to D) Analysis of Trp-fluorescence upon GM1 binding by EtxB, EtxB(G33D), and EtxB(H57S) by fluorescence spectroscopy.	bind
80763	2	3509	11	NULL	NULL	0	NULL	GM1	Protein		binds to 					EtxB(G33D)	Protein				NULL	fluorescence spectroscopy	0	NULL	NULL	NULL	gw60_infectimmun_71_3_1527_s_145	12595472	(B to D) Analysis of Trp-fluorescence upon GM1 binding by EtxB, EtxB(G33D), and EtxB(H57S) by fluorescence spectroscopy.	bind
80764	3	3509	11	NULL	NULL	0	NULL	GM1	Protein		binds to 					EtxB(H57S)	Protein				NULL	fluorescence spectroscopy	0	NULL	NULL	NULL	gw60_infectimmun_71_3_1527_s_145	12595472	(B to D) Analysis of Trp-fluorescence upon GM1 binding by EtxB, EtxB(G33D), and EtxB(H57S) by fluorescence spectroscopy.	bind
7853	1	3510	6	11	NULL	0	NULL	AML family 	GP		bind					NP-3	GP			promoter sequences	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_322_s_101	9418879	(B to D) Binding of AML family members to NP-3 promoter sequences determined by electrophoretic mobility shift assays.	bind
11025	1	3510	7	11	NULL	0	NULL	AML family	GP		bind					NP-3	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_322_s_101	9418879	(B to D) Binding of AML family members to NP-3 promoter sequences determined by electrophoretic mobility shift assays.	bind
81257	2	3510	11	NULL	NULL	0	NULL	AML family members	Protein		binds to 					NP-3	Gene			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_322_s_101	9418879	(B to D) Binding of AML family members to NP-3 promoter sequences determined by electrophoretic mobility shift assays.	bind
7854	1	3513	6	11	NULL	0	NULL	ASH1	GP	transcription of	is dependent on					Swi5p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_5_699_s_141	8625408	(B)  ASH1 transcription is dependent on Swi5p and Ace2p transcription  factors.	bind
7855	2	3513	6	11	NULL	0	NULL	ASH1	GP	transcription of	is dependent on					Ace2p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_5_699_s_141	8625408	(B)  ASH1 transcription is dependent on Swi5p and Ace2p transcription  factors.	bind
11089	1	3513	7	11	NULL	0	NULL	ASH1	GP	transcription of	is dependent on					Swi5p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_5_699_s_141	8625408	(B)  ASH1 transcription is dependent on Swi5p and Ace2p transcription  factors.	bind
11090	2	3513	7	11	NULL	0	NULL	ASH1	GP	transcription of	is dependent on					Ace2p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_5_699_s_141	8625408	(B)  ASH1 transcription is dependent on Swi5p and Ace2p transcription  factors.	bind
80766	1	3513	11	NULL	NULL	0	NULL	ASH1	Gene		undergoes					transcription	MolecularProcess				NULL		0	NULL	NULL	NULL	gw60_cell_84_5_699_s_141	8625408	(B)  ASH1 transcription is dependent on Swi5p and Ace2p transcription  factors.	bind
80767	2	3513	11	NULL	NULL	0	NULL	statement 1	Process		depends on					Swi5p transcription factor	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_84_5_699_s_141	8625408	(B)  ASH1 transcription is dependent on Swi5p and Ace2p transcription  factors.	bind
80768	3	3513	11	NULL	NULL	NULL	NULL	statement 1	Process		depends on					Ace2p transcription factor	Protein				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_5_699_s_141	8625408	(B)  ASH1 transcription is dependent on Swi5p and Ace2p transcription  factors.	bind
7856	1	3515	6	11	NULL	NULL	NULL	bacteria	Organism		bind					NK cells	Cell	purified;; human			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_7_4133_s_156	16790787	(B)  Binding of bacteria to purified NK cells from two different human donors.	bind
11092	1	3515	7	11	NULL	NULL	NULL	bacteria	Organism		bind					NK cells	Cell	human;; purified			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_7_4133_s_156	16790787	(B)  Binding of bacteria to purified NK cells from two different human donors.	bind
80769	1	3515	11	NULL	NULL	0	NULL	 NK cells	cell	purified;;from human donor	binds to 					bacteria	Organism				NULL		0	NULL	NULL	NULL	gw70_infectimmun_74_7_4133_s_156	16790787	(B)  Binding of bacteria to purified NK cells from two different human donors.	bind
11093	1	3516	7	11	NULL	NULL	NULL	Smurf1	GP		bind			CA		Smad5	GP	WT			NULL	transfected COS7 cells	NULL	NULL	NULL	NULL	gw60_molbiolcell_14_7_2809_s_105	12857866	(B)  Binding of Smurf1(CA) to Smad5(WT) and Smad5(deltaPY) was examined in  transfected COS7 cells.	bind
11094	2	3516	7	11	NULL	NULL	NULL	Smurf1	GP		bind			CA		Smad5	GP		deltaPY		NULL	transfected COS7 cells	NULL	NULL	NULL	NULL	gw60_molbiolcell_14_7_2809_s_105	12857866	(B)  Binding of Smurf1(CA) to Smad5(WT) and Smad5(deltaPY) was examined in  transfected COS7 cells.	bind
80770	1	3516	11	NULL	NULL	0	NULL	Smurf1(CA)	Protein		binds to 					Smad5(WT)					NULL	transfected COS7 cells	0	NULL	NULL	NULL	gw60_molbiolcell_14_7_2809_s_105	12857866	(B)  Binding of Smurf1(CA) to Smad5(WT) and Smad5(deltaPY) was examined in  transfected COS7 cells.	bind
80771	2	3516	11	NULL	NULL	0	NULL	Smurf1(CA)	Protein		binds to 					Smad5(deltaPY)	Protein				NULL	transfected COS7 cells	0	NULL	NULL	NULL	gw60_molbiolcell_14_7_2809_s_105	12857866	(B)  Binding of Smurf1(CA) to Smad5(WT) and Smad5(deltaPY) was examined in  transfected COS7 cells.	bind
7878	1	3518	6	11	NULL	NULL	NULL	myoB	GP	Dictyostelium	bind			SH3 domain		p116	GP		proline-rich motifs		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_3_245_s_212	11257438	(B)  Dictyostelium myoB and myoC bind via their SH3 domain to proline-rich motifs within p116, a scaffold protein that also binds capping protein (CP) and the Arp2/3 complex.	bind
7885	2	3518	6	11	NULL	NULL	NULL	myoC	GP	Dictyostelium	bind			SH3 domain		p116	GP		proline-rich motifs		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_3_245_s_212	11257438	(B)  Dictyostelium myoB and myoC bind via their SH3 domain to proline-rich motifs within p116, a scaffold protein that also binds capping protein (CP) and the Arp2/3 complex.	bind
7886	3	3518	6	11	NULL	NULL	NULL	p116	GP		bind					CP	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_3_245_s_212	11257438	(B)  Dictyostelium myoB and myoC bind via their SH3 domain to proline-rich motifs within p116, a scaffold protein that also binds capping protein (CP) and the Arp2/3 complex.	bind
7887	4	3518	6	11	NULL	NULL	NULL	p116	GP		bind					Arp2/3 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_3_245_s_212	11257438	(B)  Dictyostelium myoB and myoC bind via their SH3 domain to proline-rich motifs within p116, a scaffold protein that also binds capping protein (CP) and the Arp2/3 complex.	bind
40771	5	3518	6	11	NULL	NULL	NULL	p116	GP		is a type of					scaffold protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_3_245_s_212	11257438	(B)  Dictyostelium myoB and myoC bind via their SH3 domain to proline-rich motifs within p116, a scaffold protein that also binds capping protein (CP) and the Arp2/3 complex.	bind
40772	6	3518	6	11	NULL	NULL	NULL	CP	GP		is					capping protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_3_245_s_212	11257438	(B)  Dictyostelium myoB and myoC bind via their SH3 domain to proline-rich motifs within p116, a scaffold protein that also binds capping protein (CP) and the Arp2/3 complex.	bind
11095	1	3518	7	11	NULL	NULL	NULL	myoB	GP	Dictyostelium	bind			SH3 domain		p116	GP		proline-rich motifs		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_3_245_s_212	11257438	(B)  Dictyostelium myoB and myoC bind via their SH3 domain to proline-rich motifs within p116, a scaffold protein that also binds capping protein (CP) and the Arp2/3 complex.	bind
11096	2	3518	7	11	NULL	NULL	NULL	myoC	GP	Dictyostelium	bind			SH3 domain		p116	GP		 proline-rich motifs		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_3_245_s_212	11257438	(B)  Dictyostelium myoB and myoC bind via their SH3 domain to proline-rich motifs within p116, a scaffold protein that also binds capping protein (CP) and the Arp2/3 complex.	bind
11099	3	3518	7	11	NULL	NULL	NULL	p116	GP		bind					capping protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_3_245_s_212	11257438	(B)  Dictyostelium myoB and myoC bind via their SH3 domain to proline-rich motifs within p116, a scaffold protein that also binds capping protein (CP) and the Arp2/3 complex.	bind
11100	4	3518	7	11	NULL	NULL	NULL	p116	GP		bind					Arp2/3 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_3_245_s_212	11257438	(B)  Dictyostelium myoB and myoC bind via their SH3 domain to proline-rich motifs within p116, a scaffold protein that also binds capping protein (CP) and the Arp2/3 complex.	bind
11102	5	3518	7	11	NULL	NULL	NULL	p116	GP		is a type of					scaffold protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_3_245_s_212	11257438	(B)  Dictyostelium myoB and myoC bind via their SH3 domain to proline-rich motifs within p116, a scaffold protein that also binds capping protein (CP) and the Arp2/3 complex.	bind
11104	6	3518	7	11	NULL	NULL	NULL	capping protein	GP		is					CP	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_3_245_s_212	11257438	(B)  Dictyostelium myoB and myoC bind via their SH3 domain to proline-rich motifs within p116, a scaffold protein that also binds capping protein (CP) and the Arp2/3 complex.	bind
80772	1	3518	11	NULL	NULL	0	NULL	p116	Protein		is a type of 					scaffold protein	Protein				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_3_245_s_212	11257438	(B)  Dictyostelium myoB and myoC bind via their SH3 domain to proline-rich motifs within p116, a scaffold protein that also binds capping protein (CP) and the Arp2/3 complex.	bind
80773	2	3518	11	NULL	NULL	0	NULL	p116	Protein		binds to 					capping protein	Protein				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_3_245_s_212	11257438	(B)  Dictyostelium myoB and myoC bind via their SH3 domain to proline-rich motifs within p116, a scaffold protein that also binds capping protein (CP) and the Arp2/3 complex.	bind
80774	3	3518	11	NULL	NULL	0	NULL	p116	Protein		binds to 					Arp2/3 complex	Protein				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_3_245_s_212	11257438	(B)  Dictyostelium myoB and myoC bind via their SH3 domain to proline-rich motifs within p116, a scaffold protein that also binds capping protein (CP) and the Arp2/3 complex.	bind
80775	4	3518	11	NULL	NULL	0	NULL	capping protein	Protein		is					CP	Protein				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_3_245_s_212	11257438	(B)  Dictyostelium myoB and myoC bind via their SH3 domain to proline-rich motifs within p116, a scaffold protein that also binds capping protein (CP) and the Arp2/3 complex.	bind
80776	5	3518	11	NULL	NULL	0	NULL	myoB	Protein	Dictyostelium	binds to 			SH3 domain		p116	Protein		proline-rich motifs		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_3_245_s_212	11257438	(B)  Dictyostelium myoB and myoC bind via their SH3 domain to proline-rich motifs within p116, a scaffold protein that also binds capping protein (CP) and the Arp2/3 complex.	bind
80777	6	3518	11	NULL	NULL	0	NULL	myoC	Protein	Dictyostelium	binds to 			SH3 domain		p116	Protein		proline-rich motif		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_3_245_s_212	11257438	(B)  Dictyostelium myoB and myoC bind via their SH3 domain to proline-rich motifs within p116, a scaffold protein that also binds capping protein (CP) and the Arp2/3 complex.	bind
7964	1	3519	6	11	NULL	NULL	NULL	Wsp	GP	Drosophila	bind					CDC42	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_1_1_s_87	11149916	(B)  Drosophila Wsp binds the activated form of CDC42 in a blot overlay assay.	bind
11106	1	3519	7	11	NULL	NULL	NULL	Wsp	GP	Drosophila	bind					CDC42	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_1_1_s_87	11149916	(B)  Drosophila Wsp binds the activated form of CDC42 in a blot overlay assay.	bind
80778	1	3519	11	NULL	NULL	0	NULL	Wsp	Protein	Drosophila	binds to 					CDC42	Protein	activated			NULL	blot overlay assay	0	NULL	NULL	NULL	gw60_cellbiol_152_1_1_s_87	11149916	(B)  Drosophila Wsp binds the activated form of CDC42 in a blot overlay assay.	bind
7965	1	3520	6	11	NULL	NULL	NULL	Smad7	GP	endogenous	bind					p38	GP	phosphorylated			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molbiolcell_14_2_529_s_245	12589052	(B)  Endogenous Smad7 binds to phosphorylated p38 in vivo.	bind
11111	1	3520	7	11	NULL	NULL	NULL	Smad7	GP	endogenous	bind					p38	GP	phosphorylated			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molbiolcell_14_2_529_s_245	12589052	(B)  Endogenous Smad7 binds to phosphorylated p38 in vivo.	bind
80779	1	3520	11	NULL	NULL	0	NULL	Smad7	Protein	Endogenous	binds to 					p38	Protein	phosphorylated			NULL	in vivo	0	NULL	NULL	NULL	gw70_molbiolcell_14_2_529_s_245	12589052	(B)  Endogenous Smad7 binds to phosphorylated p38 in vivo.	bind
7966	1	3521	6	11	NULL	NULL	NULL	GST-Mst27p-AAXX	GP		does not bind					coatomer	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3097_s_242	12925749	(B)  GST-Mst27p-AAXX and GST-Prm8p do not bind to coatomer.	bind
7967	2	3521	6	11	NULL	NULL	NULL	GST-Prm8p	GP		does not bind					coatomer	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3097_s_242	12925749	(B)  GST-Mst27p-AAXX and GST-Prm8p do not bind to coatomer.	bind
11113	1	3521	7	11	NULL	NULL	NULL	GST-Mst27p-AAXX	GP		does not bind					coatomer	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3097_s_242	12925749	(B)  GST-Mst27p-AAXX and GST-Prm8p do not bind to coatomer.	bind
11115	2	3521	7	11	NULL	NULL	NULL	GST-Prm8p	GP		does not bind					coatomer	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3097_s_242	12925749	(B)  GST-Mst27p-AAXX and GST-Prm8p do not bind to coatomer.	bind
80780	1	3521	11	NULL	NULL	0	NULL	GST-Mst27p-AAXX	Protein		does not bind to					coatomer	Protein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_8_3097_s_242	12925749	(B)  GST-Mst27p-AAXX and GST-Prm8p do not bind to coatomer.	bind
80781	2	3521	11	NULL	NULL	0	NULL	GST-Prm8p	Protein		does not bind to					coatomer	Protein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_8_3097_s_242	12925749	(B)  GST-Mst27p-AAXX and GST-Prm8p do not bind to coatomer.	bind
7968	1	3522	6	11	NULL	NULL	NULL	Stat1	GP		bind					DNA	NucleicAcid				NULL	HEp-2 cells	NULL	NULL	NULL	NULL	gw70_infectimmun_72_1_537_s_154	14688135	(B)  HEp-2 cells demonstrated inducible STAT1 DNA binding in response to stimulation with  IFN-gamma (20 ng/ml, 30 min) (arrow, lane 2).	bind
8174	2	3522	6	11	NULL	NULL	NULL	IFN-gamma	GP		induces					statement 1	Process				NULL	HEp-2 cells	NULL	NULL	NULL	NULL	gw70_infectimmun_72_1_537_s_154	14688135	(B)  HEp-2 cells demonstrated inducible STAT1 DNA binding in response to stimulation with  IFN-gamma (20 ng/ml, 30 min) (arrow, lane 2).	bind
11118	1	3522	7	11	NULL	NULL	NULL	STAT1	GP		bind					DNA	NucleicAcid				NULL	HEp-2 cells	NULL	NULL	NULL	NULL	gw70_infectimmun_72_1_537_s_154	14688135	(B)  HEp-2 cells demonstrated inducible STAT1 DNA binding in response to stimulation with  IFN-gamma (20 ng/ml, 30 min) (arrow, lane 2).	bind
11120	2	3522	7	11	NULL	NULL	NULL	HEp-2 cells	Cell		stimulated with					IFN-gamma	GP				NULL	HEp-2 cells	NULL	NULL	NULL	NULL	gw70_infectimmun_72_1_537_s_154	14688135	(B)  HEp-2 cells demonstrated inducible STAT1 DNA binding in response to stimulation with  IFN-gamma (20 ng/ml, 30 min) (arrow, lane 2).	bind
11121	3	3522	7	11	NULL	NULL	NULL	statement 2	Process		induce					statement 1	Process				NULL	HEp-2 cells	NULL	NULL	NULL	NULL	gw70_infectimmun_72_1_537_s_154	14688135	(B)  HEp-2 cells demonstrated inducible STAT1 DNA binding in response to stimulation with  IFN-gamma (20 ng/ml, 30 min) (arrow, lane 2).	bind
80782	1	3522	11	NULL	NULL	0	NULL	STAT1	Protein		binds to 					DNA	NucleicAcidSubstance				NULL	HEp-2 cells	0	NULL	NULL	NULL	gw70_infectimmun_72_1_537_s_154	14688135	(B)  HEp-2 cells demonstrated inducible STAT1 DNA binding in response to stimulation with  IFN-gamma (20 ng/ml, 30 min) (arrow, lane 2).	bind
80783	2	3522	11	NULL	NULL	0	NULL	IFN-gamma	Protein		stimulates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_1_537_s_154	14688135	(B)  HEp-2 cells demonstrated inducible STAT1 DNA binding in response to stimulation with  IFN-gamma (20 ng/ml, 30 min) (arrow, lane 2).	bind
7969	1	3523	6	11	NULL	NULL	NULL	GFP-coronin	GP		bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1275_s_130	10749929	(B)  limB null and KAx-3 cells expressing GFP-coronin, which binds to F-actin.	bind
7970	2	3523	6	11	NULL	NULL	NULL	limB null cells	Cell		express					GFP-coronin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1275_s_130	10749929	(B)  limB null and KAx-3 cells expressing GFP-coronin, which binds to F-actin.	bind
7971	3	3523	6	11	NULL	NULL	NULL	KAx-3 cells	Cell		express					GFP-coronin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1275_s_130	10749929	(B)  limB null and KAx-3 cells expressing GFP-coronin, which binds to F-actin.	bind
11124	1	3523	7	11	NULL	NULL	NULL	limB null cells	Cell		express					GFP-coronin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1275_s_130	10749929	(B)  limB null and KAx-3 cells expressing GFP-coronin, which binds to F-actin.	bind
11126	2	3523	7	11	NULL	NULL	NULL	KAx-3 cells	Cell	 	express					GFP-coronin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1275_s_130	10749929	(B)  limB null and KAx-3 cells expressing GFP-coronin, which binds to F-actin.	bind
15046	3	3523	7	11	NULL	NULL	NULL	GFP-coronin	GP		binds					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1275_s_130	10749929	(B)  limB null and KAx-3 cells expressing GFP-coronin, which binds to F-actin.	bind
80784	1	3523	11	NULL	NULL	0	NULL	GFP-coronin	Protein		binds to 					F-actin	Protein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1275_s_130	10749929	(B)  limB null and KAx-3 cells expressing GFP-coronin, which binds to F-actin.	bind
80785	2	3523	11	NULL	NULL	0	NULL	limB null cells	cell		express					GFP-coronin	Protein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1275_s_130	10749929	(B)  limB null and KAx-3 cells expressing GFP-coronin, which binds to F-actin.	bind
80786	3	3523	11	NULL	NULL	0	NULL	KAx-3 cell	cell		express					GFP-coronin	Protein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1275_s_130	10749929	(B)  limB null and KAx-3 cells expressing GFP-coronin, which binds to F-actin.	bind
7972	1	3524	6	11	NULL	NULL	NULL	M. tuberculosis	Organism		bind					M cell surface	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_immunity_10_6_641_s_64	10403639	(B)  M. tuberculosis (arrowheads) binds to the M cell surface and is internalized.	bind
7973	2	3524	6	11	NULL	NULL	NULL	statement 1	Process		leads to					M. tuberculosis	Organism	internalization of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_10_6_641_s_64	10403639	(B)  M. tuberculosis (arrowheads) binds to the M cell surface and is internalized.	bind
11127	1	3524	7	11	NULL	NULL	NULL	M. tuberculosis	Organism		bind					M cell surface	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_immunity_10_6_641_s_64	10403639	(B)  M. tuberculosis (arrowheads) binds to the M cell surface and is internalized.	bind
11128	2	3524	7	11	NULL	NULL	NULL	statement 1	Process		leads to 					M. tuberculosis	Organism	internalization of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_10_6_641_s_64	10403639	(B)  M. tuberculosis (arrowheads) binds to the M cell surface and is internalized.	bind
80787	1	3524	11	NULL	NULL	0	NULL	M. tuberculosis	Organism		binds to 					M cell 	Cell	surface			NULL		0	NULL	NULL	NULL	gw60_immunity_10_6_641_s_64	10403639	(B)  M. tuberculosis (arrowheads) binds to the M cell surface and is internalized.	bind
80788	2	3524	11	NULL	NULL	0	NULL	statement 1	Process		leads to					internalization 	BiologicalProcess	M cell			NULL		0	NULL	NULL	NULL	gw60_immunity_10_6_641_s_64	10403639	(B)  M. tuberculosis (arrowheads) binds to the M cell surface and is internalized.	bind
7974	1	3526	6	11	NULL	NULL	NULL	A-Myb	GP		bind					GST-CBP	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4705_s_195	16055500	(B)  NLK blocks the binding of A-Myb to GST-CBP.	bind
7975	2	3526	6	11	NULL	NULL	NULL	NLK	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4705_s_195	16055500	(B)  NLK blocks the binding of A-Myb to GST-CBP.	bind
11130	1	3526	7	11	NULL	NULL	NULL	A-Myb	GP		binds					GST-CBP	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4705_s_195	16055500	(B)  NLK blocks the binding of A-Myb to GST-CBP.	bind
11132	2	3526	7	11	NULL	NULL	NULL	 NLK	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4705_s_195	16055500	(B)  NLK blocks the binding of A-Myb to GST-CBP.	bind
80789	1	3526	11	NULL	NULL	0	NULL	A-Myb	Protein		binds to 					GST-CBP	Protein				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4705_s_195	16055500	(B)  NLK blocks the binding of A-Myb to GST-CBP.	bind
80790	2	3526	11	NULL	NULL	0	NULL	NLK	Protein		blocks					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4705_s_195	16055500	(B)  NLK blocks the binding of A-Myb to GST-CBP.	bind
7976	1	3527	6	11	NULL	NULL	NULL	PAX	GP		bind					PIX	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_851_s_265	10330411	(B)  PAK bound to PIX as previously reported.	bind
11133	1	3527	7	11	NULL	NULL	NULL	PAK 	GP		bind					PIX	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_851_s_265	10330411	(B)  PAK bound to PIX as previously reported.	bind
80791	1	3527	11	NULL	NULL	0	NULL	PAK	Protein		binds to 					 PIX	Protein				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_4_851_s_265	10330411	(B)  PAK bound to PIX as previously reported.	bind
7977	1	3528	6	11	NULL	NULL	NULL	Stat3	GP		bind					p53	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_17_7432_s_160	16107692	(B)  PDGF stimulation (10 ng/ml for 8 h), which activates Stat3, also leads to Stat3 binding  to the p53 promoter region as shown by ChIP.	bind
7978	2	3528	6	11	NULL	NULL	NULL	PDGF	GP	stimulation of	leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_17_7432_s_160	16107692	(B)  PDGF stimulation (10 ng/ml for 8 h), which activates Stat3, also leads to Stat3 binding  to the p53 promoter region as shown by ChIP.	bind
7979	3	3528	6	11	NULL	NULL	NULL	PDGF	GP	stimulation of	activates					Stat3	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_17_7432_s_160	16107692	(B)  PDGF stimulation (10 ng/ml for 8 h), which activates Stat3, also leads to Stat3 binding  to the p53 promoter region as shown by ChIP.	bind
11165	1	3528	7	11	NULL	NULL	NULL	Stat3 	GP		bind					p53	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_17_7432_s_160	16107692	(B)  PDGF stimulation (10 ng/ml for 8 h), which activates Stat3, also leads to Stat3 binding  to the p53 promoter region as shown by ChIP.	bind
11166	2	3528	7	11	NULL	NULL	NULL	PDGF	GP	stimulation of	activates					Stat3	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_17_7432_s_160	16107692	(B)  PDGF stimulation (10 ng/ml for 8 h), which activates Stat3, also leads to Stat3 binding  to the p53 promoter region as shown by ChIP.	bind
11167	3	3528	7	11	NULL	NULL	NULL	PDGF	GP	stimulation of	activates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_17_7432_s_160	16107692	(B)  PDGF stimulation (10 ng/ml for 8 h), which activates Stat3, also leads to Stat3 binding  to the p53 promoter region as shown by ChIP.	bind
80792	1	3528	11	NULL	NULL	NULL	NULL	Stat3	Protein		binds to 					p53 promoter	NucleicAcidSubstance				NULL	ChIP	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_17_7432_s_160	16107692	(B)  PDGF stimulation (10 ng/ml for 8 h), which activates Stat3, also leads to Stat3 binding  to the p53 promoter region as shown by ChIP.	bind
80793	2	3528	11	NULL	NULL	0	NULL	PDGF	Protein	active	activates					Stat3	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_17_7432_s_160	16107692	(B)  PDGF stimulation (10 ng/ml for 8 h), which activates Stat3, also leads to Stat3 binding  to the p53 promoter region as shown by ChIP.	bind
80794	3	3528	11	NULL	NULL	0	NULL	statement 2	Process		leads to					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_17_7432_s_160	16107692	(B)  PDGF stimulation (10 ng/ml for 8 h), which activates Stat3, also leads to Stat3 binding  to the p53 promoter region as shown by ChIP.	bind
7980	1	3530	6	11	NULL	NULL	NULL	TFIID	GP	S. cerevisiae	bind		specifically			Ad2 MLP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_16_6000_s_163	12138208	(B)  S. cerevisiae TFIID binds the Ad2 MLP specifically.	bind
11168	1	3530	7	11	NULL	NULL	NULL	TFIID	GP	S. cerevisiae	binds		specifically			Ad2 MLP 	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_16_6000_s_163	12138208	(B)  S. cerevisiae TFIID binds the Ad2 MLP specifically.	bind
80795	1	3530	11	NULL	NULL	0	NULL	TFIID	Protein	S. cerevisiae	binds to 		specifically			Ad2 MLP	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_16_6000_s_163	12138208	(B)  S. cerevisiae TFIID binds the Ad2 MLP specifically.	bind
7981	1	3532	6	11	NULL	NULL	NULL	RANTES	GP	125I-labeled	bind					CHO-CCR5 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_151_6_1281_s_184	11121442	(B) 125I-RANTES (closed symbols) and 125I - AOP-RANTES (open symbols) were bound to CHO-CCR5 (  and  ) or CHO-K1 (.,  ) cells as described in A.	bind
7982	2	3532	6	11	NULL	NULL	NULL	RANTES	GP	125I-labeled	bind					CHO-K1 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_151_6_1281_s_184	11121442	(B) 125I-RANTES (closed symbols) and 125I - AOP-RANTES (open symbols) were bound to CHO-CCR5 (  and  ) or CHO-K1 (.,  ) cells as described in A.	bind
7983	3	3532	6	11	NULL	NULL	NULL	AOP-RANTES	GP	125I-labeled	bind					CHO-CCR5 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_151_6_1281_s_184	11121442	(B) 125I-RANTES (closed symbols) and 125I - AOP-RANTES (open symbols) were bound to CHO-CCR5 (  and  ) or CHO-K1 (.,  ) cells as described in A.	bind
7984	4	3532	6	11	NULL	NULL	NULL	AOP-RANTES	GP	125I-labeled	bind					CHO-K1 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_151_6_1281_s_184	11121442	(B) 125I-RANTES (closed symbols) and 125I - AOP-RANTES (open symbols) were bound to CHO-CCR5 (  and  ) or CHO-K1 (.,  ) cells as described in A.	bind
11169	1	3532	7	11	NULL	NULL	NULL	RANTES	GP	125I-labeled	bind					CHO-CCR5 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_151_6_1281_s_184	11121442	(B) 125I-RANTES (closed symbols) and 125I - AOP-RANTES (open symbols) were bound to CHO-CCR5 (  and  ) or CHO-K1 (.,  ) cells as described in A.	bind
11170	2	3532	7	11	NULL	NULL	NULL	RANTES	GP	125I-labeled	bind					CHO-K1 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_151_6_1281_s_184	11121442	(B) 125I-RANTES (closed symbols) and 125I - AOP-RANTES (open symbols) were bound to CHO-CCR5 (  and  ) or CHO-K1 (.,  ) cells as described in A.	bind
11171	3	3532	7	11	NULL	NULL	NULL	AOP-RANTES	GP	125I-labeled	bind					CHO-CCR5 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_151_6_1281_s_184	11121442	(B) 125I-RANTES (closed symbols) and 125I - AOP-RANTES (open symbols) were bound to CHO-CCR5 (  and  ) or CHO-K1 (.,  ) cells as described in A.	bind
11172	4	3532	7	11	NULL	NULL	NULL	AOP-RANTES	GP	125I-labeled	bind					CHO-K1 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_151_6_1281_s_184	11121442	(B) 125I-RANTES (closed symbols) and 125I - AOP-RANTES (open symbols) were bound to CHO-CCR5 (  and  ) or CHO-K1 (.,  ) cells as described in A.	bind
80796	1	3532	11	NULL	NULL	0	NULL	125I-RANTES	Protein		binds to 					CHO-CCR5 cells	Cell				NULL		0	NULL	NULL	NULL	gw60_cellbiol_151_6_1281_s_184	11121442	(B) 125I-RANTES (closed symbols) and 125I - AOP-RANTES (open symbols) were bound to CHO-CCR5 (  and  ) or CHO-K1 (.,  ) cells as described in A.	bind
80797	2	3532	11	NULL	NULL	0	NULL	125I-RANTES	Protein		binds to 					CHO-K1 cell	Cell				NULL		0	NULL	NULL	NULL	gw60_cellbiol_151_6_1281_s_184	11121442	(B) 125I-RANTES (closed symbols) and 125I - AOP-RANTES (open symbols) were bound to CHO-CCR5 (  and  ) or CHO-K1 (.,  ) cells as described in A.	bind
80798	3	3532	11	NULL	NULL	0	NULL	125I - AOP-RANTES	Protein		binds to 					CHO-CCR5 cells	Cell				NULL		0	NULL	NULL	NULL	gw60_cellbiol_151_6_1281_s_184	11121442	(B) 125I-RANTES (closed symbols) and 125I - AOP-RANTES (open symbols) were bound to CHO-CCR5 (  and  ) or CHO-K1 (.,  ) cells as described in A.	bind
80799	4	3532	11	NULL	NULL	0	NULL	125I - AOP-RANTES	Protein		binds to 					CHO-K1 cell	Cell				NULL		0	NULL	NULL	NULL	gw60_cellbiol_151_6_1281_s_184	11121442	(B) 125I-RANTES (closed symbols) and 125I - AOP-RANTES (open symbols) were bound to CHO-CCR5 (  and  ) or CHO-K1 (.,  ) cells as described in A.	bind
7985	1	3537	6	11	NULL	NULL	NULL	SEP-1 protein	GP	35S-labeled	bind					GST-IFY-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_24_2118_s_145	12498686	(b) 35S-labeled SEP-1 protein binds GST-IFY-1.	bind
11173	1	3537	7	11	NULL	NULL	NULL	 SEP-1 protein	GP	35S-labeled	binds					GST-IFY-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_24_2118_s_145	12498686	(b) 35S-labeled SEP-1 protein binds GST-IFY-1.	bind
80800	1	3537	11	NULL	NULL	0	NULL	SEP-1 protein	Protein	35S-labeled	binds to 					GST-IFY-1	Protein				NULL		0	NULL	NULL	NULL	gw60_currbiol_12_24_2118_s_145	12498686	(b) 35S-labeled SEP-1 protein binds GST-IFY-1.	bind
7986	1	3539	6	11	NULL	NULL	NULL	SR protein	GP		bind									exon N1	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_6_1874_s_155	12612063	(B) A 35-kDa SR protein binds to exon N1.	bind
11174	1	3539	7	11	NULL	NULL	NULL	SR protein	GP		binds to									exon N1	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_6_1874_s_155	12612063	(B) A 35-kDa SR protein binds to exon N1.	bind
80801	1	3539	11	NULL	NULL	0	NULL	SR protein	Protein		binds to 					exon N1	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_6_1874_s_155	12612063	(B) A 35-kDa SR protein binds to exon N1.	bind
7987	1	3540	6	11	NULL	NULL	NULL	PlexB	GP		bind					RhoA	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_1_39_s_89	11604137	(B) A bigger region of PlexB, PlexB  also binds to RhoA.	bind
11175	1	3540	7	11	NULL	NULL	NULL	PlexB	GP		binds					RhoA	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_1_39_s_89	11604137	(B) A bigger region of PlexB, PlexB  also binds to RhoA.	bind
80802	1	3540	11	NULL	NULL	0	NULL	PlexB	Protein		binds to 					RhoA	Protein				NULL		0	NULL	NULL	NULL	gw60_neuron_32_1_39_s_89	11604137	(B) A bigger region of PlexB, PlexB  also binds to RhoA.	bind
7988	1	3542	6	11	NULL	NULL	NULL	CCT	GP		bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_6_927_s_198	9200611	(B) A fraction of  CCT-bound  -tubulin acquires GTP binding competence in AMP - PNP.	bind
7989	2	3542	6	11	NULL	NULL	NULL	statement 1	Process		bind					GTP	Chemical				NULL	AMP-PNP	NULL	NULL	NULL	NULL	gw60_cell_89_6_927_s_198	9200611	(B) A fraction of  CCT-bound  -tubulin acquires GTP binding competence in AMP - PNP.	bind
11176	1	3542	7	11	NULL	NULL	NULL	CCT	GP		bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_6_927_s_198	9200611	(B) A fraction of  CCT-bound  -tubulin acquires GTP binding competence in AMP - PNP.	bind
11177	2	3542	7	11	NULL	NULL	NULL	statement 1	Process		acquires					GTP	Chemical	competence for binding of			NULL	AMP - PNP	NULL	NULL	NULL	NULL	gw60_cell_89_6_927_s_198	9200611	(B) A fraction of  CCT-bound  -tubulin acquires GTP binding competence in AMP - PNP.	bind
80803	1	3542	11	NULL	NULL	0	NULL	CCT	NucleicAcidSubstance		binds to 					tubulin	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_89_6_927_s_198	9200611	(B) A fraction of  CCT-bound  -tubulin acquires GTP binding competence in AMP - PNP.	bind
80804	2	3542	11	NULL	NULL	0	NULL	GTP	Chemical		binds to 					AMP - PNP	Chemical				NULL		0	NULL	NULL	NULL	gw60_cell_89_6_927_s_198	9200611	(B) A fraction of  CCT-bound  -tubulin acquires GTP binding competence in AMP - PNP.	bind
7990	1	3543	6	11	NULL	NULL	NULL	Fu monomer	GP		bind					Cos2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_23_10397_s_89	15542847	(B) A Fu monomer binds to Cos2 at the expense of Fu dimer formation.	bind
7991	2	3543	6	11	NULL	NULL	NULL	Fu	GP		forms a					dimer	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_23_10397_s_89	15542847	(B) A Fu monomer binds to Cos2 at the expense of Fu dimer formation.	bind
7992	3	3543	6	11	NULL	NULL	NULL	statement 1	Process		occurs at expense of					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_23_10397_s_89	15542847	(B) A Fu monomer binds to Cos2 at the expense of Fu dimer formation.	bind
11179	1	3543	7	11	NULL	NULL	NULL	Fu monomer	GP		binds					Cos2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_23_10397_s_89	15542847	(B) A Fu monomer binds to Cos2 at the expense of Fu dimer formation.	bind
11180	2	3543	7	11	NULL	NULL	NULL	Fu	GP		forms					dimer	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_23_10397_s_89	15542847	(B) A Fu monomer binds to Cos2 at the expense of Fu dimer formation.	bind
52977	3	3543	7	11	NULL	NULL	NULL	statement 1	Process		occurs at expense of					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_23_10397_s_89	15542847	(B) A Fu monomer binds to Cos2 at the expense of Fu dimer formation.	bind
80805	1	3543	11	NULL	NULL	0	NULL	Fu	Protein		forms					dimer	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_23_10397_s_89	15542847	(B) A Fu monomer binds to Cos2 at the expense of Fu dimer formation.	bind
80806	2	3543	11	NULL	NULL	0	NULL	Fu	Protein	monomer	binds to					Cos2	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_23_10397_s_89	15542847	(B) A Fu monomer binds to Cos2 at the expense of Fu dimer formation.	bind
80807	3	3543	11	NULL	NULL	0	NULL	statement 1	Process		leads to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_23_10397_s_89	15542847	(B) A Fu monomer binds to Cos2 at the expense of Fu dimer formation.	bind
7993	1	3545	6	11	NULL	NULL	NULL	CREB peptide	GP	recombinant	bind					BDNF	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_4_727_s_144	9581764	(B) A recombinant CREB peptide can bind to the  BDNF promoter in a  CRE-dependent manner.	bind
7994	2	3545	6	11	NULL	NULL	NULL	statement 1	Process		is dependent on									CRE	NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_4_727_s_144	9581764	(B) A recombinant CREB peptide can bind to the  BDNF promoter in a  CRE-dependent manner.	bind
11181	1	3545	7	11	NULL	NULL	NULL	CREB peptide	GP	recombinant	bind					BDNF	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_4_727_s_144	9581764	(B) A recombinant CREB peptide can bind to the  BDNF promoter in a  CRE-dependent manner.	bind
11182	2	3545	7	11	NULL	NULL	NULL	statement 1	Process		is dependent on									CRE	NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_4_727_s_144	9581764	(B) A recombinant CREB peptide can bind to the  BDNF promoter in a  CRE-dependent manner.	bind
80808	1	3545	11	NULL	NULL	0	NULL	CREB peptide	PartOfProtein	recombinant 	binds to 					BDNF promoter	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_neuron_20_4_727_s_144	9581764	(B) A recombinant CREB peptide can bind to the  BDNF promoter in a  CRE-dependent manner.	bind
80809	2	3545	11	NULL	NULL	0	NULL	statement 1	Process		depends on					CRE	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_neuron_20_4_727_s_144	9581764	(B) A recombinant CREB peptide can bind to the  BDNF promoter in a  CRE-dependent manner.	bind
7995	1	3546	6	11	NULL	NULL	NULL	HEL	GP		bind					I-Ak	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_8_3_305_s_48	9529148	(B) A ribbon diagram ( Carson 1987  ) of HEL bound to I-Ak.	bind
11183	1	3546	7	11	NULL	NULL	NULL	HEL	GP		bind					I-Ak	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_8_3_305_s_48	9529148	(B) A ribbon diagram ( Carson 1987  ) of HEL bound to I-Ak.	bind
80810	1	3546	11	NULL	NULL	0	NULL	HEL	PartOfProtein		binds to 					I-Ak	Protein				NULL		0	NULL	NULL	NULL	gw60_immunity_8_3_305_s_48	9529148	(B) A ribbon diagram ( Carson 1987  ) of HEL bound to I-Ak.	bind
7996	1	3547	6	11	NULL	NULL	NULL				bind			Gi 1 subunit		GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_structure_4_11_1277_s_89	8939752	(b) A superposition of the C  traces of the Gi 1 subunit bound to GDP (blue), Gi 1bound to GTP  S-Mg2+ (red), and the GDP-Pi complex of G203AGi 1 (green).	bind
7997	2	3547	6	11	NULL	NULL	NULL				bind			Gi 1 subunit		GTP S-Mg+2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_structure_4_11_1277_s_89	8939752	(b) A superposition of the C  traces of the Gi 1 subunit bound to GDP (blue), Gi 1bound to GTP  S-Mg2+ (red), and the GDP-Pi complex of G203AGi 1 (green).	bind
11184	1	3547	7	11	NULL	NULL	NULL				bind			Gi 1 subunit		GDP 	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_structure_4_11_1277_s_89	8939752	(b) A superposition of the C  traces of the Gi 1 subunit bound to GDP (blue), Gi 1bound to GTP  S-Mg2+ (red), and the GDP-Pi complex of G203AGi 1 (green).	bind
11185	2	3547	7	11	NULL	NULL	NULL				bind			Gi 1 subunit		GTP S-Mg2+ 	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_structure_4_11_1277_s_89	8939752	(b) A superposition of the C  traces of the Gi 1 subunit bound to GDP (blue), Gi 1bound to GTP  S-Mg2+ (red), and the GDP-Pi complex of G203AGi 1 (green).	bind
80811	1	3547	11	NULL	NULL	0	NULL	Gi 1 subunit	Protein		binds to 					GDP	Chemical				NULL		0	NULL	NULL	NULL	gw60_structure_4_11_1277_s_89	8939752	(b) A superposition of the C  traces of the Gi 1 subunit bound to GDP (blue), Gi 1bound to GTP  S-Mg2+ (red), and the GDP-Pi complex of G203AGi 1 (green).	bind
80812	2	3547	11	NULL	NULL	0	NULL	Gi	Protein		binds to 					GTP S-Mg2+	Chemical				NULL		0	NULL	NULL	NULL	gw60_structure_4_11_1277_s_89	8939752	(b) A superposition of the C  traces of the Gi 1 subunit bound to GDP (blue), Gi 1bound to GTP  S-Mg2+ (red), and the GDP-Pi complex of G203AGi 1 (green).	bind
80813	3	3547	11	NULL	NULL	0	NULL	GDP-Pi	Chemical		complex with 					G203AGi 1	Chemical				NULL		0	NULL	NULL	NULL	gw60_structure_4_11_1277_s_89	8939752	(b) A superposition of the C  traces of the Gi 1 subunit bound to GDP (blue), Gi 1bound to GTP  S-Mg2+ (red), and the GDP-Pi complex of G203AGi 1 (green).	bind
7999	1	3548	6	11	NULL	NULL	NULL	MCM3	GP		bind					chromatin	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_16_903_s_103	10469595	(b) A time-course experiment of the binding kinetics of MCM3 and Cdc6 to chromatin.	bind
8000	2	3548	6	11	NULL	NULL	NULL	Cdc6	GP		bind					chromatin	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_16_903_s_103	10469595	(b) A time-course experiment of the binding kinetics of MCM3 and Cdc6 to chromatin.	bind
11187	1	3548	7	11	NULL	NULL	NULL	MCM3	GP		bind					chromatin	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_16_903_s_103	10469595	(b) A time-course experiment of the binding kinetics of MCM3 and Cdc6 to chromatin.	bind
11188	2	3548	7	11	NULL	NULL	NULL	Cdc6	GP		bind					chromatin	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_16_903_s_103	10469595	(b) A time-course experiment of the binding kinetics of MCM3 and Cdc6 to chromatin.	bind
80814	1	3548	11	NULL	NULL	0	NULL	MCM3	Protein		binds to 					chromatin	Chromosome				NULL		0	NULL	NULL	NULL	gw60_currbiol_9_16_903_s_103	10469595	(b) A time-course experiment of the binding kinetics of MCM3 and Cdc6 to chromatin.	bind
80815	2	3548	11	NULL	NULL	NULL	NULL	Cdc6 	Protein		binds to 					chromatin	Chromosome				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_16_903_s_103	10469595	(b) A time-course experiment of the binding kinetics of MCM3 and Cdc6 to chromatin.	bind
8001	1	3549	6	11	NULL	NULL	NULL	lamin	GP	in vitro-translated;; Drosophila	bind					H2B peptides	GP	unmodified			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_17_1529_s_106	12225670	(B) A total of 3  l in vitro-translated  Drosophila lamin was bound to the unmodified (H2B) and acetylated (H2B-Ac) peptides.	bind
8002	2	3549	6	11	NULL	NULL	NULL	lamin	GP	in vitro-translated;; Drosophila	bind					H2B-Ac peptides	GP	acetylated			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_17_1529_s_106	12225670	(B) A total of 3  l in vitro-translated  Drosophila lamin was bound to the unmodified (H2B) and acetylated (H2B-Ac) peptides.	bind
52978	3	3549	6	11	NULL	NULL	NULL	H2B-Ac	GP		is					acetylated H2B peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_17_1529_s_106	12225670	(B) A total of 3  l in vitro-translated  Drosophila lamin was bound to the unmodified (H2B) and acetylated (H2B-Ac) peptides.	bind
11189	1	3549	7	11	NULL	NULL	NULL	lamin	GP	in vitro-translated;; Drosophila	bind					H2B peptides	GP	unmodified			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_17_1529_s_106	12225670	(B) A total of 3  l in vitro-translated  Drosophila lamin was bound to the unmodified (H2B) and acetylated (H2B-Ac) peptides.	bind
11190	2	3549	7	11	NULL	NULL	NULL	lamin	GP	in vitro-translated;; Drosophila	bind					H2B-Ac peptides	GP	acetylated			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_17_1529_s_106	12225670	(B) A total of 3  l in vitro-translated  Drosophila lamin was bound to the unmodified (H2B) and acetylated (H2B-Ac) peptides.	bind
11191	3	3549	7	11	NULL	NULL	NULL	H2B-Ac	GP		is					acetylated H2B peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_17_1529_s_106	12225670	(B) A total of 3  l in vitro-translated  Drosophila lamin was bound to the unmodified (H2B) and acetylated (H2B-Ac) peptides.	bind
80816	1	3549	11	NULL	NULL	0	NULL	 lamin	Protein	in vitro-translated;;Drosophila	binds to 					H2B peptide	PartOfProtein	unmodified			NULL		0	NULL	NULL	NULL	gw60_currbiol_12_17_1529_s_106	12225670	(B) A total of 3  l in vitro-translated  Drosophila lamin was bound to the unmodified (H2B) and acetylated (H2B-Ac) peptides.	bind
80817	2	3549	11	NULL	NULL	0	NULL	lamin	Protein	in vitro-translated;;Drosophila	binds to 					H2B-Ac peptide	PartOfProtein	acetylated			NULL		0	NULL	NULL	NULL	gw60_currbiol_12_17_1529_s_106	12225670	(B) A total of 3  l in vitro-translated  Drosophila lamin was bound to the unmodified (H2B) and acetylated (H2B-Ac) peptides.	bind
8003	1	3551	6	11	NULL	NULL	NULL	Abf1p	GP		bind					ADE5,7	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_17_6279_s_81	12917348	(B) Abf1p binds in vitro to  ADE5, 7 but not to  IMD2.	bind
8005	2	3551	6	11	NULL	NULL	NULL	Abf1p	GP		does not bind					IMD2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_17_6279_s_81	12917348	(B) Abf1p binds in vitro to  ADE5, 7 but not to  IMD2.	bind
11192	1	3551	7	11	NULL	NULL	NULL	Abf1p	GP		binds					ADE5,7	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_17_6279_s_81	12917348	(B) Abf1p binds in vitro to  ADE5, 7 but not to  IMD2.	bind
11193	2	3551	7	11	NULL	NULL	NULL	Abf1p	GP		does not bind					IMD2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_17_6279_s_81	12917348	(B) Abf1p binds in vitro to  ADE5, 7 but not to  IMD2.	bind
80818	1	3551	11	NULL	NULL	0	NULL	Abf1p	Protein		binds to 					ADE5,7	NucleicAcidSubstance				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_23_17_6279_s_81	12917348	(B) Abf1p binds in vitro to  ADE5, 7 but not to  IMD2.	bind
80819	2	3551	11	NULL	NULL	0	NULL	Abf1p	Protein		does not bind to						Gene				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_23_17_6279_s_81	12917348	(B) Abf1p binds in vitro to  ADE5, 7 but not to  IMD2.	bind
8006	1	3552	6	11	NULL	NULL	NULL	Rac1	GP		bind					GST-PAK	GP		GBD		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_79	10508610	(b) Ability of Rac1 and Cdc42 17-32 peptides to compete for the binding of Rac1 and Cdc42 to GST-PAK GTPase-binding domains (GBD).	bind
8007	2	3552	6	11	NULL	NULL	NULL	Cdc42	GP		bind					GST-PAK	GP		GBD		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_79	10508610	(b) Ability of Rac1 and Cdc42 17-32 peptides to compete for the binding of Rac1 and Cdc42 to GST-PAK GTPase-binding domains (GBD).	bind
8008	3	3552	6	11	NULL	NULL	NULL	GBD	GP		is					GTPase-binding domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_79	10508610	(b) Ability of Rac1 and Cdc42 17-32 peptides to compete for the binding of Rac1 and Cdc42 to GST-PAK GTPase-binding domains (GBD).	bind
8009	4	3552	6	11	NULL	NULL	NULL	Rac1 peptides	GP		bind					GST-PAK	GP		GBD		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_79	10508610	(b) Ability of Rac1 and Cdc42 17-32 peptides to compete for the binding of Rac1 and Cdc42 to GST-PAK GTPase-binding domains (GBD).	bind
8010	5	3552	6	11	NULL	NULL	NULL	statement 4	Process		competes with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_79	10508610	(b) Ability of Rac1 and Cdc42 17-32 peptides to compete for the binding of Rac1 and Cdc42 to GST-PAK GTPase-binding domains (GBD).	bind
8011	6	3552	6	11	NULL	NULL	NULL	Cdc42 	GP		bind			17-32 peptide		GST-PAK	GP		GBD		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_79	10508610	(b) Ability of Rac1 and Cdc42 17-32 peptides to compete for the binding of Rac1 and Cdc42 to GST-PAK GTPase-binding domains (GBD).	bind
8012	7	3552	6	11	NULL	NULL	NULL	statement 6	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_79	10508610	(b) Ability of Rac1 and Cdc42 17-32 peptides to compete for the binding of Rac1 and Cdc42 to GST-PAK GTPase-binding domains (GBD).	bind
11194	1	3552	7	11	NULL	NULL	NULL	Rac1	GP		bind					GST-PAK	GP		GBD		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_79	10508610	(b) Ability of Rac1 and Cdc42 17-32 peptides to compete for the binding of Rac1 and Cdc42 to GST-PAK GTPase-binding domains (GBD).	bind
11195	2	3552	7	11	NULL	NULL	NULL	Cdc42	GP		bind					GST-PAK	GP		GBD		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_79	10508610	(b) Ability of Rac1 and Cdc42 17-32 peptides to compete for the binding of Rac1 and Cdc42 to GST-PAK GTPase-binding domains (GBD).	bind
11196	3	3552	7	11	NULL	NULL	NULL	Rac1 peptide	GP		bind					GST-PAK	GP		GBD		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_79	10508610	(b) Ability of Rac1 and Cdc42 17-32 peptides to compete for the binding of Rac1 and Cdc42 to GST-PAK GTPase-binding domains (GBD).	bind
11197	4	3552	7	11	NULL	NULL	NULL	GTPase-binding domain	GP		is					GBD	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_79	10508610	(b) Ability of Rac1 and Cdc42 17-32 peptides to compete for the binding of Rac1 and Cdc42 to GST-PAK GTPase-binding domains (GBD).	bind
52980	5	3552	7	11	NULL	NULL	NULL	statement 3	Process		competes with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_79	10508610	(b) Ability of Rac1 and Cdc42 17-32 peptides to compete for the binding of Rac1 and Cdc42 to GST-PAK GTPase-binding domains (GBD).	bind
52981	6	3552	7	11	NULL	NULL	NULL	Cdc42 peptides	GP		bind			17-32		GST-PAK	GP		GBD		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_79	10508610	(b) Ability of Rac1 and Cdc42 17-32 peptides to compete for the binding of Rac1 and Cdc42 to GST-PAK GTPase-binding domains (GBD).	bind
52982	7	3552	7	11	NULL	NULL	NULL	statement 6	Process		competes with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_79	10508610	(b) Ability of Rac1 and Cdc42 17-32 peptides to compete for the binding of Rac1 and Cdc42 to GST-PAK GTPase-binding domains (GBD).	bind
80820	1	3552	11	NULL	NULL	0	NULL	GST-PAK 	Protein		binds to 			GTPase-binding domain		Rac1	Protein				NULL		0	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_79	10508610	(b) Ability of Rac1 and Cdc42 17-32 peptides to compete for the binding of Rac1 and Cdc42 to GST-PAK GTPase-binding domains (GBD).	bind
80821	2	3552	11	NULL	NULL	0	NULL	GST-PAK	Protein		binds to 			GTPase-binding domain		Cdc42	Protein				NULL		0	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_79	10508610	(b) Ability of Rac1 and Cdc42 17-32 peptides to compete for the binding of Rac1 and Cdc42 to GST-PAK GTPase-binding domains (GBD).	bind
80822	3	3552	11	NULL	NULL	0	NULL	GTPase-binding domain	PartOfProtein		is					GBD	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_79	10508610	(b) Ability of Rac1 and Cdc42 17-32 peptides to compete for the binding of Rac1 and Cdc42 to GST-PAK GTPase-binding domains (GBD).	bind
8014	1	3554	6	11	NULL	NULL	NULL	HS1	GP		bind			actin binding domain		PIP2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_3829_s_202	9632767	(B) Actin-binding domain of HS1 binds PIP2.	bind
11198	1	3554	7	11	NULL	NULL	NULL	HS1	GP		binds			Actin-binding domain		 PIP2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_3829_s_202	9632767	(B) Actin-binding domain of HS1 binds PIP2.	bind
80828	1	3554	11	NULL	NULL	NULL	NULL	HS1	Protein		binds to 			Actin-binding domain		PIP2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_3829_s_202	9632767	(B) Actin-binding domain of HS1 binds PIP2.	bind
8077	1	3556	6	11	NULL	NULL	NULL	PI3K-C2	GP	deletion of	stimulates			N-terminal clathrin binding region		PI3K-C2	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_2_443_s_70	11239472	(b) Activity of PI3K-C2  is greatly stimulated by deletion of the N-terminal clathrin binding region of PI3K-C2  (stippled bar).	bind
11199	1	3556	7	11	NULL	NULL	NULL	PI3K-C2	GP	activity of	is stimulated by					PI3K-C2	GP	deletion of	N-terminal clathrin binding region		NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_2_443_s_70	11239472	(b) Activity of PI3K-C2  is greatly stimulated by deletion of the N-terminal clathrin binding region of PI3K-C2  (stippled bar).	bind
80834	1	3556	11	NULL	NULL	0	NULL	PI3K-C2	Protein		has binding site for			N-terminal 		clathrin	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_7_2_443_s_70	11239472	(b) Activity of PI3K-C2  is greatly stimulated by deletion of the N-terminal clathrin binding region of PI3K-C2  (stippled bar).	bind
80835	2	3556	11	NULL	NULL	0	NULL	PI3K-C2	Protein		undergoes			N-terminal clathrin binding region		deletion	MolecularProcess				NULL		0	NULL	NULL	NULL	gw60_molcell_7_2_443_s_70	11239472	(b) Activity of PI3K-C2  is greatly stimulated by deletion of the N-terminal clathrin binding region of PI3K-C2  (stippled bar).	bind
80836	3	3556	11	NULL	NULL	0	NULL	statement 2	Process		activates					PI3K-C2	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_7_2_443_s_70	11239472	(b) Activity of PI3K-C2  is greatly stimulated by deletion of the N-terminal clathrin binding region of PI3K-C2  (stippled bar).	bind
8078	1	3557	6	11	NULL	NULL	NULL	Ad2	GP		bind			E1B		PCAF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_300	10891493	(B) Ad2 E1B binds to PCAF.	bind
11200	1	3557	7	11	NULL	NULL	NULL	Ad2 	GP		binds			E1B		PCAF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_300	10891493	(B) Ad2 E1B binds to PCAF.	bind
80837	1	3557	11	NULL	NULL	0	NULL	Ad2 E1B	Protein		binds to 					PCAF	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_300	10891493	(B) Ad2 E1B binds to PCAF.	bind
8079	1	3558	6	11	NULL	NULL	NULL	uPA	GP		bind					uPAR	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
8080	2	3558	6	11	NULL	NULL	NULL	R3	GP		is 					anti-uPAR	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
8081	3	3558	6	11	NULL	NULL	NULL	R3	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
8082	4	3558	6	11	NULL	NULL	NULL	uPA	GP		induces					uPAR-expressing cells	Cell	wt;; migration of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
8083	5	3558	6	11	NULL	NULL	NULL	uPA	GP		induces					hcr-uPAR-expressing cells	Cell	migration of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
8084	6	3558	6	11	NULL	NULL	NULL	R3	GP	addition of	blocks					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
8085	7	3558	6	11	NULL	NULL	NULL	R3	GP	addition of	blocks					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
40778	8	3558	6	11	NULL	NULL	NULL	anti-uPAR	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
11201	1	3558	7	11	NULL	NULL	NULL	uPA	GP		bind					uPAR	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
11202	2	3558	7	11	NULL	NULL	NULL	monoclonal anti-uPAR antibody	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
11203	3	3558	7	11	NULL	NULL	NULL	uPA	GP		induce					uPAR-expressing cells	Cell	migration of;;wt			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
11204	4	3558	7	11	NULL	NULL	NULL	uPA	GP		induce					hcr-uPAR-expressing cells	Cell	migration of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
11205	5	3558	7	11	NULL	NULL	NULL	R3	GP	addition of	blocks					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
11206	6	3558	7	11	NULL	NULL	NULL	R3	GP	addition of	blocks					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
52983	7	3558	7	11	NULL	NULL	NULL	R3	GP		is					anti-uPAR	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
52984	8	3558	7	11	NULL	NULL	NULL	anti-uPAR	GP		is a type of					monoclonal antibody \t	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
80840	1	3558	11	NULL	NULL	0	NULL	uPA	Protein		binds to 					uPAR	Protein				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
80841	2	3558	11	NULL	NULL	0	NULL	anti-uPAR antibody	PartOfProtein	monoclonal	blocks					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
80842	3	3558	11	NULL	NULL	0	NULL	R3	PartOfProtein		is					anti-uPAR antibody	PartOfProtein	monoclonal			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
80843	4	3558	11	NULL	NULL	NULL	NULL	cells	cell	hcr-uPAR-expressing	undergoes					migration	BiologicalProcess				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
80845	5	3558	11	NULL	NULL	0	NULL	cells	cell	wt-uPAR-expressing	undergoes					migration	BiologicalProcess				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
80846	6	3558	11	NULL	NULL	0	NULL	uPA	Protein		induces					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
80847	7	3558	11	NULL	NULL	0	NULL	uPA	Protein		induces					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
80848	8	3558	11	NULL	NULL	0	NULL	R3	PartOfProtein		blocks					statement 6	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
80849	9	3558	11	NULL	NULL	0	NULL	R3	PartOfProtein		blocks					statement 7	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_367_s_141	16267271	(B) Addition of R3 (monoclonal anti-uPAR antibody blocking uPA binding to  uPAR) blocks uPA-induced migration of both wt- and  hcr-uPAR-expressing cells.	bind
8086	1	3559	6	11	NULL	NULL	NULL	R1/1	GP		bind					ICAM-1	GP		D1		NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_2_830_s_135	16428725	(B) Adhesion of NTHI was also determined  after incubating CHO-ICAM-1 cells with MAbs R1/1 and 8.4A6, which bind ICAM-1 D1  and D2, respectively.	bind
8087	2	3559	6	11	NULL	NULL	NULL	8.4A6	GP		bind					ICAM-1	GP		D2		NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_2_830_s_135	16428725	(B) Adhesion of NTHI was also determined  after incubating CHO-ICAM-1 cells with MAbs R1/1 and 8.4A6, which bind ICAM-1 D1  and D2, respectively.	bind
52985	3	3559	6	10	NULL	0	NULL	R1/1	NULL		is a type of	NULL				monoclonal antibody	NULL				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_2_830_s_135	16428725	(B) Adhesion of NTHI was also determined  after incubating CHO-ICAM-1 cells with MAbs R1/1 and 8.4A6, which bind ICAM-1 D1  and D2, respectively.	bind
52986	4	3559	6	10	NULL	0	NULL	8.4A6	NULL		is a type of	NULL				monoclonal antibody	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_74_2_830_s_135	16428725	(B) Adhesion of NTHI was also determined  after incubating CHO-ICAM-1 cells with MAbs R1/1 and 8.4A6, which bind ICAM-1 D1  and D2, respectively.	bind
11207	1	3559	7	NULL	NULL	0	NULL	R1/1 	NULL		bind	NULL				ICAM-1 	NULL		D1		NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_2_830_s_135	16428725	(B) Adhesion of NTHI was also determined  after incubating CHO-ICAM-1 cells with MAbs R1/1 and 8.4A6, which bind ICAM-1 D1  and D2, respectively.	bind
11208	2	3559	7	NULL	NULL	0	NULL	8.4A6	NULL		bind	NULL				ICAM-1	NULL		D2		NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_2_830_s_135	16428725	(B) Adhesion of NTHI was also determined  after incubating CHO-ICAM-1 cells with MAbs R1/1 and 8.4A6, which bind ICAM-1 D1  and D2, respectively.	bind
52987	3	3559	7	10	NULL	0	NULL	R1/1	NULL		is a type of	NULL				monoclonal antibody	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_74_2_830_s_135	16428725	(B) Adhesion of NTHI was also determined  after incubating CHO-ICAM-1 cells with MAbs R1/1 and 8.4A6, which bind ICAM-1 D1  and D2, respectively.	bind
52988	4	3559	7	10	NULL	0	NULL	8.4A6	NULL		is a type of	NULL				monoclonal antibody	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_74_2_830_s_135	16428725	(B) Adhesion of NTHI was also determined  after incubating CHO-ICAM-1 cells with MAbs R1/1 and 8.4A6, which bind ICAM-1 D1  and D2, respectively.	bind
80873	1	3559	11	NULL	NULL	0	NULL	MAbs R1/1	PartOfProtein		binds to 					ICAM-1 D1	Protein				NULL		0	NULL	NULL	NULL	gw70_infectimmun_74_2_830_s_135	16428725	(B) Adhesion of NTHI was also determined  after incubating CHO-ICAM-1 cells with MAbs R1/1 and 8.4A6, which bind ICAM-1 D1  and D2, respectively.	bind
80874	2	3559	11	NULL	NULL	0	NULL	8.4A6	PartOfProtein		binds to 					ICAM-1 D2	Protein				NULL		0	NULL	NULL	NULL	gw70_infectimmun_74_2_830_s_135	16428725	(B) Adhesion of NTHI was also determined  after incubating CHO-ICAM-1 cells with MAbs R1/1 and 8.4A6, which bind ICAM-1 D1  and D2, respectively.	bind
8088	1	3563	6	11	NULL	NULL	NULL	Myc-Pak1	GP		bind					Nck	GP				NULL	COS-7 cell lysates	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8058_s_283	14585966	(B) Akt expression in  COS-7 cells leads to reduced binding of Myc-Pak1 with Nck in a GST-Nck pull-down  assay with cell lysates.	bind
8089	2	3563	6	11	NULL	NULL	NULL	Akt	GP	expression of	reduces					statement 1	Process				NULL	COS-7 cell lysates	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8058_s_283	14585966	(B) Akt expression in  COS-7 cells leads to reduced binding of Myc-Pak1 with Nck in a GST-Nck pull-down  assay with cell lysates.	bind
11213	1	3563	7	11	NULL	NULL	NULL	Myc-Pak1	GP		bind					Nck	GP				NULL	COS-7 cells lysates	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8058_s_283	14585966	(B) Akt expression in  COS-7 cells leads to reduced binding of Myc-Pak1 with Nck in a GST-Nck pull-down  assay with cell lysates.	bind
11214	2	3563	7	11	NULL	NULL	NULL	Akt	GP	expression of	reduces					statement 1	Process				NULL	COS-7 cells lysates	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8058_s_283	14585966	(B) Akt expression in  COS-7 cells leads to reduced binding of Myc-Pak1 with Nck in a GST-Nck pull-down  assay with cell lysates.	bind
80875	1	3563	11	NULL	NULL	0	NULL	Myc-Pak1	Protein		binds to 					Nck	Protein				NULL	GST-Nck pull-down assay	0	NULL	NULL	NULL	gw70_molcellbiol_23_22_8058_s_283	14585966	(B) Akt expression in  COS-7 cells leads to reduced binding of Myc-Pak1 with Nck in a GST-Nck pull-down  assay with cell lysates.	bind
80876	2	3563	11	NULL	NULL	0	NULL	Akt	Protein		expressed on					COS-7 cells	Cell				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_22_8058_s_283	14585966	(B) Akt expression in  COS-7 cells leads to reduced binding of Myc-Pak1 with Nck in a GST-Nck pull-down  assay with cell lysates.	bind
80877	3	3563	11	NULL	NULL	0	NULL	statement 2	Process		reduces					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_22_8058_s_283	14585966	(B) Akt expression in  COS-7 cells leads to reduced binding of Myc-Pak1 with Nck in a GST-Nck pull-down  assay with cell lysates.	bind
8090	1	3564	6	11	NULL	NULL	NULL	Rac	GP		bind					PAK	GP		PBD		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_4_749_s_59	14765121	(B) AlF treatment causes increased binding of Rac to the p21-binding domain  of PAK (PAK PBD).	bind
8091	2	3564	6	11	NULL	NULL	NULL	AIF	GP		increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_4_749_s_59	14765121	(B) AlF treatment causes increased binding of Rac to the p21-binding domain  of PAK (PAK PBD).	bind
8092	3	3564	6	11	NULL	NULL	NULL	PBD	GP		is					p21-binding domain	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_4_749_s_59	14765121	(B) AlF treatment causes increased binding of Rac to the p21-binding domain  of PAK (PAK PBD).	bind
11218	1	3564	7	11	NULL	NULL	NULL	Rac	GP		bind					PAK	GP		PBD		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_4_749_s_59	14765121	(B) AlF treatment causes increased binding of Rac to the p21-binding domain  of PAK (PAK PBD).	bind
11219	2	3564	7	11	NULL	NULL	NULL	AlF	GP		increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_4_749_s_59	14765121	(B) AlF treatment causes increased binding of Rac to the p21-binding domain  of PAK (PAK PBD).	bind
11221	3	3564	7	11	NULL	NULL	NULL	PBD	GP		is					p21-binding domain	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_4_749_s_59	14765121	(B) AlF treatment causes increased binding of Rac to the p21-binding domain  of PAK (PAK PBD).	bind
80878	1	3564	11	NULL	NULL	0	NULL	Rac	Protein		binds to 					PAK	Protein		p21-binding domain		NULL		0	NULL	NULL	NULL	gw70_embo_23_4_749_s_59	14765121	(B) AlF treatment causes increased binding of Rac to the p21-binding domain  of PAK (PAK PBD).	bind
80879	2	3564	11	NULL	NULL	0	NULL	AlF	Chemical		increases					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_embo_23_4_749_s_59	14765121	(B) AlF treatment causes increased binding of Rac to the p21-binding domain  of PAK (PAK PBD).	bind
80880	3	3564	11	NULL	NULL	0	NULL	PAK	Protein		is			p21-binding domain		PAK PBD	Protein				NULL		0	NULL	NULL	NULL	gw70_embo_23_4_749_s_59	14765121	(B) AlF treatment causes increased binding of Rac to the p21-binding domain  of PAK (PAK PBD).	bind
8093	1	3565	6	11	NULL	NULL	NULL	target genes	GP	mouse	bind				sox-oct cis elements	Sox2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6031_s_192	15988017	(B) Alignment of  the composite sox-oct  cis elements from the respective mouse target genes that are known to bind Sox2 and Oct4,  including that described in this paper and present in the CR4-B region in panel A  (complementary strand).	bind
8094	2	3565	6	11	NULL	NULL	NULL	target genes	GP	mouse	bind				sox-oct cis elements	Oct4	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6031_s_192	15988017	(B) Alignment of  the composite sox-oct  cis elements from the respective mouse target genes that are known to bind Sox2 and Oct4,  including that described in this paper and present in the CR4-B region in panel A  (complementary strand).	bind
11226	1	3565	7	11	NULL	NULL	NULL	target genes	GP	mouse	bind				sox-oct cis elements	Sox2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6031_s_192	15988017	(B) Alignment of  the composite sox-oct  cis elements from the respective mouse target genes that are known to bind Sox2 and Oct4,  including that described in this paper and present in the CR4-B region in panel A  (complementary strand).	bind
11229	2	3565	7	11	NULL	NULL	NULL	target genes	GP	mouse	bind				sox-oct cis elements	Oct4	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6031_s_192	15988017	(B) Alignment of  the composite sox-oct  cis elements from the respective mouse target genes that are known to bind Sox2 and Oct4,  including that described in this paper and present in the CR4-B region in panel A  (complementary strand).	bind
8095	1	3571	6	11	NULL	NULL	NULL	EKLF	GP	mutant	bind			amino-terminal 		betamaj	NucleicAcid	cognate		CACC motif	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_1_161_s_187	11739731	(B) All amino-terminal mutants of EKLF bind the cognate betamaj CACC motif.	bind
11236	1	3571	7	11	NULL	NULL	NULL	EKLF	GP	 mutant	bind			amino-terminal		betamaj	NucleicAcid	cognate		CACC motif	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_1_161_s_187	11739731	(B) All amino-terminal mutants of EKLF bind the cognate betamaj CACC motif.	bind
80881	1	3571	11	NULL	NULL	0	NULL	EKLF	Protein	mutants	binds to 			amino-terminal		betamaj	Protein		CACC motif		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_1_161_s_187	11739731	(B) All amino-terminal mutants of EKLF bind the cognate betamaj CACC motif.	bind
8175	1	3573	6	11	NULL	NULL	NULL	Ran	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_4_570_s_209	11729264	(B) Amino acid sequence of Ran showing the  Switch 1 and  Switch 2 regions that undergo a conformational switch between the GTP and GDP binding states, and  the basic patch.	bind
8176	2	3573	6	11	NULL	NULL	NULL	Ran	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_4_570_s_209	11729264	(B) Amino acid sequence of Ran showing the  Switch 1 and  Switch 2 regions that undergo a conformational switch between the GTP and GDP binding states, and  the basic patch.	bind
8177	3	3573	6	11	NULL	NULL	NULL	statement 1	Process		changes					Ran	GP	conformation of 			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_4_570_s_209	11729264	(B) Amino acid sequence of Ran showing the  Switch 1 and  Switch 2 regions that undergo a conformational switch between the GTP and GDP binding states, and  the basic patch.	bind
8178	4	3573	6	11	NULL	NULL	NULL	statement 2	Process		changes					Ran	GP	conformation of 			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_4_570_s_209	11729264	(B) Amino acid sequence of Ran showing the  Switch 1 and  Switch 2 regions that undergo a conformational switch between the GTP and GDP binding states, and  the basic patch.	bind
8301	5	3573	6	11	NULL	NULL	NULL	Ran	GP		undergoes			Switch 1		conformational change	Process				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_4_570_s_209	11729264	(B) Amino acid sequence of Ran showing the  Switch 1 and  Switch 2 regions that undergo a conformational switch between the GTP and GDP binding states, and  the basic patch.	bind
8302	6	3573	6	11	NULL	NULL	NULL	Ran	GP		undergoes			Switch 2		conformational change	Process				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_4_570_s_209	11729264	(B) Amino acid sequence of Ran showing the  Switch 1 and  Switch 2 regions that undergo a conformational switch between the GTP and GDP binding states, and  the basic patch.	bind
11331	1	3573	7	11	NULL	NULL	NULL	Ran	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_4_570_s_209	11729264	(B) Amino acid sequence of Ran showing the  Switch 1 and  Switch 2 regions that undergo a conformational switch between the GTP and GDP binding states, and  the basic patch.	bind
11332	2	3573	7	11	NULL	NULL	NULL	Ran	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_4_570_s_209	11729264	(B) Amino acid sequence of Ran showing the  Switch 1 and  Switch 2 regions that undergo a conformational switch between the GTP and GDP binding states, and  the basic patch.	bind
11333	3	3573	7	11	NULL	NULL	NULL	Ran	GP		undergoes			switch 1 region		conformational change	Process				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_4_570_s_209	11729264	(B) Amino acid sequence of Ran showing the  Switch 1 and  Switch 2 regions that undergo a conformational switch between the GTP and GDP binding states, and  the basic patch.	bind
11334	4	3573	7	11	NULL	NULL	NULL	Ran	GP		undergoes			switch 2 region		conformational change	Process				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_4_570_s_209	11729264	(B) Amino acid sequence of Ran showing the  Switch 1 and  Switch 2 regions that undergo a conformational switch between the GTP and GDP binding states, and  the basic patch.	bind
11335	5	3573	7	11	NULL	NULL	NULL	statement 1	Process		changes					Ran	GP	conformation of			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_4_570_s_209	11729264	(B) Amino acid sequence of Ran showing the  Switch 1 and  Switch 2 regions that undergo a conformational switch between the GTP and GDP binding states, and  the basic patch.	bind
11336	6	3573	7	11	NULL	NULL	NULL	statement 2	Process		changes					Ran	GP	conformation of			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_4_570_s_209	11729264	(B) Amino acid sequence of Ran showing the  Switch 1 and  Switch 2 regions that undergo a conformational switch between the GTP and GDP binding states, and  the basic patch.	bind
8098	1	3574	6	11	NULL	NULL	NULL	Tem1	GP		bind					Cdc15	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_5_697_s_200	12628189	(B) Amn1 regulates the binding between Tem1 and Cdc15.	bind
8099	2	3574	6	11	NULL	NULL	NULL	Amn1	GP		regulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_5_697_s_200	12628189	(B) Amn1 regulates the binding between Tem1 and Cdc15.	bind
11239	1	3574	7	11	NULL	NULL	NULL	Tem1	GP		bind					Cdc15	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_5_697_s_200	12628189	(B) Amn1 regulates the binding between Tem1 and Cdc15.	bind
11240	2	3574	7	11	NULL	NULL	NULL	Amn1	GP		regulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_5_697_s_200	12628189	(B) Amn1 regulates the binding between Tem1 and Cdc15.	bind
80882	1	3574	11	NULL	NULL	0	NULL	Tem1	Protein		binds to 					Cdc15	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_112_5_697_s_200	12628189	(B) Amn1 regulates the binding between Tem1 and Cdc15.	bind
80883	2	3574	11	NULL	NULL	0	NULL	Amn1	Protein		regulates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cell_112_5_697_s_200	12628189	(B) Amn1 regulates the binding between Tem1 and Cdc15.	bind
8101	1	3575	6	11	NULL	NULL	NULL	L-ficolin	Chemical		bind					T-1	Organism				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_2_1052_s_161	15664949	(B) Amounts of L-ficolin bound to T-1 and Wood.	bind
8102	2	3575	6	11	NULL	NULL	NULL	L-ficolin	Chemical		bind					Wood	Organism				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_2_1052_s_161	15664949	(B) Amounts of L-ficolin bound to T-1 and Wood.	bind
11243	1	3575	7	11	NULL	NULL	NULL	L-ficolin	Chemical		bind					T-1	Organism				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_2_1052_s_161	15664949	(B) Amounts of L-ficolin bound to T-1 and Wood.	bind
11246	2	3575	7	11	NULL	NULL	NULL	L-ficolin	Chemical		bind					Wood	Organism				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_2_1052_s_161	15664949	(B) Amounts of L-ficolin bound to T-1 and Wood.	bind
80884	1	3575	11	NULL	NULL	0	NULL	L-ficolin	Protein		binds to 					T-1	Organism				NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_2_1052_s_161	15664949	(B) Amounts of L-ficolin bound to T-1 and Wood.	bind
80885	2	3575	11	NULL	NULL	0	NULL	L-ficolin	Protein		binds to 					Wood	Organism				NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_2_1052_s_161	15664949	(B) Amounts of L-ficolin bound to T-1 and Wood.	bind
8103	1	3577	6	11	NULL	NULL	NULL	neutrophil collagenase 	GP	active	bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_5_2319_s_233	10225890	(B) Analysis of active and latent forms of neutrophil collagenase binding to collagen.	bind
8104	2	3577	6	11	NULL	NULL	NULL	neutrophil collagenase 	GP	latent	bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_5_2319_s_233	10225890	(B) Analysis of active and latent forms of neutrophil collagenase binding to collagen.	bind
11252	1	3577	7	11	NULL	NULL	NULL	neutrophil collagenase	GP	active	bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_5_2319_s_233	10225890	(B) Analysis of active and latent forms of neutrophil collagenase binding to collagen.	bind
11254	2	3577	7	11	NULL	NULL	NULL	neutrophil collagenase	GP	latent	bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_5_2319_s_233	10225890	(B) Analysis of active and latent forms of neutrophil collagenase binding to collagen.	bind
80886	1	3577	11	NULL	NULL	0	NULL	collagenase	Protein	neutrophil	binds to 					collagen	Protein				NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_5_2319_s_233	10225890	(B) Analysis of active and latent forms of neutrophil collagenase binding to collagen.	bind
8105	1	3578	6	11	NULL	NULL	NULL	GCNF	GP		bind					Nanog 	GP		DR0 sequence		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8507_s_251	16166633	(B) Analysis of binding of GCNF to the  Nanog DR0 sequence by EMSA.	bind
11262	1	3578	7	11	NULL	NULL	NULL	GCNF	GP		bind					Nanog	GP		DR0 sequence		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8507_s_251	16166633	(B) Analysis of binding of GCNF to the  Nanog DR0 sequence by EMSA.	bind
80887	1	3578	11	NULL	NULL	NULL	NULL	GCNF	Protein		binds to 					Nanog DR0 sequence	NucleicAcidSubstance				NULL	by EMSA	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8507_s_251	16166633	(B) Analysis of binding of GCNF to the  Nanog DR0 sequence by EMSA.	bind
8106	1	3579	6	11	NULL	NULL	NULL	Spt20p	GP		bind					HXT genes	GP				NULL	mot1- 1 mutant strain	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_173	15923605	(B) Analysis of Spt20p binding to  HXT genes in a  mot1- 1 mutant strain after a shift to low glucose.	bind
11265	1	3579	7	11	NULL	NULL	NULL	Spt20p	GP		bind					HXT genes	GP				NULL	 mot1- 1 mutant strain	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_173	15923605	(B) Analysis of Spt20p binding to  HXT genes in a  mot1- 1 mutant strain after a shift to low glucose.	bind
80888	1	3579	11	NULL	NULL	0	NULL	Spt20p	Protein		binds to 					HXT gene	Gene				NULL	mot1- 1 mutant strain	0	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_173	15923605	(B) Analysis of Spt20p binding to  HXT genes in a  mot1- 1 mutant strain after a shift to low glucose.	bind
8108	1	3580	6	11	NULL	NULL	NULL	nuclear cyclin T	GP		bind					Tat protein	GP	HIV-1;; wild type			NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
8109	2	3580	6	11	NULL	NULL	NULL	nuclear cyclin T	GP		bind					Tat protein	GP	HIV-1;; mutant	activation domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
8110	3	3580	6	11	NULL	NULL	NULL	nuclear cyclin T	GP		bind					Tat protein	GP	HIV-2;; wild type			NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
8111	4	3580	6	11	NULL	NULL	NULL	nuclear cyclin T	GP		bind					Tat protein	GP	 HIV-2;; mutant 	activation domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
8112	5	3580	6	11	NULL	NULL	NULL	CDK9	GP		bind					Tat protein	GP	HIV-1;; wild type			NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
8113	6	3580	6	11	NULL	NULL	NULL	CDK9	GP		bind					Tat protein	GP	HIV-1;; mutant	activation domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
8114	7	3580	6	11	NULL	NULL	NULL	CDK9	GP		bind					Tat protein	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
8115	8	3580	6	11	NULL	NULL	NULL	CDK9	GP		bind					Tat protein	GP	HIV-2;; mutant	activation domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
11269	1	3580	7	11	NULL	NULL	NULL	nuclear cyclin T	GP		bind					Tat protein	GP	wild-type;; HIV-1			NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
11271	2	3580	7	11	NULL	NULL	NULL	nuclear cyclin T	GP		bind					Tat protein	GP	wild-type;; HIV-2 			NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
11273	3	3580	7	11	NULL	NULL	NULL	nuclear cyclin T	GP		bind					Tat protein	GP	mutant;; HIV-1 	activation domain 		NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
11276	4	3580	7	11	NULL	NULL	NULL	nuclear cyclin T	GP		bind					Tat protein	GP	mutant;; HIV-2	activation domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
11279	5	3580	7	11	NULL	NULL	NULL	CDK9	GP		bind					Tat protein	GP	wild-type;; HIV-1			NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
11281	6	3580	7	11	NULL	NULL	NULL	CDK9	GP		bind					Tat protein	GP	wild-type;; HIV-2			NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
11283	7	3580	7	11	NULL	NULL	NULL	CDK9	GP		bind					Tat protein	GP	HIV-1;; mutant	activation domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
11289	8	3580	7	11	NULL	NULL	NULL	CDK9	GP		bind					Tat protein	GP	HIV-2;; mutant	activation domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
80889	1	3580	11	NULL	NULL	0	NULL	cyclin T	Protein	nuclear	binds to 					Tat protein	Protein	 wild-type;HIV-1			NULL		0	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
80890	2	3580	11	NULL	NULL	0	NULL	cyclin T	Protein	nuclear	binds to 					Tat protein	Protein	wild-type;;HIV-2			NULL		0	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
80891	3	3580	11	NULL	NULL	0	NULL	cyclin T	Protein	nuclear	binds to 					Tat protein	Protein	HIV-1	activation domain mutant 		NULL		0	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
80892	4	3580	11	NULL	NULL	0	NULL	cyclin T	Protein	nuclear	binds to 					Tat protein	Protein	 HIV-2	activation domain mutant		NULL		0	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
80893	5	3580	11	NULL	NULL	0	NULL	CDK9	Protein	nuclear	binds to 					Tat protein	Protein	wild-type;HIV-1			NULL		0	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
80894	6	3580	11	NULL	NULL	NULL	NULL	CDK9	Protein	nuclear	binds to 					Tat protein	Protein	wild-type;;HIV-2			NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
80895	7	3580	11	NULL	NULL	0	NULL	CDK9	Protein	nuclear	binds to 					Tat protein	Protein	HIV-1	activation domain mutant		NULL		0	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
80896	8	3580	11	NULL	NULL	NULL	NULL	CDK9	Protein	nuclear	binds to 					Tat protein	Protein	HIV-2	activation domain mutant		NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_104	9491887	(B) Analysis of the binding of nuclear cyclin T and CDK9  to wild-type and activation domain mutant HIV-1 and HIV-2 Tat proteins.	bind
8116	1	3582	6	11	NULL	NULL	NULL	GST-PBD	GP		bind					small G proteins	GP	transfected			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_971_s_234	11238453	(B) Analysis of the effects of PSGAP on GST-PBD or GST-RBD binding to transfected small G proteins.	bind
8117	2	3582	6	11	NULL	NULL	NULL	GST-RBD	GP		bind					small G proteins	GP	transfected			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_971_s_234	11238453	(B) Analysis of the effects of PSGAP on GST-PBD or GST-RBD binding to transfected small G proteins.	bind
11299	1	3582	7	11	NULL	NULL	NULL	GST-PBD	GP		bind					small G protein	GP	transfected			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_971_s_234	11238453	(B) Analysis of the effects of PSGAP on GST-PBD or GST-RBD binding to transfected small G proteins.	bind
11301	2	3582	7	11	NULL	NULL	NULL	GST-RBD	GP		bind					small G protein	GP	transfected			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_971_s_234	11238453	(B) Analysis of the effects of PSGAP on GST-PBD or GST-RBD binding to transfected small G proteins.	bind
80897	1	3582	11	NULL	NULL	0	NULL	GST-PBD	Protein		binds to 					small G protein	Protein	transfected			NULL		0	NULL	NULL	NULL	gw60_cellbiol_152_5_971_s_234	11238453	(B) Analysis of the effects of PSGAP on GST-PBD or GST-RBD binding to transfected small G proteins.	bind
80898	2	3582	11	NULL	NULL	0	NULL	GST-RBD	Protein		binds to 					small G protein	Protein	transfected			NULL		0	NULL	NULL	NULL	gw60_cellbiol_152_5_971_s_234	11238453	(B) Analysis of the effects of PSGAP on GST-PBD or GST-RBD binding to transfected small G proteins.	bind
8118	1	3583	6	11	NULL	NULL	NULL	Bm	GP		bind					BLMA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2311_s_292	11706014	(B) and the type II'' beta-turn from Arg43A to Ile46A exhibit large conformational changes due to the binding of Bm to BLMA (Fig.  5,  a and  b).	bind
8119	2	3583	6	11	NULL	NULL	NULL	statement 1	Process		changes					Arg43A	AminoAcid	conformation of 	type II'' beta-turn		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2311_s_292	11706014	(B) and the type II'' beta-turn from Arg43A to Ile46A exhibit large conformational changes due to the binding of Bm to BLMA (Fig.  5,  a and  b).	bind
8120	3	3583	6	11	NULL	NULL	NULL	statement 1	Process		changes					Ile46A	AminoAcid	conformation of 	type II'' beta-turn		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2311_s_292	11706014	(B) and the type II'' beta-turn from Arg43A to Ile46A exhibit large conformational changes due to the binding of Bm to BLMA (Fig.  5,  a and  b).	bind
11307	1	3583	7	11	NULL	NULL	NULL	Bm	GP		bind					BLMA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2311_s_292	11706014	(B) and the type II'' beta-turn from Arg43A to Ile46A exhibit large conformational changes due to the binding of Bm to BLMA (Fig.  5,  a and  b).	bind
11313	2	3583	7	11	NULL	NULL	NULL	statement 1	Process		change					type II'' beta-turn	AminoAcid	conformation of	Arg43A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2311_s_292	11706014	(B) and the type II'' beta-turn from Arg43A to Ile46A exhibit large conformational changes due to the binding of Bm to BLMA (Fig.  5,  a and  b).	bind
15047	3	3583	7	11	NULL	NULL	NULL	statement 1	Process		change					type II'' beta-turn	AminoAcid	conformation of	Ile46A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2311_s_292	11706014	(B) and the type II'' beta-turn from Arg43A to Ile46A exhibit large conformational changes due to the binding of Bm to BLMA (Fig.  5,  a and  b).	bind
80899	1	3583	11	NULL	NULL	0	NULL	Bm	Chemical		binds to 					BLMA	Protein				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2311_s_292	11706014	(B) and the type II'' beta-turn from Arg43A to Ile46A exhibit large conformational changes due to the binding of Bm to BLMA (Fig.  5,  a and  b).	bind
8121	1	3584	6	11	NULL	NULL	NULL	p53	GP		bind					p300	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_361	16267266	(b) Another effect of ATM-induced p53 phosphorylation  is to stimulate the binding of p53 to p300 (which probably competes with Mdm2 for  p53 binding).	bind
8122	2	3584	6	11	NULL	NULL	NULL	ATM	GP		induces					p53	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_361	16267266	(b) Another effect of ATM-induced p53 phosphorylation  is to stimulate the binding of p53 to p300 (which probably competes with Mdm2 for  p53 binding).	bind
8123	3	3584	6	11	NULL	NULL	NULL	statement 2	Process		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_361	16267266	(b) Another effect of ATM-induced p53 phosphorylation  is to stimulate the binding of p53 to p300 (which probably competes with Mdm2 for  p53 binding).	bind
8124	4	3584	6	11	NULL	NULL	NULL	Mdm2	GP		bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_361	16267266	(b) Another effect of ATM-induced p53 phosphorylation  is to stimulate the binding of p53 to p300 (which probably competes with Mdm2 for  p53 binding).	bind
8125	5	3584	6	11	NULL	NULL	NULL	statement 1	Process		competes with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_361	16267266	(b) Another effect of ATM-induced p53 phosphorylation  is to stimulate the binding of p53 to p300 (which probably competes with Mdm2 for  p53 binding).	bind
11317	1	3584	7	11	NULL	NULL	NULL	 p53	GP		bind					p300	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_361	16267266	(b) Another effect of ATM-induced p53 phosphorylation  is to stimulate the binding of p53 to p300 (which probably competes with Mdm2 for  p53 binding).	bind
11319	2	3584	7	11	NULL	NULL	NULL	ATM	GP		induce					p53	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_361	16267266	(b) Another effect of ATM-induced p53 phosphorylation  is to stimulate the binding of p53 to p300 (which probably competes with Mdm2 for  p53 binding).	bind
11321	3	3584	7	11	NULL	NULL	NULL	statement 2	Process		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_361	16267266	(b) Another effect of ATM-induced p53 phosphorylation  is to stimulate the binding of p53 to p300 (which probably competes with Mdm2 for  p53 binding).	bind
11322	4	3584	7	11	NULL	NULL	NULL	Mdm2	GP		bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_361	16267266	(b) Another effect of ATM-induced p53 phosphorylation  is to stimulate the binding of p53 to p300 (which probably competes with Mdm2 for  p53 binding).	bind
11325	5	3584	7	11	NULL	NULL	NULL	statement 1	Process		compete with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_361	16267266	(b) Another effect of ATM-induced p53 phosphorylation  is to stimulate the binding of p53 to p300 (which probably competes with Mdm2 for  p53 binding).	bind
80903	1	3584	11	NULL	NULL	0	NULL	ATM	Protein		phosphorylate					p53	Protein				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_361	16267266	(b) Another effect of ATM-induced p53 phosphorylation  is to stimulate the binding of p53 to p300 (which probably competes with Mdm2 for  p53 binding).	bind
80904	2	3584	11	NULL	NULL	0	NULL	p53	Protein		binds to 					p300	Protein				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_361	16267266	(b) Another effect of ATM-induced p53 phosphorylation  is to stimulate the binding of p53 to p300 (which probably competes with Mdm2 for  p53 binding).	bind
80905	3	3584	11	NULL	NULL	0	NULL	statement 1	Process		stimulates					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_361	16267266	(b) Another effect of ATM-induced p53 phosphorylation  is to stimulate the binding of p53 to p300 (which probably competes with Mdm2 for  p53 binding).	bind
80906	4	3584	11	NULL	NULL	0	NULL	Mdm2	Protein		binds to 					p53	Protein				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_361	16267266	(b) Another effect of ATM-induced p53 phosphorylation  is to stimulate the binding of p53 to p300 (which probably competes with Mdm2 for  p53 binding).	bind
80907	5	3584	11	NULL	NULL	0	NULL	statement 2	Process		competes with					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_1_s_361	16267266	(b) Another effect of ATM-induced p53 phosphorylation  is to stimulate the binding of p53 to p300 (which probably competes with Mdm2 for  p53 binding).	bind
8126	1	3585	6	11	NULL	NULL	NULL	transactivator	GP	positive	bind					P2 sequence	NucleicAcid				NULL	BCL1 nuclear extract	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_284_s_252	9858552	(B) Anti-CDP pre- and postincubation using 1 mug of a nuclear extract from a B-cell line (BCL1) that lacks NF-muNR but contains a positive transactivator (Bright) that binds the same P2 sequence.	bind
8127	2	3585	6	11	NULL	NULL	NULL	BCL1	GP		is a type of					B-cell line	Cell				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_284_s_252	9858552	(B) Anti-CDP pre- and postincubation using 1 mug of a nuclear extract from a B-cell line (BCL1) that lacks NF-muNR but contains a positive transactivator (Bright) that binds the same P2 sequence.	bind
11329	1	3585	7	11	NULL	NULL	NULL	transactivator	GP	positive	bind					P2 sequence	NucleicAcid				NULL	BCL1 nuclear extract	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_284_s_252	9858552	(B) Anti-CDP pre- and postincubation using 1 mug of a nuclear extract from a B-cell line (BCL1) that lacks NF-muNR but contains a positive transactivator (Bright) that binds the same P2 sequence.	bind
44766	2	3585	7	11	NULL	NULL	NULL	BCL1	GP		is a type of					B-cell line	Cell				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_284_s_252	9858552	(B) Anti-CDP pre- and postincubation using 1 mug of a nuclear extract from a B-cell line (BCL1) that lacks NF-muNR but contains a positive transactivator (Bright) that binds the same P2 sequence.	bind
80908	1	3585	11	NULL	NULL	0	NULL	positive transactivator	GeneOrProtein		binds to 					P2 sequence	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_284_s_252	9858552	(B) Anti-CDP pre- and postincubation using 1 mug of a nuclear extract from a B-cell line (BCL1) that lacks NF-muNR but contains a positive transactivator (Bright) that binds the same P2 sequence.	bind
8128	1	3588	6	11	NULL	NULL	NULL	Anti-mCD100 	GP		bind		specifically			CD100-CHO cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_5_621_s_54	11114375	(B) Anti-mCD100 mAb binds specifically to CD100-CHO cells.	bind
40784	2	3588	6	11	NULL	NULL	NULL	Anti-mCD100	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_5_621_s_54	11114375	(B) Anti-mCD100 mAb binds specifically to CD100-CHO cells.	bind
11762	1	3588	7	11	NULL	NULL	NULL	Anti-mCD100 mAb	GP		bind		specifically			CD100-CHO cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_5_621_s_54	11114375	(B) Anti-mCD100 mAb binds specifically to CD100-CHO cells.	bind
44767	2	3588	7	11	NULL	NULL	NULL	Anti-mCD100	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_5_621_s_54	11114375	(B) Anti-mCD100 mAb binds specifically to CD100-CHO cells.	bind
80909	1	3588	11	NULL	NULL	0	NULL	Anti-mCD100 mAb	PartOfProtein		binds to 		specifically			CD100-CHO cells	Cell				NULL		0	NULL	NULL	NULL	gw60_immunity_13_5_621_s_54	11114375	(B) Anti-mCD100 mAb binds specifically to CD100-CHO cells.	bind
8129	1	3589	6	11	NULL	NULL	NULL	myosin-Va	GP		bind					syntaxin-1A	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_281	16030255	(B) Anti-myosin-V neck antiserum inhibits the binding of myosin-Va by syntaxin-1A.	bind
8130	2	3589	6	11	NULL	NULL	NULL	Anti-myosin-V	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_281	16030255	(B) Anti-myosin-V neck antiserum inhibits the binding of myosin-Va by syntaxin-1A.	bind
40785	3	3589	6	11	NULL	NULL	NULL	Anti-myosin-V	GP		is a type of					neck antiserum	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_281	16030255	(B) Anti-myosin-V neck antiserum inhibits the binding of myosin-Va by syntaxin-1A.	bind
11763	1	3589	7	11	NULL	NULL	NULL	myosin-Va	GP		bind					syntaxin-1A	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_281	16030255	(B) Anti-myosin-V neck antiserum inhibits the binding of myosin-Va by syntaxin-1A.	bind
11764	2	3589	7	11	NULL	NULL	NULL	Anti-myosin-V 	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_281	16030255	(B) Anti-myosin-V neck antiserum inhibits the binding of myosin-Va by syntaxin-1A.	bind
44769	3	3589	7	11	NULL	NULL	NULL	Anti-myosin-V	GP		is a type of					neck antiserum	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_281	16030255	(B) Anti-myosin-V neck antiserum inhibits the binding of myosin-Va by syntaxin-1A.	bind
80910	1	3589	11	NULL	NULL	0	NULL	myosin-Va	Protein		binds to 					syntaxin-1A	Protein				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_281	16030255	(B) Anti-myosin-V neck antiserum inhibits the binding of myosin-Va by syntaxin-1A.	bind
80911	2	3589	11	NULL	NULL	0	NULL	Anti-myosin-V	PartOfProtein	neck antiserum	inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_281	16030255	(B) Anti-myosin-V neck antiserum inhibits the binding of myosin-Va by syntaxin-1A.	bind
8131	1	3590	6	11	NULL	NULL	NULL	Asf1p	GP		bind					Cac2p	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_2_614_s_214	11756556	(B) Asf1p binds Cac2p in vitro.	bind
11765	1	3590	7	11	NULL	NULL	NULL	Asf1p	GP		binds					Cac2p	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_2_614_s_214	11756556	(B) Asf1p binds Cac2p in vitro.	bind
80912	1	3590	11	NULL	NULL	0	NULL	Asf1p	Protein		binds to 					Cac2p	Protein				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_22_2_614_s_214	11756556	(B) Asf1p binds Cac2p in vitro.	bind
8132	1	3591	6	11	NULL	NULL	NULL	GST-myogenin	GP		bind					MEF-1 oligodeoxynucleotide	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_1074_s_278	9448005	(B) Assays involving the binding of GST-myogenin fusion protein to the MEF-1 oligodeoxynucleotide.	bind
40787	2	3591	6	11	NULL	NULL	NULL	GST-myogenin	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_1074_s_278	9448005	(B) Assays involving the binding of GST-myogenin fusion protein to the MEF-1 oligodeoxynucleotide.	bind
11766	1	3591	7	11	NULL	NULL	NULL	GST-myogenin	GP		binds					MEF-1 oligodeoxynucleotide	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_1074_s_278	9448005	(B) Assays involving the binding of GST-myogenin fusion protein to the MEF-1 oligodeoxynucleotide.	bind
80913	1	3591	11	NULL	NULL	0	NULL	GST-myogenin fusion protein	Protein		binds to 					MEF-1 oligodeoxynucleotide	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_2_1074_s_278	9448005	(B) Assays involving the binding of GST-myogenin fusion protein to the MEF-1 oligodeoxynucleotide.	bind
80914	1	3592	11	NULL	NULL	0	NULL	TRAF4	Protein	knockdown	phosphorylate		serine			p47phox	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_6_2320_s_258	15743827	(B) Assessment of serine  phosphorylation of p47phox after knockdown of TRAF4.	bind
8133	1	3593	6	11	NULL	NULL	NULL	PAK4	GP	endogenous	bind					integrin beta5	GP		membrane-proximal region within cytoplasmic domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_158_7_1287_s_75	12356872	(B) Association of endogenous PAK4 with the membrane-proximal region within integrin beta5 cytoplasmic domain was examined by a GST pull-down assay, including GST fused to a beta5 deletion mutant lacking the PAK4-binding region mapped by yeast two-hybrid analysis.	bind
11768	1	3593	7	11	NULL	NULL	NULL	PAK4	GP	endogenous	bind					integrin beta5 	GP		membrane-proximal region within cytoplasmic domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_158_7_1287_s_75	12356872	(B) Association of endogenous PAK4 with the membrane-proximal region within integrin beta5 cytoplasmic domain was examined by a GST pull-down assay, including GST fused to a beta5 deletion mutant lacking the PAK4-binding region mapped by yeast two-hybrid analysis.	bind
80915	1	3593	11	NULL	NULL	NULL	NULL	PAK4	Protein	endogenous	associated with					integrin beta5	Protein	membrane-proximal region	cytoplasmic domain		NULL	GST pull-down assay	NULL	NULL	NULL	NULL	gw60_cellbiol_158_7_1287_s_75	12356872	(B) Association of endogenous PAK4 with the membrane-proximal region within integrin beta5 cytoplasmic domain was examined by a GST pull-down assay, including GST fused to a beta5 deletion mutant lacking the PAK4-binding region mapped by yeast two-hybrid analysis.	bind
80916	2	3593	11	NULL	NULL	0	NULL	GST	Protein		fused to					beta5 deletion mutant	Protein	lacking the PAK4-binding region			NULL	yeast two-hybrid analysis	0	NULL	NULL	NULL	gw60_cellbiol_158_7_1287_s_75	12356872	(B) Association of endogenous PAK4 with the membrane-proximal region within integrin beta5 cytoplasmic domain was examined by a GST pull-down assay, including GST fused to a beta5 deletion mutant lacking the PAK4-binding region mapped by yeast two-hybrid analysis.	bind
8134	1	3594	6	11	NULL	NULL	NULL	p85alpha subunit	GP		bind					p110alpha	GP				NULL	NIH 3T3 cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7119_s_144	9819398	(B) Association of p85alpha subunit with p110alpha and p110beta in NIH 3T3 cells.	bind
8135	2	3594	6	11	NULL	NULL	NULL	p85alpha subunit	GP		bind					p110beta	GP				NULL	NIH 3T3 cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7119_s_144	9819398	(B) Association of p85alpha subunit with p110alpha and p110beta in NIH 3T3 cells.	bind
11769	1	3594	7	11	NULL	NULL	NULL	p85 alpha subunit	GP		bind					p110alpha	GP				NULL	NIH 3T3 cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7119_s_144	9819398	(B) Association of p85alpha subunit with p110alpha and p110beta in NIH 3T3 cells.	bind
11770	2	3594	7	11	NULL	NULL	NULL	p85 alpha subunit	GP		bind					p110beta	GP				NULL	NIH 3T3 cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7119_s_144	9819398	(B) Association of p85alpha subunit with p110alpha and p110beta in NIH 3T3 cells.	bind
80917	1	3594	11	NULL	NULL	NULL	NULL	p85alpha	Protein		associated with					 p110alpha	Protein				NULL	in NIH 3T3 cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7119_s_144	9819398	(B) Association of p85alpha subunit with p110alpha and p110beta in NIH 3T3 cells.	bind
80918	2	3594	11	NULL	NULL	0	NULL	p85alpha	Protein		associated with					p110beta	Protein				NULL	in NIH 3T3 cells	0	NULL	NULL	NULL	gw60_molcellbiol_18_12_7119_s_144	9819398	(B) Association of p85alpha subunit with p110alpha and p110beta in NIH 3T3 cells.	bind
8136	1	3595	6	11	NULL	NULL	NULL	Stat3	GP		associates with					Etk	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2043_s_174	10688651	(B) Association of STAT3 with Etk or its deletion mutants.	bind
8137	2	3595	6	11	NULL	NULL	NULL	Stat3	GP		associates with					Etk	GP	deletion mutants			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2043_s_174	10688651	(B) Association of STAT3 with Etk or its deletion mutants.	bind
8138	3	3595	6	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2043_s_174	10688651	(B) Association of STAT3 with Etk or its deletion mutants.	bind
11771	1	3595	7	11	NULL	NULL	NULL	STAT3	GP		associates with					Etk	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2043_s_174	10688651	(B) Association of STAT3 with Etk or its deletion mutants.	bind
11772	2	3595	7	11	NULL	NULL	NULL	STAT3	GP		associates with					Etk	GP	deletion mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2043_s_174	10688651	(B) Association of STAT3 with Etk or its deletion mutants.	bind
15048	3	3595	7	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2043_s_174	10688651	(B) Association of STAT3 with Etk or its deletion mutants.	bind
80919	1	3595	11	NULL	NULL	0	NULL	STAT3	Protein		associated with					 Etk 	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_6_2043_s_174	10688651	(B) Association of STAT3 with Etk or its deletion mutants.	bind
80920	2	3595	11	NULL	NULL	0	NULL	STAT3	Protein		associated with					Etk	Protein	deletion mutant			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_6_2043_s_174	10688651	(B) Association of STAT3 with Etk or its deletion mutants.	bind
80921	3	3595	11	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_6_2043_s_174	10688651	(B) Association of STAT3 with Etk or its deletion mutants.	bind
8139	1	3596	6	11	NULL	NULL	NULL	ATP	Chemical		bind					TAP1	GP				NULL	wild type transporter	NULL	NULL	NULL	NULL	gw60_currbiol_11_4_242_s_67	11250152	(b) ATP binding capacity of TAP1 and TAP2 in wild-type transporter.	bind
8140	2	3596	6	11	NULL	NULL	NULL	ATP	Chemical		bind					TAP2	GP				NULL	wild type transporter	NULL	NULL	NULL	NULL	gw60_currbiol_11_4_242_s_67	11250152	(b) ATP binding capacity of TAP1 and TAP2 in wild-type transporter.	bind
11773	1	3596	7	11	NULL	NULL	NULL	TAP1	GP		bind					ATP	Chemical				NULL	wild-type transporter	NULL	NULL	NULL	NULL	gw60_currbiol_11_4_242_s_67	11250152	(b) ATP binding capacity of TAP1 and TAP2 in wild-type transporter.	bind
11774	2	3596	7	11	NULL	NULL	NULL	TAP2	GP		bind					ATP	Chemical				NULL	wild-type transporter	NULL	NULL	NULL	NULL	gw60_currbiol_11_4_242_s_67	11250152	(b) ATP binding capacity of TAP1 and TAP2 in wild-type transporter.	bind
80922	1	3596	11	NULL	NULL	0	NULL	ATP	Chemical		binds to 					TAP1	Protein	in wild-type transporter			NULL		0	NULL	NULL	NULL	gw60_currbiol_11_4_242_s_67	11250152	(b) ATP binding capacity of TAP1 and TAP2 in wild-type transporter.	bind
80923	2	3596	11	NULL	NULL	0	NULL	ATP	Protein		binds to 					TAP2	Protein	in wild-type transporter			NULL		0	NULL	NULL	NULL	gw60_currbiol_11_4_242_s_67	11250152	(b) ATP binding capacity of TAP1 and TAP2 in wild-type transporter.	bind
8141	1	3598	6	11	NULL	NULL	NULL	ATP	Chemical		bind					GroEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_869_s_29	11779463	(b) ATP binding to GroEL alters  its conformation, weakens the binding of substrate, and permits  the binding of GroES to the ATP-bound  ring.	bind
8142	2	3598	6	11	NULL	NULL	NULL	statement 1	Process		alters					GroEL	GP	conformation of 			NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_869_s_29	11779463	(b) ATP binding to GroEL alters  its conformation, weakens the binding of substrate, and permits  the binding of GroES to the ATP-bound  ring.	bind
8143	3	3598	6	11	NULL	NULL	NULL	statement 1	Process		weakens					substrate	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_869_s_29	11779463	(b) ATP binding to GroEL alters  its conformation, weakens the binding of substrate, and permits  the binding of GroES to the ATP-bound  ring.	bind
8144	4	3598	6	11	NULL	NULL	NULL	ATP	Chemical		bind					ring	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_869_s_29	11779463	(b) ATP binding to GroEL alters  its conformation, weakens the binding of substrate, and permits  the binding of GroES to the ATP-bound  ring.	bind
8145	5	3598	6	11	NULL	NULL	NULL	GroES	GP		bind					statement 4	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_869_s_29	11779463	(b) ATP binding to GroEL alters  its conformation, weakens the binding of substrate, and permits  the binding of GroES to the ATP-bound  ring.	bind
8146	6	3598	6	11	NULL	NULL	NULL	statement 1	Process		permits					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_869_s_29	11779463	(b) ATP binding to GroEL alters  its conformation, weakens the binding of substrate, and permits  the binding of GroES to the ATP-bound  ring.	bind
11775	1	3598	7	11	NULL	NULL	NULL	ATP	Chemical		binds to					GroEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_869_s_29	11779463	(b) ATP binding to GroEL alters  its conformation, weakens the binding of substrate, and permits  the binding of GroES to the ATP-bound  ring.	bind
11776	2	3598	7	11	NULL	NULL	NULL	statement 1	Process		alters					GroEL	GP	conformation of			NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_869_s_29	11779463	(b) ATP binding to GroEL alters  its conformation, weakens the binding of substrate, and permits  the binding of GroES to the ATP-bound  ring.	bind
11777	3	3598	7	11	NULL	NULL	NULL	statement 1	Process		weakens 					substrate	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_869_s_29	11779463	(b) ATP binding to GroEL alters  its conformation, weakens the binding of substrate, and permits  the binding of GroES to the ATP-bound  ring.	bind
11778	4	3598	7	11	NULL	NULL	NULL	GroES	GP		bind					statement 6	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_869_s_29	11779463	(b) ATP binding to GroEL alters  its conformation, weakens the binding of substrate, and permits  the binding of GroES to the ATP-bound  ring.	bind
11779	5	3598	7	11	NULL	NULL	NULL	statement 1	Process		permits					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_869_s_29	11779463	(b) ATP binding to GroEL alters  its conformation, weakens the binding of substrate, and permits  the binding of GroES to the ATP-bound  ring.	bind
52995	6	3598	7	11	NULL	NULL	NULL	ATP	Chemical		bind					ring	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_869_s_29	11779463	(b) ATP binding to GroEL alters  its conformation, weakens the binding of substrate, and permits  the binding of GroES to the ATP-bound  ring.	bind
80924	1	3598	11	NULL	NULL	0	NULL	ATP	Chemical		binds to 					GroEL	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_107_7_869_s_29	11779463	(b) ATP binding to GroEL alters  its conformation, weakens the binding of substrate, and permits  the binding of GroES to the ATP-bound  ring.	bind
80925	2	3598	11	NULL	NULL	0	NULL	statement 1	Process		alters					conformation	Process	GroEL			NULL		0	NULL	NULL	NULL	gw60_cell_107_7_869_s_29	11779463	(b) ATP binding to GroEL alters  its conformation, weakens the binding of substrate, and permits  the binding of GroES to the ATP-bound  ring.	bind
80926	3	3598	11	NULL	NULL	0	NULL	statement 1	Process		weakens					binding	BiologicalProcess	substrate			NULL		0	NULL	NULL	NULL	gw60_cell_107_7_869_s_29	11779463	(b) ATP binding to GroEL alters  its conformation, weakens the binding of substrate, and permits  the binding of GroES to the ATP-bound  ring.	bind
80927	4	3598	11	NULL	NULL	0	NULL	GroES 	Protein		binds to 					ATP-bound ring	Chemical				NULL		0	NULL	NULL	NULL	gw60_cell_107_7_869_s_29	11779463	(b) ATP binding to GroEL alters  its conformation, weakens the binding of substrate, and permits  the binding of GroES to the ATP-bound  ring.	bind
80928	5	3598	11	NULL	NULL	0	NULL	statement 1	Process		permits					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_cell_107_7_869_s_29	11779463	(b) ATP binding to GroEL alters  its conformation, weakens the binding of substrate, and permits  the binding of GroES to the ATP-bound  ring.	bind
80929	1	3599	11	NULL	NULL	0	NULL	HisP	Protein	binding pocket	binds to 					ATP	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1561_1_47_s_82	11988180	(B) ATP-binding pocket of HisP.	bind
8154	1	3602	6	11	NULL	NULL	NULL	Dam1p	GP	in vitro-translated	bind					Ndc80 complex-associated beads	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3342_s_230	12925767	(B) Bar graph shows the percentage of IVT  Dam1p bound to Ndc80 complex-associated beads.	bind
11781	1	3602	7	11	NULL	NULL	NULL	Dam1p	GP	in vitro-translated	bind					Ndc80 complex-associated beads	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3342_s_230	12925767	(B) Bar graph shows the percentage of IVT  Dam1p bound to Ndc80 complex-associated beads.	bind
80930	1	3602	11	NULL	NULL	0	NULL	Ndc80 complex	Protein		associated with					beads	Chemical				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_8_3342_s_230	12925767	(B) Bar graph shows the percentage of IVT  Dam1p bound to Ndc80 complex-associated beads.	bind
80931	2	3602	11	NULL	NULL	0	NULL	Dam1p	Protein	IVT	binds to 					statement 1	Chemical				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_8_3342_s_230	12925767	(B) Bar graph shows the percentage of IVT  Dam1p bound to Ndc80 complex-associated beads.	bind
8155	1	3603	6	11	NULL	NULL	NULL	PP1	GP		bind		weakly			Cdc25	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_4_1779_s_263	16467385	(B) Based on data presented here, we speculate that PP1 binds  weakly to Cdc25 and inefficient dephosphorylation of S287 is allowed after 14-3-3  removal.	bind
11782	1	3603	7	11	NULL	NULL	NULL	PP1	GP		binds		weakly			Cdc25	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_4_1779_s_263	16467385	(B) Based on data presented here, we speculate that PP1 binds  weakly to Cdc25 and inefficient dephosphorylation of S287 is allowed after 14-3-3  removal.	bind
80932	1	3603	11	NULL	NULL	0	NULL	PP1	Protein		binds to 		weakly			Cdc25	Protein				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_4_1779_s_263	16467385	(B) Based on data presented here, we speculate that PP1 binds  weakly to Cdc25 and inefficient dephosphorylation of S287 is allowed after 14-3-3  removal.	bind
80933	2	3603	11	NULL	NULL	0	NULL	14-3-3	Protein		removed from					Cdc25	Protein				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_4_1779_s_263	16467385	(B) Based on data presented here, we speculate that PP1 binds  weakly to Cdc25 and inefficient dephosphorylation of S287 is allowed after 14-3-3  removal.	bind
80934	3	3603	11	NULL	NULL	0	NULL	PP1	Protein		dephosphorylate		inefficiently			S287	Protein				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_4_1779_s_263	16467385	(B) Based on data presented here, we speculate that PP1 binds  weakly to Cdc25 and inefficient dephosphorylation of S287 is allowed after 14-3-3  removal.	bind
80935	4	3603	11	NULL	NULL	0	NULL	statement 3	Process		occurs after					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_4_1779_s_263	16467385	(B) Based on data presented here, we speculate that PP1 binds  weakly to Cdc25 and inefficient dephosphorylation of S287 is allowed after 14-3-3  removal.	bind
80936	1	3604	11	NULL	NULL	0	NULL	beta-galactosidase	Protein		is					beta-gal	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7214_s_92	10982838	(B) beta-Galactosidase activity of  sec61-2 mutant cells carrying plasmids expressing beta-galactosidase (beta-gal), the beta-galactosidase-SL17 fusion protein (beta-gal-SL17) ( 11), or beta-galactosidase with an N-terminal lysine residue (K-beta-gal) ( 2) at permissive and nonpermissive temperatures.	bind
80937	2	3604	11	NULL	NULL	0	NULL	beta-gal-SL17	Protein		is					beta-galactosidase-SL17 fusion protein	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7214_s_92	10982838	(B) beta-Galactosidase activity of  sec61-2 mutant cells carrying plasmids expressing beta-galactosidase (beta-gal), the beta-galactosidase-SL17 fusion protein (beta-gal-SL17) ( 11), or beta-galactosidase with an N-terminal lysine residue (K-beta-gal) ( 2) at permissive and nonpermissive temperatures.	bind
80938	3	3604	11	NULL	NULL	0	NULL	beta-galactosidase	Protein		is			N-terminal lysine residue		K-beta-gal	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7214_s_92	10982838	(B) beta-Galactosidase activity of  sec61-2 mutant cells carrying plasmids expressing beta-galactosidase (beta-gal), the beta-galactosidase-SL17 fusion protein (beta-gal-SL17) ( 11), or beta-galactosidase with an N-terminal lysine residue (K-beta-gal) ( 2) at permissive and nonpermissive temperatures.	bind
80939	4	3604	11	NULL	NULL	0	NULL	sec61-2 mutant cells	cell		carrying					plasmid	NucleicAcidSubstance	beta-galactosidase			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7214_s_92	10982838	(B) beta-Galactosidase activity of  sec61-2 mutant cells carrying plasmids expressing beta-galactosidase (beta-gal), the beta-galactosidase-SL17 fusion protein (beta-gal-SL17) ( 11), or beta-galactosidase with an N-terminal lysine residue (K-beta-gal) ( 2) at permissive and nonpermissive temperatures.	bind
80940	5	3604	11	NULL	NULL	0	NULL	sec61-2 mutant cells	cell		carrying					plasmid	NucleicAcidSubstance	beta-galactosidase-SL17 fusion protein			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7214_s_92	10982838	(B) beta-Galactosidase activity of  sec61-2 mutant cells carrying plasmids expressing beta-galactosidase (beta-gal), the beta-galactosidase-SL17 fusion protein (beta-gal-SL17) ( 11), or beta-galactosidase with an N-terminal lysine residue (K-beta-gal) ( 2) at permissive and nonpermissive temperatures.	bind
80941	6	3604	11	NULL	NULL	0	NULL	sec61-2 mutant cells	cell		carrying					plasmid	NucleicAcidSubstance	K-beta-gal			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7214_s_92	10982838	(B) beta-Galactosidase activity of  sec61-2 mutant cells carrying plasmids expressing beta-galactosidase (beta-gal), the beta-galactosidase-SL17 fusion protein (beta-gal-SL17) ( 11), or beta-galactosidase with an N-terminal lysine residue (K-beta-gal) ( 2) at permissive and nonpermissive temperatures.	bind
8156	1	3605	6	11	NULL	NULL	NULL	 3[H]QNB	Chemical		bind					mAChR	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_950_1_10_s_179	12231224	(B) Bilirubin protects 3[H]QNB binding to the mAChR from inhibition by 2  M heme and 100  M hydrogen peroxide.	bind
8157	2	3605	6	11	NULL	NULL	NULL	heme	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brainres_950_1_10_s_179	12231224	(B) Bilirubin protects 3[H]QNB binding to the mAChR from inhibition by 2  M heme and 100  M hydrogen peroxide.	bind
8158	3	3605	6	11	NULL	NULL	NULL	hydrogen peroxide	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brainres_950_1_10_s_179	12231224	(B) Bilirubin protects 3[H]QNB binding to the mAChR from inhibition by 2  M heme and 100  M hydrogen peroxide.	bind
8159	4	3605	6	11	NULL	NULL	NULL	Bilirubin	Chemical		protects					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_brainres_950_1_10_s_179	12231224	(B) Bilirubin protects 3[H]QNB binding to the mAChR from inhibition by 2  M heme and 100  M hydrogen peroxide.	bind
8160	5	3605	6	11	NULL	NULL	NULL	Bilirubin	Chemical		protects					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_brainres_950_1_10_s_179	12231224	(B) Bilirubin protects 3[H]QNB binding to the mAChR from inhibition by 2  M heme and 100  M hydrogen peroxide.	bind
11795	1	3605	7	11	NULL	NULL	NULL	3[H]QNB	Chemical		bind					mAChR	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_950_1_10_s_179	12231224	(B) Bilirubin protects 3[H]QNB binding to the mAChR from inhibition by 2  M heme and 100  M hydrogen peroxide.	bind
11796	2	3605	7	11	NULL	NULL	NULL	statement 1	Process		is inhibited by					heme	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_brainres_950_1_10_s_179	12231224	(B) Bilirubin protects 3[H]QNB binding to the mAChR from inhibition by 2  M heme and 100  M hydrogen peroxide.	bind
11797	3	3605	7	11	NULL	NULL	NULL	statement 1	Process		is inhibited by					hydrogen peroxide	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_brainres_950_1_10_s_179	12231224	(B) Bilirubin protects 3[H]QNB binding to the mAChR from inhibition by 2  M heme and 100  M hydrogen peroxide.	bind
11798	4	3605	7	11	NULL	NULL	NULL	Bilirubin	Chemical		protects					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_brainres_950_1_10_s_179	12231224	(B) Bilirubin protects 3[H]QNB binding to the mAChR from inhibition by 2  M heme and 100  M hydrogen peroxide.	bind
11799	5	3605	7	11	NULL	NULL	NULL	Bilirubin	Chemical		protects					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_brainres_950_1_10_s_179	12231224	(B) Bilirubin protects 3[H]QNB binding to the mAChR from inhibition by 2  M heme and 100  M hydrogen peroxide.	bind
80942	1	3605	11	NULL	NULL	0	NULL	3[H]QNB	Chemical		binds to 					mAChR	Protein				NULL		0	NULL	NULL	NULL	gw60_brainres_950_1_10_s_179	12231224	(B) Bilirubin protects 3[H]QNB binding to the mAChR from inhibition by 2  M heme and 100  M hydrogen peroxide.	bind
80943	2	3605	11	NULL	NULL	0	NULL	heme	Protein		inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_brainres_950_1_10_s_179	12231224	(B) Bilirubin protects 3[H]QNB binding to the mAChR from inhibition by 2  M heme and 100  M hydrogen peroxide.	bind
80944	3	3605	11	NULL	NULL	0	NULL	hydrogen peroxide	Chemical		inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_brainres_950_1_10_s_179	12231224	(B) Bilirubin protects 3[H]QNB binding to the mAChR from inhibition by 2  M heme and 100  M hydrogen peroxide.	bind
80945	4	3605	11	NULL	NULL	0	NULL	Bilirubin	Chemical		prevents					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_brainres_950_1_10_s_179	12231224	(B) Bilirubin protects 3[H]QNB binding to the mAChR from inhibition by 2  M heme and 100  M hydrogen peroxide.	bind
80946	5	3605	11	NULL	NULL	0	NULL	Bilirubin	Chemical		prevents					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_brainres_950_1_10_s_179	12231224	(B) Bilirubin protects 3[H]QNB binding to the mAChR from inhibition by 2  M heme and 100  M hydrogen peroxide.	bind
8161	1	3607	6	11	NULL	NULL	NULL	peptide ligands	GP		bind					Mena	GP		EVH1 domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_97_4_471_s_63	10338211	(B) Binding affinities of  peptide ligands to Mena EVH1 domain measured by fluorescence perturbation. '''	bind
11801	1	3607	7	11	NULL	NULL	NULL	peptide ligands	GP		bind					Mena	GP		EVH1		NULL		NULL	NULL	NULL	NULL	gw60_cell_97_4_471_s_63	10338211	(B) Binding affinities of  peptide ligands to Mena EVH1 domain measured by fluorescence perturbation. '''	bind
80947	1	3607	11	NULL	NULL	0	NULL	peptide ligands	Chemical		binds to 					Mena EVH1 domain	PartOfProtein				NULL	fluorescence perturbation	0	NULL	NULL	NULL	gw60_cell_97_4_471_s_63	10338211	(B) Binding affinities of  peptide ligands to Mena EVH1 domain measured by fluorescence perturbation. '''	bind
40847	1	3608	6	11	NULL	NULL	NULL	Rab9	GP		bind					TIP47	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5420_s_259	15456905	(B) Binding affinity of Rab9 and TIP47.	bind
11802	1	3608	7	11	NULL	NULL	NULL	Rab9	GP		bind					TIP47	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5420_s_259	15456905	(B) Binding affinity of Rab9 and TIP47.	bind
80948	1	3608	11	NULL	NULL	0	NULL	Rab9	Protein		has affinity for					binding	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_12_5420_s_259	15456905	(B) Binding affinity of Rab9 and TIP47.	bind
80949	2	3608	11	NULL	NULL	0	NULL	TIP47	Protein		has affinity for					binding	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_12_5420_s_259	15456905	(B) Binding affinity of Rab9 and TIP47.	bind
8162	1	3609	6	11	NULL	NULL	NULL	APP	GP		bind			C-terminus		KLC1	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_2_449_s_131	11144355	(B) Binding analysis of APP C terminus to KLC1.	bind
11803	1	3609	7	11	NULL	NULL	NULL	 APP 	GP		bind			C terminus		KLC1	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_2_449_s_131	11144355	(B) Binding analysis of APP C terminus to KLC1.	bind
80950	1	3609	11	NULL	NULL	0	NULL	APP	Protein	C terminus	binds to 					KLC1	Protein				NULL		0	NULL	NULL	NULL	gw60_neuron_28_2_449_s_131	11144355	(B) Binding analysis of APP C terminus to KLC1.	bind
80951	1	3614	11	NULL	NULL	NULL	NULL	ER	CellComponent		binds to 					p300	Protein				NULL	mammalian one-hybrid system	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_3_656_s_90	14680815	(B) Binding between ER  and p300  was examined using the mammalian one-hybrid system.	bind
8165	1	3615	6	11	NULL	NULL	NULL	p110alpha PI3-K	GP		bind					R-Ras	GP	mutant	effector loop		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6333_s_212	10454580	(B) Binding between p110alpha PI3-K and different R-Ras effector loop mutants was evaluated by an in vitro pull-down assay.	bind
52996	1	3615	7	11	NULL	NULL	NULL	p110alpha PI3-K	GP		bind					R-Ras	GP	mutant	effector loop		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6333_s_212	10454580	(B) Binding between p110alpha PI3-K and different R-Ras effector loop mutants was evaluated by an in vitro pull-down assay.	bind
80952	1	3615	11	NULL	NULL	0	NULL	PI3-K	Protein		binds to 			p110alpha		R-Ras effector loop mutants	Protein				NULL	in vitro pull-down assay	0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6333_s_212	10454580	(B) Binding between p110alpha PI3-K and different R-Ras effector loop mutants was evaluated by an in vitro pull-down assay.	bind
8166	1	3616	6	11	NULL	NULL	NULL	PALA	AminoAcid		bind					ATCase	GP		active site		NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_3_404_s_90	11528003	(B) Binding mode of the bisubstrate analogue PALA (purple) to the active site of  ATCase.	bind
40866	2	3616	6	11	NULL	NULL	NULL	PALA	AminoAcid		is a type of					bisubstrate analogue	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_3_404_s_90	11528003	(B) Binding mode of the bisubstrate analogue PALA (purple) to the active site of  ATCase.	bind
11807	1	3616	7	11	NULL	NULL	NULL	PALA	AminoAcid		bind					ATCase	GP		active site of		NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_3_404_s_90	11528003	(B) Binding mode of the bisubstrate analogue PALA (purple) to the active site of  ATCase.	bind
44770	2	3616	7	11	NULL	NULL	NULL	PALA	AminoAcid		is a type of					bisubstrate analogue	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_3_404_s_90	11528003	(B) Binding mode of the bisubstrate analogue PALA (purple) to the active site of  ATCase.	bind
80953	1	3616	11	NULL	NULL	0	NULL	 PALA	Chemical	bisubstrate analogue	binds to 					ATCase	Protein	active site			NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_3_404_s_90	11528003	(B) Binding mode of the bisubstrate analogue PALA (purple) to the active site of  ATCase.	bind
8167	1	3618	6	11	NULL	NULL	NULL	VASP	GP	purified	bind					M10	GP		tail		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_319_1_214_s_80	15158464	(B) Binding of  purified VASP and M10 tail.	bind
11808	1	3618	7	11	NULL	NULL	NULL	VASP	GP	purified	bind					M10	GP		tail		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_319_1_214_s_80	15158464	(B) Binding of  purified VASP and M10 tail.	bind
80954	1	3618	11	NULL	NULL	0	NULL	VASP	Protein	purified	binds to 					M10 tail	Protein				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_319_1_214_s_80	15158464	(B) Binding of  purified VASP and M10 tail.	bind
8168	1	3619	6	11	NULL	NULL	NULL	UFD2	GP	recombinant	bind					Ubi-GST	GP	ubiquitinated			NULL		NULL	NULL	NULL	NULL	gw60_cell_96_5_635_s_78	10089879	(B) Binding of  recombinant UFD2 to ubiquitinated Ubi-GST.	bind
11809	1	3619	7	11	NULL	NULL	NULL	UFD2	GP	recombinant	bind					Ubi-GST	GP	ubiquitinated			NULL		NULL	NULL	NULL	NULL	gw60_cell_96_5_635_s_78	10089879	(B) Binding of  recombinant UFD2 to ubiquitinated Ubi-GST.	bind
80955	1	3619	11	NULL	NULL	0	NULL	UFD2	Protein	recombinant	binds to 					Ubi-GST	Protein	ubiquitinated			NULL		0	NULL	NULL	NULL	gw60_cell_96_5_635_s_78	10089879	(B) Binding of  recombinant UFD2 to ubiquitinated Ubi-GST.	bind
8169	1	3620	6	11	NULL	NULL	NULL	eIF-4E	GP		bind					m7-GTP-Sepharose resin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6041_s_119	10454551	(B) Binding of 4BP-1 to eIF-4E (already bound to m7-GTP-Sepharose resin) was determined.	bind
8170	2	3620	6	11	NULL	NULL	NULL	4BP-1	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6041_s_119	10454551	(B) Binding of 4BP-1 to eIF-4E (already bound to m7-GTP-Sepharose resin) was determined.	bind
11810	1	3620	7	11	NULL	NULL	NULL	eIF-4E	GP		bind					m7-GTP-Sepharose resin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6041_s_119	10454551	(B) Binding of 4BP-1 to eIF-4E (already bound to m7-GTP-Sepharose resin) was determined.	bind
15049	2	3620	7	11	NULL	NULL	NULL	4BP-1	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6041_s_119	10454551	(B) Binding of 4BP-1 to eIF-4E (already bound to m7-GTP-Sepharose resin) was determined.	bind
80956	1	3620	11	NULL	NULL	0	NULL	4BP-1	Protein		binds to 					eIF-4E	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6041_s_119	10454551	(B) Binding of 4BP-1 to eIF-4E (already bound to m7-GTP-Sepharose resin) was determined.	bind
80957	2	3620	11	NULL	NULL	0	NULL	eIF-4E	Protein		binds to 					m7-GTP-Sepharose resin	Chemical				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6041_s_119	10454551	(B) Binding of 4BP-1 to eIF-4E (already bound to m7-GTP-Sepharose resin) was determined.	bind
8171	1	3621	6	11	NULL	NULL	NULL	CstF-64	GP		bind			RNA-BD		pA1 transcript	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_10_2_261_s_159	10072078	(B) Binding of a GST-RNA binding domain protein (-RNA BD) of CstF-64 to pA1 and pA2 transcripts.	bind
8172	2	3621	6	11	NULL	NULL	NULL	CstF-64	GP		bind			RNA-BD		pA2 transcript	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_10_2_261_s_159	10072078	(B) Binding of a GST-RNA binding domain protein (-RNA BD) of CstF-64 to pA1 and pA2 transcripts.	bind
8173	3	3621	6	11	NULL	NULL	NULL	RNA BD	GP		is					RNA binding domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_10_2_261_s_159	10072078	(B) Binding of a GST-RNA binding domain protein (-RNA BD) of CstF-64 to pA1 and pA2 transcripts.	bind
11811	1	3621	7	11	NULL	NULL	NULL	 CstF-64	GP		bind			RNA BD		pA1 transcript	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_10_2_261_s_159	10072078	(B) Binding of a GST-RNA binding domain protein (-RNA BD) of CstF-64 to pA1 and pA2 transcripts.	bind
11812	2	3621	7	11	NULL	NULL	NULL	CstF-64	GP		bind			RNA BD		pA2 transcript	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_10_2_261_s_159	10072078	(B) Binding of a GST-RNA binding domain protein (-RNA BD) of CstF-64 to pA1 and pA2 transcripts.	bind
11813	3	3621	7	11	NULL	NULL	NULL	RNA BD	GP		is					RNA binding domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_10_2_261_s_159	10072078	(B) Binding of a GST-RNA binding domain protein (-RNA BD) of CstF-64 to pA1 and pA2 transcripts.	bind
80958	1	3621	11	NULL	NULL	0	NULL	CstF-64	Protein		binds to 			GST-RNA binding domain		pA1	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_immunity_10_2_261_s_159	10072078	(B) Binding of a GST-RNA binding domain protein (-RNA BD) of CstF-64 to pA1 and pA2 transcripts.	bind
80959	2	3621	11	NULL	NULL	0	NULL	CstF-64	Protein		binds to 			GST-RNA binding domain		pA2	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_immunity_10_2_261_s_159	10072078	(B) Binding of a GST-RNA binding domain protein (-RNA BD) of CstF-64 to pA1 and pA2 transcripts.	bind
8193	1	3622	6	11	NULL	NULL	NULL	NES	GP		bind					CRM1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_22_7862_s_163	11604520	(B) Binding of a NES to CRM1 occurs in a tripartite complex with RanGTP.	bind
8370	2	3622	6	11	NULL	NULL	NULL	statement 1	GP		bind					RanGTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_22_7862_s_163	11604520	(B) Binding of a NES to CRM1 occurs in a tripartite complex with RanGTP.	bind
8371	3	3622	6	11	NULL	NULL	NULL	statement 2	Process		forms					tripartite complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_22_7862_s_163	11604520	(B) Binding of a NES to CRM1 occurs in a tripartite complex with RanGTP.	bind
11814	1	3622	7	11	NULL	NULL	NULL	NES	GP		bind					CRM1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_22_7862_s_163	11604520	(B) Binding of a NES to CRM1 occurs in a tripartite complex with RanGTP.	bind
11815	2	3622	7	11	NULL	NULL	NULL	statement 1	GP		bind					RanGTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_22_7862_s_163	11604520	(B) Binding of a NES to CRM1 occurs in a tripartite complex with RanGTP.	bind
11816	3	3622	7	11	NULL	NULL	NULL	statement 2	Process		forms					tripartite complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_22_7862_s_163	11604520	(B) Binding of a NES to CRM1 occurs in a tripartite complex with RanGTP.	bind
80960	1	3622	11	NULL	NULL	0	NULL	NES	Chemical		binds to 					CRM1	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_22_7862_s_163	11604520	(B) Binding of a NES to CRM1 occurs in a tripartite complex with RanGTP.	bind
80961	2	3622	11	NULL	NULL	0	NULL	statement 1	Protein		complex with 		tripartite			RanGTP	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_22_7862_s_163	11604520	(B) Binding of a NES to CRM1 occurs in a tripartite complex with RanGTP.	bind
8229	1	3624	6	11	NULL	NULL	NULL	biotin	Chemical		bind			RGD		uPAR - alpha5beta1 - Fn complexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_3_501_s_156	15684035	(B) Binding of biotin-RGD to uPAR - alpha5beta1 - Fn complexes.	bind
11817	1	3624	7	11	NULL	NULL	NULL	biotin	Chemical		bind			RGD		uPAR - alpha5beta1 - Fn complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_3_501_s_156	15684035	(B) Binding of biotin-RGD to uPAR - alpha5beta1 - Fn complexes.	bind
80962	1	3624	11	NULL	NULL	0	NULL	uPAR	Protein		binds to 					alpha5beta1	Protein				NULL		0	NULL	NULL	NULL	gw70_cellbiol_168_3_501_s_156	15684035	(B) Binding of biotin-RGD to uPAR - alpha5beta1 - Fn complexes.	bind
80963	2	3624	11	NULL	NULL	0	NULL	statement 1	Protein		complex with 					Fn	Protein				NULL		0	NULL	NULL	NULL	gw70_cellbiol_168_3_501_s_156	15684035	(B) Binding of biotin-RGD to uPAR - alpha5beta1 - Fn complexes.	bind
80964	3	3624	11	NULL	NULL	0	NULL	statement 2	Protein		binds to 					biotin-RGD	Chemical				NULL		0	NULL	NULL	NULL	gw70_cellbiol_168_3_501_s_156	15684035	(B) Binding of biotin-RGD to uPAR - alpha5beta1 - Fn complexes.	bind
8230	1	3625	6	11	NULL	NULL	NULL	C/EBP-beta	GP	purified	bind					K15	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_8_3168_s_263	15060141	(B) Binding of C/EBP-beta to the K15 promoter  region by gel shift analysis with the purified CEB/Pbeta protein and the -266/-353  probe.	bind
11818	1	3625	7	11	NULL	NULL	NULL	C/EBP-beta	GP	purified	bind					K15	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_8_3168_s_263	15060141	(B) Binding of C/EBP-beta to the K15 promoter  region by gel shift analysis with the purified CEB/Pbeta protein and the -266/-353  probe.	bind
81009	1	3625	11	NULL	NULL	0	NULL	C/EBP-beta	Protein		binds to 					K15 promoter	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_8_3168_s_263	15060141	(B) Binding of C/EBP-beta to the K15 promoter  region by gel shift analysis with the purified CEB/Pbeta protein and the -266/-353  probe.	bind
8231	1	3626	6	11	NULL	NULL	NULL	C/EBPbeta	GP		bind					p40	GP	endogenous		promoter	NULL	bone marrow-derived macrophages	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_6_2385_s_205	14993278	(B) Binding of C/EBPbeta to the endogenous p40 promoter was monitored by ChIP and  semiquantitative PCR by using C/EBPbeta antibodies and chromatin samples prepared  from bone marrow-derived macrophages.	bind
11819	1	3626	7	11	NULL	NULL	NULL	C/EBPbeta	GP		bind					p40	GP	endogenous		promoter	NULL	bone marrow-derived macrophages	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_6_2385_s_205	14993278	(B) Binding of C/EBPbeta to the endogenous p40 promoter was monitored by ChIP and  semiquantitative PCR by using C/EBPbeta antibodies and chromatin samples prepared  from bone marrow-derived macrophages.	bind
81010	1	3626	11	NULL	NULL	0	NULL	C/EBPbeta	Protein		binds to 					p40 promoter 	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_6_2385_s_205	14993278	(B) Binding of C/EBPbeta to the endogenous p40 promoter was monitored by ChIP and  semiquantitative PCR by using C/EBPbeta antibodies and chromatin samples prepared  from bone marrow-derived macrophages.	bind
8232	1	3627	6	11	NULL	NULL	NULL	CCR5 antisera	GP		bind					CCR5 receptor transfectants	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_2_112_s_51	9024623	(b) Binding of CCR5 antisera to CCR5 receptor transfectants.	bind
11820	1	3627	7	11	NULL	NULL	NULL	CCR5 antisera	GP		bind					CCR5 receptor transfectant	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_2_112_s_51	9024623	(b) Binding of CCR5 antisera to CCR5 receptor transfectants.	bind
81011	1	3627	11	NULL	NULL	0	NULL	CCR5 antisera	PartOfProtein		binds to 					CCR5 receptor transfectants	Cell				NULL		0	NULL	NULL	NULL	gw60_currbiol_7_2_112_s_51	9024623	(b) Binding of CCR5 antisera to CCR5 receptor transfectants.	bind
8233	1	3628	6	11	NULL	NULL	NULL	Cdc20 fragments	GP		bind					CCT	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_87_s_247	12887895	(B) Binding of Cdc20 fragments to the CCT, the APC/C, and Mad2.	bind
8234	2	3628	6	11	NULL	NULL	NULL	Cdc20 fragments	GP		bind					APC/C	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_87_s_247	12887895	(B) Binding of Cdc20 fragments to the CCT, the APC/C, and Mad2.	bind
8235	3	3628	6	11	NULL	NULL	NULL	Cdc20 fragments	GP		bind					Mad2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_87_s_247	12887895	(B) Binding of Cdc20 fragments to the CCT, the APC/C, and Mad2.	bind
11821	1	3628	7	11	NULL	NULL	NULL	 Cdc20 fragments	GP		bind					CCT	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_87_s_247	12887895	(B) Binding of Cdc20 fragments to the CCT, the APC/C, and Mad2.	bind
11822	2	3628	7	11	NULL	NULL	NULL	Cdc20 fragments	GP		bind					APC/C	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_87_s_247	12887895	(B) Binding of Cdc20 fragments to the CCT, the APC/C, and Mad2.	bind
11823	3	3628	7	11	NULL	NULL	NULL	Cdc20 fragments	GP		bind		  			Mad2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_87_s_247	12887895	(B) Binding of Cdc20 fragments to the CCT, the APC/C, and Mad2.	bind
81012	1	3628	11	NULL	NULL	0	NULL	Cdc20 fragment	PartOfProtein		binds to 					CCT	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcell_12_1_87_s_247	12887895	(B) Binding of Cdc20 fragments to the CCT, the APC/C, and Mad2.	bind
81013	2	3628	11	NULL	NULL	0	NULL	Cdc20 fragment	PartOfProtein		binds to 					APC/C	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_12_1_87_s_247	12887895	(B) Binding of Cdc20 fragments to the CCT, the APC/C, and Mad2.	bind
81014	3	3628	11	NULL	NULL	0	NULL	Cdc20 fragment	PartOfProtein		binds to 					Mad2	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_12_1_87_s_247	12887895	(B) Binding of Cdc20 fragments to the CCT, the APC/C, and Mad2.	bind
8236	1	3629	6	11	NULL	NULL	NULL	CIDR1alpha	GP		bind					IgG	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_9_5412_s_163	15322039	(B) Binding of CIDR1alpha to IgG of different species.	bind
11824	1	3629	7	11	NULL	NULL	NULL	 CIDR1alpha	GP		bind					IgG	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_9_5412_s_163	15322039	(B) Binding of CIDR1alpha to IgG of different species.	bind
81015	1	3629	11	NULL	NULL	0	NULL	CIDR1alpha	Protein		binds to 					IgG	PartOfProtein				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_9_5412_s_163	15322039	(B) Binding of CIDR1alpha to IgG of different species.	bind
8237	1	3630	6	11	NULL	NULL	NULL	CksHs2	GP		bind					p33 cdk2	GP	monomeric			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_3659_s_221	9632748	(B) Binding of CksHs2 to monomeric p33 cdk2.	bind
11825	1	3630	7	11	NULL	NULL	NULL	CksHs2	GP		bind					p33 cdk2	GP	monomeric			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_3659_s_221	9632748	(B) Binding of CksHs2 to monomeric p33 cdk2.	bind
81016	1	3630	11	NULL	NULL	0	NULL	CksHs2	Protein		binds to 					p33 cdk2	Protein	monomeric			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_3659_s_221	9632748	(B) Binding of CksHs2 to monomeric p33 cdk2.	bind
8238	1	3631	6	11	NULL	NULL	NULL	cyclin A	GP		bind					Skp2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_635_s_220	9858587	(B) Binding of cyclin A and cyclin E to Skp2.	bind
8239	2	3631	6	11	NULL	NULL	NULL	Cyclin E	GP		bind					Skp2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_635_s_220	9858587	(B) Binding of cyclin A and cyclin E to Skp2.	bind
11826	1	3631	7	11	NULL	NULL	NULL	cyclin A	GP		bind					Skp2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_635_s_220	9858587	(B) Binding of cyclin A and cyclin E to Skp2.	bind
11827	2	3631	7	11	NULL	NULL	NULL	cyclin E	GP		bind					Skp2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_635_s_220	9858587	(B) Binding of cyclin A and cyclin E to Skp2.	bind
81017	1	3631	11	NULL	NULL	0	NULL	cyclin A	Protein		binds to 					Skp2	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_635_s_220	9858587	(B) Binding of cyclin A and cyclin E to Skp2.	bind
81018	2	3631	11	NULL	NULL	0	NULL	cyclin E	Protein		binds to 					Skp2	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_635_s_220	9858587	(B) Binding of cyclin A and cyclin E to Skp2.	bind
8240	1	3632	6	11	NULL	NULL	NULL	Dbl	GP		bind					Rho proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7870_s_271	10523675	(B) Binding of Dbl to Rho proteins.	bind
11828	1	3632	7	11	NULL	NULL	NULL	Dbl	GP		bind					Rho protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7870_s_271	10523675	(B) Binding of Dbl to Rho proteins.	bind
81019	1	3632	11	NULL	NULL	0	NULL	Dbl	Protein		binds to 					Rho protein	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_11_7870_s_271	10523675	(B) Binding of Dbl to Rho proteins.	bind
8241	1	3633	6	11	NULL	NULL	NULL	Nef alleles	GP		bind					V1H	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_13_6_2045_s_112	12058068	(B) Binding of different Nef alleles and Nef mutants to V1H indicates that the integrity of the flexible loop structure is required for the interaction.	bind
8242	2	3633	6	11	NULL	NULL	NULL	Nef	GP	mutants	bind					V1H	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_13_6_2045_s_112	12058068	(B) Binding of different Nef alleles and Nef mutants to V1H indicates that the integrity of the flexible loop structure is required for the interaction.	bind
8243	3	3633	6	11	NULL	NULL	NULL	flexible loop structure	GP	integrity of	is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_13_6_2045_s_112	12058068	(B) Binding of different Nef alleles and Nef mutants to V1H indicates that the integrity of the flexible loop structure is required for the interaction.	bind
8244	4	3633	6	11	NULL	NULL	NULL	flexible loop structure	GP	integrity of	is required for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_13_6_2045_s_112	12058068	(B) Binding of different Nef alleles and Nef mutants to V1H indicates that the integrity of the flexible loop structure is required for the interaction.	bind
11829	1	3633	7	11	NULL	NULL	NULL	Nef alleles	GP		bind					V1H	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_13_6_2045_s_112	12058068	(B) Binding of different Nef alleles and Nef mutants to V1H indicates that the integrity of the flexible loop structure is required for the interaction.	bind
11830	2	3633	7	11	NULL	NULL	NULL	Nef 	GP	mutant	bind					V1H	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_13_6_2045_s_112	12058068	(B) Binding of different Nef alleles and Nef mutants to V1H indicates that the integrity of the flexible loop structure is required for the interaction.	bind
11831	3	3633	7	11	NULL	NULL	NULL	flexible loop structure	GP	integrity of	is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_13_6_2045_s_112	12058068	(B) Binding of different Nef alleles and Nef mutants to V1H indicates that the integrity of the flexible loop structure is required for the interaction.	bind
11832	4	3633	7	11	NULL	NULL	NULL	flexible loop structure	GP	integrity of	is required for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_13_6_2045_s_112	12058068	(B) Binding of different Nef alleles and Nef mutants to V1H indicates that the integrity of the flexible loop structure is required for the interaction.	bind
81020	1	3633	11	NULL	NULL	0	NULL	Nef allele	NucleicAcidSubstance		binds to 					V1H	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_13_6_2045_s_112	12058068	(B) Binding of different Nef alleles and Nef mutants to V1H indicates that the integrity of the flexible loop structure is required for the interaction.	bind
81021	2	3633	11	NULL	NULL	0	NULL	Nef mutants	Protein		binds to 					V1H	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_13_6_2045_s_112	12058068	(B) Binding of different Nef alleles and Nef mutants to V1H indicates that the integrity of the flexible loop structure is required for the interaction.	bind
8245	1	3634	6	11	NULL	NULL	NULL	dMyc	GP		bind					nnp-1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3401_s_181	15831447	(B) Binding of dMyc to the  nnp-1 promoter.	bind
11833	1	3634	7	11	NULL	NULL	NULL	dMyc	GP		bind					nnp-1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3401_s_181	15831447	(B) Binding of dMyc to the  nnp-1 promoter.	bind
81022	1	3634	11	NULL	NULL	0	NULL	dMyc	GeneOrProtein		binds to 					nnp-1 promoter	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_9_3401_s_181	15831447	(B) Binding of dMyc to the  nnp-1 promoter.	bind
8246	1	3635	6	11	NULL	NULL	NULL	DpiA protein	GP		bind					pSC101	GP			origin region	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_20_6025_s_72	14526013	(B) Binding of DpiA protein and the mutant proteins to the origin regions  of pSC101 and P1 are shown.	bind
8247	2	3635	6	11	NULL	NULL	NULL	DipA protein	GP	mutant	bind					P1	GP			origin region	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_20_6025_s_72	14526013	(B) Binding of DpiA protein and the mutant proteins to the origin regions  of pSC101 and P1 are shown.	bind
52997	3	3635	6	11	NULL	NULL	NULL	DpiA protein	GP		bind					P1	GP			origin region	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_20_6025_s_72	14526013	(B) Binding of DpiA protein and the mutant proteins to the origin regions  of pSC101 and P1 are shown.	bind
52998	4	3635	6	11	NULL	NULL	NULL	DpiA protein	GP	mutant	bind					pSC101	GP			origin region	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_20_6025_s_72	14526013	(B) Binding of DpiA protein and the mutant proteins to the origin regions  of pSC101 and P1 are shown.	bind
11834	1	3635	7	11	NULL	NULL	NULL	DpiA protein	GP		bind					pSC101	GP			origin region	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_20_6025_s_72	14526013	(B) Binding of DpiA protein and the mutant proteins to the origin regions  of pSC101 and P1 are shown.	bind
11835	2	3635	7	11	NULL	NULL	NULL	DpiA protein	GP		bind					P1	GP			origin region	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_20_6025_s_72	14526013	(B) Binding of DpiA protein and the mutant proteins to the origin regions  of pSC101 and P1 are shown.	bind
11836	3	3635	7	11	NULL	NULL	NULL	DpiA protein	GP	mutant	bind					pSC101	GP			origin region	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_20_6025_s_72	14526013	(B) Binding of DpiA protein and the mutant proteins to the origin regions  of pSC101 and P1 are shown.	bind
11837	4	3635	7	11	NULL	NULL	NULL	DpiA protein	GP	mutant	bind					P1	GP			origin region	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_20_6025_s_72	14526013	(B) Binding of DpiA protein and the mutant proteins to the origin regions  of pSC101 and P1 are shown.	bind
81023	1	3635	11	NULL	NULL	0	NULL	DpiA protein	Protein		binds to 					pSC101	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_20_6025_s_72	14526013	(B) Binding of DpiA protein and the mutant proteins to the origin regions  of pSC101 and P1 are shown.	bind
81024	2	3635	11	NULL	NULL	0	NULL	DpiA protein	Protein		binds to 					P1	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_20_6025_s_72	14526013	(B) Binding of DpiA protein and the mutant proteins to the origin regions  of pSC101 and P1 are shown.	bind
8248	1	3636	6	11	NULL	NULL	NULL	EF-Tu-GTP-aminoacyl-tRNA	NucleicAcid		bind					A/T (30S/50S)	NucleicAcid	hybrid state			NULL		NULL	NULL	NULL	NULL	gw60_structure_4_3_229_s_271	8805530	(b) Binding of EF-Tu-GTP-aminoacyl-tRNA to A/T (30S/50S) hybrid state.	bind
11838	1	3636	7	11	NULL	NULL	NULL	EF-Tu-GTP-aminoacyl-tRNA	NucleicAcid		bind					A/T (30S/50S)	NucleicAcid	hybrid state			NULL		NULL	NULL	NULL	NULL	gw60_structure_4_3_229_s_271	8805530	(b) Binding of EF-Tu-GTP-aminoacyl-tRNA to A/T (30S/50S) hybrid state.	bind
81025	1	3636	11	NULL	NULL	0	NULL	EF-Tu-GTP-aminoacyl-tRNA	NucleicAcidSubstance		binds to 					A/T	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_structure_4_3_229_s_271	8805530	(b) Binding of EF-Tu-GTP-aminoacyl-tRNA to A/T (30S/50S) hybrid state.	bind
8249	1	3637	6	11	NULL	NULL	NULL	eIF4G	GP		bind					Mnk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_225	11154262	(B) Binding of eIF4G and ERK to Mnk2.	bind
8250	2	3637	6	11	NULL	NULL	NULL	ERK	GP		bind					Mnk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_225	11154262	(B) Binding of eIF4G and ERK to Mnk2.	bind
11840	1	3637	7	11	NULL	NULL	NULL	eIF4G	GP		bind					Mnk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_225	11154262	(B) Binding of eIF4G and ERK to Mnk2.	bind
11841	2	3637	7	11	NULL	NULL	NULL	ERK	GP		bind					Mnk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_225	11154262	(B) Binding of eIF4G and ERK to Mnk2.	bind
81026	1	3637	11	NULL	NULL	0	NULL	eIF4G	Protein		binds to 					Mnk2	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_225	11154262	(B) Binding of eIF4G and ERK to Mnk2.	bind
81027	2	3637	11	NULL	NULL	0	NULL	ERK	Protein		binds to 					Mnk2	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_225	11154262	(B) Binding of eIF4G and ERK to Mnk2.	bind
8251	1	3638	6	11	NULL	NULL	NULL	eIF4G	GP		bind					Mnk1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_278	11154262	(B) Binding of eIF4G to Mnk1 and Mnk2 is reduced upon stimulation with phorbol ester.	bind
8252	2	3638	6	11	NULL	NULL	NULL	eIF4G	GP		bind					Mnk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_278	11154262	(B) Binding of eIF4G to Mnk1 and Mnk2 is reduced upon stimulation with phorbol ester.	bind
8253	3	3638	6	11	NULL	NULL	NULL	statement 1	Process		reduced upon					phorbol ester	Chemical	stimulation with			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_278	11154262	(B) Binding of eIF4G to Mnk1 and Mnk2 is reduced upon stimulation with phorbol ester.	bind
8254	4	3638	6	11	NULL	NULL	NULL	statement 2	Process		reduced upon					phorbol ester	Chemical	stimulation with			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_278	11154262	(B) Binding of eIF4G to Mnk1 and Mnk2 is reduced upon stimulation with phorbol ester.	bind
11842	1	3638	7	11	NULL	NULL	NULL	eIF4G	GP		bind					Mnk1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_278	11154262	(B) Binding of eIF4G to Mnk1 and Mnk2 is reduced upon stimulation with phorbol ester.	bind
11843	2	3638	7	11	NULL	NULL	NULL	eIF4G	GP		bind					Mnk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_278	11154262	(B) Binding of eIF4G to Mnk1 and Mnk2 is reduced upon stimulation with phorbol ester.	bind
11844	3	3638	7	11	NULL	NULL	NULL	statement 1	Process		is reduced upon					phorbol ester	Chemical	stimulation with			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_278	11154262	(B) Binding of eIF4G to Mnk1 and Mnk2 is reduced upon stimulation with phorbol ester.	bind
11845	4	3638	7	11	NULL	NULL	NULL	statement 2	Process		is reduced upon					phorbol ester	Chemical	stimulation with			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_278	11154262	(B) Binding of eIF4G to Mnk1 and Mnk2 is reduced upon stimulation with phorbol ester.	bind
81028	1	3638	11	NULL	NULL	0	NULL	eIF4G	Protein		binds to 					Mnk1	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_278	11154262	(B) Binding of eIF4G to Mnk1 and Mnk2 is reduced upon stimulation with phorbol ester.	bind
81029	2	3638	11	NULL	NULL	0	NULL	eIF4G	Protein		binds to 					Mnk2	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_278	11154262	(B) Binding of eIF4G to Mnk1 and Mnk2 is reduced upon stimulation with phorbol ester.	bind
81030	3	3638	11	NULL	NULL	0	NULL	 phorbol ester	Chemical		reduced					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_278	11154262	(B) Binding of eIF4G to Mnk1 and Mnk2 is reduced upon stimulation with phorbol ester.	bind
81031	4	3638	11	NULL	NULL	0	NULL	phorbol ester	Chemical		reduced					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_278	11154262	(B) Binding of eIF4G to Mnk1 and Mnk2 is reduced upon stimulation with phorbol ester.	bind
8255	1	3639	6	11	NULL	NULL	NULL	Rad24	GP		bind					Byr2	GP	FL			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
8256	2	3639	6	11	NULL	NULL	NULL	Rad24	GP		bind					Byr2	GP		NT		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
8257	3	3639	6	11	NULL	NULL	NULL	Rad24	GP		bind					Byr2	GP		CT		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
8258	4	3639	6	11	NULL	NULL	NULL	Rad25	GP		bind					Byr2	GP	FL			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
8259	5	3639	6	11	NULL	NULL	NULL	Rad25	GP		bind					Byr2	GP		NT		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
8260	6	3639	6	11	NULL	NULL	NULL	Rad25	GP		bind					Byr2	GP		CT		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
8261	7	3639	6	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
8262	8	3639	6	11	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
8263	9	3639	6	11	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
11940	1	3639	7	11	NULL	NULL	NULL	Rad24	GP		bind					Byr2	GP	FL			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
11941	2	3639	7	11	NULL	NULL	NULL	Rad24	GP		bind					Byr2	GP		NT		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
11942	3	3639	7	11	NULL	NULL	NULL	Rad24	GP		bind					Byr2	GP		CT		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
11943	4	3639	7	11	NULL	NULL	NULL	Rad25	GP		bind					Byr2	GP	FL			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
11944	5	3639	7	11	NULL	NULL	NULL	Rad25	GP		bind					Byr2	GP		NT		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
11945	6	3639	7	11	NULL	NULL	NULL	Rad25	GP		bind					Byr2	GP		CT		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
53010	7	3639	7	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
53011	8	3639	7	11	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
53012	9	3639	7	11	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
81032	1	3639	11	NULL	NULL	0	NULL	Rad24	Protein		binds to 					Byr2FL	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
81033	2	3639	11	NULL	NULL	0	NULL	Rad24	Protein		binds to 					Byr2NT	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
81034	3	3639	11	NULL	NULL	0	NULL	Rad24	Protein		binds to 					Byr2CT	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
81035	4	3639	11	NULL	NULL	0	NULL	Rad25	Protein		binds to 					Byr2FL	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
81036	5	3639	11	NULL	NULL	0	NULL	Rad25	Protein		binds to 					Byr2NT	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
81037	6	3639	11	NULL	NULL	0	NULL	Rad25	Protein		binds to 					Byr2CT\t	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_20_7105_s_264	12242289	(B) Binding of either Rad24 or Rad25 to Byr2FL, Byr2NT, and Byr2CT.	bind
8264	1	3640	6	11	NULL	NULL	NULL	urokinase-type plasminogen activator	GP	exogenous	bind					BMEC	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_2_1014_s_175	15664945	(B) Binding of exogenous urokinase-type  plasminogen activator to human BMEC after spirochete addition.	bind
8265	2	3640	6	11	NULL	NULL	NULL	statement 1	Process		occurs after					spirochete	Organism	addition of			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_2_1014_s_175	15664945	(B) Binding of exogenous urokinase-type  plasminogen activator to human BMEC after spirochete addition.	bind
11946	1	3640	7	11	NULL	NULL	NULL	urokinase-type plasminogen activator	GP	exogenous	bind					BMEC	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_2_1014_s_175	15664945	(B) Binding of exogenous urokinase-type  plasminogen activator to human BMEC after spirochete addition.	bind
11947	2	3640	7	11	NULL	NULL	NULL	statement 1	Process		occurs after					spirochete	Organism	addition of			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_2_1014_s_175	15664945	(B) Binding of exogenous urokinase-type  plasminogen activator to human BMEC after spirochete addition.	bind
81038	1	3640	11	NULL	NULL	0	NULL	urokinase-type plasminogen activator	Protein	exogenous	binds to 					BMEC	Cell	human			NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_2_1014_s_175	15664945	(B) Binding of exogenous urokinase-type  plasminogen activator to human BMEC after spirochete addition.	bind
81039	2	3640	11	NULL	NULL	0	NULL	spirochete	Organism		induces					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_2_1014_s_175	15664945	(B) Binding of exogenous urokinase-type  plasminogen activator to human BMEC after spirochete addition.	bind
8266	1	3641	6	11	NULL	NULL	NULL	fibrinogen	GP		bind					beta3 integrins	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_5_599_s_199	12230977	(B) Binding of fibrinogen to beta3 integrins.	bind
11948	1	3641	7	11	NULL	NULL	NULL	fibrinogen	GP		bind					beta3 integrins	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_5_599_s_199	12230977	(B) Binding of fibrinogen to beta3 integrins.	bind
81040	1	3641	11	NULL	NULL	0	NULL	fibrinogen	Protein		binds to 					beta3 integrin	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_110_5_599_s_199	12230977	(B) Binding of fibrinogen to beta3 integrins.	bind
8267	1	3642	6	11	NULL	NULL	NULL	fibronectin	GP		bind					UspA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_9_4374_s_277	9712790	(B) Binding of fibronectin to UspA1.	bind
11949	1	3642	7	11	NULL	NULL	NULL	fibronectin	GP		bind					UspA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_9_4374_s_277	9712790	(B) Binding of fibronectin to UspA1.	bind
81041	1	3642	11	NULL	NULL	0	NULL	fibronectin	Protein		binds to 					UspA1	Protein				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_9_4374_s_277	9712790	(B) Binding of fibronectin to UspA1.	bind
8268	1	3643	6	11	NULL	NULL	NULL	fip1-206	GP		bind					Pap1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_6_2026_s_328	11238938	(B) Binding of fip1-206 to Pap1 prevents specific polyadenylation.	bind
8269	2	3643	6	11	NULL	NULL	NULL	statement 1	Process		prevents					polyadenylation	Process	specific			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_6_2026_s_328	11238938	(B) Binding of fip1-206 to Pap1 prevents specific polyadenylation.	bind
11950	1	3643	7	11	NULL	NULL	NULL	fip1-206	GP		bind					Pap1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_6_2026_s_328	11238938	(B) Binding of fip1-206 to Pap1 prevents specific polyadenylation.	bind
11951	2	3643	7	11	NULL	NULL	NULL	statement 1	Process		prevents					polyadenylation	Process	specific			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_6_2026_s_328	11238938	(B) Binding of fip1-206 to Pap1 prevents specific polyadenylation.	bind
81042	1	3643	11	NULL	NULL	0	NULL	fip1-206	Protein		binds to 					Pap1 	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_6_2026_s_328	11238938	(B) Binding of fip1-206 to Pap1 prevents specific polyadenylation.	bind
81043	2	3643	11	NULL	NULL	0	NULL	statement 1	Process		prevents					polyadenylation	Process	specific			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_6_2026_s_328	11238938	(B) Binding of fip1-206 to Pap1 prevents specific polyadenylation.	bind
8270	1	3644	6	11	NULL	NULL	NULL	Fli1	GP		bind					collagenase	GP	human		tandem elements	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_7_2467_s_138	16537893	(B) Binding of Fli1 and Fos-Jun to the human collagenase tandem  elements.	bind
8271	2	3644	6	11	NULL	NULL	NULL	Fos-Jun	GP		bind					collagenase	GP	human		tandem elements	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_7_2467_s_138	16537893	(B) Binding of Fli1 and Fos-Jun to the human collagenase tandem  elements.	bind
11952	1	3644	7	11	NULL	NULL	NULL	Fli1	GP		bind					collagenase	GP	human		tandem elements	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_7_2467_s_138	16537893	(B) Binding of Fli1 and Fos-Jun to the human collagenase tandem  elements.	bind
11953	2	3644	7	11	NULL	NULL	NULL	Fos-Jun	GP		bind					collagenase	GP	human		tandem elements	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_7_2467_s_138	16537893	(B) Binding of Fli1 and Fos-Jun to the human collagenase tandem  elements.	bind
81044	1	3644	11	NULL	NULL	0	NULL	Fli1	Protein		binds to 					collagenase tandem element	GeneOrProtein	human			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_7_2467_s_138	16537893	(B) Binding of Fli1 and Fos-Jun to the human collagenase tandem  elements.	bind
81045	2	3644	11	NULL	NULL	0	NULL	Fos-Jun	Protein		binds to 					collagenase tandem element	GeneOrProtein	human			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_7_2467_s_138	16537893	(B) Binding of Fli1 and Fos-Jun to the human collagenase tandem  elements.	bind
8272	1	3645	6	11	NULL	NULL	NULL	GAGA protein	GP		bind					iab-7	GP			PRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1311_s_173	11158316	(B) Binding of GAGA protein to the  iab-7 PRE depends on the two consensus GAGA binding sites.	bind
8273	2	3645	6	11	NULL	NULL	NULL	statement 1	Process		depends on							consensus		GAGA binding sites	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1311_s_173	11158316	(B) Binding of GAGA protein to the  iab-7 PRE depends on the two consensus GAGA binding sites.	bind
11954	1	3645	7	11	NULL	NULL	NULL	GAGA protein	GP		bind					 iab-7	GP			PRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1311_s_173	11158316	(B) Binding of GAGA protein to the  iab-7 PRE depends on the two consensus GAGA binding sites.	bind
11955	2	3645	7	11	NULL	NULL	NULL	statement 1	Process		depends on							consensus		GAGA binding site	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1311_s_173	11158316	(B) Binding of GAGA protein to the  iab-7 PRE depends on the two consensus GAGA binding sites.	bind
81046	1	3645	11	NULL	NULL	0	NULL	GAGA protein	Protein		binds to 					iab-7 PRE 	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1311_s_173	11158316	(B) Binding of GAGA protein to the  iab-7 PRE depends on the two consensus GAGA binding sites.	bind
81047	2	3645	11	NULL	NULL	0	NULL	statement 1	Process		depends on					GAGA binding site		consensus			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1311_s_173	11158316	(B) Binding of GAGA protein to the  iab-7 PRE depends on the two consensus GAGA binding sites.	bind
8274	1	3646	6	11	NULL	NULL	NULL	Gal4-VP16	GP		bind					H2A nucleosomes	GP	conventional			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_3_1156_s_120	16428466	(B) Binding of Gal4-VP16 to conventional H2A nucleosomes.	bind
11956	1	3646	7	11	NULL	NULL	NULL	Gal4-VP16	GP		bind					H2A nucleosomes	GP	conventional			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_3_1156_s_120	16428466	(B) Binding of Gal4-VP16 to conventional H2A nucleosomes.	bind
81048	1	3646	11	NULL	NULL	0	NULL	Gal4-VP16	Protein		binds to 					H2A nucleosomes	CellComponent	conventional			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_3_1156_s_120	16428466	(B) Binding of Gal4-VP16 to conventional H2A nucleosomes.	bind
8275	1	3647	6	11	NULL	NULL	NULL	GAS41	GP		bind					p14 ARF gene	GP			promoter	NULL	unstressed IMR-90 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4006_s_228	16705155	(B) Binding of GAS41 to the  p14 ARF gene promoter in unstressed IMR-90 cells.	bind
11957	1	3647	7	11	NULL	NULL	NULL	GAS41	GP		bind					p14 ARF gene	GP			promoter	NULL	unstressed IMR-90 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4006_s_228	16705155	(B) Binding of GAS41 to the  p14 ARF gene promoter in unstressed IMR-90 cells.	bind
81049	1	3647	11	NULL	NULL	0	NULL	GAS41	Protein		binds to 					p14 ARF gene promoter	NucleicAcidSubstance				NULL	in unstressed IMR-90 cells	0	NULL	NULL	NULL	gw70_molcellbiol_26_11_4006_s_228	16705155	(B) Binding of GAS41 to the  p14 ARF gene promoter in unstressed IMR-90 cells.	bind
81050	1	3648	11	NULL	NULL	0	NULL	GST fusion protein	Protein		binds to 					chitin	Chemical				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_64_2_472_s_171	9464381	(b) Binding of GST fusion protein to chitin, chitosan, and Avicel.	bind
81051	2	3648	11	NULL	NULL	0	NULL	GST fusion protein	Protein		binds to 					chitosan	Chemical				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_64_2_472_s_171	9464381	(b) Binding of GST fusion protein to chitin, chitosan, and Avicel.	bind
81052	3	3648	11	NULL	NULL	0	NULL	GST fusion protein	Protein		binds to 					Avicel	Chemical				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_64_2_472_s_171	9464381	(b) Binding of GST fusion protein to chitin, chitosan, and Avicel.	bind
8279	1	3649	6	11	NULL	NULL	NULL	AR protein	GP	deletion mutant	bind					Hey1	GP	35S-labeled			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1425_s_137	15684393	(B) Binding of GST fusion proteins of AR deletion mutants to  35S-labeled Hey1.	bind
53017	2	3649	6	11	NULL	NULL	NULL	AR protein	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1425_s_137	15684393	(B) Binding of GST fusion proteins of AR deletion mutants to  35S-labeled Hey1.	bind
11961	1	3649	7	11	NULL	NULL	NULL	AR protein	GP	deletion mutant	bind					Hey1	GP	35S-labeled			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1425_s_137	15684393	(B) Binding of GST fusion proteins of AR deletion mutants to  35S-labeled Hey1.	bind
53019	2	3649	7	11	NULL	NULL	NULL	AR protein	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1425_s_137	15684393	(B) Binding of GST fusion proteins of AR deletion mutants to  35S-labeled Hey1.	bind
81053	1	3649	11	NULL	NULL	0	NULL	GST fusion proteins	Protein	AR deletion mutant	binds to 					Hey1	Protein	 35S-labeled 			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_4_1425_s_137	15684393	(B) Binding of GST fusion proteins of AR deletion mutants to  35S-labeled Hey1.	bind
8304	1	3650	6	11	NULL	NULL	NULL	GST-Rab9	GP		bind					GM130	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
8758	2	3650	6	11	NULL	NULL	NULL	GST-Rab9	GP		bind					golgin-84	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
8759	3	3650	6	11	NULL	NULL	NULL	GST-Rab9	GP		bind					p115	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
8760	4	3650	6	11	NULL	NULL	NULL	GST-Rab1	GP		bind					GM130	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
8761	5	3650	6	11	NULL	NULL	NULL	GST-Rab1	GP		bind					golgin-84	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
8762	6	3650	6	11	NULL	NULL	NULL	GST-Rab1	GP		bind					p115	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
8763	7	3650	6	11	NULL	NULL	NULL	GST-Rab9/1	GP		bind					GM130	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
8764	8	3650	6	11	NULL	NULL	NULL	GST-Rab9/1	GP		bind					golgin-84	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
8765	9	3650	6	11	NULL	NULL	NULL	GST-Rab9/1	GP		bind					p115	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
8766	10	3650	6	11	NULL	NULL	NULL	GST-Rab1/9	GP		bind					GM130	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
8767	11	3650	6	11	NULL	NULL	NULL	GST-Rab1/9	GP		bind					golgin-84	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
8768	12	3650	6	11	NULL	NULL	NULL	GST-Rab1/9	GP		bind					p115	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
53022	13	3650	6	11	NULL	NULL	NULL	GM130	GP		is a type of					Rab1 effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
53023	14	3650	6	11	NULL	NULL	NULL	golgin-84	GP		is a type of					Rab1 effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
53024	15	3650	6	11	NULL	NULL	NULL	p115	GP		is a type of					Rab1 effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
11962	1	3650	7	11	NULL	NULL	NULL	GST-Rab9	GP		bind					GM130	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
11963	2	3650	7	11	NULL	NULL	NULL	GST-Rab1	GP		bind					GM130	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
11964	3	3650	7	11	NULL	NULL	NULL	GST-Rab9/1	GP		bind					GM130	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
11965	4	3650	7	11	NULL	NULL	NULL	GST-Rab1/9	GP		bind					GM130	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
11966	5	3650	7	11	NULL	NULL	NULL	GST-Rab9	GP		bind					golgin-84	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
11967	6	3650	7	11	NULL	NULL	NULL	GST-Rab1	GP		bind					golgin-84	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
11968	7	3650	7	11	NULL	NULL	NULL	GST-Rab9/1	GP		bind					golgin-84	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
11969	8	3650	7	11	NULL	NULL	NULL	GST-Rab1/9	GP		bind					golgin-84	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
11970	9	3650	7	11	NULL	NULL	NULL	GST-Rab9	GP		bind					p115	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
11971	10	3650	7	11	NULL	NULL	NULL	GST-Rab1	GP		bind					 p115 	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
11972	11	3650	7	11	NULL	NULL	NULL	GST-Rab9/1	GP		bind					p115	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
11973	12	3650	7	11	NULL	NULL	NULL	GST-Rab1/9	GP		bind					p115	GP				NULL	rat liver Golgi detergent extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
11974	13	3650	7	11	NULL	NULL	NULL	GM130	GP		is a type of					Rab1 effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
11975	14	3650	7	11	NULL	NULL	NULL	golgin-84	GP		is a type of					Rab1 effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
11976	15	3650	7	11	NULL	NULL	NULL	p115	GP		is a type of					Rab1 effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
81054	1	3650	11	NULL	NULL	0	NULL	Rab1	Protein		binds to 					GM130	Protein	Golgi detergent extract			NULL	rat liver	0	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
81055	2	3650	11	NULL	NULL	0	NULL	Rab1	Protein		binds to 					golgin-84	Protein	Golgi detergent extract			NULL	rat liver	0	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
81056	3	3650	11	NULL	NULL	0	NULL	Rab1	Protein		binds to 					p115	Protein	Golgi detergent extract			NULL	rat liver	0	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
81057	4	3650	11	NULL	NULL	0	NULL	Rab9	Protein	GST version	binds to 					GM130	Protein	Golgi detergent extract			NULL	rat liver	0	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
81058	5	3650	11	NULL	NULL	0	NULL	 Rab9	Protein	GST version	binds to 					golgin-84	Protein	Golgi detergent extract			NULL	rat liver	0	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
81059	6	3650	11	NULL	NULL	0	NULL	 Rab9	Protein	GST version	binds to 					p115	Protein	Golgi detergent extract			NULL	rat liver	0	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
81060	7	3650	11	NULL	NULL	0	NULL	Rab1	Protein	GST version	binds to 					GM130	Protein	Golgi detergent extract			NULL	rat liver	0	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
81061	8	3650	11	NULL	NULL	0	NULL	Rab1	Protein	GST version	binds to 					golgin-84	Protein	Golgi detergent extract			NULL	rat liver	0	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
81062	9	3650	11	NULL	NULL	0	NULL	Rab1	Protein	GST version	binds to 					p115	Protein	Golgi detergent extract			NULL	rat liver	0	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
81063	10	3650	11	NULL	NULL	0	NULL	Rab9/1	Protein	GST version	binds to 					GM130	Protein	Golgi detergent extract			NULL	rat liver	0	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
81064	11	3650	11	NULL	NULL	NULL	NULL	Rab9/1	Protein	GST version	binds to 					p115	Protein	Golgi detergent extract			NULL	rat liver	NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
81065	12	3650	11	NULL	NULL	0	NULL	Rab9/1	Protein	GST version	binds to 					golgin-84	Protein	Golgi detergent extract			NULL	rat liver	0	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
81066	13	3650	11	NULL	NULL	0	NULL	Rab1/9	Protein	GST version	binds to 					GM130	Protein	Golgi detergent extract			NULL	rat liver	0	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
81067	14	3650	11	NULL	NULL	0	NULL	Rab1/9	Protein	GST version	binds to 					golgin-84	Protein	Golgi detergent extract			NULL	rat liver	0	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
81068	15	3650	11	NULL	NULL	0	NULL	Rab1/9	Protein	GST version	binds to 					p115	Protein	Golgi detergent extract			NULL	rat liver	0	NULL	NULL	NULL	gw70_cellbiol_173_6_917_s_78	16769818	(B) Binding of GST versions of Rab9, Rab1, Rab9/1, and  Rab1/9 to Rab1 effectors GM130, golgin-84, and p115 from rat liver Golgi detergent  extracts.	bind
8305	1	3651	6	11	NULL	NULL	NULL	Cdc42	GP	GTP-loaded 	bind					PAK1	GP		PBD		NULL		NULL	NULL	NULL	NULL	gw60_cell_102_3_387_s_242	10975528	(B) Binding of GTP-loaded Cdc42 (or Rac) with the PAK1 p21 binding domain  (PBD) disrupts the dimer and unfolds the IS domain (symbolized by its reversion  to a formless oval).	bind
8306	2	3651	6	11	NULL	NULL	NULL	Rac	GP	GTP-loaded	bind					PAK1	GP		PBD		NULL		NULL	NULL	NULL	NULL	gw60_cell_102_3_387_s_242	10975528	(B) Binding of GTP-loaded Cdc42 (or Rac) with the PAK1 p21 binding domain  (PBD) disrupts the dimer and unfolds the IS domain (symbolized by its reversion  to a formless oval).	bind
8307	3	3651	6	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_102_3_387_s_242	10975528	(B) Binding of GTP-loaded Cdc42 (or Rac) with the PAK1 p21 binding domain  (PBD) disrupts the dimer and unfolds the IS domain (symbolized by its reversion  to a formless oval).	bind
8308	4	3651	6	11	NULL	NULL	NULL	PBD	GP		is					p21 binding domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_102_3_387_s_242	10975528	(B) Binding of GTP-loaded Cdc42 (or Rac) with the PAK1 p21 binding domain  (PBD) disrupts the dimer and unfolds the IS domain (symbolized by its reversion  to a formless oval).	bind
8309	5	3651	6	11	NULL	NULL	NULL	statement 1	Process		disrupts					dimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_102_3_387_s_242	10975528	(B) Binding of GTP-loaded Cdc42 (or Rac) with the PAK1 p21 binding domain  (PBD) disrupts the dimer and unfolds the IS domain (symbolized by its reversion  to a formless oval).	bind
8310	6	3651	6	11	NULL	NULL	NULL	statement 2	Process		disrupts					dimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_102_3_387_s_242	10975528	(B) Binding of GTP-loaded Cdc42 (or Rac) with the PAK1 p21 binding domain  (PBD) disrupts the dimer and unfolds the IS domain (symbolized by its reversion  to a formless oval).	bind
8311	7	3651	6	11	NULL	NULL	NULL	statement 1	Process		unfolds								IS domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_102_3_387_s_242	10975528	(B) Binding of GTP-loaded Cdc42 (or Rac) with the PAK1 p21 binding domain  (PBD) disrupts the dimer and unfolds the IS domain (symbolized by its reversion  to a formless oval).	bind
8312	8	3651	6	11	NULL	NULL	NULL	statement 2	Process		unfolds								IS domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_102_3_387_s_242	10975528	(B) Binding of GTP-loaded Cdc42 (or Rac) with the PAK1 p21 binding domain  (PBD) disrupts the dimer and unfolds the IS domain (symbolized by its reversion  to a formless oval).	bind
11977	1	3651	7	11	NULL	NULL	NULL	Cdc42	GP	GTP-loaded	bind					PAK1	GP		p21 binding domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_102_3_387_s_242	10975528	(B) Binding of GTP-loaded Cdc42 (or Rac) with the PAK1 p21 binding domain  (PBD) disrupts the dimer and unfolds the IS domain (symbolized by its reversion  to a formless oval).	bind
11978	2	3651	7	11	NULL	NULL	NULL	Rac	GP	GTP-loaded	bind					PAK1	GP		p21 binding domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_102_3_387_s_242	10975528	(B) Binding of GTP-loaded Cdc42 (or Rac) with the PAK1 p21 binding domain  (PBD) disrupts the dimer and unfolds the IS domain (symbolized by its reversion  to a formless oval).	bind
11979	3	3651	7	11	NULL	NULL	NULL	statement 1	Process		disrupts					dimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_102_3_387_s_242	10975528	(B) Binding of GTP-loaded Cdc42 (or Rac) with the PAK1 p21 binding domain  (PBD) disrupts the dimer and unfolds the IS domain (symbolized by its reversion  to a formless oval).	bind
11980	4	3651	7	11	NULL	NULL	NULL	statement 1	Process		unfolds								IS domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_102_3_387_s_242	10975528	(B) Binding of GTP-loaded Cdc42 (or Rac) with the PAK1 p21 binding domain  (PBD) disrupts the dimer and unfolds the IS domain (symbolized by its reversion  to a formless oval).	bind
11981	5	3651	7	11	NULL	NULL	NULL	statement 2	Process		disrupts					dimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_102_3_387_s_242	10975528	(B) Binding of GTP-loaded Cdc42 (or Rac) with the PAK1 p21 binding domain  (PBD) disrupts the dimer and unfolds the IS domain (symbolized by its reversion  to a formless oval).	bind
11982	6	3651	7	11	NULL	NULL	NULL	statement 2	Process		unfolds								IS domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_102_3_387_s_242	10975528	(B) Binding of GTP-loaded Cdc42 (or Rac) with the PAK1 p21 binding domain  (PBD) disrupts the dimer and unfolds the IS domain (symbolized by its reversion  to a formless oval).	bind
11983	7	3651	7	11	NULL	NULL	NULL	p21 binding domain	GP		is					PBD	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_102_3_387_s_242	10975528	(B) Binding of GTP-loaded Cdc42 (or Rac) with the PAK1 p21 binding domain  (PBD) disrupts the dimer and unfolds the IS domain (symbolized by its reversion  to a formless oval).	bind
53026	8	3651	7	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_102_3_387_s_242	10975528	(B) Binding of GTP-loaded Cdc42 (or Rac) with the PAK1 p21 binding domain  (PBD) disrupts the dimer and unfolds the IS domain (symbolized by its reversion  to a formless oval).	bind
81069	1	3651	11	NULL	NULL	0	NULL	Cdc42	Protein	GTP-loaded	binds to 					PAK1	Protein		p21 binding domain		NULL		0	NULL	NULL	NULL	gw60_cell_102_3_387_s_242	10975528	(B) Binding of GTP-loaded Cdc42 (or Rac) with the PAK1 p21 binding domain  (PBD) disrupts the dimer and unfolds the IS domain (symbolized by its reversion  to a formless oval).	bind
81070	2	3651	11	NULL	NULL	0	NULL	p21 binding domain	PartOfProtein		is					PBD	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_cell_102_3_387_s_242	10975528	(B) Binding of GTP-loaded Cdc42 (or Rac) with the PAK1 p21 binding domain  (PBD) disrupts the dimer and unfolds the IS domain (symbolized by its reversion  to a formless oval).	bind
81071	3	3651	11	NULL	NULL	0	NULL	Rac	Protein		binds to 					 PAK1	Protein		p21 binding domain		NULL		0	NULL	NULL	NULL	gw60_cell_102_3_387_s_242	10975528	(B) Binding of GTP-loaded Cdc42 (or Rac) with the PAK1 p21 binding domain  (PBD) disrupts the dimer and unfolds the IS domain (symbolized by its reversion  to a formless oval).	bind
8317	1	3652	6	11	NULL	NULL	NULL	H6-CodY	GP		bind					P oppD fragment	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_2_512_s_202	15629923	(B) Binding of H6-CodY to labeled PCR products encompassing the mutated promoter  regions presented in panel A in an in vitro binding assay, relative to its binding  to the wild-type P oppD fragment.	bind
11985	1	3652	7	11	NULL	NULL	NULL	H6-CodY	GP		bind					P oppD fragment	GP	wild-type			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_2_512_s_202	15629923	(B) Binding of H6-CodY to labeled PCR products encompassing the mutated promoter  regions presented in panel A in an in vitro binding assay, relative to its binding  to the wild-type P oppD fragment.	bind
81072	1	3652	11	NULL	NULL	0	NULL	H6-CodY	Protein		binds to 					labeled PCR product	SmallMolecule				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_2_512_s_202	15629923	(B) Binding of H6-CodY to labeled PCR products encompassing the mutated promoter  regions presented in panel A in an in vitro binding assay, relative to its binding  to the wild-type P oppD fragment.	bind
8321	1	3653	6	11	NULL	NULL	NULL	Hsp40	GP		bind					GST-70C139	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2023_s_142	9528774	(B) Binding of Hsp40 to GST-70C139 was performed in the absence ( ) of Hsc70 or in the presence (+) of equimolar amounts of Hsc70 and the GST fusion protein, and Hsp40 was detected in the flowthrough fractions by Coomassie blue staining.	bind
11986	1	3653	7	11	NULL	NULL	NULL	Hsp40	GP		bind					GST-70C139	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2023_s_142	9528774	(B) Binding of Hsp40 to GST-70C139 was performed in the absence ( ) of Hsc70 or in the presence (+) of equimolar amounts of Hsc70 and the GST fusion protein, and Hsp40 was detected in the flowthrough fractions by Coomassie blue staining.	bind
81073	1	3653	11	NULL	NULL	0	NULL	Hsp40	Protein		binds to 					GST-70C139	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_2023_s_142	9528774	(B) Binding of Hsp40 to GST-70C139 was performed in the absence ( ) of Hsc70 or in the presence (+) of equimolar amounts of Hsc70 and the GST fusion protein, and Hsp40 was detected in the flowthrough fractions by Coomassie blue staining.	bind
81075	2	3653	11	NULL	NULL	NULL	NULL	Hsp40	Protein		was detected in					Coomassie blue staining	ResearchActivity	flowthrough fraction by			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2023_s_142	9528774	(B) Binding of Hsp40 to GST-70C139 was performed in the absence ( ) of Hsc70 or in the presence (+) of equimolar amounts of Hsc70 and the GST fusion protein, and Hsp40 was detected in the flowthrough fractions by Coomassie blue staining.	bind
8322	1	3654	6	11	NULL	NULL	NULL	IgG fractions	GP		bind					RO	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_1_11_s_105	9423833	(B) Binding of IgG fractions to R0; (C) binding of IgG fractions to R2-coated plates.	bind
8324	2	3654	6	11	NULL	NULL	NULL	IgG fractions	GP		bind					R2	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_1_11_s_105	9423833	(B) Binding of IgG fractions to R0; (C) binding of IgG fractions to R2-coated plates.	bind
11987	1	3654	7	11	NULL	NULL	NULL	IgG fractions	GP		bind					R0	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_1_11_s_105	9423833	(B) Binding of IgG fractions to R0; (C) binding of IgG fractions to R2-coated plates.	bind
11988	2	3654	7	11	NULL	NULL	NULL	IgG fraction	GP		bind					R2	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_1_11_s_105	9423833	(B) Binding of IgG fractions to R0; (C) binding of IgG fractions to R2-coated plates.	bind
81076	1	3654	11	NULL	NULL	0	NULL	IgG fraction	PartOfProtein		binds to 					R0	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_1_11_s_105	9423833	(B) Binding of IgG fractions to R0; (C) binding of IgG fractions to R2-coated plates.	bind
81077	2	3654	11	NULL	NULL	0	NULL	IgG fraction	PartOfProtein		binds to 					R2	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_1_11_s_105	9423833	(B) Binding of IgG fractions to R0; (C) binding of IgG fractions to R2-coated plates.	bind
8326	1	3656	6	11	NULL	NULL	NULL	IRF-3	GP		bind					importin-alpha receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_4159_s_234	10805757	(B) Binding of IRF-3 to importin-alpha receptors is NLS specific.	bind
11989	1	3656	7	NULL	NULL	0	NULL	IRF-3	NULL		bind	NULL				importin-alpha receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_11_4159_s_234	10805757	(B) Binding of IRF-3 to importin-alpha receptors is NLS specific.	bind
11990	2	3656	7	NULL	NULL	0	NULL	statement 1	NULL		is specific to	NULL				NLS	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_4159_s_234	10805757	(B) Binding of IRF-3 to importin-alpha receptors is NLS specific.	bind
81078	1	3656	11	NULL	NULL	0	NULL	IRF-3	Protein		binds to 					importin-alpha receptor	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_11_4159_s_234	10805757	(B) Binding of IRF-3 to importin-alpha receptors is NLS specific.	bind
81079	2	3656	11	NULL	NULL	0	NULL	statement 1	Process		is specific to					NLS	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_11_4159_s_234	10805757	(B) Binding of IRF-3 to importin-alpha receptors is NLS specific.	bind
8327	2	3657	6	11	NULL	NULL	NULL	statement 1	Process		is specific to					NLS	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_881_s_126	8945515	(B) Binding of labeled E. coli DnaB to  the GST, GST - wtRTP, and GST - mutant RTP matrices.	bind
8329	1	3657	6	11	NULL	NULL	NULL	DnaB	GP	labeled;; E. coli	bind					GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_881_s_126	8945515	(B) Binding of labeled E. coli DnaB to  the GST, GST - wtRTP, and GST - mutant RTP matrices.	bind
8330	2	3657	6	11	NULL	NULL	NULL	DnaB	GP	labeled;; E. coli	bind					GST-RTP	GP	wt			NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_881_s_126	8945515	(B) Binding of labeled E. coli DnaB to  the GST, GST - wtRTP, and GST - mutant RTP matrices.	bind
8331	3	3657	6	11	NULL	NULL	NULL	DnaB	GP	labeled;; E. coli	bind					GST-RTP	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_881_s_126	8945515	(B) Binding of labeled E. coli DnaB to  the GST, GST - wtRTP, and GST - mutant RTP matrices.	bind
11992	2	3657	7	11	NULL	NULL	NULL	DnaB	GP	labeled;; E. coli	bind					GST - RTP	GP	wt			NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_881_s_126	8945515	(B) Binding of labeled E. coli DnaB to  the GST, GST - wtRTP, and GST - mutant RTP matrices.	bind
11993	3	3657	7	11	NULL	NULL	NULL	DnaB	GP	labeled;; E. coli	bind					GST - RTP	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_881_s_126	8945515	(B) Binding of labeled E. coli DnaB to  the GST, GST - wtRTP, and GST - mutant RTP matrices.	bind
81080	1	3657	11	NULL	NULL	0	NULL	DnaB	Protein	labeled E. coli	binds to 					GST	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_87_5_881_s_126	8945515	(B) Binding of labeled E. coli DnaB to  the GST, GST - wtRTP, and GST - mutant RTP matrices.	bind
81081	2	3657	11	NULL	NULL	0	NULL	 DnaB	Protein	labeled E. coli	binds to 					GST - wtRTP	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_87_5_881_s_126	8945515	(B) Binding of labeled E. coli DnaB to  the GST, GST - wtRTP, and GST - mutant RTP matrices.	bind
81082	3	3657	11	NULL	NULL	0	NULL	DnaB	Protein	labeled E. coli	binds to 					GST - mutant RTP	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_87_5_881_s_126	8945515	(B) Binding of labeled E. coli DnaB to  the GST, GST - wtRTP, and GST - mutant RTP matrices.	bind
8334	1	3658	6	11	NULL	NULL	NULL	LIS1	GP		bind					GST-mNudE	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_3_665_s_90	11163258	(B) Binding of LIS1 to GST-mNudE.	bind
11994	1	3658	7	11	NULL	NULL	NULL	LIS1	GP		bind					GST-mNudE	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_3_665_s_90	11163258	(B) Binding of LIS1 to GST-mNudE.	bind
81083	1	3658	11	NULL	NULL	0	NULL	LIS1	Protein		binds to 					GST-mNudE	Protein				NULL		0	NULL	NULL	NULL	gw60_neuron_28_3_665_s_90	11163258	(B) Binding of LIS1 to GST-mNudE.	bind
8339	1	3659	6	11	NULL	NULL	NULL	 MdcR	GP		bind					P mdcR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_7_2302_s_87	10094715	(B) Binding of MdcR to P mdcR.	bind
11991	1	3659	7	11	NULL	NULL	NULL	DnaB	GP	labeled;; E. coli	bind					GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_7_2302_s_87	10094715	(B) Binding of MdcR to P mdcR.	bind
11995	1	3659	7	11	NULL	NULL	NULL	MdcR	GP		bind					P mdcR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_7_2302_s_87	10094715	(B) Binding of MdcR to P mdcR.	bind
81084	1	3659	11	NULL	NULL	0	NULL	MdcR	Gene		binds to 					P mdcR	Protein				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_7_2302_s_87	10094715	(B) Binding of MdcR to P mdcR.	bind
8342	1	3660	6	11	NULL	NULL	NULL	MDMX 	GP		bind					MDM2	GP	point mutants			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_15_5113_s_126	12860999	(B) Binding of MDMX to MDM2 point mutants.	bind
11996	1	3660	7	11	NULL	NULL	NULL	MDMX	GP		bind					MDM2	GP	point mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_15_5113_s_126	12860999	(B) Binding of MDMX to MDM2 point mutants.	bind
81085	1	3660	11	NULL	NULL	0	NULL	MDMX	Protein		binds to 					MDM2 point mutant	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_15_5113_s_126	12860999	(B) Binding of MDMX to MDM2 point mutants.	bind
8344	1	3661	6	11	NULL	NULL	NULL	MEF2D	GP	in vitro-translated;;35S-labeled	bind					HDAC7	GP		C-ter		NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_5_687_s_134	12753745	(B) Binding of MEF2D to the carboxyl (C-ter) or amino (N-ter) terminus of HDAC7 was measured in pull-down assays with in vitro translated 35S-labeled MEF2D.	bind
8345	2	3661	6	11	NULL	NULL	NULL	MEF2D	GP	in vitro-translated;;35S-labeled	bind					HDAC7	GP		N-ter		NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_5_687_s_134	12753745	(B) Binding of MEF2D to the carboxyl (C-ter) or amino (N-ter) terminus of HDAC7 was measured in pull-down assays with in vitro translated 35S-labeled MEF2D.	bind
8346	3	3661	6	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_5_687_s_134	12753745	(B) Binding of MEF2D to the carboxyl (C-ter) or amino (N-ter) terminus of HDAC7 was measured in pull-down assays with in vitro translated 35S-labeled MEF2D.	bind
40911	4	3661	6	11	NULL	NULL	NULL	C-ter	AminoAcid		is					Carboxyl terminus	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_5_687_s_134	12753745	(B) Binding of MEF2D to the carboxyl (C-ter) or amino (N-ter) terminus of HDAC7 was measured in pull-down assays with in vitro translated 35S-labeled MEF2D.	bind
40912	5	3661	6	11	NULL	NULL	NULL	N-ter	AminoAcid		is					amino terminus	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_5_687_s_134	12753745	(B) Binding of MEF2D to the carboxyl (C-ter) or amino (N-ter) terminus of HDAC7 was measured in pull-down assays with in vitro translated 35S-labeled MEF2D.	bind
12076	1	3661	7	11	NULL	NULL	NULL	 MEF2D	GP	in vitro translated;;35S-labeled	bind					HDAC7	GP		 amino terminus		NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_5_687_s_134	12753745	(B) Binding of MEF2D to the carboxyl (C-ter) or amino (N-ter) terminus of HDAC7 was measured in pull-down assays with in vitro translated 35S-labeled MEF2D.	bind
12077	2	3661	7	11	NULL	NULL	NULL	MEF2D	GP	in vitro-translated;;35S labeled	bind					HDAC7	GP		carboxyl terminus		NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_5_687_s_134	12753745	(B) Binding of MEF2D to the carboxyl (C-ter) or amino (N-ter) terminus of HDAC7 was measured in pull-down assays with in vitro translated 35S-labeled MEF2D.	bind
12078	3	3661	7	11	NULL	NULL	NULL	carboxyl terminus	AminoAcid		is					C-ter	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_5_687_s_134	12753745	(B) Binding of MEF2D to the carboxyl (C-ter) or amino (N-ter) terminus of HDAC7 was measured in pull-down assays with in vitro translated 35S-labeled MEF2D.	bind
12079	4	3661	7	11	NULL	NULL	NULL	amino terminus	AminoAcid		is					N-ter	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_5_687_s_134	12753745	(B) Binding of MEF2D to the carboxyl (C-ter) or amino (N-ter) terminus of HDAC7 was measured in pull-down assays with in vitro translated 35S-labeled MEF2D.	bind
15050	5	3661	7	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_5_687_s_134	12753745	(B) Binding of MEF2D to the carboxyl (C-ter) or amino (N-ter) terminus of HDAC7 was measured in pull-down assays with in vitro translated 35S-labeled MEF2D.	bind
81086	1	3661	11	NULL	NULL	0	NULL	MEF2D	Protein		binds to 					HDAC7	Protein		carboxyl terminus		NULL		0	NULL	NULL	NULL	gw60_immunity_18_5_687_s_134	12753745	(B) Binding of MEF2D to the carboxyl (C-ter) or amino (N-ter) terminus of HDAC7 was measured in pull-down assays with in vitro translated 35S-labeled MEF2D.	bind
81087	2	3661	11	NULL	NULL	0	NULL	MEF2D	Protein		binds to 					HDAC7	Protein		amino terminus		NULL		0	NULL	NULL	NULL	gw60_immunity_18_5_687_s_134	12753745	(B) Binding of MEF2D to the carboxyl (C-ter) or amino (N-ter) terminus of HDAC7 was measured in pull-down assays with in vitro translated 35S-labeled MEF2D.	bind
81088	3	3661	11	NULL	NULL	0	NULL	statement 1	Process		was measured in					pull-down assay	LaboratoryExperimentalFactor				NULL		0	NULL	NULL	NULL	gw60_immunity_18_5_687_s_134	12753745	(B) Binding of MEF2D to the carboxyl (C-ter) or amino (N-ter) terminus of HDAC7 was measured in pull-down assays with in vitro translated 35S-labeled MEF2D.	bind
81089	4	3661	11	NULL	NULL	0	NULL	statement 2	Process		measured in					pull-down assay	LaboratoryExperimentalFactor				NULL		0	NULL	NULL	NULL	gw60_immunity_18_5_687_s_134	12753745	(B) Binding of MEF2D to the carboxyl (C-ter) or amino (N-ter) terminus of HDAC7 was measured in pull-down assays with in vitro translated 35S-labeled MEF2D.	bind
8347	1	3662	6	11	NULL	NULL	NULL	MKL1	GP		bind					SRF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6597_s_128	12944485	(B) Binding of MKL1 to SRF in gel mobility shift assays.	bind
12080	1	3662	7	11	NULL	NULL	NULL	MKL1	GP		bind					SRF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6597_s_128	12944485	(B) Binding of MKL1 to SRF in gel mobility shift assays.	bind
81090	1	3662	11	NULL	NULL	0	NULL	MKL1	Protein		binds to 					SRF	Protein				NULL	gel mobility shift assay	0	NULL	NULL	NULL	gw60_molcellbiol_23_18_6597_s_128	12944485	(B) Binding of MKL1 to SRF in gel mobility shift assays.	bind
8348	1	3663	6	11	NULL	NULL	NULL	MOG-6	GP		bind					MEP-1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_131_12_2935_s_129	15151984	(B) Binding of MOG-6 to MEP-1 in vitro.	bind
12081	1	3663	7	11	NULL	NULL	NULL	MOG-6	GP		bind					MEP-1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_131_12_2935_s_129	15151984	(B) Binding of MOG-6 to MEP-1 in vitro.	bind
81091	1	3663	11	NULL	NULL	0	NULL	MOG-6	Protein		binds to 					MEP-1	Protein				NULL	in vitro	0	NULL	NULL	NULL	gw70_development_131_12_2935_s_129	15151984	(B) Binding of MOG-6 to MEP-1 in vitro.	bind
8349	1	3664	6	11	NULL	NULL	NULL	n-sec1	GP		bind					syntaxin 1a	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_6_1229_s_89	8663999	(B) Binding of n-sec1 to syntaxin 1a in the presence of 500  M S-NC.	bind
8350	2	3664	6	11	NULL	NULL	NULL	statement 1	Process		occurs in presence of					S-NC	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_6_1229_s_89	8663999	(B) Binding of n-sec1 to syntaxin 1a in the presence of 500  M S-NC.	bind
12082	1	3664	7	11	NULL	NULL	NULL	n-sec1	GP		bind					syntaxin 1a	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_6_1229_s_89	8663999	(B) Binding of n-sec1 to syntaxin 1a in the presence of 500  M S-NC.	bind
81092	1	3664	11	NULL	NULL	0	NULL	n-sec1	Protein		binds to 					syntaxin 1a	Protein				NULL		0	NULL	NULL	NULL	gw60_neuron_16_6_1229_s_89	8663999	(B) Binding of n-sec1 to syntaxin 1a in the presence of 500  M S-NC.	bind
81093	2	3664	11	NULL	NULL	0	NULL	statement 1	Process		occurs in the presence of					S-nitrosocysteine	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_neuron_16_6_1229_s_89	8663999	(B) Binding of n-sec1 to syntaxin 1a in the presence of 500  M S-NC.	bind
8351	1	3665	6	11	NULL	NULL	NULL	NIF-1	GP		bind					NRC	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_19_6883_s_68	12215545	(B) Binding of NIF-1 with NRC in vitro.	bind
12083	1	3665	7	11	NULL	NULL	NULL	NIF-1	GP		bind					NRC	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_19_6883_s_68	12215545	(B) Binding of NIF-1 with NRC in vitro.	bind
81094	1	3665	11	NULL	NULL	NULL	NULL	NIF-1	Protein		binds to 					NRC	Protein				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_19_6883_s_68	12215545	(B) Binding of NIF-1 with NRC in vitro.	bind
8352	1	3666	6	11	NULL	NULL	NULL	nuclear proteins	GP		bind					Sp1 sites	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1574_2_164_s_207	11955626	(B) Binding of nuclear proteins to both Sp1 sites.	bind
12085	1	3666	7	11	NULL	NULL	NULL	nuclear proteins	GP		bind					Sp1 sites	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1574_2_164_s_207	11955626	(B) Binding of nuclear proteins to both Sp1 sites.	bind
81095	1	3666	11	NULL	NULL	0	NULL	nuclear protein	Protein		binds to 					Sp1 site	Protein				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1574_2_164_s_207	11955626	(B) Binding of nuclear proteins to both Sp1 sites.	bind
8353	1	3667	6	11	NULL	NULL	NULL	nuclear proteins	GP		bind							radiolabeled		B-CRE	NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_4_709_s_254	9581763	(B) Binding of nuclear proteins to radiolabeled B-CRE in an electrophoretic mobility shift assay.	bind
12087	1	3667	7	11	NULL	NULL	NULL	nuclear proteins	GP		bind							 radiolabeled		B-CRE	NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_4_709_s_254	9581763	(B) Binding of nuclear proteins to radiolabeled B-CRE in an electrophoretic mobility shift assay.	bind
81096	1	3667	11	NULL	NULL	0	NULL	nuclear protein	Protein		binds to 					B-CRE	NucleicAcidSubstance	radiolabeled			NULL	electrophoretic mobility shift assay	0	NULL	NULL	NULL	gw60_neuron_20_4_709_s_254	9581763	(B) Binding of nuclear proteins to radiolabeled B-CRE in an electrophoretic mobility shift assay.	bind
8354	1	3668	6	11	NULL	NULL	NULL	p115	GP		bind					CSW	GP		SH2 domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_85_6_899_s_88	8681384	(B) Binding of p115 to the  CSW SH2 domains.	bind
12089	1	3668	7	11	NULL	NULL	NULL	p115	GP		bind					CSW	GP		SH2 domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_85_6_899_s_88	8681384	(B) Binding of p115 to the  CSW SH2 domains.	bind
81097	1	3668	11	NULL	NULL	0	NULL	p115	Protein		binds to 					CSW	Protein		SH2 domain		NULL		0	NULL	NULL	NULL	gw60_cell_85_6_899_s_88	8681384	(B) Binding of p115 to the  CSW SH2 domains.	bind
8355	1	3669	6	11	NULL	NULL	NULL	Pbx1	GP		bind					Hox11	GP			PX1 oligo within the promoter	NULL		NULL	NULL	NULL	NULL	gw70_development_132_13_3113_s_192	15944191	(B) Binding of Pbx1 and Hox11 to the (PX1) oligo within the  Hox11 promoter.	bind
17775	2	3669	6	11	NULL	NULL	NULL	Hox11	GP		bind					Hox11	GP			PX1 oligo within the promoter	NULL		NULL	NULL	NULL	NULL	gw70_development_132_13_3113_s_192	15944191	(B) Binding of Pbx1 and Hox11 to the (PX1) oligo within the  Hox11 promoter.	bind
12091	1	3669	7	11	NULL	NULL	NULL	Pbx1	GP		bind					Hox11	GP			PX1 oligo in the promoter of 	NULL		NULL	NULL	NULL	NULL	gw70_development_132_13_3113_s_192	15944191	(B) Binding of Pbx1 and Hox11 to the (PX1) oligo within the  Hox11 promoter.	bind
12092	2	3669	7	11	NULL	NULL	NULL	Hox11	GP		bind					Hox11	GP			PX1 oligo in the promoter of 	NULL		NULL	NULL	NULL	NULL	gw70_development_132_13_3113_s_192	15944191	(B) Binding of Pbx1 and Hox11 to the (PX1) oligo within the  Hox11 promoter.	bind
81098	1	3669	11	NULL	NULL	0	NULL	Pbx1	Protein		binds to 					Hox11 promoter	NucleicAcidSubstance			PX1 oligo	NULL		0	NULL	NULL	NULL	gw70_development_132_13_3113_s_192	15944191	(B) Binding of Pbx1 and Hox11 to the (PX1) oligo within the  Hox11 promoter.	bind
81099	2	3669	11	NULL	NULL	0	NULL	Hox11	Protein		binds to 					Hox11 promoter	NucleicAcidSubstance			PX1 oligo	NULL		0	NULL	NULL	NULL	gw70_development_132_13_3113_s_192	15944191	(B) Binding of Pbx1 and Hox11 to the (PX1) oligo within the  Hox11 promoter.	bind
8356	1	3670	6	11	NULL	NULL	NULL	Pex7p	GP		bind					PTS2 protein	GP	synthetic			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6056_s_96	12167700	(B) Binding of Pex7p to a synthetic PTS2 protein in vitro.	bind
12093	1	3670	7	11	NULL	NULL	NULL	Pex7p	GP		bind					PTS2 protein	GP	synthetic			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6056_s_96	12167700	(B) Binding of Pex7p to a synthetic PTS2 protein in vitro.	bind
81100	1	3670	11	NULL	NULL	0	NULL	Pex7p	Protein		binds to 					synthetic PTS2 protein	Protein				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6056_s_96	12167700	(B) Binding of Pex7p to a synthetic PTS2 protein in vitro.	bind
8357	1	3671	6	11	NULL	NULL	NULL	Pex7p	GP		bind					Pex13p	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6056_s_229	12167700	(B) Binding of Pex7p to Pex13p in vitro.	bind
12094	1	3671	7	11	NULL	NULL	NULL	Pex7p	GP		bind					Pex13p	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6056_s_229	12167700	(B) Binding of Pex7p to Pex13p in vitro.	bind
81101	1	3671	11	NULL	NULL	0	NULL	Pex7p	Protein		binds to 					Pex13p	Protein				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6056_s_229	12167700	(B) Binding of Pex7p to Pex13p in vitro.	bind
81102	1	3672	11	NULL	NULL	0	NULL	protein	Protein		binds to 					consensus AP-1	Protein				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1524_1_57_s_137	11078959	(B) Binding of protein(s) to a consensus AP-1 element was inhibited by exposure of EC to quinacrine.	bind
81103	2	3672	11	NULL	NULL	0	NULL	quinacrine	Chemical	exposure of	inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1524_1_57_s_137	11078959	(B) Binding of protein(s) to a consensus AP-1 element was inhibited by exposure of EC to quinacrine.	bind
12095	1	3673	7	11	NULL	NULL	NULL	Eve protein	GP	purified	bind					GST-dTBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_1_77_s_93	10024881	(b) Binding of purified Eve proteins to GST-dTBP.	bind
81104	1	3673	11	NULL	NULL	0	NULL	Eve protein	Protein	purified	binds to 					GST-dTBP	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_3_1_77_s_93	10024881	(b) Binding of purified Eve proteins to GST-dTBP.	bind
8360	1	3674	6	11	NULL	NULL	NULL	Eve proteins	GP	purified	bind					GST-dTBP	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_10_3664_s_190	16672620	(B) Binding of purified Fur protein to the  ycgT regulatory region.	bind
8361	1	3674	6	11	NULL	NULL	NULL	Fur protein	GP	purified	bind					ycgT	GP			regulatory region	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_10_3664_s_190	16672620	(B) Binding of purified Fur protein to the  ycgT regulatory region.	bind
12096	1	3674	7	11	NULL	NULL	NULL	Fur protein	GP	purified	bind					ycgT	GP			regulatory region	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_10_3664_s_190	16672620	(B) Binding of purified Fur protein to the  ycgT regulatory region.	bind
81105	1	3674	11	NULL	NULL	0	NULL	Fur protein	Protein		binds to 					ycgT regulatory region	Protein				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_10_3664_s_190	16672620	(B) Binding of purified Fur protein to the  ycgT regulatory region.	bind
8362	1	3675	6	11	NULL	NULL	NULL	RGS4	GP	purified	bind					GST-beta''-COP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_9_3155_s_136	10982407	(B) Binding of purified RGS4 to GST-beta''-COP.	bind
12097	1	3675	7	11	NULL	NULL	NULL	RGS4	GP	purified	bind					GST-beta''-COP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_9_3155_s_136	10982407	(B) Binding of purified RGS4 to GST-beta''-COP.	bind
81106	1	3675	11	NULL	NULL	0	NULL	RGS4	Protein	purified	binds to 					GST-beta''-COP	Protein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_9_3155_s_136	10982407	(B) Binding of purified RGS4 to GST-beta''-COP.	bind
8363	1	3676	6	11	NULL	NULL	NULL	DDR2-Fc	GP	radiolabelled	bind					cell surface	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_38	9659900	(B) Binding of radiolabelled DDR2-Fc to cell surfaces can be specifically competed by both DDR1 and DDR2 Rbodies (and not a control Rbody), demonstrating the specificity of binding and that both DDR receptors are binding to the same putative cell-associated ligand.	bind
8364	2	3676	6	11	NULL	NULL	NULL	DDR1 Rbodies	GP		bind					cell surface	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_38	9659900	(B) Binding of radiolabelled DDR2-Fc to cell surfaces can be specifically competed by both DDR1 and DDR2 Rbodies (and not a control Rbody), demonstrating the specificity of binding and that both DDR receptors are binding to the same putative cell-associated ligand.	bind
8366	3	3676	6	11	NULL	NULL	NULL	statement 1	Process		competes		specifically			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_38	9659900	(B) Binding of radiolabelled DDR2-Fc to cell surfaces can be specifically competed by both DDR1 and DDR2 Rbodies (and not a control Rbody), demonstrating the specificity of binding and that both DDR receptors are binding to the same putative cell-associated ligand.	bind
8367	4	3676	6	11	NULL	NULL	NULL	DDR2 Rbodies	GP		bind					cell surface	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_38	9659900	(B) Binding of radiolabelled DDR2-Fc to cell surfaces can be specifically competed by both DDR1 and DDR2 Rbodies (and not a control Rbody), demonstrating the specificity of binding and that both DDR receptors are binding to the same putative cell-associated ligand.	bind
8368	5	3676	6	11	NULL	NULL	NULL	statement 1	Process		competes		specifically			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_38	9659900	(B) Binding of radiolabelled DDR2-Fc to cell surfaces can be specifically competed by both DDR1 and DDR2 Rbodies (and not a control Rbody), demonstrating the specificity of binding and that both DDR receptors are binding to the same putative cell-associated ligand.	bind
53027	6	3676	6	11	NULL	NULL	NULL	DDR receptors	GP		bind					cell-associated ligand	GP	putative			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_38	9659900	(B) Binding of radiolabelled DDR2-Fc to cell surfaces can be specifically competed by both DDR1 and DDR2 Rbodies (and not a control Rbody), demonstrating the specificity of binding and that both DDR receptors are binding to the same putative cell-associated ligand.	bind
12100	2	3676	7	11	NULL	NULL	NULL	DDR1 Rbody 	GP		bind					cell surface  	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_38	9659900	(B) Binding of radiolabelled DDR2-Fc to cell surfaces can be specifically competed by both DDR1 and DDR2 Rbodies (and not a control Rbody), demonstrating the specificity of binding and that both DDR receptors are binding to the same putative cell-associated ligand.	bind
12101	3	3676	7	11	NULL	NULL	NULL	DDR2 Rbody	GP		bind					cell surface  	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_38	9659900	(B) Binding of radiolabelled DDR2-Fc to cell surfaces can be specifically competed by both DDR1 and DDR2 Rbodies (and not a control Rbody), demonstrating the specificity of binding and that both DDR receptors are binding to the same putative cell-associated ligand.	bind
12102	4	3676	7	11	NULL	NULL	NULL	statement 2	Process		compete with		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_38	9659900	(B) Binding of radiolabelled DDR2-Fc to cell surfaces can be specifically competed by both DDR1 and DDR2 Rbodies (and not a control Rbody), demonstrating the specificity of binding and that both DDR receptors are binding to the same putative cell-associated ligand.	bind
12103	5	3676	7	11	NULL	NULL	NULL	statement 3	Process		compete with		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_38	9659900	(B) Binding of radiolabelled DDR2-Fc to cell surfaces can be specifically competed by both DDR1 and DDR2 Rbodies (and not a control Rbody), demonstrating the specificity of binding and that both DDR receptors are binding to the same putative cell-associated ligand.	bind
12104	6	3676	7	11	NULL	NULL	NULL	DDR receptors	GP		bind					cell-associated ligand	GP	putative			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_38	9659900	(B) Binding of radiolabelled DDR2-Fc to cell surfaces can be specifically competed by both DDR1 and DDR2 Rbodies (and not a control Rbody), demonstrating the specificity of binding and that both DDR receptors are binding to the same putative cell-associated ligand.	bind
81108	1	3676	11	NULL	NULL	0	NULL	DDR2-Fc	Protein	 radiolabelled	binds to 					cell surface	CellComponent				NULL		0	NULL	NULL	NULL	gw60_molcell_1_1_25_s_38	9659900	(B) Binding of radiolabelled DDR2-Fc to cell surfaces can be specifically competed by both DDR1 and DDR2 Rbodies (and not a control Rbody), demonstrating the specificity of binding and that both DDR receptors are binding to the same putative cell-associated ligand.	bind
81109	2	3676	11	NULL	NULL	0	NULL	DDR1 Rbodies	Protein		binds to 					cell surface	CellComponent				NULL		0	NULL	NULL	NULL	gw60_molcell_1_1_25_s_38	9659900	(B) Binding of radiolabelled DDR2-Fc to cell surfaces can be specifically competed by both DDR1 and DDR2 Rbodies (and not a control Rbody), demonstrating the specificity of binding and that both DDR receptors are binding to the same putative cell-associated ligand.	bind
81110	3	3676	11	NULL	NULL	0	NULL	DDR2 Rbodies	Protein		binds to 					cell surface	CellComponent				NULL		0	NULL	NULL	NULL	gw60_molcell_1_1_25_s_38	9659900	(B) Binding of radiolabelled DDR2-Fc to cell surfaces can be specifically competed by both DDR1 and DDR2 Rbodies (and not a control Rbody), demonstrating the specificity of binding and that both DDR receptors are binding to the same putative cell-associated ligand.	bind
81111	4	3676	11	NULL	NULL	0	NULL	DDR1 Rbodies	Protein		competes with					DDR2-Fc	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_1_1_25_s_38	9659900	(B) Binding of radiolabelled DDR2-Fc to cell surfaces can be specifically competed by both DDR1 and DDR2 Rbodies (and not a control Rbody), demonstrating the specificity of binding and that both DDR receptors are binding to the same putative cell-associated ligand.	bind
81112	5	3676	11	NULL	NULL	0	NULL	DDR2 Rbodies	Protein		competes with					DDR2-Fc	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_1_1_25_s_38	9659900	(B) Binding of radiolabelled DDR2-Fc to cell surfaces can be specifically competed by both DDR1 and DDR2 Rbodies (and not a control Rbody), demonstrating the specificity of binding and that both DDR receptors are binding to the same putative cell-associated ligand.	bind
81113	6	3676	11	NULL	NULL	0	NULL	DDR1 Rbodies	Protein		binds to 					cell-associated ligand	GeneOrProtein	putative 			NULL		0	NULL	NULL	NULL	gw60_molcell_1_1_25_s_38	9659900	(B) Binding of radiolabelled DDR2-Fc to cell surfaces can be specifically competed by both DDR1 and DDR2 Rbodies (and not a control Rbody), demonstrating the specificity of binding and that both DDR receptors are binding to the same putative cell-associated ligand.	bind
81114	7	3676	11	NULL	NULL	0	NULL	DDR2 Rbodies	Protein		binds to 					cell-associated ligand	GeneOrProtein	putative 			NULL		0	NULL	NULL	NULL	gw60_molcell_1_1_25_s_38	9659900	(B) Binding of radiolabelled DDR2-Fc to cell surfaces can be specifically competed by both DDR1 and DDR2 Rbodies (and not a control Rbody), demonstrating the specificity of binding and that both DDR receptors are binding to the same putative cell-associated ligand.	bind
8528	1	3677	6	11	NULL	NULL	NULL	elongin B 	GP	radiolabelled	bind					GST-elongin C	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_732_s_209	9447969	(B) Binding of radiolabelled elongin B to the indicated GST-elongin C fusion proteins (lanes 2 to 10).	bind
40916	2	3677	6	11	NULL	NULL	NULL	GST-elongin C	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_732_s_209	9447969	(B) Binding of radiolabelled elongin B to the indicated GST-elongin C fusion proteins (lanes 2 to 10).	bind
12106	1	3677	7	11	NULL	NULL	NULL	elongin B	GP	radiolabelled 	bind					GST-elongin C	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_732_s_209	9447969	(B) Binding of radiolabelled elongin B to the indicated GST-elongin C fusion proteins (lanes 2 to 10).	bind
53028	2	3677	7	11	NULL	NULL	NULL	GST-elongin C	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_732_s_209	9447969	(B) Binding of radiolabelled elongin B to the indicated GST-elongin C fusion proteins (lanes 2 to 10).	bind
81115	1	3677	11	NULL	NULL	0	NULL	elongin B	Protein	radiolabelled	binds to 					GST-elongin C fusion proteins	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_2_732_s_209	9447969	(B) Binding of radiolabelled elongin B to the indicated GST-elongin C fusion proteins (lanes 2 to 10).	bind
8529	1	3678	6	11	NULL	NULL	NULL	Raf-1	GP		bind					Rb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_108	9819434	(B) Binding of Raf-1 to Rb and p130 but not to p107, E2F1, or DP proteins in a similar assay.	bind
8533	3	3678	6	11	NULL	NULL	NULL	Raf-1	GP		bind					p130	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_108	9819434	(B) Binding of Raf-1 to Rb and p130 but not to p107, E2F1, or DP proteins in a similar assay.	bind
8534	4	3678	6	11	NULL	NULL	NULL	Raf-1	GP		does not bind					p107	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_108	9819434	(B) Binding of Raf-1 to Rb and p130 but not to p107, E2F1, or DP proteins in a similar assay.	bind
8535	5	3678	6	11	NULL	NULL	NULL	Raf-1	GP		does not bind					E2F1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_108	9819434	(B) Binding of Raf-1 to Rb and p130 but not to p107, E2F1, or DP proteins in a similar assay.	bind
8536	6	3678	6	11	NULL	NULL	NULL	Raf-1	GP		does not bind					DP proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_108	9819434	(B) Binding of Raf-1 to Rb and p130 but not to p107, E2F1, or DP proteins in a similar assay.	bind
12099	1	3678	7	11	NULL	NULL	NULL	DDR2-Fc	GP	radiolabelled 	bind					cell surface  	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_108	9819434	(B) Binding of Raf-1 to Rb and p130 but not to p107, E2F1, or DP proteins in a similar assay.	bind
12107	1	3678	7	11	NULL	NULL	NULL	Raf-1	GP		bind					Rb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_108	9819434	(B) Binding of Raf-1 to Rb and p130 but not to p107, E2F1, or DP proteins in a similar assay.	bind
12109	2	3678	7	11	NULL	NULL	NULL	Raf-1	GP		bind					p130	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_108	9819434	(B) Binding of Raf-1 to Rb and p130 but not to p107, E2F1, or DP proteins in a similar assay.	bind
12110	3	3678	7	11	NULL	NULL	NULL	Raf-1	GP		does not bind					p107	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_108	9819434	(B) Binding of Raf-1 to Rb and p130 but not to p107, E2F1, or DP proteins in a similar assay.	bind
12111	4	3678	7	11	NULL	NULL	NULL	Raf-1	GP		does not bind					E2F1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_108	9819434	(B) Binding of Raf-1 to Rb and p130 but not to p107, E2F1, or DP proteins in a similar assay.	bind
12112	5	3678	7	11	NULL	NULL	NULL	Raf-1	GP		does not bind					DP protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_108	9819434	(B) Binding of Raf-1 to Rb and p130 but not to p107, E2F1, or DP proteins in a similar assay.	bind
81116	1	3678	11	NULL	NULL	0	NULL	Raf-1	Protein		binds to 					Rb	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_108	9819434	(B) Binding of Raf-1 to Rb and p130 but not to p107, E2F1, or DP proteins in a similar assay.	bind
81117	2	3678	11	NULL	NULL	0	NULL	Raf-1	Protein		binds to 					p130	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_108	9819434	(B) Binding of Raf-1 to Rb and p130 but not to p107, E2F1, or DP proteins in a similar assay.	bind
81118	3	3678	11	NULL	NULL	NULL	NULL	Raf-1	Protein		does not bind to					p107 protein	Protein				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_108	9819434	(B) Binding of Raf-1 to Rb and p130 but not to p107, E2F1, or DP proteins in a similar assay.	bind
81119	4	3678	11	NULL	NULL	NULL	NULL	Raf-1	Protein		does not bind to					E2F1 protein	Protein				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_108	9819434	(B) Binding of Raf-1 to Rb and p130 but not to p107, E2F1, or DP proteins in a similar assay.	bind
81120	5	3678	11	NULL	NULL	0	NULL	Raf-1	Protein		does not bind to					DP protein	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_108	9819434	(B) Binding of Raf-1 to Rb and p130 but not to p107, E2F1, or DP proteins in a similar assay.	bind
8540	1	3679	6	11	NULL	NULL	NULL	CBF3 proteins	GP	recombinant	bind					DNA	NucleicAcid			CDEIII 	NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_11_4557_s_108	13679521	(B) Binding of recombinant CBF3 proteins to CDEIII DNA (probe 2). "`	bind
12113	1	3679	7	11	NULL	NULL	NULL	CBF3 protein	GP	recombinant	bind					DNA	NucleicAcid			CDEIII 	NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_11_4557_s_108	13679521	(B) Binding of recombinant CBF3 proteins to CDEIII DNA (probe 2). "`	bind
81121	1	3679	11	NULL	NULL	0	NULL	CBF3 protein	Protein	 recombinant	binds to 					CDEIII DNA	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_11_4557_s_108	13679521	(B) Binding of recombinant CBF3 proteins to CDEIII DNA (probe 2). "`	bind
8543	1	3680	6	11	NULL	NULL	NULL	NF-I	GP	recombinant	bind			C220		UC	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_72_1_65_s_137	10521600	(B) Binding of recombinant NF-I C220 to UC, UCY and UBE.	bind
8546	2	3680	6	11	NULL	NULL	NULL	NF-I	GP	recombinant	bind			C220		UCY	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_72_1_65_s_137	10521600	(B) Binding of recombinant NF-I C220 to UC, UCY and UBE.	bind
8547	3	3680	6	11	NULL	NULL	NULL	NF-I	GP	recombinant	bind			C220		UBE	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_72_1_65_s_137	10521600	(B) Binding of recombinant NF-I C220 to UC, UCY and UBE.	bind
12114	1	3680	7	11	NULL	NULL	NULL	NF-I 	GP	recombinant	bind			C220 		UC	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_72_1_65_s_137	10521600	(B) Binding of recombinant NF-I C220 to UC, UCY and UBE.	bind
12115	2	3680	7	11	NULL	NULL	NULL	NF-I 	GP	recombinant	bind			C220 		UCY	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_72_1_65_s_137	10521600	(B) Binding of recombinant NF-I C220 to UC, UCY and UBE.	bind
12116	3	3680	7	11	NULL	NULL	NULL	NF-I	GP	recombinant	bind			C220		UBE	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_72_1_65_s_137	10521600	(B) Binding of recombinant NF-I C220 to UC, UCY and UBE.	bind
81217	1	3680	11	NULL	NULL	0	NULL	NF-I C220	Protein		binds to 					UC	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_72_1_65_s_137	10521600	(B) Binding of recombinant NF-I C220 to UC, UCY and UBE.	bind
81218	2	3680	11	NULL	NULL	0	NULL	NF-I C220	Protein		binds to 					UCY	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_72_1_65_s_137	10521600	(B) Binding of recombinant NF-I C220 to UC, UCY and UBE.	bind
81219	3	3680	11	NULL	NULL	NULL	NULL	NF-I C220	Protein		binds to 					UBE	NucleicAcidSubstance				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_72_1_65_s_137	10521600	(B) Binding of recombinant NF-I C220 to UC, UCY and UBE.	bind
8552	1	3681	6	11	NULL	NULL	NULL	SP-1	GP	recombinant	bind					TK-SP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8442_s_188	10567569	(B) Binding of recombinant SP-1 to a TK-SP1 or to the indicated E2F elements.	bind
8558	2	3681	6	11	NULL	NULL	NULL	SP-1	GP	recombinant	bind									E2F element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8442_s_188	10567569	(B) Binding of recombinant SP-1 to a TK-SP1 or to the indicated E2F elements.	bind
40923	3	3681	6	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8442_s_188	10567569	(B) Binding of recombinant SP-1 to a TK-SP1 or to the indicated E2F elements.	bind
12117	1	3681	7	11	NULL	NULL	NULL	SP-1	GP	recombinant	bind					TK-SP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8442_s_188	10567569	(B) Binding of recombinant SP-1 to a TK-SP1 or to the indicated E2F elements.	bind
12118	2	3681	7	11	NULL	NULL	NULL	SP-1	GP	recombinant	bind									E2F element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8442_s_188	10567569	(B) Binding of recombinant SP-1 to a TK-SP1 or to the indicated E2F elements.	bind
12119	3	3681	7	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8442_s_188	10567569	(B) Binding of recombinant SP-1 to a TK-SP1 or to the indicated E2F elements.	bind
81220	1	3681	11	NULL	NULL	0	NULL	SP-1	Protein		binds to 					TK-SP1 	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_12_8442_s_188	10567569	(B) Binding of recombinant SP-1 to a TK-SP1 or to the indicated E2F elements.	bind
81221	2	3681	11	NULL	NULL	0	NULL	SP-1	Protein		binds to 					E2F	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_12_8442_s_188	10567569	(B) Binding of recombinant SP-1 to a TK-SP1 or to the indicated E2F elements.	bind
8559	1	3682	6	11	NULL	NULL	NULL	RPA	GP		bind					p53	GP			UV lesions	NULL	HEK293T cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_39_s_95	16354678	(B) Binding of RPA to UV and  N-AAAF lesions in the p53 of HEK293T cells.	bind
8560	2	3682	6	11	NULL	NULL	NULL	RPA	GP		bind					p53	GP			N-AAAF lesions	NULL	HEK293T cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_39_s_95	16354678	(B) Binding of RPA to UV and  N-AAAF lesions in the p53 of HEK293T cells.	bind
12120	1	3682	7	11	NULL	NULL	NULL	RPA	GP		bind					p53	GP			UV lesion 	NULL	HEK293T cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_39_s_95	16354678	(B) Binding of RPA to UV and  N-AAAF lesions in the p53 of HEK293T cells.	bind
12121	2	3682	7	11	NULL	NULL	NULL	RPA	GP		bind					p53	GP			N-AAAF lesion	NULL	HEK293T cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_39_s_95	16354678	(B) Binding of RPA to UV and  N-AAAF lesions in the p53 of HEK293T cells.	bind
81222	1	3682	11	NULL	NULL	0	NULL	UV	EnvironmentalFactor		makes lesions in					p53	Protein	HEK293T cells			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_1_39_s_95	16354678	(B) Binding of RPA to UV and  N-AAAF lesions in the p53 of HEK293T cells.	bind
81223	2	3682	11	NULL	NULL	0	NULL	N-AAAF	Chemical		makes lesions in					p53	Protein	HEK293T cells			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_1_39_s_95	16354678	(B) Binding of RPA to UV and  N-AAAF lesions in the p53 of HEK293T cells.	bind
81224	3	3682	11	NULL	NULL	0	NULL	RPA	Protein		binds to 					statement 1	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_1_39_s_95	16354678	(B) Binding of RPA to UV and  N-AAAF lesions in the p53 of HEK293T cells.	bind
81225	4	3682	11	NULL	NULL	0	NULL	RPA	Protein		binds to 					statement 2	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_1_39_s_95	16354678	(B) Binding of RPA to UV and  N-AAAF lesions in the p53 of HEK293T cells.	bind
8561	1	3683	6	11	NULL	NULL	NULL	Skp1	GP		bind					Skp2	GP	truncation mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_635_s_169	9858587	(B) Binding of Skp1 and cyclin A-Cdk2 to Skp2 truncation mutants.	bind
8562	2	3683	6	11	NULL	NULL	NULL	cyclin A-Cdk2	GP		bind					Skp2	GP	truncation mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_635_s_169	9858587	(B) Binding of Skp1 and cyclin A-Cdk2 to Skp2 truncation mutants.	bind
12122	1	3683	7	11	NULL	NULL	NULL	Skp1	GP		bind					Skp2	GP	truncation mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_635_s_169	9858587	(B) Binding of Skp1 and cyclin A-Cdk2 to Skp2 truncation mutants.	bind
12123	2	3683	7	11	NULL	NULL	NULL	cyclin A-Cdk2	GP		bind					Skp2	GP	truncation mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_635_s_169	9858587	(B) Binding of Skp1 and cyclin A-Cdk2 to Skp2 truncation mutants.	bind
81226	1	3683	11	NULL	NULL	0	NULL	Skp1	Protein		binds to 					Skp2 mutants	Protein	truncation			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_635_s_169	9858587	(B) Binding of Skp1 and cyclin A-Cdk2 to Skp2 truncation mutants.	bind
81227	2	3683	11	NULL	NULL	0	NULL	cyclin A-Cdk2	Protein		binds to 					Skp2 mutants	Protein	truncation			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_635_s_169	9858587	(B) Binding of Skp1 and cyclin A-Cdk2 to Skp2 truncation mutants.	bind
8563	1	3684	6	11	NULL	NULL	NULL	Skp2	GP		bind					cyclin D2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1189_s_257	12769844	(B) Binding of Skp2, Sug1, and Ub to the cyclin D2 promoter is Myc dependent.	bind
8564	2	3684	6	11	NULL	NULL	NULL	Sug1	GP		bind					cyclin D2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1189_s_257	12769844	(B) Binding of Skp2, Sug1, and Ub to the cyclin D2 promoter is Myc dependent.	bind
8565	3	3684	6	11	NULL	NULL	NULL	Ub	GP		bind					cyclin D2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1189_s_257	12769844	(B) Binding of Skp2, Sug1, and Ub to the cyclin D2 promoter is Myc dependent.	bind
8566	4	3684	6	11	NULL	NULL	NULL	statement 1	Process		is dependent on					Myc	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1189_s_257	12769844	(B) Binding of Skp2, Sug1, and Ub to the cyclin D2 promoter is Myc dependent.	bind
8567	5	3684	6	11	NULL	NULL	NULL	statement 2	Process		is dependent on					Myc	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1189_s_257	12769844	(B) Binding of Skp2, Sug1, and Ub to the cyclin D2 promoter is Myc dependent.	bind
8568	6	3684	6	11	NULL	NULL	NULL	statement 3	Process		is dependent on					Myc	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1189_s_257	12769844	(B) Binding of Skp2, Sug1, and Ub to the cyclin D2 promoter is Myc dependent.	bind
12124	1	3684	7	11	NULL	NULL	NULL	Skp2	GP		bind					cyclin D2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1189_s_257	12769844	(B) Binding of Skp2, Sug1, and Ub to the cyclin D2 promoter is Myc dependent.	bind
12125	2	3684	7	11	NULL	NULL	NULL	Sug1	GP		bind					cyclin D2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1189_s_257	12769844	(B) Binding of Skp2, Sug1, and Ub to the cyclin D2 promoter is Myc dependent.	bind
12126	3	3684	7	11	NULL	NULL	NULL	Ub	GP		bind					cyclin D2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1189_s_257	12769844	(B) Binding of Skp2, Sug1, and Ub to the cyclin D2 promoter is Myc dependent.	bind
12127	4	3684	7	11	NULL	NULL	NULL	statement 1	Process		is dependent on					Myc	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1189_s_257	12769844	(B) Binding of Skp2, Sug1, and Ub to the cyclin D2 promoter is Myc dependent.	bind
12128	5	3684	7	11	NULL	NULL	NULL	statement 2	Process		is dependent on					Myc	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1189_s_257	12769844	(B) Binding of Skp2, Sug1, and Ub to the cyclin D2 promoter is Myc dependent.	bind
12129	6	3684	7	11	NULL	NULL	NULL	statement 3	Process		is dependent on					Myc	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1189_s_257	12769844	(B) Binding of Skp2, Sug1, and Ub to the cyclin D2 promoter is Myc dependent.	bind
81228	1	3684	11	NULL	NULL	0	NULL	Skp2	Protein		binds to 					cyclin D2 promoter	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1189_s_257	12769844	(B) Binding of Skp2, Sug1, and Ub to the cyclin D2 promoter is Myc dependent.	bind
81229	2	3684	11	NULL	NULL	0	NULL	Sug1	Protein		binds to 					cyclin D2 promoter	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1189_s_257	12769844	(B) Binding of Skp2, Sug1, and Ub to the cyclin D2 promoter is Myc dependent.	bind
81230	3	3684	11	NULL	NULL	0	NULL	Ub	Protein		binds to 					cyclin D2 promoter	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1189_s_257	12769844	(B) Binding of Skp2, Sug1, and Ub to the cyclin D2 promoter is Myc dependent.	bind
81231	4	3684	11	NULL	NULL	0	NULL	statement 1	Process		depends on					Myc	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1189_s_257	12769844	(B) Binding of Skp2, Sug1, and Ub to the cyclin D2 promoter is Myc dependent.	bind
81232	5	3684	11	NULL	NULL	0	NULL	statement 2	Process		depends on					Myc	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1189_s_257	12769844	(B) Binding of Skp2, Sug1, and Ub to the cyclin D2 promoter is Myc dependent.	bind
81233	6	3684	11	NULL	NULL	0	NULL	statement 3	Process		depends on					Myc	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1189_s_257	12769844	(B) Binding of Skp2, Sug1, and Ub to the cyclin D2 promoter is Myc dependent.	bind
8569	1	3685	6	11	NULL	NULL	NULL	bHA	GP	soluble	bind					layilin-IgG	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_891_s_168	11294894	(B) Binding of soluble bHA to layilin-IgG (L-IgG) or CD44-IgG immobilized in microtiter wells.	bind
8570	2	3685	6	11	NULL	NULL	NULL	bHA	GP	soluble	bind					CD44-IgG	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_891_s_168	11294894	(B) Binding of soluble bHA to layilin-IgG (L-IgG) or CD44-IgG immobilized in microtiter wells.	bind
8571	3	3685	6	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_891_s_168	11294894	(B) Binding of soluble bHA to layilin-IgG (L-IgG) or CD44-IgG immobilized in microtiter wells.	bind
40936	4	3685	6	11	NULL	NULL	NULL	L-IgG	GP		is					layilin-IgG	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_891_s_168	11294894	(B) Binding of soluble bHA to layilin-IgG (L-IgG) or CD44-IgG immobilized in microtiter wells.	bind
12130	1	3685	7	11	NULL	NULL	NULL	bHA	GP	soluble	bind					layilin-IgG	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_891_s_168	11294894	(B) Binding of soluble bHA to layilin-IgG (L-IgG) or CD44-IgG immobilized in microtiter wells.	bind
12131	2	3685	7	11	NULL	NULL	NULL	bHA	GP	soluble	bind					CD44-IgG	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_891_s_168	11294894	(B) Binding of soluble bHA to layilin-IgG (L-IgG) or CD44-IgG immobilized in microtiter wells.	bind
12132	3	3685	7	11	NULL	NULL	NULL	layilin-IgG	GP		is					L-IgG	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_891_s_168	11294894	(B) Binding of soluble bHA to layilin-IgG (L-IgG) or CD44-IgG immobilized in microtiter wells.	bind
12133	4	3685	7	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_4_891_s_168	11294894	(B) Binding of soluble bHA to layilin-IgG (L-IgG) or CD44-IgG immobilized in microtiter wells.	bind
81234	1	3685	11	NULL	NULL	0	NULL	layilin-IgG	PartOfProtein		is					L-IgG	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_4_891_s_168	11294894	(B) Binding of soluble bHA to layilin-IgG (L-IgG) or CD44-IgG immobilized in microtiter wells.	bind
81235	2	3685	11	NULL	NULL	0	NULL	bHA	NonProteinOrNucleicAcidChemical	soluble	binds to 					layilin-IgG	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_4_891_s_168	11294894	(B) Binding of soluble bHA to layilin-IgG (L-IgG) or CD44-IgG immobilized in microtiter wells.	bind
81236	3	3685	11	NULL	NULL	0	NULL	bHA	NonProteinOrNucleicAcidChemical	soluble	binds to 					CD44-IgG	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_4_891_s_168	11294894	(B) Binding of soluble bHA to layilin-IgG (L-IgG) or CD44-IgG immobilized in microtiter wells.	bind
8572	1	3686	6	11	NULL	NULL	NULL	Sp1	GP		bind									TSA-response element	NULL	Hep3B cells	NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_4_1005_s_114	12200149	(B) Binding of Sp1 and Sp3 to the TSA-response element in Hep3B cells.	bind
8573	2	3686	6	11	NULL	NULL	NULL	Sp3	GP		bind									TSA-response element	NULL	Hep3B cells	NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_4_1005_s_114	12200149	(B) Binding of Sp1 and Sp3 to the TSA-response element in Hep3B cells.	bind
12134	1	3686	7	11	NULL	NULL	NULL	Sp1 	GP		bind									TSA-response element	NULL	Hep3B cells	NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_4_1005_s_114	12200149	(B) Binding of Sp1 and Sp3 to the TSA-response element in Hep3B cells.	bind
12135	2	3686	7	11	NULL	NULL	NULL	Sp3	GP		bind									TSA-response element	NULL	Hep3B cells	NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_4_1005_s_114	12200149	(B) Binding of Sp1 and Sp3 to the TSA-response element in Hep3B cells.	bind
81237	1	3686	11	NULL	NULL	0	NULL	Sp1	Protein		binds to 					TSA-response element	NucleicAcidSubstance	Hep3B cells			NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_4_1005_s_114	12200149	(B) Binding of Sp1 and Sp3 to the TSA-response element in Hep3B cells.	bind
81238	2	3686	11	NULL	NULL	0	NULL	Sp3	Protein		binds to 					TSA-response element	NucleicAcidSubstance	Hep3B cells			NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_4_1005_s_114	12200149	(B) Binding of Sp1 and Sp3 to the TSA-response element in Hep3B cells.	bind
8574	1	3687	6	11	NULL	NULL	NULL	sperm cells	Cell		bind					zona pellucida	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_267_1_203_s_232	14975727	(B) Binding of sperm cells to the zona pellucida.	bind
12136	1	3687	7	11	NULL	NULL	NULL	sperm cells	Cell		bind					zona pellucida	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_267_1_203_s_232	14975727	(B) Binding of sperm cells to the zona pellucida.	bind
81239	1	3687	11	NULL	NULL	0	NULL	sperm cells	cell		binds to 					zona pellucida	AnatomicalPart				NULL		0	NULL	NULL	NULL	gw70_devbiol_267_1_203_s_232	14975727	(B) Binding of sperm cells to the zona pellucida.	bind
8575	1	3688	6	11	NULL	NULL	NULL	syncollin	GP		bind					GST-syntaxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_2_325_s_135	9244306	(B) Binding of syncollin to GST-syntaxin in  the presence of 1 mM EGTA or 100 muM free Ca2+.	bind
8576	2	3688	6	11	NULL	NULL	NULL	statement 1	Process		occurs in presence of					EGTA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_2_325_s_135	9244306	(B) Binding of syncollin to GST-syntaxin in  the presence of 1 mM EGTA or 100 muM free Ca2+.	bind
8577	3	3688	6	11	NULL	NULL	NULL	statement 1	Process		occurs in presence of					Ca+2	Chemical	free			NULL		NULL	NULL	NULL	NULL	gw60_cell_90_2_325_s_135	9244306	(B) Binding of syncollin to GST-syntaxin in  the presence of 1 mM EGTA or 100 muM free Ca2+.	bind
53029	4	3688	6	11	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_2_325_s_135	9244306	(B) Binding of syncollin to GST-syntaxin in  the presence of 1 mM EGTA or 100 muM free Ca2+.	bind
12137	1	3688	7	11	NULL	NULL	NULL	syncollin 	GP		bind					GST-syntaxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_2_325_s_135	9244306	(B) Binding of syncollin to GST-syntaxin in  the presence of 1 mM EGTA or 100 muM free Ca2+.	bind
44731	3	3688	7	11	NULL	NULL	NULL	statement 1	GP		in the presence of					EGTA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_2_325_s_135	9244306	(B) Binding of syncollin to GST-syntaxin in  the presence of 1 mM EGTA or 100 muM free Ca2+.	bind
44732	2	3688	7	11	NULL	NULL	NULL	statement 1	Process		in the presence of 					free Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_2_325_s_135	9244306	(B) Binding of syncollin to GST-syntaxin in  the presence of 1 mM EGTA or 100 muM free Ca2+.	bind
44733	4	3688	7	11	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_2_325_s_135	9244306	(B) Binding of syncollin to GST-syntaxin in  the presence of 1 mM EGTA or 100 muM free Ca2+.	bind
81240	1	3688	11	NULL	NULL	0	NULL	syncollin	Protein		binds to 					GST-syntaxin	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_90_2_325_s_135	9244306	(B) Binding of syncollin to GST-syntaxin in  the presence of 1 mM EGTA or 100 muM free Ca2+.	bind
81241	2	3688	11	NULL	NULL	0	NULL	statement 1	Process		occurs in the presence of					EGTA	Chemical				NULL		0	NULL	NULL	NULL	gw60_cell_90_2_325_s_135	9244306	(B) Binding of syncollin to GST-syntaxin in  the presence of 1 mM EGTA or 100 muM free Ca2+.	bind
81242	3	3688	11	NULL	NULL	0	NULL	statement 1	Process		occurs in the presence of					free Ca2+	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	gw60_cell_90_2_325_s_135	9244306	(B) Binding of syncollin to GST-syntaxin in  the presence of 1 mM EGTA or 100 muM free Ca2+.	bind
8578	1	3689	6	11	NULL	NULL	NULL	TBL1	GP		bind					H4	GP	biotinylated	tail peptide		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_82	15601853	(B) Binding of TBL1 and TBLR1 to a biotinylated H4 tail peptide  with or without acetylation on lysines 5, 8, 12, and 16.	bind
8579	2	3689	6	11	NULL	NULL	NULL	TBLR1	GP		bind					H4 	GP	biotinylated	tail peptide		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_82	15601853	(B) Binding of TBL1 and TBLR1 to a biotinylated H4 tail peptide  with or without acetylation on lysines 5, 8, 12, and 16.	bind
12140	1	3689	7	11	NULL	NULL	NULL	TBL1	GP		bind					H4	GP	biotinylated	tail peptide		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_82	15601853	(B) Binding of TBL1 and TBLR1 to a biotinylated H4 tail peptide  with or without acetylation on lysines 5, 8, 12, and 16.	bind
12142	2	3689	7	11	NULL	NULL	NULL	TBLR1	GP		bind					H4	GP	biotinylated	tail peptide		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_82	15601853	(B) Binding of TBL1 and TBLR1 to a biotinylated H4 tail peptide  with or without acetylation on lysines 5, 8, 12, and 16.	bind
81243	1	3689	11	NULL	NULL	0	NULL	TBL1	Protein		binds to 					H4 tail peptide	PartOfProtein	biotinylated			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_82	15601853	(B) Binding of TBL1 and TBLR1 to a biotinylated H4 tail peptide  with or without acetylation on lysines 5, 8, 12, and 16.	bind
81244	2	3689	11	NULL	NULL	0	NULL	TBLR1	Protein		binds to 					H4 tail peptide	PartOfProtein	biotinylated			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_82	15601853	(B) Binding of TBL1 and TBLR1 to a biotinylated H4 tail peptide  with or without acetylation on lysines 5, 8, 12, and 16.	bind
81245	3	3689	11	NULL	NULL	0	NULL	statement 1	Process		is independent of					lysines	AminoAcid	acetylation			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_82	15601853	(B) Binding of TBL1 and TBLR1 to a biotinylated H4 tail peptide  with or without acetylation on lysines 5, 8, 12, and 16.	bind
8580	1	3690	6	11	NULL	NULL	NULL	BAZF	GP		bind					Bcl6	GP		1-520		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_303_2_600_s_121	12659862	(B) Binding of the 27  aa of BAZF to Bcl6(1-520) by the pull-down assay.	bind
12151	1	3690	7	11	NULL	NULL	NULL	BAZF	GP		bind					Bcl6	GP		1-520		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_303_2_600_s_121	12659862	(B) Binding of the 27  aa of BAZF to Bcl6(1-520) by the pull-down assay.	bind
81246	1	3690	11	NULL	NULL	0	NULL	27 aa	AminoAcid	BAZF	binds to 					Bcl6	Protein				NULL	 pull-down assay	0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_303_2_600_s_121	12659862	(B) Binding of the 27  aa of BAZF to Bcl6(1-520) by the pull-down assay.	bind
8581	1	3691	6	11	NULL	NULL	NULL	Abl	GP		bind			SH3 domain		proline-rich sequences	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_152_s_201	9418863	(B) Binding of the Abl SH3 domain to proline-rich sequences is not required for phosphorylation of Ena.	bind
8585	2	3691	6	11	NULL	NULL	NULL	statement 1	Process		is not required for					Ena	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_152_s_201	9418863	(B) Binding of the Abl SH3 domain to proline-rich sequences is not required for phosphorylation of Ena.	bind
12152	1	3691	7	11	NULL	NULL	NULL	Abl	GP		bind			SH3 domain		proline-rich sequence	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_152_s_201	9418863	(B) Binding of the Abl SH3 domain to proline-rich sequences is not required for phosphorylation of Ena.	bind
12153	2	3691	7	11	NULL	NULL	NULL	statement 1	Process		is not required for					Ena	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_152_s_201	9418863	(B) Binding of the Abl SH3 domain to proline-rich sequences is not required for phosphorylation of Ena.	bind
81247	1	3691	11	NULL	NULL	0	NULL	Abl	Protein	SH3 domain	binds to 					proline-rich sequence	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_152_s_201	9418863	(B) Binding of the Abl SH3 domain to proline-rich sequences is not required for phosphorylation of Ena.	bind
81248	2	3691	11	NULL	NULL	0	NULL	Ena	Protein		undergoes					phosphorylation	MolecularProcess				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_152_s_201	9418863	(B) Binding of the Abl SH3 domain to proline-rich sequences is not required for phosphorylation of Ena.	bind
81249	3	3691	11	NULL	NULL	0	NULL	statement 1	Process		is not required for					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_152_s_201	9418863	(B) Binding of the Abl SH3 domain to proline-rich sequences is not required for phosphorylation of Ena.	bind
8595	1	3692	6	11	NULL	NULL	NULL	CED-4	GP	mutant	bind					E1B 19K	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_6052_s_213	9742122	(B) Binding of the CED-4 mutant proteins to E1B 19K.	bind
12154	1	3692	7	11	NULL	NULL	NULL	CED-4	GP	mutant	bind					E1B 19K	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_6052_s_213	9742122	(B) Binding of the CED-4 mutant proteins to E1B 19K.	bind
81250	1	3692	11	NULL	NULL	0	NULL	CED-4 proteins	Protein	mutant 	binds to 					E1B 19K	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_10_6052_s_213	9742122	(B) Binding of the CED-4 mutant proteins to E1B 19K.	bind
8599	1	3693	6	11	NULL	NULL	NULL	HAP1-PPR1	GP		bind					UAS1/ CYC1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_3819_s_312	9632766	(B) Binding of the HAP1-PPR1 hybrid protein to UAS1/ CYC1 and UAS/ CYC7.	bind
8602	2	3693	6	11	NULL	NULL	NULL	HAP1-PPR1	GP		bind					UAS/CYC7	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_3819_s_312	9632766	(B) Binding of the HAP1-PPR1 hybrid protein to UAS1/ CYC1 and UAS/ CYC7.	bind
40942	3	3693	6	11	NULL	NULL	NULL	HAP1-PPR1	GP		is a type of					hybrid protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_3819_s_312	9632766	(B) Binding of the HAP1-PPR1 hybrid protein to UAS1/ CYC1 and UAS/ CYC7.	bind
12155	1	3693	7	11	NULL	NULL	NULL	HAP1-PPR1	GP		bind					UAS1/ CYC1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_3819_s_312	9632766	(B) Binding of the HAP1-PPR1 hybrid protein to UAS1/ CYC1 and UAS/ CYC7.	bind
12156	2	3693	7	11	NULL	NULL	NULL	HAP1-PPR1 	GP		bind					UAS/ CYC7	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_3819_s_312	9632766	(B) Binding of the HAP1-PPR1 hybrid protein to UAS1/ CYC1 and UAS/ CYC7.	bind
53030	3	3693	7	11	NULL	NULL	NULL	HAP1-PPR1	GP		is a type of					hybrid protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_3819_s_312	9632766	(B) Binding of the HAP1-PPR1 hybrid protein to UAS1/ CYC1 and UAS/ CYC7.	bind
81251	1	3693	11	NULL	NULL	0	NULL	HAP1-PPR1 hybrid protein	Protein		binds to 					 UAS1/ CYC1	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_3819_s_312	9632766	(B) Binding of the HAP1-PPR1 hybrid protein to UAS1/ CYC1 and UAS/ CYC7.	bind
81252	2	3693	11	NULL	NULL	0	NULL	HAP1-PPR1 hybrid protein	Protein		binds to 					UAS/ CYC7	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_3819_s_312	9632766	(B) Binding of the HAP1-PPR1 hybrid protein to UAS1/ CYC1 and UAS/ CYC7.	bind
8605	1	3694	6	11	NULL	NULL	NULL	p120 E4F protein	GP	purified	bind					Cyclin A	GP			CRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_8_2956_s_227	11283272	(B) Binding of the purified p120 E4F protein to cyclin A CRE.	bind
12157	1	3694	7	11	NULL	NULL	NULL	p120 E4F protein	GP	purified	bind					cyclin A	GP			CRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_8_2956_s_227	11283272	(B) Binding of the purified p120 E4F protein to cyclin A CRE.	bind
81253	1	3694	11	NULL	NULL	0	NULL	p120 E4F protein	Protein	purified	binds to 					cyclin A CRE	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_8_2956_s_227	11283272	(B) Binding of the purified p120 E4F protein to cyclin A CRE.	bind
8607	1	3695	6	11	NULL	NULL	NULL	Pax6 isoforms	GP		bind					F-crystallin	GP			enhancer	NULL		NULL	NULL	NULL	NULL	gw60_gene_286_2_271_s_108	11943482	(B) Binding of the two Pax6 isoforms to the  F-crystallin enhancer.	bind
12158	1	3695	7	11	NULL	NULL	NULL	Pax6 isoform	GP		bind					F-crystallin	GP			enhancer	NULL		NULL	NULL	NULL	NULL	gw60_gene_286_2_271_s_108	11943482	(B) Binding of the two Pax6 isoforms to the  F-crystallin enhancer.	bind
81338	1	3695	11	NULL	NULL	0	NULL	Pax6	Protein		binds to 					F-crystallin enhancer	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_gene_286_2_271_s_108	11943482	(B) Binding of the two Pax6 isoforms to the  F-crystallin enhancer.	bind
12159	1	3696	7	11	NULL	NULL	NULL	TIE2 receptor	GP		bind					Angiopoietin-1	GP	cloned			NULL		NULL	NULL	NULL	NULL	gw60_cell_87_7_1161_s_100	8980223	(B) Binding of TIE2 receptors by cloned  Angiopoietin-1.	bind
81339	1	3696	11	NULL	NULL	0	NULL	TIE2 receptors	GeneOrProtein		binds to 					Angiopoietin-1	GeneOrProtein	cloned			NULL		0	NULL	NULL	NULL	gw60_cell_87_7_1161_s_100	8980223	(B) Binding of TIE2 receptors by cloned  Angiopoietin-1.	bind
8611	1	3697	6	11	NULL	NULL	NULL	TIE2 receptors	GP		bind					Angiopoietin-1	GP	cloned			NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_5_905_s_109	9620695	(B) Binding of tomosyn to truncated forms of syntaxin-1a.	bind
8618	1	3697	6	11	NULL	NULL	NULL	tomosyn	GP		bind					syntaxin-1A	GP	truncated forms of 			NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_5_905_s_109	9620695	(B) Binding of tomosyn to truncated forms of syntaxin-1a.	bind
12160	1	3697	7	11	NULL	NULL	NULL	tomosyn	GP		bind					syntaxin-1a	GP	truncated forms of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_5_905_s_109	9620695	(B) Binding of tomosyn to truncated forms of syntaxin-1a.	bind
81341	1	3697	11	NULL	NULL	0	NULL	tomosyn	GeneOrProtein		binds to 					syntaxin-1a	GeneOrProtein	 truncated			NULL		0	NULL	NULL	NULL	gw60_neuron_20_5_905_s_109	9620695	(B) Binding of tomosyn to truncated forms of syntaxin-1a.	bind
8619	1	3698	6	11	NULL	NULL	NULL	v-Src	GP		bind					His6Cdc37	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_6_1051_s_89	12499358	(B) Binding of v-Src and Hsp90 to human His6Cdc37 and His6Cdc371 - 173.	bind
8620	2	3698	6	11	NULL	NULL	NULL	Hsp90	GP		bind					His6Cdc37	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_6_1051_s_89	12499358	(B) Binding of v-Src and Hsp90 to human His6Cdc37 and His6Cdc371 - 173.	bind
8621	2	3698	6	11	NULL	NULL	NULL	v-Src	GP		bind					His6Cdc37	GP	human	1 - 173		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_6_1051_s_89	12499358	(B) Binding of v-Src and Hsp90 to human His6Cdc37 and His6Cdc371 - 173.	bind
8622	4	3698	6	11	NULL	NULL	NULL	Hsp90	GP		bind					His6Cdc37	GP	human	1 - 173		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_6_1051_s_89	12499358	(B) Binding of v-Src and Hsp90 to human His6Cdc37 and His6Cdc371 - 173.	bind
12161	1	3698	7	11	NULL	NULL	NULL	v-Src	GP		bind					His6Cdc37	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_6_1051_s_89	12499358	(B) Binding of v-Src and Hsp90 to human His6Cdc37 and His6Cdc371 - 173.	bind
12162	2	3698	7	11	NULL	NULL	NULL	v-Src	GP		bind					His6Cdc37	GP	human	1-173		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_6_1051_s_89	12499358	(B) Binding of v-Src and Hsp90 to human His6Cdc37 and His6Cdc371 - 173.	bind
12163	3	3698	7	11	NULL	NULL	NULL	Hsp90	GP		bind					His6Cdc37	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_6_1051_s_89	12499358	(B) Binding of v-Src and Hsp90 to human His6Cdc37 and His6Cdc371 - 173.	bind
12164	4	3698	7	11	NULL	NULL	NULL	Hsp90	GP		bind					His6Cdc37	GP	human	1-173		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_6_1051_s_89	12499358	(B) Binding of v-Src and Hsp90 to human His6Cdc37 and His6Cdc371 - 173.	bind
81359	1	3698	11	NULL	NULL	NULL	NULL	 v-Src	GeneOrProtein		binds to 					Cdc37	Protein	human	His6		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_6_1051_s_89	12499358	(B) Binding of v-Src and Hsp90 to human His6Cdc37 and His6Cdc371 - 173.	bind
81360	2	3698	11	NULL	NULL	0	NULL	Hsp90	GeneOrProtein		binds to 					Cdc37	Protein	human	His6		NULL		0	NULL	NULL	NULL	gw60_cellbiol_159_6_1051_s_89	12499358	(B) Binding of v-Src and Hsp90 to human His6Cdc37 and His6Cdc371 - 173.	bind
8769	1	3699	6	11	NULL	NULL	NULL	Vav	GP		bind					GST-hSiah2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3798_s_132	10207103	(B) Binding of Vav to GST-hSiah2 fusion proteins.	bind
40946	2	3699	6	11	NULL	NULL	NULL	GST-hSiah2	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3798_s_132	10207103	(B) Binding of Vav to GST-hSiah2 fusion proteins.	bind
12165	1	3699	7	11	NULL	NULL	NULL	Vav	GP		bind					 GST-hSiah2 	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3798_s_132	10207103	(B) Binding of Vav to GST-hSiah2 fusion proteins.	bind
44771	2	3699	7	11	NULL	NULL	NULL	GST-hSiah2	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3798_s_132	10207103	(B) Binding of Vav to GST-hSiah2 fusion proteins.	bind
81361	1	3699	11	NULL	NULL	0	NULL	Vav	Protein		binds to 					GST-hSiah2 	Protein	fusion protein			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3798_s_132	10207103	(B) Binding of Vav to GST-hSiah2 fusion proteins.	bind
8770	1	3700	6	11	NULL	NULL	NULL	VCP	GP		bind					Thio-ataxin-3Q20	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6469_s_379	12944474	(B) Binding of VCP by Thio-ataxin-3Q20.	bind
12166	1	3700	7	11	NULL	NULL	NULL	VCP	GP		bind					Thio-ataxin-3Q20	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6469_s_379	12944474	(B) Binding of VCP by Thio-ataxin-3Q20.	bind
81363	1	3700	11	NULL	NULL	0	NULL	VCP	GeneOrProtein		binds to 					Thio-ataxin-3Q20	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_18_6469_s_379	12944474	(B) Binding of VCP by Thio-ataxin-3Q20.	bind
8530	1	3701	5	11	NULL	NULL	NULL	Yrb1	GP		bind					Gsp	GP		G12V		NULL		NULL	NULL	NULL	NULL	gw60_genetics_157_3_1089_s_214	11238397	(B) Binding of Yrb1 to Gsp(G12V) was assessed by copurification.	bind
8771	1	3701	6	11	NULL	NULL	NULL	Yrb1	GP		bind					Gsp	GP		G12V		NULL		NULL	NULL	NULL	NULL	gw60_genetics_157_3_1089_s_214	11238397	(B) Binding of Yrb1 to Gsp(G12V) was assessed by copurification.	bind
81364	1	3701	11	NULL	NULL	0	NULL	Yrb1	GeneOrProtein		binds to 					Gsp	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_genetics_157_3_1089_s_214	11238397	(B) Binding of Yrb1 to Gsp(G12V) was assessed by copurification.	bind
8532	1	3702	5	11	NULL	NULL	NULL	NAC	GP		bind					CSF proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_44_1_105_s_68	9030704	(B) Binding of []NAC to CSF proteins.	bind
8772	1	3702	6	11	NULL	NULL	NULL	NAC	GP		bind					CSF proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_44_1_105_s_68	9030704	(B) Binding of []NAC to CSF proteins.	bind
81365	1	3702	11	NULL	NULL	0	NULL	NAC	GeneOrProtein		binds to 					CSF protein	Protein				NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_44_1_105_s_68	9030704	(B) Binding of []NAC to CSF proteins.	bind
81367	1	3704	11	NULL	NULL	0	NULL	WAF1 gene	Gene		has binding site for					p53 	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_12_s_194	9858527	(B) Binding to the p53 binding site of the  WAF1 gene.	bind
8537	1	3705	5	11	NULL	NULL	NULL	TAK/P-TEFb complex	GP		contain					CDK9	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_209	9491887	(B) Biochemical view of the interaction of Tat with the cyclin T  subunit of the CDK9-containing TAK/P-TEFb complex, and the subsequent cooperative binding of Tat  and TAKPPTEFb to TAR RNA.	bind
8538	2	3705	5	11	NULL	NULL	NULL	cyclin T subunit	GP		is present in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_209	9491887	(B) Biochemical view of the interaction of Tat with the cyclin T  subunit of the CDK9-containing TAK/P-TEFb complex, and the subsequent cooperative binding of Tat  and TAKPPTEFb to TAR RNA.	bind
8539	3	3705	5	11	NULL	NULL	NULL	Tat	GP		interact with					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_209	9491887	(B) Biochemical view of the interaction of Tat with the cyclin T  subunit of the CDK9-containing TAK/P-TEFb complex, and the subsequent cooperative binding of Tat  and TAKPPTEFb to TAR RNA.	bind
8541	4	3705	5	11	NULL	NULL	NULL	Tat	GP		bind					TAR RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_209	9491887	(B) Biochemical view of the interaction of Tat with the cyclin T  subunit of the CDK9-containing TAK/P-TEFb complex, and the subsequent cooperative binding of Tat  and TAKPPTEFb to TAR RNA.	bind
8542	5	3705	5	11	NULL	NULL	NULL	TAKPPTEFb	GP		bind					TAR RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_209	9491887	(B) Biochemical view of the interaction of Tat with the cyclin T  subunit of the CDK9-containing TAK/P-TEFb complex, and the subsequent cooperative binding of Tat  and TAKPPTEFb to TAR RNA.	bind
8544	6	3705	5	11	NULL	NULL	NULL	statement 4	Process		occurs in cooperation with					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_209	9491887	(B) Biochemical view of the interaction of Tat with the cyclin T  subunit of the CDK9-containing TAK/P-TEFb complex, and the subsequent cooperative binding of Tat  and TAKPPTEFb to TAR RNA.	bind
8545	7	3705	5	11	NULL	NULL	NULL	statement 6	Process		occurs after					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_209	9491887	(B) Biochemical view of the interaction of Tat with the cyclin T  subunit of the CDK9-containing TAK/P-TEFb complex, and the subsequent cooperative binding of Tat  and TAKPPTEFb to TAR RNA.	bind
8773	2	3705	6	11	NULL	NULL	NULL	Tat	GP		interacts with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_209	9491887	(B) Biochemical view of the interaction of Tat with the cyclin T  subunit of the CDK9-containing TAK/P-TEFb complex, and the subsequent cooperative binding of Tat  and TAKPPTEFb to TAR RNA.	bind
8774	3	3705	6	11	NULL	NULL	NULL	Tat	GP		bind					TAR RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_209	9491887	(B) Biochemical view of the interaction of Tat with the cyclin T  subunit of the CDK9-containing TAK/P-TEFb complex, and the subsequent cooperative binding of Tat  and TAKPPTEFb to TAR RNA.	bind
8775	4	3705	6	11	NULL	NULL	NULL	TAKPPTEFb	GP		bind					TAR RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_209	9491887	(B) Biochemical view of the interaction of Tat with the cyclin T  subunit of the CDK9-containing TAK/P-TEFb complex, and the subsequent cooperative binding of Tat  and TAKPPTEFb to TAR RNA.	bind
8776	5	3705	6	11	NULL	NULL	NULL	statement 3	Process		acts in cooperation with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_209	9491887	(B) Biochemical view of the interaction of Tat with the cyclin T  subunit of the CDK9-containing TAK/P-TEFb complex, and the subsequent cooperative binding of Tat  and TAKPPTEFb to TAR RNA.	bind
53452	1	3705	6	11	NULL	NULL	NULL	TAK/P-TEFb complex	GP		contain					CDK9	GP		cyclin T subunit		NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_209	9491887	(B) Biochemical view of the interaction of Tat with the cyclin T  subunit of the CDK9-containing TAK/P-TEFb complex, and the subsequent cooperative binding of Tat  and TAKPPTEFb to TAR RNA.	bind
53457	6	3705	6	11	NULL	NULL	NULL	statement 5	Process		occurs after					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_209	9491887	(B) Biochemical view of the interaction of Tat with the cyclin T  subunit of the CDK9-containing TAK/P-TEFb complex, and the subsequent cooperative binding of Tat  and TAKPPTEFb to TAR RNA.	bind
81368	1	3705	11	NULL	NULL	0	NULL	Tat	GeneOrProtein		interact with					cyclin T	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_cell_92_4_451_s_209	9491887	(B) Biochemical view of the interaction of Tat with the cyclin T  subunit of the CDK9-containing TAK/P-TEFb complex, and the subsequent cooperative binding of Tat  and TAKPPTEFb to TAR RNA.	bind
81370	2	3705	11	NULL	NULL	0	NULL	TAK/P-TEFb complex	Protein		contain					CDK9	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_92_4_451_s_209	9491887	(B) Biochemical view of the interaction of Tat with the cyclin T  subunit of the CDK9-containing TAK/P-TEFb complex, and the subsequent cooperative binding of Tat  and TAKPPTEFb to TAR RNA.	bind
81371	3	3705	11	NULL	NULL	0	NULL	cyclin T	Protein		is a subunit of					statement 2	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_92_4_451_s_209	9491887	(B) Biochemical view of the interaction of Tat with the cyclin T  subunit of the CDK9-containing TAK/P-TEFb complex, and the subsequent cooperative binding of Tat  and TAKPPTEFb to TAR RNA.	bind
81372	4	3705	11	NULL	NULL	0	NULL	Tat	GeneOrProtein		binds to 					TAR 	NucleicAcidSubstance	RNA			NULL		0	NULL	NULL	NULL	gw60_cell_92_4_451_s_209	9491887	(B) Biochemical view of the interaction of Tat with the cyclin T  subunit of the CDK9-containing TAK/P-TEFb complex, and the subsequent cooperative binding of Tat  and TAKPPTEFb to TAR RNA.	bind
81373	5	3705	11	NULL	NULL	0	NULL	TAKPPTEFb	Protein		binds to 					TAR	NucleicAcidSubstance	RNA			NULL		0	NULL	NULL	NULL	gw60_cell_92_4_451_s_209	9491887	(B) Biochemical view of the interaction of Tat with the cyclin T  subunit of the CDK9-containing TAK/P-TEFb complex, and the subsequent cooperative binding of Tat  and TAKPPTEFb to TAR RNA.	bind
8553	1	3706	5	11	NULL	NULL	NULL	dopamine	Chemical		stimulate					GTP S	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_brainres_920_1_41_s_181	11716810	(B) Blockade of dopamine (1 mM)-stimulated [35]GTP S binding by the D2/D3 receptor antagonists, raclopride and L741,626.	bind
8554	2	3706	5	11	NULL	NULL	NULL	raclopride	Chemical		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brainres_920_1_41_s_181	11716810	(B) Blockade of dopamine (1 mM)-stimulated [35]GTP S binding by the D2/D3 receptor antagonists, raclopride and L741,626.	bind
8555	3	3706	5	11	NULL	NULL	NULL	L741,626	Chemical		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brainres_920_1_41_s_181	11716810	(B) Blockade of dopamine (1 mM)-stimulated [35]GTP S binding by the D2/D3 receptor antagonists, raclopride and L741,626.	bind
44772	4	3706	5	11	NULL	NULL	NULL	raclopride \t	Chemical		is a type of					D2/D3 receptor antagonist	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_brainres_920_1_41_s_181	11716810	(B) Blockade of dopamine (1 mM)-stimulated [35]GTP S binding by the D2/D3 receptor antagonists, raclopride and L741,626.	bind
44773	5	3706	5	11	NULL	NULL	NULL	L741,626	Chemical		is a type of					D2/D3 receptor antagonist	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_brainres_920_1_41_s_181	11716810	(B) Blockade of dopamine (1 mM)-stimulated [35]GTP S binding by the D2/D3 receptor antagonists, raclopride and L741,626.	bind
8777	1	3706	6	11	NULL	NULL	NULL	dopamine	Chemical		stimulates					GTP S	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_brainres_920_1_41_s_181	11716810	(B) Blockade of dopamine (1 mM)-stimulated [35]GTP S binding by the D2/D3 receptor antagonists, raclopride and L741,626.	bind
8778	2	3706	6	11	NULL	NULL	NULL	raclopride	Chemical		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brainres_920_1_41_s_181	11716810	(B) Blockade of dopamine (1 mM)-stimulated [35]GTP S binding by the D2/D3 receptor antagonists, raclopride and L741,626.	bind
8779	3	3706	6	11	NULL	NULL	NULL	L741,626	Chemical		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brainres_920_1_41_s_181	11716810	(B) Blockade of dopamine (1 mM)-stimulated [35]GTP S binding by the D2/D3 receptor antagonists, raclopride and L741,626.	bind
40947	4	3706	6	11	NULL	NULL	NULL	raclopride	Chemical		is a type of					D2/D3 receptor antagonist	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_brainres_920_1_41_s_181	11716810	(B) Blockade of dopamine (1 mM)-stimulated [35]GTP S binding by the D2/D3 receptor antagonists, raclopride and L741,626.	bind
40948	5	3706	6	11	NULL	NULL	NULL	L741,626	Chemical		is a type of					D2/D3 receptor antagonist	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_brainres_920_1_41_s_181	11716810	(B) Blockade of dopamine (1 mM)-stimulated [35]GTP S binding by the D2/D3 receptor antagonists, raclopride and L741,626.	bind
81375	1	3706	11	NULL	NULL	0	NULL	raclopride	NonProteinOrNucleicAcidChemical		is an agonist of					D2/D3 receptor 	Protein				NULL		0	NULL	NULL	NULL	gw60_brainres_920_1_41_s_181	11716810	(B) Blockade of dopamine (1 mM)-stimulated [35]GTP S binding by the D2/D3 receptor antagonists, raclopride and L741,626.	bind
81376	2	3706	11	NULL	NULL	0	NULL	L741,626	NonProteinOrNucleicAcidChemical		is an agonist of					D2/D3 receptor 	Protein				NULL		0	NULL	NULL	NULL	gw60_brainres_920_1_41_s_181	11716810	(B) Blockade of dopamine (1 mM)-stimulated [35]GTP S binding by the D2/D3 receptor antagonists, raclopride and L741,626.	bind
81377	3	3706	11	NULL	NULL	0	NULL	dopamine	NonProteinOrNucleicAcidChemical		stimulate					GTP	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	gw60_brainres_920_1_41_s_181	11716810	(B) Blockade of dopamine (1 mM)-stimulated [35]GTP S binding by the D2/D3 receptor antagonists, raclopride and L741,626.	bind
81379	4	3706	11	NULL	NULL	0	NULL	raclopride	NonProteinOrNucleicAcidChemical		blocks					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_brainres_920_1_41_s_181	11716810	(B) Blockade of dopamine (1 mM)-stimulated [35]GTP S binding by the D2/D3 receptor antagonists, raclopride and L741,626.	bind
81380	5	3706	11	NULL	NULL	0	NULL	L741,626	NonProteinOrNucleicAcidChemical		blocks					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_brainres_920_1_41_s_181	11716810	(B) Blockade of dopamine (1 mM)-stimulated [35]GTP S binding by the D2/D3 receptor antagonists, raclopride and L741,626.	bind
8556	1	3707	5	11	NULL	NULL	NULL	UL18-Fc	GP		bind					NK cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_immunity_7_2_273_s_121	9285411	(B) Blocking of binding of UL18-Fc to NK cells by anti-LIR-1.	bind
8557	2	3707	5	11	NULL	NULL	NULL	anti-LIR-1	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_7_2_273_s_121	9285411	(B) Blocking of binding of UL18-Fc to NK cells by anti-LIR-1.	bind
8780	1	3707	6	11	NULL	NULL	NULL	UL18-Fc	GP		bind					NK cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_immunity_7_2_273_s_121	9285411	(B) Blocking of binding of UL18-Fc to NK cells by anti-LIR-1.	bind
8781	2	3707	6	11	NULL	NULL	NULL	anti-LIR-1	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_7_2_273_s_121	9285411	(B) Blocking of binding of UL18-Fc to NK cells by anti-LIR-1.	bind
81382	1	3707	11	NULL	NULL	0	NULL	UL18-Fc	GeneOrProtein		binds to 					NK cells	Cell				NULL		0	NULL	NULL	NULL	gw60_immunity_7_2_273_s_121	9285411	(B) Blocking of binding of UL18-Fc to NK cells by anti-LIR-1.	bind
81383	2	3707	11	NULL	NULL	0	NULL	anti-LIR-1	GeneOrProtein		blocks					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_immunity_7_2_273_s_121	9285411	(B) Blocking of binding of UL18-Fc to NK cells by anti-LIR-1.	bind
8582	1	3708	5	11	NULL	NULL	NULL	Rac1	GP		bind					GST-PAK	GP		GBD		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_125	10508610	(b) Both PAK and N-WASP CRIB peptides inhibit binding of Rac1 and Cdc42 to GST-PAK GBD.	bind
8583	2	3708	5	11	NULL	NULL	NULL	Cdc42	GP		bind					GST-PAK	GP		GBD		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_125	10508610	(b) Both PAK and N-WASP CRIB peptides inhibit binding of Rac1 and Cdc42 to GST-PAK GBD.	bind
8584	3	3708	5	11	NULL	NULL	NULL	PAK	GP		inhibit			CRIB peptide		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_125	10508610	(b) Both PAK and N-WASP CRIB peptides inhibit binding of Rac1 and Cdc42 to GST-PAK GBD.	bind
8586	4	3708	5	11	NULL	NULL	NULL	PAK	GP		inhibit			CRIB peptide		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_125	10508610	(b) Both PAK and N-WASP CRIB peptides inhibit binding of Rac1 and Cdc42 to GST-PAK GBD.	bind
8587	5	3708	5	11	NULL	NULL	NULL	N-WASP	GP		inhibit			CRIB peptide		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_125	10508610	(b) Both PAK and N-WASP CRIB peptides inhibit binding of Rac1 and Cdc42 to GST-PAK GBD.	bind
8588	6	3708	5	11	NULL	NULL	NULL	N-WASP	GP		inhibit			CRIB peptide		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_125	10508610	(b) Both PAK and N-WASP CRIB peptides inhibit binding of Rac1 and Cdc42 to GST-PAK GBD.	bind
8782	1	3708	6	11	NULL	NULL	NULL	Rac1	GP		bind					GST-PAK	GP		GBD		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_125	10508610	(b) Both PAK and N-WASP CRIB peptides inhibit binding of Rac1 and Cdc42 to GST-PAK GBD.	bind
8783	2	3708	6	11	NULL	NULL	NULL	Cdc42	GP		bind					GST-PAK	GP		GBD		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_125	10508610	(b) Both PAK and N-WASP CRIB peptides inhibit binding of Rac1 and Cdc42 to GST-PAK GBD.	bind
8784	3	3708	6	11	NULL	NULL	NULL	PAK	GP		inhibits			 CRIB peptide		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_125	10508610	(b) Both PAK and N-WASP CRIB peptides inhibit binding of Rac1 and Cdc42 to GST-PAK GBD.	bind
8785	4	3708	6	11	NULL	NULL	NULL	PAK	GP		inhibits			CRIB peptide		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_125	10508610	(b) Both PAK and N-WASP CRIB peptides inhibit binding of Rac1 and Cdc42 to GST-PAK GBD.	bind
8786	5	3708	6	11	NULL	NULL	NULL	N-WASP	GP		inhibits			 CRIB peptide		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_125	10508610	(b) Both PAK and N-WASP CRIB peptides inhibit binding of Rac1 and Cdc42 to GST-PAK GBD.	bind
8787	6	3708	6	11	NULL	NULL	NULL	N-WASP	GP		inhibits			 CRIB peptide		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_125	10508610	(b) Both PAK and N-WASP CRIB peptides inhibit binding of Rac1 and Cdc42 to GST-PAK GBD.	bind
81384	1	3708	11	NULL	NULL	0	NULL	Rac1	GeneOrProtein		binds to 					GST-PAK GBD	Protein				NULL		0	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_125	10508610	(b) Both PAK and N-WASP CRIB peptides inhibit binding of Rac1 and Cdc42 to GST-PAK GBD.	bind
81385	2	3708	11	NULL	NULL	0	NULL	Cdc42	GeneOrProtein		binds to 					GST-PAK GBD	Protein				NULL		0	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_125	10508610	(b) Both PAK and N-WASP CRIB peptides inhibit binding of Rac1 and Cdc42 to GST-PAK GBD.	bind
81386	3	3708	11	NULL	NULL	0	NULL	PAK	PartOfProtein	peptide	inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_125	10508610	(b) Both PAK and N-WASP CRIB peptides inhibit binding of Rac1 and Cdc42 to GST-PAK GBD.	bind
81387	4	3708	11	NULL	NULL	0	NULL	PAK	PartOfProtein	peptide	inhibit					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_125	10508610	(b) Both PAK and N-WASP CRIB peptides inhibit binding of Rac1 and Cdc42 to GST-PAK GBD.	bind
81388	5	3708	11	NULL	NULL	0	NULL	N-WASP CRIB	PartOfProtein	peptide	inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_125	10508610	(b) Both PAK and N-WASP CRIB peptides inhibit binding of Rac1 and Cdc42 to GST-PAK GBD.	bind
81389	6	3708	11	NULL	NULL	0	NULL	N-WASP CRIB	PartOfProtein	peptide	inhibit					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_currbiol_9_18_991_s_125	10508610	(b) Both PAK and N-WASP CRIB peptides inhibit binding of Rac1 and Cdc42 to GST-PAK GBD.	bind
8589	1	3709	5	11	NULL	NULL	NULL	Vg1RBP/Vera	GP		bind		specifically			Xcat2	GP			 3'UTR	NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_239	15292452	(B) Both Vg1RBP/Vera and VgRBP60/hnRNP I specifically bind to the Xcat2  3'UTR.	bind
8590	2	3709	5	11	NULL	NULL	NULL	VgRBP60/hnRNP I	GP		bind		specifically			Xcat2	GP			3'UTR	NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_239	15292452	(B) Both Vg1RBP/Vera and VgRBP60/hnRNP I specifically bind to the Xcat2  3'UTR.	bind
8788	1	3709	6	11	NULL	NULL	NULL	Vg1RBP/Vera	GP		bind		specifically			Xcat2 	GP			3'UTR	NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_239	15292452	(B) Both Vg1RBP/Vera and VgRBP60/hnRNP I specifically bind to the Xcat2  3'UTR.	bind
8789	2	3709	6	11	NULL	NULL	NULL	VgRBP60/hnRNP I	GP		bind		specifically			Xcat2 	GP			3'UTR	NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_239	15292452	(B) Both Vg1RBP/Vera and VgRBP60/hnRNP I specifically bind to the Xcat2  3'UTR.	bind
81390	1	3709	11	NULL	NULL	0	NULL	Vg1RBP/Vera	GeneOrProtein		binds to 		specifically			Xcat2 	Gene			3'UTR	NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_239	15292452	(B) Both Vg1RBP/Vera and VgRBP60/hnRNP I specifically bind to the Xcat2  3'UTR.	bind
81391	2	3709	11	NULL	NULL	0	NULL	VgRBP60/hnRNP I	GeneOrProtein		binds to 					Xcat2 	Gene			3'UTR	NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_239	15292452	(B) Both Vg1RBP/Vera and VgRBP60/hnRNP I specifically bind to the Xcat2  3'UTR.	bind
8591	1	3711	5	11	NULL	NULL	NULL	BRG1	GP		bind					p21	GP	endogenous		promoter	NULL	HeLa cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1188_s_96	14729964	(B) BRG1 is bound to the endogenous p21 promoter (p21 pr) in HeLa cells.	bind
10035	2	3711	5	11	NULL	NULL	NULL	p21 pr	GP		is					promoter p21	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1188_s_96	14729964	(B) BRG1 is bound to the endogenous p21 promoter (p21 pr) in HeLa cells.	bind
8790	1	3711	6	11	NULL	NULL	NULL	BRG1	GP		bind					p21	GP	endogenous		promoter	NULL	HeLa cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1188_s_96	14729964	(B) BRG1 is bound to the endogenous p21 promoter (p21 pr) in HeLa cells.	bind
8791	2	3711	6	11	NULL	NULL	NULL	p21 pr	GP		is					p21 promoter	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1188_s_96	14729964	(B) BRG1 is bound to the endogenous p21 promoter (p21 pr) in HeLa cells.	bind
81392	1	3711	11	NULL	NULL	0	NULL	BRG1	GeneOrProtein		binds to 					p21	Gene	endogenous		promoter	NULL	HeLa cell	0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1188_s_96	14729964	(B) BRG1 is bound to the endogenous p21 promoter (p21 pr) in HeLa cells.	bind
8592	1	3712	5	11	NULL	NULL	NULL	c-IAP1	GP		bind					c-IAP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3348_s_242	15798218	(B) c-IAP1 binds c-IAP2 only in the presence of TRAF1 or TRAF2.	bind
8593	2	3712	5	11	NULL	NULL	NULL	statement 1	Process		in the presence of		only			TRAF1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3348_s_242	15798218	(B) c-IAP1 binds c-IAP2 only in the presence of TRAF1 or TRAF2.	bind
8594	3	3712	5	11	NULL	NULL	NULL	statement 1	Process		in the presence of		only			TRAF2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3348_s_242	15798218	(B) c-IAP1 binds c-IAP2 only in the presence of TRAF1 or TRAF2.	bind
8596	4	3712	5	11	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3348_s_242	15798218	(B) c-IAP1 binds c-IAP2 only in the presence of TRAF1 or TRAF2.	bind
8793	1	3712	6	11	NULL	NULL	NULL	c-IAP1	GP		bind					c-IAP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3348_s_242	15798218	(B) c-IAP1 binds c-IAP2 only in the presence of TRAF1 or TRAF2.	bind
8794	2	3712	6	11	NULL	NULL	NULL	statement 1	Process		occurs in presence of		only			TRAF1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3348_s_242	15798218	(B) c-IAP1 binds c-IAP2 only in the presence of TRAF1 or TRAF2.	bind
8795	3	3712	6	11	NULL	NULL	NULL	statement 1	Process		occurs in presence of		only			TRAF2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3348_s_242	15798218	(B) c-IAP1 binds c-IAP2 only in the presence of TRAF1 or TRAF2.	bind
8796	4	3712	6	11	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3348_s_242	15798218	(B) c-IAP1 binds c-IAP2 only in the presence of TRAF1 or TRAF2.	bind
81393	1	3712	11	NULL	NULL	0	NULL	c-IAP1	GeneOrProtein		binds to 					c-IAP2 	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3348_s_242	15798218	(B) c-IAP1 binds c-IAP2 only in the presence of TRAF1 or TRAF2.	bind
81394	2	3712	11	NULL	NULL	0	NULL	statement 1	Process		occurs in the presence of					TRAF1	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3348_s_242	15798218	(B) c-IAP1 binds c-IAP2 only in the presence of TRAF1 or TRAF2.	bind
81395	3	3712	11	NULL	NULL	0	NULL	statement 1	Process		occurs in the presence of					TRAF2	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3348_s_242	15798218	(B) c-IAP1 binds c-IAP2 only in the presence of TRAF1 or TRAF2.	bind
8597	1	3713	5	11	NULL	NULL	NULL	Sso	GP		bind					Vsm1	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_193	12925750	(B) C2-ceramide inhibits the binding of Sso to Vsm1 in vivo.	bind
8598	2	3713	5	11	NULL	NULL	NULL	C2-ceramide	Chemical		inhibit					statement 1	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_193	12925750	(B) C2-ceramide inhibits the binding of Sso to Vsm1 in vivo.	bind
8797	1	3713	6	11	NULL	NULL	NULL	Sso	GP		bind					Vsm1	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_193	12925750	(B) C2-ceramide inhibits the binding of Sso to Vsm1 in vivo.	bind
8798	2	3713	6	11	NULL	NULL	NULL	C2-ceramide	Chemical		inhibits					statement 1	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_193	12925750	(B) C2-ceramide inhibits the binding of Sso to Vsm1 in vivo.	bind
81396	1	3713	11	NULL	NULL	0	NULL	C2-ceramide	Chemical		inhibit					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_193	12925750	(B) C2-ceramide inhibits the binding of Sso to Vsm1 in vivo.	bind
81397	2	3713	11	NULL	NULL	0	NULL	Sso	GeneOrProtein		binds to 					Vsm1	GeneOrProtein				NULL	in vivo	0	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_193	12925750	(B) C2-ceramide inhibits the binding of Sso to Vsm1 in vivo.	bind
8600	1	3714	5	11	NULL	NULL	NULL	brain proteins	GP		bind					syntaxin-1A	GP		191-240		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_155	16030255	(B) Ca2+-dependent binding of brain proteins to syntaxin-1A [191-240] and syntaxin-1A [191-240  L222].	bind
8601	2	3714	5	11	NULL	NULL	NULL	statement 1	Process		is dependent on					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_155	16030255	(B) Ca2+-dependent binding of brain proteins to syntaxin-1A [191-240] and syntaxin-1A [191-240  L222].	bind
8603	3	3714	5	11	NULL	NULL	NULL	brain proteins	GP		bind					syntaxin-1A	GP		191-240;; L222		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_155	16030255	(B) Ca2+-dependent binding of brain proteins to syntaxin-1A [191-240] and syntaxin-1A [191-240  L222].	bind
8604	4	3714	5	11	NULL	NULL	NULL	statement 3	Process		is dependent on					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_155	16030255	(B) Ca2+-dependent binding of brain proteins to syntaxin-1A [191-240] and syntaxin-1A [191-240  L222].	bind
8799	1	3714	6	11	NULL	NULL	NULL	brain proteins	GP		bind					syntaxin-1A	GP		191-240		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_155	16030255	(B) Ca2+-dependent binding of brain proteins to syntaxin-1A [191-240] and syntaxin-1A [191-240  L222].	bind
8800	2	3714	6	11	NULL	NULL	NULL	brain proteins	GP		bind					syntaxin-1A	GP		191-240;;L222		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_155	16030255	(B) Ca2+-dependent binding of brain proteins to syntaxin-1A [191-240] and syntaxin-1A [191-240  L222].	bind
8801	3	3714	6	11	NULL	NULL	NULL	statement 1	Process		is dependent on					Ca+2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_155	16030255	(B) Ca2+-dependent binding of brain proteins to syntaxin-1A [191-240] and syntaxin-1A [191-240  L222].	bind
8802	4	3714	6	11	NULL	NULL	NULL	statement 2	Process		is dependent on					Ca+2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_155	16030255	(B) Ca2+-dependent binding of brain proteins to syntaxin-1A [191-240] and syntaxin-1A [191-240  L222].	bind
81398	1	3714	11	NULL	NULL	0	NULL	brain proteins	Protein		binds to 					syntaxin-1A	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_155	16030255	(B) Ca2+-dependent binding of brain proteins to syntaxin-1A [191-240] and syntaxin-1A [191-240  L222].	bind
81399	2	3714	11	NULL	NULL	0	NULL	brain proteins	Protein		binds to 					syntaxin-1A	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_155	16030255	(B) Ca2+-dependent binding of brain proteins to syntaxin-1A [191-240] and syntaxin-1A [191-240  L222].	bind
81400	3	3714	11	NULL	NULL	0	NULL	statement 1	Process		depends on					Ca2+	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_155	16030255	(B) Ca2+-dependent binding of brain proteins to syntaxin-1A [191-240] and syntaxin-1A [191-240  L222].	bind
81401	4	3714	11	NULL	NULL	0	NULL	statement 2	Process		depends on					Ca2+	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_155	16030255	(B) Ca2+-dependent binding of brain proteins to syntaxin-1A [191-240] and syntaxin-1A [191-240  L222].	bind
8606	1	3718	5	11	NULL	NULL	NULL	CAT	GP		bind					SHP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
8608	2	3718	5	11	NULL	NULL	NULL	FBS	CellComponent		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
8609	3	3718	5	11	NULL	NULL	NULL	LA	GP		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
8610	4	3718	5	11	NULL	NULL	NULL	LA	GP		is					laminin	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
8612	5	3718	5	11	NULL	NULL	NULL	HA	Chemical		does not stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
8613	6	3718	5	11	NULL	NULL	NULL	HA	Chemical		is					hyaluronic acid	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
8614	7	3718	5	11	NULL	NULL	NULL	EL	GP		does not stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
8615	8	3718	5	11	NULL	NULL	NULL	EL	GP		is					elastin	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
8803	1	3718	6	11	NULL	NULL	NULL	CAT	GP		bind					SHP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
8804	2	3718	6	11	NULL	NULL	NULL	FBS	CellComponent		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
8805	3	3718	6	11	NULL	NULL	NULL	LA	GP		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
8806	4	3718	6	11	NULL	NULL	NULL	LA	GP		is					laminin	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
8807	5	3718	6	11	NULL	NULL	NULL	HA	Chemical		does not stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
8808	6	3718	6	11	NULL	NULL	NULL	EL	GP		does not stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
8809	7	3718	6	11	NULL	NULL	NULL	HA	Chemical		is					hyaluronic acid	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
8810	8	3718	6	11	NULL	NULL	NULL	EL 	GP		is					elastin	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
8811	9	3718	6	11	NULL	NULL	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
81402	1	3718	11	NULL	NULL	0	NULL	CAT	GeneOrProtein		binds to 					SHP2	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
81403	2	3718	11	NULL	NULL	0	NULL	FBS	Chemical		stimulates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
81404	3	3718	11	NULL	NULL	0	NULL	laminin	GeneOrProtein		stimulates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
81405	4	3718	11	NULL	NULL	0	NULL	laminin	GeneOrProtein		is					LA	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
81406	5	3718	11	NULL	NULL	0	NULL	hyaluronic acid	NonProteinOrNucleicAcidChemical		is					HA	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
81407	6	3718	11	NULL	NULL	NULL	NULL	EL	GeneOrProtein		is					elastin	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
81408	7	3718	11	NULL	NULL	0	NULL	hyaluronic acid	NonProteinOrNucleicAcidChemical		does not stimulate					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
81409	8	3718	11	NULL	NULL	NULL	NULL	elastin	GeneOrProtein		does not stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_91	15556604	(B) CAT binds SHP2 upon stimulation with FBS or laminin  (LA), but not with hyaluronic acid (HA) or elastin (EL).	bind
8616	1	3719	5	11	NULL	NULL	NULL	SATB1 DNA	NucleicAcid		bind					MMTV	Organism			LTR	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4918_s_214	10373541	(B) CDP overexpression prevents SATB1 DNA binding to the MMTV LTR.	bind
8617	2	3719	5	11	NULL	NULL	NULL	CDP	GP	overexpression of	prevent					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4918_s_214	10373541	(B) CDP overexpression prevents SATB1 DNA binding to the MMTV LTR.	bind
8812	1	3719	6	11	NULL	NULL	NULL	SATB1 DNA	NucleicAcid		bind					MMTV	Organism			LTR	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4918_s_214	10373541	(B) CDP overexpression prevents SATB1 DNA binding to the MMTV LTR.	bind
8813	2	3719	6	11	NULL	NULL	NULL	CDP	GP	overexpression of	prevents					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4918_s_214	10373541	(B) CDP overexpression prevents SATB1 DNA binding to the MMTV LTR.	bind
81410	1	3719	11	NULL	NULL	NULL	NULL	SATB1	Gene	DNA	binds to 					MMTV	Gene	LTR			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4918_s_214	10373541	(B) CDP overexpression prevents SATB1 DNA binding to the MMTV LTR.	bind
81411	2	3719	11	NULL	NULL	0	NULL	CDP	Gene	overexpression	prevents					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4918_s_214	10373541	(B) CDP overexpression prevents SATB1 DNA binding to the MMTV LTR.	bind
10032	1	3720	5	11	NULL	NULL	NULL	amphiphysin	GP	mutant	does not bind			SH3 domain					proline-rich sequences		NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_45_6_787_s_146	14529717	(B) Cells overexpressing transfected G684R/P687L mutant amphiphysin SH3 domain (which  no longer binds to proline-rich sequences), stained for either the mutant SH3 domain  (left), or for internalized transferrin (Tf, right).	bind
8814	1	3720	6	11	NULL	NULL	NULL	amphiphysin	GP	mutant	does not bind			SH3 domain					proline-rich sequences		NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_45_6_787_s_146	14529717	(B) Cells overexpressing transfected G684R/P687L mutant amphiphysin SH3 domain (which  no longer binds to proline-rich sequences), stained for either the mutant SH3 domain  (left), or for internalized transferrin (Tf, right).	bind
81412	1	3720	11	NULL	NULL	0	NULL	amphiphysin	Protein	 G684R/P687L mutant 	does not bind to			SH3 domain		proline-rich sequence	PartOfProtein				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_6_787_s_146	14529717	(B) Cells overexpressing transfected G684R/P687L mutant amphiphysin SH3 domain (which  no longer binds to proline-rich sequences), stained for either the mutant SH3 domain  (left), or for internalized transferrin (Tf, right).	bind
8623	1	3721	5	11	NULL	NULL	NULL	Ssb1/2p	GP		bind					HSF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_5_1739_s_270	10793148	(B) Cells were grown in 0.5% glucose to induce the binding of Ssb1/2p to HSF.	bind
8624	2	3721	5	11	NULL	NULL	NULL	glucose	Chemical		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_5_1739_s_270	10793148	(B) Cells were grown in 0.5% glucose to induce the binding of Ssb1/2p to HSF.	bind
8815	1	3721	6	11	NULL	NULL	NULL	Ssb1/2p	GP		bind					HSF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_5_1739_s_270	10793148	(B) Cells were grown in 0.5% glucose to induce the binding of Ssb1/2p to HSF.	bind
8816	2	3721	6	11	NULL	NULL	NULL	glucose	Chemical		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_5_1739_s_270	10793148	(B) Cells were grown in 0.5% glucose to induce the binding of Ssb1/2p to HSF.	bind
81413	1	3721	11	NULL	NULL	0	NULL	 Ssb1/2p	Protein		binds to 					HSF	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_5_1739_s_270	10793148	(B) Cells were grown in 0.5% glucose to induce the binding of Ssb1/2p to HSF.	bind
81414	2	3721	11	NULL	NULL	0	NULL	glucose	NonProteinOrNucleicAcidChemical		induces					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_5_1739_s_270	10793148	(B) Cells were grown in 0.5% glucose to induce the binding of Ssb1/2p to HSF.	bind
8625	1	3724	5	11	NULL	NULL	NULL	CREB	GP		bind					NF-IL6beta gene locus	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3365_s_199	15901830	(B) ChIP analysis of CREB or Sp1 binding to  the  NF-IL6beta gene locus.	bind
10030	2	3724	5	11	NULL	NULL	NULL	Sp1	GP		bind					NF-IL6beta gene locus	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3365_s_199	15901830	(B) ChIP analysis of CREB or Sp1 binding to  the  NF-IL6beta gene locus.	bind
10031	3	3724	5	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3365_s_199	15901830	(B) ChIP analysis of CREB or Sp1 binding to  the  NF-IL6beta gene locus.	bind
8817	1	3724	6	11	NULL	NULL	NULL	CREB	GP		bind					NF-IL6beta gene	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3365_s_199	15901830	(B) ChIP analysis of CREB or Sp1 binding to  the  NF-IL6beta gene locus.	bind
8818	2	3724	6	11	NULL	NULL	NULL	Sp1	GP		bind					NF-IL6beta gene	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3365_s_199	15901830	(B) ChIP analysis of CREB or Sp1 binding to  the  NF-IL6beta gene locus.	bind
8819	3	3724	6	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3365_s_199	15901830	(B) ChIP analysis of CREB or Sp1 binding to  the  NF-IL6beta gene locus.	bind
81415	1	3724	11	NULL	NULL	0	NULL	CREB	GeneOrProtein		binds to 					NF-IL6beta gene	Gene			locus	NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_7_3365_s_199	15901830	(B) ChIP analysis of CREB or Sp1 binding to  the  NF-IL6beta gene locus.	bind
81416	2	3724	11	NULL	NULL	0	NULL	Sp1	GeneOrProtein		binds to 					NF-IL6beta gene	Gene			locus	NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_7_3365_s_199	15901830	(B) ChIP analysis of CREB or Sp1 binding to  the  NF-IL6beta gene locus.	bind
8626	1	3725	5	11	NULL	NULL	NULL	PU.1	GP		bind					mcl-1 gene locus	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_6_1896_s_112	12612065	(B) ChIP analysis of PU.1 binding to the  mcl-1 gene locus.	bind
8820	1	3725	6	11	NULL	NULL	NULL	PU.1	GP		bind					mcl-1 gene locus	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_6_1896_s_112	12612065	(B) ChIP analysis of PU.1 binding to the  mcl-1 gene locus.	bind
81417	1	3725	11	NULL	NULL	0	NULL	 PU.1	GeneOrProtein		binds to 					mcl-1 gene	Gene			locus	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_6_1896_s_112	12612065	(B) ChIP analysis of PU.1 binding to the  mcl-1 gene locus.	bind
8627	1	3726	5	11	NULL	NULL	NULL	c-Rel	GP		bind					bfl-1 locus	GP				NULL	in human Jurkat T cells stimulated with PMA plus ionomycin (P+I)	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8629	2	3726	5	11	NULL	NULL	NULL	p65/RelA	GP		bind					bfl-1 locus	GP				NULL	in human Jurkat T cells stimulated with PMA plus ionomycin (P+I)	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8630	3	3726	5	11	NULL	NULL	NULL	c-Jun	GP		bind					bfl-1 locus	GP				NULL	in human Jurkat T cells stimulated with PMA plus ionomycin (P+I)	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8631	4	3726	5	11	NULL	NULL	NULL	C/EBPbeta	GP		bind					bfl-1 locus	GP				NULL	in human Jurkat T cells stimulated with PMA plus ionomycin (P+I)	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8632	5	3726	5	11	NULL	NULL	NULL	HMGI-C	GP		bind					bfl-1 locus	GP				NULL	in human Jurkat T cells stimulated with PMA plus ionomycin (P+I)	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8633	6	3726	5	11	NULL	NULL	NULL	c-Rel	GP		bind					bfl-1 locus	GP				NULL	in human Jurkat T cells stimulated with DMSO control	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8634	7	3726	5	11	NULL	NULL	NULL	p65/RelA	GP		bind					bfl-1 locus	GP				NULL	in human Jurkat T cells stimulated with DMSO control	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8635	8	3726	5	11	NULL	NULL	NULL	c-Jun	GP		bind					bfl-1 locus	GP				NULL	in human Jurkat T cells stimulated with DMSO control	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8636	9	3726	5	11	NULL	NULL	NULL	C/EBPbeta	GP		bind					bfl-1 locus	GP				NULL	in human Jurkat T cells stimulated with DMSO control	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8637	10	3726	5	11	NULL	NULL	NULL	HMGI-C	GP		bind					bfl-1 locus	GP				NULL	in human Jurkat T cells stimulated with DMSO control	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8638	11	3726	5	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8639	12	3726	5	11	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8640	13	3726	5	11	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8641	14	3726	5	11	NULL	NULL	NULL	statement 4	Process		bind					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8642	15	3726	5	11	NULL	NULL	NULL	statement 5	Process		is an alternative to					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
53465	16	3726	5	11	NULL	NULL	NULL	c-Rel	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
53466	17	3726	5	11	NULL	NULL	NULL	p65/RelA	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
53467	18	3726	5	11	NULL	NULL	NULL	C/EBPbeta	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
53468	19	3726	5	11	NULL	NULL	NULL	HMGI-C	GP		is a type of					architectural factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
53470	20	3726	5	11	NULL	NULL	NULL	c-Jun	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8821	1	3726	6	11	NULL	NULL	NULL	c-Rel	GP		bind					bfl-1 locus	GP				NULL	human Jurkat T cells stimulated with PMA plus ionomycin	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8822	2	3726	6	11	NULL	NULL	NULL	p65/RelA	GP		bind					bfl-1 locus	GP				NULL	human Jurkat T cells stimulated with PMA plus ionomycin	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8823	3	3726	6	11	NULL	NULL	NULL	c-Jun	GP		bind					bfl-1 locus	GP				NULL	human Jurkat T cells stimulated with PMA plus ionomycin	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8824	4	3726	6	11	NULL	NULL	NULL	C/EBPbeta	GP		bind					bfl-1 locus	GP				NULL	human Jurkat T cells stimulated with PMA plus ionomycin	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8825	5	3726	6	11	NULL	NULL	NULL	HMGI-C	GP		bind					bfl-1 locus	GP				NULL	human Jurkat T cells stimulated with PMA plus ionomycin	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
9694	6	3726	6	11	NULL	NULL	NULL	c-Rel	GP		bind					bfl-1 locus	GP				NULL	human Jurkat T cells stimulated with DMSO control	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
9695	7	3726	6	11	NULL	NULL	NULL	p65/RelA	GP		bind					bfl-1 locus	GP				NULL	human Jurkat T cells stimulated with DMSO control	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
9696	8	3726	6	11	NULL	NULL	NULL	c-Jun	GP		bind					bfl-1 locus	GP				NULL	human Jurkat T cells stimulated with DMSO control	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
9697	9	3726	6	11	NULL	NULL	NULL	C/EBPbeta	GP		bind					bfl-1 locus	GP				NULL	human Jurkat T cells stimulated with DMSO control	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
9698	10	3726	6	11	NULL	NULL	NULL	HMGI-C	GP		bind					bfl-1 locus	GP				NULL	human Jurkat T cells stimulated with DMSO control	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
40953	11	3726	6	11	NULL	NULL	NULL	c-Rel	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
40954	12	3726	6	11	NULL	NULL	NULL	p65/RelA	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
40955	13	3726	6	11	NULL	NULL	NULL	c-Jun	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
40956	14	3726	6	11	NULL	NULL	NULL	C/EBPbeta	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
40957	15	3726	6	11	NULL	NULL	NULL	HMGI-C 	GP		is a type of					architectural factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
53469	16	3726	6	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
53471	17	3726	6	11	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
53472	18	3726	6	11	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
53473	19	3726	6	11	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
53474	20	3726	6	11	NULL	NULL	NULL	statement 5	Process		is an alternative to					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
81418	1	3726	11	NULL	NULL	0	NULL	c-Rel	Protein		is a type of 					transcription factor	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
81419	2	3726	11	NULL	NULL	0	NULL	 p65/RelA	Protein		is a type of 					transcription factor	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
81420	3	3726	11	NULL	NULL	0	NULL	c-Jun	Protein		is a type of 					transcription factor	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
81421	4	3726	11	NULL	NULL	0	NULL	C/EBPbeta	Protein		is a type of 					transcription factor	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
81422	5	3726	11	NULL	NULL	0	NULL	HMGI-C	GeneOrProtein		binds to 					bfl-1	Gene	human;;Jurkat T cell		locus	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
81423	6	3726	11	NULL	NULL	0	NULL	PMA 	NonProteinOrNucleicAcidChemical		stimulates					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
81424	7	3726	11	NULL	NULL	0	NULL	 ionomycin	NonProteinOrNucleicAcidChemical		stimulates					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
81425	8	3726	11	NULL	NULL	0	NULL	statement 6	Process		occurs along with					statement 7	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_8_2749_s_222	12665576	(B) ChIP analysis of transcription factors c-Rel, p65/RelA, c-Jun, and  C/EBPbeta and of architectural factor HMGI-C binding to the  bfl-1 locus in human Jurkat T cells stimulated with PMA plus ionomycin (P+I) for 2 or 18  h or with a DMSO control.	bind
8643	1	3727	5	11	NULL	NULL	NULL	Myc	GP		bind					P57KIP2 gene	GP			DNA surrounding the start site of transcription of	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7648_s_228	14560010	(B) ChIp experiments documenting in vivo binding of Myc and Miz1 to DNA surrounding  the start site of transcription of the  P57KIP2and  P21CIP1 genes.	bind
8644	2	3727	5	11	NULL	NULL	NULL	Myc	GP		bind					P21CIP1 gene	GP			DNA surrounding the start site of transcription of	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7648_s_228	14560010	(B) ChIp experiments documenting in vivo binding of Myc and Miz1 to DNA surrounding  the start site of transcription of the  P57KIP2and  P21CIP1 genes.	bind
8645	3	3727	5	11	NULL	NULL	NULL	Miz1	GP		bind					P57KIP2 gene	GP			DNA surrounding the start site of transcription of	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7648_s_228	14560010	(B) ChIp experiments documenting in vivo binding of Myc and Miz1 to DNA surrounding  the start site of transcription of the  P57KIP2and  P21CIP1 genes.	bind
8646	4	3727	5	11	NULL	NULL	NULL	Miz1	GP		bind					P21CIP1 gene	GP			DNA surrounding the start site of transcription of	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7648_s_228	14560010	(B) ChIp experiments documenting in vivo binding of Myc and Miz1 to DNA surrounding  the start site of transcription of the  P57KIP2and  P21CIP1 genes.	bind
8826	1	3727	6	11	NULL	NULL	NULL	Myc	GP		bind					P57KIP2 gene	GP			DNA surrounding transcription start site	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7648_s_228	14560010	(B) ChIp experiments documenting in vivo binding of Myc and Miz1 to DNA surrounding  the start site of transcription of the  P57KIP2and  P21CIP1 genes.	bind
8827	2	3727	6	NULL	NULL	0	NULL	Myc	NULL		bind	NULL				p21Cip1	NULL			DNA surrounding transcription start site	NULL	in vivo	0	NULL	NULL	NULL	gw70_molcellbiol_23_21_7648_s_228	14560010	(B) ChIp experiments documenting in vivo binding of Myc and Miz1 to DNA surrounding  the start site of transcription of the  P57KIP2and  P21CIP1 genes.	bind
8828	3	3727	6	11	NULL	NULL	NULL	Miz1	GP		bind					P57KIP2 gene	GP			DNA surrounding transcription start site	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7648_s_228	14560010	(B) ChIp experiments documenting in vivo binding of Myc and Miz1 to DNA surrounding  the start site of transcription of the  P57KIP2and  P21CIP1 genes.	bind
8829	4	3727	6	11	NULL	NULL	NULL	Miz1	GP		bind					p21Cip1	GP			DNA surrounding transcription start site	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7648_s_228	14560010	(B) ChIp experiments documenting in vivo binding of Myc and Miz1 to DNA surrounding  the start site of transcription of the  P57KIP2and  P21CIP1 genes.	bind
81426	1	3727	11	NULL	NULL	0	NULL	P57KIP2 gene	Gene		undergoes					transcription	MolecularProcess				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_21_7648_s_228	14560010	(B) ChIp experiments documenting in vivo binding of Myc and Miz1 to DNA surrounding  the start site of transcription of the  P57KIP2and  P21CIP1 genes.	bind
81427	2	3727	11	NULL	NULL	0	NULL	P21CIP1 gene	Gene		undergoes					transcription	MolecularProcess				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_21_7648_s_228	14560010	(B) ChIp experiments documenting in vivo binding of Myc and Miz1 to DNA surrounding  the start site of transcription of the  P57KIP2and  P21CIP1 genes.	bind
81428	3	3727	11	NULL	NULL	0	NULL	Myc	Protein		binds to 					P57KIP2 gene	Gene			transcription start site	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_21_7648_s_228	14560010	(B) ChIp experiments documenting in vivo binding of Myc and Miz1 to DNA surrounding  the start site of transcription of the  P57KIP2and  P21CIP1 genes.	bind
81429	4	3727	11	NULL	NULL	0	NULL	Myc	Protein		binds to 					P21CIP1 gene	Gene			transcription start site	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_21_7648_s_228	14560010	(B) ChIp experiments documenting in vivo binding of Myc and Miz1 to DNA surrounding  the start site of transcription of the  P57KIP2and  P21CIP1 genes.	bind
81430	5	3727	11	NULL	NULL	0	NULL	Miz1	Protein		binds to 					P57KIP2 gene	Gene			transcription start site	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_21_7648_s_228	14560010	(B) ChIp experiments documenting in vivo binding of Myc and Miz1 to DNA surrounding  the start site of transcription of the  P57KIP2and  P21CIP1 genes.	bind
81431	6	3727	11	NULL	NULL	0	NULL	Miz1	Gene		binds to 					P21CIP1 gene	Gene			transcription start site	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_21_7648_s_228	14560010	(B) ChIp experiments documenting in vivo binding of Myc and Miz1 to DNA surrounding  the start site of transcription of the  P57KIP2and  P21CIP1 genes.	bind
8647	1	3728	5	11	NULL	NULL	NULL	GATA-6	GP		bind									I-BRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6646_s_232	12944489	(B) ChIP of GATA-6 bound to I-BRE.	bind
8830	1	3728	6	11	NULL	NULL	NULL	GATA-6	GP		bind									I-BRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6646_s_232	12944489	(B) ChIP of GATA-6 bound to I-BRE.	bind
81432	1	3728	11	NULL	NULL	0	NULL	GATA-6	GeneOrProtein		binds to 					I-BRE	Gene				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_18_6646_s_232	12944489	(B) ChIP of GATA-6 bound to I-BRE.	bind
8648	1	3729	5	11	NULL	NULL	NULL	Smad1	GP		bind									BRE-1	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6646_s_161	12944489	(B) ChIP of Smad1 bound to BRE-1.	bind
8831	1	3729	6	11	NULL	NULL	NULL	Smad1	GP		bind									BRE-1	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6646_s_161	12944489	(B) ChIP of Smad1 bound to BRE-1.	bind
81433	1	3729	11	NULL	NULL	0	NULL	Smad1	GeneOrProtein		binds to 					BRE-1	Gene				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_18_6646_s_161	12944489	(B) ChIP of Smad1 bound to BRE-1.	bind
8649	1	3730	5	11	NULL	NULL	NULL	NF-Y	GP		bind					cyclin B2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_gene_312_0_225_s_254	12909359	(B) Chromatin immunoprecipitation (ChIP) assays showing binding of NF-Y to the  cyclin B2 promoter.	bind
8832	1	3730	6	11	NULL	NULL	NULL	NF-Y	GP		bind					cyclin B2 	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_gene_312_0_225_s_254	12909359	(B) Chromatin immunoprecipitation (ChIP) assays showing binding of NF-Y to the  cyclin B2 promoter.	bind
81434	1	3730	11	NULL	NULL	0	NULL	 NF-Y	GeneOrProtein		binds to 					cyclin B2	Gene			promoter	NULL		0	NULL	NULL	NULL	gw60_gene_312_0_225_s_254	12909359	(B) Chromatin immunoprecipitation (ChIP) assays showing binding of NF-Y to the  cyclin B2 promoter.	bind
8650	1	3731	5	11	NULL	NULL	NULL	Cks1	GP		bind					Skp2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_7_3_639_s_181	11463388	(B) Cks1 binds Skp2 in vitro.	bind
8833	1	3731	6	11	NULL	NULL	NULL	Cks1	GP		bind					Skp2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_7_3_639_s_181	11463388	(B) Cks1 binds Skp2 in vitro.	bind
81435	1	3731	11	NULL	NULL	0	NULL	Cks1	GeneOrProtein		binds to 					Skp2	GeneOrProtein				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcell_7_3_639_s_181	11463388	(B) Cks1 binds Skp2 in vitro.	bind
8651	1	3733	5	11	NULL	NULL	NULL	EDA-A5	GP		bind					TROY receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_gene_371_1_42_s_111	16423472	(B) Co-immunoprecipitation analysis  for binding of EDA-A5  to TROY receptor.	bind
8834	1	3733	6	11	NULL	NULL	NULL	EDA-A5	GP		bind					TROY receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_gene_371_1_42_s_111	16423472	(B) Co-immunoprecipitation analysis  for binding of EDA-A5  to TROY receptor.	bind
81436	1	3733	11	NULL	NULL	0	NULL	EDA-A5	GeneOrProtein		binds to 					TROY receptor	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw70_gene_371_1_42_s_111	16423472	(B) Co-immunoprecipitation analysis  for binding of EDA-A5  to TROY receptor.	bind
8652	1	3734	5	11	NULL	NULL	NULL	CoA	GP		bind					CoaA protein	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_11_3410_s_125	12754240	(B) CoA binding of  CoaA protein mutants compared to that of wild-type CoaA.	bind
8653	2	3734	5	11	NULL	NULL	NULL	CoA	GP		bind					CoaA	GP	wild-type			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_11_3410_s_125	12754240	(B) CoA binding of  CoaA protein mutants compared to that of wild-type CoaA.	bind
8835	1	3734	6	11	NULL	NULL	NULL	CoA	GP		bind					CoaA protein	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_11_3410_s_125	12754240	(B) CoA binding of  CoaA protein mutants compared to that of wild-type CoaA.	bind
8989	2	3734	6	11	NULL	NULL	NULL	CoA	GP		bind					CoaA protein	GP	wild-type			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_11_3410_s_125	12754240	(B) CoA binding of  CoaA protein mutants compared to that of wild-type CoaA.	bind
8654	1	3736	5	11	NULL	NULL	NULL	Coatomer	GP		bind					Bet1p-GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_395_s_243	11970962	(B) Coatomer binds to Bet1p-GST via Glo3p.	bind
8655	2	3736	5	11	NULL	NULL	NULL	statement 1	Process		occurs via					Glo3p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_395_s_243	11970962	(B) Coatomer binds to Bet1p-GST via Glo3p.	bind
9016	1	3736	6	11	NULL	NULL	NULL	Coatomer	GP		bind					Bet1p-GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_395_s_243	11970962	(B) Coatomer binds to Bet1p-GST via Glo3p.	bind
9017	2	3736	6	11	NULL	NULL	NULL	statement 1	Process		occurs via					Glo3p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_395_s_243	11970962	(B) Coatomer binds to Bet1p-GST via Glo3p.	bind
81437	1	3736	11	NULL	NULL	0	NULL	Coatomer	Protein		binds to 					Bet1p-GST	Protein				NULL		0	NULL	NULL	NULL	gw60_cellbiol_157_3_395_s_243	11970962	(B) Coatomer binds to Bet1p-GST via Glo3p.	bind
81438	2	3736	11	NULL	NULL	0	NULL	Coatomer	Protein		binds to 					Glo3p	Protein				NULL		0	NULL	NULL	NULL	gw60_cellbiol_157_3_395_s_243	11970962	(B) Coatomer binds to Bet1p-GST via Glo3p.	bind
81439	3	3736	11	NULL	NULL	0	NULL	Glo3p	Protein		binds to 					Bet1p-GST	Protein				NULL		0	NULL	NULL	NULL	gw60_cellbiol_157_3_395_s_243	11970962	(B) Coatomer binds to Bet1p-GST via Glo3p.	bind
8656	2	3737	5	11	NULL	NULL	NULL	K2-3f	GP		bind			scFv		statement 1	Cell				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1638_3_257_s_277	12878327	(B) Cocaine  inhibition of scFv K2-3f binding to the hDAT expressed on the surface of a transfected  neuroblastoma N1E-115 cell line.	bind
8657	3	3737	5	11	NULL	NULL	NULL	Cocaine	Chemical		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1638_3_257_s_277	12878327	(B) Cocaine  inhibition of scFv K2-3f binding to the hDAT expressed on the surface of a transfected  neuroblastoma N1E-115 cell line.	bind
10029	1	3737	5	11	NULL	NULL	NULL	hDAT	GP		expressed					on surface of neuroblastoma N1E-115 cells	Cell	transfected			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1638_3_257_s_277	12878327	(B) Cocaine  inhibition of scFv K2-3f binding to the hDAT expressed on the surface of a transfected  neuroblastoma N1E-115 cell line.	bind
9018	1	3737	6	11	NULL	NULL	NULL	 K2-3f	GP		bind			scFv		hDAT	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1638_3_257_s_277	12878327	(B) Cocaine  inhibition of scFv K2-3f binding to the hDAT expressed on the surface of a transfected  neuroblastoma N1E-115 cell line.	bind
9019	2	3737	6	11	NULL	NULL	NULL	hDAT	GP		expressed on 					neuroblastoma N1E-115 cell line	Cell	surface of transfected			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1638_3_257_s_277	12878327	(B) Cocaine  inhibition of scFv K2-3f binding to the hDAT expressed on the surface of a transfected  neuroblastoma N1E-115 cell line.	bind
53475	3	3737	6	11	NULL	NULL	NULL	Cocaine	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1638_3_257_s_277	12878327	(B) Cocaine  inhibition of scFv K2-3f binding to the hDAT expressed on the surface of a transfected  neuroblastoma N1E-115 cell line.	bind
81440	1	3737	11	NULL	NULL	0	NULL	scFv K2-3f	GeneOrProtein		binds to 					hDAT	GeneOrProtein	 neuroblastoma;;N1E-115 cell line			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1638_3_257_s_277	12878327	(B) Cocaine  inhibition of scFv K2-3f binding to the hDAT expressed on the surface of a transfected  neuroblastoma N1E-115 cell line.	bind
81441	2	3737	11	NULL	NULL	0	NULL	Cocaine	NonProteinOrNucleicAcidChemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1638_3_257_s_277	12878327	(B) Cocaine  inhibition of scFv K2-3f binding to the hDAT expressed on the surface of a transfected  neuroblastoma N1E-115 cell line.	bind
8658	1	3740	5	11	NULL	NULL	NULL	Cdc50p-GFP	GP		colocalize with					myc-Vps21p	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_730_s_248	12589066	(B) Colocalization of Cdc50p-GFP with myc-Vps21p.	bind
9020	1	3740	6	11	NULL	NULL	NULL	Cdc50p-GFP	GP		colocalizes with					myc-Vps21p	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_730_s_248	12589066	(B) Colocalization of Cdc50p-GFP with myc-Vps21p.	bind
81442	1	3740	11	NULL	NULL	0	NULL	Cdc50p-GFP	GeneOrProtein		colocalizes with					myc-Vps21p	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_2_730_s_248	12589066	(B) Colocalization of Cdc50p-GFP with myc-Vps21p.	bind
81443	1	3743	11	NULL	NULL	0	NULL	 leucine	AminoAcid		binds to 					BacA	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_9_4509_s_111	12200307	(B) Comparison of one of the three leucine-specific consensus sequences found in the leucine binding domains of BacA, LicA, LchAA, LicB, LchAB, SrfAA, and SrfAB ( 52) with the corresponding residues in the sequenced part of amphisin synthetase.	bind
81444	2	3743	11	NULL	NULL	0	NULL	 leucine	AminoAcid		binds to 					LicA	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_9_4509_s_111	12200307	(B) Comparison of one of the three leucine-specific consensus sequences found in the leucine binding domains of BacA, LicA, LchAA, LicB, LchAB, SrfAA, and SrfAB ( 52) with the corresponding residues in the sequenced part of amphisin synthetase.	bind
81445	3	3743	11	NULL	NULL	0	NULL	leucine	AminoAcid		binds to 					LchAA	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_9_4509_s_111	12200307	(B) Comparison of one of the three leucine-specific consensus sequences found in the leucine binding domains of BacA, LicA, LchAA, LicB, LchAB, SrfAA, and SrfAB ( 52) with the corresponding residues in the sequenced part of amphisin synthetase.	bind
81446	4	3743	11	NULL	NULL	0	NULL	leucine	AminoAcid		binds to 					LicB	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_9_4509_s_111	12200307	(B) Comparison of one of the three leucine-specific consensus sequences found in the leucine binding domains of BacA, LicA, LchAA, LicB, LchAB, SrfAA, and SrfAB ( 52) with the corresponding residues in the sequenced part of amphisin synthetase.	bind
81447	5	3743	11	NULL	NULL	0	NULL	leucine	AminoAcid		binds to 					LchAB	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_9_4509_s_111	12200307	(B) Comparison of one of the three leucine-specific consensus sequences found in the leucine binding domains of BacA, LicA, LchAA, LicB, LchAB, SrfAA, and SrfAB ( 52) with the corresponding residues in the sequenced part of amphisin synthetase.	bind
81448	6	3743	11	NULL	NULL	0	NULL	leucine	AminoAcid		binds to 					SrfAA	Gene				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_9_4509_s_111	12200307	(B) Comparison of one of the three leucine-specific consensus sequences found in the leucine binding domains of BacA, LicA, LchAA, LicB, LchAB, SrfAA, and SrfAB ( 52) with the corresponding residues in the sequenced part of amphisin synthetase.	bind
81449	7	3743	11	NULL	NULL	0	NULL	leucine	AminoAcid		binds to 					SrfAB	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_9_4509_s_111	12200307	(B) Comparison of one of the three leucine-specific consensus sequences found in the leucine binding domains of BacA, LicA, LchAA, LicB, LchAB, SrfAA, and SrfAB ( 52) with the corresponding residues in the sequenced part of amphisin synthetase.	bind
8659	2	3744	5	11	NULL	NULL	NULL	PCAF	GP		bind			bromodomain		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_9_3_575_s_37	11931765	(B) Comparison of PCAF bromodomain binding to lysine-acetylated peptide derived from HIV-1 Tat at K50 (SYGR-AcK-KRRQR) (left) versus one derived from histone H4 at K16 (SGRGKGGKGLGKGGA-AcK-RHRK) (right).	bind
8660	4	3744	5	11	NULL	NULL	NULL	PCAF	GP		bind			bromodomain		statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_9_3_575_s_37	11931765	(B) Comparison of PCAF bromodomain binding to lysine-acetylated peptide derived from HIV-1 Tat at K50 (SYGR-AcK-KRRQR) (left) versus one derived from histone H4 at K16 (SGRGKGGKGLGKGGA-AcK-RHRK) (right).	bind
10024	1	3744	5	11	NULL	NULL	NULL	peptide	GP	acetylated	derived from			lysine		HIV-1 Tat	GP		k50(SYGR-AcK-KRRQR)		NULL		NULL	NULL	NULL	NULL	gw60_molcell_9_3_575_s_37	11931765	(B) Comparison of PCAF bromodomain binding to lysine-acetylated peptide derived from HIV-1 Tat at K50 (SYGR-AcK-KRRQR) (left) versus one derived from histone H4 at K16 (SGRGKGGKGLGKGGA-AcK-RHRK) (right).	bind
10025	3	3744	5	11	NULL	NULL	NULL	peptide	GP	acetylated	derived from			lysine		histone H4	GP		K16 (SGRGKGGKGLGKGGA-AcK-RHRK)		NULL		NULL	NULL	NULL	NULL	gw60_molcell_9_3_575_s_37	11931765	(B) Comparison of PCAF bromodomain binding to lysine-acetylated peptide derived from HIV-1 Tat at K50 (SYGR-AcK-KRRQR) (left) versus one derived from histone H4 at K16 (SGRGKGGKGLGKGGA-AcK-RHRK) (right).	bind
9021	1	3744	6	11	NULL	NULL	NULL	 peptide	GP	acetylated	derived from			lysine		HIV-1-Tat	GP		K50 (SYGR-AcK-KRRQR)		NULL		NULL	NULL	NULL	NULL	gw60_molcell_9_3_575_s_37	11931765	(B) Comparison of PCAF bromodomain binding to lysine-acetylated peptide derived from HIV-1 Tat at K50 (SYGR-AcK-KRRQR) (left) versus one derived from histone H4 at K16 (SGRGKGGKGLGKGGA-AcK-RHRK) (right).	bind
9022	2	3744	6	11	NULL	NULL	NULL	peptide	GP	acetylated 	derived from			lysine		histone H4	GP		K16 (SGRGKGGKGLGKGGA-AcK-RHRK)		NULL		NULL	NULL	NULL	NULL	gw60_molcell_9_3_575_s_37	11931765	(B) Comparison of PCAF bromodomain binding to lysine-acetylated peptide derived from HIV-1 Tat at K50 (SYGR-AcK-KRRQR) (left) versus one derived from histone H4 at K16 (SGRGKGGKGLGKGGA-AcK-RHRK) (right).	bind
9023	3	3744	6	11	NULL	NULL	NULL	PCAF	GP		bind			bromodomain		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_9_3_575_s_37	11931765	(B) Comparison of PCAF bromodomain binding to lysine-acetylated peptide derived from HIV-1 Tat at K50 (SYGR-AcK-KRRQR) (left) versus one derived from histone H4 at K16 (SGRGKGGKGLGKGGA-AcK-RHRK) (right).	bind
9024	4	3744	6	11	NULL	NULL	NULL	PCAF	GP		bind			bromodomain		statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_9_3_575_s_37	11931765	(B) Comparison of PCAF bromodomain binding to lysine-acetylated peptide derived from HIV-1 Tat at K50 (SYGR-AcK-KRRQR) (left) versus one derived from histone H4 at K16 (SGRGKGGKGLGKGGA-AcK-RHRK) (right).	bind
81450	1	3744	11	NULL	NULL	0	NULL	PCAF 	Protein		binds to 			bromodomain		lysine-acetylated peptide	PartOfProtein	HIV-1 Tat			NULL		0	NULL	NULL	NULL	gw60_molcell_9_3_575_s_37	11931765	(B) Comparison of PCAF bromodomain binding to lysine-acetylated peptide derived from HIV-1 Tat at K50 (SYGR-AcK-KRRQR) (left) versus one derived from histone H4 at K16 (SGRGKGGKGLGKGGA-AcK-RHRK) (right).	bind
8661	1	3745	5	11	NULL	NULL	NULL	H-NS	GP		bind					PCR fragments	NucleicAcid	representing -310 fusion			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_22_6497_s_197	14594821	(B) Comparison of the binding of H-NS to PCR fragments representing the  -310 and -310d4 fusions.	bind
8662	2	3745	5	11	NULL	NULL	NULL	H-NS	GP		bind					PCR fragments	NucleicAcid	representing -310d4 fusion			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_22_6497_s_197	14594821	(B) Comparison of the binding of H-NS to PCR fragments representing the  -310 and -310d4 fusions.	bind
9025	1	3745	6	11	NULL	NULL	NULL	H-NS	GP		bind					PCR fragments	NucleicAcid	-310 fusions			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_22_6497_s_197	14594821	(B) Comparison of the binding of H-NS to PCR fragments representing the  -310 and -310d4 fusions.	bind
9699	2	3745	6	11	NULL	NULL	NULL	H-NS	GP		bind					PCR fragments	NucleicAcid	-310d4 fusions			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_22_6497_s_197	14594821	(B) Comparison of the binding of H-NS to PCR fragments representing the  -310 and -310d4 fusions.	bind
81451	1	3745	11	NULL	NULL	0	NULL	 H-NS	GeneOrProtein		binds to 					PCR fragment	PartOfProtein				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_22_6497_s_197	14594821	(B) Comparison of the binding of H-NS to PCR fragments representing the  -310 and -310d4 fusions.	bind
8663	1	3747	5	11	NULL	NULL	NULL	L1 lipid	Chemical		bind		tightly			sIgA	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_3_153_s_213	16039903	(B) Comparison of the incorporation of 32P label into L1 and L2 lipids tightly bound to sIgA by TLC on a Kieselgel plates using  chloroform-methanol-7 M NH4OH (60:35:5).	bind
8664	2	3747	5	11	NULL	NULL	NULL	L2 lipid	Chemical		bind		tightly			sIgA	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_3_153_s_213	16039903	(B) Comparison of the incorporation of 32P label into L1 and L2 lipids tightly bound to sIgA by TLC on a Kieselgel plates using  chloroform-methanol-7 M NH4OH (60:35:5).	bind
9026	1	3747	6	11	NULL	NULL	NULL	L1 lipid	Chemical		bind		tightly			sIgA	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_3_153_s_213	16039903	(B) Comparison of the incorporation of 32P label into L1 and L2 lipids tightly bound to sIgA by TLC on a Kieselgel plates using  chloroform-methanol-7 M NH4OH (60:35:5).	bind
9027	2	3747	6	11	NULL	NULL	NULL	L2 lipid	Chemical		bind		tightly			sIgA	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_3_153_s_213	16039903	(B) Comparison of the incorporation of 32P label into L1 and L2 lipids tightly bound to sIgA by TLC on a Kieselgel plates using  chloroform-methanol-7 M NH4OH (60:35:5).	bind
81452	1	3747	11	NULL	NULL	0	NULL	L1 lipid	NonProteinOrNucleicAcidChemical		binds to 		tightly			sIgA	Protein				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_3_153_s_213	16039903	(B) Comparison of the incorporation of 32P label into L1 and L2 lipids tightly bound to sIgA by TLC on a Kieselgel plates using  chloroform-methanol-7 M NH4OH (60:35:5).	bind
81453	2	3747	11	NULL	NULL	NULL	NULL	L2 lipid	NonProteinOrNucleicAcidChemical		binds to 		tightly			sIgA	Protein				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_3_153_s_213	16039903	(B) Comparison of the incorporation of 32P label into L1 and L2 lipids tightly bound to sIgA by TLC on a Kieselgel plates using  chloroform-methanol-7 M NH4OH (60:35:5).	bind
8665	1	3750	5	11	NULL	NULL	NULL	Mcm1	GP		bind					ARS120	NucleicAcid		fragment I		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_14_6514_s_215	15226450	(B) Competition  for binding of Mcm1 by fragment I of ARS120 and ARS131a.	bind
8666	2	3750	5	11	NULL	NULL	NULL	Mcm1	GP		bind					ARS131a	NucleicAcid		fragment I		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_14_6514_s_215	15226450	(B) Competition  for binding of Mcm1 by fragment I of ARS120 and ARS131a.	bind
8667	3	3750	5	11	NULL	NULL	NULL	statement 1	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_14_6514_s_215	15226450	(B) Competition  for binding of Mcm1 by fragment I of ARS120 and ARS131a.	bind
9414	1	3750	6	11	NULL	NULL	NULL	Mcm1	GP		bind					ARS120	NucleicAcid		fragment 1 		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_14_6514_s_215	15226450	(B) Competition  for binding of Mcm1 by fragment I of ARS120 and ARS131a.	bind
9415	2	3750	6	11	NULL	NULL	NULL	Mcm1	GP		bind					ARS131a	NucleicAcid		fragment 1 		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_14_6514_s_215	15226450	(B) Competition  for binding of Mcm1 by fragment I of ARS120 and ARS131a.	bind
9416	3	3750	6	11	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_14_6514_s_215	15226450	(B) Competition  for binding of Mcm1 by fragment I of ARS120 and ARS131a.	bind
81454	1	3750	11	NULL	NULL	0	NULL	 Mcm1	GeneOrProtein		binds to 					fragment I	NucleicAcidSubstance	ARS120			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_14_6514_s_215	15226450	(B) Competition  for binding of Mcm1 by fragment I of ARS120 and ARS131a.	bind
81455	2	3750	11	NULL	NULL	0	NULL	Mcm1	GeneOrProtein		binds to 					fragment I	NucleicAcidSubstance	ARS131a			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_14_6514_s_215	15226450	(B) Competition  for binding of Mcm1 by fragment I of ARS120 and ARS131a.	bind
8668	1	3751	5	11	NULL	NULL	NULL	gp120	GP	biotinylated;; HIV-1	bind					DC-SIGN	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_5_653_s_181	12433371	(B) Competition assay of biotinylated HIV-1 gp120 binding to DC-SIGN.	bind
9028	1	3751	6	11	NULL	NULL	NULL	gp120	GP	biotinylated;; HIV-1	bind					DC-SIGN	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_5_653_s_181	12433371	(B) Competition assay of biotinylated HIV-1 gp120 binding to DC-SIGN.	bind
81456	1	3751	11	NULL	NULL	0	NULL	gp120	GeneOrProtein	HIV-1;;biotinylated	binds to 					DC-SIGN	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_immunity_17_5_653_s_181	12433371	(B) Competition assay of biotinylated HIV-1 gp120 binding to DC-SIGN.	bind
8669	1	3753	5	11	NULL	NULL	NULL	C/EBPdelta	GP		bind				APRE	Stat3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2108_s_244	9528783	(B) Competition for Stat3 binding by the C/EBPdelta APRE.	bind
9029	1	3753	6	11	NULL	NULL	NULL	Stat3	GP		bind					C/EBPdelta	GP			APRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2108_s_244	9528783	(B) Competition for Stat3 binding by the C/EBPdelta APRE.	bind
81457	1	3753	11	NULL	NULL	0	NULL	C/EBPdelta	Gene		binds to 				APRE	Stat3	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_2108_s_244	9528783	(B) Competition for Stat3 binding by the C/EBPdelta APRE.	bind
8879	1	3754	5	11	NULL	NULL	NULL	p53	GP		bind					PUMA	GP			 binding site 2	NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_94	11463392	(B) Competitive inhibition of p53 binding to the PUMA binding site 2 with the wild-type PUMA BS2 but not the mutant PUMA BS2 oligonucleotide	bind
8881	2	3754	5	11	NULL	NULL	NULL	p53	GP		bind					PUMA	GP	wild-type		BS2	NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_94	11463392	(B) Competitive inhibition of p53 binding to the PUMA binding site 2 with the wild-type PUMA BS2 but not the mutant PUMA BS2 oligonucleotide	bind
8882	3	3754	5	11	NULL	NULL	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_94	11463392	(B) Competitive inhibition of p53 binding to the PUMA binding site 2 with the wild-type PUMA BS2 but not the mutant PUMA BS2 oligonucleotide	bind
8883	4	3754	5	11	NULL	NULL	NULL	p53	GP		does not bind					PUMA	GP	mutant		BS2 oligonucleotide	NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_94	11463392	(B) Competitive inhibition of p53 binding to the PUMA binding site 2 with the wild-type PUMA BS2 but not the mutant PUMA BS2 oligonucleotide	bind
8884	5	3754	5	11	NULL	NULL	NULL	statement 4	Process		does not compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_94	11463392	(B) Competitive inhibition of p53 binding to the PUMA binding site 2 with the wild-type PUMA BS2 but not the mutant PUMA BS2 oligonucleotide	bind
9030	1	3754	6	11	NULL	NULL	NULL	p53	GP		bind					PUMA	GP			binding site 2	NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_94	11463392	(B) Competitive inhibition of p53 binding to the PUMA binding site 2 with the wild-type PUMA BS2 but not the mutant PUMA BS2 oligonucleotide	bind
9031	2	3754	6	11	NULL	NULL	NULL	p53	GP		bind					PUMA	GP	wild-type		BS2	NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_94	11463392	(B) Competitive inhibition of p53 binding to the PUMA binding site 2 with the wild-type PUMA BS2 but not the mutant PUMA BS2 oligonucleotide	bind
9032	3	3754	6	11	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_94	11463392	(B) Competitive inhibition of p53 binding to the PUMA binding site 2 with the wild-type PUMA BS2 but not the mutant PUMA BS2 oligonucleotide	bind
9033	4	3754	6	11	NULL	NULL	NULL	p53	GP		does not bind					PUMA 	GP	mutant		BS2  oligonucletide	NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_94	11463392	(B) Competitive inhibition of p53 binding to the PUMA binding site 2 with the wild-type PUMA BS2 but not the mutant PUMA BS2 oligonucleotide	bind
53476	5	3754	6	11	NULL	NULL	NULL	statement 4	Process		does not compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_94	11463392	(B) Competitive inhibition of p53 binding to the PUMA binding site 2 with the wild-type PUMA BS2 but not the mutant PUMA BS2 oligonucleotide	bind
81458	1	3754	11	NULL	NULL	NULL	NULL	 p53	GeneOrProtein		binds to 					PUMA	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_94	11463392	(B) Competitive inhibition of p53 binding to the PUMA binding site 2 with the wild-type PUMA BS2 but not the mutant PUMA BS2 oligonucleotide	bind
81459	2	3754	11	NULL	NULL	NULL	NULL	PUMA BS2	GeneOrProtein	wild-type	Competitively inhibit					PUMA	GeneOrProtein	binding site 2			NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_683_s_94	11463392	(B) Competitive inhibition of p53 binding to the PUMA binding site 2 with the wild-type PUMA BS2 but not the mutant PUMA BS2 oligonucleotide	bind
81460	3	3754	11	NULL	NULL	0	NULL	PUMA BS2	NucleicAcidSubstance	mutant	Competitively inhibit					PUMA	GeneOrProtein	binding site 2			NULL		0	NULL	NULL	NULL	gw60_molcell_7_3_683_s_94	11463392	(B) Competitive inhibition of p53 binding to the PUMA binding site 2 with the wild-type PUMA BS2 but not the mutant PUMA BS2 oligonucleotide	bind
8670	1	3755	5	11	NULL	NULL	NULL	Complexin	GP		bind					ternary SNARE complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_283_s_158	16267273	(B) Complexin binding to the ternary SNARE complex.	bind
9034	1	3755	6	11	NULL	NULL	NULL	Complexin	GP		bind					ternary SNARE complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_283_s_158	16267273	(B) Complexin binding to the ternary SNARE complex.	bind
81461	1	3755	11	NULL	NULL	0	NULL	Complexin	GeneOrProtein		binds to 					SNARE	Protein	ternary complex			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_283_s_158	16267273	(B) Complexin binding to the ternary SNARE complex.	bind
8671	1	3756	5	11	NULL	NULL	NULL	KorB (pSB24.2)	GP		bind					pIJ101 kilB	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_13_3780_s_110	12813071	(B) Concentration-dependent characteristics of KorB (pSB24.2) binding  to the pIJ101  kilB promoter.	bind
8672	2	3756	5	11	NULL	NULL	NULL	statement 1	Process		is dependent on					concentration	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_13_3780_s_110	12813071	(B) Concentration-dependent characteristics of KorB (pSB24.2) binding  to the pIJ101  kilB promoter.	bind
9035	1	3756	6	11	NULL	NULL	NULL	KorB (pSB24.2)	GP		bind					pIJ101 kilB	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_13_3780_s_110	12813071	(B) Concentration-dependent characteristics of KorB (pSB24.2) binding  to the pIJ101  kilB promoter.	bind
53477	2	3756	6	11	NULL	NULL	NULL	statement 1	Process		depends on					Concentration	QuantityOrMeasure				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_13_3780_s_110	12813071	(B) Concentration-dependent characteristics of KorB (pSB24.2) binding  to the pIJ101  kilB promoter.	bind
81462	1	3756	11	NULL	NULL	0	NULL	KorB	GeneOrProtein		binds to 					pIJ101 kilB	Gene			promoter	NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_13_3780_s_110	12813071	(B) Concentration-dependent characteristics of KorB (pSB24.2) binding  to the pIJ101  kilB promoter.	bind
8673	1	3758	5	11	NULL	NULL	NULL	GTP S	NucleicAcid		bind					MBP-T43NTR-Gi	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_104	11287004	(B) Concentration-response curves for NT-induced [35]GTP S binding to MBP-T43NTR-Gi (squares) or MBP-T43NTR-Gi/q (triangles).	bind
8674	2	3758	5	11	NULL	NULL	NULL	NT	GP		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_104	11287004	(B) Concentration-response curves for NT-induced [35]GTP S binding to MBP-T43NTR-Gi (squares) or MBP-T43NTR-Gi/q (triangles).	bind
8675	3	3758	5	11	NULL	NULL	NULL	GTP S	NucleicAcid		bind					MBP-T43NTR-Gi/q	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_104	11287004	(B) Concentration-response curves for NT-induced [35]GTP S binding to MBP-T43NTR-Gi (squares) or MBP-T43NTR-Gi/q (triangles).	bind
8676	4	3758	5	11	NULL	NULL	NULL	NT	GP		induce					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_104	11287004	(B) Concentration-response curves for NT-induced [35]GTP S binding to MBP-T43NTR-Gi (squares) or MBP-T43NTR-Gi/q (triangles).	bind
53478	5	3758	5	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_104	11287004	(B) Concentration-response curves for NT-induced [35]GTP S binding to MBP-T43NTR-Gi (squares) or MBP-T43NTR-Gi/q (triangles).	bind
9036	1	3758	6	11	NULL	NULL	NULL	GTP S	NucleicAcid		bind					MBP-T43NTR-Gi	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_104	11287004	(B) Concentration-response curves for NT-induced [35]GTP S binding to MBP-T43NTR-Gi (squares) or MBP-T43NTR-Gi/q (triangles).	bind
9037	2	3758	6	11	NULL	NULL	NULL	GTP S	NucleicAcid		bind					MBP-T43NTR-Gi/q	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_104	11287004	(B) Concentration-response curves for NT-induced [35]GTP S binding to MBP-T43NTR-Gi (squares) or MBP-T43NTR-Gi/q (triangles).	bind
9038	3	3758	6	11	NULL	NULL	NULL	NT	GP		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_104	11287004	(B) Concentration-response curves for NT-induced [35]GTP S binding to MBP-T43NTR-Gi (squares) or MBP-T43NTR-Gi/q (triangles).	bind
9039	4	3758	6	11	NULL	NULL	NULL	NT	GP		induces					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_104	11287004	(B) Concentration-response curves for NT-induced [35]GTP S binding to MBP-T43NTR-Gi (squares) or MBP-T43NTR-Gi/q (triangles).	bind
9040	5	3758	6	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_493_2_101_s_104	11287004	(B) Concentration-response curves for NT-induced [35]GTP S binding to MBP-T43NTR-Gi (squares) or MBP-T43NTR-Gi/q (triangles).	bind
81463	1	3758	11	NULL	NULL	0	NULL	GTP	NonProteinOrNucleicAcidChemical		binds to 					MBP-T43NTR-Gi	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_febslett_493_2_101_s_104	11287004	(B) Concentration-response curves for NT-induced [35]GTP S binding to MBP-T43NTR-Gi (squares) or MBP-T43NTR-Gi/q (triangles).	bind
81464	2	3758	11	NULL	NULL	0	NULL	GTP	Chemical		binds to 					MBP-T43NTR-Gi/q	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_febslett_493_2_101_s_104	11287004	(B) Concentration-response curves for NT-induced [35]GTP S binding to MBP-T43NTR-Gi (squares) or MBP-T43NTR-Gi/q (triangles).	bind
81465	3	3758	11	NULL	NULL	0	NULL	NT	PartOfProtein		induces					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_493_2_101_s_104	11287004	(B) Concentration-response curves for NT-induced [35]GTP S binding to MBP-T43NTR-Gi (squares) or MBP-T43NTR-Gi/q (triangles).	bind
81466	4	3758	11	NULL	NULL	0	NULL	NT	PartOfProtein		induces					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_493_2_101_s_104	11287004	(B) Concentration-response curves for NT-induced [35]GTP S binding to MBP-T43NTR-Gi (squares) or MBP-T43NTR-Gi/q (triangles).	bind
8677	1	3762	5	11	NULL	NULL	NULL	IRF-3	GP		bind					IFNA1	GP			VRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_400	12138184	(B) Cooperation between IRF-3 and IRF-5 binding to IFNA1 VRE enhances IRF-5-induced IFNA1 expression.	bind
8678	2	3762	5	11	NULL	NULL	NULL	IRF-5	GP		bind					IFNA1	GP			VRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_400	12138184	(B) Cooperation between IRF-3 and IRF-5 binding to IFNA1 VRE enhances IRF-5-induced IFNA1 expression.	bind
8679	3	3762	5	11	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_400	12138184	(B) Cooperation between IRF-3 and IRF-5 binding to IFNA1 VRE enhances IRF-5-induced IFNA1 expression.	bind
8680	4	3762	5	11	NULL	NULL	NULL	IRF-5	GP		induce					IFNA1	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_400	12138184	(B) Cooperation between IRF-3 and IRF-5 binding to IFNA1 VRE enhances IRF-5-induced IFNA1 expression.	bind
8681	5	3762	5	11	NULL	NULL	NULL	statement 3	Process		enhances					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_400	12138184	(B) Cooperation between IRF-3 and IRF-5 binding to IFNA1 VRE enhances IRF-5-induced IFNA1 expression.	bind
9041	1	3762	6	11	NULL	NULL	NULL	IRF-3	GP		bind					IFNA1	GP			VRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_400	12138184	(B) Cooperation between IRF-3 and IRF-5 binding to IFNA1 VRE enhances IRF-5-induced IFNA1 expression.	bind
9042	2	3762	6	11	NULL	NULL	NULL	IRF-5	GP		bind					IFNA1	GP			VRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_400	12138184	(B) Cooperation between IRF-3 and IRF-5 binding to IFNA1 VRE enhances IRF-5-induced IFNA1 expression.	bind
9043	3	3762	6	11	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_400	12138184	(B) Cooperation between IRF-3 and IRF-5 binding to IFNA1 VRE enhances IRF-5-induced IFNA1 expression.	bind
9044	4	3762	6	11	NULL	NULL	NULL	IRF-5	GP		induces					IFNA1	GP	expression of 			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_400	12138184	(B) Cooperation between IRF-3 and IRF-5 binding to IFNA1 VRE enhances IRF-5-induced IFNA1 expression.	bind
9045	5	3762	6	11	NULL	NULL	NULL	statement 3	Process		enhances					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_400	12138184	(B) Cooperation between IRF-3 and IRF-5 binding to IFNA1 VRE enhances IRF-5-induced IFNA1 expression.	bind
81467	1	3762	11	NULL	NULL	0	NULL	 IRF-3 	GeneOrProtein		binds to 					IFNA1	Gene			VRE	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_400	12138184	(B) Cooperation between IRF-3 and IRF-5 binding to IFNA1 VRE enhances IRF-5-induced IFNA1 expression.	bind
81468	2	3762	11	NULL	NULL	0	NULL	IRF-5 	GeneOrProtein		binds to 					IFNA1	Gene			VRE	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_400	12138184	(B) Cooperation between IRF-3 and IRF-5 binding to IFNA1 VRE enhances IRF-5-induced IFNA1 expression.	bind
81469	3	3762	11	NULL	NULL	0	NULL	IRF-3	GeneOrProtein		Cooperate with					IRF-5	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_400	12138184	(B) Cooperation between IRF-3 and IRF-5 binding to IFNA1 VRE enhances IRF-5-induced IFNA1 expression.	bind
81470	4	3762	11	NULL	NULL	0	NULL	IRF-5	GeneOrProtein		induces					IFNA1	Gene	expression			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_400	12138184	(B) Cooperation between IRF-3 and IRF-5 binding to IFNA1 VRE enhances IRF-5-induced IFNA1 expression.	bind
81471	5	3762	11	NULL	NULL	0	NULL	statement 1	Process		enhances					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_400	12138184	(B) Cooperation between IRF-3 and IRF-5 binding to IFNA1 VRE enhances IRF-5-induced IFNA1 expression.	bind
81472	6	3762	11	NULL	NULL	0	NULL	statement 2	Process		enhances					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_16_5721_s_400	12138184	(B) Cooperation between IRF-3 and IRF-5 binding to IFNA1 VRE enhances IRF-5-induced IFNA1 expression.	bind
8682	1	3764	5	11	NULL	NULL	NULL	SF-1	GP	COS1-overexpressed	bind					PE1 probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_146	15831456	(B) COS1-overexpressed SF-1 and  LRH-1 binding to the PE1, PE2, and DR0 probes in the absence or presence of antibodies.	bind
8683	2	3764	5	11	NULL	NULL	NULL	LRH-1	GP	COS1-overexpressed	bind					PE1 probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_146	15831456	(B) COS1-overexpressed SF-1 and  LRH-1 binding to the PE1, PE2, and DR0 probes in the absence or presence of antibodies.	bind
8684	3	3764	5	11	NULL	NULL	NULL	SF-1	GP	COS1-overexpressed	bind					PE2 probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_146	15831456	(B) COS1-overexpressed SF-1 and  LRH-1 binding to the PE1, PE2, and DR0 probes in the absence or presence of antibodies.	bind
8685	4	3764	5	11	NULL	NULL	NULL	LRH-1	GP	COS1-overexpressed	bind					PE2 probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_146	15831456	(B) COS1-overexpressed SF-1 and  LRH-1 binding to the PE1, PE2, and DR0 probes in the absence or presence of antibodies.	bind
8686	5	3764	5	11	NULL	NULL	NULL	SF-1	GP	COS1-overexpressed	bind					DRO probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_146	15831456	(B) COS1-overexpressed SF-1 and  LRH-1 binding to the PE1, PE2, and DR0 probes in the absence or presence of antibodies.	bind
8687	6	3764	5	11	NULL	NULL	NULL	LRH-1	GP	COS1-overexpressed	bind					DRO probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_146	15831456	(B) COS1-overexpressed SF-1 and  LRH-1 binding to the PE1, PE2, and DR0 probes in the absence or presence of antibodies.	bind
9046	1	3764	6	11	NULL	NULL	NULL	SF-1	GP	COS-1 overexpressed	bind					PE1 probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_146	15831456	(B) COS1-overexpressed SF-1 and  LRH-1 binding to the PE1, PE2, and DR0 probes in the absence or presence of antibodies.	bind
9048	2	3764	6	11	NULL	NULL	NULL	SF-1	GP	COS-1 overexpressed	bind					PE2 probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_146	15831456	(B) COS1-overexpressed SF-1 and  LRH-1 binding to the PE1, PE2, and DR0 probes in the absence or presence of antibodies.	bind
9049	3	3764	6	11	NULL	NULL	NULL	SF-1	GP	COS-1 overexpressed	bind					DR0 probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_146	15831456	(B) COS1-overexpressed SF-1 and  LRH-1 binding to the PE1, PE2, and DR0 probes in the absence or presence of antibodies.	bind
9050	4	3764	6	11	NULL	NULL	NULL	LRH-1	GP	COS-1 overexpressed	bind					PE1 probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_146	15831456	(B) COS1-overexpressed SF-1 and  LRH-1 binding to the PE1, PE2, and DR0 probes in the absence or presence of antibodies.	bind
9051	5	3764	6	11	NULL	NULL	NULL	LRH-1	GP	COS-1 overexpressed	bind					PE2 probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_146	15831456	(B) COS1-overexpressed SF-1 and  LRH-1 binding to the PE1, PE2, and DR0 probes in the absence or presence of antibodies.	bind
9052	6	3764	6	11	NULL	NULL	NULL	LRH-1	GP	COS-1 overexpressed	bind					DR0 probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_146	15831456	(B) COS1-overexpressed SF-1 and  LRH-1 binding to the PE1, PE2, and DR0 probes in the absence or presence of antibodies.	bind
81473	1	3764	11	NULL	NULL	NULL	NULL	SF-1	GeneOrProtein	COS1-overexpressed	binds to 					PE1 probe	NucleicAcidSubstance				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_146	15831456	(B) COS1-overexpressed SF-1 and  LRH-1 binding to the PE1, PE2, and DR0 probes in the absence or presence of antibodies.	bind
81474	2	3764	11	NULL	NULL	NULL	NULL	 LRH-1	GeneOrProtein	COS1-overexpressed	binds to 					PE1 probe	NucleicAcidSubstance				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_146	15831456	(B) COS1-overexpressed SF-1 and  LRH-1 binding to the PE1, PE2, and DR0 probes in the absence or presence of antibodies.	bind
81475	3	3764	11	NULL	NULL	0	NULL	SF-1	GeneOrProtein	COS1-overexpressed	binds to 					PE2 probe	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_146	15831456	(B) COS1-overexpressed SF-1 and  LRH-1 binding to the PE1, PE2, and DR0 probes in the absence or presence of antibodies.	bind
81476	4	3764	11	NULL	NULL	0	NULL	 LRH-1	GeneOrProtein	COS1-overexpressed	binds to 					PE2 probe	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_146	15831456	(B) COS1-overexpressed SF-1 and  LRH-1 binding to the PE1, PE2, and DR0 probes in the absence or presence of antibodies.	bind
81477	5	3764	11	NULL	NULL	0	NULL	SF-1	GeneOrProtein	COS1-overexpressed	binds to 					DR0 probe	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_146	15831456	(B) COS1-overexpressed SF-1 and  LRH-1 binding to the PE1, PE2, and DR0 probes in the absence or presence of antibodies.	bind
81478	6	3764	11	NULL	NULL	0	NULL	LRH-1	GeneOrProtein	COS1-overexpressed	binds to 					DR0 probe	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_146	15831456	(B) COS1-overexpressed SF-1 and  LRH-1 binding to the PE1, PE2, and DR0 probes in the absence or presence of antibodies.	bind
8688	1	3765	5	11	NULL	NULL	NULL	HIF-1	GP		bind					f-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_273_2_285_s_73	15328013	(B) Costaining for HIF-1  (green) and phalloidin-Alexa Fluor 568 (red),  which binds f-actin and delineates the myocardium.	bind
8689	2	3765	5	11	NULL	NULL	NULL	HIF-1	GP		delineates					myocardium	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_273_2_285_s_73	15328013	(B) Costaining for HIF-1  (green) and phalloidin-Alexa Fluor 568 (red),  which binds f-actin and delineates the myocardium.	bind
8690	3	3765	5	11	NULL	NULL	NULL	phalloidin-Alexa Fluor 568	Chemical		bind					f-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_273_2_285_s_73	15328013	(B) Costaining for HIF-1  (green) and phalloidin-Alexa Fluor 568 (red),  which binds f-actin and delineates the myocardium.	bind
8691	4	3765	5	11	NULL	NULL	NULL	phalloidin-Alexa Fluor 568	Chemical		delineates					myocardium	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_273_2_285_s_73	15328013	(B) Costaining for HIF-1  (green) and phalloidin-Alexa Fluor 568 (red),  which binds f-actin and delineates the myocardium.	bind
9053	1	3765	6	11	NULL	NULL	NULL	HIF-1	GP		bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_273_2_285_s_73	15328013	(B) Costaining for HIF-1  (green) and phalloidin-Alexa Fluor 568 (red),  which binds f-actin and delineates the myocardium.	bind
9054	2	3765	6	11	NULL	NULL	NULL	phalloidin-Alexa Fluor 568	Chemical		bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_273_2_285_s_73	15328013	(B) Costaining for HIF-1  (green) and phalloidin-Alexa Fluor 568 (red),  which binds f-actin and delineates the myocardium.	bind
9055	3	3765	6	11	NULL	NULL	NULL	statement 1	Process		delineates					myocardium	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_273_2_285_s_73	15328013	(B) Costaining for HIF-1  (green) and phalloidin-Alexa Fluor 568 (red),  which binds f-actin and delineates the myocardium.	bind
9056	4	3765	6	11	NULL	NULL	NULL	statement 2	Process		delineates					myocardium	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_273_2_285_s_73	15328013	(B) Costaining for HIF-1  (green) and phalloidin-Alexa Fluor 568 (red),  which binds f-actin and delineates the myocardium.	bind
81479	1	3765	11	NULL	NULL	NULL	NULL	phalloidin-Alexa Fluor 568	NonProteinOrNucleicAcidChemical		binds to 					f-actin	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_273_2_285_s_73	15328013	(B) Costaining for HIF-1  (green) and phalloidin-Alexa Fluor 568 (red),  which binds f-actin and delineates the myocardium.	bind
81480	2	3765	11	NULL	NULL	0	NULL	statement 1	Process		delineates					myocardium	AnatomicalPart				NULL		0	NULL	NULL	NULL	gw70_devbiol_273_2_285_s_73	15328013	(B) Costaining for HIF-1  (green) and phalloidin-Alexa Fluor 568 (red),  which binds f-actin and delineates the myocardium.	bind
8692	1	3766	5	11	NULL	NULL	NULL	BV	Chemical		bind		covalently			PHY-2	GP		1-515		NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_12_2140_s_190	16339731	(B) Covalent binding of BV and  PCB to PHY-2 (1-515).	bind
8693	2	3766	5	11	NULL	NULL	NULL	PCB	GP		bind		covalently			PHY-2	GP		1-515		NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_12_2140_s_190	16339731	(B) Covalent binding of BV and  PCB to PHY-2 (1-515).	bind
9057	1	3766	6	11	NULL	NULL	NULL	BV	Chemical		bind		covalently			PHY-2	GP		1-515		NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_12_2140_s_190	16339731	(B) Covalent binding of BV and  PCB to PHY-2 (1-515).	bind
9058	2	3766	6	11	NULL	NULL	NULL	PCB	GP		bind		covalently			PHY-2	GP		1-515		NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_12_2140_s_190	16339731	(B) Covalent binding of BV and  PCB to PHY-2 (1-515).	bind
81481	1	3766	11	NULL	NULL	0	NULL	BV	Chemical		binds to 		Covalently			PHY-2	Protein				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_12_2140_s_190	16339731	(B) Covalent binding of BV and  PCB to PHY-2 (1-515).	bind
81482	2	3766	11	NULL	NULL	0	NULL	PCB	Chemical		binds to 		Covalently			PHY-2	Protein				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_12_2140_s_190	16339731	(B) Covalent binding of BV and  PCB to PHY-2 (1-515).	bind
8694	1	3767	5	11	NULL	NULL	NULL	CP110	GP		bind					cyclin E/CDK2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_devcell_3_3_339_s_69	12361598	(B) CP110 binds to cyclin E/CDK2, cyclin A/CDK2, and cyclin B/CDC2 in vitro.	bind
8695	2	3767	5	11	NULL	NULL	NULL	CP110	GP		bind					cyclin A/CDK2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_devcell_3_3_339_s_69	12361598	(B) CP110 binds to cyclin E/CDK2, cyclin A/CDK2, and cyclin B/CDC2 in vitro.	bind
8696	3	3767	5	11	NULL	NULL	NULL	CP110	GP		bind					cyclin B/CDC2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_devcell_3_3_339_s_69	12361598	(B) CP110 binds to cyclin E/CDK2, cyclin A/CDK2, and cyclin B/CDC2 in vitro.	bind
9059	1	3767	6	11	NULL	NULL	NULL	CP110	GP		bind					cyclin E/CDK2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_devcell_3_3_339_s_69	12361598	(B) CP110 binds to cyclin E/CDK2, cyclin A/CDK2, and cyclin B/CDC2 in vitro.	bind
9060	2	3767	6	11	NULL	NULL	NULL	CP110	GP		bind					cyclin A/CDK2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_devcell_3_3_339_s_69	12361598	(B) CP110 binds to cyclin E/CDK2, cyclin A/CDK2, and cyclin B/CDC2 in vitro.	bind
9061	3	3767	6	11	NULL	NULL	NULL	CP110	GP		bind					cyclin B/CDC2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_devcell_3_3_339_s_69	12361598	(B) CP110 binds to cyclin E/CDK2, cyclin A/CDK2, and cyclin B/CDC2 in vitro.	bind
81483	1	3767	11	NULL	NULL	0	NULL	CP110	GeneOrProtein		binds to 					cyclin E/CDK2	GeneOrProtein				NULL	in vitro	0	NULL	NULL	NULL	gw60_devcell_3_3_339_s_69	12361598	(B) CP110 binds to cyclin E/CDK2, cyclin A/CDK2, and cyclin B/CDC2 in vitro.	bind
81484	2	3767	11	NULL	NULL	0	NULL	CP110	GeneOrProtein		binds to 					 cyclin A/CDK2	GeneOrProtein				NULL	in vitro	0	NULL	NULL	NULL	gw60_devcell_3_3_339_s_69	12361598	(B) CP110 binds to cyclin E/CDK2, cyclin A/CDK2, and cyclin B/CDC2 in vitro.	bind
81485	3	3767	11	NULL	NULL	0	NULL	CP110	GeneOrProtein		binds to 					 cyclin B/CDC2	GeneOrProtein				NULL	in vitro	0	NULL	NULL	NULL	gw60_devcell_3_3_339_s_69	12361598	(B) CP110 binds to cyclin E/CDK2, cyclin A/CDK2, and cyclin B/CDC2 in vitro.	bind
8697	1	3768	5	11	NULL	NULL	NULL	CR	GP		bind					TRAF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_5_409_s_73	11882293	(B) CR binds TRAF2 through the N-terminal non-death domain region.	bind
8698	2	3768	5	11	NULL	NULL	NULL	statement 1	Process		occurs through								N-terminal non-death domain region		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_5_409_s_73	11882293	(B) CR binds TRAF2 through the N-terminal non-death domain region.	bind
9062	1	3768	6	11	NULL	NULL	NULL	CR	GP		bind			N-terminal non-death domain region		TRAF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_5_409_s_73	11882293	(B) CR binds TRAF2 through the N-terminal non-death domain region.	bind
81486	1	3768	11	NULL	NULL	0	NULL	crinkled	GeneOrProtein		binds to 			N-terminal non-death domain		TRAF2	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_currbiol_12_5_409_s_73	11882293	(B) CR binds TRAF2 through the N-terminal non-death domain region.	bind
8699	1	3769	5	11	NULL	NULL	NULL	CREB1a 	GP		forms					homo-dimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_211_s_98	9790528	(B) CREB1a and CREB1b bind CRE as homo- and heterodimers.	bind
8700	2	3769	5	11	NULL	NULL	NULL	CREB1b	GP		forms					homo-dimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_211_s_98	9790528	(B) CREB1a and CREB1b bind CRE as homo- and heterodimers.	bind
8701	3	3769	5	11	NULL	NULL	NULL	CREB1a	GP		forms					heterodimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_211_s_98	9790528	(B) CREB1a and CREB1b bind CRE as homo- and heterodimers.	bind
8702	5	3769	5	11	NULL	NULL	NULL	statement 1	GP		bind									CRE	NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_211_s_98	9790528	(B) CREB1a and CREB1b bind CRE as homo- and heterodimers.	bind
11088	4	3769	5	11	NULL	NULL	NULL	CREB1b	GP		forms					heterodimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_211_s_98	9790528	(B) CREB1a and CREB1b bind CRE as homo- and heterodimers.	bind
53479	6	3769	5	11	NULL	NULL	NULL	statement 2	GP		bind									CRE	NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_211_s_98	9790528	(B) CREB1a and CREB1b bind CRE as homo- and heterodimers.	bind
53480	7	3769	5	11	NULL	NULL	NULL	statement 3	GP		bind									CRE	NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_211_s_98	9790528	(B) CREB1a and CREB1b bind CRE as homo- and heterodimers.	bind
53481	8	3769	5	11	NULL	NULL	NULL	statement 4	GP		bind									CRE	NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_211_s_98	9790528	(B) CREB1a and CREB1b bind CRE as homo- and heterodimers.	bind
9063	1	3769	6	11	NULL	NULL	NULL	CREB1a	GP		form					homodimers	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_211_s_98	9790528	(B) CREB1a and CREB1b bind CRE as homo- and heterodimers.	bind
9064	2	3769	6	11	NULL	NULL	NULL	statement 1	GP		bind									CRE	NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_211_s_98	9790528	(B) CREB1a and CREB1b bind CRE as homo- and heterodimers.	bind
9358	3	3769	6	11	NULL	NULL	NULL	CREB1b	GP		form					homodimers	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_211_s_98	9790528	(B) CREB1a and CREB1b bind CRE as homo- and heterodimers.	bind
9359	5	3769	6	11	NULL	NULL	NULL	CREB1a	GP		forms					heterodimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_211_s_98	9790528	(B) CREB1a and CREB1b bind CRE as homo- and heterodimers.	bind
9360	6	3769	6	11	NULL	NULL	NULL	CREB1b	GP		forms					heterodimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_211_s_98	9790528	(B) CREB1a and CREB1b bind CRE as homo- and heterodimers.	bind
9362	4	3769	6	11	NULL	NULL	NULL	statement 3	GP		bind									CRE	NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_211_s_98	9790528	(B) CREB1a and CREB1b bind CRE as homo- and heterodimers.	bind
9363	7	3769	6	11	NULL	NULL	NULL	statement 5	GP		bind									CRE	NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_211_s_98	9790528	(B) CREB1a and CREB1b bind CRE as homo- and heterodimers.	bind
53482	8	3769	6	11	NULL	NULL	NULL	statement 6	GP		bind									CRE	NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_211_s_98	9790528	(B) CREB1a and CREB1b bind CRE as homo- and heterodimers.	bind
81487	1	3769	11	NULL	NULL	0	NULL	CREB1a	GeneOrProtein		binds to 					CRE	Gene				NULL		0	NULL	NULL	NULL	gw60_cell_95_2_211_s_98	9790528	(B) CREB1a and CREB1b bind CRE as homo- and heterodimers.	bind
81488	2	3769	11	NULL	NULL	0	NULL	CREB1b	GeneOrProtein		binds to 					CRE	Gene				NULL		0	NULL	NULL	NULL	gw60_cell_95_2_211_s_98	9790528	(B) CREB1a and CREB1b bind CRE as homo- and heterodimers.	bind
8872	1	3770	5	11	NULL	NULL	NULL	DBP	GP	purified;;serum	bind					cell surface	OrganismPart				NULL	wild-type kidneys	NULL	NULL	NULL	NULL	gw60_cell_96_4_507_s_91	10052453	(B) Cryosections  through wild-type and megalin-/- kidneys were incubated with purified serum DBP, and cell  surface binding of DBP was detected using rabbit anti-DBP antiserum and peroxidase-conjugated  anti-rabbit IgG.	bind
53634	2	3770	5	11	NULL	NULL	NULL	DBP	GP	purified;;serum	bind					cell surface	OrganismPart				NULL	megalin-/- kidneys	NULL	NULL	NULL	NULL	gw60_cell_96_4_507_s_91	10052453	(B) Cryosections  through wild-type and megalin-/- kidneys were incubated with purified serum DBP, and cell  surface binding of DBP was detected using rabbit anti-DBP antiserum and peroxidase-conjugated  anti-rabbit IgG.	bind
9065	1	3770	6	11	NULL	NULL	NULL	DBP	GP	purified;;serum	bind					cell surface	OrganismPart				NULL	wild type kidneys	NULL	NULL	NULL	NULL	gw60_cell_96_4_507_s_91	10052453	(B) Cryosections  through wild-type and megalin-/- kidneys were incubated with purified serum DBP, and cell  surface binding of DBP was detected using rabbit anti-DBP antiserum and peroxidase-conjugated  anti-rabbit IgG.	bind
9066	2	3770	6	11	NULL	NULL	NULL	DBP	GP	purified;;serum	bind					cell surface	OrganismPart				NULL	megalin-/- kidneys	NULL	NULL	NULL	NULL	gw60_cell_96_4_507_s_91	10052453	(B) Cryosections  through wild-type and megalin-/- kidneys were incubated with purified serum DBP, and cell  surface binding of DBP was detected using rabbit anti-DBP antiserum and peroxidase-conjugated  anti-rabbit IgG.	bind
81489	1	3770	11	NULL	NULL	0	NULL	DBP	Protein	serum 	binds to 					cell surface	CellComponent				NULL		0	NULL	NULL	NULL	gw60_cell_96_4_507_s_91	10052453	(B) Cryosections  through wild-type and megalin-/- kidneys were incubated with purified serum DBP, and cell  surface binding of DBP was detected using rabbit anti-DBP antiserum and peroxidase-conjugated  anti-rabbit IgG.	bind
8703	1	3771	5	11	NULL	NULL	NULL	CSC-1	GP		bind					BIR-1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_229_s_106	12707312	(B) CSC-1 binds to BIR-1 in vitro, and this interaction requires Zinc binding  by BIR-1.	bind
8704	2	3771	5	11	NULL	NULL	NULL	BIR-1	GP		bind					Zinc	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_229_s_106	12707312	(B) CSC-1 binds to BIR-1 in vitro, and this interaction requires Zinc binding  by BIR-1.	bind
8705	3	3771	5	11	NULL	NULL	NULL	statement 1	Process		require					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_229_s_106	12707312	(B) CSC-1 binds to BIR-1 in vitro, and this interaction requires Zinc binding  by BIR-1.	bind
9067	1	3771	6	11	NULL	NULL	NULL	Zinc	Chemical		bind					BIR-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_229_s_106	12707312	(B) CSC-1 binds to BIR-1 in vitro, and this interaction requires Zinc binding  by BIR-1.	bind
9068	2	3771	6	11	NULL	NULL	NULL	BIR-1	GP		bind					CSC-1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_229_s_106	12707312	(B) CSC-1 binds to BIR-1 in vitro, and this interaction requires Zinc binding  by BIR-1.	bind
9700	3	3771	6	11	NULL	NULL	NULL	statement 2	Process		require					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_229_s_106	12707312	(B) CSC-1 binds to BIR-1 in vitro, and this interaction requires Zinc binding  by BIR-1.	bind
81490	1	3771	11	NULL	NULL	0	NULL	CSC-1	GeneOrProtein		binds to 					BIR-1	GeneOrProtein				NULL	in vitro	0	NULL	NULL	NULL	gw70_cellbiol_161_2_229_s_106	12707312	(B) CSC-1 binds to BIR-1 in vitro, and this interaction requires Zinc binding  by BIR-1.	bind
81491	2	3771	11	NULL	NULL	0	NULL	Zinc	NonProteinOrNucleicAcidChemical		binds to 					BIR-1	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw70_cellbiol_161_2_229_s_106	12707312	(B) CSC-1 binds to BIR-1 in vitro, and this interaction requires Zinc binding  by BIR-1.	bind
81492	3	3771	11	NULL	NULL	0	NULL	statement 2	Process		requires					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_cellbiol_161_2_229_s_106	12707312	(B) CSC-1 binds to BIR-1 in vitro, and this interaction requires Zinc binding  by BIR-1.	bind
8706	1	3773	5	11	NULL	NULL	NULL	CtBP2	GP		bind					Znf219	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_15_5296_s_284	12101226	(B) CtBP2 binds Znf219 in vitro.	bind
9069	1	3773	6	11	NULL	NULL	NULL	CtBP2	GP		bind					Znf219	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_15_5296_s_284	12101226	(B) CtBP2 binds Znf219 in vitro.	bind
81493	1	3773	11	NULL	NULL	0	NULL	CtBP2	GeneOrProtein		binds to 					Znf219	GeneOrProtein				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_22_15_5296_s_284	12101226	(B) CtBP2 binds Znf219 in vitro.	bind
8712	1	3774	5	11	NULL	NULL	NULL	CUG-BP	GP		bind									U/G motifs in 3 splice site of intron 2	NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_1_45_s_148	12150906	(B) CUG-BP binds U/G motifs in the 3  splice site of intron 2.	bind
9070	1	3774	6	11	NULL	NULL	NULL	CUG-BP	GP		bind									U/G motifs in 3 splice site of intron 2	NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_1_45_s_148	12150906	(B) CUG-BP binds U/G motifs in the 3  splice site of intron 2.	bind
81494	1	3774	11	NULL	NULL	0	NULL	CUG-BP	GeneOrProtein		binds to 					intron 2	NucleicAcidSubstance			U/G motifs	NULL		0	NULL	NULL	NULL	gw60_molcell_10_1_45_s_148	12150906	(B) CUG-BP binds U/G motifs in the 3  splice site of intron 2.	bind
8713	1	3775	5	11	NULL	NULL	NULL	BCE	GP		bind					Hb	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2528_s_169	12670977	(b) Curve for the binding of BCE surface  proteins to Hb after neutralization of Hb binding.	bind
53635	2	3775	5	11	NULL	NULL	NULL	BCE	GP		is a type of					surface protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2528_s_169	12670977	(b) Curve for the binding of BCE surface  proteins to Hb after neutralization of Hb binding.	bind
9071	1	3775	6	11	NULL	NULL	NULL	BCE 	GP		bind					Hb	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2528_s_169	12670977	(b) Curve for the binding of BCE surface  proteins to Hb after neutralization of Hb binding.	bind
41005	2	3775	6	11	NULL	NULL	NULL	BCE	GP		is a type of					surface protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2528_s_169	12670977	(b) Curve for the binding of BCE surface  proteins to Hb after neutralization of Hb binding.	bind
81495	1	3775	11	NULL	NULL	0	NULL	BCE surface protein	Protein		binds to 					Hb	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_8_2528_s_169	12670977	(b) Curve for the binding of BCE surface  proteins to Hb after neutralization of Hb binding.	bind
8714	1	3776	5	11	NULL	NULL	NULL	AgrA	GP		bind							isolated		P2 repeats	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_22_7549_s_157	15516566	(B) Curves showing binding  of AgrA to isolated P2 and P3 repeats and to a P2 mutant fragment.	bind
8715	2	3776	5	11	NULL	NULL	NULL	AgrA	GP		bind							isolated		P3 repeats	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_22_7549_s_157	15516566	(B) Curves showing binding  of AgrA to isolated P2 and P3 repeats and to a P2 mutant fragment.	bind
8716	3	3776	5	11	NULL	NULL	NULL	AgrA	GP		bind							mutant		P2 fragment	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_22_7549_s_157	15516566	(B) Curves showing binding  of AgrA to isolated P2 and P3 repeats and to a P2 mutant fragment.	bind
9072	1	3776	6	11	NULL	NULL	NULL	AgrA	GP		bind							isolated		P2 repeats	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_22_7549_s_157	15516566	(B) Curves showing binding  of AgrA to isolated P2 and P3 repeats and to a P2 mutant fragment.	bind
9073	2	3776	6	11	NULL	NULL	NULL	AgrA	GP		bind							isolated		P3 repeats	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_22_7549_s_157	15516566	(B) Curves showing binding  of AgrA to isolated P2 and P3 repeats and to a P2 mutant fragment.	bind
9074	3	3776	6	11	NULL	NULL	NULL	AgrA	GP		bind							mutant		P2 fragment	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_22_7549_s_157	15516566	(B) Curves showing binding  of AgrA to isolated P2 and P3 repeats and to a P2 mutant fragment.	bind
81503	1	3776	11	NULL	NULL	0	NULL	AgrA	GeneOrProtein		binds to 					P2 repeat	Gene				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_22_7549_s_157	15516566	(B) Curves showing binding  of AgrA to isolated P2 and P3 repeats and to a P2 mutant fragment.	bind
81504	2	3776	11	NULL	NULL	0	NULL	AgrA	GeneOrProtein		binds to 					P3 repeat	Gene				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_22_7549_s_157	15516566	(B) Curves showing binding  of AgrA to isolated P2 and P3 repeats and to a P2 mutant fragment.	bind
81506	3	3776	11	NULL	NULL	0	NULL	AgrA	GeneOrProtein		binds to 					P2 fragment	Gene	mutant			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_22_7549_s_157	15516566	(B) Curves showing binding  of AgrA to isolated P2 and P3 repeats and to a P2 mutant fragment.	bind
8717	1	3777	5	11	NULL	NULL	NULL	p130 constructs	GP	transfected	bind					Cyclin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_269	9710622	(B) Cyclin-binding activity of transfected p130 constructs.	bind
9075	1	3777	6	11	NULL	NULL	NULL	p130 constructs	GP	transfected	bind					Cyclin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_269	9710622	(B) Cyclin-binding activity of transfected p130 constructs.	bind
81507	1	3777	11	NULL	NULL	0	NULL	Cyclin	GeneOrProtein		binds to 					p130	GeneOrProtein	transfected			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_269	9710622	(B) Cyclin-binding activity of transfected p130 constructs.	bind
8718	1	3778	5	11	NULL	NULL	NULL	Cyp-40	GP		bind					c-Myb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_203_s_102	9659917	(B) Cyclosporin-A does not affect Cyp-40 binding to c-Myb.	bind
8719	2	3778	5	11	NULL	NULL	NULL	Cyclosporin-A	Chemical		does not affect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_203_s_102	9659917	(B) Cyclosporin-A does not affect Cyp-40 binding to c-Myb.	bind
9076	1	3778	6	11	NULL	NULL	NULL	Cyp-40	GP		bind					c-Myb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_203_s_102	9659917	(B) Cyclosporin-A does not affect Cyp-40 binding to c-Myb.	bind
9077	2	3778	6	11	NULL	NULL	NULL	Cyclosporin-A	Chemical		does not affect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_2_203_s_102	9659917	(B) Cyclosporin-A does not affect Cyp-40 binding to c-Myb.	bind
81508	1	3778	11	NULL	NULL	0	NULL	Cyp-40	GeneOrProtein		binds to 					c-Myb	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_molcell_1_2_203_s_102	9659917	(B) Cyclosporin-A does not affect Cyp-40 binding to c-Myb.	bind
81509	2	3778	11	NULL	NULL	0	NULL	Cyclosporin-A	Chemical		does not affect					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_1_2_203_s_102	9659917	(B) Cyclosporin-A does not affect Cyp-40 binding to c-Myb.	bind
8720	1	3779	5	11	NULL	NULL	NULL	Dap1p	GP		bind					heme	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1669_s_139	15713626	(B) Dap1p bound to heme (left bar), while the Dap1pD91G lost heme-binding activity (right bar).	bind
8721	2	3779	5	11	NULL	NULL	NULL	Dap1p	GP		does not bind			D91G		heme	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1669_s_139	15713626	(B) Dap1p bound to heme (left bar), while the Dap1pD91G lost heme-binding activity (right bar).	bind
9078	1	3779	6	11	NULL	NULL	NULL	Dap1p	GP		bind					heme	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1669_s_139	15713626	(B) Dap1p bound to heme (left bar), while the Dap1pD91G lost heme-binding activity (right bar).	bind
9079	2	3779	6	11	NULL	NULL	NULL	Dap1p	GP		does not bind			D91G		heme	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1669_s_139	15713626	(B) Dap1p bound to heme (left bar), while the Dap1pD91G lost heme-binding activity (right bar).	bind
81510	1	3779	11	NULL	NULL	0	NULL	Dap1p	Protein		binds to 					heme	Protein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_5_1669_s_139	15713626	(B) Dap1p bound to heme (left bar), while the Dap1pD91G lost heme-binding activity (right bar).	bind
8722	1	3780	5	11	NULL	NULL	NULL	DAPA	Chemical		bind					DTBS	GP				NULL		NULL	NULL	NULL	NULL	gw60_structure_3_11_1207_s_85	8591031	(b) DAPA bound to DTBS, in 20 mM MgSO4 and in a CO2-free nitrogen atmosphere.	bind
8723	2	3780	5	11	NULL	NULL	NULL	statement 1	Process		occurs in					MgSO4	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_structure_3_11_1207_s_85	8591031	(b) DAPA bound to DTBS, in 20 mM MgSO4 and in a CO2-free nitrogen atmosphere.	bind
8724	3	3780	5	11	NULL	NULL	NULL	statement 1	Process		occurs in					CO2-free nitrogen atmosphere	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_structure_3_11_1207_s_85	8591031	(b) DAPA bound to DTBS, in 20 mM MgSO4 and in a CO2-free nitrogen atmosphere.	bind
9080	1	3780	6	11	NULL	NULL	NULL	DAPA	Chemical		bind					DTBS	GP				NULL		NULL	NULL	NULL	NULL	gw60_structure_3_11_1207_s_85	8591031	(b) DAPA bound to DTBS, in 20 mM MgSO4 and in a CO2-free nitrogen atmosphere.	bind
9081	2	3780	6	11	NULL	NULL	NULL	statement 1	Process		occurs in					CO2-free nitrogen atmosphere	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_structure_3_11_1207_s_85	8591031	(b) DAPA bound to DTBS, in 20 mM MgSO4 and in a CO2-free nitrogen atmosphere.	bind
9082	3	3780	6	11	NULL	NULL	NULL	statement 1	Process		occurs in					MgSO4	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_structure_3_11_1207_s_85	8591031	(b) DAPA bound to DTBS, in 20 mM MgSO4 and in a CO2-free nitrogen atmosphere.	bind
81512	1	3780	11	NULL	NULL	0	NULL	DAPA	NonProteinOrNucleicAcidChemical		binds to 					DTBS	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_structure_3_11_1207_s_85	8591031	(b) DAPA bound to DTBS, in 20 mM MgSO4 and in a CO2-free nitrogen atmosphere.	bind
81513	2	3780	11	NULL	NULL	0	NULL	statement 1	Process		occurs in the presence of					MgSO4	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	gw60_structure_3_11_1207_s_85	8591031	(b) DAPA bound to DTBS, in 20 mM MgSO4 and in a CO2-free nitrogen atmosphere.	bind
81514	3	3780	11	NULL	NULL	0	NULL	statement 1	Process		occurs in the presence of					CO2-free nitrogen	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	gw60_structure_3_11_1207_s_85	8591031	(b) DAPA bound to DTBS, in 20 mM MgSO4 and in a CO2-free nitrogen atmosphere.	bind
8725	1	3782	5	11	NULL	NULL	NULL	Daxx	GP		bind					p53	GP		COOH terminus		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_1_322_s_120	12482984	(B) Daxx binds to the COOH terminus of p53.	bind
9083	1	3782	6	11	NULL	NULL	NULL	Daxx	GP		bind					p53	GP		COOH terminus		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_1_322_s_120	12482984	(B) Daxx binds to the COOH terminus of p53.	bind
81515	1	3782	11	NULL	NULL	0	NULL	Daxx	GeneOrProtein		binds to 					p53	Protein		COOH terminus		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_1_322_s_120	12482984	(B) Daxx binds to the COOH terminus of p53.	bind
8726	1	3783	5	NULL	NULL	0	NULL	Daxx	NULL		bind	NULL				p53	NULL	mutants			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_1_322_s_166	12482984	(B) Daxx binds to various p53 mutants.	bind
9084	1	3783	6	NULL	NULL	0	NULL	Daxx	NULL		bind	NULL				p53	NULL	mutant			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_1_322_s_166	12482984	(B) Daxx binds to various p53 mutants.	bind
81516	1	3783	11	NULL	NULL	0	NULL	Daxx	GeneOrProtein		binds to 					p53	Gene	mutant			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_1_322_s_166	12482984	(B) Daxx binds to various p53 mutants.	bind
8727	1	3784	5	11	NULL	NULL	NULL	Ddi1	GP		bind			UBL domain		19S RP	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5355_s_131	15964793	(B) Ddi1 binds the 19S RP via its UBL domain.	bind
9085	1	3784	6	11	NULL	NULL	NULL	Ddi1	GP		bind			UBL domain		19S RP	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5355_s_131	15964793	(B) Ddi1 binds the 19S RP via its UBL domain.	bind
81517	1	3784	11	NULL	NULL	0	NULL	Ddi1	PartOfProtein		binds to 					19S RP	Protein		UBL domain		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_13_5355_s_131	15964793	(B) Ddi1 binds the 19S RP via its UBL domain.	bind
8728	1	3785	5	11	NULL	NULL	NULL	ZO-1	GP		bind					GST-C-Occludin(NP)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
8729	2	3785	5	11	NULL	NULL	NULL	ZO-2	GP		bind					GST-C-Occludin(NP)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
8730	3	3785	5	11	NULL	NULL	NULL	ZO-3	GP		bind					GST-C-Occludin(NP)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
8731	4	3785	5	11	NULL	NULL	NULL	ZO-1	GP		bind					GST-C-Occludin(PY)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
8732	5	3785	5	11	NULL	NULL	NULL	ZO-2	GP		bind					GST-C-Occludin(PY)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
8733	6	3785	5	11	NULL	NULL	NULL	ZO-3	GP		bind					GST-C-Occludin(PY)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
9086	1	3785	6	11	NULL	NULL	NULL	ZO-1	GP		bind					GST-C-Occludin(NP)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
9087	2	3785	6	11	NULL	NULL	NULL	ZO-1	GP		bind					GST-C-Occludin(PY)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
9088	3	3785	6	11	NULL	NULL	NULL	ZO-2	GP		bind					GST-C-Occludin(NP)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
9089	4	3785	6	11	NULL	NULL	NULL	ZO-2	GP		bind					GST-C-Occludin(PY)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
9090	5	3785	6	11	NULL	NULL	NULL	ZO-3	GP		bind					GST-C-Occludin(NP)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
9091	6	3785	6	11	NULL	NULL	NULL	ZO-3	GP		bind					GST-C-Occludin(PY)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
81518	1	3785	11	NULL	NULL	0	NULL	GST-C-Occludin	Protein		is					NP	Protein				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
81519	2	3785	11	NULL	NULL	0	NULL	GST-C-Occludin	Protein		binds to 					PY	Protein				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
81521	3	3785	11	NULL	NULL	NULL	NULL	ZO-1	Protein		binds to 					GST-C-Occludin	Protein				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
81522	4	3785	11	NULL	NULL	0	NULL	ZO-1	Protein		binds to 					GST-C-Occludin	Protein				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
81523	5	3785	11	NULL	NULL	0	NULL	ZO-2	Protein		binds to 					GST-C-Occludin	Protein				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
81524	6	3785	11	NULL	NULL	0	NULL	ZO-2	Protein		binds to 					GST-C-Occludin	Protein				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
81525	7	3785	11	NULL	NULL	0	NULL	ZO-3	Protein		binds to 					GST-C-Occludin	Protein				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
81526	8	3785	11	NULL	NULL	0	NULL	ZO-3	Protein		binds to 					GST-C-Occludin	Protein				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric  analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY)  in A. Values (arbitrary density units) are average of three independent experiments.	bind
8734	1	3787	5	11	NULL	NULL	NULL	ZO-1	GP		bind					GST-C-Occludin(NP)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_79	12604349	(B) Densitometric analysis of ZO-1, ZO-2, and ZO-3  bound to GST-C-Occludin(NP) and GST-C-Occludin(PY) in A. Values (arbitrary density  units) are average of values from two independent experiments.	bind
8735	2	3787	5	11	NULL	NULL	NULL	ZO-2	GP		bind					GST-C-Occludin(NP)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_79	12604349	(B) Densitometric analysis of ZO-1, ZO-2, and ZO-3  bound to GST-C-Occludin(NP) and GST-C-Occludin(PY) in A. Values (arbitrary density  units) are average of values from two independent experiments.	bind
8736	3	3787	5	11	NULL	NULL	NULL	ZO-3	GP		bind					GST-C-Occludin(NP)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_79	12604349	(B) Densitometric analysis of ZO-1, ZO-2, and ZO-3  bound to GST-C-Occludin(NP) and GST-C-Occludin(PY) in A. Values (arbitrary density  units) are average of values from two independent experiments.	bind
8737	4	3787	5	11	NULL	NULL	NULL	ZO-1	GP		bind					GST-C-Occludin(PY)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_79	12604349	(B) Densitometric analysis of ZO-1, ZO-2, and ZO-3  bound to GST-C-Occludin(NP) and GST-C-Occludin(PY) in A. Values (arbitrary density  units) are average of values from two independent experiments.	bind
8738	5	3787	5	11	NULL	NULL	NULL	ZO-2	GP		bind					GST-C-Occludin(PY)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_79	12604349	(B) Densitometric analysis of ZO-1, ZO-2, and ZO-3  bound to GST-C-Occludin(NP) and GST-C-Occludin(PY) in A. Values (arbitrary density  units) are average of values from two independent experiments.	bind
8739	6	3787	5	11	NULL	NULL	NULL	ZO-3	GP		bind					GST-C-Occludin(PY)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_79	12604349	(B) Densitometric analysis of ZO-1, ZO-2, and ZO-3  bound to GST-C-Occludin(NP) and GST-C-Occludin(PY) in A. Values (arbitrary density  units) are average of values from two independent experiments.	bind
9092	1	3787	6	11	NULL	NULL	NULL	ZO-1	GP		bind					GST-C-Occludin(NP)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_79	12604349	(B) Densitometric analysis of ZO-1, ZO-2, and ZO-3  bound to GST-C-Occludin(NP) and GST-C-Occludin(PY) in A. Values (arbitrary density  units) are average of values from two independent experiments.	bind
9093	2	3787	6	11	NULL	NULL	NULL	ZO-1	GP		bind					GST-C-Occludin(PY)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_79	12604349	(B) Densitometric analysis of ZO-1, ZO-2, and ZO-3  bound to GST-C-Occludin(NP) and GST-C-Occludin(PY) in A. Values (arbitrary density  units) are average of values from two independent experiments.	bind
9094	3	3787	6	11	NULL	NULL	NULL	ZO-2	GP		bind					GST-C-Occludin(NP)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_79	12604349	(B) Densitometric analysis of ZO-1, ZO-2, and ZO-3  bound to GST-C-Occludin(NP) and GST-C-Occludin(PY) in A. Values (arbitrary density  units) are average of values from two independent experiments.	bind
9095	4	3787	6	11	NULL	NULL	NULL	ZO-2	GP		bind					GST-C-Occludin(PY)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_79	12604349	(B) Densitometric analysis of ZO-1, ZO-2, and ZO-3  bound to GST-C-Occludin(NP) and GST-C-Occludin(PY) in A. Values (arbitrary density  units) are average of values from two independent experiments.	bind
9096	5	3787	6	11	NULL	NULL	NULL	ZO-3	GP		bind					GST-C-Occludin(NP)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_79	12604349	(B) Densitometric analysis of ZO-1, ZO-2, and ZO-3  bound to GST-C-Occludin(NP) and GST-C-Occludin(PY) in A. Values (arbitrary density  units) are average of values from two independent experiments.	bind
9097	6	3787	6	11	NULL	NULL	NULL	ZO-3	GP		bind					GST-C-Occludin(PY)	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_2_324_s_79	12604349	(B) Densitometric analysis of ZO-1, ZO-2, and ZO-3  bound to GST-C-Occludin(NP) and GST-C-Occludin(PY) in A. Values (arbitrary density  units) are average of values from two independent experiments.	bind
9098	1	3788	6	11	NULL	NULL	NULL	ZO-1	GP		bind					GST-C-Occludin(NP)	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY) in A. Values (arbitrary density units) are average of three independent experiments.	bind
9099	2	3788	6	11	NULL	NULL	NULL	ZO-1	GP		bind					GST-C-Occludin(PY)	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY) in A. Values (arbitrary density units) are average of three independent experiments.	bind
9100	3	3788	6	11	NULL	NULL	NULL	ZO-2	GP		bind					GST-C-Occludin(NP)	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY) in A. Values (arbitrary density units) are average of three independent experiments.	bind
9101	4	3788	6	11	NULL	NULL	NULL	ZO-2	GP		bind					GST-C-Occludin(PY)	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY) in A. Values (arbitrary density units) are average of three independent experiments.	bind
9102	5	3788	6	11	NULL	NULL	NULL	ZO-3	GP		bind					GST-C-Occludin(NP)	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY) in A. Values (arbitrary density units) are average of three independent experiments.	bind
9103	6	3788	6	11	NULL	NULL	NULL	ZO-3	GP		bind					GST-C-Occludin(PY)	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_302_2_324_s_67	12604349	(B) Densitometric analysis of ZO-1, ZO-2, and ZO-3 bound to GST-C-Occludin(NP) and GST-C-Occludin(PY) in A. Values (arbitrary density units) are average of three independent experiments.	bind
8746	1	3790	5	11	NULL	NULL	NULL	TcTS	GP		interact with					lactose	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_4_757_s_147	12419220	(b) Detailed view of the interaction between TcTS and lactose, demonstrating that the acceptor substrate only binds to TcTS when sialic acid is present.	bind
8747	2	3790	5	11	NULL	NULL	NULL	acceptor substrate	Chemical		bind					TcTS	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_4_757_s_147	12419220	(b) Detailed view of the interaction between TcTS and lactose, demonstrating that the acceptor substrate only binds to TcTS when sialic acid is present.	bind
8748	3	3790	5	11	NULL	NULL	NULL	statement 2	Process		in the presence of		only			sialic acid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_4_757_s_147	12419220	(b) Detailed view of the interaction between TcTS and lactose, demonstrating that the acceptor substrate only binds to TcTS when sialic acid is present.	bind
9104	1	3790	6	11	NULL	NULL	NULL	TcTS	GP		interacts with					lactose	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_4_757_s_147	12419220	(b) Detailed view of the interaction between TcTS and lactose, demonstrating that the acceptor substrate only binds to TcTS when sialic acid is present.	bind
9105	2	3790	6	11	NULL	NULL	NULL	acceptor substrate	Chemical		bind					TcTS	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_4_757_s_147	12419220	(b) Detailed view of the interaction between TcTS and lactose, demonstrating that the acceptor substrate only binds to TcTS when sialic acid is present.	bind
9106	3	3790	6	11	NULL	NULL	NULL	statement 2	Process		occurs in presence of		only			sialic acid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_4_757_s_147	12419220	(b) Detailed view of the interaction between TcTS and lactose, demonstrating that the acceptor substrate only binds to TcTS when sialic acid is present.	bind
81529	1	3790	11	NULL	NULL	0	NULL	TcTS	GeneOrProtein		interacts with					lactose	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	gw60_molcell_10_4_757_s_147	12419220	(b) Detailed view of the interaction between TcTS and lactose, demonstrating that the acceptor substrate only binds to TcTS when sialic acid is present.	bind
81530	2	3790	11	NULL	NULL	0	NULL	acceptor substrate	Thing		binds to 					TcTS	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_molcell_10_4_757_s_147	12419220	(b) Detailed view of the interaction between TcTS and lactose, demonstrating that the acceptor substrate only binds to TcTS when sialic acid is present.	bind
81531	3	3790	11	NULL	NULL	0	NULL	statement 2	Process		occurs in the presence of					sialic acid	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	gw60_molcell_10_4_757_s_147	12419220	(b) Detailed view of the interaction between TcTS and lactose, demonstrating that the acceptor substrate only binds to TcTS when sialic acid is present.	bind
8749	1	3791	5	11	NULL	NULL	NULL	ras	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4282_s_212	9632812	(B) Detection of an active, GTP-bound form of ras during treatment with rhTPO or rhIL-3.	bind
9174	1	3791	6	11	NULL	NULL	NULL	GTP	Chemical		bind					ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4282_s_212	9632812	(B) Detection of an active, GTP-bound form of ras during treatment with rhTPO or rhIL-3.	bind
81532	1	3791	11	NULL	NULL	0	NULL	GTP	NonProteinOrNucleicAcidChemical		binds to 					ras	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_4282_s_212	9632812	(B) Detection of an active, GTP-bound form of ras during treatment with rhTPO or rhIL-3.	bind
8750	1	3794	5	11	NULL	NULL	NULL	RCH1	GP		bind					CAS	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7782_s_161	10523667	(B) Determination of the binding affinities of importin alpha1/Rch1 (RCH1), importin alpha5/hSRP1 (hSRP1), and importin alpha3 to CAS.	bind
8751	2	3794	5	11	NULL	NULL	NULL	RCH1	GP		is					importin alpha1/Rch1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7782_s_161	10523667	(B) Determination of the binding affinities of importin alpha1/Rch1 (RCH1), importin alpha5/hSRP1 (hSRP1), and importin alpha3 to CAS.	bind
8752	3	3794	5	11	NULL	NULL	NULL	hSRP1	GP		bind					CAS	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7782_s_161	10523667	(B) Determination of the binding affinities of importin alpha1/Rch1 (RCH1), importin alpha5/hSRP1 (hSRP1), and importin alpha3 to CAS.	bind
8753	4	3794	5	11	NULL	NULL	NULL	hSRP1	GP		is					importin alpha5/hSRP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7782_s_161	10523667	(B) Determination of the binding affinities of importin alpha1/Rch1 (RCH1), importin alpha5/hSRP1 (hSRP1), and importin alpha3 to CAS.	bind
8754	5	3794	5	11	NULL	NULL	NULL	importin alpha3	GP		bind					CAS	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7782_s_161	10523667	(B) Determination of the binding affinities of importin alpha1/Rch1 (RCH1), importin alpha5/hSRP1 (hSRP1), and importin alpha3 to CAS.	bind
9175	1	3794	6	11	NULL	NULL	NULL	importin alpha1/Rch1	GP		bind					CAS	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7782_s_161	10523667	(B) Determination of the binding affinities of importin alpha1/Rch1 (RCH1), importin alpha5/hSRP1 (hSRP1), and importin alpha3 to CAS.	bind
9176	2	3794	6	11	NULL	NULL	NULL	importin alpha5/hSRP1	GP		bind					CAS	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7782_s_161	10523667	(B) Determination of the binding affinities of importin alpha1/Rch1 (RCH1), importin alpha5/hSRP1 (hSRP1), and importin alpha3 to CAS.	bind
9177	3	3794	6	11	NULL	NULL	NULL	importin alpha3	GP		bind					CAS	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7782_s_161	10523667	(B) Determination of the binding affinities of importin alpha1/Rch1 (RCH1), importin alpha5/hSRP1 (hSRP1), and importin alpha3 to CAS.	bind
11649	4	3794	6	11	NULL	NULL	NULL	RCH1	GP		is					importin alpha1/Rch1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7782_s_161	10523667	(B) Determination of the binding affinities of importin alpha1/Rch1 (RCH1), importin alpha5/hSRP1 (hSRP1), and importin alpha3 to CAS.	bind
11650	5	3794	6	11	NULL	NULL	NULL	hSRP1	GP		is					importin alpha5/hSRP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7782_s_161	10523667	(B) Determination of the binding affinities of importin alpha1/Rch1 (RCH1), importin alpha5/hSRP1 (hSRP1), and importin alpha3 to CAS.	bind
81533	1	3794	11	NULL	NULL	0	NULL	importin alpha1/Rch1	Protein		is					RCH1	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_11_7782_s_161	10523667	(B) Determination of the binding affinities of importin alpha1/Rch1 (RCH1), importin alpha5/hSRP1 (hSRP1), and importin alpha3 to CAS.	bind
81534	2	3794	11	NULL	NULL	0	NULL	importin alpha5/hSRP1	Protein		binds to 					hSRP1	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_11_7782_s_161	10523667	(B) Determination of the binding affinities of importin alpha1/Rch1 (RCH1), importin alpha5/hSRP1 (hSRP1), and importin alpha3 to CAS.	bind
81535	3	3794	11	NULL	NULL	0	NULL	importin alpha1/Rch1	GeneOrProtein		binds to 					CAS	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_11_7782_s_161	10523667	(B) Determination of the binding affinities of importin alpha1/Rch1 (RCH1), importin alpha5/hSRP1 (hSRP1), and importin alpha3 to CAS.	bind
81536	4	3794	11	NULL	NULL	0	NULL	importin alpha5/hSRP1	GeneOrProtein		binds to 					CAS	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_11_7782_s_161	10523667	(B) Determination of the binding affinities of importin alpha1/Rch1 (RCH1), importin alpha5/hSRP1 (hSRP1), and importin alpha3 to CAS.	bind
81537	5	3794	11	NULL	NULL	0	NULL	importin alpha3	GeneOrProtein		binds to 					CAS	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_11_7782_s_161	10523667	(B) Determination of the binding affinities of importin alpha1/Rch1 (RCH1), importin alpha5/hSRP1 (hSRP1), and importin alpha3 to CAS.	bind
8755	1	3795	5	11	NULL	NULL	NULL	dHK protein	GP		bind					microtubules	CellComponent	endogenous;; Drosophila			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_923_s_240	11238449	(B) dHK protein also bound to endogenous  Drosophila microtubules when they were stabilized by the addition of GTP - taxol.	bind
8756	2	3795	5	11	NULL	NULL	NULL	GTP - taxol	Chemical	addition of	stabilize					microtubules	CellComponent	endogenous;;Drosophila			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_923_s_240	11238449	(B) dHK protein also bound to endogenous  Drosophila microtubules when they were stabilized by the addition of GTP - taxol.	bind
8757	3	3795	5	11	NULL	NULL	NULL	statement 1	Process		occurs after					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_923_s_240	11238449	(B) dHK protein also bound to endogenous  Drosophila microtubules when they were stabilized by the addition of GTP - taxol.	bind
9178	1	3795	6	11	NULL	NULL	NULL	dHK protein	GP		bind					microtubules	CellComponent	endogenous;; Drosophila			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_923_s_240	11238449	(B) dHK protein also bound to endogenous  Drosophila microtubules when they were stabilized by the addition of GTP - taxol.	bind
9179	2	3795	6	11	NULL	NULL	NULL	GTP-taxol	Chemical		stabilizes					microtubules	CellComponent	endogenous;; drosophila			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_923_s_240	11238449	(B) dHK protein also bound to endogenous  Drosophila microtubules when they were stabilized by the addition of GTP - taxol.	bind
9180	3	3795	6	11	NULL	NULL	NULL	statement 2	Process		leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_923_s_240	11238449	(B) dHK protein also bound to endogenous  Drosophila microtubules when they were stabilized by the addition of GTP - taxol.	bind
81538	1	3795	11	NULL	NULL	NULL	NULL	GTP - taxol	NonProteinOrNucleicAcidChemical		stabilizes 					endogenous microtubules	CellComponent	Drosophila			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_923_s_240	11238449	(B) dHK protein also bound to endogenous  Drosophila microtubules when they were stabilized by the addition of GTP - taxol.	bind
81539	2	3795	11	NULL	NULL	0	NULL	dHK protein	Protein		binds to 					endogenous microtubules\t\t\t 	CellComponent	Drosophila			NULL		0	NULL	NULL	NULL	gw60_cellbiol_152_5_923_s_240	11238449	(B) dHK protein also bound to endogenous  Drosophila microtubules when they were stabilized by the addition of GTP - taxol.	bind
81540	3	3795	11	NULL	NULL	0	NULL	statement 2	Process		occurs after					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_152_5_923_s_240	11238449	(B) dHK protein also bound to endogenous  Drosophila microtubules when they were stabilized by the addition of GTP - taxol.	bind
8903	1	3796	5	11	NULL	NULL	NULL	preimmune serum	CellComponent	rabbit	bind					Dap.3	Cell				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_6_2769_s_108	10338479	(B) Dilution studies of antisera raised against CKDLL EQKRAAVDTYC, CLGSIS ESRRALQDSQR, and CKDIL EDERAAVDTYC peptides and pooled preimmune rabbit serum binding to mouse fibroblast transfected cell line Dap.3 expressing HLA-DRB1*0401 (DR4/Dw4).	bind
8904	2	3796	5	11	NULL	NULL	NULL	Dap.3	cell		is a type of					 fibroblast transfected cell line 	Cell	mouse			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_6_2769_s_108	10338479	(B) Dilution studies of antisera raised against CKDLL EQKRAAVDTYC, CLGSIS ESRRALQDSQR, and CKDIL EDERAAVDTYC peptides and pooled preimmune rabbit serum binding to mouse fibroblast transfected cell line Dap.3 expressing HLA-DRB1*0401 (DR4/Dw4).	bind
53641	3	3796	5	11	NULL	NULL	NULL	Dap.3	cell		express					HLA-DRB1*0401 (DR4/Dw4)	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_6_2769_s_108	10338479	(B) Dilution studies of antisera raised against CKDLL EQKRAAVDTYC, CLGSIS ESRRALQDSQR, and CKDIL EDERAAVDTYC peptides and pooled preimmune rabbit serum binding to mouse fibroblast transfected cell line Dap.3 expressing HLA-DRB1*0401 (DR4/Dw4).	bind
9181	1	3796	6	11	NULL	NULL	NULL	Dap.3	cell		expresses					HLA-DRB1*0401 (DR4/Dw4)	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_6_2769_s_108	10338479	(B) Dilution studies of antisera raised against CKDLL EQKRAAVDTYC, CLGSIS ESRRALQDSQR, and CKDIL EDERAAVDTYC peptides and pooled preimmune rabbit serum binding to mouse fibroblast transfected cell line Dap.3 expressing HLA-DRB1*0401 (DR4/Dw4).	bind
9182	2	3796	6	11	NULL	NULL	NULL	preimmune serum	CellComponent	 rabbit	bind					Dap.3	Cell				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_6_2769_s_108	10338479	(B) Dilution studies of antisera raised against CKDLL EQKRAAVDTYC, CLGSIS ESRRALQDSQR, and CKDIL EDERAAVDTYC peptides and pooled preimmune rabbit serum binding to mouse fibroblast transfected cell line Dap.3 expressing HLA-DRB1*0401 (DR4/Dw4).	bind
41006	3	3796	6	11	NULL	NULL	NULL	Dap.3	cell		is a type of					fibroblast transfected cell line	Cell	mouse			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_6_2769_s_108	10338479	(B) Dilution studies of antisera raised against CKDLL EQKRAAVDTYC, CLGSIS ESRRALQDSQR, and CKDIL EDERAAVDTYC peptides and pooled preimmune rabbit serum binding to mouse fibroblast transfected cell line Dap.3 expressing HLA-DRB1*0401 (DR4/Dw4).	bind
81541	1	3796	11	NULL	NULL	NULL	NULL	preimmune serum	CellComponent	rabbit	binds to 					statement 3	Cell				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_6_2769_s_108	10338479	(B) Dilution studies of antisera raised against CKDLL EQKRAAVDTYC, CLGSIS ESRRALQDSQR, and CKDIL EDERAAVDTYC peptides and pooled preimmune rabbit serum binding to mouse fibroblast transfected cell line Dap.3 expressing HLA-DRB1*0401 (DR4/Dw4).	bind
81542	2	3796	11	NULL	NULL	0	NULL	fibroblast cell\t	cell	mouse	is					Dap.3	Cell				NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_6_2769_s_108	10338479	(B) Dilution studies of antisera raised against CKDLL EQKRAAVDTYC, CLGSIS ESRRALQDSQR, and CKDIL EDERAAVDTYC peptides and pooled preimmune rabbit serum binding to mouse fibroblast transfected cell line Dap.3 expressing HLA-DRB1*0401 (DR4/Dw4).	bind
81543	3	3796	11	NULL	NULL	0	NULL	Dap.3	cell		express					HLA-DRB1	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_6_2769_s_108	10338479	(B) Dilution studies of antisera raised against CKDLL EQKRAAVDTYC, CLGSIS ESRRALQDSQR, and CKDIL EDERAAVDTYC peptides and pooled preimmune rabbit serum binding to mouse fibroblast transfected cell line Dap.3 expressing HLA-DRB1*0401 (DR4/Dw4).	bind
81544	4	3796	11	NULL	NULL	0	NULL	peptides	PartOfProtein		binds to 			CKDLL EQKRAAVDTYC		statement 3	Cell				NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_6_2769_s_108	10338479	(B) Dilution studies of antisera raised against CKDLL EQKRAAVDTYC, CLGSIS ESRRALQDSQR, and CKDIL EDERAAVDTYC peptides and pooled preimmune rabbit serum binding to mouse fibroblast transfected cell line Dap.3 expressing HLA-DRB1*0401 (DR4/Dw4).	bind
81545	5	3796	11	NULL	NULL	0	NULL	peptides	PartOfProtein		binds to 			CLGSIS ESRRALQDSQR		statement 3	Cell				NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_6_2769_s_108	10338479	(B) Dilution studies of antisera raised against CKDLL EQKRAAVDTYC, CLGSIS ESRRALQDSQR, and CKDIL EDERAAVDTYC peptides and pooled preimmune rabbit serum binding to mouse fibroblast transfected cell line Dap.3 expressing HLA-DRB1*0401 (DR4/Dw4).	bind
81546	6	3796	11	NULL	NULL	0	NULL	peptides	PartOfProtein		binds to 			CKDIL EDERAAVDTYC		statement 3	Cell				NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_6_2769_s_108	10338479	(B) Dilution studies of antisera raised against CKDLL EQKRAAVDTYC, CLGSIS ESRRALQDSQR, and CKDIL EDERAAVDTYC peptides and pooled preimmune rabbit serum binding to mouse fibroblast transfected cell line Dap.3 expressing HLA-DRB1*0401 (DR4/Dw4).	bind
8905	1	3797	5	11	NULL	NULL	NULL	calmodulin	GP		bind		directly			L-selectin	GP		cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_cell_92_6_809_s_104	9529256	(B) Direct binding of calmodulin to  the L-selectin cytoplasmic tail.	bind
9183	1	3797	6	11	NULL	NULL	NULL	calmodulin	GP		bind		directly			L-selectin	GP		cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_cell_92_6_809_s_104	9529256	(B) Direct binding of calmodulin to  the L-selectin cytoplasmic tail.	bind
81547	1	3797	11	NULL	NULL	0	NULL	calmodulin	GeneOrProtein		binds to 		direct			L-selectin	Protein		cytoplasmic tail		NULL		0	NULL	NULL	NULL	gw60_cell_92_6_809_s_104	9529256	(B) Direct binding of calmodulin to  the L-selectin cytoplasmic tail.	bind
8906	1	3798	5	11	NULL	NULL	NULL	Dam1	GP		bind		directly			Ipl1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_5_763_s_139	11724818	(B) Direct binding of Dam1 to Ipl1 and Sli15.	bind
8907	2	3798	5	11	NULL	NULL	NULL	Dam1	GP		bind		directly			Sli15	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_5_763_s_139	11724818	(B) Direct binding of Dam1 to Ipl1 and Sli15.	bind
9184	1	3798	6	11	NULL	NULL	NULL	Dam1	GP		bind		directly			Ipl1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_5_763_s_139	11724818	(B) Direct binding of Dam1 to Ipl1 and Sli15.	bind
9185	2	3798	6	11	NULL	NULL	NULL	Dam1	GP		bind		directly			Sli15	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_5_763_s_139	11724818	(B) Direct binding of Dam1 to Ipl1 and Sli15.	bind
81548	1	3798	11	NULL	NULL	0	NULL	Dam1	GeneOrProtein		binds to 		direct			Ipl1	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_5_763_s_139	11724818	(B) Direct binding of Dam1 to Ipl1 and Sli15.	bind
81549	2	3798	11	NULL	NULL	0	NULL	Dam1	GeneOrProtein		binds to 		direct			Sli15	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_5_763_s_139	11724818	(B) Direct binding of Dam1 to Ipl1 and Sli15.	bind
8908	1	3799	5	11	NULL	NULL	NULL	alphaCP-1	GP	recombinant	bind		directly							alpha3'UTR	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4572_s_219	10373506	(B) Direct binding of recombinant alphaCP-1 and alphaCP-2 to the alpha3'UTR (determined as detailed for panel A).	bind
8909	2	3799	5	11	NULL	NULL	NULL	alphaCP-2	GP	recombinant	bind		directly							alpha3'UTR	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4572_s_219	10373506	(B) Direct binding of recombinant alphaCP-1 and alphaCP-2 to the alpha3'UTR (determined as detailed for panel A).	bind
53642	3	3799	5	11	NULL	NULL	NULL	alphaCP-1	GP		is a type of					recombinant protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4572_s_219	10373506	(B) Direct binding of recombinant alphaCP-1 and alphaCP-2 to the alpha3'UTR (determined as detailed for panel A).	bind
53644	4	3799	5	11	NULL	NULL	NULL	alphaCP-2	GP		is a type of					recombinant protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4572_s_219	10373506	(B) Direct binding of recombinant alphaCP-1 and alphaCP-2 to the alpha3'UTR (determined as detailed for panel A).	bind
9186	1	3799	6	11	NULL	NULL	NULL	alphaCP-1	GP		bind		directly							alpha3'UTR	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4572_s_219	10373506	(B) Direct binding of recombinant alphaCP-1 and alphaCP-2 to the alpha3'UTR (determined as detailed for panel A).	bind
9187	2	3799	6	11	NULL	NULL	NULL	alphaCP-2	GP		bind		directly							alpha3'UTR	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4572_s_219	10373506	(B) Direct binding of recombinant alphaCP-1 and alphaCP-2 to the alpha3'UTR (determined as detailed for panel A).	bind
41007	3	3799	6	11	NULL	NULL	NULL	alphaCP-1	GP		is a type of					recombinant protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4572_s_219	10373506	(B) Direct binding of recombinant alphaCP-1 and alphaCP-2 to the alpha3'UTR (determined as detailed for panel A).	bind
41008	4	3799	6	11	NULL	NULL	NULL	alphaCP-2	GP		is a type of					recombinant protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4572_s_219	10373506	(B) Direct binding of recombinant alphaCP-1 and alphaCP-2 to the alpha3'UTR (determined as detailed for panel A).	bind
81550	1	3799	11	NULL	NULL	0	NULL	alphaCP-1	GeneOrProtein	recombinant	binds to 		direct			alpha3'UTR	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4572_s_219	10373506	(B) Direct binding of recombinant alphaCP-1 and alphaCP-2 to the alpha3'UTR (determined as detailed for panel A).	bind
81551	2	3799	11	NULL	NULL	0	NULL	alphaCP-2	GeneOrProtein	recombinant	binds to 		direct			alpha3'UTR	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4572_s_219	10373506	(B) Direct binding of recombinant alphaCP-1 and alphaCP-2 to the alpha3'UTR (determined as detailed for panel A).	bind
8910	1	3800	5	11	NULL	NULL	NULL	RIM1	GP		bind		directly			CAST	GP		COOH terminus		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_158_3_577_s_208	12163476	(b) Direct binding of RIM1 to the COOH terminus of CAST.	bind
9188	1	3800	6	11	NULL	NULL	NULL	RIM1	GP		bind		directly			CAST	GP		COOH terminus		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_158_3_577_s_208	12163476	(b) Direct binding of RIM1 to the COOH terminus of CAST.	bind
81552	1	3800	11	NULL	NULL	0	NULL	RIM1	GeneOrProtein		binds to 					CAST	Protein		COOH terminus		NULL		0	NULL	NULL	NULL	gw60_cellbiol_158_3_577_s_208	12163476	(b) Direct binding of RIM1 to the COOH terminus of CAST.	bind
8911	1	3801	5	11	NULL	NULL	NULL	tomosyn	GP		bind		directly			syntaxin-1a	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_5_905_s_79	9620695	(B) Direct binding of tomosyn to syntaxin-1a in a blot overlay assay.	bind
9189	1	3801	6	11	NULL	NULL	NULL	tomosyn	GP		bind		directly			syntaxin 1a	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_5_905_s_79	9620695	(B) Direct binding of tomosyn to syntaxin-1a in a blot overlay assay.	bind
81553	1	3801	11	NULL	NULL	0	NULL	tomosyn	GeneOrProtein		binds to 		direct			syntaxin-1a	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_neuron_20_5_905_s_79	9620695	(B) Direct binding of tomosyn to syntaxin-1a in a blot overlay assay.	bind
8912	1	3802	5	11	NULL	NULL	NULL	SHP-1	GP		bind					CD22	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_18_1009_s_191	9740800	(b) Distinction between function of SHP-1 bound to tyrosine-phosphorylated CD22 and CD72, respectively.	bind
8913	2	3802	5	11	NULL	NULL	NULL	SHP-1	GP		bind					CD72	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_18_1009_s_191	9740800	(b) Distinction between function of SHP-1 bound to tyrosine-phosphorylated CD22 and CD72, respectively.	bind
9190	1	3802	6	11	NULL	NULL	NULL	SHP-1	GP		bind					CD22	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_18_1009_s_191	9740800	(b) Distinction between function of SHP-1 bound to tyrosine-phosphorylated CD22 and CD72, respectively.	bind
9191	2	3802	6	11	NULL	NULL	NULL	SHP-1	GP		bind					CD72	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_18_1009_s_191	9740800	(b) Distinction between function of SHP-1 bound to tyrosine-phosphorylated CD22 and CD72, respectively.	bind
81554	1	3802	11	NULL	NULL	0	NULL	SHP-1	GeneOrProtein		binds to 					CD22	Protein		tyrosine-phosphorylated 		NULL		0	NULL	NULL	NULL	gw60_currbiol_8_18_1009_s_191	9740800	(b) Distinction between function of SHP-1 bound to tyrosine-phosphorylated CD22 and CD72, respectively.	bind
81555	2	3802	11	NULL	NULL	0	NULL	SHP-1	GeneOrProtein		binds to 					CD72	Protein		tyrosine-phosphorylated		NULL		0	NULL	NULL	NULL	gw60_currbiol_8_18_1009_s_191	9740800	(b) Distinction between function of SHP-1 bound to tyrosine-phosphorylated CD22 and CD72, respectively.	bind
8914	1	3804	5	11	NULL	NULL	NULL	p53 protein	GP	endogenous	bind									p53BE	NULL		NULL	NULL	NULL	NULL	gw60_cell_113_3_301_s_279	12732139	(B) DNAP showing Activin-independent binding of endogenous p53 protein to  p53BE.	bind
8915	2	3804	5	11	NULL	NULL	NULL	statement 1	Process		is independent of					activin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_3_301_s_279	12732139	(B) DNAP showing Activin-independent binding of endogenous p53 protein to  p53BE.	bind
9192	1	3804	6	11	NULL	NULL	NULL	p53 protein	GP	endogenous	bind									p53BE	NULL		NULL	NULL	NULL	NULL	gw60_cell_113_3_301_s_279	12732139	(B) DNAP showing Activin-independent binding of endogenous p53 protein to  p53BE.	bind
9193	2	3804	6	11	NULL	NULL	NULL	statement 1	Process		is independent of					activin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_3_301_s_279	12732139	(B) DNAP showing Activin-independent binding of endogenous p53 protein to  p53BE.	bind
81556	1	3804	11	NULL	NULL	NULL	NULL	p53 protein	Protein	 endogenous	binds to 					p53BE	Gene				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_3_301_s_279	12732139	(B) DNAP showing Activin-independent binding of endogenous p53 protein to  p53BE.	bind
81557	2	3804	11	NULL	NULL	0	NULL	statement 1	Process		is independent of					statement 3	Protein				NULL		0	NULL	NULL	NULL	gw60_cell_113_3_301_s_279	12732139	(B) DNAP showing Activin-independent binding of endogenous p53 protein to  p53BE.	bind
81558	3	3804	11	NULL	NULL	0	NULL	DNAP	GeneOrProtein		shows					Activin	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_cell_113_3_301_s_279	12732139	(B) DNAP showing Activin-independent binding of endogenous p53 protein to  p53BE.	bind
8916	1	3805	5	11	NULL	NULL	NULL	NAC	GP		bind					gdhA	GP			promoter region	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_24_6966_s_100	12446647	(B) DNase I footprint of NAC bound to the  gdhA promoter region.	bind
9194	1	3805	6	11	NULL	NULL	NULL	NAC	GP		bind					gdhA	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_24_6966_s_100	12446647	(B) DNase I footprint of NAC bound to the  gdhA promoter region.	bind
81559	1	3805	11	NULL	NULL	0	NULL	NAC	GeneOrProtein		binds to 				DNase I footprint	 gdhA	Gene			promoter region	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_24_6966_s_100	12446647	(B) DNase I footprint of NAC bound to the  gdhA promoter region.	bind
8917	1	3807	5	11	NULL	NULL	NULL	Zur	GP		bind					yciA	GP			promoter region	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_23_6508_s_153	12426338	(B) DNase I footprinting analysis of Zur binding to the  yciA promoter region.	bind
9195	1	3807	6	11	NULL	NULL	NULL	Zur	GP		bind					yciA	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_23_6508_s_153	12426338	(B) DNase I footprinting analysis of Zur binding to the  yciA promoter region.	bind
81560	1	3807	11	NULL	NULL	0	NULL	Zur	GeneOrProtein		binds to 				DNase I footprinting	 yciA	Gene			promoter region	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_23_6508_s_153	12426338	(B) DNase I footprinting analysis of Zur binding to the  yciA promoter region.	bind
8918	1	3808	5	11	NULL	NULL	NULL	YycF	GP		bind					ssaA	GP			promoter region	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_4_1175_s_151	14762013	(B) DNase I footprinting of YycF bound to the  ssaA promoter region.	bind
9196	1	3808	6	11	NULL	NULL	NULL	YycF	GP		bind					ssaA	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_4_1175_s_151	14762013	(B) DNase I footprinting of YycF bound to the  ssaA promoter region.	bind
81561	1	3808	11	NULL	NULL	0	NULL	YycF	GeneOrProtein		binds to 				DNase I footprint	ssaA	Gene			promoter region	NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_4_1175_s_151	14762013	(B) DNase I footprinting of YycF bound to the  ssaA promoter region.	bind
8919	1	3809	5	11	NULL	NULL	NULL	Doa1	GP		bind					Ub	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4122_s_134	16705165	(B) Doa1  binds Ub in vitro.	bind
9197	1	3809	6	11	NULL	NULL	NULL	Doa1	GP		bind					Ub	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4122_s_134	16705165	(B) Doa1  binds Ub in vitro.	bind
81562	1	3809	11	NULL	NULL	0	NULL	Doa1	GeneOrProtein		binds to 					Ub	GeneOrProtein				NULL	in vitro	0	NULL	NULL	NULL	gw70_molcellbiol_26_11_4122_s_134	16705165	(B) Doa1  binds Ub in vitro.	bind
8920	1	3810	5	11	NULL	NULL	NULL	DOKL	GP		bind					c-Abl	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8314_s_276	10567556	(B) DOKL binding to c-Abl requires Abl kinase activity.	bind
8921	2	3810	5	11	NULL	NULL	NULL	statement 1	Process		require					Abl kinase	GP	 activity of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8314_s_276	10567556	(B) DOKL binding to c-Abl requires Abl kinase activity.	bind
9198	1	3810	6	11	NULL	NULL	NULL	DOKL	GP		bind					c-Abl	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8314_s_276	10567556	(B) DOKL binding to c-Abl requires Abl kinase activity.	bind
41009	3	3810	6	11	NULL	NULL	NULL	statement 1	Process		requires					Abl kinase	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8314_s_276	10567556	(B) DOKL binding to c-Abl requires Abl kinase activity.	bind
81563	1	3810	11	NULL	NULL	0	NULL	DOKL	GeneOrProtein		binds to 					c-Abl	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_12_8314_s_276	10567556	(B) DOKL binding to c-Abl requires Abl kinase activity.	bind
81564	2	3810	11	NULL	NULL	0	NULL	statement 1	Process		requires					Abl kinase	Protein				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_12_8314_s_276	10567556	(B) DOKL binding to c-Abl requires Abl kinase activity.	bind
8922	1	3811	5	11	NULL	NULL	NULL				bind		dose dependently	LR974P		SHP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1545_1_20_s_143	11342028	(B) Dose dependence of binding of LR974P to SHP-2.	bind
9200	1	3811	6	11	NULL	NULL	NULL				bind		dose dependently	LR974P		SHP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1545_1_20_s_143	11342028	(B) Dose dependence of binding of LR974P to SHP-2.	bind
81600	1	3811	11	NULL	NULL	0	NULL	LR974P	GeneOrProtein		binds to 					SHP2	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1545_1_20_s_143	11342028	(B) Dose dependence of binding of LR974P to SHP-2.	bind
8924	1	3812	5	11	NULL	NULL	NULL	Raf-1	GP		bind					GST-Rb	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_137	15485920	(B) Dose-dependent inhibition of the binding of  Raf-1 to GST-Rb by the Raf-1 peptide in a GST pull-down assay.	bind
8925	2	3812	5	11	NULL	NULL	NULL	Raf-1 peptide	GP		inhibits		dose-dependently			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_137	15485920	(B) Dose-dependent inhibition of the binding of  Raf-1 to GST-Rb by the Raf-1 peptide in a GST pull-down assay.	bind
9201	1	3812	6	11	NULL	NULL	NULL	Raf-1	GP		bind					GST-Rb	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_137	15485920	(B) Dose-dependent inhibition of the binding of  Raf-1 to GST-Rb by the Raf-1 peptide in a GST pull-down assay.	bind
9202	2	3812	6	11	NULL	NULL	NULL	Raf-1 peptide	GP		inhibits 		dose-dependently			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_137	15485920	(B) Dose-dependent inhibition of the binding of  Raf-1 to GST-Rb by the Raf-1 peptide in a GST pull-down assay.	bind
81601	1	3812	11	NULL	NULL	0	NULL	Raf-1	GeneOrProtein		binds to 					GST-Rb	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_137	15485920	(B) Dose-dependent inhibition of the binding of  Raf-1 to GST-Rb by the Raf-1 peptide in a GST pull-down assay.	bind
81602	2	3812	11	NULL	NULL	0	NULL	Raf-1 peptide	PartOfProtein		inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_137	15485920	(B) Dose-dependent inhibition of the binding of  Raf-1 to GST-Rb by the Raf-1 peptide in a GST pull-down assay.	bind
8927	1	3813	5	11	NULL	NULL	NULL	BMP-7	GP	125I-labeled	bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_4_858_s_197	12927798	(B) Dose-response curve for 125I-labeled BMP-7 binding with heparin.	bind
9203	1	3813	6	11	NULL	NULL	NULL	BMP-7	GP	125I-labeled	bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_4_858_s_197	12927798	(B) Dose-response curve for 125I-labeled BMP-7 binding with heparin.	bind
81603	1	3813	11	NULL	NULL	0	NULL	BMP-7	GeneOrProtein	125I-labeled	binds to 					heparin	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_4_858_s_197	12927798	(B) Dose-response curve for 125I-labeled BMP-7 binding with heparin.	bind
8928	1	3814	5	11	NULL	NULL	NULL	FASII	GP		bind			C-terminal 98-amino-acid residues		DLG	GP		PDZ domains		NULL		NULL	NULL	NULL	NULL	gw60_neuron_19_4_787_s_155	9354326	(B) Dose-response curves of C-terminal 98-amino-acid residues of FASII binding to the PDZ domains in DLG and SAP97.	bind
8929	2	3814	5	11	NULL	NULL	NULL	FASII	GP		bind			C-terminal 98-amino-acid residues		SAP97	GP		PDZ domain		NULL		NULL	NULL	NULL	NULL	gw60_neuron_19_4_787_s_155	9354326	(B) Dose-response curves of C-terminal 98-amino-acid residues of FASII binding to the PDZ domains in DLG and SAP97.	bind
9204	1	3814	6	11	NULL	NULL	NULL	FASII	GP		bind			C-terminal 98-amino-acid residues		DLG	GP		PDZ domain		NULL		NULL	NULL	NULL	NULL	gw60_neuron_19_4_787_s_155	9354326	(B) Dose-response curves of C-terminal 98-amino-acid residues of FASII binding to the PDZ domains in DLG and SAP97.	bind
9205	2	3814	6	11	NULL	NULL	NULL	FASII	GP		bind			C-terminal 98-amino-acid residues		SAP97	GP		PDZ domain		NULL		NULL	NULL	NULL	NULL	gw60_neuron_19_4_787_s_155	9354326	(B) Dose-response curves of C-terminal 98-amino-acid residues of FASII binding to the PDZ domains in DLG and SAP97.	bind
81604	1	3814	11	NULL	NULL	0	NULL	FASII	Protein		binds to 			C-terminal 98-amino-acid		DLG	Protein		PDZ domain		NULL		0	NULL	NULL	NULL	gw60_neuron_19_4_787_s_155	9354326	(B) Dose-response curves of C-terminal 98-amino-acid residues of FASII binding to the PDZ domains in DLG and SAP97.	bind
81605	2	3814	11	NULL	NULL	0	NULL	FASII	Protein		binds to 			C-terminal 98-amino-acid		SAP97	Protein		PDZ domain		NULL		0	NULL	NULL	NULL	gw60_neuron_19_4_787_s_155	9354326	(B) Dose-response curves of C-terminal 98-amino-acid residues of FASII binding to the PDZ domains in DLG and SAP97.	bind
8930	1	3816	5	11	NULL	NULL	NULL	Hsp70	GP		bind					PBMC	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_3_353_s_37	12354387	(B) Dot plot profile showing the binding of Hsp70 to human PBMC.	bind
9206	1	3816	6	11	NULL	NULL	NULL	Hsp70	GP		bind					PBMC	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_3_353_s_37	12354387	(B) Dot plot profile showing the binding of Hsp70 to human PBMC.	bind
81606	1	3816	11	NULL	NULL	0	NULL	Hsp70	GeneOrProtein		binds to 					PBMC	Cell	human			NULL		0	NULL	NULL	NULL	gw60_immunity_17_3_353_s_37	12354387	(B) Dot plot profile showing the binding of Hsp70 to human PBMC.	bind
8931	1	3817	5	11	NULL	NULL	NULL	TBPCORE	GP	human	bind					 DNA	NucleicAcid			TATA box	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_1_151_s_77	12535529	(B) Downstream or front view of the human TBPCORE (white) bound to the TATA box-containing DNA (green)  (Nikolov et al., 1996  ).	bind
9207	1	3817	6	11	NULL	NULL	NULL	TBPCORE	GP	human	bind					DNA	NucleicAcid			TATA box	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_1_151_s_77	12535529	(B) Downstream or front view of the human TBPCORE (white) bound to the TATA box-containing DNA (green)  (Nikolov et al., 1996  ).	bind
81607	1	3817	11	NULL	NULL	0	NULL	TBPCORE	GeneOrProtein	Human	binds to 					DNA	NucleicAcidSubstance	TATA box			NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_151_s_77	12535529	(B) Downstream or front view of the human TBPCORE (white) bound to the TATA box-containing DNA (green)  (Nikolov et al., 1996  ).	bind
8932	1	3819	5	11	NULL	NULL	NULL	GFP - X-PAK5	GP		bind					MTs	CellComponent				NULL	live A6 cells	NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_1029_s_210	11733543	(B) Dynamics of GFP - X-PAK5 - bound MTs in live A6 cells.	bind
9208	1	3819	6	11	NULL	NULL	NULL	GFP - X-PAK5	GP		bind					MTs	CellComponent				NULL	live A6 cells	NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_1029_s_210	11733543	(B) Dynamics of GFP - X-PAK5 - bound MTs in live A6 cells.	bind
81608	1	3819	11	NULL	NULL	0	NULL	GFP - X-PAK5	GeneOrProtein		binds to 					MT	CellComponent	live A6 cell			NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_6_1029_s_210	11733543	(B) Dynamics of GFP - X-PAK5 - bound MTs in live A6 cells.	bind
8933	1	3820	5	11	NULL	NULL	NULL	E2F-4	GP		bind					p130	GP				NULL	insect cell lysate expressing p130,E2F-4,DP-1	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6233_s_31	10938100	(B) E2F-4 is bound to p130 in insect cell lysate expressing p130, E2F-4, and DP-1.	bind
9241	1	3820	6	11	NULL	NULL	NULL	E2F-4	GP		bind					p130	GP				NULL	insect cell lysate expressing p130,E2F-4,DP-1	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6233_s_31	10938100	(B) E2F-4 is bound to p130 in insect cell lysate expressing p130, E2F-4, and DP-1.	bind
81609	1	3820	11	NULL	NULL	0	NULL	E2F-4	GeneOrProtein		binds to 					p130	GeneOrProtein	insect cell lysate			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6233_s_31	10938100	(B) E2F-4 is bound to p130 in insect cell lysate expressing p130, E2F-4, and DP-1.	bind
81610	2	3820	11	NULL	NULL	0	NULL	insect cell	cell		express					p130	Gene				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6233_s_31	10938100	(B) E2F-4 is bound to p130 in insect cell lysate expressing p130, E2F-4, and DP-1.	bind
81611	3	3820	11	NULL	NULL	0	NULL	insect cell	cell		express					E2F-4	Gene				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6233_s_31	10938100	(B) E2F-4 is bound to p130 in insect cell lysate expressing p130, E2F-4, and DP-1.	bind
81612	4	3820	11	NULL	NULL	0	NULL	insect cell	cell		express					DP-1	Gene				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6233_s_31	10938100	(B) E2F-4 is bound to p130 in insect cell lysate expressing p130, E2F-4, and DP-1.	bind
8936	1	3821	5	11	NULL	NULL	NULL	E64	Chemical		stabilize					FH	GP	binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_11_6206_s_299	12379699	(B) E64 stabilizes FH binding activity.	bind
9245	1	3821	6	11	NULL	NULL	NULL	E64	Chemical		stabilizes					FH	GP	binding activity of 			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_11_6206_s_299	12379699	(B) E64 stabilizes FH binding activity.	bind
81613	1	3821	11	NULL	NULL	0	NULL	E64	Chemical		stabilizes					FH	GeneOrProtein	binding activity			NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_11_6206_s_299	12379699	(B) E64 stabilizes FH binding activity.	bind
8937	1	3822	5	11	NULL	NULL	NULL	cIR-MAP2c (-Au11)	GP	unlabeled	bind					2.6 tubulin monomers	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_7_1187_s_103	12082079	(B) Each unlabeled cIR-MAP2c (-Au11) bound 2.6 tubulin monomers and each gold-labeled cIR-MAP2c (+Au11) bound 2.5 tubulin monomers.	bind
8938	2	3822	5	11	NULL	NULL	NULL	IR-MAP2c (+Au11)	GP	gold-labeled	bind					2.5 tubulin monomers	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_7_1187_s_103	12082079	(B) Each unlabeled cIR-MAP2c (-Au11) bound 2.6 tubulin monomers and each gold-labeled cIR-MAP2c (+Au11) bound 2.5 tubulin monomers.	bind
9246	1	3822	6	11	NULL	NULL	NULL	cIR-MAP2c	GP	unlabeled	bind					2.6 tubulin monomer	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_7_1187_s_103	12082079	(B) Each unlabeled cIR-MAP2c (-Au11) bound 2.6 tubulin monomers and each gold-labeled cIR-MAP2c (+Au11) bound 2.5 tubulin monomers.	bind
9247	2	3822	6	11	NULL	NULL	NULL	cIR-MAP2c	GP	gold labeled	bind					2.5 tubulin monomer	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_7_1187_s_103	12082079	(B) Each unlabeled cIR-MAP2c (-Au11) bound 2.6 tubulin monomers and each gold-labeled cIR-MAP2c (+Au11) bound 2.5 tubulin monomers.	bind
81614	1	3822	11	NULL	NULL	NULL	NULL	cIR-MAP2c	GeneOrProtein	unlabeled	binds to 					2.6 tubulin monomer	Protein				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_7_1187_s_103	12082079	(B) Each unlabeled cIR-MAP2c (-Au11) bound 2.6 tubulin monomers and each gold-labeled cIR-MAP2c (+Au11) bound 2.5 tubulin monomers.	bind
81615	2	3822	11	NULL	NULL	0	NULL	cIR-MAP2c	GeneOrProtein	gold-labeled	binds to 					2.5 tubulin monomer	Protein				NULL		0	NULL	NULL	NULL	gw60_cellbiol_157_7_1187_s_103	12082079	(B) Each unlabeled cIR-MAP2c (-Au11) bound 2.6 tubulin monomers and each gold-labeled cIR-MAP2c (+Au11) bound 2.5 tubulin monomers.	bind
8939	1	3823	5	11	NULL	NULL	NULL	EBAG9	GP		bind			predicted TM region		Snapin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_3_1245_s_200	15635093	(B) EBAG9 binds to Snapin via  its predicted TM region.	bind
9249	1	3823	6	11	NULL	NULL	NULL	EBAG9	GP		bind			predicted TM region		Snapin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_3_1245_s_200	15635093	(B) EBAG9 binds to Snapin via  its predicted TM region.	bind
81616	1	3823	11	NULL	NULL	0	NULL	EBAG9	Gene		binds to 				TM region	Snapin	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_3_1245_s_200	15635093	(B) EBAG9 binds to Snapin via  its predicted TM region.	bind
8941	1	3824	5	11	NULL	NULL	NULL	Ecm22p	GP		bind		directly			ERG2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6395_s_273	11533229	(B) Ecm22p also bound directly to the  ERG2 promoter in a SRE-dependent manner.	bind
8942	2	3824	5	11	NULL	NULL	NULL	statement 1	Process		is dependent on									SRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6395_s_273	11533229	(B) Ecm22p also bound directly to the  ERG2 promoter in a SRE-dependent manner.	bind
9250	1	3824	6	11	NULL	NULL	NULL	Ecm22p	GP		bind		directly			ERG2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6395_s_273	11533229	(B) Ecm22p also bound directly to the  ERG2 promoter in a SRE-dependent manner.	bind
9251	2	3824	6	11	NULL	NULL	NULL	statement 1	Process		is dependent on									SRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6395_s_273	11533229	(B) Ecm22p also bound directly to the  ERG2 promoter in a SRE-dependent manner.	bind
81617	1	3824	11	NULL	NULL	0	NULL	Ecm22p	Protein		binds to 		directly			ERG2	Gene			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_19_6395_s_273	11533229	(B) Ecm22p also bound directly to the  ERG2 promoter in a SRE-dependent manner.	bind
81618	2	3824	11	NULL	NULL	0	NULL	statement 1	Process		depends on					SRE	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_19_6395_s_273	11533229	(B) Ecm22p also bound directly to the  ERG2 promoter in a SRE-dependent manner.	bind
8943	1	3825	5	11	NULL	NULL	NULL	Ras	GP	inhibition of	induce					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9271_s_220	11094078	(B) Ectopic expression of  bcl-2 blocks apoptosis induced by inhibition of Ras and PI 3-kinase.	bind
8944	2	3825	5	11	NULL	NULL	NULL	PI 3-kinase	GP	inhibition of	induce					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9271_s_220	11094078	(B) Ectopic expression of  bcl-2 blocks apoptosis induced by inhibition of Ras and PI 3-kinase.	bind
8945	3	3825	5	11	NULL	NULL	NULL	 bcl-2	GP	ectopic expression of	blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9271_s_220	11094078	(B) Ectopic expression of  bcl-2 blocks apoptosis induced by inhibition of Ras and PI 3-kinase.	bind
8946	4	3825	5	11	NULL	NULL	NULL	bcl-2	GP	ectopic expression of	blocks					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9271_s_220	11094078	(B) Ectopic expression of  bcl-2 blocks apoptosis induced by inhibition of Ras and PI 3-kinase.	bind
9252	1	3825	6	11	NULL	NULL	NULL	Ras	GP	inhibition of	induces					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9271_s_220	11094078	(B) Ectopic expression of  bcl-2 blocks apoptosis induced by inhibition of Ras and PI 3-kinase.	bind
9253	2	3825	6	11	NULL	NULL	NULL	PI 3-kinase	GP	inhibition of	induces					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9271_s_220	11094078	(B) Ectopic expression of  bcl-2 blocks apoptosis induced by inhibition of Ras and PI 3-kinase.	bind
9254	3	3825	6	11	NULL	NULL	NULL	Bcl-2	GP	ectopic expression of	blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9271_s_220	11094078	(B) Ectopic expression of  bcl-2 blocks apoptosis induced by inhibition of Ras and PI 3-kinase.	bind
9255	4	3825	6	11	NULL	NULL	NULL	Bcl-2	GP	ectopic expression of	blocks					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9271_s_220	11094078	(B) Ectopic expression of  bcl-2 blocks apoptosis induced by inhibition of Ras and PI 3-kinase.	bind
81619	1	3825	11	NULL	NULL	0	NULL	bcl-2	GeneOrProtein	Ectopic expression	blocks					apoptosis	BiologicalProcess				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_24_9271_s_220	11094078	(B) Ectopic expression of  bcl-2 blocks apoptosis induced by inhibition of Ras and PI 3-kinase.	bind
81620	2	3825	11	NULL	NULL	0	NULL	Ras	GeneOrProtein	inhibition	induces					apoptosis	BiologicalProcess				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_24_9271_s_220	11094078	(B) Ectopic expression of  bcl-2 blocks apoptosis induced by inhibition of Ras and PI 3-kinase.	bind
81621	3	3825	11	NULL	NULL	0	NULL	PI 3-kinase	GeneOrProtein	inhibition	induces					apoptosis	BiologicalProcess				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_24_9271_s_220	11094078	(B) Ectopic expression of  bcl-2 blocks apoptosis induced by inhibition of Ras and PI 3-kinase.	bind
8947	1	3826	5	11	NULL	NULL	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_206_s_140	9864217	(B) Effect of antibodies against TNF-alpha or IL-1R on the induction of DNA binding of NF-kappaB by LPS with or without priming by IFN-gamma.	bind
8948	2	3826	5	11	NULL	NULL	NULL	LPS	Chemical		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_206_s_140	9864217	(B) Effect of antibodies against TNF-alpha or IL-1R on the induction of DNA binding of NF-kappaB by LPS with or without priming by IFN-gamma.	bind
9256	1	3826	6	11	NULL	NULL	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_206_s_140	9864217	(B) Effect of antibodies against TNF-alpha or IL-1R on the induction of DNA binding of NF-kappaB by LPS with or without priming by IFN-gamma.	bind
9257	2	3826	6	11	NULL	NULL	NULL	LPS	Chemical		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_206_s_140	9864217	(B) Effect of antibodies against TNF-alpha or IL-1R on the induction of DNA binding of NF-kappaB by LPS with or without priming by IFN-gamma.	bind
81622	1	3826	11	NULL	NULL	0	NULL	NF-kappaB	Protein		binds to 					DNA	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_1_206_s_140	9864217	(B) Effect of antibodies against TNF-alpha or IL-1R on the induction of DNA binding of NF-kappaB by LPS with or without priming by IFN-gamma.	bind
81623	2	3826	11	NULL	NULL	0	NULL	LPS	NonProteinOrNucleicAcidChemical		induces					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_1_206_s_140	9864217	(B) Effect of antibodies against TNF-alpha or IL-1R on the induction of DNA binding of NF-kappaB by LPS with or without priming by IFN-gamma.	bind
8949	1	3827	5	11	NULL	NULL	NULL	syntaxin	GP		bind					synaptotagmin	GP		C2A domain		NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_86_1_39_s_133	9692742	(B) Effect of antibodies on Ca2+-dependent syntaxin binding to synaptotagmin C2A domain.	bind
8950	2	3827	5	11	NULL	NULL	NULL	statement 1	Process		is dependent on					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_86_1_39_s_133	9692742	(B) Effect of antibodies on Ca2+-dependent syntaxin binding to synaptotagmin C2A domain.	bind
9258	1	3827	6	11	NULL	NULL	NULL	syntaxin	GP		bind					synaptotagmin	GP		C2A domain		NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_86_1_39_s_133	9692742	(B) Effect of antibodies on Ca2+-dependent syntaxin binding to synaptotagmin C2A domain.	bind
9259	2	3827	6	11	NULL	NULL	NULL	statement 1	Process		is dependent on					Ca+2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_86_1_39_s_133	9692742	(B) Effect of antibodies on Ca2+-dependent syntaxin binding to synaptotagmin C2A domain.	bind
81624	1	3827	11	NULL	NULL	NULL	NULL	syntaxin	GeneOrProtein		binds to 					synaptotagmin	Protein		C2A domain		NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_86_1_39_s_133	9692742	(B) Effect of antibodies on Ca2+-dependent syntaxin binding to synaptotagmin C2A domain.	bind
81625	2	3827	11	NULL	NULL	0	NULL	statement 1	Process		depends on					Ca2+	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	gw60_neuroscience_86_1_39_s_133	9692742	(B) Effect of antibodies on Ca2+-dependent syntaxin binding to synaptotagmin C2A domain.	bind
8951	1	3828	5	11	NULL	NULL	NULL	dynein	GP		bind					liposomes	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_1_173_s_74	11172722	(B) Effect of antibodies on the binding of dynein and dynactin to liposomes.	bind
8952	2	3828	5	11	NULL	NULL	NULL	dynactin	GP		bind					liposomes	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_1_173_s_74	11172722	(B) Effect of antibodies on the binding of dynein and dynactin to liposomes.	bind
9260	1	3828	6	11	NULL	NULL	NULL	dynein	GP		bind					liposomes	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_1_173_s_74	11172722	(B) Effect of antibodies on the binding of dynein and dynactin to liposomes.	bind
9261	2	3828	6	11	NULL	NULL	NULL	dynactin	GP		bind					liposomes	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_1_173_s_74	11172722	(B) Effect of antibodies on the binding of dynein and dynactin to liposomes.	bind
81626	1	3828	11	NULL	NULL	0	NULL	 dynein	Protein		binds to 					liposomes	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	gw60_molcell_7_1_173_s_74	11172722	(B) Effect of antibodies on the binding of dynein and dynactin to liposomes.	bind
81627	2	3828	11	NULL	NULL	0	NULL	dynactin	Protein		binds to 					liposomes	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	gw60_molcell_7_1_173_s_74	11172722	(B) Effect of antibodies on the binding of dynein and dynactin to liposomes.	bind
8953	1	3829	5	11	NULL	NULL	NULL	tubulin	GP		bind					colchicine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1432_2_350_s_114	10407156	(B) Effect of bisANS and GTP on the colchicine binding activity of tubulin.	bind
9262	1	3829	6	11	NULL	NULL	NULL	tubulin	GP		bind					colchicine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1432_2_350_s_114	10407156	(B) Effect of bisANS and GTP on the colchicine binding activity of tubulin.	bind
81628	1	3829	11	NULL	NULL	0	NULL	colchicine	NonProteinOrNucleicAcidChemical		binds to 					tubulin	Protein				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1432_2_350_s_114	10407156	(B) Effect of bisANS and GTP on the colchicine binding activity of tubulin.	bind
8954	1	3830	5	11	NULL	NULL	NULL	AFP	GP		bind					MDM	Cell				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_3_507_s_103	12176010	(B) Effect of bovine fetuin (500 nM) (AFP + fetuin) or AGP (AFP + AGP) on [125]AFP binding to MDM (AFP).	bind
9263	1	3830	6	11	NULL	NULL	NULL	AFP	GP		bind					MDM	Cell				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_3_507_s_103	12176010	(B) Effect of bovine fetuin (500 nM) (AFP + fetuin) or AGP (AFP + AGP) on [125]AFP binding to MDM (AFP).	bind
81629	1	3830	11	NULL	NULL	0	NULL	AFP	Protein		binds to 					MDM	Cell				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_3_507_s_103	12176010	(B) Effect of bovine fetuin (500 nM) (AFP + fetuin) or AGP (AFP + AGP) on [125]AFP binding to MDM (AFP).	bind
8955	1	3831	5	11	NULL	NULL	NULL	C5	GP		bind					GST-p16	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_3_421_s_182	9660926	(B) Effect of R24C mutation on the binding of C5 to GST-p16.	bind
9264	1	3831	6	11	NULL	NULL	NULL	C5	GP		bind					GST-p16	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_3_421_s_182	9660926	(B) Effect of R24C mutation on the binding of C5 to GST-p16.	bind
81630	1	3831	11	NULL	NULL	0	NULL	C5	Protein		binds to 					 GST-p16	Protein				NULL		0	NULL	NULL	NULL	gw60_molcell_1_3_421_s_182	9660926	(B) Effect of R24C mutation on the binding of C5 to GST-p16.	bind
8956	1	3832	5	11	NULL	NULL	NULL	p97	GP		bind					p62	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2379_s_193	9398662	(B) Effect of Ran on the binding of p97 to p62.	bind
9265	1	3832	6	11	NULL	NULL	NULL	p97	GP		bind					p62	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2379_s_193	9398662	(B) Effect of Ran on the binding of p97 to p62.	bind
81631	1	3832	11	NULL	NULL	0	NULL	p97	GeneOrProtein		binds to 					p62	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_8_12_2379_s_193	9398662	(B) Effect of Ran on the binding of p97 to p62.	bind
8957	1	3833	5	11	NULL	NULL	NULL	Bas2p	GP		bind					Bas1p	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_23_7901_s_330	11689683	(B) Effect of SAICAR and AICAR on in vitro binding of Bas2p to Bas1p on the  ADE5,7 promoter.	bind
13173	2	3833	5	11	NULL	NULL	NULL	statement 1	GP		bind					ADE5,7	GP			promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_23_7901_s_330	11689683	(B) Effect of SAICAR and AICAR on in vitro binding of Bas2p to Bas1p on the  ADE5,7 promoter.	bind
9266	1	3833	6	11	NULL	NULL	NULL	Bas2p	GP		bind					Bas1p	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_23_7901_s_330	11689683	(B) Effect of SAICAR and AICAR on in vitro binding of Bas2p to Bas1p on the  ADE5,7 promoter.	bind
11761	2	3833	6	11	NULL	NULL	NULL	statement 1	GP		binds					ADE5,7	GP			promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_23_7901_s_330	11689683	(B) Effect of SAICAR and AICAR on in vitro binding of Bas2p to Bas1p on the  ADE5,7 promoter.	bind
81632	1	3833	11	NULL	NULL	0	NULL	Bas2p	GeneOrProtein		binds to 					Bas1p	Gene			ADE5,7 promoter	NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_21_23_7901_s_330	11689683	(B) Effect of SAICAR and AICAR on in vitro binding of Bas2p to Bas1p on the  ADE5,7 promoter.	bind
8958	1	3834	5	11	NULL	NULL	NULL	TN-R 160	GP		bind					FN fragments	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_863_1_42_s_111	10773191	(B) Effect of soluble GAGs on the binding of TN-R 160 to FN fragments and heparin-binding peptides.	bind
8959	2	3834	5	11	NULL	NULL	NULL	TN-R 160	GP		bind					heparin-binding peptides	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_863_1_42_s_111	10773191	(B) Effect of soluble GAGs on the binding of TN-R 160 to FN fragments and heparin-binding peptides.	bind
9267	1	3834	6	11	NULL	NULL	NULL	TN-R 160	GP		bind					FN fragments	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_863_1_42_s_111	10773191	(B) Effect of soluble GAGs on the binding of TN-R 160 to FN fragments and heparin-binding peptides.	bind
9268	2	3834	6	11	NULL	NULL	NULL	heparin	Chemical		bind					peptides	amino acid				NULL		NULL	NULL	NULL	NULL	gw60_brainres_863_1_42_s_111	10773191	(B) Effect of soluble GAGs on the binding of TN-R 160 to FN fragments and heparin-binding peptides.	bind
9269	3	3834	6	11	NULL	NULL	NULL	TN-R 160	GP		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_863_1_42_s_111	10773191	(B) Effect of soluble GAGs on the binding of TN-R 160 to FN fragments and heparin-binding peptides.	bind
81633	1	3834	11	NULL	NULL	0	NULL	 TN-R	GeneOrProtein		binds to 					FN fragment	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_brainres_863_1_42_s_111	10773191	(B) Effect of soluble GAGs on the binding of TN-R 160 to FN fragments and heparin-binding peptides.	bind
81634	2	3834	11	NULL	NULL	0	NULL	TN-R 	GeneOrProtein		binds to 					heparin-binding peptide	PartOfProtein				NULL		0	NULL	NULL	NULL	gw60_brainres_863_1_42_s_111	10773191	(B) Effect of soluble GAGs on the binding of TN-R 160 to FN fragments and heparin-binding peptides.	bind
8960	1	3835	5	11	NULL	NULL	NULL	TN-R 160	GP		bind					TN-C	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_863_1_42_s_143	10773191	(B) Effect of soluble GAGs on the binding of TN-R 160 to TN-C.	bind
9270	1	3835	6	11	NULL	NULL	NULL	TN-R 160	GP		bind					TN-C	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_863_1_42_s_143	10773191	(B) Effect of soluble GAGs on the binding of TN-R 160 to TN-C.	bind
81635	1	3835	11	NULL	NULL	0	NULL	TN-R 160	GeneOrProtein		binds to 					TN-C	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_brainres_863_1_42_s_143	10773191	(B) Effect of soluble GAGs on the binding of TN-R 160 to TN-C.	bind
8961	1	3836	5	11	NULL	NULL	NULL	Css IV	GP		bind					rIIA 	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_4_919_s_145	9808476	(B) Effect of the different mutations on Css IV binding affinity to rIIA sodium channels.	bind
53645	2	3836	5	11	NULL	NULL	NULL	rIIA	GP		is a type of					sodium channel	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_4_919_s_145	9808476	(B) Effect of the different mutations on Css IV binding affinity to rIIA sodium channels.	bind
9271	1	3836	6	11	NULL	NULL	NULL	Css IV	GP		bind					rIIA	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_4_919_s_145	9808476	(B) Effect of the different mutations on Css IV binding affinity to rIIA sodium channels.	bind
41010	2	3836	6	11	NULL	NULL	NULL	rIIA	GP		is a type of					sodium channel	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_4_919_s_145	9808476	(B) Effect of the different mutations on Css IV binding affinity to rIIA sodium channels.	bind
81636	1	3836	11	NULL	NULL	0	NULL	Css IV	GeneOrProtein		binds to 					rIIA 	GeneOrProtein	sodium channels			NULL		0	NULL	NULL	NULL	gw60_neuron_21_4_919_s_145	9808476	(B) Effect of the different mutations on Css IV binding affinity to rIIA sodium channels.	bind
8962	1	3837	5	11	NULL	NULL	NULL	GTP	Chemical		bind					His6-BCTD	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_6_1347_s_153	9515899	(B) Effect on the GTP binding of His6-BCTD.	bind
9272	1	3837	6	11	NULL	NULL	NULL	His6-BCTD	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_6_1347_s_153	9515899	(B) Effect on the GTP binding of His6-BCTD.	bind
81637	1	3837	11	NULL	NULL	0	NULL	His6-BCTD	Protein		binds to 					GTP	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_6_1347_s_153	9515899	(B) Effect on the GTP binding of His6-BCTD.	bind
8963	1	3838	5	11	NULL	NULL	NULL	NSAP1	GP	purified	bind					probe IV	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_18_7878_s_117	15340051	(B) Effects of competitor RNAs on binding of purified NSAP1 to probe  IV.	bind
9273	1	3838	6	11	NULL	NULL	NULL	NSAP1	GP	purified	bind					probe IV	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_18_7878_s_117	15340051	(B) Effects of competitor RNAs on binding of purified NSAP1 to probe  IV.	bind
81638	1	3838	11	NULL	NULL	0	NULL	NSAP1	GeneOrProtein		binds to 					probe IV	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_18_7878_s_117	15340051	(B) Effects of competitor RNAs on binding of purified NSAP1 to probe  IV.	bind
8964	1	3839	5	11	NULL	NULL	NULL	MAb	GP		bind					O-PG	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_clindiagnlabimmun_8_3_647_s_75	11329475	(B) Effects of fungal glucan on MAb binding to O-PG-coated wells.	bind
9274	1	3839	6	11	NULL	NULL	NULL	MAb	GP		bind 					O-PG	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_clindiagnlabimmun_8_3_647_s_75	11329475	(B) Effects of fungal glucan on MAb binding to O-PG-coated wells.	bind
81639	1	3839	11	NULL	NULL	0	NULL	MAb	Protein		binds to 					O-PG	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	gw60_clindiagnlabimmun_8_3_647_s_75	11329475	(B) Effects of fungal glucan on MAb binding to O-PG-coated wells.	bind
8965	1	3840	5	11	NULL	NULL	NULL	Gab1	GP		undergoes					phosphorylation	Process		tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_103_s_62	12370245	(b) EGF selectively enhances Gab1 tyrosine phosphorylation and binding to SHP-2.	bind
8966	2	3840	5	11	NULL	NULL	NULL	Gab1	GP		bind					SHP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_103_s_62	12370245	(b) EGF selectively enhances Gab1 tyrosine phosphorylation and binding to SHP-2.	bind
8967	3	3840	5	11	NULL	NULL	NULL	EGF	GP		enhances		selectively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_103_s_62	12370245	(b) EGF selectively enhances Gab1 tyrosine phosphorylation and binding to SHP-2.	bind
8968	4	3840	5	11	NULL	NULL	NULL	EGF	GP		enhances		selectively			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_103_s_62	12370245	(b) EGF selectively enhances Gab1 tyrosine phosphorylation and binding to SHP-2.	bind
9275	1	3840	6	11	NULL	NULL	NULL	Gab1	GP		bind					SHP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_103_s_62	12370245	(b) EGF selectively enhances Gab1 tyrosine phosphorylation and binding to SHP-2.	bind
9276	2	3840	6	11	NULL	NULL	NULL	EGF	GP		enhances		selectively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_103_s_62	12370245	(b) EGF selectively enhances Gab1 tyrosine phosphorylation and binding to SHP-2.	bind
9277	4	3840	6	11	NULL	NULL	NULL	EGF	GP		enhances		selectively			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_103_s_62	12370245	(b) EGF selectively enhances Gab1 tyrosine phosphorylation and binding to SHP-2.	bind
53647	3	3840	6	11	NULL	NULL	NULL	Gab1	GP		undergoes					phosphorylation	Process		tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_103_s_62	12370245	(b) EGF selectively enhances Gab1 tyrosine phosphorylation and binding to SHP-2.	bind
81640	1	3840	11	NULL	NULL	0	NULL	Gab1	Protein	tyrosine phosphorylate	binds to 					SHP-2	GeneOrProtein				NULL		0	NULL	NULL	NULL	gw60_cellbiol_159_1_103_s_62	12370245	(b) EGF selectively enhances Gab1 tyrosine phosphorylation and binding to SHP-2.	bind
81641	2	3840	11	NULL	NULL	0	NULL	EGF	Protein		enhances		selectively			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_159_1_103_s_62	12370245	(b) EGF selectively enhances Gab1 tyrosine phosphorylation and binding to SHP-2.	bind
9386	1	3841	5	11	NULL	NULL	NULL	GDP	Chemical		bind					eIF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1492_1_56_s_172	10858531	(B) eIF2B activity was analyzed in lysates from infected Sf9 cells as described in A. Aliquots (40  l) of lysates containing wild-type AcNPV baculovirus (AcNPV), five subunit eIF2B with wild-type (lane 1, GST 1-716) and truncated (lane 2, GST 1-164; lane 3, GST 159-716) GST-eIF2B  fusion proteins were assayed for guanine nucleotide exchange activity, measured as the exchange of [3]GDP bound to eIF2 for nonradiolabeled GDP over time.	bind
9357	1	3841	6	11	NULL	NULL	NULL	GDP	Chemical		bind					eIF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1492_1_56_s_172	10858531	(B) eIF2B activity was analyzed in lysates from infected Sf9 cells as described in A. Aliquots (40  l) of lysates containing wild-type AcNPV baculovirus (AcNPV), five subunit eIF2B with wild-type (lane 1, GST 1-716) and truncated (lane 2, GST 1-164; lane 3, GST 159-716) GST-eIF2B  fusion proteins were assayed for guanine nucleotide exchange activity, measured as the exchange of [3]GDP bound to eIF2 for nonradiolabeled GDP over time.	bind
81642	1	3841	11	NULL	NULL	0	NULL	GDP	NonProteinOrNucleicAcidChemical		binds to 					eIF2	Protein				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1492_1_56_s_172	10858531	(B) eIF2B activity was analyzed in lysates from infected Sf9 cells as described in A. Aliquots (40  l) of lysates containing wild-type AcNPV baculovirus (AcNPV), five subunit eIF2B with wild-type (lane 1, GST 1-716) and truncated (lane 2, GST 1-164; lane 3, GST 159-716) GST-eIF2B  fusion proteins were assayed for guanine nucleotide exchange activity, measured as the exchange of [3]GDP bound to eIF2 for nonradiolabeled GDP over time.	bind
8969	1	3842	5	11	NULL	NULL	NULL	TFIIB	GP		bind							unbent		TBP-TATA box complex	NULL		NULL	NULL	NULL	NULL	gw60_cell_108_5_615_s_202	11893333	(B) Electrophoretic mobility retardation analysis of TFIIB binding to the unbent TBP-TATA box complex.	bind
9364	1	3842	6	11	NULL	NULL	NULL	TFIIB	GP		bind							unbent		TBP-TATA box complex	NULL		NULL	NULL	NULL	NULL	gw60_cell_108_5_615_s_202	11893333	(B) Electrophoretic mobility retardation analysis of TFIIB binding to the unbent TBP-TATA box complex.	bind
81643	1	3842	11	NULL	NULL	0	NULL	TFIIB	GeneOrProtein		binds to 					TBP-TATA box	GeneOrProtein	unbent			NULL		0	NULL	NULL	NULL	gw60_cell_108_5_615_s_202	11893333	(B) Electrophoretic mobility retardation analysis of TFIIB binding to the unbent TBP-TATA box complex.	bind
8970	1	3843	5	11	NULL	NULL	NULL	Atf1pHa	GP		bind					ntp1+	GP			CRE element at promoter	NULL		NULL	NULL	NULL	NULL	gw70_yeast_21_7_593_s_145	15164362	(B) EMSA analysis of Atf1pHa binding to CRE element at  ntp1+ promoter.	bind
9365	1	3843	6	11	NULL	NULL	NULL	Atf1pHa	GP		bind					ntp1+	GP			CRE element of promoter	NULL		NULL	NULL	NULL	NULL	gw70_yeast_21_7_593_s_145	15164362	(B) EMSA analysis of Atf1pHa binding to CRE element at  ntp1+ promoter.	bind
81644	1	3843	11	NULL	NULL	0	NULL	Atf1pHa	GeneOrProtein		binds to 					CRE	Gene			ntp1+ promoter	NULL		0	NULL	NULL	NULL	gw70_yeast_21_7_593_s_145	15164362	(B) EMSA analysis of Atf1pHa binding to CRE element at  ntp1+ promoter.	bind
8971	1	3844	5	11	NULL	NULL	NULL	MEF2C	GP		bind					CRT	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_1_37_s_163	15998798	(B) EMSA analysis of MEF2C binding to the CRT promoter.	bind
9366	1	3844	6	11	NULL	NULL	NULL	MEF2C	GP		bind					CRT	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_1_37_s_163	15998798	(B) EMSA analysis of MEF2C binding to the CRT promoter.	bind
81645	1	3844	11	NULL	NULL	0	NULL	MEF2C	GeneOrProtein		binds to 					CRT	Gene			promoter	NULL		0	NULL	NULL	NULL	gw70_cellbiol_170_1_37_s_163	15998798	(B) EMSA analysis of MEF2C binding to the CRT promoter.	bind
9439	1	3845	5	11	NULL	NULL	NULL	p53	GP		bind					DNA	NucleicAcid				NULL	whole cell extracts from Rb/ ARF E13.5 brains	NULL	NULL	NULL	NULL	gw60_currbiol_12_2_159_s_74	11818069	(B) EMSA demonstrates that  p53 DNA binding activity in whole cell extracts from  Rb/ ARF E13.5 brains using a radiolabeled  p53 consensus binding site oligonucleotide is upregulated (lanes 11 and 12) compared to wild-type controls (lanes 3 and 4) and comparable to levels observed in  Rb mutant samples (lanes 7 and 8).	bind
9367	1	3845	6	11	NULL	NULL	NULL	p53	GP		bind					DNA	NucleicAcid				NULL	whole cell extracts from Rb/ ARF E13.5 brains	NULL	NULL	NULL	NULL	gw60_currbiol_12_2_159_s_74	11818069	(B) EMSA demonstrates that  p53 DNA binding activity in whole cell extracts from  Rb/ ARF E13.5 brains using a radiolabeled  p53 consensus binding site oligonucleotide is upregulated (lanes 11 and 12) compared to wild-type controls (lanes 3 and 4) and comparable to levels observed in  Rb mutant samples (lanes 7 and 8).	bind
8972	1	3846	5	11	NULL	NULL	NULL	DAF-16	GP		bind		specifically			daf-15 	GP			IRS	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_131_16_3897_s_201	15253933	(B) EMSA indicates DAF-16 binds specifically to the  daf-15 IRS in vitro (see text).	bind
9368	1	3846	6	11	NULL	NULL	NULL	DAF-16	GP		bind		specifically			daf-15	GP			IRS	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_131_16_3897_s_201	15253933	(B) EMSA indicates DAF-16 binds specifically to the  daf-15 IRS in vitro (see text).	bind
81646	1	3846	11	NULL	NULL	0	NULL	DAF-16	GeneOrProtein		binds to 					daf-15 IRS	GeneOrProtein				NULL	in vitro	0	NULL	NULL	NULL	gw70_development_131_16_3897_s_201	15253933	(B) EMSA indicates DAF-16 binds specifically to the  daf-15 IRS in vitro (see text).	bind
8973	1	3849	5	11	NULL	NULL	NULL	GRBP	GP	purified;; cytosolic	bind					DNA	NucleicAcid			GRE	NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1624_1_29_s_151	14642810	(B) EMSA of purified cytosolic GRBP and expressed  Translin binding to GRE (MLTF-like site) DNA.	bind
8974	2	3849	5	11	NULL	NULL	NULL	Translin	GP	expressed	bind					DNA	NucleicAcid			GRE	NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1624_1_29_s_151	14642810	(B) EMSA of purified cytosolic GRBP and expressed  Translin binding to GRE (MLTF-like site) DNA.	bind
53648	3	3849	5	11	NULL	NULL	NULL	GRE	GP		is					MLTF-like site	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1624_1_29_s_151	14642810	(B) EMSA of purified cytosolic GRBP and expressed  Translin binding to GRE (MLTF-like site) DNA.	bind
9369	1	3849	6	11	NULL	NULL	NULL	GRBP	GP	purified;; cytosolic	bind					DNA	NucleicAcid			GRE	NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1624_1_29_s_151	14642810	(B) EMSA of purified cytosolic GRBP and expressed  Translin binding to GRE (MLTF-like site) DNA.	bind
9370	2	3849	6	11	NULL	NULL	NULL	translin	GP		bind					DNA	NucleicAcid			GRE	NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1624_1_29_s_151	14642810	(B) EMSA of purified cytosolic GRBP and expressed  Translin binding to GRE (MLTF-like site) DNA.	bind
9371	3	3849	6	11	NULL	NULL	NULL	GRE	GP		is					MLTF-like site	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1624_1_29_s_151	14642810	(B) EMSA of purified cytosolic GRBP and expressed  Translin binding to GRE (MLTF-like site) DNA.	bind
8975	1	3850	5	11	NULL	NULL	NULL	Stat5	GP		bind					BCL-X gene	GP	human		BCL-X(-316 to -346)	NULL		NULL	NULL	NULL	NULL	gw60_cell_98_2_181_s_112	10428030	(B) EMSA showing  Stat5 binding to  BCL-X(-316 to -346) from the human  BCL-X gene.	bind
9372	1	3850	6	11	NULL	NULL	NULL	Stat5	GP		bind					BCL-X gene	GP	human		BCL-X(-316 to -346)	NULL		NULL	NULL	NULL	NULL	gw60_cell_98_2_181_s_112	10428030	(B) EMSA showing  Stat5 binding to  BCL-X(-316 to -346) from the human  BCL-X gene.	bind
8976	1	3851	5	11	NULL	NULL	NULL	MSY2	GP		bind					Prm1	GP	wt		1-37	NULL	testis extracts	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_7010_s_253	11564883	(B) EMSA with testis extracts showing the binding of MSY2 and MSY4 to  Prm11-37wt but not to the mutant version used in the transgene.	bind
8977	2	3851	5	11	NULL	NULL	NULL	MSY4	GP		bind					Prm1	GP	wt		1-37	NULL	testis extracts	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_7010_s_253	11564883	(B) EMSA with testis extracts showing the binding of MSY2 and MSY4 to  Prm11-37wt but not to the mutant version used in the transgene.	bind
8978	3	3851	5	11	NULL	NULL	NULL	MSY2	GP		does not bind					Prm1	GP	mutant		1-37	NULL	testis extracts	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_7010_s_253	11564883	(B) EMSA with testis extracts showing the binding of MSY2 and MSY4 to  Prm11-37wt but not to the mutant version used in the transgene.	bind
8979	4	3851	5	11	NULL	NULL	NULL	MSY4	GP		does not bind					Prm1	GP	mutant		1-37	NULL	testis extracts	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_7010_s_253	11564883	(B) EMSA with testis extracts showing the binding of MSY2 and MSY4 to  Prm11-37wt but not to the mutant version used in the transgene.	bind
9373	1	3851	6	11	NULL	NULL	NULL	MSY2	GP		bind					Prm1	GP	wild type		1-37	NULL	testis extracts	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_7010_s_253	11564883	(B) EMSA with testis extracts showing the binding of MSY2 and MSY4 to  Prm11-37wt but not to the mutant version used in the transgene.	bind
9374	2	3851	6	11	NULL	NULL	NULL	MSY4	GP		bind					Prm1	GP	wild type		1-37	NULL	testis extracts	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_7010_s_253	11564883	(B) EMSA with testis extracts showing the binding of MSY2 and MSY4 to  Prm11-37wt but not to the mutant version used in the transgene.	bind
9375	3	3851	6	11	NULL	NULL	NULL	MSY2	GP		does not bind					Prm1	GP	mutant		1-37	NULL	testis extracts	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_7010_s_253	11564883	(B) EMSA with testis extracts showing the binding of MSY2 and MSY4 to  Prm11-37wt but not to the mutant version used in the transgene.	bind
9376	4	3851	6	11	NULL	NULL	NULL	MSY4	GP		does not bind					Prm1	GP	mutant		1-37	NULL	testis extracts	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_7010_s_253	11564883	(B) EMSA with testis extracts showing the binding of MSY2 and MSY4 to  Prm11-37wt but not to the mutant version used in the transgene.	bind
9111	1	3853	5	11	NULL	NULL	NULL	Galphas	GP	endogenous;; rat brain lysates	bind					GST-Hrs	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5538_s_159	15469987	(B) Endogenous Galphas from rat brain lysates binds to GST-Hrs but not to GST.	bind
9112	2	3853	5	11	NULL	NULL	NULL	Galphas	GP	endogenous;; rat brain lysates	does not bind					GST	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5538_s_159	15469987	(B) Endogenous Galphas from rat brain lysates binds to GST-Hrs but not to GST.	bind
9377	1	3853	6	11	NULL	NULL	NULL	Galphas	GP	endogenous;; rat brain lysates	bind					GST-Hrs	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5538_s_159	15469987	(B) Endogenous Galphas from rat brain lysates binds to GST-Hrs but not to GST.	bind
9378	2	3853	6	11	NULL	NULL	NULL	Galphas	GP	endogenous;; rat brain lysates	does not bind					GST	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5538_s_159	15469987	(B) Endogenous Galphas from rat brain lysates binds to GST-Hrs but not to GST.	bind
9113	1	3854	5	NULL	NULL	0	NULL	Smad7	NULL	endogenous	bind	NULL				p38	NULL	phosphorylated			NULL	in vivo	0	NULL	NULL	NULL	gw60_molbiolcell_14_2_529_s_245	12589052	(B) Endogenous Smad7 binds to phosphorylated p38 in vivo.	bind
9379	1	3854	6	NULL	NULL	0	NULL	Smad7	NULL	endogenous	bind	NULL				p38	NULL	phosphorylated			NULL	in vivo	0	NULL	NULL	NULL	gw60_molbiolcell_14_2_529_s_245	12589052	(B) Endogenous Smad7 binds to phosphorylated p38 in vivo.	bind
9114	1	3855	5	11	NULL	NULL	NULL	Nrf2	GP		bind					PSMB5	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8786_s_182	14612418	(B) Enhanced binding of Nrf2 to the  PSMB5 promoter following sulforaphane (Sul) treatment compared to that in vehicle (V)-treated  cells.	bind
9115	2	3855	5	11	NULL	NULL	NULL	Nrf2	GP		bind					PSMB5	GP			promoter	NULL	in vehicle (V)-treated cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8786_s_182	14612418	(B) Enhanced binding of Nrf2 to the  PSMB5 promoter following sulforaphane (Sul) treatment compared to that in vehicle (V)-treated  cells.	bind
9116	3	3855	5	11	NULL	NULL	NULL	Sul	Chemical	treatment with	enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8786_s_182	14612418	(B) Enhanced binding of Nrf2 to the  PSMB5 promoter following sulforaphane (Sul) treatment compared to that in vehicle (V)-treated  cells.	bind
53649	4	3855	5	11	NULL	NULL	NULL	Sul	Chemical		is					sulforaphane	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8786_s_182	14612418	(B) Enhanced binding of Nrf2 to the  PSMB5 promoter following sulforaphane (Sul) treatment compared to that in vehicle (V)-treated  cells.	bind
9380	1	3855	6	11	NULL	NULL	NULL	Nrf2	GP		bind					PSMB5	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8786_s_182	14612418	(B) Enhanced binding of Nrf2 to the  PSMB5 promoter following sulforaphane (Sul) treatment compared to that in vehicle (V)-treated  cells.	bind
9381	2	3855	6	11	NULL	NULL	NULL	statement 1	Process		occurs following					Sul	Chemical	treatment with			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8786_s_182	14612418	(B) Enhanced binding of Nrf2 to the  PSMB5 promoter following sulforaphane (Sul) treatment compared to that in vehicle (V)-treated  cells.	bind
9382	3	3855	6	11	NULL	NULL	NULL	Nrf2	GP		bind					PSMB5	GP			promoter	NULL	vehicle (V)-treated cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8786_s_182	14612418	(B) Enhanced binding of Nrf2 to the  PSMB5 promoter following sulforaphane (Sul) treatment compared to that in vehicle (V)-treated  cells.	bind
53650	4	3855	6	11	NULL	NULL	NULL	Sul	Chemical		is					sulforaphane	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8786_s_182	14612418	(B) Enhanced binding of Nrf2 to the  PSMB5 promoter following sulforaphane (Sul) treatment compared to that in vehicle (V)-treated  cells.	bind
9117	1	3856	5	11	NULL	NULL	NULL	GR	GP		bind					MMTV chromatin 	Chromosome				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3255_s_73	11971959	(B) Enhancement of GR binding to MMTV chromatin by HeLa nuclear extract.	bind
9118	2	3856	5	11	NULL	NULL	NULL	HeLa nuclear extract	CellComponent		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3255_s_73	11971959	(B) Enhancement of GR binding to MMTV chromatin by HeLa nuclear extract.	bind
9383	1	3856	6	11	NULL	NULL	NULL	GR	GP		bind					MMTV chromatin	Chromosome				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3255_s_73	11971959	(B) Enhancement of GR binding to MMTV chromatin by HeLa nuclear extract.	bind
9384	2	3856	6	11	NULL	NULL	NULL	HeLa nuclear extract	CellComponent		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3255_s_73	11971959	(B) Enhancement of GR binding to MMTV chromatin by HeLa nuclear extract.	bind
9119	1	3857	5	11	NULL	NULL	NULL	Ephrin-B1-Fc	GP		bind		specifically			neural crest cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_8_571_s_159	9259560	(b) Ephrin-B1-Fc bound specifically to neural crest cells, indicating that receptor expression was maintained  in vitro.	bind
9120	2	3857	5	11	NULL	NULL	NULL	statement 1	Process		indicate					maintained receptor expression 	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_currbiol_7_8_571_s_159	9259560	(b) Ephrin-B1-Fc bound specifically to neural crest cells, indicating that receptor expression was maintained  in vitro.	bind
9385	1	3857	6	11	NULL	NULL	NULL	Ephrin-B1-Fc	GP		bind		specifically			neural crest cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_8_571_s_159	9259560	(b) Ephrin-B1-Fc bound specifically to neural crest cells, indicating that receptor expression was maintained  in vitro.	bind
11651	2	3857	6	11	NULL	NULL	NULL	statement 1	Process		indicates					maintained receptor expression	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_currbiol_7_8_571_s_159	9259560	(b) Ephrin-B1-Fc bound specifically to neural crest cells, indicating that receptor expression was maintained  in vitro.	bind
9121	1	3860	5	11	NULL	NULL	NULL	P6EtG/HLA-A2	GP		bind					A6	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_4_475_s_110	11070166	(B) Equilibrium binding data for P6EtG/HLA-A2 binding to A6.	bind
9387	1	3860	6	11	NULL	NULL	NULL	P6EtG/HLA-A2	GP		bind					A6	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_4_475_s_110	11070166	(B) Equilibrium binding data for P6EtG/HLA-A2 binding to A6.	bind
9447	1	3861	5	11	NULL	NULL	NULL	ER	Chemical		does not bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_1_97_s_157	15240572	(B) ER and LG3 do not bind to an analytical heparin-agarose column.	bind
9448	2	3861	5	11	NULL	NULL	NULL	LG3	GP		does not bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_1_97_s_157	15240572	(B) ER and LG3 do not bind to an analytical heparin-agarose column.	bind
9388	1	3861	6	11	NULL	NULL	NULL	ER	Chemical		does not bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_1_97_s_157	15240572	(B) ER and LG3 do not bind to an analytical heparin-agarose column.	bind
9389	2	3861	6	11	NULL	NULL	NULL	LG3	GP		does not bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_1_97_s_157	15240572	(B) ER and LG3 do not bind to an analytical heparin-agarose column.	bind
9122	1	3862	5	11	NULL	NULL	NULL	ER-E2F3	GP		bind							E2F-responsive		promoters	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_7_2660_s_209	15767672	(B) ER-E2F3 binds to E2F-responsive promoters  and recruits pRB upon activation.	bind
9123	2	3862	5	11	NULL	NULL	NULL	ER-E2F3	GP	activated	recruit					pRB	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_7_2660_s_209	15767672	(B) ER-E2F3 binds to E2F-responsive promoters  and recruits pRB upon activation.	bind
9390	1	3862	6	11	NULL	NULL	NULL	ER-E2F3	GP		bind							E2F responsive		promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_7_2660_s_209	15767672	(B) ER-E2F3 binds to E2F-responsive promoters  and recruits pRB upon activation.	bind
9391	2	3862	6	11	NULL	NULL	NULL	ER-E2F3	GP	activated	recruits					pRB	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_7_2660_s_209	15767672	(B) ER-E2F3 binds to E2F-responsive promoters  and recruits pRB upon activation.	bind
9125	1	3863	5	11	NULL	NULL	NULL	ERalpha	GP		bind					hTERT	GP			ERE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3764_s_83	10805720	(b) ERalpha binding to the hTERT ERE.	bind
9392	1	3863	6	11	NULL	NULL	NULL	ERalpha	GP		bind					hTERT	GP			ERE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3764_s_83	10805720	(b) ERalpha binding to the hTERT ERE.	bind
9126	1	3864	5	10	NULL	0	NULL	ERKs	NULL		does not bind	NULL				Mxi2	NULL	mutant	 WI		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_9_3079_s_299	12697810	(B) ERKs cannot bind to the Mxi2 WI mutant form.	bind
9393	1	3864	6	11	NULL	NULL	NULL	ERK	GP		does not bind					Mxi2	GP	mutant	WI		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_9_3079_s_299	12697810	(B) ERKs cannot bind to the Mxi2 WI mutant form.	bind
9127	1	3865	5	11	NULL	NULL	NULL	ETO-2	GP		bind					HDAC1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_172	11533236	(B) ETO-2 binds HDACs 1, 2, 3, 6, and 8.	bind
9128	2	3865	5	11	NULL	NULL	NULL	ETO-2	GP		bind					HDAC2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_172	11533236	(B) ETO-2 binds HDACs 1, 2, 3, 6, and 8.	bind
9129	3	3865	5	11	NULL	NULL	NULL	ETO-2	GP		bind					HDAC3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_172	11533236	(B) ETO-2 binds HDACs 1, 2, 3, 6, and 8.	bind
9130	4	3865	5	11	NULL	NULL	NULL	ETO-2	GP		bind					HDAC6	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_172	11533236	(B) ETO-2 binds HDACs 1, 2, 3, 6, and 8.	bind
9131	5	3865	5	11	NULL	NULL	NULL	ETO-2	GP		bind					HDAC8	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_172	11533236	(B) ETO-2 binds HDACs 1, 2, 3, 6, and 8.	bind
9394	1	3865	6	11	NULL	NULL	NULL	ETO-2	GP		bind					HDAC1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_172	11533236	(B) ETO-2 binds HDACs 1, 2, 3, 6, and 8.	bind
9395	2	3865	6	11	NULL	NULL	NULL	ETO-2	GP		bind					HDAC2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_172	11533236	(B) ETO-2 binds HDACs 1, 2, 3, 6, and 8.	bind
9396	3	3865	6	11	NULL	NULL	NULL	ETO-2	GP		bind					HDAC3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_172	11533236	(B) ETO-2 binds HDACs 1, 2, 3, 6, and 8.	bind
9397	4	3865	6	11	NULL	NULL	NULL	ETO-2	GP		bind					HDAC6	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_172	11533236	(B) ETO-2 binds HDACs 1, 2, 3, 6, and 8.	bind
9398	5	3865	6	11	NULL	NULL	NULL	ETO-2	GP		bind					HDAC8	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_172	11533236	(B) ETO-2 binds HDACs 1, 2, 3, 6, and 8.	bind
9442	1	3866	5	11	NULL	NULL	NULL	MyoD	GP		direct					MyHC 	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6600_s_196	10938134	(B) Even though cain cotransfection blocks MyoD-directed MyHC expression, these cells still express myogenin, suggesting no loss of transfected cells or in their respecification to the myogenic lineage.	bind
9443	2	3866	5	11	NULL	NULL	NULL	cain	GP	transfection	blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6600_s_196	10938134	(B) Even though cain cotransfection blocks MyoD-directed MyHC expression, these cells still express myogenin, suggesting no loss of transfected cells or in their respecification to the myogenic lineage.	bind
9444	3	3866	5	11	NULL	NULL	NULL	cells	cell		express					myogenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6600_s_196	10938134	(B) Even though cain cotransfection blocks MyoD-directed MyHC expression, these cells still express myogenin, suggesting no loss of transfected cells or in their respecification to the myogenic lineage.	bind
9445	4	3866	5	11	NULL	NULL	NULL	statement 3	Process		suggest					 transfected cells	Cell	 no loss of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6600_s_196	10938134	(B) Even though cain cotransfection blocks MyoD-directed MyHC expression, these cells still express myogenin, suggesting no loss of transfected cells or in their respecification to the myogenic lineage.	bind
9446	5	3866	5	11	NULL	NULL	NULL	statement 3	Process		suggest					myogenic lineage	Cell	respecification to			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6600_s_196	10938134	(B) Even though cain cotransfection blocks MyoD-directed MyHC expression, these cells still express myogenin, suggesting no loss of transfected cells or in their respecification to the myogenic lineage.	bind
9670	1	3866	6	11	NULL	NULL	NULL	MyoD-	GP		directs					MyHC	GP	expression of 			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6600_s_196	10938134	(B) Even though cain cotransfection blocks MyoD-directed MyHC expression, these cells still express myogenin, suggesting no loss of transfected cells or in their respecification to the myogenic lineage.	bind
9671	2	3866	6	11	NULL	NULL	NULL	cain	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6600_s_196	10938134	(B) Even though cain cotransfection blocks MyoD-directed MyHC expression, these cells still express myogenin, suggesting no loss of transfected cells or in their respecification to the myogenic lineage.	bind
9132	1	3868	5	11	NULL	NULL	NULL	Exip	GP		bind					IRAK	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_575_1_136_s_124	15388348	(B) Exip binds to IRAK.	bind
9399	1	3868	6	11	NULL	NULL	NULL	Exip	GP		bind					IRAK	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_575_1_136_s_124	15388348	(B) Exip binds to IRAK.	bind
9133	1	3869	5	11	NULL	NULL	NULL	Exip	GP		bind					Tollip	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_575_1_136_s_111	15388348	(B) Exip binds to Tollip irrespective to IL-1  stimulation.	bind
9134	2	3869	5	11	NULL	NULL	NULL	statement 1	Process		irrespective to					IL-1	GP	stimulation of			NULL		NULL	NULL	NULL	NULL	gw70_febslett_575_1_136_s_111	15388348	(B) Exip binds to Tollip irrespective to IL-1  stimulation.	bind
9400	1	3869	6	11	NULL	NULL	NULL	Exip	GP		bind					Tollip	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_575_1_136_s_111	15388348	(B) Exip binds to Tollip irrespective to IL-1  stimulation.	bind
11652	2	3869	6	11	NULL	NULL	NULL	statement 1	GP		irrespective to					IL-1	GP	stimulation of 			NULL		NULL	NULL	NULL	NULL	gw70_febslett_575_1_136_s_111	15388348	(B) Exip binds to Tollip irrespective to IL-1  stimulation.	bind
9135	1	3870	5	11	NULL	NULL	NULL	NGFI-B/RXR	GP		bind					DR1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_6_849_s_260	9660968	(B) Expected role of NGFI-B's 5  flanking sequence in NGFI-B/RXR binding to DR1-DR5.	bind
9136	2	3870	5	11	NULL	NULL	NULL	NGFI-B/RXR	GP		bind					DR2	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_6_849_s_260	9660968	(B) Expected role of NGFI-B's 5  flanking sequence in NGFI-B/RXR binding to DR1-DR5.	bind
9137	3	3870	5	11	NULL	NULL	NULL	NGFI-B/RXR	GP		bind					DR3	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_6_849_s_260	9660968	(B) Expected role of NGFI-B's 5  flanking sequence in NGFI-B/RXR binding to DR1-DR5.	bind
9138	4	3870	5	11	NULL	NULL	NULL	NGFI-B/RXR	GP		bind					DR4	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_6_849_s_260	9660968	(B) Expected role of NGFI-B's 5  flanking sequence in NGFI-B/RXR binding to DR1-DR5.	bind
9139	5	3870	5	11	NULL	NULL	NULL	NGFI-B/RXR	GP		bind					DR5	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_6_849_s_260	9660968	(B) Expected role of NGFI-B's 5  flanking sequence in NGFI-B/RXR binding to DR1-DR5.	bind
9401	1	3870	6	11	NULL	NULL	NULL	NGFI-B/RXR	GP		bind					DR1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_6_849_s_260	9660968	(B) Expected role of NGFI-B's 5  flanking sequence in NGFI-B/RXR binding to DR1-DR5.	bind
44775	2	3870	6	11	NULL	NULL	NULL	NGFI-B/RXR	GP		bind					DR2	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_6_849_s_260	9660968	(B) Expected role of NGFI-B's 5  flanking sequence in NGFI-B/RXR binding to DR1-DR5.	bind
44776	3	3870	6	11	NULL	NULL	NULL	NGFI-B/RXR	GP		bind					DR3	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_6_849_s_260	9660968	(B) Expected role of NGFI-B's 5  flanking sequence in NGFI-B/RXR binding to DR1-DR5.	bind
44777	4	3870	6	11	NULL	NULL	NULL	NGFI-B/RXR	GP		bind					DR4	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_6_849_s_260	9660968	(B) Expected role of NGFI-B's 5  flanking sequence in NGFI-B/RXR binding to DR1-DR5.	bind
44778	5	3870	6	11	NULL	NULL	NULL	NGFI-B/RXR	GP		bind					DR5	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_6_849_s_260	9660968	(B) Expected role of NGFI-B's 5  flanking sequence in NGFI-B/RXR binding to DR1-DR5.	bind
9140	1	3871	5	11	NULL	NULL	NULL	AKAP79	GP	wt	bind					RII	GP				NULL	in stable cells	NULL	NULL	NULL	NULL	gw60_neuron_19_1_185_s_51	9247274	(B) Expression and RII binding properties of AKAP79wt and AKAP79pro in the stable cells.	bind
9141	2	3871	5	11	NULL	NULL	NULL	AKAP79	GP	pro	bind					RII	GP				NULL	in stable cells	NULL	NULL	NULL	NULL	gw60_neuron_19_1_185_s_51	9247274	(B) Expression and RII binding properties of AKAP79wt and AKAP79pro in the stable cells.	bind
9402	1	3871	6	11	NULL	NULL	NULL	AKAP79	GP	wild type	bind					RII	GP				NULL	stable cells	NULL	NULL	NULL	NULL	gw60_neuron_19_1_185_s_51	9247274	(B) Expression and RII binding properties of AKAP79wt and AKAP79pro in the stable cells.	bind
9403	2	3871	6	11	NULL	NULL	NULL	AKAP79	GP	pro	bind					RII	GP				NULL	stable cells	NULL	NULL	NULL	NULL	gw60_neuron_19_1_185_s_51	9247274	(B) Expression and RII binding properties of AKAP79wt and AKAP79pro in the stable cells.	bind
9211	1	3873	5	11	NULL	NULL	NULL	GRIP1	GP		bind		specifically			liprin-4	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_neuron_34_1_39_s_45	11931740	(B) Filter overlay assay showing specific in vitro binding between GRIP1 and liprin- 4.	bind
9404	1	3873	6	11	NULL	NULL	NULL	GRIP1	GP		bind		specifically			liprin-4	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_neuron_34_1_39_s_45	11931740	(B) Filter overlay assay showing specific in vitro binding between GRIP1 and liprin- 4.	bind
9212	1	3874	5	11	NULL	NULL	NULL	Fli1	GP		bind					SCL	GP			+19 core enhancer	NULL	in blood cell lines	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_7_2615_s_203	16537906	(B) Fli1, Elf1, and GATA2 bind the SCL +19 core enhancer in  both blood and bone cell lines.	bind
9213	2	3874	5	11	NULL	NULL	NULL	Fli1	GP		bind					SCL	GP			+19 core enhancer	NULL	in bone cell lines	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_7_2615_s_203	16537906	(B) Fli1, Elf1, and GATA2 bind the SCL +19 core enhancer in  both blood and bone cell lines.	bind
9215	4	3874	5	11	NULL	NULL	NULL	Elf1	GP		bind					SCL	GP			+19 core enhancer	NULL	in bone cell lines	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_7_2615_s_203	16537906	(B) Fli1, Elf1, and GATA2 bind the SCL +19 core enhancer in  both blood and bone cell lines.	bind
9216	5	3874	5	11	NULL	NULL	NULL	GATA2	GP		bind					SCL	GP			+19 core enhancer	NULL	in blood cell lines	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_7_2615_s_203	16537906	(B) Fli1, Elf1, and GATA2 bind the SCL +19 core enhancer in  both blood and bone cell lines.	bind
9217	6	3874	5	11	NULL	NULL	NULL	GATA2	GP		bind					SCL	GP			+19 core enhancer	NULL	in bone cell lines	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_7_2615_s_203	16537906	(B) Fli1, Elf1, and GATA2 bind the SCL +19 core enhancer in  both blood and bone cell lines.	bind
9405	1	3874	6	11	NULL	NULL	NULL	Fli1	GP		bind					SCL	GP			+19 core enhancer	NULL	blood cell lines	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_7_2615_s_203	16537906	(B) Fli1, Elf1, and GATA2 bind the SCL +19 core enhancer in  both blood and bone cell lines.	bind
9406	2	3874	6	11	NULL	NULL	NULL	Elf1	GP		bind					SCL 	GP			+19 core enhancer	NULL	blood cell lines	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_7_2615_s_203	16537906	(B) Fli1, Elf1, and GATA2 bind the SCL +19 core enhancer in  both blood and bone cell lines.	bind
9407	3	3874	6	11	NULL	NULL	NULL	GATA2	GP		bind					SCL 	GP			+19 core enhancer	NULL	blood cell lines	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_7_2615_s_203	16537906	(B) Fli1, Elf1, and GATA2 bind the SCL +19 core enhancer in  both blood and bone cell lines.	bind
11653	4	3874	6	11	NULL	NULL	NULL	Fli1	GP		bind					SCL	GP			+19 core enhancer	NULL	bone cell line	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_7_2615_s_203	16537906	(B) Fli1, Elf1, and GATA2 bind the SCL +19 core enhancer in  both blood and bone cell lines.	bind
11654	5	3874	6	11	NULL	NULL	NULL	Elf1	GP		bind					SCL	GP			+19 core enhancer	NULL	bone cell line	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_7_2615_s_203	16537906	(B) Fli1, Elf1, and GATA2 bind the SCL +19 core enhancer in  both blood and bone cell lines.	bind
11655	6	3874	6	11	NULL	NULL	NULL	GATA-2	GP		bind					SCL	GP			+19 core enhancer	NULL	bone cell line	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_7_2615_s_203	16537906	(B) Fli1, Elf1, and GATA2 bind the SCL +19 core enhancer in  both blood and bone cell lines.	bind
9218	1	3875	5	11	NULL	NULL	NULL	BLyS	GP		bind					 B cells	Cell	splenic			NULL		NULL	NULL	NULL	NULL	gw60_immunity_14_5_573_s_108	11371359	(B) Flow cytometric analysis of BLyS binding to splenic B cells.	bind
9408	1	3875	6	11	NULL	NULL	NULL	BLyS	GP		bind					B cells	Cell	splenic			NULL		NULL	NULL	NULL	NULL	gw60_immunity_14_5_573_s_108	11371359	(B) Flow cytometric analysis of BLyS binding to splenic B cells.	bind
9214	3	3876	5	11	NULL	NULL	NULL	Elf1	GP		bind					SCL	GP			+19 core enhancer	NULL	in blood cell lines	NULL	NULL	NULL	NULL	gw60_neuron_37_4_555_s_36	12597853	(B) FMRP binds to CYFIP, which interacts directly with F-actin.	bind
9219	1	3876	5	11	NULL	NULL	NULL	FMRP	GP		bind					CYFIP	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_37_4_555_s_36	12597853	(B) FMRP binds to CYFIP, which interacts directly with F-actin.	bind
9220	2	3876	5	11	NULL	NULL	NULL	CYFIP	GP		interact with		directly			F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_37_4_555_s_36	12597853	(B) FMRP binds to CYFIP, which interacts directly with F-actin.	bind
9409	1	3876	6	11	NULL	NULL	NULL	FMRP	GP		bind					CYFIP	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_37_4_555_s_36	12597853	(B) FMRP binds to CYFIP, which interacts directly with F-actin.	bind
9410	2	3876	6	11	NULL	NULL	NULL	CYFIP	GP		interacts		directly			F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_37_4_555_s_36	12597853	(B) FMRP binds to CYFIP, which interacts directly with F-actin.	bind
9221	1	3877	5	11	NULL	NULL	NULL	xUBF	GP		bind							Xenopus		core promoter region	NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_5_1059_s_160	11106745	(B) Footprint analysis of xUBF bound to the  Xenopus core promoter region.	bind
9411	1	3877	6	11	NULL	NULL	NULL	xUBF	GP		bind							Xenopus 		core promoter region	NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_5_1059_s_160	11106745	(B) Footprint analysis of xUBF bound to the  Xenopus core promoter region.	bind
9222	1	3878	5	11	NULL	NULL	NULL	Mpc54p-GFP components	GP		bind					SPBs	CellComponent				NULL	in wild-type cells in meiosis II	NULL	NULL	NULL	NULL	gw70_cellbiol_171_4_627_s_148	16286509	(B) FRAP analysis of the binding of Mpc54p-GFP components to SPBs in wild-type cells  in meiosis II.	bind
9412	1	3878	6	11	NULL	NULL	NULL	Mpc54p-GFP	GP		bind					SPBs	CellComponent				NULL	wild-type cells in meiosis II	NULL	NULL	NULL	NULL	gw70_cellbiol_171_4_627_s_148	16286509	(B) FRAP analysis of the binding of Mpc54p-GFP components to SPBs in wild-type cells  in meiosis II.	bind
9223	1	3879	5	11	NULL	NULL	NULL	FRS2alpha	GP		bind					TrkA	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_979_s_238	10629055	(B) FRS2alpha binds to tyrosine-phosphorylated TrkA.	bind
9413	1	3879	6	11	NULL	NULL	NULL	FRS2alpha	GP		bind					TrkA	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_979_s_238	10629055	(B) FRS2alpha binds to tyrosine-phosphorylated TrkA.	bind
9224	1	3880	5	11	NULL	NULL	NULL	GFP-Crz1p		full-length	bind		constitutively	S409		importin Nmd5p	GP				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_3_5_1147_s_197	15470242	(B) Full-length GFP-Crz1pS409,410,423A constitutively binds the importin Nmd5p.	bind
9225	2	3880	5	11	NULL	NULL	NULL	GFP-Crz1p	GP	full-length	bind		constitutively	S410		importin Nmd5p	GP				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_3_5_1147_s_197	15470242	(B) Full-length GFP-Crz1pS409,410,423A constitutively binds the importin Nmd5p.	bind
9226	3	3880	5	11	NULL	NULL	NULL	GFP-Crz1p	GP	full-length	bind		constitutively	S423A		importin Nmd5p	GP				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_3_5_1147_s_197	15470242	(B) Full-length GFP-Crz1pS409,410,423A constitutively binds the importin Nmd5p.	bind
9417	1	3880	6	11	NULL	NULL	NULL	GFP-Crz1p	GP	full length	bind		constitutively	S409		importin Nmd5p	GP				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_3_5_1147_s_197	15470242	(B) Full-length GFP-Crz1pS409,410,423A constitutively binds the importin Nmd5p.	bind
9418	2	3880	6	11	NULL	NULL	NULL	GFP-Crz1p	GP	full length	bind		constitutively	S410		importin Nmd5p	GP				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_3_5_1147_s_197	15470242	(B) Full-length GFP-Crz1pS409,410,423A constitutively binds the importin Nmd5p.	bind
9419	3	3880	6	11	NULL	NULL	NULL	GFP-Crz1p	GP	full length	bind		constitutively	S423A		importin Nmd5p	GP				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_3_5_1147_s_197	15470242	(B) Full-length GFP-Crz1pS409,410,423A constitutively binds the importin Nmd5p.	bind
9227	1	3882	5	11	NULL	NULL	NULL	FUS3	GP		bind					At2S3	GP			RY-G-box complex in promoter	NULL		NULL	NULL	NULL	NULL	gw70_development_130_24_6065_s_100	14597573	(B) FUS3 and LEC2 bind to the  RY-G-box complex in the  At2S3 promoter.	bind
9228	2	3882	5	11	NULL	NULL	NULL	LEC2	GP		bind					At2S3	GP			RY-G-box complex in promoter	NULL		NULL	NULL	NULL	NULL	gw70_development_130_24_6065_s_100	14597573	(B) FUS3 and LEC2 bind to the  RY-G-box complex in the  At2S3 promoter.	bind
9420	1	3882	6	11	NULL	NULL	NULL	FUS3	GP		bind					At2S3	GP			RY-G-box complex of the promoter	NULL		NULL	NULL	NULL	NULL	gw70_development_130_24_6065_s_100	14597573	(B) FUS3 and LEC2 bind to the  RY-G-box complex in the  At2S3 promoter.	bind
9421	2	3882	6	11	NULL	NULL	NULL	LEC2	GP		bind					At2S3	GP			RY-G-box complex of the promoter	NULL		NULL	NULL	NULL	NULL	gw70_development_130_24_6065_s_100	14597573	(B) FUS3 and LEC2 bind to the  RY-G-box complex in the  At2S3 promoter.	bind
9229	1	3883	5	11	NULL	NULL	NULL	Gads/Grb2	GP		bind					SLP-76	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_7_2515_s_241	12640133	(B) Gab2 competes for  Gads/Grb2 binding with SLP-76.	bind
9230	2	3883	5	11	NULL	NULL	NULL	Gab2	GP		bind					SLP-76	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_7_2515_s_241	12640133	(B) Gab2 competes for  Gads/Grb2 binding with SLP-76.	bind
9231	3	3883	5	11	NULL	NULL	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_7_2515_s_241	12640133	(B) Gab2 competes for  Gads/Grb2 binding with SLP-76.	bind
9625	1	3883	6	11	NULL	NULL	NULL	Gads/Grb2	GP		bind					SLP-76	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_7_2515_s_241	12640133	(B) Gab2 competes for  Gads/Grb2 binding with SLP-76.	bind
9626	2	3883	6	11	NULL	NULL	NULL	Gab2	GP		bind					SLP-76	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_7_2515_s_241	12640133	(B) Gab2 competes for  Gads/Grb2 binding with SLP-76.	bind
9627	3	3883	6	11	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_7_2515_s_241	12640133	(B) Gab2 competes for  Gads/Grb2 binding with SLP-76.	bind
9232	1	3884	5	11	NULL	NULL	NULL	Gads/Grb2	GP		bind					SLP-76	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_7_2515_s_241	12640133	(B) Gab2 competes for Gads/Grb2 binding with SLP-76.	bind
9233	2	3884	5	11	NULL	NULL	NULL	Gab2	GP		bind					SLP-76	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_7_2515_s_241	12640133	(B) Gab2 competes for Gads/Grb2 binding with SLP-76.	bind
9234	3	3884	5	11	NULL	NULL	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_7_2515_s_241	12640133	(B) Gab2 competes for Gads/Grb2 binding with SLP-76.	bind
9659	1	3884	6	11	NULL	NULL	NULL	Gads/Grb2	GP		bind					SLP-76	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_7_2515_s_241	12640133	(B) Gab2 competes for Gads/Grb2 binding with SLP-76.	bind
9660	2	3884	6	11	NULL	NULL	NULL	Gab2	GP		bind					SLP-76	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_7_2515_s_241	12640133	(B) Gab2 competes for Gads/Grb2 binding with SLP-76.	bind
9661	3	3884	6	11	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_7_2515_s_241	12640133	(B) Gab2 competes for Gads/Grb2 binding with SLP-76.	bind
9235	1	3885	5	11	NULL	NULL	NULL	trypomastigote	Organism	T. cruzi	bind					CASM cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_11_6717_s_47	15501810	(B) Galectin-3 enhances  T. cruzi trypomastigote binding to human CASM cells.	bind
9236	2	3885	5	11	NULL	NULL	NULL	Galectin-3	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_11_6717_s_47	15501810	(B) Galectin-3 enhances  T. cruzi trypomastigote binding to human CASM cells.	bind
9422	1	3885	6	11	NULL	NULL	NULL	trypomastigote	Organism	T. cruzi	bind					CASM cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_11_6717_s_47	15501810	(B) Galectin-3 enhances  T. cruzi trypomastigote binding to human CASM cells.	bind
9423	2	3885	6	11	NULL	NULL	NULL	Galectin-3	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_11_6717_s_47	15501810	(B) Galectin-3 enhances  T. cruzi trypomastigote binding to human CASM cells.	bind
9237	1	3886	5	11	NULL	NULL	NULL	GATA-1	GP		bind					GGE probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_2_713_s_212	10611250	(B) GATA-1, GATA-2, and GATA-3 can bind to the GGE probe.	bind
9238	2	3886	5	11	NULL	NULL	NULL	GATA-2	GP		bind					GGE probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_2_713_s_212	10611250	(B) GATA-1, GATA-2, and GATA-3 can bind to the GGE probe.	bind
9239	3	3886	5	11	NULL	NULL	NULL	GATA-3	GP		bind					GGE probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_2_713_s_212	10611250	(B) GATA-1, GATA-2, and GATA-3 can bind to the GGE probe.	bind
9424	1	3886	6	11	NULL	NULL	NULL	GATA-1	GP		bind					GGE probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_2_713_s_212	10611250	(B) GATA-1, GATA-2, and GATA-3 can bind to the GGE probe.	bind
9425	2	3886	6	11	NULL	NULL	NULL	GATA-2	GP		bind					GGE probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_2_713_s_212	10611250	(B) GATA-1, GATA-2, and GATA-3 can bind to the GGE probe.	bind
9426	3	3886	6	11	NULL	NULL	NULL	GATA-3	GP		bind					GGE probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_2_713_s_212	10611250	(B) GATA-1, GATA-2, and GATA-3 can bind to the GGE probe.	bind
9240	2	3887	5	11	NULL	NULL	NULL	Gcn4	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_390	11884596	(B) Gcn4 binds to Ty1 sequences harboring Gcn4 binding sites.	bind
53651	1	3887	5	11	NULL	NULL	NULL	Ty1 sequences	GP		harbor								Gcn4 binding sites		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_390	11884596	(B) Gcn4 binds to Ty1 sequences harboring Gcn4 binding sites.	bind
9427	1	3887	6	11	NULL	NULL	NULL	Ty1 sequences	GP		harbor								Gcn4 binding sites		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_390	11884596	(B) Gcn4 binds to Ty1 sequences harboring Gcn4 binding sites.	bind
9428	2	3887	6	11	NULL	NULL	NULL	Gcn4	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_390	11884596	(B) Gcn4 binds to Ty1 sequences harboring Gcn4 binding sites.	bind
9596	1	3888	5	11	NULL	NULL	NULL	3H-IP6	Chemical		bind					DNA-PK	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_102_6_721_s_151	11030616	(B) Gel  filtration analyses of 3H-IP6 binding by DNA-PK.	bind
9429	1	3888	6	11	NULL	NULL	NULL	3H-IP6	Chemical		bind					DNA-PK	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_102_6_721_s_151	11030616	(B) Gel  filtration analyses of 3H-IP6 binding by DNA-PK.	bind
9597	1	3889	5	11	NULL	NULL	NULL	SoxS	GP		bind					yggX	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_22_6624_s_139	14594836	(B) Gel mobility shift assay of SoxS binding to the  yggX promoter.	bind
9430	1	3889	6	11	NULL	NULL	NULL	SoxS	GP		bind					yggX	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_22_6624_s_139	14594836	(B) Gel mobility shift assay of SoxS binding to the  yggX promoter.	bind
9598	1	3890	5	11	NULL	NULL	NULL	PirR	GP		bind					pirAB- pirR	GP			intergenic region	NULL		NULL	NULL	NULL	NULL	gw70_febslett_574_1_101_s_155	15358547	(B) Gel mobility shift assays of PirR binding to  the  pirAB- pirR intergenic region.	bind
9431	1	3890	6	11	NULL	NULL	NULL	PirR	GP		bind					pirAB- pirR	GP			intergenic region	NULL		NULL	NULL	NULL	NULL	gw70_febslett_574_1_101_s_155	15358547	(B) Gel mobility shift assays of PirR binding to  the  pirAB- pirR intergenic region.	bind
9601	1	3891	5	11	NULL	NULL	NULL	primary pro-B cells proteins	GP		bind									E i NF- B site	NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_131_s_146	9047235	(B) Gel mobility supershift analysis of primary pro- and pre-B cell proteins binding to the E i NF- B site.	bind
9602	2	3891	5	11	NULL	NULL	NULL	primary pre-B cells proteins	GP		bind									E i NF- B site	NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_131_s_146	9047235	(B) Gel mobility supershift analysis of primary pro- and pre-B cell proteins binding to the E i NF- B site.	bind
9432	1	3891	6	11	NULL	NULL	NULL	primary pro-B cell proteins	GP		bind									E i NF- B site	NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_131_s_146	9047235	(B) Gel mobility supershift analysis of primary pro- and pre-B cell proteins binding to the E i NF- B site.	bind
9433	2	3891	6	11	NULL	NULL	NULL	primary pre-B cell proteins	GP		bind 									E i NF- B site	NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_131_s_146	9047235	(B) Gel mobility supershift analysis of primary pro- and pre-B cell proteins binding to the E i NF- B site.	bind
9603	1	3893	5	11	NULL	NULL	NULL				bind			POU domain		DNA fragment	NucleicAcid			promoter 	NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_2_397_s_153	12191484	(B) Gel shift analysis of POU domain (POU*) and TBP binding to promoter DNA fragment.	bind
9604	2	3893	5	11	NULL	NULL	NULL	TBP	GP		bind					DNA fragment	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_2_397_s_153	12191484	(B) Gel shift analysis of POU domain (POU*) and TBP binding to promoter DNA fragment.	bind
9434	1	3893	6	11	NULL	NULL	NULL				bind			POU domain		DNA fragment	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_2_397_s_153	12191484	(B) Gel shift analysis of POU domain (POU*) and TBP binding to promoter DNA fragment.	bind
9435	2	3893	6	11	NULL	NULL	NULL	TBP	GP		bind					DNA fragment	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_2_397_s_153	12191484	(B) Gel shift analysis of POU domain (POU*) and TBP binding to promoter DNA fragment.	bind
9605	1	3894	5	11	NULL	NULL	NULL	LuxR	GP		bind					luxI DNA	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_3_631_s_87	14729687	(B) Gel shift assay of LuxR binding to  luxI promoter DNA.	bind
9436	1	3894	6	11	NULL	NULL	NULL	LuxR	GP		bind					luxI DNA	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_3_631_s_87	14729687	(B) Gel shift assay of LuxR binding to  luxI promoter DNA.	bind
9599	1	3896	5	11	NULL	NULL	NULL	Tem1	GP		bind					Bfa1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_177	14734533	(B) Gic1  can disrupt binding of Tem1 to Bfa1.	bind
9600	2	3896	5	11	NULL	NULL	NULL	Gic1	GP		disrupt					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_177	14734533	(B) Gic1  can disrupt binding of Tem1 to Bfa1.	bind
9437	1	3896	6	11	NULL	NULL	NULL	Tem1	GP		bind					Bfa1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_177	14734533	(B) Gic1  can disrupt binding of Tem1 to Bfa1.	bind
9438	2	3896	6	11	NULL	NULL	NULL	Gic1	GP		disrupts					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_177	14734533	(B) Gic1  can disrupt binding of Tem1 to Bfa1.	bind
9606	1	3897	5	11	NULL	NULL	NULL	Gic1	GP		bind		directly			Bfa1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_142	14734533	(B) Gic1 binds directly  to Bfa1, Bub2, Tem1, and Cdc14.	bind
9607	2	3897	5	11	NULL	NULL	NULL	Gic1	GP		bind		directly			Bub2	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_142	14734533	(B) Gic1 binds directly  to Bfa1, Bub2, Tem1, and Cdc14.	bind
9608	3	3897	5	11	NULL	NULL	NULL	Gic1	GP		bind		directly			Tem1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_142	14734533	(B) Gic1 binds directly  to Bfa1, Bub2, Tem1, and Cdc14.	bind
9609	4	3897	5	11	NULL	NULL	NULL	Gic1	GP		bind		directly			Cdc14	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_142	14734533	(B) Gic1 binds directly  to Bfa1, Bub2, Tem1, and Cdc14.	bind
9449	1	3897	6	11	NULL	NULL	NULL	Gic1	GP		bind		directly			Bfa1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_142	14734533	(B) Gic1 binds directly  to Bfa1, Bub2, Tem1, and Cdc14.	bind
9450	2	3897	6	11	NULL	NULL	NULL	Gic1	GP		bind		directly			Bub2	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_142	14734533	(B) Gic1 binds directly  to Bfa1, Bub2, Tem1, and Cdc14.	bind
9451	3	3897	6	11	NULL	NULL	NULL	Gic1	GP		bind		directly			Tem1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_142	14734533	(B) Gic1 binds directly  to Bfa1, Bub2, Tem1, and Cdc14.	bind
9452	4	3897	6	11	NULL	NULL	NULL	Gic1	GP		bind		directly			Cdc14	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_142	14734533	(B) Gic1 binds directly  to Bfa1, Bub2, Tem1, and Cdc14.	bind
9610	1	3898	5	11	NULL	NULL	NULL	GIPC	GP		bind			L142A		TrkA	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_3_615_s_219	11251075	(B) GIPC(L142A/G143E) binds TrkA.	bind
9611	2	3898	5	11	NULL	NULL	NULL	GIPC	GP		bind			G143E		TrkA	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_3_615_s_219	11251075	(B) GIPC(L142A/G143E) binds TrkA.	bind
9453	1	3898	6	11	NULL	NULL	NULL	GIPC	GP		bind			L142A		TrkA	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_3_615_s_219	11251075	(B) GIPC(L142A/G143E) binds TrkA.	bind
9454	2	3898	6	11	NULL	NULL	NULL	GIPC	GP		bind			G143E		TrkA	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_3_615_s_219	11251075	(B) GIPC(L142A/G143E) binds TrkA.	bind
9612	1	3899	5	11	NULL	NULL	NULL	GLD-1	GP		bind									GRE	NULL		NULL	NULL	NULL	NULL	gw70_development_131_14_3263_s_235	15201219	(B) GLD-1 binds the GRE and  may repress  pal-1 translation after ribosome loading.	bind
9613	2	3899	5	11	NULL	NULL	NULL	GLD-1	GP		repress		may			pal-1	GP	translation of			NULL		NULL	NULL	NULL	NULL	gw70_development_131_14_3263_s_235	15201219	(B) GLD-1 binds the GRE and  may repress  pal-1 translation after ribosome loading.	bind
9614	3	3899	5	11	NULL	NULL	NULL	statement 2	Process		occurs after					ribosome loading	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_131_14_3263_s_235	15201219	(B) GLD-1 binds the GRE and  may repress  pal-1 translation after ribosome loading.	bind
9455	1	3899	6	11	NULL	NULL	NULL	GLD-1	GP		bind									GRE	NULL		NULL	NULL	NULL	NULL	gw70_development_131_14_3263_s_235	15201219	(B) GLD-1 binds the GRE and  may repress  pal-1 translation after ribosome loading.	bind
9456	2	3899	6	11	NULL	NULL	NULL	GLD-1	GP		repress		may			pal-1	GP	translation of			NULL		NULL	NULL	NULL	NULL	gw70_development_131_14_3263_s_235	15201219	(B) GLD-1 binds the GRE and  may repress  pal-1 translation after ribosome loading.	bind
9457	3	3899	6	11	NULL	NULL	NULL	statement 2	Process		occurs after					ribosome loading	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_131_14_3263_s_235	15201219	(B) GLD-1 binds the GRE and  may repress  pal-1 translation after ribosome loading.	bind
9615	1	3900	5	11	NULL	NULL	NULL	GMAP-210	GP		bind					microtubules	CellComponent	taxol-polymerized			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_1_83_s_270	10189370	(B) GMAP-210  binds to taxol-polymerized microtubules.	bind
9458	1	3900	6	11	NULL	NULL	NULL	GMAP-210	GP		bind					microtubules	CellComponent	taxol-polymerized			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_1_83_s_270	10189370	(B) GMAP-210  binds to taxol-polymerized microtubules.	bind
9616	1	3901	5	11	NULL	NULL	NULL	Bim	GP		bind					Bcl-w	GP				NULL	in epileptic brain	NULL	NULL	NULL	NULL	gw70_jclininvest_113_7_1059_s_268	15057313	(B) Graph showing quantification of higher Bim binding to Bcl-w (OD  units) in epileptic brain.	bind
9459	1	3901	6	11	NULL	NULL	NULL	Bim	GP		bind					Bcl-w	GP				NULL	epileptic brain	NULL	NULL	NULL	NULL	gw70_jclininvest_113_7_1059_s_268	15057313	(B) Graph showing quantification of higher Bim binding to Bcl-w (OD  units) in epileptic brain.	bind
10556	1	3902	5	11	NULL	NULL	NULL	U1A	GP	mutant	bind					PIE RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_9_3163_s_128	12697817	(B) Graphic summary  of the EMSAs in which the  y axis shows the PIE RNA binding activities of the mutant proteins in forming the (U1A)2-PIE RNA complex relative to that of U1Awt, which was set to 1.0.	bind
10557	2	3902	5	11	NULL	NULL	NULL	statement 1	Process		forms					(U1A)2-PIE RNA complex	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_9_3163_s_128	12697817	(B) Graphic summary  of the EMSAs in which the  y axis shows the PIE RNA binding activities of the mutant proteins in forming the (U1A)2-PIE RNA complex relative to that of U1Awt, which was set to 1.0.	bind
9662	1	3902	6	11	NULL	NULL	NULL	U1A	GP	mutant	bind					PIE RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_9_3163_s_128	12697817	(B) Graphic summary  of the EMSAs in which the  y axis shows the PIE RNA binding activities of the mutant proteins in forming the (U1A)2-PIE RNA complex relative to that of U1Awt, which was set to 1.0.	bind
9663	2	3902	6	11	NULL	NULL	NULL	statement 1	Process		forms 					(U1A)2-PIE RNA complex	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_9_3163_s_128	12697817	(B) Graphic summary  of the EMSAs in which the  y axis shows the PIE RNA binding activities of the mutant proteins in forming the (U1A)2-PIE RNA complex relative to that of U1Awt, which was set to 1.0.	bind
9617	1	3904	5	11	NULL	NULL	NULL	GrnCDE			bind					GST-cyclin T1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_5_1688_s_39	12588988	(B) GrnCDE and GEP binding to GST-cyclin T1.	bind
9618	2	3904	5	NULL	NULL	0	NULL	GEP	NULL		bind	NULL				GST-cyclin T1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_5_1688_s_39	12588988	(B) GrnCDE and GEP binding to GST-cyclin T1.	bind
9460	1	3904	6	NULL	NULL	0	NULL	GrnCDE	NULL		bind	NULL				GST-cyclin T1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_5_1688_s_39	12588988	(B) GrnCDE and GEP binding to GST-cyclin T1.	bind
9461	2	3904	6	NULL	NULL	0	NULL	GEP	NULL		bind	NULL				GST-cyclin T1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_5_1688_s_39	12588988	(B) GrnCDE and GEP binding to GST-cyclin T1.	bind
9619	1	3907	5	11	NULL	NULL	NULL	cypin	GP		bind					PSD-95	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_3_659_s_97	10595517	(B) GST fusion protein affinity chromatography shows that cypin binding to PSD-95 requires PDZ1 and PDZ2.	bind
9620	2	3907	5	11	NULL	NULL	NULL	statement 1	Process		require								PDZ1		NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_3_659_s_97	10595517	(B) GST fusion protein affinity chromatography shows that cypin binding to PSD-95 requires PDZ1 and PDZ2.	bind
9621	3	3907	5	11	NULL	NULL	NULL	statement 1	Process		require								PDZ2		NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_3_659_s_97	10595517	(B) GST fusion protein affinity chromatography shows that cypin binding to PSD-95 requires PDZ1 and PDZ2.	bind
9462	1	3907	6	11	NULL	NULL	NULL	cypin	GP		bind					PSD-95	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_3_659_s_97	10595517	(B) GST fusion protein affinity chromatography shows that cypin binding to PSD-95 requires PDZ1 and PDZ2.	bind
9463	2	3907	6	11	NULL	NULL	NULL	statement 1	Process		requires								PDZ1		NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_3_659_s_97	10595517	(B) GST fusion protein affinity chromatography shows that cypin binding to PSD-95 requires PDZ1 and PDZ2.	bind
9464	3	3907	6	11	NULL	NULL	NULL	statement 1	Process		requires								PDZ2		NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_3_659_s_97	10595517	(B) GST fusion protein affinity chromatography shows that cypin binding to PSD-95 requires PDZ1 and PDZ2.	bind
9622	1	3908	5	11	NULL	NULL	NULL	E1B 19K	GP	deletion mutant	bind					Bax	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_6052_s_267	9742122	(B) GST fusion protein binding assay of deletion mutants of E1B 19K binding to Bax and CED-4.	bind
9623	2	3908	5	11	NULL	NULL	NULL	E1B 19K	GP	deletion mutant	bind					CED-4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_6052_s_267	9742122	(B) GST fusion protein binding assay of deletion mutants of E1B 19K binding to Bax and CED-4.	bind
9465	1	3908	6	11	NULL	NULL	NULL	E1B 19K	GP	deletion mutant	bind					Bax	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_6052_s_267	9742122	(B) GST fusion protein binding assay of deletion mutants of E1B 19K binding to Bax and CED-4.	bind
9466	2	3908	6	11	NULL	NULL	NULL	E1B 19K	GP	deletion mutant	bind					CED-4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_6052_s_267	9742122	(B) GST fusion protein binding assay of deletion mutants of E1B 19K binding to Bax and CED-4.	bind
9624	1	3909	5	11	NULL	NULL	NULL	yMBF1 protein	GP		bind			D112A		GCN4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_4971_s_169	9710580	(B) GST pull-down assays for binding of the yMBF1 D112A protein and yMBF1deltaNT to GCN4.	bind
9628	2	3909	5	11	NULL	NULL	NULL	yMBF1	GP		bind			deltaNT		GCN4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_4971_s_169	9710580	(B) GST pull-down assays for binding of the yMBF1 D112A protein and yMBF1deltaNT to GCN4.	bind
9467	1	3909	6	11	NULL	NULL	NULL	yMBF1	GP		bind			D112A		GCN4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_4971_s_169	9710580	(B) GST pull-down assays for binding of the yMBF1 D112A protein and yMBF1deltaNT to GCN4.	bind
9468	2	3909	6	11	NULL	NULL	NULL	yMBF1	GP		bind			deltaNT		GCN4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_4971_s_169	9710580	(B) GST pull-down assays for binding of the yMBF1 D112A protein and yMBF1deltaNT to GCN4.	bind
9629	1	3911	5	11	NULL	NULL	NULL	GST-12S E1A protein	GP		bind					p300	GP		carboxy-terminal fragments ending at amino acid 2414		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_75	10330164	(B) GST-12S and -13S E1A proteins bind to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1542.	bind
9630	2	3911	5	11	NULL	NULL	NULL	GST-12S E1A protein	GP		bind					p300	GP		carboxy-terminal fragments ending at amino acid 1906		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_75	10330164	(B) GST-12S and -13S E1A proteins bind to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1542.	bind
9631	3	3911	5	11	NULL	NULL	NULL	GST-12S E1A protein	GP		bind					p300	GP		carboxy-terminal fragments ending at amino acid 1542		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_75	10330164	(B) GST-12S and -13S E1A proteins bind to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1542.	bind
9632	4	3911	5	11	NULL	NULL	NULL	GST-13S E1A protein	GP		bind					p300	GP		carboxy-terminal fragments ending at amino acid 2414		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_75	10330164	(B) GST-12S and -13S E1A proteins bind to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1542.	bind
9633	5	3911	5	11	NULL	NULL	NULL	GST-13S E1A protein	GP		bind					p300	GP		carboxy-terminal fragments ending at amino acid 1906		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_75	10330164	(B) GST-12S and -13S E1A proteins bind to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1542.	bind
9634	6	3911	5	11	NULL	NULL	NULL	GST-13S E1A protein	GP		bind					p300	GP		carboxy-terminal fragments ending at amino acid 1542		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_75	10330164	(B) GST-12S and -13S E1A proteins bind to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1542.	bind
9469	1	3911	6	11	NULL	NULL	NULL	GST-12S E1A protein	GP		bind					p300	GP		carboxy terminal fragments ending at amino acid 2414		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_75	10330164	(B) GST-12S and -13S E1A proteins bind to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1542.	bind
9470	2	3911	6	11	NULL	NULL	NULL	GST-12S E1A protein	GP		bind					p300	GP		carboxy terminal fragments ending at amino acid 1906		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_75	10330164	(B) GST-12S and -13S E1A proteins bind to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1542.	bind
12304	3	3911	6	11	NULL	NULL	NULL	GST-12S E1A protein	GP		bind					p300	GP		carboxy-terminal fragments ending at amino acid 1542		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_75	10330164	(B) GST-12S and -13S E1A proteins bind to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1542.	bind
12305	4	3911	6	11	NULL	NULL	NULL	GST-13S E1A protein	GP		bind					p300	GP		carboxy terminal fragments ending at amino acid 2414		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_75	10330164	(B) GST-12S and -13S E1A proteins bind to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1542.	bind
12306	5	3911	6	11	NULL	NULL	NULL	GST-13S E1A protein	GP		bind					p300	GP		carboxy terminal fragments ending at amino acid 1906		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_75	10330164	(B) GST-12S and -13S E1A proteins bind to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1542.	bind
12307	6	3911	6	11	NULL	NULL	NULL	GST-13S E1A protein	GP		bind					p300	GP		carboxy terminal fragments ending at amino acid 1542		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_75	10330164	(B) GST-12S and -13S E1A proteins bind to p300 carboxy-terminal fragments ending at amino acids 2414, 1906, and 1542.	bind
9635	1	3918	5	11	NULL	NULL	NULL	HA-Sec4-N133Ip	GP		bind					myc-Ssop	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molbiolcell_10_12_4149_s_248	10588649	(B) HA-Sec4-N133Ip binds myc-Ssop in vitro.	bind
9471	1	3918	6	11	NULL	NULL	NULL	HA-Sec4-N133Ip	GP		bind					myc-Ssop	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molbiolcell_10_12_4149_s_248	10588649	(B) HA-Sec4-N133Ip binds myc-Ssop in vitro.	bind
9636	1	3919	5	11	NULL	NULL	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_104_3_731_s_111	11440805	(b) HDB/SI/MCPO shows a significant increase (+242.6%, paired  t-test;  t=-3.03, DF=4,  P<0.03) in NF- B DNA binding activity following adenosine treatment when compared to ACSF treated samples.	bind
9637	2	3919	5	11	NULL	NULL	NULL	adenosine	NucleicAcid	treatment with	increase		significantly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_104_3_731_s_111	11440805	(b) HDB/SI/MCPO shows a significant increase (+242.6%, paired  t-test;  t=-3.03, DF=4,  P<0.03) in NF- B DNA binding activity following adenosine treatment when compared to ACSF treated samples.	bind
9472	1	3919	6	11	NULL	NULL	NULL	NF-kappaB	GP		bind					DNA 	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_104_3_731_s_111	11440805	(b) HDB/SI/MCPO shows a significant increase (+242.6%, paired  t-test;  t=-3.03, DF=4,  P<0.03) in NF- B DNA binding activity following adenosine treatment when compared to ACSF treated samples.	bind
9473	2	3919	6	11	NULL	NULL	NULL	adenosine 	NucleicAcid	treatment with	increase		significantly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_104_3_731_s_111	11440805	(b) HDB/SI/MCPO shows a significant increase (+242.6%, paired  t-test;  t=-3.03, DF=4,  P<0.03) in NF- B DNA binding activity following adenosine treatment when compared to ACSF treated samples.	bind
9639	1	3921	5	11	NULL	NULL	NULL	SHH:AP	GP		bind					EGL	GP				NULL	P6 cerebellum	NULL	NULL	NULL	NULL	gw60_development_129_9_2223_s_209	11959830	(B) Heparinase I and III treatment results in significantly decreased binding of SHH:AP to the EGL and IGL in sections of P6 cerebellum.	bind
9640	2	3921	5	11	NULL	NULL	NULL	SHH:AP	GP		bind					IGL	GP				NULL	P6 cerebellum	NULL	NULL	NULL	NULL	gw60_development_129_9_2223_s_209	11959830	(B) Heparinase I and III treatment results in significantly decreased binding of SHH:AP to the EGL and IGL in sections of P6 cerebellum.	bind
9641	3	3921	5	11	NULL	NULL	NULL	Heparinase I	GP	treatment	decrease		significantly			statement 1	Process				NULL	P6 cerebellum	NULL	NULL	NULL	NULL	gw60_development_129_9_2223_s_209	11959830	(B) Heparinase I and III treatment results in significantly decreased binding of SHH:AP to the EGL and IGL in sections of P6 cerebellum.	bind
9642	4	3921	5	11	NULL	NULL	NULL	Heparinase I	GP	treatment	decrease		significantly			statement 2	Process				NULL	P6 cerebellum	NULL	NULL	NULL	NULL	gw60_development_129_9_2223_s_209	11959830	(B) Heparinase I and III treatment results in significantly decreased binding of SHH:AP to the EGL and IGL in sections of P6 cerebellum.	bind
9643	5	3921	5	11	NULL	NULL	NULL	Heparinase III	GP	treatment	decrease		significantly			statement 1	Process				NULL	P6 cerebellum	NULL	NULL	NULL	NULL	gw60_development_129_9_2223_s_209	11959830	(B) Heparinase I and III treatment results in significantly decreased binding of SHH:AP to the EGL and IGL in sections of P6 cerebellum.	bind
9644	6	3921	5	11	NULL	NULL	NULL	Heparinase III	GP	treatment	decrease		significantly			statement 2	Process				NULL	P6 cerebellum	NULL	NULL	NULL	NULL	gw60_development_129_9_2223_s_209	11959830	(B) Heparinase I and III treatment results in significantly decreased binding of SHH:AP to the EGL and IGL in sections of P6 cerebellum.	bind
9474	1	3921	6	11	NULL	NULL	NULL	SHH:AP	GP		bind					EGL	GP				NULL	sections of P6 cerebellum	NULL	NULL	NULL	NULL	gw60_development_129_9_2223_s_209	11959830	(B) Heparinase I and III treatment results in significantly decreased binding of SHH:AP to the EGL and IGL in sections of P6 cerebellum.	bind
9475	2	3921	6	NULL	NULL	0	NULL	SHH:AP	NULL		bind	NULL				IGL	NULL				NULL	sections of P6 cerebellum	0	NULL	NULL	NULL	gw60_development_129_9_2223_s_209	11959830	(B) Heparinase I and III treatment results in significantly decreased binding of SHH:AP to the EGL and IGL in sections of P6 cerebellum.	bind
9476	3	3921	6	NULL	NULL	0	NULL	Heparinase I	NULL		decreases	NULL	significantly			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_development_129_9_2223_s_209	11959830	(B) Heparinase I and III treatment results in significantly decreased binding of SHH:AP to the EGL and IGL in sections of P6 cerebellum.	bind
9477	4	3921	6	NULL	NULL	0	NULL	Heparinase III	NULL		decreases	NULL	significantly			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_development_129_9_2223_s_209	11959830	(B) Heparinase I and III treatment results in significantly decreased binding of SHH:AP to the EGL and IGL in sections of P6 cerebellum.	bind
12308	5	3921	6	11	NULL	NULL	NULL	Heparinase I	GP		decreases		significantly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_development_129_9_2223_s_209	11959830	(B) Heparinase I and III treatment results in significantly decreased binding of SHH:AP to the EGL and IGL in sections of P6 cerebellum.	bind
12309	6	3921	6	NULL	NULL	0	NULL	Heparinase III	NULL		decreases	NULL	significantly			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_development_129_9_2223_s_209	11959830	(B) Heparinase I and III treatment results in significantly decreased binding of SHH:AP to the EGL and IGL in sections of P6 cerebellum.	bind
9645	1	3922	5	11	NULL	NULL	NULL	BTAF1	GP		bind					TBP	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_22_10072_s_112	15509807	(B) Hexokinase activity is  necessary to abolish NC2alpha-mediated binding of BTAF1 and TBP. RK13 cell lysate (1 mul) containing overexpressed  BTAF1 was incubated with glutathione-agarose beads coated with GST-TBP (lanes 3 to  6 and 8 to 11) or GST-deltaTFIIS (lanes 7 and 12) in the absence (lanes 3, 7, 8, and 12) or presence of 6.5 pmol  of hisNC2alpha (lanes 4 and 9), hisNC2beta (lanes 5 and 10), and NC2(alpha/hisbeta) (lanes 6 and 11).	bind
9646	2	3922	5	11	NULL	NULL	NULL	NC2alpha	GP		mediate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_22_10072_s_112	15509807	(B) Hexokinase activity is  necessary to abolish NC2alpha-mediated binding of BTAF1 and TBP. RK13 cell lysate (1 mul) containing overexpressed  BTAF1 was incubated with glutathione-agarose beads coated with GST-TBP (lanes 3 to  6 and 8 to 11) or GST-deltaTFIIS (lanes 7 and 12) in the absence (lanes 3, 7, 8, and 12) or presence of 6.5 pmol  of hisNC2alpha (lanes 4 and 9), hisNC2beta (lanes 5 and 10), and NC2(alpha/hisbeta) (lanes 6 and 11).	bind
9647	3	3922	5	11	NULL	NULL	NULL	hexokinase 	GP	activity of	abolish					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_22_10072_s_112	15509807	(B) Hexokinase activity is  necessary to abolish NC2alpha-mediated binding of BTAF1 and TBP. RK13 cell lysate (1 mul) containing overexpressed  BTAF1 was incubated with glutathione-agarose beads coated with GST-TBP (lanes 3 to  6 and 8 to 11) or GST-deltaTFIIS (lanes 7 and 12) in the absence (lanes 3, 7, 8, and 12) or presence of 6.5 pmol  of hisNC2alpha (lanes 4 and 9), hisNC2beta (lanes 5 and 10), and NC2(alpha/hisbeta) (lanes 6 and 11).	bind
9664	1	3922	6	11	NULL	NULL	NULL	BTAF1	GP		bind					TBP	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_22_10072_s_112	15509807	(B) Hexokinase activity is  necessary to abolish NC2alpha-mediated binding of BTAF1 and TBP. RK13 cell lysate (1 mul) containing overexpressed  BTAF1 was incubated with glutathione-agarose beads coated with GST-TBP (lanes 3 to  6 and 8 to 11) or GST-deltaTFIIS (lanes 7 and 12) in the absence (lanes 3, 7, 8, and 12) or presence of 6.5 pmol  of hisNC2alpha (lanes 4 and 9), hisNC2beta (lanes 5 and 10), and NC2(alpha/hisbeta) (lanes 6 and 11).	bind
9665	2	3922	6	11	NULL	NULL	NULL	NC2alpha	GP		mediates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_22_10072_s_112	15509807	(B) Hexokinase activity is  necessary to abolish NC2alpha-mediated binding of BTAF1 and TBP. RK13 cell lysate (1 mul) containing overexpressed  BTAF1 was incubated with glutathione-agarose beads coated with GST-TBP (lanes 3 to  6 and 8 to 11) or GST-deltaTFIIS (lanes 7 and 12) in the absence (lanes 3, 7, 8, and 12) or presence of 6.5 pmol  of hisNC2alpha (lanes 4 and 9), hisNC2beta (lanes 5 and 10), and NC2(alpha/hisbeta) (lanes 6 and 11).	bind
9666	3	3922	6	11	NULL	NULL	NULL	hexokinase	GP	activity of	abolish					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_22_10072_s_112	15509807	(B) Hexokinase activity is  necessary to abolish NC2alpha-mediated binding of BTAF1 and TBP. RK13 cell lysate (1 mul) containing overexpressed  BTAF1 was incubated with glutathione-agarose beads coated with GST-TBP (lanes 3 to  6 and 8 to 11) or GST-deltaTFIIS (lanes 7 and 12) in the absence (lanes 3, 7, 8, and 12) or presence of 6.5 pmol  of hisNC2alpha (lanes 4 and 9), hisNC2beta (lanes 5 and 10), and NC2(alpha/hisbeta) (lanes 6 and 11).	bind
9648	1	3923	5	11	NULL	NULL	NULL	Hif-1	GP		bind									HRE	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3163_s_219	15798202	(B) Hif-1 and Hif-2 HRE binding activity by EMSA.	bind
9649	2	3923	5	11	NULL	NULL	NULL	Hif-2	GP		bind									HRE	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3163_s_219	15798202	(B) Hif-1 and Hif-2 HRE binding activity by EMSA.	bind
9478	1	3923	6	11	NULL	NULL	NULL	HIF-1	GP		bind									HRE	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3163_s_219	15798202	(B) Hif-1 and Hif-2 HRE binding activity by EMSA.	bind
9479	2	3923	6	11	NULL	NULL	NULL	HIF-2	GP		bind									HRE	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3163_s_219	15798202	(B) Hif-1 and Hif-2 HRE binding activity by EMSA.	bind
9650	1	3924	5	11	NULL	NULL	NULL	Hir1p	GP		bind					Asf1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_7_463_s_193	11412995	(b) Hir1p and Hir2p coimmunoprecipitate with Asf1p.	bind
9651	2	3924	5	11	NULL	NULL	NULL	Hir2p	GP		bind					Asf1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_7_463_s_193	11412995	(b) Hir1p and Hir2p coimmunoprecipitate with Asf1p.	bind
9480	1	3924	6	11	NULL	NULL	NULL	Hir1p	GP		bind					Asf1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_7_463_s_193	11412995	(b) Hir1p and Hir2p coimmunoprecipitate with Asf1p.	bind
9481	2	3924	6	11	NULL	NULL	NULL	Hir2p	GP		bind					Asf1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_7_463_s_193	11412995	(b) Hir1p and Hir2p coimmunoprecipitate with Asf1p.	bind
9652	1	3926	5	11	NULL	NULL	NULL	Arr2	GP		bind					membranes	CellComponent	rhodopsin-containing			NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_1_129_s_159	11086989	(B) Histogram quantifying the percent of Arr2 bound to rhodopsin-containing membranes after treatment with blue light (B) or blue light followed by orange light (BO).	bind
9482	1	3926	6	11	NULL	NULL	NULL	Arr2	GP		bind					membranes	CellComponent	rhodopsin-containing			NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_1_129_s_159	11086989	(B) Histogram quantifying the percent of Arr2 bound to rhodopsin-containing membranes after treatment with blue light (B) or blue light followed by orange light (BO).	bind
9653	1	3927	5	11	NULL	NULL	NULL	hMSH2-hMSH6	GP		bind					DNA mismatched 	NucleicAcid	nicked;; circular 		O-G/T	NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_2_255_s_100	10078208	(B) hMSH2-hMSH6 (65 nM) binding a nicked circular 2.9 kb mismatched (O-G/T) or homoduplex (O-G/C) DNA.	bind
9654	2	3927	5	11	NULL	NULL	NULL	hMSH2-hMSH6	GP		bind					DNA homoduplex	NucleicAcid	nicked;; circular		O-G/C	NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_2_255_s_100	10078208	(B) hMSH2-hMSH6 (65 nM) binding a nicked circular 2.9 kb mismatched (O-G/T) or homoduplex (O-G/C) DNA.	bind
9536	1	3927	6	11	NULL	NULL	NULL	 hMSH2-hMSH6	GP		bind					mismatched DNA	NucleicAcid	nicked;; circular 		O-G/T	NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_2_255_s_100	10078208	(B) hMSH2-hMSH6 (65 nM) binding a nicked circular 2.9 kb mismatched (O-G/T) or homoduplex (O-G/C) DNA.	bind
9537	2	3927	6	11	NULL	NULL	NULL	hMSH2-hMSH6	GP		bind					homoduplex DNA	NucleicAcid	nicked;; circular		O-G/C	NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_2_255_s_100	10078208	(B) hMSH2-hMSH6 (65 nM) binding a nicked circular 2.9 kb mismatched (O-G/T) or homoduplex (O-G/C) DNA.	bind
9655	1	3929	5	11	NULL	NULL	NULL	HrpR	GP		bind					protein	GP	E. coli			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_19_5589_s_245	11544221	(B) HrpR binding to an  E. coli protein-loaded column.	bind
9538	1	3929	6	11	NULL	NULL	NULL	HrpR	GP		bind					protein	GP	E.coli			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_19_5589_s_245	11544221	(B) HrpR binding to an  E. coli protein-loaded column.	bind
9656	1	3930	5	11	NULL	NULL	NULL	Hsp104	GP		bind					Sti1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_22_7569_s_134	11604493	(B) Hsp104 and Hsp90 binding to Sti1 requires TPR1 and TPR2, respectively.	bind
9657	2	3930	5	11	NULL	NULL	NULL	statement 1	Process		require					TPR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_22_7569_s_134	11604493	(B) Hsp104 and Hsp90 binding to Sti1 requires TPR1 and TPR2, respectively.	bind
9658	3	3930	5	11	NULL	NULL	NULL	Hsp90	GP		bind					Sti1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_22_7569_s_134	11604493	(B) Hsp104 and Hsp90 binding to Sti1 requires TPR1 and TPR2, respectively.	bind
9691	4	3930	5	11	NULL	NULL	NULL	statement 3	Process		require					TPR2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_22_7569_s_134	11604493	(B) Hsp104 and Hsp90 binding to Sti1 requires TPR1 and TPR2, respectively.	bind
9539	1	3930	6	11	NULL	NULL	NULL	Hsp104	GP		bind					Sti1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_22_7569_s_134	11604493	(B) Hsp104 and Hsp90 binding to Sti1 requires TPR1 and TPR2, respectively.	bind
9540	2	3930	6	11	NULL	NULL	NULL	Hsp90	GP		bind					Sti1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_22_7569_s_134	11604493	(B) Hsp104 and Hsp90 binding to Sti1 requires TPR1 and TPR2, respectively.	bind
9541	3	3930	6	11	NULL	NULL	NULL	statement 1	Process		requires					TPR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_22_7569_s_134	11604493	(B) Hsp104 and Hsp90 binding to Sti1 requires TPR1 and TPR2, respectively.	bind
9544	4	3930	6	11	NULL	NULL	NULL	statement 2	Process		requires					TPR2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_22_7569_s_134	11604493	(B) Hsp104 and Hsp90 binding to Sti1 requires TPR1 and TPR2, respectively.	bind
9701	1	3931	5	11	NULL	NULL	NULL	mediator		human	bind					DNA	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_9_772_s_19	12725737	(B) Human mediator and DA bind cooperatively to promoter DNA.	bind
9702	2	3931	5	11	NULL	NULL	NULL	DA	GP	human	bind					DNA	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_9_772_s_19	12725737	(B) Human mediator and DA bind cooperatively to promoter DNA.	bind
9703	3	3931	5	11	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_9_772_s_19	12725737	(B) Human mediator and DA bind cooperatively to promoter DNA.	bind
9545	1	3931	6	11	NULL	NULL	NULL	mediator		human	bind					DNA	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_9_772_s_19	12725737	(B) Human mediator and DA bind cooperatively to promoter DNA.	bind
9546	2	3931	6	11	NULL	NULL	NULL	DA	GP		bind					DNA	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_9_772_s_19	12725737	(B) Human mediator and DA bind cooperatively to promoter DNA.	bind
9547	3	3931	6	11	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_9_772_s_19	12725737	(B) Human mediator and DA bind cooperatively to promoter DNA.	bind
9704	1	3932	5	11	NULL	NULL	NULL	p70 MGR	GP	human	bind					En-1	GP	human		promoter	NULL		NULL	NULL	NULL	NULL	gw60_mechdev_114_1_37_s_177	12175488	(B) Human p70 MGR binds to the human En-1 promoter.	bind
9548	1	3932	6	11	NULL	NULL	NULL	p70 MGR	GP	human	bind					En-1	GP	human		promoter	NULL		NULL	NULL	NULL	NULL	gw60_mechdev_114_1_37_s_177	12175488	(B) Human p70 MGR binds to the human En-1 promoter.	bind
9705	1	3933	5	11	NULL	NULL	NULL	hRNF5	GP		bind					paxillin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5331_s_131	12861019	(B) Human RNF5  (hRNF5) binds to paxillin.	bind
9706	2	3933	5	11	NULL	NULL	NULL	hRNF5	GP		is					human RNF5	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5331_s_131	12861019	(B) Human RNF5  (hRNF5) binds to paxillin.	bind
9549	1	3933	6	11	NULL	NULL	NULL	hRNF5	GP		bind					paxillin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5331_s_131	12861019	(B) Human RNF5  (hRNF5) binds to paxillin.	bind
9550	2	3933	6	11	NULL	NULL	NULL	hRNF5	GP		is					human RNF5	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5331_s_131	12861019	(B) Human RNF5  (hRNF5) binds to paxillin.	bind
9707	1	3935	5	11	NULL	NULL	NULL	HVEM:Fc	Organism		bind					T cells	Cell	activated;; human;; peripheral blood			NULL		NULL	NULL	NULL	NULL	gw60_immunity_8_1_21_s_52	9462508	(B) HVEM:Fc binds activated T cells from human peripheral blood.	bind
9551	1	3935	6	11	NULL	NULL	NULL	HVEM:Fc	Organism		bind					T cells 	Cell	activated;; human;; peripheral blood			NULL		NULL	NULL	NULL	NULL	gw60_immunity_8_1_21_s_52	9462508	(B) HVEM:Fc binds activated T cells from human peripheral blood.	bind
9708	1	3936	5	11	NULL	NULL	NULL	E47 homodimers	GP		bind		sequence specific			MEF-1 oligodeoxynucleotide	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_313	11940648	(B) Id2 inhibits the sequence-specific binding of E47 homodimers and MyoD-E47 heterodimers to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition.	bind
9709	2	3936	5	11	NULL	NULL	NULL	MyoD-E47 heterodimers	GP		bind		sequence specific			MEF-1 oligodeoxynucleotide	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_313	11940648	(B) Id2 inhibits the sequence-specific binding of E47 homodimers and MyoD-E47 heterodimers to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition.	bind
9710	3	3936	5	11	NULL	NULL	NULL	Id2	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_313	11940648	(B) Id2 inhibits the sequence-specific binding of E47 homodimers and MyoD-E47 heterodimers to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition.	bind
9711	4	3936	5	11	NULL	NULL	NULL	Id2	GP		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_313	11940648	(B) Id2 inhibits the sequence-specific binding of E47 homodimers and MyoD-E47 heterodimers to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition.	bind
9712	5	3936	5	11	NULL	NULL	NULL	p204	GP		overcomes					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_313	11940648	(B) Id2 inhibits the sequence-specific binding of E47 homodimers and MyoD-E47 heterodimers to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition.	bind
9713	6	3936	5	11	NULL	NULL	NULL	p204	GP		overcomes					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_313	11940648	(B) Id2 inhibits the sequence-specific binding of E47 homodimers and MyoD-E47 heterodimers to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition.	bind
9557	1	3936	6	11	NULL	NULL	NULL	E47 homodimers	GP		bind					MEF-1 oligodeoxynucleotide	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_313	11940648	(B) Id2 inhibits the sequence-specific binding of E47 homodimers and MyoD-E47 heterodimers to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition.	bind
9558	2	3936	6	11	NULL	NULL	NULL	MyoD-E47 heterodimers	GP		bind					MEF-1 oligodeoxynucleotide	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_313	11940648	(B) Id2 inhibits the sequence-specific binding of E47 homodimers and MyoD-E47 heterodimers to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition.	bind
9559	3	3936	6	NULL	NULL	0	NULL	Id2	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_313	11940648	(B) Id2 inhibits the sequence-specific binding of E47 homodimers and MyoD-E47 heterodimers to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition.	bind
9560	4	3936	6	NULL	NULL	0	NULL	Id2	NULL		inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_313	11940648	(B) Id2 inhibits the sequence-specific binding of E47 homodimers and MyoD-E47 heterodimers to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition.	bind
9561	5	3936	6	NULL	NULL	0	NULL	p204	NULL		overcomes	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_313	11940648	(B) Id2 inhibits the sequence-specific binding of E47 homodimers and MyoD-E47 heterodimers to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition.	bind
9562	6	3936	6	NULL	NULL	0	NULL	p204	NULL		overcomes	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_313	11940648	(B) Id2 inhibits the sequence-specific binding of E47 homodimers and MyoD-E47 heterodimers to the MEF-1 oligodeoxynucleotide in vitro, and p204 overcomes the inhibition.	bind
9714	1	3940	5	11	NULL	NULL	NULL	IHF	GP		bind					 Ppac	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_7_2215_s_94	15028709	(B) IHF binding to the  Ppac promoter.	bind
9563	1	3940	6	11	NULL	NULL	NULL	IHF	GP		bind					Ppac	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_7_2215_s_94	15028709	(B) IHF binding to the  Ppac promoter.	bind
9715	1	3945	5	11	NULL	NULL	NULL	EMILIN-1	GP		bind					elastin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_638_s_238	14701737	(B) Immunoprecipitation assays  showing binding of EMILIN-1 to elastin and fibulin-5.	bind
9716	2	3945	5	11	NULL	NULL	NULL	EMILIN-1	GP		bind					fibulin-5	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_638_s_238	14701737	(B) Immunoprecipitation assays  showing binding of EMILIN-1 to elastin and fibulin-5.	bind
9564	1	3945	6	11	NULL	NULL	NULL	EMILIN-1	GP		bind					elastin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_638_s_238	14701737	(B) Immunoprecipitation assays  showing binding of EMILIN-1 to elastin and fibulin-5.	bind
9565	2	3945	6	11	NULL	NULL	NULL	EMILIN-1	GP		bind					fibulin-5	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_638_s_238	14701737	(B) Immunoprecipitation assays  showing binding of EMILIN-1 to elastin and fibulin-5.	bind
9718	2	3946	5	10	NULL	0	NULL	statement 1			in the absence of					antiserum					NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_44_6_817_s_249	12681380	(B) Immunoprecipitations performed in the absence of antiserum demonstrate that  syntaxin 1 binds directly to protein A sepharose.	bind
9566	1	3946	6	NULL	NULL	0	NULL	syntaxin 1	NULL		bind	NULL	directly			Protein A	NULL				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_44_6_817_s_249	12681380	(B) Immunoprecipitations performed in the absence of antiserum demonstrate that  syntaxin 1 binds directly to protein A sepharose.	bind
53714	2	3946	6	10	NULL	0	NULL	statement 1			in the absence of					antiserum					NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_44_6_817_s_249	12681380	(B) Immunoprecipitations performed in the absence of antiserum demonstrate that  syntaxin 1 binds directly to protein A sepharose.	bind
9717	1	3948	5	11	NULL	NULL	NULL	syntaxin 1	GP		bind		directly			protein A	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_3_349_s_173	12176322	(B) Importin-alpha can bind NLS and the N terminus of Npap60 simultaneously.	bind
9719	1	3948	5	11	NULL	NULL	NULL	importin-alpha	GP		bind					Npap60	GP		NLS		NULL		NULL	NULL	NULL	NULL	gw60_cell_110_3_349_s_173	12176322	(B) Importin-alpha can bind NLS and the N terminus of Npap60 simultaneously.	bind
9720	2	3948	5	11	NULL	NULL	NULL	importin-alpha	GP		bind					Npap60	GP		N terminus		NULL		NULL	NULL	NULL	NULL	gw60_cell_110_3_349_s_173	12176322	(B) Importin-alpha can bind NLS and the N terminus of Npap60 simultaneously.	bind
9721	3	3948	5	11	NULL	NULL	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_3_349_s_173	12176322	(B) Importin-alpha can bind NLS and the N terminus of Npap60 simultaneously.	bind
9567	1	3948	6	11	NULL	NULL	NULL	Importin-alpha	GP		bind					NLS	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_3_349_s_173	12176322	(B) Importin-alpha can bind NLS and the N terminus of Npap60 simultaneously.	bind
9568	2	3948	6	11	NULL	NULL	NULL	Importin alpha	GP		bind					Npap60	GP		N-terminus		NULL		NULL	NULL	NULL	NULL	gw60_cell_110_3_349_s_173	12176322	(B) Importin-alpha can bind NLS and the N terminus of Npap60 simultaneously.	bind
12503	3	3948	6	11	NULL	NULL	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_3_349_s_173	12176322	(B) Importin-alpha can bind NLS and the N terminus of Npap60 simultaneously.	bind
9722	1	3949	5	11	NULL	NULL	NULL	cyclin D1	GP		bind					CCND1 gene	GP			upstream regulatory region	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_16_7260_s_258	15282324	(B) In  vitro binding of cyclin D1 and pRb to the upstream regulatory region of the  CCND1 gene.	bind
9723	2	3949	5	11	NULL	NULL	NULL	pRb	GP		bind					CCND1 gene	GP			upstream regulatory region	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_16_7260_s_258	15282324	(B) In  vitro binding of cyclin D1 and pRb to the upstream regulatory region of the  CCND1 gene.	bind
9569	1	3949	6	11	NULL	NULL	NULL	Cyclin D1	GP		bind					CCND1 gene	GP			upstream regulatory region	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_16_7260_s_258	15282324	(B) In  vitro binding of cyclin D1 and pRb to the upstream regulatory region of the  CCND1 gene.	bind
9570	2	3949	6	11	NULL	NULL	NULL	pRb	GP		bind					CCND1 gene	GP			upstream regulatory region	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_16_7260_s_258	15282324	(B) In  vitro binding of cyclin D1 and pRb to the upstream regulatory region of the  CCND1 gene.	bind
9724	1	3950	5	11	NULL	NULL	NULL	FGF-1	GP		bind		high affinity			FGFR2	GP				NULL	cells expressing cell surface proteoglycans	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_368	10490614	(B) In cells where cell surface proteoglycans are present, FGF-1 binds to FGFR2 with a high affinity through interaction with the heparan sulfate glycosaminoglycan moiety and transmits moderate downstream signals.	bind
9728	2	3950	5	11	NULL	NULL	NULL	FGF-1	GP		interacts with					heparan sulfate glycosaminoglycan	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_368	10490614	(B) In cells where cell surface proteoglycans are present, FGF-1 binds to FGFR2 with a high affinity through interaction with the heparan sulfate glycosaminoglycan moiety and transmits moderate downstream signals.	bind
9729	4	3950	5	11	NULL	NULL	NULL	statement 2	Process		transmits					downstream signals	Process	moderate			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_368	10490614	(B) In cells where cell surface proteoglycans are present, FGF-1 binds to FGFR2 with a high affinity through interaction with the heparan sulfate glycosaminoglycan moiety and transmits moderate downstream signals.	bind
13001	3	3950	5	11	NULL	NULL	NULL	statement 1	Process		occurs through					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_368	10490614	(B) In cells where cell surface proteoglycans are present, FGF-1 binds to FGFR2 with a high affinity through interaction with the heparan sulfate glycosaminoglycan moiety and transmits moderate downstream signals.	bind
9571	1	3950	6	11	NULL	NULL	NULL	FGF-1	GP		bind		high affinity			FGFR2	GP				NULL	cells expressing cell surface proteoglycans	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_368	10490614	(B) In cells where cell surface proteoglycans are present, FGF-1 binds to FGFR2 with a high affinity through interaction with the heparan sulfate glycosaminoglycan moiety and transmits moderate downstream signals.	bind
9667	2	3950	6	11	NULL	NULL	NULL	FGF-1	GP		interacts with					heparan sulfate glycosaminoglycan	Chemical				NULL	cells expressing cell surface proteoglycans	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_368	10490614	(B) In cells where cell surface proteoglycans are present, FGF-1 binds to FGFR2 with a high affinity through interaction with the heparan sulfate glycosaminoglycan moiety and transmits moderate downstream signals.	bind
9668	3	3950	6	11	NULL	NULL	NULL	statement 1	Process		occurs through					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_368	10490614	(B) In cells where cell surface proteoglycans are present, FGF-1 binds to FGFR2 with a high affinity through interaction with the heparan sulfate glycosaminoglycan moiety and transmits moderate downstream signals.	bind
9669	4	3950	6	11	NULL	NULL	NULL	FGF-1	GP		transmits					downstream signals	Process	moderate			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_368	10490614	(B) In cells where cell surface proteoglycans are present, FGF-1 binds to FGFR2 with a high affinity through interaction with the heparan sulfate glycosaminoglycan moiety and transmits moderate downstream signals.	bind
10558	1	3951	5	11	NULL	NULL	NULL	RITS complex	GP		assembles at 									cenH	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
10559	2	3951	5	11	NULL	NULL	NULL	RITS complex	GP		assembles at									centromeric sequences	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
10560	5	3951	5	11	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
10561	3	3951	5	11	NULL	NULL	NULL	statement 1	Process		is dependent on					RNAi	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
10562	4	3951	5	11	NULL	NULL	NULL	statement 2	Process		is dependent on					RNAi	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
10563	6	3951	5	11	NULL	NULL	NULL	Clr4	GP		is recruited to									cenH	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
10564	7	3951	5	11	NULL	NULL	NULL	statement 3	Process		promote					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
10565	8	3951	5	11	NULL	NULL	NULL	Clr4	GP		is recruited to									centromeric sequences	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
10566	9	3951	5	11	NULL	NULL	NULL	statement 4	Process		promote					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
10567	10	3951	5	11	NULL	NULL	NULL	statement 7	Process		important for					silencing	Process	establishment of 			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
10568	11	3951	5	11	NULL	NULL	NULL	statement 9	Process		important for					silencing	Process	establishment of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
53776	12	3951	5	11	NULL	NULL	NULL	statement 4	Process		promote					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
53777	13	3951	5	11	NULL	NULL	NULL	statement 3	Process		promote					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
53778	14	3951	5	11	NULL	NULL	NULL	statement 12	Process		important for					silencing	Process	establishment of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
53779	15	3951	5	11	NULL	NULL	NULL	statement 13	Process		important for					silencing	Process	establishment of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
16271	1	3951	6	11	NULL	NULL	NULL	RITS complex	GP		assembles at									cenH sequences	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
16272	2	3951	6	11	NULL	NULL	NULL	RITS complex	GP		assembles at									centromeric sequences	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
16273	3	3951	6	11	NULL	NULL	NULL	statement 1	Process		is dependent on					RNAi	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
16274	4	3951	6	11	NULL	NULL	NULL	statement 2	Process		is dependent on					RNAi	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
16275	5	3951	6	11	NULL	NULL	NULL	Clr4	GP		is recruited on									cenH sequences	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
16277	6	3951	6	11	NULL	NULL	NULL	Clr4	GP		is recruited on									centromeric sequences	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
16278	7	3951	6	11	NULL	NULL	NULL	statement 1	Process		promotes					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
16279	8	3951	6	11	NULL	NULL	NULL	statement 1	Process		promotes					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
16280	9	3951	6	11	NULL	NULL	NULL	statement 2	Process		promotes					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
16281	10	3951	6	11	NULL	NULL	NULL	statement 2	Process		promotes					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
53775	11	3951	6	11	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
53780	12	3951	6	11	NULL	NULL	NULL	statement 7	Process		important for					silencing	Process	establishment of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
53781	13	3951	6	11	NULL	NULL	NULL	statement 8	Process		important for					silencing	Process	establishment of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
53782	14	3951	6	11	NULL	NULL	NULL	statement 9	Process		important for					silencing	Process	establishment of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
53783	15	3951	6	11	NULL	NULL	NULL	statement 10	Process		important for					silencing	Process	establishment of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2331_s_46	15743828	(B) In contrast, the RNAi-dependent assembly of the RITS complex at  cenH or centromeric sequences promotes recruitment of Clr4 to these sequences and is important  for establishment of silencing.	bind
9730	1	3952	5	11	NULL	NULL	NULL	HNF4	GP		bind		constitutively			fatty acids	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_2_219_s_36	12191466	(B) In contrast, the work by  Wisely et al. (2002  ) shows that HNF4 constitutively binds fatty acids as structural cofactors, raising the question of how the switch is made from corepressor to coactivator complex.	bind
53883	2	3952	5	11	NULL	NULL	NULL	HNF4	GP		acts as a					structural cofactor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_2_219_s_36	12191466	(B) In contrast, the work by  Wisely et al. (2002  ) shows that HNF4 constitutively binds fatty acids as structural cofactors, raising the question of how the switch is made from corepressor to coactivator complex.	bind
9572	1	3952	6	11	NULL	NULL	NULL	HNF4	GP		bind		constitutively			fatty acids	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_2_219_s_36	12191466	(B) In contrast, the work by  Wisely et al. (2002  ) shows that HNF4 constitutively binds fatty acids as structural cofactors, raising the question of how the switch is made from corepressor to coactivator complex.	bind
9674	2	3952	6	11	NULL	NULL	NULL	HNF-4	GP		acts as a					structural cofactor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_2_219_s_36	12191466	(B) In contrast, the work by  Wisely et al. (2002  ) shows that HNF4 constitutively binds fatty acids as structural cofactors, raising the question of how the switch is made from corepressor to coactivator complex.	bind
9731	1	3953	5	11	NULL	NULL	NULL	PP2A 	GP		bind			regulatory B subunit		KSR1	GP				NULL	stimulated cells	NULL	NULL	NULL	NULL	gw60_currbiol_13_16_1356_s_199	12932319	(B) In stimulated cells, Ras activation induces binding of the PP2A regulatory B subunit to the KSR1 and Raf-1 complexes, increasing PP2A activity and resulting in the dephosphorylation of KSR1 on S392 and Raf-1 on S259.	bind
9732	5	3953	5	11	NULL	NULL	NULL	PP2A 	GP		bind			regulatory B subunit		Raf-1 complex	GP				NULL	stimulated cells	NULL	NULL	NULL	NULL	gw60_currbiol_13_16_1356_s_199	12932319	(B) In stimulated cells, Ras activation induces binding of the PP2A regulatory B subunit to the KSR1 and Raf-1 complexes, increasing PP2A activity and resulting in the dephosphorylation of KSR1 on S392 and Raf-1 on S259.	bind
9733	2	3953	5	11	NULL	NULL	NULL	Ras	GP	activation of	induce					statement 1	Process				NULL	stimulated cells	NULL	NULL	NULL	NULL	gw60_currbiol_13_16_1356_s_199	12932319	(B) In stimulated cells, Ras activation induces binding of the PP2A regulatory B subunit to the KSR1 and Raf-1 complexes, increasing PP2A activity and resulting in the dephosphorylation of KSR1 on S392 and Raf-1 on S259.	bind
9734	6	3953	5	11	NULL	NULL	NULL	Ras	GP	activation of	induce					statement 5	Process				NULL	stimulated cells	NULL	NULL	NULL	NULL	gw60_currbiol_13_16_1356_s_199	12932319	(B) In stimulated cells, Ras activation induces binding of the PP2A regulatory B subunit to the KSR1 and Raf-1 complexes, increasing PP2A activity and resulting in the dephosphorylation of KSR1 on S392 and Raf-1 on S259.	bind
9735	3	3953	5	11	NULL	NULL	NULL	statement 2	Process		increase					PP2A	GP	activity of			NULL	stimulated cells	NULL	NULL	NULL	NULL	gw60_currbiol_13_16_1356_s_199	12932319	(B) In stimulated cells, Ras activation induces binding of the PP2A regulatory B subunit to the KSR1 and Raf-1 complexes, increasing PP2A activity and resulting in the dephosphorylation of KSR1 on S392 and Raf-1 on S259.	bind
9736	7	3953	5	11	NULL	NULL	NULL	statement 6	Process		increase					PP2A	GP	activity of			NULL	stimulated cells	NULL	NULL	NULL	NULL	gw60_currbiol_13_16_1356_s_199	12932319	(B) In stimulated cells, Ras activation induces binding of the PP2A regulatory B subunit to the KSR1 and Raf-1 complexes, increasing PP2A activity and resulting in the dephosphorylation of KSR1 on S392 and Raf-1 on S259.	bind
9737	4	3953	5	11	NULL	NULL	NULL	statement 3	Process		results in					KSR1	GP	dephosphorylation of	S392		NULL	stimulated cells	NULL	NULL	NULL	NULL	gw60_currbiol_13_16_1356_s_199	12932319	(B) In stimulated cells, Ras activation induces binding of the PP2A regulatory B subunit to the KSR1 and Raf-1 complexes, increasing PP2A activity and resulting in the dephosphorylation of KSR1 on S392 and Raf-1 on S259.	bind
9738	8	3953	5	11	NULL	NULL	NULL	statement 7	Process		results in					Raf-1	GP	dephosphorylation of	S259		NULL	stimulated cells	NULL	NULL	NULL	NULL	gw60_currbiol_13_16_1356_s_199	12932319	(B) In stimulated cells, Ras activation induces binding of the PP2A regulatory B subunit to the KSR1 and Raf-1 complexes, increasing PP2A activity and resulting in the dephosphorylation of KSR1 on S392 and Raf-1 on S259.	bind
9680	4	3953	6	11	NULL	NULL	NULL	Ras	GP	activation of	dephosphorylates					KSR1	GP		S392		NULL	stimulated cells	NULL	NULL	NULL	NULL	gw60_currbiol_13_16_1356_s_199	12932319	(B) In stimulated cells, Ras activation induces binding of the PP2A regulatory B subunit to the KSR1 and Raf-1 complexes, increasing PP2A activity and resulting in the dephosphorylation of KSR1 on S392 and Raf-1 on S259.	bind
9681	5	3953	6	11	NULL	NULL	NULL	Ras	GP	activation of	dephosphorylates					Raf-1	GP		S259		NULL	stimulated cells	NULL	NULL	NULL	NULL	gw60_currbiol_13_16_1356_s_199	12932319	(B) In stimulated cells, Ras activation induces binding of the PP2A regulatory B subunit to the KSR1 and Raf-1 complexes, increasing PP2A activity and resulting in the dephosphorylation of KSR1 on S392 and Raf-1 on S259.	bind
10497	1	3953	6	11	NULL	NULL	NULL	PP2A	GP		bind			 regulatory B subunit 		KSR1	GP				NULL	stimulated cells	NULL	NULL	NULL	NULL	gw60_currbiol_13_16_1356_s_199	12932319	(B) In stimulated cells, Ras activation induces binding of the PP2A regulatory B subunit to the KSR1 and Raf-1 complexes, increasing PP2A activity and resulting in the dephosphorylation of KSR1 on S392 and Raf-1 on S259.	bind
10498	2	3953	6	11	NULL	NULL	NULL	PP2A 	GP		bind			regulatory B subunit		Raf-1 complexes	GP				NULL	stimulated cells	NULL	NULL	NULL	NULL	gw60_currbiol_13_16_1356_s_199	12932319	(B) In stimulated cells, Ras activation induces binding of the PP2A regulatory B subunit to the KSR1 and Raf-1 complexes, increasing PP2A activity and resulting in the dephosphorylation of KSR1 on S392 and Raf-1 on S259.	bind
10499	3	3953	6	11	NULL	NULL	NULL	statement 1	Process		increases					PP2A	GP	activity of			NULL	stimulated cells	NULL	NULL	NULL	NULL	gw60_currbiol_13_16_1356_s_199	12932319	(B) In stimulated cells, Ras activation induces binding of the PP2A regulatory B subunit to the KSR1 and Raf-1 complexes, increasing PP2A activity and resulting in the dephosphorylation of KSR1 on S392 and Raf-1 on S259.	bind
12505	6	3953	6	11	NULL	NULL	NULL	Ras	GP	activation of	induces					statement 1	Process				NULL	stimulated cells	NULL	NULL	NULL	NULL	gw60_currbiol_13_16_1356_s_199	12932319	(B) In stimulated cells, Ras activation induces binding of the PP2A regulatory B subunit to the KSR1 and Raf-1 complexes, increasing PP2A activity and resulting in the dephosphorylation of KSR1 on S392 and Raf-1 on S259.	bind
53905	7	3953	6	11	NULL	NULL	NULL	statement 2	Process		increases					PP2A	GP	activity of			NULL	stimulated cells	NULL	NULL	NULL	NULL	gw60_currbiol_13_16_1356_s_199	12932319	(B) In stimulated cells, Ras activation induces binding of the PP2A regulatory B subunit to the KSR1 and Raf-1 complexes, increasing PP2A activity and resulting in the dephosphorylation of KSR1 on S392 and Raf-1 on S259.	bind
53906	8	3953	6	11	NULL	NULL	NULL	Ras	GP	activation of	induces					statement 2	Process				NULL	stimulated cells	NULL	NULL	NULL	NULL	gw60_currbiol_13_16_1356_s_199	12932319	(B) In stimulated cells, Ras activation induces binding of the PP2A regulatory B subunit to the KSR1 and Raf-1 complexes, increasing PP2A activity and resulting in the dephosphorylation of KSR1 on S392 and Raf-1 on S259.	bind
9739	1	3954	5	11	NULL	NULL	NULL	CreERT2 	GP		bind					HSP90	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_22_4_430_s_29	12727441	(B) In the absence of appropriate ligand, the CreERT2  fusion protein is bound to the heatshock protein HSP90 and inhibited from entering  the nucleus.	bind
9740	4	3954	5	11	NULL	NULL	NULL	statement 1	Process		in the absence of					appropriate ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_22_4_430_s_29	12727441	(B) In the absence of appropriate ligand, the CreERT2  fusion protein is bound to the heatshock protein HSP90 and inhibited from entering  the nucleus.	bind
9741	2	3954	5	11	NULL	NULL	NULL	CreERT2	GP		is inhibited from					 nucleus	CellComponent	entering into			NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_22_4_430_s_29	12727441	(B) In the absence of appropriate ligand, the CreERT2  fusion protein is bound to the heatshock protein HSP90 and inhibited from entering  the nucleus.	bind
9742	3	3954	5	11	NULL	NULL	NULL	statement 2	Process		occurs following					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_22_4_430_s_29	12727441	(B) In the absence of appropriate ligand, the CreERT2  fusion protein is bound to the heatshock protein HSP90 and inhibited from entering  the nucleus.	bind
53914	5	3954	5	11	NULL	NULL	NULL	HSP90	GP		is a type of					heatshock protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_22_4_430_s_29	12727441	(B) In the absence of appropriate ligand, the CreERT2  fusion protein is bound to the heatshock protein HSP90 and inhibited from entering  the nucleus.	bind
53915	6	3954	5	11	NULL	NULL	NULL	CreERT2	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_22_4_430_s_29	12727441	(B) In the absence of appropriate ligand, the CreERT2  fusion protein is bound to the heatshock protein HSP90 and inhibited from entering  the nucleus.	bind
9573	1	3954	6	11	NULL	NULL	NULL	CreERT2 	GP		bind					 HSP90	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_22_4_430_s_29	12727441	(B) In the absence of appropriate ligand, the CreERT2  fusion protein is bound to the heatshock protein HSP90 and inhibited from entering  the nucleus.	bind
12506	2	3954	6	11	NULL	NULL	NULL	CreERT2	GP		is inhibited from					nucleus	CellComponent	entering into			NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_22_4_430_s_29	12727441	(B) In the absence of appropriate ligand, the CreERT2  fusion protein is bound to the heatshock protein HSP90 and inhibited from entering  the nucleus.	bind
53920	3	3954	6	11	NULL	NULL	NULL	statement 2	Process		occurs following					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_22_4_430_s_29	12727441	(B) In the absence of appropriate ligand, the CreERT2  fusion protein is bound to the heatshock protein HSP90 and inhibited from entering  the nucleus.	bind
53921	4	3954	6	11	NULL	NULL	NULL	statement 1	Process		in the absence of					appropriate ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_22_4_430_s_29	12727441	(B) In the absence of appropriate ligand, the CreERT2  fusion protein is bound to the heatshock protein HSP90 and inhibited from entering  the nucleus.	bind
53922	5	3954	6	11	NULL	NULL	NULL	HSP90	GP		is a type of					heatshock protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_22_4_430_s_29	12727441	(B) In the absence of appropriate ligand, the CreERT2  fusion protein is bound to the heatshock protein HSP90 and inhibited from entering  the nucleus.	bind
53923	6	3954	6	11	NULL	NULL	NULL	CreERT2	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_22_4_430_s_29	12727441	(B) In the absence of appropriate ligand, the CreERT2  fusion protein is bound to the heatshock protein HSP90 and inhibited from entering  the nucleus.	bind
9743	1	3956	5	11	NULL	NULL	NULL	ScaA	GP	enzyme-laden	bind					ScaD	GP	type II cohesins of			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_17_5782_s_193	15317783	(B) In the additional mechanism of attachment, the enzyme-laden ScaA is bound to  the type II cohesins of ScaD, which can also accept a single enzyme via its third  type I cohesin.	bind
9744	2	3956	5	11	NULL	NULL	NULL	ScaD	GP		accept					single enzyme	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_17_5782_s_193	15317783	(B) In the additional mechanism of attachment, the enzyme-laden ScaA is bound to  the type II cohesins of ScaD, which can also accept a single enzyme via its third  type I cohesin.	bind
9745	3	3956	5	11	NULL	NULL	NULL	statement 2	Process		occurs via					 cohesin	GP		third type I		NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_17_5782_s_193	15317783	(B) In the additional mechanism of attachment, the enzyme-laden ScaA is bound to  the type II cohesins of ScaD, which can also accept a single enzyme via its third  type I cohesin.	bind
9574	1	3956	6	11	NULL	NULL	NULL	ScaA	GP	enzyme-laden 	bind					 ScaD	GP	type II cohesins of			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_17_5782_s_193	15317783	(B) In the additional mechanism of attachment, the enzyme-laden ScaA is bound to  the type II cohesins of ScaD, which can also accept a single enzyme via its third  type I cohesin.	bind
12511	2	3956	6	11	NULL	NULL	NULL	ScaD	GP		accept					single enzyme	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_17_5782_s_193	15317783	(B) In the additional mechanism of attachment, the enzyme-laden ScaA is bound to  the type II cohesins of ScaD, which can also accept a single enzyme via its third  type I cohesin.	bind
12512	3	3956	6	11	NULL	NULL	NULL	statement 2	Process		occurs via					cohesin	GP		third type I		NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_17_5782_s_193	15317783	(B) In the additional mechanism of attachment, the enzyme-laden ScaA is bound to  the type II cohesins of ScaD, which can also accept a single enzyme via its third  type I cohesin.	bind
9746	1	3957	5	11	NULL	NULL	NULL	APC	Organism		bind					beta-catenin	GP				NULL	adult colonocyte	NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_699_s_346	10330400	(B) In the adult  colonocyte, Wnt is not present, GSK-3beta activity is constitutively high, and APC binds beta-catenin and targets it for degradation.	bind
9747	2	3957	5	11	NULL	NULL	NULL	statement 1	Process		targets					beta-catenin	GP	 degradation of			NULL	adult colonocyte	NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_699_s_346	10330400	(B) In the adult  colonocyte, Wnt is not present, GSK-3beta activity is constitutively high, and APC binds beta-catenin and targets it for degradation.	bind
53931	3	3957	5	11	NULL	NULL	NULL	Wnt	GP		not present in					adult colonocyte	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_699_s_346	10330400	(B) In the adult  colonocyte, Wnt is not present, GSK-3beta activity is constitutively high, and APC binds beta-catenin and targets it for degradation.	bind
53932	4	3957	5	11	NULL	NULL	NULL	GSK-3beta	GP	activity of	is high in		constitutively			adult colonocyte	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_699_s_346	10330400	(B) In the adult  colonocyte, Wnt is not present, GSK-3beta activity is constitutively high, and APC binds beta-catenin and targets it for degradation.	bind
9575	1	3957	6	11	NULL	NULL	NULL	APC	Organism		bind					beta-catenin	GP				NULL	adult colonocyte	NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_699_s_346	10330400	(B) In the adult  colonocyte, Wnt is not present, GSK-3beta activity is constitutively high, and APC binds beta-catenin and targets it for degradation.	bind
9576	2	3957	6	11	NULL	NULL	NULL	Wnt	GP		is not present in					adult colonocyte	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_699_s_346	10330400	(B) In the adult  colonocyte, Wnt is not present, GSK-3beta activity is constitutively high, and APC binds beta-catenin and targets it for degradation.	bind
9577	3	3957	6	11	NULL	NULL	NULL	GSK-3beta	GP	activity of	is high		constitutively			adult colonocyte	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_699_s_346	10330400	(B) In the adult  colonocyte, Wnt is not present, GSK-3beta activity is constitutively high, and APC binds beta-catenin and targets it for degradation.	bind
53933	4	3957	6	11	NULL	NULL	NULL	statement 1	Process		targets					beta-catenin	GP	degradation of			NULL	adult colonocyte	NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_699_s_346	10330400	(B) In the adult  colonocyte, Wnt is not present, GSK-3beta activity is constitutively high, and APC binds beta-catenin and targets it for degradation.	bind
9748	1	3958	5	11	NULL	NULL	NULL	NT2	GP		bind					Col11a2	GP	WT		promoter sequence	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4256_s_236	12024037	(B) In the left panel, lane 2 shows that NT2 bound to the WT  Col11a2 promoter sequence.	bind
9578	1	3958	6	11	NULL	NULL	NULL	NT2	GP		bind					Col11a2	GP	wild type		promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4256_s_236	12024037	(B) In the left panel, lane 2 shows that NT2 bound to the WT  Col11a2 promoter sequence.	bind
9749	1	3959	5	11	NULL	NULL	NULL	transposase	GP		forms complex with					transposon	GP		end fragments		NULL		NULL	NULL	NULL	NULL	gw60_cell_84_2_223_s_64	8565068	(B) In the presence of IHF, transposase builds a synaptic  complex with a pair of transposon end fragments (paired ends complex or  PEC;  Sakai et al., 1995   ).	bind
9750	2	3959	5	11	NULL	NULL	NULL	statement 1	Process		in the presence of					IHF	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_2_223_s_64	8565068	(B) In the presence of IHF, transposase builds a synaptic  complex with a pair of transposon end fragments (paired ends complex or  PEC;  Sakai et al., 1995   ).	bind
53934	3	3959	5	11	NULL	NULL	NULL	statement 1	Process		forms					synaptic complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_2_223_s_64	8565068	(B) In the presence of IHF, transposase builds a synaptic  complex with a pair of transposon end fragments (paired ends complex or  PEC;  Sakai et al., 1995   ).	bind
53935	4	3959	5	11	NULL	NULL	NULL	PEC	GP		is					paired ends complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_2_223_s_64	8565068	(B) In the presence of IHF, transposase builds a synaptic  complex with a pair of transposon end fragments (paired ends complex or  PEC;  Sakai et al., 1995   ).	bind
9579	1	3959	6	11	NULL	NULL	NULL	transposase	GP		forms a complex with					transposon	GP		end fragments		NULL		NULL	NULL	NULL	NULL	gw60_cell_84_2_223_s_64	8565068	(B) In the presence of IHF, transposase builds a synaptic  complex with a pair of transposon end fragments (paired ends complex or  PEC;  Sakai et al., 1995   ).	bind
9580	2	3959	6	11	NULL	NULL	NULL	PEC	GP		is					paired ends complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_2_223_s_64	8565068	(B) In the presence of IHF, transposase builds a synaptic  complex with a pair of transposon end fragments (paired ends complex or  PEC;  Sakai et al., 1995   ).	bind
9581	3	3959	6	11	NULL	NULL	NULL	statement 1	Process		occurs in presence of					IHF	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_2_223_s_64	8565068	(B) In the presence of IHF, transposase builds a synaptic  complex with a pair of transposon end fragments (paired ends complex or  PEC;  Sakai et al., 1995   ).	bind
53936	4	3959	6	11	NULL	NULL	NULL	statement 1	Process		forms					synaptic complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_2_223_s_64	8565068	(B) In the presence of IHF, transposase builds a synaptic  complex with a pair of transposon end fragments (paired ends complex or  PEC;  Sakai et al., 1995   ).	bind
9751	1	3960	5	11	NULL	NULL	NULL	WAK1	GP		bind					OEE2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_305_4_862_s_127	12767910	(B) In vitro binding of  WAK1 to OEE2.	bind
9582	1	3960	6	11	NULL	NULL	NULL	WAK1	GP		bind					OEE2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_305_4_862_s_127	12767910	(B) In vitro binding of  WAK1 to OEE2.	bind
9752	1	3961	5	11	NULL	NULL	NULL	ASAP1b	GP		bind					GST-Src	GP		SH3		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7038_s_327	9819391	(B) In vitro binding of ASAP1b to GST-Src SH3 and GST-Crk.	bind
9753	2	3961	5	11	NULL	NULL	NULL	ASAP1b	GP		bind					GST-Crk	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7038_s_327	9819391	(B) In vitro binding of ASAP1b to GST-Src SH3 and GST-Crk.	bind
9583	1	3961	6	11	NULL	NULL	NULL	 ASAP1b	GP		bind					GST-Src	GP		SH3 domain		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7038_s_327	9819391	(B) In vitro binding of ASAP1b to GST-Src SH3 and GST-Crk.	bind
9584	2	3961	6	11	NULL	NULL	NULL	ASAP1b	GP		bind					GST-Crk	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7038_s_327	9819391	(B) In vitro binding of ASAP1b to GST-Src SH3 and GST-Crk.	bind
9754	1	3962	5	11	NULL	NULL	NULL	E2F	GP		bind					PPAR 1	GP			promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_devcell_3_1_39_s_70	12110166	(B) In vitro binding of E2F to the  PPAR 1 promoter.	bind
9585	1	3962	6	11	NULL	NULL	NULL	E2F	GP		bind					PPAR1	GP			promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_devcell_3_1_39_s_70	12110166	(B) In vitro binding of E2F to the  PPAR 1 promoter.	bind
9755	1	3963	5	11	NULL	NULL	NULL	Gab1	GP		bind			MBD		Met	GP	WT			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_7_6_1293_s_35	11430831	(B) In vitro binding of Gab1, Grb2, Src, and p85PI3K by MetWT and Metd. GST-fusion proteins of the Gab1 Met binding domain (MBD), the carboxyl-terminal p85PI3K SH2, the Src SH2, and full size Grb2 were immobilized on glutathione-Sepharose and incubated with lysates of untreated or HGF-stimulated  metWT/WT and  metd/d hepatocytes.	bind
9756	2	3963	5	11	NULL	NULL	NULL	Gab1	GP		bind			MBD		Metd	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_7_6_1293_s_35	11430831	(B) In vitro binding of Gab1, Grb2, Src, and p85PI3K by MetWT and Metd. GST-fusion proteins of the Gab1 Met binding domain (MBD), the carboxyl-terminal p85PI3K SH2, the Src SH2, and full size Grb2 were immobilized on glutathione-Sepharose and incubated with lysates of untreated or HGF-stimulated  metWT/WT and  metd/d hepatocytes.	bind
9757	3	3963	5	11	NULL	NULL	NULL	Grb2	GP	full size	bind					Met	GP	WT			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_7_6_1293_s_35	11430831	(B) In vitro binding of Gab1, Grb2, Src, and p85PI3K by MetWT and Metd. GST-fusion proteins of the Gab1 Met binding domain (MBD), the carboxyl-terminal p85PI3K SH2, the Src SH2, and full size Grb2 were immobilized on glutathione-Sepharose and incubated with lysates of untreated or HGF-stimulated  metWT/WT and  metd/d hepatocytes.	bind
9758	4	3963	5	11	NULL	NULL	NULL	Grb2	GP	full size	bind					Metd	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_7_6_1293_s_35	11430831	(B) In vitro binding of Gab1, Grb2, Src, and p85PI3K by MetWT and Metd. GST-fusion proteins of the Gab1 Met binding domain (MBD), the carboxyl-terminal p85PI3K SH2, the Src SH2, and full size Grb2 were immobilized on glutathione-Sepharose and incubated with lysates of untreated or HGF-stimulated  metWT/WT and  metd/d hepatocytes.	bind
9759	5	3963	5	11	NULL	NULL	NULL	Src	GP		bind			SH2		Met	GP	WT			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_7_6_1293_s_35	11430831	(B) In vitro binding of Gab1, Grb2, Src, and p85PI3K by MetWT and Metd. GST-fusion proteins of the Gab1 Met binding domain (MBD), the carboxyl-terminal p85PI3K SH2, the Src SH2, and full size Grb2 were immobilized on glutathione-Sepharose and incubated with lysates of untreated or HGF-stimulated  metWT/WT and  metd/d hepatocytes.	bind
9760	6	3963	5	11	NULL	NULL	NULL	Src	GP		bind			SH2		Metd	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_7_6_1293_s_35	11430831	(B) In vitro binding of Gab1, Grb2, Src, and p85PI3K by MetWT and Metd. GST-fusion proteins of the Gab1 Met binding domain (MBD), the carboxyl-terminal p85PI3K SH2, the Src SH2, and full size Grb2 were immobilized on glutathione-Sepharose and incubated with lysates of untreated or HGF-stimulated  metWT/WT and  metd/d hepatocytes.	bind
9761	7	3963	5	11	NULL	NULL	NULL	p85PI3K	GP		bind			carboxyl-terminal;;SH2		Met	GP	WT			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_7_6_1293_s_35	11430831	(B) In vitro binding of Gab1, Grb2, Src, and p85PI3K by MetWT and Metd. GST-fusion proteins of the Gab1 Met binding domain (MBD), the carboxyl-terminal p85PI3K SH2, the Src SH2, and full size Grb2 were immobilized on glutathione-Sepharose and incubated with lysates of untreated or HGF-stimulated  metWT/WT and  metd/d hepatocytes.	bind
9762	8	3963	5	11	NULL	NULL	NULL	p85PI3K	GP		bind			 carboxyl-terminal;;SH2		Metd	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_7_6_1293_s_35	11430831	(B) In vitro binding of Gab1, Grb2, Src, and p85PI3K by MetWT and Metd. GST-fusion proteins of the Gab1 Met binding domain (MBD), the carboxyl-terminal p85PI3K SH2, the Src SH2, and full size Grb2 were immobilized on glutathione-Sepharose and incubated with lysates of untreated or HGF-stimulated  metWT/WT and  metd/d hepatocytes.	bind
53971	9	3963	5	11	NULL	NULL	NULL	MBD	GP		is					Met binding domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_6_1293_s_35	11430831	(B) In vitro binding of Gab1, Grb2, Src, and p85PI3K by MetWT and Metd. GST-fusion proteins of the Gab1 Met binding domain (MBD), the carboxyl-terminal p85PI3K SH2, the Src SH2, and full size Grb2 were immobilized on glutathione-Sepharose and incubated with lysates of untreated or HGF-stimulated  metWT/WT and  metd/d hepatocytes.	bind
9682	1	3963	6	11	NULL	NULL	NULL	Gab1	GP		bind			MBD		Met	GP	wild type			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_7_6_1293_s_35	11430831	(B) In vitro binding of Gab1, Grb2, Src, and p85PI3K by MetWT and Metd. GST-fusion proteins of the Gab1 Met binding domain (MBD), the carboxyl-terminal p85PI3K SH2, the Src SH2, and full size Grb2 were immobilized on glutathione-Sepharose and incubated with lysates of untreated or HGF-stimulated  metWT/WT and  metd/d hepatocytes.	bind
9683	2	3963	6	11	NULL	NULL	NULL	Gab1	GP		bind			MBD		Metd	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_6_1293_s_35	11430831	(B) In vitro binding of Gab1, Grb2, Src, and p85PI3K by MetWT and Metd. GST-fusion proteins of the Gab1 Met binding domain (MBD), the carboxyl-terminal p85PI3K SH2, the Src SH2, and full size Grb2 were immobilized on glutathione-Sepharose and incubated with lysates of untreated or HGF-stimulated  metWT/WT and  metd/d hepatocytes.	bind
9684	3	3963	6	11	NULL	NULL	NULL	Grb2	GP	full size	bind					Met	GP	wild type			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_7_6_1293_s_35	11430831	(B) In vitro binding of Gab1, Grb2, Src, and p85PI3K by MetWT and Metd. GST-fusion proteins of the Gab1 Met binding domain (MBD), the carboxyl-terminal p85PI3K SH2, the Src SH2, and full size Grb2 were immobilized on glutathione-Sepharose and incubated with lysates of untreated or HGF-stimulated  metWT/WT and  metd/d hepatocytes.	bind
9685	4	3963	6	11	NULL	NULL	NULL	Grb2	GP	full size	bind					Metd	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_7_6_1293_s_35	11430831	(B) In vitro binding of Gab1, Grb2, Src, and p85PI3K by MetWT and Metd. GST-fusion proteins of the Gab1 Met binding domain (MBD), the carboxyl-terminal p85PI3K SH2, the Src SH2, and full size Grb2 were immobilized on glutathione-Sepharose and incubated with lysates of untreated or HGF-stimulated  metWT/WT and  metd/d hepatocytes.	bind
9686	5	3963	6	11	NULL	NULL	NULL	MBD	GP		is					Met binding domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_6_1293_s_35	11430831	(B) In vitro binding of Gab1, Grb2, Src, and p85PI3K by MetWT and Metd. GST-fusion proteins of the Gab1 Met binding domain (MBD), the carboxyl-terminal p85PI3K SH2, the Src SH2, and full size Grb2 were immobilized on glutathione-Sepharose and incubated with lysates of untreated or HGF-stimulated  metWT/WT and  metd/d hepatocytes.	bind
9687	6	3963	6	11	NULL	NULL	NULL	Src	GP		bind			SH2 domain		Met	GP	wild type			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_7_6_1293_s_35	11430831	(B) In vitro binding of Gab1, Grb2, Src, and p85PI3K by MetWT and Metd. GST-fusion proteins of the Gab1 Met binding domain (MBD), the carboxyl-terminal p85PI3K SH2, the Src SH2, and full size Grb2 were immobilized on glutathione-Sepharose and incubated with lysates of untreated or HGF-stimulated  metWT/WT and  metd/d hepatocytes.	bind
9688	7	3963	6	11	NULL	NULL	NULL	Src	GP		bind			SH2 domain		Metd	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_7_6_1293_s_35	11430831	(B) In vitro binding of Gab1, Grb2, Src, and p85PI3K by MetWT and Metd. GST-fusion proteins of the Gab1 Met binding domain (MBD), the carboxyl-terminal p85PI3K SH2, the Src SH2, and full size Grb2 were immobilized on glutathione-Sepharose and incubated with lysates of untreated or HGF-stimulated  metWT/WT and  metd/d hepatocytes.	bind
9689	8	3963	6	11	NULL	NULL	NULL	p85PI3K	GP		bind			carboxyl-terminal domain;;SH2		Met	GP	wild type			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_7_6_1293_s_35	11430831	(B) In vitro binding of Gab1, Grb2, Src, and p85PI3K by MetWT and Metd. GST-fusion proteins of the Gab1 Met binding domain (MBD), the carboxyl-terminal p85PI3K SH2, the Src SH2, and full size Grb2 were immobilized on glutathione-Sepharose and incubated with lysates of untreated or HGF-stimulated  metWT/WT and  metd/d hepatocytes.	bind
9690	9	3963	6	11	NULL	NULL	NULL	p85PI3K	GP		bind			carboxyl-terminal domain;;SH2		Metd	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_7_6_1293_s_35	11430831	(B) In vitro binding of Gab1, Grb2, Src, and p85PI3K by MetWT and Metd. GST-fusion proteins of the Gab1 Met binding domain (MBD), the carboxyl-terminal p85PI3K SH2, the Src SH2, and full size Grb2 were immobilized on glutathione-Sepharose and incubated with lysates of untreated or HGF-stimulated  metWT/WT and  metd/d hepatocytes.	bind
9763	1	3964	5	11	NULL	NULL	NULL	h411/414	GP		bind					RanBP3	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8751_s_270	14612415	(B) In vitro binding of h411/414 to RanBP3.	bind
9586	1	3964	6	11	NULL	NULL	NULL	h411/414	GP		bind					RanBP3	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8751_s_270	14612415	(B) In vitro binding of h411/414 to RanBP3.	bind
9764	1	3965	5	11	NULL	NULL	NULL	Siah-1	GP		bind					Sina protein	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_724_s_176	9858595	(B) In vitro binding of Siah-1 to the Sina protein.	bind
9587	1	3965	6	11	NULL	NULL	NULL	Siah-1	GP		bind					Sina protein	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_724_s_176	9858595	(B) In vitro binding of Siah-1 to the Sina protein.	bind
9765	1	3966	5	11	NULL	NULL	NULL	Numb	GP		bind			PTB domain		Nak	GP		C terminus		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_598_s_143	9418906	(B) In vitro binding of the Numb PTB domain to the Nak C terminus.	bind
9588	1	3966	6	11	NULL	NULL	NULL	Numb	GP		bind			PTB domain		Nak	GP		C terminus		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_598_s_143	9418906	(B) In vitro binding of the Numb PTB domain to the Nak C terminus.	bind
9766	1	3967	5	11	NULL	NULL	NULL	titin	GP		bind					obscurin	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cellbiol_154_1_123_s_175	11448995	(B) In vitro binding of titin to obscurin.	bind
9589	1	3967	6	11	NULL	NULL	NULL	titin	GP		bind					obscurin	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cellbiol_154_1_123_s_175	11448995	(B) In vitro binding of titin to obscurin.	bind
9767	1	3968	5	11	NULL	NULL	NULL	WAK1	GP		bind					OEE2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_305_4_862_s_127	12767910	(B) In vitro binding of WAK1 to OEE2.	bind
9590	1	3968	6	11	NULL	NULL	NULL	WAK1	GP		bind					OEE2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_305_4_862_s_127	12767910	(B) In vitro binding of WAK1 to OEE2.	bind
9768	1	3970	5	11	NULL	NULL	NULL	NF-kB	GP		bind					DNA	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_2957_s_266	15798185	(B) In vitro DNA binding assay of NF-kB.	bind
9591	1	3970	6	11	NULL	NULL	NULL	NF-kB	GP		bind					DNA	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_2957_s_266	15798185	(B) In vitro DNA binding assay of NF-kB.	bind
9769	1	3971	5	11	NULL	NULL	NULL	Miz-1	GP		bind					GST-TopBP1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_10_3_509_s_71	12408820	(B) In vitro GST binding assays demonstrating POZ-dependent binding of Miz-1 to GST-TopBP1 but not to GST alone.	bind
9770	2	3971	5	11	NULL	NULL	NULL	Miz-1	GP		does not bind					GST	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_10_3_509_s_71	12408820	(B) In vitro GST binding assays demonstrating POZ-dependent binding of Miz-1 to GST-TopBP1 but not to GST alone.	bind
9771	3	3971	5	11	NULL	NULL	NULL	statement 1	Process		is dependent on								POZ		NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_3_509_s_71	12408820	(B) In vitro GST binding assays demonstrating POZ-dependent binding of Miz-1 to GST-TopBP1 but not to GST alone.	bind
9592	1	3971	6	11	NULL	NULL	NULL	Miz-1	GP		bind					GST-TopBP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_3_509_s_71	12408820	(B) In vitro GST binding assays demonstrating POZ-dependent binding of Miz-1 to GST-TopBP1 but not to GST alone.	bind
9593	2	3971	6	11	NULL	NULL	NULL	statement 1	Process		is dependent on								POZ		NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_3_509_s_71	12408820	(B) In vitro GST binding assays demonstrating POZ-dependent binding of Miz-1 to GST-TopBP1 but not to GST alone.	bind
9594	3	3971	6	11	NULL	NULL	NULL	Miz-1	GP		does not bind					GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_3_509_s_71	12408820	(B) In vitro GST binding assays demonstrating POZ-dependent binding of Miz-1 to GST-TopBP1 but not to GST alone.	bind
9772	1	3974	5	11	NULL	NULL	NULL	Adaptin protein	GP	in vitro-translated	bind					GST-Numb	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_2_221_s_161	12194853	(B) In vitro-translated  -Adaptin protein binds GST-Numb, but binding to GST-Numb 5  (Frise et al., 1996  ) lacking amino acids (aa) 426-546 is strongly reduced.	bind
9773	2	3974	5	11	NULL	NULL	NULL	Adaptin protein	GP	in vitro-translated	bind					GST-Numb 5	GP	lacking amino acids	426-546		NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_2_221_s_161	12194853	(B) In vitro-translated  -Adaptin protein binds GST-Numb, but binding to GST-Numb 5  (Frise et al., 1996  ) lacking amino acids (aa) 426-546 is strongly reduced.	bind
9774	3	3974	5	11	NULL	NULL	NULL	statement 2	Process	binding of	reduced than		strongly			statement 1	Process	binding of			NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_2_221_s_161	12194853	(B) In vitro-translated  -Adaptin protein binds GST-Numb, but binding to GST-Numb 5  (Frise et al., 1996  ) lacking amino acids (aa) 426-546 is strongly reduced.	bind
9595	1	3974	6	11	NULL	NULL	NULL	Adaptin protein	GP	in vitro-translated	bind					GST-Numb 5	GP	lacking amino acids	426-546		NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_2_221_s_161	12194853	(B) In vitro-translated  -Adaptin protein binds GST-Numb, but binding to GST-Numb 5  (Frise et al., 1996  ) lacking amino acids (aa) 426-546 is strongly reduced.	bind
16267	2	3974	6	11	NULL	NULL	NULL	Adaptin protein	GP	in vitro-translated	bind					GST-Numb	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_2_221_s_161	12194853	(B) In vitro-translated  -Adaptin protein binds GST-Numb, but binding to GST-Numb 5  (Frise et al., 1996  ) lacking amino acids (aa) 426-546 is strongly reduced.	bind
16276	3	3974	6	11	NULL	NULL	NULL	statement 2	Process	binding of	reduced than		strongly			statement 1	Process	binding of			NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_2_221_s_161	12194853	(B) In vitro-translated  -Adaptin protein binds GST-Numb, but binding to GST-Numb 5  (Frise et al., 1996  ) lacking amino acids (aa) 426-546 is strongly reduced.	bind
9775	1	3977	5	11	NULL	NULL	NULL	IRF-1	GP		bind					IL-4	GP			promoter	NULL	in vivo Jurkat T cells transfected with IRF-1 expression vectors	NULL	NULL	NULL	NULL	gw60_immunity_17_6_703_s_186	12479817	(B) In vivo binding of IRF-1 and IRF-2 to the IL-4 promoter was assessed by ChIP with Jurkat T cells transfected with IRF-1 and IRF-2 expression vectors.	bind
9776	2	3977	5	11	NULL	NULL	NULL	IRF-2	GP		bind					IL-4	GP			promoter	NULL	in vivo Jurkat T cells transfected with IRF-2 expression vectors	NULL	NULL	NULL	NULL	gw60_immunity_17_6_703_s_186	12479817	(B) In vivo binding of IRF-1 and IRF-2 to the IL-4 promoter was assessed by ChIP with Jurkat T cells transfected with IRF-1 and IRF-2 expression vectors.	bind
9777	1	3977	6	11	NULL	NULL	NULL	IRF-1	GP		bind					IL-4	GP			promoter	NULL	Jurkat T cells transfected with  IRF-1 expression vector	NULL	NULL	NULL	NULL	gw60_immunity_17_6_703_s_186	12479817	(B) In vivo binding of IRF-1 and IRF-2 to the IL-4 promoter was assessed by ChIP with Jurkat T cells transfected with IRF-1 and IRF-2 expression vectors.	bind
9778	1	3978	5	11	NULL	NULL	NULL	MEK5 protein sequences	GP		bind					ERK5	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_6_2065_s_71	16507987	(B) In vivo binding of MEK5 protein sequences and ERK5.	bind
9782	1	3978	6	11	NULL	NULL	NULL	MEK5 protein sequences	GP		bind					ERK5	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_6_2065_s_71	16507987	(B) In vivo binding of MEK5 protein sequences and ERK5.	bind
9780	1	3979	5	11	NULL	NULL	NULL	GTP	Chemical		bind					Ras	GP				NULL	transiently transfected NIH 3T3 cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4611_s_271	10373510	(B) In vivo measurement of GTP and GDP bound to Ras in transiently transfected NIH 3T3 cells.	bind
9781	2	3979	5	11	NULL	NULL	NULL	GDP	Chemical		bind					Ras	GP				NULL	transiently transfected NIH 3T3 cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4611_s_271	10373510	(B) In vivo measurement of GTP and GDP bound to Ras in transiently transfected NIH 3T3 cells.	bind
9783	1	3979	6	11	NULL	NULL	NULL	GTP	Chemical		bind					Ras	GP				NULL	transiently transfected NIH 3T3 cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4611_s_271	10373510	(B) In vivo measurement of GTP and GDP bound to Ras in transiently transfected NIH 3T3 cells.	bind
9784	2	3979	6	11	NULL	NULL	NULL	GDP	Chemical		bind					Ras	GP				NULL	transiently transfected NIH 3T3 cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4611_s_271	10373510	(B) In vivo measurement of GTP and GDP bound to Ras in transiently transfected NIH 3T3 cells.	bind
9789	1	3981	5	11	NULL	NULL	NULL	Nck-1	GP		bind			SH3(1)		GST-IRE1alpha	GP	bound to glutathione-Sepharose beads			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_9_4248_s_200	15201339	(B) Individual SH3 domains of  Nck-1, Nck-1-SH3(1), Nck-1-SH3(2), and Nck-1-SH3(3), fused to GST were cleaved with  thrombin, GST and thrombin were depleted and the products were pulled down with GST-IRE1alpha or GST-IRE1beta bound to glutathione-Sepharose beads.	bind
9790	2	3981	5	11	NULL	NULL	NULL	Nck-1	GP		bind			SH3(1)		GST-IRE1beta	GP	bound to glutathione-Sepharose beads			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_9_4248_s_200	15201339	(B) Individual SH3 domains of  Nck-1, Nck-1-SH3(1), Nck-1-SH3(2), and Nck-1-SH3(3), fused to GST were cleaved with  thrombin, GST and thrombin were depleted and the products were pulled down with GST-IRE1alpha or GST-IRE1beta bound to glutathione-Sepharose beads.	bind
9791	3	3981	5	11	NULL	NULL	NULL	Nck-1	GP		bind			SH3(2)		GST-IRE1alpha	GP	bound to glutathione-Sepharose beads			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_9_4248_s_200	15201339	(B) Individual SH3 domains of  Nck-1, Nck-1-SH3(1), Nck-1-SH3(2), and Nck-1-SH3(3), fused to GST were cleaved with  thrombin, GST and thrombin were depleted and the products were pulled down with GST-IRE1alpha or GST-IRE1beta bound to glutathione-Sepharose beads.	bind
9792	4	3981	5	11	NULL	NULL	NULL	Nck-1	GP		bind			SH3(2)		GST-IRE1beta	GP	bound to glutathione-Sepharose beads			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_9_4248_s_200	15201339	(B) Individual SH3 domains of  Nck-1, Nck-1-SH3(1), Nck-1-SH3(2), and Nck-1-SH3(3), fused to GST were cleaved with  thrombin, GST and thrombin were depleted and the products were pulled down with GST-IRE1alpha or GST-IRE1beta bound to glutathione-Sepharose beads.	bind
9794	5	3981	5	11	NULL	NULL	NULL	Nck-1	GP		bind			SH3(3)		GST-IRE1alpha	GP	bound to glutathione-Sepharose beads			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_9_4248_s_200	15201339	(B) Individual SH3 domains of  Nck-1, Nck-1-SH3(1), Nck-1-SH3(2), and Nck-1-SH3(3), fused to GST were cleaved with  thrombin, GST and thrombin were depleted and the products were pulled down with GST-IRE1alpha or GST-IRE1beta bound to glutathione-Sepharose beads.	bind
9795	6	3981	5	11	NULL	NULL	NULL	Nck-1	GP		bind			SH3(3)		GST-IRE1beta	GP	bound to glutathione-Sepharose beads			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_9_4248_s_200	15201339	(B) Individual SH3 domains of  Nck-1, Nck-1-SH3(1), Nck-1-SH3(2), and Nck-1-SH3(3), fused to GST were cleaved with  thrombin, GST and thrombin were depleted and the products were pulled down with GST-IRE1alpha or GST-IRE1beta bound to glutathione-Sepharose beads.	bind
9779	2	3981	6	11	NULL	NULL	NULL	IRF-2	GP		bind					IL-4	GP			promoter	NULL	Jurkat T cells transfected with  IRF-2 expression vector	NULL	NULL	NULL	NULL	gw70_molbiolcell_15_9_4248_s_200	15201339	(B) Individual SH3 domains of  Nck-1, Nck-1-SH3(1), Nck-1-SH3(2), and Nck-1-SH3(3), fused to GST were cleaved with  thrombin, GST and thrombin were depleted and the products were pulled down with GST-IRE1alpha or GST-IRE1beta bound to glutathione-Sepharose beads.	bind
9785	1	3981	6	11	NULL	NULL	NULL	GST-IRE1alpha	GP		bind					NCk-1	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_9_4248_s_200	15201339	(B) Individual SH3 domains of  Nck-1, Nck-1-SH3(1), Nck-1-SH3(2), and Nck-1-SH3(3), fused to GST were cleaved with  thrombin, GST and thrombin were depleted and the products were pulled down with GST-IRE1alpha or GST-IRE1beta bound to glutathione-Sepharose beads.	bind
9786	2	3981	6	11	NULL	NULL	NULL	GST-IRE1beta	GP		bind					NCk-1	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_9_4248_s_200	15201339	(B) Individual SH3 domains of  Nck-1, Nck-1-SH3(1), Nck-1-SH3(2), and Nck-1-SH3(3), fused to GST were cleaved with  thrombin, GST and thrombin were depleted and the products were pulled down with GST-IRE1alpha or GST-IRE1beta bound to glutathione-Sepharose beads.	bind
9787	3	3981	6	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_9_4248_s_200	15201339	(B) Individual SH3 domains of  Nck-1, Nck-1-SH3(1), Nck-1-SH3(2), and Nck-1-SH3(3), fused to GST were cleaved with  thrombin, GST and thrombin were depleted and the products were pulled down with GST-IRE1alpha or GST-IRE1beta bound to glutathione-Sepharose beads.	bind
9797	1	3982	5	11	NULL	NULL	NULL	IRFs	GP		bind					IL-4	GP			IRF binding sites	NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_6_703_s_101	12479817	(B) Inducible binding of IRFs to the IL-4 IRF binding sites upon IFN-  stimulation.	bind
9798	2	3982	5	11	NULL	NULL	NULL	IFN	GP	stimulation	induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_6_703_s_101	12479817	(B) Inducible binding of IRFs to the IL-4 IRF binding sites upon IFN-  stimulation.	bind
9788	1	3982	6	11	NULL	NULL	NULL	IRFs	GP		bind					IL-4	GP			IRF binding site	NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_6_703_s_101	12479817	(B) Inducible binding of IRFs to the IL-4 IRF binding sites upon IFN-  stimulation.	bind
9793	2	3982	6	11	NULL	NULL	NULL	IFN	GP	stimulation of	induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_6_703_s_101	12479817	(B) Inducible binding of IRFs to the IL-4 IRF binding sites upon IFN-  stimulation.	bind
9799	1	3983	5	11	NULL	NULL	NULL	PpsR	GP		bind					puc	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_110_5_613_s_170	12230978	(B) Influence of light on PpsR binding to a  puc promoter probe.	bind
9796	1	3983	6	11	NULL	NULL	NULL	PpsR	GP		bind					puc	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_110_5_613_s_170	12230978	(B) Influence of light on PpsR binding to a  puc promoter probe.	bind
9800	1	3985	5	11	NULL	NULL	NULL	Pit1	GP		inhibit					GATA2	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_cell_97_5_587_s_134	10367888	(B) Inhibition of  GATA2 binding by Pit1.	bind
9813	1	3985	6	11	NULL	NULL	NULL	Pit1	GP		inhibits					GATA2	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_cell_97_5_587_s_134	10367888	(B) Inhibition of  GATA2 binding by Pit1.	bind
9801	1	3986	5	11	NULL	NULL	NULL	125I- -bungarotoxin 	Chemical		bind					SH-SY5Y-h 7 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_191	11044725	(B) Inhibition of 125I- -bungarotoxin ( -BTx) binding to SH-SY5Y-h 7 cells by verapamil.	bind
9802	2	3986	5	11	NULL	NULL	NULL	verapamil	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_191	11044725	(B) Inhibition of 125I- -bungarotoxin ( -BTx) binding to SH-SY5Y-h 7 cells by verapamil.	bind
54012	3	3986	5	11	NULL	NULL	NULL	BTx	Chemical		is					bungarotoxin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_191	11044725	(B) Inhibition of 125I- -bungarotoxin ( -BTx) binding to SH-SY5Y-h 7 cells by verapamil.	bind
9817	1	3986	6	11	NULL	NULL	NULL	125I- -bungarotoxin	Chemical		bind					SH-SY5Y-h 7 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_191	11044725	(B) Inhibition of 125I- -bungarotoxin ( -BTx) binding to SH-SY5Y-h 7 cells by verapamil.	bind
9819	2	3986	6	11	NULL	NULL	NULL	BTx	Chemical		is					bungarotoxin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_191	11044725	(B) Inhibition of 125I- -bungarotoxin ( -BTx) binding to SH-SY5Y-h 7 cells by verapamil.	bind
9820	3	3986	6	11	NULL	NULL	NULL	verapamil	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_13_2533_s_191	11044725	(B) Inhibition of 125I- -bungarotoxin ( -BTx) binding to SH-SY5Y-h 7 cells by verapamil.	bind
9803	1	3987	5	11	NULL	NULL	NULL	FKHR	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_1_104_s_255	12482965	(B) Inhibition of FKHR DNA binding by activated androgen receptor.	bind
9804	2	3987	5	11	NULL	NULL	NULL	androgen receptor	GP	activated	inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_1_104_s_255	12482965	(B) Inhibition of FKHR DNA binding by activated androgen receptor.	bind
9827	1	3987	6	11	NULL	NULL	NULL	FKHR	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_1_104_s_255	12482965	(B) Inhibition of FKHR DNA binding by activated androgen receptor.	bind
9828	2	3987	6	11	NULL	NULL	NULL	androgen receptor	GP	activated	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_1_104_s_255	12482965	(B) Inhibition of FKHR DNA binding by activated androgen receptor.	bind
9805	1	3988	5	11	NULL	NULL	NULL	Hgl2	GP	cysteine-rich	bind		specifically			GalNAc19BSA	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_8_3836_s_175	10417146	(b) Inhibition of GalNAc-specific binding of cysteine-rich Hgl2 to GalNAc19BSA with asialofetuin (ASF) and holotransferrin (hT) at 25 or 50 muM.	bind
9807	2	3988	5	11	NULL	NULL	NULL	ASF	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_8_3836_s_175	10417146	(b) Inhibition of GalNAc-specific binding of cysteine-rich Hgl2 to GalNAc19BSA with asialofetuin (ASF) and holotransferrin (hT) at 25 or 50 muM.	bind
9808	3	3988	5	11	NULL	NULL	NULL	ASF	GP		is					asialofetuin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_8_3836_s_175	10417146	(b) Inhibition of GalNAc-specific binding of cysteine-rich Hgl2 to GalNAc19BSA with asialofetuin (ASF) and holotransferrin (hT) at 25 or 50 muM.	bind
9809	4	3988	5	11	NULL	NULL	NULL	hT	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_8_3836_s_175	10417146	(b) Inhibition of GalNAc-specific binding of cysteine-rich Hgl2 to GalNAc19BSA with asialofetuin (ASF) and holotransferrin (hT) at 25 or 50 muM.	bind
9810	5	3988	5	11	NULL	NULL	NULL	hT	GP		is					holotransferrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_8_3836_s_175	10417146	(b) Inhibition of GalNAc-specific binding of cysteine-rich Hgl2 to GalNAc19BSA with asialofetuin (ASF) and holotransferrin (hT) at 25 or 50 muM.	bind
9829	1	3988	6	11	NULL	NULL	NULL	Hgl2	GP	cysteine-rich	bind		specifically			GalNAc19BSA	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_8_3836_s_175	10417146	(b) Inhibition of GalNAc-specific binding of cysteine-rich Hgl2 to GalNAc19BSA with asialofetuin (ASF) and holotransferrin (hT) at 25 or 50 muM.	bind
9830	2	3988	6	11	NULL	NULL	NULL	ASF	GP		is					asialofetuin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_8_3836_s_175	10417146	(b) Inhibition of GalNAc-specific binding of cysteine-rich Hgl2 to GalNAc19BSA with asialofetuin (ASF) and holotransferrin (hT) at 25 or 50 muM.	bind
9831	3	3988	6	11	NULL	NULL	NULL	hT	GP		is					holotransferrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_8_3836_s_175	10417146	(b) Inhibition of GalNAc-specific binding of cysteine-rich Hgl2 to GalNAc19BSA with asialofetuin (ASF) and holotransferrin (hT) at 25 or 50 muM.	bind
9832	4	3988	6	11	NULL	NULL	NULL	ASF	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_8_3836_s_175	10417146	(b) Inhibition of GalNAc-specific binding of cysteine-rich Hgl2 to GalNAc19BSA with asialofetuin (ASF) and holotransferrin (hT) at 25 or 50 muM.	bind
9833	5	3988	6	11	NULL	NULL	NULL	hT	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_8_3836_s_175	10417146	(b) Inhibition of GalNAc-specific binding of cysteine-rich Hgl2 to GalNAc19BSA with asialofetuin (ASF) and holotransferrin (hT) at 25 or 50 muM.	bind
9811	1	3989	5	11	NULL	NULL	NULL	H-2	GP	biotinylated	bind			N-terminal		EF-Tu	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_chembiol_10_2_161_s_101	12618188	(B) Inhibition of N-terminal biotinylated  H-2 (0.5  M) binding to immobilized EF-Tu by N-terminal acetylated  H-2.	bind
9812	2	3989	5	11	NULL	NULL	NULL	H-2	GP	acetylated	inhibit			N-terminal		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_10_2_161_s_101	12618188	(B) Inhibition of N-terminal biotinylated  H-2 (0.5  M) binding to immobilized EF-Tu by N-terminal acetylated  H-2.	bind
9834	1	3989	6	11	NULL	NULL	NULL	H-2	GP	biotinylated	bind			N-terminus		EF-Tu	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_chembiol_10_2_161_s_101	12618188	(B) Inhibition of N-terminal biotinylated  H-2 (0.5  M) binding to immobilized EF-Tu by N-terminal acetylated  H-2.	bind
9835	2	3989	6	11	NULL	NULL	NULL	H-2	GP	acetylated	inhibits			N-terminal 		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_10_2_161_s_101	12618188	(B) Inhibition of N-terminal biotinylated  H-2 (0.5  M) binding to immobilized EF-Tu by N-terminal acetylated  H-2.	bind
9814	1	3990	5	11	NULL	NULL	NULL	peptide V	GP		mediate					HDL	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_290	10191300	(B) Inhibition of peptide V-mediated binding of HDL by HDL, LDL, and AcLDL.	bind
9815	2	3990	5	11	NULL	NULL	NULL	HDL	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_290	10191300	(B) Inhibition of peptide V-mediated binding of HDL by HDL, LDL, and AcLDL.	bind
9816	3	3990	5	11	NULL	NULL	NULL	LDL	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_290	10191300	(B) Inhibition of peptide V-mediated binding of HDL by HDL, LDL, and AcLDL.	bind
9818	4	3990	5	11	NULL	NULL	NULL	AcLDL	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_290	10191300	(B) Inhibition of peptide V-mediated binding of HDL by HDL, LDL, and AcLDL.	bind
9836	1	3990	6	11	NULL	NULL	NULL	peptide V	GP		mediates					HDL	Chemical	binding of 			NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_290	10191300	(B) Inhibition of peptide V-mediated binding of HDL by HDL, LDL, and AcLDL.	bind
9837	2	3990	6	11	NULL	NULL	NULL	HDL	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_290	10191300	(B) Inhibition of peptide V-mediated binding of HDL by HDL, LDL, and AcLDL.	bind
9838	3	3990	6	11	NULL	NULL	NULL	LDL	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_290	10191300	(B) Inhibition of peptide V-mediated binding of HDL by HDL, LDL, and AcLDL.	bind
9839	4	3990	6	11	NULL	NULL	NULL	AcLDL	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_290	10191300	(B) Inhibition of peptide V-mediated binding of HDL by HDL, LDL, and AcLDL.	bind
9821	1	3991	5	11	NULL	NULL	NULL	GTP	Chemical		bind					Rac	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_381_s_167	12707308	(B) Inhibition of ROCK activity in the presence of high concentration of  SDF-1alpha (500 ng/ml) increases the GTP-bound form of Rac.	bind
9822	2	3991	5	11	NULL	NULL	NULL	SDF-1alpha	GP	high concentration of	inhibit					ROCK	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_381_s_167	12707308	(B) Inhibition of ROCK activity in the presence of high concentration of  SDF-1alpha (500 ng/ml) increases the GTP-bound form of Rac.	bind
9823	3	3991	5	11	NULL	NULL	NULL	statement 2	Process		increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_381_s_167	12707308	(B) Inhibition of ROCK activity in the presence of high concentration of  SDF-1alpha (500 ng/ml) increases the GTP-bound form of Rac.	bind
9921	1	3991	6	11	NULL	NULL	NULL	GTP	Chemical		bind					Rac	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_381_s_167	12707308	(B) Inhibition of ROCK activity in the presence of high concentration of  SDF-1alpha (500 ng/ml) increases the GTP-bound form of Rac.	bind
9922	2	3991	6	11	NULL	NULL	NULL	ROCK activity	GP	inhibition of	increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_381_s_167	12707308	(B) Inhibition of ROCK activity in the presence of high concentration of  SDF-1alpha (500 ng/ml) increases the GTP-bound form of Rac.	bind
9923	3	3991	6	11	NULL	NULL	NULL	statement 2	Process		occurs in presence of					SDF-1 alpha	GP	high concentration of			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_2_381_s_167	12707308	(B) Inhibition of ROCK activity in the presence of high concentration of  SDF-1alpha (500 ng/ml) increases the GTP-bound form of Rac.	bind
9824	1	3993	5	11	NULL	NULL	NULL	GR 113808	Chemical		bind		specifically			h5-HT4(n) receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_42_1_60_s_174	11750916	(B) Inhibition of specific [3]GR 113808 binding to h5-HT4(n) receptors.	bind
9841	1	3993	6	11	NULL	NULL	NULL	GR 113808	Chemical		bind		specifically			h5-HT4(n) receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_42_1_60_s_174	11750916	(B) Inhibition of specific [3]GR 113808 binding to h5-HT4(n) receptors.	bind
9825	1	3994	5	11	NULL	NULL	NULL	TnrA	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_4_427_s_54	11719184	(B) Inhibition of TnrA DNA binding by GS  in the presence and absence of feedback  inhibitors.	bind
9826	2	3994	5	11	NULL	NULL	NULL	GS	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_4_427_s_54	11719184	(B) Inhibition of TnrA DNA binding by GS  in the presence and absence of feedback  inhibitors.	bind
9844	1	3994	6	11	NULL	NULL	NULL	TnrA	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_4_427_s_54	11719184	(B) Inhibition of TnrA DNA binding by GS  in the presence and absence of feedback  inhibitors.	bind
9845	2	3994	6	11	NULL	NULL	NULL	GS	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_4_427_s_54	11719184	(B) Inhibition of TnrA DNA binding by GS  in the presence and absence of feedback  inhibitors.	bind
9842	1	3995	5	11	NULL	NULL	NULL	Syk-NC-SH2	GP		bind					Fc RII	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1451_2_353_s_110	10556589	(B) Inhibitory effect of peptides corresponding to ITAM on the binding of Syk-NC-SH2 to Fc RII.	bind
9843	2	3995	5	11	NULL	NULL	NULL	ITAM peptides	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1451_2_353_s_110	10556589	(B) Inhibitory effect of peptides corresponding to ITAM on the binding of Syk-NC-SH2 to Fc RII.	bind
9846	1	3995	6	11	NULL	NULL	NULL	Syk-NC-SH2	GP		bind					Fc-RII	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1451_2_353_s_110	10556589	(B) Inhibitory effect of peptides corresponding to ITAM on the binding of Syk-NC-SH2 to Fc RII.	bind
9847	2	3995	6	11	NULL	NULL	NULL	ITAM peptides	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1451_2_353_s_110	10556589	(B) Inhibitory effect of peptides corresponding to ITAM on the binding of Syk-NC-SH2 to Fc RII.	bind
9890	1	3996	5	11	NULL	NULL	NULL	GTP S	Chemical		bind					KA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_38_7_991_s_111	10428417	(B) Intracellular Ca2+ was required for attenuation of DPDPE-stimulated [35]GTP S binding by KA or PMA.	bind
9891	2	3996	5	11	NULL	NULL	NULL	GTP S	Chemical		bind					PMA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_38_7_991_s_111	10428417	(B) Intracellular Ca2+ was required for attenuation of DPDPE-stimulated [35]GTP S binding by KA or PMA.	bind
9892	3	3996	5	11	NULL	NULL	NULL	DPDPE	Chemical		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_38_7_991_s_111	10428417	(B) Intracellular Ca2+ was required for attenuation of DPDPE-stimulated [35]GTP S binding by KA or PMA.	bind
9893	4	3996	5	11	NULL	NULL	NULL	DPDPE	Chemical		stimulate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_38_7_991_s_111	10428417	(B) Intracellular Ca2+ was required for attenuation of DPDPE-stimulated [35]GTP S binding by KA or PMA.	bind
9894	5	3996	5	11	NULL	NULL	NULL	Ca2+	Chemical	intracellular	attenuate					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_38_7_991_s_111	10428417	(B) Intracellular Ca2+ was required for attenuation of DPDPE-stimulated [35]GTP S binding by KA or PMA.	bind
9895	6	3996	5	11	NULL	NULL	NULL	Ca2+	Chemical	intracellular	attenuate					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_38_7_991_s_111	10428417	(B) Intracellular Ca2+ was required for attenuation of DPDPE-stimulated [35]GTP S binding by KA or PMA.	bind
54017	7	3996	5	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_38_7_991_s_111	10428417	(B) Intracellular Ca2+ was required for attenuation of DPDPE-stimulated [35]GTP S binding by KA or PMA.	bind
9848	1	3996	6	11	NULL	NULL	NULL	GTP S	Chemical		bind					KA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_38_7_991_s_111	10428417	(B) Intracellular Ca2+ was required for attenuation of DPDPE-stimulated [35]GTP S binding by KA or PMA.	bind
9849	2	3996	6	11	NULL	NULL	NULL	GTP S	Chemical		bind					PMA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_38_7_991_s_111	10428417	(B) Intracellular Ca2+ was required for attenuation of DPDPE-stimulated [35]GTP S binding by KA or PMA.	bind
9850	3	3996	6	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_38_7_991_s_111	10428417	(B) Intracellular Ca2+ was required for attenuation of DPDPE-stimulated [35]GTP S binding by KA or PMA.	bind
9851	4	3996	6	11	NULL	NULL	NULL	DPDPE	Chemical		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_38_7_991_s_111	10428417	(B) Intracellular Ca2+ was required for attenuation of DPDPE-stimulated [35]GTP S binding by KA or PMA.	bind
9852	5	3996	6	11	NULL	NULL	NULL	DPDPE	Chemical		stimulates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_38_7_991_s_111	10428417	(B) Intracellular Ca2+ was required for attenuation of DPDPE-stimulated [35]GTP S binding by KA or PMA.	bind
9853	6	3996	6	11	NULL	NULL	NULL	Intracellular Ca2+	Chemical		attenuates					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_38_7_991_s_111	10428417	(B) Intracellular Ca2+ was required for attenuation of DPDPE-stimulated [35]GTP S binding by KA or PMA.	bind
9854	7	3996	6	11	NULL	NULL	NULL	Intracellular Ca2+	Chemical		attenuates					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_38_7_991_s_111	10428417	(B) Intracellular Ca2+ was required for attenuation of DPDPE-stimulated [35]GTP S binding by KA or PMA.	bind
9840	1	3998	5	11	NULL	NULL	NULL	IRF-1	GP		bind					mu	NucleicAcid			enhancer	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_11_6870_s_212	9774700	(B) IRF-1 binding to the mu enhancer.	bind
9855	1	3998	6	11	NULL	NULL	NULL	IRF-1	GP		bind					mu	NucleicAcid			enhancer	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_11_6870_s_212	9774700	(B) IRF-1 binding to the mu enhancer.	bind
9896	1	4000	5	11	NULL	NULL	NULL	JNK	GP		bind					MKK7beta	GP		NH2 terminus		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1569_s_185	9891090	(B) JNK binds to the NH2 terminus of MKK7beta.	bind
9856	1	4000	6	11	NULL	NULL	NULL	JNK	GP		bind					MKK7beta	GP		NH2 terminus		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1569_s_185	9891090	(B) JNK binds to the NH2 terminus of MKK7beta.	bind
9897	1	4001	5	11	NULL	NULL	NULL	p34/p20 complex	GP		bind					ADP-Pi	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_5_1041_s_166	11741539	(B) Kd measurements for p34/p20 and Arp2/3 complex binding to ADP-Pi and ADP F-actin.	bind
9898	2	4001	5	11	NULL	NULL	NULL	p34/p20 complex	GP		bind					ADP F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_5_1041_s_166	11741539	(B) Kd measurements for p34/p20 and Arp2/3 complex binding to ADP-Pi and ADP F-actin.	bind
9899	3	4001	5	11	NULL	NULL	NULL	Arp2/3 complex	GP		bind					ADP-Pi	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_5_1041_s_166	11741539	(B) Kd measurements for p34/p20 and Arp2/3 complex binding to ADP-Pi and ADP F-actin.	bind
9900	4	4001	5	11	NULL	NULL	NULL	Arp2/3 complex	GP		bind					ADP F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_5_1041_s_166	11741539	(B) Kd measurements for p34/p20 and Arp2/3 complex binding to ADP-Pi and ADP F-actin.	bind
12173	1	4001	7	11	NULL	NULL	NULL	p34/p20 complex	GP		bind					ADP-Pi	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_5_1041_s_166	11741539	(B) Kd measurements for p34/p20 and Arp2/3 complex binding to ADP-Pi and ADP F-actin.	bind
12174	2	4001	7	11	NULL	NULL	NULL	p34/p20 complex	GP		bind					ADP F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_5_1041_s_166	11741539	(B) Kd measurements for p34/p20 and Arp2/3 complex binding to ADP-Pi and ADP F-actin.	bind
12175	3	4001	7	11	NULL	NULL	NULL	Arp2/3 complex	GP		bind					 ADP-Pi	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_5_1041_s_166	11741539	(B) Kd measurements for p34/p20 and Arp2/3 complex binding to ADP-Pi and ADP F-actin.	bind
12176	4	4001	7	11	NULL	NULL	NULL	Arp2/3 complex	GP		bind					ADP F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_5_1041_s_166	11741539	(B) Kd measurements for p34/p20 and Arp2/3 complex binding to ADP-Pi and ADP F-actin.	bind
9901	1	4003	5	11	NULL	NULL	NULL	Syt 1	GP		does not bind					GST-NECAB 	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_112_1_51_s_150	12044471	(B) Lack of binding of Syt 1 and Mint 2 to GST-NECAB fusion proteins.	bind
9902	2	4003	5	11	NULL	NULL	NULL	Mint 2	GP		does not bind					GST-NECAB	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_112_1_51_s_150	12044471	(B) Lack of binding of Syt 1 and Mint 2 to GST-NECAB fusion proteins.	bind
44538	3	4003	5	11	NULL	NULL	NULL	GST-NECAB	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_112_1_51_s_150	12044471	(B) Lack of binding of Syt 1 and Mint 2 to GST-NECAB fusion proteins.	bind
12177	1	4003	7	11	NULL	NULL	NULL	Syt 1	GP		does not bind					 GST-NECAB	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_112_1_51_s_150	12044471	(B) Lack of binding of Syt 1 and Mint 2 to GST-NECAB fusion proteins.	bind
12178	2	4003	7	11	NULL	NULL	NULL	Mint 2	GP		does not bind					GST-NECAB	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_112_1_51_s_150	12044471	(B) Lack of binding of Syt 1 and Mint 2 to GST-NECAB fusion proteins.	bind
44404	3	4003	7	11	NULL	NULL	NULL	GST-NECAB	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_112_1_51_s_150	12044471	(B) Lack of binding of Syt 1 and Mint 2 to GST-NECAB fusion proteins.	bind
9903	1	4004	5	11	NULL	NULL	NULL	Shc	GP		does not bind					TrkB receptors	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_2_335_s_74	9728915	(B) Lack of Shc binding to mutant TrkB receptors.	bind
12179	1	4004	7	11	NULL	NULL	NULL	Shc	GP		does not bind					TrkB receptor	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_2_335_s_74	9728915	(B) Lack of Shc binding to mutant TrkB receptors.	bind
10077	1	4006	5	11	NULL	NULL	NULL	Top2p	GP		bind									CEN4 region	NULL		NULL	NULL	NULL	NULL	gw70_genetics_172_2_783_s_108	16204216	(B) Layout of the PCR probes used for ChIP analysis of Top2p binding to the  CEN4 region.	bind
12180	1	4006	7	11	NULL	NULL	NULL	Top2p	GP		bind									CEN4 region	NULL		NULL	NULL	NULL	NULL	gw70_genetics_172_2_783_s_108	16204216	(B) Layout of the PCR probes used for ChIP analysis of Top2p binding to the  CEN4 region.	bind
10078	1	4008	5	11	NULL	NULL	NULL	Lef1	GP		bind					Brn-2	GP			promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_7_2915_s_100	15024079	(B) Lef1 binds the  Brn-2 promoter in vitro.	bind
12181	1	4008	7	11	NULL	NULL	NULL	Lef1	GP		bind					Brn-2 	GP			promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_7_2915_s_100	15024079	(B) Lef1 binds the  Brn-2 promoter in vitro.	bind
10079	1	4009	5	11	NULL	NULL	NULL	TAFII250	GP	in vitro-expressed	bind					GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_846_s_128	9858607	(B) Levels of in vitro-expressed TAFII250 bound to GST, TBP, or Rb, as detected by Western analysis (monoclonal anti-hTAFII250 antibody) of nonradioactive, duplicate kinase reactions performed concurrently with those shown in panel A.	bind
10080	2	4009	5	11	NULL	NULL	NULL	TAFII250	GP	in vitro-expressed	bind					TBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_846_s_128	9858607	(B) Levels of in vitro-expressed TAFII250 bound to GST, TBP, or Rb, as detected by Western analysis (monoclonal anti-hTAFII250 antibody) of nonradioactive, duplicate kinase reactions performed concurrently with those shown in panel A.	bind
10081	3	4009	5	11	NULL	NULL	NULL	TAFII250	GP	in vitro-expressed	bind					Rb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_846_s_128	9858607	(B) Levels of in vitro-expressed TAFII250 bound to GST, TBP, or Rb, as detected by Western analysis (monoclonal anti-hTAFII250 antibody) of nonradioactive, duplicate kinase reactions performed concurrently with those shown in panel A.	bind
12182	1	4009	7	11	NULL	NULL	NULL	TAFII250	GP	in vitro-expressed	bind					GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_846_s_128	9858607	(B) Levels of in vitro-expressed TAFII250 bound to GST, TBP, or Rb, as detected by Western analysis (monoclonal anti-hTAFII250 antibody) of nonradioactive, duplicate kinase reactions performed concurrently with those shown in panel A.	bind
12183	2	4009	7	11	NULL	NULL	NULL	TAFII250	GP	in vitro-expressed	bind					TBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_846_s_128	9858607	(B) Levels of in vitro-expressed TAFII250 bound to GST, TBP, or Rb, as detected by Western analysis (monoclonal anti-hTAFII250 antibody) of nonradioactive, duplicate kinase reactions performed concurrently with those shown in panel A.	bind
12184	3	4009	7	11	NULL	NULL	NULL	TAFII250	GP	in vitro-expressed	bind					Rb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_846_s_128	9858607	(B) Levels of in vitro-expressed TAFII250 bound to GST, TBP, or Rb, as detected by Western analysis (monoclonal anti-hTAFII250 antibody) of nonradioactive, duplicate kinase reactions performed concurrently with those shown in panel A.	bind
10082	1	4010	5	11	NULL	NULL	NULL	Snapin	GP		bind					GST-SNAP23	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_3_1245_s_359	15635093	(B) Likewise, inhibition of Snapin binding to GST-SNAP23 (10 mug)  was determined in the presence of EBAG9.	bind
10083	2	4010	5	11	NULL	NULL	NULL	EBAG9	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_3_1245_s_359	15635093	(B) Likewise, inhibition of Snapin binding to GST-SNAP23 (10 mug)  was determined in the presence of EBAG9.	bind
12185	1	4010	7	11	NULL	NULL	NULL	Snapin	GP		bind					GST-SNAP23	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_3_1245_s_359	15635093	(B) Likewise, inhibition of Snapin binding to GST-SNAP23 (10 mug)  was determined in the presence of EBAG9.	bind
12186	2	4010	7	11	NULL	NULL	NULL	EBAG9	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_3_1245_s_359	15635093	(B) Likewise, inhibition of Snapin binding to GST-SNAP23 (10 mug)  was determined in the presence of EBAG9.	bind
10086	1	4012	5	11	NULL	NULL	NULL	peptides	amino acid	proline-rich	is derived from					C3G	GP		Crk-binding region		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_5_3044_s_172	9566923	(B) Linker insertion mutations in the Crk SH3 domain disrupt binding to proline-rich peptides derived from the Crk-binding region of C3G.	bind
10087	2	4012	5	11	NULL	NULL	NULL	Crk	GP		bind			SH3 domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_5_3044_s_172	9566923	(B) Linker insertion mutations in the Crk SH3 domain disrupt binding to proline-rich peptides derived from the Crk-binding region of C3G.	bind
10088	3	4012	5	11	NULL	NULL	NULL	Crk	GP	linker insertion mutations in	disrupt			SH3 domain		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_5_3044_s_172	9566923	(B) Linker insertion mutations in the Crk SH3 domain disrupt binding to proline-rich peptides derived from the Crk-binding region of C3G.	bind
12262	1	4012	7	11	NULL	NULL	NULL	 Crk	GP		bind			SH3		 peptides	amino acid	proline-rich			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_5_3044_s_172	9566923	(B) Linker insertion mutations in the Crk SH3 domain disrupt binding to proline-rich peptides derived from the Crk-binding region of C3G.	bind
12263	2	4012	7	11	NULL	NULL	NULL	Crk	GP	Linker insertion mutations in	disrupt			SH3 domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_5_3044_s_172	9566923	(B) Linker insertion mutations in the Crk SH3 domain disrupt binding to proline-rich peptides derived from the Crk-binding region of C3G.	bind
12264	3	4012	7	11	NULL	NULL	NULL	proline-rich peptide	amino acid		is derived from					C3G	GP		Crk-binding region of		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_5_3044_s_172	9566923	(B) Linker insertion mutations in the Crk SH3 domain disrupt binding to proline-rich peptides derived from the Crk-binding region of C3G.	bind
10089	1	4013	5	11	NULL	NULL	NULL	GTP	Chemical		bind					Rheb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_6_1457_s_54	12820960	(B) Loss of TSC2 function leads to elevated levels of GTP bound Rheb.	bind
10090	2	4013	5	11	NULL	NULL	NULL	TSC2	GP	loss of 	leads to					statement 1	Process	elevated levels of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_6_1457_s_54	12820960	(B) Loss of TSC2 function leads to elevated levels of GTP bound Rheb.	bind
12265	1	4013	7	11	NULL	NULL	NULL	GTP	Chemical		bind					Rheb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_6_1457_s_54	12820960	(B) Loss of TSC2 function leads to elevated levels of GTP bound Rheb.	bind
12266	2	4013	7	11	NULL	NULL	NULL	TSC2	GP	Loss of	leads to					statement 1	Process	elevated levels of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_6_1457_s_54	12820960	(B) Loss of TSC2 function leads to elevated levels of GTP bound Rheb.	bind
10091	1	4014	5	11	NULL	NULL	NULL	MAb 24c5	GP		bind					GC	Chemical	dilute concentrations of 			NULL	in M. tuberculosis	NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_143	11953397	(B) MAb 24c5 binding to dilute concentrations of GC in the  M. tuberculosis GC ELISA.	bind
12267	1	4014	7	11	NULL	NULL	NULL	MAb 24c5	GP		bind					GC	Chemical	dilute concentrations of			NULL	M. tuberculosis	NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_143	11953397	(B) MAb 24c5 binding to dilute concentrations of GC in the  M. tuberculosis GC ELISA.	bind
10092	1	4020	5	11	NULL	NULL	NULL	JAK	GP		bind					AT1aR	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9829_s_210	16260600	(B) Maximal AII-induced ANF transactivation  requires JAK binding to AT1aR.	bind
10093	2	4020	5	11	NULL	NULL	NULL	Maximal AII	GP		induce					ANF	GP	transactivation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9829_s_210	16260600	(B) Maximal AII-induced ANF transactivation  requires JAK binding to AT1aR.	bind
10094	3	4020	5	11	NULL	NULL	NULL	statement 2	Process		require					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9829_s_210	16260600	(B) Maximal AII-induced ANF transactivation  requires JAK binding to AT1aR.	bind
12468	1	4020	7	11	NULL	NULL	NULL	JAK	GP		bind					AT1aR	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9829_s_210	16260600	(B) Maximal AII-induced ANF transactivation  requires JAK binding to AT1aR.	bind
12469	2	4020	7	11	NULL	NULL	NULL	Maximal AII	GP		induce					ANF	GP	transactivation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9829_s_210	16260600	(B) Maximal AII-induced ANF transactivation  requires JAK binding to AT1aR.	bind
12470	3	4020	7	11	NULL	NULL	NULL	statement 2	Process		requires					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9829_s_210	16260600	(B) Maximal AII-induced ANF transactivation  requires JAK binding to AT1aR.	bind
10095	1	4021	5	11	NULL	NULL	NULL	MBP	GP		does not bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_18_4427_s_138	12900458	(B) MBP does not bind  to F-actin.	bind
12471	1	4021	7	11	NULL	NULL	NULL	MBP	GP		does not bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_18_4427_s_138	12900458	(B) MBP does not bind  to F-actin.	bind
10097	1	4023	5	11	NULL	NULL	NULL	Mbp-Ndt80	GP	E. coli	bind					MSE	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_5_685_s_176	9660952	(B) Mbp-Ndt80 isolated from  E. colibinds the MSE.	bind
12472	1	4023	7	11	NULL	NULL	NULL	Mbp-Ndt80	GP	E.coli	bind					MSE	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_5_685_s_176	9660952	(B) Mbp-Ndt80 isolated from  E. colibinds the MSE.	bind
10099	1	4026	5	11	NULL	NULL	NULL	Mediator complex	GP		contains					CDK8	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_14_4604_s_175	11416138	(B) Mediator complexes containing CDK8 and cyclin C are bound by the VDR LBD.	bind
10100	2	4026	5	11	NULL	NULL	NULL	Mediator complex	GP		contains					cyclin C	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_14_4604_s_175	11416138	(B) Mediator complexes containing CDK8 and cyclin C are bound by the VDR LBD.	bind
10101	3	4026	5	11	NULL	NULL	NULL	VDR	GP		bind			LBD		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_14_4604_s_175	11416138	(B) Mediator complexes containing CDK8 and cyclin C are bound by the VDR LBD.	bind
10102	4	4026	5	11	NULL	NULL	NULL	VDR	GP		bind			LBD		statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_14_4604_s_175	11416138	(B) Mediator complexes containing CDK8 and cyclin C are bound by the VDR LBD.	bind
12478	1	4026	7	11	NULL	NULL	NULL	mediator complex	GP		bind					VDR	GP		LBD		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_14_4604_s_175	11416138	(B) Mediator complexes containing CDK8 and cyclin C are bound by the VDR LBD.	bind
12479	2	4026	7	11	NULL	NULL	NULL	mediator complex	GP		bind					VDR	GP		LBD		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_14_4604_s_175	11416138	(B) Mediator complexes containing CDK8 and cyclin C are bound by the VDR LBD.	bind
12480	3	4026	7	11	NULL	NULL	NULL	mediator complex	GP		contain					CDK8	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_14_4604_s_175	11416138	(B) Mediator complexes containing CDK8 and cyclin C are bound by the VDR LBD.	bind
12481	4	4026	7	11	NULL	NULL	NULL	mediator complex	GP		contain					cyclin C	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_14_4604_s_175	11416138	(B) Mediator complexes containing CDK8 and cyclin C are bound by the VDR LBD.	bind
10103	1	4027	5	11	NULL	NULL	NULL	GRP1	GP		bind			PH domain		PtdIns-3,4,5-P3	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_1_89_s_138	12507995	(B) Membrane recruitment of the PtdIns-3,4,5-P3 - binding PH domain of GRP1.	bind
10104	2	4027	5	11	NULL	NULL	NULL	statement 1	GP		is recruited to					membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_1_89_s_138	12507995	(B) Membrane recruitment of the PtdIns-3,4,5-P3 - binding PH domain of GRP1.	bind
12482	2	4027	7	11	NULL	NULL	NULL	statement 1	GP		is recruited to					membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_1_89_s_138	12507995	(B) Membrane recruitment of the PtdIns-3,4,5-P3 - binding PH domain of GRP1.	bind
44405	1	4027	7	11	NULL	NULL	NULL	GRP1	GP		bind			PH domain		PtdIns-3,4,5-P3	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_1_89_s_138	12507995	(B) Membrane recruitment of the PtdIns-3,4,5-P3 - binding PH domain of GRP1.	bind
10105	1	4028	5	11	NULL	NULL	NULL	Methoprene	Chemical		bind					dUSP	GP				NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_33_s_233	11719067	(B) Methoprene (40  M) binds to dUSP and causes suppression in fluorescence.	bind
12483	1	4028	7	11	NULL	NULL	NULL	Methoprene	Chemical		bind					dUSP	GP				NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_33_s_233	11719067	(B) Methoprene (40  M) binds to dUSP and causes suppression in fluorescence.	bind
10107	1	4030	5	11	NULL	NULL	NULL	MIM	GP		bind					F-actin	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_cellbiol_168_3_453_s_118	15684034	(B) MIM binds F-actin  in vitro .	bind
12484	1	4030	7	11	NULL	NULL	NULL	MIM	GP		bind					F-actin	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_cellbiol_168_3_453_s_118	15684034	(B) MIM binds F-actin  in vitro .	bind
10108	1	4031	5	11	NULL	NULL	NULL	 p97	GP	mitotically phosphorylated	bind					p47	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_6_1067_s_146	12810701	(B) Mitotically phosphorylated  p97 binds to p47.	bind
12485	1	4031	7	11	NULL	NULL	NULL	 p97	GP	mitotically phosphorylated	bind					p47	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_6_1067_s_146	12810701	(B) Mitotically phosphorylated  p97 binds to p47.	bind
10109	1	4032	5	11	NULL	NULL	NULL	p97	GP	mitotically phosphorylated	bind					p47	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_161_6_1067_s_145	12810701	(B) Mitotically phosphorylated p97 binds to p47.	bind
10110	1	4033	5	11	NULL	NULL	NULL	Mlc2p	GP		bind					Myo1p	GP		IQ2		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_165_6_843_s_80	15210731	(B) Mlc2p  binds to Myo1p through IQ2.	bind
12486	1	4033	7	11	NULL	NULL	NULL	Mlc2p	GP		bind					Myo1p	GP		IQ2		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_165_6_843_s_80	15210731	(B) Mlc2p  binds to Myo1p through IQ2.	bind
10112	1	4035	5	11	NULL	NULL	NULL	ZEBRA	GP		bind									Z-3 binding site	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_375	10825199	(B) Model depicting how HMG-1 induces cooperative binding of ZEBRA to the Z-3 and Z-4 pair of binding sites.	bind
10113	2	4035	5	11	NULL	NULL	NULL	ZEBRA	GP		bind									Z-4 binding site	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_375	10825199	(B) Model depicting how HMG-1 induces cooperative binding of ZEBRA to the Z-3 and Z-4 pair of binding sites.	bind
10114	3	4035	5	11	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_375	10825199	(B) Model depicting how HMG-1 induces cooperative binding of ZEBRA to the Z-3 and Z-4 pair of binding sites.	bind
10115	4	4035	5	11	NULL	NULL	NULL	HMG-1	GP		induce					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_375	10825199	(B) Model depicting how HMG-1 induces cooperative binding of ZEBRA to the Z-3 and Z-4 pair of binding sites.	bind
12487	1	4035	7	11	NULL	NULL	NULL	ZEBRA	GP		bind									Z-3 binding site	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_375	10825199	(B) Model depicting how HMG-1 induces cooperative binding of ZEBRA to the Z-3 and Z-4 pair of binding sites.	bind
12488	2	4035	7	11	NULL	NULL	NULL	ZEBRA	GP		bind								 	Z-4 binding site	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_375	10825199	(B) Model depicting how HMG-1 induces cooperative binding of ZEBRA to the Z-3 and Z-4 pair of binding sites.	bind
12489	3	4035	7	11	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_375	10825199	(B) Model depicting how HMG-1 induces cooperative binding of ZEBRA to the Z-3 and Z-4 pair of binding sites.	bind
12490	4	4035	7	11	NULL	NULL	NULL	HMG-1	GP		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_375	10825199	(B) Model depicting how HMG-1 induces cooperative binding of ZEBRA to the Z-3 and Z-4 pair of binding sites.	bind
12491	5	4035	7	11	NULL	NULL	NULL	HMG-1	GP		induces					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_375	10825199	(B) Model depicting how HMG-1 induces cooperative binding of ZEBRA to the Z-3 and Z-4 pair of binding sites.	bind
10116	1	4036	5	11	NULL	NULL	NULL	snapin	GP		bind					cypin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5103_s_291	16120643	(B) Model for snapin and  tubulin binding to cypin.	bind
10117	2	4036	5	11	NULL	NULL	NULL	tubulin	GP		bind					cypin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5103_s_291	16120643	(B) Model for snapin and  tubulin binding to cypin.	bind
12492	1	4036	7	11	NULL	NULL	NULL	snapin	GP		bind					cypin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5103_s_291	16120643	(B) Model for snapin and  tubulin binding to cypin.	bind
12493	2	4036	7	11	NULL	NULL	NULL	tubulin	GP		bind					cypin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5103_s_291	16120643	(B) Model for snapin and  tubulin binding to cypin.	bind
10118	1	4037	5	11	NULL	NULL	NULL	Mot3	GP		bind					Ty912delta	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_1879_s_271	9528759	(B) Mot3 binding to the  Ty912delta promoter is zinc dependent.	bind
10119	2	4037	5	11	NULL	NULL	NULL	statement 1	Process		is dependent on					zinc	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_1879_s_271	9528759	(B) Mot3 binding to the  Ty912delta promoter is zinc dependent.	bind
12494	1	4037	7	11	NULL	NULL	NULL	Mot3	GP		bind					Ty912delta	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_1879_s_271	9528759	(B) Mot3 binding to the  Ty912delta promoter is zinc dependent.	bind
12495	2	4037	7	11	NULL	NULL	NULL	statement 1	Process		is dependent on					zinc	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_1879_s_271	9528759	(B) Mot3 binding to the  Ty912delta promoter is zinc dependent.	bind
10120	1	4038	5	11	NULL	NULL	NULL	mSin3A	GP		bind								ETO domains		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_205	11533236	(B) mSin3A and N-CoR bind to distinct ETO domains.	bind
10121	2	4038	5	11	NULL	NULL	NULL	N-CoR	GP		bind								ETO domains		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_205	11533236	(B) mSin3A and N-CoR bind to distinct ETO domains.	bind
12496	1	4038	7	11	NULL	NULL	NULL	mSin3A	GP		bind								ETO domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_205	11533236	(B) mSin3A and N-CoR bind to distinct ETO domains.	bind
12497	2	4038	7	11	NULL	NULL	NULL	Nn-CoR	GP		bind								ETO domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6470_s_205	11533236	(B) mSin3A and N-CoR bind to distinct ETO domains.	bind
10122	1	4039	5	11	NULL	NULL	NULL	MSP	GP		bind					VAB-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_132_23_5225_s_383	16267094	(B) MSP binding to VAB-1 triggers a switch (SW) from  negative to positive regulation.	bind
10123	3	4039	5	11	NULL	NULL	NULL	statement 1	Process		triggers					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_132_23_5225_s_383	16267094	(B) MSP binding to VAB-1 triggers a switch (SW) from  negative to positive regulation.	bind
10124	4	4039	5	11	NULL	NULL	NULL	SW	Process		is					switch	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_132_23_5225_s_383	16267094	(B) MSP binding to VAB-1 triggers a switch (SW) from  negative to positive regulation.	bind
44761	2	4039	5	11	NULL	NULL	NULL	negative regulation	Process		switches to					positive regulation	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_132_23_5225_s_383	16267094	(B) MSP binding to VAB-1 triggers a switch (SW) from  negative to positive regulation.	bind
12498	1	4039	7	11	NULL	NULL	NULL	MSP	GP		bind					VAB-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_132_23_5225_s_383	16267094	(B) MSP binding to VAB-1 triggers a switch (SW) from  negative to positive regulation.	bind
12499	2	4039	7	11	NULL	NULL	NULL	negative regulation	Process		switches to					positive regulation	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_132_23_5225_s_383	16267094	(B) MSP binding to VAB-1 triggers a switch (SW) from  negative to positive regulation.	bind
12500	3	4039	7	11	NULL	NULL	NULL	switch	Process		is					SW	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_132_23_5225_s_383	16267094	(B) MSP binding to VAB-1 triggers a switch (SW) from  negative to positive regulation.	bind
54247	4	4039	7	11	NULL	NULL	NULL	statement 1	Process		triggers					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_132_23_5225_s_383	16267094	(B) MSP binding to VAB-1 triggers a switch (SW) from  negative to positive regulation.	bind
10571	1	4040	5	11	NULL	NULL	NULL	MST1	GP		bind					NORE	GP		carboxy-terminal to RA domain		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_4_253_s_55	11864565	(B) MST1 binds NORE carboxy-terminal to the NORE-RA domain.	bind
18467	1	4040	7	11	NULL	NULL	NULL	MST1	GP		binds					NORE	GP		carboxy-terminal to the RA domain		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_4_253_s_55	11864565	(B) MST1 binds NORE carboxy-terminal to the NORE-RA domain.	bind
10125	1	4041	5	11	NULL	NULL	NULL	TBP	GP		bind					nhp6ab mot1 strain	GP		R1243I		NULL		NULL	NULL	NULL	NULL	gw70_genetics_172_2_837_s_242	16272410	(B) Multicopy TBP plasmid restores TBP binding in the   nhp6ab mot1(R1243I) strain.	bind
10126	2	4041	5	11	NULL	NULL	NULL	TBP plasmid	CellComponent	multicopy	restores					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_genetics_172_2_837_s_242	16272410	(B) Multicopy TBP plasmid restores TBP binding in the   nhp6ab mot1(R1243I) strain.	bind
12504	1	4041	7	11	NULL	NULL	NULL	TBP	GP		bind					nhp6ab mot1  strain	GP		R1243I		NULL		NULL	NULL	NULL	NULL	gw70_genetics_172_2_837_s_242	16272410	(B) Multicopy TBP plasmid restores TBP binding in the   nhp6ab mot1(R1243I) strain.	bind
15600	2	4041	7	11	NULL	NULL	NULL	TBP plasmid	GP	multicopy	restores					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_genetics_172_2_837_s_242	16272410	(B) Multicopy TBP plasmid restores TBP binding in the   nhp6ab mot1(R1243I) strain.	bind
10133	1	4043	5	11	NULL	NULL	NULL	ATP	Chemical		bind					ABC transporters	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_152_4_1417_s_176	10430572	(B) Multiple sequence alignment of partial ORF1 with the five most similar database entries, all of which are ATP-binding subunits of ABC transporters.	bind
12507	1	4043	7	11	NULL	NULL	NULL	ATP	Chemical		bind					ABC transporter	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_152_4_1417_s_176	10430572	(B) Multiple sequence alignment of partial ORF1 with the five most similar database entries, all of which are ATP-binding subunits of ABC transporters.	bind
10136	1	4044	5	11	NULL	NULL	NULL	RB proteins	GP	mutant	does not bind					E2F-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_5_1390_s_134	11839806	(B) Mutant RB proteins do not bind more E2F-1.	bind
12508	1	4044	7	11	NULL	NULL	NULL	RB protein	GP	mutant	does not bind					E2F-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_5_1390_s_134	11839806	(B) Mutant RB proteins do not bind more E2F-1.	bind
10579	1	4045	5	11	NULL	NULL	NULL	ZEBRA	GP		bind		cooperatively			HMG-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_190	10825199	(B) Mutation of individual ZEBRA binding sites abolishes cooperative binding of ZEBRA and HMG-1.	bind
10580	2	4045	5	11	NULL	NULL	NULL	ZEBRA	GP	mutant	abolish			binding sites		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_190	10825199	(B) Mutation of individual ZEBRA binding sites abolishes cooperative binding of ZEBRA and HMG-1.	bind
12509	1	4045	7	11	NULL	NULL	NULL	ZEBRA	GP		bind		cooperatively			HMG-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_190	10825199	(B) Mutation of individual ZEBRA binding sites abolishes cooperative binding of ZEBRA and HMG-1.	bind
12510	2	4045	7	11	NULL	NULL	NULL	ZEBRA	GP	mutant	abolishes			binding site		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_190	10825199	(B) Mutation of individual ZEBRA binding sites abolishes cooperative binding of ZEBRA and HMG-1.	bind
10141	1	4046	5	11	NULL	NULL	NULL	D-STAT	GP		undergoes							phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_cell_84_3_421_s_104	8608596	(B) Mutation of Tyr-704  to Phe-704 abolished the tyrosine phosphorylation of D-STAT.	bind
10142	2	4046	5	11	NULL	NULL	NULL			mutation of	abolish			Tyr-704		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_3_421_s_104	8608596	(B) Mutation of Tyr-704  to Phe-704 abolished the tyrosine phosphorylation of D-STAT.	bind
10143	3	4046	5	11	NULL	NULL	NULL			mutation of	abolish			Phe-704		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_3_421_s_104	8608596	(B) Mutation of Tyr-704  to Phe-704 abolished the tyrosine phosphorylation of D-STAT.	bind
12513	1	4046	7	11	NULL	NULL	NULL	D-STAT	GP		undergoes							phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_cell_84_3_421_s_104	8608596	(B) Mutation of Tyr-704  to Phe-704 abolished the tyrosine phosphorylation of D-STAT.	bind
15601	2	4046	7	11	NULL	NULL	NULL			mutation	abolish			Tyr-704 		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_3_421_s_104	8608596	(B) Mutation of Tyr-704  to Phe-704 abolished the tyrosine phosphorylation of D-STAT.	bind
15602	3	4046	7	11	NULL	NULL	NULL			mutation	abolish			Phe-704		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_3_421_s_104	8608596	(B) Mutation of Tyr-704  to Phe-704 abolished the tyrosine phosphorylation of D-STAT.	bind
10144	1	4047	5	11	NULL	NULL	NULL	vIRF	GP		bind					p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_21_8254_s_120	11027294	(B) Mutational analysis of vIRF binding to p300.	bind
12514	1	4047	7	11	NULL	NULL	NULL	vIRF	GP		bind					p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_21_8254_s_120	11027294	(B) Mutational analysis of vIRF binding to p300.	bind
10148	1	4048	5	11	NULL	NULL	NULL	Arp2/3 complex	GP		mediate					actin	GP	nucleation of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_89_s_70	11581288	(B) Mutations in the actin monomer-binding region of ActA decrease the efficiency of Arp2/3 complex -  mediated actin nucleation.	bind
10149	2	4048	5	11	NULL	NULL	NULL	ActA	GP	mutation in	decreases			actin monomer-binding region		statement 1	Process	efficieny of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_89_s_70	11581288	(B) Mutations in the actin monomer-binding region of ActA decrease the efficiency of Arp2/3 complex -  mediated actin nucleation.	bind
12515	1	4048	7	11	NULL	NULL	NULL	Arp2/3 complex	GP		mediate					actin	GP	nucleation of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_89_s_70	11581288	(B) Mutations in the actin monomer-binding region of ActA decrease the efficiency of Arp2/3 complex -  mediated actin nucleation.	bind
12516	2	4048	7	11	NULL	NULL	NULL	ActA	GP	mutations in	decrease			actin monomer-binding region		statement 1	Process	efficiency of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_1_89_s_70	11581288	(B) Mutations in the actin monomer-binding region of ActA decrease the efficiency of Arp2/3 complex -  mediated actin nucleation.	bind
10581	1	4049	5	11	NULL	NULL	NULL	AMP	Chemical		bind					gamma2	GP		CBS domains		NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_178	14722619	(b) Mutations that caused an increase in the  B0.5 for binding of AMP to the CBS domains of gamma2 also caused an increase in the  A0.5 for activation of recombinant alpha1beta1gamma2 complexes, with the same order of potency, i.e.,  B0.5 or  A0.5 for WT   L ins < R302Q < H383R < T400N < R531G.	bind
12517	1	4049	7	11	NULL	NULL	NULL	AMP	Chemical		bind					gamma2	GP		CBS domain		NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_2_274_s_178	14722619	(b) Mutations that caused an increase in the  B0.5 for binding of AMP to the CBS domains of gamma2 also caused an increase in the  A0.5 for activation of recombinant alpha1beta1gamma2 complexes, with the same order of potency, i.e.,  B0.5 or  A0.5 for WT   L ins < R302Q < H383R < T400N < R531G.	bind
10150	1	4050	5	11	NULL	NULL	NULL	MutS/MutL	GP		bind									Sb-G/T-bS	NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_233_s_147	12887908	(B) MutS/MutL binding to biotin-streptavidin double blocked-end G/T mismatch DNA (Sb-G/T-bS).	bind
10151	2	4050	5	11	NULL	NULL	NULL	Sb-G/T-bS	NucleicAcid		is					biotin-streptavidin double blocked-end G/T mismatch DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_233_s_147	12887908	(B) MutS/MutL binding to biotin-streptavidin double blocked-end G/T mismatch DNA (Sb-G/T-bS).	bind
12518	1	4050	7	11	NULL	NULL	NULL	MutS/MutL	GP		bind									Sb-G/T-bS	NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_233_s_147	12887908	(B) MutS/MutL binding to biotin-streptavidin double blocked-end G/T mismatch DNA (Sb-G/T-bS).	bind
12519	2	4050	7	11	NULL	NULL	NULL	Sb-G/T-bS	NucleicAcid		is					biotin-streptavidin double blocked-end G/T mismatch DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_233_s_147	12887908	(B) MutS/MutL binding to biotin-streptavidin double blocked-end G/T mismatch DNA (Sb-G/T-bS).	bind
10152	1	4051	5	11	NULL	NULL	NULL	NFATp	GP		bind					TNF-alpha	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2620_s_122	11909956	(B) Mutually exclusive binding of NFATp and Ets-1 to shared sites in the TNF-alpha promoter.	bind
10153	2	4051	5	11	NULL	NULL	NULL	Ets-1	GP		bind					TNF-alpha	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2620_s_122	11909956	(B) Mutually exclusive binding of NFATp and Ets-1 to shared sites in the TNF-alpha promoter.	bind
10154	3	4051	5	11	NULL	NULL	NULL	statement 1	Process		mutually exclusive to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2620_s_122	11909956	(B) Mutually exclusive binding of NFATp and Ets-1 to shared sites in the TNF-alpha promoter.	bind
12522	1	4051	7	11	NULL	NULL	NULL	NFATp	GP		bind					TNF-alpha	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2620_s_122	11909956	(B) Mutually exclusive binding of NFATp and Ets-1 to shared sites in the TNF-alpha promoter.	bind
12524	2	4051	7	11	NULL	NULL	NULL	Ets-1	GP		bind					TNF-alpha	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2620_s_122	11909956	(B) Mutually exclusive binding of NFATp and Ets-1 to shared sites in the TNF-alpha promoter.	bind
12526	3	4051	7	11	NULL	NULL	NULL	statement 1	Process		mutually exclusive to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2620_s_122	11909956	(B) Mutually exclusive binding of NFATp and Ets-1 to shared sites in the TNF-alpha promoter.	bind
10155	1	4052	5	11	NULL	NULL	NULL	N-WASp	GP		bind					Arp2/3 complex	GP				NULL	at an actin filament branch point	NULL	NULL	NULL	NULL	gw60_currbiol_12_15_1270_s_226	12176354	(B) N-WASp and cortactin bound to Arp2/3 complex at an actin filament branch point.	bind
10156	2	4052	5	11	NULL	NULL	NULL	cortactin	GP		bind					Arp2/3 complex	GP				NULL	at an actin filament branch point	NULL	NULL	NULL	NULL	gw60_currbiol_12_15_1270_s_226	12176354	(B) N-WASp and cortactin bound to Arp2/3 complex at an actin filament branch point.	bind
12529	1	4052	7	11	NULL	NULL	NULL	N-WASp	GP		bind					Arp2/3 complex	GP				NULL	actin filament branch point	NULL	NULL	NULL	NULL	gw60_currbiol_12_15_1270_s_226	12176354	(B) N-WASp and cortactin bound to Arp2/3 complex at an actin filament branch point.	bind
12530	2	4052	7	11	NULL	NULL	NULL	cortactin	GP		bind					Arp2/3 complex	GP				NULL	actin filament branch point	NULL	NULL	NULL	NULL	gw60_currbiol_12_15_1270_s_226	12176354	(B) N-WASp and cortactin bound to Arp2/3 complex at an actin filament branch point.	bind
10157	1	4053	5	11	NULL	NULL	NULL	NBP1	GP		bind		tightly			Nef	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_8_5_647_s_45	9620685	(B) NBP1 binds to Nef tightly in the yeast two-hybrid system.	bind
12531	1	4053	7	11	NULL	NULL	NULL	NBP1	GP		bind		tightly			Nef	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_8_5_647_s_45	9620685	(B) NBP1 binds to Nef tightly in the yeast two-hybrid system.	bind
10158	1	4054	5	11	NULL	NULL	NULL	LDL	Chemical		bind		specifically			mSR-BI	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_111	10191300	(B) Net specific binding activity of LDL to mSR-BI mediated by peptide V.	bind
10159	2	4054	5	11	NULL	NULL	NULL	statement 1	Process		is mediated by					peptide V	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_111	10191300	(B) Net specific binding activity of LDL to mSR-BI mediated by peptide V.	bind
12532	1	4054	7	11	NULL	NULL	NULL	LDL	Chemical		bind		specifically			mSR-BI	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_111	10191300	(B) Net specific binding activity of LDL to mSR-BI mediated by peptide V.	bind
12533	2	4054	7	11	NULL	NULL	NULL	statement 1	Process		is mediated by					peptide V	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_111	10191300	(B) Net specific binding activity of LDL to mSR-BI mediated by peptide V.	bind
10160	1	4055	5	11	NULL	NULL	NULL	NeuAc4D ligand	Chemical		bind					BHA surface	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_structure_2_8_719_s_119	7994572	(b) NeuAc4D (carbon atoms colored yellow) ligand bound to the BHA surface.	bind
12534	1	4055	7	11	NULL	NULL	NULL	NeuAc4D	Chemical		bind					BHA surface	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_structure_2_8_719_s_119	7994572	(b) NeuAc4D (carbon atoms colored yellow) ligand bound to the BHA surface.	bind
10161	1	4058	5	11	NULL	NULL	NULL	NFI/CTF	GP		bind					CSF1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_106_3_309_s_126	11509180	(B) NFI/CTF is bound to  CSF1 promoter in the absence of BAF  complex.	bind
10162	2	4058	5	11	NULL	NULL	NULL	statement 1	Process		in the absence of					BAF complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_106_3_309_s_126	11509180	(B) NFI/CTF is bound to  CSF1 promoter in the absence of BAF  complex.	bind
12535	1	4058	7	11	NULL	NULL	NULL	NFI/CTF	GP		bind					CSF1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_106_3_309_s_126	11509180	(B) NFI/CTF is bound to  CSF1 promoter in the absence of BAF  complex.	bind
12536	2	4058	7	11	NULL	NULL	NULL	statement 1	Process		occurs in the absence of					BAF complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_106_3_309_s_126	11509180	(B) NFI/CTF is bound to  CSF1 promoter in the absence of BAF  complex.	bind
10163	1	4059	5	11	NULL	NULL	NULL	Nmd5p	GP		bind					Crz1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_951_s_112	11535618	(B) Nmd5p binds Crz1p in a calcineurin-dependent manner.	bind
10164	2	4059	5	11	NULL	NULL	NULL	statement 1	Process		is dependent on					calcineurin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_951_s_112	11535618	(B) Nmd5p binds Crz1p in a calcineurin-dependent manner.	bind
12537	1	4059	7	11	NULL	NULL	NULL	Nmd5p	GP		bind					Crz1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_951_s_112	11535618	(B) Nmd5p binds Crz1p in a calcineurin-dependent manner.	bind
12538	2	4059	7	11	NULL	NULL	NULL	statement 1	Process		is dependent on					calcineurin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_951_s_112	11535618	(B) Nmd5p binds Crz1p in a calcineurin-dependent manner.	bind
10165	1	4060	5	11	NULL	NULL	NULL	Npap60	GP		bind					importin-alpha:beta	GP				NULL	HeLa cytosol	NULL	NULL	NULL	NULL	gw60_cell_110_3_349_s_47	12176322	(B) Npap60 binds importin-alpha:beta from HeLa cytosol.	bind
12539	1	4060	7	11	NULL	NULL	NULL	Npap60	GP		binds					importin-alpha:beta	GP				NULL	HeLa cytosol	NULL	NULL	NULL	NULL	gw60_cell_110_3_349_s_47	12176322	(B) Npap60 binds importin-alpha:beta from HeLa cytosol.	bind
10166	1	4061	5	11	NULL	NULL	NULL	NSF	GP		bind					R2C-PICK1 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_57	11931741	(B) NSF binds R2C-PICK1 complex more strongly than R2C alone.	bind
10167	2	4061	5	11	NULL	NULL	NULL	NSF	GP		bind					R2C	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_57	11931741	(B) NSF binds R2C-PICK1 complex more strongly than R2C alone.	bind
10168	3	4061	5	11	NULL	NULL	NULL	statement 1	Process		is stronger than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_57	11931741	(B) NSF binds R2C-PICK1 complex more strongly than R2C alone.	bind
12541	1	4061	7	11	NULL	NULL	NULL	NSF	GP		bind					R2C-PICK1 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_57	11931741	(B) NSF binds R2C-PICK1 complex more strongly than R2C alone.	bind
12543	2	4061	7	11	NULL	NULL	NULL	NSF	GP		bind					R2C	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_57	11931741	(B) NSF binds R2C-PICK1 complex more strongly than R2C alone.	bind
12544	3	4061	7	11	NULL	NULL	NULL	statement 1	Process		occurs  more strongly than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_57	11931741	(B) NSF binds R2C-PICK1 complex more strongly than R2C alone.	bind
10169	1	4062	5	11	NULL	NULL	NULL	NTF2	GP		bind					Ran GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1241_s_147	12769848	(B) NTF2 bound to Ran GDP.	bind
12546	1	4062	7	11	NULL	NULL	NULL	NTF2	GP		bind					Ran GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1241_s_147	12769848	(B) NTF2 bound to Ran GDP.	bind
10170	1	4064	5	11	NULL	NULL	NULL	HMG-17	GP	heat-treated	bind					Cp	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3466_s_223	10207070	(B) Nucleoprotein gel assay showing that heat-treated (95 degrees C, 5 min) HMG-17 bound to core particles (Cp) in a manner that is indistinguishable from the untreated HMG-17.	bind
10171	2	4064	5	11	NULL	NULL	NULL	Cp	CellComponent		is					core particles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3466_s_223	10207070	(B) Nucleoprotein gel assay showing that heat-treated (95 degrees C, 5 min) HMG-17 bound to core particles (Cp) in a manner that is indistinguishable from the untreated HMG-17.	bind
10172	3	4064	5	11	NULL	NULL	NULL	HMG-17	GP	untreated	bind					Cp	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3466_s_223	10207070	(B) Nucleoprotein gel assay showing that heat-treated (95 degrees C, 5 min) HMG-17 bound to core particles (Cp) in a manner that is indistinguishable from the untreated HMG-17.	bind
10173	4	4064	5	11	NULL	NULL	NULL	statement 1	Process		is indistinguishable from					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3466_s_223	10207070	(B) Nucleoprotein gel assay showing that heat-treated (95 degrees C, 5 min) HMG-17 bound to core particles (Cp) in a manner that is indistinguishable from the untreated HMG-17.	bind
12547	1	4064	7	11	NULL	NULL	NULL	HMG-17	GP	heat-treated	bind					Cp	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3466_s_223	10207070	(B) Nucleoprotein gel assay showing that heat-treated (95 degrees C, 5 min) HMG-17 bound to core particles (Cp) in a manner that is indistinguishable from the untreated HMG-17.	bind
12548	2	4064	7	11	NULL	NULL	NULL	Cp	CellComponent		is					core particles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3466_s_223	10207070	(B) Nucleoprotein gel assay showing that heat-treated (95 degrees C, 5 min) HMG-17 bound to core particles (Cp) in a manner that is indistinguishable from the untreated HMG-17.	bind
15603	3	4064	7	11	NULL	NULL	NULL	HMG-17	GP	untreated	bind					Cp	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3466_s_223	10207070	(B) Nucleoprotein gel assay showing that heat-treated (95 degrees C, 5 min) HMG-17 bound to core particles (Cp) in a manner that is indistinguishable from the untreated HMG-17.	bind
15605	4	4064	7	11	NULL	NULL	NULL	statement 1	Process		is indistinguishable from					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3466_s_223	10207070	(B) Nucleoprotein gel assay showing that heat-treated (95 degrees C, 5 min) HMG-17 bound to core particles (Cp) in a manner that is indistinguishable from the untreated HMG-17.	bind
10174	1	4065	5	11	NULL	NULL	NULL	NXF	GP		bind		directly			Drebrin	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_608_s_94	14701734	(b) NXF directly binds to the Drebrin promoter in vivo.	bind
12554	1	4065	7	11	NULL	NULL	NULL	NXF	GP		bind		directly			Drebrin	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_608_s_94	14701734	(b) NXF directly binds to the Drebrin promoter in vivo.	bind
10175	1	4066	5	11	NULL	NULL	NULL	NXT1	GP		bind		directly			Crm1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_1_141_s_240	11149927	(B) NXT1 binds directly to Crm1, and binding is stimulated by the addition of Ran preloaded with GMP-PNP.	bind
10176	3	4066	5	11	NULL	NULL	NULL	statement 1	Process		is stimulated by					statement 2	Process	addition of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_1_141_s_240	11149927	(B) NXT1 binds directly to Crm1, and binding is stimulated by the addition of Ran preloaded with GMP-PNP.	bind
10177	2	4066	5	11	NULL	NULL	NULL	Ran	GP		preloaded with					GMP-PNP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_1_141_s_240	11149927	(B) NXT1 binds directly to Crm1, and binding is stimulated by the addition of Ran preloaded with GMP-PNP.	bind
12555	1	4066	7	11	NULL	NULL	NULL	NXT1	GP		bind		directly			Crm1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_1_141_s_240	11149927	(B) NXT1 binds directly to Crm1, and binding is stimulated by the addition of Ran preloaded with GMP-PNP.	bind
12556	2	4066	7	11	NULL	NULL	NULL	Ran	GP		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_1_141_s_240	11149927	(B) NXT1 binds directly to Crm1, and binding is stimulated by the addition of Ran preloaded with GMP-PNP.	bind
12558	3	4066	7	11	NULL	NULL	NULL	Ran	GP		is preloaded with					GMP-PNP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_1_141_s_240	11149927	(B) NXT1 binds directly to Crm1, and binding is stimulated by the addition of Ran preloaded with GMP-PNP.	bind
10178	1	4067	5	11	NULL	NULL	NULL	OAS1D	GP		bind					OAS1A	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4615_s_262	15899864	(B) OAS1D binds OAS1A in vitro.	bind
12561	1	4067	7	11	NULL	NULL	NULL	OAS1D	GP		binds					OAS1A	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4615_s_262	15899864	(B) OAS1D binds OAS1A in vitro.	bind
10179	1	4068	5	11	NULL	NULL	NULL	Sed5p	GP		bind		only			Sly1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_4_645_s_40	11994317	(B) Of the yeast ER to Golgi SNAREs, only Sed5p binds Sly1p.	bind
12563	1	4068	7	11	NULL	NULL	NULL	Sed5p	GP		binds					Sly1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_4_645_s_40	11994317	(B) Of the yeast ER to Golgi SNAREs, only Sed5p binds Sly1p.	bind
10180	1	4070	5	11	NULL	NULL	NULL	stimulus	Process		activate					Rac	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
10181	2	4070	5	11	NULL	NULL	NULL	GTP	Chemical		bind					Rac	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
10183	3	4070	5	11	NULL	NULL	NULL	statement 2	Process		bind					Nap125	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
10184	4	4070	5	11	NULL	NULL	NULL	statement 2	Process		bind					PIR121	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
10185	5	4070	5	11	NULL	NULL	NULL	statement 2	GP		bind					Abi2	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
10186	6	4070	5	11	NULL	NULL	NULL	statement 3	Process		release					WAVE1	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
10187	7	4070	5	11	NULL	NULL	NULL	statement 3	Process		release					HSPC300	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
10188	8	4070	5	11	NULL	NULL	NULL	statement 4	Process		release					WAVE1	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
10189	9	4070	5	11	NULL	NULL	NULL	statement 4	Process		release					HSPC300	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
10190	10	4070	5	11	NULL	NULL	NULL	statement 5	Process		release					WAVE1	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
10191	11	4070	5	11	NULL	NULL	NULL	statement 5	Process		release					HSPC300	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
12564	1	4070	7	11	NULL	NULL	NULL	stimulus	Process		activates					Rac	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
12565	3	4070	7	11	NULL	NULL	NULL	statement 2	Process		binds					Nap125	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
12566	4	4070	7	11	NULL	NULL	NULL	statement 2	GP		binds					PIR121	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
12567	5	4070	7	11	NULL	NULL	NULL	statement 2	GP		binds					Abi2	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
12569	6	4070	7	11	NULL	NULL	NULL	statement 3	Process		release					WAVE1	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
12572	7	4070	7	11	NULL	NULL	NULL	statement 4	Process		release					WAVE1	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
12573	8	4070	7	11	NULL	NULL	NULL	statement 5	Process		release					WAVE1	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
12574	9	4070	7	11	NULL	NULL	NULL	statement 3	Process		release					HSPC300	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
12575	10	4070	7	11	NULL	NULL	NULL	statement 4	Process		release					HSPC300	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
12577	11	4070	7	11	NULL	NULL	NULL	statement 5	Process		release					HSPC300	GP				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
44406	2	4070	7	11	NULL	NULL	NULL	Rac	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_46_3_299_s_169	14975685	(B) Once a stimulus activates Rac, GTP bound Rac binds to Nap125,  PIR121 and Abi2, thus releasing WAVE1 and HSPC300.	bind
10192	1	4071	5	11	NULL	NULL	NULL	STAT1	GP		bind					DMA antibodies	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_104_5_731_s_68	11257227	(B) Only  methylated STAT1(NH2)-GST competes for STAT1 binding to  DMA antibodies.	bind
10193	2	4071	5	11	NULL	NULL	NULL	STAT1-GST	GP	methylated	bind			NH2		DMA antibodies	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_104_5_731_s_68	11257227	(B) Only  methylated STAT1(NH2)-GST competes for STAT1 binding to  DMA antibodies.	bind
10194	3	4071	5	11	NULL	NULL	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_104_5_731_s_68	11257227	(B) Only  methylated STAT1(NH2)-GST competes for STAT1 binding to  DMA antibodies.	bind
12578	1	4071	7	11	NULL	NULL	NULL	STAT1	GP		bind					DMA antibodies	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_104_5_731_s_68	11257227	(B) Only  methylated STAT1(NH2)-GST competes for STAT1 binding to  DMA antibodies.	bind
12579	2	4071	7	11	NULL	NULL	NULL	STAT1-GST	GP	methylated	bind			NH2		DMA antibodies	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_104_5_731_s_68	11257227	(B) Only  methylated STAT1(NH2)-GST competes for STAT1 binding to  DMA antibodies.	bind
12581	3	4071	7	11	NULL	NULL	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_104_5_731_s_68	11257227	(B) Only  methylated STAT1(NH2)-GST competes for STAT1 binding to  DMA antibodies.	bind
10195	1	4072	5	11	NULL	NULL	NULL	p53	GP		bind					DNA	NucleicAcid	platinated			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1517_3_392_s_99	11342217	(B) p53 binding to platinated DNA.	bind
12600	1	4072	7	11	NULL	NULL	NULL	p53	GP		bind					 DNA	NucleicAcid	platinated			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1517_3_392_s_99	11342217	(B) p53 binding to platinated DNA.	bind
10196	1	4073	5	11	NULL	NULL	NULL	p70 MGR	GP		bind					Dopa decarboxylase	GP	Drosophila		promoter	NULL		NULL	NULL	NULL	NULL	gw60_mechdev_114_1_37_s_154	12175488	(B) p70 MGR binds to the  Drosophila Dopa decarboxylase promoter.	bind
12601	1	4073	7	11	NULL	NULL	NULL	p70 MGR	GP		binds					Dopa decarboxylase	GP	Drosophila		promoter	NULL		NULL	NULL	NULL	NULL	gw60_mechdev_114_1_37_s_154	12175488	(B) p70 MGR binds to the  Drosophila Dopa decarboxylase promoter.	bind
10197	1	4074	5	11	NULL	NULL	NULL	PAI-2	GP		bind					Rb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_148	12944478	(B) PAI-2 binds Rb and p130 but not p107.	bind
10198	2	4074	5	11	NULL	NULL	NULL	PAI-2	GP		bind					p130	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_148	12944478	(B) PAI-2 binds Rb and p130 but not p107.	bind
10199	3	4074	5	11	NULL	NULL	NULL	PAI-2	GP		does not bind					p107	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_148	12944478	(B) PAI-2 binds Rb and p130 but not p107.	bind
12602	1	4074	7	11	NULL	NULL	NULL	PAI-2	GP		binds					Rb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_148	12944478	(B) PAI-2 binds Rb and p130 but not p107.	bind
12603	2	4074	7	11	NULL	NULL	NULL	PAI-2	GP		binds					p130	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_148	12944478	(B) PAI-2 binds Rb and p130 but not p107.	bind
12606	3	4074	7	11	NULL	NULL	NULL	PAI-2	GP		does not bind					p107	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_148	12944478	(B) PAI-2 binds Rb and p130 but not p107.	bind
10200	1	4075	5	11	NULL	NULL	NULL	Pax4	GP		bind			PD		Pax6	GP	putative 	target sites		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8281_s_158	10567553	(B) Pax4 PD binds to the putative Pax6 target sites.	bind
12607	1	4075	7	11	NULL	NULL	NULL	Pax4 	GP		binds to			PD		Pax6	GP	putative	target site		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8281_s_158	10567553	(B) Pax4 PD binds to the putative Pax6 target sites.	bind
10201	1	4076	5	11	NULL	NULL	NULL	p53	GP		bind					CBP	GP		KIX domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4849_s_91	10848610	(B) pCREB, but not unphosphorylated CREB, enhances p53 binding to the KIX domain of CBP.	bind
10202	2	4076	5	11	NULL	NULL	NULL	pCREB	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4849_s_91	10848610	(B) pCREB, but not unphosphorylated CREB, enhances p53 binding to the KIX domain of CBP.	bind
10203	3	4076	5	11	NULL	NULL	NULL	CREB	GP	unphosphorylated	does not enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4849_s_91	10848610	(B) pCREB, but not unphosphorylated CREB, enhances p53 binding to the KIX domain of CBP.	bind
12608	1	4076	7	11	NULL	NULL	NULL	p53	GP		bind					CBP	GP		KIX		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4849_s_91	10848610	(B) pCREB, but not unphosphorylated CREB, enhances p53 binding to the KIX domain of CBP.	bind
12609	2	4076	7	11	NULL	NULL	NULL	pCREB	GP		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4849_s_91	10848610	(B) pCREB, but not unphosphorylated CREB, enhances p53 binding to the KIX domain of CBP.	bind
12610	3	4076	7	11	NULL	NULL	NULL	CREB	GP	unphosphorylated	does not enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4849_s_91	10848610	(B) pCREB, but not unphosphorylated CREB, enhances p53 binding to the KIX domain of CBP.	bind
11430	1	4077	5	11	NULL	NULL	NULL	PTP1B	GP		bind					IR peptides	GP	monophosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1401_s_58	11163213	(B) Peptide competition assay with the PTP1B substrate-trapping mutant form (D181A) quantifying the relative binding affinity of PTP1B for the mono-, bis-, and trisphosphorylated IR peptides.	bind
11431	2	4077	5	11	NULL	NULL	NULL	PTP1B	GP		bind					IR peptides	GP	bisphosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1401_s_58	11163213	(B) Peptide competition assay with the PTP1B substrate-trapping mutant form (D181A) quantifying the relative binding affinity of PTP1B for the mono-, bis-, and trisphosphorylated IR peptides.	bind
11432	3	4077	5	11	NULL	NULL	NULL	PTP1B	GP		bind					IR peptides	GP	trisphosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1401_s_58	11163213	(B) Peptide competition assay with the PTP1B substrate-trapping mutant form (D181A) quantifying the relative binding affinity of PTP1B for the mono-, bis-, and trisphosphorylated IR peptides.	bind
12611	1	4077	7	11	NULL	NULL	NULL	PTP1B	GP		bind					IR peptides	GP	monophosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1401_s_58	11163213	(B) Peptide competition assay with the PTP1B substrate-trapping mutant form (D181A) quantifying the relative binding affinity of PTP1B for the mono-, bis-, and trisphosphorylated IR peptides.	bind
12612	2	4077	7	11	NULL	NULL	NULL	PTP1B	GP		bind					IR peptides	GP	bisphosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1401_s_58	11163213	(B) Peptide competition assay with the PTP1B substrate-trapping mutant form (D181A) quantifying the relative binding affinity of PTP1B for the mono-, bis-, and trisphosphorylated IR peptides.	bind
12613	3	4077	7	11	NULL	NULL	NULL	PTP1B	GP		bind					IR peptides	GP	trisphosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1401_s_58	11163213	(B) Peptide competition assay with the PTP1B substrate-trapping mutant form (D181A) quantifying the relative binding affinity of PTP1B for the mono-, bis-, and trisphosphorylated IR peptides.	bind
10204	1	4078	5	11	NULL	NULL	NULL	[3]BPTI	GP	unfolded	bind					EF-Tu	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_3_749_s_30	12176046	(B) Peptides  (DnaK binder) and  (not DnaK binder) were tested for their abillity to compete in solution for the binding of unfolded [3]BPTI to EF-Tu by gel permeation chromatography.	bind
12638	1	4078	7	11	NULL	NULL	NULL	[3]BPTI 	GP	unfolded	bind					EF-Tu	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_3_749_s_30	12176046	(B) Peptides  (DnaK binder) and  (not DnaK binder) were tested for their abillity to compete in solution for the binding of unfolded [3]BPTI to EF-Tu by gel permeation chromatography.	bind
10205	1	4079	5	11	NULL	NULL	NULL	MBL	GP		bind					bacteria	Organism				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_2_1052_s_206	15664949	(B) Percentages of MBL, L-ficolin, and H-ficolin bound to bacteria.	bind
10206	2	4079	5	11	NULL	NULL	NULL	L-ficolin	GP		bind					bacteria	Organism				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_2_1052_s_206	15664949	(B) Percentages of MBL, L-ficolin, and H-ficolin bound to bacteria.	bind
10207	3	4079	5	11	NULL	NULL	NULL	H-ficolin	GP		bind					bacteria	Organism				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_2_1052_s_206	15664949	(B) Percentages of MBL, L-ficolin, and H-ficolin bound to bacteria.	bind
12639	1	4079	7	11	NULL	NULL	NULL	MBL	GP		bind					bacteria	Organism				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_2_1052_s_206	15664949	(B) Percentages of MBL, L-ficolin, and H-ficolin bound to bacteria.	bind
12640	2	4079	7	11	NULL	NULL	NULL	L-ficolin	GP		bind					bacteria	Organism				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_2_1052_s_206	15664949	(B) Percentages of MBL, L-ficolin, and H-ficolin bound to bacteria.	bind
12641	3	4079	7	11	NULL	NULL	NULL	H-ficolin	GP		bind					bacteria	Organism				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_2_1052_s_206	15664949	(B) Percentages of MBL, L-ficolin, and H-ficolin bound to bacteria.	bind
10208	1	4082	5	11	NULL	NULL	NULL	Pex22p	GP		bind					Pex4p	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_cellbiol_146_1_99_s_311	10402463	(B) Pex22p binds to Pex4p in vivo.	bind
12642	1	4082	7	11	NULL	NULL	NULL	Pex22p	GP		binds to					Pex4p	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_cellbiol_146_1_99_s_311	10402463	(B) Pex22p binds to Pex4p in vivo.	bind
10209	1	4083	5	11	NULL	NULL	NULL	Mot1p	GP		bind					HXT	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_201	15923605	(B) PhosphorImager quantification of Mot1p, Taf1p, TBP, and Pol II binding to the  indicated  HXT promoters.	bind
10210	2	4083	5	11	NULL	NULL	NULL	Taf1p	GP		bind					HXT	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_201	15923605	(B) PhosphorImager quantification of Mot1p, Taf1p, TBP, and Pol II binding to the  indicated  HXT promoters.	bind
10211	3	4083	5	11	NULL	NULL	NULL	TBP	GP		bind					HXT	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_201	15923605	(B) PhosphorImager quantification of Mot1p, Taf1p, TBP, and Pol II binding to the  indicated  HXT promoters.	bind
10212	4	4083	5	11	NULL	NULL	NULL	Pol II	GP		bind					HXT	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_201	15923605	(B) PhosphorImager quantification of Mot1p, Taf1p, TBP, and Pol II binding to the  indicated  HXT promoters.	bind
12643	1	4083	7	11	NULL	NULL	NULL	Mot1p	GP		bind					HXT	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_201	15923605	(B) PhosphorImager quantification of Mot1p, Taf1p, TBP, and Pol II binding to the  indicated  HXT promoters.	bind
12644	2	4083	7	11	NULL	NULL	NULL	Taf1p	GP		bind					HXT	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_201	15923605	(B) PhosphorImager quantification of Mot1p, Taf1p, TBP, and Pol II binding to the  indicated  HXT promoters.	bind
12645	3	4083	7	11	NULL	NULL	NULL	TBP	GP		bind					HXT	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_201	15923605	(B) PhosphorImager quantification of Mot1p, Taf1p, TBP, and Pol II binding to the  indicated  HXT promoters.	bind
12646	4	4083	7	11	NULL	NULL	NULL	Pol II	GP		bind					HXT	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_201	15923605	(B) PhosphorImager quantification of Mot1p, Taf1p, TBP, and Pol II binding to the  indicated  HXT promoters.	bind
10213	1	4085	5	11	NULL	NULL	NULL	AP-1	GP		bind					Golgi	CellComponent	semi-intact cells			NULL		NULL	NULL	NULL	NULL	gw60_cell_114_3_299_s_167	12914695	(B) PI(4)P addback restores AP-1 binding to the Golgi of semi-intact cells.	bind
10214	2	4085	5	11	NULL	NULL	NULL	PI(4)P	Chemical		restores					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_3_299_s_167	12914695	(B) PI(4)P addback restores AP-1 binding to the Golgi of semi-intact cells.	bind
12647	1	4085	7	11	NULL	NULL	NULL	AP-1	GP		bind					Golgi 	CellComponent	semi-intact cells			NULL		NULL	NULL	NULL	NULL	gw60_cell_114_3_299_s_167	12914695	(B) PI(4)P addback restores AP-1 binding to the Golgi of semi-intact cells.	bind
12648	2	4085	7	11	NULL	NULL	NULL	PI(4)P	Chemical		restores					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_3_299_s_167	12914695	(B) PI(4)P addback restores AP-1 binding to the Golgi of semi-intact cells.	bind
10215	1	4086	5	11	NULL	NULL	NULL	PlexB	GP		bind					Rac	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_1_39_s_57	11604137	(B) PlexB binds to Rac in a GTP-dependent manner.	bind
10216	2	4086	5	11	NULL	NULL	NULL	statement 1	Process		is dependent on					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_1_39_s_57	11604137	(B) PlexB binds to Rac in a GTP-dependent manner.	bind
12649	1	4086	7	11	NULL	NULL	NULL	PlexB	GP		bind					Rac 	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_1_39_s_57	11604137	(B) PlexB binds to Rac in a GTP-dependent manner.	bind
12650	2	4086	7	11	NULL	NULL	NULL	statement 1	Process		is dependent on					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_1_39_s_57	11604137	(B) PlexB binds to Rac in a GTP-dependent manner.	bind
10217	1	4088	5	11	NULL	NULL	NULL	TRAF6	GP		mediate					IKK	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_351_s_131	11057907	(B) Point mutation at Cys-87 of  Ubc13 abolishes its ability to support TRAF6-mediated IKK activation.	bind
10218	2	4088	5	11	NULL	NULL	NULL	Ubc13	GP	point mutation	abolish			Cys-87		statement 1	Process	ability to support			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_351_s_131	11057907	(B) Point mutation at Cys-87 of  Ubc13 abolishes its ability to support TRAF6-mediated IKK activation.	bind
12651	1	4088	7	11	NULL	NULL	NULL	TRAF6	GP		mediates					IKK	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_351_s_131	11057907	(B) Point mutation at Cys-87 of  Ubc13 abolishes its ability to support TRAF6-mediated IKK activation.	bind
12652	2	4088	7	11	NULL	NULL	NULL	Ubc13	GP	Point mutation at	abolishes			Cys-87		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_351_s_131	11057907	(B) Point mutation at Cys-87 of  Ubc13 abolishes its ability to support TRAF6-mediated IKK activation.	bind
10219	1	4089	5	11	NULL	NULL	NULL	Poly(ADP-ribose)	Chemical		bind					hTRF2	GP	purified;;recombinant			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_4_1595_s_237	14749375	(B) Poly(ADP-ribose) binds to purified recombinant hTRF2.	bind
12653	1	4089	7	11	NULL	NULL	NULL	Poly ADP-ribose	Chemical		binds					 hTRF2	GP	purified			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_4_1595_s_237	14749375	(B) Poly(ADP-ribose) binds to purified recombinant hTRF2.	bind
10220	1	4090	5	11	NULL	NULL	NULL	p53	GP		bind		rapidly			mdm2	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_472_1_93_s_153	10781812	(B) Poly-G (5  g) precaptured by mdm2 bound to mAb 4B2 linked to the surface of a CM5 Biosensor chip, enhanced the binding of all the p53 mutations apart from p53C 64, showing that a tetramerisation domain is an absolute requirement for rapid binding of p53 to mdm2.	bind
10221	2	4090	5	11	NULL	NULL	NULL	mdm2	GP		bind					mAb 4B2	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_472_1_93_s_153	10781812	(B) Poly-G (5  g) precaptured by mdm2 bound to mAb 4B2 linked to the surface of a CM5 Biosensor chip, enhanced the binding of all the p53 mutations apart from p53C 64, showing that a tetramerisation domain is an absolute requirement for rapid binding of p53 to mdm2.	bind
10222	3	4090	5	11	NULL	NULL	NULL	Poly-G	NucleicAcid		precaptured by					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_472_1_93_s_153	10781812	(B) Poly-G (5  g) precaptured by mdm2 bound to mAb 4B2 linked to the surface of a CM5 Biosensor chip, enhanced the binding of all the p53 mutations apart from p53C 64, showing that a tetramerisation domain is an absolute requirement for rapid binding of p53 to mdm2.	bind
10223	4	4090	5	11	NULL	NULL	NULL	statement 3	Process		enhances					p53	GP	binding of;; mutant			NULL		NULL	NULL	NULL	NULL	gw60_febslett_472_1_93_s_153	10781812	(B) Poly-G (5  g) precaptured by mdm2 bound to mAb 4B2 linked to the surface of a CM5 Biosensor chip, enhanced the binding of all the p53 mutations apart from p53C 64, showing that a tetramerisation domain is an absolute requirement for rapid binding of p53 to mdm2.	bind
10224	5	4090	5	11	NULL	NULL	NULL	statement 3	Process		does not enhance					p53	GP	binding of;; mutant	C 64		NULL		NULL	NULL	NULL	NULL	gw60_febslett_472_1_93_s_153	10781812	(B) Poly-G (5  g) precaptured by mdm2 bound to mAb 4B2 linked to the surface of a CM5 Biosensor chip, enhanced the binding of all the p53 mutations apart from p53C 64, showing that a tetramerisation domain is an absolute requirement for rapid binding of p53 to mdm2.	bind
10225	6	4090	5	11	NULL	NULL	NULL				is required for		absolutely	tetramerisation domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_472_1_93_s_153	10781812	(B) Poly-G (5  g) precaptured by mdm2 bound to mAb 4B2 linked to the surface of a CM5 Biosensor chip, enhanced the binding of all the p53 mutations apart from p53C 64, showing that a tetramerisation domain is an absolute requirement for rapid binding of p53 to mdm2.	bind
10226	7	4090	5	11	NULL	NULL	NULL	statement 4	Process		shows					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_472_1_93_s_153	10781812	(B) Poly-G (5  g) precaptured by mdm2 bound to mAb 4B2 linked to the surface of a CM5 Biosensor chip, enhanced the binding of all the p53 mutations apart from p53C 64, showing that a tetramerisation domain is an absolute requirement for rapid binding of p53 to mdm2.	bind
10227	8	4090	5	11	NULL	NULL	NULL	statement 5	Process		shows					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_472_1_93_s_153	10781812	(B) Poly-G (5  g) precaptured by mdm2 bound to mAb 4B2 linked to the surface of a CM5 Biosensor chip, enhanced the binding of all the p53 mutations apart from p53C 64, showing that a tetramerisation domain is an absolute requirement for rapid binding of p53 to mdm2.	bind
12654	1	4090	7	11	NULL	NULL	NULL	Poly-G	NucleicAcid		bind					mAb 4B2	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_472_1_93_s_153	10781812	(B) Poly-G (5  g) precaptured by mdm2 bound to mAb 4B2 linked to the surface of a CM5 Biosensor chip, enhanced the binding of all the p53 mutations apart from p53C 64, showing that a tetramerisation domain is an absolute requirement for rapid binding of p53 to mdm2.	bind
12655	2	4090	7	11	NULL	NULL	NULL	Poly-G	NucleicAcid		is precaptured by					mdm2	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_472_1_93_s_153	10781812	(B) Poly-G (5  g) precaptured by mdm2 bound to mAb 4B2 linked to the surface of a CM5 Biosensor chip, enhanced the binding of all the p53 mutations apart from p53C 64, showing that a tetramerisation domain is an absolute requirement for rapid binding of p53 to mdm2.	bind
12661	5	4090	7	11	NULL	NULL	NULL	p53	GP		bind		rapidly			mdm2	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_472_1_93_s_153	10781812	(B) Poly-G (5  g) precaptured by mdm2 bound to mAb 4B2 linked to the surface of a CM5 Biosensor chip, enhanced the binding of all the p53 mutations apart from p53C 64, showing that a tetramerisation domain is an absolute requirement for rapid binding of p53 to mdm2.	bind
12664	6	4090	7	11	NULL	NULL	NULL				is required for			tetramerisation domain		statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_472_1_93_s_153	10781812	(B) Poly-G (5  g) precaptured by mdm2 bound to mAb 4B2 linked to the surface of a CM5 Biosensor chip, enhanced the binding of all the p53 mutations apart from p53C 64, showing that a tetramerisation domain is an absolute requirement for rapid binding of p53 to mdm2.	bind
44471	3	4090	7	11	NULL	NULL	NULL	statement 1	Process		enhance					p53	GP	binding of;;mutated			NULL		NULL	NULL	NULL	NULL	gw60_febslett_472_1_93_s_153	10781812	(B) Poly-G (5  g) precaptured by mdm2 bound to mAb 4B2 linked to the surface of a CM5 Biosensor chip, enhanced the binding of all the p53 mutations apart from p53C 64, showing that a tetramerisation domain is an absolute requirement for rapid binding of p53 to mdm2.	bind
44472	4	4090	7	11	NULL	NULL	NULL	statement 1	Process		does not enhance					p53	GP	binding of;;mutated	C64		NULL		NULL	NULL	NULL	NULL	gw60_febslett_472_1_93_s_153	10781812	(B) Poly-G (5  g) precaptured by mdm2 bound to mAb 4B2 linked to the surface of a CM5 Biosensor chip, enhanced the binding of all the p53 mutations apart from p53C 64, showing that a tetramerisation domain is an absolute requirement for rapid binding of p53 to mdm2.	bind
10228	1	4092	5	11	NULL	NULL	NULL	GST-Rad24	GP		bind		preferentially			phospho-Ste11	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_1_3_389_s_207	11702950	(B) Preferential binding between GST-Rad24 and phospho-Ste11.	bind
12665	1	4092	7	11	NULL	NULL	NULL	GST-Rad24	GP		bind		preferentially			phospho-Ste11	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_1_3_389_s_207	11702950	(B) Preferential binding between GST-Rad24 and phospho-Ste11.	bind
10229	1	4093	5	11	NULL	NULL	NULL	AF-6	GP		bind					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4663_s_272	12808105	(B) Prevention of phosphorylation of AF-6 by  Bcr reduces binding of AF-6 to Ras.	bind
10230	2	4093	5	11	NULL	NULL	NULL	Bcr	GP		prevent					AF-6	GP	phosphorylation of 			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4663_s_272	12808105	(B) Prevention of phosphorylation of AF-6 by  Bcr reduces binding of AF-6 to Ras.	bind
10231	3	4093	5	11	NULL	NULL	NULL	statement 2	Process		reduce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4663_s_272	12808105	(B) Prevention of phosphorylation of AF-6 by  Bcr reduces binding of AF-6 to Ras.	bind
12666	1	4093	7	11	NULL	NULL	NULL	AF-6	GP		bind					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4663_s_272	12808105	(B) Prevention of phosphorylation of AF-6 by  Bcr reduces binding of AF-6 to Ras.	bind
12667	2	4093	7	11	NULL	NULL	NULL	Bcr	GP		prevents					AF6	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4663_s_272	12808105	(B) Prevention of phosphorylation of AF-6 by  Bcr reduces binding of AF-6 to Ras.	bind
12668	3	4093	7	11	NULL	NULL	NULL	statement 2	Process		reduce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4663_s_272	12808105	(B) Prevention of phosphorylation of AF-6 by  Bcr reduces binding of AF-6 to Ras.	bind
10232	1	4096	5	11	NULL	NULL	NULL	Apaf1	GP		bind				promoter	p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_2_207_s_91	11591730	(B) Protein was extracted from neurons 48 h after infection with Ad-p53 or Ad-p53-173L and p53 binding activity to the Apaf1 promoter elements was assayed by electrophoretic mobility shift assay.	bind
12669	1	4096	7	11	NULL	NULL	NULL	 p53	GP		bind					Apaf1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_2_207_s_91	11591730	(B) Protein was extracted from neurons 48 h after infection with Ad-p53 or Ad-p53-173L and p53 binding activity to the Apaf1 promoter elements was assayed by electrophoretic mobility shift assay.	bind
10233	1	4097	5	11	NULL	NULL	NULL	c-Src	GP		phosphorylate					GST-PECAM	GP		1Cyt		NULL		NULL	NULL	NULL	NULL	gw60_febslett_408_3_331_s_73	9188788	(B) Proteins bound to the c-Src phosphorylated GST-PECAM-1Cyt affinity matrix.	bind
12670	1	4097	7	11	NULL	NULL	NULL	c-Src	GP		phosphorylate					GST-PECAM	GP		1Cyt		NULL		NULL	NULL	NULL	NULL	gw60_febslett_408_3_331_s_73	9188788	(B) Proteins bound to the c-Src phosphorylated GST-PECAM-1Cyt affinity matrix.	bind
10234	1	4104	5	11	NULL	NULL	NULL	Tra2	GP	purified	bind					RNA	NucleicAcid			A element	NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1625_2_141_s_196	12531473	(B) Purified Tra2  binds to A element RNA.	bind
12671	1	4104	7	11	NULL	NULL	NULL	Tra2 	GP	purified	bind					RNA	NucleicAcid			A element	NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1625_2_141_s_196	12531473	(B) Purified Tra2  binds to A element RNA.	bind
10235	1	4105	5	11	NULL	NULL	NULL	TWD1-3 protein	GP	purified	bind		specifically			vacuolar membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_7_3393_s_255	15133126	(B) Purified TWD1-3 protein binds specifically to vacuolar membranes.	bind
12672	1	4105	7	11	NULL	NULL	NULL	TWD1-3 	GP	purified	binds		specifically			vacuolar membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_7_3393_s_255	15133126	(B) Purified TWD1-3 protein binds specifically to vacuolar membranes.	bind
10236	1	4106	5	11	NULL	NULL	NULL	Ena 	GP	purified;;recombinant	bind					GST-Dlar	GP		D1-D2		NULL		NULL	NULL	NULL	NULL	gw60_neuron_22_2_301_s_196	10069336	(B) Purified, recombinant Ena (arrow) binds to GST-Dlar D1-D2 (lane 2), and binds weakly to GST-DPTP10D (lane 3) but does not bind significantly to GST alone (lane 1).	bind
10237	2	4106	5	11	NULL	NULL	NULL	Ena	GP	purified;;recombinant	bind		weakly			GST-DPTP10D	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_22_2_301_s_196	10069336	(B) Purified, recombinant Ena (arrow) binds to GST-Dlar D1-D2 (lane 2), and binds weakly to GST-DPTP10D (lane 3) but does not bind significantly to GST alone (lane 1).	bind
10238	3	4106	5	11	NULL	NULL	NULL	Ena	GP	purified;;recombinant	does not bind		significantly			GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_22_2_301_s_196	10069336	(B) Purified, recombinant Ena (arrow) binds to GST-Dlar D1-D2 (lane 2), and binds weakly to GST-DPTP10D (lane 3) but does not bind significantly to GST alone (lane 1).	bind
44473	1	4106	7	11	NULL	NULL	NULL	Ena	GP	purified;;recombinant	bind					GST-Dlar 	GP		D1-D2		NULL		NULL	NULL	NULL	NULL	gw60_neuron_22_2_301_s_196	10069336	(B) Purified, recombinant Ena (arrow) binds to GST-Dlar D1-D2 (lane 2), and binds weakly to GST-DPTP10D (lane 3) but does not bind significantly to GST alone (lane 1).	bind
44474	2	4106	7	11	NULL	NULL	NULL	Ena	GP	purified;;recombinant	bind		weakly			GST-DPTP10D	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_22_2_301_s_196	10069336	(B) Purified, recombinant Ena (arrow) binds to GST-Dlar D1-D2 (lane 2), and binds weakly to GST-DPTP10D (lane 3) but does not bind significantly to GST alone (lane 1).	bind
44476	3	4106	7	11	NULL	NULL	NULL	Ena	GP	purified;;recombinant	does not bind		significantly			GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_22_2_301_s_196	10069336	(B) Purified, recombinant Ena (arrow) binds to GST-Dlar D1-D2 (lane 2), and binds weakly to GST-DPTP10D (lane 3) but does not bind significantly to GST alone (lane 1).	bind
10239	1	4107	5	11	NULL	NULL	NULL	mSin3A	GP		bind									5' LTR	NULL	SLB-1 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_14_6117_s_190	15226416	(B) Quantification of mSin3A and  NCoR binding at the 5' and 3'' LTRs in SLB-1 cells.	bind
10240	2	4107	5	11	NULL	NULL	NULL	mSin3A	GP		bind									3'' LTR	NULL	SLB-1 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_14_6117_s_190	15226416	(B) Quantification of mSin3A and  NCoR binding at the 5' and 3'' LTRs in SLB-1 cells.	bind
10241	3	4107	5	11	NULL	NULL	NULL	NCoR	GP		bind									5' LTR	NULL	SLB-1 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_14_6117_s_190	15226416	(B) Quantification of mSin3A and  NCoR binding at the 5' and 3'' LTRs in SLB-1 cells.	bind
10242	4	4107	5	11	NULL	NULL	NULL	NCoR	GP		bind									3'' LTR	NULL	SLB-1 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_14_6117_s_190	15226416	(B) Quantification of mSin3A and  NCoR binding at the 5' and 3'' LTRs in SLB-1 cells.	bind
12677	1	4107	7	11	NULL	NULL	NULL	mSin3A	GP		bind									 5' LTR	NULL	SLB-1 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_14_6117_s_190	15226416	(B) Quantification of mSin3A and  NCoR binding at the 5' and 3'' LTRs in SLB-1 cells.	bind
12678	2	4107	7	11	NULL	NULL	NULL	mSin3A	GP		bind									3'' LTR	NULL	SLB-1 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_14_6117_s_190	15226416	(B) Quantification of mSin3A and  NCoR binding at the 5' and 3'' LTRs in SLB-1 cells.	bind
12680	4	4107	7	11	NULL	NULL	NULL	NCoR	GP		bind									3'' LTR	NULL	SLB-1 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_14_6117_s_190	15226416	(B) Quantification of mSin3A and  NCoR binding at the 5' and 3'' LTRs in SLB-1 cells.	bind
10243	1	4108	5	11	NULL	NULL	NULL	NodD1	GP		bind					nodF	GP		nod box		NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_15_5417_s_169	16855231	(B) Quantitation  of NodD1 binding to the  nodF nod box from the experiment shown in panel A.	bind
12679	3	4108	7	11	NULL	NULL	NULL	NCoR	GP		bind									5' LTR	NULL	SLB-1 cells	NULL	NULL	NULL	NULL	gw70_jbacteriol_188_15_5417_s_169	16855231	(B) Quantitation  of NodD1 binding to the  nodF nod box from the experiment shown in panel A.	bind
12681	1	4108	7	11	NULL	NULL	NULL	NodD1	GP		bind					nodF	GP		nod box		NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_15_5417_s_169	16855231	(B) Quantitation  of NodD1 binding to the  nodF nod box from the experiment shown in panel A.	bind
10244	1	4109	5	11	NULL	NULL	NULL	Spt10	GP		bind					HTA2-HTB2	GP			promoter	NULL	G1 phase	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_1_135_s_161	14673149	(B) Quantitation of Spt10  and Spt21 binding at the  HTA2-HTB2 promoter at both G1 (white bars) and S (gray bars) phases.	bind
10245	2	4109	5	11	NULL	NULL	NULL	Spt10	GP		bind					HTA2-HTB2	GP			promoter	NULL	S phase	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_1_135_s_161	14673149	(B) Quantitation of Spt10  and Spt21 binding at the  HTA2-HTB2 promoter at both G1 (white bars) and S (gray bars) phases.	bind
10246	3	4109	5	11	NULL	NULL	NULL	Spt21	GP		bind					HTA2-HTB2	GP			promoter	NULL	G1 phase	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_1_135_s_161	14673149	(B) Quantitation of Spt10  and Spt21 binding at the  HTA2-HTB2 promoter at both G1 (white bars) and S (gray bars) phases.	bind
10247	4	4109	5	11	NULL	NULL	NULL	Spt21	GP		bind					HTA2-HTB2	GP			promoter	NULL	S phase	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_1_135_s_161	14673149	(B) Quantitation of Spt10  and Spt21 binding at the  HTA2-HTB2 promoter at both G1 (white bars) and S (gray bars) phases.	bind
12682	1	4109	7	11	NULL	NULL	NULL	Spt10	GP		bind					HTA2-HTB2	GP			promoter	NULL	G1 phase	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_1_135_s_161	14673149	(B) Quantitation of Spt10  and Spt21 binding at the  HTA2-HTB2 promoter at both G1 (white bars) and S (gray bars) phases.	bind
12683	2	4109	7	11	NULL	NULL	NULL	Spt10	GP		bind					HTA2-HTB2	GP			promoter	NULL	S phase	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_1_135_s_161	14673149	(B) Quantitation of Spt10  and Spt21 binding at the  HTA2-HTB2 promoter at both G1 (white bars) and S (gray bars) phases.	bind
12684	3	4109	7	11	NULL	NULL	NULL	Spt21	GP		bind					HTA2-HTB2	GP			promoter	NULL	G1 phase	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_1_135_s_161	14673149	(B) Quantitation of Spt10  and Spt21 binding at the  HTA2-HTB2 promoter at both G1 (white bars) and S (gray bars) phases.	bind
12685	4	4109	7	11	NULL	NULL	NULL	Spt21	GP		bind					HTA2-HTB2	GP			promoter	NULL	S phase	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_1_135_s_161	14673149	(B) Quantitation of Spt10  and Spt21 binding at the  HTA2-HTB2 promoter at both G1 (white bars) and S (gray bars) phases.	bind
10248	1	4110	5	11	NULL	NULL	NULL	Pitx2 proteins 	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_7001_s_115	10490637	(B) Quantitation of the DNA binding of Pitx2 and truncated Pitx2 proteins from the EMSA experiments.	bind
10249	2	4110	5	11	NULL	NULL	NULL	Pitx2 proteins	GP	truncated	bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_7001_s_115	10490637	(B) Quantitation of the DNA binding of Pitx2 and truncated Pitx2 proteins from the EMSA experiments.	bind
12686	1	4110	7	11	NULL	NULL	NULL	Pitx2	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_7001_s_115	10490637	(B) Quantitation of the DNA binding of Pitx2 and truncated Pitx2 proteins from the EMSA experiments.	bind
12687	2	4110	7	11	NULL	NULL	NULL	Pitx2	GP	truncated	bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_7001_s_115	10490637	(B) Quantitation of the DNA binding of Pitx2 and truncated Pitx2 proteins from the EMSA experiments.	bind
10250	1	4111	5	11	NULL	NULL	NULL	acetyl-histone H3	GP		bind					bcl-2	GP			P1 promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_204	15713621	(B) Quantitative  ChIP assay of acetyl-histone H3 and acetyl-histone H4 binding to the  bcl-2 P1 promoter.	bind
10251	2	4111	5	11	NULL	NULL	NULL	acetyl-histone H4	GP		bind					bcl-2	GP			P1 promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_204	15713621	(B) Quantitative  ChIP assay of acetyl-histone H3 and acetyl-histone H4 binding to the  bcl-2 P1 promoter.	bind
12701	1	4111	7	11	NULL	NULL	NULL	acetyl-histone H3	GP		bind					bcl-2	GP			P1 promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_204	15713621	(B) Quantitative  ChIP assay of acetyl-histone H3 and acetyl-histone H4 binding to the  bcl-2 P1 promoter.	bind
12702	2	4111	7	11	NULL	NULL	NULL	acetyl-histone H4	GP		bind					bcl-2 	GP			P1 promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_204	15713621	(B) Quantitative  ChIP assay of acetyl-histone H3 and acetyl-histone H4 binding to the  bcl-2 P1 promoter.	bind
10252	1	4112	5	11	NULL	NULL	NULL	tubulin	GP		bind					GST-CNP	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_4_661_s_65	16103231	(B) Quantitative analysis of tubulin binding to GST-CNP.	bind
12703	1	4112	7	11	NULL	NULL	NULL	tubulin	GP		bind					GST-CNP	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_4_661_s_65	16103231	(B) Quantitative analysis of tubulin binding to GST-CNP.	bind
10253	1	4113	5	11	NULL	NULL	NULL	R/M	GP		bind					DNA	NucleicAcid	circular			NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_5_1129_s_104	11741547	(B) R/M bound to the 1.8 kb circular DNA.	bind
12704	1	4113	7	11	NULL	NULL	NULL	R/M	GP		bind					 DNA	NucleicAcid	circular			NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_5_1129_s_104	11741547	(B) R/M bound to the 1.8 kb circular DNA.	bind
10256	1	4114	5	11	NULL	NULL	NULL	Munc18-1 proteins	GP	radiolabelled;;wild-type	bind					GST	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_470_s_137	15563604	(B) Radiolabeled Munc18-1  wild-type and mutant proteins were bound to GST, GST-Mint 2, and GST-Mint1 residues  226-314 immobilized on glutathione-Sepharose.	bind
10257	2	4114	5	11	NULL	NULL	NULL	Munc18-1 proteins	GP	radiolabelled;;mutant	bind					GST	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_470_s_137	15563604	(B) Radiolabeled Munc18-1  wild-type and mutant proteins were bound to GST, GST-Mint 2, and GST-Mint1 residues  226-314 immobilized on glutathione-Sepharose.	bind
10258	3	4114	5	11	NULL	NULL	NULL	Munc18-1 proteins	GP	radiolabelled;;wild-type	bind					GST-Mint 2	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_470_s_137	15563604	(B) Radiolabeled Munc18-1  wild-type and mutant proteins were bound to GST, GST-Mint 2, and GST-Mint1 residues  226-314 immobilized on glutathione-Sepharose.	bind
10259	4	4114	5	11	NULL	NULL	NULL	Munc18-1 proteins	GP	radiolabelled;;mutant	bind					GST-Mint 2	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_470_s_137	15563604	(B) Radiolabeled Munc18-1  wild-type and mutant proteins were bound to GST, GST-Mint 2, and GST-Mint1 residues  226-314 immobilized on glutathione-Sepharose.	bind
10260	5	4114	5	11	NULL	NULL	NULL	Munc18-1 proteins	GP	radiolabelled;;wild-type	bind					GST-Mint1	GP	immobilized	226-314		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_470_s_137	15563604	(B) Radiolabeled Munc18-1  wild-type and mutant proteins were bound to GST, GST-Mint 2, and GST-Mint1 residues  226-314 immobilized on glutathione-Sepharose.	bind
10261	6	4114	5	11	NULL	NULL	NULL	Munc18-1 proteins	GP	radiolabelled;;mutant	bind					GST-Mint1	GP	immobilized	226-314		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_470_s_137	15563604	(B) Radiolabeled Munc18-1  wild-type and mutant proteins were bound to GST, GST-Mint 2, and GST-Mint1 residues  226-314 immobilized on glutathione-Sepharose.	bind
12705	1	4114	7	11	NULL	NULL	NULL	Munc18-1	GP	radiolabeled;;wild-type	bind					GST	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_470_s_137	15563604	(B) Radiolabeled Munc18-1  wild-type and mutant proteins were bound to GST, GST-Mint 2, and GST-Mint1 residues  226-314 immobilized on glutathione-Sepharose.	bind
12706	2	4114	7	11	NULL	NULL	NULL	Munc18-1	GP	radiolabeled;;wild-type	bind					GST-Mint 2	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_470_s_137	15563604	(B) Radiolabeled Munc18-1  wild-type and mutant proteins were bound to GST, GST-Mint 2, and GST-Mint1 residues  226-314 immobilized on glutathione-Sepharose.	bind
12707	3	4114	7	11	NULL	NULL	NULL	Munc18-1	GP	radiolabeled;;wild-type	bind					GST-Mint1	GP	immobilized	226-314		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_470_s_137	15563604	(B) Radiolabeled Munc18-1  wild-type and mutant proteins were bound to GST, GST-Mint 2, and GST-Mint1 residues  226-314 immobilized on glutathione-Sepharose.	bind
12708	4	4114	7	11	NULL	NULL	NULL	Munc18-1	GP	radiolabeled;;mutant	bind					GST	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_470_s_137	15563604	(B) Radiolabeled Munc18-1  wild-type and mutant proteins were bound to GST, GST-Mint 2, and GST-Mint1 residues  226-314 immobilized on glutathione-Sepharose.	bind
12709	5	4114	7	11	NULL	NULL	NULL	Munc18-1	GP	radiolabeled;;mutant	bind					GST-Mint 2	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_470_s_137	15563604	(B) Radiolabeled Munc18-1  wild-type and mutant proteins were bound to GST, GST-Mint 2, and GST-Mint1 residues  226-314 immobilized on glutathione-Sepharose.	bind
12710	6	4114	7	11	NULL	NULL	NULL	Munc18-1	GP	radiolabeled;;mutant	bind					GST-Mint 1	GP	immobilized	226-314		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_470_s_137	15563604	(B) Radiolabeled Munc18-1  wild-type and mutant proteins were bound to GST, GST-Mint 2, and GST-Mint1 residues  226-314 immobilized on glutathione-Sepharose.	bind
10254	1	4115	5	11	NULL	NULL	NULL	CRT	GP		bind								DBD		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6286_s_135	12167720	(B) RanGTP is not a cofactor for CRT binding to the DBD.	bind
10255	2	4115	5	11	NULL	NULL	NULL	RanGTP 	Chemical		is not a cofactor for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6286_s_135	12167720	(B) RanGTP is not a cofactor for CRT binding to the DBD.	bind
12711	1	4115	7	11	NULL	NULL	NULL	CRT	GP		bind					DBD	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6286_s_135	12167720	(B) RanGTP is not a cofactor for CRT binding to the DBD.	bind
12712	2	4115	7	11	NULL	NULL	NULL	RanGTP	Chemical		is not a cofactor for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6286_s_135	12167720	(B) RanGTP is not a cofactor for CRT binding to the DBD.	bind
10262	1	4117	5	11	NULL	NULL	NULL	rec-Pin1	GP		bind					neuronal nuclei	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_expneurol_199_2_328_s_136	16480979	(b) Rec-Pin1 binding: levels of rec-Pin1 binding to neuronal nuclei (Nu;  black bars), cytoplasm (Cyt; grey bars), and lipofuscin granules (Lipo; white bars).	bind
10263	2	4117	5	11	NULL	NULL	NULL	rec-Pin1	GP		bind					neuronal cytoplasm	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_expneurol_199_2_328_s_136	16480979	(b) Rec-Pin1 binding: levels of rec-Pin1 binding to neuronal nuclei (Nu;  black bars), cytoplasm (Cyt; grey bars), and lipofuscin granules (Lipo; white bars).	bind
10264	3	4117	5	11	NULL	NULL	NULL	rec-Pin1	GP		bind					neuronal lipofuscin granules	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_expneurol_199_2_328_s_136	16480979	(b) Rec-Pin1 binding: levels of rec-Pin1 binding to neuronal nuclei (Nu;  black bars), cytoplasm (Cyt; grey bars), and lipofuscin granules (Lipo; white bars).	bind
12713	1	4117	7	11	NULL	NULL	NULL	rec-Pin1 	GP		bind					neuronal nuclei	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_expneurol_199_2_328_s_136	16480979	(b) Rec-Pin1 binding: levels of rec-Pin1 binding to neuronal nuclei (Nu;  black bars), cytoplasm (Cyt; grey bars), and lipofuscin granules (Lipo; white bars).	bind
12714	2	4117	7	11	NULL	NULL	NULL	rec-Pin1 	GP		bind					neuronal cytoplasm	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_expneurol_199_2_328_s_136	16480979	(b) Rec-Pin1 binding: levels of rec-Pin1 binding to neuronal nuclei (Nu;  black bars), cytoplasm (Cyt; grey bars), and lipofuscin granules (Lipo; white bars).	bind
12715	3	4117	7	11	NULL	NULL	NULL	rec-Pin1 	GP		bind					lipofuscin granules	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_expneurol_199_2_328_s_136	16480979	(b) Rec-Pin1 binding: levels of rec-Pin1 binding to neuronal nuclei (Nu;  black bars), cytoplasm (Cyt; grey bars), and lipofuscin granules (Lipo; white bars).	bind
10271	1	4118	5	11	NULL	NULL	NULL	IRP1	GP	recombinant;;Manduca	bind					ferritin	GP	human		IRE transcripts	NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_85_s_188	11719072	(B) Recombinant  Manduca IRP1 binds human ferritin IRE transcripts.	bind
44477	1	4118	7	11	NULL	NULL	NULL	IRP1	GP	recombinant;;Manduca	bind					ferritin	GP	human		IRE	NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_85_s_188	11719072	(B) Recombinant  Manduca IRP1 binds human ferritin IRE transcripts.	bind
10279	1	4119	5	11	NULL	NULL	NULL	IRF-3	GP	recombinant	bind			N-terminal		RANTES probe	GP			ISRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_959_s_143	9891032	(B) Recombinant N-terminal IRF-3 binds to the RANTES ISRE probe.	bind
12742	1	4119	7	11	NULL	NULL	NULL	IRF-3 	GP	recombinant	binds			N-terminal		RANTES 	GP			ISRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_959_s_143	9891032	(B) Recombinant N-terminal IRF-3 binds to the RANTES ISRE probe.	bind
10267	1	4121	5	11	NULL	NULL	NULL	RuBisCo	GP		bind					EL229C-B	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_138	11672529	(B) Refolding of 0.5 muM RuBisCo  bound to EL229C-B with the addition of  either 5 muM SA (.)	bind
10268	2	4121	5	11	NULL	NULL	NULL	SA	Chemical	addition of	refolds					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_138	11672529	(B) Refolding of 0.5 muM RuBisCo  bound to EL229C-B with the addition of  either 5 muM SA (.)	bind
12743	1	4121	7	11	NULL	NULL	NULL	RuBisCo	GP		bind					EL229C-B	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_138	11672529	(B) Refolding of 0.5 muM RuBisCo  bound to EL229C-B with the addition of  either 5 muM SA (.)	bind
12744	2	4121	7	11	NULL	NULL	NULL	statement 1	Process	refolding of 	after addition of					SA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_138	11672529	(B) Refolding of 0.5 muM RuBisCo  bound to EL229C-B with the addition of  either 5 muM SA (.)	bind
10280	1	4122	5	11	NULL	NULL	NULL	RelA	GP		bind					Cyclin T1	GP		cyclin box		NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_327_s_102	11545735	(B) RelA binds to the cyclin box of Cyclin T1.	bind
12745	1	4122	7	11	NULL	NULL	NULL	RelA	GP		bind					Cyclin T1	GP		cyclin box		NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_327_s_102	11545735	(B) RelA binds to the cyclin box of Cyclin T1.	bind
10281	1	4124	5	11	NULL	NULL	NULL	ResD	GP		does not bind					yclJ	GP	mutations in		promoters putative ResD box	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_19_6477_s_193	15375128	(B) ResD does not bind to  yclJ promoters carrying mutations in the putative ResD box.	bind
12746	1	4124	7	11	NULL	NULL	NULL	ResD	GP		does not bind					 yclJ	GP	mutant		putative ResD box promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_19_6477_s_193	15375128	(B) ResD does not bind to  yclJ promoters carrying mutations in the putative ResD box.	bind
10336	1	4125	5	11	NULL	NULL	NULL	TCR	GP		bind					P6A/HLA-A2	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_4_475_s_54	11070166	(B) Residuals for TCR binding to P6A/HLA-A2 assuming no interaction (circles, 3.2  M TCR + 3.3  M P6A/HLA-A2, representing 1.4% complex; triangles, 9.3  M TCR + 9.5  M P6A/HLA-A2, representing 3.6% complex).	bind
12747	1	4125	7	11	NULL	NULL	NULL	TCR	GP		bind					P6A/HLA-A2	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_4_475_s_54	11070166	(B) Residuals for TCR binding to P6A/HLA-A2 assuming no interaction (circles, 3.2  M TCR + 3.3  M P6A/HLA-A2, representing 1.4% complex; triangles, 9.3  M TCR + 9.5  M P6A/HLA-A2, representing 3.6% complex).	bind
10343	1	4126	5	11	NULL	NULL	NULL	CodY	GP		bind									fla/chePA promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_10_3118_s_199	12730172	(B) Results of CodY binding to  fla/chePA, the sigmaA-dependent promoter.	bind
13002	2	4126	5	11	NULL	NULL	NULL				is dependent on				fla/chePA	sigmaA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_10_3118_s_199	12730172	(B) Results of CodY binding to  fla/chePA, the sigmaA-dependent promoter.	bind
12748	1	4126	7	11	NULL	NULL	NULL	CodY	GP		bind									fla/chePA promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_10_3118_s_199	12730172	(B) Results of CodY binding to  fla/chePA, the sigmaA-dependent promoter.	bind
12749	2	4126	7	11	NULL	NULL	NULL				is dependent on				fla/chePA	sigmaA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_10_3118_s_199	12730172	(B) Results of CodY binding to  fla/chePA, the sigmaA-dependent promoter.	bind
10385	1	4127	5	11	NULL	NULL	NULL	RFC (p140)	GP		bind					RelA	GP		RHD		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_2_721_s_110	12509469	(B) RFC (p140) binds the RHD of RelA.	bind
12750	1	4127	7	11	NULL	NULL	NULL	RFC (p140)	GP		binds					RelA	GP		RHD		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_2_721_s_110	12509469	(B) RFC (p140) binds the RHD of RelA.	bind
10386	1	4128	5	11	NULL	NULL	NULL	RFXANK	GP		bind					RFXAP	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4455_s_108	10825209	(B) RFXANK binds to RFXAP but not to RFX5 in vitro.	bind
10387	2	4128	5	11	NULL	NULL	NULL	RFXANK	GP		does not bind					RFX5	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4455_s_108	10825209	(B) RFXANK binds to RFXAP but not to RFX5 in vitro.	bind
12752	1	4128	7	11	NULL	NULL	NULL	RFXANK	GP		binds					RFXAP	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4455_s_108	10825209	(B) RFXANK binds to RFXAP but not to RFX5 in vitro.	bind
12753	2	4128	7	11	NULL	NULL	NULL	RFXANK	GP		does not bind					RFX5	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4455_s_108	10825209	(B) RFXANK binds to RFXAP but not to RFX5 in vitro.	bind
10388	1	4129	5	11	NULL	NULL	NULL	GST-Rhotekin	GP		bind		only			Rho-GTP	GP	active			NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_6_733_s_142	12062086	(B) Rho activation assay: after normalization of cell lysates from the conditions shown by anti-Rho Western blot, the lysates were probed with GST-Rhotekin, which only binds active Rho-GTP.	bind
12754	1	4129	7	11	NULL	NULL	NULL	GST-Rhotekin	GP		binds		only			Rho-GTP	GP	active			NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_6_733_s_142	12062086	(B) Rho activation assay: after normalization of cell lysates from the conditions shown by anti-Rho Western blot, the lysates were probed with GST-Rhotekin, which only binds active Rho-GTP.	bind
10389	1	4130	5	11	NULL	NULL	NULL	rIB2	GP		bind					MLK3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4073_s_197	12024021	(B) rIB2 binds to MLK3.	bind
12755	1	4130	7	11	NULL	NULL	NULL	 rIB2	GP		binds to					MLK3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4073_s_197	12024021	(B) rIB2 binds to MLK3.	bind
10390	1	4131	5	11	NULL	NULL	NULL	CksHs1	GP		bind					CDK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_6_863_s_36	8601310	(B) Ribbon diagram  of CksHs1 (yellow) bound to CDK2, with the N-lobe in purple and the C-lobe  in blue and green.	bind
12756	1	4131	7	11	NULL	NULL	NULL	CksHs1	GP		bind					CDK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_6_863_s_36	8601310	(B) Ribbon diagram  of CksHs1 (yellow) bound to CDK2, with the N-lobe in purple and the C-lobe  in blue and green.	bind
10391	1	4132	5	11	NULL	NULL	NULL	HSA	Chemical		is saturated with					palmitic acid	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1688_2_102_s_126	14990340	(B) Rifampin binding to HSA saturated  with palmitic acid.	bind
10392	2	4132	5	11	NULL	NULL	NULL	Rifampin	Chemical		bind					statement 1	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1688_2_102_s_126	14990340	(B) Rifampin binding to HSA saturated  with palmitic acid.	bind
12758	1	4132	7	11	NULL	NULL	NULL	HSA	Chemical		is saturated with					palmitic acid	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1688_2_102_s_126	14990340	(B) Rifampin binding to HSA saturated  with palmitic acid.	bind
12759	2	4132	7	11	NULL	NULL	NULL	Rifampin	Chemical		bind					statement 1	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1688_2_102_s_126	14990340	(B) Rifampin binding to HSA saturated  with palmitic acid.	bind
10393	1	4133	5	11	NULL	NULL	NULL	chromaffin cell cytoplasmic protein	GP		bind					TH mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_120_2_91_s_151	14741398	(B) RNA-EMSA of chromaffin cell cytoplasmic protein binding to TH mRNA.  32P-labeled RNA probes THC, TH1, TH2 and TH3 were incubated alone (lanes 1,3,5 and 7)  or with 40  g S100 cytoplasmic extracts (lanes 2, 4, 6 and 8) and separated on non-denaturing  gels.	bind
12777	1	4133	7	11	NULL	NULL	NULL	chromaffin cell cytoplasmic protein	GP		bind					TH mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_120_2_91_s_151	14741398	(B) RNA-EMSA of chromaffin cell cytoplasmic protein binding to TH mRNA.  32P-labeled RNA probes THC, TH1, TH2 and TH3 were incubated alone (lanes 1,3,5 and 7)  or with 40  g S100 cytoplasmic extracts (lanes 2, 4, 6 and 8) and separated on non-denaturing  gels.	bind
10400	1	4134	5	11	NULL	NULL	NULL	cyclin T protein	GP	GST-cleaved	bind					TAR-2 RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_188	9491887	(B) RNase footprint analysis of the binding  of GST-cleaved cyclin T and GST-Tat-2 (aa 1 - 99) proteins to TAR-2 RNA.	bind
10401	2	4134	5	11	NULL	NULL	NULL	GST-Tat-2 protein	GP		bind			aa 1 - 99		TAR-2 RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_188	9491887	(B) RNase footprint analysis of the binding  of GST-cleaved cyclin T and GST-Tat-2 (aa 1 - 99) proteins to TAR-2 RNA.	bind
12760	1	4134	7	11	NULL	NULL	NULL	 cyclin T	GP	GST-cleaved	bind					TAR-2 RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_188	9491887	(B) RNase footprint analysis of the binding  of GST-cleaved cyclin T and GST-Tat-2 (aa 1 - 99) proteins to TAR-2 RNA.	bind
12761	2	4134	7	11	NULL	NULL	NULL	GST-Tat-2	GP		bind			1 - 99		TAR-2 RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_92_4_451_s_188	9491887	(B) RNase footprint analysis of the binding  of GST-cleaved cyclin T and GST-Tat-2 (aa 1 - 99) proteins to TAR-2 RNA.	bind
10403	1	4135	5	11	NULL	NULL	NULL	Robo1	GP		bind		specifically			srGAPs	GP		SH3 domains		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_209_s_98	11672528	(B) Robo1 specifically binds to SH3 domains  in srGAPs but not to SH3 motif  in Src or Graf.	bind
10404	2	4135	5	11	NULL	NULL	NULL	Robo1	GP		does not bind					Src	GP		SH3 motif		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_209_s_98	11672528	(B) Robo1 specifically binds to SH3 domains  in srGAPs but not to SH3 motif  in Src or Graf.	bind
10406	3	4135	5	11	NULL	NULL	NULL	Robo1	GP		does not bind					Graf	GP		SH3 motif		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_209_s_98	11672528	(B) Robo1 specifically binds to SH3 domains  in srGAPs but not to SH3 motif  in Src or Graf.	bind
10407	4	4135	5	11	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_209_s_98	11672528	(B) Robo1 specifically binds to SH3 domains  in srGAPs but not to SH3 motif  in Src or Graf.	bind
12762	1	4135	7	11	NULL	NULL	NULL	Robo1	GP		binds		specifically			srGAPs	GP		SH3		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_209_s_98	11672528	(B) Robo1 specifically binds to SH3 domains  in srGAPs but not to SH3 motif  in Src or Graf.	bind
12763	2	4135	7	11	NULL	NULL	NULL	Robo1	GP		does not bind					Src	GP		SH3 moif		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_209_s_98	11672528	(B) Robo1 specifically binds to SH3 domains  in srGAPs but not to SH3 motif  in Src or Graf.	bind
12764	3	4135	7	11	NULL	NULL	NULL	Robo1	GP		does not bind					Graf	GP		SH3 moif		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_209_s_98	11672528	(B) Robo1 specifically binds to SH3 domains  in srGAPs but not to SH3 motif  in Src or Graf.	bind
10409	1	4136	5	11	NULL	NULL	NULL	CBP	GP		enhance					GCMa	GP	transcriptional activity of	C-terminal TAD		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8401_s_336	16166624	(B) Roles of lysine367, lysine406, and lysine409 in the CBP-enhanced transcriptional activity of GCMa C-terminal TAD. CV1 cells were  transfected with different combinations of 0.5 mug of pGal4-GCMa-Flag(300-436), pGal4-GCMa-Flag(300-436)K2R,  pGal4-GCMa-Flag(300-436)K3R, and pCBP-HA.	bind
12765	1	4136	7	11	NULL	NULL	NULL	CBP	GP		enhance					GCMa	GP	transcriptional activity of	C-terminal TAD		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8401_s_336	16166624	(B) Roles of lysine367, lysine406, and lysine409 in the CBP-enhanced transcriptional activity of GCMa C-terminal TAD. CV1 cells were  transfected with different combinations of 0.5 mug of pGal4-GCMa-Flag(300-436), pGal4-GCMa-Flag(300-436)K2R,  pGal4-GCMa-Flag(300-436)K3R, and pCBP-HA.	bind
10411	1	4137	5	11	NULL	NULL	NULL	PABPC1	GP		bind					Gl pre-mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_8_3085_s_179	16581783	(B) RT-PCR of Gl pre-mRNA  from intron 1 into intron 2 (introns 1 and 2) and MUP mRNA to determine the extent  of PABPC1 binding to Gl pre-mRNA that occurs after cell lysis.	bind
10412	2	4137	5	11	NULL	NULL	NULL	statement 1	Process		occurs after					cell lysis	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_8_3085_s_179	16581783	(B) RT-PCR of Gl pre-mRNA  from intron 1 into intron 2 (introns 1 and 2) and MUP mRNA to determine the extent  of PABPC1 binding to Gl pre-mRNA that occurs after cell lysis.	bind
12766	1	4137	7	11	NULL	NULL	NULL	PABPC1	GP		bind					Gl pre-mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_8_3085_s_179	16581783	(B) RT-PCR of Gl pre-mRNA  from intron 1 into intron 2 (introns 1 and 2) and MUP mRNA to determine the extent  of PABPC1 binding to Gl pre-mRNA that occurs after cell lysis.	bind
12767	2	4137	7	11	NULL	NULL	NULL	statement 1	Process		occurs after					cell lysis	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_8_3085_s_179	16581783	(B) RT-PCR of Gl pre-mRNA  from intron 1 into intron 2 (introns 1 and 2) and MUP mRNA to determine the extent  of PABPC1 binding to Gl pre-mRNA that occurs after cell lysis.	bind
10414	1	4139	5	11	NULL	NULL	NULL	sAPP695T	GP		bind					HK cleavage products	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1571_3_225_s_276	12090937	(B) sAPP695T binding to the HK cleavage products.	bind
12768	1	4139	7	11	NULL	NULL	NULL	sAPP695T 	GP		bind					HK cleavage products	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1571_3_225_s_276	12090937	(B) sAPP695T binding to the HK cleavage products.	bind
10415	1	4140	5	11	NULL	NULL	NULL	SATB1	GP		bind					IL-2 	GP			promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1620_s_178	15713622	(B) SATB1 binds to the IL-2 promoter in vitro.	bind
12769	1	4140	7	11	NULL	NULL	NULL	 SATB1	GP		binds					 IL-2	GP			promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1620_s_178	15713622	(B) SATB1 binds to the IL-2 promoter in vitro.	bind
10416	1	4142	5	11	NULL	NULL	NULL	[3]R-PIA	GP		bind		specifically			A1Rs	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_14_5164_s_242	10866672	(B) Saturation isotherm of [3]R-PIA specific binding to purified A1Rs in the absence or presence of 30 nM hsc73.	bind
12770	1	4142	7	11	NULL	NULL	NULL	[3]R-PIA	GP		bind		specifically			A1Rs	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_14_5164_s_242	10866672	(B) Saturation isotherm of [3]R-PIA specific binding to purified A1Rs in the absence or presence of 30 nM hsc73.	bind
10417	1	4143	5	11	NULL	NULL	NULL	sbp1p	GP		bind					spi1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_148_2_645_s_186	9504913	(B) sbp1p binds to spi1p.	bind
12771	1	4143	7	11	NULL	NULL	NULL	sbp1p	GP		binds to					spi1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_148_2_645_s_186	9504913	(B) sbp1p binds to spi1p.	bind
10418	1	4144	5	11	NULL	NULL	NULL	sc1	GP		bind					FMRP proteins	GP		N terminus		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_4_489_s_141	11719189	(B) sc1 binding to FMRP  N and C termini fusion proteins (see  Experimental Procedures).	bind
10419	2	4144	5	11	NULL	NULL	NULL	sc1	GP		bind					FMRP proteins	GP		C terminus		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_4_489_s_141	11719189	(B) sc1 binding to FMRP  N and C termini fusion proteins (see  Experimental Procedures).	bind
44428	3	4144	5	11	NULL	NULL	NULL	FMRP	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_4_489_s_141	11719189	(B) sc1 binding to FMRP  N and C termini fusion proteins (see  Experimental Procedures).	bind
12772	1	4144	7	11	NULL	NULL	NULL	sc1 	GP		bind					FMRP  protein	GP		N terminus		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_4_489_s_141	11719189	(B) sc1 binding to FMRP  N and C termini fusion proteins (see  Experimental Procedures).	bind
12773	2	4144	7	11	NULL	NULL	NULL	sc1 	GP		bind					FMRP  protein	GP		C terminus		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_4_489_s_141	11719189	(B) sc1 binding to FMRP  N and C termini fusion proteins (see  Experimental Procedures).	bind
10452	1	4145	5	11	NULL	NULL	NULL	YFP- lac rep-SRC570-780 protein	GP		bind									lac operator sequences	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3437_s_84	11971975	(B) Schematic of the YFP- lac rep-SRC570-780 fusion protein, which binds to  lac operator sequences and can recruit wild-type ER or CFP-ER.	bind
10453	2	4145	5	11	NULL	NULL	NULL	statement 1	Process		recruit					ER	GP	wild-type			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3437_s_84	11971975	(B) Schematic of the YFP- lac rep-SRC570-780 fusion protein, which binds to  lac operator sequences and can recruit wild-type ER or CFP-ER.	bind
10454	3	4145	5	11	NULL	NULL	NULL	statement 1	Process		recruit					CFP-ER	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3437_s_84	11971975	(B) Schematic of the YFP- lac rep-SRC570-780 fusion protein, which binds to  lac operator sequences and can recruit wild-type ER or CFP-ER.	bind
44429	4	4145	5	11	NULL	NULL	NULL	YFP- lac rep-SRC570-780	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3437_s_84	11971975	(B) Schematic of the YFP- lac rep-SRC570-780 fusion protein, which binds to  lac operator sequences and can recruit wild-type ER or CFP-ER.	bind
12774	1	4145	7	11	NULL	NULL	NULL	YFP- lac rep-SRC570-780	GP		binds									lac operator sequences	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3437_s_84	11971975	(B) Schematic of the YFP- lac rep-SRC570-780 fusion protein, which binds to  lac operator sequences and can recruit wild-type ER or CFP-ER.	bind
12775	2	4145	7	11	NULL	NULL	NULL	statement 1	Process		recruits					ER	GP	wild-type			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3437_s_84	11971975	(B) Schematic of the YFP- lac rep-SRC570-780 fusion protein, which binds to  lac operator sequences and can recruit wild-type ER or CFP-ER.	bind
12776	3	4145	7	11	NULL	NULL	NULL	statement 1	Process		recruits					CFP-ER	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3437_s_84	11971975	(B) Schematic of the YFP- lac rep-SRC570-780 fusion protein, which binds to  lac operator sequences and can recruit wild-type ER or CFP-ER.	bind
44407	4	4145	7	11	NULL	NULL	NULL	YFP- lac rep-SRC570-780	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3437_s_84	11971975	(B) Schematic of the YFP- lac rep-SRC570-780 fusion protein, which binds to  lac operator sequences and can recruit wild-type ER or CFP-ER.	bind
11438	1	4151	5	11	NULL	NULL	NULL	endo-oxabicyclic inhibitor	Chemical		bind					CM	CellComponent	E. coli			NULL		NULL	NULL	NULL	NULL	gw60_structure_5_11_1437_s_96	9384560	(b) Scheme of interactions between the inhibitor and active site residues of YCM.  (c) Stereo view of the binding mode of the inhibitor to the active site in ITRP.  (d,e) Binding of the  endo-oxabicyclic inhibitor to  E. coli CM (d) and to  B. subtilis CM (e).	bind
11439	2	4151	5	11	NULL	NULL	NULL	endo-oxabicyclic inhibitor	Chemical		bind					CM	CellComponent	B. subtilis			NULL		NULL	NULL	NULL	NULL	gw60_structure_5_11_1437_s_96	9384560	(b) Scheme of interactions between the inhibitor and active site residues of YCM.  (c) Stereo view of the binding mode of the inhibitor to the active site in ITRP.  (d,e) Binding of the  endo-oxabicyclic inhibitor to  E. coli CM (d) and to  B. subtilis CM (e).	bind
12880	1	4151	7	11	NULL	NULL	NULL	endo-oxabicyclic inhibitor	Chemical		bind					CM	CellComponent	E.coli			NULL		NULL	NULL	NULL	NULL	gw60_structure_5_11_1437_s_96	9384560	(b) Scheme of interactions between the inhibitor and active site residues of YCM.  (c) Stereo view of the binding mode of the inhibitor to the active site in ITRP.  (d,e) Binding of the  endo-oxabicyclic inhibitor to  E. coli CM (d) and to  B. subtilis CM (e).	bind
12881	2	4151	7	11	NULL	NULL	NULL	endo-oxabicyclic inhibitor	Chemical		bind					CM	CellComponent	B. subtilis			NULL		NULL	NULL	NULL	NULL	gw60_structure_5_11_1437_s_96	9384560	(b) Scheme of interactions between the inhibitor and active site residues of YCM.  (c) Stereo view of the binding mode of the inhibitor to the active site in ITRP.  (d,e) Binding of the  endo-oxabicyclic inhibitor to  E. coli CM (d) and to  B. subtilis CM (e).	bind
10455	1	4153	5	11	NULL	NULL	NULL	EphA3-AP	GP		bind					ephrins-A	GP				NULL	muscle	NULL	NULL	NULL	NULL	gw60_neuron_25_2_295_s_52	10719886	(B) Sections of muscle stained with EphA3-AP or EphA5-Fc fusion proteins, which bind to ephrins-A but not to ephrins-B.	bind
10456	2	4153	5	11	NULL	NULL	NULL	EphA3-AP	GP		does not bind					ephrins-B	GP				NULL	muscle	NULL	NULL	NULL	NULL	gw60_neuron_25_2_295_s_52	10719886	(B) Sections of muscle stained with EphA3-AP or EphA5-Fc fusion proteins, which bind to ephrins-A but not to ephrins-B.	bind
10457	3	4153	5	11	NULL	NULL	NULL	EphA5-Fc	GP		bind					ephrins-A	GP				NULL	muscle	NULL	NULL	NULL	NULL	gw60_neuron_25_2_295_s_52	10719886	(B) Sections of muscle stained with EphA3-AP or EphA5-Fc fusion proteins, which bind to ephrins-A but not to ephrins-B.	bind
10458	4	4153	5	11	NULL	NULL	NULL	EphA5-Fc	GP		does not bind					ephrins-B	GP				NULL	muscle	NULL	NULL	NULL	NULL	gw60_neuron_25_2_295_s_52	10719886	(B) Sections of muscle stained with EphA3-AP or EphA5-Fc fusion proteins, which bind to ephrins-A but not to ephrins-B.	bind
10459	5	4153	5	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_2_295_s_52	10719886	(B) Sections of muscle stained with EphA3-AP or EphA5-Fc fusion proteins, which bind to ephrins-A but not to ephrins-B.	bind
10460	6	4153	5	11	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_2_295_s_52	10719886	(B) Sections of muscle stained with EphA3-AP or EphA5-Fc fusion proteins, which bind to ephrins-A but not to ephrins-B.	bind
44430	7	4153	5	11	NULL	NULL	NULL	EphA3-AP	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_2_295_s_52	10719886	(B) Sections of muscle stained with EphA3-AP or EphA5-Fc fusion proteins, which bind to ephrins-A but not to ephrins-B.	bind
44431	8	4153	5	11	NULL	NULL	NULL	EphA5-Fc	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_2_295_s_52	10719886	(B) Sections of muscle stained with EphA3-AP or EphA5-Fc fusion proteins, which bind to ephrins-A but not to ephrins-B.	bind
12883	1	4153	7	11	NULL	NULL	NULL	EphA3-AP	GP		bind					ephrins-A 	GP				NULL	muscle	NULL	NULL	NULL	NULL	gw60_neuron_25_2_295_s_52	10719886	(B) Sections of muscle stained with EphA3-AP or EphA5-Fc fusion proteins, which bind to ephrins-A but not to ephrins-B.	bind
12884	2	4153	7	11	NULL	NULL	NULL	EphA5-Fc	GP		bind					ephrins-A 	GP				NULL	muscle	NULL	NULL	NULL	NULL	gw60_neuron_25_2_295_s_52	10719886	(B) Sections of muscle stained with EphA3-AP or EphA5-Fc fusion proteins, which bind to ephrins-A but not to ephrins-B.	bind
12885	3	4153	7	11	NULL	NULL	NULL	EphA3-AP	GP		does not bind					ephrins-B	GP				NULL	muscle	NULL	NULL	NULL	NULL	gw60_neuron_25_2_295_s_52	10719886	(B) Sections of muscle stained with EphA3-AP or EphA5-Fc fusion proteins, which bind to ephrins-A but not to ephrins-B.	bind
12886	4	4153	7	11	NULL	NULL	NULL	EphA5-Fc	GP		does not bind					ephrins-B	GP				NULL	muscle	NULL	NULL	NULL	NULL	gw60_neuron_25_2_295_s_52	10719886	(B) Sections of muscle stained with EphA3-AP or EphA5-Fc fusion proteins, which bind to ephrins-A but not to ephrins-B.	bind
44408	5	4153	7	11	NULL	NULL	NULL	EphA3-AP	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_2_295_s_52	10719886	(B) Sections of muscle stained with EphA3-AP or EphA5-Fc fusion proteins, which bind to ephrins-A but not to ephrins-B.	bind
44479	6	4153	7	11	NULL	NULL	NULL	EphA5-Fc	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_2_295_s_52	10719886	(B) Sections of muscle stained with EphA3-AP or EphA5-Fc fusion proteins, which bind to ephrins-A but not to ephrins-B.	bind
54280	7	4153	7	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_2_295_s_52	10719886	(B) Sections of muscle stained with EphA3-AP or EphA5-Fc fusion proteins, which bind to ephrins-A but not to ephrins-B.	bind
54281	8	4153	7	11	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_2_295_s_52	10719886	(B) Sections of muscle stained with EphA3-AP or EphA5-Fc fusion proteins, which bind to ephrins-A but not to ephrins-B.	bind
10461	1	4154	5	11	NULL	NULL	NULL	VASP	GP	eukaryotic;;recombinant	bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_6_1245_s_325	10087267	(b) Sedimentation assay for the  binding of eukaryotic recombinant VASP to F-actin.	bind
44478	1	4154	7	11	NULL	NULL	NULL	VASP	GP	eukaryotic;;recombinant	bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_6_1245_s_325	10087267	(b) Sedimentation assay for the  binding of eukaryotic recombinant VASP to F-actin.	bind
10462	1	4155	5	11	NULL	NULL	NULL	CSL	GP		bind					Caco-2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_10_5282_s_235	10496907	(B) Self-displaceable binding of CSL to Caco-2 cells.	bind
12888	1	4155	7	11	NULL	NULL	NULL	CSL	GP		bind					Caco-2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_10_5282_s_235	10496907	(B) Self-displaceable binding of CSL to Caco-2 cells.	bind
10463	1	4158	5	11	NULL	NULL	NULL	p53	GP		bind		sequence specific			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_267	14612423	(B) Sequence-specific DNA binding changes the conformation of p53 ( ), thus permitting acetylation to occur in a PXXP-dependent manner.	bind
10464	2	4158	5	11	NULL	NULL	NULL	statement 1	Process		change					p53	GP	conformation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_267	14612423	(B) Sequence-specific DNA binding changes the conformation of p53 ( ), thus permitting acetylation to occur in a PXXP-dependent manner.	bind
10465	3	4158	5	11	NULL	NULL	NULL	statement 2	Process		permit					p53	GP	acetylation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_267	14612423	(B) Sequence-specific DNA binding changes the conformation of p53 ( ), thus permitting acetylation to occur in a PXXP-dependent manner.	bind
10466	4	4158	5	11	NULL	NULL	NULL	statement 3	Process		is dependent on								PXXP		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_267	14612423	(B) Sequence-specific DNA binding changes the conformation of p53 ( ), thus permitting acetylation to occur in a PXXP-dependent manner.	bind
12890	1	4158	7	11	NULL	NULL	NULL	p53	GP		bind		sequence-specific			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_267	14612423	(B) Sequence-specific DNA binding changes the conformation of p53 ( ), thus permitting acetylation to occur in a PXXP-dependent manner.	bind
12891	2	4158	7	11	NULL	NULL	NULL	statement 1	Process		changes					p53	GP	conformation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_267	14612423	(B) Sequence-specific DNA binding changes the conformation of p53 ( ), thus permitting acetylation to occur in a PXXP-dependent manner.	bind
12892	3	4158	7	11	NULL	NULL	NULL	statement 2	Process		permits					p53	GP	acetylation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_267	14612423	(B) Sequence-specific DNA binding changes the conformation of p53 ( ), thus permitting acetylation to occur in a PXXP-dependent manner.	bind
16307	4	4158	7	11	NULL	NULL	NULL	statement 3	Process		is dependent on								PXXP		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_267	14612423	(B) Sequence-specific DNA binding changes the conformation of p53 ( ), thus permitting acetylation to occur in a PXXP-dependent manner.	bind
11440	1	4161	5	11	NULL	NULL	NULL	diazepam	Chemical		bind					HSA	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1750_1_93_s_169	15890566	(B) shows the binding isotherm of diazepam to  HSA as a function of GnHCl concentration at a fixed diazepam/albumin molar ratio  of 2:1.	bind
12893	1	4161	7	NULL	NULL	0	NULL	diazepam	NULL		bind	NULL				HSA	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1750_1_93_s_169	15890566	(B) shows the binding isotherm of diazepam to  HSA as a function of GnHCl concentration at a fixed diazepam/albumin molar ratio  of 2:1.	bind
10467	1	4162	5	11	NULL	NULL	NULL	HoxB1 peptide	GP		bind					Pbx1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_96_4_587_s_116	10052460	(B) Side  view of the HoxB1 peptide bound to Pbx1.	bind
12894	1	4162	7	11	NULL	NULL	NULL	HoxB1 peptide	GP		bind					Pbx1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_96_4_587_s_116	10052460	(B) Side  view of the HoxB1 peptide bound to Pbx1.	bind
10468	1	4163	5	11	NULL	NULL	NULL	Ni2+	Chemical		bind					HypA	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_3_726_s_145	12533448	(B) Sigmoidal curve for Ni2+ binding by HypA (wild type).	bind
12895	1	4163	7	11	NULL	NULL	NULL	Ni2+	Chemical		bind					HypA	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_3_726_s_145	12533448	(B) Sigmoidal curve for Ni2+ binding by HypA (wild type).	bind
10469	1	4165	5	11	NULL	NULL	NULL	O2	Chemical		bind					heme a3	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_3_261_s_93	11115638	(B) Simulated curves for O2 binding to heme  a3 with a second-order rate constant of 108 M-1s-1, limited by the CO-off rate from CuB (different values of  koff c.f.  kmax in  Eq. 1).	bind
12896	1	4165	7	11	NULL	NULL	NULL	O2	Chemical		bind					heme a3	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1503_3_261_s_93	11115638	(B) Simulated curves for O2 binding to heme  a3 with a second-order rate constant of 108 M-1s-1, limited by the CO-off rate from CuB (different values of  koff c.f.  kmax in  Eq. 1).	bind
10471	1	4166	5	11	NULL	NULL	NULL	BR-II	GP	singly expressed 	bind		weakly			BMP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_3_1023_s_208	10712517	(B) Singly expressed BR-II binds the BMP-2 only weakly.	bind
12897	1	4166	7	11	NULL	NULL	NULL	BR-II	GP	Singly expressed	binds		weakly			 BMP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_3_1023_s_208	10712517	(B) Singly expressed BR-II binds the BMP-2 only weakly.	bind
10472	1	4167	5	11	NULL	NULL	NULL	Skp2	GP		bind		specifically			p27CP	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_12_661_s_72	10375532	(b) Skp2 specifically binds to p27CP.	bind
12898	1	4167	7	11	NULL	NULL	NULL	Skp2	GP		binds		specifically			p27CP	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_12_661_s_72	10375532	(b) Skp2 specifically binds to p27CP.	bind
10473	1	4168	5	11	NULL	NULL	NULL	Snf1	GP		bind					GST-Gln3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_4_1246_s_181	11809814	(B) Snf1 binds to GST-Gln3.	bind
12899	1	4168	7	11	NULL	NULL	NULL	Snf1	GP		bind					GST-Gln3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_4_1246_s_181	11809814	(B) Snf1 binds to GST-Gln3.	bind
10474	1	4169	5	11	NULL	NULL	NULL	PKC	GP	activity of	regulate					SOCE	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_7_1033_s_192	15051735	(B) SOCE is regulated  by PKC activity.	bind
12900	1	4169	7	11	NULL	NULL	NULL	PKC	GP	activity of	regulates					SOCE	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_7_1033_s_192	15051735	(B) SOCE is regulated  by PKC activity.	bind
10475	1	4172	5	11	NULL	NULL	NULL	L1Fc	GP		is					L1	GP	Soluble			NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6348_s_127	12456642	(b) Soluble L1 (L1Fc) binds both L1 and NP-1 on the growth cone and switches Sema3A repulsion to attraction.	bind
10476	2	4172	5	11	NULL	NULL	NULL	L1Fc	GP		bind					L1	GP	soluble			NULL	on the growth cone	NULL	NULL	NULL	NULL	gw60_embo_21_23_6348_s_127	12456642	(b) Soluble L1 (L1Fc) binds both L1 and NP-1 on the growth cone and switches Sema3A repulsion to attraction.	bind
10477	3	4172	5	11	NULL	NULL	NULL	L1Fc	GP		bind					NP-1	GP				NULL	on the growth cone	NULL	NULL	NULL	NULL	gw60_embo_21_23_6348_s_127	12456642	(b) Soluble L1 (L1Fc) binds both L1 and NP-1 on the growth cone and switches Sema3A repulsion to attraction.	bind
10478	4	4172	5	11	NULL	NULL	NULL	Sema3A	GP	repulsion of	switches to					Sema3A	GP	attraction of			NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6348_s_127	12456642	(b) Soluble L1 (L1Fc) binds both L1 and NP-1 on the growth cone and switches Sema3A repulsion to attraction.	bind
13003	5	4172	5	11	NULL	NULL	NULL	L1	GP	soluble	causes					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6348_s_127	12456642	(b) Soluble L1 (L1Fc) binds both L1 and NP-1 on the growth cone and switches Sema3A repulsion to attraction.	bind
12903	3	4172	7	11	NULL	NULL	NULL	Sema3A	GP	repulsion of	switches to					Sema3A	GP	attraction of			NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6348_s_127	12456642	(b) Soluble L1 (L1Fc) binds both L1 and NP-1 on the growth cone and switches Sema3A repulsion to attraction.	bind
12905	5	4172	7	11	NULL	NULL	NULL	L1	GP	soluble	is					L1Fc	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6348_s_127	12456642	(b) Soluble L1 (L1Fc) binds both L1 and NP-1 on the growth cone and switches Sema3A repulsion to attraction.	bind
44480	1	4172	7	11	NULL	NULL	NULL	L1	GP	soluble	bind					L1	GP				NULL	on the growth cone	NULL	NULL	NULL	NULL	gw60_embo_21_23_6348_s_127	12456642	(b) Soluble L1 (L1Fc) binds both L1 and NP-1 on the growth cone and switches Sema3A repulsion to attraction.	bind
44481	2	4172	7	11	NULL	NULL	NULL	L1	GP	soluble	bind					NP-1	GP				NULL	on the growth cone	NULL	NULL	NULL	NULL	gw60_embo_21_23_6348_s_127	12456642	(b) Soluble L1 (L1Fc) binds both L1 and NP-1 on the growth cone and switches Sema3A repulsion to attraction.	bind
44482	4	4172	7	11	NULL	NULL	NULL	L1	GP	soluble	causes					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6348_s_127	12456642	(b) Soluble L1 (L1Fc) binds both L1 and NP-1 on the growth cone and switches Sema3A repulsion to attraction.	bind
10479	1	4174	5	11	NULL	NULL	NULL	Sp proteins	GP		is expressed in		transiently			SL2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_4_583_s_120	10744779	(B) Sp proteins transiently expressed in SL2 cells bind to the  Ctpct probe containing multiple binding elements.	bind
10480	2	4174	5	11	NULL	NULL	NULL	statement 1	GP		bind					Ctpct probe	GP		multiple binding elements		NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_4_583_s_120	10744779	(B) Sp proteins transiently expressed in SL2 cells bind to the  Ctpct probe containing multiple binding elements.	bind
12906	1	4174	7	11	NULL	NULL	NULL	SL2 cells	cell		bind					 Ctpct probe	GP		multiple binding elements		NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_4_583_s_120	10744779	(B) Sp proteins transiently expressed in SL2 cells bind to the  Ctpct probe containing multiple binding elements.	bind
12907	2	4174	7	11	NULL	NULL	NULL	Sp proteins	GP		 expressed in		transiently			SL2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_4_583_s_120	10744779	(B) Sp proteins transiently expressed in SL2 cells bind to the  Ctpct probe containing multiple binding elements.	bind
10481	1	4176	5	11	NULL	NULL	NULL	Oct-1	GP		bind		specifically							Oct-1 site	NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_1_55_s_123	15527761	(B) Specific binding of Oct-1  to the Oct-1 site.	bind
12908	1	4176	7	11	NULL	NULL	NULL	Oct-1	GP		bind		specifically							Oct-1 site	NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_1_55_s_123	15527761	(B) Specific binding of Oct-1  to the Oct-1 site.	bind
10482	1	4177	5	11	NULL	NULL	NULL	PPARgamma2/RXRalpha	GP		bind		specifically							PPRE	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1313_s_238	14729975	(B) Specific binding of PPARgamma2/RXRalpha to the PPRE. PPARgamma2 and RXRalpha were synthesized in a rabbit reticulocyte lysate system.	bind
12909	1	4177	7	11	NULL	NULL	NULL	PPARgamma2/RXRalpha	GP		bind		specifically							PPRE	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1313_s_238	14729975	(B) Specific binding of PPARgamma2/RXRalpha to the PPRE. PPARgamma2 and RXRalpha were synthesized in a rabbit reticulocyte lysate system.	bind
10483	1	4179	5	11	NULL	NULL	NULL	psi RNA	NucleicAcid		bind					NC protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_4_1181_s_88	15249214	(B) Specific inhibition by aptamer  N70-13 of psi RNA binding to NC protein.	bind
10484	2	4179	5	11	NULL	NULL	NULL	aptamer N70-13	NucleicAcid		inhibit		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_4_1181_s_88	15249214	(B) Specific inhibition by aptamer  N70-13 of psi RNA binding to NC protein.	bind
12910	1	4179	7	11	NULL	NULL	NULL	psi RNA	NucleicAcid		binds					NC protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_4_1181_s_88	15249214	(B) Specific inhibition by aptamer  N70-13 of psi RNA binding to NC protein.	bind
12911	2	4179	7	11	NULL	NULL	NULL	aptamer N70-13	NucleicAcid		inhibits		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_4_1181_s_88	15249214	(B) Specific inhibition by aptamer  N70-13 of psi RNA binding to NC protein.	bind
10485	1	4180	5	11	NULL	NULL	NULL	transferrin	GP	specific	bind					L4-L5 fusion	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_2_732_s_218	11796606	(B) Specific transferrin binding to L4-L5 fusion	bind
12912	1	4180	7	11	NULL	NULL	NULL	transferrin	GP	specific	bind					L4-L5 fusion	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_2_732_s_218	11796606	(B) Specific transferrin binding to L4-L5 fusion	bind
10486	1	4181	5	11	NULL	NULL	NULL	SPN	GP		bind					Xpo1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4660_s_90	16030253	(B) SPN binding  to Xpo1 is extremely sensitive to mutation.	bind
10487	2	4181	5	11	NULL	NULL	NULL	statement 1	Process		is sensitive to		extremely			mutation	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4660_s_90	16030253	(B) SPN binding  to Xpo1 is extremely sensitive to mutation.	bind
12913	1	4181	7	11	NULL	NULL	NULL	SPN	GP		bind					Xpo1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4660_s_90	16030253	(B) SPN binding  to Xpo1 is extremely sensitive to mutation.	bind
12914	2	4181	7	11	NULL	NULL	NULL	statement 1	Process		is sensitive to		extremely			mutation	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4660_s_90	16030253	(B) SPN binding  to Xpo1 is extremely sensitive to mutation.	bind
10488	1	4182	5	11	NULL	NULL	NULL	Spt10p	GP		bind		specifically			HTA1-HTB1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_20_9127_s_271	16199888	(B) Spt10p binds specifically  to the  HTA1-HTB1 promoter.	bind
12915	1	4182	7	11	NULL	NULL	NULL	Spt10p	GP		binds		specifically			HTA1-HTB1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_20_9127_s_271	16199888	(B) Spt10p binds specifically  to the  HTA1-HTB1 promoter.	bind
10492	1	4184	5	11	NULL	NULL	NULL	Src	GP		bind					mDia2	GP		proline-rich FH1 domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_1_13_s_57	10678165	(B) Src binds the proline-rich FH1 domain of mDia2.	bind
12919	1	4184	7	11	NULL	NULL	NULL	 Src	GP		bind					mDia2	GP		proline-rich FH1 domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_1_13_s_57	10678165	(B) Src binds the proline-rich FH1 domain of mDia2.	bind
10493	1	4185	5	11	NULL	NULL	NULL	SREBP-1a	GP		bind					CBP/p300	GP	full-length	KIX domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_10_3392_s_114	12724399	(B) SREBP-1a binding to the KIX domain of full-length CBP/p300 prevents binding of the coactivators to the Tax/CREB/viral CRE DNA complex.	bind
10494	2	4185	5	11	NULL	NULL	NULL	coactivators	GP		bind					Tax/CREB/viral CRE DNA complex	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_10_3392_s_114	12724399	(B) SREBP-1a binding to the KIX domain of full-length CBP/p300 prevents binding of the coactivators to the Tax/CREB/viral CRE DNA complex.	bind
10495	3	4185	5	11	NULL	NULL	NULL	statement 1	Process		prevent					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_10_3392_s_114	12724399	(B) SREBP-1a binding to the KIX domain of full-length CBP/p300 prevents binding of the coactivators to the Tax/CREB/viral CRE DNA complex.	bind
12920	1	4185	7	11	NULL	NULL	NULL	 SREBP-1a	GP		bind					CBP/p300	GP	full-length	KIX domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_10_3392_s_114	12724399	(B) SREBP-1a binding to the KIX domain of full-length CBP/p300 prevents binding of the coactivators to the Tax/CREB/viral CRE DNA complex.	bind
12921	2	4185	7	11	NULL	NULL	NULL	coactivators 	GP		bind					Tax/CREB/viral CRE DNA complex	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_10_3392_s_114	12724399	(B) SREBP-1a binding to the KIX domain of full-length CBP/p300 prevents binding of the coactivators to the Tax/CREB/viral CRE DNA complex.	bind
12922	3	4185	7	11	NULL	NULL	NULL	statement 1	Process		prevents					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_10_3392_s_114	12724399	(B) SREBP-1a binding to the KIX domain of full-length CBP/p300 prevents binding of the coactivators to the Tax/CREB/viral CRE DNA complex.	bind
10496	1	4186	5	11	NULL	NULL	NULL	SspB	GP		bind					ssrA peptide	GP		NKKGRHGAANDENYALAA		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_9_11_1237_s_60	12445774	(B) SspB binding to the NKKGRHGAANDENYALAA ssrA peptide assayed by isothermal titration calorimetry (25 degrees C).	bind
12923	1	4186	7	11	NULL	NULL	NULL	SspB	GP		bind					 ssrA peptide	GP		NKKGRHGAANDENYALAA		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_9_11_1237_s_60	12445774	(B) SspB binding to the NKKGRHGAANDENYALAA ssrA peptide assayed by isothermal titration calorimetry (25 degrees C).	bind
10500	1	4187	5	11	NULL	NULL	NULL	Ste12	GP		bind									UAS2-1	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_216	15485921	(B) Ste12 and Tec1 binding to UAS2-1 is independent of Flo8 and Mss11.	bind
10501	2	4187	5	11	NULL	NULL	NULL	statement 1	Process		is independent of					Flo8	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_216	15485921	(B) Ste12 and Tec1 binding to UAS2-1 is independent of Flo8 and Mss11.	bind
10502	3	4187	5	11	NULL	NULL	NULL	statement 1	Process		is independent of					Mss11	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_216	15485921	(B) Ste12 and Tec1 binding to UAS2-1 is independent of Flo8 and Mss11.	bind
10503	4	4187	5	11	NULL	NULL	NULL	Tec1	GP		bind									UAS2-1	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_216	15485921	(B) Ste12 and Tec1 binding to UAS2-1 is independent of Flo8 and Mss11.	bind
10504	5	4187	5	11	NULL	NULL	NULL	statement 4	Process		is independent of					Flo8	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_216	15485921	(B) Ste12 and Tec1 binding to UAS2-1 is independent of Flo8 and Mss11.	bind
10505	6	4187	5	11	NULL	NULL	NULL	statement 4	Process		is independent of					Mss11	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_216	15485921	(B) Ste12 and Tec1 binding to UAS2-1 is independent of Flo8 and Mss11.	bind
12924	1	4187	7	11	NULL	NULL	NULL	Ste12 	GP		bind									UAS2-1	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_216	15485921	(B) Ste12 and Tec1 binding to UAS2-1 is independent of Flo8 and Mss11.	bind
12925	2	4187	7	11	NULL	NULL	NULL	Tec1	GP		bind									UAS2-1	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_216	15485921	(B) Ste12 and Tec1 binding to UAS2-1 is independent of Flo8 and Mss11.	bind
12926	3	4187	7	11	NULL	NULL	NULL	statement 1	Process		is independent of					Flo8	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_216	15485921	(B) Ste12 and Tec1 binding to UAS2-1 is independent of Flo8 and Mss11.	bind
12927	4	4187	7	11	NULL	NULL	NULL	statement 2	Process		is independent of					Flo8	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_216	15485921	(B) Ste12 and Tec1 binding to UAS2-1 is independent of Flo8 and Mss11.	bind
12928	5	4187	7	11	NULL	NULL	NULL	statement 1	Process		is independent of					Mss11	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_216	15485921	(B) Ste12 and Tec1 binding to UAS2-1 is independent of Flo8 and Mss11.	bind
12929	6	4187	7	11	NULL	NULL	NULL	statement 2	Process		is independent of					Mss11	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9542_s_216	15485921	(B) Ste12 and Tec1 binding to UAS2-1 is independent of Flo8 and Mss11.	bind
10506	1	4191	5	11	NULL	NULL	NULL	NAD+	Chemical		bind					LeuDH	GP				NULL		NULL	NULL	NULL	NULL	gw60_structure_3_7_693_s_188	8591046	(b) Stereo representation of NAD+ bound to LeuDH.	bind
12930	1	4191	7	11	NULL	NULL	NULL	NAD+	Chemical		bind					LeuDH	GP				NULL		NULL	NULL	NULL	NULL	gw60_structure_3_7_693_s_188	8591046	(b) Stereo representation of NAD+ bound to LeuDH.	bind
10507	1	4192	5	11	NULL	NULL	NULL	HP0525	GP		bind					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1461_s_64	11163218	(B) Stereo ribbon diagram of the structure of HP0525 bound to ADP and a 9-mer of PEG ( Carson 1997  ).	bind
10508	2	4192	5	11	NULL	NULL	NULL	HP0525	GP		bind					PEG	Chemical	9-mer of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1461_s_64	11163218	(B) Stereo ribbon diagram of the structure of HP0525 bound to ADP and a 9-mer of PEG ( Carson 1997  ).	bind
12931	1	4192	7	11	NULL	NULL	NULL	HP0525	GP		bind					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1461_s_64	11163218	(B) Stereo ribbon diagram of the structure of HP0525 bound to ADP and a 9-mer of PEG ( Carson 1997  ).	bind
12932	2	4192	7	11	NULL	NULL	NULL	HP0525	GP		bind					 PEG	Chemical	9-mer of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1461_s_64	11163218	(B) Stereo ribbon diagram of the structure of HP0525 bound to ADP and a 9-mer of PEG ( Carson 1997  ).	bind
10509	1	4193	5	11	NULL	NULL	NULL	compound 1	Chemical		bind					JNK3	GP		ATP binding site of		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_10_8_705_s_55	12954329	(B) Stereo view of compound 1 bound to the ATP binding site of JNK3.	bind
12933	1	4193	7	11	NULL	NULL	NULL	compound 1	Chemical		bind					JNK3	GP		ATP binding site		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_10_8_705_s_55	12954329	(B) Stereo view of compound 1 bound to the ATP binding site of JNK3.	bind
10510	1	4194	5	11	NULL	NULL	NULL	[35] GTP S	Chemical		bind					PM	QuantityOrMeasure	from limbic forebrain			NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_50_7_834_s_217	16448676	(b) Stimulation of [35] GTP S binding to PM from the limbic forebrain by various concentrations of WIN55,212-2.	bind
10511	2	4194	5	11	NULL	NULL	NULL	WIN55,212-2	Chemical		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_50_7_834_s_217	16448676	(b) Stimulation of [35] GTP S binding to PM from the limbic forebrain by various concentrations of WIN55,212-2.	bind
12934	1	4194	7	11	NULL	NULL	NULL	[35] GTP S	Chemical		binds to					PM	QuantityOrMeasure	limbic forebrain			NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_50_7_834_s_217	16448676	(b) Stimulation of [35] GTP S binding to PM from the limbic forebrain by various concentrations of WIN55,212-2.	bind
16309	2	4194	7	11	NULL	NULL	NULL	WIN55,212-2	Chemical		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_50_7_834_s_217	16448676	(b) Stimulation of [35] GTP S binding to PM from the limbic forebrain by various concentrations of WIN55,212-2.	bind
10512	1	4196	5	11	NULL	NULL	NULL	E-cadherin	GP	phosphorylated	bind			region IV		beta-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_105_3_391_s_135	11348595	(B) Structure of  phosphorylated E-cadherin region IV bound to beta-catenin.	bind
12935	1	4196	7	11	NULL	NULL	NULL	 E-cadherin	GP	phosphorylated	bind			region IV		beta-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_105_3_391_s_135	11348595	(B) Structure of  phosphorylated E-cadherin region IV bound to beta-catenin.	bind
10513	1	4197	5	11	NULL	NULL	NULL	Lyn	GP		bind					CD19	GP	phosphorylated	Y513		NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_1_47_s_265	10933394	(B) Subsequently, Lyn binds phosphorylated CD19-Y513 via its SH2 domain and phosphorylates CD19-Y482 through  processive phosphorylation.	bind
10514	2	4197	5	11	NULL	NULL	NULL	statement 1	Process		via					CD19	GP		SH2 domain		NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_1_47_s_265	10933394	(B) Subsequently, Lyn binds phosphorylated CD19-Y513 via its SH2 domain and phosphorylates CD19-Y482 through  processive phosphorylation.	bind
10515	3	4197	5	11	NULL	NULL	NULL	Lyn	GP		phosphorylate					CD19	GP		Y482		NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_1_47_s_265	10933394	(B) Subsequently, Lyn binds phosphorylated CD19-Y513 via its SH2 domain and phosphorylates CD19-Y482 through  processive phosphorylation.	bind
10516	4	4197	5	11	NULL	NULL	NULL	statement 3	Process		occurs through					processive phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_1_47_s_265	10933394	(B) Subsequently, Lyn binds phosphorylated CD19-Y513 via its SH2 domain and phosphorylates CD19-Y482 through  processive phosphorylation.	bind
12936	1	4197	7	11	NULL	NULL	NULL	Lyn	GP		binds					CD19	GP	 phosphorylated	Y513 SH2 domain		NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_1_47_s_265	10933394	(B) Subsequently, Lyn binds phosphorylated CD19-Y513 via its SH2 domain and phosphorylates CD19-Y482 through  processive phosphorylation.	bind
12937	2	4197	7	11	NULL	NULL	NULL	statement 1	GP		phosphorylates					CD19	GP		Y482		NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_1_47_s_265	10933394	(B) Subsequently, Lyn binds phosphorylated CD19-Y513 via its SH2 domain and phosphorylates CD19-Y482 through  processive phosphorylation.	bind
12938	3	4197	7	11	NULL	NULL	NULL	statement 1	Process		occurs through					processive phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_1_47_s_265	10933394	(B) Subsequently, Lyn binds phosphorylated CD19-Y513 via its SH2 domain and phosphorylates CD19-Y482 through  processive phosphorylation.	bind
10517	1	4200	5	11	NULL	NULL	NULL	Pho81	GP		bind					Pho80-Pho85	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6695_s_247	11533256	(B) Summary of the binding of different Pho81 domains to Pho80-Pho85.	bind
12939	1	4200	7	11	NULL	NULL	NULL	Pho81	GP		binds					Pho80-Pho85	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6695_s_247	11533256	(B) Summary of the binding of different Pho81 domains to Pho80-Pho85.	bind
12458	1	4201	5	11	NULL	NULL	NULL			SUMO- modified	bind			CRD1 domain		HDAC6	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_11_4_1043_s_220	12718889	(B) SUMO- modified CRD1 domain binds HDAC6 in vitro.	bind
12940	1	4201	7	11	NULL	NULL	NULL			SUMO- modified	binds			CRD1 domain		HDAC6	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_11_4_1043_s_220	12718889	(B) SUMO- modified CRD1 domain binds HDAC6 in vitro.	bind
12459	1	4203	5	11	NULL	NULL	NULL	caspase-7	GP	active	bind					XIAP fragment	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_3_399_s_181	11701129	(B) Superposition  of the active caspase-7 without bound cofactors  (pink), the procaspase-7 zymogen (blue), and the active caspase-7  (green) bound with an XIAP fragment.	bind
12941	1	4203	7	11	NULL	NULL	NULL	caspase-7	GP	active	bind					XIAP fragment	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_3_399_s_181	11701129	(B) Superposition  of the active caspase-7 without bound cofactors  (pink), the procaspase-7 zymogen (blue), and the active caspase-7  (green) bound with an XIAP fragment.	bind
12460	1	4204	5	11	NULL	NULL	NULL	threonyl-tRNA synthetase	GP		bind			C-terminal domain		cognate tRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_1_43_s_71	11172710	(B) Superposition of domain 3 of Pol B with the C-terminal domain of threonyl-tRNA synthetase bound to its cognate tRNA ( Yaremchuk et al. 2000  ; PDB code 1QF6).	bind
12942	1	4204	7	11	NULL	NULL	NULL	threonyl-tRNA synthetase	GP		binds			C-terminal domain		cognate tRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_1_43_s_71	11172710	(B) Superposition of domain 3 of Pol B with the C-terminal domain of threonyl-tRNA synthetase bound to its cognate tRNA ( Yaremchuk et al. 2000  ; PDB code 1QF6).	bind
12461	1	4205	5	11	NULL	NULL	NULL	GL-7-ACA	Chemical		bind					CAD	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_12_1253_s_225	11755403	(B) Superposition of GL-7-ACA bound CAD onto PMSF bound PGA with four catalytic residues  [28]  .	bind
12462	2	4205	5	11	NULL	NULL	NULL	PMSF	Chemical		bind					PGA	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_12_1253_s_225	11755403	(B) Superposition of GL-7-ACA bound CAD onto PMSF bound PGA with four catalytic residues  [28]  .	bind
12943	1	4205	7	11	NULL	NULL	NULL	GL-7-ACA	Chemical		bind					CAD	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_12_1253_s_225	11755403	(B) Superposition of GL-7-ACA bound CAD onto PMSF bound PGA with four catalytic residues  [28]  .	bind
12944	2	4205	7	11	NULL	NULL	NULL	PMSF	Chemical		bind					PGA	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_12_1253_s_225	11755403	(B) Superposition of GL-7-ACA bound CAD onto PMSF bound PGA with four catalytic residues  [28]  .	bind
13447	1	4206	5	11	NULL	NULL	NULL	TS: TS	GP	Escherichia coli	bind					dUMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
43350	2	4206	5	11	NULL	NULL	NULL	TS: TS	GP	Escherichia coli	bind					CB3717	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
43351	3	4206	5	11	NULL	NULL	NULL	TS: TS	GP	Escherichia coli	bind					BW1843U89	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
43353	4	4206	5	11	NULL	NULL	NULL	TS: TS	GP	Escherichia coli	bind					ZD1694	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
43354	5	4206	5	11	NULL	NULL	NULL	PcTS	Organism		bind					dUMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
43355	6	4206	5	11	NULL	NULL	NULL	PcTS	Organism		bind					CB3717	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
43357	7	4206	5	11	NULL	NULL	NULL	PcTS	Organism		bind					BW1843U89	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
43358	8	4206	5	11	NULL	NULL	NULL	TS	Organism	Lactobacillus casei	bind								A156		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
43360	9	4206	5	11	NULL	NULL	NULL	TS	Organism	Lactobacillus casei	bind					MR29	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
12945	1	4206	7	11	NULL	NULL	NULL	TS: TS	Organism	Escherichia coli	bind					dUMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
12946	2	4206	7	11	NULL	NULL	NULL	TS: TS 	GP	Escherichia coli	bind					CB3717	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
12947	3	4206	7	11	NULL	NULL	NULL	TS: TS	GP	Escherichia coli	bind					BW1843U89	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
12948	4	4206	7	11	NULL	NULL	NULL	TS: TS	GP	Escherichia coli 	bind					ZD1694	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
12949	5	4206	7	11	NULL	NULL	NULL	PcTS	Organism		bind					dUMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
12950	6	4206	7	11	NULL	NULL	NULL	PcTS	Organism		bind					CB3717	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
12951	7	4206	7	11	NULL	NULL	NULL	PcTS	Organism		bind					BW1843U89 	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
12952	8	4206	7	11	NULL	NULL	NULL	TS	GP	Lactobacillus casei	bind								A156		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
12953	10	4206	7	11	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
12954	11	4206	7	11	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
12955	9	4206	7	11	NULL	NULL	NULL	TS	GP	Lactobacillus casei	bind					MR29	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
54321	12	4206	7	11	NULL	NULL	NULL	statement 6	Process		is an alternative to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
54322	13	4206	7	11	NULL	NULL	NULL	statement 8	Process		is an alternative to					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_5_445_s_144	11358692	(b) Superposition of seven structures of TS: TS from  Escherichia coli bound to dUMP and either CB3717, BW1843U89 or ZD1694, PcTS bound to dUMP and either CB3717 or BW1843U89 and TS from  Lactobacillus casei bound to A156 or MR29.	bind
12463	1	4207	5	11	NULL	NULL	NULL	EPA	Chemical		bind					PPAR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_3_397_s_151	10198642	(b) Superposition of the structures of GW2433 and EPA bound to PPAR .	bind
16472	2	4207	5	11	NULL	NULL	NULL	GW2433	Chemical		bind					PPAR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_3_397_s_151	10198642	(b) Superposition of the structures of GW2433 and EPA bound to PPAR .	bind
12956	1	4207	7	11	NULL	NULL	NULL	GW2433	Chemical		bind					PPAR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_3_397_s_151	10198642	(b) Superposition of the structures of GW2433 and EPA bound to PPAR .	bind
12957	2	4207	7	11	NULL	NULL	NULL	EPA	Chemical		bind					PPAR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_3_397_s_151	10198642	(b) Superposition of the structures of GW2433 and EPA bound to PPAR .	bind
12464	1	4208	5	11	NULL	NULL	NULL	caspase-7	GP	active	bind					XIAP fragment	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_3_399_s_47	11701129	(B) Superposition of the unprocessed procaspase-7 zymogen  (blue) with the active caspase-7 (green) bound with an  XIAP fragment.	bind
12958	1	4208	7	11	NULL	NULL	NULL	caspase-7	GP	active	bind					 XIAP fragment	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_3_399_s_47	11701129	(B) Superposition of the unprocessed procaspase-7 zymogen  (blue) with the active caspase-7 (green) bound with an  XIAP fragment.	bind
12465	1	4210	5	11	NULL	NULL	NULL	CBP20	GP	TAPmyc-tagged	bind					SL RNA	NucleicAcid	32P-labeled			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2216_s_109	15743819	(B) Supershift analysis of CBP20 binding to the SL RNA. 32P-labeled SL RNA (lane 1) was incubated with TAPmyc-tagged CBP20, partially purified by the TAP method, in the absence of antibodies  (lane 2) or in the presence of anti-myc (lane 3) and anti-HA (lane 4) antibodies.	bind
12959	1	4210	7	11	NULL	NULL	NULL	CBP20	GP	TAPmyc-tagged	bind					SL RNA	NucleicAcid	32P-labeled			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2216_s_109	15743819	(B) Supershift analysis of CBP20 binding to the SL RNA. 32P-labeled SL RNA (lane 1) was incubated with TAPmyc-tagged CBP20, partially purified by the TAP method, in the absence of antibodies  (lane 2) or in the presence of anti-myc (lane 3) and anti-HA (lane 4) antibodies.	bind
12466	1	4211	5	11	NULL	NULL	NULL	AP-1	GP		bind		specifically			c-Jun	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_872_1_282_s_81	10924710	(B) Supershift of AP-1 binding by specific antibodies against c-Jun and ATF-2.	bind
12467	2	4211	5	11	NULL	NULL	NULL	AP-1	GP		bind		specifically			ATF-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_872_1_282_s_81	10924710	(B) Supershift of AP-1 binding by specific antibodies against c-Jun and ATF-2.	bind
12960	1	4211	7	11	NULL	NULL	NULL	AP-1	GP		bind		specifically			c-Jun antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_872_1_282_s_81	10924710	(B) Supershift of AP-1 binding by specific antibodies against c-Jun and ATF-2.	bind
12961	2	4211	7	11	NULL	NULL	NULL	AP-1	GP		bind		specifically			ATF-2 antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_872_1_282_s_81	10924710	(B) Supershift of AP-1 binding by specific antibodies against c-Jun and ATF-2.	bind
12523	1	4212	5	11	NULL	NULL	NULL	CUS2 alleles	GP		supress									G53A	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5000_s_145	9710584	(B) Suppression of G53A and C62U by different  CUS2 alleles.	bind
12525	2	4212	5	11	NULL	NULL	NULL	CUS2 alleles	GP		supress									C62U	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5000_s_145	9710584	(B) Suppression of G53A and C62U by different  CUS2 alleles.	bind
12962	1	4212	7	11	NULL	NULL	NULL	CUS2 alleles	GP		suppress									G53A 	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5000_s_145	9710584	(B) Suppression of G53A and C62U by different  CUS2 alleles.	bind
12963	2	4212	7	11	NULL	NULL	NULL	CUS2 alleles	GP		suppress									C62U	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5000_s_145	9710584	(B) Suppression of G53A and C62U by different  CUS2 alleles.	bind
12527	1	4213	5	11	NULL	NULL	NULL	SWI/SNF	GP		bind					HO	GP			URS1	NULL	during the cell cycle	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_143	16705163	(B) SWI/SNF binding to  HO URS1 and URS2 during the cell cycle.	bind
12528	2	4213	5	11	NULL	NULL	NULL	SWI/SNF	GP		bind					HO	GP			URS2	NULL	during the cell cycle	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_143	16705163	(B) SWI/SNF binding to  HO URS1 and URS2 during the cell cycle.	bind
12964	1	4213	7	11	NULL	NULL	NULL	SWI/SNF	GP		bind					HO	GP			URS1	NULL	during cell cycle	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_143	16705163	(B) SWI/SNF binding to  HO URS1 and URS2 during the cell cycle.	bind
12965	2	4213	7	11	NULL	NULL	NULL	SWI/SNF	GP		bind					HO	GP			URS2	NULL	during cell cycle	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_143	16705163	(B) SWI/SNF binding to  HO URS1 and URS2 during the cell cycle.	bind
12540	1	4214	5	11	NULL	NULL	NULL	PGL-1	GP	native	bind					Schwann cell-DRG neuron co-cultures	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_511_s_106	11081637	(B) Synthetic trisaccharides inhibit native PGL-1 binding  to Schwann cell-DRG neuron co-cultures.	bind
12542	2	4214	5	11	NULL	NULL	NULL	trisaccharides	Chemical	synthetic	inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_511_s_106	11081637	(B) Synthetic trisaccharides inhibit native PGL-1 binding  to Schwann cell-DRG neuron co-cultures.	bind
12966	1	4214	7	11	NULL	NULL	NULL	PGL-1	GP	native	binds					Schwann cell-DRG neuron co-culture	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_511_s_106	11081637	(B) Synthetic trisaccharides inhibit native PGL-1 binding  to Schwann cell-DRG neuron co-cultures.	bind
12967	2	4214	7	11	NULL	NULL	NULL	trisaccharides	Chemical	synthetic	inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_511_s_106	11081637	(B) Synthetic trisaccharides inhibit native PGL-1 binding  to Schwann cell-DRG neuron co-cultures.	bind
12545	1	4215	5	11	NULL	NULL	NULL	telomeric DNA	NucleicAcid		bind					xTRF chimeric proteins	GP				NULL	in Xenopus egg extracts	NULL	NULL	NULL	NULL	gw70_embo_25_3_575_s_139	16424898	(B) Telomeric  DNA binding of chimeric xTRF proteins in  Xenopus egg extracts.	bind
12968	1	4215	7	11	NULL	NULL	NULL	chimeric xTRF protein	GP		bind					Telomeric DNA	NucleicAcid				NULL	Xenopus egg extracts	NULL	NULL	NULL	NULL	gw70_embo_25_3_575_s_139	16424898	(B) Telomeric  DNA binding of chimeric xTRF proteins in  Xenopus egg extracts.	bind
12549	1	4216	5	11	NULL	NULL	NULL	FLO11	GP		bind				FRE of promoter	Ste12p protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_1_161_s_212	9436998	(B) The   FLO11 promoter region contains a filamentous response element (FRE), a site for the cooperative binding of the proteins Ste12p and Tec1p which transcriptionally activate genes during the filamentous response (Madhani and Fink, 1997  ).	bind
12550	2	4216	5	11	NULL	NULL	NULL	FRE	GP		is					filamentous response element	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_1_161_s_212	9436998	(B) The   FLO11 promoter region contains a filamentous response element (FRE), a site for the cooperative binding of the proteins Ste12p and Tec1p which transcriptionally activate genes during the filamentous response (Madhani and Fink, 1997  ).	bind
12551	3	4216	5	11	NULL	NULL	NULL	FLO11	GP		bind				FRE of promoter	Tec1p  protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_1_161_s_212	9436998	(B) The   FLO11 promoter region contains a filamentous response element (FRE), a site for the cooperative binding of the proteins Ste12p and Tec1p which transcriptionally activate genes during the filamentous response (Madhani and Fink, 1997  ).	bind
54278	4	4216	5	11	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_1_161_s_212	9436998	(B) The   FLO11 promoter region contains a filamentous response element (FRE), a site for the cooperative binding of the proteins Ste12p and Tec1p which transcriptionally activate genes during the filamentous response (Madhani and Fink, 1997  ).	bind
12969	1	4216	7	11	NULL	NULL	NULL	Ste12p	GP		bind					FLO11	GP			FRE of promoter	NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_1_161_s_212	9436998	(B) The   FLO11 promoter region contains a filamentous response element (FRE), a site for the cooperative binding of the proteins Ste12p and Tec1p which transcriptionally activate genes during the filamentous response (Madhani and Fink, 1997  ).	bind
12970	2	4216	7	11	NULL	NULL	NULL	Tec1p	GP		bind					FLO11	GP			FRE of promoter	NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_1_161_s_212	9436998	(B) The   FLO11 promoter region contains a filamentous response element (FRE), a site for the cooperative binding of the proteins Ste12p and Tec1p which transcriptionally activate genes during the filamentous response (Madhani and Fink, 1997  ).	bind
12972	4	4216	7	11	NULL	NULL	NULL	FRE	GP		is					filamentous response element	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_1_161_s_212	9436998	(B) The   FLO11 promoter region contains a filamentous response element (FRE), a site for the cooperative binding of the proteins Ste12p and Tec1p which transcriptionally activate genes during the filamentous response (Madhani and Fink, 1997  ).	bind
54279	3	4216	7	11	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_1_161_s_212	9436998	(B) The   FLO11 promoter region contains a filamentous response element (FRE), a site for the cooperative binding of the proteins Ste12p and Tec1p which transcriptionally activate genes during the filamentous response (Madhani and Fink, 1997  ).	bind
12557	1	4217	5	11	NULL	NULL	NULL	eIF5	GP		bind					NIP1	GP		NTD		NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9437_s_254	15485912	(B) The  NIP1-Box2 mutation diminishes binding of eIF5 and eIF2 to the NIP1-NTD in vivo.	bind
12559	2	4217	5	11	NULL	NULL	NULL	eIF2	GP		bind					NIP1	GP		NTD		NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9437_s_254	15485912	(B) The  NIP1-Box2 mutation diminishes binding of eIF5 and eIF2 to the NIP1-NTD in vivo.	bind
12560	3	4217	5	11	NULL	NULL	NULL	NIP1	GP	mutant	diminishes			Box2		statement 1	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9437_s_254	15485912	(B) The  NIP1-Box2 mutation diminishes binding of eIF5 and eIF2 to the NIP1-NTD in vivo.	bind
12562	4	4217	5	11	NULL	NULL	NULL	NIP1	GP	mutant	diminishes			Box2		statement 2	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9437_s_254	15485912	(B) The  NIP1-Box2 mutation diminishes binding of eIF5 and eIF2 to the NIP1-NTD in vivo.	bind
12975	1	4217	7	11	NULL	NULL	NULL	eIF5	GP		bind					NIP1	GP		NTD		NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9437_s_254	15485912	(B) The  NIP1-Box2 mutation diminishes binding of eIF5 and eIF2 to the NIP1-NTD in vivo.	bind
12976	2	4217	7	11	NULL	NULL	NULL	eIF2	GP		bind					NIP1	GP		NTD		NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9437_s_254	15485912	(B) The  NIP1-Box2 mutation diminishes binding of eIF5 and eIF2 to the NIP1-NTD in vivo.	bind
12977	3	4217	7	11	NULL	NULL	NULL	NIP1	GP	mutation of	diminishes			Box2		statement 1	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9437_s_254	15485912	(B) The  NIP1-Box2 mutation diminishes binding of eIF5 and eIF2 to the NIP1-NTD in vivo.	bind
12978	4	4217	7	11	NULL	NULL	NULL	NIP1	GP	mutation of	diminishes			Box2		statement 2	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9437_s_254	15485912	(B) The  NIP1-Box2 mutation diminishes binding of eIF5 and eIF2 to the NIP1-NTD in vivo.	bind
12568	1	4218	5	11	NULL	NULL	NULL	41 kDa proteins	GP		bind					NF 3-GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_3_419_s_78	12636922	(B) The 41 and 39 kDa proteins bound by NF 3-GST are identical to human TAF1.	bind
12570	2	4218	5	11	NULL	NULL	NULL	statement 1	GP		identical to					TAF1	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_3_419_s_78	12636922	(B) The 41 and 39 kDa proteins bound by NF 3-GST are identical to human TAF1.	bind
12571	3	4218	5	11	NULL	NULL	NULL	39 kDa proteins	GP		bind					NF 3-GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_3_419_s_78	12636922	(B) The 41 and 39 kDa proteins bound by NF 3-GST are identical to human TAF1.	bind
12576	4	4218	5	11	NULL	NULL	NULL	statement 3	GP		identical to					TAF1	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_3_419_s_78	12636922	(B) The 41 and 39 kDa proteins bound by NF 3-GST are identical to human TAF1.	bind
12979	1	4218	7	11	NULL	NULL	NULL	NF 3-GST	GP		bind					41 kDa protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_3_419_s_78	12636922	(B) The 41 and 39 kDa proteins bound by NF 3-GST are identical to human TAF1.	bind
12980	2	4218	7	11	NULL	NULL	NULL	NF3-GST	GP		bind					39 kDa protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_3_419_s_78	12636922	(B) The 41 and 39 kDa proteins bound by NF 3-GST are identical to human TAF1.	bind
12981	3	4218	7	11	NULL	NULL	NULL	41kDa protein	GP		is identical to					TAF1	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_3_419_s_78	12636922	(B) The 41 and 39 kDa proteins bound by NF 3-GST are identical to human TAF1.	bind
12580	1	4220	5	11	NULL	NULL	NULL	C3	GP		bind					yeast cells	Organism				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_7_4310_s_224	16790805	(B) The amount  of C3 binding to yeast cells in the presence of each test antibody was determined  by flow cytometry.	bind
12983	1	4220	7	11	NULL	NULL	NULL	C3	GP		bind					yeast cells	Organism				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_7_4310_s_224	16790805	(B) The amount  of C3 binding to yeast cells in the presence of each test antibody was determined  by flow cytometry.	bind
12582	1	4221	5	11	NULL	NULL	NULL	FKBP12	GP		bind					RyR1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_6_919_s_106	12629052	(B) The amount of FKBP12 bound to  RyR1 was assessed by coimmunoprecipitation followed by immunoblotting.	bind
12984	1	4221	7	11	NULL	NULL	NULL	FKBP12	GP		bind					RyR1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_6_919_s_106	12629052	(B) The amount of FKBP12 bound to  RyR1 was assessed by coimmunoprecipitation followed by immunoblotting.	bind
12583	1	4223	5	11	NULL	NULL	NULL	Cdc68	GP		bind					Nhp6a	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3491_s_263	11313475	(B) The assemblage of Cdc68 and Pob3-Nhp6a protein binds Nhp6a.	bind
12584	2	4223	5	11	NULL	NULL	NULL	Pob3-Nhp6a protein	GP		bind					Nhp6a	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3491_s_263	11313475	(B) The assemblage of Cdc68 and Pob3-Nhp6a protein binds Nhp6a.	bind
12982	4	4223	7	11	NULL	NULL	NULL	39 kDa protein	GP		is identical to					TAF1	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3491_s_263	11313475	(B) The assemblage of Cdc68 and Pob3-Nhp6a protein binds Nhp6a.	bind
12985	1	4223	7	11	NULL	NULL	NULL	Cdc68	GP		bind					Nhp6a	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3491_s_263	11313475	(B) The assemblage of Cdc68 and Pob3-Nhp6a protein binds Nhp6a.	bind
12986	2	4223	7	11	NULL	NULL	NULL	Pob3-Nhp6a	GP		bind					Nhp6a	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3491_s_263	11313475	(B) The assemblage of Cdc68 and Pob3-Nhp6a protein binds Nhp6a.	bind
12585	1	4225	5	11	NULL	NULL	NULL	HDAC1	GP		bind					AR	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8563_s_163	14612401	(B) The binding of HDAC1 to the AR is shown as percent binding for multiple  separate transfections.	bind
12987	1	4225	7	11	NULL	NULL	NULL	HDAC1	GP		bind					AR	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8563_s_163	14612401	(B) The binding of HDAC1 to the AR is shown as percent binding for multiple  separate transfections.	bind
12586	1	4226	5	11	NULL	NULL	NULL	Hha	GP		bind					DNA	NucleicAcid	labeled		hilA promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_22_6620_s_262	11673432	(B) The binding of Hha to labeled  hilA promoter DNA was competed with unlabeled  hilA promoter DNA.	bind
12587	2	4226	5	11	NULL	NULL	NULL	Hha	GP		bind					DNA	NucleicAcid	unlabeled		hilA promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_22_6620_s_262	11673432	(B) The binding of Hha to labeled  hilA promoter DNA was competed with unlabeled  hilA promoter DNA.	bind
12588	3	4226	5	11	NULL	NULL	NULL	statement 1	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_22_6620_s_262	11673432	(B) The binding of Hha to labeled  hilA promoter DNA was competed with unlabeled  hilA promoter DNA.	bind
12988	1	4226	7	11	NULL	NULL	NULL	Hha	GP		bind					hilA DNA	NucleicAcid	labeled		promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_22_6620_s_262	11673432	(B) The binding of Hha to labeled  hilA promoter DNA was competed with unlabeled  hilA promoter DNA.	bind
12989	2	4226	7	11	NULL	NULL	NULL	Hha	GP		bind					hilA DNA	NucleicAcid	unlabeled		promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_22_6620_s_262	11673432	(B) The binding of Hha to labeled  hilA promoter DNA was competed with unlabeled  hilA promoter DNA.	bind
12990	3	4226	7	11	NULL	NULL	NULL	statement 1	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_22_6620_s_262	11673432	(B) The binding of Hha to labeled  hilA promoter DNA was competed with unlabeled  hilA promoter DNA.	bind
12604	1	4227	5	11	NULL	NULL	NULL	Munc18c	GP		bind					Snc2p-PrA	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_927_s_80	16769821	(B) The binding of Munc18c to Snc2p-PrA and GST-tagged syntaxin 4 (Sx4) was  assessed.	bind
12605	2	4227	5	11	NULL	NULL	NULL	Munc18c	GP		bind					GST-tagged syntaxin 4	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_927_s_80	16769821	(B) The binding of Munc18c to Snc2p-PrA and GST-tagged syntaxin 4 (Sx4) was  assessed.	bind
16471	3	4227	5	11	NULL	NULL	NULL	syntaxin 4	GP		is					Sx4	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_927_s_80	16769821	(B) The binding of Munc18c to Snc2p-PrA and GST-tagged syntaxin 4 (Sx4) was  assessed.	bind
12991	1	4227	7	11	NULL	NULL	NULL	Munc18c	GP		bind					Snc2p-PrA	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_927_s_80	16769821	(B) The binding of Munc18c to Snc2p-PrA and GST-tagged syntaxin 4 (Sx4) was  assessed.	bind
12992	2	4227	7	11	NULL	NULL	NULL	Munc18c	GP		bind					syntaxin 4	GP	GST-tagged			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_927_s_80	16769821	(B) The binding of Munc18c to Snc2p-PrA and GST-tagged syntaxin 4 (Sx4) was  assessed.	bind
12993	3	4227	7	11	NULL	NULL	NULL	syntaxin 4	GP		is					Sx4	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_6_927_s_80	16769821	(B) The binding of Munc18c to Snc2p-PrA and GST-tagged syntaxin 4 (Sx4) was  assessed.	bind
12994	1	4228	7	11	NULL	NULL	NULL	PPAR	GP		bind					Site I 	NucleicAcid	truncated derivative of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1583_2_229_s_113	12117567	(B) The binding of PPAR , LXR  and RXR  to a truncated derivative of the Site I comprising the 5' half site of the LXRE plus the next six consecutive nucleotides (see  Table 1 for sequence).	bind
12995	2	4228	7	11	NULL	NULL	NULL	PPAR	GP		bind					statement 1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1583_2_229_s_113	12117567	(B) The binding of PPAR , LXR  and RXR  to a truncated derivative of the Site I comprising the 5' half site of the LXRE plus the next six consecutive nucleotides (see  Table 1 for sequence).	bind
12996	3	4228	7	11	NULL	NULL	NULL	LXR	GP		bind					statement 1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1583_2_229_s_113	12117567	(B) The binding of PPAR , LXR  and RXR  to a truncated derivative of the Site I comprising the 5' half site of the LXRE plus the next six consecutive nucleotides (see  Table 1 for sequence).	bind
12997	1	4228	7	11	NULL	NULL	NULL	Site I	NucleicAcid	truncated derivative of	comprises of									5' half site of the LXRE plus the next six consecutive nucleotides 	NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1583_2_229_s_113	12117567	(B) The binding of PPAR , LXR  and RXR  to a truncated derivative of the Site I comprising the 5' half site of the LXRE plus the next six consecutive nucleotides (see  Table 1 for sequence).	bind
54264	4	4228	7	11	NULL	NULL	NULL	RXR	GP		bind					statement 1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1583_2_229_s_113	12117567	(B) The binding of PPAR , LXR  and RXR  to a truncated derivative of the Site I comprising the 5' half site of the LXRE plus the next six consecutive nucleotides (see  Table 1 for sequence).	bind
12615	1	4229	5	11	NULL	NULL	NULL	TRAF6	GP		bind					CD40	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9806_s_237	16260598	(B) The binding of TRAF6 to CD40 mediates NF-kappaB signaling in TRAF2-deficient cells.	bind
12616	2	4229	5	11	NULL	NULL	NULL	statement 1	Process		mediate					NF-kappaB	GP	signaling of			NULL	in TRAF2-deficient cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9806_s_237	16260598	(B) The binding of TRAF6 to CD40 mediates NF-kappaB signaling in TRAF2-deficient cells.	bind
12998	1	4229	7	11	NULL	NULL	NULL	TRAF6	GP		bind					CD40	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9806_s_237	16260598	(B) The binding of TRAF6 to CD40 mediates NF-kappaB signaling in TRAF2-deficient cells.	bind
12999	2	4229	7	11	NULL	NULL	NULL	statement 1	Process		mediates					NF-kappaB	GP	signaling of			NULL	TRAF2-deficient cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9806_s_237	16260598	(B) The binding of TRAF6 to CD40 mediates NF-kappaB signaling in TRAF2-deficient cells.	bind
12617	1	4230	5	11	NULL	NULL	NULL	CTCF	GP		bind			C terminus		CTCF	GP		11 ZF domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_8_3497_s_98	15060168	(B) The C terminus of CTCF binds to the 11 ZF domain of CTCF.	bind
13000	1	4230	7	11	NULL	NULL	NULL	CTCF	GP		bind			C terminus		CTCF	GP		11 ZF domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_8_3497_s_98	15060168	(B) The C terminus of CTCF binds to the 11 ZF domain of CTCF.	bind
12618	1	4231	5	11	NULL	NULL	NULL	MIBP1	GP		bind			C-terminal zinc finger		SSTR-2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3736_s_118	10207097	(B) The C-terminal MIBP1 zinc finger binds to the SSTR-2 promoter.	bind
13024	1	4231	7	11	NULL	NULL	NULL	MIBP1	GP		binds to			C-terminal zinc finger		SSTR-2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3736_s_118	10207097	(B) The C-terminal MIBP1 zinc finger binds to the SSTR-2 promoter.	bind
12619	1	4233	5	11	NULL	NULL	NULL	CDC25A	GP		bind			carboxyl terminus		ASK1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_14_4818_s_228	11416155	(B) The carboxyl terminus of CDC25A binds to ASK1 in vitro.	bind
13025	1	4233	7	11	NULL	NULL	NULL	CDC25A	GP		binds			carboxyl terminus		ASK1 	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_14_4818_s_228	11416155	(B) The carboxyl terminus of CDC25A binds to ASK1 in vitro.	bind
13452	1	4234	5	11	NULL	NULL	NULL	NF-E2	GP		bind					HS2 core region	GP	of the transfected muLCR			NULL	in stably transfected MEL cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_9_3083_s_203	11287613	(B) The CCAAT box mutation does not affect the binding of NF-E2 to the HS2 core region of the transfected muLCR in stably transfected MEL cells.	bind
13453	2	4234	5	11	NULL	NULL	NULL			mutant	does not affect				CCAAT box	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_9_3083_s_203	11287613	(B) The CCAAT box mutation does not affect the binding of NF-E2 to the HS2 core region of the transfected muLCR in stably transfected MEL cells.	bind
13026	1	4234	7	11	NULL	NULL	NULL	NF-E2	GP		bind					HS2 core region	GP	transfected muLCR			NULL	transfected MEL cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_9_3083_s_203	11287613	(B) The CCAAT box mutation does not affect the binding of NF-E2 to the HS2 core region of the transfected muLCR in stably transfected MEL cells.	bind
13027	2	4234	7	11	NULL	NULL	NULL			mutation of	does not affect				CCAAT box 	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_9_3083_s_203	11287613	(B) The CCAAT box mutation does not affect the binding of NF-E2 to the HS2 core region of the transfected muLCR in stably transfected MEL cells.	bind
12621	1	4235	5	11	NULL	NULL	NULL	co-activator	GP		bind					Notch 1	GP		IC		NULL		NULL	NULL	NULL	NULL	gw60_mechdev_104_1_3_s_378	11404076	(B) The co-activator (dotted) binds to both Notch 1 IC and Notch 3 IC, but is not sufficient for activation.	bind
12623	2	4235	5	11	NULL	NULL	NULL	co-activator	GP		bind					Notch 3	GP		IC		NULL		NULL	NULL	NULL	NULL	gw60_mechdev_104_1_3_s_378	11404076	(B) The co-activator (dotted) binds to both Notch 1 IC and Notch 3 IC, but is not sufficient for activation.	bind
12624	3	4235	5	11	NULL	NULL	NULL	co-activator	GP		is not sufficient for					activation	Process				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_104_1_3_s_378	11404076	(B) The co-activator (dotted) binds to both Notch 1 IC and Notch 3 IC, but is not sufficient for activation.	bind
13028	1	4235	7	11	NULL	NULL	NULL	co-activator	GP		binds					Notch 1	GP		 IC		NULL		NULL	NULL	NULL	NULL	gw60_mechdev_104_1_3_s_378	11404076	(B) The co-activator (dotted) binds to both Notch 1 IC and Notch 3 IC, but is not sufficient for activation.	bind
13029	2	4235	7	11	NULL	NULL	NULL	co-activator	GP		binds					Notch 3	GP		IC		NULL		NULL	NULL	NULL	NULL	gw60_mechdev_104_1_3_s_378	11404076	(B) The co-activator (dotted) binds to both Notch 1 IC and Notch 3 IC, but is not sufficient for activation.	bind
16310	3	4235	7	11	NULL	NULL	NULL	co-activator	GP		is not sufficient for					activation	Process				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_104_1_3_s_378	11404076	(B) The co-activator (dotted) binds to both Notch 1 IC and Notch 3 IC, but is not sufficient for activation.	bind
12626	1	4236	5	11	NULL	NULL	NULL	E7	Organism	mutant	does not bind			deltaDLYC		Rb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_378_s_182	9418885	(B) The control for E7 expression was the same expression vector into which a mutant E7 (deltaDLYC) unable to bind Rb was cloned ( 23).	bind
13034	1	4236	7	11	NULL	NULL	NULL	E7	Organism	mutant	does not bind			deltaDLYC		Rb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_378_s_182	9418885	(B) The control for E7 expression was the same expression vector into which a mutant E7 (deltaDLYC) unable to bind Rb was cloned ( 23).	bind
12628	1	4237	5	11	NULL	NULL	NULL	3H-RTX	Chemical		bind							mutant	S512C		NULL		NULL	NULL	NULL	NULL	gw60_cell_108_3_421_s_171	11853675	(B) The cysteine-reactive reagent MTSET reversibly inhibits 3H-RTX binding to S512C mutant.	bind
12630	2	4237	5	11	NULL	NULL	NULL	MTSET	Chemical		inhibit		reversibly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_108_3_421_s_171	11853675	(B) The cysteine-reactive reagent MTSET reversibly inhibits 3H-RTX binding to S512C mutant.	bind
44432	3	4237	5	11	NULL	NULL	NULL	MTSET	Chemical		is a type of					cysteine-reactive reagent	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_108_3_421_s_171	11853675	(B) The cysteine-reactive reagent MTSET reversibly inhibits 3H-RTX binding to S512C mutant.	bind
13035	1	4237	7	11	NULL	NULL	NULL	3H-RTX	Chemical		binds							mutant	S512C		NULL		NULL	NULL	NULL	NULL	gw60_cell_108_3_421_s_171	11853675	(B) The cysteine-reactive reagent MTSET reversibly inhibits 3H-RTX binding to S512C mutant.	bind
13037	2	4237	7	11	NULL	NULL	NULL	MTSET	Chemical		inhibits		reversibly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_108_3_421_s_171	11853675	(B) The cysteine-reactive reagent MTSET reversibly inhibits 3H-RTX binding to S512C mutant.	bind
44409	3	4237	7	11	NULL	NULL	NULL	MTSET	Chemical		is a type of					cysteine-reactive reagent	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_108_3_421_s_171	11853675	(B) The cysteine-reactive reagent MTSET reversibly inhibits 3H-RTX binding to S512C mutant.	bind
12632	1	4240	5	11	NULL	NULL	NULL	YPT1	GP	wild-type	bind					DSS4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7444_s_142	9819430	(B) The dominant interfering YPT1-N22 protein binds DSS4 under conditions where the interaction of wild-type YPT1 and DSS4 is disrupted.	bind
12633	2	4240	5	11	NULL	NULL	NULL	YPT1 protein	GP	dominant interfering	bind			N22		DSS4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7444_s_142	9819430	(B) The dominant interfering YPT1-N22 protein binds DSS4 under conditions where the interaction of wild-type YPT1 and DSS4 is disrupted.	bind
12634	3	4240	5	11	NULL	NULL	NULL	statement 2	Process		occurs after		only			statement 1	Process	disruption			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7444_s_142	9819430	(B) The dominant interfering YPT1-N22 protein binds DSS4 under conditions where the interaction of wild-type YPT1 and DSS4 is disrupted.	bind
13043	1	4240	7	11	NULL	NULL	NULL	YPT1	GP	 dominant interfering	binds			N22		DSS4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7444_s_142	9819430	(B) The dominant interfering YPT1-N22 protein binds DSS4 under conditions where the interaction of wild-type YPT1 and DSS4 is disrupted.	bind
13045	2	4240	7	11	NULL	NULL	NULL	YPT1	GP	Wild-type	binds					DSS4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7444_s_142	9819430	(B) The dominant interfering YPT1-N22 protein binds DSS4 under conditions where the interaction of wild-type YPT1 and DSS4 is disrupted.	bind
13047	3	4240	7	11	NULL	NULL	NULL	statement 1	Process		occurs upon					statement 2	Process	disrupted			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7444_s_142	9819430	(B) The dominant interfering YPT1-N22 protein binds DSS4 under conditions where the interaction of wild-type YPT1 and DSS4 is disrupted.	bind
12635	1	4242	5	11	NULL	NULL	NULL	MutS	GP		bind					G/T mismatch DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_233_s_112	12887908	(B) The effect of ATP and ATP S on the stability of the MutS bound to G/T mismatch DNA.	bind
13048	1	4242	7	11	NULL	NULL	NULL	MutS 	GP		bind					G/T mismatch DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_233_s_112	12887908	(B) The effect of ATP and ATP S on the stability of the MutS bound to G/T mismatch DNA.	bind
12636	1	4243	5	11	NULL	NULL	NULL	anti-TcpA 15 serum	CellComponent		bind					TCP	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_10_6050_s_255	15385509	(B) The effect of the D175A alteration on binding  of anti-TcpA 15 serum to TCP was tested.	bind
13050	1	4243	7	11	NULL	NULL	NULL	anti-TcpA 15 serum	CellComponent		bind					TCP	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_10_6050_s_255	15385509	(B) The effect of the D175A alteration on binding  of anti-TcpA 15 serum to TCP was tested.	bind
12637	1	4244	5	11	NULL	NULL	NULL	ELT-2 GATA factor protein	GP		bind		specifically			pho-1	GP	critical		GATA1 site in promoter	NULL		NULL	NULL	NULL	NULL	gw70_devbiol_279_2_446_s_181	15733671	(B) The ELT-2 GATA factor protein binds specifically  to the critical GATA1 site in the  pho-1 promoter.	bind
13053	1	4244	7	11	NULL	NULL	NULL	ELT-2 GATA factor	GP		binds		specifically			pho-1	GP			critical GATA1 site in the promoter of 	NULL		NULL	NULL	NULL	NULL	gw70_devbiol_279_2_446_s_181	15733671	(B) The ELT-2 GATA factor protein binds specifically  to the critical GATA1 site in the  pho-1 promoter.	bind
12825	1	4245	5	11	NULL	NULL	NULL	Pac-525	amino acid		bind					SDS	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_1_328_s_191	16352849	(B) The final refined average structure for Pac-525 bound to SDS.	bind
13054	1	4245	7	11	NULL	NULL	NULL	Pac-525	amino acid		bind					SDS	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_1_328_s_191	16352849	(B) The final refined average structure for Pac-525 bound to SDS.	bind
12826	1	4247	5	11	NULL	NULL	NULL	XylRdeltaA	GP		bind					restriction fragments	NucleicAcid			Pu enhancer	NULL		NULL	NULL	NULL	NULL	gw60_cell_86_2_331_s_63	8706137	(B) The footprints  shown are the result of the binding of 0.5 muM XylRdeltaA to  restriction fragments spanning exclusively the  Pu enhancer, in the presence of 5 mM  of each of the nucleotides indicated.	bind
13079	1	4247	7	11	NULL	NULL	NULL	 XylRdeltaA	GP		bind					restriction fragments	NucleicAcid	  		Pu enhancer	NULL		NULL	NULL	NULL	NULL	gw60_cell_86_2_331_s_63	8706137	(B) The footprints  shown are the result of the binding of 0.5 muM XylRdeltaA to  restriction fragments spanning exclusively the  Pu enhancer, in the presence of 5 mM  of each of the nucleotides indicated.	bind
13454	1	4249	5	11	NULL	NULL	NULL	I4AA	Chemical		is					imidazol-4-acetic acid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_37_9_1111_s_115	9833641	(B) The GABA-C receptor antagonist imidazol-4-acetic acid (I4AA, 3 mM) caused a GABA-A mediated depression of the fEPSP slope (42%) and GABA (3 mM) applied in conjunction with I4AA led to a further 22% inhibition ( n=9).	bind
13455	2	4249	5	11	NULL	NULL	NULL	I4AA	Chemical		antagonist of					GABA-C receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_37_9_1111_s_115	9833641	(B) The GABA-C receptor antagonist imidazol-4-acetic acid (I4AA, 3 mM) caused a GABA-A mediated depression of the fEPSP slope (42%) and GABA (3 mM) applied in conjunction with I4AA led to a further 22% inhibition ( n=9).	bind
13456	3	4249	5	11	NULL	NULL	NULL	GABA	Chemical		mediate					fEPSP	Chemical	depression of			NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_37_9_1111_s_115	9833641	(B) The GABA-C receptor antagonist imidazol-4-acetic acid (I4AA, 3 mM) caused a GABA-A mediated depression of the fEPSP slope (42%) and GABA (3 mM) applied in conjunction with I4AA led to a further 22% inhibition ( n=9).	bind
13457	4	4249	5	11	NULL	NULL	NULL	I4AA	Chemical		caused					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_37_9_1111_s_115	9833641	(B) The GABA-C receptor antagonist imidazol-4-acetic acid (I4AA, 3 mM) caused a GABA-A mediated depression of the fEPSP slope (42%) and GABA (3 mM) applied in conjunction with I4AA led to a further 22% inhibition ( n=9).	bind
13458	5	4249	5	11	NULL	NULL	NULL	GABA	Chemical		inhibit		further			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_37_9_1111_s_115	9833641	(B) The GABA-C receptor antagonist imidazol-4-acetic acid (I4AA, 3 mM) caused a GABA-A mediated depression of the fEPSP slope (42%) and GABA (3 mM) applied in conjunction with I4AA led to a further 22% inhibition ( n=9).	bind
44433	6	4249	5	11	NULL	NULL	NULL	statement 5	Process		occurs in conjunction with 					I4AA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_37_9_1111_s_115	9833641	(B) The GABA-C receptor antagonist imidazol-4-acetic acid (I4AA, 3 mM) caused a GABA-A mediated depression of the fEPSP slope (42%) and GABA (3 mM) applied in conjunction with I4AA led to a further 22% inhibition ( n=9).	bind
13080	3	4249	7	11	NULL	NULL	NULL	imidazol-4-acetic acid	Chemical		cause					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_37_9_1111_s_115	9833641	(B) The GABA-C receptor antagonist imidazol-4-acetic acid (I4AA, 3 mM) caused a GABA-A mediated depression of the fEPSP slope (42%) and GABA (3 mM) applied in conjunction with I4AA led to a further 22% inhibition ( n=9).	bind
44410	1	4249	7	11	NULL	NULL	NULL	imidazol-4-acetic acid	Chemical		is an antagonist of					GABA-C receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_37_9_1111_s_115	9833641	(B) The GABA-C receptor antagonist imidazol-4-acetic acid (I4AA, 3 mM) caused a GABA-A mediated depression of the fEPSP slope (42%) and GABA (3 mM) applied in conjunction with I4AA led to a further 22% inhibition ( n=9).	bind
44411	2	4249	7	11	NULL	NULL	NULL	GABA-A 	Chemical		mediate					fEPSP	Chemical	depression of			NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_37_9_1111_s_115	9833641	(B) The GABA-C receptor antagonist imidazol-4-acetic acid (I4AA, 3 mM) caused a GABA-A mediated depression of the fEPSP slope (42%) and GABA (3 mM) applied in conjunction with I4AA led to a further 22% inhibition ( n=9).	bind
44412	4	4249	7	11	NULL	NULL	NULL	imidazol-4-acetic acid	Chemical		is					I4AA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_37_9_1111_s_115	9833641	(B) The GABA-C receptor antagonist imidazol-4-acetic acid (I4AA, 3 mM) caused a GABA-A mediated depression of the fEPSP slope (42%) and GABA (3 mM) applied in conjunction with I4AA led to a further 22% inhibition ( n=9).	bind
12827	1	4250	5	11	NULL	NULL	NULL	GST-RMP probe	GP		bind		specifically			RPB5	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7546_s_164	9819440	(B) The GST-RMP probe bound specifically to RPB5 but not to HBx, CTD, TBP, or GST.	bind
12828	2	4250	5	11	NULL	NULL	NULL	GST-RMP probe	GP		does not bind					HBx	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7546_s_164	9819440	(B) The GST-RMP probe bound specifically to RPB5 but not to HBx, CTD, TBP, or GST.	bind
12829	3	4250	5	11	NULL	NULL	NULL	GST-RMP probe	GP		does not bind								CTD		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7546_s_164	9819440	(B) The GST-RMP probe bound specifically to RPB5 but not to HBx, CTD, TBP, or GST.	bind
12830	4	4250	5	11	NULL	NULL	NULL	GST-RMP probe	GP		does not bind					TBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7546_s_164	9819440	(B) The GST-RMP probe bound specifically to RPB5 but not to HBx, CTD, TBP, or GST.	bind
12831	5	4250	5	11	NULL	NULL	NULL	GST-RMP probe	GP		does not bind					GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7546_s_164	9819440	(B) The GST-RMP probe bound specifically to RPB5 but not to HBx, CTD, TBP, or GST.	bind
13081	1	4250	7	11	NULL	NULL	NULL	GST-RMP probe	GP		bind		specifically			RPB5	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7546_s_164	9819440	(B) The GST-RMP probe bound specifically to RPB5 but not to HBx, CTD, TBP, or GST.	bind
13082	2	4250	7	11	NULL	NULL	NULL	GST-RMP probe	GP		does not bind					HBx	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7546_s_164	9819440	(B) The GST-RMP probe bound specifically to RPB5 but not to HBx, CTD, TBP, or GST.	bind
13083	3	4250	7	11	NULL	NULL	NULL	GST-RMP probe	GP		does not bind								CTD		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7546_s_164	9819440	(B) The GST-RMP probe bound specifically to RPB5 but not to HBx, CTD, TBP, or GST.	bind
13084	4	4250	7	11	NULL	NULL	NULL	GST-RMP probe	GP		does not bind					TBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7546_s_164	9819440	(B) The GST-RMP probe bound specifically to RPB5 but not to HBx, CTD, TBP, or GST.	bind
13085	5	4250	7	11	NULL	NULL	NULL	GST-RMP probe	GP		does not bind					GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7546_s_164	9819440	(B) The GST-RMP probe bound specifically to RPB5 but not to HBx, CTD, TBP, or GST.	bind
12832	1	4251	5	11	NULL	NULL	NULL	Tub2	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_175_1_17_s_29	17030980	(B) The GTP-binding pocket  of Tub2.	bind
13086	1	4251	7	11	NULL	NULL	NULL	GTP	Chemical		bind					Tub2	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_175_1_17_s_29	17030980	(B) The GTP-binding pocket  of Tub2.	bind
12833	1	4252	5	11	NULL	NULL	NULL	HOXD4	GP		bind			homeodomain		CBP	GP		HAT domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_21_7509_s_250	11585930	(B) The HOXD4 homeodomain binds to the CBP HAT domain.	bind
13087	1	4252	7	11	NULL	NULL	NULL	HOXD4 	GP		bind			homeodomain		CBP	GP		HAT domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_21_7509_s_250	11585930	(B) The HOXD4 homeodomain binds to the CBP HAT domain.	bind
12834	1	4253	5	11	NULL	NULL	NULL	Chl4p	GP		interact with					CEN DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_460_s_104	12589047	(B) The interaction of Chl4p with  CEN DNA depends on Ndc10p.	bind
12835	2	4253	5	11	NULL	NULL	NULL	statement 1	Process		depends on					Ndc10p	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_460_s_104	12589047	(B) The interaction of Chl4p with  CEN DNA depends on Ndc10p.	bind
13088	1	4253	7	11	NULL	NULL	NULL	Chl4p 	GP		bind					CEN DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_460_s_104	12589047	(B) The interaction of Chl4p with  CEN DNA depends on Ndc10p.	bind
13089	2	4253	7	11	NULL	NULL	NULL	statement 1	Process		depends on					Ndc10p	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_460_s_104	12589047	(B) The interaction of Chl4p with  CEN DNA depends on Ndc10p.	bind
12836	1	4255	5	11	NULL	NULL	NULL	alpha-actinin	GP	isolated	bind		homogenously	ABD		F-actin	GP				NULL	in resting cells 	NULL	NULL	NULL	NULL	gw60_molbiolcell_14_6_2482_s_99	12808045	(B) The isolated ABD of  alpha-actinin binds almost homogenously to F-actin in resting cells (top  row).	bind
13090	1	4255	7	11	NULL	NULL	NULL	alpha-actinin	GP	isolated	binds		homogenously	ABD		F-actin	GP	 			NULL	resting cells	NULL	NULL	NULL	NULL	gw60_molbiolcell_14_6_2482_s_99	12808045	(B) The isolated ABD of  alpha-actinin binds almost homogenously to F-actin in resting cells (top  row).	bind
12837	1	4256	5	11	NULL	NULL	NULL	PTB	GP		bind					DCS RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_20_7463_s_437	11003644	(B) The left panel shows that hnRNP H enhances PTB and nPTB binding to the DCS RNA.	bind
12838	2	4256	5	11	NULL	NULL	NULL	hnRNP H	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_20_7463_s_437	11003644	(B) The left panel shows that hnRNP H enhances PTB and nPTB binding to the DCS RNA.	bind
12839	3	4256	5	11	NULL	NULL	NULL	nPTB	GP		bind					DCS RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_20_7463_s_437	11003644	(B) The left panel shows that hnRNP H enhances PTB and nPTB binding to the DCS RNA.	bind
12840	4	4256	5	11	NULL	NULL	NULL	hnRNP H	GP		enhances					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_20_7463_s_437	11003644	(B) The left panel shows that hnRNP H enhances PTB and nPTB binding to the DCS RNA.	bind
13091	1	4256	7	11	NULL	NULL	NULL	PTB 	GP		bind					DCS RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_20_7463_s_437	11003644	(B) The left panel shows that hnRNP H enhances PTB and nPTB binding to the DCS RNA.	bind
13092	2	4256	7	11	NULL	NULL	NULL	nPTB	GP		bind					DCS RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_20_7463_s_437	11003644	(B) The left panel shows that hnRNP H enhances PTB and nPTB binding to the DCS RNA.	bind
13093	3	4256	7	11	NULL	NULL	NULL	 hnRNP H	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_20_7463_s_437	11003644	(B) The left panel shows that hnRNP H enhances PTB and nPTB binding to the DCS RNA.	bind
13094	4	4256	7	11	NULL	NULL	NULL	hnRNP H	GP		enhances					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_20_7463_s_437	11003644	(B) The left panel shows that hnRNP H enhances PTB and nPTB binding to the DCS RNA.	bind
12841	1	4257	5	11	NULL	NULL	NULL	cyt-PTP molecule	GP		bind		intramolecular	D1 domain		cyt-PTP molecule	GP		D2 domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5460_s_314	12861030	(B) The less favored possibility of  intramolecular binding between D1 and D2 domains within a single cyt-PTP  molecule, which inhibits cyt-PTP  activity.	bind
12843	2	4257	5	11	NULL	NULL	NULL	statement 1	Process		inhibit					cyt-PTP	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5460_s_314	12861030	(B) The less favored possibility of  intramolecular binding between D1 and D2 domains within a single cyt-PTP  molecule, which inhibits cyt-PTP  activity.	bind
13095	1	4257	7	11	NULL	NULL	NULL	 cyt-PTP molecule	GP		bind		 intramolecular	D1		 cyt-PTP molecule	GP		D2		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5460_s_314	12861030	(B) The less favored possibility of  intramolecular binding between D1 and D2 domains within a single cyt-PTP  molecule, which inhibits cyt-PTP  activity.	bind
13096	2	4257	7	11	NULL	NULL	NULL	statement 1	Process		inhibits					cyt-PTP 	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_15_5460_s_314	12861030	(B) The less favored possibility of  intramolecular binding between D1 and D2 domains within a single cyt-PTP  molecule, which inhibits cyt-PTP  activity.	bind
12844	1	4261	5	11	NULL	NULL	NULL	MS2-RS domain hybrid proteins	GP		bind		specifically			MS2 RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_5_765_s_62	9660960	(B) The MS2-RS domain hybrid proteins bind specifically to MS2 RNA.	bind
13097	1	4261	7	11	NULL	NULL	NULL	MS2-RS domain hybrid protein	GP		bind		specifically			MS2 RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_5_765_s_62	9660960	(B) The MS2-RS domain hybrid proteins bind specifically to MS2 RNA.	bind
12845	1	4262	5	11	NULL	NULL	NULL	Neb1 protein	GP		bind		directly			NS1 protein	GP	viral	effector domain		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_1_7_991_s_44	9651582	(B) The Neb1 protein binds directly to the effector domain of the viral NS1 protein in vitro.	bind
13098	1	4262	7	11	NULL	NULL	NULL	Neb1 protein	GP		binds		directly			 NS1	GP	viral	effector domain		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_1_7_991_s_44	9651582	(B) The Neb1 protein binds directly to the effector domain of the viral NS1 protein in vitro.	bind
12846	1	4267	5	11	NULL	NULL	NULL	PLD1	GP		bind		specifically	PH domain		lipid monolayers	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_1_43_s_62	10660303	(b) The PH domain of PLD1 bound specifically to PI(4,5)P2-containing supported lipid monolayers.	bind
43532	2	4267	5	11	NULL	NULL	NULL	lipid monolayers	Chemical		contains					PI(4,5)P2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_1_43_s_62	10660303	(b) The PH domain of PLD1 bound specifically to PI(4,5)P2-containing supported lipid monolayers.	bind
43533	3	4267	5	11	NULL	NULL	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_1_43_s_62	10660303	(b) The PH domain of PLD1 bound specifically to PI(4,5)P2-containing supported lipid monolayers.	bind
13100	1	4267	7	11	NULL	NULL	NULL	PLD1	GP		bind		specifically	PH domain		PI(4,5)P2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_1_43_s_62	10660303	(b) The PH domain of PLD1 bound specifically to PI(4,5)P2-containing supported lipid monolayers.	bind
13101	2	4267	7	11	NULL	NULL	NULL	lipid monolayers	Chemical		contain					PI(4,5)P2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_1_43_s_62	10660303	(b) The PH domain of PLD1 bound specifically to PI(4,5)P2-containing supported lipid monolayers.	bind
43552	3	4267	7	11	NULL	NULL	NULL	statement 1	Process		occur simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_1_43_s_62	10660303	(b) The PH domain of PLD1 bound specifically to PI(4,5)P2-containing supported lipid monolayers.	bind
12847	1	4268	5	11	NULL	NULL	NULL	ARF1	GP		bind			active site		GTP analog	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_237_s_84	9790530	(B) The picture shows the active site region of the overlapped structures of  ARF1 bound to GTP analog (yellow) or GDP (blue).	bind
12848	2	4268	5	11	NULL	NULL	NULL	ARF1	GP		bind			active site		GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_237_s_84	9790530	(B) The picture shows the active site region of the overlapped structures of  ARF1 bound to GTP analog (yellow) or GDP (blue).	bind
54273	3	4268	5	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_237_s_84	9790530	(B) The picture shows the active site region of the overlapped structures of  ARF1 bound to GTP analog (yellow) or GDP (blue).	bind
13102	1	4268	7	11	NULL	NULL	NULL	 ARF1	GP		binds			active site		GTP analog	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_237_s_84	9790530	(B) The picture shows the active site region of the overlapped structures of  ARF1 bound to GTP analog (yellow) or GDP (blue).	bind
13103	2	4268	7	11	NULL	NULL	NULL	ARF1	GP		bind			active site		GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_237_s_84	9790530	(B) The picture shows the active site region of the overlapped structures of  ARF1 bound to GTP analog (yellow) or GDP (blue).	bind
13104	3	4268	7	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_2_237_s_84	9790530	(B) The picture shows the active site region of the overlapped structures of  ARF1 bound to GTP analog (yellow) or GDP (blue).	bind
12849	1	4269	5	11	NULL	NULL	NULL	DRIP205	GP		bind					PPARgamma-RXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_21_8008_s_146	11027271	(B) The PPARgamma AF-2 mutation abolishes DRIP205, but not SRC-1 or ACTR binding to PPARgamma-RXR.	bind
12850	2	4269	5	11	NULL	NULL	NULL	PPARgamma	GP	mutant	abolish			AF-2		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_21_8008_s_146	11027271	(B) The PPARgamma AF-2 mutation abolishes DRIP205, but not SRC-1 or ACTR binding to PPARgamma-RXR.	bind
12851	3	4269	5	11	NULL	NULL	NULL	SRC-1	GP		bind					PPARgamma-RXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_21_8008_s_146	11027271	(B) The PPARgamma AF-2 mutation abolishes DRIP205, but not SRC-1 or ACTR binding to PPARgamma-RXR.	bind
12852	4	4269	5	11	NULL	NULL	NULL	PPARgamma	GP	mutant	does not abolish			AF-2		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_21_8008_s_146	11027271	(B) The PPARgamma AF-2 mutation abolishes DRIP205, but not SRC-1 or ACTR binding to PPARgamma-RXR.	bind
12853	5	4269	5	11	NULL	NULL	NULL	ACTR	GP		bind					PPARgamma-RXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_21_8008_s_146	11027271	(B) The PPARgamma AF-2 mutation abolishes DRIP205, but not SRC-1 or ACTR binding to PPARgamma-RXR.	bind
12854	6	4269	5	11	NULL	NULL	NULL	PPARgamma	GP	mutant	does not abolish			AF-2		statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_21_8008_s_146	11027271	(B) The PPARgamma AF-2 mutation abolishes DRIP205, but not SRC-1 or ACTR binding to PPARgamma-RXR.	bind
13106	1	4269	7	11	NULL	NULL	NULL	DRIP205	GP		bind					PPARgamma-RXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_21_8008_s_146	11027271	(B) The PPARgamma AF-2 mutation abolishes DRIP205, but not SRC-1 or ACTR binding to PPARgamma-RXR.	bind
13107	2	4269	7	11	NULL	NULL	NULL	SRC-1	GP		bind					PPARgamma-RXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_21_8008_s_146	11027271	(B) The PPARgamma AF-2 mutation abolishes DRIP205, but not SRC-1 or ACTR binding to PPARgamma-RXR.	bind
13108	3	4269	7	11	NULL	NULL	NULL	ACTR	GP		bind					PPARgamma-RXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_21_8008_s_146	11027271	(B) The PPARgamma AF-2 mutation abolishes DRIP205, but not SRC-1 or ACTR binding to PPARgamma-RXR.	bind
13109	4	4269	7	11	NULL	NULL	NULL	PPARgamma	GP	mutation of	abolishes			AF-2		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_21_8008_s_146	11027271	(B) The PPARgamma AF-2 mutation abolishes DRIP205, but not SRC-1 or ACTR binding to PPARgamma-RXR.	bind
13110	5	4269	7	11	NULL	NULL	NULL	PPARgamma	GP	mutation of	does not abolish			AF-2		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_21_8008_s_146	11027271	(B) The PPARgamma AF-2 mutation abolishes DRIP205, but not SRC-1 or ACTR binding to PPARgamma-RXR.	bind
13111	6	4269	7	11	NULL	NULL	NULL	PPARgamma	GP	mutation of	does not abolish			AF-2		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_21_8008_s_146	11027271	(B) The PPARgamma AF-2 mutation abolishes DRIP205, but not SRC-1 or ACTR binding to PPARgamma-RXR.	bind
12855	1	4270	5	11	NULL	NULL	NULL	Grb2	GP		bind					Gab2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
12856	2	4270	5	11	NULL	NULL	NULL	Grb2	GP		bind					Gab3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
12857	3	4270	5	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
12858	4	4270	5	11	NULL	NULL	NULL				mediates			PRD		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
12859	5	4270	5	11	NULL	NULL	NULL				mediates			PRD		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
12860	6	4270	5	11	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
12861	7	4270	5	11	NULL	NULL	NULL	Mona	GP		bind					Gab2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
12862	8	4270	5	11	NULL	NULL	NULL	Mona	GP		bind					Gab3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
12863	9	4270	5	11	NULL	NULL	NULL	statement 7	Process		is an alternative to					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
12864	10	4270	5	11	NULL	NULL	NULL				mediates			PRD		statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
12865	11	4270	5	11	NULL	NULL	NULL				mediates			PRD		statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
12866	12	4270	5	11	NULL	NULL	NULL	statement 10	Process		is an alternative to					statement 11	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
13112	1	4270	7	11	NULL	NULL	NULL	Grb2 	GP		bind					Gab2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
13113	2	4270	7	11	NULL	NULL	NULL	Mona	GP		bind					Gab2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
13114	3	4270	7	11	NULL	NULL	NULL	Grb2 	GP		bind					Gab3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
13115	4	4270	7	11	NULL	NULL	NULL	Mona	GP		bind					Gab3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
13116	5	4270	7	11	NULL	NULL	NULL				mediates			PRD		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
13117	6	4270	7	11	NULL	NULL	NULL				mediates			PRD		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
13118	7	4270	7	11	NULL	NULL	NULL				mediates			PRD		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
13119	8	4270	7	11	NULL	NULL	NULL				mediates			PRD		statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
54274	9	4270	7	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
54275	10	4270	7	11	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
54276	11	4270	7	11	NULL	NULL	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
54277	12	4270	7	11	NULL	NULL	NULL	statement 7	Process		is an alternative to					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_53	11997510	(B) The PRD is sufficient to mediate binding of Grb2 and Mona to either Gab2 or Gab3.	bind
12867	1	4271	5	11	NULL	NULL	NULL	Reelin	GP		bind					VLDLR-expressing cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_2_471_s_127	10571240	(B) The relative amount of Reelin bound to VLDLR-expressing cells from two independent experiments was plotted against the concentration of Reelin (nM).	bind
13120	2	4271	7	11	NULL	NULL	NULL	Reelin 	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_2_471_s_127	10571240	(B) The relative amount of Reelin bound to VLDLR-expressing cells from two independent experiments was plotted against the concentration of Reelin (nM).	bind
44413	1	4271	7	11	NULL	NULL	NULL	cells	cell		express					VLDLR	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_2_471_s_127	10571240	(B) The relative amount of Reelin bound to VLDLR-expressing cells from two independent experiments was plotted against the concentration of Reelin (nM).	bind
12868	1	4275	5	11	NULL	NULL	NULL				bind			SWI/SNF subunit		SNZ1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8829_s_134	14612422	(B) The same process was used as for panel A except that  the SWI/SNF subunit binding to the  SNZ1 promoter was analyzed.	bind
13121	1	4275	7	11	NULL	NULL	NULL				bind			SWI/SNF subunit		 SNZ1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8829_s_134	14612422	(B) The same process was used as for panel A except that  the SWI/SNF subunit binding to the  SNZ1 promoter was analyzed.	bind
16449	1	4278	5	11	NULL	NULL	NULL	Pol II	GP		bind					GAL10	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1301_s_135	12769853	(B) The strain was deleted for  gal11, and the binding of Pol II and of SAGA was measured at the  GAL10 promoter following induction.	bind
16451	2	4278	5	11	NULL	NULL	NULL	SAGA	GP		bind					GAL10	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1301_s_135	12769853	(B) The strain was deleted for  gal11, and the binding of Pol II and of SAGA was measured at the  GAL10 promoter following induction.	bind
13336	1	4278	7	11	NULL	NULL	NULL	 Pol II	GP		bind					GAL10	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1301_s_135	12769853	(B) The strain was deleted for  gal11, and the binding of Pol II and of SAGA was measured at the  GAL10 promoter following induction.	bind
13337	2	4278	7	11	NULL	NULL	NULL	SAGA	GP		bind					GAL10	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1301_s_135	12769853	(B) The strain was deleted for  gal11, and the binding of Pol II and of SAGA was measured at the  GAL10 promoter following induction.	bind
16453	1	4281	5	11	NULL	NULL	NULL	Ubc9	GP		bind					Nup358	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6498_s_264	12192048	(B) The synergistic effect of SUMO-1-modified RanGAP1 on the binding of Ubc9 to Nup358 was investigated.	bind
16454	2	4281	5	11	NULL	NULL	NULL	RanGAP1 	GP	SUMO-1-modified	effect		synergistically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6498_s_264	12192048	(B) The synergistic effect of SUMO-1-modified RanGAP1 on the binding of Ubc9 to Nup358 was investigated.	bind
13124	1	4281	7	11	NULL	NULL	NULL	Ubc9	GP		bind					Nup358	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6498_s_264	12192048	(B) The synergistic effect of SUMO-1-modified RanGAP1 on the binding of Ubc9 to Nup358 was investigated.	bind
13125	2	4281	7	11	NULL	NULL	NULL	RanGAP1 	GP	SUMO-1-modified	effect		synergistically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6498_s_264	12192048	(B) The synergistic effect of SUMO-1-modified RanGAP1 on the binding of Ubc9 to Nup358 was investigated.	bind
16455	1	4282	5	11	NULL	NULL	NULL	F1 phage	Organism		bind					AMA1	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6981_s_147	16177378	(B) The synthetic peptides R1, F1, and F1(s), a scrambled  version of the F1 peptide, were tested for their ability to block binding of F1 phage  to AMA1.	bind
13126	1	4282	7	11	NULL	NULL	NULL	F1 phage	Organism		bind					AMA1	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6981_s_147	16177378	(B) The synthetic peptides R1, F1, and F1(s), a scrambled  version of the F1 peptide, were tested for their ability to block binding of F1 phage  to AMA1.	bind
16456	2	4283	5	11	NULL	NULL	NULL	TNFR2	GP		is required for			TRAF2 binding region		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_11_6_783_s_83	10626900	(B) The TRAF2 binding region of TNFR2 is required for TNF-mediated cell death.	bind
44434	1	4283	5	11	NULL	NULL	NULL	TNF	GP		mediate					cell death	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_11_6_783_s_83	10626900	(B) The TRAF2 binding region of TNFR2 is required for TNF-mediated cell death.	bind
13127	2	4283	7	11	NULL	NULL	NULL	TNFR2	GP		is required for			TRAF2 binding region		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_11_6_783_s_83	10626900	(B) The TRAF2 binding region of TNFR2 is required for TNF-mediated cell death.	bind
44414	1	4283	7	11	NULL	NULL	NULL	TNF	GP		mediate					cell death	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_11_6_783_s_83	10626900	(B) The TRAF2 binding region of TNFR2 is required for TNF-mediated cell death.	bind
16457	1	4284	5	11	NULL	NULL	NULL	TCR	GP		bind			V domain		HLA-A2	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_8_4_403_s_43	9586631	(B) The V  and V  domains of each TCR bound to HLA-A2 (colors as in	bind
13128	1	4284	7	11	NULL	NULL	NULL	 TCR 	GP		binds			V and V domain		HLA-A2	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_8_4_403_s_43	9586631	(B) The V  and V  domains of each TCR bound to HLA-A2 (colors as in	bind
16458	1	4286	5	11	NULL	NULL	NULL	Stat3	GP	mutant	bind		decreased			c-Jun	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_7138_s_135	10490649	(B) Three Stat3 mutants showed decreased c-Jun binding.	bind
13129	1	4286	7	11	NULL	NULL	NULL	Stat3	GP	mutant	bind		decreased			c-Jun	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_7138_s_135	10490649	(B) Three Stat3 mutants showed decreased c-Jun binding.	bind
16459	1	4288	5	11	NULL	NULL	NULL	125I-P40	GP		bind					CEM cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_9_4456_s_120	10456886	(B) Time course of 125I-P40 (106 cpm; 10 9 M) binding to CEM cells (8 x 106).	bind
13130	1	4288	7	11	NULL	NULL	NULL	125I-P40 	GP		bind					CEM cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_9_4456_s_120	10456886	(B) Time course of 125I-P40 (106 cpm; 10 9 M) binding to CEM cells (8 x 106).	bind
16460	2	4289	5	11	NULL	NULL	NULL	[3]AII	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_179	12721105	(b) Time course of PMA effect on [3]AII (4 nM) binding to HEK 293 cells stably expressing AT1R - YFP. (c) Effect of PMA on [3]Lys-des-Arg9-bradykinin binding to HEK 293 cells stably expressing B1R - YFP.	bind
16461	3	4289	5	11	NULL	NULL	NULL	[3]Lys-des-Arg9-bradykinin	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_179	12721105	(b) Time course of PMA effect on [3]AII (4 nM) binding to HEK 293 cells stably expressing AT1R - YFP. (c) Effect of PMA on [3]Lys-des-Arg9-bradykinin binding to HEK 293 cells stably expressing B1R - YFP.	bind
44435	1	4289	5	11	NULL	NULL	NULL	HEK 293 cells	cell		express		stably			AT1R - YFP	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_179	12721105	(b) Time course of PMA effect on [3]AII (4 nM) binding to HEK 293 cells stably expressing AT1R - YFP. (c) Effect of PMA on [3]Lys-des-Arg9-bradykinin binding to HEK 293 cells stably expressing B1R - YFP.	bind
13132	2	4289	7	11	NULL	NULL	NULL	[3]AII	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_179	12721105	(b) Time course of PMA effect on [3]AII (4 nM) binding to HEK 293 cells stably expressing AT1R - YFP. (c) Effect of PMA on [3]Lys-des-Arg9-bradykinin binding to HEK 293 cells stably expressing B1R - YFP.	bind
13133	3	4289	7	11	NULL	NULL	NULL	[3]Lys-des-Arg9-bradykinin	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_179	12721105	(b) Time course of PMA effect on [3]AII (4 nM) binding to HEK 293 cells stably expressing AT1R - YFP. (c) Effect of PMA on [3]Lys-des-Arg9-bradykinin binding to HEK 293 cells stably expressing B1R - YFP.	bind
44415	1	4289	7	11	NULL	NULL	NULL	HEK 293 cells	cell		express		stably			AT1R - YFP	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_8_1495_s_179	12721105	(b) Time course of PMA effect on [3]AII (4 nM) binding to HEK 293 cells stably expressing AT1R - YFP. (c) Effect of PMA on [3]Lys-des-Arg9-bradykinin binding to HEK 293 cells stably expressing B1R - YFP.	bind
16462	1	4290	5	11	NULL	NULL	NULL	cPot1	GP		bind					MBS oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_5_2091_s_282	14966288	(B) Titration curve for cPot1 binding to the MBS  oligonucleotide.	bind
13134	1	4290	7	11	NULL	NULL	NULL	cPot1	GP		bind					MBS oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_5_2091_s_282	14966288	(B) Titration curve for cPot1 binding to the MBS  oligonucleotide.	bind
16463	1	4291	5	11	NULL	NULL	NULL	p53	GP		bind			Arg		p53CON DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1092_s_174	9891044	(B) Titration of p53Pro and p53Arg binding to p53CON DNA.	bind
16464	2	4291	5	11	NULL	NULL	NULL	p53	GP		bind			Pro		p53CON DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1092_s_174	9891044	(B) Titration of p53Pro and p53Arg binding to p53CON DNA.	bind
13135	1	4291	7	11	NULL	NULL	NULL	p53	GP		bind			Pro		p53CON DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1092_s_174	9891044	(B) Titration of p53Pro and p53Arg binding to p53CON DNA.	bind
13136	2	4291	7	11	NULL	NULL	NULL	p53	GP		bind			Arg		p53CON DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1092_s_174	9891044	(B) Titration of p53Pro and p53Arg binding to p53CON DNA.	bind
16465	1	4292	5	11	NULL	NULL	NULL	TM-1	GP		does not bind					B7-1	Cell				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_5_11_1303_s_166	8574588	(b) TM-1 does not bind to B7-1, B7-2 or ICAM-1, as determined by flow cytometry.	bind
16466	2	4292	5	11	NULL	NULL	NULL	TM-1	GP		does not bind					B7-2	Cell				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_5_11_1303_s_166	8574588	(b) TM-1 does not bind to B7-1, B7-2 or ICAM-1, as determined by flow cytometry.	bind
16467	3	4292	5	11	NULL	NULL	NULL	TM-1	GP		does not bind					ICAM-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_5_11_1303_s_166	8574588	(b) TM-1 does not bind to B7-1, B7-2 or ICAM-1, as determined by flow cytometry.	bind
13137	1	4292	7	11	NULL	NULL	NULL	TM-1	GP		does not bind					B7-1	Cell				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_5_11_1303_s_166	8574588	(b) TM-1 does not bind to B7-1, B7-2 or ICAM-1, as determined by flow cytometry.	bind
13138	2	4292	7	11	NULL	NULL	NULL	TM-1	GP		does not bind					B7-2	Cell				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_5_11_1303_s_166	8574588	(b) TM-1 does not bind to B7-1, B7-2 or ICAM-1, as determined by flow cytometry.	bind
13139	3	4292	7	11	NULL	NULL	NULL	TM-1	GP		does not bind					ICAM-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_5_11_1303_s_166	8574588	(b) TM-1 does not bind to B7-1, B7-2 or ICAM-1, as determined by flow cytometry.	bind
16468	1	4293	5	11	NULL	NULL	NULL	PIP3	GP		bind					PKB	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7794_s_199	14560023	(B) To assess the importance  of PKCzeta activation in influencing the binding of PIP3 to PKB, the experiment in panel A was repeated but with TBST buffer that either lacked  ATP, PS, and MgCl2 or which had been supplemented with Ro 31.8220 (Ro, 5 muM), as indicated.	bind
13140	1	4293	7	11	NULL	NULL	NULL	PIP3	GP		bind					PKB	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7794_s_199	14560023	(B) To assess the importance  of PKCzeta activation in influencing the binding of PIP3 to PKB, the experiment in panel A was repeated but with TBST buffer that either lacked  ATP, PS, and MgCl2 or which had been supplemented with Ro 31.8220 (Ro, 5 muM), as indicated.	bind
16469	1	4298	5	11	NULL	NULL	NULL	c-Myb proteins	GP	35S-labeled	bind					GST-KIX	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5601_s_102	10409749	(B) Top, representative autoradiogram obtained following SDS-PAGE of 35S-labeled c-Myb proteins bound to GST-KIX resin.	bind
13142	1	4298	7	11	NULL	NULL	NULL	c-Myb protein	GP	35S-labeled	bind					GST-KIX	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5601_s_102	10409749	(B) Top, representative autoradiogram obtained following SDS-PAGE of 35S-labeled c-Myb proteins bound to GST-KIX resin.	bind
16470	1	4299	5	11	NULL	NULL	NULL	c-jun	GP		bind					ET-1	GP			Ap1 element in promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_14_5518_s_174	16809784	(B) Transcription factor c-jun binds the Ap1 element in the ET-1  promoter.	bind
44436	2	4299	5	11	NULL	NULL	NULL	c-jun	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_14_5518_s_174	16809784	(B) Transcription factor c-jun binds the Ap1 element in the ET-1  promoter.	bind
13143	1	4299	7	11	NULL	NULL	NULL	c-jun	GP		binds					ET-1	GP			Ap1 element in the promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_14_5518_s_174	16809784	(B) Transcription factor c-jun binds the Ap1 element in the ET-1  promoter.	bind
44416	2	4299	7	11	NULL	NULL	NULL	c-jun	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_14_5518_s_174	16809784	(B) Transcription factor c-jun binds the Ap1 element in the ET-1  promoter.	bind
10518	1	4300	5	11	NULL	NULL	NULL	p27	GP		bind		transiently			CRM1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_1_201_s_141	12529437	(B) Transient binding of p27 to CRM1 occurs early in G1.	bind
10519	2	4300	5	11	NULL	NULL	NULL	statement 1	Process		occurs early in					G1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_1_201_s_141	12529437	(B) Transient binding of p27 to CRM1 occurs early in G1.	bind
9857	1	4300	6	11	NULL	NULL	NULL	p27	GP		bind		transiently			CRM1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_1_201_s_141	12529437	(B) Transient binding of p27 to CRM1 occurs early in G1.	bind
9858	2	4300	6	11	NULL	NULL	NULL	statement 1	Process		occurs early in					G1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_1_201_s_141	12529437	(B) Transient binding of p27 to CRM1 occurs early in G1.	bind
10520	1	4301	5	NULL	NULL	0	NULL	TRF2	NULL		bind	NULL				POT1	NULL				NULL	293 cells	0	NULL	NULL	NULL	gw70_molcellbiol_25_3_1070_s_215	15657433	(B) TRF2 and TRF2deltaBdeltaM bound to POT1 in 293 cells.	bind
10521	2	4301	5	NULL	NULL	0	NULL	TRF2deltaBdeltaM	NULL		bind	NULL				POT1	NULL				NULL	293 cells	0	NULL	NULL	NULL	gw70_molcellbiol_25_3_1070_s_215	15657433	(B) TRF2 and TRF2deltaBdeltaM bound to POT1 in 293 cells.	bind
9859	1	4301	6	NULL	NULL	0	NULL	TRF2	GP		bind					POT1	GP				NULL	293 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_3_1070_s_215	15657433	(B) TRF2 and TRF2deltaBdeltaM bound to POT1 in 293 cells.	bind
9860	2	4301	6	NULL	NULL	0	NULL	TRF2deltaBdeltaM	GP		bind					POT1	GP				NULL	293 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_3_1070_s_215	15657433	(B) TRF2 and TRF2deltaBdeltaM bound to POT1 in 293 cells.	bind
10522	1	4302	5	NULL	NULL	0	NULL	Tubulin	NULL		bind	NULL				Op18  derivatives	NULL	Flag-epitope - tagged			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_146_6_1289_s_111	10491392	(B) Tubulin binding to the indicated Op18 Flag-epitope - tagged derivatives was analyzed at equimolar concentration (10 muM) in PEM, pH 6.8, containing 17% glycerol.	bind
9861	1	4302	6	NULL	NULL	0	NULL	Tubulin	GP		bind					Op18 derivates	GP	Flag-eptitope			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_146_6_1289_s_111	10491392	(B) Tubulin binding to the indicated Op18 Flag-epitope - tagged derivatives was analyzed at equimolar concentration (10 muM) in PEM, pH 6.8, containing 17% glycerol.	bind
10526	1	4306	5	NULL	NULL	0	NULL		NULL		bind	NULL		Uba domain		polyubiquitin chains	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_9_3868_s_64	12972570	(B) Uba domain binding to polyubiquitin chains does not  correlate with proteasome pull down.	bind
11443	2	4306	5	NULL	NULL	0	NULL	statement 1	NULL		does not correlate with	NULL				proteasome	NULL	pull down of			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_9_3868_s_64	12972570	(B) Uba domain binding to polyubiquitin chains does not  correlate with proteasome pull down.	bind
9862	1	4306	6	NULL	NULL	0	NULL		NULL		bind	NULL		Uba		polyubiquitin chains	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_9_3868_s_64	12972570	(B) Uba domain binding to polyubiquitin chains does not  correlate with proteasome pull down.	bind
54260	2	4306	6	10	NULL	0	NULL	statement 1			does not correlate with					proteasome		pull down of			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_9_3868_s_64	12972570	(B) Uba domain binding to polyubiquitin chains does not  correlate with proteasome pull down.	bind
10527	1	4307	5	NULL	NULL	0	NULL	CP2	NULL		bind	NULL				GATA-1 oligonucleotide	NULL			HS2 enhancer 	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_10_3942_s_119	16648487	(B) Unlabeled  oligonucleotides comprising the wild-type (wt) or mutated GATA-1 palindrome do not  affect the binding of CP2 to the GATA-1 HS2 enhancer oligonucleotide in competition  experiments.	bind
9863	1	4307	6	NULL	NULL	0	NULL	CP2	GP		bind					GATA-1 oligonucleotide	NucleicAcid			HS2 enhancer	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_10_3942_s_119	16648487	(B) Unlabeled  oligonucleotides comprising the wild-type (wt) or mutated GATA-1 palindrome do not  affect the binding of CP2 to the GATA-1 HS2 enhancer oligonucleotide in competition  experiments.	bind
10528	1	4309	5	NULL	NULL	0	NULL	v-E10	NULL		bind	NULL		PQE binding motif		TRAF6	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_1115_s_92	11238466	(B) v-E10 binds TRAF6 via a PQE binding motif.	bind
9864	1	4309	6	NULL	NULL	0	NULL	v-E10	GP		bind			PQE binding motif		TRAF6	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_1115_s_92	11238466	(B) v-E10 binds TRAF6 via a PQE binding motif.	bind
10532	1	4310	5	NULL	NULL	0	NULL	VDE	NULL		bind	NULL				Srp1p	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_23_5_1726_s_222	12588991	(B) VDE binds Srp1p in vitro.	bind
9865	1	4310	6	NULL	NULL	0	NULL	VDE	GP		bind					Srp1p	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_5_1726_s_222	12588991	(B) VDE binds Srp1p in vitro.	bind
10533	1	4311	5	NULL	NULL	0	NULL	VDR	NULL		is present in	NULL				Jun-Fos DNA-bound complex	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4191_s_190	10330159	(B) VDR is present in the Jun-Fos DNA-bound complex.	bind
10534	1	4312	5	NULL	NULL	0	NULL	Vg	NULL		associate with	NULL				Sd	NULL				NULL		0	NULL	NULL	NULL	gw60_development_130_17_4135_s_493	12874133	(B) Vg associates with Sd to form a bipartite transcription factor (Vg/Sd) that controls the expression of an unknown diffusible factor.	bind
10627	2	4312	5	NULL	NULL	0	NULL	statement 1	NULL		forms	NULL				Vg/Sd bipartite transcription factor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4135_s_493	12874133	(B) Vg associates with Sd to form a bipartite transcription factor (Vg/Sd) that controls the expression of an unknown diffusible factor.	bind
10628	3	4312	5	10	NULL	0	NULL	statement 2			control					unknown diffusible factor		expression of 			NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4135_s_493	12874133	(B) Vg associates with Sd to form a bipartite transcription factor (Vg/Sd) that controls the expression of an unknown diffusible factor.	bind
9867	1	4312	6	NULL	NULL	NULL	NULL	Vg	GP		associate with					Sd	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4135_s_493	12874133	(B) Vg associates with Sd to form a bipartite transcription factor (Vg/Sd) that controls the expression of an unknown diffusible factor.	bind
9868	2	4312	6	NULL	NULL	NULL	NULL	statement 1	Process		forms					bipartite transcription factor (Vg/Sd)	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4135_s_493	12874133	(B) Vg associates with Sd to form a bipartite transcription factor (Vg/Sd) that controls the expression of an unknown diffusible factor.	bind
10630	1	4313	5	NULL	NULL	0	NULL	Vpr	NULL		bind	NULL				ANT	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_583_s_238	12729593	(B) Vpr binds to the adenine nucleotide translocator (ANT) to induce mitochondrial  membrane potential (MMP).	bind
10631	2	4313	5	NULL	NULL	0	NULL	ANT	NULL		is	NULL				adenine nucleotide translocator	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_583_s_238	12729593	(B) Vpr binds to the adenine nucleotide translocator (ANT) to induce mitochondrial  membrane potential (MMP).	bind
10632	3	4313	5	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL				MMP	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_583_s_238	12729593	(B) Vpr binds to the adenine nucleotide translocator (ANT) to induce mitochondrial  membrane potential (MMP).	bind
10633	4	4313	5	NULL	NULL	0	NULL	MMP	NULL		is	NULL				mitochondrial membrane potential	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_583_s_238	12729593	(B) Vpr binds to the adenine nucleotide translocator (ANT) to induce mitochondrial  membrane potential (MMP).	bind
9870	1	4313	6	NULL	NULL	NULL	NULL	Vpr	GP		bind					ANT	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_583_s_238	12729593	(B) Vpr binds to the adenine nucleotide translocator (ANT) to induce mitochondrial  membrane potential (MMP).	bind
9871	2	4313	6	NULL	NULL	NULL	NULL	ANT	GP		is					adenine nucleotide translocator	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_583_s_238	12729593	(B) Vpr binds to the adenine nucleotide translocator (ANT) to induce mitochondrial  membrane potential (MMP).	bind
9872	3	4313	6	NULL	NULL	NULL	NULL	statement 1	Process		induce					MMP	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_583_s_238	12729593	(B) Vpr binds to the adenine nucleotide translocator (ANT) to induce mitochondrial  membrane potential (MMP).	bind
9873	4	4313	6	NULL	NULL	NULL	NULL	MMP	Process		is					mitochondrial membrane potential	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_583_s_238	12729593	(B) Vpr binds to the adenine nucleotide translocator (ANT) to induce mitochondrial  membrane potential (MMP).	bind
10635	1	4315	5	NULL	NULL	0	NULL	Vps45p	NULL		bind	NULL				Vac1p	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_9_3_159_s_68	10021387	(b) Vps45p binds Vac1p.	bind
9874	1	4315	6	NULL	NULL	NULL	NULL	Vps45p	GP		bind					Vac1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_3_159_s_68	10021387	(b) Vps45p binds Vac1p.	bind
10638	1	4316	5	NULL	NULL	0	NULL	cyclin E	NULL		bind	NULL				p107 derivatives	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_295	9710622	(B) Western blot analysis of cyclin E bound to p107 derivatives.	bind
9875	1	4316	6	NULL	NULL	NULL	NULL	Cyclin E	GP		bind					p107 derivatives	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5380_s_295	9710622	(B) Western blot analysis of cyclin E bound to p107 derivatives.	bind
10642	1	4318	5	NULL	NULL	0	NULL	uPAR	NULL	occupied	bind	NULL				LRP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1467_s_304	11359936	(B) When binding of occupied uPAR to LRP is prevented, uPA:PAI-1 bridges uPAR and LRP and occupied uPAR moves into clathrin-coated pits.	bind
10643	2	4318	5	NULL	NULL	0	NULL	uPA:PAI-1	NULL		bridges	NULL				uPAR	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1467_s_304	11359936	(B) When binding of occupied uPAR to LRP is prevented, uPA:PAI-1 bridges uPAR and LRP and occupied uPAR moves into clathrin-coated pits.	bind
10644	4	4318	5	NULL	NULL	0	NULL	statement 2	NULL		in the absence of	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1467_s_304	11359936	(B) When binding of occupied uPAR to LRP is prevented, uPA:PAI-1 bridges uPAR and LRP and occupied uPAR moves into clathrin-coated pits.	bind
10647	6	4318	5	NULL	NULL	0	NULL	uPAR	NULL	occupied	moves into	NULL				clathrin-coated pits	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1467_s_304	11359936	(B) When binding of occupied uPAR to LRP is prevented, uPA:PAI-1 bridges uPAR and LRP and occupied uPAR moves into clathrin-coated pits.	bind
10650	5	4318	5	10	NULL	0	NULL	statement 3			in the absence of					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1467_s_304	11359936	(B) When binding of occupied uPAR to LRP is prevented, uPA:PAI-1 bridges uPAR and LRP and occupied uPAR moves into clathrin-coated pits.	bind
13040	3	4318	5	NULL	NULL	0	NULL	uPA:PAI-1	NULL		bridges	NULL				LRP	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_5_1467_s_304	11359936	(B) When binding of occupied uPAR to LRP is prevented, uPA:PAI-1 bridges uPAR and LRP and occupied uPAR moves into clathrin-coated pits.	bind
54261	7	4318	5	10	NULL	0	NULL	statement 6			in absence of					statement 1					NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_5_1467_s_304	11359936	(B) When binding of occupied uPAR to LRP is prevented, uPA:PAI-1 bridges uPAR and LRP and occupied uPAR moves into clathrin-coated pits.	bind
10803	1	4318	6	NULL	NULL	NULL	NULL	uPAR	GP	occupied	bind					LRP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1467_s_304	11359936	(B) When binding of occupied uPAR to LRP is prevented, uPA:PAI-1 bridges uPAR and LRP and occupied uPAR moves into clathrin-coated pits.	bind
10804	2	4318	6	NULL	NULL	NULL	NULL	uPA:PAI-1	GP		bridges					uPAR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1467_s_304	11359936	(B) When binding of occupied uPAR to LRP is prevented, uPA:PAI-1 bridges uPAR and LRP and occupied uPAR moves into clathrin-coated pits.	bind
10805	3	4318	6	NULL	NULL	NULL	NULL	uPA:PAI-1	GP		bridges					LRP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1467_s_304	11359936	(B) When binding of occupied uPAR to LRP is prevented, uPA:PAI-1 bridges uPAR and LRP and occupied uPAR moves into clathrin-coated pits.	bind
10806	4	4318	6	NULL	NULL	NULL	NULL	statement 2	Process		occurs in absence of					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1467_s_304	11359936	(B) When binding of occupied uPAR to LRP is prevented, uPA:PAI-1 bridges uPAR and LRP and occupied uPAR moves into clathrin-coated pits.	bind
10807	5	4318	6	NULL	NULL	NULL	NULL	statement 3	Process		occurs in absence of					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1467_s_304	11359936	(B) When binding of occupied uPAR to LRP is prevented, uPA:PAI-1 bridges uPAR and LRP and occupied uPAR moves into clathrin-coated pits.	bind
10808	6	4318	6	NULL	NULL	NULL	NULL	uPAR	GP	occupied	moves to					clathrin-coated pits	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1467_s_304	11359936	(B) When binding of occupied uPAR to LRP is prevented, uPA:PAI-1 bridges uPAR and LRP and occupied uPAR moves into clathrin-coated pits.	bind
10809	7	4318	6	NULL	NULL	NULL	NULL	statement 6	Process		occurs in absence of					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1467_s_304	11359936	(B) When binding of occupied uPAR to LRP is prevented, uPA:PAI-1 bridges uPAR and LRP and occupied uPAR moves into clathrin-coated pits.	bind
10653	1	4319	5	NULL	NULL	0	NULL	SatA	NULL		bind	NULL	tightly			SatB/atC	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_10_6727_s_194	16177350	(B) When SatA binds tightly with  SatB/atC, it may transition to an open conformation, which has decreased affinity  for sialic acid, and SatB/atC may reorient to expose a sugar binding site.	bind
10656	2	4319	5	NULL	NULL	0	NULL	SatB/atC	NULL		transition to	NULL	may			open conformation	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_10_6727_s_194	16177350	(B) When SatA binds tightly with  SatB/atC, it may transition to an open conformation, which has decreased affinity  for sialic acid, and SatB/atC may reorient to expose a sugar binding site.	bind
10662	3	4319	5	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_10_6727_s_194	16177350	(B) When SatA binds tightly with  SatB/atC, it may transition to an open conformation, which has decreased affinity  for sialic acid, and SatB/atC may reorient to expose a sugar binding site.	bind
10665	4	4319	5	NULL	NULL	0	NULL	statement 2	NULL		decreased affinity for	NULL				sialic acid	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_10_6727_s_194	16177350	(B) When SatA binds tightly with  SatB/atC, it may transition to an open conformation, which has decreased affinity  for sialic acid, and SatB/atC may reorient to expose a sugar binding site.	bind
10667	5	4319	5	10	NULL	0	NULL	SatB/atC			expose		may						sugar binding site		NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6727_s_194	16177350	(B) When SatA binds tightly with  SatB/atC, it may transition to an open conformation, which has decreased affinity  for sialic acid, and SatB/atC may reorient to expose a sugar binding site.	bind
9876	1	4319	6	NULL	NULL	NULL	NULL	SatA	GP		bind		tightly			SatB/atC	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6727_s_194	16177350	(B) When SatA binds tightly with  SatB/atC, it may transition to an open conformation, which has decreased affinity  for sialic acid, and SatB/atC may reorient to expose a sugar binding site.	bind
9877	2	4319	6	NULL	NULL	NULL	NULL	SatB/atC	GP		transition to		may			open conformation					NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6727_s_194	16177350	(B) When SatA binds tightly with  SatB/atC, it may transition to an open conformation, which has decreased affinity  for sialic acid, and SatB/atC may reorient to expose a sugar binding site.	bind
9878	3	4319	6	NULL	NULL	NULL	NULL	SatA	GP	open conformation	has decreased affinity for					sialic acid	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6727_s_194	16177350	(B) When SatA binds tightly with  SatB/atC, it may transition to an open conformation, which has decreased affinity  for sialic acid, and SatB/atC may reorient to expose a sugar binding site.	bind
9924	4	4319	6	NULL	NULL	NULL	NULL	SatB/atC	GP		expose		may						sugar binding site		NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6727_s_194	16177350	(B) When SatA binds tightly with  SatB/atC, it may transition to an open conformation, which has decreased affinity  for sialic acid, and SatB/atC may reorient to expose a sugar binding site.	bind
12778	5	4319	6	NULL	NULL	NULL	NULL	statement 1	Process		lead to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6727_s_194	16177350	(B) When SatA binds tightly with  SatB/atC, it may transition to an open conformation, which has decreased affinity  for sialic acid, and SatB/atC may reorient to expose a sugar binding site.	bind
10668	1	4320	5	NULL	NULL	0	NULL	phospho-LIS1 isoform	NULL		bind	NULL				MT bundles	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_9_3089_s_298	11940666	(b) When the distal zinc finger motif of CLIP-170 is mutated, the phospho-LIS1 isoform can no longer bind to MT bundles.	bind
10669	2	4320	5	10	NULL	0	NULL	CLIP-170		mutation of 	prevent			distal zinc finger motif		statement 1					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_3089_s_298	11940666	(b) When the distal zinc finger motif of CLIP-170 is mutated, the phospho-LIS1 isoform can no longer bind to MT bundles.	bind
9879	1	4320	6	NULL	NULL	NULL	NULL	phospho-LIS1 isoform	GP		bind					MT bundles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_3089_s_298	11940666	(b) When the distal zinc finger motif of CLIP-170 is mutated, the phospho-LIS1 isoform can no longer bind to MT bundles.	bind
9880	2	4320	6	NULL	NULL	NULL	NULL	CLIP-170	GP	mutant	attenuates			distal zinc finger motif		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_3089_s_298	11940666	(b) When the distal zinc finger motif of CLIP-170 is mutated, the phospho-LIS1 isoform can no longer bind to MT bundles.	bind
10670	1	4321	5	NULL	NULL	0	NULL	BimL protein	NULL	wild-type	bind	NULL	tightly			Bcl-w	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_162_5_877_s_98	12952938	(B) Wild-type BimL protein and its BH3 peptide bind tightly to Bcl-w.	bind
10671	2	4321	5	NULL	NULL	0	NULL	BH3 peptide	NULL		bind	NULL	tightly			Bcl-w	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_162_5_877_s_98	12952938	(B) Wild-type BimL protein and its BH3 peptide bind tightly to Bcl-w.	bind
9881	1	4321	6	NULL	NULL	NULL	NULL	BimL protein	GP	wild type	bind		tightly			Bcl-w	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_5_877_s_98	12952938	(B) Wild-type BimL protein and its BH3 peptide bind tightly to Bcl-w.	bind
9882	2	4321	6	NULL	NULL	NULL	NULL	BH3 peptide	AminoAcid		bind		tightly			Bcl-w	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_5_877_s_98	12952938	(B) Wild-type BimL protein and its BH3 peptide bind tightly to Bcl-w.	bind
10676	1	4323	5	NULL	NULL	0	NULL	CLK	NULL		bind	NULL					NULL			per sequences	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_18_6935_s_222	10958689	(B) Yeast one-hybrid assays showing the binding of CLK and CYC to  per and  to upstream sequences.	bind
10677	2	4323	5	NULL	NULL	0	NULL	CYC	NULL		bind	NULL					NULL			per sequences	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_18_6935_s_222	10958689	(B) Yeast one-hybrid assays showing the binding of CLK and CYC to  per and  to upstream sequences.	bind
12657	1	4323	6	NULL	NULL	NULL	NULL	CLK	GP		bind						GP			per sequences	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6935_s_222	10958689	(B) Yeast one-hybrid assays showing the binding of CLK and CYC to  per and  to upstream sequences.	bind
12658	2	4323	6	NULL	NULL	NULL	NULL	CYC	GP		bind						GP			per sequences	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6935_s_222	10958689	(B) Yeast one-hybrid assays showing the binding of CLK and CYC to  per and  to upstream sequences.	bind
10680	1	4324	5	NULL	NULL	0	NULL	membrane pore complex	NULL		formed by	NULL				Sec61	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_108_5_591_s_32	11893330	(B) Yeast ribosome bound to the membrane pore complex formed by Sec61 (red).	bind
10681	2	4324	5	NULL	NULL	0	NULL	ribosome	NULL	yeast	bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_108_5_591_s_32	11893330	(B) Yeast ribosome bound to the membrane pore complex formed by Sec61 (red).	bind
9885	1	4324	6	NULL	NULL	NULL	NULL	Sec61	GP		form					membrane pore complex	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_108_5_591_s_32	11893330	(B) Yeast ribosome bound to the membrane pore complex formed by Sec61 (red).	bind
9886	2	4324	6	NULL	NULL	NULL	NULL	ribosome	CellComponent	yeast	bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_108_5_591_s_32	11893330	(B) Yeast ribosome bound to the membrane pore complex formed by Sec61 (red).	bind
10682	1	4325	5	NULL	NULL	0	NULL	DCAPS	NULL		bind	NULL				Axin	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_2_229_s_72	12711303	(B) Yeast two-hybrid assay for the binding of DCAPS to Axin,  Dfz2, and Dsh.	bind
10683	2	4325	5	NULL	NULL	0	NULL	DCAPS	NULL		bind	NULL				Dfz2	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_2_229_s_72	12711303	(B) Yeast two-hybrid assay for the binding of DCAPS to Axin,  Dfz2, and Dsh.	bind
10684	3	4325	5	NULL	NULL	0	NULL	DCAPS	NULL		bind	NULL				Dsh	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_2_229_s_72	12711303	(B) Yeast two-hybrid assay for the binding of DCAPS to Axin,  Dfz2, and Dsh.	bind
9887	1	4325	6	NULL	NULL	NULL	NULL	DCAPS	GP		bind					Axin	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_2_229_s_72	12711303	(B) Yeast two-hybrid assay for the binding of DCAPS to Axin,  Dfz2, and Dsh.	bind
9888	2	4325	6	NULL	NULL	NULL	NULL	DCAPS	GP		bind					Dfz2	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_2_229_s_72	12711303	(B) Yeast two-hybrid assay for the binding of DCAPS to Axin,  Dfz2, and Dsh.	bind
9889	3	4325	6	NULL	NULL	NULL	NULL	DCAPS	GP		bind					Dsh	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_2_229_s_72	12711303	(B) Yeast two-hybrid assay for the binding of DCAPS to Axin,  Dfz2, and Dsh.	bind
10685	1	4327	5	10	NULL	0	NULL	rootletin fragments			derived from								rod domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_3_431_s_184	12427867	(B) Yeast two-hybrid assays show homotypic binding between rootletin fragments derived from the rod domain.	bind
54262	2	4327	5	10	NULL	0	NULL	rootletin fragments			bind		homotypically			rootletin fragments					NULL		0	NULL	NULL	NULL	gw60_cellbiol_159_3_431_s_184	12427867	(B) Yeast two-hybrid assays show homotypic binding between rootletin fragments derived from the rod domain.	bind
12660	1	4327	6	NULL	NULL	NULL	NULL	rootletin fragments	GP		are derived from								rod domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_3_431_s_184	12427867	(B) Yeast two-hybrid assays show homotypic binding between rootletin fragments derived from the rod domain.	bind
41326	2	4327	6	NULL	NULL	NULL	NULL	rootletin fragments	GP		bind		homotypically			rootletin fragments	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_3_431_s_184	12427867	(B) Yeast two-hybrid assays show homotypic binding between rootletin fragments derived from the rod domain.	bind
10692	1	4328	5	NULL	NULL	0	NULL		NULL	mutant	bind	NULL		pericentrin domain		GCP2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_8_3642_s_118	15146056	(B) Yeast two-hybrid data showing significantly  reduced binding of mutant pericentrin domain for GCP2 and GCP3.	bind
10693	2	4328	5	NULL	NULL	0	NULL		NULL	mutant	bind	NULL		pericentrin domain		GCP3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_8_3642_s_118	15146056	(B) Yeast two-hybrid data showing significantly  reduced binding of mutant pericentrin domain for GCP2 and GCP3.	bind
12662	1	4328	6	NULL	NULL	NULL	NULL			mutant	bind			pericentrin domain		GCP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_8_3642_s_118	15146056	(B) Yeast two-hybrid data showing significantly  reduced binding of mutant pericentrin domain for GCP2 and GCP3.	bind
12663	2	4328	6	NULL	NULL	NULL	NULL			mutant	bind			pericentrin domain		GCP3	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_8_3642_s_118	15146056	(B) Yeast two-hybrid data showing significantly  reduced binding of mutant pericentrin domain for GCP2 and GCP3.	bind
10705	1	4330	5	NULL	NULL	0	NULL	YY1	NULL		bind	NULL					NULL			SR3	NULL		0	NULL	NULL	NULL	gw70_development_131_19_4709_s_208	15329343	(B) YY1 binds to SR3.	bind
9904	1	4330	6	NULL	NULL	NULL	NULL	YY1	GP		bind									SR3	NULL		NULL	NULL	NULL	NULL	gw70_development_131_19_4709_s_208	15329343	(B) YY1 binds to SR3.	bind
10706	1	4331	5	NULL	NULL	0	NULL	ZEN-4	NULL		bind	NULL		E502K		CYK-4	NULL		S15L		NULL		0	NULL	NULL	NULL	gw60_devcell_2_1_41_s_138	11782313	(B) ZEN-4(E502K) binds to CYK-4(S15L).	bind
9905	1	4331	6	NULL	NULL	NULL	NULL	ZEN-4	GP		bind			E502K		CYK-4	GP		S15L		NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_1_41_s_138	11782313	(B) ZEN-4(E502K) binds to CYK-4(S15L).	bind
10707	1	4332	5	NULL	NULL	0	NULL	ZO-1	NULL		bind	NULL	directly	PDZ domains		ARVCF	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_12_5503_s_107	15456900	(B) ZO-1 PDZ domains bind directly to ARVCF in blot overlays.	bind
9906	1	4332	6	NULL	NULL	NULL	NULL	ZO-1	GP		bind		directly	PDZ domain		ARVCF	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5503_s_107	15456900	(B) ZO-1 PDZ domains bind directly to ARVCF in blot overlays.	bind
10708	1	4333	5	10	NULL	0	NULL	[125] adrenomedullin	NULL	rat	bind	NULL				CHO-K1 cell membranes	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1539_1_131_s_73	11389975	(B) [125]Rat adrenomedullin binding to CHO-K1 cell membranes was assayed.	bind
9907	1	4333	6	NULL	NULL	NULL	NULL	[125] adrenomedullin	AminoAcid	rat	bind					CHO-K1 cell membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1539_1_131_s_73	11389975	(B) [125]Rat adrenomedullin binding to CHO-K1 cell membranes was assayed.	bind
10709	1	4335	5	NULL	NULL	0	NULL	HEK-293 cell membranes	NULL		express	NULL				D2R	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_38_2_291_s_175	12718862	(B) [35]GTP S binding to HEK-293 cell membranes expressing D2R was determined after stimulation with dopamine.	bind
10710	2	4335	5	10	NULL	0	NULL	GTP S			bind					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_neuron_38_2_291_s_175	12718862	(B) [35]GTP S binding to HEK-293 cell membranes expressing D2R was determined after stimulation with dopamine.	bind
10711	3	4335	5	NULL	NULL	0	NULL	dopamine	NULL	stimulation by	is required for	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_38_2_291_s_175	12718862	(B) [35]GTP S binding to HEK-293 cell membranes expressing D2R was determined after stimulation with dopamine.	bind
9908	1	4335	6	NULL	NULL	NULL	NULL	HEK-293 cell membranes	CellComponent		express					D2R	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_38_2_291_s_175	12718862	(B) [35]GTP S binding to HEK-293 cell membranes expressing D2R was determined after stimulation with dopamine.	bind
9909	2	4335	6	NULL	NULL	NULL	NULL	GTP S	Chemical		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_38_2_291_s_175	12718862	(B) [35]GTP S binding to HEK-293 cell membranes expressing D2R was determined after stimulation with dopamine.	bind
9910	3	4335	6	NULL	NULL	NULL	NULL	statement 2	Process		after stimulation with					dopamine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_neuron_38_2_291_s_175	12718862	(B) [35]GTP S binding to HEK-293 cell membranes expressing D2R was determined after stimulation with dopamine.	bind
10713	1	4339	5	NULL	NULL	0	NULL	ZEB-1/deltaEF1	NULL		bind	NULL				R-Smads	NULL	activated			NULL		0	NULL	NULL	NULL	gw60_embo_22_10_2443_s_29	12743038	(B, C and D) ZEB-1/deltaEF1 and ZEB-2/SIP1 bind to activated R-Smads.	bind
10714	2	4339	5	NULL	NULL	0	NULL	ZEB-2/SIP1	NULL		bind	NULL				R-Smads	NULL	activated			NULL		0	NULL	NULL	NULL	gw60_embo_22_10_2443_s_29	12743038	(B, C and D) ZEB-1/deltaEF1 and ZEB-2/SIP1 bind to activated R-Smads.	bind
9911	1	4339	6	NULL	NULL	NULL	NULL	ZEB-1/deltaEF1	GP		bind					R-Smads	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_embo_22_10_2443_s_29	12743038	(B, C and D) ZEB-1/deltaEF1 and ZEB-2/SIP1 bind to activated R-Smads.	bind
9912	2	4339	6	NULL	NULL	NULL	NULL	ZEB-2/SIP1	GP		bind					R-Smads	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_embo_22_10_2443_s_29	12743038	(B, C and D) ZEB-1/deltaEF1 and ZEB-2/SIP1 bind to activated R-Smads.	bind
10715	1	4340	5	NULL	NULL	0	NULL	NF-kappaB	NULL		bind	NULL				DNA	NULL				NULL	in lymphocytes exposed to PMA/ionomycin	0	NULL	NULL	NULL	gw60_brjpharmacol_137_6_761_s_177	12411406	(B, C) Identical concentrations of PHE and BZD reduce the DNA binding activity of NF-kappaB and AP-1 in lymphocytes exposed 1 or 2 h to PMA/ionomycin.	bind
10716	2	4340	5	NULL	NULL	0	NULL	AP-1	NULL		bind	NULL				DNA	NULL				NULL	in lymphocytes exposed to PMA/ionomycin	0	NULL	NULL	NULL	gw60_brjpharmacol_137_6_761_s_177	12411406	(B, C) Identical concentrations of PHE and BZD reduce the DNA binding activity of NF-kappaB and AP-1 in lymphocytes exposed 1 or 2 h to PMA/ionomycin.	bind
10717	3	4340	5	NULL	NULL	0	NULL	PHE	NULL		reduce	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_137_6_761_s_177	12411406	(B, C) Identical concentrations of PHE and BZD reduce the DNA binding activity of NF-kappaB and AP-1 in lymphocytes exposed 1 or 2 h to PMA/ionomycin.	bind
10718	4	4340	5	NULL	NULL	0	NULL	PHE	NULL		reduce	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_137_6_761_s_177	12411406	(B, C) Identical concentrations of PHE and BZD reduce the DNA binding activity of NF-kappaB and AP-1 in lymphocytes exposed 1 or 2 h to PMA/ionomycin.	bind
10719	5	4340	5	NULL	NULL	0	NULL	BZD	NULL		reduce	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_137_6_761_s_177	12411406	(B, C) Identical concentrations of PHE and BZD reduce the DNA binding activity of NF-kappaB and AP-1 in lymphocytes exposed 1 or 2 h to PMA/ionomycin.	bind
10720	6	4340	5	NULL	NULL	0	NULL	BZD	NULL		reduce	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_137_6_761_s_177	12411406	(B, C) Identical concentrations of PHE and BZD reduce the DNA binding activity of NF-kappaB and AP-1 in lymphocytes exposed 1 or 2 h to PMA/ionomycin.	bind
9913	1	4340	6	NULL	NULL	NULL	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL	lymphocytes exposed to PMA/ionomycin	NULL	NULL	NULL	NULL	gw60_brjpharmacol_137_6_761_s_177	12411406	(B, C) Identical concentrations of PHE and BZD reduce the DNA binding activity of NF-kappaB and AP-1 in lymphocytes exposed 1 or 2 h to PMA/ionomycin.	bind
9914	2	4340	6	NULL	NULL	NULL	NULL	AP-1	GP		bind					DNA	NucleicAcid				NULL	lymphocytes exposed to PMA/ionomycin	NULL	NULL	NULL	NULL	gw60_brjpharmacol_137_6_761_s_177	12411406	(B, C) Identical concentrations of PHE and BZD reduce the DNA binding activity of NF-kappaB and AP-1 in lymphocytes exposed 1 or 2 h to PMA/ionomycin.	bind
9915	3	4340	6	NULL	NULL	NULL	NULL	PHE			reduce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_137_6_761_s_177	12411406	(B, C) Identical concentrations of PHE and BZD reduce the DNA binding activity of NF-kappaB and AP-1 in lymphocytes exposed 1 or 2 h to PMA/ionomycin.	bind
9916	4	4340	6	NULL	NULL	NULL	NULL	PHE			reduce					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_137_6_761_s_177	12411406	(B, C) Identical concentrations of PHE and BZD reduce the DNA binding activity of NF-kappaB and AP-1 in lymphocytes exposed 1 or 2 h to PMA/ionomycin.	bind
9917	5	4340	6	NULL	NULL	NULL	NULL	BZD	GP		reduce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_137_6_761_s_177	12411406	(B, C) Identical concentrations of PHE and BZD reduce the DNA binding activity of NF-kappaB and AP-1 in lymphocytes exposed 1 or 2 h to PMA/ionomycin.	bind
9918	6	4340	6	NULL	NULL	NULL	NULL	BZD	GP		reduce					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_137_6_761_s_177	12411406	(B, C) Identical concentrations of PHE and BZD reduce the DNA binding activity of NF-kappaB and AP-1 in lymphocytes exposed 1 or 2 h to PMA/ionomycin.	bind
10721	1	4341	5	NULL	NULL	0	NULL	LacI-GFP	NULL		bind	NULL					NULL			 lac operator	NULL	in spo0J+ (strain DCL696) cells	NULL	NULL	NULL	NULL	gw70_jbacteriol_185_4_1326_s_163	12562803	(B, C) Position of sister origin regions (359 degrees ) visualized  with LacI-GFP bound to  lac operator arrays in  spo0J+ (strain DCL696) and  spo0J mutant (strain DCL705) cells.	bind
10722	2	4341	5	NULL	NULL	0	NULL	LacI-GFP	NULL		bind	NULL					NULL			lac operator	NULL	in spo0J mutant (strain DCL705) cells	0	NULL	NULL	NULL	gw70_jbacteriol_185_4_1326_s_163	12562803	(B, C) Position of sister origin regions (359 degrees ) visualized  with LacI-GFP bound to  lac operator arrays in  spo0J+ (strain DCL696) and  spo0J mutant (strain DCL705) cells.	bind
12779	1	4341	6	NULL	NULL	NULL	NULL	LacI-GFP			bind						NucleicAcid			lac operator	NULL	spo0J+ (strain DCL696) cells)	NULL	NULL	NULL	NULL	gw70_jbacteriol_185_4_1326_s_163	12562803	(B, C) Position of sister origin regions (359 degrees ) visualized  with LacI-GFP bound to  lac operator arrays in  spo0J+ (strain DCL696) and  spo0J mutant (strain DCL705) cells.	bind
12780	2	4341	6	NULL	NULL	NULL	NULL	LacI-GFP			bind						NucleicAcid			lac operator	NULL	spo0J mutant (strain DCL705) cells	NULL	NULL	NULL	NULL	gw70_jbacteriol_185_4_1326_s_163	12562803	(B, C) Position of sister origin regions (359 degrees ) visualized  with LacI-GFP bound to  lac operator arrays in  spo0J+ (strain DCL696) and  spo0J mutant (strain DCL705) cells.	bind
10723	1	4343	5	NULL	NULL	0	NULL	EGFR	NULL		does not bind	NULL		tryptic domains		F-actin	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_4_930_s_135	14651960	(B,C)  Tryptic domains of the EGFR do not bind F-actin.	bind
9919	1	4343	6	NULL	NULL	NULL	NULL	EGFR	GP		does not bind			tryptic domains		F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_4_930_s_135	14651960	(B,C)  Tryptic domains of the EGFR do not bind F-actin.	bind
10724	1	4345	5	NULL	NULL	0	NULL		NULL		bind	NULL		envelope domains		HBcAg protein	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_319_3_959_s_123	15184075	(B,C) Binding of envelope domains and HBcAg protein.	bind
9920	1	4345	6	NULL	NULL	NULL	NULL				bind			envelop domains		HBcAg protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_319_3_959_s_123	15184075	(B,C) Binding of envelope domains and HBcAg protein.	bind
10725	1	4346	5	10	NULL	0	NULL	P30-34			bind					DCs					NULL		NULL	NULL	NULL	NULL	gw70_febslett_579_7_1658_s_75	15757657	(B-D) FACS analysis of  P30-34 binding to DCs. (B) DCs were incubated with 3  M of the indicated proteins  for 1.5 h. DCs were then incubated with a rabbit anti-bvPLA2 serum and with a phycoerythrin anti-rabbit IgG antibody.	bind
9942	1	4346	6	NULL	NULL	NULL	NULL	P30-34			bind					DCs	Cell				NULL		NULL	NULL	NULL	NULL	gw70_febslett_579_7_1658_s_75	15757657	(B-D) FACS analysis of  P30-34 binding to DCs. (B) DCs were incubated with 3  M of the indicated proteins  for 1.5 h. DCs were then incubated with a rabbit anti-bvPLA2 serum and with a phycoerythrin anti-rabbit IgG antibody.	bind
10726	1	4348	5	NULL	NULL	0	NULL	Xlim-1	NULL		bind	NULL				cerberus	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_devbiol_257_1_190_s_296	12710967	(B-D) Xlim-1, Mix.1, Siamois, and Xotx2 bind to the  cerberus promoter.	bind
10727	2	4348	5	NULL	NULL	0	NULL	Mix.1	NULL		bind	NULL				cerberus	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_devbiol_257_1_190_s_296	12710967	(B-D) Xlim-1, Mix.1, Siamois, and Xotx2 bind to the  cerberus promoter.	bind
10728	3	4348	5	NULL	NULL	0	NULL	Siamois	NULL		bind	NULL				cerberus	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_devbiol_257_1_190_s_296	12710967	(B-D) Xlim-1, Mix.1, Siamois, and Xotx2 bind to the  cerberus promoter.	bind
10729	4	4348	5	NULL	NULL	0	NULL	Xotx2	NULL		bind	NULL				cerberus	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_devbiol_257_1_190_s_296	12710967	(B-D) Xlim-1, Mix.1, Siamois, and Xotx2 bind to the  cerberus promoter.	bind
9943	1	4348	6	NULL	NULL	NULL	NULL	Xlim-1	GP		bind					cerberus	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_devbiol_257_1_190_s_296	12710967	(B-D) Xlim-1, Mix.1, Siamois, and Xotx2 bind to the  cerberus promoter.	bind
9944	2	4348	6	NULL	NULL	NULL	NULL	Mix.1	GP		bind					cerberus	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_devbiol_257_1_190_s_296	12710967	(B-D) Xlim-1, Mix.1, Siamois, and Xotx2 bind to the  cerberus promoter.	bind
9945	3	4348	6	NULL	NULL	NULL	NULL	Siamois	GP		bind					cerberus	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_devbiol_257_1_190_s_296	12710967	(B-D) Xlim-1, Mix.1, Siamois, and Xotx2 bind to the  cerberus promoter.	bind
9946	4	4348	6	NULL	NULL	NULL	NULL	Xotx2	GP		bind					cerberus	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_devbiol_257_1_190_s_296	12710967	(B-D) Xlim-1, Mix.1, Siamois, and Xotx2 bind to the  cerberus promoter.	bind
11444	1	4349	5	10	NULL	0	NULL	neuropilin-2 ectodomain-Fc		soluble	bind					neuropilin-2					NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_25	9883722	(B-G) Binding of neuropilins in  trans was observed through binding of a soluble neuropilin-2 ectodomain-Fc fusion protein to neuropilin-2(a0) expressed in COS cells (B and E), neuropilin-1 expressed in COS cells (C and F), or control COS cells (D and G) in the absence (B-D) or presence (E-G) of Sema E (similar results were obtained with Sema IV (data not shown)).	bind
11445	2	4349	5	10	NULL	0	NULL	neuropilin-2 ectodomain-Fc		soluble	bind					neuropilin-1					NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_25	9883722	(B-G) Binding of neuropilins in  trans was observed through binding of a soluble neuropilin-2 ectodomain-Fc fusion protein to neuropilin-2(a0) expressed in COS cells (B and E), neuropilin-1 expressed in COS cells (C and F), or control COS cells (D and G) in the absence (B-D) or presence (E-G) of Sema E (similar results were obtained with Sema IV (data not shown)).	bind
44437	3	4349	5	10	NULL	0	NULL	neuropilin-2	NULL		is expressed in	NULL				COS cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_25	9883722	(B-G) Binding of neuropilins in  trans was observed through binding of a soluble neuropilin-2 ectodomain-Fc fusion protein to neuropilin-2(a0) expressed in COS cells (B and E), neuropilin-1 expressed in COS cells (C and F), or control COS cells (D and G) in the absence (B-D) or presence (E-G) of Sema E (similar results were obtained with Sema IV (data not shown)).	bind
44438	4	4349	5	10	NULL	0	NULL	neuropilin-1 	NULL		is expressed in	NULL				COS cells	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_25	9883722	(B-G) Binding of neuropilins in  trans was observed through binding of a soluble neuropilin-2 ectodomain-Fc fusion protein to neuropilin-2(a0) expressed in COS cells (B and E), neuropilin-1 expressed in COS cells (C and F), or control COS cells (D and G) in the absence (B-D) or presence (E-G) of Sema E (similar results were obtained with Sema IV (data not shown)).	bind
57787	5	4349	5	10	NULL	0	NULL	\tneuropilin-2 ectodomain-Fc			is a type of					fusion protein					NULL		0	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_25	9883722	(B-G) Binding of neuropilins in  trans was observed through binding of a soluble neuropilin-2 ectodomain-Fc fusion protein to neuropilin-2(a0) expressed in COS cells (B and E), neuropilin-1 expressed in COS cells (C and F), or control COS cells (D and G) in the absence (B-D) or presence (E-G) of Sema E (similar results were obtained with Sema IV (data not shown)).	bind
9947	1	4349	6	NULL	NULL	NULL	NULL	neuropilin-2 ectodomain-Fc 	GP	soluble	bind					neuropilin-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_25	9883722	(B-G) Binding of neuropilins in  trans was observed through binding of a soluble neuropilin-2 ectodomain-Fc fusion protein to neuropilin-2(a0) expressed in COS cells (B and E), neuropilin-1 expressed in COS cells (C and F), or control COS cells (D and G) in the absence (B-D) or presence (E-G) of Sema E (similar results were obtained with Sema IV (data not shown)).	bind
9948	2	4349	6	NULL	NULL	NULL	NULL	neuropilin-2 ectodomain-Fc	GP	soluble	bind					neuropilin-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_25	9883722	(B-G) Binding of neuropilins in  trans was observed through binding of a soluble neuropilin-2 ectodomain-Fc fusion protein to neuropilin-2(a0) expressed in COS cells (B and E), neuropilin-1 expressed in COS cells (C and F), or control COS cells (D and G) in the absence (B-D) or presence (E-G) of Sema E (similar results were obtained with Sema IV (data not shown)).	bind
9949	3	4349	6	NULL	NULL	NULL	NULL	neuropilin-1	GP		is expressed in					COS cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_25	9883722	(B-G) Binding of neuropilins in  trans was observed through binding of a soluble neuropilin-2 ectodomain-Fc fusion protein to neuropilin-2(a0) expressed in COS cells (B and E), neuropilin-1 expressed in COS cells (C and F), or control COS cells (D and G) in the absence (B-D) or presence (E-G) of Sema E (similar results were obtained with Sema IV (data not shown)).	bind
57788	4	4349	6	NULL	NULL	NULL	NULL	neuropilin-2	GP		is expressed in					COS cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_25	9883722	(B-G) Binding of neuropilins in  trans was observed through binding of a soluble neuropilin-2 ectodomain-Fc fusion protein to neuropilin-2(a0) expressed in COS cells (B and E), neuropilin-1 expressed in COS cells (C and F), or control COS cells (D and G) in the absence (B-D) or presence (E-G) of Sema E (similar results were obtained with Sema IV (data not shown)).	bind
57789	5	4349	6	NULL	NULL	NULL	NULL	neuropilin-2 ectodomain-Fc	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_25	9883722	(B-G) Binding of neuropilins in  trans was observed through binding of a soluble neuropilin-2 ectodomain-Fc fusion protein to neuropilin-2(a0) expressed in COS cells (B and E), neuropilin-1 expressed in COS cells (C and F), or control COS cells (D and G) in the absence (B-D) or presence (E-G) of Sema E (similar results were obtained with Sema IV (data not shown)).	bind
10754	1	4350	5	10	NULL	0	NULL	Sema IV-AP fusion	NULL	full length	bind	NULL				neuropilin-2	NULL	truncated forms of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_129	9883722	(B-J) Binding of AP fusions of full length and truncated versions of Sema IV to truncated forms of neuropilin-2(a0).	bind
10755	2	4350	5	10	NULL	0	NULL	Sema IV-AP fusion		 truncated 	bind					neuropilin-2		truncated forms of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_129	9883722	(B-J) Binding of AP fusions of full length and truncated versions of Sema IV to truncated forms of neuropilin-2(a0).	bind
9950	1	4350	6	NULL	NULL	NULL	NULL	Sema IV-AP fusion	GP	full length	bind					neuropilin-2	GP	truncated forms of 			NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_129	9883722	(B-J) Binding of AP fusions of full length and truncated versions of Sema IV to truncated forms of neuropilin-2(a0).	bind
9951	2	4350	6	NULL	NULL	NULL	NULL	Sema IV-AP fusion	GP	truncated 	bind					neuropilin-2	GP	truncated forms of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_129	9883722	(B-J) Binding of AP fusions of full length and truncated versions of Sema IV to truncated forms of neuropilin-2(a0).	bind
10753	1	4352	5	NULL	NULL	0	NULL	RNA	NULL		bind	NULL				BBR	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_5_2_395_s_58	10882080	(b-m) RNA binding to the BBR (b-g) and DNA binding to the DNA target sequence ATCTAATCCC (h-m) of the wild-type BCD HD (HDwt) and single amino acid replacement mutants.	bind
11446	2	4352	5	NULL	NULL	0	NULL	DNA	NULL		bind	NULL				BCD	NULL	wild-type		DNA target sequence ATCTAATCCC in HD	NULL		0	NULL	NULL	NULL	gw60_molcell_5_2_395_s_58	10882080	(b-m) RNA binding to the BBR (b-g) and DNA binding to the DNA target sequence ATCTAATCCC (h-m) of the wild-type BCD HD (HDwt) and single amino acid replacement mutants.	bind
9952	1	4352	6	NULL	NULL	NULL	NULL	RNA	NucleicAcid		bind					BBR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_2_395_s_58	10882080	(b-m) RNA binding to the BBR (b-g) and DNA binding to the DNA target sequence ATCTAATCCC (h-m) of the wild-type BCD HD (HDwt) and single amino acid replacement mutants.	bind
9953	2	4352	6	NULL	NULL	NULL	NULL	DNA	NucleicAcid		bind					BCD	NucleicAcid	wild type		DNA target sequence ATCTAATCCC in HD	NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_2_395_s_58	10882080	(b-m) RNA binding to the BBR (b-g) and DNA binding to the DNA target sequence ATCTAATCCC (h-m) of the wild-type BCD HD (HDwt) and single amino acid replacement mutants.	bind
11448	1	4354	5	NULL	NULL	0	NULL	Gcn4p	NULL		bind	NULL					NULL			TATA region	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_8_3135_s_72	16581788	(Because the UAS and TATA elements are separated by <200 bp and the sheared chromatin fragments are  500 bp, most fragments containing the TATA element also contain the UAS, likely accounting for the apparent binding of Gcn4p to the TATA region.)	bind
9954	1	4354	6	NULL	NULL	NULL	NULL	Gcn4p	GP		bind						NucleicAcid			TATA box	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_8_3135_s_72	16581788	(Because the UAS and TATA elements are separated by <200 bp and the sheared chromatin fragments are  500 bp, most fragments containing the TATA element also contain the UAS, likely accounting for the apparent binding of Gcn4p to the TATA region.)	bind
10756	1	4355	5	NULL	NULL	0	NULL	CcpC	NULL		bind	NULL				 ccpC	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_1_179_s_234	16352834	(Binding of CcpC to the  ccpC promoter relies on a Box I sequence only and is not affected by citrate [ ]).	bind
10757	2	4355	5	NULL	NULL	0	NULL	statement 1	NULL		relies on	NULL	only				NULL			Box I sequence	NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_1_179_s_234	16352834	(Binding of CcpC to the  ccpC promoter relies on a Box I sequence only and is not affected by citrate [ ]).	bind
10758	3	4355	5	NULL	NULL	0	NULL	statement 1	NULL		is not affected by	NULL				citrate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_1_179_s_234	16352834	(Binding of CcpC to the  ccpC promoter relies on a Box I sequence only and is not affected by citrate [ ]).	bind
9955	1	4355	6	NULL	NULL	NULL	NULL	CcpC	GP		bind					ccpC	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_1_179_s_234	16352834	(Binding of CcpC to the  ccpC promoter relies on a Box I sequence only and is not affected by citrate [ ]).	bind
9956	2	4355	6	NULL	NULL	NULL	NULL	statement 1	Process		is not affected by					citrate	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_1_179_s_234	16352834	(Binding of CcpC to the  ccpC promoter relies on a Box I sequence only and is not affected by citrate [ ]).	bind
9957	3	4355	6	NULL	NULL	NULL	NULL	statement 1	Process		is dependent on		only				NucleicAcid			Box I sequence	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_1_179_s_234	16352834	(Binding of CcpC to the  ccpC promoter relies on a Box I sequence only and is not affected by citrate [ ]).	bind
10759	1	4358	5	NULL	NULL	0	NULL	I-mfa	NULL		bind	NULL				Axin	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_271	12192039	(Bottom panel) I-mfa binding to Axin does not affect the binding of GSK-3beta, and the activation of JNK is decreased.	bind
10760	2	4358	5	NULL	NULL	0	NULL	statement 1	NULL		does not affect	NULL				GSK-3beta	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_271	12192039	(Bottom panel) I-mfa binding to Axin does not affect the binding of GSK-3beta, and the activation of JNK is decreased.	bind
10837	3	4358	5	NULL	NULL	0	NULL	statement 1	NULL		decrease	NULL				JNK	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_271	12192039	(Bottom panel) I-mfa binding to Axin does not affect the binding of GSK-3beta, and the activation of JNK is decreased.	bind
9958	1	4358	6	NULL	NULL	NULL	NULL	 I-mfa	GP		bind					Axin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_271	12192039	(Bottom panel) I-mfa binding to Axin does not affect the binding of GSK-3beta, and the activation of JNK is decreased.	bind
9959	2	4358	6	NULL	NULL	NULL	NULL	statement 1	Process		does not affect					GSK-3beta	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_271	12192039	(Bottom panel) I-mfa binding to Axin does not affect the binding of GSK-3beta, and the activation of JNK is decreased.	bind
12676	3	4358	6	NULL	NULL	NULL	NULL	statement 1	Process		decrease					JNK	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_271	12192039	(Bottom panel) I-mfa binding to Axin does not affect the binding of GSK-3beta, and the activation of JNK is decreased.	bind
10838	1	4361	5	NULL	NULL	0	NULL	HVEM:Fc	NULL		bind	NULL				II-23 cells	NULL	activated			NULL		0	NULL	NULL	NULL	gw60_immunity_8_1_21_s_65	9462508	(Bottom) dose dependence of LT  competition for HVEM:Fc binding to activated II-23 cells as determined by flow cytofluorometry.	bind
10839	2	4361	5	NULL	NULL	0	NULL	LT	NULL		bind	NULL				II-23 cells	NULL	activated			NULL		0	NULL	NULL	NULL	gw60_immunity_8_1_21_s_65	9462508	(Bottom) dose dependence of LT  competition for HVEM:Fc binding to activated II-23 cells as determined by flow cytofluorometry.	bind
10840	3	4361	5	NULL	NULL	0	NULL	statement 2	NULL		compete with	NULL	dose dependently			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_8_1_21_s_65	9462508	(Bottom) dose dependence of LT  competition for HVEM:Fc binding to activated II-23 cells as determined by flow cytofluorometry.	bind
9960	1	4361	6	NULL	NULL	NULL	NULL	HVEM:Fc	GP		bind					II-23 cells	Cell	activated			NULL		NULL	NULL	NULL	NULL	gw60_immunity_8_1_21_s_65	9462508	(Bottom) dose dependence of LT  competition for HVEM:Fc binding to activated II-23 cells as determined by flow cytofluorometry.	bind
9961	2	4361	6	NULL	NULL	NULL	NULL	LT	GP		bind					II-23 cells	Cell	activated			NULL		NULL	NULL	NULL	NULL	gw60_immunity_8_1_21_s_65	9462508	(Bottom) dose dependence of LT  competition for HVEM:Fc binding to activated II-23 cells as determined by flow cytofluorometry.	bind
9962	3	4361	6	NULL	NULL	NULL	NULL	statement 1	Process		competes		dose dependently			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_8_1_21_s_65	9462508	(Bottom) dose dependence of LT  competition for HVEM:Fc binding to activated II-23 cells as determined by flow cytofluorometry.	bind
10841	1	4362	5	NULL	NULL	0	NULL	LT R:Fc	NULL		inhibit	NULL	dose dependently			HVEM:Fc	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_immunity_8_1_21_s_59	9462508	(Bottom) dose-dependent inhibition of HVEM:Fc binding by LT R:Fc.	bind
9963	1	4362	6	NULL	NULL	NULL	NULL	LT R:Fc	GP		inhibits		dose dependently			HVEM:Fc	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_8_1_21_s_59	9462508	(Bottom) dose-dependent inhibition of HVEM:Fc binding by LT R:Fc.	bind
10842	1	4364	5	NULL	NULL	0	NULL	eIF2beta	NULL		bind	NULL				p97	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_25_17_4008_s_76	16932749	(Bottom) eIF2beta bound to p97 was quantified with a densitometer.	bind
9964	1	4364	6	NULL	NULL	NULL	NULL	eIF2beta	GP		bind					p97	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_17_4008_s_76	16932749	(Bottom) eIF2beta bound to p97 was quantified with a densitometer.	bind
10843	1	4365	5	NULL	NULL	0	NULL	S. pneumoniae cells	NULL	FITC-labeled	adhere to	NULL				CHO-ICAM-1 cells	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_74_2_830_s_121	16428725	(Bottom) Few FITC-labeled  S. pneumoniae cells (green) adhere to CHO-ICAM-1 cells.	bind
9965	1	4365	6	NULL	NULL	NULL	NULL	S. pneumoniae cells	Cell	FITC labeled	adhere to					CHO-ICAM-1 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_2_830_s_121	16428725	(Bottom) Few FITC-labeled  S. pneumoniae cells (green) adhere to CHO-ICAM-1 cells.	bind
10876	2	4366	5	10	NULL	0	NULL	statement 1			bind					PP1					NULL		NULL	NULL	NULL	NULL	gw60_cell_105_1_115_s_84	11301007	(Bottom) Fluctuations  in the simulation of three states of  the enzyme: (i) The inactive and assembled structure (including  SH2 and SH3) bound to PP1 (blue), (ii) the isolated  kinase domain in the absence of the  SH3 and SH2 domains bound to PP1  (green), and (iii) the isolated kinase domain in the  absence of PP1 (red).	bind
10877	1	4366	5	10	NULL	0	NULL	assembled structure			include								SH2 and SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_105_1_115_s_84	11301007	(Bottom) Fluctuations  in the simulation of three states of  the enzyme: (i) The inactive and assembled structure (including  SH2 and SH3) bound to PP1 (blue), (ii) the isolated  kinase domain in the absence of the  SH3 and SH2 domains bound to PP1  (green), and (iii) the isolated kinase domain in the  absence of PP1 (red).	bind
10878	3	4366	5	10	NULL	0	NULL			isolated	bind			kinase domain		PP1					NULL		NULL	NULL	NULL	NULL	gw60_cell_105_1_115_s_84	11301007	(Bottom) Fluctuations  in the simulation of three states of  the enzyme: (i) The inactive and assembled structure (including  SH2 and SH3) bound to PP1 (blue), (ii) the isolated  kinase domain in the absence of the  SH3 and SH2 domains bound to PP1  (green), and (iii) the isolated kinase domain in the  absence of PP1 (red).	bind
10879	4	4366	5	10	NULL	0	NULL	statement 3			in the absence of								SH2 domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_105_1_115_s_84	11301007	(Bottom) Fluctuations  in the simulation of three states of  the enzyme: (i) The inactive and assembled structure (including  SH2 and SH3) bound to PP1 (blue), (ii) the isolated  kinase domain in the absence of the  SH3 and SH2 domains bound to PP1  (green), and (iii) the isolated kinase domain in the  absence of PP1 (red).	bind
10880	5	4366	5	10	NULL	0	NULL	statement 3			in the absence of								SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_105_1_115_s_84	11301007	(Bottom) Fluctuations  in the simulation of three states of  the enzyme: (i) The inactive and assembled structure (including  SH2 and SH3) bound to PP1 (blue), (ii) the isolated  kinase domain in the absence of the  SH3 and SH2 domains bound to PP1  (green), and (iii) the isolated kinase domain in the  absence of PP1 (red).	bind
9966	1	4366	6	10	NULL	0	NULL	assembled structure			include								SH2 and SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_105_1_115_s_84	11301007	(Bottom) Fluctuations  in the simulation of three states of  the enzyme: (i) The inactive and assembled structure (including  SH2 and SH3) bound to PP1 (blue), (ii) the isolated  kinase domain in the absence of the  SH3 and SH2 domains bound to PP1  (green), and (iii) the isolated kinase domain in the  absence of PP1 (red).	bind
9967	2	4366	6	NULL	NULL	NULL	NULL	statement 1	Process		bind					PP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_105_1_115_s_84	11301007	(Bottom) Fluctuations  in the simulation of three states of  the enzyme: (i) The inactive and assembled structure (including  SH2 and SH3) bound to PP1 (blue), (ii) the isolated  kinase domain in the absence of the  SH3 and SH2 domains bound to PP1  (green), and (iii) the isolated kinase domain in the  absence of PP1 (red).	bind
9968	3	4366	6	NULL	NULL	NULL	NULL			isolated	bind			kinase domain		PP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_105_1_115_s_84	11301007	(Bottom) Fluctuations  in the simulation of three states of  the enzyme: (i) The inactive and assembled structure (including  SH2 and SH3) bound to PP1 (blue), (ii) the isolated  kinase domain in the absence of the  SH3 and SH2 domains bound to PP1  (green), and (iii) the isolated kinase domain in the  absence of PP1 (red).	bind
54265	4	4366	6	NULL	NULL	NULL	NULL	statement 3			in the absence of								SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_105_1_115_s_84	11301007	(Bottom) Fluctuations  in the simulation of three states of  the enzyme: (i) The inactive and assembled structure (including  SH2 and SH3) bound to PP1 (blue), (ii) the isolated  kinase domain in the absence of the  SH3 and SH2 domains bound to PP1  (green), and (iii) the isolated kinase domain in the  absence of PP1 (red).	bind
54266	5	4366	6	10	NULL	0	NULL	statement 3			in the absence of								SH2 domain		NULL		0	NULL	NULL	NULL	gw60_cell_105_1_115_s_84	11301007	(Bottom) Fluctuations  in the simulation of three states of  the enzyme: (i) The inactive and assembled structure (including  SH2 and SH3) bound to PP1 (blue), (ii) the isolated  kinase domain in the absence of the  SH3 and SH2 domains bound to PP1  (green), and (iii) the isolated kinase domain in the  absence of PP1 (red).	bind
10881	1	4367	5	10	NULL	0	NULL	Bmp Smads	NULL		bind	NULL	specifically				NULL			SBE	NULL	embryonic hindlimb 	NULL	NULL	NULL	NULL	gw70_development_133_8_1575_s_239	16556916	(Bottom) In vivo ChIP analysis utilizing extracts from  embryonic hindlimb and an antibody specific for Bmp Smads demonstrated specific binding  of Bmp Smads to a region containing the Smad binding element (SBE; 2).	bind
10882	2	4367	5	NULL	NULL	0	NULL	SBE	NULL		is	NULL				Smad binding element	NULL				NULL		0	NULL	NULL	NULL	gw70_development_133_8_1575_s_239	16556916	(Bottom) In vivo ChIP analysis utilizing extracts from  embryonic hindlimb and an antibody specific for Bmp Smads demonstrated specific binding  of Bmp Smads to a region containing the Smad binding element (SBE; 2).	bind
9969	1	4367	6	NULL	NULL	NULL	NULL	Bmp Smads	GP		bind		specifically							SBE	NULL	extracts from embryonic hindlimb	NULL	NULL	NULL	NULL	gw70_development_133_8_1575_s_239	16556916	(Bottom) In vivo ChIP analysis utilizing extracts from  embryonic hindlimb and an antibody specific for Bmp Smads demonstrated specific binding  of Bmp Smads to a region containing the Smad binding element (SBE; 2).	bind
9970	2	4367	6	NULL	NULL	0	NULL	SBE	NULL		is	NULL				Smad binding element	NULL				NULL		0	NULL	NULL	NULL	gw70_development_133_8_1575_s_239	16556916	(Bottom) In vivo ChIP analysis utilizing extracts from  embryonic hindlimb and an antibody specific for Bmp Smads demonstrated specific binding  of Bmp Smads to a region containing the Smad binding element (SBE; 2).	bind
10883	1	4368	5	NULL	NULL	0	NULL	RNA	NULL		bind	NULL					NULL		RBD (E29C) 		NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_9_1899_s_171	10756189	(Bottom) Representative plot of fraction RNA bound by RBD (E29C) as a function of protein concentration.	bind
9971	1	4368	6	NULL	NULL	NULL	NULL	 RNA	NucleicAcid		bind								RBD (E29C)		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_9_1899_s_171	10756189	(Bottom) Representative plot of fraction RNA bound by RBD (E29C) as a function of protein concentration.	bind
10887	1	4371	5	NULL	NULL	0	NULL	K+ channel Kv1.4	NULL		bind	NULL	specifically			PSD-95	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_24_3_659_s_46	10595517	(Bottom) Western blotting shows that the K+ channel Kv1.4 also specifically binds to the PSD-95 column.	bind
9972	1	4371	6	NULL	NULL	NULL	NULL	K+ channel Kv1.4	GP		bind		specifically			PSD-95	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_3_659_s_46	10595517	(Bottom) Western blotting shows that the K+ channel Kv1.4 also specifically binds to the PSD-95 column.	bind
10889	1	4373	5	10	NULL	0	NULL	L. monocytogenes genome			contain					target sites for CcpC regulation				between positions - 300 and +100 to translational start site	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_1_179_s_162	16352834	(Box I: ATAA-N7-TTAT) ( ). Using this CcpC consensus binding site, we searched the  L. monocytogenes genome and identified 92 potential target sites for CcpC regulation located between positions  - 300 and +100 with respect to a translational start site.	bind
12781	1	4373	6	NULL	NULL	NULL	NULL	L. monocytogenes genome	Organism		contains					targets sites for CcpC regulation	GP			between positions - 300 and +100 to translational start site	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_1_179_s_162	16352834	(Box I: ATAA-N7-TTAT) ( ). Using this CcpC consensus binding site, we searched the  L. monocytogenes genome and identified 92 potential target sites for CcpC regulation located between positions  - 300 and +100 with respect to a translational start site.	bind
10892	1	4376	5	NULL	NULL	0	NULL	tropomyosin	NULL		bind	NULL				actin-myosin S-1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_12867_s_68	8662810	(By equilibrium linkage ( 6,  7) this in turn implies that troponin promotes tropomyosin binding to actin-myosin S-1.)	bind
10893	2	4376	5	NULL	NULL	0	NULL	troponin	NULL		promote	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_12867_s_68	8662810	(By equilibrium linkage ( 6,  7) this in turn implies that troponin promotes tropomyosin binding to actin-myosin S-1.)	bind
9973	1	4376	6	NULL	NULL	NULL	NULL	tropomyosin	GP		bind					actin-myosin S-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_12867_s_68	8662810	(By equilibrium linkage ( 6,  7) this in turn implies that troponin promotes tropomyosin binding to actin-myosin S-1.)	bind
9974	2	4376	6	NULL	NULL	NULL	NULL	troponin	GP		promotes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_12867_s_68	8662810	(By equilibrium linkage ( 6,  7) this in turn implies that troponin promotes tropomyosin binding to actin-myosin S-1.)	bind
10896	1	4377	5	NULL	NULL	0	NULL	E. coli	NULL		bind	NULL				BECs	NULL	human			NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_4_1947_s_142	15784534	(C  and D) Binding of  E. coli to human BECs visualized by using rhodamine-labeled  A. actinomycetemcomitans against a fluorescein-cytokeratin-labeled BEC background.	bind
9975	1	4377	6	NULL	NULL	NULL	NULL	E.coli	Organism		bind					BECs	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_4_1947_s_142	15784534	(C  and D) Binding of  E. coli to human BECs visualized by using rhodamine-labeled  A. actinomycetemcomitans against a fluorescein-cytokeratin-labeled BEC background.	bind
10897	1	4378	5	NULL	NULL	0	NULL	COS cells	NULL		express	NULL				neuropilin	NULL	rat			NULL		0	NULL	NULL	NULL	gw60_cell_90_4_739_s_90	9288753	(C - H) Binding of various AP  fusion proteins to COS cells expressing rat neuropilin.	bind
10898	2	4378	5	NULL	NULL	0	NULL	AP fusion proteins	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_90_4_739_s_90	9288753	(C - H) Binding of various AP  fusion proteins to COS cells expressing rat neuropilin.	bind
9995	2	4378	6	NULL	NULL	NULL	NULL	AP fusion proteins	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_4_739_s_90	9288753	(C - H) Binding of various AP  fusion proteins to COS cells expressing rat neuropilin.	bind
54267	1	4378	6	NULL	NULL	NULL	NULL	COS cells	Cell		express					neuropilin	GP	rat			NULL		NULL	NULL	NULL	NULL	gw60_cell_90_4_739_s_90	9288753	(C - H) Binding of various AP  fusion proteins to COS cells expressing rat neuropilin.	bind
10899	1	4379	5	10	NULL	0	NULL	Tbx5	NULL		bind	NULL				 ANF	NULL			TBE	NULL		NULL	NULL	NULL	NULL	gw60_cell_106_6_709_s_188	11572777	(C and  D) Tbx5 binds to the  ANF and  cx40  TBEs.	bind
10901	2	4379	5	10	NULL	0	NULL	Tbx5	NULL		bind	NULL				cx40	NULL			TBE	NULL		NULL	NULL	NULL	NULL	gw60_cell_106_6_709_s_188	11572777	(C and  D) Tbx5 binds to the  ANF and  cx40  TBEs.	bind
9996	1	4379	6	NULL	NULL	NULL	NULL	Tbx5	GP		bind					ANF	GP			TBE	NULL		NULL	NULL	NULL	NULL	gw60_cell_106_6_709_s_188	11572777	(C and  D) Tbx5 binds to the  ANF and  cx40  TBEs.	bind
9997	2	4379	6	NULL	NULL	NULL	NULL	Tbx5	GP		bind					cx40	GP			TBE	NULL		NULL	NULL	NULL	NULL	gw60_cell_106_6_709_s_188	11572777	(C and  D) Tbx5 binds to the  ANF and  cx40  TBEs.	bind
10902	1	4380	5	NULL	NULL	0	NULL	Raf-1	NULL		bind	NULL				Rb	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_177	15485920	(C and D)  The presence of 1 muM penetratin-Raf-1 peptide conjugate markedly inhibits the binding  of Raf-1 to Rb (C), whereas a scrambled peptide conjugate is unable to do so (D).	bind
10903	2	4380	5	NULL	NULL	0	NULL	penetratin-Raf-1 peptide conjugate	NULL		inhibit	NULL	markedly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_177	15485920	(C and D)  The presence of 1 muM penetratin-Raf-1 peptide conjugate markedly inhibits the binding  of Raf-1 to Rb (C), whereas a scrambled peptide conjugate is unable to do so (D).	bind
10904	3	4380	5	NULL	NULL	0	NULL	scrambled peptide conjugate	NULL		does not inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_177	15485920	(C and D)  The presence of 1 muM penetratin-Raf-1 peptide conjugate markedly inhibits the binding  of Raf-1 to Rb (C), whereas a scrambled peptide conjugate is unable to do so (D).	bind
9998	1	4380	6	NULL	NULL	NULL	NULL	Raf-1	GP		bind					Rb	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_177	15485920	(C and D)  The presence of 1 muM penetratin-Raf-1 peptide conjugate markedly inhibits the binding  of Raf-1 to Rb (C), whereas a scrambled peptide conjugate is unable to do so (D).	bind
9999	2	4380	6	NULL	NULL	NULL	NULL	penetratin-Raf-1 peptide 	AminoAcid		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_177	15485920	(C and D)  The presence of 1 muM penetratin-Raf-1 peptide conjugate markedly inhibits the binding  of Raf-1 to Rb (C), whereas a scrambled peptide conjugate is unable to do so (D).	bind
10000	3	4380	6	NULL	NULL	NULL	NULL	scrambled peptide conjugate	AminoAcid		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_177	15485920	(C and D)  The presence of 1 muM penetratin-Raf-1 peptide conjugate markedly inhibits the binding  of Raf-1 to Rb (C), whereas a scrambled peptide conjugate is unable to do so (D).	bind
10905	1	4381	5	NULL	NULL	0	NULL	AfaF	NULL		bind	NULL				Lrp	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_229	12618452	(C and D) AfaF bound to Lrp allows Lrp binding to GATCdist in phase-ON cells (C) and increases Lrp binding to GATCprox in phase-OFF cells (D).	bind
10909	2	4381	5	NULL	NULL	0	NULL	Lrp	NULL		bind	NULL					NULL			GATCdist	NULL	phase-ON cells	0	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_229	12618452	(C and D) AfaF bound to Lrp allows Lrp binding to GATCdist in phase-ON cells (C) and increases Lrp binding to GATCprox in phase-OFF cells (D).	bind
10911	3	4381	5	NULL	NULL	0	NULL	statement 1	NULL		allows	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_229	12618452	(C and D) AfaF bound to Lrp allows Lrp binding to GATCdist in phase-ON cells (C) and increases Lrp binding to GATCprox in phase-OFF cells (D).	bind
10913	4	4381	5	NULL	NULL	0	NULL	Lrp	NULL		bind	NULL					NULL			GATCprox	NULL	phase-OFF cells	0	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_229	12618452	(C and D) AfaF bound to Lrp allows Lrp binding to GATCdist in phase-ON cells (C) and increases Lrp binding to GATCprox in phase-OFF cells (D).	bind
10914	5	4381	5	NULL	NULL	0	NULL	statement 1	NULL		increase	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_229	12618452	(C and D) AfaF bound to Lrp allows Lrp binding to GATCdist in phase-ON cells (C) and increases Lrp binding to GATCprox in phase-OFF cells (D).	bind
10001	1	4381	6	NULL	NULL	NULL	NULL	AfaF	GP		bind					Lrp	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_229	12618452	(C and D) AfaF bound to Lrp allows Lrp binding to GATCdist in phase-ON cells (C) and increases Lrp binding to GATCprox in phase-OFF cells (D).	bind
10002	2	4381	6	NULL	NULL	NULL	NULL	Lrp	GP		bind									GATCdist	NULL	phase-ON cells	NULL	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_229	12618452	(C and D) AfaF bound to Lrp allows Lrp binding to GATCdist in phase-ON cells (C) and increases Lrp binding to GATCprox in phase-OFF cells (D).	bind
10003	3	4381	6	NULL	NULL	NULL	NULL	Lrp	GP		bind									GATCprox	NULL	phase-OFF cells	NULL	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_229	12618452	(C and D) AfaF bound to Lrp allows Lrp binding to GATCdist in phase-ON cells (C) and increases Lrp binding to GATCprox in phase-OFF cells (D).	bind
10004	4	4381	6	NULL	NULL	NULL	NULL	statement 1	Process		allows					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_229	12618452	(C and D) AfaF bound to Lrp allows Lrp binding to GATCdist in phase-ON cells (C) and increases Lrp binding to GATCprox in phase-OFF cells (D).	bind
10005	5	4381	6	NULL	NULL	NULL	NULL	statement 1	Process		increases					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_6_1886_s_229	12618452	(C and D) AfaF bound to Lrp allows Lrp binding to GATCdist in phase-ON cells (C) and increases Lrp binding to GATCprox in phase-OFF cells (D).	bind
10941	1	4382	5	NULL	NULL	0	NULL	E(spl)bHLH proteins	NULL		bind	NULL				B1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4600_s_149	10373509	(C and D) Binding of E(spl)bHLH proteins to B1, A1, and A2 (Table  1).	bind
10942	2	4382	5	NULL	NULL	0	NULL	E(spl)bHLH proteins	NULL		bind	NULL				A1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4600_s_149	10373509	(C and D) Binding of E(spl)bHLH proteins to B1, A1, and A2 (Table  1).	bind
10943	3	4382	5	NULL	NULL	0	NULL	E(spl)bHLH proteins	NULL		bind	NULL				A2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4600_s_149	10373509	(C and D) Binding of E(spl)bHLH proteins to B1, A1, and A2 (Table  1).	bind
10795	1	4382	6	NULL	NULL	NULL	NULL	E(spl)bHLH proteins	GP		bind					B1					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4600_s_149	10373509	(C and D) Binding of E(spl)bHLH proteins to B1, A1, and A2 (Table  1).	bind
10796	2	4382	6	NULL	NULL	NULL	NULL	E(spl)bHLH proteins	GP		bind					A1					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4600_s_149	10373509	(C and D) Binding of E(spl)bHLH proteins to B1, A1, and A2 (Table  1).	bind
10797	3	4382	6	NULL	NULL	NULL	NULL	E(spl)bHLH proteins	GP		bind					A2					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4600_s_149	10373509	(C and D) Binding of E(spl)bHLH proteins to B1, A1, and A2 (Table  1).	bind
10944	1	4383	5	NULL	NULL	0	NULL	Bl	NULL		bind	NULL				ribonucleotide homopolymers	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_11_7846_s_145	10523673	(C and D) Binding of the Bl and human K proteins to ribonucleotide homopolymers.	bind
10945	2	4383	5	NULL	NULL	0	NULL	K proteins	NULL	human	bind	NULL				ribonucleotide homopolymers	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_11_7846_s_145	10523673	(C and D) Binding of the Bl and human K proteins to ribonucleotide homopolymers.	bind
10127	1	4383	6	NULL	NULL	NULL	NULL	B1			bind					ribonucleotide polymers	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7846_s_145	10523673	(C and D) Binding of the Bl and human K proteins to ribonucleotide homopolymers.	bind
10128	2	4383	6	NULL	NULL	NULL	NULL	K protein	GP	human	bind					ribonucleotide polymers	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7846_s_145	10523673	(C and D) Binding of the Bl and human K proteins to ribonucleotide homopolymers.	bind
11602	1	4384	5	NULL	NULL	0	NULL	myc-Gcn4p	NULL		bind	NULL				ARG1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8829_s_79	14612422	(C and D) ChIP analysis was conducted as described above to measure binding  of myc-Gcn4p to  ARG1 (C) or  SNZ1 (D) in the following strains: transformants of the  gcn4delta strains containing either all WT SWI/SNF genes (249),  snf2delta (SY169),  swi3delta (SY294),  snf6delta (SY295),  snf11delta (SY296),  snf5delta (SY327), or  swp73delta (SY298), all bearing single-copy plasmid pSK1 containing  GCN4-myc, lanes 2 through 8;  gcn4delta strain (249) transformed with empty vector YCp50 or single-copy plasmid pSY284 containing   gcn4-14Ala-myc, respectively, lanes 1 and 9.	bind
11603	2	4384	5	NULL	NULL	0	NULL	myc-Gcn4p	NULL		bind	NULL				SNZ1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8829_s_79	14612422	(C and D) ChIP analysis was conducted as described above to measure binding  of myc-Gcn4p to  ARG1 (C) or  SNZ1 (D) in the following strains: transformants of the  gcn4delta strains containing either all WT SWI/SNF genes (249),  snf2delta (SY169),  swi3delta (SY294),  snf6delta (SY295),  snf11delta (SY296),  snf5delta (SY327), or  swp73delta (SY298), all bearing single-copy plasmid pSK1 containing  GCN4-myc, lanes 2 through 8;  gcn4delta strain (249) transformed with empty vector YCp50 or single-copy plasmid pSY284 containing   gcn4-14Ala-myc, respectively, lanes 1 and 9.	bind
11604	3	4384	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8829_s_79	14612422	(C and D) ChIP analysis was conducted as described above to measure binding  of myc-Gcn4p to  ARG1 (C) or  SNZ1 (D) in the following strains: transformants of the  gcn4delta strains containing either all WT SWI/SNF genes (249),  snf2delta (SY169),  swi3delta (SY294),  snf6delta (SY295),  snf11delta (SY296),  snf5delta (SY327), or  swp73delta (SY298), all bearing single-copy plasmid pSK1 containing  GCN4-myc, lanes 2 through 8;  gcn4delta strain (249) transformed with empty vector YCp50 or single-copy plasmid pSY284 containing   gcn4-14Ala-myc, respectively, lanes 1 and 9.	bind
10798	1	4384	6	NULL	NULL	NULL	NULL	myc-Gcn4p	GP		bind					ARG1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8829_s_79	14612422	(C and D) ChIP analysis was conducted as described above to measure binding  of myc-Gcn4p to  ARG1 (C) or  SNZ1 (D) in the following strains: transformants of the  gcn4delta strains containing either all WT SWI/SNF genes (249),  snf2delta (SY169),  swi3delta (SY294),  snf6delta (SY295),  snf11delta (SY296),  snf5delta (SY327), or  swp73delta (SY298), all bearing single-copy plasmid pSK1 containing  GCN4-myc, lanes 2 through 8;  gcn4delta strain (249) transformed with empty vector YCp50 or single-copy plasmid pSY284 containing   gcn4-14Ala-myc, respectively, lanes 1 and 9.	bind
10799	2	4384	6	NULL	NULL	NULL	NULL	myc-Gcn4p	GP		bind					SNZ1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8829_s_79	14612422	(C and D) ChIP analysis was conducted as described above to measure binding  of myc-Gcn4p to  ARG1 (C) or  SNZ1 (D) in the following strains: transformants of the  gcn4delta strains containing either all WT SWI/SNF genes (249),  snf2delta (SY169),  swi3delta (SY294),  snf6delta (SY295),  snf11delta (SY296),  snf5delta (SY327), or  swp73delta (SY298), all bearing single-copy plasmid pSK1 containing  GCN4-myc, lanes 2 through 8;  gcn4delta strain (249) transformed with empty vector YCp50 or single-copy plasmid pSY284 containing   gcn4-14Ala-myc, respectively, lanes 1 and 9.	bind
10800	3	4384	6	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8829_s_79	14612422	(C and D) ChIP analysis was conducted as described above to measure binding  of myc-Gcn4p to  ARG1 (C) or  SNZ1 (D) in the following strains: transformants of the  gcn4delta strains containing either all WT SWI/SNF genes (249),  snf2delta (SY169),  swi3delta (SY294),  snf6delta (SY295),  snf11delta (SY296),  snf5delta (SY327), or  swp73delta (SY298), all bearing single-copy plasmid pSK1 containing  GCN4-myc, lanes 2 through 8;  gcn4delta strain (249) transformed with empty vector YCp50 or single-copy plasmid pSY284 containing   gcn4-14Ala-myc, respectively, lanes 1 and 9.	bind
10946	1	4385	5	NULL	NULL	0	NULL	T1 reovirus strains	NULL		bind	NULL				NT2 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_104_3_441_s_110	11239401	(C and D) Effect of anti-hJAM mAbs on binding of T1 and T3 reovirus strains to NT2 cells.	bind
10947	2	4385	5	NULL	NULL	0	NULL	T3 reovirus strains	NULL		bind	NULL				NT2 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_104_3_441_s_110	11239401	(C and D) Effect of anti-hJAM mAbs on binding of T1 and T3 reovirus strains to NT2 cells.	bind
10130	1	4385	6	NULL	NULL	NULL	NULL	T1 reovirus	Organism		bind					NT2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cell_104_3_441_s_110	11239401	(C and D) Effect of anti-hJAM mAbs on binding of T1 and T3 reovirus strains to NT2 cells.	bind
10131	2	4385	6	NULL	NULL	NULL	NULL	T3 reovirus	Organism		bind					NT2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cell_104_3_441_s_110	11239401	(C and D) Effect of anti-hJAM mAbs on binding of T1 and T3 reovirus strains to NT2 cells.	bind
10950	1	4386	5	NULL	NULL	0	NULL	P300 protein	NULL	endogenous	bind	NULL				p53 protein isoforms	NULL	total			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_298	14612423	(C and D) Endogenous P300 protein was immunoprecipitated with an anti-p300  antibody, and levels of total p53 protein isoforms (C) or acetylated p53 isoforms  (D) bound to p300 were quantitated by immunoblotting with either the acetylation-specific  antibody or a p53 protein antibody to normalize to the total p53 protein.	bind
10951	2	4386	5	NULL	NULL	0	NULL	P300 protein	NULL	endogenous	bind	NULL				p53 protein isoforms	NULL	acetylated			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_298	14612423	(C and D) Endogenous P300 protein was immunoprecipitated with an anti-p300  antibody, and levels of total p53 protein isoforms (C) or acetylated p53 isoforms  (D) bound to p300 were quantitated by immunoblotting with either the acetylation-specific  antibody or a p53 protein antibody to normalize to the total p53 protein.	bind
10132	1	4386	6	NULL	NULL	NULL	NULL	p53	GP	acetylated	bind					p300	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_298	14612423	(C and D) Endogenous P300 protein was immunoprecipitated with an anti-p300  antibody, and levels of total p53 protein isoforms (C) or acetylated p53 isoforms  (D) bound to p300 were quantitated by immunoblotting with either the acetylation-specific  antibody or a p53 protein antibody to normalize to the total p53 protein.	bind
12782	2	4386	6	NULL	NULL	NULL	NULL	p53	GP	total	bind					p300	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_298	14612423	(C and D) Endogenous P300 protein was immunoprecipitated with an anti-p300  antibody, and levels of total p53 protein isoforms (C) or acetylated p53 isoforms  (D) bound to p300 were quantitated by immunoblotting with either the acetylation-specific  antibody or a p53 protein antibody to normalize to the total p53 protein.	bind
10952	1	4387	5	10	NULL	0	NULL	Etheno-ATP			bind					Arp2/3 complex		purified;;mutant			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_315_s_81	15657399	(C and D) Etheno-ATP binding to purified Arp2/3 complex mutants.	bind
10134	1	4387	6	NULL	NULL	NULL	NULL	Etheno-ATP	Chemical		bind					Arp2/3 complex	GP	purified;;mutant			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_315_s_81	15657399	(C and D) Etheno-ATP binding to purified Arp2/3 complex mutants.	bind
10953	1	4388	5	NULL	NULL	0	NULL	GADD34	NULL		bind	NULL				Smad7	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_164_2_291_s_76	14718519	(c and d) Experiments were performed in both yeast  (c) and mammalian (d) systems, as in  Fig. 1, to map GADD34 binding to Smad7.	bind
10135	1	4388	6	NULL	NULL	NULL	NULL	GADD34	GP		bind					Smad7	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_291_s_76	14718519	(c and d) Experiments were performed in both yeast  (c) and mammalian (d) systems, as in  Fig. 1, to map GADD34 binding to Smad7.	bind
10954	1	4389	5	10	NULL	0	NULL	plasmid p28			confers					Sema III		binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_cell_90_4_739_s_67	9288753	(C and D) Following isolation of plasmid p28, which confers Sema III - binding  activity, Sema III - AP (D) but not AP (C) was found to bind cells transiently transfected  with p28.	bind
10955	3	4389	5	NULL	NULL	0	NULL	Sema III - AP	NULL		bind	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_4_739_s_67	9288753	(C and D) Following isolation of plasmid p28, which confers Sema III - binding  activity, Sema III - AP (D) but not AP (C) was found to bind cells transiently transfected  with p28.	bind
10956	4	4389	5	NULL	NULL	0	NULL	AP	NULL		does not bind	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_4_739_s_67	9288753	(C and D) Following isolation of plasmid p28, which confers Sema III - binding  activity, Sema III - AP (D) but not AP (C) was found to bind cells transiently transfected  with p28.	bind
44439	2	4389	5	10	NULL	0	NULL	cells	NULL		transfected with	NULL	transiently			p28	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_90_4_739_s_67	9288753	(C and D) Following isolation of plasmid p28, which confers Sema III - binding  activity, Sema III - AP (D) but not AP (C) was found to bind cells transiently transfected  with p28.	bind
10801	1	4389	6	NULL	NULL	NULL	NULL	p28	GP		confers					SemaIII	GP	binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_cell_90_4_739_s_67	9288753	(C and D) Following isolation of plasmid p28, which confers Sema III - binding  activity, Sema III - AP (D) but not AP (C) was found to bind cells transiently transfected  with p28.	bind
10802	2	4389	6	NULL	NULL	NULL	NULL	cells	Cell		transfected with		transiently			p28	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_4_739_s_67	9288753	(C and D) Following isolation of plasmid p28, which confers Sema III - binding  activity, Sema III - AP (D) but not AP (C) was found to bind cells transiently transfected  with p28.	bind
11663	3	4389	6	NULL	NULL	NULL	NULL	Sema III - AP	GP		bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_4_739_s_67	9288753	(C and D) Following isolation of plasmid p28, which confers Sema III - binding  activity, Sema III - AP (D) but not AP (C) was found to bind cells transiently transfected  with p28.	bind
54285	4	4389	6	NULL	NULL	NULL	NULL	AP	GP		does not bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_4_739_s_67	9288753	(C and D) Following isolation of plasmid p28, which confers Sema III - binding  activity, Sema III - AP (D) but not AP (C) was found to bind cells transiently transfected  with p28.	bind
10957	1	4390	5	NULL	NULL	0	NULL	EhRab7A	NULL	recombinant	bind	NULL				EhVps26	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5294_s_149	16120649	(C and D) In vitro binding of recombinant EhRab7A with EhVps26  and EhVps29 (C), and of recombinant EhRab7A with EhVps26FL and EhVps26deltaC (D).	bind
10958	2	4390	5	NULL	NULL	0	NULL	EhRab7A	NULL	recombinant	bind	NULL				EhVps29	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5294_s_149	16120649	(C and D) In vitro binding of recombinant EhRab7A with EhVps26  and EhVps29 (C), and of recombinant EhRab7A with EhVps26FL and EhVps26deltaC (D).	bind
10959	3	4390	5	10	NULL	0	NULL	EhRab7A		recombinant	bind					EhVps26FL					NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5294_s_149	16120649	(C and D) In vitro binding of recombinant EhRab7A with EhVps26  and EhVps29 (C), and of recombinant EhRab7A with EhVps26FL and EhVps26deltaC (D).	bind
10960	4	4390	5	10	NULL	0	NULL	EhRab7A		recombinant	bind					EhVps26deltaC					NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5294_s_149	16120649	(C and D) In vitro binding of recombinant EhRab7A with EhVps26  and EhVps29 (C), and of recombinant EhRab7A with EhVps26FL and EhVps26deltaC (D).	bind
10137	1	4390	6	NULL	NULL	NULL	NULL	EhRab7A	GP	recombinant	bind					EhVps26	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5294_s_149	16120649	(C and D) In vitro binding of recombinant EhRab7A with EhVps26  and EhVps29 (C), and of recombinant EhRab7A with EhVps26FL and EhVps26deltaC (D).	bind
10138	2	4390	6	NULL	NULL	NULL	NULL	EhVps7A	GP	recombinant	bind					Ehvps29	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5294_s_149	16120649	(C and D) In vitro binding of recombinant EhRab7A with EhVps26  and EhVps29 (C), and of recombinant EhRab7A with EhVps26FL and EhVps26deltaC (D).	bind
10139	3	4390	6	NULL	NULL	NULL	NULL	EhRab7A	GP	recombinant	bind					EhVps26FL	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5294_s_149	16120649	(C and D) In vitro binding of recombinant EhRab7A with EhVps26  and EhVps29 (C), and of recombinant EhRab7A with EhVps26FL and EhVps26deltaC (D).	bind
10140	4	4390	6	NULL	NULL	NULL	NULL	EhRab7A	GP	recombinant	bind					EhVps26deltaC 	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5294_s_149	16120649	(C and D) In vitro binding of recombinant EhRab7A with EhVps26  and EhVps29 (C), and of recombinant EhRab7A with EhVps26FL and EhVps26deltaC (D).	bind
10961	1	4391	5	NULL	NULL	0	NULL	SsrA peptide	NULL		bind	NULL				SspB	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_12_1_75_s_50	12887894	(C and D) Isothermal titration calorimetric studies of SsrA peptide binding to SspB (C) and SspB127 (D) reveal dissociation constants of 6.16 and 6.22  M, respectively.	bind
10962	2	4391	5	NULL	NULL	0	NULL	SsrA peptide	NULL		bind	NULL				SspB127	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_12_1_75_s_50	12887894	(C and D) Isothermal titration calorimetric studies of SsrA peptide binding to SspB (C) and SspB127 (D) reveal dissociation constants of 6.16 and 6.22  M, respectively.	bind
10145	1	4391	6	NULL	NULL	NULL	NULL	SsrA peptide	GP		bind					SspB	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_75_s_50	12887894	(C and D) Isothermal titration calorimetric studies of SsrA peptide binding to SspB (C) and SspB127 (D) reveal dissociation constants of 6.16 and 6.22  M, respectively.	bind
10146	2	4391	6	NULL	NULL	NULL	NULL	SsrA peptide	GP		bind					SspB127	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_75_s_50	12887894	(C and D) Isothermal titration calorimetric studies of SsrA peptide binding to SspB (C) and SspB127 (D) reveal dissociation constants of 6.16 and 6.22  M, respectively.	bind
10963	1	4392	5	NULL	NULL	0	NULL	type IV collagen	NULL		bind	NULL				fibronectin	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_10_4467_s_137	15282337	(C and D) Quantification of type IV collagen binding to fibronectin beads (including  means and standard deviations of four experiments).	bind
10147	1	4392	6	NULL	NULL	NULL	NULL	type IV collagen	GP		bind					fibronectin beads	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_10_4467_s_137	15282337	(C and D) Quantification of type IV collagen binding to fibronectin beads (including  means and standard deviations of four experiments).	bind
10964	1	4393	5	NULL	NULL	0	NULL	Rad24p	NULL		bind	NULL				Eco1p	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_8_2999_s_162	12665596	(C and D) Rad24p binding to Eco1p was  not disrupted by DNase I treatment, while this level of DNase I under identical conditions  was sufficient to completely digest 500 ng of lambda DNA.	bind
10965	2	4393	5	10	NULL	0	NULL	DNase I			does not disrupt					statement 1					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2999_s_162	12665596	(C and D) Rad24p binding to Eco1p was  not disrupted by DNase I treatment, while this level of DNase I under identical conditions  was sufficient to completely digest 500 ng of lambda DNA.	bind
10966	3	4393	5	10	NULL	0	NULL	DNase I			digest		completely			lambda DNA					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2999_s_162	12665596	(C and D) Rad24p binding to Eco1p was  not disrupted by DNase I treatment, while this level of DNase I under identical conditions  was sufficient to completely digest 500 ng of lambda DNA.	bind
10265	1	4393	6	NULL	NULL	NULL	NULL	Rad24p	GP		bind					Eco1p	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2999_s_162	12665596	(C and D) Rad24p binding to Eco1p was  not disrupted by DNase I treatment, while this level of DNase I under identical conditions  was sufficient to completely digest 500 ng of lambda DNA.	bind
10266	2	4393	6	NULL	NULL	NULL	NULL	DNase I	GP		does not disrupt					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2999_s_162	12665596	(C and D) Rad24p binding to Eco1p was  not disrupted by DNase I treatment, while this level of DNase I under identical conditions  was sufficient to completely digest 500 ng of lambda DNA.	bind
54286	3	4393	6	NULL	NULL	NULL	NULL	DNase I 	GP		digest		completely			lambda DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_8_2999_s_162	12665596	(C and D) Rad24p binding to Eco1p was  not disrupted by DNase I treatment, while this level of DNase I under identical conditions  was sufficient to completely digest 500 ng of lambda DNA.	bind
10967	1	4395	5	10	NULL	0	NULL	 fra-1 			bind					fra-1				TRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_12_4401_s_230	12773579	(C and D) Serum induction of  fra-1 and mRNA and protein binding to  fra-1 TRE.	bind
10970	2	4395	5	10	NULL	0	NULL	serum			induce					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_12_4401_s_230	12773579	(C and D) Serum induction of  fra-1 and mRNA and protein binding to  fra-1 TRE.	bind
10269	1	4395	6	NULL	NULL	NULL	NULL	Fra-1	GP		bind					fra-1	GP			TRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_12_4401_s_230	12773579	(C and D) Serum induction of  fra-1 and mRNA and protein binding to  fra-1 TRE.	bind
10273	2	4395	6	NULL	NULL	NULL	NULL	serum	Chemical		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_12_4401_s_230	12773579	(C and D) Serum induction of  fra-1 and mRNA and protein binding to  fra-1 TRE.	bind
10971	1	4396	5	NULL	NULL	0	NULL	Ste12	NULL		bind	NULL				filamentation genes	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_113_3_395_s_133	12732146	(C and D) Ste12 binding to filamentation genes during butanol treatment.	bind
10972	2	4396	5	10	NULL	0	NULL	statement 1			occurs during					butanol		treatment with			NULL		NULL	NULL	NULL	NULL	gw60_cell_113_3_395_s_133	12732146	(C and D) Ste12 binding to filamentation genes during butanol treatment.	bind
10276	1	4396	6	NULL	NULL	NULL	NULL	Ste12	GP		bind					filamentous genes	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_3_395_s_133	12732146	(C and D) Ste12 binding to filamentation genes during butanol treatment.	bind
10277	2	4396	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs during					butanol	Chemical	treatment with			NULL		NULL	NULL	NULL	NULL	gw60_cell_113_3_395_s_133	12732146	(C and D) Ste12 binding to filamentation genes during butanol treatment.	bind
10973	1	4397	5	10	NULL	0	NULL	 DR		nuclear	bind					hsp90					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5811_s_174	10409767	(c and d) The nuclear DR remains bound to hsp90.	bind
10278	1	4397	6	NULL	NULL	NULL	NULL	DR	GP	nuclear	bind					hsp90	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5811_s_174	10409767	(c and d) The nuclear DR remains bound to hsp90.	bind
10986	1	4399	5	NULL	NULL	0	NULL	S1-S2-GluR2	NULL		bind	NULL				NR2A	NULL		glutamate		NULL		0	NULL	NULL	NULL	gw60_neuron_32_6_1085_s_264	11754839	(C and D) Three-dimensional model of the ligand binding domain of NR2A (C) and NR1 (D) based on the structure of S1-S2-GluR2 bound to glutamate for NR2A and the apo structure for NR1 (Protein Data Bank ID codes: 1FTJ for NR2A and 1FTO for NR1).	bind
12783	1	4399	6	NULL	NULL	NULL	NULL	S1-S2-GluR2	AminoAcid		bind					NR2A	GP		glutamate		NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_6_1085_s_264	11754839	(C and D) Three-dimensional model of the ligand binding domain of NR2A (C) and NR1 (D) based on the structure of S1-S2-GluR2 bound to glutamate for NR2A and the apo structure for NR1 (Protein Data Bank ID codes: 1FTJ for NR2A and 1FTO for NR1).	bind
10991	1	4400	5	NULL	NULL	0	NULL	myc-Srb6p	NULL		bind	NULL				SNZ1	NULL			UAS	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_15_6871_s_178	15254252	(C and F) The procedures described for panels B and E were employed to analyze  binding of myc-Srb6p (C) or myc-Gal11p (F) to the  SNZ1 UAS.	bind
10994	2	4400	5	NULL	NULL	0	NULL	myc-Gal11p	NULL		bind	NULL				SNZ1	NULL			UAS	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_15_6871_s_178	15254252	(C and F) The procedures described for panels B and E were employed to analyze  binding of myc-Srb6p (C) or myc-Gal11p (F) to the  SNZ1 UAS.	bind
13105	3	4400	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_15_6871_s_178	15254252	(C and F) The procedures described for panels B and E were employed to analyze  binding of myc-Srb6p (C) or myc-Gal11p (F) to the  SNZ1 UAS.	bind
10282	1	4400	6	NULL	NULL	NULL	NULL	myc-Srb6p	GP		bind					SNZ1	GP			UAS	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_15_6871_s_178	15254252	(C and F) The procedures described for panels B and E were employed to analyze  binding of myc-Srb6p (C) or myc-Gal11p (F) to the  SNZ1 UAS.	bind
10283	2	4400	6	NULL	NULL	NULL	NULL	myc-Gal11p	GP		bind					SNZ1	GP			UAS	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_15_6871_s_178	15254252	(C and F) The procedures described for panels B and E were employed to analyze  binding of myc-Srb6p (C) or myc-Gal11p (F) to the  SNZ1 UAS.	bind
10284	3	4400	6	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_15_6871_s_178	15254252	(C and F) The procedures described for panels B and E were employed to analyze  binding of myc-Srb6p (C) or myc-Gal11p (F) to the  SNZ1 UAS.	bind
10995	1	4401	5	NULL	NULL	0	NULL	phospho-CheY	NULL		bind	NULL				FliM	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_21_5580_s_399	9791106	(C to E) Hypotheses for the movements that might be triggered by binding of phospho-CheY to FliM, to cause switching to the CW direction of motor rotation.	bind
11001	2	4401	5	NULL	NULL	0	NULL	statement 1	NULL		causes	NULL				CW direction of motor rotation	NULL	switching to			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_21_5580_s_399	9791106	(C to E) Hypotheses for the movements that might be triggered by binding of phospho-CheY to FliM, to cause switching to the CW direction of motor rotation.	bind
10285	1	4401	6	NULL	NULL	NULL	NULL	phospho-CheY	GP		bind					FliM	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_21_5580_s_399	9791106	(C to E) Hypotheses for the movements that might be triggered by binding of phospho-CheY to FliM, to cause switching to the CW direction of motor rotation.	bind
12784	2	4401	6	NULL	NULL	NULL	NULL	statement 1	Process		causes					CW direction of motor rotation		switching to			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_21_5580_s_399	9791106	(C to E) Hypotheses for the movements that might be triggered by binding of phospho-CheY to FliM, to cause switching to the CW direction of motor rotation.	bind
11005	1	4402	5	NULL	NULL	0	NULL	Tem1	NULL		bind	NULL				Cdc15	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_112_5_697_s_204	12628189	(C)  AMN1 overexpression inhibits the binding between Tem1 and Cdc15.	bind
11006	2	4402	5	NULL	NULL	0	NULL	AMN1	NULL	overexpression of	inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_112_5_697_s_204	12628189	(C)  AMN1 overexpression inhibits the binding between Tem1 and Cdc15.	bind
10286	1	4402	6	NULL	NULL	NULL	NULL	Tem1	GP		bind					Cdc15	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_5_697_s_204	12628189	(C)  AMN1 overexpression inhibits the binding between Tem1 and Cdc15.	bind
10287	2	4402	6	NULL	NULL	NULL	NULL	AMN1	GP	overexpression of	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_5_697_s_204	12628189	(C)  AMN1 overexpression inhibits the binding between Tem1 and Cdc15.	bind
11007	1	4403	5	NULL	NULL	0	NULL	nuclear proteins	NULL		bind	NULL				TGF- 1	NULL	human		AP-1 site B of promoter	NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_2_301_s_95	12711314	(C)  Binding of nuclear proteins to the AP-1 site B of the human TGF- 1 promoter.	bind
10288	1	4403	6	NULL	NULL	NULL	NULL	nuclear protein	GP		bind					TGF-1 	GP	human		AP-1 site B of promoter	NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_2_301_s_95	12711314	(C)  Binding of nuclear proteins to the AP-1 site B of the human TGF- 1 promoter.	bind
11008	1	4404	5	NULL	NULL	0	NULL	H3 Ab	NULL		bind	NULL				H3 peptide	NULL	unphosphorylated 			NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_2_225_s_117	10209020	(C)  ELISA of H3 Ab binding to the unphosphorylated H3 peptide  (open square), phosphorylated H3 peptide (closed square), total  cellular proteins from cycling cells (open circle) or from cells  treated with nocodazole (closed circle).	bind
11010	2	4404	5	NULL	NULL	0	NULL	H3 Ab	NULL		bind	NULL				H3 peptide	NULL	phosphorylated			NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_2_225_s_117	10209020	(C)  ELISA of H3 Ab binding to the unphosphorylated H3 peptide  (open square), phosphorylated H3 peptide (closed square), total  cellular proteins from cycling cells (open circle) or from cells  treated with nocodazole (closed circle).	bind
11011	5	4404	5	10	NULL	0	NULL	H3 Ab	NULL		bind	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_2_225_s_117	10209020	(C)  ELISA of H3 Ab binding to the unphosphorylated H3 peptide  (open square), phosphorylated H3 peptide (closed square), total  cellular proteins from cycling cells (open circle) or from cells  treated with nocodazole (closed circle).	bind
11013	6	4404	5	10	NULL	0	NULL	H3 Ab	NULL		bind	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_2_225_s_117	10209020	(C)  ELISA of H3 Ab binding to the unphosphorylated H3 peptide  (open square), phosphorylated H3 peptide (closed square), total  cellular proteins from cycling cells (open circle) or from cells  treated with nocodazole (closed circle).	bind
44440	3	4404	5	10	NULL	0	NULL	total cellular proteins	NULL		are from	NULL				cells treated with nocodazole	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_2_225_s_117	10209020	(C)  ELISA of H3 Ab binding to the unphosphorylated H3 peptide  (open square), phosphorylated H3 peptide (closed square), total  cellular proteins from cycling cells (open circle) or from cells  treated with nocodazole (closed circle).	bind
44441	4	4404	5	10	NULL	0	NULL	total cellular proteins	NULL		are from	NULL				cycling cells	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_2_225_s_117	10209020	(C)  ELISA of H3 Ab binding to the unphosphorylated H3 peptide  (open square), phosphorylated H3 peptide (closed square), total  cellular proteins from cycling cells (open circle) or from cells  treated with nocodazole (closed circle).	bind
10289	1	4404	6	NULL	NULL	NULL	NULL	H3 Ab 	GP		bind					H3 peptide	AminoAcid	unphosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_2_225_s_117	10209020	(C)  ELISA of H3 Ab binding to the unphosphorylated H3 peptide  (open square), phosphorylated H3 peptide (closed square), total  cellular proteins from cycling cells (open circle) or from cells  treated with nocodazole (closed circle).	bind
10290	2	4404	6	NULL	NULL	NULL	NULL	H3 Ab	GP		bind					H3 peptide	AminoAcid	phosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_2_225_s_117	10209020	(C)  ELISA of H3 Ab binding to the unphosphorylated H3 peptide  (open square), phosphorylated H3 peptide (closed square), total  cellular proteins from cycling cells (open circle) or from cells  treated with nocodazole (closed circle).	bind
10291	3	4404	6	NULL	NULL	NULL	NULL	total cellular proteins	GP		are from					cycling cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_2_225_s_117	10209020	(C)  ELISA of H3 Ab binding to the unphosphorylated H3 peptide  (open square), phosphorylated H3 peptide (closed square), total  cellular proteins from cycling cells (open circle) or from cells  treated with nocodazole (closed circle).	bind
10292	4	4404	6	NULL	NULL	NULL	NULL	total cellular proteins	GP		are from					cells treated with nocodazole	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_2_225_s_117	10209020	(C)  ELISA of H3 Ab binding to the unphosphorylated H3 peptide  (open square), phosphorylated H3 peptide (closed square), total  cellular proteins from cycling cells (open circle) or from cells  treated with nocodazole (closed circle).	bind
54287	5	4404	6	NULL	NULL	NULL	NULL	H3 Ab	GP		bind					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_2_225_s_117	10209020	(C)  ELISA of H3 Ab binding to the unphosphorylated H3 peptide  (open square), phosphorylated H3 peptide (closed square), total  cellular proteins from cycling cells (open circle) or from cells  treated with nocodazole (closed circle).	bind
54288	6	4404	6	NULL	NULL	NULL	NULL	H3 Ab	GP		bind					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_2_225_s_117	10209020	(C)  ELISA of H3 Ab binding to the unphosphorylated H3 peptide  (open square), phosphorylated H3 peptide (closed square), total  cellular proteins from cycling cells (open circle) or from cells  treated with nocodazole (closed circle).	bind
11038	1	4406	5	NULL	NULL	0	NULL	SEK1	NULL		bind	NULL				anti-SEK1 antibody	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_170_1_61_s_247	15998799	(C)  Immunoprecipitates were analyzed for SEK1 binding with anti-SEK1 or anti - rabbit  Akt antibody (top).	bind
11039	2	4406	5	NULL	NULL	0	NULL	SEK1	NULL		bind	NULL				anti - rabbit Akt antibody	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_170_1_61_s_247	15998799	(C)  Immunoprecipitates were analyzed for SEK1 binding with anti-SEK1 or anti - rabbit  Akt antibody (top).	bind
54289	1	4406	6	NULL	NULL	NULL	NULL	SEK1	GP		bind					anti-SEK1 antibody	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_1_61_s_247	15998799	(C)  Immunoprecipitates were analyzed for SEK1 binding with anti-SEK1 or anti - rabbit  Akt antibody (top).	bind
54290	2	4406	6	NULL	NULL	NULL	NULL	SEK1 	GP		bind					anti - rabbit Akt antibody	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_1_61_s_247	15998799	(C)  Immunoprecipitates were analyzed for SEK1 binding with anti-SEK1 or anti - rabbit  Akt antibody (top).	bind
11040	1	4407	5	NULL	NULL	0	NULL	DHFR-TS protein	NULL	plasmodium	bind	NULL	specifically			DHFR-TS RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_science_296_5567_545_s_36	11964483	(C)  Plasmodium DHFR-TS protein bound  DHFR-TS RNA with specificity.	bind
10293	1	4407	6	NULL	NULL	NULL	NULL	DHFR-TS protein	GP	plasmodium	bind		specifically			DHFR-TS RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_science_296_5567_545_s_36	11964483	(C)  Plasmodium DHFR-TS protein bound  DHFR-TS RNA with specificity.	bind
11041	1	4408	5	NULL	NULL	0	NULL	Runx2	NULL		bind	NULL					NULL	mouse		A elements	NULL	hypertrophic MCT cells	0	NULL	NULL	NULL	gw70_cellbiol_162_5_833_s_108	12952936	(C)  Runx2 binds to the mouse A and B elements in hypertrophic MCT cells.	bind
11042	2	4408	5	NULL	NULL	0	NULL	Runx2	NULL		bind	NULL					NULL	mouse		B elements	NULL	hypertrophic MCT cells	0	NULL	NULL	NULL	gw70_cellbiol_162_5_833_s_108	12952936	(C)  Runx2 binds to the mouse A and B elements in hypertrophic MCT cells.	bind
10294	1	4408	6	NULL	NULL	NULL	NULL	Runx2	GP		bind							mouse		A element	NULL	hypertrophic MCT cells	NULL	NULL	NULL	NULL	gw70_cellbiol_162_5_833_s_108	12952936	(C)  Runx2 binds to the mouse A and B elements in hypertrophic MCT cells.	bind
10296	2	4408	6	NULL	NULL	NULL	NULL	Runx2	GP		bind							mouse		B element	NULL	hypertrophic MCT cells	NULL	NULL	NULL	NULL	gw70_cellbiol_162_5_833_s_108	12952936	(C)  Runx2 binds to the mouse A and B elements in hypertrophic MCT cells.	bind
11043	1	4409	5	NULL	NULL	0	NULL	syntaxin-1A	NULL		bind	NULL		191-240		myosin-Va	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_159	16030255	(C)  Syntaxin-1A [191-240] but not syntaxin-1A [191-240 L222] binds myosin-Va.	bind
11045	2	4409	5	NULL	NULL	0	NULL	syntaxin-1A	NULL		does not bind	NULL		191-240 L222		myosin-Va	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_159	16030255	(C)  Syntaxin-1A [191-240] but not syntaxin-1A [191-240 L222] binds myosin-Va.	bind
10297	1	4409	6	NULL	NULL	NULL	NULL	Syntaxin-1A	GP		bind			191-240		myosin-Va	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_159	16030255	(C)  Syntaxin-1A [191-240] but not syntaxin-1A [191-240 L222] binds myosin-Va.	bind
10298	2	4409	6	NULL	NULL	NULL	NULL	syntaxin-1A	GP		does not bind			191-240 L222		myosin-Va	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_159	16030255	(C)  Syntaxin-1A [191-240] but not syntaxin-1A [191-240 L222] binds myosin-Va.	bind
11048	1	4410	5	NULL	NULL	0	NULL	Sso	NULL		is not assembled into	NULL				SNARE complexes	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_8_3114_s_198	12925750	(C)  Vsm1 binds to Sso that is not assembled into  SNARE complexes.	bind
11049	2	4410	5	NULL	NULL	0	NULL	Vsm1	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_8_3114_s_198	12925750	(C)  Vsm1 binds to Sso that is not assembled into  SNARE complexes.	bind
10300	2	4410	6	NULL	NULL	NULL	NULL	Vsm1	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_8_3114_s_198	12925750	(C)  Vsm1 binds to Sso that is not assembled into  SNARE complexes.	bind
10301	1	4410	6	NULL	NULL	NULL	NULL	Sso	GP		is not assembled into					SNARE complexes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_8_3114_s_198	12925750	(C)  Vsm1 binds to Sso that is not assembled into  SNARE complexes.	bind
11053	1	4413	5	NULL	NULL	0	NULL	PiC	NULL	35S-labeled	bind	NULL				Tom70	NULL	human	cytosolic segment (Hs-3)		NULL		0	NULL	NULL	NULL	gw60_cell_112_1_41_s_207	12526792	(C) 35S-labeled PiC (lane 1) was bound to human Tom70 cytosolic segment (Hs-3) and recovered with NiNTA-agarose as in	bind
10306	1	4413	6	NULL	NULL	NULL	NULL	PiC	GP	35S-labeled	bind					Tom70	GP	human	cytosolic segment (Hs-3)		NULL		NULL	NULL	NULL	NULL	gw60_cell_112_1_41_s_207	12526792	(C) 35S-labeled PiC (lane 1) was bound to human Tom70 cytosolic segment (Hs-3) and recovered with NiNTA-agarose as in	bind
11054	1	4414	5	NULL	NULL	0	NULL	GM1	NULL	3H-labeled	bind	NULL				CD1b	NULL	soluble			NULL		0	NULL	NULL	NULL	gw60_immunity_13_2_255_s_165	10981968	(C) 3H-labeled GM1 bound to soluble CD1b is displaced by cold GM2.	bind
11055	2	4414	5	NULL	NULL	0	NULL	GM2	NULL	cold	displaces	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_13_2_255_s_165	10981968	(C) 3H-labeled GM1 bound to soluble CD1b is displaced by cold GM2.	bind
10307	1	4414	6	NULL	NULL	NULL	NULL	GM1	GP	3H-labeled 	bind					CD1b	GP	soluble			NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_2_255_s_165	10981968	(C) 3H-labeled GM1 bound to soluble CD1b is displaced by cold GM2.	bind
10309	2	4414	6	NULL	NULL	NULL	NULL	GM2	GP	cold	displaces					GM1	GP				NULL	statement 1	NULL	NULL	NULL	NULL	gw60_immunity_13_2_255_s_165	10981968	(C) 3H-labeled GM1 bound to soluble CD1b is displaced by cold GM2.	bind
11056	1	4415	5	NULL	NULL	0	NULL	PlexB	NULL		bind	NULL				RhoA	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_32_1_39_s_93	11604137	(C) A 40 amino acid deletion in PlexB  (PlexB d40) eliminates its binding to RhoA.	bind
11058	2	4415	5	NULL	NULL	0	NULL	PlexB d40	NULL		eliminate	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_32_1_39_s_93	11604137	(C) A 40 amino acid deletion in PlexB  (PlexB d40) eliminates its binding to RhoA.	bind
11059	3	4415	5	NULL	NULL	0	NULL	PlexB d40	NULL		is	NULL				40 amino acid deletion in PlexB	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_32_1_39_s_93	11604137	(C) A 40 amino acid deletion in PlexB  (PlexB d40) eliminates its binding to RhoA.	bind
10310	1	4415	6	NULL	NULL	NULL	NULL	PlexB	GP		bind					RhoA	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_1_39_s_93	11604137	(C) A 40 amino acid deletion in PlexB  (PlexB d40) eliminates its binding to RhoA.	bind
10311	2	4415	6	NULL	NULL	NULL	NULL	PlexBd40	GP		eliminates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_1_39_s_93	11604137	(C) A 40 amino acid deletion in PlexB  (PlexB d40) eliminates its binding to RhoA.	bind
54291	3	4415	6	NULL	NULL	NULL	NULL	PlexB d40	GP		is					40 amino acid deletion in PlexB	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_1_39_s_93	11604137	(C) A 40 amino acid deletion in PlexB  (PlexB d40) eliminates its binding to RhoA.	bind
11063	1	4417	5	NULL	NULL	0	NULL	EGFP-MuB	NULL		bind	NULL				target DNA molecules	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_10_6_1367_s_203	12504012	(C) A graph of the total fluorescence signal from the EGFP-MuB bound to the target DNA molecules versus time.	bind
10312	1	4417	6	NULL	NULL	NULL	NULL	EGFP-MuB	GP		bind					target DNA molecules	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_6_1367_s_203	12504012	(C) A graph of the total fluorescence signal from the EGFP-MuB bound to the target DNA molecules versus time.	bind
11065	1	4418	5	10	NULL	0	NULL	minichromosome		mardel derived;;human engineered	bind					CENP-A					NULL		NULL	NULL	NULL	NULL	gw60_devcell_1_2_165_s_20	11702777	(C) A mardel(10)-derived human engineered minichromosome (arrowed) (left panel; DAPI staining) binds CENP-A (red doublet signal; middle panel) and shows absence of  -satellite (yellow/green; right panel).	bind
10313	1	4418	6	NULL	NULL	NULL	NULL	minichromosome	Chromosome	mardel derived;;human engineered	bind					CENP-A	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_1_2_165_s_20	11702777	(C) A mardel(10)-derived human engineered minichromosome (arrowed) (left panel; DAPI staining) binds CENP-A (red doublet signal; middle panel) and shows absence of  -satellite (yellow/green; right panel).	bind
11069	1	4419	5	NULL	NULL	0	NULL	JM22z	NULL		bind	NULL				HLA-A2-flu	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_10_3_357_s_123	10204491	(C) A reaction profile illustrating the potential energy changes as JM22z binds to HLA-A2-flu.	bind
10317	1	4419	6	NULL	NULL	NULL	NULL	JM22z	GP		bind					HLA-A2-flu	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_10_3_357_s_123	10204491	(C) A reaction profile illustrating the potential energy changes as JM22z binds to HLA-A2-flu.	bind
11073	1	4421	5	10	NULL	0	NULL	P48 proteins		mutant;;human	heterodimerize with					E12					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_276	16354684	(C) Ability of the mutant human P48 proteins to form heterodimers  with E12 and trimers with E12 and either RBP-J or RBP-L that bind the  Ela1 PTF1-site.	bind
11074	5	4421	5	10	NULL	0	NULL	P48 proteins		mutant;; human	form trimers with					 statement 2					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_276	16354684	(C) Ability of the mutant human P48 proteins to form heterodimers  with E12 and trimers with E12 and either RBP-J or RBP-L that bind the  Ela1 PTF1-site.	bind
11075	4	4421	5	10	NULL	0	NULL	P48 proteins		mutant;;human	form trimers with					E12					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_276	16354684	(C) Ability of the mutant human P48 proteins to form heterodimers  with E12 and trimers with E12 and either RBP-J or RBP-L that bind the  Ela1 PTF1-site.	bind
11077	6	4421	5	10	NULL	0	NULL	statement 4			occur simultaneously with					statement 5					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_276	16354684	(C) Ability of the mutant human P48 proteins to form heterodimers  with E12 and trimers with E12 and either RBP-J or RBP-L that bind the  Ela1 PTF1-site.	bind
11078	3	4421	5	NULL	NULL	0	NULL	RBP-J	NULL		bind	NULL				Ela1	NULL			PTF1-site	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_276	16354684	(C) Ability of the mutant human P48 proteins to form heterodimers  with E12 and trimers with E12 and either RBP-J or RBP-L that bind the  Ela1 PTF1-site.	bind
11079	2	4421	5	NULL	NULL	0	NULL	RBP-L	NULL		bind	NULL				Ela1	NULL			PTF1-site	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_276	16354684	(C) Ability of the mutant human P48 proteins to form heterodimers  with E12 and trimers with E12 and either RBP-J or RBP-L that bind the  Ela1 PTF1-site.	bind
54293	7	4421	5	10	NULL	0	NULL	P48 proteins		human;;mutant	form trimers with					statement 3					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_276	16354684	(C) Ability of the mutant human P48 proteins to form heterodimers  with E12 and trimers with E12 and either RBP-J or RBP-L that bind the  Ela1 PTF1-site.	bind
54294	8	4421	5	10	NULL	0	NULL	statement 4			occur simultaneously with					statement 7					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_276	16354684	(C) Ability of the mutant human P48 proteins to form heterodimers  with E12 and trimers with E12 and either RBP-J or RBP-L that bind the  Ela1 PTF1-site.	bind
54295	9	4421	5	10	NULL	0	NULL	statement 6			is an alternative to					statement 8					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_276	16354684	(C) Ability of the mutant human P48 proteins to form heterodimers  with E12 and trimers with E12 and either RBP-J or RBP-L that bind the  Ela1 PTF1-site.	bind
10319	1	4421	6	NULL	NULL	NULL	NULL	P48 proteins	GP	mutant;; human	form heterodimers with					E12	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_276	16354684	(C) Ability of the mutant human P48 proteins to form heterodimers  with E12 and trimers with E12 and either RBP-J or RBP-L that bind the  Ela1 PTF1-site.	bind
10322	2	4421	6	NULL	NULL	NULL	NULL	RBP-J	GP		bind					Ela1	GP		PTF1-site		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_276	16354684	(C) Ability of the mutant human P48 proteins to form heterodimers  with E12 and trimers with E12 and either RBP-J or RBP-L that bind the  Ela1 PTF1-site.	bind
10324	3	4421	6	NULL	NULL	NULL	NULL	RBP-L	GP		bind					Ela1	GP		PTF1-site		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_276	16354684	(C) Ability of the mutant human P48 proteins to form heterodimers  with E12 and trimers with E12 and either RBP-J or RBP-L that bind the  Ela1 PTF1-site.	bind
10325	4	4421	6	NULL	NULL	NULL	NULL	P48 proteins	GP	mutant;;human	form trimers with					E12	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_276	16354684	(C) Ability of the mutant human P48 proteins to form heterodimers  with E12 and trimers with E12 and either RBP-J or RBP-L that bind the  Ela1 PTF1-site.	bind
12869	5	4421	6	NULL	NULL	NULL	NULL	P48 proteins	GP	mutant;;human	form trimers with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_276	16354684	(C) Ability of the mutant human P48 proteins to form heterodimers  with E12 and trimers with E12 and either RBP-J or RBP-L that bind the  Ela1 PTF1-site.	bind
12870	6	4421	6	NULL	NULL	NULL	NULL	statement 4	Process		occur simultaneously with					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_276	16354684	(C) Ability of the mutant human P48 proteins to form heterodimers  with E12 and trimers with E12 and either RBP-J or RBP-L that bind the  Ela1 PTF1-site.	bind
54296	7	4421	6	NULL	NULL	NULL	NULL	P48 proteins	GP	mutant;;human	form trimers with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_276	16354684	(C) Ability of the mutant human P48 proteins to form heterodimers  with E12 and trimers with E12 and either RBP-J or RBP-L that bind the  Ela1 PTF1-site.	bind
54297	8	4421	6	NULL	NULL	NULL	NULL	statement 4	Process		occur simultaneously with					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_276	16354684	(C) Ability of the mutant human P48 proteins to form heterodimers  with E12 and trimers with E12 and either RBP-J or RBP-L that bind the  Ela1 PTF1-site.	bind
54298	9	4421	6	NULL	NULL	NULL	NULL	statement 6	Process		is an alternative to					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_117_s_276	16354684	(C) Ability of the mutant human P48 proteins to form heterodimers  with E12 and trimers with E12 and either RBP-J or RBP-L that bind the  Ela1 PTF1-site.	bind
11080	1	4424	5	NULL	NULL	0	NULL	cortactin	NULL	mutant	does not bind	NULL		W22A		Arp2/3 complex	NULL				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_21_1852_s_28	12419186	(C) Actin dynamics in cells expressing mutant forms of cortactin that do not bind Arp2/3 complex (cortactin W22A) or dynamin2 (cortactin W525K).	bind
11081	2	4424	5	NULL	NULL	0	NULL	cortactin	NULL	mutant	does not bind	NULL		W525K		dynamin2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_21_1852_s_28	12419186	(C) Actin dynamics in cells expressing mutant forms of cortactin that do not bind Arp2/3 complex (cortactin W22A) or dynamin2 (cortactin W525K).	bind
10326	1	4424	6	NULL	NULL	NULL	NULL	cortactin	GP	mutant	does not bind			W22A		Arp2/3 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_21_1852_s_28	12419186	(C) Actin dynamics in cells expressing mutant forms of cortactin that do not bind Arp2/3 complex (cortactin W22A) or dynamin2 (cortactin W525K).	bind
10327	2	4424	6	NULL	NULL	NULL	NULL	cortactin	GP	mutant	does not bind			W525K		dynamin2	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_21_1852_s_28	12419186	(C) Actin dynamics in cells expressing mutant forms of cortactin that do not bind Arp2/3 complex (cortactin W22A) or dynamin2 (cortactin W525K).	bind
11082	1	4425	5	NULL	NULL	0	NULL	Adf-1	NULL		bind	NULL				TAFII110	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_molcellbiol_18_4_2252_s_269	9528796	(C) Adf-1 binds the same regions of TAFII110 and TAFII250 in vivo as it does in vitro.	bind
11083	2	4425	5	NULL	NULL	0	NULL	Adf-1	NULL		bind	NULL				TAFII250	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2252_s_269	9528796	(C) Adf-1 binds the same regions of TAFII110 and TAFII250 in vivo as it does in vitro.	bind
11084	3	4425	5	NULL	NULL	0	NULL	Adf-1	NULL		bind	NULL				TAFII110	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_18_4_2252_s_269	9528796	(C) Adf-1 binds the same regions of TAFII110 and TAFII250 in vivo as it does in vitro.	bind
11085	4	4425	5	NULL	NULL	0	NULL	Adf-1	NULL		bind	NULL				TAFII250	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_18_4_2252_s_269	9528796	(C) Adf-1 binds the same regions of TAFII110 and TAFII250 in vivo as it does in vitro.	bind
10328	1	4425	6	NULL	NULL	NULL	NULL	Adf-1	GP		bind					TAFII110	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2252_s_269	9528796	(C) Adf-1 binds the same regions of TAFII110 and TAFII250 in vivo as it does in vitro.	bind
10329	2	4425	6	NULL	NULL	NULL	NULL	Adf-1	GP		bind					TAFII250	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2252_s_269	9528796	(C) Adf-1 binds the same regions of TAFII110 and TAFII250 in vivo as it does in vitro.	bind
10330	3	4425	6	NULL	NULL	NULL	NULL	Adf-1	GP		bind					TAFII250	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2252_s_269	9528796	(C) Adf-1 binds the same regions of TAFII110 and TAFII250 in vivo as it does in vitro.	bind
10331	4	4425	6	NULL	NULL	NULL	NULL	Adf-1	GP		bind					TAFII110	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2252_s_269	9528796	(C) Adf-1 binds the same regions of TAFII110 and TAFII250 in vivo as it does in vitro.	bind
11086	1	4426	5	NULL	NULL	0	NULL	p53	NULL		bind	NULL				Snk/Plk2	NULL			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_16_5556_s_203	12897130	(c) Adriamycin treatment enhances p53 binding  to the Snk/Plk2 promoter in vivo.	bind
11087	2	4426	5	NULL	NULL	0	NULL	Adriamycin	NULL	treatment of	enhances	NULL				statement 1	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_16_5556_s_203	12897130	(c) Adriamycin treatment enhances p53 binding  to the Snk/Plk2 promoter in vivo.	bind
10332	1	4426	6	NULL	NULL	NULL	NULL	p53	GP		bind					Snk/Plk2	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_16_5556_s_203	12897130	(c) Adriamycin treatment enhances p53 binding  to the Snk/Plk2 promoter in vivo.	bind
10333	2	4426	6	NULL	NULL	NULL	NULL	adriamycin	Chemical	treatment of	enhances					statement 1	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_16_5556_s_203	12897130	(c) Adriamycin treatment enhances p53 binding  to the Snk/Plk2 promoter in vivo.	bind
11215	1	4428	5	10	NULL	0	NULL	GST-SOX9	NULL		bind	NULL				AMH	NULL			SOX-BS in proximal promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_11_6653_s_185	9774680	(C) Affinity binding of GST-SOX9 to the SOX-binding site (SOX-BS) in the AMH proximal promoter probe.	bind
11216	2	4428	5	NULL	NULL	0	NULL	SOX-BS	NULL		is	NULL				SOX-binding site	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_11_6653_s_185	9774680	(C) Affinity binding of GST-SOX9 to the SOX-binding site (SOX-BS) in the AMH proximal promoter probe.	bind
10334	1	4428	6	NULL	NULL	NULL	NULL	GST-SOX9	GP		bind					AMH 	GP			SOX-BS in the proximal promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_11_6653_s_185	9774680	(C) Affinity binding of GST-SOX9 to the SOX-binding site (SOX-BS) in the AMH proximal promoter probe.	bind
10335	2	4428	6	NULL	NULL	NULL	NULL	SOX-BS			is					SOX-binding site					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_11_6653_s_185	9774680	(C) Affinity binding of GST-SOX9 to the SOX-binding site (SOX-BS) in the AMH proximal promoter probe.	bind
11217	1	4431	5	NULL	NULL	0	NULL	SOS	NULL	Drosophila	bind	NULL	strongly			Drk	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_6_1_65_s_234	10949028	(C) Alignment of the C terminus of ARK-1 with a region of  Drosophila SOS that binds strongly to Drk, the  Drosophila ortholog of SEM-5 (see  Raabe et al. 1995  ).	bind
13122	2	4431	5	10	NULL	0	NULL	Drk		Drosophila	is ortholog of					SEM-5					NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_1_65_s_234	10949028	(C) Alignment of the C terminus of ARK-1 with a region of  Drosophila SOS that binds strongly to Drk, the  Drosophila ortholog of SEM-5 (see  Raabe et al. 1995  ).	bind
10337	1	4431	6	NULL	NULL	NULL	NULL	SOS	GP	Drosophila	bind		strongly			Drk	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_1_65_s_234	10949028	(C) Alignment of the C terminus of ARK-1 with a region of  Drosophila SOS that binds strongly to Drk, the  Drosophila ortholog of SEM-5 (see  Raabe et al. 1995  ).	bind
10338	2	4431	6	NULL	NULL	NULL	NULL	Drk	GP	Drosophila	is ortholog of					SEM-5	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_1_65_s_234	10949028	(C) Alignment of the C terminus of ARK-1 with a region of  Drosophila SOS that binds strongly to Drk, the  Drosophila ortholog of SEM-5 (see  Raabe et al. 1995  ).	bind
11220	1	4436	5	NULL	NULL	0	NULL	Ets2-Fli1 fusion protein	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_7_2467_s_232	16537893	(C) An Ets2-Fli1 fusion protein binds DNA cooperatively  with Fos-Jun.	bind
11222	2	4436	5	NULL	NULL	0	NULL	Fos-Jun	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_7_2467_s_232	16537893	(C) An Ets2-Fli1 fusion protein binds DNA cooperatively  with Fos-Jun.	bind
11223	3	4436	5	NULL	NULL	0	NULL	statement 1	NULL		occurs in cooperation with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_7_2467_s_232	16537893	(C) An Ets2-Fli1 fusion protein binds DNA cooperatively  with Fos-Jun.	bind
10339	1	4436	6	NULL	NULL	NULL	NULL	 Ets2-Fli1	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_7_2467_s_232	16537893	(C) An Ets2-Fli1 fusion protein binds DNA cooperatively  with Fos-Jun.	bind
10340	2	4436	6	NULL	NULL	NULL	NULL	Fos-Jun	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_7_2467_s_232	16537893	(C) An Ets2-Fli1 fusion protein binds DNA cooperatively  with Fos-Jun.	bind
12785	3	4436	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_7_2467_s_232	16537893	(C) An Ets2-Fli1 fusion protein binds DNA cooperatively  with Fos-Jun.	bind
11224	1	4437	5	10	NULL	0	NULL	anti-VCP IgY 		affinity-purified	bind					rVCP					NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_30_s_115	12922167	(c) Analysis of affinity-purified anti-VCP IgY (primary antibody) binding to rVCP, and anti-chicken IgG (secondary antibody) binding to anti-VCP IgY primary antibody.	bind
11225	2	4437	5	10	NULL	0	NULL	anti-chicken IgG 			bind					anti-VCP IgY 					NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_30_s_115	12922167	(c) Analysis of affinity-purified anti-VCP IgY (primary antibody) binding to rVCP, and anti-chicken IgG (secondary antibody) binding to anti-VCP IgY primary antibody.	bind
54299	3	4437	5	10	NULL	0	NULL	anti-VCP IgY			is a type of					primary antibody					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_30_s_115	12922167	(c) Analysis of affinity-purified anti-VCP IgY (primary antibody) binding to rVCP, and anti-chicken IgG (secondary antibody) binding to anti-VCP IgY primary antibody.	bind
54300	4	4437	5	10	NULL	0	NULL	anti-chicken IgG 			is a type of					secondary antibody					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_30_s_115	12922167	(c) Analysis of affinity-purified anti-VCP IgY (primary antibody) binding to rVCP, and anti-chicken IgG (secondary antibody) binding to anti-VCP IgY primary antibody.	bind
10341	1	4437	6	NULL	NULL	NULL	NULL	anti-VCP IgY	GP	affinity-purified	bind					rVCP	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_30_s_115	12922167	(c) Analysis of affinity-purified anti-VCP IgY (primary antibody) binding to rVCP, and anti-chicken IgG (secondary antibody) binding to anti-VCP IgY primary antibody.	bind
10342	2	4437	6	NULL	NULL	NULL	NULL	anti-chicken IgG	GP		bind					anti-VCP IgY 	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_30_s_115	12922167	(c) Analysis of affinity-purified anti-VCP IgY (primary antibody) binding to rVCP, and anti-chicken IgG (secondary antibody) binding to anti-VCP IgY primary antibody.	bind
54301	3	4437	6	NULL	NULL	NULL	NULL	anti-VCP IgY	GP		is a type of					primary antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_30_s_115	12922167	(c) Analysis of affinity-purified anti-VCP IgY (primary antibody) binding to rVCP, and anti-chicken IgG (secondary antibody) binding to anti-VCP IgY primary antibody.	bind
54302	4	4437	6	NULL	NULL	NULL	NULL	anti-chicken IgG	GP		is a type of					secondary antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_30_s_115	12922167	(c) Analysis of affinity-purified anti-VCP IgY (primary antibody) binding to rVCP, and anti-chicken IgG (secondary antibody) binding to anti-VCP IgY primary antibody.	bind
11227	1	4438	5	10	NULL	0	NULL	eIF2		purified	bind					eIF2B complex		FLAG-tagged;; wild-type			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3965_s_323	10805739	(C) Analysis of binding between the indicated concentration of purified eIF2 and FLAG-tagged wild-type eIF2B complex (lanes 7 to 10) or eIF2BepsilonF250L (lanes 11 to 14).	bind
11228	2	4438	5	NULL	NULL	0	NULL	eIF2	NULL	purified	bind	NULL				eIF2Bepsilon	NULL		F250L		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_11_3965_s_323	10805739	(C) Analysis of binding between the indicated concentration of purified eIF2 and FLAG-tagged wild-type eIF2B complex (lanes 7 to 10) or eIF2BepsilonF250L (lanes 11 to 14).	bind
54303	3	4438	5	10	NULL	0	NULL	statement 1			is an alternative to					statement 2					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_11_3965_s_323	10805739	(C) Analysis of binding between the indicated concentration of purified eIF2 and FLAG-tagged wild-type eIF2B complex (lanes 7 to 10) or eIF2BepsilonF250L (lanes 11 to 14).	bind
10523	1	4438	6	NULL	NULL	NULL	NULL	eIF2	GP		bind					eIF2B complex	GP	FLAG-tagged;;wild type			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3965_s_323	10805739	(C) Analysis of binding between the indicated concentration of purified eIF2 and FLAG-tagged wild-type eIF2B complex (lanes 7 to 10) or eIF2BepsilonF250L (lanes 11 to 14).	bind
10524	2	4438	6	NULL	NULL	NULL	NULL	eIF2	GP		bind					eIF2Bepsilon	GP		F250L		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3965_s_323	10805739	(C) Analysis of binding between the indicated concentration of purified eIF2 and FLAG-tagged wild-type eIF2B complex (lanes 7 to 10) or eIF2BepsilonF250L (lanes 11 to 14).	bind
10525	3	4438	6	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3965_s_323	10805739	(C) Analysis of binding between the indicated concentration of purified eIF2 and FLAG-tagged wild-type eIF2B complex (lanes 7 to 10) or eIF2BepsilonF250L (lanes 11 to 14).	bind
11230	1	4439	5	NULL	NULL	0	NULL	NFATp/c	NULL		bind	NULL					NULL			IL190 element	NULL	PMA/I-activated Jurkat cell nuclear extracts	0	NULL	NULL	NULL	gw60_immunity_6_2_175_s_150	9047239	(C) Analysis of NFATp/c and Oct binding to the IL190 element using PMA/I-activated Jurkat cell nuclear extracts in the presence and absence of 1  l of Oct-1 and 0.2  l of NFATp antisera.	bind
11231	2	4439	5	NULL	NULL	0	NULL	Oct	NULL		bind	NULL					NULL			IL190 element	NULL	PMA/I-activated Jurkat cell nuclear extracts 	0	NULL	NULL	NULL	gw60_immunity_6_2_175_s_150	9047239	(C) Analysis of NFATp/c and Oct binding to the IL190 element using PMA/I-activated Jurkat cell nuclear extracts in the presence and absence of 1  l of Oct-1 and 0.2  l of NFATp antisera.	bind
10529	1	4439	6	NULL	NULL	NULL	NULL	NFATp/c	GP		bind									IL190 element	NULL	PMA/I-activated Jurkat cell nuclear extracts	NULL	NULL	NULL	NULL	gw60_immunity_6_2_175_s_150	9047239	(C) Analysis of NFATp/c and Oct binding to the IL190 element using PMA/I-activated Jurkat cell nuclear extracts in the presence and absence of 1  l of Oct-1 and 0.2  l of NFATp antisera.	bind
10531	2	4439	6	NULL	NULL	NULL	NULL	Oct	GP		bind									IL190 element	NULL	PMA/I-activated Jurkat cell nuclear extracts	NULL	NULL	NULL	NULL	gw60_immunity_6_2_175_s_150	9047239	(C) Analysis of NFATp/c and Oct binding to the IL190 element using PMA/I-activated Jurkat cell nuclear extracts in the presence and absence of 1  l of Oct-1 and 0.2  l of NFATp antisera.	bind
11232	1	4440	5	10	NULL	0	NULL				bind			E-NTD 		RseA-cyto-His6					NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_4_1067_s_148	12718891	(C) Anti- E Western blot showing that both  E-NTD and -CTD domains bind to RseA-cyto-His6.	bind
11233	2	4440	5	10	NULL	0	NULL				bind			E-CTD		RseA-cyto-His6					NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_4_1067_s_148	12718891	(C) Anti- E Western blot showing that both  E-NTD and -CTD domains bind to RseA-cyto-His6.	bind
10535	1	4440	6	NULL	NULL	NULL	NULL				bind			E-NTD		RseA-cyto-His6	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_4_1067_s_148	12718891	(C) Anti- E Western blot showing that both  E-NTD and -CTD domains bind to RseA-cyto-His6.	bind
10536	2	4440	6	NULL	NULL	NULL	NULL				bind			E-CTD		RseA-cyto-His6	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_4_1067_s_148	12718891	(C) Anti- E Western blot showing that both  E-NTD and -CTD domains bind to RseA-cyto-His6.	bind
11234	1	4441	5	NULL	NULL	0	NULL	AP-1	NULL		bind	NULL				normal membranes	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_cell_114_3_299_s_170	12914695	(C) Anti-PI(4)P blocks AP-1 binding to normal membranes in vitro.	bind
11235	2	4441	5	NULL	NULL	0	NULL	anti-PI(4)P	NULL		blocks	NULL				statement 1	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cell_114_3_299_s_170	12914695	(C) Anti-PI(4)P blocks AP-1 binding to normal membranes in vitro.	bind
10537	1	4441	6	NULL	NULL	NULL	NULL	AP-1	GP		bind					normal membranes	CellComponent				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cell_114_3_299_s_170	12914695	(C) Anti-PI(4)P blocks AP-1 binding to normal membranes in vitro.	bind
10538	2	4441	6	NULL	NULL	NULL	NULL	Anti-PI(4)P	GP		blocks					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cell_114_3_299_s_170	12914695	(C) Anti-PI(4)P blocks AP-1 binding to normal membranes in vitro.	bind
11237	1	4442	5	NULL	NULL	0	NULL	PF2 antibody	NULL		bind	NULL				zonular microfibrils 	NULL	bovine			NULL	middle of the interbead 	NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_1045_s_156	11238459	(C) Antibody PF2 (purple) binds bovine zonular microfibrils near the middle of the interbead.	bind
10539	1	4442	6	NULL	NULL	NULL	NULL	PF2 antibody	GP		bind					zonular microfibrils	CellComponent	bovine			NULL	middle of the interbead	NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_1045_s_156	11238459	(C) Antibody PF2 (purple) binds bovine zonular microfibrils near the middle of the interbead.	bind
11238	1	4443	5	NULL	NULL	0	NULL	AP-2	NULL		bind	NULL				C40 enhancer	NULL			AP-2(B) motif in	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_8_3308_s_272	16581802	(C) AP-2 binds to the AP-2(B) motif within the C40 enhancer.	bind
10540	1	4443	6	NULL	NULL	NULL	NULL	AP-2	GP		bind					C40 enhancer	GP			AP-2(B) motif in	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_8_3308_s_272	16581802	(C) AP-2 binds to the AP-2(B) motif within the C40 enhancer.	bind
11241	1	4444	5	NULL	NULL	0	NULL	APA-1	NULL		bind	NULL				MMP1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_21_7385_s_321	12370286	(C) APA-1 binds to the  MMP1 promoter.	bind
10541	1	4444	6	NULL	NULL	NULL	NULL	APA-1	GP		bind					MMP1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_21_7385_s_321	12370286	(C) APA-1 binds to the  MMP1 promoter.	bind
11242	1	4445	5	10	NULL	0	NULL	ArpA			does not bind			W119A		A-factor					NULL		NULL	NULL	NULL	NULL	gw60_gene_222_1_133_s_210	9813285	(c) ArpA/W119A does not bind A-factor, since almost no radioactivity elutes in fractions 3 and 4 in either the presence ( ) or the absence ( ) of non-labelled A-factor.	bind
10542	1	4445	6	NULL	NULL	NULL	NULL	ArpA	GP		does not bind			W119A		A-factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_gene_222_1_133_s_210	9813285	(c) ArpA/W119A does not bind A-factor, since almost no radioactivity elutes in fractions 3 and 4 in either the presence ( ) or the absence ( ) of non-labelled A-factor.	bind
11245	1	4446	5	NULL	NULL	0	NULL	Hsp70/Hsc70	NULL	endogenous	bind	NULL				GADD34-BAG-1 complex	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_10_3477_s_145	12724406	(C) ATP modulation of the binding of endogenous Hsp70/Hsc70 and PP1 to the GADD34-BAG-1 complex.	bind
11247	2	4446	5	NULL	NULL	0	NULL	PP1	NULL	endogenous	bind	NULL				GADD34-BAG-1 complex	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_10_3477_s_145	12724406	(C) ATP modulation of the binding of endogenous Hsp70/Hsc70 and PP1 to the GADD34-BAG-1 complex.	bind
11248	3	4446	5	NULL	NULL	0	NULL	ATP	NULL		modulate	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_10_3477_s_145	12724406	(C) ATP modulation of the binding of endogenous Hsp70/Hsc70 and PP1 to the GADD34-BAG-1 complex.	bind
11249	4	4446	5	NULL	NULL	0	NULL	ATP	NULL		modulate	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_10_3477_s_145	12724406	(C) ATP modulation of the binding of endogenous Hsp70/Hsc70 and PP1 to the GADD34-BAG-1 complex.	bind
10543	1	4446	6	NULL	NULL	NULL	NULL	Hsp70/Hsc70	GP	endogenous	bind					GADD34-BAG-1 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_10_3477_s_145	12724406	(C) ATP modulation of the binding of endogenous Hsp70/Hsc70 and PP1 to the GADD34-BAG-1 complex.	bind
10544	2	4446	6	NULL	NULL	NULL	NULL	PP1	GP	endogenous	bind					GADD34-BAG-1 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_10_3477_s_145	12724406	(C) ATP modulation of the binding of endogenous Hsp70/Hsc70 and PP1 to the GADD34-BAG-1 complex.	bind
12786	3	4446	6	NULL	NULL	NULL	NULL	ATP	Chemical		modulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_10_3477_s_145	12724406	(C) ATP modulation of the binding of endogenous Hsp70/Hsc70 and PP1 to the GADD34-BAG-1 complex.	bind
12787	4	4446	6	NULL	NULL	NULL	NULL	ATP	Chemical		modulates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_10_3477_s_145	12724406	(C) ATP modulation of the binding of endogenous Hsp70/Hsc70 and PP1 to the GADD34-BAG-1 complex.	bind
11250	1	4447	5	NULL	NULL	0	NULL	CAND1	NULL		bind	NULL				CUL1	NULL				NULL	HeLa extracts	0	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_135	12504026	(C) ATP prevents the binding of CAND1 to CUL1 in HeLa extracts.	bind
11251	2	4447	5	NULL	NULL	0	NULL	ATP	NULL		prevent	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_135	12504026	(C) ATP prevents the binding of CAND1 to CUL1 in HeLa extracts.	bind
10545	1	4447	6	NULL	NULL	NULL	NULL	CAND1	GP		bind					CUL1	GP				NULL	HeLa nuclear extracts	NULL	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_135	12504026	(C) ATP prevents the binding of CAND1 to CUL1 in HeLa extracts.	bind
10546	2	4447	6	NULL	NULL	NULL	NULL	ATP	Chemical		prevents					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_135	12504026	(C) ATP prevents the binding of CAND1 to CUL1 in HeLa extracts.	bind
11253	1	4448	5	NULL	NULL	0	NULL	Aurora-A	NULL		bind	NULL				CNN	NULL		COOH-terminal domain		NULL		0	NULL	NULL	NULL	gw70_cellbiol_162_5_757_s_32	12939255	(C) Aurora-A  binds to the COOH-terminal domain of CNN.	bind
10547	1	4448	6	NULL	NULL	NULL	NULL	Aurora-A	GP		bind					CNN	GP		COOH-terminal domain		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_5_757_s_32	12939255	(C) Aurora-A  binds to the COOH-terminal domain of CNN.	bind
11255	1	4449	5	NULL	NULL	0	NULL	PAPs	NULL	35S-labeled	bind	NULL				GST-cyclin B1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_14_5310_s_133	10866687	(C) Autoradiogram of 35S-labeled PAPs bound to either GST-cyclin B1 (lanes 1, 3, 5, and 7) or GST (lanes 2, 4, 6, and 8).	bind
11256	2	4449	5	NULL	NULL	0	NULL	PAPs	NULL	35S-labeled	bind	NULL				GST	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_14_5310_s_133	10866687	(C) Autoradiogram of 35S-labeled PAPs bound to either GST-cyclin B1 (lanes 1, 3, 5, and 7) or GST (lanes 2, 4, 6, and 8).	bind
13123	3	4449	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_14_5310_s_133	10866687	(C) Autoradiogram of 35S-labeled PAPs bound to either GST-cyclin B1 (lanes 1, 3, 5, and 7) or GST (lanes 2, 4, 6, and 8).	bind
10548	1	4449	6	NULL	NULL	NULL	NULL	PAPs	GP	35S-labeled	bind					GST-cyclin B1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_14_5310_s_133	10866687	(C) Autoradiogram of 35S-labeled PAPs bound to either GST-cyclin B1 (lanes 1, 3, 5, and 7) or GST (lanes 2, 4, 6, and 8).	bind
10549	2	4449	6	NULL	NULL	NULL	NULL	PAPs	GP	35S-labeled	bind					GST					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_14_5310_s_133	10866687	(C) Autoradiogram of 35S-labeled PAPs bound to either GST-cyclin B1 (lanes 1, 3, 5, and 7) or GST (lanes 2, 4, 6, and 8).	bind
10550	3	4449	6	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_14_5310_s_133	10866687	(C) Autoradiogram of 35S-labeled PAPs bound to either GST-cyclin B1 (lanes 1, 3, 5, and 7) or GST (lanes 2, 4, 6, and 8).	bind
11257	1	4450	5	10	NULL	0	NULL	hybrid 8			bind					32P DNA					NULL		NULL	NULL	NULL	NULL	gw60_chembiol_10_8_713_s_142	12954330	(C) Autoradiogram showing the binding of hybrid  8 to 32P DNAs (45 pM).	bind
10551	1	4450	6	NULL	NULL	NULL	NULL	hybrid 8			bind					32P DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_10_8_713_s_142	12954330	(C) Autoradiogram showing the binding of hybrid  8 to 32P DNAs (45 pM).	bind
11258	1	4453	5	NULL	NULL	0	NULL	PriA protein	NULL		bind	NULL				Fork 4	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_9_2_241_s_197	11864599	(C) Band-shift assay showing binding of PriA and SrgA proteins to Fork 4 in the presence of EDTA.	bind
11259	2	4453	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				EDTA	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_9_2_241_s_197	11864599	(C) Band-shift assay showing binding of PriA and SrgA proteins to Fork 4 in the presence of EDTA.	bind
11260	3	4453	5	NULL	NULL	0	NULL	SrgA protein	NULL		bind	NULL				Fork 4	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_9_2_241_s_197	11864599	(C) Band-shift assay showing binding of PriA and SrgA proteins to Fork 4 in the presence of EDTA.	bind
11261	4	4453	5	NULL	NULL	0	NULL	statement 3	NULL		in the presence of	NULL				EDTA	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_9_2_241_s_197	11864599	(C) Band-shift assay showing binding of PriA and SrgA proteins to Fork 4 in the presence of EDTA.	bind
10552	1	4453	6	NULL	NULL	NULL	NULL	PriA	GP		bind					Fork 4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_9_2_241_s_197	11864599	(C) Band-shift assay showing binding of PriA and SrgA proteins to Fork 4 in the presence of EDTA.	bind
10553	2	4453	6	NULL	NULL	NULL	NULL	SrgA	GP		bind					Fork 4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_9_2_241_s_197	11864599	(C) Band-shift assay showing binding of PriA and SrgA proteins to Fork 4 in the presence of EDTA.	bind
10554	3	4453	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs in presence of					EDTA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_9_2_241_s_197	11864599	(C) Band-shift assay showing binding of PriA and SrgA proteins to Fork 4 in the presence of EDTA.	bind
10555	4	4453	6	NULL	NULL	NULL	NULL	statement 2	Process		occurs in presence of					EDTA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_9_2_241_s_197	11864599	(C) Band-shift assay showing binding of PriA and SrgA proteins to Fork 4 in the presence of EDTA.	bind
11263	1	4454	5	NULL	NULL	0	NULL	NR	NULL		bind	NULL					NULL		RBD-2		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_203	10891484	(C) Basic/polar residues N terminal to the core LXXLL motif are critical for NR binding to RBD-2.	bind
11264	2	4454	5	NULL	NULL	0	NULL		NULL		critical for	NULL		basic/polar residues N terminal to core LXXLL motif		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_203	10891484	(C) Basic/polar residues N terminal to the core LXXLL motif are critical for NR binding to RBD-2.	bind
10761	1	4454	6	NULL	NULL	NULL	NULL	NR	GP		bind								RBD-2		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_203	10891484	(C) Basic/polar residues N terminal to the core LXXLL motif are critical for NR binding to RBD-2.	bind
10762	2	4454	6	NULL	NULL	NULL	NULL				are critical for			Basic/polar residues N terminal to the core LXXLL motif		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_203	10891484	(C) Basic/polar residues N terminal to the core LXXLL motif are critical for NR binding to RBD-2.	bind
11267	1	4455	5	NULL	NULL	0	NULL	Bcl-3 protein	NULL		bind	NULL				cyclin D1	NULL			proximal NF-kappaB site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_24_8428_s_190	11713278	(C) Bcl-3 and p52 proteins bind to the proximal NF-kappaB site of the cyclin D1 promoter.	bind
11268	2	4455	5	NULL	NULL	0	NULL	p52 protein	NULL		bind	NULL				cyclin D1	NULL			proximal NF-kappaB site of promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_24_8428_s_190	11713278	(C) Bcl-3 and p52 proteins bind to the proximal NF-kappaB site of the cyclin D1 promoter.	bind
10763	1	4455	6	NULL	NULL	NULL	NULL	Bcl-3	GP		bind					cyclin D1	GP			proximal NF-kappaB site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_24_8428_s_190	11713278	(C) Bcl-3 and p52 proteins bind to the proximal NF-kappaB site of the cyclin D1 promoter.	bind
10764	2	4455	6	NULL	NULL	NULL	NULL	p52	GP		bind					cyclin D1	GP			proximal NF-kappaB site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_24_8428_s_190	11713278	(C) Bcl-3 and p52 proteins bind to the proximal NF-kappaB site of the cyclin D1 promoter.	bind
11270	1	4457	5	NULL	NULL	0	NULL	BCS1(84-126)-DHFR	NULL		bind	NULL				OMV	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_7_2239_s_277	12640110	(C) BCS1(84-126)-DHFR bound to OMV can be coimmunoprecipitated  with components of the TOM complex.	bind
11272	2	4457	5	NULL	NULL	0	NULL	statement 1	NULL		coimmunoprecipitates with	NULL				TOM complex	NULL	components of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_7_2239_s_277	12640110	(C) BCS1(84-126)-DHFR bound to OMV can be coimmunoprecipitated  with components of the TOM complex.	bind
10765	1	4457	6	NULL	NULL	NULL	NULL	BCS1-DHFR	GP		bind					OMV	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_7_2239_s_277	12640110	(C) BCS1(84-126)-DHFR bound to OMV can be coimmunoprecipitated  with components of the TOM complex.	bind
10766	2	4457	6	NULL	NULL	NULL	NULL	statement 1	Process		coimmunoprecipitates					TOM complex	CellComponent	components of 			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_7_2239_s_277	12640110	(C) BCS1(84-126)-DHFR bound to OMV can be coimmunoprecipitated  with components of the TOM complex.	bind
11274	1	4460	5	NULL	NULL	0	NULL	Bfa1p	NULL		bind	NULL	directly			Cdc14p	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_157_3_367_s_102	11970961	(C) Bfa1p and Tem1p bind directly to Cdc14p.	bind
11275	2	4460	5	NULL	NULL	0	NULL	Tem1p	NULL		bind	NULL	directly			Cdc14p	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_157_3_367_s_102	11970961	(C) Bfa1p and Tem1p bind directly to Cdc14p.	bind
10767	1	4460	6	NULL	NULL	NULL	NULL	Bfa1p	GP		bind		directly			Cdc14p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_367_s_102	11970961	(C) Bfa1p and Tem1p bind directly to Cdc14p.	bind
10768	2	4460	6	NULL	NULL	NULL	NULL	Tem1p	GP		bind		directly			Cdc14p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_367_s_102	11970961	(C) Bfa1p and Tem1p bind directly to Cdc14p.	bind
11277	1	4461	5	NULL	NULL	0	NULL	CRMP-2	NULL		bind	NULL				tubulin	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_22_9973_s_149	16260611	(C) Biacore sensorgram of CRMP-2 binding to tubulin.	bind
10769	1	4461	6	NULL	NULL	NULL	NULL	CRMP-2	GP		bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9973_s_149	16260611	(C) Biacore sensorgram of CRMP-2 binding to tubulin.	bind
11278	1	4462	5	NULL	NULL	0	NULL	wtBH3	NULL		is	NULL				Bim BH3 peptide	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_162_5_877_s_100	12952938	(C) Bim BH3 peptide (wtBH3) binds Bcl-w as well as BimLdeltaC27.	bind
11280	2	4462	5	NULL	NULL	0	NULL	wtBH3	NULL		bind	NULL				Bcl-w	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_162_5_877_s_100	12952938	(C) Bim BH3 peptide (wtBH3) binds Bcl-w as well as BimLdeltaC27.	bind
11282	3	4462	5	10	NULL	0	NULL	wtBH3			bind					BimLdeltaC27					NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_5_877_s_100	12952938	(C) Bim BH3 peptide (wtBH3) binds Bcl-w as well as BimLdeltaC27.	bind
10770	1	4462	6	NULL	NULL	NULL	NULL	Bim BH3 peptide	AminoAcid	wild type	bind					Bcl-w	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_5_877_s_100	12952938	(C) Bim BH3 peptide (wtBH3) binds Bcl-w as well as BimLdeltaC27.	bind
10771	2	4462	6	NULL	NULL	NULL	NULL	Bim BH3 peptide	AminoAcid	wild type	bind					BimLdeltaC27	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_5_877_s_100	12952938	(C) Bim BH3 peptide (wtBH3) binds Bcl-w as well as BimLdeltaC27.	bind
54304	3	4462	6	NULL	NULL	NULL	NULL	wtBH3	GP		is					Bim BH3 peptide	AminoAcid	wild type			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_5_877_s_100	12952938	(C) Bim BH3 peptide (wtBH3) binds Bcl-w as well as BimLdeltaC27.	bind
11284	1	4463	5	NULL	NULL	0	NULL	IgG2 MAbs	NULL		bind	NULL				PNAG antigen	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_74_5_2742_s_161	16622211	(C) Binding  of IgG2 MAbs to PNAG antigen.	bind
10772	1	4463	6	NULL	NULL	NULL	NULL	IgG2 MAbs	GP		bind					PNAG antigen	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_5_2742_s_161	16622211	(C) Binding  of IgG2 MAbs to PNAG antigen.	bind
11285	1	4464	5	NULL	NULL	0	NULL	MECA-79 antibody	NULL		bind	NULL				MECA-79-positive CD34.IgG	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_105_7_957_s_100	11439191	(C) Binding  of MECA-79 antibody to MECA-79-positive CD34.IgG coated  on plates was measured in the absence  and presence of synthetic oligosaccharides, shown at right, at  different concentrations	bind
12871	1	4464	6	NULL	NULL	0	NULL	MECA-79 antibody	NULL		bind	NULL				MECA-79-positive CD34.IgG	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_105_7_957_s_100	11439191	(C) Binding  of MECA-79 antibody to MECA-79-positive CD34.IgG coated  on plates was measured in the absence  and presence of synthetic oligosaccharides, shown at right, at  different concentrations	bind
11286	1	4465	5	NULL	NULL	0	NULL	NK cells	NULL		bind	NULL				annexin V-FITC	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_3_810_s_139	15240120	(C) Binding  of NK cells to annexin V-FITC and propidium iodide (PI).	bind
11287	2	4465	5	NULL	NULL	0	NULL	NK cells	NULL		bind	NULL				PI	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_3_810_s_139	15240120	(C) Binding  of NK cells to annexin V-FITC and propidium iodide (PI).	bind
11288	3	4465	5	NULL	NULL	0	NULL	PI	NULL		is	NULL				propidium iodide	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_3_810_s_139	15240120	(C) Binding  of NK cells to annexin V-FITC and propidium iodide (PI).	bind
10773	1	4465	6	NULL	NULL	NULL	NULL	NK cells	Cell		bind					annexin V-FITC	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_3_810_s_139	15240120	(C) Binding  of NK cells to annexin V-FITC and propidium iodide (PI).	bind
10774	2	4465	6	NULL	NULL	NULL	NULL	NK cells	Cell		bind					propidium iodide	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_3_810_s_139	15240120	(C) Binding  of NK cells to annexin V-FITC and propidium iodide (PI).	bind
10775	3	4465	6	NULL	NULL	NULL	NULL	PI	Chemical		is					propidium iodide	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_3_810_s_139	15240120	(C) Binding  of NK cells to annexin V-FITC and propidium iodide (PI).	bind
11290	1	4467	5	NULL	NULL	0	NULL	ERK2	NULL		bind	NULL				GST-Elk-1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_710_s_317	9447967	(C) Binding and phosphorylation of GST-Elk-1 fusion proteins by ERK2.	bind
11291	2	4467	5	NULL	NULL	0	NULL	ERK2	NULL		phosphorylate	NULL				GST-Elk-1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_710_s_317	9447967	(C) Binding and phosphorylation of GST-Elk-1 fusion proteins by ERK2.	bind
44556	3	4467	5	10	NULL	0	NULL	GST-Elk-1	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_2_710_s_317	9447967	(C) Binding and phosphorylation of GST-Elk-1 fusion proteins by ERK2.	bind
10776	1	4467	6	NULL	NULL	NULL	NULL	ERK2	GP		bind					GST-Elk-1 	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_710_s_317	9447967	(C) Binding and phosphorylation of GST-Elk-1 fusion proteins by ERK2.	bind
10777	2	4467	6	NULL	NULL	NULL	NULL	ERK2	GP		phosphorylates					GST-Elk-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_710_s_317	9447967	(C) Binding and phosphorylation of GST-Elk-1 fusion proteins by ERK2.	bind
41477	3	4467	6	NULL	NULL	NULL	NULL	GST-Elk-1	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_710_s_317	9447967	(C) Binding and phosphorylation of GST-Elk-1 fusion proteins by ERK2.	bind
11292	1	4468	5	NULL	NULL	0	NULL	ER	NULL		bind	NULL				TIF2	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_3_656_s_63	14680815	(C) Binding between ER  and TIF2 was examined using the mammalian two-hybrid  system.	bind
10778	1	4468	6	NULL	NULL	NULL	NULL	ER	GP		bind					TIF2	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_3_656_s_63	14680815	(C) Binding between ER  and TIF2 was examined using the mammalian two-hybrid  system.	bind
11293	1	4469	5	10	NULL	0	NULL	IL-8	NULL		bind	NULL				CXCR1-CFP receptors	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5752_s_80	15964828	(c) Binding curve of IL-8 with CXCR1-CFP receptors  expressed in CX1-HEK cells.	bind
44558	2	4469	5	10	NULL	0	NULL	 CXCR1-CFP receptors	NULL		expressed in	NULL				CX1-HEK cells	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5752_s_80	15964828	(c) Binding curve of IL-8 with CXCR1-CFP receptors  expressed in CX1-HEK cells.	bind
10779	1	4469	6	NULL	NULL	NULL	NULL	IL-8	GP		bind					CXCR1-CFP receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5752_s_80	15964828	(c) Binding curve of IL-8 with CXCR1-CFP receptors  expressed in CX1-HEK cells.	bind
41478	2	4469	6	NULL	NULL	NULL	NULL	CXCR1-CFP receptors	GP		are expressed in					CX1-HEK cells 	Cell				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5752_s_80	15964828	(c) Binding curve of IL-8 with CXCR1-CFP receptors  expressed in CX1-HEK cells.	bind
11294	1	4470	5	10	NULL	0	NULL	MDMX			bind					p53					NULL	H1299 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6509_s_157	16024788	(c) Binding efficiency between  MDMX and p53 was determined by transient cotransfection of H1299 cells with MDMX  and p53 expression plasmids, followed by MDMX IP/p53 Western blotting.	bind
10780	1	4470	6	NULL	NULL	NULL	NULL	MDMX	GP		bind					p53	GP				NULL	H1299 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6509_s_157	16024788	(c) Binding efficiency between  MDMX and p53 was determined by transient cotransfection of H1299 cells with MDMX  and p53 expression plasmids, followed by MDMX IP/p53 Western blotting.	bind
11295	1	4472	5	NULL	NULL	0	NULL	Sox-2	NULL		bind	NULL				UTF1	NULL			regulatory element	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_179	10409735	(C) Binding modes of Sox-2 and Oct-3/4 to the UTF1 regulatory element.	bind
11296	2	4472	5	NULL	NULL	0	NULL	Oct-3/4	NULL		bind	NULL				UTF1	NULL			regulatory element	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_179	10409735	(C) Binding modes of Sox-2 and Oct-3/4 to the UTF1 regulatory element.	bind
10781	1	4472	6	NULL	NULL	NULL	NULL	Sox-2	GP		bind					UTF-1	GP			regulatory element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_179	10409735	(C) Binding modes of Sox-2 and Oct-3/4 to the UTF1 regulatory element.	bind
10782	2	4472	6	NULL	NULL	NULL	NULL	Oct-3/4	GP		bind					UTF-1	GP			regulatory element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_179	10409735	(C) Binding modes of Sox-2 and Oct-3/4 to the UTF1 regulatory element.	bind
11297	1	4473	5	NULL	NULL	0	NULL	 calmodulin	NULL		bind	NULL				L-selectin	NULL		cytoplasmic tail		NULL		0	NULL	NULL	NULL	gw60_cell_92_6_809_s_108	9529256	(C) Binding of  calmodulin to the L-selectin cytoplasmic tail is inhibited by trifluoperazine.	bind
11298	2	4473	5	NULL	NULL	0	NULL	trifluoperazine	NULL		inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_92_6_809_s_108	9529256	(C) Binding of  calmodulin to the L-selectin cytoplasmic tail is inhibited by trifluoperazine.	bind
10783	1	4473	6	NULL	NULL	NULL	NULL	calmodulin	GP		bind					L-selectin	GP		cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_cell_92_6_809_s_108	9529256	(C) Binding of  calmodulin to the L-selectin cytoplasmic tail is inhibited by trifluoperazine.	bind
10784	2	4473	6	NULL	NULL	NULL	NULL	trifluoperazine	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_92_6_809_s_108	9529256	(C) Binding of  calmodulin to the L-selectin cytoplasmic tail is inhibited by trifluoperazine.	bind
11300	2	4474	5	NULL	NULL	0	NULL	4.1R/GST	NULL		bind	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_1_29_s_225	10189366	(C) Binding of 4.1R/GST to NuMA amino acid  sequence 1697-1889 translated from NuMA2/TOPO.	bind
11302	1	4474	5	NULL	NULL	0	NULL	NuMA	NULL		translated from	NULL		amino acid sequence 1697-1889		NuMA2/TOPO	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_1_29_s_225	10189366	(C) Binding of 4.1R/GST to NuMA amino acid  sequence 1697-1889 translated from NuMA2/TOPO.	bind
10785	1	4474	6	NULL	NULL	NULL	NULL	4.1R/GST	GP		bind					NuMA 	GP		amino acid sequence 1697-1889		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_1_29_s_225	10189366	(C) Binding of 4.1R/GST to NuMA amino acid  sequence 1697-1889 translated from NuMA2/TOPO.	bind
10786	2	4474	6	NULL	NULL	NULL	NULL	NuMA 	GP		translated from			amino acid sequence 1697-1889		NuMA2/TOPO	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_1_29_s_225	10189366	(C) Binding of 4.1R/GST to NuMA amino acid  sequence 1697-1889 translated from NuMA2/TOPO.	bind
11304	2	4475	5	10	NULL	0	NULL	4BP-1			bind					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6041_s_135	10454551	(C) Binding of 4BP-1 to eIF-4E (bound to m7-GTP resin) was determined in the presence or absence of rapamycin (0.2 muM).	bind
54305	1	4475	5	10	NULL	0	NULL	 eIF-4E			bind					m7-GTP resin					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6041_s_135	10454551	(C) Binding of 4BP-1 to eIF-4E (bound to m7-GTP resin) was determined in the presence or absence of rapamycin (0.2 muM).	bind
10787	1	4475	6	NULL	NULL	NULL	NULL	eIF-4E	GP		bind					m7-GTP resin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6041_s_135	10454551	(C) Binding of 4BP-1 to eIF-4E (bound to m7-GTP resin) was determined in the presence or absence of rapamycin (0.2 muM).	bind
10788	2	4475	6	NULL	NULL	NULL	NULL	4BP-1	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6041_s_135	10454551	(C) Binding of 4BP-1 to eIF-4E (bound to m7-GTP resin) was determined in the presence or absence of rapamycin (0.2 muM).	bind
11306	1	4476	5	NULL	NULL	0	NULL	Abf2p	NULL		bind	NULL				four-way junction DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1522_3_175_s_225	11779632	(C) Binding of Abf2p and phosphorylated Abf2p to four-way junction DNA.	bind
11308	2	4476	5	NULL	NULL	0	NULL	Abf2p	NULL	phosphorylated	bind	NULL				four-way junction DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1522_3_175_s_225	11779632	(C) Binding of Abf2p and phosphorylated Abf2p to four-way junction DNA.	bind
10789	1	4476	6	NULL	NULL	NULL	NULL	Abf2p	GP		bind					four-way junction DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1522_3_175_s_225	11779632	(C) Binding of Abf2p and phosphorylated Abf2p to four-way junction DNA.	bind
10790	2	4476	6	NULL	NULL	NULL	NULL	Abf2p	GP	phosphorylated	bind					four-way junction DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1522_3_175_s_225	11779632	(C) Binding of Abf2p and phosphorylated Abf2p to four-way junction DNA.	bind
11309	1	4478	5	NULL	NULL	0	NULL	B-Myb	NULL		bind	NULL				NLK	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4705_s_137	16055500	(C) Binding of B-Myb to NLK  and HIPK2.	bind
11310	2	4478	5	NULL	NULL	0	NULL	B-Myb	NULL		bind	NULL				HIPK2	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4705_s_137	16055500	(C) Binding of B-Myb to NLK  and HIPK2.	bind
10791	1	4478	6	NULL	NULL	NULL	NULL	B-Myb	GP		bind					NLK	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4705_s_137	16055500	(C) Binding of B-Myb to NLK  and HIPK2.	bind
10792	2	4478	6	NULL	NULL	NULL	NULL	B-Myb	GP		bind					HIPK2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4705_s_137	16055500	(C) Binding of B-Myb to NLK  and HIPK2.	bind
11311	1	4479	5	NULL	NULL	0	NULL	Sir3p protein	NULL		bind	NULL				telomeric sequences	NULL				NULL	nocodazole-arrested (G2/M) phase cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4202_s_217	12024033	(C) Binding of both Sir3p and Dna2-Myc protein to telomeric sequences in nocodazole-arrested (G2/M) phase cells.	bind
11312	2	4479	5	NULL	NULL	0	NULL	Dna2-Myc protein	NULL		bind	NULL				telomeric sequences	NULL				NULL	nocodazole-arrested (G2/M) phase cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4202_s_217	12024033	(C) Binding of both Sir3p and Dna2-Myc protein to telomeric sequences in nocodazole-arrested (G2/M) phase cells.	bind
10793	1	4479	6	NULL	NULL	NULL	NULL	Sir3p	GP		bind					telomeric sequences					NULL	nocodazole-arrested (G2/M) phase cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4202_s_217	12024033	(C) Binding of both Sir3p and Dna2-Myc protein to telomeric sequences in nocodazole-arrested (G2/M) phase cells.	bind
10794	2	4479	6	NULL	NULL	NULL	NULL	Dna2-Myc protein	GP		bind					telomeric sequences					NULL	nocodazole-arrested (G2/M) phase cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4202_s_217	12024033	(C) Binding of both Sir3p and Dna2-Myc protein to telomeric sequences in nocodazole-arrested (G2/M) phase cells.	bind
11314	1	4480	5	NULL	NULL	0	NULL	CBP	NULL		bind	NULL				xUBF	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_6_5_1059_s_134	11106745	(C) Binding of CBP and Rb to xUBF are mutually exclusive.	bind
11315	2	4480	5	NULL	NULL	0	NULL	Rb	NULL		bind	NULL				xUBF	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_6_5_1059_s_134	11106745	(C) Binding of CBP and Rb to xUBF are mutually exclusive.	bind
11316	3	4480	5	NULL	NULL	0	NULL	statement 1	NULL		mutually exclusive to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_6_5_1059_s_134	11106745	(C) Binding of CBP and Rb to xUBF are mutually exclusive.	bind
10974	1	4480	6	NULL	NULL	NULL	NULL	CBP	GP		bind					xUBF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_5_1059_s_134	11106745	(C) Binding of CBP and Rb to xUBF are mutually exclusive.	bind
10975	2	4480	6	NULL	NULL	NULL	NULL	Rb	GP		bind					xUBF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_5_1059_s_134	11106745	(C) Binding of CBP and Rb to xUBF are mutually exclusive.	bind
10976	3	4480	6	NULL	NULL	NULL	NULL	statement 1	Process		is independent of					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_5_1059_s_134	11106745	(C) Binding of CBP and Rb to xUBF are mutually exclusive.	bind
11318	1	4481	5	NULL	NULL	0	NULL	Cdh1	NULL		bind	NULL				TPX2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_23_10516_s_204	16287863	(C) Binding of Cdh1 to TPX2 and TPX2-N.	bind
11320	2	4481	5	10	NULL	0	NULL	Cdh1			bind					TPX2			N-terminus		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10516_s_204	16287863	(C) Binding of Cdh1 to TPX2 and TPX2-N.	bind
10977	1	4481	6	NULL	NULL	NULL	NULL	Cdh1	GP		bind					TPX2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10516_s_204	16287863	(C) Binding of Cdh1 to TPX2 and TPX2-N.	bind
10978	2	4481	6	NULL	NULL	NULL	NULL	Cdh1	GP		bind					TPX2	GP		N-terminus		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10516_s_204	16287863	(C) Binding of Cdh1 to TPX2 and TPX2-N.	bind
11323	1	4482	5	NULL	NULL	0	NULL	CMV gB	NULL		bind	NULL				DC-SIGNR	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_17_5_653_s_186	12433371	(C) Binding of CMV gB to DC-SIGNR.	bind
10979	1	4482	6	NULL	NULL	NULL	NULL	CMV gB	GP		bind					DC-SIGNR	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_5_653_s_186	12433371	(C) Binding of CMV gB to DC-SIGNR.	bind
11324	1	4483	5	10	NULL	0	NULL	collagen	NULL		bind	NULL				collagen substrates	NULL				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_5_2319_s_238	10225890	(C) Binding of collagen to different collagen substrates.	bind
10980	1	4483	6	NULL	NULL	NULL	NULL	collagen	GP		bind					collagen substrates	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_5_2319_s_238	10225890	(C) Binding of collagen to different collagen substrates.	bind
11326	1	4484	5	NULL	NULL	0	NULL	CPEB	NULL		bind	NULL				 XPum	NULL		Puf		NULL		0	NULL	NULL	NULL	gw70_mechdev_120_8_865_s_80	12963108	(C) Binding of CPEB to XPum Puf  but not to XPum NN and NC.	bind
11327	2	4484	5	NULL	NULL	0	NULL	CPEB	NULL		does not bind	NULL				XPum	NULL		NN		NULL		0	NULL	NULL	NULL	gw70_mechdev_120_8_865_s_80	12963108	(C) Binding of CPEB to XPum Puf  but not to XPum NN and NC.	bind
11328	3	4484	5	10	NULL	0	NULL	CPEB			does not bind					XPum			NC		NULL		NULL	NULL	NULL	NULL	gw70_mechdev_120_8_865_s_80	12963108	(C) Binding of CPEB to XPum Puf  but not to XPum NN and NC.	bind
10981	1	4484	6	NULL	NULL	NULL	NULL	CPEB	GP		bind					XPum	GP		puf		NULL		NULL	NULL	NULL	NULL	gw70_mechdev_120_8_865_s_80	12963108	(C) Binding of CPEB to XPum Puf  but not to XPum NN and NC.	bind
10982	2	4484	6	NULL	NULL	NULL	NULL	CPEB	GP		does not bind					XPum	GP		NN		NULL		NULL	NULL	NULL	NULL	gw70_mechdev_120_8_865_s_80	12963108	(C) Binding of CPEB to XPum Puf  but not to XPum NN and NC.	bind
10983	3	4484	6	NULL	NULL	NULL	NULL	CPEB	GP		does not bind					XPum	GP		NC		NULL		NULL	NULL	NULL	NULL	gw70_mechdev_120_8_865_s_80	12963108	(C) Binding of CPEB to XPum Puf  but not to XPum NN and NC.	bind
11337	1	4485	5	NULL	NULL	0	NULL	CtBP1	NULL		bind	NULL				deltaEF1	NULL	full-length			NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_19_12_8581_s_125	10567582	(C) Binding of CtBP1 and CtBP2 to full-length deltaEF1 in vitro.	bind
11338	2	4485	5	NULL	NULL	0	NULL	CtBP2	NULL		bind	NULL				deltaEF1	NULL	full-length			NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_19_12_8581_s_125	10567582	(C) Binding of CtBP1 and CtBP2 to full-length deltaEF1 in vitro.	bind
10984	1	4485	6	NULL	NULL	NULL	NULL	CtBP1	GP		bind					deltaEF1	GP	full length			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8581_s_125	10567582	(C) Binding of CtBP1 and CtBP2 to full-length deltaEF1 in vitro.	bind
10985	2	4485	6	NULL	NULL	NULL	NULL	CtBP2	GP		bind					deltaEF1	GP	full length			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8581_s_125	10567582	(C) Binding of CtBP1 and CtBP2 to full-length deltaEF1 in vitro.	bind
11339	1	4486	5	NULL	NULL	0	NULL	CtBP1	NULL		bind	NULL		K428R		Smad6	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1389_s_122	12769861	(C) Binding of CtBP1(K428R) to Smad6 remains unchanged.	bind
10987	1	4486	6	NULL	NULL	NULL	NULL	CtBP1	GP		bind			K428R		Smad6	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1389_s_122	12769861	(C) Binding of CtBP1(K428R) to Smad6 remains unchanged.	bind
11340	1	4487	5	NULL	NULL	0	NULL	DNA replication proteins	NULL		bind	NULL				chromatin	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_11_2_329_s_222	12620222	(C) Binding of DNA replication proteins and other checkpoint proteins to chromatin in the absence of Claspin.	bind
11341	2	4487	5	NULL	NULL	0	NULL	statement 1	NULL		in the absence of	NULL				Claspin	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_11_2_329_s_222	12620222	(C) Binding of DNA replication proteins and other checkpoint proteins to chromatin in the absence of Claspin.	bind
11342	3	4487	5	10	NULL	0	NULL	checkpoint proteins			bind					chromatin					NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_2_329_s_222	12620222	(C) Binding of DNA replication proteins and other checkpoint proteins to chromatin in the absence of Claspin.	bind
11343	4	4487	5	NULL	NULL	0	NULL	statement 3	NULL		in the absence of	NULL				Claspin	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_11_2_329_s_222	12620222	(C) Binding of DNA replication proteins and other checkpoint proteins to chromatin in the absence of Claspin.	bind
10988	1	4487	6	NULL	NULL	NULL	NULL	DNA replication proteins	GP		bind					chromatin	Chromosome				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_2_329_s_222	12620222	(C) Binding of DNA replication proteins and other checkpoint proteins to chromatin in the absence of Claspin.	bind
10989	2	4487	6	NULL	NULL	NULL	NULL	checkpoint proteins	GP		bind					chromatin	Chromosome				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_2_329_s_222	12620222	(C) Binding of DNA replication proteins and other checkpoint proteins to chromatin in the absence of Claspin.	bind
10990	3	4487	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs in absence of					Claspin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_2_329_s_222	12620222	(C) Binding of DNA replication proteins and other checkpoint proteins to chromatin in the absence of Claspin.	bind
10992	4	4487	6	NULL	NULL	NULL	NULL	statement 2	Process		occurs in absence of					Claspin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_2_329_s_222	12620222	(C) Binding of DNA replication proteins and other checkpoint proteins to chromatin in the absence of Claspin.	bind
11344	1	4488	5	NULL	NULL	0	NULL	DpiA protein	NULL		bind	NULL				pSC101 origin fragment	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_20_6025_s_75	14526013	(C) Binding of DpiA protein and the mutant proteins to pSC101 origin fragment.	bind
11345	2	4488	5	NULL	NULL	0	NULL	DpiA protein	NULL	mutant	bind	NULL				pSC101 origin fragment	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_20_6025_s_75	14526013	(C) Binding of DpiA protein and the mutant proteins to pSC101 origin fragment.	bind
10993	1	4488	6	NULL	NULL	NULL	NULL	DpiA protein	GP		bind					pSC101 origin fragment	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_20_6025_s_75	14526013	(C) Binding of DpiA protein and the mutant proteins to pSC101 origin fragment.	bind
10996	2	4488	6	NULL	NULL	NULL	NULL	DpiA protein	GP	mutant	bind					pSC101 origin fragment	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_20_6025_s_75	14526013	(C) Binding of DpiA protein and the mutant proteins to pSC101 origin fragment.	bind
11346	1	4489	5	10	NULL	0	NULL	E2F1			bind					MCM4					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_99	15121871	(C) Binding of E2F1 to E2F targets ( MCM4,  MCM3,  PCNA, and  p107) and control promoter ( AchR).	bind
11347	2	4489	5	10	NULL	0	NULL	E2F1			bind					MCM3					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_99	15121871	(C) Binding of E2F1 to E2F targets ( MCM4,  MCM3,  PCNA, and  p107) and control promoter ( AchR).	bind
11348	3	4489	5	10	NULL	0	NULL	E2F1			bind					PCNA					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_99	15121871	(C) Binding of E2F1 to E2F targets ( MCM4,  MCM3,  PCNA, and  p107) and control promoter ( AchR).	bind
11349	4	4489	5	10	NULL	0	NULL	E2F1			bind					 p107					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_99	15121871	(C) Binding of E2F1 to E2F targets ( MCM4,  MCM3,  PCNA, and  p107) and control promoter ( AchR).	bind
11350	5	4489	5	NULL	NULL	0	NULL	E2F1	NULL		bind	NULL				AchR	NULL	control		promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_99	15121871	(C) Binding of E2F1 to E2F targets ( MCM4,  MCM3,  PCNA, and  p107) and control promoter ( AchR).	bind
54364	6	4489	5	10	NULL	0	NULL	MCM4			is a type of					E2F target					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_99	15121871	(C) Binding of E2F1 to E2F targets ( MCM4,  MCM3,  PCNA, and  p107) and control promoter ( AchR).	bind
54365	7	4489	5	10	NULL	0	NULL	MCM3			is a type of					E2F target					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_99	15121871	(C) Binding of E2F1 to E2F targets ( MCM4,  MCM3,  PCNA, and  p107) and control promoter ( AchR).	bind
54366	8	4489	5	10	NULL	0	NULL	PCNA			is a type of					E2F target					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_99	15121871	(C) Binding of E2F1 to E2F targets ( MCM4,  MCM3,  PCNA, and  p107) and control promoter ( AchR).	bind
54367	9	4489	5	10	NULL	0	NULL	p107			is a type of					E2F target					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_99	15121871	(C) Binding of E2F1 to E2F targets ( MCM4,  MCM3,  PCNA, and  p107) and control promoter ( AchR).	bind
10997	1	4489	6	NULL	NULL	NULL	NULL	E2F1	GP		bind					MCM4	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_99	15121871	(C) Binding of E2F1 to E2F targets ( MCM4,  MCM3,  PCNA, and  p107) and control promoter ( AchR).	bind
10998	2	4489	6	NULL	NULL	NULL	NULL	E2F1	GP		bind					MCM3	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_99	15121871	(C) Binding of E2F1 to E2F targets ( MCM4,  MCM3,  PCNA, and  p107) and control promoter ( AchR).	bind
10999	3	4489	6	NULL	NULL	NULL	NULL	E2F1	GP		bind					PCNA	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_99	15121871	(C) Binding of E2F1 to E2F targets ( MCM4,  MCM3,  PCNA, and  p107) and control promoter ( AchR).	bind
11000	4	4489	6	NULL	NULL	NULL	NULL	E2F1	GP		bind					p107	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_99	15121871	(C) Binding of E2F1 to E2F targets ( MCM4,  MCM3,  PCNA, and  p107) and control promoter ( AchR).	bind
11002	5	4489	6	NULL	NULL	NULL	NULL	E2F1	GP		bind					AchR	GP	control		promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_99	15121871	(C) Binding of E2F1 to E2F targets ( MCM4,  MCM3,  PCNA, and  p107) and control promoter ( AchR).	bind
54368	6	4489	6	NULL	NULL	NULL	NULL	MCM4	GP		is a type of					E2F target	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_99	15121871	(C) Binding of E2F1 to E2F targets ( MCM4,  MCM3,  PCNA, and  p107) and control promoter ( AchR).	bind
54369	7	4489	6	NULL	NULL	NULL	NULL	MCM3	GP		is a type of					E2F target	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_99	15121871	(C) Binding of E2F1 to E2F targets ( MCM4,  MCM3,  PCNA, and  p107) and control promoter ( AchR).	bind
54370	8	4489	6	NULL	NULL	NULL	NULL	PCNA	GP		is a type of					E2F target	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_99	15121871	(C) Binding of E2F1 to E2F targets ( MCM4,  MCM3,  PCNA, and  p107) and control promoter ( AchR).	bind
54371	9	4489	6	NULL	NULL	NULL	NULL	p107	GP		is a type of					E2F target	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_10_4546_s_99	15121871	(C) Binding of E2F1 to E2F targets ( MCM4,  MCM3,  PCNA, and  p107) and control promoter ( AchR).	bind
11351	1	4490	5	NULL	NULL	0	NULL	EL229C-B	NULL		bind	NULL				GroES	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_107_2_223_s_78	11672529	(C) Binding of EL229C-B and  EL229C-B:SA complex to GroES analyzed by surface  plasmon resonance in the presence of ATP.	bind
11352	2	4490	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_107_2_223_s_78	11672529	(C) Binding of EL229C-B and  EL229C-B:SA complex to GroES analyzed by surface  plasmon resonance in the presence of ATP.	bind
11353	3	4490	5	NULL	NULL	0	NULL	EL229C-B:SA complex	NULL		bind	NULL				GroES	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_107_2_223_s_78	11672529	(C) Binding of EL229C-B and  EL229C-B:SA complex to GroES analyzed by surface  plasmon resonance in the presence of ATP.	bind
11354	4	4490	5	NULL	NULL	0	NULL	statement 3	NULL		in the presence of	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_107_2_223_s_78	11672529	(C) Binding of EL229C-B and  EL229C-B:SA complex to GroES analyzed by surface  plasmon resonance in the presence of ATP.	bind
11003	1	4490	6	NULL	NULL	NULL	NULL	EL229C-B	GP		bind					GroES	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_78	11672529	(C) Binding of EL229C-B and  EL229C-B:SA complex to GroES analyzed by surface  plasmon resonance in the presence of ATP.	bind
11004	2	4490	6	NULL	NULL	NULL	NULL	EL229C-B:SA complex	GP		bind					GroES	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_78	11672529	(C) Binding of EL229C-B and  EL229C-B:SA complex to GroES analyzed by surface  plasmon resonance in the presence of ATP.	bind
12872	3	4490	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs in presence of					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_78	11672529	(C) Binding of EL229C-B and  EL229C-B:SA complex to GroES analyzed by surface  plasmon resonance in the presence of ATP.	bind
12873	4	4490	6	NULL	NULL	NULL	NULL	statement 2	Process		occurs in presence of					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_78	11672529	(C) Binding of EL229C-B and  EL229C-B:SA complex to GroES analyzed by surface  plasmon resonance in the presence of ATP.	bind
11355	1	4491	5	NULL	NULL	0	NULL	fibronectin	NULL		bind	NULL				UspA2	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_9_4374_s_280	9712790	(C) Binding of fibronectin to UspA2.	bind
11018	1	4491	6	NULL	NULL	NULL	NULL	fibronectin	GP		bind					UspA2	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_9_4374_s_280	9712790	(C) Binding of fibronectin to UspA2.	bind
11356	1	4493	5	NULL	NULL	0	NULL	S2R+ cells	NULL		transfected with	NULL				Frizzled2-FLAG	NULL				NULL		0	NULL	NULL	NULL	gw70_development_132_24_5479_s_176	16291792	(C) Binding of GFP-Wingless to S2R+ cells transfected  with Frizzled2-FLAG.	bind
11357	2	4493	5	NULL	NULL	0	NULL	GFP-Wingless	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_development_132_24_5479_s_176	16291792	(C) Binding of GFP-Wingless to S2R+ cells transfected  with Frizzled2-FLAG.	bind
11023	1	4493	6	NULL	NULL	NULL	NULL	S2R+ cells	Cell		transfected with					Frizzled2	GP	FLAG tagged			NULL		NULL	NULL	NULL	NULL	gw70_development_132_24_5479_s_176	16291792	(C) Binding of GFP-Wingless to S2R+ cells transfected  with Frizzled2-FLAG.	bind
11024	2	4493	6	NULL	NULL	NULL	NULL	GFP-wingless	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_132_24_5479_s_176	16291792	(C) Binding of GFP-Wingless to S2R+ cells transfected  with Frizzled2-FLAG.	bind
11358	1	4494	5	NULL	NULL	0	NULL	GLD-1	NULL		bind	NULL				mes-3	NULL			3' UTR	NULL		0	NULL	NULL	NULL	gw60_genetics_159_3_1007_s_196	11729149	(C) Binding of GLD-1 to the  mes-3 3' UTR was tested using RNA gel mobility shift assay.	bind
11026	1	4494	6	NULL	NULL	NULL	NULL	GLD-1	GP		bind					mes-3 	GP			3' UTR	NULL		NULL	NULL	NULL	NULL	gw60_genetics_159_3_1007_s_196	11729149	(C) Binding of GLD-1 to the  mes-3 3' UTR was tested using RNA gel mobility shift assay.	bind
11359	1	4495	5	NULL	NULL	0	NULL	GST-MBD2a	NULL		bind	NULL				RHA	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_23_8_2645_s_164	12665568	(C) Binding of GST-MBD2a to RHA in vitro.	bind
11027	1	4495	6	NULL	NULL	NULL	NULL	GST-MBD2a	GP		bind					RHA	Chemical				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_8_2645_s_164	12665568	(C) Binding of GST-MBD2a to RHA in vitro.	bind
11360	1	4496	5	NULL	NULL	0	NULL	GST-VCA	NULL		bind	NULL				Arp2/3	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_150_6_1299_s_76	10995436	(C) Binding of GST-VCA (0.2 muM) to Arp2/3 (0.1 muM) was tested (as in B) in the presence of the indicated concentrations of HT-WG or HT-WGP.	bind
11361	2	4496	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				HT-WG	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_150_6_1299_s_76	10995436	(C) Binding of GST-VCA (0.2 muM) to Arp2/3 (0.1 muM) was tested (as in B) in the presence of the indicated concentrations of HT-WG or HT-WGP.	bind
11362	3	4496	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				HT-WGP	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_150_6_1299_s_76	10995436	(C) Binding of GST-VCA (0.2 muM) to Arp2/3 (0.1 muM) was tested (as in B) in the presence of the indicated concentrations of HT-WG or HT-WGP.	bind
11363	4	4496	5	NULL	NULL	0	NULL	statement 2	NULL		is an alternative to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_150_6_1299_s_76	10995436	(C) Binding of GST-VCA (0.2 muM) to Arp2/3 (0.1 muM) was tested (as in B) in the presence of the indicated concentrations of HT-WG or HT-WGP.	bind
11030	1	4496	6	NULL	NULL	NULL	NULL	GST-VCA	GP		bind					Arp2/3	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_6_1299_s_76	10995436	(C) Binding of GST-VCA (0.2 muM) to Arp2/3 (0.1 muM) was tested (as in B) in the presence of the indicated concentrations of HT-WG or HT-WGP.	bind
12874	2	4496	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs in presence of					HT-WG	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_6_1299_s_76	10995436	(C) Binding of GST-VCA (0.2 muM) to Arp2/3 (0.1 muM) was tested (as in B) in the presence of the indicated concentrations of HT-WG or HT-WGP.	bind
12875	3	4496	6	NULL	NULL	NULL	NULL	statement 2	Process		occurs in presence of					HT-WGP	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_6_1299_s_76	10995436	(C) Binding of GST-VCA (0.2 muM) to Arp2/3 (0.1 muM) was tested (as in B) in the presence of the indicated concentrations of HT-WG or HT-WGP.	bind
12876	4	4496	6	NULL	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_6_1299_s_76	10995436	(C) Binding of GST-VCA (0.2 muM) to Arp2/3 (0.1 muM) was tested (as in B) in the presence of the indicated concentrations of HT-WG or HT-WGP.	bind
11364	1	4497	5	10	NULL	0	NULL	Ikaros		immunopurified	bind					mononucleosomes 					NULL		NULL	NULL	NULL	NULL	gw60_immunity_10_3_345_s_141	10204490	(C) Binding of immunopurified Ikaros to mononucleosomes (Nc).	bind
11031	1	4497	6	NULL	NULL	NULL	NULL	Ikaros	GP	immunopurified	bind					mononucleosomes	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_10_3_345_s_141	10204490	(C) Binding of immunopurified Ikaros to mononucleosomes (Nc).	bind
11365	1	4498	5	NULL	NULL	0	NULL	Mad2	NULL		bind	NULL				Cdc20 fragments	NULL				NULL	in wild-type cells	0	NULL	NULL	NULL	gw60_molcell_12_1_87_s_251	12887895	(C) Binding of Mad2 to Cdc20 fragments in wild-type and  cct1-2 cells.	bind
11366	2	4498	5	NULL	NULL	0	NULL	Mad2	NULL		bind	NULL				Cdc20 fragments	NULL				NULL	in cct1-2 cells	0	NULL	NULL	NULL	gw60_molcell_12_1_87_s_251	12887895	(C) Binding of Mad2 to Cdc20 fragments in wild-type and  cct1-2 cells.	bind
11032	1	4498	6	NULL	NULL	NULL	NULL	Mad2	GP		bind					Cdc20 fragment	AminoAcid				NULL	wild-type cells	NULL	NULL	NULL	NULL	gw60_molcell_12_1_87_s_251	12887895	(C) Binding of Mad2 to Cdc20 fragments in wild-type and  cct1-2 cells.	bind
12877	2	4498	6	NULL	NULL	NULL	NULL	Mad2	GP		bind					Cdc20 fragment	AminoAcid				NULL	cct1-2 cells	NULL	NULL	NULL	NULL	gw60_molcell_12_1_87_s_251	12887895	(C) Binding of Mad2 to Cdc20 fragments in wild-type and  cct1-2 cells.	bind
11367	1	4499	5	NULL	NULL	0	NULL	mPER	NULL		bind	NULL				CKI	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_2_584_s_246	14701732	(C) Binding of mPER with CKI .	bind
11033	1	4499	6	NULL	NULL	NULL	NULL	mPER	GP		bind					CKI	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_584_s_246	14701732	(C) Binding of mPER with CKI .	bind
11368	1	4500	5	10	NULL	0	NULL	mSin3A-HDAC-1	NULL		bind	NULL					NULL		ETS domains		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_8_2802_s_140	11283259	(C) Binding of mSin3A-HDAC-1 to different ETS domains.	bind
11034	1	4500	6	NULL	NULL	NULL	NULL	mSin3A-HDAC-1	GP		bind								ETS domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_8_2802_s_140	11283259	(C) Binding of mSin3A-HDAC-1 to different ETS domains.	bind
11369	1	4501	5	NULL	NULL	0	NULL	n-sec1	NULL		bind	NULL				syntaxin 1a	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_16_6_1229_s_90	8663999	(C) Binding of n-sec1 to syntaxin 1a in the presence of 1 mM S-NC.	bind
11370	2	4501	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				S-NC	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_16_6_1229_s_90	8663999	(C) Binding of n-sec1 to syntaxin 1a in the presence of 1 mM S-NC.	bind
11035	1	4501	6	NULL	NULL	NULL	NULL	n-sec1	GP		bind					syntaxin 1a	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_6_1229_s_90	8663999	(C) Binding of n-sec1 to syntaxin 1a in the presence of 1 mM S-NC.	bind
11036	2	4501	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs in presence of					S-NC	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_6_1229_s_90	8663999	(C) Binding of n-sec1 to syntaxin 1a in the presence of 1 mM S-NC.	bind
11371	1	4502	5	NULL	NULL	0	NULL	nuclear proteins	NULL		bind	NULL				TGF- 1	NULL	human		AP-1 site B of promoter	NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_304_2_301_s_95	12711314	(C) Binding of nuclear proteins to the AP-1 site B of the human TGF- 1 promoter.	bind
11037	1	4502	6	NULL	NULL	NULL	NULL	nuclear proteins	GP		bind					TGF-1	GP	human		AP-1 site B of promoter	NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_304_2_301_s_95	12711314	(C) Binding of nuclear proteins to the AP-1 site B of the human TGF- 1 promoter.	bind
11372	1	4503	5	NULL	NULL	0	NULL	Nup98	NULL		bind	NULL				VSV M protein	NULL				NULL		0	NULL	NULL	NULL	gw70_microbesinfect_6_8_715_s_170	15207818	(C) Binding of Nup98 to VSV M protein.	bind
11044	1	4503	6	NULL	NULL	NULL	NULL	Nup98	GP		bind					VSV M protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbesinfect_6_8_715_s_170	15207818	(C) Binding of Nup98 to VSV M protein.	bind
11373	1	4504	5	NULL	NULL	0	NULL	p107	NULL		bind	NULL				cyclin - Cdk2 complexes	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_168_1_55_s_72	15631990	(C) Binding of p107 to cyclin - Cdk2 complexes.	bind
11046	1	4504	6	NULL	NULL	NULL	NULL	p107	GP		bind					cyclin - Cdk2 complexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_1_55_s_72	15631990	(C) Binding of p107 to cyclin - Cdk2 complexes.	bind
11374	1	4505	5	NULL	NULL	0	NULL	p202	NULL		bind	NULL				MyoD protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_2_1074_s_258	9448005	(C) Binding of p202 to MyoD protein as assayed by coimmunoprecipitation.	bind
11047	1	4505	6	NULL	NULL	NULL	NULL	p202	GP		bind					MyoD	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_1074_s_258	9448005	(C) Binding of p202 to MyoD protein as assayed by coimmunoprecipitation.	bind
11375	1	4506	5	NULL	NULL	0	NULL	p53/p73	NULL		bind	NULL		DBD		MDM2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_24_8533_s_193	11713288	(C) Binding of p53/p73DBD or p53/p73betaeCT to MDM2 was examined as described for Fig.  3.	bind
11376	2	4506	5	NULL	NULL	0	NULL	p53/p73beta	NULL		bind	NULL		eCT		MDM2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_24_8533_s_193	11713288	(C) Binding of p53/p73DBD or p53/p73betaeCT to MDM2 was examined as described for Fig.  3.	bind
54372	3	4506	5	10	NULL	0	NULL	statement 1			is an alternative to					statement 2					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_24_8533_s_193	11713288	(C) Binding of p53/p73DBD or p53/p73betaeCT to MDM2 was examined as described for Fig.  3.	bind
11050	1	4506	6	NULL	NULL	NULL	NULL	p53/p73	GP		bind			DBD		MDM2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_24_8533_s_193	11713288	(C) Binding of p53/p73DBD or p53/p73betaeCT to MDM2 was examined as described for Fig.  3.	bind
11051	2	4506	6	NULL	NULL	NULL	NULL	p53/p73beta	GP		bind			eCT		MDM2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_24_8533_s_193	11713288	(C) Binding of p53/p73DBD or p53/p73betaeCT to MDM2 was examined as described for Fig.  3.	bind
11052	3	4506	6	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_24_8533_s_193	11713288	(C) Binding of p53/p73DBD or p53/p73betaeCT to MDM2 was examined as described for Fig.  3.	bind
11377	1	4507	5	NULL	NULL	0	NULL	p73beta/p53	NULL		bind	NULL		CT		MDM2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_24_8533_s_162	11713288	(C) Binding of p73beta/p53CT to MDM2 was analyzed by incubating lysates from cells expressing Flag-p73beta/p53CT with GST-MDM2.	bind
11057	1	4507	6	NULL	NULL	NULL	NULL	p73beta/p53	GP		bind			CT		MDM2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_24_8533_s_162	11713288	(C) Binding of p73beta/p53CT to MDM2 was analyzed by incubating lysates from cells expressing Flag-p73beta/p53CT with GST-MDM2.	bind
11378	1	4508	5	NULL	NULL	0	NULL	PAI-2	NULL		bind	NULL				Rb	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_152	12944478	(C) Binding of PAI-2 and the C-D interhelical deletion mutant of PAI-2 to Rb and Rb LXCXE mutants.	bind
11379	2	4508	5	NULL	NULL	0	NULL	PAI-2	NULL		bind	NULL				Rb	NULL	mutant	LXCXE		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_152	12944478	(C) Binding of PAI-2 and the C-D interhelical deletion mutant of PAI-2 to Rb and Rb LXCXE mutants.	bind
11380	3	4508	5	NULL	NULL	0	NULL	PAI-2	NULL	deletion mutants of	bind	NULL		C-D interhelical		Rb	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_152	12944478	(C) Binding of PAI-2 and the C-D interhelical deletion mutant of PAI-2 to Rb and Rb LXCXE mutants.	bind
11381	4	4508	5	NULL	NULL	0	NULL	PAI-2	NULL	deletion mutants of	bind	NULL		C-D interhelical		Rb	NULL	mutant	LXCXE		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_152	12944478	(C) Binding of PAI-2 and the C-D interhelical deletion mutant of PAI-2 to Rb and Rb LXCXE mutants.	bind
11060	1	4508	6	NULL	NULL	NULL	NULL	PAI-2	GP		bind					Rb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_152	12944478	(C) Binding of PAI-2 and the C-D interhelical deletion mutant of PAI-2 to Rb and Rb LXCXE mutants.	bind
11061	2	4508	6	NULL	NULL	NULL	NULL	PAI-2	GP	deletion mutant	bind			C-D interhelical		Rb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_152	12944478	(C) Binding of PAI-2 and the C-D interhelical deletion mutant of PAI-2 to Rb and Rb LXCXE mutants.	bind
11062	3	4508	6	NULL	NULL	NULL	NULL	PAI-2	GP		bind					Rb	GP	mutant	LXCXE		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_152	12944478	(C) Binding of PAI-2 and the C-D interhelical deletion mutant of PAI-2 to Rb and Rb LXCXE mutants.	bind
11064	4	4508	6	NULL	NULL	NULL	NULL	PAI-2	GP	deletion mutant	bind			C-D interhelical		Rb	GP	mutant	LXCXE		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_152	12944478	(C) Binding of PAI-2 and the C-D interhelical deletion mutant of PAI-2 to Rb and Rb LXCXE mutants.	bind
11382	1	4509	5	NULL	NULL	0	NULL	PCNA	NULL		bind	NULL				CAF-1	NULL		p150 subunit		NULL		NULL	NULL	NULL	NULL	gw60_cell_96_4_575_s_144	10052459	(C) Binding of PCNA  to the p150 subunit of CAF-1.	bind
11066	1	4509	6	NULL	NULL	NULL	NULL	PCNA	GP		bind					CAF-1	GP		p150 subunit		NULL		NULL	NULL	NULL	NULL	gw60_cell_96_4_575_s_144	10052459	(C) Binding of PCNA  to the p150 subunit of CAF-1.	bind
11383	1	4510	5	NULL	NULL	0	NULL	sera	NULL	human;; pooled	bind	NULL				RESA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_9_4679_s_222	10456916	(C) Binding of pooled human sera to RESA and two synthetic mimotopes, 17(3) and 15(1).	bind
11384	2	4510	5	10	NULL	0	NULL	sera		human;; pooled	bind					mimotopes		synthetic			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_9_4679_s_222	10456916	(C) Binding of pooled human sera to RESA and two synthetic mimotopes, 17(3) and 15(1).	bind
11068	1	4510	6	NULL	NULL	NULL	NULL	sera	GP	pooled;; human	bind					RESA	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_9_4679_s_222	10456916	(C) Binding of pooled human sera to RESA and two synthetic mimotopes, 17(3) and 15(1).	bind
11070	2	4510	6	NULL	NULL	NULL	NULL	sera	GP	pooled;; human	bind					mimotopes	GP	synthetic			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_9_4679_s_222	10456916	(C) Binding of pooled human sera to RESA and two synthetic mimotopes, 17(3) and 15(1).	bind
11386	1	4511	5	NULL	NULL	0	NULL	p120 E4F protein	NULL	purified	bind	NULL				cyclin A	NULL			CRE site	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_8_2956_s_316	11283272	(C) Binding of purified p120 E4F protein to the cyclin A CRE site is enhanced by pRB.	bind
11387	2	4511	5	NULL	NULL	0	NULL	pRB	NULL		enhances	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_8_2956_s_316	11283272	(C) Binding of purified p120 E4F protein to the cyclin A CRE site is enhanced by pRB.	bind
11071	1	4511	6	NULL	NULL	NULL	NULL	p120 E4F protein	GP	purified	bind					cyclin A	GP			CRE site	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_8_2956_s_316	11283272	(C) Binding of purified p120 E4F protein to the cyclin A CRE site is enhanced by pRB.	bind
11072	2	4511	6	NULL	NULL	NULL	NULL	pRB	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_8_2956_s_316	11283272	(C) Binding of purified p120 E4F protein to the cyclin A CRE site is enhanced by pRB.	bind
11388	1	4512	5	NULL	NULL	0	NULL	Rad9	NULL		bind	NULL				GST-BRCT	NULL				NULL	wild-type yeast extracts	0	NULL	NULL	NULL	gw60_currbiol_9_10_551_s_73	10339432	(c) Binding of Rad9 by GST-BRCT from wild-type yeast extracts.	bind
11076	1	4512	6	NULL	NULL	NULL	NULL	Rad9	GP		bind					GST-BRCT	GP				NULL	wild type yeast extracts	NULL	NULL	NULL	NULL	gw60_currbiol_9_10_551_s_73	10339432	(c) Binding of Rad9 by GST-BRCT from wild-type yeast extracts.	bind
11389	1	4513	5	NULL	NULL	0	NULL	E47	NULL	recombinant	bind	NULL				mb-1	NULL			promoter distal region	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_24_8539_s_241	12446773	(C) Binding of recombinant E47 to the  mb-1 promoter distal region.	bind
11091	1	4513	6	NULL	NULL	NULL	NULL	E47	GP	recombinant	bind					mb-1	GP			distal region of promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_24_8539_s_241	12446773	(C) Binding of recombinant E47 to the  mb-1 promoter distal region.	bind
11390	1	4514	5	NULL	NULL	0	NULL	GST-Myc	NULL	recombinant	bind	NULL				FasL	NULL			Myc-binding site in promoter	NULL		0	NULL	NULL	NULL	gw60_currbiol_10_19_1205_s_40	11050389	(c) Binding of recombinant GST-Myc and GST-Max to the Myc-binding site in the FasL promoter.	bind
11391	2	4514	5	NULL	NULL	0	NULL	GST-Max	NULL	recombinant	bind	NULL				FasL	NULL			Myc-binding site in promoter	NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_19_1205_s_40	11050389	(c) Binding of recombinant GST-Myc and GST-Max to the Myc-binding site in the FasL promoter.	bind
11097	1	4514	6	NULL	NULL	NULL	NULL	GST-Myc	GP	recombinant	bind					FasL	GP			Myc-binding site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_19_1205_s_40	11050389	(c) Binding of recombinant GST-Myc and GST-Max to the Myc-binding site in the FasL promoter.	bind
11098	2	4514	6	NULL	NULL	NULL	NULL	GST-Max	GP	recombinant	bind					FasL	GP			Myc-binding site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_19_1205_s_40	11050389	(c) Binding of recombinant GST-Myc and GST-Max to the Myc-binding site in the FasL promoter.	bind
11392	1	4515	5	NULL	NULL	0	NULL	RAS	NULL		activated by	NULL				EGF	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_3_916_s_144	11784866	(C) Binding of RIN1 to RAS activated by EGF.	bind
11393	2	4515	5	NULL	NULL	0	NULL	RIN1	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_3_916_s_144	11784866	(C) Binding of RIN1 to RAS activated by EGF.	bind
11101	1	4515	6	NULL	NULL	NULL	NULL	EGF	GP		activates					RAS	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_3_916_s_144	11784866	(C) Binding of RIN1 to RAS activated by EGF.	bind
11103	2	4515	6	NULL	NULL	NULL	NULL	RIN1	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_3_916_s_144	11784866	(C) Binding of RIN1 to RAS activated by EGF.	bind
11394	1	4516	5	NULL	NULL	0	NULL	S-layer proteins	NULL		bind	NULL				type IV collagen	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_22_6440_s_237	11053389	(C) Binding of S-layer proteins to type IV and I collagens, laminin, fibronectin, and BSA immobilized on plastic.	bind
11395	2	4516	5	NULL	NULL	0	NULL	S-layer proteins	NULL		bind	NULL				type I collagen	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_22_6440_s_237	11053389	(C) Binding of S-layer proteins to type IV and I collagens, laminin, fibronectin, and BSA immobilized on plastic.	bind
11396	3	4516	5	NULL	NULL	0	NULL	S-layer proteins	NULL		bind	NULL				laminin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_22_6440_s_237	11053389	(C) Binding of S-layer proteins to type IV and I collagens, laminin, fibronectin, and BSA immobilized on plastic.	bind
11397	4	4516	5	NULL	NULL	0	NULL	S-layer proteins	NULL		bind	NULL				fibronectin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_22_6440_s_237	11053389	(C) Binding of S-layer proteins to type IV and I collagens, laminin, fibronectin, and BSA immobilized on plastic.	bind
11398	5	4516	5	10	NULL	0	NULL	S-layer proteins	NULL		bind	NULL				BSA	NULL	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_22_6440_s_237	11053389	(C) Binding of S-layer proteins to type IV and I collagens, laminin, fibronectin, and BSA immobilized on plastic.	bind
11105	1	4516	6	NULL	NULL	NULL	NULL	S-layer proteins	GP		bind					type IV collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_22_6440_s_237	11053389	(C) Binding of S-layer proteins to type IV and I collagens, laminin, fibronectin, and BSA immobilized on plastic.	bind
11107	2	4516	6	NULL	NULL	NULL	NULL	S-layer proteins	GP		bind					type I collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_22_6440_s_237	11053389	(C) Binding of S-layer proteins to type IV and I collagens, laminin, fibronectin, and BSA immobilized on plastic.	bind
11108	3	4516	6	NULL	NULL	NULL	NULL	S-layer proteins	GP		bind					laminin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_22_6440_s_237	11053389	(C) Binding of S-layer proteins to type IV and I collagens, laminin, fibronectin, and BSA immobilized on plastic.	bind
11109	4	4516	6	NULL	NULL	NULL	NULL	S-layer proteins	GP		bind					fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_22_6440_s_237	11053389	(C) Binding of S-layer proteins to type IV and I collagens, laminin, fibronectin, and BSA immobilized on plastic.	bind
11110	5	4516	6	NULL	NULL	NULL	NULL	BSA	GP		immobilized on					plastic	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_22_6440_s_237	11053389	(C) Binding of S-layer proteins to type IV and I collagens, laminin, fibronectin, and BSA immobilized on plastic.	bind
11112	6	4516	6	NULL	NULL	NULL	NULL	S-layer proteins	GP		bind					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_22_6440_s_237	11053389	(C) Binding of S-layer proteins to type IV and I collagens, laminin, fibronectin, and BSA immobilized on plastic.	bind
11399	1	4517	5	NULL	NULL	0	NULL	NIH-3T3 cells	NULL		express	NULL				ErbB-2	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_1_191_s_124	11342269	(c) Binding of scFv-COS-1 cells to ErbB-2-expressing NIH-3T3 cells.	bind
11400	2	4517	5	NULL	NULL	0	NULL	scFv-COS-1 cells	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_1_191_s_124	11342269	(c) Binding of scFv-COS-1 cells to ErbB-2-expressing NIH-3T3 cells.	bind
11114	1	4517	6	NULL	NULL	NULL	NULL	NIH-3T3 cells	Cell		express					ErbB-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_1_191_s_124	11342269	(c) Binding of scFv-COS-1 cells to ErbB-2-expressing NIH-3T3 cells.	bind
11116	2	4517	6	NULL	NULL	NULL	NULL	scFv-COS-1 cells	Cell		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1525_1_191_s_124	11342269	(c) Binding of scFv-COS-1 cells to ErbB-2-expressing NIH-3T3 cells.	bind
11401	1	4518	5	NULL	NULL	0	NULL	sperm cells	NULL		bind	NULL				ZP	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1469_3_197_s_830	11063883	(C) Binding of sperm cells to the ZP triggers the acrosome reaction and acrosomal enzymes are secreted.	bind
11402	2	4518	5	NULL	NULL	0	NULL	statement 1	NULL		triggers	NULL				acrosome	NULL	reaction of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1469_3_197_s_830	11063883	(C) Binding of sperm cells to the ZP triggers the acrosome reaction and acrosomal enzymes are secreted.	bind
11403	3	4518	5	10	NULL	0	NULL	statement 2			leads to					acrosomal enzymes		secretion of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1469_3_197_s_830	11063883	(C) Binding of sperm cells to the ZP triggers the acrosome reaction and acrosomal enzymes are secreted.	bind
11117	1	4518	6	NULL	NULL	NULL	NULL	sperm cells	Cell		bind					ZP	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1469_3_197_s_830	11063883	(C) Binding of sperm cells to the ZP triggers the acrosome reaction and acrosomal enzymes are secreted.	bind
11119	2	4518	6	NULL	NULL	NULL	NULL	statement 1	Process		triggers					acrosome	CellComponent	reaction of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1469_3_197_s_830	11063883	(C) Binding of sperm cells to the ZP triggers the acrosome reaction and acrosomal enzymes are secreted.	bind
11122	3	4518	6	NULL	NULL	NULL	NULL	statement 2	Process		leads to 					acrosomal enzyme 	GP	secretion of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1469_3_197_s_830	11063883	(C) Binding of sperm cells to the ZP triggers the acrosome reaction and acrosomal enzymes are secreted.	bind
11404	1	4519	5	NULL	NULL	0	NULL	JunB derivatives	NULL		bind	NULL				JNK2	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_87_5_929_s_128	8945519	(C) Binding of the different JunB  derivatives to JNK2.	bind
11123	1	4519	6	NULL	NULL	NULL	NULL	JunB derivatives	GP		bind					JNK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_929_s_128	8945519	(C) Binding of the different JunB  derivatives to JNK2.	bind
11405	1	4520	5	NULL	NULL	0	NULL		NULL		bind	NULL		linker sequence		ERK2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_7_2_387_s_37	11239467	(C) Binding of the linker sequence to ERK2.	bind
11125	1	4520	6	NULL	NULL	NULL	NULL				bind			linker sequence		ERK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_2_387_s_37	11239467	(C) Binding of the linker sequence to ERK2.	bind
11406	1	4521	5	NULL	NULL	0	NULL	M4	NULL	mutant	bind	NULL				nuclear matrix	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_4165_s_276	9632801	(C) Binding of the M4 and M5 mutants to the nuclear matrix.	bind
11407	2	4521	5	NULL	NULL	0	NULL	M5	NULL	mutant	bind	NULL				nuclear matrix	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_4165_s_276	9632801	(C) Binding of the M4 and M5 mutants to the nuclear matrix.	bind
11129	1	4521	6	NULL	NULL	NULL	NULL	M4		mutant	bind					nuclear matrix	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4165_s_276	9632801	(C) Binding of the M4 and M5 mutants to the nuclear matrix.	bind
11131	2	4521	6	NULL	NULL	NULL	NULL	M5		mutant	bind					nuclear matrix	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4165_s_276	9632801	(C) Binding of the M4 and M5 mutants to the nuclear matrix.	bind
11408	1	4522	5	10	NULL	0	NULL	THP-1 cells			bind					von Willebrand factor		deletion of	domain A2 		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_5_905_s_241	11381078	(C) Binding of THP-1 cells to domain A2 - deleted von Willebrand factor.	bind
11134	1	4522	6	NULL	NULL	NULL	NULL	THP-1 cells	Cell		bind					von Willebrand factor	GP	deletion of	domain A2		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_5_905_s_241	11381078	(C) Binding of THP-1 cells to domain A2 - deleted von Willebrand factor.	bind
11420	1	4523	5	10	NULL	0	NULL	vitronectin	NULL	 NHS	bind	NULL				H. influenzae strains	NULL	recombinant 			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_3_1597_s_270	16495531	(C) Binding of vitronectin from NHS by these recombinant  H. influenzae strains.	bind
11135	1	4523	6	NULL	NULL	NULL	NULL	H. influenzae strains	Organism	recombinant	bind					vitronectin	GP	NHS			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_3_1597_s_270	16495531	(C) Binding of vitronectin from NHS by these recombinant  H. influenzae strains.	bind
11409	1	4524	5	NULL	NULL	0	NULL	Vav-3	NULL	wild type	bind	NULL				RhoA	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_11_7870_s_274	10523675	(C) Binding of wild type Vav-3 to RhoA.	bind
11136	1	4524	6	NULL	NULL	NULL	NULL	Vav-3	GP	wild type	bind					RhoA	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7870_s_274	10523675	(C) Binding of wild type Vav-3 to RhoA.	bind
11410	1	4525	5	NULL	NULL	0	NULL	Wnt8	NULL		bind	NULL				LRP6	NULL				NULL		0	NULL	NULL	NULL	gw70_development_130_18_4295_s_276	12900447	(C) Binding of Wnt8 and  LRP6 is attenuated in the presence of Wise, but binding of Wnt8 and Frizzled8 is  not.	bind
11411	2	4525	5	NULL	NULL	0	NULL	Wise	NULL	presence of	attenuate	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_development_130_18_4295_s_276	12900447	(C) Binding of Wnt8 and  LRP6 is attenuated in the presence of Wise, but binding of Wnt8 and Frizzled8 is  not.	bind
11412	3	4525	5	NULL	NULL	0	NULL	Wnt8	NULL		bind	NULL				Frizzled8	NULL				NULL		0	NULL	NULL	NULL	gw70_development_130_18_4295_s_276	12900447	(C) Binding of Wnt8 and  LRP6 is attenuated in the presence of Wise, but binding of Wnt8 and Frizzled8 is  not.	bind
11413	4	4525	5	NULL	NULL	0	NULL	Wise	NULL	presence of	does not attenuate	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_development_130_18_4295_s_276	12900447	(C) Binding of Wnt8 and  LRP6 is attenuated in the presence of Wise, but binding of Wnt8 and Frizzled8 is  not.	bind
11137	1	4525	6	NULL	NULL	NULL	NULL	Wnt8	GP		bind					LRP6	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_18_4295_s_276	12900447	(C) Binding of Wnt8 and  LRP6 is attenuated in the presence of Wise, but binding of Wnt8 and Frizzled8 is  not.	bind
11138	2	4525	6	NULL	NULL	NULL	NULL	Wise	GP		attenuates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_130_18_4295_s_276	12900447	(C) Binding of Wnt8 and  LRP6 is attenuated in the presence of Wise, but binding of Wnt8 and Frizzled8 is  not.	bind
11139	3	4525	6	NULL	NULL	NULL	NULL	Wnt8	GP		bind					Frizzled8	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_130_18_4295_s_276	12900447	(C) Binding of Wnt8 and  LRP6 is attenuated in the presence of Wise, but binding of Wnt8 and Frizzled8 is  not.	bind
11140	4	4525	6	NULL	NULL	NULL	NULL	wise	GP		does not attenuate					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_130_18_4295_s_276	12900447	(C) Binding of Wnt8 and  LRP6 is attenuated in the presence of Wise, but binding of Wnt8 and Frizzled8 is  not.	bind
11605	1	4527	5	NULL	NULL	0	NULL	RNAP	NULL	WT	bind	NULL				srf	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_193	16740936	(C) Binding of WT and mutant  rpoA( C265A) RNAP with ComA P to the  srf promoter as determined by SPPR analysis.	bind
11606	2	4527	5	NULL	NULL	0	NULL	statement 1	NULL		occurs with	NULL				ComA P	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_193	16740936	(C) Binding of WT and mutant  rpoA( C265A) RNAP with ComA P to the  srf promoter as determined by SPPR analysis.	bind
11607	3	4527	5	10	NULL	0	NULL	rpoA RNAP		mutant	bind			 C265A		srf				promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_193	16740936	(C) Binding of WT and mutant  rpoA( C265A) RNAP with ComA P to the  srf promoter as determined by SPPR analysis.	bind
11608	4	4527	5	NULL	NULL	0	NULL	statement 3	NULL		occurs with	NULL				ComA P	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_193	16740936	(C) Binding of WT and mutant  rpoA( C265A) RNAP with ComA P to the  srf promoter as determined by SPPR analysis.	bind
11141	1	4527	6	NULL	NULL	NULL	NULL	RNAP	GP	wild type	bind					srf	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_193	16740936	(C) Binding of WT and mutant  rpoA( C265A) RNAP with ComA P to the  srf promoter as determined by SPPR analysis.	bind
11142	2	4527	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs with					ComA P	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_193	16740936	(C) Binding of WT and mutant  rpoA( C265A) RNAP with ComA P to the  srf promoter as determined by SPPR analysis.	bind
11143	3	4527	6	NULL	NULL	NULL	NULL	rpoA RNAP	GP	mutant	bind			C265A		srf	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_193	16740936	(C) Binding of WT and mutant  rpoA( C265A) RNAP with ComA P to the  srf promoter as determined by SPPR analysis.	bind
11144	4	4527	6	NULL	NULL	NULL	NULL	statement 3	Process		occurs with					ComA P	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_193	16740936	(C) Binding of WT and mutant  rpoA( C265A) RNAP with ComA P to the  srf promoter as determined by SPPR analysis.	bind
11414	1	4528	5	NULL	NULL	0	NULL	BiP	NULL	wt	bind	NULL				Ig HC	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_3_921_s_95	15657421	(C) Binding of wt and mutant BiP to Ig HC and ATF6.	bind
11415	2	4528	5	NULL	NULL	0	NULL	BiP	NULL	mutant	bind	NULL				Ig HC	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_3_921_s_95	15657421	(C) Binding of wt and mutant BiP to Ig HC and ATF6.	bind
11416	3	4528	5	NULL	NULL	0	NULL	BiP	NULL	wt	bind	NULL				ATF6	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_3_921_s_95	15657421	(C) Binding of wt and mutant BiP to Ig HC and ATF6.	bind
11417	4	4528	5	NULL	NULL	0	NULL	BiP	NULL	mutant	bind	NULL				ATF6	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_3_921_s_95	15657421	(C) Binding of wt and mutant BiP to Ig HC and ATF6.	bind
11145	1	4528	6	NULL	NULL	NULL	NULL	BiP	GP	wild type	bind					Ig HC	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_3_921_s_95	15657421	(C) Binding of wt and mutant BiP to Ig HC and ATF6.	bind
11146	2	4528	6	NULL	NULL	0	NULL	BiP	NULL	mutant	bind	NULL				Ig HC	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_3_921_s_95	15657421	(C) Binding of wt and mutant BiP to Ig HC and ATF6.	bind
11147	3	4528	6	NULL	NULL	0	NULL	BiP	NULL	wild type	bind	NULL				ATF6	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_3_921_s_95	15657421	(C) Binding of wt and mutant BiP to Ig HC and ATF6.	bind
11148	4	4528	6	NULL	NULL	0	NULL	BiP	NULL	mutant	bind	NULL				ATF6	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_3_921_s_95	15657421	(C) Binding of wt and mutant BiP to Ig HC and ATF6.	bind
11419	1	4530	5	NULL	NULL	0	NULL		NULL		bind	NULL		CTD amino acids Y1-S7		Pin1	NULL		WW domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_6_1549_s_162	12820968	(C) Blue ribbon representation of the backbone and solid bond representation for CTD amino acids Y1-S7 bound to the WW domain of Pin1 (PDB code 1f8a).	bind
11149	1	4530	6	NULL	NULL	NULL	NULL				bind			CTD amino acids Y1-S7		Pin1	GP		WW domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_6_1549_s_162	12820968	(C) Blue ribbon representation of the backbone and solid bond representation for CTD amino acids Y1-S7 bound to the WW domain of Pin1 (PDB code 1f8a).	bind
11460	1	4531	5	NULL	NULL	0	NULL	endophilin	NULL		contains	NULL					NULL		NH2-terminus lipid binding region		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_2_193_s_84	11604418	(C) Both the NH2-terminal lipid binding region and the SH3 domain of endophilin (which binds dynamin) are required to form a complex of endophilin and dynamin on the lipid bilayer.	bind
11461	2	4531	5	NULL	NULL	0	NULL	endophilin	NULL		contains	NULL					NULL	 	SH3 domain dynamin binding region		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_2_193_s_84	11604418	(C) Both the NH2-terminal lipid binding region and the SH3 domain of endophilin (which binds dynamin) are required to form a complex of endophilin and dynamin on the lipid bilayer.	bind
11462	3	4531	5	10	NULL	0	NULL	endophilin	NULL		forms complex with	NULL				dynamin	NULL				NULL	lipid bilayer	NULL	NULL	NULL	NULL	gw60_cellbiol_155_2_193_s_84	11604418	(C) Both the NH2-terminal lipid binding region and the SH3 domain of endophilin (which binds dynamin) are required to form a complex of endophilin and dynamin on the lipid bilayer.	bind
11463	4	4531	5	10	NULL	0	NULL	statement 1	NULL		is required for	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_2_193_s_84	11604418	(C) Both the NH2-terminal lipid binding region and the SH3 domain of endophilin (which binds dynamin) are required to form a complex of endophilin and dynamin on the lipid bilayer.	bind
11464	5	4531	5	10	NULL	0	NULL	statement 2	NULL		is required for	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_2_193_s_84	11604418	(C) Both the NH2-terminal lipid binding region and the SH3 domain of endophilin (which binds dynamin) are required to form a complex of endophilin and dynamin on the lipid bilayer.	bind
11150	1	4531	6	NULL	NULL	NULL	NULL	endophilin	GP		contains								NH2-terminal lipid binding region		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_2_193_s_84	11604418	(C) Both the NH2-terminal lipid binding region and the SH3 domain of endophilin (which binds dynamin) are required to form a complex of endophilin and dynamin on the lipid bilayer.	bind
11151	2	4531	6	NULL	NULL	NULL	NULL	endophilin	GP		contains								SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_2_193_s_84	11604418	(C) Both the NH2-terminal lipid binding region and the SH3 domain of endophilin (which binds dynamin) are required to form a complex of endophilin and dynamin on the lipid bilayer.	bind
11152	3	4531	6	NULL	NULL	NULL	NULL	endophilin	GP		forms a complex with					dynamin	GP				NULL	lipid bilayer	NULL	NULL	NULL	NULL	gw60_cellbiol_155_2_193_s_84	11604418	(C) Both the NH2-terminal lipid binding region and the SH3 domain of endophilin (which binds dynamin) are required to form a complex of endophilin and dynamin on the lipid bilayer.	bind
54429	4	4531	6	NULL	NULL	NULL	NULL	statement 1	Process		is required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_2_193_s_84	11604418	(C) Both the NH2-terminal lipid binding region and the SH3 domain of endophilin (which binds dynamin) are required to form a complex of endophilin and dynamin on the lipid bilayer.	bind
54430	5	4531	6	NULL	NULL	NULL	NULL	statement 2	Process		is required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_2_193_s_84	11604418	(C) Both the NH2-terminal lipid binding region and the SH3 domain of endophilin (which binds dynamin) are required to form a complex of endophilin and dynamin on the lipid bilayer.	bind
11468	1	4533	5	NULL	NULL	0	NULL	USF	NULL		bind	NULL					NULL			E1-box	NULL	in non-HGF expressing cell types	0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_2_374_s_143	12163028	(C) But in non-HGF expressing cell types USF bound to the E1-box mediates gene repression supported by its interaction with an inhibitory transcriptional factor.	bind
11469	2	4533	5	NULL	NULL	0	NULL	statement 1	NULL		mediate	NULL				gene repression	NULL				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_2_374_s_143	12163028	(C) But in non-HGF expressing cell types USF bound to the E1-box mediates gene repression supported by its interaction with an inhibitory transcriptional factor.	bind
11470	3	4533	5	NULL	NULL	0	NULL	USF	NULL		interacts with	NULL				inhibitory transcriptional factor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_2_374_s_143	12163028	(C) But in non-HGF expressing cell types USF bound to the E1-box mediates gene repression supported by its interaction with an inhibitory transcriptional factor.	bind
13131	4	4533	5	NULL	NULL	0	NULL	statement 2	NULL		is supported by	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_2_374_s_143	12163028	(C) But in non-HGF expressing cell types USF bound to the E1-box mediates gene repression supported by its interaction with an inhibitory transcriptional factor.	bind
11153	1	4533	6	NULL	NULL	NULL	NULL	USF	GP		bind									E1-box	NULL	non-HGF expressing cell types	NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_2_374_s_143	12163028	(C) But in non-HGF expressing cell types USF bound to the E1-box mediates gene repression supported by its interaction with an inhibitory transcriptional factor.	bind
11154	2	4533	6	NULL	NULL	NULL	NULL	USF	GP		interacts with					inhibitory transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_2_374_s_143	12163028	(C) But in non-HGF expressing cell types USF bound to the E1-box mediates gene repression supported by its interaction with an inhibitory transcriptional factor.	bind
12878	3	4533	6	NULL	NULL	NULL	NULL	statement 1	Process		mediates					gene expression	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_2_374_s_143	12163028	(C) But in non-HGF expressing cell types USF bound to the E1-box mediates gene repression supported by its interaction with an inhibitory transcriptional factor.	bind
13004	4	4533	6	NULL	NULL	NULL	NULL	statement 3	Process		is supported by					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_2_374_s_143	12163028	(C) But in non-HGF expressing cell types USF bound to the E1-box mediates gene repression supported by its interaction with an inhibitory transcriptional factor.	bind
11471	1	4534	5	NULL	NULL	0	NULL	C-Vps/HOPS proteins	NULL		bind	NULL				mon1delta vacuoles	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_163_5_973_s_69	14662743	(C) C-Vps/HOPS proteins are bound to the  mon1delta vacuoles.	bind
11155	1	4534	6	NULL	NULL	NULL	NULL	C-Vps/HOPS protein	GP		bind to					mon1delta vacuoles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_163_5_973_s_69	14662743	(C) C-Vps/HOPS proteins are bound to the  mon1delta vacuoles.	bind
11472	2	4535	5	10	NULL	0	NULL	C4BP			does not bind					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_6_837_s_76	12818164	(C) C4BP and anti-CD40 fail to bind to B cells from a CD40-deficient patient.	bind
11473	2	4535	5	10	NULL	0	NULL	anti-CD40			does not bind					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_6_837_s_76	12818164	(C) C4BP and anti-CD40 fail to bind to B cells from a CD40-deficient patient.	bind
54431	1	4535	5	10	NULL	0	NULL	B cells 			derived from					CD40-deficient patient					NULL		0	NULL	NULL	NULL	gw60_immunity_18_6_837_s_76	12818164	(C) C4BP and anti-CD40 fail to bind to B cells from a CD40-deficient patient.	bind
11156	1	4535	6	NULL	NULL	NULL	NULL	B cells 	Cell		derived from					CD40 deficient patients	Person				NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_6_837_s_76	12818164	(C) C4BP and anti-CD40 fail to bind to B cells from a CD40-deficient patient.	bind
11157	2	4535	6	NULL	NULL	NULL	NULL	C4BP	GP		does not bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_6_837_s_76	12818164	(C) C4BP and anti-CD40 fail to bind to B cells from a CD40-deficient patient.	bind
11158	3	4535	6	NULL	NULL	NULL	NULL	anti-CD40	GP		does not bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_6_837_s_76	12818164	(C) C4BP and anti-CD40 fail to bind to B cells from a CD40-deficient patient.	bind
11474	1	4537	5	NULL	NULL	0	NULL	CAND1	NULL		bind	NULL				CUL1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_46	12504026	(C) CAND1 binding to CUL1 requires the carboxyl terminus of CUL1.	bind
11475	2	4537	5	NULL	NULL	0	NULL	statement 1	NULL		require	NULL				CUL1	NULL		carboxyl terminus		NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_46	12504026	(C) CAND1 binding to CUL1 requires the carboxyl terminus of CUL1.	bind
11159	1	4537	6	NULL	NULL	NULL	NULL	CAND1	GP		bind					CUL1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_46	12504026	(C) CAND1 binding to CUL1 requires the carboxyl terminus of CUL1.	bind
13005	2	4537	6	NULL	NULL	NULL	NULL	statement 1	Process		requires					CUL1	GP		carboxyl terminus of 		NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_46	12504026	(C) CAND1 binding to CUL1 requires the carboxyl terminus of CUL1.	bind
11476	1	4538	5	NULL	NULL	0	NULL	CAS	NULL		bind	NULL	preferentially			importin	NULL	NLS-free			NULL		NULL	NULL	NULL	NULL	gw60_cell_90_6_1061_s_143	9323134	(C) CAS binds preferentially to NLS-free  importin  .	bind
11160	1	4538	6	NULL	NULL	NULL	NULL	CAS	GP		bind		preferentially			importin	GP	NLS free			NULL		NULL	NULL	NULL	NULL	gw60_cell_90_6_1061_s_143	9323134	(C) CAS binds preferentially to NLS-free  importin  .	bind
11477	1	4539	5	NULL	NULL	0	NULL	Cdc24	NULL		bind	NULL		N-terminal two-thirds		Pcn1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1038_s_229	9891039	(C) Cdc24 binds Pcn1 and Rfc1 via its N-terminal two-thirds.	bind
11478	2	4539	5	NULL	NULL	0	NULL	Cdc24	NULL		bind	NULL		N-terminal two-thirds		Rfc1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1038_s_229	9891039	(C) Cdc24 binds Pcn1 and Rfc1 via its N-terminal two-thirds.	bind
11161	1	4539	6	NULL	NULL	NULL	NULL	Cdc24	GP		bind			N-terminal two third		Pcn1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1038_s_229	9891039	(C) Cdc24 binds Pcn1 and Rfc1 via its N-terminal two-thirds.	bind
11162	2	4539	6	NULL	NULL	NULL	NULL	Cdc24	GP		bind			N-terminal two third		Rfc1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1038_s_229	9891039	(C) Cdc24 binds Pcn1 and Rfc1 via its N-terminal two-thirds.	bind
11479	1	4540	5	NULL	NULL	0	NULL	CDH1	NULL		bind	NULL				SnoN	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_8_5_1027_s_142	11741538	(C) CDH1 binds to SnoN in the presence of Smad3.	bind
11480	2	4540	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				Smad3	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_8_5_1027_s_142	11741538	(C) CDH1 binds to SnoN in the presence of Smad3.	bind
11163	1	4540	6	NULL	NULL	NULL	NULL	CDH1	GP		bind					SnoN	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_5_1027_s_142	11741538	(C) CDH1 binds to SnoN in the presence of Smad3.	bind
11164	2	4540	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs in presence of					Smad3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_5_1027_s_142	11741538	(C) CDH1 binds to SnoN in the presence of Smad3.	bind
11483	1	4541	5	NULL	NULL	0	NULL	p53	NULL		bind	NULL				Apaf1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_2_207_s_93	11591730	(C) Cell extracts (20 mug protein) obtained from untreated neurons or neurons exposed to camptothecin (10 muM) for 12 h were tested for p53 binding activity to the Apaf1 promoter elements as described above.	bind
54433	1	4541	6	NULL	NULL	NULL	NULL	p53	GP		bind					Apaf1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_2_207_s_93	11591730	(C) Cell extracts (20 mug protein) obtained from untreated neurons or neurons exposed to camptothecin (10 muM) for 12 h were tested for p53 binding activity to the Apaf1 promoter elements as described above.	bind
11484	1	4542	5	NULL	NULL	0	NULL	Pol II	NULL		bind	NULL					NULL			HS2	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_18_6484_s_105	12944475	(C) ChIP analysis of Pol II binding to HS2, HS3, and HS4, the active  Ey promoter, and intergenic site IVR5.	bind
11485	2	4542	5	NULL	NULL	0	NULL	Pol II	NULL		bind	NULL					NULL			HS3	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_18_6484_s_105	12944475	(C) ChIP analysis of Pol II binding to HS2, HS3, and HS4, the active  Ey promoter, and intergenic site IVR5.	bind
11486	3	4542	5	NULL	NULL	0	NULL	Pol II	NULL		bind	NULL					NULL			HS4	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_18_6484_s_105	12944475	(C) ChIP analysis of Pol II binding to HS2, HS3, and HS4, the active  Ey promoter, and intergenic site IVR5.	bind
11487	4	4542	5	NULL	NULL	0	NULL	Pol II	NULL		bind	NULL				Ey	NULL	active		promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_18_6484_s_105	12944475	(C) ChIP analysis of Pol II binding to HS2, HS3, and HS4, the active  Ey promoter, and intergenic site IVR5.	bind
11488	5	4542	5	NULL	NULL	0	NULL	Pol II	NULL		bind	NULL					NULL			intergenic site IVR5	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6484_s_105	12944475	(C) ChIP analysis of Pol II binding to HS2, HS3, and HS4, the active  Ey promoter, and intergenic site IVR5.	bind
11421	1	4542	6	10	NULL	0	NULL	Pol II			bind									HS2	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6484_s_105	12944475	(C) ChIP analysis of Pol II binding to HS2, HS3, and HS4, the active  Ey promoter, and intergenic site IVR5.	bind
11422	2	4542	6	10	NULL	0	NULL	Pol II			bind									HS3	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6484_s_105	12944475	(C) ChIP analysis of Pol II binding to HS2, HS3, and HS4, the active  Ey promoter, and intergenic site IVR5.	bind
11423	3	4542	6	10	NULL	0	NULL	Pol II			bind									HS4	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6484_s_105	12944475	(C) ChIP analysis of Pol II binding to HS2, HS3, and HS4, the active  Ey promoter, and intergenic site IVR5.	bind
11424	4	4542	6	NULL	NULL	0	NULL	Pol II	NULL		bind	NULL				Ey	NULL	active		promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_18_6484_s_105	12944475	(C) ChIP analysis of Pol II binding to HS2, HS3, and HS4, the active  Ey promoter, and intergenic site IVR5.	bind
11425	5	4542	6	NULL	NULL	0	NULL	Pol II	NULL		bind	NULL					NULL			intergenic site IVR5	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_18_6484_s_105	12944475	(C) ChIP analysis of Pol II binding to HS2, HS3, and HS4, the active  Ey promoter, and intergenic site IVR5.	bind
11489	1	4543	5	NULL	NULL	0	NULL	Rpb1	NULL		bind	NULL				GAL1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_18_6270_s_213	11509669	(C) ChIP analysis of the binding of Rpb1 to the  GAL1 and  GAL10 promoters.	bind
11490	2	4543	5	NULL	NULL	0	NULL	Rpb1	NULL		bind	NULL				GAL10	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_18_6270_s_213	11509669	(C) ChIP analysis of the binding of Rpb1 to the  GAL1 and  GAL10 promoters.	bind
11426	1	4543	6	NULL	NULL	NULL	NULL	Rpb1	GP		bind					GAL1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_18_6270_s_213	11509669	(C) ChIP analysis of the binding of Rpb1 to the  GAL1 and  GAL10 promoters.	bind
11427	2	4543	6	NULL	NULL	NULL	NULL	Rpb1	GP		bind					GAL10	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_18_6270_s_213	11509669	(C) ChIP analysis of the binding of Rpb1 to the  GAL1 and  GAL10 promoters.	bind
11492	1	4544	5	NULL	NULL	0	NULL	Sox1	NULL		bind	NULL	directly			Hes1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_devbiol_269_2_580_s_178	15110721	(C) ChIP assay demonstrates that Sox1 binds directly to the Hes1 promoter.	bind
11428	1	4544	6	NULL	NULL	NULL	NULL	Sox1	GP		bind		directly			Hes1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_devbiol_269_2_580_s_178	15110721	(C) ChIP assay demonstrates that Sox1 binds directly to the Hes1 promoter.	bind
11494	1	4545	5	NULL	NULL	0	NULL	MEF2	NULL		bind	NULL				 lklf	NULL			promoter	NULL	in vivo	0	NULL	NULL	NULL	gw70_molcellbiol_25_19_8553_s_303	16166637	(C) ChIP assays were performed to demonstrate in vivo binding of MEF2 to the  lklf promoter.	bind
11429	1	4545	6	NULL	NULL	NULL	NULL	MEF2	GP		bind					lklf	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8553_s_303	16166637	(C) ChIP assays were performed to demonstrate in vivo binding of MEF2 to the  lklf promoter.	bind
11495	1	4546	5	NULL	NULL	0	NULL	GATA-1	NULL		bind	NULL				TIMP-1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_17_7412_s_142	16107690	(C) ChIP of GATA-1 bound to the  TIMP-1 promoter.	bind
11449	1	4546	6	NULL	NULL	NULL	NULL	GATA-1	GP		bind					TIMP-1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_17_7412_s_142	16107690	(C) ChIP of GATA-1 bound to the  TIMP-1 promoter.	bind
11497	1	4547	5	NULL	NULL	0	NULL	chPER3	NULL		bind	NULL				CKI	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_2_584_s_144	14701732	(C) chPER3 binds to CKI  more efficiently than mPER3, whereas chPER2 binds to CKI  much less efficiently than mPER2.	bind
11498	2	4547	5	NULL	NULL	0	NULL	mPER3	NULL		bind	NULL				CKI	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_2_584_s_144	14701732	(C) chPER3 binds to CKI  more efficiently than mPER3, whereas chPER2 binds to CKI  much less efficiently than mPER2.	bind
11500	3	4547	5	NULL	NULL	0	NULL	statement 1	NULL		is more efficient than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_2_584_s_144	14701732	(C) chPER3 binds to CKI  more efficiently than mPER3, whereas chPER2 binds to CKI  much less efficiently than mPER2.	bind
11501	4	4547	5	NULL	NULL	0	NULL	chPER2	NULL		bind	NULL				CKI	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_2_584_s_144	14701732	(C) chPER3 binds to CKI  more efficiently than mPER3, whereas chPER2 binds to CKI  much less efficiently than mPER2.	bind
11503	5	4547	5	NULL	NULL	0	NULL	mPER2	NULL		bind	NULL				CKI	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_2_584_s_144	14701732	(C) chPER3 binds to CKI  more efficiently than mPER3, whereas chPER2 binds to CKI  much less efficiently than mPER2.	bind
11504	6	4547	5	NULL	NULL	0	NULL	statement 4	NULL		is less efficient than	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_2_584_s_144	14701732	(C) chPER3 binds to CKI  more efficiently than mPER3, whereas chPER2 binds to CKI  much less efficiently than mPER2.	bind
11450	1	4547	6	NULL	NULL	NULL	NULL	chPER3	GP		bind					CKI	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_584_s_144	14701732	(C) chPER3 binds to CKI  more efficiently than mPER3, whereas chPER2 binds to CKI  much less efficiently than mPER2.	bind
11451	2	4547	6	NULL	NULL	NULL	NULL	mPER3	GP		bind					CKI	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_584_s_144	14701732	(C) chPER3 binds to CKI  more efficiently than mPER3, whereas chPER2 binds to CKI  much less efficiently than mPER2.	bind
11452	3	4547	6	NULL	NULL	NULL	NULL	statement 1	Process		is more efficient than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_584_s_144	14701732	(C) chPER3 binds to CKI  more efficiently than mPER3, whereas chPER2 binds to CKI  much less efficiently than mPER2.	bind
11453	4	4547	6	NULL	NULL	NULL	NULL	chPER2	GP		bind					CKI	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_584_s_144	14701732	(C) chPER3 binds to CKI  more efficiently than mPER3, whereas chPER2 binds to CKI  much less efficiently than mPER2.	bind
11454	5	4547	6	NULL	NULL	NULL	NULL	mPER2	GP		bind					CKI	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_584_s_144	14701732	(C) chPER3 binds to CKI  more efficiently than mPER3, whereas chPER2 binds to CKI  much less efficiently than mPER2.	bind
11455	6	4547	6	NULL	NULL	NULL	NULL	statement 4	Process		is less efficient than					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_584_s_144	14701732	(C) chPER3 binds to CKI  more efficiently than mPER3, whereas chPER2 binds to CKI  much less efficiently than mPER2.	bind
11507	1	4549	5	NULL	NULL	0	NULL	Tcf3	NULL		bind	NULL				beta-catenin	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_217	11524435	(C) CK1epsilon stimulates the binding of Tcf3 to beta-catenin.	bind
11508	2	4549	5	NULL	NULL	0	NULL	CK1epsilon	NULL		stimulate	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_217	11524435	(C) CK1epsilon stimulates the binding of Tcf3 to beta-catenin.	bind
11456	1	4549	6	NULL	NULL	NULL	NULL	Tcf3	GP		bind					beta-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_217	11524435	(C) CK1epsilon stimulates the binding of Tcf3 to beta-catenin.	bind
11457	2	4549	6	NULL	NULL	NULL	NULL	CK1epsilon	GP		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_217	11524435	(C) CK1epsilon stimulates the binding of Tcf3 to beta-catenin.	bind
11510	1	4553	5	NULL	NULL	0	NULL	LR974P	NULL		bind	NULL				SHP-2	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1545_1_20_s_146	11342028	(C) Comparison of binding of LR986P and LR974P to SHP-2.	bind
11511	2	4553	5	NULL	NULL	0	NULL	LR986P	NULL		bind	NULL				SHP-2	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1545_1_20_s_146	11342028	(C) Comparison of binding of LR986P and LR974P to SHP-2.	bind
11458	1	4553	6	NULL	NULL	NULL	NULL	LR974P			bind					SHP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1545_1_20_s_146	11342028	(C) Comparison of binding of LR986P and LR974P to SHP-2.	bind
11459	2	4553	6	NULL	NULL	NULL	NULL	LR986P			bind					SHP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1545_1_20_s_146	11342028	(C) Comparison of binding of LR986P and LR974P to SHP-2.	bind
11600	1	4554	6	NULL	NULL	NULL	NULL	MAb9E			bind					MYC epitope	AminoAcid		C terminus of the intracellular domain		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_7_1709_s_146	9658166	(C) Comparison of Delta isoforms immunoprecipitated using MAb8A from cultured cells that express DeltaWTNdeMYC (lane 1) with Delta isoforms immunoprecipitated from DeltaWTNdeMYC+ cells with MAb9E, which binds to the MYC epitope at the C terminus of the intracellular domain (lane 2).	bind
11514	1	4555	5	10	NULL	0	NULL	Translin		 rat;; liver	bind									Bcl-CL1	NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1624_1_29_s_157	14642810	(C) Comparison of expressed rat liver Translin binding  to Bcl-CL1 and GRE (MLTF-like site) DNA.	bind
11515	2	4555	5	10	NULL	0	NULL	Translin		 rat;;liver	bind					DNA				GRE (MLTF-like site)	NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1624_1_29_s_157	14642810	(C) Comparison of expressed rat liver Translin binding  to Bcl-CL1 and GRE (MLTF-like site) DNA.	bind
11481	1	4555	6	NULL	NULL	NULL	NULL	translin	GP	rat;; liver	bind									Bcl-CL1	NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1624_1_29_s_157	14642810	(C) Comparison of expressed rat liver Translin binding  to Bcl-CL1 and GRE (MLTF-like site) DNA.	bind
11482	2	4555	6	NULL	NULL	NULL	NULL	translin	GP	rat;; liver	bind					DNA	NucleicAcid			GRE (MLTF-like site)	NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1624_1_29_s_157	14642810	(C) Comparison of expressed rat liver Translin binding  to Bcl-CL1 and GRE (MLTF-like site) DNA.	bind
11517	1	4557	5	NULL	NULL	0	NULL	MEKK-1	NULL		phosphorylate	NULL				SMRT	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6612_s_250	10938135	(C) Comparison of MEKK-1 phosphorylation of SMRT and of SEK-1.	bind
11518	2	4557	5	NULL	NULL	0	NULL	MEKK-1	NULL		phosphorylate	NULL				SEK-1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6612_s_250	10938135	(C) Comparison of MEKK-1 phosphorylation of SMRT and of SEK-1.	bind
11491	1	4557	6	NULL	NULL	NULL	NULL	MEKK-1	GP		phosphorylates					SMRT	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6612_s_250	10938135	(C) Comparison of MEKK-1 phosphorylation of SMRT and of SEK-1.	bind
11493	2	4557	6	NULL	NULL	NULL	NULL	MEKK-1	GP		phosphorylates					SEK-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6612_s_250	10938135	(C) Comparison of MEKK-1 phosphorylation of SMRT and of SEK-1.	bind
11519	1	4558	5	NULL	NULL	0	NULL	PP1c	NULL		bind	NULL				AKAP220 peptide	NULL	human			NULL		0	NULL	NULL	NULL	gw60_currbiol_9_6_321_s_53	10209101	(c) Comparison of PP1c  binding to the human AKAP220 peptide, the rat AKAP220 peptide, and the GM subunit peptide ( plus-or-minus  standard error).	bind
11520	2	4558	5	NULL	NULL	0	NULL	PP1c	NULL		bind	NULL				AKAP220 peptide	NULL	rat			NULL		0	NULL	NULL	NULL	gw60_currbiol_9_6_321_s_53	10209101	(c) Comparison of PP1c  binding to the human AKAP220 peptide, the rat AKAP220 peptide, and the GM subunit peptide ( plus-or-minus  standard error).	bind
11521	3	4558	5	NULL	NULL	0	NULL	PP1c	NULL		bind	NULL				GM subunit peptide	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_9_6_321_s_53	10209101	(c) Comparison of PP1c  binding to the human AKAP220 peptide, the rat AKAP220 peptide, and the GM subunit peptide ( plus-or-minus  standard error).	bind
11496	1	4558	6	NULL	NULL	NULL	NULL	PP1c	GP		bind					AKAP220 peptide	AminoAcid	human			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_6_321_s_53	10209101	(c) Comparison of PP1c  binding to the human AKAP220 peptide, the rat AKAP220 peptide, and the GM subunit peptide ( plus-or-minus  standard error).	bind
11499	2	4558	6	NULL	NULL	NULL	NULL	PP1c	GP		bind					AKAP220 peptide	AminoAcid	rat			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_6_321_s_53	10209101	(c) Comparison of PP1c  binding to the human AKAP220 peptide, the rat AKAP220 peptide, and the GM subunit peptide ( plus-or-minus  standard error).	bind
11502	3	4558	6	NULL	NULL	NULL	NULL	PP1c	GP		bind					GM subunit peptide	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_9_6_321_s_53	10209101	(c) Comparison of PP1c  binding to the human AKAP220 peptide, the rat AKAP220 peptide, and the GM subunit peptide ( plus-or-minus  standard error).	bind
11522	1	4559	5	NULL	NULL	0	NULL	JNK isoform	NULL	human	bind	NULL				JIP1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_10_7245_s_166	10490659	(C) Comparison of the binding of 10 human JNK isoforms to JIP1 and JIP2.	bind
11523	2	4559	5	NULL	NULL	0	NULL	JNK isoform	NULL	human	bind	NULL				JIP2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_10_7245_s_166	10490659	(C) Comparison of the binding of 10 human JNK isoforms to JIP1 and JIP2.	bind
11505	1	4559	6	NULL	NULL	NULL	NULL	JNK isoforms	GP	human	bind					JIP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_7245_s_166	10490659	(C) Comparison of the binding of 10 human JNK isoforms to JIP1 and JIP2.	bind
11506	2	4559	6	NULL	NULL	NULL	NULL	JNK isoforms	GP	human	bind					JIP2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_7245_s_166	10490659	(C) Comparison of the binding of 10 human JNK isoforms to JIP1 and JIP2.	bind
11524	1	4560	5	NULL	NULL	0	NULL	JNK isoform	NULL		bind	NULL				JIP3	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_3_1030_s_160	10629060	(C) Comparison of the binding of 10 JNK isoforms to JIP3.	bind
11509	1	4560	6	NULL	NULL	NULL	NULL	JNK isoforms	GP		bind					JIP3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_1030_s_160	10629060	(C) Comparison of the binding of 10 JNK isoforms to JIP3.	bind
11525	1	4561	5	NULL	NULL	0	NULL	TBL1	NULL		bind	NULL	preferentially			histones	NULL	hypoacetylated			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_197	15601853	(C) Competition  experiments showing that TBL1 and TBLR1 bound preferentially to hypoacetylated histones.	bind
11526	2	4561	5	NULL	NULL	0	NULL	TBLR1	NULL		bind	NULL	preferentially			histones	NULL	hypoacetylated			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_197	15601853	(C) Competition  experiments showing that TBL1 and TBLR1 bound preferentially to hypoacetylated histones.	bind
11512	1	4561	6	NULL	NULL	NULL	NULL	TBL1	GP		bind		preferentially			histones	GP	hypoacetylated			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_197	15601853	(C) Competition  experiments showing that TBL1 and TBLR1 bound preferentially to hypoacetylated histones.	bind
11513	2	4561	6	NULL	NULL	NULL	NULL	TBLR1	GP		bind		preferentially			histones	GP	hypoacetylated			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_324_s_197	15601853	(C) Competition  experiments showing that TBL1 and TBLR1 bound preferentially to hypoacetylated histones.	bind
11527	1	4562	5	NULL	NULL	0	NULL	tRNAAla	NULL	unlabeled	bind	NULL				mitochondria	NULL	isolated			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_11_4000_s_243	12748301	(C) Competition experiments of tRNAAla binding onto isolated mitochondria using unlabeled tRNAAla, tRNAPhe, or tRNAMet-e as competitors.	bind
11528	2	4562	5	NULL	NULL	0	NULL	tRNAPhe	NULL	unlabeled	bind	NULL				mitochondria	NULL	isolated			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_11_4000_s_243	12748301	(C) Competition experiments of tRNAAla binding onto isolated mitochondria using unlabeled tRNAAla, tRNAPhe, or tRNAMet-e as competitors.	bind
11529	3	4562	5	NULL	NULL	0	NULL	tRNAMet-e	NULL	unlabeled	bind	NULL				mitochondria	NULL	isolated			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_11_4000_s_243	12748301	(C) Competition experiments of tRNAAla binding onto isolated mitochondria using unlabeled tRNAAla, tRNAPhe, or tRNAMet-e as competitors.	bind
11530	4	4562	5	NULL	NULL	0	NULL	statement 2	NULL		compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_11_4000_s_243	12748301	(C) Competition experiments of tRNAAla binding onto isolated mitochondria using unlabeled tRNAAla, tRNAPhe, or tRNAMet-e as competitors.	bind
11531	5	4562	5	NULL	NULL	0	NULL	statement 3	NULL		compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_11_4000_s_243	12748301	(C) Competition experiments of tRNAAla binding onto isolated mitochondria using unlabeled tRNAAla, tRNAPhe, or tRNAMet-e as competitors.	bind
11547	1	4562	6	NULL	NULL	NULL	NULL	tRNAAla	NucleicAcid		bind					mitochondria	CellComponent	isolated			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_11_4000_s_243	12748301	(C) Competition experiments of tRNAAla binding onto isolated mitochondria using unlabeled tRNAAla, tRNAPhe, or tRNAMet-e as competitors.	bind
11548	2	4562	6	NULL	NULL	NULL	NULL	tRNAAla	NucleicAcid	unlabeled	bind					mitochondria	CellComponent	isolated			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_11_4000_s_243	12748301	(C) Competition experiments of tRNAAla binding onto isolated mitochondria using unlabeled tRNAAla, tRNAPhe, or tRNAMet-e as competitors.	bind
11549	3	4562	6	NULL	NULL	NULL	NULL	statement 2	Process		competes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_11_4000_s_243	12748301	(C) Competition experiments of tRNAAla binding onto isolated mitochondria using unlabeled tRNAAla, tRNAPhe, or tRNAMet-e as competitors.	bind
11550	4	4562	6	NULL	NULL	NULL	NULL	tRNAPhe	NucleicAcid	unlabeled	bind					mitochondria	CellComponent	isolated			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_11_4000_s_243	12748301	(C) Competition experiments of tRNAAla binding onto isolated mitochondria using unlabeled tRNAAla, tRNAPhe, or tRNAMet-e as competitors.	bind
11551	5	4562	6	NULL	NULL	NULL	NULL	statement 4	Process		competes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_11_4000_s_243	12748301	(C) Competition experiments of tRNAAla binding onto isolated mitochondria using unlabeled tRNAAla, tRNAPhe, or tRNAMet-e as competitors.	bind
11552	6	4562	6	NULL	NULL	NULL	NULL	tRNAMet-e	NucleicAcid	unlabeled	bind					mitochondria	CellComponent	isolated			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_11_4000_s_243	12748301	(C) Competition experiments of tRNAAla binding onto isolated mitochondria using unlabeled tRNAAla, tRNAPhe, or tRNAMet-e as competitors.	bind
11553	7	4562	6	NULL	NULL	NULL	NULL	statement 6	Process		competes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_11_4000_s_243	12748301	(C) Competition experiments of tRNAAla binding onto isolated mitochondria using unlabeled tRNAAla, tRNAPhe, or tRNAMet-e as competitors.	bind
11532	1	4563	5	NULL	NULL	0	NULL	NF D	NULL		bind	NULL				rDNA probe A123BP	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_16_7284_s_178	15282326	(C) Competition for binding of NF D to rDNA probe A123BP with increasing amounts of unlabeled rDNA A123BP or rA123BPH as indicated.	bind
11533	2	4563	5	NULL	NULL	0	NULL	NF D	NULL		bind	NULL				rDNA A123BP	NULL	unlabeled			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_16_7284_s_178	15282326	(C) Competition for binding of NF D to rDNA probe A123BP with increasing amounts of unlabeled rDNA A123BP or rA123BPH as indicated.	bind
11534	3	4563	5	NULL	NULL	0	NULL	NF D	NULL		bind	NULL				rA123BPH	NULL	unlabeled			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_16_7284_s_178	15282326	(C) Competition for binding of NF D to rDNA probe A123BP with increasing amounts of unlabeled rDNA A123BP or rA123BPH as indicated.	bind
11535	4	4563	5	NULL	NULL	0	NULL	statement 2	NULL		compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_16_7284_s_178	15282326	(C) Competition for binding of NF D to rDNA probe A123BP with increasing amounts of unlabeled rDNA A123BP or rA123BPH as indicated.	bind
11536	5	4563	5	NULL	NULL	0	NULL	statement 3	NULL		compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_16_7284_s_178	15282326	(C) Competition for binding of NF D to rDNA probe A123BP with increasing amounts of unlabeled rDNA A123BP or rA123BPH as indicated.	bind
54436	6	4563	5	10	NULL	0	NULL	statement 2			is an alternative to					statement 3					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_16_7284_s_178	15282326	(C) Competition for binding of NF D to rDNA probe A123BP with increasing amounts of unlabeled rDNA A123BP or rA123BPH as indicated.	bind
11554	1	4563	6	NULL	NULL	NULL	NULL	NF D			bind					rDNA A123BP	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_16_7284_s_178	15282326	(C) Competition for binding of NF D to rDNA probe A123BP with increasing amounts of unlabeled rDNA A123BP or rA123BPH as indicated.	bind
11555	2	4563	6	NULL	NULL	NULL	NULL	NF D			bind					rDNA A123BP	NucleicAcid	unlabeled			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_16_7284_s_178	15282326	(C) Competition for binding of NF D to rDNA probe A123BP with increasing amounts of unlabeled rDNA A123BP or rA123BPH as indicated.	bind
11556	3	4563	6	NULL	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_16_7284_s_178	15282326	(C) Competition for binding of NF D to rDNA probe A123BP with increasing amounts of unlabeled rDNA A123BP or rA123BPH as indicated.	bind
11557	4	4563	6	NULL	NULL	NULL	NULL	NF D			bind					rDNA A123BPH	NucleicAcid	unlabeled			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_16_7284_s_178	15282326	(C) Competition for binding of NF D to rDNA probe A123BP with increasing amounts of unlabeled rDNA A123BP or rA123BPH as indicated.	bind
11558	5	4563	6	NULL	NULL	NULL	NULL	statement 1	Process		competes					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_16_7284_s_178	15282326	(C) Competition for binding of NF D to rDNA probe A123BP with increasing amounts of unlabeled rDNA A123BP or rA123BPH as indicated.	bind
11559	6	4563	6	NULL	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_16_7284_s_178	15282326	(C) Competition for binding of NF D to rDNA probe A123BP with increasing amounts of unlabeled rDNA A123BP or rA123BPH as indicated.	bind
11537	1	4564	5	NULL	NULL	0	NULL	KKLF	NULL		bind	NULL					NULL			GA element	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7319_s_142	10982849	(C) Competitive binding of KKLF and MAZ at the GA element.	bind
11538	2	4564	5	NULL	NULL	0	NULL	MAZ	NULL		bind	NULL					NULL			GA element	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7319_s_142	10982849	(C) Competitive binding of KKLF and MAZ at the GA element.	bind
11539	3	4564	5	NULL	NULL	0	NULL	statement 1	NULL		compete with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7319_s_142	10982849	(C) Competitive binding of KKLF and MAZ at the GA element.	bind
11560	1	4564	6	NULL	NULL	NULL	NULL	KKLF	GP		bind									GA element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7319_s_142	10982849	(C) Competitive binding of KKLF and MAZ at the GA element.	bind
11561	2	4564	6	NULL	NULL	NULL	NULL	MAZ	GP		bind									GA element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7319_s_142	10982849	(C) Competitive binding of KKLF and MAZ at the GA element.	bind
11562	3	4564	6	NULL	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7319_s_142	10982849	(C) Competitive binding of KKLF and MAZ at the GA element.	bind
11540	1	4566	5	NULL	NULL	0	NULL	Gsp1	NULL		bind	NULL				GTP	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_12_4295_s_221	10825193	(C) Complex formation is dependent on the GTP-bound form of Gsp1.	bind
11541	2	4566	5	NULL	NULL	0	NULL	complex formation	NULL		is dependent on	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_12_4295_s_221	10825193	(C) Complex formation is dependent on the GTP-bound form of Gsp1.	bind
11563	1	4566	6	NULL	NULL	NULL	NULL	Gsp1	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4295_s_221	10825193	(C) Complex formation is dependent on the GTP-bound form of Gsp1.	bind
11542	1	4567	5	NULL	NULL	0	NULL	syntaxin-1A	NULL		bind	NULL				myosin-Va	NULL				NULL	in brain homogenate (Crude)	0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_94	16030255	(C) Confirmation of the 10 - 6 M Ca2+/2 mM Mg2+/0.5 mM ATP-dependent binding of syntaxin-1A to myosin-Va in brain homogenate (Crude)  or to purified myosin-Va (Purified).	bind
11543	2	4567	5	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_94	16030255	(C) Confirmation of the 10 - 6 M Ca2+/2 mM Mg2+/0.5 mM ATP-dependent binding of syntaxin-1A to myosin-Va in brain homogenate (Crude)  or to purified myosin-Va (Purified).	bind
11544	3	4567	5	NULL	NULL	0	NULL	syntaxin-1A	NULL		bind	NULL				myosin-Va	NULL	purified			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_94	16030255	(C) Confirmation of the 10 - 6 M Ca2+/2 mM Mg2+/0.5 mM ATP-dependent binding of syntaxin-1A to myosin-Va in brain homogenate (Crude)  or to purified myosin-Va (Purified).	bind
11545	4	4567	5	NULL	NULL	0	NULL	statement 3	NULL		is dependent on	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_94	16030255	(C) Confirmation of the 10 - 6 M Ca2+/2 mM Mg2+/0.5 mM ATP-dependent binding of syntaxin-1A to myosin-Va in brain homogenate (Crude)  or to purified myosin-Va (Purified).	bind
11546	5	4567	5	NULL	NULL	0	NULL	statement 4	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_94	16030255	(C) Confirmation of the 10 - 6 M Ca2+/2 mM Mg2+/0.5 mM ATP-dependent binding of syntaxin-1A to myosin-Va in brain homogenate (Crude)  or to purified myosin-Va (Purified).	bind
11564	1	4567	6	NULL	NULL	NULL	NULL	syntaxin-1A	GP		bind					myosin-Va	GP				NULL	brain homogenate	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_94	16030255	(C) Confirmation of the 10 - 6 M Ca2+/2 mM Mg2+/0.5 mM ATP-dependent binding of syntaxin-1A to myosin-Va in brain homogenate (Crude)  or to purified myosin-Va (Purified).	bind
11565	2	4567	6	NULL	NULL	NULL	NULL	syntaxin-1A	GP		bind					myosin-Va	GP	purified			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_94	16030255	(C) Confirmation of the 10 - 6 M Ca2+/2 mM Mg2+/0.5 mM ATP-dependent binding of syntaxin-1A to myosin-Va in brain homogenate (Crude)  or to purified myosin-Va (Purified).	bind
11566	3	4567	6	NULL	NULL	NULL	NULL	statement 1	Process		is dependent on					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_94	16030255	(C) Confirmation of the 10 - 6 M Ca2+/2 mM Mg2+/0.5 mM ATP-dependent binding of syntaxin-1A to myosin-Va in brain homogenate (Crude)  or to purified myosin-Va (Purified).	bind
11567	4	4567	6	NULL	NULL	NULL	NULL	statement 2	Process		is dependent on					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_94	16030255	(C) Confirmation of the 10 - 6 M Ca2+/2 mM Mg2+/0.5 mM ATP-dependent binding of syntaxin-1A to myosin-Va in brain homogenate (Crude)  or to purified myosin-Va (Purified).	bind
54437	5	4567	6	NULL	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_94	16030255	(C) Confirmation of the 10 - 6 M Ca2+/2 mM Mg2+/0.5 mM ATP-dependent binding of syntaxin-1A to myosin-Va in brain homogenate (Crude)  or to purified myosin-Va (Purified).	bind
11614	1	4569	5	10	NULL	0	NULL	methyltransferase	NULL		bind	NULL		HsdM subunits			NULL		linker region		NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_2_412_s_131	10839821	(c) Consequent model of the methyltransferase, in which the two HsdM subunits bind  to the linker region to generate an enzyme with pseudodyad symmetry.	bind
11615	2	4569	5	NULL	NULL	0	NULL	statement 1	NULL		generate	NULL				enzyme	NULL	 pseudodyad symmetry			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_2_412_s_131	10839821	(c) Consequent model of the methyltransferase, in which the two HsdM subunits bind  to the linker region to generate an enzyme with pseudodyad symmetry.	bind
11568	1	4569	6	NULL	NULL	NULL	NULL	methyltransferase	GP		bind			HsdM subunits					linker region		NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_2_412_s_131	10839821	(c) Consequent model of the methyltransferase, in which the two HsdM subunits bind  to the linker region to generate an enzyme with pseudodyad symmetry.	bind
11569	2	4569	6	NULL	NULL	NULL	NULL	statement 1	Process		generates					enzyme	GP	pseudodyad symmetry			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_2_412_s_131	10839821	(c) Consequent model of the methyltransferase, in which the two HsdM subunits bind  to the linker region to generate an enzyme with pseudodyad symmetry.	bind
11609	1	4571	5	NULL	NULL	0	NULL	Vera	NULL		bind	NULL				E2	NULL	deletion mutants			NULL		0	NULL	NULL	NULL	gw60_currbiol_8_9_489_s_60	9560341	(c) Correlation between localization  in vivo and Vera binding of E2 deletion mutants.	bind
11570	1	4571	6	NULL	NULL	NULL	NULL	E2	GP	deletion mutant	bind					Vera	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_9_489_s_60	9560341	(c) Correlation between localization  in vivo and Vera binding of E2 deletion mutants.	bind
11610	1	4573	5	NULL	NULL	0	NULL	VEGFR2	NULL		bind	NULL	selectively			F-actin	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_267_2_294_s_182	15013795	(C) Costaining for VEGFR2 (green) and phalloidin-Alexa Fluor 568 (red), which binds  to F-actin selectively and delineates the myocardium.	bind
11611	2	4573	5	NULL	NULL	0	NULL	VEGFR2	NULL		delineates	NULL				myocardium	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_267_2_294_s_182	15013795	(C) Costaining for VEGFR2 (green) and phalloidin-Alexa Fluor 568 (red), which binds  to F-actin selectively and delineates the myocardium.	bind
11612	3	4573	5	NULL	NULL	0	NULL	phalloidin-Alexa Fluor 568	NULL		bind	NULL	selectively			F-actin	NULL				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_267_2_294_s_182	15013795	(C) Costaining for VEGFR2 (green) and phalloidin-Alexa Fluor 568 (red), which binds  to F-actin selectively and delineates the myocardium.	bind
11613	4	4573	5	NULL	NULL	0	NULL	statement 3	NULL		delineates	NULL				myocardium	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_267_2_294_s_182	15013795	(C) Costaining for VEGFR2 (green) and phalloidin-Alexa Fluor 568 (red), which binds  to F-actin selectively and delineates the myocardium.	bind
54438	1	4573	6	NULL	NULL	NULL	NULL	VEGFR2	GP		bind		selectively			F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_267_2_294_s_182	15013795	(C) Costaining for VEGFR2 (green) and phalloidin-Alexa Fluor 568 (red), which binds  to F-actin selectively and delineates the myocardium.	bind
54439	2	4573	6	NULL	NULL	NULL	NULL	statement 1	Process		delineates					myocardium	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_267_2_294_s_182	15013795	(C) Costaining for VEGFR2 (green) and phalloidin-Alexa Fluor 568 (red), which binds  to F-actin selectively and delineates the myocardium.	bind
11616	1	4574	5	NULL	NULL	0	NULL	MyoD	NULL	cotransfection of	does not alter	NULL				myogenin-positive cells	NULL	number of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6600_s_197	10938134	(C) Cotransfection of MyoD and calcineurin (CnA) also does not alter the number of myogenin-positive cells.	bind
11617	2	4574	5	NULL	NULL	0	NULL	calcineurin (CnA)	NULL	cotransfection of	does not alter	NULL				myogenin-positive cells	NULL	number of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6600_s_197	10938134	(C) Cotransfection of MyoD and calcineurin (CnA) also does not alter the number of myogenin-positive cells.	bind
16268	1	4574	6	NULL	NULL	NULL	NULL	MyoD	GP	cotransfection of	does not alter					myogenin-positive cells	Cell	number of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6600_s_197	10938134	(C) Cotransfection of MyoD and calcineurin (CnA) also does not alter the number of myogenin-positive cells.	bind
16269	2	4574	6	NULL	NULL	NULL	NULL	calcineurin (CnA)	GP	cotransfection of	does not alter					myogenin-positive cells	Cell	number of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6600_s_197	10938134	(C) Cotransfection of MyoD and calcineurin (CnA) also does not alter the number of myogenin-positive cells.	bind
11618	1	4575	5	NULL	NULL	0	NULL	CPR	NULL		bind	NULL				10-mer peptides	NULL				NULL	cellulose membrane	NULL	NULL	NULL	NULL	gw60_chembiol_9_10_1129_s_110	12401497	(C) CPR binding to PCI-derived 10-mer peptides on a cellulose membrane.	bind
44562	2	4575	5	10	NULL	0	NULL	10-mer peptides	NULL		is derived from	NULL				PCI	NULL				NULL		0	NULL	NULL	NULL	gw60_chembiol_9_10_1129_s_110	12401497	(C) CPR binding to PCI-derived 10-mer peptides on a cellulose membrane.	bind
11574	2	4575	6	NULL	NULL	NULL	NULL	CPR	GP		bind					statement 1	Process				NULL	cellulose membrane	NULL	NULL	NULL	NULL	gw60_chembiol_9_10_1129_s_110	12401497	(C) CPR binding to PCI-derived 10-mer peptides on a cellulose membrane.	bind
54440	1	4575	6	NULL	NULL	NULL	NULL	10-mer peptides	AminoAcid		derived from					PCI	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_9_10_1129_s_110	12401497	(C) CPR binding to PCI-derived 10-mer peptides on a cellulose membrane.	bind
11619	1	4576	5	NULL	NULL	0	NULL	CREB	NULL		bind	NULL				cyclin D1	NULL			CRE of promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_17_7514_s_218	15314161	(C) CREB and ATF-2 bind the CRE  of the cyclin D1 promoter.	bind
11620	2	4576	5	NULL	NULL	0	NULL	ATF-2	NULL		bind	NULL				cyclin D1	NULL			CRE of promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_17_7514_s_218	15314161	(C) CREB and ATF-2 bind the CRE  of the cyclin D1 promoter.	bind
11575	1	4576	6	NULL	NULL	NULL	NULL	CREB	GP		bind					cyclin D1	GP			CRE element of promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_17_7514_s_218	15314161	(C) CREB and ATF-2 bind the CRE  of the cyclin D1 promoter.	bind
11576	2	4576	6	NULL	NULL	NULL	NULL	ATF-2	GP		bind					cyclin D1	GP			CRE element of promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_17_7514_s_218	15314161	(C) CREB and ATF-2 bind the CRE  of the cyclin D1 promoter.	bind
11621	1	4578	5	NULL	NULL	0	NULL	CSP	NULL		bind	NULL	dose dependently			Syntaxin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_23_3_593_s_218	10433270	(C) CSP binds Syntaxin in a dose-dependent and saturable manner.	bind
11623	2	4578	5	NULL	NULL	0	NULL	statement 1	NULL		occurs in	NULL				saturable manner	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_23_3_593_s_218	10433270	(C) CSP binds Syntaxin in a dose-dependent and saturable manner.	bind
11577	1	4578	6	NULL	NULL	NULL	NULL	CSP	GP		bind		dose dependently			Syntaxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_23_3_593_s_218	10433270	(C) CSP binds Syntaxin in a dose-dependent and saturable manner.	bind
16270	2	4578	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs in					saturable manner					NULL		NULL	NULL	NULL	NULL	gw60_neuron_23_3_593_s_218	10433270	(C) CSP binds Syntaxin in a dose-dependent and saturable manner.	bind
11624	1	4579	5	NULL	NULL	0	NULL	Tg	NULL		bind	NULL				BiP	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_22_9793_s_263	16260597	(C) CST causes a dramatic increase  of Tg binding to BiP and GRP94.	bind
11625	2	4579	5	NULL	NULL	0	NULL	CST	NULL		increase	NULL	dramatically			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_22_9793_s_263	16260597	(C) CST causes a dramatic increase  of Tg binding to BiP and GRP94.	bind
11626	3	4579	5	NULL	NULL	0	NULL	Tg	NULL		bind	NULL				GRP94	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_22_9793_s_263	16260597	(C) CST causes a dramatic increase  of Tg binding to BiP and GRP94.	bind
11627	4	4579	5	NULL	NULL	0	NULL	CST	NULL		increase	NULL	dramatically			statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_22_9793_s_263	16260597	(C) CST causes a dramatic increase  of Tg binding to BiP and GRP94.	bind
11578	1	4579	6	NULL	NULL	NULL	NULL	Tg	GP		bind					BiP	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9793_s_263	16260597	(C) CST causes a dramatic increase  of Tg binding to BiP and GRP94.	bind
11579	2	4579	6	NULL	NULL	NULL	NULL	Tg	GP		bind					GRP94	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9793_s_263	16260597	(C) CST causes a dramatic increase  of Tg binding to BiP and GRP94.	bind
11580	3	4579	6	NULL	NULL	NULL	NULL	CST	GP		increases		dramatically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9793_s_263	16260597	(C) CST causes a dramatic increase  of Tg binding to BiP and GRP94.	bind
11581	4	4579	6	NULL	NULL	NULL	NULL	CST	GP		increases		dramatically			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9793_s_263	16260597	(C) CST causes a dramatic increase  of Tg binding to BiP and GRP94.	bind
11628	1	4580	5	NULL	NULL	0	NULL	CTGF	NULL		bind	NULL				LRP6	NULL		EGF repeat 1		NULL		0	NULL	NULL	NULL	gw70_development_131_9_2137_s_237	15105373	(C) CTGF binds to both EGF repeats 1, 2 and 3, 4 of LRP6.	bind
11629	2	4580	5	NULL	NULL	0	NULL	CTGF	NULL		bind	NULL				LRP6	NULL		EGF repeat 2		NULL		0	NULL	NULL	NULL	gw70_development_131_9_2137_s_237	15105373	(C) CTGF binds to both EGF repeats 1, 2 and 3, 4 of LRP6.	bind
11630	3	4580	5	NULL	NULL	0	NULL	CTGF	NULL		bind	NULL				LRP6	NULL		EGF repeat 3		NULL		0	NULL	NULL	NULL	gw70_development_131_9_2137_s_237	15105373	(C) CTGF binds to both EGF repeats 1, 2 and 3, 4 of LRP6.	bind
11631	4	4580	5	NULL	NULL	0	NULL	CTGF	NULL		bind	NULL				LRP6	NULL		EGF repeat 4		NULL		0	NULL	NULL	NULL	gw70_development_131_9_2137_s_237	15105373	(C) CTGF binds to both EGF repeats 1, 2 and 3, 4 of LRP6.	bind
11582	1	4580	6	NULL	NULL	NULL	NULL	CTGF	GP		bind					LRP6	GP		EGF repeat 1		NULL		NULL	NULL	NULL	NULL	gw70_development_131_9_2137_s_237	15105373	(C) CTGF binds to both EGF repeats 1, 2 and 3, 4 of LRP6.	bind
13007	2	4580	6	NULL	NULL	NULL	NULL	CTGF	GP		bind					LRP6	GP		EGF repeat 2		NULL		NULL	NULL	NULL	NULL	gw70_development_131_9_2137_s_237	15105373	(C) CTGF binds to both EGF repeats 1, 2 and 3, 4 of LRP6.	bind
13008	3	4580	6	NULL	NULL	NULL	NULL	CTGF	GP		bind					LRP6	GP		EGF repeat 3		NULL		NULL	NULL	NULL	NULL	gw70_development_131_9_2137_s_237	15105373	(C) CTGF binds to both EGF repeats 1, 2 and 3, 4 of LRP6.	bind
13009	4	4580	6	NULL	NULL	NULL	NULL	CTGF	GP		bind					LRP6	GP		EGF repeat 4		NULL		NULL	NULL	NULL	NULL	gw70_development_131_9_2137_s_237	15105373	(C) CTGF binds to both EGF repeats 1, 2 and 3, 4 of LRP6.	bind
11632	1	4581	5	NULL	NULL	0	NULL	Cux/CDP	NULL		bind	NULL					NULL			P1 site	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_284_s_182	9858552	(C) Cux/CDP binds to P1, P2, and P4 sites.	bind
11633	2	4581	5	NULL	NULL	0	NULL	Cux/CDP	NULL		bind	NULL					NULL			P2 site	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_284_s_182	9858552	(C) Cux/CDP binds to P1, P2, and P4 sites.	bind
11634	3	4581	5	NULL	NULL	0	NULL	Cux/CDP	NULL		bind	NULL					NULL			P4 site	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_284_s_182	9858552	(C) Cux/CDP binds to P1, P2, and P4 sites.	bind
11583	1	4581	6	NULL	NULL	NULL	NULL	Cux/CDP	GP		bind									P1 site	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_284_s_182	9858552	(C) Cux/CDP binds to P1, P2, and P4 sites.	bind
11584	2	4581	6	NULL	NULL	NULL	NULL	Cux/CDP	GP		bind									P2 site	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_284_s_182	9858552	(C) Cux/CDP binds to P1, P2, and P4 sites.	bind
11585	3	4581	6	NULL	NULL	NULL	NULL	Cux/CDP	GP		bind									P4 site	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_284_s_182	9858552	(C) Cux/CDP binds to P1, P2, and P4 sites.	bind
11635	1	4582	5	NULL	NULL	0	NULL	Cyclin E	NULL	alone	does not bind	NULL				p300	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_136	10330164	(C) Cyclin E alone does not bind to p300.	bind
11586	1	4582	6	NULL	NULL	NULL	NULL	Cyclin E	GP		does not bind					p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_136	10330164	(C) Cyclin E alone does not bind to p300.	bind
11636	1	4583	5	NULL	NULL	0	NULL	Sir3	NULL		bind	NULL				Sir4	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_199	15899856	(C) Defects in Sir3 binding to Sir4 derepress telomeric silencing.	bind
11637	2	4583	5	NULL	NULL	0	NULL	statement 1	NULL	defects in	derepress	NULL				telomeric silencing	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_199	15899856	(C) Defects in Sir3 binding to Sir4 derepress telomeric silencing.	bind
11587	1	4583	6	NULL	NULL	NULL	NULL	Sir3	GP		bind					Sir4	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_199	15899856	(C) Defects in Sir3 binding to Sir4 derepress telomeric silencing.	bind
11588	2	4583	6	NULL	NULL	NULL	NULL	statement 1	Process	defects in	derepress					telomeric silencing	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_199	15899856	(C) Defects in Sir3 binding to Sir4 derepress telomeric silencing.	bind
11638	1	4584	5	NULL	NULL	0	NULL	mGluR7a	NULL		bind	NULL				PICK1	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_28_2_485_s_47	11144358	(C) Deletion of last 3 amino acids of the distal tail of mGluR7a (distal 7a 3) eliminated the binding with PICK1.	bind
11639	2	4584	5	NULL	NULL	0	NULL		NULL		eliminate	NULL		distal 7a 3		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_2_485_s_47	11144358	(C) Deletion of last 3 amino acids of the distal tail of mGluR7a (distal 7a 3) eliminated the binding with PICK1.	bind
11640	3	4584	5	NULL	NULL	0	NULL	distal 7a 3	NULL		is	NULL				deletion of last 3 amino acids of the distal tail of mGluR7a	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_28_2_485_s_47	11144358	(C) Deletion of last 3 amino acids of the distal tail of mGluR7a (distal 7a 3) eliminated the binding with PICK1.	bind
11589	1	4584	6	NULL	NULL	NULL	NULL	mGluR7a	GP		bind					PICK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_2_485_s_47	11144358	(C) Deletion of last 3 amino acids of the distal tail of mGluR7a (distal 7a 3) eliminated the binding with PICK1.	bind
11590	2	4584	6	NULL	NULL	NULL	NULL	mGluR7a	GP	deletion mutant	eliminates			distal 7a 3		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_2_485_s_47	11144358	(C) Deletion of last 3 amino acids of the distal tail of mGluR7a (distal 7a 3) eliminated the binding with PICK1.	bind
13010	3	4584	6	NULL	NULL	NULL	NULL	distal 7a			is					deletion of last 3 amino acids of the distal tail of mGluR7a					NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_2_485_s_47	11144358	(C) Deletion of last 3 amino acids of the distal tail of mGluR7a (distal 7a 3) eliminated the binding with PICK1.	bind
11641	1	4585	5	NULL	NULL	0	NULL	paxillin	NULL		bind	NULL		NH2 terminus		p95PKL	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_851_s_269	10330411	(C) Deletion of LD4 from the paxillin NH2 terminus fusion protein eliminated the binding to p95PKL.	bind
11642	2	4585	5	NULL	NULL	0	NULL	paxillin	NULL	deletion of LD4 from	eliminate	NULL		NH2 terminus		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_851_s_269	10330411	(C) Deletion of LD4 from the paxillin NH2 terminus fusion protein eliminated the binding to p95PKL.	bind
44563	3	4585	5	10	NULL	0	NULL	paxillin	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_4_851_s_269	10330411	(C) Deletion of LD4 from the paxillin NH2 terminus fusion protein eliminated the binding to p95PKL.	bind
11591	1	4585	6	NULL	NULL	NULL	NULL	paxillin	GP		bind			NH2 terminus		p95PKL	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_851_s_269	10330411	(C) Deletion of LD4 from the paxillin NH2 terminus fusion protein eliminated the binding to p95PKL.	bind
11592	2	4585	6	NULL	NULL	NULL	NULL	paxillin 	GP	deletion of LD4 from	eliminates			NH2 terminus		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_851_s_269	10330411	(C) Deletion of LD4 from the paxillin NH2 terminus fusion protein eliminated the binding to p95PKL.	bind
54441	3	4585	6	NULL	NULL	NULL	NULL	 paxillin	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_851_s_269	10330411	(C) Deletion of LD4 from the paxillin NH2 terminus fusion protein eliminated the binding to p95PKL.	bind
11644	1	4589	5	NULL	NULL	0	NULL	JIP-1	NULL		bind	NULL	differentially			APP polypeptides	NULL	phosphorylated			NULL		0	NULL	NULL	NULL	gw70_cellbiol_171_4_615_s_92	16301330	(C) Differential  binding of JIP-1 and Fe65 to phosphorylated and nonphosphorylated APP polypeptides  (ELISA).	bind
11645	2	4589	5	NULL	NULL	0	NULL	JIP-1	NULL		bind	NULL	differentially			APP polypeptides	NULL	nonphosphorylated			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_4_615_s_92	16301330	(C) Differential  binding of JIP-1 and Fe65 to phosphorylated and nonphosphorylated APP polypeptides  (ELISA).	bind
11646	3	4589	5	NULL	NULL	0	NULL	Fe65	NULL		bind	NULL	differentially			APP polypeptides	NULL	phosphorylated			NULL		0	NULL	NULL	NULL	gw70_cellbiol_171_4_615_s_92	16301330	(C) Differential  binding of JIP-1 and Fe65 to phosphorylated and nonphosphorylated APP polypeptides  (ELISA).	bind
11647	4	4589	5	NULL	NULL	0	NULL	Fe65	NULL		bind	NULL	differentially			APP polypeptides	NULL	nonphosphorylated			NULL		0	NULL	NULL	NULL	gw70_cellbiol_171_4_615_s_92	16301330	(C) Differential  binding of JIP-1 and Fe65 to phosphorylated and nonphosphorylated APP polypeptides  (ELISA).	bind
11593	1	4589	6	NULL	NULL	NULL	NULL	JIP1	GP		bind		differentially			APP polypeptides	AminoAcid	phosphorylated			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_4_615_s_92	16301330	(C) Differential  binding of JIP-1 and Fe65 to phosphorylated and nonphosphorylated APP polypeptides  (ELISA).	bind
11594	2	4589	6	NULL	NULL	NULL	NULL	JIP1	GP		bind		differentially			APP polypeptides	AminoAcid	nonphosphorylated			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_4_615_s_92	16301330	(C) Differential  binding of JIP-1 and Fe65 to phosphorylated and nonphosphorylated APP polypeptides  (ELISA).	bind
11595	3	4589	6	NULL	NULL	NULL	NULL	Fe65	GP		bind		differentially			APP polypeptides	AminoAcid	phosphorylated			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_4_615_s_92	16301330	(C) Differential  binding of JIP-1 and Fe65 to phosphorylated and nonphosphorylated APP polypeptides  (ELISA).	bind
11596	4	4589	6	NULL	NULL	NULL	NULL	Fe65	GP		bind		differentially			APP polypeptides	AminoAcid	nonphosphorylated			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_4_615_s_92	16301330	(C) Differential  binding of JIP-1 and Fe65 to phosphorylated and nonphosphorylated APP polypeptides  (ELISA).	bind
11648	1	4590	5	NULL	NULL	0	NULL	s-synaphin constructs	NULL	recombinant	bind	NULL	differentially			syntaxin	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_104_3_421_s_58	11239399	(C) Differential binding of recombinant s-synaphin constructs to syntaxin.	bind
11597	1	4590	6	NULL	NULL	NULL	NULL	s-synaphin	GP	recombinant	bind		differentially			syntaxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_104_3_421_s_58	11239399	(C) Differential binding of recombinant s-synaphin constructs to syntaxin.	bind
11658	1	4591	5	NULL	NULL	0	NULL	TCF	NULL		bind	NULL				beta-catenin	NULL	untethered 			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8462_s_163	14612392	(C) Differential requirements of TCF and APC binding for untethered  and membrane-tethered beta-catenin.	bind
11659	2	4591	5	NULL	NULL	0	NULL	APC	NULL		bind	NULL				beta-catenin	NULL	untethered			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8462_s_163	14612392	(C) Differential requirements of TCF and APC binding for untethered  and membrane-tethered beta-catenin.	bind
11660	3	4591	5	NULL	NULL	0	NULL	TCF	NULL		bind	NULL				beta-catenin	NULL	membrane-tethered			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8462_s_163	14612392	(C) Differential requirements of TCF and APC binding for untethered  and membrane-tethered beta-catenin.	bind
11661	4	4591	5	NULL	NULL	0	NULL	APC	NULL		bind	NULL				beta-catenin	NULL	membrane-tethered			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8462_s_163	14612392	(C) Differential requirements of TCF and APC binding for untethered  and membrane-tethered beta-catenin.	bind
43796	1	4591	6	NULL	NULL	NULL	NULL	beta-catenin	GP	untethered	bind					TCF	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8462_s_163	14612392	(C) Differential requirements of TCF and APC binding for untethered  and membrane-tethered beta-catenin.	bind
43797	2	4591	6	NULL	NULL	NULL	NULL	beta-catenin	GP	membrane-tethered	bind					TCF	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8462_s_163	14612392	(C) Differential requirements of TCF and APC binding for untethered  and membrane-tethered beta-catenin.	bind
43798	3	4591	6	NULL	NULL	NULL	NULL	beta-catenin	GP	untethered	bind					APC	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8462_s_163	14612392	(C) Differential requirements of TCF and APC binding for untethered  and membrane-tethered beta-catenin.	bind
43799	4	4591	6	NULL	NULL	NULL	NULL	beta-catenin	GP	membrane-tethered	bind					APC	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8462_s_163	14612392	(C) Differential requirements of TCF and APC binding for untethered  and membrane-tethered beta-catenin.	bind
11656	1	4592	5	10	NULL	0	NULL	DDR1 Rbodies			bind		differentially			dermal collagen I		 bovine			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_131	9659900	(C) Differential slot-blot binding of DDR1 and DDR2 Rbodies to commercially-derived bovine dermal collagen I (Vitrogen).	bind
11657	2	4592	5	10	NULL	0	NULL	DDR2 Rbodies			bind		differentially			dermal collagen I		 bovine			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_131	9659900	(C) Differential slot-blot binding of DDR1 and DDR2 Rbodies to commercially-derived bovine dermal collagen I (Vitrogen).	bind
11674	1	4592	6	NULL	NULL	NULL	NULL	DDR1 Rbodies	GP		bind		differentially			dermal collagen I	GP	bovine			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_131	9659900	(C) Differential slot-blot binding of DDR1 and DDR2 Rbodies to commercially-derived bovine dermal collagen I (Vitrogen).	bind
11675	2	4592	6	NULL	NULL	NULL	NULL	DDR2 Rbodies	GP		bind		differentially			dermal collagen I	GP	bovine			NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_1_25_s_131	9659900	(C) Differential slot-blot binding of DDR1 and DDR2 Rbodies to commercially-derived bovine dermal collagen I (Vitrogen).	bind
11662	1	4593	5	NULL	NULL	0	NULL	GST-p53	NULL	recombinant	bind	NULL	directly				NULL			 p53BE	NULL		NULL	NULL	NULL	NULL	gw60_cell_113_3_301_s_280	12732139	(C) Direct binding of recombinant GST-p53 and p73 to the  p53BE in gel shift experiments.	bind
11664	2	4593	5	NULL	NULL	0	NULL	GST-p73	NULL	recombinant	bind	NULL	directly				NULL			p53BE	NULL		NULL	NULL	NULL	NULL	gw60_cell_113_3_301_s_280	12732139	(C) Direct binding of recombinant GST-p53 and p73 to the  p53BE in gel shift experiments.	bind
11676	1	4593	6	NULL	NULL	NULL	NULL	GST-p53	GP	recombinant	bind		directly							p53BE	NULL		NULL	NULL	NULL	NULL	gw60_cell_113_3_301_s_280	12732139	(C) Direct binding of recombinant GST-p53 and p73 to the  p53BE in gel shift experiments.	bind
11677	2	4593	6	NULL	NULL	NULL	NULL	GST-p73	GP	recombinant	bind		directly							p53BE	NULL		NULL	NULL	NULL	NULL	gw60_cell_113_3_301_s_280	12732139	(C) Direct binding of recombinant GST-p53 and p73 to the  p53BE in gel shift experiments.	bind
11665	1	4594	5	NULL	NULL	0	NULL	Stx6	NULL		bind	NULL	directly			Syt IV	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw70_cellbiol_173_2_241_s_130	16618809	(C) Direct binding of Stx6  to Syt IV in vitro.	bind
11678	1	4594	6	NULL	NULL	NULL	NULL	Stx6	GP		bind		directly			Syt IV	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_cellbiol_173_2_241_s_130	16618809	(C) Direct binding of Stx6  to Syt IV in vitro.	bind
11666	1	4596	5	NULL	NULL	0	NULL	[125]AFP	NULL		bind	NULL				MDM	NULL				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_3_507_s_104	12176010	(C) Displacement curve shows inhibition of the binding of [125]AFP (1.5 nM) to MDM by unlabeled AFP.	bind
11667	2	4596	5	NULL	NULL	0	NULL	AFP	NULL	unlabeled	inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_3_507_s_104	12176010	(C) Displacement curve shows inhibition of the binding of [125]AFP (1.5 nM) to MDM by unlabeled AFP.	bind
11679	1	4596	6	NULL	NULL	NULL	NULL	[125]AFP	Chemical		bind					MDM	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_3_507_s_104	12176010	(C) Displacement curve shows inhibition of the binding of [125]AFP (1.5 nM) to MDM by unlabeled AFP.	bind
11680	2	4596	6	NULL	NULL	NULL	NULL	AFP	Chemical	unlabeled	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_3_507_s_104	12176010	(C) Displacement curve shows inhibition of the binding of [125]AFP (1.5 nM) to MDM by unlabeled AFP.	bind
11668	1	4597	5	10	NULL	0	NULL	RFX			bind					DRA				promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_17_5699_s_350	11486010	(C) Dissociation rates were determined by EMSA for the higher-order protein-DNA complexes formed by simultaneous binding of RFX, NF-Y, and X2BP to the DRA promoter.	bind
11669	2	4597	5	NULL	NULL	0	NULL	NF-Y	NULL		bind	NULL				DRA	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_17_5699_s_350	11486010	(C) Dissociation rates were determined by EMSA for the higher-order protein-DNA complexes formed by simultaneous binding of RFX, NF-Y, and X2BP to the DRA promoter.	bind
11670	3	4597	5	NULL	NULL	0	NULL	X2BP	NULL		bind	NULL				DRA	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_17_5699_s_350	11486010	(C) Dissociation rates were determined by EMSA for the higher-order protein-DNA complexes formed by simultaneous binding of RFX, NF-Y, and X2BP to the DRA promoter.	bind
11681	1	4597	6	NULL	NULL	NULL	NULL	RFX	GP		bind					DRA	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_17_5699_s_350	11486010	(C) Dissociation rates were determined by EMSA for the higher-order protein-DNA complexes formed by simultaneous binding of RFX, NF-Y, and X2BP to the DRA promoter.	bind
11682	2	4597	6	NULL	NULL	NULL	NULL	NF-Y	GP		bind					DRA	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_17_5699_s_350	11486010	(C) Dissociation rates were determined by EMSA for the higher-order protein-DNA complexes formed by simultaneous binding of RFX, NF-Y, and X2BP to the DRA promoter.	bind
11683	3	4597	6	NULL	NULL	NULL	NULL	X2BP	GP		bind					DRA	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_17_5699_s_350	11486010	(C) Dissociation rates were determined by EMSA for the higher-order protein-DNA complexes formed by simultaneous binding of RFX, NF-Y, and X2BP to the DRA promoter.	bind
11671	1	4599	5	NULL	NULL	0	NULL	Dll3	NULL	expression of	is restricted to	NULL				Purkinje cells	NULL				NULL	adult cerebellum	0	NULL	NULL	NULL	gw60_mechdev_114_1_153_s_128	12175503	(C) Dll3 expression is restricted to Purkinje cells (PC; arrow) in the adult cerebellum and, (D) Jagged1 is prominently expressed by granule cells in the IGL.	bind
11672	2	4599	5	10	NULL	0	NULL	Jagged1			is expressed by		prominently			granule cells					NULL	IGL	NULL	NULL	NULL	NULL	gw60_mechdev_114_1_153_s_128	12175503	(C) Dll3 expression is restricted to Purkinje cells (PC; arrow) in the adult cerebellum and, (D) Jagged1 is prominently expressed by granule cells in the IGL.	bind
11684	1	4599	6	NULL	NULL	NULL	NULL	Purkinje cells	Cell		express					dll3	GP				NULL	adult cerebellum	NULL	NULL	NULL	NULL	gw60_mechdev_114_1_153_s_128	12175503	(C) Dll3 expression is restricted to Purkinje cells (PC; arrow) in the adult cerebellum and, (D) Jagged1 is prominently expressed by granule cells in the IGL.	bind
11685	2	4599	6	NULL	NULL	NULL	NULL	granule cells	Cell		express					Jagged1	GP				NULL	IGL	NULL	NULL	NULL	NULL	gw60_mechdev_114_1_153_s_128	12175503	(C) Dll3 expression is restricted to Purkinje cells (PC; arrow) in the adult cerebellum and, (D) Jagged1 is prominently expressed by granule cells in the IGL.	bind
11673	1	4600	5	10	NULL	0	NULL	PerR	NULL	purified	bind	NULL				perR	NULL			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_12_3276_s_146	12029044	(C) DNase I footprint of purified PerR binding to the  perR promoter.	bind
11686	1	4600	6	NULL	NULL	NULL	NULL	PerR	GP	purified	bind					perR	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_12_3276_s_146	12029044	(C) DNase I footprint of purified PerR binding to the  perR promoter.	bind
11933	1	4601	5	NULL	NULL	0	NULL	Dock	NULL		bind	NULL	directly	SH2		Dscam	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_101_6_671_s_111	10892653	(C) Dock SH2  directly binds Dscam.	bind
11687	1	4601	6	NULL	NULL	NULL	NULL	Dock	GP		bind		directly	SH2 domain		Dscam	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_101_6_671_s_111	10892653	(C) Dock SH2  directly binds Dscam.	bind
11934	1	4602	5	NULL	NULL	0	NULL	DOKL	NULL		bind	NULL				c-Abl	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_12_8314_s_280	10567556	(C) DOKL binding to c-Abl can be detected with anti-Abl antisera.	bind
11688	1	4602	6	NULL	NULL	NULL	NULL	DOKL	GP		bind					c-Abl	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8314_s_280	10567556	(C) DOKL binding to c-Abl can be detected with anti-Abl antisera.	bind
12084	2	4603	5	NULL	NULL	0	NULL	SfbX	NULL	recombinant	bind	NULL				fibronectin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1208_s_215	12562790	(c) Dose-dependent competitive inhibition of GAS fibronectin-binding by recombinant SfbX.	bind
14577	3	4603	5	10	NULL	0	NULL	statement 2	NULL		inhibit	NULL	competitively;;dose dependently			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1208_s_215	12562790	(c) Dose-dependent competitive inhibition of GAS fibronectin-binding by recombinant SfbX.	bind
14578	1	4603	5	NULL	NULL	0	NULL	GAS	NULL		bind	NULL				fibronectin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_185_4_1208_s_215	12562790	(c) Dose-dependent competitive inhibition of GAS fibronectin-binding by recombinant SfbX.	bind
11689	1	4603	6	NULL	NULL	NULL	NULL	GAS	GP		bind					fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1208_s_215	12562790	(c) Dose-dependent competitive inhibition of GAS fibronectin-binding by recombinant SfbX.	bind
11690	2	4603	6	NULL	NULL	NULL	NULL	Sfbx	GP	recombinant	bind					fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1208_s_215	12562790	(c) Dose-dependent competitive inhibition of GAS fibronectin-binding by recombinant SfbX.	bind
11691	3	4603	6	NULL	NULL	NULL	NULL	statement 2	Process		inhibits		competitively;;dose dependently			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1208_s_215	12562790	(c) Dose-dependent competitive inhibition of GAS fibronectin-binding by recombinant SfbX.	bind
12086	1	4604	5	10	NULL	0	NULL	Ndc10p			bind					Chromosome V					NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_11_4557_s_180	13679521	(C) Doubling time under nonselective conditions (YPD); chromosome  loss rates determined from B. (D) Binding of Ndc10p and the cohesin subunit Mcd1p  to a region of Chromosome V previously subjected to detailed analysis (Tanaka  et al., 1999 ) by ChIP in 200-base pair DNA fragments spaced every 1 kb.	bind
12088	2	4604	5	10	NULL	0	NULL	Mcd1p			bind			cohesin subunit		Chromosome V					NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_11_4557_s_180	13679521	(C) Doubling time under nonselective conditions (YPD); chromosome  loss rates determined from B. (D) Binding of Ndc10p and the cohesin subunit Mcd1p  to a region of Chromosome V previously subjected to detailed analysis (Tanaka  et al., 1999 ) by ChIP in 200-base pair DNA fragments spaced every 1 kb.	bind
11692	1	4604	6	NULL	NULL	NULL	NULL	Ndc10p	GP		bind					region of Chromosome V	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_11_4557_s_180	13679521	(C) Doubling time under nonselective conditions (YPD); chromosome  loss rates determined from B. (D) Binding of Ndc10p and the cohesin subunit Mcd1p  to a region of Chromosome V previously subjected to detailed analysis (Tanaka  et al., 1999 ) by ChIP in 200-base pair DNA fragments spaced every 1 kb.	bind
11693	2	4604	6	NULL	NULL	NULL	NULL	Mcd1p	GP		bind			cohesin subunit		region of Chromosome V	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_11_4557_s_180	13679521	(C) Doubling time under nonselective conditions (YPD); chromosome  loss rates determined from B. (D) Binding of Ndc10p and the cohesin subunit Mcd1p  to a region of Chromosome V previously subjected to detailed analysis (Tanaka  et al., 1999 ) by ChIP in 200-base pair DNA fragments spaced every 1 kb.	bind
12090	1	4605	5	NULL	NULL	0	NULL	RFP - X-PAK5	NULL		bind	NULL				GFP MT bundles	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_6_1029_s_214	11733543	(C) Dynamic of RFP - X-PAK5 - bound GFP MT bundles (the dot pinpoints the initial position of the free end of a bundle) versus unbound GFP MTs (the cross pinpoints the initial position of one MT) were overlaid.	bind
11694	1	4605	6	NULL	NULL	NULL	NULL	RFP - X-PAK5	GP		bind					GFP MT bundles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_1029_s_214	11733543	(C) Dynamic of RFP - X-PAK5 - bound GFP MT bundles (the dot pinpoints the initial position of the free end of a bundle) versus unbound GFP MTs (the cross pinpoints the initial position of one MT) were overlaid.	bind
12098	1	4606	5	NULL	NULL	0	NULL	Rb	NULL		inhibit	NULL				E2F	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_18_6799_s_117	10958676	(C) E1a cannot block Rb inhibition of E2F when the LXCXE binding site is mutated.	bind
12105	2	4606	5	NULL	NULL	0	NULL	E1a	NULL	mutant	does not block	NULL		LXCXE binding site		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_18_6799_s_117	10958676	(C) E1a cannot block Rb inhibition of E2F when the LXCXE binding site is mutated.	bind
12187	3	4606	5	NULL	NULL	0	NULL	E1a	NULL		blocks	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_18_6799_s_117	10958676	(C) E1a cannot block Rb inhibition of E2F when the LXCXE binding site is mutated.	bind
12301	1	4606	6	NULL	NULL	NULL	NULL	Rb	GP		inhibits					E2F	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6799_s_117	10958676	(C) E1a cannot block Rb inhibition of E2F when the LXCXE binding site is mutated.	bind
12302	2	4606	6	NULL	NULL	NULL	NULL	E1a	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6799_s_117	10958676	(C) E1a cannot block Rb inhibition of E2F when the LXCXE binding site is mutated.	bind
12303	3	4606	6	NULL	NULL	NULL	NULL	E1a	GP	mutant	does not block			LXCXE binding site		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6799_s_117	10958676	(C) E1a cannot block Rb inhibition of E2F when the LXCXE binding site is mutated.	bind
12108	1	4607	5	NULL	NULL	0	NULL	E1B 55-kDa proteins	NULL		bind	NULL				PCAF	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_306	10891493	(C) E1B 55-kDa proteins bind to PCAF in vivo.	bind
11695	1	4607	6	NULL	NULL	NULL	NULL	E1B 55-kDa proteins	GP		bind					PCAF	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_306	10891493	(C) E1B 55-kDa proteins bind to PCAF in vivo.	bind
12138	1	4608	5	NULL	NULL	0	NULL	EBNA-1	NULL		bind	NULL		delta16-372		oriP plasmids	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_10_3576_s_222	11313483	(C) EBNA-1(delta16-372) can bind  oriP plasmids but cannot recruit them onto mitotic chromosomes.	bind
12141	3	4608	5	NULL	NULL	0	NULL	EBNA-1	NULL		does not recruit	NULL		delta16-372		statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3576_s_222	11313483	(C) EBNA-1(delta16-372) can bind  oriP plasmids but cannot recruit them onto mitotic chromosomes.	bind
44564	2	4608	5	10	NULL	0	NULL	oriP	NULL		recruits to	NULL				mitotic chromosomes	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_10_3576_s_222	11313483	(C) EBNA-1(delta16-372) can bind  oriP plasmids but cannot recruit them onto mitotic chromosomes.	bind
11696	1	4608	6	NULL	NULL	NULL	NULL	EBNA-1	GP		bind			delta16-372		oriP plasmids	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3576_s_222	11313483	(C) EBNA-1(delta16-372) can bind  oriP plasmids but cannot recruit them onto mitotic chromosomes.	bind
54450	2	4608	6	NULL	NULL	NULL	NULL	oriP	NucleicAcid		recruits to					mitotic chromosomes	Chromosome				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3576_s_222	11313483	(C) EBNA-1(delta16-372) can bind  oriP plasmids but cannot recruit them onto mitotic chromosomes.	bind
54451	3	4608	6	NULL	NULL	NULL	NULL	EBNA-1	GP		does not recruit			delta16-372		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3576_s_222	11313483	(C) EBNA-1(delta16-372) can bind  oriP plasmids but cannot recruit them onto mitotic chromosomes.	bind
12144	1	4610	5	NULL	NULL	0	NULL	Npl3p	NULL		bind	NULL				Mtr10p	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_150_4_707_s_209	10952997	(c) Effect of double modification on Npl3p binding to Mtr10p.	bind
11697	1	4610	6	NULL	NULL	NULL	NULL	Npl3p	GP		bind					Mtr10p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_4_707_s_209	10952997	(c) Effect of double modification on Npl3p binding to Mtr10p.	bind
12148	1	4611	5	NULL	NULL	0	NULL	LARG	NULL		bind	NULL				IGF-1 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_5_809_s_122	11724822	(C) Effect of IGF-1 on the binding state of LARG and the IGF-1 receptor.	bind
11698	1	4611	6	NULL	NULL	NULL	NULL	LARG	GP		bind					IGF-1 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_5_809_s_122	11724822	(C) Effect of IGF-1 on the binding state of LARG and the IGF-1 receptor.	bind
12167	1	4612	5	NULL	NULL	0	NULL	sAPP695T	NULL		bind	NULL				HK	NULL	cleavage products of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1571_3_225_s_253	12090937	(C) Effect of plasma kallikrein treatment on binding of sAPP695T to HK cleavage products.	bind
11699	1	4612	6	NULL	NULL	NULL	NULL	sAPP695T			bind					HK 	GP	clevage products of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1571_3_225_s_253	12090937	(C) Effect of plasma kallikrein treatment on binding of sAPP695T to HK cleavage products.	bind
12168	1	4614	5	NULL	NULL	0	NULL	fascin	NULL		bind	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_150_4_807_s_276	10953005	(C) Effect of the antibodies on the binding of fascin to actin in a blot-overlay assay.	bind
11700	1	4614	6	NULL	NULL	NULL	NULL	fascin	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_4_807_s_276	10953005	(C) Effect of the antibodies on the binding of fascin to actin in a blot-overlay assay.	bind
12169	1	4615	5	NULL	NULL	0	NULL	A1Rs	NULL		bind	NULL				hsc73	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_14_5164_s_206	10866672	(C) Effect of two different concentrations of ADA upon binding of A1Rs to hsc73.	bind
11701	1	4615	6	NULL	NULL	NULL	NULL	A1Rs	GP		bind					hsc73	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_14_5164_s_206	10866672	(C) Effect of two different concentrations of ADA upon binding of A1Rs to hsc73.	bind
12170	1	4616	5	NULL	NULL	0	NULL	IAAP	NULL		bind	NULL				Cdr1p-GFP	NULL				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_2_6_1361_s_192	14665469	(c) Effects of Cdr1p substrates on the binding of IAAP to  Cdr1p-GFP.	bind
11702	1	4616	6	NULL	NULL	NULL	NULL	IAAP	GP		bind					Cdr1p-GFP	GP				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_2_6_1361_s_192	14665469	(c) Effects of Cdr1p substrates on the binding of IAAP to  Cdr1p-GFP.	bind
12171	1	4617	5	NULL	NULL	0	NULL	BMP-7	NULL		bind	NULL				ROS 17/2	NULL				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_4_858_s_198	12927798	(C) Effects of GAGs on BMP-7 binding to ROS 17/2.	bind
11703	1	4617	6	NULL	NULL	NULL	NULL	BMP-7	GP		bind					ROS 17/2	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_4_858_s_198	12927798	(C) Effects of GAGs on BMP-7 binding to ROS 17/2.	bind
12172	1	4618	5	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				CHO-CD36 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_117	10191300	(C) Effects of peptide V on the binding of LDL to CHO-CD36 cells.	bind
11704	1	4618	6	NULL	NULL	NULL	NULL	LDL	Chemical		bind					CHO-CD36 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_4_753_s_117	10191300	(C) Effects of peptide V on the binding of LDL to CHO-CD36 cells.	bind
12188	1	4619	5	NULL	NULL	0	NULL	Axn follicle cell clones	NULL	mutant	express	NULL				Hts	NULL	higher levels of			NULL	Egg chambers	0	NULL	NULL	NULL	gw60_development_130_14_3259_s_211	12783796	(C) Egg chambers with mutant  Axn follicle cell clones that express higher levels of Hts (outlined).	bind
11705	1	4619	6	NULL	NULL	NULL	NULL	 Axn follicle cell clones	Cell	mutant	express					Hts	GP	high levels of			NULL	Egg chambers	NULL	NULL	NULL	NULL	gw60_development_130_14_3259_s_211	12783796	(C) Egg chambers with mutant  Axn follicle cell clones that express higher levels of Hts (outlined).	bind
12189	1	4620	5	NULL	NULL	0	NULL	Elc1	NULL		bind	NULL				Snf4	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1491_1_161_s_309	10760578	(C) Elc1 binding to Snf4 is not for required for glucose derepression.	bind
12190	2	4620	5	NULL	NULL	0	NULL	statement 1	NULL		is not required for	NULL				glucose derepression	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1491_1_161_s_309	10760578	(C) Elc1 binding to Snf4 is not for required for glucose derepression.	bind
11706	1	4620	6	NULL	NULL	NULL	NULL	Elc1	GP		bind					Snf4	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1491_1_161_s_309	10760578	(C) Elc1 binding to Snf4 is not for required for glucose derepression.	bind
11707	2	4620	6	NULL	NULL	NULL	NULL	statement 1	Process		is not required for					glucose derepression	AbstractConcept				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1491_1_161_s_309	10760578	(C) Elc1 binding to Snf4 is not for required for glucose derepression.	bind
12191	1	4625	5	NULL	NULL	0	NULL	AlgR	NULL		bind	NULL				algD sequences	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_16_4544_s_181	12142425	(C) EMSA of AlgR or AlgR derivatives binding to  algD sequences.	bind
12192	2	4625	5	NULL	NULL	0	NULL	AlgR derivatives	NULL		bind	NULL				algD sequences	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_16_4544_s_181	12142425	(C) EMSA of AlgR or AlgR derivatives binding to  algD sequences.	bind
12194	3	4625	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_16_4544_s_181	12142425	(C) EMSA of AlgR or AlgR derivatives binding to  algD sequences.	bind
11708	1	4625	6	NULL	NULL	NULL	NULL	AlgR	GP		bind					algD sequences	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_16_4544_s_181	12142425	(C) EMSA of AlgR or AlgR derivatives binding to  algD sequences.	bind
11709	2	4625	6	NULL	NULL	NULL	NULL	AlgR derivatives 	GP		bind					algD sequences	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_16_4544_s_181	12142425	(C) EMSA of AlgR or AlgR derivatives binding to  algD sequences.	bind
11710	3	4625	6	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_16_4544_s_181	12142425	(C) EMSA of AlgR or AlgR derivatives binding to  algD sequences.	bind
12193	1	4627	5	NULL	NULL	0	NULL	c- myc RNA	NULL		does not bind	NULL			IRES	unr	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_10_3364_s_143	11313462	(C) EMSA of c- myc IRES RNA does not show any binding to unr or PTB. (D) EMSA of G3PDH mRNA used a control does not show any binding to unr or PTB.	bind
12195	2	4627	5	NULL	NULL	0	NULL	c- myc RNA	NULL		does not bind	NULL			IRES	PTB	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3364_s_143	11313462	(C) EMSA of c- myc IRES RNA does not show any binding to unr or PTB. (D) EMSA of G3PDH mRNA used a control does not show any binding to unr or PTB.	bind
12196	3	4627	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_10_3364_s_143	11313462	(C) EMSA of c- myc IRES RNA does not show any binding to unr or PTB. (D) EMSA of G3PDH mRNA used a control does not show any binding to unr or PTB.	bind
12197	4	4627	5	NULL	NULL	0	NULL	G3PDH mRNA	NULL	control	does not bind	NULL				unr	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_10_3364_s_143	11313462	(C) EMSA of c- myc IRES RNA does not show any binding to unr or PTB. (D) EMSA of G3PDH mRNA used a control does not show any binding to unr or PTB.	bind
12198	5	4627	5	NULL	NULL	0	NULL	G3PDH mRNA	NULL	control	does not bind	NULL				PTB	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_10_3364_s_143	11313462	(C) EMSA of c- myc IRES RNA does not show any binding to unr or PTB. (D) EMSA of G3PDH mRNA used a control does not show any binding to unr or PTB.	bind
12199	6	4627	5	NULL	NULL	0	NULL	statement 4	NULL		is an alternative to	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_10_3364_s_143	11313462	(C) EMSA of c- myc IRES RNA does not show any binding to unr or PTB. (D) EMSA of G3PDH mRNA used a control does not show any binding to unr or PTB.	bind
11711	1	4627	6	NULL	NULL	NULL	NULL	c- myc RNA	NucleicAcid		does not bind				IRES 	unr	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3364_s_143	11313462	(C) EMSA of c- myc IRES RNA does not show any binding to unr or PTB. (D) EMSA of G3PDH mRNA used a control does not show any binding to unr or PTB.	bind
11712	2	4627	6	NULL	NULL	NULL	NULL	c- myc RNA	NucleicAcid		does not bind				IRES	PTB	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3364_s_143	11313462	(C) EMSA of c- myc IRES RNA does not show any binding to unr or PTB. (D) EMSA of G3PDH mRNA used a control does not show any binding to unr or PTB.	bind
11713	3	4627	6	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3364_s_143	11313462	(C) EMSA of c- myc IRES RNA does not show any binding to unr or PTB. (D) EMSA of G3PDH mRNA used a control does not show any binding to unr or PTB.	bind
11714	4	4627	6	NULL	NULL	NULL	NULL	G3PDH mRNA	NucleicAcid		does not bind					unr	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3364_s_143	11313462	(C) EMSA of c- myc IRES RNA does not show any binding to unr or PTB. (D) EMSA of G3PDH mRNA used a control does not show any binding to unr or PTB.	bind
11715	5	4627	6	NULL	NULL	NULL	NULL	G3PDH mRNA	NucleicAcid		does not bind					PTB	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3364_s_143	11313462	(C) EMSA of c- myc IRES RNA does not show any binding to unr or PTB. (D) EMSA of G3PDH mRNA used a control does not show any binding to unr or PTB.	bind
11716	6	4627	6	NULL	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3364_s_143	11313462	(C) EMSA of c- myc IRES RNA does not show any binding to unr or PTB. (D) EMSA of G3PDH mRNA used a control does not show any binding to unr or PTB.	bind
12200	1	4628	5	10	NULL	0	NULL	GST-Desrt-ARID	NULL	recombinant	bind	NULL				(TTA)9 oligonucleotide	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genomeres_11_8_1327_s_42	11483573	(C) EMSA of recombinant GST-Desrt-ARID fusion protein binding to a (TTA)9 oligonucleotide (lane  2).	bind
44565	2	4628	5	10	NULL	0	NULL	GST-Desrt-ARID	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_genomeres_11_8_1327_s_42	11483573	(C) EMSA of recombinant GST-Desrt-ARID fusion protein binding to a (TTA)9 oligonucleotide (lane  2).	bind
11717	1	4628	6	NULL	NULL	NULL	NULL	GST-Desrt-ARID 	GP	recombinant	bind					(TTA)9 oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genomeres_11_8_1327_s_42	11483573	(C) EMSA of recombinant GST-Desrt-ARID fusion protein binding to a (TTA)9 oligonucleotide (lane  2).	bind
54452	2	4628	6	NULL	NULL	NULL	NULL	GST-Desrt-ARID	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_genomeres_11_8_1327_s_42	11483573	(C) EMSA of recombinant GST-Desrt-ARID fusion protein binding to a (TTA)9 oligonucleotide (lane  2).	bind
12201	1	4629	5	NULL	NULL	0	NULL	ETS-1	NULL	in vitro-translated	bind	NULL				IL-3	NULL			ETS binding site in promoter	NULL		0	NULL	NULL	NULL	gw60_immunity_17_4_437_s_192	12387738	(C) EMSAs demonstrating that in vitro-translated ETS-1 binds to an ETS binding site in the IL-3 promoter (lane 1) but not to the EBS1 (lanes 4-6) or EBS2 (lanes 8-10) sites in the murine perforin promoter.	bind
12202	2	4629	5	NULL	NULL	0	NULL	ETS-1	NULL	in vitro-translated	does not bind	NULL				perforin	NULL	murine		EBS1 sites in promoter	NULL		0	NULL	NULL	NULL	gw60_immunity_17_4_437_s_192	12387738	(C) EMSAs demonstrating that in vitro-translated ETS-1 binds to an ETS binding site in the IL-3 promoter (lane 1) but not to the EBS1 (lanes 4-6) or EBS2 (lanes 8-10) sites in the murine perforin promoter.	bind
12203	3	4629	5	NULL	NULL	0	NULL	ETS-1	NULL	in vitro-translated	does not bind	NULL				perforin	NULL	murine		EBS2 sites in promoter	NULL		0	NULL	NULL	NULL	gw60_immunity_17_4_437_s_192	12387738	(C) EMSAs demonstrating that in vitro-translated ETS-1 binds to an ETS binding site in the IL-3 promoter (lane 1) but not to the EBS1 (lanes 4-6) or EBS2 (lanes 8-10) sites in the murine perforin promoter.	bind
11718	1	4629	6	NULL	NULL	NULL	NULL	ETS-1	GP	in vitro-translated	bind					IL-3	GP			ETS binding site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_4_437_s_192	12387738	(C) EMSAs demonstrating that in vitro-translated ETS-1 binds to an ETS binding site in the IL-3 promoter (lane 1) but not to the EBS1 (lanes 4-6) or EBS2 (lanes 8-10) sites in the murine perforin promoter.	bind
11719	2	4629	6	NULL	NULL	NULL	NULL	ETS-1	GP	in vitro-translated	does not bind					perforin	GP	murine		EBS1 site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_4_437_s_192	12387738	(C) EMSAs demonstrating that in vitro-translated ETS-1 binds to an ETS binding site in the IL-3 promoter (lane 1) but not to the EBS1 (lanes 4-6) or EBS2 (lanes 8-10) sites in the murine perforin promoter.	bind
11720	3	4629	6	NULL	NULL	NULL	NULL	ETS-1	GP	in vitro-translated	does not bind					perforin	GP	murine		EBS2 site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_4_437_s_192	12387738	(C) EMSAs demonstrating that in vitro-translated ETS-1 binds to an ETS binding site in the IL-3 promoter (lane 1) but not to the EBS1 (lanes 4-6) or EBS2 (lanes 8-10) sites in the murine perforin promoter.	bind
12204	1	4630	5	NULL	NULL	0	NULL	CREB	NULL	endogenous	bind	NULL				cpg15	NULL			promoter	NULL	in vivo	0	NULL	NULL	NULL	gw70_molcellneurosci_24_3_538_s_162	14664806	(C) Endogenous CREB binds to the  cpg15 promoter in vivo.	bind
11722	1	4630	6	NULL	NULL	NULL	NULL	CREB	GP	endogenous	bind					cpg15	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_538_s_162	14664806	(C) Endogenous CREB binds to the  cpg15 promoter in vivo.	bind
12205	1	4631	5	NULL	NULL	0	NULL	NGF	NULL	endogenous	bind	NULL	tightly			surface NGF receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_85_3_345_s_93	8616890	(C) Endogenous NGF  is tightly bound to surface NGF receptors.	bind
11723	1	4631	6	NULL	NULL	NULL	NULL	NGF	GP	endogenous	bind		tightly			surface NGF receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_85_3_345_s_93	8616890	(C) Endogenous NGF  is tightly bound to surface NGF receptors.	bind
12207	1	4634	5	NULL	NULL	0	NULL	GDP	NULL		bind	NULL	exclusively			gamma-tubulin	NULL				NULL	in gammaTuSC	NULL	NULL	NULL	NULL	gw60_cellbiol_144_4_721_s_379	10037793	(C) Exclusively, GDP binds to gamma-tubulin in  gammaTuSC (for quantitation see Table  II:  20 muM GDP, experiment 3).	bind
11724	1	4634	6	NULL	NULL	NULL	NULL	GDP	Chemical		bind		exclusively			gamma-tubulin	CellComponent				NULL	gammaTuSC 	NULL	NULL	NULL	NULL	gw60_cellbiol_144_4_721_s_379	10037793	(C) Exclusively, GDP binds to gamma-tubulin in  gammaTuSC (for quantitation see Table  II:  20 muM GDP, experiment 3).	bind
12209	1	4636	5	NULL	NULL	0	NULL	MEKK2	NULL		bind	NULL				Lad	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_7_2298_s_228	12640115	(C) Expression of MEKK2aa228-282 in HEK293 cells blocked MEKK2 binding to Lad. HEK293 cells stably transfected with MEKK2aa228-282, MEKK3aa239-293, or an empty vector were transiently transfected with or without Flag-Lad.	bind
12210	2	4636	5	NULL	NULL	0	NULL	MEKK2	NULL	expression of	blocks	NULL		aa228-282		statement 1	NULL				NULL	in HEK293 cells	0	NULL	NULL	NULL	gw60_molcellbiol_23_7_2298_s_228	12640115	(C) Expression of MEKK2aa228-282 in HEK293 cells blocked MEKK2 binding to Lad. HEK293 cells stably transfected with MEKK2aa228-282, MEKK3aa239-293, or an empty vector were transiently transfected with or without Flag-Lad.	bind
11730	1	4636	6	NULL	NULL	NULL	NULL	MEKK2	GP		bind					Lad	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_7_2298_s_228	12640115	(C) Expression of MEKK2aa228-282 in HEK293 cells blocked MEKK2 binding to Lad. HEK293 cells stably transfected with MEKK2aa228-282, MEKK3aa239-293, or an empty vector were transiently transfected with or without Flag-Lad.	bind
11731	2	4636	6	NULL	NULL	NULL	NULL	MEKK2	GP		expressed in			aa228-282		HEK293 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_7_2298_s_228	12640115	(C) Expression of MEKK2aa228-282 in HEK293 cells blocked MEKK2 binding to Lad. HEK293 cells stably transfected with MEKK2aa228-282, MEKK3aa239-293, or an empty vector were transiently transfected with or without Flag-Lad.	bind
11732	3	4636	6	NULL	NULL	NULL	NULL	statement 2	Process		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_7_2298_s_228	12640115	(C) Expression of MEKK2aa228-282 in HEK293 cells blocked MEKK2 binding to Lad. HEK293 cells stably transfected with MEKK2aa228-282, MEKK3aa239-293, or an empty vector were transiently transfected with or without Flag-Lad.	bind
12211	1	4638	5	NULL	NULL	0	NULL	GI 262570	NULL		bind	NULL				hPPAR	NULL		LBD		NULL		0	NULL	NULL	NULL	gw60_molcell_8_4_737_s_86	11684010	(C) F-L-Leu competes with the binding of GI 262570 to the hPPAR  LBD.	bind
12212	2	4638	5	NULL	NULL	0	NULL		NULL		bind	NULL		F-L-Leu		hPPAR	NULL		LBD		NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_4_737_s_86	11684010	(C) F-L-Leu competes with the binding of GI 262570 to the hPPAR  LBD.	bind
12213	3	4638	5	NULL	NULL	0	NULL	statement 1	NULL		compete with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_8_4_737_s_86	11684010	(C) F-L-Leu competes with the binding of GI 262570 to the hPPAR  LBD.	bind
11733	1	4638	6	NULL	NULL	NULL	NULL	GI 262570	GP		bind					hPPAR	GP		LBD		NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_4_737_s_86	11684010	(C) F-L-Leu competes with the binding of GI 262570 to the hPPAR  LBD.	bind
11734	2	4638	6	NULL	NULL	NULL	NULL				bind			F-L-Leu		hPPAR	GP		LBD		NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_4_737_s_86	11684010	(C) F-L-Leu competes with the binding of GI 262570 to the hPPAR  LBD.	bind
11735	3	4638	6	NULL	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_4_737_s_86	11684010	(C) F-L-Leu competes with the binding of GI 262570 to the hPPAR  LBD.	bind
12214	1	4639	5	NULL	NULL	0	NULL	curcumin	NULL		bind	NULL				HUVECs	NULL				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_10_8_695_s_120	12954328	(C) FACS analysis of the competitive binding of curcumin with APN-specific antibody (WM15) to HUVECs.	bind
12215	2	4639	5	10	NULL	0	NULL	WM15			is a type of					APN-specific antibody					NULL		NULL	NULL	NULL	NULL	gw60_chembiol_10_8_695_s_120	12954328	(C) FACS analysis of the competitive binding of curcumin with APN-specific antibody (WM15) to HUVECs.	bind
14575	3	4639	5	NULL	NULL	0	NULL	WM15	NULL		bind	NULL				HUVECs	NULL				NULL		0	NULL	NULL	NULL	gw60_chembiol_10_8_695_s_120	12954328	(C) FACS analysis of the competitive binding of curcumin with APN-specific antibody (WM15) to HUVECs.	bind
14576	4	4639	5	NULL	NULL	0	NULL	statement 1	NULL		compete with	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_chembiol_10_8_695_s_120	12954328	(C) FACS analysis of the competitive binding of curcumin with APN-specific antibody (WM15) to HUVECs.	bind
11736	1	4639	6	NULL	NULL	NULL	NULL	curcumin	GP		bind					HUVEC	Cell				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_10_8_695_s_120	12954328	(C) FACS analysis of the competitive binding of curcumin with APN-specific antibody (WM15) to HUVECs.	bind
11737	2	4639	6	NULL	NULL	NULL	NULL	WM15	AminoAcid		bind					HUVEC	Cell				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_10_8_695_s_120	12954328	(C) FACS analysis of the competitive binding of curcumin with APN-specific antibody (WM15) to HUVECs.	bind
11738	3	4639	6	NULL	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_10_8_695_s_120	12954328	(C) FACS analysis of the competitive binding of curcumin with APN-specific antibody (WM15) to HUVECs.	bind
54461	4	4639	6	NULL	NULL	NULL	NULL	WM15	AminoAcid		is a type of					APN-specific antibody	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_10_8_695_s_120	12954328	(C) FACS analysis of the competitive binding of curcumin with APN-specific antibody (WM15) to HUVECs.	bind
12216	1	4641	5	NULL	NULL	0	NULL	FH	NULL		bind	NULL				Fba	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_11_6206_s_210	12379699	(C) FH binding to Fba is shown.	bind
11739	1	4641	6	NULL	NULL	NULL	NULL	FH	GP		bind					Fba	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_11_6206_s_210	12379699	(C) FH binding to Fba is shown.	bind
12217	1	4642	5	10	NULL	0	NULL	Mia1p-GST		 Filter-immobilized;;recombinant	bind					microtubules		taxol-stabilized			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_5_2212_s_73	16481403	(C) Filter-immobilized  recombinant Mia1p-GST bound taxol-stabilized microtubules in the Far Western assay.	bind
11740	1	4642	6	NULL	NULL	NULL	NULL	Mia1p-GST	GP	Filter-immobilized ;;recombinant	bind					microtubules	CellComponent	taxol-stabilized			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_5_2212_s_73	16481403	(C) Filter-immobilized  recombinant Mia1p-GST bound taxol-stabilized microtubules in the Far Western assay.	bind
12218	1	4644	5	NULL	NULL	0	NULL	FMRP	NULL		bind	NULL				MAP1B mRNA	NULL			5 UTR	NULL		0	NULL	NULL	NULL	gw60_neuron_37_4_555_s_39	12597853	(C) FMRP binds to the 5 UTR of MAP1B mRNA via its G-quartet structure.	bind
12219	2	4644	5	NULL	NULL	0	NULL	statement 1	NULL		via	NULL				G-quartet structure	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_37_4_555_s_39	12597853	(C) FMRP binds to the 5 UTR of MAP1B mRNA via its G-quartet structure.	bind
11741	1	4644	6	NULL	NULL	NULL	NULL	FMRP	GP		bind					MAP1B mRNA	NucleicAcid			5 UTR	NULL		NULL	NULL	NULL	NULL	gw60_neuron_37_4_555_s_39	12597853	(C) FMRP binds to the 5 UTR of MAP1B mRNA via its G-quartet structure.	bind
54462	2	4644	6	NULL	NULL	NULL	NULL	statement 1	Process		via					G-quartet structure					NULL		NULL	NULL	NULL	NULL	gw60_neuron_37_4_555_s_39	12597853	(C) FMRP binds to the 5 UTR of MAP1B mRNA via its G-quartet structure.	bind
12222	1	4647	5	10	NULL	0	NULL	FRS2alpha	NULL		bind	NULL		PTB domain		TrkA	NULL	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_979_s_242	10629055	(C) FRS2alpha binds to tyrosine-phosphorylated TrkA via the PTB domain.	bind
11742	1	4647	6	NULL	NULL	NULL	NULL	FRS2alpha	GP		bind			PTB domain		TrkA	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_979_s_242	10629055	(C) FRS2alpha binds to tyrosine-phosphorylated TrkA via the PTB domain.	bind
12223	1	4648	5	NULL	NULL	0	NULL	Myc-epsin1	NULL	full-length	is expressed in	NULL				COS cells	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
12224	2	4648	5	NULL	NULL	0	NULL	Myc-epsinR	NULL	full-length	is expressed in	NULL				COS cells	NULL				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
12225	3	4648	5	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				alpha-adaptin	NULL		GST-appendage domains		NULL		0	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
12226	4	4648	5	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				beta-adaptin	NULL		GST-appendage domains		NULL		0	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
12227	5	4648	5	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				gamma-adaptin	NULL		GST-appendage domains		NULL		0	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
12228	6	4648	5	NULL	NULL	0	NULL	statement 1	NULL		does not bind	NULL				gamma-adaptin	NULL		L762E appendage		NULL		0	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
12229	7	4648	5	NULL	NULL	0	NULL	statement 2	NULL		bind	NULL				alpha-adaptin	NULL		GST-appendage domains		NULL		0	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
12230	8	4648	5	NULL	NULL	0	NULL	statement 2	NULL		bind	NULL				beta-adaptin	NULL		GST-appendage domains		NULL		0	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
12231	9	4648	5	NULL	NULL	0	NULL	statement 2	NULL		bind	NULL				gamma-adaptin	NULL		GST-appendage domains		NULL		0	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
12232	10	4648	5	NULL	NULL	0	NULL	statement 2	NULL		does not bind	NULL				gamma-adaptin	NULL		L762E appendage		NULL		0	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
11743	1	4648	6	NULL	NULL	NULL	NULL	Myc-epsin1	GP	full length	expressed in					COS cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
11744	2	4648	6	NULL	NULL	NULL	NULL	statement 1	Process		bind					alpha-adaptin	GP		GST-appendage domain		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
11745	3	4648	6	NULL	NULL	NULL	NULL	statement 1	Process		bind					beta-adaptin	GP		GST-appendage domain		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
11746	4	4648	6	NULL	NULL	NULL	NULL	statement 1	Process		bind					gamma-adaptin	GP		GST-appendage domain		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
11747	5	4648	6	NULL	NULL	NULL	NULL	statement 1	Process		does not bind					gamma-adaptin	GP		L762E appendage		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
11748	6	4648	6	NULL	NULL	NULL	NULL	Myc-epsinR	GP		expressed in					COS cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
11749	7	4648	6	NULL	NULL	NULL	NULL	statement 6	Process		bind					alpha-adaptin	GP		GST-appendage domain		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
11750	8	4648	6	NULL	NULL	NULL	NULL	statement 6	Process		bind					beta-adaptin	GP		GST-appendage domain		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
11751	9	4648	6	NULL	NULL	NULL	NULL	statement 6	Process		bind					gamma-adaptin	GP		GST-appendage domain		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
11752	10	4648	6	NULL	NULL	NULL	NULL	statement 6	Process		does not bind					gamma-adaptin	GP		L762E appendage		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_2_213_s_106	12538641	(C) Full-length  Myc-epsin1 and Myc-epsinR expressed in COS cells bind to the GST-appendage domains  of alpha-, beta-, and gamma-adaptin, but not the L762E gamma-adaptin appendage.	bind
12243	1	4650	5	NULL	NULL	0	NULL	ARF1	NULL	activated	bind	NULL				cargo proteins	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_115	15657398	(C) GAP does not affect the binding of activated ARF1 to cargo proteins.	bind
12244	2	4650	5	NULL	NULL	0	NULL	GAP	NULL		does not affect	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_115	15657398	(C) GAP does not affect the binding of activated ARF1 to cargo proteins.	bind
11787	1	4650	6	NULL	NULL	NULL	NULL	ARF1	GP	activated	bind					cargo proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_115	15657398	(C) GAP does not affect the binding of activated ARF1 to cargo proteins.	bind
11789	2	4650	6	NULL	NULL	NULL	NULL	GAP	GP		does not affect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_115	15657398	(C) GAP does not affect the binding of activated ARF1 to cargo proteins.	bind
12245	2	4652	5	10	NULL	0	NULL	GFP-Wg	NULL		bind	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_development_132_24_5479_s_279	16291792	(C) GFP-Wg binding to S2 cells transfected  with Frizzled2 (top) or Arrow (bottom), as quantified by fluorescence intensity after immunocytochemistry  using an anti-GFP antibody.	bind
44566	1	4652	5	10	NULL	0	NULL	S2 cells	NULL		transfected with	NULL				Frizzled2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_development_132_24_5479_s_279	16291792	(C) GFP-Wg binding to S2 cells transfected  with Frizzled2 (top) or Arrow (bottom), as quantified by fluorescence intensity after immunocytochemistry  using an anti-GFP antibody.	bind
44567	3	4652	5	10	NULL	0	NULL	S2 cells	NULL		transfected with	NULL				Arrow	NULL				NULL		0	NULL	NULL	NULL	gw70_development_132_24_5479_s_279	16291792	(C) GFP-Wg binding to S2 cells transfected  with Frizzled2 (top) or Arrow (bottom), as quantified by fluorescence intensity after immunocytochemistry  using an anti-GFP antibody.	bind
44568	4	4652	5	10	NULL	0	NULL	GFP-Wg	NULL		bind	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_development_132_24_5479_s_279	16291792	(C) GFP-Wg binding to S2 cells transfected  with Frizzled2 (top) or Arrow (bottom), as quantified by fluorescence intensity after immunocytochemistry  using an anti-GFP antibody.	bind
11792	1	4652	6	NULL	NULL	NULL	NULL	S2 cells	Cell		transfected with					Frizzled2	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_132_24_5479_s_279	16291792	(C) GFP-Wg binding to S2 cells transfected  with Frizzled2 (top) or Arrow (bottom), as quantified by fluorescence intensity after immunocytochemistry  using an anti-GFP antibody.	bind
11793	2	4652	6	NULL	NULL	NULL	NULL	S2 cells	Cell		transfected with					Arrow	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_132_24_5479_s_279	16291792	(C) GFP-Wg binding to S2 cells transfected  with Frizzled2 (top) or Arrow (bottom), as quantified by fluorescence intensity after immunocytochemistry  using an anti-GFP antibody.	bind
11794	3	4652	6	NULL	NULL	NULL	NULL	GFP-Wg	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_132_24_5479_s_279	16291792	(C) GFP-Wg binding to S2 cells transfected  with Frizzled2 (top) or Arrow (bottom), as quantified by fluorescence intensity after immunocytochemistry  using an anti-GFP antibody.	bind
11846	4	4652	6	NULL	NULL	NULL	NULL	GFP-Wg	GP		bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_132_24_5479_s_279	16291792	(C) GFP-Wg binding to S2 cells transfected  with Frizzled2 (top) or Arrow (bottom), as quantified by fluorescence intensity after immunocytochemistry  using an anti-GFP antibody.	bind
12246	1	4653	5	NULL	NULL	0	NULL	Bfa1	NULL		bind	NULL				Bub2	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_179	14734533	(C) Gic1 can disrupt binding between Bfa1 and Bub2.	bind
12247	2	4653	5	NULL	NULL	0	NULL	Gic1	NULL		disrupt	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_179	14734533	(C) Gic1 can disrupt binding between Bfa1 and Bub2.	bind
11847	1	4653	6	NULL	NULL	NULL	NULL	Bfa1	GP		bind					Bub2	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_179	14734533	(C) Gic1 can disrupt binding between Bfa1 and Bub2.	bind
11848	2	4653	6	NULL	NULL	NULL	NULL	Gic1	GP		disrupts					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_179	14734533	(C) Gic1 can disrupt binding between Bfa1 and Bub2.	bind
12248	1	4654	5	NULL	NULL	0	NULL	GMEB-1	NULL		bind	NULL	specifically			MURF-1	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_157_1_125_s_178	11927605	(C) GMEB-1 specifically binds to MURF-1 in GST pull-down assays.	bind
11849	1	4654	6	NULL	NULL	NULL	NULL	GMEB-1	GP		bind		specifically			MURF-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_1_125_s_178	11927605	(C) GMEB-1 specifically binds to MURF-1 in GST pull-down assays.	bind
12249	1	4658	5	NULL	NULL	0	NULL	Grb-2	NULL		bind	NULL				PY proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_1_26_s_256	11113178	(C) Grb-2 binding with PY proteins.	bind
11851	1	4658	6	NULL	NULL	NULL	NULL	Grb-2	GP		bind					PY proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_1_26_s_256	11113178	(C) Grb-2 binding with PY proteins.	bind
12250	1	4659	5	10	NULL	0	NULL	NF-1			bind					MMTV naked DNA					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3255_s_114	11971959	(C) Greater binding of NF-1 to MMTV naked DNA than to chromatin.	bind
12251	2	4659	5	NULL	NULL	0	NULL	NF-1	NULL		bind	NULL				chromatin	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_10_3255_s_114	11971959	(C) Greater binding of NF-1 to MMTV naked DNA than to chromatin.	bind
12252	3	4659	5	NULL	NULL	0	NULL	statement 1	NULL		greater than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_10_3255_s_114	11971959	(C) Greater binding of NF-1 to MMTV naked DNA than to chromatin.	bind
11852	1	4659	6	NULL	NULL	NULL	NULL	NF-1	GP		bind					MMTV naked DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3255_s_114	11971959	(C) Greater binding of NF-1 to MMTV naked DNA than to chromatin.	bind
11853	2	4659	6	NULL	NULL	NULL	NULL	NF-1	GP		bind					chromatin	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3255_s_114	11971959	(C) Greater binding of NF-1 to MMTV naked DNA than to chromatin.	bind
11854	3	4659	6	NULL	NULL	NULL	NULL	statement 1	Process		is greater than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3255_s_114	11971959	(C) Greater binding of NF-1 to MMTV naked DNA than to chromatin.	bind
12253	1	4660	5	NULL	NULL	0	NULL	Nup2p	NULL		bind	NULL				Nup60p	NULL				NULL	in yeast extracts	0	NULL	NULL	NULL	gw60_cellbiol_154_5_937_s_123	11535617	(C) Gsp1p - GTP enhances binding of Nup2p to Nup60p in yeast extracts.	bind
12254	2	4660	5	NULL	NULL	0	NULL	Gsp1p - GTP	NULL		enhances	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_5_937_s_123	11535617	(C) Gsp1p - GTP enhances binding of Nup2p to Nup60p in yeast extracts.	bind
11855	1	4660	6	NULL	NULL	NULL	NULL	Nup2p	GP		bind					Nup60p	GP				NULL	yeast extracts	NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_937_s_123	11535617	(C) Gsp1p - GTP enhances binding of Nup2p to Nup60p in yeast extracts.	bind
11856	2	4660	6	NULL	NULL	NULL	NULL	Gsp1p - GTP	Chemical		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_937_s_123	11535617	(C) Gsp1p - GTP enhances binding of Nup2p to Nup60p in yeast extracts.	bind
12256	1	4664	5	NULL	NULL	0	NULL	GlyT2	NULL	EGFP-tagged full-length	bind	NULL				GST-syntenin-1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellneurosci_26_4_518_s_41	15276154	(C) GST pull-down assay showing that EGFP-tagged full-length  GlyT2 bound to GST-syntenin-1, whereas its C-terminal deletion mutant (EGFP-GlyT2  TQC) did not bind.	bind
12257	2	4664	5	NULL	NULL	0	NULL	EGFP-GlyT2 TQC	NULL		is	NULL				C-terminal deletion mutant of EGFP-tagged GlyT2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellneurosci_26_4_518_s_41	15276154	(C) GST pull-down assay showing that EGFP-tagged full-length  GlyT2 bound to GST-syntenin-1, whereas its C-terminal deletion mutant (EGFP-GlyT2  TQC) did not bind.	bind
12258	3	4664	5	NULL	NULL	0	NULL	EGFP-GlyT2 TQC	NULL		does not bind	NULL				GST-syntenin-1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellneurosci_26_4_518_s_41	15276154	(C) GST pull-down assay showing that EGFP-tagged full-length  GlyT2 bound to GST-syntenin-1, whereas its C-terminal deletion mutant (EGFP-GlyT2  TQC) did not bind.	bind
11857	1	4664	6	NULL	NULL	NULL	NULL	GlyT2	GP	EGFP-tagged;; full-length	bind					GST-syntenin-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_26_4_518_s_41	15276154	(C) GST pull-down assay showing that EGFP-tagged full-length  GlyT2 bound to GST-syntenin-1, whereas its C-terminal deletion mutant (EGFP-GlyT2  TQC) did not bind.	bind
11858	2	4664	6	NULL	NULL	NULL	NULL	EGFP-GlyT2 TQC	AminoAcid		does not bind					GST-syntenin-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_26_4_518_s_41	15276154	(C) GST pull-down assay showing that EGFP-tagged full-length  GlyT2 bound to GST-syntenin-1, whereas its C-terminal deletion mutant (EGFP-GlyT2  TQC) did not bind.	bind
11859	3	4664	6	NULL	NULL	NULL	NULL	EGFP-GlyT2 TQC	AminoAcid		is					C-terminal deletion mutant EGFP-tagged GlyT2 					NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_26_4_518_s_41	15276154	(C) GST pull-down assay showing that EGFP-tagged full-length  GlyT2 bound to GST-syntenin-1, whereas its C-terminal deletion mutant (EGFP-GlyT2  TQC) did not bind.	bind
12259	1	4666	5	NULL	NULL	0	NULL	GST-FHA	NULL		bind	NULL				Chk2	NULL	activated			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_12_4419_s_71	12024051	(C) GST-FHA binds to activated Chk2.	bind
11860	1	4666	6	NULL	NULL	NULL	NULL	GST-FHA	GP		bind					Chk2	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4419_s_71	12024051	(C) GST-FHA binds to activated Chk2.	bind
12260	1	4670	5	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				DLP1 protein	NULL	WT			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_9_2894_s_195	11553726	(C) GTP binding of DLP1 WT and mutant proteins was tested with the use of GTP as a substrate.	bind
12261	2	4670	5	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				DLP1 protein	NULL	mutant			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_9_2894_s_195	11553726	(C) GTP binding of DLP1 WT and mutant proteins was tested with the use of GTP as a substrate.	bind
11861	1	4670	6	NULL	NULL	NULL	NULL	GTP	Chemical		bind					DLP1	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_9_2894_s_195	11553726	(C) GTP binding of DLP1 WT and mutant proteins was tested with the use of GTP as a substrate.	bind
11862	2	4670	6	NULL	NULL	NULL	NULL	GTP	Chemical		bind					DLP1	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_9_2894_s_195	11553726	(C) GTP binding of DLP1 WT and mutant proteins was tested with the use of GTP as a substrate.	bind
12345	1	4671	5	NULL	NULL	0	NULL	HDAC1	NULL		bind	NULL				Nkx3.2	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8704_s_144	14612411	(C) HDAC1 binds to Nkx3.2 in a BMP-dependent  manner in vivo.	bind
12346	2	4671	5	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				BMP	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8704_s_144	14612411	(C) HDAC1 binds to Nkx3.2 in a BMP-dependent  manner in vivo.	bind
11863	1	4671	6	NULL	NULL	NULL	NULL	HDAC1	GP		bind					Nkx3.2	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8704_s_144	14612411	(C) HDAC1 binds to Nkx3.2 in a BMP-dependent  manner in vivo.	bind
11864	2	4671	6	NULL	NULL	NULL	NULL	statement 1	Process		is dependent on					BMP	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8704_s_144	14612411	(C) HDAC1 binds to Nkx3.2 in a BMP-dependent  manner in vivo.	bind
12347	1	4672	5	NULL	NULL	0	NULL	Hip1R	NULL		does not bind	NULL				clathrin HC	NULL		GST-TD (amino acids 1 - 579)		NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_6_1209_s_74	11564758	(c) Hip1R does not bind to GST-TD of clathrin HC (amino acids 1 - 579) immobilized on glutathione-agarose beads (Coomassie stained gel).	bind
11865	1	4672	6	NULL	NULL	NULL	NULL	Hip1R	GP		does not bind					clathrin HC	GP		GST-TD		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_6_1209_s_74	11564758	(c) Hip1R does not bind to GST-TD of clathrin HC (amino acids 1 - 579) immobilized on glutathione-agarose beads (Coomassie stained gel).	bind
12348	1	4675	5	NULL	NULL	0	NULL	Rta	NULL	intact	bind	NULL				BHLF-1	NULL			enhancer	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_12_4390_s_42	12024049	(C) HMGB1 facilitates binding of intact Rta to its sites on the BHLF-1 enhancer.	bind
12349	2	4675	5	NULL	NULL	0	NULL	HMGB1	NULL		facilitate	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_12_4390_s_42	12024049	(C) HMGB1 facilitates binding of intact Rta to its sites on the BHLF-1 enhancer.	bind
11866	1	4675	6	NULL	NULL	NULL	NULL	Rta	GP	intact	bind					BHLF-1	GP			site on enhancer	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4390_s_42	12024049	(C) HMGB1 facilitates binding of intact Rta to its sites on the BHLF-1 enhancer.	bind
11867	2	4675	6	NULL	NULL	NULL	NULL	HMGB1	GP		facilitate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4390_s_42	12024049	(C) HMGB1 facilitates binding of intact Rta to its sites on the BHLF-1 enhancer.	bind
12350	1	4676	5	10	NULL	0	NULL	HNF6			bind					Glut2				promoter	NULL	wild-type chromatin	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7069_s_42	16055718	(c) HNF6 binding to the Glut2 promoter is  13-fold higher in wild-type than in  HNF6 - / -  chromatin, confirming the specificity of the anti-HNF6 antibody.	bind
12351	2	4676	5	10	NULL	0	NULL	HNF6			bind					Glut2					NULL	HNF6 - / - chromatin	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7069_s_42	16055718	(c) HNF6 binding to the Glut2 promoter is  13-fold higher in wild-type than in  HNF6 - / -  chromatin, confirming the specificity of the anti-HNF6 antibody.	bind
12352	3	4676	5	10	NULL	0	NULL	statement 1			is greater than					statement 2					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7069_s_42	16055718	(c) HNF6 binding to the Glut2 promoter is  13-fold higher in wild-type than in  HNF6 - / -  chromatin, confirming the specificity of the anti-HNF6 antibody.	bind
12353	4	4676	5	10	NULL	0	NULL	statement 3			confirms					anti-HNF6 antibody		specificity of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7069_s_42	16055718	(c) HNF6 binding to the Glut2 promoter is  13-fold higher in wild-type than in  HNF6 - / -  chromatin, confirming the specificity of the anti-HNF6 antibody.	bind
11868	1	4676	6	NULL	NULL	NULL	NULL	HNF6	GP		bind					Glut2	GP			promoter	NULL	wild type chromatin	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7069_s_42	16055718	(c) HNF6 binding to the Glut2 promoter is  13-fold higher in wild-type than in  HNF6 - / -  chromatin, confirming the specificity of the anti-HNF6 antibody.	bind
11869	2	4676	6	NULL	NULL	NULL	NULL	HNF6	GP		bind					Glut2	GP			promoter	NULL	HNF6-/- chromatin	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7069_s_42	16055718	(c) HNF6 binding to the Glut2 promoter is  13-fold higher in wild-type than in  HNF6 - / -  chromatin, confirming the specificity of the anti-HNF6 antibody.	bind
11870	3	4676	6	NULL	NULL	NULL	NULL	statement 1	Process		is greater than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7069_s_42	16055718	(c) HNF6 binding to the Glut2 promoter is  13-fold higher in wild-type than in  HNF6 - / -  chromatin, confirming the specificity of the anti-HNF6 antibody.	bind
54463	4	4676	6	NULL	NULL	NULL	NULL	statement 3	Process		confirms					anti-HNF6 antibody	GP	specificity of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7069_s_42	16055718	(c) HNF6 binding to the Glut2 promoter is  13-fold higher in wild-type than in  HNF6 - / -  chromatin, confirming the specificity of the anti-HNF6 antibody.	bind
12354	1	4678	5	NULL	NULL	0	NULL	HsMAD2	NULL		bind	NULL				GST - TXBP181	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_93_1_81_s_111	9546394	(C) HsMAD2 binds to GST - TXBP181 but not  GST.	bind
12355	2	4678	5	NULL	NULL	0	NULL	HsMAD2	NULL		does not bind	NULL				GST	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_93_1_81_s_111	9546394	(C) HsMAD2 binds to GST - TXBP181 but not  GST.	bind
11871	1	4678	6	NULL	NULL	NULL	NULL	HsMAD2	GP		bind					GST - TXBP181	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_93_1_81_s_111	9546394	(C) HsMAD2 binds to GST - TXBP181 but not  GST.	bind
12356	1	4679	5	NULL	NULL	0	NULL	TGFalpha	NULL	human	bind	NULL				EGF	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_110_6_763_s_91	12297049	(C) Human TGFalpha, EGF, and heparin binding EGF.	bind
12357	2	4679	5	NULL	NULL	0	NULL	EGF	NULL	human	bind	NULL				EGF	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_110_6_763_s_91	12297049	(C) Human TGFalpha, EGF, and heparin binding EGF.	bind
12358	3	4679	5	NULL	NULL	0	NULL	heparin	NULL	human	bind	NULL				EGF	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_110_6_763_s_91	12297049	(C) Human TGFalpha, EGF, and heparin binding EGF.	bind
11873	1	4679	6	NULL	NULL	NULL	NULL	TGFalpha	GP	human	bind					EGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_6_763_s_91	12297049	(C) Human TGFalpha, EGF, and heparin binding EGF.	bind
11874	2	4679	6	NULL	NULL	NULL	NULL	EGF	GP	human	bind					EGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_6_763_s_91	12297049	(C) Human TGFalpha, EGF, and heparin binding EGF.	bind
11875	3	4679	6	NULL	NULL	NULL	NULL	heparin	GP	human	bind					EGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_6_763_s_91	12297049	(C) Human TGFalpha, EGF, and heparin binding EGF.	bind
12359	1	4680	5	NULL	NULL	0	NULL	HVEM	NULL		bind	NULL				LT	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_8_1_21_s_101	9462508	(C) HVEM binds LT  and gD-1.	bind
12360	2	4680	5	NULL	NULL	0	NULL	HVEM	NULL		bind	NULL				gD-1	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_8_1_21_s_101	9462508	(C) HVEM binds LT  and gD-1.	bind
11876	1	4680	6	NULL	NULL	NULL	NULL	HVEM	GP		bind					LT	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_8_1_21_s_101	9462508	(C) HVEM binds LT  and gD-1.	bind
11877	2	4680	6	NULL	NULL	NULL	NULL	HVEM	GP		bind					gD-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_8_1_21_s_101	9462508	(C) HVEM binds LT  and gD-1.	bind
12361	1	4682	5	NULL	NULL	0	NULL	IE2	NULL		bind	NULL	directly			Spi-1	NULL		antiparallel beta3 and beta4 of wing motif		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_6803_s_248	10490619	(c) IE2 directly bound to Spi-1 through a portion (antiparallel beta3 and beta4) of the wing motif (lane 6).	bind
11878	1	4682	6	NULL	NULL	NULL	NULL	IE2	GP		bind		directly			Spi-1	GP		antiparallel beta3 and beta4 of the wing motif		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_6803_s_248	10490619	(c) IE2 directly bound to Spi-1 through a portion (antiparallel beta3 and beta4) of the wing motif (lane 6).	bind
12365	1	4684	5	NULL	NULL	0	NULL	FKBP12	NULL		bind	NULL				RyR1	NULL	WT			NULL		0	NULL	NULL	NULL	gw70_cellbiol_160_6_919_s_51	12629052	(C) Immunoblot showing binding of  FKBP12 to WT and mutant RyR1, assessed by centrifugation (FKBP12 cosediments with  RyR1) and FKBP12 immunoblotting.	bind
12366	2	4684	5	NULL	NULL	0	NULL	FKBP12	NULL		bind	NULL				RyR1	NULL	mutant			NULL		0	NULL	NULL	NULL	gw70_cellbiol_160_6_919_s_51	12629052	(C) Immunoblot showing binding of  FKBP12 to WT and mutant RyR1, assessed by centrifugation (FKBP12 cosediments with  RyR1) and FKBP12 immunoblotting.	bind
11879	1	4684	6	NULL	NULL	NULL	NULL	FKBP12	GP		bind					RyR1	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_6_919_s_51	12629052	(C) Immunoblot showing binding of  FKBP12 to WT and mutant RyR1, assessed by centrifugation (FKBP12 cosediments with  RyR1) and FKBP12 immunoblotting.	bind
11880	2	4684	6	NULL	NULL	NULL	NULL	FKBP12	GP		bind					RyR1	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_6_919_s_51	12629052	(C) Immunoblot showing binding of  FKBP12 to WT and mutant RyR1, assessed by centrifugation (FKBP12 cosediments with  RyR1) and FKBP12 immunoblotting.	bind
12370	1	4685	5	NULL	NULL	0	NULL	anti-PMT polyclonal antibodies	NULL		bind	NULL				peptides	NULL	recombinant			NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7839_s_187	11705966	(C) Immunoblot showing the binding of anti-PMT and anti-peptide polyclonal antibodies to recombinant peptides.	bind
12372	2	4685	5	NULL	NULL	0	NULL	anti-peptide polyclonal antibodies	NULL		bind	NULL				peptides	NULL	recombinant			NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7839_s_187	11705966	(C) Immunoblot showing the binding of anti-PMT and anti-peptide polyclonal antibodies to recombinant peptides.	bind
12375	1	4686	5	NULL	NULL	0	NULL	cyclin E	NULL		bind	NULL				p21	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3916_s_334	10207115	(C) Immunodepletion of cyclin E bound to p21 following 3 days of p16 induction.	bind
12376	2	4686	5	NULL	NULL	0	NULL	p16	NULL	induction	immunodeplete	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3916_s_334	10207115	(C) Immunodepletion of cyclin E bound to p21 following 3 days of p16 induction.	bind
11881	1	4686	6	NULL	NULL	NULL	NULL	cyclin E	GP		bind					p21	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3916_s_334	10207115	(C) Immunodepletion of cyclin E bound to p21 following 3 days of p16 induction.	bind
54464	1	4686	6	NULL	NULL	NULL	NULL	p16	GP	induction of	immunodeplete					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3916_s_334	10207115	(C) Immunodepletion of cyclin E bound to p21 following 3 days of p16 induction.	bind
13428	1	4687	5	NULL	NULL	0	NULL	Rep-kappaBBP-Jkappa	NULL		bind	NULL				NF-kappaB2-specific oligonucleotide	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2077_s_319	9528780	(C) In cell lysates transfected with a Notch-1-IC expression plasmid, Rep-kappaBBP-Jkappa-specific DNA binding activity bound to the NF-kappaB2-specific oligonucleotide (complex A) was abolished, but no higher-order complex, could be identified; it was probably masked by additional NF-kappaB-specific DNA binding activity (complex B).	bind
13431	2	4687	5	10	NULL	0	NULL	Notch-1-IC 	NULL		inhibit	NULL				statement 1	NULL				NULL	cell lysates	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2077_s_319	9528780	(C) In cell lysates transfected with a Notch-1-IC expression plasmid, Rep-kappaBBP-Jkappa-specific DNA binding activity bound to the NF-kappaB2-specific oligonucleotide (complex A) was abolished, but no higher-order complex, could be identified; it was probably masked by additional NF-kappaB-specific DNA binding activity (complex B).	bind
12273	1	4687	6	NULL	NULL	NULL	NULL	Rep-kappaBBP-Jkappa-	GP		bind					NF-kappaB2-specific oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2077_s_319	9528780	(C) In cell lysates transfected with a Notch-1-IC expression plasmid, Rep-kappaBBP-Jkappa-specific DNA binding activity bound to the NF-kappaB2-specific oligonucleotide (complex A) was abolished, but no higher-order complex, could be identified; it was probably masked by additional NF-kappaB-specific DNA binding activity (complex B).	bind
12448	2	4687	6	NULL	NULL	NULL	NULL	Notch-1-IC 	GP		inhibits					statement 1	Process				NULL	cell lysates	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2077_s_319	9528780	(C) In cell lysates transfected with a Notch-1-IC expression plasmid, Rep-kappaBBP-Jkappa-specific DNA binding activity bound to the NF-kappaB2-specific oligonucleotide (complex A) was abolished, but no higher-order complex, could be identified; it was probably masked by additional NF-kappaB-specific DNA binding activity (complex B).	bind
13422	1	4688	5	NULL	NULL	0	NULL		NULL		replaces	NULL			G residue		NULL			A in the lexA binding site upstream of recA	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_22_6235_s_41	12399494	(C) In the  recA281(Oc) mutation, a G residue replaces A in the  lexA binding site upstream of  recA.	bind
13423	2	4688	5	NULL	NULL	0	NULL	statement 1	NULL		occurs in	NULL				recA281(Oc)	NULL	mutation			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_22_6235_s_41	12399494	(C) In the  recA281(Oc) mutation, a G residue replaces A in the  lexA binding site upstream of  recA.	bind
13406	1	4689	5	10	NULL	0	NULL	GSK-3		inactive	in the presence of					Li+					NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_673_s_234	14664817	(C) In the presence of Li+ and excess (transfected) Axin, GSK-3 is inactive and protein X is unphosphorylated,  but Axin binds to protein X preventing induction of neurite outgrowth.	bind
13407	2	4689	5	10	NULL	0	NULL	protein X		unphosphorylated	in the presence of					Li+					NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_673_s_234	14664817	(C) In the presence of Li+ and excess (transfected) Axin, GSK-3 is inactive and protein X is unphosphorylated,  but Axin binds to protein X preventing induction of neurite outgrowth.	bind
13408	3	4689	5	10	NULL	0	NULL	GSK-3		inactive	in the presence of					Axin		excess			NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_673_s_234	14664817	(C) In the presence of Li+ and excess (transfected) Axin, GSK-3 is inactive and protein X is unphosphorylated,  but Axin binds to protein X preventing induction of neurite outgrowth.	bind
13415	4	4689	5	10	NULL	0	NULL	protein X		unphosphorylated	in the presence of					Axin		excess			NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_673_s_234	14664817	(C) In the presence of Li+ and excess (transfected) Axin, GSK-3 is inactive and protein X is unphosphorylated,  but Axin binds to protein X preventing induction of neurite outgrowth.	bind
13417	5	4689	5	NULL	NULL	0	NULL	Axin	NULL		bind	NULL				protein X	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellneurosci_24_3_673_s_234	14664817	(C) In the presence of Li+ and excess (transfected) Axin, GSK-3 is inactive and protein X is unphosphorylated,  but Axin binds to protein X preventing induction of neurite outgrowth.	bind
13418	6	4689	5	NULL	NULL	0	NULL	statement 5	NULL		prevents	NULL				neurite outgrowth	NULL	induction of			NULL		0	NULL	NULL	NULL	gw70_molcellneurosci_24_3_673_s_234	14664817	(C) In the presence of Li+ and excess (transfected) Axin, GSK-3 is inactive and protein X is unphosphorylated,  but Axin binds to protein X preventing induction of neurite outgrowth.	bind
11882	1	4689	6	NULL	NULL	NULL	NULL	Axin	GP		bind					protein X	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_673_s_234	14664817	(C) In the presence of Li+ and excess (transfected) Axin, GSK-3 is inactive and protein X is unphosphorylated,  but Axin binds to protein X preventing induction of neurite outgrowth.	bind
11883	2	4689	6	NULL	NULL	NULL	NULL	statement 1	Process		prevents					neurite outgrowth	Process	induction of 			NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_673_s_234	14664817	(C) In the presence of Li+ and excess (transfected) Axin, GSK-3 is inactive and protein X is unphosphorylated,  but Axin binds to protein X preventing induction of neurite outgrowth.	bind
12279	3	4689	6	NULL	NULL	NULL	NULL	GSK-3	GP	inactive	in the presence of					Li+	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_673_s_234	14664817	(C) In the presence of Li+ and excess (transfected) Axin, GSK-3 is inactive and protein X is unphosphorylated,  but Axin binds to protein X preventing induction of neurite outgrowth.	bind
57790	4	4689	6	NULL	NULL	NULL	NULL	protein X	GP	unphosphorylated	in the presence of					Li+	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_673_s_234	14664817	(C) In the presence of Li+ and excess (transfected) Axin, GSK-3 is inactive and protein X is unphosphorylated,  but Axin binds to protein X preventing induction of neurite outgrowth.	bind
57791	5	4689	6	NULL	NULL	NULL	NULL	GSK-3	GP	inactive	in the presence of					Axin	GP	excess			NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_673_s_234	14664817	(C) In the presence of Li+ and excess (transfected) Axin, GSK-3 is inactive and protein X is unphosphorylated,  but Axin binds to protein X preventing induction of neurite outgrowth.	bind
57793	6	4689	6	NULL	NULL	NULL	NULL	protein X	GP	unphosphorylated	in the presence of					Axin	GP	excess			NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_673_s_234	14664817	(C) In the presence of Li+ and excess (transfected) Axin, GSK-3 is inactive and protein X is unphosphorylated,  but Axin binds to protein X preventing induction of neurite outgrowth.	bind
12383	1	4690	5	10	NULL	0	NULL	C-sos1			displace from					 grb2 CH2					NULL	in vitro	NULL	NULL	NULL	NULL	gw70_cellbiol_172_6_817_s_123	16520382	(C) In vitro binding assay showing displacement  of CH2 from grb2 by C-sos1.	bind
11884	1	4690	6	NULL	NULL	NULL	NULL	C-sos1	GP		displace from					grb2 CH2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_cellbiol_172_6_817_s_123	16520382	(C) In vitro binding assay showing displacement  of CH2 from grb2 by C-sos1.	bind
12384	1	4691	5	NULL	NULL	0	NULL	AP-3	NULL		bind	NULL				AGAP1	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_devcell_5_3_513_s_44	12967569	(C) In vitro binding between AP-3 and GST fusion proteins of AGAP1.	bind
44569	2	4691	5	10	NULL	0	NULL	AGAP1	NULL		is a type of	NULL				GST fusion protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_3_513_s_44	12967569	(C) In vitro binding between AP-3 and GST fusion proteins of AGAP1.	bind
11885	1	4691	6	NULL	NULL	NULL	NULL	AP-3	GP		bind					AGAP1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_devcell_5_3_513_s_44	12967569	(C) In vitro binding between AP-3 and GST fusion proteins of AGAP1.	bind
54467	2	4691	6	NULL	NULL	NULL	NULL	AGAP1	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_3_513_s_44	12967569	(C) In vitro binding between AP-3 and GST fusion proteins of AGAP1.	bind
12385	1	4692	5	NULL	NULL	0	NULL	S35Metataxin	NULL		bind	NULL		1539-816		p80 coilin	NULL		266-597		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1638_1_35_s_110	12757932	(C) In vitro binding between S35Metataxin-1539-816 and GST-fusion-p80 coilin266-597.	bind
44570	2	4692	5	10	NULL	0	NULL	p80 coilin	NULL		is a type of	NULL		266-597		GST-fusion protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1638_1_35_s_110	12757932	(C) In vitro binding between S35Metataxin-1539-816 and GST-fusion-p80 coilin266-597.	bind
11886	1	4692	6	NULL	NULL	NULL	NULL	S35Metataxin	GP		bind			1539-816		p80 coilin	GP		266-597		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1638_1_35_s_110	12757932	(C) In vitro binding between S35Metataxin-1539-816 and GST-fusion-p80 coilin266-597.	bind
54468	2	4692	6	NULL	NULL	NULL	NULL	p80 coilin	GP		is a type of			266-597		GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1638_1_35_s_110	12757932	(C) In vitro binding between S35Metataxin-1539-816 and GST-fusion-p80 coilin266-597.	bind
12387	1	4693	5	NULL	NULL	0	NULL	PaaX	NULL		bind	NULL				Ppac	NULL			promoter	NULL	in vitro	0	NULL	NULL	NULL	gw70_jbacteriol_186_7_2215_s_47	15028709	(C) In vitro binding of PaaX to the  Ppac promoter by gel retardation assay.	bind
11887	1	4693	6	NULL	NULL	NULL	NULL	PaaX	GP		bind					Ppac	GP			promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbacteriol_186_7_2215_s_47	15028709	(C) In vitro binding of PaaX to the  Ppac promoter by gel retardation assay.	bind
12388	1	4694	5	10	NULL	0	NULL	ARF		radiolabeled;;human	bind					GST					NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1258_s_176	15684379	(C) In vitro binding of radiolabeled  human ARF to GST, GST-wild-type NPM (WT), or various GST-NPM mutants (NPM residues  fused to GST are indicated) was detected by autoradiography.	bind
12389	2	4694	5	10	NULL	0	NULL	ARF		radiolabeled;;human	bind					GST- NPM		wild-type			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1258_s_176	15684379	(C) In vitro binding of radiolabeled  human ARF to GST, GST-wild-type NPM (WT), or various GST-NPM mutants (NPM residues  fused to GST are indicated) was detected by autoradiography.	bind
12390	3	4694	5	10	NULL	0	NULL	ARF		radiolabeled;;human	bind					GST-NPM		mutant			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1258_s_176	15684379	(C) In vitro binding of radiolabeled  human ARF to GST, GST-wild-type NPM (WT), or various GST-NPM mutants (NPM residues  fused to GST are indicated) was detected by autoradiography.	bind
11888	1	4694	6	NULL	NULL	NULL	NULL	ARF	GP	radiolabeled;; human	bind					GST					NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1258_s_176	15684379	(C) In vitro binding of radiolabeled  human ARF to GST, GST-wild-type NPM (WT), or various GST-NPM mutants (NPM residues  fused to GST are indicated) was detected by autoradiography.	bind
11889	2	4694	6	NULL	NULL	NULL	NULL	ARF	GP	radiolabeled;; human	bind					GST-NPM	GP	wild type			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1258_s_176	15684379	(C) In vitro binding of radiolabeled  human ARF to GST, GST-wild-type NPM (WT), or various GST-NPM mutants (NPM residues  fused to GST are indicated) was detected by autoradiography.	bind
11890	3	4694	6	NULL	NULL	NULL	NULL	ARF	GP	radiolabeled;; human	bind					GST-NPM	GP	mutant			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1258_s_176	15684379	(C) In vitro binding of radiolabeled  human ARF to GST, GST-wild-type NPM (WT), or various GST-NPM mutants (NPM residues  fused to GST are indicated) was detected by autoradiography.	bind
12392	1	4696	5	NULL	NULL	0	NULL	Src	NULL		bind	NULL				RACK1	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_6_3245_s_206	9584165	(C) In vitro protein kinase activity of Src bound to RACK1.	bind
11891	1	4696	6	NULL	NULL	NULL	NULL	Src	GP		bind					RACK1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_6_3245_s_206	9584165	(C) In vitro protein kinase activity of Src bound to RACK1.	bind
12395	1	4699	5	NULL	NULL	0	NULL	HIRA protein	NULL	in vitro-labeled	bind	NULL				core histone H4	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_9_5546_s_193	9710638	(C) In vitro-labeled HIRA protein binds core histone H4 immobilized on beads.	bind
11892	1	4699	6	NULL	NULL	NULL	NULL	HIRA	GP	In vitro-labeled 	bind					core histone H4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5546_s_193	9710638	(C) In vitro-labeled HIRA protein binds core histone H4 immobilized on beads.	bind
12396	1	4700	5	NULL	NULL	0	NULL	IRF-1	NULL		bind	NULL				IL-4	NULL			promoter	NULL	in vivo in peripheral blood T cells 	NULL	NULL	NULL	NULL	gw60_immunity_17_6_703_s_189	12479817	(C) In vivo binding of IRF-1 and IRF-2 to the IL-4 promoter in peripheral blood T cells upon IFN-  stimulation.	bind
12397	2	4700	5	NULL	NULL	0	NULL	statement 1	NULL		occurs upon	NULL				IFN	NULL	stimulation			NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_6_703_s_189	12479817	(C) In vivo binding of IRF-1 and IRF-2 to the IL-4 promoter in peripheral blood T cells upon IFN-  stimulation.	bind
12398	3	4700	5	NULL	NULL	0	NULL	IRF-2	NULL		bind	NULL				IL-4	NULL			promoter	NULL	in vivo in peripheral blood T cells	0	NULL	NULL	NULL	gw60_immunity_17_6_703_s_189	12479817	(C) In vivo binding of IRF-1 and IRF-2 to the IL-4 promoter in peripheral blood T cells upon IFN-  stimulation.	bind
12399	4	4700	5	NULL	NULL	0	NULL	statement 3	NULL		occurs upon	NULL				IFN	NULL	stimulation			NULL		0	NULL	NULL	NULL	gw60_immunity_17_6_703_s_189	12479817	(C) In vivo binding of IRF-1 and IRF-2 to the IL-4 promoter in peripheral blood T cells upon IFN-  stimulation.	bind
11893	1	4700	6	NULL	NULL	NULL	NULL	IRF-1	GP		bind					IL-4	GP			promoter	NULL	peripheral blood T cells, in vivo	NULL	NULL	NULL	NULL	gw60_immunity_17_6_703_s_189	12479817	(C) In vivo binding of IRF-1 and IRF-2 to the IL-4 promoter in peripheral blood T cells upon IFN-  stimulation.	bind
11894	2	4700	6	NULL	NULL	NULL	NULL	IRF-2	GP		bind					IL-4	GP			promoter	NULL	peripheral blood T cells, in vivo	NULL	NULL	NULL	NULL	gw60_immunity_17_6_703_s_189	12479817	(C) In vivo binding of IRF-1 and IRF-2 to the IL-4 promoter in peripheral blood T cells upon IFN-  stimulation.	bind
11895	3	4700	6	NULL	NULL	NULL	NULL	IFN	GP		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_6_703_s_189	12479817	(C) In vivo binding of IRF-1 and IRF-2 to the IL-4 promoter in peripheral blood T cells upon IFN-  stimulation.	bind
11896	4	4700	6	NULL	NULL	NULL	NULL	IFN	GP		stimulates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_6_703_s_189	12479817	(C) In vivo binding of IRF-1 and IRF-2 to the IL-4 promoter in peripheral blood T cells upon IFN-  stimulation.	bind
12400	1	4701	5	NULL	NULL	0	NULL	SATB1	NULL		bind	NULL				IL-2	NULL	distal		promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1620_s_182	15713622	(C) In vivo binding of SATB1 to  the distal IL-2 promoter.	bind
11897	1	4701	6	NULL	NULL	NULL	NULL	SATB1	GP		bind					IL-2	GP	distal		promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1620_s_182	15713622	(C) In vivo binding of SATB1 to  the distal IL-2 promoter.	bind
13229	1	4702	5	NULL	NULL	0	NULL	PDX-1	NULL	endogenous	bind	NULL				LRH-1	NULL	murine		promoter	NULL	in the gut from E13.5 embryos	0	NULL	NULL	NULL	gw70_molcellbiol_23_19_6713_s_189	12972592	(C) In vivo ChIP assay demonstrating  binding of endogenous PDX-1 to the murine LRH-1 promoter in the gut and pancreas  from E13.5 embryos.	bind
13230	2	4702	5	NULL	NULL	0	NULL	PDX-1	NULL	endogenous	bind	NULL				LRH-1	NULL	murine		promoter	NULL	in the pancreas from E13.5 embryos	0	NULL	NULL	NULL	gw70_molcellbiol_23_19_6713_s_189	12972592	(C) In vivo ChIP assay demonstrating  binding of endogenous PDX-1 to the murine LRH-1 promoter in the gut and pancreas  from E13.5 embryos.	bind
11898	1	4702	6	NULL	NULL	NULL	NULL	PDX-1	GP	endogenous	bind					LRH-1	GP	murine		promoter	NULL	gut from E13.5 embryos	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_19_6713_s_189	12972592	(C) In vivo ChIP assay demonstrating  binding of endogenous PDX-1 to the murine LRH-1 promoter in the gut and pancreas  from E13.5 embryos.	bind
15183	2	4702	6	NULL	NULL	NULL	NULL	PDX-1	GP	endogenous	bind					LRH-1	GP	murine		promoter	NULL	pancreas from E13.5 embryos	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_19_6713_s_189	12972592	(C) In vivo ChIP assay demonstrating  binding of endogenous PDX-1 to the murine LRH-1 promoter in the gut and pancreas  from E13.5 embryos.	bind
13231	1	4703	5	NULL	NULL	0	NULL	beta3-integrin	NULL		induce	NULL				PEA3	NULL	DNA-binding activity of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_6_2118_s_219	11238946	(C) Induction of PEA3 DNA-binding activity by beta3-integrin.	bind
11900	1	4703	6	NULL	NULL	NULL	NULL	beta3-integrin	GP		induces					PEA3	GP	DNA binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_6_2118_s_219	11238946	(C) Induction of PEA3 DNA-binding activity by beta3-integrin.	bind
13232	1	4704	5	NULL	NULL	0	NULL	BMP4	NULL		bind	NULL				BMPR1B	NULL		ectodomain		NULL		0	NULL	NULL	NULL	gw70_development_131_1_229_s_146	14660436	(C) Inhibition of BMP4 binding to BMPR1B  ectodomain by mCHL2-FLAG.	bind
13233	2	4704	5	NULL	NULL	0	NULL	mCHL2-FLAG	NULL		inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_1_229_s_146	14660436	(C) Inhibition of BMP4 binding to BMPR1B  ectodomain by mCHL2-FLAG.	bind
11901	1	4704	6	NULL	NULL	NULL	NULL	BMP4	GP		bind					BMPR1B	GP		ectodomain		NULL		NULL	NULL	NULL	NULL	gw70_development_131_1_229_s_146	14660436	(C) Inhibition of BMP4 binding to BMPR1B  ectodomain by mCHL2-FLAG.	bind
11902	2	4704	6	NULL	NULL	NULL	NULL	mCHL2-FLAG	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_131_1_229_s_146	14660436	(C) Inhibition of BMP4 binding to BMPR1B  ectodomain by mCHL2-FLAG.	bind
13234	1	4705	5	NULL	NULL	0	NULL	Ac-DEVD-CHO	NULL		inhibit	NULL				eIF4G	NULL	cleavage of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_7565_s_279	9819442	(C) Inhibition of eIF4G cleavage by Ac-DEVD-CHO.	bind
11903	1	4705	6	NULL	NULL	NULL	NULL	Ac-DEVD-CHO	GP		inhibits					eIF4G	GP	clevage of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7565_s_279	9819442	(C) Inhibition of eIF4G cleavage by Ac-DEVD-CHO.	bind
13235	1	4706	5	NULL	NULL	0	NULL	Gt	NULL		bind	NULL				rhodopsin	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_3_5_649_s_56	10360181	(C) Inhibition of Gt binding to rhodopsin by phosducin.	bind
13236	2	4706	5	NULL	NULL	0	NULL	phosducin	NULL		inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_3_5_649_s_56	10360181	(C) Inhibition of Gt binding to rhodopsin by phosducin.	bind
11904	1	4706	6	NULL	NULL	NULL	NULL	Gt	GP		bind					rhodopsin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_5_649_s_56	10360181	(C) Inhibition of Gt binding to rhodopsin by phosducin.	bind
11905	2	4706	6	NULL	NULL	NULL	NULL	phosducin	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_5_649_s_56	10360181	(C) Inhibition of Gt binding to rhodopsin by phosducin.	bind
13237	1	4707	5	NULL	NULL	0	NULL	anti-BSAP antibody	NULL		inhibit	NULL				NF-JC	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_5_4_377_s_97	8885870	(C) Inhibition of NF-JC binding by anti-BSAP antibody.	bind
11906	1	4707	6	NULL	NULL	NULL	NULL	anti-BSAP antibody	GP		inhibits					NF-JC	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_5_4_377_s_97	8885870	(C) Inhibition of NF-JC binding by anti-BSAP antibody.	bind
13238	2	4708	5	10	NULL	NULL	NULL	7-Cl-Kyn	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_110_2_159_s_146	12591153	(C) Inhibition of NMDA receptor-mediated currents by 7-Cl-Kyn, a competitive antagonist of NMDA receptors acting on the glycine binding site of NR1.	bind
13239	4	4708	5	10	NULL	NULL	NULL	7-Cl-Kyn	Chemical		is					NMDA receptors	GP	competitive antagonist of 			NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_110_2_159_s_146	12591153	(C) Inhibition of NMDA receptor-mediated currents by 7-Cl-Kyn, a competitive antagonist of NMDA receptors acting on the glycine binding site of NR1.	bind
13240	3	4708	5	10	NULL	NULL	NULL	7-Cl-Kyn	Chemical		acts on					NR1	GP		glycine binding site 		NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_110_2_159_s_146	12591153	(C) Inhibition of NMDA receptor-mediated currents by 7-Cl-Kyn, a competitive antagonist of NMDA receptors acting on the glycine binding site of NR1.	bind
54477	1	4708	5	10	NULL	NULL	NULL	NMDA receptor	GP		mediates					currents	AbstractConcept				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_110_2_159_s_146	12591153	(C) Inhibition of NMDA receptor-mediated currents by 7-Cl-Kyn, a competitive antagonist of NMDA receptors acting on the glycine binding site of NR1.	bind
12278	1	4708	6	10	NULL	NULL	NULL	NMDA receptors	GP		mediates					currents	AbstractConcept				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_110_2_159_s_146	12591153	(C) Inhibition of NMDA receptor-mediated currents by 7-Cl-Kyn, a competitive antagonist of NMDA receptors acting on the glycine binding site of NR1.	bind
12449	2	4708	6	10	NULL	NULL	NULL	7-Cl-Kyn	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_110_2_159_s_146	12591153	(C) Inhibition of NMDA receptor-mediated currents by 7-Cl-Kyn, a competitive antagonist of NMDA receptors acting on the glycine binding site of NR1.	bind
12450	3	4708	6	NULL	NULL	NULL	NULL	7-Cl-Kyn	Chemical		is					NMDA receptors	GP	competitive antagonist of 			NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_110_2_159_s_146	12591153	(C) Inhibition of NMDA receptor-mediated currents by 7-Cl-Kyn, a competitive antagonist of NMDA receptors acting on the glycine binding site of NR1.	bind
12451	4	4708	6	NULL	NULL	NULL	NULL	7-Cl-Kyn	Chemical		acts on					NR1	GP		glycine binding site		NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_110_2_159_s_146	12591153	(C) Inhibition of NMDA receptor-mediated currents by 7-Cl-Kyn, a competitive antagonist of NMDA receptors acting on the glycine binding site of NR1.	bind
13241	1	4709	5	NULL	NULL	0	NULL	LLN	NULL		is	NULL				LLNL	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_24_9236_s_230	11094075	(C) Inhibition of proteasome by LLNL (LLN) stabilizes p27Kip1 protein levels.	bind
13242	2	4709	5	NULL	NULL	0	NULL		NULL		inhibit	NULL		LLN		proteasome	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_24_9236_s_230	11094075	(C) Inhibition of proteasome by LLNL (LLN) stabilizes p27Kip1 protein levels.	bind
13243	3	4709	5	NULL	NULL	0	NULL	statement 2	NULL		stabilize	NULL				p27Kip1	NULL	protein levels of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_24_9236_s_230	11094075	(C) Inhibition of proteasome by LLNL (LLN) stabilizes p27Kip1 protein levels.	bind
12280	1	4709	6	NULL	NULL	NULL	NULL				inhibits			LLNL		proteasome	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9236_s_230	11094075	(C) Inhibition of proteasome by LLNL (LLN) stabilizes p27Kip1 protein levels.	bind
12281	2	4709	6	NULL	NULL	NULL	NULL	statement 1	Process		stabilizes					p27Kip1	GP	protein levels of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9236_s_230	11094075	(C) Inhibition of proteasome by LLNL (LLN) stabilizes p27Kip1 protein levels.	bind
54478	3	4709	6	10	NULL	0	NULL	LLN			is					LLNL					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_24_9236_s_230	11094075	(C) Inhibition of proteasome by LLNL (LLN) stabilizes p27Kip1 protein levels.	bind
13403	1	4710	5	NULL	NULL	0	NULL	Ras activation	NULL	inhibition of	does not block	NULL					NULL	induction of		RNA Pol I-dependent promoter	NULL	in cells overexpressing TBP	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7086_s_202	9819395	(C) Inhibition of Ras activation does not block induction of RNA Pol I-dependent promoters in cells overexpressing TBP.	bind
15184	1	4710	6	10	NULL	0	NULL	Ras activation		inhibition of	does not block							induction of 		RNA Pol I-dependent promoter	NULL	cells overexpressing TBP	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7086_s_202	9819395	(C) Inhibition of Ras activation does not block induction of RNA Pol I-dependent promoters in cells overexpressing TBP.	bind
13244	1	4711	5	NULL	NULL	0	NULL	Idax	NULL		bind	NULL				Dvl	NULL				NULL	in intact cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_1_330_s_205	11113207	(C) Inhibition of the binding of Idax to Dvl by Axin in intact cells.	bind
13245	2	4711	5	NULL	NULL	0	NULL	Axin	NULL		inhibit	NULL				statement 1	NULL				NULL	in intact cells	0	NULL	NULL	NULL	gw60_molcellbiol_21_1_330_s_205	11113207	(C) Inhibition of the binding of Idax to Dvl by Axin in intact cells.	bind
11907	1	4711	6	NULL	NULL	NULL	NULL	Idax	GP		bind					Dvl	GP				NULL	intact cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_1_330_s_205	11113207	(C) Inhibition of the binding of Idax to Dvl by Axin in intact cells.	bind
11908	2	4711	6	NULL	NULL	NULL	NULL	Axin	GP		inhibits					statement 1	Process				NULL	intact cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_1_330_s_205	11113207	(C) Inhibition of the binding of Idax to Dvl by Axin in intact cells.	bind
13246	1	4712	5	NULL	NULL	0	NULL	Ubc13/Uev1A	NULL	interference of	inhibit	NULL				NF- B	NULL	activation of			NULL	in cells	0	NULL	NULL	NULL	gw60_cell_103_2_351_s_160	11057907	(C) Interference of Ubc13/Uev1A inhibits NF- B activation in cells.	bind
11909	1	4712	6	NULL	NULL	NULL	NULL	Ubc13/Uev1A	GP	Interference of	inhibits					NF-B	GP	activation of			NULL	in cells	NULL	NULL	NULL	NULL	gw60_cell_103_2_351_s_160	11057907	(C) Interference of Ubc13/Uev1A inhibits NF- B activation in cells.	bind
13247	1	4713	5	NULL	NULL	0	NULL	JAK2	NULL		bind	NULL	directly			EpoR	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_8_6_1327_s_109	11779507	(C) JAK2 and JAK2 (JH3-JH7) bind EpoR directly.	bind
13248	2	4713	5	NULL	NULL	0	NULL	JAK2	NULL		bind	NULL	directly	JH3-JH7		EpoR	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_8_6_1327_s_109	11779507	(C) JAK2 and JAK2 (JH3-JH7) bind EpoR directly.	bind
11910	1	4713	6	NULL	NULL	NULL	NULL	JAK2	GP		bind		directly			EpoR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_6_1327_s_109	11779507	(C) JAK2 and JAK2 (JH3-JH7) bind EpoR directly.	bind
11911	2	4713	6	NULL	NULL	NULL	NULL	JAK2	GP		bind		directly	JH3-JH7		EpoR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_6_1327_s_109	11779507	(C) JAK2 and JAK2 (JH3-JH7) bind EpoR directly.	bind
13249	1	4715	5	NULL	NULL	0	NULL	rhodanese 	NULL	[35]methionine-labeled 	bind	NULL				GroEL	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_90_3_491_s_117	9267029	(C) Kinetics of binding and release of [35]methionine-labeled rhodanese and CAT from GroEL.	bind
13250	2	4715	5	NULL	NULL	0	NULL	rhodanese	NULL	[35]methionine-labeled	release	NULL				GroEL	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_90_3_491_s_117	9267029	(C) Kinetics of binding and release of [35]methionine-labeled rhodanese and CAT from GroEL.	bind
13251	3	4715	5	NULL	NULL	0	NULL	CAT	NULL	[35]methionine-labeled	bind	NULL				GroEL	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_90_3_491_s_117	9267029	(C) Kinetics of binding and release of [35]methionine-labeled rhodanese and CAT from GroEL.	bind
13252	4	4715	5	NULL	NULL	0	NULL	CAT	NULL	[35]methionine-labeled	release	NULL				GroEL	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_90_3_491_s_117	9267029	(C) Kinetics of binding and release of [35]methionine-labeled rhodanese and CAT from GroEL.	bind
16234	1	4715	6	NULL	NULL	NULL	NULL	rhodanese	GP	[35]methionine-labeled	bind					GroEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_3_491_s_117	9267029	(C) Kinetics of binding and release of [35]methionine-labeled rhodanese and CAT from GroEL.	bind
16235	2	4715	6	NULL	NULL	NULL	NULL	rhodanese	GP	[35]methionine-labeled	release					GroEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_3_491_s_117	9267029	(C) Kinetics of binding and release of [35]methionine-labeled rhodanese and CAT from GroEL.	bind
16237	3	4715	6	NULL	NULL	NULL	NULL	CAT	GP	[35]methionine-labeled	bind					GroEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_3_491_s_117	9267029	(C) Kinetics of binding and release of [35]methionine-labeled rhodanese and CAT from GroEL.	bind
54479	4	4715	6	NULL	NULL	NULL	NULL	CAT	GP	[35]methionine-labeled	release					GroEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_3_491_s_117	9267029	(C) Kinetics of binding and release of [35]methionine-labeled rhodanese and CAT from GroEL.	bind
13253	1	4716	5	NULL	NULL	0	NULL	Krox-20	NULL		inhibit	NULL				Schwann cell	NULL	death of			NULL		0	NULL	NULL	NULL	gw70_cellbiol_164_3_385_s_66	14757751	(C) Krox-20 inhibits Schwann cell death after serum withdrawal.	bind
13254	2	4716	5	NULL	NULL	0	NULL	statement 1	NULL		occurs after	NULL				serum	NULL	withdrawal of			NULL		0	NULL	NULL	NULL	gw70_cellbiol_164_3_385_s_66	14757751	(C) Krox-20 inhibits Schwann cell death after serum withdrawal.	bind
11912	1	4716	6	NULL	NULL	NULL	NULL	Krox-20	GP		inhibits					Schwann cell	Cell	death of			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_3_385_s_66	14757751	(C) Krox-20 inhibits Schwann cell death after serum withdrawal.	bind
15185	2	4716	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs after					serum 	OrganismPart	withdrawal of			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_3_385_s_66	14757751	(C) Krox-20 inhibits Schwann cell death after serum withdrawal.	bind
13255	1	4717	5	NULL	NULL	0	NULL	trypomastigote	NULL	T. cruzi	bind	NULL				CASM cells	NULL	human			NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_11_6717_s_49	15501810	(C) Lactose, but not sucrose, inhibits  T. cruzi trypomastigote binding to human CASM cells.	bind
13256	2	4717	5	NULL	NULL	0	NULL	lactose	NULL		inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_11_6717_s_49	15501810	(C) Lactose, but not sucrose, inhibits  T. cruzi trypomastigote binding to human CASM cells.	bind
13257	3	4717	5	NULL	NULL	0	NULL	sucrose	NULL		does not inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_11_6717_s_49	15501810	(C) Lactose, but not sucrose, inhibits  T. cruzi trypomastigote binding to human CASM cells.	bind
11913	1	4717	6	NULL	NULL	NULL	NULL	trypomastigote	OrganismPart	T. cruzi	bind					CASM cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_11_6717_s_49	15501810	(C) Lactose, but not sucrose, inhibits  T. cruzi trypomastigote binding to human CASM cells.	bind
11914	2	4717	6	NULL	NULL	NULL	NULL	lactose	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_11_6717_s_49	15501810	(C) Lactose, but not sucrose, inhibits  T. cruzi trypomastigote binding to human CASM cells.	bind
11915	3	4717	6	NULL	NULL	NULL	NULL	sucrose	Chemical		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_11_6717_s_49	15501810	(C) Lactose, but not sucrose, inhibits  T. cruzi trypomastigote binding to human CASM cells.	bind
13825	1	4718	5	10	NULL	0	NULL	TIF2			bind			coactivator motif		GST-GR			LBD		NULL		NULL	NULL	NULL	NULL	gw60_cell_110_1_93_s_68	12151000	(C) Ligand-dependent binding of TIF2 coactivator motif to GST-GR LBD in the presence of a 5-fold excess of dexamethasone (triangles), RU486 (squares), and no compound (circles) was measured by surface plasmon resonance.	bind
54480	2	4718	5	10	NULL	0	NULL	statement 1			depends on					ligand					NULL		NULL	NULL	NULL	NULL	gw60_cell_110_1_93_s_68	12151000	(C) Ligand-dependent binding of TIF2 coactivator motif to GST-GR LBD in the presence of a 5-fold excess of dexamethasone (triangles), RU486 (squares), and no compound (circles) was measured by surface plasmon resonance.	bind
11916	1	4718	6	NULL	NULL	NULL	NULL	TIF2	GP		bind			coactivator motif		GST-GR	GP		LBD		NULL		NULL	NULL	NULL	NULL	gw60_cell_110_1_93_s_68	12151000	(C) Ligand-dependent binding of TIF2 coactivator motif to GST-GR LBD in the presence of a 5-fold excess of dexamethasone (triangles), RU486 (squares), and no compound (circles) was measured by surface plasmon resonance.	bind
11917	2	4718	6	NULL	NULL	NULL	NULL	statement 1	Process		is dependent on					ligand					NULL		NULL	NULL	NULL	NULL	gw60_cell_110_1_93_s_68	12151000	(C) Ligand-dependent binding of TIF2 coactivator motif to GST-GR LBD in the presence of a 5-fold excess of dexamethasone (triangles), RU486 (squares), and no compound (circles) was measured by surface plasmon resonance.	bind
13830	1	4719	5	NULL	NULL	0	NULL	MAb 24c5	NULL		bind	NULL				MTB	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
13831	2	4719	5	NULL	NULL	0	NULL	MTB	NULL		is	NULL				M. tuberculosis Erdman day-20 7H9 medium 	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
13833	3	4719	5	NULL	NULL	0	NULL	MAb 24c5	NULL		bind	NULL				INTPHSE	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
13834	4	4719	5	10	NULL	0	NULL	INTPHSE			is a type of					cell culture supernatant extract					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
13837	5	4719	5	NULL	NULL	0	NULL	MAb 24c5	NULL		bind	NULL				GC	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
13838	6	4719	5	NULL	NULL	0	NULL	MAb 24c5	NULL		bind	NULL				AM	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
13839	7	4719	5	NULL	NULL	0	NULL	MAb 24c5	NULL		bind	NULL				LAM	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
13840	8	4719	5	NULL	NULL	0	NULL	LAM	NULL		is	NULL				lipoarabinomannan	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
13841	9	4719	5	NULL	NULL	0	NULL	MAb 24c5	NULL		bind	NULL				PIM	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
13842	10	4719	5	NULL	NULL	0	NULL	PIM	NULL		is	NULL				phosphatidylinositol mannoside	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
13843	11	4719	5	NULL	NULL	0	NULL	MAb 24c5	NULL		bind	NULL				LM	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
13844	12	4719	5	NULL	NULL	0	NULL	LM	NULL		is	NULL				fast-growing mycobacterial lipomannan	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
13845	13	4719	5	NULL	NULL	0	NULL	MAb 24c5	NULL		bind	NULL				mAGP	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
13846	14	4719	5	NULL	NULL	0	NULL	mAGP	NULL		is	NULL				mycolyl-arabinogalactan-peptidoglycan complex	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
13847	15	4719	5	NULL	NULL	0	NULL	MAb 24c5	NULL		bind	NULL				TLF	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
13848	16	4719	5	NULL	NULL	0	NULL	TLF	NULL		is	NULL				total lipid fraction	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
12282	1	4719	6	NULL	NULL	NULL	NULL	MAb 24c5	GP		bind					MTB					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
12283	2	4719	6	NULL	NULL	0	NULL	MTB	NULL		is	NULL				Erdman day-20 7H9 medium	NULL	M. tuberculosis			NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
12285	3	4719	6	NULL	NULL	NULL	NULL	MAb 24c5	GP		bind					INTPHSE					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
12286	4	4719	6	10	NULL	0	NULL	INTPHSE			is a type of					cell culture supernatant extract 					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
12287	5	4719	6	NULL	NULL	NULL	NULL	MAb 24c5	GP		bind					GC	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
12288	6	4719	6	NULL	NULL	NULL	NULL	MAb 24c5	GP		bind					AM	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
12289	7	4719	6	NULL	NULL	NULL	NULL	MAb 24c5	GP		bind					LAM	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
12290	8	4719	6	NULL	NULL	NULL	NULL	LAM	Chemical		is					lipoarabinomannan	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
12291	9	4719	6	NULL	NULL	NULL	NULL	MAb 24c5	GP		bind					PIM	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
12292	10	4719	6	NULL	NULL	NULL	NULL	PIM	Chemical		is					phosphatidylinositol mannoside	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
12293	11	4719	6	NULL	NULL	NULL	NULL	MAb 24c5	GP		bind					LM	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
12294	12	4719	6	NULL	NULL	NULL	NULL	LM	Chemical		is					fast-growing mycobacterial lipomannan	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
12295	13	4719	6	NULL	NULL	NULL	NULL	MAb 24c5	GP		bind					mAGP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
12296	14	4719	6	NULL	NULL	NULL	NULL	mAGP	Chemical		is					mycolyl-arabinogalactan-peptidoglycan complex	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
12297	15	4719	6	NULL	NULL	NULL	NULL	MAb 24c5	GP		bind					TLF	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
12298	16	4719	6	NULL	NULL	NULL	NULL	TLF	OrganismPart		is					total lipid fraction	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_145	11953397	(C) MAb 24c5 binding to  M. tuberculosis Erdman day-20 7H9 medium (MTB), cell culture supernatant extract (INTPHSE), GC, AM, lipoarabinomannan (LAM), phosphatidylinositol mannoside (PIM), fast-growing mycobacterial lipomannan (LM), mycolyl-arabinogalactan-peptidoglycan complex (mAGP), and total lipid fraction (TLF).	bind
13849	1	4720	5	NULL	NULL	0	NULL	Hsp70	NULL		bind	NULL				DC	NULL	immature			NULL		0	NULL	NULL	NULL	gw60_immunity_17_3_353_s_40	12354387	(C) Maleylated BSA inhibits Hsp70 binding to immature DC.	bind
13850	2	4720	5	NULL	NULL	0	NULL	BSA	NULL	maleylated	inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_17_3_353_s_40	12354387	(C) Maleylated BSA inhibits Hsp70 binding to immature DC.	bind
11918	1	4720	6	NULL	NULL	NULL	NULL	Hsp70	GP		bind					DC	Cell	immature			NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_3_353_s_40	12354387	(C) Maleylated BSA inhibits Hsp70 binding to immature DC.	bind
11919	2	4720	6	NULL	NULL	NULL	NULL	BSA	OrganismPart	maleylated	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_3_353_s_40	12354387	(C) Maleylated BSA inhibits Hsp70 binding to immature DC.	bind
13851	1	4721	5	NULL	NULL	0	NULL		NULL		bind	NULL		Kalirin domains		TrkA	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_5106_s_277	15923627	(C) Mapping of Kalirin domains that bind TrkA by a GST  pulldown assay.	bind
11920	1	4721	6	NULL	NULL	NULL	NULL				bind			Kalirin domains		TrkA	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_5106_s_277	15923627	(C) Mapping of Kalirin domains that bind TrkA by a GST  pulldown assay.	bind
13852	1	4724	5	NULL	NULL	0	NULL	Mdl1	NULL		bind	NULL				F1F0-ATP synthase	NULL		F0 moiety		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_37_38338_s_173	15247210	(C) Mdl1 binds to the F0 moiety of the F1F0-ATP synthase.	bind
11921	1	4724	6	NULL	NULL	NULL	NULL	Mdl1	GP		bind					F1F0-ATP synthase	GP		F0 moiety		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_37_38338_s_173	15247210	(C) Mdl1 binds to the F0 moiety of the F1F0-ATP synthase.	bind
13853	1	4725	5	10	NULL	0	NULL	p53			bind					Apaf-1				promoter	NULL	MEF	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_9_3492_s_119	16611991	(C) MEFs (p53+/+) and primary MEFs (p53+/+) were analyzed by ChIP for p53 binding to the  Apaf-1 gene promoter in the absence of stress.	bind
54483	2	4725	5	10	NULL	0	NULL	p53			bind					Apaf-1				promoter	NULL	primary MEF	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_9_3492_s_119	16611991	(C) MEFs (p53+/+) and primary MEFs (p53+/+) were analyzed by ChIP for p53 binding to the  Apaf-1 gene promoter in the absence of stress.	bind
11997	1	4725	6	NULL	NULL	NULL	NULL	p53	GP		bind					Apaf-1 	GP			promoter	NULL	MEF	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_9_3492_s_119	16611991	(C) MEFs (p53+/+) and primary MEFs (p53+/+) were analyzed by ChIP for p53 binding to the  Apaf-1 gene promoter in the absence of stress.	bind
11998	2	4725	6	NULL	NULL	NULL	NULL	p53	GP		bind					Apaf-1	GP			promoter	NULL	primary MEF	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_9_3492_s_119	16611991	(C) MEFs (p53+/+) and primary MEFs (p53+/+) were analyzed by ChIP for p53 binding to the  Apaf-1 gene promoter in the absence of stress.	bind
13854	1	4726	5	NULL	NULL	0	NULL	MIBP1	NULL		bind	NULL				SSTR-2	NULL			promoter	NULL	in vivo	0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3736_s_122	10207097	(C) MIBP1 binds to the SSTR-2 promoter in vivo.	bind
11999	1	4726	6	NULL	NULL	NULL	NULL	MIBP1	GP		bind					SSTR-2	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3736_s_122	10207097	(C) MIBP1 binds to the SSTR-2 promoter in vivo.	bind
13855	1	4727	5	NULL	NULL	0	NULL	MKP5	NULL		bind	NULL				JNK	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_19_8619_s_258	16166642	(c) MKP5 binding to JNK increases  in cells that were treated with JAMP siRNA.	bind
44571	2	4727	5	10	NULL	0	NULL	JAMP siRNA	NULL		increase	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_19_8619_s_258	16166642	(c) MKP5 binding to JNK increases  in cells that were treated with JAMP siRNA.	bind
12000	1	4727	6	NULL	NULL	NULL	NULL	MKP5	GP		bind					JNK	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8619_s_258	16166642	(c) MKP5 binding to JNK increases  in cells that were treated with JAMP siRNA.	bind
12001	2	4727	6	NULL	NULL	NULL	NULL	JAMP siRNA	NucleicAcid		increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8619_s_258	16166642	(c) MKP5 binding to JNK increases  in cells that were treated with JAMP siRNA.	bind
13857	1	4728	5	10	NULL	0	NULL	MOD1			bind					CAF-1			p150 N-terminal domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_4_529_s_65	10549285	(C) MOD1 binds to CAF-1 primarily through the p150 N-terminal domain.	bind
12002	1	4728	6	NULL	NULL	NULL	NULL	MOD1	GP		bind					CAF-1	GP		p150 N-terminal domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_4_529_s_65	10549285	(C) MOD1 binds to CAF-1 primarily through the p150 N-terminal domain.	bind
13859	1	4729	5	10	NULL	0	NULL	 transcription factor		dimeric	bind					ERK2 dimer					NULL		NULL	NULL	NULL	NULL	gw60_cell_93_4_605_s_166	9604935	(C) Model of a dimeric transcription factor bound to an ERK2 dimer.	bind
15186	1	4729	6	NULL	NULL	NULL	NULL	transcription factor	GP	dimeric	bind					ERK2 dimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_93_4_605_s_166	9604935	(C) Model of a dimeric transcription factor bound to an ERK2 dimer.	bind
13860	1	4730	5	10	NULL	0	NULL	CopG			bind					DNA					NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_18_4943_s_40	12193609	(C) Model of CopG binding to its target DNA.	bind
12003	1	4730	6	NULL	NULL	NULL	NULL	CopG	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_18_4943_s_40	12193609	(C) Model of CopG binding to its target DNA.	bind
13861	1	4731	5	NULL	NULL	0	NULL	Mona	NULL		does not bind	NULL		SH2 domain		Gab3	NULL	phosphorylated	tyrosine		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_160	11997510	(C) Mona SH2 domain does not bind to tyrosine phosphorylated Gab3.	bind
12004	1	4731	6	NULL	NULL	NULL	NULL	Mona	GP		does not bind			SH2 domain		Gab3	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3744_s_160	11997510	(C) Mona SH2 domain does not bind to tyrosine phosphorylated Gab3.	bind
13862	1	4732	5	NULL	NULL	0	NULL	Six3	NULL	mouse	bind	NULL				Grg4	NULL				NULL	in mammalian cells	0	NULL	NULL	NULL	gw60_development_129_12_2835_s_153	12050133	(C) Mouse Six3 bound to Grg4 in mammalian cells.	bind
12005	1	4732	6	NULL	NULL	NULL	NULL	Six3	GP	mouse	bind					Grg4	GP				NULL	mammalian cells	NULL	NULL	NULL	NULL	gw60_development_129_12_2835_s_153	12050133	(C) Mouse Six3 bound to Grg4 in mammalian cells.	bind
13863	1	4734	5	NULL	NULL	0	NULL	Munc13-1	NULL		bind	NULL				RIM1	NULL		84 residue zinc finger domain		NULL		0	NULL	NULL	NULL	gw60_neuron_30_1_183_s_146	11343654	(C) Munc13-1 and Rab3A bind to the same 84 residue zinc finger domain of RIM1.	bind
13864	2	4734	5	NULL	NULL	0	NULL	Rab3A	NULL		bind	NULL				RIM1	NULL		84 residue zinc finger domain		NULL		0	NULL	NULL	NULL	gw60_neuron_30_1_183_s_146	11343654	(C) Munc13-1 and Rab3A bind to the same 84 residue zinc finger domain of RIM1.	bind
12006	1	4734	6	NULL	NULL	NULL	NULL	Munc13-1	GP		bind					RIM1	GP		84 residue zinc finger domain		NULL		NULL	NULL	NULL	NULL	gw60_neuron_30_1_183_s_146	11343654	(C) Munc13-1 and Rab3A bind to the same 84 residue zinc finger domain of RIM1.	bind
12007	2	4734	6	NULL	NULL	NULL	NULL	Rab3A	GP		bind					RIM1	GP		84 residue zinc finger domain		NULL		NULL	NULL	NULL	NULL	gw60_neuron_30_1_183_s_146	11343654	(C) Munc13-1 and Rab3A bind to the same 84 residue zinc finger domain of RIM1.	bind
13865	1	4735	5	NULL	NULL	0	NULL	RNF5	NULL	mutant	bind	NULL				paxillin	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_15_5331_s_134	12861019	(C) Mutant forms of RNF5 exhibit stronger binding to paxillin than wild-type RNF5.	bind
13866	2	4735	5	NULL	NULL	0	NULL	RNF5	NULL	wild-type	bind	NULL				paxillin	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_15_5331_s_134	12861019	(C) Mutant forms of RNF5 exhibit stronger binding to paxillin than wild-type RNF5.	bind
13867	3	4735	5	NULL	NULL	0	NULL	statement 1	NULL		is stronger than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_15_5331_s_134	12861019	(C) Mutant forms of RNF5 exhibit stronger binding to paxillin than wild-type RNF5.	bind
12008	1	4735	6	NULL	NULL	NULL	NULL	RNF5	GP	wild type	bind					paxillin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_15_5331_s_134	12861019	(C) Mutant forms of RNF5 exhibit stronger binding to paxillin than wild-type RNF5.	bind
12009	2	4735	6	NULL	NULL	NULL	NULL	RNF5	GP	mutant	bind					paxillin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_15_5331_s_134	12861019	(C) Mutant forms of RNF5 exhibit stronger binding to paxillin than wild-type RNF5.	bind
12010	3	4735	6	NULL	NULL	NULL	NULL	statement 2	Process		is greater than					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_15_5331_s_134	12861019	(C) Mutant forms of RNF5 exhibit stronger binding to paxillin than wild-type RNF5.	bind
13868	1	4736	5	NULL	NULL	0	NULL	Tom22	NULL	mutant	alter	NULL		cytosolic domain		Tom40	NULL	oligomeric structure of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_9_5256_s_140	9710610	(C) Mutations in the cytosolic domain of Tom22 alter the oligomeric structure of Tom40.	bind
12011	1	4736	6	NULL	NULL	NULL	NULL	Tom22	GP	mutant	alter			cytosolic domain		Tom40	GP	oligomeric structure of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5256_s_140	9710610	(C) Mutations in the cytosolic domain of Tom22 alter the oligomeric structure of Tom40.	bind
13869	1	4737	5	NULL	NULL	0	NULL	Vg1RBP/Vera	NULL		bind	NULL				Vg1 LS	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_242	15292452	(C) Mutations within E2 or R1 motifs do not affect binding of Vg1RBP/Vera  to the Vg1 LS and Xcat2 3'UTR.	bind
13870	2	4737	5	NULL	NULL	0	NULL	Vg1RBP/Vera	NULL		bind	NULL				Xcat2	NULL			3'UTR	NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_242	15292452	(C) Mutations within E2 or R1 motifs do not affect binding of Vg1RBP/Vera  to the Vg1 LS and Xcat2 3'UTR.	bind
13871	3	4737	5	NULL	NULL	0	NULL		NULL	mutant	does not affect	NULL			E2 motif	statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_242	15292452	(C) Mutations within E2 or R1 motifs do not affect binding of Vg1RBP/Vera  to the Vg1 LS and Xcat2 3'UTR.	bind
13872	4	4737	5	NULL	NULL	0	NULL		NULL	mutant	does not affect	NULL			R1 motif	statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_242	15292452	(C) Mutations within E2 or R1 motifs do not affect binding of Vg1RBP/Vera  to the Vg1 LS and Xcat2 3'UTR.	bind
13873	5	4737	5	NULL	NULL	0	NULL	statement 3	NULL		is an alternative to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_242	15292452	(C) Mutations within E2 or R1 motifs do not affect binding of Vg1RBP/Vera  to the Vg1 LS and Xcat2 3'UTR.	bind
13874	6	4737	5	NULL	NULL	0	NULL		NULL	mutant	does not affect	NULL			E2 motif	statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_242	15292452	(C) Mutations within E2 or R1 motifs do not affect binding of Vg1RBP/Vera  to the Vg1 LS and Xcat2 3'UTR.	bind
13875	7	4737	5	NULL	NULL	0	NULL		NULL	mutant	does not affect	NULL			R1 motif	statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_242	15292452	(C) Mutations within E2 or R1 motifs do not affect binding of Vg1RBP/Vera  to the Vg1 LS and Xcat2 3'UTR.	bind
13876	8	4737	5	NULL	NULL	0	NULL	statement 6	NULL		is an alternative to	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_242	15292452	(C) Mutations within E2 or R1 motifs do not affect binding of Vg1RBP/Vera  to the Vg1 LS and Xcat2 3'UTR.	bind
12012	1	4737	6	NULL	NULL	NULL	NULL	Vg1RBP/Vera	GP		bind					Vg1	GP		LS		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_242	15292452	(C) Mutations within E2 or R1 motifs do not affect binding of Vg1RBP/Vera  to the Vg1 LS and Xcat2 3'UTR.	bind
12013	2	4737	6	NULL	NULL	NULL	NULL	Vg1RBP/Vera	GP		bind					Xcat2	GP			3'UTR	NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_242	15292452	(C) Mutations within E2 or R1 motifs do not affect binding of Vg1RBP/Vera  to the Vg1 LS and Xcat2 3'UTR.	bind
15187	3	4737	6	NULL	NULL	NULL	NULL			mutations of	do not affect			E2 motif		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_242	15292452	(C) Mutations within E2 or R1 motifs do not affect binding of Vg1RBP/Vera  to the Vg1 LS and Xcat2 3'UTR.	bind
15188	4	4737	6	NULL	NULL	NULL	NULL			mutations of	do not affect			R1 motif		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_242	15292452	(C) Mutations within E2 or R1 motifs do not affect binding of Vg1RBP/Vera  to the Vg1 LS and Xcat2 3'UTR.	bind
15189	5	4737	6	NULL	NULL	NULL	NULL			mutations of	do not affect			E2 motif		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_242	15292452	(C) Mutations within E2 or R1 motifs do not affect binding of Vg1RBP/Vera  to the Vg1 LS and Xcat2 3'UTR.	bind
15190	6	4737	6	NULL	NULL	NULL	NULL			mutations of	do not affect			R1 motif		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_242	15292452	(C) Mutations within E2 or R1 motifs do not affect binding of Vg1RBP/Vera  to the Vg1 LS and Xcat2 3'UTR.	bind
54491	7	4737	6	NULL	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_242	15292452	(C) Mutations within E2 or R1 motifs do not affect binding of Vg1RBP/Vera  to the Vg1 LS and Xcat2 3'UTR.	bind
54492	8	4737	6	NULL	NULL	NULL	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_10_4669_s_242	15292452	(C) Mutations within E2 or R1 motifs do not affect binding of Vg1RBP/Vera  to the Vg1 LS and Xcat2 3'UTR.	bind
13877	1	4738	5	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				probe B	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2098_s_209	10022897	(C) Mutual exclusive binding of Sp1 and NF-kappaB p50 to probe B.	bind
13878	2	4738	5	NULL	NULL	0	NULL	NF-kappaB p50	NULL		bind	NULL				probe B	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2098_s_209	10022897	(C) Mutual exclusive binding of Sp1 and NF-kappaB p50 to probe B.	bind
13879	3	4738	5	NULL	NULL	0	NULL	statement 1	NULL		mutually exclusive to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2098_s_209	10022897	(C) Mutual exclusive binding of Sp1 and NF-kappaB p50 to probe B.	bind
12015	1	4738	6	NULL	NULL	NULL	NULL	Sp1	GP		bind					probe B					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2098_s_209	10022897	(C) Mutual exclusive binding of Sp1 and NF-kappaB p50 to probe B.	bind
12016	2	4738	6	NULL	NULL	NULL	NULL	NF-kappaB p50	GP		bind					probe B					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2098_s_209	10022897	(C) Mutual exclusive binding of Sp1 and NF-kappaB p50 to probe B.	bind
12017	3	4738	6	NULL	NULL	NULL	NULL	statement 1	Process		is independent of					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2098_s_209	10022897	(C) Mutual exclusive binding of Sp1 and NF-kappaB p50 to probe B.	bind
13880	1	4739	5	NULL	NULL	0	NULL	Myricetin	NULL		bind	NULL				PI3K	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_6_4_909_s_221	11090628	(C) Myricetin binding to PI3K  as compared with quercetin binding to PI3K .	bind
13881	2	4739	5	NULL	NULL	0	NULL	quercetin	NULL		bind	NULL				PI3K	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_6_4_909_s_221	11090628	(C) Myricetin binding to PI3K  as compared with quercetin binding to PI3K .	bind
12018	1	4739	6	NULL	NULL	NULL	NULL	Myricetin	GP		bind					PI3K	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_4_909_s_221	11090628	(C) Myricetin binding to PI3K  as compared with quercetin binding to PI3K .	bind
12019	2	4739	6	NULL	NULL	NULL	NULL	quercetin	GP		bind					PI3K	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_4_909_s_221	11090628	(C) Myricetin binding to PI3K  as compared with quercetin binding to PI3K .	bind
13882	1	4740	5	NULL	NULL	0	NULL	AP-2 protein	NULL		does not bind	NULL		N-terminally deleted		RB	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_3647_s_227	9632747	(C) N-terminally deleted AP-2 protein does not bind to RB.	bind
12020	1	4740	6	NULL	NULL	NULL	NULL	AP-2 protein	GP		does not bind			N-terminally deleted		RB	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_3647_s_227	9632747	(C) N-terminally deleted AP-2 protein does not bind to RB.	bind
13883	1	4741	5	NULL	NULL	0	NULL	Nef	NULL		bind	NULL				PAK1	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_20_7_2619_s_111	10713183	(C) Nef binds to PAK1 in vitro.	bind
12021	1	4741	6	NULL	NULL	NULL	NULL	Nef	GP		bind					PAK1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_7_2619_s_111	10713183	(C) Nef binds to PAK1 in vitro.	bind
13884	1	4742	5	NULL	NULL	0	NULL	Neurexin	NULL		bind	NULL				neuroligin	NULL	mutants of			NULL		0	NULL	NULL	NULL	gw60_cell_101_6_657_s_190	10892652	(C) Neurexin binding of neuroligin mutants.	bind
12022	1	4742	6	NULL	NULL	NULL	NULL	Neurexin	GP		bind					neuroligin	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_cell_101_6_657_s_190	10892652	(C) Neurexin binding of neuroligin mutants.	bind
13885	1	4743	5	NULL	NULL	0	NULL	aconitase	NULL	newly translated in E. coli	bind	NULL				GroEL	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_107_2_235_s_48	11672530	(c) Newly translated aconitase in  E. coli is  bound to GroEL and released from it  in the presence but not absence of  GroES.	bind
13886	2	4743	5	NULL	NULL	0	NULL	aconitase	NULL	newly translated in E. coli	is released from	NULL				GroEL	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_107_2_235_s_48	11672530	(c) Newly translated aconitase in  E. coli is  bound to GroEL and released from it  in the presence but not absence of  GroES.	bind
13887	3	4743	5	NULL	NULL	0	NULL	statement 2	NULL		in the presence of	NULL	only			GroES	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_107_2_235_s_48	11672530	(c) Newly translated aconitase in  E. coli is  bound to GroEL and released from it  in the presence but not absence of  GroES.	bind
12023	1	4743	6	NULL	NULL	NULL	NULL	aconitase	GP	newly translated;; E.coli	bind					GroEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_235_s_48	11672530	(c) Newly translated aconitase in  E. coli is  bound to GroEL and released from it  in the presence but not absence of  GroES.	bind
12024	2	4743	6	NULL	NULL	NULL	NULL	aconitase	GP	newly translated;; E.coli	released from					GroEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_235_s_48	11672530	(c) Newly translated aconitase in  E. coli is  bound to GroEL and released from it  in the presence but not absence of  GroES.	bind
12025	3	4743	6	NULL	NULL	NULL	NULL	statement 2	Process		occurs in presence of					GroES	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_235_s_48	11672530	(c) Newly translated aconitase in  E. coli is  bound to GroEL and released from it  in the presence but not absence of  GroES.	bind
13888	1	4744	5	NULL	NULL	0	NULL	class II UNC-86 	NULL	mutant	bind	NULL	very weakly			CS1 oligonucleotide	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_13_4806_s_161	10848606	(C) No or very weak binding of class II and III UNC-86 mutants to the CS1 oligonucleotide could be detected at the protein concentrations used.	bind
13889	2	4744	5	NULL	NULL	0	NULL	class III UNC-86	NULL	mutant	bind	NULL	very weakly			CS1 oligonucleotide	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_13_4806_s_161	10848606	(C) No or very weak binding of class II and III UNC-86 mutants to the CS1 oligonucleotide could be detected at the protein concentrations used.	bind
54493	3	4744	5	10	NULL	0	NULL	class II UNC-86		mutant	does not bind					CS1 oligonucleotide					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4806_s_161	10848606	(C) No or very weak binding of class II and III UNC-86 mutants to the CS1 oligonucleotide could be detected at the protein concentrations used.	bind
54494	4	4744	5	10	NULL	0	NULL	class III UNC-86		mutant	does not bind					CS1 oligonucleotide					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_13_4806_s_161	10848606	(C) No or very weak binding of class II and III UNC-86 mutants to the CS1 oligonucleotide could be detected at the protein concentrations used.	bind
54495	5	4744	5	10	NULL	0	NULL	statement 1			is an alternative to					statement 3					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_13_4806_s_161	10848606	(C) No or very weak binding of class II and III UNC-86 mutants to the CS1 oligonucleotide could be detected at the protein concentrations used.	bind
54496	6	4744	5	10	NULL	0	NULL	statement 2			is an alternative to					statement 4					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_13_4806_s_161	10848606	(C) No or very weak binding of class II and III UNC-86 mutants to the CS1 oligonucleotide could be detected at the protein concentrations used.	bind
12026	1	4744	6	NULL	NULL	NULL	NULL	class II UNC-86	GP	mutant	bind		weakly			CS1 oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4806_s_161	10848606	(C) No or very weak binding of class II and III UNC-86 mutants to the CS1 oligonucleotide could be detected at the protein concentrations used.	bind
12027	2	4744	6	NULL	NULL	NULL	NULL	class III UNC-86	GP	mutant	bind		weakly			CS1 oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4806_s_161	10848606	(C) No or very weak binding of class II and III UNC-86 mutants to the CS1 oligonucleotide could be detected at the protein concentrations used.	bind
12028	3	4744	6	NULL	NULL	NULL	NULL	class II UNC-86	GP	mutant	does not bind					CS1 oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4806_s_161	10848606	(C) No or very weak binding of class II and III UNC-86 mutants to the CS1 oligonucleotide could be detected at the protein concentrations used.	bind
12029	4	4744	6	NULL	NULL	NULL	NULL	class III UNC-86	GP	mutant	does not bind					CS1 oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4806_s_161	10848606	(C) No or very weak binding of class II and III UNC-86 mutants to the CS1 oligonucleotide could be detected at the protein concentrations used.	bind
12030	5	4744	6	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4806_s_161	10848606	(C) No or very weak binding of class II and III UNC-86 mutants to the CS1 oligonucleotide could be detected at the protein concentrations used.	bind
12031	6	4744	6	NULL	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4806_s_161	10848606	(C) No or very weak binding of class II and III UNC-86 mutants to the CS1 oligonucleotide could be detected at the protein concentrations used.	bind
13890	1	4745	5	NULL	NULL	0	NULL	NSF	NULL		does not bind	NULL	alone			PICK1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_63	11931741	(C) NSF does not bind PICK1 alone.	bind
12032	1	4745	6	NULL	NULL	NULL	NULL	NSF	GP		does not bind		alone			PICK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_63	11931741	(C) NSF does not bind PICK1 alone.	bind
13891	3	4746	5	10	NULL	0	NULL	statement 1			is not increased by					HNF3betaloxP/loxP; Alb					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_14_5175_s_161	10866673	(C) Nuclear binding activities of HNF3alpha and HNF3gamma are not increased in HNF3betaloxP/loxP; Alb.	bind
13892	4	4746	5	10	NULL	0	NULL	statement 2			is not increased by					HNF3betaloxP/loxP; Alb					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_14_5175_s_161	10866673	(C) Nuclear binding activities of HNF3alpha and HNF3gamma are not increased in HNF3betaloxP/loxP; Alb.	bind
54497	1	4746	5	10	NULL	0	NULL	HNF3alpha 			possess					 Nuclear binding activity					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_14_5175_s_161	10866673	(C) Nuclear binding activities of HNF3alpha and HNF3gamma are not increased in HNF3betaloxP/loxP; Alb.	bind
54498	2	4746	5	10	NULL	0	NULL	HNF3gamma			possess					Nuclear binding activity					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_14_5175_s_161	10866673	(C) Nuclear binding activities of HNF3alpha and HNF3gamma are not increased in HNF3betaloxP/loxP; Alb.	bind
15191	1	4746	6	NULL	NULL	NULL	NULL	HNF3alpha	GP		possess					Nuclear binding activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_14_5175_s_161	10866673	(C) Nuclear binding activities of HNF3alpha and HNF3gamma are not increased in HNF3betaloxP/loxP; Alb.	bind
15192	2	4746	6	NULL	NULL	NULL	NULL	HNF3gamma	GP		possess					Nuclear binding activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_14_5175_s_161	10866673	(C) Nuclear binding activities of HNF3alpha and HNF3gamma are not increased in HNF3betaloxP/loxP; Alb.	bind
41570	3	4746	6	NULL	NULL	NULL	NULL	statement 1	Process		is not increased by					HNF3betaloxP/loxP; Alb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_14_5175_s_161	10866673	(C) Nuclear binding activities of HNF3alpha and HNF3gamma are not increased in HNF3betaloxP/loxP; Alb.	bind
41571	4	4746	6	NULL	NULL	NULL	NULL	statement 2	Process		is not increased by					HNF3betaloxP/loxP; Alb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_14_5175_s_161	10866673	(C) Nuclear binding activities of HNF3alpha and HNF3gamma are not increased in HNF3betaloxP/loxP; Alb.	bind
13893	1	4749	5	NULL	NULL	0	NULL	Optineurin	NULL		bind	NULL				myosin VI	NULL	purified	tail		NULL		0	NULL	NULL	NULL	gw70_cellbiol_169_2_285_s_63	15837803	(C) Optineurin binds to purified  myosin VI tail.	bind
12033	1	4749	6	NULL	NULL	NULL	NULL	optineurin	GP		bind					myosin VI 	GP	purified	tail		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_169_2_285_s_63	15837803	(C) Optineurin binds to purified  myosin VI tail.	bind
13894	1	4750	5	NULL	NULL	0	NULL	UBF	NULL		bind	NULL				rRNA gene	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_7_2539_s_178	15767661	(C) Overexpression of TIP5 impairs binding  of UBF to the rRNA gene promoter.	bind
13895	2	4750	5	NULL	NULL	0	NULL	TIP5	NULL	overexpression of	impairs	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_7_2539_s_178	15767661	(C) Overexpression of TIP5 impairs binding  of UBF to the rRNA gene promoter.	bind
12034	1	4750	6	NULL	NULL	NULL	NULL	UBF	GP		bind					rRNA 	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_7_2539_s_178	15767661	(C) Overexpression of TIP5 impairs binding  of UBF to the rRNA gene promoter.	bind
12035	2	4750	6	NULL	NULL	NULL	NULL	TIP5 	GP	overexpression of	impairs					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_7_2539_s_178	15767661	(C) Overexpression of TIP5 impairs binding  of UBF to the rRNA gene promoter.	bind
13896	1	4755	5	NULL	NULL	0	NULL	OxyR	NULL		bind	NULL				ahpC	NULL	M. marinum		promoter region	NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_7_2674_s_134	16547055	(C) OxyR binds to the  M. marinum ahpC promoter region.	bind
12036	1	4755	6	NULL	NULL	NULL	NULL	OxyR	GP		bind					ahpC	GP	M. marinum		promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_7_2674_s_134	16547055	(C) OxyR binds to the  M. marinum ahpC promoter region.	bind
13897	1	4756	5	10	NULL	0	NULL	p27		phosphorylated	bind			serine 10		GRB2					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_11_3735_s_293	12748278	(C) p27 bound to GRB2 is phosphorylated on serine  10.	bind
12037	1	4756	6	NULL	NULL	NULL	NULL	p27	GP	phosphorylated	bind			serine 10		GRB2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_11_3735_s_293	12748278	(C) p27 bound to GRB2 is phosphorylated on serine  10.	bind
13899	1	4758	5	NULL	NULL	0	NULL	p53	NULL		bind	NULL	specifically				NULL			p53RE-1	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5602_s_205	10891498	(C) p53 binds specifically to both p53RE-1 and p53RE-2 in vitro.	bind
13900	2	4758	5	NULL	NULL	0	NULL	p53	NULL		bind	NULL	specifically				NULL			p53RE-2	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5602_s_205	10891498	(C) p53 binds specifically to both p53RE-1 and p53RE-2 in vitro.	bind
12038	1	4758	6	NULL	NULL	NULL	NULL	p53	GP		bind		specifically							p53RE-1	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5602_s_205	10891498	(C) p53 binds specifically to both p53RE-1 and p53RE-2 in vitro.	bind
12039	2	4758	6	NULL	NULL	NULL	NULL	p53	GP		bind		specifically							p53RE-2	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5602_s_205	10891498	(C) p53 binds specifically to both p53RE-1 and p53RE-2 in vitro.	bind
13901	1	4759	5	NULL	NULL	0	NULL	CREB	NULL		bind	NULL				CBP	NULL		KIX domain		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_13_4849_s_96	10848610	(C) p53 does not enhance the binding of CREB to the KIX domain of CBP.	bind
13902	2	4759	5	NULL	NULL	0	NULL	p53	NULL		does not enhance	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_13_4849_s_96	10848610	(C) p53 does not enhance the binding of CREB to the KIX domain of CBP.	bind
12040	1	4759	6	NULL	NULL	NULL	NULL	CREB	GP		bind					CBP	GP		KIX domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4849_s_96	10848610	(C) p53 does not enhance the binding of CREB to the KIX domain of CBP.	bind
12041	2	4759	6	NULL	NULL	NULL	NULL	p53	GP		does not enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4849_s_96	10848610	(C) p53 does not enhance the binding of CREB to the KIX domain of CBP.	bind
13903	1	4760	5	NULL	NULL	0	NULL	SRC-1	NULL		bind	NULL				Nur77	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_7_2593_s_271	15024051	(C) p65  interfered with the binding of the coactivator SRC-1 to Nur77 in GST pull-down assays.	bind
13904	2	4760	5	NULL	NULL	0	NULL	p65	NULL		interferes with	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_7_2593_s_271	15024051	(C) p65  interfered with the binding of the coactivator SRC-1 to Nur77 in GST pull-down assays.	bind
54505	3	4760	5	10	NULL	0	NULL	SRC-1			is a type of					coactivator					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_7_2593_s_271	15024051	(C) p65  interfered with the binding of the coactivator SRC-1 to Nur77 in GST pull-down assays.	bind
12042	1	4760	6	NULL	NULL	NULL	NULL	SRC-1	GP		bind					Nur77	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_7_2593_s_271	15024051	(C) p65  interfered with the binding of the coactivator SRC-1 to Nur77 in GST pull-down assays.	bind
12043	2	4760	6	NULL	NULL	NULL	NULL	p65	GP		interferes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_7_2593_s_271	15024051	(C) p65  interfered with the binding of the coactivator SRC-1 to Nur77 in GST pull-down assays.	bind
41575	3	4760	6	NULL	NULL	NULL	NULL	SRC-1	GP		is a type of					coactivator	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_7_2593_s_271	15024051	(C) p65  interfered with the binding of the coactivator SRC-1 to Nur77 in GST pull-down assays.	bind
13905	1	4761	5	NULL	NULL	0	NULL	p73	NULL		bind	NULL				p73	NULL		Ndelta		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_8_3536_s_329	15060172	(C) p73 binds to p73Ndelta but not to p73 lacking the putative tetramerization domain.	bind
13906	2	4761	5	10	NULL	0	NULL	p73			does not bind					p73		lacking;;putative	 tetramerization domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_8_3536_s_329	15060172	(C) p73 binds to p73Ndelta but not to p73 lacking the putative tetramerization domain.	bind
12044	1	4761	6	NULL	NULL	0	NULL	p73	NULL		bind	NULL				p73	NULL		Ndelta		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_8_3536_s_329	15060172	(C) p73 binds to p73Ndelta but not to p73 lacking the putative tetramerization domain.	bind
12045	2	4761	6	NULL	NULL	0	NULL	p73	NULL		does not bind	NULL				p73	NULL	lacking;; putative	tetramerization domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_8_3536_s_329	15060172	(C) p73 binds to p73Ndelta but not to p73 lacking the putative tetramerization domain.	bind
13907	1	4762	5	NULL	NULL	0	NULL	PAG3	NULL		bind	NULL				paxillin isoforms	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1315_s_142	10749932	(C) PAG3 binding to paxillin isoforms.	bind
12046	1	4762	6	NULL	NULL	NULL	NULL	PAG3	GP		bind					paxillin isoforms	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1315_s_142	10749932	(C) PAG3 binding to paxillin isoforms.	bind
13908	1	4763	5	NULL	NULL	0	NULL	PAK	NULL		bind	NULL				PIX-GIT1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_11_3906_s_247	10805734	(C) PAK binding to PIX-GIT1 is negatively regulated by kinase activation.	bind
13909	2	4763	5	10	NULL	0	NULL	statement 1			regulated by		negatively			kinase		activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3906_s_247	10805734	(C) PAK binding to PIX-GIT1 is negatively regulated by kinase activation.	bind
12047	1	4763	6	NULL	NULL	NULL	NULL	PAK	GP		bind					PIX-GIT1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3906_s_247	10805734	(C) PAK binding to PIX-GIT1 is negatively regulated by kinase activation.	bind
12048	2	4763	6	NULL	NULL	NULL	NULL	statement 1	Process		regulated by		negatively 			kinase	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_3906_s_247	10805734	(C) PAK binding to PIX-GIT1 is negatively regulated by kinase activation.	bind
13910	1	4764	5	NULL	NULL	0	NULL	Pax1	NULL		bind	NULL				oligonucleotide B4	NULL				NULL		0	NULL	NULL	NULL	gw70_development_130_3_473_s_126	12490554	(C) Pax1  binds to oligonucleotide B4.	bind
12049	1	4764	6	NULL	NULL	NULL	NULL	Pax1	GP		bind					oligonucleotide B4	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_development_130_3_473_s_126	12490554	(C) Pax1  binds to oligonucleotide B4.	bind
13911	1	4766	5	NULL	NULL	0	NULL		NULL		bind	NULL		N		GST-RDGCcat	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_32_6_1097_s_227	11754840	(C) Percent of N or NI12E bound to GST-RDGCcat in the presence of Ca2+/aM (from [B]).	bind
13912	2	4766	5	NULL	NULL	0	NULL		NULL		bind	NULL		NI12E		GST-RDGCcat 	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_32_6_1097_s_227	11754840	(C) Percent of N or NI12E bound to GST-RDGCcat in the presence of Ca2+/aM (from [B]).	bind
15587	3	4766	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				Ca2+	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_32_6_1097_s_227	11754840	(C) Percent of N or NI12E bound to GST-RDGCcat in the presence of Ca2+/aM (from [B]).	bind
15588	4	4766	5	NULL	NULL	0	NULL	statement 2	NULL		in the presence of	NULL				Ca2+	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_32_6_1097_s_227	11754840	(C) Percent of N or NI12E bound to GST-RDGCcat in the presence of Ca2+/aM (from [B]).	bind
12299	1	4766	6	NULL	NULL	NULL	NULL				bind			NI12E		GST-RDGCcat	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_6_1097_s_227	11754840	(C) Percent of N or NI12E bound to GST-RDGCcat in the presence of Ca2+/aM (from [B]).	bind
12300	2	4766	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs in presence of					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_6_1097_s_227	11754840	(C) Percent of N or NI12E bound to GST-RDGCcat in the presence of Ca2+/aM (from [B]).	bind
16241	3	4766	6	NULL	NULL	NULL	NULL				bind			N terminal domain		GST-RDGCcat	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_6_1097_s_227	11754840	(C) Percent of N or NI12E bound to GST-RDGCcat in the presence of Ca2+/aM (from [B]).	bind
16242	4	4766	6	NULL	NULL	NULL	NULL	statement 2	Process		occurs in presence of					Ca+2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_6_1097_s_227	11754840	(C) Percent of N or NI12E bound to GST-RDGCcat in the presence of Ca2+/aM (from [B]).	bind
13913	1	4767	5	NULL	NULL	0	NULL	PEX7	NULL		bind	NULL	inefficient			pex5-1	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_2_573_s_228	15548601	(C) PEX7 binding  with pex5-1 is inefficient, resulting in decreased PTS2 protein import and IBA resistance.	bind
13914	2	4767	5	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				PTS2 protein	NULL	decreased import of			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_2_573_s_228	15548601	(C) PEX7 binding  with pex5-1 is inefficient, resulting in decreased PTS2 protein import and IBA resistance.	bind
13915	3	4767	5	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				IBA resistance	NULL	decreased			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_2_573_s_228	15548601	(C) PEX7 binding  with pex5-1 is inefficient, resulting in decreased PTS2 protein import and IBA resistance.	bind
12050	1	4767	6	NULL	NULL	NULL	NULL	PEX7	GP		bind		inefficiently			pex5-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_573_s_228	15548601	(C) PEX7 binding  with pex5-1 is inefficient, resulting in decreased PTS2 protein import and IBA resistance.	bind
12051	2	4767	6	NULL	NULL	NULL	NULL	statement 1	Process		leads to					PTS2 protein 	GP	decreased import of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_573_s_228	15548601	(C) PEX7 binding  with pex5-1 is inefficient, resulting in decreased PTS2 protein import and IBA resistance.	bind
12052	3	4767	6	NULL	NULL	NULL	NULL	statement 1	Process		leads to					IBA 	Chemical	resistance of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_573_s_228	15548601	(C) PEX7 binding  with pex5-1 is inefficient, resulting in decreased PTS2 protein import and IBA resistance.	bind
14579	1	4768	5	10	NULL	0	NULL	EGFR		 blocking function of	diminishes					Ras/MAPK		active			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_103_s_65	12370245	(c) Pharmacologic blockade of EGFR function diminishes active Ras/MAPK, Gab1 tyrosine phosphorylation, and binding to SHP-2.	bind
14580	2	4768	5	10	NULL	0	NULL	EGFR		blocking  function of	diminishes					Gab1		phosphorylation	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_103_s_65	12370245	(c) Pharmacologic blockade of EGFR function diminishes active Ras/MAPK, Gab1 tyrosine phosphorylation, and binding to SHP-2.	bind
14581	3	4768	5	NULL	NULL	0	NULL	Gab1	NULL		bind	NULL				SHP-2	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_159_1_103_s_65	12370245	(c) Pharmacologic blockade of EGFR function diminishes active Ras/MAPK, Gab1 tyrosine phosphorylation, and binding to SHP-2.	bind
14582	4	4768	5	10	NULL	0	NULL	EGFR		blocking function of	diminishes					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_103_s_65	12370245	(c) Pharmacologic blockade of EGFR function diminishes active Ras/MAPK, Gab1 tyrosine phosphorylation, and binding to SHP-2.	bind
12053	1	4768	6	NULL	NULL	NULL	NULL	Gab1	GP		bind					SHP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_103_s_65	12370245	(c) Pharmacologic blockade of EGFR function diminishes active Ras/MAPK, Gab1 tyrosine phosphorylation, and binding to SHP-2.	bind
12054	2	4768	6	NULL	NULL	NULL	NULL	EGFR 	GP	blocking function of	diminishes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_103_s_65	12370245	(c) Pharmacologic blockade of EGFR function diminishes active Ras/MAPK, Gab1 tyrosine phosphorylation, and binding to SHP-2.	bind
12055	3	4768	6	NULL	NULL	NULL	NULL	Gab1	GP		is phosphorylated on								tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_103_s_65	12370245	(c) Pharmacologic blockade of EGFR function diminishes active Ras/MAPK, Gab1 tyrosine phosphorylation, and binding to SHP-2.	bind
12056	4	4768	6	NULL	NULL	NULL	NULL	EGFR	GP	blocking function of	diminishes					Ras/MAPK	GP	active			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_103_s_65	12370245	(c) Pharmacologic blockade of EGFR function diminishes active Ras/MAPK, Gab1 tyrosine phosphorylation, and binding to SHP-2.	bind
12452	5	4768	6	NULL	NULL	NULL	NULL	EGFR	GP	blocking function of	diminishes					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_1_103_s_65	12370245	(c) Pharmacologic blockade of EGFR function diminishes active Ras/MAPK, Gab1 tyrosine phosphorylation, and binding to SHP-2.	bind
13916	1	4769	5	NULL	NULL	0	NULL	PhoP P	NULL		bind	NULL				phoB-PS	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_15_5166_s_209	16030210	(C) PhoP P binds to the  phoB-PS promoter independent of the downstream direct repeats.	bind
13917	2	4769	5	NULL	NULL	0	NULL	statement 1	NULL		is independent of	NULL					NULL	downstream		direct repeats	NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_15_5166_s_209	16030210	(C) PhoP P binds to the  phoB-PS promoter independent of the downstream direct repeats.	bind
12057	1	4769	6	NULL	NULL	NULL	NULL	PhoP P 	GP		bind					phoB-PS	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_15_5166_s_209	16030210	(C) PhoP P binds to the  phoB-PS promoter independent of the downstream direct repeats.	bind
12058	2	4769	6	NULL	NULL	NULL	NULL	statement 1	Process		is independent of							downstream		direct repeats	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_15_5166_s_209	16030210	(C) PhoP P binds to the  phoB-PS promoter independent of the downstream direct repeats.	bind
13918	1	4770	5	NULL	NULL	0	NULL	DnaB	NULL	E. coli	bind	NULL				RTP	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_87_5_881_s_130	8945515	(C) Phosphorimager analyses  of the autoradiograms shown in (B); note that the mutations E30K and Y33N  have caused significant reduction in the binding of E. coli DnaB to the  RTP matrices.	bind
13919	2	4770	5	NULL	NULL	0	NULL		NULL	mutant	reduce	NULL	significantly	E30K		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_87_5_881_s_130	8945515	(C) Phosphorimager analyses  of the autoradiograms shown in (B); note that the mutations E30K and Y33N  have caused significant reduction in the binding of E. coli DnaB to the  RTP matrices.	bind
13920	3	4770	5	NULL	NULL	0	NULL		NULL	mutant	reduce	NULL	significantly	Y33N		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_87_5_881_s_130	8945515	(C) Phosphorimager analyses  of the autoradiograms shown in (B); note that the mutations E30K and Y33N  have caused significant reduction in the binding of E. coli DnaB to the  RTP matrices.	bind
12059	1	4770	6	NULL	NULL	NULL	NULL	DnaB	GP	E.coli	bind					RTP matrices	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_881_s_130	8945515	(C) Phosphorimager analyses  of the autoradiograms shown in (B); note that the mutations E30K and Y33N  have caused significant reduction in the binding of E. coli DnaB to the  RTP matrices.	bind
12060	2	4770	6	NULL	NULL	NULL	NULL			mutant	causes		significant	E30K		statement 1	Process	reduction in			NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_881_s_130	8945515	(C) Phosphorimager analyses  of the autoradiograms shown in (B); note that the mutations E30K and Y33N  have caused significant reduction in the binding of E. coli DnaB to the  RTP matrices.	bind
12061	3	4770	6	NULL	NULL	NULL	NULL			mutant	causes		significant	Y33N		statement 1	Process	reduction in			NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_881_s_130	8945515	(C) Phosphorimager analyses  of the autoradiograms shown in (B); note that the mutations E30K and Y33N  have caused significant reduction in the binding of E. coli DnaB to the  RTP matrices.	bind
13921	1	4771	5	NULL	NULL	0	NULL	PIP2	NULL		bind	NULL				syt I/IX constructs	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_162_2_199_s_211	12860971	(C) PIP2-binding activity of the indicated syt I/IX constructs was assayed as described in the legend to  Fig. 2 A. (D) PIP2 binding is correlated with inhibition of secretion.	bind
12062	1	4771	6	NULL	NULL	NULL	NULL	syt I/IX constructs			bind					PIP2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_162_2_199_s_211	12860971	(C) PIP2-binding activity of the indicated syt I/IX constructs was assayed as described in the legend to  Fig. 2 A. (D) PIP2 binding is correlated with inhibition of secretion.	bind
13922	1	4772	5	NULL	NULL	0	NULL	SRP	NULL		bind	NULL				bt-SR	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_162_4_575_s_173	12913112	(C) Plots of kon for SRP binding to bt-SR in the presence (solid symbols) or absence (open symbols)  of 25 muM GTP.	bind
12063	1	4772	6	NULL	NULL	NULL	NULL	SRP	GP		bind					bt-SR	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_4_575_s_173	12913112	(C) Plots of kon for SRP binding to bt-SR in the presence (solid symbols) or absence (open symbols)  of 25 muM GTP.	bind
13923	1	4774	5	NULL	NULL	0	NULL	p53	NULL	wild-type	bind	NULL				DNA	NULL	biotinylated target			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_7168_s_203	10490652	(C) PMA stimulates wild-type p53 binding to biotinylated target DNA.	bind
13924	2	4774	5	NULL	NULL	0	NULL	PMA	NULL		stimulate	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_10_7168_s_203	10490652	(C) PMA stimulates wild-type p53 binding to biotinylated target DNA.	bind
12064	1	4774	6	NULL	NULL	NULL	NULL	p53	GP	wild type	bind					target DNA	NucleicAcid	biotinylated			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_7168_s_203	10490652	(C) PMA stimulates wild-type p53 binding to biotinylated target DNA.	bind
12065	2	4774	6	NULL	NULL	NULL	NULL	PMA	Chemical		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_7168_s_203	10490652	(C) PMA stimulates wild-type p53 binding to biotinylated target DNA.	bind
13925	1	4775	5	NULL	NULL	0	NULL	Poly(ADP-ribose)	NULL		bind	NULL				hTRF2	NULL		myb domain		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1595_s_240	14749375	(C) Poly(ADP-ribose) binds  to the myb domain of hTRF2.	bind
12066	1	4775	6	NULL	NULL	NULL	NULL	Poly (ADP-ribose)	Chemical		bind					hTRF2	GP		myb domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_4_1595_s_240	14749375	(C) Poly(ADP-ribose) binds  to the myb domain of hTRF2.	bind
13926	1	4776	5	NULL	NULL	0	NULL	cdk4	NULL		bind	NULL				p16	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_1_3_421_s_189	9660926	(C) Positive control for the effect of R24C mutation on the binding of cdk4 to p16.	bind
12067	1	4776	6	NULL	NULL	NULL	NULL	cdk4	GP		bind					p16	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_3_421_s_189	9660926	(C) Positive control for the effect of R24C mutation on the binding of cdk4 to p16.	bind
13927	1	4777	5	NULL	NULL	0	NULL	pp32	NULL		bind	NULL				TAF-I	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_cell_104_1_119_s_128	11163245	(C) pp32 binds to TAF-I , and Set/TAF-Ibeta in vitro.	bind
13928	2	4777	5	NULL	NULL	0	NULL	pp32	NULL		bind	NULL				Set/TAF-Ibeta	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_cell_104_1_119_s_128	11163245	(C) pp32 binds to TAF-I , and Set/TAF-Ibeta in vitro.	bind
12068	1	4777	6	NULL	NULL	NULL	NULL	pp32	GP		bind					TAF-I	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cell_104_1_119_s_128	11163245	(C) pp32 binds to TAF-I , and Set/TAF-Ibeta in vitro.	bind
12069	2	4777	6	NULL	NULL	NULL	NULL	pp32	GP		bind					Set/TAF-Ibeta	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cell_104_1_119_s_128	11163245	(C) pp32 binds to TAF-I , and Set/TAF-Ibeta in vitro.	bind
13930	1	4778	5	NULL	NULL	0	NULL	pRb	NULL		bind	NULL				E2F4	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_6_3_729_s_142	11030352	(C) pRb binds to E2F4 following the expression of p16INK4a.	bind
13931	2	4778	5	NULL	NULL	0	NULL	p16INK4a	NULL	expression of	leads to	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_6_3_729_s_142	11030352	(C) pRb binds to E2F4 following the expression of p16INK4a.	bind
12070	1	4778	6	NULL	NULL	NULL	NULL	pRb	GP		bind					E2F4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_3_729_s_142	11030352	(C) pRb binds to E2F4 following the expression of p16INK4a.	bind
12071	2	4778	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs following					p16INK4a	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_3_729_s_142	11030352	(C) pRb binds to E2F4 following the expression of p16INK4a.	bind
14583	1	4779	5	10	NULL	0	NULL	Prohibitin			bind					HP1gamma			chromodomain		NULL	MCF-7 cell lysates	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4161_s_141	16705168	(C) Prohibitin  in the MCF-7 cell lysates binds to the chromodomain and chromoshadow domain of HP1gamma while Rb binds only to the chromoshadow domain.	bind
14584	2	4779	5	10	NULL	0	NULL	Prohibitin			bind					HP1gamma			chromoshadow domain		NULL	MCF-7 cell lysates	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4161_s_141	16705168	(C) Prohibitin  in the MCF-7 cell lysates binds to the chromodomain and chromoshadow domain of HP1gamma while Rb binds only to the chromoshadow domain.	bind
14585	3	4779	5	10	NULL	0	NULL	Rb			bind		only			HP1gamma			chromoshadow domain		NULL	MCF-7 cell lysates	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4161_s_141	16705168	(C) Prohibitin  in the MCF-7 cell lysates binds to the chromodomain and chromoshadow domain of HP1gamma while Rb binds only to the chromoshadow domain.	bind
12072	1	4779	6	NULL	NULL	NULL	NULL	Prohibitin	GP		bind					HP1gamma	GP		chromodomain		NULL	MCF-7 cell lysates	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4161_s_141	16705168	(C) Prohibitin  in the MCF-7 cell lysates binds to the chromodomain and chromoshadow domain of HP1gamma while Rb binds only to the chromoshadow domain.	bind
12073	2	4779	6	NULL	NULL	NULL	NULL	prohibitin	GP		bind					HP1gamma	GP		chromoshadow domain		NULL	MCF-7 cell lysates	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4161_s_141	16705168	(C) Prohibitin  in the MCF-7 cell lysates binds to the chromodomain and chromoshadow domain of HP1gamma while Rb binds only to the chromoshadow domain.	bind
12074	3	4779	6	NULL	NULL	NULL	NULL	Rb	GP		bind					HP1gamma	GP		chromoshadow domain		NULL	MCF-7 cell lysates	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4161_s_141	16705168	(C) Prohibitin  in the MCF-7 cell lysates binds to the chromodomain and chromoshadow domain of HP1gamma while Rb binds only to the chromoshadow domain.	bind
12075	1	4781	6	NULL	NULL	NULL	NULL	nuclear extracts	CellComponent		bind					CaSR-C	GP	radiolabeled			NULL	rMTC cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7410_s_189	9819427	(C) Protein-DNA complexes formed between nuclear extracts from rMTC cells and radiolabeled CaSR-C, CAM-III-A, CAM-III-B, E-CAD-A, or CT/CGRP-C (lanes 3 to 12) were compared to those formed with the downstream TTF-1 binding site of the TSHR (TSHR DS) (lanes 1 and 2) in the presence of an antiserum to a specific TTF-1 peptide or its preimmune control.	bind
12268	2	4781	6	NULL	NULL	NULL	NULL	nuclear extracts	CellComponent		bind					CAM-III-A	GP	radiolabeled			NULL	rMTC cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7410_s_189	9819427	(C) Protein-DNA complexes formed between nuclear extracts from rMTC cells and radiolabeled CaSR-C, CAM-III-A, CAM-III-B, E-CAD-A, or CT/CGRP-C (lanes 3 to 12) were compared to those formed with the downstream TTF-1 binding site of the TSHR (TSHR DS) (lanes 1 and 2) in the presence of an antiserum to a specific TTF-1 peptide or its preimmune control.	bind
12269	3	4781	6	NULL	NULL	NULL	NULL	nuclear extracts	CellComponent		bind					CAM-III-B	GP	radiolabeled			NULL	rMTC cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7410_s_189	9819427	(C) Protein-DNA complexes formed between nuclear extracts from rMTC cells and radiolabeled CaSR-C, CAM-III-A, CAM-III-B, E-CAD-A, or CT/CGRP-C (lanes 3 to 12) were compared to those formed with the downstream TTF-1 binding site of the TSHR (TSHR DS) (lanes 1 and 2) in the presence of an antiserum to a specific TTF-1 peptide or its preimmune control.	bind
12270	4	4781	6	NULL	NULL	NULL	NULL	nuclear extracts	CellComponent		bind					E-CAD-A	GP	radiolabeled			NULL	rMTC cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7410_s_189	9819427	(C) Protein-DNA complexes formed between nuclear extracts from rMTC cells and radiolabeled CaSR-C, CAM-III-A, CAM-III-B, E-CAD-A, or CT/CGRP-C (lanes 3 to 12) were compared to those formed with the downstream TTF-1 binding site of the TSHR (TSHR DS) (lanes 1 and 2) in the presence of an antiserum to a specific TTF-1 peptide or its preimmune control.	bind
12271	5	4781	6	NULL	NULL	NULL	NULL	nuclear extracts	CellComponent		bind					CT/CGRP-C	GP	radiolabeled			NULL	rMTC cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7410_s_189	9819427	(C) Protein-DNA complexes formed between nuclear extracts from rMTC cells and radiolabeled CaSR-C, CAM-III-A, CAM-III-B, E-CAD-A, or CT/CGRP-C (lanes 3 to 12) were compared to those formed with the downstream TTF-1 binding site of the TSHR (TSHR DS) (lanes 1 and 2) in the presence of an antiserum to a specific TTF-1 peptide or its preimmune control.	bind
12453	6	4781	6	NULL	NULL	NULL	NULL	nuclear extracts	CellComponent		bind					TSHR	GP			downstream TTF-1 binding site	NULL	rMTC cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7410_s_189	9819427	(C) Protein-DNA complexes formed between nuclear extracts from rMTC cells and radiolabeled CaSR-C, CAM-III-A, CAM-III-B, E-CAD-A, or CT/CGRP-C (lanes 3 to 12) were compared to those formed with the downstream TTF-1 binding site of the TSHR (TSHR DS) (lanes 1 and 2) in the presence of an antiserum to a specific TTF-1 peptide or its preimmune control.	bind
13939	1	4784	5	NULL	NULL	0	NULL	GFP - X-PAK5	NULL		bind	NULL				MTs	NULL				NULL	cells expressing GFP - X-PAK5 alone	0	NULL	NULL	NULL	gw60_cellbiol_155_6_1029_s_250	11733543	(C) Quantification of cells that present GFP - X-PAK5 binding to the MTs in cells expressing either GFP - X-PAK5 alone or coexpressed with active GTPases.	bind
13940	2	4784	5	NULL	NULL	0	NULL	GFP - X-PAK5	NULL		bind	NULL				MTs	NULL				NULL	in cells expressing GFP - X-PAK5 coexpressed with active GTPases	0	NULL	NULL	NULL	gw60_cellbiol_155_6_1029_s_250	11733543	(C) Quantification of cells that present GFP - X-PAK5 binding to the MTs in cells expressing either GFP - X-PAK5 alone or coexpressed with active GTPases.	bind
13941	3	4784	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_6_1029_s_250	11733543	(C) Quantification of cells that present GFP - X-PAK5 binding to the MTs in cells expressing either GFP - X-PAK5 alone or coexpressed with active GTPases.	bind
12272	1	4784	6	NULL	NULL	NULL	NULL	GFP - X-PAK5	GP		bind					MTs	CellComponent				NULL	in cells expressing GFP - X-PAK5 alone	NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_1029_s_250	11733543	(C) Quantification of cells that present GFP - X-PAK5 binding to the MTs in cells expressing either GFP - X-PAK5 alone or coexpressed with active GTPases.	bind
15193	2	4784	6	NULL	NULL	NULL	NULL	GFP - X-PAK5	GP		bind					MTs	CellComponent				NULL	in cells  expressing GFP - X-PAK5 coexpressed with active GTPases	NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_1029_s_250	11733543	(C) Quantification of cells that present GFP - X-PAK5 binding to the MTs in cells expressing either GFP - X-PAK5 alone or coexpressed with active GTPases.	bind
54506	3	4784	6	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_1029_s_250	11733543	(C) Quantification of cells that present GFP - X-PAK5 binding to the MTs in cells expressing either GFP - X-PAK5 alone or coexpressed with active GTPases.	bind
14586	1	4786	5	NULL	NULL	0	NULL	Smad4	NULL		bind	NULL					NULL			SBE/p53RE	NULL	WT mouse liver tissue	0	NULL	NULL	NULL	gw70_molcellbiol_25_3_1200_s_71	15657445	(C) Quantifying in vivo ChIP of Smad4 and P-Smad2 binding to the  SBE/p53RE and distal genomic sites in WT and p53-null mouse liver tissue.	bind
14587	2	4786	5	NULL	NULL	0	NULL	Smad4	NULL		bind	NULL					NULL			SBE/p53RE	NULL	p53-null mouse liver tissue	0	NULL	NULL	NULL	gw70_molcellbiol_25_3_1200_s_71	15657445	(C) Quantifying in vivo ChIP of Smad4 and P-Smad2 binding to the  SBE/p53RE and distal genomic sites in WT and p53-null mouse liver tissue.	bind
14588	3	4786	5	NULL	NULL	0	NULL	P-Smad2	NULL		bind	NULL					NULL			SBE/p53RE	NULL	WT mouse liver tissue	0	NULL	NULL	NULL	gw70_molcellbiol_25_3_1200_s_71	15657445	(C) Quantifying in vivo ChIP of Smad4 and P-Smad2 binding to the  SBE/p53RE and distal genomic sites in WT and p53-null mouse liver tissue.	bind
14589	4	4786	5	NULL	NULL	0	NULL	P-Smad2	NULL		bind	NULL					NULL			SBE/p53RE	NULL	p53-null mouse liver tissue	0	NULL	NULL	NULL	gw70_molcellbiol_25_3_1200_s_71	15657445	(C) Quantifying in vivo ChIP of Smad4 and P-Smad2 binding to the  SBE/p53RE and distal genomic sites in WT and p53-null mouse liver tissue.	bind
12274	1	4786	6	NULL	NULL	NULL	NULL	Smad4	GP		bind									SBE/p53RE	NULL	wild type mouse liver tissue	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_3_1200_s_71	15657445	(C) Quantifying in vivo ChIP of Smad4 and P-Smad2 binding to the  SBE/p53RE and distal genomic sites in WT and p53-null mouse liver tissue.	bind
12275	2	4786	6	NULL	NULL	NULL	NULL	Smad4	GP		bind									SBE/p53RE	NULL	p53-null mouse liver tissue	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_3_1200_s_71	15657445	(C) Quantifying in vivo ChIP of Smad4 and P-Smad2 binding to the  SBE/p53RE and distal genomic sites in WT and p53-null mouse liver tissue.	bind
12276	3	4786	6	NULL	NULL	NULL	NULL	P-Smad2	GP		bind									SBE/p53RE	NULL	wild type mouse liver tissue	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_3_1200_s_71	15657445	(C) Quantifying in vivo ChIP of Smad4 and P-Smad2 binding to the  SBE/p53RE and distal genomic sites in WT and p53-null mouse liver tissue.	bind
12277	4	4786	6	NULL	NULL	NULL	NULL	P-Smad2	GP		bind									SBE/p53RE	NULL	p53-null mouse liver tissue	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_3_1200_s_71	15657445	(C) Quantifying in vivo ChIP of Smad4 and P-Smad2 binding to the  SBE/p53RE and distal genomic sites in WT and p53-null mouse liver tissue.	bind
13942	1	4787	5	NULL	NULL	0	NULL	acetyl-histone H3	NULL		bind	NULL				bcl-2	NULL			P2 promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_210	15713621	(C) Quantitative ChIP  assay of acetyl-histone H3 and acetyl-histone H4 binding to the  bcl-2 P2 promoter.	bind
13943	2	4787	5	NULL	NULL	0	NULL	acetyl-histone H4	NULL		bind	NULL				bcl-2	NULL			P2 promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_210	15713621	(C) Quantitative ChIP  assay of acetyl-histone H3 and acetyl-histone H4 binding to the  bcl-2 P2 promoter.	bind
12310	1	4787	6	NULL	NULL	NULL	NULL	acetyl-histone H3	GP		bind					bcl-2 	GP			P2 promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_210	15713621	(C) Quantitative ChIP  assay of acetyl-histone H3 and acetyl-histone H4 binding to the  bcl-2 P2 promoter.	bind
12311	2	4787	6	NULL	NULL	NULL	NULL	acetyl-histone H4	GP		bind					bcl-2	GP			P2 promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_210	15713621	(C) Quantitative ChIP  assay of acetyl-histone H3 and acetyl-histone H4 binding to the  bcl-2 P2 promoter.	bind
13944	1	4788	5	10	NULL	0	NULL	38 kDa protein			bind					GST - BRCA1 					NULL		NULL	NULL	NULL	NULL	gw60_cell_88_2_265_s_130	9008167	(C) Rad51 antiserum recognizes a 38 kDa protein bound to  GST - BRCA1 #4.	bind
13945	2	4788	5	NULL	NULL	0	NULL	Rad51 antiserum	NULL		recognizes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_88_2_265_s_130	9008167	(C) Rad51 antiserum recognizes a 38 kDa protein bound to  GST - BRCA1 #4.	bind
12312	1	4788	6	NULL	NULL	NULL	NULL	38 kDa protein	GP		bind					GST-BRCA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_88_2_265_s_130	9008167	(C) Rad51 antiserum recognizes a 38 kDa protein bound to  GST - BRCA1 #4.	bind
16282	2	4788	6	NULL	NULL	NULL	NULL	Rad51 antiserum	GP		recognizes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_88_2_265_s_130	9008167	(C) Rad51 antiserum recognizes a 38 kDa protein bound to  GST - BRCA1 #4.	bind
13946	1	4790	5	NULL	NULL	0	NULL	Ran-GTP	NULL		bind	NULL				Kap123p	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_5_715_s_100	9182759	(C) Ran-GTP binds to Kap123p.	bind
12313	1	4790	6	NULL	NULL	NULL	NULL	Ran-GTP	GP		bind					Kap123p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_5_715_s_100	9182759	(C) Ran-GTP binds to Kap123p.	bind
14189	1	4791	5	10	NULL	0	NULL	nicotine			bind					choline acetyltransferase		activity of			NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_94_3_685_s_88	10579560	(c) Ratios of [3](-)nicotine, [3]epibatidine, [3]cytisine, and [3]vesamicol binding to choline acetyltransferase activity as averages of the individual cases.	bind
14190	2	4791	5	10	NULL	0	NULL	epibatidine			bind					choline acetyltransferase		activity of			NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_94_3_685_s_88	10579560	(c) Ratios of [3](-)nicotine, [3]epibatidine, [3]cytisine, and [3]vesamicol binding to choline acetyltransferase activity as averages of the individual cases.	bind
14191	3	4791	5	10	NULL	0	NULL	cytisine			bind					choline acetyltransferase		activity of			NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_94_3_685_s_88	10579560	(c) Ratios of [3](-)nicotine, [3]epibatidine, [3]cytisine, and [3]vesamicol binding to choline acetyltransferase activity as averages of the individual cases.	bind
14192	4	4791	5	10	NULL	0	NULL	vesamicol			bind					choline acetyltransferase		activity of			NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_94_3_685_s_88	10579560	(c) Ratios of [3](-)nicotine, [3]epibatidine, [3]cytisine, and [3]vesamicol binding to choline acetyltransferase activity as averages of the individual cases.	bind
12314	1	4791	6	NULL	NULL	NULL	NULL	nicotine	Chemical		bind					choline acetyltransferase	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_94_3_685_s_88	10579560	(c) Ratios of [3](-)nicotine, [3]epibatidine, [3]cytisine, and [3]vesamicol binding to choline acetyltransferase activity as averages of the individual cases.	bind
12315	2	4791	6	NULL	NULL	NULL	NULL	epibatidine	Chemical		bind					choline acetyltransferase	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_94_3_685_s_88	10579560	(c) Ratios of [3](-)nicotine, [3]epibatidine, [3]cytisine, and [3]vesamicol binding to choline acetyltransferase activity as averages of the individual cases.	bind
12316	3	4791	6	NULL	NULL	NULL	NULL	cytisine	AminoAcid		bind					choline acetyltransferase	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_94_3_685_s_88	10579560	(c) Ratios of [3](-)nicotine, [3]epibatidine, [3]cytisine, and [3]vesamicol binding to choline acetyltransferase activity as averages of the individual cases.	bind
12317	4	4791	6	NULL	NULL	NULL	NULL	vesamicol	Chemical		bind					choline acetyltransferase	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_94_3_685_s_88	10579560	(c) Ratios of [3](-)nicotine, [3]epibatidine, [3]cytisine, and [3]vesamicol binding to choline acetyltransferase activity as averages of the individual cases.	bind
14193	1	4792	5	NULL	NULL	0	NULL	eIF4GI	NULL	recombinant	does not bind	NULL		(1040-1560) FVR1239AAA		eIF4A	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_20_2_468_s_194	10611225	(C) Recombinant eIF4GI(1040-1560) FVR1239AAA does not bind eIF4A in vitro.	bind
12318	1	4792	6	NULL	NULL	NULL	NULL	eIF4GI	GP	recombinant	does not bind			1040-1560 FVR1239AAA		eIF4A	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_2_468_s_194	10611225	(C) Recombinant eIF4GI(1040-1560) FVR1239AAA does not bind eIF4A in vitro.	bind
14194	1	4793	5	NULL	NULL	0	NULL	rhodanese	NULL	refolding of	bind	NULL				EL229C-B	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_139	11672529	(C) Refolding of rhodanese bound to EL229C-B  was initiated as in (B) followed by addition  of EL229C/SA ( ) or SR-EL/SA ( ) at 1.5 min.	bind
14196	2	4793	5	NULL	NULL	0	NULL	EL229C/SA	NULL	addition of	initiates	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_139	11672529	(C) Refolding of rhodanese bound to EL229C-B  was initiated as in (B) followed by addition  of EL229C/SA ( ) or SR-EL/SA ( ) at 1.5 min.	bind
14197	3	4793	5	NULL	NULL	0	NULL	SR-EL/SA	NULL	addition of	initiates	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_139	11672529	(C) Refolding of rhodanese bound to EL229C-B  was initiated as in (B) followed by addition  of EL229C/SA ( ) or SR-EL/SA ( ) at 1.5 min.	bind
14198	4	4793	5	NULL	NULL	0	NULL	statement 3	NULL		is an alternative to	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_139	11672529	(C) Refolding of rhodanese bound to EL229C-B  was initiated as in (B) followed by addition  of EL229C/SA ( ) or SR-EL/SA ( ) at 1.5 min.	bind
12319	1	4793	6	NULL	NULL	NULL	NULL	rhodanese	GP	refolding of	bind					EL229C-B					NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_139	11672529	(C) Refolding of rhodanese bound to EL229C-B  was initiated as in (B) followed by addition  of EL229C/SA ( ) or SR-EL/SA ( ) at 1.5 min.	bind
16283	2	4793	6	NULL	NULL	NULL	NULL	EL229C/SA		addition of	initiates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_139	11672529	(C) Refolding of rhodanese bound to EL229C-B  was initiated as in (B) followed by addition  of EL229C/SA ( ) or SR-EL/SA ( ) at 1.5 min.	bind
16284	3	4793	6	NULL	NULL	NULL	NULL	SR-EL/SA	GP	addition of	initiates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_139	11672529	(C) Refolding of rhodanese bound to EL229C-B  was initiated as in (B) followed by addition  of EL229C/SA ( ) or SR-EL/SA ( ) at 1.5 min.	bind
54507	4	4793	6	NULL	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_139	11672529	(C) Refolding of rhodanese bound to EL229C-B  was initiated as in (B) followed by addition  of EL229C/SA ( ) or SR-EL/SA ( ) at 1.5 min.	bind
14199	1	4795	5	NULL	NULL	0	NULL	[35]GTP S	NULL		bind	NULL				coronal brain sections	NULL	VEH treated mice			NULL	in caudate-putamen	0	NULL	NULL	NULL	gw70_neuropharmacology_50_7_788_s_407	16443242	(C) Representative autoradiograms for cannabinoid receptor agonist-stimulated  [35]GTP S binding of coronal brain sections from VEH and ND treated mice in the caudate-putamen.	bind
14202	2	4795	5	NULL	NULL	0	NULL	[35]GTP S	NULL		bind	NULL				coronal brain sections	NULL	ND treated mice			NULL	in caudate-putamen	0	NULL	NULL	NULL	gw70_neuropharmacology_50_7_788_s_407	16443242	(C) Representative autoradiograms for cannabinoid receptor agonist-stimulated  [35]GTP S binding of coronal brain sections from VEH and ND treated mice in the caudate-putamen.	bind
14203	3	4795	5	NULL	NULL	0	NULL	cannabinoid receptor agonist	NULL		stimulate	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_50_7_788_s_407	16443242	(C) Representative autoradiograms for cannabinoid receptor agonist-stimulated  [35]GTP S binding of coronal brain sections from VEH and ND treated mice in the caudate-putamen.	bind
14204	4	4795	5	NULL	NULL	0	NULL	cannabinoid receptor agonist	NULL		stimulate	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_50_7_788_s_407	16443242	(C) Representative autoradiograms for cannabinoid receptor agonist-stimulated  [35]GTP S binding of coronal brain sections from VEH and ND treated mice in the caudate-putamen.	bind
17054	1	4795	6	NULL	NULL	NULL	NULL	GTP S	Chemical		bind					coronal brain sections	OrganismPart	VEH treated mice 			NULL	in caudate-putamen	NULL	NULL	NULL	NULL	gw70_neuropharmacology_50_7_788_s_407	16443242	(C) Representative autoradiograms for cannabinoid receptor agonist-stimulated  [35]GTP S binding of coronal brain sections from VEH and ND treated mice in the caudate-putamen.	bind
17055	2	4795	6	NULL	NULL	NULL	NULL	GTP S	Chemical		bind					coronal brain sections	OrganismPart	ND treated mice			NULL	in caudate-putamen	NULL	NULL	NULL	NULL	gw70_neuropharmacology_50_7_788_s_407	16443242	(C) Representative autoradiograms for cannabinoid receptor agonist-stimulated  [35]GTP S binding of coronal brain sections from VEH and ND treated mice in the caudate-putamen.	bind
17057	3	4795	6	NULL	NULL	NULL	NULL	cannabinoid receptor agonist	GP		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_50_7_788_s_407	16443242	(C) Representative autoradiograms for cannabinoid receptor agonist-stimulated  [35]GTP S binding of coronal brain sections from VEH and ND treated mice in the caudate-putamen.	bind
17058	4	4795	6	NULL	NULL	NULL	NULL	cannabinoid receptor agonist	GP		stimulates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_50_7_788_s_407	16443242	(C) Representative autoradiograms for cannabinoid receptor agonist-stimulated  [35]GTP S binding of coronal brain sections from VEH and ND treated mice in the caudate-putamen.	bind
14205	1	4796	5	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				D2	NULL				NULL		0	NULL	NULL	NULL	gw60_genetics_155_1_203_s_121	10790395	(C) Residues involved in ATP binding by D2 are shown in contact with ATP.	bind
12320	1	4796	6	NULL	NULL	NULL	NULL	ATP	Chemical		bind					D2	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_1_203_s_121	10790395	(C) Residues involved in ATP binding by D2 are shown in contact with ATP.	bind
14207	1	4797	5	NULL	NULL	0	NULL		NULL		bind	NULL		GST-RBD		RhoA	NULL				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_1_87_s_139	15527766	(C) RhoA activities are  indicated by the amount of GST-RBD bound RhoA normalized to the amount of total RhoA  content in the lysates.	bind
12321	1	4797	6	NULL	NULL	NULL	NULL				bind			GST-RBD		RhoA	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_1_87_s_139	15527766	(C) RhoA activities are  indicated by the amount of GST-RBD bound RhoA normalized to the amount of total RhoA  content in the lysates.	bind
14208	1	4798	5	NULL	NULL	0	NULL	CksHs1 monomer	NULL		bind	NULL				CDK2	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_84_6_863_s_102	8601310	(C) Ribbon model of  the monomeric fold of CksHs1 monomer (yellow) bound to CDK2 (displayed as C   trace except for helix  5 and loop L14 and oriented to match   Figure 1B, with the same color code) with a superimposed CksHs2 interlocked dimer (pink  and light purple ribbons).	bind
12322	1	4798	6	NULL	NULL	NULL	NULL	CksHs1 monomer	GP		bind					CDK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_6_863_s_102	8601310	(C) Ribbon model of  the monomeric fold of CksHs1 monomer (yellow) bound to CDK2 (displayed as C   trace except for helix  5 and loop L14 and oriented to match   Figure 1B, with the same color code) with a superimposed CksHs2 interlocked dimer (pink  and light purple ribbons).	bind
14209	1	4799	5	NULL	NULL	0	NULL	NF1	NULL		bind	NULL				MMTV	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_16_5417_s_168	11463824	(C) Roscovitine inhibits NF1 binding to the MMTV promoter.	bind
14210	2	4799	5	NULL	NULL	0	NULL	Roscovitine	NULL		inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_16_5417_s_168	11463824	(C) Roscovitine inhibits NF1 binding to the MMTV promoter.	bind
12323	1	4799	6	NULL	NULL	NULL	NULL	NF1	GP		bind					MMTV	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_16_5417_s_168	11463824	(C) Roscovitine inhibits NF1 binding to the MMTV promoter.	bind
12324	2	4799	6	NULL	NULL	NULL	NULL	Roscovitine	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_16_5417_s_168	11463824	(C) Roscovitine inhibits NF1 binding to the MMTV promoter.	bind
14211	1	4801	5	NULL	NULL	0	NULL	SATB1	NULL		bind	NULL				IL2Ralpha	NULL			promoter	NULL	in vivo	0	NULL	NULL	NULL	gw70_molcellbiol_25_5_1620_s_135	15713622	(C) SATB1 binds to the IL2Ralpha promoter in vivo.	bind
12325	1	4801	6	NULL	NULL	NULL	NULL	SATB1	GP		bind					IL2Ralpha	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1620_s_135	15713622	(C) SATB1 binds to the IL2Ralpha promoter in vivo.	bind
14591	1	4802	5	10	NULL	0	NULL	Mtb HSP70		unlabeled	inhibit					FITC-Mtb HSP70		binding of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_6_971_s_143	11754818	(C) Saturation binding of FITC-labeled Mtb HSP70 and the inhibition of FITC-Mtb HSP70 binding by unlabeled Mtb HSP70, HSA, or  E. coli HSP70.	bind
14592	2	4802	5	10	NULL	0	NULL	HSA		unlabeled	inhibit					FITC-Mtb HSP70		binding of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_6_971_s_143	11754818	(C) Saturation binding of FITC-labeled Mtb HSP70 and the inhibition of FITC-Mtb HSP70 binding by unlabeled Mtb HSP70, HSA, or  E. coli HSP70.	bind
14593	3	4802	5	10	NULL	0	NULL	HSP70		E. coli	inhibit					FITC-Mtb HSP70		binding of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_6_971_s_143	11754818	(C) Saturation binding of FITC-labeled Mtb HSP70 and the inhibition of FITC-Mtb HSP70 binding by unlabeled Mtb HSP70, HSA, or  E. coli HSP70.	bind
14594	4	4802	5	10	NULL	0	NULL	statement 2			is an alternative to					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_6_971_s_143	11754818	(C) Saturation binding of FITC-labeled Mtb HSP70 and the inhibition of FITC-Mtb HSP70 binding by unlabeled Mtb HSP70, HSA, or  E. coli HSP70.	bind
12326	1	4802	6	NULL	NULL	NULL	NULL	Mtb HSP70	GP	unlabeled	inhibits					FITC-Mtb HSP70	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_6_971_s_143	11754818	(C) Saturation binding of FITC-labeled Mtb HSP70 and the inhibition of FITC-Mtb HSP70 binding by unlabeled Mtb HSP70, HSA, or  E. coli HSP70.	bind
12327	2	4802	6	NULL	NULL	NULL	NULL	HSA	GP	unlabeled	inhibits					FITC-Mtb HSP70	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_6_971_s_143	11754818	(C) Saturation binding of FITC-labeled Mtb HSP70 and the inhibition of FITC-Mtb HSP70 binding by unlabeled Mtb HSP70, HSA, or  E. coli HSP70.	bind
12328	3	4802	6	NULL	NULL	NULL	NULL	HSP70	GP	E.coli	inhibits					FITC-Mtb HSP70	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_6_971_s_143	11754818	(C) Saturation binding of FITC-labeled Mtb HSP70 and the inhibition of FITC-Mtb HSP70 binding by unlabeled Mtb HSP70, HSA, or  E. coli HSP70.	bind
12329	4	4802	6	NULL	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_6_971_s_143	11754818	(C) Saturation binding of FITC-labeled Mtb HSP70 and the inhibition of FITC-Mtb HSP70 binding by unlabeled Mtb HSP70, HSA, or  E. coli HSP70.	bind
14212	1	4803	5	10	NULL	0	NULL	NFPS			bind					GLYT1 membranes					NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_49_6_922_s_174	16143353	(C) Saturation curve of [3]NFPS binding to GLYT1 membranes.	bind
12330	1	4803	6	NULL	NULL	NULL	NULL	NFPS	Chemical		bind					GLYT1 membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_49_6_922_s_174	16143353	(C) Saturation curve of [3]NFPS binding to GLYT1 membranes.	bind
14213	1	4804	5	NULL	NULL	0	NULL	COS-7 cells	NULL		express	NULL				NP-1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_99_1_59_s_167	10520994	(C) Scatchard analysis of AP-Sema3A binding to NP-1- or NP-1/Plex  1 DN - expressing COS-7 cells.	bind
14214	3	4804	5	NULL	NULL	0	NULL	AP-Sema3A	NULL		bind	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_99_1_59_s_167	10520994	(C) Scatchard analysis of AP-Sema3A binding to NP-1- or NP-1/Plex  1 DN - expressing COS-7 cells.	bind
44572	2	4804	5	10	NULL	0	NULL	 COS-7 cells	NULL		express	NULL				NP-1/Plex 1 DN	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_99_1_59_s_167	10520994	(C) Scatchard analysis of AP-Sema3A binding to NP-1- or NP-1/Plex  1 DN - expressing COS-7 cells.	bind
44573	4	4804	5	10	NULL	0	NULL	AP-Sema3A	NULL		bind	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_99_1_59_s_167	10520994	(C) Scatchard analysis of AP-Sema3A binding to NP-1- or NP-1/Plex  1 DN - expressing COS-7 cells.	bind
44574	5	4804	5	10	NULL	0	NULL	statement 3	NULL		is an alternative to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_99_1_59_s_167	10520994	(C) Scatchard analysis of AP-Sema3A binding to NP-1- or NP-1/Plex  1 DN - expressing COS-7 cells.	bind
12331	1	4804	6	NULL	NULL	NULL	NULL	COS-7 cells	Cell		express					NP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_99_1_59_s_167	10520994	(C) Scatchard analysis of AP-Sema3A binding to NP-1- or NP-1/Plex  1 DN - expressing COS-7 cells.	bind
12332	2	4804	6	NULL	NULL	NULL	NULL	COS-7 cells	Cell		express					NP-1/Plex 1 DN	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_99_1_59_s_167	10520994	(C) Scatchard analysis of AP-Sema3A binding to NP-1- or NP-1/Plex  1 DN - expressing COS-7 cells.	bind
12333	3	4804	6	NULL	NULL	NULL	NULL	AP-Sema3A	GP		bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_99_1_59_s_167	10520994	(C) Scatchard analysis of AP-Sema3A binding to NP-1- or NP-1/Plex  1 DN - expressing COS-7 cells.	bind
12334	5	4804	6	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_99_1_59_s_167	10520994	(C) Scatchard analysis of AP-Sema3A binding to NP-1- or NP-1/Plex  1 DN - expressing COS-7 cells.	bind
54526	4	4804	6	NULL	NULL	NULL	NULL	AP-Sema3A	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_99_1_59_s_167	10520994	(C) Scatchard analysis of AP-Sema3A binding to NP-1- or NP-1/Plex  1 DN - expressing COS-7 cells.	bind
14215	1	4805	5	NULL	NULL	0	NULL	Angiopoietin-1	NULL		bind	NULL				TIE2-Fc	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_87_7_1161_s_104	8980223	(C) Scatchard analysis of binding  of Angiopoietin-1 to TIE2-Fc.	bind
12335	1	4805	6	NULL	NULL	NULL	NULL	Angiopoietin-1	GP		bind					TIE2-Fc	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_7_1161_s_104	8980223	(C) Scatchard analysis of binding  of Angiopoietin-1 to TIE2-Fc.	bind
14216	1	4806	5	NULL	NULL	0	NULL	Ce-Sema1aa	NULL		bind	NULL		deltaC-Fc-AP		PLX-1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_development_129_9_2053_s_237	11959816	(C) Scatchard analysis of the binding of Ce-Sema1aadeltaC-Fc-AP to PLX-1.	bind
12336	1	4806	6	NULL	NULL	NULL	NULL	Ce-Sema1aa	GP		bind			deltaC-Fc-AP		PLX-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_129_9_2053_s_237	11959816	(C) Scatchard analysis of the binding of Ce-Sema1aadeltaC-Fc-AP to PLX-1.	bind
14217	1	4807	5	NULL	NULL	0	NULL	ubiquitin	NULL		bind	NULL				HAUSP	NULL		catalytic core domain		NULL		0	NULL	NULL	NULL	gw60_cell_111_7_1041_s_119	12507430	(C) Schematic diagram of how ubiquitin is bound by the HAUSP catalytic core domain.	bind
12337	1	4807	6	NULL	NULL	NULL	NULL	HAUSP	GP		bind			catalytic core domain		ubiquitin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_7_1041_s_119	12507430	(C) Schematic diagram of how ubiquitin is bound by the HAUSP catalytic core domain.	bind
14218	1	4812	5	10	NULL	0	NULL	 Nck			bind					PDGFR-beta		human			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_21_7867_s_197	11027258	(C) Schematic representation of binding of the two Ncks to human PDGFR-beta together with their shared binding partners.	bind
12338	1	4812	6	NULL	NULL	NULL	NULL	Nck	GP		bind					PDGFR-beta	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_21_7867_s_197	11027258	(C) Schematic representation of binding of the two Ncks to human PDGFR-beta together with their shared binding partners.	bind
14219	1	4814	5	NULL	NULL	0	NULL	agrin	NULL		bind	NULL				dystroglycan complex	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_85_4_513_s_144	8653787	(C) Schematic representation of one of several  possible models of the MuSK receptor complex for agrin, depicting requirement for a  myotube-associated specificity component (MASC) and possible interactions to additional components that may be  required for signaling or coupling to various effectors or substrates; these couplings may  be mediated extracellularly (for example, via agrin binding to the dystroglycan complex) or intracellularly  (for example, via interactions of SH2 domain - containing proteins to phosphorylated tyrosines on MuSK).	bind
14220	2	4814	5	10	NULL	0	NULL	proteins	NULL		bind	NULL		SH2 domain		MuSK	NULL	phosphorylated	tyrosines		NULL		NULL	NULL	NULL	NULL	gw60_cell_85_4_513_s_144	8653787	(C) Schematic representation of one of several  possible models of the MuSK receptor complex for agrin, depicting requirement for a  myotube-associated specificity component (MASC) and possible interactions to additional components that may be  required for signaling or coupling to various effectors or substrates; these couplings may  be mediated extracellularly (for example, via agrin binding to the dystroglycan complex) or intracellularly  (for example, via interactions of SH2 domain - containing proteins to phosphorylated tyrosines on MuSK).	bind
12339	1	4814	6	NULL	NULL	NULL	NULL	agrin	GP		bind					dystroglycan complex	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_85_4_513_s_144	8653787	(C) Schematic representation of one of several  possible models of the MuSK receptor complex for agrin, depicting requirement for a  myotube-associated specificity component (MASC) and possible interactions to additional components that may be  required for signaling or coupling to various effectors or substrates; these couplings may  be mediated extracellularly (for example, via agrin binding to the dystroglycan complex) or intracellularly  (for example, via interactions of SH2 domain - containing proteins to phosphorylated tyrosines on MuSK).	bind
12340	2	4814	6	NULL	NULL	NULL	NULL	protein			bind			SH2 domain		MuSK	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_cell_85_4_513_s_144	8653787	(C) Schematic representation of one of several  possible models of the MuSK receptor complex for agrin, depicting requirement for a  myotube-associated specificity component (MASC) and possible interactions to additional components that may be  required for signaling or coupling to various effectors or substrates; these couplings may  be mediated extracellularly (for example, via agrin binding to the dystroglycan complex) or intracellularly  (for example, via interactions of SH2 domain - containing proteins to phosphorylated tyrosines on MuSK).	bind
14221	1	4815	5	NULL	NULL	0	NULL	Skp2	NULL		bind	NULL	selectively			p27CP	NULL				NULL	in HeLa extracts	NULL	NULL	NULL	NULL	gw60_currbiol_9_12_661_s_75	10375532	(c) Selective binding of Skp2, Skp1 and Cul-1 to p27CP in HeLa extracts.	bind
14222	2	4815	5	NULL	NULL	0	NULL	Skp1	NULL		bind	NULL	selectively			p27CP	NULL				NULL	in HeLa extracts	NULL	NULL	NULL	NULL	gw60_currbiol_9_12_661_s_75	10375532	(c) Selective binding of Skp2, Skp1 and Cul-1 to p27CP in HeLa extracts.	bind
14223	3	4815	5	NULL	NULL	0	NULL	Cul-1	NULL		bind	NULL	selectively			p27CP	NULL				NULL	in HeLa extracts	NULL	NULL	NULL	NULL	gw60_currbiol_9_12_661_s_75	10375532	(c) Selective binding of Skp2, Skp1 and Cul-1 to p27CP in HeLa extracts.	bind
12341	1	4815	6	NULL	NULL	NULL	NULL	Skp2	GP		bind		selectively			p27CP	GP				NULL	HeLa  extracts	NULL	NULL	NULL	NULL	gw60_currbiol_9_12_661_s_75	10375532	(c) Selective binding of Skp2, Skp1 and Cul-1 to p27CP in HeLa extracts.	bind
12342	2	4815	6	NULL	NULL	NULL	NULL	Skp1	GP		bind		selectively			p27CP	GP				NULL	HeLa  extracts	NULL	NULL	NULL	NULL	gw60_currbiol_9_12_661_s_75	10375532	(c) Selective binding of Skp2, Skp1 and Cul-1 to p27CP in HeLa extracts.	bind
12343	3	4815	6	NULL	NULL	NULL	NULL	Cul-1	GP		bind		selectively			p27CP	GP				NULL	HeLa  extracts	NULL	NULL	NULL	NULL	gw60_currbiol_9_12_661_s_75	10375532	(c) Selective binding of Skp2, Skp1 and Cul-1 to p27CP in HeLa extracts.	bind
14224	1	4820	5	NULL	NULL	0	NULL	NF-kappaB proteins	NULL		bind	NULL				RANTES gene	NULL			NF-kappaB binding sites within A sites	NULL		0	NULL	NULL	NULL	gw70_infectimmun_71_7_3748_s_177	12819056	(C) Sequence specificity of NF-kappaB binding activity and characterization of NF-kappaB proteins that bound to the NF-kappaB binding sites within A and B sites of the RANTES gene.	bind
14225	2	4820	5	NULL	NULL	0	NULL	NF-kappaB proteins	NULL		bind	NULL				RANTES gene	NULL			NF-kappaB binding sites within B sites	NULL		0	NULL	NULL	NULL	gw70_infectimmun_71_7_3748_s_177	12819056	(C) Sequence specificity of NF-kappaB binding activity and characterization of NF-kappaB proteins that bound to the NF-kappaB binding sites within A and B sites of the RANTES gene.	bind
12344	1	4820	6	NULL	NULL	NULL	NULL	NF-kappaB proteins	GP		bind					RANTES gene	GP			NF-kappaB binding sites within A sites	NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_7_3748_s_177	12819056	(C) Sequence specificity of NF-kappaB binding activity and characterization of NF-kappaB proteins that bound to the NF-kappaB binding sites within A and B sites of the RANTES gene.	bind
16285	2	4820	6	NULL	NULL	NULL	NULL	NF-kappaB proteins	GP		bind					RANTES gene	GP			NF-kappaB binding sites within B sites	NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_7_3748_s_177	12819056	(C) Sequence specificity of NF-kappaB binding activity and characterization of NF-kappaB proteins that bound to the NF-kappaB binding sites within A and B sites of the RANTES gene.	bind
14226	1	4821	5	NULL	NULL	0	NULL	sFRP/Frzb proteins	NULL		bind	NULL				Wnt molecules	NULL	specific			NULL		0	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
14227	2	4821	5	NULL	NULL	0	NULL	Cerberus	NULL		bind	NULL				Wnt molecules	NULL	specific			NULL		0	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
14228	3	4821	5	NULL	NULL	0	NULL	WIF-1	NULL		bind	NULL				Wnt molecules	NULL	specific			NULL		0	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
14229	4	4821	5	10	NULL	0	NULL	Wnt binding antagonists			bind					Wnt molecules		specific			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
14230	5	4821	5	NULL	NULL	0	NULL	Wnt	NULL		interacts with	NULL				Fz	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
14231	6	4821	5	NULL	NULL	0	NULL	Wnt	NULL		interacts with	NULL				LRP5/6	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
14232	7	4821	5	NULL	NULL	0	NULL	statement 5	NULL		is an alternative to	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
14235	8	4821	5	NULL	NULL	0	NULL	sFRP/Frzb proteins	NULL		prevent	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
14236	9	4821	5	NULL	NULL	0	NULL	sFRP/Frzb proteins	NULL		prevent	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
14237	10	4821	5	10	NULL	0	NULL	 sFRP/Frzb proteins			prevent					Fz-LRP5/6 complex		formation of			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
14239	11	4821	5	10	NULL	0	NULL	Cerberus			prevent					statement 5					NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
14240	12	4821	5	10	NULL	0	NULL	Cerberus			prevent					statement 6					NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
14241	13	4821	5	10	NULL	0	NULL	Cerberus			prevent					Fz-LRP5/6 complex		formation of			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
14243	16	4821	5	NULL	NULL	0	NULL	WIF-1	NULL		prevent	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
14244	17	4821	5	NULL	NULL	0	NULL	WIF-1	NULL		prevent	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
14245	18	4821	5	10	NULL	0	NULL	WIF-1			prevent					Fz-LRP5/6 complex		formation of			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
14246	19	4821	5	10	NULL	0	NULL	Wnt binding antagonists			prevent					Fz-LRP5/6 complex		formation of			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
14247	14	4821	5	10	NULL	0	NULL	Wnt binding antagonists			prevent					statement 5					NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
14248	15	4821	5	10	NULL	0	NULL	Wnt binding antagonists			prevent					statement 6					NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
12402	1	4821	6	NULL	NULL	NULL	NULL	sFRP/Frzb proteins	GP		bind					Wnt molecule	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
12403	2	4821	6	NULL	NULL	NULL	NULL	Cerberus	GP		bind					Wnt molecule	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
12404	3	4821	6	NULL	NULL	NULL	NULL	WIF-1	GP		bind					Wnt molecule	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
12436	4	4821	6	NULL	NULL	NULL	NULL	Wnt	GP		interacts with					Fz	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
12437	5	4821	6	NULL	NULL	NULL	NULL	Wnt	GP		interacts with					LRP5/6	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
12438	6	4821	6	NULL	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
12439	7	4821	6	NULL	NULL	NULL	NULL	statement 1	Process		prevents					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
12440	8	4821	6	NULL	NULL	NULL	NULL	statement 1	Process		prevents					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
12441	9	4821	6	NULL	NULL	NULL	NULL	statement 2	Process		prevents					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
12442	10	4821	6	NULL	NULL	NULL	NULL	statement 2	Process		prevents					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
12443	11	4821	6	NULL	NULL	NULL	NULL	statement 3	Process		prevents					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
12444	12	4821	6	NULL	NULL	NULL	NULL	statement 3	Process		prevents					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
12445	13	4821	6	NULL	NULL	NULL	NULL	sFRP/Frzb proteins	GP		prevents					Fz-LRP5/6 complex	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
12446	14	4821	6	NULL	NULL	NULL	NULL	Cerberus	GP		prevents					Fz-LRP5/6 complex	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
12447	15	4821	6	NULL	NULL	NULL	NULL	WIF-1	GP		prevents					Fz-LRP5/6 complex	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
54527	16	4821	6	NULL	NULL	NULL	NULL	Wnt binding antagonists	GP		bind		specific			Wnt molecules	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
54528	17	4821	6	NULL	NULL	NULL	NULL	statement 16	Process		prevents					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
54529	18	4821	6	NULL	NULL	NULL	NULL	statement 16	Process		prevents					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
54530	19	4821	6	NULL	NULL	NULL	NULL	Wnt binding antagonists	GP		prevent					Fz-LRP5/6 complex	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_275	11448771	(c) sFRP/Frzb proteins, Cerberus, WIF-1 and other Wnt binding antagonists bind specific Wnt molecules and prevent Wnt interaction with Fz and/or LRP5/6; they thereby prevent formation of the Fz-LRP5/6 complex.	bind
14251	1	4822	5	NULL	NULL	0	NULL	Ctf13	NULL		bind	NULL				Skp1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_18_8069_s_230	15340069	(C) Sgt1 and Hsp90 stimulate the  binding of Ctf13 to Skp1.	bind
14252	2	4822	5	NULL	NULL	0	NULL	Sgt1	NULL		stimulate	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_18_8069_s_230	15340069	(C) Sgt1 and Hsp90 stimulate the  binding of Ctf13 to Skp1.	bind
14253	3	4822	5	NULL	NULL	0	NULL	Hsp90	NULL		stimulate	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_18_8069_s_230	15340069	(C) Sgt1 and Hsp90 stimulate the  binding of Ctf13 to Skp1.	bind
12405	1	4822	6	NULL	NULL	NULL	NULL	Ctf13	GP		bind					Skp1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_18_8069_s_230	15340069	(C) Sgt1 and Hsp90 stimulate the  binding of Ctf13 to Skp1.	bind
12406	2	4822	6	NULL	NULL	NULL	NULL	Sgt1	GP		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_18_8069_s_230	15340069	(C) Sgt1 and Hsp90 stimulate the  binding of Ctf13 to Skp1.	bind
12407	3	4822	6	NULL	NULL	NULL	NULL	Hsp90	GP		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_18_8069_s_230	15340069	(C) Sgt1 and Hsp90 stimulate the  binding of Ctf13 to Skp1.	bind
14254	1	4825	5	NULL	NULL	0	NULL	MazE	NULL		bind	NULL		random coil region between strand S4 and helix H2		MazF	NULL		helix H3		NULL		0	NULL	NULL	NULL	gw60_molcell_11_4_875_s_157	12718874	(C) Site 3: the random coil region of MazE between   strand S4 and   helix H2 bound to   helix H3 of MazF.	bind
12408	1	4825	6	NULL	NULL	NULL	NULL	MazE	GP		bind			random coil region between strand S4 and helix H2		MazF	GP		helix H3		NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_4_875_s_157	12718874	(C) Site 3: the random coil region of MazE between   strand S4 and   helix H2 bound to   helix H3 of MazF.	bind
14257	2	4827	5	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				Ctpct probe	NULL			single binding elements	NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_4_583_s_125	10744779	(C) Sp proteins transiently expressed in SL2 cells bind to the  Ctpct probe containing single binding elements.	bind
44575	1	4827	5	10	NULL	0	NULL	SL2 cells	NULL		express	NULL	transiently			Sp proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_41_4_583_s_125	10744779	(C) Sp proteins transiently expressed in SL2 cells bind to the  Ctpct probe containing single binding elements.	bind
12409	1	4827	6	NULL	NULL	NULL	NULL	SL2 cells	Cell		express		transiently			Sp proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_4_583_s_125	10744779	(C) Sp proteins transiently expressed in SL2 cells bind to the  Ctpct probe containing single binding elements.	bind
12410	2	4827	6	NULL	NULL	NULL	NULL	statement 1	Process		bind					Ctpct probe	NucleicAcid			single binding elements	NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_4_583_s_125	10744779	(C) Sp proteins transiently expressed in SL2 cells bind to the  Ctpct probe containing single binding elements.	bind
14258	1	4829	5	NULL	NULL	0	NULL	NF-kappaB	NULL		bind	NULL	specifically			cyclin D1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_4_2690_s_106	10082535	(C) Specific binding of NF-kappaB to the cyclin D1 promoter.	bind
12411	1	4829	6	NULL	NULL	NULL	NULL	NF-kappaB	GP		bind		specifically			cyclin D1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_2690_s_106	10082535	(C) Specific binding of NF-kappaB to the cyclin D1 promoter.	bind
14259	1	4830	5	NULL	NULL	0	NULL	SE RNA #1	NULL		bind	NULL	specifically			NFATc	NULL		DBD		NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_298_4_486_s_69	12408978	(C) Specific binding of SE RNA #1 to NFATc DBD.	bind
12412	1	4830	6	NULL	NULL	NULL	NULL	SE RNA #1	NucleicAcid		bind		specifically			NFATc	GP		DBD		NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_298_4_486_s_69	12408978	(C) Specific binding of SE RNA #1 to NFATc DBD.	bind
14260	1	4831	5	NULL	NULL	0	NULL	LXR	NULL		bind	NULL	specifically		PPRE	PPAR /RXR heterodimers	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_1_161_s_69	11172721	(C) Specific binding of the LXR  PPRE by PPAR /RXR heterodimers.	bind
12413	1	4831	6	NULL	NULL	NULL	NULL	PPAR /RXR heterodimers	GP		bind		specifically			LXR	GP			PPRE	NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_1_161_s_69	11172721	(C) Specific binding of the LXR  PPRE by PPAR /RXR heterodimers.	bind
14261	1	4832	5	NULL	NULL	0	NULL	TAR RNA	NULL		bind	NULL				NC protein	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_4_1181_s_92	15249214	(C) Specific inhibition by aptamer N70-13 of TAR  RNA binding to NC protein.	bind
14262	2	4832	5	NULL	NULL	0	NULL	aptamer N70-13	NULL		inhibit	NULL	specifically			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_4_1181_s_92	15249214	(C) Specific inhibition by aptamer N70-13 of TAR  RNA binding to NC protein.	bind
12414	1	4832	6	NULL	NULL	NULL	NULL	TAR RNA	NucleicAcid		bind					NC protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_4_1181_s_92	15249214	(C) Specific inhibition by aptamer N70-13 of TAR  RNA binding to NC protein.	bind
12415	2	4832	6	NULL	NULL	NULL	NULL	aptamer N70-13	NucleicAcid		inhibit		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_4_1181_s_92	15249214	(C) Specific inhibition by aptamer N70-13 of TAR  RNA binding to NC protein.	bind
14263	1	4833	5	NULL	NULL	0	NULL	XAP1	NULL		bind	NULL				CRM1	NULL				NULL		0	NULL	NULL	NULL	gw60_chembiol_7_5_345_s_62	10801471	(c) Specificity of XAP1 binding to CRM1.	bind
12416	1	4833	6	NULL	NULL	NULL	NULL	XAP1	GP		bind					CRM1	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_7_5_345_s_62	10801471	(c) Specificity of XAP1 binding to CRM1.	bind
14264	1	4836	5	NULL	NULL	0	NULL	Stat5a dimers	NULL		bind	NULL				M10 PRRIII probe	NULL	mutant			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_1910_s_165	10022878	(C) Stat5a and Stat5b can bind to the mutant M10 PRRIII probe equally well as dimers and 2x dimers.	bind
14265	2	4836	5	NULL	NULL	0	NULL	Stat5a 2x dimers	NULL		bind	NULL				M10 PRRIII probe	NULL	mutant			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_1910_s_165	10022878	(C) Stat5a and Stat5b can bind to the mutant M10 PRRIII probe equally well as dimers and 2x dimers.	bind
14266	3	4836	5	NULL	NULL	0	NULL	Stat5b dimers	NULL		bind	NULL				M10 PRRIII probe	NULL	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_1910_s_165	10022878	(C) Stat5a and Stat5b can bind to the mutant M10 PRRIII probe equally well as dimers and 2x dimers.	bind
14267	4	4836	5	NULL	NULL	0	NULL	Stat5b 2x dimers	NULL		bind	NULL				M10 PRRIII probe	NULL	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_1910_s_165	10022878	(C) Stat5a and Stat5b can bind to the mutant M10 PRRIII probe equally well as dimers and 2x dimers.	bind
54536	5	4836	5	10	NULL	0	NULL	statement 1		binding of	is equivalent to					statement 2		binding of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_1910_s_165	10022878	(C) Stat5a and Stat5b can bind to the mutant M10 PRRIII probe equally well as dimers and 2x dimers.	bind
54537	6	4836	5	10	NULL	0	NULL	statement 3		binding of	is equivalent to					statement 4		binding of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_1910_s_165	10022878	(C) Stat5a and Stat5b can bind to the mutant M10 PRRIII probe equally well as dimers and 2x dimers.	bind
12417	1	4836	6	NULL	NULL	NULL	NULL	Stat5a dimers	GP		bind					M10 PRRIII probe	NucleicAcid	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_1910_s_165	10022878	(C) Stat5a and Stat5b can bind to the mutant M10 PRRIII probe equally well as dimers and 2x dimers.	bind
12418	2	4836	6	NULL	NULL	NULL	NULL	Stat5b dimers	GP		bind					M10 PRRIII probe	NucleicAcid	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_1910_s_165	10022878	(C) Stat5a and Stat5b can bind to the mutant M10 PRRIII probe equally well as dimers and 2x dimers.	bind
54534	3	4836	6	NULL	NULL	NULL	NULL	Stat5a 2x dimers	GP		bind					M10 PRRIII probe	NucleicAcid	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_1910_s_165	10022878	(C) Stat5a and Stat5b can bind to the mutant M10 PRRIII probe equally well as dimers and 2x dimers.	bind
54535	4	4836	6	NULL	NULL	NULL	NULL	Stat5b 2xdimers	GP		bind					M10 PRRIII probe	NucleicAcid	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_1910_s_165	10022878	(C) Stat5a and Stat5b can bind to the mutant M10 PRRIII probe equally well as dimers and 2x dimers.	bind
54538	5	4836	6	NULL	NULL	NULL	NULL	statement 1	Process	binding of	is equivalent to					statement 3	Process	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_1910_s_165	10022878	(C) Stat5a and Stat5b can bind to the mutant M10 PRRIII probe equally well as dimers and 2x dimers.	bind
54539	6	4836	6	NULL	NULL	NULL	NULL	statement 2	Process	binding of	is equivalent to					statement 4	Process	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_1910_s_165	10022878	(C) Stat5a and Stat5b can bind to the mutant M10 PRRIII probe equally well as dimers and 2x dimers.	bind
14268	1	4837	5	NULL	NULL	0	NULL	GTP S	NULL		bind	NULL				myr-bARF1	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcell_3_3_275_s_73	10198630	(C) Strains listed in (B) were incubated with or without BFA (100  g/mL) for 2 min, pulse labeled for 10 min, and chased for 30 min. (D) Inhibition of Gea1p or G-AR-Gp chimera-stimulated GTP S binding to myr-bARF1 by BFA in vitro was monitored.	bind
14269	2	4837	5	NULL	NULL	0	NULL	Gea1p	NULL		stimulate	NULL				statement 1	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcell_3_3_275_s_73	10198630	(C) Strains listed in (B) were incubated with or without BFA (100  g/mL) for 2 min, pulse labeled for 10 min, and chased for 30 min. (D) Inhibition of Gea1p or G-AR-Gp chimera-stimulated GTP S binding to myr-bARF1 by BFA in vitro was monitored.	bind
14270	3	4837	5	NULL	NULL	0	NULL	G-AR-Gp chimera	NULL		stimulate	NULL				statement 1	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcell_3_3_275_s_73	10198630	(C) Strains listed in (B) were incubated with or without BFA (100  g/mL) for 2 min, pulse labeled for 10 min, and chased for 30 min. (D) Inhibition of Gea1p or G-AR-Gp chimera-stimulated GTP S binding to myr-bARF1 by BFA in vitro was monitored.	bind
14271	4	4837	5	NULL	NULL	0	NULL	BFA	NULL		inhibit	NULL				statement 2	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcell_3_3_275_s_73	10198630	(C) Strains listed in (B) were incubated with or without BFA (100  g/mL) for 2 min, pulse labeled for 10 min, and chased for 30 min. (D) Inhibition of Gea1p or G-AR-Gp chimera-stimulated GTP S binding to myr-bARF1 by BFA in vitro was monitored.	bind
14272	5	4837	5	NULL	NULL	0	NULL	BFA	NULL		inhibit	NULL				statement 3	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcell_3_3_275_s_73	10198630	(C) Strains listed in (B) were incubated with or without BFA (100  g/mL) for 2 min, pulse labeled for 10 min, and chased for 30 min. (D) Inhibition of Gea1p or G-AR-Gp chimera-stimulated GTP S binding to myr-bARF1 by BFA in vitro was monitored.	bind
12419	1	4837	6	NULL	NULL	NULL	NULL	GTP S 	GP		bind					myr-bARF1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_3_3_275_s_73	10198630	(C) Strains listed in (B) were incubated with or without BFA (100  g/mL) for 2 min, pulse labeled for 10 min, and chased for 30 min. (D) Inhibition of Gea1p or G-AR-Gp chimera-stimulated GTP S binding to myr-bARF1 by BFA in vitro was monitored.	bind
54545	2	4837	6	NULL	NULL	NULL	NULL	Gea1p	GP		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_3_275_s_73	10198630	(C) Strains listed in (B) were incubated with or without BFA (100  g/mL) for 2 min, pulse labeled for 10 min, and chased for 30 min. (D) Inhibition of Gea1p or G-AR-Gp chimera-stimulated GTP S binding to myr-bARF1 by BFA in vitro was monitored.	bind
54546	3	4837	6	NULL	NULL	NULL	NULL	G-AR-Gp chimera	GP		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_3_275_s_73	10198630	(C) Strains listed in (B) were incubated with or without BFA (100  g/mL) for 2 min, pulse labeled for 10 min, and chased for 30 min. (D) Inhibition of Gea1p or G-AR-Gp chimera-stimulated GTP S binding to myr-bARF1 by BFA in vitro was monitored.	bind
54547	4	4837	6	NULL	NULL	NULL	NULL	BFA	GP		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_3_275_s_73	10198630	(C) Strains listed in (B) were incubated with or without BFA (100  g/mL) for 2 min, pulse labeled for 10 min, and chased for 30 min. (D) Inhibition of Gea1p or G-AR-Gp chimera-stimulated GTP S binding to myr-bARF1 by BFA in vitro was monitored.	bind
54548	5	4837	6	NULL	NULL	NULL	NULL	BFA	GP		inhibit					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_3_275_s_73	10198630	(C) Strains listed in (B) were incubated with or without BFA (100  g/mL) for 2 min, pulse labeled for 10 min, and chased for 30 min. (D) Inhibition of Gea1p or G-AR-Gp chimera-stimulated GTP S binding to myr-bARF1 by BFA in vitro was monitored.	bind
14273	1	4839	5	10	NULL	0	NULL	ARF	NULL		bind	NULL				N5 fragment	NULL	wild-type		nodal ASE	NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_1_35_s_193	10678167	(C) Supershift analysis of ARF binding to the  N5  wild-type fragment of  nodal ASE.	bind
12420	1	4839	6	NULL	NULL	NULL	NULL	ARF	GP		bind					 N5 fragment	NucleicAcid	wild-type		nodal ASE	NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_1_35_s_193	10678167	(C) Supershift analysis of ARF binding to the  N5  wild-type fragment of  nodal ASE.	bind
14274	1	4840	5	NULL	NULL	0	NULL	HNF1	NULL		bind	NULL					NULL			HNF1 element	NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_1_233_s_92	14575719	(C) Supershift experiments carried out with  antibodies to HNF1  and HNF1  indicate that HNF1  is binding to the HNF1 element.	bind
12421	1	4840	6	NULL	NULL	NULL	NULL	HNF1	GP		bind									HNF1 element	NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_1_233_s_92	14575719	(C) Supershift experiments carried out with  antibodies to HNF1  and HNF1  indicate that HNF1  is binding to the HNF1 element.	bind
14275	1	4841	5	NULL	NULL	0	NULL	Taf1p	NULL		bind	NULL				HXT	NULL				NULL	in Wt cells	0	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_174	15923605	(C) Taf1p binding to  HXT in Wt,  gcn5delta,  spt3delta, and  spt8delta cells.	bind
14276	2	4841	5	NULL	NULL	0	NULL	Taf1p	NULL		bind	NULL				HXT 	NULL				NULL	in gcn5delta cells	0	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_174	15923605	(C) Taf1p binding to  HXT in Wt,  gcn5delta,  spt3delta, and  spt8delta cells.	bind
14277	3	4841	5	NULL	NULL	0	NULL	Taf1p	NULL		bind	NULL				HXT	NULL				NULL	in spt3delta cells	0	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_174	15923605	(C) Taf1p binding to  HXT in Wt,  gcn5delta,  spt3delta, and  spt8delta cells.	bind
14278	4	4841	5	NULL	NULL	0	NULL	Taf1p	NULL		bind	NULL				HXT	NULL				NULL	in spt8delta cells	0	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_174	15923605	(C) Taf1p binding to  HXT in Wt,  gcn5delta,  spt3delta, and  spt8delta cells.	bind
12422	1	4841	6	NULL	NULL	NULL	NULL	Taf1p	GP		bind					HXT	GP				NULL	wild type cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_174	15923605	(C) Taf1p binding to  HXT in Wt,  gcn5delta,  spt3delta, and  spt8delta cells.	bind
12423	2	4841	6	NULL	NULL	NULL	NULL	Taf1p	GP		bind					HXT	GP				NULL	gcn5delta cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_174	15923605	(C) Taf1p binding to  HXT in Wt,  gcn5delta,  spt3delta, and  spt8delta cells.	bind
12424	3	4841	6	NULL	NULL	NULL	NULL	Taf1p	GP		bind					HXT	GP				NULL	spt3delta cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_174	15923605	(C) Taf1p binding to  HXT in Wt,  gcn5delta,  spt3delta, and  spt8delta cells.	bind
12425	4	4841	6	NULL	NULL	NULL	NULL	Taf1p	GP		bind					HXT	GP				NULL	spt8delta cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4863_s_174	15923605	(C) Taf1p binding to  HXT in Wt,  gcn5delta,  spt3delta, and  spt8delta cells.	bind
14279	1	4842	5	NULL	NULL	0	NULL	TAL1beta-BM	NULL		does not bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_6939_s_298	9819382	(C) TAL1beta-BM does not bind to DNA. 293E cells were transfected with expression vectors for wild-type or mutant TAL1beta and E47S.	bind
12426	1	4842	6	NULL	NULL	NULL	NULL	TAL1beta-BM	GP		does not bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6939_s_298	9819382	(C) TAL1beta-BM does not bind to DNA. 293E cells were transfected with expression vectors for wild-type or mutant TAL1beta and E47S.	bind
14280	1	4843	5	NULL	NULL	0	NULL	oligomer mut 4	NULL		contains	NULL				mutated 3' end of the binding motif	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5823_s_283	10409768	(C) TASS-1 binds weakly to oligomers mut 4 and mut 5, in which the 3' end of the binding motif has been mutated (solid box); however, Co-F cannot bind to the DNA-TASS-1 complex.	bind
14281	2	4843	5	NULL	NULL	0	NULL	oligomer mut 5	NULL		contains	NULL				mutated 3' end of the binding motif	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5823_s_283	10409768	(C) TASS-1 binds weakly to oligomers mut 4 and mut 5, in which the 3' end of the binding motif has been mutated (solid box); however, Co-F cannot bind to the DNA-TASS-1 complex.	bind
14282	3	4843	5	NULL	NULL	0	NULL	TASS-1	NULL		bind	NULL	weakly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5823_s_283	10409768	(C) TASS-1 binds weakly to oligomers mut 4 and mut 5, in which the 3' end of the binding motif has been mutated (solid box); however, Co-F cannot bind to the DNA-TASS-1 complex.	bind
14283	4	4843	5	NULL	NULL	0	NULL	TASS-1	NULL		bind	NULL	weakly			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5823_s_283	10409768	(C) TASS-1 binds weakly to oligomers mut 4 and mut 5, in which the 3' end of the binding motif has been mutated (solid box); however, Co-F cannot bind to the DNA-TASS-1 complex.	bind
14284	5	4843	5	NULL	NULL	0	NULL	Co-F	NULL		does not bind	NULL				DNA-TASS-1 complex	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5823_s_283	10409768	(C) TASS-1 binds weakly to oligomers mut 4 and mut 5, in which the 3' end of the binding motif has been mutated (solid box); however, Co-F cannot bind to the DNA-TASS-1 complex.	bind
12427	1	4843	6	NULL	NULL	NULL	NULL	TASS-1	GP		bind		weakly			mut 4 oligomer	NucleicAcid	mutant	3' end of the binding motif		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5823_s_283	10409768	(C) TASS-1 binds weakly to oligomers mut 4 and mut 5, in which the 3' end of the binding motif has been mutated (solid box); however, Co-F cannot bind to the DNA-TASS-1 complex.	bind
12428	2	4843	6	NULL	NULL	NULL	NULL	TASS-1	GP		bind		weakly			mut 5 oligomer	NucleicAcid	mutant	3' end of the binding motif		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5823_s_283	10409768	(C) TASS-1 binds weakly to oligomers mut 4 and mut 5, in which the 3' end of the binding motif has been mutated (solid box); however, Co-F cannot bind to the DNA-TASS-1 complex.	bind
12429	3	4843	6	NULL	NULL	NULL	NULL	Co-F	GP		does not bind					DNA-TASS-1 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5823_s_283	10409768	(C) TASS-1 binds weakly to oligomers mut 4 and mut 5, in which the 3' end of the binding motif has been mutated (solid box); however, Co-F cannot bind to the DNA-TASS-1 complex.	bind
14285	1	4844	5	NULL	NULL	0	NULL	TCR-CD3	NULL		bind	NULL				Nck	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_109_7_901_s_136	12110186	(C) TCR-CD3 binding to Nck is detected before protein tyrosine phosphorylation.	bind
14286	2	4844	5	NULL	NULL	0	NULL	statement 1	NULL		occurs before	NULL				protein	NULL	phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_cell_109_7_901_s_136	12110186	(C) TCR-CD3 binding to Nck is detected before protein tyrosine phosphorylation.	bind
12430	1	4844	6	NULL	NULL	NULL	NULL	TCR-CD3	GP		bind					Nck	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_136	12110186	(C) TCR-CD3 binding to Nck is detected before protein tyrosine phosphorylation.	bind
16286	2	4844	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs before					 protein	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_136	12110186	(C) TCR-CD3 binding to Nck is detected before protein tyrosine phosphorylation.	bind
14287	1	4845	5	NULL	NULL	0	NULL	TCR	NULL		bind	NULL				peptide-MHC complexes	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_5_10_1116_s_56	8548281	(c) The    TCR binds peptide-MHC complexes.	bind
12431	1	4845	6	NULL	NULL	NULL	NULL	TCR	GP		bind					peptide-MHC complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_5_10_1116_s_56	8548281	(c) The    TCR binds peptide-MHC complexes.	bind
54549	1	4846	5	10	NULL	0	NULL	annexin V			bind					PI					NULL		0	NULL	NULL	NULL	gw70_cellbiol_173_1_133_s_61	16606695	(C) The  duration from rounding to annexin V binding and annexin V binding to PI uptake was  calculated for individual cells and is presented as means  plus-or-minus  SEM (error  bars;  n = 25).	bind
12432	1	4846	6	NULL	NULL	NULL	NULL	annexin V	GP		bind					PI	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_1_133_s_61	16606695	(C) The  duration from rounding to annexin V binding and annexin V binding to PI uptake was  calculated for individual cells and is presented as means  plus-or-minus  SEM (error  bars;  n = 25).	bind
14288	1	4847	5	NULL	NULL	0	NULL	p27	NULL	cellular	bind	NULL				CRM1	NULL	recombinant			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_1_201_s_192	12529437	(C) The  effect of LMB on binding of recombinant CRM1 to cellular p27 was assayed as in A.  Equal amounts of heat stable p27 recovered from midG1 cells were reacted with recombinant  RanGTP and CRM1 without (lane 1) or with (lane 2) pretreatment of the CRM1 with LMB.	bind
12433	1	4847	6	NULL	NULL	NULL	NULL	CRM1	GP	recombinant	bind					p27	GP	cellular			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_1_201_s_192	12529437	(C) The  effect of LMB on binding of recombinant CRM1 to cellular p27 was assayed as in A.  Equal amounts of heat stable p27 recovered from midG1 cells were reacted with recombinant  RanGTP and CRM1 without (lane 1) or with (lane 2) pretreatment of the CRM1 with LMB.	bind
14289	1	4848	5	NULL	NULL	0	NULL	Daxx	NULL		bind	NULL		acidic domain		p53	NULL		COOH terminus		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_1_322_s_122	12482984	(C) The acidic domain of Daxx binds to the COOH terminus of p53.	bind
12434	1	4848	6	NULL	NULL	NULL	NULL	Daxx	GP		bind			acidic domain		p53	GP		COOH terminus		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_1_322_s_122	12482984	(C) The acidic domain of Daxx binds to the COOH terminus of p53.	bind
14290	1	4849	5	NULL	NULL	0	NULL	axin	NULL		bind	NULL		GID		GSK-3beta	NULL				NULL	in oocytes	0	NULL	NULL	NULL	gw60_molcellbiol_19_10_7147_s_100	10490650	(C) The axin GID binds GSK-3beta in oocytes.	bind
12435	1	4849	6	NULL	NULL	NULL	NULL	axin	GP		bind			GID		GSK-3beta	GP				NULL	oocytes	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_7147_s_100	10490650	(C) The axin GID binds GSK-3beta in oocytes.	bind
16291	1	4850	5	10	NULL	0	NULL			bidirectional	require				BAL1/BBAP promoter 			intact		IRF-1 binding site	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_14_5348_s_214	16809771	(C) The bidirectional  BAL1/BBAP promoter requires intact IRF-1 and STAT binding sites for IFN-gamma-induced activity.	bind
16292	2	4850	5	10	NULL	0	NULL			bidirectional	require				BAL1/BBAP promoter	IFN-gamma		induced activity of		STAT binding sites	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_14_5348_s_214	16809771	(C) The bidirectional  BAL1/BBAP promoter requires intact IRF-1 and STAT binding sites for IFN-gamma-induced activity.	bind
41611	1	4850	6	NULL	NULL	NULL	NULL			bidirectional	requires				BAL1/BBAP promoter					IRF-1 binding site	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_14_5348_s_214	16809771	(C) The bidirectional  BAL1/BBAP promoter requires intact IRF-1 and STAT binding sites for IFN-gamma-induced activity.	bind
41612	2	4850	6	NULL	NULL	NULL	NULL			bidirectional	 require				BAL1/BBAP promoter	IFN-gamma	GP	induced activity of		STAT binding sites	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_14_5348_s_214	16809771	(C) The bidirectional  BAL1/BBAP promoter requires intact IRF-1 and STAT binding sites for IFN-gamma-induced activity.	bind
14291	1	4851	5	NULL	NULL	0	NULL	ATRIP-LG	NULL		bind	NULL				ATR	NULL				NULL	in A549-derived cells	0	NULL	NULL	NULL	gw70_molbiolcell_16_12_5551_s_88	16176973	(C) The binding ability of ATRIP-LG to ATR. A549-derived cells were lysed  and subjected to immunoprecipitation using anti-ATR or anti-Myc antibody.	bind
12454	1	4851	6	NULL	NULL	NULL	NULL	ATRIP-LG	GP		bind					ATR	GP				NULL	A549-derived cells	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_12_5551_s_88	16176973	(C) The binding ability of ATRIP-LG to ATR. A549-derived cells were lysed  and subjected to immunoprecipitation using anti-ATR or anti-Myc antibody.	bind
14294	1	4853	5	NULL	NULL	0	NULL	p53	NULL		bind	NULL				Ankyrin-like repeat protein gene	NULL			promoter	NULL	primary MEF	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_9_3492_s_219	16611991	(C) The binding of p53 to the  Ankyrin-like repeat protein gene promoter was compared in primary and transformed MEFs.	bind
44588	2	4853	5	10	NULL	0	NULL	p53	NULL		bind	NULL				Ankyrin-like repeat protein gene	NULL			promoter	NULL	transformed MEFs	0	NULL	NULL	NULL	gw70_molcellbiol_26_9_3492_s_219	16611991	(C) The binding of p53 to the  Ankyrin-like repeat protein gene promoter was compared in primary and transformed MEFs.	bind
12455	1	4853	6	NULL	NULL	NULL	NULL	p53	GP		bind					Ankyrin-like repeat protein gene	GP			promoter	NULL	primary MEF	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_9_3492_s_219	16611991	(C) The binding of p53 to the  Ankyrin-like repeat protein gene promoter was compared in primary and transformed MEFs.	bind
12456	2	4853	6	NULL	NULL	NULL	NULL	p53	GP		bind					Ankyrin-like repeat protein gene	GP			promoter	NULL	transformed MEF	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_9_3492_s_219	16611991	(C) The binding of p53 to the  Ankyrin-like repeat protein gene promoter was compared in primary and transformed MEFs.	bind
14295	1	4854	5	NULL	NULL	0	NULL	DHM5	NULL		is	NULL				truncated myosin-Va	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_194	16030255	(C) The binding of truncated myosin-Va  (DHM5) by syntaxin-1A requires a pCa of 6.6.	bind
14296	2	4854	5	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				syntaxin-1A	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_194	16030255	(C) The binding of truncated myosin-Va  (DHM5) by syntaxin-1A requires a pCa of 6.6.	bind
12457	1	4854	6	NULL	NULL	NULL	NULL	myosin-Va	GP	truncated	bind					syntaxin-1A	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_194	16030255	(C) The binding of truncated myosin-Va  (DHM5) by syntaxin-1A requires a pCa of 6.6.	bind
16299	2	4854	6	NULL	NULL	NULL	NULL	myosin-Va	GP	truncated	is					DHM5	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_194	16030255	(C) The binding of truncated myosin-Va  (DHM5) by syntaxin-1A requires a pCa of 6.6.	bind
14298	1	4855	5	NULL	NULL	0	NULL	p97	NULL	wt	bind	NULL				p62	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_8_12_2379_s_213	9398662	(C) The binding of wt p97 and deltaN p97 to p62 adsorbed to microtiter wells was analyzed as in panel B.	bind
14299	2	4855	5	NULL	NULL	0	NULL	p97	NULL		bind	NULL		deltaN		p62	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_8_12_2379_s_213	9398662	(C) The binding of wt p97 and deltaN p97 to p62 adsorbed to microtiter wells was analyzed as in panel B.	bind
12589	1	4855	6	NULL	NULL	NULL	NULL	p97	GP	wild type	bind					p62	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2379_s_213	9398662	(C) The binding of wt p97 and deltaN p97 to p62 adsorbed to microtiter wells was analyzed as in panel B.	bind
12590	2	4855	6	NULL	NULL	NULL	NULL	p97	GP		bind			deltaN		p62	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2379_s_213	9398662	(C) The binding of wt p97 and deltaN p97 to p62 adsorbed to microtiter wells was analyzed as in panel B.	bind
14300	1	4856	5	NULL	NULL	0	NULL	NBS1	NULL	Xenopus	bind	NULL		C-terminal 50 amino acid		ATM	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_234	15964794	(C) The C-terminal 50 amino acids  of  Xenopus NBS1 bind ATM but not Mre11, whereas the C-terminal 147 amino acids of NBS1 bind  to both ATM and Mre11.	bind
14301	2	4856	5	NULL	NULL	0	NULL	NBS1	NULL	Xenopus	does not bind	NULL		C-terminal 50 amino acids		Mre11	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_234	15964794	(C) The C-terminal 50 amino acids  of  Xenopus NBS1 bind ATM but not Mre11, whereas the C-terminal 147 amino acids of NBS1 bind  to both ATM and Mre11.	bind
14302	3	4856	5	10	NULL	0	NULL	NBS1		Xenopus	bind			C-terminal 147 amino acids		ATM					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_234	15964794	(C) The C-terminal 50 amino acids  of  Xenopus NBS1 bind ATM but not Mre11, whereas the C-terminal 147 amino acids of NBS1 bind  to both ATM and Mre11.	bind
14303	4	4856	5	10	NULL	0	NULL	NBS1		Xenopus	bind			C-terminal 147 amino acids		Mre11					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_234	15964794	(C) The C-terminal 50 amino acids  of  Xenopus NBS1 bind ATM but not Mre11, whereas the C-terminal 147 amino acids of NBS1 bind  to both ATM and Mre11.	bind
12591	1	4856	6	NULL	NULL	NULL	NULL	NBS1	GP	Xenopus	bind			C-terminal 50 amino acids 		ATM	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_234	15964794	(C) The C-terminal 50 amino acids  of  Xenopus NBS1 bind ATM but not Mre11, whereas the C-terminal 147 amino acids of NBS1 bind  to both ATM and Mre11.	bind
12592	2	4856	6	NULL	NULL	NULL	NULL	NBS1	GP	Xenopus	does not bind			C-terminal 50 amino acids		Mre11	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_234	15964794	(C) The C-terminal 50 amino acids  of  Xenopus NBS1 bind ATM but not Mre11, whereas the C-terminal 147 amino acids of NBS1 bind  to both ATM and Mre11.	bind
12593	3	4856	6	NULL	NULL	NULL	NULL	NBS1	GP	Xenopus	bind			C-terminal 147 amino acids		ATM	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_234	15964794	(C) The C-terminal 50 amino acids  of  Xenopus NBS1 bind ATM but not Mre11, whereas the C-terminal 147 amino acids of NBS1 bind  to both ATM and Mre11.	bind
12594	4	4856	6	NULL	NULL	NULL	NULL	NBS1	GP	Xenopus	bind			C-terminal 147 amino acids		Mre11	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_234	15964794	(C) The C-terminal 50 amino acids  of  Xenopus NBS1 bind ATM but not Mre11, whereas the C-terminal 147 amino acids of NBS1 bind  to both ATM and Mre11.	bind
14304	1	4857	5	10	NULL	0	NULL	CheY			bind					CheA			P2 domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_4_485_s_155	9809070	(c) The CheY binding P2 domain of CheA has an  /  structure.	bind
14305	1	4858	5	10	NULL	0	NULL	Vav S3			is					Vav protein  		mutant;;lacking	C-terminal SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_6_729_s_58	10394361	(C) The CN from HIV fails to bind to the mutant Vav protein lacking the C-terminal SH3 domain (Vav S3) (lanes 5-8) but interacts with Vav2 (lanes 1-4) in COS cells.	bind
14306	2	4858	5	NULL	NULL	0	NULL	CN	NULL	 HIV	does not bind	NULL				Vav S3	NULL				NULL	in COS cells	NULL	NULL	NULL	NULL	gw60_molcell_3_6_729_s_58	10394361	(C) The CN from HIV fails to bind to the mutant Vav protein lacking the C-terminal SH3 domain (Vav S3) (lanes 5-8) but interacts with Vav2 (lanes 1-4) in COS cells.	bind
14307	3	4858	5	NULL	NULL	0	NULL	CN	NULL	HIV	interacts with	NULL				Vav2	NULL				NULL	in COS cells	NULL	NULL	NULL	NULL	gw60_molcell_3_6_729_s_58	10394361	(C) The CN from HIV fails to bind to the mutant Vav protein lacking the C-terminal SH3 domain (Vav S3) (lanes 5-8) but interacts with Vav2 (lanes 1-4) in COS cells.	bind
12595	3	4858	6	NULL	NULL	NULL	NULL	CN	GP	HIV	does not bind					Vav S3	GP				NULL	COS cells	NULL	NULL	NULL	NULL	gw60_molcell_3_6_729_s_58	10394361	(C) The CN from HIV fails to bind to the mutant Vav protein lacking the C-terminal SH3 domain (Vav S3) (lanes 5-8) but interacts with Vav2 (lanes 1-4) in COS cells.	bind
12596	2	4858	6	NULL	NULL	NULL	NULL	CN	GP	HIV	interacts with					Vav2	GP				NULL	COS cells	NULL	NULL	NULL	NULL	gw60_molcell_3_6_729_s_58	10394361	(C) The CN from HIV fails to bind to the mutant Vav protein lacking the C-terminal SH3 domain (Vav S3) (lanes 5-8) but interacts with Vav2 (lanes 1-4) in COS cells.	bind
54551	1	4858	6	NULL	NULL	NULL	NULL	Vav S3	GP		is					Vav protein	GP	mutant;;lacking	C-terminal SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_6_729_s_58	10394361	(C) The CN from HIV fails to bind to the mutant Vav protein lacking the C-terminal SH3 domain (Vav S3) (lanes 5-8) but interacts with Vav2 (lanes 1-4) in COS cells.	bind
14308	1	4860	5	NULL	NULL	0	NULL	Sac6	NULL		bind	NULL				actin filaments	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_7_2617_s_253	12857851	(C) The concentrations of Sac6 ( ) and Scp1 ( ) bound to  actin filaments were calculated from gel densitometry and plotted versus  the  total concentration of His6-Scp1 in the reactions.	bind
14309	2	4860	5	NULL	NULL	0	NULL	Scp1	NULL		bind	NULL				actin filaments	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_7_2617_s_253	12857851	(C) The concentrations of Sac6 ( ) and Scp1 ( ) bound to  actin filaments were calculated from gel densitometry and plotted versus  the  total concentration of His6-Scp1 in the reactions.	bind
12597	1	4860	6	NULL	NULL	NULL	NULL	sac6	GP		bind					actin filament	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_7_2617_s_253	12857851	(C) The concentrations of Sac6 ( ) and Scp1 ( ) bound to  actin filaments were calculated from gel densitometry and plotted versus  the  total concentration of His6-Scp1 in the reactions.	bind
12598	2	4860	6	NULL	NULL	NULL	NULL	Scp1	GP		bind					actin filament	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_7_2617_s_253	12857851	(C) The concentrations of Sac6 ( ) and Scp1 ( ) bound to  actin filaments were calculated from gel densitometry and plotted versus  the  total concentration of His6-Scp1 in the reactions.	bind
14310	1	4861	5	NULL	NULL	0	NULL	Sac6	NULL		bind	NULL				actin filaments	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_7_2617_s_253	12857851	(C) The concentrations of Sac6 ( ) and Scp1 ( ) bound to  actin filaments were calculated from gel densitometry and plotted versus the  total concentration of His6-Scp1 in the reactions.	bind
14311	2	4861	5	NULL	NULL	0	NULL	Scp1	NULL		bind	NULL				actin filaments	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_7_2617_s_253	12857851	(C) The concentrations of Sac6 ( ) and Scp1 ( ) bound to  actin filaments were calculated from gel densitometry and plotted versus the  total concentration of His6-Scp1 in the reactions.	bind
14312	1	4862	5	10	NULL	0	NULL	GST-GraudeltaN 			bind			E493K		DNA					NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_4_1831_s_163	10924478	(C) The DNA-binding activity of the GST-GraudeltaN E493K and C298Y fusions was analyzed by gel-shift assay.	bind
14313	2	4862	5	10	NULL	0	NULL	GST-GraudeltaN 			bind			C298Y		DNA					NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_4_1831_s_163	10924478	(C) The DNA-binding activity of the GST-GraudeltaN E493K and C298Y fusions was analyzed by gel-shift assay.	bind
54552	3	4862	5	10	NULL	0	NULL	GST-GraudeltaN			is a type of			E493K		fusion protein					NULL		0	NULL	NULL	NULL	gw60_genetics_155_4_1831_s_163	10924478	(C) The DNA-binding activity of the GST-GraudeltaN E493K and C298Y fusions was analyzed by gel-shift assay.	bind
54553	4	4862	5	10	NULL	0	NULL	GST-GraudeltaN			is a type of			C298Y		fusion protein					NULL		0	NULL	NULL	NULL	gw60_genetics_155_4_1831_s_163	10924478	(C) The DNA-binding activity of the GST-GraudeltaN E493K and C298Y fusions was analyzed by gel-shift assay.	bind
12599	1	4862	6	NULL	NULL	NULL	NULL	GST-GraudeltaN	GP		bind			E493K		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_4_1831_s_163	10924478	(C) The DNA-binding activity of the GST-GraudeltaN E493K and C298Y fusions was analyzed by gel-shift assay.	bind
12821	2	4862	6	NULL	NULL	NULL	NULL	GST-GraudeltaN	GP		bind			C298Y		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_4_1831_s_163	10924478	(C) The DNA-binding activity of the GST-GraudeltaN E493K and C298Y fusions was analyzed by gel-shift assay.	bind
54554	3	4862	6	NULL	NULL	NULL	NULL	GST-GraudeltaN 	GP		is a type of			E493K		fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_4_1831_s_163	10924478	(C) The DNA-binding activity of the GST-GraudeltaN E493K and C298Y fusions was analyzed by gel-shift assay.	bind
54555	4	4862	6	NULL	NULL	NULL	NULL	GST-GraudeltaN	GP		is a type of			 C298Y		fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_4_1831_s_163	10924478	(C) The DNA-binding activity of the GST-GraudeltaN E493K and C298Y fusions was analyzed by gel-shift assay.	bind
16293	1	4863	5	NULL	NULL	0	NULL	annexin V	NULL		bind	NULL				PI	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_173_1_133_s_123	16606695	(C) The duration from  rounding to annexin V binding and annexin V binding to PI uptake was calculated for  individual cells and is presented as means  plus-or-minus  SEM (error bars;  n = 33).	bind
12822	1	4863	6	NULL	NULL	NULL	NULL	annexin V	GP		bind					PI	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_1_133_s_123	16606695	(C) The duration from  rounding to annexin V binding and annexin V binding to PI uptake was calculated for  individual cells and is presented as means  plus-or-minus  SEM (error bars;  n = 33).	bind
14314	1	4866	5	10	NULL	0	NULL	NahR			bind					Psal					NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1725_2_247_s_188	15978733	(C) The effect of salicylate  (0.1, 1 or 10 mM) on the sensorgram of NahR (1  M) binding to  Psal (1000 RU) is shown at a flow rate of 20  l/min.	bind
12614	1	4866	6	NULL	NULL	NULL	NULL	NahR	GP		bind					Psal	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1725_2_247_s_188	15978733	(C) The effect of salicylate  (0.1, 1 or 10 mM) on the sensorgram of NahR (1  M) binding to  Psal (1000 RU) is shown at a flow rate of 20  l/min.	bind
14315	1	4867	5	10	NULL	0	NULL	LPA			induce					IP		generation of			NULL	in HeLa cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_11_5069_s_203	15143197	(C) The effects of  a mutation at the C-terminal PDZ-binding motif of LPA2 on LPA-induced IPs generation in HeLa cells.	bind
12620	1	4867	6	NULL	NULL	NULL	NULL	LPA	Chemical		induces					IP	GP	generation of			NULL	HeLa cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_11_5069_s_203	15143197	(C) The effects of  a mutation at the C-terminal PDZ-binding motif of LPA2 on LPA-induced IPs generation in HeLa cells.	bind
14316	1	4868	5	NULL	NULL	0	NULL	FRL	NULL		bind	NULL		FH1 domain		profilin	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_18_6872_s_269	10958683	(C) The FH1 domain of FRL binds to profilin.	bind
12622	1	4868	6	NULL	NULL	NULL	NULL	FRL	GP		bind			FH1 domain		profilin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6872_s_269	10958683	(C) The FH1 domain of FRL binds to profilin.	bind
14317	1	4869	5	10	NULL	0	NULL	Alp11B			bind		efficiently			alpha-tubulin					NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_9_2987_s_264	10473641	(C) The glycine-rich domain is important for efficient binding between Alp11B and alpha-tubulin.	bind
54556	2	4869	5	10	NULL	0	NULL				is important for			glycine-rich domain		statement 1					NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_9_2987_s_264	10473641	(C) The glycine-rich domain is important for efficient binding between Alp11B and alpha-tubulin.	bind
12625	1	4869	6	NULL	NULL	NULL	NULL	Alp11B	GP		bind		efficiently			alpha-tubulin	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_9_2987_s_264	10473641	(C) The glycine-rich domain is important for efficient binding between Alp11B and alpha-tubulin.	bind
12627	2	4869	6	NULL	NULL	NULL	NULL				is important for			glycine-rich domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_9_2987_s_264	10473641	(C) The glycine-rich domain is important for efficient binding between Alp11B and alpha-tubulin.	bind
14318	1	4870	5	NULL	NULL	0	NULL	Grp1	NULL		bind	NULL		PH domain		Ins(1,3,4,5)P4	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_8_4_829_s_234	11684018	(C) The Grp1 PH domain bound to Ins(1,3,4,5)P4.	bind
12629	1	4870	6	NULL	NULL	NULL	NULL	Grp1	GP		bind			PH domain		Ins(1,3,4,5)P4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_4_829_s_234	11684018	(C) The Grp1 PH domain bound to Ins(1,3,4,5)P4.	bind
14319	1	4871	5	NULL	NULL	0	NULL	DdLIMP	NULL		sediments with	NULL				PIP2	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_1_167_s_313	10189376	(C) The highest amount  of DdLIMP is sedimented with PIP2, there is only  minute binding to PC, and moderate binding to  the anionic phospholipid PS.	bind
14320	2	4871	5	10	NULL	0	NULL	DdLIMP			bind					PC					NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_1_167_s_313	10189376	(C) The highest amount  of DdLIMP is sedimented with PIP2, there is only  minute binding to PC, and moderate binding to  the anionic phospholipid PS.	bind
14321	3	4871	5	NULL	NULL	0	NULL	DdLIMP	NULL		bind	NULL	moderate			phospholipid PS	NULL	anionic			NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_1_167_s_313	10189376	(C) The highest amount  of DdLIMP is sedimented with PIP2, there is only  minute binding to PC, and moderate binding to  the anionic phospholipid PS.	bind
12631	1	4871	6	NULL	NULL	NULL	NULL	DdLIMP	GP		bind					PIP2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_1_167_s_313	10189376	(C) The highest amount  of DdLIMP is sedimented with PIP2, there is only  minute binding to PC, and moderate binding to  the anionic phospholipid PS.	bind
12688	2	4871	6	NULL	NULL	NULL	NULL	DdLIMP	GP		bind					PC	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_1_167_s_313	10189376	(C) The highest amount  of DdLIMP is sedimented with PIP2, there is only  minute binding to PC, and moderate binding to  the anionic phospholipid PS.	bind
12689	3	4871	6	NULL	NULL	NULL	NULL	DdLIMP	GP		bind		moderate			phospholipid PS	CellComponent	anionic			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_1_167_s_313	10189376	(C) The highest amount  of DdLIMP is sedimented with PIP2, there is only  minute binding to PC, and moderate binding to  the anionic phospholipid PS.	bind
14322	1	4872	5	NULL	NULL	0	NULL	SMRT	NULL		bind	NULL				RARbeta	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_8_2844_s_163	12665583	(C) The I412T mutant enhances SMRT binding by RARbeta, but not RARalpha, in a GST-protein interaction assay in vitro.	bind
14323	2	4872	5	NULL	NULL	0	NULL		NULL	mutant	enhances	NULL		I412T		statement 1	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_8_2844_s_163	12665583	(C) The I412T mutant enhances SMRT binding by RARbeta, but not RARalpha, in a GST-protein interaction assay in vitro.	bind
14324	3	4872	5	NULL	NULL	0	NULL	SMRT	NULL		bind	NULL				RARalpha	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_8_2844_s_163	12665583	(C) The I412T mutant enhances SMRT binding by RARbeta, but not RARalpha, in a GST-protein interaction assay in vitro.	bind
14325	4	4872	5	NULL	NULL	0	NULL		NULL	mutant	does not enhance	NULL		I412T		statement 3	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_8_2844_s_163	12665583	(C) The I412T mutant enhances SMRT binding by RARbeta, but not RARalpha, in a GST-protein interaction assay in vitro.	bind
12690	1	4872	6	NULL	NULL	NULL	NULL	SMRT	GP		bind					RARbeta	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_8_2844_s_163	12665583	(C) The I412T mutant enhances SMRT binding by RARbeta, but not RARalpha, in a GST-protein interaction assay in vitro.	bind
12691	2	4872	6	NULL	NULL	NULL	NULL	SMRT	GP		bind					RARalpha	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_8_2844_s_163	12665583	(C) The I412T mutant enhances SMRT binding by RARbeta, but not RARalpha, in a GST-protein interaction assay in vitro.	bind
12692	3	4872	6	NULL	NULL	NULL	NULL			mutant	enhances			I412T		statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_8_2844_s_163	12665583	(C) The I412T mutant enhances SMRT binding by RARbeta, but not RARalpha, in a GST-protein interaction assay in vitro.	bind
12693	4	4872	6	NULL	NULL	NULL	NULL			mutant	does not enhance			I412T		statement 2	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_8_2844_s_163	12665583	(C) The I412T mutant enhances SMRT binding by RARbeta, but not RARalpha, in a GST-protein interaction assay in vitro.	bind
14326	1	4873	5	NULL	NULL	0	NULL	HIF-1	NULL		bind	NULL				PSMA7	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_febslett_498_1_62_s_82	11389899	(C) The in vivo binding of HIF-1  to PSMA7 was confirmed by co-immunoprecipitation.	bind
12694	1	4873	6	NULL	NULL	NULL	NULL	HIF-1	GP		bind					PSMA7	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_febslett_498_1_62_s_82	11389899	(C) The in vivo binding of HIF-1  to PSMA7 was confirmed by co-immunoprecipitation.	bind
14327	1	4874	5	NULL	NULL	0	NULL	Chl4p	NULL		interacts with	NULL				CEN DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_2_460_s_108	12589047	(C) The interaction of Chl4p with  CEN DNA depends on Ctf19p.	bind
14328	2	4874	5	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				Ctf19p	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_2_460_s_108	12589047	(C) The interaction of Chl4p with  CEN DNA depends on Ctf19p.	bind
12695	1	4874	6	NULL	NULL	NULL	NULL	Chl4p	GP		interacts with					CEN DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_460_s_108	12589047	(C) The interaction of Chl4p with  CEN DNA depends on Ctf19p.	bind
12696	2	4874	6	NULL	NULL	NULL	NULL	statement 1	Process		is dependent on					Ctf19p	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_460_s_108	12589047	(C) The interaction of Chl4p with  CEN DNA depends on Ctf19p.	bind
14329	1	4875	5	NULL	NULL	0	NULL	nm23-H2	NULL	kinase negative mutant 	bind	NULL				Lbc	NULL	mutant	H118F		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_4_1063_s_98	15249197	(C) The kinase negative  mutant of nm23-H2 binds to Lbc. H118F mutant was expressed and subjected to binding  assay.	bind
12697	1	4875	6	NULL	NULL	NULL	NULL	nm23-H2		kinase negative mutant	bind					Lbc	GP	mutant	H118F		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_4_1063_s_98	15249197	(C) The kinase negative  mutant of nm23-H2 binds to Lbc. H118F mutant was expressed and subjected to binding  assay.	bind
14330	1	4876	5	10	NULL	0	NULL	nucleosomes 			does not bind				last 13 bp of DNA	histone octamer					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_22_10047_s_124	15509805	(c) The last 13 bp of DNA on nucleosomes slid by ISW2 were not bound to the histone  octamer, as shown by exonuclease III footprinting.	bind
12699	2	4876	6	NULL	NULL	NULL	NULL	nucleosomes			does not bind				last 13 bp of DNA on	histone octamer					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_22_10047_s_124	15509805	(c) The last 13 bp of DNA on nucleosomes slid by ISW2 were not bound to the histone  octamer, as shown by exonuclease III footprinting.	bind
14331	1	4877	5	NULL	NULL	0	NULL	Nyv1p	NULL		bind	NULL		longin domain		AP3	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw70_molbiolcell_17_10_4282_s_291	16855025	(C) The longin domain of Nyv1p binds to  AP3 in vitro.	bind
12700	1	4877	6	NULL	NULL	NULL	NULL	Nyv1p	GP		bind			longin domain		AP3	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molbiolcell_17_10_4282_s_291	16855025	(C) The longin domain of Nyv1p binds to  AP3 in vitro.	bind
14332	1	4878	5	NULL	NULL	0	NULL	G-CSF	NULL	biotin-labeled	bind	NULL				G-CSF receptor	NULL				NULL	UT-7/GR cell surface	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_319_2_582_s_145	15178446	(C) The mean fluorescence  intensity (MFI) that represents biotin-labeled G-CSF bound to G-CSF receptor expressed  on the UT-7/GR cell surface was competitively suppressed by G-CSF-PE40 in a dose-dependent  manner.	bind
14333	2	4878	5	10	NULL	0	NULL	G-CSF-PE40			supress		competitively;;dose dependently			statement 1					NULL	UT-7/GR cell surface	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_319_2_582_s_145	15178446	(C) The mean fluorescence  intensity (MFI) that represents biotin-labeled G-CSF bound to G-CSF receptor expressed  on the UT-7/GR cell surface was competitively suppressed by G-CSF-PE40 in a dose-dependent  manner.	bind
12823	1	4878	6	NULL	NULL	NULL	NULL	G-CSF	GP	biotin-labeled	bind					G-CSF receptor	GP				NULL	UT-7/GR cell surface	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_319_2_582_s_145	15178446	(C) The mean fluorescence  intensity (MFI) that represents biotin-labeled G-CSF bound to G-CSF receptor expressed  on the UT-7/GR cell surface was competitively suppressed by G-CSF-PE40 in a dose-dependent  manner.	bind
12824	2	4878	6	NULL	NULL	NULL	NULL	G-CSF-PE40	GP		suppresses		competitively;;dose dependently			statement 1	Process				NULL	UT-7/GR cell surface	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_319_2_582_s_145	15178446	(C) The mean fluorescence  intensity (MFI) that represents biotin-labeled G-CSF bound to G-CSF receptor expressed  on the UT-7/GR cell surface was competitively suppressed by G-CSF-PE40 in a dose-dependent  manner.	bind
14334	1	4879	5	NULL	NULL	0	NULL	Msb3	NULL		bind	NULL		N-terminal non-GAP region		Spa2	NULL		SHD-I region		NULL	in vitro	0	NULL	NULL	NULL	gw70_molcellbiol_25_19_8567_s_40	16166638	(C) The N-terminal, non-GAP  region of Msb3 or Msb4 binds to the SHD-I region of Spa2 in vitro.	bind
14335	2	4879	5	NULL	NULL	0	NULL	Msb4	NULL		bind	NULL		N-terminal non-GAP region		Spa2	NULL		SHD-I region		NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8567_s_40	16166638	(C) The N-terminal, non-GAP  region of Msb3 or Msb4 binds to the SHD-I region of Spa2 in vitro.	bind
14336	3	4879	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_19_8567_s_40	16166638	(C) The N-terminal, non-GAP  region of Msb3 or Msb4 binds to the SHD-I region of Spa2 in vitro.	bind
12716	1	4879	6	NULL	NULL	NULL	NULL	Msb3	GP		bind			N-terminal non-GAP region		Spa2	GP		SHD-I		NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8567_s_40	16166638	(C) The N-terminal, non-GAP  region of Msb3 or Msb4 binds to the SHD-I region of Spa2 in vitro.	bind
12717	2	4879	6	NULL	NULL	NULL	NULL	Msb4	GP		bind			N-terminal non-GAP region		Spa2	GP		SHD-I		NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8567_s_40	16166638	(C) The N-terminal, non-GAP  region of Msb3 or Msb4 binds to the SHD-I region of Spa2 in vitro.	bind
12718	3	4879	6	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8567_s_40	16166638	(C) The N-terminal, non-GAP  region of Msb3 or Msb4 binds to the SHD-I region of Spa2 in vitro.	bind
14337	1	4880	5	NULL	NULL	0	NULL	anti-Nischarin antibody	NULL	chicken	bind	NULL				Nischarin	NULL	endogenous			NULL	in RIE cells	0	NULL	NULL	NULL	gw60_cellbiol_151_6_1141_s_265	11121431	(C) The peptide used for immunization can block the binding of chicken anti-Nischarin antibody both to endogenous Nischarin in RIE cells and to expressed Nischarin in Cos7 cells.	bind
14339	2	4880	5	10	NULL	0	NULL	anti-Nischarin antibody	NULL	chicken	bind	NULL				Nischarin 	NULL				NULL	expressed in Cos7 cells	NULL	NULL	NULL	NULL	gw60_cellbiol_151_6_1141_s_265	11121431	(C) The peptide used for immunization can block the binding of chicken anti-Nischarin antibody both to endogenous Nischarin in RIE cells and to expressed Nischarin in Cos7 cells.	bind
12719	1	4880	6	NULL	NULL	NULL	NULL	anti-Nischarin antibody	GP	chicken	bind					Nischarin	GP	endogenous			NULL	RIE cells	NULL	NULL	NULL	NULL	gw60_cellbiol_151_6_1141_s_265	11121431	(C) The peptide used for immunization can block the binding of chicken anti-Nischarin antibody both to endogenous Nischarin in RIE cells and to expressed Nischarin in Cos7 cells.	bind
12720	2	4880	6	NULL	NULL	NULL	NULL	anti-Nischarin antibody	GP	chicken	bind					Nischarin	GP				NULL	expressed in Cos7 cells	NULL	NULL	NULL	NULL	gw60_cellbiol_151_6_1141_s_265	11121431	(C) The peptide used for immunization can block the binding of chicken anti-Nischarin antibody both to endogenous Nischarin in RIE cells and to expressed Nischarin in Cos7 cells.	bind
14418	1	4881	5	NULL	NULL	0	NULL	PPT1	NULL	bovine	bind	NULL				palmitate	NULL				NULL		0	NULL	NULL	NULL	gw60_gene_312_0_271_s_96	12909364	(C) The predicted amino acid sequence of CG12108 and human PPT1 were superimposed onto the crystal structure of bovine PPT1 bound to palmitate (PDB#1EH5) using MSA-3D, and the results viewed using Protein Explorer.	bind
12722	1	4881	6	NULL	NULL	NULL	NULL	PPT1	GP	bovine	bind					palmitate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_gene_312_0_271_s_96	12909364	(C) The predicted amino acid sequence of CG12108 and human PPT1 were superimposed onto the crystal structure of bovine PPT1 bound to palmitate (PDB#1EH5) using MSA-3D, and the results viewed using Protein Explorer.	bind
14419	1	4884	5	NULL	NULL	0	NULL	GTP S	NULL		bind	NULL				myr-yARF2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_3_3_275_s_128	10198630	(C) The Sec7 domain of yeast Gea1p (wild type) or the same domain carrying the mutation M699L was purified from  E. coli and tested for stimulation of GTP S binding to myr-yARF2 in the presence or absence of BFA.	bind
12723	1	4884	6	NULL	NULL	NULL	NULL	GTP S	Chemical		bind					myr-yARF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_3_275_s_128	10198630	(C) The Sec7 domain of yeast Gea1p (wild type) or the same domain carrying the mutation M699L was purified from  E. coli and tested for stimulation of GTP S binding to myr-yARF2 in the presence or absence of BFA.	bind
14420	1	4885	5	NULL	NULL	0	NULL	BiP	NULL		bind	NULL				HC	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_15_1_105_s_227	11485742	(C) The signals for HC and labeled BiP were quantitated by densiotometry, and the relative amount of BiP bound to HC was determined with the value at 150 min set to 100	bind
12724	1	4885	6	NULL	NULL	NULL	NULL	BiP	GP		bind					HC	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_1_105_s_227	11485742	(C) The signals for HC and labeled BiP were quantitated by densiotometry, and the relative amount of BiP bound to HC was determined with the value at 150 min set to 100	bind
14421	1	4886	5	NULL	NULL	0	NULL	TopBP1	NULL		bind	NULL		sixth BRCT domain		E2F1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_9_3287_s_167	12697828	(C) The sixth BRCT domain of TopBP1  binds E2F1.	bind
12725	1	4886	6	NULL	NULL	NULL	NULL	TopBP1	GP		bind			sixth BRCT domain		E2F1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_9_3287_s_167	12697828	(C) The sixth BRCT domain of TopBP1  binds E2F1.	bind
14422	1	4888	5	NULL	NULL	0	NULL	Sox-2	NULL		bind	NULL				UTF1	NULL			regulatory element	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_219	10409735	(C) The Sox-2 and chimera 1 bearing the POU DNA binding domain of Oct-6 bind to the UTF1 regulatory element in a mutually exclusive manner.	bind
14423	2	4888	5	NULL	NULL	0	NULL	chimera 1	NULL		bind	NULL		POU DNA binding domain of Oct-6		UTF1	NULL			regulatory element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_219	10409735	(C) The Sox-2 and chimera 1 bearing the POU DNA binding domain of Oct-6 bind to the UTF1 regulatory element in a mutually exclusive manner.	bind
14424	3	4888	5	NULL	NULL	0	NULL	statement 1	NULL		mutually exclusive to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_219	10409735	(C) The Sox-2 and chimera 1 bearing the POU DNA binding domain of Oct-6 bind to the UTF1 regulatory element in a mutually exclusive manner.	bind
12726	1	4888	6	NULL	NULL	NULL	NULL	Sox-2	GP		bind					UTF-1	GP			regulatory element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_219	10409735	(C) The Sox-2 and chimera 1 bearing the POU DNA binding domain of Oct-6 bind to the UTF1 regulatory element in a mutually exclusive manner.	bind
12727	2	4888	6	NULL	NULL	NULL	NULL	chimera 1	GP		bind			POU DNA binding domain of Oct-6		UTF-1	GP			regulatory element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_219	10409735	(C) The Sox-2 and chimera 1 bearing the POU DNA binding domain of Oct-6 bind to the UTF1 regulatory element in a mutually exclusive manner.	bind
12728	3	4888	6	NULL	NULL	NULL	NULL	statement 1	Process		is independent of					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_219	10409735	(C) The Sox-2 and chimera 1 bearing the POU DNA binding domain of Oct-6 bind to the UTF1 regulatory element in a mutually exclusive manner.	bind
14425	1	4889	5	NULL	NULL	0	NULL	GBD hybrid	NULL		bind	NULL					NULL			Gal4 binding sites	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_23_8292_s_125	12417731	(C) The strain is the same as in panel B except that a GBD hybrid binds to the Gal4 binding sites and causes silencing of the  URA3 gene.	bind
14426	2	4889	5	NULL	NULL	0	NULL	statement 1	NULL		causes	NULL				URA3 gene	NULL	silencing of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_23_8292_s_125	12417731	(C) The strain is the same as in panel B except that a GBD hybrid binds to the Gal4 binding sites and causes silencing of the  URA3 gene.	bind
12729	1	4889	6	NULL	NULL	NULL	NULL	GBD hybrid			bind									Gal4 binding sites	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_23_8292_s_125	12417731	(C) The strain is the same as in panel B except that a GBD hybrid binds to the Gal4 binding sites and causes silencing of the  URA3 gene.	bind
12730	2	4889	6	NULL	NULL	NULL	NULL	statement 1			causes					URA3 gene	GP	silencing of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_23_8292_s_125	12417731	(C) The strain is the same as in panel B except that a GBD hybrid binds to the Gal4 binding sites and causes silencing of the  URA3 gene.	bind
14417	2	4890	5	10	NULL	0	NULL	Ras		distal	bind					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_cell_112_5_685_s_33	12628188	(C) The structure of the distal Ras bound to the GTP analog GppNp from the RasY64A complex is shown on the left (structure D).	bind
54557	1	4890	5	10	NULL	0	NULL	GppNp 			is from					RasY64A complex					NULL		0	NULL	NULL	NULL	gw60_cell_112_5_685_s_33	12628188	(C) The structure of the distal Ras bound to the GTP analog GppNp from the RasY64A complex is shown on the left (structure D).	bind
54558	3	4890	5	10	NULL	0	NULL	GppNp			is a type of					GTP analog					NULL		0	NULL	NULL	NULL	gw60_cell_112_5_685_s_33	12628188	(C) The structure of the distal Ras bound to the GTP analog GppNp from the RasY64A complex is shown on the left (structure D).	bind
12731	1	4890	6	NULL	NULL	NULL	NULL	GppNp	Chemical		is from					Ras complex	GP		Y64A		NULL		NULL	NULL	NULL	NULL	gw60_cell_112_5_685_s_33	12628188	(C) The structure of the distal Ras bound to the GTP analog GppNp from the RasY64A complex is shown on the left (structure D).	bind
12732	2	4890	6	NULL	NULL	NULL	NULL	Ras	GP	distal	bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_5_685_s_33	12628188	(C) The structure of the distal Ras bound to the GTP analog GppNp from the RasY64A complex is shown on the left (structure D).	bind
41696	3	4890	6	NULL	NULL	NULL	NULL	GppNp	Chemical		is a type of					GTP analog	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_5_685_s_33	12628188	(C) The structure of the distal Ras bound to the GTP analog GppNp from the RasY64A complex is shown on the left (structure D).	bind
14427	1	4891	5	NULL	NULL	0	NULL	DinR	NULL		bind	NULL				dinR	NULL			promoter/operator	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_8_2201_s_227	9555905	(C) Three-dimensional representation of the bases within the  recA operator that are protected by DinR during hydroxyl radical cleavage, indicating that the protected sites lie on one face of [[ the DNA.                     The nondenaturing gel mobility shift assay ]] suggests that DinR apparently binds to the  dinR promoter/operator to form two major protein-DNA species (Fig.  5).	bind
14428	2	4891	5	10	NULL	0	NULL	statement 1			forms					 protein-DNA species		two major			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_8_2201_s_227	9555905	(C) Three-dimensional representation of the bases within the  recA operator that are protected by DinR during hydroxyl radical cleavage, indicating that the protected sites lie on one face of [[ the DNA.                     The nondenaturing gel mobility shift assay ]] suggests that DinR apparently binds to the  dinR promoter/operator to form two major protein-DNA species (Fig.  5).	bind
16294	3	4891	5	NULL	NULL	0	NULL	recA	NULL		protected by	NULL			operator	DinR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_8_2201_s_227	9555905	(C) Three-dimensional representation of the bases within the  recA operator that are protected by DinR during hydroxyl radical cleavage, indicating that the protected sites lie on one face of [[ the DNA.                     The nondenaturing gel mobility shift assay ]] suggests that DinR apparently binds to the  dinR promoter/operator to form two major protein-DNA species (Fig.  5).	bind
16295	4	4891	5	NULL	NULL	0	NULL	statement 3	NULL		occurs during	NULL				hydroxyl radical cleavage	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_8_2201_s_227	9555905	(C) Three-dimensional representation of the bases within the  recA operator that are protected by DinR during hydroxyl radical cleavage, indicating that the protected sites lie on one face of [[ the DNA.                     The nondenaturing gel mobility shift assay ]] suggests that DinR apparently binds to the  dinR promoter/operator to form two major protein-DNA species (Fig.  5).	bind
12733	1	4891	6	NULL	NULL	NULL	NULL	DinR	GP		bind					dinR	GP			promoter/operator	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_8_2201_s_227	9555905	(C) Three-dimensional representation of the bases within the  recA operator that are protected by DinR during hydroxyl radical cleavage, indicating that the protected sites lie on one face of [[ the DNA.                     The nondenaturing gel mobility shift assay ]] suggests that DinR apparently binds to the  dinR promoter/operator to form two major protein-DNA species (Fig.  5).	bind
12734	2	4891	6	NULL	NULL	NULL	NULL	recA	GP		protected by				operator	DinR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_8_2201_s_227	9555905	(C) Three-dimensional representation of the bases within the  recA operator that are protected by DinR during hydroxyl radical cleavage, indicating that the protected sites lie on one face of [[ the DNA.                     The nondenaturing gel mobility shift assay ]] suggests that DinR apparently binds to the  dinR promoter/operator to form two major protein-DNA species (Fig.  5).	bind
12735	3	4891	6	NULL	NULL	NULL	NULL	statement 2	Process		occurs during					hydroxyl radical cleavage	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_8_2201_s_227	9555905	(C) Three-dimensional representation of the bases within the  recA operator that are protected by DinR during hydroxyl radical cleavage, indicating that the protected sites lie on one face of [[ the DNA.                     The nondenaturing gel mobility shift assay ]] suggests that DinR apparently binds to the  dinR promoter/operator to form two major protein-DNA species (Fig.  5).	bind
16300	4	4891	6	NULL	NULL	NULL	NULL	statement 1	Process		forms					protein-DNA species		two major			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_8_2201_s_227	9555905	(C) Three-dimensional representation of the bases within the  recA operator that are protected by DinR during hydroxyl radical cleavage, indicating that the protected sites lie on one face of [[ the DNA.                     The nondenaturing gel mobility shift assay ]] suggests that DinR apparently binds to the  dinR promoter/operator to form two major protein-DNA species (Fig.  5).	bind
14429	1	4892	5	NULL	NULL	0	NULL	GTP S	NULL		bind	NULL				ARF6-His	NULL				NULL		NULL	NULL	NULL	NULL	gw70_febslett_579_2_343_s_34	15642342	(C) Time course of [35]GTP S binding to ARF6-His.	bind
12736	1	4892	6	NULL	NULL	NULL	NULL	GTP S	Chemical		bind					ARF6-His	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_579_2_343_s_34	15642342	(C) Time course of [35]GTP S binding to ARF6-His.	bind
14430	1	4893	5	NULL	NULL	0	NULL	collagen	NULL		bind	NULL					NULL		upper front edge of I domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_101_1_47_s_95	10778855	(C) Top view of complex, showing how collagen  binds to the upper front edge of the I domain.	bind
12737	1	4893	6	NULL	NULL	NULL	NULL	collagen	GP		bind								upper front edge of the I domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_101_1_47_s_95	10778855	(C) Top view of complex, showing how collagen  binds to the upper front edge of the I domain.	bind
14431	1	4895	5	NULL	NULL	0	NULL	TR	NULL		bind	NULL				TRAP220	NULL	deletion mutants containing one or both	LXXLL motifs		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_153	10891484	(C) TR binds only TRAP220 deletion mutants containing one or both of the LXXLL motifs.	bind
12738	1	4895	6	NULL	NULL	NULL	NULL	TR	GP		bind					TRAP220	GP	deletion mutants	LXXLL motifs		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_153	10891484	(C) TR binds only TRAP220 deletion mutants containing one or both of the LXXLL motifs.	bind
14432	2	4896	5	10	NULL	0	NULL	CD40		mutant	does not bind		directly			TRAF6					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9806_s_298	16260598	(C) TRAF6 and TRAF2 coimmunoprecipitate  in CD40L-stimulated carcinoma cells carrying a mutated CD40 that does not directly  bind TRAF6.	bind
44576	1	4896	5	10	NULL	0	NULL	TRAF6			bind					TRAF2					NULL	CD40L-stimulated carcinoma cells carrying a mutated CD40	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9806_s_298	16260598	(C) TRAF6 and TRAF2 coimmunoprecipitate  in CD40L-stimulated carcinoma cells carrying a mutated CD40 that does not directly  bind TRAF6.	bind
12739	1	4896	6	NULL	NULL	NULL	NULL	TRAF6	GP		bind					TRAF2	GP				NULL	CD40L-stimulated carcinoma cells carrying a mutated CD40	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9806_s_298	16260598	(C) TRAF6 and TRAF2 coimmunoprecipitate  in CD40L-stimulated carcinoma cells carrying a mutated CD40 that does not directly  bind TRAF6.	bind
12740	2	4896	6	NULL	NULL	NULL	NULL	CD40	GP	mutant	does not bind		directly			TRAF6	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9806_s_298	16260598	(C) TRAF6 and TRAF2 coimmunoprecipitate  in CD40L-stimulated carcinoma cells carrying a mutated CD40 that does not directly  bind TRAF6.	bind
14437	1	4897	5	NULL	NULL	0	NULL	Raf	NULL		induce	NULL				mdm2	NULL	transcription of			NULL		0	NULL	NULL	NULL	gw60_cell_103_2_321_s_49	11057904	(C) Transcriptional induction of  mdm2 by Raf is independent of p53.	bind
14438	2	4897	5	NULL	NULL	0	NULL	statement 1	NULL		is independent of	NULL				p53	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_103_2_321_s_49	11057904	(C) Transcriptional induction of  mdm2 by Raf is independent of p53.	bind
12788	1	4897	6	NULL	NULL	NULL	NULL	Raf	GP		induces		transcriptionally			mdm2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_321_s_49	11057904	(C) Transcriptional induction of  mdm2 by Raf is independent of p53.	bind
12789	2	4897	6	NULL	NULL	NULL	NULL	statement 1	Process		is independent of					p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_321_s_49	11057904	(C) Transcriptional induction of  mdm2 by Raf is independent of p53.	bind
14439	1	4898	5	NULL	NULL	0	NULL	C2C12 nuclear proteins	NULL		bind	NULL				MEF-1 oligodeoxynucleotide	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_316	11940648	(C) Transfection of a Flag-Id2 expression plasmid inhibits the binding of C2C12 nuclear proteins to the MEF-1 oligodeoxynucleotide, and induced p204 overcomes the inhibition.	bind
14440	2	4898	5	10	NULL	0	NULL	Flag-Id2 expression plasmid			inhibit					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_316	11940648	(C) Transfection of a Flag-Id2 expression plasmid inhibits the binding of C2C12 nuclear proteins to the MEF-1 oligodeoxynucleotide, and induced p204 overcomes the inhibition.	bind
14441	3	4898	5	NULL	NULL	0	NULL	p204	NULL	induced	overcomes	NULL				statement 1	NULL	inhibition of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_316	11940648	(C) Transfection of a Flag-Id2 expression plasmid inhibits the binding of C2C12 nuclear proteins to the MEF-1 oligodeoxynucleotide, and induced p204 overcomes the inhibition.	bind
12790	1	4898	6	NULL	NULL	NULL	NULL	C2C12 nuclear proteins	GP		bind					MEF-1 oligodeoxynucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_316	11940648	(C) Transfection of a Flag-Id2 expression plasmid inhibits the binding of C2C12 nuclear proteins to the MEF-1 oligodeoxynucleotide, and induced p204 overcomes the inhibition.	bind
12791	2	4898	6	NULL	NULL	NULL	NULL	Flag-Id2 expression plasmid 			inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_316	11940648	(C) Transfection of a Flag-Id2 expression plasmid inhibits the binding of C2C12 nuclear proteins to the MEF-1 oligodeoxynucleotide, and induced p204 overcomes the inhibition.	bind
12792	3	4898	6	NULL	NULL	NULL	NULL	p204	GP	induced	overcomes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_316	11940648	(C) Transfection of a Flag-Id2 expression plasmid inhibits the binding of C2C12 nuclear proteins to the MEF-1 oligodeoxynucleotide, and induced p204 overcomes the inhibition.	bind
14442	1	4899	5	NULL	NULL	0	NULL	mant-ADP	NULL		bind	NULL				PI3K	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_103_6_931_s_120	11136978	(C) Transient and steady-state  measurements of mant-ATP and mant-ADP binding to PI3K.	bind
14443	2	4899	5	NULL	NULL	0	NULL	mant-ATP	NULL		bind	NULL				PI3K	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_103_6_931_s_120	11136978	(C) Transient and steady-state  measurements of mant-ATP and mant-ADP binding to PI3K.	bind
12793	1	4899	6	NULL	NULL	NULL	NULL	mant-ATP	Chemical		bind					PI3K	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_6_931_s_120	11136978	(C) Transient and steady-state  measurements of mant-ATP and mant-ADP binding to PI3K.	bind
12794	2	4899	6	NULL	NULL	NULL	NULL	mant-ADP	Chemical		bind					PI3K	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_6_931_s_120	11136978	(C) Transient and steady-state  measurements of mant-ATP and mant-ADP binding to PI3K.	bind
14444	1	4900	5	NULL	NULL	0	NULL	SUV39H1	NULL		bind	NULL				HP1alpha	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw70_molcellbiol_25_7_2525_s_354	15767660	(C) TSA did not affect the in vitro binding of SUV39H1  to HP1alpha as determined by GST pull-down assay.	bind
14445	2	4900	5	NULL	NULL	0	NULL	TSA	NULL		does not affect	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_7_2525_s_354	15767660	(C) TSA did not affect the in vitro binding of SUV39H1  to HP1alpha as determined by GST pull-down assay.	bind
12795	1	4900	6	NULL	NULL	NULL	NULL	SUV39H1	GP		bind					HP1alpha	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_7_2525_s_354	15767660	(C) TSA did not affect the in vitro binding of SUV39H1  to HP1alpha as determined by GST pull-down assay.	bind
12796	2	4900	6	NULL	NULL	NULL	NULL	TSA	Chemical		did not affect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_7_2525_s_354	15767660	(C) TSA did not affect the in vitro binding of SUV39H1  to HP1alpha as determined by GST pull-down assay.	bind
14446	1	4902	5	NULL	NULL	0	NULL	snapin	NULL	unphosphorylated	bind	NULL				cypin	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_11_5103_s_341	16120643	(C) Unphosphorylated snapin binds to cypin better  than a phosphomimetic form of snapin.	bind
14447	2	4902	5	NULL	NULL	0	NULL	snapin	NULL	phosphomimetic form of	bind	NULL				cypin	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5103_s_341	16120643	(C) Unphosphorylated snapin binds to cypin better  than a phosphomimetic form of snapin.	bind
14448	3	4902	5	NULL	NULL	0	NULL	statement 1	NULL		better than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_11_5103_s_341	16120643	(C) Unphosphorylated snapin binds to cypin better  than a phosphomimetic form of snapin.	bind
12797	1	4902	6	NULL	NULL	NULL	NULL	snapin	GP	unphosphorylated	bind					cypin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5103_s_341	16120643	(C) Unphosphorylated snapin binds to cypin better  than a phosphomimetic form of snapin.	bind
12798	2	4902	6	NULL	NULL	NULL	NULL	snapin	GP	phosphomimetic form of	bind					cypin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5103_s_341	16120643	(C) Unphosphorylated snapin binds to cypin better  than a phosphomimetic form of snapin.	bind
12799	3	4902	6	NULL	NULL	NULL	NULL	statement 1	Process		is better than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_11_5103_s_341	16120643	(C) Unphosphorylated snapin binds to cypin better  than a phosphomimetic form of snapin.	bind
14449	1	4903	5	NULL	NULL	0	NULL	TM-1	NULL	untagged	bind	NULL				Enigma	NULL		PDZ domain		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_6_1973_s_136	10359609	(C) Untagged TM-1 binds to the PDZ domain of Enigma to the same extent as the corresponding fusion protein.	bind
12800	1	4903	6	NULL	NULL	NULL	NULL	TM-1	GP	untagged	bind					Enigma	GP		PDZ domain		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_6_1973_s_136	10359609	(C) Untagged TM-1 binds to the PDZ domain of Enigma to the same extent as the corresponding fusion protein.	bind
14450	1	4904	5	10	NULL	0	NULL	Bru			bind		specifically			grk				3 UTR	NULL		NULL	NULL	NULL	NULL	gw70_mechdev_120_3_289_s_152	12591598	(C) UV cross-linking  RNA competition experiment showing that Bru binds the 3  portion of the  grk 3 UTR specifically.	bind
12801	1	4904	6	NULL	NULL	NULL	NULL	Bru	GP		bind		specifically			grk	GP			3 UTR	NULL		NULL	NULL	NULL	NULL	gw70_mechdev_120_3_289_s_152	12591598	(C) UV cross-linking  RNA competition experiment showing that Bru binds the 3  portion of the  grk 3 UTR specifically.	bind
14451	1	4905	5	NULL	NULL	0	NULL	PTB	NULL		bind	NULL				Sec RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7388_s_266	10982855	(C) UV cross-linking and competition experiments demonstrated that PTB binding to the Sec RNA can be competed using self-competition or using a cold ISS1 competitor.	bind
14452	2	4905	5	10	NULL	0	NULL	 ISS1		cold	bind					Sec RNA					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7388_s_266	10982855	(C) UV cross-linking and competition experiments demonstrated that PTB binding to the Sec RNA can be competed using self-competition or using a cold ISS1 competitor.	bind
14453	3	4905	5	10	NULL	0	NULL	statement 1			compete with					statement 2					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7388_s_266	10982855	(C) UV cross-linking and competition experiments demonstrated that PTB binding to the Sec RNA can be competed using self-competition or using a cold ISS1 competitor.	bind
16296	4	4905	5	NULL	NULL	0	NULL	Sec RNA	NULL		bind	NULL				Sec RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7388_s_266	10982855	(C) UV cross-linking and competition experiments demonstrated that PTB binding to the Sec RNA can be competed using self-competition or using a cold ISS1 competitor.	bind
16297	5	4905	5	NULL	NULL	0	NULL	statement 4	NULL		competes with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7388_s_266	10982855	(C) UV cross-linking and competition experiments demonstrated that PTB binding to the Sec RNA can be competed using self-competition or using a cold ISS1 competitor.	bind
16298	6	4905	5	NULL	NULL	0	NULL	statement 3	NULL		is an alternative to	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7388_s_266	10982855	(C) UV cross-linking and competition experiments demonstrated that PTB binding to the Sec RNA can be competed using self-competition or using a cold ISS1 competitor.	bind
12802	1	4905	6	NULL	NULL	NULL	NULL	PTB	GP		bind					Sec RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7388_s_266	10982855	(C) UV cross-linking and competition experiments demonstrated that PTB binding to the Sec RNA can be competed using self-competition or using a cold ISS1 competitor.	bind
12803	2	4905	6	NULL	NULL	NULL	NULL	 ISS1	GP	cold	bind					Sec RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7388_s_266	10982855	(C) UV cross-linking and competition experiments demonstrated that PTB binding to the Sec RNA can be competed using self-competition or using a cold ISS1 competitor.	bind
12804	3	4905	6	NULL	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7388_s_266	10982855	(C) UV cross-linking and competition experiments demonstrated that PTB binding to the Sec RNA can be competed using self-competition or using a cold ISS1 competitor.	bind
12805	4	4905	6	NULL	NULL	NULL	NULL	Sec RNA	NucleicAcid		bind					Sec RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7388_s_266	10982855	(C) UV cross-linking and competition experiments demonstrated that PTB binding to the Sec RNA can be competed using self-competition or using a cold ISS1 competitor.	bind
12806	5	4905	6	NULL	NULL	NULL	NULL	statement 1	Process		competes					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7388_s_266	10982855	(C) UV cross-linking and competition experiments demonstrated that PTB binding to the Sec RNA can be competed using self-competition or using a cold ISS1 competitor.	bind
12807	6	4905	6	NULL	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7388_s_266	10982855	(C) UV cross-linking and competition experiments demonstrated that PTB binding to the Sec RNA can be competed using self-competition or using a cold ISS1 competitor.	bind
14454	1	4906	5	NULL	NULL	0	NULL	VRI	NULL		bind	NULL				cry	NULL			E4BP4-consensus sites in promoter	NULL		0	NULL	NULL	NULL	gw60_neuron_37_2_249_s_190	12546820	(C) VRI binds E4BP4-consensus sites in the  cry promoter.	bind
12808	1	4906	6	NULL	NULL	NULL	NULL	VRI	GP		bind					cry	GP			E4BP4-consensus site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_neuron_37_2_249_s_190	12546820	(C) VRI binds E4BP4-consensus sites in the  cry promoter.	bind
14455	2	4907	5	NULL	NULL	0	NULL	Vsm1	NULL		bind	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_198	12925750	(C) Vsm1 binds to Sso that is not assembled into  SNARE complexes.	bind
44577	1	4907	5	10	NULL	0	NULL	Sso	NULL		is not assembled into	NULL				SNARE complexes	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_198	12925750	(C) Vsm1 binds to Sso that is not assembled into  SNARE complexes.	bind
12809	1	4907	6	NULL	NULL	NULL	NULL	Sso	GP		is not assembled into					SNARE complexes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_198	12925750	(C) Vsm1 binds to Sso that is not assembled into  SNARE complexes.	bind
12810	2	4907	6	NULL	NULL	NULL	NULL	Vsm1	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_198	12925750	(C) Vsm1 binds to Sso that is not assembled into  SNARE complexes.	bind
14456	1	4908	5	NULL	NULL	0	NULL	Sec9	NULL		bind	NULL				Sso1	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_75	12925750	(C) Vsm1 displaces Sec9 binding to Sso1.	bind
14457	2	4908	5	NULL	NULL	0	NULL	Vsm1	NULL		bind	NULL				Sso1	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_75	12925750	(C) Vsm1 displaces Sec9 binding to Sso1.	bind
14458	3	4908	5	NULL	NULL	0	NULL	statement 2	NULL		displaces	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_75	12925750	(C) Vsm1 displaces Sec9 binding to Sso1.	bind
12811	1	4908	6	NULL	NULL	NULL	NULL	Sec9	GP		bind					Sso1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_75	12925750	(C) Vsm1 displaces Sec9 binding to Sso1.	bind
12812	2	4908	6	NULL	NULL	NULL	NULL	Vsm1	GP		bind					Sso1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_75	12925750	(C) Vsm1 displaces Sec9 binding to Sso1.	bind
16304	3	4908	6	NULL	NULL	NULL	NULL	statement 2	Process		displace					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_75	12925750	(C) Vsm1 displaces Sec9 binding to Sso1.	bind
14459	1	4910	5	NULL	NULL	0	NULL	Ezh2 antibodies	NULL		precipitate	NULL				Ezh2	NULL				NULL		0	NULL	NULL	NULL	gw70_development_130_18_4235_s_258	12900441	(C) Western blot analysis  of IP-bound beads and supernatant (SN) showed that the Ezh2 antibodies precipitate  Ezh2 and that Eed and HDAC1 are bound to this complex.	bind
14460	2	4910	5	NULL	NULL	0	NULL	Eed	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_development_130_18_4235_s_258	12900441	(C) Western blot analysis  of IP-bound beads and supernatant (SN) showed that the Ezh2 antibodies precipitate  Ezh2 and that Eed and HDAC1 are bound to this complex.	bind
14461	3	4910	5	NULL	NULL	0	NULL	HDAC1	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_development_130_18_4235_s_258	12900441	(C) Western blot analysis  of IP-bound beads and supernatant (SN) showed that the Ezh2 antibodies precipitate  Ezh2 and that Eed and HDAC1 are bound to this complex.	bind
12813	1	4910	6	NULL	NULL	NULL	NULL	Ezh2 antibodies	GP		precipitate					Ezh2	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_18_4235_s_258	12900441	(C) Western blot analysis  of IP-bound beads and supernatant (SN) showed that the Ezh2 antibodies precipitate  Ezh2 and that Eed and HDAC1 are bound to this complex.	bind
12814	2	4910	6	NULL	NULL	NULL	NULL	Eed	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_130_18_4235_s_258	12900441	(C) Western blot analysis  of IP-bound beads and supernatant (SN) showed that the Ezh2 antibodies precipitate  Ezh2 and that Eed and HDAC1 are bound to this complex.	bind
12815	3	4910	6	NULL	NULL	NULL	NULL	HDAC1	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_130_18_4235_s_258	12900441	(C) Western blot analysis  of IP-bound beads and supernatant (SN) showed that the Ezh2 antibodies precipitate  Ezh2 and that Eed and HDAC1 are bound to this complex.	bind
14462	2	4914	5	NULL	NULL	0	NULL	SER	NULL		does not bind	NULL				Notch	NULL				NULL		NULL	NULL	NULL	NULL	gw70_development_130_26_6411_s_310	14627724	(C) When  O-fucose is extended by Fringe, SER can not bind or activate Notch.	bind
14463	4	4914	5	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_development_130_26_6411_s_310	14627724	(C) When  O-fucose is extended by Fringe, SER can not bind or activate Notch.	bind
14464	3	4914	5	NULL	NULL	0	NULL	SER	NULL		does not activate	NULL				Notch	NULL				NULL		0	NULL	NULL	NULL	gw70_development_130_26_6411_s_310	14627724	(C) When  O-fucose is extended by Fringe, SER can not bind or activate Notch.	bind
14465	5	4914	5	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_development_130_26_6411_s_310	14627724	(C) When  O-fucose is extended by Fringe, SER can not bind or activate Notch.	bind
44578	1	4914	5	10	NULL	0	NULL	O-fucose	NULL		extended by	NULL				fringe	NULL				NULL		0	NULL	NULL	NULL	gw70_development_130_26_6411_s_310	14627724	(C) When  O-fucose is extended by Fringe, SER can not bind or activate Notch.	bind
12816	1	4914	6	NULL	NULL	NULL	NULL	o-fucose	Chemical		extended by					Fringe	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_26_6411_s_310	14627724	(C) When  O-fucose is extended by Fringe, SER can not bind or activate Notch.	bind
12817	2	4914	6	NULL	NULL	NULL	NULL	SER	CellComponent		does not bind					Notch	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_26_6411_s_310	14627724	(C) When  O-fucose is extended by Fringe, SER can not bind or activate Notch.	bind
12818	3	4914	6	NULL	NULL	NULL	NULL	SER	CellComponent		does not activate					Notch	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_26_6411_s_310	14627724	(C) When  O-fucose is extended by Fringe, SER can not bind or activate Notch.	bind
12819	4	4914	6	NULL	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_130_26_6411_s_310	14627724	(C) When  O-fucose is extended by Fringe, SER can not bind or activate Notch.	bind
12820	5	4914	6	NULL	NULL	NULL	NULL	statement 1	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_130_26_6411_s_310	14627724	(C) When  O-fucose is extended by Fringe, SER can not bind or activate Notch.	bind
14466	1	4915	5	NULL	NULL	0	NULL	FGF-1	NULL		bind	NULL	high affinity			FGFR2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_369	10490614	(C) When heparin is added to the system where no cell surface proteoglycans are available, heparin promotes high-affinity binding of FGF-1 to FGFR2.	bind
14467	2	4915	5	NULL	NULL	0	NULL	heparin	NULL		promote	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_369	10490614	(C) When heparin is added to the system where no cell surface proteoglycans are available, heparin promotes high-affinity binding of FGF-1 to FGFR2.	bind
17657	3	4915	5	NULL	NULL	0	NULL	statement 2	NULL		in the absence of	NULL				cell surface proteoglycans 	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_369	10490614	(C) When heparin is added to the system where no cell surface proteoglycans are available, heparin promotes high-affinity binding of FGF-1 to FGFR2.	bind
13011	1	4915	6	NULL	NULL	NULL	NULL	FGF-1	GP		bind		high affinity			FGFR2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_369	10490614	(C) When heparin is added to the system where no cell surface proteoglycans are available, heparin promotes high-affinity binding of FGF-1 to FGFR2.	bind
13012	2	4915	6	NULL	NULL	NULL	NULL	heparin	Chemical		promotes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_369	10490614	(C) When heparin is added to the system where no cell surface proteoglycans are available, heparin promotes high-affinity binding of FGF-1 to FGFR2.	bind
13013	3	4915	6	NULL	NULL	NULL	NULL	statement 2	Process		occurs in absence of					cell surface proteoglycans	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_6754_s_369	10490614	(C) When heparin is added to the system where no cell surface proteoglycans are available, heparin promotes high-affinity binding of FGF-1 to FGFR2.	bind
14468	1	4916	5	NULL	NULL	0	NULL	hsc70	NULL	wild-type	bind	NULL				auxilin	NULL		J-domain		NULL		0	NULL	NULL	NULL	gw60_cellbiol_159_3_477_s_211	12427870	(C) Wild-type and mutant hsc70 bind the J-domain of auxilin.	bind
14469	2	4916	5	NULL	NULL	0	NULL	hsc70	NULL	mutant	bind	NULL				auxilin	NULL		J-domain		NULL		0	NULL	NULL	NULL	gw60_cellbiol_159_3_477_s_211	12427870	(C) Wild-type and mutant hsc70 bind the J-domain of auxilin.	bind
13014	1	4916	6	NULL	NULL	NULL	NULL	hsc70	GP	wild type	bind					auxilin	GP		J-domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_3_477_s_211	12427870	(C) Wild-type and mutant hsc70 bind the J-domain of auxilin.	bind
13015	2	4916	6	NULL	NULL	NULL	NULL	hsc70	GP	mutant	bind					auxilin	GP		J-domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_3_477_s_211	12427870	(C) Wild-type and mutant hsc70 bind the J-domain of auxilin.	bind
14470	1	4917	5	NULL	NULL	0	NULL	Sir1p	NULL	wild-type	bind	NULL					NULL			HMR	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_2_774_s_290	14701749	(C) Wild-type and mutant Sir1p binding to  HMR a was examined using ChIP assays with anti-HA.	bind
14471	2	4917	5	NULL	NULL	0	NULL	Sir1p	NULL	mutant	bind	NULL					NULL			HMR	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_2_774_s_290	14701749	(C) Wild-type and mutant Sir1p binding to  HMR a was examined using ChIP assays with anti-HA.	bind
13016	1	4917	6	NULL	NULL	NULL	NULL	Sir1p	GP	wild type	bind									HMR	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_774_s_290	14701749	(C) Wild-type and mutant Sir1p binding to  HMR a was examined using ChIP assays with anti-HA.	bind
13017	2	4917	6	NULL	NULL	NULL	NULL	Sir1p	GP	mutant	bind									HMR	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_774_s_290	14701749	(C) Wild-type and mutant Sir1p binding to  HMR a was examined using ChIP assays with anti-HA.	bind
14472	1	4918	5	NULL	NULL	0	NULL	RS	NULL		bind	NULL				chromatin	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_8_3536_s_276	15060172	(C) Wild-type p53 triggers binding of RS and RH to chromatin.	bind
14473	2	4918	5	NULL	NULL	0	NULL	p53	NULL	wild-type	triggers	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_8_3536_s_276	15060172	(C) Wild-type p53 triggers binding of RS and RH to chromatin.	bind
14474	3	4918	5	NULL	NULL	0	NULL	RH	NULL		bind	NULL				chromatin	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_8_3536_s_276	15060172	(C) Wild-type p53 triggers binding of RS and RH to chromatin.	bind
14475	4	4918	5	NULL	NULL	0	NULL	p53	NULL	wild-type	triggers	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_8_3536_s_276	15060172	(C) Wild-type p53 triggers binding of RS and RH to chromatin.	bind
13018	1	4918	6	NULL	NULL	NULL	NULL	RS	GP		bind					chromatin	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_8_3536_s_276	15060172	(C) Wild-type p53 triggers binding of RS and RH to chromatin.	bind
13019	2	4918	6	NULL	NULL	NULL	NULL	RH	GP		bind					chromatin	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_8_3536_s_276	15060172	(C) Wild-type p53 triggers binding of RS and RH to chromatin.	bind
13020	3	4918	6	NULL	NULL	NULL	NULL	p53	GP	wild type	triggers					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_8_3536_s_276	15060172	(C) Wild-type p53 triggers binding of RS and RH to chromatin.	bind
13021	4	4918	6	NULL	NULL	NULL	NULL	p53	GP	wild type	triggers					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_8_3536_s_276	15060172	(C) Wild-type p53 triggers binding of RS and RH to chromatin.	bind
14476	1	4919	5	NULL	NULL	0	NULL	DNedd4	NULL		bind	NULL		WW2		Comm	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_35_3_447_s_91	12165468	(C) WW2 and WW3 from DNedd4 can each bind Comm.	bind
14477	2	4919	5	NULL	NULL	0	NULL	DNedd4	NULL		bind	NULL		WW3		Comm	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_35_3_447_s_91	12165468	(C) WW2 and WW3 from DNedd4 can each bind Comm.	bind
13022	1	4919	6	NULL	NULL	NULL	NULL	DNedd4	GP		bind			WW2		Comm	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_35_3_447_s_91	12165468	(C) WW2 and WW3 from DNedd4 can each bind Comm.	bind
13023	2	4919	6	NULL	NULL	NULL	NULL	DNedd4	GP		bind			WW3		Comm	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_35_3_447_s_91	12165468	(C) WW2 and WW3 from DNedd4 can each bind Comm.	bind
14478	1	4920	5	NULL	NULL	0	NULL	Nkd	NULL		bind	NULL				Dsh	NULL				NULL		0	NULL	NULL	NULL	gw70_genetics_174_1_331_s_209	16849595	(C) Y2H of Nkd or Nkddelta30aa binding to Dsh or DshbPDZ.	bind
14479	2	4920	5	NULL	NULL	0	NULL	Nkd	NULL		bind	NULL		delta30aa		Dsh	NULL				NULL		0	NULL	NULL	NULL	gw70_genetics_174_1_331_s_209	16849595	(C) Y2H of Nkd or Nkddelta30aa binding to Dsh or DshbPDZ.	bind
14480	3	4920	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_genetics_174_1_331_s_209	16849595	(C) Y2H of Nkd or Nkddelta30aa binding to Dsh or DshbPDZ.	bind
14481	4	4920	5	NULL	NULL	0	NULL	Nkd	NULL		bind	NULL				Dshb	NULL		PDZ		NULL		0	NULL	NULL	NULL	gw70_genetics_174_1_331_s_209	16849595	(C) Y2H of Nkd or Nkddelta30aa binding to Dsh or DshbPDZ.	bind
14482	5	4920	5	NULL	NULL	0	NULL	Nkd	NULL		bind	NULL		delta30aa		Dshb	NULL		PDZ		NULL		0	NULL	NULL	NULL	gw70_genetics_174_1_331_s_209	16849595	(C) Y2H of Nkd or Nkddelta30aa binding to Dsh or DshbPDZ.	bind
14483	6	4920	5	NULL	NULL	0	NULL	statement 4	NULL		is an alternative to	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_genetics_174_1_331_s_209	16849595	(C) Y2H of Nkd or Nkddelta30aa binding to Dsh or DshbPDZ.	bind
13030	1	4920	6	NULL	NULL	NULL	NULL	Nkd	GP		bind					Dsh	GP				NULL		NULL	NULL	NULL	NULL	gw70_genetics_174_1_331_s_209	16849595	(C) Y2H of Nkd or Nkddelta30aa binding to Dsh or DshbPDZ.	bind
13031	2	4920	6	NULL	NULL	NULL	NULL	Nkd	GP		bind			delta30aa		Dsh	GP				NULL		NULL	NULL	NULL	NULL	gw70_genetics_174_1_331_s_209	16849595	(C) Y2H of Nkd or Nkddelta30aa binding to Dsh or DshbPDZ.	bind
13032	3	4920	6	NULL	NULL	NULL	NULL	Nkd	GP		bind					Dshb	GP		PDZ domain		NULL		NULL	NULL	NULL	NULL	gw70_genetics_174_1_331_s_209	16849595	(C) Y2H of Nkd or Nkddelta30aa binding to Dsh or DshbPDZ.	bind
13033	4	4920	6	NULL	NULL	NULL	NULL	Nkd	GP		bind			delta30aa		Dshb	GP		PDZ domain		NULL		NULL	NULL	NULL	NULL	gw70_genetics_174_1_331_s_209	16849595	(C) Y2H of Nkd or Nkddelta30aa binding to Dsh or DshbPDZ.	bind
54592	5	4920	6	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_genetics_174_1_331_s_209	16849595	(C) Y2H of Nkd or Nkddelta30aa binding to Dsh or DshbPDZ.	bind
54593	6	4920	6	NULL	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_genetics_174_1_331_s_209	16849595	(C) Y2H of Nkd or Nkddelta30aa binding to Dsh or DshbPDZ.	bind
14484	1	4921	5	NULL	NULL	0	NULL	LFY	NULL		bind	NULL				AP3	NULL			site I	NULL		0	NULL	NULL	NULL	gw60_development_129_9_2079_s_126	11959818	(C) Yeast one-hybrid assays demonstrate that LFY binds to  AP3 site I.	bind
13036	1	4921	6	NULL	NULL	NULL	NULL	LFY	GP		bind					AP3	GP			site I 	NULL		NULL	NULL	NULL	NULL	gw60_development_129_9_2079_s_126	11959818	(C) Yeast one-hybrid assays demonstrate that LFY binds to  AP3 site I.	bind
14485	1	4923	5	NULL	NULL	0	NULL	Smad3	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_13_4494_s_178	12808092	(C) YY1  inhibits DNA binding of Smad3 and Smad4.	bind
14486	2	4923	5	NULL	NULL	0	NULL	Smad4	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_13_4494_s_178	12808092	(C) YY1  inhibits DNA binding of Smad3 and Smad4.	bind
14487	3	4923	5	NULL	NULL	0	NULL	YY1	NULL		inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_13_4494_s_178	12808092	(C) YY1  inhibits DNA binding of Smad3 and Smad4.	bind
14488	4	4923	5	NULL	NULL	0	NULL	YY1	NULL		inhibit	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_13_4494_s_178	12808092	(C) YY1  inhibits DNA binding of Smad3 and Smad4.	bind
13038	1	4923	6	NULL	NULL	NULL	NULL	Smad3	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4494_s_178	12808092	(C) YY1  inhibits DNA binding of Smad3 and Smad4.	bind
13039	2	4923	6	NULL	NULL	NULL	NULL	Smad4	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4494_s_178	12808092	(C) YY1  inhibits DNA binding of Smad3 and Smad4.	bind
13041	3	4923	6	NULL	NULL	NULL	NULL	YY1	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4494_s_178	12808092	(C) YY1  inhibits DNA binding of Smad3 and Smad4.	bind
13042	4	4923	6	NULL	NULL	NULL	NULL	YY1	GP		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4494_s_178	12808092	(C) YY1  inhibits DNA binding of Smad3 and Smad4.	bind
14489	2	4925	5	10	NULL	0	NULL	GTP S			bind					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_neuron_38_2_291_s_179	12718862	(C) [35]GTP S binding to HEK-293 cell membranes expressing D3R/Go  was determined after stimulation with dopamine.	bind
14490	3	4925	5	10	NULL	0	NULL	statement 1	NULL		occurs after stimulation with	NULL				dopamine	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_38_2_291_s_179	12718862	(C) [35]GTP S binding to HEK-293 cell membranes expressing D3R/Go  was determined after stimulation with dopamine.	bind
44579	1	4925	5	10	NULL	0	NULL	HEK-293 cell membranes	NULL		express	NULL				D3R/Go	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_38_2_291_s_179	12718862	(C) [35]GTP S binding to HEK-293 cell membranes expressing D3R/Go  was determined after stimulation with dopamine.	bind
13044	1	4925	6	NULL	NULL	NULL	NULL	HEK-293 cell membranes	CellComponent		express					D3R/Go	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_38_2_291_s_179	12718862	(C) [35]GTP S binding to HEK-293 cell membranes expressing D3R/Go  was determined after stimulation with dopamine.	bind
13046	2	4925	6	NULL	NULL	NULL	NULL	GTP S	Chemical		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_38_2_291_s_179	12718862	(C) [35]GTP S binding to HEK-293 cell membranes expressing D3R/Go  was determined after stimulation with dopamine.	bind
13049	3	4925	6	NULL	NULL	NULL	NULL	dopamine	Chemical		stimulates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_38_2_291_s_179	12718862	(C) [35]GTP S binding to HEK-293 cell membranes expressing D3R/Go  was determined after stimulation with dopamine.	bind
14491	1	4926	5	10	NULL	0	NULL	GTP			bind					Xl Sept2					NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_21_1858_s_34	12419187	(C) [3]GTP binding of  Xl Sept2 and  cc-Sep2, as determined by a filter binding assay.	bind
14492	2	4926	5	10	NULL	0	NULL	GTP			bind					cc-Sep2					NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_21_1858_s_34	12419187	(C) [3]GTP binding of  Xl Sept2 and  cc-Sep2, as determined by a filter binding assay.	bind
13051	1	4926	6	NULL	NULL	NULL	NULL	GTP	Chemical		bind					Xl Sept2	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_21_1858_s_34	12419187	(C) [3]GTP binding of  Xl Sept2 and  cc-Sep2, as determined by a filter binding assay.	bind
13052	2	4926	6	NULL	NULL	NULL	NULL	GTP	Chemical		bind					cc-Sep2	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_21_1858_s_34	12419187	(C) [3]GTP binding of  Xl Sept2 and  cc-Sep2, as determined by a filter binding assay.	bind
14493	1	4927	5	NULL	NULL	0	NULL	Siah-1	NULL		bind	NULL				pAPC	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcell_7_5_927_s_47	11389840	(C), (D), and (E) show in vitro and in vivo binding of Siah-1 to pAPC.	bind
14494	2	4927	5	NULL	NULL	0	NULL	Siah-1	NULL		bind	NULL				pAPC	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_molcell_7_5_927_s_47	11389840	(C), (D), and (E) show in vitro and in vivo binding of Siah-1 to pAPC.	bind
13055	1	4927	6	NULL	NULL	NULL	NULL	Siah-1	GP		bind					pAPC	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_7_5_927_s_47	11389840	(C), (D), and (E) show in vitro and in vivo binding of Siah-1 to pAPC.	bind
13056	2	4927	6	NULL	NULL	NULL	NULL	Siah-1	GP		bind					pAPC	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcell_7_5_927_s_47	11389840	(C), (D), and (E) show in vitro and in vivo binding of Siah-1 to pAPC.	bind
14495	1	4929	5	NULL	NULL	0	NULL	TFIIIA	NULL		bind	NULL				DNA	NULL	nucleosomal			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_6_2167_s_85	10688663	(C, D, and E) Removal of the core histone tails or the H2A-H2B dimer facilitates TFIIIA binding to nucleosomal DNA.	bind
14496	2	4929	5	NULL	NULL	0	NULL	core histone tails	NULL	removal of	facilitate	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_6_2167_s_85	10688663	(C, D, and E) Removal of the core histone tails or the H2A-H2B dimer facilitates TFIIIA binding to nucleosomal DNA.	bind
14497	3	4929	5	NULL	NULL	0	NULL	H2A-H2B dimer	NULL	removal of	facilitate	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_6_2167_s_85	10688663	(C, D, and E) Removal of the core histone tails or the H2A-H2B dimer facilitates TFIIIA binding to nucleosomal DNA.	bind
14498	4	4929	5	NULL	NULL	0	NULL	statement 2	NULL		is an alternative to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_6_2167_s_85	10688663	(C, D, and E) Removal of the core histone tails or the H2A-H2B dimer facilitates TFIIIA binding to nucleosomal DNA.	bind
13057	1	4929	6	NULL	NULL	NULL	NULL	TFIIIA	GP		bind					nucleosomal DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2167_s_85	10688663	(C, D, and E) Removal of the core histone tails or the H2A-H2B dimer facilitates TFIIIA binding to nucleosomal DNA.	bind
13058	2	4929	6	NULL	NULL	NULL	NULL	core histone tails		removal of	facilitate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2167_s_85	10688663	(C, D, and E) Removal of the core histone tails or the H2A-H2B dimer facilitates TFIIIA binding to nucleosomal DNA.	bind
13059	3	4929	6	NULL	NULL	NULL	NULL	H2A-H2B dimer	GP	removal of	facilitate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2167_s_85	10688663	(C, D, and E) Removal of the core histone tails or the H2A-H2B dimer facilitates TFIIIA binding to nucleosomal DNA.	bind
13060	4	4929	6	NULL	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2167_s_85	10688663	(C, D, and E) Removal of the core histone tails or the H2A-H2B dimer facilitates TFIIIA binding to nucleosomal DNA.	bind
14499	1	4930	5	NULL	NULL	0	NULL	Par3L isoforms	NULL		bind	NULL	differentially			Par6	NULL				NULL		0	NULL	NULL	NULL	gw60_gene_294_1_99_s_202	12234671	(C,D) Par3L isoforms show differential binding to Par6.	bind
13061	1	4930	6	NULL	NULL	NULL	NULL	Par3L isoforms	GP		bind		differentially			Par6	GP				NULL		NULL	NULL	NULL	NULL	gw60_gene_294_1_99_s_202	12234671	(C,D) Par3L isoforms show differential binding to Par6.	bind
14500	1	4931	5	NULL	NULL	0	NULL	GFR 1-Fc receptor bodies	NULL		bind	NULL	directly			GDNF ligands	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1291_s_171	9883723	(C-E) Direct binding of GFR 1-Fc (C), GFR 2-Fc (D), and GFR 3-Fc (E) receptor bodies to the GDNF ligands.	bind
14501	2	4931	5	NULL	NULL	0	NULL	GFR 2-Fc receptor bodies	NULL		bind	NULL	directly			GDNF ligands	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_21_6_1291_s_171	9883723	(C-E) Direct binding of GFR 1-Fc (C), GFR 2-Fc (D), and GFR 3-Fc (E) receptor bodies to the GDNF ligands.	bind
14502	3	4931	5	NULL	NULL	0	NULL	GFR 3-Fc receptor bodies	NULL		bind	NULL	directly			GDNF ligands	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_21_6_1291_s_171	9883723	(C-E) Direct binding of GFR 1-Fc (C), GFR 2-Fc (D), and GFR 3-Fc (E) receptor bodies to the GDNF ligands.	bind
13062	1	4931	6	NULL	NULL	NULL	NULL	GFR 1-Fc receptor body	GP		bind		directly			GDNF ligands	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1291_s_171	9883723	(C-E) Direct binding of GFR 1-Fc (C), GFR 2-Fc (D), and GFR 3-Fc (E) receptor bodies to the GDNF ligands.	bind
13063	2	4931	6	NULL	NULL	NULL	NULL	GFR 2-Fc receptor body	GP		bind		directly			GDNF ligands	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1291_s_171	9883723	(C-E) Direct binding of GFR 1-Fc (C), GFR 2-Fc (D), and GFR 3-Fc (E) receptor bodies to the GDNF ligands.	bind
13064	3	4931	6	NULL	NULL	NULL	NULL	GFR 3-Fc receptor body	GP		bind		directly			GDNF ligands	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1291_s_171	9883723	(C-E) Direct binding of GFR 1-Fc (C), GFR 2-Fc (D), and GFR 3-Fc (E) receptor bodies to the GDNF ligands.	bind
14503	1	4932	5	10	NULL	0	NULL	SKP1			bind					CUL1					NULL	HeLa cells	NULL	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_175	12504026	(C-E) Silencing of CAND1 in HeLa cells caused increased binding of SKP1 and SKP2 to CUL1 and downregulation of SKP2.	bind
14504	2	4932	5	NULL	NULL	0	NULL	CAND1	NULL	silencing of	increase	NULL				statement 1	NULL				NULL	in HeLa cells	NULL	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_175	12504026	(C-E) Silencing of CAND1 in HeLa cells caused increased binding of SKP1 and SKP2 to CUL1 and downregulation of SKP2.	bind
14505	3	4932	5	10	NULL	0	NULL	SKP2			bind					CUL1					NULL	HeLa cells	NULL	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_175	12504026	(C-E) Silencing of CAND1 in HeLa cells caused increased binding of SKP1 and SKP2 to CUL1 and downregulation of SKP2.	bind
14506	4	4932	5	NULL	NULL	0	NULL	CAND1	NULL	silencing of	increase	NULL				statement 3	NULL				NULL	in HeLa cells	NULL	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_175	12504026	(C-E) Silencing of CAND1 in HeLa cells caused increased binding of SKP1 and SKP2 to CUL1 and downregulation of SKP2.	bind
14507	5	4932	5	NULL	NULL	0	NULL	CAND1	NULL	silencing of	downregulates	NULL				Skp2	NULL				NULL	in HeLa cells	NULL	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_175	12504026	(C-E) Silencing of CAND1 in HeLa cells caused increased binding of SKP1 and SKP2 to CUL1 and downregulation of SKP2.	bind
13065	1	4932	6	NULL	NULL	NULL	NULL	SKP1	GP		bind					CUL1	GP				NULL	HeLa cells	NULL	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_175	12504026	(C-E) Silencing of CAND1 in HeLa cells caused increased binding of SKP1 and SKP2 to CUL1 and downregulation of SKP2.	bind
13066	2	4932	6	NULL	NULL	NULL	NULL	SKP2	GP		bind					CUL1	GP				NULL	HeLa cells	NULL	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_175	12504026	(C-E) Silencing of CAND1 in HeLa cells caused increased binding of SKP1 and SKP2 to CUL1 and downregulation of SKP2.	bind
13067	3	4932	6	NULL	NULL	NULL	NULL	CAND1	GP	silencing of	increases					statement 1	Process				NULL	HeLa cells	NULL	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_175	12504026	(C-E) Silencing of CAND1 in HeLa cells caused increased binding of SKP1 and SKP2 to CUL1 and downregulation of SKP2.	bind
13068	4	4932	6	NULL	NULL	NULL	NULL	CAND1	GP	silencing of	increases					statement 2	Process				NULL	HeLa cells	NULL	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_175	12504026	(C-E) Silencing of CAND1 in HeLa cells caused increased binding of SKP1 and SKP2 to CUL1 and downregulation of SKP2.	bind
13069	5	4932	6	NULL	NULL	NULL	NULL	CAND1	GP	silencing of	downregulates					SKP2	GP				NULL	HeLa cells	NULL	NULL	NULL	NULL	gw60_molcell_10_6_1519_s_175	12504026	(C-E) Silencing of CAND1 in HeLa cells caused increased binding of SKP1 and SKP2 to CUL1 and downregulation of SKP2.	bind
14508	1	4935	5	NULL	NULL	0	NULL	(CAG)(n)-hairpin DNA	NULL		bind	NULL				Msh2-Msh3	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_nat-struct-mol-biol_12_8_16025128_s_1	16025128	(CAG)(n)-hairpin DNA binds to Msh2-Msh3 and changes properties of mismatch recognition..	bind
14509	2	4935	5	NULL	NULL	0	NULL	(CAG)(n)-hairpin DNA	NULL		change	NULL				mismatch recognition	NULL	properties of			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_nat-struct-mol-biol_12_8_16025128_s_1	16025128	(CAG)(n)-hairpin DNA binds to Msh2-Msh3 and changes properties of mismatch recognition..	bind
13071	1	4935	6	NULL	NULL	NULL	NULL	(CAG)(n)-hairpin DNA	NucleicAcid		bind					Msh2-Msh3	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_nat-struct-mol-biol_12_8_16025128_s_1	16025128	(CAG)(n)-hairpin DNA binds to Msh2-Msh3 and changes properties of mismatch recognition..	bind
13072	2	4935	6	NULL	NULL	NULL	NULL	statement 1	Process		changes					mismatch recognition	Process	properties of 			NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_nat-struct-mol-biol_12_8_16025128_s_1	16025128	(CAG)(n)-hairpin DNA binds to Msh2-Msh3 and changes properties of mismatch recognition..	bind
14510	1	4938	5	NULL	NULL	0	NULL	Crk-associated substrate	NULL		bind	NULL		SH3 domain		FAK	NULL		proline-rich region		NULL		NULL	NULL	NULL	NULL	gw60_febslett_498_1_26_s_13	11389892	(Crk-associated substrate) binds the proline-rich region of FAK through an SH3 domain.	bind
13073	1	4938	6	NULL	NULL	NULL	NULL	Crk-associated substrate	GP		bind			SH3 domain		FAK	GP		proline-rich region		NULL		NULL	NULL	NULL	NULL	gw60_febslett_498_1_26_s_13	11389892	(Crk-associated substrate) binds the proline-rich region of FAK through an SH3 domain.	bind
14511	1	4939	5	NULL	NULL	0	NULL	Csk-associated substrate	NULL		bind	NULL		SH2 domain		Src kinase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_10_8837_s_374	12496276	(Csk-associated substrate) binds Src kinase through its SH2 and SH3 domains ( ).	bind
14512	2	4939	5	NULL	NULL	0	NULL	Csk-associated substrate	NULL		bind	NULL		SH3 domain		Src kinase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_10_8837_s_374	12496276	(Csk-associated substrate) binds Src kinase through its SH2 and SH3 domains ( ).	bind
13074	1	4939	6	NULL	NULL	NULL	NULL	Csk-associated substrate	GP		bind			SH2 domain		Src kinase	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_10_8837_s_374	12496276	(Csk-associated substrate) binds Src kinase through its SH2 and SH3 domains ( ).	bind
13075	2	4939	6	NULL	NULL	NULL	NULL	Csk-associated substrate	GP		bind			SH3 domain		Src kinase	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_10_8837_s_374	12496276	(Csk-associated substrate) binds Src kinase through its SH2 and SH3 domains ( ).	bind
14513	1	4941	5	10	NULL	0	NULL				bind				(CT)n regions	GAGA factor					NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_nucleic-acids-res_31_10_12736297_s_3	12736297	(CT)n  regions are known to bind GAGA factor, a dominant enhancer of PEV thought  to play a role in generating an accessible chromatin structure.	bind
14514	2	4941	5	10	NULL	0	NULL	GAGA factor			is a type of					PEV		dominant		  enhancer 	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_nucleic-acids-res_31_10_12736297_s_3	12736297	(CT)n  regions are known to bind GAGA factor, a dominant enhancer of PEV thought  to play a role in generating an accessible chromatin structure.	bind
54594	3	4941	5	10	NULL	0	NULL	statement 1			plays a role in					chromatin structure		generating;; accessible			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_nucleic-acids-res_31_10_12736297_s_3	12736297	(CT)n  regions are known to bind GAGA factor, a dominant enhancer of PEV thought  to play a role in generating an accessible chromatin structure.	bind
13076	1	4941	6	NULL	NULL	NULL	NULL	GAGA factor	GP		is a type of					PEV	GP	dominant		enhancer	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_nucleic-acids-res_31_10_12736297_s_3	12736297	(CT)n  regions are known to bind GAGA factor, a dominant enhancer of PEV thought  to play a role in generating an accessible chromatin structure.	bind
13077	2	4941	6	NULL	NULL	NULL	NULL	statement 1	Process		plays a role in					chromatin	OrganismPart	generating an;; accessible;;  structure of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_nucleic-acids-res_31_10_12736297_s_3	12736297	(CT)n  regions are known to bind GAGA factor, a dominant enhancer of PEV thought  to play a role in generating an accessible chromatin structure.	bind
13078	3	4941	6	NULL	NULL	NULL	NULL				bind				(CT)n regions	GAGA factor	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_nucleic-acids-res_31_10_12736297_s_3	12736297	(CT)n  regions are known to bind GAGA factor, a dominant enhancer of PEV thought  to play a role in generating an accessible chromatin structure.	bind
14517	1	4943	5	NULL	NULL	0	NULL	Krox-20	NULL		activate	NULL				periaxin protein	NULL	expression of			NULL	in Swiss 3T3 cells	0	NULL	NULL	NULL	gw70_cellbiol_164_3_385_s_91	14757751	(D - G) Krox-20 activates periaxin and P0 myelin protein expression in Swiss 3T3 cells.	bind
14518	2	4943	5	NULL	NULL	0	NULL	Krox-20	NULL		activate	NULL				P0 myelin protein	NULL	expression of			NULL	in Swiss 3T3 cells	0	NULL	NULL	NULL	gw70_cellbiol_164_3_385_s_91	14757751	(D - G) Krox-20 activates periaxin and P0 myelin protein expression in Swiss 3T3 cells.	bind
13144	1	4943	6	NULL	NULL	NULL	NULL	Krox-20	GP		activates					periaxin protein	GP	expression of			NULL	Swiss 3T3 cells	NULL	NULL	NULL	NULL	gw70_cellbiol_164_3_385_s_91	14757751	(D - G) Krox-20 activates periaxin and P0 myelin protein expression in Swiss 3T3 cells.	bind
13145	2	4943	6	NULL	NULL	NULL	NULL	Krox-20	GP		activates					P0 myelin protein	GP	expression of			NULL	Swiss 3T3 cells	NULL	NULL	NULL	NULL	gw70_cellbiol_164_3_385_s_91	14757751	(D - G) Krox-20 activates periaxin and P0 myelin protein expression in Swiss 3T3 cells.	bind
14519	1	4944	5	NULL	NULL	0	NULL	Pol I	NULL		bind	NULL				35S rDNA	NULL			promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_19_5851_s_242	15520468	(D and E)  In vitro binding of Pol I to the 35S rDNA promoter.	bind
13146	1	4944	6	NULL	NULL	NULL	NULL	Pol I	GP		bind					35S rDNA	NucleicAcid			promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_19_5851_s_242	15520468	(D and E)  In vitro binding of Pol I to the 35S rDNA promoter.	bind
14520	1	4945	5	NULL	NULL	0	NULL		NULL		bind	NULL		GST-ARD		Tiam1	NULL	recombinant	C1199		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cellbiol_150_1_177_s_279	10893266	(D and E) Binding analysis between GST-ARD and the recombinant C1199 Tiam1 in vitro.	bind
13147	1	4945	6	NULL	NULL	NULL	NULL				bind			GST-ARD		Tiam1	GP	recombinant	C1199		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cellbiol_150_1_177_s_279	10893266	(D and E) Binding analysis between GST-ARD and the recombinant C1199 Tiam1 in vitro.	bind
14521	2	4946	5	NULL	NULL	0	NULL	Cdc31p	NULL		bind	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_7_1211_s_164	14504268	(d and e) Cdc31p binding to Sfi1p fusions containing 1 - 3  repeats.	bind
44580	1	4946	5	10	NULL	0	NULL	Sfi1p fusions	NULL		contain	NULL					NULL		1-3 repeats		NULL		0	NULL	NULL	NULL	gw70_cellbiol_162_7_1211_s_164	14504268	(d and e) Cdc31p binding to Sfi1p fusions containing 1 - 3  repeats.	bind
13148	1	4946	6	NULL	NULL	NULL	NULL	Sfi1p fusions	GP		contain								1-3 repeats		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_7_1211_s_164	14504268	(d and e) Cdc31p binding to Sfi1p fusions containing 1 - 3  repeats.	bind
13149	2	4946	6	NULL	NULL	NULL	NULL	Cdc31p	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_7_1211_s_164	14504268	(d and e) Cdc31p binding to Sfi1p fusions containing 1 - 3  repeats.	bind
14522	2	4947	5	10	NULL	0	NULL	statement 1			dephosphorylate					TbetaRI					NULL	in vivo	NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_291_s_142	14718519	(d and e) In in vivo  dephosphorylation assay, dominant-negative SARA with a mutation in the PP1c-binding  domain (F728A) inhibits the dephosphorylation of TbetaRI by Smad7-recruited PP1 complex.	bind
14523	3	4947	5	10	NULL	0	NULL	SARA		dominant-negative mutant 	inhibit			PP1c-binding domain;;F728A		statement 1					NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_291_s_142	14718519	(d and e) In in vivo  dephosphorylation assay, dominant-negative SARA with a mutation in the PP1c-binding  domain (F728A) inhibits the dephosphorylation of TbetaRI by Smad7-recruited PP1 complex.	bind
54595	1	4947	5	10	NULL	0	NULL	Smad7			recruit					PP1 complex					NULL		0	NULL	NULL	NULL	gw70_cellbiol_164_2_291_s_142	14718519	(d and e) In in vivo  dephosphorylation assay, dominant-negative SARA with a mutation in the PP1c-binding  domain (F728A) inhibits the dephosphorylation of TbetaRI by Smad7-recruited PP1 complex.	bind
13322	2	4947	6	NULL	NULL	NULL	NULL	statement 1	Process		dephosphorylates					TbetaRI	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_291_s_142	14718519	(d and e) In in vivo  dephosphorylation assay, dominant-negative SARA with a mutation in the PP1c-binding  domain (F728A) inhibits the dephosphorylation of TbetaRI by Smad7-recruited PP1 complex.	bind
13323	3	4947	6	NULL	NULL	NULL	NULL	SARA	GP	dominant-negative mutant	inhibits			PP1c-binding domain;;F728A		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_291_s_142	14718519	(d and e) In in vivo  dephosphorylation assay, dominant-negative SARA with a mutation in the PP1c-binding  domain (F728A) inhibits the dephosphorylation of TbetaRI by Smad7-recruited PP1 complex.	bind
54596	1	4947	6	NULL	NULL	NULL	NULL	Smad7	GP		recruits					PP1 complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_291_s_142	14718519	(d and e) In in vivo  dephosphorylation assay, dominant-negative SARA with a mutation in the PP1c-binding  domain (F728A) inhibits the dephosphorylation of TbetaRI by Smad7-recruited PP1 complex.	bind
14524	1	4948	5	NULL	NULL	0	NULL	MEF2C	NULL		bind	NULL				p300	NULL				NULL	in cardiocytes	0	NULL	NULL	NULL	gw60_molcellbiol_20_23_8643_s_174	11073966	(D and E) MEF2C binds p300 in cardiocytes.	bind
13150	1	4948	6	NULL	NULL	NULL	NULL	MEF2C	GP		bind					p300	GP				NULL	cardiocytes	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_23_8643_s_174	11073966	(D and E) MEF2C binds p300 in cardiocytes.	bind
14525	1	4950	5	NULL	NULL	0	NULL	myc-Snf5p	NULL		bind	NULL				SNZ1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8829_s_246	14612422	(D and H) The strains described for panels A and E that harbor the  SNF5-myc allele were subjected to ChIP analysis to measure binding of myc-Snf5p to  SNZ1.	bind
13151	1	4950	6	NULL	NULL	NULL	NULL	myc-Snf5p	GP		bind					SNZ1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8829_s_246	14612422	(D and H) The strains described for panels A and E that harbor the  SNF5-myc allele were subjected to ChIP analysis to measure binding of myc-Snf5p to  SNZ1.	bind
14526	1	4951	5	NULL	NULL	0	NULL	Dynamin	NULL		bind	NULL				Amphiphysin	NULL		SH3 domain		NULL		0	NULL	NULL	NULL	gw60_development_128_24_5005_s_90	11748137	(D)  Drosophila Amphiphysin does not interact with  Drosophila Dynamin: western analysis and Coomassie staining of Dynamin binding to the SH3 domain of Amphiphysin.	bind
14527	2	4951	5	NULL	NULL	0	NULL	Amphiphysin	NULL	Drosophila	does not interact with	NULL				Dynamin	NULL	Drosophila			NULL		0	NULL	NULL	NULL	gw60_development_128_24_5005_s_90	11748137	(D)  Drosophila Amphiphysin does not interact with  Drosophila Dynamin: western analysis and Coomassie staining of Dynamin binding to the SH3 domain of Amphiphysin.	bind
13152	1	4951	6	NULL	NULL	NULL	NULL	Amphiphysin	GP	Drosophila	does not interact					Dynamin	GP	Drosophila			NULL		NULL	NULL	NULL	NULL	gw60_development_128_24_5005_s_90	11748137	(D)  Drosophila Amphiphysin does not interact with  Drosophila Dynamin: western analysis and Coomassie staining of Dynamin binding to the SH3 domain of Amphiphysin.	bind
13153	2	4951	6	NULL	NULL	NULL	NULL	Dynamin	GP		bind					Amphiphysin	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_development_128_24_5005_s_90	11748137	(D)  Drosophila Amphiphysin does not interact with  Drosophila Dynamin: western analysis and Coomassie staining of Dynamin binding to the SH3 domain of Amphiphysin.	bind
14528	1	4953	5	10	NULL	0	NULL	Nkx2-5			bind					Hop				Nkx2.5 binding site in proximal promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_110_6_713_s_112	12297045	(D) (left) EMSA revealing that Nkx2-5 can bind to a Nkx2.5 binding site (NKE-WT) present in the proximal Hop promoter, while it can not bind a mutant Nkx2.5 binding site (mut).	bind
14529	2	4953	5	10	NULL	0	NULL	Nkx2-5			does not bind					Hop		mutant		Nkx2.5 binding site	NULL		NULL	NULL	NULL	NULL	gw60_cell_110_6_713_s_112	12297045	(D) (left) EMSA revealing that Nkx2-5 can bind to a Nkx2.5 binding site (NKE-WT) present in the proximal Hop promoter, while it can not bind a mutant Nkx2.5 binding site (mut).	bind
54597	3	4953	5	10	NULL	0	NULL	NKE-WT			is					wild type Nkx2.5 binding site					NULL		0	NULL	NULL	NULL	gw60_cell_110_6_713_s_112	12297045	(D) (left) EMSA revealing that Nkx2-5 can bind to a Nkx2.5 binding site (NKE-WT) present in the proximal Hop promoter, while it can not bind a mutant Nkx2.5 binding site (mut).	bind
13154	1	4953	6	NULL	NULL	NULL	NULL	Nkx2-5	GP		bind					Hop	GP			NKE-WT of proximal promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_110_6_713_s_112	12297045	(D) (left) EMSA revealing that Nkx2-5 can bind to a Nkx2.5 binding site (NKE-WT) present in the proximal Hop promoter, while it can not bind a mutant Nkx2.5 binding site (mut).	bind
13155	2	4953	6	NULL	NULL	NULL	NULL	NKE-WT	GP		is							wild type		 Nkx2.5 binding site 	NULL		NULL	NULL	NULL	NULL	gw60_cell_110_6_713_s_112	12297045	(D) (left) EMSA revealing that Nkx2-5 can bind to a Nkx2.5 binding site (NKE-WT) present in the proximal Hop promoter, while it can not bind a mutant Nkx2.5 binding site (mut).	bind
13156	3	4953	6	NULL	NULL	NULL	NULL	Nkx2-5	GP		does not bind					Hop	GP	mutant		Nkx2.5 binding site	NULL		NULL	NULL	NULL	NULL	gw60_cell_110_6_713_s_112	12297045	(D) (left) EMSA revealing that Nkx2-5 can bind to a Nkx2.5 binding site (NKE-WT) present in the proximal Hop promoter, while it can not bind a mutant Nkx2.5 binding site (mut).	bind
14530	1	4954	5	NULL	NULL	0	NULL	GST-RB	NULL		does not bind	NULL	directly			p53	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_3_2_181_s_183	10078201	(D) (right panel) shows that GST-RB does not bind to p53 directly, and it can only coprecipitate with p53 in the presence of MDM2.	bind
14531	2	4954	5	10	NULL	0	NULL	GST-RB			bind					p53					NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_2_181_s_183	10078201	(D) (right panel) shows that GST-RB does not bind to p53 directly, and it can only coprecipitate with p53 in the presence of MDM2.	bind
14532	3	4954	5	NULL	NULL	0	NULL	statement 2	NULL		in the presence of	NULL	only			MDM2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_3_2_181_s_183	10078201	(D) (right panel) shows that GST-RB does not bind to p53 directly, and it can only coprecipitate with p53 in the presence of MDM2.	bind
13158	1	4954	6	NULL	NULL	NULL	NULL	GST-RB	GP		does not bind		directly			p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_2_181_s_183	10078201	(D) (right panel) shows that GST-RB does not bind to p53 directly, and it can only coprecipitate with p53 in the presence of MDM2.	bind
13159	2	4954	6	NULL	NULL	NULL	NULL	GST-RB	GP		bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_2_181_s_183	10078201	(D) (right panel) shows that GST-RB does not bind to p53 directly, and it can only coprecipitate with p53 in the presence of MDM2.	bind
13160	3	4954	6	NULL	NULL	NULL	NULL	statement 2	Process		occurs in presence of		only			MDM2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_2_181_s_183	10078201	(D) (right panel) shows that GST-RB does not bind to p53 directly, and it can only coprecipitate with p53 in the presence of MDM2.	bind
14533	1	4955	5	NULL	NULL	0	NULL	Vav	NULL		bind	NULL		SH2 domain		SLP-76	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_6_2_155_s_134	9047237	(D) (Top panel) Peptides corresponding to the first pYESP motifs can compete for Vav SH2 domain binding to SLP-76.	bind
14534	2	4955	5	NULL	NULL	0	NULL	Peptides	NULL		bind	NULL		pYESP motifs		SLP-76	NULL				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_155_s_134	9047237	(D) (Top panel) Peptides corresponding to the first pYESP motifs can compete for Vav SH2 domain binding to SLP-76.	bind
14535	3	4955	5	NULL	NULL	0	NULL	statement 2	NULL		compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_6_2_155_s_134	9047237	(D) (Top panel) Peptides corresponding to the first pYESP motifs can compete for Vav SH2 domain binding to SLP-76.	bind
13161	1	4955	6	NULL	NULL	NULL	NULL	Vav	GP		bind			SH2 domain		SLP-76	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_155_s_134	9047237	(D) (Top panel) Peptides corresponding to the first pYESP motifs can compete for Vav SH2 domain binding to SLP-76.	bind
13162	2	4955	6	NULL	NULL	NULL	NULL	peptide			bind			pYESP motifs		SLP-76	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_155_s_134	9047237	(D) (Top panel) Peptides corresponding to the first pYESP motifs can compete for Vav SH2 domain binding to SLP-76.	bind
13163	3	4955	6	NULL	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_2_155_s_134	9047237	(D) (Top panel) Peptides corresponding to the first pYESP motifs can compete for Vav SH2 domain binding to SLP-76.	bind
14536	1	4957	5	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				p21WAF1/CIP1	NULL			GC-rich region of the promoter	NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_7_979_s_36	15051732	(d) 1 ng/ml of TGFbeta1 enhanced  the binding of Sp1 to a GC-rich region in the p21WAF1/CIP1 promoter as determined by chromatin immunoprecipitation.	bind
14537	2	4957	5	NULL	NULL	0	NULL	TGFbeta1	NULL		enhances	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_164_7_979_s_36	15051732	(d) 1 ng/ml of TGFbeta1 enhanced  the binding of Sp1 to a GC-rich region in the p21WAF1/CIP1 promoter as determined by chromatin immunoprecipitation.	bind
13164	1	4957	6	NULL	NULL	NULL	NULL	Sp1	GP		bind					p21WAF1/CIP1	GP			GC-rich region of the promoter	NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_7_979_s_36	15051732	(d) 1 ng/ml of TGFbeta1 enhanced  the binding of Sp1 to a GC-rich region in the p21WAF1/CIP1 promoter as determined by chromatin immunoprecipitation.	bind
13165	2	4957	6	NULL	NULL	NULL	NULL	TGFbeta1	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_7_979_s_36	15051732	(d) 1 ng/ml of TGFbeta1 enhanced  the binding of Sp1 to a GC-rich region in the p21WAF1/CIP1 promoter as determined by chromatin immunoprecipitation.	bind
14538	1	4958	5	NULL	NULL	0	NULL	24 hpf embryo	NULL		express	NULL	ectopically			Nkx6 (fly gene) RNA	NULL	ectopic 			NULL		NULL	NULL	NULL	NULL	gw70_development_131_21_5221_s_286	15456722	(D) 24 hpf embryo ectopically expressing  Nkx6 (fly gene) RNA generates ectopic PMNs (compare with  Fig. 7D).	bind
17658	2	4958	5	NULL	NULL	0	NULL	statement 1	NULL		generates	NULL				PMN	NULL	ectopic			NULL		0	NULL	NULL	NULL	gw70_development_131_21_5221_s_286	15456722	(D) 24 hpf embryo ectopically expressing  Nkx6 (fly gene) RNA generates ectopic PMNs (compare with  Fig. 7D).	bind
13166	1	4958	6	NULL	NULL	NULL	NULL	24 hpf embryo	Organism		express		ectopically			Nkx6 (fly gene) RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_development_131_21_5221_s_286	15456722	(D) 24 hpf embryo ectopically expressing  Nkx6 (fly gene) RNA generates ectopic PMNs (compare with  Fig. 7D).	bind
13167	2	4958	6	NULL	NULL	NULL	NULL	statement 1	Process		generates					PMN	Cell	ectopic			NULL		NULL	NULL	NULL	NULL	gw70_development_131_21_5221_s_286	15456722	(D) 24 hpf embryo ectopically expressing  Nkx6 (fly gene) RNA generates ectopic PMNs (compare with  Fig. 7D).	bind
14539	1	4959	5	NULL	NULL	0	NULL	prohibitin	NULL	35S-labeled	bind	NULL				GST-Suv39H	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw70_molcellbiol_26_11_4161_s_142	16705168	(D) 35S-labeled prohibitin binds to GST-Suv39H in vitro.	bind
13168	1	4959	6	NULL	NULL	NULL	NULL	prohibitin	GP	35S-labeled	bind					GST-Suv39H	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4161_s_142	16705168	(D) 35S-labeled prohibitin binds to GST-Suv39H in vitro.	bind
14540	3	4960	5	NULL	NULL	0	NULL	statement 1	NULL		occur along with	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_140	10330164	(D) A chimeric protein containing the amino terminus of TFIIB and the cyclin homology domain of cyclin E does not bind to p300.	bind
44581	1	4960	5	10	NULL	0	NULL	chimeric protein	NULL		contains	NULL				TFIIB	NULL		 amino terminus		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_140	10330164	(D) A chimeric protein containing the amino terminus of TFIIB and the cyclin homology domain of cyclin E does not bind to p300.	bind
44582	2	4960	5	10	NULL	0	NULL	chimeric protein	NULL		contain	NULL				cyclin E	NULL		cyclin homology domain		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_140	10330164	(D) A chimeric protein containing the amino terminus of TFIIB and the cyclin homology domain of cyclin E does not bind to p300.	bind
44583	4	4960	5	10	NULL	0	NULL	statement 3	NULL		does not bind	NULL				p300	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_140	10330164	(D) A chimeric protein containing the amino terminus of TFIIB and the cyclin homology domain of cyclin E does not bind to p300.	bind
13169	3	4960	6	NULL	NULL	NULL	NULL	statement 1	Process		occur along with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_140	10330164	(D) A chimeric protein containing the amino terminus of TFIIB and the cyclin homology domain of cyclin E does not bind to p300.	bind
41943	4	4960	6	NULL	NULL	NULL	NULL	statement 3	Process		does not bind					p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_140	10330164	(D) A chimeric protein containing the amino terminus of TFIIB and the cyclin homology domain of cyclin E does not bind to p300.	bind
54598	1	4960	6	NULL	NULL	NULL	NULL	chimeric protein	GP		contains					TFIIB	GP		amino terminus of		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_140	10330164	(D) A chimeric protein containing the amino terminus of TFIIB and the cyclin homology domain of cyclin E does not bind to p300.	bind
54600	2	4960	6	NULL	NULL	NULL	NULL	chimeric protein	GP		contains					cyclin E	GP		cyclin homology domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_140	10330164	(D) A chimeric protein containing the amino terminus of TFIIB and the cyclin homology domain of cyclin E does not bind to p300.	bind
14541	2	4961	5	NULL	NULL	0	NULL	VASP	NULL	His-tagged	bind	NULL		EVH1 domain		Ni	NULL				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_18_1617_s_21	12372256	(D) A Coomassie-stained gel showing that the His-tagged EVH1 domain of VASP, from a soluble  E.  coli extract (sol), binds to the nickel resin (Ni) and the positive control ActA peptide FPPPP, but not to the negative control ActA peptide APPPP or residues 451-461 of WIP (peptide F).	bind
14542	3	4961	5	NULL	NULL	0	NULL	Ni	NULL		is	NULL				nickel resin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_18_1617_s_21	12372256	(D) A Coomassie-stained gel showing that the His-tagged EVH1 domain of VASP, from a soluble  E.  coli extract (sol), binds to the nickel resin (Ni) and the positive control ActA peptide FPPPP, but not to the negative control ActA peptide APPPP or residues 451-461 of WIP (peptide F).	bind
14543	4	4961	5	NULL	NULL	0	NULL	VASP	NULL	His-tagged 	bind	NULL		EVH1 domain		ActA peptide FPPPP	NULL	positive control			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_18_1617_s_21	12372256	(D) A Coomassie-stained gel showing that the His-tagged EVH1 domain of VASP, from a soluble  E.  coli extract (sol), binds to the nickel resin (Ni) and the positive control ActA peptide FPPPP, but not to the negative control ActA peptide APPPP or residues 451-461 of WIP (peptide F).	bind
14544	5	4961	5	NULL	NULL	0	NULL	VASP	NULL	His-tagged	does not bind	NULL		EVH1 domain		ActA peptide APPPP	NULL	negative control			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_18_1617_s_21	12372256	(D) A Coomassie-stained gel showing that the His-tagged EVH1 domain of VASP, from a soluble  E.  coli extract (sol), binds to the nickel resin (Ni) and the positive control ActA peptide FPPPP, but not to the negative control ActA peptide APPPP or residues 451-461 of WIP (peptide F).	bind
14545	6	4961	5	NULL	NULL	0	NULL	VASP	NULL	His-tagged	does not bind	NULL		EVH1 domain		WIP	NULL		residues 451-461		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_18_1617_s_21	12372256	(D) A Coomassie-stained gel showing that the His-tagged EVH1 domain of VASP, from a soluble  E.  coli extract (sol), binds to the nickel resin (Ni) and the positive control ActA peptide FPPPP, but not to the negative control ActA peptide APPPP or residues 451-461 of WIP (peptide F).	bind
44584	1	4961	5	10	NULL	0	NULL	VASP	NULL		is derived from	NULL		EVH1 domain		soluble E.coli extract	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_12_18_1617_s_21	12372256	(D) A Coomassie-stained gel showing that the His-tagged EVH1 domain of VASP, from a soluble  E.  coli extract (sol), binds to the nickel resin (Ni) and the positive control ActA peptide FPPPP, but not to the negative control ActA peptide APPPP or residues 451-461 of WIP (peptide F).	bind
13325	1	4961	6	NULL	NULL	NULL	NULL	VASP	GP		bind			EVH1 domain		ActA peptide FPPPP	GP	positive control			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_18_1617_s_21	12372256	(D) A Coomassie-stained gel showing that the His-tagged EVH1 domain of VASP, from a soluble  E.  coli extract (sol), binds to the nickel resin (Ni) and the positive control ActA peptide FPPPP, but not to the negative control ActA peptide APPPP or residues 451-461 of WIP (peptide F).	bind
13326	2	4961	6	NULL	NULL	NULL	NULL	VASP	GP		does not bind			EVH1 domain		ActA peptide FPPPP	GP	negative control			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_18_1617_s_21	12372256	(D) A Coomassie-stained gel showing that the His-tagged EVH1 domain of VASP, from a soluble  E.  coli extract (sol), binds to the nickel resin (Ni) and the positive control ActA peptide FPPPP, but not to the negative control ActA peptide APPPP or residues 451-461 of WIP (peptide F).	bind
13327	3	4961	6	NULL	NULL	NULL	NULL	VASP	GP		does not bind			EVH1 domain		WIP	GP		residues 451-461		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_18_1617_s_21	12372256	(D) A Coomassie-stained gel showing that the His-tagged EVH1 domain of VASP, from a soluble  E.  coli extract (sol), binds to the nickel resin (Ni) and the positive control ActA peptide FPPPP, but not to the negative control ActA peptide APPPP or residues 451-461 of WIP (peptide F).	bind
13329	4	4961	6	NULL	NULL	NULL	NULL	VASP	GP		is derived from			EVH1 domain		E.coli extract	OrganismPart	soluble			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_18_1617_s_21	12372256	(D) A Coomassie-stained gel showing that the His-tagged EVH1 domain of VASP, from a soluble  E.  coli extract (sol), binds to the nickel resin (Ni) and the positive control ActA peptide FPPPP, but not to the negative control ActA peptide APPPP or residues 451-461 of WIP (peptide F).	bind
17347	5	4961	6	NULL	NULL	NULL	NULL	Ni	Chemical		is					Nickel resin					NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_18_1617_s_21	12372256	(D) A Coomassie-stained gel showing that the His-tagged EVH1 domain of VASP, from a soluble  E.  coli extract (sol), binds to the nickel resin (Ni) and the positive control ActA peptide FPPPP, but not to the negative control ActA peptide APPPP or residues 451-461 of WIP (peptide F).	bind
17348	6	4961	6	NULL	NULL	NULL	NULL	VASP	GP		bind			EVH1 domain		Ni	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_18_1617_s_21	12372256	(D) A Coomassie-stained gel showing that the His-tagged EVH1 domain of VASP, from a soluble  E.  coli extract (sol), binds to the nickel resin (Ni) and the positive control ActA peptide FPPPP, but not to the negative control ActA peptide APPPP or residues 451-461 of WIP (peptide F).	bind
14546	1	4962	5	NULL	NULL	0	NULL	Rb	NULL		mediate	NULL				E2F	NULL	repression of;; activity of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_195	9819434	(D) A dominant-acting form of Ras can reverse Rb-mediated repression of E2F activity.	bind
14547	2	4962	5	NULL	NULL	0	NULL	Ras	NULL	dominant-acting form of	reverse	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_195	9819434	(D) A dominant-acting form of Ras can reverse Rb-mediated repression of E2F activity.	bind
13171	1	4962	6	NULL	NULL	NULL	NULL	Rb	GP		mediates					E2F	GP	repression of;; activity of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_195	9819434	(D) A dominant-acting form of Ras can reverse Rb-mediated repression of E2F activity.	bind
13172	2	4962	6	NULL	NULL	NULL	NULL	Ras	GP	a dominant acting form of	reverse					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7487_s_195	9819434	(D) A dominant-acting form of Ras can reverse Rb-mediated repression of E2F activity.	bind
14548	1	4963	5	NULL	NULL	0	NULL	CRM1	NULL		bind	NULL	specifically	493-600		XAP1	NULL				NULL		0	NULL	NULL	NULL	gw60_chembiol_7_5_345_s_147	10801471	(d) A fragment of 108 amino acids (CRM1[493-600]) comprising amino acids known to affect LMB sensitivity in  S. pombe binds specifically to XAP1.	bind
17659	2	4963	5	10	NULL	0	NULL	CRM1			affect			amino acid 493-600		LMB 		sensitivity of			NULL	S. pombe	NULL	NULL	NULL	NULL	gw60_chembiol_7_5_345_s_147	10801471	(d) A fragment of 108 amino acids (CRM1[493-600]) comprising amino acids known to affect LMB sensitivity in  S. pombe binds specifically to XAP1.	bind
13330	1	4963	6	NULL	NULL	NULL	NULL	CRM1	GP		bind		specifically	amino acid 493-600		XAP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_7_5_345_s_147	10801471	(d) A fragment of 108 amino acids (CRM1[493-600]) comprising amino acids known to affect LMB sensitivity in  S. pombe binds specifically to XAP1.	bind
13331	2	4963	6	NULL	NULL	NULL	NULL	CRM1	GP		affect			amino acid 493-600		LMB	GP	sensitivity of			NULL	S. pombe	NULL	NULL	NULL	NULL	gw60_chembiol_7_5_345_s_147	10801471	(d) A fragment of 108 amino acids (CRM1[493-600]) comprising amino acids known to affect LMB sensitivity in  S. pombe binds specifically to XAP1.	bind
14549	1	4964	5	NULL	NULL	0	NULL	SHP2-SH2-GST	NULL		bind	NULL				CAT	NULL	biotinylated;; wt			NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_148	15556604	(D) A pre-incubation of SHP2-SH2-GST with  wt CAT, but not wife Y280F, inhibits a further binding of SHP2-SH2-GST to biotinylated  wt CAT.	bind
14550	4	4964	5	NULL	NULL	0	NULL	statement 2	NULL		inhibit	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_148	15556604	(D) A pre-incubation of SHP2-SH2-GST with  wt CAT, but not wife Y280F, inhibits a further binding of SHP2-SH2-GST to biotinylated  wt CAT.	bind
14551	5	4964	5	NULL	NULL	0	NULL	statement 3	NULL		does not inhibit	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_148	15556604	(D) A pre-incubation of SHP2-SH2-GST with  wt CAT, but not wife Y280F, inhibits a further binding of SHP2-SH2-GST to biotinylated  wt CAT.	bind
44585	2	4964	5	10	NULL	0	NULL	SHP2-SH2-GST	NULL		pre-incubated with	NULL				CAT	NULL	wt			NULL		0	NULL	NULL	NULL	gw70_febslett_577_3_327_s_148	15556604	(D) A pre-incubation of SHP2-SH2-GST with  wt CAT, but not wife Y280F, inhibits a further binding of SHP2-SH2-GST to biotinylated  wt CAT.	bind
44586	3	4964	5	10	NULL	0	NULL	SHP2-SH2-GST	NULL		pre-incubated with	NULL				wife	NULL		Y280F		NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_148	15556604	(D) A pre-incubation of SHP2-SH2-GST with  wt CAT, but not wife Y280F, inhibits a further binding of SHP2-SH2-GST to biotinylated  wt CAT.	bind
13174	1	4964	6	NULL	NULL	NULL	NULL	SHP2-SH2-GST 			bind					CAT	GP	biotinylated;; wild type			NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_148	15556604	(D) A pre-incubation of SHP2-SH2-GST with  wt CAT, but not wife Y280F, inhibits a further binding of SHP2-SH2-GST to biotinylated  wt CAT.	bind
13175	2	4964	6	NULL	NULL	NULL	NULL	SHP2-SH2-GST 			pre incubated with					CAT	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_148	15556604	(D) A pre-incubation of SHP2-SH2-GST with  wt CAT, but not wife Y280F, inhibits a further binding of SHP2-SH2-GST to biotinylated  wt CAT.	bind
13176	3	4964	6	NULL	NULL	NULL	NULL	statement 2	Process		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_148	15556604	(D) A pre-incubation of SHP2-SH2-GST with  wt CAT, but not wife Y280F, inhibits a further binding of SHP2-SH2-GST to biotinylated  wt CAT.	bind
13177	4	4964	6	NULL	NULL	NULL	NULL	SHP2-SH2-GST			pre incubated with					wife	GP		Y280F		NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_148	15556604	(D) A pre-incubation of SHP2-SH2-GST with  wt CAT, but not wife Y280F, inhibits a further binding of SHP2-SH2-GST to biotinylated  wt CAT.	bind
13178	5	4964	6	NULL	NULL	NULL	NULL	statement 4	Process		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_577_3_327_s_148	15556604	(D) A pre-incubation of SHP2-SH2-GST with  wt CAT, but not wife Y280F, inhibits a further binding of SHP2-SH2-GST to biotinylated  wt CAT.	bind
14552	1	4966	5	NULL	NULL	0	NULL	PR	NULL	full-length	bind	NULL				Src	NULL		SH3 domain		NULL		0	NULL	NULL	NULL	gw60_molcell_8_2_269_s_48	11545730	(D) A synthetic peptide containing the PR proline-rich motif inhibits interaction of full-length PR with the SH3 domain of Src. PR-B binding to GST-Src (U-SH3-SH2 domains) by a pull-down assay was performed as in (C), except in the presence and absence of varying concentrations of a synthetic peptide (200- to 3000-fold molar excess over PR-B) containing either the wild-type PR proline-rich motif (WT) or a mutant motif (Mut).	bind
14553	2	4966	5	NULL	NULL	0	NULL	peptide	NULL	synthetic	inhibit	NULL		PR proline-rich motif		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_8_2_269_s_48	11545730	(D) A synthetic peptide containing the PR proline-rich motif inhibits interaction of full-length PR with the SH3 domain of Src. PR-B binding to GST-Src (U-SH3-SH2 domains) by a pull-down assay was performed as in (C), except in the presence and absence of varying concentrations of a synthetic peptide (200- to 3000-fold molar excess over PR-B) containing either the wild-type PR proline-rich motif (WT) or a mutant motif (Mut).	bind
14554	3	4966	5	NULL	NULL	0	NULL	PR-B	NULL		bind	NULL				GST-Src	NULL		U-SH3-SH2 domains		NULL		0	NULL	NULL	NULL	gw60_molcell_8_2_269_s_48	11545730	(D) A synthetic peptide containing the PR proline-rich motif inhibits interaction of full-length PR with the SH3 domain of Src. PR-B binding to GST-Src (U-SH3-SH2 domains) by a pull-down assay was performed as in (C), except in the presence and absence of varying concentrations of a synthetic peptide (200- to 3000-fold molar excess over PR-B) containing either the wild-type PR proline-rich motif (WT) or a mutant motif (Mut).	bind
13179	1	4966	6	NULL	NULL	NULL	NULL	PR	GP	full length	interacts with					Src	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_269_s_48	11545730	(D) A synthetic peptide containing the PR proline-rich motif inhibits interaction of full-length PR with the SH3 domain of Src. PR-B binding to GST-Src (U-SH3-SH2 domains) by a pull-down assay was performed as in (C), except in the presence and absence of varying concentrations of a synthetic peptide (200- to 3000-fold molar excess over PR-B) containing either the wild-type PR proline-rich motif (WT) or a mutant motif (Mut).	bind
13180	2	4966	6	NULL	NULL	NULL	NULL	PR-B	GP		bind					GST-Src	GP		U-SH3-SH2 domains		NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_269_s_48	11545730	(D) A synthetic peptide containing the PR proline-rich motif inhibits interaction of full-length PR with the SH3 domain of Src. PR-B binding to GST-Src (U-SH3-SH2 domains) by a pull-down assay was performed as in (C), except in the presence and absence of varying concentrations of a synthetic peptide (200- to 3000-fold molar excess over PR-B) containing either the wild-type PR proline-rich motif (WT) or a mutant motif (Mut).	bind
13181	3	4966	6	NULL	NULL	NULL	NULL	peptide		synthetic	contains					PR	GP		proline-rich motifs		NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_269_s_48	11545730	(D) A synthetic peptide containing the PR proline-rich motif inhibits interaction of full-length PR with the SH3 domain of Src. PR-B binding to GST-Src (U-SH3-SH2 domains) by a pull-down assay was performed as in (C), except in the presence and absence of varying concentrations of a synthetic peptide (200- to 3000-fold molar excess over PR-B) containing either the wild-type PR proline-rich motif (WT) or a mutant motif (Mut).	bind
13182	4	4966	6	NULL	NULL	NULL	NULL	statement 3	Process		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_269_s_48	11545730	(D) A synthetic peptide containing the PR proline-rich motif inhibits interaction of full-length PR with the SH3 domain of Src. PR-B binding to GST-Src (U-SH3-SH2 domains) by a pull-down assay was performed as in (C), except in the presence and absence of varying concentrations of a synthetic peptide (200- to 3000-fold molar excess over PR-B) containing either the wild-type PR proline-rich motif (WT) or a mutant motif (Mut).	bind
14555	1	4967	5	NULL	NULL	0	NULL	UNC-115	NULL		bind	NULL		VHD		actin	NULL				NULL		0	NULL	NULL	NULL	gw70_development_130_4_693_s_269	12506000	(D) A western blot showing that the  UNC-115 VHD bound to actin.	bind
13183	1	4967	6	NULL	NULL	NULL	NULL	UNC-115	GP		bind			VHD		actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_4_693_s_269	12506000	(D) A western blot showing that the  UNC-115 VHD bound to actin.	bind
14556	1	4969	5	NULL	NULL	0	NULL	Mgamma proteins	NULL		bind	NULL				N-box probe	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4600_s_110	10373509	(D) Addition of a fivefold molar excess of unlabeled B1 oligonucleotide has a greater effect on binding of the Mgamma and Mbeta proteins (approximately 500 ng of soluble pGex fusion protein) to the N-box probe than addition of a fivefold excess molar excess of unlabeled N-box oligonucleotide.	bind
14557	2	4969	5	NULL	NULL	0	NULL	Mbeta proteins	NULL		bind	NULL				N-box probe	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4600_s_110	10373509	(D) Addition of a fivefold molar excess of unlabeled B1 oligonucleotide has a greater effect on binding of the Mgamma and Mbeta proteins (approximately 500 ng of soluble pGex fusion protein) to the N-box probe than addition of a fivefold excess molar excess of unlabeled N-box oligonucleotide.	bind
13184	1	4969	6	NULL	NULL	NULL	NULL	Mgamma proteins	GP		bind					N-box probe					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4600_s_110	10373509	(D) Addition of a fivefold molar excess of unlabeled B1 oligonucleotide has a greater effect on binding of the Mgamma and Mbeta proteins (approximately 500 ng of soluble pGex fusion protein) to the N-box probe than addition of a fivefold excess molar excess of unlabeled N-box oligonucleotide.	bind
13185	2	4969	6	NULL	NULL	NULL	NULL	Mbeta proteins	GP		bind					N-box probe					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4600_s_110	10373509	(D) Addition of a fivefold molar excess of unlabeled B1 oligonucleotide has a greater effect on binding of the Mgamma and Mbeta proteins (approximately 500 ng of soluble pGex fusion protein) to the N-box probe than addition of a fivefold excess molar excess of unlabeled N-box oligonucleotide.	bind
14558	1	4970	5	10	NULL	0	NULL	Claspin	NULL		bind	NULL				chromatin	NULL				NULL	RPA-depleted extracts	NULL	NULL	NULL	NULL	gw60_molcell_11_2_329_s_164	12620222	(D) Addition of rhRPA to RPA-depleted extracts restores normally regulated binding of Claspin and Pol   to chromatin.	bind
14559	2	4970	5	NULL	NULL	0	NULL	Pol 	NULL		bind	NULL				chromatin	NULL				NULL	RPA-depleted extracts	NULL	NULL	NULL	NULL	gw60_molcell_11_2_329_s_164	12620222	(D) Addition of rhRPA to RPA-depleted extracts restores normally regulated binding of Claspin and Pol   to chromatin.	bind
14560	3	4970	5	10	NULL	0	NULL	rhRPA	NULL	addition of	restores	NULL				statement 1	NULL	normally regulated			NULL	RPA-depleted extracts	NULL	NULL	NULL	NULL	gw60_molcell_11_2_329_s_164	12620222	(D) Addition of rhRPA to RPA-depleted extracts restores normally regulated binding of Claspin and Pol   to chromatin.	bind
14561	4	4970	5	10	NULL	0	NULL	rhRPA	NULL	addition of	restores	NULL				statement 2	NULL	normally regulated			NULL	RPA-depleted extracts	NULL	NULL	NULL	NULL	gw60_molcell_11_2_329_s_164	12620222	(D) Addition of rhRPA to RPA-depleted extracts restores normally regulated binding of Claspin and Pol   to chromatin.	bind
13187	1	4970	6	NULL	NULL	NULL	NULL	Claspin	GP		bind					chromatin	OrganismPart				NULL	RPA-depleted extracts	NULL	NULL	NULL	NULL	gw60_molcell_11_2_329_s_164	12620222	(D) Addition of rhRPA to RPA-depleted extracts restores normally regulated binding of Claspin and Pol   to chromatin.	bind
13188	2	4970	6	NULL	NULL	NULL	NULL	Pol	GP		bind					chromatin	OrganismPart				NULL	RPA-depleted extracts	NULL	NULL	NULL	NULL	gw60_molcell_11_2_329_s_164	12620222	(D) Addition of rhRPA to RPA-depleted extracts restores normally regulated binding of Claspin and Pol   to chromatin.	bind
13189	3	4970	6	NULL	NULL	NULL	NULL	rhRPA	GP	addition of	restores					statement 1	Process	normally regulated			NULL	RPA-depleted extracts	NULL	NULL	NULL	NULL	gw60_molcell_11_2_329_s_164	12620222	(D) Addition of rhRPA to RPA-depleted extracts restores normally regulated binding of Claspin and Pol   to chromatin.	bind
13190	4	4970	6	NULL	NULL	NULL	NULL	rhRPA	GP	addition of	restores					statement 2	Process	normally regulated			NULL	RPA-depleted extracts	NULL	NULL	NULL	NULL	gw60_molcell_11_2_329_s_164	12620222	(D) Addition of rhRPA to RPA-depleted extracts restores normally regulated binding of Claspin and Pol   to chromatin.	bind
14562	1	4971	5	NULL	NULL	0	NULL	GST-SF-1 protein	NULL	recombinant	bind	NULL				AMH	NULL			SF-1-BS in promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_11_6653_s_188	9774680	(D) Affinity binding of GST-SF-1 recombinant protein to the SF-1-binding site (SF-1-BS) in the AMH promoter.	bind
14563	2	4971	5	NULL	NULL	0	NULL	SF-1-BS	NULL		is	NULL				SF-1-binding site	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_11_6653_s_188	9774680	(D) Affinity binding of GST-SF-1 recombinant protein to the SF-1-binding site (SF-1-BS) in the AMH promoter.	bind
13191	1	4971	6	NULL	NULL	NULL	NULL	GST-SF-1 protein	GP	recombinant	bind					AMH	GP			SF-1-BS of promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_11_6653_s_188	9774680	(D) Affinity binding of GST-SF-1 recombinant protein to the SF-1-binding site (SF-1-BS) in the AMH promoter.	bind
13192	2	4971	6	NULL	NULL	NULL	NULL	SF-1-BS			is					SF-1-binding site					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_11_6653_s_188	9774680	(D) Affinity binding of GST-SF-1 recombinant protein to the SF-1-binding site (SF-1-BS) in the AMH promoter.	bind
14564	1	4972	5	NULL	NULL	0	NULL	importin-alpha receptors	NULL		bind	NULL				SV40	NULL		NLS		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_11_4159_s_238	10805757	(D) All the importin-alpha receptors tested can bind to the SV40 NLS.	bind
13193	1	4972	6	NULL	NULL	NULL	NULL	importin-alpha receptors	GP		bind					SV40	GP		NLS		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_4159_s_238	10805757	(D) All the importin-alpha receptors tested can bind to the SV40 NLS.	bind
14565	1	4973	5	10	NULL	0	NULL	TSP1	NULL		mediate	NULL		alpha4beta1 integrin binding regions		CD4+T cells	NULL	adhesion of ;;activated			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_509_s_53	11980922	(D) alpha4beta1 integrin binding regions of TSP1 and TSP2 mediate adhesion of activated CD4+T cells.	bind
14566	2	4973	5	10	NULL	0	NULL	TSP2	NULL		mediate	NULL		alpha4beta1 integrin binding regions		CD4+T cells	NULL	adhesion of ;;activated			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_509_s_53	11980922	(D) alpha4beta1 integrin binding regions of TSP1 and TSP2 mediate adhesion of activated CD4+T cells.	bind
13194	1	4973	6	NULL	NULL	NULL	NULL	TSP1	GP		mediate			alpha4beta1 integrin binding regions		CD4+T cells	Cell	adhesion of;; activated			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_509_s_53	11980922	(D) alpha4beta1 integrin binding regions of TSP1 and TSP2 mediate adhesion of activated CD4+T cells.	bind
13195	2	4973	6	NULL	NULL	NULL	NULL	TSP2	GP		mediate			alpha4beta1 integrin binding regions		CD4+T cells	Cell	adhesion of;; activated			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_509_s_53	11980922	(D) alpha4beta1 integrin binding regions of TSP1 and TSP2 mediate adhesion of activated CD4+T cells.	bind
14567	1	4974	5	NULL	NULL	0	NULL	RPA	NULL		bind	NULL				GST-Stuho	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_152_5_985_s_226	11238454	(D) Amount of RPA bound to GST-Stuho.	bind
13196	1	4974	6	NULL	NULL	NULL	NULL	RPA	GP		bind					GST-Stuho	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_985_s_226	11238454	(D) Amount of RPA bound to GST-Stuho.	bind
14569	1	4976	5	NULL	NULL	0	NULL	Axin	NULL		bind	NULL				LRP6deltaEGF-FKBP	NULL				NULL	in 293 cells	0	NULL	NULL	NULL	gw70_development_131_20_5103_s_180	15459103	(D) AP20187 increases the binding of Axin to LRP6deltaEGF-FKBP during beta-catenin stabilization in 293 cells.	bind
14570	2	4976	5	NULL	NULL	0	NULL	statement 1	NULL		occurs during	NULL				beta-catenin 	NULL	stabilization of			NULL	in 293 cells	0	NULL	NULL	NULL	gw70_development_131_20_5103_s_180	15459103	(D) AP20187 increases the binding of Axin to LRP6deltaEGF-FKBP during beta-catenin stabilization in 293 cells.	bind
14571	3	4976	5	NULL	NULL	0	NULL	AP20187	NULL		increase	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_20_5103_s_180	15459103	(D) AP20187 increases the binding of Axin to LRP6deltaEGF-FKBP during beta-catenin stabilization in 293 cells.	bind
13197	1	4976	6	NULL	NULL	NULL	NULL	Axin	GP		bind					LRP6deltaEGF-FKBP	GP				NULL	293 cells	NULL	NULL	NULL	NULL	gw70_development_131_20_5103_s_180	15459103	(D) AP20187 increases the binding of Axin to LRP6deltaEGF-FKBP during beta-catenin stabilization in 293 cells.	bind
13198	2	4976	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs during					beta-catenin	GP	stabilization of 			NULL		NULL	NULL	NULL	NULL	gw70_development_131_20_5103_s_180	15459103	(D) AP20187 increases the binding of Axin to LRP6deltaEGF-FKBP during beta-catenin stabilization in 293 cells.	bind
13199	3	4976	6	NULL	NULL	NULL	NULL	AP20187			increases					statement 1	Process				NULL	293 cells	NULL	NULL	NULL	NULL	gw70_development_131_20_5103_s_180	15459103	(D) AP20187 increases the binding of Axin to LRP6deltaEGF-FKBP during beta-catenin stabilization in 293 cells.	bind
14572	1	4980	5	NULL	NULL	0	NULL	SRP	NULL		bind	NULL				bt-SR 	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_162_4_575_s_173	12913112	(D) Association and dissociation curves for binding of SRP to bt-SR in the presence of buffer E adjusted to (a) 25 muM GTP, (b) 25 muM GDP, or (c) 25 muM Gpp(NH)p.	bind
13200	1	4980	6	NULL	NULL	NULL	NULL	SRP	GP		bind					bt-SR	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_162_4_575_s_173	12913112	(D) Association and dissociation curves for binding of SRP to bt-SR in the presence of buffer E adjusted to (a) 25 muM GTP, (b) 25 muM GDP, or (c) 25 muM Gpp(NH)p.	bind
14574	1	4982	5	NULL	NULL	0	NULL	B7h-Ig	NULL		bind	NULL				T cells	NULL	activated			NULL		0	NULL	NULL	NULL	gw60_immunity_11_4_423_s_121	10549624	(D) B7h-Ig binds to activated T cells.	bind
13201	1	4982	6	NULL	NULL	NULL	NULL	B7h-Ig	GP		bind					T cells	Cell	activated			NULL		NULL	NULL	NULL	NULL	gw60_immunity_11_4_423_s_121	10549624	(D) B7h-Ig binds to activated T cells.	bind
14653	1	4984	5	NULL	NULL	0	NULL	Chk2	NULL	bacterially produced	bind	NULL		FHA domain		HA-Chk2	NULL		SCD		NULL	293 cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4419_s_77	12024051	(D) Bacterially produced FHA domain of Chk2 binds to SCD in HA-Chk2 and its mutants expressed in 293 cells after gamma irradiation.	bind
14654	2	4984	5	NULL	NULL	0	NULL	gamma irradiation	NULL		is required for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_12_4419_s_77	12024051	(D) Bacterially produced FHA domain of Chk2 binds to SCD in HA-Chk2 and its mutants expressed in 293 cells after gamma irradiation.	bind
14655	3	4984	5	NULL	NULL	0	NULL	Chk2	NULL	bacterially produced	bind	NULL		FHA domain		HA-Chk2	NULL	mutants expressed	SCD		NULL	293 cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4419_s_77	12024051	(D) Bacterially produced FHA domain of Chk2 binds to SCD in HA-Chk2 and its mutants expressed in 293 cells after gamma irradiation.	bind
14656	4	4984	5	NULL	NULL	0	NULL	gamma irradiation	NULL		is required for	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_12_4419_s_77	12024051	(D) Bacterially produced FHA domain of Chk2 binds to SCD in HA-Chk2 and its mutants expressed in 293 cells after gamma irradiation.	bind
13202	1	4984	6	NULL	NULL	NULL	NULL	Chk2	GP	Bacterially produced	bind			FHA domain		HA-Chk2 	GP		SCD		NULL	293 cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4419_s_77	12024051	(D) Bacterially produced FHA domain of Chk2 binds to SCD in HA-Chk2 and its mutants expressed in 293 cells after gamma irradiation.	bind
13203	2	4984	6	NULL	NULL	NULL	NULL	Chk2	GP	Bacterially produced	bind			FHA domain		HA-Chk2 	GP	mutant	SCD		NULL	293T cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4419_s_77	12024051	(D) Bacterially produced FHA domain of Chk2 binds to SCD in HA-Chk2 and its mutants expressed in 293 cells after gamma irradiation.	bind
17349	3	4984	6	NULL	NULL	NULL	NULL	gamma radiation			is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4419_s_77	12024051	(D) Bacterially produced FHA domain of Chk2 binds to SCD in HA-Chk2 and its mutants expressed in 293 cells after gamma irradiation.	bind
17350	4	4984	6	NULL	NULL	NULL	NULL	gamma radiation			is required for					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4419_s_77	12024051	(D) Bacterially produced FHA domain of Chk2 binds to SCD in HA-Chk2 and its mutants expressed in 293 cells after gamma irradiation.	bind
14657	1	4985	5	NULL	NULL	0	NULL	BAF complex	NULL		does not bind	NULL				CSF1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_cell_106_3_309_s_136	11509180	(D) BAF complex and NFI/CTF are not  bound to the CSF1 promoter when the  NFI/CTF site is mutated.	bind
14658	2	4985	5	NULL	NULL	0	NULL	statement 1	NULL		occurs on	NULL					NULL	mutation		NFI/CTF site	NULL		0	NULL	NULL	NULL	gw60_cell_106_3_309_s_136	11509180	(D) BAF complex and NFI/CTF are not  bound to the CSF1 promoter when the  NFI/CTF site is mutated.	bind
14659	3	4985	5	NULL	NULL	0	NULL	NFI/CTF	NULL		does not bind	NULL				CSF1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_cell_106_3_309_s_136	11509180	(D) BAF complex and NFI/CTF are not  bound to the CSF1 promoter when the  NFI/CTF site is mutated.	bind
14660	4	4985	5	NULL	NULL	0	NULL	statement 3	NULL		occurs on	NULL					NULL	mutation		NFI/CTF site	NULL		0	NULL	NULL	NULL	gw60_cell_106_3_309_s_136	11509180	(D) BAF complex and NFI/CTF are not  bound to the CSF1 promoter when the  NFI/CTF site is mutated.	bind
13332	1	4985	6	NULL	NULL	NULL	NULL	BAF complex	GP		does not bind					CSF1 	GP	mutant		NFI/CTF site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_106_3_309_s_136	11509180	(D) BAF complex and NFI/CTF are not  bound to the CSF1 promoter when the  NFI/CTF site is mutated.	bind
13333	2	4985	6	NULL	NULL	NULL	NULL	NFI/CTF	GP		does not bind					CSF1	GP	mutant		NFI/CTF site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_106_3_309_s_136	11509180	(D) BAF complex and NFI/CTF are not  bound to the CSF1 promoter when the  NFI/CTF site is mutated.	bind
14661	1	4986	5	NULL	NULL	0	NULL	Che-1	NULL		bind	NULL				Tau	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellneurosci_24_4_1038_s_60	14697667	(D) Binding  of Che-1 by Tau affinity chromatography.	bind
13204	1	4986	6	NULL	NULL	NULL	NULL	Che-1	GP		bind					Tau	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_4_1038_s_60	14697667	(D) Binding  of Che-1 by Tau affinity chromatography.	bind
14662	1	4987	5	NULL	NULL	0	NULL	dATF-2	NULL		bind	NULL					NULL			CRE	NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_6_2934_s_166	15788564	(D) Binding  of dATF-2 to the CRE.	bind
13205	1	4987	6	NULL	NULL	NULL	NULL	dATF-2	GP		bind									CRE	NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_6_2934_s_166	15788564	(D) Binding  of dATF-2 to the CRE.	bind
14663	1	4991	5	NULL	NULL	0	NULL	ER	NULL		bind	NULL				SMRT	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_3_656_s_67	14680815	(D) Binding between ER  and SMRT was examined  using the mammalian two-hybrid system.	bind
13206	1	4991	6	NULL	NULL	NULL	NULL	ER	CellComponent		bind					SMRT	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_3_656_s_67	14680815	(D) Binding between ER  and SMRT was examined  using the mammalian two-hybrid system.	bind
14664	1	4992	5	NULL	NULL	0	NULL	NuMA	NULL		translated from	NULL		amino acid sequence 1831-2102		NuMA3/TOPO	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_1_29_s_226	10189366	(D) Binding of 4.1R/GST to NuMA amino acid sequence 1831-2102 translated from NuMA3/TOPO.	bind
14665	2	4992	5	NULL	NULL	0	NULL	4.1R/GST	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_1_29_s_226	10189366	(D) Binding of 4.1R/GST to NuMA amino acid sequence 1831-2102 translated from NuMA3/TOPO.	bind
13207	1	4992	6	NULL	NULL	NULL	NULL	4.1R/GST	GP		bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_1_29_s_226	10189366	(D) Binding of 4.1R/GST to NuMA amino acid sequence 1831-2102 translated from NuMA3/TOPO.	bind
13208	2	4992	6	NULL	NULL	NULL	NULL	NuMA	GP		translated from			amino acid sequence 1831-2102		NuMA3/TOPO	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_1_29_s_226	10189366	(D) Binding of 4.1R/GST to NuMA amino acid sequence 1831-2102 translated from NuMA3/TOPO.	bind
14666	1	4993	5	NULL	NULL	0	NULL	espin constructs	NULL	6X His-tagged	bind	NULL				GST-profilin IIa	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_163_5_1045_s_175	14657236	(D) Binding of 6X His-tagged espin constructs  to GST-profilin IIa, GST-profilin I, or GST in a pull-down assay.	bind
14667	2	4993	5	NULL	NULL	0	NULL	espin constructs	NULL	6X His-tagged	bind	NULL				GST-profilin I	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_163_5_1045_s_175	14657236	(D) Binding of 6X His-tagged espin constructs  to GST-profilin IIa, GST-profilin I, or GST in a pull-down assay.	bind
14668	3	4993	5	NULL	NULL	0	NULL	espin constructs	NULL	6X His-tagged	bind	NULL				GST	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_163_5_1045_s_175	14657236	(D) Binding of 6X His-tagged espin constructs  to GST-profilin IIa, GST-profilin I, or GST in a pull-down assay.	bind
14669	4	4993	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_163_5_1045_s_175	14657236	(D) Binding of 6X His-tagged espin constructs  to GST-profilin IIa, GST-profilin I, or GST in a pull-down assay.	bind
14670	5	4993	5	NULL	NULL	0	NULL	statement 2	NULL		is an alternative to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_163_5_1045_s_175	14657236	(D) Binding of 6X His-tagged espin constructs  to GST-profilin IIa, GST-profilin I, or GST in a pull-down assay.	bind
13209	1	4993	6	NULL	NULL	NULL	NULL	espin constructs	GP	His-tagged	bind					GST-profilin IIa	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_163_5_1045_s_175	14657236	(D) Binding of 6X His-tagged espin constructs  to GST-profilin IIa, GST-profilin I, or GST in a pull-down assay.	bind
13210	2	4993	6	NULL	NULL	NULL	NULL	epsin constructs	GP	His-tagged	bind					GST-profilin I	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_163_5_1045_s_175	14657236	(D) Binding of 6X His-tagged espin constructs  to GST-profilin IIa, GST-profilin I, or GST in a pull-down assay.	bind
13211	3	4993	6	NULL	NULL	NULL	NULL	epsin constructs	GP	His-tagged	bind					GST					NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_163_5_1045_s_175	14657236	(D) Binding of 6X His-tagged espin constructs  to GST-profilin IIa, GST-profilin I, or GST in a pull-down assay.	bind
54624	4	4993	6	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_163_5_1045_s_175	14657236	(D) Binding of 6X His-tagged espin constructs  to GST-profilin IIa, GST-profilin I, or GST in a pull-down assay.	bind
54625	5	4993	6	NULL	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_163_5_1045_s_175	14657236	(D) Binding of 6X His-tagged espin constructs  to GST-profilin IIa, GST-profilin I, or GST in a pull-down assay.	bind
14671	1	4994	5	10	NULL	0	NULL	ornithodorin	NULL		is a type of	NULL				thrombin inhibitor	NULL	soft tick 			NULL		NULL	NULL	NULL	NULL	gw70_insectbiochemmolbiol_34_1_1_s_293	14723893	(d) Binding of a soft tick thrombin inhibitor  (ornithodorin) with thrombin ( [ Van de Locht et al., 1996]).	bind
14672	2	4994	5	NULL	NULL	0	NULL	ornithodorin	NULL		bind	NULL				thrombin	NULL				NULL		0	NULL	NULL	NULL	gw70_insectbiochemmolbiol_34_1_1_s_293	14723893	(d) Binding of a soft tick thrombin inhibitor  (ornithodorin) with thrombin ( [ Van de Locht et al., 1996]).	bind
13212	1	4994	6	NULL	NULL	NULL	NULL	ornithodorin	GP		bind					thrombin	GP				NULL		NULL	NULL	NULL	NULL	gw70_insectbiochemmolbiol_34_1_1_s_293	14723893	(d) Binding of a soft tick thrombin inhibitor  (ornithodorin) with thrombin ( [ Van de Locht et al., 1996]).	bind
13213	2	4994	6	NULL	NULL	NULL	NULL	ornithodorin	GP		is a type of					thrombin inhibitor	GP	soft tick			NULL		NULL	NULL	NULL	NULL	gw70_insectbiochemmolbiol_34_1_1_s_293	14723893	(d) Binding of a soft tick thrombin inhibitor  (ornithodorin) with thrombin ( [ Van de Locht et al., 1996]).	bind
14673	1	4995	5	NULL	NULL	0	NULL	C/EBPbeta	NULL		bind	NULL				p40	NULL	endogenous		promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_6_2385_s_177	14993278	(D) Binding of C/EBPbeta to the endogenous p40 promoter was monitored  by ChIP and semiquantitative PCR by using C/EBPbeta and GST antibodies and chromatin  samples as described in the legend to Fig.  2.	bind
13214	1	4995	6	NULL	NULL	NULL	NULL	C/EBPbeta	GP		bind					p40	GP	endogenous		promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_6_2385_s_177	14993278	(D) Binding of C/EBPbeta to the endogenous p40 promoter was monitored  by ChIP and semiquantitative PCR by using C/EBPbeta and GST antibodies and chromatin  samples as described in the legend to Fig.  2.	bind
14674	1	4996	5	NULL	NULL	0	NULL	Ce-Sema1aadeltaC-Fc-AP	NULL		bind	NULL				PLX-1	NULL				NULL		0	NULL	NULL	NULL	gw60_development_129_9_2053_s_239	11959816	(D) Binding of Ce-Sema1aadeltaC-Fc-AP to PLX-1.	bind
13215	1	4996	6	NULL	NULL	NULL	NULL	Ce-Sema1aadeltaC-Fc-AP	GP		bind					PLX-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_129_9_2053_s_239	11959816	(D) Binding of Ce-Sema1aadeltaC-Fc-AP to PLX-1.	bind
14675	1	4997	5	NULL	NULL	0	NULL	CPEB	NULL		bind	NULL				XPum	NULL		Puf		NULL		0	NULL	NULL	NULL	gw70_mechdev_120_8_865_s_84	12963108	(D) Binding of CPEB to XPum Puf as revealed by anti-CPEB  immunoprecipitation.	bind
13216	1	4997	6	NULL	NULL	NULL	NULL	CPEB	GP		bind					Xpum	GP		puf		NULL		NULL	NULL	NULL	NULL	gw70_mechdev_120_8_865_s_84	12963108	(D) Binding of CPEB to XPum Puf as revealed by anti-CPEB  immunoprecipitation.	bind
14676	1	4998	5	NULL	NULL	0	NULL	fl- -SsrA	NULL		bind	NULL				hexameric ClpA	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_9_3_673_s_145	11931773	(D) Binding of fl- -SsrA to hexameric ClpA is inhibited by ClpS.	bind
14677	2	4998	5	NULL	NULL	0	NULL	ClpS	NULL		inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_9_3_673_s_145	11931773	(D) Binding of fl- -SsrA to hexameric ClpA is inhibited by ClpS.	bind
13217	1	4998	6	NULL	NULL	NULL	NULL	fl- -SsrA 	GP		bind					hexameric ClpA	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_9_3_673_s_145	11931773	(D) Binding of fl- -SsrA to hexameric ClpA is inhibited by ClpS.	bind
13218	2	4998	6	NULL	NULL	NULL	NULL	ClpS	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_9_3_673_s_145	11931773	(D) Binding of fl- -SsrA to hexameric ClpA is inhibited by ClpS.	bind
14678	1	4999	5	NULL	NULL	0	NULL	gp82 proteins	NULL	recombinant	bind	NULL				HeLa cells	NULL				NULL		0	NULL	NULL	NULL	gw70_microbesinfect_8_6_1502_s_102	16697683	(D) Binding of gp82 recombinant proteins to HeLa cells.	bind
13219	1	4999	6	NULL	NULL	NULL	NULL	gp82 proteins	GP	recombinant	bind					HeLa cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_microbesinfect_8_6_1502_s_102	16697683	(D) Binding of gp82 recombinant proteins to HeLa cells.	bind
14679	1	5000	5	NULL	NULL	0	NULL	GSK-3beta	NULL		bind	NULL				NEMO	NULL				NULL	extracts of astrocytes	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4649_s_271	12808104	(D) Binding of GSK-3beta to NEMO was analyzed using extracts  of astrocytes.	bind
13220	1	5000	6	NULL	NULL	NULL	NULL	GSK-3beta	GP		bind					NEMO	GP				NULL	extracts of astrocytes	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4649_s_271	12808104	(D) Binding of GSK-3beta to NEMO was analyzed using extracts  of astrocytes.	bind
13338	1	5001	7	NULL	NULL	0	NULL	GSK-3beta	NULL		bind	NULL				NEMO	NULL				NULL	extracts of astrocytes	0	NULL	NULL	NULL	gw60_molcellbiol_23_13_4649_s_271	12808104	(D) Binding of GSK-3beta to NEMO was analyzed using extracts of astrocytes.	bind
13222	1	5002	6	NULL	NULL	NULL	NULL	KSR	GP		bind					MEK	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5523_s_323	10409742	(D) Binding of KSR to MEK does not alter the ability of MEK to activate ERK in response to growth factor stimulation.	bind
13223	2	5002	6	NULL	NULL	NULL	NULL	MEK	GP		activate					ERK	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5523_s_323	10409742	(D) Binding of KSR to MEK does not alter the ability of MEK to activate ERK in response to growth factor stimulation.	bind
13224	3	5002	6	NULL	NULL	NULL	NULL	statement 2	Process		occurs in response to					growth factor 	GP	stimulation of 			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5523_s_323	10409742	(D) Binding of KSR to MEK does not alter the ability of MEK to activate ERK in response to growth factor stimulation.	bind
17351	4	5002	6	NULL	NULL	NULL	NULL	statement 1	Process		does not alter					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5523_s_323	10409742	(D) Binding of KSR to MEK does not alter the ability of MEK to activate ERK in response to growth factor stimulation.	bind
13339	1	5002	7	NULL	NULL	0	NULL	 KSR 	NULL		bind	NULL				MEK	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5523_s_323	10409742	(D) Binding of KSR to MEK does not alter the ability of MEK to activate ERK in response to growth factor stimulation.	bind
13340	2	5002	7	NULL	NULL	0	NULL	MEK	NULL		activate	NULL				ERK	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5523_s_323	10409742	(D) Binding of KSR to MEK does not alter the ability of MEK to activate ERK in response to growth factor stimulation.	bind
13341	3	5002	7	NULL	NULL	0	NULL	statement 2	NULL		occurs in response to	NULL				growth factor	NULL	stimulation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5523_s_323	10409742	(D) Binding of KSR to MEK does not alter the ability of MEK to activate ERK in response to growth factor stimulation.	bind
13342	4	5002	7	NULL	NULL	0	NULL	statement 1	NULL		does not alter	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5523_s_323	10409742	(D) Binding of KSR to MEK does not alter the ability of MEK to activate ERK in response to growth factor stimulation.	bind
13225	1	5003	6	NULL	NULL	NULL	NULL	MCP-1 variants	GP		bind					M3	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_343_s_163	12419245	(D) Binding of MCP-1 variants to M3.	bind
13343	1	5003	7	NULL	NULL	0	NULL	MCP-1 variants	NULL		bind	NULL				M3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_343_s_163	12419245	(D) Binding of MCP-1 variants to M3.	bind
13226	1	5004	6	NULL	NULL	NULL	NULL	p27	GP		bind					Cdk2 complexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_1_55_s_74	15631990	(D) Binding of p27 to Cdk2  complexes.	bind
13344	1	5004	7	NULL	NULL	0	NULL	p27	NULL		bind	NULL				Cdk2 complex	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_168_1_55_s_74	15631990	(D) Binding of p27 to Cdk2  complexes.	bind
13227	1	5005	6	NULL	NULL	NULL	NULL	peptidyl-tRNA	NucleicAcid		bind							classical	P site		NULL		NULL	NULL	NULL	NULL	gw60_structure_4_3_229_s_277	8805530	(d) Binding of peptidyl-tRNA and aminoacyl-tRNA in classical P and A sites.	bind
13228	2	5005	6	NULL	NULL	NULL	NULL	aminoacyl-tRNA	NucleicAcid		bind							classical	A site		NULL		NULL	NULL	NULL	NULL	gw60_structure_4_3_229_s_277	8805530	(d) Binding of peptidyl-tRNA and aminoacyl-tRNA in classical P and A sites.	bind
13345	1	5005	7	NULL	NULL	0	NULL	peptidyl-tRNA	NULL		bind	NULL					NULL	classical	P site		NULL		NULL	NULL	NULL	NULL	gw60_structure_4_3_229_s_277	8805530	(d) Binding of peptidyl-tRNA and aminoacyl-tRNA in classical P and A sites.	bind
13348	4	5005	7	NULL	NULL	0	NULL	aminoacyl-tRNA	NULL		bind	NULL					NULL	classical	A site		NULL		0	NULL	NULL	NULL	gw60_structure_4_3_229_s_277	8805530	(d) Binding of peptidyl-tRNA and aminoacyl-tRNA in classical P and A sites.	bind
13258	1	5006	6	NULL	NULL	NULL	NULL	pp90RSK	GP		bind					p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_86_3_465_s_110	8756728	(d) Binding of pp90RSK to  P300 does not interfere with binding of phospho-CREB to P300.	bind
13259	2	5006	6	NULL	NULL	NULL	NULL	phospho-CREB	GP		bind					p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_86_3_465_s_110	8756728	(d) Binding of pp90RSK to  P300 does not interfere with binding of phospho-CREB to P300.	bind
13260	3	5006	6	NULL	NULL	NULL	NULL	statement 1	Process		does not interfere with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_86_3_465_s_110	8756728	(d) Binding of pp90RSK to  P300 does not interfere with binding of phospho-CREB to P300.	bind
13349	1	5006	7	NULL	NULL	0	NULL	phospho-CREB	NULL		bind	NULL				P300	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_86_3_465_s_110	8756728	(d) Binding of pp90RSK to  P300 does not interfere with binding of phospho-CREB to P300.	bind
13350	2	5006	7	NULL	NULL	0	NULL	pp90RSK	NULL		bind	NULL				P300	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_86_3_465_s_110	8756728	(d) Binding of pp90RSK to  P300 does not interfere with binding of phospho-CREB to P300.	bind
13351	3	5006	7	NULL	NULL	0	NULL	statement 2	NULL		does not interfere with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_86_3_465_s_110	8756728	(d) Binding of pp90RSK to  P300 does not interfere with binding of phospho-CREB to P300.	bind
13261	1	5007	6	NULL	NULL	NULL	NULL	GRASP55	GP	purified	bind					p24 proteins	GP		cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_68	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the cytoplasmic tails of the various p24 proteins, TGF-alpha, and GM130.	bind
13262	2	5007	6	NULL	NULL	NULL	NULL	GRASP55	GP	purified	bind					TGF-alpha	GP		cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_68	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the cytoplasmic tails of the various p24 proteins, TGF-alpha, and GM130.	bind
13263	3	5007	6	NULL	NULL	NULL	NULL	GRASP55	GP	purified	bind					GM130	GP		cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_68	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the cytoplasmic tails of the various p24 proteins, TGF-alpha, and GM130.	bind
13264	4	5007	6	NULL	NULL	NULL	NULL	GRASP65	GP	purified	bind					p24 proteins	GP		cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_68	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the cytoplasmic tails of the various p24 proteins, TGF-alpha, and GM130.	bind
13265	5	5007	6	NULL	NULL	NULL	NULL	GRASP65	GP	purified	bind					TGF-alpha	GP		cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_68	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the cytoplasmic tails of the various p24 proteins, TGF-alpha, and GM130.	bind
13266	6	5007	6	NULL	NULL	NULL	NULL	GRASP65	GP	purified	bind					GM130	GP		cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_68	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the cytoplasmic tails of the various p24 proteins, TGF-alpha, and GM130.	bind
44615	7	5007	6	NULL	NULL	NULL	NULL	p24 proteins	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_68	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the cytoplasmic tails of the various p24 proteins, TGF-alpha, and GM130.	bind
44617	8	5007	6	NULL	NULL	NULL	NULL	TGF-alpha	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_68	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the cytoplasmic tails of the various p24 proteins, TGF-alpha, and GM130.	bind
44620	9	5007	6	NULL	NULL	NULL	NULL	GM130	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_68	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the cytoplasmic tails of the various p24 proteins, TGF-alpha, and GM130.	bind
13352	1	5007	7	10	NULL	0	NULL	GRASP55	NULL	purified	bind	NULL				p24 protein	NULL		cytoplasmic tails		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_68	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the cytoplasmic tails of the various p24 proteins, TGF-alpha, and GM130.	bind
13353	2	5007	7	10	NULL	0	NULL	GRASP55	NULL	purified	bind	NULL				TGF-alpha	NULL		cytoplasmic tails		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_68	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the cytoplasmic tails of the various p24 proteins, TGF-alpha, and GM130.	bind
13354	3	5007	7	10	NULL	0	NULL	GRASP55	NULL	purified	bind	NULL				GM130	NULL		cytoplasmic tails		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_68	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the cytoplasmic tails of the various p24 proteins, TGF-alpha, and GM130.	bind
13355	4	5007	7	10	NULL	0	NULL	GRASP65	NULL	purified	bind	NULL				p24 protein	NULL		cytoplasmic tails		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_68	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the cytoplasmic tails of the various p24 proteins, TGF-alpha, and GM130.	bind
13356	5	5007	7	10	NULL	0	NULL	GRASP65	NULL	purified	bind	NULL				TGF-alpha	NULL		cytoplasmic tails		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_68	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the cytoplasmic tails of the various p24 proteins, TGF-alpha, and GM130.	bind
13357	6	5007	7	10	NULL	0	NULL	GRASP65	NULL	purified	bind	NULL				GM130	NULL		cytoplasmic tails		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_68	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the cytoplasmic tails of the various p24 proteins, TGF-alpha, and GM130.	bind
44616	7	5007	7	10	NULL	0	NULL	p24 proteins	NULL		is a type of	NULL				GST fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_68	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the cytoplasmic tails of the various p24 proteins, TGF-alpha, and GM130.	bind
44619	8	5007	7	10	NULL	0	NULL	TGF-alpha	NULL		is a type of	NULL				GST fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_68	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the cytoplasmic tails of the various p24 proteins, TGF-alpha, and GM130.	bind
44621	9	5007	7	10	NULL	0	NULL	GM130	NULL		is a type of	NULL				GST fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_68	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the cytoplasmic tails of the various p24 proteins, TGF-alpha, and GM130.	bind
13267	1	5008	6	NULL	NULL	NULL	NULL	GRASP55	GP	purified	bind					p24a	GP	wild-type	cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
13268	2	5008	6	NULL	NULL	NULL	NULL	Grasp55	GP	purified	bind					GM130	GP	wild-type			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
13269	3	5008	6	NULL	NULL	NULL	NULL	GRASP55	GP	purified	bind					p24a	GP	point mutant	cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
13270	4	5008	6	NULL	NULL	NULL	NULL	GRASP55	GP	purified	bind					GM130	GP	point mutant			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
17352	5	5008	6	NULL	NULL	NULL	NULL	GRASP65	GP	purified	bind					p24a	GP	wild-type	cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
17353	6	5008	6	NULL	NULL	NULL	NULL	GRASP65	GP	purified	bind					GM130	GP	wild-type			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
17354	7	5008	6	NULL	NULL	NULL	NULL	GRASP65	GP	purified	bind					p24a	GP	point mutant	cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
17355	8	5008	6	NULL	NULL	NULL	NULL	GRASP65	GP	purified	bind					GM130	GP	point mutant			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
44622	9	5008	6	NULL	NULL	NULL	NULL	p24a	GP		is a type of					GST fusion protein					NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
44624	10	5008	6	NULL	NULL	NULL	NULL	GM130	GP		is a type of					GST fusion protein					NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
13358	1	5008	7	10	NULL	0	NULL	GRASP55	NULL	purified	bind	NULL				 p24a	NULL	wild-type	cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
13359	2	5008	7	10	NULL	0	NULL	GRASP55	NULL	purified	bind	NULL				p24a	NULL	point mutant	cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
13360	3	5008	7	10	NULL	0	NULL	GRASP55	NULL	purified	bind	NULL				GM130	NULL	wild-type			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
13361	4	5008	7	10	NULL	0	NULL	GRASP55	NULL	purified	bind	NULL				GM130	NULL	point mutant			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
13362	5	5008	7	10	NULL	0	NULL	GRASP65	NULL	purified	bind	NULL				p24a	NULL	wild-type	cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
13363	6	5008	7	10	NULL	0	NULL	GRASP65	NULL	purified	bind	NULL				p24a	NULL	point mutant	cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
13364	7	5008	7	10	NULL	0	NULL	GRASP65	NULL	purified	bind	NULL				GM130	NULL	wild-type			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
13365	8	5008	7	10	NULL	0	NULL	GRASP65	NULL	purified	bind	NULL				GM130	NULL	point mutant			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
44625	10	5008	7	10	NULL	0	NULL	GM130	NULL		is a type of	NULL				GST fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
44626	9	5008	7	10	NULL	0	NULL	p24a	NULL		is a type of	NULL				GST fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_6_885_s_82	11739402	(D) Binding of purified GRASP55 and GRASP65 to GST fusion proteins bearing the wild-type and point mutant forms of the p24a cytoplasmic tail, and GM130.	bind
13271	1	5009	6	NULL	NULL	NULL	NULL	Rpb1	GP		bind					GAL1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_18_6270_s_216	11509669	(D) Binding of Rpb1 to the  GAL1 and  GAL10 promoters.	bind
13272	2	5009	6	NULL	NULL	NULL	NULL	Rpb1	GP		bind					GAL10	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_18_6270_s_216	11509669	(D) Binding of Rpb1 to the  GAL1 and  GAL10 promoters.	bind
13366	1	5009	7	NULL	NULL	0	NULL	Rpb1	NULL		bind	NULL				GAL1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_18_6270_s_216	11509669	(D) Binding of Rpb1 to the  GAL1 and  GAL10 promoters.	bind
13367	2	5009	7	NULL	NULL	0	NULL	Rpb1	NULL		bind	NULL				GAL10	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_18_6270_s_216	11509669	(D) Binding of Rpb1 to the  GAL1 and  GAL10 promoters.	bind
13273	1	5010	6	NULL	NULL	NULL	NULL	Sar1p	GP		bind					Sec23/24p complex	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_395_s_203	11970962	(D) Binding of Sar1p and Sec23/24p complex is enhanced in the presence of Glo3p.	bind
13274	2	5010	6	NULL	NULL	NULL	NULL	Glo3p	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_395_s_203	11970962	(D) Binding of Sar1p and Sec23/24p complex is enhanced in the presence of Glo3p.	bind
13368	1	5010	7	NULL	NULL	0	NULL	Sar1p 	NULL		bind	NULL				Sec23/24p complex	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_157_3_395_s_203	11970962	(D) Binding of Sar1p and Sec23/24p complex is enhanced in the presence of Glo3p.	bind
13369	2	5010	7	10	NULL	0	NULL	Glo3p	NULL		enhance	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_3_395_s_203	11970962	(D) Binding of Sar1p and Sec23/24p complex is enhanced in the presence of Glo3p.	bind
13275	1	5011	6	NULL	NULL	NULL	NULL	Sla2p	GP		bind					PtdIns3P	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_717_s_113	15574875	(D) Binding of Sla2p to PtdIns3P, PtdIns4P, and PtdIns5P.	bind
13276	2	5011	6	NULL	NULL	NULL	NULL	Sla2p	GP		bind					PtdIns4P	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_717_s_113	15574875	(D) Binding of Sla2p to PtdIns3P, PtdIns4P, and PtdIns5P.	bind
13277	3	5011	6	NULL	NULL	NULL	NULL	Sla2p	GP		bind					PtdIns5P	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_717_s_113	15574875	(D) Binding of Sla2p to PtdIns3P, PtdIns4P, and PtdIns5P.	bind
13370	1	5011	7	NULL	NULL	0	NULL	Sla2p	NULL		bind	NULL				PtdIns3P	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_2_717_s_113	15574875	(D) Binding of Sla2p to PtdIns3P, PtdIns4P, and PtdIns5P.	bind
13371	2	5011	7	NULL	NULL	0	NULL	Sla2p 	NULL		bind	NULL				PtdIns4P	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_2_717_s_113	15574875	(D) Binding of Sla2p to PtdIns3P, PtdIns4P, and PtdIns5P.	bind
13372	3	5011	7	NULL	NULL	0	NULL	Sla2p	NULL		bind	NULL				PtdIns5P	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_2_717_s_113	15574875	(D) Binding of Sla2p to PtdIns3P, PtdIns4P, and PtdIns5P.	bind
13278	1	5012	6	NULL	NULL	NULL	NULL	Synaptotagmin	GP		bind					GST-SyxH3-C	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_23_3_593_s_220	10433270	(D) Binding of Synaptotagmin to GST-SyxH3-C is strongly reduced compared to GST-Syx.	bind
13279	2	5012	6	NULL	NULL	NULL	NULL	Synaptotagmin	GP		bind					GST-Syx	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_23_3_593_s_220	10433270	(D) Binding of Synaptotagmin to GST-SyxH3-C is strongly reduced compared to GST-Syx.	bind
13280	3	5012	6	NULL	NULL	NULL	NULL	statement 1	Process		is reduced than		strongly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_23_3_593_s_220	10433270	(D) Binding of Synaptotagmin to GST-SyxH3-C is strongly reduced compared to GST-Syx.	bind
13373	1	5012	7	NULL	NULL	0	NULL	Synaptotagmin	NULL		bind	NULL				GST-SyxH3-C	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_593_s_220	10433270	(D) Binding of Synaptotagmin to GST-SyxH3-C is strongly reduced compared to GST-Syx.	bind
13374	2	5012	7	NULL	NULL	0	NULL	Synaptotagmin	NULL		bind	NULL				GST-Syx	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_593_s_220	10433270	(D) Binding of Synaptotagmin to GST-SyxH3-C is strongly reduced compared to GST-Syx.	bind
13375	3	5012	7	10	NULL	0	NULL	statement 1	NULL		is reduced than	NULL	strongly			statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_23_3_593_s_220	10433270	(D) Binding of Synaptotagmin to GST-SyxH3-C is strongly reduced compared to GST-Syx.	bind
13281	1	5013	6	NULL	NULL	NULL	NULL	translation factors	GP		bind					eIF4GI	GP	point mutant			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_2_468_s_224	10611225	(D) Binding of translation factors to eIF4GI point mutants in vitro.	bind
13376	1	5013	7	NULL	NULL	0	NULL	 translation factors	NULL		bind	NULL				eIF4GI	NULL	point mutant			NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_20_2_468_s_224	10611225	(D) Binding of translation factors to eIF4GI point mutants in vitro.	bind
13282	1	5015	6	NULL	NULL	NULL	NULL	TSG101	GP		bind					Hrs	GP	deletion mutant			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_162_3_425_s_83	12900394	(D) Binding of Tsg101 to Hrs deletion mutants.	bind
13377	1	5015	7	NULL	NULL	0	NULL	Tsg101	NULL		bind	NULL				Hrs	NULL	deletion mutant			NULL		0	NULL	NULL	NULL	gw60_cellbiol_162_3_425_s_83	12900394	(D) Binding of Tsg101 to Hrs deletion mutants.	bind
13283	1	5016	6	NULL	NULL	NULL	NULL	GST-Spo20p	GP	wt	bind			61-91		PA	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_4_1802_s_249	14742704	(D) Binding of wt and mutant  GST-Spo20p61-91 to PA.	bind
13284	2	5016	6	10	NULL	0	NULL	GST-Spo20p	NULL	mutant	bind	NULL		61-91		PA	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_4_1802_s_249	14742704	(D) Binding of wt and mutant  GST-Spo20p61-91 to PA.	bind
13378	1	5016	7	10	NULL	0	NULL	GST-Spo20p	NULL	wt	bind	NULL		61-91		PA	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_4_1802_s_249	14742704	(D) Binding of wt and mutant  GST-Spo20p61-91 to PA.	bind
13379	2	5016	7	10	NULL	0	NULL	GST-Spo20p	NULL	mutant	bind	NULL		61-91		PA	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_4_1802_s_249	14742704	(D) Binding of wt and mutant  GST-Spo20p61-91 to PA.	bind
13285	1	5017	6	NULL	NULL	NULL	NULL	Xrn1p	GP		bind					actin RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5930_s_244	10454540	(D) Binding of Xrn1p and Xrn1-D208Ap to actin RNA (nuclease substrate of panel C) was determined by filter binding.	bind
13286	2	5017	6	NULL	NULL	NULL	NULL	Xrn1	GP		bind			D208Ap		actin RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5930_s_244	10454540	(D) Binding of Xrn1p and Xrn1-D208Ap to actin RNA (nuclease substrate of panel C) was determined by filter binding.	bind
13380	1	5017	7	NULL	NULL	0	NULL	Xrn1p	NULL		bind	NULL				actin RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_5930_s_244	10454540	(D) Binding of Xrn1p and Xrn1-D208Ap to actin RNA (nuclease substrate of panel C) was determined by filter binding.	bind
13381	2	5017	7	NULL	NULL	0	NULL	Xrn1p	NULL		bind	NULL		D208A		actin RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_5930_s_244	10454540	(D) Binding of Xrn1p and Xrn1-D208Ap to actin RNA (nuclease substrate of panel C) was determined by filter binding.	bind
13287	1	5018	6	NULL	NULL	NULL	NULL				bind			RGG box		sc1 RNAs	NucleicAcid	truncated	bp 1 - 58		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_4_489_s_144	11719189	(D) Binding specificity  of the RGG box (cterm 10) to truncated  sc1 RNAs (bp 1 - 58), or mutants G37-G38 or  G42-G43 to CC.	bind
13382	1	5018	7	NULL	NULL	0	NULL		NULL		bind	NULL		RGG box 		sc1 RNAs	NULL	truncated	bp 1 - 58		NULL		NULL	NULL	NULL	NULL	gw60_cell_107_4_489_s_144	11719189	(D) Binding specificity  of the RGG box (cterm 10) to truncated  sc1 RNAs (bp 1 - 58), or mutants G37-G38 or  G42-G43 to CC.	bind
13288	1	5019	6	NULL	NULL	NULL	NULL	RXR-VDR heterodimer	GP		bind							specific		VDRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_257	10891484	(D) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-VDR heterodimer bound to a specific VDRE.	bind
13289	2	5019	6	NULL	NULL	NULL	NULL	TRAP220	GP		bind		efficiently	RBD		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_257	10891484	(D) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-VDR heterodimer bound to a specific VDRE.	bind
13290	3	5019	6	NULL	NULL	NULL	NULL			proper spacing of 	is necessary for			RBD-1		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_257	10891484	(D) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-VDR heterodimer bound to a specific VDRE.	bind
17356	4	5019	6	NULL	NULL	NULL	NULL			proper spacing of	is necessary for			RBD-2		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_257	10891484	(D) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-VDR heterodimer bound to a specific VDRE.	bind
44711	5	5019	6	NULL	NULL	NULL	NULL			presence of	is necessary for			RBD-1		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_257	10891484	(D) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-VDR heterodimer bound to a specific VDRE.	bind
44712	6	5019	6	NULL	NULL	NULL	NULL			presence of	is necessary for			RBD-2		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_257	10891484	(D) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-VDR heterodimer bound to a specific VDRE.	bind
13384	1	5019	7	NULL	NULL	0	NULL	RXR-VDR heterodimer	NULL		bind	NULL					NULL	specific		VDRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_257	10891484	(D) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-VDR heterodimer bound to a specific VDRE.	bind
13385	2	5019	7	NULL	NULL	0	NULL	TRAP220	NULL		bind	NULL	efficiently	RBD		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_257	10891484	(D) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-VDR heterodimer bound to a specific VDRE.	bind
13386	3	5019	7	NULL	NULL	0	NULL		NULL	proper spacing of	is necessary for	NULL		RBD-1		statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_257	10891484	(D) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-VDR heterodimer bound to a specific VDRE.	bind
13387	4	5019	7	NULL	NULL	0	NULL		NULL	proper spacing of	is necessary for	NULL		RBD-2		statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_257	10891484	(D) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-VDR heterodimer bound to a specific VDRE.	bind
44717	5	5019	7	NULL	NULL	0	NULL		NULL	presence of	is necessary for	NULL		RBD-1		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_257	10891484	(D) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-VDR heterodimer bound to a specific VDRE.	bind
44718	6	5019	7	NULL	NULL	0	NULL		NULL	presence of 	is necessary for	NULL		RBD-2		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5433_s_257	10891484	(D) Both the presence and proper spacing of RBD-1 and RBD-2 are necessary for efficient binding of TRAP220 RBD to an RXR-VDR heterodimer bound to a specific VDRE.	bind
13291	1	5020	6	NULL	NULL	NULL	NULL	eIF4G	GP		bind					Mnk2a	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_16_5692_s_289	12897141	(D) C-terminal deletions affect binding of eIF4G to Mnk2a.	bind
13292	2	5020	6	NULL	NULL	NULL	NULL			deletion of	affect			C-terminus		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_16_5692_s_289	12897141	(D) C-terminal deletions affect binding of eIF4G to Mnk2a.	bind
13388	1	5020	7	NULL	NULL	0	NULL	eIF4G	NULL		bind	NULL				Mnk2a	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_16_5692_s_289	12897141	(D) C-terminal deletions affect binding of eIF4G to Mnk2a.	bind
13389	2	5020	7	NULL	NULL	0	NULL		NULL	deletion of	affect	NULL		C-terminal 		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_16_5692_s_289	12897141	(D) C-terminal deletions affect binding of eIF4G to Mnk2a.	bind
13293	1	5021	6	NULL	NULL	NULL	NULL	C4BP	GP		bind		directly			CD40	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_6_837_s_46	12818164	(D) C4BP  binds directly to CD40.	bind
13390	1	5021	7	NULL	NULL	0	NULL	C4BP	NULL		binds	NULL	directly			CD40	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_18_6_837_s_46	12818164	(D) C4BP  binds directly to CD40.	bind
13294	1	5022	6	NULL	NULL	NULL	NULL	myosin-Va	GP		bind					syntaxin-1A	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_96	16030255	(D) Ca2+-dependence of myosin-Va binding to syntaxin-1A.	bind
13295	2	5022	6	NULL	NULL	NULL	NULL	statement 1	Process		is dependent on					Ca+2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_96	16030255	(D) Ca2+-dependence of myosin-Va binding to syntaxin-1A.	bind
13391	1	5022	7	NULL	NULL	0	NULL	myosin-Va	NULL		bind	NULL				syntaxin-1A	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_96	16030255	(D) Ca2+-dependence of myosin-Va binding to syntaxin-1A.	bind
13392	2	5022	7	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				Ca2+	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_96	16030255	(D) Ca2+-dependence of myosin-Va binding to syntaxin-1A.	bind
13296	1	5023	6	NULL	NULL	NULL	NULL	CAML	GP		does not bind					FGFR1	GP				NULL	PC-12 cells	NULL	NULL	NULL	NULL	gw60_devcell_5_2_245_s_154	12919676	(D) CAML does not bind the FGFR1 in PC-12 cells.	bind
13393	1	5023	7	NULL	NULL	0	NULL	CAML	NULL		does not bind	NULL				FGFR1	NULL				NULL	PC-12 cells	0	NULL	NULL	NULL	gw60_devcell_5_2_245_s_154	12919676	(D) CAML does not bind the FGFR1 in PC-12 cells.	bind
13297	1	5025	6	NULL	NULL	NULL	NULL	Cdc24	GP		bind			FW253AA		Pcn1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1038_s_235	9891039	(D) Cdc24(FW253AA) binds Pcn1 and Rfc1.	bind
13298	2	5025	6	NULL	NULL	NULL	NULL	Cdc24	GP		bind			FW253AA		Rfc1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1038_s_235	9891039	(D) Cdc24(FW253AA) binds Pcn1 and Rfc1.	bind
13394	1	5025	7	NULL	NULL	0	NULL	Cdc24	NULL		binds	NULL		FW253AA		Pcn1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1038_s_235	9891039	(D) Cdc24(FW253AA) binds Pcn1 and Rfc1.	bind
13395	2	5025	7	NULL	NULL	0	NULL	 Cdc24	NULL		binds	NULL		FW253AA		Rfc1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1038_s_235	9891039	(D) Cdc24(FW253AA) binds Pcn1 and Rfc1.	bind
13299	1	5027	6	NULL	NULL	NULL	NULL	SF-1	GP	endogenous	bind		directly			Oct4	GP			PE	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_150	15831456	(D) ChIP analysis of direct binding of endogenous  SF-1 and LRH-1 to the Oct4 PE and PP in vivo.	bind
13300	2	5027	6	NULL	NULL	NULL	NULL	SF-1	GP	endogenous	bind		directly			Oct4	GP			PP	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_150	15831456	(D) ChIP analysis of direct binding of endogenous  SF-1 and LRH-1 to the Oct4 PE and PP in vivo.	bind
13301	3	5027	6	NULL	NULL	NULL	NULL	LRH-1	GP	endogenous	bind		directly			Oct4	GP			PE	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_150	15831456	(D) ChIP analysis of direct binding of endogenous  SF-1 and LRH-1 to the Oct4 PE and PP in vivo.	bind
13302	4	5027	6	NULL	NULL	NULL	NULL	LRH-1	GP	endogenous	bind		directly			Oct4	GP			PP	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_150	15831456	(D) ChIP analysis of direct binding of endogenous  SF-1 and LRH-1 to the Oct4 PE and PP in vivo.	bind
13396	1	5027	7	NULL	NULL	0	NULL	SF-1	NULL	endogenous	binds	NULL	directly			Oct4	NULL			PE	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_150	15831456	(D) ChIP analysis of direct binding of endogenous  SF-1 and LRH-1 to the Oct4 PE and PP in vivo.	bind
13397	2	5027	7	NULL	NULL	0	NULL	SF-1	NULL	endogenous	binds	NULL	directly			Oct4	NULL			PP	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_150	15831456	(D) ChIP analysis of direct binding of endogenous  SF-1 and LRH-1 to the Oct4 PE and PP in vivo.	bind
13398	3	5027	7	NULL	NULL	0	NULL	LRH-1	NULL	endogenous	binds	NULL	directly			Oct4 	NULL			PE	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_150	15831456	(D) ChIP analysis of direct binding of endogenous  SF-1 and LRH-1 to the Oct4 PE and PP in vivo.	bind
13399	4	5027	7	NULL	NULL	0	NULL	LRH-1	NULL	endogenous	binds	NULL	directly			Oct4	NULL			PP	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_9_3492_s_150	15831456	(D) ChIP analysis of direct binding of endogenous  SF-1 and LRH-1 to the Oct4 PE and PP in vivo.	bind
13303	1	5028	6	NULL	NULL	NULL	NULL	PDX-1	GP	endogenous	bind					LRH-1	GP	human		promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_19_6713_s_161	12972592	(D) ChIP assay demonstrating binding of endogenous PDX-1  to the human LRH-1 promoter.	bind
13400	1	5028	7	NULL	NULL	0	NULL	PDX-1	NULL	endogenous	bind	NULL				LRH-1	NULL	human		promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_19_6713_s_161	12972592	(D) ChIP assay demonstrating binding of endogenous PDX-1  to the human LRH-1 promoter.	bind
13304	1	5029	6	NULL	NULL	NULL	NULL	Runx2	GP	endogenous	bind					beta-casein	GP	endogenous		promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3182_s_152	15798204	(D) ChIP assay demonstrating the binding of endogenous Runx2 and Oct-1  to the endogenous beta-casein promoter.	bind
13305	2	5029	6	NULL	NULL	NULL	NULL	Oct-1	GP	endogenous	bind					beta-casein	GP	endogenous		promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3182_s_152	15798204	(D) ChIP assay demonstrating the binding of endogenous Runx2 and Oct-1  to the endogenous beta-casein promoter.	bind
13401	1	5029	7	NULL	NULL	0	NULL	Runx2	NULL	endogenous	bind	NULL				beta-casein	NULL	endogenous		promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3182_s_152	15798204	(D) ChIP assay demonstrating the binding of endogenous Runx2 and Oct-1  to the endogenous beta-casein promoter.	bind
13402	2	5029	7	NULL	NULL	0	NULL	Oct-1	NULL	endogenous	bind	NULL				beta-casein	NULL	endogenous		promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3182_s_152	15798204	(D) ChIP assay demonstrating the binding of endogenous Runx2 and Oct-1  to the endogenous beta-casein promoter.	bind
13306	1	5030	6	NULL	NULL	NULL	NULL	AP-1	GP		bind					hTERT	GP			promoter	NULL	in vivo using HeLa cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_18_8037_s_165	16135795	(D) ChIP assay to verify the  binding of AP-1 to the  hTERT promoter in vivo using HeLa cells.	bind
13404	1	5030	7	10	NULL	0	NULL	AP-1	NULL		bind	NULL				hTERT	NULL			promoter	NULL	in vivo using HeLa cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_18_8037_s_165	16135795	(D) ChIP assay to verify the  binding of AP-1 to the  hTERT promoter in vivo using HeLa cells.	bind
13307	1	5031	6	NULL	NULL	NULL	NULL	RB	GP		bind					LPL	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_6_903_s_113	12479814	(D) Chromatin immunoprecipitation (ChIP) assays demonstrating binding of RB, PPAR , or HDAC3 to the LPL promoter.	bind
13308	2	5031	6	NULL	NULL	NULL	NULL	PPAR	GP		bind					LPL	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_6_903_s_113	12479814	(D) Chromatin immunoprecipitation (ChIP) assays demonstrating binding of RB, PPAR , or HDAC3 to the LPL promoter.	bind
13309	3	5031	6	NULL	NULL	NULL	NULL	HDAC3	GP		bind					LPL	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_6_903_s_113	12479814	(D) Chromatin immunoprecipitation (ChIP) assays demonstrating binding of RB, PPAR , or HDAC3 to the LPL promoter.	bind
13310	4	5031	6	NULL	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_6_903_s_113	12479814	(D) Chromatin immunoprecipitation (ChIP) assays demonstrating binding of RB, PPAR , or HDAC3 to the LPL promoter.	bind
44713	5	5031	6	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_6_903_s_113	12479814	(D) Chromatin immunoprecipitation (ChIP) assays demonstrating binding of RB, PPAR , or HDAC3 to the LPL promoter.	bind
13405	1	5031	7	NULL	NULL	0	NULL	 RB	NULL		bind	NULL				LPL	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_devcell_3_6_903_s_113	12479814	(D) Chromatin immunoprecipitation (ChIP) assays demonstrating binding of RB, PPAR , or HDAC3 to the LPL promoter.	bind
13409	2	5031	7	NULL	NULL	0	NULL	PPAR	NULL		bind	NULL				LPL	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_devcell_3_6_903_s_113	12479814	(D) Chromatin immunoprecipitation (ChIP) assays demonstrating binding of RB, PPAR , or HDAC3 to the LPL promoter.	bind
13410	3	5031	7	NULL	NULL	0	NULL	HDAC3	NULL		bind	NULL				LPL	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_devcell_3_6_903_s_113	12479814	(D) Chromatin immunoprecipitation (ChIP) assays demonstrating binding of RB, PPAR , or HDAC3 to the LPL promoter.	bind
44719	4	5031	7	NULL	NULL	0	NULL	statement 2	NULL		is an alternative to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_devcell_3_6_903_s_113	12479814	(D) Chromatin immunoprecipitation (ChIP) assays demonstrating binding of RB, PPAR , or HDAC3 to the LPL promoter.	bind
53049	5	5031	7	10	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_devcell_3_6_903_s_113	12479814	(D) Chromatin immunoprecipitation (ChIP) assays demonstrating binding of RB, PPAR , or HDAC3 to the LPL promoter.	bind
13311	1	5032	6	NULL	NULL	NULL	NULL	MEF	GP		bind					PFP	GP			promoter	NULL	PFP-positive CTLL-2 cell line	NULL	NULL	NULL	NULL	gw60_immunity_17_4_437_s_194	12387738	(D) Chromatin immunoprecipitation analysis of MEF binding to PFP promoter in the PFP-positive CTLL-2 cell line but not the PFP-negative EL-4 cell line.	bind
13312	2	5032	6	NULL	NULL	NULL	NULL	MEF	GP		does not bind					PFP	GP			promoter	NULL	PFP-negative EL-4 cell line	NULL	NULL	NULL	NULL	gw60_immunity_17_4_437_s_194	12387738	(D) Chromatin immunoprecipitation analysis of MEF binding to PFP promoter in the PFP-positive CTLL-2 cell line but not the PFP-negative EL-4 cell line.	bind
13411	1	5032	7	NULL	NULL	0	NULL	MEF	NULL		bind	NULL				PFP	NULL			promoter	NULL	PFP-positive CTLL-2 cell line	NULL	NULL	NULL	NULL	gw60_immunity_17_4_437_s_194	12387738	(D) Chromatin immunoprecipitation analysis of MEF binding to PFP promoter in the PFP-positive CTLL-2 cell line but not the PFP-negative EL-4 cell line.	bind
13412	2	5032	7	NULL	NULL	0	NULL	MEF	NULL		does not bind	NULL				PFP	NULL			promoter	NULL	PFP-negative EL-4 cell line	0	NULL	NULL	NULL	gw60_immunity_17_4_437_s_194	12387738	(D) Chromatin immunoprecipitation analysis of MEF binding to PFP promoter in the PFP-positive CTLL-2 cell line but not the PFP-negative EL-4 cell line.	bind
13313	1	5033	6	NULL	NULL	NULL	NULL	Hip1R	GP		bind					cages		truncated			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_6_1209_s_78	11564758	(d) Clathrin LC restores Hip1R binding to truncated cages.	bind
13314	2	5033	6	NULL	NULL	NULL	NULL	Clathrin LC	GP		restores					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_6_1209_s_78	11564758	(d) Clathrin LC restores Hip1R binding to truncated cages.	bind
13413	1	5033	7	10	NULL	0	NULL	Hip1R	NULL		bind	NULL				cages	NULL	truncated			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_6_1209_s_78	11564758	(d) Clathrin LC restores Hip1R binding to truncated cages.	bind
13414	2	5033	7	NULL	NULL	0	NULL	Clathrin LC	NULL		restores	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_6_1209_s_78	11564758	(d) Clathrin LC restores Hip1R binding to truncated cages.	bind
13315	1	5034	6	NULL	NULL	NULL	NULL	CLOCK	GP		bind					mPer1	GP			E box at CT 06	NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_855_s_164	11779462	(D) CLOCK and BMAL1 are  bound to  mPer1 E box at CT  06 and 15.	bind
13316	2	5034	6	NULL	NULL	NULL	NULL	CLOCK	GP		bind					mPer1	GP			E box at CT 15	NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_855_s_164	11779462	(D) CLOCK and BMAL1 are  bound to  mPer1 E box at CT  06 and 15.	bind
13317	3	5034	6	NULL	NULL	NULL	NULL	BMAL1	GP		bind					mPer1	GP			E box at CT 06	NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_855_s_164	11779462	(D) CLOCK and BMAL1 are  bound to  mPer1 E box at CT  06 and 15.	bind
13318	4	5034	6	NULL	NULL	NULL	NULL	BMAL1	GP		bind					mPer1	GP			E box at CT 15	NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_855_s_164	11779462	(D) CLOCK and BMAL1 are  bound to  mPer1 E box at CT  06 and 15.	bind
13416	1	5034	7	NULL	NULL	0	NULL	CLOCK	NULL		bind	NULL				mPer1	NULL			E box at CT 06	NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_855_s_164	11779462	(D) CLOCK and BMAL1 are  bound to  mPer1 E box at CT  06 and 15.	bind
13419	2	5034	7	NULL	NULL	0	NULL	CLOCK	NULL		bind	NULL				 mPer1	NULL			E box at CT 15	NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_855_s_164	11779462	(D) CLOCK and BMAL1 are  bound to  mPer1 E box at CT  06 and 15.	bind
13420	3	5034	7	NULL	NULL	0	NULL	BMAL1	NULL		bind	NULL				mPer1	NULL			E box at CT 06	NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_855_s_164	11779462	(D) CLOCK and BMAL1 are  bound to  mPer1 E box at CT  06 and 15.	bind
13421	4	5034	7	NULL	NULL	0	NULL	BMAL1	NULL		bind	NULL				mPer1	NULL			E box at CT 15	NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_855_s_164	11779462	(D) CLOCK and BMAL1 are  bound to  mPer1 E box at CT  06 and 15.	bind
13319	1	5035	6	NULL	NULL	NULL	NULL	Tubulin	OrganismPart	soluble	bind					GST-CNP	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_4_661_s_71	16103231	(D) Comparative binding of soluble tubulin and preassembled MTs to GST-CNP.	bind
13320	2	5035	6	NULL	NULL	NULL	NULL	MTs	OrganismPart	preassembled	bind					GST-CNP	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_4_661_s_71	16103231	(D) Comparative binding of soluble tubulin and preassembled MTs to GST-CNP.	bind
13424	1	5035	7	NULL	NULL	0	NULL	tubulin	NULL	soluble	bind	NULL				GST-CNP	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_170_4_661_s_71	16103231	(D) Comparative binding of soluble tubulin and preassembled MTs to GST-CNP.	bind
13425	2	5035	7	NULL	NULL	0	NULL	MTs	NULL	preassembled	bind	NULL				GST-CNP	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_170_4_661_s_71	16103231	(D) Comparative binding of soluble tubulin and preassembled MTs to GST-CNP.	bind
13334	1	5039	6	NULL	NULL	NULL	NULL	myosin-Va	GP		bind					syntaxin-1A	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_161	16030255	(D) Competitive inhibition of myosin-Va binding to syntaxin-1A by syntaxin-1A [191-240].	bind
13335	2	5039	6	NULL	NULL	NULL	NULL	myosin-Va	GP		bind					syntaxin-1A	GP		191-240		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_161	16030255	(D) Competitive inhibition of myosin-Va binding to syntaxin-1A by syntaxin-1A [191-240].	bind
44703	3	5039	6	NULL	NULL	NULL	NULL	statement 2	Process		inhibit		competitively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_161	16030255	(D) Competitive inhibition of myosin-Va binding to syntaxin-1A by syntaxin-1A [191-240].	bind
13426	1	5039	7	NULL	NULL	0	NULL	myosin-Va	NULL		bind	NULL				syntaxin-1A	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_161	16030255	(D) Competitive inhibition of myosin-Va binding to syntaxin-1A by syntaxin-1A [191-240].	bind
13427	2	5039	7	NULL	NULL	0	NULL	myosin-Va	NULL		bind	NULL				syntaxin-1A 	NULL		191-240		NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_161	16030255	(D) Competitive inhibition of myosin-Va binding to syntaxin-1A by syntaxin-1A [191-240].	bind
13429	3	5039	7	NULL	NULL	0	NULL	statement 2	NULL		inhibits	NULL	competitively			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_161	16030255	(D) Competitive inhibition of myosin-Va binding to syntaxin-1A by syntaxin-1A [191-240].	bind
13491	1	5040	6	NULL	NULL	NULL	NULL	IAAP	GP		bind					Cdr1p-GFP	GP				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_2_6_1361_s_197	14665469	(d) Concentration-dependent  inhibition of IAAP binding to Cdr1p-GFP by nystatin.	bind
13492	2	5040	6	NULL	NULL	NULL	NULL	nystatin	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_2_6_1361_s_197	14665469	(d) Concentration-dependent  inhibition of IAAP binding to Cdr1p-GFP by nystatin.	bind
13493	3	5040	6	NULL	NULL	NULL	NULL	statement 2	Process		is dependent on					concentration					NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_2_6_1361_s_197	14665469	(d) Concentration-dependent  inhibition of IAAP binding to Cdr1p-GFP by nystatin.	bind
13430	1	5040	7	NULL	NULL	0	NULL	IAAP	NULL		bind	NULL				Cdr1p-GFP	NULL				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_2_6_1361_s_197	14665469	(d) Concentration-dependent  inhibition of IAAP binding to Cdr1p-GFP by nystatin.	bind
13432	2	5040	7	NULL	NULL	0	NULL	nystatin	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_2_6_1361_s_197	14665469	(d) Concentration-dependent  inhibition of IAAP binding to Cdr1p-GFP by nystatin.	bind
13433	3	5040	7	NULL	NULL	0	NULL	statement 2	NULL		is dependent on	NULL				Concentration	NULL				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_2_6_1361_s_197	14665469	(d) Concentration-dependent  inhibition of IAAP binding to Cdr1p-GFP by nystatin.	bind
13494	1	5043	6	NULL	NULL	NULL	NULL	Ccz1	GP		bind					vacuole	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_163_5_973_s_71	14662743	(D) Cooperative binding of Ccz1 and Mon1 to the vacuole.	bind
13495	2	5043	6	NULL	NULL	NULL	NULL	Mon1	GP		bind					vacuole	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_163_5_973_s_71	14662743	(D) Cooperative binding of Ccz1 and Mon1 to the vacuole.	bind
13496	3	5043	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_163_5_973_s_71	14662743	(D) Cooperative binding of Ccz1 and Mon1 to the vacuole.	bind
13434	1	5043	7	NULL	NULL	0	NULL	Ccz1	NULL		binds	NULL				vacuole	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_163_5_973_s_71	14662743	(D) Cooperative binding of Ccz1 and Mon1 to the vacuole.	bind
13436	2	5043	7	NULL	NULL	0	NULL	Mon1	NULL		binds	NULL				vacuole	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_163_5_973_s_71	14662743	(D) Cooperative binding of Ccz1 and Mon1 to the vacuole.	bind
13437	3	5043	7	NULL	NULL	0	NULL	statement 1	NULL		occurs in cooperation with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_163_5_973_s_71	14662743	(D) Cooperative binding of Ccz1 and Mon1 to the vacuole.	bind
13497	1	5044	6	NULL	NULL	NULL	NULL	NF-Y	GP		bind					AADC 	GP			neuronal promoter	NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_89_1_58_s_213	11311976	(D) Cooperative binding of NF-Y and the POU-domain of Brn-2 on AADC neuronal promoter.	bind
13498	2	5044	6	NULL	NULL	NULL	NULL	Brn-2	GP		bind			POU domain		AADC	GP			neuronal promoter	NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_89_1_58_s_213	11311976	(D) Cooperative binding of NF-Y and the POU-domain of Brn-2 on AADC neuronal promoter.	bind
13499	3	5044	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_89_1_58_s_213	11311976	(D) Cooperative binding of NF-Y and the POU-domain of Brn-2 on AADC neuronal promoter.	bind
13439	1	5044	7	10	NULL	0	NULL	NF-Y	NULL		binds	NULL				AADC	NULL			 neuronal promoter	NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_89_1_58_s_213	11311976	(D) Cooperative binding of NF-Y and the POU-domain of Brn-2 on AADC neuronal promoter.	bind
13440	2	5044	7	10	NULL	0	NULL	Brn-2	NULL		binds	NULL		POU		AADC	NULL			neuronal promoter	NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_89_1_58_s_213	11311976	(D) Cooperative binding of NF-Y and the POU-domain of Brn-2 on AADC neuronal promoter.	bind
13441	3	5044	7	NULL	NULL	0	NULL	statement 1	NULL		occurs in cooperation with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_89_1_58_s_213	11311976	(D) Cooperative binding of NF-Y and the POU-domain of Brn-2 on AADC neuronal promoter.	bind
13500	1	5046	6	NULL	NULL	NULL	NULL	CPI-17	GP		bind		directly			CKI	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_1_39_s_143	15003508	(D) CPI-17 directly binds to CKI.	bind
13442	1	5046	7	NULL	NULL	0	NULL	CPI-17	NULL		binds	NULL	directly			CKI	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_1_39_s_143	15003508	(D) CPI-17 directly binds to CKI.	bind
13501	1	5047	6	NULL	NULL	NULL	NULL	CUGBP1	GP		bind					p21 mRNA	NucleicAcid			GCN repeats;;5' region	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_6927_s_254	11564876	(D) CUGBP1 binds to GCN repeats with the 5' region of p21 mRNA.	bind
13443	1	5047	7	10	NULL	0	NULL	CUGBP1	NULL		binds	NULL				p21 mRNA	NULL			GCN repeats;;5' region 	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_6927_s_254	11564876	(D) CUGBP1 binds to GCN repeats with the 5' region of p21 mRNA.	bind
13502	1	5048	6	NULL	NULL	NULL	NULL	CUGBP2	GP		bind					COX-2	GP			first 60 nt of 3' UTR	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_1_113_s_191	12535526	(D) CUGBP2 and hnRNP A1 bind cooperatively to the first 60 nt of COX-2 3 UTR.	bind
13503	2	5048	6	NULL	NULL	NULL	NULL	hnRNP A1	GP		bind					COX-2	GP			first 60 nt of 3' UTR	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_1_113_s_191	12535526	(D) CUGBP2 and hnRNP A1 bind cooperatively to the first 60 nt of COX-2 3 UTR.	bind
13504	3	5048	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_1_113_s_191	12535526	(D) CUGBP2 and hnRNP A1 bind cooperatively to the first 60 nt of COX-2 3 UTR.	bind
13444	1	5048	7	NULL	NULL	0	NULL	CUGBP2	NULL		bind	NULL				COX-2	NULL			first 60 nt of 3 UTR	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_1_113_s_191	12535526	(D) CUGBP2 and hnRNP A1 bind cooperatively to the first 60 nt of COX-2 3 UTR.	bind
13445	2	5048	7	NULL	NULL	0	NULL	 hnRNP A1	NULL		bind	NULL				COX-2	NULL			first 60 nt of 3 UTR	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_1_113_s_191	12535526	(D) CUGBP2 and hnRNP A1 bind cooperatively to the first 60 nt of COX-2 3 UTR.	bind
13446	3	5048	7	NULL	NULL	0	NULL	statement 1 	NULL		occurs in cooperation with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_113_s_191	12535526	(D) CUGBP2 and hnRNP A1 bind cooperatively to the first 60 nt of COX-2 3 UTR.	bind
13505	1	5049	6	NULL	NULL	NULL	NULL	Cyclin B chimeras	GP		bind					CDK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_945_s_197	11238451	(D) Cyclin B chimeras bind and activate CDK1 to a similar extent as wild-type cyclins.	bind
13506	2	5049	6	NULL	NULL	NULL	NULL	Cyclin B chimeras	GP		activate					CDK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_945_s_197	11238451	(D) Cyclin B chimeras bind and activate CDK1 to a similar extent as wild-type cyclins.	bind
13507	3	5049	6	NULL	NULL	NULL	NULL	cyclins	GP	wild type	bind					CDK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_945_s_197	11238451	(D) Cyclin B chimeras bind and activate CDK1 to a similar extent as wild-type cyclins.	bind
13508	4	5049	6	NULL	NULL	NULL	NULL	cyclins	GP	wild type	activate					CDK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_945_s_197	11238451	(D) Cyclin B chimeras bind and activate CDK1 to a similar extent as wild-type cyclins.	bind
44714	5	5049	6	NULL	NULL	NULL	NULL	statement 1	Process		is similar to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_945_s_197	11238451	(D) Cyclin B chimeras bind and activate CDK1 to a similar extent as wild-type cyclins.	bind
44715	6	5049	6	NULL	NULL	NULL	NULL	statement 2	Process		is similar to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_945_s_197	11238451	(D) Cyclin B chimeras bind and activate CDK1 to a similar extent as wild-type cyclins.	bind
13459	1	5049	7	NULL	NULL	0	NULL	Cyclin B chimera	NULL		bind	NULL				CDK1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_945_s_197	11238451	(D) Cyclin B chimeras bind and activate CDK1 to a similar extent as wild-type cyclins.	bind
13460	2	5049	7	NULL	NULL	0	NULL	Cyclin B chimera	NULL		activate	NULL				CDK1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_945_s_197	11238451	(D) Cyclin B chimeras bind and activate CDK1 to a similar extent as wild-type cyclins.	bind
13462	3	5049	7	NULL	NULL	0	NULL	cyclins	NULL	wild-type	bind	NULL				CDK1	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_152_5_945_s_197	11238451	(D) Cyclin B chimeras bind and activate CDK1 to a similar extent as wild-type cyclins.	bind
13464	5	5049	7	NULL	NULL	0	NULL	statement 1	NULL		occurs to a similar extent as	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_945_s_197	11238451	(D) Cyclin B chimeras bind and activate CDK1 to a similar extent as wild-type cyclins.	bind
17357	4	5049	7	NULL	NULL	0	NULL	cyclins	NULL	wild-type	activate	NULL				CDK1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_945_s_197	11238451	(D) Cyclin B chimeras bind and activate CDK1 to a similar extent as wild-type cyclins.	bind
44721	6	5049	7	NULL	NULL	0	NULL	statement 2	NULL		occurs to a similar extent as	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_152_5_945_s_197	11238451	(D) Cyclin B chimeras bind and activate CDK1 to a similar extent as wild-type cyclins.	bind
13509	1	5050	6	NULL	NULL	NULL	NULL	DDB1	GP		bind		directly			DDB2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_3_357_s_61	12732143	(D) DDB1 directly binds not only to DDB2, but also to CSA.	bind
13510	2	5050	6	NULL	NULL	NULL	NULL	DDB1	GP		bind		directly			CSA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_3_357_s_61	12732143	(D) DDB1 directly binds not only to DDB2, but also to CSA.	bind
13465	1	5050	7	NULL	NULL	0	NULL	DDB1	NULL		binds	NULL	directly			DDB2	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_113_3_357_s_61	12732143	(D) DDB1 directly binds not only to DDB2, but also to CSA.	bind
13466	2	5050	7	NULL	NULL	0	NULL	DDB1	NULL		binds	NULL	directly			CSA	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_113_3_357_s_61	12732143	(D) DDB1 directly binds not only to DDB2, but also to CSA.	bind
13511	1	5051	6	NULL	NULL	NULL	NULL	FoxM1 protein	GP		bind					Skp2	GP	endogenous		promoter	NULL	U2OS cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_24_10875_s_386	16314512	(D) Depletion of FoxM1 in U2OS cells by siFoxM1 #2 transfection  inhibits binding of FoxM1 protein to the endogenous Skp2 or Cks1 promoter regions.	bind
13512	2	5051	6	NULL	NULL	NULL	NULL	FoxM1 protein	GP		bind					Cks1	GP	endogenous		promoter	NULL	U2OS cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_24_10875_s_386	16314512	(D) Depletion of FoxM1 in U2OS cells by siFoxM1 #2 transfection  inhibits binding of FoxM1 protein to the endogenous Skp2 or Cks1 promoter regions.	bind
13513	3	5051	6	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_24_10875_s_386	16314512	(D) Depletion of FoxM1 in U2OS cells by siFoxM1 #2 transfection  inhibits binding of FoxM1 protein to the endogenous Skp2 or Cks1 promoter regions.	bind
13514	4	5051	6	NULL	NULL	NULL	NULL	FoxM1 protein	GP	depletion of 	inhibits					statement 1	Process				NULL	U2OS cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_24_10875_s_386	16314512	(D) Depletion of FoxM1 in U2OS cells by siFoxM1 #2 transfection  inhibits binding of FoxM1 protein to the endogenous Skp2 or Cks1 promoter regions.	bind
13515	5	5051	6	NULL	NULL	NULL	NULL	FoxM1 protein	GP	depletion of	inhibits					statement 2	Process				NULL	U2OS cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_24_10875_s_386	16314512	(D) Depletion of FoxM1 in U2OS cells by siFoxM1 #2 transfection  inhibits binding of FoxM1 protein to the endogenous Skp2 or Cks1 promoter regions.	bind
13467	1	5051	7	NULL	NULL	0	NULL	FoxM1	NULL		bind	NULL				Skp2	NULL	endogenous		promoter	NULL	U2OS cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_24_10875_s_386	16314512	(D) Depletion of FoxM1 in U2OS cells by siFoxM1 #2 transfection  inhibits binding of FoxM1 protein to the endogenous Skp2 or Cks1 promoter regions.	bind
13468	2	5051	7	NULL	NULL	0	NULL	FoxM1	NULL		bind	NULL				Cks1	NULL	endogenous		promoter	NULL	U2OS cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_24_10875_s_386	16314512	(D) Depletion of FoxM1 in U2OS cells by siFoxM1 #2 transfection  inhibits binding of FoxM1 protein to the endogenous Skp2 or Cks1 promoter regions.	bind
13469	3	5051	7	10	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_24_10875_s_386	16314512	(D) Depletion of FoxM1 in U2OS cells by siFoxM1 #2 transfection  inhibits binding of FoxM1 protein to the endogenous Skp2 or Cks1 promoter regions.	bind
13470	4	5051	7	10	NULL	0	NULL	FoxM1	NULL	depletion of	inhibits	NULL				statement 1	NULL				NULL	U2OS cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_24_10875_s_386	16314512	(D) Depletion of FoxM1 in U2OS cells by siFoxM1 #2 transfection  inhibits binding of FoxM1 protein to the endogenous Skp2 or Cks1 promoter regions.	bind
13471	5	5051	7	10	NULL	0	NULL	FoxM1	NULL	depletion of	inhibits	NULL				statement 2	NULL				NULL	U2OS cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_24_10875_s_386	16314512	(D) Depletion of FoxM1 in U2OS cells by siFoxM1 #2 transfection  inhibits binding of FoxM1 protein to the endogenous Skp2 or Cks1 promoter regions.	bind
13516	1	5053	6	NULL	NULL	NULL	NULL	TIP60	GP		bind		differentially			p21 gene	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4006_s_234	16705155	(D) Differential binding of TIP60 and GAS41 to  p21 and  p14 ARF gene promoters.	bind
13517	2	5053	6	NULL	NULL	NULL	NULL	GAS41	GP		bind		differentially			p21 gene	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4006_s_234	16705155	(D) Differential binding of TIP60 and GAS41 to  p21 and  p14 ARF gene promoters.	bind
13518	3	5053	6	NULL	NULL	NULL	NULL	TIP60	GP		bind		differentially			p14 ARF gene	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4006_s_234	16705155	(D) Differential binding of TIP60 and GAS41 to  p21 and  p14 ARF gene promoters.	bind
13519	4	5053	6	NULL	NULL	NULL	NULL	GAS41	GP		bind		differentially			p14 ARF gene	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4006_s_234	16705155	(D) Differential binding of TIP60 and GAS41 to  p21 and  p14 ARF gene promoters.	bind
13472	1	5053	7	10	NULL	0	NULL	TIP60 	NULL		binds	NULL	differentially			p21 gene	NULL			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4006_s_234	16705155	(D) Differential binding of TIP60 and GAS41 to  p21 and  p14 ARF gene promoters.	bind
13473	2	5053	7	10	NULL	0	NULL	TIP60 	NULL		binds	NULL	differentially			p14 ARF gene	NULL			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4006_s_234	16705155	(D) Differential binding of TIP60 and GAS41 to  p21 and  p14 ARF gene promoters.	bind
13474	3	5053	7	10	NULL	0	NULL	GAS41	NULL		binds	NULL	differentially			p21 gene	NULL			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4006_s_234	16705155	(D) Differential binding of TIP60 and GAS41 to  p21 and  p14 ARF gene promoters.	bind
13475	4	5053	7	10	NULL	0	NULL	GAS41	NULL		binds	NULL	differentially			p14 ARF gene	NULL			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4006_s_234	16705155	(D) Differential binding of TIP60 and GAS41 to  p21 and  p14 ARF gene promoters.	bind
13520	1	5054	6	NULL	NULL	NULL	NULL	GCNF	GP		bind		directly			Nanog gene	GP	endogenous		DR0 element	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8507_s_254	16166633	(D) Direct binding of GCNF to the endogenous   Nanog gene DR0 elements was demonstrated by ChIP assay with GCNF antibodies.	bind
13476	1	5054	7	10	NULL	0	NULL	GCNF	NULL		binds	NULL	directly			Nanog gene	NULL	endogenous		DR0 element	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8507_s_254	16166633	(D) Direct binding of GCNF to the endogenous   Nanog gene DR0 elements was demonstrated by ChIP assay with GCNF antibodies.	bind
13521	1	5055	6	NULL	NULL	NULL	NULL	His6-Ipl1	GP		bind		directly			GST-Sli15	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_7_1381_s_298	10385519	(D) Direct binding of His6-Ipl1  to GST-Sli15.	bind
13477	1	5055	7	NULL	NULL	0	NULL	His6-Ipl1	NULL		binds	NULL	directly			GST-Sli15	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_7_1381_s_298	10385519	(D) Direct binding of His6-Ipl1  to GST-Sli15.	bind
13522	1	5056	6	NULL	NULL	NULL	NULL	Dkk-1	GP		bind					LRP5/6	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_278	11448771	(d) Dkk-1 binds to LRP5/6 and prevents Fz-LRP5/6 complex formation but does not affect the Wnt-Fz interaction.	bind
13524	3	5056	6	NULL	NULL	NULL	NULL	statement 1	Process		prevents					Fz-LRP5/6 complex	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_278	11448771	(d) Dkk-1 binds to LRP5/6 and prevents Fz-LRP5/6 complex formation but does not affect the Wnt-Fz interaction.	bind
13526	5	5056	6	NULL	NULL	NULL	NULL	statement 1	Process		has no effect on					Wnt-Fz	GP	interaction of			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_278	11448771	(d) Dkk-1 binds to LRP5/6 and prevents Fz-LRP5/6 complex formation but does not affect the Wnt-Fz interaction.	bind
13478	1	5056	7	NULL	NULL	0	NULL	Dkk-1	NULL		binds	NULL				LRP5/6	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_278	11448771	(d) Dkk-1 binds to LRP5/6 and prevents Fz-LRP5/6 complex formation but does not affect the Wnt-Fz interaction.	bind
13479	2	5056	7	NULL	NULL	0	NULL	statement 1	NULL		prevents	NULL				Fz-LRP5/6 complex	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_278	11448771	(d) Dkk-1 binds to LRP5/6 and prevents Fz-LRP5/6 complex formation but does not affect the Wnt-Fz interaction.	bind
13481	4	5056	7	10	NULL	0	NULL	statement 1	NULL		does not affect	NULL				Wnt-Fz	NULL	interaction of			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_278	11448771	(d) Dkk-1 binds to LRP5/6 and prevents Fz-LRP5/6 complex formation but does not affect the Wnt-Fz interaction.	bind
13527	1	5057	6	NULL	NULL	NULL	NULL	Dock	GP		bind			SH3 domain		Dscam	GP				NULL	yeast 	NULL	NULL	NULL	NULL	gw60_cell_101_6_671_s_115	10892653	(D) Dock  SH3 domains bind Dscam in yeast.	bind
13482	1	5057	7	10	NULL	0	NULL	Dock	NULL		bind	NULL		SH3 domain		Dscam	NULL				NULL	yeast	NULL	NULL	NULL	NULL	gw60_cell_101_6_671_s_115	10892653	(D) Dock  SH3 domains bind Dscam in yeast.	bind
13528	1	5058	6	NULL	NULL	NULL	NULL	E. coli SE5000(pCS267)	Organism	Psa-fimbriated	bind					A549 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_10_5636_s_128	16988239	(D) Dose-dependent  inhibition of Psa-fimbriated  E. coli SE5000(pCS267) binding to A549 cells using rabbit-specific anti-Psa (filled circles)  or preimmune (empty circles) antiserum as inhibitors.	bind
13529	2	5058	6	NULL	NULL	NULL	NULL	rabbit-specific anti-Psa	GP		inhibits		dose dependently			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_10_5636_s_128	16988239	(D) Dose-dependent  inhibition of Psa-fimbriated  E. coli SE5000(pCS267) binding to A549 cells using rabbit-specific anti-Psa (filled circles)  or preimmune (empty circles) antiserum as inhibitors.	bind
13530	3	5058	6	NULL	NULL	NULL	NULL	preimmune antiserum			inhibits		dose dependently			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_10_5636_s_128	16988239	(D) Dose-dependent  inhibition of Psa-fimbriated  E. coli SE5000(pCS267) binding to A549 cells using rabbit-specific anti-Psa (filled circles)  or preimmune (empty circles) antiserum as inhibitors.	bind
13483	1	5058	7	10	NULL	0	NULL	E. coli SE5000(pCS267)	NULL	Psa-fimbriated	bind	NULL				A549 cells 	NULL				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_10_5636_s_128	16988239	(D) Dose-dependent  inhibition of Psa-fimbriated  E. coli SE5000(pCS267) binding to A549 cells using rabbit-specific anti-Psa (filled circles)  or preimmune (empty circles) antiserum as inhibitors.	bind
13484	2	5058	7	NULL	NULL	0	NULL	rabbit-specific anti-Psa	NULL		inhibits	NULL	dose-dependently			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_74_10_5636_s_128	16988239	(D) Dose-dependent  inhibition of Psa-fimbriated  E. coli SE5000(pCS267) binding to A549 cells using rabbit-specific anti-Psa (filled circles)  or preimmune (empty circles) antiserum as inhibitors.	bind
13485	3	5058	7	NULL	NULL	0	NULL	preimmune antiserum	NULL		inhibits	NULL	dose-dependently			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_74_10_5636_s_128	16988239	(D) Dose-dependent  inhibition of Psa-fimbriated  E. coli SE5000(pCS267) binding to A549 cells using rabbit-specific anti-Psa (filled circles)  or preimmune (empty circles) antiserum as inhibitors.	bind
13531	1	5059	6	NULL	NULL	NULL	NULL	Hsf4b	GP		bind									HSE	NULL	H1299 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_8_3282_s_206	16581800	(D) DUSP26 affects  Hsf4b binding to HSE. H1299 cells were cotransfected with Flag-Hsf4b and increasing  amounts of HA-DUSP26 (same samples as in panel A, lanes 1 to 4).	bind
13532	2	5059	6	NULL	NULL	NULL	NULL	DUSP26	GP		affects					statement 1	Process				NULL	H1299 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_8_3282_s_206	16581800	(D) DUSP26 affects  Hsf4b binding to HSE. H1299 cells were cotransfected with Flag-Hsf4b and increasing  amounts of HA-DUSP26 (same samples as in panel A, lanes 1 to 4).	bind
13486	1	5059	7	NULL	NULL	0	NULL	Flag-Hsf4b	NULL		binds	NULL					NULL			HSE	NULL	H1299 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_8_3282_s_206	16581800	(D) DUSP26 affects  Hsf4b binding to HSE. H1299 cells were cotransfected with Flag-Hsf4b and increasing  amounts of HA-DUSP26 (same samples as in panel A, lanes 1 to 4).	bind
13487	2	5059	7	NULL	NULL	0	NULL	HA-DUSP26	NULL		affects	NULL				statement 1	NULL				NULL	H1299 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_8_3282_s_206	16581800	(D) DUSP26 affects  Hsf4b binding to HSE. H1299 cells were cotransfected with Flag-Hsf4b and increasing  amounts of HA-DUSP26 (same samples as in panel A, lanes 1 to 4).	bind
13533	1	5060	6	NULL	NULL	NULL	NULL	GR	GP		bind					MMTV	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3255_s_79	11971959	(D) Effect of HMG-1 on binding of GR to MMTV promoter.	bind
13488	1	5060	7	NULL	NULL	0	NULL	GR	NULL		bind	NULL				MMTV	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_10_3255_s_79	11971959	(D) Effect of HMG-1 on binding of GR to MMTV promoter.	bind
13534	1	5061	6	NULL	NULL	NULL	NULL	MAb 24c5	GP		bind					M. tuberculosis Erdman day-20 7H9 medium					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_147	11953397	(D) Effects of proteinase K on binding of MAb 24c5 to  M. tuberculosis Erdman day-20 7H9 medium.	bind
13489	1	5061	7	NULL	NULL	0	NULL	MAb 24c5	NULL		bind	NULL				M. tuberculosis Erdman day-20 7H9 medium	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2566_s_147	11953397	(D) Effects of proteinase K on binding of MAb 24c5 to  M. tuberculosis Erdman day-20 7H9 medium.	bind
13535	1	5062	6	NULL	NULL	NULL	NULL	GAL4-FAST2	GP		bind					n2 oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_1_35_s_74	10678167	(D) EMSA analysis of the binding of a GAL4-FAST2 fusion protein to the oligonucleotide  n2.	bind
44670	2	5062	6	NULL	NULL	NULL	NULL	GAL4-FAST2	GP		is a type of					fusion protein					NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_1_35_s_74	10678167	(D) EMSA analysis of the binding of a GAL4-FAST2 fusion protein to the oligonucleotide  n2.	bind
13490	1	5062	7	NULL	NULL	0	NULL	GAL4-FAST2	NULL		binds	NULL				oligonucleotide n2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_5_1_35_s_74	10678167	(D) EMSA analysis of the binding of a GAL4-FAST2 fusion protein to the oligonucleotide  n2.	bind
44671	2	5062	7	10	NULL	0	NULL	GAL4-FAST2	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_5_1_35_s_74	10678167	(D) EMSA analysis of the binding of a GAL4-FAST2 fusion protein to the oligonucleotide  n2.	bind
13536	1	5063	6	NULL	NULL	NULL	NULL	Sp1	GP		bind					DNA	NucleicAcid				NULL	kidney nuclear extracts	NULL	NULL	NULL	NULL	gw70_devbiol_267_2_505_s_227	15013809	(D) EMSA analysis with kidney (K) and liver (L) nuclear extracts shows  equivalent Sp1 and Sp3 DNA binding activity.	bind
13537	2	5063	6	NULL	NULL	NULL	NULL	Sp1	GP		bind					DNA	NucleicAcid				NULL	liver nuclear extracts	NULL	NULL	NULL	NULL	gw70_devbiol_267_2_505_s_227	15013809	(D) EMSA analysis with kidney (K) and liver (L) nuclear extracts shows  equivalent Sp1 and Sp3 DNA binding activity.	bind
13538	3	5063	6	NULL	NULL	NULL	NULL	Sp3	GP		bind					DNA	NucleicAcid				NULL	kidney nuclear extracts	NULL	NULL	NULL	NULL	gw70_devbiol_267_2_505_s_227	15013809	(D) EMSA analysis with kidney (K) and liver (L) nuclear extracts shows  equivalent Sp1 and Sp3 DNA binding activity.	bind
13539	4	5063	6	NULL	NULL	NULL	NULL	sp3	GP		bind					DNA	NucleicAcid				NULL	liver nuclear extracts	NULL	NULL	NULL	NULL	gw70_devbiol_267_2_505_s_227	15013809	(D) EMSA analysis with kidney (K) and liver (L) nuclear extracts shows  equivalent Sp1 and Sp3 DNA binding activity.	bind
17715	5	5063	6	NULL	NULL	0	NULL	K	NULL		is	NULL				Kidney	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_267_2_505_s_227	15013809	(D) EMSA analysis with kidney (K) and liver (L) nuclear extracts shows  equivalent Sp1 and Sp3 DNA binding activity.	bind
17716	6	5063	6	NULL	NULL	0	NULL	L	NULL		is	NULL				liver	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_267_2_505_s_227	15013809	(D) EMSA analysis with kidney (K) and liver (L) nuclear extracts shows  equivalent Sp1 and Sp3 DNA binding activity.	bind
13614	1	5063	7	10	NULL	0	NULL	Sp1 	NULL		bind	NULL				DNA	NULL				NULL	Kidney nuclear extract	NULL	NULL	NULL	NULL	gw70_devbiol_267_2_505_s_227	15013809	(D) EMSA analysis with kidney (K) and liver (L) nuclear extracts shows  equivalent Sp1 and Sp3 DNA binding activity.	bind
13615	2	5063	7	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				DNA	NULL				NULL	Liver nuclear extract	0	NULL	NULL	NULL	gw70_devbiol_267_2_505_s_227	15013809	(D) EMSA analysis with kidney (K) and liver (L) nuclear extracts shows  equivalent Sp1 and Sp3 DNA binding activity.	bind
13616	3	5063	7	10	NULL	0	NULL	 Sp3	NULL		bind	NULL				DNA	NULL				NULL	Kidney nuclear extract	NULL	NULL	NULL	NULL	gw70_devbiol_267_2_505_s_227	15013809	(D) EMSA analysis with kidney (K) and liver (L) nuclear extracts shows  equivalent Sp1 and Sp3 DNA binding activity.	bind
13617	4	5063	7	NULL	NULL	0	NULL	Sp3	NULL		bind	NULL				DNA	NULL				NULL	Liver nuclear extract	0	NULL	NULL	NULL	gw70_devbiol_267_2_505_s_227	15013809	(D) EMSA analysis with kidney (K) and liver (L) nuclear extracts shows  equivalent Sp1 and Sp3 DNA binding activity.	bind
13618	5	5063	7	NULL	NULL	0	NULL	Kidney	NULL		is	NULL				K	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_267_2_505_s_227	15013809	(D) EMSA analysis with kidney (K) and liver (L) nuclear extracts shows  equivalent Sp1 and Sp3 DNA binding activity.	bind
13619	6	5063	7	NULL	NULL	0	NULL	Liver	NULL		is	NULL				L	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_267_2_505_s_227	15013809	(D) EMSA analysis with kidney (K) and liver (L) nuclear extracts shows  equivalent Sp1 and Sp3 DNA binding activity.	bind
13540	1	5064	6	NULL	NULL	NULL	NULL	Runx2	GP	endogenous	bind					beta-casein	GP			Runx2-binding site of promoter	NULL	HC11 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3182_s_108	15798204	(D) EMSA demonstrating  that endogenous Runx2 from HC11 cells binds to the Runx2-binding site in the beta-casein  promoter.	bind
13620	1	5064	7	10	NULL	0	NULL	Runx2	NULL	endogenous	binds	NULL				beta-casein	NULL			Runx2-binding site in the promoter of 	NULL	 HC11 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3182_s_108	15798204	(D) EMSA demonstrating  that endogenous Runx2 from HC11 cells binds to the Runx2-binding site in the beta-casein  promoter.	bind
13541	1	5066	6	NULL	NULL	NULL	NULL	GST-HoxB5	GP	recombinant	bind		specifically			HBE					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_16_5680_s_184	12897140	(D) EMSA with recombinant GST-HoxB5 (or GST alone) indicating specific  binding to the HBE that is competed away by excess specific (+) competitor but not  by a mutant sequence (NS).	bind
13622	1	5066	7	NULL	NULL	0	NULL	GST-HoxB5	NULL	recombinant	binds	NULL	specifically			HBE	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_16_5680_s_184	12897140	(D) EMSA with recombinant GST-HoxB5 (or GST alone) indicating specific  binding to the HBE that is competed away by excess specific (+) competitor but not  by a mutant sequence (NS).	bind
13542	1	5068	6	NULL	NULL	NULL	NULL	calsyntenin-1	GP		bind					KLC1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_8_3651_s_120	16760430	(D) Estimation of the  apparent binding affinity of calsyntenin-1 to KLC1.	bind
13625	1	5068	7	NULL	NULL	0	NULL	calsyntenin-1	NULL		bind	NULL				KLC1	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_8_3651_s_120	16760430	(D) Estimation of the  apparent binding affinity of calsyntenin-1 to KLC1.	bind
13543	1	5070	6	NULL	NULL	NULL	NULL	FH	GP		bind					Fba	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_12_7119_s_166	14638802	(D) FH  binding to immobilized Fba.	bind
13630	1	5070	7	NULL	NULL	0	NULL	FH	NULL		binds	NULL				Fba	NULL	immobilized			NULL		0	NULL	NULL	NULL	gw70_infectimmun_71_12_7119_s_166	14638802	(D) FH  binding to immobilized Fba.	bind
13586	1	5071	6	NULL	NULL	NULL	NULL	NrbI protein	GP		induces					Filopodia	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2349_s_137	15743906	(D) Filopodia induced by NrbI and Spino proteins unable to bind PP1 because  of the F-to-A substitutions within the PP1-binding motif were compared with control  GFP-expressing cells as described above.	bind
13587	2	5071	6	NULL	NULL	NULL	NULL	spino proteins	GP		induce					Filopodia	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2349_s_137	15743906	(D) Filopodia induced by NrbI and Spino proteins unable to bind PP1 because  of the F-to-A substitutions within the PP1-binding motif were compared with control  GFP-expressing cells as described above.	bind
13588	3	5071	6	NULL	NULL	NULL	NULL	statement 6	Process		does not bind					PP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2349_s_137	15743906	(D) Filopodia induced by NrbI and Spino proteins unable to bind PP1 because  of the F-to-A substitutions within the PP1-binding motif were compared with control  GFP-expressing cells as described above.	bind
13773	4	5071	6	NULL	NULL	NULL	NULL	statement 1	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2349_s_137	15743906	(D) Filopodia induced by NrbI and Spino proteins unable to bind PP1 because  of the F-to-A substitutions within the PP1-binding motif were compared with control  GFP-expressing cells as described above.	bind
13774	5	5071	6	NULL	NULL	NULL	NULL	statement 2	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2349_s_137	15743906	(D) Filopodia induced by NrbI and Spino proteins unable to bind PP1 because  of the F-to-A substitutions within the PP1-binding motif were compared with control  GFP-expressing cells as described above.	bind
53050	6	5071	6	NULL	NULL	NULL	NULL	Filopodia	OrganismPart		is substituted to			F within PP1-binding motif		Filopodia	OrganismPart		A within PP1-binding motif		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2349_s_137	15743906	(D) Filopodia induced by NrbI and Spino proteins unable to bind PP1 because  of the F-to-A substitutions within the PP1-binding motif were compared with control  GFP-expressing cells as described above.	bind
13637	1	5071	7	NULL	NULL	0	NULL	NrbI protein	NULL		induce	NULL				Filopodia	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2349_s_137	15743906	(D) Filopodia induced by NrbI and Spino proteins unable to bind PP1 because  of the F-to-A substitutions within the PP1-binding motif were compared with control  GFP-expressing cells as described above.	bind
13639	2	5071	7	NULL	NULL	0	NULL	Spino protein	NULL		induce	NULL				Filopodia	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2349_s_137	15743906	(D) Filopodia induced by NrbI and Spino proteins unable to bind PP1 because  of the F-to-A substitutions within the PP1-binding motif were compared with control  GFP-expressing cells as described above.	bind
13653	3	5071	7	10	NULL	0	NULL	statement 6	NULL		does not bind	NULL				PP1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2349_s_137	15743906	(D) Filopodia induced by NrbI and Spino proteins unable to bind PP1 because  of the F-to-A substitutions within the PP1-binding motif were compared with control  GFP-expressing cells as described above.	bind
13654	4	5071	7	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_5_2349_s_137	15743906	(D) Filopodia induced by NrbI and Spino proteins unable to bind PP1 because  of the F-to-A substitutions within the PP1-binding motif were compared with control  GFP-expressing cells as described above.	bind
13789	5	5071	7	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_5_2349_s_137	15743906	(D) Filopodia induced by NrbI and Spino proteins unable to bind PP1 because  of the F-to-A substitutions within the PP1-binding motif were compared with control  GFP-expressing cells as described above.	bind
53051	6	5071	7	10	NULL	0	NULL	Filopodia	NULL		is substituted to	NULL		F within PP1-binding motif		Filopodia	NULL		A within PP1-binding motif		NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_5_2349_s_137	15743906	(D) Filopodia induced by NrbI and Spino proteins unable to bind PP1 because  of the F-to-A substitutions within the PP1-binding motif were compared with control  GFP-expressing cells as described above.	bind
13544	1	5072	6	NULL	NULL	NULL	NULL	O2	Chemical		bind					hemes	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_68_3_453_s_89	15353565	(D) FixL acts  as a homodimer that is inactive when O2 is bound to the hemes.	bind
13545	2	5072	6	NULL	NULL	NULL	NULL	FixL	GP		acts as a					homodimer	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_68_3_453_s_89	15353565	(D) FixL acts  as a homodimer that is inactive when O2 is bound to the hemes.	bind
13546	3	5072	6	NULL	NULL	NULL	NULL	statement 1	Process		inactivates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_68_3_453_s_89	15353565	(D) FixL acts  as a homodimer that is inactive when O2 is bound to the hemes.	bind
13655	1	5072	7	NULL	NULL	0	NULL	O2	NULL		binds	NULL				heme	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_68_3_453_s_89	15353565	(D) FixL acts  as a homodimer that is inactive when O2 is bound to the hemes.	bind
13656	2	5072	7	NULL	NULL	0	NULL	FixL	NULL		acts as a 	NULL				homodimer	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_68_3_453_s_89	15353565	(D) FixL acts  as a homodimer that is inactive when O2 is bound to the hemes.	bind
13657	3	5072	7	NULL	NULL	0	NULL	statement 1	NULL		inactivates	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_68_3_453_s_89	15353565	(D) FixL acts  as a homodimer that is inactive when O2 is bound to the hemes.	bind
13547	1	5074	6	NULL	NULL	NULL	NULL	FXR	GP		bind					GRIP1	GP		NID region		NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_4_1093_s_58	12718893	(D) FXR binding to different NID regions of GRIP1 in the presence of CDCA.	bind
13548	2	5074	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs in presence of					CDCA	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_4_1093_s_58	12718893	(D) FXR binding to different NID regions of GRIP1 in the presence of CDCA.	bind
13660	1	5074	7	10	NULL	0	NULL	FXR	NULL		bind	NULL				GRIP1	NULL		NID region		NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_4_1093_s_58	12718893	(D) FXR binding to different NID regions of GRIP1 in the presence of CDCA.	bind
13661	2	5074	7	NULL	NULL	0	NULL	statement 1	NULL		occurs in the presence of	NULL				CDCA	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_11_4_1093_s_58	12718893	(D) FXR binding to different NID regions of GRIP1 in the presence of CDCA.	bind
13589	1	5075	6	NULL	NULL	NULL	NULL	L1	GP		bind					NP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6348_s_129	12456642	(d) G121S, a mutation that destroys homophilic binding, does not affect L1 binding to NP-1 or alter the ability of the chimera to induce the switch.	bind
13590	2	5075	6	NULL	NULL	0	NULL		NULL	mutant	destroys	NULL		G121S		homophilic binding	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6348_s_129	12456642	(d) G121S, a mutation that destroys homophilic binding, does not affect L1 binding to NP-1 or alter the ability of the chimera to induce the switch.	bind
13591	3	5075	6	NULL	NULL	0	NULL		NULL	mutant	does not affect	NULL		G121S		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_21_23_6348_s_129	12456642	(d) G121S, a mutation that destroys homophilic binding, does not affect L1 binding to NP-1 or alter the ability of the chimera to induce the switch.	bind
13592	4	5075	6	NULL	NULL	0	NULL	chimera	NULL		induce	NULL				switch	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_21_23_6348_s_129	12456642	(d) G121S, a mutation that destroys homophilic binding, does not affect L1 binding to NP-1 or alter the ability of the chimera to induce the switch.	bind
13593	5	5075	6	NULL	NULL	0	NULL		NULL	mutant	does not alter	NULL		G121S		statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_21_23_6348_s_129	12456642	(d) G121S, a mutation that destroys homophilic binding, does not affect L1 binding to NP-1 or alter the ability of the chimera to induce the switch.	bind
13662	1	5075	7	10	NULL	0	NULL		NULL	mutant	destroys	NULL		G121S		homophilic binding	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6348_s_129	12456642	(d) G121S, a mutation that destroys homophilic binding, does not affect L1 binding to NP-1 or alter the ability of the chimera to induce the switch.	bind
13663	2	5075	7	NULL	NULL	0	NULL	L1	NULL		bind	NULL				NP-1	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_21_23_6348_s_129	12456642	(d) G121S, a mutation that destroys homophilic binding, does not affect L1 binding to NP-1 or alter the ability of the chimera to induce the switch.	bind
13664	3	5075	7	10	NULL	0	NULL		NULL	mutant	does not affect	NULL		G121S		statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6348_s_129	12456642	(d) G121S, a mutation that destroys homophilic binding, does not affect L1 binding to NP-1 or alter the ability of the chimera to induce the switch.	bind
13665	4	5075	7	NULL	NULL	0	NULL	chimera	NULL		induce	NULL				switch	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_21_23_6348_s_129	12456642	(d) G121S, a mutation that destroys homophilic binding, does not affect L1 binding to NP-1 or alter the ability of the chimera to induce the switch.	bind
13666	5	5075	7	10	NULL	0	NULL		NULL	mutant	does not alter	NULL		G121S		statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6348_s_129	12456642	(d) G121S, a mutation that destroys homophilic binding, does not affect L1 binding to NP-1 or alter the ability of the chimera to induce the switch.	bind
13549	1	5076	6	NULL	NULL	NULL	NULL	GST-Prox1	GP	purified	bind					FGFR-3	GP	putative		Prox1 binding sequences of the promoter	NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_2_576_s_140	16291864	(D) Gel electrophoresis mobility shift assays  showed that the purified GST-Prox1 fusion protein (GST-ProxBD) but not the GST protein  alone binds to the putative Prox1 binding sequences found in the FGFR-3 promoter.	bind
13550	3	5076	6	NULL	NULL	NULL	NULL	GST-ProxBD	GP		is					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_2_576_s_140	16291864	(D) Gel electrophoresis mobility shift assays  showed that the purified GST-Prox1 fusion protein (GST-ProxBD) but not the GST protein  alone binds to the putative Prox1 binding sequences found in the FGFR-3 promoter.	bind
13595	4	5076	6	NULL	NULL	NULL	NULL	GST			does not bind		alone			FGFR-3	GP	putative		Prox1 binding sequences of the promoter	NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_2_576_s_140	16291864	(D) Gel electrophoresis mobility shift assays  showed that the purified GST-Prox1 fusion protein (GST-ProxBD) but not the GST protein  alone binds to the putative Prox1 binding sequences found in the FGFR-3 promoter.	bind
44672	2	5076	6	NULL	NULL	NULL	NULL	GST-Prox1	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_2_576_s_140	16291864	(D) Gel electrophoresis mobility shift assays  showed that the purified GST-Prox1 fusion protein (GST-ProxBD) but not the GST protein  alone binds to the putative Prox1 binding sequences found in the FGFR-3 promoter.	bind
13667	1	5076	7	10	NULL	0	NULL	GST-ProxBD	NULL	purified	bind	NULL				FGFR-3	NULL	putative		Prox1 binding sequences in the promoter of	NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_2_576_s_140	16291864	(D) Gel electrophoresis mobility shift assays  showed that the purified GST-Prox1 fusion protein (GST-ProxBD) but not the GST protein  alone binds to the putative Prox1 binding sequences found in the FGFR-3 promoter.	bind
13668	2	5076	7	10	NULL	0	NULL	GST	NULL		does not bind	NULL				FGFR-3	NULL	putative		Prox1 binding sequences in the promoter of	NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_2_576_s_140	16291864	(D) Gel electrophoresis mobility shift assays  showed that the purified GST-Prox1 fusion protein (GST-ProxBD) but not the GST protein  alone binds to the putative Prox1 binding sequences found in the FGFR-3 promoter.	bind
17774	4	5076	7	10	NULL	0	NULL	statement 3	NULL		is	NULL				GST-ProxBD	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_2_576_s_140	16291864	(D) Gel electrophoresis mobility shift assays  showed that the purified GST-Prox1 fusion protein (GST-ProxBD) but not the GST protein  alone binds to the putative Prox1 binding sequences found in the FGFR-3 promoter.	bind
44673	3	5076	7	10	NULL	0	NULL	GST-Prox1	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_2_576_s_140	16291864	(D) Gel electrophoresis mobility shift assays  showed that the purified GST-Prox1 fusion protein (GST-ProxBD) but not the GST protein  alone binds to the putative Prox1 binding sequences found in the FGFR-3 promoter.	bind
13551	1	5077	6	NULL	NULL	NULL	NULL	TR-RXR heterodimer	GP		bind									TRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2718_s_119	10733574	(D) Gel mobility shift assay of GST-DRIP205 binding to a TR-RXR heterodimer bound to a TRE in the presence of 10 6 M T3 (+) or ethanol ( ), as described in for panel C.	bind
13552	2	5077	6	NULL	NULL	NULL	NULL	GST-DRIP205	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2718_s_119	10733574	(D) Gel mobility shift assay of GST-DRIP205 binding to a TR-RXR heterodimer bound to a TRE in the presence of 10 6 M T3 (+) or ethanol ( ), as described in for panel C.	bind
13553	3	5077	6	NULL	NULL	NULL	NULL	statement 2	Process		occurs in presence of					T3	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2718_s_119	10733574	(D) Gel mobility shift assay of GST-DRIP205 binding to a TR-RXR heterodimer bound to a TRE in the presence of 10 6 M T3 (+) or ethanol ( ), as described in for panel C.	bind
13554	4	5077	6	NULL	NULL	NULL	NULL	statement 2	Process		occurs in presence of					ethanol	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2718_s_119	10733574	(D) Gel mobility shift assay of GST-DRIP205 binding to a TR-RXR heterodimer bound to a TRE in the presence of 10 6 M T3 (+) or ethanol ( ), as described in for panel C.	bind
13555	5	5077	6	NULL	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2718_s_119	10733574	(D) Gel mobility shift assay of GST-DRIP205 binding to a TR-RXR heterodimer bound to a TRE in the presence of 10 6 M T3 (+) or ethanol ( ), as described in for panel C.	bind
13669	1	5077	7	NULL	NULL	0	NULL	TR-RXR heterodimer	NULL		bind	NULL					NULL			TRE 	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2718_s_119	10733574	(D) Gel mobility shift assay of GST-DRIP205 binding to a TR-RXR heterodimer bound to a TRE in the presence of 10 6 M T3 (+) or ethanol ( ), as described in for panel C.	bind
13670	2	5077	7	NULL	NULL	0	NULL	GST-DRIP205	NULL		bind	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2718_s_119	10733574	(D) Gel mobility shift assay of GST-DRIP205 binding to a TR-RXR heterodimer bound to a TRE in the presence of 10 6 M T3 (+) or ethanol ( ), as described in for panel C.	bind
17776	5	5077	7	NULL	NULL	0	NULL	statement 3	NULL		is an alternative to	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2718_s_119	10733574	(D) Gel mobility shift assay of GST-DRIP205 binding to a TR-RXR heterodimer bound to a TRE in the presence of 10 6 M T3 (+) or ethanol ( ), as described in for panel C.	bind
19969	3	5077	7	NULL	NULL	0	NULL	statement 2	NULL		occurs in the presence of	NULL				T3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2718_s_119	10733574	(D) Gel mobility shift assay of GST-DRIP205 binding to a TR-RXR heterodimer bound to a TRE in the presence of 10 6 M T3 (+) or ethanol ( ), as described in for panel C.	bind
19970	4	5077	7	NULL	NULL	0	NULL	statement 2	NULL		occurs in the presence of	NULL				ethanol	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2718_s_119	10733574	(D) Gel mobility shift assay of GST-DRIP205 binding to a TR-RXR heterodimer bound to a TRE in the presence of 10 6 M T3 (+) or ethanol ( ), as described in for panel C.	bind
13556	1	5079	6	NULL	NULL	NULL	NULL	GST-Akt	GP		bind					Grb10	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_4_979_s_180	11809791	(D) GST-Akt binds to Grb10 and Grb10deltaPH.	bind
13557	2	5079	6	NULL	NULL	NULL	NULL	GST-Akt	GP		bind					Grb10	GP		deltaPH		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_4_979_s_180	11809791	(D) GST-Akt binds to Grb10 and Grb10deltaPH.	bind
13672	1	5079	7	NULL	NULL	0	NULL	GST-Akt	NULL		binds	NULL				Grb10	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_4_979_s_180	11809791	(D) GST-Akt binds to Grb10 and Grb10deltaPH.	bind
13673	2	5079	7	NULL	NULL	0	NULL	GST-Akt	NULL		binds	NULL				Grb10	NULL		deltaPH		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_4_979_s_180	11809791	(D) GST-Akt binds to Grb10 and Grb10deltaPH.	bind
13598	1	5080	6	NULL	NULL	NULL	NULL	GST-p40PX	GP		bind		specifically			PI(3)P	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_1_35_s_197	12535519	(D) GST-p40PX and GST-FYVE3 bind specifically to PI(3)P. Hybond-C membranes spotted with the indicated lipids (pmoles) were incubated with GST-p40PX (10  g/ml) or GST-FYVE3 (10  g/ml) and extensively washed, and bound protein was detected by immunoblotting with an HRP-conjugated anti-GST antibody.	bind
13599	2	5080	6	NULL	NULL	NULL	NULL	GST-FYVE3	GP		bind		specifically			PI(3)P	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_1_35_s_197	12535519	(D) GST-p40PX and GST-FYVE3 bind specifically to PI(3)P. Hybond-C membranes spotted with the indicated lipids (pmoles) were incubated with GST-p40PX (10  g/ml) or GST-FYVE3 (10  g/ml) and extensively washed, and bound protein was detected by immunoblotting with an HRP-conjugated anti-GST antibody.	bind
13674	1	5080	7	NULL	NULL	0	NULL	GST-p40PX	NULL		bind	NULL	specifically			PI(3)P	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_35_s_197	12535519	(D) GST-p40PX and GST-FYVE3 bind specifically to PI(3)P. Hybond-C membranes spotted with the indicated lipids (pmoles) were incubated with GST-p40PX (10  g/ml) or GST-FYVE3 (10  g/ml) and extensively washed, and bound protein was detected by immunoblotting with an HRP-conjugated anti-GST antibody.	bind
13675	2	5080	7	NULL	NULL	0	NULL	GST-FYVE3	NULL		bind	NULL	specifically			PI(3)P	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_35_s_197	12535519	(D) GST-p40PX and GST-FYVE3 bind specifically to PI(3)P. Hybond-C membranes spotted with the indicated lipids (pmoles) were incubated with GST-p40PX (10  g/ml) or GST-FYVE3 (10  g/ml) and extensively washed, and bound protein was detected by immunoblotting with an HRP-conjugated anti-GST antibody.	bind
13558	1	5081	6	NULL	NULL	NULL	NULL	HNF-6	GP		bind					g6pc	GP	endogenous		promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_6037_s_90	16880515	(D) HNF-6 binds endogenous  g6pc promoter.	bind
13676	1	5081	7	NULL	NULL	0	NULL	HNF-6	NULL		binds	NULL				g6pc	NULL	endogenous		promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_16_6037_s_90	16880515	(D) HNF-6 binds endogenous  g6pc promoter.	bind
13559	1	5082	6	NULL	NULL	NULL	NULL	HP1	GP		bind					H3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_729_s_210	11336697	(D) HP1  and Pc1/M33 bind to H3 in a CD integrity-dependent manner.	bind
13560	2	5082	6	NULL	NULL	NULL	NULL	Pc1/M33	GP		bind					H3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_729_s_210	11336697	(D) HP1  and Pc1/M33 bind to H3 in a CD integrity-dependent manner.	bind
13561	3	5082	6	NULL	NULL	NULL	NULL	statement 1	Process		is dependent on					CD 		integrity of 			NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_729_s_210	11336697	(D) HP1  and Pc1/M33 bind to H3 in a CD integrity-dependent manner.	bind
13562	4	5082	6	NULL	NULL	NULL	NULL	statement 2	Process		is dependent on					CD		integrity of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_729_s_210	11336697	(D) HP1  and Pc1/M33 bind to H3 in a CD integrity-dependent manner.	bind
13677	1	5082	7	NULL	NULL	0	NULL	HP1	NULL		bind	NULL				H3	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_7_4_729_s_210	11336697	(D) HP1  and Pc1/M33 bind to H3 in a CD integrity-dependent manner.	bind
13678	2	5082	7	NULL	NULL	0	NULL	Pc1/M33	NULL		bind	NULL				H3	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_7_4_729_s_210	11336697	(D) HP1  and Pc1/M33 bind to H3 in a CD integrity-dependent manner.	bind
13679	3	5082	7	NULL	NULL	0	NULL	statement 1	NULL		depends on	NULL				 CD  	NULL	integrity of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_729_s_210	11336697	(D) HP1  and Pc1/M33 bind to H3 in a CD integrity-dependent manner.	bind
13680	4	5082	7	NULL	NULL	0	NULL	statement 2	NULL		depends on	NULL				CD 	NULL	integrity of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_729_s_210	11336697	(D) HP1  and Pc1/M33 bind to H3 in a CD integrity-dependent manner.	bind
13563	1	5083	6	NULL	NULL	NULL	NULL	hTid-1	GP		bind		high affinity			IkappaB proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_44_s_131	15601829	(D) hTid-1 binds to IkappaB proteins with high affinity.	bind
13681	1	5083	7	NULL	NULL	0	NULL	hTid-1	NULL		binds	NULL	high affinity			IkappaB proteins	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_1_44_s_131	15601829	(D) hTid-1 binds to IkappaB proteins with high affinity.	bind
13597	1	5085	6	NULL	NULL	NULL	NULL	p53	GP	mutant	does not bind			S46A		p53AIP1	GP			p53BDS	NULL		NULL	NULL	NULL	NULL	gw60_cell_102_6_849_s_276	11030628	(D) Impaired binding activity of the  mutant p53 (S46A) protein to p53BDS of p53AIP1 but not p21Waf1.	bind
13772	2	5085	6	NULL	NULL	NULL	NULL	p53	GP	mutant	bind			S46A		p21Waf1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_102_6_849_s_276	11030628	(D) Impaired binding activity of the  mutant p53 (S46A) protein to p53BDS of p53AIP1 but not p21Waf1.	bind
13682	1	5085	7	NULL	NULL	0	NULL	p53	NULL	mutant	does not bind	NULL		S46A		p53AIP1	NULL			p53BDS	NULL		NULL	NULL	NULL	NULL	gw60_cell_102_6_849_s_276	11030628	(D) Impaired binding activity of the  mutant p53 (S46A) protein to p53BDS of p53AIP1 but not p21Waf1.	bind
13683	2	5085	7	NULL	NULL	0	NULL	p53	NULL	mutant	bind	NULL		S46A		p21Waf1	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_102_6_849_s_276	11030628	(D) Impaired binding activity of the  mutant p53 (S46A) protein to p53BDS of p53AIP1 but not p21Waf1.	bind
13564	1	5086	6	NULL	NULL	NULL	NULL	NFATc3	GP	full length	enhances					myogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6600_s_218	10938134	(D) In contrast, cotransfection of a expression vector encoding full-length NFATc3 produced a noticeable enhancement of myogenesis (extent of differentiation).	bind
13684	1	5086	7	NULL	NULL	0	NULL	NFATc3	NULL	full-length	enhance	NULL				myogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6600_s_218	10938134	(D) In contrast, cotransfection of a expression vector encoding full-length NFATc3 produced a noticeable enhancement of myogenesis (extent of differentiation).	bind
13565	1	5087	6	NULL	NULL	NULL	NULL	PNT-P2	GP		bind					MAE	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_130_5_845_s_342	12538513	(D) In the absence of signaling, PNT-P2 can bind to MAE and is prevented from activating transcription, either as a consequence of its interaction with MAE or because it is out competed by YAN, or both.	bind
13600	2	5087	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs in absence of					signaling	Process				NULL		NULL	NULL	NULL	NULL	gw60_development_130_5_845_s_342	12538513	(D) In the absence of signaling, PNT-P2 can bind to MAE and is prevented from activating transcription, either as a consequence of its interaction with MAE or because it is out competed by YAN, or both.	bind
13601	3	5087	6	NULL	NULL	NULL	NULL	PNT-P2	GP		activates					transcription	Process				NULL		NULL	NULL	NULL	NULL	gw60_development_130_5_845_s_342	12538513	(D) In the absence of signaling, PNT-P2 can bind to MAE and is prevented from activating transcription, either as a consequence of its interaction with MAE or because it is out competed by YAN, or both.	bind
13602	4	5087	6	NULL	NULL	NULL	NULL	statement 1	Process		prevents					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_development_130_5_845_s_342	12538513	(D) In the absence of signaling, PNT-P2 can bind to MAE and is prevented from activating transcription, either as a consequence of its interaction with MAE or because it is out competed by YAN, or both.	bind
13603	5	5087	6	NULL	NULL	NULL	NULL	PNT-P2	GP		bind					Yan	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_130_5_845_s_342	12538513	(D) In the absence of signaling, PNT-P2 can bind to MAE and is prevented from activating transcription, either as a consequence of its interaction with MAE or because it is out competed by YAN, or both.	bind
13604	6	5087	6	NULL	NULL	NULL	NULL	statement 5	Process		prevents					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_development_130_5_845_s_342	12538513	(D) In the absence of signaling, PNT-P2 can bind to MAE and is prevented from activating transcription, either as a consequence of its interaction with MAE or because it is out competed by YAN, or both.	bind
13605	7	5087	6	NULL	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_development_130_5_845_s_342	12538513	(D) In the absence of signaling, PNT-P2 can bind to MAE and is prevented from activating transcription, either as a consequence of its interaction with MAE or because it is out competed by YAN, or both.	bind
17717	8	5087	6	NULL	NULL	NULL	NULL	statement 5	GP		competes					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_130_5_845_s_342	12538513	(D) In the absence of signaling, PNT-P2 can bind to MAE and is prevented from activating transcription, either as a consequence of its interaction with MAE or because it is out competed by YAN, or both.	bind
13685	1	5087	7	NULL	NULL	0	NULL	PNT-P2	NULL		bind	NULL				MAE	NULL				NULL		0	NULL	NULL	NULL	gw60_development_130_5_845_s_342	12538513	(D) In the absence of signaling, PNT-P2 can bind to MAE and is prevented from activating transcription, either as a consequence of its interaction with MAE or because it is out competed by YAN, or both.	bind
13686	2	5087	7	NULL	NULL	0	NULL	statement 1	NULL		occurs in the absence of	NULL				signaling	NULL				NULL		NULL	NULL	NULL	NULL	gw60_development_130_5_845_s_342	12538513	(D) In the absence of signaling, PNT-P2 can bind to MAE and is prevented from activating transcription, either as a consequence of its interaction with MAE or because it is out competed by YAN, or both.	bind
13687	4	5087	7	NULL	NULL	0	NULL	statement 1	NULL		prevents	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_development_130_5_845_s_342	12538513	(D) In the absence of signaling, PNT-P2 can bind to MAE and is prevented from activating transcription, either as a consequence of its interaction with MAE or because it is out competed by YAN, or both.	bind
13688	5	5087	7	NULL	NULL	0	NULL	PNT-P2	NULL		bind	NULL				YAN	NULL				NULL		NULL	NULL	NULL	NULL	gw60_development_130_5_845_s_342	12538513	(D) In the absence of signaling, PNT-P2 can bind to MAE and is prevented from activating transcription, either as a consequence of its interaction with MAE or because it is out competed by YAN, or both.	bind
13689	6	5087	7	NULL	NULL	0	NULL	statement 4	NULL		occurs	NULL				statement 1	NULL	because of			NULL		NULL	NULL	NULL	NULL	gw60_development_130_5_845_s_342	12538513	(D) In the absence of signaling, PNT-P2 can bind to MAE and is prevented from activating transcription, either as a consequence of its interaction with MAE or because it is out competed by YAN, or both.	bind
13690	7	5087	7	NULL	NULL	0	NULL	statement 4	NULL		occurs 	NULL				statement 5	NULL	because of			NULL		NULL	NULL	NULL	NULL	gw60_development_130_5_845_s_342	12538513	(D) In the absence of signaling, PNT-P2 can bind to MAE and is prevented from activating transcription, either as a consequence of its interaction with MAE or because it is out competed by YAN, or both.	bind
13691	8	5087	7	NULL	NULL	0	NULL	statement 6	NULL		is an alternative to	NULL				statement 7	NULL				NULL		NULL	NULL	NULL	NULL	gw60_development_130_5_845_s_342	12538513	(D) In the absence of signaling, PNT-P2 can bind to MAE and is prevented from activating transcription, either as a consequence of its interaction with MAE or because it is out competed by YAN, or both.	bind
17777	3	5087	7	NULL	NULL	0	NULL	PNT-P2 	NULL		activates	NULL				transcription 	NULL				NULL		0	NULL	NULL	NULL	gw60_development_130_5_845_s_342	12538513	(D) In the absence of signaling, PNT-P2 can bind to MAE and is prevented from activating transcription, either as a consequence of its interaction with MAE or because it is out competed by YAN, or both.	bind
17781	9	5087	7	NULL	NULL	0	NULL	statement 1	NULL		compete with	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_development_130_5_845_s_342	12538513	(D) In the absence of signaling, PNT-P2 can bind to MAE and is prevented from activating transcription, either as a consequence of its interaction with MAE or because it is out competed by YAN, or both.	bind
13566	1	5088	6	NULL	NULL	NULL	NULL	RNA polymerase	GP		bind		selectively			P3	GP			promoter	NULL	wild-type aroP fragment	NULL	NULL	NULL	NULL	gw60_jbacteriol_180_20_5466_s_91	9765583	(d) In the presence of TyrR and tyrosine, RNA polymerase binds selectively to the P3 promoter on a wild-type  aroP fragment (P1+ P3+) (same pattern as for panel b).	bind
13567	2	5088	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs in presence of					TyrR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_20_5466_s_91	9765583	(d) In the presence of TyrR and tyrosine, RNA polymerase binds selectively to the P3 promoter on a wild-type  aroP fragment (P1+ P3+) (same pattern as for panel b).	bind
13568	3	5088	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs in presence of					tyrosine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_20_5466_s_91	9765583	(d) In the presence of TyrR and tyrosine, RNA polymerase binds selectively to the P3 promoter on a wild-type  aroP fragment (P1+ P3+) (same pattern as for panel b).	bind
13692	1	5088	7	NULL	NULL	0	NULL	RNA polymerase	NULL		binds	NULL	selectively			P3	NULL			promoter	NULL	wild-type aroP fragment 	0	NULL	NULL	NULL	gw60_jbacteriol_180_20_5466_s_91	9765583	(d) In the presence of TyrR and tyrosine, RNA polymerase binds selectively to the P3 promoter on a wild-type  aroP fragment (P1+ P3+) (same pattern as for panel b).	bind
13693	2	5088	7	NULL	NULL	0	NULL	statement 1	NULL		occurs in the presence of	NULL				TyrR	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_20_5466_s_91	9765583	(d) In the presence of TyrR and tyrosine, RNA polymerase binds selectively to the P3 promoter on a wild-type  aroP fragment (P1+ P3+) (same pattern as for panel b).	bind
13694	3	5088	7	NULL	NULL	0	NULL	statement 1	NULL		occurs in the presence of	NULL				tyrosine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_20_5466_s_91	9765583	(d) In the presence of TyrR and tyrosine, RNA polymerase binds selectively to the P3 promoter on a wild-type  aroP fragment (P1+ P3+) (same pattern as for panel b).	bind
13569	1	5089	6	NULL	NULL	NULL	NULL	mto1p	GP	truncated	bind					GST-mto2p	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_6_3040_s_186	15659644	(D) In vitro binding  of mto1p truncations to GST-mto2p by pull-down assays.	bind
13695	1	5089	7	NULL	NULL	0	NULL	mto1p	NULL	truncated	binds	NULL				GST-mto2p	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw70_molbiolcell_16_6_3040_s_186	15659644	(D) In vitro binding  of mto1p truncations to GST-mto2p by pull-down assays.	bind
13570	2	5090	6	NULL	NULL	NULL	NULL	Pex19p	GP		bind					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molbiolcell_15_7_3406_s_111	15133130	(D) In vitro binding of Pex19p to Pex13p-derived synthetic peptides.	bind
44674	1	5090	6	NULL	NULL	NULL	NULL	synthetic peptides			is derived from					Pex13p	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_7_3406_s_111	15133130	(D) In vitro binding of Pex19p to Pex13p-derived synthetic peptides.	bind
13696	2	5090	7	10	NULL	0	NULL	Pex19p	NULL		bind	NULL				statement 1	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molbiolcell_15_7_3406_s_111	15133130	(D) In vitro binding of Pex19p to Pex13p-derived synthetic peptides.	bind
44675	1	5090	7	10	NULL	0	NULL	synthetic peptides	NULL		is derived from	NULL				Pex13p	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_7_3406_s_111	15133130	(D) In vitro binding of Pex19p to Pex13p-derived synthetic peptides.	bind
13571	1	5091	6	NULL	NULL	NULL	NULL	KIF13A	GP	purified;;recombinant	bind					beta1-adaptin	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cell_103_4_569_s_133	11106728	(D) In vitro binding of purified recombinant KIF13A and beta1-adaptin.	bind
13697	1	5091	7	10	NULL	0	NULL	KIF13A	NULL	purified;;recombinant	bind	NULL				beta1-adaptin	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cell_103_4_569_s_133	11106728	(D) In vitro binding of purified recombinant KIF13A and beta1-adaptin.	bind
13572	1	5092	6	NULL	NULL	NULL	NULL	v-Rel proteins	GP	mutant	bind					DNA	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_5_1520_s_212	12588973	(D) In vitro DNA-binding activity of mutant v-Rel proteins.	bind
13698	1	5092	7	NULL	NULL	0	NULL	v-Rel protein	NULL	mutant	bind	NULL				DNA	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_23_5_1520_s_212	12588973	(D) In vitro DNA-binding activity of mutant v-Rel proteins.	bind
13573	1	5093	6	NULL	NULL	NULL	NULL	cyclin D1	GP		bind					GAL-ER	CellComponent				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_cell_88_3_405_s_212	9039267	(D) In vivo binding between cyclin D1 and  GAL-ER fusion proteins.	bind
44676	2	5093	6	NULL	NULL	NULL	NULL	GAL-ER	CellComponent		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_88_3_405_s_212	9039267	(D) In vivo binding between cyclin D1 and  GAL-ER fusion proteins.	bind
13699	1	5093	7	10	NULL	0	NULL	cyclin D1	NULL		bind	NULL				GAL-ER	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_cell_88_3_405_s_212	9039267	(D) In vivo binding between cyclin D1 and  GAL-ER fusion proteins.	bind
44677	2	5093	7	10	NULL	0	NULL	GAL-ER	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_88_3_405_s_212	9039267	(D) In vivo binding between cyclin D1 and  GAL-ER fusion proteins.	bind
13574	1	5094	6	NULL	NULL	NULL	NULL	Ey	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_3_297_s_181	10198632	(D) Increased DNA-binding activity of Ey due to a single amino acid substitution.	bind
13575	2	5094	6	NULL	NULL	NULL	NULL	Ey	GP	single amino acid substitution of	increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_3_297_s_181	10198632	(D) Increased DNA-binding activity of Ey due to a single amino acid substitution.	bind
13700	1	5094	7	NULL	NULL	0	NULL	Ey 	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_3_3_297_s_181	10198632	(D) Increased DNA-binding activity of Ey due to a single amino acid substitution.	bind
13701	2	5094	7	10	NULL	0	NULL	Ey	NULL	single amino acid substitution of	increases	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_3_297_s_181	10198632	(D) Increased DNA-binding activity of Ey due to a single amino acid substitution.	bind
13576	1	5095	6	NULL	NULL	NULL	NULL	p53	GP		bind					Cyclin A1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8917_s_195	15456866	(D) Increased p53 binding to the cyclin  A1 promoter following irradiation.	bind
13577	2	5095	6	NULL	NULL	NULL	NULL	statement 1	Process		increases following					irradiation					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8917_s_195	15456866	(D) Increased p53 binding to the cyclin  A1 promoter following irradiation.	bind
13702	1	5095	7	NULL	NULL	0	NULL	p53	NULL		bind	NULL				cyclin A1	NULL			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8917_s_195	15456866	(D) Increased p53 binding to the cyclin  A1 promoter following irradiation.	bind
13703	2	5095	7	NULL	NULL	0	NULL	statement 1	NULL		is increased upon	NULL				irradiation	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_20_8917_s_195	15456866	(D) Increased p53 binding to the cyclin  A1 promoter following irradiation.	bind
13578	1	5096	6	NULL	NULL	NULL	NULL	mSin3a	GP	endogenous	bind					Elk-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_8_2802_s_281	11283259	(D) Inducible binding of endogenous mSin3A to Elk-1 following EGF induction.	bind
13579	2	5096	6	NULL	NULL	NULL	NULL	EGF	GP		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_8_2802_s_281	11283259	(D) Inducible binding of endogenous mSin3A to Elk-1 following EGF induction.	bind
13704	1	5096	7	NULL	NULL	0	NULL	mSin3A	NULL	endogenous	bind	NULL				 Elk-1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_8_2802_s_281	11283259	(D) Inducible binding of endogenous mSin3A to Elk-1 following EGF induction.	bind
13705	2	5096	7	NULL	NULL	0	NULL	EGF	NULL		induce	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_8_2802_s_281	11283259	(D) Inducible binding of endogenous mSin3A to Elk-1 following EGF induction.	bind
13580	1	5097	6	NULL	NULL	NULL	NULL	Hsp70	GP		bind					macrophages	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_3_353_s_45	12354387	(D) Inhibition of Hsp70 binding to human macrophages (M ) and peripheral blood myeloid DC.	bind
13581	2	5097	6	NULL	NULL	NULL	NULL	Hsp70	GP		bind					peripheral blood myeloid DC	Cell				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_3_353_s_45	12354387	(D) Inhibition of Hsp70 binding to human macrophages (M ) and peripheral blood myeloid DC.	bind
17718	3	5097	6	NULL	NULL	0	NULL	M	NULL		is	NULL				macrophages	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_17_3_353_s_45	12354387	(D) Inhibition of Hsp70 binding to human macrophages (M ) and peripheral blood myeloid DC.	bind
13706	1	5097	7	NULL	NULL	0	NULL	Hsp70	NULL		bind	NULL				macrophages	NULL	human			NULL		0	NULL	NULL	NULL	gw60_immunity_17_3_353_s_45	12354387	(D) Inhibition of Hsp70 binding to human macrophages (M ) and peripheral blood myeloid DC.	bind
13707	2	5097	7	NULL	NULL	0	NULL	Hsp70	NULL		bind	NULL				peripheral blood myeloid DC	NULL				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_3_353_s_45	12354387	(D) Inhibition of Hsp70 binding to human macrophages (M ) and peripheral blood myeloid DC.	bind
13708	3	5097	7	NULL	NULL	0	NULL	macrophages	NULL		is	NULL				M	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_17_3_353_s_45	12354387	(D) Inhibition of Hsp70 binding to human macrophages (M ) and peripheral blood myeloid DC.	bind
13582	1	5098	6	NULL	NULL	NULL	NULL	MyoD	GP		bind					Tncs	GP			regulatory region	NULL		NULL	NULL	NULL	NULL	gw60_molcell_9_3_587_s_199	11931766	(D) Inhibition of p38 kinase does not alter MyoD binding to the  Tncs regulatory region as assessed by ChIP analysis of SB 203580-treated samples.	bind
13583	2	5098	6	NULL	NULL	NULL	NULL	p38 kinase	GP	inhibition of	does not alter					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_9_3_587_s_199	11931766	(D) Inhibition of p38 kinase does not alter MyoD binding to the  Tncs regulatory region as assessed by ChIP analysis of SB 203580-treated samples.	bind
13709	1	5098	7	NULL	NULL	0	NULL	MyoD	NULL		bind	NULL				Tncs	NULL			regulatory region	NULL		0	NULL	NULL	NULL	gw60_molcell_9_3_587_s_199	11931766	(D) Inhibition of p38 kinase does not alter MyoD binding to the  Tncs regulatory region as assessed by ChIP analysis of SB 203580-treated samples.	bind
13710	2	5098	7	NULL	NULL	0	NULL	p38 kinase	NULL	inhibition of	does not alter	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_9_3_587_s_199	11931766	(D) Inhibition of p38 kinase does not alter MyoD binding to the  Tncs regulatory region as assessed by ChIP analysis of SB 203580-treated samples.	bind
13606	1	5099	6	NULL	NULL	NULL	NULL	Tob	GP		interacts with					Smad1	GP	deletion mutants			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_7_1085_s_192	11163184	(D) Interaction of  Tob with various Smad1 deletion mutants.	bind
13711	1	5099	7	NULL	NULL	0	NULL	Tob	NULL		interacts with	NULL				Smad1	NULL	deletion mutant			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_7_1085_s_192	11163184	(D) Interaction of  Tob with various Smad1 deletion mutants.	bind
13607	1	5100	6	NULL	NULL	NULL	NULL	L-periaxin	GP		bind			binding domain		DRP2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_neuron_30_3_677_s_45	11430802	(D) Interaction of the binding domains of L-periaxin and DRP2 in vitro.	bind
13712	1	5100	7	NULL	NULL	0	NULL	L-periaxin	NULL		bind	NULL		binding domain		DRP2	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_neuron_30_3_677_s_45	11430802	(D) Interaction of the binding domains of L-periaxin and DRP2 in vitro.	bind
13608	1	5102	6	NULL	NULL	NULL	NULL	Kap121p	GP		bind					Nup53p	GP				NULL	NPC	NULL	NULL	NULL	NULL	gw60_cellbiol_159_2_267_s_237	12403813	(D) Kap121p bound to Nup53p at the NPC could then be released by stochastic changes that allow Nup53p to bind Nup170p.	bind
13609	2	5102	6	NULL	NULL	NULL	NULL	Nup53p	GP		released by					stochastic changes	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_2_267_s_237	12403813	(D) Kap121p bound to Nup53p at the NPC could then be released by stochastic changes that allow Nup53p to bind Nup170p.	bind
13610	3	5102	6	NULL	NULL	NULL	NULL	Nup53p	GP		bind					Nup170p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_2_267_s_237	12403813	(D) Kap121p bound to Nup53p at the NPC could then be released by stochastic changes that allow Nup53p to bind Nup170p.	bind
13611	4	5102	6	NULL	NULL	NULL	NULL	statement 2	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_2_267_s_237	12403813	(D) Kap121p bound to Nup53p at the NPC could then be released by stochastic changes that allow Nup53p to bind Nup170p.	bind
13713	1	5102	7	NULL	NULL	0	NULL	Kap121p 	NULL		bind	NULL				Nup53p	NULL				NULL	at NPC	NULL	NULL	NULL	NULL	gw60_cellbiol_159_2_267_s_237	12403813	(D) Kap121p bound to Nup53p at the NPC could then be released by stochastic changes that allow Nup53p to bind Nup170p.	bind
13714	2	5102	7	NULL	NULL	0	NULL	Nup53p	NULL		bind	NULL				Nup170p	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_159_2_267_s_237	12403813	(D) Kap121p bound to Nup53p at the NPC could then be released by stochastic changes that allow Nup53p to bind Nup170p.	bind
13715	3	5102	7	NULL	NULL	0	NULL	Nup53p	NULL	release of	occurs by	NULL				stochastic changes	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_2_267_s_237	12403813	(D) Kap121p bound to Nup53p at the NPC could then be released by stochastic changes that allow Nup53p to bind Nup170p.	bind
44722	4	5102	7	NULL	NULL	0	NULL	statement 3	NULL		leads to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_159_2_267_s_237	12403813	(D) Kap121p bound to Nup53p at the NPC could then be released by stochastic changes that allow Nup53p to bind Nup170p.	bind
13612	1	5103	6	NULL	NULL	NULL	NULL	Grb2	GP		bind			SH3 domain		Sos-1	GP		proline-rich COOH-terminal (aa 1131 - 1333)		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_156_1_125_s_86	11777939	(D) Kinetic analysis and rate constants for the binding of the SH3 domains of Grb2 and E3b1 to the proline-rich COOH-terminal of Sos-1 (aa 1131 - 1333).	bind
13613	2	5103	6	NULL	NULL	NULL	NULL	E3b1	GP		bind			SH3 domain		Sos-1	GP		proline-rich COOH-terminal (aa 1131 - 1333)		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_156_1_125_s_86	11777939	(D) Kinetic analysis and rate constants for the binding of the SH3 domains of Grb2 and E3b1 to the proline-rich COOH-terminal of Sos-1 (aa 1131 - 1333).	bind
13716	1	5103	7	10	NULL	0	NULL	Grb2	NULL		bind	NULL		SH3 domain		Sos-1	NULL		proline-rich COOH-terminal (aa 1131 - 1333)		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_156_1_125_s_86	11777939	(D) Kinetic analysis and rate constants for the binding of the SH3 domains of Grb2 and E3b1 to the proline-rich COOH-terminal of Sos-1 (aa 1131 - 1333).	bind
13717	2	5103	7	10	NULL	0	NULL	E3b1	NULL		bind	NULL		SH3 domain		Sos-1	NULL		proline-rich COOH-terminal (aa 1131 - 1333)		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_156_1_125_s_86	11777939	(D) Kinetic analysis and rate constants for the binding of the SH3 domains of Grb2 and E3b1 to the proline-rich COOH-terminal of Sos-1 (aa 1131 - 1333).	bind
13621	1	5104	6	NULL	NULL	NULL	NULL	KLF7	GP		bind					p27Kip1	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5699_s_253	15964824	(d) KLF7 binds in vivo to the  p27 kip1 promoter.	bind
13718	1	5104	7	NULL	NULL	0	NULL	KLF7	NULL		bind	NULL				p27 kip1	NULL			promoter	NULL	in vivo	0	NULL	NULL	NULL	gw70_molcellbiol_25_13_5699_s_253	15964824	(d) KLF7 binds in vivo to the  p27 kip1 promoter.	bind
13623	1	5108	6	NULL	NULL	NULL	NULL	Pdcd4	GP		bind					eIF4A	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_1_26_s_163	12482958	(D) Mammalian two-hybrid assay of Pdcd4 binding to eIF4A.	bind
13719	1	5108	7	NULL	NULL	0	NULL	Pdcd4	NULL		bind	NULL				eIF4A	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_1_26_s_163	12482958	(D) Mammalian two-hybrid assay of Pdcd4 binding to eIF4A.	bind
13624	1	5110	6	NULL	NULL	NULL	NULL	MBP-3	GP		does not bind					dsRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_6_1908_s_268	11238927	(D) MBP-3 cannot bind dsRNA. MBP, MBP-3, and wt PACT were tested for poly(I-C)-agarose binding activity.	bind
13721	1	5110	7	NULL	NULL	0	NULL	MBP-3	NULL		does not bind	NULL				dsRNA	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_6_1908_s_268	11238927	(D) MBP-3 cannot bind dsRNA. MBP, MBP-3, and wt PACT were tested for poly(I-C)-agarose binding activity.	bind
13626	1	5111	6	NULL	NULL	NULL	NULL	MBP-3	GP		does not bind					DD	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_6_1908_s_332	11238927	(D) MBP-3 cannot bind to DD.	bind
13722	1	5111	7	NULL	NULL	0	NULL	MBP-3	NULL		does not bind	NULL				DD	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_6_1908_s_332	11238927	(D) MBP-3 cannot bind to DD.	bind
13627	1	5112	6	NULL	NULL	NULL	NULL	MKK3	GP		stimulates					NFATc-CBP	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6442_s_305	12944472	(D) MKK3(E) stimulated NFATc-CBP binding.	bind
13724	1	5112	7	NULL	NULL	0	NULL	MKK3	NULL		stimulate	NULL				NFATc-CBP	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6442_s_305	12944472	(D) MKK3(E) stimulated NFATc-CBP binding.	bind
13628	1	5113	6	NULL	NULL	NULL	NULL	IP3	GP		bind					PRR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_9_7_829_s_149	12144927	(D) Molecular models of IP3 and IP6 bound to PRR-2.	bind
13629	2	5113	6	NULL	NULL	NULL	NULL	IP6	GP		bind					PRR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_9_7_829_s_149	12144927	(D) Molecular models of IP3 and IP6 bound to PRR-2.	bind
13725	1	5113	7	NULL	NULL	0	NULL	IP3	NULL		bind	NULL				PRR-2	NULL				NULL		0	NULL	NULL	NULL	gw60_chembiol_9_7_829_s_149	12144927	(D) Molecular models of IP3 and IP6 bound to PRR-2.	bind
13726	2	5113	7	NULL	NULL	0	NULL	IP6	NULL		bind	NULL				PRR-2	NULL				NULL		0	NULL	NULL	NULL	gw60_chembiol_9_7_829_s_149	12144927	(D) Molecular models of IP3 and IP6 bound to PRR-2.	bind
13631	1	5114	6	NULL	NULL	NULL	NULL	APP	GP		bind					KLC	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_2_449_s_137	11144355	(D) Monoclonal antibody to the TPR domain of KLC (KLC-All) inhibits APP binding to KLC.	bind
13632	2	5114	6	NULL	NULL	NULL	NULL	KLC-All	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_2_449_s_137	11144355	(D) Monoclonal antibody to the TPR domain of KLC (KLC-All) inhibits APP binding to KLC.	bind
13633	3	5114	6	NULL	NULL	NULL	NULL	KLC-All	GP		is					monoclonal antibody to the TPR domain of KLC	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_2_449_s_137	11144355	(D) Monoclonal antibody to the TPR domain of KLC (KLC-All) inhibits APP binding to KLC.	bind
13727	1	5114	7	NULL	NULL	0	NULL	APP	NULL		bind	NULL				KLC	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_28_2_449_s_137	11144355	(D) Monoclonal antibody to the TPR domain of KLC (KLC-All) inhibits APP binding to KLC.	bind
13728	2	5114	7	10	NULL	0	NULL	KLC-All	NULL		inhibits	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_2_449_s_137	11144355	(D) Monoclonal antibody to the TPR domain of KLC (KLC-All) inhibits APP binding to KLC.	bind
17782	3	5114	7	10	NULL	0	NULL	KLC-All	NULL		is	NULL				monoclonal antibody to the TPR domain of KLC	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_2_449_s_137	11144355	(D) Monoclonal antibody to the TPR domain of KLC (KLC-All) inhibits APP binding to KLC.	bind
14085	1	5115	6	NULL	NULL	NULL	NULL	IFN-gamma	GP		induce					Stat1alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_3_1442_s_205	12595462	(D) Moreover, neither IFN-gamma-induced Stat1alpha nor IFN-gamma-induced IRF-1 bound either NF-kappaB-binding site, although, as expected, there was binding to GAS and ISRE sites, respectively.	bind
14086	2	5115	6	NULL	NULL	NULL	NULL	IFN-gamma	GP		induce					IRF-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_3_1442_s_205	12595462	(D) Moreover, neither IFN-gamma-induced Stat1alpha nor IFN-gamma-induced IRF-1 bound either NF-kappaB-binding site, although, as expected, there was binding to GAS and ISRE sites, respectively.	bind
14087	3	5115	6	NULL	NULL	NULL	NULL	statement 1	Process		does not bind									NF-kappaB-binding site	NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_3_1442_s_205	12595462	(D) Moreover, neither IFN-gamma-induced Stat1alpha nor IFN-gamma-induced IRF-1 bound either NF-kappaB-binding site, although, as expected, there was binding to GAS and ISRE sites, respectively.	bind
14088	4	5115	6	NULL	NULL	NULL	NULL	statement 2	Process		does not bind									NF-kappaB-binding site	NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_3_1442_s_205	12595462	(D) Moreover, neither IFN-gamma-induced Stat1alpha nor IFN-gamma-induced IRF-1 bound either NF-kappaB-binding site, although, as expected, there was binding to GAS and ISRE sites, respectively.	bind
14089	5	5115	6	NULL	NULL	NULL	NULL	statement 1	Process		bind									GAS site	NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_3_1442_s_205	12595462	(D) Moreover, neither IFN-gamma-induced Stat1alpha nor IFN-gamma-induced IRF-1 bound either NF-kappaB-binding site, although, as expected, there was binding to GAS and ISRE sites, respectively.	bind
14090	6	5115	6	NULL	NULL	NULL	NULL	statement 2	Process		bind									ISRE site	NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_3_1442_s_205	12595462	(D) Moreover, neither IFN-gamma-induced Stat1alpha nor IFN-gamma-induced IRF-1 bound either NF-kappaB-binding site, although, as expected, there was binding to GAS and ISRE sites, respectively.	bind
13729	1	5115	7	NULL	NULL	0	NULL	IFN-gamma	NULL		induce	NULL				Stat1alpha 	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_71_3_1442_s_205	12595462	(D) Moreover, neither IFN-gamma-induced Stat1alpha nor IFN-gamma-induced IRF-1 bound either NF-kappaB-binding site, although, as expected, there was binding to GAS and ISRE sites, respectively.	bind
13730	2	5115	7	NULL	NULL	0	NULL	IFN-gamma	NULL		induce	NULL				IRF-1	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_71_3_1442_s_205	12595462	(D) Moreover, neither IFN-gamma-induced Stat1alpha nor IFN-gamma-induced IRF-1 bound either NF-kappaB-binding site, although, as expected, there was binding to GAS and ISRE sites, respectively.	bind
13731	3	5115	7	NULL	NULL	0	NULL	statement 1	NULL		does not bind	NULL					NULL			NF-kappaB binding site	NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_3_1442_s_205	12595462	(D) Moreover, neither IFN-gamma-induced Stat1alpha nor IFN-gamma-induced IRF-1 bound either NF-kappaB-binding site, although, as expected, there was binding to GAS and ISRE sites, respectively.	bind
13732	4	5115	7	NULL	NULL	0	NULL	statement 2	NULL		does not bind	NULL					NULL			NF-kappaB binding site	NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_3_1442_s_205	12595462	(D) Moreover, neither IFN-gamma-induced Stat1alpha nor IFN-gamma-induced IRF-1 bound either NF-kappaB-binding site, although, as expected, there was binding to GAS and ISRE sites, respectively.	bind
13733	5	5115	7	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL					NULL			GAS site	NULL		0	NULL	NULL	NULL	gw60_infectimmun_71_3_1442_s_205	12595462	(D) Moreover, neither IFN-gamma-induced Stat1alpha nor IFN-gamma-induced IRF-1 bound either NF-kappaB-binding site, although, as expected, there was binding to GAS and ISRE sites, respectively.	bind
13734	6	5115	7	10	NULL	0	NULL	statement 2	NULL		bind	NULL					NULL			ISRE site	NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_3_1442_s_205	12595462	(D) Moreover, neither IFN-gamma-induced Stat1alpha nor IFN-gamma-induced IRF-1 bound either NF-kappaB-binding site, although, as expected, there was binding to GAS and ISRE sites, respectively.	bind
13635	1	5117	6	NULL	NULL	NULL	NULL	transcription factor	GP		bind									AP/dE composite element	NULL	nuclear extracts from hormone-treated hBC cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_16_7260_s_185	15282324	(D) Mutant analysis of in vitro  transcription factor binding to the AP/dE composite element by EMSAs with nuclear  extracts from hormone-treated hBC cells.	bind
13737	1	5117	7	10	NULL	0	NULL	transcription factor	NULL		bind	NULL					NULL			AP/dE composite element 	NULL	nuclear extracts from hormone-treated hBC cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_16_7260_s_185	15282324	(D) Mutant analysis of in vitro  transcription factor binding to the AP/dE composite element by EMSAs with nuclear  extracts from hormone-treated hBC cells.	bind
13636	1	5118	6	NULL	NULL	NULL	NULL	Brf1	GP		bind					C-DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_231	16880507	(D) Mutant peptides do not inhibit Brf1 binding to C-DNA.	bind
13638	2	5118	6	NULL	NULL	NULL	NULL	peptides	GP	mutant	do not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_231	16880507	(D) Mutant peptides do not inhibit Brf1 binding to C-DNA.	bind
13738	1	5118	7	NULL	NULL	0	NULL	Brf1	NULL		bind	NULL				C-DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_231	16880507	(D) Mutant peptides do not inhibit Brf1 binding to C-DNA.	bind
13739	2	5118	7	NULL	NULL	0	NULL	peptides	NULL	mutant	does not inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_231	16880507	(D) Mutant peptides do not inhibit Brf1 binding to C-DNA.	bind
13640	1	5119	6	NULL	NULL	NULL	NULL	Nck	GP		bind								PRS		NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_86	12110186	(D) Nck binds to the PRS.	bind
13740	1	5119	7	NULL	NULL	0	NULL	Nck	NULL		binds	NULL					NULL		PRS		NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_86	12110186	(D) Nck binds to the PRS.	bind
13641	1	5120	6	NULL	NULL	NULL	NULL	NFAT5	GP		bind					aldose reductase	GP			enhancer	NULL	living cells	NULL	NULL	NULL	NULL	gw60_immunity_15_1_47_s_167	11485737	(D) NFAT5 binds to the aldose reductase enhancer and the  TNF  proximal promoter in living cells.	bind
13642	2	5120	6	NULL	NULL	NULL	NULL	NFAT5	GP		bind					TNF	GP			proximal promoter	NULL	living cells	NULL	NULL	NULL	NULL	gw60_immunity_15_1_47_s_167	11485737	(D) NFAT5 binds to the aldose reductase enhancer and the  TNF  proximal promoter in living cells.	bind
13741	1	5120	7	NULL	NULL	0	NULL	NFAT5	NULL		bind	NULL				aldose reductase	NULL			enhancer	NULL	living cells	0	NULL	NULL	NULL	gw60_immunity_15_1_47_s_167	11485737	(D) NFAT5 binds to the aldose reductase enhancer and the  TNF  proximal promoter in living cells.	bind
13742	2	5120	7	NULL	NULL	0	NULL	NFAT5	NULL		bind	NULL				TNF	NULL			proximal promoter	NULL	living cells	0	NULL	NULL	NULL	gw60_immunity_15_1_47_s_167	11485737	(D) NFAT5 binds to the aldose reductase enhancer and the  TNF  proximal promoter in living cells.	bind
13643	1	5121	6	NULL	NULL	NULL	NULL	NORE1	GP		bind					MST1	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_4_253_s_67	11864565	(D) NORE1 binds MST 1, but not related kinases.	bind
13644	2	5121	6	NULL	NULL	NULL	NULL	NORE1	GP		does not bind					MST1 related kinases	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_4_253_s_67	11864565	(D) NORE1 binds MST 1, but not related kinases.	bind
13743	1	5121	7	NULL	NULL	0	NULL	NORE1	NULL		binds	NULL				MST 1	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_12_4_253_s_67	11864565	(D) NORE1 binds MST 1, but not related kinases.	bind
13744	2	5121	7	NULL	NULL	0	NULL	NORE1	NULL		does not bind	NULL				MST 1 related kinases	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_12_4_253_s_67	11864565	(D) NORE1 binds MST 1, but not related kinases.	bind
13645	1	5123	6	NULL	NULL	0	NULL	Npap60	NULL		bind	NULL				importin-alpha isoforms	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_110_3_349_s_141	12176322	(D) Npap60 binds several importin-alpha isoforms.	bind
13745	1	5123	7	NULL	NULL	0	NULL	Npap60	NULL		binds	NULL				importin-alpha isoform	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_110_3_349_s_141	12176322	(D) Npap60 binds several importin-alpha isoforms.	bind
14091	1	5125	6	NULL	NULL	NULL	NULL	NFAT	GP		bind					PPARgamma2 gene	GP			proximal NFAT binding element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3892_s_361	11997522	(D) Nuclear extracts prepared from differentiated 3T3-L1 adipocytes form NFAT-DNA complexes on the proximal and the distal NFAT binding elements of the PPARgamma2 gene.	bind
14092	2	5125	6	NULL	NULL	NULL	NULL	NFAT	GP		bind					PPARgamma2 gene	GP			distal NFAT binding element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3892_s_361	11997522	(D) Nuclear extracts prepared from differentiated 3T3-L1 adipocytes form NFAT-DNA complexes on the proximal and the distal NFAT binding elements of the PPARgamma2 gene.	bind
53081	3	5125	6	NULL	NULL	NULL	NULL	nuclear extracts	CellComponent		are prepared from					3T3-L1 adipocytes	Cell	differentiated			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3892_s_361	11997522	(D) Nuclear extracts prepared from differentiated 3T3-L1 adipocytes form NFAT-DNA complexes on the proximal and the distal NFAT binding elements of the PPARgamma2 gene.	bind
53082	4	5125	6	NULL	NULL	NULL	NULL	statement 3	Process		form					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3892_s_361	11997522	(D) Nuclear extracts prepared from differentiated 3T3-L1 adipocytes form NFAT-DNA complexes on the proximal and the distal NFAT binding elements of the PPARgamma2 gene.	bind
53083	5	5125	6	NULL	NULL	NULL	NULL	statement 3	Process		form					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3892_s_361	11997522	(D) Nuclear extracts prepared from differentiated 3T3-L1 adipocytes form NFAT-DNA complexes on the proximal and the distal NFAT binding elements of the PPARgamma2 gene.	bind
13746	1	5125	7	10	NULL	0	NULL	NFAT	NULL		bind	NULL				PPARgamma2	NULL			proximal NFAT binding elements	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3892_s_361	11997522	(D) Nuclear extracts prepared from differentiated 3T3-L1 adipocytes form NFAT-DNA complexes on the proximal and the distal NFAT binding elements of the PPARgamma2 gene.	bind
17784	2	5125	7	10	NULL	0	NULL	NFAT	NULL		bind	NULL				PPARgamma2	NULL			distal NFAT binding element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3892_s_361	11997522	(D) Nuclear extracts prepared from differentiated 3T3-L1 adipocytes form NFAT-DNA complexes on the proximal and the distal NFAT binding elements of the PPARgamma2 gene.	bind
53084	3	5125	7	10	NULL	0	NULL	nuclear extracts	NULL		are prepared from	NULL				3T3-L1 adipocytes	NULL	differentiated			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_11_3892_s_361	11997522	(D) Nuclear extracts prepared from differentiated 3T3-L1 adipocytes form NFAT-DNA complexes on the proximal and the distal NFAT binding elements of the PPARgamma2 gene.	bind
53085	4	5125	7	10	NULL	0	NULL	statement 3	NULL		form	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_11_3892_s_361	11997522	(D) Nuclear extracts prepared from differentiated 3T3-L1 adipocytes form NFAT-DNA complexes on the proximal and the distal NFAT binding elements of the PPARgamma2 gene.	bind
53086	5	5125	7	10	NULL	0	NULL	statement 3	NULL		form	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_11_3892_s_361	11997522	(D) Nuclear extracts prepared from differentiated 3T3-L1 adipocytes form NFAT-DNA complexes on the proximal and the distal NFAT binding elements of the PPARgamma2 gene.	bind
13646	1	5126	6	NULL	NULL	NULL	NULL	Nup60p	GP		bind					Prp20p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_937_s_193	11535617	(D) Nup60p binds Prp20p.	bind
13790	1	5126	7	NULL	NULL	0	NULL	Nup60p	NULL		binds	NULL				Prp20p	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_5_937_s_193	11535617	(D) Nup60p binds Prp20p.	bind
13650	1	5128	6	NULL	NULL	NULL	NULL	Bcl2	GP	hypophosphorylated	bind		only			Bax	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_6_3509_s_128	9584191	(D) Only hypophosphorylated Bcl2 binds to Bax.	bind
13793	1	5128	7	10	NULL	0	NULL	 Bcl2	NULL	hypophosphorylated	binds	NULL	only			Bax	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_6_3509_s_128	9584191	(D) Only hypophosphorylated Bcl2 binds to Bax.	bind
13651	1	5129	6	NULL	NULL	NULL	NULL	p150	GP		bind					p21	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_9_3885_s_174	15082782	(D) p150 binds p21 promoter region in vivo.	bind
13794	1	5129	7	NULL	NULL	0	NULL	p150	NULL		binds	NULL				p21	NULL			promoter	NULL	in vivo	0	NULL	NULL	NULL	gw70_molcellbiol_24_9_3885_s_174	15082782	(D) p150 binds p21 promoter region in vivo.	bind
13652	1	5130	6	NULL	NULL	NULL	NULL	p68	GP		bind					CBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5363_s_218	10409727	(D) p68 binds to CBP.	bind
13795	1	5130	7	NULL	NULL	0	NULL	p68	NULL		binds	NULL				CBP	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5363_s_218	10409727	(D) p68 binds to CBP.	bind
13748	1	5131	6	NULL	NULL	NULL	NULL	PAK2	GP		does not bind					TGF-betaR complex	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8878_s_119	14612425	(D) PAK2 does not bind the TGF-betaR complex.	bind
13796	1	5131	7	NULL	NULL	0	NULL	PAK2	NULL		does not bind	NULL				TGF-betaR complex	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8878_s_119	14612425	(D) PAK2 does not bind the TGF-betaR complex.	bind
13749	1	5132	6	NULL	NULL	NULL	NULL	aldolase	GP	parasite	bind		directly			actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_4_885_s_68	12718875	(D) Parasite aldolase binds directly to actin.	bind
13797	1	5132	7	NULL	NULL	0	NULL	aldolase	NULL	Parasite	binds	NULL	directly			actin	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_11_4_885_s_68	12718875	(D) Parasite aldolase binds directly to actin.	bind
13750	1	5133	6	NULL	NULL	NULL	NULL	Paxillin	GP		bind					PAG3	GP		COOH-terminal region		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1315_s_146	10749932	(D) Paxillin binds to the COOH-terminal region of PAG3.	bind
13798	1	5133	7	NULL	NULL	0	NULL	Paxillin	NULL		binds to	NULL				PAG3	NULL		COOH-terminal 		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1315_s_146	10749932	(D) Paxillin binds to the COOH-terminal region of PAG3.	bind
13751	1	5134	6	NULL	NULL	NULL	NULL	Ptc2	GP	phosphorylated	bind					Rad53	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_3_827_s_114	12667463	(D) Phosphorylated Ptc2 binds to Rad53 irrespective of its phosphorylation state.	bind
13752	2	5134	6	NULL	NULL	NULL	NULL	statement 1	Process		irrespective of					Ptc2	GP	phosphorylation status of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_3_827_s_114	12667463	(D) Phosphorylated Ptc2 binds to Rad53 irrespective of its phosphorylation state.	bind
13799	1	5134	7	NULL	NULL	0	NULL	Ptc2	NULL	phosphorylated	binds to	NULL				Rad53	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_11_3_827_s_114	12667463	(D) Phosphorylated Ptc2 binds to Rad53 irrespective of its phosphorylation state.	bind
13800	2	5134	7	NULL	NULL	0	NULL	statement 1	NULL		irrespective of	NULL				Ptc2	NULL	 phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_3_827_s_114	12667463	(D) Phosphorylated Ptc2 binds to Rad53 irrespective of its phosphorylation state.	bind
13753	1	5135	6	NULL	NULL	NULL	NULL	BAF complex	Cell		bind					chromatin	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_5_625_s_92	9845365	(D) PIP2 enhances BAF complex binding to chromatin.	bind
13754	2	5135	6	NULL	NULL	NULL	NULL	PIP2	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_95_5_625_s_92	9845365	(D) PIP2 enhances BAF complex binding to chromatin.	bind
13801	1	5135	7	NULL	NULL	0	NULL	BAF complex	NULL		binds	NULL				chromatin	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_95_5_625_s_92	9845365	(D) PIP2 enhances BAF complex binding to chromatin.	bind
13802	2	5135	7	NULL	NULL	0	NULL	PIP2	NULL		enhances	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_95_5_625_s_92	9845365	(D) PIP2 enhances BAF complex binding to chromatin.	bind
13755	1	5136	6	NULL	NULL	NULL	NULL	PLC 1	GP		bind					TrkB receptors	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_2_335_s_85	9728915	(D) PLC 1 binding to mutant TrkB receptors.	bind
13803	1	5136	7	NULL	NULL	0	NULL	PLC 1	NULL		bind	NULL				 TrkB receptor	NULL	mutant			NULL		0	NULL	NULL	NULL	gw60_neuron_21_2_335_s_85	9728915	(D) PLC 1 binding to mutant TrkB receptors.	bind
14093	1	5137	6	NULL	NULL	NULL	NULL	PP2A	GP		bind					ST	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_147	15684382	(D) PP2A binding  to ST can be uncoupled from the ST-mediated transfer of PP2A onto AR.	bind
19010	3	5137	6	NULL	NULL	NULL	NULL	PP2A	GP		transfer to					AR	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_147	15684382	(D) PP2A binding  to ST can be uncoupled from the ST-mediated transfer of PP2A onto AR.	bind
19011	4	5137	6	NULL	NULL	NULL	NULL	ST	GP		mediates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_147	15684382	(D) PP2A binding  to ST can be uncoupled from the ST-mediated transfer of PP2A onto AR.	bind
53052	5	5137	6	NULL	NULL	NULL	NULL	statement 1	Process		uncoupled by					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_147	15684382	(D) PP2A binding  to ST can be uncoupled from the ST-mediated transfer of PP2A onto AR.	bind
13805	1	5137	7	NULL	NULL	0	NULL	PP2A	NULL		bind	NULL				ST	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_147	15684382	(D) PP2A binding  to ST can be uncoupled from the ST-mediated transfer of PP2A onto AR.	bind
13811	2	5137	7	NULL	NULL	0	NULL	PP2A	NULL		transfer to	NULL				AR	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_147	15684382	(D) PP2A binding  to ST can be uncoupled from the ST-mediated transfer of PP2A onto AR.	bind
13813	4	5137	7	10	NULL	0	NULL	statement 1	NULL		 uncoupled by	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_147	15684382	(D) PP2A binding  to ST can be uncoupled from the ST-mediated transfer of PP2A onto AR.	bind
19030	3	5137	7	NULL	NULL	0	NULL	ST	NULL		mediates	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_147	15684382	(D) PP2A binding  to ST can be uncoupled from the ST-mediated transfer of PP2A onto AR.	bind
13756	1	5138	6	NULL	NULL	NULL	NULL	Procaspase 3	GP	endogenous	bind					AKAP95	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9469_s_151	16227597	(D) Procaspase 3 binds to AKAP95 at endogenous  protein levels.	bind
13816	1	5138	7	10	NULL	0	NULL	Procaspase 3	NULL	endogenous	binds	NULL				AKAP95	NULL	endogenous			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9469_s_151	16227597	(D) Procaspase 3 binds to AKAP95 at endogenous  protein levels.	bind
13757	1	5139	6	NULL	NULL	NULL	NULL	Smurf2	GP		induces					receptor complex	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1365_s_177	11163210	(D) Proteasome and lysosome inhibitors block Smurf2-induced degradation of the receptor complex.	bind
13758	2	5139	6	NULL	NULL	NULL	NULL	proteasome inhibitors	Chemical		block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1365_s_177	11163210	(D) Proteasome and lysosome inhibitors block Smurf2-induced degradation of the receptor complex.	bind
13759	3	5139	6	NULL	NULL	NULL	NULL	lysosome inhibitors	GP		block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1365_s_177	11163210	(D) Proteasome and lysosome inhibitors block Smurf2-induced degradation of the receptor complex.	bind
13817	1	5139	7	NULL	NULL	0	NULL	Smurf2	NULL		induce	NULL				receptor complex	NULL	degradation of			NULL		0	NULL	NULL	NULL	gw60_molcell_6_6_1365_s_177	11163210	(D) Proteasome and lysosome inhibitors block Smurf2-induced degradation of the receptor complex.	bind
13818	2	5139	7	NULL	NULL	0	NULL	Proteasome inhibitor	NULL		block	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_6_6_1365_s_177	11163210	(D) Proteasome and lysosome inhibitors block Smurf2-induced degradation of the receptor complex.	bind
13819	3	5139	7	NULL	NULL	0	NULL	 lysosome inhibitor	NULL		block	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_6_6_1365_s_177	11163210	(D) Proteasome and lysosome inhibitors block Smurf2-induced degradation of the receptor complex.	bind
13760	1	5140	6	NULL	NULL	NULL	NULL	PU.1	GP		bind								CH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3729_s_184	11997509	(D) PU.1 binds to both the CH3 domain and the AT domain.	bind
13761	2	5140	6	NULL	NULL	NULL	NULL	PU.1	GP		bind								AT domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_11_3729_s_184	11997509	(D) PU.1 binds to both the CH3 domain and the AT domain.	bind
13820	1	5140	7	NULL	NULL	0	NULL	PU.1	NULL		binds	NULL					NULL		CH3 domain		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_11_3729_s_184	11997509	(D) PU.1 binds to both the CH3 domain and the AT domain.	bind
13821	2	5140	7	NULL	NULL	0	NULL	PU.1	NULL		binds	NULL					NULL		AT domain		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_11_3729_s_184	11997509	(D) PU.1 binds to both the CH3 domain and the AT domain.	bind
13762	1	5141	6	NULL	NULL	NULL	NULL	CDC48	GP	purified	bind					Ubi-GST	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cell_107_5_667_s_240	11733065	(D) Purified CDC48  binds Ubi-GST but not GST in vitro.	bind
13763	2	5141	6	NULL	NULL	NULL	NULL	CDC48	GP	purified	does not bind					GST	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cell_107_5_667_s_240	11733065	(D) Purified CDC48  binds Ubi-GST but not GST in vitro.	bind
13822	1	5141	7	NULL	NULL	0	NULL	CDC48	NULL	purified	binds	NULL				Ubi-GST	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_cell_107_5_667_s_240	11733065	(D) Purified CDC48  binds Ubi-GST but not GST in vitro.	bind
13823	2	5141	7	NULL	NULL	0	NULL	CDC48	NULL	purified	does not bind	NULL				GST	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_cell_107_5_667_s_240	11733065	(D) Purified CDC48  binds Ubi-GST but not GST in vitro.	bind
13764	1	5142	6	NULL	NULL	NULL	NULL	aldolase-His6	GP	purified;;recombinant;;Toxoplasma	bind		specifically			GST-MIC2t	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_4_885_s_117	12718875	(D) Purified recombinant  Toxoplasma aldolase-His6 (TgAld) also bound specifically to GST-MIC2t but not the W/A mutant.	bind
13765	2	5142	6	NULL	NULL	NULL	NULL	aldolase-His6	GP	purified;;recombinant;;Toxoplasma	does not bind					W/A 		mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_4_885_s_117	12718875	(D) Purified recombinant  Toxoplasma aldolase-His6 (TgAld) also bound specifically to GST-MIC2t but not the W/A mutant.	bind
13766	3	5142	6	NULL	NULL	NULL	NULL	TgAld	GP		is					Toxoplasma aldolase-His6	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_4_885_s_117	12718875	(D) Purified recombinant  Toxoplasma aldolase-His6 (TgAld) also bound specifically to GST-MIC2t but not the W/A mutant.	bind
13824	1	5142	7	10	NULL	0	NULL	aldolase-His6	NULL	purified;;recombinant;;Toxoplasma	bind	NULL	specifically			GST-MIC2t	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_4_885_s_117	12718875	(D) Purified recombinant  Toxoplasma aldolase-His6 (TgAld) also bound specifically to GST-MIC2t but not the W/A mutant.	bind
13828	2	5142	7	10	NULL	0	NULL	aldolase-His6	NULL	purified;;recombinant;;Toxoplasma	does not bind	NULL				W/A	NULL	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_4_885_s_117	12718875	(D) Purified recombinant  Toxoplasma aldolase-His6 (TgAld) also bound specifically to GST-MIC2t but not the W/A mutant.	bind
13829	3	5142	7	NULL	NULL	0	NULL	TgAld	NULL		is	NULL				Toxoplasma aldolase-His6	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_4_885_s_117	12718875	(D) Purified recombinant  Toxoplasma aldolase-His6 (TgAld) also bound specifically to GST-MIC2t but not the W/A mutant.	bind
13767	1	5145	6	NULL	NULL	NULL	NULL	VDR	GP		bind					beta-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_2_369_s_253	11470825	(D) Quantification of the amount of VDR bound to beta-catenin after 1alpha,25(OH)2D3 addition.	bind
44685	2	5145	6	NULL	NULL	NULL	NULL	1alpha,25(OH)2D3	Chemical	addition of	leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_2_369_s_253	11470825	(D) Quantification of the amount of VDR bound to beta-catenin after 1alpha,25(OH)2D3 addition.	bind
13832	1	5145	7	NULL	NULL	0	NULL	VDR	NULL		bind	NULL				beta-catenin	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_2_369_s_253	11470825	(D) Quantification of the amount of VDR bound to beta-catenin after 1alpha,25(OH)2D3 addition.	bind
13835	2	5145	7	10	NULL	0	NULL	statement 1	NULL		occurs after	NULL				1alpha,25(OH)2D3	NULL	addition of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_2_369_s_253	11470825	(D) Quantification of the amount of VDR bound to beta-catenin after 1alpha,25(OH)2D3 addition.	bind
13768	1	5146	6	NULL	NULL	NULL	NULL	TOPBP1	GP		bind					Miz-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_3_509_s_113	12408820	(D) Quantitation of five independent immunoprecipitation experiments performed as in (C); the amount of TOPBP1 bound to Miz-1 in the absence of UV irradiation was arbitrarily set to one.	bind
13769	2	5146	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs in absence of					UV irradiation	MachineActivity				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_3_509_s_113	12408820	(D) Quantitation of five independent immunoprecipitation experiments performed as in (C); the amount of TOPBP1 bound to Miz-1 in the absence of UV irradiation was arbitrarily set to one.	bind
13836	1	5146	7	NULL	NULL	0	NULL	TOPBP1	NULL		bind	NULL				Miz-1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_3_509_s_113	12408820	(D) Quantitation of five independent immunoprecipitation experiments performed as in (C); the amount of TOPBP1 bound to Miz-1 in the absence of UV irradiation was arbitrarily set to one.	bind
19765	2	5146	7	NULL	NULL	0	NULL	statement 1	NULL		occurs in absence of	NULL				UV irradiation	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_10_3_509_s_113	12408820	(D) Quantitation of five independent immunoprecipitation experiments performed as in (C); the amount of TOPBP1 bound to Miz-1 in the absence of UV irradiation was arbitrarily set to one.	bind
14098	1	5147	6	NULL	NULL	NULL	NULL	InR	GP		bind					GST-IRS	GP	wild type	1108 - 516		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_2_213_s_177	15249583	(D) Quantitation of InR binding to  GST-IRS-1108 - 516 (WT) or a mutant GST-IRS-1108 - 516 in which serine 302 is mutated to alanine (S302A) after in vitro phosphorylation  by S6K2.	bind
14099	2	5147	6	NULL	NULL	NULL	NULL	InR	GP		bind					GST-IRS	GP	mutant	S302A 1108 - 516		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_2_213_s_177	15249583	(D) Quantitation of InR binding to  GST-IRS-1108 - 516 (WT) or a mutant GST-IRS-1108 - 516 in which serine 302 is mutated to alanine (S302A) after in vitro phosphorylation  by S6K2.	bind
14100	3	5147	6	NULL	NULL	0	NULL	S302A	NULL		is	NULL				serine 302 is mutated to alanine	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_166_2_213_s_177	15249583	(D) Quantitation of InR binding to  GST-IRS-1108 - 516 (WT) or a mutant GST-IRS-1108 - 516 in which serine 302 is mutated to alanine (S302A) after in vitro phosphorylation  by S6K2.	bind
14101	4	5147	6	NULL	NULL	0	NULL	S6K2	NULL		phosphorylates	NULL				GST-IRS	NULL		1108 - 516		NULL	in vitro	NULL	NULL	NULL	NULL	gw70_cellbiol_166_2_213_s_177	15249583	(D) Quantitation of InR binding to  GST-IRS-1108 - 516 (WT) or a mutant GST-IRS-1108 - 516 in which serine 302 is mutated to alanine (S302A) after in vitro phosphorylation  by S6K2.	bind
14102	5	5147	6	NULL	NULL	NULL	NULL	statement 4	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_2_213_s_177	15249583	(D) Quantitation of InR binding to  GST-IRS-1108 - 516 (WT) or a mutant GST-IRS-1108 - 516 in which serine 302 is mutated to alanine (S302A) after in vitro phosphorylation  by S6K2.	bind
13929	1	5147	7	NULL	NULL	0	NULL	InR	NULL		bind	NULL				GST-IRS	NULL	WT	1108 - 516		NULL		0	NULL	NULL	NULL	gw70_cellbiol_166_2_213_s_177	15249583	(D) Quantitation of InR binding to  GST-IRS-1108 - 516 (WT) or a mutant GST-IRS-1108 - 516 in which serine 302 is mutated to alanine (S302A) after in vitro phosphorylation  by S6K2.	bind
13932	2	5147	7	NULL	NULL	0	NULL	S6K2	NULL		phosphorylates	NULL				 GST-IRS	NULL	mutant	1108 - 516 S302A		NULL	in vitro	0	NULL	NULL	NULL	gw70_cellbiol_166_2_213_s_177	15249583	(D) Quantitation of InR binding to  GST-IRS-1108 - 516 (WT) or a mutant GST-IRS-1108 - 516 in which serine 302 is mutated to alanine (S302A) after in vitro phosphorylation  by S6K2.	bind
13933	3	5147	7	NULL	NULL	0	NULL	InR	NULL		bind	NULL				GST-IRS	NULL	mutant	1108 - 516 S302A		NULL		0	NULL	NULL	NULL	gw70_cellbiol_166_2_213_s_177	15249583	(D) Quantitation of InR binding to  GST-IRS-1108 - 516 (WT) or a mutant GST-IRS-1108 - 516 in which serine 302 is mutated to alanine (S302A) after in vitro phosphorylation  by S6K2.	bind
13934	4	5147	7	NULL	NULL	0	NULL	statement 3	NULL		occurs after	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_166_2_213_s_177	15249583	(D) Quantitation of InR binding to  GST-IRS-1108 - 516 (WT) or a mutant GST-IRS-1108 - 516 in which serine 302 is mutated to alanine (S302A) after in vitro phosphorylation  by S6K2.	bind
53053	5	5147	7	10	NULL	0	NULL	S302A	NULL		is	NULL				serine 302 is mutated to alanine	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_166_2_213_s_177	15249583	(D) Quantitation of InR binding to  GST-IRS-1108 - 516 (WT) or a mutant GST-IRS-1108 - 516 in which serine 302 is mutated to alanine (S302A) after in vitro phosphorylation  by S6K2.	bind
13770	1	5148	6	NULL	NULL	NULL	NULL	Rad32	GP		bind			D25A		Rad50	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_15_5186_s_185	12861005	(D) Rad32-D25A binds to Rad50 in immunoprecipitation assay.	bind
13935	1	5148	7	NULL	NULL	0	NULL	Rad32	NULL		binds	NULL		D25A		Rad50	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_15_5186_s_185	12861005	(D) Rad32-D25A binds to Rad50 in immunoprecipitation assay.	bind
13771	1	5152	6	NULL	NULL	NULL	NULL	Gal4-Knirps chimera	GP		mediates			202-358		repression	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7247_s_258	10982842	(D) Repression mediated by the Gal4-Knirps (202-358) chimera, a protein that contains the dCtBP interaction motif.	bind
13775	2	5152	6	NULL	NULL	NULL	NULL	Gal4-Knirps chimera	GP		contain			202-358					dCtBP interaction motif		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7247_s_258	10982842	(D) Repression mediated by the Gal4-Knirps (202-358) chimera, a protein that contains the dCtBP interaction motif.	bind
13947	1	5152	7	NULL	NULL	0	NULL	chimera Gal4-Knirps	NULL		contains	NULL		202-358			NULL		dCtBP interaction motif		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7247_s_258	10982842	(D) Repression mediated by the Gal4-Knirps (202-358) chimera, a protein that contains the dCtBP interaction motif.	bind
13948	2	5152	7	NULL	NULL	0	NULL	chimera Gal4-Knirps	NULL		mediates	NULL		202-358		repression	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7247_s_258	10982842	(D) Repression mediated by the Gal4-Knirps (202-358) chimera, a protein that contains the dCtBP interaction motif.	bind
13776	1	5153	6	NULL	NULL	NULL	NULL	BCS1	GP		bind					OMV	Organism				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_7_2239_s_283	12640110	(D) Residues 87 to 126 of BCS1 increase binding  to OMV.	bind
13777	2	5153	6	NULL	NULL	NULL	NULL	BCS1	GP		increase			residues 87 to 126		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_7_2239_s_283	12640110	(D) Residues 87 to 126 of BCS1 increase binding  to OMV.	bind
13949	1	5153	7	NULL	NULL	0	NULL	BCS1	NULL		bind	NULL				OMV	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_7_2239_s_283	12640110	(D) Residues 87 to 126 of BCS1 increase binding  to OMV.	bind
13950	2	5153	7	NULL	NULL	0	NULL	BCS1	NULL		increase	NULL		Residues 87 to 126		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_7_2239_s_283	12640110	(D) Residues 87 to 126 of BCS1 increase binding  to OMV.	bind
13778	1	5156	6	NULL	NULL	NULL	NULL	CSL	GP		bind					Caco-2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_10_5282_s_240	10496907	(D) Saturability of CSL binding to Caco-2 cells.	bind
13951	1	5156	7	NULL	NULL	0	NULL	CSL	NULL		bind	NULL				Caco-2 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_10_5282_s_240	10496907	(D) Saturability of CSL binding to Caco-2 cells.	bind
13779	1	5158	6	NULL	NULL	NULL	NULL	Sem-AP	GP		bind					NP	GP	mutants			NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_5_1093_s_73	9856464	(D) Sem-AP binding to NP mutants.	bind
13952	1	5158	7	NULL	NULL	0	NULL	Sem-AP	NULL		bind	NULL				 NP	NULL	mutant			NULL		0	NULL	NULL	NULL	gw60_neuron_21_5_1093_s_73	9856464	(D) Sem-AP binding to NP mutants.	bind
13780	1	5161	6	NULL	NULL	NULL	NULL	Skp2	GP		bind		directly			Smad4	GP	cancer mutants			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_17_7524_s_129	15314162	(D) Skp2 binds to Smad4 cancer mutants directly in  vitro.	bind
13955	1	5161	7	NULL	NULL	0	NULL	Skp2 	NULL		binds	NULL	directly			Smad4	NULL	cancer mutant			NULL	in vitro	0	NULL	NULL	NULL	gw70_molcellbiol_24_17_7524_s_129	15314162	(D) Skp2 binds to Smad4 cancer mutants directly in  vitro.	bind
13781	1	5162	6	NULL	NULL	NULL	NULL	Smurf2	GP		increases					IFN	GP	inhibitory effect of 			NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1365_s_258	11163210	(D) Smurf2 increases IFN  inhibitory effect.	bind
13956	1	5162	7	NULL	NULL	0	NULL	Smurf2 	NULL		increase	NULL				IFN	NULL	inhibitory effect of			NULL		0	NULL	NULL	NULL	gw60_molcell_6_6_1365_s_258	11163210	(D) Smurf2 increases IFN  inhibitory effect.	bind
13782	1	5163	6	NULL	NULL	NULL	NULL	CRM1	GP		bind					Nup214	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_18_6772_s_317	16943420	(D) Solid-phase binding  of CRM1 to Nup214 was analyzed in the absence or presence of RanGTPgammaS, RanGDP, or NES peptide, as indicated.	bind
13957	1	5163	7	NULL	NULL	0	NULL	CRM1	NULL		bind	NULL				Nup214	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_18_6772_s_317	16943420	(D) Solid-phase binding  of CRM1 to Nup214 was analyzed in the absence or presence of RanGTPgammaS, RanGDP, or NES peptide, as indicated.	bind
13783	2	5164	6	NULL	NULL	NULL	NULL	statement 1	Process		bind		specifically			hsp27	GP			EcRE	NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_28_11_849_s_166	9818386	(d) Specific binding of hsp27 EcRE to the EcR complex that had been pretreated with  -protein phosphatase.	bind
13784	1	5164	6	NULL	NULL	NULL	NULL	EcR complex	GP		pre-treated with					protein phosphatase	GP				NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_28_11_849_s_166	9818386	(d) Specific binding of hsp27 EcRE to the EcR complex that had been pretreated with  -protein phosphatase.	bind
13958	1	5164	7	NULL	NULL	0	NULL	hsp27 	NULL		bind	NULL	specifically		EcRE	EcR complex 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_28_11_849_s_166	9818386	(d) Specific binding of hsp27 EcRE to the EcR complex that had been pretreated with  -protein phosphatase.	bind
13959	2	5164	7	NULL	NULL	0	NULL	EcR complex	NULL		pretreated with	NULL				protein phosphatase	NULL				NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_28_11_849_s_166	9818386	(d) Specific binding of hsp27 EcRE to the EcR complex that had been pretreated with  -protein phosphatase.	bind
13785	1	5165	6	NULL	NULL	NULL	NULL	NFATc	GP		bind		specifically	DBD		SE RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_298_4_486_s_73	12408978	(D) Specific binding of NFATc DBD to SE RNA #1.	bind
13960	1	5165	7	10	NULL	0	NULL	NFATc 	NULL		bind	NULL	specifically	DBD		SE RNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_298_4_486_s_73	12408978	(D) Specific binding of NFATc DBD to SE RNA #1.	bind
13786	1	5166	6	NULL	NULL	NULL	NULL	HMG-I	GP		bind					HPV18 	Organism	wt			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_7_2329_s_184	12640118	(D) Specific competition of the AP1 and HMG-I(Y) binding  on the HPV18 wt probe.	bind
13787	2	5166	6	NULL	NULL	NULL	NULL	AP1	GP		bind					HPV18	Organism	wt			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_7_2329_s_184	12640118	(D) Specific competition of the AP1 and HMG-I(Y) binding  on the HPV18 wt probe.	bind
13788	3	5166	6	NULL	NULL	NULL	NULL	statement 1	Process		competes with		specifically			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_7_2329_s_184	12640118	(D) Specific competition of the AP1 and HMG-I(Y) binding  on the HPV18 wt probe.	bind
13961	1	5166	7	NULL	NULL	0	NULL	AP1	NULL		bind	NULL				HPV18	NULL	wt			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_7_2329_s_184	12640118	(D) Specific competition of the AP1 and HMG-I(Y) binding  on the HPV18 wt probe.	bind
13962	2	5166	7	NULL	NULL	0	NULL	HMG-I	NULL		bind	NULL				HPV18	NULL	wt			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_7_2329_s_184	12640118	(D) Specific competition of the AP1 and HMG-I(Y) binding  on the HPV18 wt probe.	bind
13974	3	5166	7	NULL	NULL	0	NULL	statement 1	NULL		compete with	NULL	specifically			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_7_2329_s_184	12640118	(D) Specific competition of the AP1 and HMG-I(Y) binding  on the HPV18 wt probe.	bind
19012	1	5167	6	NULL	NULL	NULL	NULL	AKAP79	GP		bind		specifically			PSD-95	GP	mutant	SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_neuron_27_1_107_s_175	10939335	(D) Specificity of AKAP79 binding to the SH3 domain binding was tested in pulldown experiments using SH3 domain mutants of PSD-95.	bind
13976	1	5167	7	NULL	NULL	0	NULL	AKAP79	NULL		bind	NULL	specifically			PSD-95	NULL	mutant	SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_neuron_27_1_107_s_175	10939335	(D) Specificity of AKAP79 binding to the SH3 domain binding was tested in pulldown experiments using SH3 domain mutants of PSD-95.	bind
13804	1	5168	6	NULL	NULL	NULL	NULL	NAD+	Chemical		bind		specifically			RIBEYE	GP		B domain		NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_3_857_s_260	11163272	(D) Specificity of NAD+ binding to the B domain of RIBEYE.	bind
13977	1	5168	7	NULL	NULL	0	NULL	NAD+	NULL		bind	NULL	specifically			RIBEYE	NULL		B domain		NULL		0	NULL	NULL	NULL	gw60_neuron_28_3_857_s_260	11163272	(D) Specificity of NAD+ binding to the B domain of RIBEYE.	bind
13806	1	5169	6	NULL	NULL	NULL	NULL	p53	GP		bind					Apaf1	GP			promoter	NULL	p53+/+ neurons treated with camptothecin	NULL	NULL	NULL	NULL	gw60_cellbiol_155_2_207_s_94	11591730	(D) Specificity of p53 binding activity to the Apaf1 promoter was examined in p53+/+ and p53-/- neurons treated with camptothecin.	bind
13807	2	5169	6	NULL	NULL	NULL	NULL	p53	GP		bind					Apaf1	GP			promoter	NULL	p53-/- neurons treated with camptothecin	NULL	NULL	NULL	NULL	gw60_cellbiol_155_2_207_s_94	11591730	(D) Specificity of p53 binding activity to the Apaf1 promoter was examined in p53+/+ and p53-/- neurons treated with camptothecin.	bind
13978	1	5169	7	NULL	NULL	0	NULL	p53	NULL		bind	NULL				Apaf1	NULL			promoter	NULL	p53+/+ neurons treated with camptothecin	NULL	NULL	NULL	NULL	gw60_cellbiol_155_2_207_s_94	11591730	(D) Specificity of p53 binding activity to the Apaf1 promoter was examined in p53+/+ and p53-/- neurons treated with camptothecin.	bind
13979	2	5169	7	NULL	NULL	0	NULL	p53	NULL		bind	NULL				Apaf1	NULL			promoter	NULL	p53-/- neurons treated with camptothecin	NULL	NULL	NULL	NULL	gw60_cellbiol_155_2_207_s_94	11591730	(D) Specificity of p53 binding activity to the Apaf1 promoter was examined in p53+/+ and p53-/- neurons treated with camptothecin.	bind
13808	1	5171	6	NULL	NULL	NULL	NULL	MMP-2	GP		cleaves					Ln-5	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_1_197_s_209	12695504	(D) Stimulated migration of  MMP-2 cleaved Ln-5 depends on EGFR. MCF10A cells were allowed to migrate on Transwell  membranes, which were coated with either uncleaved (top panels; -MMP-2) or MMP-2-cleaved  Ln-5 (bottom panels; +MMP-2).	bind
13809	2	5171	6	NULL	NULL	NULL	NULL	Ln-5	GP	migration of;;MMP-2 cleaved	is dependent on					EGFR	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_1_197_s_209	12695504	(D) Stimulated migration of  MMP-2 cleaved Ln-5 depends on EGFR. MCF10A cells were allowed to migrate on Transwell  membranes, which were coated with either uncleaved (top panels; -MMP-2) or MMP-2-cleaved  Ln-5 (bottom panels; +MMP-2).	bind
14050	1	5171	7	NULL	NULL	0	NULL	MMP-2 	NULL		cleaves	NULL				Ln-5	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_161_1_197_s_209	12695504	(D) Stimulated migration of  MMP-2 cleaved Ln-5 depends on EGFR. MCF10A cells were allowed to migrate on Transwell  membranes, which were coated with either uncleaved (top panels; -MMP-2) or MMP-2-cleaved  Ln-5 (bottom panels; +MMP-2).	bind
14051	2	5171	7	10	NULL	0	NULL	Ln-5	NULL	migration of;;MMP-2 cleaved	depends on	NULL				EGFR	NULL				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_1_197_s_209	12695504	(D) Stimulated migration of  MMP-2 cleaved Ln-5 depends on EGFR. MCF10A cells were allowed to migrate on Transwell  membranes, which were coated with either uncleaved (top panels; -MMP-2) or MMP-2-cleaved  Ln-5 (bottom panels; +MMP-2).	bind
13810	1	5172	6	NULL	NULL	NULL	NULL	GTP S 	Chemical		bind					Rab5	GP				NULL	early endosomes	NULL	NULL	NULL	NULL	gw60_cell_90_6_1149_s_172	9323142	(d) Stimulation of [35]GTP S  binding to Rab5 on early endosomes by the Rabaptin-5 - p60 complex.	bind
13812	2	5172	6	NULL	NULL	NULL	NULL	Rabaptin-5 - p60 complex	GP		stimulates					statement 1	Process				NULL	early endosomes	NULL	NULL	NULL	NULL	gw60_cell_90_6_1149_s_172	9323142	(d) Stimulation of [35]GTP S  binding to Rab5 on early endosomes by the Rabaptin-5 - p60 complex.	bind
14052	1	5172	7	10	NULL	0	NULL	GTP S 	NULL		bind	NULL				Rab5	NULL				NULL	early endosomes	NULL	NULL	NULL	NULL	gw60_cell_90_6_1149_s_172	9323142	(d) Stimulation of [35]GTP S  binding to Rab5 on early endosomes by the Rabaptin-5 - p60 complex.	bind
14053	2	5172	7	10	NULL	0	NULL	Rabaptin-5 - p60 complex	NULL		stimulate	NULL				statement 1	NULL				NULL	early endosomes	NULL	NULL	NULL	NULL	gw60_cell_90_6_1149_s_172	9323142	(d) Stimulation of [35]GTP S  binding to Rab5 on early endosomes by the Rabaptin-5 - p60 complex.	bind
13814	1	5173	6	NULL	NULL	NULL	NULL	SNARE proteins	GP		bind					MYC-Sec1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_146_2_333_s_157	10427089	(D) Stoichiometry of SNARE proteins bound to MYC-Sec1p.	bind
14054	1	5173	7	NULL	NULL	0	NULL	SNARE protein	NULL		bind	NULL				MYC-Sec1p	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_146_2_333_s_157	10427089	(D) Stoichiometry of SNARE proteins bound to MYC-Sec1p.	bind
13815	1	5174	6	NULL	NULL	NULL	NULL	SA	Chemical		bind					EL229C-B					NULL		NULL	NULL	NULL	NULL	gw60_cell_107_2_223_s_81	11672529	(D) Stopped-flow kinetics of SA binding to  EL229C-B.	bind
14055	1	5174	7	NULL	NULL	0	NULL	SA	NULL		bind	NULL				EL229C-B	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_107_2_223_s_81	11672529	(D) Stopped-flow kinetics of SA binding to  EL229C-B.	bind
13963	1	5175	6	NULL	NULL	NULL	NULL	Stx	GP		bind					glomeruli 	OrganismPart	immature;;outer cortex			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_1_612_s_63	15618202	(D) Stx binding to immature glomeruli (IG) of outer cortex.	bind
19013	2	5175	6	NULL	NULL	NULL	NULL	IG	OrganismPart		is					immature glomeruli	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_1_612_s_63	15618202	(D) Stx binding to immature glomeruli (IG) of outer cortex.	bind
14056	1	5175	7	10	NULL	0	NULL	Stx	NULL		bind	NULL				 glomeruli	NULL	immature;;outer cortex			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_1_612_s_63	15618202	(D) Stx binding to immature glomeruli (IG) of outer cortex.	bind
14057	2	5175	7	NULL	NULL	0	NULL	IG	NULL		is	NULL				 immature glomeruli 	NULL				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_1_612_s_63	15618202	(D) Stx binding to immature glomeruli (IG) of outer cortex.	bind
13964	1	5176	6	NULL	NULL	NULL	NULL	Sec15p	GP		bind					Sec2p constructs	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_6_2757_s_228	16611746	(D) Summary of Sec15p and Ypt32p binding to Sec2p  constructs.	bind
13965	2	5176	6	NULL	NULL	NULL	NULL	Ypt32p	GP		bind					Sec2p constructs	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_6_2757_s_228	16611746	(D) Summary of Sec15p and Ypt32p binding to Sec2p  constructs.	bind
14058	1	5176	7	NULL	NULL	0	NULL	Sec15p	NULL		bind	NULL				Sec2p constructs	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_6_2757_s_228	16611746	(D) Summary of Sec15p and Ypt32p binding to Sec2p  constructs.	bind
14059	2	5176	7	NULL	NULL	0	NULL	Ypt32p	NULL		bind	NULL				Sec2p constructs	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_6_2757_s_228	16611746	(D) Summary of Sec15p and Ypt32p binding to Sec2p  constructs.	bind
13966	1	5178	6	NULL	NULL	NULL	NULL	caspase-7	GP	active	bind			catalytic groove		XIAP fragment					NULL		NULL	NULL	NULL	NULL	gw60_cell_107_3_399_s_56	11701129	(D) Surface representation of the catalytic groove  in the active caspase-7 bound with an  XIAP fragment.	bind
14060	1	5178	7	10	NULL	0	NULL	caspase-7	NULL	active	bind	NULL		catalytic groove		XIAP fragment	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_3_399_s_56	11701129	(D) Surface representation of the catalytic groove  in the active caspase-7 bound with an  XIAP fragment.	bind
13967	1	5179	6	NULL	NULL	NULL	NULL	Swi/nf	GP		displace					nucleosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_392	11884596	(D) Swi/nf and SAGA displace nucleosomes, allowing binding of Ste12 and Tec1 to their sites.	bind
13968	2	5179	6	NULL	NULL	NULL	NULL	SAGA	GP		displace					nucleosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_392	11884596	(D) Swi/nf and SAGA displace nucleosomes, allowing binding of Ste12 and Tec1 to their sites.	bind
13969	3	5179	6	NULL	NULL	NULL	NULL	Ste12	GP		bind									site	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_392	11884596	(D) Swi/nf and SAGA displace nucleosomes, allowing binding of Ste12 and Tec1 to their sites.	bind
13970	4	5179	6	NULL	NULL	NULL	NULL	Tec1	GP		bind									site	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_392	11884596	(D) Swi/nf and SAGA displace nucleosomes, allowing binding of Ste12 and Tec1 to their sites.	bind
13971	5	5179	6	NULL	NULL	NULL	NULL	statement 1	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_392	11884596	(D) Swi/nf and SAGA displace nucleosomes, allowing binding of Ste12 and Tec1 to their sites.	bind
13972	6	5179	6	NULL	NULL	NULL	NULL	statement 1	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_392	11884596	(D) Swi/nf and SAGA displace nucleosomes, allowing binding of Ste12 and Tec1 to their sites.	bind
13973	7	5179	6	NULL	NULL	NULL	NULL	statement 2	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_392	11884596	(D) Swi/nf and SAGA displace nucleosomes, allowing binding of Ste12 and Tec1 to their sites.	bind
13975	8	5179	6	NULL	NULL	NULL	NULL	statement 2	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_392	11884596	(D) Swi/nf and SAGA displace nucleosomes, allowing binding of Ste12 and Tec1 to their sites.	bind
14061	1	5179	7	NULL	NULL	0	NULL	Swi/nf 	NULL		displace	NULL				nucleosomes	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_392	11884596	(D) Swi/nf and SAGA displace nucleosomes, allowing binding of Ste12 and Tec1 to their sites.	bind
14062	2	5179	7	NULL	NULL	0	NULL	SAGA	NULL		displace	NULL				nucleosomes	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_392	11884596	(D) Swi/nf and SAGA displace nucleosomes, allowing binding of Ste12 and Tec1 to their sites.	bind
14063	3	5179	7	10	NULL	0	NULL	Ste12			bind					Swi/nf 					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_392	11884596	(D) Swi/nf and SAGA displace nucleosomes, allowing binding of Ste12 and Tec1 to their sites.	bind
14064	4	5179	7	10	NULL	0	NULL	Ste12			bind					SAGA					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_392	11884596	(D) Swi/nf and SAGA displace nucleosomes, allowing binding of Ste12 and Tec1 to their sites.	bind
14065	5	5179	7	NULL	NULL	0	NULL	statement 1	NULL		allows	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_392	11884596	(D) Swi/nf and SAGA displace nucleosomes, allowing binding of Ste12 and Tec1 to their sites.	bind
14066	6	5179	7	NULL	NULL	0	NULL	statement 2	NULL		allows	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_392	11884596	(D) Swi/nf and SAGA displace nucleosomes, allowing binding of Ste12 and Tec1 to their sites.	bind
14067	7	5179	7	NULL	NULL	0	NULL	Tec1	NULL		bind	NULL				Swi/nf 	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_392	11884596	(D) Swi/nf and SAGA displace nucleosomes, allowing binding of Ste12 and Tec1 to their sites.	bind
14068	8	5179	7	NULL	NULL	0	NULL	Tec1	NULL		bind	NULL				SAGA	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_392	11884596	(D) Swi/nf and SAGA displace nucleosomes, allowing binding of Ste12 and Tec1 to their sites.	bind
14069	9	5179	7	NULL	NULL	0	NULL	statement 1	NULL		allows	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_392	11884596	(D) Swi/nf and SAGA displace nucleosomes, allowing binding of Ste12 and Tec1 to their sites.	bind
14070	10	5179	7	NULL	NULL	0	NULL	statement 2	NULL		allows	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_7_2078_s_392	11884596	(D) Swi/nf and SAGA displace nucleosomes, allowing binding of Ste12 and Tec1 to their sites.	bind
13980	1	5180	6	NULL	NULL	NULL	NULL	SWI/SNF	GP		bind					HO	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_38	16705163	(D) SWI/SNF binding to  HO is restored in a  gcn5 sin3 strain.	bind
13981	2	5180	6	NULL	NULL	NULL	NULL	statement 1	Process		restored in					gcn5 sin3 strain	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_38	16705163	(D) SWI/SNF binding to  HO is restored in a  gcn5 sin3 strain.	bind
14071	1	5180	7	NULL	NULL	0	NULL	SWI/SNF	NULL		bind	NULL				HO	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_38	16705163	(D) SWI/SNF binding to  HO is restored in a  gcn5 sin3 strain.	bind
14072	2	5180	7	NULL	NULL	0	NULL	statement 1	NULL		is restored in	NULL				 gcn5 sin3 strain	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_38	16705163	(D) SWI/SNF binding to  HO is restored in a  gcn5 sin3 strain.	bind
13982	1	5181	6	NULL	NULL	NULL	NULL	Syntaxin	GP		bind					syt IX	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4755_s_213	16093350	(D) Syntaxin bound to  syt IX (C) was quantified by densitometry.	bind
14073	1	5181	7	NULL	NULL	0	NULL	Syntaxin	NULL		bind	NULL				syt IX	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4755_s_213	16093350	(D) Syntaxin bound to  syt IX (C) was quantified by densitometry.	bind
13983	1	5182	6	NULL	NULL	NULL	NULL	TCR	GP		bind					Nck	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_139	12110186	(D) Temperature dependence of TCR binding to Nck.	bind
13984	2	5182	6	NULL	NULL	NULL	NULL	statement 1	Process		is dependent on					temperature	AbstractConcept				NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_139	12110186	(D) Temperature dependence of TCR binding to Nck.	bind
14074	1	5182	7	NULL	NULL	0	NULL	TCR	NULL		bind	NULL				Nck	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_109_7_901_s_139	12110186	(D) Temperature dependence of TCR binding to Nck.	bind
14075	2	5182	7	NULL	NULL	0	NULL	statement 1	NULL		depends on	NULL				temperature	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_109_7_901_s_139	12110186	(D) Temperature dependence of TCR binding to Nck.	bind
13985	1	5183	6	NULL	NULL	NULL	NULL	annexin V	GP		bind					PKC	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1151_s_190	12769841	(D) The  5 integrin cytoplasmic domain inhibits binding of annexin V to PKC.	bind
13986	2	5183	6	NULL	NULL	NULL	NULL	5 integrin	GP		inhibits			cytoplasmic domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1151_s_190	12769841	(D) The  5 integrin cytoplasmic domain inhibits binding of annexin V to PKC.	bind
14076	1	5183	7	NULL	NULL	0	NULL	annexin V	NULL		bind	NULL				PKC	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1151_s_190	12769841	(D) The  5 integrin cytoplasmic domain inhibits binding of annexin V to PKC.	bind
14077	2	5183	7	NULL	NULL	0	NULL	5 integrin	NULL		inhibits	NULL		cytoplasmic domain		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1151_s_190	12769841	(D) The  5 integrin cytoplasmic domain inhibits binding of annexin V to PKC.	bind
13987	1	5184	6	NULL	NULL	NULL	NULL	semaphorin	GP		bind					NP/Plex 1 complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_99_1_59_s_89	10520994	(D) The  affinity of semaphorin binding to various NP/Plex 1 complexes.	bind
14078	1	5184	7	NULL	NULL	0	NULL	semaphorin	NULL		bind	NULL				NP/Plex 1 complex 	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_99_1_59_s_89	10520994	(D) The  affinity of semaphorin binding to various NP/Plex 1 complexes.	bind
13988	1	5185	6	NULL	NULL	NULL	NULL	BRG1 proteins	GP	mutant	does not bind					pRB	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1188_s_293	14729964	(D) The  mutant BRG1 proteins that do not bind pRB are capable of inducing formation of flat  cells.	bind
13989	2	5185	6	NULL	NULL	NULL	NULL	BRG1 proteins	GP	mutant	induce					flat cells	Cell	formation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1188_s_293	14729964	(D) The  mutant BRG1 proteins that do not bind pRB are capable of inducing formation of flat  cells.	bind
14079	1	5185	7	10	NULL	0	NULL	BRG1 protein	NULL	mutant	does not bind	NULL				pRB	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1188_s_293	14729964	(D) The  mutant BRG1 proteins that do not bind pRB are capable of inducing formation of flat  cells.	bind
14080	2	5185	7	10	NULL	0	NULL	BRG1 protein	NULL	mutant	induce	NULL				flat cells	NULL	formation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1188_s_293	14729964	(D) The  mutant BRG1 proteins that do not bind pRB are capable of inducing formation of flat  cells.	bind
13990	1	5186	6	NULL	NULL	NULL	NULL	eIF5	GP		bind					NIP1	GP		NTD		NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9437_s_261	15485912	(D) The  NIP1-Box6 mutation diminishes binding of eIF5 and eIF2 to the NIP1-NTD in vivo.	bind
13991	2	5186	6	NULL	NULL	NULL	NULL	eIF2	GP		bind					NIP1	GP		NTD		NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9437_s_261	15485912	(D) The  NIP1-Box6 mutation diminishes binding of eIF5 and eIF2 to the NIP1-NTD in vivo.	bind
13992	3	5186	6	NULL	NULL	NULL	NULL	NIP1	GP	mutant	diminishes			Box6		statement 1	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9437_s_261	15485912	(D) The  NIP1-Box6 mutation diminishes binding of eIF5 and eIF2 to the NIP1-NTD in vivo.	bind
13993	4	5186	6	NULL	NULL	NULL	NULL	NIP1	GP	mutant	diminishes			Box6		statement 2	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9437_s_261	15485912	(D) The  NIP1-Box6 mutation diminishes binding of eIF5 and eIF2 to the NIP1-NTD in vivo.	bind
14081	1	5186	7	NULL	NULL	0	NULL	 eIF5	NULL		bind	NULL				NIP1	NULL		NTD		NULL	in vivo	0	NULL	NULL	NULL	gw70_molcellbiol_24_21_9437_s_261	15485912	(D) The  NIP1-Box6 mutation diminishes binding of eIF5 and eIF2 to the NIP1-NTD in vivo.	bind
14082	2	5186	7	NULL	NULL	0	NULL	eIF2	NULL		bind	NULL				NIP1	NULL		NTD		NULL	in vivo	0	NULL	NULL	NULL	gw70_molcellbiol_24_21_9437_s_261	15485912	(D) The  NIP1-Box6 mutation diminishes binding of eIF5 and eIF2 to the NIP1-NTD in vivo.	bind
14083	3	5186	7	10	NULL	0	NULL	NIP1	NULL	mutant	diminishes	NULL		Box6		statement 1	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9437_s_261	15485912	(D) The  NIP1-Box6 mutation diminishes binding of eIF5 and eIF2 to the NIP1-NTD in vivo.	bind
14084	4	5186	7	10	NULL	0	NULL	NIP1	NULL	mutant	diminishes	NULL		Box6		statement 2	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9437_s_261	15485912	(D) The  NIP1-Box6 mutation diminishes binding of eIF5 and eIF2 to the NIP1-NTD in vivo.	bind
13994	1	5187	6	NULL	NULL	NULL	NULL	38 kDa protein	GP		bind					GST - BRCA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_88_2_265_s_134	9008167	(D) The 38 kDa protein bound to GST - BRCA1  #4 is a product of the human cell extract and can be  reimmunoprecipitated with Rad51 antiserum.	bind
13995	2	5187	6	NULL	NULL	NULL	NULL	38 kDa protein	GP		is a product of					cell extract	OrganismPart	human			NULL		NULL	NULL	NULL	NULL	gw60_cell_88_2_265_s_134	9008167	(D) The 38 kDa protein bound to GST - BRCA1  #4 is a product of the human cell extract and can be  reimmunoprecipitated with Rad51 antiserum.	bind
13996	3	5187	6	NULL	NULL	NULL	NULL	38 kDa protein	GP		reimmunoprecipitates with					Rad51 antiserum	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_88_2_265_s_134	9008167	(D) The 38 kDa protein bound to GST - BRCA1  #4 is a product of the human cell extract and can be  reimmunoprecipitated with Rad51 antiserum.	bind
14103	1	5187	7	10	NULL	0	NULL	38 kDa protein	NULL		bind	NULL				GST - BRCA1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_88_2_265_s_134	9008167	(D) The 38 kDa protein bound to GST - BRCA1  #4 is a product of the human cell extract and can be  reimmunoprecipitated with Rad51 antiserum.	bind
53056	2	5187	7	10	NULL	0	NULL	38 kDa protein	NULL		is a product of	NULL				cell extract	NULL	human			NULL		0	NULL	NULL	NULL	gw60_cell_88_2_265_s_134	9008167	(D) The 38 kDa protein bound to GST - BRCA1  #4 is a product of the human cell extract and can be  reimmunoprecipitated with Rad51 antiserum.	bind
53057	2	5187	7	10	NULL	0	NULL	38 kDa protein	NULL		reimmunoprecipitates with\t	NULL				Rad51 antiserum	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_88_2_265_s_134	9008167	(D) The 38 kDa protein bound to GST - BRCA1  #4 is a product of the human cell extract and can be  reimmunoprecipitated with Rad51 antiserum.	bind
13997	1	5188	6	NULL	NULL	NULL	NULL	Arp2/3	GP		bind					GST-VCA	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_6_1299_s_78	10995436	(D) The ability of HT-WG (2 muM) to inhibit the binding of Arp2/3 (0.1 muM) to GST-VCA (0.2 muM) was tested in the presence of GTPgammaS-loaded Cdc42 (5 muM) or PI(4,5)P2-containing vesicles (100 muM; PI(4,5)P2/PI/PC = 10:45:45).	bind
13998	2	5188	6	NULL	NULL	NULL	NULL	HT-WG	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_6_1299_s_78	10995436	(D) The ability of HT-WG (2 muM) to inhibit the binding of Arp2/3 (0.1 muM) to GST-VCA (0.2 muM) was tested in the presence of GTPgammaS-loaded Cdc42 (5 muM) or PI(4,5)P2-containing vesicles (100 muM; PI(4,5)P2/PI/PC = 10:45:45).	bind
14104	1	5188	7	NULL	NULL	0	NULL	Arp2/3	NULL		bind	NULL				GST-VCA	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_150_6_1299_s_78	10995436	(D) The ability of HT-WG (2 muM) to inhibit the binding of Arp2/3 (0.1 muM) to GST-VCA (0.2 muM) was tested in the presence of GTPgammaS-loaded Cdc42 (5 muM) or PI(4,5)P2-containing vesicles (100 muM; PI(4,5)P2/PI/PC = 10:45:45).	bind
14105	2	5188	7	NULL	NULL	0	NULL	HT-WG	NULL		inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_150_6_1299_s_78	10995436	(D) The ability of HT-WG (2 muM) to inhibit the binding of Arp2/3 (0.1 muM) to GST-VCA (0.2 muM) was tested in the presence of GTPgammaS-loaded Cdc42 (5 muM) or PI(4,5)P2-containing vesicles (100 muM; PI(4,5)P2/PI/PC = 10:45:45).	bind
14001	1	5189	6	NULL	NULL	NULL	NULL	His6-Ap-uch			bind					proteasome	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_1_115_s_174	9094720	(D) The binding of His6-Ap-uch to the proteasome  reaches saturation.	bind
14106	1	5189	7	NULL	NULL	0	NULL	His6-Ap-uch 	NULL		bind	NULL				proteasome	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_89_1_115_s_174	9094720	(D) The binding of His6-Ap-uch to the proteasome  reaches saturation.	bind
14002	1	5190	6	NULL	NULL	NULL	NULL	p27	GP		bind					cyclin A-cdk2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_13_6058_s_208	15199159	(D) The binding of p27 to cyclin A-cdk2  and skp2 is compromised by the ck( - ) mutation.	bind
14003	2	5190	6	NULL	NULL	NULL	NULL	p27	GP		bind					skp2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_13_6058_s_208	15199159	(D) The binding of p27 to cyclin A-cdk2  and skp2 is compromised by the ck( - ) mutation.	bind
14004	3	5190	6	NULL	NULL	NULL	NULL	statement 1	Process		is compromised by					ck	GP	mutation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_13_6058_s_208	15199159	(D) The binding of p27 to cyclin A-cdk2  and skp2 is compromised by the ck( - ) mutation.	bind
14005	4	5190	6	NULL	NULL	NULL	NULL	statement 2	Process		is compromised by					ck	GP	mutation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_13_6058_s_208	15199159	(D) The binding of p27 to cyclin A-cdk2  and skp2 is compromised by the ck( - ) mutation.	bind
14107	1	5190	7	NULL	NULL	0	NULL	p27	NULL		bind	NULL				cyclin A-cdk2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_13_6058_s_208	15199159	(D) The binding of p27 to cyclin A-cdk2  and skp2 is compromised by the ck( - ) mutation.	bind
14108	2	5190	7	NULL	NULL	0	NULL	p27	NULL		bind	NULL				 skp2 	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_13_6058_s_208	15199159	(D) The binding of p27 to cyclin A-cdk2  and skp2 is compromised by the ck( - ) mutation.	bind
14109	3	5190	7	10	NULL	0	NULL	statement 1	NULL		is compromised by	NULL				ck	NULL	mutation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_13_6058_s_208	15199159	(D) The binding of p27 to cyclin A-cdk2  and skp2 is compromised by the ck( - ) mutation.	bind
14110	4	5190	7	10	NULL	0	NULL	statement 2	NULL		is compromised by	NULL				ck	NULL	mutation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_13_6058_s_208	15199159	(D) The binding of p27 to cyclin A-cdk2  and skp2 is compromised by the ck( - ) mutation.	bind
14006	1	5191	6	NULL	NULL	NULL	NULL	ss-affixin	GP	T7-tagged	bind					ILK	GP	FLAG tagged;;point mutants			NULL	COS-7 cells	NULL	NULL	NULL	NULL	gw60_cellbiol_153_6_1251_s_147	11402068	(D) The binding of T7-tagged ss-affixin with Flag-tagged ILK point mutants was examined by immunoprecipitation assays in COS-7 cells.	bind
14111	1	5191	7	10	NULL	0	NULL	ss-affixin	NULL	T7-tagged 	bind	NULL				ILK	NULL	Flag-tagged;;point mutant			NULL	COS-7 cells	NULL	NULL	NULL	NULL	gw60_cellbiol_153_6_1251_s_147	11402068	(D) The binding of T7-tagged ss-affixin with Flag-tagged ILK point mutants was examined by immunoprecipitation assays in COS-7 cells.	bind
14007	1	5192	6	NULL	NULL	NULL	NULL	Comm 	GP	variants	coimmunoprecipates with					Robo	GP				NULL	S2 cells	NULL	NULL	NULL	NULL	gw60_neuron_35_3_447_s_162	12165468	(D) The Comm variants that cannot bind DNedd4 or are not ubiquitinated still coimmunoprecipitate with Robo in S2 cells.	bind
14008	2	5192	6	NULL	NULL	NULL	NULL	Comm 	GP	variants	does not bind					DNedd4	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_35_3_447_s_162	12165468	(D) The Comm variants that cannot bind DNedd4 or are not ubiquitinated still coimmunoprecipitate with Robo in S2 cells.	bind
14009	3	5192	6	NULL	NULL	NULL	NULL	Comm 	GP	variants	is not					ubiquitinated					NULL		NULL	NULL	NULL	NULL	gw60_neuron_35_3_447_s_162	12165468	(D) The Comm variants that cannot bind DNedd4 or are not ubiquitinated still coimmunoprecipitate with Robo in S2 cells.	bind
14112	1	5192	7	NULL	NULL	0	NULL	Comm 	NULL	variants of	does not bind	NULL				DNedd4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_35_3_447_s_162	12165468	(D) The Comm variants that cannot bind DNedd4 or are not ubiquitinated still coimmunoprecipitate with Robo in S2 cells.	bind
14113	2	5192	7	NULL	NULL	0	NULL	Comm 	NULL	variants of	is not	NULL				ubiquitinated	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_35_3_447_s_162	12165468	(D) The Comm variants that cannot bind DNedd4 or are not ubiquitinated still coimmunoprecipitate with Robo in S2 cells.	bind
14121	3	5192	7	10	NULL	0	NULL	 Comm	NULL	variants of	coimmunoprecipitate with	NULL				Robo	NULL				NULL	S2 cells	NULL	NULL	NULL	NULL	gw60_neuron_35_3_447_s_162	12165468	(D) The Comm variants that cannot bind DNedd4 or are not ubiquitinated still coimmunoprecipitate with Robo in S2 cells.	bind
14010	1	5193	6	NULL	NULL	NULL	NULL	Daxx	GP		bind			COOH terminus		p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_1_322_s_126	12482984	(D) The COOH terminus of Daxx binds to p53.	bind
14120	1	5193	7	NULL	NULL	0	NULL	Daxx	NULL		binds	NULL		COOH terminus		p53	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_1_322_s_126	12482984	(D) The COOH terminus of Daxx binds to p53.	bind
14011	1	5194	6	NULL	NULL	NULL	NULL	depolarization	Process		occurs in response to					cAMP pulse					NULL		NULL	NULL	NULL	NULL	gw60_neuron_36_3_451_s_186	12408847	(D) The depolarization (bottom, solid black trace) in response to a 250 nM cAMP pulse (upper, solid black trace) is due to an accumulation of channels in the open, cAMP-bound state (AO, solid red lines).	bind
14012	2	5194	6	NULL	NULL	NULL	NULL	channels	CellComponent		accumulate in					cAMP-bound state	Process	open			NULL		NULL	NULL	NULL	NULL	gw60_neuron_36_3_451_s_186	12408847	(D) The depolarization (bottom, solid black trace) in response to a 250 nM cAMP pulse (upper, solid black trace) is due to an accumulation of channels in the open, cAMP-bound state (AO, solid red lines).	bind
14013	3	5194	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs due to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_36_3_451_s_186	12408847	(D) The depolarization (bottom, solid black trace) in response to a 250 nM cAMP pulse (upper, solid black trace) is due to an accumulation of channels in the open, cAMP-bound state (AO, solid red lines).	bind
15473	1	5194	7	NULL	NULL	0	NULL	Depolarization	NULL		in response to	NULL				cAMP pulse	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_36_3_451_s_186	12408847	(D) The depolarization (bottom, solid black trace) in response to a 250 nM cAMP pulse (upper, solid black trace) is due to an accumulation of channels in the open, cAMP-bound state (AO, solid red lines).	bind
15474	2	5194	7	NULL	NULL	0	NULL	channels	NULL		accumulate in	NULL				 cAMP-bound state 	NULL	open			NULL		NULL	NULL	NULL	NULL	gw60_neuron_36_3_451_s_186	12408847	(D) The depolarization (bottom, solid black trace) in response to a 250 nM cAMP pulse (upper, solid black trace) is due to an accumulation of channels in the open, cAMP-bound state (AO, solid red lines).	bind
19031	3	5194	7	NULL	NULL	0	NULL	statement 1	NULL		due to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_36_3_451_s_186	12408847	(D) The depolarization (bottom, solid black trace) in response to a 250 nM cAMP pulse (upper, solid black trace) is due to an accumulation of channels in the open, cAMP-bound state (AO, solid red lines).	bind
14014	1	5195	6	NULL	NULL	NULL	NULL				does not bind		cooperatively	E7R		TBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_2_397_s_200	12191484	(D) The E7R, E22R POU domain does not cooperatively bind with TBP.	bind
14015	2	5195	6	NULL	NULL	NULL	NULL				does not bind		cooperatively	E22R POU domain		TBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_2_397_s_200	12191484	(D) The E7R, E22R POU domain does not cooperatively bind with TBP.	bind
14122	1	5195	7	10	NULL	0	NULL		NULL		does not bind	NULL	cooperatively	 E7R		TBP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_2_397_s_200	12191484	(D) The E7R, E22R POU domain does not cooperatively bind with TBP.	bind
14123	2	5195	7	10	NULL	0	NULL		NULL		does not bind	NULL	cooperatively	E22R POU domain		TBP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_2_397_s_200	12191484	(D) The E7R, E22R POU domain does not cooperatively bind with TBP.	bind
14016	1	5196	6	NULL	NULL	NULL	NULL	tetrameric IP3 receptor 	GP		bind			four subunits		IP3	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_7_510_s_52	9210378	(d) The Hill coefficients derived from the curves shown in (c) suggest that three and possibly all four subunits of the tetrameric IP3 receptor must bind IP3 before the channel can open and release Ca2+ into the cytosol.	bind
14017	2	5196	6	NULL	NULL	NULL	NULL	channel	CellComponent	open	release					Ca+2 	Chemical				NULL	cytosol	NULL	NULL	NULL	NULL	gw60_currbiol_7_7_510_s_52	9210378	(d) The Hill coefficients derived from the curves shown in (c) suggest that three and possibly all four subunits of the tetrameric IP3 receptor must bind IP3 before the channel can open and release Ca2+ into the cytosol.	bind
14018	3	5196	6	NULL	NULL	NULL	NULL	statement 1	Process		occur before		must			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_7_510_s_52	9210378	(d) The Hill coefficients derived from the curves shown in (c) suggest that three and possibly all four subunits of the tetrameric IP3 receptor must bind IP3 before the channel can open and release Ca2+ into the cytosol.	bind
14124	1	5196	7	10	NULL	0	NULL	tetrameric IP3 receptor	NULL		bind	NULL		four subunits		IP3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_7_510_s_52	9210378	(d) The Hill coefficients derived from the curves shown in (c) suggest that three and possibly all four subunits of the tetrameric IP3 receptor must bind IP3 before the channel can open and release Ca2+ into the cytosol.	bind
14125	2	5196	7	NULL	NULL	0	NULL	channel	NULL	open	release	NULL				Ca2+	NULL				NULL	cytosol	NULL	NULL	NULL	NULL	gw60_currbiol_7_7_510_s_52	9210378	(d) The Hill coefficients derived from the curves shown in (c) suggest that three and possibly all four subunits of the tetrameric IP3 receptor must bind IP3 before the channel can open and release Ca2+ into the cytosol.	bind
14126	3	5196	7	10	NULL	0	NULL	statement 1	NULL		occur before	NULL	must 			statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_7_510_s_52	9210378	(d) The Hill coefficients derived from the curves shown in (c) suggest that three and possibly all four subunits of the tetrameric IP3 receptor must bind IP3 before the channel can open and release Ca2+ into the cytosol.	bind
14019	1	5197	6	NULL	NULL	NULL	NULL	Egr protein	GP		bind					nuclear proteins	GP	mouse;; hippocampus			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10286_s_213	16287845	(D) The mutation within E2m1 completely abrogated Egr protein  binding with nuclear proteins obtained from seized mouse hippocampus.	bind
14020	2	5197	6	NULL	NULL	NULL	NULL	E2m1	GP	mutant	abrogates		completely			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10286_s_213	16287845	(D) The mutation within E2m1 completely abrogated Egr protein  binding with nuclear proteins obtained from seized mouse hippocampus.	bind
14128	1	5197	7	10	NULL	0	NULL	Egr protein 	NULL		bind	NULL				nuclear proteins	NULL	mouse;;hippocampus			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10286_s_213	16287845	(D) The mutation within E2m1 completely abrogated Egr protein  binding with nuclear proteins obtained from seized mouse hippocampus.	bind
14129	2	5197	7	10	NULL	0	NULL	E2m1	NULL	mutant	abrogates	NULL	completely			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10286_s_213	16287845	(D) The mutation within E2m1 completely abrogated Egr protein  binding with nuclear proteins obtained from seized mouse hippocampus.	bind
14021	1	5198	6	NULL	NULL	NULL	NULL	FRS2 protein	GP		bind			PTB domain		TrkA	GP		NPQ pY sequence		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_979_s_246	10629055	(D) The PTB domains of FRS2 proteins bind to the NPQ pY sequence of TrkA.	bind
14130	1	5198	7	NULL	NULL	0	NULL	 FRS2 protein	NULL		bind	NULL		PTB domain		TrkA	NULL		NPQ pY sequence 		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_3_979_s_246	10629055	(D) The PTB domains of FRS2 proteins bind to the NPQ pY sequence of TrkA.	bind
14022	1	5199	6	NULL	NULL	NULL	NULL	B-Raf	GP		bind					GST-Rb	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_140	15485920	(D) The Raf-1 peptide is unable to disrupt the binding of  B-Raf to GST-Rb and GST-MEK1 in vitro.	bind
14023	2	5199	6	NULL	NULL	NULL	NULL	B-Raf	GP		bind					GST-MEK1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_140	15485920	(D) The Raf-1 peptide is unable to disrupt the binding of  B-Raf to GST-Rb and GST-MEK1 in vitro.	bind
14024	3	5199	6	NULL	NULL	NULL	NULL	Raf-1 peptide	GP		does not disrupt					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_140	15485920	(D) The Raf-1 peptide is unable to disrupt the binding of  B-Raf to GST-Rb and GST-MEK1 in vitro.	bind
14025	4	5199	6	NULL	NULL	NULL	NULL	Raf-1 peptide	GP		does not disrupt					statement 2	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_140	15485920	(D) The Raf-1 peptide is unable to disrupt the binding of  B-Raf to GST-Rb and GST-MEK1 in vitro.	bind
14131	1	5199	7	NULL	NULL	0	NULL	B-Raf 	NULL		bind	NULL				GST-Rb	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_140	15485920	(D) The Raf-1 peptide is unable to disrupt the binding of  B-Raf to GST-Rb and GST-MEK1 in vitro.	bind
14132	2	5199	7	NULL	NULL	0	NULL	B-Raf 	NULL		bind	NULL				GST-MEK1	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_140	15485920	(D) The Raf-1 peptide is unable to disrupt the binding of  B-Raf to GST-Rb and GST-MEK1 in vitro.	bind
14133	3	5199	7	10	NULL	0	NULL	Raf-1 peptide	NULL		does not disrupt	NULL				statement 1	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_140	15485920	(D) The Raf-1 peptide is unable to disrupt the binding of  B-Raf to GST-Rb and GST-MEK1 in vitro.	bind
14134	4	5199	7	10	NULL	0	NULL	Raf-1 peptide	NULL		does not disrupt	NULL				statement 2	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_140	15485920	(D) The Raf-1 peptide is unable to disrupt the binding of  B-Raf to GST-Rb and GST-MEK1 in vitro.	bind
14026	1	5200	6	NULL	NULL	NULL	NULL	Rip11	GP		bind			C2 domain		PC/PE liposomes	CellComponent	neutral			NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1437_s_50	11163216	(D) The Rip11 C2 domain binds to neutral PC/PE liposomes in a Mg2+-dependent manner.	bind
14027	2	5200	6	NULL	NULL	NULL	NULL	statement 1	Process		is dependent on					Mg+2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1437_s_50	11163216	(D) The Rip11 C2 domain binds to neutral PC/PE liposomes in a Mg2+-dependent manner.	bind
14135	1	5200	7	NULL	NULL	0	NULL	Rip 11	NULL		binds	NULL		C2 domain		PC/PE liposomes 	NULL	neutral			NULL		0	NULL	NULL	NULL	gw60_molcell_6_6_1437_s_50	11163216	(D) The Rip11 C2 domain binds to neutral PC/PE liposomes in a Mg2+-dependent manner.	bind
14136	2	5200	7	NULL	NULL	0	NULL	statement 1	NULL		depends on	NULL				Mg2+	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_6_6_1437_s_50	11163216	(D) The Rip11 C2 domain binds to neutral PC/PE liposomes in a Mg2+-dependent manner.	bind
14028	1	5201	6	NULL	NULL	NULL	NULL	Rs-Lys2 transcripts	GP		bind		strongly			Rs-Lys2 probe	NucleicAcid	antisense			NULL		NULL	NULL	NULL	NULL	gw70_insectbiochemmolbiol_32_12_1615_s_197	12429113	(D) The Rs-Lys2 transcripts bound strongly to the antisense  Rs-Lys2 probe.	bind
14137	1	5201	7	NULL	NULL	0	NULL	 Rs-Lys2 transcripts	NULL		bind	NULL	strongly			Rs-Lys2 probe	NULL	antisense			NULL		NULL	NULL	NULL	NULL	gw70_insectbiochemmolbiol_32_12_1615_s_197	12429113	(D) The Rs-Lys2 transcripts bound strongly to the antisense  Rs-Lys2 probe.	bind
14029	1	5203	6	NULL	NULL	NULL	NULL	PAI-2	GP		bind			RSL mutant		Rb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_155	12944478	(D) The RSL mutant of PAI-2 retains binding to Rb. Input IVT PAI-2 (lane 3, top panel), a C-D interhelical deletion mutant of PAI-2 (C-D PAI-2) (middle panel), or the RSL mutant of PAI-2 (PAI-2Ala380) was incubated with GST-Rb379-928.	bind
14138	1	5203	7	NULL	NULL	0	NULL	PAI-2	NULL		bind	NULL		RSL mutant 		Rb	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_155	12944478	(D) The RSL mutant of PAI-2 retains binding to Rb. Input IVT PAI-2 (lane 3, top panel), a C-D interhelical deletion mutant of PAI-2 (C-D PAI-2) (middle panel), or the RSL mutant of PAI-2 (PAI-2Ala380) was incubated with GST-Rb379-928.	bind
14030	1	5204	6	NULL	NULL	NULL	NULL	FAK protein	GP		bind					GEX-p85	GP	full-length			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_20_7015_s_121	12242282	(D) The same total cell lysates were also subjected to GST pull-down (PD) assay by using GST fusion protein with full-length p85 (GEX-p85), and the FAK proteins bound to GEX-p85 were detected by immunoblotting with anti-HA antibody.	bind
14139	1	5204	7	NULL	NULL	0	NULL	FAK protein	NULL		bind	NULL				GEX-p85	NULL	full-length			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_20_7015_s_121	12242282	(D) The same total cell lysates were also subjected to GST pull-down (PD) assay by using GST fusion protein with full-length p85 (GEX-p85), and the FAK proteins bound to GEX-p85 were detected by immunoblotting with anti-HA antibody.	bind
14031	1	5205	6	NULL	NULL	NULL	NULL	SAP90	GP		bind			SH3 domain		H6KA2	GP		proline-rich sequences		NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_4_727_s_118	9808460	(D) The SAP90 SH3 domain binds to both proline-rich sequences present in H6KA2(c-term).	bind
14140	1	5205	7	NULL	NULL	0	NULL	SAP90	NULL		binds	NULL		SH3 domain		 H6KA2	NULL		proline-rich sequence in c-term		NULL		0	NULL	NULL	NULL	gw60_neuron_21_4_727_s_118	9808460	(D) The SAP90 SH3 domain binds to both proline-rich sequences present in H6KA2(c-term).	bind
14032	1	5206	6	NULL	NULL	NULL	NULL	Pax2	GP		bind									sequence A5	NULL		NULL	NULL	NULL	NULL	gw70_development_130_13_2903_s_79	12756174	(D) The specificity of Pax2 and Pax6 binding to sequence A5 (lane 1 and 4, -ab) is  confirmed by the addition of anti-Pax2 antibody (lane 2, +P2-ab) and anti-Pax6 antibody  (lane 5, +P6-ab), which inhibits the formation of the complex.	bind
14033	2	5206	6	NULL	NULL	NULL	NULL	Pax6	GP		bind									sequence A5	NULL		NULL	NULL	NULL	NULL	gw70_development_130_13_2903_s_79	12756174	(D) The specificity of Pax2 and Pax6 binding to sequence A5 (lane 1 and 4, -ab) is  confirmed by the addition of anti-Pax2 antibody (lane 2, +P2-ab) and anti-Pax6 antibody  (lane 5, +P6-ab), which inhibits the formation of the complex.	bind
14141	1	5206	7	NULL	NULL	0	NULL	Pax2	NULL		bind	NULL					NULL			sequence A5	NULL		NULL	NULL	NULL	NULL	gw70_development_130_13_2903_s_79	12756174	(D) The specificity of Pax2 and Pax6 binding to sequence A5 (lane 1 and 4, -ab) is  confirmed by the addition of anti-Pax2 antibody (lane 2, +P2-ab) and anti-Pax6 antibody  (lane 5, +P6-ab), which inhibits the formation of the complex.	bind
14142	2	5206	7	NULL	NULL	0	NULL	Pax6 	NULL		bind	NULL					NULL			sequence A5	NULL		NULL	NULL	NULL	NULL	gw70_development_130_13_2903_s_79	12756174	(D) The specificity of Pax2 and Pax6 binding to sequence A5 (lane 1 and 4, -ab) is  confirmed by the addition of anti-Pax2 antibody (lane 2, +P2-ab) and anti-Pax6 antibody  (lane 5, +P6-ab), which inhibits the formation of the complex.	bind
14034	1	5209	6	NULL	NULL	NULL	NULL	carcinoma cells	Cell		carries					CD40	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9806_s_303	16260598	(D) TRAF6 and TRAF2 do not coimmunoprecipitate in  CD40L-stimulated carcinoma cells carrying a mutated CD40 that does not directly bind  TRAF2/TRAF3.	bind
14035	2	5209	6	NULL	NULL	NULL	NULL	TRAF2	GP		does not coimmunoprecipitate in					statement 1	Process	CD40L-stimulated			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9806_s_303	16260598	(D) TRAF6 and TRAF2 do not coimmunoprecipitate in  CD40L-stimulated carcinoma cells carrying a mutated CD40 that does not directly bind  TRAF2/TRAF3.	bind
14095	3	5209	6	NULL	NULL	NULL	NULL	TRAF6	GP		does not coimmuprecipitate in					statement 1	Process	CD40L-stimulated			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9806_s_303	16260598	(D) TRAF6 and TRAF2 do not coimmunoprecipitate in  CD40L-stimulated carcinoma cells carrying a mutated CD40 that does not directly bind  TRAF2/TRAF3.	bind
14096	4	5209	6	NULL	NULL	NULL	NULL	CD40	GP	mutant	does not bind		directly			TRAF2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9806_s_303	16260598	(D) TRAF6 and TRAF2 do not coimmunoprecipitate in  CD40L-stimulated carcinoma cells carrying a mutated CD40 that does not directly bind  TRAF2/TRAF3.	bind
14097	5	5209	6	NULL	NULL	NULL	NULL	CD40	GP	mutant	does not bind		directly			TRAF3	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9806_s_303	16260598	(D) TRAF6 and TRAF2 do not coimmunoprecipitate in  CD40L-stimulated carcinoma cells carrying a mutated CD40 that does not directly bind  TRAF2/TRAF3.	bind
14143	1	5209	7	NULL	NULL	0	NULL	CD40	NULL	mutated	does not bind	NULL	directly			TRAF2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9806_s_303	16260598	(D) TRAF6 and TRAF2 do not coimmunoprecipitate in  CD40L-stimulated carcinoma cells carrying a mutated CD40 that does not directly bind  TRAF2/TRAF3.	bind
15583	2	5209	7	NULL	NULL	0	NULL	CD40	NULL	mutated	does not bind	NULL	directly			TRAF3	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_22_9806_s_303	16260598	(D) TRAF6 and TRAF2 do not coimmunoprecipitate in  CD40L-stimulated carcinoma cells carrying a mutated CD40 that does not directly bind  TRAF2/TRAF3.	bind
15584	3	5209	7	10	NULL	0	NULL	 TRAF6 	NULL		does not coimmunoprecipitate in	NULL				carcinoma cells	NULL	CD40L-stimulated 			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9806_s_303	16260598	(D) TRAF6 and TRAF2 do not coimmunoprecipitate in  CD40L-stimulated carcinoma cells carrying a mutated CD40 that does not directly bind  TRAF2/TRAF3.	bind
15585	4	5209	7	10	NULL	0	NULL	TRAF2	NULL		does not coimmunoprecipitate in	NULL				carcinoma cells	NULL	CD40L-stimulated			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9806_s_303	16260598	(D) TRAF6 and TRAF2 do not coimmunoprecipitate in  CD40L-stimulated carcinoma cells carrying a mutated CD40 that does not directly bind  TRAF2/TRAF3.	bind
15586	5	5209	7	10	NULL	0	NULL	carcinoma cells	NULL		carries	NULL				CD40	NULL	mutated			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9806_s_303	16260598	(D) TRAF6 and TRAF2 do not coimmunoprecipitate in  CD40L-stimulated carcinoma cells carrying a mutated CD40 that does not directly bind  TRAF2/TRAF3.	bind
14036	1	5210	6	NULL	NULL	NULL	NULL	Cd3	GP		bind					Nck	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_210	12110186	(D) Transduction of antibody APA1/1 interferes with CD3  binding to Nck. Human PBMC were either mock-transduced or transduced with APA1/1 before stimulation with UCHT1.	bind
14037	2	5210	6	NULL	NULL	NULL	NULL	antibody APA1/1	GP		interferes with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_210	12110186	(D) Transduction of antibody APA1/1 interferes with CD3  binding to Nck. Human PBMC were either mock-transduced or transduced with APA1/1 before stimulation with UCHT1.	bind
14147	1	5210	7	NULL	NULL	0	NULL	CD3 	NULL		bind	NULL				Nck	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_109_7_901_s_210	12110186	(D) Transduction of antibody APA1/1 interferes with CD3  binding to Nck. Human PBMC were either mock-transduced or transduced with APA1/1 before stimulation with UCHT1.	bind
14148	2	5210	7	NULL	NULL	0	NULL	antibody APA1/1	NULL		interferes with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_109_7_901_s_210	12110186	(D) Transduction of antibody APA1/1 interferes with CD3  binding to Nck. Human PBMC were either mock-transduced or transduced with APA1/1 before stimulation with UCHT1.	bind
14038	1	5212	6	NULL	NULL	0	NULL	TRIKA1 (Ubc13/Uev1A)	NULL		is 	NULL				E2	NULL	specific			NULL		0	NULL	NULL	NULL	gw60_cell_103_2_351_s_139	11057907	(D) TRIKA1 (Ubc13/Uev1A) is a specific E2 that activates IKK in conjunction with TRAF6.	bind
14039	2	5212	6	NULL	NULL	NULL	NULL	statement 1	Process		activates					IKK	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_351_s_139	11057907	(D) TRIKA1 (Ubc13/Uev1A) is a specific E2 that activates IKK in conjunction with TRAF6.	bind
14040	3	5212	6	NULL	NULL	NULL	NULL	TRAF6	GP		activates					IKK	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_351_s_139	11057907	(D) TRIKA1 (Ubc13/Uev1A) is a specific E2 that activates IKK in conjunction with TRAF6.	bind
19014	4	5212	6	NULL	NULL	NULL	NULL	statement 2	Process		occurs in conjunction with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_351_s_139	11057907	(D) TRIKA1 (Ubc13/Uev1A) is a specific E2 that activates IKK in conjunction with TRAF6.	bind
14151	1	5212	7	NULL	NULL	0	NULL	TRIKA1(Ubc13/Uev1A) 	NULL		activates	NULL				IKK 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_351_s_139	11057907	(D) TRIKA1 (Ubc13/Uev1A) is a specific E2 that activates IKK in conjunction with TRAF6.	bind
14152	2	5212	7	NULL	NULL	0	NULL	TRAF6	NULL		activates	NULL				IKK	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_103_2_351_s_139	11057907	(D) TRIKA1 (Ubc13/Uev1A) is a specific E2 that activates IKK in conjunction with TRAF6.	bind
14153	3	5212	7	NULL	NULL	0	NULL	statement 1	NULL		occurs in conjunction with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_103_2_351_s_139	11057907	(D) TRIKA1 (Ubc13/Uev1A) is a specific E2 that activates IKK in conjunction with TRAF6.	bind
14154	4	5212	7	10	NULL	0	NULL	TRIKA1(Ubc13/Uev1A)	NULL		is	NULL				E2	NULL	specific			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_351_s_139	11057907	(D) TRIKA1 (Ubc13/Uev1A) is a specific E2 that activates IKK in conjunction with TRAF6.	bind
14041	1	5213	6	NULL	NULL	NULL	NULL	TrkA	GP		bind		specifically			Kalirin	GP		N-terminal PH domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_5106_s_283	15923627	(D) TrkA binds specifically to the N-terminal  PH domains of Kalirin and Trio.	bind
14042	2	5213	6	NULL	NULL	NULL	NULL	TrkA	GP		bind		specifically			Trio	GP		N-terminal PH domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_5106_s_283	15923627	(D) TrkA binds specifically to the N-terminal  PH domains of Kalirin and Trio.	bind
14155	1	5213	7	NULL	NULL	0	NULL	TrkA	NULL		binds	NULL	specifically			Kalirin	NULL		N-terminal PH domain		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_12_5106_s_283	15923627	(D) TrkA binds specifically to the N-terminal  PH domains of Kalirin and Trio.	bind
14156	2	5213	7	NULL	NULL	0	NULL	TrkA	NULL		bind	NULL	specifically			Trio	NULL		N-terminal PH domain		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_12_5106_s_283	15923627	(D) TrkA binds specifically to the N-terminal  PH domains of Kalirin and Trio.	bind
14043	1	5214	6	NULL	NULL	NULL	NULL	SUV39H1	GP		bind					HP1alpha	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_7_2525_s_355	15767660	(D) TSA did not affect the in vivo binding  of SUV39H1 to HP1alpha as determined by coimmunoprecipitation.	bind
14044	2	5214	6	NULL	NULL	NULL	NULL	TSA	Chemical		did not affect					statement 1	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_7_2525_s_355	15767660	(D) TSA did not affect the in vivo binding  of SUV39H1 to HP1alpha as determined by coimmunoprecipitation.	bind
14157	1	5214	7	NULL	NULL	0	NULL	SUV39H1	NULL		bind	NULL				HP1alpha	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw70_molcellbiol_25_7_2525_s_355	15767660	(D) TSA did not affect the in vivo binding  of SUV39H1 to HP1alpha as determined by coimmunoprecipitation.	bind
14158	2	5214	7	10	NULL	0	NULL	TSA	NULL		does not affect	NULL				statement 1	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_7_2525_s_355	15767660	(D) TSA did not affect the in vivo binding  of SUV39H1 to HP1alpha as determined by coimmunoprecipitation.	bind
14045	1	5215	6	NULL	NULL	NULL	NULL	VCP	GP		bind					(Ub)2-7 chains					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6469_s_388	12944474	(D) VCP binds to (Ub)2-7 chains more weakly than ataxin-3.	bind
14046	2	5215	6	NULL	NULL	NULL	NULL	ataxin-3	GP		bind					(Ub)2-7 chains					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6469_s_388	12944474	(D) VCP binds to (Ub)2-7 chains more weakly than ataxin-3.	bind
14047	3	5215	6	NULL	NULL	NULL	NULL	statement 1	Process		is weaker than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6469_s_388	12944474	(D) VCP binds to (Ub)2-7 chains more weakly than ataxin-3.	bind
14159	1	5215	7	10	NULL	0	NULL	VCP	NULL		binds	NULL				(Ub)2-7 chains	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6469_s_388	12944474	(D) VCP binds to (Ub)2-7 chains more weakly than ataxin-3.	bind
14160	2	5215	7	10	NULL	0	NULL	ataxin-3	NULL		binds	NULL				(Ub)2-7 chains	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6469_s_388	12944474	(D) VCP binds to (Ub)2-7 chains more weakly than ataxin-3.	bind
14161	3	5215	7	NULL	NULL	0	NULL	statement 1	NULL		occurs	NULL				statement 2	NULL	more weakly than			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6469_s_388	12944474	(D) VCP binds to (Ub)2-7 chains more weakly than ataxin-3.	bind
14048	1	5216	6	NULL	NULL	NULL	NULL	VP16	GP		bind					HCF-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_14_4700_s_279	11416146	(D) VP16 binding to HCF-1 was assayed as described in the legend to Fig.  6.	bind
14162	1	5216	7	NULL	NULL	0	NULL	VP16	NULL		bind	NULL				HCF-1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_14_4700_s_279	11416146	(D) VP16 binding to HCF-1 was assayed as described in the legend to Fig.  6.	bind
14049	1	5217	6	NULL	NULL	NULL	NULL	Vsm1	GP		bind					Sso1	GP	native			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_202	12925750	(D) Vsm1 binds better to native Sso1 than constitutively open mutants.	bind
19015	2	5217	6	NULL	NULL	NULL	NULL	Vsm1	GP		bind					Sso1	GP	constitutively open mutant			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_202	12925750	(D) Vsm1 binds better to native Sso1 than constitutively open mutants.	bind
19016	3	5217	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs better than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_202	12925750	(D) Vsm1 binds better to native Sso1 than constitutively open mutants.	bind
14163	1	5217	7	NULL	NULL	0	NULL	Vsm1	NULL		binds	NULL				Sso1	NULL	native			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_202	12925750	(D) Vsm1 binds better to native Sso1 than constitutively open mutants.	bind
14164	2	5217	7	NULL	NULL	0	NULL	Vsm1	NULL		binds	NULL				Sso1	NULL	constitutively open mutant			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_202	12925750	(D) Vsm1 binds better to native Sso1 than constitutively open mutants.	bind
14165	3	5217	7	NULL	NULL	0	NULL	statement 1	NULL		occurs better than 	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_8_3114_s_202	12925750	(D) Vsm1 binds better to native Sso1 than constitutively open mutants.	bind
14114	1	5220	6	NULL	NULL	NULL	NULL	GCP2	GP		bind					pericentrin A fragment	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_8_3642_s_121	15146056	(D) Yeast two-hybrid data showing binding of GCP2  by a pericentrin A fragment and lack of GCP2 binding by the homologous pericentrin  B fragment as well as mutants lacking a pericentrin B specific exon (see MATERIALS  AND METHODS for details).	bind
14115	2	5220	6	NULL	NULL	NULL	NULL	pericentrin B fragment	GP	homologous	does not bind					GCP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_8_3642_s_121	15146056	(D) Yeast two-hybrid data showing binding of GCP2  by a pericentrin A fragment and lack of GCP2 binding by the homologous pericentrin  B fragment as well as mutants lacking a pericentrin B specific exon (see MATERIALS  AND METHODS for details).	bind
14116	3	5220	6	NULL	NULL	NULL	NULL	eletion	GP	mutant	does not bind				pericentrin B specific exon	GCP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_8_3642_s_121	15146056	(D) Yeast two-hybrid data showing binding of GCP2  by a pericentrin A fragment and lack of GCP2 binding by the homologous pericentrin  B fragment as well as mutants lacking a pericentrin B specific exon (see MATERIALS  AND METHODS for details).	bind
14168	1	5220	7	NULL	NULL	0	NULL	GCP2	NULL		bind	NULL				pericentrin A fragment 	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3642_s_121	15146056	(D) Yeast two-hybrid data showing binding of GCP2  by a pericentrin A fragment and lack of GCP2 binding by the homologous pericentrin  B fragment as well as mutants lacking a pericentrin B specific exon (see MATERIALS  AND METHODS for details).	bind
14169	2	5220	7	NULL	NULL	0	NULL	GCP2	NULL		does not bind	NULL				pericentrin B fragment	NULL	homologous			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3642_s_121	15146056	(D) Yeast two-hybrid data showing binding of GCP2  by a pericentrin A fragment and lack of GCP2 binding by the homologous pericentrin  B fragment as well as mutants lacking a pericentrin B specific exon (see MATERIALS  AND METHODS for details).	bind
14170	3	5220	7	NULL	NULL	0	NULL	GCP2	NULL		does not bind	NULL					NULL	mutant		pericentrin B specific exon	NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_8_3642_s_121	15146056	(D) Yeast two-hybrid data showing binding of GCP2  by a pericentrin A fragment and lack of GCP2 binding by the homologous pericentrin  B fragment as well as mutants lacking a pericentrin B specific exon (see MATERIALS  AND METHODS for details).	bind
14117	1	5221	6	NULL	NULL	NULL	NULL	Smad4	GP	nuclear	bind					DNA	NucleicAcid			SBE	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4494_s_182	12808092	(D) YY1  inhibits binding of nuclear Smad4 to SBE DNA.	bind
14118	2	5221	6	NULL	NULL	NULL	NULL	YY1	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4494_s_182	12808092	(D) YY1  inhibits binding of nuclear Smad4 to SBE DNA.	bind
14171	1	5221	7	NULL	NULL	0	NULL	Smad4	NULL	nuclear	binds	NULL				DNA	NULL			SBE	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_13_4494_s_182	12808092	(D) YY1  inhibits binding of nuclear Smad4 to SBE DNA.	bind
14172	2	5221	7	NULL	NULL	0	NULL	YY1	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_13_4494_s_182	12808092	(D) YY1  inhibits binding of nuclear Smad4 to SBE DNA.	bind
14119	1	5225	6	NULL	NULL	NULL	NULL	sgt1-3 protein	GP		does not bind					Hsc82	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_18_8069_s_233	15340069	(D, top) sgt1-3 protein (sgt1-3p) does  not bind to Hsc82 in vitro.	bind
19017	2	5225	6	NULL	NULL	NULL	NULL	sgt1-3p	GP		is					sgt1-3 protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_18_8069_s_233	15340069	(D, top) sgt1-3 protein (sgt1-3p) does  not bind to Hsc82 in vitro.	bind
14173	1	5225	7	NULL	NULL	0	NULL	sgt1-3p	NULL		does not bind	NULL				Hsc82	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw70_molcellbiol_24_18_8069_s_233	15340069	(D, top) sgt1-3 protein (sgt1-3p) does  not bind to Hsc82 in vitro.	bind
14174	2	5225	7	NULL	NULL	0	NULL	sgt1-3p	NULL		is	NULL				sgt1-3 protein	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_18_8069_s_233	15340069	(D, top) sgt1-3 protein (sgt1-3p) does  not bind to Hsc82 in vitro.	bind
14812	1	5226	6	NULL	NULL	NULL	NULL	Pcl2	GP	chick	downregulates					Shh	GP				NULL	embryos	NULL	NULL	NULL	NULL	gw70_development_131_17_4381_s_188	15294861	(D,F,H,J) Embryos overexpressing chick  Pcl2 show downregulation of  Shh (D) in the node and notochord, of  Nodal (F) and  Pitx2 (H) in the left LPM, and of  Lefty1 (J) in the prospective floor plate.	bind
15475	1	5226	7	NULL	NULL	0	NULL	Pcl2	NULL	chick	downregulates	NULL				Shh	NULL				NULL	embryos	NULL	NULL	NULL	NULL	gw70_development_131_17_4381_s_188	15294861	(D,F,H,J) Embryos overexpressing chick  Pcl2 show downregulation of  Shh (D) in the node and notochord, of  Nodal (F) and  Pitx2 (H) in the left LPM, and of  Lefty1 (J) in the prospective floor plate.	bind
14183	1	5227	6	NULL	NULL	NULL	NULL	ORC	GP		bind		significantly			ars1 DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_13589_s_110	11717425	(dI-dC) also reduced ORC binding to  ars1 DNA significantly (plateauing at  90% inhibition at high levels).	bind
14175	1	5227	7	10	NULL	0	NULL	ORC	NULL		bind	NULL	significantly			 ars1 DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_13589_s_110	11717425	(dI-dC) also reduced ORC binding to  ars1 DNA significantly (plateauing at  90% inhibition at high levels).	bind
14184	1	5228	6	NULL	NULL	NULL	NULL	VAB-1-AP	GP		bind		specifically			VAB-2/EFN-1 expressing cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cell_99_7_781_s_84	10619431	(E - G) VAB-1-AP specifically binds to VAB-2/EFN-1 expressing cells.	bind
14176	1	5228	7	NULL	NULL	0	NULL	VAB-1-AP	NULL		binds	NULL	specifically			VAB-2/EFN-1 expressing cells	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_99_7_781_s_84	10619431	(E - G) VAB-1-AP specifically binds to VAB-2/EFN-1 expressing cells.	bind
14185	1	5230	6	NULL	NULL	NULL	NULL	E.coli	Organism		bind					BEC	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_4_1947_s_143	15784534	(E and F) Binding of  E. coli to human BECs visualized by staining with crystal violet.	bind
14177	1	5230	7	NULL	NULL	0	NULL	E. coli 	NULL		binds	NULL				BECs	NULL	human			NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_4_1947_s_143	15784534	(E and F) Binding of  E. coli to human BECs visualized by staining with crystal violet.	bind
14186	1	5231	6	NULL	NULL	NULL	NULL	C/EBP-alpha	GP		bind					NP-3	GP			promoter sequences	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_322_s_104	9418879	(E and F) Binding of C/EBP-alpha to NP-3 promoter sequences.	bind
14178	1	5231	7	NULL	NULL	0	NULL	C/EBP-alpha	NULL		binds	NULL				NP-3 	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_322_s_104	9418879	(E and F) Binding of C/EBP-alpha to NP-3 promoter sequences.	bind
14813	1	5232	6	NULL	NULL	NULL	NULL	DNase I	GP	purified;;fluorescein labeled	bind					G-actin	GP	unlabeled chicken			NULL		NULL	NULL	NULL	NULL	gw70_devbiol_271_1_59_s_377	15196950	(E and F) Control zygote microinjected  with rhodamine-labeled G-actin at stage 0.1 and with purified fluorescein-labeled  DNase I bound to unlabeled chicken G-actin at stage 0.8.	bind
19018	2	5232	6	NULL	NULL	NULL	NULL	G-actin	GP	rhodamine-labeled	bind					G-actin	GP	unlabeled chicken			NULL		NULL	NULL	NULL	NULL	gw70_devbiol_271_1_59_s_377	15196950	(E and F) Control zygote microinjected  with rhodamine-labeled G-actin at stage 0.1 and with purified fluorescein-labeled  DNase I bound to unlabeled chicken G-actin at stage 0.8.	bind
14179	1	5232	7	NULL	NULL	0	NULL	G-actin 	NULL	rhodamine-labeled	bind	NULL				G-actin	NULL	unlabeled chicken			NULL		0	NULL	NULL	NULL	gw70_devbiol_271_1_59_s_377	15196950	(E and F) Control zygote microinjected  with rhodamine-labeled G-actin at stage 0.1 and with purified fluorescein-labeled  DNase I bound to unlabeled chicken G-actin at stage 0.8.	bind
14180	2	5232	7	10	NULL	0	NULL	DNase I	NULL	purified;;fluorescein-labeled	bind	NULL				G-actin	NULL	unlabeled chicken 			NULL		NULL	NULL	NULL	NULL	gw70_devbiol_271_1_59_s_377	15196950	(E and F) Control zygote microinjected  with rhodamine-labeled G-actin at stage 0.1 and with purified fluorescein-labeled  DNase I bound to unlabeled chicken G-actin at stage 0.8.	bind
14187	1	5234	6	NULL	NULL	NULL	NULL	His-GFP-SsrA protein	GP		bind					SspB	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_75_s_51	12887894	(E and F) Isothermal titration calorimetric studies of His-GFP-SsrA protein binding to SspB (E) and SspB127 (F) reveal dissociation constants of 728 and 695 nM, respectively.	bind
14188	2	5234	6	NULL	NULL	NULL	NULL	His-GFP-SsrA protein	GP		bind					SspB127	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_75_s_51	12887894	(E and F) Isothermal titration calorimetric studies of His-GFP-SsrA protein binding to SspB (E) and SspB127 (F) reveal dissociation constants of 728 and 695 nM, respectively.	bind
14181	1	5234	7	NULL	NULL	0	NULL	His-GFP-SsrA	NULL		bind	NULL				SspB	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_12_1_75_s_51	12887894	(E and F) Isothermal titration calorimetric studies of His-GFP-SsrA protein binding to SspB (E) and SspB127 (F) reveal dissociation constants of 728 and 695 nM, respectively.	bind
14182	2	5234	7	NULL	NULL	0	NULL	His-GFP-SsrA	NULL		bind	NULL				SspB127	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_12_1_75_s_51	12887894	(E and F) Isothermal titration calorimetric studies of His-GFP-SsrA protein binding to SspB (E) and SspB127 (F) reveal dissociation constants of 728 and 695 nM, respectively.	bind
14814	1	5236	6	NULL	NULL	NULL	NULL	IFNAR1-EC	GP		bind					IFNAR1-EC receptor surface	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1888_s_28	16479007	(E to G) Dissociation  of wt IFN-alpha2 (E), IFN-beta (F), and the HEQ mutant (G) from the ternary complex, with both IFNAR1-EC  and IFNAR2-EC bound to the surface (IFNAR2-EC I47A was used for IFN-beta), at IFNAR1-EC  receptor surface concentrations of 4 fmol/mm2 (black), 2 fmol/mm2 (red), and 1 fmol/mm2 (blue).	bind
14815	2	5236	6	NULL	NULL	NULL	NULL	IFNAR2-EC	GP		bind					IFNAR1-EC receptor surface	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1888_s_28	16479007	(E to G) Dissociation  of wt IFN-alpha2 (E), IFN-beta (F), and the HEQ mutant (G) from the ternary complex, with both IFNAR1-EC  and IFNAR2-EC bound to the surface (IFNAR2-EC I47A was used for IFN-beta), at IFNAR1-EC  receptor surface concentrations of 4 fmol/mm2 (black), 2 fmol/mm2 (red), and 1 fmol/mm2 (blue).	bind
16181	3	5236	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1888_s_28	16479007	(E to G) Dissociation  of wt IFN-alpha2 (E), IFN-beta (F), and the HEQ mutant (G) from the ternary complex, with both IFNAR1-EC  and IFNAR2-EC bound to the surface (IFNAR2-EC I47A was used for IFN-beta), at IFNAR1-EC  receptor surface concentrations of 4 fmol/mm2 (black), 2 fmol/mm2 (red), and 1 fmol/mm2 (blue).	bind
16182	4	5236	6	NULL	NULL	NULL	NULL	IFN-alpha2	GP	wt	dissociates from					ternary complex					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1888_s_28	16479007	(E to G) Dissociation  of wt IFN-alpha2 (E), IFN-beta (F), and the HEQ mutant (G) from the ternary complex, with both IFNAR1-EC  and IFNAR2-EC bound to the surface (IFNAR2-EC I47A was used for IFN-beta), at IFNAR1-EC  receptor surface concentrations of 4 fmol/mm2 (black), 2 fmol/mm2 (red), and 1 fmol/mm2 (blue).	bind
16183	5	5236	6	NULL	NULL	NULL	NULL	IFN-beta	GP		dissociates from					ternary complex					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1888_s_28	16479007	(E to G) Dissociation  of wt IFN-alpha2 (E), IFN-beta (F), and the HEQ mutant (G) from the ternary complex, with both IFNAR1-EC  and IFNAR2-EC bound to the surface (IFNAR2-EC I47A was used for IFN-beta), at IFNAR1-EC  receptor surface concentrations of 4 fmol/mm2 (black), 2 fmol/mm2 (red), and 1 fmol/mm2 (blue).	bind
16184	6	5236	6	10	NULL	0	NULL		NULL	mutant	dissociates from	NULL		HEQ		ternary complex	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1888_s_28	16479007	(E to G) Dissociation  of wt IFN-alpha2 (E), IFN-beta (F), and the HEQ mutant (G) from the ternary complex, with both IFNAR1-EC  and IFNAR2-EC bound to the surface (IFNAR2-EC I47A was used for IFN-beta), at IFNAR1-EC  receptor surface concentrations of 4 fmol/mm2 (black), 2 fmol/mm2 (red), and 1 fmol/mm2 (blue).	bind
15108	1	5236	7	NULL	NULL	0	NULL	 IFN-alpha2 	NULL	wt	dissociates from	NULL				ternary complex	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1888_s_28	16479007	(E to G) Dissociation  of wt IFN-alpha2 (E), IFN-beta (F), and the HEQ mutant (G) from the ternary complex, with both IFNAR1-EC  and IFNAR2-EC bound to the surface (IFNAR2-EC I47A was used for IFN-beta), at IFNAR1-EC  receptor surface concentrations of 4 fmol/mm2 (black), 2 fmol/mm2 (red), and 1 fmol/mm2 (blue).	bind
15109	2	5236	7	10	NULL	0	NULL	IFN-beta 	NULL		dissociates from	NULL				ternary complex	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1888_s_28	16479007	(E to G) Dissociation  of wt IFN-alpha2 (E), IFN-beta (F), and the HEQ mutant (G) from the ternary complex, with both IFNAR1-EC  and IFNAR2-EC bound to the surface (IFNAR2-EC I47A was used for IFN-beta), at IFNAR1-EC  receptor surface concentrations of 4 fmol/mm2 (black), 2 fmol/mm2 (red), and 1 fmol/mm2 (blue).	bind
15110	3	5236	7	10	NULL	0	NULL		NULL	mutant	dissociates from	NULL		HEQ		ternary complex	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1888_s_28	16479007	(E to G) Dissociation  of wt IFN-alpha2 (E), IFN-beta (F), and the HEQ mutant (G) from the ternary complex, with both IFNAR1-EC  and IFNAR2-EC bound to the surface (IFNAR2-EC I47A was used for IFN-beta), at IFNAR1-EC  receptor surface concentrations of 4 fmol/mm2 (black), 2 fmol/mm2 (red), and 1 fmol/mm2 (blue).	bind
15111	4	5236	7	NULL	NULL	0	NULL	IFNAR1-EC	NULL		bind	NULL				IFNAR1-EC receptor surface	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1888_s_28	16479007	(E to G) Dissociation  of wt IFN-alpha2 (E), IFN-beta (F), and the HEQ mutant (G) from the ternary complex, with both IFNAR1-EC  and IFNAR2-EC bound to the surface (IFNAR2-EC I47A was used for IFN-beta), at IFNAR1-EC  receptor surface concentrations of 4 fmol/mm2 (black), 2 fmol/mm2 (red), and 1 fmol/mm2 (blue).	bind
15112	5	5236	7	NULL	NULL	0	NULL	IFNAR2-EC	NULL		bind	NULL				IFNAR1-EC receptor surface	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1888_s_28	16479007	(E to G) Dissociation  of wt IFN-alpha2 (E), IFN-beta (F), and the HEQ mutant (G) from the ternary complex, with both IFNAR1-EC  and IFNAR2-EC bound to the surface (IFNAR2-EC I47A was used for IFN-beta), at IFNAR1-EC  receptor surface concentrations of 4 fmol/mm2 (black), 2 fmol/mm2 (red), and 1 fmol/mm2 (blue).	bind
15594	6	5236	7	NULL	NULL	0	NULL	statement 4	NULL		occurs simultaneous with	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1888_s_28	16479007	(E to G) Dissociation  of wt IFN-alpha2 (E), IFN-beta (F), and the HEQ mutant (G) from the ternary complex, with both IFNAR1-EC  and IFNAR2-EC bound to the surface (IFNAR2-EC I47A was used for IFN-beta), at IFNAR1-EC  receptor surface concentrations of 4 fmol/mm2 (black), 2 fmol/mm2 (red), and 1 fmol/mm2 (blue).	bind
14341	1	5237	6	NULL	NULL	NULL	NULL	HRX	GP		bind					GADD34	GP	endogenous			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_7050_s_173	10490642	(E to G) HRX fusion proteins bind endogenous GADD34 in vivo.	bind
44686	2	5237	6	NULL	NULL	NULL	NULL	HRX	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_7050_s_173	10490642	(E to G) HRX fusion proteins bind endogenous GADD34 in vivo.	bind
15113	1	5237	7	10	NULL	0	NULL	HRX	NULL		bind	NULL				GADD34	NULL	endogenous			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_10_7050_s_173	10490642	(E to G) HRX fusion proteins bind endogenous GADD34 in vivo.	bind
44687	3	5237	7	10	NULL	0	NULL	HRX	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_10_7050_s_173	10490642	(E to G) HRX fusion proteins bind endogenous GADD34 in vivo.	bind
14342	1	5238	6	NULL	NULL	NULL	NULL	35S-A-Raf	GP		does not bind					GST-Rb	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_141	15485920	(E) 35S-A-Raf does not bind to GST-Rb but binds to the positive control GST-MEK1.	bind
14343	2	5238	6	NULL	NULL	NULL	NULL	35S-A-Raf	GP		bind					GST-MEK1	GP	positive control			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_141	15485920	(E) 35S-A-Raf does not bind to GST-Rb but binds to the positive control GST-MEK1.	bind
15114	1	5238	7	NULL	NULL	0	NULL	35S-A-Raf	NULL		does not bind	NULL				GST-Rb	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_141	15485920	(E) 35S-A-Raf does not bind to GST-Rb but binds to the positive control GST-MEK1.	bind
15115	2	5238	7	10	NULL	0	NULL	35S-A-Raf	NULL		bind	NULL				GST-MEK1	NULL	positive control			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_141	15485920	(E) 35S-A-Raf does not bind to GST-Rb but binds to the positive control GST-MEK1.	bind
14344	1	5240	6	NULL	NULL	NULL	NULL	Ad2	GP		bind		specifically			M21-L4 litter cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_158_6_1119_s_98	12221069	(E) Ad2 binds specifically to both M21-L4 and M21 litter cells.	bind
14345	2	5240	6	NULL	NULL	NULL	NULL	Ad2	GP		bind		specifically			M21 litter cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_158_6_1119_s_98	12221069	(E) Ad2 binds specifically to both M21-L4 and M21 litter cells.	bind
15116	1	5240	7	NULL	NULL	0	NULL	Ad2	NULL		binds	NULL	specifically			M21-L4 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_158_6_1119_s_98	12221069	(E) Ad2 binds specifically to both M21-L4 and M21 litter cells.	bind
15117	2	5240	7	NULL	NULL	0	NULL	Ad2	NULL		binds	NULL	specifically			M21 litter cells	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_158_6_1119_s_98	12221069	(E) Ad2 binds specifically to both M21-L4 and M21 litter cells.	bind
14346	1	5241	6	NULL	NULL	NULL	NULL	KLC-1	GP		bind					calsyntenin-1	GP	point mutants			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_8_3651_s_163	16760430	(E) Analysis of KLC1-binding of calsyntenin-1 point mutants by quantitative GST  pulldown assay.	bind
15118	1	5241	7	NULL	NULL	0	NULL	KLC1	NULL		bind	NULL				calsyntenin-1	NULL	point mutant			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_8_3651_s_163	16760430	(E) Analysis of KLC1-binding of calsyntenin-1 point mutants by quantitative GST  pulldown assay.	bind
14347	1	5243	6	NULL	NULL	NULL	NULL	ATF6	GP		bind									ATF6 site	NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_881_s_253	11779464	(E) Binding  of ATF6 and XBP1 to the ATF6  site.	bind
14348	2	5243	6	NULL	NULL	NULL	NULL	XBP1	GP		bind									ATF6 site	NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_881_s_253	11779464	(E) Binding  of ATF6 and XBP1 to the ATF6  site.	bind
15119	1	5243	7	NULL	NULL	0	NULL	ATF6	NULL		bind	NULL					NULL			ATF6 site	NULL		0	NULL	NULL	NULL	gw60_cell_107_7_881_s_253	11779464	(E) Binding  of ATF6 and XBP1 to the ATF6  site.	bind
15120	2	5243	7	NULL	NULL	0	NULL	XBP1	NULL		bind	NULL					NULL			ATF6 site	NULL		0	NULL	NULL	NULL	gw60_cell_107_7_881_s_253	11779464	(E) Binding  of ATF6 and XBP1 to the ATF6  site.	bind
14349	1	5244	6	NULL	NULL	NULL	NULL	E2F1	GP	endogenous;;cellular lysates	bind					GST-Phb	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_2_459_s_98	14637159	(E) Binding  of endogenous E2F1 present in cellular lysates to GST-Phb and GST-Phb-CC beads in  vitro; the binding was detected by Western blotting.	bind
14350	2	5244	6	NULL	NULL	NULL	NULL	E2F1	GP	endogenous;;cellular lysates	bind					GST-Phb-CC	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_2_459_s_98	14637159	(E) Binding  of endogenous E2F1 present in cellular lysates to GST-Phb and GST-Phb-CC beads in  vitro; the binding was detected by Western blotting.	bind
15121	1	5244	7	10	NULL	0	NULL	E2F1	NULL	endogenous;;cellular lysates	bind	NULL				GST-Phb	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_2_459_s_98	14637159	(E) Binding  of endogenous E2F1 present in cellular lysates to GST-Phb and GST-Phb-CC beads in  vitro; the binding was detected by Western blotting.	bind
15122	2	5244	7	10	NULL	0	NULL	E2F1	NULL	endogenous;;cellular lysates	bind	NULL				GST-Phb-CC	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_2_459_s_98	14637159	(E) Binding  of endogenous E2F1 present in cellular lysates to GST-Phb and GST-Phb-CC beads in  vitro; the binding was detected by Western blotting.	bind
14351	1	5245	6	NULL	NULL	NULL	NULL	SLP-76	GP		bind					Vav	GP				NULL	jurkat cells	NULL	NULL	NULL	NULL	gw60_immunity_6_2_155_s_190	9047237	(E) Binding between SLP-76 and Vav in Jurkat cells.	bind
15123	1	5245	7	NULL	NULL	0	NULL	SLP-76	NULL		bind	NULL				Vav	NULL				NULL	Jurkat cells	0	NULL	NULL	NULL	gw60_immunity_6_2_155_s_190	9047237	(E) Binding between SLP-76 and Vav in Jurkat cells.	bind
14352	1	5246	6	NULL	NULL	NULL	NULL	Ad4BP/SF-1	GP		bind									XRE site	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_10040_s_288	16260617	(E) Binding of Ad4BP/SF-1 to  the XRE and Ad4 sites in the presence or absence of AhR, revealed by ChIP assays.	bind
14353	2	5246	6	NULL	NULL	NULL	NULL	Ad4BP/SF-1	GP		bind									Ad4 site	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_10040_s_288	16260617	(E) Binding of Ad4BP/SF-1 to  the XRE and Ad4 sites in the presence or absence of AhR, revealed by ChIP assays.	bind
15124	1	5246	7	NULL	NULL	0	NULL	Ad4BP/SF-1	NULL		bind	NULL					NULL			Ad4 site	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_22_10040_s_288	16260617	(E) Binding of Ad4BP/SF-1 to  the XRE and Ad4 sites in the presence or absence of AhR, revealed by ChIP assays.	bind
15125	2	5246	7	NULL	NULL	0	NULL	Ad4BP/SF-1	NULL		bind	NULL					NULL			 XRE site 	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_22_10040_s_288	16260617	(E) Binding of Ad4BP/SF-1 to  the XRE and Ad4 sites in the presence or absence of AhR, revealed by ChIP assays.	bind
14354	1	5247	6	NULL	NULL	NULL	NULL	Adf-1	GP		bind					ftz	GP	proximal		enhancer	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_6_3384_s_242	9584179	(E) Binding of Adf-1 to the  ftz proximal enhancer and that to the Adh distal promoter sites were compared.	bind
14355	2	5247	6	NULL	NULL	NULL	NULL	Adf-1	GP		bind					Adh	GP	distal		promoter 	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_6_3384_s_242	9584179	(E) Binding of Adf-1 to the  ftz proximal enhancer and that to the Adh distal promoter sites were compared.	bind
15126	1	5247	7	10	NULL	0	NULL	Adf-1	NULL		bind	NULL				 ftz	NULL	proximal		enhancer	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_6_3384_s_242	9584179	(E) Binding of Adf-1 to the  ftz proximal enhancer and that to the Adh distal promoter sites were compared.	bind
15127	2	5247	7	10	NULL	0	NULL	Adf-1	NULL		bind	NULL				Adh 	NULL	distal		promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_6_3384_s_242	9584179	(E) Binding of Adf-1 to the  ftz proximal enhancer and that to the Adh distal promoter sites were compared.	bind
14356	1	5248	6	NULL	NULL	NULL	NULL	C3dg-SA-PE	GP		bind					B cells	Cell	splenic			NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_6_713_s_74	12479818	(E) Binding of C3dg-SA-PE to splenic B cells.	bind
15128	1	5248	7	NULL	NULL	0	NULL	C3dg-SA-PE	NULL		bind	NULL				B cells	NULL	splenic			NULL		0	NULL	NULL	NULL	gw60_immunity_17_6_713_s_74	12479818	(E) Binding of C3dg-SA-PE to splenic B cells.	bind
14357	1	5249	6	NULL	NULL	NULL	NULL	Dpr	GP		bind			PDZ-B		XDsh	GP		PDZ		NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_4_449_s_90	11970895	(E) Binding of Dpr PDZ-B to XDsh PDZ.	bind
15129	1	5249	7	NULL	NULL	0	NULL	Dpr 	NULL		bind	NULL		PDZ-B		XDsh	NULL		PDZ		NULL		0	NULL	NULL	NULL	gw60_devcell_2_4_449_s_90	11970895	(E) Binding of Dpr PDZ-B to XDsh PDZ.	bind
14816	1	5250	6	NULL	NULL	NULL	NULL	Mgamma proteins	GP		bind					B1 probe	NucleicAcid	labeled			NULL	soluble bacterial extract	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4600_s_111	10373509	(E) Binding of Mgamma and Mbeta proteins (approximately 50 ng of pGex fusion protein in a soluble bacterial extract) to labeled B1 probe in the presence of nonspecific competitor DNA [poly(dI-dC)] or 5-, 10-, 20-, or 40-fold molar excess of unlabeled B1, N-box, or Hairy oligonucleotide as indicated.	bind
14817	2	5250	6	NULL	NULL	NULL	NULL	Mbeta proteins	GP		bind					B1 probe	NucleicAcid	labeled			NULL	soluble bacterial extract	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4600_s_111	10373509	(E) Binding of Mgamma and Mbeta proteins (approximately 50 ng of pGex fusion protein in a soluble bacterial extract) to labeled B1 probe in the presence of nonspecific competitor DNA [poly(dI-dC)] or 5-, 10-, 20-, or 40-fold molar excess of unlabeled B1, N-box, or Hairy oligonucleotide as indicated.	bind
15130	1	5250	7	10	NULL	0	NULL	Mgamma proteins	NULL		bind	NULL				B1 probe 	NULL	labeled			NULL	soluble bacterial extract	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4600_s_111	10373509	(E) Binding of Mgamma and Mbeta proteins (approximately 50 ng of pGex fusion protein in a soluble bacterial extract) to labeled B1 probe in the presence of nonspecific competitor DNA [poly(dI-dC)] or 5-, 10-, 20-, or 40-fold molar excess of unlabeled B1, N-box, or Hairy oligonucleotide as indicated.	bind
15131	2	5250	7	10	NULL	0	NULL	Mbeta proteins	NULL		bind	NULL				B1 probe 	NULL	labeled			NULL	soluble bacterial extract	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4600_s_111	10373509	(E) Binding of Mgamma and Mbeta proteins (approximately 50 ng of pGex fusion protein in a soluble bacterial extract) to labeled B1 probe in the presence of nonspecific competitor DNA [poly(dI-dC)] or 5-, 10-, 20-, or 40-fold molar excess of unlabeled B1, N-box, or Hairy oligonucleotide as indicated.	bind
14358	1	5251	6	NULL	NULL	NULL	NULL	myosin-Va	GP		bind					syntaxin-1A	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_101	16030255	(E) Binding of myosin-Va by syntaxin-1A requires ATP analogues in presence of 10 - 6 M Ca2+.	bind
14359	2	5251	6	NULL	NULL	NULL	NULL	statement 1	Process		requires					ATP analogues	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_101	16030255	(E) Binding of myosin-Va by syntaxin-1A requires ATP analogues in presence of 10 - 6 M Ca2+.	bind
14360	3	5251	6	NULL	NULL	NULL	NULL	statement 2	Process		occurs in presence of					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_101	16030255	(E) Binding of myosin-Va by syntaxin-1A requires ATP analogues in presence of 10 - 6 M Ca2+.	bind
15132	1	5251	7	NULL	NULL	0	NULL	myosin-Va	NULL		bind	NULL				syntaxin-1A	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_101	16030255	(E) Binding of myosin-Va by syntaxin-1A requires ATP analogues in presence of 10 - 6 M Ca2+.	bind
15133	2	5251	7	NULL	NULL	0	NULL	statement 1	NULL		requires	NULL				ATP analogues	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_101	16030255	(E) Binding of myosin-Va by syntaxin-1A requires ATP analogues in presence of 10 - 6 M Ca2+.	bind
19775	3	5251	7	NULL	NULL	0	NULL	statement 2	NULL		occurs in presence of	NULL				Ca2+	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_101	16030255	(E) Binding of myosin-Va by syntaxin-1A requires ATP analogues in presence of 10 - 6 M Ca2+.	bind
14361	1	5252	6	NULL	NULL	NULL	NULL	Xpum	GP		bind			Puf		CPEB	GP				NULL		NULL	NULL	NULL	NULL	gw70_mechdev_120_8_865_s_90	12963108	(E) Binding of XPum Puf and  CPEB in immature	bind
15597	1	5252	7	NULL	NULL	0	NULL	XPum	NULL		bind	NULL		 Puf		CPEB	NULL				NULL		NULL	NULL	NULL	NULL	gw70_mechdev_120_8_865_s_90	12963108	(E) Binding of XPum Puf and  CPEB in immature	bind
14362	1	5253	6	NULL	NULL	NULL	NULL	APP	GP		bind		directly	C terminus		KLC1	GP		TPR domain		NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_2_449_s_140	11144355	(E) C terminus of APP directly binds the TPR domain of KLC1.	bind
15134	1	5253	7	NULL	NULL	0	NULL	APP	NULL		binds	NULL	directly	C terminus		KLC1	NULL		TPR		NULL		0	NULL	NULL	NULL	gw60_neuron_28_2_449_s_140	11144355	(E) C terminus of APP directly binds the TPR domain of KLC1.	bind
14363	2	5254	6	NULL	NULL	NULL	NULL	C/EBP	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_4_495_s_194	12757710	(E) C/EBP  binds to E2F consensus within the DHFR promoter.	bind
53058	1	5254	6	NULL	NULL	NULL	NULL	E2F consensus	NucleicAcid		resides within					DHFR	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_113_4_495_s_194	12757710	(E) C/EBP  binds to E2F consensus within the DHFR promoter.	bind
15135	2	5254	7	10	NULL	0	NULL	C/EBP	NULL		binds	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_4_495_s_194	12757710	(E) C/EBP  binds to E2F consensus within the DHFR promoter.	bind
53059	1	5254	7	10	NULL	0	NULL	E2F consensus	NULL		resides within	NULL				DHFR	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_cell_113_4_495_s_194	12757710	(E) C/EBP  binds to E2F consensus within the DHFR promoter.	bind
14364	1	5255	6	NULL	NULL	NULL	NULL	His6 - syntaxin 1 	GP		bind					GST-syncollin	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_cell_90_2_325_s_147	9244306	(E) Ca2+ sensitivity of  the binding of His6 - syntaxin 1 to GST-syncollinshort, immobilized on glutathione - agarose.	bind
53060	2	5255	6	NULL	NULL	NULL	NULL	statement 1	Process		is sensitive to					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_2_325_s_147	9244306	(E) Ca2+ sensitivity of  the binding of His6 - syntaxin 1 to GST-syncollinshort, immobilized on glutathione - agarose.	bind
15136	1	5255	7	NULL	NULL	0	NULL	His6 - syntaxin 1	NULL		bind	NULL				GST-syncollinshort	NULL	immobilized			NULL		0	NULL	NULL	NULL	gw60_cell_90_2_325_s_147	9244306	(E) Ca2+ sensitivity of  the binding of His6 - syntaxin 1 to GST-syncollinshort, immobilized on glutathione - agarose.	bind
15137	2	5255	7	NULL	NULL	0	NULL	statement 1	NULL		is sensitive to	NULL				Ca2+	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_90_2_325_s_147	9244306	(E) Ca2+ sensitivity of  the binding of His6 - syntaxin 1 to GST-syncollinshort, immobilized on glutathione - agarose.	bind
14365	1	5256	6	NULL	NULL	NULL	NULL	Cdc42p	GP	wild type	bind					Ste20p	GP		CRIB domain		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_6_2824_s_308	16571678	(E) Cdc42[V36]p GTPgammaS binds the Ste20p CRIB domain similar to wild-type Cdc42p.	bind
14366	2	5256	6	NULL	NULL	NULL	NULL	Cdc42[V36]p GTPgammaS	GP		bind					Ste20p	GP		CRIB domain		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_6_2824_s_308	16571678	(E) Cdc42[V36]p GTPgammaS binds the Ste20p CRIB domain similar to wild-type Cdc42p.	bind
15138	1	5256	7	NULL	NULL	0	NULL	Cdc42[V36]p GTPgammaS	NULL		bind	NULL				Ste20p	NULL		CRIB 		NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_6_2824_s_308	16571678	(E) Cdc42[V36]p GTPgammaS binds the Ste20p CRIB domain similar to wild-type Cdc42p.	bind
15139	2	5256	7	NULL	NULL	0	NULL	Cdc42p 	NULL	wild-type	bind	NULL				Ste20p	NULL		CRIB		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_6_2824_s_308	16571678	(E) Cdc42[V36]p GTPgammaS binds the Ste20p CRIB domain similar to wild-type Cdc42p.	bind
14367	1	5258	6	NULL	NULL	NULL	NULL	E2F1	GP		bind					Rb	GP			promoter	NULL	E13.5 embryonic brain	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_12_4448_s_265	16738312	(E) ChIP analysis demonstrates that E2F1 and E2F4, as well  as acetylated histone H3 are bound to the  Rb and  Cdc2 promoters, but not to intron 3 of the  Rb gene in the E13.5 embryonic brain.	bind
14368	2	5258	6	NULL	NULL	NULL	NULL	E2F1	GP		bind					cdc2	GP			promoter	NULL	E13.5 embryonic brain	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_12_4448_s_265	16738312	(E) ChIP analysis demonstrates that E2F1 and E2F4, as well  as acetylated histone H3 are bound to the  Rb and  Cdc2 promoters, but not to intron 3 of the  Rb gene in the E13.5 embryonic brain.	bind
14369	3	5258	6	NULL	NULL	NULL	NULL	histone H3	GP	acetylated	bind					Rb	GP			promoter	NULL	E13.5 embryonic brain	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_12_4448_s_265	16738312	(E) ChIP analysis demonstrates that E2F1 and E2F4, as well  as acetylated histone H3 are bound to the  Rb and  Cdc2 promoters, but not to intron 3 of the  Rb gene in the E13.5 embryonic brain.	bind
14370	4	5258	6	NULL	NULL	NULL	NULL	histone H3	GP	acetylated	bind					cdc42	GP			promoter	NULL	E13.5 embryonic brain	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_12_4448_s_265	16738312	(E) ChIP analysis demonstrates that E2F1 and E2F4, as well  as acetylated histone H3 are bound to the  Rb and  Cdc2 promoters, but not to intron 3 of the  Rb gene in the E13.5 embryonic brain.	bind
14371	5	5258	6	NULL	NULL	NULL	NULL	E2F4	GP		bind					Rb	GP			promoter	NULL	E13.5 embryonic brain	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_12_4448_s_265	16738312	(E) ChIP analysis demonstrates that E2F1 and E2F4, as well  as acetylated histone H3 are bound to the  Rb and  Cdc2 promoters, but not to intron 3 of the  Rb gene in the E13.5 embryonic brain.	bind
14372	6	5258	6	NULL	NULL	NULL	NULL	E2F4	GP		bind					Cdc2	GP			promoter	NULL	E13.5 embryonic brain	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_12_4448_s_265	16738312	(E) ChIP analysis demonstrates that E2F1 and E2F4, as well  as acetylated histone H3 are bound to the  Rb and  Cdc2 promoters, but not to intron 3 of the  Rb gene in the E13.5 embryonic brain.	bind
14373	7	5258	6	NULL	NULL	NULL	NULL	E2F1	GP		does not bind					Rb	GP			intron 3	NULL	E13.5 embryonic brain	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_12_4448_s_265	16738312	(E) ChIP analysis demonstrates that E2F1 and E2F4, as well  as acetylated histone H3 are bound to the  Rb and  Cdc2 promoters, but not to intron 3 of the  Rb gene in the E13.5 embryonic brain.	bind
14374	8	5258	6	NULL	NULL	NULL	NULL	E2F4	GP		does not bind					Rb	GP			intron 3	NULL	E13.5 embryonic brain	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_12_4448_s_265	16738312	(E) ChIP analysis demonstrates that E2F1 and E2F4, as well  as acetylated histone H3 are bound to the  Rb and  Cdc2 promoters, but not to intron 3 of the  Rb gene in the E13.5 embryonic brain.	bind
14375	9	5258	6	NULL	NULL	NULL	NULL	histone H3	GP	acetylated	bind					Rb	GP			intron 3	NULL	E13.5 embryonic brain	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_12_4448_s_265	16738312	(E) ChIP analysis demonstrates that E2F1 and E2F4, as well  as acetylated histone H3 are bound to the  Rb and  Cdc2 promoters, but not to intron 3 of the  Rb gene in the E13.5 embryonic brain.	bind
15141	1	5258	7	NULL	NULL	0	NULL	E2F1	NULL		bind	NULL				 Rb	NULL			promoter	NULL	E13.5 embryonic brain	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_12_4448_s_265	16738312	(E) ChIP analysis demonstrates that E2F1 and E2F4, as well  as acetylated histone H3 are bound to the  Rb and  Cdc2 promoters, but not to intron 3 of the  Rb gene in the E13.5 embryonic brain.	bind
15142	2	5258	7	NULL	NULL	0	NULL	E2F1	NULL		bind	NULL				Cdc2	NULL			promoter	NULL	E13.5 embryonic brain	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_12_4448_s_265	16738312	(E) ChIP analysis demonstrates that E2F1 and E2F4, as well  as acetylated histone H3 are bound to the  Rb and  Cdc2 promoters, but not to intron 3 of the  Rb gene in the E13.5 embryonic brain.	bind
15143	3	5258	7	NULL	NULL	0	NULL	E2F1	NULL		does not bind	NULL				Rb	NULL			 intron 3	NULL	E13.5 embryonic brain	0	NULL	NULL	NULL	gw70_molcellbiol_26_12_4448_s_265	16738312	(E) ChIP analysis demonstrates that E2F1 and E2F4, as well  as acetylated histone H3 are bound to the  Rb and  Cdc2 promoters, but not to intron 3 of the  Rb gene in the E13.5 embryonic brain.	bind
15144	4	5258	7	NULL	NULL	0	NULL	E2F4	NULL		bind	NULL				Rb	NULL			promoter	NULL	E13.5 embryonic brain	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_12_4448_s_265	16738312	(E) ChIP analysis demonstrates that E2F1 and E2F4, as well  as acetylated histone H3 are bound to the  Rb and  Cdc2 promoters, but not to intron 3 of the  Rb gene in the E13.5 embryonic brain.	bind
15145	5	5258	7	NULL	NULL	0	NULL	E2F4	NULL		bind	NULL				Cdc2	NULL			promoter	NULL	E13.5 embryonic brain	0	NULL	NULL	NULL	gw70_molcellbiol_26_12_4448_s_265	16738312	(E) ChIP analysis demonstrates that E2F1 and E2F4, as well  as acetylated histone H3 are bound to the  Rb and  Cdc2 promoters, but not to intron 3 of the  Rb gene in the E13.5 embryonic brain.	bind
15146	6	5258	7	NULL	NULL	0	NULL	E2F4	NULL		does not bind	NULL				Rb	NULL			intron 3	NULL	E13.5 embryonic brain	0	NULL	NULL	NULL	gw70_molcellbiol_26_12_4448_s_265	16738312	(E) ChIP analysis demonstrates that E2F1 and E2F4, as well  as acetylated histone H3 are bound to the  Rb and  Cdc2 promoters, but not to intron 3 of the  Rb gene in the E13.5 embryonic brain.	bind
15147	7	5258	7	NULL	NULL	0	NULL	histone H3	NULL	acetylated	bind	NULL				Rb	NULL			promoter	NULL	E13.5 embryonic brain	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_12_4448_s_265	16738312	(E) ChIP analysis demonstrates that E2F1 and E2F4, as well  as acetylated histone H3 are bound to the  Rb and  Cdc2 promoters, but not to intron 3 of the  Rb gene in the E13.5 embryonic brain.	bind
15148	8	5258	7	NULL	NULL	0	NULL	histone H3	NULL	acetylated	bind	NULL				Cdc2	NULL			promoter	NULL	E13.5 embryonic brain	0	NULL	NULL	NULL	gw70_molcellbiol_26_12_4448_s_265	16738312	(E) ChIP analysis demonstrates that E2F1 and E2F4, as well  as acetylated histone H3 are bound to the  Rb and  Cdc2 promoters, but not to intron 3 of the  Rb gene in the E13.5 embryonic brain.	bind
15149	9	5258	7	NULL	NULL	0	NULL	histone H3	NULL	acetylated	does not bind	NULL				Rb	NULL			intron 3	NULL	E13.5 embryonic brain	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_12_4448_s_265	16738312	(E) ChIP analysis demonstrates that E2F1 and E2F4, as well  as acetylated histone H3 are bound to the  Rb and  Cdc2 promoters, but not to intron 3 of the  Rb gene in the E13.5 embryonic brain.	bind
14376	1	5259	6	NULL	NULL	NULL	NULL	TBP	GP		bind					GAL1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_18_6270_s_218	11509669	(E) ChIP analysis of the binding of TBP to the  GAL1 and  GAL10 promoters.	bind
14377	2	5259	6	NULL	NULL	NULL	NULL	TBP	GP		bind					GAL10	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_18_6270_s_218	11509669	(E) ChIP analysis of the binding of TBP to the  GAL1 and  GAL10 promoters.	bind
15150	1	5259	7	NULL	NULL	0	NULL	TBP	NULL		bind	NULL				GAL1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_18_6270_s_218	11509669	(E) ChIP analysis of the binding of TBP to the  GAL1 and  GAL10 promoters.	bind
15151	2	5259	7	NULL	NULL	0	NULL	TBP	NULL		bind	NULL				GAL10	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_18_6270_s_218	11509669	(E) ChIP analysis of the binding of TBP to the  GAL1 and  GAL10 promoters.	bind
14378	1	5260	6	NULL	NULL	NULL	NULL	H3	GP	methylated	bind			R17		TgCARM1	GP				NULL	extracellular tachyzoites treated with AMI-1	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10301_s_50	16287846	(E) ChIP experiments with extracellular tachyzoites treated with  AMI-1 or dimethyl sulfoxide (control) display the binding of methylated H3 [R17]  on TgCARM1 target  SAG1 and  SAG2A genes (Fig.  6A).	bind
14818	2	5260	6	NULL	NULL	NULL	NULL	H3	GP	methylated	bind			R17		TgCARM1	GP				NULL	extracellular tachyzoites treated with dimethyl sulfoxide	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10301_s_50	16287846	(E) ChIP experiments with extracellular tachyzoites treated with  AMI-1 or dimethyl sulfoxide (control) display the binding of methylated H3 [R17]  on TgCARM1 target  SAG1 and  SAG2A genes (Fig.  6A).	bind
14821	3	5260	6	NULL	NULL	NULL	NULL	statement 1	Process		target					SAG1 gene	GP				NULL	extracellular tachyzoites treated with AMI-1	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10301_s_50	16287846	(E) ChIP experiments with extracellular tachyzoites treated with  AMI-1 or dimethyl sulfoxide (control) display the binding of methylated H3 [R17]  on TgCARM1 target  SAG1 and  SAG2A genes (Fig.  6A).	bind
14822	4	5260	6	NULL	NULL	NULL	NULL	statement 1	Process		target					SAG2A gene	GP				NULL	extracellular tachyzoites treated with AMI-1	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10301_s_50	16287846	(E) ChIP experiments with extracellular tachyzoites treated with  AMI-1 or dimethyl sulfoxide (control) display the binding of methylated H3 [R17]  on TgCARM1 target  SAG1 and  SAG2A genes (Fig.  6A).	bind
16199	5	5260	6	NULL	NULL	NULL	NULL	statement 2	Process		target					SAG1 gene	GP				NULL	extracellular tachyzoites treated with AMI-1	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10301_s_50	16287846	(E) ChIP experiments with extracellular tachyzoites treated with  AMI-1 or dimethyl sulfoxide (control) display the binding of methylated H3 [R17]  on TgCARM1 target  SAG1 and  SAG2A genes (Fig.  6A).	bind
16200	6	5260	6	NULL	NULL	NULL	NULL	statement 2	Process		target					SAG2A gene	GP				NULL	extracellular tachyzoites treated with AMI-1	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10301_s_50	16287846	(E) ChIP experiments with extracellular tachyzoites treated with  AMI-1 or dimethyl sulfoxide (control) display the binding of methylated H3 [R17]  on TgCARM1 target  SAG1 and  SAG2A genes (Fig.  6A).	bind
15152	1	5260	7	NULL	NULL	0	NULL	H3 	NULL	methylated	bind	NULL		R17		TgCARM1	NULL			 	NULL	extracellular tachyzoites treated with  AMI-1	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10301_s_50	16287846	(E) ChIP experiments with extracellular tachyzoites treated with  AMI-1 or dimethyl sulfoxide (control) display the binding of methylated H3 [R17]  on TgCARM1 target  SAG1 and  SAG2A genes (Fig.  6A).	bind
15153	2	5260	7	NULL	NULL	0	NULL	H3 	NULL	methylated	bind	NULL		R17		TgCARM1	NULL				NULL	extracellular tachyzoites treated with  dimethyl sulfoxide	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10301_s_50	16287846	(E) ChIP experiments with extracellular tachyzoites treated with  AMI-1 or dimethyl sulfoxide (control) display the binding of methylated H3 [R17]  on TgCARM1 target  SAG1 and  SAG2A genes (Fig.  6A).	bind
15154	3	5260	7	10	NULL	0	NULL	statement 1	NULL		bind	NULL				SAG1 gene	NULL				NULL	extracellular tachyzoites treated with AMI-1	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10301_s_50	16287846	(E) ChIP experiments with extracellular tachyzoites treated with  AMI-1 or dimethyl sulfoxide (control) display the binding of methylated H3 [R17]  on TgCARM1 target  SAG1 and  SAG2A genes (Fig.  6A).	bind
15155	4	5260	7	10	NULL	0	NULL	statement 2	NULL		bind	NULL				SAG1 gene	NULL				NULL	extracellular tachyzoites treated with AMI-1	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10301_s_50	16287846	(E) ChIP experiments with extracellular tachyzoites treated with  AMI-1 or dimethyl sulfoxide (control) display the binding of methylated H3 [R17]  on TgCARM1 target  SAG1 and  SAG2A genes (Fig.  6A).	bind
15595	5	5260	7	10	NULL	0	NULL	statement 1	NULL		bind	NULL				SAG2A gene	NULL				NULL	extracellular tachyzoites treated with AMI-1	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10301_s_50	16287846	(E) ChIP experiments with extracellular tachyzoites treated with  AMI-1 or dimethyl sulfoxide (control) display the binding of methylated H3 [R17]  on TgCARM1 target  SAG1 and  SAG2A genes (Fig.  6A).	bind
15596	6	5260	7	10	NULL	0	NULL	statement 2	NULL		bind	NULL				SAG2A gene	NULL				NULL	extracellular tachyzoites treated with AMI-1	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10301_s_50	16287846	(E) ChIP experiments with extracellular tachyzoites treated with  AMI-1 or dimethyl sulfoxide (control) display the binding of methylated H3 [R17]  on TgCARM1 target  SAG1 and  SAG2A genes (Fig.  6A).	bind
14379	1	5261	6	NULL	NULL	NULL	NULL	TAp73alpha	GP		bind					p21	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_24_10593_s_397	15572666	(E) ChIP with  anti-HA antibodies in cells overexpressing HA-TAp73alpha alone or in combination with PIAS-1 or PIAS-1 and SUMO-1, showing reduced binding  of TAp73alpha to the p21 promoter in the presence of PIAS-1.	bind
14380	2	5261	6	NULL	NULL	NULL	NULL	statement 1	Process		is reduced in					PIAS-1	GP	presence of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_24_10593_s_397	15572666	(E) ChIP with  anti-HA antibodies in cells overexpressing HA-TAp73alpha alone or in combination with PIAS-1 or PIAS-1 and SUMO-1, showing reduced binding  of TAp73alpha to the p21 promoter in the presence of PIAS-1.	bind
15156	1	5261	7	NULL	NULL	0	NULL	TAp73alpha 	NULL		binding 	NULL				p21	NULL			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_24_10593_s_397	15572666	(E) ChIP with  anti-HA antibodies in cells overexpressing HA-TAp73alpha alone or in combination with PIAS-1 or PIAS-1 and SUMO-1, showing reduced binding  of TAp73alpha to the p21 promoter in the presence of PIAS-1.	bind
15598	2	5261	7	10	NULL	0	NULL	statement 1	NULL		is reduced in	NULL				PIAS-1	NULL	presence of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_24_10593_s_397	15572666	(E) ChIP with  anti-HA antibodies in cells overexpressing HA-TAp73alpha alone or in combination with PIAS-1 or PIAS-1 and SUMO-1, showing reduced binding  of TAp73alpha to the p21 promoter in the presence of PIAS-1.	bind
14381	1	5262	6	NULL	NULL	NULL	NULL	CLOCK	GP		bind					mPer1	GP			E box	NULL	circadian cycle	NULL	NULL	NULL	NULL	gw60_cell_107_7_855_s_168	11779462	(E) CLOCK and  BMAL1 are bound to the  mPer1 E  box over the circadian cycle.	bind
14382	2	5262	6	NULL	NULL	NULL	NULL	BMAL1	GP		bind					mPer1	GP			E box	NULL	circadian cycle	NULL	NULL	NULL	NULL	gw60_cell_107_7_855_s_168	11779462	(E) CLOCK and  BMAL1 are bound to the  mPer1 E  box over the circadian cycle.	bind
15157	1	5262	7	NULL	NULL	0	NULL	CLOCK 	NULL		bind	NULL				mPer1 	NULL			E box	NULL	circadian cycle	NULL	NULL	NULL	NULL	gw60_cell_107_7_855_s_168	11779462	(E) CLOCK and  BMAL1 are bound to the  mPer1 E  box over the circadian cycle.	bind
15158	2	5262	7	NULL	NULL	0	NULL	BMAL1	NULL		bind	NULL				mPer1 	NULL			E box 	NULL	circadian cycle	NULL	NULL	NULL	NULL	gw60_cell_107_7_855_s_168	11779462	(E) CLOCK and  BMAL1 are bound to the  mPer1 E  box over the circadian cycle.	bind
14383	1	5263	6	NULL	NULL	NULL	NULL	GST-CNP	GP		bind					MTs	CellComponent	preassembled			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_4_661_s_74	16103231	(E) Comparison of CNP and tau binding to MTs. Different amounts of GST-CNP (left) and tau (right) were cosedimented with preassembled MTs and analyzed by immunoblotting.	bind
14384	2	5263	6	NULL	NULL	NULL	NULL	tau	GP		bind					MTs	CellComponent	preassembled			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_4_661_s_74	16103231	(E) Comparison of CNP and tau binding to MTs. Different amounts of GST-CNP (left) and tau (right) were cosedimented with preassembled MTs and analyzed by immunoblotting.	bind
15159	1	5263	7	10	NULL	0	NULL	GST-CNP	NULL		bind	NULL				MTs	NULL	preassembled			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_4_661_s_74	16103231	(E) Comparison of CNP and tau binding to MTs. Different amounts of GST-CNP (left) and tau (right) were cosedimented with preassembled MTs and analyzed by immunoblotting.	bind
15160	2	5263	7	10	NULL	0	NULL	tau	NULL		bind	NULL				MTs	NULL	preassembled			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_4_661_s_74	16103231	(E) Comparison of CNP and tau binding to MTs. Different amounts of GST-CNP (left) and tau (right) were cosedimented with preassembled MTs and analyzed by immunoblotting.	bind
14385	1	5264	6	NULL	NULL	NULL	NULL	Arr2	GP		bind					PIP3 resin	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_1_121_s_94	12848937	(E) Competition of Arr2 binding to the PIP3 resin with various concentrations of PIP3 and IP6 as indicated.	bind
14386	2	5264	6	NULL	NULL	NULL	NULL	PIP3	GP		bind					PIP3 resin	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_1_121_s_94	12848937	(E) Competition of Arr2 binding to the PIP3 resin with various concentrations of PIP3 and IP6 as indicated.	bind
14387	3	5264	6	NULL	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_1_121_s_94	12848937	(E) Competition of Arr2 binding to the PIP3 resin with various concentrations of PIP3 and IP6 as indicated.	bind
14388	4	5264	6	NULL	NULL	NULL	NULL	IP6	GP		bind					PIP3 resin	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_1_121_s_94	12848937	(E) Competition of Arr2 binding to the PIP3 resin with various concentrations of PIP3 and IP6 as indicated.	bind
14389	5	5264	6	NULL	NULL	NULL	NULL	statement 1	Process		competes					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_1_121_s_94	12848937	(E) Competition of Arr2 binding to the PIP3 resin with various concentrations of PIP3 and IP6 as indicated.	bind
15161	1	5264	7	NULL	NULL	0	NULL	Arr2	NULL		bind	NULL				 PIP3 resin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_1_121_s_94	12848937	(E) Competition of Arr2 binding to the PIP3 resin with various concentrations of PIP3 and IP6 as indicated.	bind
15162	2	5264	7	NULL	NULL	0	NULL	PIP3	NULL		bind	NULL				PIP3 resin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_1_121_s_94	12848937	(E) Competition of Arr2 binding to the PIP3 resin with various concentrations of PIP3 and IP6 as indicated.	bind
44723	3	5264	7	NULL	NULL	0	NULL	 IP6	NULL		bind	NULL				PIP3 resin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_1_121_s_94	12848937	(E) Competition of Arr2 binding to the PIP3 resin with various concentrations of PIP3 and IP6 as indicated.	bind
44724	4	5264	7	NULL	NULL	0	NULL	statement 1	NULL		compete with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_39_1_121_s_94	12848937	(E) Competition of Arr2 binding to the PIP3 resin with various concentrations of PIP3 and IP6 as indicated.	bind
44725	5	5264	7	NULL	NULL	0	NULL	statement 1	NULL		compete with	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_39_1_121_s_94	12848937	(E) Competition of Arr2 binding to the PIP3 resin with various concentrations of PIP3 and IP6 as indicated.	bind
14390	1	5265	6	NULL	NULL	NULL	NULL	Crt1	GP		bind					Ssn6-Tup1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cell_94_5_595_s_59	9741624	(E) Crt1 binds Ssn6-Tup1 in vitro.	bind
15163	1	5265	7	NULL	NULL	0	NULL	Crt1	NULL		binds	NULL				Ssn6-Tup1	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_cell_94_5_595_s_59	9741624	(E) Crt1 binds Ssn6-Tup1 in vitro.	bind
14391	1	5266	6	NULL	NULL	NULL	NULL	PRA1	GP		bind					Pic-Zn1	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_1_203_s_172	10707984	(E) Detergent sensitivity of PRA1 binding to Pic-Zn1 in 0.01% Triton X-100 (closed squares), 0.05% Triton X-100 (open circles), 0.1% Triton X-100 (closed triangles), and 0.5% Triton X-100 (open diamonds).	bind
15164	1	5266	7	NULL	NULL	0	NULL	PRA1	NULL		bind	NULL				Pic-Zn1	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_25_1_203_s_172	10707984	(E) Detergent sensitivity of PRA1 binding to Pic-Zn1 in 0.01% Triton X-100 (closed squares), 0.05% Triton X-100 (open circles), 0.1% Triton X-100 (closed triangles), and 0.5% Triton X-100 (open diamonds).	bind
14392	1	5267	6	NULL	NULL	NULL	NULL	cyclin D1	GP		bind		directly			ER	GP		EF-region		NULL		NULL	NULL	NULL	NULL	gw60_cell_88_3_405_s_217	9039267	(E) Direct binding between cyclin D1 and EF-region of  ER.	bind
15165	1	5267	7	NULL	NULL	0	NULL	cyclin D1	NULL		binds	NULL	directly			ER	NULL		EF region		NULL		0	NULL	NULL	NULL	gw60_cell_88_3_405_s_217	9039267	(E) Direct binding between cyclin D1 and EF-region of  ER.	bind
14393	1	5268	6	NULL	NULL	NULL	NULL	Grb2	GP		bind		directly			FRS2	GP				NULL	FGF-stimulated cells	NULL	NULL	NULL	NULL	gw60_cell_89_5_693_s_43	9182757	(E) Direct binding of Grb2 to FRS2 in FGF-stimulated cells.	bind
15166	1	5268	7	NULL	NULL	0	NULL	Grb2	NULL		binds	NULL	directly			 FRS2 	NULL				NULL	FGF-stimulated cells	0	NULL	NULL	NULL	gw60_cell_89_5_693_s_43	9182757	(E) Direct binding of Grb2 to FRS2 in FGF-stimulated cells.	bind
14394	1	5269	6	NULL	NULL	NULL	NULL	LRP5	GP		bind		directly			Wnt1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_2_303_s_166	11956231	(E) Direct binding of LRP5 to Wnt1 or Wnt4.	bind
14395	2	5269	6	NULL	NULL	NULL	NULL	LRP5	GP		bind		directly			Wnt4	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_2_303_s_166	11956231	(E) Direct binding of LRP5 to Wnt1 or Wnt4.	bind
14396	3	5269	6	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_2_303_s_166	11956231	(E) Direct binding of LRP5 to Wnt1 or Wnt4.	bind
15167	1	5269	7	NULL	NULL	0	NULL	LRP5	NULL		binds	NULL	directly			Wnt1	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_157_2_303_s_166	11956231	(E) Direct binding of LRP5 to Wnt1 or Wnt4.	bind
15168	2	5269	7	NULL	NULL	0	NULL	LRP5	NULL		binds	NULL	directly			Wnt4	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_157_2_303_s_166	11956231	(E) Direct binding of LRP5 to Wnt1 or Wnt4.	bind
15169	3	5269	7	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_157_2_303_s_166	11956231	(E) Direct binding of LRP5 to Wnt1 or Wnt4.	bind
14397	1	5270	6	NULL	NULL	NULL	NULL	TBP plus TFB	GP		bind									T1 BRE-TATA box sequences	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_18_6419_s_41	16159776	(E) DNase I footprints of the complexes formed by TBP  plus TFB binding to the T1, T2, and T3 BRE-TATA box sequences.	bind
14398	2	5270	6	NULL	NULL	NULL	NULL	TBP plus TFB	GP		bind									T2 BRE-TATA box sequences	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_18_6419_s_41	16159776	(E) DNase I footprints of the complexes formed by TBP  plus TFB binding to the T1, T2, and T3 BRE-TATA box sequences.	bind
14399	3	5270	6	NULL	NULL	NULL	NULL	TBP plus TFB	GP		bind									T3 BRE-TATA box sequences	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_18_6419_s_41	16159776	(E) DNase I footprints of the complexes formed by TBP  plus TFB binding to the T1, T2, and T3 BRE-TATA box sequences.	bind
15171	2	5270	7	NULL	NULL	0	NULL	TBP plus TFB	NULL		bind	NULL					NULL			 T1 BRE-TATA box sequences	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_18_6419_s_41	16159776	(E) DNase I footprints of the complexes formed by TBP  plus TFB binding to the T1, T2, and T3 BRE-TATA box sequences.	bind
15172	3	5270	7	NULL	NULL	0	NULL	TBP plus TFB	NULL		bind	NULL					NULL			T2 BRE-TATA box sequences	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_18_6419_s_41	16159776	(E) DNase I footprints of the complexes formed by TBP  plus TFB binding to the T1, T2, and T3 BRE-TATA box sequences.	bind
15173	4	5270	7	NULL	NULL	0	NULL	TBP plus TFB	NULL		bind	NULL					NULL			T3 BRE-TATA box sequences	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_18_6419_s_41	16159776	(E) DNase I footprints of the complexes formed by TBP  plus TFB binding to the T1, T2, and T3 BRE-TATA box sequences.	bind
14400	1	5272	6	NULL	NULL	NULL	NULL	Dock	GP		bind			SH3 domain		Dscam	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cell_101_6_671_s_120	10892653	(E) Dock SH3 domains bind to Dscam  in vitro.	bind
15174	1	5272	7	NULL	NULL	0	NULL	Dock 	NULL		bind	NULL		SH3 domain		Dscam	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_cell_101_6_671_s_120	10892653	(E) Dock SH3 domains bind to Dscam  in vitro.	bind
14401	1	5273	6	NULL	NULL	NULL	NULL	RNAP	GP		bind					srf	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_222	16740936	(E) Effect of  rpoA mutations on ComA-dependent RNAP binding to the  srf and  rpsD promoter and on Spx-dependent RNAP release from promoter DNA.	bind
14402	2	5273	6	NULL	NULL	NULL	NULL	RNAP	GP		bind					rpsD	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_222	16740936	(E) Effect of  rpoA mutations on ComA-dependent RNAP binding to the  srf and  rpsD promoter and on Spx-dependent RNAP release from promoter DNA.	bind
14403	3	5273	6	NULL	NULL	NULL	NULL	statement 1	Process		is dependent on					ComA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_222	16740936	(E) Effect of  rpoA mutations on ComA-dependent RNAP binding to the  srf and  rpsD promoter and on Spx-dependent RNAP release from promoter DNA.	bind
14404	4	5273	6	NULL	NULL	NULL	NULL	statement 2	Process		is dependent on					ComA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_222	16740936	(E) Effect of  rpoA mutations on ComA-dependent RNAP binding to the  srf and  rpsD promoter and on Spx-dependent RNAP release from promoter DNA.	bind
14405	5	5273	6	NULL	NULL	NULL	NULL	DNA	NucleicAcid		release				promoter	RNAP	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_222	16740936	(E) Effect of  rpoA mutations on ComA-dependent RNAP binding to the  srf and  rpsD promoter and on Spx-dependent RNAP release from promoter DNA.	bind
14406	6	5273	6	NULL	NULL	NULL	NULL	statement 5	Process		is dependent on					Spx	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_222	16740936	(E) Effect of  rpoA mutations on ComA-dependent RNAP binding to the  srf and  rpsD promoter and on Spx-dependent RNAP release from promoter DNA.	bind
15175	1	5273	7	10	NULL	0	NULL	RNAP	NULL		bind	NULL				srf 	NULL			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_222	16740936	(E) Effect of  rpoA mutations on ComA-dependent RNAP binding to the  srf and  rpsD promoter and on Spx-dependent RNAP release from promoter DNA.	bind
15176	2	5273	7	10	NULL	0	NULL	RNAP	NULL		bind	NULL				rpsD	NULL			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_222	16740936	(E) Effect of  rpoA mutations on ComA-dependent RNAP binding to the  srf and  rpsD promoter and on Spx-dependent RNAP release from promoter DNA.	bind
15177	3	5273	7	10	NULL	0	NULL	RNAP	NULL		is release from	NULL				DNA	NULL			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_222	16740936	(E) Effect of  rpoA mutations on ComA-dependent RNAP binding to the  srf and  rpsD promoter and on Spx-dependent RNAP release from promoter DNA.	bind
53061	4	5273	7	10	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				ComA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_222	16740936	(E) Effect of  rpoA mutations on ComA-dependent RNAP binding to the  srf and  rpsD promoter and on Spx-dependent RNAP release from promoter DNA.	bind
53062	5	5273	7	10	NULL	0	NULL	statement 2	NULL		is dependent on	NULL				ComA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_222	16740936	(E) Effect of  rpoA mutations on ComA-dependent RNAP binding to the  srf and  rpsD promoter and on Spx-dependent RNAP release from promoter DNA.	bind
53063	6	5273	7	10	NULL	0	NULL	statement 3	NULL		is dependent on	NULL				Spx	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_12_4300_s_222	16740936	(E) Effect of  rpoA mutations on ComA-dependent RNAP binding to the  srf and  rpsD promoter and on Spx-dependent RNAP release from promoter DNA.	bind
14407	1	5274	6	NULL	NULL	NULL	NULL	tau	GP		coimmunoprecipitates with					Fe65	GP				NULL	CGNs	NULL	NULL	NULL	NULL	gw70_neurobioldis_18_2_399_s_137	15686969	(E) Effect of the roscovitine (40  M) and lithium (10  M)  on the binding of Tau to Fe65 in CGNs. Immunoprecipitation and Western blot analysis  in B and E were performed as described in A. (E, F) Quantitative evaluation of the  effect of roscovitine and lithium on phosphorylation of tau at Tau-1 and AT8 sites  and their effect on the amount of tau co-immunoprecipitated with Fe65 (F).	bind
15205	1	5274	7	10	NULL	0	NULL	 Tau	NULL		coimmunoprecipitates with	NULL				Fe65 	NULL				NULL	CGNs	NULL	NULL	NULL	NULL	gw70_neurobioldis_18_2_399_s_137	15686969	(E) Effect of the roscovitine (40  M) and lithium (10  M)  on the binding of Tau to Fe65 in CGNs. Immunoprecipitation and Western blot analysis  in B and E were performed as described in A. (E, F) Quantitative evaluation of the  effect of roscovitine and lithium on phosphorylation of tau at Tau-1 and AT8 sites  and their effect on the amount of tau co-immunoprecipitated with Fe65 (F).	bind
14408	1	5275	6	NULL	NULL	NULL	NULL	Mgamma	GP		bind					B1 probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4600_s_156	10373509	(E) Effects of 5-, 10-, 20-, or 40-fold molar excess of either unlabeled A1 or A2 oligonucleotide on binding of Mgamma (50 ng) to the B1 probe.	bind
15178	1	5275	7	NULL	NULL	0	NULL	Mgamma	NULL		bind	NULL				B1 probe	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4600_s_156	10373509	(E) Effects of 5-, 10-, 20-, or 40-fold molar excess of either unlabeled A1 or A2 oligonucleotide on binding of Mgamma (50 ng) to the B1 probe.	bind
14409	1	5276	6	NULL	NULL	NULL	NULL	CPSF	GP		bind					RNA	NucleicAcid	pre-wt			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2660_s_220	10733568	(E) Effects of DNA oligonucleotide competitors (Oligo) on the binding of CPSF to the pre-wt RNA.	bind
15179	1	5276	7	NULL	NULL	0	NULL	CPSF	NULL		bind	NULL				RNA	NULL	pre-wt			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_8_2660_s_220	10733568	(E) Effects of DNA oligonucleotide competitors (Oligo) on the binding of CPSF to the pre-wt RNA.	bind
14410	1	5277	6	NULL	NULL	NULL	NULL	CRT	GP		bind								DBD		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6286_s_238	12167720	(E) EGTA-sensitive binding of CRT to the DBD is partially lost on removal of the C-terminal domain (residues 1 to 273).	bind
14411	2	5277	6	NULL	NULL	NULL	NULL	statement 1	Process		is sensitive to					EGTA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6286_s_238	12167720	(E) EGTA-sensitive binding of CRT to the DBD is partially lost on removal of the C-terminal domain (residues 1 to 273).	bind
14412	3	5277	6	NULL	NULL	NULL	NULL	statement 1	Process		is lost upon		partially					removal of	C-terminal domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6286_s_238	12167720	(E) EGTA-sensitive binding of CRT to the DBD is partially lost on removal of the C-terminal domain (residues 1 to 273).	bind
15180	1	5277	7	10	NULL	0	NULL	 CRT	NULL		bind	NULL					NULL		DBD		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6286_s_238	12167720	(E) EGTA-sensitive binding of CRT to the DBD is partially lost on removal of the C-terminal domain (residues 1 to 273).	bind
15181	2	5277	7	NULL	NULL	0	NULL	statement 1	NULL		is sensitive to	NULL				EGTA	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6286_s_238	12167720	(E) EGTA-sensitive binding of CRT to the DBD is partially lost on removal of the C-terminal domain (residues 1 to 273).	bind
15182	3	5277	7	10	NULL	0	NULL	statement 1	NULL		is lost upon	NULL	partially				NULL	removal of 	C-terminal domain residues 1 to 273		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6286_s_238	12167720	(E) EGTA-sensitive binding of CRT to the DBD is partially lost on removal of the C-terminal domain (residues 1 to 273).	bind
14823	1	5278	6	NULL	NULL	NULL	NULL			deletion mutant	bind			delta1-4		SK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_3039_s_135	10082571	(E) EMSA carried out as described for panel D but performed at [[ 0 degrees C.                    The deletion mutants delta1-4 ]] and delta1-7 (Fig.  3A) both bound well to SK1 (Fig.  3B, lanes 8 and 9), and an EMSA titration indicated that delta1-7 and the Skn domain bound to this site with very similar affinities (Fig.  4A, lanes 1 to 10), indicating that the more distal (amino-terminal) residues in the arm (positions 1 to 7) (Fig.  3A) are not required for binding affinity.	bind
14824	2	5278	6	NULL	NULL	NULL	NULL			deletion mutant	bind			delta1-7		SK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_3039_s_135	10082571	(E) EMSA carried out as described for panel D but performed at [[ 0 degrees C.                    The deletion mutants delta1-4 ]] and delta1-7 (Fig.  3A) both bound well to SK1 (Fig.  3B, lanes 8 and 9), and an EMSA titration indicated that delta1-7 and the Skn domain bound to this site with very similar affinities (Fig.  4A, lanes 1 to 10), indicating that the more distal (amino-terminal) residues in the arm (positions 1 to 7) (Fig.  3A) are not required for binding affinity.	bind
53064	3	5278	6	NULL	NULL	NULL	NULL				is not required for			amino-terminal residues in the arm (1 to 7)		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_3039_s_135	10082571	(E) EMSA carried out as described for panel D but performed at [[ 0 degrees C.                    The deletion mutants delta1-4 ]] and delta1-7 (Fig.  3A) both bound well to SK1 (Fig.  3B, lanes 8 and 9), and an EMSA titration indicated that delta1-7 and the Skn domain bound to this site with very similar affinities (Fig.  4A, lanes 1 to 10), indicating that the more distal (amino-terminal) residues in the arm (positions 1 to 7) (Fig.  3A) are not required for binding affinity.	bind
15233	1	5278	7	NULL	NULL	0	NULL		NULL	deletion mutant	bind	NULL		delta1-4		SK1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_3039_s_135	10082571	(E) EMSA carried out as described for panel D but performed at [[ 0 degrees C.                    The deletion mutants delta1-4 ]] and delta1-7 (Fig.  3A) both bound well to SK1 (Fig.  3B, lanes 8 and 9), and an EMSA titration indicated that delta1-7 and the Skn domain bound to this site with very similar affinities (Fig.  4A, lanes 1 to 10), indicating that the more distal (amino-terminal) residues in the arm (positions 1 to 7) (Fig.  3A) are not required for binding affinity.	bind
15234	2	5278	7	NULL	NULL	0	NULL		NULL	deletion mutant	bind	NULL		delta1-7 		SK1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_3039_s_135	10082571	(E) EMSA carried out as described for panel D but performed at [[ 0 degrees C.                    The deletion mutants delta1-4 ]] and delta1-7 (Fig.  3A) both bound well to SK1 (Fig.  3B, lanes 8 and 9), and an EMSA titration indicated that delta1-7 and the Skn domain bound to this site with very similar affinities (Fig.  4A, lanes 1 to 10), indicating that the more distal (amino-terminal) residues in the arm (positions 1 to 7) (Fig.  3A) are not required for binding affinity.	bind
15235	3	5278	7	10	NULL	0	NULL		NULL		is not required for	NULL		amino-terminal residues in the arm (1 to 7)		statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_3039_s_135	10082571	(E) EMSA carried out as described for panel D but performed at [[ 0 degrees C.                    The deletion mutants delta1-4 ]] and delta1-7 (Fig.  3A) both bound well to SK1 (Fig.  3B, lanes 8 and 9), and an EMSA titration indicated that delta1-7 and the Skn domain bound to this site with very similar affinities (Fig.  4A, lanes 1 to 10), indicating that the more distal (amino-terminal) residues in the arm (positions 1 to 7) (Fig.  3A) are not required for binding affinity.	bind
14413	1	5279	6	NULL	NULL	NULL	NULL	HOX	GP		bind							wild type		40 bp oligonucleotide	NULL		NULL	NULL	NULL	NULL	gw70_devbiol_283_2_474_s_167	15913596	(E) EMSA of HOX and PBX1 binding to a 40-bp wild-type or mutant oligonucleotide  derived from 125 bp  Hb9 enhancer.	bind
14414	2	5279	6	NULL	NULL	NULL	NULL	HOX	GP		bind							mutant		40 bp oligonucleotide	NULL		NULL	NULL	NULL	NULL	gw70_devbiol_283_2_474_s_167	15913596	(E) EMSA of HOX and PBX1 binding to a 40-bp wild-type or mutant oligonucleotide  derived from 125 bp  Hb9 enhancer.	bind
14415	3	5279	6	NULL	NULL	NULL	NULL	PBX1	GP		bind							wild type		40 bp oligonucleotide	NULL		NULL	NULL	NULL	NULL	gw70_devbiol_283_2_474_s_167	15913596	(E) EMSA of HOX and PBX1 binding to a 40-bp wild-type or mutant oligonucleotide  derived from 125 bp  Hb9 enhancer.	bind
14416	4	5279	6	NULL	NULL	NULL	NULL	PBX1	GP		bind							mutant		40 bp oligonucleotide	NULL		NULL	NULL	NULL	NULL	gw70_devbiol_283_2_474_s_167	15913596	(E) EMSA of HOX and PBX1 binding to a 40-bp wild-type or mutant oligonucleotide  derived from 125 bp  Hb9 enhancer.	bind
54282	5	5279	6	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_283_2_474_s_167	15913596	(E) EMSA of HOX and PBX1 binding to a 40-bp wild-type or mutant oligonucleotide  derived from 125 bp  Hb9 enhancer.	bind
54283	6	5279	6	NULL	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_283_2_474_s_167	15913596	(E) EMSA of HOX and PBX1 binding to a 40-bp wild-type or mutant oligonucleotide  derived from 125 bp  Hb9 enhancer.	bind
54284	7	5279	6	NULL	NULL	NULL	NULL				is derived from				40 bp oligonucleotide	Hb9	GP			125 bp enhancer	NULL		NULL	NULL	NULL	NULL	gw70_devbiol_283_2_474_s_167	15913596	(E) EMSA of HOX and PBX1 binding to a 40-bp wild-type or mutant oligonucleotide  derived from 125 bp  Hb9 enhancer.	bind
15236	1	5279	7	NULL	NULL	0	NULL	HOX	NULL		bind	NULL					NULL	wild-type		40-bp oligonucleotide	NULL		0	NULL	NULL	NULL	gw70_devbiol_283_2_474_s_167	15913596	(E) EMSA of HOX and PBX1 binding to a 40-bp wild-type or mutant oligonucleotide  derived from 125 bp  Hb9 enhancer.	bind
15237	2	5279	7	NULL	NULL	0	NULL	HOX	NULL		bind	NULL					NULL	mutant		40-bp oligonucleotide	NULL		0	NULL	NULL	NULL	gw70_devbiol_283_2_474_s_167	15913596	(E) EMSA of HOX and PBX1 binding to a 40-bp wild-type or mutant oligonucleotide  derived from 125 bp  Hb9 enhancer.	bind
15238	3	5279	7	NULL	NULL	0	NULL	PBX1	NULL		bind	NULL					NULL	wild-type		40-bp oligonucleotide	NULL		0	NULL	NULL	NULL	gw70_devbiol_283_2_474_s_167	15913596	(E) EMSA of HOX and PBX1 binding to a 40-bp wild-type or mutant oligonucleotide  derived from 125 bp  Hb9 enhancer.	bind
15239	4	5279	7	NULL	NULL	0	NULL	PBX1	NULL		bind	NULL					NULL	mutant		40-bp oligonucleotide	NULL		0	NULL	NULL	NULL	gw70_devbiol_283_2_474_s_167	15913596	(E) EMSA of HOX and PBX1 binding to a 40-bp wild-type or mutant oligonucleotide  derived from 125 bp  Hb9 enhancer.	bind
15240	5	5279	7	NULL	NULL	0	NULL		NULL		is derived from	NULL			40-bp oligonucleotide	Hb9 	NULL			125 bp enhancer	NULL		0	NULL	NULL	NULL	gw70_devbiol_283_2_474_s_167	15913596	(E) EMSA of HOX and PBX1 binding to a 40-bp wild-type or mutant oligonucleotide  derived from 125 bp  Hb9 enhancer.	bind
15241	6	5279	7	NULL	NULL	0	NULL		NULL	mutant	is derived from	NULL			40-bp oligonucleotide	Hb9 	NULL			125 bp enhancer	NULL		0	NULL	NULL	NULL	gw70_devbiol_283_2_474_s_167	15913596	(E) EMSA of HOX and PBX1 binding to a 40-bp wild-type or mutant oligonucleotide  derived from 125 bp  Hb9 enhancer.	bind
15242	7	5279	7	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_283_2_474_s_167	15913596	(E) EMSA of HOX and PBX1 binding to a 40-bp wild-type or mutant oligonucleotide  derived from 125 bp  Hb9 enhancer.	bind
15243	8	5279	7	NULL	NULL	0	NULL	statement 3	NULL		is an alternative to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_283_2_474_s_167	15913596	(E) EMSA of HOX and PBX1 binding to a 40-bp wild-type or mutant oligonucleotide  derived from 125 bp  Hb9 enhancer.	bind
14601	1	5282	6	NULL	NULL	NULL	NULL	Miz-1	GP		bind					p21Cip1	GP			start site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_3_509_s_196	12408820	(E) Gel shift assays documenting binding of Miz-1 and TopBP1 to the start site of the  p21Cip1 promoter.	bind
14602	2	5282	6	NULL	NULL	NULL	NULL	TopBP1	GP		bind					p21Cip1	GP			start site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_3_509_s_196	12408820	(E) Gel shift assays documenting binding of Miz-1 and TopBP1 to the start site of the  p21Cip1 promoter.	bind
15244	1	5282	7	NULL	NULL	0	NULL	Miz-1 	NULL		bind	NULL				p21Cip1	NULL			start site of the promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_3_509_s_196	12408820	(E) Gel shift assays documenting binding of Miz-1 and TopBP1 to the start site of the  p21Cip1 promoter.	bind
15245	2	5282	7	NULL	NULL	0	NULL	TopBP1	NULL		bind	NULL				p21Cip1	NULL			start site of the promoter	NULL		0	NULL	NULL	NULL	gw60_molcell_10_3_509_s_196	12408820	(E) Gel shift assays documenting binding of Miz-1 and TopBP1 to the start site of the  p21Cip1 promoter.	bind
14603	1	5283	6	NULL	NULL	NULL	NULL	GST E1A 	GP		bind			C terminus		TnT CtBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_4_857_s_186	12419229	(E) GST E1A C  binding to TnT CtBP at various concentrations of NAD+, NADH, ADP-Ribose,  NMN, and Nicotinamide.	bind
15246	1	5283	7	NULL	NULL	0	NULL	GST E1A 	NULL		bind	NULL		C		TnT CtBP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_4_857_s_186	12419229	(E) GST E1A C  binding to TnT CtBP at various concentrations of NAD+, NADH, ADP-Ribose,  NMN, and Nicotinamide.	bind
14604	1	5286	6	NULL	NULL	NULL	NULL	hMSH2-hMSH6	GP		bind					DNA	NucleicAcid			b-GT	NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_2_255_s_36	10078208	(E) hMSH2-hMSH6 binding a  b-GT or  b-GC DNA in the presence or absence of MgCl2.	bind
14605	2	5286	6	NULL	NULL	NULL	NULL	hMSH2-hMSH6	GP		bind					DNA	NucleicAcid			b-GC	NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_2_255_s_36	10078208	(E) hMSH2-hMSH6 binding a  b-GT or  b-GC DNA in the presence or absence of MgCl2.	bind
15251	1	5286	7	NULL	NULL	0	NULL	hMSH2-hMSH6	NULL		bind	NULL				DNA	NULL			b-GT	NULL		0	NULL	NULL	NULL	gw60_molcell_3_2_255_s_36	10078208	(E) hMSH2-hMSH6 binding a  b-GT or  b-GC DNA in the presence or absence of MgCl2.	bind
15252	2	5286	7	NULL	NULL	0	NULL	hMSH2-hMSH6	NULL		bind	NULL				DNA	NULL			b-GC	NULL		0	NULL	NULL	NULL	gw60_molcell_3_2_255_s_36	10078208	(E) hMSH2-hMSH6 binding a  b-GT or  b-GC DNA in the presence or absence of MgCl2.	bind
14606	1	5287	6	NULL	NULL	NULL	NULL	HNF6	GP		bind					Glut2	GP			promoter	NULL	wild type liver chromatin	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7069_s_43	16055718	(e) HNF6 binds to  the Glut2 promoter in both wild-type and Foxa2-deficient liver chromatin, with a  trend towards less binding in the absence of Foxa2.	bind
14607	2	5287	6	NULL	NULL	NULL	NULL	HNF-6	GP		bind					Glut2	GP			promoter	NULL	Foxa2-deficient liver chromatin	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7069_s_43	16055718	(e) HNF6 binds to  the Glut2 promoter in both wild-type and Foxa2-deficient liver chromatin, with a  trend towards less binding in the absence of Foxa2.	bind
14608	3	5287	6	NULL	NULL	NULL	NULL	statement 2	Process		is less as compared to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7069_s_43	16055718	(e) HNF6 binds to  the Glut2 promoter in both wild-type and Foxa2-deficient liver chromatin, with a  trend towards less binding in the absence of Foxa2.	bind
15253	1	5287	7	NULL	NULL	0	NULL	HNF6 	NULL		binds	NULL				Glut2	NULL			promoter	NULL	 wild-type liver chromatin	0	NULL	NULL	NULL	gw70_molcellbiol_25_16_7069_s_43	16055718	(e) HNF6 binds to  the Glut2 promoter in both wild-type and Foxa2-deficient liver chromatin, with a  trend towards less binding in the absence of Foxa2.	bind
15254	2	5287	7	NULL	NULL	0	NULL	HNF6	NULL		binds	NULL				Glut2	NULL			promoter	NULL	Foxa2-deficient liver chromatin	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7069_s_43	16055718	(e) HNF6 binds to  the Glut2 promoter in both wild-type and Foxa2-deficient liver chromatin, with a  trend towards less binding in the absence of Foxa2.	bind
19987	4	5287	7	NULL	NULL	0	NULL	statement 2	NULL		is less than	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_16_7069_s_43	16055718	(e) HNF6 binds to  the Glut2 promoter in both wild-type and Foxa2-deficient liver chromatin, with a  trend towards less binding in the absence of Foxa2.	bind
14609	1	5288	6	NULL	NULL	NULL	NULL				bind		weakly	10C		MSL complexes	GP	partial			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_3_136_s_128	10679323	(e) Hoechst and (f) anti-Msl1 antibody staining pattern showing that 10C binds partial MSL complexes only weakly.	bind
15256	1	5288	7	NULL	NULL	0	NULL		NULL		binds	NULL	weakly	10C		MSL complexes	NULL	partial			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_3_136_s_128	10679323	(e) Hoechst and (f) anti-Msl1 antibody staining pattern showing that 10C binds partial MSL complexes only weakly.	bind
14610	1	5289	6	NULL	NULL	NULL	NULL	Rac1	GP	constitutively activated	bind					Pak	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_101_3_283_s_220	10847683	(E) In a yeast two-hybrid assay, constitutively activated Rac1  but not Mtl binds to Pak.	bind
14611	2	5289	6	NULL	NULL	NULL	NULL	Mtl	GP		does not bind					Pak	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_101_3_283_s_220	10847683	(E) In a yeast two-hybrid assay, constitutively activated Rac1  but not Mtl binds to Pak.	bind
15257	1	5289	7	NULL	NULL	0	NULL	Rac1	NULL	constitutively activated	binds to	NULL				Pak	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_101_3_283_s_220	10847683	(E) In a yeast two-hybrid assay, constitutively activated Rac1  but not Mtl binds to Pak.	bind
15258	2	5289	7	NULL	NULL	0	NULL	Mtl	NULL		does not bind	NULL				Pak	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_101_3_283_s_220	10847683	(E) In a yeast two-hybrid assay, constitutively activated Rac1  but not Mtl binds to Pak.	bind
14612	1	5290	6	NULL	NULL	NULL	NULL	Ras2	GP		bind					Lte1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cellbiol_161_5_889_s_47	12782684	(e) In vitro binding of Ras2 and Lte1.	bind
15259	1	5290	7	NULL	NULL	0	NULL	Ras2	NULL		binds	NULL				Lte1	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_cellbiol_161_5_889_s_47	12782684	(e) In vitro binding of Ras2 and Lte1.	bind
14613	1	5291	6	NULL	NULL	NULL	NULL	ERK5	GP		induces					lklf gene	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8553_s_257	16166637	(E) Induction of the endogenous  lklf gene by ERK5.	bind
15260	1	5291	7	NULL	NULL	0	NULL	ERK5	NULL		induce	NULL				lklf gene	NULL	endogenous			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_19_8553_s_257	16166637	(E) Induction of the endogenous  lklf gene by ERK5.	bind
14614	1	5292	6	NULL	NULL	NULL	NULL	CIDR1alpha	GP		bind					B cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_9_5412_s_83	15322039	(E) Inhibition of CIDR1alpha binding to B cells with increasing concentrations of soluble IgG (upper panel) and  IgM (lower panel).	bind
14615	2	5292	6	NULL	NULL	NULL	NULL	IgG	GP	soluble	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_9_5412_s_83	15322039	(E) Inhibition of CIDR1alpha binding to B cells with increasing concentrations of soluble IgG (upper panel) and  IgM (lower panel).	bind
14616	3	5292	6	NULL	NULL	NULL	NULL	IgM	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_72_9_5412_s_83	15322039	(E) Inhibition of CIDR1alpha binding to B cells with increasing concentrations of soluble IgG (upper panel) and  IgM (lower panel).	bind
15261	1	5292	7	NULL	NULL	0	NULL	CIDR1alpha	NULL		bind	NULL				B cells	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_9_5412_s_83	15322039	(E) Inhibition of CIDR1alpha binding to B cells with increasing concentrations of soluble IgG (upper panel) and  IgM (lower panel).	bind
15262	2	5292	7	NULL	NULL	0	NULL	 IgG	NULL	soluble	inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_9_5412_s_83	15322039	(E) Inhibition of CIDR1alpha binding to B cells with increasing concentrations of soluble IgG (upper panel) and  IgM (lower panel).	bind
15263	3	5292	7	NULL	NULL	0	NULL	IgM	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_9_5412_s_83	15322039	(E) Inhibition of CIDR1alpha binding to B cells with increasing concentrations of soluble IgG (upper panel) and  IgM (lower panel).	bind
14617	1	5293	6	NULL	NULL	NULL	NULL	FITC- E. coli	Organism		bind					dSR-CI	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_6_1027_s_165	11754822	(E) Inhibition profile of FITC- E. coli binding to dSR-CI.	bind
15264	1	5293	7	NULL	NULL	0	NULL	FITC- E. coli	NULL		bind	NULL				dSR-CI	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_15_6_1027_s_165	11754822	(E) Inhibition profile of FITC- E. coli binding to dSR-CI.	bind
14618	1	5294	6	NULL	NULL	NULL	NULL	Nck	GP		bind					CD3	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_213	12110186	(E) Interference with Nck binding to CD3  inhibits T cell proliferation.	bind
14619	2	5294	6	NULL	NULL	NULL	NULL	statement 1	Process	Interference with	inhibits					T cell	Cell	proliferation of			NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_213	12110186	(E) Interference with Nck binding to CD3  inhibits T cell proliferation.	bind
15265	1	5294	7	NULL	NULL	0	NULL	Nck	NULL		bind	NULL				CD3	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_109_7_901_s_213	12110186	(E) Interference with Nck binding to CD3  inhibits T cell proliferation.	bind
15266	2	5294	7	10	NULL	0	NULL	statement 1	NULL	interference with	inhibits	NULL				T cell	NULL	profileration of			NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_213	12110186	(E) Interference with Nck binding to CD3  inhibits T cell proliferation.	bind
14620	1	5296	6	NULL	NULL	NULL	NULL	MEK5	GP		bind			PB1 		ERK5	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_6_2065_s_114	16507987	(E) Mapping of residues  required for the MEK5 PB1 domain binding of ERK5.	bind
15267	1	5296	7	NULL	NULL	0	NULL	MEK5	NULL		bind	NULL		PB1 domain		ERK5	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_6_2065_s_114	16507987	(E) Mapping of residues  required for the MEK5 PB1 domain binding of ERK5.	bind
14621	1	5297	6	NULL	NULL	NULL	NULL	mDia1-N	GP		bind					GST-RhoA	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_15_1335_s_105	12906795	(E) mDia1-N binding to GST-RhoA.	bind
15268	1	5297	7	NULL	NULL	0	NULL	mDia1-N	NULL		bind	NULL				GST-RhoA	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_13_15_1335_s_105	12906795	(E) mDia1-N binding to GST-RhoA.	bind
14622	1	5298	6	NULL	NULL	NULL	NULL	Meox1	GP		bind		specifically			B7 oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_7_2757_s_89	15024065	(E) Meox1 and Meox2 bound specifically to the B7 oligonucleotide.	bind
14623	2	5298	6	NULL	NULL	NULL	NULL	Meox2	GP		bind		specifically			B7 oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_7_2757_s_89	15024065	(E) Meox1 and Meox2 bound specifically to the B7 oligonucleotide.	bind
15269	1	5298	7	NULL	NULL	0	NULL	Meox1	NULL		bind	NULL	specifically			B7 oligonucleotide	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_7_2757_s_89	15024065	(E) Meox1 and Meox2 bound specifically to the B7 oligonucleotide.	bind
15270	2	5298	7	NULL	NULL	0	NULL	Meox2	NULL		bind	NULL	specifically			B7 oligonucleotide	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_7_2757_s_89	15024065	(E) Meox1 and Meox2 bound specifically to the B7 oligonucleotide.	bind
14624	1	5299	6	NULL	NULL	NULL	NULL	Oct-3/4	GP		forms a complex with					Sox-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_225	10409735	(E) Model showing how the UTF1 regulatory element can selectively bind the complex comprising Oct-3/4 and Sox-2 and preclude the binding of Oct-6 together with Sox-2.	bind
14625	2	5299	6	NULL	NULL	NULL	NULL	UTF1	GP		bind		selectively		regulatory element	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_225	10409735	(E) Model showing how the UTF1 regulatory element can selectively bind the complex comprising Oct-3/4 and Sox-2 and preclude the binding of Oct-6 together with Sox-2.	bind
14626	3	5299	6	NULL	NULL	NULL	NULL	Oct-6	GP		bind					Sox-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_225	10409735	(E) Model showing how the UTF1 regulatory element can selectively bind the complex comprising Oct-3/4 and Sox-2 and preclude the binding of Oct-6 together with Sox-2.	bind
14627	4	5299	6	NULL	NULL	NULL	NULL	statement 2	Process		precludes					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_225	10409735	(E) Model showing how the UTF1 regulatory element can selectively bind the complex comprising Oct-3/4 and Sox-2 and preclude the binding of Oct-6 together with Sox-2.	bind
15271	1	5299	7	10	NULL	0	NULL	Oct-3/4	NULL		forms a complex with	NULL				Sox-2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_225	10409735	(E) Model showing how the UTF1 regulatory element can selectively bind the complex comprising Oct-3/4 and Sox-2 and preclude the binding of Oct-6 together with Sox-2.	bind
15272	2	5299	7	NULL	NULL	0	NULL	UTF1	NULL		bind	NULL	selectively		regulatory element	statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_225	10409735	(E) Model showing how the UTF1 regulatory element can selectively bind the complex comprising Oct-3/4 and Sox-2 and preclude the binding of Oct-6 together with Sox-2.	bind
15273	3	5299	7	NULL	NULL	0	NULL	Oct-6	NULL		bind	NULL				Sox-2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_225	10409735	(E) Model showing how the UTF1 regulatory element can selectively bind the complex comprising Oct-3/4 and Sox-2 and preclude the binding of Oct-6 together with Sox-2.	bind
15274	4	5299	7	10	NULL	0	NULL	statement 2	NULL		precludes	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_225	10409735	(E) Model showing how the UTF1 regulatory element can selectively bind the complex comprising Oct-3/4 and Sox-2 and preclude the binding of Oct-6 together with Sox-2.	bind
14628	1	5300	6	NULL	NULL	NULL	NULL	Monoclonal antibody AT8	GP		bind					PBs	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_3_646_s_77	12914799	(E) Monoclonal antibody AT8 (for hyperphosphorylated tau) bound to PBs and neuropil threads (arrow head).	bind
14629	2	5300	6	NULL	NULL	NULL	NULL	Monoclonal antibody AT8	GP		bind					neuropil threads	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_3_646_s_77	12914799	(E) Monoclonal antibody AT8 (for hyperphosphorylated tau) bound to PBs and neuropil threads (arrow head).	bind
15275	1	5300	7	10	NULL	0	NULL	Monoclonal antibody AT8	NULL		bind	NULL				PBs	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_3_646_s_77	12914799	(E) Monoclonal antibody AT8 (for hyperphosphorylated tau) bound to PBs and neuropil threads (arrow head).	bind
15276	2	5300	7	10	NULL	0	NULL	Monoclonal antibody AT8	NULL		bind	NULL				 neuropil threads	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_3_646_s_77	12914799	(E) Monoclonal antibody AT8 (for hyperphosphorylated tau) bound to PBs and neuropil threads (arrow head).	bind
14680	1	5301	5	10	NULL	0	NULL	p53		mutant	bind					Net					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1132_s_191	14729959	(E) Mutant p53s bind to Net. SAOS2 cells were transfected  with expression vectors for wild-type or mutant p53s and GST or GST-N6.	bind
14630	1	5301	6	NULL	NULL	NULL	NULL	p53	GP	mutant	bind					Net	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1132_s_191	14729959	(E) Mutant p53s bind to Net. SAOS2 cells were transfected  with expression vectors for wild-type or mutant p53s and GST or GST-N6.	bind
14681	1	5302	5	NULL	NULL	0	NULL		NULL	newly translated	bind	NULL			G t		NULL			CCT	NULL	primary rat retinal culture	NULL	NULL	NULL	NULL	gw60_cell_89_6_927_s_92	9200611	(E) Newly translated G t in a primary rat  retinal culture becomes bound to CCT and is subsequently dissociated.	bind
14682	2	5302	5	NULL	NULL	0	NULL	statement 1	NULL		undergoes	NULL				dissociation	NULL	subsequent			NULL		0	NULL	NULL	NULL	gw60_cell_89_6_927_s_92	9200611	(E) Newly translated G t in a primary rat  retinal culture becomes bound to CCT and is subsequently dissociated.	bind
16208	1	5302	6	NULL	NULL	NULL	NULL	G t	GP	newly translated	bind									CCT	NULL	primary rat retinal culture	NULL	NULL	NULL	NULL	gw60_cell_89_6_927_s_92	9200611	(E) Newly translated G t in a primary rat  retinal culture becomes bound to CCT and is subsequently dissociated.	bind
16211	2	5302	6	NULL	NULL	NULL	NULL	G t	GP	newly translated	is dissociated from					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_6_927_s_92	9200611	(E) Newly translated G t in a primary rat  retinal culture becomes bound to CCT and is subsequently dissociated.	bind
14683	1	5303	5	NULL	NULL	0	NULL	p53	NULL		bind	NULL				IGFBP3	NULL			promoter	NULL	in vivo	0	NULL	NULL	NULL	gw70_molcellbiol_25_5_2014_s_357	15713654	(E) p53 and p53(deltaAD1deltaBD) bind the IGFBP3 promoter in vivo.	bind
14684	2	5303	5	NULL	NULL	0	NULL	p53	NULL		bind	NULL		deltaAD1deltaBD		IGFBP3	NULL			promoter	NULL	in vivo	0	NULL	NULL	NULL	gw70_molcellbiol_25_5_2014_s_357	15713654	(E) p53 and p53(deltaAD1deltaBD) bind the IGFBP3 promoter in vivo.	bind
14631	1	5303	6	NULL	NULL	NULL	NULL	p53	GP		bind					IGFBP3	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_2014_s_357	15713654	(E) p53 and p53(deltaAD1deltaBD) bind the IGFBP3 promoter in vivo.	bind
14632	2	5303	6	NULL	NULL	NULL	NULL	p53	GP		bind			deltaAD1deltaBD		IGFBP3	GP			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_2014_s_357	15713654	(E) p53 and p53(deltaAD1deltaBD) bind the IGFBP3 promoter in vivo.	bind
14685	1	5304	5	NULL	NULL	0	NULL	p53/6KR protein	NULL		bind	NULL				MDM2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_24_8533_s_228	11713288	(E) p53/6KR or 6KA protein binding to MDM2 was assessed as described in Materials and Methods.	bind
14686	2	5304	5	NULL	NULL	0	NULL	6KA protein	NULL		bind	NULL				MDM2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_24_8533_s_228	11713288	(E) p53/6KR or 6KA protein binding to MDM2 was assessed as described in Materials and Methods.	bind
14687	3	5304	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_24_8533_s_228	11713288	(E) p53/6KR or 6KA protein binding to MDM2 was assessed as described in Materials and Methods.	bind
14633	1	5304	6	NULL	NULL	NULL	NULL	p53/6KR protein	GP		bind					MDM2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_24_8533_s_228	11713288	(E) p53/6KR or 6KA protein binding to MDM2 was assessed as described in Materials and Methods.	bind
14634	2	5304	6	NULL	NULL	NULL	NULL	6KA protein	GP		bind					MDM2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_24_8533_s_228	11713288	(E) p53/6KR or 6KA protein binding to MDM2 was assessed as described in Materials and Methods.	bind
19020	3	5304	6	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_24_8533_s_228	11713288	(E) p53/6KR or 6KA protein binding to MDM2 was assessed as described in Materials and Methods.	bind
14688	1	5305	5	NULL	NULL	0	NULL	p54nrb	NULL		bind	NULL				I-RNA	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_cell_106_4_465_s_225	11525732	(E) p54nrb binds I-RNA in vivo.	bind
14635	1	5305	6	NULL	NULL	NULL	NULL	p54nrb	GP		bind					I-RNA	NucleicAcid				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_cell_106_4_465_s_225	11525732	(E) p54nrb binds I-RNA in vivo.	bind
14689	1	5306	5	NULL	NULL	0	NULL	eIF4E	NULL		bind	NULL	selectively			cyclin D1	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_169_2_245_s_54	15837800	(E) Parallel  RT-PCR methods to the experiments in A - C confirm the above results indicating eIF4E  selectively binds cyclin D1 in a cap-dependent manner.	bind
14690	2	5306	5	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				cap	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_169_2_245_s_54	15837800	(E) Parallel  RT-PCR methods to the experiments in A - C confirm the above results indicating eIF4E  selectively binds cyclin D1 in a cap-dependent manner.	bind
14636	1	5306	6	NULL	NULL	NULL	NULL	eIF4E	GP		bind		selectively			cyclin D1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_169_2_245_s_54	15837800	(E) Parallel  RT-PCR methods to the experiments in A - C confirm the above results indicating eIF4E  selectively binds cyclin D1 in a cap-dependent manner.	bind
14637	2	5306	6	NULL	NULL	NULL	NULL	statement 1	Process		is dependent on					cap	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_169_2_245_s_54	15837800	(E) Parallel  RT-PCR methods to the experiments in A - C confirm the above results indicating eIF4E  selectively binds cyclin D1 in a cap-dependent manner.	bind
14691	1	5308	5	NULL	NULL	0	NULL	Phb-CC	NULL		bind	NULL				HDAC1	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_2_459_s_137	14637159	(E) Phb-CC  binds to HDAC1 in vitro.	bind
14638	1	5308	6	NULL	NULL	NULL	NULL	Phb-CC	GP		bind					HDAC1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_2_459_s_137	14637159	(E) Phb-CC  binds to HDAC1 in vitro.	bind
14692	1	5309	5	NULL	NULL	0	NULL	SMRT	NULL		associate with	NULL	physically			MEKK-1	NULL				NULL	in mammalian cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6612_s_258	10938135	(E) Physical association of SMRT with MEKK-1 and MEK-1 in mammalian cells.	bind
14693	2	5309	5	NULL	NULL	0	NULL	SMRT	NULL		associate with	NULL	physically			MEK-1	NULL				NULL	in mammalian cells	0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6612_s_258	10938135	(E) Physical association of SMRT with MEKK-1 and MEK-1 in mammalian cells.	bind
14639	1	5309	6	NULL	NULL	NULL	NULL	SMRT	GP		associate with		physically			MEKK-1	GP				NULL	mammalian cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6612_s_258	10938135	(E) Physical association of SMRT with MEKK-1 and MEK-1 in mammalian cells.	bind
14640	2	5309	6	NULL	NULL	NULL	NULL	SMRT	GP		associate with		physically			MEK-1	GP				NULL	mammalian cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6612_s_258	10938135	(E) Physical association of SMRT with MEKK-1 and MEK-1 in mammalian cells.	bind
14752	1	5311	5	NULL	NULL	0	NULL	Ap-uch	NULL		bind	NULL				proteasome	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_89_1_115_s_177	9094720	(E) Quantification of Ap-uch bound to the proteasome (from blot  shown in panel D).	bind
14641	1	5311	6	NULL	NULL	NULL	NULL	Ap-uch	GP		bind					proteasome	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_1_115_s_177	9094720	(E) Quantification of Ap-uch bound to the proteasome (from blot  shown in panel D).	bind
14753	1	5312	5	NULL	NULL	0	NULL	TCF-4	NULL		bind	NULL				beta-catenin	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_2_369_s_254	11470825	(E) Quantification of the amount of TCF-4 bound to beta-catenin after 1alpha,25(OH)2D3 addition.	bind
14754	2	5312	5	NULL	NULL	0	NULL	statement 1	NULL		occurs after	NULL				1alpha,25(OH)2D3	NULL	addition of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_2_369_s_254	11470825	(E) Quantification of the amount of TCF-4 bound to beta-catenin after 1alpha,25(OH)2D3 addition.	bind
14642	1	5312	6	NULL	NULL	NULL	NULL	TCF-4	GP		bind					beta-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_2_369_s_254	11470825	(E) Quantification of the amount of TCF-4 bound to beta-catenin after 1alpha,25(OH)2D3 addition.	bind
19021	2	5312	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs after 					1alpha,25(OH)2D3	Chemical	addition of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_2_369_s_254	11470825	(E) Quantification of the amount of TCF-4 bound to beta-catenin after 1alpha,25(OH)2D3 addition.	bind
14756	1	5313	5	NULL	NULL	0	NULL	HDAC1	NULL		bind	NULL				bcl-2	NULL			P1 promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_287	15713621	(E) Quantitative ChIP assays of the binding of HDAC1 and HDAC2  to the  bcl-2 P1 promoter.	bind
14757	2	5313	5	NULL	NULL	0	NULL	HDAC2	NULL		bind	NULL				bcl-2	NULL			P1 promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_287	15713621	(E) Quantitative ChIP assays of the binding of HDAC1 and HDAC2  to the  bcl-2 P1 promoter.	bind
14643	1	5313	6	NULL	NULL	NULL	NULL	HDAC1	GP		bind					bcl-2 	GP			P1 promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_287	15713621	(E) Quantitative ChIP assays of the binding of HDAC1 and HDAC2  to the  bcl-2 P1 promoter.	bind
14644	2	5313	6	NULL	NULL	NULL	NULL	HDAC2	GP		bind					bcl-2 	GP			P1 promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_287	15713621	(E) Quantitative ChIP assays of the binding of HDAC1 and HDAC2  to the  bcl-2 P1 promoter.	bind
14758	1	5314	5	NULL	NULL	0	NULL	eIF4GI	NULL	recombinant	does not bind	NULL		(157-1090) Y776A		eIF4A	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_2_468_s_165	10611225	(E) Recombinant eIF4GI(157-1090) Y776A does not bind eIF4A.	bind
14645	1	5314	6	NULL	NULL	NULL	NULL	eIF4GI	GP	recombinant	does not bind			157-1090 Y776A		eIF4A	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_2_468_s_165	10611225	(E) Recombinant eIF4GI(157-1090) Y776A does not bind eIF4A.	bind
14759	1	5316	5	NULL	NULL	0	NULL		NULL		bind	NULL		PH domains		PI(3,4)P2	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_8_3242_s_172	12925760	(E) Residues   conserved in PH domains binding to PI(3,4)P2 and  PI(3,4,5)P3 (Isakoff  et  al., 1998 ) are aligned to the SWAP-70 sequence.	bind
14760	2	5316	5	NULL	NULL	0	NULL		NULL		bind	NULL		PH domains		PI(3,4,5)P3	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_8_3242_s_172	12925760	(E) Residues   conserved in PH domains binding to PI(3,4)P2 and  PI(3,4,5)P3 (Isakoff  et  al., 1998 ) are aligned to the SWAP-70 sequence.	bind
19022	1	5316	6	NULL	NULL	NULL	NULL				bind			PH domain		PI(3,4)P2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_8_3242_s_172	12925760	(E) Residues   conserved in PH domains binding to PI(3,4)P2 and  PI(3,4,5)P3 (Isakoff  et  al., 1998 ) are aligned to the SWAP-70 sequence.	bind
19023	2	5316	6	NULL	NULL	NULL	NULL				bind			PH domain		PI(3,4,5)P3	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_8_3242_s_172	12925760	(E) Residues   conserved in PH domains binding to PI(3,4)P2 and  PI(3,4,5)P3 (Isakoff  et  al., 1998 ) are aligned to the SWAP-70 sequence.	bind
14763	1	5319	5	10	NULL	0	NULL	CUGBP2			bind		specifically							A-II region	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_1_113_s_162	12535526	(E) Scanning mutagenesis identifies specific CUGBP2 binding to A-II and A-III regions.	bind
14764	2	5319	5	10	NULL	0	NULL	CUGBP2			bind		specifically							A-III region	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_1_113_s_162	12535526	(E) Scanning mutagenesis identifies specific CUGBP2 binding to A-II and A-III regions.	bind
14646	1	5319	6	NULL	NULL	NULL	NULL	CUGBP2	GP		bind		specifically							A-II region	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_1_113_s_162	12535526	(E) Scanning mutagenesis identifies specific CUGBP2 binding to A-II and A-III regions.	bind
14647	2	5319	6	NULL	NULL	NULL	NULL	CUGBP2	GP		bind		specifically							A-III region	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_1_113_s_162	12535526	(E) Scanning mutagenesis identifies specific CUGBP2 binding to A-II and A-III regions.	bind
14766	1	5320	5	NULL	NULL	0	NULL	Sno	NULL		bind	NULL		C-terminal domain		Su(H)	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_110_5_625_s_257	12230979	(E) Sno binds to Su(H) via its C-terminal domain.	bind
14648	1	5320	6	NULL	NULL	NULL	NULL	Sno	GP		bind			C-terminal domain		Su(H)	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_5_625_s_257	12230979	(E) Sno binds to Su(H) via its C-terminal domain.	bind
14767	1	5321	5	NULL	NULL	0	NULL	dATF-2	NULL		bind	NULL	specifically				NULL			CRE	NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_6_2934_s_168	15788564	(E) Specific binding of  dATF-2 to CRE.	bind
14649	1	5321	6	NULL	NULL	NULL	NULL	dATF-2	GP		bind		specifically							CRE	NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_6_2934_s_168	15788564	(E) Specific binding of  dATF-2 to CRE.	bind
14769	1	5322	5	10	NULL	0	NULL	p53			bind		specifically			FAK				promoter	NULL	in HeLa cells	NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_111_s_344	15157737	(E) Specific binding of p53 with the FAK-promoter  probe in HeLa cells.	bind
14650	1	5322	6	NULL	NULL	NULL	NULL	p53	GP		bind		specifically			FAK	GP			promoter	NULL	HeLa cells	NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1678_2_111_s_344	15157737	(E) Specific binding of p53 with the FAK-promoter  probe in HeLa cells.	bind
14771	1	5323	5	NULL	NULL	0	NULL	FarB	NULL		bind	NULL				probe J7-8	NULL				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_5_794_s_239	16682457	(E) Specific competition of binding of FarB and FarA to probe J7-8.	bind
14772	2	5323	5	NULL	NULL	0	NULL	FarA	NULL		bind	NULL				probe J7-8	NULL				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_5_794_s_239	16682457	(E) Specific competition of binding of FarB and FarA to probe J7-8.	bind
14773	3	5323	5	NULL	NULL	0	NULL	statement 1	NULL		compete with	NULL	specifically			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_5_794_s_239	16682457	(E) Specific competition of binding of FarB and FarA to probe J7-8.	bind
14651	1	5323	6	NULL	NULL	NULL	NULL	FarB	GP		bind					probe J7-8	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_5_5_794_s_239	16682457	(E) Specific competition of binding of FarB and FarA to probe J7-8.	bind
14652	2	5323	6	NULL	NULL	NULL	NULL	FarA	GP		bind					probe J7-8	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_5_5_794_s_239	16682457	(E) Specific competition of binding of FarB and FarA to probe J7-8.	bind
19024	3	5323	6	NULL	NULL	NULL	NULL	statement 1	Process		competes		specifically			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_5_5_794_s_239	16682457	(E) Specific competition of binding of FarB and FarA to probe J7-8.	bind
14774	1	5325	5	NULL	NULL	0	NULL		NULL		bind	NULL		PDZ		CtBP1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1389_s_153	12769861	(E) SUMOylation blocks PDZ binding to CtBP1.	bind
14775	2	5325	5	NULL	NULL	0	NULL	SUMOylation	NULL		blocks	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1389_s_153	12769861	(E) SUMOylation blocks PDZ binding to CtBP1.	bind
14694	1	5325	6	NULL	NULL	NULL	NULL				bind			PDZ		CtBP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1389_s_153	12769861	(E) SUMOylation blocks PDZ binding to CtBP1.	bind
14695	2	5325	6	NULL	NULL	NULL	NULL	SUMOylation	Process		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1389_s_153	12769861	(E) SUMOylation blocks PDZ binding to CtBP1.	bind
14776	1	5326	5	10	NULL	0	NULL	msl-2			bind				3 UTR 	SXL					NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1397_s_78	12769862	(E) The 3  UTR  msl-2 sequences provide a function in addition to SXL binding.	bind
14696	1	5326	6	NULL	NULL	NULL	NULL	msl-2	GP		bind				3 UTR	SXL	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1397_s_78	12769862	(E) The 3  UTR  msl-2 sequences provide a function in addition to SXL binding.	bind
14777	1	5328	5	NULL	NULL	0	NULL	p53	NULL		bind	NULL				p21	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_22_9958_s_144	15509798	(E) The effect of NAD or TDP on p53 binding  to p21 versus hdm2 DNA is quantified below each lane.	bind
14778	2	5328	5	NULL	NULL	0	NULL	p53	NULL		bind	NULL				hdm2 DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_22_9958_s_144	15509798	(E) The effect of NAD or TDP on p53 binding  to p21 versus hdm2 DNA is quantified below each lane.	bind
14697	1	5328	6	NULL	NULL	NULL	NULL	p53	GP		bind					p21	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_22_9958_s_144	15509798	(E) The effect of NAD or TDP on p53 binding  to p21 versus hdm2 DNA is quantified below each lane.	bind
14698	2	5328	6	NULL	NULL	NULL	NULL	p53	GP		bind					hdm2 DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_22_9958_s_144	15509798	(E) The effect of NAD or TDP on p53 binding  to p21 versus hdm2 DNA is quantified below each lane.	bind
14779	1	5331	5	NULL	NULL	0	NULL	PLIC1	NULL		bind	NULL		UBA domain		K7	NULL				NULL	in 293T cells	0	NULL	NULL	NULL	gw70_molcellbiol_24_9_3938_s_133	15082787	(E) The PLIC1 UBA domain binds to K7 in 293T  cells.	bind
14699	1	5331	6	NULL	NULL	NULL	NULL	PLIC1	GP		bind			UBA		K7	GP				NULL	293T cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_9_3938_s_133	15082787	(E) The PLIC1 UBA domain binds to K7 in 293T  cells.	bind
14780	1	5332	5	NULL	NULL	0	NULL		NULL		bind	NULL		SH3 domains			NULL		DH domain		NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_4_1624_s_227	12686614	(E) The SH3 domains  bind the DH domain.	bind
14700	1	5332	6	NULL	NULL	NULL	NULL				bind			SH3 domain					DH domain		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_4_1624_s_227	12686614	(E) The SH3 domains  bind the DH domain.	bind
14781	1	5334	5	NULL	NULL	0	NULL	PBX	NULL		bind	NULL				CBP	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_21_7509_s_122	11585930	(E) The TALE motif does not prevent PBX binding to CBP, but changing an arginine to lysine within HD helix 3 increases CBP binding to PBX.	bind
14782	2	5334	5	NULL	NULL	0	NULL		NULL		does not prevent	NULL		TALE motif		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_21_7509_s_122	11585930	(E) The TALE motif does not prevent PBX binding to CBP, but changing an arginine to lysine within HD helix 3 increases CBP binding to PBX.	bind
14783	3	5334	5	NULL	NULL	0	NULL	arginine	NULL		changes to	NULL				lysine	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_21_7509_s_122	11585930	(E) The TALE motif does not prevent PBX binding to CBP, but changing an arginine to lysine within HD helix 3 increases CBP binding to PBX.	bind
19092	4	5334	5	NULL	NULL	0	NULL	statement 3	NULL		occurs in	NULL					NULL		HD helix 3		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_21_7509_s_122	11585930	(E) The TALE motif does not prevent PBX binding to CBP, but changing an arginine to lysine within HD helix 3 increases CBP binding to PBX.	bind
19093	5	5334	5	NULL	NULL	0	NULL	statement 4	NULL		increases	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_21_7509_s_122	11585930	(E) The TALE motif does not prevent PBX binding to CBP, but changing an arginine to lysine within HD helix 3 increases CBP binding to PBX.	bind
14701	1	5334	6	NULL	NULL	NULL	NULL	CBP	GP		bind					PBX	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_21_7509_s_122	11585930	(E) The TALE motif does not prevent PBX binding to CBP, but changing an arginine to lysine within HD helix 3 increases CBP binding to PBX.	bind
14702	2	5334	6	NULL	NULL	NULL	NULL				does not prevent			TALE motif		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_21_7509_s_122	11585930	(E) The TALE motif does not prevent PBX binding to CBP, but changing an arginine to lysine within HD helix 3 increases CBP binding to PBX.	bind
14703	3	5334	6	NULL	NULL	NULL	NULL	arginine	AminoAcid		changes to					lysine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_21_7509_s_122	11585930	(E) The TALE motif does not prevent PBX binding to CBP, but changing an arginine to lysine within HD helix 3 increases CBP binding to PBX.	bind
19025	4	5334	6	NULL	NULL	NULL	NULL	statement 3	Process		occurs in								HD helix 3		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_21_7509_s_122	11585930	(E) The TALE motif does not prevent PBX binding to CBP, but changing an arginine to lysine within HD helix 3 increases CBP binding to PBX.	bind
19026	5	5334	6	NULL	NULL	NULL	NULL	statement 4	Process		increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_21_7509_s_122	11585930	(E) The TALE motif does not prevent PBX binding to CBP, but changing an arginine to lysine within HD helix 3 increases CBP binding to PBX.	bind
14784	1	5337	5	NULL	NULL	0	NULL	iron	NULL		bind	NULL				Lf	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_21_6091_s_128	11029429	(e) Viable counts of  E. coli strain E2348/69 after 18 h of incubation from an inoculum of 102 CFU/ml in unsupplemented serum-SAPI medium (control) or in serum-SAPI medium supplemented with NE complexes of (i) the Tf isoform mixture used as markers in panel c above, (ii) Apo-Tf, (iii) iron-bound Lf, or (iv) BSA. (f) Binding of [3]NE, expressed as 3H cpm per 30 mug of protein, to (i) partially iron-saturated Tf, (ii) Apo-Tf, (iii) iron-bound Lf, or (iv) BSA; the values shown are the means of triplicate assays.	bind
14785	2	5337	5	10	NULL	0	NULL	NE			bind					Tf		partially iron-saturated			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_21_6091_s_128	11029429	(e) Viable counts of  E. coli strain E2348/69 after 18 h of incubation from an inoculum of 102 CFU/ml in unsupplemented serum-SAPI medium (control) or in serum-SAPI medium supplemented with NE complexes of (i) the Tf isoform mixture used as markers in panel c above, (ii) Apo-Tf, (iii) iron-bound Lf, or (iv) BSA. (f) Binding of [3]NE, expressed as 3H cpm per 30 mug of protein, to (i) partially iron-saturated Tf, (ii) Apo-Tf, (iii) iron-bound Lf, or (iv) BSA; the values shown are the means of triplicate assays.	bind
56060	3	5337	5	10	NULL	0	NULL	NE			bind					Apo-Tf					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_21_6091_s_128	11029429	(e) Viable counts of  E. coli strain E2348/69 after 18 h of incubation from an inoculum of 102 CFU/ml in unsupplemented serum-SAPI medium (control) or in serum-SAPI medium supplemented with NE complexes of (i) the Tf isoform mixture used as markers in panel c above, (ii) Apo-Tf, (iii) iron-bound Lf, or (iv) BSA. (f) Binding of [3]NE, expressed as 3H cpm per 30 mug of protein, to (i) partially iron-saturated Tf, (ii) Apo-Tf, (iii) iron-bound Lf, or (iv) BSA; the values shown are the means of triplicate assays.	bind
56061	4	5337	5	10	NULL	0	NULL	NE			bind					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_21_6091_s_128	11029429	(e) Viable counts of  E. coli strain E2348/69 after 18 h of incubation from an inoculum of 102 CFU/ml in unsupplemented serum-SAPI medium (control) or in serum-SAPI medium supplemented with NE complexes of (i) the Tf isoform mixture used as markers in panel c above, (ii) Apo-Tf, (iii) iron-bound Lf, or (iv) BSA. (f) Binding of [3]NE, expressed as 3H cpm per 30 mug of protein, to (i) partially iron-saturated Tf, (ii) Apo-Tf, (iii) iron-bound Lf, or (iv) BSA; the values shown are the means of triplicate assays.	bind
14704	1	5337	6	NULL	NULL	NULL	NULL	iron	Chemical		bind					Lf	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_21_6091_s_128	11029429	(e) Viable counts of  E. coli strain E2348/69 after 18 h of incubation from an inoculum of 102 CFU/ml in unsupplemented serum-SAPI medium (control) or in serum-SAPI medium supplemented with NE complexes of (i) the Tf isoform mixture used as markers in panel c above, (ii) Apo-Tf, (iii) iron-bound Lf, or (iv) BSA. (f) Binding of [3]NE, expressed as 3H cpm per 30 mug of protein, to (i) partially iron-saturated Tf, (ii) Apo-Tf, (iii) iron-bound Lf, or (iv) BSA; the values shown are the means of triplicate assays.	bind
19160	2	5337	6	NULL	NULL	NULL	NULL	NE	OrganismPart		bind					Tf	GP	partially iron-saturated			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_21_6091_s_128	11029429	(e) Viable counts of  E. coli strain E2348/69 after 18 h of incubation from an inoculum of 102 CFU/ml in unsupplemented serum-SAPI medium (control) or in serum-SAPI medium supplemented with NE complexes of (i) the Tf isoform mixture used as markers in panel c above, (ii) Apo-Tf, (iii) iron-bound Lf, or (iv) BSA. (f) Binding of [3]NE, expressed as 3H cpm per 30 mug of protein, to (i) partially iron-saturated Tf, (ii) Apo-Tf, (iii) iron-bound Lf, or (iv) BSA; the values shown are the means of triplicate assays.	bind
19161	3	5337	6	NULL	NULL	NULL	NULL	NE	OrganismPart		bind					Apo-Tf	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_21_6091_s_128	11029429	(e) Viable counts of  E. coli strain E2348/69 after 18 h of incubation from an inoculum of 102 CFU/ml in unsupplemented serum-SAPI medium (control) or in serum-SAPI medium supplemented with NE complexes of (i) the Tf isoform mixture used as markers in panel c above, (ii) Apo-Tf, (iii) iron-bound Lf, or (iv) BSA. (f) Binding of [3]NE, expressed as 3H cpm per 30 mug of protein, to (i) partially iron-saturated Tf, (ii) Apo-Tf, (iii) iron-bound Lf, or (iv) BSA; the values shown are the means of triplicate assays.	bind
19162	4	5337	6	NULL	NULL	NULL	NULL	NE	OrganismPart		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_21_6091_s_128	11029429	(e) Viable counts of  E. coli strain E2348/69 after 18 h of incubation from an inoculum of 102 CFU/ml in unsupplemented serum-SAPI medium (control) or in serum-SAPI medium supplemented with NE complexes of (i) the Tf isoform mixture used as markers in panel c above, (ii) Apo-Tf, (iii) iron-bound Lf, or (iv) BSA. (f) Binding of [3]NE, expressed as 3H cpm per 30 mug of protein, to (i) partially iron-saturated Tf, (ii) Apo-Tf, (iii) iron-bound Lf, or (iv) BSA; the values shown are the means of triplicate assays.	bind
14786	1	5338	5	NULL	NULL	0	NULL	Jacob	NULL	E. histolytica	bind	NULL				chitin	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_6_3259_s_40	12011021	(E) Western blot analysis of chitin binding by  E. histolytica Jacob, detected with anti-myc antibodies and chemiluminescence.	bind
14705	1	5338	6	NULL	NULL	NULL	NULL	Jacob	GP	E. histolytica	bind					chitin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_6_3259_s_40	12011021	(E) Western blot analysis of chitin binding by  E. histolytica Jacob, detected with anti-myc antibodies and chemiluminescence.	bind
14787	1	5339	5	NULL	NULL	0	NULL	Sam68	NULL		bind	NULL				cyclin B1	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_14_s_186	16221888	(E) Western blot analysis of the IgG, cyclin B1 and Erk1/2  immunoprecipitates from the kinase assay (D) probed with anti-Sam68 antibody: Sam68  binds both cyclin B1 and Erk1/2, but this interaction is inhibited by OA stimulation.	bind
14788	2	5339	5	NULL	NULL	0	NULL	Sam68	NULL		bind	NULL				Erk1/2	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_14_s_186	16221888	(E) Western blot analysis of the IgG, cyclin B1 and Erk1/2  immunoprecipitates from the kinase assay (D) probed with anti-Sam68 antibody: Sam68  binds both cyclin B1 and Erk1/2, but this interaction is inhibited by OA stimulation.	bind
14789	3	5339	5	NULL	NULL	0	NULL	OA	NULL	stimulation by	inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_14_s_186	16221888	(E) Western blot analysis of the IgG, cyclin B1 and Erk1/2  immunoprecipitates from the kinase assay (D) probed with anti-Sam68 antibody: Sam68  binds both cyclin B1 and Erk1/2, but this interaction is inhibited by OA stimulation.	bind
14790	4	5339	5	NULL	NULL	0	NULL	OA	NULL	stimulation by	inhibit	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_14_s_186	16221888	(E) Western blot analysis of the IgG, cyclin B1 and Erk1/2  immunoprecipitates from the kinase assay (D) probed with anti-Sam68 antibody: Sam68  binds both cyclin B1 and Erk1/2, but this interaction is inhibited by OA stimulation.	bind
14706	1	5339	6	NULL	NULL	NULL	NULL	Sam68	GP		bind					cyclin B1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_14_s_186	16221888	(E) Western blot analysis of the IgG, cyclin B1 and Erk1/2  immunoprecipitates from the kinase assay (D) probed with anti-Sam68 antibody: Sam68  binds both cyclin B1 and Erk1/2, but this interaction is inhibited by OA stimulation.	bind
14707	2	5339	6	NULL	NULL	NULL	NULL	Sam68	GP		bind					Erk1/2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_14_s_186	16221888	(E) Western blot analysis of the IgG, cyclin B1 and Erk1/2  immunoprecipitates from the kinase assay (D) probed with anti-Sam68 antibody: Sam68  binds both cyclin B1 and Erk1/2, but this interaction is inhibited by OA stimulation.	bind
14708	3	5339	6	NULL	NULL	NULL	NULL	OA	Chemical	stimulation of	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_14_s_186	16221888	(E) Western blot analysis of the IgG, cyclin B1 and Erk1/2  immunoprecipitates from the kinase assay (D) probed with anti-Sam68 antibody: Sam68  binds both cyclin B1 and Erk1/2, but this interaction is inhibited by OA stimulation.	bind
14709	4	5339	6	NULL	NULL	NULL	NULL	OA	Chemical	stimulation of	inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_1_14_s_186	16221888	(E) Western blot analysis of the IgG, cyclin B1 and Erk1/2  immunoprecipitates from the kinase assay (D) probed with anti-Sam68 antibody: Sam68  binds both cyclin B1 and Erk1/2, but this interaction is inhibited by OA stimulation.	bind
14791	1	5340	5	NULL	NULL	0	NULL	MBP	NULL	bovine	does not bind	NULL				MAG	NULL				NULL		0	NULL	NULL	NULL	gw70_neurobioldis_12_1_1_s_166	12609484	(E) Western blot of bovine MBP after incubation with serum and IgM (data not shown)  bound to several spinal cord proteins, they did not bind to MAG (  Fig. 4B) nor CSPG (  Fig. 4C).	bind
14792	2	5340	5	NULL	NULL	0	NULL	MBP	NULL	bovine	does not bind	NULL				CSPG	NULL				NULL		NULL	NULL	NULL	NULL	gw70_neurobioldis_12_1_1_s_166	12609484	(E) Western blot of bovine MBP after incubation with serum and IgM (data not shown)  bound to several spinal cord proteins, they did not bind to MAG (  Fig. 4B) nor CSPG (  Fig. 4C).	bind
19094	3	5340	5	NULL	NULL	0	NULL	MBP	NULL	bovine	bind	NULL				spinal cord proteins	NULL				NULL		0	NULL	NULL	NULL	gw70_neurobioldis_12_1_1_s_166	12609484	(E) Western blot of bovine MBP after incubation with serum and IgM (data not shown)  bound to several spinal cord proteins, they did not bind to MAG (  Fig. 4B) nor CSPG (  Fig. 4C).	bind
14710	1	5340	6	NULL	NULL	NULL	NULL	MBP	GP	bovine	bind					spinal cord proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_neurobioldis_12_1_1_s_166	12609484	(E) Western blot of bovine MBP after incubation with serum and IgM (data not shown)  bound to several spinal cord proteins, they did not bind to MAG (  Fig. 4B) nor CSPG (  Fig. 4C).	bind
14711	2	5340	6	NULL	NULL	NULL	NULL	MBP	GP	bovine	does not bind					MAG	GP				NULL		NULL	NULL	NULL	NULL	gw70_neurobioldis_12_1_1_s_166	12609484	(E) Western blot of bovine MBP after incubation with serum and IgM (data not shown)  bound to several spinal cord proteins, they did not bind to MAG (  Fig. 4B) nor CSPG (  Fig. 4C).	bind
14712	3	5340	6	NULL	NULL	NULL	NULL	MBP	GP	bovine	does not bind					CSPG	GP				NULL		NULL	NULL	NULL	NULL	gw70_neurobioldis_12_1_1_s_166	12609484	(E) Western blot of bovine MBP after incubation with serum and IgM (data not shown)  bound to several spinal cord proteins, they did not bind to MAG (  Fig. 4B) nor CSPG (  Fig. 4C).	bind
14793	1	5342	5	NULL	NULL	0	NULL	cain	NULL		blocks	NULL				MyHC	NULL	expression of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6600_s_188	10938134	(E) Western blot quantitation revealed a dramatic increase in the amount of total MyHC protein between MyoD and calcineurin, while cain blocked MyHC expression.	bind
14713	1	5342	6	NULL	NULL	NULL	NULL	cain	GP		blocks					MyHC	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6600_s_188	10938134	(E) Western blot quantitation revealed a dramatic increase in the amount of total MyHC protein between MyoD and calcineurin, while cain blocked MyHC expression.	bind
14794	2	5343	5	10	NULL	0	NULL	statement 1			 activate					CRF-R2					NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_3_401_s_115	12895416	(E) When CRF is not bound to CRF-BP, it does not activate CRF-R2.	bind
14795	1	5343	5	10	NULL	0	NULL	CRF			bind					CRF-BP					NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_3_401_s_115	12895416	(E) When CRF is not bound to CRF-BP, it does not activate CRF-R2.	bind
14714	1	5343	6	NULL	NULL	NULL	NULL	CRF	GP		bind					CRF-BP	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_3_401_s_115	12895416	(E) When CRF is not bound to CRF-BP, it does not activate CRF-R2.	bind
14715	2	5343	6	NULL	NULL	NULL	NULL	statement 1	Process		activates					CRF-R2	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_3_401_s_115	12895416	(E) When CRF is not bound to CRF-BP, it does not activate CRF-R2.	bind
14797	1	5344	5	NULL	NULL	0	NULL	WISH	NULL		bind	NULL		SH3 domain		N-WASP	NULL		proline-rich region		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_3_471_s_87	11157975	(E) WISH SH3 domain binds to the proline-rich region of N-WASP.	bind
14716	1	5344	6	NULL	NULL	NULL	NULL	WISH	GP		bind			SH3 domain		N-WASP	GP		proline-rich region		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_3_471_s_87	11157975	(E) WISH SH3 domain binds to the proline-rich region of N-WASP.	bind
14798	1	5346	5	10	NULL	0	NULL	olfactory receptor neurons		subset of	bind					lectin UEA-1					NULL	P2-Lis1 mice	NULL	NULL	NULL	NULL	gw60_brainres_932_1_1_s_133	11911856	(E, F) The subset of olfactory receptor neurons binding the lectin UEA-1 converge on multiple glomeruli in the ventral region of the olfactory bulb (solid arrows) in both control and P2-Lis1 mice.	bind
14799	4	5346	5	10	NULL	0	NULL	statement 2			converge on					multiple glomeruli		in the ventral region of the olfactory bulb			NULL	in control mice	NULL	NULL	NULL	NULL	gw60_brainres_932_1_1_s_133	11911856	(E, F) The subset of olfactory receptor neurons binding the lectin UEA-1 converge on multiple glomeruli in the ventral region of the olfactory bulb (solid arrows) in both control and P2-Lis1 mice.	bind
14800	3	5346	5	10	NULL	0	NULL	statement 1			converge on					multiple glomeruli		in the ventral region of the olfactory bulb			NULL	in P2-Lis1 mice	NULL	NULL	NULL	NULL	gw60_brainres_932_1_1_s_133	11911856	(E, F) The subset of olfactory receptor neurons binding the lectin UEA-1 converge on multiple glomeruli in the ventral region of the olfactory bulb (solid arrows) in both control and P2-Lis1 mice.	bind
56076	2	5346	5	10	NULL	0	NULL	olfactory receptor neurons			bind					lectin UEA-1					NULL	control mice	0	NULL	NULL	NULL	gw60_brainres_932_1_1_s_133	11911856	(E, F) The subset of olfactory receptor neurons binding the lectin UEA-1 converge on multiple glomeruli in the ventral region of the olfactory bulb (solid arrows) in both control and P2-Lis1 mice.	bind
14717	1	5346	6	NULL	NULL	NULL	NULL	olfactory receptor neurons	OrganismPart		bind					lectin UEA-1	GP				NULL	control mice	NULL	NULL	NULL	NULL	gw60_brainres_932_1_1_s_133	11911856	(E, F) The subset of olfactory receptor neurons binding the lectin UEA-1 converge on multiple glomeruli in the ventral region of the olfactory bulb (solid arrows) in both control and P2-Lis1 mice.	bind
14718	2	5346	6	NULL	NULL	NULL	NULL	olfactory receptor neurons	OrganismPart		bind					lectin UEA-1	GP				NULL	P2-Lis1 mice	NULL	NULL	NULL	NULL	gw60_brainres_932_1_1_s_133	11911856	(E, F) The subset of olfactory receptor neurons binding the lectin UEA-1 converge on multiple glomeruli in the ventral region of the olfactory bulb (solid arrows) in both control and P2-Lis1 mice.	bind
56077	3	5346	6	NULL	NULL	NULL	NULL	statement 1	Process		converge on					multiple glomeruli 	CellComponent	ventral region of the olfactory bulb			NULL	control mice	NULL	NULL	NULL	NULL	gw60_brainres_932_1_1_s_133	11911856	(E, F) The subset of olfactory receptor neurons binding the lectin UEA-1 converge on multiple glomeruli in the ventral region of the olfactory bulb (solid arrows) in both control and P2-Lis1 mice.	bind
56078	4	5346	6	NULL	NULL	NULL	NULL	statement 2	Process		converge on					 multiple glomeruli 	CellComponent	ventral region of the olfactory bulb			NULL	P2-Lis1 mice	NULL	NULL	NULL	NULL	gw60_brainres_932_1_1_s_133	11911856	(E, F) The subset of olfactory receptor neurons binding the lectin UEA-1 converge on multiple glomeruli in the ventral region of the olfactory bulb (solid arrows) in both control and P2-Lis1 mice.	bind
14801	1	5347	5	NULL	NULL	0	NULL	Pin1-/- PGCs	NULL		do not undergo	NULL				apoptosis	NULL	increased			NULL		0	NULL	NULL	NULL	gw60_development_130_15_3579_s_192	12810604	(E,F) Wild-type (E) and  Pin1-mutant (F) PGCs (green, round cells) are not positive for the apoptosis marker LysoTracker (red), indicating that  Pin1-/- PGCs do not undergo increased apoptosis.	bind
14719	1	5347	6	NULL	NULL	NULL	NULL	Pin1-/- PGCs	Cell		do not undergo					apoptosis	Process	increased			NULL		NULL	NULL	NULL	NULL	gw60_development_130_15_3579_s_192	12810604	(E,F) Wild-type (E) and  Pin1-mutant (F) PGCs (green, round cells) are not positive for the apoptosis marker LysoTracker (red), indicating that  Pin1-/- PGCs do not undergo increased apoptosis.	bind
14802	1	5350	5	NULL	NULL	0	NULL	G-CSF	NULL		bind	NULL		E46A		(gp130-Ig)GR	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_73	10364174	(E46A)G-CSF bound to (gp130-Ig)GR with a similar affinity ( K d = 0.50 nM) to WT G-CSF ( K d = 0.42 nM), indicating that this residue was not required for binding to the CRHM site and probably interacts with the Ig domain.	bind
14803	2	5350	5	NULL	NULL	0	NULL	G-CSF	NULL		bind	NULL		E46A		G-CSF	NULL	WT			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_73	10364174	(E46A)G-CSF bound to (gp130-Ig)GR with a similar affinity ( K d = 0.50 nM) to WT G-CSF ( K d = 0.42 nM), indicating that this residue was not required for binding to the CRHM site and probably interacts with the Ig domain.	bind
14804	3	5350	5	NULL	NULL	0	NULL	statement 1	NULL		affinity to	NULL	similar			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_73	10364174	(E46A)G-CSF bound to (gp130-Ig)GR with a similar affinity ( K d = 0.50 nM) to WT G-CSF ( K d = 0.42 nM), indicating that this residue was not required for binding to the CRHM site and probably interacts with the Ig domain.	bind
14805	4	5350	5	NULL	NULL	0	NULL	G-CSF	NULL		is not required for	NULL		E46A			NULL	binding to	CRHM site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_73	10364174	(E46A)G-CSF bound to (gp130-Ig)GR with a similar affinity ( K d = 0.50 nM) to WT G-CSF ( K d = 0.42 nM), indicating that this residue was not required for binding to the CRHM site and probably interacts with the Ig domain.	bind
14806	5	5350	5	NULL	NULL	0	NULL	G-CSF	NULL		interacts with	NULL	probably	E46A			NULL		Ig domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_73	10364174	(E46A)G-CSF bound to (gp130-Ig)GR with a similar affinity ( K d = 0.50 nM) to WT G-CSF ( K d = 0.42 nM), indicating that this residue was not required for binding to the CRHM site and probably interacts with the Ig domain.	bind
14720	1	5350	6	NULL	NULL	NULL	NULL	G-CSF	GP		bind			E46A		(gp130-Ig)GR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_73	10364174	(E46A)G-CSF bound to (gp130-Ig)GR with a similar affinity ( K d = 0.50 nM) to WT G-CSF ( K d = 0.42 nM), indicating that this residue was not required for binding to the CRHM site and probably interacts with the Ig domain.	bind
14721	2	5350	6	NULL	NULL	NULL	NULL	G-CSF	GP		bind			E46A		G-CSF	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_73	10364174	(E46A)G-CSF bound to (gp130-Ig)GR with a similar affinity ( K d = 0.50 nM) to WT G-CSF ( K d = 0.42 nM), indicating that this residue was not required for binding to the CRHM site and probably interacts with the Ig domain.	bind
14722	3	5350	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs with similar affinity to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_73	10364174	(E46A)G-CSF bound to (gp130-Ig)GR with a similar affinity ( K d = 0.50 nM) to WT G-CSF ( K d = 0.42 nM), indicating that this residue was not required for binding to the CRHM site and probably interacts with the Ig domain.	bind
14825	4	5350	6	NULL	NULL	NULL	NULL	G-CSF	GP		is not required for			E46A				binding to	CRHM site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_73	10364174	(E46A)G-CSF bound to (gp130-Ig)GR with a similar affinity ( K d = 0.50 nM) to WT G-CSF ( K d = 0.42 nM), indicating that this residue was not required for binding to the CRHM site and probably interacts with the Ig domain.	bind
14826	5	5350	6	NULL	NULL	NULL	NULL	G-CSF	GP		interacts with		probably	E46A					Ig domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_73	10364174	(E46A)G-CSF bound to (gp130-Ig)GR with a similar affinity ( K d = 0.50 nM) to WT G-CSF ( K d = 0.42 nM), indicating that this residue was not required for binding to the CRHM site and probably interacts with the Ig domain.	bind
14827	1	5351	5	NULL	NULL	0	NULL	PrPC	NULL		bind	NULL				6H4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_48_38081_s_196	10967124	(Eq. 1)    According to our hypothesis,  A should obey equation 2,           (Eq. 2)    where alpha is a proportionality constant representing the efficiency of PrPC binding to 6H4, of C15S binding to PrPC, of the swine antibody binding to the rabbit antibody, and finally the horseradish peroxidase color reaction.	bind
14828	2	5351	5	NULL	NULL	0	NULL		NULL		bind	NULL		C15S		PrPC	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_48_38081_s_196	10967124	(Eq. 1)    According to our hypothesis,  A should obey equation 2,           (Eq. 2)    where alpha is a proportionality constant representing the efficiency of PrPC binding to 6H4, of C15S binding to PrPC, of the swine antibody binding to the rabbit antibody, and finally the horseradish peroxidase color reaction.	bind
14723	1	5351	6	NULL	NULL	NULL	NULL	PrPC	GP		bind					6H4	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_38081_s_196	10967124	(Eq. 1)    According to our hypothesis,  A should obey equation 2,           (Eq. 2)    where alpha is a proportionality constant representing the efficiency of PrPC binding to 6H4, of C15S binding to PrPC, of the swine antibody binding to the rabbit antibody, and finally the horseradish peroxidase color reaction.	bind
14724	2	5351	6	NULL	NULL	NULL	NULL				bind			C15S		PrPC	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_38081_s_196	10967124	(Eq. 1)    According to our hypothesis,  A should obey equation 2,           (Eq. 2)    where alpha is a proportionality constant representing the efficiency of PrPC binding to 6H4, of C15S binding to PrPC, of the swine antibody binding to the rabbit antibody, and finally the horseradish peroxidase color reaction.	bind
14829	1	5354	5	NULL	NULL	0	NULL	GALT	NULL	free	does not bind	NULL				UMP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_10_6559_s_210	10037750	(Eq. 1)   But free GALT will not bind UMP to form UMP-GALT ( 34,  35); therefore,  k 5 = 0.	bind
14726	1	5354	6	NULL	NULL	NULL	NULL	GALT	GP	free	does not bind					UMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_10_6559_s_210	10037750	(Eq. 1)   But free GALT will not bind UMP to form UMP-GALT ( 34,  35); therefore,  k 5 = 0.	bind
14830	1	5355	5	NULL	NULL	0	NULL	Pn	NULL		bind	NULL	irreversibly			AP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_14_13340_s_75	14715654	(Eq. 1) or Pn irreversibly binds to AP and is depleted from the reaction as the PnAP complex as indicated in  Equation 2.	bind
14831	2	5355	5	NULL	NULL	0	NULL	statement 1	NULL		forms	NULL				PnAP complex	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13340_s_75	14715654	(Eq. 1) or Pn irreversibly binds to AP and is depleted from the reaction as the PnAP complex as indicated in  Equation 2.	bind
14727	1	5355	6	NULL	NULL	NULL	NULL	Pn	GP		bind		irreversibly			AP	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13340_s_75	14715654	(Eq. 1) or Pn irreversibly binds to AP and is depleted from the reaction as the PnAP complex as indicated in  Equation 2.	bind
14728	2	5355	6	NULL	NULL	NULL	NULL	statement 1	Process		forms a 					PnAP complex	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13340_s_75	14715654	(Eq. 1) or Pn irreversibly binds to AP and is depleted from the reaction as the PnAP complex as indicated in  Equation 2.	bind
14832	1	5365	5	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				acto-S1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_26974_s_182	15897189	(Eq. 2) and  K1'' k+2'' is the second order rate constant for binding of ATP to acto-S1.	bind
14729	1	5365	6	NULL	NULL	NULL	NULL	ATP	Chemical		bind					acto-S1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_29_26974_s_182	15897189	(Eq. 2) and  K1'' k+2'' is the second order rate constant for binding of ATP to acto-S1.	bind
14833	1	5366	5	NULL	NULL	0	NULL	ATP	NULL		induce	NULL				acto-S1	NULL	dissociation reaction of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50293_s_93	14506231	(Eq. 2) where  kobs represents the observed rate constant for the ATP-induced acto-S1 dissociation reaction,  K1 k+2 is the second order rate constant for the binding of ATP to acto-S1, and  KAD is the equilibrium dissociation constant for ADP binding to acto-S1.	bind
14835	2	5366	5	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				acto-S1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_50293_s_93	14506231	(Eq. 2) where  kobs represents the observed rate constant for the ATP-induced acto-S1 dissociation reaction,  K1 k+2 is the second order rate constant for the binding of ATP to acto-S1, and  KAD is the equilibrium dissociation constant for ADP binding to acto-S1.	bind
14837	3	5366	5	NULL	NULL	0	NULL	ADP	NULL		bind	NULL				acto-S1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_50293_s_93	14506231	(Eq. 2) where  kobs represents the observed rate constant for the ATP-induced acto-S1 dissociation reaction,  K1 k+2 is the second order rate constant for the binding of ATP to acto-S1, and  KAD is the equilibrium dissociation constant for ADP binding to acto-S1.	bind
14730	1	5366	6	NULL	NULL	NULL	NULL	ATP	Chemical		bind					acto-S1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_50293_s_93	14506231	(Eq. 2) where  kobs represents the observed rate constant for the ATP-induced acto-S1 dissociation reaction,  K1 k+2 is the second order rate constant for the binding of ATP to acto-S1, and  KAD is the equilibrium dissociation constant for ADP binding to acto-S1.	bind
14731	2	5366	6	NULL	NULL	NULL	NULL	ADP	Chemical		bind					acto-S1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_50293_s_93	14506231	(Eq. 2) where  kobs represents the observed rate constant for the ATP-induced acto-S1 dissociation reaction,  K1 k+2 is the second order rate constant for the binding of ATP to acto-S1, and  KAD is the equilibrium dissociation constant for ADP binding to acto-S1.	bind
56079	3	5366	6	NULL	NULL	NULL	NULL	ATP	Chemical		induce					acto-S1 	GP	dissociation reaction of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_50293_s_93	14506231	(Eq. 2) where  kobs represents the observed rate constant for the ATP-induced acto-S1 dissociation reaction,  K1 k+2 is the second order rate constant for the binding of ATP to acto-S1, and  KAD is the equilibrium dissociation constant for ADP binding to acto-S1.	bind
15606	1	5367	5	NULL	NULL	0	NULL	CheA	NULL		bind	NULL				CF	NULL	WT			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_41_30512_s_72	16920717	(Eq. 2) where Act o and Act* are the CheA activities bound to 100% WT-CF and 100% NS-CF arrays, respectively; and [ CoA] and [ C*A are the CheA concentrations bound to WT- and NS-CFs, respectively (in the presence of CheW), estimated through the model with constraints imposed by the activity and binding data.	bind
15607	2	5367	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				CheW	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_41_30512_s_72	16920717	(Eq. 2) where Act o and Act* are the CheA activities bound to 100% WT-CF and 100% NS-CF arrays, respectively; and [ CoA] and [ C*A are the CheA concentrations bound to WT- and NS-CFs, respectively (in the presence of CheW), estimated through the model with constraints imposed by the activity and binding data.	bind
15608	3	5367	5	NULL	NULL	0	NULL	CheA	NULL		bind	NULL				CF	NULL	NS			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_41_30512_s_72	16920717	(Eq. 2) where Act o and Act* are the CheA activities bound to 100% WT-CF and 100% NS-CF arrays, respectively; and [ CoA] and [ C*A are the CheA concentrations bound to WT- and NS-CFs, respectively (in the presence of CheW), estimated through the model with constraints imposed by the activity and binding data.	bind
19163	4	5367	5	NULL	NULL	0	NULL	statement 3	NULL		in the presence of	NULL				CheW	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_41_30512_s_72	16920717	(Eq. 2) where Act o and Act* are the CheA activities bound to 100% WT-CF and 100% NS-CF arrays, respectively; and [ CoA] and [ C*A are the CheA concentrations bound to WT- and NS-CFs, respectively (in the presence of CheW), estimated through the model with constraints imposed by the activity and binding data.	bind
19028	1	5367	6	NULL	NULL	NULL	NULL	CheA	GP		bind					CF	GP	NS			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_41_30512_s_72	16920717	(Eq. 2) where Act o and Act* are the CheA activities bound to 100% WT-CF and 100% NS-CF arrays, respectively; and [ CoA] and [ C*A are the CheA concentrations bound to WT- and NS-CFs, respectively (in the presence of CheW), estimated through the model with constraints imposed by the activity and binding data.	bind
19029	2	5367	6	NULL	NULL	NULL	NULL	CheA	GP		bind					CF	GP	WT			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_41_30512_s_72	16920717	(Eq. 2) where Act o and Act* are the CheA activities bound to 100% WT-CF and 100% NS-CF arrays, respectively; and [ CoA] and [ C*A are the CheA concentrations bound to WT- and NS-CFs, respectively (in the presence of CheW), estimated through the model with constraints imposed by the activity and binding data.	bind
19816	3	5367	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs in presence of					CheW	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_41_30512_s_72	16920717	(Eq. 2) where Act o and Act* are the CheA activities bound to 100% WT-CF and 100% NS-CF arrays, respectively; and [ CoA] and [ C*A are the CheA concentrations bound to WT- and NS-CFs, respectively (in the presence of CheW), estimated through the model with constraints imposed by the activity and binding data.	bind
19817	4	5367	6	NULL	NULL	NULL	NULL	statement 2	Process		occurs in presence of					CheW	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_41_30512_s_72	16920717	(Eq. 2) where Act o and Act* are the CheA activities bound to 100% WT-CF and 100% NS-CF arrays, respectively; and [ CoA] and [ C*A are the CheA concentrations bound to WT- and NS-CFs, respectively (in the presence of CheW), estimated through the model with constraints imposed by the activity and binding data.	bind
14840	1	5369	5	NULL	NULL	0	NULL	ARNT-bHLH dimers	NULL		bind	NULL				ARNT-bHLH dimer	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40537_s_125	11502749	(Eq. 3)    where nu2 is the average number of ARNT-bHLH dimers bound to the ARNT-bHLH dimer.	bind
14841	2	5369	5	NULL	NULL	0	NULL	nu2	NULL		is	NULL				average number of ARNT-bHLH dimers bound to the ARNT-bHLH dimer	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40537_s_125	11502749	(Eq. 3)    where nu2 is the average number of ARNT-bHLH dimers bound to the ARNT-bHLH dimer.	bind
14732	1	5369	6	NULL	NULL	NULL	NULL	ARNT-bHLH dimers	GP		bind					ARNT-bHLH dimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40537_s_125	11502749	(Eq. 3)    where nu2 is the average number of ARNT-bHLH dimers bound to the ARNT-bHLH dimer.	bind
56080	2	5369	6	NULL	NULL	NULL	NULL	nu2	GP		is					average number of ARNT-bHLH dimers bound to the ARNT-bHLH dimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40537_s_125	11502749	(Eq. 3)    where nu2 is the average number of ARNT-bHLH dimers bound to the ARNT-bHLH dimer.	bind
14843	1	5370	5	10	NULL	0	NULL	 IdeR		active	bind					fxbA				operator region	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_51_53554_s_146	15456786	(Eq. 3)  Kd is the equilibrium dissociation constant where half of the IdeR is activated and bound to the  fxbA operator region,  M is the divalent metal ion concentration, and  h is the Hill coefficient, which is often used as a measurement of cooperativity.	bind
14733	1	5370	6	NULL	NULL	NULL	NULL	IdeR	GP	activated	bind					fxbA	GP			operator	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_51_53554_s_146	15456786	(Eq. 3)  Kd is the equilibrium dissociation constant where half of the IdeR is activated and bound to the  fxbA operator region,  M is the divalent metal ion concentration, and  h is the Hill coefficient, which is often used as a measurement of cooperativity.	bind
14844	1	5371	5	NULL	NULL	0	NULL	pAB	NULL		bind	NULL				FXa subforms	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_28_16621_s_63	8663222	(Eq. 3)  pAB Binding to FXa Subforms	bind
14734	1	5371	6	NULL	NULL	NULL	NULL	pAB	GP		bind					FXa subforms	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_28_16621_s_63	8663222	(Eq. 3)  pAB Binding to FXa Subforms	bind
14845	1	5372	5	NULL	NULL	0	NULL	i CytR dimers	NULL		bind	NULL				udp	NULL	unliganded 		promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_23_16010_s_149	10347150	(Eq. 3) delta G i,M is the free energy change for binding of  i CytR dimers to the unliganded  udp promoter ( i.e. related to the macroscopic product association equilibrium constant by  K i,M =          The value of  N in   N was treated as an adjustable parameter in the analysis, representing the average CytR stoichiometry of the higher order complexes.	bind
14735	1	5372	6	NULL	NULL	NULL	NULL	i CytR dimers	GP		bind					udp	GP	unliganded		promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_23_16010_s_149	10347150	(Eq. 3) delta G i,M is the free energy change for binding of  i CytR dimers to the unliganded  udp promoter ( i.e. related to the macroscopic product association equilibrium constant by  K i,M =          The value of  N in   N was treated as an adjustable parameter in the analysis, representing the average CytR stoichiometry of the higher order complexes.	bind
14847	1	5373	5	NULL	NULL	0	NULL	GCLC	NULL		bind	NULL				GCLM	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_40_33766_s_133	16081425	(Eq. 3) The total GCL activity (GCLtot) when all GCLC is bound with GCLM is as follows.	bind
14736	1	5373	6	NULL	NULL	NULL	NULL	GCLC	GP		bind					GCLM	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_40_33766_s_133	16081425	(Eq. 3) The total GCL activity (GCLtot) when all GCLC is bound with GCLM is as follows.	bind
15604	1	5379	5	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				Gi	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_2_922_s_92	11689554	(Eq. 5)    The dissociation constant for GTP binding to Gi ( K i) was determined from the inhibition of the initial rate of GTPgammaS binding (Equation  6), where I is GTP,  K s is the Michaelis constant for GTPgammaS, and  V is the maximum velocity.	bind
14737	1	5379	6	NULL	NULL	NULL	NULL	GTP	Chemical		bind					Gi					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_2_922_s_92	11689554	(Eq. 5)    The dissociation constant for GTP binding to Gi ( K i) was determined from the inhibition of the initial rate of GTPgammaS binding (Equation  6), where I is GTP,  K s is the Michaelis constant for GTPgammaS, and  V is the maximum velocity.	bind
14849	1	5380	5	NULL	NULL	0	NULL	PRPP	NULL		bind	NULL				UMP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_6921_s_177	12482852	(Eq. 5)    We consider this agreement to be acceptable given that the value for the Michaelis  constant for PPi could not be determined very accurately and that the dissociation constants for binding of PRPP and UMP used for estimates of the corresponding inhibition constants were determined at pH 7.5 and 0  degrees C.	bind
19032	1	5380	6	NULL	NULL	NULL	NULL	PRPP	GP		bind					UMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_6921_s_177	12482852	(Eq. 5)    We consider this agreement to be acceptable given that the value for the Michaelis  constant for PPi could not be determined very accurately and that the dissociation constants for binding of PRPP and UMP used for estimates of the corresponding inhibition constants were determined at pH 7.5 and 0  degrees C.	bind
14850	1	5382	5	10	NULL	0	NULL	ADP			bind					GSTKar3 complex		Mt			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51354_s_135	15385545	(Eq. 5) where Mt.E.ADP is the concentration of ADP bound to Mt.GSTKar3 complex,  E0 is the total GSTKar3 concentration, ADP is the total nucleotide present, and  Kd is the dissociation constant for ADP.	bind
14738	1	5382	6	NULL	NULL	NULL	NULL	ADP	Chemical		bind					GSTKar3 complex	GP	Mt			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51354_s_135	15385545	(Eq. 5) where Mt.E.ADP is the concentration of ADP bound to Mt.GSTKar3 complex,  E0 is the total GSTKar3 concentration, ADP is the total nucleotide present, and  Kd is the dissociation constant for ADP.	bind
14853	1	5383	5	NULL	NULL	0	NULL	Rb+	NULL		bind	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_8_5922_s_77	11739378	(Eq. 6)    quation  6 contains all the terms predicted by the stoichiometry of binding of Rb+ and ATP, which suggests that all the possible states of the enzyme with bound ATP and/or bound or occluded Rb+ are present in equilibrium with free Rb+ and ATP.	bind
14739	1	5383	6	NULL	NULL	NULL	NULL	Rb+	Chemical		bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_8_5922_s_77	11739378	(Eq. 6)    quation  6 contains all the terms predicted by the stoichiometry of binding of Rb+ and ATP, which suggests that all the possible states of the enzyme with bound ATP and/or bound or occluded Rb+ are present in equilibrium with free Rb+ and ATP.	bind
14868	1	5385	5	NULL	NULL	0	NULL	hirudin	NULL		bind	NULL				thrombin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_26997_s_60	15923186	(Eq. 7) where  k1 is the second-order rate constant for hirudin binding to thrombin.	bind
14742	1	5385	6	NULL	NULL	NULL	NULL	hirudin	GP		bind					thrombin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_29_26997_s_60	15923186	(Eq. 7) where  k1 is the second-order rate constant for hirudin binding to thrombin.	bind
14870	1	5387	5	NULL	NULL	0	NULL	GST-HuR	NULL		bind	NULL				RNA substrates	NULL	Fl-labeled 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_23_22406_s_110	15809297	(Eq. 9) Quantitative assessment of binding between GST-HuR and Fl-labeled RNA substrates was similarly preformed using fluorescence anisotropy, but with two significant variations.	bind
14743	1	5387	6	NULL	NULL	NULL	NULL	GST-HuR	GP		bind					RNA	NucleicAcid	F1-labeled			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_23_22406_s_110	15809297	(Eq. 9) Quantitative assessment of binding between GST-HuR and Fl-labeled RNA substrates was similarly preformed using fluorescence anisotropy, but with two significant variations.	bind
14871	1	5388	5	NULL	NULL	0	NULL	PMCA	NULL		bind	NULL				calmodulin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_43_39797_s_296	11514555	(Eq. A1)[[             ]](Eq. A2)    The concentration of PMCA bound to calmodulin, [PC], can be expressed in terms of [PCCa] and [P] by using the following mass conservation equation.	bind
14744	1	5388	6	NULL	NULL	NULL	NULL	PMCA	GP		bind					calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_43_39797_s_296	11514555	(Eq. A1)[[             ]](Eq. A2)    The concentration of PMCA bound to calmodulin, [PC], can be expressed in terms of [PCCa] and [P] by using the following mass conservation equation.	bind
14745	1	5389	6	NULL	NULL	NULL	NULL	phosphoprotein 50	GP		bind					ERM	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_6_2372_s_159	12808036	(ERM-binding phosphoprotein 50) and a number of  membrane proteins and a C-terminal domain (C-ERMAD) harboring the F-actin  binding site (for reviews see Bretscher  et al.,  2000  ,  2002  ;  Tsukita  et al., 1997  ;  Mangeat  et al.,  1999  ).	bind
14872	1	5390	5	NULL	NULL	0	NULL	ER 	NULL		bind	NULL				alpha2 integrin	NULL		I domain		NULL		0	NULL	NULL	NULL	gw70_cellbiol_166_1_97_s_126	15240572	(F and G) Analyses of ER and LG3 binding to the I domain  of alpha2 integrin by SPR.	bind
14873	2	5390	5	NULL	NULL	0	NULL	LG3	NULL		bind	NULL				alpha2 integrin	NULL		I domain		NULL		0	NULL	NULL	NULL	gw70_cellbiol_166_1_97_s_126	15240572	(F and G) Analyses of ER and LG3 binding to the I domain  of alpha2 integrin by SPR.	bind
14746	1	5390	6	NULL	NULL	NULL	NULL	ER	CellComponent		bind					alpha2 integrin	GP		I domain		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_1_97_s_126	15240572	(F and G) Analyses of ER and LG3 binding to the I domain  of alpha2 integrin by SPR.	bind
14747	2	5390	6	NULL	NULL	NULL	NULL	LG3	GP		bind					alpha2 integrin	GP		I domain		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_1_97_s_126	15240572	(F and G) Analyses of ER and LG3 binding to the I domain  of alpha2 integrin by SPR.	bind
14874	1	5391	5	NULL	NULL	0	NULL	Smad7	NULL		bind	NULL				GADD34	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_164_2_291_s_47	14718519	(f and g) Similar experiments were performed in both yeast  (f) and mammalian (g) systems to map Smad7 binding to GADD34.	bind
14748	1	5391	6	NULL	NULL	NULL	NULL	Smad7	GP		bind					GADD34	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_291_s_47	14718519	(f and g) Similar experiments were performed in both yeast  (f) and mammalian (g) systems to map Smad7 binding to GADD34.	bind
14875	1	5392	5	10	NULL	0	NULL	neurofilament fragments	NULL	sonicated	bind	NULL				microtubules	NULL	along the side of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_11_5092_s_136	15342782	(f and g) Sonicated neurofilament fragments bind along the  side of microtubules in the presence of dynein/dynactin In the absence of dynein/dynactin  less binding of sonicated NF fragments to microtubules is seen (our unpublished results).	bind
14876	2	5392	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				dynein/dynactin	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_11_5092_s_136	15342782	(f and g) Sonicated neurofilament fragments bind along the  side of microtubules in the presence of dynein/dynactin In the absence of dynein/dynactin  less binding of sonicated NF fragments to microtubules is seen (our unpublished results).	bind
14877	3	5392	5	NULL	NULL	0	NULL	NF fragments	NULL	sonicated	bind	NULL	lesser			microtubules	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_11_5092_s_136	15342782	(f and g) Sonicated neurofilament fragments bind along the  side of microtubules in the presence of dynein/dynactin In the absence of dynein/dynactin  less binding of sonicated NF fragments to microtubules is seen (our unpublished results).	bind
14878	4	5392	5	NULL	NULL	0	NULL	statement 3	NULL		in the absence of	NULL				dynein/dynactin	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_11_5092_s_136	15342782	(f and g) Sonicated neurofilament fragments bind along the  side of microtubules in the presence of dynein/dynactin In the absence of dynein/dynactin  less binding of sonicated NF fragments to microtubules is seen (our unpublished results).	bind
14749	1	5392	6	NULL	NULL	NULL	NULL	neurofilament fragments	CellComponent	sonicated	bind					 microtubules 	CellComponent	side of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_11_5092_s_136	15342782	(f and g) Sonicated neurofilament fragments bind along the  side of microtubules in the presence of dynein/dynactin In the absence of dynein/dynactin  less binding of sonicated NF fragments to microtubules is seen (our unpublished results).	bind
19033	2	5392	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs in presence of					dynein/dynactin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_11_5092_s_136	15342782	(f and g) Sonicated neurofilament fragments bind along the  side of microtubules in the presence of dynein/dynactin In the absence of dynein/dynactin  less binding of sonicated NF fragments to microtubules is seen (our unpublished results).	bind
19034	3	5392	6	NULL	NULL	NULL	NULL	NF fragments	CellComponent	sonicated	bind		less			microtubules	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_11_5092_s_136	15342782	(f and g) Sonicated neurofilament fragments bind along the  side of microtubules in the presence of dynein/dynactin In the absence of dynein/dynactin  less binding of sonicated NF fragments to microtubules is seen (our unpublished results).	bind
19035	4	5392	6	NULL	NULL	NULL	NULL	statement 3	Process		occurs in absence of					dynein/dynactin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_11_5092_s_136	15342782	(f and g) Sonicated neurofilament fragments bind along the  side of microtubules in the presence of dynein/dynactin In the absence of dynein/dynactin  less binding of sonicated NF fragments to microtubules is seen (our unpublished results).	bind
14879	1	5393	5	10	NULL	0	NULL	(F Pmp) -TAM			bind					ZAP-70			tandem SH2 domains		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_944_s_69	7822334	(F Pmp) -TAM    bound the tandem  SH2 domains of ZAP-70 with an affinity similar to the  (pTyr) -TAM    itself.	bind
14880	2	5393	5	10	NULL	0	NULL	TAM			bind			pTyr		ZAP-70			tandem SH2 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_944_s_69	7822334	(F Pmp) -TAM    bound the tandem  SH2 domains of ZAP-70 with an affinity similar to the  (pTyr) -TAM    itself.	bind
14881	3	5393	5	10	NULL	0	NULL	statement 1			is similar to					statement 2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_944_s_69	7822334	(F Pmp) -TAM    bound the tandem  SH2 domains of ZAP-70 with an affinity similar to the  (pTyr) -TAM    itself.	bind
14750	1	5393	6	NULL	NULL	NULL	NULL	(F Pmp) -TAM	GP		bind					ZAP-70	GP		tandem SH2 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_944_s_69	7822334	(F Pmp) -TAM    bound the tandem  SH2 domains of ZAP-70 with an affinity similar to the  (pTyr) -TAM    itself.	bind
19036	2	5393	6	NULL	NULL	NULL	NULL	TAM	GP		bind			pTyr		ZAP-70	GP		tandem SH2 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_944_s_69	7822334	(F Pmp) -TAM    bound the tandem  SH2 domains of ZAP-70 with an affinity similar to the  (pTyr) -TAM    itself.	bind
19037	3	5393	6	NULL	NULL	NULL	NULL	statement 1	Process		is similar to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_944_s_69	7822334	(F Pmp) -TAM    bound the tandem  SH2 domains of ZAP-70 with an affinity similar to the  (pTyr) -TAM    itself.	bind
14882	1	5394	5	NULL	NULL	0	NULL	CNP	NULL		bind	NULL				tubulin	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_170_4_661_s_75	16103231	(F)  Comparison of CNP and tau binding to tubulin.	bind
14883	2	5394	5	NULL	NULL	0	NULL	tau	NULL		bind	NULL				tubulin	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_170_4_661_s_75	16103231	(F)  Comparison of CNP and tau binding to tubulin.	bind
14751	1	5394	6	NULL	NULL	NULL	NULL	CNP	GP		bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_4_661_s_75	16103231	(F)  Comparison of CNP and tau binding to tubulin.	bind
14755	2	5394	6	NULL	NULL	NULL	NULL	tau	GP		bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_170_4_661_s_75	16103231	(F)  Comparison of CNP and tau binding to tubulin.	bind
14884	1	5395	5	NULL	NULL	0	NULL	InR	NULL		bind	NULL				GST-IRS	NULL	WT	1108 - 516		NULL		0	NULL	NULL	NULL	gw70_cellbiol_166_2_213_s_181	15249583	(F)  Quantitation of InR binding to GST-IRS-1108 - 516 (WT) or S302A and S302E mutants.	bind
14885	2	5395	5	NULL	NULL	0	NULL	InR	NULL		bind	NULL				GST-IRS	NULL	mutant	S302A		NULL		0	NULL	NULL	NULL	gw70_cellbiol_166_2_213_s_181	15249583	(F)  Quantitation of InR binding to GST-IRS-1108 - 516 (WT) or S302A and S302E mutants.	bind
14886	3	5395	5	NULL	NULL	0	NULL	InR	NULL		bind	NULL				GST-IRS	NULL	mutant	S302E		NULL		0	NULL	NULL	NULL	gw70_cellbiol_166_2_213_s_181	15249583	(F)  Quantitation of InR binding to GST-IRS-1108 - 516 (WT) or S302A and S302E mutants.	bind
14761	1	5395	6	NULL	NULL	NULL	NULL	InR	GP		bind					GST-IRS	GP	wild type	1108 - 516		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_2_213_s_181	15249583	(F)  Quantitation of InR binding to GST-IRS-1108 - 516 (WT) or S302A and S302E mutants.	bind
14762	2	5395	6	NULL	NULL	NULL	NULL	InR	GP		bind					GST-IRS	GP	mutant	S302A		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_2_213_s_181	15249583	(F)  Quantitation of InR binding to GST-IRS-1108 - 516 (WT) or S302A and S302E mutants.	bind
14765	3	5395	6	NULL	NULL	NULL	NULL	InR	GP		bind					GST-IRS	GP	mutant	S302E		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_2_213_s_181	15249583	(F)  Quantitation of InR binding to GST-IRS-1108 - 516 (WT) or S302A and S302E mutants.	bind
14887	1	5396	5	NULL	NULL	0	NULL	PMP	NULL	cytosolic	bind	NULL				PEX19	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_164_1_57_s_53	14709540	(F)  The majority of cytosolic PMP is bound to PEX19.	bind
14768	1	5396	6	NULL	NULL	NULL	NULL	PMP	GP	cytosolic	bind					PEX19	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_1_57_s_53	14709540	(F)  The majority of cytosolic PMP is bound to PEX19.	bind
14888	1	5397	5	NULL	NULL	0	NULL	ERK2	NULL		bind	NULL				Mxi2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_9_3079_s_225	12697810	(F) Affinity of ERK2 binding to Mxi2.	bind
14770	1	5397	6	NULL	NULL	NULL	NULL	ERK2	GP		bind					Mxi2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_9_3079_s_225	12697810	(F) Affinity of ERK2 binding to Mxi2.	bind
14889	1	5398	5	10	NULL	0	NULL	Robo1/Fc			bind					Slit2-expressing cells					NULL		NULL	NULL	NULL	NULL	gw70_devbiol_296_2_499_s_544	16854408	(F) Anti-Fc labeling reveals that Robo1/Fc successfully binds  to Slit2-expressing cells, but not  Mock  cells (data not shown) in a collagen gel.	bind
14890	2	5398	5	10	NULL	0	NULL	Robo1/Fc			does not bind					Mock cells 					NULL		NULL	NULL	NULL	NULL	gw70_devbiol_296_2_499_s_544	16854408	(F) Anti-Fc labeling reveals that Robo1/Fc successfully binds  to Slit2-expressing cells, but not  Mock  cells (data not shown) in a collagen gel.	bind
14807	1	5398	6	NULL	NULL	NULL	NULL	Robo1/Fc	GP		bind					Slit2-expressing cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_296_2_499_s_544	16854408	(F) Anti-Fc labeling reveals that Robo1/Fc successfully binds  to Slit2-expressing cells, but not  Mock  cells (data not shown) in a collagen gel.	bind
14808	2	5398	6	NULL	NULL	NULL	NULL	Robo1/Fc	GP		does not bind					Mock cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_296_2_499_s_544	16854408	(F) Anti-Fc labeling reveals that Robo1/Fc successfully binds  to Slit2-expressing cells, but not  Mock  cells (data not shown) in a collagen gel.	bind
14891	1	5399	5	NULL	NULL	0	NULL	EF-G-GTP	NULL		bind	NULL				ribosome	NULL	pre-translocational state of			NULL		0	NULL	NULL	NULL	gw60_structure_4_3_229_s_280	8805530	(f) Binding of EF-G-GTP to the pre-translocational state of the ribosome.	bind
14809	1	5399	6	NULL	NULL	NULL	NULL	EF-G-GTP	Chemical		bind					ribosome	CellComponent	pre-translocational state of			NULL		NULL	NULL	NULL	NULL	gw60_structure_4_3_229_s_280	8805530	(f) Binding of EF-G-GTP to the pre-translocational state of the ribosome.	bind
14892	1	5400	5	10	NULL	NULL	NULL	Hrs	GP		bind					STAM2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_9_3675_s_87	12972556	(F) Binding of Hrs to STAM2 and its mutants.	bind
14893	2	5400	5	10	NULL	NULL	NULL	Hrs	GP		bind					STAM2	GP	mutants			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_9_3675_s_87	12972556	(F) Binding of Hrs to STAM2 and its mutants.	bind
14810	1	5400	6	10	NULL	NULL	NULL	Hrs	GP		bind					STAM2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_9_3675_s_87	12972556	(F) Binding of Hrs to STAM2 and its mutants.	bind
14811	2	5400	6	10	NULL	NULL	NULL	Hrs	GP		bind					STAM2	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_9_3675_s_87	12972556	(F) Binding of Hrs to STAM2 and its mutants.	bind
14954	1	5401	6	10	NULL	NULL	NULL	Pax1	GP		bind					oligonucleotide S1	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_3_473_s_135	12490554	(F) Binding of Pax1 and Pax9 to oligonucleotide  S1.	bind
14955	2	5401	6	10	NULL	NULL	NULL	Pax9	GP		bind					oligonucleotide S1	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_3_473_s_135	12490554	(F) Binding of Pax1 and Pax9 to oligonucleotide  S1.	bind
15277	1	5401	7	10	NULL	NULL	NULL	Pax1	GP		bind					 oligonucleotide S1	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_3_473_s_135	12490554	(F) Binding of Pax1 and Pax9 to oligonucleotide  S1.	bind
15278	2	5401	7	10	NULL	NULL	NULL	Pax9	GP		bind					oligonucleotide S1	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_3_473_s_135	12490554	(F) Binding of Pax1 and Pax9 to oligonucleotide  S1.	bind
14956	1	5403	6	10	NULL	NULL	NULL	TBP	GP		bind					GAL1 	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_18_6270_s_220	11509669	(F) Binding of TBP to the  GAL1 and  GAL10 promoters.	bind
14957	2	5403	6	10	NULL	NULL	NULL	TBP	GP		bind					GAL10	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_18_6270_s_220	11509669	(F) Binding of TBP to the  GAL1 and  GAL10 promoters.	bind
15284	1	5403	7	10	NULL	NULL	NULL	TBP	GP		bind					GAL1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_18_6270_s_220	11509669	(F) Binding of TBP to the  GAL1 and  GAL10 promoters.	bind
15285	2	5403	7	10	NULL	NULL	NULL	TBP	GP		bind					GAL10	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_18_6270_s_220	11509669	(F) Binding of TBP to the  GAL1 and  GAL10 promoters.	bind
14961	1	5404	6	10	NULL	NULL	NULL	SBP	GP		bind					sperm LD-DIM	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_43_42050_s_101	12917406	(f) Binding of the SBP to the Sperm LD-DIM and the Sialidase-treated One --	bind
15286	1	5404	7	10	NULL	NULL	NULL	SBP	GP		bind					Sperm LD-DIM	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_43_42050_s_101	12917406	(f) Binding of the SBP to the Sperm LD-DIM and the Sialidase-treated One --	bind
14962	1	5405	6	10	NULL	NULL	NULL	Sed5	GP		bind			LxxME		Sec24	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_4_483_s_234	12941276	(F) Binding of the Sed5 LxxME sequence to Sec24 is not affected by the assembly state.	bind
19038	2	5405	6	10	NULL	NULL	NULL	statement 1	Process		is not affected by					assembly state	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_4_483_s_234	12941276	(F) Binding of the Sed5 LxxME sequence to Sec24 is not affected by the assembly state.	bind
15287	1	5405	7	10	NULL	NULL	NULL	Sed5 	GP		bind			LxxME sequence		Sec24	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_4_483_s_234	12941276	(F) Binding of the Sed5 LxxME sequence to Sec24 is not affected by the assembly state.	bind
15288	2	5405	7	10	NULL	NULL	NULL	statement 1	Process		is not affected by					assembly state	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_4_483_s_234	12941276	(F) Binding of the Sed5 LxxME sequence to Sec24 is not affected by the assembly state.	bind
14963	1	5406	6	10	NULL	NULL	NULL	syntaxin-1A	GP		bind					myosin-V	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_212	16030255	(F) Ca2+ requirement for binding of syntaxin-1A to myosin-V is due to Ca2+-dependent release of CaM from the neck domain of myosin-Va.	bind
14964	2	5406	6	10	NULL	NULL	NULL	statement 1	Process		requires					Ca+2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_212	16030255	(F) Ca2+ requirement for binding of syntaxin-1A to myosin-V is due to Ca2+-dependent release of CaM from the neck domain of myosin-Va.	bind
14966	3	5406	6	10	NULL	NULL	NULL	myosin-Va	GP		release			neck domain		CaM	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_212	16030255	(F) Ca2+ requirement for binding of syntaxin-1A to myosin-V is due to Ca2+-dependent release of CaM from the neck domain of myosin-Va.	bind
14967	4	5406	6	10	NULL	NULL	NULL	statement 3	Process		is dependent on					Ca+2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_212	16030255	(F) Ca2+ requirement for binding of syntaxin-1A to myosin-V is due to Ca2+-dependent release of CaM from the neck domain of myosin-Va.	bind
14968	5	5406	6	10	NULL	NULL	NULL	statement 2	Process		is due to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_212	16030255	(F) Ca2+ requirement for binding of syntaxin-1A to myosin-V is due to Ca2+-dependent release of CaM from the neck domain of myosin-Va.	bind
15291	1	5406	7	10	NULL	NULL	NULL	syntaxin-1A 	GP		bind					myosin-V	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_212	16030255	(F) Ca2+ requirement for binding of syntaxin-1A to myosin-V is due to Ca2+-dependent release of CaM from the neck domain of myosin-Va.	bind
15292	2	5406	7	10	NULL	NULL	NULL	statement 1	Process		is dependent on					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_212	16030255	(F) Ca2+ requirement for binding of syntaxin-1A to myosin-V is due to Ca2+-dependent release of CaM from the neck domain of myosin-Va.	bind
15293	3	5406	7	10	NULL	NULL	NULL	myosin-Va	GP		release			neck domain		CaM	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_212	16030255	(F) Ca2+ requirement for binding of syntaxin-1A to myosin-V is due to Ca2+-dependent release of CaM from the neck domain of myosin-Va.	bind
15294	5	5406	7	10	NULL	NULL	NULL	statement 2	Process		is due to 					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_212	16030255	(F) Ca2+ requirement for binding of syntaxin-1A to myosin-V is due to Ca2+-dependent release of CaM from the neck domain of myosin-Va.	bind
44716	4	5406	7	10	NULL	NULL	NULL	statement 3	Process		is dependent on					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_212	16030255	(F) Ca2+ requirement for binding of syntaxin-1A to myosin-V is due to Ca2+-dependent release of CaM from the neck domain of myosin-Va.	bind
14971	1	5407	6	10	NULL	NULL	NULL	CCD vesicles	CellComponent		bind		specifically			COG complex	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_747_s_114	15728195	(F) CCD vesicles  specifically bind to the COG complex in vitro.	bind
15295	1	5407	7	10	NULL	NULL	NULL	CCD vesicles	CellComponent		bind		specifically			COG complex	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_747_s_114	15728195	(F) CCD vesicles  specifically bind to the COG complex in vitro.	bind
14974	1	5408	6	10	NULL	NULL	NULL	INCENP	GP	chicken	bind					AIRK2	GP	human			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_currbiol_10_17_1075_s_27	10996078	(f) Chicken INCENP (cINCENP) binds human AIRK2  in vitro.	bind
19039	2	5408	6	10	NULL	NULL	NULL	Chicken INCENP	GP		is					cINCENP	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_17_1075_s_27	10996078	(f) Chicken INCENP (cINCENP) binds human AIRK2  in vitro.	bind
15296	1	5408	7	10	NULL	NULL	NULL	INCENP	GP	chicken	bind					AIRK2	GP	human			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_currbiol_10_17_1075_s_27	10996078	(f) Chicken INCENP (cINCENP) binds human AIRK2  in vitro.	bind
15297	2	5408	7	10	NULL	NULL	NULL	Chicken INCENP	GP		is					cINCENP	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_17_1075_s_27	10996078	(f) Chicken INCENP (cINCENP) binds human AIRK2  in vitro.	bind
14977	1	5409	6	10	NULL	NULL	NULL	Myc	GP		bind					p21 initiator	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcell_10_3_509_s_201	12408820	(F) Chromatin-immunoprecipitation assay (ChIP) documenting binding of Myc and Miz-1 to the p21 initiator in vivo; control panels show ChIP reactions for the E box of the prothymosin-  gene and the coding region of the p15Ink4b gene as negative control  (Staller et al., 2001  ).	bind
14978	2	5409	6	10	NULL	NULL	NULL	Miz-1	GP		bind					p21 initiator	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcell_10_3_509_s_201	12408820	(F) Chromatin-immunoprecipitation assay (ChIP) documenting binding of Myc and Miz-1 to the p21 initiator in vivo; control panels show ChIP reactions for the E box of the prothymosin-  gene and the coding region of the p15Ink4b gene as negative control  (Staller et al., 2001  ).	bind
15298	1	5409	7	10	NULL	NULL	NULL	Myc	GP		bind					p21 initiator	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcell_10_3_509_s_201	12408820	(F) Chromatin-immunoprecipitation assay (ChIP) documenting binding of Myc and Miz-1 to the p21 initiator in vivo; control panels show ChIP reactions for the E box of the prothymosin-  gene and the coding region of the p15Ink4b gene as negative control  (Staller et al., 2001  ).	bind
15299	2	5409	7	10	NULL	NULL	NULL	Miz-1	GP		bind					p21 initiator	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcell_10_3_509_s_201	12408820	(F) Chromatin-immunoprecipitation assay (ChIP) documenting binding of Myc and Miz-1 to the p21 initiator in vivo; control panels show ChIP reactions for the E box of the prothymosin-  gene and the coding region of the p15Ink4b gene as negative control  (Staller et al., 2001  ).	bind
15051	1	5410	6	10	NULL	NULL	NULL	CRM1 exportin	GP		bind					IRF-3	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_4159_s_174	10805757	(f) CRM1 exportin binding to IRF-3 in vitro.	bind
15300	1	5410	7	10	NULL	NULL	NULL	CRM1 exportin	GP		bind					IRF-3 	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_4159_s_174	10805757	(f) CRM1 exportin binding to IRF-3 in vitro.	bind
15052	1	5411	6	10	NULL	NULL	NULL	GTP	Chemical		bind					Rac	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9247_s_214	11094076	(F) EDG5 cells were transiently transfected with expression vectors for myc-tagged wild-type (wt) Rac or V12-Rac and 48 h later were stimulated with S1P (0.1 muM) for 5 min or were not stimulated and assayed for the amounts of GTP-bound forms of Rac and V12-Rac.	bind
15053	2	5411	6	10	NULL	NULL	NULL	GTP	Chemical		bind					Rac	GP		V12		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9247_s_214	11094076	(F) EDG5 cells were transiently transfected with expression vectors for myc-tagged wild-type (wt) Rac or V12-Rac and 48 h later were stimulated with S1P (0.1 muM) for 5 min or were not stimulated and assayed for the amounts of GTP-bound forms of Rac and V12-Rac.	bind
15301	1	5411	7	10	NULL	NULL	NULL	GTP	Chemical		bind					Rac	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9247_s_214	11094076	(F) EDG5 cells were transiently transfected with expression vectors for myc-tagged wild-type (wt) Rac or V12-Rac and 48 h later were stimulated with S1P (0.1 muM) for 5 min or were not stimulated and assayed for the amounts of GTP-bound forms of Rac and V12-Rac.	bind
15302	2	5411	7	10	NULL	NULL	NULL	GTP	Chemical		bind					Rac	GP		V12		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9247_s_214	11094076	(F) EDG5 cells were transiently transfected with expression vectors for myc-tagged wild-type (wt) Rac or V12-Rac and 48 h later were stimulated with S1P (0.1 muM) for 5 min or were not stimulated and assayed for the amounts of GTP-bound forms of Rac and V12-Rac.	bind
15054	1	5412	6	10	NULL	NULL	NULL	CbaR	GP		bind					P cbaA DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_67_8_3530_s_219	11472929	(F) Effects of benzoate and various hydroxylated benzoates on CbaR binding to P cbaA DNA.	bind
15303	1	5412	7	10	NULL	NULL	NULL	CbaR	GP		bind					P cbaA DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_67_8_3530_s_219	11472929	(F) Effects of benzoate and various hydroxylated benzoates on CbaR binding to P cbaA DNA.	bind
15055	1	5413	6	10	NULL	NULL	NULL	Runx2	GP		bind					BSP DNA	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9460_s_158	16227596	(F) EMSA used  to test the ability of wild-type Msx2, but not mutant Msx2 (His), to block the binding  of Runx2 to its target DNA derived from the BSP promoter.	bind
15056	2	5413	6	10	NULL	NULL	NULL	Msx2	GP	wild type	block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9460_s_158	16227596	(F) EMSA used  to test the ability of wild-type Msx2, but not mutant Msx2 (His), to block the binding  of Runx2 to its target DNA derived from the BSP promoter.	bind
15057	3	5413	6	10	NULL	NULL	NULL	Msx2	GP	mutant	does not block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9460_s_158	16227596	(F) EMSA used  to test the ability of wild-type Msx2, but not mutant Msx2 (His), to block the binding  of Runx2 to its target DNA derived from the BSP promoter.	bind
15304	1	5413	7	10	NULL	NULL	NULL	Runx2	GP		binds					BSP DNA	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9460_s_158	16227596	(F) EMSA used  to test the ability of wild-type Msx2, but not mutant Msx2 (His), to block the binding  of Runx2 to its target DNA derived from the BSP promoter.	bind
15305	2	5413	7	10	NULL	NULL	NULL	Msx2	GP	Wild-type	blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9460_s_158	16227596	(F) EMSA used  to test the ability of wild-type Msx2, but not mutant Msx2 (His), to block the binding  of Runx2 to its target DNA derived from the BSP promoter.	bind
53080	3	5413	7	10	NULL	NULL	NULL	Msx2	GP	mutant	does not block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9460_s_158	16227596	(F) EMSA used  to test the ability of wild-type Msx2, but not mutant Msx2 (His), to block the binding  of Runx2 to its target DNA derived from the BSP promoter.	bind
15058	1	5414	6	10	NULL	NULL	NULL	GRH	GP		bind								FP3 motif		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_4_1434_s_171	16449654	(F) GRH binding to the FP3 motif in a gel shift assay can be deduced from the  competition of the marked shifts by nonoverlapping GRH binding site FP1 (the applied  competitor fragments are referred to by their proximal and distal binding sites and  are indicated above the lanes).	bind
15213	2	5414	6	NULL	NULL	0	NULL		NULL		bind	NULL			GRH binding site FP1		NULL		FP3 motif		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_4_1434_s_171	16449654	(F) GRH binding to the FP3 motif in a gel shift assay can be deduced from the  competition of the marked shifts by nonoverlapping GRH binding site FP1 (the applied  competitor fragments are referred to by their proximal and distal binding sites and  are indicated above the lanes).	bind
15214	3	5414	6	10	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_4_1434_s_171	16449654	(F) GRH binding to the FP3 motif in a gel shift assay can be deduced from the  competition of the marked shifts by nonoverlapping GRH binding site FP1 (the applied  competitor fragments are referred to by their proximal and distal binding sites and  are indicated above the lanes).	bind
15306	1	5414	7	10	NULL	NULL	NULL	GRH	GP		bind								 FP3 motif		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_4_1434_s_171	16449654	(F) GRH binding to the FP3 motif in a gel shift assay can be deduced from the  competition of the marked shifts by nonoverlapping GRH binding site FP1 (the applied  competitor fragments are referred to by their proximal and distal binding sites and  are indicated above the lanes).	bind
19993	2	5414	7	NULL	NULL	0	NULL		NULL		bind	NULL			GRH binding site FP1		NULL		FP3 motif		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_4_1434_s_171	16449654	(F) GRH binding to the FP3 motif in a gel shift assay can be deduced from the  competition of the marked shifts by nonoverlapping GRH binding site FP1 (the applied  competitor fragments are referred to by their proximal and distal binding sites and  are indicated above the lanes).	bind
19994	3	5414	7	10	NULL	NULL	NULL	statement 1	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_4_1434_s_171	16449654	(F) GRH binding to the FP3 motif in a gel shift assay can be deduced from the  competition of the marked shifts by nonoverlapping GRH binding site FP1 (the applied  competitor fragments are referred to by their proximal and distal binding sites and  are indicated above the lanes).	bind
15059	1	5415	6	10	NULL	NULL	NULL	Rho1	GP		bind					alpha-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_129_16_3771_s_214	12135916	(F) GST pulldown experiments demonstrating the regions of Rho1 required for binding of alpha-catenin (top panel) and p120ctn (second panel from top).	bind
15060	2	5415	6	10	NULL	NULL	NULL	Rho1	GP		bind					p120ctn	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_129_16_3771_s_214	12135916	(F) GST pulldown experiments demonstrating the regions of Rho1 required for binding of alpha-catenin (top panel) and p120ctn (second panel from top).	bind
15307	1	5415	7	10	NULL	NULL	NULL	Rho1	GP		bind					alpha-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_129_16_3771_s_214	12135916	(F) GST pulldown experiments demonstrating the regions of Rho1 required for binding of alpha-catenin (top panel) and p120ctn (second panel from top).	bind
15308	2	5415	7	10	NULL	NULL	NULL	Rho1	GP		bind					 p120ctn	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_129_16_3771_s_214	12135916	(F) GST pulldown experiments demonstrating the regions of Rho1 required for binding of alpha-catenin (top panel) and p120ctn (second panel from top).	bind
15061	1	5416	6	10	NULL	NULL	NULL	IGF-I	GP		induces					Shc	GP	phosphorylation of			NULL	Shc-3F - expressing cells	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3353_s_177	15888547	(F) IGF-I - induced Shc phosphorylation and Shc  binding to Grb2 as well as phosphorylation of Erk1,2 in vector and in Shc-3F - expressing  cells are shown.	bind
15062	2	5416	6	10	NULL	NULL	NULL	Shc	GP		bind					Grb2	GP				NULL	Shc-3F - expressing cells	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3353_s_177	15888547	(F) IGF-I - induced Shc phosphorylation and Shc  binding to Grb2 as well as phosphorylation of Erk1,2 in vector and in Shc-3F - expressing  cells are shown.	bind
15063	3	5416	6	10	NULL	NULL	NULL	IGF-I	GP		induces					statement 2	Process				NULL	Shc-3F - expressing cells	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3353_s_177	15888547	(F) IGF-I - induced Shc phosphorylation and Shc  binding to Grb2 as well as phosphorylation of Erk1,2 in vector and in Shc-3F - expressing  cells are shown.	bind
15064	4	5416	6	10	NULL	NULL	NULL	IGF-I	GP		induces					Erk1/2	GP	phosphorylation of			NULL	Shc-3F - expressing cells	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3353_s_177	15888547	(F) IGF-I - induced Shc phosphorylation and Shc  binding to Grb2 as well as phosphorylation of Erk1,2 in vector and in Shc-3F - expressing  cells are shown.	bind
15309	1	5416	7	10	NULL	NULL	NULL	Shc	GP		bind					Grb2	GP				NULL	Shc-3F - expressing cells	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3353_s_177	15888547	(F) IGF-I - induced Shc phosphorylation and Shc  binding to Grb2 as well as phosphorylation of Erk1,2 in vector and in Shc-3F - expressing  cells are shown.	bind
15310	2	5416	7	10	NULL	NULL	NULL	IGF-I 	GP		induce					statement 1	Process				NULL	Shc-3F - expressing cells	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3353_s_177	15888547	(F) IGF-I - induced Shc phosphorylation and Shc  binding to Grb2 as well as phosphorylation of Erk1,2 in vector and in Shc-3F - expressing  cells are shown.	bind
15311	3	5416	7	10	NULL	NULL	NULL	IGF-I	GP		induce					Shc	GP	phosphorylation of			NULL	Shc-3F - expressing cells	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3353_s_177	15888547	(F) IGF-I - induced Shc phosphorylation and Shc  binding to Grb2 as well as phosphorylation of Erk1,2 in vector and in Shc-3F - expressing  cells are shown.	bind
15313	5	5416	7	10	NULL	NULL	NULL	IGF-I	GP		induce					Erk1,2	GP	phosphorylation of			NULL	Shc-3F - expressing cells	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3353_s_177	15888547	(F) IGF-I - induced Shc phosphorylation and Shc  binding to Grb2 as well as phosphorylation of Erk1,2 in vector and in Shc-3F - expressing  cells are shown.	bind
15065	1	5418	6	10	NULL	NULL	NULL	KSRP	GP		bind					fos RNA	NucleicAcid			ARE	NULL		NULL	NULL	NULL	NULL	gw60_cell_107_4_451_s_227	11719186	(F) KSRP binds AREfos RNA.	bind
15315	1	5418	7	10	NULL	NULL	NULL	KSRP	GP		binds					fos RNA	NucleicAcid			ARE	NULL		NULL	NULL	NULL	NULL	gw60_cell_107_4_451_s_227	11719186	(F) KSRP binds AREfos RNA.	bind
15066	1	5420	6	10	NULL	NULL	NULL	Myosin-I	GP		does not bind					syntaxin-1A	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_103	16030255	(F) Myosin-I (myr1A) and myosin-IIB do  not bind to syntaxin-1A, even though they are present in the brain homogenate.	bind
15067	2	5420	6	10	NULL	NULL	NULL	myosin-IIB	GP		does not bind					syntaxin-1A	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_103	16030255	(F) Myosin-I (myr1A) and myosin-IIB do  not bind to syntaxin-1A, even though they are present in the brain homogenate.	bind
19040	3	5420	6	10	NULL	NULL	NULL	Myosin-I	GP		is					myr1A	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_103	16030255	(F) Myosin-I (myr1A) and myosin-IIB do  not bind to syntaxin-1A, even though they are present in the brain homogenate.	bind
15316	1	5420	7	10	NULL	NULL	NULL	Myosin-I	GP		does not bind					syntaxin-1A	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_103	16030255	(F) Myosin-I (myr1A) and myosin-IIB do  not bind to syntaxin-1A, even though they are present in the brain homogenate.	bind
15319	2	5420	7	10	NULL	NULL	NULL	myosin-IIB	GP		does not bind					syntaxin-1A	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_103	16030255	(F) Myosin-I (myr1A) and myosin-IIB do  not bind to syntaxin-1A, even though they are present in the brain homogenate.	bind
15321	3	5420	7	10	NULL	NULL	NULL	Myosin-I	GP		is					myr1A	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4519_s_103	16030255	(F) Myosin-I (myr1A) and myosin-IIB do  not bind to syntaxin-1A, even though they are present in the brain homogenate.	bind
15068	2	5421	6	10	NULL	NULL	NULL	p53	GP		bind					statement 2	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_2014_s_359	15713654	(F) p53 and p53(deltaAD1deltaBD) bind the p53-responsive element within the p21 promoter in vivo.	bind
15069	3	5421	6	10	NULL	NULL	NULL	p53	GP		bind			deltaAD1deltaBD		statement 1	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_2014_s_359	15713654	(F) p53 and p53(deltaAD1deltaBD) bind the p53-responsive element within the p21 promoter in vivo.	bind
53087	1	5421	6	10	NULL	NULL	NULL				resides within				p53-responsive element	p21	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_2014_s_359	15713654	(F) p53 and p53(deltaAD1deltaBD) bind the p53-responsive element within the p21 promoter in vivo.	bind
15323	2	5421	7	10	NULL	NULL	NULL	p53	GP		bind					statement 1	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_2014_s_359	15713654	(F) p53 and p53(deltaAD1deltaBD) bind the p53-responsive element within the p21 promoter in vivo.	bind
15325	3	5421	7	10	NULL	NULL	NULL	 p53	GP		bind			deltaAD1deltaBD		statement 1	Process			 	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_2014_s_359	15713654	(F) p53 and p53(deltaAD1deltaBD) bind the p53-responsive element within the p21 promoter in vivo.	bind
53088	1	5421	7	10	NULL	NULL	NULL				resides within				p53-responsive element	p21	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_2014_s_359	15713654	(F) p53 and p53(deltaAD1deltaBD) bind the p53-responsive element within the p21 promoter in vivo.	bind
15070	1	5422	6	10	NULL	NULL	NULL	AGAP1	GP		bind			PH domain		AP-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_3_513_s_58	12967569	(F) PH domain of AGAP1 binds to AP-3.	bind
15328	1	5422	7	10	NULL	NULL	NULL	AGAP1	GP		bind			PH domain		AP-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_5_3_513_s_58	12967569	(F) PH domain of AGAP1 binds to AP-3.	bind
15071	1	5423	6	10	NULL	NULL	NULL	HDAC1	GP		bind					bcl-2	GP			P2 promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_290	15713621	(F) Quantitative ChIP assays of the binding of HDAC1 and HDAC2 to the  bcl-2 P2 promoter.	bind
15072	2	5423	6	10	NULL	NULL	NULL	HDAC2	GP		bind					bcl-2	GP			P2 promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_290	15713621	(F) Quantitative ChIP assays of the binding of HDAC1 and HDAC2 to the  bcl-2 P2 promoter.	bind
15331	1	5423	7	10	NULL	NULL	NULL	 HDAC1	GP		bind					bcl-2 	GP			P2 promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_290	15713621	(F) Quantitative ChIP assays of the binding of HDAC1 and HDAC2 to the  bcl-2 P2 promoter.	bind
15332	2	5423	7	10	NULL	NULL	NULL	HDAC2 	GP		bind					bcl-2 	GP			P2 promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1608_s_290	15713621	(F) Quantitative ChIP assays of the binding of HDAC1 and HDAC2 to the  bcl-2 P2 promoter.	bind
15073	2	5424	6	10	NULL	NULL	NULL	Brg	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_2_169_s_177	12932351	(F) Real-time PCR quantifying the binding of Brg to the proximal  TCF site at the  Myc promoter.	bind
53089	1	5424	6	10	NULL	NULL	NULL			proximal	resides within				TCF site	Myc	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_2_169_s_177	12932351	(F) Real-time PCR quantifying the binding of Brg to the proximal  TCF site at the  Myc promoter.	bind
15333	2	5424	7	10	NULL	NULL	NULL	Brg 	GP 		bind					statement 1	Process			 	NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_2_169_s_177	12932351	(F) Real-time PCR quantifying the binding of Brg to the proximal  TCF site at the  Myc promoter.	bind
53090	1	5424	7	10	NULL	NULL	NULL			proximal	resides within				TCF site	Myc	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_2_169_s_177	12932351	(F) Real-time PCR quantifying the binding of Brg to the proximal  TCF site at the  Myc promoter.	bind
15215	1	5425	6	10	NULL	NULL	NULL	ApoER2-Fc	GP		bind					protein A	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_2_481_s_72	10571241	(F) Recombinant Fc fusion proteins from 1 ml 293 culture supernatant transfected (lanes 1-5) or not transfected (lane 6) with the ApoER2-Fc expression plasmid were bound to 40  l protein A Sepharose slurry, followed by incubation with 500  l Reelin containing (lanes 1-4 and 6) or not containing (lane 5) 293 cell culture supernatant without additions (lane 1) or in the presence of 30  g/ml GST-RAP (lane 2), 30  g/ml GST (lane 3), or 30 mM EDTA (lane 4).	bind
15334	1	5425	7	10	NULL	NULL	NULL	ApoER2-Fc	GP		bind					 protein A 	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_2_481_s_72	10571241	(F) Recombinant Fc fusion proteins from 1 ml 293 culture supernatant transfected (lanes 1-5) or not transfected (lane 6) with the ApoER2-Fc expression plasmid were bound to 40  l protein A Sepharose slurry, followed by incubation with 500  l Reelin containing (lanes 1-4 and 6) or not containing (lane 5) 293 cell culture supernatant without additions (lane 1) or in the presence of 30  g/ml GST-RAP (lane 2), 30  g/ml GST (lane 3), or 30 mM EDTA (lane 4).	bind
15074	1	5426	6	10	NULL	NULL	NULL	RF-Cp145	GP		bind			domain B		GST-Rb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_715_s_107	11336696	(F) RF-Cp145 domain B binds to GST-Rb in an LxCxE-dependent manner.	bind
15075	2	5426	6	10	NULL	NULL	NULL	statement 1	Process		is dependent on								LxCxE		NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_715_s_107	11336696	(F) RF-Cp145 domain B binds to GST-Rb in an LxCxE-dependent manner.	bind
15335	1	5426	7	10	NULL	NULL	NULL	RF-Cp145	GP		binds to			domain B		GST-Rb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_715_s_107	11336696	(F) RF-Cp145 domain B binds to GST-Rb in an LxCxE-dependent manner.	bind
15336	2	5426	7	10	NULL	NULL	NULL	statement 1	Process		depends on								LxCxE		NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_4_715_s_107	11336696	(F) RF-Cp145 domain B binds to GST-Rb in an LxCxE-dependent manner.	bind
15076	1	5427	6	10	NULL	NULL	NULL	NAF1	GP		bind					NAP57	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_2_207_s_50	16618814	(F) Schematic depiction  of the mutually exclusive binding of NAF1 and GAR1 to NAP57 in the context of the  core trimer.	bind
15077	2	5427	6	10	NULL	NULL	NULL	GAR1	GP		bind					NAP57	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_2_207_s_50	16618814	(F) Schematic depiction  of the mutually exclusive binding of NAF1 and GAR1 to NAP57 in the context of the  core trimer.	bind
15078	3	5427	6	10	NULL	NULL	NULL	statement 1	Process		mutually exclusive to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_2_207_s_50	16618814	(F) Schematic depiction  of the mutually exclusive binding of NAF1 and GAR1 to NAP57 in the context of the  core trimer.	bind
15337	1	5427	7	10	NULL	NULL	NULL	NAF1	GP		bind					NAP57	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_2_207_s_50	16618814	(F) Schematic depiction  of the mutually exclusive binding of NAF1 and GAR1 to NAP57 in the context of the  core trimer.	bind
15338	2	5427	7	10	NULL	NULL	NULL	GAR1	GP		bind					NAP57	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_2_207_s_50	16618814	(F) Schematic depiction  of the mutually exclusive binding of NAF1 and GAR1 to NAP57 in the context of the  core trimer.	bind
15339	3	5427	7	10	NULL	NULL	NULL	statement 1	Process		is mutually exclusive to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_2_207_s_50	16618814	(F) Schematic depiction  of the mutually exclusive binding of NAF1 and GAR1 to NAP57 in the context of the  core trimer.	bind
15079	1	5428	6	10	NULL	NULL	NULL	Sec23/24	GP		bind					Sec22	GP	intact			NULL		NULL	NULL	NULL	NULL	gw60_cell_114_4_483_s_49	12941276	(F) Sec23/24 binds to intact Sec22, but not to Bos1.	bind
15080	2	5428	6	10	NULL	NULL	NULL	Sec23/24	GP		does not bind					Bos1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_4_483_s_49	12941276	(F) Sec23/24 binds to intact Sec22, but not to Bos1.	bind
15340	1	5428	7	10	NULL	NULL	NULL	Sec23/24	GP		bind					Sec22	GP	intact			NULL		NULL	NULL	NULL	NULL	gw60_cell_114_4_483_s_49	12941276	(F) Sec23/24 binds to intact Sec22, but not to Bos1.	bind
15341	2	5428	7	10	NULL	NULL	NULL	Sec23/24	GP		does not bind					Bos1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_4_483_s_49	12941276	(F) Sec23/24 binds to intact Sec22, but not to Bos1.	bind
15081	1	5429	6	10	NULL	NULL	NULL	GDP	Chemical		bind					gamma-tubulin	GP				NULL	gammaTuSC	NULL	NULL	NULL	NULL	gw60_cellbiol_144_4_721_s_383	10037793	(F) Small  amounts of both GDP and GTP are detected bound to gamma-tubulin in the gammaTuSC (for quantitation see Table  II: 20 muM GTP, experiment  1).	bind
15082	2	5429	6	10	NULL	NULL	NULL	GTP	Chemical		bind					gamma-tubulin	GP				NULL	gammaTuSC	NULL	NULL	NULL	NULL	gw60_cellbiol_144_4_721_s_383	10037793	(F) Small  amounts of both GDP and GTP are detected bound to gamma-tubulin in the gammaTuSC (for quantitation see Table  II: 20 muM GTP, experiment  1).	bind
15342	1	5429	7	10	NULL	NULL	NULL	GDP	Chemical		bind					gamma-tubulin	GP				NULL	in gammaTuSC	NULL	NULL	NULL	NULL	gw60_cellbiol_144_4_721_s_383	10037793	(F) Small  amounts of both GDP and GTP are detected bound to gamma-tubulin in the gammaTuSC (for quantitation see Table  II: 20 muM GTP, experiment  1).	bind
15343	2	5429	7	10	NULL	NULL	NULL	GTP	Chemical		bind					gamma-tubulin	GP				NULL	in gammaTuSC	NULL	NULL	NULL	NULL	gw60_cellbiol_144_4_721_s_383	10037793	(F) Small  amounts of both GDP and GTP are detected bound to gamma-tubulin in the gammaTuSC (for quantitation see Table  II: 20 muM GTP, experiment  1).	bind
19041	1	5430	6	10	NULL	NULL	NULL	RII	GP	recombinant	bind					Rab32	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_158_4_659_s_70	12186851	(F) Solution binding of recombinant RII and Rab32.	bind
15344	1	5430	7	10	NULL	NULL	NULL	 RII	GP	recombinant	bind					Rab32	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_158_4_659_s_70	12186851	(F) Solution binding of recombinant RII and Rab32.	bind
15216	1	5431	6	10	NULL	NULL	NULL	Gfi1	GP	silencing of	diminishes					G9a	GP	binding of			NULL	HL-60 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10338_s_287	16287849	(F) Specific silencing of Gfi1 by siRNA, but [[ not nonspecific  control ]] siRNA (as shown by Western blotting, right panel), diminishes binding of  G9a and HDAC1, diminishes incorporation of dimethylated histone H3-K9, and modestly  increases incorporation of AcyH3, on the p21Cip/WAF1 promoter in HL-60 cells (as revealed by ChIP, left and middle panels).	bind
15217	2	5431	6	10	NULL	NULL	NULL	AcyH3	GP		incorporated on					p21Cip/WAF1	GP			promoter	NULL	HL-60 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10338_s_287	16287849	(F) Specific silencing of Gfi1 by siRNA, but [[ not nonspecific  control ]] siRNA (as shown by Western blotting, right panel), diminishes binding of  G9a and HDAC1, diminishes incorporation of dimethylated histone H3-K9, and modestly  increases incorporation of AcyH3, on the p21Cip/WAF1 promoter in HL-60 cells (as revealed by ChIP, left and middle panels).	bind
15218	3	5431	6	10	NULL	NULL	NULL	histone H3-K9	GP	dimethylated	incorporated on					p21Cip/WAF1	GP			promoter	NULL	HL-60 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10338_s_287	16287849	(F) Specific silencing of Gfi1 by siRNA, but [[ not nonspecific  control ]] siRNA (as shown by Western blotting, right panel), diminishes binding of  G9a and HDAC1, diminishes incorporation of dimethylated histone H3-K9, and modestly  increases incorporation of AcyH3, on the p21Cip/WAF1 promoter in HL-60 cells (as revealed by ChIP, left and middle panels).	bind
15219	4	5431	6	10	NULL	NULL	NULL	Gfi1	GP	silencing of	diminishes					HDAC1	GP	binding of			NULL	HL-60 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10338_s_287	16287849	(F) Specific silencing of Gfi1 by siRNA, but [[ not nonspecific  control ]] siRNA (as shown by Western blotting, right panel), diminishes binding of  G9a and HDAC1, diminishes incorporation of dimethylated histone H3-K9, and modestly  increases incorporation of AcyH3, on the p21Cip/WAF1 promoter in HL-60 cells (as revealed by ChIP, left and middle panels).	bind
15220	5	5431	6	10	NULL	NULL	NULL	Gfi1	GP	silencing of	diminishes					statement 3	Process				NULL	HL-60 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10338_s_287	16287849	(F) Specific silencing of Gfi1 by siRNA, but [[ not nonspecific  control ]] siRNA (as shown by Western blotting, right panel), diminishes binding of  G9a and HDAC1, diminishes incorporation of dimethylated histone H3-K9, and modestly  increases incorporation of AcyH3, on the p21Cip/WAF1 promoter in HL-60 cells (as revealed by ChIP, left and middle panels).	bind
15221	6	5431	6	10	NULL	NULL	NULL	Gfi1	GP	silencing of	increases		modestly			statement 2	Process				NULL	HL-60 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10338_s_287	16287849	(F) Specific silencing of Gfi1 by siRNA, but [[ not nonspecific  control ]] siRNA (as shown by Western blotting, right panel), diminishes binding of  G9a and HDAC1, diminishes incorporation of dimethylated histone H3-K9, and modestly  increases incorporation of AcyH3, on the p21Cip/WAF1 promoter in HL-60 cells (as revealed by ChIP, left and middle panels).	bind
15345	1	5431	7	10	NULL	NULL	NULL	Gfi1	GP	silencing of	diminishes					G9a	GP	binding of			NULL	HL-60 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10338_s_287	16287849	(F) Specific silencing of Gfi1 by siRNA, but [[ not nonspecific  control ]] siRNA (as shown by Western blotting, right panel), diminishes binding of  G9a and HDAC1, diminishes incorporation of dimethylated histone H3-K9, and modestly  increases incorporation of AcyH3, on the p21Cip/WAF1 promoter in HL-60 cells (as revealed by ChIP, left and middle panels).	bind
15346	2	5431	7	10	NULL	NULL	NULL	Gfi1	GP	silencing of	diminishes					HDAC1	GP	binding of			NULL	HL-60 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10338_s_287	16287849	(F) Specific silencing of Gfi1 by siRNA, but [[ not nonspecific  control ]] siRNA (as shown by Western blotting, right panel), diminishes binding of  G9a and HDAC1, diminishes incorporation of dimethylated histone H3-K9, and modestly  increases incorporation of AcyH3, on the p21Cip/WAF1 promoter in HL-60 cells (as revealed by ChIP, left and middle panels).	bind
15347	3	5431	7	10	NULL	NULL	NULL	AcyH3	GP		incorporated on					p21Cip/WAF1	GP			promoter	NULL	HL-60 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10338_s_287	16287849	(F) Specific silencing of Gfi1 by siRNA, but [[ not nonspecific  control ]] siRNA (as shown by Western blotting, right panel), diminishes binding of  G9a and HDAC1, diminishes incorporation of dimethylated histone H3-K9, and modestly  increases incorporation of AcyH3, on the p21Cip/WAF1 promoter in HL-60 cells (as revealed by ChIP, left and middle panels).	bind
15348	5	5431	7	10	NULL	NULL	NULL	histone H3-K9	GP	dimethylated	incorporated on					p21Cip/WAF1	GP			promoter	NULL	HL-60 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10338_s_287	16287849	(F) Specific silencing of Gfi1 by siRNA, but [[ not nonspecific  control ]] siRNA (as shown by Western blotting, right panel), diminishes binding of  G9a and HDAC1, diminishes incorporation of dimethylated histone H3-K9, and modestly  increases incorporation of AcyH3, on the p21Cip/WAF1 promoter in HL-60 cells (as revealed by ChIP, left and middle panels).	bind
53091	4	5431	7	10	NULL	NULL	NULL	Gfi1	GP	silencing of	diminishes					statement 3	Process				NULL	HL-60 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10338_s_287	16287849	(F) Specific silencing of Gfi1 by siRNA, but [[ not nonspecific  control ]] siRNA (as shown by Western blotting, right panel), diminishes binding of  G9a and HDAC1, diminishes incorporation of dimethylated histone H3-K9, and modestly  increases incorporation of AcyH3, on the p21Cip/WAF1 promoter in HL-60 cells (as revealed by ChIP, left and middle panels).	bind
53092	6	5431	7	10	NULL	NULL	NULL	Gfi1	GP	silencing of	diminishes					statement 5	Process				NULL	HL-60 cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10338_s_287	16287849	(F) Specific silencing of Gfi1 by siRNA, but [[ not nonspecific  control ]] siRNA (as shown by Western blotting, right panel), diminishes binding of  G9a and HDAC1, diminishes incorporation of dimethylated histone H3-K9, and modestly  increases incorporation of AcyH3, on the p21Cip/WAF1 promoter in HL-60 cells (as revealed by ChIP, left and middle panels).	bind
15222	1	5433	6	10	NULL	NULL	NULL	nucleoporin repeats	GP		bind			x-Phe-Gly residues		TAP	GP		NTF2-like domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_3_645_s_135	11583626	(F) Superposition of the x-Phe-Gly residues of nucleoporin repeats bound to TAP NTF2-like domain (black) and to importin   (gray;  Bayliss et al., 2000  ) shows they have a similar conformation when bound to the two different transport factors.	bind
15223	2	5433	6	10	NULL	NULL	NULL	nucleoporin repeats	GP		bind			x-Phe-Gly residues		importin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_3_645_s_135	11583626	(F) Superposition of the x-Phe-Gly residues of nucleoporin repeats bound to TAP NTF2-like domain (black) and to importin   (gray;  Bayliss et al., 2000  ) shows they have a similar conformation when bound to the two different transport factors.	bind
15349	1	5433	7	10	NULL	NULL	NULL	nucleoporin repeats	GP		bind			x-Phe-Gly residues		TAP	GP		NTF2-like domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_3_645_s_135	11583626	(F) Superposition of the x-Phe-Gly residues of nucleoporin repeats bound to TAP NTF2-like domain (black) and to importin   (gray;  Bayliss et al., 2000  ) shows they have a similar conformation when bound to the two different transport factors.	bind
15350	2	5433	7	10	NULL	NULL	NULL	 nucleoporin repeats	GP		bind			x-Phe-Gly residues		importin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_3_645_s_135	11583626	(F) Superposition of the x-Phe-Gly residues of nucleoporin repeats bound to TAP NTF2-like domain (black) and to importin   (gray;  Bayliss et al., 2000  ) shows they have a similar conformation when bound to the two different transport factors.	bind
15083	1	5434	6	10	NULL	NULL	NULL	eIF2B	GP		bind					eIF2alpha	GP	phosphorylated			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3063_s_337	15798194	(F) Surface representation of eIF2alpha highlighting residues (purple) important for binding and inhibition of eIF2B by phosphorylated  eIF2alpha.	bind
15084	2	5434	6	10	NULL	NULL	NULL	eIF2alpha	GP	phosphorylated	inhibits					eIF2B	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3063_s_337	15798194	(F) Surface representation of eIF2alpha highlighting residues (purple) important for binding and inhibition of eIF2B by phosphorylated  eIF2alpha.	bind
15351	1	5434	7	10	NULL	NULL	NULL	eIF2alpha	GP	phosphorylated	bind					eIF2B	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3063_s_337	15798194	(F) Surface representation of eIF2alpha highlighting residues (purple) important for binding and inhibition of eIF2B by phosphorylated  eIF2alpha.	bind
15352	2	5434	7	10	NULL	NULL	NULL	eIF2alpha	GP	phosphorylated	inhibits					eIF2B	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3063_s_337	15798194	(F) Surface representation of eIF2alpha highlighting residues (purple) important for binding and inhibition of eIF2B by phosphorylated  eIF2alpha.	bind
15224	1	5435	6	10	NULL	NULL	NULL	TAL1beta-BM	GP		induces					RALDH2-T	GP	endogenous expression of			NULL	HPB-ALL cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6939_s_307	9819382	(F) TAL1beta-BM induces endogeneous  RALDH2-T expression with LMO in HPB-ALL cells.	bind
15225	2	5435	6	10	NULL	NULL	NULL	statement 1	Process		occurs with					LMO	GP				NULL	HPB-ALL cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6939_s_307	9819382	(F) TAL1beta-BM induces endogeneous  RALDH2-T expression with LMO in HPB-ALL cells.	bind
15353	1	5435	7	10	NULL	NULL	NULL	TAL1beta-BM	GP		induces					RALDH2-T	GP	endogenous expression of			NULL	HPB-ALL cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6939_s_307	9819382	(F) TAL1beta-BM induces endogeneous  RALDH2-T expression with LMO in HPB-ALL cells.	bind
15394	2	5435	7	10	NULL	NULL	NULL	statement 1	Process		occurs with					LMO	GP				NULL	HPB-ALL cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6939_s_307	9819382	(F) TAL1beta-BM induces endogeneous  RALDH2-T expression with LMO in HPB-ALL cells.	bind
15085	1	5436	6	10	NULL	NULL	NULL	HDAC1	GP		bind					GST-Rb	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_142	15485920	(F) The  Raf-1 peptide specifically disrupts the Rb-Raf-1 interaction but does not affect  the binding of HDAC1, cyclin D, and prohibitin to GST-Rb.	bind
15086	2	5436	6	10	NULL	NULL	NULL	cyclin D	GP		bind					GST-Rb	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_142	15485920	(F) The  Raf-1 peptide specifically disrupts the Rb-Raf-1 interaction but does not affect  the binding of HDAC1, cyclin D, and prohibitin to GST-Rb.	bind
15087	3	5436	6	10	NULL	NULL	NULL	Prohibitin	GP		bind					GST-Rb	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_142	15485920	(F) The  Raf-1 peptide specifically disrupts the Rb-Raf-1 interaction but does not affect  the binding of HDAC1, cyclin D, and prohibitin to GST-Rb.	bind
15088	4	5436	6	10	NULL	NULL	NULL	Raf-1 peptide	GP		does not affect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_142	15485920	(F) The  Raf-1 peptide specifically disrupts the Rb-Raf-1 interaction but does not affect  the binding of HDAC1, cyclin D, and prohibitin to GST-Rb.	bind
15089	5	5436	6	10	NULL	NULL	NULL	Raf-1 peptide	GP		does not affect					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_142	15485920	(F) The  Raf-1 peptide specifically disrupts the Rb-Raf-1 interaction but does not affect  the binding of HDAC1, cyclin D, and prohibitin to GST-Rb.	bind
15090	6	5436	6	10	NULL	NULL	NULL	Raf-1 peptide	GP		does not affect					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_142	15485920	(F) The  Raf-1 peptide specifically disrupts the Rb-Raf-1 interaction but does not affect  the binding of HDAC1, cyclin D, and prohibitin to GST-Rb.	bind
15091	7	5436	6	10	NULL	NULL	NULL	Raf-1 peptide	GP		disrupts		specifically			Rb-Raf-1	GP	interaction of 			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_142	15485920	(F) The  Raf-1 peptide specifically disrupts the Rb-Raf-1 interaction but does not affect  the binding of HDAC1, cyclin D, and prohibitin to GST-Rb.	bind
15477	1	5436	7	10	NULL	NULL	NULL	Raf-1 peptide	GP		disrupts		specifically			Rb-Raf-1	GP	interaction of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_142	15485920	(F) The  Raf-1 peptide specifically disrupts the Rb-Raf-1 interaction but does not affect  the binding of HDAC1, cyclin D, and prohibitin to GST-Rb.	bind
15478	2	5436	7	10	NULL	NULL	NULL	HDAC1	GP		bind					GST-Rb	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_142	15485920	(F) The  Raf-1 peptide specifically disrupts the Rb-Raf-1 interaction but does not affect  the binding of HDAC1, cyclin D, and prohibitin to GST-Rb.	bind
15479	3	5436	7	10	NULL	NULL	NULL	 cyclin D	GP		bind					GST-Rb	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_142	15485920	(F) The  Raf-1 peptide specifically disrupts the Rb-Raf-1 interaction but does not affect  the binding of HDAC1, cyclin D, and prohibitin to GST-Rb.	bind
15480	4	5436	7	10	NULL	NULL	NULL	prohibitin	GP		binds					GST-Rb	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_142	15485920	(F) The  Raf-1 peptide specifically disrupts the Rb-Raf-1 interaction but does not affect  the binding of HDAC1, cyclin D, and prohibitin to GST-Rb.	bind
15481	5	5436	7	10	NULL	NULL	NULL	Raf-1 peptide	GP		does not affect					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_142	15485920	(F) The  Raf-1 peptide specifically disrupts the Rb-Raf-1 interaction but does not affect  the binding of HDAC1, cyclin D, and prohibitin to GST-Rb.	bind
15482	6	5436	7	10	NULL	NULL	NULL	Raf-1 peptide	GP		does not affect					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_142	15485920	(F) The  Raf-1 peptide specifically disrupts the Rb-Raf-1 interaction but does not affect  the binding of HDAC1, cyclin D, and prohibitin to GST-Rb.	bind
15483	7	5436	7	10	NULL	NULL	NULL	Raf-1 peptide	GP		does not affect					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_142	15485920	(F) The  Raf-1 peptide specifically disrupts the Rb-Raf-1 interaction but does not affect  the binding of HDAC1, cyclin D, and prohibitin to GST-Rb.	bind
15092	1	5437	6	10	NULL	NULL	NULL	ATM	GP		bind					plasmid DNA	NucleicAcid	linearized			NULL	Nbs1-depleted extract	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_336	15964794	(F) The C147 fragment  of Nbs1 restores ATM binding to linearized plasmid DNA and damaged sperm chromatin  in an Nbs1-depleted extract.	bind
15093	2	5437	6	10	NULL	NULL	NULL	ATM	GP		bind					sperm chromatin	Chromosome	damaged			NULL	Nbs1-depleted extract	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_336	15964794	(F) The C147 fragment  of Nbs1 restores ATM binding to linearized plasmid DNA and damaged sperm chromatin  in an Nbs1-depleted extract.	bind
15094	3	5437	6	10	NULL	NULL	NULL	Nbs1	GP		restores			C147 fragment		statement 1	Process				NULL	Nbs1-depleted extract	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_336	15964794	(F) The C147 fragment  of Nbs1 restores ATM binding to linearized plasmid DNA and damaged sperm chromatin  in an Nbs1-depleted extract.	bind
15095	4	5437	6	10	NULL	NULL	NULL	Nbs1	GP		restores			C147 fragment		statement 2	Process				NULL	Nbs1-depleted extract	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_336	15964794	(F) The C147 fragment  of Nbs1 restores ATM binding to linearized plasmid DNA and damaged sperm chromatin  in an Nbs1-depleted extract.	bind
15484	1	5437	7	10	NULL	NULL	NULL	ATM	GP		bind					plasmid DNA	NucleicAcid	 linearized			NULL	Nbs1-depleted extract	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_336	15964794	(F) The C147 fragment  of Nbs1 restores ATM binding to linearized plasmid DNA and damaged sperm chromatin  in an Nbs1-depleted extract.	bind
15485	2	5437	7	10	NULL	NULL	NULL	ATM	GP		bind					sperm chromatin	Chromosome	damaged			NULL	Nbs1-depleted extract	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_336	15964794	(F) The C147 fragment  of Nbs1 restores ATM binding to linearized plasmid DNA and damaged sperm chromatin  in an Nbs1-depleted extract.	bind
15486	3	5437	7	10	NULL	NULL	NULL	Nbs1	GP		restores			 C147 fragment		statement 1	Process				NULL	Nbs1-depleted extract	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_336	15964794	(F) The C147 fragment  of Nbs1 restores ATM binding to linearized plasmid DNA and damaged sperm chromatin  in an Nbs1-depleted extract.	bind
15487	4	5437	7	10	NULL	NULL	NULL	Nbs1	GP		restores			C147 fragment		statement 2	Process				NULL	Nbs1-depleted extract	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5363_s_336	15964794	(F) The C147 fragment  of Nbs1 restores ATM binding to linearized plasmid DNA and damaged sperm chromatin  in an Nbs1-depleted extract.	bind
15096	1	5438	6	10	NULL	NULL	NULL	GST-Jun proteins	GP		bind					JNK	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_929_s_109	8945519	(F) The different GST - Jun  proteins bind JNK.	bind
15488	1	5438	7	10	NULL	NULL	NULL	GST - Jun proteins	GP		bind					JNK	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_929_s_109	8945519	(F) The different GST - Jun  proteins bind JNK.	bind
15097	1	5441	6	10	NULL	NULL	NULL	lck-GFP D10 cell	Cell		forms a conjugate with					TR-transferrin	GP	internalized			NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_6_809_s_290	12479826	(F) Time points from conjugate formation of an lck-GFP D10 cell with internalized TR-transferrin.	bind
15599	1	5441	7	10	NULL	NULL	NULL	lck-GFP D10 cell	Cell		forms a conjugate with					TR-transferrin	GP	 internalized 			NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_6_809_s_290	12479826	(F) Time points from conjugate formation of an lck-GFP D10 cell with internalized TR-transferrin.	bind
15098	1	5442	6	10	NULL	NULL	NULL	MAE	GP		bind					PNT-P2	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_5_845_s_345	12538513	(F) To prevent runaway signaling, a negative feedback loop may  occur in which MAE binds to PNT-P2 and inhibits transcriptional activation.	bind
15099	2	5442	6	10	NULL	NULL	NULL	statement 1	Process		inhibits					transcription	Process	activation of			NULL		NULL	NULL	NULL	NULL	gw70_development_130_5_845_s_345	12538513	(F) To prevent runaway signaling, a negative feedback loop may  occur in which MAE binds to PNT-P2 and inhibits transcriptional activation.	bind
19042	3	5442	6	10	NULL	NULL	NULL	negative feedback loop	Process		lead to 		may 			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_130_5_845_s_345	12538513	(F) To prevent runaway signaling, a negative feedback loop may  occur in which MAE binds to PNT-P2 and inhibits transcriptional activation.	bind
15489	1	5442	7	10	NULL	NULL	NULL	MAE	GP		binds					PNT-P2	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_5_845_s_345	12538513	(F) To prevent runaway signaling, a negative feedback loop may  occur in which MAE binds to PNT-P2 and inhibits transcriptional activation.	bind
15490	2	5442	7	10	NULL	NULL	NULL	negative feedback loop	GP		lead to		may			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_130_5_845_s_345	12538513	(F) To prevent runaway signaling, a negative feedback loop may  occur in which MAE binds to PNT-P2 and inhibits transcriptional activation.	bind
15491	3	5442	7	10	NULL	NULL	NULL	statement 1	Process		inhibits					transcription 	Process	activation of			NULL		NULL	NULL	NULL	NULL	gw70_development_130_5_845_s_345	12538513	(F) To prevent runaway signaling, a negative feedback loop may  occur in which MAE binds to PNT-P2 and inhibits transcriptional activation.	bind
15100	1	5444	6	10	NULL	NULL	NULL	CRF	GP		bind					CRF-BP	GP				NULL	dopamine neurons	NULL	NULL	NULL	NULL	gw60_neuron_39_3_401_s_116	12895416	(F) When CRF is bound to CRF-BP it can activate CRF-R2 and the PLC pathway to potentiate NMDARs in dopamine neurons.	bind
15101	2	5444	6	10	NULL	NULL	NULL	CRF	GP		activate					CRF-R2	GP				NULL	dopamine neurons	NULL	NULL	NULL	NULL	gw60_neuron_39_3_401_s_116	12895416	(F) When CRF is bound to CRF-BP it can activate CRF-R2 and the PLC pathway to potentiate NMDARs in dopamine neurons.	bind
15102	3	5444	6	10	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_3_401_s_116	12895416	(F) When CRF is bound to CRF-BP it can activate CRF-R2 and the PLC pathway to potentiate NMDARs in dopamine neurons.	bind
15226	4	5444	6	10	NULL	NULL	NULL	CRF	GP		activate					PLC pathway	Process				NULL	dopamine neurons	NULL	NULL	NULL	NULL	gw60_neuron_39_3_401_s_116	12895416	(F) When CRF is bound to CRF-BP it can activate CRF-R2 and the PLC pathway to potentiate NMDARs in dopamine neurons.	bind
15227	5	5444	6	10	NULL	NULL	NULL	statement 1	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_3_401_s_116	12895416	(F) When CRF is bound to CRF-BP it can activate CRF-R2 and the PLC pathway to potentiate NMDARs in dopamine neurons.	bind
15228	6	5444	6	10	NULL	NULL	NULL	CRF	GP		potentiate					NMDARs	GP				NULL	dopamine neurons	NULL	NULL	NULL	NULL	gw60_neuron_39_3_401_s_116	12895416	(F) When CRF is bound to CRF-BP it can activate CRF-R2 and the PLC pathway to potentiate NMDARs in dopamine neurons.	bind
15229	7	5444	6	10	NULL	NULL	NULL	statement 4	Process		leads to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_3_401_s_116	12895416	(F) When CRF is bound to CRF-BP it can activate CRF-R2 and the PLC pathway to potentiate NMDARs in dopamine neurons.	bind
15492	1	5444	7	10	NULL	NULL	NULL	CRF	GP		binds					CRF-BP	GP				NULL	dopamine neurons	NULL	NULL	NULL	NULL	gw60_neuron_39_3_401_s_116	12895416	(F) When CRF is bound to CRF-BP it can activate CRF-R2 and the PLC pathway to potentiate NMDARs in dopamine neurons.	bind
15493	2	5444	7	10	NULL	NULL	NULL	statement 1	Process		activates					CRF-R2	GP				NULL	dopamine neurons	NULL	NULL	NULL	NULL	gw60_neuron_39_3_401_s_116	12895416	(F) When CRF is bound to CRF-BP it can activate CRF-R2 and the PLC pathway to potentiate NMDARs in dopamine neurons.	bind
15494	3	5444	7	10	NULL	NULL	NULL	statement 1	Process		activates					PLC pathway	Process				NULL	dopamine neurons	NULL	NULL	NULL	NULL	gw60_neuron_39_3_401_s_116	12895416	(F) When CRF is bound to CRF-BP it can activate CRF-R2 and the PLC pathway to potentiate NMDARs in dopamine neurons.	bind
15495	4	5444	7	10	NULL	NULL	NULL	statement 2	Process		potentiate					NMDARs	GP				NULL	dopamine neurons	NULL	NULL	NULL	NULL	gw60_neuron_39_3_401_s_116	12895416	(F) When CRF is bound to CRF-BP it can activate CRF-R2 and the PLC pathway to potentiate NMDARs in dopamine neurons.	bind
15496	5	5444	7	10	NULL	NULL	NULL	statement 3	Process		potentiate					NMDARs	GP				NULL	dopamine neurons	NULL	NULL	NULL	NULL	gw60_neuron_39_3_401_s_116	12895416	(F) When CRF is bound to CRF-BP it can activate CRF-R2 and the PLC pathway to potentiate NMDARs in dopamine neurons.	bind
15103	1	5445	6	10	NULL	NULL	NULL	F5CG	GP		bind					DNMT1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33011_s_244	10551869	(F/MeCG)12 has two characteristics as follows: on the one hand, it acts as a dead-end inhibitor since F5CG binds to DNMT1 in the presence of AdoMet and traps the enzyme into a stable DNMT1-AdoMet-DNA complex that does not proceed through catalysis ( 52-54).	bind
15104	2	5445	6	10	NULL	NULL	NULL	statement 1	Process		occurs in presence of					AdoMet	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33011_s_244	10551869	(F/MeCG)12 has two characteristics as follows: on the one hand, it acts as a dead-end inhibitor since F5CG binds to DNMT1 in the presence of AdoMet and traps the enzyme into a stable DNMT1-AdoMet-DNA complex that does not proceed through catalysis ( 52-54).	bind
15231	3	5445	6	10	NULL	NULL	NULL	(F/MeCG)12	Chemical		acts as a					inhibitor	Chemical	dead-end			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33011_s_244	10551869	(F/MeCG)12 has two characteristics as follows: on the one hand, it acts as a dead-end inhibitor since F5CG binds to DNMT1 in the presence of AdoMet and traps the enzyme into a stable DNMT1-AdoMet-DNA complex that does not proceed through catalysis ( 52-54).	bind
15232	4	5445	6	10	NULL	NULL	NULL	statement 2	Process		forms a					DNMT1-AdoMet-DNA complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33011_s_244	10551869	(F/MeCG)12 has two characteristics as follows: on the one hand, it acts as a dead-end inhibitor since F5CG binds to DNMT1 in the presence of AdoMet and traps the enzyme into a stable DNMT1-AdoMet-DNA complex that does not proceed through catalysis ( 52-54).	bind
53093	5	5445	6	10	NULL	NULL	NULL	statement 4	Process		does not proceed through					catalysis	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33011_s_244	10551869	(F/MeCG)12 has two characteristics as follows: on the one hand, it acts as a dead-end inhibitor since F5CG binds to DNMT1 in the presence of AdoMet and traps the enzyme into a stable DNMT1-AdoMet-DNA complex that does not proceed through catalysis ( 52-54).	bind
15497	1	5445	7	10	NULL	NULL	NULL	F5CG	GP		binds to					DNMT1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33011_s_244	10551869	(F/MeCG)12 has two characteristics as follows: on the one hand, it acts as a dead-end inhibitor since F5CG binds to DNMT1 in the presence of AdoMet and traps the enzyme into a stable DNMT1-AdoMet-DNA complex that does not proceed through catalysis ( 52-54).	bind
15498	3	5445	7	10	NULL	NULL	NULL	statement 1	Process		forms					DNMT1-AdoMet-DNA complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33011_s_244	10551869	(F/MeCG)12 has two characteristics as follows: on the one hand, it acts as a dead-end inhibitor since F5CG binds to DNMT1 in the presence of AdoMet and traps the enzyme into a stable DNMT1-AdoMet-DNA complex that does not proceed through catalysis ( 52-54).	bind
15499	4	5445	7	10	NULL	NULL	NULL	statement 3	Process		does not proceed through					catalysis	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33011_s_244	10551869	(F/MeCG)12 has two characteristics as follows: on the one hand, it acts as a dead-end inhibitor since F5CG binds to DNMT1 in the presence of AdoMet and traps the enzyme into a stable DNMT1-AdoMet-DNA complex that does not proceed through catalysis ( 52-54).	bind
20002	2	5445	7	10	NULL	NULL	NULL	statement 1	Process		occurs in the presence of					AdoMet	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33011_s_244	10551869	(F/MeCG)12 has two characteristics as follows: on the one hand, it acts as a dead-end inhibitor since F5CG binds to DNMT1 in the presence of AdoMet and traps the enzyme into a stable DNMT1-AdoMet-DNA complex that does not proceed through catalysis ( 52-54).	bind
15105	1	5446	6	10	NULL	NULL	NULL	Fas-associated factor 1	GP		bind					Fas	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_425_6959_727_s_69	14562105	(Fas-associated factor 1), a protein  that binds to Fas and regulates apoptosis 5,  6.	bind
15106	2	5446	6	10	NULL	NULL	NULL	Fas-associated factor 1	GP		regulates					apoptosis 5,6	Process				NULL		NULL	NULL	NULL	NULL	gw70_nature_425_6959_727_s_69	14562105	(Fas-associated factor 1), a protein  that binds to Fas and regulates apoptosis 5,  6.	bind
15500	1	5446	7	10	NULL	NULL	NULL	Fas-associated factor 1	GP		binds					Fas	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_425_6959_727_s_69	14562105	(Fas-associated factor 1), a protein  that binds to Fas and regulates apoptosis 5,  6.	bind
15501	2	5446	7	10	NULL	NULL	NULL	statement 1	Process		regulates					apoptosis5,6	Process				NULL		NULL	NULL	NULL	NULL	gw70_nature_425_6959_727_s_69	14562105	(Fas-associated factor 1), a protein  that binds to Fas and regulates apoptosis 5,  6.	bind
15107	1	5447	6	10	NULL	NULL	NULL	(Fe3+ citrate)2	Chemical		bind					FecA	GP	outer membrane protein			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_7_2387_s_7	12644513	(Fe3+ citrate)2 binds to the outer membrane protein FecA and without further transport into the cell induces transcription of the  fec transport genes ( ,  ).	bind
15194	2	5447	6	10	NULL	NULL	NULL	statement 1	Process		induces					fec transport genes	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_7_2387_s_7	12644513	(Fe3+ citrate)2 binds to the outer membrane protein FecA and without further transport into the cell induces transcription of the  fec transport genes ( ,  ).	bind
44764	3	5447	6	10	NULL	NULL	NULL	(Fe3+ citrate)2	Chemical		is transported into					cell	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_7_2387_s_7	12644513	(Fe3+ citrate)2 binds to the outer membrane protein FecA and without further transport into the cell induces transcription of the  fec transport genes ( ,  ).	bind
44765	4	5447	6	10	NULL	NULL	NULL	statement 2	Process		occurs without					statement 3	Process	further			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_7_2387_s_7	12644513	(Fe3+ citrate)2 binds to the outer membrane protein FecA and without further transport into the cell induces transcription of the  fec transport genes ( ,  ).	bind
15502	1	5447	7	10	NULL	NULL	NULL	(Fe3+ citrate)2	Chemical		binds					FecA	GP	outer membrane protein			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_7_2387_s_7	12644513	(Fe3+ citrate)2 binds to the outer membrane protein FecA and without further transport into the cell induces transcription of the  fec transport genes ( ,  ).	bind
15503	2	5447	7	10	NULL	NULL	NULL	statement 1	Process		induces					fec transport gene	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_7_2387_s_7	12644513	(Fe3+ citrate)2 binds to the outer membrane protein FecA and without further transport into the cell induces transcription of the  fec transport genes ( ,  ).	bind
44762	3	5447	7	10	NULL	NULL	NULL	(Fe3+ citrate)2	Chemical		is transported into					cell	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_7_2387_s_7	12644513	(Fe3+ citrate)2 binds to the outer membrane protein FecA and without further transport into the cell induces transcription of the  fec transport genes ( ,  ).	bind
44763	4	5447	7	10	NULL	NULL	NULL	statement 2	Process		occurs without					statement 3	Process	further			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_7_2387_s_7	12644513	(Fe3+ citrate)2 binds to the outer membrane protein FecA and without further transport into the cell induces transcription of the  fec transport genes ( ,  ).	bind
15195	1	5450	6	10	NULL	NULL	NULL	p-toluic acid	Chemical		bind					AcmACP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12508_s_263	10212227	(Fig.  6,  lanes 2 and  2'') This findings clearly show that the  p-toluic acid bound to AcmACP directly acylates the threonine covalently bound to ACMS II.	bind
15196	2	5450	6	10	NULL	NULL	NULL	threonine	AminoAcid		bind		covalently			ACMS II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12508_s_263	10212227	(Fig.  6,  lanes 2 and  2'') This findings clearly show that the  p-toluic acid bound to AcmACP directly acylates the threonine covalently bound to ACMS II.	bind
15197	3	5450	6	10	NULL	NULL	NULL	statement 1	Process		acylates		directly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12508_s_263	10212227	(Fig.  6,  lanes 2 and  2'') This findings clearly show that the  p-toluic acid bound to AcmACP directly acylates the threonine covalently bound to ACMS II.	bind
15504	1	5450	7	10	NULL	NULL	NULL	p-toluic acid	Chemical		bind					AcmACP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12508_s_263	10212227	(Fig.  6,  lanes 2 and  2'') This findings clearly show that the  p-toluic acid bound to AcmACP directly acylates the threonine covalently bound to ACMS II.	bind
15505	2	5450	7	10	NULL	NULL	NULL	threonine	AminoAcid		bind		covalently			ACMS II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12508_s_263	10212227	(Fig.  6,  lanes 2 and  2'') This findings clearly show that the  p-toluic acid bound to AcmACP directly acylates the threonine covalently bound to ACMS II.	bind
15506	3	5450	7	10	NULL	NULL	NULL	statement 1	Process		acylates		directly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12508_s_263	10212227	(Fig.  6,  lanes 2 and  2'') This findings clearly show that the  p-toluic acid bound to AcmACP directly acylates the threonine covalently bound to ACMS II.	bind
15198	1	5452	6	10	NULL	NULL	NULL	AtVTI1a	GP		does not bind					T7 antibody	GP				NULL	wild-type plant extract	NULL	NULL	NULL	NULL	gw60_molbiolcell_10_7_2251_s_376	10397763	(Figure  10, right side) As we expected, in the control experiment in which wild-type plant extract was used (Figure  10, left side), AtVTI1a did not bind to the T7 antibody.	bind
15507	1	5452	7	10	NULL	NULL	NULL	AtVTI1a	GP		does not bind					T7 antibody	GP				NULL	wild-type plant extract	NULL	NULL	NULL	NULL	gw60_molbiolcell_10_7_2251_s_376	10397763	(Figure  10, right side) As we expected, in the control experiment in which wild-type plant extract was used (Figure  10, left side), AtVTI1a did not bind to the T7 antibody.	bind
15199	1	5453	6	10	NULL	NULL	NULL	p65	GP		bind					NF-kappaB	GP			consensus sequence	NULL	Nucleus	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1148_s_204	15802625	(Figure II) but increases p65 phosphorylation and p65 binding to NF-kappaB consensus sequence in the nuclei ( Figure 3A and 3B)	bind
15508	1	5453	7	10	NULL	NULL	NULL	p65 	GP		bind					NF-kappaB	GP			consensus sequence	NULL	nucleus	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1148_s_204	15802625	(Figure II) but increases p65 phosphorylation and p65 binding to NF-kappaB consensus sequence in the nuclei ( Figure 3A and 3B)	bind
15200	1	5454	6	10	NULL	NULL	NULL	QKI	GP		regulates					mRNA homeostasis	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_8_1801_s_213	12682013	(Figures  1 and  2), the modulation of the RNA-binding activity of QKI by Src-PTKs (Figures  5 and  6) and the developmental regulation of QKI tyrosine phosphorylation (Figure  8) support the hypothesis that QKI is a pivotal intermediate for developmental signals to control CNS myelination via regulating mRNA homeostasis.	bind
15201	2	5454	6	10	NULL	NULL	NULL	QKI	GP		controls					CNS	OrganismPart	myelination of 			NULL		NULL	NULL	NULL	NULL	gw60_embo_22_8_1801_s_213	12682013	(Figures  1 and  2), the modulation of the RNA-binding activity of QKI by Src-PTKs (Figures  5 and  6) and the developmental regulation of QKI tyrosine phosphorylation (Figure  8) support the hypothesis that QKI is a pivotal intermediate for developmental signals to control CNS myelination via regulating mRNA homeostasis.	bind
15202	3	5454	6	10	NULL	NULL	NULL	statement 2	Process		occurs via					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_8_1801_s_213	12682013	(Figures  1 and  2), the modulation of the RNA-binding activity of QKI by Src-PTKs (Figures  5 and  6) and the developmental regulation of QKI tyrosine phosphorylation (Figure  8) support the hypothesis that QKI is a pivotal intermediate for developmental signals to control CNS myelination via regulating mRNA homeostasis.	bind
53094	4	5454	6	10	NULL	NULL	NULL	QKI	GP		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_8_1801_s_213	12682013	(Figures  1 and  2), the modulation of the RNA-binding activity of QKI by Src-PTKs (Figures  5 and  6) and the developmental regulation of QKI tyrosine phosphorylation (Figure  8) support the hypothesis that QKI is a pivotal intermediate for developmental signals to control CNS myelination via regulating mRNA homeostasis.	bind
53095	5	5454	6	10	NULL	NULL	NULL	Src-PTKs	GP		modulate					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_8_1801_s_213	12682013	(Figures  1 and  2), the modulation of the RNA-binding activity of QKI by Src-PTKs (Figures  5 and  6) and the developmental regulation of QKI tyrosine phosphorylation (Figure  8) support the hypothesis that QKI is a pivotal intermediate for developmental signals to control CNS myelination via regulating mRNA homeostasis.	bind
53096	6	5454	6	10	NULL	NULL	NULL	QKI	GP		acts as					pivotal intermediate	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_8_1801_s_213	12682013	(Figures  1 and  2), the modulation of the RNA-binding activity of QKI by Src-PTKs (Figures  5 and  6) and the developmental regulation of QKI tyrosine phosphorylation (Figure  8) support the hypothesis that QKI is a pivotal intermediate for developmental signals to control CNS myelination via regulating mRNA homeostasis.	bind
15509	1	5454	7	10	NULL	NULL	NULL	QKI	GP		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_8_1801_s_213	12682013	(Figures  1 and  2), the modulation of the RNA-binding activity of QKI by Src-PTKs (Figures  5 and  6) and the developmental regulation of QKI tyrosine phosphorylation (Figure  8) support the hypothesis that QKI is a pivotal intermediate for developmental signals to control CNS myelination via regulating mRNA homeostasis.	bind
15510	2	5454	7	10	NULL	NULL	NULL	Src-PTKs	GP		modulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_8_1801_s_213	12682013	(Figures  1 and  2), the modulation of the RNA-binding activity of QKI by Src-PTKs (Figures  5 and  6) and the developmental regulation of QKI tyrosine phosphorylation (Figure  8) support the hypothesis that QKI is a pivotal intermediate for developmental signals to control CNS myelination via regulating mRNA homeostasis.	bind
53097	3	5454	7	10	NULL	NULL	NULL	QKI	GP		regulates					mRNA homeostasis	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_8_1801_s_213	12682013	(Figures  1 and  2), the modulation of the RNA-binding activity of QKI by Src-PTKs (Figures  5 and  6) and the developmental regulation of QKI tyrosine phosphorylation (Figure  8) support the hypothesis that QKI is a pivotal intermediate for developmental signals to control CNS myelination via regulating mRNA homeostasis.	bind
53098	4	5454	7	10	NULL	NULL	NULL	QKI	GP		controls					CNS	OrganismPart	myelination of 			NULL		NULL	NULL	NULL	NULL	gw60_embo_22_8_1801_s_213	12682013	(Figures  1 and  2), the modulation of the RNA-binding activity of QKI by Src-PTKs (Figures  5 and  6) and the developmental regulation of QKI tyrosine phosphorylation (Figure  8) support the hypothesis that QKI is a pivotal intermediate for developmental signals to control CNS myelination via regulating mRNA homeostasis.	bind
53099	5	5454	7	10	NULL	NULL	NULL	statement 4	Process		via					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_8_1801_s_213	12682013	(Figures  1 and  2), the modulation of the RNA-binding activity of QKI by Src-PTKs (Figures  5 and  6) and the developmental regulation of QKI tyrosine phosphorylation (Figure  8) support the hypothesis that QKI is a pivotal intermediate for developmental signals to control CNS myelination via regulating mRNA homeostasis.	bind
53100	6	5454	7	10	NULL	NULL	NULL	QKI	GP		acts as					pivotal intermediate	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_8_1801_s_213	12682013	(Figures  1 and  2), the modulation of the RNA-binding activity of QKI by Src-PTKs (Figures  5 and  6) and the developmental regulation of QKI tyrosine phosphorylation (Figure  8) support the hypothesis that QKI is a pivotal intermediate for developmental signals to control CNS myelination via regulating mRNA homeostasis.	bind
15203	1	5455	6	10	NULL	NULL	NULL	MCAK	GP		bind					MT lattice	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_2_700_s_182	16291860	(Figures  1 and  4); therefore, the high-affinity end binding sites for MCAK on the MT are saturated, and MCAK is binding to the MT lattice as well.	bind
15514	1	5455	7	10	NULL	NULL	NULL	MCAK	GP		binds					MT lattice	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_2_700_s_182	16291860	(Figures  1 and  4); therefore, the high-affinity end binding sites for MCAK on the MT are saturated, and MCAK is binding to the MT lattice as well.	bind
15204	1	5457	6	10	NULL	NULL	NULL	p70	GP		bind					splicosomal complex	CellComponent	mature	3 splice site		NULL		NULL	NULL	NULL	NULL	gw60_embo_16_14_4421_s_118	9250686	(Figures  2 and  3A); the kinetics of p70 crosslinking parallel those of the second step of splicing (Figures  1B); both the second step of splicing and crosslinking of p70 require a normal RNA branch structure (Figure  4); p70 is bound to the 3  splice site in the mature spliceosomal complex (Figure  3); certain  cis-acting mutations impair both the binding of p70 and the second step of splicing	bind
15208	2	5457	6	10	NULL	NULL	NULL	cis-acting mutations	Process		impair					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_14_4421_s_118	9250686	(Figures  2 and  3A); the kinetics of p70 crosslinking parallel those of the second step of splicing (Figures  1B); both the second step of splicing and crosslinking of p70 require a normal RNA branch structure (Figure  4); p70 is bound to the 3  splice site in the mature spliceosomal complex (Figure  3); certain  cis-acting mutations impair both the binding of p70 and the second step of splicing	bind
19043	3	5457	6	10	NULL	NULL	NULL	second step of splicing	Process		require					RNA branch structure	NucleicAcid	normal			NULL		NULL	NULL	NULL	NULL	gw60_embo_16_14_4421_s_118	9250686	(Figures  2 and  3A); the kinetics of p70 crosslinking parallel those of the second step of splicing (Figures  1B); both the second step of splicing and crosslinking of p70 require a normal RNA branch structure (Figure  4); p70 is bound to the 3  splice site in the mature spliceosomal complex (Figure  3); certain  cis-acting mutations impair both the binding of p70 and the second step of splicing	bind
19044	4	5457	6	10	NULL	NULL	NULL	p70	GP	crosslinking of	require					RNA branch structure	NucleicAcid	normal			NULL		NULL	NULL	NULL	NULL	gw60_embo_16_14_4421_s_118	9250686	(Figures  2 and  3A); the kinetics of p70 crosslinking parallel those of the second step of splicing (Figures  1B); both the second step of splicing and crosslinking of p70 require a normal RNA branch structure (Figure  4); p70 is bound to the 3  splice site in the mature spliceosomal complex (Figure  3); certain  cis-acting mutations impair both the binding of p70 and the second step of splicing	bind
19045	5	5457	6	10	NULL	NULL	NULL	cis acting mutations	Process		impair					second step of splicing	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_14_4421_s_118	9250686	(Figures  2 and  3A); the kinetics of p70 crosslinking parallel those of the second step of splicing (Figures  1B); both the second step of splicing and crosslinking of p70 require a normal RNA branch structure (Figure  4); p70 is bound to the 3  splice site in the mature spliceosomal complex (Figure  3); certain  cis-acting mutations impair both the binding of p70 and the second step of splicing	bind
15515	1	5457	7	10	NULL	NULL	NULL	second step of splicing	Process		require					RNA branch structure	NucleicAcid	normal			NULL		NULL	NULL	NULL	NULL	gw60_embo_16_14_4421_s_118	9250686	(Figures  2 and  3A); the kinetics of p70 crosslinking parallel those of the second step of splicing (Figures  1B); both the second step of splicing and crosslinking of p70 require a normal RNA branch structure (Figure  4); p70 is bound to the 3  splice site in the mature spliceosomal complex (Figure  3); certain  cis-acting mutations impair both the binding of p70 and the second step of splicing	bind
15516	2	5457	7	10	NULL	NULL	NULL	p70	GP	crosslinking of	requires					RNA branch structure	NucleicAcid	normal			NULL		NULL	NULL	NULL	NULL	gw60_embo_16_14_4421_s_118	9250686	(Figures  2 and  3A); the kinetics of p70 crosslinking parallel those of the second step of splicing (Figures  1B); both the second step of splicing and crosslinking of p70 require a normal RNA branch structure (Figure  4); p70 is bound to the 3  splice site in the mature spliceosomal complex (Figure  3); certain  cis-acting mutations impair both the binding of p70 and the second step of splicing	bind
15517	3	5457	7	10	NULL	NULL	NULL	p70	GP		binds					spliceosomal complex	CellComponent	mature	3 splice site		NULL		NULL	NULL	NULL	NULL	gw60_embo_16_14_4421_s_118	9250686	(Figures  2 and  3A); the kinetics of p70 crosslinking parallel those of the second step of splicing (Figures  1B); both the second step of splicing and crosslinking of p70 require a normal RNA branch structure (Figure  4); p70 is bound to the 3  splice site in the mature spliceosomal complex (Figure  3); certain  cis-acting mutations impair both the binding of p70 and the second step of splicing	bind
15518	4	5457	7	10	NULL	NULL	NULL	cis-acting mutations	Process		impair					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_14_4421_s_118	9250686	(Figures  2 and  3A); the kinetics of p70 crosslinking parallel those of the second step of splicing (Figures  1B); both the second step of splicing and crosslinking of p70 require a normal RNA branch structure (Figure  4); p70 is bound to the 3  splice site in the mature spliceosomal complex (Figure  3); certain  cis-acting mutations impair both the binding of p70 and the second step of splicing	bind
15519	5	5457	7	10	NULL	NULL	NULL	cis-acting mutations	Process		impair					second step of splicing	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_14_4421_s_118	9250686	(Figures  2 and  3A); the kinetics of p70 crosslinking parallel those of the second step of splicing (Figures  1B); both the second step of splicing and crosslinking of p70 require a normal RNA branch structure (Figure  4); p70 is bound to the 3  splice site in the mature spliceosomal complex (Figure  3); certain  cis-acting mutations impair both the binding of p70 and the second step of splicing	bind
15209	1	5459	6	10	NULL	NULL	NULL	IgE antibodies	GP		did not bind					HSA	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_5_1348_s_92	12054661	(First of all, from this study, we could confirm that patients'' IgE antibodies did not bind to HSA which was used in "`blocking"` step.)	bind
15520	1	5459	7	10	NULL	NULL	NULL	IgE antibodies	GP		does not bind					HSA	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_5_1348_s_92	12054661	(First of all, from this study, we could confirm that patients'' IgE antibodies did not bind to HSA which was used in "`blocking"` step.)	bind
15210	1	5460	6	10	NULL	NULL	NULL	KDR	GP		is					kinase insert domain-containing receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_6_3154_s_40	8621715	(Fms-like tyrosine kinase) ( 24) and KDR  (kinase insert domain-containing receptor) proteins ( 25,  26) (the mouse homologue of the latter is called  Flk-1; see ( 27) ), bind VEGF with high affinity.	bind
15211	2	5460	6	10	NULL	NULL	NULL	KDR	GP		bind		high affinity			VEGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_6_3154_s_40	8621715	(Fms-like tyrosine kinase) ( 24) and KDR  (kinase insert domain-containing receptor) proteins ( 25,  26) (the mouse homologue of the latter is called  Flk-1; see ( 27) ), bind VEGF with high affinity.	bind
15212	3	5460	6	10	NULL	NULL	NULL	Flk-1	GP	mouse	is homologous to					KDR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_6_3154_s_40	8621715	(Fms-like tyrosine kinase) ( 24) and KDR  (kinase insert domain-containing receptor) proteins ( 25,  26) (the mouse homologue of the latter is called  Flk-1; see ( 27) ), bind VEGF with high affinity.	bind
15522	1	5460	7	10	NULL	NULL	NULL	KDR	GP		bind		high affinity			VEGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_6_3154_s_40	8621715	(Fms-like tyrosine kinase) ( 24) and KDR  (kinase insert domain-containing receptor) proteins ( 25,  26) (the mouse homologue of the latter is called  Flk-1; see ( 27) ), bind VEGF with high affinity.	bind
15524	2	5460	7	10	NULL	NULL	NULL	KDR	GP		is					kinase insert domain-containing receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_6_3154_s_40	8621715	(Fms-like tyrosine kinase) ( 24) and KDR  (kinase insert domain-containing receptor) proteins ( 25,  26) (the mouse homologue of the latter is called  Flk-1; see ( 27) ), bind VEGF with high affinity.	bind
19607	3	5460	7	10	NULL	NULL	NULL	Flk-1	GP	mouse	is homologous to					KDR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_6_3154_s_40	8621715	(Fms-like tyrosine kinase) ( 24) and KDR  (kinase insert domain-containing receptor) proteins ( 25,  26) (the mouse homologue of the latter is called  Flk-1; see ( 27) ), bind VEGF with high affinity.	bind
16348	1	5461	6	10	NULL	NULL	NULL	IGFBP-5	GP	human	bind					IGF-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_1_5_655_s_36	11709186	(For example, human IGFBP-5 binds IGF-2 with a dissociation constant of 8 x 10 11 M;  Kalus et al., 1998  ).	bind
15525	1	5461	7	10	NULL	NULL	NULL	IGFBP-5	GP	human	bind					IGF-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_1_5_655_s_36	11709186	(For example, human IGFBP-5 binds IGF-2 with a dissociation constant of 8 x 10 11 M;  Kalus et al., 1998  ).	bind
16349	1	5462	6	10	NULL	NULL	NULL	Ab-p44	GP		bind					TFIIH	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_102_5_599_s_140	11007478	(G and H) Analysis of the binding of Ab-p44 to TFIIH.	bind
15526	1	5462	7	10	NULL	NULL	NULL	 Ab-p44	GP		bind					TFIIH	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_102_5_599_s_140	11007478	(G and H) Analysis of the binding of Ab-p44 to TFIIH.	bind
16350	1	5465	6	10	NULL	NULL	NULL	GTP	Chemical	active	bind					Rac	GP				NULL	lysates of LS174T	NULL	NULL	NULL	NULL	gw60_cell_111_2_251_s_61	12408869	(G) Active GTP-bound Rac was precipitated from lysates of LS174T using PAK1 Rac binding domain coupled to agarose (upper image).	bind
15527	1	5465	7	10	NULL	NULL	NULL	GTP	Chemical	active	bind					Rac	GP				NULL	lysates of LS174T	NULL	NULL	NULL	NULL	gw60_cell_111_2_251_s_61	12408869	(G) Active GTP-bound Rac was precipitated from lysates of LS174T using PAK1 Rac binding domain coupled to agarose (upper image).	bind
16351	1	5466	6	10	NULL	NULL	NULL	Sox2	GP		bind									composite sox-oct element	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6031_s_271	15988017	(G) Analysis of the cooperativity  of Sox2 and Oct4 binding to the composite sox-oct element.	bind
16352	2	5466	6	10	NULL	NULL	NULL	Oct4	GP		bind									composite sox-oct element	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6031_s_271	15988017	(G) Analysis of the cooperativity  of Sox2 and Oct4 binding to the composite sox-oct element.	bind
19046	3	5466	6	10	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6031_s_271	15988017	(G) Analysis of the cooperativity  of Sox2 and Oct4 binding to the composite sox-oct element.	bind
15529	1	5466	7	10	NULL	NULL	NULL	Sox2	GP		bind									composite sox-oct element	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6031_s_271	15988017	(G) Analysis of the cooperativity  of Sox2 and Oct4 binding to the composite sox-oct element.	bind
15530	2	5466	7	10	NULL	NULL	NULL	Oct4	GP		bind									composite sox-oct element	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6031_s_271	15988017	(G) Analysis of the cooperativity  of Sox2 and Oct4 binding to the composite sox-oct element.	bind
15531	3	5466	7	10	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6031_s_271	15988017	(G) Analysis of the cooperativity  of Sox2 and Oct4 binding to the composite sox-oct element.	bind
16353	1	5467	6	10	NULL	NULL	NULL	c-Jun	GP		bind					JNK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_929_s_112	8945519	(G) Binding of c-Jun, JunB, or JunD to  JNK2.	bind
16354	2	5467	6	10	NULL	NULL	NULL	JunB	GP		bind					JNK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_929_s_112	8945519	(G) Binding of c-Jun, JunB, or JunD to  JNK2.	bind
16355	3	5467	6	10	NULL	NULL	NULL	JunD	GP		bind					JNK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_929_s_112	8945519	(G) Binding of c-Jun, JunB, or JunD to  JNK2.	bind
15532	1	5467	7	10	NULL	NULL	NULL	c-Jun	GP		bind					JNK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_929_s_112	8945519	(G) Binding of c-Jun, JunB, or JunD to  JNK2.	bind
15533	2	5467	7	10	NULL	NULL	NULL	JunB	GP		bind					JNK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_929_s_112	8945519	(G) Binding of c-Jun, JunB, or JunD to  JNK2.	bind
15534	3	5467	7	10	NULL	NULL	NULL	 JunD	GP		bind					JNK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_5_929_s_112	8945519	(G) Binding of c-Jun, JunB, or JunD to  JNK2.	bind
16356	1	5468	6	10	NULL	NULL	NULL	Mnk2a	GP		bind					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_16_5692_s_160	12897141	(G) Binding of Mnk2a to eIF4G enhances eIF4E phosphorylation.	bind
16357	2	5468	6	10	NULL	NULL	NULL	statement 1	Process		enhances					eIF4E	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_16_5692_s_160	12897141	(G) Binding of Mnk2a to eIF4G enhances eIF4E phosphorylation.	bind
15535	1	5468	7	10	NULL	NULL	NULL	Mnk2a	GP		bind					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_16_5692_s_160	12897141	(G) Binding of Mnk2a to eIF4G enhances eIF4E phosphorylation.	bind
15536	2	5468	7	10	NULL	NULL	NULL	statement 1	Process		enhances					eIF4E	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_16_5692_s_160	12897141	(G) Binding of Mnk2a to eIF4G enhances eIF4E phosphorylation.	bind
16365	1	5469	6	10	NULL	NULL	NULL	Cdc31p	GP		bind					hSfi1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_7_1211_s_165	14504268	(g) Cdc31p binding to GST fusions of hSfi1.	bind
53101	2	5469	6	10	NULL	NULL	NULL	hSfi1	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_7_1211_s_165	14504268	(g) Cdc31p binding to GST fusions of hSfi1.	bind
15537	1	5469	7	10	NULL	NULL	NULL	Cdc31p	GP		bind					hSfi1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_7_1211_s_165	14504268	(g) Cdc31p binding to GST fusions of hSfi1.	bind
53102	2	5469	7	10	NULL	NULL	NULL	hSfi1	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_7_1211_s_165	14504268	(g) Cdc31p binding to GST fusions of hSfi1.	bind
16772	1	5470	6	10	NULL	NULL	NULL	noggin RNA	NucleicAcid		increases					BF-1	GP	induction of			NULL		NULL	NULL	NULL	NULL	gw70_development_131_21_5309_s_133	15456729	(G) Co-injection of 2 ng Cv-2 RNA plus 0.1 ng noggin RNA increases the induction  of BF-1 when compared with injection of 0.1 ng noggin RNA alone.	bind
16774	2	5470	6	10	NULL	NULL	NULL	Cv-2 RNA	NucleicAcid		increases					BF-1	GP	induction of			NULL		NULL	NULL	NULL	NULL	gw70_development_131_21_5309_s_133	15456729	(G) Co-injection of 2 ng Cv-2 RNA plus 0.1 ng noggin RNA increases the induction  of BF-1 when compared with injection of 0.1 ng noggin RNA alone.	bind
16775	3	5470	6	10	NULL	NULL	NULL	statement 2	Process		occurs togther with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_131_21_5309_s_133	15456729	(G) Co-injection of 2 ng Cv-2 RNA plus 0.1 ng noggin RNA increases the induction  of BF-1 when compared with injection of 0.1 ng noggin RNA alone.	bind
16777	4	5470	6	10	NULL	NULL	NULL	statement 3	Process		is more as compared with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_131_21_5309_s_133	15456729	(G) Co-injection of 2 ng Cv-2 RNA plus 0.1 ng noggin RNA increases the induction  of BF-1 when compared with injection of 0.1 ng noggin RNA alone.	bind
15538	1	5470	7	10	NULL	NULL	NULL	Cv-2 RNA	NucleicAcid		increase					BF-1	GP	induction of			NULL		NULL	NULL	NULL	NULL	gw70_development_131_21_5309_s_133	15456729	(G) Co-injection of 2 ng Cv-2 RNA plus 0.1 ng noggin RNA increases the induction  of BF-1 when compared with injection of 0.1 ng noggin RNA alone.	bind
15539	2	5470	7	10	NULL	NULL	NULL	noggin RNA	NucleicAcid		increase					BF-1	GP	induction of			NULL		NULL	NULL	NULL	NULL	gw70_development_131_21_5309_s_133	15456729	(G) Co-injection of 2 ng Cv-2 RNA plus 0.1 ng noggin RNA increases the induction  of BF-1 when compared with injection of 0.1 ng noggin RNA alone.	bind
15540	3	5470	7	10	NULL	NULL	NULL	statement 1	Process		occurs togther with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_131_21_5309_s_133	15456729	(G) Co-injection of 2 ng Cv-2 RNA plus 0.1 ng noggin RNA increases the induction  of BF-1 when compared with injection of 0.1 ng noggin RNA alone.	bind
53103	4	5470	7	10	NULL	NULL	NULL	statement 3	Process		is more as compared with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_131_21_5309_s_133	15456729	(G) Co-injection of 2 ng Cv-2 RNA plus 0.1 ng noggin RNA increases the induction  of BF-1 when compared with injection of 0.1 ng noggin RNA alone.	bind
16366	1	5471	6	10	NULL	NULL	NULL	Lz	GP		bind					SME				RD sites 	NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
16367	2	5471	6	10	NULL	NULL	NULL	SME	GP		is					eye-specific enhancer	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
16780	3	5471	6	10	NULL	NULL	NULL	EGFR	GP		inactivates					Yan	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
16782	4	5471	6	10	NULL	NULL	NULL	EGFR	GP		activates					PntP2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
16820	5	5471	6	10	NULL	NULL	NULL	PntP2	GP		bind					SME	GP			ETS domain binding sites	NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
16821	6	5471	6	10	NULL	NULL	NULL	Notch signal	Process		activates					Su(H)	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
16822	7	5471	6	10	NULL	NULL	NULL	Su(H)	GP		bind					SME	GP			Su(H) binding sites	NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
16823	8	5471	6	10	NULL	NULL	NULL	D-Pax2	GP	expression of	is dependent on					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
16826	9	5471	6	10	NULL	NULL	NULL	D-Pax2	GP	expression of	is dependent on					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
16827	10	5471	6	10	NULL	NULL	NULL	D-Pax2	GP	expression of	is dependent on					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
16831	11	5471	6	10	NULL	NULL	NULL	D-Pax2	GP	expression of	is dependent on					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
16832	12	5471	6	10	NULL	NULL	NULL	D-Pax2	GP	expression of	is dependent on					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
16834	13	5471	6	10	NULL	NULL	NULL	D-Pax2	GP	expression of	is dependent on					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
15541	1	5471	7	10	NULL	NULL	NULL	Lz	GP		bind					SME	GP			RD sites 	NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
15542	2	5471	7	10	NULL	NULL	NULL	EGFR	GP		inactivate					Yan	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
15543	3	5471	7	10	NULL	NULL	NULL	EGFR	GP		activates					PntP2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
15544	4	5471	7	10	NULL	NULL	NULL	statement 3	Process		binds to					SME	GP			ETS domain binding site	NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
15545	5	5471	7	10	NULL	NULL	NULL	Notch signal	Process		activates					Su(H)	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
15546	6	5471	7	10	NULL	NULL	NULL	statement 5	Process		bind					SME	GP			Su(H) binding site	NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
15547	7	5471	7	10	NULL	NULL	NULL	SME	GP		is					eye-specific enhancer	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
19608	8	5471	7	10	NULL	NULL	NULL	D-Pax2	GP	expression of	is dependent on					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
19609	9	5471	7	10	NULL	NULL	NULL	D-Pax2	GP	expression of	is dependent on					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
19610	10	5471	7	10	NULL	NULL	NULL	D-Pax2	GP	expression of	is dependent on 					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
19611	11	5471	7	10	NULL	NULL	NULL	D-Pax2	GP	expression of	is dependent on					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
19612	12	5471	7	10	NULL	NULL	NULL	D-Pax2	GP	expression of	is dependent on					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
19613	13	5471	7	10	NULL	NULL	NULL	D-Pax2	GP	expression of	is dependent on					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_270	11051549	(G) Cone  cell-specific activation of  D-Pax2 expression is dependent on three inputs: (i) Lz binding to  the RD sites in the eye-specific enhancer (SME), (ii) EGFR signal-dependent inactivation of Yan  and activation of PntP2, which then binds to ETS domain binding sites in  the SME, and (iii) Notch signal-dependent activation of Su(H), which binds to the Su(H) binding sites  in the SME.	bind
16369	1	5472	6	10	NULL	NULL	NULL	SRF	GP	epitope tagged	bind							radioactively labeled		SRE	NULL		NULL	NULL	NULL	NULL	gw60_cell_110_6_713_s_242	12297045	(G) EMSA reveals binding of epitope tagged SRF to radioactively labeled SRE (lanes 1,3).	bind
15548	1	5472	7	10	NULL	NULL	NULL	SRF	GP	epitope tagged	bind							radioactively labeled		SRE	NULL		NULL	NULL	NULL	NULL	gw60_cell_110_6_713_s_242	12297045	(G) EMSA reveals binding of epitope tagged SRF to radioactively labeled SRE (lanes 1,3).	bind
16370	1	5473	6	10	NULL	NULL	NULL	Tem1	GP		bind					Bub2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_271	14734533	(G) Gic1-pr and Gic1-pr-SS disrupt the binding  between Tem1 and Bub2 in vitro.	bind
16371	2	5473	6	10	NULL	NULL	NULL	Gic1-pr	GP		disrupts					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_271	14734533	(G) Gic1-pr and Gic1-pr-SS disrupt the binding  between Tem1 and Bub2 in vitro.	bind
16372	3	5473	6	10	NULL	NULL	NULL	Gic1-pr-SS	GP		disrupts					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_271	14734533	(G) Gic1-pr and Gic1-pr-SS disrupt the binding  between Tem1 and Bub2 in vitro.	bind
15549	1	5473	7	10	NULL	NULL	NULL	Tem1	GP		bind					Bub2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_271	14734533	(G) Gic1-pr and Gic1-pr-SS disrupt the binding  between Tem1 and Bub2 in vitro.	bind
15550	2	5473	7	10	NULL	NULL	NULL	Gic1-pr	GP		disrupts					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_271	14734533	(G) Gic1-pr and Gic1-pr-SS disrupt the binding  between Tem1 and Bub2 in vitro.	bind
15551	3	5473	7	10	NULL	NULL	NULL	Gic1-pr-SS	GP		disrupts					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_cellbiol_164_2_219_s_271	14734533	(G) Gic1-pr and Gic1-pr-SS disrupt the binding  between Tem1 and Bub2 in vitro.	bind
16373	1	5475	6	10	NULL	NULL	NULL	NSF	GP		does not bind					PICK1-SNAP complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_127	11931741	(G) NSF does not bind PICK1-SNAP complexes.	bind
15552	1	5475	7	10	NULL	NULL	NULL	NSF	GP		does not bind					PICK1-SNAP complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_34_1_53_s_127	11931741	(G) NSF does not bind PICK1-SNAP complexes.	bind
16374	1	5476	6	10	NULL	NULL	NULL	PGL-1	GP		bind					laminin 2 chain	GP		LG1 module		NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_511_s_129	11081637	(G) PGL-1 binds  to LG1, LG4 and LG5 modules of the laminin  2 chain.	bind
16375	2	5476	6	10	NULL	NULL	NULL	PGL-1	GP		bind					laminin 2 chain	GP		LG4 module		NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_511_s_129	11081637	(G) PGL-1 binds  to LG1, LG4 and LG5 modules of the laminin  2 chain.	bind
16376	3	5476	6	10	NULL	NULL	NULL	PGL-1	GP		bind					laminin 2 chain	GP		LG5 module		NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_511_s_129	11081637	(G) PGL-1 binds  to LG1, LG4 and LG5 modules of the laminin  2 chain.	bind
15553	1	5476	7	10	NULL	NULL	NULL	PGL-1	GP		bind					laminin 2 chain	GP		LG1 module		NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_511_s_129	11081637	(G) PGL-1 binds  to LG1, LG4 and LG5 modules of the laminin  2 chain.	bind
15554	2	5476	7	10	NULL	NULL	NULL	PGL-1	GP		bind					laminin 2 chain	GP		LG4 module		NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_511_s_129	11081637	(G) PGL-1 binds  to LG1, LG4 and LG5 modules of the laminin  2 chain.	bind
15555	3	5476	7	10	NULL	NULL	NULL	PGL-1	GP		bind					laminin 2 chain	GP		LG5 module		NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_511_s_129	11081637	(G) PGL-1 binds  to LG1, LG4 and LG5 modules of the laminin  2 chain.	bind
16377	1	5477	6	10	NULL	NULL	NULL	Skp1p	GP		bind					sgt1-5 protein	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_1_21_s_145	10445024	(G) Skp1p binds to  sgt1-5 mutant protein, but not  sgt1-3 mutant protein.	bind
16378	2	5477	6	10	NULL	NULL	NULL	Skp1p	GP		does not bind					sgt1-3 protein	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_1_21_s_145	10445024	(G) Skp1p binds to  sgt1-5 mutant protein, but not  sgt1-3 mutant protein.	bind
15556	1	5477	7	10	NULL	NULL	NULL	 Skp1p	GP		bind					 sgt1-5	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_1_21_s_145	10445024	(G) Skp1p binds to  sgt1-5 mutant protein, but not  sgt1-3 mutant protein.	bind
15557	2	5477	7	10	NULL	NULL	NULL	Skp1p	GP		does not bind					sgt1-3	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_1_21_s_145	10445024	(G) Skp1p binds to  sgt1-5 mutant protein, but not  sgt1-3 mutant protein.	bind
16379	1	5479	6	10	NULL	NULL	NULL	KSRP	GP		bind		specifically			RNA	NucleicAcid			AREfos	NULL		NULL	NULL	NULL	NULL	gw60_cell_107_4_451_s_229	11719186	(G) Specific binding of KSRP to  AREfos RNA.	bind
15558	1	5479	7	10	NULL	NULL	NULL	KSRP	GP		bind		specifically			  RNA	NucleicAcid			AREfos	NULL		NULL	NULL	NULL	NULL	gw60_cell_107_4_451_s_229	11719186	(G) Specific binding of KSRP to  AREfos RNA.	bind
16384	1	5481	6	10	NULL	NULL	NULL	Raichu-RhoA	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_7_975_s_98	15452141	(G), Schematic representations of Raichu-RhoA bound to GDP  or GTP.	bind
16385	2	5481	6	10	NULL	NULL	NULL	Raichu-RhoA	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_7_975_s_98	15452141	(G), Schematic representations of Raichu-RhoA bound to GDP  or GTP.	bind
16386	3	5481	6	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_7_975_s_98	15452141	(G), Schematic representations of Raichu-RhoA bound to GDP  or GTP.	bind
15559	1	5481	7	10	NULL	NULL	NULL	Raichu-RhoA	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_7_975_s_98	15452141	(G), Schematic representations of Raichu-RhoA bound to GDP  or GTP.	bind
15560	2	5481	7	10	NULL	NULL	NULL	Raichu-RhoA	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_7_975_s_98	15452141	(G), Schematic representations of Raichu-RhoA bound to GDP  or GTP.	bind
19614	3	5481	7	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_7_975_s_98	15452141	(G), Schematic representations of Raichu-RhoA bound to GDP  or GTP.	bind
16387	1	5486	6	10	NULL	NULL	NULL	HSF1	GP		bind									HSE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_4949_s_223	9710578	(GA) enhances the heat-inducible HSE-binding activity of HSF1 and delays deactivation during recovery.	bind
16388	2	5486	6	10	NULL	NULL	NULL	statement 1	Process		is induced by					Heat					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_4949_s_223	9710578	(GA) enhances the heat-inducible HSE-binding activity of HSF1 and delays deactivation during recovery.	bind
16389	3	5486	6	10	NULL	NULL	NULL	GA	Chemical		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_4949_s_223	9710578	(GA) enhances the heat-inducible HSE-binding activity of HSF1 and delays deactivation during recovery.	bind
19615	1	5486	7	10	NULL	NULL	NULL				bind				HSE	HSF1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_4949_s_223	9710578	(GA) enhances the heat-inducible HSE-binding activity of HSF1 and delays deactivation during recovery.	bind
19616	2	5486	7	10	NULL	NULL	NULL	statement 1	Process		is induced by					heat					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_4949_s_223	9710578	(GA) enhances the heat-inducible HSE-binding activity of HSF1 and delays deactivation during recovery.	bind
19617	3	5486	7	10	NULL	NULL	NULL	GA	Chemical		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_4949_s_223	9710578	(GA) enhances the heat-inducible HSE-binding activity of HSF1 and delays deactivation during recovery.	bind
16390	1	5487	6	10	NULL	NULL	NULL	GAL4	GP		bind									CGGN11CCG	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5279_s_124	10409719	(GAL4 binds to the sequence CGGN11CCG, and PUT3 binds the sequence CGGN10CCG [ 49].)	bind
16391	2	5487	6	10	NULL	NULL	NULL	PUT3	GP		bind									CGGN10CCG	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5279_s_124	10409719	(GAL4 binds to the sequence CGGN11CCG, and PUT3 binds the sequence CGGN10CCG [ 49].)	bind
15563	1	5487	7	10	NULL	NULL	NULL	GAL4	GP		bind									CGGN11CCG	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5279_s_124	10409719	(GAL4 binds to the sequence CGGN11CCG, and PUT3 binds the sequence CGGN10CCG [ 49].)	bind
15564	2	5487	7	10	NULL	NULL	NULL	PUT3	GP		bind									CGGN10CCG	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5279_s_124	10409719	(GAL4 binds to the sequence CGGN11CCG, and PUT3 binds the sequence CGGN10CCG [ 49].)	bind
16392	1	5488	6	10	NULL	NULL	NULL	GAL4-VP16	GP		bind					linker DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_14773_s_162	11279013	(GAL4-VP16 binding to linker DNA protects it from MNase digestion and increases the yield of fragments corresponding to dinucleosomes).	bind
16393	2	5488	6	10	NULL	NULL	NULL	MNase	GP		digests					linker DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_14773_s_162	11279013	(GAL4-VP16 binding to linker DNA protects it from MNase digestion and increases the yield of fragments corresponding to dinucleosomes).	bind
16394	3	5488	6	10	NULL	NULL	NULL	statement 1	Process		protects					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_14773_s_162	11279013	(GAL4-VP16 binding to linker DNA protects it from MNase digestion and increases the yield of fragments corresponding to dinucleosomes).	bind
16395	4	5488	6	10	NULL	NULL	NULL	GAL4-VP16	GP		increases					dinucleosome fragments	CellComponent	yield of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_14773_s_162	11279013	(GAL4-VP16 binding to linker DNA protects it from MNase digestion and increases the yield of fragments corresponding to dinucleosomes).	bind
15565	1	5488	7	10	NULL	NULL	NULL	GAL4-VP16	GP		bind					linker DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_14773_s_162	11279013	(GAL4-VP16 binding to linker DNA protects it from MNase digestion and increases the yield of fragments corresponding to dinucleosomes).	bind
15566	4	5488	7	10	NULL	NULL	NULL	statement 1	Process		protects					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_14773_s_162	11279013	(GAL4-VP16 binding to linker DNA protects it from MNase digestion and increases the yield of fragments corresponding to dinucleosomes).	bind
15567	3	5488	7	10	NULL	NULL	NULL	statement 1	Process		increases					dinucleosome fragments	CellComponent	yield of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_14773_s_162	11279013	(GAL4-VP16 binding to linker DNA protects it from MNase digestion and increases the yield of fragments corresponding to dinucleosomes).	bind
44828	2	5488	7	10	NULL	NULL	NULL	linker DNA	NucleicAcid		digest					MNase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_14773_s_162	11279013	(GAL4-VP16 binding to linker DNA protects it from MNase digestion and increases the yield of fragments corresponding to dinucleosomes).	bind
16396	1	5490	6	10	NULL	NULL	NULL	Oct4	GP		bind									composite sox-oct element	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6031_s_276	15988017	(H) Analysis of the cooperativity of Oct4 and Sox2 binding  to the composite sox-oct element.	bind
16397	2	5490	6	10	NULL	NULL	NULL	Sox2	GP		bind									composite sox-oct element	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6031_s_276	15988017	(H) Analysis of the cooperativity of Oct4 and Sox2 binding  to the composite sox-oct element.	bind
16398	3	5490	6	10	NULL	NULL	NULL	statement 1	Process		acts in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6031_s_276	15988017	(H) Analysis of the cooperativity of Oct4 and Sox2 binding  to the composite sox-oct element.	bind
15568	1	5490	7	10	NULL	NULL	NULL	Oct4	GP		bind									composite sox-oct  element	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6031_s_276	15988017	(H) Analysis of the cooperativity of Oct4 and Sox2 binding  to the composite sox-oct element.	bind
15569	2	5490	7	10	NULL	NULL	NULL	Sox2	GP		bind									composite sox-oct element	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6031_s_276	15988017	(H) Analysis of the cooperativity of Oct4 and Sox2 binding  to the composite sox-oct element.	bind
15570	3	5490	7	10	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6031_s_276	15988017	(H) Analysis of the cooperativity of Oct4 and Sox2 binding  to the composite sox-oct element.	bind
16399	1	5491	6	10	NULL	NULL	NULL	anti-CD34	GP	mouse	bind					tumor cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5350_577_s_47	9438854	(H) Binding of mouse anti-CD34 to tumor cells demonstrated by RPE-labeled anti-mouse IgG (red).	bind
15571	1	5491	7	10	NULL	NULL	NULL	anti-CD34	GP	mouse	bind					tumor cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5350_577_s_47	9438854	(H) Binding of mouse anti-CD34 to tumor cells demonstrated by RPE-labeled anti-mouse IgG (red).	bind
16400	1	5492	6	10	NULL	NULL	NULL	Dlt	GP		bind		directly			Par-6	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_130_18_4363_s_166	12900452	(H) Direct binding of Dlt to Par-6, but not to aPKC or Baz.	bind
16401	2	5492	6	10	NULL	NULL	NULL	Dlt	GP		does not bind					aPKC	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_130_18_4363_s_166	12900452	(H) Direct binding of Dlt to Par-6, but not to aPKC or Baz.	bind
16402	3	5492	6	10	NULL	NULL	NULL	Dlt	GP		does not bind					Baz	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_130_18_4363_s_166	12900452	(H) Direct binding of Dlt to Par-6, but not to aPKC or Baz.	bind
15572	1	5492	7	10	NULL	NULL	NULL	Dlt 	GP		bind		directly			Par-6	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_130_18_4363_s_166	12900452	(H) Direct binding of Dlt to Par-6, but not to aPKC or Baz.	bind
15573	2	5492	7	10	NULL	NULL	NULL	Dlt	GP		does not bind					PKC	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_130_18_4363_s_166	12900452	(H) Direct binding of Dlt to Par-6, but not to aPKC or Baz.	bind
15574	3	5492	7	10	NULL	NULL	NULL	Dlt	GP		does not bind					Baz	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_130_18_4363_s_166	12900452	(H) Direct binding of Dlt to Par-6, but not to aPKC or Baz.	bind
16403	1	5493	6	10	NULL	NULL	NULL	Pit1	GP		bind					TSHbeta 	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_97_5_587_s_145	10367888	(H) DNA binding of Pit1  and GATA2 on the  TSHbeta promoter.	bind
16404	2	5493	6	10	NULL	NULL	NULL	GATA2	GP		bind					TSHbeta	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_97_5_587_s_145	10367888	(H) DNA binding of Pit1  and GATA2 on the  TSHbeta promoter.	bind
15575	1	5493	7	10	NULL	NULL	NULL	Pit1 	GP		bind					 TSHbeta	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_97_5_587_s_145	10367888	(H) DNA binding of Pit1  and GATA2 on the  TSHbeta promoter.	bind
15576	2	5493	7	10	NULL	NULL	NULL	GATA2	GP		bind					TSHbeta	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_97_5_587_s_145	10367888	(H) DNA binding of Pit1  and GATA2 on the  TSHbeta promoter.	bind
16405	1	5495	6	10	NULL	NULL	NULL	Wg	GP		expressed in					Wing	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4135_s_372	12874133	(H) Expression of UAS- dve with  sd-Gal4 abolishes expression of Wg in the wing.	bind
16406	2	5495	6	10	NULL	NULL	NULL	UAS-dve	GP	expression of	occurs simultaneously with					Sd-Gal4	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4135_s_372	12874133	(H) Expression of UAS- dve with  sd-Gal4 abolishes expression of Wg in the wing.	bind
16407	3	5495	6	10	NULL	NULL	NULL	statement 2	Process		abolishes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4135_s_372	12874133	(H) Expression of UAS- dve with  sd-Gal4 abolishes expression of Wg in the wing.	bind
15577	2	5495	7	10	NULL	NULL	NULL	Wg	GP		is expressed in					wing	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4135_s_372	12874133	(H) Expression of UAS- dve with  sd-Gal4 abolishes expression of Wg in the wing.	bind
15578	1	5495	7	10	NULL	NULL	NULL	UAS- dve	GP	expression of	occurs simultaneously with					sd-Gal4	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4135_s_372	12874133	(H) Expression of UAS- dve with  sd-Gal4 abolishes expression of Wg in the wing.	bind
53104	3	5495	7	10	NULL	NULL	NULL	statement 1	Process		abolishes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4135_s_372	12874133	(H) Expression of UAS- dve with  sd-Gal4 abolishes expression of Wg in the wing.	bind
16408	1	5496	6	10	NULL	NULL	NULL	Hp1	GP		bind					lineage progenitors	Cell	MAA-positive			NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_3_263_s_119	10198629	(H) Hp1 (yellow) binding to MAA-positive lineage progenitors (green) that predominate in normal, embryonic day 18.5 FVB/N gastric epithelium.	bind
16409	2	5496	6	10	NULL	NULL	NULL	lineage progenitors	Cell	MAA-positive	predominate in					embryonic day 18.5 FVB/N gastric epithelium	OrganismPart	normal			NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_3_263_s_119	10198629	(H) Hp1 (yellow) binding to MAA-positive lineage progenitors (green) that predominate in normal, embryonic day 18.5 FVB/N gastric epithelium.	bind
15579	1	5496	7	10	NULL	NULL	NULL	Hp1	GP		bind					lineage progenitors	Cell	MAA-positive			NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_3_263_s_119	10198629	(H) Hp1 (yellow) binding to MAA-positive lineage progenitors (green) that predominate in normal, embryonic day 18.5 FVB/N gastric epithelium.	bind
19618	2	5496	7	10	NULL	NULL	NULL	lineage progenitors	Cell	MAA-positive	predominate in					embryonic day 18.5 FVB/N gastric epithelium	OrganismPart	normal			NULL		NULL	NULL	NULL	NULL	gw60_molcell_3_3_263_s_119	10198629	(H) Hp1 (yellow) binding to MAA-positive lineage progenitors (green) that predominate in normal, embryonic day 18.5 FVB/N gastric epithelium.	bind
16410	1	5497	6	10	NULL	NULL	NULL	centrin 2	GP	human	bind					hSfi1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_7_1211_s_166	14504268	(h) Human centrin 2 binding  to GST fusions of hSfi1.	bind
44792	2	5497	6	10	NULL	NULL	NULL	hSfi1	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_7_1211_s_166	14504268	(h) Human centrin 2 binding  to GST fusions of hSfi1.	bind
15580	1	5497	7	10	NULL	NULL	NULL	centrin 2 	GP	human	bind					hSfi1	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_7_1211_s_166	14504268	(h) Human centrin 2 binding  to GST fusions of hSfi1.	bind
44793	2	5497	7	10	NULL	NULL	NULL	hSfi1	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_7_1211_s_166	14504268	(h) Human centrin 2 binding  to GST fusions of hSfi1.	bind
16448	1	5498	6	10	NULL	NULL	NULL	p53	GP		bind		directly			myosin VI	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_6_2175_s_151	16507995	(H) p53 binds directly to the myosin  VI promoter.	bind
15581	1	5498	7	10	NULL	NULL	NULL	p53	GP		binds		directly			myosin VI	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_6_2175_s_151	16507995	(H) p53 binds directly to the myosin  VI promoter.	bind
16510	1	5499	6	10	NULL	NULL	NULL	Pros-S	GP		bind									seq56B	NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_6_853_s_111	12791270	(H) Pros-S binding to seq56B.	bind
15582	1	5499	7	10	NULL	NULL	NULL	Pros-S	GP		bind									seq56B	NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_6_853_s_111	12791270	(H) Pros-S binding to seq56B.	bind
16511	1	5500	6	10	NULL	NULL	NULL	Patr-B0101	GP		bind								I1452V variant		NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_6_883_s_135	11754811	(H) Relative binding capacity to Patr-B0101 binding of the I1452V or D1449E variants and the NS31444 parental peptide.	bind
16512	2	5500	6	10	NULL	NULL	NULL	Patr-B0101	GP		bind								D1449E variant		NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_6_883_s_135	11754811	(H) Relative binding capacity to Patr-B0101 binding of the I1452V or D1449E variants and the NS31444 parental peptide.	bind
16513	3	5500	6	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_6_883_s_135	11754811	(H) Relative binding capacity to Patr-B0101 binding of the I1452V or D1449E variants and the NS31444 parental peptide.	bind
16514	4	5500	6	10	NULL	NULL	NULL	Patr-B0101	GP		bind					NS31444 parental peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_6_883_s_135	11754811	(H) Relative binding capacity to Patr-B0101 binding of the I1452V or D1449E variants and the NS31444 parental peptide.	bind
15782	1	5500	7	10	NULL	NULL	NULL				bind			I1452V		 Patr-B0101	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_6_883_s_135	11754811	(H) Relative binding capacity to Patr-B0101 binding of the I1452V or D1449E variants and the NS31444 parental peptide.	bind
15783	2	5500	7	10	NULL	NULL	NULL				bind			D1449E 		Patr-B0101	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_6_883_s_135	11754811	(H) Relative binding capacity to Patr-B0101 binding of the I1452V or D1449E variants and the NS31444 parental peptide.	bind
15784	3	5500	7	10	NULL	NULL	NULL	NS31444 parental peptide	GP		bind					Patr-B0101	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_6_883_s_135	11754811	(H) Relative binding capacity to Patr-B0101 binding of the I1452V or D1449E variants and the NS31444 parental peptide.	bind
44794	4	5500	7	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_15_6_883_s_135	11754811	(H) Relative binding capacity to Patr-B0101 binding of the I1452V or D1449E variants and the NS31444 parental peptide.	bind
16515	1	5501	6	10	NULL	NULL	NULL	Yan	GP		bind									ETS domain binding sites 1 within SME	NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_161	11051549	(H) Yan binds to ETS domain binding  sites 1, 2, 4, and 6 within the SME, causing shifted bands.	bind
16516	2	5501	6	10	NULL	NULL	NULL	Yan	GP		bind									ETS domain binding sites 2 within SME	NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_161	11051549	(H) Yan binds to ETS domain binding  sites 1, 2, 4, and 6 within the SME, causing shifted bands.	bind
16517	3	5501	6	10	NULL	NULL	NULL	Yan	GP		bind									ETS domain binding sites 4 within SME	NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_161	11051549	(H) Yan binds to ETS domain binding  sites 1, 2, 4, and 6 within the SME, causing shifted bands.	bind
16518	4	5501	6	10	NULL	NULL	NULL	Yan	GP		bind									ETS domain binding sites 6 within SME	NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_161	11051549	(H) Yan binds to ETS domain binding  sites 1, 2, 4, and 6 within the SME, causing shifted bands.	bind
15778	1	5501	7	10	NULL	NULL	NULL	Yan	GP		bind									ETS domain 1 within SME	NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_161	11051549	(H) Yan binds to ETS domain binding  sites 1, 2, 4, and 6 within the SME, causing shifted bands.	bind
15779	2	5501	7	10	NULL	NULL	NULL	Yan 	GP		bind									ETS domain 2 within SME	NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_161	11051549	(H) Yan binds to ETS domain binding  sites 1, 2, 4, and 6 within the SME, causing shifted bands.	bind
15780	3	5501	7	10	NULL	NULL	NULL	Yan	GP		bind									ETS domain 4 within SME	NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_161	11051549	(H) Yan binds to ETS domain binding  sites 1, 2, 4, and 6 within the SME, causing shifted bands.	bind
15781	4	5501	7	10	NULL	NULL	NULL	Yan	GP		bind									ETS domain 6 within SME	NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_161	11051549	(H) Yan binds to ETS domain binding  sites 1, 2, 4, and 6 within the SME, causing shifted bands.	bind
16519	1	5502	6	10	NULL	NULL	NULL	dTCF-HMG protein	GP		bind					wing	OrganismPart			794 bp Ser of enhancer	NULL		NULL	NULL	NULL	NULL	gw70_development_131_2_285_s_165	14701680	(H-K) DNase I footprinting analysis of the  dTCF-HMG protein bound to the 794 bp  Ser wing enhancer.	bind
15785	1	5502	7	10	NULL	NULL	NULL	dTCF-HMG protein	GP		bind					wing	OrganismPart			794 bp Ser of enhancer	NULL		NULL	NULL	NULL	NULL	gw70_development_131_2_285_s_165	14701680	(H-K) DNase I footprinting analysis of the  dTCF-HMG protein bound to the 794 bp  Ser wing enhancer.	bind
16520	1	5506	6	10	NULL	NULL	NULL				bind			K3L		PKR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_2_295_s_234	12191475	(His 47), also reduced the binding affinity of K3L for PKR.	bind
67197	2	5506	6	10	NULL	NULL	NULL				reduce			His 47		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_2_295_s_234	12191475	(His 47), also reduced the binding affinity of K3L for PKR.	bind
15786	1	5506	7	10	NULL	NULL	NULL				bind			K3L		PKR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_2_295_s_234	12191475	(His 47), also reduced the binding affinity of K3L for PKR.	bind
15787	2	5506	7	10	NULL	NULL	NULL				reduce			His 47		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_2_295_s_234	12191475	(His 47), also reduced the binding affinity of K3L for PKR.	bind
16521	1	5508	6	10	NULL	NULL	NULL				does not bind			His- lC		F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_33_23549_s_205	10438535	(His- lC) does not bind to F-actin in the co-sedimentation assay excludes the tag as a mediator of F-actin binding.	bind
15788	1	5508	7	10	NULL	NULL	NULL				does not bind			His- lC		F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_33_23549_s_205	10438535	(His- lC) does not bind to F-actin in the co-sedimentation assay excludes the tag as a mediator of F-actin binding.	bind
16522	1	5509	6	10	NULL	NULL	NULL	HSF	GP		bind									heat shock element	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_7_792_s_131	10766736	(HSE) The heat shock element to which HSF binds; (GA) a GAGA element to which GAGA factor binds (Wilkins and Lis 1997  ).	bind
16523	2	5509	6	10	NULL	NULL	NULL	GAGA factor	GP		bind									GAGA element	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_7_792_s_131	10766736	(HSE) The heat shock element to which HSF binds; (GA) a GAGA element to which GAGA factor binds (Wilkins and Lis 1997  ).	bind
15789	1	5509	7	10	NULL	NULL	NULL	HSF	GP		bind									heat shock element	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_7_792_s_131	10766736	(HSE) The heat shock element to which HSF binds; (GA) a GAGA element to which GAGA factor binds (Wilkins and Lis 1997  ).	bind
15790	2	5509	7	10	NULL	NULL	NULL	GAGA factor	GP		bind									GAGA element	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_7_792_s_131	10766736	(HSE) The heat shock element to which HSF binds; (GA) a GAGA element to which GAGA factor binds (Wilkins and Lis 1997  ).	bind
16524	1	5511	6	10	NULL	NULL	NULL	GST-EB1	GP		bind					Mlp-FLAG	GP				NULL	SF9 whole cell extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_171_2_201_s_104	16247022	(I and J) GST-EB1 but not GST binds Mlp-FLAG whether present in SF9 whole  cell extracts	bind
16525	2	5511	6	10	NULL	NULL	NULL	GST	Chemical		does not bind					Mlp-FLAG	GP				NULL	SF9 whole cell extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_171_2_201_s_104	16247022	(I and J) GST-EB1 but not GST binds Mlp-FLAG whether present in SF9 whole  cell extracts	bind
15791	1	5511	7	10	NULL	NULL	NULL	GST-EB1	GP		bind					Mlp-FLAG	GP				NULL	 SF9 whole cell extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_171_2_201_s_104	16247022	(I and J) GST-EB1 but not GST binds Mlp-FLAG whether present in SF9 whole  cell extracts	bind
15792	2	5511	7	10	NULL	NULL	NULL	GST	Chemical		does not bind					Mlp-FLAG	GP				NULL	SF9 whole cell extracts	NULL	NULL	NULL	NULL	gw70_cellbiol_171_2_201_s_104	16247022	(I and J) GST-EB1 but not GST binds Mlp-FLAG whether present in SF9 whole  cell extracts	bind
16526	1	5512	6	10	NULL	NULL	NULL	P450 2E1	GP		bind					ethanol	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_23833_s_173	10446146	(i)  K d values for binding of P450 2E1 and either ethanol, acetaldehyde, or acetic acid are all high (millimolar to molar range).	bind
16527	2	5512	6	10	NULL	NULL	NULL	P450 2E1	GP		bind					acetaldehyde	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_23833_s_173	10446146	(i)  K d values for binding of P450 2E1 and either ethanol, acetaldehyde, or acetic acid are all high (millimolar to molar range).	bind
16528	3	5512	6	10	NULL	NULL	NULL	P450 2E1	GP		bind					acetic acid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_23833_s_173	10446146	(i)  K d values for binding of P450 2E1 and either ethanol, acetaldehyde, or acetic acid are all high (millimolar to molar range).	bind
16301	1	5512	7	10	NULL	NULL	NULL	P450 2E1	GP		bind					ethanol	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_23833_s_173	10446146	(i)  K d values for binding of P450 2E1 and either ethanol, acetaldehyde, or acetic acid are all high (millimolar to molar range).	bind
16302	2	5512	7	10	NULL	NULL	NULL	P450 2E1	GP		bind					acetaldehyde	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_23833_s_173	10446146	(i)  K d values for binding of P450 2E1 and either ethanol, acetaldehyde, or acetic acid are all high (millimolar to molar range).	bind
16303	3	5512	7	10	NULL	NULL	NULL	P450 2E1	GP		bind					acetic acid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_23833_s_173	10446146	(i)  K d values for binding of P450 2E1 and either ethanol, acetaldehyde, or acetic acid are all high (millimolar to molar range).	bind
16529	1	5513	6	10	NULL	NULL	NULL	MAQ1	GP		bind					P-TEFb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_14_4859_s_370	12832472	(i) 7SK RNA is essential for MAQ1 binding to P-TEFb, whereas although TAR RNA enhances the interaction between Tat and cyclin T1 ( 63), Tat binding to P-TEFb can occur in the absence of TAR RNA ( 25,  61).	bind
16530	2	5513	6	10	NULL	NULL	NULL	7SK RNA	NucleicAcid		is essential for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_14_4859_s_370	12832472	(i) 7SK RNA is essential for MAQ1 binding to P-TEFb, whereas although TAR RNA enhances the interaction between Tat and cyclin T1 ( 63), Tat binding to P-TEFb can occur in the absence of TAR RNA ( 25,  61).	bind
16531	3	5513	6	10	NULL	NULL	NULL	Tat	GP		bind					cyclin T1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_14_4859_s_370	12832472	(i) 7SK RNA is essential for MAQ1 binding to P-TEFb, whereas although TAR RNA enhances the interaction between Tat and cyclin T1 ( 63), Tat binding to P-TEFb can occur in the absence of TAR RNA ( 25,  61).	bind
16532	4	5513	6	10	NULL	NULL	NULL	Tat	GP		bind					P-TEFb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_14_4859_s_370	12832472	(i) 7SK RNA is essential for MAQ1 binding to P-TEFb, whereas although TAR RNA enhances the interaction between Tat and cyclin T1 ( 63), Tat binding to P-TEFb can occur in the absence of TAR RNA ( 25,  61).	bind
16533	5	5513	6	10	NULL	NULL	NULL	statement 4	Process		occur in the absence of					TAR RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_14_4859_s_370	12832472	(i) 7SK RNA is essential for MAQ1 binding to P-TEFb, whereas although TAR RNA enhances the interaction between Tat and cyclin T1 ( 63), Tat binding to P-TEFb can occur in the absence of TAR RNA ( 25,  61).	bind
16534	6	5513	6	10	NULL	NULL	NULL	TAR RNA	NucleicAcid		enhances					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_14_4859_s_370	12832472	(i) 7SK RNA is essential for MAQ1 binding to P-TEFb, whereas although TAR RNA enhances the interaction between Tat and cyclin T1 ( 63), Tat binding to P-TEFb can occur in the absence of TAR RNA ( 25,  61).	bind
15793	1	5513	7	10	NULL	NULL	NULL	MAQ1 	GP		bind					P-TEFb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_14_4859_s_370	12832472	(i) 7SK RNA is essential for MAQ1 binding to P-TEFb, whereas although TAR RNA enhances the interaction between Tat and cyclin T1 ( 63), Tat binding to P-TEFb can occur in the absence of TAR RNA ( 25,  61).	bind
15794	2	5513	7	10	NULL	NULL	NULL	7SK RNA	NucleicAcid		is essential for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_14_4859_s_370	12832472	(i) 7SK RNA is essential for MAQ1 binding to P-TEFb, whereas although TAR RNA enhances the interaction between Tat and cyclin T1 ( 63), Tat binding to P-TEFb can occur in the absence of TAR RNA ( 25,  61).	bind
15795	3	5513	7	10	NULL	NULL	NULL	 Tat	GP		bind					cyclin T1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_14_4859_s_370	12832472	(i) 7SK RNA is essential for MAQ1 binding to P-TEFb, whereas although TAR RNA enhances the interaction between Tat and cyclin T1 ( 63), Tat binding to P-TEFb can occur in the absence of TAR RNA ( 25,  61).	bind
15796	4	5513	7	10	NULL	NULL	NULL	 TAR RNA	NucleicAcid		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_14_4859_s_370	12832472	(i) 7SK RNA is essential for MAQ1 binding to P-TEFb, whereas although TAR RNA enhances the interaction between Tat and cyclin T1 ( 63), Tat binding to P-TEFb can occur in the absence of TAR RNA ( 25,  61).	bind
15797	5	5513	7	10	NULL	NULL	NULL	Tat	GP		bind					P-TEFb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_14_4859_s_370	12832472	(i) 7SK RNA is essential for MAQ1 binding to P-TEFb, whereas although TAR RNA enhances the interaction between Tat and cyclin T1 ( 63), Tat binding to P-TEFb can occur in the absence of TAR RNA ( 25,  61).	bind
15798	6	5513	7	10	NULL	NULL	NULL	statement 5	Process		occur in the absence of					TAR RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_14_4859_s_370	12832472	(i) 7SK RNA is essential for MAQ1 binding to P-TEFb, whereas although TAR RNA enhances the interaction between Tat and cyclin T1 ( 63), Tat binding to P-TEFb can occur in the absence of TAR RNA ( 25,  61).	bind
16535	1	5515	6	10	NULL	NULL	NULL	GST-L18	GP		bind		directly			PKR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1116_s_290	9891046	(i) A GST-L18 fusion protein directly bound to PKR.	bind
44806	2	5515	6	10	NULL	NULL	NULL	GST-L18 	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1116_s_290	9891046	(i) A GST-L18 fusion protein directly bound to PKR.	bind
15799	1	5515	7	10	NULL	NULL	NULL	GST-L18	GP		bind		directly			PKR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1116_s_290	9891046	(i) A GST-L18 fusion protein directly bound to PKR.	bind
44807	2	5515	7	10	NULL	NULL	NULL	GST-L18 	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1116_s_290	9891046	(i) A GST-L18 fusion protein directly bound to PKR.	bind
16536	1	5516	6	10	NULL	NULL	NULL	antibodies	GP		bind					Vn	GP	close proximity to	cell adhesion domain		NULL	unfractionated plasma	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_21_13705_s_6	9153222	(i) Antibodies that bind in close proximity to the cell adhesion domain of Vn fail to bind to native Vn present in unfractionated plasma.	bind
16537	2	5516	6	10	NULL	NULL	NULL	antibodies	GP		does not bind					Vn	GP	native			NULL	unfractionated plasma	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_21_13705_s_6	9153222	(i) Antibodies that bind in close proximity to the cell adhesion domain of Vn fail to bind to native Vn present in unfractionated plasma.	bind
15800	1	5516	7	10	NULL	NULL	NULL	Antibodies	GP		bind					Vn 	GP	close proximity to	cell adhesion domain		NULL	unfractionated plasma	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_21_13705_s_6	9153222	(i) Antibodies that bind in close proximity to the cell adhesion domain of Vn fail to bind to native Vn present in unfractionated plasma.	bind
15802	3	5516	7	10	NULL	NULL	NULL	Antibodies	GP		does not bind					Vn	GP	native			NULL	 unfractionated plasma	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_21_13705_s_6	9153222	(i) Antibodies that bind in close proximity to the cell adhesion domain of Vn fail to bind to native Vn present in unfractionated plasma.	bind
16538	1	5517	6	10	NULL	NULL	NULL	AP-Sema3A	GP		bind		high affinity			corpus callosum axons	OrganismPart				NULL	E17.5 wild type mice	NULL	NULL	NULL	NULL	gw60_devcell_5_1_45_s_156	12852851	(I) AP-Sema3A section binding reveals a high level of Sema3A binding to axons of the E17.5 corpus callosum in wild-type mice.	bind
15803	1	5517	7	10	NULL	NULL	NULL	AP-Sema3A	GP		bind		high affinity			corpus callosum axons	OrganismPart				NULL	E17.5  wild-type mice	NULL	NULL	NULL	NULL	gw60_devcell_5_1_45_s_156	12852851	(I) AP-Sema3A section binding reveals a high level of Sema3A binding to axons of the E17.5 corpus callosum in wild-type mice.	bind
16539	1	5518	6	10	NULL	NULL	NULL	ATP	Chemical		bind								D1 domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_90_3_523_s_122	9267032	(i) ATP  bound to both D1 and D2 domains maintains the closed cylinder.	bind
16540	2	5518	6	10	NULL	NULL	NULL	ATP	Chemical		bind								D2 domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_90_3_523_s_122	9267032	(i) ATP  bound to both D1 and D2 domains maintains the closed cylinder.	bind
16541	3	5518	6	10	NULL	NULL	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_3_523_s_122	9267032	(i) ATP  bound to both D1 and D2 domains maintains the closed cylinder.	bind
16542	4	5518	6	10	NULL	NULL	NULL	statement 3	Process		maintains					closed cylinder					NULL		NULL	NULL	NULL	NULL	gw60_cell_90_3_523_s_122	9267032	(i) ATP  bound to both D1 and D2 domains maintains the closed cylinder.	bind
15804	1	5518	7	10	NULL	NULL	NULL	ATP	Chemical		bind								D1 domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_90_3_523_s_122	9267032	(i) ATP  bound to both D1 and D2 domains maintains the closed cylinder.	bind
15805	2	5518	7	10	NULL	NULL	NULL	ATP	Chemical		bind								D2 domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_90_3_523_s_122	9267032	(i) ATP  bound to both D1 and D2 domains maintains the closed cylinder.	bind
15806	3	5518	7	10	NULL	NULL	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_90_3_523_s_122	9267032	(i) ATP  bound to both D1 and D2 domains maintains the closed cylinder.	bind
15807	4	5518	7	10	NULL	NULL	NULL	statement 3	Process		maintains					closed cylinder					NULL		NULL	NULL	NULL	NULL	gw60_cell_90_3_523_s_122	9267032	(i) ATP  bound to both D1 and D2 domains maintains the closed cylinder.	bind
16543	1	5519	6	10	NULL	NULL	NULL	PrPSc	GP		bind					PrP-Fc2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_1_49_s_160	12679034	(I) Binding of PrPSc to PrP-Fc2 is highly sensitive to chaotropic salts.	bind
16544	2	5519	6	10	NULL	NULL	NULL	statement 1	Process		is sensitive to 		highly			chaotropic salts	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_1_49_s_160	12679034	(I) Binding of PrPSc to PrP-Fc2 is highly sensitive to chaotropic salts.	bind
15808	1	5519	7	10	NULL	NULL	NULL	PrPSc	GP		bind					PrP-Fc2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_1_49_s_160	12679034	(I) Binding of PrPSc to PrP-Fc2 is highly sensitive to chaotropic salts.	bind
15809	2	5519	7	10	NULL	NULL	NULL	statement 1	Process		is sensitive to		highly			chaotropic salts	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_113_1_49_s_160	12679034	(I) Binding of PrPSc to PrP-Fc2 is highly sensitive to chaotropic salts.	bind
16545	1	5520	6	10	NULL	NULL	NULL	Cu(I)	Chemical		bind					chaperone	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_23163_s_256	12686548	(i) Can the two-coordinate Cu(I)-bound chaperone ever be  prepared free from ligation by an exogenous third ligand, and if so, what is  the structure?	bind
15810	1	5520	7	10	NULL	NULL	NULL	chaperone	GP		bind					Cu(I)	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_23163_s_256	12686548	(i) Can the two-coordinate Cu(I)-bound chaperone ever be  prepared free from ligation by an exogenous third ligand, and if so, what is  the structure?	bind
16546	1	5521	6	10	NULL	NULL	NULL	glucose catabolites	Chemical		activate					HPr kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_7_2513_s_193	9647823	(i) Catabolites of glucose activate the HPr kinase, and then the phosphorylated form of HPr(Ser) binds to CcpA, mediating the dimerization of CcpA ( 12,  34,  37).	bind
16547	2	5521	6	10	NULL	NULL	NULL	HPr	GP	phosphorylated	bind			Ser		CcpA	GP				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_7_2513_s_193	9647823	(i) Catabolites of glucose activate the HPr kinase, and then the phosphorylated form of HPr(Ser) binds to CcpA, mediating the dimerization of CcpA ( 12,  34,  37).	bind
16548	3	5521	6	10	NULL	NULL	NULL	statement 2	Process		mediates					CcpA	GP	dimerization of			NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_7_2513_s_193	9647823	(i) Catabolites of glucose activate the HPr kinase, and then the phosphorylated form of HPr(Ser) binds to CcpA, mediating the dimerization of CcpA ( 12,  34,  37).	bind
15811	1	5521	7	10	NULL	NULL	NULL	glucose catabolites	Chemical		activates					HPr kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_7_2513_s_193	9647823	(i) Catabolites of glucose activate the HPr kinase, and then the phosphorylated form of HPr(Ser) binds to CcpA, mediating the dimerization of CcpA ( 12,  34,  37).	bind
15812	2	5521	7	10	NULL	NULL	NULL	HPr	GP	phosphorylated	bind			Ser		CcpA	GP				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_7_2513_s_193	9647823	(i) Catabolites of glucose activate the HPr kinase, and then the phosphorylated form of HPr(Ser) binds to CcpA, mediating the dimerization of CcpA ( 12,  34,  37).	bind
15813	3	5521	7	10	NULL	NULL	NULL	statement 2	Process		mediates					CcpA	GP	dimerization of			NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_7_2513_s_193	9647823	(i) Catabolites of glucose activate the HPr kinase, and then the phosphorylated form of HPr(Ser) binds to CcpA, mediating the dimerization of CcpA ( 12,  34,  37).	bind
16549	1	5522	6	10	NULL	NULL	NULL	CcpA	GP		bind		efficiently			phoPR	GP			CRE site of promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbacteriol_188_4_1266_s_296	16452408	(i) CcpA without cofactors binds efficiently to the  phoPR promoter  cre site ( Kd  0.5 nM) but required more than 1 muM CcpA to inhibit PA6 transcription in vitro in the absence of coeffectors.	bind
16550	2	5522	6	10	NULL	NULL	NULL	CcpA	GP		inhibit					PA6	GP	transcription of			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbacteriol_188_4_1266_s_296	16452408	(i) CcpA without cofactors binds efficiently to the  phoPR promoter  cre site ( Kd  0.5 nM) but required more than 1 muM CcpA to inhibit PA6 transcription in vitro in the absence of coeffectors.	bind
16551	3	5522	6	10	NULL	NULL	NULL	statement 2	Process		occurs in absence of					coeffectors	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbacteriol_188_4_1266_s_296	16452408	(i) CcpA without cofactors binds efficiently to the  phoPR promoter  cre site ( Kd  0.5 nM) but required more than 1 muM CcpA to inhibit PA6 transcription in vitro in the absence of coeffectors.	bind
53105	4	5522	6	10	NULL	NULL	NULL	statement 1	Process		occurs without					CcpA	GP	cofactors of			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbacteriol_188_4_1266_s_296	16452408	(i) CcpA without cofactors binds efficiently to the  phoPR promoter  cre site ( Kd  0.5 nM) but required more than 1 muM CcpA to inhibit PA6 transcription in vitro in the absence of coeffectors.	bind
15814	1	5522	7	10	NULL	NULL	NULL	CcpA	GP		binds		efficiently			 phoPR	GP			promoter cre site	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbacteriol_188_4_1266_s_296	16452408	(i) CcpA without cofactors binds efficiently to the  phoPR promoter  cre site ( Kd  0.5 nM) but required more than 1 muM CcpA to inhibit PA6 transcription in vitro in the absence of coeffectors.	bind
15815	2	5522	7	10	NULL	NULL	NULL	statement 1	Process		occur without					CcpA	GP	cofactors of			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbacteriol_188_4_1266_s_296	16452408	(i) CcpA without cofactors binds efficiently to the  phoPR promoter  cre site ( Kd  0.5 nM) but required more than 1 muM CcpA to inhibit PA6 transcription in vitro in the absence of coeffectors.	bind
15816	3	5522	7	10	NULL	NULL	NULL	CcpA	GP		inhibit					PA6	GP	transcription of			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbacteriol_188_4_1266_s_296	16452408	(i) CcpA without cofactors binds efficiently to the  phoPR promoter  cre site ( Kd  0.5 nM) but required more than 1 muM CcpA to inhibit PA6 transcription in vitro in the absence of coeffectors.	bind
15817	4	5522	7	10	NULL	NULL	NULL	statement 3	Process		occurs in the absence of					coeffectors	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbacteriol_188_4_1266_s_296	16452408	(i) CcpA without cofactors binds efficiently to the  phoPR promoter  cre site ( Kd  0.5 nM) but required more than 1 muM CcpA to inhibit PA6 transcription in vitro in the absence of coeffectors.	bind
16552	1	5523	6	10	NULL	NULL	NULL	E.coli	Organism		bind					CHO cells	Cell	SR-A transfected			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_4_1953_s_119	10722588	(i) Characteristics of binding of  E. coli by SR-A-transfected CHO cells.	bind
15818	1	5523	7	10	NULL	NULL	NULL	E.coli	Organism		bind					CHO cells	Cell	SR-A-transfected			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_4_1953_s_119	10722588	(i) Characteristics of binding of  E. coli by SR-A-transfected CHO cells.	bind
16756	1	5524	6	10	NULL	NULL	NULL	PU.1	GP		associates with					GATA-1 target gene	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7460_s_372	14559995	(i) ChIP experiments indicate that PU.1 and pRB can be found associated with a GATA-1 target gene, but only when both GATA-1 and an intact GATA-1 DNA binding site are present.	bind
16757	2	5524	6	10	NULL	NULL	NULL	pRB	GP		associates with					GATA-1 target gene	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7460_s_372	14559995	(i) ChIP experiments indicate that PU.1 and pRB can be found associated with a GATA-1 target gene, but only when both GATA-1 and an intact GATA-1 DNA binding site are present.	bind
16760	3	5524	6	10	NULL	NULL	NULL	statement 1	Process		occurs in presence of		only					intact		GATA-1 DNA binding site	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7460_s_372	14559995	(i) ChIP experiments indicate that PU.1 and pRB can be found associated with a GATA-1 target gene, but only when both GATA-1 and an intact GATA-1 DNA binding site are present.	bind
16761	4	5524	6	10	NULL	NULL	NULL	statement 1	Process		occurs in presence of		only			GATA-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7460_s_372	14559995	(i) ChIP experiments indicate that PU.1 and pRB can be found associated with a GATA-1 target gene, but only when both GATA-1 and an intact GATA-1 DNA binding site are present.	bind
17044	5	5524	6	10	NULL	NULL	NULL	statement 3	Process		occurs simultaneously with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7460_s_372	14559995	(i) ChIP experiments indicate that PU.1 and pRB can be found associated with a GATA-1 target gene, but only when both GATA-1 and an intact GATA-1 DNA binding site are present.	bind
17045	6	5524	6	10	NULL	NULL	NULL	statement 2	Process		occurs in presence of		only					intact		GATA-1 DNA binding site	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7460_s_372	14559995	(i) ChIP experiments indicate that PU.1 and pRB can be found associated with a GATA-1 target gene, but only when both GATA-1 and an intact GATA-1 DNA binding site are present.	bind
17046	7	5524	6	10	NULL	NULL	NULL	statement 2	Process		occurs in presence of		only			GATA-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7460_s_372	14559995	(i) ChIP experiments indicate that PU.1 and pRB can be found associated with a GATA-1 target gene, but only when both GATA-1 and an intact GATA-1 DNA binding site are present.	bind
17047	8	5524	6	10	NULL	NULL	NULL	statement 6	Process		occurs simultaneously with					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7460_s_372	14559995	(i) ChIP experiments indicate that PU.1 and pRB can be found associated with a GATA-1 target gene, but only when both GATA-1 and an intact GATA-1 DNA binding site are present.	bind
15819	1	5524	7	10	NULL	NULL	NULL	PU.1	GP		associate with					GATA-1 target gene	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7460_s_372	14559995	(i) ChIP experiments indicate that PU.1 and pRB can be found associated with a GATA-1 target gene, but only when both GATA-1 and an intact GATA-1 DNA binding site are present.	bind
15820	2	5524	7	10	NULL	NULL	NULL	pRB	GP		associate with					GATA-1 target gene	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7460_s_372	14559995	(i) ChIP experiments indicate that PU.1 and pRB can be found associated with a GATA-1 target gene, but only when both GATA-1 and an intact GATA-1 DNA binding site are present.	bind
15821	3	5524	7	10	NULL	NULL	NULL	statement 1	Process		occurs in the presence of		only			GATA-1 	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7460_s_372	14559995	(i) ChIP experiments indicate that PU.1 and pRB can be found associated with a GATA-1 target gene, but only when both GATA-1 and an intact GATA-1 DNA binding site are present.	bind
15822	4	5524	7	10	NULL	NULL	NULL	statement 2	Process		occurs in the presence of		only			GATA-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7460_s_372	14559995	(i) ChIP experiments indicate that PU.1 and pRB can be found associated with a GATA-1 target gene, but only when both GATA-1 and an intact GATA-1 DNA binding site are present.	bind
15823	5	5524	7	10	NULL	NULL	NULL	statement 1	Process		occurs in the presence of		only					intact		GATA-1 DNA binding site	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7460_s_372	14559995	(i) ChIP experiments indicate that PU.1 and pRB can be found associated with a GATA-1 target gene, but only when both GATA-1 and an intact GATA-1 DNA binding site are present.	bind
15824	6	5524	7	10	NULL	NULL	NULL	statement 2	Process		occurs in the presence of		only					intact		GATA-1 DNA binding site	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7460_s_372	14559995	(i) ChIP experiments indicate that PU.1 and pRB can be found associated with a GATA-1 target gene, but only when both GATA-1 and an intact GATA-1 DNA binding site are present.	bind
15825	7	5524	7	10	NULL	NULL	NULL	statement 3	Process		occurs simultaneous with					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7460_s_372	14559995	(i) ChIP experiments indicate that PU.1 and pRB can be found associated with a GATA-1 target gene, but only when both GATA-1 and an intact GATA-1 DNA binding site are present.	bind
15826	8	5524	7	10	NULL	NULL	NULL	statement 4	Process		occurs simultaneous with					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7460_s_372	14559995	(i) ChIP experiments indicate that PU.1 and pRB can be found associated with a GATA-1 target gene, but only when both GATA-1 and an intact GATA-1 DNA binding site are present.	bind
16553	1	5525	6	10	NULL	NULL	NULL	uracil	Chemical		bind					UDGs	GP		active site pocket		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_24_7216_s_188	14654697	(i) Co-crystal structures of uracil and UDG have shown that at least one site of uracil binding to UDGs is the active site pocket ( 14, 15).	bind
15827	1	5525	7	10	NULL	NULL	NULL	uracil	Chemical		bind					UDGs	GP		active site pocket		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_24_7216_s_188	14654697	(i) Co-crystal structures of uracil and UDG have shown that at least one site of uracil binding to UDGs is the active site pocket ( 14, 15).	bind
16554	1	5526	6	10	NULL	NULL	NULL	Coagulation factor G	GP		bind					beta-1,3-glucans	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_38_24948_s_233	9733802	(i) Coagulation factor G binds beta-1,3-glucans but not LPS ( 43).	bind
16555	2	5526	6	10	NULL	NULL	NULL	Coagulation factor G	GP		does not bind					LPS	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_38_24948_s_233	9733802	(i) Coagulation factor G binds beta-1,3-glucans but not LPS ( 43).	bind
15832	1	5526	7	10	NULL	NULL	NULL	Coagulation factor G	GP		binds					beta-1,3-glucans	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_38_24948_s_233	9733802	(i) Coagulation factor G binds beta-1,3-glucans but not LPS ( 43).	bind
15833	2	5526	7	10	NULL	NULL	NULL	Coagulation factor G	GP		does not bind					LPS	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_38_24948_s_233	9733802	(i) Coagulation factor G binds beta-1,3-glucans but not LPS ( 43).	bind
16556	1	5527	6	10	NULL	NULL	NULL	collagen cDNA	NucleicAcid		bind		specifically			alpha1	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_17_12475_s_48	10777533	(I) collagen cDNA that specifically binds human alpha1	bind
15834	1	5527	7	10	NULL	NULL	NULL	collagen cDNA	NucleicAcid		binds		specifically			alpha1	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_17_12475_s_48	10777533	(I) collagen cDNA that specifically binds human alpha1	bind
16557	1	5528	6	10	NULL	NULL	NULL	decorin	GP		bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_29_21801_s_60	10823816	(I) Collagen Chain-- Binding of decorin to collagen interferes with horizontal accretion of collagen molecules and prevents lateral growth of the fibrils ( 2).	bind
16558	2	5528	6	10	NULL	NULL	NULL	statement 1	Process		interferes with					collagen molecules	GP	horizontal accretion of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_29_21801_s_60	10823816	(I) Collagen Chain-- Binding of decorin to collagen interferes with horizontal accretion of collagen molecules and prevents lateral growth of the fibrils ( 2).	bind
16559	3	5528	6	10	NULL	NULL	NULL	statement 1	Process		prevents					fibrils	OrganismPart	lateral growth of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_29_21801_s_60	10823816	(I) Collagen Chain-- Binding of decorin to collagen interferes with horizontal accretion of collagen molecules and prevents lateral growth of the fibrils ( 2).	bind
15835	1	5528	7	10	NULL	NULL	NULL	decorin	GP		binds					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_29_21801_s_60	10823816	(I) Collagen Chain-- Binding of decorin to collagen interferes with horizontal accretion of collagen molecules and prevents lateral growth of the fibrils ( 2).	bind
15836	2	5528	7	10	NULL	NULL	NULL	statement 1	Process		interferes with					collagen molecules	GP	horizontal accretion of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_29_21801_s_60	10823816	(I) Collagen Chain-- Binding of decorin to collagen interferes with horizontal accretion of collagen molecules and prevents lateral growth of the fibrils ( 2).	bind
15837	3	5528	7	10	NULL	NULL	NULL	statement 2	Process		prevents					fibrils	OrganismPart	lateral growth of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_29_21801_s_60	10823816	(I) Collagen Chain-- Binding of decorin to collagen interferes with horizontal accretion of collagen molecules and prevents lateral growth of the fibrils ( 2).	bind
16560	1	5529	6	10	NULL	NULL	NULL	BTEB	GP		is					basic transcription element binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2818_s_57	10733585	(I) collagen gene, and the GC box was bound by a DNA binding protein, termed BTEB (basic transcription element binding protein) ( 8).	bind
16561	2	5529	6	10	NULL	NULL	NULL	BTEB	GP		bind					collagen gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2818_s_57	10733585	(I) collagen gene, and the GC box was bound by a DNA binding protein, termed BTEB (basic transcription element binding protein) ( 8).	bind
16562	3	5529	6	10	NULL	NULL	NULL	BTEB	GP		bind									GC box	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2818_s_57	10733585	(I) collagen gene, and the GC box was bound by a DNA binding protein, termed BTEB (basic transcription element binding protein) ( 8).	bind
44808	4	5529	6	10	NULL	NULL	NULL	BTEB	GP		is a type of					DNA binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2818_s_57	10733585	(I) collagen gene, and the GC box was bound by a DNA binding protein, termed BTEB (basic transcription element binding protein) ( 8).	bind
15838	1	5529	7	10	NULL	NULL	NULL	BTEB	GP		bind					collagen gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2818_s_57	10733585	(I) collagen gene, and the GC box was bound by a DNA binding protein, termed BTEB (basic transcription element binding protein) ( 8).	bind
15839	2	5529	7	10	NULL	NULL	NULL	BTEB	GP		binds									GC box	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2818_s_57	10733585	(I) collagen gene, and the GC box was bound by a DNA binding protein, termed BTEB (basic transcription element binding protein) ( 8).	bind
15840	3	5529	7	10	NULL	NULL	NULL	BTEB	GP		is					basic transcription element binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2818_s_57	10733585	(I) collagen gene, and the GC box was bound by a DNA binding protein, termed BTEB (basic transcription element binding protein) ( 8).	bind
15841	4	5529	7	10	NULL	NULL	NULL	BTEB	GP		is a type of					DNA binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2818_s_57	10733585	(I) collagen gene, and the GC box was bound by a DNA binding protein, termed BTEB (basic transcription element binding protein) ( 8).	bind
16563	1	5531	6	10	NULL	NULL	NULL	HMG-I(Y)	GP		modulates					NF-Y function	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_29	9388234	(I) collagen promoter and multimerized version of the alpha2(I) collagen NF-Y(CBF) binding site have been used to investigate the role of HMG-I(Y) as a protein cofactor in modulating NF-Y function.	bind
16564	2	5531	6	10	NULL	NULL	NULL	HMG-I(Y)	GP		is a type of					protien cofactor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_29	9388234	(I) collagen promoter and multimerized version of the alpha2(I) collagen NF-Y(CBF) binding site have been used to investigate the role of HMG-I(Y) as a protein cofactor in modulating NF-Y function.	bind
20334	1	5531	7	10	NULL	NULL	NULL	HMG-I(Y)	GP		modulates					NF-Y function	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_29	9388234	(I) collagen promoter and multimerized version of the alpha2(I) collagen NF-Y(CBF) binding site have been used to investigate the role of HMG-I(Y) as a protein cofactor in modulating NF-Y function.	bind
20335	2	5531	7	10	NULL	NULL	NULL	HMG-I(Y)	GP		is a type of					protein cofactor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_29	9388234	(I) collagen promoter and multimerized version of the alpha2(I) collagen NF-Y(CBF) binding site have been used to investigate the role of HMG-I(Y) as a protein cofactor in modulating NF-Y function.	bind
16565	1	5532	6	10	NULL	NULL	NULL	NF-Y	GP		bind					cell-cycle genes	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_33_30435_s_136	12771133	(i) Contrary to predictions based upon  in  vitro binding activity in EMSAs and ChIP data on other promoters, the   in vivo binding of NF-Y to cell-cycle genes is strictly regulated  during the different phases of the cell-cycle.	bind
16566	2	5532	6	10	NULL	NULL	NULL	statement 1	Process		is regulated during		strictly			cell cycle	Process	different phases of 			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_33_30435_s_136	12771133	(i) Contrary to predictions based upon  in  vitro binding activity in EMSAs and ChIP data on other promoters, the   in vivo binding of NF-Y to cell-cycle genes is strictly regulated  during the different phases of the cell-cycle.	bind
15842	1	5532	7	10	NULL	NULL	NULL	NF-Y	GP		bind					cell-cycle genes	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_33_30435_s_136	12771133	(i) Contrary to predictions based upon  in  vitro binding activity in EMSAs and ChIP data on other promoters, the   in vivo binding of NF-Y to cell-cycle genes is strictly regulated  during the different phases of the cell-cycle.	bind
15843	2	5532	7	10	NULL	NULL	NULL	statement 1	Process		is regulated during		strictly			cell-cycle	Process	different phases of			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_33_30435_s_136	12771133	(i) Contrary to predictions based upon  in  vitro binding activity in EMSAs and ChIP data on other promoters, the   in vivo binding of NF-Y to cell-cycle genes is strictly regulated  during the different phases of the cell-cycle.	bind
16837	1	5533	6	NULL	NULL	0	NULL		NULL		bind	NULL	directly	region I			NULL		region II		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_4_1414_s_268	16449652	(i) Direct interactions  between regions I and II are important for masking the NLS, and the signal-dependent  binding of unknown factor "`X"` to the region spanning aa residues 183 to  382 disrupts this masking.	bind
16839	2	5533	6	10	NULL	NULL	NULL	statement 1	Process		is important for					NLS	GP	masking of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_4_1414_s_268	16449652	(i) Direct interactions  between regions I and II are important for masking the NLS, and the signal-dependent  binding of unknown factor "`X"` to the region spanning aa residues 183 to  382 disrupts this masking.	bind
16840	3	5533	6	10	NULL	NULL	NULL	unknown factor X	GP		bind								aa residues 183 to 382		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_4_1414_s_268	16449652	(i) Direct interactions  between regions I and II are important for masking the NLS, and the signal-dependent  binding of unknown factor "`X"` to the region spanning aa residues 183 to  382 disrupts this masking.	bind
16841	4	5533	6	10	NULL	NULL	NULL	statement 3	Process		is dependent on					signal	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_4_1414_s_268	16449652	(i) Direct interactions  between regions I and II are important for masking the NLS, and the signal-dependent  binding of unknown factor "`X"` to the region spanning aa residues 183 to  382 disrupts this masking.	bind
16842	5	5533	6	10	NULL	NULL	NULL	statement 4	Process		disrupts					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_4_1414_s_268	16449652	(i) Direct interactions  between regions I and II are important for masking the NLS, and the signal-dependent  binding of unknown factor "`X"` to the region spanning aa residues 183 to  382 disrupts this masking.	bind
15844	1	5533	7	NULL	NULL	0	NULL		NULL		bind	NULL	directly	region I			NULL		region II		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_4_1414_s_268	16449652	(i) Direct interactions  between regions I and II are important for masking the NLS, and the signal-dependent  binding of unknown factor "`X"` to the region spanning aa residues 183 to  382 disrupts this masking.	bind
15845	2	5533	7	10	NULL	NULL	NULL	statement 1	Process		is important for					NLS	GP	masking			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_4_1414_s_268	16449652	(i) Direct interactions  between regions I and II are important for masking the NLS, and the signal-dependent  binding of unknown factor "`X"` to the region spanning aa residues 183 to  382 disrupts this masking.	bind
15846	3	5533	7	10	NULL	NULL	NULL	unknown factor X	GP		binds								region spanning aa residues 183 to 382 		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_4_1414_s_268	16449652	(i) Direct interactions  between regions I and II are important for masking the NLS, and the signal-dependent  binding of unknown factor "`X"` to the region spanning aa residues 183 to  382 disrupts this masking.	bind
15847	4	5533	7	10	NULL	NULL	NULL	statement 3	Process		is dependent on					signal	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_4_1414_s_268	16449652	(i) Direct interactions  between regions I and II are important for masking the NLS, and the signal-dependent  binding of unknown factor "`X"` to the region spanning aa residues 183 to  382 disrupts this masking.	bind
15848	5	5533	7	10	NULL	NULL	NULL	statement 3	Process		disrupts					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_4_1414_s_268	16449652	(i) Direct interactions  between regions I and II are important for masking the NLS, and the signal-dependent  binding of unknown factor "`X"` to the region spanning aa residues 183 to  382 disrupts this masking.	bind
16567	1	5535	6	10	NULL	NULL	NULL	MAb FRP5	GP		activates					ErbB-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5042_s_322	9710588	(i) ErbB-2 activated by MAb FRP5 and ErbB-2 activated by NDF displayed similar levels of total phosphotyrosine; however, GST-Grb2 SH2 bound significantly higher amounts of FRP5-activated ErbB-2.	bind
16568	2	5535	6	10	NULL	NULL	NULL	NDF	GP		activates					ErbB-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5042_s_322	9710588	(i) ErbB-2 activated by MAb FRP5 and ErbB-2 activated by NDF displayed similar levels of total phosphotyrosine; however, GST-Grb2 SH2 bound significantly higher amounts of FRP5-activated ErbB-2.	bind
16569	3	5535	6	10	NULL	NULL	NULL	FRP5	GP		activates					ErbB-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5042_s_322	9710588	(i) ErbB-2 activated by MAb FRP5 and ErbB-2 activated by NDF displayed similar levels of total phosphotyrosine; however, GST-Grb2 SH2 bound significantly higher amounts of FRP5-activated ErbB-2.	bind
16570	4	5535	6	10	NULL	NULL	NULL	GST-Grb2	GP		bind		significantly	SH2 domain		ErB-2	GP	FRP5 activated			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5042_s_322	9710588	(i) ErbB-2 activated by MAb FRP5 and ErbB-2 activated by NDF displayed similar levels of total phosphotyrosine; however, GST-Grb2 SH2 bound significantly higher amounts of FRP5-activated ErbB-2.	bind
15849	1	5535	7	10	NULL	NULL	NULL	MAb FRP5	GP		activates					ErbB-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5042_s_322	9710588	(i) ErbB-2 activated by MAb FRP5 and ErbB-2 activated by NDF displayed similar levels of total phosphotyrosine; however, GST-Grb2 SH2 bound significantly higher amounts of FRP5-activated ErbB-2.	bind
15850	2	5535	7	10	NULL	NULL	NULL	NDF	GP		activates					ErbB-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5042_s_322	9710588	(i) ErbB-2 activated by MAb FRP5 and ErbB-2 activated by NDF displayed similar levels of total phosphotyrosine; however, GST-Grb2 SH2 bound significantly higher amounts of FRP5-activated ErbB-2.	bind
15851	3	5535	7	10	NULL	NULL	NULL	statement 1	Process	levels of total	is similar to			phosphotyrosine		statement 2	Process	levels of total	phosphotyrosine		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5042_s_322	9710588	(i) ErbB-2 activated by MAb FRP5 and ErbB-2 activated by NDF displayed similar levels of total phosphotyrosine; however, GST-Grb2 SH2 bound significantly higher amounts of FRP5-activated ErbB-2.	bind
15852	4	5535	7	10	NULL	NULL	NULL	FRP5	GP		activates					ErbB-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5042_s_322	9710588	(i) ErbB-2 activated by MAb FRP5 and ErbB-2 activated by NDF displayed similar levels of total phosphotyrosine; however, GST-Grb2 SH2 bound significantly higher amounts of FRP5-activated ErbB-2.	bind
15853	5	5535	7	10	NULL	NULL	NULL	GST-Grb2	GP		bind		significantly	SH2		ErbB-2	GP	FRP5-activated 			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5042_s_322	9710588	(i) ErbB-2 activated by MAb FRP5 and ErbB-2 activated by NDF displayed similar levels of total phosphotyrosine; however, GST-Grb2 SH2 bound significantly higher amounts of FRP5-activated ErbB-2.	bind
16749	1	5538	6	10	NULL	NULL	NULL	substrate protein	GP		loaded into					GroEL	GP		heptamer ring		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45737_s_18	15347650	(i) For  cis-ternary complex formation, the binding of ATP to the substrate protein-loaded heptamer ring of GroEL permits the binding of GroES to this ring ( cis-ring) generating an enlarged, closed central cavity ( cis-cavity) in which the substrate protein is discharged ( cis-ATP complex) ( ).	bind
16751	2	5538	6	10	NULL	NULL	NULL	ATP	Chemical		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45737_s_18	15347650	(i) For  cis-ternary complex formation, the binding of ATP to the substrate protein-loaded heptamer ring of GroEL permits the binding of GroES to this ring ( cis-ring) generating an enlarged, closed central cavity ( cis-cavity) in which the substrate protein is discharged ( cis-ATP complex) ( ).	bind
16752	3	5538	6	10	NULL	NULL	NULL	GroES	GP		bind					GroEL	GP		heptamer ring		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45737_s_18	15347650	(i) For  cis-ternary complex formation, the binding of ATP to the substrate protein-loaded heptamer ring of GroEL permits the binding of GroES to this ring ( cis-ring) generating an enlarged, closed central cavity ( cis-cavity) in which the substrate protein is discharged ( cis-ATP complex) ( ).	bind
16754	4	5538	6	10	NULL	NULL	NULL	statement 2	Process		permits					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45737_s_18	15347650	(i) For  cis-ternary complex formation, the binding of ATP to the substrate protein-loaded heptamer ring of GroEL permits the binding of GroES to this ring ( cis-ring) generating an enlarged, closed central cavity ( cis-cavity) in which the substrate protein is discharged ( cis-ATP complex) ( ).	bind
44823	5	5538	6	10	NULL	NULL	NULL	statement 3	Process		generates					cis-cavity					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45737_s_18	15347650	(i) For  cis-ternary complex formation, the binding of ATP to the substrate protein-loaded heptamer ring of GroEL permits the binding of GroES to this ring ( cis-ring) generating an enlarged, closed central cavity ( cis-cavity) in which the substrate protein is discharged ( cis-ATP complex) ( ).	bind
44824	6	5538	6	10	NULL	NULL	NULL	substrate protein	GP		is discharged into					cis-cavity					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45737_s_18	15347650	(i) For  cis-ternary complex formation, the binding of ATP to the substrate protein-loaded heptamer ring of GroEL permits the binding of GroES to this ring ( cis-ring) generating an enlarged, closed central cavity ( cis-cavity) in which the substrate protein is discharged ( cis-ATP complex) ( ).	bind
44825	7	5538	6	10	NULL	0	NULL	cis-cavity	NULL		is an	NULL				closed central cavity	NULL	enlarged			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_44_45737_s_18	15347650	(i) For  cis-ternary complex formation, the binding of ATP to the substrate protein-loaded heptamer ring of GroEL permits the binding of GroES to this ring ( cis-ring) generating an enlarged, closed central cavity ( cis-cavity) in which the substrate protein is discharged ( cis-ATP complex) ( ).	bind
44826	8	5538	6	10	NULL	NULL	NULL	cis-ternary complex	GP	formation of	involves					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45737_s_18	15347650	(i) For  cis-ternary complex formation, the binding of ATP to the substrate protein-loaded heptamer ring of GroEL permits the binding of GroES to this ring ( cis-ring) generating an enlarged, closed central cavity ( cis-cavity) in which the substrate protein is discharged ( cis-ATP complex) ( ).	bind
15886	1	5538	7	10	NULL	NULL	NULL	substrate protein	GP		is loaded with					GroEL	GP		heptamer ring 		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45737_s_18	15347650	(i) For  cis-ternary complex formation, the binding of ATP to the substrate protein-loaded heptamer ring of GroEL permits the binding of GroES to this ring ( cis-ring) generating an enlarged, closed central cavity ( cis-cavity) in which the substrate protein is discharged ( cis-ATP complex) ( ).	bind
15887	2	5538	7	10	NULL	NULL	NULL	ATP	Chemical		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45737_s_18	15347650	(i) For  cis-ternary complex formation, the binding of ATP to the substrate protein-loaded heptamer ring of GroEL permits the binding of GroES to this ring ( cis-ring) generating an enlarged, closed central cavity ( cis-cavity) in which the substrate protein is discharged ( cis-ATP complex) ( ).	bind
15889	3	5538	7	10	NULL	NULL	NULL	GroES	GP		bind					GroEL	GP	 	cis- ring		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45737_s_18	15347650	(i) For  cis-ternary complex formation, the binding of ATP to the substrate protein-loaded heptamer ring of GroEL permits the binding of GroES to this ring ( cis-ring) generating an enlarged, closed central cavity ( cis-cavity) in which the substrate protein is discharged ( cis-ATP complex) ( ).	bind
15893	4	5538	7	10	NULL	NULL	NULL	statement 2	Process		permits					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45737_s_18	15347650	(i) For  cis-ternary complex formation, the binding of ATP to the substrate protein-loaded heptamer ring of GroEL permits the binding of GroES to this ring ( cis-ring) generating an enlarged, closed central cavity ( cis-cavity) in which the substrate protein is discharged ( cis-ATP complex) ( ).	bind
15898	5	5538	7	10	NULL	NULL	NULL	statement 3	Process		generates					cis-cavity					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45737_s_18	15347650	(i) For  cis-ternary complex formation, the binding of ATP to the substrate protein-loaded heptamer ring of GroEL permits the binding of GroES to this ring ( cis-ring) generating an enlarged, closed central cavity ( cis-cavity) in which the substrate protein is discharged ( cis-ATP complex) ( ).	bind
15901	6	5538	7	10	NULL	NULL	NULL	substrate protein	GP		is discharged into					cis-cavity					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45737_s_18	15347650	(i) For  cis-ternary complex formation, the binding of ATP to the substrate protein-loaded heptamer ring of GroEL permits the binding of GroES to this ring ( cis-ring) generating an enlarged, closed central cavity ( cis-cavity) in which the substrate protein is discharged ( cis-ATP complex) ( ).	bind
15904	7	5538	7	NULL	NULL	0	NULL	cis-cavity	NULL		is an	NULL				closed central cavity	NULL	enlarged			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_44_45737_s_18	15347650	(i) For  cis-ternary complex formation, the binding of ATP to the substrate protein-loaded heptamer ring of GroEL permits the binding of GroES to this ring ( cis-ring) generating an enlarged, closed central cavity ( cis-cavity) in which the substrate protein is discharged ( cis-ATP complex) ( ).	bind
15908	8	5538	7	10	NULL	NULL	NULL	cis-ternary complex 	GP	formation of	involves					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45737_s_18	15347650	(i) For  cis-ternary complex formation, the binding of ATP to the substrate protein-loaded heptamer ring of GroEL permits the binding of GroES to this ring ( cis-ring) generating an enlarged, closed central cavity ( cis-cavity) in which the substrate protein is discharged ( cis-ATP complex) ( ).	bind
16571	1	5539	6	10	NULL	NULL	NULL	fVIII	GP		bind					LRP	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_249	10608826	(i) fVIII binds to purified LRP with the affinity similar (within 2-fold) to that determined in our study.	bind
15909	1	5539	7	10	NULL	NULL	NULL	fVIII	GP		bind					LRP	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_249	10608826	(i) fVIII binds to purified LRP with the affinity similar (within 2-fold) to that determined in our study.	bind
16734	1	5540	6	10	NULL	NULL	NULL	Galectin-1	GP		is found in					cytosol	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_18	7890630	(i) Galectin-1 is found  mainly in the cytosol of most cells in which it occurs (Briles  et  al., 1979), (ii) the lectin has free sulfhydryls and is inactive  in the absence of reducing agents (Hirabayashi and Kasai, 1991;  Barondes, 1984), (iii) the lectin lacks an identifiable signal sequence  and does not appear to be secreted through the normal secretory pathway  in differentiated myoblasts (Cooper and Barondes, 1990), (iv) the  lectin binds to beta-galactosyl-containing glycoconjugates on the cell  surface and in the extracellular matrix (Cerra  et al., 1984;  Merkle and Cummings, 1988;	bind
16735	2	5540	6	10	NULL	NULL	NULL	lectin	GP		bind					beta-galactosyl-containing glycoconjugates	Chemical				NULL	cell surface	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_18	7890630	(i) Galectin-1 is found  mainly in the cytosol of most cells in which it occurs (Briles  et  al., 1979), (ii) the lectin has free sulfhydryls and is inactive  in the absence of reducing agents (Hirabayashi and Kasai, 1991;  Barondes, 1984), (iii) the lectin lacks an identifiable signal sequence  and does not appear to be secreted through the normal secretory pathway  in differentiated myoblasts (Cooper and Barondes, 1990), (iv) the  lectin binds to beta-galactosyl-containing glycoconjugates on the cell  surface and in the extracellular matrix (Cerra  et al., 1984;  Merkle and Cummings, 1988;	bind
16736	3	5540	6	10	NULL	NULL	NULL	lectin	GP		bind					beta-galactosyl-containing glycoconjugates	Chemical				NULL	extracellular matrix	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_18	7890630	(i) Galectin-1 is found  mainly in the cytosol of most cells in which it occurs (Briles  et  al., 1979), (ii) the lectin has free sulfhydryls and is inactive  in the absence of reducing agents (Hirabayashi and Kasai, 1991;  Barondes, 1984), (iii) the lectin lacks an identifiable signal sequence  and does not appear to be secreted through the normal secretory pathway  in differentiated myoblasts (Cooper and Barondes, 1990), (iv) the  lectin binds to beta-galactosyl-containing glycoconjugates on the cell  surface and in the extracellular matrix (Cerra  et al., 1984;  Merkle and Cummings, 1988;	bind
16738	4	5540	6	10	NULL	NULL	NULL	lectin	GP		is inactive					reducing agents	Chemical	in absence of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_18	7890630	(i) Galectin-1 is found  mainly in the cytosol of most cells in which it occurs (Briles  et  al., 1979), (ii) the lectin has free sulfhydryls and is inactive  in the absence of reducing agents (Hirabayashi and Kasai, 1991;  Barondes, 1984), (iii) the lectin lacks an identifiable signal sequence  and does not appear to be secreted through the normal secretory pathway  in differentiated myoblasts (Cooper and Barondes, 1990), (iv) the  lectin binds to beta-galactosyl-containing glycoconjugates on the cell  surface and in the extracellular matrix (Cerra  et al., 1984;  Merkle and Cummings, 1988;	bind
16739	5	5540	6	10	NULL	NULL	NULL	lectin	GP		is not secreted through					secretory pathway	Process	normal			NULL	differentiated myoblasts	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_18	7890630	(i) Galectin-1 is found  mainly in the cytosol of most cells in which it occurs (Briles  et  al., 1979), (ii) the lectin has free sulfhydryls and is inactive  in the absence of reducing agents (Hirabayashi and Kasai, 1991;  Barondes, 1984), (iii) the lectin lacks an identifiable signal sequence  and does not appear to be secreted through the normal secretory pathway  in differentiated myoblasts (Cooper and Barondes, 1990), (iv) the  lectin binds to beta-galactosyl-containing glycoconjugates on the cell  surface and in the extracellular matrix (Cerra  et al., 1984;  Merkle and Cummings, 1988;	bind
16743	6	5540	6	10	NULL	NULL	NULL	lectin	GP		lacks an							identifiable		signal sequence	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_18	7890630	(i) Galectin-1 is found  mainly in the cytosol of most cells in which it occurs (Briles  et  al., 1979), (ii) the lectin has free sulfhydryls and is inactive  in the absence of reducing agents (Hirabayashi and Kasai, 1991;  Barondes, 1984), (iii) the lectin lacks an identifiable signal sequence  and does not appear to be secreted through the normal secretory pathway  in differentiated myoblasts (Cooper and Barondes, 1990), (iv) the  lectin binds to beta-galactosyl-containing glycoconjugates on the cell  surface and in the extracellular matrix (Cerra  et al., 1984;  Merkle and Cummings, 1988;	bind
15924	1	5540	7	10	NULL	NULL	NULL	Galectin-1	GP		is found in					cytosol	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_18	7890630	(i) Galectin-1 is found  mainly in the cytosol of most cells in which it occurs (Briles  et  al., 1979), (ii) the lectin has free sulfhydryls and is inactive  in the absence of reducing agents (Hirabayashi and Kasai, 1991;  Barondes, 1984), (iii) the lectin lacks an identifiable signal sequence  and does not appear to be secreted through the normal secretory pathway  in differentiated myoblasts (Cooper and Barondes, 1990), (iv) the  lectin binds to beta-galactosyl-containing glycoconjugates on the cell  surface and in the extracellular matrix (Cerra  et al., 1984;  Merkle and Cummings, 1988;	bind
15930	2	5540	7	10	NULL	NULL	NULL	Lectin	GP		contains					sulfhydryls	Chemical	free			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_18	7890630	(i) Galectin-1 is found  mainly in the cytosol of most cells in which it occurs (Briles  et  al., 1979), (ii) the lectin has free sulfhydryls and is inactive  in the absence of reducing agents (Hirabayashi and Kasai, 1991;  Barondes, 1984), (iii) the lectin lacks an identifiable signal sequence  and does not appear to be secreted through the normal secretory pathway  in differentiated myoblasts (Cooper and Barondes, 1990), (iv) the  lectin binds to beta-galactosyl-containing glycoconjugates on the cell  surface and in the extracellular matrix (Cerra  et al., 1984;  Merkle and Cummings, 1988;	bind
15931	3	5540	7	10	NULL	NULL	NULL	statement 2	Process		is inactive					reducing agents	Chemical	in the absence of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_18	7890630	(i) Galectin-1 is found  mainly in the cytosol of most cells in which it occurs (Briles  et  al., 1979), (ii) the lectin has free sulfhydryls and is inactive  in the absence of reducing agents (Hirabayashi and Kasai, 1991;  Barondes, 1984), (iii) the lectin lacks an identifiable signal sequence  and does not appear to be secreted through the normal secretory pathway  in differentiated myoblasts (Cooper and Barondes, 1990), (iv) the  lectin binds to beta-galactosyl-containing glycoconjugates on the cell  surface and in the extracellular matrix (Cerra  et al., 1984;  Merkle and Cummings, 1988;	bind
15933	4	5540	7	10	NULL	NULL	NULL	Lectin	GP		lacks					Signal sequence	GP	 an identifiable			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_18	7890630	(i) Galectin-1 is found  mainly in the cytosol of most cells in which it occurs (Briles  et  al., 1979), (ii) the lectin has free sulfhydryls and is inactive  in the absence of reducing agents (Hirabayashi and Kasai, 1991;  Barondes, 1984), (iii) the lectin lacks an identifiable signal sequence  and does not appear to be secreted through the normal secretory pathway  in differentiated myoblasts (Cooper and Barondes, 1990), (iv) the  lectin binds to beta-galactosyl-containing glycoconjugates on the cell  surface and in the extracellular matrix (Cerra  et al., 1984;  Merkle and Cummings, 1988;	bind
15934	5	5540	7	10	NULL	NULL	NULL	Lectin	GP		is not secreted through					secretory pathway	Process	normal 			NULL	differentiated myoblasts 	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_18	7890630	(i) Galectin-1 is found  mainly in the cytosol of most cells in which it occurs (Briles  et  al., 1979), (ii) the lectin has free sulfhydryls and is inactive  in the absence of reducing agents (Hirabayashi and Kasai, 1991;  Barondes, 1984), (iii) the lectin lacks an identifiable signal sequence  and does not appear to be secreted through the normal secretory pathway  in differentiated myoblasts (Cooper and Barondes, 1990), (iv) the  lectin binds to beta-galactosyl-containing glycoconjugates on the cell  surface and in the extracellular matrix (Cerra  et al., 1984;  Merkle and Cummings, 1988;	bind
15936	7	5540	7	10	NULL	NULL	NULL	beta-galactosyl-containing glycoconjugates	Chemical		bind					lectin	GP				NULL	 cell surface	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_18	7890630	(i) Galectin-1 is found  mainly in the cytosol of most cells in which it occurs (Briles  et  al., 1979), (ii) the lectin has free sulfhydryls and is inactive  in the absence of reducing agents (Hirabayashi and Kasai, 1991;  Barondes, 1984), (iii) the lectin lacks an identifiable signal sequence  and does not appear to be secreted through the normal secretory pathway  in differentiated myoblasts (Cooper and Barondes, 1990), (iv) the  lectin binds to beta-galactosyl-containing glycoconjugates on the cell  surface and in the extracellular matrix (Cerra  et al., 1984;  Merkle and Cummings, 1988;	bind
15937	8	5540	7	10	NULL	NULL	NULL	beta-galactosyl-containing glycoconjugates	Chemical		binds					lectin	GP				NULL	extracellular matrix 	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_18	7890630	(i) Galectin-1 is found  mainly in the cytosol of most cells in which it occurs (Briles  et  al., 1979), (ii) the lectin has free sulfhydryls and is inactive  in the absence of reducing agents (Hirabayashi and Kasai, 1991;  Barondes, 1984), (iii) the lectin lacks an identifiable signal sequence  and does not appear to be secreted through the normal secretory pathway  in differentiated myoblasts (Cooper and Barondes, 1990), (iv) the  lectin binds to beta-galactosyl-containing glycoconjugates on the cell  surface and in the extracellular matrix (Cerra  et al., 1984;  Merkle and Cummings, 1988;	bind
16572	1	5541	6	10	NULL	NULL	NULL	GDP	Chemical		bind					Arf-1	GP	membrane attached			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_7_1199_s_239	11748249	(I) GDP bound to Arf-1 attached to the membrane is replaced with GTP by Arf-1 guanine exchange factor.	bind
16573	2	5541	6	10	NULL	NULL	NULL	GTP	Chemical		bind					Arf-1	GP	membrane attached			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_7_1199_s_239	11748249	(I) GDP bound to Arf-1 attached to the membrane is replaced with GTP by Arf-1 guanine exchange factor.	bind
16574	3	5541	6	10	NULL	NULL	NULL	statement 1	Process		is replaced by					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_7_1199_s_239	11748249	(I) GDP bound to Arf-1 attached to the membrane is replaced with GTP by Arf-1 guanine exchange factor.	bind
44827	4	5541	6	10	NULL	NULL	NULL	statement 2	Process		occurs through					Arf-1 guanine exchange factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_7_1199_s_239	11748249	(I) GDP bound to Arf-1 attached to the membrane is replaced with GTP by Arf-1 guanine exchange factor.	bind
15940	1	5541	7	10	NULL	NULL	NULL	GDP	Chemical		bind					Arf-1	GP	membrane attached			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_7_1199_s_239	11748249	(I) GDP bound to Arf-1 attached to the membrane is replaced with GTP by Arf-1 guanine exchange factor.	bind
15941	2	5541	7	NULL	NULL	0	NULL	GTP	NULL		binds	NULL				 Arf-1	NULL	membrane attached			NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_7_1199_s_239	11748249	(I) GDP bound to Arf-1 attached to the membrane is replaced with GTP by Arf-1 guanine exchange factor.	bind
15942	3	5541	7	10	NULL	NULL	NULL	statement 1	Process		is replaced by					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_7_1199_s_239	11748249	(I) GDP bound to Arf-1 attached to the membrane is replaced with GTP by Arf-1 guanine exchange factor.	bind
15943	4	5541	7	10	NULL	NULL	NULL	statement 2	Process		occurs through					Arf-1 guanine exchange factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_7_1199_s_239	11748249	(I) GDP bound to Arf-1 attached to the membrane is replaced with GTP by Arf-1 guanine exchange factor.	bind
16722	1	5542	6	10	NULL	NULL	NULL	GTP	Chemical		bind					eRF3	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
16723	2	5542	6	10	NULL	NULL	NULL	statement 1	Process		associates with					eRF1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
16724	3	5542	6	10	NULL	NULL	NULL	eRF1	GP		enters to					ribosome	CellComponent		 A site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
16725	4	5542	6	10	NULL	NULL	NULL	statement 2	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
16727	5	5542	6	10	NULL	NULL	NULL	GTPase-activating proteins	GP		consists of					ribosome	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
16728	6	5542	6	10	NULL	NULL	NULL	eRF3	GP		associates with					statement 11	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
16731	7	5542	6	10	NULL	NULL	NULL	statement 6	Process		activates					GTP	Chemical	hydrolysis of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
16732	8	5542	6	10	NULL	NULL	NULL	GDP	Chemical		bind					eRF3	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
16733	9	5542	6	10	NULL	NULL	NULL	statement 8	Process		dissociates from					eRF1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
53107	10	5542	6	10	NULL	NULL	NULL	GTPase-activating proteins	GP		consists of					eRF1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
53108	11	5542	6	10	NULL	NULL	NULL	statement 5	Process		occurs along with					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
15944	1	5542	7	10	NULL	NULL	NULL	GTP	Chemical		bind					 eRF3	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
15945	3	5542	7	10	NULL	NULL	NULL	eRF1	GP		enters					ribosome	CellComponent		A site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
15946	4	5542	7	10	NULL	NULL	NULL	GTPase-activating protein	GP		consist of					ribosome	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
15947	5	5542	7	10	NULL	NULL	NULL	GTPase-activating protein	GP		consist of					eRF1 	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
15948	6	5542	7	10	NULL	NULL	NULL	statement 3	Process		occurs along with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
15949	7	5542	7	10	NULL	NULL	NULL	eRF3	GP		associate with					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
15950	8	5542	7	10	NULL	NULL	NULL	statement 7	Process		activates					GTP	Chemical	hydrolysis of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
15951	10	5542	7	10	NULL	NULL	NULL	statement 9	Process		dissociates from					eRF1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
44848	2	5542	7	10	NULL	NULL	NULL	statement 1	Process		associate with					eRF1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
44849	9	5542	7	10	NULL	NULL	NULL	GDP	Chemical		bind					eRF3	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
53106	11	5542	7	10	NULL	NULL	NULL	statement 2			leads to					statement 3					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_269	15337765	(i) GTP-bound eRF3 associates with eRF1 and brings it to the ribosomal A site, (ii) the association of eRF3 with the GTPase-activating proteins consisting of ribosome and eRF1 leads to the activation of GTP hydrolysis, and (iii) the resulting GDP-bound form of eRF3 dissociates from eRF1, although its lifetime may be quite short in the presence of Mg2+.	bind
16718	1	5543	6	10	NULL	NULL	NULL	t-RNA	NucleicAcid		bind					A-site	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_19_5241_s_227	11013226	(i) His229 might be involved in the binding of adenosine 76 of the A-site-bound tRNA.	bind
16719	2	5543	6	10	NULL	NULL	NULL				be involved in		might	His229		statement 1	Process	binding of	adenosine 76		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_19_5241_s_227	11013226	(i) His229 might be involved in the binding of adenosine 76 of the A-site-bound tRNA.	bind
15953	2	5543	7	10	NULL	NULL	NULL				be involved in		might	His229		statement 1	Process		adenosine 76 		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_19_5241_s_227	11013226	(i) His229 might be involved in the binding of adenosine 76 of the A-site-bound tRNA.	bind
19758	1	5543	7	10	NULL	NULL	NULL	tRNA	NucleicAcid		bind					A site	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_19_5241_s_227	11013226	(i) His229 might be involved in the binding of adenosine 76 of the A-site-bound tRNA.	bind
16598	1	5544	6	10	NULL	NULL	NULL	HSP-CBF	GP		bind					NF-Y	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_28_26332_s_237	11306579	(i) HSP-CBF might intervene early during the establishment of an open chromatin configuration within the heat shock regulatory regions following NF-Y binding (Fig.  7 A).	bind
16599	2	5544	6	10	NULL	NULL	NULL	statement 1	Process		intervene during		might			open chromatin configuration	Process	establishement of		heat shock regulatory region	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_28_26332_s_237	11306579	(i) HSP-CBF might intervene early during the establishment of an open chromatin configuration within the heat shock regulatory regions following NF-Y binding (Fig.  7 A).	bind
44810	3	5544	6	10	NULL	NULL	NULL	statement 2	Process		occurs following					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_28_26332_s_237	11306579	(i) HSP-CBF might intervene early during the establishment of an open chromatin configuration within the heat shock regulatory regions following NF-Y binding (Fig.  7 A).	bind
15954	1	5544	7	10	NULL	NULL	NULL	HSP-CBF	GP		intervene during		might;;early			open chromatin configuration	Process	establishment of		heat shock regulatory regions	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_28_26332_s_237	11306579	(i) HSP-CBF might intervene early during the establishment of an open chromatin configuration within the heat shock regulatory regions following NF-Y binding (Fig.  7 A).	bind
15956	2	5544	7	10	NULL	NULL	NULL	statement 1	Process		occurs upon					NF-Y	GP	binding of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_28_26332_s_237	11306579	(i) HSP-CBF might intervene early during the establishment of an open chromatin configuration within the heat shock regulatory regions following NF-Y binding (Fig.  7 A).	bind
16601	1	5545	6	10	NULL	NULL	NULL	bd receptor	GP		is a type of					K88 adhesin receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_165_s_283	9864211	(i) In addition to being found in phenotype D animals, receptor  d (IGLad) is also found in phenotype A animals, and (ii) receptor  d is not present in phenotype C animals, indicating that there may be a fourth K88 adhesin receptor, possibly a  bd receptor that binds both K88ab and K88ad adhesin and is found exclusively in phenotype C animals.	bind
16602	2	5545	6	10	NULL	NULL	NULL	bd receptor	GP		bind					adhesin	GP		K88ab		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_165_s_283	9864211	(i) In addition to being found in phenotype D animals, receptor  d (IGLad) is also found in phenotype A animals, and (ii) receptor  d is not present in phenotype C animals, indicating that there may be a fourth K88 adhesin receptor, possibly a  bd receptor that binds both K88ab and K88ad adhesin and is found exclusively in phenotype C animals.	bind
16603	3	5545	6	10	NULL	NULL	NULL	bd receptor	GP		bind					adhesin	GP		K88ad		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_165_s_283	9864211	(i) In addition to being found in phenotype D animals, receptor  d (IGLad) is also found in phenotype A animals, and (ii) receptor  d is not present in phenotype C animals, indicating that there may be a fourth K88 adhesin receptor, possibly a  bd receptor that binds both K88ab and K88ad adhesin and is found exclusively in phenotype C animals.	bind
16606	4	5545	6	10	NULL	NULL	NULL	bd receptor	GP		is found		exclusively			phenotype C animals	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_165_s_283	9864211	(i) In addition to being found in phenotype D animals, receptor  d (IGLad) is also found in phenotype A animals, and (ii) receptor  d is not present in phenotype C animals, indicating that there may be a fourth K88 adhesin receptor, possibly a  bd receptor that binds both K88ab and K88ad adhesin and is found exclusively in phenotype C animals.	bind
16607	5	5545	6	10	NULL	NULL	NULL	receptor d	GP		is					IGLad	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_165_s_283	9864211	(i) In addition to being found in phenotype D animals, receptor  d (IGLad) is also found in phenotype A animals, and (ii) receptor  d is not present in phenotype C animals, indicating that there may be a fourth K88 adhesin receptor, possibly a  bd receptor that binds both K88ab and K88ad adhesin and is found exclusively in phenotype C animals.	bind
16608	6	5545	6	10	NULL	NULL	NULL	receptor d	GP		is found in					phenotype A animals	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_165_s_283	9864211	(i) In addition to being found in phenotype D animals, receptor  d (IGLad) is also found in phenotype A animals, and (ii) receptor  d is not present in phenotype C animals, indicating that there may be a fourth K88 adhesin receptor, possibly a  bd receptor that binds both K88ab and K88ad adhesin and is found exclusively in phenotype C animals.	bind
16609	7	5545	6	10	NULL	NULL	NULL	receptor d	GP		is not present in					phenotype C animals	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_165_s_283	9864211	(i) In addition to being found in phenotype D animals, receptor  d (IGLad) is also found in phenotype A animals, and (ii) receptor  d is not present in phenotype C animals, indicating that there may be a fourth K88 adhesin receptor, possibly a  bd receptor that binds both K88ab and K88ad adhesin and is found exclusively in phenotype C animals.	bind
15957	2	5545	7	10	NULL	NULL	NULL	bd receptor	GP		bind					adhesin 	GP		K88ab		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_165_s_283	9864211	(i) In addition to being found in phenotype D animals, receptor  d (IGLad) is also found in phenotype A animals, and (ii) receptor  d is not present in phenotype C animals, indicating that there may be a fourth K88 adhesin receptor, possibly a  bd receptor that binds both K88ab and K88ad adhesin and is found exclusively in phenotype C animals.	bind
15958	3	5545	7	10	NULL	NULL	NULL	bd receptor	GP		bind					adhesin	GP		K88ad		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_165_s_283	9864211	(i) In addition to being found in phenotype D animals, receptor  d (IGLad) is also found in phenotype A animals, and (ii) receptor  d is not present in phenotype C animals, indicating that there may be a fourth K88 adhesin receptor, possibly a  bd receptor that binds both K88ab and K88ad adhesin and is found exclusively in phenotype C animals.	bind
44926	1	5545	7	10	NULL	NULL	NULL	bd receptor	GP		is a type of					K88 adhesin receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_165_s_283	9864211	(i) In addition to being found in phenotype D animals, receptor  d (IGLad) is also found in phenotype A animals, and (ii) receptor  d is not present in phenotype C animals, indicating that there may be a fourth K88 adhesin receptor, possibly a  bd receptor that binds both K88ab and K88ad adhesin and is found exclusively in phenotype C animals.	bind
44927	5	5545	7	10	NULL	NULL	NULL	receptor d	GP		is 					IGLad	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_165_s_283	9864211	(i) In addition to being found in phenotype D animals, receptor  d (IGLad) is also found in phenotype A animals, and (ii) receptor  d is not present in phenotype C animals, indicating that there may be a fourth K88 adhesin receptor, possibly a  bd receptor that binds both K88ab and K88ad adhesin and is found exclusively in phenotype C animals.	bind
44928	4	5545	7	10	NULL	NULL	NULL	bd receptor	GP		found in		exclusively			phenotype C animals	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_165_s_283	9864211	(i) In addition to being found in phenotype D animals, receptor  d (IGLad) is also found in phenotype A animals, and (ii) receptor  d is not present in phenotype C animals, indicating that there may be a fourth K88 adhesin receptor, possibly a  bd receptor that binds both K88ab and K88ad adhesin and is found exclusively in phenotype C animals.	bind
44929	6	5545	7	10	NULL	NULL	NULL	receptor d	GP		is found in					phenotype D animals	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_165_s_283	9864211	(i) In addition to being found in phenotype D animals, receptor  d (IGLad) is also found in phenotype A animals, and (ii) receptor  d is not present in phenotype C animals, indicating that there may be a fourth K88 adhesin receptor, possibly a  bd receptor that binds both K88ab and K88ad adhesin and is found exclusively in phenotype C animals.	bind
44930	7	5545	7	10	NULL	NULL	NULL	receptor d	GP		is found in					phenotype A animals	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_165_s_283	9864211	(i) In addition to being found in phenotype D animals, receptor  d (IGLad) is also found in phenotype A animals, and (ii) receptor  d is not present in phenotype C animals, indicating that there may be a fourth K88 adhesin receptor, possibly a  bd receptor that binds both K88ab and K88ad adhesin and is found exclusively in phenotype C animals.	bind
44931	8	5545	7	10	NULL	NULL	NULL	receptor d	GP		is not found in					phenotype C animals	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_1_165_s_283	9864211	(i) In addition to being found in phenotype D animals, receptor  d (IGLad) is also found in phenotype A animals, and (ii) receptor  d is not present in phenotype C animals, indicating that there may be a fourth K88 adhesin receptor, possibly a  bd receptor that binds both K88ab and K88ad adhesin and is found exclusively in phenotype C animals.	bind
16708	1	5546	6	10	NULL	NULL	NULL	A. naeslundii genospecies 2	Organism	human	bind		avidly			PRPs	GP	acidic			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
16709	2	5546	6	10	NULL	NULL	NULL	A. naeslundii genospecies 2	Organism	monkey	bind		avidly			PRPs	GP	acidic			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
16710	3	5546	6	10	NULL	NULL	NULL	A. naeslundii genospecies 2	Organism	human	bind		weakly			statherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
16711	4	5546	6	10	NULL	NULL	NULL	A. naeslundii genospecies 2	Organism	monkey	bind		weakly			statherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
16712	5	5546	6	10	NULL	NULL	NULL	A. naeslundii genospecies 1	Organism		bind		avidly			PRPs	GP	acidic			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
16713	6	5546	6	10	NULL	NULL	NULL	A. naeslundii genospecies 1	Organism		bind		weakly			PRP	GP	acidic			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
16714	7	5546	6	10	NULL	NULL	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
16715	8	5546	6	10	NULL	NULL	NULL	A. viscosus strains	Organism	rat	bind		avidly;;preferentially			statherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
16716	9	5546	6	10	NULL	NULL	NULL	A. viscosus strains	Organism	hamster	bind		avidly;;preferentially			statherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
16717	10	5546	6	10	NULL	NULL	NULL	actinomycosis	Organism	human	bind		avidly;;preferentially			statherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
15959	1	5546	7	10	NULL	NULL	NULL	 A. naeslundii	Organism	genospecies 2 of human origin	bind		avidly			PRPs	GP	acidic			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
15960	2	5546	7	10	NULL	NULL	NULL	A. naeslundii	Organism	genospecies 2 of monkey origin	bind		avidly			PRPs	GP	acidic			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
15961	3	5546	7	10	NULL	NULL	NULL	A. naeslundii 	Organism	genospecies 2 of human origin	bind		weakly			statherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
15962	4	5546	7	10	NULL	NULL	NULL	A. naeslundii	Organism	genospecies 2 of monkey origin	bind		weakly			statherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
15963	5	5546	7	10	NULL	NULL	NULL	A. naeslundii	Organism	genospecies 1	bind		avidly			PRPs	GP	acidic			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
15964	6	5546	7	10	NULL	NULL	NULL	A. naeslundii	Organism	genospecies 1	bind		weakly			PRPs	GP	acidic			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
15965	7	5546	7	10	NULL	NULL	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
15966	8	5546	7	10	NULL	NULL	NULL	A. viscosus	Organism	rat	bind		avidly;;preferentially			statherin 	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
15967	9	5546	7	10	NULL	NULL	NULL	A. viscosus	Organism	hamster plaque	bind		avidly;;preferentially			statherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
15968	10	5546	7	10	NULL	NULL	NULL	actinomycosis 	Organism	human	bind		avidly;;preferentially			statherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_108	11705891	(i) In preferential acidic-PRP binding, oral strains of  A. naeslundii genospecies 2 of human ( n = 11) and monkey ( n = 2) origin bound avidly to acidic PRPs but deviated in their relative, although weak, capacities for binding to statherin and oral strains of  A. naeslundii genospecies 1 bound either avidly ( n = 2) or weakly ( n = 4) to acidic PRPs. (ii) In preferential statherin binding,  A. viscosus strains from rat or hamster plaque ( n = 6) and a case of human actinomycosis bound statherin avidly and preferentially.	bind
16611	1	5547	6	10	NULL	NULL	NULL	ArgR1	GP		bind					target DNA sequence	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_18_6059_s_261	15342575	(i) Integrity of the DBDs of both ArgR1 and ArgR2 was necessary for arginine repression, so we conclude that both ArgR proteins bind to target DNA sequences.	bind
16614	2	5547	6	10	NULL	NULL	NULL	ArgR2	GP		bind					target DNA sequence	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_18_6059_s_261	15342575	(i) Integrity of the DBDs of both ArgR1 and ArgR2 was necessary for arginine repression, so we conclude that both ArgR proteins bind to target DNA sequences.	bind
16617	3	5547	6	10	NULL	NULL	NULL	ArgR1	GP	integrity of	is necessary for			DBD		arginine	AminoAcid	repression of 			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_18_6059_s_261	15342575	(i) Integrity of the DBDs of both ArgR1 and ArgR2 was necessary for arginine repression, so we conclude that both ArgR proteins bind to target DNA sequences.	bind
19667	4	5547	6	10	NULL	NULL	NULL	ArgR2	GP	integrity of	is necessary for			DBD		arginine	AminoAcid	repression of			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_18_6059_s_261	15342575	(i) Integrity of the DBDs of both ArgR1 and ArgR2 was necessary for arginine repression, so we conclude that both ArgR proteins bind to target DNA sequences.	bind
19668	5	5547	6	10	NULL	NULL	NULL	statement 3	Process		is simultaneous with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_18_6059_s_261	15342575	(i) Integrity of the DBDs of both ArgR1 and ArgR2 was necessary for arginine repression, so we conclude that both ArgR proteins bind to target DNA sequences.	bind
15970	1	5547	7	10	NULL	NULL	NULL	ArgR1	GP		bind					target DNA sequence	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_18_6059_s_261	15342575	(i) Integrity of the DBDs of both ArgR1 and ArgR2 was necessary for arginine repression, so we conclude that both ArgR proteins bind to target DNA sequences.	bind
15971	2	5547	7	10	NULL	NULL	NULL	ArgR1	GP	Integrity of	is necessary for			DBD		arginine	AminoAcid	repression of			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_18_6059_s_261	15342575	(i) Integrity of the DBDs of both ArgR1 and ArgR2 was necessary for arginine repression, so we conclude that both ArgR proteins bind to target DNA sequences.	bind
15972	3	5547	7	10	NULL	NULL	NULL	ArgR2	GP	Integrity of	is necessary for			DBD		arginine	AminoAcid	repression of			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_18_6059_s_261	15342575	(i) Integrity of the DBDs of both ArgR1 and ArgR2 was necessary for arginine repression, so we conclude that both ArgR proteins bind to target DNA sequences.	bind
19759	4	5547	7	10	NULL	NULL	NULL	statement 2	Process		occurs simultaneous with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_18_6059_s_261	15342575	(i) Integrity of the DBDs of both ArgR1 and ArgR2 was necessary for arginine repression, so we conclude that both ArgR proteins bind to target DNA sequences.	bind
53109	5	5547	7	10	NULL	NULL	NULL	ArgR2	GP		bind					target DNA sequence	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_18_6059_s_261	15342575	(i) Integrity of the DBDs of both ArgR1 and ArgR2 was necessary for arginine repression, so we conclude that both ArgR proteins bind to target DNA sequences.	bind
16619	1	5548	6	10	NULL	NULL	NULL	KIF13A	GP		bind					beta1-adaptin	GP		ear domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_103_4_569_s_161	11106728	(I) KIF13A binds to the ear domain of beta1-adaptin.	bind
15973	1	5548	7	10	NULL	NULL	NULL	KIF13A	GP		binds to					beta1-adaptin	GP		ear domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_103_4_569_s_161	11106728	(I) KIF13A binds to the ear domain of beta1-adaptin.	bind
16620	1	5549	6	10	NULL	NULL	NULL	SSBs	NucleicAcid		activate					PARP-1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_53_55117_s_31	15498778	(i) Ku heterodimer does not represent the sole DSBs recognition complex in cell extracts because it was originally pointed out that PARP-1 is activated  in vitro not only by SSBs but also by DSBs ( ) and that purified PARP-1 binds to DSBs with an efficacy higherR than to SSBs ( ,  ) and with an affinity even greater than that of DNA-PK ( ).	bind
16621	2	5549	6	10	NULL	NULL	NULL	DSBs	NucleicAcid		activate					PARP-1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_53_55117_s_31	15498778	(i) Ku heterodimer does not represent the sole DSBs recognition complex in cell extracts because it was originally pointed out that PARP-1 is activated  in vitro not only by SSBs but also by DSBs ( ) and that purified PARP-1 binds to DSBs with an efficacy higherR than to SSBs ( ,  ) and with an affinity even greater than that of DNA-PK ( ).	bind
16623	3	5549	6	10	NULL	NULL	NULL	PARP-1	GP	purified	bind					DSBs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_53_55117_s_31	15498778	(i) Ku heterodimer does not represent the sole DSBs recognition complex in cell extracts because it was originally pointed out that PARP-1 is activated  in vitro not only by SSBs but also by DSBs ( ) and that purified PARP-1 binds to DSBs with an efficacy higherR than to SSBs ( ,  ) and with an affinity even greater than that of DNA-PK ( ).	bind
16624	4	5549	6	10	NULL	NULL	NULL	PARP-1	GP	purified	bind					SSBs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_53_55117_s_31	15498778	(i) Ku heterodimer does not represent the sole DSBs recognition complex in cell extracts because it was originally pointed out that PARP-1 is activated  in vitro not only by SSBs but also by DSBs ( ) and that purified PARP-1 binds to DSBs with an efficacy higherR than to SSBs ( ,  ) and with an affinity even greater than that of DNA-PK ( ).	bind
16626	5	5549	6	10	NULL	NULL	NULL	statement 3	Process		is higher than					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_53_55117_s_31	15498778	(i) Ku heterodimer does not represent the sole DSBs recognition complex in cell extracts because it was originally pointed out that PARP-1 is activated  in vitro not only by SSBs but also by DSBs ( ) and that purified PARP-1 binds to DSBs with an efficacy higherR than to SSBs ( ,  ) and with an affinity even greater than that of DNA-PK ( ).	bind
17048	6	5549	6	10	NULL	NULL	NULL	PARP-1	GP	purified	bind					DNA-PK	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_53_55117_s_31	15498778	(i) Ku heterodimer does not represent the sole DSBs recognition complex in cell extracts because it was originally pointed out that PARP-1 is activated  in vitro not only by SSBs but also by DSBs ( ) and that purified PARP-1 binds to DSBs with an efficacy higherR than to SSBs ( ,  ) and with an affinity even greater than that of DNA-PK ( ).	bind
17049	7	5549	6	10	NULL	NULL	NULL	statement 6	Process		has great efficacy than					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_53_55117_s_31	15498778	(i) Ku heterodimer does not represent the sole DSBs recognition complex in cell extracts because it was originally pointed out that PARP-1 is activated  in vitro not only by SSBs but also by DSBs ( ) and that purified PARP-1 binds to DSBs with an efficacy higherR than to SSBs ( ,  ) and with an affinity even greater than that of DNA-PK ( ).	bind
15974	1	5549	7	10	NULL	NULL	NULL	PARP-1	GP		is activated by					SSBs	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_53_55117_s_31	15498778	(i) Ku heterodimer does not represent the sole DSBs recognition complex in cell extracts because it was originally pointed out that PARP-1 is activated  in vitro not only by SSBs but also by DSBs ( ) and that purified PARP-1 binds to DSBs with an efficacy higherR than to SSBs ( ,  ) and with an affinity even greater than that of DNA-PK ( ).	bind
15975	2	5549	7	10	NULL	NULL	NULL	PARP-1	GP		is activated by					DSBs	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_53_55117_s_31	15498778	(i) Ku heterodimer does not represent the sole DSBs recognition complex in cell extracts because it was originally pointed out that PARP-1 is activated  in vitro not only by SSBs but also by DSBs ( ) and that purified PARP-1 binds to DSBs with an efficacy higherR than to SSBs ( ,  ) and with an affinity even greater than that of DNA-PK ( ).	bind
15976	3	5549	7	10	NULL	NULL	NULL	PARP-1	GP	purified	bind					DSBs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_53_55117_s_31	15498778	(i) Ku heterodimer does not represent the sole DSBs recognition complex in cell extracts because it was originally pointed out that PARP-1 is activated  in vitro not only by SSBs but also by DSBs ( ) and that purified PARP-1 binds to DSBs with an efficacy higherR than to SSBs ( ,  ) and with an affinity even greater than that of DNA-PK ( ).	bind
15977	4	5549	7	10	NULL	NULL	NULL	PARP-1	GP	purified	bind					SSBs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_53_55117_s_31	15498778	(i) Ku heterodimer does not represent the sole DSBs recognition complex in cell extracts because it was originally pointed out that PARP-1 is activated  in vitro not only by SSBs but also by DSBs ( ) and that purified PARP-1 binds to DSBs with an efficacy higherR than to SSBs ( ,  ) and with an affinity even greater than that of DNA-PK ( ).	bind
15978	5	5549	7	10	NULL	NULL	NULL	PARP-1	GP	purified	bind					DNA-PK	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_53_55117_s_31	15498778	(i) Ku heterodimer does not represent the sole DSBs recognition complex in cell extracts because it was originally pointed out that PARP-1 is activated  in vitro not only by SSBs but also by DSBs ( ) and that purified PARP-1 binds to DSBs with an efficacy higherR than to SSBs ( ,  ) and with an affinity even greater than that of DNA-PK ( ).	bind
15979	6	5549	7	10	NULL	NULL	NULL	statement 3	Process		has  greater efficacy than					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_53_55117_s_31	15498778	(i) Ku heterodimer does not represent the sole DSBs recognition complex in cell extracts because it was originally pointed out that PARP-1 is activated  in vitro not only by SSBs but also by DSBs ( ) and that purified PARP-1 binds to DSBs with an efficacy higherR than to SSBs ( ,  ) and with an affinity even greater than that of DNA-PK ( ).	bind
15980	7	5549	7	10	NULL	NULL	NULL	statement 3	Process		greater affinity than					statement 5	Process	 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_53_55117_s_31	15498778	(i) Ku heterodimer does not represent the sole DSBs recognition complex in cell extracts because it was originally pointed out that PARP-1 is activated  in vitro not only by SSBs but also by DSBs ( ) and that purified PARP-1 binds to DSBs with an efficacy higherR than to SSBs ( ,  ) and with an affinity even greater than that of DNA-PK ( ).	bind
16628	1	5550	6	10	NULL	NULL	NULL	LPS	Chemical		induces					c-Rel	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5523_s_228	9710636	(i) LPS induces more c-Rel, and in 1B4.	bind
15982	1	5550	7	10	NULL	NULL	NULL	 LPS	Chemical		induce					c-Rel	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5523_s_228	9710636	(i) LPS induces more c-Rel, and in 1B4.	bind
16631	1	5551	6	10	NULL	NULL	NULL	m-UBR1	GP		bind					Arg	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8255_s_38	14585983	(I) m-UBR1 and m-UBR2 bind to Arg (type 1) and Phe (type  2) destabilizing N-terminal residues but not to the other tested N-terminal residues.	bind
16633	2	5551	6	10	NULL	NULL	NULL	m-UBR1	GP		bind					Phe	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8255_s_38	14585983	(I) m-UBR1 and m-UBR2 bind to Arg (type 1) and Phe (type  2) destabilizing N-terminal residues but not to the other tested N-terminal residues.	bind
16635	3	5551	6	10	NULL	NULL	NULL	m-UBR2	GP		bind					Arg	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8255_s_38	14585983	(I) m-UBR1 and m-UBR2 bind to Arg (type 1) and Phe (type  2) destabilizing N-terminal residues but not to the other tested N-terminal residues.	bind
16637	4	5551	6	10	NULL	NULL	NULL	m-UBR2	GP		bind					Phe	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8255_s_38	14585983	(I) m-UBR1 and m-UBR2 bind to Arg (type 1) and Phe (type  2) destabilizing N-terminal residues but not to the other tested N-terminal residues.	bind
16638	5	5551	6	10	NULL	NULL	NULL	statement 1	Process		destabilizes								N-terminal residues		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8255_s_38	14585983	(I) m-UBR1 and m-UBR2 bind to Arg (type 1) and Phe (type  2) destabilizing N-terminal residues but not to the other tested N-terminal residues.	bind
16639	6	5551	6	10	NULL	NULL	NULL	statement 2	Process		destabilizes								N-terminal residues		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8255_s_38	14585983	(I) m-UBR1 and m-UBR2 bind to Arg (type 1) and Phe (type  2) destabilizing N-terminal residues but not to the other tested N-terminal residues.	bind
16640	7	5551	6	10	NULL	NULL	NULL	statement 3	Process		destabilizes								N-terminal residues		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8255_s_38	14585983	(I) m-UBR1 and m-UBR2 bind to Arg (type 1) and Phe (type  2) destabilizing N-terminal residues but not to the other tested N-terminal residues.	bind
16641	8	5551	6	10	NULL	NULL	NULL	statement 4	Process		destabilizes								N-terminal residues		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8255_s_38	14585983	(I) m-UBR1 and m-UBR2 bind to Arg (type 1) and Phe (type  2) destabilizing N-terminal residues but not to the other tested N-terminal residues.	bind
15984	1	5551	7	10	NULL	NULL	NULL	m-UBR1	GP		bind					Arg	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8255_s_38	14585983	(I) m-UBR1 and m-UBR2 bind to Arg (type 1) and Phe (type  2) destabilizing N-terminal residues but not to the other tested N-terminal residues.	bind
15985	2	5551	7	10	NULL	NULL	NULL	m-UBR1	GP		bind					Phe	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8255_s_38	14585983	(I) m-UBR1 and m-UBR2 bind to Arg (type 1) and Phe (type  2) destabilizing N-terminal residues but not to the other tested N-terminal residues.	bind
15986	3	5551	7	10	NULL	NULL	NULL	m-UBR2	GP		bind					Arg	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8255_s_38	14585983	(I) m-UBR1 and m-UBR2 bind to Arg (type 1) and Phe (type  2) destabilizing N-terminal residues but not to the other tested N-terminal residues.	bind
15987	4	5551	7	10	NULL	NULL	NULL	m-UBR2	GP		bind					Phe	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8255_s_38	14585983	(I) m-UBR1 and m-UBR2 bind to Arg (type 1) and Phe (type  2) destabilizing N-terminal residues but not to the other tested N-terminal residues.	bind
15988	5	5551	7	10	NULL	NULL	NULL	statement 1	Process		destabilize								N-terminal residues		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8255_s_38	14585983	(I) m-UBR1 and m-UBR2 bind to Arg (type 1) and Phe (type  2) destabilizing N-terminal residues but not to the other tested N-terminal residues.	bind
15989	6	5551	7	10	NULL	NULL	NULL	statement 2	Process		destabilize								N-terminal residues		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8255_s_38	14585983	(I) m-UBR1 and m-UBR2 bind to Arg (type 1) and Phe (type  2) destabilizing N-terminal residues but not to the other tested N-terminal residues.	bind
15990	7	5551	7	10	NULL	NULL	NULL	statement 3	Process		destabilize								N-terminal residues		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8255_s_38	14585983	(I) m-UBR1 and m-UBR2 bind to Arg (type 1) and Phe (type  2) destabilizing N-terminal residues but not to the other tested N-terminal residues.	bind
15991	8	5551	7	10	NULL	NULL	NULL	statement 4	Process		destabilize								N-terminal residues		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8255_s_38	14585983	(I) m-UBR1 and m-UBR2 bind to Arg (type 1) and Phe (type  2) destabilizing N-terminal residues but not to the other tested N-terminal residues.	bind
16643	1	5552	6	10	NULL	NULL	NULL	CRP	GP	purified	bind		directly			traJ	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_5_1616_s_204	12591879	(i) Mobility shift experiments demonstrated that there was direct binding of CRP to the  traJ promoter region; (ii) DNase I footprint experiments showed that binding of purified CRP to a fragment carrying the  traJ promoter region provided protection against DNase I activity; and (iii) targeted mutagenesis of the putative CRP binding sites in the  traJ promoter region reduced the activation of TraJ under starvation conditions.	bind
16644	2	5552	6	10	NULL	NULL	NULL	statement 1	Process		provides protection against					DNase I activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_5_1616_s_204	12591879	(i) Mobility shift experiments demonstrated that there was direct binding of CRP to the  traJ promoter region; (ii) DNase I footprint experiments showed that binding of purified CRP to a fragment carrying the  traJ promoter region provided protection against DNase I activity; and (iii) targeted mutagenesis of the putative CRP binding sites in the  traJ promoter region reduced the activation of TraJ under starvation conditions.	bind
16645	3	5552	6	10	NULL	NULL	NULL	traJ	GP	targeted mutagenesis of;;putative	reduced				CRP binding sites of the promoter	TraJ	GP	activation of 			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_5_1616_s_204	12591879	(i) Mobility shift experiments demonstrated that there was direct binding of CRP to the  traJ promoter region; (ii) DNase I footprint experiments showed that binding of purified CRP to a fragment carrying the  traJ promoter region provided protection against DNase I activity; and (iii) targeted mutagenesis of the putative CRP binding sites in the  traJ promoter region reduced the activation of TraJ under starvation conditions.	bind
16646	4	5552	6	10	NULL	NULL	NULL	statement 3	Process		occurs under					starvation conditions	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_5_1616_s_204	12591879	(i) Mobility shift experiments demonstrated that there was direct binding of CRP to the  traJ promoter region; (ii) DNase I footprint experiments showed that binding of purified CRP to a fragment carrying the  traJ promoter region provided protection against DNase I activity; and (iii) targeted mutagenesis of the putative CRP binding sites in the  traJ promoter region reduced the activation of TraJ under starvation conditions.	bind
15992	1	5552	7	10	NULL	NULL	NULL	CRP	GP	purified	bind		directly			traJ	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_5_1616_s_204	12591879	(i) Mobility shift experiments demonstrated that there was direct binding of CRP to the  traJ promoter region; (ii) DNase I footprint experiments showed that binding of purified CRP to a fragment carrying the  traJ promoter region provided protection against DNase I activity; and (iii) targeted mutagenesis of the putative CRP binding sites in the  traJ promoter region reduced the activation of TraJ under starvation conditions.	bind
15994	3	5552	7	10	NULL	NULL	NULL	traJ fragment	GP		is protected against				promoter	DNase I	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_5_1616_s_204	12591879	(i) Mobility shift experiments demonstrated that there was direct binding of CRP to the  traJ promoter region; (ii) DNase I footprint experiments showed that binding of purified CRP to a fragment carrying the  traJ promoter region provided protection against DNase I activity; and (iii) targeted mutagenesis of the putative CRP binding sites in the  traJ promoter region reduced the activation of TraJ under starvation conditions.	bind
15995	4	5552	7	10	NULL	NULL	NULL	 traJ	GP	 targeted mutagenesis of;;putataive	reduced				CRP site in the promoter	TraJ	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_5_1616_s_204	12591879	(i) Mobility shift experiments demonstrated that there was direct binding of CRP to the  traJ promoter region; (ii) DNase I footprint experiments showed that binding of purified CRP to a fragment carrying the  traJ promoter region provided protection against DNase I activity; and (iii) targeted mutagenesis of the putative CRP binding sites in the  traJ promoter region reduced the activation of TraJ under starvation conditions.	bind
44811	5	5552	7	10	NULL	NULL	NULL	statement 4	Process		occurs under					starvation condition	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_5_1616_s_204	12591879	(i) Mobility shift experiments demonstrated that there was direct binding of CRP to the  traJ promoter region; (ii) DNase I footprint experiments showed that binding of purified CRP to a fragment carrying the  traJ promoter region provided protection against DNase I activity; and (iii) targeted mutagenesis of the putative CRP binding sites in the  traJ promoter region reduced the activation of TraJ under starvation conditions.	bind
16703	1	5553	6	10	NULL	NULL	NULL	Lef	GP		bind					CBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35170_s_155	10906119	(i) Most population of CBP is occupied by beta-catenin because of a much higher levels of beta-catenin than those of Lef/TCF. (ii) High levels of beta-catenin inhibit the binding between Lef and CBP by the association of beta-catenin with Lef and/or CBP and cause the conversion from a Lef-CBP suppression complex to a Lef-beta-catenin-CBP activation complex.	bind
16704	2	5553	6	10	NULL	NULL	NULL	beta-catenin	GP	high levels of	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35170_s_155	10906119	(i) Most population of CBP is occupied by beta-catenin because of a much higher levels of beta-catenin than those of Lef/TCF. (ii) High levels of beta-catenin inhibit the binding between Lef and CBP by the association of beta-catenin with Lef and/or CBP and cause the conversion from a Lef-CBP suppression complex to a Lef-beta-catenin-CBP activation complex.	bind
16705	3	5553	6	10	NULL	NULL	NULL	statement 1	Process		forms a 					suppression complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35170_s_155	10906119	(i) Most population of CBP is occupied by beta-catenin because of a much higher levels of beta-catenin than those of Lef/TCF. (ii) High levels of beta-catenin inhibit the binding between Lef and CBP by the association of beta-catenin with Lef and/or CBP and cause the conversion from a Lef-CBP suppression complex to a Lef-beta-catenin-CBP activation complex.	bind
16706	4	5553	6	10	NULL	NULL	NULL	beta-catenin	GP		associates with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35170_s_155	10906119	(i) Most population of CBP is occupied by beta-catenin because of a much higher levels of beta-catenin than those of Lef/TCF. (ii) High levels of beta-catenin inhibit the binding between Lef and CBP by the association of beta-catenin with Lef and/or CBP and cause the conversion from a Lef-CBP suppression complex to a Lef-beta-catenin-CBP activation complex.	bind
16707	5	5553	6	10	NULL	NULL	NULL	statement 4	Process		forms a 					Lef-beta-catenin-CBP activation complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35170_s_155	10906119	(i) Most population of CBP is occupied by beta-catenin because of a much higher levels of beta-catenin than those of Lef/TCF. (ii) High levels of beta-catenin inhibit the binding between Lef and CBP by the association of beta-catenin with Lef and/or CBP and cause the conversion from a Lef-CBP suppression complex to a Lef-beta-catenin-CBP activation complex.	bind
44847	6	5553	6	10	NULL	NULL	NULL	Lef-CBP suppression complex	GP		converts to					Lef-beta-catenin-CBP activation complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35170_s_155	10906119	(i) Most population of CBP is occupied by beta-catenin because of a much higher levels of beta-catenin than those of Lef/TCF. (ii) High levels of beta-catenin inhibit the binding between Lef and CBP by the association of beta-catenin with Lef and/or CBP and cause the conversion from a Lef-CBP suppression complex to a Lef-beta-catenin-CBP activation complex.	bind
15996	1	5553	7	10	NULL	NULL	NULL	Lef 	GP		bind					CBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35170_s_155	10906119	(i) Most population of CBP is occupied by beta-catenin because of a much higher levels of beta-catenin than those of Lef/TCF. (ii) High levels of beta-catenin inhibit the binding between Lef and CBP by the association of beta-catenin with Lef and/or CBP and cause the conversion from a Lef-CBP suppression complex to a Lef-beta-catenin-CBP activation complex.	bind
15997	2	5553	7	10	NULL	NULL	NULL	beta-catenin	GP		associate with					Lef	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35170_s_155	10906119	(i) Most population of CBP is occupied by beta-catenin because of a much higher levels of beta-catenin than those of Lef/TCF. (ii) High levels of beta-catenin inhibit the binding between Lef and CBP by the association of beta-catenin with Lef and/or CBP and cause the conversion from a Lef-CBP suppression complex to a Lef-beta-catenin-CBP activation complex.	bind
15998	3	5553	7	10	NULL	NULL	NULL	beta-catenin	GP		associate with					CBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35170_s_155	10906119	(i) Most population of CBP is occupied by beta-catenin because of a much higher levels of beta-catenin than those of Lef/TCF. (ii) High levels of beta-catenin inhibit the binding between Lef and CBP by the association of beta-catenin with Lef and/or CBP and cause the conversion from a Lef-CBP suppression complex to a Lef-beta-catenin-CBP activation complex.	bind
15999	4	5553	7	10	NULL	NULL	NULL	beta-catenin	GP	high levels of	inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35170_s_155	10906119	(i) Most population of CBP is occupied by beta-catenin because of a much higher levels of beta-catenin than those of Lef/TCF. (ii) High levels of beta-catenin inhibit the binding between Lef and CBP by the association of beta-catenin with Lef and/or CBP and cause the conversion from a Lef-CBP suppression complex to a Lef-beta-catenin-CBP activation complex.	bind
16000	5	5553	7	10	NULL	NULL	NULL	statement 4	Process		occurs by					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35170_s_155	10906119	(i) Most population of CBP is occupied by beta-catenin because of a much higher levels of beta-catenin than those of Lef/TCF. (ii) High levels of beta-catenin inhibit the binding between Lef and CBP by the association of beta-catenin with Lef and/or CBP and cause the conversion from a Lef-CBP suppression complex to a Lef-beta-catenin-CBP activation complex.	bind
16001	6	5553	7	10	NULL	NULL	NULL	statement 4	Process		occurs by					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35170_s_155	10906119	(i) Most population of CBP is occupied by beta-catenin because of a much higher levels of beta-catenin than those of Lef/TCF. (ii) High levels of beta-catenin inhibit the binding between Lef and CBP by the association of beta-catenin with Lef and/or CBP and cause the conversion from a Lef-CBP suppression complex to a Lef-beta-catenin-CBP activation complex.	bind
16002	7	5553	7	10	NULL	NULL	NULL	Lef-CBP suppression complex	GP		converts to					Lef-beta-catenin-CBP activation complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35170_s_155	10906119	(i) Most population of CBP is occupied by beta-catenin because of a much higher levels of beta-catenin than those of Lef/TCF. (ii) High levels of beta-catenin inhibit the binding between Lef and CBP by the association of beta-catenin with Lef and/or CBP and cause the conversion from a Lef-CBP suppression complex to a Lef-beta-catenin-CBP activation complex.	bind
16003	8	5553	7	10	NULL	NULL	NULL	statement 2	Process		cause					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35170_s_155	10906119	(i) Most population of CBP is occupied by beta-catenin because of a much higher levels of beta-catenin than those of Lef/TCF. (ii) High levels of beta-catenin inhibit the binding between Lef and CBP by the association of beta-catenin with Lef and/or CBP and cause the conversion from a Lef-CBP suppression complex to a Lef-beta-catenin-CBP activation complex.	bind
16004	9	5553	7	10	NULL	NULL	NULL	statement 3	Process		cause					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35170_s_155	10906119	(i) Most population of CBP is occupied by beta-catenin because of a much higher levels of beta-catenin than those of Lef/TCF. (ii) High levels of beta-catenin inhibit the binding between Lef and CBP by the association of beta-catenin with Lef and/or CBP and cause the conversion from a Lef-CBP suppression complex to a Lef-beta-catenin-CBP activation complex.	bind
17579	1	5554	6	10	NULL	NULL	NULL	p40	GP		bind					p37	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6303_s_225	9045649	(i) No stable complex with two subunits was formed, although weak interactions could be observed for several pairs of subunits; (ii) the only stable three-subunit core complex was formed with p40, p37, and p36; (iii) p140 and p38 bound only cooperatively to the core complex p40.p37.p36 ( 31).	bind
17580	2	5554	6	10	NULL	NULL	NULL	statement 1	Process		bind					p36	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6303_s_225	9045649	(i) No stable complex with two subunits was formed, although weak interactions could be observed for several pairs of subunits; (ii) the only stable three-subunit core complex was formed with p40, p37, and p36; (iii) p140 and p38 bound only cooperatively to the core complex p40.p37.p36 ( 31).	bind
17581	3	5554	6	10	NULL	NULL	NULL	statement 2	Process		forms a 					three-subunit core complex	GP	stable			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6303_s_225	9045649	(i) No stable complex with two subunits was formed, although weak interactions could be observed for several pairs of subunits; (ii) the only stable three-subunit core complex was formed with p40, p37, and p36; (iii) p140 and p38 bound only cooperatively to the core complex p40.p37.p36 ( 31).	bind
17587	4	5554	6	10	NULL	NULL	NULL	p140	GP		bind					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6303_s_225	9045649	(i) No stable complex with two subunits was formed, although weak interactions could be observed for several pairs of subunits; (ii) the only stable three-subunit core complex was formed with p40, p37, and p36; (iii) p140 and p38 bound only cooperatively to the core complex p40.p37.p36 ( 31).	bind
17588	5	5554	6	10	NULL	NULL	NULL	p38	GP		bind					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6303_s_225	9045649	(i) No stable complex with two subunits was formed, although weak interactions could be observed for several pairs of subunits; (ii) the only stable three-subunit core complex was formed with p40, p37, and p36; (iii) p140 and p38 bound only cooperatively to the core complex p40.p37.p36 ( 31).	bind
17590	6	5554	6	10	NULL	NULL	NULL	statement 4	Process		occurs in cooperation with					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6303_s_225	9045649	(i) No stable complex with two subunits was formed, although weak interactions could be observed for several pairs of subunits; (ii) the only stable three-subunit core complex was formed with p40, p37, and p36; (iii) p140 and p38 bound only cooperatively to the core complex p40.p37.p36 ( 31).	bind
16005	1	5554	7	10	NULL	NULL	NULL	p40	GP		bind					p37	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6303_s_225	9045649	(i) No stable complex with two subunits was formed, although weak interactions could be observed for several pairs of subunits; (ii) the only stable three-subunit core complex was formed with p40, p37, and p36; (iii) p140 and p38 bound only cooperatively to the core complex p40.p37.p36 ( 31).	bind
16006	2	5554	7	10	NULL	NULL	NULL	statement 1	Process		bind					p36	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6303_s_225	9045649	(i) No stable complex with two subunits was formed, although weak interactions could be observed for several pairs of subunits; (ii) the only stable three-subunit core complex was formed with p40, p37, and p36; (iii) p140 and p38 bound only cooperatively to the core complex p40.p37.p36 ( 31).	bind
16007	3	5554	7	10	NULL	NULL	NULL	statement 2	Process		forms					three-subunit  core complex	GP	stable			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6303_s_225	9045649	(i) No stable complex with two subunits was formed, although weak interactions could be observed for several pairs of subunits; (ii) the only stable three-subunit core complex was formed with p40, p37, and p36; (iii) p140 and p38 bound only cooperatively to the core complex p40.p37.p36 ( 31).	bind
16008	4	5554	7	10	NULL	NULL	NULL	p140	GP		bind					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6303_s_225	9045649	(i) No stable complex with two subunits was formed, although weak interactions could be observed for several pairs of subunits; (ii) the only stable three-subunit core complex was formed with p40, p37, and p36; (iii) p140 and p38 bound only cooperatively to the core complex p40.p37.p36 ( 31).	bind
16009	5	5554	7	10	NULL	NULL	NULL	p38	GP		bind					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6303_s_225	9045649	(i) No stable complex with two subunits was formed, although weak interactions could be observed for several pairs of subunits; (ii) the only stable three-subunit core complex was formed with p40, p37, and p36; (iii) p140 and p38 bound only cooperatively to the core complex p40.p37.p36 ( 31).	bind
16010	6	5554	7	10	NULL	NULL	NULL	statement 4	Process		occurs in cooperation with					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6303_s_225	9045649	(i) No stable complex with two subunits was formed, although weak interactions could be observed for several pairs of subunits; (ii) the only stable three-subunit core complex was formed with p40, p37, and p36; (iii) p140 and p38 bound only cooperatively to the core complex p40.p37.p36 ( 31).	bind
17059	1	5555	6	10	NULL	NULL	NULL	OATP-C	GP		is expressed in		only			hepatocytes	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_40_37206_s_26	11483603	(i) OATP-C is expressed only in hepatocytes and binding sites for HNF1 have been shown in the promoters or enhancers of numerous genes expressed exclusively in the liver ( 13,  14); (ii) the phenotype of increased serum bile acid concentrations and a 3-10-fold elevation of serum bilirubin in HNF1alpha-deficient (Tcf1 / ) mice ( 11,  15) is consistent with a reduced function of Oatp4 ( Slc21a6), the liver-specific mouse orthologue of human OATP-C ( SLC21A6).	bind
45644	2	5555	6	10	NULL	NULL	NULL	Oatp4	GP		is					Slc21a6	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_40_37206_s_26	11483603	(i) OATP-C is expressed only in hepatocytes and binding sites for HNF1 have been shown in the promoters or enhancers of numerous genes expressed exclusively in the liver ( 13,  14); (ii) the phenotype of increased serum bile acid concentrations and a 3-10-fold elevation of serum bilirubin in HNF1alpha-deficient (Tcf1 / ) mice ( 11,  15) is consistent with a reduced function of Oatp4 ( Slc21a6), the liver-specific mouse orthologue of human OATP-C ( SLC21A6).	bind
45645	3	5555	6	10	NULL	NULL	NULL	Oatp4	GP	mouse;; liver specific	is orthologous to					OATP-C	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_40_37206_s_26	11483603	(i) OATP-C is expressed only in hepatocytes and binding sites for HNF1 have been shown in the promoters or enhancers of numerous genes expressed exclusively in the liver ( 13,  14); (ii) the phenotype of increased serum bile acid concentrations and a 3-10-fold elevation of serum bilirubin in HNF1alpha-deficient (Tcf1 / ) mice ( 11,  15) is consistent with a reduced function of Oatp4 ( Slc21a6), the liver-specific mouse orthologue of human OATP-C ( SLC21A6).	bind
16262	1	5555	7	10	NULL	NULL	NULL	OATP-C	GP		is expressed in		only			hepatocytes	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_40_37206_s_26	11483603	(i) OATP-C is expressed only in hepatocytes and binding sites for HNF1 have been shown in the promoters or enhancers of numerous genes expressed exclusively in the liver ( 13,  14); (ii) the phenotype of increased serum bile acid concentrations and a 3-10-fold elevation of serum bilirubin in HNF1alpha-deficient (Tcf1 / ) mice ( 11,  15) is consistent with a reduced function of Oatp4 ( Slc21a6), the liver-specific mouse orthologue of human OATP-C ( SLC21A6).	bind
16266	2	5555	7	10	NULL	NULL	NULL	Oatp4 	GP	mouse;;liver-specific	is orthologous to					OATP-C	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_40_37206_s_26	11483603	(i) OATP-C is expressed only in hepatocytes and binding sites for HNF1 have been shown in the promoters or enhancers of numerous genes expressed exclusively in the liver ( 13,  14); (ii) the phenotype of increased serum bile acid concentrations and a 3-10-fold elevation of serum bilirubin in HNF1alpha-deficient (Tcf1 / ) mice ( 11,  15) is consistent with a reduced function of Oatp4 ( Slc21a6), the liver-specific mouse orthologue of human OATP-C ( SLC21A6).	bind
45646	3	5555	7	10	NULL	NULL	NULL	Oatp4 	GP		is					Slc21a6	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_40_37206_s_26	11483603	(i) OATP-C is expressed only in hepatocytes and binding sites for HNF1 have been shown in the promoters or enhancers of numerous genes expressed exclusively in the liver ( 13,  14); (ii) the phenotype of increased serum bile acid concentrations and a 3-10-fold elevation of serum bilirubin in HNF1alpha-deficient (Tcf1 / ) mice ( 11,  15) is consistent with a reduced function of Oatp4 ( Slc21a6), the liver-specific mouse orthologue of human OATP-C ( SLC21A6).	bind
45647	4	5555	7	10	NULL	NULL	NULL	OATP-C	GP		is					SLC21A6	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_40_37206_s_26	11483603	(i) OATP-C is expressed only in hepatocytes and binding sites for HNF1 have been shown in the promoters or enhancers of numerous genes expressed exclusively in the liver ( 13,  14); (ii) the phenotype of increased serum bile acid concentrations and a 3-10-fold elevation of serum bilirubin in HNF1alpha-deficient (Tcf1 / ) mice ( 11,  15) is consistent with a reduced function of Oatp4 ( Slc21a6), the liver-specific mouse orthologue of human OATP-C ( SLC21A6).	bind
17060	1	5559	6	10	NULL	NULL	NULL	p105	GP		resides		exclusively			cytosolic compartment	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
17061	2	5559	6	10	NULL	NULL	NULL	statement 1	Process		is independent of					cellular activation	Process	status of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
17063	4	5559	6	10	NULL	NULL	NULL	p105	GP		inhibits			ankyrin motif-rich carboxyl-terminal domain		nuclear expression	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
17064	5	5559	6	10	NULL	NULL	NULL	p105	GP		inhibits			ankyrin motif-rich carboxyl-terminal domain				DNA binding activity of	amino terminal half		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
17602	6	5559	6	10	NULL	NULL	NULL				undergoes		constitutively	IkappaBalpha-related domain		degradation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
17605	7	5559	6	10	NULL	NULL	NULL	p105	GP		sequesters		physically			RelA	GP				NULL	cytoplasm	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
17608	8	5559	6	10	NULL	NULL	NULL	IkappaBalpha	GP		sequesters		physically			RelA	GP				NULL	cytoplasm	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
17719	9	5559	6	10	NULL	NULL	NULL	p105 gene	GP	inducible	contain							functional		NF-kappaB binding sites	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
17720	10	5559	6	10	NULL	NULL	NULL	IkappaBalpha gene	GP	inducible	contain							functional		NF-kappaB-binding site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
53117	11	5559	6	10	NULL	NULL	NULL	statement 6	Process		generates					NF-kappaB	GP		p50 DNA binding subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
16034	1	5559	7	10	NULL	NULL	NULL	p105	GP		resides		exclusively			cytosolic compartment	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
16036	2	5559	7	10	NULL	NULL	NULL	statement 1	Process		is independent of					cellular activation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
16038	3	5559	7	10	NULL	NULL	NULL	p105	GP		inhibits			ankyrin motif-rich carboxyl-terminal domain 		 nuclear expression	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
16042	4	5559	7	10	NULL	NULL	NULL	p105	GP		inhibits			ankyrin motif-rich carboxyl-terminal domain 				DNA binding activity of	half of amino-terminal		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
16045	5	5559	7	10	NULL	NULL	NULL				undergoes		constitutively	IkappaBalpha-related domain		degradation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
16048	6	5559	7	10	NULL	NULL	NULL	 p105	GP		sequesters		physically			RelA	GP				NULL	cytoplasmic compartment 	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
16049	7	5559	7	10	NULL	NULL	NULL	IkappaBalpha	GP		sequesters		physically			RelA	GP				NULL	cytoplasmic compartment 	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
16050	8	5559	7	10	NULL	NULL	NULL	p105 gene	GP	inducible  	contain							functional	NF-kappaB binding sites		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
16051	9	5559	7	10	NULL	NULL	NULL	IkappaBalpha gene	GP	inducible 	contain							functional	NF-kappaB binding sites		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
53118	10	5559	7	10	NULL	NULL	NULL	statement 5	Process		generates					NF-kappaB	GP		p50 DNA binding subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	bind
17609	1	5560	6	10	NULL	NULL	NULL	VWF	GP	purified	bind					platelets	OrganismPart	human			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_4699_s_239	16373331	(i) Peptides derived from these regions inhibited ristocetin-induced binding of purified VWF to human platelets ( ), (ii) stepwise N-terminal deletions in the aa 1204 - 1271 region of a recombinant VWF fragment comprising the A1 domain (aa 1204 - 1496) resulted in stepwise increased ristocetin-induced binding to human platelets ( ); (iii) Ala mutations in the N-terminal flanking region of the A1 domain (aa 1260 - 1271) in full-length VWF resulted in an increased ristocetin-induced binding to human platelets ( ); (iv) deletions in the aa 1222 - 1271 region in full-length VWF in which an additional R1308A mutation was added resulted in an increased ristocetin-induced or even spontaneous binding to human platelets when compared with the R1308A VWF point mutant ( ); (v) specific  O-linked glycosylation in the aa 1248 - 1256 region negatively modulated the binding to human platelets as demonstrated using glycosylphosphatidylinositol COS-7 cell-anchored FLAG-tagged VWF A1 domains ( ).	bind
17610	2	5560	6	10	NULL	NULL	NULL	statement 1	Process		is induced by					ristocetin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_4699_s_239	16373331	(i) Peptides derived from these regions inhibited ristocetin-induced binding of purified VWF to human platelets ( ), (ii) stepwise N-terminal deletions in the aa 1204 - 1271 region of a recombinant VWF fragment comprising the A1 domain (aa 1204 - 1496) resulted in stepwise increased ristocetin-induced binding to human platelets ( ); (iii) Ala mutations in the N-terminal flanking region of the A1 domain (aa 1260 - 1271) in full-length VWF resulted in an increased ristocetin-induced binding to human platelets ( ); (iv) deletions in the aa 1222 - 1271 region in full-length VWF in which an additional R1308A mutation was added resulted in an increased ristocetin-induced or even spontaneous binding to human platelets when compared with the R1308A VWF point mutant ( ); (v) specific  O-linked glycosylation in the aa 1248 - 1256 region negatively modulated the binding to human platelets as demonstrated using glycosylphosphatidylinositol COS-7 cell-anchored FLAG-tagged VWF A1 domains ( ).	bind
17625	3	5560	6	10	NULL	NULL	NULL	VWF fragment	GP	N-terminal deletion;;recombinant	increases			aa 1204 - 1271		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_4699_s_239	16373331	(i) Peptides derived from these regions inhibited ristocetin-induced binding of purified VWF to human platelets ( ), (ii) stepwise N-terminal deletions in the aa 1204 - 1271 region of a recombinant VWF fragment comprising the A1 domain (aa 1204 - 1496) resulted in stepwise increased ristocetin-induced binding to human platelets ( ); (iii) Ala mutations in the N-terminal flanking region of the A1 domain (aa 1260 - 1271) in full-length VWF resulted in an increased ristocetin-induced binding to human platelets ( ); (iv) deletions in the aa 1222 - 1271 region in full-length VWF in which an additional R1308A mutation was added resulted in an increased ristocetin-induced or even spontaneous binding to human platelets when compared with the R1308A VWF point mutant ( ); (v) specific  O-linked glycosylation in the aa 1248 - 1256 region negatively modulated the binding to human platelets as demonstrated using glycosylphosphatidylinositol COS-7 cell-anchored FLAG-tagged VWF A1 domains ( ).	bind
17660	4	5560	6	10	NULL	NULL	NULL	VWF	GP	full length;;mutant	increases			Ala		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_4699_s_239	16373331	(i) Peptides derived from these regions inhibited ristocetin-induced binding of purified VWF to human platelets ( ), (ii) stepwise N-terminal deletions in the aa 1204 - 1271 region of a recombinant VWF fragment comprising the A1 domain (aa 1204 - 1496) resulted in stepwise increased ristocetin-induced binding to human platelets ( ); (iii) Ala mutations in the N-terminal flanking region of the A1 domain (aa 1260 - 1271) in full-length VWF resulted in an increased ristocetin-induced binding to human platelets ( ); (iv) deletions in the aa 1222 - 1271 region in full-length VWF in which an additional R1308A mutation was added resulted in an increased ristocetin-induced or even spontaneous binding to human platelets when compared with the R1308A VWF point mutant ( ); (v) specific  O-linked glycosylation in the aa 1248 - 1256 region negatively modulated the binding to human platelets as demonstrated using glycosylphosphatidylinositol COS-7 cell-anchored FLAG-tagged VWF A1 domains ( ).	bind
17661	5	5560	6	10	NULL	NULL	NULL	VWF	GP	deletion mutant;;full-length	increases			aa1222-1271;;R1308A		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_4699_s_239	16373331	(i) Peptides derived from these regions inhibited ristocetin-induced binding of purified VWF to human platelets ( ), (ii) stepwise N-terminal deletions in the aa 1204 - 1271 region of a recombinant VWF fragment comprising the A1 domain (aa 1204 - 1496) resulted in stepwise increased ristocetin-induced binding to human platelets ( ); (iii) Ala mutations in the N-terminal flanking region of the A1 domain (aa 1260 - 1271) in full-length VWF resulted in an increased ristocetin-induced binding to human platelets ( ); (iv) deletions in the aa 1222 - 1271 region in full-length VWF in which an additional R1308A mutation was added resulted in an increased ristocetin-induced or even spontaneous binding to human platelets when compared with the R1308A VWF point mutant ( ); (v) specific  O-linked glycosylation in the aa 1248 - 1256 region negatively modulated the binding to human platelets as demonstrated using glycosylphosphatidylinositol COS-7 cell-anchored FLAG-tagged VWF A1 domains ( ).	bind
17662	6	5560	6	10	NULL	NULL	NULL	VWF	GP	glycosylated	negatively modulates			aa 1248-1256		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_4699_s_239	16373331	(i) Peptides derived from these regions inhibited ristocetin-induced binding of purified VWF to human platelets ( ), (ii) stepwise N-terminal deletions in the aa 1204 - 1271 region of a recombinant VWF fragment comprising the A1 domain (aa 1204 - 1496) resulted in stepwise increased ristocetin-induced binding to human platelets ( ); (iii) Ala mutations in the N-terminal flanking region of the A1 domain (aa 1260 - 1271) in full-length VWF resulted in an increased ristocetin-induced binding to human platelets ( ); (iv) deletions in the aa 1222 - 1271 region in full-length VWF in which an additional R1308A mutation was added resulted in an increased ristocetin-induced or even spontaneous binding to human platelets when compared with the R1308A VWF point mutant ( ); (v) specific  O-linked glycosylation in the aa 1248 - 1256 region negatively modulated the binding to human platelets as demonstrated using glycosylphosphatidylinositol COS-7 cell-anchored FLAG-tagged VWF A1 domains ( ).	bind
16103	1	5560	7	10	NULL	NULL	NULL	VWF	GP	purified 	bind					platelets	OrganismPart	human			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_4699_s_239	16373331	(i) Peptides derived from these regions inhibited ristocetin-induced binding of purified VWF to human platelets ( ), (ii) stepwise N-terminal deletions in the aa 1204 - 1271 region of a recombinant VWF fragment comprising the A1 domain (aa 1204 - 1496) resulted in stepwise increased ristocetin-induced binding to human platelets ( ); (iii) Ala mutations in the N-terminal flanking region of the A1 domain (aa 1260 - 1271) in full-length VWF resulted in an increased ristocetin-induced binding to human platelets ( ); (iv) deletions in the aa 1222 - 1271 region in full-length VWF in which an additional R1308A mutation was added resulted in an increased ristocetin-induced or even spontaneous binding to human platelets when compared with the R1308A VWF point mutant ( ); (v) specific  O-linked glycosylation in the aa 1248 - 1256 region negatively modulated the binding to human platelets as demonstrated using glycosylphosphatidylinositol COS-7 cell-anchored FLAG-tagged VWF A1 domains ( ).	bind
16105	2	5560	7	10	NULL	NULL	NULL	ristocetin	Chemical		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_4699_s_239	16373331	(i) Peptides derived from these regions inhibited ristocetin-induced binding of purified VWF to human platelets ( ), (ii) stepwise N-terminal deletions in the aa 1204 - 1271 region of a recombinant VWF fragment comprising the A1 domain (aa 1204 - 1496) resulted in stepwise increased ristocetin-induced binding to human platelets ( ); (iii) Ala mutations in the N-terminal flanking region of the A1 domain (aa 1260 - 1271) in full-length VWF resulted in an increased ristocetin-induced binding to human platelets ( ); (iv) deletions in the aa 1222 - 1271 region in full-length VWF in which an additional R1308A mutation was added resulted in an increased ristocetin-induced or even spontaneous binding to human platelets when compared with the R1308A VWF point mutant ( ); (v) specific  O-linked glycosylation in the aa 1248 - 1256 region negatively modulated the binding to human platelets as demonstrated using glycosylphosphatidylinositol COS-7 cell-anchored FLAG-tagged VWF A1 domains ( ).	bind
16117	3	5560	7	10	NULL	NULL	NULL	VWF fragment	GP	deletion of;;recombinant	increase			N-terminal aa 1204 - 1271 		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_4699_s_239	16373331	(i) Peptides derived from these regions inhibited ristocetin-induced binding of purified VWF to human platelets ( ), (ii) stepwise N-terminal deletions in the aa 1204 - 1271 region of a recombinant VWF fragment comprising the A1 domain (aa 1204 - 1496) resulted in stepwise increased ristocetin-induced binding to human platelets ( ); (iii) Ala mutations in the N-terminal flanking region of the A1 domain (aa 1260 - 1271) in full-length VWF resulted in an increased ristocetin-induced binding to human platelets ( ); (iv) deletions in the aa 1222 - 1271 region in full-length VWF in which an additional R1308A mutation was added resulted in an increased ristocetin-induced or even spontaneous binding to human platelets when compared with the R1308A VWF point mutant ( ); (v) specific  O-linked glycosylation in the aa 1248 - 1256 region negatively modulated the binding to human platelets as demonstrated using glycosylphosphatidylinositol COS-7 cell-anchored FLAG-tagged VWF A1 domains ( ).	bind
16119	4	5560	7	10	NULL	NULL	NULL	VWF fragment	GP		comprise								 A1 domain aa 1204 - 1496		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_4699_s_239	16373331	(i) Peptides derived from these regions inhibited ristocetin-induced binding of purified VWF to human platelets ( ), (ii) stepwise N-terminal deletions in the aa 1204 - 1271 region of a recombinant VWF fragment comprising the A1 domain (aa 1204 - 1496) resulted in stepwise increased ristocetin-induced binding to human platelets ( ); (iii) Ala mutations in the N-terminal flanking region of the A1 domain (aa 1260 - 1271) in full-length VWF resulted in an increased ristocetin-induced binding to human platelets ( ); (iv) deletions in the aa 1222 - 1271 region in full-length VWF in which an additional R1308A mutation was added resulted in an increased ristocetin-induced or even spontaneous binding to human platelets when compared with the R1308A VWF point mutant ( ); (v) specific  O-linked glycosylation in the aa 1248 - 1256 region negatively modulated the binding to human platelets as demonstrated using glycosylphosphatidylinositol COS-7 cell-anchored FLAG-tagged VWF A1 domains ( ).	bind
16123	5	5560	7	10	NULL	NULL	NULL	Ala	AminoAcid	mutations of	increase			N- terminal flanking region of the A1 domain aa 1260 - 1271		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_4699_s_239	16373331	(i) Peptides derived from these regions inhibited ristocetin-induced binding of purified VWF to human platelets ( ), (ii) stepwise N-terminal deletions in the aa 1204 - 1271 region of a recombinant VWF fragment comprising the A1 domain (aa 1204 - 1496) resulted in stepwise increased ristocetin-induced binding to human platelets ( ); (iii) Ala mutations in the N-terminal flanking region of the A1 domain (aa 1260 - 1271) in full-length VWF resulted in an increased ristocetin-induced binding to human platelets ( ); (iv) deletions in the aa 1222 - 1271 region in full-length VWF in which an additional R1308A mutation was added resulted in an increased ristocetin-induced or even spontaneous binding to human platelets when compared with the R1308A VWF point mutant ( ); (v) specific  O-linked glycosylation in the aa 1248 - 1256 region negatively modulated the binding to human platelets as demonstrated using glycosylphosphatidylinositol COS-7 cell-anchored FLAG-tagged VWF A1 domains ( ).	bind
16126	6	5560	7	10	NULL	NULL	NULL	VWF	GP	deletion mutant;;full-length	increase			aa 1222 - 1271		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_4699_s_239	16373331	(i) Peptides derived from these regions inhibited ristocetin-induced binding of purified VWF to human platelets ( ), (ii) stepwise N-terminal deletions in the aa 1204 - 1271 region of a recombinant VWF fragment comprising the A1 domain (aa 1204 - 1496) resulted in stepwise increased ristocetin-induced binding to human platelets ( ); (iii) Ala mutations in the N-terminal flanking region of the A1 domain (aa 1260 - 1271) in full-length VWF resulted in an increased ristocetin-induced binding to human platelets ( ); (iv) deletions in the aa 1222 - 1271 region in full-length VWF in which an additional R1308A mutation was added resulted in an increased ristocetin-induced or even spontaneous binding to human platelets when compared with the R1308A VWF point mutant ( ); (v) specific  O-linked glycosylation in the aa 1248 - 1256 region negatively modulated the binding to human platelets as demonstrated using glycosylphosphatidylinositol COS-7 cell-anchored FLAG-tagged VWF A1 domains ( ).	bind
16132	7	5560	7	10	NULL	NULL	NULL	VWF	GP	deletion mutant;;full-length	result in			aa1222-1271		statement 2	Process	spontaneous			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_4699_s_239	16373331	(i) Peptides derived from these regions inhibited ristocetin-induced binding of purified VWF to human platelets ( ), (ii) stepwise N-terminal deletions in the aa 1204 - 1271 region of a recombinant VWF fragment comprising the A1 domain (aa 1204 - 1496) resulted in stepwise increased ristocetin-induced binding to human platelets ( ); (iii) Ala mutations in the N-terminal flanking region of the A1 domain (aa 1260 - 1271) in full-length VWF resulted in an increased ristocetin-induced binding to human platelets ( ); (iv) deletions in the aa 1222 - 1271 region in full-length VWF in which an additional R1308A mutation was added resulted in an increased ristocetin-induced or even spontaneous binding to human platelets when compared with the R1308A VWF point mutant ( ); (v) specific  O-linked glycosylation in the aa 1248 - 1256 region negatively modulated the binding to human platelets as demonstrated using glycosylphosphatidylinositol COS-7 cell-anchored FLAG-tagged VWF A1 domains ( ).	bind
16133	8	5560	7	10	NULL	NULL	NULL	statement 6	Process	additional mutation to	increase			R1308A		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_4699_s_239	16373331	(i) Peptides derived from these regions inhibited ristocetin-induced binding of purified VWF to human platelets ( ), (ii) stepwise N-terminal deletions in the aa 1204 - 1271 region of a recombinant VWF fragment comprising the A1 domain (aa 1204 - 1496) resulted in stepwise increased ristocetin-induced binding to human platelets ( ); (iii) Ala mutations in the N-terminal flanking region of the A1 domain (aa 1260 - 1271) in full-length VWF resulted in an increased ristocetin-induced binding to human platelets ( ); (iv) deletions in the aa 1222 - 1271 region in full-length VWF in which an additional R1308A mutation was added resulted in an increased ristocetin-induced or even spontaneous binding to human platelets when compared with the R1308A VWF point mutant ( ); (v) specific  O-linked glycosylation in the aa 1248 - 1256 region negatively modulated the binding to human platelets as demonstrated using glycosylphosphatidylinositol COS-7 cell-anchored FLAG-tagged VWF A1 domains ( ).	bind
16136	9	5560	7	10	NULL	NULL	NULL	statement 7	Process	additional mutation to	increase			R1308A		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_4699_s_239	16373331	(i) Peptides derived from these regions inhibited ristocetin-induced binding of purified VWF to human platelets ( ), (ii) stepwise N-terminal deletions in the aa 1204 - 1271 region of a recombinant VWF fragment comprising the A1 domain (aa 1204 - 1496) resulted in stepwise increased ristocetin-induced binding to human platelets ( ); (iii) Ala mutations in the N-terminal flanking region of the A1 domain (aa 1260 - 1271) in full-length VWF resulted in an increased ristocetin-induced binding to human platelets ( ); (iv) deletions in the aa 1222 - 1271 region in full-length VWF in which an additional R1308A mutation was added resulted in an increased ristocetin-induced or even spontaneous binding to human platelets when compared with the R1308A VWF point mutant ( ); (v) specific  O-linked glycosylation in the aa 1248 - 1256 region negatively modulated the binding to human platelets as demonstrated using glycosylphosphatidylinositol COS-7 cell-anchored FLAG-tagged VWF A1 domains ( ).	bind
16137	10	5560	7	10	NULL	NULL	NULL	VWF	GP	point mutant	increase			R1308A		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_4699_s_239	16373331	(i) Peptides derived from these regions inhibited ristocetin-induced binding of purified VWF to human platelets ( ), (ii) stepwise N-terminal deletions in the aa 1204 - 1271 region of a recombinant VWF fragment comprising the A1 domain (aa 1204 - 1496) resulted in stepwise increased ristocetin-induced binding to human platelets ( ); (iii) Ala mutations in the N-terminal flanking region of the A1 domain (aa 1260 - 1271) in full-length VWF resulted in an increased ristocetin-induced binding to human platelets ( ); (iv) deletions in the aa 1222 - 1271 region in full-length VWF in which an additional R1308A mutation was added resulted in an increased ristocetin-induced or even spontaneous binding to human platelets when compared with the R1308A VWF point mutant ( ); (v) specific  O-linked glycosylation in the aa 1248 - 1256 region negatively modulated the binding to human platelets as demonstrated using glycosylphosphatidylinositol COS-7 cell-anchored FLAG-tagged VWF A1 domains ( ).	bind
16138	11	5560	7	10	NULL	NULL	NULL	statement 8	Process		is increased 					statement 10	Process	compared with			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_4699_s_239	16373331	(i) Peptides derived from these regions inhibited ristocetin-induced binding of purified VWF to human platelets ( ), (ii) stepwise N-terminal deletions in the aa 1204 - 1271 region of a recombinant VWF fragment comprising the A1 domain (aa 1204 - 1496) resulted in stepwise increased ristocetin-induced binding to human platelets ( ); (iii) Ala mutations in the N-terminal flanking region of the A1 domain (aa 1260 - 1271) in full-length VWF resulted in an increased ristocetin-induced binding to human platelets ( ); (iv) deletions in the aa 1222 - 1271 region in full-length VWF in which an additional R1308A mutation was added resulted in an increased ristocetin-induced or even spontaneous binding to human platelets when compared with the R1308A VWF point mutant ( ); (v) specific  O-linked glycosylation in the aa 1248 - 1256 region negatively modulated the binding to human platelets as demonstrated using glycosylphosphatidylinositol COS-7 cell-anchored FLAG-tagged VWF A1 domains ( ).	bind
16139	12	5560	7	10	NULL	NULL	NULL	statement 9	Process		is increased					statement 10	Process	compared with			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_4699_s_239	16373331	(i) Peptides derived from these regions inhibited ristocetin-induced binding of purified VWF to human platelets ( ), (ii) stepwise N-terminal deletions in the aa 1204 - 1271 region of a recombinant VWF fragment comprising the A1 domain (aa 1204 - 1496) resulted in stepwise increased ristocetin-induced binding to human platelets ( ); (iii) Ala mutations in the N-terminal flanking region of the A1 domain (aa 1260 - 1271) in full-length VWF resulted in an increased ristocetin-induced binding to human platelets ( ); (iv) deletions in the aa 1222 - 1271 region in full-length VWF in which an additional R1308A mutation was added resulted in an increased ristocetin-induced or even spontaneous binding to human platelets when compared with the R1308A VWF point mutant ( ); (v) specific  O-linked glycosylation in the aa 1248 - 1256 region negatively modulated the binding to human platelets as demonstrated using glycosylphosphatidylinositol COS-7 cell-anchored FLAG-tagged VWF A1 domains ( ).	bind
16140	13	5560	7	10	NULL	NULL	NULL			O-linked glycosylation	negatively modulates			aa 1248 - 1256		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_4699_s_239	16373331	(i) Peptides derived from these regions inhibited ristocetin-induced binding of purified VWF to human platelets ( ), (ii) stepwise N-terminal deletions in the aa 1204 - 1271 region of a recombinant VWF fragment comprising the A1 domain (aa 1204 - 1496) resulted in stepwise increased ristocetin-induced binding to human platelets ( ); (iii) Ala mutations in the N-terminal flanking region of the A1 domain (aa 1260 - 1271) in full-length VWF resulted in an increased ristocetin-induced binding to human platelets ( ); (iv) deletions in the aa 1222 - 1271 region in full-length VWF in which an additional R1308A mutation was added resulted in an increased ristocetin-induced or even spontaneous binding to human platelets when compared with the R1308A VWF point mutant ( ); (v) specific  O-linked glycosylation in the aa 1248 - 1256 region negatively modulated the binding to human platelets as demonstrated using glycosylphosphatidylinositol COS-7 cell-anchored FLAG-tagged VWF A1 domains ( ).	bind
17065	1	5561	6	10	NULL	NULL	NULL	86 kDa protein	GP	phosphorylated	bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_757_1_24_s_178	9200495	(i) Phospho- and dephospho-86 kDa protein bind to F-actin, with apparent dissociation constants of  Kd 280 nM and  Kd 690 nM, respectively.	bind
17066	2	5561	6	10	NULL	NULL	NULL	86 kDa protein	GP	dephosphorylated	bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_757_1_24_s_178	9200495	(i) Phospho- and dephospho-86 kDa protein bind to F-actin, with apparent dissociation constants of  Kd 280 nM and  Kd 690 nM, respectively.	bind
16142	1	5561	7	10	NULL	NULL	NULL	86 kDa protein	GP	phosphorylated	bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_757_1_24_s_178	9200495	(i) Phospho- and dephospho-86 kDa protein bind to F-actin, with apparent dissociation constants of  Kd 280 nM and  Kd 690 nM, respectively.	bind
16143	2	5561	7	10	NULL	NULL	NULL	86 kDa protein	GP	dephosphorylated	bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_757_1_24_s_178	9200495	(i) Phospho- and dephospho-86 kDa protein bind to F-actin, with apparent dissociation constants of  Kd 280 nM and  Kd 690 nM, respectively.	bind
17067	1	5563	6	10	NULL	NULL	NULL	Rtp-YFP	GP		bind							endogenous		ter sites	NULL	strain IRN424	NULL	NULL	NULL	NULL	gw70_jbacteriol_185_4_1326_s_167	12562803	(I) Position of Rtp-YFP  bound to endogenous  ter sites (strain IRN424).	bind
16144	1	5563	7	10	NULL	NULL	NULL	Rtp-YFP	GP		bind							endogenous		ter sites	NULL	strain IRN424	NULL	NULL	NULL	NULL	gw70_jbacteriol_185_4_1326_s_167	12562803	(I) Position of Rtp-YFP  bound to endogenous  ter sites (strain IRN424).	bind
17069	1	5565	6	10	NULL	NULL	NULL	PPARalpha	GP		bind							natural		PPRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
17070	2	5565	6	10	NULL	NULL	NULL	PPARbeta	GP		bind							natural		PPRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
17074	3	5565	6	10	NULL	NULL	NULL	PPARgamma	GP		bind							natural		PPRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
17075	4	5565	6	10	NULL	NULL	NULL	RXRalpha	GP		bind							natural		PPRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
17076	6	5565	6	10	NULL	NULL	NULL	statement 5	Process		is stronger than					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
17077	7	5565	6	10	NULL	NULL	NULL	statement 5	Process		is stronger than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
17078	10	5565	6	10	NULL	NULL	NULL	statement 9	Process		is stronger than					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
17079	11	5565	6	10	NULL	NULL	NULL	statement 9	Process		is stronger than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
53122	5	5565	6	10	NULL	NULL	NULL	statement 3	Process		in combination with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
53123	8	5565	6	10	NULL	NULL	NULL	RXRgamma	GP		bind							natural		PPRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
53124	9	5565	6	10	NULL	NULL	NULL	statement 3	Process		in combination with					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
16147	1	5565	7	10	NULL	NULL	NULL	PPARgamma	GP		bind							natural		PPRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
16148	2	5565	7	10	NULL	NULL	NULL	RXRgamma	GP		bind							natural		PPRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
16149	3	5565	7	10	NULL	NULL	NULL	PPARalpha	GP		bind							natural		PPRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
16150	4	5565	7	10	NULL	NULL	NULL	PPARbeta	GP		bind							natural		PPRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
16151	8	5565	7	10	NULL	NULL	NULL	statement 6	Process		is stronger than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
16152	9	5565	7	10	NULL	NULL	NULL	statement 6	Process		is stronger than					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
16153	10	5565	7	10	NULL	NULL	NULL	statement 7	Process		is stronger than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
16154	11	5565	7	10	NULL	NULL	NULL	statement 7	Process		is stronger than					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
53119	5	5565	7	10	NULL	NULL	NULL	RXRalpha	GP		bind							natural		PPRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
53120	6	5565	7	10	NULL	NULL	NULL	statement 1	Process		in combination with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
53121	7	5565	7	10	NULL	NULL	NULL	statement 1	Process		in combination with					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25252_s_6	9312141	(i) PPARgamma in combination with either RXRalpha or RXRgamma binds more strongly than PPARalpha or PPARbeta to all natural PPREs tested.	bind
17080	1	5566	6	10	NULL	NULL	NULL	Sp1	GP		bind					FP-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_49_40650_s_290	16216869	(I) promoter activity nor Sp1 binding to FP-2 by PPARgamma.	bind
16155	1	5566	7	10	NULL	NULL	NULL	 Sp1	GP		bind					FP-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_49_40650_s_290	16216869	(I) promoter activity nor Sp1 binding to FP-2 by PPARgamma.	bind
17083	1	5568	6	10	NULL	NULL	NULL	Rab1B	GP	wt	bind					REP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_242	11389151	(i) Rab1B(wt) binds to REP and is di-geranylgeranylated exclusively by GGTase II. (ii) Rab1B(Y78D) cannot bind REP and therefore fails to undergo prenylation.	bind
17084	2	5568	6	10	NULL	NULL	NULL	GGTase II	GP		di-geranylgeranylate		exclusively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_242	11389151	(i) Rab1B(wt) binds to REP and is di-geranylgeranylated exclusively by GGTase II. (ii) Rab1B(Y78D) cannot bind REP and therefore fails to undergo prenylation.	bind
17085	3	5568	6	10	NULL	NULL	NULL	Rab1B	GP		does not bind			Y78D		REP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_242	11389151	(i) Rab1B(wt) binds to REP and is di-geranylgeranylated exclusively by GGTase II. (ii) Rab1B(Y78D) cannot bind REP and therefore fails to undergo prenylation.	bind
17086	4	5568	6	10	NULL	NULL	NULL	Rab1B	GP		does not undergo			Y78D		prenylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_242	11389151	(i) Rab1B(wt) binds to REP and is di-geranylgeranylated exclusively by GGTase II. (ii) Rab1B(Y78D) cannot bind REP and therefore fails to undergo prenylation.	bind
17087	5	5568	6	10	NULL	NULL	NULL	statement 4	Process		occurs due to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_242	11389151	(i) Rab1B(wt) binds to REP and is di-geranylgeranylated exclusively by GGTase II. (ii) Rab1B(Y78D) cannot bind REP and therefore fails to undergo prenylation.	bind
16157	1	5568	7	10	NULL	NULL	NULL	Rab1B	GP	wt	bind					REP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_242	11389151	(i) Rab1B(wt) binds to REP and is di-geranylgeranylated exclusively by GGTase II. (ii) Rab1B(Y78D) cannot bind REP and therefore fails to undergo prenylation.	bind
16158	2	5568	7	10	NULL	NULL	NULL	GGTase II	GP		di-geranylgeranylates		exclusively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_242	11389151	(i) Rab1B(wt) binds to REP and is di-geranylgeranylated exclusively by GGTase II. (ii) Rab1B(Y78D) cannot bind REP and therefore fails to undergo prenylation.	bind
16159	3	5568	7	10	NULL	NULL	NULL	Rab1B	GP		does not bind			Y78D		REP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_242	11389151	(i) Rab1B(wt) binds to REP and is di-geranylgeranylated exclusively by GGTase II. (ii) Rab1B(Y78D) cannot bind REP and therefore fails to undergo prenylation.	bind
16160	4	5568	7	10	NULL	NULL	NULL	statement 3	Process		fails to undergo					prenylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_242	11389151	(i) Rab1B(wt) binds to REP and is di-geranylgeranylated exclusively by GGTase II. (ii) Rab1B(Y78D) cannot bind REP and therefore fails to undergo prenylation.	bind
17663	1	5571	6	10	NULL	NULL	NULL	SCR 8-14 	GP		inhibits		partially			SCR 8-15/PspC	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_10_5604_s_216	12228288	(i) SCR 13 and SCR 15 may come together to form the strongest PspC binding site, and this protein may partially displace the weaker binding SCR 8-14 (containing only SCR 13) from PspC. (ii) There may be an additional binding site for SCR 15 on PspC, which is distinct from the SCR 13 binding site, explaining why SCR 8-14 is only partially inhibitory of SCR 8-15/PspC binding.	bind
17721	2	5571	6	10	NULL	NULL	NULL	SCR 13	GP		bind					SCR 15	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_10_5604_s_216	12228288	(i) SCR 13 and SCR 15 may come together to form the strongest PspC binding site, and this protein may partially displace the weaker binding SCR 8-14 (containing only SCR 13) from PspC. (ii) There may be an additional binding site for SCR 15 on PspC, which is distinct from the SCR 13 binding site, explaining why SCR 8-14 is only partially inhibitory of SCR 8-15/PspC binding.	bind
17722	3	5571	6	10	NULL	NULL	NULL	statement 2	Process		forms							strongest		PspC binding site	NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_10_5604_s_216	12228288	(i) SCR 13 and SCR 15 may come together to form the strongest PspC binding site, and this protein may partially displace the weaker binding SCR 8-14 (containing only SCR 13) from PspC. (ii) There may be an additional binding site for SCR 15 on PspC, which is distinct from the SCR 13 binding site, explaining why SCR 8-14 is only partially inhibitory of SCR 8-15/PspC binding.	bind
17723	4	5571	6	10	NULL	NULL	NULL	SCR 8-14	GP		contains		only			SCR 13	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_10_5604_s_216	12228288	(i) SCR 13 and SCR 15 may come together to form the strongest PspC binding site, and this protein may partially displace the weaker binding SCR 8-14 (containing only SCR 13) from PspC. (ii) There may be an additional binding site for SCR 15 on PspC, which is distinct from the SCR 13 binding site, explaining why SCR 8-14 is only partially inhibitory of SCR 8-15/PspC binding.	bind
17724	5	5571	6	10	NULL	NULL	NULL	statement 4	Process		bind		weakly			PspC	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_10_5604_s_216	12228288	(i) SCR 13 and SCR 15 may come together to form the strongest PspC binding site, and this protein may partially displace the weaker binding SCR 8-14 (containing only SCR 13) from PspC. (ii) There may be an additional binding site for SCR 15 on PspC, which is distinct from the SCR 13 binding site, explaining why SCR 8-14 is only partially inhibitory of SCR 8-15/PspC binding.	bind
17725	6	5571	6	10	NULL	NULL	NULL	statement 3	Process		displace		may;; partially			statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_10_5604_s_216	12228288	(i) SCR 13 and SCR 15 may come together to form the strongest PspC binding site, and this protein may partially displace the weaker binding SCR 8-14 (containing only SCR 13) from PspC. (ii) There may be an additional binding site for SCR 15 on PspC, which is distinct from the SCR 13 binding site, explaining why SCR 8-14 is only partially inhibitory of SCR 8-15/PspC binding.	bind
16161	1	5571	7	10	NULL	NULL	NULL	SCR 13 	GP		bind 					SCR 15	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_10_5604_s_216	12228288	(i) SCR 13 and SCR 15 may come together to form the strongest PspC binding site, and this protein may partially displace the weaker binding SCR 8-14 (containing only SCR 13) from PspC. (ii) There may be an additional binding site for SCR 15 on PspC, which is distinct from the SCR 13 binding site, explaining why SCR 8-14 is only partially inhibitory of SCR 8-15/PspC binding.	bind
16162	2	5571	7	10	NULL	NULL	NULL	statement 1	Process		forms							strongest	PspC binding site		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_10_5604_s_216	12228288	(i) SCR 13 and SCR 15 may come together to form the strongest PspC binding site, and this protein may partially displace the weaker binding SCR 8-14 (containing only SCR 13) from PspC. (ii) There may be an additional binding site for SCR 15 on PspC, which is distinct from the SCR 13 binding site, explaining why SCR 8-14 is only partially inhibitory of SCR 8-15/PspC binding.	bind
16163	4	5571	7	10	NULL	NULL	NULL	statement 2	Process		displace		may;;partially			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_10_5604_s_216	12228288	(i) SCR 13 and SCR 15 may come together to form the strongest PspC binding site, and this protein may partially displace the weaker binding SCR 8-14 (containing only SCR 13) from PspC. (ii) There may be an additional binding site for SCR 15 on PspC, which is distinct from the SCR 13 binding site, explaining why SCR 8-14 is only partially inhibitory of SCR 8-15/PspC binding.	bind
16164	5	5571	7	10	NULL	NULL	NULL	statement 3	Process		contains only					SCR 13	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_10_5604_s_216	12228288	(i) SCR 13 and SCR 15 may come together to form the strongest PspC binding site, and this protein may partially displace the weaker binding SCR 8-14 (containing only SCR 13) from PspC. (ii) There may be an additional binding site for SCR 15 on PspC, which is distinct from the SCR 13 binding site, explaining why SCR 8-14 is only partially inhibitory of SCR 8-15/PspC binding.	bind
16165	6	5571	7	10	NULL	NULL	NULL	SCR 8-15	GP		bind					PspC	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_10_5604_s_216	12228288	(i) SCR 13 and SCR 15 may come together to form the strongest PspC binding site, and this protein may partially displace the weaker binding SCR 8-14 (containing only SCR 13) from PspC. (ii) There may be an additional binding site for SCR 15 on PspC, which is distinct from the SCR 13 binding site, explaining why SCR 8-14 is only partially inhibitory of SCR 8-15/PspC binding.	bind
16166	7	5571	7	10	NULL	NULL	NULL	SCR 8-14	GP		inhibits		partially			SCR 8-15/PspC	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_10_5604_s_216	12228288	(i) SCR 13 and SCR 15 may come together to form the strongest PspC binding site, and this protein may partially displace the weaker binding SCR 8-14 (containing only SCR 13) from PspC. (ii) There may be an additional binding site for SCR 15 on PspC, which is distinct from the SCR 13 binding site, explaining why SCR 8-14 is only partially inhibitory of SCR 8-15/PspC binding.	bind
44934	3	5571	7	10	NULL	NULL	NULL	SCR 8-14	GP		bind		weakly			PspC	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_10_5604_s_216	12228288	(i) SCR 13 and SCR 15 may come together to form the strongest PspC binding site, and this protein may partially displace the weaker binding SCR 8-14 (containing only SCR 13) from PspC. (ii) There may be an additional binding site for SCR 15 on PspC, which is distinct from the SCR 13 binding site, explaining why SCR 8-14 is only partially inhibitory of SCR 8-15/PspC binding.	bind
17157	1	5572	6	10	NULL	NULL	NULL	Actin	GP		bind					Kelch	GP	nonphosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_156_4_703_s_86	11854310	(I) showed that actin was bound only to the nonphosphorylated form of Kelch.	bind
16167	1	5572	7	10	NULL	NULL	NULL	actin	GP		bind					Kelch	GP	nonphosphorylated 			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_156_4_703_s_86	11854310	(I) showed that actin was bound only to the nonphosphorylated form of Kelch.	bind
17158	1	5573	6	10	NULL	NULL	NULL	TFIIB	GP		bind		robustly			Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_19_6958_s_286	12972613	(I) site in DAPA revealed robust binding of TFIIB to the Sp1	bind
16168	1	5573	7	10	NULL	NULL	NULL	 TFIIB	GP		bind		robustly			Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_19_6958_s_286	12972613	(I) site in DAPA revealed robust binding of TFIIB to the Sp1	bind
17159	1	5574	6	10	NULL	NULL	NULL	Stat5B	GP		bind					insulin receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_253	10821852	(i) Stat5B binds to the insulin receptor, as shown by a yeast two-hybrid assay.	bind
16170	1	5574	7	10	NULL	NULL	NULL	 Stat5B	GP		binds to					insulin receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_253	10821852	(i) Stat5B binds to the insulin receptor, as shown by a yeast two-hybrid assay.	bind
20034	1	5575	6	10	NULL	NULL	NULL	poly L-proline	AminoAcid		does not bind					type II prolyl 4-hydroxylase tetramer	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_2_306_s_177	9889187	(I) subunit by glutamate and glutamine, respectively, in the alpha(II) subunit appears to explain most of the lack of poly(L-proline) binding of the type II prolyl 4-hydroxylase tetramer.	bind
16171	1	5575	7	10	NULL	NULL	NULL	poly L-proline	AminoAcid		does not bind					type II prolyl 4-hydroxylase tetramer	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_2_306_s_177	9889187	(I) subunit by glutamate and glutamine, respectively, in the alpha(II) subunit appears to explain most of the lack of poly(L-proline) binding of the type II prolyl 4-hydroxylase tetramer.	bind
17160	1	5577	6	10	NULL	NULL	NULL	At-P4H-1	GP		bind			Lys270		2-oxoglutarate	Chemical		C-5 carboxyl group		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_26_23965_s_130	11976332	(I) subunit, the At-P4H-1 Lys270 corresponds to the lysine that binds the C-5 carboxyl group of 2-oxoglutarate, and the At-P4H-1 Arg278 corresponds to the fifth critical residue, a histidine or an arginine depending on the species, which is probably involved in both the binding of the C-1 carboxyl group of 2-oxoglutarate to the Fe2+ atom and the decarboxylation of this cosubstrate ( 12,  26,  34).	bind
17167	2	5577	6	10	NULL	NULL	NULL	2-oxoglutarate	Chemical		bind			C-1 carboxyl group		Fe+2 atom	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_26_23965_s_130	11976332	(I) subunit, the At-P4H-1 Lys270 corresponds to the lysine that binds the C-5 carboxyl group of 2-oxoglutarate, and the At-P4H-1 Arg278 corresponds to the fifth critical residue, a histidine or an arginine depending on the species, which is probably involved in both the binding of the C-1 carboxyl group of 2-oxoglutarate to the Fe2+ atom and the decarboxylation of this cosubstrate ( 12,  26,  34).	bind
17187	3	5577	6	10	NULL	NULL	NULL	At-P4H-1	GP		is involved in			Arg278		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_26_23965_s_130	11976332	(I) subunit, the At-P4H-1 Lys270 corresponds to the lysine that binds the C-5 carboxyl group of 2-oxoglutarate, and the At-P4H-1 Arg278 corresponds to the fifth critical residue, a histidine or an arginine depending on the species, which is probably involved in both the binding of the C-1 carboxyl group of 2-oxoglutarate to the Fe2+ atom and the decarboxylation of this cosubstrate ( 12,  26,  34).	bind
17188	4	5577	6	10	NULL	NULL	NULL	At-P4H-1	GP		is involved in			Arg278		cosubstrate	Chemical	decarboxylation of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_26_23965_s_130	11976332	(I) subunit, the At-P4H-1 Lys270 corresponds to the lysine that binds the C-5 carboxyl group of 2-oxoglutarate, and the At-P4H-1 Arg278 corresponds to the fifth critical residue, a histidine or an arginine depending on the species, which is probably involved in both the binding of the C-1 carboxyl group of 2-oxoglutarate to the Fe2+ atom and the decarboxylation of this cosubstrate ( 12,  26,  34).	bind
16172	1	5577	7	10	NULL	NULL	NULL	At-P4H-1 	GP		binds			Lys270		2-oxoglutarate	Chemical		C-5 carboxyl group		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_26_23965_s_130	11976332	(I) subunit, the At-P4H-1 Lys270 corresponds to the lysine that binds the C-5 carboxyl group of 2-oxoglutarate, and the At-P4H-1 Arg278 corresponds to the fifth critical residue, a histidine or an arginine depending on the species, which is probably involved in both the binding of the C-1 carboxyl group of 2-oxoglutarate to the Fe2+ atom and the decarboxylation of this cosubstrate ( 12,  26,  34).	bind
16173	2	5577	7	10	NULL	NULL	NULL	2-oxoglutarate	Chemical		binds			C-1 carboxyl group		Fe2+ atom	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_26_23965_s_130	11976332	(I) subunit, the At-P4H-1 Lys270 corresponds to the lysine that binds the C-5 carboxyl group of 2-oxoglutarate, and the At-P4H-1 Arg278 corresponds to the fifth critical residue, a histidine or an arginine depending on the species, which is probably involved in both the binding of the C-1 carboxyl group of 2-oxoglutarate to the Fe2+ atom and the decarboxylation of this cosubstrate ( 12,  26,  34).	bind
16174	3	5577	7	10	NULL	NULL	NULL	At-P4H-1	GP		is involved in			Arg278		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_26_23965_s_130	11976332	(I) subunit, the At-P4H-1 Lys270 corresponds to the lysine that binds the C-5 carboxyl group of 2-oxoglutarate, and the At-P4H-1 Arg278 corresponds to the fifth critical residue, a histidine or an arginine depending on the species, which is probably involved in both the binding of the C-1 carboxyl group of 2-oxoglutarate to the Fe2+ atom and the decarboxylation of this cosubstrate ( 12,  26,  34).	bind
16175	4	5577	7	10	NULL	NULL	NULL	At-P4H-1	GP		is involved in			Arg278		cosubstrate	Chemical	decarboxylation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_26_23965_s_130	11976332	(I) subunit, the At-P4H-1 Lys270 corresponds to the lysine that binds the C-5 carboxyl group of 2-oxoglutarate, and the At-P4H-1 Arg278 corresponds to the fifth critical residue, a histidine or an arginine depending on the species, which is probably involved in both the binding of the C-1 carboxyl group of 2-oxoglutarate to the Fe2+ atom and the decarboxylation of this cosubstrate ( 12,  26,  34).	bind
17189	1	5578	6	10	NULL	NULL	NULL	Sxl protein	GP		bind					msl-2 mRNA	NucleicAcid			3'UTR	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_3018_s_264	10082569	(i) Sxl protein binds to the 3' UTRs of  msl-2 and  Sxl mRNAs in vivo.	bind
17190	2	5578	6	10	NULL	NULL	NULL	Sxl protein	GP		bind					Sxl mRNA	NucleicAcid			3' UTR	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_3018_s_264	10082569	(i) Sxl protein binds to the 3' UTRs of  msl-2 and  Sxl mRNAs in vivo.	bind
16176	1	5578	7	10	NULL	NULL	NULL	Sxl protein	GP		bind					 msl-2 mRNA	NucleicAcid			 3' UTRs	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_3018_s_264	10082569	(i) Sxl protein binds to the 3' UTRs of  msl-2 and  Sxl mRNAs in vivo.	bind
16177	2	5578	7	10	NULL	NULL	NULL	Sxl protein	GP		bind					Sxl mRNA	NucleicAcid			 3' UTRs	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_3018_s_264	10082569	(i) Sxl protein binds to the 3' UTRs of  msl-2 and  Sxl mRNAs in vivo.	bind
17191	1	5579	6	10	NULL	NULL	NULL	ADR1	GP		bind			TADIV		TFIID components	GP	yeast			NULL	yeast crude extracts	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5861_s_193	9742103	(i) TADIV of ADR1 binds TFIID components from yeast crude extracts; (ii) the ability of derivatives of TADIV to bind TFIID components correlates with TADIV activation potential; (iii) deletion of TADIV from ADR1 severely compromises ADR1 function; (iv) the transcriptional potential of LexA-ADR1-TADIV was more severely compromised than that of other activation domains by a  taf130/145 allele; (v) ADR1 coimmunoprecipitates with either TAFII90 or TBP; and (vi) TFIID appears to be required for ADR1-dependent activation of  ADH2 in vivo, as depletion of yeast cells of TAFII90 prevents  ADH2 derepression.	bind
17664	2	5579	6	10	NULL	NULL	NULL	statement 1	Process		corelates with					TADIV	GP	activation potential of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5861_s_193	9742103	(i) TADIV of ADR1 binds TFIID components from yeast crude extracts; (ii) the ability of derivatives of TADIV to bind TFIID components correlates with TADIV activation potential; (iii) deletion of TADIV from ADR1 severely compromises ADR1 function; (iv) the transcriptional potential of LexA-ADR1-TADIV was more severely compromised than that of other activation domains by a  taf130/145 allele; (v) ADR1 coimmunoprecipitates with either TAFII90 or TBP; and (vi) TFIID appears to be required for ADR1-dependent activation of  ADH2 in vivo, as depletion of yeast cells of TAFII90 prevents  ADH2 derepression.	bind
17665	3	5579	6	10	NULL	NULL	NULL	ADR1	GP	deletion of	compromises		severely	TADIV		ADR1	GP	function of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5861_s_193	9742103	(i) TADIV of ADR1 binds TFIID components from yeast crude extracts; (ii) the ability of derivatives of TADIV to bind TFIID components correlates with TADIV activation potential; (iii) deletion of TADIV from ADR1 severely compromises ADR1 function; (iv) the transcriptional potential of LexA-ADR1-TADIV was more severely compromised than that of other activation domains by a  taf130/145 allele; (v) ADR1 coimmunoprecipitates with either TAFII90 or TBP; and (vi) TFIID appears to be required for ADR1-dependent activation of  ADH2 in vivo, as depletion of yeast cells of TAFII90 prevents  ADH2 derepression.	bind
17666	4	5579	6	10	NULL	NULL	NULL	ADR1	GP		coimmunoprecipates with					TAFII90	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5861_s_193	9742103	(i) TADIV of ADR1 binds TFIID components from yeast crude extracts; (ii) the ability of derivatives of TADIV to bind TFIID components correlates with TADIV activation potential; (iii) deletion of TADIV from ADR1 severely compromises ADR1 function; (iv) the transcriptional potential of LexA-ADR1-TADIV was more severely compromised than that of other activation domains by a  taf130/145 allele; (v) ADR1 coimmunoprecipitates with either TAFII90 or TBP; and (vi) TFIID appears to be required for ADR1-dependent activation of  ADH2 in vivo, as depletion of yeast cells of TAFII90 prevents  ADH2 derepression.	bind
17667	5	5579	6	10	NULL	NULL	NULL	ADR1	GP		coimmunoprecipitates with					TBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5861_s_193	9742103	(i) TADIV of ADR1 binds TFIID components from yeast crude extracts; (ii) the ability of derivatives of TADIV to bind TFIID components correlates with TADIV activation potential; (iii) deletion of TADIV from ADR1 severely compromises ADR1 function; (iv) the transcriptional potential of LexA-ADR1-TADIV was more severely compromised than that of other activation domains by a  taf130/145 allele; (v) ADR1 coimmunoprecipitates with either TAFII90 or TBP; and (vi) TFIID appears to be required for ADR1-dependent activation of  ADH2 in vivo, as depletion of yeast cells of TAFII90 prevents  ADH2 derepression.	bind
17668	6	5579	6	10	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5861_s_193	9742103	(i) TADIV of ADR1 binds TFIID components from yeast crude extracts; (ii) the ability of derivatives of TADIV to bind TFIID components correlates with TADIV activation potential; (iii) deletion of TADIV from ADR1 severely compromises ADR1 function; (iv) the transcriptional potential of LexA-ADR1-TADIV was more severely compromised than that of other activation domains by a  taf130/145 allele; (v) ADR1 coimmunoprecipitates with either TAFII90 or TBP; and (vi) TFIID appears to be required for ADR1-dependent activation of  ADH2 in vivo, as depletion of yeast cells of TAFII90 prevents  ADH2 derepression.	bind
17669	7	5579	6	10	NULL	NULL	NULL	ADH2	GP	activation of	is dependent on					ADR1	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5861_s_193	9742103	(i) TADIV of ADR1 binds TFIID components from yeast crude extracts; (ii) the ability of derivatives of TADIV to bind TFIID components correlates with TADIV activation potential; (iii) deletion of TADIV from ADR1 severely compromises ADR1 function; (iv) the transcriptional potential of LexA-ADR1-TADIV was more severely compromised than that of other activation domains by a  taf130/145 allele; (v) ADR1 coimmunoprecipitates with either TAFII90 or TBP; and (vi) TFIID appears to be required for ADR1-dependent activation of  ADH2 in vivo, as depletion of yeast cells of TAFII90 prevents  ADH2 derepression.	bind
17670	8	5579	6	10	NULL	NULL	NULL	TFIID	GP		is required for					statement 7	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5861_s_193	9742103	(i) TADIV of ADR1 binds TFIID components from yeast crude extracts; (ii) the ability of derivatives of TADIV to bind TFIID components correlates with TADIV activation potential; (iii) deletion of TADIV from ADR1 severely compromises ADR1 function; (iv) the transcriptional potential of LexA-ADR1-TADIV was more severely compromised than that of other activation domains by a  taf130/145 allele; (v) ADR1 coimmunoprecipitates with either TAFII90 or TBP; and (vi) TFIID appears to be required for ADR1-dependent activation of  ADH2 in vivo, as depletion of yeast cells of TAFII90 prevents  ADH2 derepression.	bind
17726	9	5579	6	10	NULL	NULL	NULL	TAFII90	GP	depletion of	prevents					ADH2	GP	depression of			NULL	yeast cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5861_s_193	9742103	(i) TADIV of ADR1 binds TFIID components from yeast crude extracts; (ii) the ability of derivatives of TADIV to bind TFIID components correlates with TADIV activation potential; (iii) deletion of TADIV from ADR1 severely compromises ADR1 function; (iv) the transcriptional potential of LexA-ADR1-TADIV was more severely compromised than that of other activation domains by a  taf130/145 allele; (v) ADR1 coimmunoprecipitates with either TAFII90 or TBP; and (vi) TFIID appears to be required for ADR1-dependent activation of  ADH2 in vivo, as depletion of yeast cells of TAFII90 prevents  ADH2 derepression.	bind
16178	1	5579	7	10	NULL	NULL	NULL	ADR1	GP		binds			TADIV		TFIID components	GP				NULL	yeast crude extract	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5861_s_193	9742103	(i) TADIV of ADR1 binds TFIID components from yeast crude extracts; (ii) the ability of derivatives of TADIV to bind TFIID components correlates with TADIV activation potential; (iii) deletion of TADIV from ADR1 severely compromises ADR1 function; (iv) the transcriptional potential of LexA-ADR1-TADIV was more severely compromised than that of other activation domains by a  taf130/145 allele; (v) ADR1 coimmunoprecipitates with either TAFII90 or TBP; and (vi) TFIID appears to be required for ADR1-dependent activation of  ADH2 in vivo, as depletion of yeast cells of TAFII90 prevents  ADH2 derepression.	bind
16179	2	5579	7	10	NULL	NULL	NULL	statement 1	Process		correlates with							activation potential	TADIV 		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5861_s_193	9742103	(i) TADIV of ADR1 binds TFIID components from yeast crude extracts; (ii) the ability of derivatives of TADIV to bind TFIID components correlates with TADIV activation potential; (iii) deletion of TADIV from ADR1 severely compromises ADR1 function; (iv) the transcriptional potential of LexA-ADR1-TADIV was more severely compromised than that of other activation domains by a  taf130/145 allele; (v) ADR1 coimmunoprecipitates with either TAFII90 or TBP; and (vi) TFIID appears to be required for ADR1-dependent activation of  ADH2 in vivo, as depletion of yeast cells of TAFII90 prevents  ADH2 derepression.	bind
16180	3	5579	7	10	NULL	NULL	NULL	ADR1	GP	deletion of	compromise		severely	TADIV 		ADR1	GP	function of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5861_s_193	9742103	(i) TADIV of ADR1 binds TFIID components from yeast crude extracts; (ii) the ability of derivatives of TADIV to bind TFIID components correlates with TADIV activation potential; (iii) deletion of TADIV from ADR1 severely compromises ADR1 function; (iv) the transcriptional potential of LexA-ADR1-TADIV was more severely compromised than that of other activation domains by a  taf130/145 allele; (v) ADR1 coimmunoprecipitates with either TAFII90 or TBP; and (vi) TFIID appears to be required for ADR1-dependent activation of  ADH2 in vivo, as depletion of yeast cells of TAFII90 prevents  ADH2 derepression.	bind
16186	5	5579	7	10	NULL	NULL	NULL	ADR1	GP		\tcoimmunoprecipitates with					TAFII90	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5861_s_193	9742103	(i) TADIV of ADR1 binds TFIID components from yeast crude extracts; (ii) the ability of derivatives of TADIV to bind TFIID components correlates with TADIV activation potential; (iii) deletion of TADIV from ADR1 severely compromises ADR1 function; (iv) the transcriptional potential of LexA-ADR1-TADIV was more severely compromised than that of other activation domains by a  taf130/145 allele; (v) ADR1 coimmunoprecipitates with either TAFII90 or TBP; and (vi) TFIID appears to be required for ADR1-dependent activation of  ADH2 in vivo, as depletion of yeast cells of TAFII90 prevents  ADH2 derepression.	bind
16187	6	5579	7	10	NULL	NULL	NULL	ADR1	GP		\tcoimmunoprecipitates with					TBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5861_s_193	9742103	(i) TADIV of ADR1 binds TFIID components from yeast crude extracts; (ii) the ability of derivatives of TADIV to bind TFIID components correlates with TADIV activation potential; (iii) deletion of TADIV from ADR1 severely compromises ADR1 function; (iv) the transcriptional potential of LexA-ADR1-TADIV was more severely compromised than that of other activation domains by a  taf130/145 allele; (v) ADR1 coimmunoprecipitates with either TAFII90 or TBP; and (vi) TFIID appears to be required for ADR1-dependent activation of  ADH2 in vivo, as depletion of yeast cells of TAFII90 prevents  ADH2 derepression.	bind
16188	7	5579	7	10	NULL	NULL	NULL	ADH2	GP	activation of	is dependent on					ADR1	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5861_s_193	9742103	(i) TADIV of ADR1 binds TFIID components from yeast crude extracts; (ii) the ability of derivatives of TADIV to bind TFIID components correlates with TADIV activation potential; (iii) deletion of TADIV from ADR1 severely compromises ADR1 function; (iv) the transcriptional potential of LexA-ADR1-TADIV was more severely compromised than that of other activation domains by a  taf130/145 allele; (v) ADR1 coimmunoprecipitates with either TAFII90 or TBP; and (vi) TFIID appears to be required for ADR1-dependent activation of  ADH2 in vivo, as depletion of yeast cells of TAFII90 prevents  ADH2 derepression.	bind
16189	8	5579	7	10	NULL	NULL	NULL	TFIID	GP		is required for					statement 7	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5861_s_193	9742103	(i) TADIV of ADR1 binds TFIID components from yeast crude extracts; (ii) the ability of derivatives of TADIV to bind TFIID components correlates with TADIV activation potential; (iii) deletion of TADIV from ADR1 severely compromises ADR1 function; (iv) the transcriptional potential of LexA-ADR1-TADIV was more severely compromised than that of other activation domains by a  taf130/145 allele; (v) ADR1 coimmunoprecipitates with either TAFII90 or TBP; and (vi) TFIID appears to be required for ADR1-dependent activation of  ADH2 in vivo, as depletion of yeast cells of TAFII90 prevents  ADH2 derepression.	bind
16190	9	5579	7	10	NULL	NULL	NULL	TAFII90	GP	depletion of	prevents					ADH2	GP	derepression of			NULL	yeast cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5861_s_193	9742103	(i) TADIV of ADR1 binds TFIID components from yeast crude extracts; (ii) the ability of derivatives of TADIV to bind TFIID components correlates with TADIV activation potential; (iii) deletion of TADIV from ADR1 severely compromises ADR1 function; (iv) the transcriptional potential of LexA-ADR1-TADIV was more severely compromised than that of other activation domains by a  taf130/145 allele; (v) ADR1 coimmunoprecipitates with either TAFII90 or TBP; and (vi) TFIID appears to be required for ADR1-dependent activation of  ADH2 in vivo, as depletion of yeast cells of TAFII90 prevents  ADH2 derepression.	bind
17771	10	5579	7	10	NULL	NULL	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_5861_s_193	9742103	(i) TADIV of ADR1 binds TFIID components from yeast crude extracts; (ii) the ability of derivatives of TADIV to bind TFIID components correlates with TADIV activation potential; (iii) deletion of TADIV from ADR1 severely compromises ADR1 function; (iv) the transcriptional potential of LexA-ADR1-TADIV was more severely compromised than that of other activation domains by a  taf130/145 allele; (v) ADR1 coimmunoprecipitates with either TAFII90 or TBP; and (vi) TFIID appears to be required for ADR1-dependent activation of  ADH2 in vivo, as depletion of yeast cells of TAFII90 prevents  ADH2 derepression.	bind
17671	1	5580	6	10	NULL	NULL	NULL	CheY	GP		bind					CheZ	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7357_s_57	8631757	(i) The  CheY(N23D) mutant protein is impaired in its interaction with CheZ,  thus affecting the ability of CheZ to bind and dephosphorylate it; or  (ii) the binding of CheY(N23D) to CheZ is stronger compared to  wild-type CheY, so that most of the CheZ present in the reaction would  be ```sequestered'''  leaving residual CheY(N23D), which would  be dephosphorylated only by spontaneous hydrolysis.	bind
17672	2	5580	6	10	NULL	NULL	NULL	CheY	GP	mutant	affects			N23D		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7357_s_57	8631757	(i) The  CheY(N23D) mutant protein is impaired in its interaction with CheZ,  thus affecting the ability of CheZ to bind and dephosphorylate it; or  (ii) the binding of CheY(N23D) to CheZ is stronger compared to  wild-type CheY, so that most of the CheZ present in the reaction would  be ```sequestered'''  leaving residual CheY(N23D), which would  be dephosphorylated only by spontaneous hydrolysis.	bind
17673	3	5580	6	10	NULL	NULL	NULL	CheZ	GP		dephosphorylate					CheY	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7357_s_57	8631757	(i) The  CheY(N23D) mutant protein is impaired in its interaction with CheZ,  thus affecting the ability of CheZ to bind and dephosphorylate it; or  (ii) the binding of CheY(N23D) to CheZ is stronger compared to  wild-type CheY, so that most of the CheZ present in the reaction would  be ```sequestered'''  leaving residual CheY(N23D), which would  be dephosphorylated only by spontaneous hydrolysis.	bind
17674	4	5580	6	10	NULL	NULL	NULL	CheY	GP	mutant	affects			N23D		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7357_s_57	8631757	(i) The  CheY(N23D) mutant protein is impaired in its interaction with CheZ,  thus affecting the ability of CheZ to bind and dephosphorylate it; or  (ii) the binding of CheY(N23D) to CheZ is stronger compared to  wild-type CheY, so that most of the CheZ present in the reaction would  be ```sequestered'''  leaving residual CheY(N23D), which would  be dephosphorylated only by spontaneous hydrolysis.	bind
17675	5	5580	6	10	NULL	NULL	NULL	CheY	GP	mutant	bind			N23D		CheZ	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7357_s_57	8631757	(i) The  CheY(N23D) mutant protein is impaired in its interaction with CheZ,  thus affecting the ability of CheZ to bind and dephosphorylate it; or  (ii) the binding of CheY(N23D) to CheZ is stronger compared to  wild-type CheY, so that most of the CheZ present in the reaction would  be ```sequestered'''  leaving residual CheY(N23D), which would  be dephosphorylated only by spontaneous hydrolysis.	bind
17676	6	5580	6	10	NULL	NULL	NULL	CheY	GP	wild type	bind					CheZ	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7357_s_57	8631757	(i) The  CheY(N23D) mutant protein is impaired in its interaction with CheZ,  thus affecting the ability of CheZ to bind and dephosphorylate it; or  (ii) the binding of CheY(N23D) to CheZ is stronger compared to  wild-type CheY, so that most of the CheZ present in the reaction would  be ```sequestered'''  leaving residual CheY(N23D), which would  be dephosphorylated only by spontaneous hydrolysis.	bind
17677	7	5580	6	10	NULL	NULL	NULL	statement 5	Process		is stronger than					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7357_s_57	8631757	(i) The  CheY(N23D) mutant protein is impaired in its interaction with CheZ,  thus affecting the ability of CheZ to bind and dephosphorylate it; or  (ii) the binding of CheY(N23D) to CheZ is stronger compared to  wild-type CheY, so that most of the CheZ present in the reaction would  be ```sequestered'''  leaving residual CheY(N23D), which would  be dephosphorylated only by spontaneous hydrolysis.	bind
20035	8	5580	6	10	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7357_s_57	8631757	(i) The  CheY(N23D) mutant protein is impaired in its interaction with CheZ,  thus affecting the ability of CheZ to bind and dephosphorylate it; or  (ii) the binding of CheY(N23D) to CheZ is stronger compared to  wild-type CheY, so that most of the CheZ present in the reaction would  be ```sequestered'''  leaving residual CheY(N23D), which would  be dephosphorylated only by spontaneous hydrolysis.	bind
16191	1	5580	7	10	NULL	NULL	NULL	CheY	GP	mutant	impairs			N23D		CheZ	GP	interaction of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7357_s_57	8631757	(i) The  CheY(N23D) mutant protein is impaired in its interaction with CheZ,  thus affecting the ability of CheZ to bind and dephosphorylate it; or  (ii) the binding of CheY(N23D) to CheZ is stronger compared to  wild-type CheY, so that most of the CheZ present in the reaction would  be ```sequestered'''  leaving residual CheY(N23D), which would  be dephosphorylated only by spontaneous hydrolysis.	bind
16192	2	5580	7	10	NULL	NULL	NULL	statement 1	Process		affects					CheZ	GP	the binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7357_s_57	8631757	(i) The  CheY(N23D) mutant protein is impaired in its interaction with CheZ,  thus affecting the ability of CheZ to bind and dephosphorylate it; or  (ii) the binding of CheY(N23D) to CheZ is stronger compared to  wild-type CheY, so that most of the CheZ present in the reaction would  be ```sequestered'''  leaving residual CheY(N23D), which would  be dephosphorylated only by spontaneous hydrolysis.	bind
16193	3	5580	7	10	NULL	NULL	NULL	CheZ	GP		dephosphorylates					CheY	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7357_s_57	8631757	(i) The  CheY(N23D) mutant protein is impaired in its interaction with CheZ,  thus affecting the ability of CheZ to bind and dephosphorylate it; or  (ii) the binding of CheY(N23D) to CheZ is stronger compared to  wild-type CheY, so that most of the CheZ present in the reaction would  be ```sequestered'''  leaving residual CheY(N23D), which would  be dephosphorylated only by spontaneous hydrolysis.	bind
16196	8	5580	7	10	NULL	NULL	NULL	statement 5	Process		leaves behind					CheY	GP	 residual	N23D		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7357_s_57	8631757	(i) The  CheY(N23D) mutant protein is impaired in its interaction with CheZ,  thus affecting the ability of CheZ to bind and dephosphorylate it; or  (ii) the binding of CheY(N23D) to CheZ is stronger compared to  wild-type CheY, so that most of the CheZ present in the reaction would  be ```sequestered'''  leaving residual CheY(N23D), which would  be dephosphorylated only by spontaneous hydrolysis.	bind
16197	9	5580	7	10	NULL	NULL	NULL	CheY	GP	residual	dephosphorylated by		only	N23D		hydrolysis	Process	spontaneous			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7357_s_57	8631757	(i) The  CheY(N23D) mutant protein is impaired in its interaction with CheZ,  thus affecting the ability of CheZ to bind and dephosphorylate it; or  (ii) the binding of CheY(N23D) to CheZ is stronger compared to  wild-type CheY, so that most of the CheZ present in the reaction would  be ```sequestered'''  leaving residual CheY(N23D), which would  be dephosphorylated only by spontaneous hydrolysis.	bind
16198	10	5580	7	10	NULL	NULL	NULL	statement 8	Process		leads to					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7357_s_57	8631757	(i) The  CheY(N23D) mutant protein is impaired in its interaction with CheZ,  thus affecting the ability of CheZ to bind and dephosphorylate it; or  (ii) the binding of CheY(N23D) to CheZ is stronger compared to  wild-type CheY, so that most of the CheZ present in the reaction would  be ```sequestered'''  leaving residual CheY(N23D), which would  be dephosphorylated only by spontaneous hydrolysis.	bind
16305	4	5580	7	10	NULL	NULL	NULL	statement 1	Process		affects					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7357_s_57	8631757	(i) The  CheY(N23D) mutant protein is impaired in its interaction with CheZ,  thus affecting the ability of CheZ to bind and dephosphorylate it; or  (ii) the binding of CheY(N23D) to CheZ is stronger compared to  wild-type CheY, so that most of the CheZ present in the reaction would  be ```sequestered'''  leaving residual CheY(N23D), which would  be dephosphorylated only by spontaneous hydrolysis.	bind
20095	5	5580	7	10	NULL	NULL	NULL	CheY	GP	mutant	binds			N23D		CheZ	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7357_s_57	8631757	(i) The  CheY(N23D) mutant protein is impaired in its interaction with CheZ,  thus affecting the ability of CheZ to bind and dephosphorylate it; or  (ii) the binding of CheY(N23D) to CheZ is stronger compared to  wild-type CheY, so that most of the CheZ present in the reaction would  be ```sequestered'''  leaving residual CheY(N23D), which would  be dephosphorylated only by spontaneous hydrolysis.	bind
20096	6	5580	7	10	NULL	NULL	NULL	CheY	GP	wild-type	binds					CheZ	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7357_s_57	8631757	(i) The  CheY(N23D) mutant protein is impaired in its interaction with CheZ,  thus affecting the ability of CheZ to bind and dephosphorylate it; or  (ii) the binding of CheY(N23D) to CheZ is stronger compared to  wild-type CheY, so that most of the CheZ present in the reaction would  be ```sequestered'''  leaving residual CheY(N23D), which would  be dephosphorylated only by spontaneous hydrolysis.	bind
20097	7	5580	7	10	NULL	NULL	NULL	statement 5	Process		is stronger					statement 6	Process	compared to			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7357_s_57	8631757	(i) The  CheY(N23D) mutant protein is impaired in its interaction with CheZ,  thus affecting the ability of CheZ to bind and dephosphorylate it; or  (ii) the binding of CheY(N23D) to CheZ is stronger compared to  wild-type CheY, so that most of the CheZ present in the reaction would  be ```sequestered'''  leaving residual CheY(N23D), which would  be dephosphorylated only by spontaneous hydrolysis.	bind
17236	1	5581	6	10	NULL	NULL	NULL				bind			CI		ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_2017_s_264	16628225	(i) The ATP binding modes between CI and CII differ ( Figure 1B) (  et al).	bind
17237	2	5581	6	10	NULL	NULL	NULL				bind			CII		ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_2017_s_264	16628225	(i) The ATP binding modes between CI and CII differ ( Figure 1B) (  et al).	bind
20036	3	5581	6	10	NULL	NULL	NULL	statement 1	Process	binding mode of	is different from					statement 2	Process	binding mode of 			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_2017_s_264	16628225	(i) The ATP binding modes between CI and CII differ ( Figure 1B) (  et al).	bind
16202	1	5581	7	10	NULL	NULL	NULL	ATP	Chemical		bind								CI		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_2017_s_264	16628225	(i) The ATP binding modes between CI and CII differ ( Figure 1B) (  et al).	bind
16203	2	5581	7	10	NULL	NULL	NULL	ATP	Chemical		bind								CII		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_2017_s_264	16628225	(i) The ATP binding modes between CI and CII differ ( Figure 1B) (  et al).	bind
16205	3	5581	7	10	NULL	NULL	NULL	statement 1	Process	binding mode of	differs with					statement 2	Process	binding mode of			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_2017_s_264	16628225	(i) The ATP binding modes between CI and CII differ ( Figure 1B) (  et al).	bind
17316	1	5582	6	10	NULL	NULL	NULL	ASF-1	GP		bind									as-1 element	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_775_s_171	11809891	(i) The binding affinity of ASF-1 and different TGA factors to the  as-1 element is highest if the spacing between the two palindromes is either 10 or 12 bp.	bind
17317	2	5582	6	10	NULL	NULL	NULL	TGA factors	GP		bind									as-1 element	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_775_s_171	11809891	(i) The binding affinity of ASF-1 and different TGA factors to the  as-1 element is highest if the spacing between the two palindromes is either 10 or 12 bp.	bind
16209	1	5582	7	10	NULL	NULL	NULL	ASF-1	GP		bind									as-1 element	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_775_s_171	11809891	(i) The binding affinity of ASF-1 and different TGA factors to the  as-1 element is highest if the spacing between the two palindromes is either 10 or 12 bp.	bind
16210	2	5582	7	10	NULL	NULL	NULL	TGA factors	GP		bind									as-1 element	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_775_s_171	11809891	(i) The binding affinity of ASF-1 and different TGA factors to the  as-1 element is highest if the spacing between the two palindromes is either 10 or 12 bp.	bind
17318	1	5583	6	10	NULL	NULL	NULL	alpha-Syn	GP		bind					phospholipids	Chemical	acidic			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_44_34328_s_135	10915790	(i) The binding of alpha-Syn with acidic phospholipids is dose-dependent; (ii) the extent of lipid binding depends rather on the availability of the phospholipids than on the size of lipid vesicles (SUVs  versus MLVs); (iii) alpha-Syn binding to phospholipid vesicles increases drastically when an acidic phospholipid is mixed with PE instead of PC; and (iv) alpha-Syn binding to acidic phospholipid (with PC or PE) vesicles is inversely proportional to the ionic strength.	bind
17320	2	5583	6	10	NULL	NULL	NULL	statement 1	Process		is dependent on					dose	QuantityOrMeasure				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_44_34328_s_135	10915790	(i) The binding of alpha-Syn with acidic phospholipids is dose-dependent; (ii) the extent of lipid binding depends rather on the availability of the phospholipids than on the size of lipid vesicles (SUVs  versus MLVs); (iii) alpha-Syn binding to phospholipid vesicles increases drastically when an acidic phospholipid is mixed with PE instead of PC; and (iv) alpha-Syn binding to acidic phospholipid (with PC or PE) vesicles is inversely proportional to the ionic strength.	bind
17323	3	5583	6	10	NULL	NULL	NULL	alpha-Syn	GP		bind					phospholipid vesicles	CellComponent	acidic			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_44_34328_s_135	10915790	(i) The binding of alpha-Syn with acidic phospholipids is dose-dependent; (ii) the extent of lipid binding depends rather on the availability of the phospholipids than on the size of lipid vesicles (SUVs  versus MLVs); (iii) alpha-Syn binding to phospholipid vesicles increases drastically when an acidic phospholipid is mixed with PE instead of PC; and (iv) alpha-Syn binding to acidic phospholipid (with PC or PE) vesicles is inversely proportional to the ionic strength.	bind
17727	4	5583	6	10	NULL	NULL	NULL	statement 3	Process		is inversely propotional to					ionic strength	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_44_34328_s_135	10915790	(i) The binding of alpha-Syn with acidic phospholipids is dose-dependent; (ii) the extent of lipid binding depends rather on the availability of the phospholipids than on the size of lipid vesicles (SUVs  versus MLVs); (iii) alpha-Syn binding to phospholipid vesicles increases drastically when an acidic phospholipid is mixed with PE instead of PC; and (iv) alpha-Syn binding to acidic phospholipid (with PC or PE) vesicles is inversely proportional to the ionic strength.	bind
20037	5	5583	6	10	NULL	NULL	NULL	alpha-Syn	GP		bind					phospholipid vesicles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_44_34328_s_135	10915790	(i) The binding of alpha-Syn with acidic phospholipids is dose-dependent; (ii) the extent of lipid binding depends rather on the availability of the phospholipids than on the size of lipid vesicles (SUVs  versus MLVs); (iii) alpha-Syn binding to phospholipid vesicles increases drastically when an acidic phospholipid is mixed with PE instead of PC; and (iv) alpha-Syn binding to acidic phospholipid (with PC or PE) vesicles is inversely proportional to the ionic strength.	bind
16214	1	5583	7	10	NULL	NULL	NULL	alpha-Syn	GP		bind					 phospholipids	Chemical	acidic			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_44_34328_s_135	10915790	(i) The binding of alpha-Syn with acidic phospholipids is dose-dependent; (ii) the extent of lipid binding depends rather on the availability of the phospholipids than on the size of lipid vesicles (SUVs  versus MLVs); (iii) alpha-Syn binding to phospholipid vesicles increases drastically when an acidic phospholipid is mixed with PE instead of PC; and (iv) alpha-Syn binding to acidic phospholipid (with PC or PE) vesicles is inversely proportional to the ionic strength.	bind
16215	2	5583	7	10	NULL	NULL	NULL	statement 1	Process		is dependent on					dose	QuantityOrMeasure				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_44_34328_s_135	10915790	(i) The binding of alpha-Syn with acidic phospholipids is dose-dependent; (ii) the extent of lipid binding depends rather on the availability of the phospholipids than on the size of lipid vesicles (SUVs  versus MLVs); (iii) alpha-Syn binding to phospholipid vesicles increases drastically when an acidic phospholipid is mixed with PE instead of PC; and (iv) alpha-Syn binding to acidic phospholipid (with PC or PE) vesicles is inversely proportional to the ionic strength.	bind
16218	3	5583	7	10	NULL	NULL	NULL	alpha-Syn	GP		bind					phospholipid vesicles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_44_34328_s_135	10915790	(i) The binding of alpha-Syn with acidic phospholipids is dose-dependent; (ii) the extent of lipid binding depends rather on the availability of the phospholipids than on the size of lipid vesicles (SUVs  versus MLVs); (iii) alpha-Syn binding to phospholipid vesicles increases drastically when an acidic phospholipid is mixed with PE instead of PC; and (iv) alpha-Syn binding to acidic phospholipid (with PC or PE) vesicles is inversely proportional to the ionic strength.	bind
16221	4	5583	7	10	NULL	NULL	NULL	alpha-Syn	GP		bind					phospholipid vesicles	CellComponent	acidic			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_44_34328_s_135	10915790	(i) The binding of alpha-Syn with acidic phospholipids is dose-dependent; (ii) the extent of lipid binding depends rather on the availability of the phospholipids than on the size of lipid vesicles (SUVs  versus MLVs); (iii) alpha-Syn binding to phospholipid vesicles increases drastically when an acidic phospholipid is mixed with PE instead of PC; and (iv) alpha-Syn binding to acidic phospholipid (with PC or PE) vesicles is inversely proportional to the ionic strength.	bind
16222	5	5583	7	10	NULL	NULL	NULL	statement 4	Process		is inversely proportional to					ionic strength	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_44_34328_s_135	10915790	(i) The binding of alpha-Syn with acidic phospholipids is dose-dependent; (ii) the extent of lipid binding depends rather on the availability of the phospholipids than on the size of lipid vesicles (SUVs  versus MLVs); (iii) alpha-Syn binding to phospholipid vesicles increases drastically when an acidic phospholipid is mixed with PE instead of PC; and (iv) alpha-Syn binding to acidic phospholipid (with PC or PE) vesicles is inversely proportional to the ionic strength.	bind
17327	1	5584	6	10	NULL	NULL	NULL	elongin C	GP		bind					VHL	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_30388_s_81	12048197	(i) The binding of Elongin C to VHL is stabilized by Elongin B both  in vitro and in cells ( 16,  35).	bind
17329	2	5584	6	10	NULL	NULL	NULL	Elongin B	GP		stabilizes					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_30388_s_81	12048197	(i) The binding of Elongin C to VHL is stabilized by Elongin B both  in vitro and in cells ( 16,  35).	bind
17330	4	5584	6	10	NULL	NULL	NULL	Elongin B	GP		stabilizes					statement 3	Process				NULL	in cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_30388_s_81	12048197	(i) The binding of Elongin C to VHL is stabilized by Elongin B both  in vitro and in cells ( 16,  35).	bind
17690	3	5584	6	10	NULL	NULL	NULL	elongin C	GP		bind					VHL	GP				NULL	in cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_30388_s_81	12048197	(i) The binding of Elongin C to VHL is stabilized by Elongin B both  in vitro and in cells ( 16,  35).	bind
16223	1	5584	7	10	NULL	NULL	NULL	Elongin C	GP		bind					VHL	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_30388_s_81	12048197	(i) The binding of Elongin C to VHL is stabilized by Elongin B both  in vitro and in cells ( 16,  35).	bind
16224	2	5584	7	10	NULL	NULL	NULL	Elongin C	GP		bind					VHL	GP				NULL	in cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_30388_s_81	12048197	(i) The binding of Elongin C to VHL is stabilized by Elongin B both  in vitro and in cells ( 16,  35).	bind
16225	3	5584	7	10	NULL	NULL	NULL	statement 1	Process		is stabilized by					Elongin B	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_30388_s_81	12048197	(i) The binding of Elongin C to VHL is stabilized by Elongin B both  in vitro and in cells ( 16,  35).	bind
16226	4	5584	7	10	NULL	NULL	NULL	statement 2	Process		is stabilized by					Elongin B	GP				NULL	in cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_30388_s_81	12048197	(i) The binding of Elongin C to VHL is stabilized by Elongin B both  in vitro and in cells ( 16,  35).	bind
17362	1	5585	6	10	NULL	NULL	NULL	Mg2+	Chemical		are located 			binding sites residues 457-464		central alpha2beta complex	GP	upstream of 	binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3583_s_269	10652354	(i) The binding sites of Mg2+ (residues 457-464) ( 40,  41), located upstream of the central alpha2beta complex binding site, form a part of the catalytic site of RNA polymerization.	bind
17363	2	5585	6	10	NULL	NULL	NULL	statement 1	Process		forms					RNA polymerization	Process		catalytic site 		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3583_s_269	10652354	(i) The binding sites of Mg2+ (residues 457-464) ( 40,  41), located upstream of the central alpha2beta complex binding site, form a part of the catalytic site of RNA polymerization.	bind
16227	1	5585	7	10	NULL	NULL	NULL	Mg2+	Chemical	 	is located			binding site residues 457-464		central alpha2beta complex	GP	upstream of 	 binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3583_s_269	10652354	(i) The binding sites of Mg2+ (residues 457-464) ( 40,  41), located upstream of the central alpha2beta complex binding site, form a part of the catalytic site of RNA polymerization.	bind
16228	2	5585	7	10	NULL	NULL	NULL	statement 1	Process		forms 					RNA polymerization	Process	part of 	catalytic site of		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3583_s_269	10652354	(i) The binding sites of Mg2+ (residues 457-464) ( 40,  41), located upstream of the central alpha2beta complex binding site, form a part of the catalytic site of RNA polymerization.	bind
17364	1	5587	6	10	NULL	NULL	NULL	NCAM	GP		bind			IgI domain		heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_251	9092558	(i) The IgI domain bound heparin but did not bind other negatively charged carbohydrates such as carboxymethylated dextran (the surface of a CM5 sensor chip) and PSA. (ii) Other extracellular domains of NCAM (with the exception of the IgII domain) did not bind to heparin.	bind
17365	2	5587	6	10	NULL	NULL	NULL	NCAM	GP		does not bind			IgI domain		carboxymethylated dextran	Chemical	negatively charged			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_251	9092558	(i) The IgI domain bound heparin but did not bind other negatively charged carbohydrates such as carboxymethylated dextran (the surface of a CM5 sensor chip) and PSA. (ii) Other extracellular domains of NCAM (with the exception of the IgII domain) did not bind to heparin.	bind
17366	3	5587	6	10	NULL	NULL	NULL	NCAM	GP		does not bind			IgI domain		PSA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_251	9092558	(i) The IgI domain bound heparin but did not bind other negatively charged carbohydrates such as carboxymethylated dextran (the surface of a CM5 sensor chip) and PSA. (ii) Other extracellular domains of NCAM (with the exception of the IgII domain) did not bind to heparin.	bind
17367	4	5587	6	10	NULL	NULL	NULL	NCAM	GP		bind			IgII domain		heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_251	9092558	(i) The IgI domain bound heparin but did not bind other negatively charged carbohydrates such as carboxymethylated dextran (the surface of a CM5 sensor chip) and PSA. (ii) Other extracellular domains of NCAM (with the exception of the IgII domain) did not bind to heparin.	bind
17368	5	5587	6	10	NULL	NULL	NULL	NCAM	GP		does not bind			extracellular domain		heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_251	9092558	(i) The IgI domain bound heparin but did not bind other negatively charged carbohydrates such as carboxymethylated dextran (the surface of a CM5 sensor chip) and PSA. (ii) Other extracellular domains of NCAM (with the exception of the IgII domain) did not bind to heparin.	bind
16229	1	5587	7	10	NULL	NULL	NULL	NCAM	GP		bind			 IgI 		heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_251	9092558	(i) The IgI domain bound heparin but did not bind other negatively charged carbohydrates such as carboxymethylated dextran (the surface of a CM5 sensor chip) and PSA. (ii) Other extracellular domains of NCAM (with the exception of the IgII domain) did not bind to heparin.	bind
16230	2	5587	7	10	NULL	NULL	NULL	NCAM	GP		does not bind			IgI		carboxymethylated dextran	Chemical	negatively charged			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_251	9092558	(i) The IgI domain bound heparin but did not bind other negatively charged carbohydrates such as carboxymethylated dextran (the surface of a CM5 sensor chip) and PSA. (ii) Other extracellular domains of NCAM (with the exception of the IgII domain) did not bind to heparin.	bind
16231	3	5587	7	10	NULL	NULL	NULL	NCAM	GP		does not bind			IgI		PSA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_251	9092558	(i) The IgI domain bound heparin but did not bind other negatively charged carbohydrates such as carboxymethylated dextran (the surface of a CM5 sensor chip) and PSA. (ii) Other extracellular domains of NCAM (with the exception of the IgII domain) did not bind to heparin.	bind
16232	4	5587	7	10	NULL	NULL	NULL	NCAM	GP	 	does not bind			extracellular domain		heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_251	9092558	(i) The IgI domain bound heparin but did not bind other negatively charged carbohydrates such as carboxymethylated dextran (the surface of a CM5 sensor chip) and PSA. (ii) Other extracellular domains of NCAM (with the exception of the IgII domain) did not bind to heparin.	bind
16233	5	5587	7	10	NULL	NULL	NULL	NCAM	GP		bind			IgII		heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_251	9092558	(i) The IgI domain bound heparin but did not bind other negatively charged carbohydrates such as carboxymethylated dextran (the surface of a CM5 sensor chip) and PSA. (ii) Other extracellular domains of NCAM (with the exception of the IgII domain) did not bind to heparin.	bind
17369	1	5588	6	10	NULL	NULL	NULL	ctMycBR Max heterodimer	GP		does not bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_48_28797_s_230	7499403	(i) The presence of Max does  not confer DNA binding activity to the  ctMycBR  Max heterodimer.	bind
20038	2	5588	6	10	NULL	NULL	NULL	Max	GP	presence of	does not confer					ctMycBR Max heterodimer	GP	DNA binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_48_28797_s_230	7499403	(i) The presence of Max does  not confer DNA binding activity to the  ctMycBR  Max heterodimer.	bind
16236	1	5588	7	10	NULL	NULL	NULL	ctMycBR Max heterodimer 	GP		does not bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_48_28797_s_230	7499403	(i) The presence of Max does  not confer DNA binding activity to the  ctMycBR  Max heterodimer.	bind
16238	2	5588	7	10	NULL	NULL	NULL	Max	GP	presence of 	does not confer					ctMycBR Max heterodimer	GP	DNA binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_48_28797_s_230	7499403	(i) The presence of Max does  not confer DNA binding activity to the  ctMycBR  Max heterodimer.	bind
17370	1	5589	6	10	NULL	NULL	NULL	Zw5 protein	GP		bind									scs	NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_358_s_195	15650749	(I) The proteins Zw5 and BEAF, which  bind to the insulator elements  scs and  scs'', interact with each other  in vitro and their binding sites are located in close proximity to each other  in vivo (  et al).	bind
17371	2	5589	6	10	NULL	NULL	NULL	BEAF protein	GP		bind									scs''	NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_358_s_195	15650749	(I) The proteins Zw5 and BEAF, which  bind to the insulator elements  scs and  scs'', interact with each other  in vitro and their binding sites are located in close proximity to each other  in vivo (  et al).	bind
17374	3	5589	6	10	NULL	NULL	NULL	Zw5	GP		interact with					BEAF	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_embo_24_2_358_s_195	15650749	(I) The proteins Zw5 and BEAF, which  bind to the insulator elements  scs and  scs'', interact with each other  in vitro and their binding sites are located in close proximity to each other  in vivo (  et al).	bind
20039	4	5589	6	NULL	NULL	0	NULL		NULL		is in close proximity to	NULL			scs		NULL			scs''	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_embo_24_2_358_s_195	15650749	(I) The proteins Zw5 and BEAF, which  bind to the insulator elements  scs and  scs'', interact with each other  in vitro and their binding sites are located in close proximity to each other  in vivo (  et al).	bind
53188	5	5589	6	10	NULL	NULL	NULL	scs	GP		is a type of					insulator element	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_358_s_195	15650749	(I) The proteins Zw5 and BEAF, which  bind to the insulator elements  scs and  scs'', interact with each other  in vitro and their binding sites are located in close proximity to each other  in vivo (  et al).	bind
53189	6	5589	6	10	NULL	NULL	NULL	scs''	GP		is a type of					insulator element	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_358_s_195	15650749	(I) The proteins Zw5 and BEAF, which  bind to the insulator elements  scs and  scs'', interact with each other  in vitro and their binding sites are located in close proximity to each other  in vivo (  et al).	bind
16239	1	5589	7	10	NULL	NULL	NULL	Zw5 protein	GP		bind									scs	NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_358_s_195	15650749	(I) The proteins Zw5 and BEAF, which  bind to the insulator elements  scs and  scs'', interact with each other  in vitro and their binding sites are located in close proximity to each other  in vivo (  et al).	bind
16240	2	5589	7	10	NULL	NULL	NULL	BEAF protein	GP		bind									scs''	NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_358_s_195	15650749	(I) The proteins Zw5 and BEAF, which  bind to the insulator elements  scs and  scs'', interact with each other  in vitro and their binding sites are located in close proximity to each other  in vivo (  et al).	bind
16243	5	5589	7	10	NULL	NULL	NULL	Zw5	GP		interacts with					BEAF	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_embo_24_2_358_s_195	15650749	(I) The proteins Zw5 and BEAF, which  bind to the insulator elements  scs and  scs'', interact with each other  in vitro and their binding sites are located in close proximity to each other  in vivo (  et al).	bind
16244	6	5589	7	NULL	NULL	0	NULL		NULL		is in close proximity to	NULL			scs		NULL			scs''	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_embo_24_2_358_s_195	15650749	(I) The proteins Zw5 and BEAF, which  bind to the insulator elements  scs and  scs'', interact with each other  in vitro and their binding sites are located in close proximity to each other  in vivo (  et al).	bind
53190	3	5589	7	10	NULL	NULL	NULL	scs	GP		is a type of					insulator element	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_358_s_195	15650749	(I) The proteins Zw5 and BEAF, which  bind to the insulator elements  scs and  scs'', interact with each other  in vitro and their binding sites are located in close proximity to each other  in vivo (  et al).	bind
53191	4	5589	7	10	NULL	NULL	NULL	scs''	GP		is a type of					insulator element	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_358_s_195	15650749	(I) The proteins Zw5 and BEAF, which  bind to the insulator elements  scs and  scs'', interact with each other  in vitro and their binding sites are located in close proximity to each other  in vivo (  et al).	bind
17375	1	5590	6	10	NULL	NULL	NULL	NADPH	Chemical		bind		tightly			EH2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_37317_s_243	10969088	(i) The redox potentials of  EH2/ EH4,  325 mV for the  E. coli and human enzymes, ( 24) and of NADP+/NADPH,  309 mV at pH 6.9 and 25  degrees C ( 25), together with the high NADPH concentration determine the effective redox potential of the system; (ii) the binding of NADPH to  EH2 is very tight, and we assume that it is tighter than the binding to  EH4; this causes the redox potential of the system to be shifted to even more negative values ( 26).	bind
17376	2	5590	6	10	NULL	NULL	NULL	NADPH	Chemical		bind					EH4	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_37317_s_243	10969088	(i) The redox potentials of  EH2/ EH4,  325 mV for the  E. coli and human enzymes, ( 24) and of NADP+/NADPH,  309 mV at pH 6.9 and 25  degrees C ( 25), together with the high NADPH concentration determine the effective redox potential of the system; (ii) the binding of NADPH to  EH2 is very tight, and we assume that it is tighter than the binding to  EH4; this causes the redox potential of the system to be shifted to even more negative values ( 26).	bind
17377	3	5590	6	10	NULL	NULL	NULL	statement 1	Process		is stronger than		probably			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_37317_s_243	10969088	(i) The redox potentials of  EH2/ EH4,  325 mV for the  E. coli and human enzymes, ( 24) and of NADP+/NADPH,  309 mV at pH 6.9 and 25  degrees C ( 25), together with the high NADPH concentration determine the effective redox potential of the system; (ii) the binding of NADPH to  EH2 is very tight, and we assume that it is tighter than the binding to  EH4; this causes the redox potential of the system to be shifted to even more negative values ( 26).	bind
20040	4	5590	6	10	NULL	NULL	NULL	statement 1	Process		cause					redox potential	QuantityOrMeasure	negative value of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_37317_s_243	10969088	(i) The redox potentials of  EH2/ EH4,  325 mV for the  E. coli and human enzymes, ( 24) and of NADP+/NADPH,  309 mV at pH 6.9 and 25  degrees C ( 25), together with the high NADPH concentration determine the effective redox potential of the system; (ii) the binding of NADPH to  EH2 is very tight, and we assume that it is tighter than the binding to  EH4; this causes the redox potential of the system to be shifted to even more negative values ( 26).	bind
16245	1	5590	7	10	NULL	NULL	NULL	NADPH	Chemical		bind		tightly			EH2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_37317_s_243	10969088	(i) The redox potentials of  EH2/ EH4,  325 mV for the  E. coli and human enzymes, ( 24) and of NADP+/NADPH,  309 mV at pH 6.9 and 25  degrees C ( 25), together with the high NADPH concentration determine the effective redox potential of the system; (ii) the binding of NADPH to  EH2 is very tight, and we assume that it is tighter than the binding to  EH4; this causes the redox potential of the system to be shifted to even more negative values ( 26).	bind
16246	2	5590	7	10	NULL	NULL	NULL	NADPH	Chemical		bind					EH4	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_37317_s_243	10969088	(i) The redox potentials of  EH2/ EH4,  325 mV for the  E. coli and human enzymes, ( 24) and of NADP+/NADPH,  309 mV at pH 6.9 and 25  degrees C ( 25), together with the high NADPH concentration determine the effective redox potential of the system; (ii) the binding of NADPH to  EH2 is very tight, and we assume that it is tighter than the binding to  EH4; this causes the redox potential of the system to be shifted to even more negative values ( 26).	bind
16247	3	5590	7	10	NULL	NULL	NULL	statement 1	Process		is tighter than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_37317_s_243	10969088	(i) The redox potentials of  EH2/ EH4,  325 mV for the  E. coli and human enzymes, ( 24) and of NADP+/NADPH,  309 mV at pH 6.9 and 25  degrees C ( 25), together with the high NADPH concentration determine the effective redox potential of the system; (ii) the binding of NADPH to  EH2 is very tight, and we assume that it is tighter than the binding to  EH4; this causes the redox potential of the system to be shifted to even more negative values ( 26).	bind
16248	4	5590	7	10	NULL	NULL	NULL	statement 1	Process		cause					 redox potential	QuantityOrMeasure	negative value of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_37317_s_243	10969088	(i) The redox potentials of  EH2/ EH4,  325 mV for the  E. coli and human enzymes, ( 24) and of NADP+/NADPH,  309 mV at pH 6.9 and 25  degrees C ( 25), together with the high NADPH concentration determine the effective redox potential of the system; (ii) the binding of NADPH to  EH2 is very tight, and we assume that it is tighter than the binding to  EH4; this causes the redox potential of the system to be shifted to even more negative values ( 26).	bind
17678	1	5591	6	10	NULL	NULL	NULL	RelA	GP		forms heteromer with					C/EBP	GP				NULL	LPS-induced rabbit liver	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
17679	2	5591	6	10	NULL	NULL	NULL	RelA	GP		transactivate					SAA gene	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
17680	3	5591	6	10	NULL	NULL	NULL	C/EBP	GP		transactivate					SAA gene	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
17681	4	5591	6	10	NULL	NULL	NULL	statement 2	Process		acts in cooperation with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
17682	5	5591	6	10	NULL	NULL	NULL	NF-kappaB	GP		forms a heteromeric complex with					C/EBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
17683	6	5591	6	10	NULL	NULL	NULL	statement 5	Process		bind					SAA	GP			NF-kappaB-binding element of promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
17684	7	5591	6	10	NULL	NULL	NULL	statement 5	Process		bind					SAA	GP			C/EBP binding element of promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
17731	8	5591	6	10	NULL	NULL	NULL	statement 1	Process		bind					SAA	GP			promoter	NULL	LPS-induced rabbit liver	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
17732	9	5591	6	10	NULL	NULL	NULL	statement 6	Process		has much higher affinity than					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
20301	10	5591	6	10	NULL	NULL	NULL	NF-kappaB C/EBP heteromeric complex	GP	transactivation potential of	is higher than					homomeric counterparts	GP	transactivation potential of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
53193	11	5591	6	10	NULL	NULL	NULL	statement 5	Process		activates					SAA	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
16249	1	5591	7	10	NULL	NULL	NULL	RelA	GP		transactivate					SAA 	GP	 expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
16250	2	5591	7	10	NULL	NULL	NULL	C/EBP	GP		transactivate					SAA	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
16251	3	5591	7	10	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
16252	4	5591	7	10	NULL	NULL	NULL	NF-kappaB	GP		forms heteromeric complex with					C/EBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
16253	5	5591	7	10	NULL	NULL	NULL	statement 4	Process		activates					SAA	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
16254	6	5591	7	10	NULL	NULL	NULL	NF-kappaB C/EBP heteromeric complex	GP	transactivation potential of	is high than					homomeric counterparts	GP	transactivation potential of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
16255	7	5591	7	10	NULL	NULL	NULL	statement 4	Process		bind					SAA	GP			NF-kappaB binding element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
16256	8	5591	7	10	NULL	NULL	NULL	statement 4	Process		bind					SAA	GP			C/EBP binding element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
16257	9	5591	7	10	NULL	NULL	NULL	statement 7	Process		has higher affinity than					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
20094	10	5591	7	10	NULL	NULL	NULL	RelA	GP		forms heteromer with					C/EBP	GP				NULL	LPS-induced rabbit liver	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
53192	11	5591	7	10	NULL	NULL	NULL	statement 8	Process		bind					SAA	GP			promoter	NULL	LPS-induced rabbit liver	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7365_s_267	7706280	(i) There is  in vivo  evidence of  RelA C/EBP heteromer formation at the SAA promoter in the  LPS-induced rabbit liver; (ii) RelA and C/EBP-   cooperatively  transactivate the expression of SAA gene; (iii) the heteromeric complex  of NF-kappaB and C/EBP has a higher transactivation potential in  activating SAA expression than their homomeric counterparts; (iv) the  heteromeric complex of NF-kappaB and C/EBP can bind to both NF-kappaB  and C/EBP binding elements; (v) the NF-kappaB C/EBP heteromer  interacts with the NF-kappaB element with a much higher affinity than  that with the C/EBP element of SAA promoter.	bind
17378	1	5593	6	10	NULL	NULL	NULL	Hsc70	GP		bind					HRI	GP	transformed			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_356	10454533	(i) Under conditions of heme deficiency, the binding of Hsc70 to transformed HRI may directly suppress its autokinase activity, preventing the hyperphosphorylation of transformed HRI (Fig.  10B,  1).	bind
17380	2	5593	6	10	NULL	NULL	NULL	statement 1	Process		suppress		may directly			Hsc70	GP	autokinase activity of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_356	10454533	(i) Under conditions of heme deficiency, the binding of Hsc70 to transformed HRI may directly suppress its autokinase activity, preventing the hyperphosphorylation of transformed HRI (Fig.  10B,  1).	bind
17382	3	5593	6	10	NULL	NULL	NULL	statement 2	Process		prevents					HRI	GP	hyperphosphorylation transformed			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_356	10454533	(i) Under conditions of heme deficiency, the binding of Hsc70 to transformed HRI may directly suppress its autokinase activity, preventing the hyperphosphorylation of transformed HRI (Fig.  10B,  1).	bind
17384	4	5593	6	10	NULL	NULL	NULL	statement 2	Process		occurs under					heme	Chemical	deficiency of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_356	10454533	(i) Under conditions of heme deficiency, the binding of Hsc70 to transformed HRI may directly suppress its autokinase activity, preventing the hyperphosphorylation of transformed HRI (Fig.  10B,  1).	bind
16258	1	5593	7	10	NULL	NULL	NULL	Hsc70	GP		bind					HRI	GP	transformed			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_356	10454533	(i) Under conditions of heme deficiency, the binding of Hsc70 to transformed HRI may directly suppress its autokinase activity, preventing the hyperphosphorylation of transformed HRI (Fig.  10B,  1).	bind
16259	2	5593	7	10	NULL	NULL	NULL	statement 1	Process		occurs under					heme	Chemical	deficiency of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_356	10454533	(i) Under conditions of heme deficiency, the binding of Hsc70 to transformed HRI may directly suppress its autokinase activity, preventing the hyperphosphorylation of transformed HRI (Fig.  10B,  1).	bind
16260	3	5593	7	10	NULL	NULL	NULL	statement 1	Process		suppress		may directly			Hsc70	GP	autokinase activity of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_356	10454533	(i) Under conditions of heme deficiency, the binding of Hsc70 to transformed HRI may directly suppress its autokinase activity, preventing the hyperphosphorylation of transformed HRI (Fig.  10B,  1).	bind
16261	4	5593	7	10	NULL	NULL	NULL	statement 1	Process		prevents					HRI	GP	hyperphosphorylation of transformed			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_356	10454533	(i) Under conditions of heme deficiency, the binding of Hsc70 to transformed HRI may directly suppress its autokinase activity, preventing the hyperphosphorylation of transformed HRI (Fig.  10B,  1).	bind
17386	1	5594	6	10	NULL	NULL	NULL	basal AP-2	GP	binding of	does not change with					ischemia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_45_16345_s_136	16258061	(I) versus nonischemic (N) limbs, no binding of YB-1, and no  change in basal AP-2 binding with ischemia.	bind
16446	1	5594	7	10	NULL	NULL	NULL	basal AP-2	GP	 binding of	does not change with					ischemia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_45_16345_s_136	16258061	(I) versus nonischemic (N) limbs, no binding of YB-1, and no  change in basal AP-2 binding with ischemia.	bind
17393	1	5595	6	10	NULL	NULL	NULL	homodimeric SRF	GP		bind									SRE motif	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_17_12941_s_104	10777594	(I) was formed by a homodimeric SRF bound to the SRE motif.	bind
16312	1	5595	7	10	NULL	NULL	NULL	 homodimeric SRF	GP		bind									SRE motif	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_17_12941_s_104	10777594	(I) was formed by a homodimeric SRF bound to the SRE motif.	bind
17396	1	5596	6	10	NULL	NULL	NULL	low molecular weight protein cDNA	NucleicAcid		bind		specifically			hYAP	GP		WW domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_24_14733_s_133	7782338	(i) We have recently  identified and cloned two cDNAs for low molecular weight proteins that  bind specifically to the WW domain of hYAP.	bind
16313	1	5596	7	10	NULL	NULL	NULL	low molecular weight protein cDNA	NucleicAcid		bind		specifically			hYAP	GP		 WW domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_24_14733_s_133	7782338	(i) We have recently  identified and cloned two cDNAs for low molecular weight proteins that  bind specifically to the WW domain of hYAP.	bind
17400	1	5597	6	NULL	NULL	0	NULL		NULL		lies between	NULL		Bm-binding pocket			NULL		regions I and IV		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2311_s_314	11706014	(i) When Bm-I binds to the Bm-binding pocket between regions I and IV, because the connectivity between regions III and IV is significantly strong, a significant amount of energy is necessary to cause the rotational change of region IV, which results in weak binding of Bm-I to the pocket.	bind
17401	2	5597	6	10	NULL	NULL	NULL	Bm-I	GP		bind		weakly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2311_s_314	11706014	(i) When Bm-I binds to the Bm-binding pocket between regions I and IV, because the connectivity between regions III and IV is significantly strong, a significant amount of energy is necessary to cause the rotational change of region IV, which results in weak binding of Bm-I to the pocket.	bind
16314	1	5597	7	10	NULL	NULL	NULL	Bm-I	GP		binds		weakly						Bm-binding pocket		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2311_s_314	11706014	(i) When Bm-I binds to the Bm-binding pocket between regions I and IV, because the connectivity between regions III and IV is significantly strong, a significant amount of energy is necessary to cause the rotational change of region IV, which results in weak binding of Bm-I to the pocket.	bind
16315	2	5597	7	10	NULL	NULL	NULL	statement 1	Process		occurs between								region I and IV		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2311_s_314	11706014	(i) When Bm-I binds to the Bm-binding pocket between regions I and IV, because the connectivity between regions III and IV is significantly strong, a significant amount of energy is necessary to cause the rotational change of region IV, which results in weak binding of Bm-I to the pocket.	bind
17687	1	5598	6	10	NULL	NULL	NULL	NTCB fragment	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_32182_s_210	9405419	(i) When the peptide of Met1-Pro41 was split into Met1-Gly25 and Pro26-Pro41, both peptides lost the antagonism for the actin binding of the NTCB (Fig.  4) and NN fragments (Fig.  1 c).	bind
17688	2	5598	6	10	NULL	NULL	NULL	NN fragment	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_32182_s_210	9405419	(i) When the peptide of Met1-Pro41 was split into Met1-Gly25 and Pro26-Pro41, both peptides lost the antagonism for the actin binding of the NTCB (Fig.  4) and NN fragments (Fig.  1 c).	bind
54099	3	5598	6	10	NULL	NULL	NULL	peptide	GP		split into			Met1-Pro41					Met1-Gly25		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_32182_s_210	9405419	(i) When the peptide of Met1-Pro41 was split into Met1-Gly25 and Pro26-Pro41, both peptides lost the antagonism for the actin binding of the NTCB (Fig.  4) and NN fragments (Fig.  1 c).	bind
54100	4	5598	6	10	NULL	NULL	NULL	peptide	GP		split into			Met1-Pro41					Pro26-Pro41		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_32182_s_210	9405419	(i) When the peptide of Met1-Pro41 was split into Met1-Gly25 and Pro26-Pro41, both peptides lost the antagonism for the actin binding of the NTCB (Fig.  4) and NN fragments (Fig.  1 c).	bind
54101	5	5598	6	10	NULL	NULL	NULL	statement 3	Process		loses antagonism for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_32182_s_210	9405419	(i) When the peptide of Met1-Pro41 was split into Met1-Gly25 and Pro26-Pro41, both peptides lost the antagonism for the actin binding of the NTCB (Fig.  4) and NN fragments (Fig.  1 c).	bind
54102	6	5598	6	10	NULL	NULL	NULL	statement 3	Process		loses antagonism for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_32182_s_210	9405419	(i) When the peptide of Met1-Pro41 was split into Met1-Gly25 and Pro26-Pro41, both peptides lost the antagonism for the actin binding of the NTCB (Fig.  4) and NN fragments (Fig.  1 c).	bind
54103	7	5598	6	10	NULL	NULL	NULL	statement 4	Process		loses antagonism for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_32182_s_210	9405419	(i) When the peptide of Met1-Pro41 was split into Met1-Gly25 and Pro26-Pro41, both peptides lost the antagonism for the actin binding of the NTCB (Fig.  4) and NN fragments (Fig.  1 c).	bind
54104	8	5598	6	10	NULL	NULL	NULL	statement 4	Process		loses antagonism for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_32182_s_210	9405419	(i) When the peptide of Met1-Pro41 was split into Met1-Gly25 and Pro26-Pro41, both peptides lost the antagonism for the actin binding of the NTCB (Fig.  4) and NN fragments (Fig.  1 c).	bind
16319	1	5598	7	10	NULL	NULL	NULL	actin	GP		bind					NTCB	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_32182_s_210	9405419	(i) When the peptide of Met1-Pro41 was split into Met1-Gly25 and Pro26-Pro41, both peptides lost the antagonism for the actin binding of the NTCB (Fig.  4) and NN fragments (Fig.  1 c).	bind
16320	2	5598	7	10	NULL	NULL	NULL	actin	GP		bind					NN fragments	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_32182_s_210	9405419	(i) When the peptide of Met1-Pro41 was split into Met1-Gly25 and Pro26-Pro41, both peptides lost the antagonism for the actin binding of the NTCB (Fig.  4) and NN fragments (Fig.  1 c).	bind
16321	3	5598	7	10	NULL	NULL	NULL	peptide	GP		split into			Met1-Pro41					Met1-Gly25		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_32182_s_210	9405419	(i) When the peptide of Met1-Pro41 was split into Met1-Gly25 and Pro26-Pro41, both peptides lost the antagonism for the actin binding of the NTCB (Fig.  4) and NN fragments (Fig.  1 c).	bind
16322	4	5598	7	10	NULL	NULL	NULL	peptide	GP		split into			Met1-Pro41					Pro26-Pro41		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_32182_s_210	9405419	(i) When the peptide of Met1-Pro41 was split into Met1-Gly25 and Pro26-Pro41, both peptides lost the antagonism for the actin binding of the NTCB (Fig.  4) and NN fragments (Fig.  1 c).	bind
16323	5	5598	7	10	NULL	NULL	NULL	statement 3	Process		loses					statement 1	Process	antagonism for 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_32182_s_210	9405419	(i) When the peptide of Met1-Pro41 was split into Met1-Gly25 and Pro26-Pro41, both peptides lost the antagonism for the actin binding of the NTCB (Fig.  4) and NN fragments (Fig.  1 c).	bind
16327	6	5598	7	10	NULL	NULL	NULL	statement 3	Process		loses					statement 2	Process	antagonism for 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_32182_s_210	9405419	(i) When the peptide of Met1-Pro41 was split into Met1-Gly25 and Pro26-Pro41, both peptides lost the antagonism for the actin binding of the NTCB (Fig.  4) and NN fragments (Fig.  1 c).	bind
16335	7	5598	7	10	NULL	NULL	NULL	statement 4	Process		loses					statement 1	Process	antagonism for			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_32182_s_210	9405419	(i) When the peptide of Met1-Pro41 was split into Met1-Gly25 and Pro26-Pro41, both peptides lost the antagonism for the actin binding of the NTCB (Fig.  4) and NN fragments (Fig.  1 c).	bind
16337	8	5598	7	10	NULL	NULL	NULL	statement 4	Process		loses					statement 2	Process	antagonism for 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_32182_s_210	9405419	(i) When the peptide of Met1-Pro41 was split into Met1-Gly25 and Pro26-Pro41, both peptides lost the antagonism for the actin binding of the NTCB (Fig.  4) and NN fragments (Fig.  1 c).	bind
17431	1	5599	6	10	NULL	NULL	NULL	CarS	GP		does not bind					DNA	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_9_7262_s_8	11748235	(i) Whereas CarS exhibits no DNA binding  in vitro, CarA binds specifically to a region encompassing PB to form at least two distinct complexes.	bind
17489	2	5599	6	10	NULL	NULL	NULL	CarA	GP		bind		specifically					region encompassing		PB	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_9_7262_s_8	11748235	(i) Whereas CarS exhibits no DNA binding  in vitro, CarA binds specifically to a region encompassing PB to form at least two distinct complexes.	bind
17490	3	5599	6	10	NULL	NULL	NULL	statement 2	Process		forms 					two distinct complexes	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_9_7262_s_8	11748235	(i) Whereas CarS exhibits no DNA binding  in vitro, CarA binds specifically to a region encompassing PB to form at least two distinct complexes.	bind
16341	1	5599	7	10	NULL	NULL	NULL	CarS	GP		does not bind					DNA	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_9_7262_s_8	11748235	(i) Whereas CarS exhibits no DNA binding  in vitro, CarA binds specifically to a region encompassing PB to form at least two distinct complexes.	bind
16342	2	5599	7	10	NULL	NULL	NULL	CarA	GP		bind		specifically					region encompassing		PB	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_9_7262_s_8	11748235	(i) Whereas CarS exhibits no DNA binding  in vitro, CarA binds specifically to a region encompassing PB to form at least two distinct complexes.	bind
16343	3	5599	7	10	NULL	NULL	NULL	statement 2	Process		forms					two distint complex	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_9_7262_s_8	11748235	(i) Whereas CarS exhibits no DNA binding  in vitro, CarA binds specifically to a region encompassing PB to form at least two distinct complexes.	bind
16344	1	5600	7	10	NULL	NULL	NULL	histidine	AminoAcid	spacing between 13residues	serve as					heme	Chemical	axial ligands for			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_14_3815_s_139	12081951	(i) Whereas the spacing (13 residues) between the histidines supposed to serve as axial ligands to the hemes is conserved in all cyt  b sequences in helix II, there are 14 residues between the heme binding histidines in helix IV in  R. gelatinosus (Fig.  4A), as already observed in cyt  b6 ( 41) and in the cyt  b subunits of the beta, gamma, and   subdivisions of proteobacteria, with the exception of  A. vinosum ( 41).	bind
16345	2	5600	7	10	NULL	NULL	NULL	statement 1	Process		is conserved in								cyt b sequences in helix II		NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_14_3815_s_139	12081951	(i) Whereas the spacing (13 residues) between the histidines supposed to serve as axial ligands to the hemes is conserved in all cyt  b sequences in helix II, there are 14 residues between the heme binding histidines in helix IV in  R. gelatinosus (Fig.  4A), as already observed in cyt  b6 ( 41) and in the cyt  b subunits of the beta, gamma, and   subdivisions of proteobacteria, with the exception of  A. vinosum ( 41).	bind
16346	3	5600	7	10	NULL	NULL	NULL			R. gelatinosus	bind			histidine in helix IV		heme	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_14_3815_s_139	12081951	(i) Whereas the spacing (13 residues) between the histidines supposed to serve as axial ligands to the hemes is conserved in all cyt  b sequences in helix II, there are 14 residues between the heme binding histidines in helix IV in  R. gelatinosus (Fig.  4A), as already observed in cyt  b6 ( 41) and in the cyt  b subunits of the beta, gamma, and   subdivisions of proteobacteria, with the exception of  A. vinosum ( 41).	bind
16347	4	5600	7	NULL	NULL	0	NULL		NULL		present in 	NULL		14 residues			NULL		histidine in helix IV		NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_14_3815_s_139	12081951	(i) Whereas the spacing (13 residues) between the histidines supposed to serve as axial ligands to the hemes is conserved in all cyt  b sequences in helix II, there are 14 residues between the heme binding histidines in helix IV in  R. gelatinosus (Fig.  4A), as already observed in cyt  b6 ( 41) and in the cyt  b subunits of the beta, gamma, and   subdivisions of proteobacteria, with the exception of  A. vinosum ( 41).	bind
17491	1	5601	6	10	NULL	NULL	NULL	DicB	GP		bind		might			MinC	GP	cytoplasmic			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_11_2951_s_263	12003935	(i) Without itself being targeted to a specific cellular location, DicB might bind cytoplasmic MinC and modify it to a form with affinity for a septal ring component.	bind
20302	2	5601	6	10	NULL	NULL	NULL	MinC	GP	modified form of;;cytoplasmic	has affinity for					septal ring component	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_11_2951_s_263	12003935	(i) Without itself being targeted to a specific cellular location, DicB might bind cytoplasmic MinC and modify it to a form with affinity for a septal ring component.	bind
20303	3	5601	6	10	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_11_2951_s_263	12003935	(i) Without itself being targeted to a specific cellular location, DicB might bind cytoplasmic MinC and modify it to a form with affinity for a septal ring component.	bind
16358	1	5601	7	10	NULL	NULL	NULL	DicB	GP		bind		might			MinC	GP	cytoplasmic			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_11_2951_s_263	12003935	(i) Without itself being targeted to a specific cellular location, DicB might bind cytoplasmic MinC and modify it to a form with affinity for a septal ring component.	bind
16359	2	5601	7	10	NULL	NULL	NULL	MinC	GP	modified form of;;cytoplasmic	has affinity for					 septal ring component	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_11_2951_s_263	12003935	(i) Without itself being targeted to a specific cellular location, DicB might bind cytoplasmic MinC and modify it to a form with affinity for a septal ring component.	bind
16360	3	5601	7	10	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_11_2951_s_263	12003935	(i) Without itself being targeted to a specific cellular location, DicB might bind cytoplasmic MinC and modify it to a form with affinity for a septal ring component.	bind
17492	1	5602	6	10	NULL	NULL	NULL	poly(L-proline)	AminoAcid		inhibits		effectively			2beta2 tetramer	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17342_s_146	9211872	(I))2beta2 tetramer is effectively inhibited by poly(L-proline) ( 1,  2) and becomes bound to poly(L-proline) affinity columns ( 20).	bind
17493	2	5602	6	10	NULL	NULL	NULL	2beta2 tetramer	GP		bind					poly(L-proline)	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17342_s_146	9211872	(I))2beta2 tetramer is effectively inhibited by poly(L-proline) ( 1,  2) and becomes bound to poly(L-proline) affinity columns ( 20).	bind
16361	1	5602	7	10	NULL	NULL	NULL	poly L-proline	AminoAcid		inhibits		effectively			2beta2 tetramer	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17342_s_146	9211872	(I))2beta2 tetramer is effectively inhibited by poly(L-proline) ( 1,  2) and becomes bound to poly(L-proline) affinity columns ( 20).	bind
16362	2	5602	7	10	NULL	NULL	NULL	2beta2 tetramer	GP		bind					poly(L-proline)	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17342_s_146	9211872	(I))2beta2 tetramer is effectively inhibited by poly(L-proline) ( 1,  2) and becomes bound to poly(L-proline) affinity columns ( 20).	bind
17494	1	5604	6	10	NULL	NULL	NULL	AcLDL	Chemical		bind					SR fusion proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_31_19592_s_193	9677385	(I), indicating that the human IgG fragment is not responsible for any of the binding of the AcLDL to the SR fusion proteins.	bind
17495	2	5604	6	10	NULL	NULL	NULL	IgG fragment	GP	human	is not responsible for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_31_19592_s_193	9677385	(I), indicating that the human IgG fragment is not responsible for any of the binding of the AcLDL to the SR fusion proteins.	bind
16363	1	5604	7	10	NULL	NULL	NULL	AcLDL	Chemical		bind					SR fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_31_19592_s_193	9677385	(I), indicating that the human IgG fragment is not responsible for any of the binding of the AcLDL to the SR fusion proteins.	bind
16364	2	5604	7	10	NULL	NULL	NULL	IgG fragment	GP	human	is not responsible for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_31_19592_s_193	9677385	(I), indicating that the human IgG fragment is not responsible for any of the binding of the AcLDL to the SR fusion proteins.	bind
17496	1	5605	6	10	NULL	NULL	NULL	C/EBP family	GP		bind					P3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_31629_s_27	9822619	(I), which is required for the liver-specific expression of the PEPCK gene ( 21); members of the C/EBP family are the only transcription factors that are known to bind to the P3	bind
45628	2	5605	6	10	NULL	NULL	NULL	C/EBP family	GP		is a type of					transcription factors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_31629_s_27	9822619	(I), which is required for the liver-specific expression of the PEPCK gene ( 21); members of the C/EBP family are the only transcription factors that are known to bind to the P3	bind
16368	1	5605	7	10	NULL	NULL	NULL	C/EBP family	GP		bind					P3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_31629_s_27	9822619	(I), which is required for the liver-specific expression of the PEPCK gene ( 21); members of the C/EBP family are the only transcription factors that are known to bind to the P3	bind
45629	2	5605	7	10	NULL	NULL	NULL	C/EBP family	GP		is a type of					transcription factors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_31629_s_27	9822619	(I), which is required for the liver-specific expression of the PEPCK gene ( 21); members of the C/EBP family are the only transcription factors that are known to bind to the P3	bind
17497	1	5609	6	10	NULL	NULL	NULL	collagen	GP		bind					alpha2beta1	GP		A-domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33287_s_241	9837901	(I)-5/6, perhaps reflecting enhancement of collagen binding to alpha2beta1 A-domain by site(s) in the adjacent EF hand domain ( 35).	bind
20304	2	5609	6	10	NULL	NULL	NULL			site adjacent to	enhance			EF hand domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33287_s_241	9837901	(I)-5/6, perhaps reflecting enhancement of collagen binding to alpha2beta1 A-domain by site(s) in the adjacent EF hand domain ( 35).	bind
16411	1	5609	7	10	NULL	NULL	NULL	collagen	GP		bind					alpha2beta1	GP		A-domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33287_s_241	9837901	(I)-5/6, perhaps reflecting enhancement of collagen binding to alpha2beta1 A-domain by site(s) in the adjacent EF hand domain ( 35).	bind
16412	2	5609	7	10	NULL	NULL	NULL			site adjacent to	enhance			EF hand domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33287_s_241	9837901	(I)-5/6, perhaps reflecting enhancement of collagen binding to alpha2beta1 A-domain by site(s) in the adjacent EF hand domain ( 35).	bind
17498	1	5610	6	10	NULL	NULL	NULL	GFOGER-GPP peptide	GP		supports 					platelet 	OrganismPart	adhesion of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_101	10617582	(I)-5/6-GPP, peptide GFOGER-GPP supported platelet adhesion and exhibited alpha2beta1 binding as good as that to collagen I, whereas binding of the alpha2 A-domain was consistently higher than that to the collagen (Figs.  1 and  2).	bind
17499	2	5610	6	10	NULL	NULL	NULL	GFOGER-GPP peptide	GP		bind					alpha2beta1 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_101	10617582	(I)-5/6-GPP, peptide GFOGER-GPP supported platelet adhesion and exhibited alpha2beta1 binding as good as that to collagen I, whereas binding of the alpha2 A-domain was consistently higher than that to the collagen (Figs.  1 and  2).	bind
17500	3	5610	6	10	NULL	NULL	NULL	GFOGER-GPP peptide	GP		bind					collagen I	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_101	10617582	(I)-5/6-GPP, peptide GFOGER-GPP supported platelet adhesion and exhibited alpha2beta1 binding as good as that to collagen I, whereas binding of the alpha2 A-domain was consistently higher than that to the collagen (Figs.  1 and  2).	bind
17728	4	5610	6	10	NULL	NULL	NULL	statement 2	Process		is as good as					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_101	10617582	(I)-5/6-GPP, peptide GFOGER-GPP supported platelet adhesion and exhibited alpha2beta1 binding as good as that to collagen I, whereas binding of the alpha2 A-domain was consistently higher than that to the collagen (Figs.  1 and  2).	bind
17729	5	5610	6	10	NULL	NULL	NULL	GFOGER-GPP peptide	GP		bind					alpha 2	GP		A-domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_101	10617582	(I)-5/6-GPP, peptide GFOGER-GPP supported platelet adhesion and exhibited alpha2beta1 binding as good as that to collagen I, whereas binding of the alpha2 A-domain was consistently higher than that to the collagen (Figs.  1 and  2).	bind
17730	6	5610	6	10	NULL	NULL	NULL	statement 5	Process		is higher than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_101	10617582	(I)-5/6-GPP, peptide GFOGER-GPP supported platelet adhesion and exhibited alpha2beta1 binding as good as that to collagen I, whereas binding of the alpha2 A-domain was consistently higher than that to the collagen (Figs.  1 and  2).	bind
16413	1	5610	7	10	NULL	NULL	NULL	GFOGER-GPP peptide	GP		support					platelets	OrganismPart	adhesion of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_101	10617582	(I)-5/6-GPP, peptide GFOGER-GPP supported platelet adhesion and exhibited alpha2beta1 binding as good as that to collagen I, whereas binding of the alpha2 A-domain was consistently higher than that to the collagen (Figs.  1 and  2).	bind
16414	2	5610	7	10	NULL	NULL	NULL	GFOGER-GPP peptide	GP		bind					alpha2beta1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_101	10617582	(I)-5/6-GPP, peptide GFOGER-GPP supported platelet adhesion and exhibited alpha2beta1 binding as good as that to collagen I, whereas binding of the alpha2 A-domain was consistently higher than that to the collagen (Figs.  1 and  2).	bind
16415	3	5610	7	10	NULL	NULL	NULL	GFOGER-GPP peptide	GP		bind					collagen I	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_101	10617582	(I)-5/6-GPP, peptide GFOGER-GPP supported platelet adhesion and exhibited alpha2beta1 binding as good as that to collagen I, whereas binding of the alpha2 A-domain was consistently higher than that to the collagen (Figs.  1 and  2).	bind
16416	4	5610	7	10	NULL	NULL	NULL	GFOGER-GPP peptide	GP		bind					alpha2	GP		A-domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_101	10617582	(I)-5/6-GPP, peptide GFOGER-GPP supported platelet adhesion and exhibited alpha2beta1 binding as good as that to collagen I, whereas binding of the alpha2 A-domain was consistently higher than that to the collagen (Figs.  1 and  2).	bind
16417	5	5610	7	10	NULL	NULL	NULL	statement 2	Process		is as good as					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_101	10617582	(I)-5/6-GPP, peptide GFOGER-GPP supported platelet adhesion and exhibited alpha2beta1 binding as good as that to collagen I, whereas binding of the alpha2 A-domain was consistently higher than that to the collagen (Figs.  1 and  2).	bind
16418	6	5610	7	10	NULL	NULL	NULL	GFOGER-GPP peptide	GP		bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_101	10617582	(I)-5/6-GPP, peptide GFOGER-GPP supported platelet adhesion and exhibited alpha2beta1 binding as good as that to collagen I, whereas binding of the alpha2 A-domain was consistently higher than that to the collagen (Figs.  1 and  2).	bind
16419	7	5610	7	10	NULL	NULL	NULL	statement 4	Process		is higher than					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_101	10617582	(I)-5/6-GPP, peptide GFOGER-GPP supported platelet adhesion and exhibited alpha2beta1 binding as good as that to collagen I, whereas binding of the alpha2 A-domain was consistently higher than that to the collagen (Figs.  1 and  2).	bind
17501	1	5611	6	10	NULL	NULL	NULL	IL-2	GP		bind					Collagen	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_49_38170_s_110	10982811	(I)-derived CNBr Peptides Inhibit Binding of IL-2 to Immobilized Collagen-- Incubation of IL-2 with the constituent chains of collagen type I, namely alpha1 and alpha2, with native collagen types III and IV, previously immobilized at 50 ng/200 mul/well, in the presence of increasing amounts of solubilized collagen chains or their CNBr peptides resulted in a dose-dependent inhibition of the IL-2-collagen interaction.	bind
17502	2	5611	6	10	NULL	NULL	NULL	CNBr peptides	GP		inhibits		dose dependently			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_49_38170_s_110	10982811	(I)-derived CNBr Peptides Inhibit Binding of IL-2 to Immobilized Collagen-- Incubation of IL-2 with the constituent chains of collagen type I, namely alpha1 and alpha2, with native collagen types III and IV, previously immobilized at 50 ng/200 mul/well, in the presence of increasing amounts of solubilized collagen chains or their CNBr peptides resulted in a dose-dependent inhibition of the IL-2-collagen interaction.	bind
16420	1	5611	7	10	NULL	NULL	NULL	IL-2	GP		bind					Collagen	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_49_38170_s_110	10982811	(I)-derived CNBr Peptides Inhibit Binding of IL-2 to Immobilized Collagen-- Incubation of IL-2 with the constituent chains of collagen type I, namely alpha1 and alpha2, with native collagen types III and IV, previously immobilized at 50 ng/200 mul/well, in the presence of increasing amounts of solubilized collagen chains or their CNBr peptides resulted in a dose-dependent inhibition of the IL-2-collagen interaction.	bind
16421	2	5611	7	10	NULL	NULL	NULL	CNBr Peptides	GP		inhibits		dose-dependently			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_49_38170_s_110	10982811	(I)-derived CNBr Peptides Inhibit Binding of IL-2 to Immobilized Collagen-- Incubation of IL-2 with the constituent chains of collagen type I, namely alpha1 and alpha2, with native collagen types III and IV, previously immobilized at 50 ng/200 mul/well, in the presence of increasing amounts of solubilized collagen chains or their CNBr peptides resulted in a dose-dependent inhibition of the IL-2-collagen interaction.	bind
17503	1	5612	6	10	NULL	NULL	NULL				bind			RBD		GST-L18	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1116_s_156	9891046	(I)-poly(C) (5 and 15 mug/ml) significantly reduced the amount of RBD bound to GST-L18 (Fig.  3A, lanes 2 and 3).	bind
17504	2	5612	6	10	NULL	NULL	NULL	poly(C)	Chemical		reduces		significantly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1116_s_156	9891046	(I)-poly(C) (5 and 15 mug/ml) significantly reduced the amount of RBD bound to GST-L18 (Fig.  3A, lanes 2 and 3).	bind
16422	1	5612	7	10	NULL	NULL	NULL				bind			RBD		GST-L18	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1116_s_156	9891046	(I)-poly(C) (5 and 15 mug/ml) significantly reduced the amount of RBD bound to GST-L18 (Fig.  3A, lanes 2 and 3).	bind
16423	2	5612	7	10	NULL	NULL	NULL	poly(C)	Chemical		reduces		significantly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1116_s_156	9891046	(I)-poly(C) (5 and 15 mug/ml) significantly reduced the amount of RBD bound to GST-L18 (Fig.  3A, lanes 2 and 3).	bind
17505	1	5615	6	10	NULL	NULL	NULL	THP	GP		bind			127 - 138		alpha2 integrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_33_30516_s_199	12788934	(I)127 - 138 THP bound  7  times more strongly to the alpha2 integrin subunit than to  alpha1beta1 integrins or  alphaVbeta3 integrins, which had equivalent binding  strengths.	bind
17506	2	5615	6	10	NULL	NULL	NULL	THP	GP		bind			127 - 138		alpha1beta1 integrins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_33_30516_s_199	12788934	(I)127 - 138 THP bound  7  times more strongly to the alpha2 integrin subunit than to  alpha1beta1 integrins or  alphaVbeta3 integrins, which had equivalent binding  strengths.	bind
17507	3	5615	6	10	NULL	NULL	NULL	THP	GP		bind			127 - 138		alphaVbeta3 integrins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_33_30516_s_199	12788934	(I)127 - 138 THP bound  7  times more strongly to the alpha2 integrin subunit than to  alpha1beta1 integrins or  alphaVbeta3 integrins, which had equivalent binding  strengths.	bind
17508	4	5615	6	10	NULL	NULL	NULL	statement 1	Process		is stronger than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_33_30516_s_199	12788934	(I)127 - 138 THP bound  7  times more strongly to the alpha2 integrin subunit than to  alpha1beta1 integrins or  alphaVbeta3 integrins, which had equivalent binding  strengths.	bind
17509	5	5615	6	10	NULL	NULL	NULL	statement 1	Process		is stronger than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_33_30516_s_199	12788934	(I)127 - 138 THP bound  7  times more strongly to the alpha2 integrin subunit than to  alpha1beta1 integrins or  alphaVbeta3 integrins, which had equivalent binding  strengths.	bind
20305	6	5615	6	10	NULL	NULL	NULL	statement 2	Process		has equivalent strength to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_33_30516_s_199	12788934	(I)127 - 138 THP bound  7  times more strongly to the alpha2 integrin subunit than to  alpha1beta1 integrins or  alphaVbeta3 integrins, which had equivalent binding  strengths.	bind
16426	1	5615	7	10	NULL	NULL	NULL	THP	GP		bind			127 - 138		alpha2 integrin subunit	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_33_30516_s_199	12788934	(I)127 - 138 THP bound  7  times more strongly to the alpha2 integrin subunit than to  alpha1beta1 integrins or  alphaVbeta3 integrins, which had equivalent binding  strengths.	bind
16427	2	5615	7	10	NULL	NULL	NULL	THP	GP		bind			127 - 138		alpha1beta1 integrins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_33_30516_s_199	12788934	(I)127 - 138 THP bound  7  times more strongly to the alpha2 integrin subunit than to  alpha1beta1 integrins or  alphaVbeta3 integrins, which had equivalent binding  strengths.	bind
16428	3	5615	7	10	NULL	NULL	NULL	THP	GP		bind			127 - 138		alphaVbeta3 integrins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_33_30516_s_199	12788934	(I)127 - 138 THP bound  7  times more strongly to the alpha2 integrin subunit than to  alpha1beta1 integrins or  alphaVbeta3 integrins, which had equivalent binding  strengths.	bind
16429	4	5615	7	10	NULL	NULL	NULL	statement 1	Process		is stronger than		significantly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_33_30516_s_199	12788934	(I)127 - 138 THP bound  7  times more strongly to the alpha2 integrin subunit than to  alpha1beta1 integrins or  alphaVbeta3 integrins, which had equivalent binding  strengths.	bind
16430	5	5615	7	10	NULL	NULL	NULL	statement 1	Process		is stronger than		significantly			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_33_30516_s_199	12788934	(I)127 - 138 THP bound  7  times more strongly to the alpha2 integrin subunit than to  alpha1beta1 integrins or  alphaVbeta3 integrins, which had equivalent binding  strengths.	bind
16431	6	5615	7	10	NULL	NULL	NULL	statement 2	Process		has equivalent strength to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_33_30516_s_199	12788934	(I)127 - 138 THP bound  7  times more strongly to the alpha2 integrin subunit than to  alpha1beta1 integrins or  alphaVbeta3 integrins, which had equivalent binding  strengths.	bind
17510	1	5616	6	10	NULL	NULL	NULL	THP	GP		bind		high affinity	925-937		heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_13_7275_s_121	9636139	(I)925-937 THP bound heparin with high affinity.	bind
16432	1	5616	7	10	NULL	NULL	NULL	THP	GP		bind		high affinity	925-937		heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_13_7275_s_121	9636139	(I)925-937 THP bound heparin with high affinity.	bind
17511	1	5617	6	10	NULL	NULL	NULL	THP	GP		bind		tightly	925-937		medium Mr heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_13_7275_s_101	9636139	(I)925-937 THP or type I collagen bound even more tightly to medium  Mr heparin ( Kd   250 nM and 14 nM, respectively).	bind
17512	2	5617	6	10	NULL	NULL	NULL	type I collagen	GP		bind		tightly			medium Mr heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_13_7275_s_101	9636139	(I)925-937 THP or type I collagen bound even more tightly to medium  Mr heparin ( Kd   250 nM and 14 nM, respectively).	bind
16433	1	5617	7	10	NULL	NULL	NULL	THP	GP		bind		tightly	925-937		medium Mr heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_13_7275_s_101	9636139	(I)925-937 THP or type I collagen bound even more tightly to medium  Mr heparin ( Kd   250 nM and 14 nM, respectively).	bind
16434	2	5617	7	10	NULL	NULL	NULL	 type I collagen	GP		bind		tightly			medium Mr heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_13_7275_s_101	9636139	(I)925-937 THP or type I collagen bound even more tightly to medium  Mr heparin ( Kd   250 nM and 14 nM, respectively).	bind
17513	1	5618	6	10	NULL	NULL	NULL	TLR3	GP	WT	bind		directly	ECD		pI:pC	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_23_8792_s_79	16720699	(I):p(C), a major portion of WT TLR3-ECD elutes in the void volume, at the same position as pI:pC (fraction 4), indicating that WT TLR3-ECD directly binds pI:pC.	bind
16435	1	5618	7	10	NULL	NULL	NULL	TLR3	GP	WT	binds		directly	ECD		pI:pC	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_23_8792_s_79	16720699	(I):p(C), a major portion of WT TLR3-ECD elutes in the void volume, at the same position as pI:pC (fraction 4), indicating that WT TLR3-ECD directly binds pI:pC.	bind
17521	1	5620	6	10	NULL	NULL	NULL	TnI	GP	skeletal	bind			residues 128-148		actin-tropomyosin	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_424_6944_35_s_163	12840750	(I); the corresponding peptide (residues 128-148  in skeletal TnI) binds to actin-tropomyosin and induces a weak inhibitory activity  on its own 32.	bind
16436	1	5620	7	10	NULL	NULL	NULL	 TnI	GP	skeletal	bind			128-148		actin-tropomyosin	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_424_6944_35_s_163	12840750	(I); the corresponding peptide (residues 128-148  in skeletal TnI) binds to actin-tropomyosin and induces a weak inhibitory activity  on its own 32.	bind
17522	1	5621	6	10	NULL	NULL	NULL	eutT genes	GP		encode					adenosyl-transferases	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_49_40948_s_24	16207720	(I)alamin adenosyl-transferases encoded by the  eutT and  pduO genes ( - ).	bind
17523	2	5621	6	10	NULL	NULL	NULL	pduO genes	GP		encode					adenosyl-transferases	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_49_40948_s_24	16207720	(I)alamin adenosyl-transferases encoded by the  eutT and  pduO genes ( - ).	bind
16438	1	5621	7	10	NULL	NULL	NULL	eutT gene	GP		encode					alamin adenosyl-transferases	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_49_40948_s_24	16207720	(I)alamin adenosyl-transferases encoded by the  eutT and  pduO genes ( - ).	bind
16439	2	5621	7	10	NULL	NULL	NULL	pduO gene	GP		encode					alamin adenosyl-transferases	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_49_40948_s_24	16207720	(I)alamin adenosyl-transferases encoded by the  eutT and  pduO genes ( - ).	bind
17524	1	5622	6	10	NULL	NULL	NULL	amide	Chemical		bind					CoFeSPCh	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_39_14331_s_166	16983091	(I)amide bound to CoFeSPCh and CH3-H4folate bound to MeTr.	bind
17525	2	5622	6	10	NULL	NULL	NULL	MeTr	GP		bind					CH3-H4folate	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_39_14331_s_166	16983091	(I)amide bound to CoFeSPCh and CH3-H4folate bound to MeTr.	bind
16440	1	5622	7	10	NULL	NULL	NULL	amide	Chemical		bind					CoFeSPCh	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_39_14331_s_166	16983091	(I)amide bound to CoFeSPCh and CH3-H4folate bound to MeTr.	bind
16441	2	5622	7	10	NULL	NULL	NULL	CH3-H4folate	Chemical		bind					MeTr 	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_39_14331_s_166	16983091	(I)amide bound to CoFeSPCh and CH3-H4folate bound to MeTr.	bind
17526	1	5623	6	10	NULL	NULL	NULL	collagen type I	GP		bind			CB6		heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1613_s_8	8576160	(I)CB6 of collagen type I, which also  binds heparin.	bind
16442	1	5623	7	10	NULL	NULL	NULL	type I collagen	GP		bind			CB6		heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1613_s_8	8576160	(I)CB6 of collagen type I, which also  binds heparin.	bind
17527	1	5624	6	10	NULL	NULL	NULL	KGF	GP		bind					alpha1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_30_26872_s_121	11973338	(I)CB8 as inhibitors of KGF binding to alpha1	bind
20306	2	5624	6	10	NULL	NULL	NULL	CB8	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_30_26872_s_121	11973338	(I)CB8 as inhibitors of KGF binding to alpha1	bind
16443	1	5624	7	10	NULL	NULL	NULL	KGF	GP		bind					alpha1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_30_26872_s_121	11973338	(I)CB8 as inhibitors of KGF binding to alpha1	bind
16444	2	5624	7	10	NULL	NULL	NULL	CB8	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_30_26872_s_121	11973338	(I)CB8 as inhibitors of KGF binding to alpha1	bind
17528	1	5625	6	10	NULL	NULL	NULL	Dkk-1-AP	GP		bind					LRP6N-IgG	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_90	11448771	(I, II) or hIgG (III, IV) Abs.  (c) Dkk-1-AP binding to LRP6N-IgG (circles, line) or IgG (squares).	bind
17529	2	5625	6	10	NULL	NULL	NULL	Dkk-1-AP	GP		bind					IgG	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_90	11448771	(I, II) or hIgG (III, IV) Abs.  (c) Dkk-1-AP binding to LRP6N-IgG (circles, line) or IgG (squares).	bind
17530	3	5625	6	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_90	11448771	(I, II) or hIgG (III, IV) Abs.  (c) Dkk-1-AP binding to LRP6N-IgG (circles, line) or IgG (squares).	bind
16445	1	5625	7	10	NULL	NULL	NULL	Dkk-1-AP	GP		bind					LRP6N-IgG	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_90	11448771	(I, II) or hIgG (III, IV) Abs.  (c) Dkk-1-AP binding to LRP6N-IgG (circles, line) or IgG (squares).	bind
20275	2	5625	7	10	NULL	NULL	NULL	Dkk-1-AP	GP		bind					IgG	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_90	11448771	(I, II) or hIgG (III, IV) Abs.  (c) Dkk-1-AP binding to LRP6N-IgG (circles, line) or IgG (squares).	bind
20276	3	5625	7	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_90	11448771	(I, II) or hIgG (III, IV) Abs.  (c) Dkk-1-AP binding to LRP6N-IgG (circles, line) or IgG (squares).	bind
17531	1	5627	6	10	NULL	NULL	NULL	pCVI-HSA	GP		bind					HSC	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_17_12743_s_275	10777570	(I, III, VI, and IV) interfered with 125I-pCVI-HSA binding to HSC (data not shown).	bind
16447	1	5627	7	10	NULL	NULL	NULL	25I-pCVI-HSA	GP		bind					HSC	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_17_12743_s_275	10777570	(I, III, VI, and IV) interfered with 125I-pCVI-HSA binding to HSC (data not shown).	bind
17685	1	5628	6	10	NULL	NULL	NULL	p12I	GP		bind		may			calcineurin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_18_15550_s_122	12601010	(I/ L)T Binds Calcineurin To test whether p12I binds calcineurin, we transiently transfected p12I into both 293T and Jurkat T cells and performed both immunoprecipitation and calmodulin bead pull-down experiments (Fig.  2).	bind
25321	1	5628	7	10	NULL	NULL	NULL	p12I	GP		bind		may			calcineurin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_18_15550_s_122	12601010	(I/ L)T Binds Calcineurin To test whether p12I binds calcineurin, we transiently transfected p12I into both 293T and Jurkat T cells and performed both immunoprecipitation and calmodulin bead pull-down experiments (Fig.  2).	bind
17693	1	5629	6	10	NULL	NULL	NULL	CXCL9	GP		bind					memory CD8+ T cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_9_2456_s_170	16955143	(I:C) diminished staining of CXCR3 on memory CD8+ T cells (Figure  3E), suggesting binding of its ligand CXCL9 and consequent downregulation of CXCR3 ( ).	bind
45748	2	5629	6	10	NULL	NULL	NULL	statement 1	Process		downregulates					CXCR3	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_9_2456_s_170	16955143	(I:C) diminished staining of CXCR3 on memory CD8+ T cells (Figure  3E), suggesting binding of its ligand CXCL9 and consequent downregulation of CXCR3 ( ).	bind
17023	1	5629	7	10	NULL	NULL	NULL	CXCL9	GP		bind					memory CD8+ T cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_9_2456_s_170	16955143	(I:C) diminished staining of CXCR3 on memory CD8+ T cells (Figure  3E), suggesting binding of its ligand CXCL9 and consequent downregulation of CXCR3 ( ).	bind
17024	2	5629	7	10	NULL	NULL	NULL	statement 1	Process		downregulates					CXCR3 	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_9_2456_s_170	16955143	(I:C) diminished staining of CXCR3 on memory CD8+ T cells (Figure  3E), suggesting binding of its ligand CXCL9 and consequent downregulation of CXCR3 ( ).	bind
17695	1	5630	6	10	NULL	NULL	NULL	TRIF-TRAF6	GP		play a role in					TAK1	GP	activation of 			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_22_2668_s_106	16260493	(I:C) leads to TAK1 activation through TRIF - TRAF6 (Sato et al. 2003 ), followed by NF-kappaB activation (Jiang et al. 2003 ).	bind
20307	2	5630	6	10	NULL	NULL	NULL	statement 1	Process		is followed by					NF-kappaB	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_22_2668_s_106	16260493	(I:C) leads to TAK1 activation through TRIF - TRAF6 (Sato et al. 2003 ), followed by NF-kappaB activation (Jiang et al. 2003 ).	bind
17025	1	5630	7	10	NULL	NULL	NULL	TAK1	GP	activation of	occurs through					TRIF - TRAF6	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_22_2668_s_106	16260493	(I:C) leads to TAK1 activation through TRIF - TRAF6 (Sato et al. 2003 ), followed by NF-kappaB activation (Jiang et al. 2003 ).	bind
17026	2	5630	7	10	NULL	NULL	NULL	statement 1	Process		is followed by					NF-kappaB	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_22_2668_s_106	16260493	(I:C) leads to TAK1 activation through TRIF - TRAF6 (Sato et al. 2003 ), followed by NF-kappaB activation (Jiang et al. 2003 ).	bind
17696	1	5632	6	10	NULL	NULL	NULL	IFN-inducing factor	GP		induces					IL-8	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_8_867_s_406	10222332	(IFN-inducing factor) induces IL-8 and IL-1 via TNF production from non-CD14+ human blood mononuclear cells.	bind
17697	2	5632	6	10	NULL	NULL	NULL	IFN-inducing factor	GP		induces					IL-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_8_867_s_406	10222332	(IFN-inducing factor) induces IL-8 and IL-1 via TNF production from non-CD14+ human blood mononuclear cells.	bind
17698	3	5632	6	10	NULL	NULL	NULL	blood mononuclear cells	Cell	non-CD14+ human	produce					TNF	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_8_867_s_406	10222332	(IFN-inducing factor) induces IL-8 and IL-1 via TNF production from non-CD14+ human blood mononuclear cells.	bind
17699	4	5632	6	10	NULL	NULL	NULL	statement 1	Process		occurs via					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_8_867_s_406	10222332	(IFN-inducing factor) induces IL-8 and IL-1 via TNF production from non-CD14+ human blood mononuclear cells.	bind
17700	5	5632	6	10	NULL	NULL	NULL	statement 2	Process		occurs via					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_8_867_s_406	10222332	(IFN-inducing factor) induces IL-8 and IL-1 via TNF production from non-CD14+ human blood mononuclear cells.	bind
17027	1	5632	7	10	NULL	NULL	NULL	IFN-inducing factor	GP		induce					IL-8	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_8_867_s_406	10222332	(IFN-inducing factor) induces IL-8 and IL-1 via TNF production from non-CD14+ human blood mononuclear cells.	bind
17028	2	5632	7	10	NULL	NULL	NULL	IFN-inducing factor	GP		induce					IL-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_8_867_s_406	10222332	(IFN-inducing factor) induces IL-8 and IL-1 via TNF production from non-CD14+ human blood mononuclear cells.	bind
17029	4	5632	7	10	NULL	NULL	NULL	statement 1	Process		occurs via					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_8_867_s_406	10222332	(IFN-inducing factor) induces IL-8 and IL-1 via TNF production from non-CD14+ human blood mononuclear cells.	bind
17030	5	5632	7	10	NULL	NULL	NULL	statement 2	Process		occurs via					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_8_867_s_406	10222332	(IFN-inducing factor) induces IL-8 and IL-1 via TNF production from non-CD14+ human blood mononuclear cells.	bind
45836	3	5632	7	10	NULL	NULL	NULL	blood mononuclear cells	Cell	non-CD14+ human	produce					TNF	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_8_867_s_406	10222332	(IFN-inducing factor) induces IL-8 and IL-1 via TNF production from non-CD14+ human blood mononuclear cells.	bind
17701	1	5633	6	10	NULL	NULL	NULL	FK506 peptidomacrolide	Chemical		bind					PP2B	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_97_1_21_s_9	11744159	(ii) After complexation with FKBP12, the FK506 peptidomacrolide binds to the protein phosphatase calcineurin (PP2B) which results in immediate inhibition of calcineurin activity.	bind
17702	2	5633	6	10	NULL	NULL	NULL	PP2B	GP		is					protein phosphatase calcineurin 	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_97_1_21_s_9	11744159	(ii) After complexation with FKBP12, the FK506 peptidomacrolide binds to the protein phosphatase calcineurin (PP2B) which results in immediate inhibition of calcineurin activity.	bind
17703	3	5633	6	10	NULL	NULL	NULL	statement 1	Process		inhibits					calcineurin 	GP	activity of 			NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_97_1_21_s_9	11744159	(ii) After complexation with FKBP12, the FK506 peptidomacrolide binds to the protein phosphatase calcineurin (PP2B) which results in immediate inhibition of calcineurin activity.	bind
17704	4	5633	6	10	NULL	NULL	NULL	FK506 peptidomacrolide	Chemical		complexes with					FKBP12	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_97_1_21_s_9	11744159	(ii) After complexation with FKBP12, the FK506 peptidomacrolide binds to the protein phosphatase calcineurin (PP2B) which results in immediate inhibition of calcineurin activity.	bind
17705	5	5633	6	10	NULL	NULL	NULL	statement 1	Process		occurs after					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_97_1_21_s_9	11744159	(ii) After complexation with FKBP12, the FK506 peptidomacrolide binds to the protein phosphatase calcineurin (PP2B) which results in immediate inhibition of calcineurin activity.	bind
17031	1	5633	7	10	NULL	NULL	NULL	FK506 peptidomacrolide	Chemical		complex with					FKBP12	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_97_1_21_s_9	11744159	(ii) After complexation with FKBP12, the FK506 peptidomacrolide binds to the protein phosphatase calcineurin (PP2B) which results in immediate inhibition of calcineurin activity.	bind
17032	2	5633	7	10	NULL	NULL	NULL	FK506 peptidomacrolide	Chemical		binds to					PP2B	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_97_1_21_s_9	11744159	(ii) After complexation with FKBP12, the FK506 peptidomacrolide binds to the protein phosphatase calcineurin (PP2B) which results in immediate inhibition of calcineurin activity.	bind
17033	3	5633	7	10	NULL	NULL	NULL	statement 2	Process		occurs after					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_97_1_21_s_9	11744159	(ii) After complexation with FKBP12, the FK506 peptidomacrolide binds to the protein phosphatase calcineurin (PP2B) which results in immediate inhibition of calcineurin activity.	bind
17034	4	5633	7	10	NULL	NULL	NULL	statement 2	Process		inhibits					calcineurin	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_97_1_21_s_9	11744159	(ii) After complexation with FKBP12, the FK506 peptidomacrolide binds to the protein phosphatase calcineurin (PP2B) which results in immediate inhibition of calcineurin activity.	bind
17035	5	5633	7	10	NULL	NULL	NULL	PP2B	GP		is					protein phosphatase calcineurin	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_97_1_21_s_9	11744159	(ii) After complexation with FKBP12, the FK506 peptidomacrolide binds to the protein phosphatase calcineurin (PP2B) which results in immediate inhibition of calcineurin activity.	bind
17706	1	5634	6	10	NULL	NULL	NULL	ATP	Chemical	hydrolysis of	unwraps					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_601_s_229	11157766	(ii) After the ATP hydrolysis the DNA becomes unwrapped, but UvrA remains bound to the complex, thereby directing the wrapping after binding of the new ATP molecule.	bind
17707	2	5634	6	10	NULL	NULL	NULL	UvrA	GP		directs					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_601_s_229	11157766	(ii) After the ATP hydrolysis the DNA becomes unwrapped, but UvrA remains bound to the complex, thereby directing the wrapping after binding of the new ATP molecule.	bind
17708	3	5634	6	10	NULL	NULL	NULL	statement 2	Process		occurs after					ATP molecule	Chemical	wrapping of 			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_601_s_229	11157766	(ii) After the ATP hydrolysis the DNA becomes unwrapped, but UvrA remains bound to the complex, thereby directing the wrapping after binding of the new ATP molecule.	bind
17036	1	5634	7	10	NULL	NULL	NULL	ATP	Chemical	hydrolysis of	unwraps					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_601_s_229	11157766	(ii) After the ATP hydrolysis the DNA becomes unwrapped, but UvrA remains bound to the complex, thereby directing the wrapping after binding of the new ATP molecule.	bind
17037	3	5634	7	10	NULL	NULL	NULL	UvrA	GP		directs					DNA	NucleicAcid	wrapping of			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_601_s_229	11157766	(ii) After the ATP hydrolysis the DNA becomes unwrapped, but UvrA remains bound to the complex, thereby directing the wrapping after binding of the new ATP molecule.	bind
17038	2	5634	7	10	NULL	NULL	NULL	statement 1	Process		bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_601_s_229	11157766	(ii) After the ATP hydrolysis the DNA becomes unwrapped, but UvrA remains bound to the complex, thereby directing the wrapping after binding of the new ATP molecule.	bind
20285	4	5634	7	10	NULL	NULL	NULL	statement 3	Process		occurs after					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_601_s_229	11157766	(ii) After the ATP hydrolysis the DNA becomes unwrapped, but UvrA remains bound to the complex, thereby directing the wrapping after binding of the new ATP molecule.	bind
17709	1	5635	6	10	NULL	NULL	NULL	HSF	GP		bind									HSE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_28_26332_s_238	11306579	(ii) Alternatively, it could be recruited only when HSFs binds to the HSEs and increase the stability of the nucleoprotein complex (Fig.  7 B).	bind
17710	2	5635	6	10	NULL	NULL	NULL	statement 1	Process		increase					nucleoprotein complex	GP	stability of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_28_26332_s_238	11306579	(ii) Alternatively, it could be recruited only when HSFs binds to the HSEs and increase the stability of the nucleoprotein complex (Fig.  7 B).	bind
17041	1	5635	7	10	NULL	NULL	NULL	HSF	GP		bind									HSE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_28_26332_s_238	11306579	(ii) Alternatively, it could be recruited only when HSFs binds to the HSEs and increase the stability of the nucleoprotein complex (Fig.  7 B).	bind
17042	2	5635	7	10	NULL	NULL	NULL	statement 1	Process		increase					nucleoprotein complex	GP	stability of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_28_26332_s_238	11306579	(ii) Alternatively, it could be recruited only when HSFs binds to the HSEs and increase the stability of the nucleoprotein complex (Fig.  7 B).	bind
20739	1	5636	6	10	NULL	NULL	NULL	OP2	GP		allow		could			unidentified regulator protein	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_19_5948_s_158	10498706	(ii) Alternatively, OP2 could allow the binding of an unidentified regulator protein acting synergically with KdgR and whose action would strictly depend on the simultaneous presence of KdgR.	bind
20740	2	5636	6	10	NULL	NULL	NULL	unidentified regulator protein	GP		acts with		synergistically			KdgR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_19_5948_s_158	10498706	(ii) Alternatively, OP2 could allow the binding of an unidentified regulator protein acting synergically with KdgR and whose action would strictly depend on the simultaneous presence of KdgR.	bind
20741	3	5636	6	10	NULL	NULL	NULL	unidentified regulator protein	GP	action of	depend on		strictly;; could			KdgR	GP	presence of 			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_19_5948_s_158	10498706	(ii) Alternatively, OP2 could allow the binding of an unidentified regulator protein acting synergically with KdgR and whose action would strictly depend on the simultaneous presence of KdgR.	bind
17043	1	5636	7	10	NULL	NULL	NULL	OP2	GP		allows					unidentified regulator protein 	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_19_5948_s_158	10498706	(ii) Alternatively, OP2 could allow the binding of an unidentified regulator protein acting synergically with KdgR and whose action would strictly depend on the simultaneous presence of KdgR.	bind
17050	2	5636	7	10	NULL	NULL	NULL	unidentified regulator protein 	GP		acts		synergistically			KdgR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_19_5948_s_158	10498706	(ii) Alternatively, OP2 could allow the binding of an unidentified regulator protein acting synergically with KdgR and whose action would strictly depend on the simultaneous presence of KdgR.	bind
17051	3	5636	7	10	NULL	NULL	NULL	unidentified regulator protein 	GP	action of	depends on		strictly			KdgR	GP	presence of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_19_5948_s_158	10498706	(ii) Alternatively, OP2 could allow the binding of an unidentified regulator protein acting synergically with KdgR and whose action would strictly depend on the simultaneous presence of KdgR.	bind
17711	1	5637	6	10	NULL	NULL	NULL	CaM	GP		blocks 		completely			G protein	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_42_32672_s_340	10926927	(ii) At a concentration where CaM completely blocks G protein activation, the formation of the agonist/receptor/G protein complex, hence, high affinity agonist binding is virtually unaffected.	bind
20308	2	5637	6	10	NULL	NULL	NULL	CaM	GP		does not affect					agonist/receptor/G protein complex	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_42_32672_s_340	10926927	(ii) At a concentration where CaM completely blocks G protein activation, the formation of the agonist/receptor/G protein complex, hence, high affinity agonist binding is virtually unaffected.	bind
20309	3	5637	6	10	NULL	NULL	NULL	CaM	GP		does not affect					agonist	GP	high affinity binding of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_42_32672_s_340	10926927	(ii) At a concentration where CaM completely blocks G protein activation, the formation of the agonist/receptor/G protein complex, hence, high affinity agonist binding is virtually unaffected.	bind
17052	1	5637	7	10	NULL	NULL	NULL	CaM	GP		blocks		completely			G protein	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_42_32672_s_340	10926927	(ii) At a concentration where CaM completely blocks G protein activation, the formation of the agonist/receptor/G protein complex, hence, high affinity agonist binding is virtually unaffected.	bind
17053	2	5637	7	10	NULL	NULL	NULL	CaM	GP		does not affect					agonist/receptor/G protein complex	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_42_32672_s_340	10926927	(ii) At a concentration where CaM completely blocks G protein activation, the formation of the agonist/receptor/G protein complex, hence, high affinity agonist binding is virtually unaffected.	bind
17056	3	5637	7	10	NULL	NULL	NULL	CaM	GP		does not affect					agonist	GP	high affinity binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_42_32672_s_340	10926927	(ii) At a concentration where CaM completely blocks G protein activation, the formation of the agonist/receptor/G protein complex, hence, high affinity agonist binding is virtually unaffected.	bind
17712	1	5638	6	10	NULL	NULL	NULL	ATP	Chemical		bind					polypeptide-containing ring of GroEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21251_s_20	10409682	(ii) Bind-ing of ATP to the polypeptide-containing ring of GroEL permits the binding of GroES to that ring accompanying the release of polypeptide into an enclosed cage, defined by the GroEL cavity and the dome of GroES, in which folding to the native state can proceed with aggregation being avoided ( 6,  8-13).	bind
17713	2	5638	6	10	NULL	NULL	NULL	GroES	GP		bind					polypeptide-containing ring of GroEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21251_s_20	10409682	(ii) Bind-ing of ATP to the polypeptide-containing ring of GroEL permits the binding of GroES to that ring accompanying the release of polypeptide into an enclosed cage, defined by the GroEL cavity and the dome of GroES, in which folding to the native state can proceed with aggregation being avoided ( 6,  8-13).	bind
17714	3	5638	6	10	NULL	NULL	NULL	statement 1	Process		permits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21251_s_20	10409682	(ii) Bind-ing of ATP to the polypeptide-containing ring of GroEL permits the binding of GroES to that ring accompanying the release of polypeptide into an enclosed cage, defined by the GroEL cavity and the dome of GroES, in which folding to the native state can proceed with aggregation being avoided ( 6,  8-13).	bind
17068	1	5638	7	10	NULL	NULL	NULL	ATP	Chemical		bind					polypeptide-containing ring GroEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21251_s_20	10409682	(ii) Bind-ing of ATP to the polypeptide-containing ring of GroEL permits the binding of GroES to that ring accompanying the release of polypeptide into an enclosed cage, defined by the GroEL cavity and the dome of GroES, in which folding to the native state can proceed with aggregation being avoided ( 6,  8-13).	bind
17071	2	5638	7	10	NULL	NULL	NULL	GroES	GP		bind					polypeptide-containing ring GroEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21251_s_20	10409682	(ii) Bind-ing of ATP to the polypeptide-containing ring of GroEL permits the binding of GroES to that ring accompanying the release of polypeptide into an enclosed cage, defined by the GroEL cavity and the dome of GroES, in which folding to the native state can proceed with aggregation being avoided ( 6,  8-13).	bind
17072	3	5638	7	10	NULL	NULL	NULL	statement 1	Process		permits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21251_s_20	10409682	(ii) Bind-ing of ATP to the polypeptide-containing ring of GroEL permits the binding of GroES to that ring accompanying the release of polypeptide into an enclosed cage, defined by the GroEL cavity and the dome of GroES, in which folding to the native state can proceed with aggregation being avoided ( 6,  8-13).	bind
17733	1	5639	6	10	NULL	NULL	NULL	bacteria	Organism		bind					Eap-coated surface	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_6_2933_s_197	12010982	(ii) Binding of bacteria to Eap-coated surface.	bind
17089	1	5639	7	10	NULL	NULL	NULL	bacteria	Organism		bind					Eap-coated surface	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_6_2933_s_197	12010982	(ii) Binding of bacteria to Eap-coated surface.	bind
17734	1	5640	6	10	NULL	NULL	NULL	PGN	GP		bind					CD14	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17735	2	5640	6	10	NULL	NULL	NULL	CD14	GP		bind					LPS	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17736	3	5640	6	10	NULL	NULL	NULL	PGN	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17737	4	5640	6	10	NULL	NULL	NULL	PGN	GP		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17738	5	5640	6	10	NULL	NULL	NULL	lysostaphin	GP		is a type of					PGN-lytic enzyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17739	6	5640	6	10	NULL	NULL	NULL	muramidase SG	GP		is a type of					PGN-lytic enzyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17740	7	5640	6	10	NULL	NULL	NULL	lysozyme	GP		is a type of					PGN-lytic enzyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17741	8	5640	6	10	NULL	NULL	NULL	statement 5	Process		disrupts					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17742	9	5640	6	10	NULL	NULL	NULL	statement 5	Process		disrupts					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17743	10	5640	6	10	NULL	NULL	NULL	statement 6	Process		disrupts					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17744	11	5640	6	10	NULL	NULL	NULL	statement 6	Process		disrupts					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17745	12	5640	6	10	NULL	NULL	NULL	statement 7	Process		disrupts					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17746	13	5640	6	10	NULL	NULL	NULL	statement 7	Process		disrupts					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17090	1	5640	7	10	NULL	NULL	NULL	PGN	GP		bind					CD14	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17091	2	5640	7	10	NULL	NULL	NULL	LPS	Chemical		bind					CD14	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17092	3	5640	7	10	NULL	NULL	NULL	PGN	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17093	4	5640	7	10	NULL	NULL	NULL	PGN	GP		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17094	5	5640	7	10	NULL	NULL	NULL	lysostaphin	GP		is a type of					PGN-lytic enzymes	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17095	6	5640	7	10	NULL	NULL	NULL	muramidase SG	GP		is a type of					PGN-lytic enzymes	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17096	7	5640	7	10	NULL	NULL	NULL	lysozyme	GP		is a type of					PGN-lytic enzymes	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17097	8	5640	7	10	NULL	NULL	NULL	statement 5	Process		disrupts					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17098	9	5640	7	10	NULL	NULL	NULL	statement 5	Process		disrupts					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17099	10	5640	7	10	NULL	NULL	NULL	statement 6	Process		disrupts					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
45847	11	5640	7	10	NULL	NULL	NULL	statement 6	Process		disrupts					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
45848	12	5640	7	10	NULL	NULL	NULL	statement 7	Process		disrupts					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
45849	13	5640	7	10	NULL	NULL	NULL	statement 7	Process		disrupts					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8680_s_251	9535844	(ii) Binding of PGN to CD14 and the inhibitory capacity of PGN for CD14 binding to PGN and LPS are lost when the PGN preparations are digested with PGN-lytic enzymes (lysostaphin, muramidase SG, and lysozyme) but are not affected by digestion with other enzymes (heparinase, RNase, DNase, and trypsin).	bind
17747	1	5641	6	10	NULL	NULL	NULL	Raf	GP		bind					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4623_s_312	10373511	(ii) Binding of Raf to Ras does not change the intrinsic GTPase activity of Ras (50% conversion of GTP to GDP in about 30 min) ( 10) or slightly enhances it ( 40).	bind
17748	2	5641	6	10	NULL	NULL	NULL	Ras	GP		activates					GTPase	GP	intrinsic			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4623_s_312	10373511	(ii) Binding of Raf to Ras does not change the intrinsic GTPase activity of Ras (50% conversion of GTP to GDP in about 30 min) ( 10) or slightly enhances it ( 40).	bind
17749	3	5641	6	10	NULL	NULL	NULL	statement 1	Process		does not change					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4623_s_312	10373511	(ii) Binding of Raf to Ras does not change the intrinsic GTPase activity of Ras (50% conversion of GTP to GDP in about 30 min) ( 10) or slightly enhances it ( 40).	bind
20310	4	5641	6	10	NULL	NULL	NULL	statement 1	Process		slightly enhances					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4623_s_312	10373511	(ii) Binding of Raf to Ras does not change the intrinsic GTPase activity of Ras (50% conversion of GTP to GDP in about 30 min) ( 10) or slightly enhances it ( 40).	bind
20311	5	5641	6	10	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4623_s_312	10373511	(ii) Binding of Raf to Ras does not change the intrinsic GTPase activity of Ras (50% conversion of GTP to GDP in about 30 min) ( 10) or slightly enhances it ( 40).	bind
17100	1	5641	7	10	NULL	NULL	NULL	Raf	GP		bind					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4623_s_312	10373511	(ii) Binding of Raf to Ras does not change the intrinsic GTPase activity of Ras (50% conversion of GTP to GDP in about 30 min) ( 10) or slightly enhances it ( 40).	bind
17101	2	5641	7	10	NULL	NULL	NULL	statement 1	GP		does not change					Ras	GP	intrinsic GTPase activity of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4623_s_312	10373511	(ii) Binding of Raf to Ras does not change the intrinsic GTPase activity of Ras (50% conversion of GTP to GDP in about 30 min) ( 10) or slightly enhances it ( 40).	bind
17102	3	5641	7	10	NULL	NULL	NULL	statement 1	Process		enhance		slightly			Ras	GP	intrinsic GTPase activity of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4623_s_312	10373511	(ii) Binding of Raf to Ras does not change the intrinsic GTPase activity of Ras (50% conversion of GTP to GDP in about 30 min) ( 10) or slightly enhances it ( 40).	bind
17103	4	5641	7	10	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4623_s_312	10373511	(ii) Binding of Raf to Ras does not change the intrinsic GTPase activity of Ras (50% conversion of GTP to GDP in about 30 min) ( 10) or slightly enhances it ( 40).	bind
17750	1	5642	6	10	NULL	NULL	NULL	surface proteins	GP		bind					choline 	Chemical	containing teichoic acids			NULL	Streptococcus pneumoniae	NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1694_1_269_s_10	15546671	(ii) Binding of surface proteins to choline containing teichoic acids (in  Streptococcus pneumoniae) [  9].	bind
17104	1	5642	7	10	NULL	NULL	NULL	surface proteins	GP		bind					choline	Chemical	containing teichoic acids			NULL	Streptococcus pneumoniae	NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1694_1_269_s_10	15546671	(ii) Binding of surface proteins to choline containing teichoic acids (in  Streptococcus pneumoniae) [  9].	bind
17751	1	5643	6	10	NULL	NULL	NULL	Wzt	GP		bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_7_4458_s_91	11401986	(ii) Binding of Wzt to ATP.	bind
17105	1	5643	7	10	NULL	NULL	NULL	Wzt	GP		bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_7_4458_s_91	11401986	(ii) Binding of Wzt to ATP.	bind
17752	1	5645	6	10	NULL	NULL	NULL	ghrelin	GP		bind					GHSR-1a	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_6_1029_s_151	12486113	(ii) Both ghrelin and its deacylated form, des-acyl ghrelin, recognize a common high affinity binding site, although only ghrelin and not des-acyl ghrelin bind to GHSR-1a ( Kojima et al., 1999).	bind
17753	2	5645	6	10	NULL	NULL	NULL	des-acyl ghrelin	GP		does not bind					GHSR-1a	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_6_1029_s_151	12486113	(ii) Both ghrelin and its deacylated form, des-acyl ghrelin, recognize a common high affinity binding site, although only ghrelin and not des-acyl ghrelin bind to GHSR-1a ( Kojima et al., 1999).	bind
45630	3	5645	6	10	NULL	NULL	NULL	des-acyl ghrelin	GP		is deacylated form of					ghrelin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_6_1029_s_151	12486113	(ii) Both ghrelin and its deacylated form, des-acyl ghrelin, recognize a common high affinity binding site, although only ghrelin and not des-acyl ghrelin bind to GHSR-1a ( Kojima et al., 1999).	bind
17107	1	5645	7	10	NULL	NULL	NULL	ghrelin	GP		bind					GHSR-1a	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_6_1029_s_151	12486113	(ii) Both ghrelin and its deacylated form, des-acyl ghrelin, recognize a common high affinity binding site, although only ghrelin and not des-acyl ghrelin bind to GHSR-1a ( Kojima et al., 1999).	bind
17108	2	5645	7	10	NULL	NULL	NULL	des-acyl ghrelin	GP		does not bind					GHSR-1a	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_6_1029_s_151	12486113	(ii) Both ghrelin and its deacylated form, des-acyl ghrelin, recognize a common high affinity binding site, although only ghrelin and not des-acyl ghrelin bind to GHSR-1a ( Kojima et al., 1999).	bind
17109	3	5645	7	10	NULL	NULL	NULL	des-acyl ghrelin	GP		is deacylated form of					ghrelin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_6_1029_s_151	12486113	(ii) Both ghrelin and its deacylated form, des-acyl ghrelin, recognize a common high affinity binding site, although only ghrelin and not des-acyl ghrelin bind to GHSR-1a ( Kojima et al., 1999).	bind
17754	1	5646	6	10	NULL	NULL	NULL	E2	GP		bind					ER	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_4_1978_s_274	16314411	(ii) Ca2+/calmodulin stimulates E2 binding to the ER ( ).	bind
17755	2	5646	6	10	NULL	NULL	NULL	Ca2+	Chemical		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_4_1978_s_274	16314411	(ii) Ca2+/calmodulin stimulates E2 binding to the ER ( ).	bind
67377	3	5646	6	10	NULL	0	NULL	calmodulin	GP		stimulates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_4_1978_s_274	16314411	(ii) Ca2+/calmodulin stimulates E2 binding to the ER ( ).	bind
17110	1	5646	7	10	NULL	NULL	NULL	E2	GP		bind					ER	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_4_1978_s_274	16314411	(ii) Ca2+/calmodulin stimulates E2 binding to the ER ( ).	bind
17111	2	5646	7	10	NULL	NULL	NULL	Ca2+	Chemical		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_4_1978_s_274	16314411	(ii) Ca2+/calmodulin stimulates E2 binding to the ER ( ).	bind
67378	3	5646	7	10	NULL	0	NULL	calmodulin	GP		stimulates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_4_1978_s_274	16314411	(ii) Ca2+/calmodulin stimulates E2 binding to the ER ( ).	bind
17756	1	5649	6	10	NULL	NULL	NULL	statins	gP		bind					LFA-1	GP				NULL	antigen presenting cells	NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_12	15186950	(ii) Certain statins bind to the adhesion molecule leucocyte function antigen-1  (LFA-1) on antigen-presenting cells and therefore block the interaction with T cells  expressing the counter-receptor intercellular adhesion molecule-1 (ICAM-1) [  12].	bind
17757	2	5649	6	10	NULL	NULL	NULL	LFA-1	GP		is					leucocyte function antigen-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_12	15186950	(ii) Certain statins bind to the adhesion molecule leucocyte function antigen-1  (LFA-1) on antigen-presenting cells and therefore block the interaction with T cells  expressing the counter-receptor intercellular adhesion molecule-1 (ICAM-1) [  12].	bind
17758	3	5649	6	10	NULL	NULL	NULL	ICAM-1	GP		is					intercellular adhesion molecule-1 	GP				NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_12	15186950	(ii) Certain statins bind to the adhesion molecule leucocyte function antigen-1  (LFA-1) on antigen-presenting cells and therefore block the interaction with T cells  expressing the counter-receptor intercellular adhesion molecule-1 (ICAM-1) [  12].	bind
17759	4	5649	6	10	NULL	NULL	NULL	T cells	Cell		express					ICAM-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_12	15186950	(ii) Certain statins bind to the adhesion molecule leucocyte function antigen-1  (LFA-1) on antigen-presenting cells and therefore block the interaction with T cells  expressing the counter-receptor intercellular adhesion molecule-1 (ICAM-1) [  12].	bind
17760	5	5649	6	10	NULL	NULL	NULL	statement 1	Process		block					statement 4	Process	 interaction with			NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_12	15186950	(ii) Certain statins bind to the adhesion molecule leucocyte function antigen-1  (LFA-1) on antigen-presenting cells and therefore block the interaction with T cells  expressing the counter-receptor intercellular adhesion molecule-1 (ICAM-1) [  12].	bind
45631	6	5649	6	10	NULL	NULL	NULL	LFA-1	GP		is a type of					adhesion molecule	GP				NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_12	15186950	(ii) Certain statins bind to the adhesion molecule leucocyte function antigen-1  (LFA-1) on antigen-presenting cells and therefore block the interaction with T cells  expressing the counter-receptor intercellular adhesion molecule-1 (ICAM-1) [  12].	bind
45632	7	5649	6	10	NULL	NULL	NULL	ICAM-1	GP		is a type of					counter-receptor molecule	GP				NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_12	15186950	(ii) Certain statins bind to the adhesion molecule leucocyte function antigen-1  (LFA-1) on antigen-presenting cells and therefore block the interaction with T cells  expressing the counter-receptor intercellular adhesion molecule-1 (ICAM-1) [  12].	bind
17112	1	5649	7	10	NULL	NULL	NULL	statins	GP		bind					LFA-1	GP				NULL	antigen-presenting cells	NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_12	15186950	(ii) Certain statins bind to the adhesion molecule leucocyte function antigen-1  (LFA-1) on antigen-presenting cells and therefore block the interaction with T cells  expressing the counter-receptor intercellular adhesion molecule-1 (ICAM-1) [  12].	bind
17113	2	5649	7	10	NULL	NULL	NULL	antigen-presenting cells	Cell		bind					T cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_12	15186950	(ii) Certain statins bind to the adhesion molecule leucocyte function antigen-1  (LFA-1) on antigen-presenting cells and therefore block the interaction with T cells  expressing the counter-receptor intercellular adhesion molecule-1 (ICAM-1) [  12].	bind
17114	3	5649	7	10	NULL	NULL	NULL	T cells	Cell		express					ICAM-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_12	15186950	(ii) Certain statins bind to the adhesion molecule leucocyte function antigen-1  (LFA-1) on antigen-presenting cells and therefore block the interaction with T cells  expressing the counter-receptor intercellular adhesion molecule-1 (ICAM-1) [  12].	bind
17115	4	5649	7	10	NULL	NULL	NULL	statement 1	Process		blocks					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_12	15186950	(ii) Certain statins bind to the adhesion molecule leucocyte function antigen-1  (LFA-1) on antigen-presenting cells and therefore block the interaction with T cells  expressing the counter-receptor intercellular adhesion molecule-1 (ICAM-1) [  12].	bind
17117	6	5649	7	10	NULL	NULL	NULL	LFA-1	GP		is					leucocyte function antigen-1 	GP				NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_12	15186950	(ii) Certain statins bind to the adhesion molecule leucocyte function antigen-1  (LFA-1) on antigen-presenting cells and therefore block the interaction with T cells  expressing the counter-receptor intercellular adhesion molecule-1 (ICAM-1) [  12].	bind
17118	7	5649	7	10	NULL	NULL	NULL	ICAM-1	GP		is					intercellular adhesion molecule-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_12	15186950	(ii) Certain statins bind to the adhesion molecule leucocyte function antigen-1  (LFA-1) on antigen-presenting cells and therefore block the interaction with T cells  expressing the counter-receptor intercellular adhesion molecule-1 (ICAM-1) [  12].	bind
17119	8	5649	7	10	NULL	NULL	NULL	LFA-1	GP		is a type of					adhesion molecule	GP				NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_12	15186950	(ii) Certain statins bind to the adhesion molecule leucocyte function antigen-1  (LFA-1) on antigen-presenting cells and therefore block the interaction with T cells  expressing the counter-receptor intercellular adhesion molecule-1 (ICAM-1) [  12].	bind
17120	9	5649	7	10	NULL	NULL	NULL	ICAM-1	GP		is a type of					counter-receptor molecule	GP				NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_12	15186950	(ii) Certain statins bind to the adhesion molecule leucocyte function antigen-1  (LFA-1) on antigen-presenting cells and therefore block the interaction with T cells  expressing the counter-receptor intercellular adhesion molecule-1 (ICAM-1) [  12].	bind
17761	1	5650	6	10	NULL	NULL	NULL	CTCF	GP		does not bind					ICR	GP			insulator sites	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_11_4791_s_234	15143173	(ii) CTCF binds to other sequences in the ICR -- aside from the insulator sites -- to inhibit methylation.	bind
17762	2	5650	6	10	NULL	NULL	NULL	CTCF	GP		bind					ICR	GP			other sequences	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_11_4791_s_234	15143173	(ii) CTCF binds to other sequences in the ICR -- aside from the insulator sites -- to inhibit methylation.	bind
17763	3	5650	6	10	NULL	NULL	NULL	statement 2	Process		inhibits					methylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_11_4791_s_234	15143173	(ii) CTCF binds to other sequences in the ICR -- aside from the insulator sites -- to inhibit methylation.	bind
17121	1	5650	7	10	NULL	NULL	NULL	CTCF	GP		binds					 ICR	GP			sequences	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_11_4791_s_234	15143173	(ii) CTCF binds to other sequences in the ICR -- aside from the insulator sites -- to inhibit methylation.	bind
17122	2	5650	7	10	NULL	NULL	NULL	CTCF	GP		does not bind					ICR	GP			insulator sites	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_11_4791_s_234	15143173	(ii) CTCF binds to other sequences in the ICR -- aside from the insulator sites -- to inhibit methylation.	bind
17123	3	5650	7	10	NULL	NULL	NULL	statement 1	Process		inhibits					methylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_11_4791_s_234	15143173	(ii) CTCF binds to other sequences in the ICR -- aside from the insulator sites -- to inhibit methylation.	bind
17764	1	5651	6	10	NULL	NULL	NULL	Vn	GP	denatured	bind		dose dependently			glycoprotein IIb/IIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_21_13705_s_7	9153222	(ii) Denatured Vn binds to both glycoprotein IIb/IIa and alphavbeta3 in a dose-dependent manner.	bind
17765	2	5651	6	10	NULL	NULL	NULL	Vn	GP	denatured	bind		dose dependently			alphavbeta3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_21_13705_s_7	9153222	(ii) Denatured Vn binds to both glycoprotein IIb/IIa and alphavbeta3 in a dose-dependent manner.	bind
17124	1	5651	7	10	NULL	NULL	NULL	Vn 	GP	denatured	bind		dose-dependently			glycoprotein IIb/IIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_21_13705_s_7	9153222	(ii) Denatured Vn binds to both glycoprotein IIb/IIa and alphavbeta3 in a dose-dependent manner.	bind
17125	2	5651	7	10	NULL	NULL	NULL	Vn	GP	denatured	bind		dose-dependently			alphavbeta3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_21_13705_s_7	9153222	(ii) Denatured Vn binds to both glycoprotein IIb/IIa and alphavbeta3 in a dose-dependent manner.	bind
17766	1	5652	6	10	NULL	NULL	NULL	DicB	GP 		have affinity for a					septal ring factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_11_2951_s_264	12003935	(ii) DicB itself might have affinity for a septal ring factor and recruit MinC. (iii) The binding of DicB to MinC might create a site on the heteromeric complex with a high affinity for a septal ring-associated target.	bind
17767	2	5652	6	10	NULL	NULL	NULL	DicB	GP		recruit					MinC	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_11_2951_s_264	12003935	(ii) DicB itself might have affinity for a septal ring factor and recruit MinC. (iii) The binding of DicB to MinC might create a site on the heteromeric complex with a high affinity for a septal ring-associated target.	bind
17768	3	5652	6	10	NULL	NULL	NULL	DicB	GP		bind					MinC	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_11_2951_s_264	12003935	(ii) DicB itself might have affinity for a septal ring factor and recruit MinC. (iii) The binding of DicB to MinC might create a site on the heteromeric complex with a high affinity for a septal ring-associated target.	bind
17769	4	5652	6	10	NULL	NULL	NULL	statement 3	Process		create		may			heteromeric complex	GP		site		NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_11_2951_s_264	12003935	(ii) DicB itself might have affinity for a septal ring factor and recruit MinC. (iii) The binding of DicB to MinC might create a site on the heteromeric complex with a high affinity for a septal ring-associated target.	bind
17770	5	5652	6	10	NULL	NULL	NULL	heteromeric complex	GP		has high affinity for					septal ring-associated target	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_11_2951_s_264	12003935	(ii) DicB itself might have affinity for a septal ring factor and recruit MinC. (iii) The binding of DicB to MinC might create a site on the heteromeric complex with a high affinity for a septal ring-associated target.	bind
17128	1	5652	7	10	NULL	NULL	NULL	DicB	GP		 has affinity for					septal ring factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_11_2951_s_264	12003935	(ii) DicB itself might have affinity for a septal ring factor and recruit MinC. (iii) The binding of DicB to MinC might create a site on the heteromeric complex with a high affinity for a septal ring-associated target.	bind
17129	2	5652	7	10	NULL	NULL	NULL	DicB	GP		recruit					MinC	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_11_2951_s_264	12003935	(ii) DicB itself might have affinity for a septal ring factor and recruit MinC. (iii) The binding of DicB to MinC might create a site on the heteromeric complex with a high affinity for a septal ring-associated target.	bind
17130	4	5652	7	10	NULL	NULL	NULL	statement 3	Process		create					heteromeric complex	GP	a site on the			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_11_2951_s_264	12003935	(ii) DicB itself might have affinity for a septal ring factor and recruit MinC. (iii) The binding of DicB to MinC might create a site on the heteromeric complex with a high affinity for a septal ring-associated target.	bind
17131	5	5652	7	10	NULL	NULL	NULL	heteromeric complex	GP		high affinity for					septal ring-associated target	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_11_2951_s_264	12003935	(ii) DicB itself might have affinity for a septal ring factor and recruit MinC. (iii) The binding of DicB to MinC might create a site on the heteromeric complex with a high affinity for a septal ring-associated target.	bind
45850	3	5652	7	10	NULL	NULL	NULL	DicB	GP		bind					MinC	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_11_2951_s_264	12003935	(ii) DicB itself might have affinity for a septal ring factor and recruit MinC. (iii) The binding of DicB to MinC might create a site on the heteromeric complex with a high affinity for a septal ring-associated target.	bind
17358	1	5653	7	10	NULL	NULL	NULL	GPVI	GP		bind					Fc Rgamma	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_17_15441_s_214	12594225	(ii) Does GPVI interact with Fc Rgamma, calmodulin, and Lyn through discrete protein domains or does the receptor interact with these proteins in an interdependent fashion that requires formation of a complex in which some or all must be present?	bind
17359	2	5653	7	10	NULL	NULL	NULL	GPVI	GP		bind					calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_17_15441_s_214	12594225	(ii) Does GPVI interact with Fc Rgamma, calmodulin, and Lyn through discrete protein domains or does the receptor interact with these proteins in an interdependent fashion that requires formation of a complex in which some or all must be present?	bind
17360	3	5653	7	10	NULL	NULL	NULL	GPVI	GP		bind					Lyn	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_17_15441_s_214	12594225	(ii) Does GPVI interact with Fc Rgamma, calmodulin, and Lyn through discrete protein domains or does the receptor interact with these proteins in an interdependent fashion that requires formation of a complex in which some or all must be present?	bind
17778	1	5654	6	10	NULL	NULL	NULL	G6P	GP		bind		strongly;;anti-cooperatively			HKI	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_44_31155_s_32	10531306	(ii) G6P binding to HKI must be strongly anti-cooperative.	bind
17132	1	5654	7	10	NULL	NULL	NULL	G6P	GP		bind		strongly;;anti-cooperatively			HKI 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_44_31155_s_32	10531306	(ii) G6P binding to HKI must be strongly anti-cooperative.	bind
17779	1	5655	6	10	NULL	NULL	NULL	HSP90	GP		bind					eNOS	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_11_9339_s_191	12519764	(ii) HSP90 binding to eNOS increases when the quantity of CaM bound to eNOS remains constant (Fig.  5), and this results in a further increase in eNOS activity (from 139% to 254% of basal eNOS activity at 12 and 45 nM HSP90, respectively; Fig.  2).	bind
17780	2	5655	6	10	NULL	NULL	NULL	CaM	GP		bind					eNOS	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_11_9339_s_191	12519764	(ii) HSP90 binding to eNOS increases when the quantity of CaM bound to eNOS remains constant (Fig.  5), and this results in a further increase in eNOS activity (from 139% to 254% of basal eNOS activity at 12 and 45 nM HSP90, respectively; Fig.  2).	bind
17134	1	5655	7	10	NULL	NULL	NULL	HSP90	GP		bind					eNOS	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_11_9339_s_191	12519764	(ii) HSP90 binding to eNOS increases when the quantity of CaM bound to eNOS remains constant (Fig.  5), and this results in a further increase in eNOS activity (from 139% to 254% of basal eNOS activity at 12 and 45 nM HSP90, respectively; Fig.  2).	bind
17135	2	5655	7	10	NULL	NULL	NULL	CaM	GP		bind					eNOS	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_11_9339_s_191	12519764	(ii) HSP90 binding to eNOS increases when the quantity of CaM bound to eNOS remains constant (Fig.  5), and this results in a further increase in eNOS activity (from 139% to 254% of basal eNOS activity at 12 and 45 nM HSP90, respectively; Fig.  2).	bind
17906	1	5656	6	10	NULL	NULL	NULL	Sm proteins	GP		assemble onto					oligonucleotide	NucleicAcid	consensus		Sm binding site 	NULL	Xenopus oocytes	NULL	NULL	NULL	NULL	gw60_embo_20_19_5470_s_206	11574479	(ii) In a study of the assembly of U7 snRNPs in  Xenopus oocytes ( Stefanovic  et al., 1995), we have previously shown that the Sm B and G proteins could be cross-linked to the Sm binding site of U7 snRNA to similar positions as have recently been characterized for Sm proteins assembled onto a consensus Sm binding site oligonucleotide ( Urlaub  et al., 2001).	bind
17907	2	5656	6	10	NULL	NULL	NULL	Sm B proteins	GP		cross link		may			U7 snRNA	NucleicAcid		Sm binding site		NULL	Xenopus oocytes	NULL	NULL	NULL	NULL	gw60_embo_20_19_5470_s_206	11574479	(ii) In a study of the assembly of U7 snRNPs in  Xenopus oocytes ( Stefanovic  et al., 1995), we have previously shown that the Sm B and G proteins could be cross-linked to the Sm binding site of U7 snRNA to similar positions as have recently been characterized for Sm proteins assembled onto a consensus Sm binding site oligonucleotide ( Urlaub  et al., 2001).	bind
17908	3	5656	6	10	NULL	NULL	NULL	Sm G protein	GP		cross link		may			U7 snRNA	NucleicAcid		Sm binding site		NULL	Xenopus oocytes	NULL	NULL	NULL	NULL	gw60_embo_20_19_5470_s_206	11574479	(ii) In a study of the assembly of U7 snRNPs in  Xenopus oocytes ( Stefanovic  et al., 1995), we have previously shown that the Sm B and G proteins could be cross-linked to the Sm binding site of U7 snRNA to similar positions as have recently been characterized for Sm proteins assembled onto a consensus Sm binding site oligonucleotide ( Urlaub  et al., 2001).	bind
17139	1	5656	7	10	NULL	NULL	NULL	Sm B	GP		crosslink to					U7 snRNA	NucleicAcid		Sm binding site 		NULL	 Xenopus oocytes 	NULL	NULL	NULL	NULL	gw60_embo_20_19_5470_s_206	11574479	(ii) In a study of the assembly of U7 snRNPs in  Xenopus oocytes ( Stefanovic  et al., 1995), we have previously shown that the Sm B and G proteins could be cross-linked to the Sm binding site of U7 snRNA to similar positions as have recently been characterized for Sm proteins assembled onto a consensus Sm binding site oligonucleotide ( Urlaub  et al., 2001).	bind
17140	2	5656	7	10	NULL	NULL	NULL	G proteins	GP		crosslink to					U7 snRNA	NucleicAcid		Sm binding site 		NULL	 Xenopus oocytes 	NULL	NULL	NULL	NULL	gw60_embo_20_19_5470_s_206	11574479	(ii) In a study of the assembly of U7 snRNPs in  Xenopus oocytes ( Stefanovic  et al., 1995), we have previously shown that the Sm B and G proteins could be cross-linked to the Sm binding site of U7 snRNA to similar positions as have recently been characterized for Sm proteins assembled onto a consensus Sm binding site oligonucleotide ( Urlaub  et al., 2001).	bind
17141	3	5656	7	10	NULL	NULL	NULL	Sm protein	GP		assemble onto					oligonucleotide	NucleicAcid	consensus		Sm binding site	NULL	 Xenopus oocytes 	NULL	NULL	NULL	NULL	gw60_embo_20_19_5470_s_206	11574479	(ii) In a study of the assembly of U7 snRNPs in  Xenopus oocytes ( Stefanovic  et al., 1995), we have previously shown that the Sm B and G proteins could be cross-linked to the Sm binding site of U7 snRNA to similar positions as have recently been characterized for Sm proteins assembled onto a consensus Sm binding site oligonucleotide ( Urlaub  et al., 2001).	bind
17783	1	5657	6	10	NULL	NULL	NULL	ICP0	GP		bind			RING finger domain		cdc34	GP				NULL	in vitro	NULL	NULL	NULL	NULL	abs-batch0517-0529_proc-natl-acad-sci-u-s-a_98_15_11447293_s_6	11447293	(ii) In an in vitro substrate-independent  ubiquitination system, the RING finger domain encoded by exon 2 of ICP0  binds cdc34, whereas the carboxyl-terminal domain of ICP0 functions as  an E3 ligase independent of the RING finger domain.	bind
17785	2	5657	6	10	NULL	NULL	NULL	ICP0	GP		functions as			carboxyl-terminal domain		E3 ligase	GP				NULL	in vitro	NULL	NULL	NULL	NULL	abs-batch0517-0529_proc-natl-acad-sci-u-s-a_98_15_11447293_s_6	11447293	(ii) In an in vitro substrate-independent  ubiquitination system, the RING finger domain encoded by exon 2 of ICP0  binds cdc34, whereas the carboxyl-terminal domain of ICP0 functions as  an E3 ligase independent of the RING finger domain.	bind
17788	3	5657	6	10	NULL	NULL	NULL	statement 2	Process		is independent of								RING finger domain		NULL	in vitro	NULL	NULL	NULL	NULL	abs-batch0517-0529_proc-natl-acad-sci-u-s-a_98_15_11447293_s_6	11447293	(ii) In an in vitro substrate-independent  ubiquitination system, the RING finger domain encoded by exon 2 of ICP0  binds cdc34, whereas the carboxyl-terminal domain of ICP0 functions as  an E3 ligase independent of the RING finger domain.	bind
20314	4	5657	6	10	NULL	NULL	NULL	ICP0	GP		is encoded by			RING finger domain		ICP0	GP			exon 2	NULL	in vitro	NULL	NULL	NULL	NULL	abs-batch0517-0529_proc-natl-acad-sci-u-s-a_98_15_11447293_s_6	11447293	(ii) In an in vitro substrate-independent  ubiquitination system, the RING finger domain encoded by exon 2 of ICP0  binds cdc34, whereas the carboxyl-terminal domain of ICP0 functions as  an E3 ligase independent of the RING finger domain.	bind
17142	1	5657	7	10	NULL	NULL	NULL	 ICP0	GP		binds			RING finger domain		cdc34	GP				NULL	in vitro	NULL	NULL	NULL	NULL	abs-batch0517-0529_proc-natl-acad-sci-u-s-a_98_15_11447293_s_6	11447293	(ii) In an in vitro substrate-independent  ubiquitination system, the RING finger domain encoded by exon 2 of ICP0  binds cdc34, whereas the carboxyl-terminal domain of ICP0 functions as  an E3 ligase independent of the RING finger domain.	bind
17143	2	5657	7	10	NULL	NULL	NULL	ICP0 	GP		is encoded by			RING finger domain		 ICP0	GP			exon 2	NULL	in vitro	NULL	NULL	NULL	NULL	abs-batch0517-0529_proc-natl-acad-sci-u-s-a_98_15_11447293_s_6	11447293	(ii) In an in vitro substrate-independent  ubiquitination system, the RING finger domain encoded by exon 2 of ICP0  binds cdc34, whereas the carboxyl-terminal domain of ICP0 functions as  an E3 ligase independent of the RING finger domain.	bind
17145	3	5657	7	10	NULL	NULL	NULL	 ICP0	GP		functions as 			 carboxyl-terminal domain		E3 ligase	GP				NULL	in vitro	NULL	NULL	NULL	NULL	abs-batch0517-0529_proc-natl-acad-sci-u-s-a_98_15_11447293_s_6	11447293	(ii) In an in vitro substrate-independent  ubiquitination system, the RING finger domain encoded by exon 2 of ICP0  binds cdc34, whereas the carboxyl-terminal domain of ICP0 functions as  an E3 ligase independent of the RING finger domain.	bind
17146	4	5657	7	10	NULL	NULL	NULL	statement 4	Process		is independent of								RING finger domain		NULL	in vitro	NULL	NULL	NULL	NULL	abs-batch0517-0529_proc-natl-acad-sci-u-s-a_98_15_11447293_s_6	11447293	(ii) In an in vitro substrate-independent  ubiquitination system, the RING finger domain encoded by exon 2 of ICP0  binds cdc34, whereas the carboxyl-terminal domain of ICP0 functions as  an E3 ligase independent of the RING finger domain.	bind
17789	1	5658	6	10	NULL	NULL	NULL	VLDL	Chemical		bind					HSPG-LPL complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_atherosclerosis_136_2_255_s_156	9543096	(ii) In our experiments we studied binding of VLDL to HSPG-LPL complexes rather than to HSPG or heparin alone, which we consider as more relevant for extrapolation to the in vivo situation.	bind
17147	1	5658	7	10	NULL	NULL	NULL	VLDL	Chemical		bind					HSPG-LPL complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_atherosclerosis_136_2_255_s_156	9543096	(ii) In our experiments we studied binding of VLDL to HSPG-LPL complexes rather than to HSPG or heparin alone, which we consider as more relevant for extrapolation to the in vivo situation.	bind
17790	1	5659	6	10	NULL	NULL	NULL	oral Actinomyces viscosus strains	Organism	rat	bind		preferentially			statherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_6	11705891	(ii) In preferential statherin binding, oral  Actinomyces viscosus strains of rat and hamster origin (and strain 19246 from a human case of actinomycosis) bound statherin preferentially.	bind
17791	2	5659	6	10	NULL	NULL	NULL	oral Actinomyces viscosus strains	Organism	hamster	bind		preferentially			statherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_6	11705891	(ii) In preferential statherin binding, oral  Actinomyces viscosus strains of rat and hamster origin (and strain 19246 from a human case of actinomycosis) bound statherin preferentially.	bind
17792	3	5659	6	10	NULL	NULL	NULL	strain 19246 of actinomycosis	Organism	human	bind		preferentially			statherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_6	11705891	(ii) In preferential statherin binding, oral  Actinomyces viscosus strains of rat and hamster origin (and strain 19246 from a human case of actinomycosis) bound statherin preferentially.	bind
17148	1	5659	7	10	NULL	NULL	NULL	oral Actinomyces viscosus strains 	Organism	rat origin	bind		preferentially			statherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_6	11705891	(ii) In preferential statherin binding, oral  Actinomyces viscosus strains of rat and hamster origin (and strain 19246 from a human case of actinomycosis) bound statherin preferentially.	bind
17149	2	5659	7	10	NULL	NULL	NULL	oral Actinomyces viscosus strains 	Organism	hamster origin	bind		preferentially			statherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_6	11705891	(ii) In preferential statherin binding, oral  Actinomyces viscosus strains of rat and hamster origin (and strain 19246 from a human case of actinomycosis) bound statherin preferentially.	bind
17150	3	5659	7	10	NULL	NULL	NULL	strain 19246	Organism	human	bind		preferentially			statherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7224_s_6	11705891	(ii) In preferential statherin binding, oral  Actinomyces viscosus strains of rat and hamster origin (and strain 19246 from a human case of actinomycosis) bound statherin preferentially.	bind
17793	1	5660	6	10	NULL	NULL	NULL	myocyte nuclear factor	GP		bind									PNR element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7243_s_322	9819411	(ii) In the competition assay, although two inverted repeats of the Ets-binding sites were found to be necessary for the myocyte nuclear factor to bind to the PNR element, the HeLa cell nuclear factor could bind effectively to a single Ets-binding site of the palindrome.	bind
17794	2	5660	6	10	NULL	NULL	NULL	HeLa cell nuclear factor	GP		bind		effectively					single		Ets-binding site of the palindrome	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7243_s_322	9819411	(ii) In the competition assay, although two inverted repeats of the Ets-binding sites were found to be necessary for the myocyte nuclear factor to bind to the PNR element, the HeLa cell nuclear factor could bind effectively to a single Ets-binding site of the palindrome.	bind
17795	3	5660	6	10	NULL	NULL	NULL				are necessary for				two inverted repeats of Ets-binding sites	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7243_s_322	9819411	(ii) In the competition assay, although two inverted repeats of the Ets-binding sites were found to be necessary for the myocyte nuclear factor to bind to the PNR element, the HeLa cell nuclear factor could bind effectively to a single Ets-binding site of the palindrome.	bind
17151	1	5660	7	10	NULL	NULL	NULL	myocyte nuclear factor	GP		bind									PNR element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7243_s_322	9819411	(ii) In the competition assay, although two inverted repeats of the Ets-binding sites were found to be necessary for the myocyte nuclear factor to bind to the PNR element, the HeLa cell nuclear factor could bind effectively to a single Ets-binding site of the palindrome.	bind
17152	2	5660	7	10	NULL	NULL	NULL	HeLa cell nuclear factor	GP		bind		effectively					single		Ets-binding site of the palindrome	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7243_s_322	9819411	(ii) In the competition assay, although two inverted repeats of the Ets-binding sites were found to be necessary for the myocyte nuclear factor to bind to the PNR element, the HeLa cell nuclear factor could bind effectively to a single Ets-binding site of the palindrome.	bind
17153	3	5660	7	10	NULL	NULL	NULL				is necessary for				 two inverted repeats of Ets-binding sites	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7243_s_322	9819411	(ii) In the competition assay, although two inverted repeats of the Ets-binding sites were found to be necessary for the myocyte nuclear factor to bind to the PNR element, the HeLa cell nuclear factor could bind effectively to a single Ets-binding site of the palindrome.	bind
17796	1	5661	6	10	NULL	NULL	NULL	ClpA	GP	E.coli	bind					GFP	GP	unfolded			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbacteriol_183_8_2677_s_128	11274130	(ii) In vitro experiments showed that  E. coli ClpA can bind unfolded GFP and that the complex ClpAP can degrade unfolded GFP but not native GFP ( 10).	bind
17797	2	5661	6	10	NULL	NULL	NULL	complex ClpAP	GP		degrade					GFP	GP	unfolded			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbacteriol_183_8_2677_s_128	11274130	(ii) In vitro experiments showed that  E. coli ClpA can bind unfolded GFP and that the complex ClpAP can degrade unfolded GFP but not native GFP ( 10).	bind
17798	3	5661	6	10	NULL	NULL	NULL	complex ClpAP	GP		does not degrade					GFP	GP	native			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbacteriol_183_8_2677_s_128	11274130	(ii) In vitro experiments showed that  E. coli ClpA can bind unfolded GFP and that the complex ClpAP can degrade unfolded GFP but not native GFP ( 10).	bind
17154	1	5661	7	10	NULL	NULL	NULL	ClpA	GP	E. coli	bind					 GFP	GP	unfolded			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbacteriol_183_8_2677_s_128	11274130	(ii) In vitro experiments showed that  E. coli ClpA can bind unfolded GFP and that the complex ClpAP can degrade unfolded GFP but not native GFP ( 10).	bind
17155	2	5661	7	10	NULL	NULL	NULL	ClpA complex	GP		degrade					 GFP	GP	unfolded			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbacteriol_183_8_2677_s_128	11274130	(ii) In vitro experiments showed that  E. coli ClpA can bind unfolded GFP and that the complex ClpAP can degrade unfolded GFP but not native GFP ( 10).	bind
17156	3	5661	7	10	NULL	NULL	NULL	ClpAP complex	GP		does not degrade					GFP	GP	native			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbacteriol_183_8_2677_s_128	11274130	(ii) In vitro experiments showed that  E. coli ClpA can bind unfolded GFP and that the complex ClpAP can degrade unfolded GFP but not native GFP ( 10).	bind
17799	1	5662	6	10	NULL	NULL	NULL	Nrf2/MafK heterodimer	GP	putative	bind									ARE	NULL		NULL	NULL	NULL	NULL	abs-batch0540-0549_free-radic-biol-med_39_11_16274879_s_6	16274879	(ii) Nuclear localization of Nrf2  coincides with increased DNA binding of a putative Nrf2/MafK heterodimer  to its cognate cis-regulatory site, i.e., the antioxidant-responsive element  (ARE).	bind
17800	2	5662	6	10	NULL	NULL	NULL	ARE	GP		is					antioxidant-responsive element	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0540-0549_free-radic-biol-med_39_11_16274879_s_6	16274879	(ii) Nuclear localization of Nrf2  coincides with increased DNA binding of a putative Nrf2/MafK heterodimer  to its cognate cis-regulatory site, i.e., the antioxidant-responsive element  (ARE).	bind
17801	3	5662	6	10	NULL	NULL	NULL	Nrf2	GP	nuclear localization of	increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0540-0549_free-radic-biol-med_39_11_16274879_s_6	16274879	(ii) Nuclear localization of Nrf2  coincides with increased DNA binding of a putative Nrf2/MafK heterodimer  to its cognate cis-regulatory site, i.e., the antioxidant-responsive element  (ARE).	bind
20315	4	5662	6	10	NULL	NULL	NULL	ARE	GP		is a type of					cis-regulatory site	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0540-0549_free-radic-biol-med_39_11_16274879_s_6	16274879	(ii) Nuclear localization of Nrf2  coincides with increased DNA binding of a putative Nrf2/MafK heterodimer  to its cognate cis-regulatory site, i.e., the antioxidant-responsive element  (ARE).	bind
17161	1	5662	7	10	NULL	NULL	NULL	Nrf2/MafK heterodimer	GP	putative	bind									ARE	NULL		NULL	NULL	NULL	NULL	abs-batch0540-0549_free-radic-biol-med_39_11_16274879_s_6	16274879	(ii) Nuclear localization of Nrf2  coincides with increased DNA binding of a putative Nrf2/MafK heterodimer  to its cognate cis-regulatory site, i.e., the antioxidant-responsive element  (ARE).	bind
17162	2	5662	7	10	NULL	NULL	NULL	Nrf2	GP	Nuclear localization of	increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0540-0549_free-radic-biol-med_39_11_16274879_s_6	16274879	(ii) Nuclear localization of Nrf2  coincides with increased DNA binding of a putative Nrf2/MafK heterodimer  to its cognate cis-regulatory site, i.e., the antioxidant-responsive element  (ARE).	bind
17163	3	5662	7	10	NULL	NULL	NULL	ARE	GP		is					antioxidant-responsive element	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0540-0549_free-radic-biol-med_39_11_16274879_s_6	16274879	(ii) Nuclear localization of Nrf2  coincides with increased DNA binding of a putative Nrf2/MafK heterodimer  to its cognate cis-regulatory site, i.e., the antioxidant-responsive element  (ARE).	bind
17164	4	5662	7	10	NULL	NULL	NULL	ARE	GP		is a type of					 cis-regulatory site	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0540-0549_free-radic-biol-med_39_11_16274879_s_6	16274879	(ii) Nuclear localization of Nrf2  coincides with increased DNA binding of a putative Nrf2/MafK heterodimer  to its cognate cis-regulatory site, i.e., the antioxidant-responsive element  (ARE).	bind
17802	1	5663	6	10	NULL	NULL	NULL	p60	GP		bind					ICP0	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-virol_73_5_10196275_s_10	10196275	(ii) p60 also bound ICP0; the binding of ICP0 was independent  of that of ICP22.	bind
17803	2	5663	6	10	NULL	NULL	NULL	ICP0	GP	binding of	is independent of					ICP22	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-virol_73_5_10196275_s_10	10196275	(ii) p60 also bound ICP0; the binding of ICP0 was independent  of that of ICP22.	bind
17165	1	5663	7	10	NULL	NULL	NULL	p60	GP		bind					ICP0	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-virol_73_5_10196275_s_10	10196275	(ii) p60 also bound ICP0; the binding of ICP0 was independent  of that of ICP22.	bind
17166	2	5663	7	10	NULL	NULL	NULL	ICP0	GP	binding of	is independent of					 ICP22	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-virol_73_5_10196275_s_10	10196275	(ii) p60 also bound ICP0; the binding of ICP0 was independent  of that of ICP22.	bind
17804	1	5665	6	10	NULL	NULL	NULL	synapsin I	GP		bind					SV	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_42_43769_s_258	15265868	(ii) Rab3A recruitment by SV in the presence of RabGDI parallels the amount of synapsin I bound to SV.	bind
17805	2	5665	6	10	NULL	NULL	NULL	SV	OrganismPart		recruits					Rab3A	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_42_43769_s_258	15265868	(ii) Rab3A recruitment by SV in the presence of RabGDI parallels the amount of synapsin I bound to SV.	bind
17806	3	5665	6	10	NULL	NULL	NULL	statement 2	Process		occurs in presence of					RabGDI	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_42_43769_s_258	15265868	(ii) Rab3A recruitment by SV in the presence of RabGDI parallels the amount of synapsin I bound to SV.	bind
20316	4	5665	6	10	NULL	NULL	NULL	statement 1	Process		parallels					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_42_43769_s_258	15265868	(ii) Rab3A recruitment by SV in the presence of RabGDI parallels the amount of synapsin I bound to SV.	bind
17170	1	5665	7	10	NULL	NULL	NULL	SV	OrganismPart		recruits					 Rab3A 	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_42_43769_s_258	15265868	(ii) Rab3A recruitment by SV in the presence of RabGDI parallels the amount of synapsin I bound to SV.	bind
17171	2	5665	7	10	NULL	NULL	NULL	statement 1	Process		occurs in the presence of					RabGDI	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_42_43769_s_258	15265868	(ii) Rab3A recruitment by SV in the presence of RabGDI parallels the amount of synapsin I bound to SV.	bind
17172	3	5665	7	10	NULL	NULL	NULL	SV	OrganismPart		bind					synapsin I	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_42_43769_s_258	15265868	(ii) Rab3A recruitment by SV in the presence of RabGDI parallels the amount of synapsin I bound to SV.	bind
17173	4	5665	7	10	NULL	NULL	NULL	statement 1	Process		parallels					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_42_43769_s_258	15265868	(ii) Rab3A recruitment by SV in the presence of RabGDI parallels the amount of synapsin I bound to SV.	bind
17807	1	5666	6	10	NULL	NULL	NULL	fVIII	GP		bind					LRP	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_250	10608826	(ii) RAP completely inhibits fVIII binding to purified LRP.	bind
17808	2	5666	6	10	NULL	NULL	NULL	RAP	GP		inhibits		completely			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_250	10608826	(ii) RAP completely inhibits fVIII binding to purified LRP.	bind
17174	1	5666	7	10	NULL	NULL	NULL	fVIII	GP		binds to					LRP	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_250	10608826	(ii) RAP completely inhibits fVIII binding to purified LRP.	bind
17175	2	5666	7	10	NULL	NULL	NULL	RAP	GP		inhibits		completely			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_250	10608826	(ii) RAP completely inhibits fVIII binding to purified LRP.	bind
17809	1	5667	6	10	NULL	NULL	NULL	Raf-1	GP		bind					Rb	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_460	15485920	(ii) Rb phosphorylation can be observed when Raf-1, but not cyclin-cdk's, are bound to Rb.	bind
17810	2	5667	6	10	NULL	NULL	NULL	cyclin-cdk	GP		bind					Rb	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_460	15485920	(ii) Rb phosphorylation can be observed when Raf-1, but not cyclin-cdk's, are bound to Rb.	bind
17811	3	5667	6	10	NULL	NULL	NULL	Rb	GP	phosphorylation of	is observed with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_460	15485920	(ii) Rb phosphorylation can be observed when Raf-1, but not cyclin-cdk's, are bound to Rb.	bind
17812	4	5667	6	10	NULL	NULL	NULL	Rb	GP	phosphorylation of	is not observed with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_460	15485920	(ii) Rb phosphorylation can be observed when Raf-1, but not cyclin-cdk's, are bound to Rb.	bind
17176	1	5667	7	10	NULL	NULL	NULL	Raf-1	GP		bind					Rb	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_460	15485920	(ii) Rb phosphorylation can be observed when Raf-1, but not cyclin-cdk's, are bound to Rb.	bind
17177	2	5667	7	10	NULL	NULL	NULL	Rb	GP		undergoes					phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_460	15485920	(ii) Rb phosphorylation can be observed when Raf-1, but not cyclin-cdk's, are bound to Rb.	bind
17178	3	5667	7	10	NULL	NULL	NULL	statement 2	Process		occurs upon					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_460	15485920	(ii) Rb phosphorylation can be observed when Raf-1, but not cyclin-cdk's, are bound to Rb.	bind
17179	4	5667	7	10	NULL	NULL	NULL	cyclin-cdks	GP		bind					Rb	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_460	15485920	(ii) Rb phosphorylation can be observed when Raf-1, but not cyclin-cdk's, are bound to Rb.	bind
20737	5	5667	7	10	NULL	NULL	NULL	Rb	GP		does not					phosphorylation	Process	undergo			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_460	15485920	(ii) Rb phosphorylation can be observed when Raf-1, but not cyclin-cdk's, are bound to Rb.	bind
20738	6	5667	7	10	NULL	NULL	NULL	statement 5	Process		occurs upon					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_21_9527_s_460	15485920	(ii) Rb phosphorylation can be observed when Raf-1, but not cyclin-cdk's, are bound to Rb.	bind
17814	1	5668	6	10	NULL	NULL	NULL	UMSBP	GP	recombinant	bind									H14 sequence	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13419_s_200	10224106	(ii) Recombinant UMSBP, expressed in bacteria by a plasmid carrying the cloned  C. fasciculata  UMSBP gene (and subsequently purified to apparent homogeneity), binds the H14 sequence as efficiently as it binds the UMS (Fig.  3).	bind
17815	2	5668	6	10	NULL	NULL	NULL	UMSBP	GP	recombinant	bind									UMS	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13419_s_200	10224106	(ii) Recombinant UMSBP, expressed in bacteria by a plasmid carrying the cloned  C. fasciculata  UMSBP gene (and subsequently purified to apparent homogeneity), binds the H14 sequence as efficiently as it binds the UMS (Fig.  3).	bind
17816	3	5668	6	10	NULL	NULL	NULL	statement 1	Process		is as efficient as					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13419_s_200	10224106	(ii) Recombinant UMSBP, expressed in bacteria by a plasmid carrying the cloned  C. fasciculata  UMSBP gene (and subsequently purified to apparent homogeneity), binds the H14 sequence as efficiently as it binds the UMS (Fig.  3).	bind
17180	1	5668	7	10	NULL	NULL	NULL	UMSBP	GP	recombinant	binds									H14 sequence 	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13419_s_200	10224106	(ii) Recombinant UMSBP, expressed in bacteria by a plasmid carrying the cloned  C. fasciculata  UMSBP gene (and subsequently purified to apparent homogeneity), binds the H14 sequence as efficiently as it binds the UMS (Fig.  3).	bind
17181	2	5668	7	10	NULL	NULL	NULL	UMSBP	GP	recombinant	bind									UMS	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13419_s_200	10224106	(ii) Recombinant UMSBP, expressed in bacteria by a plasmid carrying the cloned  C. fasciculata  UMSBP gene (and subsequently purified to apparent homogeneity), binds the H14 sequence as efficiently as it binds the UMS (Fig.  3).	bind
17183	4	5668	7	10	NULL	NULL	NULL	statement 1	Process		is as efficient as					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13419_s_200	10224106	(ii) Recombinant UMSBP, expressed in bacteria by a plasmid carrying the cloned  C. fasciculata  UMSBP gene (and subsequently purified to apparent homogeneity), binds the H14 sequence as efficiently as it binds the UMS (Fig.  3).	bind
17818	1	5669	6	10	NULL	NULL	NULL	Sec24D	GP		does not bind					CFP-rGAT1-delta37	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28553_s_488	15073174	(ii) Sec24D did not bind to CFP-rGAT1-delta37.	bind
17184	1	5669	7	10	NULL	NULL	NULL	Sec24D	GP		does not bind					CFP-rGAT1-delta37	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28553_s_488	15073174	(ii) Sec24D did not bind to CFP-rGAT1-delta37.	bind
17819	1	5670	6	10	NULL	NULL	NULL	NELF	GP		bind		sequence specifically			RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2918_s_287	11940650	(ii) Sequence-specific RNA binding by NELF is important for transcription repression, and substitution did not work because RNA-binding specificity is different between NELF-E and CstF-64.	bind
17820	2	5670	6	10	NULL	NULL	NULL	statement 1	Process		is important for					transcription repression	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2918_s_287	11940650	(ii) Sequence-specific RNA binding by NELF is important for transcription repression, and substitution did not work because RNA-binding specificity is different between NELF-E and CstF-64.	bind
20317	3	5670	6	10	NULL	NULL	NULL	NELF-E	GP		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2918_s_287	11940650	(ii) Sequence-specific RNA binding by NELF is important for transcription repression, and substitution did not work because RNA-binding specificity is different between NELF-E and CstF-64.	bind
20318	4	5670	6	10	NULL	NULL	NULL	CstF-64	GP		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2918_s_287	11940650	(ii) Sequence-specific RNA binding by NELF is important for transcription repression, and substitution did not work because RNA-binding specificity is different between NELF-E and CstF-64.	bind
20319	5	5670	6	10	NULL	NULL	NULL	statement 3	Process	binding affinity of	is different from					statement 4	Process	binding affinity of 			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2918_s_287	11940650	(ii) Sequence-specific RNA binding by NELF is important for transcription repression, and substitution did not work because RNA-binding specificity is different between NELF-E and CstF-64.	bind
20320	6	5670	6	10	NULL	NULL	NULL	NELF-E	GP		was not substituted for					CstF-64	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2918_s_287	11940650	(ii) Sequence-specific RNA binding by NELF is important for transcription repression, and substitution did not work because RNA-binding specificity is different between NELF-E and CstF-64.	bind
20321	7	5670	6	10	NULL	NULL	NULL	statement 6	Process		because of					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2918_s_287	11940650	(ii) Sequence-specific RNA binding by NELF is important for transcription repression, and substitution did not work because RNA-binding specificity is different between NELF-E and CstF-64.	bind
17185	1	5670	7	10	NULL	NULL	NULL	NELF	GP		bind		sequence specifically			RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2918_s_287	11940650	(ii) Sequence-specific RNA binding by NELF is important for transcription repression, and substitution did not work because RNA-binding specificity is different between NELF-E and CstF-64.	bind
17186	2	5670	7	10	NULL	NULL	NULL	statement 1	Process		is important for					transcription 	Process	repression of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2918_s_287	11940650	(ii) Sequence-specific RNA binding by NELF is important for transcription repression, and substitution did not work because RNA-binding specificity is different between NELF-E and CstF-64.	bind
17192	3	5670	7	10	NULL	NULL	NULL	NELF-E	GP		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2918_s_287	11940650	(ii) Sequence-specific RNA binding by NELF is important for transcription repression, and substitution did not work because RNA-binding specificity is different between NELF-E and CstF-64.	bind
17193	4	5670	7	10	NULL	NULL	NULL	CstF-64	GP		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2918_s_287	11940650	(ii) Sequence-specific RNA binding by NELF is important for transcription repression, and substitution did not work because RNA-binding specificity is different between NELF-E and CstF-64.	bind
17194	5	5670	7	10	NULL	NULL	NULL	statement 3	Process		is different from					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2918_s_287	11940650	(ii) Sequence-specific RNA binding by NELF is important for transcription repression, and substitution did not work because RNA-binding specificity is different between NELF-E and CstF-64.	bind
20287	6	5670	7	10	NULL	NULL	NULL	NELF-E	GP		is not substituted for					CstF-64	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2918_s_287	11940650	(ii) Sequence-specific RNA binding by NELF is important for transcription repression, and substitution did not work because RNA-binding specificity is different between NELF-E and CstF-64.	bind
20288	7	5670	7	10	NULL	NULL	NULL	statement 6	Process		because of					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2918_s_287	11940650	(ii) Sequence-specific RNA binding by NELF is important for transcription repression, and substitution did not work because RNA-binding specificity is different between NELF-E and CstF-64.	bind
17889	1	5671	6	10	NULL	NULL	NULL	fibrillin-1	GP		bind					glycosaminoglycan chain	Chemical		sulfated regions		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_36035_s_272	11461921	(ii) Since fibrillin-1 only binds to highly sulfated and iduronated regions within a glycosaminoglycan chain, the patterns of high and low sulfated regions could determine a spatial arrangement of fibrillin-1 necessary to facilitate fibrillin-1 self-interactions or for disulfide bond formation, which is known as one of the initial steps in fibrillin-1 assembly ( 13).	bind
17909	2	5671	6	10	NULL	NULL	NULL	fibrillin-1	GP		interacts with					fibrillin 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_36035_s_272	11461921	(ii) Since fibrillin-1 only binds to highly sulfated and iduronated regions within a glycosaminoglycan chain, the patterns of high and low sulfated regions could determine a spatial arrangement of fibrillin-1 necessary to facilitate fibrillin-1 self-interactions or for disulfide bond formation, which is known as one of the initial steps in fibrillin-1 assembly ( 13).	bind
17910	3	5671	6	10	NULL	NULL	NULL	fibrillin-1	GP	assembly of	requires					disulfide bond	Process	formation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_36035_s_272	11461921	(ii) Since fibrillin-1 only binds to highly sulfated and iduronated regions within a glycosaminoglycan chain, the patterns of high and low sulfated regions could determine a spatial arrangement of fibrillin-1 necessary to facilitate fibrillin-1 self-interactions or for disulfide bond formation, which is known as one of the initial steps in fibrillin-1 assembly ( 13).	bind
18209	4	5671	6	10	NULL	NULL	NULL	fibrillin-1	GP		bind					glycosaminoglycan chain	GP		iduronated regions		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_36035_s_272	11461921	(ii) Since fibrillin-1 only binds to highly sulfated and iduronated regions within a glycosaminoglycan chain, the patterns of high and low sulfated regions could determine a spatial arrangement of fibrillin-1 necessary to facilitate fibrillin-1 self-interactions or for disulfide bond formation, which is known as one of the initial steps in fibrillin-1 assembly ( 13).	bind
17195	1	5671	7	10	NULL	NULL	NULL	fibrillin-1	GP		binds		only			glycosaminoglycan chain	Chemical		highly sulfated within		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_36035_s_272	11461921	(ii) Since fibrillin-1 only binds to highly sulfated and iduronated regions within a glycosaminoglycan chain, the patterns of high and low sulfated regions could determine a spatial arrangement of fibrillin-1 necessary to facilitate fibrillin-1 self-interactions or for disulfide bond formation, which is known as one of the initial steps in fibrillin-1 assembly ( 13).	bind
17196	2	5671	7	10	NULL	NULL	NULL	fibrillin-1	GP		binds		only			glycosaminoglycan chain	Chemical		iduronated regions within		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_36035_s_272	11461921	(ii) Since fibrillin-1 only binds to highly sulfated and iduronated regions within a glycosaminoglycan chain, the patterns of high and low sulfated regions could determine a spatial arrangement of fibrillin-1 necessary to facilitate fibrillin-1 self-interactions or for disulfide bond formation, which is known as one of the initial steps in fibrillin-1 assembly ( 13).	bind
17197	3	5671	7	10	NULL	NULL	NULL			patterns of high and low	determine			sulfated regions		fibrillin-1	GP	spatial arrangement of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_36035_s_272	11461921	(ii) Since fibrillin-1 only binds to highly sulfated and iduronated regions within a glycosaminoglycan chain, the patterns of high and low sulfated regions could determine a spatial arrangement of fibrillin-1 necessary to facilitate fibrillin-1 self-interactions or for disulfide bond formation, which is known as one of the initial steps in fibrillin-1 assembly ( 13).	bind
17198	4	5671	7	10	NULL	NULL	NULL	statement 3	Process		facilitate					fibrillin-1 	GP	self-interactions of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_36035_s_272	11461921	(ii) Since fibrillin-1 only binds to highly sulfated and iduronated regions within a glycosaminoglycan chain, the patterns of high and low sulfated regions could determine a spatial arrangement of fibrillin-1 necessary to facilitate fibrillin-1 self-interactions or for disulfide bond formation, which is known as one of the initial steps in fibrillin-1 assembly ( 13).	bind
17199	5	5671	7	10	NULL	NULL	NULL	statement 3	Process		facilitate					disulfide bond	Process	formation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_36035_s_272	11461921	(ii) Since fibrillin-1 only binds to highly sulfated and iduronated regions within a glycosaminoglycan chain, the patterns of high and low sulfated regions could determine a spatial arrangement of fibrillin-1 necessary to facilitate fibrillin-1 self-interactions or for disulfide bond formation, which is known as one of the initial steps in fibrillin-1 assembly ( 13).	bind
17200	6	5671	7	10	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_36035_s_272	11461921	(ii) Since fibrillin-1 only binds to highly sulfated and iduronated regions within a glycosaminoglycan chain, the patterns of high and low sulfated regions could determine a spatial arrangement of fibrillin-1 necessary to facilitate fibrillin-1 self-interactions or for disulfide bond formation, which is known as one of the initial steps in fibrillin-1 assembly ( 13).	bind
17201	7	5671	7	10	NULL	NULL	NULL	statement 4	Process		is					fibrillin-1	GP	initial steps of assembly			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_36035_s_272	11461921	(ii) Since fibrillin-1 only binds to highly sulfated and iduronated regions within a glycosaminoglycan chain, the patterns of high and low sulfated regions could determine a spatial arrangement of fibrillin-1 necessary to facilitate fibrillin-1 self-interactions or for disulfide bond formation, which is known as one of the initial steps in fibrillin-1 assembly ( 13).	bind
17202	8	5671	7	10	NULL	NULL	NULL	statement 5	Process		is					fibrillin-1	GP	initial steps of assembly			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_36035_s_272	11461921	(ii) Since fibrillin-1 only binds to highly sulfated and iduronated regions within a glycosaminoglycan chain, the patterns of high and low sulfated regions could determine a spatial arrangement of fibrillin-1 necessary to facilitate fibrillin-1 self-interactions or for disulfide bond formation, which is known as one of the initial steps in fibrillin-1 assembly ( 13).	bind
17890	1	5672	6	10	NULL	NULL	NULL	Tir	GP		bind					intimin	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_4_1725_s_258	12654785	(ii) Subsequent binding of Tir to intimin mediates the intimate attachment between eukaryotic cell and bacterium and (iii) thereby induces a signal which leads to Esp secretion and formation of the type III translocon.	bind
17891	2	5672	6	10	NULL	NULL	NULL	eukaryotic cell	Cell		attaches		intimately			bacterium	Organism				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_4_1725_s_258	12654785	(ii) Subsequent binding of Tir to intimin mediates the intimate attachment between eukaryotic cell and bacterium and (iii) thereby induces a signal which leads to Esp secretion and formation of the type III translocon.	bind
17892	3	5672	6	10	NULL	NULL	NULL	statement 1	Process		mediates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_4_1725_s_258	12654785	(ii) Subsequent binding of Tir to intimin mediates the intimate attachment between eukaryotic cell and bacterium and (iii) thereby induces a signal which leads to Esp secretion and formation of the type III translocon.	bind
17893	4	5672	6	10	NULL	NULL	NULL	statement 2	Process		signals					Esp	GP	secretion of			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_4_1725_s_258	12654785	(ii) Subsequent binding of Tir to intimin mediates the intimate attachment between eukaryotic cell and bacterium and (iii) thereby induces a signal which leads to Esp secretion and formation of the type III translocon.	bind
17894	5	5672	6	10	NULL	NULL	NULL	statement 2	Process		forms					type III translocon	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_4_1725_s_258	12654785	(ii) Subsequent binding of Tir to intimin mediates the intimate attachment between eukaryotic cell and bacterium and (iii) thereby induces a signal which leads to Esp secretion and formation of the type III translocon.	bind
17203	1	5672	7	10	NULL	NULL	NULL	Tir	GP		bind					intimin	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_4_1725_s_258	12654785	(ii) Subsequent binding of Tir to intimin mediates the intimate attachment between eukaryotic cell and bacterium and (iii) thereby induces a signal which leads to Esp secretion and formation of the type III translocon.	bind
17204	2	5672	7	10	NULL	NULL	NULL	eukaryotic cell	Cell		attaches to		intimately			bacterium	Organism				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_4_1725_s_258	12654785	(ii) Subsequent binding of Tir to intimin mediates the intimate attachment between eukaryotic cell and bacterium and (iii) thereby induces a signal which leads to Esp secretion and formation of the type III translocon.	bind
17205	3	5672	7	10	NULL	NULL	NULL	statement 1	Process		mediates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_4_1725_s_258	12654785	(ii) Subsequent binding of Tir to intimin mediates the intimate attachment between eukaryotic cell and bacterium and (iii) thereby induces a signal which leads to Esp secretion and formation of the type III translocon.	bind
17206	4	5672	7	10	NULL	NULL	NULL	statement 3	Process		induce a					signal	Process				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_4_1725_s_258	12654785	(ii) Subsequent binding of Tir to intimin mediates the intimate attachment between eukaryotic cell and bacterium and (iii) thereby induces a signal which leads to Esp secretion and formation of the type III translocon.	bind
17207	5	5672	7	10	NULL	NULL	NULL	statement 4	Process		leads to					Esp	GP	secretion of			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_4_1725_s_258	12654785	(ii) Subsequent binding of Tir to intimin mediates the intimate attachment between eukaryotic cell and bacterium and (iii) thereby induces a signal which leads to Esp secretion and formation of the type III translocon.	bind
17208	6	5672	7	10	NULL	NULL	NULL	statement 4	Process		leads to					type III translocon	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_4_1725_s_258	12654785	(ii) Subsequent binding of Tir to intimin mediates the intimate attachment between eukaryotic cell and bacterium and (iii) thereby induces a signal which leads to Esp secretion and formation of the type III translocon.	bind
17895	1	5673	6	10	NULL	NULL	NULL	putidaredoxin	GP		bind		strongly			CYP101	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36225_s_174	11459837	(ii) The aromatic character of the C-terminal tryptophan in position 106 of putidaredoxin ( 26,  44) is indispensable for the strong binding of putidaredoxin and CYP101, whereas wild type adrenodoxin has no tryptophan at all and also comprises a more extended C-terminal end (adrenodoxin consists of 128 amino acids).	bind
17896	2	5673	6	10	NULL	NULL	NULL	putidaredoxin	GP	aromatic character of	is indspensable for			C-terminal tryptophan		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36225_s_174	11459837	(ii) The aromatic character of the C-terminal tryptophan in position 106 of putidaredoxin ( 26,  44) is indispensable for the strong binding of putidaredoxin and CYP101, whereas wild type adrenodoxin has no tryptophan at all and also comprises a more extended C-terminal end (adrenodoxin consists of 128 amino acids).	bind
22994	3	5673	6	10	NULL	NULL	NULL	adrenodoxin	GP	wild type	does not have					tryptophan	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36225_s_174	11459837	(ii) The aromatic character of the C-terminal tryptophan in position 106 of putidaredoxin ( 26,  44) is indispensable for the strong binding of putidaredoxin and CYP101, whereas wild type adrenodoxin has no tryptophan at all and also comprises a more extended C-terminal end (adrenodoxin consists of 128 amino acids).	bind
22995	4	5673	6	10	NULL	NULL	NULL	adrenodoxin	GP	wild type	comprises of								extended C-terminal end		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36225_s_174	11459837	(ii) The aromatic character of the C-terminal tryptophan in position 106 of putidaredoxin ( 26,  44) is indispensable for the strong binding of putidaredoxin and CYP101, whereas wild type adrenodoxin has no tryptophan at all and also comprises a more extended C-terminal end (adrenodoxin consists of 128 amino acids).	bind
22997	5	5673	6	10	NULL	NULL	NULL	adrenodoxin	GP		consists of								128 amino acids		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36225_s_174	11459837	(ii) The aromatic character of the C-terminal tryptophan in position 106 of putidaredoxin ( 26,  44) is indispensable for the strong binding of putidaredoxin and CYP101, whereas wild type adrenodoxin has no tryptophan at all and also comprises a more extended C-terminal end (adrenodoxin consists of 128 amino acids).	bind
17210	1	5673	7	10	NULL	NULL	NULL	putidaredoxin	GP		binds		strongly			CYP101	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36225_s_174	11459837	(ii) The aromatic character of the C-terminal tryptophan in position 106 of putidaredoxin ( 26,  44) is indispensable for the strong binding of putidaredoxin and CYP101, whereas wild type adrenodoxin has no tryptophan at all and also comprises a more extended C-terminal end (adrenodoxin consists of 128 amino acids).	bind
17211	2	5673	7	10	NULL	NULL	NULL	putidaredoxin	GP	aromatic character of 	is indispensable for			C-terminal tryptophan  position 106		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36225_s_174	11459837	(ii) The aromatic character of the C-terminal tryptophan in position 106 of putidaredoxin ( 26,  44) is indispensable for the strong binding of putidaredoxin and CYP101, whereas wild type adrenodoxin has no tryptophan at all and also comprises a more extended C-terminal end (adrenodoxin consists of 128 amino acids).	bind
17212	3	5673	7	10	NULL	NULL	NULL	adrenodoxin	GP	wild type	does not have					tryptophan	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36225_s_174	11459837	(ii) The aromatic character of the C-terminal tryptophan in position 106 of putidaredoxin ( 26,  44) is indispensable for the strong binding of putidaredoxin and CYP101, whereas wild type adrenodoxin has no tryptophan at all and also comprises a more extended C-terminal end (adrenodoxin consists of 128 amino acids).	bind
17213	4	5673	7	10	NULL	NULL	NULL	adrenodoxin	GP	wild type	comprises of								extended C-terminal end		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36225_s_174	11459837	(ii) The aromatic character of the C-terminal tryptophan in position 106 of putidaredoxin ( 26,  44) is indispensable for the strong binding of putidaredoxin and CYP101, whereas wild type adrenodoxin has no tryptophan at all and also comprises a more extended C-terminal end (adrenodoxin consists of 128 amino acids).	bind
17214	5	5673	7	10	NULL	NULL	NULL	adrenodoxin	GP		consist of								128 amino acids		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36225_s_174	11459837	(ii) The aromatic character of the C-terminal tryptophan in position 106 of putidaredoxin ( 26,  44) is indispensable for the strong binding of putidaredoxin and CYP101, whereas wild type adrenodoxin has no tryptophan at all and also comprises a more extended C-terminal end (adrenodoxin consists of 128 amino acids).	bind
17897	1	5674	6	10	NULL	NULL	NULL	HRI	GP		bind					heme	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_357	10454533	(ii) The binding of Hsc70 to transformed HRI may increase the binding affinity of HRI for heme, enhancing the ability of the limiting concentration of heme present in heme-deficient RRL to suppress HRI activation (Fig.  10B,  2).	bind
17898	2	5674	6	10	NULL	NULL	NULL	Hsc70	GP		bind					HRI	GP	transformed			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_357	10454533	(ii) The binding of Hsc70 to transformed HRI may increase the binding affinity of HRI for heme, enhancing the ability of the limiting concentration of heme present in heme-deficient RRL to suppress HRI activation (Fig.  10B,  2).	bind
17899	3	5674	6	10	NULL	NULL	NULL	statement 2	Process		increase		may			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_357	10454533	(ii) The binding of Hsc70 to transformed HRI may increase the binding affinity of HRI for heme, enhancing the ability of the limiting concentration of heme present in heme-deficient RRL to suppress HRI activation (Fig.  10B,  2).	bind
17900	4	5674	6	10	NULL	NULL	NULL	RRL	GP	heme-deficient	suppress					HRI	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_357	10454533	(ii) The binding of Hsc70 to transformed HRI may increase the binding affinity of HRI for heme, enhancing the ability of the limiting concentration of heme present in heme-deficient RRL to suppress HRI activation (Fig.  10B,  2).	bind
17901	5	5674	6	10	NULL	NULL	NULL	statement 3	Process		enhances					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_357	10454533	(ii) The binding of Hsc70 to transformed HRI may increase the binding affinity of HRI for heme, enhancing the ability of the limiting concentration of heme present in heme-deficient RRL to suppress HRI activation (Fig.  10B,  2).	bind
17215	1	5674	7	10	NULL	NULL	NULL	Hsc70	GP		bind					HRI	GP	transformed			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_357	10454533	(ii) The binding of Hsc70 to transformed HRI may increase the binding affinity of HRI for heme, enhancing the ability of the limiting concentration of heme present in heme-deficient RRL to suppress HRI activation (Fig.  10B,  2).	bind
17216	2	5674	7	10	NULL	NULL	NULL	HRI	GP		bind					heme	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_357	10454533	(ii) The binding of Hsc70 to transformed HRI may increase the binding affinity of HRI for heme, enhancing the ability of the limiting concentration of heme present in heme-deficient RRL to suppress HRI activation (Fig.  10B,  2).	bind
17217	3	5674	7	10	NULL	NULL	NULL	statement 1	Process		increase		may			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_357	10454533	(ii) The binding of Hsc70 to transformed HRI may increase the binding affinity of HRI for heme, enhancing the ability of the limiting concentration of heme present in heme-deficient RRL to suppress HRI activation (Fig.  10B,  2).	bind
17218	4	5674	7	10	NULL	NULL	NULL	RRL	GP	heme-deficient 	suppress					HRI	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_357	10454533	(ii) The binding of Hsc70 to transformed HRI may increase the binding affinity of HRI for heme, enhancing the ability of the limiting concentration of heme present in heme-deficient RRL to suppress HRI activation (Fig.  10B,  2).	bind
17219	5	5674	7	10	NULL	NULL	NULL	statement 3	Process		enhances					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_357	10454533	(ii) The binding of Hsc70 to transformed HRI may increase the binding affinity of HRI for heme, enhancing the ability of the limiting concentration of heme present in heme-deficient RRL to suppress HRI activation (Fig.  10B,  2).	bind
17902	1	5675	6	10	NULL	NULL	NULL	mAb 865	GP		bind					HS/heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_37_22802_s_145	8798457	(ii) The binding of mAb 865 to HS/heparin decreases with increasing sulfate contents of the polysaccharide.	bind
17903	2	5675	6	10	NULL	NULL	NULL	polysaccharide	Chemical	increasing sulfate contents of	decreases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_37_22802_s_145	8798457	(ii) The binding of mAb 865 to HS/heparin decreases with increasing sulfate contents of the polysaccharide.	bind
17220	1	5675	7	10	NULL	NULL	NULL	mAb 865	GP		bind					HS/heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_37_22802_s_145	8798457	(ii) The binding of mAb 865 to HS/heparin decreases with increasing sulfate contents of the polysaccharide.	bind
17221	2	5675	7	10	NULL	NULL	NULL	polysaccharide	Chemical	increasing sulfate contents of	decrease					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_37_22802_s_145	8798457	(ii) The binding of mAb 865 to HS/heparin decreases with increasing sulfate contents of the polysaccharide.	bind
17911	1	5676	6	10	NULL	NULL	NULL	Pd	GP		bind					ferrous CO-P450cam	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2547_s_189	11706033	(ii) The binding of Pd to ferrous CO-P450cam exhibits a 1.5-nm red-shift in the Soret transition.	bind
17222	1	5676	7	10	NULL	NULL	NULL	 Pd	GP		bind					ferrous CO-P450cam	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2547_s_189	11706033	(ii) The binding of Pd to ferrous CO-P450cam exhibits a 1.5-nm red-shift in the Soret transition.	bind
17912	1	5677	6	10	NULL	NULL	NULL	GTP S	GP		does not inhibit					PYY	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_1_574_s_243	8550622	(ii) The inhibition of PYY binding by GTP S could not be observed,  again ruling out a major role of Galpha   in controlling the  dissociation of PYY from PYY receptors.	bind
17913	2	5677	6	10	NULL	NULL	NULL	PYY	GP		dissociates from					PYY receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_1_574_s_243	8550622	(ii) The inhibition of PYY binding by GTP S could not be observed,  again ruling out a major role of Galpha   in controlling the  dissociation of PYY from PYY receptors.	bind
17914	3	5677	6	10	NULL	NULL	NULL	Galpha	GP		does not control					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_1_574_s_243	8550622	(ii) The inhibition of PYY binding by GTP S could not be observed,  again ruling out a major role of Galpha   in controlling the  dissociation of PYY from PYY receptors.	bind
17224	1	5677	7	10	NULL	NULL	NULL	GTP S	GP		does not inhibit					PYY	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_1_574_s_243	8550622	(ii) The inhibition of PYY binding by GTP S could not be observed,  again ruling out a major role of Galpha   in controlling the  dissociation of PYY from PYY receptors.	bind
17225	2	5677	7	10	NULL	NULL	NULL	PYY	GP		dissociates from					PYY receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_1_574_s_243	8550622	(ii) The inhibition of PYY binding by GTP S could not be observed,  again ruling out a major role of Galpha   in controlling the  dissociation of PYY from PYY receptors.	bind
17226	3	5677	7	10	NULL	NULL	NULL	G alpha	GP		does not control					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_1_574_s_243	8550622	(ii) The inhibition of PYY binding by GTP S could not be observed,  again ruling out a major role of Galpha   in controlling the  dissociation of PYY from PYY receptors.	bind
17915	1	5678	6	10	NULL	NULL	NULL	insulin receptor	GP		induces					Stat5B	GP	phosphorylation of	tyrosine		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_255	10821852	(ii) The insulin receptor induces the tyrosine phosphorylation of Stat5B  in vitro and of Stat3 and Stat5B in cultured cells.	bind
17916	2	5678	6	10	NULL	NULL	NULL	insulin receptor	GP		induces					Stat3	GP	phosphorylation of	tyrosine		NULL	in cultured cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_255	10821852	(ii) The insulin receptor induces the tyrosine phosphorylation of Stat5B  in vitro and of Stat3 and Stat5B in cultured cells.	bind
17917	3	5678	6	10	NULL	NULL	NULL	insulin receptor	GP		induces					Stat5B	GP	phosphorylation of	tyrosine		NULL	in cultured cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_255	10821852	(ii) The insulin receptor induces the tyrosine phosphorylation of Stat5B  in vitro and of Stat3 and Stat5B in cultured cells.	bind
17227	1	5678	7	10	NULL	NULL	NULL	insulin receptor	GP		induces					Stat5B	GP	phosphorylation of	tyrosine 		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_255	10821852	(ii) The insulin receptor induces the tyrosine phosphorylation of Stat5B  in vitro and of Stat3 and Stat5B in cultured cells.	bind
17228	2	5678	7	10	NULL	NULL	NULL	insulin receptor	GP		induces					Stat3	GP	phosphorylation of	tyrosine		NULL	in cultured cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_255	10821852	(ii) The insulin receptor induces the tyrosine phosphorylation of Stat5B  in vitro and of Stat3 and Stat5B in cultured cells.	bind
17229	3	5678	7	10	NULL	NULL	NULL	insulin receptor	GP		induces					Stat5B	GP	phosphorylation of	tyrosine		NULL	in cultured cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_255	10821852	(ii) The insulin receptor induces the tyrosine phosphorylation of Stat5B  in vitro and of Stat3 and Stat5B in cultured cells.	bind
17918	1	5680	6	10	NULL	NULL	NULL	Ubr1p	GP		is adjacent to			RING-H2					BRR region		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6832_s_38	10581257	(ii) The RING-H2 domain of Ubr1p, adjacent to the BRR region, is strictly required for ubiquitylation of N-end rule substrates, even though this domain is not required for the binding of Ubr1p to either Ubc2p or N-end rule substrates.	bind
17919	2	5680	6	10	NULL	NULL	NULL	Ubr1p	GP		is required for		strictly	RING-H2		N-end rule substrates	GP	ubiquitination of			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6832_s_38	10581257	(ii) The RING-H2 domain of Ubr1p, adjacent to the BRR region, is strictly required for ubiquitylation of N-end rule substrates, even though this domain is not required for the binding of Ubr1p to either Ubc2p or N-end rule substrates.	bind
17920	3	5680	6	10	NULL	NULL	NULL	Ubr1p	GP		bind					Ubc2p	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6832_s_38	10581257	(ii) The RING-H2 domain of Ubr1p, adjacent to the BRR region, is strictly required for ubiquitylation of N-end rule substrates, even though this domain is not required for the binding of Ubr1p to either Ubc2p or N-end rule substrates.	bind
17921	4	5680	6	10	NULL	NULL	NULL	Ubr1p	GP		is not required for			RING-H2		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6832_s_38	10581257	(ii) The RING-H2 domain of Ubr1p, adjacent to the BRR region, is strictly required for ubiquitylation of N-end rule substrates, even though this domain is not required for the binding of Ubr1p to either Ubc2p or N-end rule substrates.	bind
17922	5	5680	6	10	NULL	NULL	NULL	Ubr1p	GP		bind					N-end rule substrates	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6832_s_38	10581257	(ii) The RING-H2 domain of Ubr1p, adjacent to the BRR region, is strictly required for ubiquitylation of N-end rule substrates, even though this domain is not required for the binding of Ubr1p to either Ubc2p or N-end rule substrates.	bind
17923	6	5680	6	10	NULL	NULL	NULL	Ubr1p	GP		is not required for			RING-H2		statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6832_s_38	10581257	(ii) The RING-H2 domain of Ubr1p, adjacent to the BRR region, is strictly required for ubiquitylation of N-end rule substrates, even though this domain is not required for the binding of Ubr1p to either Ubc2p or N-end rule substrates.	bind
17230	1	5680	7	10	NULL	NULL	NULL	Ubr1p	GP		is required for		strictly	RING-H2 domain		N-end rule substrates	GP	ubiquitylation of			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6832_s_38	10581257	(ii) The RING-H2 domain of Ubr1p, adjacent to the BRR region, is strictly required for ubiquitylation of N-end rule substrates, even though this domain is not required for the binding of Ubr1p to either Ubc2p or N-end rule substrates.	bind
17231	2	5680	7	10	NULL	NULL	NULL	Ubr1p	GP		is adjacent to			RING-H2 domain 					BRR region		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6832_s_38	10581257	(ii) The RING-H2 domain of Ubr1p, adjacent to the BRR region, is strictly required for ubiquitylation of N-end rule substrates, even though this domain is not required for the binding of Ubr1p to either Ubc2p or N-end rule substrates.	bind
17232	3	5680	7	10	NULL	NULL	NULL	Ubr1p	GP		bind					Ubc2p	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6832_s_38	10581257	(ii) The RING-H2 domain of Ubr1p, adjacent to the BRR region, is strictly required for ubiquitylation of N-end rule substrates, even though this domain is not required for the binding of Ubr1p to either Ubc2p or N-end rule substrates.	bind
17233	4	5680	7	10	NULL	NULL	NULL	Ubr1p	GP		bind					N-end rule substrates	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6832_s_38	10581257	(ii) The RING-H2 domain of Ubr1p, adjacent to the BRR region, is strictly required for ubiquitylation of N-end rule substrates, even though this domain is not required for the binding of Ubr1p to either Ubc2p or N-end rule substrates.	bind
17234	5	5680	7	10	NULL	NULL	NULL	Ubr1p	GP		is not required for			RING-H2 domain		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6832_s_38	10581257	(ii) The RING-H2 domain of Ubr1p, adjacent to the BRR region, is strictly required for ubiquitylation of N-end rule substrates, even though this domain is not required for the binding of Ubr1p to either Ubc2p or N-end rule substrates.	bind
17235	6	5680	7	10	NULL	NULL	NULL	Ubr1p	GP		is not required for			RING-H2 domain 		statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6832_s_38	10581257	(ii) The RING-H2 domain of Ubr1p, adjacent to the BRR region, is strictly required for ubiquitylation of N-end rule substrates, even though this domain is not required for the binding of Ubr1p to either Ubc2p or N-end rule substrates.	bind
17924	2	5681	6	10	NULL	NULL	NULL	statement 1	Process		bind					TMP	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-phys-chem-b-condens-matter-mater-surf-interfaces-biophys_109_1_16851014_s_6	16851014	(ii) The unsaturated UO(2)L(2) complexes with  F ligands bind more strongly TMP than H(2)O, thus preferentially leading  to the UO(2)L(2)(TMP) complex, more hydrophobic than UO(2)L(2)(H(2)O).	bind
18199	3	5681	6	10	NULL	NULL	NULL	statement 1	Process		bind					H(2)O	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-phys-chem-b-condens-matter-mater-surf-interfaces-biophys_109_1_16851014_s_6	16851014	(ii) The unsaturated UO(2)L(2) complexes with  F ligands bind more strongly TMP than H(2)O, thus preferentially leading  to the UO(2)L(2)(TMP) complex, more hydrophobic than UO(2)L(2)(H(2)O).	bind
18200	4	5681	6	10	NULL	NULL	NULL	statement 2	Process		is more stronger than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-phys-chem-b-condens-matter-mater-surf-interfaces-biophys_109_1_16851014_s_6	16851014	(ii) The unsaturated UO(2)L(2) complexes with  F ligands bind more strongly TMP than H(2)O, thus preferentially leading  to the UO(2)L(2)(TMP) complex, more hydrophobic than UO(2)L(2)(H(2)O).	bind
18201	5	5681	6	10	NULL	NULL	NULL	statement 2	Process		forms					UO(2)L(2)(TMP) complex	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-phys-chem-b-condens-matter-mater-surf-interfaces-biophys_109_1_16851014_s_6	16851014	(ii) The unsaturated UO(2)L(2) complexes with  F ligands bind more strongly TMP than H(2)O, thus preferentially leading  to the UO(2)L(2)(TMP) complex, more hydrophobic than UO(2)L(2)(H(2)O).	bind
18202	6	5681	6	10	NULL	NULL	NULL	statement 3	Process		forms					UO(2)L(2)(H(2)O)	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-phys-chem-b-condens-matter-mater-surf-interfaces-biophys_109_1_16851014_s_6	16851014	(ii) The unsaturated UO(2)L(2) complexes with  F ligands bind more strongly TMP than H(2)O, thus preferentially leading  to the UO(2)L(2)(TMP) complex, more hydrophobic than UO(2)L(2)(H(2)O).	bind
18203	7	5681	6	10	NULL	NULL	NULL	statement 5	Process		is more hydrophobic than					statement 6	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-phys-chem-b-condens-matter-mater-surf-interfaces-biophys_109_1_16851014_s_6	16851014	(ii) The unsaturated UO(2)L(2) complexes with  F ligands bind more strongly TMP than H(2)O, thus preferentially leading  to the UO(2)L(2)(TMP) complex, more hydrophobic than UO(2)L(2)(H(2)O).	bind
53245	1	5681	6	10	NULL	NULL	NULL	UO(2)L(2)	Chemical		complexes with					F ligands	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-phys-chem-b-condens-matter-mater-surf-interfaces-biophys_109_1_16851014_s_6	16851014	(ii) The unsaturated UO(2)L(2) complexes with  F ligands bind more strongly TMP than H(2)O, thus preferentially leading  to the UO(2)L(2)(TMP) complex, more hydrophobic than UO(2)L(2)(H(2)O).	bind
17238	1	5681	7	10	NULL	NULL	NULL	UO(2)L(2)	Chemical	unsaturated	complex with					F ligands	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-phys-chem-b-condens-matter-mater-surf-interfaces-biophys_109_1_16851014_s_6	16851014	(ii) The unsaturated UO(2)L(2) complexes with  F ligands bind more strongly TMP than H(2)O, thus preferentially leading  to the UO(2)L(2)(TMP) complex, more hydrophobic than UO(2)L(2)(H(2)O).	bind
17239	2	5681	7	10	NULL	NULL	NULL	statement 1	Process		binds		strongly			TMP	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-phys-chem-b-condens-matter-mater-surf-interfaces-biophys_109_1_16851014_s_6	16851014	(ii) The unsaturated UO(2)L(2) complexes with  F ligands bind more strongly TMP than H(2)O, thus preferentially leading  to the UO(2)L(2)(TMP) complex, more hydrophobic than UO(2)L(2)(H(2)O).	bind
17240	3	5681	7	10	NULL	NULL	NULL	statement 1	Process		binds					H(2)O	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-phys-chem-b-condens-matter-mater-surf-interfaces-biophys_109_1_16851014_s_6	16851014	(ii) The unsaturated UO(2)L(2) complexes with  F ligands bind more strongly TMP than H(2)O, thus preferentially leading  to the UO(2)L(2)(TMP) complex, more hydrophobic than UO(2)L(2)(H(2)O).	bind
17241	4	5681	7	10	NULL	NULL	NULL	statement 2	Process		is stronger than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-phys-chem-b-condens-matter-mater-surf-interfaces-biophys_109_1_16851014_s_6	16851014	(ii) The unsaturated UO(2)L(2) complexes with  F ligands bind more strongly TMP than H(2)O, thus preferentially leading  to the UO(2)L(2)(TMP) complex, more hydrophobic than UO(2)L(2)(H(2)O).	bind
17242	5	5681	7	10	NULL	NULL	NULL	statement 2	Process		leads to					UO(2)L(2)(TMP) complex	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-phys-chem-b-condens-matter-mater-surf-interfaces-biophys_109_1_16851014_s_6	16851014	(ii) The unsaturated UO(2)L(2) complexes with  F ligands bind more strongly TMP than H(2)O, thus preferentially leading  to the UO(2)L(2)(TMP) complex, more hydrophobic than UO(2)L(2)(H(2)O).	bind
17243	6	5681	7	10	NULL	NULL	NULL	statement 3	Process		leads to					UO(2)L(2)(H(2)O)	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-phys-chem-b-condens-matter-mater-surf-interfaces-biophys_109_1_16851014_s_6	16851014	(ii) The unsaturated UO(2)L(2) complexes with  F ligands bind more strongly TMP than H(2)O, thus preferentially leading  to the UO(2)L(2)(TMP) complex, more hydrophobic than UO(2)L(2)(H(2)O).	bind
17244	7	5681	7	10	NULL	NULL	NULL	statement 5	Process		is more hydrophobic than					statement 6	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-phys-chem-b-condens-matter-mater-surf-interfaces-biophys_109_1_16851014_s_6	16851014	(ii) The unsaturated UO(2)L(2) complexes with  F ligands bind more strongly TMP than H(2)O, thus preferentially leading  to the UO(2)L(2)(TMP) complex, more hydrophobic than UO(2)L(2)(H(2)O).	bind
17925	1	5682	6	10	NULL	NULL	NULL	ERK	GP		bind					p38MAPK	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_216	11154262	(ii) Thr403 is situated close to a region that has been proposed to allow the binding of ERK and p38MAPK ( 9,  35).	bind
17245	1	5682	7	10	NULL	NULL	NULL	ERK 	GP		bind					p38MAPK	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_3_743_s_216	11154262	(ii) Thr403 is situated close to a region that has been proposed to allow the binding of ERK and p38MAPK ( 9,  35).	bind
17926	1	5683	6	10	NULL	NULL	NULL	p14ARF	GP		bind					Mdm2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6170_s_243	12167711	(ii) Ubiquitylation of p53, which is blocked upon binding of p14ARF to Mdm2, is permitted by mutant Mdm2.	bind
24574	2	5683	6	10	NULL	NULL	NULL	p14ARF	GP		bind					Mdm2	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6170_s_243	12167711	(ii) Ubiquitylation of p53, which is blocked upon binding of p14ARF to Mdm2, is permitted by mutant Mdm2.	bind
24575	3	5683	6	10	NULL	NULL	NULL	statement 1	Process		blocks					p53	GP	ubiquitylation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6170_s_243	12167711	(ii) Ubiquitylation of p53, which is blocked upon binding of p14ARF to Mdm2, is permitted by mutant Mdm2.	bind
24576	4	5683	6	10	NULL	NULL	NULL	statement 2	Process		allows					p53	GP	ubiquitylation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6170_s_243	12167711	(ii) Ubiquitylation of p53, which is blocked upon binding of p14ARF to Mdm2, is permitted by mutant Mdm2.	bind
17247	1	5683	7	10	NULL	NULL	NULL	p14ARF 	GP		bind					Mdm2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6170_s_243	12167711	(ii) Ubiquitylation of p53, which is blocked upon binding of p14ARF to Mdm2, is permitted by mutant Mdm2.	bind
17248	2	5683	7	10	NULL	NULL	NULL	p14ARF 	GP		bind					Mdm2	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6170_s_243	12167711	(ii) Ubiquitylation of p53, which is blocked upon binding of p14ARF to Mdm2, is permitted by mutant Mdm2.	bind
17249	3	5683	7	10	NULL	NULL	NULL	statement 1	Process		blocks					p53	GP	Ubiquitylation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6170_s_243	12167711	(ii) Ubiquitylation of p53, which is blocked upon binding of p14ARF to Mdm2, is permitted by mutant Mdm2.	bind
17250	4	5683	7	10	NULL	NULL	NULL	statement 2	Process		allows					p53	GP	Ubiquitylation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6170_s_243	12167711	(ii) Ubiquitylation of p53, which is blocked upon binding of p14ARF to Mdm2, is permitted by mutant Mdm2.	bind
17930	1	5685	6	10	NULL	NULL	NULL	kinesin-I	GP		bind					APP	GP	excess			NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_3_389_s_243	11709151	(II) When APP is in excess, kinesin-I binds excess APP, thus titrating kinesin-I from non-APP vesicles, causing non-APP vesicles to stall and inducing a retrograde death signal if an A -containing region is in the organelle jam.	bind
17931	2	5685	6	10	NULL	NULL	NULL	statement 1	Process		cause					non-APP vesicles	CellComponent	stalling of 			NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_3_389_s_243	11709151	(II) When APP is in excess, kinesin-I binds excess APP, thus titrating kinesin-I from non-APP vesicles, causing non-APP vesicles to stall and inducing a retrograde death signal if an A -containing region is in the organelle jam.	bind
17932	3	5685	6	10	NULL	NULL	NULL	statement 1	Process		induces					death signal	Process	retrograde			NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_3_389_s_243	11709151	(II) When APP is in excess, kinesin-I binds excess APP, thus titrating kinesin-I from non-APP vesicles, causing non-APP vesicles to stall and inducing a retrograde death signal if an A -containing region is in the organelle jam.	bind
17934	4	5685	6	10	NULL	NULL	NULL	statement 3	Process		occurs in presence of					A -containing region in organelle jam	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_3_389_s_243	11709151	(II) When APP is in excess, kinesin-I binds excess APP, thus titrating kinesin-I from non-APP vesicles, causing non-APP vesicles to stall and inducing a retrograde death signal if an A -containing region is in the organelle jam.	bind
24577	5	5685	6	10	NULL	NULL	NULL	statement 1	Process		occurs in					APP	GP	excess of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_3_389_s_243	11709151	(II) When APP is in excess, kinesin-I binds excess APP, thus titrating kinesin-I from non-APP vesicles, causing non-APP vesicles to stall and inducing a retrograde death signal if an A -containing region is in the organelle jam.	bind
24578	6	5685	6	10	NULL	NULL	NULL	statement 1	Process		titrates					kinesin-I	GP	from non-APP vesicles			NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_3_389_s_243	11709151	(II) When APP is in excess, kinesin-I binds excess APP, thus titrating kinesin-I from non-APP vesicles, causing non-APP vesicles to stall and inducing a retrograde death signal if an A -containing region is in the organelle jam.	bind
17251	1	5685	7	10	NULL	NULL	NULL	kinesin-I	GP		bind					APP	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_3_389_s_243	11709151	(II) When APP is in excess, kinesin-I binds excess APP, thus titrating kinesin-I from non-APP vesicles, causing non-APP vesicles to stall and inducing a retrograde death signal if an A -containing region is in the organelle jam.	bind
17252	2	5685	7	10	NULL	NULL	NULL	statement 1	Process		occur					APP	GP	in excess of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_3_389_s_243	11709151	(II) When APP is in excess, kinesin-I binds excess APP, thus titrating kinesin-I from non-APP vesicles, causing non-APP vesicles to stall and inducing a retrograde death signal if an A -containing region is in the organelle jam.	bind
17253	3	5685	7	10	NULL	NULL	NULL	statement 1	Process		titrates					kinesin-I	GP	from non-APP vesicles			NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_3_389_s_243	11709151	(II) When APP is in excess, kinesin-I binds excess APP, thus titrating kinesin-I from non-APP vesicles, causing non-APP vesicles to stall and inducing a retrograde death signal if an A -containing region is in the organelle jam.	bind
17254	4	5685	7	10	NULL	NULL	NULL	statement 1	Process		stall					non-APP vesicles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_3_389_s_243	11709151	(II) When APP is in excess, kinesin-I binds excess APP, thus titrating kinesin-I from non-APP vesicles, causing non-APP vesicles to stall and inducing a retrograde death signal if an A -containing region is in the organelle jam.	bind
17255	5	5685	7	10	NULL	NULL	NULL	statement 1	Process		induce					death signal	Process	 retrograde			NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_3_389_s_243	11709151	(II) When APP is in excess, kinesin-I binds excess APP, thus titrating kinesin-I from non-APP vesicles, causing non-APP vesicles to stall and inducing a retrograde death signal if an A -containing region is in the organelle jam.	bind
17256	6	5685	7	10	NULL	NULL	NULL	statement 5	Process		occurs in the presence of					A -containing region in organelle jam	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_3_389_s_243	11709151	(II) When APP is in excess, kinesin-I binds excess APP, thus titrating kinesin-I from non-APP vesicles, causing non-APP vesicles to stall and inducing a retrograde death signal if an A -containing region is in the organelle jam.	bind
17936	1	5686	6	10	NULL	NULL	NULL	Nef	GP		bind					Lck	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_11_6333_s_206	8626429	(iii)  What are the consequences of the binding of Nef to Lck?	bind
17361	1	5686	7	10	NULL	NULL	NULL	Nef 	GP		binds					Lck	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_11_6333_s_206	8626429	(iii)  What are the consequences of the binding of Nef to Lck?	bind
17943	1	5687	6	10	NULL	NULL	NULL	ceramide	Chemical		bind					C26 fatty acid	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_23_22515_s_241	15817474	(iii) All mutations that affect fatty acid elongation and the synthesis of the ceramide-bound C26 fatty acid conditionally destabilize newly synthesized Pma1p.	bind
45749	2	5687	6	10	NULL	NULL	NULL	statement 1	Process	mutation of	destabilize		conditionally			Pma1p	GP	newly synthesized			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_23_22515_s_241	15817474	(iii) All mutations that affect fatty acid elongation and the synthesis of the ceramide-bound C26 fatty acid conditionally destabilize newly synthesized Pma1p.	bind
45750	3	5687	6	10	NULL	NULL	NULL	fatty acid elongation	Process	mutation of	destabilize		conditionally			Pma1p	GP	newly synthesized			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_23_22515_s_241	15817474	(iii) All mutations that affect fatty acid elongation and the synthesis of the ceramide-bound C26 fatty acid conditionally destabilize newly synthesized Pma1p.	bind
17257	1	5687	7	10	NULL	NULL	NULL	ceramide	Chemical		bind					C26 fatty acid	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_23_22515_s_241	15817474	(iii) All mutations that affect fatty acid elongation and the synthesis of the ceramide-bound C26 fatty acid conditionally destabilize newly synthesized Pma1p.	bind
17258	2	5687	7	10	NULL	NULL	NULL	mutations	Process		destabilize		conditionally			Pma1p	GP	newly synthesized			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_23_22515_s_241	15817474	(iii) All mutations that affect fatty acid elongation and the synthesis of the ceramide-bound C26 fatty acid conditionally destabilize newly synthesized Pma1p.	bind
17259	3	5687	7	10	NULL	NULL	NULL	mutations	Process		affect					fatty acid	Chemical	elongation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_23_22515_s_241	15817474	(iii) All mutations that affect fatty acid elongation and the synthesis of the ceramide-bound C26 fatty acid conditionally destabilize newly synthesized Pma1p.	bind
17260	4	5687	7	10	NULL	NULL	NULL	mutations	Process		affect					statement 1	Process	synthesis of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_23_22515_s_241	15817474	(iii) All mutations that affect fatty acid elongation and the synthesis of the ceramide-bound C26 fatty acid conditionally destabilize newly synthesized Pma1p.	bind
17261	5	5687	7	10	NULL	NULL	NULL	statement 3	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_23_22515_s_241	15817474	(iii) All mutations that affect fatty acid elongation and the synthesis of the ceramide-bound C26 fatty acid conditionally destabilize newly synthesized Pma1p.	bind
17262	6	5687	7	10	NULL	NULL	NULL	statement 4	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_23_22515_s_241	15817474	(iii) All mutations that affect fatty acid elongation and the synthesis of the ceramide-bound C26 fatty acid conditionally destabilize newly synthesized Pma1p.	bind
17945	1	5688	6	10	NULL	NULL	NULL	ATF-1	GP		bind									CRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_41_25715_s_218	8810350	(iii) ATF-1 bound the major CRE with a lower affinity than CREB.	bind
17946	2	5688	6	10	NULL	NULL	NULL	CREB	GP		bind									CRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_41_25715_s_218	8810350	(iii) ATF-1 bound the major CRE with a lower affinity than CREB.	bind
17948	3	5688	6	10	NULL	NULL	NULL	statement 1	Process		is lower in affinity than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_41_25715_s_218	8810350	(iii) ATF-1 bound the major CRE with a lower affinity than CREB.	bind
17263	1	5688	7	10	NULL	NULL	NULL	ATF-1	GP		bind							major		CRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_41_25715_s_218	8810350	(iii) ATF-1 bound the major CRE with a lower affinity than CREB.	bind
17264	2	5688	7	10	NULL	NULL	NULL	CREB	GP		bind									CRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_41_25715_s_218	8810350	(iii) ATF-1 bound the major CRE with a lower affinity than CREB.	bind
17265	3	5688	7	10	NULL	NULL	NULL	statement 1	Process		has lower affinity than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_41_25715_s_218	8810350	(iii) ATF-1 bound the major CRE with a lower affinity than CREB.	bind
17950	1	5689	6	10	NULL	NULL	NULL	ATP	Chemical		bind					Ssa/sb	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2510_s_226	16688211	(iii) ATP binding to Ssa/sb or Sse1p induces  a transfer of the substrate to Sse1p, before being shuttled to other chaperones such  as TRiC or Hsp90.	bind
17953	2	5689	6	10	NULL	NULL	NULL	ATP	Chemical		bind					Sse1p	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2510_s_226	16688211	(iii) ATP binding to Ssa/sb or Sse1p induces  a transfer of the substrate to Sse1p, before being shuttled to other chaperones such  as TRiC or Hsp90.	bind
17954	3	5689	6	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2510_s_226	16688211	(iii) ATP binding to Ssa/sb or Sse1p induces  a transfer of the substrate to Sse1p, before being shuttled to other chaperones such  as TRiC or Hsp90.	bind
17955	4	5689	6	10	NULL	NULL	NULL	statement 1	Process		induces					Sse1p	GP	transfer of substrate to			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2510_s_226	16688211	(iii) ATP binding to Ssa/sb or Sse1p induces  a transfer of the substrate to Sse1p, before being shuttled to other chaperones such  as TRiC or Hsp90.	bind
17956	5	5689	6	10	NULL	NULL	NULL	statement 2	Process		induces					Sse1p	GP	transfer of substrate to			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2510_s_226	16688211	(iii) ATP binding to Ssa/sb or Sse1p induces  a transfer of the substrate to Sse1p, before being shuttled to other chaperones such  as TRiC or Hsp90.	bind
45634	6	5689	6	10	NULL	NULL	NULL	Hsp90	GP		is a type of					chaperone	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2510_s_226	16688211	(iii) ATP binding to Ssa/sb or Sse1p induces  a transfer of the substrate to Sse1p, before being shuttled to other chaperones such  as TRiC or Hsp90.	bind
45635	7	5689	6	10	NULL	NULL	NULL	TRiC	GP		is a type of					chaperone	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2510_s_226	16688211	(iii) ATP binding to Ssa/sb or Sse1p induces  a transfer of the substrate to Sse1p, before being shuttled to other chaperones such  as TRiC or Hsp90.	bind
17266	1	5689	7	10	NULL	NULL	NULL	ATP	Chemical		bind					Ssa/sb 	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2510_s_226	16688211	(iii) ATP binding to Ssa/sb or Sse1p induces  a transfer of the substrate to Sse1p, before being shuttled to other chaperones such  as TRiC or Hsp90.	bind
17267	2	5689	7	10	NULL	NULL	NULL	ATP	Chemical		bind					Sse1p	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2510_s_226	16688211	(iii) ATP binding to Ssa/sb or Sse1p induces  a transfer of the substrate to Sse1p, before being shuttled to other chaperones such  as TRiC or Hsp90.	bind
17268	3	5689	7	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2510_s_226	16688211	(iii) ATP binding to Ssa/sb or Sse1p induces  a transfer of the substrate to Sse1p, before being shuttled to other chaperones such  as TRiC or Hsp90.	bind
17269	4	5689	7	10	NULL	NULL	NULL	statement 1	Process		induce					Sse1p	GP	transfer of the substrate to 			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2510_s_226	16688211	(iii) ATP binding to Ssa/sb or Sse1p induces  a transfer of the substrate to Sse1p, before being shuttled to other chaperones such  as TRiC or Hsp90.	bind
17270	5	5689	7	10	NULL	NULL	NULL	statement 2	Process		induce					Sse1p	GP	transfer of the substrate to 			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2510_s_226	16688211	(iii) ATP binding to Ssa/sb or Sse1p induces  a transfer of the substrate to Sse1p, before being shuttled to other chaperones such  as TRiC or Hsp90.	bind
17271	6	5689	7	10	NULL	NULL	NULL	Sse1p	GP		is shuttled to					TRiC	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2510_s_226	16688211	(iii) ATP binding to Ssa/sb or Sse1p induces  a transfer of the substrate to Sse1p, before being shuttled to other chaperones such  as TRiC or Hsp90.	bind
17272	7	5689	7	10	NULL	NULL	NULL	Sse1p	GP		is shuttled to					Hsp90	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2510_s_226	16688211	(iii) ATP binding to Ssa/sb or Sse1p induces  a transfer of the substrate to Sse1p, before being shuttled to other chaperones such  as TRiC or Hsp90.	bind
45633	8	5689	7	10	NULL	NULL	NULL	TRiC	GP		is a type of					chaperone	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2510_s_226	16688211	(iii) ATP binding to Ssa/sb or Sse1p induces  a transfer of the substrate to Sse1p, before being shuttled to other chaperones such  as TRiC or Hsp90.	bind
45636	9	5689	7	10	NULL	NULL	NULL	Hsp90	GP		is a type of					chaperone	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2510_s_226	16688211	(iii) ATP binding to Ssa/sb or Sse1p induces  a transfer of the substrate to Sse1p, before being shuttled to other chaperones such  as TRiC or Hsp90.	bind
17957	1	5690	6	10	NULL	NULL	NULL	ATP	Chemical		bind					cis complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_4_730_s_19	11684006	(iii) ATP bound to the  cis complex acts as a timer, giving the substrate at least 8-10 s to fold inside the cavity after which ATP hydrolysis primes GroES for release from the  cis ring.	bind
17958	2	5690	6	10	NULL	NULL	NULL	GroES	GP		releases from					cis ring	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_4_730_s_19	11684006	(iii) ATP bound to the  cis complex acts as a timer, giving the substrate at least 8-10 s to fold inside the cavity after which ATP hydrolysis primes GroES for release from the  cis ring.	bind
17959	3	5690	6	10	NULL	NULL	NULL	ATP	Chemical	hydrolysis of	primes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_4_730_s_19	11684006	(iii) ATP bound to the  cis complex acts as a timer, giving the substrate at least 8-10 s to fold inside the cavity after which ATP hydrolysis primes GroES for release from the  cis ring.	bind
17961	4	5690	6	10	NULL	NULL	NULL	statement 3	Process		occurs after					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_4_730_s_19	11684006	(iii) ATP bound to the  cis complex acts as a timer, giving the substrate at least 8-10 s to fold inside the cavity after which ATP hydrolysis primes GroES for release from the  cis ring.	bind
17274	1	5690	7	10	NULL	NULL	NULL	ATP	Chemical		bind					cis complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_4_730_s_19	11684006	(iii) ATP bound to the  cis complex acts as a timer, giving the substrate at least 8-10 s to fold inside the cavity after which ATP hydrolysis primes GroES for release from the  cis ring.	bind
17275	2	5690	7	10	NULL	NULL	NULL	GroES	GP		release from					cis ring	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_4_730_s_19	11684006	(iii) ATP bound to the  cis complex acts as a timer, giving the substrate at least 8-10 s to fold inside the cavity after which ATP hydrolysis primes GroES for release from the  cis ring.	bind
23431	3	5690	7	10	NULL	NULL	NULL	ATP	Chemical	hydrolysis of	primes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_4_730_s_19	11684006	(iii) ATP bound to the  cis complex acts as a timer, giving the substrate at least 8-10 s to fold inside the cavity after which ATP hydrolysis primes GroES for release from the  cis ring.	bind
23437	4	5690	7	10	NULL	NULL	NULL	statement 3	Process		occurs after					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_4_730_s_19	11684006	(iii) ATP bound to the  cis complex acts as a timer, giving the substrate at least 8-10 s to fold inside the cavity after which ATP hydrolysis primes GroES for release from the  cis ring.	bind
17962	1	5691	6	10	NULL	NULL	NULL	Msb3	GP		bind					Spa2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8567_s_128	16166638	(iii) Binding of Msb3 and Msb4 to Spa2.	bind
17963	2	5691	6	10	NULL	NULL	NULL	Msb4	GP		bind					Spa2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8567_s_128	16166638	(iii) Binding of Msb3 and Msb4 to Spa2.	bind
17276	1	5691	7	10	NULL	NULL	NULL	Msb3	GP		bind					Spa2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8567_s_128	16166638	(iii) Binding of Msb3 and Msb4 to Spa2.	bind
17277	2	5691	7	10	NULL	NULL	NULL	Msb4	GP		bind					Spa2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8567_s_128	16166638	(iii) Binding of Msb3 and Msb4 to Spa2.	bind
17964	1	5692	6	10	NULL	NULL	NULL				bind			PTB domain		peptides	GP	tyrosine-phosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_19_17088_s_156	11877385	(iii) Both PTB domains bind to tyrosine-phosphorylated peptides in an overall enthalpy-driven interaction, which is exemplified by an NP XpY-containing peptide from IL-4R	bind
17278	1	5692	7	10	NULL	NULL	NULL				bind			PTB domain		 peptides	GP	tyrosine-phosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_19_17088_s_156	11877385	(iii) Both PTB domains bind to tyrosine-phosphorylated peptides in an overall enthalpy-driven interaction, which is exemplified by an NP XpY-containing peptide from IL-4R	bind
17965	1	5693	6	10	NULL	NULL	NULL	c-Src	GP		phosphorylates					FAK	GP		Tyr-925 site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35624_s_184	10958798	(iii) c-Src then phosphorylates FAK at multiple sites including the Tyr-925 site (for a review see Ref.  46); and (iv) FAK phosphorylation at multiple sites results in conformational changes favoring p130Cas binding to the FAK/c-Src complex ( 29).	bind
17966	2	5693	6	10	NULL	NULL	NULL	p130Cas	GP		bind					FAK/c-Src complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35624_s_184	10958798	(iii) c-Src then phosphorylates FAK at multiple sites including the Tyr-925 site (for a review see Ref.  46); and (iv) FAK phosphorylation at multiple sites results in conformational changes favoring p130Cas binding to the FAK/c-Src complex ( 29).	bind
17967	3	5693	6	10	NULL	NULL	NULL	FAK	GP	phosphorylation of	results in			multiple sites		conformational changes	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35624_s_184	10958798	(iii) c-Src then phosphorylates FAK at multiple sites including the Tyr-925 site (for a review see Ref.  46); and (iv) FAK phosphorylation at multiple sites results in conformational changes favoring p130Cas binding to the FAK/c-Src complex ( 29).	bind
17968	4	5693	6	10	NULL	NULL	NULL	statement 3	Process		favors					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35624_s_184	10958798	(iii) c-Src then phosphorylates FAK at multiple sites including the Tyr-925 site (for a review see Ref.  46); and (iv) FAK phosphorylation at multiple sites results in conformational changes favoring p130Cas binding to the FAK/c-Src complex ( 29).	bind
17280	1	5693	7	10	NULL	NULL	NULL	 c-Src	GP		phosphorylates					FAK 	GP		Tyr-925 site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35624_s_184	10958798	(iii) c-Src then phosphorylates FAK at multiple sites including the Tyr-925 site (for a review see Ref.  46); and (iv) FAK phosphorylation at multiple sites results in conformational changes favoring p130Cas binding to the FAK/c-Src complex ( 29).	bind
17281	2	5693	7	10	NULL	NULL	NULL	c-Src	GP		phosphorylates					FAK 	GP	multiple sites			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35624_s_184	10958798	(iii) c-Src then phosphorylates FAK at multiple sites including the Tyr-925 site (for a review see Ref.  46); and (iv) FAK phosphorylation at multiple sites results in conformational changes favoring p130Cas binding to the FAK/c-Src complex ( 29).	bind
17282	3	5693	7	10	NULL	NULL	NULL	p130Cas	GP		bind					FAK/c-Src complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35624_s_184	10958798	(iii) c-Src then phosphorylates FAK at multiple sites including the Tyr-925 site (for a review see Ref.  46); and (iv) FAK phosphorylation at multiple sites results in conformational changes favoring p130Cas binding to the FAK/c-Src complex ( 29).	bind
17283	4	5693	7	10	NULL	NULL	NULL	statement 2	Process		favors					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_45_35624_s_184	10958798	(iii) c-Src then phosphorylates FAK at multiple sites including the Tyr-925 site (for a review see Ref.  46); and (iv) FAK phosphorylation at multiple sites results in conformational changes favoring p130Cas binding to the FAK/c-Src complex ( 29).	bind
18047	1	5694	6	10	NULL	NULL	NULL	Calmodulin	GP		bind					ER	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_4_1978_s_275	16314411	(iii) Calmodulin binds to the ER in a Ca2+-dependent manner ( ,  ,  ), and this increases the  Kd value of estradiol binding ( ).	bind
18048	2	5694	6	10	NULL	NULL	NULL	statement 1	Process		is dependent on					Ca+2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_4_1978_s_275	16314411	(iii) Calmodulin binds to the ER in a Ca2+-dependent manner ( ,  ,  ), and this increases the  Kd value of estradiol binding ( ).	bind
17284	1	5694	7	10	NULL	NULL	NULL	Calmodulin	GP		binds					ER	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_4_1978_s_275	16314411	(iii) Calmodulin binds to the ER in a Ca2+-dependent manner ( ,  ,  ), and this increases the  Kd value of estradiol binding ( ).	bind
17285	2	5694	7	10	NULL	NULL	NULL	statement 1	Process		depends on					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_4_1978_s_275	16314411	(iii) Calmodulin binds to the ER in a Ca2+-dependent manner ( ,  ,  ), and this increases the  Kd value of estradiol binding ( ).	bind
18049	1	5695	6	10	NULL	NULL	NULL	D-Xylose	Chemical		bind					XylR	GP				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_7_2513_s_196	9647823	(iii) D-Xylose itself binds to XylR, inactivating it to be released from the  xyl operator, thus inducing the  xyl operon.	bind
18050	2	5695	6	10	NULL	NULL	NULL	D-Xylose	Chemical		inactivates					XylR	GP				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_7_2513_s_196	9647823	(iii) D-Xylose itself binds to XylR, inactivating it to be released from the  xyl operator, thus inducing the  xyl operon.	bind
18051	3	5695	6	10	NULL	NULL	NULL	XylR	GP		released from					xyl operator	GP				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_7_2513_s_196	9647823	(iii) D-Xylose itself binds to XylR, inactivating it to be released from the  xyl operator, thus inducing the  xyl operon.	bind
18052	4	5695	6	10	NULL	NULL	NULL	statement 3	Process		induces					xyl operon	GP				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_7_2513_s_196	9647823	(iii) D-Xylose itself binds to XylR, inactivating it to be released from the  xyl operator, thus inducing the  xyl operon.	bind
23014	5	5695	6	10	NULL	NULL	NULL	statement 1	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_7_2513_s_196	9647823	(iii) D-Xylose itself binds to XylR, inactivating it to be released from the  xyl operator, thus inducing the  xyl operon.	bind
17286	1	5695	7	10	NULL	NULL	NULL	D-Xylose	Chemical		binds					XylR	GP				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_7_2513_s_196	9647823	(iii) D-Xylose itself binds to XylR, inactivating it to be released from the  xyl operator, thus inducing the  xyl operon.	bind
17287	4	5695	7	10	NULL	NULL	NULL	D-Xylose	Chemical		release from					xyl operator	GP			 	NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_7_2513_s_196	9647823	(iii) D-Xylose itself binds to XylR, inactivating it to be released from the  xyl operator, thus inducing the  xyl operon.	bind
17288	3	5695	7	10	NULL	NULL	NULL	statement 1	Process		induce					xyl operon	GP			 	NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_7_2513_s_196	9647823	(iii) D-Xylose itself binds to XylR, inactivating it to be released from the  xyl operator, thus inducing the  xyl operon.	bind
17289	2	5695	7	10	NULL	NULL	NULL	statement 1	Process		inactivate					XylR	GP				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_7_2513_s_196	9647823	(iii) D-Xylose itself binds to XylR, inactivating it to be released from the  xyl operator, thus inducing the  xyl operon.	bind
17290	5	5695	7	10	NULL	NULL	NULL	statement 1	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_7_2513_s_196	9647823	(iii) D-Xylose itself binds to XylR, inactivating it to be released from the  xyl operator, thus inducing the  xyl operon.	bind
18053	1	5696	6	10	NULL	NULL	NULL	VLDL	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biol-chem_386_5_15927888_s_6	15927888	(iii) Different mechanisms specific for a  particular lipoprotein from E3/3 or E2/3 subjects are responsible for  apoE-mediated VLDL binding and apoB-mediated LDL binding to the LDL receptor  in a solid-phase binding assay.	bind
18054	2	5696	6	10	NULL	NULL	NULL	statement 1	Process		is mediated by					apoE	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biol-chem_386_5_15927888_s_6	15927888	(iii) Different mechanisms specific for a  particular lipoprotein from E3/3 or E2/3 subjects are responsible for  apoE-mediated VLDL binding and apoB-mediated LDL binding to the LDL receptor  in a solid-phase binding assay.	bind
18055	3	5696	6	10	NULL	NULL	NULL	LDL	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biol-chem_386_5_15927888_s_6	15927888	(iii) Different mechanisms specific for a  particular lipoprotein from E3/3 or E2/3 subjects are responsible for  apoE-mediated VLDL binding and apoB-mediated LDL binding to the LDL receptor  in a solid-phase binding assay.	bind
18056	4	5696	6	10	NULL	NULL	NULL	statement 3	Process		is mediated by					apoB	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biol-chem_386_5_15927888_s_6	15927888	(iii) Different mechanisms specific for a  particular lipoprotein from E3/3 or E2/3 subjects are responsible for  apoE-mediated VLDL binding and apoB-mediated LDL binding to the LDL receptor  in a solid-phase binding assay.	bind
17291	1	5696	7	10	NULL	NULL	NULL	VLDL	GP		binds					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biol-chem_386_5_15927888_s_6	15927888	(iii) Different mechanisms specific for a  particular lipoprotein from E3/3 or E2/3 subjects are responsible for  apoE-mediated VLDL binding and apoB-mediated LDL binding to the LDL receptor  in a solid-phase binding assay.	bind
17292	2	5696	7	10	NULL	NULL	NULL	LDL	GP		binds					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biol-chem_386_5_15927888_s_6	15927888	(iii) Different mechanisms specific for a  particular lipoprotein from E3/3 or E2/3 subjects are responsible for  apoE-mediated VLDL binding and apoB-mediated LDL binding to the LDL receptor  in a solid-phase binding assay.	bind
17293	3	5696	7	10	NULL	NULL	NULL	apoE	Chemical		mediates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biol-chem_386_5_15927888_s_6	15927888	(iii) Different mechanisms specific for a  particular lipoprotein from E3/3 or E2/3 subjects are responsible for  apoE-mediated VLDL binding and apoB-mediated LDL binding to the LDL receptor  in a solid-phase binding assay.	bind
17294	4	5696	7	10	NULL	NULL	NULL	apoB	Chemical		mediates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biol-chem_386_5_15927888_s_6	15927888	(iii) Different mechanisms specific for a  particular lipoprotein from E3/3 or E2/3 subjects are responsible for  apoE-mediated VLDL binding and apoB-mediated LDL binding to the LDL receptor  in a solid-phase binding assay.	bind
18057	1	5697	6	10	NULL	NULL	NULL	Ethanol	Chemical		bind		rapidly			p450 2E1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_23833_s_175	10446146	(iii) Ethanol binds rapidly to P450 2E1, since burst kinetics are not attenuated when P450 2E1 and ethanol are mixed from separate syringes ( 10).	bind
17295	1	5697	7	10	NULL	NULL	NULL	Ethanol	Chemical		binds		rapidly			P450 2E1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_23833_s_175	10446146	(iii) Ethanol binds rapidly to P450 2E1, since burst kinetics are not attenuated when P450 2E1 and ethanol are mixed from separate syringes ( 10).	bind
18058	1	5698	6	10	NULL	NULL	NULL	catenin	GP	expression of	alters					epithelial cell 	Cell	adhesion of			NULL	MDCK cells	NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_696_s_147	14664819	(iii) Expression of dominant active forms of  -catenin in MDCK cells altered epithelial  cell adhesion, possibly as a result of  -catenin binding to E-cadherin and APC protein  [ Barth et al., 1997] although other studies suggested that this finding might be specific to certain  cell types [  Loureiro et al., 2001], as overexpression of dominant  -catenin did not alter the cell shape in  Drosophila.	bind
18059	2	5698	6	10	NULL	NULL	NULL	catenin	GP		bind					E-cadherin	GP				NULL	MDCK cells	NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_696_s_147	14664819	(iii) Expression of dominant active forms of  -catenin in MDCK cells altered epithelial  cell adhesion, possibly as a result of  -catenin binding to E-cadherin and APC protein  [ Barth et al., 1997] although other studies suggested that this finding might be specific to certain  cell types [  Loureiro et al., 2001], as overexpression of dominant  -catenin did not alter the cell shape in  Drosophila.	bind
18060	3	5698	6	10	NULL	NULL	NULL	catenin	GP		bind					APC protein	GP				NULL	MDCK cells	NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_696_s_147	14664819	(iii) Expression of dominant active forms of  -catenin in MDCK cells altered epithelial  cell adhesion, possibly as a result of  -catenin binding to E-cadherin and APC protein  [ Barth et al., 1997] although other studies suggested that this finding might be specific to certain  cell types [  Loureiro et al., 2001], as overexpression of dominant  -catenin did not alter the cell shape in  Drosophila.	bind
18061	4	5698	6	10	NULL	NULL	NULL	catenin	GP	overexpression of	did not alter					cell shape	Process				NULL	drosophila	NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_696_s_147	14664819	(iii) Expression of dominant active forms of  -catenin in MDCK cells altered epithelial  cell adhesion, possibly as a result of  -catenin binding to E-cadherin and APC protein  [ Barth et al., 1997] although other studies suggested that this finding might be specific to certain  cell types [  Loureiro et al., 2001], as overexpression of dominant  -catenin did not alter the cell shape in  Drosophila.	bind
23024	5	5698	6	10	NULL	NULL	NULL	statement 2	Process		results in		possibly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_696_s_147	14664819	(iii) Expression of dominant active forms of  -catenin in MDCK cells altered epithelial  cell adhesion, possibly as a result of  -catenin binding to E-cadherin and APC protein  [ Barth et al., 1997] although other studies suggested that this finding might be specific to certain  cell types [  Loureiro et al., 2001], as overexpression of dominant  -catenin did not alter the cell shape in  Drosophila.	bind
23025	6	5698	6	10	NULL	NULL	NULL	statement 3	Process		results in		possibly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_696_s_147	14664819	(iii) Expression of dominant active forms of  -catenin in MDCK cells altered epithelial  cell adhesion, possibly as a result of  -catenin binding to E-cadherin and APC protein  [ Barth et al., 1997] although other studies suggested that this finding might be specific to certain  cell types [  Loureiro et al., 2001], as overexpression of dominant  -catenin did not alter the cell shape in  Drosophila.	bind
17296	1	5698	7	10	NULL	NULL	NULL	catenin	GP		bind					 E-cadherin	GP				NULL	MDCK cells 	NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_696_s_147	14664819	(iii) Expression of dominant active forms of  -catenin in MDCK cells altered epithelial  cell adhesion, possibly as a result of  -catenin binding to E-cadherin and APC protein  [ Barth et al., 1997] although other studies suggested that this finding might be specific to certain  cell types [  Loureiro et al., 2001], as overexpression of dominant  -catenin did not alter the cell shape in  Drosophila.	bind
17297	2	5698	7	10	NULL	NULL	NULL	catenin	GP		bind					APC protein	GP				NULL	MDCK cells 	NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_696_s_147	14664819	(iii) Expression of dominant active forms of  -catenin in MDCK cells altered epithelial  cell adhesion, possibly as a result of  -catenin binding to E-cadherin and APC protein  [ Barth et al., 1997] although other studies suggested that this finding might be specific to certain  cell types [  Loureiro et al., 2001], as overexpression of dominant  -catenin did not alter the cell shape in  Drosophila.	bind
17298	3	5698	7	10	NULL	NULL	NULL	catenin	GP	dominant active forms of	is expressed in					MDCK cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_696_s_147	14664819	(iii) Expression of dominant active forms of  -catenin in MDCK cells altered epithelial  cell adhesion, possibly as a result of  -catenin binding to E-cadherin and APC protein  [ Barth et al., 1997] although other studies suggested that this finding might be specific to certain  cell types [  Loureiro et al., 2001], as overexpression of dominant  -catenin did not alter the cell shape in  Drosophila.	bind
17299	4	5698	7	10	NULL	NULL	NULL	statement 3	Process		alters					 epithelial cell	Cell	adhesion of			NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_696_s_147	14664819	(iii) Expression of dominant active forms of  -catenin in MDCK cells altered epithelial  cell adhesion, possibly as a result of  -catenin binding to E-cadherin and APC protein  [ Barth et al., 1997] although other studies suggested that this finding might be specific to certain  cell types [  Loureiro et al., 2001], as overexpression of dominant  -catenin did not alter the cell shape in  Drosophila.	bind
17300	5	5698	7	10	NULL	NULL	NULL	statement 1	Process		results in		possibly			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_696_s_147	14664819	(iii) Expression of dominant active forms of  -catenin in MDCK cells altered epithelial  cell adhesion, possibly as a result of  -catenin binding to E-cadherin and APC protein  [ Barth et al., 1997] although other studies suggested that this finding might be specific to certain  cell types [  Loureiro et al., 2001], as overexpression of dominant  -catenin did not alter the cell shape in  Drosophila.	bind
17301	6	5698	7	10	NULL	NULL	NULL	statement 2	Process		results in		possibly			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_696_s_147	14664819	(iii) Expression of dominant active forms of  -catenin in MDCK cells altered epithelial  cell adhesion, possibly as a result of  -catenin binding to E-cadherin and APC protein  [ Barth et al., 1997] although other studies suggested that this finding might be specific to certain  cell types [  Loureiro et al., 2001], as overexpression of dominant  -catenin did not alter the cell shape in  Drosophila.	bind
53244	7	5698	7	10	NULL	NULL	NULL	catenin	GP	overexpression of	does not alter					cell shape	Process				NULL	Drosophila	NULL	NULL	NULL	NULL	gw70_molcellneurosci_24_3_696_s_147	14664819	(iii) Expression of dominant active forms of  -catenin in MDCK cells altered epithelial  cell adhesion, possibly as a result of  -catenin binding to E-cadherin and APC protein  [ Barth et al., 1997] although other studies suggested that this finding might be specific to certain  cell types [  Loureiro et al., 2001], as overexpression of dominant  -catenin did not alter the cell shape in  Drosophila.	bind
18062	1	5699	6	10	NULL	NULL	NULL	GM1	Chemical		bind					PDGFR	GP				NULL	in GEM fractions	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11239_s_8	11782461	(iii) GM1 binds with PDGFR in GEM fractions.	bind
17302	1	5699	7	10	NULL	NULL	NULL	GM1	Chemical		bind					PDGFR 	GP				NULL	in GEM fractions	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11239_s_8	11782461	(iii) GM1 binds with PDGFR in GEM fractions.	bind
18063	1	5700	6	10	NULL	NULL	NULL	FLT4L	GP		interact with					PTB-SHC proteins	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_12956_s_185	8662748	(iii) GST-PTB SHC recombinant and epitope-tagged SHC proteins were used to confirm this interaction; Tyr1337 mutation (but not Tyr1333 or Tyr1363 mutations) decreased FLT4L capacity to interact with PTB-SHC recombinant proteins, and the deletion of SHC PTB domain (but not of SHC SH2 domain) abolished the binding of SHC to Tyr(P)1337-containing peptide.	bind
18064	2	5700	6	10	NULL	NULL	NULL	FLT4L	GP	mutant	decreases			Tyr1337		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_12956_s_185	8662748	(iii) GST-PTB SHC recombinant and epitope-tagged SHC proteins were used to confirm this interaction; Tyr1337 mutation (but not Tyr1333 or Tyr1363 mutations) decreased FLT4L capacity to interact with PTB-SHC recombinant proteins, and the deletion of SHC PTB domain (but not of SHC SH2 domain) abolished the binding of SHC to Tyr(P)1337-containing peptide.	bind
18065	3	5700	6	10	NULL	NULL	NULL	FLT4L	GP	mutant	does not decrease			Tyr1333		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_12956_s_185	8662748	(iii) GST-PTB SHC recombinant and epitope-tagged SHC proteins were used to confirm this interaction; Tyr1337 mutation (but not Tyr1333 or Tyr1363 mutations) decreased FLT4L capacity to interact with PTB-SHC recombinant proteins, and the deletion of SHC PTB domain (but not of SHC SH2 domain) abolished the binding of SHC to Tyr(P)1337-containing peptide.	bind
18066	4	5700	6	10	NULL	NULL	NULL	FLT4L	GP	mutant	does not decrease			Tyr1363		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_12956_s_185	8662748	(iii) GST-PTB SHC recombinant and epitope-tagged SHC proteins were used to confirm this interaction; Tyr1337 mutation (but not Tyr1333 or Tyr1363 mutations) decreased FLT4L capacity to interact with PTB-SHC recombinant proteins, and the deletion of SHC PTB domain (but not of SHC SH2 domain) abolished the binding of SHC to Tyr(P)1337-containing peptide.	bind
18067	5	5700	6	10	NULL	NULL	NULL	SHC	GP		bind					Tyr(P)1337-containing peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_12956_s_185	8662748	(iii) GST-PTB SHC recombinant and epitope-tagged SHC proteins were used to confirm this interaction; Tyr1337 mutation (but not Tyr1333 or Tyr1363 mutations) decreased FLT4L capacity to interact with PTB-SHC recombinant proteins, and the deletion of SHC PTB domain (but not of SHC SH2 domain) abolished the binding of SHC to Tyr(P)1337-containing peptide.	bind
18068	6	5700	6	10	NULL	NULL	NULL			deletion of	abolishes			SHC PTB domain		statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_12956_s_185	8662748	(iii) GST-PTB SHC recombinant and epitope-tagged SHC proteins were used to confirm this interaction; Tyr1337 mutation (but not Tyr1333 or Tyr1363 mutations) decreased FLT4L capacity to interact with PTB-SHC recombinant proteins, and the deletion of SHC PTB domain (but not of SHC SH2 domain) abolished the binding of SHC to Tyr(P)1337-containing peptide.	bind
18069	7	5700	6	10	NULL	NULL	NULL			deletion of	does not abolish			SHC SH2 domain		statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_12956_s_185	8662748	(iii) GST-PTB SHC recombinant and epitope-tagged SHC proteins were used to confirm this interaction; Tyr1337 mutation (but not Tyr1333 or Tyr1363 mutations) decreased FLT4L capacity to interact with PTB-SHC recombinant proteins, and the deletion of SHC PTB domain (but not of SHC SH2 domain) abolished the binding of SHC to Tyr(P)1337-containing peptide.	bind
17303	1	5700	7	10	NULL	NULL	NULL	FLT4L	GP		bind					GST-PTB SHC	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_12956_s_185	8662748	(iii) GST-PTB SHC recombinant and epitope-tagged SHC proteins were used to confirm this interaction; Tyr1337 mutation (but not Tyr1333 or Tyr1363 mutations) decreased FLT4L capacity to interact with PTB-SHC recombinant proteins, and the deletion of SHC PTB domain (but not of SHC SH2 domain) abolished the binding of SHC to Tyr(P)1337-containing peptide.	bind
17304	2	5700	7	10	NULL	NULL	NULL			mutation of	decrease			Tyr1337		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_12956_s_185	8662748	(iii) GST-PTB SHC recombinant and epitope-tagged SHC proteins were used to confirm this interaction; Tyr1337 mutation (but not Tyr1333 or Tyr1363 mutations) decreased FLT4L capacity to interact with PTB-SHC recombinant proteins, and the deletion of SHC PTB domain (but not of SHC SH2 domain) abolished the binding of SHC to Tyr(P)1337-containing peptide.	bind
17305	3	5700	7	10	NULL	NULL	NULL			mutation	does not affect			Tyr1333		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_12956_s_185	8662748	(iii) GST-PTB SHC recombinant and epitope-tagged SHC proteins were used to confirm this interaction; Tyr1337 mutation (but not Tyr1333 or Tyr1363 mutations) decreased FLT4L capacity to interact with PTB-SHC recombinant proteins, and the deletion of SHC PTB domain (but not of SHC SH2 domain) abolished the binding of SHC to Tyr(P)1337-containing peptide.	bind
17306	4	5700	7	10	NULL	NULL	NULL			mutation	does not affect			Tyr1363		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_12956_s_185	8662748	(iii) GST-PTB SHC recombinant and epitope-tagged SHC proteins were used to confirm this interaction; Tyr1337 mutation (but not Tyr1333 or Tyr1363 mutations) decreased FLT4L capacity to interact with PTB-SHC recombinant proteins, and the deletion of SHC PTB domain (but not of SHC SH2 domain) abolished the binding of SHC to Tyr(P)1337-containing peptide.	bind
17307	5	5700	7	10	NULL	NULL	NULL	SHC 	GP		bind					Tyr(P)1337-containing peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_12956_s_185	8662748	(iii) GST-PTB SHC recombinant and epitope-tagged SHC proteins were used to confirm this interaction; Tyr1337 mutation (but not Tyr1333 or Tyr1363 mutations) decreased FLT4L capacity to interact with PTB-SHC recombinant proteins, and the deletion of SHC PTB domain (but not of SHC SH2 domain) abolished the binding of SHC to Tyr(P)1337-containing peptide.	bind
17308	6	5700	7	10	NULL	NULL	NULL	SHC	GP	deletion of	abolish			PTB domain		statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_12956_s_185	8662748	(iii) GST-PTB SHC recombinant and epitope-tagged SHC proteins were used to confirm this interaction; Tyr1337 mutation (but not Tyr1333 or Tyr1363 mutations) decreased FLT4L capacity to interact with PTB-SHC recombinant proteins, and the deletion of SHC PTB domain (but not of SHC SH2 domain) abolished the binding of SHC to Tyr(P)1337-containing peptide.	bind
17309	7	5700	7	10	NULL	NULL	NULL	SHC	GP	deletion of	does not affect			SH2 domain		statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_12956_s_185	8662748	(iii) GST-PTB SHC recombinant and epitope-tagged SHC proteins were used to confirm this interaction; Tyr1337 mutation (but not Tyr1333 or Tyr1363 mutations) decreased FLT4L capacity to interact with PTB-SHC recombinant proteins, and the deletion of SHC PTB domain (but not of SHC SH2 domain) abolished the binding of SHC to Tyr(P)1337-containing peptide.	bind
18070	1	5701	6	10	NULL	NULL	NULL	flavin cofactor	Chemical		bind					TcuA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_15_5479_s_74	16855237	(iii) Identification of the flavin cofactor bound to TcuA.  or flavin analysis, a preparation of TcuA that was not reconstituted with FAD was used.	bind
17310	1	5701	7	10	NULL	NULL	NULL	flavin cofactor	Chemical		bind					TcuA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_15_5479_s_74	16855237	(iii) Identification of the flavin cofactor bound to TcuA.  or flavin analysis, a preparation of TcuA that was not reconstituted with FAD was used.	bind
18071	1	5702	6	10	NULL	NULL	NULL	UxuR	GP		bind							synthetic		 operator	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_12_3695_s_260	10368143	(iii) In gel retardation assays, MeGlcUAXyl3 was particularly effective in preventing the binding of UxuR to a synthetic operator.	bind
18072	2	5702	6	10	NULL	NULL	NULL	MeGlcUAXyl3	Chemical		prevents					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_12_3695_s_260	10368143	(iii) In gel retardation assays, MeGlcUAXyl3 was particularly effective in preventing the binding of UxuR to a synthetic operator.	bind
17311	1	5702	7	10	NULL	NULL	NULL	UxuR 	GP		bind							synthetic 		operator	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_12_3695_s_260	10368143	(iii) In gel retardation assays, MeGlcUAXyl3 was particularly effective in preventing the binding of UxuR to a synthetic operator.	bind
17312	2	5702	7	10	NULL	NULL	NULL	MeGlcUAXyl3	Chemical		prevents					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_12_3695_s_260	10368143	(iii) In gel retardation assays, MeGlcUAXyl3 was particularly effective in preventing the binding of UxuR to a synthetic operator.	bind
18073	1	5703	6	NULL	NULL	0	NULL	cysteine	NULL		bind	NULL	covalently			Flavin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_12_3336_s_243	10852862	(iii) In the FAD binding pocket of flavocytochrome  c of  A. vinosum, there are a cysteine known to covalently bind flavin and two additional cysteines that form a disulfide bridge ( 9).	bind
18074	2	5703	6	NULL	NULL	0	NULL	statement 1	NULL		occurs in	NULL				flavocytochrome c 	NULL	A. vinosum	FAD binding pocket		NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_12_3336_s_243	10852862	(iii) In the FAD binding pocket of flavocytochrome  c of  A. vinosum, there are a cysteine known to covalently bind flavin and two additional cysteines that form a disulfide bridge ( 9).	bind
18075	3	5703	6	NULL	NULL	0	NULL	cysteine	NULL		forms a 	NULL				disulfide bridge	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_12_3336_s_243	10852862	(iii) In the FAD binding pocket of flavocytochrome  c of  A. vinosum, there are a cysteine known to covalently bind flavin and two additional cysteines that form a disulfide bridge ( 9).	bind
18076	4	5703	6	NULL	NULL	0	NULL	statement 3	NULL		occurs in	NULL				flavocytochrome c	NULL	A. vinosum	FAD binding pocket		NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_12_3336_s_243	10852862	(iii) In the FAD binding pocket of flavocytochrome  c of  A. vinosum, there are a cysteine known to covalently bind flavin and two additional cysteines that form a disulfide bridge ( 9).	bind
17313	1	5703	7	NULL	NULL	NULL	NULL	cysteine	AminoAcid		bind		covalently			flavin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_12_3336_s_243	10852862	(iii) In the FAD binding pocket of flavocytochrome  c of  A. vinosum, there are a cysteine known to covalently bind flavin and two additional cysteines that form a disulfide bridge ( 9).	bind
17314	2	5703	7	NULL	NULL	NULL	NULL	statement 1	Process		present in					flavocytochrome c 	Chemical	A. vinosum	FAD binding pocket		NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_12_3336_s_243	10852862	(iii) In the FAD binding pocket of flavocytochrome  c of  A. vinosum, there are a cysteine known to covalently bind flavin and two additional cysteines that form a disulfide bridge ( 9).	bind
17315	3	5703	7	NULL	NULL	NULL	NULL	cysteines	AminoAcid		form					disulfide bridge	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_12_3336_s_243	10852862	(iii) In the FAD binding pocket of flavocytochrome  c of  A. vinosum, there are a cysteine known to covalently bind flavin and two additional cysteines that form a disulfide bridge ( 9).	bind
23451	4	5703	7	NULL	NULL	NULL	NULL	statement 3	Process		present in					flavocytochrome c 	Chemical	A. vinosum	FAD binding pocket		NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_12_3336_s_243	10852862	(iii) In the FAD binding pocket of flavocytochrome  c of  A. vinosum, there are a cysteine known to covalently bind flavin and two additional cysteines that form a disulfide bridge ( 9).	bind
18077	1	5704	6	NULL	NULL	0	NULL	statin	NULL		bind	NULL				LFA-1	NULL				NULL		0	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_181	15186950	(iii) Inflammatory processes involving bacterial infection and superantigen-induced  T cell activation may profit from treatment with a statin that binds LFA-1 (simvastatin).	bind
18078	2	5704	6	NULL	NULL	0	NULL	LFA-1	NULL		is	NULL				simvastatin	NULL				NULL		0	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_181	15186950	(iii) Inflammatory processes involving bacterial infection and superantigen-induced  T cell activation may profit from treatment with a statin that binds LFA-1 (simvastatin).	bind
18079	3	5704	6	10	NULL	0	NULL	superantigen	NULL		induce	NULL				T cell	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_181	15186950	(iii) Inflammatory processes involving bacterial infection and superantigen-induced  T cell activation may profit from treatment with a statin that binds LFA-1 (simvastatin).	bind
18080	4	5704	6	NULL	NULL	0	NULL	Inflammatory process	NULL		involve	NULL				bacterial infection	NULL				NULL		0	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_181	15186950	(iii) Inflammatory processes involving bacterial infection and superantigen-induced  T cell activation may profit from treatment with a statin that binds LFA-1 (simvastatin).	bind
18081	5	5704	6	10	NULL	0	NULL	inflammatory processes	NULL		involve	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_181	15186950	(iii) Inflammatory processes involving bacterial infection and superantigen-induced  T cell activation may profit from treatment with a statin that binds LFA-1 (simvastatin).	bind
18082	6	5704	6	NULL	NULL	0	NULL	statement 4	NULL		profit from	NULL	may			statin	NULL	treatment with			NULL		0	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_181	15186950	(iii) Inflammatory processes involving bacterial infection and superantigen-induced  T cell activation may profit from treatment with a statin that binds LFA-1 (simvastatin).	bind
45751	7	5704	6	10	NULL	0	NULL	statement 5	NULL		profit from	NULL	may			statin	NULL	treatment with			NULL		0	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_181	15186950	(iii) Inflammatory processes involving bacterial infection and superantigen-induced  T cell activation may profit from treatment with a statin that binds LFA-1 (simvastatin).	bind
17319	1	5704	7	NULL	NULL	NULL	NULL	statin	GP		binds					LFA-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_181	15186950	(iii) Inflammatory processes involving bacterial infection and superantigen-induced  T cell activation may profit from treatment with a statin that binds LFA-1 (simvastatin).	bind
17321	2	5704	7	NULL	NULL	NULL	NULL	LFA-1	GP		is					simvastatin	GP				NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_181	15186950	(iii) Inflammatory processes involving bacterial infection and superantigen-induced  T cell activation may profit from treatment with a statin that binds LFA-1 (simvastatin).	bind
23452	4	5704	7	NULL	NULL	NULL	NULL	Inflammatory process	Process		involve					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_181	15186950	(iii) Inflammatory processes involving bacterial infection and superantigen-induced  T cell activation may profit from treatment with a statin that binds LFA-1 (simvastatin).	bind
23453	5	5704	7	NULL	NULL	NULL	NULL	Inflammatory process	Process		involve					bacterial infection	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_181	15186950	(iii) Inflammatory processes involving bacterial infection and superantigen-induced  T cell activation may profit from treatment with a statin that binds LFA-1 (simvastatin).	bind
23454	6	5704	7	NULL	NULL	NULL	NULL	statement 4	Process		profit from		may			statin	GP	treatment with			NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_181	15186950	(iii) Inflammatory processes involving bacterial infection and superantigen-induced  T cell activation may profit from treatment with a statin that binds LFA-1 (simvastatin).	bind
23455	7	5704	7	NULL	NULL	NULL	NULL	statement 5	Process		profit from		may			statin	GP	treatment with			NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_181	15186950	(iii) Inflammatory processes involving bacterial infection and superantigen-induced  T cell activation may profit from treatment with a statin that binds LFA-1 (simvastatin).	bind
45851	3	5704	7	NULL	NULL	NULL	NULL	superantigen	GP		induce					T cell	Cell	activation of			NULL		NULL	NULL	NULL	NULL	gw70_atherosclerosis_175_1_83_s_181	15186950	(iii) Inflammatory processes involving bacterial infection and superantigen-induced  T cell activation may profit from treatment with a statin that binds LFA-1 (simvastatin).	bind
18083	1	5705	6	NULL	NULL	0	NULL	Stat3	NULL		exhibits	NULL				DNA binding activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_256	10821852	(iii) Insulin stimulates Stat3 and Stat5 DNA binding activities, and (iv) insulin transactivates a reporter gene containing Stat binding sites.	bind
18084	2	5705	6	NULL	NULL	0	NULL	Stat5	NULL		exhibits	NULL				DNA binding activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_256	10821852	(iii) Insulin stimulates Stat3 and Stat5 DNA binding activities, and (iv) insulin transactivates a reporter gene containing Stat binding sites.	bind
18085	3	5705	6	NULL	NULL	0	NULL	Insulin	NULL		stimulates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_256	10821852	(iii) Insulin stimulates Stat3 and Stat5 DNA binding activities, and (iv) insulin transactivates a reporter gene containing Stat binding sites.	bind
18086	4	5705	6	NULL	NULL	0	NULL	Insulin	NULL		stimulates	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_256	10821852	(iii) Insulin stimulates Stat3 and Stat5 DNA binding activities, and (iv) insulin transactivates a reporter gene containing Stat binding sites.	bind
18087	5	5705	6	NULL	NULL	0	NULL	Insulin	NULL		transactivates	NULL				reporter gene	NULL			Stat binding sites	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_256	10821852	(iii) Insulin stimulates Stat3 and Stat5 DNA binding activities, and (iv) insulin transactivates a reporter gene containing Stat binding sites.	bind
17322	1	5705	7	NULL	NULL	NULL	NULL	Stat3	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_256	10821852	(iii) Insulin stimulates Stat3 and Stat5 DNA binding activities, and (iv) insulin transactivates a reporter gene containing Stat binding sites.	bind
17324	2	5705	7	NULL	NULL	NULL	NULL	Stat5	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_256	10821852	(iii) Insulin stimulates Stat3 and Stat5 DNA binding activities, and (iv) insulin transactivates a reporter gene containing Stat binding sites.	bind
17325	3	5705	7	NULL	NULL	NULL	NULL	Insulin	GP		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_256	10821852	(iii) Insulin stimulates Stat3 and Stat5 DNA binding activities, and (iv) insulin transactivates a reporter gene containing Stat binding sites.	bind
17326	4	5705	7	NULL	NULL	NULL	NULL	Insulin	GP		stimulate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_256	10821852	(iii) Insulin stimulates Stat3 and Stat5 DNA binding activities, and (iv) insulin transactivates a reporter gene containing Stat binding sites.	bind
17328	5	5705	7	NULL	NULL	NULL	NULL	Insulin	GP		transactivate					reporter gene	GP			Stat binding sites	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_256	10821852	(iii) Insulin stimulates Stat3 and Stat5 DNA binding activities, and (iv) insulin transactivates a reporter gene containing Stat binding sites.	bind
18088	1	5706	6	NULL	NULL	0	NULL	Sa-Lrp	NULL		bind	NULL				Sa-Lrp	NULL			control region	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_13_3661_s_263	10850980	(iii) Like  E. coli Lrp, Sa-Lrp binds to its own control region in a leucine-independent manner, suggestive of leucine-independent autoregulation.	bind
18089	2	5706	6	NULL	NULL	0	NULL	statement 1	NULL		is independent of	NULL				leucine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_13_3661_s_263	10850980	(iii) Like  E. coli Lrp, Sa-Lrp binds to its own control region in a leucine-independent manner, suggestive of leucine-independent autoregulation.	bind
18090	3	5706	6	NULL	NULL	0	NULL	Lrp	NULL	E.coli	bind	NULL				Lrp	NULL	E.coli		control region	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_13_3661_s_263	10850980	(iii) Like  E. coli Lrp, Sa-Lrp binds to its own control region in a leucine-independent manner, suggestive of leucine-independent autoregulation.	bind
18091	4	5706	6	NULL	NULL	0	NULL	statement 3	NULL		is independent of	NULL				leucine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_13_3661_s_263	10850980	(iii) Like  E. coli Lrp, Sa-Lrp binds to its own control region in a leucine-independent manner, suggestive of leucine-independent autoregulation.	bind
23026	5	5706	6	NULL	NULL	0	NULL	statement 1	NULL		suggests	NULL					NULL	independent autoregulation of	leucine		NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_13_3661_s_263	10850980	(iii) Like  E. coli Lrp, Sa-Lrp binds to its own control region in a leucine-independent manner, suggestive of leucine-independent autoregulation.	bind
23027	6	5706	6	NULL	NULL	0	NULL	statement 3	NULL		suggests	NULL					NULL	independent autoregulation of	leucine		NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_13_3661_s_263	10850980	(iii) Like  E. coli Lrp, Sa-Lrp binds to its own control region in a leucine-independent manner, suggestive of leucine-independent autoregulation.	bind
17331	1	5706	7	NULL	NULL	NULL	NULL	Sa-Lrp	GP		bind					Sa-Lrp	GP			control region	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_13_3661_s_263	10850980	(iii) Like  E. coli Lrp, Sa-Lrp binds to its own control region in a leucine-independent manner, suggestive of leucine-independent autoregulation.	bind
17332	2	5706	7	NULL	NULL	NULL	NULL	statement 1	Process		is independent of					leucine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_13_3661_s_263	10850980	(iii) Like  E. coli Lrp, Sa-Lrp binds to its own control region in a leucine-independent manner, suggestive of leucine-independent autoregulation.	bind
17333	3	5706	7	NULL	NULL	NULL	NULL	Lrp	GP	E. coli	bind					Lrp	GP	E. coli		control region	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_13_3661_s_263	10850980	(iii) Like  E. coli Lrp, Sa-Lrp binds to its own control region in a leucine-independent manner, suggestive of leucine-independent autoregulation.	bind
17334	4	5706	7	NULL	NULL	NULL	NULL	statement 3	Process		is independent of					leucine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_13_3661_s_263	10850980	(iii) Like  E. coli Lrp, Sa-Lrp binds to its own control region in a leucine-independent manner, suggestive of leucine-independent autoregulation.	bind
17335	5	5706	7	NULL	NULL	NULL	NULL	statement 2	Process		suggests					leucine	AminoAcid	independent autoregulation of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_13_3661_s_263	10850980	(iii) Like  E. coli Lrp, Sa-Lrp binds to its own control region in a leucine-independent manner, suggestive of leucine-independent autoregulation.	bind
17336	6	5706	7	NULL	NULL	NULL	NULL	statement 4	Process		suggests					leucine	Aminoacid	independent autoregulation of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_13_3661_s_263	10850980	(iii) Like  E. coli Lrp, Sa-Lrp binds to its own control region in a leucine-independent manner, suggestive of leucine-independent autoregulation.	bind
18092	1	5707	6	10	NULL	0	NULL	GPVI	NULL	cell-expressed	bind	NULL				convulxin	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_251	15466473	(iii) Only the combination of 9O12 and 3F8 could strongly impair the binding of cell-expressed GPVI to convulxin.	bind
18093	2	5707	6	NULL	NULL	0	NULL	9O12	NULL		impair	NULL	strongly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_251	15466473	(iii) Only the combination of 9O12 and 3F8 could strongly impair the binding of cell-expressed GPVI to convulxin.	bind
18124	3	5707	6	NULL	NULL	0	NULL	3F8	NULL		impair	NULL	strongly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_251	15466473	(iii) Only the combination of 9O12 and 3F8 could strongly impair the binding of cell-expressed GPVI to convulxin.	bind
18125	4	5707	6	NULL	NULL	0	NULL	statement 2	NULL		occurs in combination with	NULL	only			statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_251	15466473	(iii) Only the combination of 9O12 and 3F8 could strongly impair the binding of cell-expressed GPVI to convulxin.	bind
17337	1	5707	7	NULL	NULL	NULL	NULL	GPVI	GP	cell-expressed	bind					convulxin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_251	15466473	(iii) Only the combination of 9O12 and 3F8 could strongly impair the binding of cell-expressed GPVI to convulxin.	bind
17338	2	5707	7	NULL	NULL	NULL	NULL	9O12	GP		impair		strongly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_251	15466473	(iii) Only the combination of 9O12 and 3F8 could strongly impair the binding of cell-expressed GPVI to convulxin.	bind
17339	3	5707	7	NULL	NULL	NULL	NULL	3F8	GP		impair		strongly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_251	15466473	(iii) Only the combination of 9O12 and 3F8 could strongly impair the binding of cell-expressed GPVI to convulxin.	bind
17340	4	5707	7	NULL	NULL	NULL	NULL	statement 2	Process		occur in combination with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_251	15466473	(iii) Only the combination of 9O12 and 3F8 could strongly impair the binding of cell-expressed GPVI to convulxin.	bind
18129	1	5708	6	NULL	NULL	0	NULL	BRG1	NULL		bind	NULL	directly			IFITM1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_10_4476_s_269	15121865	(iii) Our ChIP results demonstrate that BRG1 is directly bound to the IFITM1 promoter both in the absence and in the presence of IFN-alpha (Fig.  6).	bind
17341	1	5708	7	NULL	NULL	NULL	NULL	BRG1	GP		bind		directly			IFITM1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_10_4476_s_269	15121865	(iii) Our ChIP results demonstrate that BRG1 is directly bound to the IFITM1 promoter both in the absence and in the presence of IFN-alpha (Fig.  6).	bind
18134	1	5709	6	NULL	NULL	0	NULL	Pex14p	NULL		bind	NULL				Pex5p	NULL	cargo loaded			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_6_1639_s_586	11865044	(iii) Pex14p can bind to cargo-loaded Pex5p, while Pex13p binds only to unloaded Pex5p, consistent with the notion that Pex14p most likely functions as the initial docking site of Pex5p ( 29).	bind
18135	2	5709	6	NULL	NULL	0	NULL	Pex13p	NULL		bind	NULL	only			Pex5p	NULL	unloaded			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_6_1639_s_586	11865044	(iii) Pex14p can bind to cargo-loaded Pex5p, while Pex13p binds only to unloaded Pex5p, consistent with the notion that Pex14p most likely functions as the initial docking site of Pex5p ( 29).	bind
18138	3	5709	6	NULL	NULL	0	NULL	Pex14	NULL		functions as	NULL	mostly			Pex5p	NULL		docking site		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_6_1639_s_586	11865044	(iii) Pex14p can bind to cargo-loaded Pex5p, while Pex13p binds only to unloaded Pex5p, consistent with the notion that Pex14p most likely functions as the initial docking site of Pex5p ( 29).	bind
17342	1	5709	7	NULL	NULL	NULL	NULL	Pex14p	GP		bind					Pex5p	GP	cargo-loaded			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_6_1639_s_586	11865044	(iii) Pex14p can bind to cargo-loaded Pex5p, while Pex13p binds only to unloaded Pex5p, consistent with the notion that Pex14p most likely functions as the initial docking site of Pex5p ( 29).	bind
17343	2	5709	7	NULL	NULL	NULL	NULL	Pex13p	GP		binds		only			Pex5p	GP	unloaded			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_6_1639_s_586	11865044	(iii) Pex14p can bind to cargo-loaded Pex5p, while Pex13p binds only to unloaded Pex5p, consistent with the notion that Pex14p most likely functions as the initial docking site of Pex5p ( 29).	bind
17344	3	5709	7	NULL	NULL	NULL	NULL	Pex14p	GP		functions as 		mostly			Pex5p	GP		docking site		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_6_1639_s_586	11865044	(iii) Pex14p can bind to cargo-loaded Pex5p, while Pex13p binds only to unloaded Pex5p, consistent with the notion that Pex14p most likely functions as the initial docking site of Pex5p ( 29).	bind
18146	1	5710	6	NULL	NULL	0	NULL	CREB	NULL	phosphorylated	bind	NULL				c- fos	NULL			CRE in 5 regulatory region	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_41_25715_s_187	8810350	(iii) Phosphorylated CREB bound to the major CRE in the c- fos 5  regulatory region results in transcriptional activation.	bind
23036	2	5710	6	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				transcription	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_41_25715_s_187	8810350	(iii) Phosphorylated CREB bound to the major CRE in the c- fos 5  regulatory region results in transcriptional activation.	bind
17345	1	5710	7	NULL	NULL	NULL	NULL	CREB	GP	phosphorylated 	bind					c- fos	GP	major		CRE in 5 regulatory region of 	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_41_25715_s_187	8810350	(iii) Phosphorylated CREB bound to the major CRE in the c- fos 5  regulatory region results in transcriptional activation.	bind
17346	2	5710	7	NULL	NULL	NULL	NULL	statement 1	Process		activates					transcription 	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_41_25715_s_187	8810350	(iii) Phosphorylated CREB bound to the major CRE in the c- fos 5  regulatory region results in transcriptional activation.	bind
18149	1	5711	6	NULL	NULL	0	NULL	hydrolases	NULL		bind	NULL	noncovalently	C-terminal		ubiquitin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_34_20235_s_19	8702753	(iii) Proteins binding noncovalently to ubiquitin: all C-terminal hydrolases (deubiquitinating enzymes) and an S5 subunit of the 26 S proteasome bind noncovalently to ubiquitin ( 10,  11,  12).	bind
18152	2	5711	6	NULL	NULL	0	NULL	26 S proteasome	NULL		bind	NULL	noncovalently	S5 subunit		ubiquitin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20235_s_19	8702753	(iii) Proteins binding noncovalently to ubiquitin: all C-terminal hydrolases (deubiquitinating enzymes) and an S5 subunit of the 26 S proteasome bind noncovalently to ubiquitin ( 10,  11,  12).	bind
18153	3	5711	6	NULL	NULL	0	NULL	hydrolases	NULL		are	NULL		c-terminal		deubiquitinating enzymes	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_34_20235_s_19	8702753	(iii) Proteins binding noncovalently to ubiquitin: all C-terminal hydrolases (deubiquitinating enzymes) and an S5 subunit of the 26 S proteasome bind noncovalently to ubiquitin ( 10,  11,  12).	bind
17381	1	5711	7	NULL	NULL	NULL	NULL	 hydrolases 	GP		bind		noncovalently	C-terminal		Ubiquitin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20235_s_19	8702753	(iii) Proteins binding noncovalently to ubiquitin: all C-terminal hydrolases (deubiquitinating enzymes) and an S5 subunit of the 26 S proteasome bind noncovalently to ubiquitin ( 10,  11,  12).	bind
17383	2	5711	7	NULL	NULL	NULL	NULL	 26 S proteasome	GP		bind		noncovalently	S5 subunit		Ubiquitin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20235_s_19	8702753	(iii) Proteins binding noncovalently to ubiquitin: all C-terminal hydrolases (deubiquitinating enzymes) and an S5 subunit of the 26 S proteasome bind noncovalently to ubiquitin ( 10,  11,  12).	bind
17385	3	5711	7	NULL	NULL	NULL	NULL	 hydrolases	GP		are			C-terminal		deubiquitinating enzymes	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20235_s_19	8702753	(iii) Proteins binding noncovalently to ubiquitin: all C-terminal hydrolases (deubiquitinating enzymes) and an S5 subunit of the 26 S proteasome bind noncovalently to ubiquitin ( 10,  11,  12).	bind
18154	1	5712	6	10	NULL	0	NULL	ERK2	NULL	purified;;activated	bind	NULL				beta	NULL		carboxy terminal		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13539_s_268	11805112	(iii) Purified activated ERK2 can bind the carboxyl termini of beta and gamma and phosphorylate betaThr-613 and gammaThr-623.	bind
18155	2	5712	6	10	NULL	0	NULL	ERK2	NULL	purified;;activated	bind	NULL				gamma	NULL		carboxy terminal		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13539_s_268	11805112	(iii) Purified activated ERK2 can bind the carboxyl termini of beta and gamma and phosphorylate betaThr-613 and gammaThr-623.	bind
18156	3	5712	6	10	NULL	0	NULL	ERK2	NULL	purified;;activated	phosphorylate	NULL				beta	NULL		Thr-613		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13539_s_268	11805112	(iii) Purified activated ERK2 can bind the carboxyl termini of beta and gamma and phosphorylate betaThr-613 and gammaThr-623.	bind
18158	4	5712	6	10	NULL	0	NULL	ERK2	NULL	purified;;activated	phosphorylate	NULL				gamma	NULL		Thr-623		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13539_s_268	11805112	(iii) Purified activated ERK2 can bind the carboxyl termini of beta and gamma and phosphorylate betaThr-613 and gammaThr-623.	bind
17387	1	5712	7	NULL	NULL	NULL	NULL	ERK2	GP	purified;;activated	bind					beta	GP		carboxyl termini 		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13539_s_268	11805112	(iii) Purified activated ERK2 can bind the carboxyl termini of beta and gamma and phosphorylate betaThr-613 and gammaThr-623.	bind
17388	2	5712	7	NULL	NULL	NULL	NULL	ERK2	GP	purified;;activated	bind					gamma	GP		carboxyl termini 		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13539_s_268	11805112	(iii) Purified activated ERK2 can bind the carboxyl termini of beta and gamma and phosphorylate betaThr-613 and gammaThr-623.	bind
17389	3	5712	7	NULL	NULL	NULL	NULL	ERK2	GP	purified;;activated	phosphorylate					 beta	GP		Thr-613		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13539_s_268	11805112	(iii) Purified activated ERK2 can bind the carboxyl termini of beta and gamma and phosphorylate betaThr-613 and gammaThr-623.	bind
17390	4	5712	7	NULL	NULL	NULL	NULL	ERK2	GP	purified;;activated	phosphorylate					gamma	GP		Thr-623		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13539_s_268	11805112	(iii) Purified activated ERK2 can bind the carboxyl termini of beta and gamma and phosphorylate betaThr-613 and gammaThr-623.	bind
18162	1	5713	6	NULL	NULL	0	NULL	Rab1B	NULL		bind	NULL		CLLL		REP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_243	11389151	(iii) Rab1B-CLLL binds to REP and is geranylgeranylated on the single cysteine by GGTase II, but it can also be modified in a REP-independent manner by GGTase I. (iv) Rab1B(Y78D)CLLL cannot bind REP but can be geranylgeranylated by GGTase I.	bind
18163	2	5713	6	NULL	NULL	0	NULL	GGTase II	NULL		geranylgeranylate	NULL				Rab1B	NULL		CLLL		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_243	11389151	(iii) Rab1B-CLLL binds to REP and is geranylgeranylated on the single cysteine by GGTase II, but it can also be modified in a REP-independent manner by GGTase I. (iv) Rab1B(Y78D)CLLL cannot bind REP but can be geranylgeranylated by GGTase I.	bind
18164	3	5713	6	NULL	NULL	0	NULL	Rab1B	NULL	mutant	does not bind	NULL		CLLL;;Y78D		REP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_243	11389151	(iii) Rab1B-CLLL binds to REP and is geranylgeranylated on the single cysteine by GGTase II, but it can also be modified in a REP-independent manner by GGTase I. (iv) Rab1B(Y78D)CLLL cannot bind REP but can be geranylgeranylated by GGTase I.	bind
18165	4	5713	6	NULL	NULL	0	NULL	GGTase I	NULL		geranylgeranylate	NULL				Rab1B	NULL	mutant	Y78D;;CLLL		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_243	11389151	(iii) Rab1B-CLLL binds to REP and is geranylgeranylated on the single cysteine by GGTase II, but it can also be modified in a REP-independent manner by GGTase I. (iv) Rab1B(Y78D)CLLL cannot bind REP but can be geranylgeranylated by GGTase I.	bind
23037	5	5713	6	NULL	NULL	0	NULL	statement 2	NULL		is independent of	NULL				REP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_243	11389151	(iii) Rab1B-CLLL binds to REP and is geranylgeranylated on the single cysteine by GGTase II, but it can also be modified in a REP-independent manner by GGTase I. (iv) Rab1B(Y78D)CLLL cannot bind REP but can be geranylgeranylated by GGTase I.	bind
23038	6	5713	6	NULL	NULL	0	NULL	GGTase II	NULL		geranylgeranylates	NULL				statement 1	NULL		single cysteine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_243	11389151	(iii) Rab1B-CLLL binds to REP and is geranylgeranylated on the single cysteine by GGTase II, but it can also be modified in a REP-independent manner by GGTase I. (iv) Rab1B(Y78D)CLLL cannot bind REP but can be geranylgeranylated by GGTase I.	bind
17394	1	5713	7	NULL	NULL	NULL	NULL	Rab1B	GP		binds			CLLL		REP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_243	11389151	(iii) Rab1B-CLLL binds to REP and is geranylgeranylated on the single cysteine by GGTase II, but it can also be modified in a REP-independent manner by GGTase I. (iv) Rab1B(Y78D)CLLL cannot bind REP but can be geranylgeranylated by GGTase I.	bind
17395	2	5713	7	NULL	NULL	NULL	NULL	GGTase II	GP		geranylgeranylates					statement 1	Process		single cysteine 		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_243	11389151	(iii) Rab1B-CLLL binds to REP and is geranylgeranylated on the single cysteine by GGTase II, but it can also be modified in a REP-independent manner by GGTase I. (iv) Rab1B(Y78D)CLLL cannot bind REP but can be geranylgeranylated by GGTase I.	bind
17397	3	5713	7	NULL	NULL	NULL	NULL	GGTase I	GP		geranylgeranylates					Rab1B	GP		CLLL		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_243	11389151	(iii) Rab1B-CLLL binds to REP and is geranylgeranylated on the single cysteine by GGTase II, but it can also be modified in a REP-independent manner by GGTase I. (iv) Rab1B(Y78D)CLLL cannot bind REP but can be geranylgeranylated by GGTase I.	bind
17398	4	5713	7	NULL	NULL	NULL	NULL	statement 3	Process		is independent of					REP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_243	11389151	(iii) Rab1B-CLLL binds to REP and is geranylgeranylated on the single cysteine by GGTase II, but it can also be modified in a REP-independent manner by GGTase I. (iv) Rab1B(Y78D)CLLL cannot bind REP but can be geranylgeranylated by GGTase I.	bind
17399	5	5713	7	NULL	NULL	NULL	NULL	Rab1B	GP	mutant	does not bind			CLLL;;Y78D		REP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_243	11389151	(iii) Rab1B-CLLL binds to REP and is geranylgeranylated on the single cysteine by GGTase II, but it can also be modified in a REP-independent manner by GGTase I. (iv) Rab1B(Y78D)CLLL cannot bind REP but can be geranylgeranylated by GGTase I.	bind
17402	6	5713	7	NULL	NULL	NULL	NULL	GGTase I	GP		geranylgeranylates					Rab1B	GP	mutant	CLLL;;Y78D		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20379_s_243	11389151	(iii) Rab1B-CLLL binds to REP and is geranylgeranylated on the single cysteine by GGTase II, but it can also be modified in a REP-independent manner by GGTase I. (iv) Rab1B(Y78D)CLLL cannot bind REP but can be geranylgeranylated by GGTase I.	bind
18166	1	5714	6	10	NULL	0	NULL	CnNK-2	NULL	recombinant	bind	NULL	sequence specifically			CnNk-2	NULL			NK-2 sites	NULL		NULL	NULL	NULL	NULL	gw70_mechdev_121_2_195_s_165	15037320	(iii) Recombinant  CnNK-2 is binding to NK-2 sites of the  CnNk-2 as well as the  pedibin 5  flanking region in a sequence specific manner ( Fig. 2C,E).	bind
18167	2	5714	6	10	NULL	0	NULL	CnNK-2	NULL	recombinant	bind	NULL	sequence specifically			pedibin	NULL			5 flanking region	NULL		NULL	NULL	NULL	NULL	gw70_mechdev_121_2_195_s_165	15037320	(iii) Recombinant  CnNK-2 is binding to NK-2 sites of the  CnNk-2 as well as the  pedibin 5  flanking region in a sequence specific manner ( Fig. 2C,E).	bind
17403	1	5714	7	NULL	NULL	NULL	NULL	CnNK-2	GP	recombinant	bind		sequence specifically			CnNk-2 	GP			NK-2 sites 	NULL		NULL	NULL	NULL	NULL	gw70_mechdev_121_2_195_s_165	15037320	(iii) Recombinant  CnNK-2 is binding to NK-2 sites of the  CnNk-2 as well as the  pedibin 5  flanking region in a sequence specific manner ( Fig. 2C,E).	bind
17404	2	5714	7	NULL	NULL	NULL	NULL	CnNK-2	GP	recombinant	bind		sequence specifically			pedibin	GP			5 flanking region	NULL		NULL	NULL	NULL	NULL	gw70_mechdev_121_2_195_s_165	15037320	(iii) Recombinant  CnNK-2 is binding to NK-2 sites of the  CnNk-2 as well as the  pedibin 5  flanking region in a sequence specific manner ( Fig. 2C,E).	bind
18169	1	5715	6	NULL	NULL	0	NULL	Rheb	NULL		does not bind	NULL		S20N		guanine nucleotide	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_18_7965_s_284	15340059	(iii) Rheb-S20N does not function as a dominant-negative mutant although Rheb-S20N does not bind the guanine nucleotide.	bind
23039	2	5715	6	NULL	NULL	0	NULL	Rheb	NULL		does not function as	NULL		S20N		dominant-negative mutant	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_18_7965_s_284	15340059	(iii) Rheb-S20N does not function as a dominant-negative mutant although Rheb-S20N does not bind the guanine nucleotide.	bind
17406	1	5715	7	NULL	NULL	NULL	NULL	Rheb	GP		does not bind			S20N		guanine nucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_18_7965_s_284	15340059	(iii) Rheb-S20N does not function as a dominant-negative mutant although Rheb-S20N does not bind the guanine nucleotide.	bind
17407	2	5715	7	NULL	NULL	NULL	NULL	Rheb	GP		does not function as			S20N		dominant negative mutant	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_18_7965_s_284	15340059	(iii) Rheb-S20N does not function as a dominant-negative mutant although Rheb-S20N does not bind the guanine nucleotide.	bind
23040	1	5716	6	NULL	NULL	0	NULL	RhlB 	NULL		bind	NULL				RNase E	NULL				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_15_4189_s_50	16935881	(iii) RhlB is  inactive as a helicase unless it binds RNase E or a fragment thereof (in blue) carrying  an arginine-rich region.	bind
23041	2	5716	6	NULL	NULL	0	NULL	RhlB	NULL		bind	NULL				fragment 	NULL		arginine-rich region		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_15_4189_s_50	16935881	(iii) RhlB is  inactive as a helicase unless it binds RNase E or a fragment thereof (in blue) carrying  an arginine-rich region.	bind
23043	3	5716	6	NULL	NULL	0	NULL	statement 1	NULL		abolishes	NULL				RhlB helicase	NULL	inactivity of 			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_15_4189_s_50	16935881	(iii) RhlB is  inactive as a helicase unless it binds RNase E or a fragment thereof (in blue) carrying  an arginine-rich region.	bind
23044	4	5716	6	NULL	NULL	0	NULL	statement 2	NULL		abolishes	NULL				RhlB helicase	NULL	inactivity of			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_15_4189_s_50	16935881	(iii) RhlB is  inactive as a helicase unless it binds RNase E or a fragment thereof (in blue) carrying  an arginine-rich region.	bind
45755	5	5716	6	10	NULL	0	NULL	statement 3	NULL		is an alternative to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_34_15_4189_s_50	16935881	(iii) RhlB is  inactive as a helicase unless it binds RNase E or a fragment thereof (in blue) carrying  an arginine-rich region.	bind
17408	1	5716	7	NULL	NULL	NULL	NULL	RhlB	GP		bind					RNase E	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_15_4189_s_50	16935881	(iii) RhlB is  inactive as a helicase unless it binds RNase E or a fragment thereof (in blue) carrying  an arginine-rich region.	bind
17409	2	5716	7	NULL	NULL	NULL	NULL	RhlB	GP		bind					fragment	AminoAcid		arginine-rich region		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_15_4189_s_50	16935881	(iii) RhlB is  inactive as a helicase unless it binds RNase E or a fragment thereof (in blue) carrying  an arginine-rich region.	bind
17410	3	5716	7	NULL	NULL	NULL	NULL	statement 1	Process		abolishes					Rh1B helicase	GP	inactivity of			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_15_4189_s_50	16935881	(iii) RhlB is  inactive as a helicase unless it binds RNase E or a fragment thereof (in blue) carrying  an arginine-rich region.	bind
45852	4	5716	7	NULL	NULL	NULL	NULL	statement 2	Process		abolishes					RhlB helicase	GP	inactivity of			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_15_4189_s_50	16935881	(iii) RhlB is  inactive as a helicase unless it binds RNase E or a fragment thereof (in blue) carrying  an arginine-rich region.	bind
18170	1	5717	6	NULL	NULL	0	NULL	Rit	NULL		bind	NULL				B- Raf isoform	NULL	neuronal			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_2_830_s_420	15632082	(iii) Rit demonstrates isoform-specific Raf kinase binding and activation, associating with and activating the neuronal B-Raf isoform, but not C-Raf, explaining its cell type-specific activation of the ERK MAP kinase cascade.	bind
18171	2	5717	6	NULL	NULL	0	NULL	Rit	NULL		activates	NULL				B- Raf isoform	NULL	neuronal			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_2_830_s_420	15632082	(iii) Rit demonstrates isoform-specific Raf kinase binding and activation, associating with and activating the neuronal B-Raf isoform, but not C-Raf, explaining its cell type-specific activation of the ERK MAP kinase cascade.	bind
18172	3	5717	6	NULL	NULL	0	NULL	Rit	NULL		does not bind	NULL				C-Raf	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_2_830_s_420	15632082	(iii) Rit demonstrates isoform-specific Raf kinase binding and activation, associating with and activating the neuronal B-Raf isoform, but not C-Raf, explaining its cell type-specific activation of the ERK MAP kinase cascade.	bind
18173	4	5717	6	NULL	NULL	0	NULL	Rit	NULL		does not activate	NULL				C-Raf	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_2_830_s_420	15632082	(iii) Rit demonstrates isoform-specific Raf kinase binding and activation, associating with and activating the neuronal B-Raf isoform, but not C-Raf, explaining its cell type-specific activation of the ERK MAP kinase cascade.	bind
23046	5	5717	6	NULL	NULL	0	NULL	Rit	NULL		activates	NULL				ERK MAP kinase cascade	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_2_830_s_420	15632082	(iii) Rit demonstrates isoform-specific Raf kinase binding and activation, associating with and activating the neuronal B-Raf isoform, but not C-Raf, explaining its cell type-specific activation of the ERK MAP kinase cascade.	bind
17413	1	5717	7	NULL	NULL	NULL	NULL	Rit	GP		bind					B-Raf isoform	GP	neuronal			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_2_830_s_420	15632082	(iii) Rit demonstrates isoform-specific Raf kinase binding and activation, associating with and activating the neuronal B-Raf isoform, but not C-Raf, explaining its cell type-specific activation of the ERK MAP kinase cascade.	bind
17414	2	5717	7	NULL	NULL	NULL	NULL	Rit	GP		activate					B-Raf isoform	GP	neuronal			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_2_830_s_420	15632082	(iii) Rit demonstrates isoform-specific Raf kinase binding and activation, associating with and activating the neuronal B-Raf isoform, but not C-Raf, explaining its cell type-specific activation of the ERK MAP kinase cascade.	bind
17416	3	5717	7	NULL	NULL	NULL	NULL	Rit	GP		does not bind					C-Raf	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_2_830_s_420	15632082	(iii) Rit demonstrates isoform-specific Raf kinase binding and activation, associating with and activating the neuronal B-Raf isoform, but not C-Raf, explaining its cell type-specific activation of the ERK MAP kinase cascade.	bind
17417	5	5717	7	NULL	NULL	NULL	NULL	Rit	GP 		activates					ERK MAP Kinase cascade	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_2_830_s_420	15632082	(iii) Rit demonstrates isoform-specific Raf kinase binding and activation, associating with and activating the neuronal B-Raf isoform, but not C-Raf, explaining its cell type-specific activation of the ERK MAP kinase cascade.	bind
24953	4	5717	7	NULL	NULL	NULL	NULL	Rit	GP		does not activate					C-Raf	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_2_830_s_420	15632082	(iii) Rit demonstrates isoform-specific Raf kinase binding and activation, associating with and activating the neuronal B-Raf isoform, but not C-Raf, explaining its cell type-specific activation of the ERK MAP kinase cascade.	bind
18174	1	5718	6	NULL	NULL	0	NULL	ScoC	NULL		bind	NULL				aprE	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_10_3056_s_254	15126467	(iii) ScoC binds to the  aprE promoter, but its inhibitory function might be counteracted by a positive factor(s).	bind
18175	2	5718	6	NULL	NULL	0	NULL	ScoC	NULL		inhibits	NULL				aprE	NULL			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_10_3056_s_254	15126467	(iii) ScoC binds to the  aprE promoter, but its inhibitory function might be counteracted by a positive factor(s).	bind
18176	3	5718	6	NULL	NULL	0	NULL	statement 2	NULL		be counteracted by	NULL	might			positive factor	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_10_3056_s_254	15126467	(iii) ScoC binds to the  aprE promoter, but its inhibitory function might be counteracted by a positive factor(s).	bind
17418	1	5718	7	NULL	NULL	NULL	NULL	ScoC	GP		binds to					aprE	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_10_3056_s_254	15126467	(iii) ScoC binds to the  aprE promoter, but its inhibitory function might be counteracted by a positive factor(s).	bind
24954	2	5718	7	NULL	NULL	NULL	NULL	 ScoC	GP		inhibits					aprE	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_10_3056_s_254	15126467	(iii) ScoC binds to the  aprE promoter, but its inhibitory function might be counteracted by a positive factor(s).	bind
24955	3	5718	7	NULL	NULL	NULL	NULL	statement 2	Process		be counter acted by		might			positive factor(s)	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_10_3056_s_254	15126467	(iii) ScoC binds to the  aprE promoter, but its inhibitory function might be counteracted by a positive factor(s).	bind
18177	1	5719	6	NULL	NULL	0	NULL	transcription factors	NULL		bind	NULL	sequence specifically			DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_17_10236_s_163	7730328	(iii) Sequence-specific DNA binding of  transcription factors is clearly estatablished  ( 57) .	bind
17419	1	5719	7	NULL	NULL	NULL	NULL	 transcription factors 	GP		bind		sequence-specifically			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_17_10236_s_163	7730328	(iii) Sequence-specific DNA binding of  transcription factors is clearly estatablished  ( 57) .	bind
18178	1	5720	6	NULL	NULL	0	NULL	Src	NULL		does not bind	NULL		K295R		ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_2_875_s_227	14701758	(iii) Src(K295R) cannot bind ATP and has no basal or agonist activity.	bind
18179	2	5720	6	NULL	NULL	0	NULL	Src	NULL		does not exhibit	NULL		K295R		basal activity	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_2_875_s_227	14701758	(iii) Src(K295R) cannot bind ATP and has no basal or agonist activity.	bind
18180	3	5720	6	NULL	NULL	0	NULL	Src	NULL		does not exhibit	NULL		K295R		agonist activity	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_875_s_227	14701758	(iii) Src(K295R) cannot bind ATP and has no basal or agonist activity.	bind
17420	1	5720	7	NULL	NULL	NULL	NULL	Src	GP		does not bind			K295R		ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_875_s_227	14701758	(iii) Src(K295R) cannot bind ATP and has no basal or agonist activity.	bind
17421	2	5720	7	NULL	NULL	NULL	NULL	Src	GP		does not have			K295R		basal activity	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_875_s_227	14701758	(iii) Src(K295R) cannot bind ATP and has no basal or agonist activity.	bind
17422	3	5720	7	NULL	NULL	NULL	NULL	Src	GP		does not have			K295R		agonist activity	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_875_s_227	14701758	(iii) Src(K295R) cannot bind ATP and has no basal or agonist activity.	bind
18181	1	5721	6	NULL	NULL	0	NULL	LBP	NULL		bind	NULL		amino-terminal fragment		LPS	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_30_17934_s_128	7543094	(iii) The amino-terminal fragment of  LBP (residues 1-197) retains the LPS binding activity of the  native molecule( 15 ) .	bind
24956	1	5721	7	NULL	NULL	NULL	NULL	LBP	GP		binds			amino-terminal fragment		LPS	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_30_17934_s_128	7543094	(iii) The amino-terminal fragment of  LBP (residues 1-197) retains the LPS binding activity of the  native molecule( 15 ) .	bind
18182	1	5722	6	NULL	NULL	0	NULL	HRI	NULL	transformed	reassociates with	NULL				heme	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_358	10454533	(iii) The binding of Hsc70 to transformed HRI which has reassociated with heme may facilitate a conformational change in HRI that is required for heme-induced inhibition of HRI activity (Fig.  10B,  3).	bind
18183	2	5722	6	NULL	NULL	0	NULL	Hsc70	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_358	10454533	(iii) The binding of Hsc70 to transformed HRI which has reassociated with heme may facilitate a conformational change in HRI that is required for heme-induced inhibition of HRI activity (Fig.  10B,  3).	bind
18184	3	5722	6	10	NULL	0	NULL	statement 2	NULL		facilitate	NULL	may			HRI	NULL	conformational change of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_358	10454533	(iii) The binding of Hsc70 to transformed HRI which has reassociated with heme may facilitate a conformational change in HRI that is required for heme-induced inhibition of HRI activity (Fig.  10B,  3).	bind
18185	4	5722	6	NULL	NULL	0	NULL	heme	NULL		induce	NULL				HRI	NULL	inhibition of activity of 			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_358	10454533	(iii) The binding of Hsc70 to transformed HRI which has reassociated with heme may facilitate a conformational change in HRI that is required for heme-induced inhibition of HRI activity (Fig.  10B,  3).	bind
23091	5	5722	6	NULL	NULL	0	NULL	statement 3	NULL		is required for	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_358	10454533	(iii) The binding of Hsc70 to transformed HRI which has reassociated with heme may facilitate a conformational change in HRI that is required for heme-induced inhibition of HRI activity (Fig.  10B,  3).	bind
17424	2	5722	7	NULL	NULL	NULL	NULL	Hsc70	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_358	10454533	(iii) The binding of Hsc70 to transformed HRI which has reassociated with heme may facilitate a conformational change in HRI that is required for heme-induced inhibition of HRI activity (Fig.  10B,  3).	bind
17425	1	5722	7	NULL	NULL	NULL	NULL	HRI	GP	transformed	reassociate with					heme	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_358	10454533	(iii) The binding of Hsc70 to transformed HRI which has reassociated with heme may facilitate a conformational change in HRI that is required for heme-induced inhibition of HRI activity (Fig.  10B,  3).	bind
17426	3	5722	7	NULL	NULL	NULL	NULL	statement 2	Process		facilitate					HRI 	GP	conformational change in			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_358	10454533	(iii) The binding of Hsc70 to transformed HRI which has reassociated with heme may facilitate a conformational change in HRI that is required for heme-induced inhibition of HRI activity (Fig.  10B,  3).	bind
17427	4	5722	7	NULL	NULL	NULL	NULL	heme	Chemical		induce					HRI	GP	inhibition of activity of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_358	10454533	(iii) The binding of Hsc70 to transformed HRI which has reassociated with heme may facilitate a conformational change in HRI that is required for heme-induced inhibition of HRI activity (Fig.  10B,  3).	bind
17428	5	5722	7	NULL	NULL	NULL	NULL	statement 3	Process		is required for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_5861_s_358	10454533	(iii) The binding of Hsc70 to transformed HRI which has reassociated with heme may facilitate a conformational change in HRI that is required for heme-induced inhibition of HRI activity (Fig.  10B,  3).	bind
18186	1	5723	6	NULL	NULL	0	NULL	IRS-2	NULL		interact with	NULL	specifically	amino acids 591 - 786		IR	NULL		KRLB of the beta subunit		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_15_14536_s_280	15705592	(iii) The IRS-2 sequence contains a unique region (amino acids 591 - 786), not present in IRS-1, which interacts specifically with the kinase regulatory loop binding (KRLB) domain of the beta-subunit of IR. (iv) There is a difference in the phosphorylation patterns of IRS-1 and IRS-2.	bind
18187	2	5723	6	NULL	NULL	0	NULL	KRLB	NULL		is	NULL				kinase regulatory loop binding	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_15_14536_s_280	15705592	(iii) The IRS-2 sequence contains a unique region (amino acids 591 - 786), not present in IRS-1, which interacts specifically with the kinase regulatory loop binding (KRLB) domain of the beta-subunit of IR. (iv) There is a difference in the phosphorylation patterns of IRS-1 and IRS-2.	bind
23092	3	5723	6	NULL	NULL	0	NULL	IRS-2	NULL		is not present in	NULL		amino acids 591-786		IRS-1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_15_14536_s_280	15705592	(iii) The IRS-2 sequence contains a unique region (amino acids 591 - 786), not present in IRS-1, which interacts specifically with the kinase regulatory loop binding (KRLB) domain of the beta-subunit of IR. (iv) There is a difference in the phosphorylation patterns of IRS-1 and IRS-2.	bind
23093	4	5723	6	NULL	NULL	0	NULL	IRS-1	NULL	phosphorylation pattern of	differs from	NULL				IRS-2	NULL	phosphorylation pattern of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_15_14536_s_280	15705592	(iii) The IRS-2 sequence contains a unique region (amino acids 591 - 786), not present in IRS-1, which interacts specifically with the kinase regulatory loop binding (KRLB) domain of the beta-subunit of IR. (iv) There is a difference in the phosphorylation patterns of IRS-1 and IRS-2.	bind
17429	1	5723	7	NULL	NULL	NULL	NULL	IRS-2	GP		binds		specifically	amino acids 591 - 786		IR	GP		KRLB of the beta subunit		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_15_14536_s_280	15705592	(iii) The IRS-2 sequence contains a unique region (amino acids 591 - 786), not present in IRS-1, which interacts specifically with the kinase regulatory loop binding (KRLB) domain of the beta-subunit of IR. (iv) There is a difference in the phosphorylation patterns of IRS-1 and IRS-2.	bind
17430	2	5723	7	NULL	NULL	NULL	NULL	KRLB	GP		is					kinase regulatory loop binding domain	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_15_14536_s_280	15705592	(iii) The IRS-2 sequence contains a unique region (amino acids 591 - 786), not present in IRS-1, which interacts specifically with the kinase regulatory loop binding (KRLB) domain of the beta-subunit of IR. (iv) There is a difference in the phosphorylation patterns of IRS-1 and IRS-2.	bind
17432	3	5723	7	NULL	NULL	NULL	NULL	IRS-2	GP	unique region	is not present in			 amino acids 591 - 786		IRS-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_15_14536_s_280	15705592	(iii) The IRS-2 sequence contains a unique region (amino acids 591 - 786), not present in IRS-1, which interacts specifically with the kinase regulatory loop binding (KRLB) domain of the beta-subunit of IR. (iv) There is a difference in the phosphorylation patterns of IRS-1 and IRS-2.	bind
17433	4	5723	7	NULL	NULL	NULL	NULL	IRS-1	GP	phosphorylation pattern of	differs from					IRS-2	GP	phosphorylation pattern of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_15_14536_s_280	15705592	(iii) The IRS-2 sequence contains a unique region (amino acids 591 - 786), not present in IRS-1, which interacts specifically with the kinase regulatory loop binding (KRLB) domain of the beta-subunit of IR. (iv) There is a difference in the phosphorylation patterns of IRS-1 and IRS-2.	bind
18188	1	5725	6	NULL	NULL	0	NULL	Fyn	NULL		bind	NULL		SH2 domain		tr-kit	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_embo_21_20_5386_s_186	12374739	(iii) The SH2 domain of Fyn, which binds  in vitro to tr-kit, or the Src-like kinase inhibitor PP2, suppress tr-kit-induced egg activation.	bind
18189	2	5725	6	10	NULL	0	NULL	Fyn	NULL		bind	NULL		SH2 domain		PP2	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_21_20_5386_s_186	12374739	(iii) The SH2 domain of Fyn, which binds  in vitro to tr-kit, or the Src-like kinase inhibitor PP2, suppress tr-kit-induced egg activation.	bind
18190	3	5725	6	NULL	NULL	0	NULL	tr-kit	NULL		induce	NULL				egg	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw60_embo_21_20_5386_s_186	12374739	(iii) The SH2 domain of Fyn, which binds  in vitro to tr-kit, or the Src-like kinase inhibitor PP2, suppress tr-kit-induced egg activation.	bind
18191	4	5725	6	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_21_20_5386_s_186	12374739	(iii) The SH2 domain of Fyn, which binds  in vitro to tr-kit, or the Src-like kinase inhibitor PP2, suppress tr-kit-induced egg activation.	bind
24586	5	5725	6	NULL	NULL	0	NULL	Fyn	NULL		suppress	NULL		SH2 domain		statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_21_20_5386_s_186	12374739	(iii) The SH2 domain of Fyn, which binds  in vitro to tr-kit, or the Src-like kinase inhibitor PP2, suppress tr-kit-induced egg activation.	bind
24587	6	5725	6	NULL	NULL	0	NULL	PP2	NULL		is a type of	NULL				Src-like kinase inhibitor	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_21_20_5386_s_186	12374739	(iii) The SH2 domain of Fyn, which binds  in vitro to tr-kit, or the Src-like kinase inhibitor PP2, suppress tr-kit-induced egg activation.	bind
17437	1	5725	7	NULL	NULL	NULL	NULL	Fyn	GP		binds			SH2 domain		tr-kit	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_21_20_5386_s_186	12374739	(iii) The SH2 domain of Fyn, which binds  in vitro to tr-kit, or the Src-like kinase inhibitor PP2, suppress tr-kit-induced egg activation.	bind
17438	2	5725	7	NULL	NULL	NULL	NULL	Fyn	GP		binds			SH2 domain		PP2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_21_20_5386_s_186	12374739	(iii) The SH2 domain of Fyn, which binds  in vitro to tr-kit, or the Src-like kinase inhibitor PP2, suppress tr-kit-induced egg activation.	bind
17439	3	5725	7	NULL	NULL	NULL	NULL	PP2	GP		is a type of 					Src-like kinase inhibitor	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_20_5386_s_186	12374739	(iii) The SH2 domain of Fyn, which binds  in vitro to tr-kit, or the Src-like kinase inhibitor PP2, suppress tr-kit-induced egg activation.	bind
17440	4	5725	7	NULL	NULL	NULL	NULL	tr-kit	GP		induce					egg	Organism	activation of			NULL		NULL	NULL	NULL	NULL	gw60_embo_21_20_5386_s_186	12374739	(iii) The SH2 domain of Fyn, which binds  in vitro to tr-kit, or the Src-like kinase inhibitor PP2, suppress tr-kit-induced egg activation.	bind
17441	5	5725	7	NULL	NULL	NULL	NULL	Fyn	GP		suppress			SH2 domain		statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_20_5386_s_186	12374739	(iii) The SH2 domain of Fyn, which binds  in vitro to tr-kit, or the Src-like kinase inhibitor PP2, suppress tr-kit-induced egg activation.	bind
24957	6	5725	7	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_20_5386_s_186	12374739	(iii) The SH2 domain of Fyn, which binds  in vitro to tr-kit, or the Src-like kinase inhibitor PP2, suppress tr-kit-induced egg activation.	bind
18192	1	5726	6	NULL	NULL	0	NULL	Rb+	NULL		bind	NULL				E1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_8_5910_s_374	11739377	(iii) The very large values of the constants of the reactions that lead to occlusion after the binding of Rb+ to  E1 are not enough to explain the time-independent component of the occlusion curves.	bind
17442	1	5726	7	NULL	NULL	NULL	NULL	Rb+	Chemical		bind					E1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_8_5910_s_374	11739377	(iii) The very large values of the constants of the reactions that lead to occlusion after the binding of Rb+ to  E1 are not enough to explain the time-independent component of the occlusion curves.	bind
18193	1	5727	6	10	NULL	0	NULL	UV-DDB	NULL		bind	NULL	high affinity;;specifically			DNA	NULL	UV-irradiated			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9784_s_192	16260596	(iii) UV-DDB binds to UV-irradiated DNA ( ,  ) and in particular to (6-4) photoproducts ( ) with high affinity and specificity.	bind
18194	2	5727	6	NULL	NULL	0	NULL	UV-DDB	NULL		bind	NULL	high affinity;;specifically			photoproducts	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9784_s_192	16260596	(iii) UV-DDB binds to UV-irradiated DNA ( ,  ) and in particular to (6-4) photoproducts ( ) with high affinity and specificity.	bind
17443	1	5727	7	NULL	NULL	NULL	NULL	UV-DDB	GP		binds		high affinity;;specifically			DNA	NucleicAcid	UV-irradiated			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9784_s_192	16260596	(iii) UV-DDB binds to UV-irradiated DNA ( ,  ) and in particular to (6-4) photoproducts ( ) with high affinity and specificity.	bind
17444	2	5727	7	NULL	NULL	NULL	NULL	UV-DDB	GP		binds		high affinity;;specifically			photoproducts	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9784_s_192	16260596	(iii) UV-DDB binds to UV-irradiated DNA ( ,  ) and in particular to (6-4) photoproducts ( ) with high affinity and specificity.	bind
18195	1	5728	6	NULL	NULL	0	NULL	Mdm2	NULL	wild type	bind	NULL				p14ARF	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6170_s_244	12167711	(iii) Wild-type and mutant Mdm2 bind to p14ARF with equal affinities.	bind
18196	2	5728	6	NULL	NULL	0	NULL	Mdm2	NULL	mutant	bind	NULL				p14ARF	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6170_s_244	12167711	(iii) Wild-type and mutant Mdm2 bind to p14ARF with equal affinities.	bind
18197	3	5728	6	NULL	NULL	0	NULL	statement 1	NULL	affinity of	is equal to	NULL				statement 2	NULL	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6170_s_244	12167711	(iii) Wild-type and mutant Mdm2 bind to p14ARF with equal affinities.	bind
17447	1	5728	7	NULL	NULL	NULL	NULL	Mdm2	GP	Wild-type	bind					p14ARF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6170_s_244	12167711	(iii) Wild-type and mutant Mdm2 bind to p14ARF with equal affinities.	bind
17448	2	5728	7	NULL	NULL	NULL	NULL	Mdm2	GP	mutant	bind					p14 ARF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6170_s_244	12167711	(iii) Wild-type and mutant Mdm2 bind to p14ARF with equal affinities.	bind
17449	3	5728	7	NULL	NULL	NULL	NULL	statement 1	Process	affinity of	is equal to					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6170_s_244	12167711	(iii) Wild-type and mutant Mdm2 bind to p14ARF with equal affinities.	bind
18198	1	5729	6	10	NULL	0	NULL	AMP	NULL		bind	NULL					NULL		ATP-BD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_3_2234_s_203	11053407	(In fact, AMP consistently produced a small increase in the fluorescence of the ATP-pretreated sample, further illustrating that AMP was bound to ATP-BD, but did not compete with TNP-ATP.)	bind
18204	2	5729	6	10	NULL	0	NULL	TNP	NULL		bind	NULL					NULL		ATP-BD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_3_2234_s_203	11053407	(In fact, AMP consistently produced a small increase in the fluorescence of the ATP-pretreated sample, further illustrating that AMP was bound to ATP-BD, but did not compete with TNP-ATP.)	bind
18205	3	5729	6	10	NULL	0	NULL	statement 1	NULL		does not compete	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_3_2234_s_203	11053407	(In fact, AMP consistently produced a small increase in the fluorescence of the ATP-pretreated sample, further illustrating that AMP was bound to ATP-BD, but did not compete with TNP-ATP.)	bind
17450	1	5729	7	NULL	NULL	NULL	NULL	AMP	Chemical		bind								ATP-BD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_3_2234_s_203	11053407	(In fact, AMP consistently produced a small increase in the fluorescence of the ATP-pretreated sample, further illustrating that AMP was bound to ATP-BD, but did not compete with TNP-ATP.)	bind
17451	2	5729	7	NULL	NULL	NULL	NULL	TNP	Chemical		bind								ATP-BD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_3_2234_s_203	11053407	(In fact, AMP consistently produced a small increase in the fluorescence of the ATP-pretreated sample, further illustrating that AMP was bound to ATP-BD, but did not compete with TNP-ATP.)	bind
17452	3	5729	7	NULL	NULL	NULL	NULL	statement 1	Process		does not compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_3_2234_s_203	11053407	(In fact, AMP consistently produced a small increase in the fluorescence of the ATP-pretreated sample, further illustrating that AMP was bound to ATP-BD, but did not compete with TNP-ATP.)	bind
18206	1	5730	6	10	NULL	0	NULL	anti-human Fc	NULL		stabilizes	NULL	significantly			Ntm-Fc	NULL	binding of 			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_22_9312_s_213	9801370	(In other studies, we found that cross-linking with the anti-human Fc significantly stabilized the binding of the Ntm-Fc; data not shown.)	bind
17455	1	5730	7	NULL	NULL	NULL	NULL	anti-human Fc	GP		stabilize		significantly			Ntm-Fc	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_22_9312_s_213	9801370	(In other studies, we found that cross-linking with the anti-human Fc significantly stabilized the binding of the Ntm-Fc; data not shown.)	bind
18207	1	5732	6	10	NULL	0	NULL	Ddi1	NULL		lacks	NULL					NULL		UbA domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1579_s_278	16478980	(In this scenario one possible explanation for the marked reduction [ca. 90% in the binding of Ufo1 to Ddi1 lacking its UbA domain may reflect a similar lack of accessibility to the Ddi1 core.)	bind
45756	2	5732	6	10	NULL	0	NULL	Ufo1	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1579_s_278	16478980	(In this scenario one possible explanation for the marked reduction [ca. 90% in the binding of Ufo1 to Ddi1 lacking its UbA domain may reflect a similar lack of accessibility to the Ddi1 core.)	bind
17456	2	5732	7	NULL	NULL	NULL	NULL	Ufo1	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1579_s_278	16478980	(In this scenario one possible explanation for the marked reduction [ca. 90% in the binding of Ufo1 to Ddi1 lacking its UbA domain may reflect a similar lack of accessibility to the Ddi1 core.)	bind
17457	1	5732	7	NULL	NULL	NULL	NULL	Ddi1	GP		lacks								UbA domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1579_s_278	16478980	(In this scenario one possible explanation for the marked reduction [ca. 90% in the binding of Ufo1 to Ddi1 lacking its UbA domain may reflect a similar lack of accessibility to the Ddi1 core.)	bind
18208	1	5733	6	NULL	NULL	0	NULL	RAG1	NULL		is limited to	NULL		importin alpha binding site		importin alpha1	NULL		98-amino acid fragment		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_22_16752_s_220	10748034	(In unpublished data described in Ref.  48, the importin alpha binding site of RAG1 was limited to the same 98-amino acid fragment of importin alpha1 that we identified (432-529).)	bind
17817	1	5733	7	NULL	NULL	NULL	NULL	RAG1	GP		is limited to			importin alpha binding site of		importin alpha1	GP		98-amino acid fragment		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_22_16752_s_220	10748034	(In unpublished data described in Ref.  48, the importin alpha binding site of RAG1 was limited to the same 98-amino acid fragment of importin alpha1 that we identified (432-529).)	bind
18210	1	5734	6	10	NULL	0	NULL	TC-[57Co]Cbl complex	NULL		bind	NULL				HMEC	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1528_1_43_s_106	11514097	(Inset) Analysis of TC-[57Co]Cbl complex binding to HMEC.	bind
17458	1	5734	7	NULL	NULL	NULL	NULL	TC-[57Co]Cbl complex 	Chemical		bind					HMEC	Cell				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1528_1_43_s_106	11514097	(Inset) Analysis of TC-[57Co]Cbl complex binding to HMEC.	bind
18211	1	5736	6	NULL	NULL	0	NULL	Streptokinase	NULL		bind	NULL				plasminogen	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_71_4_1903_s_169	12654807	(Interaction 3) Streptokinase binds plasminogen and GAS M protein binds fibrinogen.	bind
18212	2	5736	6	NULL	NULL	0	NULL	GAS M protein	NULL		bind	NULL				fibrinogen	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_71_4_1903_s_169	12654807	(Interaction 3) Streptokinase binds plasminogen and GAS M protein binds fibrinogen.	bind
17459	1	5736	7	NULL	NULL	NULL	NULL	Streptokinase	GP		binds					plasminogen	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_4_1903_s_169	12654807	(Interaction 3) Streptokinase binds plasminogen and GAS M protein binds fibrinogen.	bind
17460	2	5736	7	NULL	NULL	NULL	NULL	GAS M protein	GP		binds					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_71_4_1903_s_169	12654807	(Interaction 3) Streptokinase binds plasminogen and GAS M protein binds fibrinogen.	bind
18213	1	5739	6	NULL	NULL	0	NULL	Mei4 protein	NULL	recombinant	bind	NULL	specifically			spo6+	NULL			FLEX-D DNA fragment	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_2118_s_360	9528784	(iv) A recombinant Mei4 protein could bind specifically to the FLEX-D DNA fragment, a putative  cis element on  spo6+.	bind
53246	2	5739	6	10	NULL	0	NULL	FLEX-D DNA fragment	NULL		is a type of	NULL				putative cis element on spo6+	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_2118_s_360	9528784	(iv) A recombinant Mei4 protein could bind specifically to the FLEX-D DNA fragment, a putative  cis element on  spo6+.	bind
17461	1	5739	7	10	NULL	0	NULL	Mei4 protein	NULL	recombinant	bind	NULL	specifically			spo6	NULL			FLEX-D DNA fragment	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2118_s_360	9528784	(iv) A recombinant Mei4 protein could bind specifically to the FLEX-D DNA fragment, a putative  cis element on  spo6+.	bind
17462	2	5739	7	10	NULL	0	NULL	FLEX-D DNA fragment	NULL		is a type of	NULL				putative cis element on spo6+	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2118_s_360	9528784	(iv) A recombinant Mei4 protein could bind specifically to the FLEX-D DNA fragment, a putative  cis element on  spo6+.	bind
18214	1	5740	6	NULL	NULL	0	NULL	MyoD	NULL		bind	NULL				DNA	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_12	11940648	(iv) Addition of p204 overcame the inhibition by the Id proteins of the binding of MyoD and E47 to DNA in vitro.	bind
18215	2	5740	6	NULL	NULL	0	NULL	E47	NULL		bind	NULL				DNA	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_12	11940648	(iv) Addition of p204 overcame the inhibition by the Id proteins of the binding of MyoD and E47 to DNA in vitro.	bind
18216	3	5740	6	10	NULL	0	NULL	Id protein	NULL		inhibit	NULL				statement 1	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_12	11940648	(iv) Addition of p204 overcame the inhibition by the Id proteins of the binding of MyoD and E47 to DNA in vitro.	bind
18217	4	5740	6	10	NULL	0	NULL	Id protein	NULL		inhibit	NULL				statement 2	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_12	11940648	(iv) Addition of p204 overcame the inhibition by the Id proteins of the binding of MyoD and E47 to DNA in vitro.	bind
18308	5	5740	6	10	NULL	0	NULL	p204	NULL		overcome	NULL				statement 3	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_12	11940648	(iv) Addition of p204 overcame the inhibition by the Id proteins of the binding of MyoD and E47 to DNA in vitro.	bind
18309	6	5740	6	10	NULL	0	NULL	p204	NULL		overcome	NULL				statement 4	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_12	11940648	(iv) Addition of p204 overcame the inhibition by the Id proteins of the binding of MyoD and E47 to DNA in vitro.	bind
17463	1	5740	7	NULL	NULL	NULL	NULL	MyoD	GP		binds					DNA	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_12	11940648	(iv) Addition of p204 overcame the inhibition by the Id proteins of the binding of MyoD and E47 to DNA in vitro.	bind
17464	2	5740	7	NULL	NULL	NULL	NULL	E47	GP		binds					DNA	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_12	11940648	(iv) Addition of p204 overcame the inhibition by the Id proteins of the binding of MyoD and E47 to DNA in vitro.	bind
17465	3	5740	7	NULL	NULL	NULL	NULL	Id proteins	Gp		inhibits					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_12	11940648	(iv) Addition of p204 overcame the inhibition by the Id proteins of the binding of MyoD and E47 to DNA in vitro.	bind
17466	4	5740	7	NULL	NULL	NULL	NULL	Id proteins	GP		inhibits					statement 2	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_12	11940648	(iv) Addition of p204 overcame the inhibition by the Id proteins of the binding of MyoD and E47 to DNA in vitro.	bind
17467	5	5740	7	NULL	NULL	NULL	NULL	p204	GP	addition of	overcame					statement 3	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_12	11940648	(iv) Addition of p204 overcame the inhibition by the Id proteins of the binding of MyoD and E47 to DNA in vitro.	bind
17468	6	5740	7	NULL	NULL	NULL	NULL	p204	GP	addition of	overcame					statement 4	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_9_2893_s_12	11940648	(iv) Addition of p204 overcame the inhibition by the Id proteins of the binding of MyoD and E47 to DNA in vitro.	bind
18310	1	5741	6	NULL	NULL	0	NULL	Tim17	NULL		bind	NULL				mtHsp70	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_9_2205_s_69	9171336	(iv) As a further control to exclude a post-lysis binding of Tim17 or Tim23 to mtHsp70, the Tim proteins were imported into  ssc1-3 mitochondria, where they were correctly integrated into the inner membrane but did not bind to the mutant Hsp70 (Figure  2D, lane 6).	bind
18311	2	5741	6	NULL	NULL	0	NULL	Tim23	NULL		bind	NULL				mtHsp70	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_9_2205_s_69	9171336	(iv) As a further control to exclude a post-lysis binding of Tim17 or Tim23 to mtHsp70, the Tim proteins were imported into  ssc1-3 mitochondria, where they were correctly integrated into the inner membrane but did not bind to the mutant Hsp70 (Figure  2D, lane 6).	bind
18312	3	5741	6	NULL	NULL	0	NULL	Tim proteins	NULL		imported into	NULL				ssc1-3 mitochondria	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_9_2205_s_69	9171336	(iv) As a further control to exclude a post-lysis binding of Tim17 or Tim23 to mtHsp70, the Tim proteins were imported into  ssc1-3 mitochondria, where they were correctly integrated into the inner membrane but did not bind to the mutant Hsp70 (Figure  2D, lane 6).	bind
18313	4	5741	6	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_9_2205_s_69	9171336	(iv) As a further control to exclude a post-lysis binding of Tim17 or Tim23 to mtHsp70, the Tim proteins were imported into  ssc1-3 mitochondria, where they were correctly integrated into the inner membrane but did not bind to the mutant Hsp70 (Figure  2D, lane 6).	bind
18314	5	5741	6	NULL	NULL	0	NULL	Tim proteins	NULL		does not bind	NULL				Hsp70	NULL	mutant			NULL		0	NULL	NULL	NULL	gw60_embo_16_9_2205_s_69	9171336	(iv) As a further control to exclude a post-lysis binding of Tim17 or Tim23 to mtHsp70, the Tim proteins were imported into  ssc1-3 mitochondria, where they were correctly integrated into the inner membrane but did not bind to the mutant Hsp70 (Figure  2D, lane 6).	bind
45759	6	5741	6	10	NULL	0	NULL	statement 3	NULL		is integrated into	NULL				inner membrane	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_9_2205_s_69	9171336	(iv) As a further control to exclude a post-lysis binding of Tim17 or Tim23 to mtHsp70, the Tim proteins were imported into  ssc1-3 mitochondria, where they were correctly integrated into the inner membrane but did not bind to the mutant Hsp70 (Figure  2D, lane 6).	bind
17469	3	5741	7	NULL	NULL	NULL	NULL	Tim proteins	GP		imported to					 ssc1-3 mitochondria	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_9_2205_s_69	9171336	(iv) As a further control to exclude a post-lysis binding of Tim17 or Tim23 to mtHsp70, the Tim proteins were imported into  ssc1-3 mitochondria, where they were correctly integrated into the inner membrane but did not bind to the mutant Hsp70 (Figure  2D, lane 6).	bind
17470	4	5741	7	NULL	NULL	NULL	NULL	statement 1	Process		 integrated to		correctly			inner membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_9_2205_s_69	9171336	(iv) As a further control to exclude a post-lysis binding of Tim17 or Tim23 to mtHsp70, the Tim proteins were imported into  ssc1-3 mitochondria, where they were correctly integrated into the inner membrane but did not bind to the mutant Hsp70 (Figure  2D, lane 6).	bind
17471	5	5741	7	NULL	NULL	NULL	NULL	Tim proteins	GP		does not bind					Hsp70	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_embo_16_9_2205_s_69	9171336	(iv) As a further control to exclude a post-lysis binding of Tim17 or Tim23 to mtHsp70, the Tim proteins were imported into  ssc1-3 mitochondria, where they were correctly integrated into the inner membrane but did not bind to the mutant Hsp70 (Figure  2D, lane 6).	bind
45853	1	5741	7	NULL	NULL	NULL	NULL	Tim17	GP		bind					mtHsp70	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_9_2205_s_69	9171336	(iv) As a further control to exclude a post-lysis binding of Tim17 or Tim23 to mtHsp70, the Tim proteins were imported into  ssc1-3 mitochondria, where they were correctly integrated into the inner membrane but did not bind to the mutant Hsp70 (Figure  2D, lane 6).	bind
45854	2	5741	7	NULL	NULL	NULL	NULL	Tim23	GP		bind					mtHsp70	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_9_2205_s_69	9171336	(iv) As a further control to exclude a post-lysis binding of Tim17 or Tim23 to mtHsp70, the Tim proteins were imported into  ssc1-3 mitochondria, where they were correctly integrated into the inner membrane but did not bind to the mutant Hsp70 (Figure  2D, lane 6).	bind
45855	6	5741	7	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_9_2205_s_69	9171336	(iv) As a further control to exclude a post-lysis binding of Tim17 or Tim23 to mtHsp70, the Tim proteins were imported into  ssc1-3 mitochondria, where they were correctly integrated into the inner membrane but did not bind to the mutant Hsp70 (Figure  2D, lane 6).	bind
18315	1	5742	6	NULL	NULL	0	NULL	myosin	NULL		bind	NULL	strongly			actin	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_19_6873_s_23	15863618	(IV) ATP hydrolysis remains reversible until myosin binds strongly  to actin ( ).	bind
18316	2	5742	6	NULL	NULL	0	NULL	ATP	NULL	hydrolysis of	is dependent on	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_19_6873_s_23	15863618	(IV) ATP hydrolysis remains reversible until myosin binds strongly  to actin ( ).	bind
17472	1	5742	7	NULL	NULL	NULL	NULL	 myosin 	GP		binds		strongly			actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_19_6873_s_23	15863618	(IV) ATP hydrolysis remains reversible until myosin binds strongly  to actin ( ).	bind
17473	2	5742	7	NULL	NULL	NULL	NULL	ATP	Chemical	hydrolysis of	remains					reversible	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_19_6873_s_23	15863618	(IV) ATP hydrolysis remains reversible until myosin binds strongly  to actin ( ).	bind
17474	3	5742	7	NULL	NULL	NULL	NULL	statement 2	Process		happens until					statement 1	Process	occurance of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_19_6873_s_23	15863618	(IV) ATP hydrolysis remains reversible until myosin binds strongly  to actin ( ).	bind
18317	1	5743	6	NULL	NULL	0	NULL	Msb3	NULL		bind	NULL				Rho GTPase	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_19_8567_s_132	16166638	(iv) Binding of Msb3 and Msb4 to Rho GTPases.	bind
18318	2	5743	6	NULL	NULL	0	NULL	Msb4	NULL		bind	NULL				Rho GTPase	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_19_8567_s_132	16166638	(iv) Binding of Msb3 and Msb4 to Rho GTPases.	bind
17475	1	5743	7	NULL	NULL	NULL	NULL	Msb3	GP		bind					Rho GTPases	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8567_s_132	16166638	(iv) Binding of Msb3 and Msb4 to Rho GTPases.	bind
17476	2	5743	7	NULL	NULL	NULL	NULL	Msb4	GP		bind					Rho GTPases	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_19_8567_s_132	16166638	(iv) Binding of Msb3 and Msb4 to Rho GTPases.	bind
18463	1	5744	6	NULL	NULL	0	NULL	plasminogen	NULL	cell surface	activates into	NULL				plasmin	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_24_7279_s_92	9405357	(iv) Binding of uPA to uPAR/CD87 activates cell surface plasminogen to plasmin which also might cleave uPAR/CD87 in the same region (Hoyer-Hansen  et al., 1992  ; Ploug and Ellis, 1994  ).	bind
18464	2	5744	6	NULL	NULL	0	NULL	uPA	NULL		bind	NULL				uPAR/CD87	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_24_7279_s_92	9405357	(iv) Binding of uPA to uPAR/CD87 activates cell surface plasminogen to plasmin which also might cleave uPAR/CD87 in the same region (Hoyer-Hansen  et al., 1992  ; Ploug and Ellis, 1994  ).	bind
18465	3	5744	6	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_24_7279_s_92	9405357	(iv) Binding of uPA to uPAR/CD87 activates cell surface plasminogen to plasmin which also might cleave uPAR/CD87 in the same region (Hoyer-Hansen  et al., 1992  ; Ploug and Ellis, 1994  ).	bind
18466	4	5744	6	NULL	NULL	0	NULL	statement 1	NULL		cleave	NULL	may			uPAR/CD87 	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_24_7279_s_92	9405357	(iv) Binding of uPA to uPAR/CD87 activates cell surface plasminogen to plasmin which also might cleave uPAR/CD87 in the same region (Hoyer-Hansen  et al., 1992  ; Ploug and Ellis, 1994  ).	bind
17477	1	5744	7	NULL	NULL	NULL	NULL	uPA	GP		bind					uPAR/CD87	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_24_7279_s_92	9405357	(iv) Binding of uPA to uPAR/CD87 activates cell surface plasminogen to plasmin which also might cleave uPAR/CD87 in the same region (Hoyer-Hansen  et al., 1992  ; Ploug and Ellis, 1994  ).	bind
17478	2	5744	7	NULL	NULL	NULL	NULL	plasminogen	GP	cell surface	converts to					plasmin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_24_7279_s_92	9405357	(iv) Binding of uPA to uPAR/CD87 activates cell surface plasminogen to plasmin which also might cleave uPAR/CD87 in the same region (Hoyer-Hansen  et al., 1992  ; Ploug and Ellis, 1994  ).	bind
17479	3	5744	7	NULL	NULL	NULL	NULL	statement 1	Process		activates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_24_7279_s_92	9405357	(iv) Binding of uPA to uPAR/CD87 activates cell surface plasminogen to plasmin which also might cleave uPAR/CD87 in the same region (Hoyer-Hansen  et al., 1992  ; Ploug and Ellis, 1994  ).	bind
17480	4	5744	7	NULL	NULL	NULL	NULL	plasmin	GP		cleave					uPAR/CD87	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_24_7279_s_92	9405357	(iv) Binding of uPA to uPAR/CD87 activates cell surface plasminogen to plasmin which also might cleave uPAR/CD87 in the same region (Hoyer-Hansen  et al., 1992  ; Ploug and Ellis, 1994  ).	bind
18319	1	5745	6	NULL	NULL	0	NULL	P22	NULL		bind	NULL				LDC	NULL	S.ruminantium			NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-biol-chem_281_7_16354653_s_11	16354653	(iv) Both P22 and mouse AZ bind to S. ruminantium  LDC but not to the LDC mutated in its binding site for P22 and AZ.	bind
18320	2	5745	6	NULL	NULL	0	NULL	AZ	NULL	mouse	bind	NULL				LDC	NULL	S.ruminantium			NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-biol-chem_281_7_16354653_s_11	16354653	(iv) Both P22 and mouse AZ bind to S. ruminantium  LDC but not to the LDC mutated in its binding site for P22 and AZ.	bind
18321	3	5745	6	NULL	NULL	0	NULL	P22	NULL		does not bind	NULL				LDC	NULL	mutant S.ruminantium	p22 binding site		NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-biol-chem_281_7_16354653_s_11	16354653	(iv) Both P22 and mouse AZ bind to S. ruminantium  LDC but not to the LDC mutated in its binding site for P22 and AZ.	bind
18322	4	5745	6	NULL	NULL	0	NULL	AZ	NULL	mouse	does not bind	NULL				LDC	NULL	mutant S.ruminantium	AZ binding site		NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-biol-chem_281_7_16354653_s_11	16354653	(iv) Both P22 and mouse AZ bind to S. ruminantium  LDC but not to the LDC mutated in its binding site for P22 and AZ.	bind
17482	1	5745	7	NULL	NULL	NULL	NULL	P22	GP		bind					LDC	GP	S. ruminantium 			NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-biol-chem_281_7_16354653_s_11	16354653	(iv) Both P22 and mouse AZ bind to S. ruminantium  LDC but not to the LDC mutated in its binding site for P22 and AZ.	bind
17483	2	5745	7	NULL	NULL	NULL	NULL	AZ	GP	mouse	bind					LDC	GP	S. ruminantium 			NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-biol-chem_281_7_16354653_s_11	16354653	(iv) Both P22 and mouse AZ bind to S. ruminantium  LDC but not to the LDC mutated in its binding site for P22 and AZ.	bind
17484	3	5745	7	NULL	NULL	NULL	NULL	P22	GP		does not bind					LDC	GP	S. ruminantium mutated at	P22 binding site		NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-biol-chem_281_7_16354653_s_11	16354653	(iv) Both P22 and mouse AZ bind to S. ruminantium  LDC but not to the LDC mutated in its binding site for P22 and AZ.	bind
17485	4	5745	7	NULL	NULL	NULL	NULL	AZ	GP		does not bind					LDC	GP	S. ruminantium mutated at	AZ binding site		NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-biol-chem_281_7_16354653_s_11	16354653	(iv) Both P22 and mouse AZ bind to S. ruminantium  LDC but not to the LDC mutated in its binding site for P22 and AZ.	bind
18323	1	5746	6	NULL	NULL	0	NULL	Ca+2	NULL		bind	NULL				EGF-1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_28_17467_s_180	9211891	(iv) Ca2+ binding to EGF-1 does not affect the VIIa interaction with TF residue Gln110.	bind
18324	2	5746	6	NULL	NULL	0	NULL	VIIa	NULL		interacts with	NULL				TF residue Gln110	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_28_17467_s_180	9211891	(iv) Ca2+ binding to EGF-1 does not affect the VIIa interaction with TF residue Gln110.	bind
18325	3	5746	6	NULL	NULL	0	NULL	statement 1	NULL		does not affect	NULL	                                                                                                                            			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_28_17467_s_180	9211891	(iv) Ca2+ binding to EGF-1 does not affect the VIIa interaction with TF residue Gln110.	bind
17486	1	5746	7	NULL	NULL	NULL	NULL	Ca2+	Chemical		binds to					EGF-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17467_s_180	9211891	(iv) Ca2+ binding to EGF-1 does not affect the VIIa interaction with TF residue Gln110.	bind
17487	2	5746	7	NULL	NULL	NULL	NULL	 VIIa	GP		interacts with					TF residue Gln110	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17467_s_180	9211891	(iv) Ca2+ binding to EGF-1 does not affect the VIIa interaction with TF residue Gln110.	bind
17488	3	5746	7	NULL	NULL	NULL	NULL	statement 1	Process		does not affect					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17467_s_180	9211891	(iv) Ca2+ binding to EGF-1 does not affect the VIIa interaction with TF residue Gln110.	bind
18326	1	5747	6	10	NULL	0	NULL	fibronectin	NULL		bind	NULL				fibrinogen	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_j-thromb-haemost_3_8_16102057_s_12	16102057	(iv) Enhanced interactions with the extracellular matrix by  binding of fibronectin to fibrin(ogen).	bind
17532	1	5747	7	NULL	NULL	NULL	NULL	fibronectin	GP		binds					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_j-thromb-haemost_3_8_16102057_s_12	16102057	(iv) Enhanced interactions with the extracellular matrix by  binding of fibronectin to fibrin(ogen).	bind
18327	1	5748	6	NULL	NULL	0	NULL	fatty acid	NULL		bind	NULL				FadL	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw70_microbiolmolbiolr_67_3_454_s_140	12966144	(iv) Fatty acid binding to FadL has been demonstrated both in vivo and in vitro ( ).	bind
18328	2	5748	6	NULL	NULL	0	NULL	fatty acid	NULL		bind	NULL				FadL	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw70_microbiolmolbiolr_67_3_454_s_140	12966144	(iv) Fatty acid binding to FadL has been demonstrated both in vivo and in vitro ( ).	bind
17534	1	5748	7	NULL	NULL	NULL	NULL	Fatty acid	Chemical		bind					FadL	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_67_3_454_s_140	12966144	(iv) Fatty acid binding to FadL has been demonstrated both in vivo and in vitro ( ).	bind
17535	2	5748	7	NULL	NULL	NULL	NULL	Fatty acid	Chemical		bind					FadL	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_67_3_454_s_140	12966144	(iv) Fatty acid binding to FadL has been demonstrated both in vivo and in vitro ( ).	bind
18329	1	5751	6	NULL	NULL	0	NULL	GadX	NULL		bind	NULL	directly			gadW	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_23_6852_s_221	14617649	(iv) GadW is also acid induced by an unknown mechanism when it is not repressed by GadX. (v) GadX directly binds to the  gadW promoter region.	bind
18384	2	5751	6	NULL	NULL	0	NULL	GadW	NULL		is induced by	NULL				acid	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_23_6852_s_221	14617649	(iv) GadW is also acid induced by an unknown mechanism when it is not repressed by GadX. (v) GadX directly binds to the  gadW promoter region.	bind
18411	3	5751	6	NULL	NULL	0	NULL	GadX	NULL		represses	NULL				GadW	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_23_6852_s_221	14617649	(iv) GadW is also acid induced by an unknown mechanism when it is not repressed by GadX. (v) GadX directly binds to the  gadW promoter region.	bind
24585	4	5751	6	NULL	NULL	0	NULL	statement 2	NULL		occurs in absence of	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_23_6852_s_221	14617649	(iv) GadW is also acid induced by an unknown mechanism when it is not repressed by GadX. (v) GadX directly binds to the  gadW promoter region.	bind
17540	1	5751	7	NULL	NULL	NULL	NULL	acid	Chemical		induce					GadW	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_23_6852_s_221	14617649	(iv) GadW is also acid induced by an unknown mechanism when it is not repressed by GadX. (v) GadX directly binds to the  gadW promoter region.	bind
17541	2	5751	7	NULL	NULL	NULL	NULL	GadX	GP		repress					GadW	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_23_6852_s_221	14617649	(iv) GadW is also acid induced by an unknown mechanism when it is not repressed by GadX. (v) GadX directly binds to the  gadW promoter region.	bind
17542	3	5751	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs in the absence of					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_23_6852_s_221	14617649	(iv) GadW is also acid induced by an unknown mechanism when it is not repressed by GadX. (v) GadX directly binds to the  gadW promoter region.	bind
17543	4	5751	7	NULL	NULL	NULL	NULL	GadX	GP		binds		directly			gadW	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_23_6852_s_221	14617649	(iv) GadW is also acid induced by an unknown mechanism when it is not repressed by GadX. (v) GadX directly binds to the  gadW promoter region.	bind
18412	1	5752	6	NULL	NULL	0	NULL	leucine	NULL		bind	NULL				Sa-Lrp protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_13_3661_s_264	10850980	(iv) Most significantly, L-leucine specifically protects the archaeal Sa-Lrp binding capacity against irreversible heat inactivation; this effect likely reflects a physiologically significant interaction of leucine with the Sa-Lrp protein and suggests that leucine might function as the main effector of a hypothetical regulon.	bind
18413	2	5752	6	NULL	NULL	0	NULL	L-leucine	NULL		protects	NULL	specifically			Sa-Lrp	NULL	binding capacity of 			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_13_3661_s_264	10850980	(iv) Most significantly, L-leucine specifically protects the archaeal Sa-Lrp binding capacity against irreversible heat inactivation; this effect likely reflects a physiologically significant interaction of leucine with the Sa-Lrp protein and suggests that leucine might function as the main effector of a hypothetical regulon.	bind
18414	3	5752	6	10	NULL	0	NULL	statement 2	NULL		occurs against	NULL				heat inactivation	NULL	irreversible			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_13_3661_s_264	10850980	(iv) Most significantly, L-leucine specifically protects the archaeal Sa-Lrp binding capacity against irreversible heat inactivation; this effect likely reflects a physiologically significant interaction of leucine with the Sa-Lrp protein and suggests that leucine might function as the main effector of a hypothetical regulon.	bind
17544	1	5752	7	NULL	NULL	NULL	NULL	leucine	AminoAcid		binds					Sa-Lrp protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_13_3661_s_264	10850980	(iv) Most significantly, L-leucine specifically protects the archaeal Sa-Lrp binding capacity against irreversible heat inactivation; this effect likely reflects a physiologically significant interaction of leucine with the Sa-Lrp protein and suggests that leucine might function as the main effector of a hypothetical regulon.	bind
17545	2	5752	7	NULL	NULL	NULL	NULL	L-leucine	AminoAcid		protects		specifically			Sa-Lrp	GP	binding of archeal			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_13_3661_s_264	10850980	(iv) Most significantly, L-leucine specifically protects the archaeal Sa-Lrp binding capacity against irreversible heat inactivation; this effect likely reflects a physiologically significant interaction of leucine with the Sa-Lrp protein and suggests that leucine might function as the main effector of a hypothetical regulon.	bind
17546	3	5752	7	NULL	NULL	NULL	NULL	statement 2	Process		protects against					 heat inactivation	Process	irreversible			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_13_3661_s_264	10850980	(iv) Most significantly, L-leucine specifically protects the archaeal Sa-Lrp binding capacity against irreversible heat inactivation; this effect likely reflects a physiologically significant interaction of leucine with the Sa-Lrp protein and suggests that leucine might function as the main effector of a hypothetical regulon.	bind
17547	4	5752	7	NULL	NULL	NULL	NULL	leucine	AminoAcid		function as		might			regulon	GP	main effector of;;hypothetical 			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_13_3661_s_264	10850980	(iv) Most significantly, L-leucine specifically protects the archaeal Sa-Lrp binding capacity against irreversible heat inactivation; this effect likely reflects a physiologically significant interaction of leucine with the Sa-Lrp protein and suggests that leucine might function as the main effector of a hypothetical regulon.	bind
18415	1	5753	6	NULL	NULL	0	NULL	GSK-3beta	NULL		bind	NULL				AKAP220	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_36955_s_237	12147701	(iv) PP1 did not inhibit the binding of GSK-3beta to AKAP220.	bind
18416	2	5753	6	NULL	NULL	0	NULL	PP1	NULL		does not inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_36955_s_237	12147701	(iv) PP1 did not inhibit the binding of GSK-3beta to AKAP220.	bind
17548	1	5753	7	NULL	NULL	NULL	NULL	GSK-3beta	GP		binds to					AKAP220	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_40_36955_s_237	12147701	(iv) PP1 did not inhibit the binding of GSK-3beta to AKAP220.	bind
17549	2	5753	7	NULL	NULL	NULL	NULL	PP1	GP		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_40_36955_s_237	12147701	(iv) PP1 did not inhibit the binding of GSK-3beta to AKAP220.	bind
18417	1	5754	6	10	NULL	0	NULL	TFIID protein	NULL	purified;;Yeast	bind	NULL					NULL			GATA sequence	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_23_17611_s_131	10748041	(iv) Purified yeast TFIID protein binds to a GATA sequence albeit less well than to a TATA sequence (Fig. 2 B of Ref.  27).	bind
18418	2	5754	6	10	NULL	0	NULL	TFIID protein	NULL	purified;;Yeast	bind	NULL					NULL			TATA sequence	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_23_17611_s_131	10748041	(iv) Purified yeast TFIID protein binds to a GATA sequence albeit less well than to a TATA sequence (Fig. 2 B of Ref.  27).	bind
18419	3	5754	6	NULL	NULL	0	NULL	statement 1	NULL		is less than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_23_17611_s_131	10748041	(iv) Purified yeast TFIID protein binds to a GATA sequence albeit less well than to a TATA sequence (Fig. 2 B of Ref.  27).	bind
17550	1	5754	7	NULL	NULL	NULL	NULL	TFIID protein	GP	purified;;yeast	binds									GATA sequence	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_23_17611_s_131	10748041	(iv) Purified yeast TFIID protein binds to a GATA sequence albeit less well than to a TATA sequence (Fig. 2 B of Ref.  27).	bind
17551	2	5754	7	NULL	NULL	NULL	NULL	TFIID protein	GP	purified;;yeast	binds									TATA sequence	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_23_17611_s_131	10748041	(iv) Purified yeast TFIID protein binds to a GATA sequence albeit less well than to a TATA sequence (Fig. 2 B of Ref.  27).	bind
17552	3	5754	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs less well than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_23_17611_s_131	10748041	(iv) Purified yeast TFIID protein binds to a GATA sequence albeit less well than to a TATA sequence (Fig. 2 B of Ref.  27).	bind
18429	1	5755	6	NULL	NULL	0	NULL	SmF	NULL		bind	NULL				SmG	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1956_s_246	9528767	(iv) SmE mutants unaffected in SmF and SmG binding (class IV).	bind
18430	2	5755	6	NULL	NULL	0	NULL	statement 1	NULL		has no effect on	NULL				SmE	NULL	mutant			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1956_s_246	9528767	(iv) SmE mutants unaffected in SmF and SmG binding (class IV).	bind
17553	1	5755	7	NULL	NULL	NULL	NULL	SmF	GP		bind					SmG	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_1956_s_246	9528767	(iv) SmE mutants unaffected in SmF and SmG binding (class IV).	bind
17554	2	5755	7	NULL	NULL	NULL	NULL	statement 1	Process		does not affect					SmE	GP	mutants			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_1956_s_246	9528767	(iv) SmE mutants unaffected in SmF and SmG binding (class IV).	bind
18431	1	5756	6	10	NULL	0	NULL	CD14	NULL	radiolabeled	bind	NULL				LPS	NULL				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_1_61_s_9	12496149	(iv) SP-C enhances the binding of radiolabeled CD14 to LPS-coated wells.	bind
18432	2	5756	6	NULL	NULL	0	NULL	SP-C	NULL		enhances	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_71_1_61_s_9	12496149	(iv) SP-C enhances the binding of radiolabeled CD14 to LPS-coated wells.	bind
17555	1	5756	7	NULL	NULL	NULL	NULL	CD14	Cell	radiolabeled	bind					LPS	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_1_61_s_9	12496149	(iv) SP-C enhances the binding of radiolabeled CD14 to LPS-coated wells.	bind
17556	2	5756	7	NULL	NULL	NULL	NULL	SP-C	GP		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_1_61_s_9	12496149	(iv) SP-C enhances the binding of radiolabeled CD14 to LPS-coated wells.	bind
18433	1	5757	6	NULL	NULL	0	NULL	SR-A	NULL		bind	NULL	directly			bacteria	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_4_1953_s_162	10722588	(iv) SR-A binds bacteria directly.	bind
17557	1	5757	7	NULL	NULL	NULL	NULL	SR-A	GP		binds		directly			bacteria	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_4_1953_s_162	10722588	(iv) SR-A binds bacteria directly.	bind
18434	1	5758	6	NULL	NULL	0	NULL	HKa	NULL		bind	NULL				urokinase receptor	NULL				NULL	vascular cell surface	0	NULL	NULL	NULL	gw60_jbiolchem_277_36_32677_s_182	12082110	(iv) The binding of HKa to the urokinase receptor ( 66) on vascular cell surfaces may approximate kallikrein and prourokinase and thereby potentiate plasmin formation.	bind
18435	2	5758	6	10	NULL	0	NULL	statement 1	NULL		potentiate	NULL				plasmin	NULL	formation of			NULL	vascular cell surface	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_36_32677_s_182	12082110	(iv) The binding of HKa to the urokinase receptor ( 66) on vascular cell surfaces may approximate kallikrein and prourokinase and thereby potentiate plasmin formation.	bind
18436	3	5758	6	NULL	NULL	0	NULL	statement 1	NULL		approximate	NULL	may			kallikrein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_36_32677_s_182	12082110	(iv) The binding of HKa to the urokinase receptor ( 66) on vascular cell surfaces may approximate kallikrein and prourokinase and thereby potentiate plasmin formation.	bind
18437	4	5758	6	NULL	NULL	0	NULL	statement 1	NULL		approximate	NULL	may			prourokinase	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_36_32677_s_182	12082110	(iv) The binding of HKa to the urokinase receptor ( 66) on vascular cell surfaces may approximate kallikrein and prourokinase and thereby potentiate plasmin formation.	bind
17558	1	5758	7	NULL	NULL	NULL	NULL	HKa	GP		bind					urokinase receptor	GP				NULL	vascular cell surface	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_36_32677_s_182	12082110	(iv) The binding of HKa to the urokinase receptor ( 66) on vascular cell surfaces may approximate kallikrein and prourokinase and thereby potentiate plasmin formation.	bind
17559	2	5758	7	NULL	NULL	NULL	NULL	statement 1	Process		approximate					kallikrein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_36_32677_s_182	12082110	(iv) The binding of HKa to the urokinase receptor ( 66) on vascular cell surfaces may approximate kallikrein and prourokinase and thereby potentiate plasmin formation.	bind
17560	3	5758	7	NULL	NULL	NULL	NULL	statement 1	Process		approximate					prourokinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_36_32677_s_182	12082110	(iv) The binding of HKa to the urokinase receptor ( 66) on vascular cell surfaces may approximate kallikrein and prourokinase and thereby potentiate plasmin formation.	bind
17561	4	5758	7	NULL	NULL	NULL	NULL	statement 1	Process		potentiate					plasmin	GP	formation of			NULL	vascular cell surface	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_36_32677_s_182	12082110	(iv) The binding of HKa to the urokinase receptor ( 66) on vascular cell surfaces may approximate kallikrein and prourokinase and thereby potentiate plasmin formation.	bind
18438	1	5759	6	NULL	NULL	0	NULL	IgI-MBP	NULL		bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_244	9092558	(iv) The binding of IgI-MBP and IgII-MBP to heparin, and of IgI-MBP to IgII-MBP, indicates that these protein constructs were folded in an active conformation.	bind
18439	2	5759	6	NULL	NULL	0	NULL	IgII-MBP	NULL		bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_244	9092558	(iv) The binding of IgI-MBP and IgII-MBP to heparin, and of IgI-MBP to IgII-MBP, indicates that these protein constructs were folded in an active conformation.	bind
18440	3	5759	6	NULL	NULL	0	NULL	IgI-MBP	NULL		bind	NULL				IgII-MBP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_244	9092558	(iv) The binding of IgI-MBP and IgII-MBP to heparin, and of IgI-MBP to IgII-MBP, indicates that these protein constructs were folded in an active conformation.	bind
24583	4	5759	6	NULL	NULL	0	NULL	statement 1	NULL		indicate	NULL				IgI-MBP	NULL	active conformation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_244	9092558	(iv) The binding of IgI-MBP and IgII-MBP to heparin, and of IgI-MBP to IgII-MBP, indicates that these protein constructs were folded in an active conformation.	bind
24584	5	5759	6	NULL	NULL	0	NULL	statement 2	NULL		indicate	NULL				IgI-MBP	NULL	active conformation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_244	9092558	(iv) The binding of IgI-MBP and IgII-MBP to heparin, and of IgI-MBP to IgII-MBP, indicates that these protein constructs were folded in an active conformation.	bind
17563	1	5759	7	NULL	NULL	NULL	NULL	IgI-MBP	GP		bind					heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_244	9092558	(iv) The binding of IgI-MBP and IgII-MBP to heparin, and of IgI-MBP to IgII-MBP, indicates that these protein constructs were folded in an active conformation.	bind
17564	2	5759	7	NULL	NULL	NULL	NULL	IgII-MBP	GP		bind					heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_244	9092558	(iv) The binding of IgI-MBP and IgII-MBP to heparin, and of IgI-MBP to IgII-MBP, indicates that these protein constructs were folded in an active conformation.	bind
17565	3	5759	7	NULL	NULL	NULL	NULL	IgI-MBP	GP		bind					IgII-MBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_244	9092558	(iv) The binding of IgI-MBP and IgII-MBP to heparin, and of IgI-MBP to IgII-MBP, indicates that these protein constructs were folded in an active conformation.	bind
17566	4	5759	7	NULL	NULL	NULL	NULL	statement 1	Process		indicate					IgI-MBP	GP	active conformation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_244	9092558	(iv) The binding of IgI-MBP and IgII-MBP to heparin, and of IgI-MBP to IgII-MBP, indicates that these protein constructs were folded in an active conformation.	bind
17567	5	5759	7	NULL	NULL	NULL	NULL	statement 2	Process		indicate					IgII-MBP	GP	active conformation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_15_10125_s_244	9092558	(iv) The binding of IgI-MBP and IgII-MBP to heparin, and of IgI-MBP to IgII-MBP, indicates that these protein constructs were folded in an active conformation.	bind
24580	1	5760	6	10	NULL	0	NULL	HMR-E silencer	NULL		is a type of	NULL			E element		NULL			Rap1 binding site	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_375	15899856	(iv) The E element of the  HMR-E silencer is a binding site for Rap1 ( ), so if a defect in the binding of Rap1 to Sir4 was the cause of the phenotypes of the  sir4 coiled-coil mutants, than we would predict that the silencing defects of these mutants in a  hmrdeltaE strain would be no more severe than  hmrdeltaE in a  SIR4 strain.	bind
24581	2	5760	6	NULL	NULL	0	NULL	Rap1	NULL		bind	NULL				Sir4	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_375	15899856	(iv) The E element of the  HMR-E silencer is a binding site for Rap1 ( ), so if a defect in the binding of Rap1 to Sir4 was the cause of the phenotypes of the  sir4 coiled-coil mutants, than we would predict that the silencing defects of these mutants in a  hmrdeltaE strain would be no more severe than  hmrdeltaE in a  SIR4 strain.	bind
24582	3	5760	6	NULL	NULL	0	NULL	statement 2	NULL	defect in	cause	NULL				sir4 phenotypes	NULL	coiled coil mutant			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_375	15899856	(iv) The E element of the  HMR-E silencer is a binding site for Rap1 ( ), so if a defect in the binding of Rap1 to Sir4 was the cause of the phenotypes of the  sir4 coiled-coil mutants, than we would predict that the silencing defects of these mutants in a  hmrdeltaE strain would be no more severe than  hmrdeltaE in a  SIR4 strain.	bind
17568	1	5760	7	NULL	NULL	NULL	NULL	HMR-E silencer	GP		is a type of				 E element  					Rap1binding site	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_375	15899856	(iv) The E element of the  HMR-E silencer is a binding site for Rap1 ( ), so if a defect in the binding of Rap1 to Sir4 was the cause of the phenotypes of the  sir4 coiled-coil mutants, than we would predict that the silencing defects of these mutants in a  hmrdeltaE strain would be no more severe than  hmrdeltaE in a  SIR4 strain.	bind
17569	2	5760	7	NULL	NULL	NULL	NULL	Rap1	GP		bind					Sir4	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_375	15899856	(iv) The E element of the  HMR-E silencer is a binding site for Rap1 ( ), so if a defect in the binding of Rap1 to Sir4 was the cause of the phenotypes of the  sir4 coiled-coil mutants, than we would predict that the silencing defects of these mutants in a  hmrdeltaE strain would be no more severe than  hmrdeltaE in a  SIR4 strain.	bind
17656	3	5760	7	NULL	NULL	NULL	NULL	statement 2	Process	defect in	cause					sir4 phenotypes	Process	coiled-coil mutant 			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4514_s_375	15899856	(iv) The E element of the  HMR-E silencer is a binding site for Rap1 ( ), so if a defect in the binding of Rap1 to Sir4 was the cause of the phenotypes of the  sir4 coiled-coil mutants, than we would predict that the silencing defects of these mutants in a  hmrdeltaE strain would be no more severe than  hmrdeltaE in a  SIR4 strain.	bind
18442	1	5762	6	NULL	NULL	0	NULL	tRNA	NULL	uncharged 	bind	NULL				Gcn2	NULL		HisRS domain		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_12_8422_s_355	10567567	(iv) Upon amino acid starvation, uncharged tRNA binds to the HisRS domain of Gcn2 and induces a conformational change that results in the release of Hsp90.	bind
18443	2	5762	6	10	NULL	0	NULL	statement 1	NULL		occurs upon	NULL				amino acid 	NULL	starvation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8422_s_355	10567567	(iv) Upon amino acid starvation, uncharged tRNA binds to the HisRS domain of Gcn2 and induces a conformational change that results in the release of Hsp90.	bind
18444	3	5762	6	10	NULL	0	NULL	statement 1	NULL		induces a 	NULL				conformational change	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8422_s_355	10567567	(iv) Upon amino acid starvation, uncharged tRNA binds to the HisRS domain of Gcn2 and induces a conformational change that results in the release of Hsp90.	bind
45760	4	5762	6	10	NULL	0	NULL	statement 3	NULL		results in	NULL				Hsp90	NULL	release of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_12_8422_s_355	10567567	(iv) Upon amino acid starvation, uncharged tRNA binds to the HisRS domain of Gcn2 and induces a conformational change that results in the release of Hsp90.	bind
17575	1	5762	7	NULL	NULL	NULL	NULL	tRNA	NucleicAcid	uncharged	binds to					Gcn2	GP		HisRS domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8422_s_355	10567567	(iv) Upon amino acid starvation, uncharged tRNA binds to the HisRS domain of Gcn2 and induces a conformational change that results in the release of Hsp90.	bind
17576	2	5762	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs upon					aminoacid	AminoAcid	starvation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8422_s_355	10567567	(iv) Upon amino acid starvation, uncharged tRNA binds to the HisRS domain of Gcn2 and induces a conformational change that results in the release of Hsp90.	bind
17577	4	5762	7	NULL	NULL	NULL	NULL	statement 3	Process		results in					Hsp90	GP	release of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8422_s_355	10567567	(iv) Upon amino acid starvation, uncharged tRNA binds to the HisRS domain of Gcn2 and induces a conformational change that results in the release of Hsp90.	bind
17578	3	5762	7	NULL	NULL	NULL	NULL	statement 1	Process		induce					conformational change 	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8422_s_355	10567567	(iv) Upon amino acid starvation, uncharged tRNA binds to the HisRS domain of Gcn2 and induces a conformational change that results in the release of Hsp90.	bind
18445	1	5763	6	NULL	NULL	0	NULL	heparin	NULL		bind	NULL				VN	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_53_37611_s_30	10608816	(iv) what are the kinetics parameters of heparin binding to VN?	bind
17582	1	5763	7	NULL	NULL	NULL	NULL	heparin 	GP		bind					VN	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_53_37611_s_30	10608816	(iv) what are the kinetics parameters of heparin binding to VN?	bind
18446	1	5764	6	NULL	NULL	0	NULL	BHK cells	NULL	transfected	overexpress	NULL				LRP	NULL				NULL	cell surface	0	NULL	NULL	NULL	gw60_embo_20_21_5863_s_186	11689427	(J - M) Increased PrP-binding by rec. SFV RNA transfected BHK cells overexpressing LRP at the cell surface.	bind
18447	2	5764	6	10	NULL	0	NULL	rec. SFV RNA	NULL		increased	NULL				PrP	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_5863_s_186	11689427	(J - M) Increased PrP-binding by rec. SFV RNA transfected BHK cells overexpressing LRP at the cell surface.	bind
17583	1	5764	7	NULL	NULL	NULL	NULL	BHK cells	Cell		is transfected with					SFV RNA	NucleicAcid	rec			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_5863_s_186	11689427	(J - M) Increased PrP-binding by rec. SFV RNA transfected BHK cells overexpressing LRP at the cell surface.	bind
17584	2	5764	7	NULL	NULL	NULL	NULL	statement 1	Process		overexpress					LRP	GP				NULL	cell surface	NULL	NULL	NULL	NULL	gw60_embo_20_21_5863_s_186	11689427	(J - M) Increased PrP-binding by rec. SFV RNA transfected BHK cells overexpressing LRP at the cell surface.	bind
45856	3	5764	7	NULL	NULL	NULL	NULL	statement 2	Process		increases					Prp	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_5863_s_186	11689427	(J - M) Increased PrP-binding by rec. SFV RNA transfected BHK cells overexpressing LRP at the cell surface.	bind
18448	1	5765	6	NULL	NULL	0	NULL	Isl1	NULL		bind	NULL					NULL			MNE	NULL		0	NULL	NULL	NULL	gw60_neuron_38_5_731_s_199	12797958	(J) The binding of Isl1 and Lhx3 to MNE was analyzed by chromatin immune precipitation analysis.	bind
18449	2	5765	6	NULL	NULL	0	NULL	Lhx3	NULL		bind	NULL					NULL			MNE	NULL		0	NULL	NULL	NULL	gw60_neuron_38_5_731_s_199	12797958	(J) The binding of Isl1 and Lhx3 to MNE was analyzed by chromatin immune precipitation analysis.	bind
17585	1	5765	7	NULL	NULL	NULL	NULL	Isl1	GP		bind									MNE	NULL		NULL	NULL	NULL	NULL	gw60_neuron_38_5_731_s_199	12797958	(J) The binding of Isl1 and Lhx3 to MNE was analyzed by chromatin immune precipitation analysis.	bind
17586	2	5765	7	NULL	NULL	NULL	NULL	Lhx3	GP		bind									MNE	NULL		NULL	NULL	NULL	NULL	gw60_neuron_38_5_731_s_199	12797958	(J) The binding of Isl1 and Lhx3 to MNE was analyzed by chromatin immune precipitation analysis.	bind
18450	1	5766	6	10	NULL	0	NULL	Spo0J-GFP			bind					PSL23 strain				parS	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1326_s_168	12562803	(J, K) Position of Spo0J-GFP bound to a  parS array (J, strain PSL23) or LacI-CFP bound to a  lac operator array (K, strain KPL716) inserted at 270 degrees .	bind
18451	2	5766	6	10	NULL	0	NULL	LacI-CFP			bind					KPL716 strain				lac operator	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1326_s_168	12562803	(J, K) Position of Spo0J-GFP bound to a  parS array (J, strain PSL23) or LacI-CFP bound to a  lac operator array (K, strain KPL716) inserted at 270 degrees .	bind
17589	1	5766	7	NULL	NULL	NULL	NULL	Spo0J-GFP	GP		bind					PSL23	GP			parS 	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1326_s_168	12562803	(J, K) Position of Spo0J-GFP bound to a  parS array (J, strain PSL23) or LacI-CFP bound to a  lac operator array (K, strain KPL716) inserted at 270 degrees .	bind
17591	2	5766	7	NULL	NULL	NULL	NULL	LacI-CFP	GP		bind					strain KPL716	Organism			lac operator	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_4_1326_s_168	12562803	(J, K) Position of Spo0J-GFP bound to a  parS array (J, strain PSL23) or LacI-CFP bound to a  lac operator array (K, strain KPL716) inserted at 270 degrees .	bind
18452	1	5767	6	NULL	NULL	0	NULL	HOXA13	NULL	wild type	bind	NULL				Bmp2	NULL			enhancer	NULL	developing limbs	NULL	NULL	NULL	NULL	gw70_development_131_18_4581_s_154	15342482	(J-L) Chromatin immunoprecipitation  using the  Hoxa13 antibody confirms that wild-type (+/+) HOXA13 binds the  Bmp2 (J) and  Bmp7s1 (K) enhancer regions in the developing limb, whereas immunoprecipitates from mutant  limbs ( - / - ) lacking the HOXA13 DNA-binding domain did not contain the  Bmp2 and  Bmp7s1 enhancer regions.	bind
18453	2	5767	6	NULL	NULL	0	NULL	HOXA13	NULL	wild type	bind	NULL				Bmp7s1	NULL			enhancer	NULL	developing limbs	NULL	NULL	NULL	NULL	gw70_development_131_18_4581_s_154	15342482	(J-L) Chromatin immunoprecipitation  using the  Hoxa13 antibody confirms that wild-type (+/+) HOXA13 binds the  Bmp2 (J) and  Bmp7s1 (K) enhancer regions in the developing limb, whereas immunoprecipitates from mutant  limbs ( - / - ) lacking the HOXA13 DNA-binding domain did not contain the  Bmp2 and  Bmp7s1 enhancer regions.	bind
18454	3	5767	6	NULL	NULL	0	NULL	HOXA13	NULL	mutant	does not bind	NULL				Bmp2 	NULL			enhancer	NULL	developing limbs	NULL	NULL	NULL	NULL	gw70_development_131_18_4581_s_154	15342482	(J-L) Chromatin immunoprecipitation  using the  Hoxa13 antibody confirms that wild-type (+/+) HOXA13 binds the  Bmp2 (J) and  Bmp7s1 (K) enhancer regions in the developing limb, whereas immunoprecipitates from mutant  limbs ( - / - ) lacking the HOXA13 DNA-binding domain did not contain the  Bmp2 and  Bmp7s1 enhancer regions.	bind
18455	4	5767	6	NULL	NULL	0	NULL	HOXA13	NULL	mutant	does not bind	NULL				Bmp7s1	NULL			enhancer	NULL	developing limbs	NULL	NULL	NULL	NULL	gw70_development_131_18_4581_s_154	15342482	(J-L) Chromatin immunoprecipitation  using the  Hoxa13 antibody confirms that wild-type (+/+) HOXA13 binds the  Bmp2 (J) and  Bmp7s1 (K) enhancer regions in the developing limb, whereas immunoprecipitates from mutant  limbs ( - / - ) lacking the HOXA13 DNA-binding domain did not contain the  Bmp2 and  Bmp7s1 enhancer regions.	bind
53248	5	5767	6	10	NULL	0	NULL	HOXA13	NULL	mutant	lacks	NULL					NULL		DNA-binding domain		NULL		0	NULL	NULL	NULL	gw70_development_131_18_4581_s_154	15342482	(J-L) Chromatin immunoprecipitation  using the  Hoxa13 antibody confirms that wild-type (+/+) HOXA13 binds the  Bmp2 (J) and  Bmp7s1 (K) enhancer regions in the developing limb, whereas immunoprecipitates from mutant  limbs ( - / - ) lacking the HOXA13 DNA-binding domain did not contain the  Bmp2 and  Bmp7s1 enhancer regions.	bind
17594	1	5767	7	NULL	NULL	NULL	NULL	HOXA13	GP	wild-type	binds					Bmp2 	GP			enhancer	NULL	in the developing limb	NULL	NULL	NULL	NULL	gw70_development_131_18_4581_s_154	15342482	(J-L) Chromatin immunoprecipitation  using the  Hoxa13 antibody confirms that wild-type (+/+) HOXA13 binds the  Bmp2 (J) and  Bmp7s1 (K) enhancer regions in the developing limb, whereas immunoprecipitates from mutant  limbs ( - / - ) lacking the HOXA13 DNA-binding domain did not contain the  Bmp2 and  Bmp7s1 enhancer regions.	bind
17595	2	5767	7	NULL	NULL	NULL	NULL	HOXA13	GP	wild-type	binds					Bmp7s1	GP			enhancer	NULL	in the developing limb	NULL	NULL	NULL	NULL	gw70_development_131_18_4581_s_154	15342482	(J-L) Chromatin immunoprecipitation  using the  Hoxa13 antibody confirms that wild-type (+/+) HOXA13 binds the  Bmp2 (J) and  Bmp7s1 (K) enhancer regions in the developing limb, whereas immunoprecipitates from mutant  limbs ( - / - ) lacking the HOXA13 DNA-binding domain did not contain the  Bmp2 and  Bmp7s1 enhancer regions.	bind
17596	3	5767	7	NULL	NULL	NULL	NULL	HOXA13	GP	mutant	does not bind					Bmp2	GP			enhancer	NULL	developing limb	NULL	NULL	NULL	NULL	gw70_development_131_18_4581_s_154	15342482	(J-L) Chromatin immunoprecipitation  using the  Hoxa13 antibody confirms that wild-type (+/+) HOXA13 binds the  Bmp2 (J) and  Bmp7s1 (K) enhancer regions in the developing limb, whereas immunoprecipitates from mutant  limbs ( - / - ) lacking the HOXA13 DNA-binding domain did not contain the  Bmp2 and  Bmp7s1 enhancer regions.	bind
17597	4	5767	7	NULL	NULL	NULL	NULL	HOXA13	GP	mutant	does not bind					Bmp7s1	GP			enhancer	NULL	developing limb	NULL	NULL	NULL	NULL	gw70_development_131_18_4581_s_154	15342482	(J-L) Chromatin immunoprecipitation  using the  Hoxa13 antibody confirms that wild-type (+/+) HOXA13 binds the  Bmp2 (J) and  Bmp7s1 (K) enhancer regions in the developing limb, whereas immunoprecipitates from mutant  limbs ( - / - ) lacking the HOXA13 DNA-binding domain did not contain the  Bmp2 and  Bmp7s1 enhancer regions.	bind
53247	5	5767	7	NULL	NULL	NULL	NULL	HOXA13	GP	mutant	lacks								DNA-binding domain		NULL		NULL	NULL	NULL	NULL	gw70_development_131_18_4581_s_154	15342482	(J-L) Chromatin immunoprecipitation  using the  Hoxa13 antibody confirms that wild-type (+/+) HOXA13 binds the  Bmp2 (J) and  Bmp7s1 (K) enhancer regions in the developing limb, whereas immunoprecipitates from mutant  limbs ( - / - ) lacking the HOXA13 DNA-binding domain did not contain the  Bmp2 and  Bmp7s1 enhancer regions.	bind
18456	1	5768	6	10	NULL	0	NULL	DC3B ADP	NULL	prolonged treatment of	ribosylates	NULL				RhoA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2437_s_164	9398666	(Just  et al., 1993  ; Gong  et al., 1996  ; present study), and our finding that prolonged treatment of DC3B ADP-ribosylates RhoA that reassociates with rhoGDI is consistent with a previous study that showed that RhoA ADP ribosylated in vitro can bind to rhoGDI (Hancock and Hall, 1993  ).	bind
18457	2	5768	6	NULL	NULL	0	NULL	RhoA	NULL		reassociates with	NULL				rhoGDI	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_8_12_2437_s_164	9398666	(Just  et al., 1993  ; Gong  et al., 1996  ; present study), and our finding that prolonged treatment of DC3B ADP-ribosylates RhoA that reassociates with rhoGDI is consistent with a previous study that showed that RhoA ADP ribosylated in vitro can bind to rhoGDI (Hancock and Hall, 1993  ).	bind
18458	3	5768	6	NULL	NULL	0	NULL	RhoA ADP	NULL	ribosylated	bind	NULL				rhoGDI	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_molbiolcell_8_12_2437_s_164	9398666	(Just  et al., 1993  ; Gong  et al., 1996  ; present study), and our finding that prolonged treatment of DC3B ADP-ribosylates RhoA that reassociates with rhoGDI is consistent with a previous study that showed that RhoA ADP ribosylated in vitro can bind to rhoGDI (Hancock and Hall, 1993  ).	bind
17598	1	5768	7	NULL	NULL	NULL	NULL	DC3B ADP	GP	prolonged treatment of	ribosylates					RhoA	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2437_s_164	9398666	(Just  et al., 1993  ; Gong  et al., 1996  ; present study), and our finding that prolonged treatment of DC3B ADP-ribosylates RhoA that reassociates with rhoGDI is consistent with a previous study that showed that RhoA ADP ribosylated in vitro can bind to rhoGDI (Hancock and Hall, 1993  ).	bind
17599	2	5768	7	NULL	NULL	NULL	NULL	statement 1	Process		reassociate with					rhoGDI	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2437_s_164	9398666	(Just  et al., 1993  ; Gong  et al., 1996  ; present study), and our finding that prolonged treatment of DC3B ADP-ribosylates RhoA that reassociates with rhoGDI is consistent with a previous study that showed that RhoA ADP ribosylated in vitro can bind to rhoGDI (Hancock and Hall, 1993  ).	bind
17600	3	5768	7	NULL	NULL	NULL	NULL	RhoA ADP 	GP	ribosylated	bind					rhoGDI	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2437_s_164	9398666	(Just  et al., 1993  ; Gong  et al., 1996  ; present study), and our finding that prolonged treatment of DC3B ADP-ribosylates RhoA that reassociates with rhoGDI is consistent with a previous study that showed that RhoA ADP ribosylated in vitro can bind to rhoGDI (Hancock and Hall, 1993  ).	bind
18459	1	5769	6	NULL	NULL	0	NULL	m-UBR2	NULL		bind	NULL				HR6B E2 enzyme	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_22_8255_s_40	14585983	(K) m-UBR2 binds to the HR6B E2  enzyme.	bind
17603	1	5769	7	NULL	NULL	NULL	NULL	m-UBR2	GP		binds to					HR6B E2 enzyme	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8255_s_40	14585983	(K) m-UBR2 binds to the HR6B E2  enzyme.	bind
18460	1	5770	6	NULL	NULL	0	NULL	Su(H)	NULL		bind	NULL					NULL			SME	NULL		0	NULL	NULL	NULL	gw60_cell_103_1_75_s_218	11051549	(K) Su(H) binding to the  SME.	bind
17606	1	5770	7	NULL	NULL	NULL	NULL	Su(H)	GP		bind									SME	NULL		NULL	NULL	NULL	NULL	gw60_cell_103_1_75_s_218	11051549	(K) Su(H) binding to the  SME.	bind
18461	1	5771	6	NULL	NULL	0	NULL	Dll3	NULL		localizes	NULL				Mesp2	NULL	expression of			NULL		0	NULL	NULL	NULL	gw60_development_130_18_4259_s_176	12900443	(K,L) Dll3 is required for localization of  Mesp2 expression into the rostral half of somites.	bind
18462	2	5771	6	NULL	NULL	0	NULL	Mesp2	NULL		expressed into	NULL				rostral half of somites	NULL				NULL		0	NULL	NULL	NULL	gw60_development_130_18_4259_s_176	12900443	(K,L) Dll3 is required for localization of  Mesp2 expression into the rostral half of somites.	bind
17607	1	5771	7	NULL	NULL	NULL	NULL	Dll3	GP		localizes					Mesp2	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_development_130_18_4259_s_176	12900443	(K,L) Dll3 is required for localization of  Mesp2 expression into the rostral half of somites.	bind
25023	2	5771	7	NULL	NULL	NULL	NULL	Mesp2	GP		expressed into					rostral half of somites	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_development_130_18_4259_s_176	12900443	(K,L) Dll3 is required for localization of  Mesp2 expression into the rostral half of somites.	bind
18472	1	5773	6	NULL	NULL	0	NULL	Kelch-like ECH-associated protein 1	NULL		bind	NULL				Nrf2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27244_s_26	15917255	(Kelch-like ECH-associated protein 1) binds to Nrf2 and facilitates the degradation of Nrf2 via the proteasome system ( ).	bind
18473	2	5773	6	10	NULL	0	NULL	statement 1	NULL		facilitate	NULL				Nrf2	NULL	degradation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_29_27244_s_26	15917255	(Kelch-like ECH-associated protein 1) binds to Nrf2 and facilitates the degradation of Nrf2 via the proteasome system ( ).	bind
18474	3	5773	6	NULL	NULL	0	NULL	statement 2	NULL		occurs via 	NULL				proteasome system	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27244_s_26	15917255	(Kelch-like ECH-associated protein 1) binds to Nrf2 and facilitates the degradation of Nrf2 via the proteasome system ( ).	bind
17611	1	5773	7	NULL	NULL	NULL	NULL	Kelch-like ECH-associated protein 1	GP		binds to					Nrf2 	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_29_27244_s_26	15917255	(Kelch-like ECH-associated protein 1) binds to Nrf2 and facilitates the degradation of Nrf2 via the proteasome system ( ).	bind
17612	2	5773	7	NULL	NULL	NULL	NULL	statement 1	Process		facilitate					Nrf2 	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_29_27244_s_26	15917255	(Kelch-like ECH-associated protein 1) binds to Nrf2 and facilitates the degradation of Nrf2 via the proteasome system ( ).	bind
17613	3	5773	7	NULL	NULL	NULL	NULL	statement 2	Process		occurs via					proteasome system	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_29_27244_s_26	15917255	(Kelch-like ECH-associated protein 1) binds to Nrf2 and facilitates the degradation of Nrf2 via the proteasome system ( ).	bind
18476	1	5774	6	10	NULL	0	NULL	telomerase RNA variant	NULL	deletion 	bind	NULL		stem loop IV		TERT	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_13_9_1116_s_71	10323863	(Lane  1) No competitor; (lane  2) a telomerase RNA variant missing stem-loop IV, which binds TERT but is less active than the wild-type RNA (see Results); (lanes  3,4) tRNA; (lanes  5,6) 5S RNA; (lanes  7,8) total yeast RNA; (lanes  9,10) a 24-nucleotide RNA oligonucleotide representing telomerase RNA residues 36-59 which have no activity (Collins and Gandhi 1998  ).	bind
45761	2	5774	6	10	NULL	0	NULL	statement 1	NULL		is less active than	NULL				RNA	NULL	wild type			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_13_9_1116_s_71	10323863	(Lane  1) No competitor; (lane  2) a telomerase RNA variant missing stem-loop IV, which binds TERT but is less active than the wild-type RNA (see Results); (lanes  3,4) tRNA; (lanes  5,6) 5S RNA; (lanes  7,8) total yeast RNA; (lanes  9,10) a 24-nucleotide RNA oligonucleotide representing telomerase RNA residues 36-59 which have no activity (Collins and Gandhi 1998  ).	bind
17614	1	5774	7	NULL	NULL	NULL	NULL	telomerase RNA variant	NucleicAcid		missing					stem-loop IV	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_13_9_1116_s_71	10323863	(Lane  1) No competitor; (lane  2) a telomerase RNA variant missing stem-loop IV, which binds TERT but is less active than the wild-type RNA (see Results); (lanes  3,4) tRNA; (lanes  5,6) 5S RNA; (lanes  7,8) total yeast RNA; (lanes  9,10) a 24-nucleotide RNA oligonucleotide representing telomerase RNA residues 36-59 which have no activity (Collins and Gandhi 1998  ).	bind
17615	2	5774	7	NULL	NULL	NULL	NULL	statement 1	Process		binds					TERT	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_13_9_1116_s_71	10323863	(Lane  1) No competitor; (lane  2) a telomerase RNA variant missing stem-loop IV, which binds TERT but is less active than the wild-type RNA (see Results); (lanes  3,4) tRNA; (lanes  5,6) 5S RNA; (lanes  7,8) total yeast RNA; (lanes  9,10) a 24-nucleotide RNA oligonucleotide representing telomerase RNA residues 36-59 which have no activity (Collins and Gandhi 1998  ).	bind
17617	3	5774	7	NULL	NULL	NULL	NULL	statement 2	Process		is less active than					RNA	NucleicAcid	wild-type			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_13_9_1116_s_71	10323863	(Lane  1) No competitor; (lane  2) a telomerase RNA variant missing stem-loop IV, which binds TERT but is less active than the wild-type RNA (see Results); (lanes  3,4) tRNA; (lanes  5,6) 5S RNA; (lanes  7,8) total yeast RNA; (lanes  9,10) a 24-nucleotide RNA oligonucleotide representing telomerase RNA residues 36-59 which have no activity (Collins and Gandhi 1998  ).	bind
18477	1	5775	6	10	NULL	0	NULL	Pse1-GFP	NULL		bind	NULL				Pho4	NULL	WT			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_17_2673_s_126	9732266	(Lane  1) Three percent of the Pse1-GFP extract loaded (L); (lane  2) Pse1-GFP bound to Pho4WT-zz (WT); (lane  3) Pse1-GFP bound to Pho4delta157-164-zz (delta); (lane  4) Pse1-GFP bound to IgG-Sepharose beads ( ).	bind
18478	2	5775	6	NULL	NULL	0	NULL	Pse1-GFP	NULL		bind	NULL				Pho4	NULL		delta157-164		NULL		0	NULL	NULL	NULL	gw60_genesdev_12_17_2673_s_126	9732266	(Lane  1) Three percent of the Pse1-GFP extract loaded (L); (lane  2) Pse1-GFP bound to Pho4WT-zz (WT); (lane  3) Pse1-GFP bound to Pho4delta157-164-zz (delta); (lane  4) Pse1-GFP bound to IgG-Sepharose beads ( ).	bind
17618	1	5775	7	NULL	NULL	NULL	NULL	Pse1-GFP	GP		bind					Pho4	GP	WT	zz		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_17_2673_s_126	9732266	(Lane  1) Three percent of the Pse1-GFP extract loaded (L); (lane  2) Pse1-GFP bound to Pho4WT-zz (WT); (lane  3) Pse1-GFP bound to Pho4delta157-164-zz (delta); (lane  4) Pse1-GFP bound to IgG-Sepharose beads ( ).	bind
17619	2	5775	7	NULL	NULL	NULL	NULL	Pse1-GFP	GP		bind					Pho4	GP		delta 157-164-zz 		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_17_2673_s_126	9732266	(Lane  1) Three percent of the Pse1-GFP extract loaded (L); (lane  2) Pse1-GFP bound to Pho4WT-zz (WT); (lane  3) Pse1-GFP bound to Pho4delta157-164-zz (delta); (lane  4) Pse1-GFP bound to IgG-Sepharose beads ( ).	bind
18479	1	5776	6	NULL	NULL	0	NULL	Oct4	NULL		bind	NULL				UTF1	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_16_2048_s_37	12923055	(Lanes   3 -  7)  Increasing amounts of Sox2-HMG protein mixed with equal amounts of Oct4 + DNA.   Although Oct4 binds alone to  UTF1 significantly more weakly than to   FGF4 (cf. the two lane  2s), heterodimerization on   UTF1 is more pronounced with even lower amounts of Sox2 (e.g., cf.  the two lane  4s or  5s).	bind
18480	2	5776	6	NULL	NULL	0	NULL	Oct4	NULL		bind	NULL				FGF4	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_16_2048_s_37	12923055	(Lanes   3 -  7)  Increasing amounts of Sox2-HMG protein mixed with equal amounts of Oct4 + DNA.   Although Oct4 binds alone to  UTF1 significantly more weakly than to   FGF4 (cf. the two lane  2s), heterodimerization on   UTF1 is more pronounced with even lower amounts of Sox2 (e.g., cf.  the two lane  4s or  5s).	bind
18481	3	5776	6	NULL	NULL	0	NULL	statement 1	NULL		is more weak than	NULL	significantly			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_16_2048_s_37	12923055	(Lanes   3 -  7)  Increasing amounts of Sox2-HMG protein mixed with equal amounts of Oct4 + DNA.   Although Oct4 binds alone to  UTF1 significantly more weakly than to   FGF4 (cf. the two lane  2s), heterodimerization on   UTF1 is more pronounced with even lower amounts of Sox2 (e.g., cf.  the two lane  4s or  5s).	bind
17621	1	5776	7	NULL	NULL	NULL	NULL	Oct4	GP		binds to					UTF1 	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_16_2048_s_37	12923055	(Lanes   3 -  7)  Increasing amounts of Sox2-HMG protein mixed with equal amounts of Oct4 + DNA.   Although Oct4 binds alone to  UTF1 significantly more weakly than to   FGF4 (cf. the two lane  2s), heterodimerization on   UTF1 is more pronounced with even lower amounts of Sox2 (e.g., cf.  the two lane  4s or  5s).	bind
17622	2	5776	7	NULL	NULL	NULL	NULL	Oct4	GP		binds to					FGF4	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_16_2048_s_37	12923055	(Lanes   3 -  7)  Increasing amounts of Sox2-HMG protein mixed with equal amounts of Oct4 + DNA.   Although Oct4 binds alone to  UTF1 significantly more weakly than to   FGF4 (cf. the two lane  2s), heterodimerization on   UTF1 is more pronounced with even lower amounts of Sox2 (e.g., cf.  the two lane  4s or  5s).	bind
17623	3	5776	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs  more weakly than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_16_2048_s_37	12923055	(Lanes   3 -  7)  Increasing amounts of Sox2-HMG protein mixed with equal amounts of Oct4 + DNA.   Although Oct4 binds alone to  UTF1 significantly more weakly than to   FGF4 (cf. the two lane  2s), heterodimerization on   UTF1 is more pronounced with even lower amounts of Sox2 (e.g., cf.  the two lane  4s or  5s).	bind
17624	4	5776	7	NULL	NULL	NULL	NULL	UTF1	GP	heterodimerization on	occurs with					Sox2	GP	even lower amounts of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_16_2048_s_37	12923055	(Lanes   3 -  7)  Increasing amounts of Sox2-HMG protein mixed with equal amounts of Oct4 + DNA.   Although Oct4 binds alone to  UTF1 significantly more weakly than to   FGF4 (cf. the two lane  2s), heterodimerization on   UTF1 is more pronounced with even lower amounts of Sox2 (e.g., cf.  the two lane  4s or  5s).	bind
18482	1	5777	6	NULL	NULL	0	NULL	Lhx3	NULL		bind	NULL				Isl1	NULL		C-terminal		NULL		0	NULL	NULL	NULL	gw60_cell_110_2_237_s_213	12150931	(Lanes 3 and 4) NLI is a competitor for Lhx3 binding to C-terminal Isl1.	bind
18483	2	5777	6	NULL	NULL	0	NULL	NLI	NULL		bind	NULL				Isl1	NULL		C-terminal		NULL		0	NULL	NULL	NULL	gw60_cell_110_2_237_s_213	12150931	(Lanes 3 and 4) NLI is a competitor for Lhx3 binding to C-terminal Isl1.	bind
18484	3	5777	6	NULL	NULL	0	NULL	statement 1	NULL		competes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_110_2_237_s_213	12150931	(Lanes 3 and 4) NLI is a competitor for Lhx3 binding to C-terminal Isl1.	bind
17626	1	5777	7	NULL	NULL	NULL	NULL	Lhx3	GP		bind					Isl1	GP		C-terminal		NULL		NULL	NULL	NULL	NULL	gw60_cell_110_2_237_s_213	12150931	(Lanes 3 and 4) NLI is a competitor for Lhx3 binding to C-terminal Isl1.	bind
17627	2	5777	7	NULL	NULL	NULL	NULL	NLI	GP		bind					Isl1	GP		C-terminal		NULL		NULL	NULL	NULL	NULL	gw60_cell_110_2_237_s_213	12150931	(Lanes 3 and 4) NLI is a competitor for Lhx3 binding to C-terminal Isl1.	bind
45857	3	5777	7	NULL	NULL	NULL	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_2_237_s_213	12150931	(Lanes 3 and 4) NLI is a competitor for Lhx3 binding to C-terminal Isl1.	bind
18485	1	5778	6	NULL	NULL	0	NULL	p16	NULL		bind	NULL				cdk4	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3916_s_215	10207115	(Left panel) Binding of p16 to cdk4.	bind
17628	1	5778	7	NULL	NULL	NULL	NULL	p16	GP		bind					cdk4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3916_s_215	10207115	(Left panel) Binding of p16 to cdk4.	bind
18486	1	5779	6	10	NULL	0	NULL		NULL		bind	NULL		CFP-PH 		PIP2	NULL				NULL	resting cell membrane	NULL	NULL	NULL	NULL	gw70_embo_24_9_1664_s_46	15861130	(Left panel) In a resting cell, CFP-PH and YFP-PH bind to PIP2 at the membrane and FRET occurs.	bind
18487	2	5779	6	10	NULL	0	NULL		NULL		bind	NULL		YFP-PH		PIP2	NULL				NULL	resting cell membrane	NULL	NULL	NULL	NULL	gw70_embo_24_9_1664_s_46	15861130	(Left panel) In a resting cell, CFP-PH and YFP-PH bind to PIP2 at the membrane and FRET occurs.	bind
17629	1	5779	7	NULL	NULL	NULL	NULL				bind			CFP-PH		PIP2	Chemical				NULL	resting cell membrane	NULL	NULL	NULL	NULL	gw70_embo_24_9_1664_s_46	15861130	(Left panel) In a resting cell, CFP-PH and YFP-PH bind to PIP2 at the membrane and FRET occurs.	bind
17630	2	5779	7	NULL	NULL	NULL	NULL				bind			YFP-PH		PIP2	Chemical				NULL	resting cell membrane	NULL	NULL	NULL	NULL	gw70_embo_24_9_1664_s_46	15861130	(Left panel) In a resting cell, CFP-PH and YFP-PH bind to PIP2 at the membrane and FRET occurs.	bind
18488	1	5780	6	10	NULL	0	NULL	Nuc	NULL		bind	NULL		RGG		G4 DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2944_s_53	12771220	(Left) Distamycin inhibition of binding of Nuc-RGG to G4 DNA.	bind
18489	2	5780	6	NULL	NULL	0	NULL	Distamycin	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2944_s_53	12771220	(Left) Distamycin inhibition of binding of Nuc-RGG to G4 DNA.	bind
17631	1	5780	7	NULL	NULL	NULL	NULL	Nuc	GP		bind			RGG		G4 DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2944_s_53	12771220	(Left) Distamycin inhibition of binding of Nuc-RGG to G4 DNA.	bind
17632	2	5780	7	NULL	NULL	NULL	NULL	Distamycin	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_11_2944_s_53	12771220	(Left) Distamycin inhibition of binding of Nuc-RGG to G4 DNA.	bind
18490	1	5781	6	10	NULL	0	NULL	SibA protein 			bind					IgG subclass 1					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_8_4851_s_132	11447160	(Left) SibA protein immunoglobulin binding with IgG subclasses 1 to 4 and IgG antibody fragments.	bind
18491	2	5781	6	10	NULL	0	NULL	SibA protein			bind					IgG subclass 2					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_8_4851_s_132	11447160	(Left) SibA protein immunoglobulin binding with IgG subclasses 1 to 4 and IgG antibody fragments.	bind
18492	3	5781	6	10	NULL	0	NULL	SibA protein			bind					IgG subclass 3					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_8_4851_s_132	11447160	(Left) SibA protein immunoglobulin binding with IgG subclasses 1 to 4 and IgG antibody fragments.	bind
18493	4	5781	6	10	NULL	0	NULL	SibA protein			bind					IgG subclass 4					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_8_4851_s_132	11447160	(Left) SibA protein immunoglobulin binding with IgG subclasses 1 to 4 and IgG antibody fragments.	bind
18494	5	5781	6	10	NULL	0	NULL	SibA protein	NULL		bind	NULL				IgG antibody fragments	NULL				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_8_4851_s_132	11447160	(Left) SibA protein immunoglobulin binding with IgG subclasses 1 to 4 and IgG antibody fragments.	bind
17633	1	5781	7	NULL	NULL	NULL	NULL	 SibA	GP		bind					IgG subclass 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_8_4851_s_132	11447160	(Left) SibA protein immunoglobulin binding with IgG subclasses 1 to 4 and IgG antibody fragments.	bind
17634	2	5781	7	NULL	NULL	NULL	NULL	SibA	GP		bind					IgG subclass 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_8_4851_s_132	11447160	(Left) SibA protein immunoglobulin binding with IgG subclasses 1 to 4 and IgG antibody fragments.	bind
17635	3	5781	7	NULL	NULL	NULL	NULL	SibA	GP		bind					IgG subclass 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_8_4851_s_132	11447160	(Left) SibA protein immunoglobulin binding with IgG subclasses 1 to 4 and IgG antibody fragments.	bind
17636	4	5781	7	NULL	NULL	NULL	NULL	SibA	GP		bind					IgG subclass 4	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_8_4851_s_132	11447160	(Left) SibA protein immunoglobulin binding with IgG subclasses 1 to 4 and IgG antibody fragments.	bind
17637	5	5781	7	NULL	NULL	NULL	NULL	SibA	GP		bind					IgG antibody fragments	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_8_4851_s_132	11447160	(Left) SibA protein immunoglobulin binding with IgG subclasses 1 to 4 and IgG antibody fragments.	bind
18495	1	5782	6	NULL	NULL	0	NULL	p300	NULL		bind	NULL				C/EBPbeta	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_1_472_s_301	15601867	(Lower panel)  Schematic representation of p300 showing the region that binds C/EBPbeta.	bind
17638	1	5782	7	NULL	NULL	NULL	NULL	p300	GP		bind					C/EBPbeta	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_1_472_s_301	15601867	(Lower panel)  Schematic representation of p300 showing the region that binds C/EBPbeta.	bind
18496	1	5783	6	10	NULL	0	NULL	Runx2	NULL	truncations	bind	NULL		N-108 series			NULL			Runx/octamer element	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3182_s_248	15798204	(Lower panel) EMSA showing binding of  the N-108 series of Runx2 truncations to the Runx/octamer element in the presence  or absence of Oct-1.	bind
17639	1	5783	7	NULL	NULL	NULL	NULL	Runx2	GP	truncations	bind			N-108 series						Runx/octamer element	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3182_s_248	15798204	(Lower panel) EMSA showing binding of  the N-108 series of Runx2 truncations to the Runx/octamer element in the presence  or absence of Oct-1.	bind
18497	1	5784	6	NULL	NULL	0	NULL	Nup116p	NULL		bind	NULL		GLEBS		Gle2p	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_17_4_1107_s_220	9463388	(Lower panel) Nup116p is drawn as a multi-domain protein which binds to Gle2p via its GLEBS and to importin/karyopherin beta-like transport factors (called beta-Kaps) via the GLFG region.	bind
18498	2	5784	6	NULL	NULL	0	NULL	Nup116p	NULL		bind	NULL		GLFG region		beta-Kaps	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_17_4_1107_s_220	9463388	(Lower panel) Nup116p is drawn as a multi-domain protein which binds to Gle2p via its GLEBS and to importin/karyopherin beta-like transport factors (called beta-Kaps) via the GLFG region.	bind
18499	3	5784	6	NULL	NULL	0	NULL	beta-Kaps	NULL		is	NULL				importin/karyopherin beta-like transport factors	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_17_4_1107_s_220	9463388	(Lower panel) Nup116p is drawn as a multi-domain protein which binds to Gle2p via its GLEBS and to importin/karyopherin beta-like transport factors (called beta-Kaps) via the GLFG region.	bind
17640	1	5784	7	NULL	NULL	NULL	NULL	Nup116p	GP		bind			GLEBS		Gle2p	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_4_1107_s_220	9463388	(Lower panel) Nup116p is drawn as a multi-domain protein which binds to Gle2p via its GLEBS and to importin/karyopherin beta-like transport factors (called beta-Kaps) via the GLFG region.	bind
17641	2	5784	7	NULL	NULL	NULL	NULL	Nup116p	GP		bind			GLFG region		beta-Kaps	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_4_1107_s_220	9463388	(Lower panel) Nup116p is drawn as a multi-domain protein which binds to Gle2p via its GLEBS and to importin/karyopherin beta-like transport factors (called beta-Kaps) via the GLFG region.	bind
17642	3	5784	7	NULL	NULL	NULL	NULL	importin/karyopherin beta-like transport factor	GP		is					beta-Kaps	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_4_1107_s_220	9463388	(Lower panel) Nup116p is drawn as a multi-domain protein which binds to Gle2p via its GLEBS and to importin/karyopherin beta-like transport factors (called beta-Kaps) via the GLFG region.	bind
18503	1	5785	6	NULL	NULL	0	NULL	IRP-1	NULL		bind	NULL					NULL			IRE	NULL		0	NULL	NULL	NULL	gw60_molcell_2_3_383_s_83	9774976	(Lower panel) The data presented in this manuscript reveal that translational inhibition by IRP-1 binding to the IRE permits eIF4F (eIF4E, eIF4G, and eIF4A) assembly but prevents the recruitment of eIF3/40S subunit complexes.	bind
18504	2	5785	6	10	NULL	0	NULL	statement 7	NULL		permits	NULL				eIF4F	NULL	assembly of 			NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_3_383_s_83	9774976	(Lower panel) The data presented in this manuscript reveal that translational inhibition by IRP-1 binding to the IRE permits eIF4F (eIF4E, eIF4G, and eIF4A) assembly but prevents the recruitment of eIF3/40S subunit complexes.	bind
18511	3	5785	6	10	NULL	0	NULL	statement 7	NULL		prevents	NULL				eIF3/40S subunit complexes	NULL	recruitment of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_3_383_s_83	9774976	(Lower panel) The data presented in this manuscript reveal that translational inhibition by IRP-1 binding to the IRE permits eIF4F (eIF4E, eIF4G, and eIF4A) assembly but prevents the recruitment of eIF3/40S subunit complexes.	bind
53251	4	5785	6	10	NULL	0	NULL	eIF4F	NULL	assembly of	consists of	NULL				eIF4E	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_2_3_383_s_83	9774976	(Lower panel) The data presented in this manuscript reveal that translational inhibition by IRP-1 binding to the IRE permits eIF4F (eIF4E, eIF4G, and eIF4A) assembly but prevents the recruitment of eIF3/40S subunit complexes.	bind
53252	5	5785	6	10	NULL	0	NULL	eIF4F	NULL	assembly of	consists of	NULL				eIF4G	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_2_3_383_s_83	9774976	(Lower panel) The data presented in this manuscript reveal that translational inhibition by IRP-1 binding to the IRE permits eIF4F (eIF4E, eIF4G, and eIF4A) assembly but prevents the recruitment of eIF3/40S subunit complexes.	bind
53253	6	5785	6	10	NULL	0	NULL	eIF4F	NULL	assembly of	consists of	NULL				eIF4A	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_3_383_s_83	9774976	(Lower panel) The data presented in this manuscript reveal that translational inhibition by IRP-1 binding to the IRE permits eIF4F (eIF4E, eIF4G, and eIF4A) assembly but prevents the recruitment of eIF3/40S subunit complexes.	bind
53254	7	5785	6	10	NULL	0	NULL	statement 1	NULL		causes	NULL				translation	NULL	inhibition of			NULL		0	NULL	NULL	NULL	gw60_molcell_2_3_383_s_83	9774976	(Lower panel) The data presented in this manuscript reveal that translational inhibition by IRP-1 binding to the IRE permits eIF4F (eIF4E, eIF4G, and eIF4A) assembly but prevents the recruitment of eIF3/40S subunit complexes.	bind
17643	1	5785	7	NULL	NULL	NULL	NULL	IRP-1 	GP		bind									IRE	NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_3_383_s_83	9774976	(Lower panel) The data presented in this manuscript reveal that translational inhibition by IRP-1 binding to the IRE permits eIF4F (eIF4E, eIF4G, and eIF4A) assembly but prevents the recruitment of eIF3/40S subunit complexes.	bind
17644	2	5785	7	NULL	NULL	NULL	NULL	statement 1	Process		cause					translation	Process	inhibition of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_3_383_s_83	9774976	(Lower panel) The data presented in this manuscript reveal that translational inhibition by IRP-1 binding to the IRE permits eIF4F (eIF4E, eIF4G, and eIF4A) assembly but prevents the recruitment of eIF3/40S subunit complexes.	bind
17645	3	5785	7	NULL	NULL	NULL	NULL	statement 2	Process		permits					eIF4F	GP	assembly of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_3_383_s_83	9774976	(Lower panel) The data presented in this manuscript reveal that translational inhibition by IRP-1 binding to the IRE permits eIF4F (eIF4E, eIF4G, and eIF4A) assembly but prevents the recruitment of eIF3/40S subunit complexes.	bind
17646	4	5785	7	NULL	NULL	NULL	NULL	eIF4F	GP	assembly of	consist of					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_3_383_s_83	9774976	(Lower panel) The data presented in this manuscript reveal that translational inhibition by IRP-1 binding to the IRE permits eIF4F (eIF4E, eIF4G, and eIF4A) assembly but prevents the recruitment of eIF3/40S subunit complexes.	bind
17647	5	5785	7	NULL	NULL	NULL	NULL	statement 2	Process		prevents					eIF3/40S subunit complex	GP	recruitment of 			NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_3_383_s_83	9774976	(Lower panel) The data presented in this manuscript reveal that translational inhibition by IRP-1 binding to the IRE permits eIF4F (eIF4E, eIF4G, and eIF4A) assembly but prevents the recruitment of eIF3/40S subunit complexes.	bind
53249	6	5785	7	NULL	NULL	NULL	NULL	eIF4F	GP	assembly of	consists of					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_3_383_s_83	9774976	(Lower panel) The data presented in this manuscript reveal that translational inhibition by IRP-1 binding to the IRE permits eIF4F (eIF4E, eIF4G, and eIF4A) assembly but prevents the recruitment of eIF3/40S subunit complexes.	bind
53250	7	5785	7	NULL	NULL	NULL	NULL	eIF4F	GP	assembly of	consists of					eIF4A	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_3_383_s_83	9774976	(Lower panel) The data presented in this manuscript reveal that translational inhibition by IRP-1 binding to the IRE permits eIF4F (eIF4E, eIF4G, and eIF4A) assembly but prevents the recruitment of eIF3/40S subunit complexes.	bind
18512	1	5787	6	NULL	NULL	0	NULL	WER	NULL		regulates	NULL	positively			GL2	NULL	transcription of			NULL	heart stage embryos	0	NULL	NULL	NULL	gw60_development_130_13_2893_s_265	12756173	(Lower row)  WER positively regulates  GL2 transcription in heart stage embryos.	bind
17648	1	5787	7	NULL	NULL	NULL	NULL	WER	GP		regulates		positively			GL2	GP	transcription of			NULL	in heart stage embryos	NULL	NULL	NULL	NULL	gw60_development_130_13_2893_s_265	12756173	(Lower row)  WER positively regulates  GL2 transcription in heart stage embryos.	bind
18514	1	5788	6	10	NULL	0	NULL	COI	NULL		bind	NULL				M3	NULL				NULL	F1 mice immunized with B6 cells	NULL	NULL	NULL	NULL	gw70_annurevimmunol_15_0_851_s_63	9143709	(LP x B6)F1 mice immunized with B6 cells react to the  B6 form of COI presented by M3wt; so far, a response in the opposite direction has not been detected, although the  two forms of COI bind equally well to M3.	bind
17649	1	5788	7	NULL	NULL	NULL	NULL	COI	GP		bind					M3	GP				NULL	F1 mice immunized with B6 cells	NULL	NULL	NULL	NULL	gw70_annurevimmunol_15_0_851_s_63	9143709	(LP x B6)F1 mice immunized with B6 cells react to the  B6 form of COI presented by M3wt; so far, a response in the opposite direction has not been detected, although the  two forms of COI bind equally well to M3.	bind
18516	1	5791	6	NULL	NULL	0	NULL	Mdmx	NULL		bind	NULL		RING finger		Mdm2	NULL		RING finger		NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_70_0_503_s_383	11395416	(Mdmx and Mdm2 interact through their  RING fingers, which could prevent E2 binding to Mdm2.)	bind
18517	2	5791	6	NULL	NULL	0	NULL	E2	NULL		bind	NULL				Mdm2	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_70_0_503_s_383	11395416	(Mdmx and Mdm2 interact through their  RING fingers, which could prevent E2 binding to Mdm2.)	bind
18519	3	5791	6	NULL	NULL	0	NULL	statement 1	NULL		prevents	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_70_0_503_s_383	11395416	(Mdmx and Mdm2 interact through their  RING fingers, which could prevent E2 binding to Mdm2.)	bind
17821	1	5791	7	NULL	NULL	NULL	NULL	Mdmx	GP		bind			RING fingers		Mdm2	GP		RING fingers		NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_70_0_503_s_383	11395416	(Mdmx and Mdm2 interact through their  RING fingers, which could prevent E2 binding to Mdm2.)	bind
17822	2	5791	7	NULL	NULL	NULL	NULL	E2	GP		bind					Mdm2	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_70_0_503_s_383	11395416	(Mdmx and Mdm2 interact through their  RING fingers, which could prevent E2 binding to Mdm2.)	bind
17823	3	5791	7	NULL	NULL	NULL	NULL	statement 1	Process		prevents					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_70_0_503_s_383	11395416	(Mdmx and Mdm2 interact through their  RING fingers, which could prevent E2 binding to Mdm2.)	bind
18520	1	5793	6	NULL	NULL	0	NULL	HIC	NULL		bind	NULL				Axin	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_270	12192039	(Middle panel) HIC binding to Axin does not affect the binding of GSK-3beta, and the activation of JNK is decreased.	bind
18521	2	5793	6	NULL	NULL	0	NULL	statement 1	NULL		does not affect	NULL				GSK-3beta	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_270	12192039	(Middle panel) HIC binding to Axin does not affect the binding of GSK-3beta, and the activation of JNK is decreased.	bind
18525	3	5793	6	NULL	NULL	0	NULL	statement 1	NULL		decreases	NULL				JNK	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_270	12192039	(Middle panel) HIC binding to Axin does not affect the binding of GSK-3beta, and the activation of JNK is decreased.	bind
17824	1	5793	7	NULL	NULL	NULL	NULL	HIC	GP		bind					Axin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_270	12192039	(Middle panel) HIC binding to Axin does not affect the binding of GSK-3beta, and the activation of JNK is decreased.	bind
17825	2	5793	7	NULL	NULL	NULL	NULL	statement 1	Process		does not affect					GSK-3beta	Process	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_270	12192039	(Middle panel) HIC binding to Axin does not affect the binding of GSK-3beta, and the activation of JNK is decreased.	bind
17826	3	5793	7	NULL	NULL	NULL	NULL	statement 1	Process		decrease					JNK	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_270	12192039	(Middle panel) HIC binding to Axin does not affect the binding of GSK-3beta, and the activation of JNK is decreased.	bind
18526	1	5795	6	10	NULL	0	NULL	Su(H)	NULL		bind	NULL	specifically				NULL			S1	NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_7_576_s_32	11937027	(N) The mobility-shift assay shows that Su(H) specifically binds to S1, S2, and S3.	bind
18527	2	5795	6	10	NULL	0	NULL	Su(H)	NULL		bind	NULL	specifically				NULL			S2	NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_7_576_s_32	11937027	(N) The mobility-shift assay shows that Su(H) specifically binds to S1, S2, and S3.	bind
18528	3	5795	6	10	NULL	0	NULL	Su(H)	NULL		bind	NULL	specifically				NULL			S3	NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_7_576_s_32	11937027	(N) The mobility-shift assay shows that Su(H) specifically binds to S1, S2, and S3.	bind
17827	1	5795	7	NULL	NULL	NULL	NULL	Su(H)	GP		binds		specifically							S1	NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_7_576_s_32	11937027	(N) The mobility-shift assay shows that Su(H) specifically binds to S1, S2, and S3.	bind
17828	2	5795	7	NULL	NULL	NULL	NULL	Su(H)	GP		binds		specifically							S2	NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_7_576_s_32	11937027	(N) The mobility-shift assay shows that Su(H) specifically binds to S1, S2, and S3.	bind
17829	3	5795	7	NULL	NULL	NULL	NULL	Su(H)	GP		binds		specifically							S3	NULL		NULL	NULL	NULL	NULL	gw60_currbiol_12_7_576_s_32	11937027	(N) The mobility-shift assay shows that Su(H) specifically binds to S1, S2, and S3.	bind
54105	1	5797	6	10	NULL	0	NULL	N3			bind		may;; directly			M2+					NULL		0	NULL	NULL	NULL	gw70_pnas_102_21_7459_s_10	15897459	(N3)H may possibly be acidified via carbonyl-coordinated M2+ to become a proton donor in the physiological pH range, at which direct (N3) -  binding of M2+ also seems possible.	bind
17830	1	5797	7	NULL	NULL	NULL	NULL	N3	Chemical		bind		may;;directly			M2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_21_7459_s_10	15897459	(N3)H may possibly be acidified via carbonyl-coordinated M2+ to become a proton donor in the physiological pH range, at which direct (N3) -  binding of M2+ also seems possible.	bind
18529	1	5798	6	10	NULL	0	NULL	StarD1	NULL	His-tagged;;full-length	bind	NULL	directly	START domain		cholesterol	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_46_8_1615_s_186	15897605	(N62)StarD1 and StarD5 containing START domains bind cholesterol   Tsujishita and Hurley ( ) reported data showing direct binding of cholesterol by a His-tagged StarD1 (full-length protein).	bind
18531	2	5798	6	10	NULL	0	NULL	StarD5	NULL		bind	NULL		START domain		cholesterol	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_46_8_1615_s_186	15897605	(N62)StarD1 and StarD5 containing START domains bind cholesterol   Tsujishita and Hurley ( ) reported data showing direct binding of cholesterol by a His-tagged StarD1 (full-length protein).	bind
17833	1	5798	7	NULL	NULL	NULL	NULL	StarD1	GP	His-tagged;;full-length	bind		directly	START domain		cholesterol	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_46_8_1615_s_186	15897605	(N62)StarD1 and StarD5 containing START domains bind cholesterol   Tsujishita and Hurley ( ) reported data showing direct binding of cholesterol by a His-tagged StarD1 (full-length protein).	bind
17834	2	5798	7	NULL	NULL	NULL	NULL	StarD5	GP		bind			START domain		cholesterol	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_46_8_1615_s_186	15897605	(N62)StarD1 and StarD5 containing START domains bind cholesterol   Tsujishita and Hurley ( ) reported data showing direct binding of cholesterol by a His-tagged StarD1 (full-length protein).	bind
24579	1	5800	6	10	NULL	0	NULL	ERK5	NULL		bind	NULL				deltakinase MEK5	NULL	mutant			NULL	cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_6_2065_s_122	16507987	(Nomenclature in the figures represents 64D65E-AA as 64.5DE-AA, etc.) (B) Binding of ERK5 and deltakinase MEK5 mutants in cells.	bind
12501	1	5800	7	NULL	NULL	NULL	NULL	ERK5	GP		bind					deltakinase MEK5 	GP	mutant			NULL	cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_6_2065_s_122	16507987	(Nomenclature in the figures represents 64D65E-AA as 64.5DE-AA, etc.) (B) Binding of ERK5 and deltakinase MEK5 mutants in cells.	bind
14894	1	5801	5	NULL	NULL	0	NULL	Annexin FITC	NULL		bind	NULL				mast cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_2_1439_s_191	11022038	(None) or with IL-3 or SCF (100 ng/ml) for 24 h. Annexin FITC binding to mast cells was determined by flow cytometry.	bind
17837	1	5801	7	NULL	NULL	NULL	NULL	 Annexin FITC	GP		bind					mast cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_2_1439_s_191	11022038	(None) or with IL-3 or SCF (100 ng/ml) for 24 h. Annexin FITC binding to mast cells was determined by flow cytometry.	bind
14895	1	5802	5	NULL	NULL	0	NULL	CFTR peptide	NULL		does not bind	NULL				beta2-syntrophin	NULL		PDZ domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_31_19797_s_124	9677412	(Not shown), we did not observe binding of the CFTR peptide to the PDZ domain of beta2-syntrophin (Fig.  4 B).	bind
17838	1	5802	7	NULL	NULL	NULL	NULL	CFTR peptide	GP		does not bind					beta2-syntrophin	GP		PDZ domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_31_19797_s_124	9677412	(Not shown), we did not observe binding of the CFTR peptide to the PDZ domain of beta2-syntrophin (Fig.  4 B).	bind
14896	1	5803	5	NULL	NULL	0	NULL	cytochrome c	NULL		bind	NULL				CCO	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_3_708_s_101	16407136	(Note that cytochrome   c is illustrated bound to CCO to denote the source of electrons, but this does not  imply cytochrome  c remains bound throughout multiple catalytic cycles.)	bind
17839	1	5803	7	NULL	NULL	NULL	NULL	cytochrome c 	GP		bind					CCO	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_3_708_s_101	16407136	(Note that cytochrome   c is illustrated bound to CCO to denote the source of electrons, but this does not  imply cytochrome  c remains bound throughout multiple catalytic cycles.)	bind
14897	1	5805	5	NULL	NULL	0	NULL	Pol II	NULL		bind	NULL					NULL			TATA region	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_13_5626_s_95	15964818	(Note that the ChIP signals for Pol II binding to the TATA region may be a composite of Pol II bound to the promoter and Pol II transcribing the 5' end of the ORF.)	bind
14898	2	5805	5	NULL	NULL	0	NULL	Pol II	NULL		bind	NULL					NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_13_5626_s_95	15964818	(Note that the ChIP signals for Pol II binding to the TATA region may be a composite of Pol II bound to the promoter and Pol II transcribing the 5' end of the ORF.)	bind
14899	3	5805	5	NULL	NULL	0	NULL	Pol II	NULL		transcribe	NULL					NULL			5' end of ORF	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_13_5626_s_95	15964818	(Note that the ChIP signals for Pol II binding to the TATA region may be a composite of Pol II bound to the promoter and Pol II transcribing the 5' end of the ORF.)	bind
14900	4	5805	5	NULL	NULL	0	NULL	statement 1	NULL		composite of 	NULL	may be			statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5626_s_95	15964818	(Note that the ChIP signals for Pol II binding to the TATA region may be a composite of Pol II bound to the promoter and Pol II transcribing the 5' end of the ORF.)	bind
14901	5	5805	5	NULL	NULL	0	NULL	statement 1	NULL		composite of	NULL	may be			statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5626_s_95	15964818	(Note that the ChIP signals for Pol II binding to the TATA region may be a composite of Pol II bound to the promoter and Pol II transcribing the 5' end of the ORF.)	bind
44720	6	5805	5	10	NULL	0	NULL	statement 2	NULL		occurs simultaneously with	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5626_s_95	15964818	(Note that the ChIP signals for Pol II binding to the TATA region may be a composite of Pol II bound to the promoter and Pol II transcribing the 5' end of the ORF.)	bind
17841	1	5805	7	NULL	NULL	NULL	NULL	Pol II	GP		bind									TATA region	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5626_s_95	15964818	(Note that the ChIP signals for Pol II binding to the TATA region may be a composite of Pol II bound to the promoter and Pol II transcribing the 5' end of the ORF.)	bind
17842	2	5805	7	NULL	NULL	NULL	NULL	Pol II	GP		bind									promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5626_s_95	15964818	(Note that the ChIP signals for Pol II binding to the TATA region may be a composite of Pol II bound to the promoter and Pol II transcribing the 5' end of the ORF.)	bind
17843	3	5805	7	NULL	NULL	NULL	NULL	Pol II	GP		transcribe									5' end of ORF	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5626_s_95	15964818	(Note that the ChIP signals for Pol II binding to the TATA region may be a composite of Pol II bound to the promoter and Pol II transcribing the 5' end of the ORF.)	bind
17844	4	5805	7	NULL	NULL	NULL	NULL	statement 2	Process		occur simultaneously with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5626_s_95	15964818	(Note that the ChIP signals for Pol II binding to the TATA region may be a composite of Pol II bound to the promoter and Pol II transcribing the 5' end of the ORF.)	bind
17845	5	5805	7	NULL	NULL	NULL	NULL	statement 1	Process		composite of		may be			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5626_s_95	15964818	(Note that the ChIP signals for Pol II binding to the TATA region may be a composite of Pol II bound to the promoter and Pol II transcribing the 5' end of the ORF.)	bind
17846	6	5805	7	NULL	NULL	NULL	NULL	statement 1	Process		composite of		may be			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5626_s_95	15964818	(Note that the ChIP signals for Pol II binding to the TATA region may be a composite of Pol II bound to the promoter and Pol II transcribing the 5' end of the ORF.)	bind
19164	1	5806	5	NULL	NULL	0	NULL	Rho protein	NULL		is the product of	NULL				rhomboid gene	NULL	Drosophila			NULL		0	NULL	NULL	NULL	gw60_genesdev_12_8_1166_s_26	9553046	(Note that the Rho protein described here is the product of  Drosophila gene  rhomboid, which bears no relationship with the mammalian membrane-bound GTPase Rho.)	bind
17848	1	5806	7	NULL	NULL	NULL	NULL	Rho protein	GP		is the product of					rhomboid gene	GP	Drosophila			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_8_1166_s_26	9553046	(Note that the Rho protein described here is the product of  Drosophila gene  rhomboid, which bears no relationship with the mammalian membrane-bound GTPase Rho.)	bind
14902	1	5807	5	NULL	NULL	0	NULL	SRF	NULL		bind	NULL				HDAC4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_22_20047_s_74	12663674	(Note that to assay the role of  Ca2+ on the binding of SRF and HDAC4, the basal protein interaction  buffer was altered by the addition of increasing concentrations of  Ca2+ (0 - 4 mM) or EGTA (10 mM).)	bind
19165	2	5807	5	NULL	NULL	0	NULL	Ca2+	NULL		has a role in	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_22_20047_s_74	12663674	(Note that to assay the role of  Ca2+ on the binding of SRF and HDAC4, the basal protein interaction  buffer was altered by the addition of increasing concentrations of  Ca2+ (0 - 4 mM) or EGTA (10 mM).)	bind
17849	1	5807	7	NULL	NULL	NULL	NULL	SRF	GP		bind					HDAC4	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20047_s_74	12663674	(Note that to assay the role of  Ca2+ on the binding of SRF and HDAC4, the basal protein interaction  buffer was altered by the addition of increasing concentrations of  Ca2+ (0 - 4 mM) or EGTA (10 mM).)	bind
17850	2	5807	7	NULL	NULL	NULL	NULL	Ca2+	Chemical		has a role in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20047_s_74	12663674	(Note that to assay the role of  Ca2+ on the binding of SRF and HDAC4, the basal protein interaction  buffer was altered by the addition of increasing concentrations of  Ca2+ (0 - 4 mM) or EGTA (10 mM).)	bind
14903	1	5808	5	NULL	NULL	0	NULL	UV	NULL		induce	NULL				RNAP IIO	NULL	degradation of 			NULL		0	NULL	NULL	NULL	gw70_genesdev_19_10_1227_s_145	15905410	(Note that UV-induced degradation of RNAP IIO appeared somewhat greater when measured with H5, likely because H5 specifically recognizes the elongating form of RNAP II that would be targeted following UV.)	bind
14905	2	5808	5	10	NULL	0	NULL	H5	NULL		recognizes	NULL	specifically			RNAP II	NULL	elongating form of 			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1227_s_145	15905410	(Note that UV-induced degradation of RNAP IIO appeared somewhat greater when measured with H5, likely because H5 specifically recognizes the elongating form of RNAP II that would be targeted following UV.)	bind
17851	1	5808	7	NULL	NULL	NULL	NULL	H5	GP		recognizes		specifically			RNAP II 	GP	elongating form of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1227_s_145	15905410	(Note that UV-induced degradation of RNAP IIO appeared somewhat greater when measured with H5, likely because H5 specifically recognizes the elongating form of RNAP II that would be targeted following UV.)	bind
17852	2	5808	7	NULL	NULL	NULL	NULL	UV			induce					RNAP IIO	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1227_s_145	15905410	(Note that UV-induced degradation of RNAP IIO appeared somewhat greater when measured with H5, likely because H5 specifically recognizes the elongating form of RNAP II that would be targeted following UV.)	bind
14908	1	5810	5	10	NULL	0	NULL	cytidine	NULL		bind	NULL					NULL		cytidine binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_27_16962_s_275	9202008	(Note:  K2 is a stepwise macroscopic equilibrium constant; it corresponds to a microscopic constant for cytidine binding to the remaining cytidine binding site equal to 2.0 x 106M 1.)	bind
17853	1	5810	7	NULL	NULL	NULL	NULL	cytidine	Chemical		bind								cytidine binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_27_16962_s_275	9202008	(Note:  K2 is a stepwise macroscopic equilibrium constant; it corresponds to a microscopic constant for cytidine binding to the remaining cytidine binding site equal to 2.0 x 106M 1.)	bind
14911	1	5812	5	10	NULL	0	NULL	semaphorin-AP 	NULL		bind	NULL				neuropilin-expressing cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_19_3_547_s_81	9331348	(P-R) Equilibrium binding of semaphorin-AP fusion proteins to neuropilin-expressing cells.	bind
44779	2	5812	5	10	NULL	0	NULL	semaphorin-AP	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_19_3_547_s_81	9331348	(P-R) Equilibrium binding of semaphorin-AP fusion proteins to neuropilin-expressing cells.	bind
17854	1	5812	7	NULL	NULL	NULL	NULL	semaphorin-AP 	GP		bind					neuropilin-expressing cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuron_19_3_547_s_81	9331348	(P-R) Equilibrium binding of semaphorin-AP fusion proteins to neuropilin-expressing cells.	bind
44780	2	5812	7	NULL	NULL	NULL	NULL	semaphorin-AP	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_19_3_547_s_81	9331348	(P-R) Equilibrium binding of semaphorin-AP fusion proteins to neuropilin-expressing cells.	bind
14912	1	5814	5	10	NULL	0	NULL	p66shc	NULL		is a type of	NULL				splice variant of p52shc/p46shc	NULL				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenomicshum_2_0_435_s_123	null	(p66shc is a splice variant of p52shc/p46shc, which binds Grb2 and may be involved  in Ras activation.)	bind
14913	2	5814	5	NULL	NULL	0	NULL	p66shc	NULL		bind	NULL				Grb2	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevgenomicshum_2_0_435_s_123	null	(p66shc is a splice variant of p52shc/p46shc, which binds Grb2 and may be involved  in Ras activation.)	bind
14914	3	5814	5	NULL	NULL	0	NULL	p66shc	NULL		involved in	NULL	may be			Ras	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_annurevgenomicshum_2_0_435_s_123	null	(p66shc is a splice variant of p52shc/p46shc, which binds Grb2 and may be involved  in Ras activation.)	bind
17857	1	5814	7	NULL	NULL	NULL	NULL	p66shc	GP		binds to					Grb2 	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenomicshum_2_0_435_s_123	null	(p66shc is a splice variant of p52shc/p46shc, which binds Grb2 and may be involved  in Ras activation.)	bind
17858	2	5814	7	NULL	NULL	NULL	NULL	p66shc	GP		 involved in		may be			Ras	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_annurevgenomicshum_2_0_435_s_123	null	(p66shc is a splice variant of p52shc/p46shc, which binds Grb2 and may be involved  in Ras activation.)	bind
17859	3	5814	7	NULL	NULL	NULL	NULL	p66shc	GP		is a type of					splice variant of p52shc/p46shc	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenomicshum_2_0_435_s_123	null	(p66shc is a splice variant of p52shc/p46shc, which binds Grb2 and may be involved  in Ras activation.)	bind
14915	1	5815	5	NULL	NULL	0	NULL	PABP-interacting protein 2	NULL		bind	NULL				PABP	NULL				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_rna_12_8_16804161_s_8	16804161	(PABP-interacting protein 2) binds PABP and inhibits  translation both in vitro and in vivo by decreasing the affinity of PABP  for polyadenylated RNA.	bind
14916	2	5815	5	NULL	NULL	0	NULL	PABP-interacting protein 2	NULL		inhibit	NULL				translation	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	abs-batch0740-0759_rna_12_8_16804161_s_8	16804161	(PABP-interacting protein 2) binds PABP and inhibits  translation both in vitro and in vivo by decreasing the affinity of PABP  for polyadenylated RNA.	bind
14917	3	5815	5	NULL	NULL	0	NULL	PABP-interacting protein 2	NULL		inhibit	NULL				translation	NULL				NULL	in vivo	0	NULL	NULL	NULL	abs-batch0740-0759_rna_12_8_16804161_s_8	16804161	(PABP-interacting protein 2) binds PABP and inhibits  translation both in vitro and in vivo by decreasing the affinity of PABP  for polyadenylated RNA.	bind
14918	4	5815	5	10	NULL	0	NULL	PABP			has affinity for					RNA		polyadenylated			NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_rna_12_8_16804161_s_8	16804161	(PABP-interacting protein 2) binds PABP and inhibits  translation both in vitro and in vivo by decreasing the affinity of PABP  for polyadenylated RNA.	bind
14919	5	5815	5	10	NULL	0	NULL	PABP-interacting protein 2	NULL		decrease	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_rna_12_8_16804161_s_8	16804161	(PABP-interacting protein 2) binds PABP and inhibits  translation both in vitro and in vivo by decreasing the affinity of PABP  for polyadenylated RNA.	bind
14922	8	5815	5	NULL	NULL	0	NULL	statement 5	NULL		leads to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_rna_12_8_16804161_s_8	16804161	(PABP-interacting protein 2) binds PABP and inhibits  translation both in vitro and in vivo by decreasing the affinity of PABP  for polyadenylated RNA.	bind
14923	9	5815	5	NULL	NULL	0	NULL	statement 5	NULL		leads to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_rna_12_8_16804161_s_8	16804161	(PABP-interacting protein 2) binds PABP and inhibits  translation both in vitro and in vivo by decreasing the affinity of PABP  for polyadenylated RNA.	bind
17860	1	5815	7	NULL	NULL	NULL	NULL	PABP-interacting protein 2	GP		binds					PABP	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_rna_12_8_16804161_s_8	16804161	(PABP-interacting protein 2) binds PABP and inhibits  translation both in vitro and in vivo by decreasing the affinity of PABP  for polyadenylated RNA.	bind
17861	2	5815	7	NULL	NULL	NULL	NULL	statement 1	Process		inhibits					translation	Process				NULL	in vitro	NULL	NULL	NULL	NULL	abs-batch0740-0759_rna_12_8_16804161_s_8	16804161	(PABP-interacting protein 2) binds PABP and inhibits  translation both in vitro and in vivo by decreasing the affinity of PABP  for polyadenylated RNA.	bind
17862	3	5815	7	NULL	NULL	NULL	NULL	statement 1	Process		inhibits					translation	Process				NULL	in vivo	NULL	NULL	NULL	NULL	abs-batch0740-0759_rna_12_8_16804161_s_8	16804161	(PABP-interacting protein 2) binds PABP and inhibits  translation both in vitro and in vivo by decreasing the affinity of PABP  for polyadenylated RNA.	bind
17863	4	5815	7	NULL	NULL	NULL	NULL	PABP	GP		has affinity for					RNA	NucleicAcid	polyadenylated			NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_rna_12_8_16804161_s_8	16804161	(PABP-interacting protein 2) binds PABP and inhibits  translation both in vitro and in vivo by decreasing the affinity of PABP  for polyadenylated RNA.	bind
17864	5	5815	7	NULL	NULL	NULL	NULL	statement 1	Process		decreases					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_rna_12_8_16804161_s_8	16804161	(PABP-interacting protein 2) binds PABP and inhibits  translation both in vitro and in vivo by decreasing the affinity of PABP  for polyadenylated RNA.	bind
17865	6	5815	7	NULL	NULL	NULL	NULL	statement 2	Process		occurs 					statement 5	Process	because of			NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_rna_12_8_16804161_s_8	16804161	(PABP-interacting protein 2) binds PABP and inhibits  translation both in vitro and in vivo by decreasing the affinity of PABP  for polyadenylated RNA.	bind
17866	7	5815	7	NULL	NULL	NULL	NULL	statement 3	Process		occurs 					statement 5	Process	because of			NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_rna_12_8_16804161_s_8	16804161	(PABP-interacting protein 2) binds PABP and inhibits  translation both in vitro and in vivo by decreasing the affinity of PABP  for polyadenylated RNA.	bind
14924	1	5816	5	NULL	NULL	0	NULL	GST	NULL	alone	does not bind	NULL	appreciably			TNNI3	NULL				NULL		0	NULL	NULL	NULL	gw70_gene_372_0_128_s_151	16516408	(Panel A), while GST alone does not appreciably bind  TNNI3.	bind
20289	1	5816	7	NULL	NULL	NULL	NULL	GST	Chemical		does not bind		appreciably			TNNI3	GP				NULL		NULL	NULL	NULL	NULL	gw70_gene_372_0_128_s_151	16516408	(Panel A), while GST alone does not appreciably bind  TNNI3.	bind
14925	1	5817	5	10	NULL	0	NULL	Polo-like		Xenopus	is required for					M-phase		exit of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7360_s_266	9819423	(Polo-like in  Xenopus) is required for M-phase exit and destruction of mitotic cyclins ( 5).	bind
14926	2	5817	5	10	NULL	0	NULL	Polo-like	NULL	Xenopus	is required for	NULL				mitotic cyclins	NULL	destruction of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7360_s_266	9819423	(Polo-like in  Xenopus) is required for M-phase exit and destruction of mitotic cyclins ( 5).	bind
17867	1	5817	7	NULL	NULL	NULL	NULL	Polo-like	OrganismPart	Xenopus	is required for					M-phase	Process	exit of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7360_s_266	9819423	(Polo-like in  Xenopus) is required for M-phase exit and destruction of mitotic cyclins ( 5).	bind
17868	2	5817	7	NULL	NULL	NULL	NULL	Polo-like	OrganismPart	Xenopus	is required for					mitotic cyclins	GP	destruction of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7360_s_266	9819423	(Polo-like in  Xenopus) is required for M-phase exit and destruction of mitotic cyclins ( 5).	bind
14927	1	5818	5	NULL	NULL	0	NULL	Ap 	NULL		bind	NULL		homeodomain		Ser wing	NULL			794 bp enhancer	NULL		0	NULL	NULL	NULL	gw70_development_131_2_285_s_194	14701680	(R-V) DNase I footprinting  analysis of the Ap homeodomain bound to the 794 bp  Ser wing enhancer.	bind
17869	1	5818	7	NULL	NULL	NULL	NULL	Ap	GP		bind			homeodomain		Ser wing	OrganismPart			 794 bp  enhancer	NULL		NULL	NULL	NULL	NULL	gw70_development_131_2_285_s_194	14701680	(R-V) DNase I footprinting  analysis of the Ap homeodomain bound to the 794 bp  Ser wing enhancer.	bind
14928	1	5819	5	10	NULL	0	NULL	Ap		HIS-tagged	bind		directly;;sequence specifically	homeodomain		Ser minimal wing				794 bp enhancer	NULL		NULL	NULL	NULL	NULL	gw70_development_131_2_285_s_193	14701680	(R-W) Binding of the Ap homeodomain (ApdeltaLIM, 6xHIS-tagged) to the 794 bp  Ser minimal wing enhancer is direct and sequence specific.	bind
54125	2	5819	5	10	NULL	0	NULL	Ap homeodomain			is					ApdeltaLIM					NULL		NULL	NULL	NULL	NULL	gw70_development_131_2_285_s_193	14701680	(R-W) Binding of the Ap homeodomain (ApdeltaLIM, 6xHIS-tagged) to the 794 bp  Ser minimal wing enhancer is direct and sequence specific.	bind
17870	1	5819	7	NULL	NULL	NULL	NULL	Ap	GP	HIS-tagged	binds		directly;;sequence specifically	homeodomain		Ser minimal wing	OrganismPart			794 bp enhancer	NULL		NULL	NULL	NULL	NULL	gw70_development_131_2_285_s_193	14701680	(R-W) Binding of the Ap homeodomain (ApdeltaLIM, 6xHIS-tagged) to the 794 bp  Ser minimal wing enhancer is direct and sequence specific.	bind
17872	2	5819	7	NULL	NULL	NULL	NULL	Ap homeodomain	GP		is					ApdeltaLIM	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_131_2_285_s_193	14701680	(R-W) Binding of the Ap homeodomain (ApdeltaLIM, 6xHIS-tagged) to the 794 bp  Ser minimal wing enhancer is direct and sequence specific.	bind
15610	1	5821	5	NULL	NULL	0	NULL	cyt P450	NULL	catalytic reaction of	involves	NULL				substrate 	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_35_36809_s_12	15194706	(REACTION 1) The cyt P450 catalytic reaction occurs via a reaction cycle that involves substrate binding, reduction of the ferric heme, O2 binding, reduction of the oxyferrous heme (second electron transfer), substrate oxidation, and finally product dissociation ( ).	bind
15611	2	5821	5	NULL	NULL	0	NULL	cyt P450	NULL	catalytic reaction of	involves	NULL				ferric heme	NULL	reduction of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_35_36809_s_12	15194706	(REACTION 1) The cyt P450 catalytic reaction occurs via a reaction cycle that involves substrate binding, reduction of the ferric heme, O2 binding, reduction of the oxyferrous heme (second electron transfer), substrate oxidation, and finally product dissociation ( ).	bind
15612	3	5821	5	NULL	NULL	0	NULL	cyt P450	NULL	catalytic reaction of	involves	NULL				O2	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_35_36809_s_12	15194706	(REACTION 1) The cyt P450 catalytic reaction occurs via a reaction cycle that involves substrate binding, reduction of the ferric heme, O2 binding, reduction of the oxyferrous heme (second electron transfer), substrate oxidation, and finally product dissociation ( ).	bind
15613	4	5821	5	NULL	NULL	0	NULL	cyt P450	NULL	catalytic reaction of	involves	NULL				oxyferrous heme	NULL	reduction of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_35_36809_s_12	15194706	(REACTION 1) The cyt P450 catalytic reaction occurs via a reaction cycle that involves substrate binding, reduction of the ferric heme, O2 binding, reduction of the oxyferrous heme (second electron transfer), substrate oxidation, and finally product dissociation ( ).	bind
15614	5	5821	5	NULL	NULL	0	NULL	cyt P450	NULL	catalytic reaction of	involves	NULL				substrate	NULL	oxidation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_35_36809_s_12	15194706	(REACTION 1) The cyt P450 catalytic reaction occurs via a reaction cycle that involves substrate binding, reduction of the ferric heme, O2 binding, reduction of the oxyferrous heme (second electron transfer), substrate oxidation, and finally product dissociation ( ).	bind
15615	6	5821	5	NULL	NULL	0	NULL	cyt P450	NULL	catalytic reaction of	involves	NULL				product	NULL	dissociation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_35_36809_s_12	15194706	(REACTION 1) The cyt P450 catalytic reaction occurs via a reaction cycle that involves substrate binding, reduction of the ferric heme, O2 binding, reduction of the oxyferrous heme (second electron transfer), substrate oxidation, and finally product dissociation ( ).	bind
17873	1	5821	7	NULL	NULL	NULL	NULL	cyt P450 	GP	catalytic reaction of	involves					substrate	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_35_36809_s_12	15194706	(REACTION 1) The cyt P450 catalytic reaction occurs via a reaction cycle that involves substrate binding, reduction of the ferric heme, O2 binding, reduction of the oxyferrous heme (second electron transfer), substrate oxidation, and finally product dissociation ( ).	bind
17874	2	5821	7	NULL	NULL	NULL	NULL	cyt P450 	GP	catalytic reaction of	involves					ferric heme	Chemical	reduction of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_35_36809_s_12	15194706	(REACTION 1) The cyt P450 catalytic reaction occurs via a reaction cycle that involves substrate binding, reduction of the ferric heme, O2 binding, reduction of the oxyferrous heme (second electron transfer), substrate oxidation, and finally product dissociation ( ).	bind
17875	3	5821	7	NULL	NULL	NULL	NULL	cyt P450	GP	catalytic reaction of	involves					O2	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_35_36809_s_12	15194706	(REACTION 1) The cyt P450 catalytic reaction occurs via a reaction cycle that involves substrate binding, reduction of the ferric heme, O2 binding, reduction of the oxyferrous heme (second electron transfer), substrate oxidation, and finally product dissociation ( ).	bind
17876	4	5821	7	NULL	NULL	NULL	NULL	cyt P450 	GP	catalytic reaction of	involves					oxyferrous heme	Chemical	reduction of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_35_36809_s_12	15194706	(REACTION 1) The cyt P450 catalytic reaction occurs via a reaction cycle that involves substrate binding, reduction of the ferric heme, O2 binding, reduction of the oxyferrous heme (second electron transfer), substrate oxidation, and finally product dissociation ( ).	bind
17877	5	5821	7	NULL	NULL	NULL	NULL	cyt P450 	GP	catalytic reaction of	involves					substrate	Chemical	oxidation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_35_36809_s_12	15194706	(REACTION 1) The cyt P450 catalytic reaction occurs via a reaction cycle that involves substrate binding, reduction of the ferric heme, O2 binding, reduction of the oxyferrous heme (second electron transfer), substrate oxidation, and finally product dissociation ( ).	bind
17878	6	5821	7	NULL	NULL	NULL	NULL	cyt P450 	Chemical	catalytic reaction of	involves					product	Chemical	dissociation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_35_36809_s_12	15194706	(REACTION 1) The cyt P450 catalytic reaction occurs via a reaction cycle that involves substrate binding, reduction of the ferric heme, O2 binding, reduction of the oxyferrous heme (second electron transfer), substrate oxidation, and finally product dissociation ( ).	bind
19166	1	5824	5	NULL	NULL	0	NULL	E7 peptide	NULL		bind	NULL		Leu			NULL		B-box helices		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_24_3199_s_206	12502741	(Red) Helices in B-box where the conserved Leu, Cys, and Glu in the E7 peptide bind; (magenta) helices from the other B-box in the asymmetric unit.	bind
19167	2	5824	5	NULL	NULL	0	NULL	E7 peptide	NULL		bind	NULL		Cys			NULL		B-box helices		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_24_3199_s_206	12502741	(Red) Helices in B-box where the conserved Leu, Cys, and Glu in the E7 peptide bind; (magenta) helices from the other B-box in the asymmetric unit.	bind
19168	3	5824	5	NULL	NULL	0	NULL	E7 peptide	NULL		bind	NULL		Glu			NULL		B-box helices		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_24_3199_s_206	12502741	(Red) Helices in B-box where the conserved Leu, Cys, and Glu in the E7 peptide bind; (magenta) helices from the other B-box in the asymmetric unit.	bind
17879	1	5824	7	NULL	NULL	NULL	NULL	E7 peptide	GP		bind			Leu					B-box helices		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_24_3199_s_206	12502741	(Red) Helices in B-box where the conserved Leu, Cys, and Glu in the E7 peptide bind; (magenta) helices from the other B-box in the asymmetric unit.	bind
17880	2	5824	7	NULL	NULL	NULL	NULL	E7 peptide	GP		bind			Cys					B-box helices		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_24_3199_s_206	12502741	(Red) Helices in B-box where the conserved Leu, Cys, and Glu in the E7 peptide bind; (magenta) helices from the other B-box in the asymmetric unit.	bind
17881	3	5824	7	NULL	NULL	NULL	NULL	E7 peptide	GP		bind			Glu					B-box helices		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_24_3199_s_206	12502741	(Red) Helices in B-box where the conserved Leu, Cys, and Glu in the E7 peptide bind; (magenta) helices from the other B-box in the asymmetric unit.	bind
14929	1	5825	5	NULL	NULL	0	NULL	Sox2	NULL		bind	NULL				FGF4	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_17_16_2048_s_25	12923055	(Remark: Sox2 binds  FGF4  and  UTF1 with similar affinity; see Supplemental Material.)	bind
14930	2	5825	5	NULL	NULL	0	NULL	Sox2	NULL		bind	NULL				UTF1	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_17_16_2048_s_25	12923055	(Remark: Sox2 binds  FGF4  and  UTF1 with similar affinity; see Supplemental Material.)	bind
14931	3	5825	5	10	NULL	0	NULL	statement 1	NULL		is similar to	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_16_2048_s_25	12923055	(Remark: Sox2 binds  FGF4  and  UTF1 with similar affinity; see Supplemental Material.)	bind
17882	1	5825	7	NULL	NULL	NULL	NULL	Sox2	GP		binds					FGF4	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_16_2048_s_25	12923055	(Remark: Sox2 binds  FGF4  and  UTF1 with similar affinity; see Supplemental Material.)	bind
17883	2	5825	7	NULL	NULL	NULL	NULL	Sox2	GP		binds					UTF1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_16_2048_s_25	12923055	(Remark: Sox2 binds  FGF4  and  UTF1 with similar affinity; see Supplemental Material.)	bind
17884	3	5825	7	NULL	NULL	NULL	NULL	statement 1	Process		is similar to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_16_2048_s_25	12923055	(Remark: Sox2 binds  FGF4  and  UTF1 with similar affinity; see Supplemental Material.)	bind
14932	1	5827	5	NULL	NULL	0	NULL	cyclin D1	NULL		bind	NULL				cdk4	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3916_s_218	10207115	(Right panel) Inhibition of cyclin D1 binding to cdk4 on p16 induction.	bind
14933	2	5827	5	NULL	NULL	0	NULL	p16	NULL	induction	inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3916_s_218	10207115	(Right panel) Inhibition of cyclin D1 binding to cdk4 on p16 induction.	bind
17885	1	5827	7	NULL	NULL	NULL	NULL	cyclin D1	GP		bind					cdk4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3916_s_218	10207115	(Right panel) Inhibition of cyclin D1 binding to cdk4 on p16 induction.	bind
17886	2	5827	7	NULL	NULL	NULL	NULL	p16	GP	induction of	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3916_s_218	10207115	(Right panel) Inhibition of cyclin D1 binding to cdk4 on p16 induction.	bind
14934	1	5829	5	10	NULL	0	NULL	PACS-1	NULL		bind	NULL				TGN/endosomal proteins	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_94_2_205_s_76	9695949	(Right) Binding of PACS-1 to additional TGN/endosomal proteins.	bind
17887	1	5829	7	NULL	NULL	NULL	NULL	PACS-1	GP		bind					TGN/endosomal proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_94_2_205_s_76	9695949	(Right) Binding of PACS-1 to additional TGN/endosomal proteins.	bind
14935	1	5832	5	10	NULL	0	NULL	Munc13-1			bind					RIM1					NULL		NULL	NULL	NULL	NULL	gw60_neuron_30_1_183_s_116	11343654	(Right) Munc13-1 binding to RIM1-GST fusion proteins in cosedimentation assays.	bind
54126	2	5832	5	10	NULL	0	NULL	RIM1			is a type of					GST fusion protein					NULL		0	NULL	NULL	NULL	gw60_neuron_30_1_183_s_116	11343654	(Right) Munc13-1 binding to RIM1-GST fusion proteins in cosedimentation assays.	bind
17929	1	5832	7	NULL	NULL	NULL	NULL	Munc13-1	GP		bind					RIM1	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_30_1_183_s_116	11343654	(Right) Munc13-1 binding to RIM1-GST fusion proteins in cosedimentation assays.	bind
54127	2	5832	7	NULL	NULL	NULL	NULL	RIM1	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_30_1_183_s_116	11343654	(Right) Munc13-1 binding to RIM1-GST fusion proteins in cosedimentation assays.	bind
14936	1	5833	5	NULL	NULL	0	NULL	Nt	NULL		bind	NULL				MTs	NULL				NULL		0	NULL	NULL	NULL	gw60_science_279_5350_580_s_48	9438855	(Right) Pellets containing Nt bound to MTs (Nt-MT complex) were incubated in the presence of 10 mM Mg-ATP, ultracentrifuged and analyzed as above.	bind
17933	1	5833	7	NULL	NULL	NULL	NULL	Nt	GP		bind					MTs	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5350_580_s_48	9438855	(Right) Pellets containing Nt bound to MTs (Nt-MT complex) were incubated in the presence of 10 mM Mg-ATP, ultracentrifuged and analyzed as above.	bind
19169	1	5834	5	NULL	NULL	0	NULL	tRNA	NULL		bind	NULL					NULL		A-site		NULL		0	NULL	NULL	NULL	gw60_science_285_5434_1722_s_57	10481006	(Right) The graph shows quantification of interference of A-site tRNA binding by modification of N1 positions of A1492 and A1493.	bind
19170	2	5834	5	NULL	NULL	0	NULL		NULL	modification of	interferes with	NULL		N1 positions of A1492		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_science_285_5434_1722_s_57	10481006	(Right) The graph shows quantification of interference of A-site tRNA binding by modification of N1 positions of A1492 and A1493.	bind
19171	3	5834	5	NULL	NULL	0	NULL		NULL	modification of	interferes with	NULL		N1 positions of A1493		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_science_285_5434_1722_s_57	10481006	(Right) The graph shows quantification of interference of A-site tRNA binding by modification of N1 positions of A1492 and A1493.	bind
17937	1	5834	7	NULL	NULL	NULL	NULL	tRNA	NucleicAcid		binds								A-site		NULL		NULL	NULL	NULL	NULL	gw60_science_285_5434_1722_s_57	10481006	(Right) The graph shows quantification of interference of A-site tRNA binding by modification of N1 positions of A1492 and A1493.	bind
17938	2	5834	7	NULL	NULL	NULL	NULL			modification of	interferes with			N1 positions of A1492		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5434_1722_s_57	10481006	(Right) The graph shows quantification of interference of A-site tRNA binding by modification of N1 positions of A1492 and A1493.	bind
17939	3	5834	7	NULL	NULL	NULL	NULL			modification of	interferes with			N1 positions of A1493		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5434_1722_s_57	10481006	(Right) The graph shows quantification of interference of A-site tRNA binding by modification of N1 positions of A1492 and A1493.	bind
14937	1	5836	5	NULL	NULL	0	NULL	Bax	NULL		bind	NULL				PTP complex	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_5_695_s_29	11724809	(Right, PTP model) According to this model, Bax binds to the PTP complex and causes its opening, resulting in the swelling of the mitochondrial matrix and rupture of the OMM.	bind
14938	2	5836	5	NULL	NULL	0	NULL	statement 1	NULL		causes	NULL				PTP complex	NULL	opening of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_5_695_s_29	11724809	(Right, PTP model) According to this model, Bax binds to the PTP complex and causes its opening, resulting in the swelling of the mitochondrial matrix and rupture of the OMM.	bind
14939	3	5836	5	NULL	NULL	0	NULL	statement 2	NULL		results in	NULL				mitochondrial matrix	NULL	swelling of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_5_695_s_29	11724809	(Right, PTP model) According to this model, Bax binds to the PTP complex and causes its opening, resulting in the swelling of the mitochondrial matrix and rupture of the OMM.	bind
14940	4	5836	5	NULL	NULL	0	NULL	statement 2	NULL		results in	NULL				OMM	NULL	rupture of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_5_695_s_29	11724809	(Right, PTP model) According to this model, Bax binds to the PTP complex and causes its opening, resulting in the swelling of the mitochondrial matrix and rupture of the OMM.	bind
17947	1	5836	7	NULL	NULL	NULL	NULL	Bax 	GP		binds to					PTP complex 	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_5_695_s_29	11724809	(Right, PTP model) According to this model, Bax binds to the PTP complex and causes its opening, resulting in the swelling of the mitochondrial matrix and rupture of the OMM.	bind
17949	2	5836	7	NULL	NULL	NULL	NULL	statement 1	Process		cause					PTP complex 	GP	opening of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_5_695_s_29	11724809	(Right, PTP model) According to this model, Bax binds to the PTP complex and causes its opening, resulting in the swelling of the mitochondrial matrix and rupture of the OMM.	bind
17951	3	5836	7	NULL	NULL	NULL	NULL	statement 1	Process		results in					mitochondrial matrix	CellComponent	swelling of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_5_695_s_29	11724809	(Right, PTP model) According to this model, Bax binds to the PTP complex and causes its opening, resulting in the swelling of the mitochondrial matrix and rupture of the OMM.	bind
17952	4	5836	7	NULL	NULL	NULL	NULL	statement 1	Process		results in					OMM	CellComponent	rupture of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_5_695_s_29	11724809	(Right, PTP model) According to this model, Bax binds to the PTP complex and causes its opening, resulting in the swelling of the mitochondrial matrix and rupture of the OMM.	bind
14941	1	5837	5	10	NULL	0	NULL	Sema IV AP 	NULL		bind	NULL				neuropilin-1- (S) expressing cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_103	9883722	(S and T) Equilibrium binding of Sema IV AP fusion proteins to neuropilin-1- (S) or neuropilin-2- (T) expressing cells.	bind
14942	2	5837	5	10	NULL	0	NULL	Sema IV AP 	NULL		bind	NULL				neuropilin-2- (T) expressing cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_103	9883722	(S and T) Equilibrium binding of Sema IV AP fusion proteins to neuropilin-1- (S) or neuropilin-2- (T) expressing cells.	bind
44781	3	5837	5	10	NULL	0	NULL	Sema IV AP	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_103	9883722	(S and T) Equilibrium binding of Sema IV AP fusion proteins to neuropilin-1- (S) or neuropilin-2- (T) expressing cells.	bind
17969	1	5837	7	NULL	NULL	NULL	NULL	Sema IV AP	GP		bind					neuropilin-1- (S) expressing cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_103	9883722	(S and T) Equilibrium binding of Sema IV AP fusion proteins to neuropilin-1- (S) or neuropilin-2- (T) expressing cells.	bind
17970	2	5837	7	NULL	NULL	NULL	NULL	Sema IV AP	GP		bind					neuropilin-2- (T) expressing cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_103	9883722	(S and T) Equilibrium binding of Sema IV AP fusion proteins to neuropilin-1- (S) or neuropilin-2- (T) expressing cells.	bind
44782	3	5837	7	NULL	NULL	NULL	NULL	Sema IV AP	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_6_1283_s_103	9883722	(S and T) Equilibrium binding of Sema IV AP fusion proteins to neuropilin-1- (S) or neuropilin-2- (T) expressing cells.	bind
14943	1	5838	5	NULL	NULL	0	NULL	CAF	NULL		bind	NULL				TH	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_j-chromatogr-b-analyt-technol-biomed-life-sci_836_1-2_16621743_s_8	16621743	(Selectivity (alpha) is the ratio of  CAF bound to TH bound.)	bind
17971	1	5838	7	NULL	NULL	NULL	NULL	CAF	Chemical		bind					TH	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-chromatogr-b-analyt-technol-biomed-life-sci_836_1-2_16621743_s_8	16621743	(Selectivity (alpha) is the ratio of  CAF bound to TH bound.)	bind
19172	1	5839	5	10	NULL	0	NULL	sFRP/Frzb	NULL		bind	NULL	may			Fz proteins	NULL				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_276	11448771	(sFRP/Frzb may also bind certain Fz proteins, not depicted here).	bind
17973	1	5839	7	NULL	NULL	NULL	NULL	sFRP/Frzb	GP		bind		may			 Fz proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_11_12_951_s_276	11448771	(sFRP/Frzb may also bind certain Fz proteins, not depicted here).	bind
14944	1	5840	5	NULL	NULL	0	NULL	apo-B	NULL		bind	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_101_5_1084_s_39	9486979	(Site B) and developed a model that explains how sequences and mutations carboxyl-terminal to the  LDL receptor-binding site modulate the receptor-binding activity of apo-B for the LDL receptor.	bind
14945	2	5840	5	NULL	NULL	0	NULL		NULL	mutant	modulate	NULL		carboxyl-terminal to LDL receptor-binding site		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_101_5_1084_s_39	9486979	(Site B) and developed a model that explains how sequences and mutations carboxyl-terminal to the  LDL receptor-binding site modulate the receptor-binding activity of apo-B for the LDL receptor.	bind
17974	1	5840	7	NULL	NULL	NULL	NULL	apo-B	Chemical		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_101_5_1084_s_39	9486979	(Site B) and developed a model that explains how sequences and mutations carboxyl-terminal to the  LDL receptor-binding site modulate the receptor-binding activity of apo-B for the LDL receptor.	bind
17975	2	5840	7	NULL	NULL	NULL	NULL			mutant	modulate			carboxyl-terminal to the LDL receptor-binding site 		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_101_5_1084_s_39	9486979	(Site B) and developed a model that explains how sequences and mutations carboxyl-terminal to the  LDL receptor-binding site modulate the receptor-binding activity of apo-B for the LDL receptor.	bind
14948	1	5843	5	NULL	NULL	0	NULL	PDK-1	NULL		bind	NULL				PIF	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_57_4_652_s_161	10727509	(Stephens et al., 1998  ), and also that binding of PIF to PDK-1 converts it into a PtdIns-3,4,5-P3-activated enzyme (Balendran et al., 1999a  ).	bind
14949	2	5843	5	NULL	NULL	0	NULL	statement 1	NULL		converted to	NULL				PtdIns-3,4,5-P3-activated enzyme	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_57_4_652_s_161	10727509	(Stephens et al., 1998  ), and also that binding of PIF to PDK-1 converts it into a PtdIns-3,4,5-P3-activated enzyme (Balendran et al., 1999a  ).	bind
17981	1	5843	7	NULL	NULL	NULL	NULL	PIF	GP		bind					PDK-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_57_4_652_s_161	10727509	(Stephens et al., 1998  ), and also that binding of PIF to PDK-1 converts it into a PtdIns-3,4,5-P3-activated enzyme (Balendran et al., 1999a  ).	bind
17982	2	5843	7	NULL	NULL	NULL	NULL	statement 1	Process		converts it to					PtdIns-3,4,5-P3-activated enzyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_57_4_652_s_161	10727509	(Stephens et al., 1998  ), and also that binding of PIF to PDK-1 converts it into a PtdIns-3,4,5-P3-activated enzyme (Balendran et al., 1999a  ).	bind
14969	1	5844	5	NULL	NULL	0	NULL	p53	NULL		bind	NULL	nonspecific			DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_8_2703_s_233	10436023	(Stimulations may be indirect: 14-3-3 may block nonspecific binding of p53 to DNA [ P16]; p300 may do the same consequential to acetylation of K382 [ P21,22].)	bind
14970	2	5844	5	NULL	NULL	0	NULL	14-3-3	NULL		blocks	NULL	may			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_8_2703_s_233	10436023	(Stimulations may be indirect: 14-3-3 may block nonspecific binding of p53 to DNA [ P16]; p300 may do the same consequential to acetylation of K382 [ P21,22].)	bind
17983	1	5844	7	NULL	NULL	NULL	NULL	p53	GP		bind		non-specifically			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_8_2703_s_233	10436023	(Stimulations may be indirect: 14-3-3 may block nonspecific binding of p53 to DNA [ P16]; p300 may do the same consequential to acetylation of K382 [ P21,22].)	bind
17984	2	5844	7	NULL	NULL	NULL	NULL	14-3-3	Chemical		block		may			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_8_2703_s_233	10436023	(Stimulations may be indirect: 14-3-3 may block nonspecific binding of p53 to DNA [ P16]; p300 may do the same consequential to acetylation of K382 [ P21,22].)	bind
17987	1	5845	7	NULL	NULL	0	NULL	NADP+	NULL		bind	NULL				CL-DHFR	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1481_1_37_s_165	10962090	(Structure of NADP+-bound CL-DHFR was obtained from the Protein Data Bank, using the PDB accession code 8DFR.)	bind
14972	1	5846	5	NULL	NULL	0	NULL	ARG1	NULL		bind	NULL					NULL		myc-Arg81p		NULL		0	NULL	NULL	NULL	gw70_pnas_101_32_11713_s_128	15289616	(Student's  t test indicates that the reduction in  ARG1 binding of myc-Arg81p and myc-Arg82p produced by exogenous arginine is statistically significant, with  P values of 0.001 and 0.02, respectively.)	bind
14973	2	5846	5	NULL	NULL	0	NULL	ARG1	NULL		bind	NULL					NULL		myc-Arg82p		NULL		0	NULL	NULL	NULL	gw70_pnas_101_32_11713_s_128	15289616	(Student's  t test indicates that the reduction in  ARG1 binding of myc-Arg81p and myc-Arg82p produced by exogenous arginine is statistically significant, with  P values of 0.001 and 0.02, respectively.)	bind
14975	3	5846	5	NULL	NULL	0	NULL		NULL	exogenous	reduce	NULL		arginine		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_32_11713_s_128	15289616	(Student's  t test indicates that the reduction in  ARG1 binding of myc-Arg81p and myc-Arg82p produced by exogenous arginine is statistically significant, with  P values of 0.001 and 0.02, respectively.)	bind
14976	4	5846	5	NULL	NULL	0	NULL		NULL	exogenous	reduce	NULL		arginine		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_32_11713_s_128	15289616	(Student's  t test indicates that the reduction in  ARG1 binding of myc-Arg81p and myc-Arg82p produced by exogenous arginine is statistically significant, with  P values of 0.001 and 0.02, respectively.)	bind
17988	1	5846	7	NULL	NULL	NULL	NULL	ARG1	AminoAcid		bind								myc-Arg81p		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_32_11713_s_128	15289616	(Student's  t test indicates that the reduction in  ARG1 binding of myc-Arg81p and myc-Arg82p produced by exogenous arginine is statistically significant, with  P values of 0.001 and 0.02, respectively.)	bind
17989	2	5846	7	NULL	NULL	NULL	NULL	ARG1	AminoAcid		bind								myc-Arg82p		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_32_11713_s_128	15289616	(Student's  t test indicates that the reduction in  ARG1 binding of myc-Arg81p and myc-Arg82p produced by exogenous arginine is statistically significant, with  P values of 0.001 and 0.02, respectively.)	bind
17990	3	5846	7	NULL	NULL	NULL	NULL	arginine	AminoAcid	exogenous	reduce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_32_11713_s_128	15289616	(Student's  t test indicates that the reduction in  ARG1 binding of myc-Arg81p and myc-Arg82p produced by exogenous arginine is statistically significant, with  P values of 0.001 and 0.02, respectively.)	bind
20290	4	5846	7	NULL	NULL	NULL	NULL	arginine	AminoAcid	exogenous	reduce					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_32_11713_s_128	15289616	(Student's  t test indicates that the reduction in  ARG1 binding of myc-Arg81p and myc-Arg82p produced by exogenous arginine is statistically significant, with  P values of 0.001 and 0.02, respectively.)	bind
14979	1	5847	5	NULL	NULL	0	NULL	SpoIIAA proteins	NULL		bind	NULL	noncovalent			SpoIIAB	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_12_3860_s_63	10368168	(Studies of noncovalent binding of the SpoIIAA proteins with SpoIIAB in the presence of ADP [ 1,  4] revealed no significant difference between SpoIIAA+, SpoIIAAG62D, and SpoIIAAG95D [results not shown.)	bind
14980	2	5847	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				ADP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_12_3860_s_63	10368168	(Studies of noncovalent binding of the SpoIIAA proteins with SpoIIAB in the presence of ADP [ 1,  4] revealed no significant difference between SpoIIAA+, SpoIIAAG62D, and SpoIIAAG95D [results not shown.)	bind
17991	1	5847	7	NULL	NULL	NULL	NULL	SpoIIAA	GP		bind		noncovalently			SpoIIAB	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_12_3860_s_63	10368168	(Studies of noncovalent binding of the SpoIIAA proteins with SpoIIAB in the presence of ADP [ 1,  4] revealed no significant difference between SpoIIAA+, SpoIIAAG62D, and SpoIIAAG95D [results not shown.)	bind
20291	2	5847	7	NULL	NULL	NULL	NULL	statement 1	Process		in presence of					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_12_3860_s_63	10368168	(Studies of noncovalent binding of the SpoIIAA proteins with SpoIIAB in the presence of ADP [ 1,  4] revealed no significant difference between SpoIIAA+, SpoIIAAG62D, and SpoIIAAG95D [results not shown.)	bind
14981	1	5848	5	NULL	NULL	0	NULL	GTF3	NULL		bind	NULL				TnI SURE	NULL		BLM		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_24_8490_s_260	11713284	(SURE  827/ 808), confirming that GTF3 binds the TnI SURE via the BLM (lanes 18 to 21).	bind
17992	1	5848	7	NULL	NULL	NULL	NULL	GTF3	GP		binds					TnI SURE	GP		BLM		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_24_8490_s_260	11713284	(SURE  827/ 808), confirming that GTF3 binds the TnI SURE via the BLM (lanes 18 to 21).	bind
14983	1	5850	5	NULL	NULL	0	NULL	HRI	NULL		bind	NULL		N-terminal domain		heme	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5171_s_258	10671563	(Table  I and Figs.  3 and  4) and that the N-terminal domain of HRI could bind heme (Fig.  8).	bind
17994	1	5850	7	NULL	NULL	NULL	NULL	HRI	GP		bind			N-terminal domain		heme	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_7_5171_s_258	10671563	(Table  I and Figs.  3 and  4) and that the N-terminal domain of HRI could bind heme (Fig.  8).	bind
14984	1	5851	5	NULL	NULL	0	NULL	importin 58	NULL		bind	NULL	poorly			T-ag	NULL		NLS		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_27_17191_s_57	9202041	(Table  I for T-ag sequences of the fusion proteins) using the dot blot technique indicated poor binding of importin 58 to the T-ag NLS in the absence of importin 97, which alone did not bind the T-ag NLS at all (Fig.  1 A).	bind
14985	2	5851	5	NULL	NULL	0	NULL	statement 1	NULL		in the absence of	NULL				importin 97	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_27_17191_s_57	9202041	(Table  I for T-ag sequences of the fusion proteins) using the dot blot technique indicated poor binding of importin 58 to the T-ag NLS in the absence of importin 97, which alone did not bind the T-ag NLS at all (Fig.  1 A).	bind
14986	3	5851	5	NULL	NULL	0	NULL	importin 97	NULL	alone	does not bind	NULL				T-ag	NULL		NLS		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_27_17191_s_57	9202041	(Table  I for T-ag sequences of the fusion proteins) using the dot blot technique indicated poor binding of importin 58 to the T-ag NLS in the absence of importin 97, which alone did not bind the T-ag NLS at all (Fig.  1 A).	bind
17995	1	5851	7	NULL	NULL	NULL	NULL	importin 58	GP		binds		poorly			T-ag	GP		NLS		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_27_17191_s_57	9202041	(Table  I for T-ag sequences of the fusion proteins) using the dot blot technique indicated poor binding of importin 58 to the T-ag NLS in the absence of importin 97, which alone did not bind the T-ag NLS at all (Fig.  1 A).	bind
17996	2	5851	7	NULL	NULL	NULL	NULL	importin 97	GP	alone	does not bind					T-ag	GP		NLS		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_27_17191_s_57	9202041	(Table  I for T-ag sequences of the fusion proteins) using the dot blot technique indicated poor binding of importin 58 to the T-ag NLS in the absence of importin 97, which alone did not bind the T-ag NLS at all (Fig.  1 A).	bind
20312	3	5851	7	NULL	NULL	NULL	NULL	statement 1	Process		 in the absence of					importin 97	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_27_17191_s_57	9202041	(Table  I for T-ag sequences of the fusion proteins) using the dot blot technique indicated poor binding of importin 58 to the T-ag NLS in the absence of importin 97, which alone did not bind the T-ag NLS at all (Fig.  1 A).	bind
14987	1	5852	5	NULL	NULL	0	NULL	mucin	NULL		bind	NULL				SLPI	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_22_13563_s_209	9593692	(Table  I) and mucin ( 35) bind to SLPI and, thus, might also be of physiologic importance.	bind
17997	1	5852	7	NULL	NULL	NULL	NULL	mucin	GP		bind					SLPI	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_13563_s_209	9593692	(Table  I) and mucin ( 35) bind to SLPI and, thus, might also be of physiologic importance.	bind
14988	1	5853	5	NULL	NULL	0	NULL	Oct-1	NULL		bind	NULL					NULL			betaA/T-rich element	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_43_30832_s_263	10521475	(Table  I) and the aforementioned A/T-rich elements, it is conceivable that Oct-1 binds the betaA/T-rich element under MOV conditions.	bind
14989	2	5853	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				MOV conditions	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_43_30832_s_263	10521475	(Table  I) and the aforementioned A/T-rich elements, it is conceivable that Oct-1 binds the betaA/T-rich element under MOV conditions.	bind
17999	1	5853	7	NULL	NULL	NULL	NULL	Oct-1	GP		binds									 betaA/T-rich element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_43_30832_s_263	10521475	(Table  I) and the aforementioned A/T-rich elements, it is conceivable that Oct-1 binds the betaA/T-rich element under MOV conditions.	bind
20313	2	5853	7	NULL	NULL	NULL	NULL	statement 1	Process		in the presence of					MOV conditions	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_43_30832_s_263	10521475	(Table  I) and the aforementioned A/T-rich elements, it is conceivable that Oct-1 binds the betaA/T-rich element under MOV conditions.	bind
14990	1	5854	5	NULL	NULL	0	NULL	DnaA	NULL		bind	NULL					NULL			oriV	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_17918_s_103	10364238	(Table  I) and the substantially reduced activity  in vitro (Fig.  2 A), suggesting that the function of DnaA box 4 is to initiate DnaA binding to  oriV.	bind
14991	2	5854	5	10	NULL	0	NULL	DnaA	NULL		initiates	NULL			box 4	statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17918_s_103	10364238	(Table  I) and the substantially reduced activity  in vitro (Fig.  2 A), suggesting that the function of DnaA box 4 is to initiate DnaA binding to  oriV.	bind
18000	1	5854	7	NULL	NULL	NULL	NULL	DnaA	NucleicAcid		binds									oriV	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17918_s_103	10364238	(Table  I) and the substantially reduced activity  in vitro (Fig.  2 A), suggesting that the function of DnaA box 4 is to initiate DnaA binding to  oriV.	bind
18001	2	5854	7	NULL	NULL	NULL	NULL	DnaA	NucleicAcid		initiates				box 4	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17918_s_103	10364238	(Table  I) and the substantially reduced activity  in vitro (Fig.  2 A), suggesting that the function of DnaA box 4 is to initiate DnaA binding to  oriV.	bind
14992	1	5855	5	NULL	NULL	0	NULL	VCAM-1	NULL	soluble	bind	NULL				VLA-4 	NULL	high affinity			NULL	on Lck-reconstituted cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_13891_s_208	11102438	(Table  I) and to the markedly higher binding of soluble VCAM-1 to high affinity VLA-4 on Lck-reconstituted cells, no significant difference was noted in the  koff of VLA-4 tethers mediated by the high or low affinity VLA-4 on Lck-reconstituted or Lck-deficient cells, respectively.	bind
18002	1	5855	7	NULL	NULL	NULL	NULL	VCAM-1	GP	soluble	bind					VLA-4 	GP	high affinity			NULL	Lck-reconstituted cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_13891_s_208	11102438	(Table  I) and to the markedly higher binding of soluble VCAM-1 to high affinity VLA-4 on Lck-reconstituted cells, no significant difference was noted in the  koff of VLA-4 tethers mediated by the high or low affinity VLA-4 on Lck-reconstituted or Lck-deficient cells, respectively.	bind
14993	1	5856	5	NULL	NULL	0	NULL	VIP	NULL	mutant	stimulate	NULL		H178A		cAMP	NULL	production of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_9_4990_s_147	9478946	(Table  I) and VIP-stimulated cAMP production (Fig.  2) observed for the H178A, H178D, and H178K mutants was not related to absence of expression at cell surface and was probably due to a drastic loss of intrinsic binding activity, contrasting with the constitutive activity and high VIP binding affinity of the H178R mutant.	bind
14997	2	5856	5	NULL	NULL	0	NULL	VIP	NULL	mutant	stimulate	NULL		H178D		cAMP	NULL	production of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_4990_s_147	9478946	(Table  I) and VIP-stimulated cAMP production (Fig.  2) observed for the H178A, H178D, and H178K mutants was not related to absence of expression at cell surface and was probably due to a drastic loss of intrinsic binding activity, contrasting with the constitutive activity and high VIP binding affinity of the H178R mutant.	bind
14998	3	5856	5	NULL	NULL	0	NULL	VIP	NULL	mutant	stimulate	NULL		H178K		cAMP	NULL	production of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_4990_s_147	9478946	(Table  I) and VIP-stimulated cAMP production (Fig.  2) observed for the H178A, H178D, and H178K mutants was not related to absence of expression at cell surface and was probably due to a drastic loss of intrinsic binding activity, contrasting with the constitutive activity and high VIP binding affinity of the H178R mutant.	bind
44783	4	5856	5	NULL	NULL	0	NULL	VIP	NULL		bind	NULL	high affinity				NULL	mutant	H178R		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_4990_s_147	9478946	(Table  I) and VIP-stimulated cAMP production (Fig.  2) observed for the H178A, H178D, and H178K mutants was not related to absence of expression at cell surface and was probably due to a drastic loss of intrinsic binding activity, contrasting with the constitutive activity and high VIP binding affinity of the H178R mutant.	bind
44784	5	5856	5	NULL	NULL	0	NULL	VIP	NULL		stimulate	NULL				cAMP	NULL	production of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_4990_s_147	9478946	(Table  I) and VIP-stimulated cAMP production (Fig.  2) observed for the H178A, H178D, and H178K mutants was not related to absence of expression at cell surface and was probably due to a drastic loss of intrinsic binding activity, contrasting with the constitutive activity and high VIP binding affinity of the H178R mutant.	bind
44785	6	5856	5	NULL	NULL	0	NULL	statement 1	NULL		occurs due to	NULL	probably			intrinsic binding activity	NULL	drastic loss of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_4990_s_147	9478946	(Table  I) and VIP-stimulated cAMP production (Fig.  2) observed for the H178A, H178D, and H178K mutants was not related to absence of expression at cell surface and was probably due to a drastic loss of intrinsic binding activity, contrasting with the constitutive activity and high VIP binding affinity of the H178R mutant.	bind
44786	7	5856	5	NULL	NULL	0	NULL	statement 2	NULL		occurs due to	NULL	probably			intrinsic binding activity	NULL	drastic loss of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_4990_s_147	9478946	(Table  I) and VIP-stimulated cAMP production (Fig.  2) observed for the H178A, H178D, and H178K mutants was not related to absence of expression at cell surface and was probably due to a drastic loss of intrinsic binding activity, contrasting with the constitutive activity and high VIP binding affinity of the H178R mutant.	bind
44787	8	5856	5	NULL	NULL	0	NULL	statement 3	NULL		occurs due to	NULL	probably			intrinsic binding activity	NULL	drastic loss of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_4990_s_147	9478946	(Table  I) and VIP-stimulated cAMP production (Fig.  2) observed for the H178A, H178D, and H178K mutants was not related to absence of expression at cell surface and was probably due to a drastic loss of intrinsic binding activity, contrasting with the constitutive activity and high VIP binding affinity of the H178R mutant.	bind
18003	1	5856	7	NULL	NULL	NULL	NULL	VIP	GP		stimulate					cAMP	Chemical	production of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_9_4990_s_147	9478946	(Table  I) and VIP-stimulated cAMP production (Fig.  2) observed for the H178A, H178D, and H178K mutants was not related to absence of expression at cell surface and was probably due to a drastic loss of intrinsic binding activity, contrasting with the constitutive activity and high VIP binding affinity of the H178R mutant.	bind
18004	2	5856	7	NULL	NULL	NULL	NULL	VIP	GP	mutant	stimulate			H178A		cAMP	Chemical	production of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_9_4990_s_147	9478946	(Table  I) and VIP-stimulated cAMP production (Fig.  2) observed for the H178A, H178D, and H178K mutants was not related to absence of expression at cell surface and was probably due to a drastic loss of intrinsic binding activity, contrasting with the constitutive activity and high VIP binding affinity of the H178R mutant.	bind
18005	3	5856	7	NULL	NULL	NULL	NULL	VIP	GP	mutant	stimulate			H178D		cAMP	Chemical	production of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_9_4990_s_147	9478946	(Table  I) and VIP-stimulated cAMP production (Fig.  2) observed for the H178A, H178D, and H178K mutants was not related to absence of expression at cell surface and was probably due to a drastic loss of intrinsic binding activity, contrasting with the constitutive activity and high VIP binding affinity of the H178R mutant.	bind
18006	4	5856	7	NULL	NULL	NULL	NULL	VIP	GP	mutant	stimulate			H178K		cAMP	Chemical	production of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_9_4990_s_147	9478946	(Table  I) and VIP-stimulated cAMP production (Fig.  2) observed for the H178A, H178D, and H178K mutants was not related to absence of expression at cell surface and was probably due to a drastic loss of intrinsic binding activity, contrasting with the constitutive activity and high VIP binding affinity of the H178R mutant.	bind
18008	5	5856	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs due to		probably			intrinsic binding activity	Process	drastic loss of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_9_4990_s_147	9478946	(Table  I) and VIP-stimulated cAMP production (Fig.  2) observed for the H178A, H178D, and H178K mutants was not related to absence of expression at cell surface and was probably due to a drastic loss of intrinsic binding activity, contrasting with the constitutive activity and high VIP binding affinity of the H178R mutant.	bind
18009	6	5856	7	NULL	NULL	NULL	NULL	VIP	GP		bind		high affinity					mutant	 H178R		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_9_4990_s_147	9478946	(Table  I) and VIP-stimulated cAMP production (Fig.  2) observed for the H178A, H178D, and H178K mutants was not related to absence of expression at cell surface and was probably due to a drastic loss of intrinsic binding activity, contrasting with the constitutive activity and high VIP binding affinity of the H178R mutant.	bind
14999	1	5857	5	NULL	NULL	0	NULL	ICAM-1 receptor	NULL		bind	NULL				rhinovirus	NULL	human			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_35_32294_s_232	12065582	(Table  I) are low and surprisingly similar to the binding of the ICAM-1 receptor to human rhinovirus ( 16).	bind
18011	1	5857	7	NULL	NULL	NULL	NULL	ICAM-1 receptor	GP		binds					rhinovirus	Organism	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_32294_s_232	12065582	(Table  I) are low and surprisingly similar to the binding of the ICAM-1 receptor to human rhinovirus ( 16).	bind
15000	1	5859	5	NULL	NULL	0	NULL	HSF	NULL		bind	NULL					NULL			HSE	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_50_32168_s_153	8943271	(Table  I) indicate that the first three complexes formed by HSF binding to an HSE contain, respectively, three, six, and nine HSF monomers per DNA molecule.	bind
15001	2	5859	5	NULL	NULL	0	NULL		NULL		contain	NULL			HSE	HSF monomers	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32168_s_153	8943271	(Table  I) indicate that the first three complexes formed by HSF binding to an HSE contain, respectively, three, six, and nine HSF monomers per DNA molecule.	bind
18012	1	5859	7	NULL	NULL	NULL	NULL	HSF	GP		bind									HSE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32168_s_153	8943271	(Table  I) indicate that the first three complexes formed by HSF binding to an HSE contain, respectively, three, six, and nine HSF monomers per DNA molecule.	bind
18015	2	5859	7	NULL	NULL	NULL	NULL				contain				HSE	 HSF monomers	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32168_s_153	8943271	(Table  I) indicate that the first three complexes formed by HSF binding to an HSE contain, respectively, three, six, and nine HSF monomers per DNA molecule.	bind
15004	1	5860	5	NULL	NULL	0	NULL	NG2	NULL		bind	NULL				alpha2 (VI)	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_42_26110_s_129	8824254	(Table  I) indicate that the soluble alpha2 (VI) chain and type VI collagen effectively inhibit the binding of NG2 to alpha2 (VI)-coated wells, whereas the alpha1 (VI) chain and the N9-N2 (VI) chain slightly enhance this interaction.	bind
15005	2	5860	5	NULL	NULL	0	NULL	alpha2 (VI) chain	NULL	soluble	inhibit	NULL	effectively			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_42_26110_s_129	8824254	(Table  I) indicate that the soluble alpha2 (VI) chain and type VI collagen effectively inhibit the binding of NG2 to alpha2 (VI)-coated wells, whereas the alpha1 (VI) chain and the N9-N2 (VI) chain slightly enhance this interaction.	bind
15006	3	5860	5	NULL	NULL	0	NULL	type VI collagen	NULL		inhibit	NULL	efficiently			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_42_26110_s_129	8824254	(Table  I) indicate that the soluble alpha2 (VI) chain and type VI collagen effectively inhibit the binding of NG2 to alpha2 (VI)-coated wells, whereas the alpha1 (VI) chain and the N9-N2 (VI) chain slightly enhance this interaction.	bind
15007	4	5860	5	NULL	NULL	0	NULL	alpha1 (VI) chain	NULL		enhance	NULL	slightly			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_26110_s_129	8824254	(Table  I) indicate that the soluble alpha2 (VI) chain and type VI collagen effectively inhibit the binding of NG2 to alpha2 (VI)-coated wells, whereas the alpha1 (VI) chain and the N9-N2 (VI) chain slightly enhance this interaction.	bind
15008	5	5860	5	10	NULL	0	NULL		NULL		enhance	NULL	slightly	N9-N2 (VI) chain		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_26110_s_129	8824254	(Table  I) indicate that the soluble alpha2 (VI) chain and type VI collagen effectively inhibit the binding of NG2 to alpha2 (VI)-coated wells, whereas the alpha1 (VI) chain and the N9-N2 (VI) chain slightly enhance this interaction.	bind
18014	1	5860	7	NULL	NULL	NULL	NULL	NG2	Chemical		bind					alpha2 (VI)	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_26110_s_129	8824254	(Table  I) indicate that the soluble alpha2 (VI) chain and type VI collagen effectively inhibit the binding of NG2 to alpha2 (VI)-coated wells, whereas the alpha1 (VI) chain and the N9-N2 (VI) chain slightly enhance this interaction.	bind
18016	2	5860	7	NULL	NULL	NULL	NULL	alpha2 (VI) chain	GP	soluble	inhibit		effectively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_26110_s_129	8824254	(Table  I) indicate that the soluble alpha2 (VI) chain and type VI collagen effectively inhibit the binding of NG2 to alpha2 (VI)-coated wells, whereas the alpha1 (VI) chain and the N9-N2 (VI) chain slightly enhance this interaction.	bind
18017	3	5860	7	NULL	NULL	NULL	NULL	type VI collagen	GP		inhibit		effectively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_26110_s_129	8824254	(Table  I) indicate that the soluble alpha2 (VI) chain and type VI collagen effectively inhibit the binding of NG2 to alpha2 (VI)-coated wells, whereas the alpha1 (VI) chain and the N9-N2 (VI) chain slightly enhance this interaction.	bind
18018	4	5860	7	NULL	NULL	NULL	NULL	alpha1 (VI) chain	GP		enhance		slightly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_26110_s_129	8824254	(Table  I) indicate that the soluble alpha2 (VI) chain and type VI collagen effectively inhibit the binding of NG2 to alpha2 (VI)-coated wells, whereas the alpha1 (VI) chain and the N9-N2 (VI) chain slightly enhance this interaction.	bind
18019	5	5860	7	NULL	NULL	NULL	NULL				enhance		slightly	N9-N2 (VI) chain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_26110_s_129	8824254	(Table  I) indicate that the soluble alpha2 (VI) chain and type VI collagen effectively inhibit the binding of NG2 to alpha2 (VI)-coated wells, whereas the alpha1 (VI) chain and the N9-N2 (VI) chain slightly enhance this interaction.	bind
15011	1	5861	5	10	NULL	0	NULL	E-selectin	NULL		improves	NULL		region 4		HL-60 cell	NULL	binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6254_s_80	9497351	(Table  I) indicate that when the three lysine residues of region 5 are present, E-selectin region 4 improves the HL-60 cell binding activity, whereas region 4 of P-selectin actually causes a loss of binding activity.	bind
15012	2	5861	5	NULL	NULL	0	NULL		NULL		is required for	NULL		three lysine residues of region 5		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_11_6254_s_80	9497351	(Table  I) indicate that when the three lysine residues of region 5 are present, E-selectin region 4 improves the HL-60 cell binding activity, whereas region 4 of P-selectin actually causes a loss of binding activity.	bind
15013	3	5861	5	10	NULL	0	NULL	P-selectin	NULL		causes	NULL		region 4		HL-60	NULL	loss of;; binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6254_s_80	9497351	(Table  I) indicate that when the three lysine residues of region 5 are present, E-selectin region 4 improves the HL-60 cell binding activity, whereas region 4 of P-selectin actually causes a loss of binding activity.	bind
18020	1	5861	7	NULL	NULL	NULL	NULL	E-selectin	GP		improves			region 4		HL-60 cell	Cell	binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6254_s_80	9497351	(Table  I) indicate that when the three lysine residues of region 5 are present, E-selectin region 4 improves the HL-60 cell binding activity, whereas region 4 of P-selectin actually causes a loss of binding activity.	bind
18021	2	5861	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs upon the presence of 								three lysine residues region 5		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6254_s_80	9497351	(Table  I) indicate that when the three lysine residues of region 5 are present, E-selectin region 4 improves the HL-60 cell binding activity, whereas region 4 of P-selectin actually causes a loss of binding activity.	bind
18022	3	5861	7	NULL	NULL	NULL	NULL	P-selectin	GP		cause			region 4		HL-60 cell	Cell	loss of;; binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6254_s_80	9497351	(Table  I) indicate that when the three lysine residues of region 5 are present, E-selectin region 4 improves the HL-60 cell binding activity, whereas region 4 of P-selectin actually causes a loss of binding activity.	bind
18023	4	5861	7	NULL	NULL	NULL	NULL	statement 3	Process		occurs upon the presence of								three lysine residues region 5		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6254_s_80	9497351	(Table  I) indicate that when the three lysine residues of region 5 are present, E-selectin region 4 improves the HL-60 cell binding activity, whereas region 4 of P-selectin actually causes a loss of binding activity.	bind
15018	1	5862	5	10	NULL	0	NULL	polyene macrolide antibiotic			bind					membrane ergosterol					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_40_37855_s_127	12133835	(Table  I) or in the sensitivities to various agents such as amphotericin B, a polyene macrolide antibiotic that binds to membrane ergosterol and induces cellular leakage ( 34) (Fig.  1 B), detergents (SDS and Triton X-100), and ethanol (data not shown).	bind
15019	2	5862	5	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL				cellular leakage	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37855_s_127	12133835	(Table  I) or in the sensitivities to various agents such as amphotericin B, a polyene macrolide antibiotic that binds to membrane ergosterol and induces cellular leakage ( 34) (Fig.  1 B), detergents (SDS and Triton X-100), and ethanol (data not shown).	bind
18024	1	5862	7	NULL	NULL	NULL	NULL	polyene macrolide antibiotic	Chemical		binds to					membrane ergosterol	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_40_37855_s_127	12133835	(Table  I) or in the sensitivities to various agents such as amphotericin B, a polyene macrolide antibiotic that binds to membrane ergosterol and induces cellular leakage ( 34) (Fig.  1 B), detergents (SDS and Triton X-100), and ethanol (data not shown).	bind
18025	2	5862	7	NULL	NULL	NULL	NULL	statement 1	Process		induce					cellular leakage	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_40_37855_s_127	12133835	(Table  I) or in the sensitivities to various agents such as amphotericin B, a polyene macrolide antibiotic that binds to membrane ergosterol and induces cellular leakage ( 34) (Fig.  1 B), detergents (SDS and Triton X-100), and ethanol (data not shown).	bind
15021	1	5863	5	NULL	NULL	0	NULL	STAT3	NULL		bind	NULL				SIE probe	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_16_10723_s_149	10196143	(Table  I) or LIF-induced STAT3 binding to the SIE probe (data not shown).	bind
15022	2	5863	5	NULL	NULL	0	NULL	LIF	NULL		induce	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_16_10723_s_149	10196143	(Table  I) or LIF-induced STAT3 binding to the SIE probe (data not shown).	bind
18026	1	5863	7	NULL	NULL	NULL	NULL	STAT3	GP		bind					SIE probe	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_16_10723_s_149	10196143	(Table  I) or LIF-induced STAT3 binding to the SIE probe (data not shown).	bind
18027	2	5863	7	NULL	NULL	NULL	NULL	LIF	GP		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_16_10723_s_149	10196143	(Table  I) or LIF-induced STAT3 binding to the SIE probe (data not shown).	bind
15023	1	5864	5	NULL	NULL	0	NULL	galanin	NULL		bind	NULL				GalR3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_136	9405385	(Table  I) revealed that, like GalR2, Gly1 of galanin is not critical for galanin to bind GalR3, whereas this residue is important for binding of galanin to GalR1 ( 15).	bind
15024	2	5864	5	NULL	NULL	0	NULL	galanin	NULL		is not critical for	NULL		Gly1		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_136	9405385	(Table  I) revealed that, like GalR2, Gly1 of galanin is not critical for galanin to bind GalR3, whereas this residue is important for binding of galanin to GalR1 ( 15).	bind
15025	3	5864	5	NULL	NULL	0	NULL	galanin	NULL		bind	NULL				GalR1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_136	9405385	(Table  I) revealed that, like GalR2, Gly1 of galanin is not critical for galanin to bind GalR3, whereas this residue is important for binding of galanin to GalR1 ( 15).	bind
15026	4	5864	5	NULL	NULL	0	NULL	galanin	NULL		is important for	NULL		Gly1		statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_136	9405385	(Table  I) revealed that, like GalR2, Gly1 of galanin is not critical for galanin to bind GalR3, whereas this residue is important for binding of galanin to GalR1 ( 15).	bind
18028	1	5864	7	NULL	NULL	NULL	NULL	galanin	GP		bind					GalR3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_136	9405385	(Table  I) revealed that, like GalR2, Gly1 of galanin is not critical for galanin to bind GalR3, whereas this residue is important for binding of galanin to GalR1 ( 15).	bind
18029	2	5864	7	NULL	NULL	NULL	NULL	galanin	GP		bind					 GalR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_136	9405385	(Table  I) revealed that, like GalR2, Gly1 of galanin is not critical for galanin to bind GalR3, whereas this residue is important for binding of galanin to GalR1 ( 15).	bind
18030	3	5864	7	NULL	NULL	NULL	NULL	galanin	GP		is not critical for			Gly1		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_136	9405385	(Table  I) revealed that, like GalR2, Gly1 of galanin is not critical for galanin to bind GalR3, whereas this residue is important for binding of galanin to GalR1 ( 15).	bind
18031	4	5864	7	NULL	NULL	NULL	NULL	galanin	GP		is important for			Gly1		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_136	9405385	(Table  I) revealed that, like GalR2, Gly1 of galanin is not critical for galanin to bind GalR3, whereas this residue is important for binding of galanin to GalR1 ( 15).	bind
15027	1	5865	5	NULL	NULL	0	NULL	galactose	NULL		bind	NULL				WBA I	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_37_28483_s_136	10837488	(Table  I) than those involved in the binding of galactose with WBA I ( 10) and jacalin.	bind
15028	2	5865	5	NULL	NULL	0	NULL	galactose	NULL		bind	NULL				jacalin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_37_28483_s_136	10837488	(Table  I) than those involved in the binding of galactose with WBA I ( 10) and jacalin.	bind
18032	1	5865	7	NULL	NULL	NULL	NULL	galactose	Chemical		bind					WBA I	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_37_28483_s_136	10837488	(Table  I) than those involved in the binding of galactose with WBA I ( 10) and jacalin.	bind
18033	2	5865	7	NULL	NULL	NULL	NULL	galactose	Chemical		bind					jacalin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_37_28483_s_136	10837488	(Table  I) than those involved in the binding of galactose with WBA I ( 10) and jacalin.	bind
18034	1	5866	7	NULL	NULL	NULL	NULL	MHC I-binding peptide	GP	unextended 	chaperoned by					hsp70	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_20_17163_s_184	11278929	(Table  I) that (i) treatment with lactacystin inhibited re-presentation of all the  extended peptides, (ii) surprisingly, treatment of cells with lactacystin inhibited re-presentation of even the  precise unextended MHC I-binding peptides when chaperoned by hsp70 or hsp90; (iii) in another surprise, re-presentation of the precise MHC I binding peptide complexed to gp96 was not inhibited by lactacystin.	bind
18035	2	5866	7	NULL	NULL	NULL	NULL	MHC I-binding peptide	GP	unextended 	chaperoned by					hsp90	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_20_17163_s_184	11278929	(Table  I) that (i) treatment with lactacystin inhibited re-presentation of all the  extended peptides, (ii) surprisingly, treatment of cells with lactacystin inhibited re-presentation of even the  precise unextended MHC I-binding peptides when chaperoned by hsp70 or hsp90; (iii) in another surprise, re-presentation of the precise MHC I binding peptide complexed to gp96 was not inhibited by lactacystin.	bind
18036	3	5866	7	NULL	NULL	NULL	NULL	lactacystin	GP		inhibits					statement 1	Process	 re-presentation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_20_17163_s_184	11278929	(Table  I) that (i) treatment with lactacystin inhibited re-presentation of all the  extended peptides, (ii) surprisingly, treatment of cells with lactacystin inhibited re-presentation of even the  precise unextended MHC I-binding peptides when chaperoned by hsp70 or hsp90; (iii) in another surprise, re-presentation of the precise MHC I binding peptide complexed to gp96 was not inhibited by lactacystin.	bind
18037	4	5866	7	NULL	NULL	NULL	NULL	lactacystin	GP		inhibits					statement 2	Process	re-presentation of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_20_17163_s_184	11278929	(Table  I) that (i) treatment with lactacystin inhibited re-presentation of all the  extended peptides, (ii) surprisingly, treatment of cells with lactacystin inhibited re-presentation of even the  precise unextended MHC I-binding peptides when chaperoned by hsp70 or hsp90; (iii) in another surprise, re-presentation of the precise MHC I binding peptide complexed to gp96 was not inhibited by lactacystin.	bind
18038	5	5866	7	NULL	NULL	NULL	NULL	MHC I binding peptide	GP		forms complex with					gp96	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_20_17163_s_184	11278929	(Table  I) that (i) treatment with lactacystin inhibited re-presentation of all the  extended peptides, (ii) surprisingly, treatment of cells with lactacystin inhibited re-presentation of even the  precise unextended MHC I-binding peptides when chaperoned by hsp70 or hsp90; (iii) in another surprise, re-presentation of the precise MHC I binding peptide complexed to gp96 was not inhibited by lactacystin.	bind
18039	6	5866	7	NULL	NULL	NULL	NULL	lactacystin	GP		does not inhibit					statement 5	Process	re-presentation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_20_17163_s_184	11278929	(Table  I) that (i) treatment with lactacystin inhibited re-presentation of all the  extended peptides, (ii) surprisingly, treatment of cells with lactacystin inhibited re-presentation of even the  precise unextended MHC I-binding peptides when chaperoned by hsp70 or hsp90; (iii) in another surprise, re-presentation of the precise MHC I binding peptide complexed to gp96 was not inhibited by lactacystin.	bind
15029	1	5867	5	NULL	NULL	0	NULL	factor Xa	NULL		bind	NULL				PS membranes	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_8_5679_s_171	12438309	(Table  I) to that reported for factor Xa bound to PS membranes ( ), we see a 20-fold increase in rate because of adding factor Va to the PS membrane.	bind
15030	2	5867	5	NULL	NULL	0	NULL	factor Va	NULL		added to	NULL				PS membrane	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5679_s_171	12438309	(Table  I) to that reported for factor Xa bound to PS membranes ( ), we see a 20-fold increase in rate because of adding factor Va to the PS membrane.	bind
20260	3	5867	5	NULL	NULL	0	NULL	statement 2	NULL		increases	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_8_5679_s_171	12438309	(Table  I) to that reported for factor Xa bound to PS membranes ( ), we see a 20-fold increase in rate because of adding factor Va to the PS membrane.	bind
18040	1	5867	7	NULL	NULL	NULL	NULL	 factor Xa	GP		bind					PS membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5679_s_171	12438309	(Table  I) to that reported for factor Xa bound to PS membranes ( ), we see a 20-fold increase in rate because of adding factor Va to the PS membrane.	bind
18041	2	5867	7	NULL	NULL	NULL	NULL	factor Va	GP		added to					PS membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5679_s_171	12438309	(Table  I) to that reported for factor Xa bound to PS membranes ( ), we see a 20-fold increase in rate because of adding factor Va to the PS membrane.	bind
18042	3	5867	7	NULL	NULL	NULL	NULL	statement 2	Process		increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5679_s_171	12438309	(Table  I) to that reported for factor Xa bound to PS membranes ( ), we see a 20-fold increase in rate because of adding factor Va to the PS membrane.	bind
15031	1	5868	5	NULL	NULL	0	NULL	factor Xa	NULL		bind	NULL				PS membranes	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_8_5679_s_171	12438309	(Table  I) to that reported for factor Xa bound to PS membranes ( 2), we see a 20-fold increase in rate because of adding factor Va to the PS membrane.	bind
15032	2	5868	5	NULL	NULL	0	NULL	factor Va	NULL		added to	NULL				PS membrane	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_8_5679_s_171	12438309	(Table  I) to that reported for factor Xa bound to PS membranes ( 2), we see a 20-fold increase in rate because of adding factor Va to the PS membrane.	bind
20261	3	5868	5	NULL	NULL	0	NULL	statement 2	NULL		increases	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_8_5679_s_171	12438309	(Table  I) to that reported for factor Xa bound to PS membranes ( 2), we see a 20-fold increase in rate because of adding factor Va to the PS membrane.	bind
15035	1	5869	5	NULL	NULL	0	NULL	mAb	NULL		bind	NULL				G-CSF-R	NULL	WT			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_39_36779_s_134	11468284	(Table  I) were normalized with respect to level of receptor expression and level of binding of each mAb to WT G-CSF-R.	bind
18043	1	5869	7	NULL	NULL	NULL	NULL	mAb	GP		bind					G-CSF-R	GP	WT			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36779_s_134	11468284	(Table  I) were normalized with respect to level of receptor expression and level of binding of each mAb to WT G-CSF-R.	bind
15036	1	5870	5	NULL	NULL	0	NULL	fragment B of PKC lambda	NULL		bind	NULL				FRS2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_27_19025_s_292	10383403	(Table  I) where only fragment B of PKC lambda binds to FRS2.	bind
18044	1	5870	7	NULL	NULL	NULL	NULL	fragment B PKC lambda	GP		binds to					FRS2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_27_19025_s_292	10383403	(Table  I) where only fragment B of PKC lambda binds to FRS2.	bind
15037	1	5871	5	NULL	NULL	0	NULL	H4B	NULL		bind	NULL					NULL	mutant	Trp-409		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_41_38280_s_200	11479310	(Table  I), and since we detect the same spectral changes induced by the binding of H4B to the Trp-409 mutants as those that we observed in the low frequency region upon binding of H4B to wild type nNOSox, we conclude that the structure of the heme pockets of the mutants is similar to that of the wild type enzyme.	bind
15038	2	5871	5	NULL	NULL	0	NULL	H4B	NULL		bind	NULL				nNOSox	NULL	wild-type			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_41_38280_s_200	11479310	(Table  I), and since we detect the same spectral changes induced by the binding of H4B to the Trp-409 mutants as those that we observed in the low frequency region upon binding of H4B to wild type nNOSox, we conclude that the structure of the heme pockets of the mutants is similar to that of the wild type enzyme.	bind
18045	1	5871	7	NULL	NULL	NULL	NULL	 H4B	GP		bind							mutant	Trp-409		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_41_38280_s_200	11479310	(Table  I), and since we detect the same spectral changes induced by the binding of H4B to the Trp-409 mutants as those that we observed in the low frequency region upon binding of H4B to wild type nNOSox, we conclude that the structure of the heme pockets of the mutants is similar to that of the wild type enzyme.	bind
18046	2	5871	7	NULL	NULL	NULL	NULL	H4B 	GP		bind					 nNOSox	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_41_38280_s_200	11479310	(Table  I), and since we detect the same spectral changes induced by the binding of H4B to the Trp-409 mutants as those that we observed in the low frequency region upon binding of H4B to wild type nNOSox, we conclude that the structure of the heme pockets of the mutants is similar to that of the wild type enzyme.	bind
15039	1	5872	5	NULL	NULL	0	NULL	GST-CtBP	NULL		bind	NULL				Ad12 E1A	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_33_20867_s_103	9694833	(Table  I), and the ability of each to inhibit the binding of GST-CtBP to Ad12 E1A was determined.	bind
18094	1	5872	7	NULL	NULL	NULL	NULL	GST-CtBP	GP		bind					 Ad12 E1A	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_33_20867_s_103	9694833	(Table  I), and the ability of each to inhibit the binding of GST-CtBP to Ad12 E1A was determined.	bind
15040	1	5873	5	NULL	NULL	0	NULL	growth factors	NULL		activate	NULL				SRF	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_43_30832_s_236	10521475	(Table  I), and the observations that the SRF is activated by growth factors, elevated levels of intracellular calcium, and mechanical stretch (three stimuli associated with MOV), we investigated whether the SRF might comprise a component of the enriched MOV-P binding activity.	bind
20336	2	5873	5	NULL	NULL	0	NULL	intracellular calcium	NULL	elevated levels of	activate	NULL				SRF	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_43_30832_s_236	10521475	(Table  I), and the observations that the SRF is activated by growth factors, elevated levels of intracellular calcium, and mechanical stretch (three stimuli associated with MOV), we investigated whether the SRF might comprise a component of the enriched MOV-P binding activity.	bind
20337	3	5873	5	NULL	NULL	0	NULL	mechanical stretch	NULL		activate	NULL				SRF	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_43_30832_s_236	10521475	(Table  I), and the observations that the SRF is activated by growth factors, elevated levels of intracellular calcium, and mechanical stretch (three stimuli associated with MOV), we investigated whether the SRF might comprise a component of the enriched MOV-P binding activity.	bind
18095	1	5873	7	NULL	NULL	NULL	NULL	growth factors	GP		activates					SRF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_43_30832_s_236	10521475	(Table  I), and the observations that the SRF is activated by growth factors, elevated levels of intracellular calcium, and mechanical stretch (three stimuli associated with MOV), we investigated whether the SRF might comprise a component of the enriched MOV-P binding activity.	bind
18096	2	5873	7	NULL	NULL	NULL	NULL	intracellular calcium	Chemical	elevated levels of	activates					SRF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_43_30832_s_236	10521475	(Table  I), and the observations that the SRF is activated by growth factors, elevated levels of intracellular calcium, and mechanical stretch (three stimuli associated with MOV), we investigated whether the SRF might comprise a component of the enriched MOV-P binding activity.	bind
20322	3	5873	7	NULL	NULL	NULL	NULL	mechanical stretch	Process		activates					SRF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_43_30832_s_236	10521475	(Table  I), and the observations that the SRF is activated by growth factors, elevated levels of intracellular calcium, and mechanical stretch (three stimuli associated with MOV), we investigated whether the SRF might comprise a component of the enriched MOV-P binding activity.	bind
15041	1	5878	5	NULL	NULL	0	NULL	DnaA protein	NULL		bind	NULL				R4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_29_17035_s_150	8663334	(Table  I), DnaA protein bound to R4 with about 3-fold higher affinity than to R1 (Fig.  7).	bind
15042	2	5878	5	NULL	NULL	0	NULL	DnaA protein	NULL		bind	NULL				R1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_29_17035_s_150	8663334	(Table  I), DnaA protein bound to R4 with about 3-fold higher affinity than to R1 (Fig.  7).	bind
15043	3	5878	5	NULL	NULL	0	NULL	statement 1	NULL		has higher affinity than	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_29_17035_s_150	8663334	(Table  I), DnaA protein bound to R4 with about 3-fold higher affinity than to R1 (Fig.  7).	bind
18097	1	5878	7	NULL	NULL	NULL	NULL	DnaA protein	GP		bind					R4	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_29_17035_s_150	8663334	(Table  I), DnaA protein bound to R4 with about 3-fold higher affinity than to R1 (Fig.  7).	bind
18098	2	5878	7	NULL	NULL	NULL	NULL	DnaA protein	GP		bind					R1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_29_17035_s_150	8663334	(Table  I), DnaA protein bound to R4 with about 3-fold higher affinity than to R1 (Fig.  7).	bind
18099	3	5878	7	NULL	NULL	NULL	NULL	statement 1	Process		has higher affinity than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_29_17035_s_150	8663334	(Table  I), DnaA protein bound to R4 with about 3-fold higher affinity than to R1 (Fig.  7).	bind
15044	1	5879	5	NULL	NULL	0	NULL	peptide inhibitor	NULL		bind	NULL				IKKbeta	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_46_32655_s_238	10551820	(Table  I), indicating that the binding of the peptide inhibitor to IKKbeta has no effect on the affinity for ATP.	bind
15045	2	5879	5	NULL	NULL	0	NULL	statement 1	NULL		does not effect	NULL				ATP	NULL	affinity for 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_46_32655_s_238	10551820	(Table  I), indicating that the binding of the peptide inhibitor to IKKbeta has no effect on the affinity for ATP.	bind
18100	1	5879	7	NULL	NULL	NULL	NULL	peptide inhibitor	GP		bind					IKKbeta	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_32655_s_238	10551820	(Table  I), indicating that the binding of the peptide inhibitor to IKKbeta has no effect on the affinity for ATP.	bind
18101	2	5879	7	NULL	NULL	NULL	NULL	statement 1	Process		has no affinity for					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_32655_s_238	10551820	(Table  I), indicating that the binding of the peptide inhibitor to IKKbeta has no effect on the affinity for ATP.	bind
15279	1	5880	5	NULL	NULL	0	NULL	vWf	NULL		bind	NULL				collagen	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_18_12300_s_238	10212199	(Table  I), indicating that the rate of association of factor VIII with vWf is not significantly affected after vWf binds to collagen.	bind
15280	2	5880	5	NULL	NULL	0	NULL	factor VIII	NULL		associate with	NULL				vWf	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_18_12300_s_238	10212199	(Table  I), indicating that the rate of association of factor VIII with vWf is not significantly affected after vWf binds to collagen.	bind
15281	3	5880	5	10	NULL	0	NULL	statement 2	NULL		does not affect	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12300_s_238	10212199	(Table  I), indicating that the rate of association of factor VIII with vWf is not significantly affected after vWf binds to collagen.	bind
18102	1	5880	7	NULL	NULL	NULL	NULL	 factor VIII 	GP		bind					vWf	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12300_s_238	10212199	(Table  I), indicating that the rate of association of factor VIII with vWf is not significantly affected after vWf binds to collagen.	bind
18103	2	5880	7	NULL	NULL	NULL	NULL	 vWf	GP		binds to					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12300_s_238	10212199	(Table  I), indicating that the rate of association of factor VIII with vWf is not significantly affected after vWf binds to collagen.	bind
18104	3	5880	7	NULL	NULL	NULL	NULL	statement 1	Process		does not affect					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12300_s_238	10212199	(Table  I), indicating that the rate of association of factor VIII with vWf is not significantly affected after vWf binds to collagen.	bind
15282	1	5881	5	NULL	NULL	0	NULL	IRS 3	NULL		does not bind	NULL				FKHR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_14_11782_s_269	12556524	(Table  I), its expression was still not induced by FKHR overexpression (Fig.  5), suggesting that IRS 3 cannot bind FKHR even when multimerized.	bind
15283	2	5881	5	NULL	NULL	0	NULL	IRS 3	NULL	multimerized	does not bind	NULL				FKHR	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_14_11782_s_269	12556524	(Table  I), its expression was still not induced by FKHR overexpression (Fig.  5), suggesting that IRS 3 cannot bind FKHR even when multimerized.	bind
18105	1	5881	7	NULL	NULL	NULL	NULL	IRS 3	GP		does not bind					FKHR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_14_11782_s_269	12556524	(Table  I), its expression was still not induced by FKHR overexpression (Fig.  5), suggesting that IRS 3 cannot bind FKHR even when multimerized.	bind
18106	2	5881	7	NULL	NULL	NULL	NULL	IRS 3	GP	multimerized 	does not bind					FKHR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_14_11782_s_269	12556524	(Table  I), its expression was still not induced by FKHR overexpression (Fig.  5), suggesting that IRS 3 cannot bind FKHR even when multimerized.	bind
15289	1	5883	5	NULL	NULL	0	NULL	PABA	NULL		bind	NULL				FXa	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_47_36876_s_359	10973949	(Table  I), PABA (Table  II), or TFPI (Table  III) binding to FXa ~4.5-fold.	bind
15290	2	5883	5	NULL	NULL	0	NULL	TFPI	NULL		bind	NULL				FXa	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_47_36876_s_359	10973949	(Table  I), PABA (Table  II), or TFPI (Table  III) binding to FXa ~4.5-fold.	bind
18110	1	5883	7	NULL	NULL	NULL	NULL	PABA	Chemical		bind					FXa	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_47_36876_s_359	10973949	(Table  I), PABA (Table  II), or TFPI (Table  III) binding to FXa ~4.5-fold.	bind
18111	2	5883	7	NULL	NULL	NULL	NULL	TFPI	GP		bind					FXa	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_47_36876_s_359	10973949	(Table  I), PABA (Table  II), or TFPI (Table  III) binding to FXa ~4.5-fold.	bind
15322	1	5884	5	NULL	NULL	0	NULL	G-CSF	NULL	mutant	bind	NULL		K23A		GR	NULL		R288A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_108	10364174	(Table  I), the mutant/WT ratios of the binding affinity of K23A, E46A, and D112A G-CSFs to (R288A)GR were greater than the corresponding ratios with WT-GR, suggesting a synergistic effect of receptor and G-CSF mutations.	bind
15324	2	5884	5	NULL	NULL	0	NULL	G-CSF	NULL	mutant	bind	NULL		E46A		GR	NULL		R288A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_108	10364174	(Table  I), the mutant/WT ratios of the binding affinity of K23A, E46A, and D112A G-CSFs to (R288A)GR were greater than the corresponding ratios with WT-GR, suggesting a synergistic effect of receptor and G-CSF mutations.	bind
15326	3	5884	5	NULL	NULL	0	NULL	G-CSF	NULL	mutant	bind	NULL		D112A		GR	NULL		R288A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_108	10364174	(Table  I), the mutant/WT ratios of the binding affinity of K23A, E46A, and D112A G-CSFs to (R288A)GR were greater than the corresponding ratios with WT-GR, suggesting a synergistic effect of receptor and G-CSF mutations.	bind
44834	4	5884	5	NULL	NULL	0	NULL	G-CSF	NULL	mutant	bind	NULL		K23A		GR	NULL	WT			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_108	10364174	(Table  I), the mutant/WT ratios of the binding affinity of K23A, E46A, and D112A G-CSFs to (R288A)GR were greater than the corresponding ratios with WT-GR, suggesting a synergistic effect of receptor and G-CSF mutations.	bind
44835	5	5884	5	NULL	NULL	0	NULL	G-CSF	NULL	mutant	bind	NULL		E46A		GR	NULL	WT			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_108	10364174	(Table  I), the mutant/WT ratios of the binding affinity of K23A, E46A, and D112A G-CSFs to (R288A)GR were greater than the corresponding ratios with WT-GR, suggesting a synergistic effect of receptor and G-CSF mutations.	bind
44836	6	5884	5	NULL	NULL	0	NULL	G-CSF	NULL	mutant	bind	NULL		D112A		GR	NULL	WT			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_108	10364174	(Table  I), the mutant/WT ratios of the binding affinity of K23A, E46A, and D112A G-CSFs to (R288A)GR were greater than the corresponding ratios with WT-GR, suggesting a synergistic effect of receptor and G-CSF mutations.	bind
44837	7	5884	5	NULL	NULL	0	NULL	statement 1	NULL		greater than	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_108	10364174	(Table  I), the mutant/WT ratios of the binding affinity of K23A, E46A, and D112A G-CSFs to (R288A)GR were greater than the corresponding ratios with WT-GR, suggesting a synergistic effect of receptor and G-CSF mutations.	bind
44838	8	5884	5	NULL	NULL	0	NULL	statement 2	NULL		greater than	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_108	10364174	(Table  I), the mutant/WT ratios of the binding affinity of K23A, E46A, and D112A G-CSFs to (R288A)GR were greater than the corresponding ratios with WT-GR, suggesting a synergistic effect of receptor and G-CSF mutations.	bind
44839	9	5884	5	NULL	NULL	0	NULL	statement 3	NULL		greater than	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_108	10364174	(Table  I), the mutant/WT ratios of the binding affinity of K23A, E46A, and D112A G-CSFs to (R288A)GR were greater than the corresponding ratios with WT-GR, suggesting a synergistic effect of receptor and G-CSF mutations.	bind
18112	1	5884	7	NULL	NULL	NULL	NULL	G-CSF	GP	mutant	bind 			K23A		GR	GP		R288A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_108	10364174	(Table  I), the mutant/WT ratios of the binding affinity of K23A, E46A, and D112A G-CSFs to (R288A)GR were greater than the corresponding ratios with WT-GR, suggesting a synergistic effect of receptor and G-CSF mutations.	bind
18113	2	5884	7	NULL	NULL	NULL	NULL	G-CSF	GP	mutant	bind			E46A		GR	GP		R288A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_108	10364174	(Table  I), the mutant/WT ratios of the binding affinity of K23A, E46A, and D112A G-CSFs to (R288A)GR were greater than the corresponding ratios with WT-GR, suggesting a synergistic effect of receptor and G-CSF mutations.	bind
18114	3	5884	7	NULL	NULL	NULL	NULL	G-CSF	GP	mutant	bind			D112A		GR	GP		R288A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_108	10364174	(Table  I), the mutant/WT ratios of the binding affinity of K23A, E46A, and D112A G-CSFs to (R288A)GR were greater than the corresponding ratios with WT-GR, suggesting a synergistic effect of receptor and G-CSF mutations.	bind
18115	4	5884	7	NULL	NULL	NULL	NULL	G-CSF	GP	mutant	bind			K23A		GR	GP	WT			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_108	10364174	(Table  I), the mutant/WT ratios of the binding affinity of K23A, E46A, and D112A G-CSFs to (R288A)GR were greater than the corresponding ratios with WT-GR, suggesting a synergistic effect of receptor and G-CSF mutations.	bind
18116	5	5884	7	NULL	NULL	NULL	NULL	G-CSF	GP	mutant	bind			E46A		GR	GP	WT			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_108	10364174	(Table  I), the mutant/WT ratios of the binding affinity of K23A, E46A, and D112A G-CSFs to (R288A)GR were greater than the corresponding ratios with WT-GR, suggesting a synergistic effect of receptor and G-CSF mutations.	bind
18117	6	5884	7	NULL	NULL	NULL	NULL	G-CSF	GP	mutant	bind			D112A 		GR	GP	WT			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_108	10364174	(Table  I), the mutant/WT ratios of the binding affinity of K23A, E46A, and D112A G-CSFs to (R288A)GR were greater than the corresponding ratios with WT-GR, suggesting a synergistic effect of receptor and G-CSF mutations.	bind
18118	7	5884	7	NULL	NULL	NULL	NULL	statement 1	Process		is greater than					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_108	10364174	(Table  I), the mutant/WT ratios of the binding affinity of K23A, E46A, and D112A G-CSFs to (R288A)GR were greater than the corresponding ratios with WT-GR, suggesting a synergistic effect of receptor and G-CSF mutations.	bind
18119	8	5884	7	NULL	NULL	NULL	NULL	statement 2	Process		is greater than					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_108	10364174	(Table  I), the mutant/WT ratios of the binding affinity of K23A, E46A, and D112A G-CSFs to (R288A)GR were greater than the corresponding ratios with WT-GR, suggesting a synergistic effect of receptor and G-CSF mutations.	bind
18120	9	5884	7	NULL	NULL	NULL	NULL	statement 3	Process		is greater than					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17445_s_108	10364174	(Table  I), the mutant/WT ratios of the binding affinity of K23A, E46A, and D112A G-CSFs to (R288A)GR were greater than the corresponding ratios with WT-GR, suggesting a synergistic effect of receptor and G-CSF mutations.	bind
15616	1	5886	5	NULL	NULL	0	NULL	mAb 8E6	NULL		does not block	NULL	directly			PAI-1	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_11_9395_s_333	11773078	(Table  I), together with the observation that mAb 8E6 does not directly block PAI-1 binding (Figs.  6 and  7), argues that the observed inhibition reflects steric interference of PAI-1 binding to one site rather than the existence of two distinct PAI-1 binding sites.	bind
18121	1	5886	7	NULL	NULL	NULL	NULL	mAb 8E6	GP		does not block		directly			PAI-1	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_11_9395_s_333	11773078	(Table  I), together with the observation that mAb 8E6 does not directly block PAI-1 binding (Figs.  6 and  7), argues that the observed inhibition reflects steric interference of PAI-1 binding to one site rather than the existence of two distinct PAI-1 binding sites.	bind
15317	1	5888	5	10	NULL	0	NULL	isoproterenol 			increased		robustly			cAMP 		levels of			NULL	CHO cells expressing beta2-adrenergic receptor	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_8_5692_s_126	11069896	(Table  I), whereas isoproterenol (2 muM) caused a robust 6-fold increase in cAMP levels in CHO cells expressing the beta2-adrenergic receptor.	bind
18126	1	5888	7	NULL	NULL	NULL	NULL	isoproterenol	Chemical		increase		robustly			cAMP	Chemical	levels of			NULL	CHO cells expressing the beta2-adrenergic receptor	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_8_5692_s_126	11069896	(Table  I), whereas isoproterenol (2 muM) caused a robust 6-fold increase in cAMP levels in CHO cells expressing the beta2-adrenergic receptor.	bind
15318	1	5892	5	NULL	NULL	0	NULL	hdm2	NULL		bind	NULL				p53	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_17_2_554_s_264	9430646	(Table  I); both hdm2 and E1B-55 kDa proteins bind to p53 (Sarnow  et al., 1982  ; Momand  et al., 1992  ).	bind
15320	2	5892	5	NULL	NULL	0	NULL	E1B-55 kDa protein	NULL		bind	NULL				p53	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_17_2_554_s_264	9430646	(Table  I); both hdm2 and E1B-55 kDa proteins bind to p53 (Sarnow  et al., 1982  ; Momand  et al., 1992  ).	bind
18127	1	5892	7	NULL	NULL	NULL	NULL	hdm2	GP		bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_2_554_s_264	9430646	(Table  I); both hdm2 and E1B-55 kDa proteins bind to p53 (Sarnow  et al., 1982  ; Momand  et al., 1992  ).	bind
18128	2	5892	7	NULL	NULL	NULL	NULL	E1B-55 kDa protein	GP		bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_2_554_s_264	9430646	(Table  I); both hdm2 and E1B-55 kDa proteins bind to p53 (Sarnow  et al., 1982  ; Momand  et al., 1992  ).	bind
15354	1	5893	5	NULL	NULL	0	NULL	enzymes	NULL	mutant	bind	NULL	efficiently			tRNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_32_22225_s_179	10428788	(Table  I, Fig.  3) indicate that the mutant enzymes still bind tRNA efficiently, which argues against a large structural change.	bind
18130	1	5893	7	NULL	NULL	0	NULL	enzymes	NULL	mutant	bind	NULL	efficiently			tRNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_32_22225_s_179	10428788	(Table  I, Fig.  3) indicate that the mutant enzymes still bind tRNA efficiently, which argues against a large structural change.	bind
15355	1	5894	5	NULL	NULL	0	NULL	HIV-1 RT	NULL		bind	NULL				dNTPs	NULL	incorrect			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_25_22662_s_222	11927582	(Table  I; Ref.  15); however, the difference is that HIV-1 RT (micromolar  K d) binds incorrect dNTPs better than the T7 DNA polymerase (millimolar  K d; Ref.  30).	bind
15356	2	5894	5	NULL	NULL	0	NULL	HIV-1 RT	NULL		bind	NULL				T7 DNA polymerase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_25_22662_s_222	11927582	(Table  I; Ref.  15); however, the difference is that HIV-1 RT (micromolar  K d) binds incorrect dNTPs better than the T7 DNA polymerase (millimolar  K d; Ref.  30).	bind
15357	3	5894	5	NULL	NULL	0	NULL	statement 1	NULL		better than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_25_22662_s_222	11927582	(Table  I; Ref.  15); however, the difference is that HIV-1 RT (micromolar  K d) binds incorrect dNTPs better than the T7 DNA polymerase (millimolar  K d; Ref.  30).	bind
18131	1	5894	7	NULL	NULL	NULL	NULL	HIV-1 RT	GP		binds					dNTPs	Chemical	incorrect			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_25_22662_s_222	11927582	(Table  I; Ref.  15); however, the difference is that HIV-1 RT (micromolar  K d) binds incorrect dNTPs better than the T7 DNA polymerase (millimolar  K d; Ref.  30).	bind
18132	2	5894	7	NULL	NULL	NULL	NULL	HIV-1 RT	GP		binds					T7 DNA polymerase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_25_22662_s_222	11927582	(Table  I; Ref.  15); however, the difference is that HIV-1 RT (micromolar  K d) binds incorrect dNTPs better than the T7 DNA polymerase (millimolar  K d; Ref.  30).	bind
18133	3	5894	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs better than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_25_22662_s_222	11927582	(Table  I; Ref.  15); however, the difference is that HIV-1 RT (micromolar  K d) binds incorrect dNTPs better than the T7 DNA polymerase (millimolar  K d; Ref.  30).	bind
15358	1	5895	5	NULL	NULL	0	NULL	CREB	NULL		bind	NULL					NULL			cAMP-response element	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_41_31708_s_161	10913126	(Table  I; TCG AGGTCA, TCA TGGCCA) ( 4) or the inhibin alpha gene, where SF-1 regulates gene transcription through its interaction with CREB bound to the cAMP-response element ( 17).	bind
15359	2	5895	5	NULL	NULL	0	NULL	SF-1	NULL		interacts with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_41_31708_s_161	10913126	(Table  I; TCG AGGTCA, TCA TGGCCA) ( 4) or the inhibin alpha gene, where SF-1 regulates gene transcription through its interaction with CREB bound to the cAMP-response element ( 17).	bind
15360	3	5895	5	NULL	NULL	0	NULL	SF-1	NULL		regulate	NULL				gene transcription	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_41_31708_s_161	10913126	(Table  I; TCG AGGTCA, TCA TGGCCA) ( 4) or the inhibin alpha gene, where SF-1 regulates gene transcription through its interaction with CREB bound to the cAMP-response element ( 17).	bind
15361	4	5895	5	NULL	NULL	0	NULL	statement 3	NULL		occurs through	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_41_31708_s_161	10913126	(Table  I; TCG AGGTCA, TCA TGGCCA) ( 4) or the inhibin alpha gene, where SF-1 regulates gene transcription through its interaction with CREB bound to the cAMP-response element ( 17).	bind
18136	1	5895	7	NULL	NULL	NULL	NULL	CREB	GP		bind									cAMP-response element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31708_s_161	10913126	(Table  I; TCG AGGTCA, TCA TGGCCA) ( 4) or the inhibin alpha gene, where SF-1 regulates gene transcription through its interaction with CREB bound to the cAMP-response element ( 17).	bind
18137	2	5895	7	NULL	NULL	NULL	NULL	SF-1	GP		regulates					gene transcription	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31708_s_161	10913126	(Table  I; TCG AGGTCA, TCA TGGCCA) ( 4) or the inhibin alpha gene, where SF-1 regulates gene transcription through its interaction with CREB bound to the cAMP-response element ( 17).	bind
18139	3	5895	7	NULL	NULL	NULL	NULL	statement 2	Process		occurs through					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31708_s_161	10913126	(Table  I; TCG AGGTCA, TCA TGGCCA) ( 4) or the inhibin alpha gene, where SF-1 regulates gene transcription through its interaction with CREB bound to the cAMP-response element ( 17).	bind
15362	1	5896	5	NULL	NULL	0	NULL	POPC-apoE4	NULL		bind	NULL				ldlA cells	NULL		Q402R/Q418		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_24_21149_s_237	11861652	(Table  II) as well as with the reduced binding of POPC-apoE4 to the ldlA [Q402R/Q418] cells (Fig.  3 D) ( 28).	bind
18140	1	5896	7	NULL	NULL	NULL	NULL	POPC-apoE4 	GP		bind					 ldlA cells	Cell		Q402R/Q418		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_24_21149_s_237	11861652	(Table  II) as well as with the reduced binding of POPC-apoE4 to the ldlA [Q402R/Q418] cells (Fig.  3 D) ( 28).	bind
15363	1	5897	5	NULL	NULL	0	NULL	htf	NULL		bind	NULL				TbpB	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_17_14712_s_140	12571247	(Table  II) in all of the experiments was found to be close to 1, confirming the previously suggested 1:1 stoichiometry for the binding of htf to TbpB ( ).	bind
18144	1	5897	7	NULL	NULL	NULL	NULL	htf 	GP		bind					TbpB	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_17_14712_s_140	12571247	(Table  II) in all of the experiments was found to be close to 1, confirming the previously suggested 1:1 stoichiometry for the binding of htf to TbpB ( ).	bind
15364	1	5899	5	NULL	NULL	0	NULL	sCPS	NULL		bind	NULL				UMP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_47_45466_s_203	12244118	(Table  II) that sCPS bound both UMP and IMP and that chCPS bound IMP were unexpected because none of these interactions had been revealed by effects on enzymatic activity.	bind
15365	2	5899	5	NULL	NULL	0	NULL	sCPS	NULL		bind	NULL				IMP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_47_45466_s_203	12244118	(Table  II) that sCPS bound both UMP and IMP and that chCPS bound IMP were unexpected because none of these interactions had been revealed by effects on enzymatic activity.	bind
15366	3	5899	5	NULL	NULL	0	NULL	chCPS	NULL		bind	NULL				IMP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_47_45466_s_203	12244118	(Table  II) that sCPS bound both UMP and IMP and that chCPS bound IMP were unexpected because none of these interactions had been revealed by effects on enzymatic activity.	bind
18145	2	5899	7	NULL	NULL	NULL	NULL	sCPS	GP		bind					 IMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_47_45466_s_203	12244118	(Table  II) that sCPS bound both UMP and IMP and that chCPS bound IMP were unexpected because none of these interactions had been revealed by effects on enzymatic activity.	bind
18147	1	5899	7	NULL	NULL	NULL	NULL	sCPS	GP		bind					 UMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_47_45466_s_203	12244118	(Table  II) that sCPS bound both UMP and IMP and that chCPS bound IMP were unexpected because none of these interactions had been revealed by effects on enzymatic activity.	bind
18148	3	5899	7	NULL	NULL	NULL	NULL	chCPS	GP		bind					IMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_47_45466_s_203	12244118	(Table  II) that sCPS bound both UMP and IMP and that chCPS bound IMP were unexpected because none of these interactions had been revealed by effects on enzymatic activity.	bind
15367	1	5900	5	NULL	NULL	0	NULL	factor VIIa	NULL	helix residues	bind	NULL				TF	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_26_18477_s_351	10373456	(Table  II) that the corresponding helix residues in factor VIIa bind to TF ( 4) and in factor Xa, they are involved in binding to factor Va. 4 Thus, a common function of this helix (162 in chymotrypsin numbering) in several blood coagulation proteases may be to serve as a binding site for the respective cofactor.	bind
15368	2	5900	5	NULL	NULL	0	NULL	factor Xa	NULL	helix residues	bind	NULL				factor Va	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_26_18477_s_351	10373456	(Table  II) that the corresponding helix residues in factor VIIa bind to TF ( 4) and in factor Xa, they are involved in binding to factor Va. 4 Thus, a common function of this helix (162 in chymotrypsin numbering) in several blood coagulation proteases may be to serve as a binding site for the respective cofactor.	bind
54129	3	5900	5	10	NULL	0	NULL	chymotrypsin			serve as		may	helix 162		cofactor			binding site		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_26_18477_s_351	10373456	(Table  II) that the corresponding helix residues in factor VIIa bind to TF ( 4) and in factor Xa, they are involved in binding to factor Va. 4 Thus, a common function of this helix (162 in chymotrypsin numbering) in several blood coagulation proteases may be to serve as a binding site for the respective cofactor.	bind
18150	1	5900	7	NULL	NULL	NULL	NULL	factor VIIa	GP		bind			helix residues		TF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_26_18477_s_351	10373456	(Table  II) that the corresponding helix residues in factor VIIa bind to TF ( 4) and in factor Xa, they are involved in binding to factor Va. 4 Thus, a common function of this helix (162 in chymotrypsin numbering) in several blood coagulation proteases may be to serve as a binding site for the respective cofactor.	bind
18151	2	5900	7	NULL	NULL	NULL	NULL	factor Xa	GP		bind			helix residues		 factor Va	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_26_18477_s_351	10373456	(Table  II) that the corresponding helix residues in factor VIIa bind to TF ( 4) and in factor Xa, they are involved in binding to factor Va. 4 Thus, a common function of this helix (162 in chymotrypsin numbering) in several blood coagulation proteases may be to serve as a binding site for the respective cofactor.	bind
18157	3	5900	7	NULL	NULL	NULL	NULL	chymotrypsin	GP		serve as			helix 162		cofactor	GP	binding site for			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_26_18477_s_351	10373456	(Table  II) that the corresponding helix residues in factor VIIa bind to TF ( 4) and in factor Xa, they are involved in binding to factor Va. 4 Thus, a common function of this helix (162 in chymotrypsin numbering) in several blood coagulation proteases may be to serve as a binding site for the respective cofactor.	bind
15369	1	5901	5	NULL	NULL	0	NULL	gp120	NULL		bind	NULL				V3-BPs	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_34_21988_s_278	9705340	(Table  II), and that the pseudopeptide inhibitor of HIV entry that mimics the V3 loop blocks the binding of gp120 to the V3-BPs (Fig.  6 B).	bind
15370	2	5901	5	NULL	NULL	0	NULL	pseudopeptide inhibitor of HIV	NULL		mimics	NULL				V3 loop	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_34_21988_s_278	9705340	(Table  II), and that the pseudopeptide inhibitor of HIV entry that mimics the V3 loop blocks the binding of gp120 to the V3-BPs (Fig.  6 B).	bind
15371	3	5901	5	NULL	NULL	0	NULL	statement 2	NULL		blocks	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_34_21988_s_278	9705340	(Table  II), and that the pseudopeptide inhibitor of HIV entry that mimics the V3 loop blocks the binding of gp120 to the V3-BPs (Fig.  6 B).	bind
18159	1	5901	7	NULL	NULL	NULL	NULL	gp120	GP		bind					V3-BPs	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_34_21988_s_278	9705340	(Table  II), and that the pseudopeptide inhibitor of HIV entry that mimics the V3 loop blocks the binding of gp120 to the V3-BPs (Fig.  6 B).	bind
18160	2	5901	7	NULL	NULL	NULL	NULL	pseudopeptide inhibitor of HIV	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_34_21988_s_278	9705340	(Table  II), and that the pseudopeptide inhibitor of HIV entry that mimics the V3 loop blocks the binding of gp120 to the V3-BPs (Fig.  6 B).	bind
18161	3	5901	7	NULL	NULL	NULL	NULL	pseudopeptide inhibitor of HIV	GP		mimics					V3 loop	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_34_21988_s_278	9705340	(Table  II), and that the pseudopeptide inhibitor of HIV entry that mimics the V3 loop blocks the binding of gp120 to the V3-BPs (Fig.  6 B).	bind
15372	1	5904	5	NULL	NULL	0	NULL	P450c27	NULL		bind	NULL				Adx	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_4_2045_s_112	9890963	(Table  II), confirming the original chromatographic observation that P450c27 binds much more tightly to Adx than P450scc.	bind
15373	2	5904	5	NULL	NULL	0	NULL	P450c27	NULL		bind	NULL				P450scc	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_4_2045_s_112	9890963	(Table  II), confirming the original chromatographic observation that P450c27 binds much more tightly to Adx than P450scc.	bind
20338	3	5904	5	NULL	NULL	0	NULL	statement 1	NULL	affinity of	is greater than	NULL				statement 2	NULL	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_4_2045_s_112	9890963	(Table  II), confirming the original chromatographic observation that P450c27 binds much more tightly to Adx than P450scc.	bind
18218	1	5904	7	NULL	NULL	NULL	NULL	P450c27 	GP		binds					Adx 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_4_2045_s_112	9890963	(Table  II), confirming the original chromatographic observation that P450c27 binds much more tightly to Adx than P450scc.	bind
18219	2	5904	7	NULL	NULL	NULL	NULL	P450scc	GP		binds					Adx	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_4_2045_s_112	9890963	(Table  II), confirming the original chromatographic observation that P450c27 binds much more tightly to Adx than P450scc.	bind
18220	3	5904	7	NULL	NULL	NULL	NULL	statement 1	Process	affinity of	is greater than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_4_2045_s_112	9890963	(Table  II), confirming the original chromatographic observation that P450c27 binds much more tightly to Adx than P450scc.	bind
15374	1	5906	5	NULL	NULL	0	NULL	ATP	NULL		bind	NULL	allosteric				NULL		Fru-2,6-P2ase domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_27_24608_s_114	11325970	(Table  II), it is likely that the ATP activation of the chicken liver 6PF-2K is caused by allosteric binding of ATP to the Fru-2,6-P2ase domain.	bind
15375	2	5906	5	10	NULL	0	NULL	ATP			activates					6PF-2K		chicken;;liver			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24608_s_114	11325970	(Table  II), it is likely that the ATP activation of the chicken liver 6PF-2K is caused by allosteric binding of ATP to the Fru-2,6-P2ase domain.	bind
20339	3	5906	5	NULL	NULL	0	NULL	statement 1	NULL		causes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_27_24608_s_114	11325970	(Table  II), it is likely that the ATP activation of the chicken liver 6PF-2K is caused by allosteric binding of ATP to the Fru-2,6-P2ase domain.	bind
18221	1	5906	7	NULL	NULL	NULL	NULL	ATP	Chemical		binds		allosterically						Fru-2,6-P2ase domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24608_s_114	11325970	(Table  II), it is likely that the ATP activation of the chicken liver 6PF-2K is caused by allosteric binding of ATP to the Fru-2,6-P2ase domain.	bind
18222	2	5906	7	NULL	NULL	NULL	NULL	ATP	Chemical		activates					6PF-2K 	GP	chicken;;liver			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24608_s_114	11325970	(Table  II), it is likely that the ATP activation of the chicken liver 6PF-2K is caused by allosteric binding of ATP to the Fru-2,6-P2ase domain.	bind
18223	3	5906	7	NULL	NULL	NULL	NULL	statement 1	Process		cause					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24608_s_114	11325970	(Table  II), it is likely that the ATP activation of the chicken liver 6PF-2K is caused by allosteric binding of ATP to the Fru-2,6-P2ase domain.	bind
15376	1	5907	5	10	NULL	0	NULL	aptamer DP3	NULL		mimics	NULL	closely			Y2 receptor	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11416_s_242	11756401	(Table  II), strongly suggest that the aptamer DP3 mimics the binding behavior of the Y2 receptor more closely than that of the Y1 and Y5 receptors.	bind
15377	2	5907	5	10	NULL	0	NULL	aptamer DP3	NULL		mimics	NULL				Y1 receptor	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11416_s_242	11756401	(Table  II), strongly suggest that the aptamer DP3 mimics the binding behavior of the Y2 receptor more closely than that of the Y1 and Y5 receptors.	bind
15378	3	5907	5	10	NULL	0	NULL	aptamer DP3	NULL		mimics	NULL				Y5 receptor	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11416_s_242	11756401	(Table  II), strongly suggest that the aptamer DP3 mimics the binding behavior of the Y2 receptor more closely than that of the Y1 and Y5 receptors.	bind
20340	4	5907	5	NULL	NULL	0	NULL	statement 1	NULL		 is more close than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_13_11416_s_242	11756401	(Table  II), strongly suggest that the aptamer DP3 mimics the binding behavior of the Y2 receptor more closely than that of the Y1 and Y5 receptors.	bind
20341	5	5907	5	NULL	NULL	0	NULL	statement 1	NULL		 is more close than	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_13_11416_s_242	11756401	(Table  II), strongly suggest that the aptamer DP3 mimics the binding behavior of the Y2 receptor more closely than that of the Y1 and Y5 receptors.	bind
18224	1	5907	7	NULL	NULL	NULL	NULL	aptamer DP3	GP		mimics					Y2 receptor	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11416_s_242	11756401	(Table  II), strongly suggest that the aptamer DP3 mimics the binding behavior of the Y2 receptor more closely than that of the Y1 and Y5 receptors.	bind
18225	2	5907	7	NULL	NULL	NULL	NULL	aptamer DP3	GP		mimics					Y1 receptor	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11416_s_242	11756401	(Table  II), strongly suggest that the aptamer DP3 mimics the binding behavior of the Y2 receptor more closely than that of the Y1 and Y5 receptors.	bind
18226	3	5907	7	NULL	NULL	NULL	NULL	aptamer DP3	GP		mimics					Y5 receptor	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11416_s_242	11756401	(Table  II), strongly suggest that the aptamer DP3 mimics the binding behavior of the Y2 receptor more closely than that of the Y1 and Y5 receptors.	bind
18227	4	5907	7	NULL	NULL	NULL	NULL	statement 1	Process		is more close than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11416_s_242	11756401	(Table  II), strongly suggest that the aptamer DP3 mimics the binding behavior of the Y2 receptor more closely than that of the Y1 and Y5 receptors.	bind
18228	5	5907	7	NULL	NULL	NULL	NULL	statement 1	Process		is more close than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11416_s_242	11756401	(Table  II), strongly suggest that the aptamer DP3 mimics the binding behavior of the Y2 receptor more closely than that of the Y1 and Y5 receptors.	bind
15379	1	5908	5	NULL	NULL	0	NULL	Cl	NULL		bind	NULL	only			EA state	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_4_2232_s_154	9442066	(Table  II), strongly suggesting that Cl  binds only to the  EA state.	bind
18229	1	5908	7	NULL	NULL	NULL	NULL	Cl	Chemical		binds		only			EA state	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_4_2232_s_154	9442066	(Table  II), strongly suggesting that Cl  binds only to the  EA state.	bind
15380	1	5910	5	NULL	NULL	0	NULL	eIF4E	NULL		bind	NULL				eIF4G1-459	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_29_21817_s_345	10764794	(Table  II), we tested the hypothesis that excess Rbp29p may increase the binding of eIF4E to eIF4G1-459.	bind
20342	2	5910	5	NULL	NULL	0	NULL	Rbp29p	NULL		increase	NULL	may			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_29_21817_s_345	10764794	(Table  II), we tested the hypothesis that excess Rbp29p may increase the binding of eIF4E to eIF4G1-459.	bind
18230	1	5910	7	NULL	NULL	NULL	NULL	eIF4E	GP		bind					eIF4G	GP		1-459		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_29_21817_s_345	10764794	(Table  II), we tested the hypothesis that excess Rbp29p may increase the binding of eIF4E to eIF4G1-459.	bind
18231	2	5910	7	NULL	NULL	NULL	NULL	Rbp29p	GP	excess of	increase		may			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_29_21817_s_345	10764794	(Table  II), we tested the hypothesis that excess Rbp29p may increase the binding of eIF4E to eIF4G1-459.	bind
15381	2	5911	5	10	NULL	0	NULL	statement 1			does not bind					protein S					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_15144_s_206	10329721	(Table  II), whereas constructs lacking SCR-1 did not bind to protein S (Figs.  3 and  4).	bind
54134	1	5911	5	10	NULL	0	NULL	constructs			lacks					SCR-1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_15144_s_206	10329721	(Table  II), whereas constructs lacking SCR-1 did not bind to protein S (Figs.  3 and  4).	bind
18232	2	5911	7	NULL	NULL	NULL	NULL	statement 1	Process		does not bind					protein S	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_15144_s_206	10329721	(Table  II), whereas constructs lacking SCR-1 did not bind to protein S (Figs.  3 and  4).	bind
54136	1	5911	7	NULL	NULL	NULL	NULL	constructs	GP		lacks					SCR-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_15144_s_206	10329721	(Table  II), whereas constructs lacking SCR-1 did not bind to protein S (Figs.  3 and  4).	bind
15382	1	5913	5	NULL	NULL	0	NULL	NT-3	NULL		bind	NULL				CR1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_11_7870_s_166	10713102	(Table  III), in agreement with NT-3 binding better to CR1 than to CR13	bind
15383	2	5913	5	NULL	NULL	0	NULL	NT-3	NULL		bind	NULL				CR13	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_11_7870_s_166	10713102	(Table  III), in agreement with NT-3 binding better to CR1 than to CR13	bind
15384	3	5913	5	NULL	NULL	0	NULL	statement 1	NULL		better than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_11_7870_s_166	10713102	(Table  III), in agreement with NT-3 binding better to CR1 than to CR13	bind
18233	1	5913	7	NULL	NULL	NULL	NULL	NT-3	GP		bind					CR1 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7870_s_166	10713102	(Table  III), in agreement with NT-3 binding better to CR1 than to CR13	bind
18234	2	5913	7	NULL	NULL	NULL	NULL	NT-3	GP		bind					CR13	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7870_s_166	10713102	(Table  III), in agreement with NT-3 binding better to CR1 than to CR13	bind
18235	3	5913	7	NULL	NULL	NULL	NULL	statement 1	Process		is better than 					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7870_s_166	10713102	(Table  III), in agreement with NT-3 binding better to CR1 than to CR13	bind
15385	1	5914	5	NULL	NULL	0	NULL	pGH	NULL		bind	NULL	poorly			GH receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_43_27077_s_164	9341147	(Table  III), so the residual 17-fold loss in affinity may be a result of generally poorer binding of pGH to GH receptors.	bind
18236	1	5914	7	NULL	NULL	NULL	NULL	pGH	GP		binds		poorly			GH receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_43_27077_s_164	9341147	(Table  III), so the residual 17-fold loss in affinity may be a result of generally poorer binding of pGH to GH receptors.	bind
15386	1	5915	5	NULL	NULL	0	NULL	CD62L	NULL		bind	NULL				GlyCAM-1 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_2_763_s_201	9422729	(Table  III), two major capping groups present in GlyCAM-1  O-linked oligosaccharides ( 53,  54), are only slightly higher (250-800 muM) than the  K d measured in the present study for CD62L binding to GlyCAM-1 (~108 muM).	bind
18237	1	5915	7	NULL	NULL	NULL	NULL	CD62L 	GP		binds					GlyCAM-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_2_763_s_201	9422729	(Table  III), two major capping groups present in GlyCAM-1  O-linked oligosaccharides ( 53,  54), are only slightly higher (250-800 muM) than the  K d measured in the present study for CD62L binding to GlyCAM-1 (~108 muM).	bind
15387	1	5918	5	10	NULL	0	NULL	mAb 2C7 	NULL		bind	NULL				WG LOS	NULL	inner structure of	15253 LOS		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_51_36550_s_186	10593954	(Table  IV), which confirmed that mAb 2C7 bound to the inner 15253 LOS structure within WG LOS.	bind
18238	1	5918	7	NULL	NULL	NULL	NULL	mAb 2C7	GP		bind					WG LOS	GP	inner structure of	15253 LOS 		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_51_36550_s_186	10593954	(Table  IV), which confirmed that mAb 2C7 bound to the inner 15253 LOS structure within WG LOS.	bind
15389	1	5919	5	NULL	NULL	0	NULL	htf	NULL		bind	NULL				His6-TbpB	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_17_14712_s_246	12571247	(Table  VI) for htf binding to N-ter was about three times largerR than the corresponding value for the binding to His6-TbpB.	bind
18239	1	5919	7	NULL	NULL	NULL	NULL	htf	GP		bind					His6-TbpB	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_17_14712_s_246	12571247	(Table  VI) for htf binding to N-ter was about three times largerR than the corresponding value for the binding to His6-TbpB.	bind
15391	1	5920	5	NULL	NULL	0	NULL	A26	NULL		bind	NULL				TeR-2 DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_25_15881_s_287	9188487	(Table  VI), A26 binds TeR-2 DNA less tightly than TeR-4 DNA ( 71).	bind
15392	2	5920	5	NULL	NULL	0	NULL	A26	NULL		bind	NULL				TeR-4 DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_25_15881_s_287	9188487	(Table  VI), A26 binds TeR-2 DNA less tightly than TeR-4 DNA ( 71).	bind
15393	3	5920	5	NULL	NULL	0	NULL	statement 1	NULL		less tightly than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_25_15881_s_287	9188487	(Table  VI), A26 binds TeR-2 DNA less tightly than TeR-4 DNA ( 71).	bind
18240	1	5920	7	NULL	NULL	NULL	NULL	A26	GP		binds					TeR-2 DNA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_25_15881_s_287	9188487	(Table  VI), A26 binds TeR-2 DNA less tightly than TeR-4 DNA ( 71).	bind
18241	2	5920	7	NULL	NULL	NULL	NULL	A26	GP		binds					TeR-4 DNA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_25_15881_s_287	9188487	(Table  VI), A26 binds TeR-2 DNA less tightly than TeR-4 DNA ( 71).	bind
18242	3	5920	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs less tightly than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_25_15881_s_287	9188487	(Table  VI), A26 binds TeR-2 DNA less tightly than TeR-4 DNA ( 71).	bind
15395	1	5921	5	NULL	NULL	0	NULL	repressor	NULL	putative	bind	NULL					NULL			RE3	NULL		NULL	NULL	NULL	NULL	gw60_embo_16_10_2554_s_191	9184203	(Table  VI), indicating that the putative repressor that binds to RE3 requires both signalling molecules for activation.	bind
15396	2	5921	5	10	NULL	0	NULL	repressor		activation of;;putative	requires					signalling molecules					NULL		NULL	NULL	NULL	NULL	gw60_embo_16_10_2554_s_191	9184203	(Table  VI), indicating that the putative repressor that binds to RE3 requires both signalling molecules for activation.	bind
18243	1	5921	7	NULL	NULL	NULL	NULL			putative	binds to				 repressor					RE3	NULL		NULL	NULL	NULL	NULL	gw60_embo_16_10_2554_s_191	9184203	(Table  VI), indicating that the putative repressor that binds to RE3 requires both signalling molecules for activation.	bind
18244	2	5921	7	NULL	NULL	NULL	NULL	repressor	GP	activation of;;putative	requires					signalling molecules	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_10_2554_s_191	9184203	(Table  VI), indicating that the putative repressor that binds to RE3 requires both signalling molecules for activation.	bind
15397	1	5923	5	NULL	NULL	0	NULL	CRP	NULL	purified	bind	NULL				cai-fix	NULL			intergenic promoter region	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbacteriol_180_10_2599_s_235	9573142	(Tables  2 and  3), the binding specificity of purified CRP to the  cai-fix intergenic promoter region was tested in vitro by performing gel mobility shift assays.	bind
18245	1	5923	7	NULL	NULL	NULL	NULL	CRP	GP	purified	binds					cai-fix	GP			 intergenic promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbacteriol_180_10_2599_s_235	9573142	(Tables  2 and  3), the binding specificity of purified CRP to the  cai-fix intergenic promoter region was tested in vitro by performing gel mobility shift assays.	bind
15398	1	5924	5	NULL	NULL	0	NULL	Pot1N molecule	NULL	additional	bind	NULL				(Tel)4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_9119_s_176	15637058	(TelAC)3 complex (compare  lanes 2 and  3), suggesting that an additional Pot1N molecule was bound to (Tel)4.	bind
18246	1	5924	7	NULL	NULL	NULL	NULL	Pot1N molecule	GP		bind					(Tel)4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_10_9119_s_176	15637058	(TelAC)3 complex (compare  lanes 2 and  3), suggesting that an additional Pot1N molecule was bound to (Tel)4.	bind
15399	1	5925	5	NULL	NULL	0	NULL	FVIIa	NULL		bind	NULL				TF	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_49_45895_s_58	11590156	(TF9 10H10 antibody binds to TF without interfering FVIIa binding to TF.)	bind
15400	2	5925	5	NULL	NULL	0	NULL	TF9 10H10 antibody	NULL		bind	NULL				TF	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_49_45895_s_58	11590156	(TF9 10H10 antibody binds to TF without interfering FVIIa binding to TF.)	bind
15401	3	5925	5	10	NULL	0	NULL	statement 2			does not interfere with					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_45895_s_58	11590156	(TF9 10H10 antibody binds to TF without interfering FVIIa binding to TF.)	bind
18247	1	5925	7	NULL	NULL	NULL	NULL	TF9 10H10 antibody	GP		binds to					TF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_45895_s_58	11590156	(TF9 10H10 antibody binds to TF without interfering FVIIa binding to TF.)	bind
18248	2	5925	7	NULL	NULL	NULL	NULL	FVIIa	GP		binds to					TF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_45895_s_58	11590156	(TF9 10H10 antibody binds to TF without interfering FVIIa binding to TF.)	bind
18249	3	5925	7	NULL	NULL	NULL	NULL	statement 1	Process		does not interfere with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_45895_s_58	11590156	(TF9 10H10 antibody binds to TF without interfering FVIIa binding to TF.)	bind
15402	1	5926	5	NULL	NULL	0	NULL	TGFbeta-receptor-associated protein	NULL		interacts with	NULL				receptor complex	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_23_2783_s_161	16322555	(TGFbeta-receptor-associated protein) (Wurthner et al. 2001 ) and TLP (TRAP-1-like protein) (Felici et al. 2003 ) have been described as adaptor proteins that interact with the receptor complex and facilitate the formation of Smad2/3 - Smad4 complexes.	bind
15403	2	5926	5	NULL	NULL	0	NULL	TGFbeta-receptor-associated protein	NULL		facilitate	NULL				Smad2/3 - Smad4 complexes	NULL	formation of			NULL		0	NULL	NULL	NULL	gw70_genesdev_19_23_2783_s_161	16322555	(TGFbeta-receptor-associated protein) (Wurthner et al. 2001 ) and TLP (TRAP-1-like protein) (Felici et al. 2003 ) have been described as adaptor proteins that interact with the receptor complex and facilitate the formation of Smad2/3 - Smad4 complexes.	bind
15404	3	5926	5	NULL	NULL	0	NULL	TLP	NULL		is	NULL				TRAP-1-like protein	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_23_2783_s_161	16322555	(TGFbeta-receptor-associated protein) (Wurthner et al. 2001 ) and TLP (TRAP-1-like protein) (Felici et al. 2003 ) have been described as adaptor proteins that interact with the receptor complex and facilitate the formation of Smad2/3 - Smad4 complexes.	bind
15405	4	5926	5	NULL	NULL	0	NULL	TLP	NULL		interacts with	NULL				receptor complex	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_23_2783_s_161	16322555	(TGFbeta-receptor-associated protein) (Wurthner et al. 2001 ) and TLP (TRAP-1-like protein) (Felici et al. 2003 ) have been described as adaptor proteins that interact with the receptor complex and facilitate the formation of Smad2/3 - Smad4 complexes.	bind
15406	5	5926	5	NULL	NULL	0	NULL	TLP	NULL		facilitate	NULL				Smad2/3 - Smad4 complexes	NULL	formation of			NULL		0	NULL	NULL	NULL	gw70_genesdev_19_23_2783_s_161	16322555	(TGFbeta-receptor-associated protein) (Wurthner et al. 2001 ) and TLP (TRAP-1-like protein) (Felici et al. 2003 ) have been described as adaptor proteins that interact with the receptor complex and facilitate the formation of Smad2/3 - Smad4 complexes.	bind
44840	6	5926	5	NULL	NULL	0	NULL	TGFbeta-receptor-associated protein	NULL		is a type of	NULL				adaptor protein	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_23_2783_s_161	16322555	(TGFbeta-receptor-associated protein) (Wurthner et al. 2001 ) and TLP (TRAP-1-like protein) (Felici et al. 2003 ) have been described as adaptor proteins that interact with the receptor complex and facilitate the formation of Smad2/3 - Smad4 complexes.	bind
44841	7	5926	5	NULL	NULL	0	NULL	TLP	NULL		is a type of	NULL				adaptor protein	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_23_2783_s_161	16322555	(TGFbeta-receptor-associated protein) (Wurthner et al. 2001 ) and TLP (TRAP-1-like protein) (Felici et al. 2003 ) have been described as adaptor proteins that interact with the receptor complex and facilitate the formation of Smad2/3 - Smad4 complexes.	bind
18250	1	5926	7	NULL	NULL	NULL	NULL	TGFbeta-receptor-associated protein	GP		interact with					receptor complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_23_2783_s_161	16322555	(TGFbeta-receptor-associated protein) (Wurthner et al. 2001 ) and TLP (TRAP-1-like protein) (Felici et al. 2003 ) have been described as adaptor proteins that interact with the receptor complex and facilitate the formation of Smad2/3 - Smad4 complexes.	bind
18251	2	5926	7	NULL	NULL	NULL	NULL	TLP	GP		interacts with					receptor complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_23_2783_s_161	16322555	(TGFbeta-receptor-associated protein) (Wurthner et al. 2001 ) and TLP (TRAP-1-like protein) (Felici et al. 2003 ) have been described as adaptor proteins that interact with the receptor complex and facilitate the formation of Smad2/3 - Smad4 complexes.	bind
18252	3	5926	7	NULL	NULL	NULL	NULL	statement 1	Process		facilitate					Smad2/3 - Smad4 complexes	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_23_2783_s_161	16322555	(TGFbeta-receptor-associated protein) (Wurthner et al. 2001 ) and TLP (TRAP-1-like protein) (Felici et al. 2003 ) have been described as adaptor proteins that interact with the receptor complex and facilitate the formation of Smad2/3 - Smad4 complexes.	bind
18253	7	5926	7	NULL	NULL	NULL	NULL	TLP	GP		is					TRAP-1-like protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_23_2783_s_161	16322555	(TGFbeta-receptor-associated protein) (Wurthner et al. 2001 ) and TLP (TRAP-1-like protein) (Felici et al. 2003 ) have been described as adaptor proteins that interact with the receptor complex and facilitate the formation of Smad2/3 - Smad4 complexes.	bind
18254	5	5926	7	NULL	NULL	NULL	NULL	TGFbeta-receptor-associated protein	GP		is a type of					adaptor protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_23_2783_s_161	16322555	(TGFbeta-receptor-associated protein) (Wurthner et al. 2001 ) and TLP (TRAP-1-like protein) (Felici et al. 2003 ) have been described as adaptor proteins that interact with the receptor complex and facilitate the formation of Smad2/3 - Smad4 complexes.	bind
18255	6	5926	7	NULL	NULL	NULL	NULL	TLP	GP		is a type of					adaptor protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_23_2783_s_161	16322555	(TGFbeta-receptor-associated protein) (Wurthner et al. 2001 ) and TLP (TRAP-1-like protein) (Felici et al. 2003 ) have been described as adaptor proteins that interact with the receptor complex and facilitate the formation of Smad2/3 - Smad4 complexes.	bind
45562	4	5926	7	NULL	NULL	NULL	NULL	statement 2	Process		facilitate					Smad2/3 - Smad4 complexes	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_23_2783_s_161	16322555	(TGFbeta-receptor-associated protein) (Wurthner et al. 2001 ) and TLP (TRAP-1-like protein) (Felici et al. 2003 ) have been described as adaptor proteins that interact with the receptor complex and facilitate the formation of Smad2/3 - Smad4 complexes.	bind
15407	1	5927	5	NULL	NULL	0	NULL	troponin	NULL	truncated	bind	NULL				tropomyosin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_145	7592713	(The   Fig. 3results can only  be analyzed qualitatively because of uncertainty in the stoichiometry  of truncated troponin binding to tropomyosin and to the thin filament.)	bind
15408	2	5927	5	NULL	NULL	0	NULL	troponin	NULL	truncated	bind	NULL				thin filament	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_145	7592713	(The   Fig. 3results can only  be analyzed qualitatively because of uncertainty in the stoichiometry  of truncated troponin binding to tropomyosin and to the thin filament.)	bind
18256	1	5927	7	NULL	NULL	NULL	NULL	troponin	GP	truncated	binds					tropomyosin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_145	7592713	(The   Fig. 3results can only  be analyzed qualitatively because of uncertainty in the stoichiometry  of truncated troponin binding to tropomyosin and to the thin filament.)	bind
18257	2	5927	7	NULL	NULL	NULL	NULL	troponin	GP	truncated	binds to					thin filament	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_145	7592713	(The   Fig. 3results can only  be analyzed qualitatively because of uncertainty in the stoichiometry  of truncated troponin binding to tropomyosin and to the thin filament.)	bind
15409	1	5930	5	NULL	NULL	0	NULL	4E-BP1	NULL		bind	NULL				eIF4E	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9373_s_119	9545260	(The exception here (as in CHO cells) is arsenite, which does not cause increased binding of 4E-BP1 to eIF4E.	bind
15410	2	5930	5	10	NULL	0	NULL	arsenite	NULL		does not increase	NULL				statement 1	NULL	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9373_s_119	9545260	(The exception here (as in CHO cells) is arsenite, which does not cause increased binding of 4E-BP1 to eIF4E.	bind
18264	1	5930	7	NULL	NULL	NULL	NULL	4E-BP1	GP		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9373_s_119	9545260	(The exception here (as in CHO cells) is arsenite, which does not cause increased binding of 4E-BP1 to eIF4E.	bind
18265	2	5930	7	NULL	NULL	NULL	NULL	arsenite	Chemical		does not increase					statement 1	Process	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9373_s_119	9545260	(The exception here (as in CHO cells) is arsenite, which does not cause increased binding of 4E-BP1 to eIF4E.	bind
15411	1	5931	5	NULL	NULL	0	NULL	Ste7	NULL		bind	NULL				GST-Ste5 	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_20_9221_s_348	15456892	(The exception was for comparisons of Ste7 binding to GST-Ste5 [see below].)	bind
18266	1	5931	7	NULL	NULL	NULL	NULL	Ste7	GP		bind					GST-Ste5	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_9221_s_348	15456892	(The exception was for comparisons of Ste7 binding to GST-Ste5 [see below].)	bind
15412	1	5932	5	10	NULL	0	NULL	ALEX	NULL		bind	NULL	weakly			GST	NULL	alone			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_14_3849_s_193	11447126	(The low level binding of ALEX to GST alone presumably reflects an unspecific sticking of the highly basic ALEX.)	bind
18267	1	5932	7	NULL	NULL	NULL	NULL	ALEX	GP		binds		weakly			GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_14_3849_s_193	11447126	(The low level binding of ALEX to GST alone presumably reflects an unspecific sticking of the highly basic ALEX.)	bind
15413	1	5933	5	NULL	NULL	0	NULL	LacR	NULL		bind	NULL					NULL			operon O1	NULL		0	NULL	NULL	NULL	gw70_pnas_103_26_9879_s_65	16785444	(The probability of occurrence of a loop depends on the energies,  GO1 and  GO3, of LacR binding to operons O1 and O3, and the difference, delta G, between  GDNA and the free energy of an unbound DNA segment of identical length.)	bind
15414	2	5933	5	NULL	NULL	0	NULL	LacR	NULL		bind	NULL					NULL			operon O3	NULL		0	NULL	NULL	NULL	gw70_pnas_103_26_9879_s_65	16785444	(The probability of occurrence of a loop depends on the energies,  GO1 and  GO3, of LacR binding to operons O1 and O3, and the difference, delta G, between  GDNA and the free energy of an unbound DNA segment of identical length.)	bind
18271	1	5933	7	NULL	NULL	NULL	NULL	LacR	GP		bind									operon O1	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_26_9879_s_65	16785444	(The probability of occurrence of a loop depends on the energies,  GO1 and  GO3, of LacR binding to operons O1 and O3, and the difference, delta G, between  GDNA and the free energy of an unbound DNA segment of identical length.)	bind
18272	2	5933	7	NULL	NULL	NULL	NULL	LacR	GP		bind									operon O3	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_26_9879_s_65	16785444	(The probability of occurrence of a loop depends on the energies,  GO1 and  GO3, of LacR binding to operons O1 and O3, and the difference, delta G, between  GDNA and the free energy of an unbound DNA segment of identical length.)	bind
15417	1	5934	5	NULL	NULL	0	NULL	dyn-2	NULL		mediate	NULL		PRD		eNOS activity	NULL	potentiation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_8_5894_s_13	12488320	(These data indicate that the binding domains of dyn-2 and eNOS reside within the dyn-2 PRD domain and the FAD binding region of the eNOS reductase domains, respectively, and that dyn-2 PRD is sufficient to mediate dyn-2-dependent potentiation of eNOS activity, at least in part, by potentiating electron transfer.)	bind
15418	2	5934	5	NULL	NULL	0	NULL	statement 1	NULL		dependent on	NULL				dyn-2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_8_5894_s_13	12488320	(These data indicate that the binding domains of dyn-2 and eNOS reside within the dyn-2 PRD domain and the FAD binding region of the eNOS reductase domains, respectively, and that dyn-2 PRD is sufficient to mediate dyn-2-dependent potentiation of eNOS activity, at least in part, by potentiating electron transfer.)	bind
18274	1	5934	7	NULL	NULL	NULL	NULL	dyn-2	GP		mediates			PRD		eNOS	GP	potentiation of;;activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_8_5894_s_13	12488320	(These data indicate that the binding domains of dyn-2 and eNOS reside within the dyn-2 PRD domain and the FAD binding region of the eNOS reductase domains, respectively, and that dyn-2 PRD is sufficient to mediate dyn-2-dependent potentiation of eNOS activity, at least in part, by potentiating electron transfer.)	bind
18275	2	5934	7	NULL	NULL	NULL	NULL	statement 1	Process		occur by					electron transfer	Process	potentiating			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_8_5894_s_13	12488320	(These data indicate that the binding domains of dyn-2 and eNOS reside within the dyn-2 PRD domain and the FAD binding region of the eNOS reductase domains, respectively, and that dyn-2 PRD is sufficient to mediate dyn-2-dependent potentiation of eNOS activity, at least in part, by potentiating electron transfer.)	bind
15415	1	5935	5	NULL	NULL	0	NULL	troponin	NULL	tropomyosin-truncated	bind	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_126	7592713	(This calculation  uses the last data point of each curve in  Fig. 3 B.)  Removal of Ca   increased this ratio by a factor of  three in each case, suggesting a 3-fold effect of Ca   on tropomyosin-truncated troponin binding to actin.	bind
15416	2	5935	5	NULL	NULL	0	NULL	Ca	NULL		effect	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_126	7592713	(This calculation  uses the last data point of each curve in  Fig. 3 B.)  Removal of Ca   increased this ratio by a factor of  three in each case, suggesting a 3-fold effect of Ca   on tropomyosin-truncated troponin binding to actin.	bind
18276	1	5935	7	NULL	NULL	NULL	NULL	troponin	GP	tropomyosin-truncated 	binds					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_126	7592713	(This calculation  uses the last data point of each curve in  Fig. 3 B.)  Removal of Ca   increased this ratio by a factor of  three in each case, suggesting a 3-fold effect of Ca   on tropomyosin-truncated troponin binding to actin.	bind
44803	2	5935	7	NULL	NULL	NULL	NULL	Ca	Chemical		plays a role in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_126	7592713	(This calculation  uses the last data point of each curve in  Fig. 3 B.)  Removal of Ca   increased this ratio by a factor of  three in each case, suggesting a 3-fold effect of Ca   on tropomyosin-truncated troponin binding to actin.	bind
15419	1	5936	5	NULL	NULL	0	NULL	Int	NULL		bind	NULL	covalently			attP	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_5_11_1312_s_203	8574589	(This is in contrast to the situation with nicked suicide substrates, where unitary strand transfer is efficiently executed by displacement of an Int covalently bound to  attP by a hydroxyl from  attB  [11]  ; the difference between these situations is the subject of another study.)	bind
15420	2	5936	5	10	NULL	0	NULL	attB	NULL		bind	NULL		hydroxyl		attP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_5_11_1312_s_203	8574589	(This is in contrast to the situation with nicked suicide substrates, where unitary strand transfer is efficiently executed by displacement of an Int covalently bound to  attP by a hydroxyl from  attB  [11]  ; the difference between these situations is the subject of another study.)	bind
20343	3	5936	5	NULL	NULL	0	NULL	statement 2	NULL		displaces	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_5_11_1312_s_203	8574589	(This is in contrast to the situation with nicked suicide substrates, where unitary strand transfer is efficiently executed by displacement of an Int covalently bound to  attP by a hydroxyl from  attB  [11]  ; the difference between these situations is the subject of another study.)	bind
20344	4	5936	5	NULL	NULL	0	NULL	unitary strand transfer	NULL		executed by	NULL	efficiently			statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_5_11_1312_s_203	8574589	(This is in contrast to the situation with nicked suicide substrates, where unitary strand transfer is efficiently executed by displacement of an Int covalently bound to  attP by a hydroxyl from  attB  [11]  ; the difference between these situations is the subject of another study.)	bind
18277	1	5936	7	NULL	NULL	NULL	NULL	Int	GP		bind		covalently			attP	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_5_11_1312_s_203	8574589	(This is in contrast to the situation with nicked suicide substrates, where unitary strand transfer is efficiently executed by displacement of an Int covalently bound to  attP by a hydroxyl from  attB  [11]  ; the difference between these situations is the subject of another study.)	bind
18278	2	5936	7	NULL	NULL	NULL	NULL	attB	GP		binds			hydroxyl		attP	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_5_11_1312_s_203	8574589	(This is in contrast to the situation with nicked suicide substrates, where unitary strand transfer is efficiently executed by displacement of an Int covalently bound to  attP by a hydroxyl from  attB  [11]  ; the difference between these situations is the subject of another study.)	bind
18279	3	5936	7	NULL	NULL	NULL	NULL	statement 2	Process		displaces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_5_11_1312_s_203	8574589	(This is in contrast to the situation with nicked suicide substrates, where unitary strand transfer is efficiently executed by displacement of an Int covalently bound to  attP by a hydroxyl from  attB  [11]  ; the difference between these situations is the subject of another study.)	bind
18280	4	5936	7	NULL	NULL	NULL	NULL	unitary strand transfer	Process		is executed by		efficiently			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_5_11_1312_s_203	8574589	(This is in contrast to the situation with nicked suicide substrates, where unitary strand transfer is efficiently executed by displacement of an Int covalently bound to  attP by a hydroxyl from  attB  [11]  ; the difference between these situations is the subject of another study.)	bind
15421	1	5937	5	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				eIF2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_27_24697_s_181	11323413	(This material is free of eIF2, thus obviating the problem of GTP binding to any eIF2 present.)	bind
18281	1	5937	7	NULL	NULL	NULL	NULL	GTP	Chemical		binds					eIF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24697_s_181	11323413	(This material is free of eIF2, thus obviating the problem of GTP binding to any eIF2 present.)	bind
15422	1	5938	5	NULL	NULL	0	NULL	titin	NULL		bind	NULL		PEVK region		actin	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_99_8_795_s_42	17038648	(This region shares homology to the PEVK region of titin, which is known to bind to actin.	bind
18282	1	5938	7	NULL	NULL	NULL	NULL	titin	GP		binds to			PEVK region		actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_99_8_795_s_42	17038648	(This region shares homology to the PEVK region of titin, which is known to bind to actin.	bind
15423	1	5939	5	NULL	NULL	0	NULL	GroEL	NULL	single ring mutant	bind	NULL	rapidly			GroES 	NULL				NULL		0	NULL	NULL	NULL	gw60_structure_4_1_1_s_81	8805512	(This was shown by using a single ring mutant GroEL that rapidly binds but very slowly releases GroES in single turnover studies to trap released GroES; results revealed that a single turnover of ATPase was sufficient for productive release of OTC from  cis, but not  trans, complexes.)	bind
15424	2	5939	5	NULL	NULL	0	NULL	GroEL	NULL	single ring mutant	release	NULL	slowly			GroES	NULL				NULL		0	NULL	NULL	NULL	gw60_structure_4_1_1_s_81	8805512	(This was shown by using a single ring mutant GroEL that rapidly binds but very slowly releases GroES in single turnover studies to trap released GroES; results revealed that a single turnover of ATPase was sufficient for productive release of OTC from  cis, but not  trans, complexes.)	bind
15425	3	5939	5	NULL	NULL	0	NULL	ATPase	NULL	single turnover of	release	NULL	productively			OTC	NULL	from cis complex			NULL		NULL	NULL	NULL	NULL	gw60_structure_4_1_1_s_81	8805512	(This was shown by using a single ring mutant GroEL that rapidly binds but very slowly releases GroES in single turnover studies to trap released GroES; results revealed that a single turnover of ATPase was sufficient for productive release of OTC from  cis, but not  trans, complexes.)	bind
20345	4	5939	5	NULL	NULL	0	NULL	ATPase	NULL	single turnover of	does not release	NULL				OTC	NULL	from trans complex			NULL		NULL	NULL	NULL	NULL	gw60_structure_4_1_1_s_81	8805512	(This was shown by using a single ring mutant GroEL that rapidly binds but very slowly releases GroES in single turnover studies to trap released GroES; results revealed that a single turnover of ATPase was sufficient for productive release of OTC from  cis, but not  trans, complexes.)	bind
18283	1	5939	7	NULL	NULL	NULL	NULL	GroEL 	GP	single ring mutant	binds		rapidly			GroES	GP				NULL		NULL	NULL	NULL	NULL	gw60_structure_4_1_1_s_81	8805512	(This was shown by using a single ring mutant GroEL that rapidly binds but very slowly releases GroES in single turnover studies to trap released GroES; results revealed that a single turnover of ATPase was sufficient for productive release of OTC from  cis, but not  trans, complexes.)	bind
18284	2	5939	7	NULL	NULL	NULL	NULL	ATPase	GP	single turnover of 	release 		productively			OTC	GP	from cis complex			NULL		NULL	NULL	NULL	NULL	gw60_structure_4_1_1_s_81	8805512	(This was shown by using a single ring mutant GroEL that rapidly binds but very slowly releases GroES in single turnover studies to trap released GroES; results revealed that a single turnover of ATPase was sufficient for productive release of OTC from  cis, but not  trans, complexes.)	bind
18285	3	5939	7	NULL	NULL	NULL	NULL	ATPase	GP	single turnover of 	does not release		productively			OTC	GP	from trans complex			NULL		NULL	NULL	NULL	NULL	gw60_structure_4_1_1_s_81	8805512	(This was shown by using a single ring mutant GroEL that rapidly binds but very slowly releases GroES in single turnover studies to trap released GroES; results revealed that a single turnover of ATPase was sufficient for productive release of OTC from  cis, but not  trans, complexes.)	bind
20373	4	5939	7	NULL	NULL	NULL	NULL	GroEL	GP	single ring mutant	releases		slowly			GroES	GP				NULL		NULL	NULL	NULL	NULL	gw60_structure_4_1_1_s_81	8805512	(This was shown by using a single ring mutant GroEL that rapidly binds but very slowly releases GroES in single turnover studies to trap released GroES; results revealed that a single turnover of ATPase was sufficient for productive release of OTC from  cis, but not  trans, complexes.)	bind
15426	1	5941	5	NULL	NULL	0	NULL	Axin	NULL		bind	NULL				MEKK	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_269	12192039	(Top panel) In the absence of GSK-3beta, Axin binds MEKK, leading to activation of the JNK pathway.	bind
15427	2	5941	5	NULL	NULL	0	NULL	statement 1	NULL		in the absence of	NULL				GSK-3beta	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_269	12192039	(Top panel) In the absence of GSK-3beta, Axin binds MEKK, leading to activation of the JNK pathway.	bind
15428	3	5941	5	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				JNK pathway	NULL	activation of 			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_269	12192039	(Top panel) In the absence of GSK-3beta, Axin binds MEKK, leading to activation of the JNK pathway.	bind
18288	1	5941	7	NULL	NULL	NULL	NULL	Axin	GP		binds					MEKK	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_269	12192039	(Top panel) In the absence of GSK-3beta, Axin binds MEKK, leading to activation of the JNK pathway.	bind
18289	2	5941	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs in the absence of					GSK-3beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_269	12192039	(Top panel) In the absence of GSK-3beta, Axin binds MEKK, leading to activation of the JNK pathway.	bind
18290	3	5941	7	NULL	NULL	NULL	NULL	statement 1	Process		leads to					JNK pathway	Process	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_269	12192039	(Top panel) In the absence of GSK-3beta, Axin binds MEKK, leading to activation of the JNK pathway.	bind
15429	1	5942	5	NULL	NULL	0	NULL	Axin	NULL		bind	NULL				beta-catenin	NULL	free			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
15430	2	5942	5	NULL	NULL	0	NULL	statement 1	NULL		in the absence of	NULL				HIC	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
15431	3	5942	5	NULL	NULL	0	NULL	statement 1	NULL		in the absence of	NULL				I-mfa	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
15432	4	5942	5	NULL	NULL	0	NULL	statement 2	NULL		is an alternative to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
15433	5	5942	5	NULL	NULL	0	NULL	beta-catenin	NULL		is released from	NULL				E-cadherin	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
15434	6	5942	5	NULL	NULL	0	NULL	Axin	NULL		bind	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
15435	7	5942	5	NULL	NULL	0	NULL	statement 6	NULL		in the absence of	NULL				HIC	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
15436	8	5942	5	NULL	NULL	0	NULL	statement 6	NULL		in the absence of	NULL				I-mfa	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
15437	9	5942	5	NULL	NULL	0	NULL	statement 7	NULL		is an alternative to	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
15438	10	5942	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
15439	11	5942	5	NULL	NULL	0	NULL	Axin	NULL		promote	NULL				beta-catenin	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
15440	12	5942	5	NULL	NULL	0	NULL	GSK-3beta	NULL		undergoes	NULL				degradation	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
15441	13	5942	5	NULL	NULL	0	NULL	beta-catenin	NULL		undergoes	NULL				degradation	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
15442	14	5942	5	NULL	NULL	0	NULL	statement 12	NULL		leads to	NULL				statement 11	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
15443	15	5942	5	NULL	NULL	0	NULL	statement 13	NULL		leads to	NULL				statement 11	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
18291	1	5942	7	NULL	NULL	NULL	NULL	Axin	GP		binds					beta-catenin	GP	free			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
18292	2	5942	7	NULL	NULL	NULL	NULL	E-cadherin	GP		release					beta-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
18293	3	5942	7	NULL	NULL	NULL	NULL	Axin	GP		binds					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
18294	4	5942	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs in the absence of					HIC	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
18295	5	5942	7	NULL	NULL	NULL	NULL	statement 3	Process		occurs in the absence of					HIC	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
18296	6	5942	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs in the absence of					I-mfa	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
18297	7	5942	7	NULL	NULL	NULL	NULL	statement 3	Process		occurs in the absence of					I-mfa	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
18298	8	5942	7	NULL	NULL	NULL	NULL	GSK-3beta 	GP		phosphorylates					beta-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
18299	9	5942	7	NULL	NULL	NULL	NULL	statement 1	Process		promotes					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
18300	10	5942	7	NULL	NULL	NULL	NULL	statement 3	Process		promotes					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
18301	11	5942	7	NULL	NULL	NULL	NULL	statement 1	Process		promotes					beta-catenin	Process	degradation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
18302	12	5942	7	NULL	NULL	NULL	NULL	statement 3	Process		promotes					beta-catenin	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6393_s_263	12192039	(Top panel) In the absence of HIC or I-mfa, Axin binds free beta-catenin or beta-catenin that is released from E-cadherin and promotes phosphorylation of beta-catenin by GSK-3beta and beta-catenin degradation.	bind
15444	1	5944	5	NULL	NULL	0	NULL	Ets-1	NULL		bind	NULL				EBS probe	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_20_4154_s_168	11600704	(Top) EMSA of Ets-1 binding to the EBS probe.	bind
18304	1	5944	7	NULL	NULL	NULL	NULL	Ets-1	GP		binds to					EBS probe	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_20_4154_s_168	11600704	(Top) EMSA of Ets-1 binding to the EBS probe.	bind
15445	1	5945	5	NULL	NULL	0	NULL	SAP1a	NULL		bind	NULL				EBS probe	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_20_4154_s_130	11600704	(Top) EMSA of SAP1a binding to the EBS probe.	bind
18305	1	5945	7	NULL	NULL	NULL	NULL	SAP1a	GP		bind					EBS probe	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_20_4154_s_130	11600704	(Top) EMSA of SAP1a binding to the EBS probe.	bind
15446	1	5946	5	NULL	NULL	0	NULL	LR1	NULL		bind	NULL				pBEND2(Sgamma1)	NULL			164 bp fragments	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_14_2651_s_89	10908319	(Top) Gel mobility shift assay of LR1 binding to 164 bp fragments of pBEND2(Sgamma1) with the LR1 site at permuted positions, as indicated above; this corresponds to digestion with:	bind
46296	2	5946	5	NULL	NULL	0	NULL		NULL		resides within	NULL			LR1 site		NULL			164 bp fragments	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_14_2651_s_89	10908319	(Top) Gel mobility shift assay of LR1 binding to 164 bp fragments of pBEND2(Sgamma1) with the LR1 site at permuted positions, as indicated above; this corresponds to digestion with:	bind
18306	1	5946	7	NULL	NULL	NULL	NULL	LR1	GP		bind					pBEND2(Sgamma1)	GP			164 bp fragments 	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_14_2651_s_89	10908319	(Top) Gel mobility shift assay of LR1 binding to 164 bp fragments of pBEND2(Sgamma1) with the LR1 site at permuted positions, as indicated above; this corresponds to digestion with:	bind
18330	2	5946	7	NULL	NULL	0	NULL		NULL		resides within	NULL			LR1 site		NULL			164 bp fragments	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_14_2651_s_89	10908319	(Top) Gel mobility shift assay of LR1 binding to 164 bp fragments of pBEND2(Sgamma1) with the LR1 site at permuted positions, as indicated above; this corresponds to digestion with:	bind
15447	1	5950	5	NULL	NULL	0	NULL	NuMA	NULL		associate with	NULL				dynein	NULL	cytoplasmic			NULL		0	NULL	NULL	NULL	gw60_cell_87_3_447_s_188	8898198	(Top) NuMA associates with cytoplasmic dynein; its binding to stationary microtubules enables the  complex to translocate free microtubules towards the chromatin or, by binding to free  microtubules, to move them polewards.	bind
15448	2	5950	5	NULL	NULL	0	NULL	NuMA	NULL		bind	NULL				microtubules	NULL	stationary			NULL		0	NULL	NULL	NULL	gw60_cell_87_3_447_s_188	8898198	(Top) NuMA associates with cytoplasmic dynein; its binding to stationary microtubules enables the  complex to translocate free microtubules towards the chromatin or, by binding to free  microtubules, to move them polewards.	bind
15449	3	5950	5	NULL	NULL	0	NULL	statement 1	NULL		translocates	NULL				free microtubules	NULL	towards chromatin			NULL		NULL	NULL	NULL	NULL	gw60_cell_87_3_447_s_188	8898198	(Top) NuMA associates with cytoplasmic dynein; its binding to stationary microtubules enables the  complex to translocate free microtubules towards the chromatin or, by binding to free  microtubules, to move them polewards.	bind
15450	4	5950	5	NULL	NULL	0	NULL	statement 2	NULL		enables	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_87_3_447_s_188	8898198	(Top) NuMA associates with cytoplasmic dynein; its binding to stationary microtubules enables the  complex to translocate free microtubules towards the chromatin or, by binding to free  microtubules, to move them polewards.	bind
15451	5	5950	5	NULL	NULL	0	NULL	NuMA	NULL		bind	NULL				microtubules	NULL	free			NULL		0	NULL	NULL	NULL	gw60_cell_87_3_447_s_188	8898198	(Top) NuMA associates with cytoplasmic dynein; its binding to stationary microtubules enables the  complex to translocate free microtubules towards the chromatin or, by binding to free  microtubules, to move them polewards.	bind
15452	6	5950	5	NULL	NULL	0	NULL	statement 5	NULL		moves	NULL				free microtubules	NULL	polewards			NULL		0	NULL	NULL	NULL	gw60_cell_87_3_447_s_188	8898198	(Top) NuMA associates with cytoplasmic dynein; its binding to stationary microtubules enables the  complex to translocate free microtubules towards the chromatin or, by binding to free  microtubules, to move them polewards.	bind
18331	1	5950	7	NULL	NULL	NULL	NULL	NuMA	GP		binds					dynein	GP	cytoplasmic			NULL		NULL	NULL	NULL	NULL	gw60_cell_87_3_447_s_188	8898198	(Top) NuMA associates with cytoplasmic dynein; its binding to stationary microtubules enables the  complex to translocate free microtubules towards the chromatin or, by binding to free  microtubules, to move them polewards.	bind
18332	2	5950	7	NULL	NULL	NULL	NULL	statement 1	Process		binds					 microtubules	CellComponent	stationary			NULL		NULL	NULL	NULL	NULL	gw60_cell_87_3_447_s_188	8898198	(Top) NuMA associates with cytoplasmic dynein; its binding to stationary microtubules enables the  complex to translocate free microtubules towards the chromatin or, by binding to free  microtubules, to move them polewards.	bind
18333	3	5950	7	NULL	NULL	NULL	NULL	statement 1	Process		translocate					free microtubules	CellComponent	 towards chromatin			NULL		NULL	NULL	NULL	NULL	gw60_cell_87_3_447_s_188	8898198	(Top) NuMA associates with cytoplasmic dynein; its binding to stationary microtubules enables the  complex to translocate free microtubules towards the chromatin or, by binding to free  microtubules, to move them polewards.	bind
18334	4	5950	7	NULL	NULL	NULL	NULL	statement 2	Process		enables					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_3_447_s_188	8898198	(Top) NuMA associates with cytoplasmic dynein; its binding to stationary microtubules enables the  complex to translocate free microtubules towards the chromatin or, by binding to free  microtubules, to move them polewards.	bind
18335	5	5950	7	NULL	NULL	NULL	NULL	statement 1	Process		binds					free microtubules	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_87_3_447_s_188	8898198	(Top) NuMA associates with cytoplasmic dynein; its binding to stationary microtubules enables the  complex to translocate free microtubules towards the chromatin or, by binding to free  microtubules, to move them polewards.	bind
18336	6	5950	7	NULL	NULL	NULL	NULL	statement 5	Process		move 					free microtubles	CellComponent	poleward			NULL		NULL	NULL	NULL	NULL	gw60_cell_87_3_447_s_188	8898198	(Top) NuMA associates with cytoplasmic dynein; its binding to stationary microtubules enables the  complex to translocate free microtubules towards the chromatin or, by binding to free  microtubules, to move them polewards.	bind
15453	1	5951	5	NULL	NULL	0	NULL	Rho	NULL		bind	NULL					NULL		RBD		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_158_1_153_s_87	12105187	(Top) Rho bound to RBD.	bind
18337	1	5951	7	NULL	NULL	NULL	NULL	Rho	GP		bind								RBD		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_158_1_153_s_87	12105187	(Top) Rho bound to RBD.	bind
15454	1	5953	5	NULL	NULL	0	NULL	S3P	NULL		bind	NULL				EPSP synthase	NULL				NULL		0	NULL	NULL	NULL	gw70_febslett_579_25_5773_s_105	16225867	(Top): S3P and glyphosate bound to EPSP synthase  (PDB 1G6S).	bind
20346	2	5953	5	NULL	NULL	0	NULL	glyphosate	NULL		bind	NULL				EPSP synthase	NULL				NULL		0	NULL	NULL	NULL	gw70_febslett_579_25_5773_s_105	16225867	(Top): S3P and glyphosate bound to EPSP synthase  (PDB 1G6S).	bind
18338	1	5953	7	NULL	NULL	NULL	NULL	S3P	GP		bind					EPSP synthase	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_579_25_5773_s_105	16225867	(Top): S3P and glyphosate bound to EPSP synthase  (PDB 1G6S).	bind
18339	2	5953	7	NULL	NULL	NULL	NULL	glyphosate	Chemical		bind					EPSP synthase 	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_579_25_5773_s_105	16225867	(Top): S3P and glyphosate bound to EPSP synthase  (PDB 1G6S).	bind
15455	1	5954	5	NULL	NULL	0	NULL	S3P	NULL		bind	NULL				EPSP synthase	NULL				NULL		0	NULL	NULL	NULL	gw70_febslett_579_25_5773_s_81	16225867	(Top): S3P bound to EPSP synthase (PDB 1G6T).	bind
18340	1	5954	7	NULL	NULL	NULL	NULL	S3P	GP		bind					EPSP synthase	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_579_25_5773_s_81	16225867	(Top): S3P bound to EPSP synthase (PDB 1G6T).	bind
16380	1	5955	5	NULL	NULL	0	NULL	RNA polymerase II	NULL		bind	NULL	relatively poorly			GST-Myc	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
16381	2	5955	5	NULL	NULL	0	NULL	RNA polymerase II	NULL		bind	NULL	relatively poorly			GST-Myc	NULL		N263		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
16382	3	5955	5	10	NULL	0	NULL	TFIIB	NULL		bind	NULL	relatively poorly			GST-Myc	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
16383	4	5955	5	10	NULL	0	NULL	TFIIB	NULL		bind	NULL	relatively poorly			GST-Myc	NULL		N263		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
20347	5	5955	5	NULL	NULL	0	NULL	TRAP 240	NULL		bind	NULL	relatively poorly			GST-Myc	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
20348	6	5955	5	NULL	NULL	0	NULL	TRAP 240	NULL		bind	NULL	relatively poorly			GST-Myc	NULL		N263		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
20349	7	5955	5	NULL	NULL	0	NULL	TRAP 230	NULL		bind	NULL	relatively poorly			GST-Myc	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
20350	8	5955	5	NULL	NULL	0	NULL	TRAP 230	NULL		bind	NULL	relatively poorly			GST-Myc	NULL		N263		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
20351	9	5955	5	NULL	NULL	0	NULL	TRAP 170	NULL		bind	NULL	relatively poorly			GST-Myc	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
20352	10	5955	5	NULL	NULL	0	NULL	TRAP 170	NULL		bind	NULL	relatively poorly			GST-Myc	NULL		N263		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
44804	11	5955	5	10	NULL	0	NULL	TFIIB	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
18341	1	5955	7	NULL	NULL	NULL	NULL	TRAP 240	GP		bind		poorly			GST-Myc	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
18342	2	5955	7	NULL	NULL	NULL	NULL	TRAP 240	GP		bind		poorly			GST-Myc	GP		N263		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
18343	3	5955	7	NULL	NULL	NULL	NULL	TRAP 230	GP		bind		poorly			GST-Myc	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
18344	4	5955	7	NULL	NULL	NULL	NULL	TRAP 230	GP		bind		poorly			GST-Myc	GP		N263		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
18345	5	5955	7	NULL	NULL	NULL	NULL	TRAP 170	GP		bind		poorly			GST-Myc	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
18346	6	5955	7	NULL	NULL	NULL	NULL	TRAP 170	GP		bind		poorly			GST-Myc	GP		N263		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
18347	7	5955	7	NULL	NULL	NULL	NULL	RNA polymerase II	GP		bind		poorly			GST-Myc	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
18348	8	5955	7	NULL	NULL	NULL	NULL	RNA polymerase II	GP		bind		poorly			GST-Myc	GP		N263		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
18349	9	5955	7	NULL	NULL	NULL	NULL	TFIIB	GP		bind		poorly			GST-Myc	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
18350	10	5955	7	NULL	NULL	NULL	NULL	TFIIB	GP		bind		poorly			GST-Myc	GP		N263		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
44805	11	5955	7	NULL	NULL	NULL	NULL	TFIIB	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20405_s_86	12660246	(TRAPs 240, 230, and 170), RNA  polymerase II, and the general transcription factor TFIIB bound relatively  poorly to GST-Myc and GST-MycN263 ( i.e. binding was either  undetectable or well below 5% of the input in corresponding panels in   lanes 3 and  6).	bind
15456	1	5956	5	NULL	NULL	0	NULL	seven-transmembrane domain superfamily receptor	NULL		bind	NULL				RANTES	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7551_s_27	8631787	(Type A and Type  B( 17,  18) ) and a single receptor that binds both  RANTES and MIP-1alpha  ( 19,  20) have been cloned and  shown to be members of the seven-transmembrane domain superfamily of  receptors.	bind
15457	2	5956	5	NULL	NULL	0	NULL	seven-transmembrane domain superfamily receptor	NULL		bind	NULL				MIP-1alpha	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7551_s_27	8631787	(Type A and Type  B( 17,  18) ) and a single receptor that binds both  RANTES and MIP-1alpha  ( 19,  20) have been cloned and  shown to be members of the seven-transmembrane domain superfamily of  receptors.	bind
18351	1	5956	7	NULL	NULL	NULL	NULL	seven-transmembrane domain superfamily receptor	GP		bind					RANTES	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7551_s_27	8631787	(Type A and Type  B( 17,  18) ) and a single receptor that binds both  RANTES and MIP-1alpha  ( 19,  20) have been cloned and  shown to be members of the seven-transmembrane domain superfamily of  receptors.	bind
18352	2	5956	7	NULL	NULL	NULL	NULL	seven-transmembrane domain superfamily receptor	GP		bind					MIP-1alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_13_7551_s_27	8631787	(Type A and Type  B( 17,  18) ) and a single receptor that binds both  RANTES and MIP-1alpha  ( 19,  20) have been cloned and  shown to be members of the seven-transmembrane domain superfamily of  receptors.	bind
18353	1	5957	7	NULL	NULL	NULL	NULL	 		conservative mutations	abolish			Glu327Gln 		Tl+ ion	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1505_1_57_s_104	11248189	(Upper left) High affinity 204Tl+ in wild type (WT) ( ) with maximum capacity 1.9 plus-or-minus 0.3 Tl+ ions per ouabain binding site and  K1/2=7.3 plus-or-minus 3.3  M. Tl+ ion binding is abolished after conservative mutations Glu327Gln ( ) or Glu327Asp ( ).	bind
18354	2	5957	7	NULL	NULL	NULL	NULL			conservative mutations	abolish			Glu327Asp		Tl+ ion	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1505_1_57_s_104	11248189	(Upper left) High affinity 204Tl+ in wild type (WT) ( ) with maximum capacity 1.9 plus-or-minus 0.3 Tl+ ions per ouabain binding site and  K1/2=7.3 plus-or-minus 3.3  M. Tl+ ion binding is abolished after conservative mutations Glu327Gln ( ) or Glu327Asp ( ).	bind
15458	1	5958	5	NULL	NULL	0	NULL	SKAP55	NULL		bind	NULL				FYB	NULL		SH3 domain		NULL	in vivo	NULL	NULL	NULL	NULL	gw60_embo_19_12_2889_s_110	10856234	(Upper panel) Mutation of tyrosine residues Y294F/Y297F attenuates  in vivo SKAP55 binding to the FYB SH3 domain.	bind
15459	2	5958	5	NULL	NULL	0	NULL		NULL	mutant	attenuate	NULL		Y294F/Y297F		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_19_12_2889_s_110	10856234	(Upper panel) Mutation of tyrosine residues Y294F/Y297F attenuates  in vivo SKAP55 binding to the FYB SH3 domain.	bind
18355	1	5958	7	NULL	NULL	NULL	NULL	SKAP55	GP		bind					FYB	GP		SH3 domain		NULL	in vivo	NULL	NULL	NULL	NULL	gw60_embo_19_12_2889_s_110	10856234	(Upper panel) Mutation of tyrosine residues Y294F/Y297F attenuates  in vivo SKAP55 binding to the FYB SH3 domain.	bind
18356	2	5958	7	NULL	NULL	NULL	NULL	tyrosine residues	AminoAcid	mutation of 	attenuate			Y294F/Y297F		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_12_2889_s_110	10856234	(Upper panel) Mutation of tyrosine residues Y294F/Y297F attenuates  in vivo SKAP55 binding to the FYB SH3 domain.	bind
15460	1	5959	5	NULL	NULL	0	NULL	PABP	NULL		bind	NULL				Cp transcript	NULL	endogenous			NULL	in U937 cells	0	NULL	NULL	NULL	gw60_molcellbiol_21_19_6440_s_264	11533233	(Upper panel) The binding of PABP to endogenous Cp transcript in U937 cells was determined.	bind
18358	1	5959	7	NULL	NULL	NULL	NULL	PABP	GP		bind					Cp transcript 	GP	endogenous			NULL	U937 cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_19_6440_s_264	11533233	(Upper panel) The binding of PABP to endogenous Cp transcript in U937 cells was determined.	bind
15461	1	5961	5	10	NULL	0	NULL	gD		soluble;; recombinant	bind								C-C'-C"` beta-strands		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_30_27006_s_49	12011057	(v) A soluble recombinant form of gD that binds to the C-C'-C"` beta-strands interfered with the binding of nectin3 and nectin4 to nectin1.	bind
15462	2	5961	5	NULL	NULL	0	NULL	nectin3	NULL		bind	NULL				nectin1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_30_27006_s_49	12011057	(v) A soluble recombinant form of gD that binds to the C-C'-C"` beta-strands interfered with the binding of nectin3 and nectin4 to nectin1.	bind
15463	3	5961	5	NULL	NULL	0	NULL	nectin4	NULL		bind	NULL				nectin1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_30_27006_s_49	12011057	(v) A soluble recombinant form of gD that binds to the C-C'-C"` beta-strands interfered with the binding of nectin3 and nectin4 to nectin1.	bind
15464	4	5961	5	NULL	NULL	0	NULL	statement 1	NULL		interfere with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_30_27006_s_49	12011057	(v) A soluble recombinant form of gD that binds to the C-C'-C"` beta-strands interfered with the binding of nectin3 and nectin4 to nectin1.	bind
15465	5	5961	5	NULL	NULL	0	NULL	statement 1	NULL		interfere with	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_30_27006_s_49	12011057	(v) A soluble recombinant form of gD that binds to the C-C'-C"` beta-strands interfered with the binding of nectin3 and nectin4 to nectin1.	bind
18359	1	5961	7	NULL	NULL	NULL	NULL	gD	GP	soluble;; recombinant	binds to								C-C'-C"` beta-strands		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_30_27006_s_49	12011057	(v) A soluble recombinant form of gD that binds to the C-C'-C"` beta-strands interfered with the binding of nectin3 and nectin4 to nectin1.	bind
18360	2	5961	7	NULL	NULL	NULL	NULL	nectin3	GP		bind					nectin1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_30_27006_s_49	12011057	(v) A soluble recombinant form of gD that binds to the C-C'-C"` beta-strands interfered with the binding of nectin3 and nectin4 to nectin1.	bind
18361	3	5961	7	NULL	NULL	NULL	NULL	nectin4	GP		bind					nectin1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_30_27006_s_49	12011057	(v) A soluble recombinant form of gD that binds to the C-C'-C"` beta-strands interfered with the binding of nectin3 and nectin4 to nectin1.	bind
18362	4	5961	7	NULL	NULL	NULL	NULL	statement 1	Process		interferes with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_30_27006_s_49	12011057	(v) A soluble recombinant form of gD that binds to the C-C'-C"` beta-strands interfered with the binding of nectin3 and nectin4 to nectin1.	bind
18363	5	5961	7	NULL	NULL	NULL	NULL	statement 1	Process		interferes with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_30_27006_s_49	12011057	(v) A soluble recombinant form of gD that binds to the C-C'-C"` beta-strands interfered with the binding of nectin3 and nectin4 to nectin1.	bind
15466	1	5962	5	NULL	NULL	0	NULL	KaiA	NULL		bind	NULL	exclusively			CII half 	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_25_9_2017_s_268	16628225	(v) EM and mutational data are consistent with KaiA binding exclusively to the  CII half (this work).	bind
18364	1	5962	7	NULL	NULL	NULL	NULL	KaiA	GP		bind		exclusively			CII half	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_2017_s_268	16628225	(v) EM and mutational data are consistent with KaiA binding exclusively to the  CII half (this work).	bind
20353	1	5963	5	NULL	NULL	0	NULL	cyclophilin-sensitive substrate	NULL	denatured	bind	NULL				GroEL	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_15_4568_s_9	9303301	(v) If a denatured cyclophilin-sensitive substrate is first bound to GroEL, however, productive folding to a cyclophilin-resistant form can be promoted, even without GroES.	bind
20354	2	5963	5	10	NULL	0	NULL	cyclophilin-sensitive substrate	NULL		folds to	NULL	productively			cyclophilin-resistant form	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_15_4568_s_9	9303301	(v) If a denatured cyclophilin-sensitive substrate is first bound to GroEL, however, productive folding to a cyclophilin-resistant form can be promoted, even without GroES.	bind
20355	3	5963	5	10	NULL	0	NULL	statement 2	NULL		occurs in absence of	NULL				GroES	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_15_4568_s_9	9303301	(v) If a denatured cyclophilin-sensitive substrate is first bound to GroEL, however, productive folding to a cyclophilin-resistant form can be promoted, even without GroES.	bind
45563	1	5963	7	NULL	NULL	NULL	NULL	cyclophilin-sensitive substrate	Chemical	denatured	bind					GroEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_15_4568_s_9	9303301	(v) If a denatured cyclophilin-sensitive substrate is first bound to GroEL, however, productive folding to a cyclophilin-resistant form can be promoted, even without GroES.	bind
45564	2	5963	7	NULL	NULL	NULL	NULL	cyclophilin-sensitive substrate	Chemical	denatured	 folds to		productively			 cyclophilin-resistant substrate	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_15_4568_s_9	9303301	(v) If a denatured cyclophilin-sensitive substrate is first bound to GroEL, however, productive folding to a cyclophilin-resistant form can be promoted, even without GroES.	bind
45565	3	5963	7	NULL	NULL	NULL	NULL	statement 2	Process		in the absence of					GroES	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_15_4568_s_9	9303301	(v) If a denatured cyclophilin-sensitive substrate is first bound to GroEL, however, productive folding to a cyclophilin-resistant form can be promoted, even without GroES.	bind
18468	1	5964	7	NULL	NULL	NULL	NULL	anti-Omp25	GP		bind					brucella	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_8_4823_s_231	11447156	(v) Macrophages infected with anti-Omp25-treated WT  B. suis produced TNF-alpha, an observation which is in line with a blockade of Omp25, since the anti-Omp25 antibody bound to an epitope of the protein which, in spite of LPS, was directly accessible on the bacteria and the comparison of the binding of anti-Omp25 and anti-Omp31 (two IgG2a MAbs) to  Brucella excluded the participation of the anti-Omp25 Fc group in TNF-alpha induction, as the levels of bound anti-Omp31 were significantly higher, yet the binding of anti-Omp31 exerted only a slight effect on the production of the cytokine during infection.	bind
18469	2	5964	7	NULL	NULL	NULL	NULL	anti-Omp31	GP		bind					brucella	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_8_4823_s_231	11447156	(v) Macrophages infected with anti-Omp25-treated WT  B. suis produced TNF-alpha, an observation which is in line with a blockade of Omp25, since the anti-Omp25 antibody bound to an epitope of the protein which, in spite of LPS, was directly accessible on the bacteria and the comparison of the binding of anti-Omp25 and anti-Omp31 (two IgG2a MAbs) to  Brucella excluded the participation of the anti-Omp25 Fc group in TNF-alpha induction, as the levels of bound anti-Omp31 were significantly higher, yet the binding of anti-Omp31 exerted only a slight effect on the production of the cytokine during infection.	bind
15467	1	5965	5	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				TNFR1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_8_2536_s_209	11909948	(v) Mutations in the P-loop motif abolish ATP binding by TNFR1.	bind
15468	2	5965	5	NULL	NULL	0	NULL		NULL	mutant	abolish	NULL		P-loop motif		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_8_2536_s_209	11909948	(v) Mutations in the P-loop motif abolish ATP binding by TNFR1.	bind
18366	1	5965	7	NULL	NULL	NULL	NULL	ATP 	Chemical		bind					TNFR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2536_s_209	11909948	(v) Mutations in the P-loop motif abolish ATP binding by TNFR1.	bind
18367	2	5965	7	NULL	NULL	NULL	NULL			mutant	abolish			P-loop motif		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2536_s_209	11909948	(v) Mutations in the P-loop motif abolish ATP binding by TNFR1.	bind
15469	1	5966	5	NULL	NULL	0	NULL	NF-kappaB proteins	NULL		bind	NULL				MMP-9	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_38_35766_s_10	12105194	(v) Recombinant IRF1, although unable to bind to an NF-kappaB consensus sequence, competes with NF-kappaB proteins for binding to the  MMP-9 promoter.	bind
15470	2	5966	5	NULL	NULL	0	NULL	IRF1	NULL	recombinant	does not bind	NULL					NULL			NF-kappaB consensus sequence	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_38_35766_s_10	12105194	(v) Recombinant IRF1, although unable to bind to an NF-kappaB consensus sequence, competes with NF-kappaB proteins for binding to the  MMP-9 promoter.	bind
15471	3	5966	5	NULL	NULL	0	NULL	IRF1	NULL	recombinant	bind	NULL				MMP-9	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_38_35766_s_10	12105194	(v) Recombinant IRF1, although unable to bind to an NF-kappaB consensus sequence, competes with NF-kappaB proteins for binding to the  MMP-9 promoter.	bind
15472	4	5966	5	NULL	NULL	0	NULL	statement 3	NULL		compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_38_35766_s_10	12105194	(v) Recombinant IRF1, although unable to bind to an NF-kappaB consensus sequence, competes with NF-kappaB proteins for binding to the  MMP-9 promoter.	bind
18368	1	5966	7	NULL	NULL	NULL	NULL	IRF1	GP	Recombinant	does not bind									NF-kappaB consensus sequence	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_38_35766_s_10	12105194	(v) Recombinant IRF1, although unable to bind to an NF-kappaB consensus sequence, competes with NF-kappaB proteins for binding to the  MMP-9 promoter.	bind
18369	2	5966	7	NULL	NULL	NULL	NULL	NF-kappaB protein	GP		binds					MMP-9	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_38_35766_s_10	12105194	(v) Recombinant IRF1, although unable to bind to an NF-kappaB consensus sequence, competes with NF-kappaB proteins for binding to the  MMP-9 promoter.	bind
18370	4	5966	7	NULL	NULL	NULL	NULL	statement 3	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_38_35766_s_10	12105194	(v) Recombinant IRF1, although unable to bind to an NF-kappaB consensus sequence, competes with NF-kappaB proteins for binding to the  MMP-9 promoter.	bind
25476	3	5966	7	NULL	NULL	NULL	NULL	IRF1	GP	recombinant	bind					MMP-9	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_38_35766_s_10	12105194	(v) Recombinant IRF1, although unable to bind to an NF-kappaB consensus sequence, competes with NF-kappaB proteins for binding to the  MMP-9 promoter.	bind
16324	1	5967	5	NULL	NULL	0	NULL	(V+C) FN	NULL		bind	NULL				PGs	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_13_11175_s_134	12482864	(V+C)  FN Binds Significantly More PGs Than Does V+C+ FN-- Analysis of small PG fractions bound to recombinant (V+C)  FN, recombinant V+C+ FN, and plasma FN revealed that the cartilage-specific isoform was able to bind small PGs despite the absence of protein segments V, III15, and I10 near the Hep II-binding domain.	bind
16325	2	5967	5	NULL	NULL	0	NULL	V+C+ FN	NULL		bind	NULL				PGs	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_13_11175_s_134	12482864	(V+C)  FN Binds Significantly More PGs Than Does V+C+ FN-- Analysis of small PG fractions bound to recombinant (V+C)  FN, recombinant V+C+ FN, and plasma FN revealed that the cartilage-specific isoform was able to bind small PGs despite the absence of protein segments V, III15, and I10 near the Hep II-binding domain.	bind
16326	3	5967	5	10	NULL	0	NULL	statement 1			more than		significantly			statement 2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_13_11175_s_134	12482864	(V+C)  FN Binds Significantly More PGs Than Does V+C+ FN-- Analysis of small PG fractions bound to recombinant (V+C)  FN, recombinant V+C+ FN, and plasma FN revealed that the cartilage-specific isoform was able to bind small PGs despite the absence of protein segments V, III15, and I10 near the Hep II-binding domain.	bind
16328	4	5967	5	NULL	NULL	0	NULL	PG fractions	NULL	small	bind	NULL				(V+C) FN	NULL	recombinant			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_13_11175_s_134	12482864	(V+C)  FN Binds Significantly More PGs Than Does V+C+ FN-- Analysis of small PG fractions bound to recombinant (V+C)  FN, recombinant V+C+ FN, and plasma FN revealed that the cartilage-specific isoform was able to bind small PGs despite the absence of protein segments V, III15, and I10 near the Hep II-binding domain.	bind
16329	5	5967	5	NULL	NULL	0	NULL	PG fractions	NULL	small	bind	NULL				V+C+ FN	NULL	recombinant			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_13_11175_s_134	12482864	(V+C)  FN Binds Significantly More PGs Than Does V+C+ FN-- Analysis of small PG fractions bound to recombinant (V+C)  FN, recombinant V+C+ FN, and plasma FN revealed that the cartilage-specific isoform was able to bind small PGs despite the absence of protein segments V, III15, and I10 near the Hep II-binding domain.	bind
16330	6	5967	5	NULL	NULL	0	NULL	PG fractions	NULL	small	bind	NULL				FN	NULL	plasma			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_13_11175_s_134	12482864	(V+C)  FN Binds Significantly More PGs Than Does V+C+ FN-- Analysis of small PG fractions bound to recombinant (V+C)  FN, recombinant V+C+ FN, and plasma FN revealed that the cartilage-specific isoform was able to bind small PGs despite the absence of protein segments V, III15, and I10 near the Hep II-binding domain.	bind
16331	7	5967	5	NULL	NULL	0	NULL	cartilage-specific isoform	NULL		bind	NULL				PGs	NULL	small			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_13_11175_s_134	12482864	(V+C)  FN Binds Significantly More PGs Than Does V+C+ FN-- Analysis of small PG fractions bound to recombinant (V+C)  FN, recombinant V+C+ FN, and plasma FN revealed that the cartilage-specific isoform was able to bind small PGs despite the absence of protein segments V, III15, and I10 near the Hep II-binding domain.	bind
16332	8	5967	5	NULL	NULL	0	NULL	statement 7	NULL		occurs despite	NULL				protein segment V	NULL	absence of	near Hep II-binding domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_13_11175_s_134	12482864	(V+C)  FN Binds Significantly More PGs Than Does V+C+ FN-- Analysis of small PG fractions bound to recombinant (V+C)  FN, recombinant V+C+ FN, and plasma FN revealed that the cartilage-specific isoform was able to bind small PGs despite the absence of protein segments V, III15, and I10 near the Hep II-binding domain.	bind
16333	9	5967	5	NULL	NULL	0	NULL	statement 7	NULL		occurs despite	NULL				protein segment III15	NULL	absence of	near Hep II-binding domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_13_11175_s_134	12482864	(V+C)  FN Binds Significantly More PGs Than Does V+C+ FN-- Analysis of small PG fractions bound to recombinant (V+C)  FN, recombinant V+C+ FN, and plasma FN revealed that the cartilage-specific isoform was able to bind small PGs despite the absence of protein segments V, III15, and I10 near the Hep II-binding domain.	bind
16334	10	5967	5	NULL	NULL	0	NULL	statement 7	NULL		occurs despite	NULL				protein segment I10	NULL	absence of	near Hep II-binding domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_13_11175_s_134	12482864	(V+C)  FN Binds Significantly More PGs Than Does V+C+ FN-- Analysis of small PG fractions bound to recombinant (V+C)  FN, recombinant V+C+ FN, and plasma FN revealed that the cartilage-specific isoform was able to bind small PGs despite the absence of protein segments V, III15, and I10 near the Hep II-binding domain.	bind
18371	1	5967	7	NULL	NULL	NULL	NULL	(V+C) FN	GP		bind					PGs	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_13_11175_s_134	12482864	(V+C)  FN Binds Significantly More PGs Than Does V+C+ FN-- Analysis of small PG fractions bound to recombinant (V+C)  FN, recombinant V+C+ FN, and plasma FN revealed that the cartilage-specific isoform was able to bind small PGs despite the absence of protein segments V, III15, and I10 near the Hep II-binding domain.	bind
18372	2	5967	7	NULL	NULL	NULL	NULL	V+C+ FN	GP		bind					PGs	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_13_11175_s_134	12482864	(V+C)  FN Binds Significantly More PGs Than Does V+C+ FN-- Analysis of small PG fractions bound to recombinant (V+C)  FN, recombinant V+C+ FN, and plasma FN revealed that the cartilage-specific isoform was able to bind small PGs despite the absence of protein segments V, III15, and I10 near the Hep II-binding domain.	bind
18373	3	5967	7	NULL	NULL	NULL	NULL	statement 1	Process		more than		significantly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_13_11175_s_134	12482864	(V+C)  FN Binds Significantly More PGs Than Does V+C+ FN-- Analysis of small PG fractions bound to recombinant (V+C)  FN, recombinant V+C+ FN, and plasma FN revealed that the cartilage-specific isoform was able to bind small PGs despite the absence of protein segments V, III15, and I10 near the Hep II-binding domain.	bind
18374	4	5967	7	NULL	NULL	NULL	NULL	PG	Chemical		bind					 FN	GP	plasma			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_13_11175_s_134	12482864	(V+C)  FN Binds Significantly More PGs Than Does V+C+ FN-- Analysis of small PG fractions bound to recombinant (V+C)  FN, recombinant V+C+ FN, and plasma FN revealed that the cartilage-specific isoform was able to bind small PGs despite the absence of protein segments V, III15, and I10 near the Hep II-binding domain.	bind
18375	5	5967	7	NULL	NULL	NULL	NULL	cartilage-specific isoform 	GP		bind					PGs	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_13_11175_s_134	12482864	(V+C)  FN Binds Significantly More PGs Than Does V+C+ FN-- Analysis of small PG fractions bound to recombinant (V+C)  FN, recombinant V+C+ FN, and plasma FN revealed that the cartilage-specific isoform was able to bind small PGs despite the absence of protein segments V, III15, and I10 near the Hep II-binding domain.	bind
18376	6	5967	7	NULL	NULL	NULL	NULL	statement 5	Process		occurs near								Hep II-binding domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_13_11175_s_134	12482864	(V+C)  FN Binds Significantly More PGs Than Does V+C+ FN-- Analysis of small PG fractions bound to recombinant (V+C)  FN, recombinant V+C+ FN, and plasma FN revealed that the cartilage-specific isoform was able to bind small PGs despite the absence of protein segments V, III15, and I10 near the Hep II-binding domain.	bind
18377	7	5967	7	NULL	NULL	NULL	NULL	statement 5	Process		occurs despite 					protein segment V	GP	absence of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_13_11175_s_134	12482864	(V+C)  FN Binds Significantly More PGs Than Does V+C+ FN-- Analysis of small PG fractions bound to recombinant (V+C)  FN, recombinant V+C+ FN, and plasma FN revealed that the cartilage-specific isoform was able to bind small PGs despite the absence of protein segments V, III15, and I10 near the Hep II-binding domain.	bind
18378	8	5967	7	NULL	NULL	NULL	NULL	statement 5	Process		occurs despite 					protein segment III15	GP	absence of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_13_11175_s_134	12482864	(V+C)  FN Binds Significantly More PGs Than Does V+C+ FN-- Analysis of small PG fractions bound to recombinant (V+C)  FN, recombinant V+C+ FN, and plasma FN revealed that the cartilage-specific isoform was able to bind small PGs despite the absence of protein segments V, III15, and I10 near the Hep II-binding domain.	bind
18379	9	5967	7	NULL	NULL	NULL	NULL	statement 5	Process		occurs despite					protein segment I10	GP	absence of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_13_11175_s_134	12482864	(V+C)  FN Binds Significantly More PGs Than Does V+C+ FN-- Analysis of small PG fractions bound to recombinant (V+C)  FN, recombinant V+C+ FN, and plasma FN revealed that the cartilage-specific isoform was able to bind small PGs despite the absence of protein segments V, III15, and I10 near the Hep II-binding domain.	bind
15617	1	5968	5	NULL	NULL	0	NULL	ITGA6/ITGB1	NULL		is	NULL				Epithelial 6 1 integrin	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_273_1_1_s_88	15302594	(vi) Epithelial  6 1 integrin (ITGA6/ITGB1)  and (vii) the long isoform of  1, (4-galactosyltransferaseB4GALT1) bind the laminin-1  (LAM1) G domain.	bind
15618	2	5968	5	NULL	NULL	0	NULL	ITGA6/ITGB1	NULL		bind	NULL				LAM1	NULL		G domain		NULL		0	NULL	NULL	NULL	gw70_devbiol_273_1_1_s_88	15302594	(vi) Epithelial  6 1 integrin (ITGA6/ITGB1)  and (vii) the long isoform of  1, (4-galactosyltransferaseB4GALT1) bind the laminin-1  (LAM1) G domain.	bind
15619	3	5968	5	NULL	NULL	0	NULL	LAM1	NULL		is	NULL				laminin-1	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_273_1_1_s_88	15302594	(vi) Epithelial  6 1 integrin (ITGA6/ITGB1)  and (vii) the long isoform of  1, (4-galactosyltransferaseB4GALT1) bind the laminin-1  (LAM1) G domain.	bind
15620	4	5968	5	NULL	NULL	0	NULL	long isoform of 1, (4-galactosyltransferaseB4GALT1)	NULL		bind	NULL				LAM1	NULL		G domain		NULL		0	NULL	NULL	NULL	gw70_devbiol_273_1_1_s_88	15302594	(vi) Epithelial  6 1 integrin (ITGA6/ITGB1)  and (vii) the long isoform of  1, (4-galactosyltransferaseB4GALT1) bind the laminin-1  (LAM1) G domain.	bind
18380	1	5968	7	NULL	NULL	NULL	NULL	Epithelial 6 1 integrin	GP		bind					laminin-1	GP		G domain		NULL		NULL	NULL	NULL	NULL	gw70_devbiol_273_1_1_s_88	15302594	(vi) Epithelial  6 1 integrin (ITGA6/ITGB1)  and (vii) the long isoform of  1, (4-galactosyltransferaseB4GALT1) bind the laminin-1  (LAM1) G domain.	bind
18381	2	5968	7	NULL	NULL	NULL	NULL	long isoform 1, (4-galactosyltransferaseB4GALT1)	GP		bind					laminin-1	GP		G domain		NULL		NULL	NULL	NULL	NULL	gw70_devbiol_273_1_1_s_88	15302594	(vi) Epithelial  6 1 integrin (ITGA6/ITGB1)  and (vii) the long isoform of  1, (4-galactosyltransferaseB4GALT1) bind the laminin-1  (LAM1) G domain.	bind
18382	3	5968	7	NULL	NULL	NULL	NULL	Epithelial 6 1 integrin	GP		is					ITGA6/ITGB1	GP				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_273_1_1_s_88	15302594	(vi) Epithelial  6 1 integrin (ITGA6/ITGB1)  and (vii) the long isoform of  1, (4-galactosyltransferaseB4GALT1) bind the laminin-1  (LAM1) G domain.	bind
18383	4	5968	7	NULL	NULL	NULL	NULL	LAM1	GP		is					 laminin-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_273_1_1_s_88	15302594	(vi) Epithelial  6 1 integrin (ITGA6/ITGB1)  and (vii) the long isoform of  1, (4-galactosyltransferaseB4GALT1) bind the laminin-1  (LAM1) G domain.	bind
15621	1	5969	5	NULL	NULL	0	NULL	Fibrinogen	NULL		bind	NULL				platelet alpha(IIb)beta3 receptor	NULL				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-thromb-haemost_3_8_16102057_s_17	16102057	(vi) Fibrinogen  binding to the platelet alpha(IIb)beta3 receptor, which is important for  incorporating platelets into a developing thrombus.	bind
15622	2	5969	5	NULL	NULL	0	NULL	statement 1	NULL		is important for	NULL				developing thrombus	NULL	incorporating platelets into			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-thromb-haemost_3_8_16102057_s_17	16102057	(vi) Fibrinogen  binding to the platelet alpha(IIb)beta3 receptor, which is important for  incorporating platelets into a developing thrombus.	bind
18385	1	5969	7	NULL	NULL	NULL	NULL	Fibrinogen	GP		bind					platelet alpha(IIb)beta3 receptor	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_j-thromb-haemost_3_8_16102057_s_17	16102057	(vi) Fibrinogen  binding to the platelet alpha(IIb)beta3 receptor, which is important for  incorporating platelets into a developing thrombus.	bind
18386	2	5969	7	NULL	NULL	NULL	NULL	statement 1	Process		is important for					developing thrombus	Process	 incorporating platelets into a			NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_j-thromb-haemost_3_8_16102057_s_17	16102057	(vi) Fibrinogen  binding to the platelet alpha(IIb)beta3 receptor, which is important for  incorporating platelets into a developing thrombus.	bind
15623	1	5970	5	NULL	NULL	0	NULL	GerK	NULL		bind	NULL				glucose	NULL				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-bacteriol_188_1_16352818_s_14	16352818	(vi) GerK binds glucose, GerB interacts  with fructose in addition to L-amino acids, and GerA interacts only with  L-valine, L-alanine, and its analogs.	bind
15624	2	5970	5	NULL	NULL	0	NULL	GerB	NULL		interacts with	NULL				fructose	NULL				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-bacteriol_188_1_16352818_s_14	16352818	(vi) GerK binds glucose, GerB interacts  with fructose in addition to L-amino acids, and GerA interacts only with  L-valine, L-alanine, and its analogs.	bind
15625	3	5970	5	NULL	NULL	0	NULL	GerB	NULL		interacts with	NULL				L-amino acids	NULL				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-bacteriol_188_1_16352818_s_14	16352818	(vi) GerK binds glucose, GerB interacts  with fructose in addition to L-amino acids, and GerA interacts only with  L-valine, L-alanine, and its analogs.	bind
15626	4	5970	5	NULL	NULL	0	NULL	GerA	NULL		interacts with	NULL				L-valine	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-bacteriol_188_1_16352818_s_14	16352818	(vi) GerK binds glucose, GerB interacts  with fructose in addition to L-amino acids, and GerA interacts only with  L-valine, L-alanine, and its analogs.	bind
15627	5	5970	5	NULL	NULL	0	NULL	GerA	NULL		interacts with	NULL				L-alanine	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-bacteriol_188_1_16352818_s_14	16352818	(vi) GerK binds glucose, GerB interacts  with fructose in addition to L-amino acids, and GerA interacts only with  L-valine, L-alanine, and its analogs.	bind
15628	6	5970	5	NULL	NULL	0	NULL	GerA	NULL		interacts with	NULL				L-alanine	NULL	analogs of			NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-bacteriol_188_1_16352818_s_14	16352818	(vi) GerK binds glucose, GerB interacts  with fructose in addition to L-amino acids, and GerA interacts only with  L-valine, L-alanine, and its analogs.	bind
15629	7	5970	5	NULL	NULL	0	NULL	GerA	NULL		interacts with	NULL				L-valine	NULL	analogs of			NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-bacteriol_188_1_16352818_s_14	16352818	(vi) GerK binds glucose, GerB interacts  with fructose in addition to L-amino acids, and GerA interacts only with  L-valine, L-alanine, and its analogs.	bind
18387	1	5970	7	NULL	NULL	NULL	NULL	GerK	GP		binds					glucose	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-bacteriol_188_1_16352818_s_14	16352818	(vi) GerK binds glucose, GerB interacts  with fructose in addition to L-amino acids, and GerA interacts only with  L-valine, L-alanine, and its analogs.	bind
18388	2	5970	7	NULL	NULL	NULL	NULL	GerB	GP		interacts with					fructose	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-bacteriol_188_1_16352818_s_14	16352818	(vi) GerK binds glucose, GerB interacts  with fructose in addition to L-amino acids, and GerA interacts only with  L-valine, L-alanine, and its analogs.	bind
18389	3	5970	7	NULL	NULL	NULL	NULL	GerB	GP		interacts with					L-amino acids	AminoAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-bacteriol_188_1_16352818_s_14	16352818	(vi) GerK binds glucose, GerB interacts  with fructose in addition to L-amino acids, and GerA interacts only with  L-valine, L-alanine, and its analogs.	bind
18390	4	5970	7	NULL	NULL	NULL	NULL	GerA	GP		interacts with					L-valine	AminoAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-bacteriol_188_1_16352818_s_14	16352818	(vi) GerK binds glucose, GerB interacts  with fructose in addition to L-amino acids, and GerA interacts only with  L-valine, L-alanine, and its analogs.	bind
18391	5	5970	7	NULL	NULL	NULL	NULL	GerA	GP		interacts with					L-alanine	AminoAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-bacteriol_188_1_16352818_s_14	16352818	(vi) GerK binds glucose, GerB interacts  with fructose in addition to L-amino acids, and GerA interacts only with  L-valine, L-alanine, and its analogs.	bind
18392	6	5970	7	NULL	NULL	NULL	NULL	GerA	GP		interacts with					L-valine	AminoAcid	analogs of			NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-bacteriol_188_1_16352818_s_14	16352818	(vi) GerK binds glucose, GerB interacts  with fructose in addition to L-amino acids, and GerA interacts only with  L-valine, L-alanine, and its analogs.	bind
18393	7	5970	7	NULL	NULL	NULL	NULL	GerA	GP		interacts with					L-alanine	AminoAcid	analogs of			NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-bacteriol_188_1_16352818_s_14	16352818	(vi) GerK binds glucose, GerB interacts  with fructose in addition to L-amino acids, and GerA interacts only with  L-valine, L-alanine, and its analogs.	bind
15630	1	5973	5	NULL	NULL	0	NULL	IGF-I	NULL		mediate	NULL				IGF-IR	NULL	ubiquitination of			NULL	p6 cells	0	NULL	NULL	NULL	gw60_molcellbiol_23_9_3363_s_270	12697834	(vii) Overexpression of a Grb10 mutant lacking the SH2 domain impairs IGF-I-mediated ubiquitination of the IGF-IR in both p6 and p6/Grb10 cells, suggesting that binding between Grb10 and Nedd4 is critical for ubiquitination of the receptor.	bind
15631	2	5973	5	NULL	NULL	0	NULL	IGF-I	NULL		mediate	NULL				IGF-IR	NULL	ubiquitination of			NULL	p6/Grb10 cells	0	NULL	NULL	NULL	gw60_molcellbiol_23_9_3363_s_270	12697834	(vii) Overexpression of a Grb10 mutant lacking the SH2 domain impairs IGF-I-mediated ubiquitination of the IGF-IR in both p6 and p6/Grb10 cells, suggesting that binding between Grb10 and Nedd4 is critical for ubiquitination of the receptor.	bind
15632	3	5973	5	10	NULL	0	NULL	Grb10	NULL	overexpression of;; mutant	impairs	NULL		SH2 domain		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_9_3363_s_270	12697834	(vii) Overexpression of a Grb10 mutant lacking the SH2 domain impairs IGF-I-mediated ubiquitination of the IGF-IR in both p6 and p6/Grb10 cells, suggesting that binding between Grb10 and Nedd4 is critical for ubiquitination of the receptor.	bind
15633	4	5973	5	10	NULL	0	NULL	Grb10	NULL	overexpression of;; mutant 	impairs	NULL		SH2 domain		statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_9_3363_s_270	12697834	(vii) Overexpression of a Grb10 mutant lacking the SH2 domain impairs IGF-I-mediated ubiquitination of the IGF-IR in both p6 and p6/Grb10 cells, suggesting that binding between Grb10 and Nedd4 is critical for ubiquitination of the receptor.	bind
15634	5	5973	5	NULL	NULL	0	NULL	Grb10	NULL		bind	NULL				Nedd4	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_9_3363_s_270	12697834	(vii) Overexpression of a Grb10 mutant lacking the SH2 domain impairs IGF-I-mediated ubiquitination of the IGF-IR in both p6 and p6/Grb10 cells, suggesting that binding between Grb10 and Nedd4 is critical for ubiquitination of the receptor.	bind
15635	6	5973	5	NULL	NULL	0	NULL	statement 5	NULL		critical for	NULL				IGF-IR	NULL	ubiquitination of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_9_3363_s_270	12697834	(vii) Overexpression of a Grb10 mutant lacking the SH2 domain impairs IGF-I-mediated ubiquitination of the IGF-IR in both p6 and p6/Grb10 cells, suggesting that binding between Grb10 and Nedd4 is critical for ubiquitination of the receptor.	bind
15636	7	5973	5	NULL	NULL	0	NULL	statement 3	NULL		suggest	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_9_3363_s_270	12697834	(vii) Overexpression of a Grb10 mutant lacking the SH2 domain impairs IGF-I-mediated ubiquitination of the IGF-IR in both p6 and p6/Grb10 cells, suggesting that binding between Grb10 and Nedd4 is critical for ubiquitination of the receptor.	bind
15637	8	5973	5	NULL	NULL	0	NULL	statement 4	NULL		suggest	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_9_3363_s_270	12697834	(vii) Overexpression of a Grb10 mutant lacking the SH2 domain impairs IGF-I-mediated ubiquitination of the IGF-IR in both p6 and p6/Grb10 cells, suggesting that binding between Grb10 and Nedd4 is critical for ubiquitination of the receptor.	bind
18394	1	5973	7	NULL	NULL	NULL	NULL	IGF-I	GP		mediates					IGF-IR	GP	 ubiquitination of			NULL	p6 cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_9_3363_s_270	12697834	(vii) Overexpression of a Grb10 mutant lacking the SH2 domain impairs IGF-I-mediated ubiquitination of the IGF-IR in both p6 and p6/Grb10 cells, suggesting that binding between Grb10 and Nedd4 is critical for ubiquitination of the receptor.	bind
18395	2	5973	7	NULL	NULL	NULL	NULL	IGF-I	GP		mediates					IGF-IR	GP	ubiquitination of			NULL	p6/Grb10 cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_23_9_3363_s_270	12697834	(vii) Overexpression of a Grb10 mutant lacking the SH2 domain impairs IGF-I-mediated ubiquitination of the IGF-IR in both p6 and p6/Grb10 cells, suggesting that binding between Grb10 and Nedd4 is critical for ubiquitination of the receptor.	bind
18396	3	5973	7	NULL	NULL	NULL	NULL	Grb10	GP	overexpression of;; mutant	impairs			SH2 domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_9_3363_s_270	12697834	(vii) Overexpression of a Grb10 mutant lacking the SH2 domain impairs IGF-I-mediated ubiquitination of the IGF-IR in both p6 and p6/Grb10 cells, suggesting that binding between Grb10 and Nedd4 is critical for ubiquitination of the receptor.	bind
18397	4	5973	7	NULL	NULL	NULL	NULL	Grb10	GP	overexpression of;; mutant	impairs			SH2 domain		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_9_3363_s_270	12697834	(vii) Overexpression of a Grb10 mutant lacking the SH2 domain impairs IGF-I-mediated ubiquitination of the IGF-IR in both p6 and p6/Grb10 cells, suggesting that binding between Grb10 and Nedd4 is critical for ubiquitination of the receptor.	bind
18398	5	5973	7	NULL	NULL	NULL	NULL	Grb10	GP		bind					Nedd4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_9_3363_s_270	12697834	(vii) Overexpression of a Grb10 mutant lacking the SH2 domain impairs IGF-I-mediated ubiquitination of the IGF-IR in both p6 and p6/Grb10 cells, suggesting that binding between Grb10 and Nedd4 is critical for ubiquitination of the receptor.	bind
18399	6	5973	7	NULL	NULL	NULL	NULL	statement 5	Process		is critical for					IGF-IR	GP	ubiquitination of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_9_3363_s_270	12697834	(vii) Overexpression of a Grb10 mutant lacking the SH2 domain impairs IGF-I-mediated ubiquitination of the IGF-IR in both p6 and p6/Grb10 cells, suggesting that binding between Grb10 and Nedd4 is critical for ubiquitination of the receptor.	bind
15638	1	5974	5	NULL	NULL	0	NULL	vWF	NULL		bind	NULL				collagen type I	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_26	7867173	(vWF can bind to collagen types I, II, and VI. 9 10  Collagen type I predominates in atherosclerotic arterial subendothelium.	bind
15639	2	5974	5	NULL	NULL	0	NULL	vWF	NULL		bind	NULL				collagen type II	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_26	7867173	(vWF can bind to collagen types I, II, and VI. 9 10  Collagen type I predominates in atherosclerotic arterial subendothelium.	bind
15640	3	5974	5	NULL	NULL	0	NULL	vWF	NULL		bind	NULL				collagen type VI	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_26	7867173	(vWF can bind to collagen types I, II, and VI. 9 10  Collagen type I predominates in atherosclerotic arterial subendothelium.	bind
15641	4	5974	5	NULL	NULL	0	NULL	Collagen type I	NULL		predominates in	NULL				atherosclerotic arterial subendothelium	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_26	7867173	(vWF can bind to collagen types I, II, and VI. 9 10  Collagen type I predominates in atherosclerotic arterial subendothelium.	bind
18400	1	5974	7	NULL	NULL	NULL	NULL	vWF	GP		bind					collagen type I	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_26	7867173	(vWF can bind to collagen types I, II, and VI. 9 10  Collagen type I predominates in atherosclerotic arterial subendothelium.	bind
18401	2	5974	7	NULL	NULL	NULL	NULL	vWF	GP		bind					collagen type II	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_26	7867173	(vWF can bind to collagen types I, II, and VI. 9 10  Collagen type I predominates in atherosclerotic arterial subendothelium.	bind
18402	3	5974	7	NULL	NULL	NULL	NULL	vWF	GP		bind					collagen type VI	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_26	7867173	(vWF can bind to collagen types I, II, and VI. 9 10  Collagen type I predominates in atherosclerotic arterial subendothelium.	bind
18403	4	5974	7	NULL	NULL	NULL	NULL	collagen type I	GP		predominates in					atherosclerotic arterial subendothelium	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_26	7867173	(vWF can bind to collagen types I, II, and VI. 9 10  Collagen type I predominates in atherosclerotic arterial subendothelium.	bind
15642	1	5976	5	NULL	NULL	0	NULL	MR	NULL		bind	NULL				cortisol	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_26	12756192	(While the MR binds cortisol with equal affinity, tissue specificity for aldosterone is conferred by the local expression of the enzyme 11beta-hydroxysteroid dehydrogenase (11betaHSD) type 2, which converts cortisol and corticosterone into the inactive cortisone and 11-dehydrocorticosterone.	bind
15643	2	5976	5	NULL	NULL	0	NULL	(11betaHSD) type 2	NULL		is	NULL				enzyme 11beta-hydroxysteroid dehydrogenase type 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_26	12756192	(While the MR binds cortisol with equal affinity, tissue specificity for aldosterone is conferred by the local expression of the enzyme 11beta-hydroxysteroid dehydrogenase (11betaHSD) type 2, which converts cortisol and corticosterone into the inactive cortisone and 11-dehydrocorticosterone.	bind
15644	3	5976	5	NULL	NULL	0	NULL	cortisol	NULL		is converted to	NULL				cortisone	NULL	inactive 			NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_26	12756192	(While the MR binds cortisol with equal affinity, tissue specificity for aldosterone is conferred by the local expression of the enzyme 11beta-hydroxysteroid dehydrogenase (11betaHSD) type 2, which converts cortisol and corticosterone into the inactive cortisone and 11-dehydrocorticosterone.	bind
15645	4	5976	5	NULL	NULL	0	NULL	(11betaHSD) type 2	NULL		is required for	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_26	12756192	(While the MR binds cortisol with equal affinity, tissue specificity for aldosterone is conferred by the local expression of the enzyme 11beta-hydroxysteroid dehydrogenase (11betaHSD) type 2, which converts cortisol and corticosterone into the inactive cortisone and 11-dehydrocorticosterone.	bind
15646	5	5976	5	NULL	NULL	0	NULL	corticosterone	NULL		is converted to	NULL				11-dehydrocorticosterone	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_26	12756192	(While the MR binds cortisol with equal affinity, tissue specificity for aldosterone is conferred by the local expression of the enzyme 11beta-hydroxysteroid dehydrogenase (11betaHSD) type 2, which converts cortisol and corticosterone into the inactive cortisone and 11-dehydrocorticosterone.	bind
15647	6	5976	5	NULL	NULL	0	NULL	(11betaHSD) type 2	NULL		is required for	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_26	12756192	(While the MR binds cortisol with equal affinity, tissue specificity for aldosterone is conferred by the local expression of the enzyme 11beta-hydroxysteroid dehydrogenase (11betaHSD) type 2, which converts cortisol and corticosterone into the inactive cortisone and 11-dehydrocorticosterone.	bind
20356	7	5976	5	NULL	NULL	0	NULL	aldosterone	NULL	tissue specificity for	is conferred by	NULL				(11betaHSD) type 2	NULL	 local expression of			NULL		0	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_26	12756192	(While the MR binds cortisol with equal affinity, tissue specificity for aldosterone is conferred by the local expression of the enzyme 11beta-hydroxysteroid dehydrogenase (11betaHSD) type 2, which converts cortisol and corticosterone into the inactive cortisone and 11-dehydrocorticosterone.	bind
18404	1	5976	7	NULL	NULL	NULL	NULL	MR	GP		binds					cortisol	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_26	12756192	(While the MR binds cortisol with equal affinity, tissue specificity for aldosterone is conferred by the local expression of the enzyme 11beta-hydroxysteroid dehydrogenase (11betaHSD) type 2, which converts cortisol and corticosterone into the inactive cortisone and 11-dehydrocorticosterone.	bind
18405	2	5976	7	NULL	NULL	NULL	NULL	cortisol	Chemical		is converted to					cortisone	Chemical	inactive			NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_26	12756192	(While the MR binds cortisol with equal affinity, tissue specificity for aldosterone is conferred by the local expression of the enzyme 11beta-hydroxysteroid dehydrogenase (11betaHSD) type 2, which converts cortisol and corticosterone into the inactive cortisone and 11-dehydrocorticosterone.	bind
18406	3	5976	7	NULL	NULL	NULL	NULL	corticosterone	Chemical		is converted to					11-dehydrocorticosterone	Chemical	inactive			NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_26	12756192	(While the MR binds cortisol with equal affinity, tissue specificity for aldosterone is conferred by the local expression of the enzyme 11beta-hydroxysteroid dehydrogenase (11betaHSD) type 2, which converts cortisol and corticosterone into the inactive cortisone and 11-dehydrocorticosterone.	bind
18407	4	5976	7	NULL	NULL	NULL	NULL	statement 2	Process		is carried out by					11betaHSD type 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_26	12756192	(While the MR binds cortisol with equal affinity, tissue specificity for aldosterone is conferred by the local expression of the enzyme 11beta-hydroxysteroid dehydrogenase (11betaHSD) type 2, which converts cortisol and corticosterone into the inactive cortisone and 11-dehydrocorticosterone.	bind
18408	5	5976	7	NULL	NULL	NULL	NULL	statement 3	Process		is carried out by					11betaHSD type 2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_26	12756192	(While the MR binds cortisol with equal affinity, tissue specificity for aldosterone is conferred by the local expression of the enzyme 11beta-hydroxysteroid dehydrogenase (11betaHSD) type 2, which converts cortisol and corticosterone into the inactive cortisone and 11-dehydrocorticosterone.	bind
18409	6	5976	7	NULL	NULL	NULL	NULL	aldosterone	Chemical	tissue specificity for	is conferred by					11betaHSD type 2	Chemical	local expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_26	12756192	(While the MR binds cortisol with equal affinity, tissue specificity for aldosterone is conferred by the local expression of the enzyme 11beta-hydroxysteroid dehydrogenase (11betaHSD) type 2, which converts cortisol and corticosterone into the inactive cortisone and 11-dehydrocorticosterone.	bind
18410	7	5976	7	NULL	NULL	NULL	NULL	11betaHSD	Chemical		is					11beta-hydroxysteroid dehydrogenase	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_26	12756192	(While the MR binds cortisol with equal affinity, tissue specificity for aldosterone is conferred by the local expression of the enzyme 11beta-hydroxysteroid dehydrogenase (11betaHSD) type 2, which converts cortisol and corticosterone into the inactive cortisone and 11-dehydrocorticosterone.	bind
15648	1	5977	5	10	NULL	0	NULL	Verprolin-homologous protein			is an effector of		downstream			IRSp53					NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-neurosci_25_4_15673667_s_10	15673667	(Wiskott-Aldrich  syndrome protein family Verprolin-homologous protein), a downstream effector  of IRSp53 that binds to the SH3 domain of IRSp53.	bind
15649	2	5977	5	NULL	NULL	0	NULL	Verprolin-homologous protein	NULL		bind	NULL				IRSp53	NULL		SH3 domain		NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-neurosci_25_4_15673667_s_10	15673667	(Wiskott-Aldrich  syndrome protein family Verprolin-homologous protein), a downstream effector  of IRSp53 that binds to the SH3 domain of IRSp53.	bind
44809	3	5977	5	10	NULL	0	NULL	Verprolin-homologous protein	NULL		belongs to 	NULL				Wiskott-Aldrich syndrome protein family	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_j-neurosci_25_4_15673667_s_10	15673667	(Wiskott-Aldrich  syndrome protein family Verprolin-homologous protein), a downstream effector  of IRSp53 that binds to the SH3 domain of IRSp53.	bind
18420	1	5977	7	NULL	NULL	NULL	NULL	Verprolin-homologous protein	GP		binds					IRSp53	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-neurosci_25_4_15673667_s_10	15673667	(Wiskott-Aldrich  syndrome protein family Verprolin-homologous protein), a downstream effector  of IRSp53 that binds to the SH3 domain of IRSp53.	bind
18421	2	5977	7	NULL	NULL	NULL	NULL	Verprolin-homologous protein	GP		belongs to					Wiskott-Aldrich syndrome protein family	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-neurosci_25_4_15673667_s_10	15673667	(Wiskott-Aldrich  syndrome protein family Verprolin-homologous protein), a downstream effector  of IRSp53 that binds to the SH3 domain of IRSp53.	bind
18422	3	5977	7	NULL	NULL	NULL	NULL	Verprolin-homologous protein	GP		is an effector of		downstream			IRSp53	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-neurosci_25_4_15673667_s_10	15673667	(Wiskott-Aldrich  syndrome protein family Verprolin-homologous protein), a downstream effector  of IRSp53 that binds to the SH3 domain of IRSp53.	bind
15650	1	5982	5	NULL	NULL	0	NULL	iso-1 cytochrome c	NULL	yeast	bind	NULL				heme lyase	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_25695_s_198	9748237	([I]), gave the dissociation constant ( K i) for the binding of yeast iso-1 cytochrome  c to heme lyase	bind
18424	1	5982	7	NULL	NULL	NULL	NULL	iso-1 cytochrome c	GP	yeast	bind					heme lyase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_25695_s_198	9748237	([I]), gave the dissociation constant ( K i) for the binding of yeast iso-1 cytochrome  c to heme lyase	bind
15651	1	5984	5	NULL	NULL	0	NULL	NGF	NULL		induce	NULL				ERK	NULL	phosphorylation			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_145	10688641	+ Ca2 chelatorsblock NGF-induced ERK phosphorylation.	bind
15652	2	5984	5	NULL	NULL	0	NULL	Ca2+ chelators	NULL		block	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_145	10688641	+ Ca2 chelatorsblock NGF-induced ERK phosphorylation.	bind
18425	1	5984	7	NULL	NULL	NULL	NULL	NGF	GP		induce					ERK	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_145	10688641	+ Ca2 chelatorsblock NGF-induced ERK phosphorylation.	bind
18426	2	5984	7	NULL	NULL	NULL	NULL	Ca2 chelators	Chemical		block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_145	10688641	+ Ca2 chelatorsblock NGF-induced ERK phosphorylation.	bind
15653	1	5986	5	NULL	NULL	0	NULL	DPPIV	NULL		bind	NULL				MBP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_27_24600_s_121	12716896	,   p <  0.01, relative to DPPIV binding to MBP.	bind
18428	1	5986	7	NULL	NULL	NULL	NULL	DPPIV	GP		bind					MBP	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_27_24600_s_121	12716896	,   p <  0.01, relative to DPPIV binding to MBP.	bind
15654	1	5988	5	NULL	NULL	0	NULL	spliceosomal 15.5 kD protein	NULL		bind	NULL				U4 snRNA fragment	NULL				NULL		NULL	NULL	NULL	NULL	gw70_nature_441_7097_1172_s_157	16810258	,  Nottrott, S. ,  Hartmuth, K. ,  Luhrmann, [[ R.  &  Ficner ]], R.   Crystal structure of the spliceosomal 15.5 kD protein bound to a U4 snRNA fragment.	bind
18500	1	5988	7	NULL	NULL	NULL	NULL	spliceosomal 15.5 kD protein	GP		bind					U4 snRNA fragment	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_nature_441_7097_1172_s_157	16810258	,  Nottrott, S. ,  Hartmuth, K. ,  Luhrmann, [[ R.  &  Ficner ]], R.   Crystal structure of the spliceosomal 15.5 kD protein bound to a U4 snRNA fragment.	bind
15655	1	5989	5	NULL	NULL	0	NULL	DPPIV	NULL		bind	NULL				MBP-FNIII12	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_27_24600_s_164	12716896	,  p < 0.01, relative to DPPIV binding to MBP-FNIII12  ( B) and relative to MTF7 adhesion to DPPIV-coated dishes  ( C).	bind
15656	2	5989	5	NULL	NULL	0	NULL	MTF7	NULL		adhere to	NULL				DPPIV	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_27_24600_s_164	12716896	,  p < 0.01, relative to DPPIV binding to MBP-FNIII12  ( B) and relative to MTF7 adhesion to DPPIV-coated dishes  ( C).	bind
18501	1	5989	7	NULL	NULL	NULL	NULL	DPPIV	GP		bind					MBP-FNIII12	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_27_24600_s_164	12716896	,  p < 0.01, relative to DPPIV binding to MBP-FNIII12  ( B) and relative to MTF7 adhesion to DPPIV-coated dishes  ( C).	bind
18502	2	5989	7	NULL	NULL	NULL	NULL	MTF7	GP		adhesion to					DPPIV-coated dishes	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_27_24600_s_164	12716896	,  p < 0.01, relative to DPPIV binding to MBP-FNIII12  ( B) and relative to MTF7 adhesion to DPPIV-coated dishes  ( C).	bind
15657	1	5992	5	NULL	NULL	0	NULL	NMDA antagonists	NULL		bind	NULL					NULL		glycine site		NULL		0	NULL	NULL	NULL	gw60_neurobioldis_12_1_82_s_8	12609492	, 1997) and noncompetitive NMDA receptor antagonists  ( Albers et al 1995 and   Lees 1997), as well as NMDA antagonists binding the glycine site  ( et al et al 2000 and   Sacco et al 2001), showed marked side effects and scant clinical efficacy.	bind
54138	2	5992	5	10	NULL	0	NULL	NMDA receptor antagonists		noncompetitive	bind								glycine site		NULL		0	NULL	NULL	NULL	gw60_neurobioldis_12_1_82_s_8	12609492	, 1997) and noncompetitive NMDA receptor antagonists  ( Albers et al 1995 and   Lees 1997), as well as NMDA antagonists binding the glycine site  ( et al et al 2000 and   Sacco et al 2001), showed marked side effects and scant clinical efficacy.	bind
18505	1	5992	7	NULL	NULL	NULL	NULL	NMDA receptor antagonists 	GP	noncompetitive	bind								glycine site		NULL		NULL	NULL	NULL	NULL	gw60_neurobioldis_12_1_82_s_8	12609492	, 1997) and noncompetitive NMDA receptor antagonists  ( Albers et al 1995 and   Lees 1997), as well as NMDA antagonists binding the glycine site  ( et al et al 2000 and   Sacco et al 2001), showed marked side effects and scant clinical efficacy.	bind
18506	2	5992	7	NULL	NULL	NULL	NULL	NMDA antagonists	GP		bind								glycine site		NULL		NULL	NULL	NULL	NULL	gw60_neurobioldis_12_1_82_s_8	12609492	, 1997) and noncompetitive NMDA receptor antagonists  ( Albers et al 1995 and   Lees 1997), as well as NMDA antagonists binding the glycine site  ( et al et al 2000 and   Sacco et al 2001), showed marked side effects and scant clinical efficacy.	bind
15658	1	5993	5	NULL	NULL	0	NULL	Wnt 	NULL		bind	NULL			response elements	Tcf-3	NULL				NULL		0	NULL	NULL	NULL	gw60_devbiol_257_1_190_s_350	12710967	, 1997) and the Wnt response elements bound by Tcf-3  ( Brannon et al 1997;  Laurent et al 1997 and   McKendry et al 1997).	bind
18507	1	5993	7	NULL	NULL	NULL	NULL	Tcf-3	GP		bind					 Wnt	GP			response element	NULL		NULL	NULL	NULL	NULL	gw60_devbiol_257_1_190_s_350	12710967	, 1997) and the Wnt response elements bound by Tcf-3  ( Brannon et al 1997;  Laurent et al 1997 and   McKendry et al 1997).	bind
15659	1	5995	5	NULL	NULL	0	NULL	MDM2	NULL		bind	NULL				pRb	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_107	12702724	, binding between MDM2 and pRb or Sp1  was  determined previously ( ).	bind
15660	2	5995	5	NULL	NULL	0	NULL	MDM2	NULL		bind	NULL				Sp1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_107	12702724	, binding between MDM2 and pRb or Sp1  was  determined previously ( ).	bind
15661	3	5995	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_107	12702724	, binding between MDM2 and pRb or Sp1  was  determined previously ( ).	bind
18508	1	5995	7	NULL	NULL	NULL	NULL	MDM2	GP		bind					pRb	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_107	12702724	, binding between MDM2 and pRb or Sp1  was  determined previously ( ).	bind
18509	2	5995	7	NULL	NULL	NULL	NULL	MDM2	GP		bind					Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_107	12702724	, binding between MDM2 and pRb or Sp1  was  determined previously ( ).	bind
18510	3	5995	7	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_107	12702724	, binding between MDM2 and pRb or Sp1  was  determined previously ( ).	bind
15663	1	5997	5	NULL	NULL	0	NULL	calpain	NULL	inactive native	associate with	NULL	reversibly			plasma membrane	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
15664	2	5997	5	NULL	NULL	0	NULL	Ca2+	NULL		induce	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
15666	3	5997	5	NULL	NULL	0	NULL	conformational changes	NULL	low Ca2+-induced	produce	NULL				calpain	NULL	active native			NULL	onto the inner surface of the plasma membrane	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
15667	4	5997	5	NULL	NULL	0	NULL	calpain	NULL	active	undergoes	NULL				autoproteolysis	NULL	irreversible			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
15668	5	5997	5	NULL	NULL	0	NULL	conformational changes	NULL	high Ca2+-induced	produce	NULL				calpain	NULL	soluble active native			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
15669	6	5997	5	NULL	NULL	0	NULL	calpain	NULL	soluble active	associate with	NULL	possibly			plasma membrane	NULL	inner surface of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
15670	7	5997	5	NULL	NULL	0	NULL	calpain	NULL	autoproteolyzed active	is released from	NULL	spontaneously			plasma membrane	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
15671	8	5997	5	NULL	NULL	0	NULL	calpain	NULL	active native	undergoes	NULL	possibly			autoproteolysis	NULL				NULL	in cytosol	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
15672	9	5997	5	NULL	NULL	0	NULL	statement 8	NULL		requires	NULL				Ca2+	NULL	high			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
15673	10	5997	5	NULL	NULL	0	NULL	calpastatin	NULL		bind	NULL	high affinity			calpain	NULL	autoproteolyzed			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
15674	11	5997	5	NULL	NULL	0	NULL	statement 10	NULL		inhibit	NULL				calpain	NULL	catalytic activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
15675	12	5997	5	NULL	NULL	0	NULL	calpastatin	NULL		is degraded to	NULL				fragments	NULL	active			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
15676	13	5997	5	NULL	NULL	0	NULL	calpastatin	NULL		is degraded to	NULL				fragments	NULL	inactive			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
15677	14	5997	5	NULL	NULL	0	NULL	calpastatin	NULL		bind	NULL				calpain	NULL	active native			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
15678	15	5997	5	NULL	NULL	0	NULL	statement 14	NULL		inhibit	NULL				calpain	NULL	catalytic activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
15679	16	5997	5	NULL	NULL	0	NULL	calpastatin	NULL		is degraded to	NULL				fragments	NULL	active, at lower rate			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
15680	17	5997	5	NULL	NULL	0	NULL	calpastatin	NULL		is degraded to	NULL				fragments	NULL	inactive, at lower rate			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
18829	1	5997	7	NULL	NULL	NULL	NULL	calpain 	GP	inactive native	binds					plasma membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
18830	2	5997	7	NULL	NULL	NULL	NULL	Ca2+	Chemical		induce					statement 1	Process	reversible association of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
18831	3	5997	7	NULL	NULL	NULL	NULL	calpain	GP	active native	on					plasma membrane	CellComponent	inner surface of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
18832	4	5997	7	NULL	NULL	NULL	NULL	Ca2+	Chemical	low	induce					statement 3	Process	conformational changes of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
18833	5	5997	7	NULL	NULL	NULL	NULL	calpain	GP	active	undergoes					autoproteolysis	Process	irreversible			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
18834	6	5997	7	NULL	NULL	NULL	NULL	Ca2+	Chemical	high	produce					calpain	GP	soluble active native			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
18835	7	5997	7	NULL	NULL	NULL	NULL	calpain	GP	soluble active	associate with					plasma membrane	CellComponent	inner surface of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
18836	8	5997	7	NULL	NULL	NULL	NULL	calpain	GP	autoproteolyzed active	release from					plasma membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
18837	9	5997	7	NULL	NULL	NULL	NULL	Ca2+	Chemical	high	autoproteolyse					calpain	GP	active native			NULL	cytosol	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
18838	10	5997	7	NULL	NULL	NULL	NULL	calpastatin	GP		binds		high affinity			calpain	GP	active autoproteolyzed 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
18839	11	5997	7	NULL	NULL	NULL	NULL	calpastatin	GP		inhibits					calpain	GP	catalytic activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
18840	12	5997	7	NULL	NULL	NULL	NULL	calpastatin	GP		degrades					calpain	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
18841	13	5997	7	NULL	NULL	NULL	NULL	statement 12	Process		produce					active fragments	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
18842	14	5997	7	NULL	NULL	NULL	NULL	statement 12	Process		produce					inactive fragments	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
18843	15	5997	7	NULL	NULL	NULL	NULL	statement 13	Process		occurs along with					statement 14	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38426_s_200	11485997	, Ca2+-induced reversible association of inactive native calpain ( ellipsoid) to plasma membrane;  , low Ca2+-induced conformational changes producing active native calpain ( hexagon) onto the inner surface of the plasma membrane;  , irreversible autoproteolysis of active calpain ( pentagon);   , high Ca2+-induced conformational changes producing soluble active native calpain;   , possible association of soluble active calpain to the inner surface of plasma membrane;   , spontaneous release of autoproteolyzed active calpain ( pentagon) from the plasma membrane;   , possible (high Ca2+-requiring) autoproteolysis of active native calpain in cytosol;   , calpastatin ( cross) binds active autoproteolyzed calpain with high affinity, inhibiting its catalytic activity, and is also degraded, producing active and inactive fragments;   , calpastatin binds active native calpain, inhibiting its catalytic activity, and is degraded to active and inactive fragments at a lower rate.	bind
15681	1	5999	5	NULL	NULL	0	NULL	cytohesin-1	NULL		bind	NULL				GST-p3(24-30ARF1)	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_28_21331_s_188	10748148	, densitometry showed that binding of cytohesin-1 and cytohesin-2 to GST-p3(24-30ARF1) was only ~60% of that of cytohesin-1 to GST-p3.	bind
15682	2	5999	5	NULL	NULL	0	NULL	cytohesin-2	NULL		bind	NULL				GST-p3(24-30ARF1)	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_28_21331_s_188	10748148	, densitometry showed that binding of cytohesin-1 and cytohesin-2 to GST-p3(24-30ARF1) was only ~60% of that of cytohesin-1 to GST-p3.	bind
15683	3	5999	5	NULL	NULL	0	NULL	cytohesin-1	NULL		bind	NULL				GST-p3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_28_21331_s_188	10748148	, densitometry showed that binding of cytohesin-1 and cytohesin-2 to GST-p3(24-30ARF1) was only ~60% of that of cytohesin-1 to GST-p3.	bind
18513	1	5999	7	NULL	NULL	NULL	NULL	cytohesin-1	GP		bind					GST-p3 (24-30ARF1)	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_28_21331_s_188	10748148	, densitometry showed that binding of cytohesin-1 and cytohesin-2 to GST-p3(24-30ARF1) was only ~60% of that of cytohesin-1 to GST-p3.	bind
18515	2	5999	7	NULL	NULL	NULL	NULL	cytohesin-2	GP		bind					GST-p3(24-30ARF1) 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_28_21331_s_188	10748148	, densitometry showed that binding of cytohesin-1 and cytohesin-2 to GST-p3(24-30ARF1) was only ~60% of that of cytohesin-1 to GST-p3.	bind
18518	3	5999	7	NULL	NULL	NULL	NULL	cytohesin-1	GP		bind					GST-p3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_28_21331_s_188	10748148	, densitometry showed that binding of cytohesin-1 and cytohesin-2 to GST-p3(24-30ARF1) was only ~60% of that of cytohesin-1 to GST-p3.	bind
15684	1	6001	5	NULL	NULL	0	NULL	GS I	NULL		interacts with	NULL				ovalbumin	NULL	pegion			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_17_14996_s_139	11836253	, laminin; +, bovine thyroglobulin;  ,  C. alata galactomannan;  , pigeon ovalbumin;  , GalNAcalpha1,3Galbeta polyacrylamide;  , GS I interaction with pigeon ovalbumin;  , GS I interaction with GalNAcalpha1,3Galbeta-polyacrylamide.	bind
15685	2	6001	5	NULL	NULL	0	NULL	GS I	NULL		interacts with	NULL				GalNAcalpha1,3Galbeta-polyacrylamide	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_17_14996_s_139	11836253	, laminin; +, bovine thyroglobulin;  ,  C. alata galactomannan;  , pigeon ovalbumin;  , GalNAcalpha1,3Galbeta polyacrylamide;  , GS I interaction with pigeon ovalbumin;  , GS I interaction with GalNAcalpha1,3Galbeta-polyacrylamide.	bind
18522	1	6001	7	NULL	NULL	NULL	NULL	GS I	GP		interacts with					ovalbumin	GP	pigeon			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14996_s_139	11836253	, laminin; +, bovine thyroglobulin;  ,  C. alata galactomannan;  , pigeon ovalbumin;  , GalNAcalpha1,3Galbeta polyacrylamide;  , GS I interaction with pigeon ovalbumin;  , GS I interaction with GalNAcalpha1,3Galbeta-polyacrylamide.	bind
18523	2	6001	7	NULL	NULL	NULL	NULL	GS I	GP		interacts with					GalNAcalpha1,3Galbeta polyacrylamide	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14996_s_139	11836253	, laminin; +, bovine thyroglobulin;  ,  C. alata galactomannan;  , pigeon ovalbumin;  , GalNAcalpha1,3Galbeta polyacrylamide;  , GS I interaction with pigeon ovalbumin;  , GS I interaction with GalNAcalpha1,3Galbeta-polyacrylamide.	bind
15686	1	6004	5	NULL	NULL	0	NULL	rGal-1 	NULL		bind	NULL				asialofetuin	NULL				NULL	in reducing buffer	0	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_149	7890630	, rGal-1 bound to asialofetuin-Sepharose in reducing buffer;   , rGal-1 bound to asialofetuin-Sepharose in nonreducing buffer;   , rGal-1 bound to laminin-Sepharose in nonreducing buffer;   , C2SrGal-1 bound to asialofetuin-Sepharose in nonreducing  buffer.	bind
15687	2	6004	5	NULL	NULL	0	NULL	rGal-1	NULL		bind	NULL				asialofetuin	NULL				NULL	in nonreducing buffer	0	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_149	7890630	, rGal-1 bound to asialofetuin-Sepharose in reducing buffer;   , rGal-1 bound to asialofetuin-Sepharose in nonreducing buffer;   , rGal-1 bound to laminin-Sepharose in nonreducing buffer;   , C2SrGal-1 bound to asialofetuin-Sepharose in nonreducing  buffer.	bind
15688	3	6004	5	NULL	NULL	0	NULL	rGal-1	NULL		bind	NULL				laminin	NULL				NULL	in reducing buffer	0	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_149	7890630	, rGal-1 bound to asialofetuin-Sepharose in reducing buffer;   , rGal-1 bound to asialofetuin-Sepharose in nonreducing buffer;   , rGal-1 bound to laminin-Sepharose in nonreducing buffer;   , C2SrGal-1 bound to asialofetuin-Sepharose in nonreducing  buffer.	bind
15689	4	6004	5	NULL	NULL	0	NULL	C2SrGal-1	NULL		bind	NULL				asialofetuin	NULL				NULL	in nonreducing buffer	0	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_149	7890630	, rGal-1 bound to asialofetuin-Sepharose in reducing buffer;   , rGal-1 bound to asialofetuin-Sepharose in nonreducing buffer;   , rGal-1 bound to laminin-Sepharose in nonreducing buffer;   , C2SrGal-1 bound to asialofetuin-Sepharose in nonreducing  buffer.	bind
18530	1	6004	7	NULL	NULL	NULL	NULL	 rGal-1	GP		bind					asialofetuin-Sepharose	Chemical				NULL	in reducing buffer	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_149	7890630	, rGal-1 bound to asialofetuin-Sepharose in reducing buffer;   , rGal-1 bound to asialofetuin-Sepharose in nonreducing buffer;   , rGal-1 bound to laminin-Sepharose in nonreducing buffer;   , C2SrGal-1 bound to asialofetuin-Sepharose in nonreducing  buffer.	bind
18538	2	6004	7	NULL	NULL	NULL	NULL	rGal-1	GP		bind					asialofetuin-Sepharose	Chemical				NULL	in nonreducing buffer	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_149	7890630	, rGal-1 bound to asialofetuin-Sepharose in reducing buffer;   , rGal-1 bound to asialofetuin-Sepharose in nonreducing buffer;   , rGal-1 bound to laminin-Sepharose in nonreducing buffer;   , C2SrGal-1 bound to asialofetuin-Sepharose in nonreducing  buffer.	bind
18539	3	6004	7	NULL	NULL	NULL	NULL	rGal-1	GP		bind					laminin-Sepharose	Chemical				NULL	in nonreducing buffer	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_149	7890630	, rGal-1 bound to asialofetuin-Sepharose in reducing buffer;   , rGal-1 bound to asialofetuin-Sepharose in nonreducing buffer;   , rGal-1 bound to laminin-Sepharose in nonreducing buffer;   , C2SrGal-1 bound to asialofetuin-Sepharose in nonreducing  buffer.	bind
18540	4	6004	7	NULL	NULL	NULL	NULL	C2SrGal-1	GP		bind					asialofetuin-Sepharose	Chemical				NULL	in nonreducing buffer	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5198_s_149	7890630	, rGal-1 bound to asialofetuin-Sepharose in reducing buffer;   , rGal-1 bound to asialofetuin-Sepharose in nonreducing buffer;   , rGal-1 bound to laminin-Sepharose in nonreducing buffer;   , C2SrGal-1 bound to asialofetuin-Sepharose in nonreducing  buffer.	bind
15690	1	6005	5	NULL	NULL	0	NULL	Quaternary ligand	NULL		bind	NULL				acetylcholinesterase	NULL		aromatic residues in active-site gorge		NULL		0	NULL	NULL	NULL	gw60_molpharmacol_55_6_982_s_293	10347238	, Schalk I, Ehret-Sabatier L, Bouet F, Goeldner M, Hirth C, Axelsen PH, Silman I and Sussman JL (1993) Quaternary ligand binding to aromatic residues in the active-site gorge of acetylcholinesterase.	bind
18542	1	6005	7	NULL	NULL	NULL	NULL	Quaternary ligand	Chemical		bind					acetylcholinesterase	GP		aromatic residues in the active-site gorge of 		NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_55_6_982_s_293	10347238	, Schalk I, Ehret-Sabatier L, Bouet F, Goeldner M, Hirth C, Axelsen PH, Silman I and Sussman JL (1993) Quaternary ligand binding to aromatic residues in the active-site gorge of acetylcholinesterase.	bind
15691	1	6009	5	NULL	NULL	0	NULL	GST-Six3	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_17_3_368_s_147	12569128	, the binding complex of GST-Six3 and DNA; arrowhead, supershifted binding complex using anti-Six3 antibody; arrow, supershifted binding complex using anti-GST antibody.	bind
18544	1	6009	7	NULL	NULL	NULL	NULL	GST-Six3	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_3_368_s_147	12569128	, the binding complex of GST-Six3 and DNA; arrowhead, supershifted binding complex using anti-Six3 antibody; arrow, supershifted binding complex using anti-GST antibody.	bind
15692	1	6010	5	NULL	NULL	0	NULL	oxipurinol	NULL		bind	NULL				xanthine oxidase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_14_7816_s_148	7713871	, without xanthine  oxidase (control);  , 2 muM  free xanthine oxidase;   , 2 muM  oxipurinol bound xanthine  oxidase.	bind
18545	1	6010	7	NULL	NULL	NULL	NULL	oxipurinol	Chemical		bind					xanthine oxidase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_14_7816_s_148	7713871	, without xanthine  oxidase (control);  , 2 muM  free xanthine oxidase;   , 2 muM  oxipurinol bound xanthine  oxidase.	bind
15693	1	6012	5	NULL	NULL	0	NULL	Abeta42	NULL		bind	NULL	state-specific 			Fe(II)	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_free-radic-biol-med_40_4_16458186_s_5	16458186	- and that Abeta42 influenced Fenton chemistry  through aggregation state-specific binding of both Fe(II) and Fe(III).	bind
15694	2	6012	5	NULL	NULL	0	NULL	Abeta42	NULL		bind	NULL	state-specific			Fe(III)	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_free-radic-biol-med_40_4_16458186_s_5	16458186	- and that Abeta42 influenced Fenton chemistry  through aggregation state-specific binding of both Fe(II) and Fe(III).	bind
15695	3	6012	5	NULL	NULL	0	NULL	Abeta42	NULL		influence	NULL				Fenton chemistry	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_free-radic-biol-med_40_4_16458186_s_5	16458186	- and that Abeta42 influenced Fenton chemistry  through aggregation state-specific binding of both Fe(II) and Fe(III).	bind
15696	4	6012	5	NULL	NULL	0	NULL	statement 3	NULL		occurs through	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_free-radic-biol-med_40_4_16458186_s_5	16458186	- and that Abeta42 influenced Fenton chemistry  through aggregation state-specific binding of both Fe(II) and Fe(III).	bind
15697	5	6012	5	NULL	NULL	0	NULL	statement 3	NULL		occurs through	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_free-radic-biol-med_40_4_16458186_s_5	16458186	- and that Abeta42 influenced Fenton chemistry  through aggregation state-specific binding of both Fe(II) and Fe(III).	bind
18546	1	6012	7	NULL	NULL	NULL	NULL	Abeta42	GP		bind		state-specific			Fe(II)	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_free-radic-biol-med_40_4_16458186_s_5	16458186	- and that Abeta42 influenced Fenton chemistry  through aggregation state-specific binding of both Fe(II) and Fe(III).	bind
18547	2	6012	7	NULL	NULL	NULL	NULL	Abeta42	GP		bind		state-specific			Fe(III)	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_free-radic-biol-med_40_4_16458186_s_5	16458186	- and that Abeta42 influenced Fenton chemistry  through aggregation state-specific binding of both Fe(II) and Fe(III).	bind
25484	3	6012	7	NULL	NULL	NULL	NULL	Abeta42	GP		influence					Fenton chemistry	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_free-radic-biol-med_40_4_16458186_s_5	16458186	- and that Abeta42 influenced Fenton chemistry  through aggregation state-specific binding of both Fe(II) and Fe(III).	bind
25485	4	6012	7	NULL	NULL	NULL	NULL	statement 3	Process		occurs through					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_free-radic-biol-med_40_4_16458186_s_5	16458186	- and that Abeta42 influenced Fenton chemistry  through aggregation state-specific binding of both Fe(II) and Fe(III).	bind
25486	5	6012	7	NULL	NULL	NULL	NULL	statement 3	Process		occurs through					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_free-radic-biol-med_40_4_16458186_s_5	16458186	- and that Abeta42 influenced Fenton chemistry  through aggregation state-specific binding of both Fe(II) and Fe(III).	bind
15698	1	6013	5	NULL	NULL	0	NULL	PLN1-26-PDZ-Myc-His6	NULL		bind	NULL				GST-SERCA2LCL	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_667_s_144	11854448	-, Mg2+- and ATP-binding protein, we examined the effects of Ca2+, Mg2+ and ATP on the binding of PLN1-26-PDZ-Myc-His6 to GST-SERCA2LCL.	bind
18548	1	6013	7	NULL	NULL	NULL	NULL	PLN1-26-PDZ-Myc-His6 	GP		bind					GST-SERCA2LCL	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_61_3_667_s_144	11854448	-, Mg2+- and ATP-binding protein, we examined the effects of Ca2+, Mg2+ and ATP on the binding of PLN1-26-PDZ-Myc-His6 to GST-SERCA2LCL.	bind
15699	1	6014	5	NULL	NULL	0	NULL	fbf	NULL		bind	NULL	specifically			gld-3S	NULL			3''-UTR	NULL		0	NULL	NULL	NULL	gw70_genetics_168_1_147_s_289	15454534	--   fbf binds specifically to  gld-3S 3''-UTR.	bind
18549	1	6014	7	NULL	NULL	NULL	NULL	fbf	GP		bind		specifically			gld-3S 	GP			3''-UTR	NULL		NULL	NULL	NULL	NULL	gw70_genetics_168_1_147_s_289	15454534	--   fbf binds specifically to  gld-3S 3''-UTR.	bind
15700	1	6015	5	10	NULL	0	NULL	p47	NULL		bind	NULL				rbcL RNA	NULL	amaranth			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_5_3476_s_253	11076953	--  Although binding of p47 to amaranth  rbcL RNA was not competed with amaranth  psbA transcript, this binding activity does share some properties with light-associated proteins that interact with the 5''-UTR of  psbA mRNA in other plant systems ( 1-4).	bind
15701	2	6015	5	10	NULL	0	NULL	p47	NULL		bind	NULL				psbA transcript	NULL	amaranth			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_5_3476_s_253	11076953	--  Although binding of p47 to amaranth  rbcL RNA was not competed with amaranth  psbA transcript, this binding activity does share some properties with light-associated proteins that interact with the 5''-UTR of  psbA mRNA in other plant systems ( 1-4).	bind
15702	3	6015	5	10	NULL	0	NULL	light-associated proteins	NULL		interacts with	NULL				psbA mRNA	NULL			5''-UTR	NULL	in other plant systems	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_5_3476_s_253	11076953	--  Although binding of p47 to amaranth  rbcL RNA was not competed with amaranth  psbA transcript, this binding activity does share some properties with light-associated proteins that interact with the 5''-UTR of  psbA mRNA in other plant systems ( 1-4).	bind
54139	4	6015	5	10	NULL	0	NULL	statement 1			does not compete with					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_5_3476_s_253	11076953	--  Although binding of p47 to amaranth  rbcL RNA was not competed with amaranth  psbA transcript, this binding activity does share some properties with light-associated proteins that interact with the 5''-UTR of  psbA mRNA in other plant systems ( 1-4).	bind
18550	1	6015	7	NULL	NULL	NULL	NULL	p47	GP		bind					rbcL RNA	NucleicAcid	 amaranth			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_5_3476_s_253	11076953	--  Although binding of p47 to amaranth  rbcL RNA was not competed with amaranth  psbA transcript, this binding activity does share some properties with light-associated proteins that interact with the 5''-UTR of  psbA mRNA in other plant systems ( 1-4).	bind
18551	4	6015	7	NULL	NULL	NULL	NULL	statement 2	Process		does not compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_5_3476_s_253	11076953	--  Although binding of p47 to amaranth  rbcL RNA was not competed with amaranth  psbA transcript, this binding activity does share some properties with light-associated proteins that interact with the 5''-UTR of  psbA mRNA in other plant systems ( 1-4).	bind
18552	3	6015	7	NULL	NULL	NULL	NULL	light-associated proteins	GP		interact with					 psbA mRNA	NucleicAcid			5''-UTR	NULL	in other plant systems	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_5_3476_s_253	11076953	--  Although binding of p47 to amaranth  rbcL RNA was not competed with amaranth  psbA transcript, this binding activity does share some properties with light-associated proteins that interact with the 5''-UTR of  psbA mRNA in other plant systems ( 1-4).	bind
55018	2	6015	7	NULL	NULL	NULL	NULL	p47	GP		bind					psbA transcript	NucleicAcid	amaranth			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_5_3476_s_253	11076953	--  Although binding of p47 to amaranth  rbcL RNA was not competed with amaranth  psbA transcript, this binding activity does share some properties with light-associated proteins that interact with the 5''-UTR of  psbA mRNA in other plant systems ( 1-4).	bind
15703	1	6017	5	NULL	NULL	0	NULL	TBP	NULL		bind	NULL				INO1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_genetics_169_4_1957_s_243	15716495	--  ChIP analysis of TBP binding to the  INO1 promoter.	bind
18553	1	6017	7	NULL	NULL	NULL	NULL	TBP	GP		bind					INO1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genetics_169_4_1957_s_243	15716495	--  ChIP analysis of TBP binding to the  INO1 promoter.	bind
15704	1	6018	5	NULL	NULL	0	NULL	Fob1p	NULL		bind	NULL				RFB	NULL				NULL		NULL	NULL	NULL	NULL	gw70_genetics_168_3_1205_s_244	15579680	--  Fob1p binding to the RFB is not diminished in  rrm3delta134-196 cells.	bind
15705	2	6018	5	NULL	NULL	0	NULL	statement 1	NULL		is not diminished in	NULL				rrm3delta134-196 cells	NULL				NULL		0	NULL	NULL	NULL	gw70_genetics_168_3_1205_s_244	15579680	--  Fob1p binding to the RFB is not diminished in  rrm3delta134-196 cells.	bind
18554	1	6018	7	NULL	NULL	NULL	NULL	Fob1p	GP		bind					RFB	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_genetics_168_3_1205_s_244	15579680	--  Fob1p binding to the RFB is not diminished in  rrm3delta134-196 cells.	bind
18555	2	6018	7	NULL	NULL	NULL	NULL	statement 1	Process		is not diminished in					rrm3delta134-196 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_genetics_168_3_1205_s_244	15579680	--  Fob1p binding to the RFB is not diminished in  rrm3delta134-196 cells.	bind
15706	1	6019	5	NULL	NULL	0	NULL	GLD-3	NULL		bind	NULL		N terminus		GLD-2	NULL				NULL		0	NULL	NULL	NULL	gw70_genetics_168_1_147_s_173	15454534	--  GLD-3 N terminus binds to GLD-2.	bind
18556	1	6019	7	NULL	NULL	NULL	NULL	GLD-3	GP		binds			N terminus		GLD-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_genetics_168_1_147_s_173	15454534	--  GLD-3 N terminus binds to GLD-2.	bind
15707	1	6020	5	NULL	NULL	0	NULL	Hap1	NULL		bind	NULL				HAP1	NULL			promoter region - 50 to - 300	NULL		0	NULL	NULL	NULL	gw70_genetics_169_3_1343_s_81	15654089	--  Hap1 binding to the  HAP1 promoter region encompassing nucleotide sequence  - 50 to  - 300.	bind
18557	1	6020	7	NULL	NULL	NULL	NULL	Hap1	GP		bind					HAP1	GP			promoter region - 50 to - 300	NULL		NULL	NULL	NULL	NULL	gw70_genetics_169_3_1343_s_81	15654089	--  Hap1 binding to the  HAP1 promoter region encompassing nucleotide sequence  - 50 to  - 300.	bind
15708	1	6021	5	NULL	NULL	0	NULL	Rad53	NULL		bind	NULL		kinase domain		ARS1	NULL				NULL		0	NULL	NULL	NULL	gw70_genetics_174_1_87_s_198	16816422	--  Rad53 kinase domain binds ARS1.	bind
18558	1	6021	7	NULL	NULL	NULL	NULL	Rad53 	GP		binds			kinase domain		ARS1	GP				NULL		NULL	NULL	NULL	NULL	gw70_genetics_174_1_87_s_198	16816422	--  Rad53 kinase domain binds ARS1.	bind
15709	1	6022	5	10	NULL	0	NULL	Rgt1 	NULL		bind	NULL	constitutively			HXT1	NULL			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genetics_169_2_583_s_103	15489524	--  Rgt1 constitutive repressors bind constitutively to the  HXT1 promoter.	bind
44814	2	6022	5	10	NULL	0	NULL	Rgt1	NULL		is a type of	NULL				constitutive repressor	NULL				NULL		NULL	NULL	NULL	NULL	gw70_genetics_169_2_583_s_103	15489524	--  Rgt1 constitutive repressors bind constitutively to the  HXT1 promoter.	bind
18559	1	6022	7	NULL	NULL	NULL	NULL	Rgt1	GP		bind		constitutively			HXT1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_genetics_169_2_583_s_103	15489524	--  Rgt1 constitutive repressors bind constitutively to the  HXT1 promoter.	bind
44817	2	6022	7	NULL	NULL	NULL	NULL	Rgt1	GP		is a type of					constitutive repressor	GP				NULL		NULL	NULL	NULL	NULL	gw70_genetics_169_2_583_s_103	15489524	--  Rgt1 constitutive repressors bind constitutively to the  HXT1 promoter.	bind
15710	1	6023	5	NULL	NULL	0	NULL	Rvs167p	NULL		bind	NULL		SH3 domain		Gyp5p	NULL				NULL		0	NULL	NULL	NULL	gw70_genetics_170_2_555_s_102	15802519	--  Rvs167p SH3 domain binds to Gyp5p and Gyl1p.	bind
15711	2	6023	5	NULL	NULL	0	NULL	Rvs167p	NULL		bind	NULL		SH3 domain		Gyl1p	NULL				NULL		0	NULL	NULL	NULL	gw70_genetics_170_2_555_s_102	15802519	--  Rvs167p SH3 domain binds to Gyp5p and Gyl1p.	bind
18560	1	6023	7	NULL	NULL	NULL	NULL	Rvs167p 	GP		bind			SH3 domain		Gyp5p	GP				NULL		NULL	NULL	NULL	NULL	gw70_genetics_170_2_555_s_102	15802519	--  Rvs167p SH3 domain binds to Gyp5p and Gyl1p.	bind
18561	2	6023	7	NULL	NULL	NULL	NULL	Rvs167p 	GP		bind			SH3 domain		Gyl1p	GP				NULL		NULL	NULL	NULL	NULL	gw70_genetics_170_2_555_s_102	15802519	--  Rvs167p SH3 domain binds to Gyp5p and Gyl1p.	bind
15712	1	6024	5	10	NULL	0	NULL	SEM-5/Grb2	NULL		bind	NULL		C-terminal SH3 domain		SOC-1/Gab1	NULL	atypical	proline-rich motif		NULL		NULL	NULL	NULL	NULL	gw70_genetics_173_1_163_s_116	16547100	--  The C-terminal SH3 domain of SEM-5/Grb2 binds an atypical proline-rich motif  within SOC-1/Gab1.	bind
18562	1	6024	7	NULL	NULL	NULL	NULL	SEM-5/Grb2	GP		binds to			C-terminal SH3 domain 		SOC-1/Gab1	GP		proline-rich motif		NULL		NULL	NULL	NULL	NULL	gw70_genetics_173_1_163_s_116	16547100	--  The C-terminal SH3 domain of SEM-5/Grb2 binds an atypical proline-rich motif  within SOC-1/Gab1.	bind
15714	1	6026	5	10	NULL	0	NULL	E1A	NULL		bind	NULL				CtBP 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38755_s_277	12161448	-- A previous report indicated that acetylation of E1A might diminish binding to the CtBP co-repressor ( 34) in contrast to this study.	bind
25642	2	6026	5	NULL	NULL	0	NULL	E1A	NULL	acetylation of	diminish	NULL	might			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_41_38755_s_277	12161448	-- A previous report indicated that acetylation of E1A might diminish binding to the CtBP co-repressor ( 34) in contrast to this study.	bind
44818	3	6026	5	10	NULL	0	NULL	CtBP	NULL		is a type of	NULL				co-repressor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_41_38755_s_277	12161448	-- A previous report indicated that acetylation of E1A might diminish binding to the CtBP co-repressor ( 34) in contrast to this study.	bind
18563	1	6026	7	NULL	NULL	NULL	NULL	E1A	GP		bind					CtBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38755_s_277	12161448	-- A previous report indicated that acetylation of E1A might diminish binding to the CtBP co-repressor ( 34) in contrast to this study.	bind
18564	2	6026	7	NULL	NULL	NULL	NULL	E1A	GP	acetylation of	diminish		might			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38755_s_277	12161448	-- A previous report indicated that acetylation of E1A might diminish binding to the CtBP co-repressor ( 34) in contrast to this study.	bind
44819	3	6026	7	NULL	NULL	NULL	NULL	CtBP	GP		is a type of					co-repressor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38755_s_277	12161448	-- A previous report indicated that acetylation of E1A might diminish binding to the CtBP co-repressor ( 34) in contrast to this study.	bind
15715	1	6027	5	NULL	NULL	0	NULL	stigmatellin	NULL		bind	NULL				bc1 complex	NULL	native			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3464_s_81	11707448	-- Binding of class II inhibitors like stigmatellin to the native  bc1 complex is known to increase the  Em value of the [2Fe-2S] cluster of the iron-sulfur subunit by about 200 mV ( 30).	bind
25643	2	6027	5	NULL	NULL	0	NULL	stigmatellin	NULL		is a type of	NULL				class II inhibitor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_5_3464_s_81	11707448	-- Binding of class II inhibitors like stigmatellin to the native  bc1 complex is known to increase the  Em value of the [2Fe-2S] cluster of the iron-sulfur subunit by about 200 mV ( 30).	bind
18565	1	6027	7	NULL	NULL	NULL	NULL	stigmatellin 	Chemical		bind					 bc1 complex	GP	native			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3464_s_81	11707448	-- Binding of class II inhibitors like stigmatellin to the native  bc1 complex is known to increase the  Em value of the [2Fe-2S] cluster of the iron-sulfur subunit by about 200 mV ( 30).	bind
18567	2	6027	7	NULL	NULL	NULL	NULL	stigmatellin 	Chemical		is a type of					class II inhibitors	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3464_s_81	11707448	-- Binding of class II inhibitors like stigmatellin to the native  bc1 complex is known to increase the  Em value of the [2Fe-2S] cluster of the iron-sulfur subunit by about 200 mV ( 30).	bind
15716	1	6028	5	NULL	NULL	0	NULL	Na+	NULL		bind	NULL				E1 form	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50283_s_240	14522987	-- It is generally accepted that the high and low affinity ATP binding reflects, respectively, binding to the E1 and E2 conformational state and that Na+ binds to the E1 form preceding phosphorylation and K+ binds to the E2 form during the Na/K-ATPase and  pNPPase reaction ( ,  ).	bind
15717	2	6028	5	NULL	NULL	0	NULL	statement 1	NULL		precede	NULL				phosphorylation	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50283_s_240	14522987	-- It is generally accepted that the high and low affinity ATP binding reflects, respectively, binding to the E1 and E2 conformational state and that Na+ binds to the E1 form preceding phosphorylation and K+ binds to the E2 form during the Na/K-ATPase and  pNPPase reaction ( ,  ).	bind
15718	3	6028	5	NULL	NULL	0	NULL	K+	NULL		bind	NULL				E2 form	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50283_s_240	14522987	-- It is generally accepted that the high and low affinity ATP binding reflects, respectively, binding to the E1 and E2 conformational state and that Na+ binds to the E1 form preceding phosphorylation and K+ binds to the E2 form during the Na/K-ATPase and  pNPPase reaction ( ,  ).	bind
15719	4	6028	5	NULL	NULL	0	NULL	statement 3	NULL		occurs during	NULL				Na/K-ATPase	NULL	reaction of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_50283_s_240	14522987	-- It is generally accepted that the high and low affinity ATP binding reflects, respectively, binding to the E1 and E2 conformational state and that Na+ binds to the E1 form preceding phosphorylation and K+ binds to the E2 form during the Na/K-ATPase and  pNPPase reaction ( ,  ).	bind
15720	5	6028	5	NULL	NULL	0	NULL	statement 3	NULL		occurs during	NULL				pNPPase	NULL	reaction of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_50283_s_240	14522987	-- It is generally accepted that the high and low affinity ATP binding reflects, respectively, binding to the E1 and E2 conformational state and that Na+ binds to the E1 form preceding phosphorylation and K+ binds to the E2 form during the Na/K-ATPase and  pNPPase reaction ( ,  ).	bind
25645	6	6028	5	NULL	NULL	0	NULL	ATP	NULL		bind	NULL	high affinity			E1 conformational state	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_50283_s_240	14522987	-- It is generally accepted that the high and low affinity ATP binding reflects, respectively, binding to the E1 and E2 conformational state and that Na+ binds to the E1 form preceding phosphorylation and K+ binds to the E2 form during the Na/K-ATPase and  pNPPase reaction ( ,  ).	bind
25646	7	6028	5	NULL	NULL	0	NULL	ATP	NULL		bind	NULL	low affinity			E2 conformational state	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_50283_s_240	14522987	-- It is generally accepted that the high and low affinity ATP binding reflects, respectively, binding to the E1 and E2 conformational state and that Na+ binds to the E1 form preceding phosphorylation and K+ binds to the E2 form during the Na/K-ATPase and  pNPPase reaction ( ,  ).	bind
18568	1	6028	7	NULL	NULL	NULL	NULL	ATP	Chemical		bind		high affinity			E1 conformational state	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_50283_s_240	14522987	-- It is generally accepted that the high and low affinity ATP binding reflects, respectively, binding to the E1 and E2 conformational state and that Na+ binds to the E1 form preceding phosphorylation and K+ binds to the E2 form during the Na/K-ATPase and  pNPPase reaction ( ,  ).	bind
18569	2	6028	7	NULL	NULL	NULL	NULL	ATP	Chemical		bind		low affinity			E2 conformational state	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_50283_s_240	14522987	-- It is generally accepted that the high and low affinity ATP binding reflects, respectively, binding to the E1 and E2 conformational state and that Na+ binds to the E1 form preceding phosphorylation and K+ binds to the E2 form during the Na/K-ATPase and  pNPPase reaction ( ,  ).	bind
18570	3	6028	7	NULL	NULL	NULL	NULL	Na+	Chemical		binds to					E1 form	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_50283_s_240	14522987	-- It is generally accepted that the high and low affinity ATP binding reflects, respectively, binding to the E1 and E2 conformational state and that Na+ binds to the E1 form preceding phosphorylation and K+ binds to the E2 form during the Na/K-ATPase and  pNPPase reaction ( ,  ).	bind
18571	4	6028	7	NULL	NULL	NULL	NULL	K+	Chemical		binds to					E2 form	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_50283_s_240	14522987	-- It is generally accepted that the high and low affinity ATP binding reflects, respectively, binding to the E1 and E2 conformational state and that Na+ binds to the E1 form preceding phosphorylation and K+ binds to the E2 form during the Na/K-ATPase and  pNPPase reaction ( ,  ).	bind
18572	5	6028	7	NULL	NULL	NULL	NULL	statement 3	Process		occurs preceding					phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_50283_s_240	14522987	-- It is generally accepted that the high and low affinity ATP binding reflects, respectively, binding to the E1 and E2 conformational state and that Na+ binds to the E1 form preceding phosphorylation and K+ binds to the E2 form during the Na/K-ATPase and  pNPPase reaction ( ,  ).	bind
18573	6	6028	7	NULL	NULL	NULL	NULL	statement 4	Process		occurs during					Na/K-ATPase	GP	reaction of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_50283_s_240	14522987	-- It is generally accepted that the high and low affinity ATP binding reflects, respectively, binding to the E1 and E2 conformational state and that Na+ binds to the E1 form preceding phosphorylation and K+ binds to the E2 form during the Na/K-ATPase and  pNPPase reaction ( ,  ).	bind
18574	7	6028	7	NULL	NULL	NULL	NULL	statement 4	Process		occurs during					pNPPase	GP	reaction of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_50283_s_240	14522987	-- It is generally accepted that the high and low affinity ATP binding reflects, respectively, binding to the E1 and E2 conformational state and that Na+ binds to the E1 form preceding phosphorylation and K+ binds to the E2 form during the Na/K-ATPase and  pNPPase reaction ( ,  ).	bind
15721	1	6029	5	NULL	NULL	0	NULL	p21	NULL		does not bind	NULL				PCNA	NULL				NULL	during arrest	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5802_s_249	14597617	-- One striking observation was the fact that p21 does not bind to PCNA during arrest.	bind
18575	1	6029	7	NULL	NULL	NULL	NULL	 p21	GP		does not bind					PCNA	GP				NULL	during arrest	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5802_s_249	14597617	-- One striking observation was the fact that p21 does not bind to PCNA during arrest.	bind
15722	1	6030	5	NULL	NULL	0	NULL	heparin	NULL		bind	NULL				vitronectin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_10_6432_s_338	10037735	-- Previous work from this laboratory had demonstrated that the dissociation constant for the binding of heparin to vitronectin was dependent on ionic strength ( 23).	bind
18576	1	6030	7	NULL	NULL	NULL	NULL	heparin	GP		bind					vitronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_10_6432_s_338	10037735	-- Previous work from this laboratory had demonstrated that the dissociation constant for the binding of heparin to vitronectin was dependent on ionic strength ( 23).	bind
19062	1	6032	5	NULL	NULL	0	NULL		NULL		lies on	NULL		GABA binding site			NULL		interface of the alpha and beta subunits		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_38_26633_s_179	10480864	-- Since the GABA binding site lies on the interface of the alpha and beta subunits, and since the mutant alpha1 subunits expressed with the beta2 subunits bind [3]muscimol, the GABA binding interface is unaffected by the Trp-69 and Trp-94 mutations.	bind
19078	2	6032	5	NULL	NULL	0	NULL		NULL	mutant	is expressed with	NULL		alpha1 subunits			NULL		beta2 subunits		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_38_26633_s_179	10480864	-- Since the GABA binding site lies on the interface of the alpha and beta subunits, and since the mutant alpha1 subunits expressed with the beta2 subunits bind [3]muscimol, the GABA binding interface is unaffected by the Trp-69 and Trp-94 mutations.	bind
19079	4	6032	5	NULL	NULL	0	NULL		NULL		is unaffected by	NULL		GABA binding interface			NULL	mutation of	Trp-69		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_38_26633_s_179	10480864	-- Since the GABA binding site lies on the interface of the alpha and beta subunits, and since the mutant alpha1 subunits expressed with the beta2 subunits bind [3]muscimol, the GABA binding interface is unaffected by the Trp-69 and Trp-94 mutations.	bind
19080	5	6032	5	NULL	NULL	0	NULL		NULL		is unaffected by	NULL		GABA binding interface			NULL	mutation of	Trp-94		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_38_26633_s_179	10480864	-- Since the GABA binding site lies on the interface of the alpha and beta subunits, and since the mutant alpha1 subunits expressed with the beta2 subunits bind [3]muscimol, the GABA binding interface is unaffected by the Trp-69 and Trp-94 mutations.	bind
19191	3	6032	5	NULL	NULL	0	NULL	statement 2	NULL		bind	NULL				muscimol	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_38_26633_s_179	10480864	-- Since the GABA binding site lies on the interface of the alpha and beta subunits, and since the mutant alpha1 subunits expressed with the beta2 subunits bind [3]muscimol, the GABA binding interface is unaffected by the Trp-69 and Trp-94 mutations.	bind
18580	1	6032	7	NULL	NULL	0	NULL		NULL	mutant	expressed with	NULL		alpha1 subunit			NULL		beta2 subunits 		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_38_26633_s_179	10480864	-- Since the GABA binding site lies on the interface of the alpha and beta subunits, and since the mutant alpha1 subunits expressed with the beta2 subunits bind [3]muscimol, the GABA binding interface is unaffected by the Trp-69 and Trp-94 mutations.	bind
18581	2	6032	7	NULL	NULL	NULL	NULL	statement 1	Process		bind					muscimol	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_38_26633_s_179	10480864	-- Since the GABA binding site lies on the interface of the alpha and beta subunits, and since the mutant alpha1 subunits expressed with the beta2 subunits bind [3]muscimol, the GABA binding interface is unaffected by the Trp-69 and Trp-94 mutations.	bind
18582	3	6032	7	NULL	NULL	0	NULL		NULL		lies on	NULL		GABA binding site			NULL		the interface of alpha and beta subunits		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_38_26633_s_179	10480864	-- Since the GABA binding site lies on the interface of the alpha and beta subunits, and since the mutant alpha1 subunits expressed with the beta2 subunits bind [3]muscimol, the GABA binding interface is unaffected by the Trp-69 and Trp-94 mutations.	bind
18583	4	6032	7	NULL	NULL	0	NULL	 	NULL		is unaffected by	NULL		GABA binding interface			NULL	mutation of	Trp-69		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_38_26633_s_179	10480864	-- Since the GABA binding site lies on the interface of the alpha and beta subunits, and since the mutant alpha1 subunits expressed with the beta2 subunits bind [3]muscimol, the GABA binding interface is unaffected by the Trp-69 and Trp-94 mutations.	bind
18584	5	6032	7	NULL	NULL	0	NULL		NULL		is unaffected by	NULL		GABA binding interface			NULL	mutation of	Trp-94		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_38_26633_s_179	10480864	-- Since the GABA binding site lies on the interface of the alpha and beta subunits, and since the mutant alpha1 subunits expressed with the beta2 subunits bind [3]muscimol, the GABA binding interface is unaffected by the Trp-69 and Trp-94 mutations.	bind
15724	1	6033	5	NULL	NULL	0	NULL	HHR23A	NULL		bind	NULL		UBA domains		Ub	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11926_s_262	14707125	-- The chemical shift mapping study presented here reveals a structural basis for the recognition and binding of UBA domains of HHR23A to Ub.	bind
18585	1	6033	7	NULL	NULL	NULL	NULL	HHR23A	GP		binds to			UBA domain		Ub	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_12_11926_s_262	14707125	-- The chemical shift mapping study presented here reveals a structural basis for the recognition and binding of UBA domains of HHR23A to Ub.	bind
15725	1	6034	5	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				Cdc42	NULL	activated			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49293_s_135	14506284	-- We had previously shown that treatment of NIH 3T3 cells with EGF led to a relatively rapid increase in the levels of GTP-bound (activated) Cdc42 ( ), as read-out by an assay that examines the binding of this GTP-binding protein to its limit-binding domain on PAK (called the PBD).	bind
15726	2	6034	5	NULL	NULL	0	NULL	GTP-binding protein	NULL		bind	NULL				PAK	NULL		PBD		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49293_s_135	14506284	-- We had previously shown that treatment of NIH 3T3 cells with EGF led to a relatively rapid increase in the levels of GTP-bound (activated) Cdc42 ( ), as read-out by an assay that examines the binding of this GTP-binding protein to its limit-binding domain on PAK (called the PBD).	bind
25647	3	6034	5	NULL	NULL	0	NULL	NIH 3T3 cells	NULL		treated with	NULL				EGF	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49293_s_135	14506284	-- We had previously shown that treatment of NIH 3T3 cells with EGF led to a relatively rapid increase in the levels of GTP-bound (activated) Cdc42 ( ), as read-out by an assay that examines the binding of this GTP-binding protein to its limit-binding domain on PAK (called the PBD).	bind
25648	4	6034	5	NULL	NULL	0	NULL	statement 3	NULL		increases	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49293_s_135	14506284	-- We had previously shown that treatment of NIH 3T3 cells with EGF led to a relatively rapid increase in the levels of GTP-bound (activated) Cdc42 ( ), as read-out by an assay that examines the binding of this GTP-binding protein to its limit-binding domain on PAK (called the PBD).	bind
18586	1	6034	7	NULL	NULL	NULL	NULL	GTP	Chemical		bind					Cdc42	GP	activated			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49293_s_135	14506284	-- We had previously shown that treatment of NIH 3T3 cells with EGF led to a relatively rapid increase in the levels of GTP-bound (activated) Cdc42 ( ), as read-out by an assay that examines the binding of this GTP-binding protein to its limit-binding domain on PAK (called the PBD).	bind
18587	2	6034	7	NULL	NULL	NULL	NULL	GTP-binding protein	GP		bind					 PAK	GP		PBD		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49293_s_135	14506284	-- We had previously shown that treatment of NIH 3T3 cells with EGF led to a relatively rapid increase in the levels of GTP-bound (activated) Cdc42 ( ), as read-out by an assay that examines the binding of this GTP-binding protein to its limit-binding domain on PAK (called the PBD).	bind
18588	3	6034	7	NULL	NULL	NULL	NULL	NIH 3T3 cells	Cell		treated with					EGF	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49293_s_135	14506284	-- We had previously shown that treatment of NIH 3T3 cells with EGF led to a relatively rapid increase in the levels of GTP-bound (activated) Cdc42 ( ), as read-out by an assay that examines the binding of this GTP-binding protein to its limit-binding domain on PAK (called the PBD).	bind
25640	4	6034	7	NULL	NULL	NULL	NULL	statement 3	Process		increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49293_s_135	14506284	-- We had previously shown that treatment of NIH 3T3 cells with EGF led to a relatively rapid increase in the levels of GTP-bound (activated) Cdc42 ( ), as read-out by an assay that examines the binding of this GTP-binding protein to its limit-binding domain on PAK (called the PBD).	bind
15727	1	6037	5	NULL	NULL	0	NULL	Actinin	NULL		bind	NULL				Tir	NULL		amino terminus		NULL		0	NULL	NULL	NULL	gw60_currbiol_10_12_735_s_76	10873808	-Actinin binds the amino terminus of Tir	bind
18589	1	6037	7	NULL	NULL	NULL	NULL	Actinin	GP		binds					Tir	GP		amino terminus		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_12_735_s_76	10873808	-Actinin binds the amino terminus of Tir	bind
15728	1	6038	5	NULL	NULL	0	NULL	Actinin	NULL		is composed of	NULL					NULL		amino-terminal actin-binding region		NULL		0	NULL	NULL	NULL	gw60_cell_98_4_537_s_30	10481917	-Actinin is composed of an amino-terminal actin-binding  region consisting of two calponin homology (CH) domains, a central rod containing four spectrin-like  repeats, and a calmodulin-like domain at the carboxy terminus (Castresana and Saraste, 1995   ;  Trave et al., 1995   ;  Davison and Critchley, 1988   ).	bind
15729	2	6038	5	NULL	NULL	0	NULL		NULL		consists of	NULL		amino-terminal actin-binding region			NULL		two CH domains		NULL		NULL	NULL	NULL	NULL	gw60_cell_98_4_537_s_30	10481917	-Actinin is composed of an amino-terminal actin-binding  region consisting of two calponin homology (CH) domains, a central rod containing four spectrin-like  repeats, and a calmodulin-like domain at the carboxy terminus (Castresana and Saraste, 1995   ;  Trave et al., 1995   ;  Davison and Critchley, 1988   ).	bind
15730	3	6038	5	NULL	NULL	0	NULL	CH domain	NULL		is	NULL				calponin homology domain	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_98_4_537_s_30	10481917	-Actinin is composed of an amino-terminal actin-binding  region consisting of two calponin homology (CH) domains, a central rod containing four spectrin-like  repeats, and a calmodulin-like domain at the carboxy terminus (Castresana and Saraste, 1995   ;  Trave et al., 1995   ;  Davison and Critchley, 1988   ).	bind
15731	4	6038	5	NULL	NULL	0	NULL		NULL		consists of	NULL		amino-terminal actin-binding region			NULL	central rod containing	four spectrin-like repeats		NULL		0	NULL	NULL	NULL	gw60_cell_98_4_537_s_30	10481917	-Actinin is composed of an amino-terminal actin-binding  region consisting of two calponin homology (CH) domains, a central rod containing four spectrin-like  repeats, and a calmodulin-like domain at the carboxy terminus (Castresana and Saraste, 1995   ;  Trave et al., 1995   ;  Davison and Critchley, 1988   ).	bind
15732	5	6038	5	NULL	NULL	0	NULL		NULL		consists of	NULL		amino-terminal actin-binding region			NULL	at carboxy terminus	calmodulin-like domain		NULL		0	NULL	NULL	NULL	gw60_cell_98_4_537_s_30	10481917	-Actinin is composed of an amino-terminal actin-binding  region consisting of two calponin homology (CH) domains, a central rod containing four spectrin-like  repeats, and a calmodulin-like domain at the carboxy terminus (Castresana and Saraste, 1995   ;  Trave et al., 1995   ;  Davison and Critchley, 1988   ).	bind
18590	1	6038	7	NULL	NULL	NULL	NULL	Actinin	GP		is composed of								amino-terminal actin-binding region		NULL		NULL	NULL	NULL	NULL	gw60_cell_98_4_537_s_30	10481917	-Actinin is composed of an amino-terminal actin-binding  region consisting of two calponin homology (CH) domains, a central rod containing four spectrin-like  repeats, and a calmodulin-like domain at the carboxy terminus (Castresana and Saraste, 1995   ;  Trave et al., 1995   ;  Davison and Critchley, 1988   ).	bind
18591	2	6038	7	NULL	NULL	NULL	NULL	statement 1	Process		consist of								two CH domains		NULL		NULL	NULL	NULL	NULL	gw60_cell_98_4_537_s_30	10481917	-Actinin is composed of an amino-terminal actin-binding  region consisting of two calponin homology (CH) domains, a central rod containing four spectrin-like  repeats, and a calmodulin-like domain at the carboxy terminus (Castresana and Saraste, 1995   ;  Trave et al., 1995   ;  Davison and Critchley, 1988   ).	bind
18592	3	6038	7	NULL	NULL	NULL	NULL	Actinin	GP		is composed of							central rod containing	four spectrin-like repeats		NULL		NULL	NULL	NULL	NULL	gw60_cell_98_4_537_s_30	10481917	-Actinin is composed of an amino-terminal actin-binding  region consisting of two calponin homology (CH) domains, a central rod containing four spectrin-like  repeats, and a calmodulin-like domain at the carboxy terminus (Castresana and Saraste, 1995   ;  Trave et al., 1995   ;  Davison and Critchley, 1988   ).	bind
18593	4	6038	7	NULL	NULL	NULL	NULL	Actinin 	GP		is composed of								calmodulin-like domain at the carboxy terminus		NULL		NULL	NULL	NULL	NULL	gw60_cell_98_4_537_s_30	10481917	-Actinin is composed of an amino-terminal actin-binding  region consisting of two calponin homology (CH) domains, a central rod containing four spectrin-like  repeats, and a calmodulin-like domain at the carboxy terminus (Castresana and Saraste, 1995   ;  Trave et al., 1995   ;  Davison and Critchley, 1988   ).	bind
18594	5	6038	7	NULL	NULL	NULL	NULL	CH domain	GP		is					calponin homology domain					NULL		NULL	NULL	NULL	NULL	gw60_cell_98_4_537_s_30	10481917	-Actinin is composed of an amino-terminal actin-binding  region consisting of two calponin homology (CH) domains, a central rod containing four spectrin-like  repeats, and a calmodulin-like domain at the carboxy terminus (Castresana and Saraste, 1995   ;  Trave et al., 1995   ;  Davison and Critchley, 1988   ).	bind
15733	1	6039	5	NULL	NULL	0	NULL	arrestin2	NULL		bind	NULL				clathrin	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_705_s_275	10611976	-arrestin2 lacks this serine, however, and it is not clear  whether its binding to clathrin is similarly controlled.	bind
18595	1	6039	7	NULL	NULL	NULL	NULL	arrestin2	GP		bind					clathrin	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_705_s_275	10611976	-arrestin2 lacks this serine, however, and it is not clear  whether its binding to clathrin is similarly controlled.	bind
15734	1	6040	5	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				PDI (3K)	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1479_1_293_s_195	11004547	-ATP bound to PDI      (3K)	bind
18596	1	6040	7	NULL	NULL	NULL	NULL	ATP	Chemical		bind					PDI	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1479_1_293_s_195	11004547	-ATP bound to PDI      (3K)	bind
15735	1	6041	5	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				PDI	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1479_1_293_s_125	11004547	-ATP bound to PDI is responsible for the decrease in the efficiency of energy transfer reflected in the measured phosphorescence yield.	bind
18597	1	6041	7	NULL	NULL	NULL	NULL	ATP	Chemical		bind					PDI	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1479_1_293_s_125	11004547	-ATP bound to PDI is responsible for the decrease in the efficiency of energy transfer reflected in the measured phosphorescence yield.	bind
15736	1	6042	5	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				PDI	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1479_1_293_s_112	11004547	-ATP bound to PDI, coordination of Tb3+ by carboxyl groups of the protein might influence the stability and phosphorescence properties of the bound ligand.	bind
25649	2	6042	5	10	NULL	0	NULL	Tb3+	NULL		coordinate	NULL		carboxyl groups		Tb3+	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1479_1_293_s_112	11004547	-ATP bound to PDI, coordination of Tb3+ by carboxyl groups of the protein might influence the stability and phosphorescence properties of the bound ligand.	bind
25650	3	6042	5	NULL	NULL	0	NULL	statement 2	NULL		influence	NULL				ligand	NULL	stability of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1479_1_293_s_112	11004547	-ATP bound to PDI, coordination of Tb3+ by carboxyl groups of the protein might influence the stability and phosphorescence properties of the bound ligand.	bind
25651	4	6042	5	NULL	NULL	0	NULL	statement 2	NULL		influence	NULL				ligand	NULL	phosphorescence properties of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1479_1_293_s_112	11004547	-ATP bound to PDI, coordination of Tb3+ by carboxyl groups of the protein might influence the stability and phosphorescence properties of the bound ligand.	bind
18682	1	6042	7	NULL	NULL	NULL	NULL	ATP	Chemical		bind					PDI	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1479_1_293_s_112	11004547	-ATP bound to PDI, coordination of Tb3+ by carboxyl groups of the protein might influence the stability and phosphorescence properties of the bound ligand.	bind
18685	2	6042	7	NULL	NULL	NULL	NULL	Tb3+	Chemical		coordinate			carboxyl groups		Tb3+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1479_1_293_s_112	11004547	-ATP bound to PDI, coordination of Tb3+ by carboxyl groups of the protein might influence the stability and phosphorescence properties of the bound ligand.	bind
18690	4	6042	7	NULL	NULL	NULL	NULL	statement 2	Process		influence					ligand	Chemical	phosphorescence properties of 			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1479_1_293_s_112	11004547	-ATP bound to PDI, coordination of Tb3+ by carboxyl groups of the protein might influence the stability and phosphorescence properties of the bound ligand.	bind
25641	3	6042	7	NULL	NULL	NULL	NULL	statement 2	Process		influence					ligand	Chemical	stability of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1479_1_293_s_112	11004547	-ATP bound to PDI, coordination of Tb3+ by carboxyl groups of the protein might influence the stability and phosphorescence properties of the bound ligand.	bind
15737	1	6044	5	NULL	NULL	0	NULL	catenin	NULL		bind	NULL				S-SCAM	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_27_4_509_s_164	15555928	-catenin also binds to the scaffolding protein S-SCAM (MAGI-2) (  Nishimura et al., 2002) which binds a variety of postsynaptic molecules including neuroligin, GKAP/SAPAP,  and NMDA receptors as well as presynaptically localized m-Lin 7 (MALS, Velis) (  Perego et al., 2000).	bind
15738	2	6044	5	NULL	NULL	0	NULL	S-SCAM	NULL		is	NULL				MAGI-2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellneurosci_27_4_509_s_164	15555928	-catenin also binds to the scaffolding protein S-SCAM (MAGI-2) (  Nishimura et al., 2002) which binds a variety of postsynaptic molecules including neuroligin, GKAP/SAPAP,  and NMDA receptors as well as presynaptically localized m-Lin 7 (MALS, Velis) (  Perego et al., 2000).	bind
15739	3	6044	5	NULL	NULL	0	NULL	S-SCAM	NULL		bind	NULL				neuroligin	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellneurosci_27_4_509_s_164	15555928	-catenin also binds to the scaffolding protein S-SCAM (MAGI-2) (  Nishimura et al., 2002) which binds a variety of postsynaptic molecules including neuroligin, GKAP/SAPAP,  and NMDA receptors as well as presynaptically localized m-Lin 7 (MALS, Velis) (  Perego et al., 2000).	bind
15740	4	6044	5	NULL	NULL	0	NULL	S-SCAM	NULL		bind	NULL				GKAP/SAPAP	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellneurosci_27_4_509_s_164	15555928	-catenin also binds to the scaffolding protein S-SCAM (MAGI-2) (  Nishimura et al., 2002) which binds a variety of postsynaptic molecules including neuroligin, GKAP/SAPAP,  and NMDA receptors as well as presynaptically localized m-Lin 7 (MALS, Velis) (  Perego et al., 2000).	bind
15741	5	6044	5	NULL	NULL	0	NULL	S-SCAM	NULL		bind	NULL				NMDA receptors	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellneurosci_27_4_509_s_164	15555928	-catenin also binds to the scaffolding protein S-SCAM (MAGI-2) (  Nishimura et al., 2002) which binds a variety of postsynaptic molecules including neuroligin, GKAP/SAPAP,  and NMDA receptors as well as presynaptically localized m-Lin 7 (MALS, Velis) (  Perego et al., 2000).	bind
15742	6	6044	5	NULL	NULL	0	NULL	S-SCAM	NULL		bind	NULL				m-Lin 7	NULL	presynaptically localized			NULL		0	NULL	NULL	NULL	gw70_molcellneurosci_27_4_509_s_164	15555928	-catenin also binds to the scaffolding protein S-SCAM (MAGI-2) (  Nishimura et al., 2002) which binds a variety of postsynaptic molecules including neuroligin, GKAP/SAPAP,  and NMDA receptors as well as presynaptically localized m-Lin 7 (MALS, Velis) (  Perego et al., 2000).	bind
25652	7	6044	5	NULL	NULL	0	NULL	S-SCAM	NULL		is a type of	NULL				scaffolding protein	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellneurosci_27_4_509_s_164	15555928	-catenin also binds to the scaffolding protein S-SCAM (MAGI-2) (  Nishimura et al., 2002) which binds a variety of postsynaptic molecules including neuroligin, GKAP/SAPAP,  and NMDA receptors as well as presynaptically localized m-Lin 7 (MALS, Velis) (  Perego et al., 2000).	bind
25653	8	6044	5	NULL	NULL	0	NULL	neuroligin	NULL		is a type of	NULL				postsynaptic molecule	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellneurosci_27_4_509_s_164	15555928	-catenin also binds to the scaffolding protein S-SCAM (MAGI-2) (  Nishimura et al., 2002) which binds a variety of postsynaptic molecules including neuroligin, GKAP/SAPAP,  and NMDA receptors as well as presynaptically localized m-Lin 7 (MALS, Velis) (  Perego et al., 2000).	bind
25654	9	6044	5	NULL	NULL	0	NULL	GKAP/SAPAP	NULL		is a type of	NULL				postsynaptic molecule	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellneurosci_27_4_509_s_164	15555928	-catenin also binds to the scaffolding protein S-SCAM (MAGI-2) (  Nishimura et al., 2002) which binds a variety of postsynaptic molecules including neuroligin, GKAP/SAPAP,  and NMDA receptors as well as presynaptically localized m-Lin 7 (MALS, Velis) (  Perego et al., 2000).	bind
25655	10	6044	5	NULL	NULL	0	NULL	NMDA receptor	NULL		is a type of	NULL				postsynaptic molecule	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellneurosci_27_4_509_s_164	15555928	-catenin also binds to the scaffolding protein S-SCAM (MAGI-2) (  Nishimura et al., 2002) which binds a variety of postsynaptic molecules including neuroligin, GKAP/SAPAP,  and NMDA receptors as well as presynaptically localized m-Lin 7 (MALS, Velis) (  Perego et al., 2000).	bind
18691	1	6044	7	NULL	NULL	NULL	NULL	catenin	GP		bind					S-SCAM	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_27_4_509_s_164	15555928	-catenin also binds to the scaffolding protein S-SCAM (MAGI-2) (  Nishimura et al., 2002) which binds a variety of postsynaptic molecules including neuroligin, GKAP/SAPAP,  and NMDA receptors as well as presynaptically localized m-Lin 7 (MALS, Velis) (  Perego et al., 2000).	bind
18692	2	6044	7	NULL	NULL	NULL	NULL	S-SCAM	GP		bind					neuroligin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_27_4_509_s_164	15555928	-catenin also binds to the scaffolding protein S-SCAM (MAGI-2) (  Nishimura et al., 2002) which binds a variety of postsynaptic molecules including neuroligin, GKAP/SAPAP,  and NMDA receptors as well as presynaptically localized m-Lin 7 (MALS, Velis) (  Perego et al., 2000).	bind
18693	3	6044	7	NULL	NULL	NULL	NULL	S-SCAM	GP		bind					GKAP/SAPAP	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_27_4_509_s_164	15555928	-catenin also binds to the scaffolding protein S-SCAM (MAGI-2) (  Nishimura et al., 2002) which binds a variety of postsynaptic molecules including neuroligin, GKAP/SAPAP,  and NMDA receptors as well as presynaptically localized m-Lin 7 (MALS, Velis) (  Perego et al., 2000).	bind
18694	4	6044	7	NULL	NULL	NULL	NULL	S-SCAM	GP		bind					NMDA receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_27_4_509_s_164	15555928	-catenin also binds to the scaffolding protein S-SCAM (MAGI-2) (  Nishimura et al., 2002) which binds a variety of postsynaptic molecules including neuroligin, GKAP/SAPAP,  and NMDA receptors as well as presynaptically localized m-Lin 7 (MALS, Velis) (  Perego et al., 2000).	bind
18695	5	6044	7	NULL	NULL	NULL	NULL	S-SCAM	GP		is a type of					scaffolding protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_27_4_509_s_164	15555928	-catenin also binds to the scaffolding protein S-SCAM (MAGI-2) (  Nishimura et al., 2002) which binds a variety of postsynaptic molecules including neuroligin, GKAP/SAPAP,  and NMDA receptors as well as presynaptically localized m-Lin 7 (MALS, Velis) (  Perego et al., 2000).	bind
18696	6	6044	7	NULL	NULL	NULL	NULL	neuroligin	GP		is a type of					postsynaptic molecule	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_27_4_509_s_164	15555928	-catenin also binds to the scaffolding protein S-SCAM (MAGI-2) (  Nishimura et al., 2002) which binds a variety of postsynaptic molecules including neuroligin, GKAP/SAPAP,  and NMDA receptors as well as presynaptically localized m-Lin 7 (MALS, Velis) (  Perego et al., 2000).	bind
18697	7	6044	7	NULL	NULL	NULL	NULL	GKAP/SAPAP	GP		is a type of					postsynaptic molecule	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_27_4_509_s_164	15555928	-catenin also binds to the scaffolding protein S-SCAM (MAGI-2) (  Nishimura et al., 2002) which binds a variety of postsynaptic molecules including neuroligin, GKAP/SAPAP,  and NMDA receptors as well as presynaptically localized m-Lin 7 (MALS, Velis) (  Perego et al., 2000).	bind
18698	8	6044	7	NULL	NULL	NULL	NULL	NMDA receptor 	GP		is a type of					postsynaptic molecule	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_27_4_509_s_164	15555928	-catenin also binds to the scaffolding protein S-SCAM (MAGI-2) (  Nishimura et al., 2002) which binds a variety of postsynaptic molecules including neuroligin, GKAP/SAPAP,  and NMDA receptors as well as presynaptically localized m-Lin 7 (MALS, Velis) (  Perego et al., 2000).	bind
18699	9	6044	7	NULL	NULL	NULL	NULL	S-SCAM	GP		binds					m-Lin 7	GP	presynaptically localized 			NULL		NULL	NULL	NULL	NULL	gw70_molcellneurosci_27_4_509_s_164	15555928	-catenin also binds to the scaffolding protein S-SCAM (MAGI-2) (  Nishimura et al., 2002) which binds a variety of postsynaptic molecules including neuroligin, GKAP/SAPAP,  and NMDA receptors as well as presynaptically localized m-Lin 7 (MALS, Velis) (  Perego et al., 2000).	bind
15743	1	6045	5	NULL	NULL	0	NULL	catenin	NULL		bind	NULL				neurogenin 1	NULL			promoter	NULL	in neural progenitor cells	0	NULL	NULL	NULL	gw70_devbiol_268_1_220_s_202	15031118	-catenin and Lef1 bind to the neurogenin 1 promoter in neural progenitor  cells.	bind
15744	2	6045	5	NULL	NULL	0	NULL	Lef1	NULL		bind	NULL				neurogenin 1	NULL			promoter	NULL	in neural progenitor cells	0	NULL	NULL	NULL	gw70_devbiol_268_1_220_s_202	15031118	-catenin and Lef1 bind to the neurogenin 1 promoter in neural progenitor  cells.	bind
18700	1	6045	7	NULL	NULL	NULL	NULL	catenin	GP		binds to					neurogenin 1	GP			promoter	NULL	neural progenitor cells	NULL	NULL	NULL	NULL	gw70_devbiol_268_1_220_s_202	15031118	-catenin and Lef1 bind to the neurogenin 1 promoter in neural progenitor  cells.	bind
18701	2	6045	7	NULL	NULL	NULL	NULL	Lef1 	GP		binds to					neurogenin 1	GP			promoter	NULL	neural progenitor cells	NULL	NULL	NULL	NULL	gw70_devbiol_268_1_220_s_202	15031118	-catenin and Lef1 bind to the neurogenin 1 promoter in neural progenitor  cells.	bind
15745	1	6046	5	NULL	NULL	0	NULL	Catenin	NULL		associate with	NULL				cadherin	NULL		cytoplasmic domain		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1495_2_168_s_58	10656974	-Catenin associates with the cytoplasmic domain of cadherins [  16], and binds the vinculin-related protein  -catenin, which in turn makes contact to actin filaments [  17].	bind
15746	2	6046	5	NULL	NULL	0	NULL	Catenin	NULL		bind	NULL				catenin	NULL	vinculin-related protein			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1495_2_168_s_58	10656974	-Catenin associates with the cytoplasmic domain of cadherins [  16], and binds the vinculin-related protein  -catenin, which in turn makes contact to actin filaments [  17].	bind
15747	3	6046	5	NULL	NULL	0	NULL	catenin	NULL		makes contact to	NULL				actin filaments	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1495_2_168_s_58	10656974	-Catenin associates with the cytoplasmic domain of cadherins [  16], and binds the vinculin-related protein  -catenin, which in turn makes contact to actin filaments [  17].	bind
25656	4	6046	5	NULL	NULL	0	NULL	catenin	NULL		is a type of	NULL				vinculin-related protein	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1495_2_168_s_58	10656974	-Catenin associates with the cytoplasmic domain of cadherins [  16], and binds the vinculin-related protein  -catenin, which in turn makes contact to actin filaments [  17].	bind
18702	1	6046	7	NULL	NULL	NULL	NULL	Catenin	GP		associate with					cadherins	GP		cytoplasmic domain		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1495_2_168_s_58	10656974	-Catenin associates with the cytoplasmic domain of cadherins [  16], and binds the vinculin-related protein  -catenin, which in turn makes contact to actin filaments [  17].	bind
18703	2	6046	7	NULL	NULL	NULL	NULL	statement 1	Process		bind					catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1495_2_168_s_58	10656974	-Catenin associates with the cytoplasmic domain of cadherins [  16], and binds the vinculin-related protein  -catenin, which in turn makes contact to actin filaments [  17].	bind
18704	3	6046	7	NULL	NULL	NULL	NULL	statement 2	Process		makes contact to					actin filaments	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1495_2_168_s_58	10656974	-Catenin associates with the cytoplasmic domain of cadherins [  16], and binds the vinculin-related protein  -catenin, which in turn makes contact to actin filaments [  17].	bind
25644	4	6046	7	NULL	NULL	NULL	NULL	catenin	GP		is a type of					vinculin related protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1495_2_168_s_58	10656974	-Catenin associates with the cytoplasmic domain of cadherins [  16], and binds the vinculin-related protein  -catenin, which in turn makes contact to actin filaments [  17].	bind
15748	1	6047	5	10	NULL	0	NULL	catenin			bind			armadillo repeats		cadherin			cytoplasmic tail 		NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_13_0_119_s_151	9442870	-catenin binds to the cadherin cytoplasmic tail via its centrally located armadillo  repeats ( Hulsken et al 1994,  Funayama et al 1995), 40 amino acid protein-protein-binding motifs originally described in the  Drosophila homologue of  -catenin Armadillo ( Peifer & Wieschaus 1990,  Peifer et al 1994).	bind
54142	2	6047	5	10	NULL	0	NULL	catenin			is located			armadillo repeats		centrally					NULL		0	NULL	NULL	NULL	gw70_annurevcelldevbiol_13_0_119_s_151	9442870	-catenin binds to the cadherin cytoplasmic tail via its centrally located armadillo  repeats ( Hulsken et al 1994,  Funayama et al 1995), 40 amino acid protein-protein-binding motifs originally described in the  Drosophila homologue of  -catenin Armadillo ( Peifer & Wieschaus 1990,  Peifer et al 1994).	bind
18705	1	6047	7	NULL	NULL	NULL	NULL	catenin 	GP		bind			armadillo repeats		cadherin	GP		cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_13_0_119_s_151	9442870	-catenin binds to the cadherin cytoplasmic tail via its centrally located armadillo  repeats ( Hulsken et al 1994,  Funayama et al 1995), 40 amino acid protein-protein-binding motifs originally described in the  Drosophila homologue of  -catenin Armadillo ( Peifer & Wieschaus 1990,  Peifer et al 1994).	bind
18706	2	6047	7	NULL	NULL	NULL	NULL	catenin	GP		is located			armadillo repeats		centrally	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_13_0_119_s_151	9442870	-catenin binds to the cadherin cytoplasmic tail via its centrally located armadillo  repeats ( Hulsken et al 1994,  Funayama et al 1995), 40 amino acid protein-protein-binding motifs originally described in the  Drosophila homologue of  -catenin Armadillo ( Peifer & Wieschaus 1990,  Peifer et al 1994).	bind
18707	3	6047	7	NULL	NULL	NULL	NULL	armadillo repeats	GP		is					catenin Armadillo	GP	Drosophila homologue of 	40 amino acid protein-protein-binding motifs		NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_13_0_119_s_151	9442870	-catenin binds to the cadherin cytoplasmic tail via its centrally located armadillo  repeats ( Hulsken et al 1994,  Funayama et al 1995), 40 amino acid protein-protein-binding motifs originally described in the  Drosophila homologue of  -catenin Armadillo ( Peifer & Wieschaus 1990,  Peifer et al 1994).	bind
15749	1	6048	5	NULL	NULL	0	NULL	transcription factors	NULL		bind	NULL				AP-1 complex	NULL				NULL		0	NULL	NULL	NULL	gw60_neuroscience_108_3_371_s_166	11738252	-Catenin could also play a role in increasing Cdk5 expression because of its ability to increase transcription factors which bind to the AP-1 complex.	bind
15750	2	6048	5	NULL	NULL	0	NULL	Catenin	NULL		increase	NULL				transcription factors	NULL				NULL		0	NULL	NULL	NULL	gw60_neuroscience_108_3_371_s_166	11738252	-Catenin could also play a role in increasing Cdk5 expression because of its ability to increase transcription factors which bind to the AP-1 complex.	bind
15751	3	6048	5	10	NULL	0	NULL	Catenin			increase					Catenin		expression of			NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_108_3_371_s_166	11738252	-Catenin could also play a role in increasing Cdk5 expression because of its ability to increase transcription factors which bind to the AP-1 complex.	bind
15752	4	6048	5	NULL	NULL	0	NULL	statement 3	NULL		because of	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_neuroscience_108_3_371_s_166	11738252	-Catenin could also play a role in increasing Cdk5 expression because of its ability to increase transcription factors which bind to the AP-1 complex.	bind
18745	1	6048	7	NULL	NULL	NULL	NULL	Catenin	GP		increase					Cdk5	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_108_3_371_s_166	11738252	-Catenin could also play a role in increasing Cdk5 expression because of its ability to increase transcription factors which bind to the AP-1 complex.	bind
18746	2	6048	7	NULL	NULL	NULL	NULL	Catenin	GP		increase					transcription factors	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_108_3_371_s_166	11738252	-Catenin could also play a role in increasing Cdk5 expression because of its ability to increase transcription factors which bind to the AP-1 complex.	bind
18747	3	6048	7	NULL	NULL	NULL	NULL	transcription factors	GP		bind					AP-1 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_108_3_371_s_166	11738252	-Catenin could also play a role in increasing Cdk5 expression because of its ability to increase transcription factors which bind to the AP-1 complex.	bind
15753	1	6049	5	NULL	NULL	0	NULL	Crystallin	NULL		bind	NULL				alphaA-crystallin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_18_10449_s_72	8631839	-Crystallin  bound to alphaA-crystallin shows an emission maximum at 337 nm,  i.e.  red-shifted only by 7 nm from that of its native state.	bind
18748	1	6049	7	NULL	NULL	NULL	NULL	Crystallin	GP		bind					alphaA-crystallin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_18_10449_s_72	8631839	-Crystallin  bound to alphaA-crystallin shows an emission maximum at 337 nm,  i.e.  red-shifted only by 7 nm from that of its native state.	bind
15754	1	6050	5	NULL	NULL	0	NULL	Crystallin	NULL		bind	NULL	specifically			NADP(H)	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26224_s_235	7592828	-Crystallin  specifically binds NADP(H) and is a novel NADPH:quinone  oxidoreductase( 35,  49) .	bind
15755	2	6050	5	NULL	NULL	0	NULL	Crystallin	NULL		is	NULL				NADPH:quinone oxidoreductase	NULL	novel			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26224_s_235	7592828	-Crystallin  specifically binds NADP(H) and is a novel NADPH:quinone  oxidoreductase( 35,  49) .	bind
18844	1	6050	7	NULL	NULL	NULL	NULL	Crystallin	GP		binds		specifically			NADP(H)	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_44_26224_s_235	7592828	-Crystallin  specifically binds NADP(H) and is a novel NADPH:quinone  oxidoreductase( 35,  49) .	bind
18845	2	6050	7	NULL	NULL	NULL	NULL	Crystallin	GP		is a type of					NADPH:quinone oxidoreductase	GP	novel			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_44_26224_s_235	7592828	-Crystallin  specifically binds NADP(H) and is a novel NADPH:quinone  oxidoreductase( 35,  49) .	bind
15756	1	6052	5	NULL	NULL	0	NULL	Crystallin	NULL		bind	NULL				MDA	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1500_1_49_s_174	10564717	-Crystallin itself binds MDA, resulting in a fluorescent adduct.	bind
18846	1	6052	7	NULL	NULL	NULL	NULL	Crystallin	GP		binds					MDA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1500_1_49_s_174	10564717	-Crystallin itself binds MDA, resulting in a fluorescent adduct.	bind
18847	2	6052	7	NULL	NULL	NULL	NULL	statement 1	Process		results in					fluorescent adduct	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1500_1_49_s_174	10564717	-Crystallin itself binds MDA, resulting in a fluorescent adduct.	bind
15757	1	6053	5	NULL	NULL	0	NULL	agrin	NULL		bind	NULL				DG	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_4_5_783_s_41	10619025	-DG binding by agrin may contribute to this process but has additional important functions in nonmuscle tissues (  Yamada et al. 1996a  ; Gesemann et al. 1998  ).	bind
18848	1	6053	7	NULL	NULL	NULL	NULL	agrin	GP		binds					DG	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_5_783_s_41	10619025	-DG binding by agrin may contribute to this process but has additional important functions in nonmuscle tissues (  Yamada et al. 1996a  ; Gesemann et al. 1998  ).	bind
15758	1	6054	5	NULL	NULL	0	NULL	agrin	NULL		interacts with	NULL				dystrophin	NULL				NULL	inside cytoplasm	0	NULL	NULL	NULL	gw60_febslett_499_3_210_s_8	11423118	-DG, which contains the transmembrane domain, interacts with dystrophin and dystrophin-related proteins inside the cytoplasm, whereas  -DG, the highly glycosylated peripheral membrane subunit, binds extracellular matrix proteins containing laminin-type LG domains [  6,   7 and   8].	bind
15759	2	6054	5	NULL	NULL	0	NULL	DG	NULL		interacts with	NULL				dystrophin-related proteins	NULL				NULL	inside cytoplasm	0	NULL	NULL	NULL	gw60_febslett_499_3_210_s_8	11423118	-DG, which contains the transmembrane domain, interacts with dystrophin and dystrophin-related proteins inside the cytoplasm, whereas  -DG, the highly glycosylated peripheral membrane subunit, binds extracellular matrix proteins containing laminin-type LG domains [  6,   7 and   8].	bind
15760	3	6054	5	10	NULL	0	NULL	DG			bind					statement 5					NULL		NULL	NULL	NULL	NULL	gw60_febslett_499_3_210_s_8	11423118	-DG, which contains the transmembrane domain, interacts with dystrophin and dystrophin-related proteins inside the cytoplasm, whereas  -DG, the highly glycosylated peripheral membrane subunit, binds extracellular matrix proteins containing laminin-type LG domains [  6,   7 and   8].	bind
25658	4	6054	5	10	NULL	0	NULL	DG			is a type of							highly glycosylated	peripheral membrane subunit		NULL		NULL	NULL	NULL	NULL	gw60_febslett_499_3_210_s_8	11423118	-DG, which contains the transmembrane domain, interacts with dystrophin and dystrophin-related proteins inside the cytoplasm, whereas  -DG, the highly glycosylated peripheral membrane subunit, binds extracellular matrix proteins containing laminin-type LG domains [  6,   7 and   8].	bind
54146	5	6054	5	10	NULL	0	NULL	extracellular matrix proteins			contains								laminin-type LG domains		NULL		0	NULL	NULL	NULL	gw60_febslett_499_3_210_s_8	11423118	-DG, which contains the transmembrane domain, interacts with dystrophin and dystrophin-related proteins inside the cytoplasm, whereas  -DG, the highly glycosylated peripheral membrane subunit, binds extracellular matrix proteins containing laminin-type LG domains [  6,   7 and   8].	bind
18849	1	6054	7	NULL	NULL	NULL	NULL	DG	GP		contains								transmembrane domain		NULL		NULL	NULL	NULL	NULL	gw60_febslett_499_3_210_s_8	11423118	-DG, which contains the transmembrane domain, interacts with dystrophin and dystrophin-related proteins inside the cytoplasm, whereas  -DG, the highly glycosylated peripheral membrane subunit, binds extracellular matrix proteins containing laminin-type LG domains [  6,   7 and   8].	bind
18850	2	6054	7	NULL	NULL	NULL	NULL	statement 1	Process		interacts with					dystrophin	GP				NULL	inside cytoplasm \t	NULL	NULL	NULL	NULL	gw60_febslett_499_3_210_s_8	11423118	-DG, which contains the transmembrane domain, interacts with dystrophin and dystrophin-related proteins inside the cytoplasm, whereas  -DG, the highly glycosylated peripheral membrane subunit, binds extracellular matrix proteins containing laminin-type LG domains [  6,   7 and   8].	bind
18851	3	6054	7	NULL	NULL	NULL	NULL	statement 1	Process		interacts with					 dystrophin-related proteins	GP				NULL	inside the cytoplasm	NULL	NULL	NULL	NULL	gw60_febslett_499_3_210_s_8	11423118	-DG, which contains the transmembrane domain, interacts with dystrophin and dystrophin-related proteins inside the cytoplasm, whereas  -DG, the highly glycosylated peripheral membrane subunit, binds extracellular matrix proteins containing laminin-type LG domains [  6,   7 and   8].	bind
18852	4	6054	7	NULL	NULL	NULL	NULL	DG	GP		is a type of							highly glycosylated	peripheral membrane subunit		NULL		NULL	NULL	NULL	NULL	gw60_febslett_499_3_210_s_8	11423118	-DG, which contains the transmembrane domain, interacts with dystrophin and dystrophin-related proteins inside the cytoplasm, whereas  -DG, the highly glycosylated peripheral membrane subunit, binds extracellular matrix proteins containing laminin-type LG domains [  6,   7 and   8].	bind
18853	5	6054	7	NULL	NULL	NULL	NULL	DG	GP		binds					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_499_3_210_s_8	11423118	-DG, which contains the transmembrane domain, interacts with dystrophin and dystrophin-related proteins inside the cytoplasm, whereas  -DG, the highly glycosylated peripheral membrane subunit, binds extracellular matrix proteins containing laminin-type LG domains [  6,   7 and   8].	bind
54147	6	6054	7	NULL	NULL	NULL	NULL	extracellular matrix protein	GP		contains								laminin-type LG domains		NULL		NULL	NULL	NULL	NULL	gw60_febslett_499_3_210_s_8	11423118	-DG, which contains the transmembrane domain, interacts with dystrophin and dystrophin-related proteins inside the cytoplasm, whereas  -DG, the highly glycosylated peripheral membrane subunit, binds extracellular matrix proteins containing laminin-type LG domains [  6,   7 and   8].	bind
15761	1	6055	5	NULL	NULL	0	NULL	Dystroglycan	NULL		bind	NULL				laminin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_20_11711_s_10	7744812	-Dystroglycan binds laminin and dystrophin binds actin filaments,  indicating that one function of the dystrophin-glycoprotein complex is  to provide a link between the extracellular matrix and the cell  cytoskeleton ( 5,  6) .	bind
15762	2	6055	5	NULL	NULL	0	NULL	dystrophin	NULL		bind	NULL				actin filaments	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_20_11711_s_10	7744812	-Dystroglycan binds laminin and dystrophin binds actin filaments,  indicating that one function of the dystrophin-glycoprotein complex is  to provide a link between the extracellular matrix and the cell  cytoskeleton ( 5,  6) .	bind
15763	4	6055	5	NULL	NULL	0	NULL	dystrophin-glycoprotein complex	NULL		plays a role in	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_20_11711_s_10	7744812	-Dystroglycan binds laminin and dystrophin binds actin filaments,  indicating that one function of the dystrophin-glycoprotein complex is  to provide a link between the extracellular matrix and the cell  cytoskeleton ( 5,  6) .	bind
45614	3	6055	5	NULL	NULL	0	NULL	extracellular matrix	NULL		is linked to	NULL				cell cytoskeleton	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_20_11711_s_10	7744812	-Dystroglycan binds laminin and dystrophin binds actin filaments,  indicating that one function of the dystrophin-glycoprotein complex is  to provide a link between the extracellular matrix and the cell  cytoskeleton ( 5,  6) .	bind
18855	1	6055	7	NULL	NULL	NULL	NULL	Dystroglycan	GP		binds					laminin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_20_11711_s_10	7744812	-Dystroglycan binds laminin and dystrophin binds actin filaments,  indicating that one function of the dystrophin-glycoprotein complex is  to provide a link between the extracellular matrix and the cell  cytoskeleton ( 5,  6) .	bind
18856	2	6055	7	NULL	NULL	NULL	NULL	dystrophin	GP		binds					actin filaments	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_20_11711_s_10	7744812	-Dystroglycan binds laminin and dystrophin binds actin filaments,  indicating that one function of the dystrophin-glycoprotein complex is  to provide a link between the extracellular matrix and the cell  cytoskeleton ( 5,  6) .	bind
18857	3	6055	7	NULL	NULL	NULL	NULL	extracellular matrix	CellComponent		is linked to					cell cytoskeleton	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_20_11711_s_10	7744812	-Dystroglycan binds laminin and dystrophin binds actin filaments,  indicating that one function of the dystrophin-glycoprotein complex is  to provide a link between the extracellular matrix and the cell  cytoskeleton ( 5,  6) .	bind
44932	4	6055	7	NULL	NULL	NULL	NULL	dystrophin-glycoprotein complex	GP		plays a role in					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_20_11711_s_10	7744812	-Dystroglycan binds laminin and dystrophin binds actin filaments,  indicating that one function of the dystrophin-glycoprotein complex is  to provide a link between the extracellular matrix and the cell  cytoskeleton ( 5,  6) .	bind
15764	1	6056	5	10	NULL	0	NULL	Dystroglycan	NULL		bind	NULL				dystrophin	NULL		cysteine-rich C-terminal domain		NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_48_0_457_s_52	9046976	-Dystroglycan binds to the cysteine-rich region of the  C-terminal domain of dystrophin ( 15,  18).	bind
18858	1	6056	7	NULL	NULL	NULL	NULL	Dystroglycan	GP		binds to					dystrophin	GP		cysteine-rich  C-terminal domain		NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_48_0_457_s_52	9046976	-Dystroglycan binds to the cysteine-rich region of the  C-terminal domain of dystrophin ( 15,  18).	bind
15765	1	6057	5	10	NULL	0	NULL	Dystroglycan	NULL		bind	NULL				dystrophin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1573_3_292_s_146	12417411	-Dystroglycan is a transmembrane protein which binds dystrophin and the intracellular cytoskeleton.	bind
15766	2	6057	5	10	NULL	0	NULL	Dystroglycan	NULL		bind	NULL				cytoskeleton	NULL	intracellular			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1573_3_292_s_146	12417411	-Dystroglycan is a transmembrane protein which binds dystrophin and the intracellular cytoskeleton.	bind
44842	3	6057	5	10	NULL	0	NULL	Dystroglycan	NULL		is a type of	NULL				transmembrane protein	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1573_3_292_s_146	12417411	-Dystroglycan is a transmembrane protein which binds dystrophin and the intracellular cytoskeleton.	bind
18859	1	6057	7	NULL	NULL	NULL	NULL	Dystroglycan	GP		binds					dystrophin	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1573_3_292_s_146	12417411	-Dystroglycan is a transmembrane protein which binds dystrophin and the intracellular cytoskeleton.	bind
18860	2	6057	7	NULL	NULL	NULL	NULL	Dystroglycan	GP		binds					cytoskeleton	CellComponent	intracellular			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1573_3_292_s_146	12417411	-Dystroglycan is a transmembrane protein which binds dystrophin and the intracellular cytoskeleton.	bind
44843	3	6057	7	NULL	NULL	NULL	NULL	Dystroglycan	GP		is a type of					transmembrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1573_3_292_s_146	12417411	-Dystroglycan is a transmembrane protein which binds dystrophin and the intracellular cytoskeleton.	bind
15767	1	6058	5	NULL	NULL	0	NULL	Glutamate uptake inhibitors	NULL		stimulate	NULL				phosphoinositide 	NULL	hydrolysis of			NULL	in baby hamster kidney cells expressing mGluR1a	0	NULL	NULL	NULL	gw60_neuropharmacology_37_12_1465_s_319	9886669	-Glutamate uptake inhibitors may stimulate phosphoinositide hydrolysis in baby hamster kidney cells expressing mGluR1a via heteroexchange with  -glutamate without direct activation of mGluR1a.	bind
15768	2	6058	5	10	NULL	0	NULL	statement 1			occurs via					glutamate		heteroexchange with 			NULL	baby hamster kidney cells expressing mGluR1a	NULL	NULL	NULL	NULL	gw60_neuropharmacology_37_12_1465_s_319	9886669	-Glutamate uptake inhibitors may stimulate phosphoinositide hydrolysis in baby hamster kidney cells expressing mGluR1a via heteroexchange with  -glutamate without direct activation of mGluR1a.	bind
15769	3	6058	5	10	NULL	0	NULL	statement 2			occurs without					mGluR1a		activation of			NULL	baby hamster kidney cells expressing mGluR1a	NULL	NULL	NULL	NULL	gw60_neuropharmacology_37_12_1465_s_319	9886669	-Glutamate uptake inhibitors may stimulate phosphoinositide hydrolysis in baby hamster kidney cells expressing mGluR1a via heteroexchange with  -glutamate without direct activation of mGluR1a.	bind
18876	1	6058	7	NULL	NULL	NULL	NULL	Glutamate uptake inhibitors	Chemical		stimulate		may			phosphoinositide	Chemical	hydrolysis of			NULL	baby hamster kidney cells expressing mGluR1a	NULL	NULL	NULL	NULL	gw60_neuropharmacology_37_12_1465_s_319	9886669	-Glutamate uptake inhibitors may stimulate phosphoinositide hydrolysis in baby hamster kidney cells expressing mGluR1a via heteroexchange with  -glutamate without direct activation of mGluR1a.	bind
18878	2	6058	7	NULL	NULL	NULL	NULL	statement 2	Process		occurs via					glutamate	AminoAcid	heteroexchange with			NULL	baby hamster kidney cells expressing mGluR1a	NULL	NULL	NULL	NULL	gw60_neuropharmacology_37_12_1465_s_319	9886669	-Glutamate uptake inhibitors may stimulate phosphoinositide hydrolysis in baby hamster kidney cells expressing mGluR1a via heteroexchange with  -glutamate without direct activation of mGluR1a.	bind
18881	3	6058	7	NULL	NULL	NULL	NULL	statement 2	Process		happens without					mGluR1a	GP	direct activation of 			NULL	baby hamster kidney cells expressing mGluR1a	NULL	NULL	NULL	NULL	gw60_neuropharmacology_37_12_1465_s_319	9886669	-Glutamate uptake inhibitors may stimulate phosphoinositide hydrolysis in baby hamster kidney cells expressing mGluR1a via heteroexchange with  -glutamate without direct activation of mGluR1a.	bind
15770	1	6059	5	NULL	NULL	0	NULL	cisplatin	NULL		bind	NULL				GSH	NULL				NULL		0	NULL	NULL	NULL	gw70_intjdevneurosci_18_2_259_s_133	10715580	-Met and  -Met, free radical scavengers, may act by several different mechanisms including direct  binding to cisplatin itself or by reversing the binding of cisplatin to GSH [ 25].	bind
15771	2	6059	5	10	NULL	0	NULL	Met			act by		may			cisplatin		direct binding to			NULL		NULL	NULL	NULL	NULL	gw70_intjdevneurosci_18_2_259_s_133	10715580	-Met and  -Met, free radical scavengers, may act by several different mechanisms including direct  binding to cisplatin itself or by reversing the binding of cisplatin to GSH [ 25].	bind
15772	3	6059	5	10	NULL	0	NULL	Met			act by		may			statement 1		reversing			NULL		NULL	NULL	NULL	NULL	gw70_intjdevneurosci_18_2_259_s_133	10715580	-Met and  -Met, free radical scavengers, may act by several different mechanisms including direct  binding to cisplatin itself or by reversing the binding of cisplatin to GSH [ 25].	bind
15773	4	6059	5	NULL	NULL	0	NULL	Met, free radical scavengers	NULL		act by	NULL	may			cisplatin	NULL	direct binding to			NULL		0	NULL	NULL	NULL	gw70_intjdevneurosci_18_2_259_s_133	10715580	-Met and  -Met, free radical scavengers, may act by several different mechanisms including direct  binding to cisplatin itself or by reversing the binding of cisplatin to GSH [ 25].	bind
15774	5	6059	5	NULL	NULL	0	NULL	Met, free radical scavengers	NULL		act by	NULL	may			statement 1	NULL	reversing			NULL		0	NULL	NULL	NULL	gw70_intjdevneurosci_18_2_259_s_133	10715580	-Met and  -Met, free radical scavengers, may act by several different mechanisms including direct  binding to cisplatin itself or by reversing the binding of cisplatin to GSH [ 25].	bind
18883	1	6059	7	NULL	NULL	NULL	NULL	Met	AminoAcid		bind		directly			cisplatin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_intjdevneurosci_18_2_259_s_133	10715580	-Met and  -Met, free radical scavengers, may act by several different mechanisms including direct  binding to cisplatin itself or by reversing the binding of cisplatin to GSH [ 25].	bind
18884	2	6059	7	NULL	NULL	NULL	NULL	Met free radical scavengers	Chemical		bind		directly			cisplatin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_intjdevneurosci_18_2_259_s_133	10715580	-Met and  -Met, free radical scavengers, may act by several different mechanisms including direct  binding to cisplatin itself or by reversing the binding of cisplatin to GSH [ 25].	bind
18887	4	6059	7	NULL	NULL	NULL	NULL	statement 1	Process		reverse					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_intjdevneurosci_18_2_259_s_133	10715580	-Met and  -Met, free radical scavengers, may act by several different mechanisms including direct  binding to cisplatin itself or by reversing the binding of cisplatin to GSH [ 25].	bind
18888	6	6059	7	NULL	NULL	NULL	NULL	statement 2	Process		reverse					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_intjdevneurosci_18_2_259_s_133	10715580	-Met and  -Met, free radical scavengers, may act by several different mechanisms including direct  binding to cisplatin itself or by reversing the binding of cisplatin to GSH [ 25].	bind
45622	3	6059	7	NULL	NULL	NULL	NULL	cisplatin	Chemical		bind					GSH	GP				NULL		NULL	NULL	NULL	NULL	gw70_intjdevneurosci_18_2_259_s_133	10715580	-Met and  -Met, free radical scavengers, may act by several different mechanisms including direct  binding to cisplatin itself or by reversing the binding of cisplatin to GSH [ 25].	bind
15775	1	6060	5	NULL	NULL	0	NULL	MSH	NULL		bind	NULL				MC1R	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevgenet_38_0_365_s_336	15568981	-MSH binds MC1R and induces the activation of the  S-coupled G protein, which  then activates adenylyl cyclase.	bind
15776	2	6060	5	10	NULL	0	NULL	statement 1			induce					S-coupled G protein		activation of			NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_38_0_365_s_336	15568981	-MSH binds MC1R and induces the activation of the  S-coupled G protein, which  then activates adenylyl cyclase.	bind
15777	3	6060	5	NULL	NULL	0	NULL	statement 2	NULL		activate	NULL				S-coupled G protein	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevgenet_38_0_365_s_336	15568981	-MSH binds MC1R and induces the activation of the  S-coupled G protein, which  then activates adenylyl cyclase.	bind
18889	1	6060	7	NULL	NULL	NULL	NULL	MSH	GP		binds					MC1R	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_38_0_365_s_336	15568981	-MSH binds MC1R and induces the activation of the  S-coupled G protein, which  then activates adenylyl cyclase.	bind
18890	2	6060	7	NULL	NULL	NULL	NULL	statement 1	Process		induce					S-coupled G protein	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_38_0_365_s_336	15568981	-MSH binds MC1R and induces the activation of the  S-coupled G protein, which  then activates adenylyl cyclase.	bind
18891	3	6060	7	NULL	NULL	NULL	NULL	statement 2	Process		activates					adenylyl cyclase	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_38_0_365_s_336	15568981	-MSH binds MC1R and induces the activation of the  S-coupled G protein, which  then activates adenylyl cyclase.	bind
15828	1	6061	5	NULL	NULL	0	NULL	MSH	NULL		bind	NULL	predominantly			receptor MC-1R	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_549_1_87_s_277	12914931	-MSH binds predominantly with its receptor MC-1R.	bind
18892	1	6061	7	NULL	NULL	NULL	NULL	MSH	GP		binds		predominantly			MC-1R receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_549_1_87_s_277	12914931	-MSH binds predominantly with its receptor MC-1R.	bind
15829	1	6062	5	NULL	NULL	0	NULL	MSH	NULL		is a type of	NULL				cell surface receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_549_1_87_s_151	12914931	-MSH binds with its cell surface receptor specifically melanocortin-1 receptor (MC-1R).	bind
15830	2	6062	5	NULL	NULL	0	NULL	MSH	NULL		bind	NULL	specifically			MC-1R	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_549_1_87_s_151	12914931	-MSH binds with its cell surface receptor specifically melanocortin-1 receptor (MC-1R).	bind
15831	3	6062	5	NULL	NULL	0	NULL	MC-1R	NULL		is	NULL				melanocortin-1 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_549_1_87_s_151	12914931	-MSH binds with its cell surface receptor specifically melanocortin-1 receptor (MC-1R).	bind
18893	1	6062	7	NULL	NULL	NULL	NULL	MSH	GP		binds		specifically			MC-1R	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_549_1_87_s_151	12914931	-MSH binds with its cell surface receptor specifically melanocortin-1 receptor (MC-1R).	bind
18894	2	6062	7	NULL	NULL	NULL	NULL	MC-1R	GP		is					melanocortin-1 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_549_1_87_s_151	12914931	-MSH binds with its cell surface receptor specifically melanocortin-1 receptor (MC-1R).	bind
25657	3	6062	7	NULL	NULL	NULL	NULL	MC-1R	GP		is a type of					cell surface receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_549_1_87_s_151	12914931	-MSH binds with its cell surface receptor specifically melanocortin-1 receptor (MC-1R).	bind
15854	1	6063	5	NULL	NULL	0	NULL	BTX	NULL		bind	NULL	specifically			AChR	NULL				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_2_147_s_22	11251289	-Neurotoxins such as  -bungarotoxin ( -BTX) bind specifically to AChR and exhibit high toxicity due to inhibition of the AChR function at the neuromuscular junction.	bind
15855	2	6063	5	NULL	NULL	0	NULL	BTX	NULL		is	NULL				bungarotoxin	NULL				NULL		0	NULL	NULL	NULL	gw60_chembiol_8_2_147_s_22	11251289	-Neurotoxins such as  -bungarotoxin ( -BTX) bind specifically to AChR and exhibit high toxicity due to inhibition of the AChR function at the neuromuscular junction.	bind
15856	3	6063	5	NULL	NULL	0	NULL	BTX	NULL		exhibit	NULL				toxicity 	NULL	high			NULL	at neuromuscular junction	0	NULL	NULL	NULL	gw60_chembiol_8_2_147_s_22	11251289	-Neurotoxins such as  -bungarotoxin ( -BTX) bind specifically to AChR and exhibit high toxicity due to inhibition of the AChR function at the neuromuscular junction.	bind
15858	4	6063	5	10	NULL	0	NULL	statement 3	NULL		occurs due to	NULL				AChR	NULL	inhibition of;; function of			NULL	at neuromuscular junction	NULL	NULL	NULL	NULL	gw60_chembiol_8_2_147_s_22	11251289	-Neurotoxins such as  -bungarotoxin ( -BTX) bind specifically to AChR and exhibit high toxicity due to inhibition of the AChR function at the neuromuscular junction.	bind
25659	5	6063	5	NULL	NULL	0	NULL	BTX	NULL		is a type of	NULL				neurotoxin	NULL				NULL		0	NULL	NULL	NULL	gw60_chembiol_8_2_147_s_22	11251289	-Neurotoxins such as  -bungarotoxin ( -BTX) bind specifically to AChR and exhibit high toxicity due to inhibition of the AChR function at the neuromuscular junction.	bind
18895	1	6063	7	NULL	NULL	NULL	NULL	BTX	GP		bind		specifically			AChR	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_2_147_s_22	11251289	-Neurotoxins such as  -bungarotoxin ( -BTX) bind specifically to AChR and exhibit high toxicity due to inhibition of the AChR function at the neuromuscular junction.	bind
18896	2	6063	7	NULL	NULL	NULL	NULL	BTX	GP		possess					high toxicity	Process				NULL	neuromuscular junction	NULL	NULL	NULL	NULL	gw60_chembiol_8_2_147_s_22	11251289	-Neurotoxins such as  -bungarotoxin ( -BTX) bind specifically to AChR and exhibit high toxicity due to inhibition of the AChR function at the neuromuscular junction.	bind
18897	3	6063	7	NULL	NULL	NULL	NULL	statement 2	Process		occurs due to					AChR	GP	inhibition of;; function of			NULL	neuromuscular junction	NULL	NULL	NULL	NULL	gw60_chembiol_8_2_147_s_22	11251289	-Neurotoxins such as  -bungarotoxin ( -BTX) bind specifically to AChR and exhibit high toxicity due to inhibition of the AChR function at the neuromuscular junction.	bind
18899	5	6063	7	NULL	NULL	NULL	NULL	BTX	GP		is					bungarotoxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_2_147_s_22	11251289	-Neurotoxins such as  -bungarotoxin ( -BTX) bind specifically to AChR and exhibit high toxicity due to inhibition of the AChR function at the neuromuscular junction.	bind
18900	6	6063	7	NULL	NULL	NULL	NULL	bungarotoxin	GP		is a type of					neurotoxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_2_147_s_22	11251289	-Neurotoxins such as  -bungarotoxin ( -BTX) bind specifically to AChR and exhibit high toxicity due to inhibition of the AChR function at the neuromuscular junction.	bind
15859	1	6064	5	NULL	NULL	0	NULL	Pak2	NULL		is	NULL				PAK	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_515_1_84_s_3	11943200	-PAK (Pak2) is a ubiquitous member of the family of p21-activated protein kinases (PAKs) which are activated by autophosphorylation following binding of the GTP-bound form of the small G-protein Cdc42 (for reviews see [  1,   2,   3,   4 and   5]).	bind
15860	2	6064	5	NULL	NULL	0	NULL	Pak2	NULL		is a type of	NULL				p21-activated protein kinases	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_515_1_84_s_3	11943200	-PAK (Pak2) is a ubiquitous member of the family of p21-activated protein kinases (PAKs) which are activated by autophosphorylation following binding of the GTP-bound form of the small G-protein Cdc42 (for reviews see [  1,   2,   3,   4 and   5]).	bind
15861	3	6064	5	NULL	NULL	0	NULL	Pak2	NULL		activated by	NULL				autophosphorylation	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_515_1_84_s_3	11943200	-PAK (Pak2) is a ubiquitous member of the family of p21-activated protein kinases (PAKs) which are activated by autophosphorylation following binding of the GTP-bound form of the small G-protein Cdc42 (for reviews see [  1,   2,   3,   4 and   5]).	bind
15862	4	6064	5	10	NULL	0	NULL	GTP	NULL		bind	NULL				Cdc42	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_515_1_84_s_3	11943200	-PAK (Pak2) is a ubiquitous member of the family of p21-activated protein kinases (PAKs) which are activated by autophosphorylation following binding of the GTP-bound form of the small G-protein Cdc42 (for reviews see [  1,   2,   3,   4 and   5]).	bind
15863	5	6064	5	10	NULL	0	NULL	statement 3	NULL		occurs upon	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_515_1_84_s_3	11943200	-PAK (Pak2) is a ubiquitous member of the family of p21-activated protein kinases (PAKs) which are activated by autophosphorylation following binding of the GTP-bound form of the small G-protein Cdc42 (for reviews see [  1,   2,   3,   4 and   5]).	bind
44844	6	6064	5	10	NULL	0	NULL	Cdc42	NULL		is a type of	NULL				small G protein	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_515_1_84_s_3	11943200	-PAK (Pak2) is a ubiquitous member of the family of p21-activated protein kinases (PAKs) which are activated by autophosphorylation following binding of the GTP-bound form of the small G-protein Cdc42 (for reviews see [  1,   2,   3,   4 and   5]).	bind
18901	1	6064	7	NULL	NULL	NULL	NULL	GTP	Chemical		bind					Cdc42	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_515_1_84_s_3	11943200	-PAK (Pak2) is a ubiquitous member of the family of p21-activated protein kinases (PAKs) which are activated by autophosphorylation following binding of the GTP-bound form of the small G-protein Cdc42 (for reviews see [  1,   2,   3,   4 and   5]).	bind
18902	2	6064	7	NULL	NULL	NULL	NULL	Pak2	GP		is a type of					p21-activated protein kinases	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_515_1_84_s_3	11943200	-PAK (Pak2) is a ubiquitous member of the family of p21-activated protein kinases (PAKs) which are activated by autophosphorylation following binding of the GTP-bound form of the small G-protein Cdc42 (for reviews see [  1,   2,   3,   4 and   5]).	bind
18903	3	6064	7	NULL	NULL	NULL	NULL	PAKs	GP		is activated by					autophosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_515_1_84_s_3	11943200	-PAK (Pak2) is a ubiquitous member of the family of p21-activated protein kinases (PAKs) which are activated by autophosphorylation following binding of the GTP-bound form of the small G-protein Cdc42 (for reviews see [  1,   2,   3,   4 and   5]).	bind
18904	4	6064	7	NULL	NULL	NULL	NULL	statement 3	Process		occurs upon					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_515_1_84_s_3	11943200	-PAK (Pak2) is a ubiquitous member of the family of p21-activated protein kinases (PAKs) which are activated by autophosphorylation following binding of the GTP-bound form of the small G-protein Cdc42 (for reviews see [  1,   2,   3,   4 and   5]).	bind
18905	5	6064	7	NULL	NULL	NULL	NULL	PAKs	GP		is					p21-activated protein kinases 	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_515_1_84_s_3	11943200	-PAK (Pak2) is a ubiquitous member of the family of p21-activated protein kinases (PAKs) which are activated by autophosphorylation following binding of the GTP-bound form of the small G-protein Cdc42 (for reviews see [  1,   2,   3,   4 and   5]).	bind
44845	6	6064	7	NULL	NULL	NULL	NULL	Cdc42	GP		is a type of					small G protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_515_1_84_s_3	11943200	-PAK (Pak2) is a ubiquitous member of the family of p21-activated protein kinases (PAKs) which are activated by autophosphorylation following binding of the GTP-bound form of the small G-protein Cdc42 (for reviews see [  1,   2,   3,   4 and   5]).	bind
15864	2	6065	5	NULL	NULL	0	NULL	PYR	NULL		bind	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_febslett_565_1_65_s_83	15135054	-PYR binding to ATP-bound DnaK monitored by tryptophan fluorescence.	bind
45615	1	6065	5	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				DnaK	NULL				NULL		0	NULL	NULL	NULL	gw70_febslett_565_1_65_s_83	15135054	-PYR binding to ATP-bound DnaK monitored by tryptophan fluorescence.	bind
18907	2	6065	7	NULL	NULL	NULL	NULL	PYR	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_565_1_65_s_83	15135054	-PYR binding to ATP-bound DnaK monitored by tryptophan fluorescence.	bind
44933	1	6065	7	NULL	NULL	NULL	NULL	ATP	Chemical		bind					DnaK	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_febslett_565_1_65_s_83	15135054	-PYR binding to ATP-bound DnaK monitored by tryptophan fluorescence.	bind
15865	1	6067	5	NULL	NULL	0	NULL	Ser	NULL		bind	NULL				NMDA receptor	NULL		glycine site		NULL		0	NULL	NULL	NULL	gw60_neuroscience_83_2_449_s_179	9460753	-Ser can also bind and modulate the glycine site of the NMDA receptor.	bind
15866	2	6067	5	NULL	NULL	0	NULL	Ser	NULL		modulate	NULL				NMDA receptor	NULL		glycine site		NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_83_2_449_s_179	9460753	-Ser can also bind and modulate the glycine site of the NMDA receptor.	bind
18909	1	6067	7	NULL	NULL	NULL	NULL	Ser	AminoAcid		bind					NMDA receptor	GP		 glycine site		NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_83_2_449_s_179	9460753	-Ser can also bind and modulate the glycine site of the NMDA receptor.	bind
18911	2	6067	7	NULL	NULL	NULL	NULL	Ser	AminoAcid		modulate					NMDA receptor	GP		glycine site		NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_83_2_449_s_179	9460753	-Ser can also bind and modulate the glycine site of the NMDA receptor.	bind
15867	1	6068	5	NULL	NULL	0	NULL	Serine	NULL		does not enhance	NULL					NULL	binding of	glutamate		NULL		NULL	NULL	NULL	NULL	gw60_brainres_771_2_292_s_228	9401750	-Serine, an agonist at the glycine binding site of NMDA receptors, failed to enhance the binding of  -glutamate (data not shown).	bind
15868	2	6068	5	NULL	NULL	0	NULL	Serine	NULL		is a type of	NULL				agonist	NULL				NULL		NULL	NULL	NULL	NULL	gw60_brainres_771_2_292_s_228	9401750	-Serine, an agonist at the glycine binding site of NMDA receptors, failed to enhance the binding of  -glutamate (data not shown).	bind
25661	3	6068	5	NULL	NULL	0	NULL	Serine	NULL		is present at	NULL				NMDA receptors	NULL		glycine binding site		NULL		0	NULL	NULL	NULL	gw60_brainres_771_2_292_s_228	9401750	-Serine, an agonist at the glycine binding site of NMDA receptors, failed to enhance the binding of  -glutamate (data not shown).	bind
18914	1	6068	7	NULL	NULL	NULL	NULL	Serine	AminoAcid		is a type of					agonist	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_brainres_771_2_292_s_228	9401750	-Serine, an agonist at the glycine binding site of NMDA receptors, failed to enhance the binding of  -glutamate (data not shown).	bind
18915	3	6068	7	NULL	NULL	NULL	NULL	Serine	AminoAcid		failed to enhance					glutamate	AminoAcid	binding of			NULL		NULL	NULL	NULL	NULL	gw60_brainres_771_2_292_s_228	9401750	-Serine, an agonist at the glycine binding site of NMDA receptors, failed to enhance the binding of  -glutamate (data not shown).	bind
25660	2	6068	7	NULL	NULL	NULL	NULL	Serine	AminoAcid		is present at					NMDA receptors	GP		glycine binding site		NULL		NULL	NULL	NULL	NULL	gw60_brainres_771_2_292_s_228	9401750	-Serine, an agonist at the glycine binding site of NMDA receptors, failed to enhance the binding of  -glutamate (data not shown).	bind
15869	1	6069	5	NULL	NULL	0	NULL	Synuclein	NULL		bind	NULL				tau	NULL				NULL		0	NULL	NULL	NULL	gw70_neurobioldis_16_1_92_s_267	15207266	-Synuclein  binds to  tau and stimulates the protein kinase A-catalyzed tau phosphorylation of serine residues  263 and 356.	bind
15870	2	6069	5	NULL	NULL	0	NULL	protein kinase A	NULL		catalyze	NULL				tau	NULL	phosphorylation of	serine 263		NULL		0	NULL	NULL	NULL	gw70_neurobioldis_16_1_92_s_267	15207266	-Synuclein  binds to  tau and stimulates the protein kinase A-catalyzed tau phosphorylation of serine residues  263 and 356.	bind
15871	3	6069	5	NULL	NULL	0	NULL	protein kinase A	NULL		catalyze	NULL				tau	NULL	phosphorylation of	serine 356		NULL		0	NULL	NULL	NULL	gw70_neurobioldis_16_1_92_s_267	15207266	-Synuclein  binds to  tau and stimulates the protein kinase A-catalyzed tau phosphorylation of serine residues  263 and 356.	bind
15872	4	6069	5	NULL	NULL	0	NULL	statement 1	NULL		stimulate	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_neurobioldis_16_1_92_s_267	15207266	-Synuclein  binds to  tau and stimulates the protein kinase A-catalyzed tau phosphorylation of serine residues  263 and 356.	bind
15873	5	6069	5	NULL	NULL	0	NULL	statement 1	NULL		stimulate	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_neurobioldis_16_1_92_s_267	15207266	-Synuclein  binds to  tau and stimulates the protein kinase A-catalyzed tau phosphorylation of serine residues  263 and 356.	bind
18916	1	6069	7	NULL	NULL	NULL	NULL	Synuclein	GP		binds to					tau 	GP				NULL		NULL	NULL	NULL	NULL	gw70_neurobioldis_16_1_92_s_267	15207266	-Synuclein  binds to  tau and stimulates the protein kinase A-catalyzed tau phosphorylation of serine residues  263 and 356.	bind
18917	2	6069	7	NULL	NULL	NULL	NULL	statement 1	Process		stimulates					tau 	GP	phosphorylation  of	serine residues 263		NULL		NULL	NULL	NULL	NULL	gw70_neurobioldis_16_1_92_s_267	15207266	-Synuclein  binds to  tau and stimulates the protein kinase A-catalyzed tau phosphorylation of serine residues  263 and 356.	bind
18918	3	6069	7	NULL	NULL	NULL	NULL	statement 1	Process		stimulates					tau	GP	phosphorylation of	serine residues 356		NULL		NULL	NULL	NULL	NULL	gw70_neurobioldis_16_1_92_s_267	15207266	-Synuclein  binds to  tau and stimulates the protein kinase A-catalyzed tau phosphorylation of serine residues  263 and 356.	bind
18919	4	6069	7	NULL	NULL	NULL	NULL	protein kinase A	GP		catalyses					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_neurobioldis_16_1_92_s_267	15207266	-Synuclein  binds to  tau and stimulates the protein kinase A-catalyzed tau phosphorylation of serine residues  263 and 356.	bind
18920	5	6069	7	NULL	NULL	NULL	NULL	protein kinase A	GP		catalyses					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_neurobioldis_16_1_92_s_267	15207266	-Synuclein  binds to  tau and stimulates the protein kinase A-catalyzed tau phosphorylation of serine residues  263 and 356.	bind
15874	1	6070	5	NULL	NULL	0	NULL	Synuclein	NULL		bind	NULL				phospholipid vesicles	NULL	synthetic			NULL		0	NULL	NULL	NULL	gw60_progneurophychbiolphych_27_1_103_s_42	12551731	-Synuclein binding to synthetic phospholipid vesicles is accompanied by a strong increase in  -helicity, an observation consistent with a role in vesicle function at synaptic terminals  ( Davidson et al., 1998).	bind
15875	2	6070	5	10	NULL	0	NULL	statement 1	NULL		is accompanied by	NULL				helicity	NULL	strong increase of			NULL		NULL	NULL	NULL	NULL	gw60_progneurophychbiolphych_27_1_103_s_42	12551731	-Synuclein binding to synthetic phospholipid vesicles is accompanied by a strong increase in  -helicity, an observation consistent with a role in vesicle function at synaptic terminals  ( Davidson et al., 1998).	bind
18921	1	6070	7	NULL	NULL	NULL	NULL	Synuclein	GP		bind					phospholipid vesicles	CellComponent	synthetic			NULL		NULL	NULL	NULL	NULL	gw60_progneurophychbiolphych_27_1_103_s_42	12551731	-Synuclein binding to synthetic phospholipid vesicles is accompanied by a strong increase in  -helicity, an observation consistent with a role in vesicle function at synaptic terminals  ( Davidson et al., 1998).	bind
18922	2	6070	7	NULL	NULL	NULL	NULL	statement 1	Process		is accompanied by					helicity	Process	strong increase in			NULL		NULL	NULL	NULL	NULL	gw60_progneurophychbiolphych_27_1_103_s_42	12551731	-Synuclein binding to synthetic phospholipid vesicles is accompanied by a strong increase in  -helicity, an observation consistent with a role in vesicle function at synaptic terminals  ( Davidson et al., 1998).	bind
15876	1	6071	5	NULL	NULL	0	NULL	Synuclein	NULL		bind	NULL				tubulin	NULL				NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_95_1_138_s_125	11687285	-Synuclein binds a tubulin affinity column	bind
18923	1	6071	7	NULL	NULL	NULL	NULL	Synuclein	GP		binds 					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_95_1_138_s_125	11687285	-Synuclein binds a tubulin affinity column	bind
15877	1	6073	5	NULL	NULL	0	NULL	Synuclein	NULL		bind	NULL				synphilin-1	NULL				NULL		0	NULL	NULL	NULL	gw60_brainres_926_1_42_s_199	11814405	-Synuclein can bind to synphilin-1 and stimulate the formation of aggregates [  9 and   41].	bind
15878	2	6073	5	10	NULL	0	NULL	statement 1			stimulate					aggregates		formation of			NULL		NULL	NULL	NULL	NULL	gw60_brainres_926_1_42_s_199	11814405	-Synuclein can bind to synphilin-1 and stimulate the formation of aggregates [  9 and   41].	bind
18924	1	6073	7	NULL	NULL	NULL	NULL	Synuclein	GP		bind					synphilin-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_926_1_42_s_199	11814405	-Synuclein can bind to synphilin-1 and stimulate the formation of aggregates [  9 and   41].	bind
18925	2	6073	7	NULL	NULL	NULL	NULL	statement 1	Process		stimulate					aggregates	Process	formation of			NULL		NULL	NULL	NULL	NULL	gw60_brainres_926_1_42_s_199	11814405	-Synuclein can bind to synphilin-1 and stimulate the formation of aggregates [  9 and   41].	bind
15879	1	6074	5	10	NULL	0	NULL	Thrombin	NULL	purified;; radiolabeled	bind	NULL				GP Ib fragments	NULL	immobilized;; recombinant			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_16_9571_s_56	7721887	-Thrombin Binding to Immobilized Recombinant GP  Ib   Fragments -Thrombin, a generous gift of Dr. John W.  Fenton II (Wadsworth Center for Laboratory and Research and Departments  of Physiology and Biochemistry, Albany Medical College, Union  University, Albany, NY), was purified and characterized as described  previously  ( 25) ; it was radiolabeled with  I using  the IODO-GEN technique  ( 20) , as reported in detail in a  previous publication  ( 4) .	bind
18926	1	6074	7	NULL	NULL	NULL	NULL	Thrombin	GP	purified;; radiolabeled	binds to					GP Ib Fragments	AminoAcid	Immobilized;; Recombinant			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_16_9571_s_56	7721887	-Thrombin Binding to Immobilized Recombinant GP  Ib   Fragments -Thrombin, a generous gift of Dr. John W.  Fenton II (Wadsworth Center for Laboratory and Research and Departments  of Physiology and Biochemistry, Albany Medical College, Union  University, Albany, NY), was purified and characterized as described  previously  ( 25) ; it was radiolabeled with  I using  the IODO-GEN technique  ( 20) , as reported in detail in a  previous publication  ( 4) .	bind
15880	1	6075	5	NULL	NULL	0	NULL	tubulin	NULL		bind	NULL		N-site		GTP	NULL				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_13_0_83_s_47	9442869	-tubulin also binds GTP, but this  GTP is bound in a non-exchangeable manner (at the N-site) and is not hydrolyzed during  polymerization ( Spiegelman et al 1977).	bind
15881	2	6075	5	NULL	NULL	0	NULL	GTP	NULL		is not hydrolyzed	NULL				polymerization	NULL	during			NULL		0	NULL	NULL	NULL	gw70_annurevcelldevbiol_13_0_83_s_47	9442869	-tubulin also binds GTP, but this  GTP is bound in a non-exchangeable manner (at the N-site) and is not hydrolyzed during  polymerization ( Spiegelman et al 1977).	bind
25664	3	6075	5	NULL	NULL	0	NULL	statement 1	NULL		occurs in	NULL				non-exchangeable manner	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevcelldevbiol_13_0_83_s_47	9442869	-tubulin also binds GTP, but this  GTP is bound in a non-exchangeable manner (at the N-site) and is not hydrolyzed during  polymerization ( Spiegelman et al 1977).	bind
18927	1	6075	7	NULL	NULL	NULL	NULL	tubulin 	GP		binds			N-site		GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_13_0_83_s_47	9442869	-tubulin also binds GTP, but this  GTP is bound in a non-exchangeable manner (at the N-site) and is not hydrolyzed during  polymerization ( Spiegelman et al 1977).	bind
18928	2	6075	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs in a					non-exchangeable manner	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_13_0_83_s_47	9442869	-tubulin also binds GTP, but this  GTP is bound in a non-exchangeable manner (at the N-site) and is not hydrolyzed during  polymerization ( Spiegelman et al 1977).	bind
18929	3	6075	7	NULL	NULL	NULL	NULL	statement 1	Process		is not hydrolysed					polymerization 	Process	during			NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_13_0_83_s_47	9442869	-tubulin also binds GTP, but this  GTP is bound in a non-exchangeable manner (at the N-site) and is not hydrolyzed during  polymerization ( Spiegelman et al 1977).	bind
15882	1	6080	5	NULL	NULL	0	NULL	HSCO	NULL		is	NULL				hepatoma subtracted clone 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_44_46204_s_242	15302862	0610025L15Rik is 92% homologous to human HSCO (hepatoma subtracted clone 1), which binds to NF-kappaB, inhibits apoptosis and is overexpressed in hepatocellular carcinomas ( ).	bind
15883	2	6080	5	NULL	NULL	0	NULL	HSCO	NULL	human	bind	NULL				NF-kappaB	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_44_46204_s_242	15302862	0610025L15Rik is 92% homologous to human HSCO (hepatoma subtracted clone 1), which binds to NF-kappaB, inhibits apoptosis and is overexpressed in hepatocellular carcinomas ( ).	bind
15884	3	6080	5	NULL	NULL	0	NULL	HSCO	NULL	human	inhibit	NULL				apoptosis	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_44_46204_s_242	15302862	0610025L15Rik is 92% homologous to human HSCO (hepatoma subtracted clone 1), which binds to NF-kappaB, inhibits apoptosis and is overexpressed in hepatocellular carcinomas ( ).	bind
15885	4	6080	5	NULL	NULL	0	NULL	HSCO	NULL	human	is overexpressed in	NULL				hepatocellular carcinomas	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_44_46204_s_242	15302862	0610025L15Rik is 92% homologous to human HSCO (hepatoma subtracted clone 1), which binds to NF-kappaB, inhibits apoptosis and is overexpressed in hepatocellular carcinomas ( ).	bind
25662	5	6080	5	NULL	NULL	0	NULL	HSCO	NULL	human	is homologous to	NULL	mostly			0610025L15Rik	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_44_46204_s_242	15302862	0610025L15Rik is 92% homologous to human HSCO (hepatoma subtracted clone 1), which binds to NF-kappaB, inhibits apoptosis and is overexpressed in hepatocellular carcinomas ( ).	bind
18930	1	6080	7	NULL	NULL	NULL	NULL	HSCO	Cell	human	binds to					NF-kappaB	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_46204_s_242	15302862	0610025L15Rik is 92% homologous to human HSCO (hepatoma subtracted clone 1), which binds to NF-kappaB, inhibits apoptosis and is overexpressed in hepatocellular carcinomas ( ).	bind
18931	2	6080	7	NULL	NULL	NULL	NULL	statement 1	Process		inhibits					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_46204_s_242	15302862	0610025L15Rik is 92% homologous to human HSCO (hepatoma subtracted clone 1), which binds to NF-kappaB, inhibits apoptosis and is overexpressed in hepatocellular carcinomas ( ).	bind
18932	3	6080	7	NULL	NULL	NULL	NULL	HSCO	Cell	human	is overexpressed in					hepatocellular carcinomas	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_46204_s_242	15302862	0610025L15Rik is 92% homologous to human HSCO (hepatoma subtracted clone 1), which binds to NF-kappaB, inhibits apoptosis and is overexpressed in hepatocellular carcinomas ( ).	bind
18933	4	6080	7	NULL	NULL	NULL	NULL	0610025L15Rik	Cell		 homologous to		mostly			HSCO	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_46204_s_242	15302862	0610025L15Rik is 92% homologous to human HSCO (hepatoma subtracted clone 1), which binds to NF-kappaB, inhibits apoptosis and is overexpressed in hepatocellular carcinomas ( ).	bind
18934	5	6080	7	NULL	NULL	NULL	NULL	HSCO	Cell		is					hepatoma subtracted clone 1	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_46204_s_242	15302862	0610025L15Rik is 92% homologous to human HSCO (hepatoma subtracted clone 1), which binds to NF-kappaB, inhibits apoptosis and is overexpressed in hepatocellular carcinomas ( ).	bind
15888	1	6103	5	NULL	NULL	0	NULL	serine protease factor VII/VIIa	NULL	plasma	bind	NULL				factor IX	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_7_1804_s_15	10397701	1  2 3  It forms a complex with the plasma serine protease factor VII/VIIa, which binds and activates factors IX and X.	bind
15890	2	6103	5	NULL	NULL	0	NULL	serine protease factor VII/VIIa	NULL	plasma	activate	NULL				factor IX	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_7_1804_s_15	10397701	1  2 3  It forms a complex with the plasma serine protease factor VII/VIIa, which binds and activates factors IX and X.	bind
15891	3	6103	5	NULL	NULL	0	NULL	serine protease factor VII/VIIa	NULL	plasma	bind	NULL				factor X	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_7_1804_s_15	10397701	1  2 3  It forms a complex with the plasma serine protease factor VII/VIIa, which binds and activates factors IX and X.	bind
15892	4	6103	5	NULL	NULL	0	NULL	serine protease factor VII/VIIa	NULL	plasma	activate	NULL				factor X	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_7_1804_s_15	10397701	1  2 3  It forms a complex with the plasma serine protease factor VII/VIIa, which binds and activates factors IX and X.	bind
19054	1	6103	7	NULL	NULL	NULL	NULL	serine protease factor VII/VIIa	GP	plasma	binds					factors IX	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_7_1804_s_15	10397701	1  2 3  It forms a complex with the plasma serine protease factor VII/VIIa, which binds and activates factors IX and X.	bind
19055	2	6103	7	NULL	NULL	NULL	NULL	serine protease factor VII/VIIa	GP	plasma	binds					factor X	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_7_1804_s_15	10397701	1  2 3  It forms a complex with the plasma serine protease factor VII/VIIa, which binds and activates factors IX and X.	bind
19056	3	6103	7	NULL	NULL	NULL	NULL	serine protease factor VII/VIIa	GP	plasma	activates					factor IX	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_7_1804_s_15	10397701	1  2 3  It forms a complex with the plasma serine protease factor VII/VIIa, which binds and activates factors IX and X.	bind
19057	4	6103	7	NULL	NULL	NULL	NULL	serine protease factor VII/VIIa	GP	plasma	activates					factor X	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_7_1804_s_15	10397701	1  2 3  It forms a complex with the plasma serine protease factor VII/VIIa, which binds and activates factors IX and X.	bind
15894	1	6104	5	NULL	NULL	0	NULL	vWF	NULL	vessel-wall bound	bind	NULL				platelet GPIb-alpha	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_3_324_s_119	10645930	1  2 5 6  Under high-shear flow conditions, the vessel-wall bound vWF binds to the platelet GPIb-alpha in the early phases of hemostasis (platelet adhesion), a process independent of ADP and induced by ristocetin.	bind
15895	2	6104	5	NULL	NULL	0	NULL	hemostasis	NULL		is independent of	NULL				ADP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_3_324_s_119	10645930	1  2 5 6  Under high-shear flow conditions, the vessel-wall bound vWF binds to the platelet GPIb-alpha in the early phases of hemostasis (platelet adhesion), a process independent of ADP and induced by ristocetin.	bind
15896	3	6104	5	NULL	NULL	0	NULL	ristocetin	NULL		induce	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_101_3_324_s_119	10645930	1  2 5 6  Under high-shear flow conditions, the vessel-wall bound vWF binds to the platelet GPIb-alpha in the early phases of hemostasis (platelet adhesion), a process independent of ADP and induced by ristocetin.	bind
25663	4	6104	5	10	NULL	0	NULL	statement 1	NULL		occurs in	NULL				hemostasis 	NULL	early phases of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_3_324_s_119	10645930	1  2 5 6  Under high-shear flow conditions, the vessel-wall bound vWF binds to the platelet GPIb-alpha in the early phases of hemostasis (platelet adhesion), a process independent of ADP and induced by ristocetin.	bind
18935	1	6104	7	NULL	NULL	NULL	NULL	vWF 	GP	 vessel-wall bound 	binds to					platelet GPIb-alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_3_324_s_119	10645930	1  2 5 6  Under high-shear flow conditions, the vessel-wall bound vWF binds to the platelet GPIb-alpha in the early phases of hemostasis (platelet adhesion), a process independent of ADP and induced by ristocetin.	bind
18936	2	6104	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs in the					hemostasis	Process	early phase of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_3_324_s_119	10645930	1  2 5 6  Under high-shear flow conditions, the vessel-wall bound vWF binds to the platelet GPIb-alpha in the early phases of hemostasis (platelet adhesion), a process independent of ADP and induced by ristocetin.	bind
18937	3	6104	7	NULL	NULL	NULL	NULL	hemostasis	Process		is independent of					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_3_324_s_119	10645930	1  2 5 6  Under high-shear flow conditions, the vessel-wall bound vWF binds to the platelet GPIb-alpha in the early phases of hemostasis (platelet adhesion), a process independent of ADP and induced by ristocetin.	bind
18938	4	6104	7	NULL	NULL	NULL	NULL	ristocetin	Chemical		induce					hemostasis	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_3_324_s_119	10645930	1  2 5 6  Under high-shear flow conditions, the vessel-wall bound vWF binds to the platelet GPIb-alpha in the early phases of hemostasis (platelet adhesion), a process independent of ADP and induced by ristocetin.	bind
15897	1	6106	5	NULL	NULL	0	NULL	heparin polysaccharide chains	NULL		bind	NULL	high affinity			antithrombin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_16_9043_s_14	7721817	1  and 2) The accelerating activity results from a sequence-specific  pentasaccharide region, present in about one-third of heparin  polysaccharide chains  ( 3,  4,  5) , which binds  antithrombin with high affinity and induces an activating  conformational change in the inhibitor  ( 6,  7,  8,  9,  10,  11) .	bind
15899	2	6106	5	10	NULL	0	NULL	statement 1			induce					inhibitor		activating;; conformational change in			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_16_9043_s_14	7721817	1  and 2) The accelerating activity results from a sequence-specific  pentasaccharide region, present in about one-third of heparin  polysaccharide chains  ( 3,  4,  5) , which binds  antithrombin with high affinity and induces an activating  conformational change in the inhibitor  ( 6,  7,  8,  9,  10,  11) .	bind
18939	1	6106	7	NULL	NULL	NULL	NULL	heparin	GP		binds		high affinity	polysaccharide chains		antithrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_16_9043_s_14	7721817	1  and 2) The accelerating activity results from a sequence-specific  pentasaccharide region, present in about one-third of heparin  polysaccharide chains  ( 3,  4,  5) , which binds  antithrombin with high affinity and induces an activating  conformational change in the inhibitor  ( 6,  7,  8,  9,  10,  11) .	bind
18940	2	6106	7	NULL	NULL	NULL	NULL	statement 1	Process		induce					inhibitor	Chemical	activating;; conformational change in			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_16_9043_s_14	7721817	1  and 2) The accelerating activity results from a sequence-specific  pentasaccharide region, present in about one-third of heparin  polysaccharide chains  ( 3,  4,  5) , which binds  antithrombin with high affinity and induces an activating  conformational change in the inhibitor  ( 6,  7,  8,  9,  10,  11) .	bind
15900	1	6107	5	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				proteoglycans	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1340_s_21	10323788	1  Binding of LDL to proteoglycans traps LDL in the arterial intima, which provides the opportunity for oxidation of LDL lipids.	bind
15902	2	6107	5	10	NULL	0	NULL	statement 1	NULL		traps	NULL				LDL	NULL				NULL	arterial intima	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1340_s_21	10323788	1  Binding of LDL to proteoglycans traps LDL in the arterial intima, which provides the opportunity for oxidation of LDL lipids.	bind
15903	3	6107	5	10	NULL	0	NULL	statement 2	NULL		plays a role in	NULL				LDL lipids	NULL	oxidation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1340_s_21	10323788	1  Binding of LDL to proteoglycans traps LDL in the arterial intima, which provides the opportunity for oxidation of LDL lipids.	bind
18949	1	6107	7	NULL	NULL	NULL	NULL	LDL	Chemical		bind					proteoglycans	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1340_s_21	10323788	1  Binding of LDL to proteoglycans traps LDL in the arterial intima, which provides the opportunity for oxidation of LDL lipids.	bind
18950	2	6107	7	NULL	NULL	NULL	NULL	statement 1	Process		traps					LDL	Chemical				NULL	in the arterial intima	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1340_s_21	10323788	1  Binding of LDL to proteoglycans traps LDL in the arterial intima, which provides the opportunity for oxidation of LDL lipids.	bind
18951	3	6107	7	NULL	NULL	NULL	NULL	statement 2	Process		plays a role in					LDL lipids	Chemical	oxidation of 			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1340_s_21	10323788	1  Binding of LDL to proteoglycans traps LDL in the arterial intima, which provides the opportunity for oxidation of LDL lipids.	bind
15905	1	6108	5	NULL	NULL	0	NULL	VLDL	NULL	from patients homozygous for apo E2/2	bind	NULL				VLDL receptor	NULL	human			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_8_1142_s_28	11222479	1  Furthermore, VLDL from patients homozygous for apo E2/2 and apo E3/3 binds the human VLDL receptor identically.	bind
15906	2	6108	5	NULL	NULL	0	NULL	VLDL	NULL	from patients homozygous for apo E3/3	bind	NULL				VLDL receptor	NULL	human			NULL		0	NULL	NULL	NULL	gw60_circulation_103_8_1142_s_28	11222479	1  Furthermore, VLDL from patients homozygous for apo E2/2 and apo E3/3 binds the human VLDL receptor identically.	bind
15907	3	6108	5	NULL	NULL	0	NULL	statement 1	NULL		identical to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_8_1142_s_28	11222479	1  Furthermore, VLDL from patients homozygous for apo E2/2 and apo E3/3 binds the human VLDL receptor identically.	bind
18952	1	6108	7	NULL	NULL	NULL	NULL	apo E2/2	Chemical		binds					 VLDL receptor	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_8_1142_s_28	11222479	1  Furthermore, VLDL from patients homozygous for apo E2/2 and apo E3/3 binds the human VLDL receptor identically.	bind
18953	2	6108	7	NULL	NULL	NULL	NULL	apo E3/3	Chemical		binds					VLDL receptor	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_8_1142_s_28	11222479	1  Furthermore, VLDL from patients homozygous for apo E2/2 and apo E3/3 binds the human VLDL receptor identically.	bind
18954	3	6108	7	NULL	NULL	NULL	NULL	statement 1	Process		is identical to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_8_1142_s_28	11222479	1  Furthermore, VLDL from patients homozygous for apo E2/2 and apo E3/3 binds the human VLDL receptor identically.	bind
15910	1	6109	5	NULL	NULL	0	NULL	PU.1	NULL		is necessary for	NULL		Ets DNA binding domain		nuclear localization 	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_280_11_15632149_s_4	15632149	1  fusions, we show that the Ets DNA binding domain of PU.1 is necessary  and sufficient for its nuclear localization.	bind
15911	2	6109	5	NULL	NULL	0	NULL	PU.1	NULL		is sufficient for	NULL		Ets DNA binding domain		nuclear localization	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_280_11_15632149_s_4	15632149	1  fusions, we show that the Ets DNA binding domain of PU.1 is necessary  and sufficient for its nuclear localization.	bind
18955	1	6109	7	NULL	NULL	NULL	NULL	PU.1	GP		is necessary for			Ets DNA binding domain		nuclear localization	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_280_11_15632149_s_4	15632149	1  fusions, we show that the Ets DNA binding domain of PU.1 is necessary  and sufficient for its nuclear localization.	bind
25665	2	6109	7	NULL	NULL	NULL	NULL	PU.1	GP		is sufficient for			Ets DNA binding domain		nuclear localization	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_280_11_15632149_s_4	15632149	1  fusions, we show that the Ets DNA binding domain of PU.1 is necessary  and sufficient for its nuclear localization.	bind
15912	1	6110	5	NULL	NULL	0	NULL	Heparin s 	NULL		bind	NULL				antithrombin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2162_s_17	10978264	1  Heparin s binding to antithrombin produces a conformational change in antithrombin that considerably accelerates the ability of the latter to inactivate coagulation enzymes.	bind
15913	2	6110	5	NULL	NULL	0	NULL	statement 1	NULL		produce	NULL				antithrombin	NULL	conformation change in			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2162_s_17	10978264	1  Heparin s binding to antithrombin produces a conformational change in antithrombin that considerably accelerates the ability of the latter to inactivate coagulation enzymes.	bind
15914	3	6110	5	NULL	NULL	0	NULL	antithrombin	NULL		inactivate	NULL				coagulation enzymes	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2162_s_17	10978264	1  Heparin s binding to antithrombin produces a conformational change in antithrombin that considerably accelerates the ability of the latter to inactivate coagulation enzymes.	bind
15915	4	6110	5	NULL	NULL	0	NULL	statement 2	NULL		accelerates	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2162_s_17	10978264	1  Heparin s binding to antithrombin produces a conformational change in antithrombin that considerably accelerates the ability of the latter to inactivate coagulation enzymes.	bind
18956	1	6110	7	NULL	NULL	NULL	NULL	Heparin s	GP		bind					antithrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2162_s_17	10978264	1  Heparin s binding to antithrombin produces a conformational change in antithrombin that considerably accelerates the ability of the latter to inactivate coagulation enzymes.	bind
18957	2	6110	7	NULL	NULL	NULL	NULL	statement 1	Process		produces					antithrombin	GP	conformational change in			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2162_s_17	10978264	1  Heparin s binding to antithrombin produces a conformational change in antithrombin that considerably accelerates the ability of the latter to inactivate coagulation enzymes.	bind
18958	3	6110	7	NULL	NULL	NULL	NULL	antithrombin	GP		inactivate					coagulation enzymes	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2162_s_17	10978264	1  Heparin s binding to antithrombin produces a conformational change in antithrombin that considerably accelerates the ability of the latter to inactivate coagulation enzymes.	bind
18959	4	6110	7	NULL	NULL	NULL	NULL	statement 2	Process		accelerates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2162_s_17	10978264	1  Heparin s binding to antithrombin produces a conformational change in antithrombin that considerably accelerates the ability of the latter to inactivate coagulation enzymes.	bind
15916	1	6111	5	10	NULL	0	NULL	G-protein-coupled receptor	NULL	human	is similar to	NULL				GPR14	NULL	rat			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_10_1378_s_17	11245639	1  In 1999, Ames et al 4  cloned a human G-protein-coupled receptor, similar to the rat GPR14, which selectively bound human UII (hUII).	bind
15917	2	6111	5	10	NULL	0	NULL	G-protein-coupled receptor	NULL	human	bind	NULL	selectively			hUII	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_10_1378_s_17	11245639	1  In 1999, Ames et al 4  cloned a human G-protein-coupled receptor, similar to the rat GPR14, which selectively bound human UII (hUII).	bind
15918	3	6111	5	NULL	NULL	0	NULL	hUII	NULL		is	NULL				human UII	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_10_1378_s_17	11245639	1  In 1999, Ames et al 4  cloned a human G-protein-coupled receptor, similar to the rat GPR14, which selectively bound human UII (hUII).	bind
18960	1	6111	7	NULL	NULL	NULL	NULL	G-protein-coupled receptor	GP	human	bind		selectively			hUII	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_10_1378_s_17	11245639	1  In 1999, Ames et al 4  cloned a human G-protein-coupled receptor, similar to the rat GPR14, which selectively bound human UII (hUII).	bind
18962	2	6111	7	NULL	NULL	NULL	NULL	GPR14	GP	rat	is similar to					G-protein-coupled receptor	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_10_1378_s_17	11245639	1  In 1999, Ames et al 4  cloned a human G-protein-coupled receptor, similar to the rat GPR14, which selectively bound human UII (hUII).	bind
18963	3	6111	7	NULL	NULL	NULL	NULL	hUII	GP		is					human UII	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_10_1378_s_17	11245639	1  In 1999, Ames et al 4  cloned a human G-protein-coupled receptor, similar to the rat GPR14, which selectively bound human UII (hUII).	bind
15919	1	6112	5	NULL	NULL	0	NULL	thrombin	NULL		bind	NULL				thrombomodulin	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_2_547_s_12	9708814	1  It is activated by thrombin bound to thrombomodulin, an endothelial cell surface protein.	bind
54150	2	6112	5	10	NULL	0	NULL	thrombomodulin			is a type of					endothelial cell surface protein					NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_2_547_s_12	9708814	1  It is activated by thrombin bound to thrombomodulin, an endothelial cell surface protein.	bind
18964	1	6112	7	NULL	NULL	NULL	NULL	thrombin	GP		bind					thrombomodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_2_547_s_12	9708814	1  It is activated by thrombin bound to thrombomodulin, an endothelial cell surface protein.	bind
18965	2	6112	7	NULL	NULL	NULL	NULL	thrombomodulin	GP		is a type of					endothelial cell surface protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_2_547_s_12	9708814	1  It is activated by thrombin bound to thrombomodulin, an endothelial cell surface protein.	bind
15920	1	6113	5	NULL	NULL	0	NULL	LDL receptors	NULL	reduced activity of	leads to	NULL	may			LDL - apo B	NULL	high levels of 			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_4_517_s_18	8624773	1  Several mechanisms may lead to high levels of LDL - apo B; these include reduced activity of LDL receptors, 3  defective apo B that prevents normal binding of LDL to LDL receptors, 4 5 6 7  and possibly overproduction of apo B - containing lipoproteins by the liver.	bind
15921	2	6113	5	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				LDL receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_4_517_s_18	8624773	1  Several mechanisms may lead to high levels of LDL - apo B; these include reduced activity of LDL receptors, 3  defective apo B that prevents normal binding of LDL to LDL receptors, 4 5 6 7  and possibly overproduction of apo B - containing lipoproteins by the liver.	bind
15922	3	6113	5	NULL	NULL	0	NULL	apo B	NULL	defective	prevent	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_4_517_s_18	8624773	1  Several mechanisms may lead to high levels of LDL - apo B; these include reduced activity of LDL receptors, 3  defective apo B that prevents normal binding of LDL to LDL receptors, 4 5 6 7  and possibly overproduction of apo B - containing lipoproteins by the liver.	bind
15923	4	6113	5	NULL	NULL	0	NULL	statement 3	NULL		leads to	NULL	may			LDL - apo B	NULL	high levels of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_4_517_s_18	8624773	1  Several mechanisms may lead to high levels of LDL - apo B; these include reduced activity of LDL receptors, 3  defective apo B that prevents normal binding of LDL to LDL receptors, 4 5 6 7  and possibly overproduction of apo B - containing lipoproteins by the liver.	bind
15925	5	6113	5	NULL	NULL	0	NULL	liver	NULL		overproduce	NULL				lipoproteins	NULL	apo B - containing			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_4_517_s_18	8624773	1  Several mechanisms may lead to high levels of LDL - apo B; these include reduced activity of LDL receptors, 3  defective apo B that prevents normal binding of LDL to LDL receptors, 4 5 6 7  and possibly overproduction of apo B - containing lipoproteins by the liver.	bind
15926	6	6113	5	NULL	NULL	0	NULL	statement 5	NULL		leads to	NULL	may			LDL - apo B	NULL	high levels of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_4_517_s_18	8624773	1  Several mechanisms may lead to high levels of LDL - apo B; these include reduced activity of LDL receptors, 3  defective apo B that prevents normal binding of LDL to LDL receptors, 4 5 6 7  and possibly overproduction of apo B - containing lipoproteins by the liver.	bind
18966	1	6113	7	NULL	NULL	NULL	NULL	LDL - apo B	GP	high levels of	is due to					LDL receptor	GP	reduced activity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_4_517_s_18	8624773	1  Several mechanisms may lead to high levels of LDL - apo B; these include reduced activity of LDL receptors, 3  defective apo B that prevents normal binding of LDL to LDL receptors, 4 5 6 7  and possibly overproduction of apo B - containing lipoproteins by the liver.	bind
18967	2	6113	7	NULL	NULL	NULL	NULL	LDL	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_4_517_s_18	8624773	1  Several mechanisms may lead to high levels of LDL - apo B; these include reduced activity of LDL receptors, 3  defective apo B that prevents normal binding of LDL to LDL receptors, 4 5 6 7  and possibly overproduction of apo B - containing lipoproteins by the liver.	bind
18969	3	6113	7	NULL	NULL	NULL	NULL	apoB	Chemical	defective	prevents					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_4_517_s_18	8624773	1  Several mechanisms may lead to high levels of LDL - apo B; these include reduced activity of LDL receptors, 3  defective apo B that prevents normal binding of LDL to LDL receptors, 4 5 6 7  and possibly overproduction of apo B - containing lipoproteins by the liver.	bind
23899	5	6113	7	NULL	NULL	NULL	NULL	liver	OrganismPart		overproduce					lipoproteins	GP	apo B - containing			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_4_517_s_18	8624773	1  Several mechanisms may lead to high levels of LDL - apo B; these include reduced activity of LDL receptors, 3  defective apo B that prevents normal binding of LDL to LDL receptors, 4 5 6 7  and possibly overproduction of apo B - containing lipoproteins by the liver.	bind
23900	4	6113	7	NULL	NULL	NULL	NULL	statement 3	Process		leads to		may			LDL - apo B	GP	high levels of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_4_517_s_18	8624773	1  Several mechanisms may lead to high levels of LDL - apo B; these include reduced activity of LDL receptors, 3  defective apo B that prevents normal binding of LDL to LDL receptors, 4 5 6 7  and possibly overproduction of apo B - containing lipoproteins by the liver.	bind
23901	6	6113	7	NULL	NULL	NULL	NULL	statement 5	Process		leads to		may			LDL-apoB	GP	high levels of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_4_517_s_18	8624773	1  Several mechanisms may lead to high levels of LDL - apo B; these include reduced activity of LDL receptors, 3  defective apo B that prevents normal binding of LDL to LDL receptors, 4 5 6 7  and possibly overproduction of apo B - containing lipoproteins by the liver.	bind
15927	1	6115	5	NULL	NULL	0	NULL	SR-A	NULL		is	NULL				macrophage scavenger receptor A	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_5_825_s_14	11348881	1  The human macrophage scavenger receptor A (SR-A) binds and internalizes modified LDL, which ultimately results in the accumulation of cholesterol esters in macrophages.	bind
15928	2	6115	5	10	NULL	0	NULL	SR-A	NULL	human;; macrophage	bind	NULL				LDL	NULL	modified			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_5_825_s_14	11348881	1  The human macrophage scavenger receptor A (SR-A) binds and internalizes modified LDL, which ultimately results in the accumulation of cholesterol esters in macrophages.	bind
15929	3	6115	5	NULL	NULL	0	NULL	SR-A	NULL		internalize	NULL				LDL	NULL	modified			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_5_825_s_14	11348881	1  The human macrophage scavenger receptor A (SR-A) binds and internalizes modified LDL, which ultimately results in the accumulation of cholesterol esters in macrophages.	bind
15932	4	6115	5	NULL	NULL	0	NULL	statement 3	NULL		results in	NULL				cholesterol esters	NULL	accumulation of 			NULL	in macrophages	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_5_825_s_14	11348881	1  The human macrophage scavenger receptor A (SR-A) binds and internalizes modified LDL, which ultimately results in the accumulation of cholesterol esters in macrophages.	bind
18972	1	6115	7	NULL	NULL	NULL	NULL	SR-A	GP	human;;macrophage	binds					LDL	GP	modified			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_5_825_s_14	11348881	1  The human macrophage scavenger receptor A (SR-A) binds and internalizes modified LDL, which ultimately results in the accumulation of cholesterol esters in macrophages.	bind
18973	2	6115	7	NULL	NULL	NULL	NULL	statement 1	Process		internalizes					LDL	GP	modified			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_5_825_s_14	11348881	1  The human macrophage scavenger receptor A (SR-A) binds and internalizes modified LDL, which ultimately results in the accumulation of cholesterol esters in macrophages.	bind
18974	3	6115	7	NULL	NULL	NULL	NULL	statement 2	Process		results in					cholesterol esters	Chemical	accumulation of			NULL	in macrophages	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_5_825_s_14	11348881	1  The human macrophage scavenger receptor A (SR-A) binds and internalizes modified LDL, which ultimately results in the accumulation of cholesterol esters in macrophages.	bind
18975	4	6115	7	NULL	NULL	NULL	NULL	SR-A	GP		is					scavenger receptor A	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_5_825_s_14	11348881	1  The human macrophage scavenger receptor A (SR-A) binds and internalizes modified LDL, which ultimately results in the accumulation of cholesterol esters in macrophages.	bind
16011	1	6116	5	NULL	NULL	0	NULL	beta2-integrin	NULL		bind	NULL				fibrinogen	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
16012	2	6116	5	NULL	NULL	0	NULL	beta3-integrin	NULL		bind	NULL				fibrinogen	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
24518	3	6116	5	NULL	NULL	0	NULL	P-selectin	NULL		bind	NULL				fibrinogen	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
24520	4	6116	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
24521	5	6116	5	NULL	NULL	0	NULL	statement 2	NULL		is an alternative to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
24527	6	6116	5	NULL	NULL	0	NULL	statement 1	NULL		contribute to	NULL				thrombus	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
24528	7	6116	5	NULL	NULL	0	NULL	statement 2	NULL		contribute to	NULL				thrombus	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
24529	8	6116	5	NULL	NULL	0	NULL	statement 3	NULL		contribute to	NULL				thrombus	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
24530	9	6116	5	NULL	NULL	0	NULL	statement 1	NULL		contribute to	NULL				fibrin	NULL	deposition of			NULL		0	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
24531	10	6116	5	NULL	NULL	0	NULL	statement 2	NULL		contribute to	NULL				fibrin	NULL	deposition of			NULL		0	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
24532	11	6116	5	NULL	NULL	0	NULL	statement 3	NULL		contribute to	NULL				fibrin	NULL	deposition of			NULL		0	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
18976	1	6116	7	NULL	NULL	NULL	NULL	P-selectin	GP		bind					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
18977	2	6116	7	NULL	NULL	NULL	NULL	beta2- integrins	GP		bind					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
18978	3	6116	7	NULL	NULL	NULL	NULL	beta3-integrins	GP		bind					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
18979	4	6116	7	NULL	NULL	NULL	NULL	statement 1	Process		contribute to					thrombus	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
18980	5	6116	7	NULL	NULL	NULL	NULL	statement 2	Process		contribute to					thrombus	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
18981	6	6116	7	NULL	NULL	NULL	NULL	statement 3	Process		contribute to					thrombus	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
18982	7	6116	7	NULL	NULL	NULL	NULL	statement 1	Process		leads to					fibrin	GP	deposition of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
18983	8	6116	7	NULL	NULL	NULL	NULL	statement 2	Process		leads to					fibrin	GP	deposition of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
18984	9	6116	7	NULL	NULL	NULL	NULL	statement 3	Process		leads to					fibrin	GP	deposition of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
18985	10	6116	7	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
18986	11	6116	7	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_13_1772_s_26	11282909	1  Their cooperative cellular interactions are mediated by adhesion molecules, ie, P-selectin or beta2- and beta3-integrins binding to fibrinogen, and contribute to thrombus formation and fibrin deposition.	bind
16013	1	6117	5	NULL	NULL	0	NULL	(IgG1,kappa) antibody	NULL		bind	NULL				CD11a	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_48_30463_s_34	9374538	1 ( 17) and TS1/22 ( 15) (IgG1,kappa) antibodies that bind to CD11a; 44 ( 18), an (IgG1,kappa) antibody that binds to CD11b; and 3.9 ( 19) an (IgG1,kappa) antibody that binds to CD11c.	bind
16014	2	6117	5	NULL	NULL	0	NULL	(IgG1,kappa) antibody	NULL		bind	NULL				CD11b	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_48_30463_s_34	9374538	1 ( 17) and TS1/22 ( 15) (IgG1,kappa) antibodies that bind to CD11a; 44 ( 18), an (IgG1,kappa) antibody that binds to CD11b; and 3.9 ( 19) an (IgG1,kappa) antibody that binds to CD11c.	bind
16015	3	6117	5	NULL	NULL	0	NULL	(IgG1,kappa) antibody	NULL		bind	NULL				CD11c	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_48_30463_s_34	9374538	1 ( 17) and TS1/22 ( 15) (IgG1,kappa) antibodies that bind to CD11a; 44 ( 18), an (IgG1,kappa) antibody that binds to CD11b; and 3.9 ( 19) an (IgG1,kappa) antibody that binds to CD11c.	bind
18989	1	6117	7	NULL	NULL	NULL	NULL	IgG1,kappa antibody	GP		bind					CD11a	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_48_30463_s_34	9374538	1 ( 17) and TS1/22 ( 15) (IgG1,kappa) antibodies that bind to CD11a; 44 ( 18), an (IgG1,kappa) antibody that binds to CD11b; and 3.9 ( 19) an (IgG1,kappa) antibody that binds to CD11c.	bind
18990	2	6117	7	NULL	NULL	NULL	NULL	IgG1,kappa antibody	GP		bind					CD11b	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_48_30463_s_34	9374538	1 ( 17) and TS1/22 ( 15) (IgG1,kappa) antibodies that bind to CD11a; 44 ( 18), an (IgG1,kappa) antibody that binds to CD11b; and 3.9 ( 19) an (IgG1,kappa) antibody that binds to CD11c.	bind
18992	3	6117	7	NULL	NULL	NULL	NULL	IgG1,kappa antibody	GP		bind					CD11c	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_48_30463_s_34	9374538	1 ( 17) and TS1/22 ( 15) (IgG1,kappa) antibodies that bind to CD11a; 44 ( 18), an (IgG1,kappa) antibody that binds to CD11b; and 3.9 ( 19) an (IgG1,kappa) antibody that binds to CD11c.	bind
16016	1	6118	5	NULL	NULL	0	NULL	tissue factor	NULL		bind	NULL				factor VII	NULL	activated			NULL		0	NULL	NULL	NULL	gw60_circulation_105_15_1756_s_24	11956113	1 -  4 This cascade is initiated by binding of tissue factor to activated factor VII, and this complex activates factor X.	bind
16017	2	6118	5	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				factor X	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_15_1756_s_24	11956113	1 -  4 This cascade is initiated by binding of tissue factor to activated factor VII, and this complex activates factor X.	bind
18993	1	6118	7	NULL	NULL	NULL	NULL	tissue factor	GP		bind					factor VII	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_15_1756_s_24	11956113	1 -  4 This cascade is initiated by binding of tissue factor to activated factor VII, and this complex activates factor X.	bind
18994	2	6118	7	NULL	NULL	NULL	NULL	statement 1	Process		activates					factor X	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_15_1756_s_24	11956113	1 -  4 This cascade is initiated by binding of tissue factor to activated factor VII, and this complex activates factor X.	bind
16019	1	6119	5	NULL	NULL	0	NULL	beta1-adrenergic receptor	NULL		bind	NULL				catecholamines	NULL	circulating			NULL		0	NULL	NULL	NULL	gw60_circulationres_89_11_997_s_10	11717156	1 -  5 The beta1- and beta2-adrenergic receptors (betaARs), which bind circulating catecholamines, activate adenylyl cyclase by coupling through the stimulatory G-protein, Galphas.	bind
16020	2	6119	5	NULL	NULL	0	NULL	beta2-adrenergic receptor	NULL		bind	NULL				catecholamines	NULL	circulating			NULL		0	NULL	NULL	NULL	gw60_circulationres_89_11_997_s_10	11717156	1 -  5 The beta1- and beta2-adrenergic receptors (betaARs), which bind circulating catecholamines, activate adenylyl cyclase by coupling through the stimulatory G-protein, Galphas.	bind
16021	3	6119	5	NULL	NULL	0	NULL	beta1-adrenergic receptor	NULL		activate	NULL				adenylyl cyclase	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_89_11_997_s_10	11717156	1 -  5 The beta1- and beta2-adrenergic receptors (betaARs), which bind circulating catecholamines, activate adenylyl cyclase by coupling through the stimulatory G-protein, Galphas.	bind
16022	4	6119	5	NULL	NULL	0	NULL	beta2-adrenergic receptor	NULL		activate	NULL				adenylyl cyclase	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_89_11_997_s_10	11717156	1 -  5 The beta1- and beta2-adrenergic receptors (betaARs), which bind circulating catecholamines, activate adenylyl cyclase by coupling through the stimulatory G-protein, Galphas.	bind
16023	5	6119	5	NULL	NULL	0	NULL	beta1-adrenergic receptor	NULL		couple through	NULL				Galphas	NULL	stimulatory G-protein			NULL		0	NULL	NULL	NULL	gw60_circulationres_89_11_997_s_10	11717156	1 -  5 The beta1- and beta2-adrenergic receptors (betaARs), which bind circulating catecholamines, activate adenylyl cyclase by coupling through the stimulatory G-protein, Galphas.	bind
16024	6	6119	5	NULL	NULL	0	NULL	beta2-adrenergic receptor	NULL		couple through	NULL				Galphas	NULL	stimulatory G-protein			NULL		0	NULL	NULL	NULL	gw60_circulationres_89_11_997_s_10	11717156	1 -  5 The beta1- and beta2-adrenergic receptors (betaARs), which bind circulating catecholamines, activate adenylyl cyclase by coupling through the stimulatory G-protein, Galphas.	bind
16025	7	6119	5	NULL	NULL	0	NULL	statement 5	NULL		leads to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_89_11_997_s_10	11717156	1 -  5 The beta1- and beta2-adrenergic receptors (betaARs), which bind circulating catecholamines, activate adenylyl cyclase by coupling through the stimulatory G-protein, Galphas.	bind
16026	8	6119	5	NULL	NULL	0	NULL	statement 6	NULL		leads to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_89_11_997_s_10	11717156	1 -  5 The beta1- and beta2-adrenergic receptors (betaARs), which bind circulating catecholamines, activate adenylyl cyclase by coupling through the stimulatory G-protein, Galphas.	bind
24533	9	6119	5	NULL	NULL	0	NULL	betaARs	NULL		is	NULL				beta-adrenergic receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_89_11_997_s_10	11717156	1 -  5 The beta1- and beta2-adrenergic receptors (betaARs), which bind circulating catecholamines, activate adenylyl cyclase by coupling through the stimulatory G-protein, Galphas.	bind
18995	1	6119	7	NULL	NULL	NULL	NULL	beta1adrenergic receptor	GP		bind					catecholamines	Chemical	circulating			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_11_997_s_10	11717156	1 -  5 The beta1- and beta2-adrenergic receptors (betaARs), which bind circulating catecholamines, activate adenylyl cyclase by coupling through the stimulatory G-protein, Galphas.	bind
18996	2	6119	7	NULL	NULL	NULL	NULL	beta2-adrenergic receptor	GP		bind					catecholamines	Chemical	circulating			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_11_997_s_10	11717156	1 -  5 The beta1- and beta2-adrenergic receptors (betaARs), which bind circulating catecholamines, activate adenylyl cyclase by coupling through the stimulatory G-protein, Galphas.	bind
18997	3	6119	7	NULL	NULL	NULL	NULL	statement 1	Process		activate					adenylyl cyclase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_11_997_s_10	11717156	1 -  5 The beta1- and beta2-adrenergic receptors (betaARs), which bind circulating catecholamines, activate adenylyl cyclase by coupling through the stimulatory G-protein, Galphas.	bind
18998	4	6119	7	NULL	NULL	NULL	NULL	statement 2	Process		activate					adenylyl cyclase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_11_997_s_10	11717156	1 -  5 The beta1- and beta2-adrenergic receptors (betaARs), which bind circulating catecholamines, activate adenylyl cyclase by coupling through the stimulatory G-protein, Galphas.	bind
18999	5	6119	7	NULL	NULL	NULL	NULL	statement 3	Process		occurs through					Galphas	GP	stimulatory G-protein			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_11_997_s_10	11717156	1 -  5 The beta1- and beta2-adrenergic receptors (betaARs), which bind circulating catecholamines, activate adenylyl cyclase by coupling through the stimulatory G-protein, Galphas.	bind
19001	6	6119	7	NULL	NULL	NULL	NULL	statement 4	Process		occurs through					Galphas	GP	stimulatory G-protein			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_11_997_s_10	11717156	1 -  5 The beta1- and beta2-adrenergic receptors (betaARs), which bind circulating catecholamines, activate adenylyl cyclase by coupling through the stimulatory G-protein, Galphas.	bind
19002	7	6119	7	NULL	NULL	NULL	NULL	betaARs	GP		is					beta-adrenergic receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_11_997_s_10	11717156	1 -  5 The beta1- and beta2-adrenergic receptors (betaARs), which bind circulating catecholamines, activate adenylyl cyclase by coupling through the stimulatory G-protein, Galphas.	bind
23902	8	6119	7	NULL	NULL	NULL	NULL	statement 5	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_11_997_s_10	11717156	1 -  5 The beta1- and beta2-adrenergic receptors (betaARs), which bind circulating catecholamines, activate adenylyl cyclase by coupling through the stimulatory G-protein, Galphas.	bind
23903	9	6119	7	NULL	NULL	NULL	NULL	statement 6	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_11_997_s_10	11717156	1 -  5 The beta1- and beta2-adrenergic receptors (betaARs), which bind circulating catecholamines, activate adenylyl cyclase by coupling through the stimulatory G-protein, Galphas.	bind
16027	1	6121	5	10	NULL	0	NULL	cAMP			bind					PKA			regulatory subunit 		NULL	eukaryotes	NULL	NULL	NULL	NULL	gw60_circulationres_88_3_319_s_12	11179200	1 2  In eukaryotes, cAMP binds the regulatory subunit of cAMP-dependent protein kinases (PKAs).	bind
16028	2	6121	5	NULL	NULL	0	NULL	PKAs	NULL		is	NULL				cAMP-dependent protein kinases	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_3_319_s_12	11179200	1 2  In eukaryotes, cAMP binds the regulatory subunit of cAMP-dependent protein kinases (PKAs).	bind
19006	1	6121	7	NULL	NULL	NULL	NULL	cAMP	Chemical		binds					PKA	GP		regulatory subunit 		NULL	in eukaryotes	NULL	NULL	NULL	NULL	gw60_circulationres_88_3_319_s_12	11179200	1 2  In eukaryotes, cAMP binds the regulatory subunit of cAMP-dependent protein kinases (PKAs).	bind
19007	2	6121	7	NULL	NULL	NULL	NULL	PKA	GP		is					cAMP-dependent protein kinases	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_3_319_s_12	11179200	1 2  In eukaryotes, cAMP binds the regulatory subunit of cAMP-dependent protein kinases (PKAs).	bind
16029	1	6122	5	NULL	NULL	0	NULL	heme	NULL		bind	NULL				NAD(P)H oxidases	NULL		p22phox subunit		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_4_365_s_3	10700437	1 2  In this issue of  Circulation Research, Cahilly and colleagues 3  provide data supporting an association between a histidine72 to tyrosine mutation at the potential site for heme binding of the p22phox subunit of NAD(P)H oxidases and increased severity and progression of CAD in patients from the Lipoprotein and Coronary Atherosclerosis Study (LCAS).	bind
16030	2	6122	5	NULL	NULL	0	NULL		NULL		is associated to	NULL		histidine72		statement 1	NULL	mutation at potential site for	tyrosine		NULL		0	NULL	NULL	NULL	gw60_circulationres_86_4_365_s_3	10700437	1 2  In this issue of  Circulation Research, Cahilly and colleagues 3  provide data supporting an association between a histidine72 to tyrosine mutation at the potential site for heme binding of the p22phox subunit of NAD(P)H oxidases and increased severity and progression of CAD in patients from the Lipoprotein and Coronary Atherosclerosis Study (LCAS).	bind
19053	1	6122	7	NULL	NULL	NULL	NULL	NAD(P)H oxidases	GP		bind			p22phox subunit 		heme 	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_4_365_s_3	10700437	1 2  In this issue of  Circulation Research, Cahilly and colleagues 3  provide data supporting an association between a histidine72 to tyrosine mutation at the potential site for heme binding of the p22phox subunit of NAD(P)H oxidases and increased severity and progression of CAD in patients from the Lipoprotein and Coronary Atherosclerosis Study (LCAS).	bind
23904	2	6122	7	NULL	NULL	NULL	NULL				is associated to			histidine72		statement 1	Process	mutation at the potential site for	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_4_365_s_3	10700437	1 2  In this issue of  Circulation Research, Cahilly and colleagues 3  provide data supporting an association between a histidine72 to tyrosine mutation at the potential site for heme binding of the p22phox subunit of NAD(P)H oxidases and increased severity and progression of CAD in patients from the Lipoprotein and Coronary Atherosclerosis Study (LCAS).	bind
16031	1	6123	5	NULL	NULL	0	NULL	GC-A	NULL		is	NULL				guanylate cyclase-A	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_930_s_25	11397699	1 2  These peptides elicit their biological effects via the elevation of intracellular cGMP by activating 2 biologically active natriuretic peptide receptors, namely, membrane-bound guanylate cyclase-A (GC-A) and guanylate cyclase-B (GC-B).	bind
16032	2	6123	5	NULL	NULL	0	NULL	GC-B	NULL		is	NULL				guanylate cyclase-B	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_930_s_25	11397699	1 2  These peptides elicit their biological effects via the elevation of intracellular cGMP by activating 2 biologically active natriuretic peptide receptors, namely, membrane-bound guanylate cyclase-A (GC-A) and guanylate cyclase-B (GC-B).	bind
16033	3	6123	5	10	NULL	0	NULL	GC-A	NULL		elevate	NULL				cGMP	NULL	intracellular			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_930_s_25	11397699	1 2  These peptides elicit their biological effects via the elevation of intracellular cGMP by activating 2 biologically active natriuretic peptide receptors, namely, membrane-bound guanylate cyclase-A (GC-A) and guanylate cyclase-B (GC-B).	bind
16035	4	6123	5	10	NULL	0	NULL	GC-B	NULL		elevate	NULL				cGMP	NULL	intracellular			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_930_s_25	11397699	1 2  These peptides elicit their biological effects via the elevation of intracellular cGMP by activating 2 biologically active natriuretic peptide receptors, namely, membrane-bound guanylate cyclase-A (GC-A) and guanylate cyclase-B (GC-B).	bind
45131	5	6123	5	10	NULL	0	NULL	GC-A	NULL		is a type of	NULL				biologically active natriuretic peptide receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_930_s_25	11397699	1 2  These peptides elicit their biological effects via the elevation of intracellular cGMP by activating 2 biologically active natriuretic peptide receptors, namely, membrane-bound guanylate cyclase-A (GC-A) and guanylate cyclase-B (GC-B).	bind
45132	6	6123	5	10	NULL	0	NULL	GC-B	NULL		is a type of	NULL				biologically active natriuretic peptide receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_930_s_25	11397699	1 2  These peptides elicit their biological effects via the elevation of intracellular cGMP by activating 2 biologically active natriuretic peptide receptors, namely, membrane-bound guanylate cyclase-A (GC-A) and guanylate cyclase-B (GC-B).	bind
19063	1	6123	7	NULL	NULL	NULL	NULL	GC-A	GP		elevates					cGMP	Chemical	intracellular			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_930_s_25	11397699	1 2  These peptides elicit their biological effects via the elevation of intracellular cGMP by activating 2 biologically active natriuretic peptide receptors, namely, membrane-bound guanylate cyclase-A (GC-A) and guanylate cyclase-B (GC-B).	bind
19064	2	6123	7	NULL	NULL	NULL	NULL	GC-B	GP		elevates					cGMP	Chemical	intracellular			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_930_s_25	11397699	1 2  These peptides elicit their biological effects via the elevation of intracellular cGMP by activating 2 biologically active natriuretic peptide receptors, namely, membrane-bound guanylate cyclase-A (GC-A) and guanylate cyclase-B (GC-B).	bind
19065	3	6123	7	NULL	NULL	NULL	NULL	GC-A	GP		is					guanylate cyclase-A	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_930_s_25	11397699	1 2  These peptides elicit their biological effects via the elevation of intracellular cGMP by activating 2 biologically active natriuretic peptide receptors, namely, membrane-bound guanylate cyclase-A (GC-A) and guanylate cyclase-B (GC-B).	bind
19066	4	6123	7	NULL	NULL	NULL	NULL	GC-B	GP		is					guanylate cyclase-B	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_930_s_25	11397699	1 2  These peptides elicit their biological effects via the elevation of intracellular cGMP by activating 2 biologically active natriuretic peptide receptors, namely, membrane-bound guanylate cyclase-A (GC-A) and guanylate cyclase-B (GC-B).	bind
45134	5	6123	7	NULL	NULL	NULL	NULL	GC-A	GP		is a type of					biologically active natriuretic peptide receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_930_s_25	11397699	1 2  These peptides elicit their biological effects via the elevation of intracellular cGMP by activating 2 biologically active natriuretic peptide receptors, namely, membrane-bound guanylate cyclase-A (GC-A) and guanylate cyclase-B (GC-B).	bind
45135	6	6123	7	NULL	NULL	NULL	NULL	GC-B	GP		is a type of					biologically active natriuretic peptide receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_930_s_25	11397699	1 2  These peptides elicit their biological effects via the elevation of intracellular cGMP by activating 2 biologically active natriuretic peptide receptors, namely, membrane-bound guanylate cyclase-A (GC-A) and guanylate cyclase-B (GC-B).	bind
16037	1	6124	5	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL				GPIIb/IIa	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_149_s_20	11145947	1 2  This adhesion step is followed by aggregation predominantly mediated by the binding of fibrinogen and vWF to GPIIb/IIa in the presence of ADP. 1 2 3 4  In addition, direct platelet aggregation in the bulk phase under conditions of abnormally elevated fluid shear stresses, analogous to those occurring in atherosclerotic or constricted arterial vessels, 5  may be important.	bind
16039	2	6124	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				ADP	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_149_s_20	11145947	1 2  This adhesion step is followed by aggregation predominantly mediated by the binding of fibrinogen and vWF to GPIIb/IIa in the presence of ADP. 1 2 3 4  In addition, direct platelet aggregation in the bulk phase under conditions of abnormally elevated fluid shear stresses, analogous to those occurring in atherosclerotic or constricted arterial vessels, 5  may be important.	bind
16040	3	6124	5	NULL	NULL	0	NULL	vWF	NULL		bind	NULL				GPIIb/IIa	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_149_s_20	11145947	1 2  This adhesion step is followed by aggregation predominantly mediated by the binding of fibrinogen and vWF to GPIIb/IIa in the presence of ADP. 1 2 3 4  In addition, direct platelet aggregation in the bulk phase under conditions of abnormally elevated fluid shear stresses, analogous to those occurring in atherosclerotic or constricted arterial vessels, 5  may be important.	bind
16041	4	6124	5	NULL	NULL	0	NULL	statement 3	NULL		in the presence of	NULL				ADP	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_149_s_20	11145947	1 2  This adhesion step is followed by aggregation predominantly mediated by the binding of fibrinogen and vWF to GPIIb/IIa in the presence of ADP. 1 2 3 4  In addition, direct platelet aggregation in the bulk phase under conditions of abnormally elevated fluid shear stresses, analogous to those occurring in atherosclerotic or constricted arterial vessels, 5  may be important.	bind
16043	5	6124	5	NULL	NULL	0	NULL	statement 2	NULL		mediate	NULL				aggregation	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_149_s_20	11145947	1 2  This adhesion step is followed by aggregation predominantly mediated by the binding of fibrinogen and vWF to GPIIb/IIa in the presence of ADP. 1 2 3 4  In addition, direct platelet aggregation in the bulk phase under conditions of abnormally elevated fluid shear stresses, analogous to those occurring in atherosclerotic or constricted arterial vessels, 5  may be important.	bind
16044	6	6124	5	NULL	NULL	0	NULL	statement 4	NULL		mediate	NULL				aggregation	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_149_s_20	11145947	1 2  This adhesion step is followed by aggregation predominantly mediated by the binding of fibrinogen and vWF to GPIIb/IIa in the presence of ADP. 1 2 3 4  In addition, direct platelet aggregation in the bulk phase under conditions of abnormally elevated fluid shear stresses, analogous to those occurring in atherosclerotic or constricted arterial vessels, 5  may be important.	bind
16046	7	6124	5	NULL	NULL	0	NULL	adhesion	NULL		is followed by	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_149_s_20	11145947	1 2  This adhesion step is followed by aggregation predominantly mediated by the binding of fibrinogen and vWF to GPIIb/IIa in the presence of ADP. 1 2 3 4  In addition, direct platelet aggregation in the bulk phase under conditions of abnormally elevated fluid shear stresses, analogous to those occurring in atherosclerotic or constricted arterial vessels, 5  may be important.	bind
16047	8	6124	5	NULL	NULL	0	NULL	adhesion	NULL		is followed by	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_149_s_20	11145947	1 2  This adhesion step is followed by aggregation predominantly mediated by the binding of fibrinogen and vWF to GPIIb/IIa in the presence of ADP. 1 2 3 4  In addition, direct platelet aggregation in the bulk phase under conditions of abnormally elevated fluid shear stresses, analogous to those occurring in atherosclerotic or constricted arterial vessels, 5  may be important.	bind
19069	1	6124	7	NULL	NULL	NULL	NULL	fibrinogen	GP		bind					GPIIb/IIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_149_s_20	11145947	1 2  This adhesion step is followed by aggregation predominantly mediated by the binding of fibrinogen and vWF to GPIIb/IIa in the presence of ADP. 1 2 3 4  In addition, direct platelet aggregation in the bulk phase under conditions of abnormally elevated fluid shear stresses, analogous to those occurring in atherosclerotic or constricted arterial vessels, 5  may be important.	bind
19070	2	6124	7	NULL	NULL	NULL	NULL	vWF	GP		bind					GPIIb/IIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_149_s_20	11145947	1 2  This adhesion step is followed by aggregation predominantly mediated by the binding of fibrinogen and vWF to GPIIb/IIa in the presence of ADP. 1 2 3 4  In addition, direct platelet aggregation in the bulk phase under conditions of abnormally elevated fluid shear stresses, analogous to those occurring in atherosclerotic or constricted arterial vessels, 5  may be important.	bind
23905	3	6124	7	NULL	NULL	NULL	NULL	statement 1	Process		in the presence of 					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_149_s_20	11145947	1 2  This adhesion step is followed by aggregation predominantly mediated by the binding of fibrinogen and vWF to GPIIb/IIa in the presence of ADP. 1 2 3 4  In addition, direct platelet aggregation in the bulk phase under conditions of abnormally elevated fluid shear stresses, analogous to those occurring in atherosclerotic or constricted arterial vessels, 5  may be important.	bind
23906	4	6124	7	NULL	NULL	NULL	NULL	statement 2	Process		in the presence of 					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_149_s_20	11145947	1 2  This adhesion step is followed by aggregation predominantly mediated by the binding of fibrinogen and vWF to GPIIb/IIa in the presence of ADP. 1 2 3 4  In addition, direct platelet aggregation in the bulk phase under conditions of abnormally elevated fluid shear stresses, analogous to those occurring in atherosclerotic or constricted arterial vessels, 5  may be important.	bind
23907	5	6124	7	NULL	NULL	NULL	NULL	statement 3	Process		mediate					aggregation	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_149_s_20	11145947	1 2  This adhesion step is followed by aggregation predominantly mediated by the binding of fibrinogen and vWF to GPIIb/IIa in the presence of ADP. 1 2 3 4  In addition, direct platelet aggregation in the bulk phase under conditions of abnormally elevated fluid shear stresses, analogous to those occurring in atherosclerotic or constricted arterial vessels, 5  may be important.	bind
23908	6	6124	7	NULL	NULL	NULL	NULL	statement 4	Process		mediate					aggregation	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_149_s_20	11145947	1 2  This adhesion step is followed by aggregation predominantly mediated by the binding of fibrinogen and vWF to GPIIb/IIa in the presence of ADP. 1 2 3 4  In addition, direct platelet aggregation in the bulk phase under conditions of abnormally elevated fluid shear stresses, analogous to those occurring in atherosclerotic or constricted arterial vessels, 5  may be important.	bind
23909	7	6124	7	NULL	NULL	NULL	NULL	Adhesion	Process		is followed by					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_149_s_20	11145947	1 2  This adhesion step is followed by aggregation predominantly mediated by the binding of fibrinogen and vWF to GPIIb/IIa in the presence of ADP. 1 2 3 4  In addition, direct platelet aggregation in the bulk phase under conditions of abnormally elevated fluid shear stresses, analogous to those occurring in atherosclerotic or constricted arterial vessels, 5  may be important.	bind
23910	8	6124	7	NULL	NULL	NULL	NULL	Adhesion	Process		is followed by					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_149_s_20	11145947	1 2  This adhesion step is followed by aggregation predominantly mediated by the binding of fibrinogen and vWF to GPIIb/IIa in the presence of ADP. 1 2 3 4  In addition, direct platelet aggregation in the bulk phase under conditions of abnormally elevated fluid shear stresses, analogous to those occurring in atherosclerotic or constricted arterial vessels, 5  may be important.	bind
16052	1	6125	5	10	NULL	0	NULL	CD8-positive T cells	NULL	cytotoxic	bind	NULL	specifically			major histocompatibility - complex	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_7_1665_s_21	8840859	1 2 3  Cytotoxic CD8-positive T cells bind specifically to foreign class I major histocompatibility - complexbearing target cells and release agents, eg, granzyme B, which disrupt cell membranes and may also induce apoptosis as demonstrated in vitro.	bind
16053	2	6125	5	NULL	NULL	0	NULL	CD8-positive T cells	NULL	cytotoxic	release	NULL				granzyme B	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_94_7_1665_s_21	8840859	1 2 3  Cytotoxic CD8-positive T cells bind specifically to foreign class I major histocompatibility - complexbearing target cells and release agents, eg, granzyme B, which disrupt cell membranes and may also induce apoptosis as demonstrated in vitro.	bind
16054	3	6125	5	NULL	NULL	0	NULL	granzyme B	NULL		disrupt	NULL				cell membranes	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_94_7_1665_s_21	8840859	1 2 3  Cytotoxic CD8-positive T cells bind specifically to foreign class I major histocompatibility - complexbearing target cells and release agents, eg, granzyme B, which disrupt cell membranes and may also induce apoptosis as demonstrated in vitro.	bind
16055	4	6125	5	NULL	NULL	0	NULL	granzyme B	NULL		induce	NULL	may			apoptosis	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_circulation_94_7_1665_s_21	8840859	1 2 3  Cytotoxic CD8-positive T cells bind specifically to foreign class I major histocompatibility - complexbearing target cells and release agents, eg, granzyme B, which disrupt cell membranes and may also induce apoptosis as demonstrated in vitro.	bind
19071	1	6125	7	NULL	NULL	NULL	NULL	CD8-positive T cells	Cell	Cytotoxic	bind		specifically			 major histocompatibility - complex	GP	foreign	class I		NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_7_1665_s_21	8840859	1 2 3  Cytotoxic CD8-positive T cells bind specifically to foreign class I major histocompatibility - complexbearing target cells and release agents, eg, granzyme B, which disrupt cell membranes and may also induce apoptosis as demonstrated in vitro.	bind
19072	2	6125	7	NULL	NULL	NULL	NULL	CD8-positive T cells	Cell	cytotoxic	release					granzyme B	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_7_1665_s_21	8840859	1 2 3  Cytotoxic CD8-positive T cells bind specifically to foreign class I major histocompatibility - complexbearing target cells and release agents, eg, granzyme B, which disrupt cell membranes and may also induce apoptosis as demonstrated in vitro.	bind
19073	3	6125	7	NULL	NULL	NULL	NULL	granzyme B	GP		disrupt					cell membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_7_1665_s_21	8840859	1 2 3  Cytotoxic CD8-positive T cells bind specifically to foreign class I major histocompatibility - complexbearing target cells and release agents, eg, granzyme B, which disrupt cell membranes and may also induce apoptosis as demonstrated in vitro.	bind
19074	4	6125	7	NULL	NULL	NULL	NULL	granzyme B	GP		induce		may			apoptosis	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_94_7_1665_s_21	8840859	1 2 3  Cytotoxic CD8-positive T cells bind specifically to foreign class I major histocompatibility - complexbearing target cells and release agents, eg, granzyme B, which disrupt cell membranes and may also induce apoptosis as demonstrated in vitro.	bind
16056	1	6126	5	10	NULL	0	NULL	NP			bind		specific			cell surface receptors		characterized;;purified;;cloned from vasculature			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_19	10785505	1 2 3  These effects are mediated by specific binding of NP to cell surface receptors that have been characterized, purified, and cloned from the vasculature, kidney, adrenal gland, and brain.	bind
16057	2	6126	5	10	NULL	0	NULL	NP			bind		specific			cell surface receptors		characterized;;purified;;cloned from vasculature			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_19	10785505	1 2 3  These effects are mediated by specific binding of NP to cell surface receptors that have been characterized, purified, and cloned from the vasculature, kidney, adrenal gland, and brain.	bind
16058	3	6126	5	10	NULL	0	NULL	NP			bind		specific			cell surface receptors		characterized;;purified;;cloned from vasculature			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_19	10785505	1 2 3  These effects are mediated by specific binding of NP to cell surface receptors that have been characterized, purified, and cloned from the vasculature, kidney, adrenal gland, and brain.	bind
16059	4	6126	5	10	NULL	0	NULL	NP			bind		specific			cell surface receptors		characterized;;purified;;cloned from vasculature			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_19	10785505	1 2 3  These effects are mediated by specific binding of NP to cell surface receptors that have been characterized, purified, and cloned from the vasculature, kidney, adrenal gland, and brain.	bind
19075	1	6126	7	NULL	NULL	NULL	NULL	 NP	GP		bind		specific			cell surface receptor	GP	characterized;;purified;;cloned from vasculature			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_19	10785505	1 2 3  These effects are mediated by specific binding of NP to cell surface receptors that have been characterized, purified, and cloned from the vasculature, kidney, adrenal gland, and brain.	bind
24120	2	6126	7	NULL	NULL	NULL	NULL	NP	GP		bind		specific			cell surface receptor	GP	characterized;;purified;;cloned from vasculature			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_19	10785505	1 2 3  These effects are mediated by specific binding of NP to cell surface receptors that have been characterized, purified, and cloned from the vasculature, kidney, adrenal gland, and brain.	bind
24121	3	6126	7	NULL	NULL	NULL	NULL	NP	GP		bind		specific			cell surface receptor	GP	characterized;;purified;;cloned from vasculature			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_19	10785505	1 2 3  These effects are mediated by specific binding of NP to cell surface receptors that have been characterized, purified, and cloned from the vasculature, kidney, adrenal gland, and brain.	bind
24122	4	6126	7	NULL	NULL	NULL	NULL	NP	GP		bind		specific			cell surface receptor	GP	characterized;;purified;;cloned from vasculature			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_19	10785505	1 2 3  These effects are mediated by specific binding of NP to cell surface receptors that have been characterized, purified, and cloned from the vasculature, kidney, adrenal gland, and brain.	bind
16060	1	6127	5	NULL	NULL	0	NULL	titin	NULL	cloned	bind	NULL				F-actin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_77_4_856_s_176	7554133	1 2 3  Using cloned titin fragments, Jin 16  recently reported binding between titin and F-actin, and this interaction may underlie the inelastic behavior of titin in the I band.	bind
24535	2	6127	5	NULL	NULL	0	NULL	statement 1	NULL		underlie	NULL	may			titin	NULL	inelastic behavior of			NULL	in I band	0	NULL	NULL	NULL	gw60_circulationres_77_4_856_s_176	7554133	1 2 3  Using cloned titin fragments, Jin 16  recently reported binding between titin and F-actin, and this interaction may underlie the inelastic behavior of titin in the I band.	bind
19076	1	6127	7	NULL	NULL	NULL	NULL	titin	GP	cloned	bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_4_856_s_176	7554133	1 2 3  Using cloned titin fragments, Jin 16  recently reported binding between titin and F-actin, and this interaction may underlie the inelastic behavior of titin in the I band.	bind
19077	2	6127	7	NULL	NULL	NULL	NULL	statement 1	Process		underlie					titin	GP	inelastic behaviour of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_4_856_s_176	7554133	1 2 3  Using cloned titin fragments, Jin 16  recently reported binding between titin and F-actin, and this interaction may underlie the inelastic behavior of titin in the I band.	bind
16061	1	6128	5	10	NULL	0	NULL	fluid shear stress			causes					platelet		aggregation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
16062	2	6128	5	NULL	NULL	0	NULL	statement 1	NULL		in the absence of	NULL				agonists	NULL	exogenous			NULL		0	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
16063	3	6128	5	NULL	NULL	0	NULL	statement 1	NULL		requires	NULL				vWf multimers	NULL	intact			NULL		0	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
16064	4	6128	5	NULL	NULL	0	NULL	statement 1	NULL		requires	NULL				Ca2+	NULL	extracellular			NULL		0	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
16065	5	6128	5	10	NULL	0	NULL	statement 1	NULL		requires	NULL				ADP	NULL	endogenous			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
16067	7	6128	5	10	NULL	0	NULL	statement 1	NULL		requires	NULL				platelets	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
16068	8	6128	5	10	NULL	0	NULL	shear stress		pathological levels of 	initiate					platelet		aggregation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
16069	9	6128	5	NULL	NULL	0	NULL	vWf	NULL		bind	NULL				GP Ib	NULL	platelet			NULL		0	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
16070	10	6128	5	NULL	NULL	0	NULL	shear stress	NULL	pathological levels of	induce	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
16071	11	6128	5	NULL	NULL	0	NULL	statement 10	NULL		leads to	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
45166	6	6128	5	10	NULL	0	NULL	GPIb	NULL		is a type of	NULL				platelet membrane glycoprotein	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
19081	1	6128	7	NULL	NULL	NULL	NULL	 vWf	GP		bind					GP Ib	GP	platelet			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
19082	2	6128	7	NULL	NULL	NULL	NULL	fluid shear stress	Process		aggregates					platelets	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
19083	3	6128	7	NULL	NULL	NULL	NULL	statement 2	Process		in absence of					agonists	Chemical	exogenous			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
19084	4	6128	7	NULL	NULL	NULL	NULL	statement 2	Process		requires					 Ca2+	Chemical	extracellular			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
19085	5	6128	7	NULL	NULL	NULL	NULL	statement 2	Process		requires					ADP	Chemical	endogenous			NULL	in platelet granules	NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
19086	6	6128	7	NULL	NULL	NULL	NULL	statement 2	Process		requires					platelets	OrganismPart	metabolically active			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
19087	7	6128	7	NULL	NULL	NULL	NULL	platelets	OrganismPart	metabolically active	has intact					GP Ib	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
19095	8	6128	7	NULL	NULL	NULL	NULL	shear stress	Process	pathological levels of	initiate					platelet 	OrganismPart	aggregation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
19096	9	6128	7	NULL	NULL	NULL	NULL	statement 8	Process		occurs upon					statement 1	Process	inducing			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
45168	10	6128	7	NULL	NULL	NULL	NULL	GPIb	GP		is a type of					platelet membrane glycoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_18	7664419	1 2 3 4  5 6 7 8 9 10 14 15 16 17  The platelet aggregation response to fluid shear stress occurs in the absence of exogenous agonists 2  3  and requires intact vWf multimers, extracellular Ca2+, endogenous ADP contained in platelet granules, and metabolically active platelets with intact platelet membrane glycoprotein (GP) Ib and [[ GP IIb/IIa. 1 2 3 4 5 6 7 8 9 10  Arterial ]] and pathological levels of shear stress (>30 dynes/cm2) initiate platelet aggregation by inducing the binding of vWf to platelet GP Ib.	bind
16072	1	6129	5	10	NULL	0	NULL	LDLs	NULL	binding of	is independent of	NULL				platelet	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_972_s_21	7541295	1 2 3 4  Binding of LDLs and HDLs was found to be independent of the state of platelet activation and was saturable.	bind
16073	2	6129	5	NULL	NULL	0	NULL	LDLs	NULL	binding of	is	NULL				saturable	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_972_s_21	7541295	1 2 3 4  Binding of LDLs and HDLs was found to be independent of the state of platelet activation and was saturable.	bind
16074	3	6129	5	10	NULL	0	NULL	HDLs	NULL	binding of	is independent of	NULL				platelet	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_972_s_21	7541295	1 2 3 4  Binding of LDLs and HDLs was found to be independent of the state of platelet activation and was saturable.	bind
16075	4	6129	5	NULL	NULL	0	NULL	HDLs	NULL	binding of	is	NULL				saturable	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_972_s_21	7541295	1 2 3 4  Binding of LDLs and HDLs was found to be independent of the state of platelet activation and was saturable.	bind
19097	1	6129	7	NULL	NULL	NULL	NULL	LDL	GP	binding of	independent of					platelet	OrganismPart	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_972_s_21	7541295	1 2 3 4  Binding of LDLs and HDLs was found to be independent of the state of platelet activation and was saturable.	bind
19098	2	6129	7	NULL	NULL	NULL	NULL	HDL	GP	binding of	independent of					platelet	OrganismPart	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_972_s_21	7541295	1 2 3 4  Binding of LDLs and HDLs was found to be independent of the state of platelet activation and was saturable.	bind
19099	3	6129	7	NULL	NULL	NULL	NULL	LDL	GP	binding of	is					saturable	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_972_s_21	7541295	1 2 3 4  Binding of LDLs and HDLs was found to be independent of the state of platelet activation and was saturable.	bind
19100	4	6129	7	NULL	NULL	NULL	NULL	HDL	GP	binding of	is					saturable	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_972_s_21	7541295	1 2 3 4  Binding of LDLs and HDLs was found to be independent of the state of platelet activation and was saturable.	bind
16076	1	6130	5	NULL	NULL	0	NULL	heparin	NULL		complex with	NULL				platelet factor 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_14_1838_s_26	11294800	1 2 3 4  HIT is caused by the binding of antibodies (most frequently IgG) to a complex of heparin and platelet factor 4.	bind
16077	2	6130	5	NULL	NULL	0	NULL	IgG antibodies	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_14_1838_s_26	11294800	1 2 3 4  HIT is caused by the binding of antibodies (most frequently IgG) to a complex of heparin and platelet factor 4.	bind
16078	3	6130	5	NULL	NULL	0	NULL	HIT	NULL		is caused by	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_14_1838_s_26	11294800	1 2 3 4  HIT is caused by the binding of antibodies (most frequently IgG) to a complex of heparin and platelet factor 4.	bind
19101	1	6130	7	NULL	NULL	NULL	NULL	heparin	GP		forms complex with					platelet factor 4	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_14_1838_s_26	11294800	1 2 3 4  HIT is caused by the binding of antibodies (most frequently IgG) to a complex of heparin and platelet factor 4.	bind
19102	2	6130	7	NULL	NULL	NULL	NULL	IgG	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_14_1838_s_26	11294800	1 2 3 4  HIT is caused by the binding of antibodies (most frequently IgG) to a complex of heparin and platelet factor 4.	bind
19103	3	6130	7	NULL	NULL	NULL	NULL	statement 2	Process		cause					HIT	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_14_1838_s_26	11294800	1 2 3 4  HIT is caused by the binding of antibodies (most frequently IgG) to a complex of heparin and platelet factor 4.	bind
16079	1	6133	5	10	NULL	0	NULL	growth factors	NULL	specific	bind	NULL				tyrosine kinases	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_19_1960_s_22	9609090	1 2 3 4 5  The binding of specific growth factors with their selective cell surface receptor tyrosine kinases results in its autophosphorylation and activation, leading to downstream signal transduction through chains of intercommunicating proteins culminating in cell proliferation.	bind
16080	2	6133	5	10	NULL	0	NULL	statement 1	NULL		results in	NULL				tyrosine kinases	NULL	autophosphorylation of 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_19_1960_s_22	9609090	1 2 3 4 5  The binding of specific growth factors with their selective cell surface receptor tyrosine kinases results in its autophosphorylation and activation, leading to downstream signal transduction through chains of intercommunicating proteins culminating in cell proliferation.	bind
16081	3	6133	5	10	NULL	0	NULL	statement 1	NULL		results in	NULL				tyrosine kinases	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_19_1960_s_22	9609090	1 2 3 4 5  The binding of specific growth factors with their selective cell surface receptor tyrosine kinases results in its autophosphorylation and activation, leading to downstream signal transduction through chains of intercommunicating proteins culminating in cell proliferation.	bind
24536	4	6133	5	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				signal transduction	NULL	downstream			NULL		0	NULL	NULL	NULL	gw60_circulation_97_19_1960_s_22	9609090	1 2 3 4 5  The binding of specific growth factors with their selective cell surface receptor tyrosine kinases results in its autophosphorylation and activation, leading to downstream signal transduction through chains of intercommunicating proteins culminating in cell proliferation.	bind
24537	5	6133	5	NULL	NULL	0	NULL	statement 4	NULL		occurs through	NULL				intercommunicating proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_97_19_1960_s_22	9609090	1 2 3 4 5  The binding of specific growth factors with their selective cell surface receptor tyrosine kinases results in its autophosphorylation and activation, leading to downstream signal transduction through chains of intercommunicating proteins culminating in cell proliferation.	bind
24538	6	6133	5	NULL	NULL	0	NULL	statement 5	NULL		results in	NULL				cell proliferation	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_97_19_1960_s_22	9609090	1 2 3 4 5  The binding of specific growth factors with their selective cell surface receptor tyrosine kinases results in its autophosphorylation and activation, leading to downstream signal transduction through chains of intercommunicating proteins culminating in cell proliferation.	bind
45200	7	6133	5	10	NULL	0	NULL	tyrosine kinase	NULL		is a type of	NULL				cell surface receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_97_19_1960_s_22	9609090	1 2 3 4 5  The binding of specific growth factors with their selective cell surface receptor tyrosine kinases results in its autophosphorylation and activation, leading to downstream signal transduction through chains of intercommunicating proteins culminating in cell proliferation.	bind
19106	1	6133	7	NULL	NULL	NULL	NULL	growth factors 	GP		bind					tyrosine kinases	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_19_1960_s_22	9609090	1 2 3 4 5  The binding of specific growth factors with their selective cell surface receptor tyrosine kinases results in its autophosphorylation and activation, leading to downstream signal transduction through chains of intercommunicating proteins culminating in cell proliferation.	bind
19107	2	6133	7	NULL	NULL	NULL	NULL	statement 1	Process		results in					tyrosine kinase	GP	autophosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_19_1960_s_22	9609090	1 2 3 4 5  The binding of specific growth factors with their selective cell surface receptor tyrosine kinases results in its autophosphorylation and activation, leading to downstream signal transduction through chains of intercommunicating proteins culminating in cell proliferation.	bind
19108	3	6133	7	NULL	NULL	NULL	NULL	statement 1	Process		results in					tyrosine kinase	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_19_1960_s_22	9609090	1 2 3 4 5  The binding of specific growth factors with their selective cell surface receptor tyrosine kinases results in its autophosphorylation and activation, leading to downstream signal transduction through chains of intercommunicating proteins culminating in cell proliferation.	bind
19109	4	6133	7	NULL	NULL	NULL	NULL	statement 2	Process		leads to					signal transduction	Process	downstream			NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_19_1960_s_22	9609090	1 2 3 4 5  The binding of specific growth factors with their selective cell surface receptor tyrosine kinases results in its autophosphorylation and activation, leading to downstream signal transduction through chains of intercommunicating proteins culminating in cell proliferation.	bind
19111	6	6133	7	NULL	NULL	NULL	NULL	signal transduction 	Process		occurs through					intercommunicating proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_19_1960_s_22	9609090	1 2 3 4 5  The binding of specific growth factors with their selective cell surface receptor tyrosine kinases results in its autophosphorylation and activation, leading to downstream signal transduction through chains of intercommunicating proteins culminating in cell proliferation.	bind
19112	7	6133	7	NULL	NULL	NULL	NULL	statement 6	Process		result in					cell profileration	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_19_1960_s_22	9609090	1 2 3 4 5  The binding of specific growth factors with their selective cell surface receptor tyrosine kinases results in its autophosphorylation and activation, leading to downstream signal transduction through chains of intercommunicating proteins culminating in cell proliferation.	bind
45201	8	6133	7	NULL	NULL	NULL	NULL	tyrosine kinase	GP		is a type of					cell surface receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_19_1960_s_22	9609090	1 2 3 4 5  The binding of specific growth factors with their selective cell surface receptor tyrosine kinases results in its autophosphorylation and activation, leading to downstream signal transduction through chains of intercommunicating proteins culminating in cell proliferation.	bind
16082	1	6134	5	NULL	NULL	0	NULL	heparin	NULL		bind	NULL				fibrin(ogen)	NULL	adsorbed			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1948_s_21	9848889	1 2 Importantly, heparin binds to adsorbed fibrin(ogen) and prevents adhesion between fibrin-coated surfaces.	bind
16083	2	6134	5	NULL	NULL	0	NULL	statement 1	NULL		prevents	NULL				fibrin-coated surfaces	NULL	adhesion between			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1948_s_21	9848889	1 2 Importantly, heparin binds to adsorbed fibrin(ogen) and prevents adhesion between fibrin-coated surfaces.	bind
19113	1	6134	7	NULL	NULL	NULL	NULL	heparin	GP		binds to					fibrinogen	GP	adsorbed			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1948_s_21	9848889	1 2 Importantly, heparin binds to adsorbed fibrin(ogen) and prevents adhesion between fibrin-coated surfaces.	bind
19114	2	6134	7	NULL	NULL	NULL	NULL	statement 1	Process		prevents					fibrin-coated surfaces	GP	adhesion between			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1948_s_21	9848889	1 2 Importantly, heparin binds to adsorbed fibrin(ogen) and prevents adhesion between fibrin-coated surfaces.	bind
16085	1	6135	5	10	NULL	0	NULL	norepinephrine	NULL		initiate	NULL				IP3 	NULL	signaling pathway of 			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_6_515_s_269	10488054	1 33  Furthermore, the observation that another agonist (norepinephrine) that binds to a different surface receptor than oxLDL but initiates the same IP3 signaling pathway as oxLDL also is incapable of generating a Ca2+ transient argues strongly that the primary defect is the IP3 signaling.	bind
16086	2	6135	5	NULL	NULL	0	NULL	statement 1	NULL		is incapable of 	NULL				Ca2+ transient	NULL	generating 			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_6_515_s_269	10488054	1 33  Furthermore, the observation that another agonist (norepinephrine) that binds to a different surface receptor than oxLDL but initiates the same IP3 signaling pathway as oxLDL also is incapable of generating a Ca2+ transient argues strongly that the primary defect is the IP3 signaling.	bind
16087	3	6135	5	NULL	NULL	0	NULL	statement 2	NULL		argues	NULL	strongly			IP3 	NULL	primary defect in signaling			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_6_515_s_269	10488054	1 33  Furthermore, the observation that another agonist (norepinephrine) that binds to a different surface receptor than oxLDL but initiates the same IP3 signaling pathway as oxLDL also is incapable of generating a Ca2+ transient argues strongly that the primary defect is the IP3 signaling.	bind
19115	1	6135	7	NULL	NULL	NULL	NULL	norepinephrine	Chemical		initiate					IP3	Chemical	signaling pathway of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_6_515_s_269	10488054	1 33  Furthermore, the observation that another agonist (norepinephrine) that binds to a different surface receptor than oxLDL but initiates the same IP3 signaling pathway as oxLDL also is incapable of generating a Ca2+ transient argues strongly that the primary defect is the IP3 signaling.	bind
19116	2	6135	7	NULL	NULL	NULL	NULL	norepinephrine	Chemical		is incapable of					Ca2+	Chemical	generating			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_6_515_s_269	10488054	1 33  Furthermore, the observation that another agonist (norepinephrine) that binds to a different surface receptor than oxLDL but initiates the same IP3 signaling pathway as oxLDL also is incapable of generating a Ca2+ transient argues strongly that the primary defect is the IP3 signaling.	bind
24172	3	6135	7	NULL	NULL	NULL	NULL	statement 3	Process		argues		strongly			IP3	Chemical	primary defect in signaling			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_6_515_s_269	10488054	1 33  Furthermore, the observation that another agonist (norepinephrine) that binds to a different surface receptor than oxLDL but initiates the same IP3 signaling pathway as oxLDL also is incapable of generating a Ca2+ transient argues strongly that the primary defect is the IP3 signaling.	bind
16088	1	6136	5	NULL	NULL	0	NULL	PU.1	NULL		bind	NULL				ganp	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_48000_s_155	11641399	1 Ab specifically inhibits binding of PU.1 to the  ganp promoter.	bind
16089	2	6136	5	NULL	NULL	0	NULL	Ab	NULL		inhibit	NULL	specifically			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_48000_s_155	11641399	1 Ab specifically inhibits binding of PU.1 to the  ganp promoter.	bind
19117	1	6136	7	NULL	NULL	NULL	NULL	PU.1	GP		bind					ganp	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_51_48000_s_155	11641399	1 Ab specifically inhibits binding of PU.1 to the  ganp promoter.	bind
19118	2	6136	7	NULL	NULL	NULL	NULL	Ab	GP		inhibits		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_51_48000_s_155	11641399	1 Ab specifically inhibits binding of PU.1 to the  ganp promoter.	bind
16090	1	6146	5	NULL	NULL	0	NULL	Ang1	NULL		is	NULL				Angiopoietin-1	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_139_2_329_s_2	12770938	1 Angiopoietin-1 (Ang1) is an angiogenic growth factor that binds to the Tie2 receptor on vascular endothelium, promoting blood vessel maturation and integrity.	bind
16091	2	6146	5	10	NULL	0	NULL	Ang1	NULL		bind	NULL				Tie2 receptor	NULL				NULL	on vascular endothelium	NULL	NULL	NULL	NULL	gw60_brjpharmacol_139_2_329_s_2	12770938	1 Angiopoietin-1 (Ang1) is an angiogenic growth factor that binds to the Tie2 receptor on vascular endothelium, promoting blood vessel maturation and integrity.	bind
16092	3	6146	5	NULL	NULL	0	NULL	statement 2	NULL		promotes	NULL				blood vessel	NULL	maturation of			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_139_2_329_s_2	12770938	1 Angiopoietin-1 (Ang1) is an angiogenic growth factor that binds to the Tie2 receptor on vascular endothelium, promoting blood vessel maturation and integrity.	bind
16093	4	6146	5	NULL	NULL	0	NULL	statement 2	NULL		promotes	NULL				integrity	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_139_2_329_s_2	12770938	1 Angiopoietin-1 (Ang1) is an angiogenic growth factor that binds to the Tie2 receptor on vascular endothelium, promoting blood vessel maturation and integrity.	bind
45204	5	6146	5	10	NULL	0	NULL	Ang1	NULL		is a type of	NULL				angiogenic growth factor	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_139_2_329_s_2	12770938	1 Angiopoietin-1 (Ang1) is an angiogenic growth factor that binds to the Tie2 receptor on vascular endothelium, promoting blood vessel maturation and integrity.	bind
19119	1	6146	7	NULL	NULL	NULL	NULL	Ang1	GP		is a type of					angiogenic growth factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_139_2_329_s_2	12770938	1 Angiopoietin-1 (Ang1) is an angiogenic growth factor that binds to the Tie2 receptor on vascular endothelium, promoting blood vessel maturation and integrity.	bind
19120	2	6146	7	NULL	NULL	NULL	NULL	Ang1	GP		bind					Tie2 receptor	GP				NULL	vascular endothelium	NULL	NULL	NULL	NULL	gw60_brjpharmacol_139_2_329_s_2	12770938	1 Angiopoietin-1 (Ang1) is an angiogenic growth factor that binds to the Tie2 receptor on vascular endothelium, promoting blood vessel maturation and integrity.	bind
19121	3	6146	7	NULL	NULL	NULL	NULL	statement 2	Process		promotes					blood vessel	OrganismPart	maturation of			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_139_2_329_s_2	12770938	1 Angiopoietin-1 (Ang1) is an angiogenic growth factor that binds to the Tie2 receptor on vascular endothelium, promoting blood vessel maturation and integrity.	bind
19122	4	6146	7	NULL	NULL	NULL	NULL	statement 2	Process		promotes					integrity	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_139_2_329_s_2	12770938	1 Angiopoietin-1 (Ang1) is an angiogenic growth factor that binds to the Tie2 receptor on vascular endothelium, promoting blood vessel maturation and integrity.	bind
19123	5	6146	7	NULL	NULL	NULL	NULL	Ang1	GP		is					Angiopoietin-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_139_2_329_s_2	12770938	1 Angiopoietin-1 (Ang1) is an angiogenic growth factor that binds to the Tie2 receptor on vascular endothelium, promoting blood vessel maturation and integrity.	bind
16094	1	6147	5	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				Sp1 probe	NULL	consensus			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_42_26236_s_233	9334192	1 antibody, unlike the anti-Sp1 antibody, failed to supershift Sp1 bound to a consensus Sp1 probe (Fig.  5 B, lanes 11-13).	bind
19124	1	6147	7	NULL	NULL	NULL	NULL	Sp1 	GP		bind					Sp1 probe	GP	consensus			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_42_26236_s_233	9334192	1 antibody, unlike the anti-Sp1 antibody, failed to supershift Sp1 bound to a consensus Sp1 probe (Fig.  5 B, lanes 11-13).	bind
16095	1	6148	5	NULL	NULL	0	NULL	Vitronectin	NULL		bind	NULL				Heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_11_6858_s_110	9054371	1 Binding of Vitronectin to Heparin Is Detected by Monitoring Changes in the Fluorescence of an Extrinsic Probe on Heparin	bind
19125	1	6148	7	NULL	NULL	NULL	NULL	Vitronectin	GP		bind					Heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_6858_s_110	9054371	1 Binding of Vitronectin to Heparin Is Detected by Monitoring Changes in the Fluorescence of an Extrinsic Probe on Heparin	bind
16096	1	6150	5	NULL	NULL	0	NULL	gp130	NULL		is	NULL				glycoprotein 130	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_12_1442_s_24	12234945	1 CT-1 binds to the glycoprotein 130 (gp130)/leukemia inhibitory factor (LIF) receptor complex 2 and activates both mitogen-activated protein kinase and janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathways.	bind
16097	2	6150	5	NULL	NULL	0	NULL	LIF	NULL		is	NULL				leukemia inhibitory factor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_12_1442_s_24	12234945	1 CT-1 binds to the glycoprotein 130 (gp130)/leukemia inhibitory factor (LIF) receptor complex 2 and activates both mitogen-activated protein kinase and janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathways.	bind
16098	3	6150	5	NULL	NULL	0	NULL	CT-1	NULL		bind	NULL				gp130/LIF receptor complex 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_12_1442_s_24	12234945	1 CT-1 binds to the glycoprotein 130 (gp130)/leukemia inhibitory factor (LIF) receptor complex 2 and activates both mitogen-activated protein kinase and janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathways.	bind
16099	4	6150	5	NULL	NULL	0	NULL	statement 3	NULL		activates	NULL				mitogen-activated protein kinase	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_12_1442_s_24	12234945	1 CT-1 binds to the glycoprotein 130 (gp130)/leukemia inhibitory factor (LIF) receptor complex 2 and activates both mitogen-activated protein kinase and janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathways.	bind
16100	5	6150	5	NULL	NULL	0	NULL	statement 3	NULL		activates	NULL				janus kinase-signal transducer	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_12_1442_s_24	12234945	1 CT-1 binds to the glycoprotein 130 (gp130)/leukemia inhibitory factor (LIF) receptor complex 2 and activates both mitogen-activated protein kinase and janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathways.	bind
16101	6	6150	5	NULL	NULL	0	NULL	statement 3	NULL		activates	NULL				JAK-STAT signaling pathways	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_12_1442_s_24	12234945	1 CT-1 binds to the glycoprotein 130 (gp130)/leukemia inhibitory factor (LIF) receptor complex 2 and activates both mitogen-activated protein kinase and janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathways.	bind
24539	7	6150	5	NULL	NULL	0	NULL	JAK-STAT signaling pathways	NULL		activates	NULL				transcription	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_12_1442_s_24	12234945	1 CT-1 binds to the glycoprotein 130 (gp130)/leukemia inhibitory factor (LIF) receptor complex 2 and activates both mitogen-activated protein kinase and janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathways.	bind
19134	1	6150	7	NULL	NULL	NULL	NULL	CT-1	GP		binds to					gp130/LIF receptor complex 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_12_1442_s_24	12234945	1 CT-1 binds to the glycoprotein 130 (gp130)/leukemia inhibitory factor (LIF) receptor complex 2 and activates both mitogen-activated protein kinase and janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathways.	bind
19135	2	6150	7	NULL	NULL	NULL	NULL	statement 1	Process		activates					mitogen-activated protein kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_12_1442_s_24	12234945	1 CT-1 binds to the glycoprotein 130 (gp130)/leukemia inhibitory factor (LIF) receptor complex 2 and activates both mitogen-activated protein kinase and janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathways.	bind
19136	3	6150	7	NULL	NULL	NULL	NULL	statement 1	Process		activates					janus kinase-signal transducer	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_12_1442_s_24	12234945	1 CT-1 binds to the glycoprotein 130 (gp130)/leukemia inhibitory factor (LIF) receptor complex 2 and activates both mitogen-activated protein kinase and janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathways.	bind
19137	4	6150	7	NULL	NULL	NULL	NULL	statement 1	Process		activates					JAK-STAT signaling pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_12_1442_s_24	12234945	1 CT-1 binds to the glycoprotein 130 (gp130)/leukemia inhibitory factor (LIF) receptor complex 2 and activates both mitogen-activated protein kinase and janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathways.	bind
19138	5	6150	7	NULL	NULL	NULL	NULL	gp130	GP		is					glycoprotein 130	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_12_1442_s_24	12234945	1 CT-1 binds to the glycoprotein 130 (gp130)/leukemia inhibitory factor (LIF) receptor complex 2 and activates both mitogen-activated protein kinase and janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathways.	bind
19139	6	6150	7	NULL	NULL	NULL	NULL	LIF	GP		is					leukemia inhibitory factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_12_1442_s_24	12234945	1 CT-1 binds to the glycoprotein 130 (gp130)/leukemia inhibitory factor (LIF) receptor complex 2 and activates both mitogen-activated protein kinase and janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathways.	bind
19140	7	6150	7	NULL	NULL	NULL	NULL	JAK-STAT pathway	Process		activates					transcription	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_12_1442_s_24	12234945	1 CT-1 binds to the glycoprotein 130 (gp130)/leukemia inhibitory factor (LIF) receptor complex 2 and activates both mitogen-activated protein kinase and janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathways.	bind
16102	1	6151	5	10	NULL	0	NULL	Vps45	NULL		bind	NULL	differential			Tlg2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1641_2_111_s_718	12914952	1 Differential binding of SM protein Vps45 to Tlg2 has recently suggested by N.J. Bryant  and D.E. James, J. Cell Biol. 161 (2003) 691-696.	bind
45205	2	6151	5	10	NULL	0	NULL	Vps45	NULL		is a type of	NULL				SM protein	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1641_2_111_s_718	12914952	1 Differential binding of SM protein Vps45 to Tlg2 has recently suggested by N.J. Bryant  and D.E. James, J. Cell Biol. 161 (2003) 691-696.	bind
19141	1	6151	7	NULL	NULL	NULL	NULL	Vps45	GP		bind		differentially			Tlg2	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1641_2_111_s_718	12914952	1 Differential binding of SM protein Vps45 to Tlg2 has recently suggested by N.J. Bryant  and D.E. James, J. Cell Biol. 161 (2003) 691-696.	bind
45206	2	6151	7	NULL	NULL	NULL	NULL	Vps45	GP		is a type of					SM protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1641_2_111_s_718	12914952	1 Differential binding of SM protein Vps45 to Tlg2 has recently suggested by N.J. Bryant  and D.E. James, J. Cell Biol. 161 (2003) 691-696.	bind
16104	1	6154	5	NULL	NULL	0	NULL	PU.1	NULL		is necessary for	NULL		Ets DNA binding domain		nuclear localization	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_11_10675_s_4	15632149	1 fusions, we show that the Ets DNA binding domain of PU.1 is necessary and sufficient for its nuclear localization.	bind
16106	2	6154	5	NULL	NULL	0	NULL	PU.1	NULL		is sufficient for	NULL		Ets DNA binding domain		nuclear localization	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_11_10675_s_4	15632149	1 fusions, we show that the Ets DNA binding domain of PU.1 is necessary and sufficient for its nuclear localization.	bind
19142	1	6154	7	NULL	NULL	NULL	NULL	PU.1	GP		is necessary for			Ets DNA binding domain		nuclear localization	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10675_s_4	15632149	1 fusions, we show that the Ets DNA binding domain of PU.1 is necessary and sufficient for its nuclear localization.	bind
19143	2	6154	7	NULL	NULL	NULL	NULL	PU.1	GP		sufficient for			Ets DNA binding domain		nuclear localization	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10675_s_4	15632149	1 fusions, we show that the Ets DNA binding domain of PU.1 is necessary and sufficient for its nuclear localization.	bind
16107	1	6155	5	NULL	NULL	0	NULL	GT335 IgGs	NULL		bind	NULL				tubulin	NULL	brain			NULL		0	NULL	NULL	NULL	gw60_cellbiol_143_6_1575_s_81	9852152	1 immunoglobulins were prepared by the caprylic acid method, and GT335 IgGs  were affinity-purified on brain tubulin bound to a Hi-Trap column ( Pharmacia Biotech, Piscataway, NJ).	bind
19144	1	6155	7	NULL	NULL	NULL	NULL	GT335 IgGs	GP		bind					tubulin	GP	brain			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_6_1575_s_81	9852152	1 immunoglobulins were prepared by the caprylic acid method, and GT335 IgGs  were affinity-purified on brain tubulin bound to a Hi-Trap column ( Pharmacia Biotech, Piscataway, NJ).	bind
16108	1	6156	5	NULL	NULL	0	NULL	Munc18-1	NULL		bind	NULL	strongly			syntaxin 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31459_s_22	9395480	1 In addition to binding strongly to syntaxin 1, Munc18-1 binds to Doc2a and Doc2b, C2 domain proteins that are associated peripherally with synaptic vesicles ( 10).	bind
16109	2	6156	5	NULL	NULL	0	NULL	Munc18-1	NULL		bind	NULL				Doc2a	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31459_s_22	9395480	1 In addition to binding strongly to syntaxin 1, Munc18-1 binds to Doc2a and Doc2b, C2 domain proteins that are associated peripherally with synaptic vesicles ( 10).	bind
16110	3	6156	5	NULL	NULL	0	NULL	Munc18-1	NULL		bind	NULL				Doc2a	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31459_s_22	9395480	1 In addition to binding strongly to syntaxin 1, Munc18-1 binds to Doc2a and Doc2b, C2 domain proteins that are associated peripherally with synaptic vesicles ( 10).	bind
16111	4	6156	5	NULL	NULL	0	NULL	C2 domain proteins	NULL		associate with	NULL	peripherally			synaptic vesicles	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31459_s_22	9395480	1 In addition to binding strongly to syntaxin 1, Munc18-1 binds to Doc2a and Doc2b, C2 domain proteins that are associated peripherally with synaptic vesicles ( 10).	bind
16112	5	6156	5	NULL	NULL	0	NULL	Munc18-1	NULL		bind	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31459_s_22	9395480	1 In addition to binding strongly to syntaxin 1, Munc18-1 binds to Doc2a and Doc2b, C2 domain proteins that are associated peripherally with synaptic vesicles ( 10).	bind
24540	6	6156	5	NULL	NULL	0	NULL	Doc2a	NULL		associate with	NULL	peripherally			synaptic vesicles	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31459_s_22	9395480	1 In addition to binding strongly to syntaxin 1, Munc18-1 binds to Doc2a and Doc2b, C2 domain proteins that are associated peripherally with synaptic vesicles ( 10).	bind
24541	7	6156	5	NULL	NULL	0	NULL	Doc2b	NULL		associate with	NULL	peripherally			synaptic vesicles	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31459_s_22	9395480	1 In addition to binding strongly to syntaxin 1, Munc18-1 binds to Doc2a and Doc2b, C2 domain proteins that are associated peripherally with synaptic vesicles ( 10).	bind
19145	1	6156	7	NULL	NULL	NULL	NULL	Munc18-1	GP		binds to					Doc2a	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31459_s_22	9395480	1 In addition to binding strongly to syntaxin 1, Munc18-1 binds to Doc2a and Doc2b, C2 domain proteins that are associated peripherally with synaptic vesicles ( 10).	bind
19146	2	6156	7	NULL	NULL	NULL	NULL	Munc18-1	GP		binds to					Doc2b	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31459_s_22	9395480	1 In addition to binding strongly to syntaxin 1, Munc18-1 binds to Doc2a and Doc2b, C2 domain proteins that are associated peripherally with synaptic vesicles ( 10).	bind
19148	3	6156	7	NULL	NULL	NULL	NULL	Munc18-1	GP		binds to		strongly			syntaxin 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31459_s_22	9395480	1 In addition to binding strongly to syntaxin 1, Munc18-1 binds to Doc2a and Doc2b, C2 domain proteins that are associated peripherally with synaptic vesicles ( 10).	bind
19149	4	6156	7	NULL	NULL	NULL	NULL	Doc2a	GP		associate with		peripherally			synaptic vesicles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31459_s_22	9395480	1 In addition to binding strongly to syntaxin 1, Munc18-1 binds to Doc2a and Doc2b, C2 domain proteins that are associated peripherally with synaptic vesicles ( 10).	bind
19150	5	6156	7	NULL	NULL	NULL	NULL	Doc2b	GP		associate with		peripherally			synaptic vesicles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31459_s_22	9395480	1 In addition to binding strongly to syntaxin 1, Munc18-1 binds to Doc2a and Doc2b, C2 domain proteins that are associated peripherally with synaptic vesicles ( 10).	bind
19151	6	6156	7	NULL	NULL	NULL	NULL	C2 domain proteins	GP		associate with		peripherally			synaptic vesicles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31459_s_22	9395480	1 In addition to binding strongly to syntaxin 1, Munc18-1 binds to Doc2a and Doc2b, C2 domain proteins that are associated peripherally with synaptic vesicles ( 10).	bind
24173	7	6156	7	NULL	NULL	NULL	NULL	Munc18-1	GP		bind					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31459_s_22	9395480	1 In addition to binding strongly to syntaxin 1, Munc18-1 binds to Doc2a and Doc2b, C2 domain proteins that are associated peripherally with synaptic vesicles ( 10).	bind
16113	1	6157	5	NULL	NULL	0	NULL	Netrin	NULL		bind	NULL				receptor Unc5b	NULL				NULL	in vascular system of fish	0	NULL	NULL	NULL	gw70_circulationres_98_4_440_s_20	16514073	1 In the vascular system of fish and mice, Netrin binding to the receptor Unc5b suppresses the formation of endothelial tip cell filopodia and branching of blood vessels.	bind
16114	2	6157	5	NULL	NULL	0	NULL	Netrin	NULL		bind	NULL				receptor Unc5b	NULL				NULL	in vascular system of mice	0	NULL	NULL	NULL	gw70_circulationres_98_4_440_s_20	16514073	1 In the vascular system of fish and mice, Netrin binding to the receptor Unc5b suppresses the formation of endothelial tip cell filopodia and branching of blood vessels.	bind
16115	3	6157	5	10	NULL	0	NULL	statement 1			supress					endothelial tip cell filopodia		formation of 			NULL	vascular system of fish	NULL	NULL	NULL	NULL	gw70_circulationres_98_4_440_s_20	16514073	1 In the vascular system of fish and mice, Netrin binding to the receptor Unc5b suppresses the formation of endothelial tip cell filopodia and branching of blood vessels.	bind
16116	4	6157	5	10	NULL	0	NULL	statement 2			supress					endothelial tip cell filopodia		formation of			NULL	vascular system of mice	NULL	NULL	NULL	NULL	gw70_circulationres_98_4_440_s_20	16514073	1 In the vascular system of fish and mice, Netrin binding to the receptor Unc5b suppresses the formation of endothelial tip cell filopodia and branching of blood vessels.	bind
16118	5	6157	5	10	NULL	0	NULL	statement 1			supress					blood vessels		branching of 			NULL	vascular system of fish	NULL	NULL	NULL	NULL	gw70_circulationres_98_4_440_s_20	16514073	1 In the vascular system of fish and mice, Netrin binding to the receptor Unc5b suppresses the formation of endothelial tip cell filopodia and branching of blood vessels.	bind
16120	6	6157	5	10	NULL	0	NULL	statement 2			supress					blood vessels		branching of			NULL	vascular system of mice	NULL	NULL	NULL	NULL	gw70_circulationres_98_4_440_s_20	16514073	1 In the vascular system of fish and mice, Netrin binding to the receptor Unc5b suppresses the formation of endothelial tip cell filopodia and branching of blood vessels.	bind
19154	1	6157	7	NULL	NULL	NULL	NULL	Netrin	GP		bind					Unc5b receptor	GP				NULL	vascular system of fish	NULL	NULL	NULL	NULL	gw70_circulationres_98_4_440_s_20	16514073	1 In the vascular system of fish and mice, Netrin binding to the receptor Unc5b suppresses the formation of endothelial tip cell filopodia and branching of blood vessels.	bind
19155	2	6157	7	NULL	NULL	NULL	NULL	Netrin	GP		bind					Unc5b receptor	GP				NULL	vascular system of mice	NULL	NULL	NULL	NULL	gw70_circulationres_98_4_440_s_20	16514073	1 In the vascular system of fish and mice, Netrin binding to the receptor Unc5b suppresses the formation of endothelial tip cell filopodia and branching of blood vessels.	bind
19156	3	6157	7	NULL	NULL	NULL	NULL	statement 1	Process		suppress					endothelial tip cell filopodia	OrganismPart	formation of			NULL	vascular system of fish	NULL	NULL	NULL	NULL	gw70_circulationres_98_4_440_s_20	16514073	1 In the vascular system of fish and mice, Netrin binding to the receptor Unc5b suppresses the formation of endothelial tip cell filopodia and branching of blood vessels.	bind
19157	4	6157	7	NULL	NULL	NULL	NULL	statement 1	Process		suppress					blood vessel	OrganismPart	branching of			NULL	vascular system of fish	NULL	NULL	NULL	NULL	gw70_circulationres_98_4_440_s_20	16514073	1 In the vascular system of fish and mice, Netrin binding to the receptor Unc5b suppresses the formation of endothelial tip cell filopodia and branching of blood vessels.	bind
19158	5	6157	7	NULL	NULL	NULL	NULL	statement 2	Process		suppress					endothelial tip cell filopodia	OrganismPart	formation of			NULL	vascular system of mice	NULL	NULL	NULL	NULL	gw70_circulationres_98_4_440_s_20	16514073	1 In the vascular system of fish and mice, Netrin binding to the receptor Unc5b suppresses the formation of endothelial tip cell filopodia and branching of blood vessels.	bind
19159	6	6157	7	NULL	NULL	NULL	NULL	statement 2	Process		suppress					blood vessel	OrganismPart	branching of			NULL	vascular system of mice	NULL	NULL	NULL	NULL	gw70_circulationres_98_4_440_s_20	16514073	1 In the vascular system of fish and mice, Netrin binding to the receptor Unc5b suppresses the formation of endothelial tip cell filopodia and branching of blood vessels.	bind
16122	1	6159	5	NULL	NULL	0	NULL	TfRs	NULL		is	NULL				Tf receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_46_33035_s_16	10551872	1 Iron uptake from Tf involves the binding of Tf to the Tf receptors (TfRs), internalization of Tf within an endocytic vesicle by receptor-mediated endocytosis, and the release of iron from Tf by a decrease in endosomal pH.	bind
16124	2	6159	5	NULL	NULL	0	NULL	TfRs	NULL		bind	NULL				TfRs	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_46_33035_s_16	10551872	1 Iron uptake from Tf involves the binding of Tf to the Tf receptors (TfRs), internalization of Tf within an endocytic vesicle by receptor-mediated endocytosis, and the release of iron from Tf by a decrease in endosomal pH.	bind
16125	3	6159	5	NULL	NULL	0	NULL	Tf	NULL	iron uptake from	involves	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_46_33035_s_16	10551872	1 Iron uptake from Tf involves the binding of Tf to the Tf receptors (TfRs), internalization of Tf within an endocytic vesicle by receptor-mediated endocytosis, and the release of iron from Tf by a decrease in endosomal pH.	bind
16127	4	6159	5	NULL	NULL	0	NULL	Tf	NULL		is internalized within	NULL				endocytic vesicle	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33035_s_16	10551872	1 Iron uptake from Tf involves the binding of Tf to the Tf receptors (TfRs), internalization of Tf within an endocytic vesicle by receptor-mediated endocytosis, and the release of iron from Tf by a decrease in endosomal pH.	bind
16128	6	6159	5	NULL	NULL	0	NULL	Tf	NULL	iron uptake from	involves	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33035_s_16	10551872	1 Iron uptake from Tf involves the binding of Tf to the Tf receptors (TfRs), internalization of Tf within an endocytic vesicle by receptor-mediated endocytosis, and the release of iron from Tf by a decrease in endosomal pH.	bind
16129	7	6159	5	NULL	NULL	0	NULL	iron	NULL		released from	NULL				Tf	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33035_s_16	10551872	1 Iron uptake from Tf involves the binding of Tf to the Tf receptors (TfRs), internalization of Tf within an endocytic vesicle by receptor-mediated endocytosis, and the release of iron from Tf by a decrease in endosomal pH.	bind
16130	8	6159	5	NULL	NULL	0	NULL	endosomal pH	NULL	decrease in	leads to	NULL				statement 7	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33035_s_16	10551872	1 Iron uptake from Tf involves the binding of Tf to the Tf receptors (TfRs), internalization of Tf within an endocytic vesicle by receptor-mediated endocytosis, and the release of iron from Tf by a decrease in endosomal pH.	bind
16131	9	6159	5	NULL	NULL	0	NULL	Tf	NULL	iron uptake from	involves	NULL				statement 8	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33035_s_16	10551872	1 Iron uptake from Tf involves the binding of Tf to the Tf receptors (TfRs), internalization of Tf within an endocytic vesicle by receptor-mediated endocytosis, and the release of iron from Tf by a decrease in endosomal pH.	bind
16134	5	6159	5	NULL	NULL	0	NULL	endocytosis	NULL	receptor-mediated	leads to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_46_33035_s_16	10551872	1 Iron uptake from Tf involves the binding of Tf to the Tf receptors (TfRs), internalization of Tf within an endocytic vesicle by receptor-mediated endocytosis, and the release of iron from Tf by a decrease in endosomal pH.	bind
20793	1	6159	7	NULL	NULL	NULL	NULL	Tf	GP		bind					TfRs	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33035_s_16	10551872	1 Iron uptake from Tf involves the binding of Tf to the Tf receptors (TfRs), internalization of Tf within an endocytic vesicle by receptor-mediated endocytosis, and the release of iron from Tf by a decrease in endosomal pH.	bind
20794	2	6159	7	NULL	NULL	NULL	NULL	Tf	GP	Iron uptake from	involves					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33035_s_16	10551872	1 Iron uptake from Tf involves the binding of Tf to the Tf receptors (TfRs), internalization of Tf within an endocytic vesicle by receptor-mediated endocytosis, and the release of iron from Tf by a decrease in endosomal pH.	bind
20797	3	6159	7	NULL	NULL	NULL	NULL	endocytosis	Process	 receptor-mediated	internalize					Tf	GP	within endocytic vesicle 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33035_s_16	10551872	1 Iron uptake from Tf involves the binding of Tf to the Tf receptors (TfRs), internalization of Tf within an endocytic vesicle by receptor-mediated endocytosis, and the release of iron from Tf by a decrease in endosomal pH.	bind
20798	4	6159	7	NULL	NULL	NULL	NULL	Tf	GP	Iron uptake from	involves					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33035_s_16	10551872	1 Iron uptake from Tf involves the binding of Tf to the Tf receptors (TfRs), internalization of Tf within an endocytic vesicle by receptor-mediated endocytosis, and the release of iron from Tf by a decrease in endosomal pH.	bind
20802	5	6159	7	NULL	NULL	NULL	NULL	pH	QuantityOrMeasure	decrease in endosomal	release					Tf	GP	iron from			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33035_s_16	10551872	1 Iron uptake from Tf involves the binding of Tf to the Tf receptors (TfRs), internalization of Tf within an endocytic vesicle by receptor-mediated endocytosis, and the release of iron from Tf by a decrease in endosomal pH.	bind
20813	6	6159	7	NULL	NULL	NULL	NULL	Tf	GP	Iron uptake from	involves					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33035_s_16	10551872	1 Iron uptake from Tf involves the binding of Tf to the Tf receptors (TfRs), internalization of Tf within an endocytic vesicle by receptor-mediated endocytosis, and the release of iron from Tf by a decrease in endosomal pH.	bind
20814	7	6159	7	NULL	NULL	NULL	NULL	TfRs	GP		is					Tf receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_33035_s_16	10551872	1 Iron uptake from Tf involves the binding of Tf to the Tf receptors (TfRs), internalization of Tf within an endocytic vesicle by receptor-mediated endocytosis, and the release of iron from Tf by a decrease in endosomal pH.	bind
16135	1	6160	5	NULL	NULL	0	NULL	ERNS antibodies	NULL		bind	NULL				ERNS antigen	NULL				NULL		0	NULL	NULL	NULL	gw60_vetmicrobiol_73_2_209_s_112	10785329	1 is conjugated with HRPO and used for detection of binding of ERNS antibodies to the ERNS antigen.	bind
20822	1	6160	7	NULL	NULL	NULL	NULL	ERNS antibodies	GP		bind					ERNS antigen	GP				NULL		NULL	NULL	NULL	NULL	gw60_vetmicrobiol_73_2_209_s_112	10785329	1 is conjugated with HRPO and used for detection of binding of ERNS antibodies to the ERNS antigen.	bind
16473	1	6162	5	NULL	NULL	0	NULL	phage-antibodies	NULL		bind	NULL				microcystin-LR-BSA conjugates	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_11_5288_s_128	12406716	1 library prior to affinity selection (pan 0) and from each subsequent pan indicated an enrichment of phage-antibodies which bound to microcystin-LR-BSA and microcystin-LR-KLH conjugates (Fig.  1).	bind
16474	2	6162	5	NULL	NULL	0	NULL	phage-antibodies	NULL		bind	NULL				microcystin-LR-KLH conjugates	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_11_5288_s_128	12406716	1 library prior to affinity selection (pan 0) and from each subsequent pan indicated an enrichment of phage-antibodies which bound to microcystin-LR-BSA and microcystin-LR-KLH conjugates (Fig.  1).	bind
20827	1	6162	7	NULL	NULL	NULL	NULL	phage-antibodies	GP		bind					microcystin-LR-BSA conjugate	GP				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_68_11_5288_s_128	12406716	1 library prior to affinity selection (pan 0) and from each subsequent pan indicated an enrichment of phage-antibodies which bound to microcystin-LR-BSA and microcystin-LR-KLH conjugates (Fig.  1).	bind
20828	2	6162	7	NULL	NULL	NULL	NULL	phage-antibodies	GP		bind					microcystin-LR-KLH conjugate	GP				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_68_11_5288_s_128	12406716	1 library prior to affinity selection (pan 0) and from each subsequent pan indicated an enrichment of phage-antibodies which bound to microcystin-LR-BSA and microcystin-LR-KLH conjugates (Fig.  1).	bind
16475	1	6163	5	NULL	NULL	0	NULL	CRP	NULL	aggregated	bind	NULL				C1q	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_17_2019_s_19	11980679	1 Ligand-bound or aggregated CRP binds C1q and in so doing activates the classical complement pathway.	bind
16476	2	6163	5	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				classical complement pathway	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_17_2019_s_19	11980679	1 Ligand-bound or aggregated CRP binds C1q and in so doing activates the classical complement pathway.	bind
16477	3	6163	5	NULL	NULL	0	NULL	CRP	NULL	ligand-bound	bind	NULL				C1q	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_17_2019_s_19	11980679	1 Ligand-bound or aggregated CRP binds C1q and in so doing activates the classical complement pathway.	bind
16478	4	6163	5	NULL	NULL	0	NULL	statement 3	NULL		activates	NULL				classical complement pathway	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_17_2019_s_19	11980679	1 Ligand-bound or aggregated CRP binds C1q and in so doing activates the classical complement pathway.	bind
20829	1	6163	7	NULL	NULL	NULL	NULL	CRP	GP	Ligand-bound	binds					C1q	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_17_2019_s_19	11980679	1 Ligand-bound or aggregated CRP binds C1q and in so doing activates the classical complement pathway.	bind
20830	2	6163	7	NULL	NULL	NULL	NULL	CRP	GP	aggregated	binds					C1q	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_17_2019_s_19	11980679	1 Ligand-bound or aggregated CRP binds C1q and in so doing activates the classical complement pathway.	bind
20831	3	6163	7	NULL	NULL	NULL	NULL	statement 1	Process		activates					classical complement pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_17_2019_s_19	11980679	1 Ligand-bound or aggregated CRP binds C1q and in so doing activates the classical complement pathway.	bind
20832	4	6163	7	NULL	NULL	NULL	NULL	statement 2	Process		activates					classical complement pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_17_2019_s_19	11980679	1 Ligand-bound or aggregated CRP binds C1q and in so doing activates the classical complement pathway.	bind
16479	1	6167	5	NULL	NULL	0	NULL	MRP-8/14 complex	NULL	native	bind	NULL				CHO-K1 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_5_3658_s_198	11723110	1 muM native MRP-8/14 complex binding to CHO-K1 ( ) and pgsA-745 cells ( ) as detected by anti-MRP-14.	bind
16480	2	6167	5	NULL	NULL	0	NULL	MRP-8/14 complex	NULL	native	bind	NULL				pgsA-745 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_5_3658_s_198	11723110	1 muM native MRP-8/14 complex binding to CHO-K1 ( ) and pgsA-745 cells ( ) as detected by anti-MRP-14.	bind
20833	1	6167	7	NULL	NULL	NULL	NULL	MRP-8/14 complex	GP	native	bind					CHO-K1 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3658_s_198	11723110	1 muM native MRP-8/14 complex binding to CHO-K1 ( ) and pgsA-745 cells ( ) as detected by anti-MRP-14.	bind
20834	2	6167	7	NULL	NULL	NULL	NULL	MRP-8/14 complex	GP	native	bind					pgsA-745 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3658_s_198	11723110	1 muM native MRP-8/14 complex binding to CHO-K1 ( ) and pgsA-745 cells ( ) as detected by anti-MRP-14.	bind
24542	1	6169	5	NULL	NULL	0	NULL	SHP	NULL		contains	NULL					NULL		two N terminus SH2 domains		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3687_s_12	9452499	1 One subfamily of cytoplasmic PTPs, referred to as SHP ( 1), contains two SH2 domains at their N terminus.	bind
24543	2	6169	5	NULL	NULL	0	NULL	SHP	NULL		is a subfamily of	NULL				cytoplasmic PTPs	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3687_s_12	9452499	1 One subfamily of cytoplasmic PTPs, referred to as SHP ( 1), contains two SH2 domains at their N terminus.	bind
20835	1	6169	7	NULL	NULL	NULL	NULL	SHP	GP		contains								2 N terminus SH2 domains		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_6_3687_s_12	9452499	1 One subfamily of cytoplasmic PTPs, referred to as SHP ( 1), contains two SH2 domains at their N terminus.	bind
20836	2	6169	7	NULL	NULL	NULL	NULL	SHP	GP		is a subfamily of					cytoplasmic PTPs	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_6_3687_s_12	9452499	1 One subfamily of cytoplasmic PTPs, referred to as SHP ( 1), contains two SH2 domains at their N terminus.	bind
16481	1	6170	5	NULL	NULL	0	NULL	EGF-like ligands	NULL	mammalian	include	NULL				TGFalpha	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_138_4_747_s_13	9265643	1 Other mammalian EGF-like ligands include transforming growth factor-alpha (TGFalpha), amphiregulin, heparin binding EGF-like  growth factor, betacellulin and epiregulin ( 3,  17,  32).	bind
16482	2	6170	5	NULL	NULL	0	NULL	TGFalpha	NULL		is	NULL				transforming growth factor-alpha	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_138_4_747_s_13	9265643	1 Other mammalian EGF-like ligands include transforming growth factor-alpha (TGFalpha), amphiregulin, heparin binding EGF-like  growth factor, betacellulin and epiregulin ( 3,  17,  32).	bind
16483	3	6170	5	NULL	NULL	0	NULL	EGF-like ligands	NULL	mammalian	include	NULL				amphiregulin	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_138_4_747_s_13	9265643	1 Other mammalian EGF-like ligands include transforming growth factor-alpha (TGFalpha), amphiregulin, heparin binding EGF-like  growth factor, betacellulin and epiregulin ( 3,  17,  32).	bind
16484	4	6170	5	NULL	NULL	0	NULL	EGF-like ligands	NULL	mammalian	include	NULL				EGF-like growth factor	NULL	heparin binding			NULL		0	NULL	NULL	NULL	gw60_cellbiol_138_4_747_s_13	9265643	1 Other mammalian EGF-like ligands include transforming growth factor-alpha (TGFalpha), amphiregulin, heparin binding EGF-like  growth factor, betacellulin and epiregulin ( 3,  17,  32).	bind
16485	5	6170	5	NULL	NULL	0	NULL	EGF-like ligands	NULL	mammalian	include	NULL				betacellulin	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_138_4_747_s_13	9265643	1 Other mammalian EGF-like ligands include transforming growth factor-alpha (TGFalpha), amphiregulin, heparin binding EGF-like  growth factor, betacellulin and epiregulin ( 3,  17,  32).	bind
16486	6	6170	5	NULL	NULL	0	NULL	EGF-like ligands	NULL	mammalian	include	NULL				epiregulin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_138_4_747_s_13	9265643	1 Other mammalian EGF-like ligands include transforming growth factor-alpha (TGFalpha), amphiregulin, heparin binding EGF-like  growth factor, betacellulin and epiregulin ( 3,  17,  32).	bind
20837	1	6170	7	NULL	NULL	NULL	NULL	EGF-like ligands	GP	mammalian	include					TGFalpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_138_4_747_s_13	9265643	1 Other mammalian EGF-like ligands include transforming growth factor-alpha (TGFalpha), amphiregulin, heparin binding EGF-like  growth factor, betacellulin and epiregulin ( 3,  17,  32).	bind
20838	2	6170	7	NULL	NULL	NULL	NULL	EGF-like ligands	GP	mammalian	include					amphiregulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_138_4_747_s_13	9265643	1 Other mammalian EGF-like ligands include transforming growth factor-alpha (TGFalpha), amphiregulin, heparin binding EGF-like  growth factor, betacellulin and epiregulin ( 3,  17,  32).	bind
20839	3	6170	7	NULL	NULL	NULL	NULL	EGF-like ligands	GP	mammalian	include					EGF-like growth factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_138_4_747_s_13	9265643	1 Other mammalian EGF-like ligands include transforming growth factor-alpha (TGFalpha), amphiregulin, heparin binding EGF-like  growth factor, betacellulin and epiregulin ( 3,  17,  32).	bind
20840	4	6170	7	NULL	NULL	NULL	NULL	EGF-like ligands	GP	mammalian	include					betacellulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_138_4_747_s_13	9265643	1 Other mammalian EGF-like ligands include transforming growth factor-alpha (TGFalpha), amphiregulin, heparin binding EGF-like  growth factor, betacellulin and epiregulin ( 3,  17,  32).	bind
20841	5	6170	7	NULL	NULL	NULL	NULL	EGF-like ligands	GP	mammalian	include					epiregulin 	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_138_4_747_s_13	9265643	1 Other mammalian EGF-like ligands include transforming growth factor-alpha (TGFalpha), amphiregulin, heparin binding EGF-like  growth factor, betacellulin and epiregulin ( 3,  17,  32).	bind
24174	6	6170	7	NULL	NULL	NULL	NULL	TGFalpha	GP		is					transforming growth factor-alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_138_4_747_s_13	9265643	1 Other mammalian EGF-like ligands include transforming growth factor-alpha (TGFalpha), amphiregulin, heparin binding EGF-like  growth factor, betacellulin and epiregulin ( 3,  17,  32).	bind
55019	7	6170	7	NULL	NULL	NULL	NULL	EGF-like growth factor	GP		bind					heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_138_4_747_s_13	9265643	1 Other mammalian EGF-like ligands include transforming growth factor-alpha (TGFalpha), amphiregulin, heparin binding EGF-like  growth factor, betacellulin and epiregulin ( 3,  17,  32).	bind
16487	1	6171	5	NULL	NULL	0	NULL	IRSs	NULL	phosphorylated	bind	NULL				enzymes	NULL		SH2 domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_28_25323_s_11	12730241	1 Phosphorylated IRSs bind and activate SH2 domain enzymes to couple the  activated receptors to such downstream metabolic effects as glucose uptake and  glycogen and triglyceride synthesis and storage.	bind
16488	2	6171	5	NULL	NULL	0	NULL	IRSs	NULL	phosphorylated	activate	NULL				enzymes	NULL		SH2 domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_28_25323_s_11	12730241	1 Phosphorylated IRSs bind and activate SH2 domain enzymes to couple the  activated receptors to such downstream metabolic effects as glucose uptake and  glycogen and triglyceride synthesis and storage.	bind
16489	3	6171	5	NULL	NULL	0	NULL	statement 1	NULL		occurs simultaneously with	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_28_25323_s_11	12730241	1 Phosphorylated IRSs bind and activate SH2 domain enzymes to couple the  activated receptors to such downstream metabolic effects as glucose uptake and  glycogen and triglyceride synthesis and storage.	bind
16490	4	6171	5	NULL	NULL	0	NULL	statement 3	NULL		leads to	NULL				glucose	NULL	uptake of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_28_25323_s_11	12730241	1 Phosphorylated IRSs bind and activate SH2 domain enzymes to couple the  activated receptors to such downstream metabolic effects as glucose uptake and  glycogen and triglyceride synthesis and storage.	bind
16491	5	6171	5	10	NULL	0	NULL	statement 3			leads to					glycogen		synthesis of;;storage of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_28_25323_s_11	12730241	1 Phosphorylated IRSs bind and activate SH2 domain enzymes to couple the  activated receptors to such downstream metabolic effects as glucose uptake and  glycogen and triglyceride synthesis and storage.	bind
16492	6	6171	5	10	NULL	0	NULL	statement 3			leads to					triglyceride		synthesis of;;storage of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_28_25323_s_11	12730241	1 Phosphorylated IRSs bind and activate SH2 domain enzymes to couple the  activated receptors to such downstream metabolic effects as glucose uptake and  glycogen and triglyceride synthesis and storage.	bind
20842	1	6171	7	NULL	NULL	NULL	NULL	IRSs	GP	phosphorylated	bind					enzymes	GP		SH2 domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_28_25323_s_11	12730241	1 Phosphorylated IRSs bind and activate SH2 domain enzymes to couple the  activated receptors to such downstream metabolic effects as glucose uptake and  glycogen and triglyceride synthesis and storage.	bind
20843	2	6171	7	NULL	NULL	NULL	NULL	IRSs	GP	phosphorylated	activate					enzymes	GP		SH2 domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_28_25323_s_11	12730241	1 Phosphorylated IRSs bind and activate SH2 domain enzymes to couple the  activated receptors to such downstream metabolic effects as glucose uptake and  glycogen and triglyceride synthesis and storage.	bind
20844	3	6171	7	NULL	NULL	NULL	NULL	statement 1	Process		is simultaneous with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_28_25323_s_11	12730241	1 Phosphorylated IRSs bind and activate SH2 domain enzymes to couple the  activated receptors to such downstream metabolic effects as glucose uptake and  glycogen and triglyceride synthesis and storage.	bind
21483	4	6171	7	NULL	NULL	NULL	NULL	statement 3	Process		effect					glucose	Chemical	uptake of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_28_25323_s_11	12730241	1 Phosphorylated IRSs bind and activate SH2 domain enzymes to couple the  activated receptors to such downstream metabolic effects as glucose uptake and  glycogen and triglyceride synthesis and storage.	bind
21484	5	6171	7	NULL	NULL	NULL	NULL	statement 3	Process		effect					glycogen	Chemical	synthesis of;;storage of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_28_25323_s_11	12730241	1 Phosphorylated IRSs bind and activate SH2 domain enzymes to couple the  activated receptors to such downstream metabolic effects as glucose uptake and  glycogen and triglyceride synthesis and storage.	bind
21485	6	6171	7	NULL	NULL	NULL	NULL	statement 3	Process		effect					triglyceride 	Chemical	synthesis of;;storage of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_28_25323_s_11	12730241	1 Phosphorylated IRSs bind and activate SH2 domain enzymes to couple the  activated receptors to such downstream metabolic effects as glucose uptake and  glycogen and triglyceride synthesis and storage.	bind
16494	1	6172	5	10	NULL	0	NULL	E2 envelope glycoprotein	NULL	HCV	bind	NULL				CD81	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_19_19401_s_29	14966136	1 Pileri  et al. ( ) and others ( ,  ,  ) showed that the E2 envelope glycoprotein of HCV binds to CD81.	bind
20849	1	6172	7	NULL	NULL	NULL	NULL	E2 envelope glycoprotein	GP	HCV	binds to					CD81	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_19_19401_s_29	14966136	1 Pileri  et al. ( ) and others ( ,  ,  ) showed that the E2 envelope glycoprotein of HCV binds to CD81.	bind
19285	1	6173	5	NULL	NULL	0	NULL	LHR A	NULL		bind	NULL				iC3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_15_8623_s_143	9535836	1 Recognizes CCP 1  and Enhances iC3 and C4b Binding by LHR A-- Of 20 mAbs to CR1 tested ( 20), 8C9.	bind
19286	2	6173	5	NULL	NULL	0	NULL	LHR A	NULL		bind	NULL				C4b	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_15_8623_s_143	9535836	1 Recognizes CCP 1  and Enhances iC3 and C4b Binding by LHR A-- Of 20 mAbs to CR1 tested ( 20), 8C9.	bind
20850	1	6173	7	NULL	NULL	NULL	NULL	C4b	GP		bind					LHR A	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8623_s_143	9535836	1 Recognizes CCP 1  and Enhances iC3 and C4b Binding by LHR A-- Of 20 mAbs to CR1 tested ( 20), 8C9.	bind
20851	2	6173	7	NULL	NULL	NULL	NULL	 iC3	GP		bind					LHR A	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8623_s_143	9535836	1 Recognizes CCP 1  and Enhances iC3 and C4b Binding by LHR A-- Of 20 mAbs to CR1 tested ( 20), 8C9.	bind
16495	1	6174	5	NULL	NULL	0	NULL	SPIR	NULL		is	NULL				Spironolactone	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_br-j-pharmacol_148_1_16520746_s_2	16520746	1 Spironolactone (SPIR) binds to cytoplasmic mineralocorticoid receptors  (MR) and functions as an aldosterone antagonist.	bind
16496	2	6174	5	NULL	NULL	0	NULL	MR	NULL		is	NULL				mineralocorticoid receptors	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_br-j-pharmacol_148_1_16520746_s_2	16520746	1 Spironolactone (SPIR) binds to cytoplasmic mineralocorticoid receptors  (MR) and functions as an aldosterone antagonist.	bind
16497	3	6174	5	NULL	NULL	0	NULL	SPIR	NULL		bind	NULL				MR	NULL	cytoplasmic			NULL		0	NULL	NULL	NULL	abs-batch0700-0719_br-j-pharmacol_148_1_16520746_s_2	16520746	1 Spironolactone (SPIR) binds to cytoplasmic mineralocorticoid receptors  (MR) and functions as an aldosterone antagonist.	bind
16498	4	6174	5	NULL	NULL	0	NULL	SPIR	NULL		function as	NULL				aldosterone antagonist	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_br-j-pharmacol_148_1_16520746_s_2	16520746	1 Spironolactone (SPIR) binds to cytoplasmic mineralocorticoid receptors  (MR) and functions as an aldosterone antagonist.	bind
20852	1	6174	7	NULL	NULL	NULL	NULL	SPIR	Chemical		binds to					MR	GP	cytoplasmic			NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_br-j-pharmacol_148_1_16520746_s_2	16520746	1 Spironolactone (SPIR) binds to cytoplasmic mineralocorticoid receptors  (MR) and functions as an aldosterone antagonist.	bind
20853	2	6174	7	NULL	NULL	NULL	NULL	SPIR	Chemical		functions as					aldosterone antagonist	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_br-j-pharmacol_148_1_16520746_s_2	16520746	1 Spironolactone (SPIR) binds to cytoplasmic mineralocorticoid receptors  (MR) and functions as an aldosterone antagonist.	bind
20855	3	6174	7	NULL	NULL	NULL	NULL	SPIR	Chemical		is					Spironolactone	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_br-j-pharmacol_148_1_16520746_s_2	16520746	1 Spironolactone (SPIR) binds to cytoplasmic mineralocorticoid receptors  (MR) and functions as an aldosterone antagonist.	bind
20862	4	6174	7	NULL	NULL	NULL	NULL	MR	GP		is					mineralocorticoid receptors	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_br-j-pharmacol_148_1_16520746_s_2	16520746	1 Spironolactone (SPIR) binds to cytoplasmic mineralocorticoid receptors  (MR) and functions as an aldosterone antagonist.	bind
16499	1	6175	5	NULL	NULL	0	NULL	AhR	NULL		is	NULL				aryl hydrocarbon receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6770_s_14	10702233	1 TCDD binds and activates the aryl hydrocarbon receptor (AhR), a member of the basic helix-loop-helix family of transcription factors.	bind
16500	2	6175	5	NULL	NULL	0	NULL	TCDD	NULL		bind	NULL				AhR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6770_s_14	10702233	1 TCDD binds and activates the aryl hydrocarbon receptor (AhR), a member of the basic helix-loop-helix family of transcription factors.	bind
16501	3	6175	5	NULL	NULL	0	NULL	TCDD	NULL		activates	NULL				AhR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6770_s_14	10702233	1 TCDD binds and activates the aryl hydrocarbon receptor (AhR), a member of the basic helix-loop-helix family of transcription factors.	bind
24544	4	6175	5	NULL	NULL	0	NULL	AhR	NULL		is a member of	NULL				basic helix-loop-helix family of transcription factors	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6770_s_14	10702233	1 TCDD binds and activates the aryl hydrocarbon receptor (AhR), a member of the basic helix-loop-helix family of transcription factors.	bind
20865	1	6175	7	NULL	NULL	NULL	NULL	TCDD	Chemical		binds					AhR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_10_6770_s_14	10702233	1 TCDD binds and activates the aryl hydrocarbon receptor (AhR), a member of the basic helix-loop-helix family of transcription factors.	bind
20867	2	6175	7	NULL	NULL	NULL	NULL	TCDD	Chemical		activates					AhR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_10_6770_s_14	10702233	1 TCDD binds and activates the aryl hydrocarbon receptor (AhR), a member of the basic helix-loop-helix family of transcription factors.	bind
20880	3	6175	7	NULL	NULL	NULL	NULL	AhR	GP		member of					basic helix-loop-helix family of transcription factors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_10_6770_s_14	10702233	1 TCDD binds and activates the aryl hydrocarbon receptor (AhR), a member of the basic helix-loop-helix family of transcription factors.	bind
20882	4	6175	7	NULL	NULL	NULL	NULL	AhR	GP		is					aryl hydrocarbon receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_10_6770_s_14	10702233	1 TCDD binds and activates the aryl hydrocarbon receptor (AhR), a member of the basic helix-loop-helix family of transcription factors.	bind
16502	1	6209	5	NULL	NULL	0	NULL	Mint proteins	NULL		bind	NULL	high affinity			Munc18-1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31459_s_140	9395480	1 The following evidence supports the notion that Mint proteins bind to Munc18-1 with high affinity.	bind
20895	1	6209	7	NULL	NULL	NULL	NULL	Mint protein	GP		bind		high affinity			Munc18-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31459_s_140	9395480	1 The following evidence supports the notion that Mint proteins bind to Munc18-1 with high affinity.	bind
16503	1	6210	5	NULL	NULL	0	NULL	CDK inhibitors	NULL		bind	NULL				cyclin-CDK complexes	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_1_175_s_17	9665478	1 The kinase activity of CDKs can be inhibited by a group of CDK inhibitors that bind to cyclin-CDK complexes and block progression through the cell cycle.	bind
16504	2	6210	5	NULL	NULL	0	NULL	statement 1	NULL		block	NULL				cell cycle	NULL	progression through			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_1_175_s_17	9665478	1 The kinase activity of CDKs can be inhibited by a group of CDK inhibitors that bind to cyclin-CDK complexes and block progression through the cell cycle.	bind
16505	3	6210	5	NULL	NULL	0	NULL	CDKs	NULL	kinase activity of	inhibited by	NULL				CDK inhibitors	NULL	group of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_1_175_s_17	9665478	1 The kinase activity of CDKs can be inhibited by a group of CDK inhibitors that bind to cyclin-CDK complexes and block progression through the cell cycle.	bind
20896	1	6210	7	NULL	NULL	NULL	NULL	CDK  inhibitors	Chemical		inhibit					CDKs	GP	kinase activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_1_175_s_17	9665478	1 The kinase activity of CDKs can be inhibited by a group of CDK inhibitors that bind to cyclin-CDK complexes and block progression through the cell cycle.	bind
20897	2	6210	7	NULL	NULL	NULL	NULL	CDK inhibitors	Chemical		bind					cyclin-CDK complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_1_175_s_17	9665478	1 The kinase activity of CDKs can be inhibited by a group of CDK inhibitors that bind to cyclin-CDK complexes and block progression through the cell cycle.	bind
20898	3	6210	7	NULL	NULL	NULL	NULL	statement 2	Process		block					cell cycle	Process	progression through			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_1_175_s_17	9665478	1 The kinase activity of CDKs can be inhibited by a group of CDK inhibitors that bind to cyclin-CDK complexes and block progression through the cell cycle.	bind
16506	1	6211	5	NULL	NULL	0	NULL	genomic DNA fragments	NULL	chicken	bind	NULL				v-Myb	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_31_21986_s_29	10419522	1 The Myb consensus sequence was first deduced by isolation of chicken genomic DNA fragments bound by v-Myb on filters ( 13) and from comparison of putative Myb binding sites within the SV40 enhancer ( 14).	bind
20907	1	6211	7	NULL	NULL	NULL	NULL	genomic DNA fragments	NucleicAcid	chicken	bind					v-Myb	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_31_21986_s_29	10419522	1 The Myb consensus sequence was first deduced by isolation of chicken genomic DNA fragments bound by v-Myb on filters ( 13) and from comparison of putative Myb binding sites within the SV40 enhancer ( 14).	bind
16507	1	6212	5	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				BSF lysate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_48_32102_s_192	9822686	1 The pattern of GTP-bound bands was essentially identical, while significantly more GTP was bound by BSF lysate than procyclic.	bind
20917	1	6212	7	NULL	NULL	NULL	NULL	BSF lysate	OrganismPart		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_32102_s_192	9822686	1 The pattern of GTP-bound bands was essentially identical, while significantly more GTP was bound by BSF lysate than procyclic.	bind
16575	1	6213	5	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL				GP IIb/IIa complex	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_104_12_1374_s_15	11560852	1 The primary mechanism of action of GP IIb/IIIa antagonists is inhibition of the final common pathway of platelet aggregation: fibrinogen or von Willebrand factor binding to the GP IIb/IIa complex.	bind
16576	2	6213	5	NULL	NULL	0	NULL	von Willebrand factor	NULL		bind	NULL				GP IIb/IIa complex	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_104_12_1374_s_15	11560852	1 The primary mechanism of action of GP IIb/IIIa antagonists is inhibition of the final common pathway of platelet aggregation: fibrinogen or von Willebrand factor binding to the GP IIb/IIa complex.	bind
16577	3	6213	5	NULL	NULL	0	NULL	GP IIb/IIIa antagonists	NULL		inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_104_12_1374_s_15	11560852	1 The primary mechanism of action of GP IIb/IIIa antagonists is inhibition of the final common pathway of platelet aggregation: fibrinogen or von Willebrand factor binding to the GP IIb/IIa complex.	bind
16578	4	6213	5	NULL	NULL	0	NULL	GP IIb/IIIa antagonists	NULL		inhibit	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_104_12_1374_s_15	11560852	1 The primary mechanism of action of GP IIb/IIIa antagonists is inhibition of the final common pathway of platelet aggregation: fibrinogen or von Willebrand factor binding to the GP IIb/IIa complex.	bind
20918	1	6213	7	NULL	NULL	NULL	NULL	fibrinogen	GP		bind					GP IIb/IIa complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_12_1374_s_15	11560852	1 The primary mechanism of action of GP IIb/IIIa antagonists is inhibition of the final common pathway of platelet aggregation: fibrinogen or von Willebrand factor binding to the GP IIb/IIa complex.	bind
20919	2	6213	7	NULL	NULL	NULL	NULL	von Willebrand factor	GP		bind					GP IIb/IIa complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_12_1374_s_15	11560852	1 The primary mechanism of action of GP IIb/IIIa antagonists is inhibition of the final common pathway of platelet aggregation: fibrinogen or von Willebrand factor binding to the GP IIb/IIa complex.	bind
20920	3	6213	7	NULL	NULL	NULL	NULL	GP IIb/IIIa antagonists	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_12_1374_s_15	11560852	1 The primary mechanism of action of GP IIb/IIIa antagonists is inhibition of the final common pathway of platelet aggregation: fibrinogen or von Willebrand factor binding to the GP IIb/IIa complex.	bind
20921	4	6213	7	NULL	NULL	NULL	NULL	GP IIb/IIIa antagonists	GP		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_12_1374_s_15	11560852	1 The primary mechanism of action of GP IIb/IIIa antagonists is inhibition of the final common pathway of platelet aggregation: fibrinogen or von Willebrand factor binding to the GP IIb/IIa complex.	bind
16579	1	6214	5	NULL	NULL	0	NULL	A-GLUT1(DTE)	NULL		bind	NULL				pCMB	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1618_1_8_s_404	14643928	1 The residual DTE in the vesicle suspension (approximately 5  M after cytoskeleton-depletion  in the presence of 0.2 mM DTE and washing once with Tris-HCl buffer [ 8) was diluted two-fold upon anion exchange chromatography to obtain A-GLUT1(DTE) and did not affect the binding of A-GLUT1(DTE) to pCMB-Sepharose 4B significantly.	bind
16580	2	6214	5	NULL	NULL	0	NULL	DTE	NULL	residual in the vesicle suspension	did not affect	NULL	significantly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1618_1_8_s_404	14643928	1 The residual DTE in the vesicle suspension (approximately 5  M after cytoskeleton-depletion  in the presence of 0.2 mM DTE and washing once with Tris-HCl buffer [ 8) was diluted two-fold upon anion exchange chromatography to obtain A-GLUT1(DTE) and did not affect the binding of A-GLUT1(DTE) to pCMB-Sepharose 4B significantly.	bind
20922	1	6214	7	NULL	NULL	NULL	NULL	A-GLUT1(DTE)	Chemical		bind					pCMB	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1618_1_8_s_404	14643928	1 The residual DTE in the vesicle suspension (approximately 5  M after cytoskeleton-depletion  in the presence of 0.2 mM DTE and washing once with Tris-HCl buffer [ 8) was diluted two-fold upon anion exchange chromatography to obtain A-GLUT1(DTE) and did not affect the binding of A-GLUT1(DTE) to pCMB-Sepharose 4B significantly.	bind
24175	2	6214	7	NULL	NULL	NULL	NULL	DTE	Chemical	residual in the vesicle suspension	did not affect		significantly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1618_1_8_s_404	14643928	1 The residual DTE in the vesicle suspension (approximately 5  M after cytoskeleton-depletion  in the presence of 0.2 mM DTE and washing once with Tris-HCl buffer [ 8) was diluted two-fold upon anion exchange chromatography to obtain A-GLUT1(DTE) and did not affect the binding of A-GLUT1(DTE) to pCMB-Sepharose 4B significantly.	bind
16581	1	6215	5	NULL	NULL	0	NULL	APC	NULL		is	NULL				activated protein C	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_9_1371_s_19	9743224	1 The zymogen protein C is converted to the active protease, activated protein C (APC), through proteolytic cleavage by thrombin bound to its endothelial membrane receptor thrombomodulin.	bind
16582	2	6215	5	10	NULL	0	NULL	zymogen protein C	NULL		is converted to	NULL				APC	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_9_1371_s_19	9743224	1 The zymogen protein C is converted to the active protease, activated protein C (APC), through proteolytic cleavage by thrombin bound to its endothelial membrane receptor thrombomodulin.	bind
16583	3	6215	5	10	NULL	0	NULL	thrombin	NULL		bind	NULL				thrombomodulin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_9_1371_s_19	9743224	1 The zymogen protein C is converted to the active protease, activated protein C (APC), through proteolytic cleavage by thrombin bound to its endothelial membrane receptor thrombomodulin.	bind
16584	4	6215	5	NULL	NULL	0	NULL	statement 2	NULL		occurs through	NULL				statement 3	NULL	proteolytic cleavage by			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_9_1371_s_19	9743224	1 The zymogen protein C is converted to the active protease, activated protein C (APC), through proteolytic cleavage by thrombin bound to its endothelial membrane receptor thrombomodulin.	bind
45208	5	6215	5	10	NULL	0	NULL	APC	NULL		is a type of	NULL				active protease	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_9_1371_s_19	9743224	1 The zymogen protein C is converted to the active protease, activated protein C (APC), through proteolytic cleavage by thrombin bound to its endothelial membrane receptor thrombomodulin.	bind
45209	6	6215	5	10	NULL	0	NULL	thrombomodulin \t	NULL		is a type of	NULL				endothelial membrane receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_9_1371_s_19	9743224	1 The zymogen protein C is converted to the active protease, activated protein C (APC), through proteolytic cleavage by thrombin bound to its endothelial membrane receptor thrombomodulin.	bind
20925	1	6215	7	NULL	NULL	NULL	NULL	zymogen protein C	GP		converts to					APC	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_9_1371_s_19	9743224	1 The zymogen protein C is converted to the active protease, activated protein C (APC), through proteolytic cleavage by thrombin bound to its endothelial membrane receptor thrombomodulin.	bind
20926	3	6215	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs through					thrombin	GP	proteolytic cleavage by			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_9_1371_s_19	9743224	1 The zymogen protein C is converted to the active protease, activated protein C (APC), through proteolytic cleavage by thrombin bound to its endothelial membrane receptor thrombomodulin.	bind
20927	2	6215	7	NULL	NULL	NULL	NULL	thrombin	GP		bind					thrombomodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_9_1371_s_19	9743224	1 The zymogen protein C is converted to the active protease, activated protein C (APC), through proteolytic cleavage by thrombin bound to its endothelial membrane receptor thrombomodulin.	bind
20930	4	6215	7	NULL	NULL	NULL	NULL	APC	GP		is					activated protein C	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_9_1371_s_19	9743224	1 The zymogen protein C is converted to the active protease, activated protein C (APC), through proteolytic cleavage by thrombin bound to its endothelial membrane receptor thrombomodulin.	bind
45210	5	6215	7	NULL	NULL	NULL	NULL	APC	GP		is a type of					active protease	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_9_1371_s_19	9743224	1 The zymogen protein C is converted to the active protease, activated protein C (APC), through proteolytic cleavage by thrombin bound to its endothelial membrane receptor thrombomodulin.	bind
54166	6	6215	7	NULL	NULL	NULL	NULL	thrombomodulin	GP		is a type of					endothelial membrane receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_9_1371_s_19	9743224	1 The zymogen protein C is converted to the active protease, activated protein C (APC), through proteolytic cleavage by thrombin bound to its endothelial membrane receptor thrombomodulin.	bind
16585	1	6217	5	10	NULL	0	NULL	Tim44	NULL		bind	NULL				mtHsp70	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31608_s_30	16027163	1 Tim44 is a peripheral membrane protein that binds both to mtHsp70 and to the translocation channel and thereby recruits the chaperone to the channel.	bind
16586	2	6217	5	10	NULL	0	NULL	Tim44	NULL		bind	NULL				translocation channel	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31608_s_30	16027163	1 Tim44 is a peripheral membrane protein that binds both to mtHsp70 and to the translocation channel and thereby recruits the chaperone to the channel.	bind
16587	3	6217	5	10	NULL	0	NULL	statement 2			leads to					statement 5					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31608_s_30	16027163	1 Tim44 is a peripheral membrane protein that binds both to mtHsp70 and to the translocation channel and thereby recruits the chaperone to the channel.	bind
45300	4	6217	5	10	NULL	0	NULL	Tim44	NULL		is a type of	NULL				peripheral membrane protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_36_31608_s_30	16027163	1 Tim44 is a peripheral membrane protein that binds both to mtHsp70 and to the translocation channel and thereby recruits the chaperone to the channel.	bind
54167	5	6217	5	10	NULL	0	NULL	chaperone			is recruited to					channel					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_36_31608_s_30	16027163	1 Tim44 is a peripheral membrane protein that binds both to mtHsp70 and to the translocation channel and thereby recruits the chaperone to the channel.	bind
20934	1	6217	7	NULL	NULL	NULL	NULL	Tim44	GP		binds					mtHsp70	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31608_s_30	16027163	1 Tim44 is a peripheral membrane protein that binds both to mtHsp70 and to the translocation channel and thereby recruits the chaperone to the channel.	bind
20935	2	6217	7	NULL	NULL	NULL	NULL	Tim44	GP		binds					translocation channel	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31608_s_30	16027163	1 Tim44 is a peripheral membrane protein that binds both to mtHsp70 and to the translocation channel and thereby recruits the chaperone to the channel.	bind
20936	3	6217	7	NULL	NULL	NULL	NULL	statement 2	Process		leads to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31608_s_30	16027163	1 Tim44 is a peripheral membrane protein that binds both to mtHsp70 and to the translocation channel and thereby recruits the chaperone to the channel.	bind
45301	4	6217	7	NULL	NULL	NULL	NULL	Tim44	GP		is a type of					peripheral membrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31608_s_30	16027163	1 Tim44 is a peripheral membrane protein that binds both to mtHsp70 and to the translocation channel and thereby recruits the chaperone to the channel.	bind
54168	5	6217	7	NULL	NULL	NULL	NULL	chaperone	GP		is recruited to					channel	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31608_s_30	16027163	1 Tim44 is a peripheral membrane protein that binds both to mtHsp70 and to the translocation channel and thereby recruits the chaperone to the channel.	bind
16588	1	6218	5	NULL	NULL	0	NULL	BPA	NULL		is	NULL				bisphenol A	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_138_7_1271_s_2	12711627	1 We investigated the effect of bisphenol A (BPA), which binds estrogen receptors, on immune responses including production of antigen-specific antibodies, proliferative responses of lymphoid cells, and Th1 and Th2 responses.	bind
16589	2	6218	5	NULL	NULL	0	NULL	BPA	NULL		bind	NULL				estrogen receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_138_7_1271_s_2	12711627	1 We investigated the effect of bisphenol A (BPA), which binds estrogen receptors, on immune responses including production of antigen-specific antibodies, proliferative responses of lymphoid cells, and Th1 and Th2 responses.	bind
20937	1	6218	7	NULL	NULL	NULL	NULL	BPA	Chemical		binds					 estrogen receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_7_1271_s_2	12711627	1 We investigated the effect of bisphenol A (BPA), which binds estrogen receptors, on immune responses including production of antigen-specific antibodies, proliferative responses of lymphoid cells, and Th1 and Th2 responses.	bind
20938	2	6218	7	NULL	NULL	NULL	NULL	BPA	Chemical		is					bisphenol A	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_7_1271_s_2	12711627	1 We investigated the effect of bisphenol A (BPA), which binds estrogen receptors, on immune responses including production of antigen-specific antibodies, proliferative responses of lymphoid cells, and Th1 and Th2 responses.	bind
16590	1	6219	5	NULL	NULL	0	NULL	TF	NULL		bind	NULL				factor VII	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_96_12_4232_s_15	9416887	1 When exposed to blood, TF binds to factor VII, and the resulting complex activates factors IX and X, leading to thrombin and fibrin generation.	bind
16591	2	6219	5	10	NULL	0	NULL	statement 1			occurs on					blood		exposure to			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_12_4232_s_15	9416887	1 When exposed to blood, TF binds to factor VII, and the resulting complex activates factors IX and X, leading to thrombin and fibrin generation.	bind
16592	3	6219	5	NULL	NULL	0	NULL	statement 1	NULL		activate	NULL				factor IX	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_96_12_4232_s_15	9416887	1 When exposed to blood, TF binds to factor VII, and the resulting complex activates factors IX and X, leading to thrombin and fibrin generation.	bind
16593	4	6219	5	NULL	NULL	0	NULL	statement 1	NULL		activate	NULL				factor X	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_96_12_4232_s_15	9416887	1 When exposed to blood, TF binds to factor VII, and the resulting complex activates factors IX and X, leading to thrombin and fibrin generation.	bind
16594	5	6219	5	NULL	NULL	0	NULL	statement 3	NULL		leads to	NULL				thrombin	NULL	generation of			NULL		0	NULL	NULL	NULL	gw60_circulation_96_12_4232_s_15	9416887	1 When exposed to blood, TF binds to factor VII, and the resulting complex activates factors IX and X, leading to thrombin and fibrin generation.	bind
16595	6	6219	5	NULL	NULL	0	NULL	statement 3	NULL		leads to	NULL				fibrin	NULL	generation of			NULL		0	NULL	NULL	NULL	gw60_circulation_96_12_4232_s_15	9416887	1 When exposed to blood, TF binds to factor VII, and the resulting complex activates factors IX and X, leading to thrombin and fibrin generation.	bind
16596	7	6219	5	NULL	NULL	0	NULL	statement 4	NULL		leads to	NULL				thrombin	NULL	generation of			NULL		0	NULL	NULL	NULL	gw60_circulation_96_12_4232_s_15	9416887	1 When exposed to blood, TF binds to factor VII, and the resulting complex activates factors IX and X, leading to thrombin and fibrin generation.	bind
16597	8	6219	5	NULL	NULL	0	NULL	statement 4	NULL		leads to	NULL				fibrin	NULL	generation of			NULL		0	NULL	NULL	NULL	gw60_circulation_96_12_4232_s_15	9416887	1 When exposed to blood, TF binds to factor VII, and the resulting complex activates factors IX and X, leading to thrombin and fibrin generation.	bind
20939	1	6219	7	NULL	NULL	NULL	NULL	TF	GP		binds to					factor VII	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_12_4232_s_15	9416887	1 When exposed to blood, TF binds to factor VII, and the resulting complex activates factors IX and X, leading to thrombin and fibrin generation.	bind
20940	2	6219	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs upon					blood	OrganismPart	exposure to			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_12_4232_s_15	9416887	1 When exposed to blood, TF binds to factor VII, and the resulting complex activates factors IX and X, leading to thrombin and fibrin generation.	bind
20941	3	6219	7	NULL	NULL	NULL	NULL	statement 1	Process		activates					factors IX	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_12_4232_s_15	9416887	1 When exposed to blood, TF binds to factor VII, and the resulting complex activates factors IX and X, leading to thrombin and fibrin generation.	bind
20942	4	6219	7	NULL	NULL	NULL	NULL	statement 1	Process		activates					factor X	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_12_4232_s_15	9416887	1 When exposed to blood, TF binds to factor VII, and the resulting complex activates factors IX and X, leading to thrombin and fibrin generation.	bind
20943	5	6219	7	NULL	NULL	NULL	NULL	statement 3	Process		leads to					thrombin	GP	generation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_12_4232_s_15	9416887	1 When exposed to blood, TF binds to factor VII, and the resulting complex activates factors IX and X, leading to thrombin and fibrin generation.	bind
20944	6	6219	7	NULL	NULL	NULL	NULL	statement 3	Process		leads to					fibrin	GP	generation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_12_4232_s_15	9416887	1 When exposed to blood, TF binds to factor VII, and the resulting complex activates factors IX and X, leading to thrombin and fibrin generation.	bind
20945	7	6219	7	NULL	NULL	NULL	NULL	statement 4	Process		leads to					thrombin	GP	generation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_12_4232_s_15	9416887	1 When exposed to blood, TF binds to factor VII, and the resulting complex activates factors IX and X, leading to thrombin and fibrin generation.	bind
20946	8	6219	7	NULL	NULL	NULL	NULL	statement 4	Process		leads to					fibrin	GP	generation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_12_4232_s_15	9416887	1 When exposed to blood, TF binds to factor VII, and the resulting complex activates factors IX and X, leading to thrombin and fibrin generation.	bind
16600	1	6220	5	NULL	NULL	0	NULL	GST CD-MPR peptide	NULL		bind	NULL					NULL		VHS domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18477_s_118	11886874	1% of the pellet ( P) and supernatant ( S) were resolved on 10% SDS gels, transferred to nitrocellulose, and probed with either the anti-Myc or anti-HA antibody as described under   *, highlights the fact that the GST CD-MPR peptide does bind to the VHS domain albeit very weakly relative to the GST CI-MPR peptide, 25% of pellet and 5% of supernatant were loaded in this case.	bind
16604	2	6220	5	NULL	NULL	0	NULL	GST CI-MPR peptide	NULL		bind	NULL					NULL		VHS domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18477_s_118	11886874	1% of the pellet ( P) and supernatant ( S) were resolved on 10% SDS gels, transferred to nitrocellulose, and probed with either the anti-Myc or anti-HA antibody as described under   *, highlights the fact that the GST CD-MPR peptide does bind to the VHS domain albeit very weakly relative to the GST CI-MPR peptide, 25% of pellet and 5% of supernatant were loaded in this case.	bind
16605	3	6220	5	NULL	NULL	0	NULL	statement 1	NULL		very weak relative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18477_s_118	11886874	1% of the pellet ( P) and supernatant ( S) were resolved on 10% SDS gels, transferred to nitrocellulose, and probed with either the anti-Myc or anti-HA antibody as described under   *, highlights the fact that the GST CD-MPR peptide does bind to the VHS domain albeit very weakly relative to the GST CI-MPR peptide, 25% of pellet and 5% of supernatant were loaded in this case.	bind
21007	1	6220	7	NULL	NULL	NULL	NULL	GST CD-MPR peptide	GP		bind		weakly						VHS domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18477_s_118	11886874	1% of the pellet ( P) and supernatant ( S) were resolved on 10% SDS gels, transferred to nitrocellulose, and probed with either the anti-Myc or anti-HA antibody as described under   *, highlights the fact that the GST CD-MPR peptide does bind to the VHS domain albeit very weakly relative to the GST CI-MPR peptide, 25% of pellet and 5% of supernatant were loaded in this case.	bind
21008	2	6220	7	NULL	NULL	NULL	NULL	GST CI-MPR peptide	GP		bind								VHS domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18477_s_118	11886874	1% of the pellet ( P) and supernatant ( S) were resolved on 10% SDS gels, transferred to nitrocellulose, and probed with either the anti-Myc or anti-HA antibody as described under   *, highlights the fact that the GST CD-MPR peptide does bind to the VHS domain albeit very weakly relative to the GST CI-MPR peptide, 25% of pellet and 5% of supernatant were loaded in this case.	bind
21009	3	6220	7	NULL	NULL	NULL	NULL	statement 1	Process		is weaker than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18477_s_118	11886874	1% of the pellet ( P) and supernatant ( S) were resolved on 10% SDS gels, transferred to nitrocellulose, and probed with either the anti-Myc or anti-HA antibody as described under   *, highlights the fact that the GST CD-MPR peptide does bind to the VHS domain albeit very weakly relative to the GST CI-MPR peptide, 25% of pellet and 5% of supernatant were loaded in this case.	bind
16610	1	6221	5	10	NULL	0	NULL	FXI	NULL	bound	is associated with	NULL				membrane rafts	NULL				NULL	TRAP-activated platelets	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_24_21744_s_192	12517745	1)   5 - 8% of bound FXI is associated with membrane rafts in  TRAP-activated platelets (Figs.   2 and   3,  A and  B);  2) FXI-raft association was disrupted by cholesterol depletion  ( Fig. 4); 3) FXI binds to lipid  rafts through the A3 domain ( Fig.  6 A); 4) the SZ-2 antibody blocks the binding of FXI to  lipid rafts suggesting FXI interacts with GPIb in lipid rafts  ( Fig. 6 B); and 5) the  initial rate of FXI activation by thrombin on activated platelets was  inhibited >85% by cholesterol depletion leading to raft disruption  ( Fig. 7).	bind
16612	2	6221	5	10	NULL	0	NULL	cholesterol	NULL	depletion of	disrupt	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_24_21744_s_192	12517745	1)   5 - 8% of bound FXI is associated with membrane rafts in  TRAP-activated platelets (Figs.   2 and   3,  A and  B);  2) FXI-raft association was disrupted by cholesterol depletion  ( Fig. 4); 3) FXI binds to lipid  rafts through the A3 domain ( Fig.  6 A); 4) the SZ-2 antibody blocks the binding of FXI to  lipid rafts suggesting FXI interacts with GPIb in lipid rafts  ( Fig. 6 B); and 5) the  initial rate of FXI activation by thrombin on activated platelets was  inhibited >85% by cholesterol depletion leading to raft disruption  ( Fig. 7).	bind
16613	3	6221	5	NULL	NULL	0	NULL	FXI	NULL		bind	NULL		A3 domain		lipid rafts	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_24_21744_s_192	12517745	1)   5 - 8% of bound FXI is associated with membrane rafts in  TRAP-activated platelets (Figs.   2 and   3,  A and  B);  2) FXI-raft association was disrupted by cholesterol depletion  ( Fig. 4); 3) FXI binds to lipid  rafts through the A3 domain ( Fig.  6 A); 4) the SZ-2 antibody blocks the binding of FXI to  lipid rafts suggesting FXI interacts with GPIb in lipid rafts  ( Fig. 6 B); and 5) the  initial rate of FXI activation by thrombin on activated platelets was  inhibited >85% by cholesterol depletion leading to raft disruption  ( Fig. 7).	bind
16615	4	6221	5	NULL	NULL	0	NULL	SZ-2 antibody	NULL		block	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_24_21744_s_192	12517745	1)   5 - 8% of bound FXI is associated with membrane rafts in  TRAP-activated platelets (Figs.   2 and   3,  A and  B);  2) FXI-raft association was disrupted by cholesterol depletion  ( Fig. 4); 3) FXI binds to lipid  rafts through the A3 domain ( Fig.  6 A); 4) the SZ-2 antibody blocks the binding of FXI to  lipid rafts suggesting FXI interacts with GPIb in lipid rafts  ( Fig. 6 B); and 5) the  initial rate of FXI activation by thrombin on activated platelets was  inhibited >85% by cholesterol depletion leading to raft disruption  ( Fig. 7).	bind
16616	5	6221	5	NULL	NULL	0	NULL	FXI	NULL		interact with	NULL				GPIb	NULL				NULL	in lipid rafts	0	NULL	NULL	NULL	gw70_jbiolchem_278_24_21744_s_192	12517745	1)   5 - 8% of bound FXI is associated with membrane rafts in  TRAP-activated platelets (Figs.   2 and   3,  A and  B);  2) FXI-raft association was disrupted by cholesterol depletion  ( Fig. 4); 3) FXI binds to lipid  rafts through the A3 domain ( Fig.  6 A); 4) the SZ-2 antibody blocks the binding of FXI to  lipid rafts suggesting FXI interacts with GPIb in lipid rafts  ( Fig. 6 B); and 5) the  initial rate of FXI activation by thrombin on activated platelets was  inhibited >85% by cholesterol depletion leading to raft disruption  ( Fig. 7).	bind
16618	6	6221	5	NULL	NULL	0	NULL	statement 4	NULL		suggest	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_24_21744_s_192	12517745	1)   5 - 8% of bound FXI is associated with membrane rafts in  TRAP-activated platelets (Figs.   2 and   3,  A and  B);  2) FXI-raft association was disrupted by cholesterol depletion  ( Fig. 4); 3) FXI binds to lipid  rafts through the A3 domain ( Fig.  6 A); 4) the SZ-2 antibody blocks the binding of FXI to  lipid rafts suggesting FXI interacts with GPIb in lipid rafts  ( Fig. 6 B); and 5) the  initial rate of FXI activation by thrombin on activated platelets was  inhibited >85% by cholesterol depletion leading to raft disruption  ( Fig. 7).	bind
16622	7	6221	5	NULL	NULL	0	NULL	thrombin	NULL		activate	NULL				FXI	NULL				NULL	on activated platelets	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_24_21744_s_192	12517745	1)   5 - 8% of bound FXI is associated with membrane rafts in  TRAP-activated platelets (Figs.   2 and   3,  A and  B);  2) FXI-raft association was disrupted by cholesterol depletion  ( Fig. 4); 3) FXI binds to lipid  rafts through the A3 domain ( Fig.  6 A); 4) the SZ-2 antibody blocks the binding of FXI to  lipid rafts suggesting FXI interacts with GPIb in lipid rafts  ( Fig. 6 B); and 5) the  initial rate of FXI activation by thrombin on activated platelets was  inhibited >85% by cholesterol depletion leading to raft disruption  ( Fig. 7).	bind
16625	8	6221	5	10	NULL	0	NULL	cholesterol	NULL	depletion of 	inhibit	NULL				statement 7	NULL	initial rate of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_24_21744_s_192	12517745	1)   5 - 8% of bound FXI is associated with membrane rafts in  TRAP-activated platelets (Figs.   2 and   3,  A and  B);  2) FXI-raft association was disrupted by cholesterol depletion  ( Fig. 4); 3) FXI binds to lipid  rafts through the A3 domain ( Fig.  6 A); 4) the SZ-2 antibody blocks the binding of FXI to  lipid rafts suggesting FXI interacts with GPIb in lipid rafts  ( Fig. 6 B); and 5) the  initial rate of FXI activation by thrombin on activated platelets was  inhibited >85% by cholesterol depletion leading to raft disruption  ( Fig. 7).	bind
16627	9	6221	5	10	NULL	0	NULL	statement 8			leads to					raft		disruption of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_24_21744_s_192	12517745	1)   5 - 8% of bound FXI is associated with membrane rafts in  TRAP-activated platelets (Figs.   2 and   3,  A and  B);  2) FXI-raft association was disrupted by cholesterol depletion  ( Fig. 4); 3) FXI binds to lipid  rafts through the A3 domain ( Fig.  6 A); 4) the SZ-2 antibody blocks the binding of FXI to  lipid rafts suggesting FXI interacts with GPIb in lipid rafts  ( Fig. 6 B); and 5) the  initial rate of FXI activation by thrombin on activated platelets was  inhibited >85% by cholesterol depletion leading to raft disruption  ( Fig. 7).	bind
21010	1	6221	7	NULL	NULL	NULL	NULL	FXI	GP	bound	associate with					membrane rafts	CellComponent				NULL	TRAP-activated platelets	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_24_21744_s_192	12517745	1)   5 - 8% of bound FXI is associated with membrane rafts in  TRAP-activated platelets (Figs.   2 and   3,  A and  B);  2) FXI-raft association was disrupted by cholesterol depletion  ( Fig. 4); 3) FXI binds to lipid  rafts through the A3 domain ( Fig.  6 A); 4) the SZ-2 antibody blocks the binding of FXI to  lipid rafts suggesting FXI interacts with GPIb in lipid rafts  ( Fig. 6 B); and 5) the  initial rate of FXI activation by thrombin on activated platelets was  inhibited >85% by cholesterol depletion leading to raft disruption  ( Fig. 7).	bind
21011	2	6221	7	NULL	NULL	NULL	NULL	cholesterol	Chemical	depletion of	disrupts					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_24_21744_s_192	12517745	1)   5 - 8% of bound FXI is associated with membrane rafts in  TRAP-activated platelets (Figs.   2 and   3,  A and  B);  2) FXI-raft association was disrupted by cholesterol depletion  ( Fig. 4); 3) FXI binds to lipid  rafts through the A3 domain ( Fig.  6 A); 4) the SZ-2 antibody blocks the binding of FXI to  lipid rafts suggesting FXI interacts with GPIb in lipid rafts  ( Fig. 6 B); and 5) the  initial rate of FXI activation by thrombin on activated platelets was  inhibited >85% by cholesterol depletion leading to raft disruption  ( Fig. 7).	bind
21012	3	6221	7	NULL	NULL	NULL	NULL	FXI 	GP		bind			A3 domain		lipid rafts	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_24_21744_s_192	12517745	1)   5 - 8% of bound FXI is associated with membrane rafts in  TRAP-activated platelets (Figs.   2 and   3,  A and  B);  2) FXI-raft association was disrupted by cholesterol depletion  ( Fig. 4); 3) FXI binds to lipid  rafts through the A3 domain ( Fig.  6 A); 4) the SZ-2 antibody blocks the binding of FXI to  lipid rafts suggesting FXI interacts with GPIb in lipid rafts  ( Fig. 6 B); and 5) the  initial rate of FXI activation by thrombin on activated platelets was  inhibited >85% by cholesterol depletion leading to raft disruption  ( Fig. 7).	bind
21013	4	6221	7	NULL	NULL	NULL	NULL	 SZ-2 antibody	GP		blocks					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_24_21744_s_192	12517745	1)   5 - 8% of bound FXI is associated with membrane rafts in  TRAP-activated platelets (Figs.   2 and   3,  A and  B);  2) FXI-raft association was disrupted by cholesterol depletion  ( Fig. 4); 3) FXI binds to lipid  rafts through the A3 domain ( Fig.  6 A); 4) the SZ-2 antibody blocks the binding of FXI to  lipid rafts suggesting FXI interacts with GPIb in lipid rafts  ( Fig. 6 B); and 5) the  initial rate of FXI activation by thrombin on activated platelets was  inhibited >85% by cholesterol depletion leading to raft disruption  ( Fig. 7).	bind
21014	5	6221	7	NULL	NULL	NULL	NULL	FXI	GP		interacts with					GPIb	GP				NULL	lipid rafts	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_24_21744_s_192	12517745	1)   5 - 8% of bound FXI is associated with membrane rafts in  TRAP-activated platelets (Figs.   2 and   3,  A and  B);  2) FXI-raft association was disrupted by cholesterol depletion  ( Fig. 4); 3) FXI binds to lipid  rafts through the A3 domain ( Fig.  6 A); 4) the SZ-2 antibody blocks the binding of FXI to  lipid rafts suggesting FXI interacts with GPIb in lipid rafts  ( Fig. 6 B); and 5) the  initial rate of FXI activation by thrombin on activated platelets was  inhibited >85% by cholesterol depletion leading to raft disruption  ( Fig. 7).	bind
21015	6	6221	7	NULL	NULL	NULL	NULL	thrombin	GP		activates					FXI	GP				NULL	activated platelets	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_24_21744_s_192	12517745	1)   5 - 8% of bound FXI is associated with membrane rafts in  TRAP-activated platelets (Figs.   2 and   3,  A and  B);  2) FXI-raft association was disrupted by cholesterol depletion  ( Fig. 4); 3) FXI binds to lipid  rafts through the A3 domain ( Fig.  6 A); 4) the SZ-2 antibody blocks the binding of FXI to  lipid rafts suggesting FXI interacts with GPIb in lipid rafts  ( Fig. 6 B); and 5) the  initial rate of FXI activation by thrombin on activated platelets was  inhibited >85% by cholesterol depletion leading to raft disruption  ( Fig. 7).	bind
21016	7	6221	7	NULL	NULL	NULL	NULL	cholesterol	Chemical	depletion of	inhibits					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_24_21744_s_192	12517745	1)   5 - 8% of bound FXI is associated with membrane rafts in  TRAP-activated platelets (Figs.   2 and   3,  A and  B);  2) FXI-raft association was disrupted by cholesterol depletion  ( Fig. 4); 3) FXI binds to lipid  rafts through the A3 domain ( Fig.  6 A); 4) the SZ-2 antibody blocks the binding of FXI to  lipid rafts suggesting FXI interacts with GPIb in lipid rafts  ( Fig. 6 B); and 5) the  initial rate of FXI activation by thrombin on activated platelets was  inhibited >85% by cholesterol depletion leading to raft disruption  ( Fig. 7).	bind
21017	8	6221	7	NULL	NULL	NULL	NULL	statement 7	Process		disrupts					rafts	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_24_21744_s_192	12517745	1)   5 - 8% of bound FXI is associated with membrane rafts in  TRAP-activated platelets (Figs.   2 and   3,  A and  B);  2) FXI-raft association was disrupted by cholesterol depletion  ( Fig. 4); 3) FXI binds to lipid  rafts through the A3 domain ( Fig.  6 A); 4) the SZ-2 antibody blocks the binding of FXI to  lipid rafts suggesting FXI interacts with GPIb in lipid rafts  ( Fig. 6 B); and 5) the  initial rate of FXI activation by thrombin on activated platelets was  inhibited >85% by cholesterol depletion leading to raft disruption  ( Fig. 7).	bind
19280	1	6222	5	NULL	NULL	0	NULL	ADIP	NULL		bind	NULL				alpha-actinin	NULL				NULL	extracts of HEK293 cells exogenously expressing full-length ADIP	NULL	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_301	12446711	1) ADIP binds to alpha-actinin as estimated by the yeast two-hybrid analysis and co-immunoprecipitation from the extracts of HEK293 cells exogenously expressing the full-length ADIP or fragments; 2) recombinant ADIP directly binds to recombinant alpha-actinin in a cell-free system; and 3) endogenous ADIP and alpha-actinin are co-immunoprecipitated from the extracts of MDCK cells.	bind
19281	2	6222	5	NULL	NULL	0	NULL	ADIP	NULL		bind	NULL				alpha-actinin	NULL				NULL	extracts of HEK293 cells exogenously expressing fragments of ADIP	0	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_301	12446711	1) ADIP binds to alpha-actinin as estimated by the yeast two-hybrid analysis and co-immunoprecipitation from the extracts of HEK293 cells exogenously expressing the full-length ADIP or fragments; 2) recombinant ADIP directly binds to recombinant alpha-actinin in a cell-free system; and 3) endogenous ADIP and alpha-actinin are co-immunoprecipitated from the extracts of MDCK cells.	bind
19282	3	6222	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_301	12446711	1) ADIP binds to alpha-actinin as estimated by the yeast two-hybrid analysis and co-immunoprecipitation from the extracts of HEK293 cells exogenously expressing the full-length ADIP or fragments; 2) recombinant ADIP directly binds to recombinant alpha-actinin in a cell-free system; and 3) endogenous ADIP and alpha-actinin are co-immunoprecipitated from the extracts of MDCK cells.	bind
19283	4	6222	5	NULL	NULL	0	NULL	ADIP	NULL	recombinant	bind	NULL	directly			alpha-actinin	NULL	recombinant			NULL	cell-free system	0	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_301	12446711	1) ADIP binds to alpha-actinin as estimated by the yeast two-hybrid analysis and co-immunoprecipitation from the extracts of HEK293 cells exogenously expressing the full-length ADIP or fragments; 2) recombinant ADIP directly binds to recombinant alpha-actinin in a cell-free system; and 3) endogenous ADIP and alpha-actinin are co-immunoprecipitated from the extracts of MDCK cells.	bind
19284	5	6222	5	NULL	NULL	0	NULL	ADIP	NULL	endogenous	bind	NULL				alpha-actinin	NULL	endogenous			NULL	extracts of MDCK cells	0	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_301	12446711	1) ADIP binds to alpha-actinin as estimated by the yeast two-hybrid analysis and co-immunoprecipitation from the extracts of HEK293 cells exogenously expressing the full-length ADIP or fragments; 2) recombinant ADIP directly binds to recombinant alpha-actinin in a cell-free system; and 3) endogenous ADIP and alpha-actinin are co-immunoprecipitated from the extracts of MDCK cells.	bind
21018	1	6222	7	NULL	NULL	NULL	NULL	 ADIP	GP		bind					alpha-actinin	GP				NULL	HEK293 cells exogenously expressing the full-length ADIP	NULL	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_301	12446711	1) ADIP binds to alpha-actinin as estimated by the yeast two-hybrid analysis and co-immunoprecipitation from the extracts of HEK293 cells exogenously expressing the full-length ADIP or fragments; 2) recombinant ADIP directly binds to recombinant alpha-actinin in a cell-free system; and 3) endogenous ADIP and alpha-actinin are co-immunoprecipitated from the extracts of MDCK cells.	bind
21019	2	6222	7	NULL	NULL	NULL	NULL	ADIP	GP		bind					alpha-actinin	GP				NULL	HEK293 cells exogenously expressing the ADIP fragments	NULL	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_301	12446711	1) ADIP binds to alpha-actinin as estimated by the yeast two-hybrid analysis and co-immunoprecipitation from the extracts of HEK293 cells exogenously expressing the full-length ADIP or fragments; 2) recombinant ADIP directly binds to recombinant alpha-actinin in a cell-free system; and 3) endogenous ADIP and alpha-actinin are co-immunoprecipitated from the extracts of MDCK cells.	bind
21020	3	6222	7	NULL	NULL	NULL	NULL	ADIP	GP	recombinant	bind		directly			alpha-actinin	GP	recombinant			NULL	in a cell-free system	NULL	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_301	12446711	1) ADIP binds to alpha-actinin as estimated by the yeast two-hybrid analysis and co-immunoprecipitation from the extracts of HEK293 cells exogenously expressing the full-length ADIP or fragments; 2) recombinant ADIP directly binds to recombinant alpha-actinin in a cell-free system; and 3) endogenous ADIP and alpha-actinin are co-immunoprecipitated from the extracts of MDCK cells.	bind
21021	4	6222	7	NULL	NULL	NULL	NULL	ADIP 	GP	endogenous	bind					alpha-actinin	GP				NULL	MDCK cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_301	12446711	1) ADIP binds to alpha-actinin as estimated by the yeast two-hybrid analysis and co-immunoprecipitation from the extracts of HEK293 cells exogenously expressing the full-length ADIP or fragments; 2) recombinant ADIP directly binds to recombinant alpha-actinin in a cell-free system; and 3) endogenous ADIP and alpha-actinin are co-immunoprecipitated from the extracts of MDCK cells.	bind
55020	5	6222	7	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_301	12446711	1) ADIP binds to alpha-actinin as estimated by the yeast two-hybrid analysis and co-immunoprecipitation from the extracts of HEK293 cells exogenously expressing the full-length ADIP or fragments; 2) recombinant ADIP directly binds to recombinant alpha-actinin in a cell-free system; and 3) endogenous ADIP and alpha-actinin are co-immunoprecipitated from the extracts of MDCK cells.	bind
16629	1	6223	5	NULL	NULL	0	NULL	Agmatine	NULL		displace	NULL				MK-801	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_544_s_150	9918557	1) Agmatine is 10- to 100-fold more potent in displacing MK-801 binding than putrescine or spermine, respectively (Anis et al., 1990  ).	bind
16630	2	6223	5	NULL	NULL	0	NULL	putrescine	NULL		displace	NULL				MK-801	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_544_s_150	9918557	1) Agmatine is 10- to 100-fold more potent in displacing MK-801 binding than putrescine or spermine, respectively (Anis et al., 1990  ).	bind
16632	3	6223	5	NULL	NULL	0	NULL	spermine	NULL		displace	NULL				MK-801	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_544_s_150	9918557	1) Agmatine is 10- to 100-fold more potent in displacing MK-801 binding than putrescine or spermine, respectively (Anis et al., 1990  ).	bind
16634	4	6223	5	NULL	NULL	0	NULL	statement 1	NULL		more potent than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_544_s_150	9918557	1) Agmatine is 10- to 100-fold more potent in displacing MK-801 binding than putrescine or spermine, respectively (Anis et al., 1990  ).	bind
16636	5	6223	5	NULL	NULL	0	NULL	statement 1	NULL		more potent than	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_544_s_150	9918557	1) Agmatine is 10- to 100-fold more potent in displacing MK-801 binding than putrescine or spermine, respectively (Anis et al., 1990  ).	bind
21022	1	6223	7	NULL	NULL	NULL	NULL	Agmatine	Chemical		displace		significantly			MK-801	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_544_s_150	9918557	1) Agmatine is 10- to 100-fold more potent in displacing MK-801 binding than putrescine or spermine, respectively (Anis et al., 1990  ).	bind
21023	2	6223	7	NULL	NULL	NULL	NULL	putrescine	Chemical		displace					MK-801	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_544_s_150	9918557	1) Agmatine is 10- to 100-fold more potent in displacing MK-801 binding than putrescine or spermine, respectively (Anis et al., 1990  ).	bind
21024	3	6223	7	NULL	NULL	NULL	NULL	spermine	Chemical		displace					MK-801	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_544_s_150	9918557	1) Agmatine is 10- to 100-fold more potent in displacing MK-801 binding than putrescine or spermine, respectively (Anis et al., 1990  ).	bind
21025	4	6223	7	NULL	NULL	NULL	NULL	statement 1	Process		is more potent than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_544_s_150	9918557	1) Agmatine is 10- to 100-fold more potent in displacing MK-801 binding than putrescine or spermine, respectively (Anis et al., 1990  ).	bind
21026	5	6223	7	NULL	NULL	NULL	NULL	statement 1	Process		is more potent than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_544_s_150	9918557	1) Agmatine is 10- to 100-fold more potent in displacing MK-801 binding than putrescine or spermine, respectively (Anis et al., 1990  ).	bind
16642	1	6224	5	NULL	NULL	0	NULL	one G protein trimer 	NULL	only	bind	NULL				B4 receptor BLT1 dimeric complex	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24108_s_259	15056658	1) Applying chemical cross-linking of purified leukotriene B4 receptor BLT1 and Galphai2, beta1, and gamma2 proteins in a reconstituted system, Baneres and Parello ( ) used a combination of mass spectrometry and neutron scattering to established that only one G protein trimer binds to the dimeric complex of this receptor.	bind
21486	1	6224	7	NULL	NULL	NULL	NULL	G protein trimer	GP		binds					 BLT1 dimeric complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_23_24108_s_259	15056658	1) Applying chemical cross-linking of purified leukotriene B4 receptor BLT1 and Galphai2, beta1, and gamma2 proteins in a reconstituted system, Baneres and Parello ( ) used a combination of mass spectrometry and neutron scattering to established that only one G protein trimer binds to the dimeric complex of this receptor.	bind
67931	2	6224	7	NULL	NULL	0	NULL	BLT1	GP		is a type of					leukotriene B4 receptor	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24108_s_259	15056658	1) Applying chemical cross-linking of purified leukotriene B4 receptor BLT1 and Galphai2, beta1, and gamma2 proteins in a reconstituted system, Baneres and Parello ( ) used a combination of mass spectrometry and neutron scattering to established that only one G protein trimer binds to the dimeric complex of this receptor.	bind
16647	1	6225	5	NULL	NULL	0	NULL	N-end rule pathway	NULL		degrade	NULL				Arg-e -DHFRha	NULL				NULL	in ATP-supplemented reticulocyte extract	0	NULL	NULL	NULL	gw60_jbiolchem_270_14_8172_s_143	7713922	1) Arg-e -DHFRha ( Fig. 1 ) is degraded by the N-end  rule pathway in ATP-supplemented reticulocyte extract in the absence  but not in the presence of MTX, a folic acid analog and a competitive  inhibitor of DHFR which binds to mammalian DHFRs with a  K   of  10 M  ( Fig. 3  A).	bind
16648	2	6225	5	NULL	NULL	0	NULL	statement 1	NULL		in the absence of	NULL				MTX	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_14_8172_s_143	7713922	1) Arg-e -DHFRha ( Fig. 1 ) is degraded by the N-end  rule pathway in ATP-supplemented reticulocyte extract in the absence  but not in the presence of MTX, a folic acid analog and a competitive  inhibitor of DHFR which binds to mammalian DHFRs with a  K   of  10 M  ( Fig. 3  A).	bind
16649	3	6225	5	NULL	NULL	0	NULL	MTX	NULL		is a type of	NULL				folic acid analog	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_14_8172_s_143	7713922	1) Arg-e -DHFRha ( Fig. 1 ) is degraded by the N-end  rule pathway in ATP-supplemented reticulocyte extract in the absence  but not in the presence of MTX, a folic acid analog and a competitive  inhibitor of DHFR which binds to mammalian DHFRs with a  K   of  10 M  ( Fig. 3  A).	bind
16650	4	6225	5	NULL	NULL	0	NULL	MTX	NULL		is a type of	NULL				DHFR inhibitor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_14_8172_s_143	7713922	1) Arg-e -DHFRha ( Fig. 1 ) is degraded by the N-end  rule pathway in ATP-supplemented reticulocyte extract in the absence  but not in the presence of MTX, a folic acid analog and a competitive  inhibitor of DHFR which binds to mammalian DHFRs with a  K   of  10 M  ( Fig. 3  A).	bind
16651	5	6225	5	NULL	NULL	0	NULL	MTX	NULL		bind	NULL				DHFR	NULL	mammalian			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_14_8172_s_143	7713922	1) Arg-e -DHFRha ( Fig. 1 ) is degraded by the N-end  rule pathway in ATP-supplemented reticulocyte extract in the absence  but not in the presence of MTX, a folic acid analog and a competitive  inhibitor of DHFR which binds to mammalian DHFRs with a  K   of  10 M  ( Fig. 3  A).	bind
21066	1	6225	7	NULL	NULL	NULL	NULL	 Arg-e -DHFRha 	GP		is degraded by					N-end rule pathway	Process				NULL	ATP-supplemented reticulocyte extract	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_14_8172_s_143	7713922	1) Arg-e -DHFRha ( Fig. 1 ) is degraded by the N-end  rule pathway in ATP-supplemented reticulocyte extract in the absence  but not in the presence of MTX, a folic acid analog and a competitive  inhibitor of DHFR which binds to mammalian DHFRs with a  K   of  10 M  ( Fig. 3  A).	bind
21067	2	6225	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs in the absence of					MTX	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_14_8172_s_143	7713922	1) Arg-e -DHFRha ( Fig. 1 ) is degraded by the N-end  rule pathway in ATP-supplemented reticulocyte extract in the absence  but not in the presence of MTX, a folic acid analog and a competitive  inhibitor of DHFR which binds to mammalian DHFRs with a  K   of  10 M  ( Fig. 3  A).	bind
21068	3	6225	7	NULL	NULL	NULL	NULL	statement 1	Process		does not occur					MTX	Chemical	in the presence of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_14_8172_s_143	7713922	1) Arg-e -DHFRha ( Fig. 1 ) is degraded by the N-end  rule pathway in ATP-supplemented reticulocyte extract in the absence  but not in the presence of MTX, a folic acid analog and a competitive  inhibitor of DHFR which binds to mammalian DHFRs with a  K   of  10 M  ( Fig. 3  A).	bind
21069	4	6225	7	NULL	NULL	NULL	NULL	MTX	Chemical		is a type of					folic acid analog	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_14_8172_s_143	7713922	1) Arg-e -DHFRha ( Fig. 1 ) is degraded by the N-end  rule pathway in ATP-supplemented reticulocyte extract in the absence  but not in the presence of MTX, a folic acid analog and a competitive  inhibitor of DHFR which binds to mammalian DHFRs with a  K   of  10 M  ( Fig. 3  A).	bind
21070	5	6225	7	NULL	NULL	NULL	NULL	MTX	Chemical		is a type of					DHFR inhibitor	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_14_8172_s_143	7713922	1) Arg-e -DHFRha ( Fig. 1 ) is degraded by the N-end  rule pathway in ATP-supplemented reticulocyte extract in the absence  but not in the presence of MTX, a folic acid analog and a competitive  inhibitor of DHFR which binds to mammalian DHFRs with a  K   of  10 M  ( Fig. 3  A).	bind
26351	6	6225	7	NULL	NULL	NULL	NULL	MTX	Chemical		bind					DHFR	GP	mammalian			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_14_8172_s_143	7713922	1) Arg-e -DHFRha ( Fig. 1 ) is degraded by the N-end  rule pathway in ATP-supplemented reticulocyte extract in the absence  but not in the presence of MTX, a folic acid analog and a competitive  inhibitor of DHFR which binds to mammalian DHFRs with a  K   of  10 M  ( Fig. 3  A).	bind
16652	1	6226	5	NULL	NULL	0	NULL	ArgBP2	NULL		is localized in	NULL				stress fibers	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
16653	2	6226	5	NULL	NULL	0	NULL	c-Abl	NULL	cytoplasmic	is localized in	NULL				stress fibers	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
16654	3	6226	5	NULL	NULL	0	NULL	ArgBP2	NULL		associate with	NULL	directly			Arg	NULL				NULL	in living cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
16655	4	6226	5	NULL	NULL	0	NULL	ArgBP2	NULL		associate with	NULL	directly			v-Abl	NULL				NULL	in living cells	0	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
16656	5	6226	5	NULL	NULL	0	NULL	ArgBP2	NULL		is a substrate for	NULL				Abl family kinases	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
16657	6	6226	5	NULL	NULL	0	NULL	ArgBP2	NULL	endogenous	undergoes	NULL		tyrosine residues		phosphorylation	NULL				NULL	in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein	0	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
16658	7	6226	5	NULL	NULL	0	NULL	ArgBP2	NULL		bind	NULL	specific			Abl family kinases	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
16659	8	6226	5	NULL	NULL	0	NULL	ArgBP2	NULL		interact with	NULL		first SH3 domain		Arg	NULL		second of three proline-rich motifs		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
16660	9	6226	5	NULL	NULL	0	NULL	ArgBP2	NULL		interact with	NULL		third SH3 domain		Arg	NULL		second of three proline-rich motifs		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
16661	10	6226	5	NULL	NULL	0	NULL	ArgBP2	NULL		interact with	NULL		first SH3 domain		c-Abl	NULL		COOH-terminal domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
16662	11	6226	5	NULL	NULL	0	NULL	ArgBP2	NULL		interact with	NULL		third SH3 domain		c-Abl	NULL		COOH-terminal domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
21071	1	6226	7	NULL	NULL	NULL	NULL	ArgBP2	GP		is localized in					stress fibers	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
21072	2	6226	7	NULL	NULL	NULL	NULL	c-Abl	GP	cytoplasmic	is localized in					stress fibers	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
21073	3	6226	7	NULL	NULL	NULL	NULL	ArgBP2	GP		associate with		directly			Arg 	AminoAcid				NULL	living cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
21074	4	6226	7	NULL	NULL	NULL	NULL	ArgBP2	GP		associate with		directly			v-Abl	GP				NULL	living cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
21075	5	6226	7	NULL	NULL	NULL	NULL	ArgBP2	GP		is a substrate for					Abl family kinases	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
21076	6	6226	7	NULL	NULL	NULL	NULL	ArgBP2	GP	endogenous	is phosphorylated on								tyrosine residues		NULL	NIH3T3 cells transformed by v-Abl	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
21077	7	6226	7	NULL	NULL	NULL	NULL	v-Abl	GP		is					Abl oncoprotein	GP	dysregulated 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
21078	8	6226	7	NULL	NULL	NULL	NULL	ArgBP2	GP		bind		specifically			Abl family kinases	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
21080	9	6226	7	NULL	NULL	NULL	NULL	ArgBP2	GP		interact with			first SH3 domain		c-Abl	GP		second proline-rich motifs located in the Arg domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
21081	10	6226	7	NULL	NULL	NULL	NULL	ArgBP2	GP		interact with			first SH3 domain		c-Abl	GP		second proline-rich motifs located in the COOH-terminal domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
55028	11	6226	7	NULL	NULL	NULL	NULL	ArgBP2	GP		interact with			third SH3 domain		c-Abl	GP		second of three proline-rich motifs located in the Arg domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
55029	12	6226	7	NULL	NULL	NULL	NULL	ArgBP2	GP		interact with			third SH3 domain		c-Abl	GP		COOH-terminal domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17542_s_250	9211900	1) ArgBP2, like cytoplasmic c-Abl, is localized in stress fibers; 2) ArgBP2 directly associates with Arg and v-Abl in living cells; 3) ArgBP2 is a substrate for Abl family kinases, consistent with the observation that it has several sequences that conform to the suggested peptide target for the Abl kinase; 4) endogenous ArgBP2 is phosphorylated on tyrosine residues in NIH3T3 cells transformed by v-Abl, a dysregulated Abl oncoprotein; and 5) the mechanism of ArgBP2 binding with Abl family kinases is specific (the first and third ArgBP2 SH3 domains interact with the second of three proline-rich motifs located in the Arg and c-Abl COOH-terminal domains).	bind
16663	1	6227	5	NULL	NULL	0	NULL	NtpK	NULL	ion binding site	bind	NULL	high affinity	Glu-139		Na+	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24405_s_162	11983695	1) At the first step of ion translocation, the ion binding site on NtpK (Glu-139) binds Na+ with a single high affinity ( Kd of Na+ = 15  plus-or-minus  5 muM) ( 15).	bind
16664	2	6227	5	NULL	NULL	0	NULL	statement 1	NULL		occurs at	NULL				first step of ion translocation	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_27_24405_s_162	11983695	1) At the first step of ion translocation, the ion binding site on NtpK (Glu-139) binds Na+ with a single high affinity ( Kd of Na+ = 15  plus-or-minus  5 muM) ( 15).	bind
21082	1	6227	7	NULL	NULL	NULL	NULL	 NtpK	GP		bind		high affinity	Glu-139		Na+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_27_24405_s_162	11983695	1) At the first step of ion translocation, the ion binding site on NtpK (Glu-139) binds Na+ with a single high affinity ( Kd of Na+ = 15  plus-or-minus  5 muM) ( 15).	bind
26352	2	6227	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs at					first step of ion translocation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_27_24405_s_162	11983695	1) At the first step of ion translocation, the ion binding site on NtpK (Glu-139) binds Na+ with a single high affinity ( Kd of Na+ = 15  plus-or-minus  5 muM) ( 15).	bind
16665	1	6228	5	NULL	NULL	0	NULL	Bernard-Soulier platelets	NULL		is deficient in	NULL				factor XI	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_1662_s_4	11696542	1) Bernard-Soulier platelets, lacking the complex, are deficient in factor XI binding; 2) two GP Ibalpha ligands, SZ-2 (a monoclonal antibody) and bovine von Willebrand factor, inhibit factor XI binding to platelets; 3) by surface plasmon resonance, factor XI bound specifically to glycocalicin (the extracellular domain of GP Ibalpha) in Zn2+-dependent fashion ( K d app ~ 52 nM).	bind
16666	2	6228	5	NULL	NULL	0	NULL	factor XI	NULL		bind	NULL				platelets	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_1662_s_4	11696542	1) Bernard-Soulier platelets, lacking the complex, are deficient in factor XI binding; 2) two GP Ibalpha ligands, SZ-2 (a monoclonal antibody) and bovine von Willebrand factor, inhibit factor XI binding to platelets; 3) by surface plasmon resonance, factor XI bound specifically to glycocalicin (the extracellular domain of GP Ibalpha) in Zn2+-dependent fashion ( K d app ~ 52 nM).	bind
16667	3	6228	5	NULL	NULL	0	NULL	two GP Ibalpha ligands	NULL		inhibit	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_1662_s_4	11696542	1) Bernard-Soulier platelets, lacking the complex, are deficient in factor XI binding; 2) two GP Ibalpha ligands, SZ-2 (a monoclonal antibody) and bovine von Willebrand factor, inhibit factor XI binding to platelets; 3) by surface plasmon resonance, factor XI bound specifically to glycocalicin (the extracellular domain of GP Ibalpha) in Zn2+-dependent fashion ( K d app ~ 52 nM).	bind
16668	4	6228	5	NULL	NULL	0	NULL	SZ-2	NULL		inhibit	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_1662_s_4	11696542	1) Bernard-Soulier platelets, lacking the complex, are deficient in factor XI binding; 2) two GP Ibalpha ligands, SZ-2 (a monoclonal antibody) and bovine von Willebrand factor, inhibit factor XI binding to platelets; 3) by surface plasmon resonance, factor XI bound specifically to glycocalicin (the extracellular domain of GP Ibalpha) in Zn2+-dependent fashion ( K d app ~ 52 nM).	bind
16669	5	6228	5	10	NULL	0	NULL	SZ-2			is a type of					monoclonal antibody					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1662_s_4	11696542	1) Bernard-Soulier platelets, lacking the complex, are deficient in factor XI binding; 2) two GP Ibalpha ligands, SZ-2 (a monoclonal antibody) and bovine von Willebrand factor, inhibit factor XI binding to platelets; 3) by surface plasmon resonance, factor XI bound specifically to glycocalicin (the extracellular domain of GP Ibalpha) in Zn2+-dependent fashion ( K d app ~ 52 nM).	bind
16670	6	6228	5	NULL	NULL	0	NULL	von Willebrand factor	NULL	bovine	inhibit	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_1662_s_4	11696542	1) Bernard-Soulier platelets, lacking the complex, are deficient in factor XI binding; 2) two GP Ibalpha ligands, SZ-2 (a monoclonal antibody) and bovine von Willebrand factor, inhibit factor XI binding to platelets; 3) by surface plasmon resonance, factor XI bound specifically to glycocalicin (the extracellular domain of GP Ibalpha) in Zn2+-dependent fashion ( K d app ~ 52 nM).	bind
16671	7	6228	5	NULL	NULL	0	NULL	factor XI	NULL		bind	NULL	specifically			glycocalicin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_1662_s_4	11696542	1) Bernard-Soulier platelets, lacking the complex, are deficient in factor XI binding; 2) two GP Ibalpha ligands, SZ-2 (a monoclonal antibody) and bovine von Willebrand factor, inhibit factor XI binding to platelets; 3) by surface plasmon resonance, factor XI bound specifically to glycocalicin (the extracellular domain of GP Ibalpha) in Zn2+-dependent fashion ( K d app ~ 52 nM).	bind
16672	8	6228	5	NULL	NULL	0	NULL	glycocalicin	NULL		is	NULL				extracellular domain of GP Ibalpha	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_1662_s_4	11696542	1) Bernard-Soulier platelets, lacking the complex, are deficient in factor XI binding; 2) two GP Ibalpha ligands, SZ-2 (a monoclonal antibody) and bovine von Willebrand factor, inhibit factor XI binding to platelets; 3) by surface plasmon resonance, factor XI bound specifically to glycocalicin (the extracellular domain of GP Ibalpha) in Zn2+-dependent fashion ( K d app ~ 52 nM).	bind
16673	9	6228	5	NULL	NULL	0	NULL	statement 7	NULL		dependent on	NULL				Zn2+	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_1662_s_4	11696542	1) Bernard-Soulier platelets, lacking the complex, are deficient in factor XI binding; 2) two GP Ibalpha ligands, SZ-2 (a monoclonal antibody) and bovine von Willebrand factor, inhibit factor XI binding to platelets; 3) by surface plasmon resonance, factor XI bound specifically to glycocalicin (the extracellular domain of GP Ibalpha) in Zn2+-dependent fashion ( K d app ~ 52 nM).	bind
21083	1	6228	7	NULL	NULL	NULL	NULL	factor XI	GP		bind					platelets	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1662_s_4	11696542	1) Bernard-Soulier platelets, lacking the complex, are deficient in factor XI binding; 2) two GP Ibalpha ligands, SZ-2 (a monoclonal antibody) and bovine von Willebrand factor, inhibit factor XI binding to platelets; 3) by surface plasmon resonance, factor XI bound specifically to glycocalicin (the extracellular domain of GP Ibalpha) in Zn2+-dependent fashion ( K d app ~ 52 nM).	bind
21084	2	6228	7	NULL	NULL	NULL	NULL	GP Ibalpha ligands	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1662_s_4	11696542	1) Bernard-Soulier platelets, lacking the complex, are deficient in factor XI binding; 2) two GP Ibalpha ligands, SZ-2 (a monoclonal antibody) and bovine von Willebrand factor, inhibit factor XI binding to platelets; 3) by surface plasmon resonance, factor XI bound specifically to glycocalicin (the extracellular domain of GP Ibalpha) in Zn2+-dependent fashion ( K d app ~ 52 nM).	bind
21085	3	6228	7	NULL	NULL	NULL	NULL	SZ-2	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1662_s_4	11696542	1) Bernard-Soulier platelets, lacking the complex, are deficient in factor XI binding; 2) two GP Ibalpha ligands, SZ-2 (a monoclonal antibody) and bovine von Willebrand factor, inhibit factor XI binding to platelets; 3) by surface plasmon resonance, factor XI bound specifically to glycocalicin (the extracellular domain of GP Ibalpha) in Zn2+-dependent fashion ( K d app ~ 52 nM).	bind
21086	4	6228	7	NULL	NULL	NULL	NULL	 von Willebrand factor	GP	bovine	inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1662_s_4	11696542	1) Bernard-Soulier platelets, lacking the complex, are deficient in factor XI binding; 2) two GP Ibalpha ligands, SZ-2 (a monoclonal antibody) and bovine von Willebrand factor, inhibit factor XI binding to platelets; 3) by surface plasmon resonance, factor XI bound specifically to glycocalicin (the extracellular domain of GP Ibalpha) in Zn2+-dependent fashion ( K d app ~ 52 nM).	bind
21087	5	6228	7	NULL	NULL	NULL	NULL	factor XI	GP		bind		specifically			glycocalicin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1662_s_4	11696542	1) Bernard-Soulier platelets, lacking the complex, are deficient in factor XI binding; 2) two GP Ibalpha ligands, SZ-2 (a monoclonal antibody) and bovine von Willebrand factor, inhibit factor XI binding to platelets; 3) by surface plasmon resonance, factor XI bound specifically to glycocalicin (the extracellular domain of GP Ibalpha) in Zn2+-dependent fashion ( K d app ~ 52 nM).	bind
21088	6	6228	7	NULL	NULL	NULL	NULL	statement 5	Process		is dependent on					Zn2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1662_s_4	11696542	1) Bernard-Soulier platelets, lacking the complex, are deficient in factor XI binding; 2) two GP Ibalpha ligands, SZ-2 (a monoclonal antibody) and bovine von Willebrand factor, inhibit factor XI binding to platelets; 3) by surface plasmon resonance, factor XI bound specifically to glycocalicin (the extracellular domain of GP Ibalpha) in Zn2+-dependent fashion ( K d app ~ 52 nM).	bind
54169	7	6228	7	NULL	NULL	NULL	NULL	SZ-2	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1662_s_4	11696542	1) Bernard-Soulier platelets, lacking the complex, are deficient in factor XI binding; 2) two GP Ibalpha ligands, SZ-2 (a monoclonal antibody) and bovine von Willebrand factor, inhibit factor XI binding to platelets; 3) by surface plasmon resonance, factor XI bound specifically to glycocalicin (the extracellular domain of GP Ibalpha) in Zn2+-dependent fashion ( K d app ~ 52 nM).	bind
54170	8	6228	7	NULL	NULL	NULL	NULL	Bernard-Soulier platelets	OrganismPart		is deficient in					factor XI	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1662_s_4	11696542	1) Bernard-Soulier platelets, lacking the complex, are deficient in factor XI binding; 2) two GP Ibalpha ligands, SZ-2 (a monoclonal antibody) and bovine von Willebrand factor, inhibit factor XI binding to platelets; 3) by surface plasmon resonance, factor XI bound specifically to glycocalicin (the extracellular domain of GP Ibalpha) in Zn2+-dependent fashion ( K d app ~ 52 nM).	bind
16674	1	6229	5	NULL	NULL	0	NULL	Wnt protein	NULL		bind	NULL				Frizzled transmembrane receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_2_325_s_17	10027390	1) Binding of the Wnt protein to the Frizzled transmembrane receptor activates the Disheveled protein, which, in turn, inhibits the activity of glycogen synthase kinase 3beta (GSK3beta).	bind
16675	2	6229	5	NULL	NULL	0	NULL	statement 1	NULL		activate	NULL				Disheveled protein	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_2_325_s_17	10027390	1) Binding of the Wnt protein to the Frizzled transmembrane receptor activates the Disheveled protein, which, in turn, inhibits the activity of glycogen synthase kinase 3beta (GSK3beta).	bind
16676	3	6229	5	NULL	NULL	0	NULL	statement 2	NULL		inhibit	NULL				GSK3beta	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_2_325_s_17	10027390	1) Binding of the Wnt protein to the Frizzled transmembrane receptor activates the Disheveled protein, which, in turn, inhibits the activity of glycogen synthase kinase 3beta (GSK3beta).	bind
16677	4	6229	5	NULL	NULL	0	NULL	GSK3beta	NULL		is	NULL				glycogen synthase kinase 3beta	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_2_325_s_17	10027390	1) Binding of the Wnt protein to the Frizzled transmembrane receptor activates the Disheveled protein, which, in turn, inhibits the activity of glycogen synthase kinase 3beta (GSK3beta).	bind
21089	1	6229	7	NULL	NULL	NULL	NULL	Wnt protein	GP		bind					Frizzled transmembrane receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_325_s_17	10027390	1) Binding of the Wnt protein to the Frizzled transmembrane receptor activates the Disheveled protein, which, in turn, inhibits the activity of glycogen synthase kinase 3beta (GSK3beta).	bind
21090	2	6229	7	NULL	NULL	NULL	NULL	statement 1	Process		activates					Disheveled protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_325_s_17	10027390	1) Binding of the Wnt protein to the Frizzled transmembrane receptor activates the Disheveled protein, which, in turn, inhibits the activity of glycogen synthase kinase 3beta (GSK3beta).	bind
21091	3	6229	7	NULL	NULL	NULL	NULL	statement 2	Process		inhibits					GSK3beta	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_325_s_17	10027390	1) Binding of the Wnt protein to the Frizzled transmembrane receptor activates the Disheveled protein, which, in turn, inhibits the activity of glycogen synthase kinase 3beta (GSK3beta).	bind
21092	4	6229	7	NULL	NULL	NULL	NULL	GSK3beta	GP		is					glycogen synthase kinase 3beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_325_s_17	10027390	1) Binding of the Wnt protein to the Frizzled transmembrane receptor activates the Disheveled protein, which, in turn, inhibits the activity of glycogen synthase kinase 3beta (GSK3beta).	bind
16678	1	6230	5	NULL	NULL	0	NULL	BMS-345541	NULL		bind	NULL				IKK-1	NULL		ATP binding site		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1450_s_234	12403772	1) BMS-345541 binds to the ATP binding site of IKK-1 but not of IKK-2, or 2) BMS-345541 binds to similar allosteric sites on IKK-1 and IKK-2, but binding to the allosteric site on IKK-2 leads to a conformational change in the enzyme that alters the peptide binding site whereas the conformational change that occurs upon binding of BMS-345541 to the corresponding site on IKK-1 causes a perturbation of the ATP binding site.	bind
16679	2	6230	5	NULL	NULL	0	NULL	BMS-345541	NULL		does not bind	NULL				IKK-2	NULL		ATP binding site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_3_1450_s_234	12403772	1) BMS-345541 binds to the ATP binding site of IKK-1 but not of IKK-2, or 2) BMS-345541 binds to similar allosteric sites on IKK-1 and IKK-2, but binding to the allosteric site on IKK-2 leads to a conformational change in the enzyme that alters the peptide binding site whereas the conformational change that occurs upon binding of BMS-345541 to the corresponding site on IKK-1 causes a perturbation of the ATP binding site.	bind
16680	3	6230	5	NULL	NULL	0	NULL	BMS-345541	NULL		bind	NULL				IKK-1	NULL		similar allosteric sites		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1450_s_234	12403772	1) BMS-345541 binds to the ATP binding site of IKK-1 but not of IKK-2, or 2) BMS-345541 binds to similar allosteric sites on IKK-1 and IKK-2, but binding to the allosteric site on IKK-2 leads to a conformational change in the enzyme that alters the peptide binding site whereas the conformational change that occurs upon binding of BMS-345541 to the corresponding site on IKK-1 causes a perturbation of the ATP binding site.	bind
16681	4	6230	5	NULL	NULL	0	NULL	BMS-345541	NULL		bind	NULL				IKK-2	NULL		similar allosteric sites		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1450_s_234	12403772	1) BMS-345541 binds to the ATP binding site of IKK-1 but not of IKK-2, or 2) BMS-345541 binds to similar allosteric sites on IKK-1 and IKK-2, but binding to the allosteric site on IKK-2 leads to a conformational change in the enzyme that alters the peptide binding site whereas the conformational change that occurs upon binding of BMS-345541 to the corresponding site on IKK-1 causes a perturbation of the ATP binding site.	bind
16682	5	6230	5	10	NULL	0	NULL	statement 4	NULL		leads to	NULL				IKK-2	NULL	conformational change of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_3_1450_s_234	12403772	1) BMS-345541 binds to the ATP binding site of IKK-1 but not of IKK-2, or 2) BMS-345541 binds to similar allosteric sites on IKK-1 and IKK-2, but binding to the allosteric site on IKK-2 leads to a conformational change in the enzyme that alters the peptide binding site whereas the conformational change that occurs upon binding of BMS-345541 to the corresponding site on IKK-1 causes a perturbation of the ATP binding site.	bind
16683	6	6230	5	NULL	NULL	0	NULL	statement 5	NULL		alters	NULL					NULL		peptide binding site		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1450_s_234	12403772	1) BMS-345541 binds to the ATP binding site of IKK-1 but not of IKK-2, or 2) BMS-345541 binds to similar allosteric sites on IKK-1 and IKK-2, but binding to the allosteric site on IKK-2 leads to a conformational change in the enzyme that alters the peptide binding site whereas the conformational change that occurs upon binding of BMS-345541 to the corresponding site on IKK-1 causes a perturbation of the ATP binding site.	bind
16684	7	6230	5	10	NULL	0	NULL	statement 3	NULL		leads to	NULL				IKK-1	NULL	conformational change of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_3_1450_s_234	12403772	1) BMS-345541 binds to the ATP binding site of IKK-1 but not of IKK-2, or 2) BMS-345541 binds to similar allosteric sites on IKK-1 and IKK-2, but binding to the allosteric site on IKK-2 leads to a conformational change in the enzyme that alters the peptide binding site whereas the conformational change that occurs upon binding of BMS-345541 to the corresponding site on IKK-1 causes a perturbation of the ATP binding site.	bind
16685	8	6230	5	NULL	NULL	0	NULL	statement 7	NULL		causes	NULL				perturbation	NULL		ATP binding site		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1450_s_234	12403772	1) BMS-345541 binds to the ATP binding site of IKK-1 but not of IKK-2, or 2) BMS-345541 binds to similar allosteric sites on IKK-1 and IKK-2, but binding to the allosteric site on IKK-2 leads to a conformational change in the enzyme that alters the peptide binding site whereas the conformational change that occurs upon binding of BMS-345541 to the corresponding site on IKK-1 causes a perturbation of the ATP binding site.	bind
21093	1	6230	7	NULL	NULL	NULL	NULL	BMS-345541	Chemical		binds					IKK-1	GP		ATP binding site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_3_1450_s_234	12403772	1) BMS-345541 binds to the ATP binding site of IKK-1 but not of IKK-2, or 2) BMS-345541 binds to similar allosteric sites on IKK-1 and IKK-2, but binding to the allosteric site on IKK-2 leads to a conformational change in the enzyme that alters the peptide binding site whereas the conformational change that occurs upon binding of BMS-345541 to the corresponding site on IKK-1 causes a perturbation of the ATP binding site.	bind
21094	2	6230	7	NULL	NULL	NULL	NULL	BMS-345541	Chemical		does not bind					IKK-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_3_1450_s_234	12403772	1) BMS-345541 binds to the ATP binding site of IKK-1 but not of IKK-2, or 2) BMS-345541 binds to similar allosteric sites on IKK-1 and IKK-2, but binding to the allosteric site on IKK-2 leads to a conformational change in the enzyme that alters the peptide binding site whereas the conformational change that occurs upon binding of BMS-345541 to the corresponding site on IKK-1 causes a perturbation of the ATP binding site.	bind
21095	3	6230	7	NULL	NULL	NULL	NULL	BMS-345541	Chemical		binds to					IKK-1	GP		allosteric site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_3_1450_s_234	12403772	1) BMS-345541 binds to the ATP binding site of IKK-1 but not of IKK-2, or 2) BMS-345541 binds to similar allosteric sites on IKK-1 and IKK-2, but binding to the allosteric site on IKK-2 leads to a conformational change in the enzyme that alters the peptide binding site whereas the conformational change that occurs upon binding of BMS-345541 to the corresponding site on IKK-1 causes a perturbation of the ATP binding site.	bind
21096	4	6230	7	NULL	NULL	NULL	NULL	BMS-345541	Chemical		binds to					IKK-2	GP		allosteric site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_3_1450_s_234	12403772	1) BMS-345541 binds to the ATP binding site of IKK-1 but not of IKK-2, or 2) BMS-345541 binds to similar allosteric sites on IKK-1 and IKK-2, but binding to the allosteric site on IKK-2 leads to a conformational change in the enzyme that alters the peptide binding site whereas the conformational change that occurs upon binding of BMS-345541 to the corresponding site on IKK-1 causes a perturbation of the ATP binding site.	bind
21097	5	6230	7	NULL	NULL	NULL	NULL	statement 4	Process		leads to					enzyme	GP	conformational change in the			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_3_1450_s_234	12403772	1) BMS-345541 binds to the ATP binding site of IKK-1 but not of IKK-2, or 2) BMS-345541 binds to similar allosteric sites on IKK-1 and IKK-2, but binding to the allosteric site on IKK-2 leads to a conformational change in the enzyme that alters the peptide binding site whereas the conformational change that occurs upon binding of BMS-345541 to the corresponding site on IKK-1 causes a perturbation of the ATP binding site.	bind
21098	6	6230	7	NULL	NULL	NULL	NULL	statement 4	Process		alters the 								peptide binding site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_3_1450_s_234	12403772	1) BMS-345541 binds to the ATP binding site of IKK-1 but not of IKK-2, or 2) BMS-345541 binds to similar allosteric sites on IKK-1 and IKK-2, but binding to the allosteric site on IKK-2 leads to a conformational change in the enzyme that alters the peptide binding site whereas the conformational change that occurs upon binding of BMS-345541 to the corresponding site on IKK-1 causes a perturbation of the ATP binding site.	bind
21099	7	6230	7	NULL	NULL	NULL	NULL	statement 3	Process		cause perturbation of								ATP binding site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_3_1450_s_234	12403772	1) BMS-345541 binds to the ATP binding site of IKK-1 but not of IKK-2, or 2) BMS-345541 binds to similar allosteric sites on IKK-1 and IKK-2, but binding to the allosteric site on IKK-2 leads to a conformational change in the enzyme that alters the peptide binding site whereas the conformational change that occurs upon binding of BMS-345541 to the corresponding site on IKK-1 causes a perturbation of the ATP binding site.	bind
16686	1	6231	5	NULL	NULL	0	NULL	pRNA	NULL	wt	bind	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
16687	2	6231	5	NULL	NULL	0	NULL	pRNA	NULL	wt	bind	NULL				ADP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
16688	3	6231	5	NULL	NULL	0	NULL	pRNA	NULL	wt	bind	NULL				AMP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
16689	4	6231	5	NULL	NULL	0	NULL	statement 1	NULL		higher affinity than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
16690	5	6231	5	NULL	NULL	0	NULL	statement 1	NULL		higher affinity than	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
16691	6	6231	5	NULL	NULL	0	NULL	aptRNA	NULL		bind	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
16692	7	6231	5	NULL	NULL	0	NULL	aptRNA	NULL		bind	NULL				ADP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
16693	8	6231	5	NULL	NULL	0	NULL	aptRNA	NULL		bind	NULL				AMP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
16694	9	6231	5	NULL	NULL	0	NULL	statement 6	NULL		higher affinity than	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
16695	10	6231	5	NULL	NULL	0	NULL	statement 6	NULL		higher affinity than	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
16696	11	6231	5	NULL	NULL	0	NULL	RNA aptamer	NULL		bind	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
16697	12	6231	5	NULL	NULL	0	NULL	RNA aptamer	NULL		bind	NULL				ADP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
16698	13	6231	5	NULL	NULL	0	NULL	RNA aptamer	NULL		bind	NULL				AMP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
16699	14	6231	5	NULL	NULL	0	NULL	RNA aptamer	NULL		bind	NULL				adenosine	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
16700	15	6231	5	NULL	NULL	0	NULL	statement 11	NULL		equal affinity to	NULL				statement 12	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
16701	16	6231	5	NULL	NULL	0	NULL	statement 12	NULL		equal affinity to	NULL				statement 13	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
16702	17	6231	5	NULL	NULL	0	NULL	statement 13	NULL		equal affinity to	NULL				statement 14	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
21100	1	6231	7	NULL	NULL	NULL	NULL	 pRNA	NucleicAcid	wt	binds		high affinity			ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
21101	2	6231	7	NULL	NULL	NULL	NULL	aptRNA	NucleicAcid		bind		high affinity			ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
21102	3	6231	7	NULL	NULL	NULL	NULL	pRNA	NucleicAcid	wt	bind					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
21103	4	6231	7	NULL	NULL	NULL	NULL	aptRNA	NucleicAcid		bind					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
21104	5	6231	7	NULL	NULL	NULL	NULL	 pRNA	NucleicAcid	wt	bind					AMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
21105	6	6231	7	NULL	NULL	NULL	NULL	aptRNA	NucleicAcid		bind					AMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
21106	7	6231	7	NULL	NULL	NULL	NULL	statement 1	Process		has higher affinity than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
21107	8	6231	7	NULL	NULL	NULL	NULL	statement 1	Process		has higher affinity than					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
21108	9	6231	7	NULL	NULL	NULL	NULL	statement 2	Process		has higher affinity than					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
21110	10	6231	7	NULL	NULL	NULL	NULL	statement 2 	Process		has higher affinity than					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
21111	11	6231	7	NULL	NULL	NULL	NULL	RNA aptamer	NucleicAcid		binds					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
21129	12	6231	7	NULL	NULL	NULL	NULL	RNA aptamer	NucleicAcid		binds					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
21130	13	6231	7	NULL	NULL	NULL	NULL	RNA aptamer	NucleicAcid		binds					AMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
21131	14	6231	7	NULL	NULL	NULL	NULL	RNA aptamer	NucleicAcid		binds					adenosine	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
21132	15	6231	7	NULL	NULL	NULL	NULL	statement 11	Process		has equal affinity as					statement 12	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
21133	16	6231	7	NULL	NULL	NULL	NULL	statement 11	Process		has equal affinity as					statement 13	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
21134	17	6231	7	NULL	NULL	NULL	NULL	statement 11	Process		has equal affinity as					statement 14	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7119_s_232	12444088	1) Both pRNAwt and aptRNA have a higher affinity for ATP than for ADP and AMP, whereas the RNA aptamer binds ATP, ADP, AMP, and adenosine equally ( ).	bind
22922	1	6233	5	NULL	NULL	0	NULL	NFAT complex	NULL		bind	NULL				IL-2	NULL	human		NFAT binding sites	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20653_s_214	7657645	1) Both proteins are able to reconstitute  an NFAT complex with murine and human IL-2 NFAT binding sites in the  presence of Fos/Jun heterodimers; both also bind specifically to a  murine NFAT oligonucleotide without Fos and Jun proteins (Jain  et  al., 1992, 1993b; Yaseen  et al., 1993;   Fig. 1and  Fig. 6).	bind
22923	2	6233	5	NULL	NULL	0	NULL	NFAT complex	NULL		bind	NULL				IL-2-	NULL	murine		NFAT binding sites	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20653_s_214	7657645	1) Both proteins are able to reconstitute  an NFAT complex with murine and human IL-2 NFAT binding sites in the  presence of Fos/Jun heterodimers; both also bind specifically to a  murine NFAT oligonucleotide without Fos and Jun proteins (Jain  et  al., 1992, 1993b; Yaseen  et al., 1993;   Fig. 1and  Fig. 6).	bind
22924	3	6233	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				Fos/Jun heterodimers	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20653_s_214	7657645	1) Both proteins are able to reconstitute  an NFAT complex with murine and human IL-2 NFAT binding sites in the  presence of Fos/Jun heterodimers; both also bind specifically to a  murine NFAT oligonucleotide without Fos and Jun proteins (Jain  et  al., 1992, 1993b; Yaseen  et al., 1993;   Fig. 1and  Fig. 6).	bind
54171	4	6233	5	10	NULL	0	NULL	statement 2			in the presence of					Fos/Jun heterodimers					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20653_s_214	7657645	1) Both proteins are able to reconstitute  an NFAT complex with murine and human IL-2 NFAT binding sites in the  presence of Fos/Jun heterodimers; both also bind specifically to a  murine NFAT oligonucleotide without Fos and Jun proteins (Jain  et  al., 1992, 1993b; Yaseen  et al., 1993;   Fig. 1and  Fig. 6).	bind
21487	1	6233	7	NULL	NULL	NULL	NULL	NFAT complex	GP		binds					 IL-2	GP	murine	NFAT binding sites		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20653_s_214	7657645	1) Both proteins are able to reconstitute  an NFAT complex with murine and human IL-2 NFAT binding sites in the  presence of Fos/Jun heterodimers; both also bind specifically to a  murine NFAT oligonucleotide without Fos and Jun proteins (Jain  et  al., 1992, 1993b; Yaseen  et al., 1993;   Fig. 1and  Fig. 6).	bind
21488	2	6233	7	NULL	NULL	NULL	NULL	NFAT complex	GP		binds					IL-2	GP	human	NFAT binding sites		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20653_s_214	7657645	1) Both proteins are able to reconstitute  an NFAT complex with murine and human IL-2 NFAT binding sites in the  presence of Fos/Jun heterodimers; both also bind specifically to a  murine NFAT oligonucleotide without Fos and Jun proteins (Jain  et  al., 1992, 1993b; Yaseen  et al., 1993;   Fig. 1and  Fig. 6).	bind
21489	3	6233	7	NULL	NULL	NULL	NULL	statement 1	Process		occur in presence of					Fos/Jun heterodimers	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20653_s_214	7657645	1) Both proteins are able to reconstitute  an NFAT complex with murine and human IL-2 NFAT binding sites in the  presence of Fos/Jun heterodimers; both also bind specifically to a  murine NFAT oligonucleotide without Fos and Jun proteins (Jain  et  al., 1992, 1993b; Yaseen  et al., 1993;   Fig. 1and  Fig. 6).	bind
21490	4	6233	7	NULL	NULL	NULL	NULL	statement 2	Process		occur in presence of					Fos/Jun heterodimers	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20653_s_214	7657645	1) Both proteins are able to reconstitute  an NFAT complex with murine and human IL-2 NFAT binding sites in the  presence of Fos/Jun heterodimers; both also bind specifically to a  murine NFAT oligonucleotide without Fos and Jun proteins (Jain  et  al., 1992, 1993b; Yaseen  et al., 1993;   Fig. 1and  Fig. 6).	bind
16720	1	6236	5	NULL	NULL	0	NULL	LTB4	NULL		bind	NULL				hBLT1	NULL	WT			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_42_41500_s_304	12902330	1) Cytoplasmic GTP content is inhibitory for the binding of LTB4 to the WT-hBLT1 but not to the mutants, as suggested by  Fig. 6; 2) intracellular signaling activates various kinases (GPCR kinase, protein kinase C, etc.) and inactivates the receptor by phosphorylating the C terminus.	bind
16721	2	6236	5	NULL	NULL	0	NULL	GTP	NULL	cytoplasmic	inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_42_41500_s_304	12902330	1) Cytoplasmic GTP content is inhibitory for the binding of LTB4 to the WT-hBLT1 but not to the mutants, as suggested by  Fig. 6; 2) intracellular signaling activates various kinases (GPCR kinase, protein kinase C, etc.) and inactivates the receptor by phosphorylating the C terminus.	bind
16729	3	6236	5	NULL	NULL	0	NULL	intracellular signaling	NULL		activates	NULL				GPCR kinase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_42_41500_s_304	12902330	1) Cytoplasmic GTP content is inhibitory for the binding of LTB4 to the WT-hBLT1 but not to the mutants, as suggested by  Fig. 6; 2) intracellular signaling activates various kinases (GPCR kinase, protein kinase C, etc.) and inactivates the receptor by phosphorylating the C terminus.	bind
16730	4	6236	5	NULL	NULL	0	NULL	intracellular signaling	NULL		activates	NULL				protein kinase C	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_42_41500_s_304	12902330	1) Cytoplasmic GTP content is inhibitory for the binding of LTB4 to the WT-hBLT1 but not to the mutants, as suggested by  Fig. 6; 2) intracellular signaling activates various kinases (GPCR kinase, protein kinase C, etc.) and inactivates the receptor by phosphorylating the C terminus.	bind
16737	5	6236	5	NULL	NULL	0	NULL	intracellular signaling	NULL		phosphorylate	NULL				receptor	NULL		C terminus		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_42_41500_s_304	12902330	1) Cytoplasmic GTP content is inhibitory for the binding of LTB4 to the WT-hBLT1 but not to the mutants, as suggested by  Fig. 6; 2) intracellular signaling activates various kinases (GPCR kinase, protein kinase C, etc.) and inactivates the receptor by phosphorylating the C terminus.	bind
16755	6	6236	5	NULL	NULL	0	NULL	intracellular signaling	NULL		inactivate	NULL				receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_42_41500_s_304	12902330	1) Cytoplasmic GTP content is inhibitory for the binding of LTB4 to the WT-hBLT1 but not to the mutants, as suggested by  Fig. 6; 2) intracellular signaling activates various kinases (GPCR kinase, protein kinase C, etc.) and inactivates the receptor by phosphorylating the C terminus.	bind
16758	7	6236	5	NULL	NULL	0	NULL	statement 5	NULL		leads to	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_42_41500_s_304	12902330	1) Cytoplasmic GTP content is inhibitory for the binding of LTB4 to the WT-hBLT1 but not to the mutants, as suggested by  Fig. 6; 2) intracellular signaling activates various kinases (GPCR kinase, protein kinase C, etc.) and inactivates the receptor by phosphorylating the C terminus.	bind
26087	8	6236	5	NULL	NULL	0	NULL	LTB4	NULL		bind	NULL				hBLT1	NULL	mutant			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_42_41500_s_304	12902330	1) Cytoplasmic GTP content is inhibitory for the binding of LTB4 to the WT-hBLT1 but not to the mutants, as suggested by  Fig. 6; 2) intracellular signaling activates various kinases (GPCR kinase, protein kinase C, etc.) and inactivates the receptor by phosphorylating the C terminus.	bind
26088	9	6236	5	NULL	NULL	0	NULL	GTP	NULL	cytoplasmic	does not inhibit	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_42_41500_s_304	12902330	1) Cytoplasmic GTP content is inhibitory for the binding of LTB4 to the WT-hBLT1 but not to the mutants, as suggested by  Fig. 6; 2) intracellular signaling activates various kinases (GPCR kinase, protein kinase C, etc.) and inactivates the receptor by phosphorylating the C terminus.	bind
21135	1	6236	7	NULL	NULL	NULL	NULL	LTB4	GP		bind					hBLT1	GP	WT			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_42_41500_s_304	12902330	1) Cytoplasmic GTP content is inhibitory for the binding of LTB4 to the WT-hBLT1 but not to the mutants, as suggested by  Fig. 6; 2) intracellular signaling activates various kinases (GPCR kinase, protein kinase C, etc.) and inactivates the receptor by phosphorylating the C terminus.	bind
21136	2	6236	7	NULL	NULL	NULL	NULL	LTB4	GP		bind					hBLT1	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_42_41500_s_304	12902330	1) Cytoplasmic GTP content is inhibitory for the binding of LTB4 to the WT-hBLT1 but not to the mutants, as suggested by  Fig. 6; 2) intracellular signaling activates various kinases (GPCR kinase, protein kinase C, etc.) and inactivates the receptor by phosphorylating the C terminus.	bind
21137	3	6236	7	NULL	NULL	NULL	NULL	GTP	Chemical	cytoplasmic	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_42_41500_s_304	12902330	1) Cytoplasmic GTP content is inhibitory for the binding of LTB4 to the WT-hBLT1 but not to the mutants, as suggested by  Fig. 6; 2) intracellular signaling activates various kinases (GPCR kinase, protein kinase C, etc.) and inactivates the receptor by phosphorylating the C terminus.	bind
21138	4	6236	7	NULL	NULL	NULL	NULL	GTP	Chemical	cytoplasmic	does not inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_42_41500_s_304	12902330	1) Cytoplasmic GTP content is inhibitory for the binding of LTB4 to the WT-hBLT1 but not to the mutants, as suggested by  Fig. 6; 2) intracellular signaling activates various kinases (GPCR kinase, protein kinase C, etc.) and inactivates the receptor by phosphorylating the C terminus.	bind
21139	5	6236	7	NULL	NULL	NULL	NULL	intracellular signaling	Process		activates					GPCR kinase	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_42_41500_s_304	12902330	1) Cytoplasmic GTP content is inhibitory for the binding of LTB4 to the WT-hBLT1 but not to the mutants, as suggested by  Fig. 6; 2) intracellular signaling activates various kinases (GPCR kinase, protein kinase C, etc.) and inactivates the receptor by phosphorylating the C terminus.	bind
21141	6	6236	7	NULL	NULL	NULL	NULL	intracellular signaling	Process		activates					protein kinase C	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_42_41500_s_304	12902330	1) Cytoplasmic GTP content is inhibitory for the binding of LTB4 to the WT-hBLT1 but not to the mutants, as suggested by  Fig. 6; 2) intracellular signaling activates various kinases (GPCR kinase, protein kinase C, etc.) and inactivates the receptor by phosphorylating the C terminus.	bind
21142	7	6236	7	NULL	NULL	NULL	NULL	intracellular signaling	Process		phosphorylates					receptor	GP		C terminus		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_42_41500_s_304	12902330	1) Cytoplasmic GTP content is inhibitory for the binding of LTB4 to the WT-hBLT1 but not to the mutants, as suggested by  Fig. 6; 2) intracellular signaling activates various kinases (GPCR kinase, protein kinase C, etc.) and inactivates the receptor by phosphorylating the C terminus.	bind
21143	8	6236	7	NULL	NULL	NULL	NULL	intracellular signaling	Process		inactivates					receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_42_41500_s_304	12902330	1) Cytoplasmic GTP content is inhibitory for the binding of LTB4 to the WT-hBLT1 but not to the mutants, as suggested by  Fig. 6; 2) intracellular signaling activates various kinases (GPCR kinase, protein kinase C, etc.) and inactivates the receptor by phosphorylating the C terminus.	bind
26356	9	6236	7	NULL	NULL	NULL	NULL	statement 6	Process		leads to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_42_41500_s_304	12902330	1) Cytoplasmic GTP content is inhibitory for the binding of LTB4 to the WT-hBLT1 but not to the mutants, as suggested by  Fig. 6; 2) intracellular signaling activates various kinases (GPCR kinase, protein kinase C, etc.) and inactivates the receptor by phosphorylating the C terminus.	bind
16759	1	6237	5	NULL	NULL	0	NULL	Defensin	NULL		bind	NULL	may			endothelial cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17650_s_64	8663495	1) Defensin may bind to endothelial cells providing novel sites to which plasminogen can bind; 2) defensin may bind to Glu- and to Lys-plasminogen directly, and the resultant complex may express novel cell binding epitopes; or 3) both mechanisms may be operative.	bind
16762	2	6237	5	10	NULL	0	NULL	statement 1	NULL		provide	NULL					NULL	novel 	plasminogen binding sites		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17650_s_64	8663495	1) Defensin may bind to endothelial cells providing novel sites to which plasminogen can bind; 2) defensin may bind to Glu- and to Lys-plasminogen directly, and the resultant complex may express novel cell binding epitopes; or 3) both mechanisms may be operative.	bind
16763	3	6237	5	10	NULL	0	NULL	Defensin	NULL		bind	NULL	may;; directly			Glu-plasminogen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17650_s_64	8663495	1) Defensin may bind to endothelial cells providing novel sites to which plasminogen can bind; 2) defensin may bind to Glu- and to Lys-plasminogen directly, and the resultant complex may express novel cell binding epitopes; or 3) both mechanisms may be operative.	bind
16764	4	6237	5	10	NULL	0	NULL	Defensin	NULL		bind	NULL	may;; directly			Lys-plasminogen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17650_s_64	8663495	1) Defensin may bind to endothelial cells providing novel sites to which plasminogen can bind; 2) defensin may bind to Glu- and to Lys-plasminogen directly, and the resultant complex may express novel cell binding epitopes; or 3) both mechanisms may be operative.	bind
16765	5	6237	5	10	NULL	0	NULL	statement 3	NULL		express	NULL	may			cell binding epitopes	NULL	novel 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17650_s_64	8663495	1) Defensin may bind to endothelial cells providing novel sites to which plasminogen can bind; 2) defensin may bind to Glu- and to Lys-plasminogen directly, and the resultant complex may express novel cell binding epitopes; or 3) both mechanisms may be operative.	bind
16766	6	6237	5	10	NULL	0	NULL	statement 4	NULL		express	NULL	may			cell binding epitopes	NULL	novel 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17650_s_64	8663495	1) Defensin may bind to endothelial cells providing novel sites to which plasminogen can bind; 2) defensin may bind to Glu- and to Lys-plasminogen directly, and the resultant complex may express novel cell binding epitopes; or 3) both mechanisms may be operative.	bind
21202	1	6237	7	NULL	NULL	NULL	NULL	Defensin	GP		bind		may			endothelial cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17650_s_64	8663495	1) Defensin may bind to endothelial cells providing novel sites to which plasminogen can bind; 2) defensin may bind to Glu- and to Lys-plasminogen directly, and the resultant complex may express novel cell binding epitopes; or 3) both mechanisms may be operative.	bind
21203	2	6237	7	NULL	NULL	NULL	NULL	statement 1	Process		provide					novel sites	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17650_s_64	8663495	1) Defensin may bind to endothelial cells providing novel sites to which plasminogen can bind; 2) defensin may bind to Glu- and to Lys-plasminogen directly, and the resultant complex may express novel cell binding epitopes; or 3) both mechanisms may be operative.	bind
21204	3	6237	7	NULL	NULL	NULL	NULL	plasminogen	GP		bind					novel sites	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17650_s_64	8663495	1) Defensin may bind to endothelial cells providing novel sites to which plasminogen can bind; 2) defensin may bind to Glu- and to Lys-plasminogen directly, and the resultant complex may express novel cell binding epitopes; or 3) both mechanisms may be operative.	bind
21205	4	6237	7	NULL	NULL	NULL	NULL	defensin	GP		bind		directly			plasminogen	GP		Glu		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17650_s_64	8663495	1) Defensin may bind to endothelial cells providing novel sites to which plasminogen can bind; 2) defensin may bind to Glu- and to Lys-plasminogen directly, and the resultant complex may express novel cell binding epitopes; or 3) both mechanisms may be operative.	bind
21206	5	6237	7	NULL	NULL	NULL	NULL	defensin	GP		bind		directly			plasminogen	GP		Lys		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17650_s_64	8663495	1) Defensin may bind to endothelial cells providing novel sites to which plasminogen can bind; 2) defensin may bind to Glu- and to Lys-plasminogen directly, and the resultant complex may express novel cell binding epitopes; or 3) both mechanisms may be operative.	bind
21207	6	6237	7	NULL	NULL	NULL	NULL	statement 4	Process		express					cell binding epitopes	CellComponent	novel			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17650_s_64	8663495	1) Defensin may bind to endothelial cells providing novel sites to which plasminogen can bind; 2) defensin may bind to Glu- and to Lys-plasminogen directly, and the resultant complex may express novel cell binding epitopes; or 3) both mechanisms may be operative.	bind
21208	7	6237	7	NULL	NULL	NULL	NULL	statement 5	Process		express					cell binding epitopes	CellComponent	novel 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17650_s_64	8663495	1) Defensin may bind to endothelial cells providing novel sites to which plasminogen can bind; 2) defensin may bind to Glu- and to Lys-plasminogen directly, and the resultant complex may express novel cell binding epitopes; or 3) both mechanisms may be operative.	bind
16767	1	6238	5	NULL	NULL	0	NULL	dIgA	NULL		bind	NULL				pIgR	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_4_901_s_171	9529387	1) Does the binding of dIgA to pIgR dimerize the pIgR?	bind
21209	1	6238	7	NULL	NULL	NULL	NULL	dIgA	GP		bind					pIgR 	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_4_901_s_171	9529387	1) Does the binding of dIgA to pIgR dimerize the pIgR?	bind
16740	1	6240	5	NULL	NULL	0	NULL	GPIb-IX	NULL		mediate	NULL				integrin alphaIIbbeta3	NULL	activation of			NULL	in a reconstituted CHO cell expression model	0	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
16741	2	6240	5	NULL	NULL	0	NULL	Raf301	NULL	dominant negative mutants	inhibit	NULL				statement 1	NULL				NULL	in a reconstituted CHO cell expression model	0	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
16742	3	6240	5	NULL	NULL	0	NULL	MEK1	NULL	dominant negative mutants	inhibit	NULL		M97K		statement 1	NULL				NULL	in a reconstituted CHO cell expression model	0	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
16744	4	6240	5	10	NULL	0	NULL	PD98059	NULL		inhibit	NULL				vWF	NULL				NULL	in platelets	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
16745	5	6240	5	NULL	NULL	0	NULL	statement 4	NULL		is independent of	NULL				cyclooxygenase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
16746	6	6240	5	10	NULL	0	NULL	U0126	NULL		inhibit	NULL				platelet aggregation	NULL	low dose thrombin-induced, integrin-dependent			NULL	in platelets	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
16747	7	6240	5	NULL	NULL	0	NULL	statement 6	NULL		is independent of	NULL				cyclooxygenase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
16748	8	6240	5	NULL	NULL	0	NULL	vWF	NULL		bind	NULL				GPIb-IX	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
16750	9	6240	5	NULL	NULL	0	NULL	statement 8	NULL		induce	NULL				ERK2	NULL	phosphorylation of 	Thr-Glu-Tyr sequence		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
16753	10	6240	5	NULL	NULL	0	NULL	statement 9	NULL		indicate	NULL				ERK MAPK pathway	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
21213	1	6240	7	NULL	NULL	NULL	NULL	GPIb-IX	GP		mediates					integrin alphaIIbbeta3	GP	activation of			NULL	reconstituted CHO cell expression 	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
21214	2	6240	7	NULL	NULL	NULL	NULL	MAP kinase pathway	Process	Dominant negative mutants of	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
21215	3	6240	7	NULL	NULL	NULL	NULL	Raf301	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
21216	4	6240	7	NULL	NULL	NULL	NULL	MEK1 M97K	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
21217	5	6240	7	NULL	NULL	NULL	NULL	PD98059	Chemical		inhibits					 vWF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
21218	6	6240	7	NULL	NULL	NULL	NULL	 U0126 	Chemical		inhibits					vWF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
21219	9	6240	7	NULL	NULL	NULL	NULL	PD98059	Chemical		inhibits					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
21220	10	6240	7	NULL	NULL	NULL	NULL	PD98059	Chemical		inhibits					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
21221	13	6240	7	NULL	NULL	NULL	NULL	statement 9	Process		is independent of					cyclooxygenase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
21223	14	6240	7	NULL	NULL	NULL	NULL	statement 10	Process		is independent of					cyclooxygenase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
21225	17	6240	7	NULL	NULL	NULL	NULL	vWF	GP		bind					GPIb-IX	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
21226	18	6240	7	NULL	NULL	NULL	NULL	statement 17	Process		induce					ERK2	GP	phosphorylation of	at the Thr-Glu-Tyr sequence		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
21231	19	6240	7	NULL	NULL	NULL	NULL	statement 18	Process		indicate					ERK MAPK pathway	Process	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
45566	8	6240	7	NULL	NULL	NULL	NULL	platelet aggregation	Process		depends on					integrin	GP				NULL	platelets	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
45567	7	6240	7	NULL	NULL	NULL	NULL	thrombin	GP		induce					platelet aggregation	Process				NULL	platelets	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
45568	11	6240	7	NULL	NULL	NULL	NULL	U0126	Chemical		inhibits					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
45569	12	6240	7	NULL	NULL	NULL	NULL	U0126	Chemical		inhibits					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
45570	15	6240	7	NULL	NULL	NULL	NULL	statement 11	Process		is independent of					cyclooxygenase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
45571	16	6240	7	NULL	NULL	NULL	NULL	statement 12	Process		is independent of					cyclooxygenase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42226_s_193	11522789	1) Dominant negative mutants of MAP kinase pathway, Raf301 and MEK1 M97K, inhibited GPIb-IX-mediated activation of integrin alphaIIbbeta3 in a reconstituted CHO cell expression model; 2) MEK inhibitors PD98059 and U0126 inhibited vWF and low dose thrombin-induced, integrin-dependent platelet aggregation in platelets in a cyclooxygenase-independent manner; and 3) vWF binding to GPIb-IX induced phosphorylation of ERK2 at the Thr-Glu-Tyr sequence, indicating that the ERK MAPK pathway is activated.	bind
16768	1	6241	5	10	NULL	0	NULL	VIP			bind					VPAC2 receptor					NULL	during some stages of brain development	NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_314_2_745_s_184	15872042	1) During some stages of brain development, the binding of VIP or PACAP to VPAC2 receptors leads to activation of separate transduction pathways.	bind
16769	2	6241	5	10	NULL	0	NULL	PACAP			bind					VPAC2 receptor					NULL	during some stages of brain development	NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_314_2_745_s_184	15872042	1) During some stages of brain development, the binding of VIP or PACAP to VPAC2 receptors leads to activation of separate transduction pathways.	bind
16770	3	6241	5	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				separate transduction pathways	NULL	activation of			NULL	during some stages of brain development	0	NULL	NULL	NULL	gw70_jpharmacolexpther_314_2_745_s_184	15872042	1) During some stages of brain development, the binding of VIP or PACAP to VPAC2 receptors leads to activation of separate transduction pathways.	bind
16771	4	6241	5	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				separate transduction pathways	NULL	activation of			NULL	during some stages of brain development	0	NULL	NULL	NULL	gw70_jpharmacolexpther_314_2_745_s_184	15872042	1) During some stages of brain development, the binding of VIP or PACAP to VPAC2 receptors leads to activation of separate transduction pathways.	bind
54172	5	6241	5	10	NULL	0	NULL	statement 1			is an alternative to					statement 2					NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_314_2_745_s_184	15872042	1) During some stages of brain development, the binding of VIP or PACAP to VPAC2 receptors leads to activation of separate transduction pathways.	bind
21232	1	6241	7	NULL	NULL	NULL	NULL	VIP	GP		bind					VPAC2 receptors	GP				NULL	during stages of brain development	NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_314_2_745_s_184	15872042	1) During some stages of brain development, the binding of VIP or PACAP to VPAC2 receptors leads to activation of separate transduction pathways.	bind
21233	2	6241	7	NULL	NULL	NULL	NULL	PACAP	GP		bind					VPAC2 receptors	GP				NULL	during stages of brain development	NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_314_2_745_s_184	15872042	1) During some stages of brain development, the binding of VIP or PACAP to VPAC2 receptors leads to activation of separate transduction pathways.	bind
21234	3	6241	7	NULL	NULL	NULL	NULL	statement 1	Process		leads to					transduction pathways	Process	activation of			NULL	during stages of brain development	NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_314_2_745_s_184	15872042	1) During some stages of brain development, the binding of VIP or PACAP to VPAC2 receptors leads to activation of separate transduction pathways.	bind
21235	4	6241	7	NULL	NULL	NULL	NULL	statement 2	Process		leads to					transduction pathways	Process	activation of			NULL	during stages of brain development	NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_314_2_745_s_184	15872042	1) During some stages of brain development, the binding of VIP or PACAP to VPAC2 receptors leads to activation of separate transduction pathways.	bind
21236	5	6241	7	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_314_2_745_s_184	15872042	1) During some stages of brain development, the binding of VIP or PACAP to VPAC2 receptors leads to activation of separate transduction pathways.	bind
16773	1	6242	5	10	NULL	0	NULL	iron			is associated with					high molecular weight fraction					NULL	in phloem	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25062_s_259	11983700	1) Essentially all iron in the phloem is associated with the high molecular weight fraction; 2) ITP-iron complexes rapidly appear in pure phloem exudate after feeding of cotyledons with 55Fe; 3) ITP carries iron  in vivo and is able to bind additional iron  in vitro; 4) purified ITP binds preferentially Fe3+, the dominant iron species in the phloem; and 5) the amino acid sequence of ITP suggests it is capable of binding several metal ions per molecule.	bind
16776	2	6242	5	NULL	NULL	0	NULL	cotyledons	NULL		fed with	NULL				55Fe	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_28_25062_s_259	11983700	1) Essentially all iron in the phloem is associated with the high molecular weight fraction; 2) ITP-iron complexes rapidly appear in pure phloem exudate after feeding of cotyledons with 55Fe; 3) ITP carries iron  in vivo and is able to bind additional iron  in vitro; 4) purified ITP binds preferentially Fe3+, the dominant iron species in the phloem; and 5) the amino acid sequence of ITP suggests it is capable of binding several metal ions per molecule.	bind
16778	3	6242	5	NULL	NULL	0	NULL	ITP-iron complexes	NULL		appear in	NULL	rapidly			phloem exudate	NULL	pure			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25062_s_259	11983700	1) Essentially all iron in the phloem is associated with the high molecular weight fraction; 2) ITP-iron complexes rapidly appear in pure phloem exudate after feeding of cotyledons with 55Fe; 3) ITP carries iron  in vivo and is able to bind additional iron  in vitro; 4) purified ITP binds preferentially Fe3+, the dominant iron species in the phloem; and 5) the amino acid sequence of ITP suggests it is capable of binding several metal ions per molecule.	bind
16779	4	6242	5	NULL	NULL	0	NULL	statement 3	NULL		occurs after	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_28_25062_s_259	11983700	1) Essentially all iron in the phloem is associated with the high molecular weight fraction; 2) ITP-iron complexes rapidly appear in pure phloem exudate after feeding of cotyledons with 55Fe; 3) ITP carries iron  in vivo and is able to bind additional iron  in vitro; 4) purified ITP binds preferentially Fe3+, the dominant iron species in the phloem; and 5) the amino acid sequence of ITP suggests it is capable of binding several metal ions per molecule.	bind
16781	5	6242	5	NULL	NULL	0	NULL	ITP	NULL		carries	NULL				iron	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_jbiolchem_277_28_25062_s_259	11983700	1) Essentially all iron in the phloem is associated with the high molecular weight fraction; 2) ITP-iron complexes rapidly appear in pure phloem exudate after feeding of cotyledons with 55Fe; 3) ITP carries iron  in vivo and is able to bind additional iron  in vitro; 4) purified ITP binds preferentially Fe3+, the dominant iron species in the phloem; and 5) the amino acid sequence of ITP suggests it is capable of binding several metal ions per molecule.	bind
16783	6	6242	5	NULL	NULL	0	NULL	ITP	NULL		bind	NULL				iron	NULL	additional			NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_277_28_25062_s_259	11983700	1) Essentially all iron in the phloem is associated with the high molecular weight fraction; 2) ITP-iron complexes rapidly appear in pure phloem exudate after feeding of cotyledons with 55Fe; 3) ITP carries iron  in vivo and is able to bind additional iron  in vitro; 4) purified ITP binds preferentially Fe3+, the dominant iron species in the phloem; and 5) the amino acid sequence of ITP suggests it is capable of binding several metal ions per molecule.	bind
16784	7	6242	5	NULL	NULL	0	NULL	ITP	NULL	purified	bind	NULL	preferentially			Fe3+	NULL				NULL	in phloem	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25062_s_259	11983700	1) Essentially all iron in the phloem is associated with the high molecular weight fraction; 2) ITP-iron complexes rapidly appear in pure phloem exudate after feeding of cotyledons with 55Fe; 3) ITP carries iron  in vivo and is able to bind additional iron  in vitro; 4) purified ITP binds preferentially Fe3+, the dominant iron species in the phloem; and 5) the amino acid sequence of ITP suggests it is capable of binding several metal ions per molecule.	bind
16785	8	6242	5	NULL	NULL	0	NULL	Fe3+	NULL		is	NULL				dominant iron species	NULL				NULL	in phloem	0	NULL	NULL	NULL	gw60_jbiolchem_277_28_25062_s_259	11983700	1) Essentially all iron in the phloem is associated with the high molecular weight fraction; 2) ITP-iron complexes rapidly appear in pure phloem exudate after feeding of cotyledons with 55Fe; 3) ITP carries iron  in vivo and is able to bind additional iron  in vitro; 4) purified ITP binds preferentially Fe3+, the dominant iron species in the phloem; and 5) the amino acid sequence of ITP suggests it is capable of binding several metal ions per molecule.	bind
16786	9	6242	5	NULL	NULL	0	NULL	ITP	NULL		bind	NULL				metal ions per molecule	NULL	several			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_28_25062_s_259	11983700	1) Essentially all iron in the phloem is associated with the high molecular weight fraction; 2) ITP-iron complexes rapidly appear in pure phloem exudate after feeding of cotyledons with 55Fe; 3) ITP carries iron  in vivo and is able to bind additional iron  in vitro; 4) purified ITP binds preferentially Fe3+, the dominant iron species in the phloem; and 5) the amino acid sequence of ITP suggests it is capable of binding several metal ions per molecule.	bind
16787	10	6242	5	NULL	NULL	0	NULL	ITP	NULL	amino acid sequence	suggest	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_28_25062_s_259	11983700	1) Essentially all iron in the phloem is associated with the high molecular weight fraction; 2) ITP-iron complexes rapidly appear in pure phloem exudate after feeding of cotyledons with 55Fe; 3) ITP carries iron  in vivo and is able to bind additional iron  in vitro; 4) purified ITP binds preferentially Fe3+, the dominant iron species in the phloem; and 5) the amino acid sequence of ITP suggests it is capable of binding several metal ions per molecule.	bind
21237	1	6242	7	NULL	NULL	NULL	NULL	ITP-iron complex	GP		appear in		rapidly			 phloem exudate	OrganismPart	pure			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25062_s_259	11983700	1) Essentially all iron in the phloem is associated with the high molecular weight fraction; 2) ITP-iron complexes rapidly appear in pure phloem exudate after feeding of cotyledons with 55Fe; 3) ITP carries iron  in vivo and is able to bind additional iron  in vitro; 4) purified ITP binds preferentially Fe3+, the dominant iron species in the phloem; and 5) the amino acid sequence of ITP suggests it is capable of binding several metal ions per molecule.	bind
21238	2	6242	7	NULL	NULL	NULL	NULL	cotyledons	OrganismPart		fed with					 Fe	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25062_s_259	11983700	1) Essentially all iron in the phloem is associated with the high molecular weight fraction; 2) ITP-iron complexes rapidly appear in pure phloem exudate after feeding of cotyledons with 55Fe; 3) ITP carries iron  in vivo and is able to bind additional iron  in vitro; 4) purified ITP binds preferentially Fe3+, the dominant iron species in the phloem; and 5) the amino acid sequence of ITP suggests it is capable of binding several metal ions per molecule.	bind
21239	3	6242	7	NULL	NULL	NULL	NULL	ITP	GP		carries					iron	Chemical				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25062_s_259	11983700	1) Essentially all iron in the phloem is associated with the high molecular weight fraction; 2) ITP-iron complexes rapidly appear in pure phloem exudate after feeding of cotyledons with 55Fe; 3) ITP carries iron  in vivo and is able to bind additional iron  in vitro; 4) purified ITP binds preferentially Fe3+, the dominant iron species in the phloem; and 5) the amino acid sequence of ITP suggests it is capable of binding several metal ions per molecule.	bind
21240	4	6242	7	NULL	NULL	NULL	NULL	statement 3	Process		binds					iron	Chemical				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25062_s_259	11983700	1) Essentially all iron in the phloem is associated with the high molecular weight fraction; 2) ITP-iron complexes rapidly appear in pure phloem exudate after feeding of cotyledons with 55Fe; 3) ITP carries iron  in vivo and is able to bind additional iron  in vitro; 4) purified ITP binds preferentially Fe3+, the dominant iron species in the phloem; and 5) the amino acid sequence of ITP suggests it is capable of binding several metal ions per molecule.	bind
21241	5	6242	7	NULL	NULL	NULL	NULL	ITP	GP	purified	binds		preferentially			Fe3+	Chemical				NULL	in the phloem	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25062_s_259	11983700	1) Essentially all iron in the phloem is associated with the high molecular weight fraction; 2) ITP-iron complexes rapidly appear in pure phloem exudate after feeding of cotyledons with 55Fe; 3) ITP carries iron  in vivo and is able to bind additional iron  in vitro; 4) purified ITP binds preferentially Fe3+, the dominant iron species in the phloem; and 5) the amino acid sequence of ITP suggests it is capable of binding several metal ions per molecule.	bind
21242	6	6242	7	NULL	NULL	NULL	NULL	ITP 	GP		bind					metal ions 	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25062_s_259	11983700	1) Essentially all iron in the phloem is associated with the high molecular weight fraction; 2) ITP-iron complexes rapidly appear in pure phloem exudate after feeding of cotyledons with 55Fe; 3) ITP carries iron  in vivo and is able to bind additional iron  in vitro; 4) purified ITP binds preferentially Fe3+, the dominant iron species in the phloem; and 5) the amino acid sequence of ITP suggests it is capable of binding several metal ions per molecule.	bind
21243	7	6242	7	NULL	NULL	NULL	NULL	iron	Chemical	phloem	associate with					high molecular weight fraction	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25062_s_259	11983700	1) Essentially all iron in the phloem is associated with the high molecular weight fraction; 2) ITP-iron complexes rapidly appear in pure phloem exudate after feeding of cotyledons with 55Fe; 3) ITP carries iron  in vivo and is able to bind additional iron  in vitro; 4) purified ITP binds preferentially Fe3+, the dominant iron species in the phloem; and 5) the amino acid sequence of ITP suggests it is capable of binding several metal ions per molecule.	bind
45559	8	6242	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs after					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25062_s_259	11983700	1) Essentially all iron in the phloem is associated with the high molecular weight fraction; 2) ITP-iron complexes rapidly appear in pure phloem exudate after feeding of cotyledons with 55Fe; 3) ITP carries iron  in vivo and is able to bind additional iron  in vitro; 4) purified ITP binds preferentially Fe3+, the dominant iron species in the phloem; and 5) the amino acid sequence of ITP suggests it is capable of binding several metal ions per molecule.	bind
16788	1	6243	5	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL				alphaIIbbeta3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_28_25715_s_179	11994301	1) Expression of constitutively active Rap1b (V12) augments fibrinogen binding to alphaIIbbeta3 when megakaryocytes are stimulated through the PAR4 thrombin receptor.	bind
16789	2	6243	5	NULL	NULL	0	NULL	PAR4 thrombin receptor	NULL		stimulate	NULL				megakaryocytes	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_28_25715_s_179	11994301	1) Expression of constitutively active Rap1b (V12) augments fibrinogen binding to alphaIIbbeta3 when megakaryocytes are stimulated through the PAR4 thrombin receptor.	bind
16790	4	6243	5	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25715_s_179	11994301	1) Expression of constitutively active Rap1b (V12) augments fibrinogen binding to alphaIIbbeta3 when megakaryocytes are stimulated through the PAR4 thrombin receptor.	bind
16791	3	6243	5	10	NULL	0	NULL	Rap1b (V12)	NULL	constitutively active	augment	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25715_s_179	11994301	1) Expression of constitutively active Rap1b (V12) augments fibrinogen binding to alphaIIbbeta3 when megakaryocytes are stimulated through the PAR4 thrombin receptor.	bind
21244	1	6243	7	NULL	NULL	NULL	NULL	fibrinogen	GP		bind					 alphaIIbbeta3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25715_s_179	11994301	1) Expression of constitutively active Rap1b (V12) augments fibrinogen binding to alphaIIbbeta3 when megakaryocytes are stimulated through the PAR4 thrombin receptor.	bind
21245	2	6243	7	NULL	NULL	NULL	NULL	Rap1b (V12) 	GP	constitutively active	augments					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25715_s_179	11994301	1) Expression of constitutively active Rap1b (V12) augments fibrinogen binding to alphaIIbbeta3 when megakaryocytes are stimulated through the PAR4 thrombin receptor.	bind
21246	3	6243	7	NULL	NULL	NULL	NULL	PAR4 thrombin receptor	GP		stimulate					megakaryocytes	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25715_s_179	11994301	1) Expression of constitutively active Rap1b (V12) augments fibrinogen binding to alphaIIbbeta3 when megakaryocytes are stimulated through the PAR4 thrombin receptor.	bind
26358	4	6243	7	NULL	NULL	NULL	NULL	statement 3	Process		lead to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25715_s_179	11994301	1) Expression of constitutively active Rap1b (V12) augments fibrinogen binding to alphaIIbbeta3 when megakaryocytes are stimulated through the PAR4 thrombin receptor.	bind
16792	1	6244	5	NULL	NULL	0	NULL	5-HT4(a)	NULL		induce	NULL					NULL	activation of		SRE	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
16793	2	6244	5	10	NULL	0	NULL	Galpha13	NULL	wild type	enhance	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
16794	3	6244	5	NULL	NULL	0	NULL	p115RhoGEF	NULL		inhibit	NULL		RGS domain		Galpha13	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
16795	4	6244	5	NULL	NULL	0	NULL	p115RhoGEF	NULL		is specific for	NULL				Galpha12	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
16796	5	6244	5	NULL	NULL	0	NULL	p115RhoGEF	NULL		is specific for	NULL		RGS domain		Galpha13	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
16797	6	6244	5	NULL	NULL	0	NULL	5-HT4(a)	NULL		activate	NULL					NULL			SRE	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
16798	7	6244	5	10	NULL	0	NULL	C3 exoenzyme			inhibit					statement 6					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
16799	8	6244	5	NULL	NULL	0	NULL	Galpha13	NULL		induce	NULL					NULL	activation of		SRE	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
16800	9	6244	5	NULL	NULL	0	NULL	p115RhoGEF	NULL		inhibit	NULL	effectively			statement 8	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
16801	10	6244	5	NULL	NULL	0	NULL	C3 exoenzyme	NULL		inhibit	NULL	effectively			statement 8	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
16802	11	6244	5	NULL	NULL	0	NULL	5-HT4(a) receptor	NULL		activate	NULL				Rho	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
54173	12	6244	5	10	NULL	0	NULL	C3 exoenzyme			is an inhibitor of		specific			Rho proteins					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
21305	1	6244	7	NULL	NULL	NULL	NULL	5-HT4	Chemical		induce							activation of		 SRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
21307	2	6244	7	NULL	NULL	NULL	NULL	Galpha13	GP	wild type	enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
21368	3	6244	7	NULL	NULL	NULL	NULL	p115RhoGEF	GP		inhibits			RGS domain		Galpha13	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
21369	4	6244	7	NULL	NULL	NULL	NULL	5-HT4	Chemical		activates									SRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
21370	5	6244	7	NULL	NULL	NULL	NULL	C3 exoenzyme	GP		inhibits					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
21371	6	6244	7	NULL	NULL	NULL	NULL	C3 exoenzyme	GP		inhibits					Rho proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
21376	7	6244	7	NULL	NULL	NULL	NULL	5-HT4 receptor	GP		activate					Rho	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
55033	8	6244	7	NULL	NULL	NULL	NULL	 p115RhoGEF	GP		is specific for			RGS domain		Galpha12	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
55035	9	6244	7	NULL	NULL	NULL	NULL	p115RhoGEF	GP		is specific for			RGS domain		Galpha13	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
55036	10	6244	7	NULL	NULL	NULL	NULL	Galpha13	GP		induce							activation of		SRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
55037	11	6244	7	NULL	NULL	NULL	NULL	p115RhoGEF	GP		inhibit		effectively			statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
55039	12	6244	7	NULL	NULL	NULL	NULL	C3 exoenzyme	GP		inhibit		effectively			statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20812_s_295	11923294	1) Expression of wild type Galpha13 enhanced 5-HT4(a)-induced SRE activation (Fig.  5); 2) Galpha13 was inhibited by the RGS domain of p115RhoGEF, which is specific for Galpha12 and Galpha13 (Fig.  4); 3) C3 exoenzyme, a specific inhibitor of Rho proteins, inhibited SRE activation by 5-HT4(a) (Fig.  6); 4) the above-mentioned inhibitors and dominant-negative constructs also effectively inhibited SRE activation induced by Galpha13; 5) finally, direct measurement of Rho activity using a rhotekin binding assay showed that the 5-HT4(a) receptor is able to activate Rho (Fig.  6 C).	bind
16803	1	6245	5	NULL	NULL	0	NULL	Gbeta	NULL		bind	NULL	specifically			CCT/TRiC complex	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_29_20221_s_330	16702223	1) Gbeta specifically binds CCT/TRiC (Figs.  5 and  6), a complex involved in protein folding ( ,  ,  ) and protein complex formation ( ,  ), shortly after its synthesis ( Fig. 8); there is a lag of several minutes before dimer formation, as would be expected if folding of Gbeta on CCT/TRiC is a requirement for production of functional Gbeta.	bind
16804	2	6245	5	NULL	NULL	0	NULL	CCT/TRiC complex	NULL		is involved in	NULL				protein folding	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_20221_s_330	16702223	1) Gbeta specifically binds CCT/TRiC (Figs.  5 and  6), a complex involved in protein folding ( ,  ,  ) and protein complex formation ( ,  ), shortly after its synthesis ( Fig. 8); there is a lag of several minutes before dimer formation, as would be expected if folding of Gbeta on CCT/TRiC is a requirement for production of functional Gbeta.	bind
16805	3	6245	5	NULL	NULL	0	NULL	CCT/TRiC complex	NULL		is involved in	NULL				protein complex formation, shortly after its synthesis	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_29_20221_s_330	16702223	1) Gbeta specifically binds CCT/TRiC (Figs.  5 and  6), a complex involved in protein folding ( ,  ,  ) and protein complex formation ( ,  ), shortly after its synthesis ( Fig. 8); there is a lag of several minutes before dimer formation, as would be expected if folding of Gbeta on CCT/TRiC is a requirement for production of functional Gbeta.	bind
21382	1	6245	7	NULL	NULL	NULL	NULL	Gbeta 	GP		binds		specifically			CCT/TRiC complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_20221_s_330	16702223	1) Gbeta specifically binds CCT/TRiC (Figs.  5 and  6), a complex involved in protein folding ( ,  ,  ) and protein complex formation ( ,  ), shortly after its synthesis ( Fig. 8); there is a lag of several minutes before dimer formation, as would be expected if folding of Gbeta on CCT/TRiC is a requirement for production of functional Gbeta.	bind
21386	2	6245	7	NULL	NULL	NULL	NULL	CCT/TRiC complex	GP		is involved in					protein folding	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_20221_s_330	16702223	1) Gbeta specifically binds CCT/TRiC (Figs.  5 and  6), a complex involved in protein folding ( ,  ,  ) and protein complex formation ( ,  ), shortly after its synthesis ( Fig. 8); there is a lag of several minutes before dimer formation, as would be expected if folding of Gbeta on CCT/TRiC is a requirement for production of functional Gbeta.	bind
21388	3	6245	7	NULL	NULL	NULL	NULL	CCT/TRiC complex	GP		is involved in					protein complex 	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_20221_s_330	16702223	1) Gbeta specifically binds CCT/TRiC (Figs.  5 and  6), a complex involved in protein folding ( ,  ,  ) and protein complex formation ( ,  ), shortly after its synthesis ( Fig. 8); there is a lag of several minutes before dimer formation, as would be expected if folding of Gbeta on CCT/TRiC is a requirement for production of functional Gbeta.	bind
16806	1	6246	5	NULL	NULL	0	NULL	hyaluronan	NULL		bind	NULL				CD44	NULL	clustered			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_37_35111_s_377	11451952	1) hyaluronan binds to clustered CD44 and possibly other unknown cell surface receptors.	bind
16807	2	6246	5	NULL	NULL	0	NULL	hyaluronan	NULL		bind	NULL	possibly			cell surface receptors	NULL	other unknown			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_37_35111_s_377	11451952	1) hyaluronan binds to clustered CD44 and possibly other unknown cell surface receptors.	bind
21394	1	6246	7	NULL	NULL	NULL	NULL	hyaluronan	Chemical		binds					CD44	Cell	clustered 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_37_35111_s_377	11451952	1) hyaluronan binds to clustered CD44 and possibly other unknown cell surface receptors.	bind
21397	2	6246	7	NULL	NULL	NULL	NULL	hyaluronan	Chemical		binds		possibly			cell surface receptor	GP	unknown			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_37_35111_s_377	11451952	1) hyaluronan binds to clustered CD44 and possibly other unknown cell surface receptors.	bind
16809	1	6248	5	NULL	NULL	0	NULL	SopE2	NULL		bind	NULL				Rac1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_36_34035_s_197	11440999	1) In the absence of free guanine nucleotide, the equilibrium binding of SopE2 to Cdc42 is ~40-fold stronger than binding of SopE2 to Rac1.	bind
16810	2	6248	5	NULL	NULL	0	NULL	SopE2	NULL		bind	NULL				Cdc42	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_36_34035_s_197	11440999	1) In the absence of free guanine nucleotide, the equilibrium binding of SopE2 to Cdc42 is ~40-fold stronger than binding of SopE2 to Rac1.	bind
16811	3	6248	5	NULL	NULL	0	NULL	statement 2	NULL	equilibrium binding of 	is stronger than	NULL				statement 1	NULL	equilibrium binding of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_36_34035_s_197	11440999	1) In the absence of free guanine nucleotide, the equilibrium binding of SopE2 to Cdc42 is ~40-fold stronger than binding of SopE2 to Rac1.	bind
16812	4	6248	5	NULL	NULL	0	NULL	statement 3	NULL		in the absence of	NULL				guanine nucleotide	NULL	free			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_36_34035_s_197	11440999	1) In the absence of free guanine nucleotide, the equilibrium binding of SopE2 to Cdc42 is ~40-fold stronger than binding of SopE2 to Rac1.	bind
21403	1	6248	7	NULL	NULL	NULL	NULL	SopE2	GP		bind					Cdc42	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_36_34035_s_197	11440999	1) In the absence of free guanine nucleotide, the equilibrium binding of SopE2 to Cdc42 is ~40-fold stronger than binding of SopE2 to Rac1.	bind
21404	2	6248	7	NULL	NULL	NULL	NULL	SopE2	GP		bind					Rac1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_36_34035_s_197	11440999	1) In the absence of free guanine nucleotide, the equilibrium binding of SopE2 to Cdc42 is ~40-fold stronger than binding of SopE2 to Rac1.	bind
21408	3	6248	7	NULL	NULL	NULL	NULL	statement 1	Process	equilibrium binding of 	is stronger than					statement 2	Process	equilibrium binding of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_36_34035_s_197	11440999	1) In the absence of free guanine nucleotide, the equilibrium binding of SopE2 to Cdc42 is ~40-fold stronger than binding of SopE2 to Rac1.	bind
26360	4	6248	7	NULL	NULL	NULL	NULL	statement 3	Process		in the absence of					 guanine nucleotide	Chemical	free			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_36_34035_s_197	11440999	1) In the absence of free guanine nucleotide, the equilibrium binding of SopE2 to Cdc42 is ~40-fold stronger than binding of SopE2 to Rac1.	bind
16813	1	6250	5	NULL	NULL	0	NULL	pPL86 RNCs	NULL		bind	NULL				RM	NULL				NULL	translocation sites	0	NULL	NULL	NULL	gw60_jbiolchem_275_43_33828_s_247	10924518	1) In the study of Murphy  et al. ( 24), pPL86 RNCs were bound to RM in stoichiometric excess to translocation sites, and mild proteolysis was then performed to determine if a population of SRP receptor had become sequestered in a protease-resistant site.	bind
21414	1	6250	7	NULL	NULL	NULL	NULL	pPL86 RNCs	GP		bind					RM	CellComponent				NULL	translocation sites	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_43_33828_s_247	10924518	1) In the study of Murphy  et al. ( 24), pPL86 RNCs were bound to RM in stoichiometric excess to translocation sites, and mild proteolysis was then performed to determine if a population of SRP receptor had become sequestered in a protease-resistant site.	bind
16814	1	6251	5	NULL	NULL	0	NULL	FITC-Gal-PLL	NULL		bind	NULL				rML	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_27_16056_s_119	7541793	1) Ligand (FITC-Gal-PLL) binding to rML was not inhibited by LOM-11 ( Fig. 4).	bind
16815	2	6251	5	NULL	NULL	0	NULL	LOM-11	NULL		does not inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_27_16056_s_119	7541793	1) Ligand (FITC-Gal-PLL) binding to rML was not inhibited by LOM-11 ( Fig. 4).	bind
21416	1	6251	7	NULL	NULL	NULL	NULL	FITC-Gal-PLL	AminoAcid		bind					rML	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_27_16056_s_119	7541793	1) Ligand (FITC-Gal-PLL) binding to rML was not inhibited by LOM-11 ( Fig. 4).	bind
21417	2	6251	7	NULL	NULL	NULL	NULL	 LOM-11	GP		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_27_16056_s_119	7541793	1) Ligand (FITC-Gal-PLL) binding to rML was not inhibited by LOM-11 ( Fig. 4).	bind
16816	1	6252	5	NULL	NULL	0	NULL	T3 	NULL		bind	NULL				TR	NULL				NULL	in solution	0	NULL	NULL	NULL	gw60_jbiolchem_273_46_30175_s_223	9804773	1) Most RTH mutations affect T3 binding to TR in solution or on DNA, as is the case with hinge mutants.	bind
16817	2	6252	5	NULL	NULL	0	NULL	T3	NULL		bind	NULL				TR	NULL				NULL	on DNA	0	NULL	NULL	NULL	gw60_jbiolchem_273_46_30175_s_223	9804773	1) Most RTH mutations affect T3 binding to TR in solution or on DNA, as is the case with hinge mutants.	bind
16818	3	6252	5	10	NULL	0	NULL	RTH 	NULL	mutation of	affect	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30175_s_223	9804773	1) Most RTH mutations affect T3 binding to TR in solution or on DNA, as is the case with hinge mutants.	bind
16819	4	6252	5	10	NULL	0	NULL	RTH	NULL	mutation of	affect	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30175_s_223	9804773	1) Most RTH mutations affect T3 binding to TR in solution or on DNA, as is the case with hinge mutants.	bind
16824	5	6252	5	NULL	NULL	0	NULL	hinge mutants	NULL		affect	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_46_30175_s_223	9804773	1) Most RTH mutations affect T3 binding to TR in solution or on DNA, as is the case with hinge mutants.	bind
16825	6	6252	5	NULL	NULL	0	NULL	hinge mutants	NULL		affect	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_46_30175_s_223	9804773	1) Most RTH mutations affect T3 binding to TR in solution or on DNA, as is the case with hinge mutants.	bind
21418	1	6252	7	NULL	NULL	NULL	NULL	T3	GP		bind					TR	GP				NULL	in solution	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30175_s_223	9804773	1) Most RTH mutations affect T3 binding to TR in solution or on DNA, as is the case with hinge mutants.	bind
21420	2	6252	7	NULL	NULL	NULL	NULL	T3	GP		bind					TR	GP				NULL	on DNA	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30175_s_223	9804773	1) Most RTH mutations affect T3 binding to TR in solution or on DNA, as is the case with hinge mutants.	bind
21423	3	6252	7	NULL	NULL	NULL	NULL	RTH	Process	mutation of	affect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30175_s_223	9804773	1) Most RTH mutations affect T3 binding to TR in solution or on DNA, as is the case with hinge mutants.	bind
21428	4	6252	7	NULL	NULL	NULL	NULL	RTH	Process	mutation of	affect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30175_s_223	9804773	1) Most RTH mutations affect T3 binding to TR in solution or on DNA, as is the case with hinge mutants.	bind
26362	5	6252	7	NULL	NULL	NULL	NULL	hinge mutants	Chemical		affect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30175_s_223	9804773	1) Most RTH mutations affect T3 binding to TR in solution or on DNA, as is the case with hinge mutants.	bind
26363	6	6252	7	NULL	NULL	NULL	NULL	hinge mutants	Chemical		affect					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30175_s_223	9804773	1) Most RTH mutations affect T3 binding to TR in solution or on DNA, as is the case with hinge mutants.	bind
16828	1	6253	5	NULL	NULL	0	NULL	HSPG	NULL		is	NULL				heparan sulfate proteoglycans	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16829	2	6253	5	NULL	NULL	0	NULL	MV	NULL		is	NULL				microvilli	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16830	3	6253	5	NULL	NULL	0	NULL	HSPG	NULL		is distributed on	NULL	mostly			MV	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16833	4	6253	5	NULL	NULL	0	NULL	LPL	NULL		bind	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16835	5	6253	5	NULL	NULL	0	NULL	LPL-TRL	NULL		bind	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16836	6	6253	5	NULL	NULL	0	NULL	nCV	NULL		is	NULL				non-coated pit vesicles	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16838	7	6253	5	NULL	NULL	0	NULL	LPL & associated TRL	NULL		is internalized by	NULL				HSPG	NULL				NULL	in nCV	0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16843	8	6253	5	NULL	NULL	0	NULL	nCV	NULL	after uptake	meet	NULL				EE	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16844	9	6253	5	NULL	NULL	0	NULL	EE	NULL		is	NULL				early endosomes	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16845	10	6253	5	NULL	NULL	0	NULL	nCV	NULL	after uptake	fuse to	NULL				EE	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16846	11	6253	5	NULL	NULL	0	NULL	statement 10	NULL		is an alternative to	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16847	12	6253	5	NULL	NULL	0	NULL	LPL	NULL		seperate from	NULL				TRL	NULL				NULL	in EE	0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16848	13	6253	5	NULL	NULL	0	NULL	LPL	NULL		is delivered to	NULL				MVB	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16849	14	6253	5	NULL	NULL	0	NULL	MVB	NULL		is	NULL				multivesicular bodies	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16850	15	6253	5	NULL	NULL	0	NULL	LPL	NULL		is delivered to	NULL	probably			Lys	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16851	16	6253	5	NULL	NULL	0	NULL	Lys	NULL		is	NULL				lysosomes	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16852	17	6253	5	NULL	NULL	0	NULL	TRL	NULL		is retained within	NULL				EE	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16853	18	6253	5	NULL	NULL	0	NULL	TRL	NULL		is retained within	NULL				compartments	NULL	other			NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16854	19	6253	5	NULL	NULL	0	NULL	statement 17	NULL		is an alternative to	NULL				statement 18	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16855	20	6253	5	NULL	NULL	0	NULL	LPL	NULL	some	bind	NULL				HSPG	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16856	21	6253	5	NULL	NULL	0	NULL	TRL	NULL	some LPL-associated	bind	NULL				HSPG	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16857	22	6253	5	NULL	NULL	0	NULL	statement 20	NULL		recognized by	NULL	could be			LRP	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16858	23	6253	5	NULL	NULL	0	NULL	statement 21	NULL		recognized by	NULL	could be			LDLr	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16859	24	6253	5	NULL	NULL	0	NULL	statement 22	NULL		is an alternative to	NULL				statement 23	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16860	25	6253	5	NULL	NULL	0	NULL	statement 20	NULL		taken up by	NULL	could be			LRP	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16861	26	6253	5	NULL	NULL	0	NULL	statement 21	NULL		taken up by	NULL	could be			LDLr	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16862	27	6253	5	NULL	NULL	0	NULL	statement 25	NULL		is an alternative to	NULL				statement 26	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16863	28	6253	5	NULL	NULL	0	NULL	cv	NULL		is	NULL				coated pit	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16864	29	6253	5	NULL	NULL	0	NULL	statement 25	NULL		follows	NULL				cv endocytosis pathway	NULL	to lysosomes			NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16865	30	6253	5	NULL	NULL	0	NULL	statement 26	NULL		follows	NULL				cv endocytosis pathway	NULL	to lysosomes			NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16866	31	6253	5	NULL	NULL	0	NULL	TRL	NULL		is recognized by	NULL				coated pit-associated receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16867	32	6253	5	NULL	NULL	0	NULL	TRL	NULL		is internalized by	NULL				coated pit-associated receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16868	33	6253	5	NULL	NULL	0	NULL	statement 31	NULL		in the absence of	NULL				LPL	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
16869	34	6253	5	NULL	NULL	0	NULL	statement 32	NULL		in the absence of	NULL				LPL	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21491	1	6253	7	NULL	NULL	NULL	NULL	LPL	GP		are distributed in			Primary binding-site		HSPG	Chemical	microvilli 			NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21492	2	6253	7	NULL	NULL	NULL	NULL	LPL-TRL	GP		are distributed in			Primary binding-site		HSPG	Chemical	microvilli 			NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21493	3	6253	7	NULL	NULL	NULL	NULL	 LPL	GP		associate with					TRL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21494	4	6253	7	NULL	NULL	NULL	NULL	statement 3	Process		is internalized					HSPG	Chemical	in nCV			NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21495	5	6253	7	NULL	NULL	NULL	NULL	nCV	CellComponent		fuse to					EE	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21496	6	6253	7	NULL	NULL	NULL	NULL	LPL	GP		separate from					TRL	GP				NULL	in EE	NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21497	7	6253	7	NULL	NULL	NULL	NULL	LPL	GP		delivered to					MVB	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21498	8	6253	7	NULL	NULL	NULL	NULL	LPL	GP		delivered to					Lys	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21499	9	6253	7	NULL	NULL	NULL	NULL	TRL	GP		is retained within					early endosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21500	10	6253	7	NULL	NULL	NULL	NULL	LPL	GP		bind					HSPG	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21501	11	6253	7	NULL	NULL	NULL	NULL	TRL	GP	LPL-associated	bind					HSPG	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21502	12	6253	7	NULL	NULL	NULL	NULL	statement 10	Process		taken up by					LRP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21503	13	6253	7	NULL	NULL	NULL	NULL	statement 11	Process		taken up by					LRP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21504	14	6253	7	NULL	NULL	NULL	NULL	statement 10	Process		taken up by					LDLr	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21505	15	6253	7	NULL	NULL	NULL	NULL	statement 11	Process		taken up by					LDLr	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21506	16	6253	7	NULL	NULL	NULL	NULL	statement 14	Process		is an alternative to					statement 12	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21507	17	6253	7	NULL	NULL	NULL	NULL	statement 15	Process		is an alternative to					statement 13	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21508	18	6253	7	NULL	NULL	NULL	NULL	statement 12	Process		follows to					coated pit endocytosis pathway to the lysosomes	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21509	19	6253	7	NULL	NULL	NULL	NULL	statement 13	Process		follows to					coated pit endocytosis pathway to the lysosomes	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21510	20	6253	7	NULL	NULL	NULL	NULL	statement 14	Process		follows to					coated pit endocytosis pathway to the lysosomes	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21511	21	6253	7	NULL	NULL	NULL	NULL	statement 15	Process		follows to					coated pit endocytosis pathway to the lysosomes	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21512	22	6253	7	NULL	NULL	NULL	NULL	 TRL 	GP		is internalized by					coated pit-associated receptors	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21513	23	6253	7	NULL	NULL	NULL	NULL	statement 22	Process		occurs in absence of					LPL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21514	24	6253	7	NULL	NULL	NULL	NULL	HSPG	Chemical		is					heparan sulfate proteoglycans	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21515	25	6253	7	NULL	NULL	NULL	NULL	MV	OrganismPart		is					microvilli	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21516	26	6253	7	NULL	NULL	NULL	NULL	nCV	CellComponent		is					non-coated pit vesicles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21517	27	6253	7	NULL	NULL	NULL	NULL	EE	CellComponent		is					early endosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21518	28	6253	7	NULL	NULL	NULL	NULL	MVB	CellComponent		is					multivesicular bodies	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21519	29	6253	7	NULL	NULL	NULL	NULL	Lys	CellComponent		is					lysosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
21520	30	6253	7	NULL	NULL	NULL	NULL	cv	CellComponent		is					 coated pit	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_4_789_s_317	9555944	1) Primary binding-sites for LPL and LPL-TRL are heparan sulfate proteoglycans (HSPG), which are distributed mostly on the microvilli (MV); 2) LPL together with associated TRL are internalized by HSPG in non-coated pit vesicles (nCV); 3) after uptake, these vesicles meet or fuse to early endosomes (EE), where LPL and TRL could separate; 4) LPL is delivered to multivesicular bodies (MVB) and probably to lysosomes (Lys); 5) TRL are retained either within the same early endosomes or in other compartments; 6) alternatively, some LPL and LPL-associated TRL bound to HSPG could be recognized and taken up by LRP or by LDLr following the coated pit (cv) endocytosis pathway to the lysosomes; 7) in the absence of LPL, TRL are recognized and internalized by coated pit-associated receptors.	bind
19264	1	6254	5	NULL	NULL	0	NULL	Rab family members	NULL		bind	NULL				GDP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
19265	2	6254	5	NULL	NULL	0	NULL	Rab GDI	NULL		bind	NULL	preferentially			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
19266	4	6254	5	NULL	NULL	0	NULL	statement 1	NULL		is converted to	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
19267	5	6254	5	NULL	NULL	0	NULL	Rab GEP	NULL	action of each	is required for	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
19268	6	6254	5	NULL	NULL	0	NULL	Rab GDI	NULL		prevents	NULL				statement 4	NULL				NULL	in cytosol	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
19269	7	6254	5	NULL	NULL	0	NULL	Rab family members	NULL		is kept as	NULL				statement 1	NULL				NULL	in cytosol	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
19270	8	6254	5	NULL	NULL	0	NULL	statement 6	NULL		results in	NULL				statement 7	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
19271	9	6254	5	NULL	NULL	0	NULL	Rab GDI	NULL		is associated with	NULL				target membranes	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
19272	10	6254	5	NULL	NULL	0	NULL	statement 9	NULL		results in	NULL				statement 7	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
19273	11	6254	5	NULL	NULL	0	NULL	Rab family members	NULL	complexed	is transported to	NULL				target membranes	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
19274	13	6254	5	NULL	NULL	0	NULL	statement 1	NULL		is dissociated from	NULL				Rab GDI	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
19275	14	6254	5	NULL	NULL	0	NULL	statement 11	NULL		leads to	NULL				statement 13	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
19276	15	6254	5	NULL	NULL	0	NULL	Rab GDI displacement factor	NULL	action of each putative	is required for	NULL				statement 13	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
19277	16	6254	5	NULL	NULL	0	NULL	statement 15	NULL		is followed by	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
19278	17	6254	5	NULL	NULL	0	NULL	statement 3	NULL		is converted to	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
19279	18	6254	5	NULL	NULL	0	NULL	Rab GAP	NULL	action of each	is required for	NULL				statement 17	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
46191	3	6254	5	NULL	NULL	0	NULL	Rab family members	NULL		bind	NULL				GTP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
46193	12	6254	5	NULL	NULL	0	NULL	Rab GDI	NULL		is required for	NULL				statement 11	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
21521	2	6254	7	NULL	NULL	NULL	NULL	Rab GDI	GP		interacts with		preferentially			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
21522	3	6254	7	NULL	NULL	NULL	NULL	statement 2	Process		keeps					statement 1	Process				NULL	in the cytosol	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
21523	5	6254	7	NULL	NULL	NULL	NULL	statement 1	Process		converts to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
21524	6	6254	7	NULL	NULL	NULL	NULL	statement 5	Process		is converted by					Rab GEP 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
21525	7	6254	7	NULL	NULL	NULL	NULL	statement 3	Process		prevents					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
21526	8	6254	7	NULL	NULL	NULL	NULL	statement 1	Process		associate with					target membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
21529	11	6254	7	NULL	NULL	NULL	NULL	Rab GDI displacement factor	GP	 putative	dissociates					statement 2	Process	GDP from			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
21530	12	6254	7	NULL	NULL	NULL	NULL	statement 11	Process		is followed by					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
45637	1	6254	7	NULL	NULL	NULL	NULL	GDP	Chemical		bind					Rab family members	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
45638	4	6254	7	NULL	NULL	NULL	NULL	GTP	Chemical		bind					Rab family members	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
45639	9	6254	7	NULL	NULL	NULL	NULL	statement 3	Process		prevents					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
45640	10	6254	7	NULL	NULL	NULL	NULL	Rab GDI	GP		transports					statement 2	Process	to target membranes			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
45641	13	6254	7	NULL	NULL	NULL	NULL	statement 4	Process		accomplishes					function	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
45642	14	6254	7	NULL	NULL	NULL	NULL	statement 13	Process		is converted to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
45643	15	6254	7	NULL	NULL	NULL	NULL	Rab GAP	GP		converts					statement 14	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34580_s_26	9852129	1) Rab GDI preferentially interacts with the GDP-bound form of Rab family members and keeps them in the GDP-bound form in the cytosol by preventing them from being converted to the GTP-bound form by the action of each Rab GEP and from being associated with each of their target membranes; 2) Rab GDI transports its complexed Rab family members to each of their target membranes where the GDP-bound form dissociates from Rab GDI by the action of each putative Rab GDI displacement factor, followed by conversion to the GTP-bound form by the action of each Rab GEP; and 3) after the GTP-bound form accomplishes its function, it is converted to the GDP-bound form by the action of each Rab GAP.	bind
16870	1	6255	5	NULL	NULL	0	NULL	RAP74	NULL		bind	NULL				TFIIB	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_20_11703_s_206	8662660	1) RAP74 could bind TFIIB to block the RAP30 binding site  on TFIIB.	bind
16871	2	6255	5	NULL	NULL	0	NULL	statement 1	NULL		block	NULL				TFIIB	NULL		RAP30 binding site		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_20_11703_s_206	8662660	1) RAP74 could bind TFIIB to block the RAP30 binding site  on TFIIB.	bind
21534	1	6255	7	NULL	NULL	NULL	NULL	RAP74	GP		bind					TFIIB	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_20_11703_s_206	8662660	1) RAP74 could bind TFIIB to block the RAP30 binding site  on TFIIB.	bind
21535	2	6255	7	NULL	NULL	NULL	NULL	statement 1	Process		blocks					TFIIB	GP		RAP30 binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_20_11703_s_206	8662660	1) RAP74 could bind TFIIB to block the RAP30 binding site  on TFIIB.	bind
16872	1	6256	5	NULL	NULL	0	NULL	TR homodimers	NULL		bind	NULL					NULL	positive		TREs	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_24_14274_s_85	7782283	1) T   binding  dissociates TR homodimers from positive TREs ( 39) (see  Fig. 7 A), allowing preferential binding of TR RXR  heterodimers; 2) TR RXR heterodimers have a stronger affinity for  TREs than TR homodimers( 8) ; 3) cotransfection of RXR enhances  the positive transcriptional response to T   on a number of  different elements( 10,  40) ; and 4) more recently yeast  expression systems demonstrate that TR RXR heterodimerization is  necessary for a full ligand-dependent transcriptional  response( 41) .	bind
16873	2	6256	5	NULL	NULL	0	NULL	T binding	NULL		dissociates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_24_14274_s_85	7782283	1) T   binding  dissociates TR homodimers from positive TREs ( 39) (see  Fig. 7 A), allowing preferential binding of TR RXR  heterodimers; 2) TR RXR heterodimers have a stronger affinity for  TREs than TR homodimers( 8) ; 3) cotransfection of RXR enhances  the positive transcriptional response to T   on a number of  different elements( 10,  40) ; and 4) more recently yeast  expression systems demonstrate that TR RXR heterodimerization is  necessary for a full ligand-dependent transcriptional  response( 41) .	bind
16874	3	6256	5	NULL	NULL	0	NULL	statement 2	NULL		allows	NULL				TR RXR heterodimers	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_24_14274_s_85	7782283	1) T   binding  dissociates TR homodimers from positive TREs ( 39) (see  Fig. 7 A), allowing preferential binding of TR RXR  heterodimers; 2) TR RXR heterodimers have a stronger affinity for  TREs than TR homodimers( 8) ; 3) cotransfection of RXR enhances  the positive transcriptional response to T   on a number of  different elements( 10,  40) ; and 4) more recently yeast  expression systems demonstrate that TR RXR heterodimerization is  necessary for a full ligand-dependent transcriptional  response( 41) .	bind
16875	4	6256	5	NULL	NULL	0	NULL	TR RXR heterodimers	NULL		bind	NULL					NULL			TREs	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_24_14274_s_85	7782283	1) T   binding  dissociates TR homodimers from positive TREs ( 39) (see  Fig. 7 A), allowing preferential binding of TR RXR  heterodimers; 2) TR RXR heterodimers have a stronger affinity for  TREs than TR homodimers( 8) ; 3) cotransfection of RXR enhances  the positive transcriptional response to T   on a number of  different elements( 10,  40) ; and 4) more recently yeast  expression systems demonstrate that TR RXR heterodimerization is  necessary for a full ligand-dependent transcriptional  response( 41) .	bind
16876	5	6256	5	NULL	NULL	0	NULL	TR RXR heterodimers	NULL		bind	NULL				TR homodimers	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_24_14274_s_85	7782283	1) T   binding  dissociates TR homodimers from positive TREs ( 39) (see  Fig. 7 A), allowing preferential binding of TR RXR  heterodimers; 2) TR RXR heterodimers have a stronger affinity for  TREs than TR homodimers( 8) ; 3) cotransfection of RXR enhances  the positive transcriptional response to T   on a number of  different elements( 10,  40) ; and 4) more recently yeast  expression systems demonstrate that TR RXR heterodimerization is  necessary for a full ligand-dependent transcriptional  response( 41) .	bind
16877	6	6256	5	NULL	NULL	0	NULL	statement 4	NULL		stronger affinity than	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_24_14274_s_85	7782283	1) T   binding  dissociates TR homodimers from positive TREs ( 39) (see  Fig. 7 A), allowing preferential binding of TR RXR  heterodimers; 2) TR RXR heterodimers have a stronger affinity for  TREs than TR homodimers( 8) ; 3) cotransfection of RXR enhances  the positive transcriptional response to T   on a number of  different elements( 10,  40) ; and 4) more recently yeast  expression systems demonstrate that TR RXR heterodimerization is  necessary for a full ligand-dependent transcriptional  response( 41) .	bind
16878	7	6256	5	10	NULL	0	NULL	RXR		cotransfection of 	enhance					T		positive transcriptional response to			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_24_14274_s_85	7782283	1) T   binding  dissociates TR homodimers from positive TREs ( 39) (see  Fig. 7 A), allowing preferential binding of TR RXR  heterodimers; 2) TR RXR heterodimers have a stronger affinity for  TREs than TR homodimers( 8) ; 3) cotransfection of RXR enhances  the positive transcriptional response to T   on a number of  different elements( 10,  40) ; and 4) more recently yeast  expression systems demonstrate that TR RXR heterodimerization is  necessary for a full ligand-dependent transcriptional  response( 41) .	bind
16879	8	6256	5	10	NULL	0	NULL	TR RXR		heterodimerization of	is necessary for					statement 9					NULL	yeast expression systems	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_24_14274_s_85	7782283	1) T   binding  dissociates TR homodimers from positive TREs ( 39) (see  Fig. 7 A), allowing preferential binding of TR RXR  heterodimers; 2) TR RXR heterodimers have a stronger affinity for  TREs than TR homodimers( 8) ; 3) cotransfection of RXR enhances  the positive transcriptional response to T   on a number of  different elements( 10,  40) ; and 4) more recently yeast  expression systems demonstrate that TR RXR heterodimerization is  necessary for a full ligand-dependent transcriptional  response( 41) .	bind
54174	9	6256	5	10	NULL	0	NULL	transcriptional response			is dependent on		fully			ligand					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_24_14274_s_85	7782283	1) T   binding  dissociates TR homodimers from positive TREs ( 39) (see  Fig. 7 A), allowing preferential binding of TR RXR  heterodimers; 2) TR RXR heterodimers have a stronger affinity for  TREs than TR homodimers( 8) ; 3) cotransfection of RXR enhances  the positive transcriptional response to T   on a number of  different elements( 10,  40) ; and 4) more recently yeast  expression systems demonstrate that TR RXR heterodimerization is  necessary for a full ligand-dependent transcriptional  response( 41) .	bind
21536	1	6256	7	NULL	NULL	NULL	NULL	TR homodimers	GP		dissociates from							positive		TREs	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_24_14274_s_85	7782283	1) T   binding  dissociates TR homodimers from positive TREs ( 39) (see  Fig. 7 A), allowing preferential binding of TR RXR  heterodimers; 2) TR RXR heterodimers have a stronger affinity for  TREs than TR homodimers( 8) ; 3) cotransfection of RXR enhances  the positive transcriptional response to T   on a number of  different elements( 10,  40) ; and 4) more recently yeast  expression systems demonstrate that TR RXR heterodimerization is  necessary for a full ligand-dependent transcriptional  response( 41) .	bind
21537	2	6256	7	NULL	NULL	NULL	NULL	T	Chemical	binding of	allows					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_24_14274_s_85	7782283	1) T   binding  dissociates TR homodimers from positive TREs ( 39) (see  Fig. 7 A), allowing preferential binding of TR RXR  heterodimers; 2) TR RXR heterodimers have a stronger affinity for  TREs than TR homodimers( 8) ; 3) cotransfection of RXR enhances  the positive transcriptional response to T   on a number of  different elements( 10,  40) ; and 4) more recently yeast  expression systems demonstrate that TR RXR heterodimerization is  necessary for a full ligand-dependent transcriptional  response( 41) .	bind
21538	3	6256	7	NULL	NULL	NULL	NULL	statement 2	Process		allows		preferentially			TR RXR heterodimers	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_24_14274_s_85	7782283	1) T   binding  dissociates TR homodimers from positive TREs ( 39) (see  Fig. 7 A), allowing preferential binding of TR RXR  heterodimers; 2) TR RXR heterodimers have a stronger affinity for  TREs than TR homodimers( 8) ; 3) cotransfection of RXR enhances  the positive transcriptional response to T   on a number of  different elements( 10,  40) ; and 4) more recently yeast  expression systems demonstrate that TR RXR heterodimerization is  necessary for a full ligand-dependent transcriptional  response( 41) .	bind
21539	4	6256	7	NULL	NULL	NULL	NULL	TR RXR heterodimers	GP		 affinity for		stronger							TRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_24_14274_s_85	7782283	1) T   binding  dissociates TR homodimers from positive TREs ( 39) (see  Fig. 7 A), allowing preferential binding of TR RXR  heterodimers; 2) TR RXR heterodimers have a stronger affinity for  TREs than TR homodimers( 8) ; 3) cotransfection of RXR enhances  the positive transcriptional response to T   on a number of  different elements( 10,  40) ; and 4) more recently yeast  expression systems demonstrate that TR RXR heterodimerization is  necessary for a full ligand-dependent transcriptional  response( 41) .	bind
21540	5	6256	7	NULL	NULL	NULL	NULL	TR homodimers	GP		has affinity for									TRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_24_14274_s_85	7782283	1) T   binding  dissociates TR homodimers from positive TREs ( 39) (see  Fig. 7 A), allowing preferential binding of TR RXR  heterodimers; 2) TR RXR heterodimers have a stronger affinity for  TREs than TR homodimers( 8) ; 3) cotransfection of RXR enhances  the positive transcriptional response to T   on a number of  different elements( 10,  40) ; and 4) more recently yeast  expression systems demonstrate that TR RXR heterodimerization is  necessary for a full ligand-dependent transcriptional  response( 41) .	bind
21541	6	6256	7	NULL	NULL	NULL	NULL	statement 4	Process		is stronger than					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_24_14274_s_85	7782283	1) T   binding  dissociates TR homodimers from positive TREs ( 39) (see  Fig. 7 A), allowing preferential binding of TR RXR  heterodimers; 2) TR RXR heterodimers have a stronger affinity for  TREs than TR homodimers( 8) ; 3) cotransfection of RXR enhances  the positive transcriptional response to T   on a number of  different elements( 10,  40) ; and 4) more recently yeast  expression systems demonstrate that TR RXR heterodimerization is  necessary for a full ligand-dependent transcriptional  response( 41) .	bind
21542	7	6256	7	NULL	NULL	NULL	NULL	RXR	GP	cotransfection of	enhances					T	Chemical	positive transcriptional response to			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_24_14274_s_85	7782283	1) T   binding  dissociates TR homodimers from positive TREs ( 39) (see  Fig. 7 A), allowing preferential binding of TR RXR  heterodimers; 2) TR RXR heterodimers have a stronger affinity for  TREs than TR homodimers( 8) ; 3) cotransfection of RXR enhances  the positive transcriptional response to T   on a number of  different elements( 10,  40) ; and 4) more recently yeast  expression systems demonstrate that TR RXR heterodimerization is  necessary for a full ligand-dependent transcriptional  response( 41) .	bind
21543	8	6256	7	NULL	NULL	NULL	NULL	TR RXR	GP	heterodimerization of	is necessary for					statement 9	Process				NULL	yeast expression systems	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_24_14274_s_85	7782283	1) T   binding  dissociates TR homodimers from positive TREs ( 39) (see  Fig. 7 A), allowing preferential binding of TR RXR  heterodimers; 2) TR RXR heterodimers have a stronger affinity for  TREs than TR homodimers( 8) ; 3) cotransfection of RXR enhances  the positive transcriptional response to T   on a number of  different elements( 10,  40) ; and 4) more recently yeast  expression systems demonstrate that TR RXR heterodimerization is  necessary for a full ligand-dependent transcriptional  response( 41) .	bind
54175	9	6256	7	NULL	NULL	NULL	NULL	transcriptional response	Process		is dependent on		fully			ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_24_14274_s_85	7782283	1) T   binding  dissociates TR homodimers from positive TREs ( 39) (see  Fig. 7 A), allowing preferential binding of TR RXR  heterodimers; 2) TR RXR heterodimers have a stronger affinity for  TREs than TR homodimers( 8) ; 3) cotransfection of RXR enhances  the positive transcriptional response to T   on a number of  different elements( 10,  40) ; and 4) more recently yeast  expression systems demonstrate that TR RXR heterodimerization is  necessary for a full ligand-dependent transcriptional  response( 41) .	bind
16880	1	6257	5	NULL	NULL	0	NULL	IL-6	NULL		bind	NULL				M1-UR21 cells	NULL	nontransfected			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22701_s_185	9712900	1) The affinity of IL-6 binding to nontransfected M1-UR21 cells, which express only low affinity receptors (IL-6R), was too low for an accurate estimation of the  K D.	bind
26374	1	6257	7	NULL	NULL	NULL	NULL	IL-6	GP		bind					M1-UR21 cells	Cell	 nontransfected			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_35_22701_s_185	9712900	1) The affinity of IL-6 binding to nontransfected M1-UR21 cells, which express only low affinity receptors (IL-6R), was too low for an accurate estimation of the  K D.	bind
16881	1	6258	5	NULL	NULL	0	NULL	glucitol	NULL		bind	NULL				GutR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_13_9620_s_274	11118449	1) The binding of glucitol to GutR can induce GutR to have conformational changes so that more residues in the DNA binding region of GutR are available to make extensive contacts with the GutR binding site.	bind
16882	2	6258	5	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL				GutR	NULL	conformational changes in			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_13_9620_s_274	11118449	1) The binding of glucitol to GutR can induce GutR to have conformational changes so that more residues in the DNA binding region of GutR are available to make extensive contacts with the GutR binding site.	bind
21546	1	6258	7	NULL	NULL	NULL	NULL	glucitol 	Chemical		bind					GutR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_13_9620_s_274	11118449	1) The binding of glucitol to GutR can induce GutR to have conformational changes so that more residues in the DNA binding region of GutR are available to make extensive contacts with the GutR binding site.	bind
21547	2	6258	7	NULL	NULL	NULL	NULL	statement 1	Process		induce					GutR	GP	availability of	 DNA binding region of 		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_13_9620_s_274	11118449	1) The binding of glucitol to GutR can induce GutR to have conformational changes so that more residues in the DNA binding region of GutR are available to make extensive contacts with the GutR binding site.	bind
21548	3	6258	7	NULL	NULL	NULL	NULL	statement 2	Process		allows							extensive contacts with 	GutR binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_13_9620_s_274	11118449	1) The binding of glucitol to GutR can induce GutR to have conformational changes so that more residues in the DNA binding region of GutR are available to make extensive contacts with the GutR binding site.	bind
16883	1	6259	5	NULL	NULL	0	NULL	natriuretic peptide	NULL		bind	NULL					NULL		ECD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_14_9752_s_28	10092664	1) The binding of the natriuretic peptide to ECD induces a conformational change.	bind
16884	2	6259	5	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL					NULL	conformational change of	ECD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_14_9752_s_28	10092664	1) The binding of the natriuretic peptide to ECD induces a conformational change.	bind
21549	1	6259	7	NULL	NULL	NULL	NULL	natriuretic peptide	GP		binds								ECD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_14_9752_s_28	10092664	1) The binding of the natriuretic peptide to ECD induces a conformational change.	bind
21550	2	6259	7	NULL	NULL	NULL	NULL	statement 1	Process		induce							conformational change	ECD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_14_9752_s_28	10092664	1) The binding of the natriuretic peptide to ECD induces a conformational change.	bind
16885	1	6260	5	NULL	NULL	0	NULL	PARP-1 inhibitors	NULL		decrease	NULL				AM-PARP	NULL	amounts of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
16886	2	6260	5	NULL	NULL	0	NULL	PARP-1 inhibitors	NULL		decrease	NULL				TNF-alpha	NULL	expression of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
16887	3	6260	5	NULL	NULL	0	NULL	PARP-1 inhibitors	NULL		decrease	NULL				iNOS	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
16888	4	6260	5	NULL	NULL	0	NULL	NF-kappaB	NULL		bind	NULL				DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
16889	5	6260	5	NULL	NULL	0	NULL	LPS	NULL		induce	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
16890	6	6260	5	NULL	NULL	0	NULL	PARP-1 inhibitors	NULL		decrease	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
16891	7	6260	5	NULL	NULL	0	NULL	PARP-1 mRNA	NULL	antisense	decrease	NULL				AM-PARP	NULL	amounts of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
16892	8	6260	5	NULL	NULL	0	NULL	PARP-1 mRNA	NULL	antisense	decrease	NULL				TNF-alpha	NULL	expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
16893	9	6260	5	NULL	NULL	0	NULL	PARP-1 mRNA	NULL	antisense	decrease	NULL				iNOS	NULL	expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
16894	10	6260	5	NULL	NULL	0	NULL	PARP-1 mRNA	NULL	antisense	decrease	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
21580	1	6260	7	NULL	NULL	NULL	NULL	PARP-1 inhibitor	Chemical		decrease					AM-PARP	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
21581	2	6260	7	NULL	NULL	NULL	NULL	PARP-1mRNA	NucleicAcid	antisense	decrease					AM-PARP	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
21582	3	6260	7	NULL	NULL	NULL	NULL	PARP-1 inhibitor	Chemical		decrease					TNF-alpha	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
21583	4	6260	7	NULL	NULL	NULL	NULL	PARP-1 mRNA	NucleicAcid	antisense	decrease					TNF-alpha	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
21584	5	6260	7	NULL	NULL	NULL	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
21585	6	6260	7	NULL	NULL	NULL	NULL	LPS	Chemical		induce					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
26366	7	6260	7	NULL	NULL	NULL	NULL	PARP-1 inhibitor	Chemical		decrease					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
26367	8	6260	7	NULL	NULL	NULL	NULL	PARP-1 mRNA	NucleicAcid	antisense	decrease					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
26369	10	6260	7	NULL	NULL	NULL	NULL	PARP-1 mRNA	NucleicAcid	antisense	decrease					iNOS	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
26372	11	6260	7	NULL	NULL	NULL	NULL	PARP-1 inhibitor	Chemical		decrease					 iNOS	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_42774_s_401	15302869	1) The inhibitors of PARP-1 and the antisense RNA for PARP-1 mRNA decreased the amounts of AM-PARP and the expression of TNF-alpha and iNOS (Figs.  1,  2,  3) and the LPS-induced DNA binding of NF-kappaB ( Fig. 5).	bind
19258	1	6261	5	NULL	NULL	0	NULL	myosin molecules	NULL		udergoes	NULL				post-translational modifications	NULL	differential			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_18_15117_s_282	11134017	1) The myosin molecules are biochemically heterogeneous as a result of differential post-translational modifications; 2) the  Drosophila myosins occupy a wider range of functionally active molecular orientations in the way they are deposited on the third bead substrate, some of which restrict the production of the full displacement; or 3) the myosin step size depends upon the geometry of myosin binding to actin and the degrees of freedom of movement within the myosin molecule.	bind
19259	2	6261	5	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				biochemically heterogeneous myosin molecules	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_18_15117_s_282	11134017	1) The myosin molecules are biochemically heterogeneous as a result of differential post-translational modifications; 2) the  Drosophila myosins occupy a wider range of functionally active molecular orientations in the way they are deposited on the third bead substrate, some of which restrict the production of the full displacement; or 3) the myosin step size depends upon the geometry of myosin binding to actin and the degrees of freedom of movement within the myosin molecule.	bind
19260	3	6261	5	10	NULL	0	NULL	myosins	NULL	Drosophila	occupy	NULL				molecular orientations	NULL	functionally active			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_15117_s_282	11134017	1) The myosin molecules are biochemically heterogeneous as a result of differential post-translational modifications; 2) the  Drosophila myosins occupy a wider range of functionally active molecular orientations in the way they are deposited on the third bead substrate, some of which restrict the production of the full displacement; or 3) the myosin step size depends upon the geometry of myosin binding to actin and the degrees of freedom of movement within the myosin molecule.	bind
19261	4	6261	5	NULL	NULL	0	NULL	myosin	NULL		bind	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_18_15117_s_282	11134017	1) The myosin molecules are biochemically heterogeneous as a result of differential post-translational modifications; 2) the  Drosophila myosins occupy a wider range of functionally active molecular orientations in the way they are deposited on the third bead substrate, some of which restrict the production of the full displacement; or 3) the myosin step size depends upon the geometry of myosin binding to actin and the degrees of freedom of movement within the myosin molecule.	bind
19262	5	6261	5	NULL	NULL	0	NULL	myosin step size	NULL		depends upon	NULL				statement 4	NULL	geometry of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_18_15117_s_282	11134017	1) The myosin molecules are biochemically heterogeneous as a result of differential post-translational modifications; 2) the  Drosophila myosins occupy a wider range of functionally active molecular orientations in the way they are deposited on the third bead substrate, some of which restrict the production of the full displacement; or 3) the myosin step size depends upon the geometry of myosin binding to actin and the degrees of freedom of movement within the myosin molecule.	bind
21586	1	6261	7	NULL	NULL	NULL	NULL	myosin molecules	GP		are					heterogeneous		biochemically			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_15117_s_282	11134017	1) The myosin molecules are biochemically heterogeneous as a result of differential post-translational modifications; 2) the  Drosophila myosins occupy a wider range of functionally active molecular orientations in the way they are deposited on the third bead substrate, some of which restrict the production of the full displacement; or 3) the myosin step size depends upon the geometry of myosin binding to actin and the degrees of freedom of movement within the myosin molecule.	bind
21587	2	6261	7	NULL	NULL	NULL	NULL	statement 1	Process		is because of 					post-translational modifications	Process	differential 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_15117_s_282	11134017	1) The myosin molecules are biochemically heterogeneous as a result of differential post-translational modifications; 2) the  Drosophila myosins occupy a wider range of functionally active molecular orientations in the way they are deposited on the third bead substrate, some of which restrict the production of the full displacement; or 3) the myosin step size depends upon the geometry of myosin binding to actin and the degrees of freedom of movement within the myosin molecule.	bind
21588	3	6261	7	NULL	NULL	NULL	NULL	myosins	GP	Drosophila	are deposited on					third bead substrate	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_15117_s_282	11134017	1) The myosin molecules are biochemically heterogeneous as a result of differential post-translational modifications; 2) the  Drosophila myosins occupy a wider range of functionally active molecular orientations in the way they are deposited on the third bead substrate, some of which restrict the production of the full displacement; or 3) the myosin step size depends upon the geometry of myosin binding to actin and the degrees of freedom of movement within the myosin molecule.	bind
21589	4	6261	7	NULL	NULL	NULL	NULL	myosins	GP	Drosophila	occupy					molecular orientations	Process	functionally active			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_15117_s_282	11134017	1) The myosin molecules are biochemically heterogeneous as a result of differential post-translational modifications; 2) the  Drosophila myosins occupy a wider range of functionally active molecular orientations in the way they are deposited on the third bead substrate, some of which restrict the production of the full displacement; or 3) the myosin step size depends upon the geometry of myosin binding to actin and the degrees of freedom of movement within the myosin molecule.	bind
21590	5	6261	7	NULL	NULL	NULL	NULL	myosin	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_15117_s_282	11134017	1) The myosin molecules are biochemically heterogeneous as a result of differential post-translational modifications; 2) the  Drosophila myosins occupy a wider range of functionally active molecular orientations in the way they are deposited on the third bead substrate, some of which restrict the production of the full displacement; or 3) the myosin step size depends upon the geometry of myosin binding to actin and the degrees of freedom of movement within the myosin molecule.	bind
16895	1	6262	5	NULL	NULL	0	NULL	prothrombin	NULL		bind	NULL				FXI	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_41_31954_s_224	10924522	1) The rA1 domain inhibits the binding of prothrombin to FXI with an IC50 of 4 x 10 7M (Fig.  1 A, Table  I).	bind
16896	2	6262	5	NULL	NULL	0	NULL		NULL		inhibit	NULL		rA1 domain		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_41_31954_s_224	10924522	1) The rA1 domain inhibits the binding of prothrombin to FXI with an IC50 of 4 x 10 7M (Fig.  1 A, Table  I).	bind
21596	1	6262	7	NULL	NULL	NULL	NULL	prothrombin 	GP		bind					FXI	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31954_s_224	10924522	1) The rA1 domain inhibits the binding of prothrombin to FXI with an IC50 of 4 x 10 7M (Fig.  1 A, Table  I).	bind
21597	2	6262	7	NULL	NULL	NULL	NULL				inhibits			rA1 domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31954_s_224	10924522	1) The rA1 domain inhibits the binding of prothrombin to FXI with an IC50 of 4 x 10 7M (Fig.  1 A, Table  I).	bind
19222	1	6263	5	NULL	NULL	0	NULL	FKHRL1	NULL		contains	NULL			regulatory region of promoter		NULL			insulin-responsive sequence-like sequences	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
19223	2	6263	5	NULL	NULL	0	NULL	FKHRL1	NULL		bind	NULL				Fas ligand gene	NULL			insulin-responsive sequence-like sequences	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
19224	3	6263	5	NULL	NULL	0	NULL	statement 2	NULL		enhances	NULL				Fas ligand	NULL	transcription of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
19225	4	6263	5	NULL	NULL	0	NULL	growth factors	NULL	removal of	up-regulates	NULL				Fas ligand mRNA	NULL	expression of			NULL	culture medium	0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
19226	5	6263	5	NULL	NULL	0	NULL	growth factors	NULL	removal of	up-regulates	NULL				Fas ligand protein	NULL	expression of			NULL	culture medium	0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
19227	6	6263	5	NULL	NULL	0	NULL	statement 4	NULL		stimulates	NULL				apoptosis	NULL				NULL	PC12 cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
19228	7	6263	5	NULL	NULL	0	NULL	statement 4	NULL		stimulates	NULL				apoptosis	NULL				NULL	primary cultured neurons	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
19229	8	6263	5	NULL	NULL	0	NULL	statement 5	NULL		stimulates	NULL				apoptosis	NULL				NULL	PC12 cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
19230	9	6263	5	NULL	NULL	0	NULL	statement 5	NULL		stimulates	NULL				apoptosis	NULL				NULL	primary cultured neurons	0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
19231	10	6263	5	NULL	NULL	0	NULL	survival factor	NULL		stimulates	NULL				PC12 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
19232	11	6263	5	NULL	NULL	0	NULL	statement 10	NULL		activates	NULL				PI3K/Akt kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
19233	12	6263	5	NULL	NULL	0	NULL	statement 10	NULL		increases	NULL				FKHRL1	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
19234	13	6263	5	NULL	NULL	0	NULL	statement 12	NULL		inhibit	NULL				Fas ligand	NULL	expression of			NULL	fibroblasts	0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
21600	1	6263	7	NULL	NULL	NULL	NULL	Fas ligand gene	GP		contains				regulatory region of promoter	FKHRL1	GP			 insulin-responsive sequences	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
21602	2	6263	7	NULL	NULL	NULL	NULL				bind			FKHRL1 sequence	 	Fas ligand gene	GP			insulin-responsive sequence	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
21604	3	6263	7	NULL	NULL	NULL	NULL	statement 2	Process		enhance					Fas ligand	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
21605	4	6263	7	NULL	NULL	NULL	NULL	growth factors	GP	removal of 	upregulates					Fas ligand mRNA 	NucleicAcid	the expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
21606	5	6263	7	NULL	NULL	NULL	NULL	growth factors	GP	removal of	upregulates					Fas ligand protein	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
21607	6	6263	7	NULL	NULL	NULL	NULL	statement 4	Process		stimulate					apoptosis	Process				NULL	in PC12 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
21608	7	6263	7	NULL	NULL	NULL	NULL	statement 5	Process		stimulate					apoptosis	Process				NULL	primary cultured neurons 	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
21609	8	6263	7	NULL	NULL	NULL	NULL	statement 4	Process		stimulate					apoptosis	Process				NULL	primary cultured neurons 	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
21610	9	6263	7	NULL	NULL	NULL	NULL	statement 5	Process		stimulate					apoptosis	Process				NULL	in PC12 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
21611	10	6263	7	NULL	NULL	NULL	NULL	PC12 cells with survival factor 	Cell	stimulation of	activates					PI3K/Akt kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
21612	11	6263	7	NULL	NULL	NULL	NULL	statement 10	Process		increases					FKHRL1	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
21613	12	6263	7	NULL	NULL	NULL	NULL	statement 11	Process		inhibits					Fas ligand	GP	the expression of			NULL	in fibroblasts	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39152_s_260	10995739	1) The regulatory region of the promoter of the Fas ligand gene contains three insulin-responsive sequence-like sequences for FKHRL1, and the binding of FKHRL1 to these sequences enhances the transcription of the Fas ligand ( 51); 2) the removal of growth factors from culture medium up-regulates the expression of Fas ligand mRNA and protein and stimulates apoptosis in several cell lines, including PC12 cells and primary cultured neurons ( 52); and 3) the stimulation of PC12 cells with a survival factor as shown in the present study activates PI3K/Akt kinase and increases the phosphorylation of FKHRL1, which was shown to inhibit the expression of the Fas ligand in fibroblasts ( 21,  52).	bind
19216	1	6264	5	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				PII	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_25_14692_s_103	8663083	1) The size of the nuclear factor that enhances Sp1 binding to PII is about 38-42 kDa, the size of the catalytic subunit of PP1; and 2) glucose-mediated activation of Sp1 binding to PII is OA-sensitive at a concentration suggesting the factor to be a PP1-like activity.	bind
19217	2	6264	5	NULL	NULL	0	NULL	nuclear factor	NULL		enhances	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_25_14692_s_103	8663083	1) The size of the nuclear factor that enhances Sp1 binding to PII is about 38-42 kDa, the size of the catalytic subunit of PP1; and 2) glucose-mediated activation of Sp1 binding to PII is OA-sensitive at a concentration suggesting the factor to be a PP1-like activity.	bind
19218	3	6264	5	NULL	NULL	0	NULL	glucose	NULL		mediate	NULL				statement 1	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_25_14692_s_103	8663083	1) The size of the nuclear factor that enhances Sp1 binding to PII is about 38-42 kDa, the size of the catalytic subunit of PP1; and 2) glucose-mediated activation of Sp1 binding to PII is OA-sensitive at a concentration suggesting the factor to be a PP1-like activity.	bind
19219	4	6264	5	NULL	NULL	0	NULL	statement 3	NULL		is sensitive to	NULL				OA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_25_14692_s_103	8663083	1) The size of the nuclear factor that enhances Sp1 binding to PII is about 38-42 kDa, the size of the catalytic subunit of PP1; and 2) glucose-mediated activation of Sp1 binding to PII is OA-sensitive at a concentration suggesting the factor to be a PP1-like activity.	bind
19220	5	6264	5	NULL	NULL	0	NULL	nuclear factor	NULL		has	NULL				PP1-like activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_25_14692_s_103	8663083	1) The size of the nuclear factor that enhances Sp1 binding to PII is about 38-42 kDa, the size of the catalytic subunit of PP1; and 2) glucose-mediated activation of Sp1 binding to PII is OA-sensitive at a concentration suggesting the factor to be a PP1-like activity.	bind
19221	6	6264	5	NULL	NULL	0	NULL	statement 4	NULL		suggests	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_25_14692_s_103	8663083	1) The size of the nuclear factor that enhances Sp1 binding to PII is about 38-42 kDa, the size of the catalytic subunit of PP1; and 2) glucose-mediated activation of Sp1 binding to PII is OA-sensitive at a concentration suggesting the factor to be a PP1-like activity.	bind
21614	1	6264	7	NULL	NULL	NULL	NULL	Sp1	GP		bind					PII	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_25_14692_s_103	8663083	1) The size of the nuclear factor that enhances Sp1 binding to PII is about 38-42 kDa, the size of the catalytic subunit of PP1; and 2) glucose-mediated activation of Sp1 binding to PII is OA-sensitive at a concentration suggesting the factor to be a PP1-like activity.	bind
21615	2	6264	7	NULL	NULL	NULL	NULL	nuclear factor	GP		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_25_14692_s_103	8663083	1) The size of the nuclear factor that enhances Sp1 binding to PII is about 38-42 kDa, the size of the catalytic subunit of PP1; and 2) glucose-mediated activation of Sp1 binding to PII is OA-sensitive at a concentration suggesting the factor to be a PP1-like activity.	bind
21616	3	6264	7	NULL	NULL	NULL	NULL	glucose	Chemical		mediates					statement 1	Process	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_25_14692_s_103	8663083	1) The size of the nuclear factor that enhances Sp1 binding to PII is about 38-42 kDa, the size of the catalytic subunit of PP1; and 2) glucose-mediated activation of Sp1 binding to PII is OA-sensitive at a concentration suggesting the factor to be a PP1-like activity.	bind
21617	4	6264	7	NULL	NULL	NULL	NULL	statement 3	Process		is sensitive to					OA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_25_14692_s_103	8663083	1) The size of the nuclear factor that enhances Sp1 binding to PII is about 38-42 kDa, the size of the catalytic subunit of PP1; and 2) glucose-mediated activation of Sp1 binding to PII is OA-sensitive at a concentration suggesting the factor to be a PP1-like activity.	bind
19215	1	6265	5	NULL	NULL	0	NULL	ouabain	NULL		bind	NULL				phosphoenzyme	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_45_31792_s_110	10542201	1) The stoichiometries of ATP binding ( 15,  24), rubidium occlusion (Fig.  2) and phosphorylation by ATP ( 10), Pi ( 14), acetyl phosphate ( 16), and  p-nitrophenyl phosphate ( 14) and the ratio of ouabain binding to phosphoenzyme ( 15,  24); 2) half-site reactivities of Na E1P to acetate ( 16) and  p-nitrophenol ( 15), namely a quarter site reactivity of the alpha-chain ( 10); 3) the fact that ATP induced four different conformational changes out of phase ( 11); 4) 32P binding and the burst size of Pi (Fig.  3,  B and  C); and 5) electron microscopy (Fig.  4).	bind
21622	1	6265	7	NULL	NULL	NULL	NULL	ouabain	GP		bind					phosphoenzyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_45_31792_s_110	10542201	1) The stoichiometries of ATP binding ( 15,  24), rubidium occlusion (Fig.  2) and phosphorylation by ATP ( 10), Pi ( 14), acetyl phosphate ( 16), and  p-nitrophenyl phosphate ( 14) and the ratio of ouabain binding to phosphoenzyme ( 15,  24); 2) half-site reactivities of Na E1P to acetate ( 16) and  p-nitrophenol ( 15), namely a quarter site reactivity of the alpha-chain ( 10); 3) the fact that ATP induced four different conformational changes out of phase ( 11); 4) 32P binding and the burst size of Pi (Fig.  3,  B and  C); and 5) electron microscopy (Fig.  4).	bind
16897	1	6266	5	NULL	NULL	0	NULL	TSG101	NULL		bind	NULL		N-terminal UEV domain			NULL		P(S/T)AP peptide motifs		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_34_36059_s_31	15218037	1) The TSG101 N-terminal UEV domain binds P(S/T)AP peptide motifs.	bind
21629	1	6266	7	NULL	NULL	NULL	NULL	TSG101	GP		binds			N-terminal UEV domain					P(S/T)AP peptide motifs		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_34_36059_s_31	15218037	1) The TSG101 N-terminal UEV domain binds P(S/T)AP peptide motifs.	bind
16898	1	6267	5	10	NULL	0	NULL	Transducin	NULL		bind	NULL				RGS9d	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_40_37365_s_245	11495924	1) Transducin binds demonstrably to RGS9d, but the difference between the binding with and without PDEgamma is small.	bind
21634	1	6267	7	NULL	NULL	NULL	NULL	Transducin	GP		binds					RGS9d	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_40_37365_s_245	11495924	1) Transducin binds demonstrably to RGS9d, but the difference between the binding with and without PDEgamma is small.	bind
16899	1	6268	5	10	NULL	0	NULL	tropomyosin molecules			bind					actin					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_179	7592713	1) Troponin  greatly promotes the binding of individual tropomyosin molecules to  actin, regardless of the Ca   concentration.	bind
16900	2	6268	5	NULL	NULL	0	NULL	Troponin	NULL		promotes	NULL	greatly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_179	7592713	1) Troponin  greatly promotes the binding of individual tropomyosin molecules to  actin, regardless of the Ca   concentration.	bind
16901	3	6268	5	NULL	NULL	0	NULL	statement 2	NULL		is independent of	NULL				Ca 	NULL	concentration of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_179	7592713	1) Troponin  greatly promotes the binding of individual tropomyosin molecules to  actin, regardless of the Ca   concentration.	bind
21638	1	6268	7	NULL	NULL	NULL	NULL	tropomyosin molecules	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_179	7592713	1) Troponin  greatly promotes the binding of individual tropomyosin molecules to  actin, regardless of the Ca   concentration.	bind
21639	2	6268	7	NULL	NULL	NULL	NULL	Troponin	GP		promotes		greatly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_179	7592713	1) Troponin  greatly promotes the binding of individual tropomyosin molecules to  actin, regardless of the Ca   concentration.	bind
21640	3	6268	7	NULL	NULL	NULL	NULL	statement 2	Process		is independent of					Ca	Chemical	 concentration 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_179	7592713	1) Troponin  greatly promotes the binding of individual tropomyosin molecules to  actin, regardless of the Ca   concentration.	bind
16902	1	6269	5	NULL	NULL	0	NULL	uPA	NULL		bind	NULL				uPAR	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_32_29863_s_292	12754207	1) uPA binds to uPAR,  2) uPAR then binds to alpha5beta1 in cis, and 3)  signal transduction is mediated through alpha5beta1  ( Fig. 8).	bind
16903	2	6269	5	NULL	NULL	0	NULL	uPAR	NULL		bind	NULL				alpha5beta1	NULL	in cis			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_32_29863_s_292	12754207	1) uPA binds to uPAR,  2) uPAR then binds to alpha5beta1 in cis, and 3)  signal transduction is mediated through alpha5beta1  ( Fig. 8).	bind
16904	3	6269	5	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_32_29863_s_292	12754207	1) uPA binds to uPAR,  2) uPAR then binds to alpha5beta1 in cis, and 3)  signal transduction is mediated through alpha5beta1  ( Fig. 8).	bind
16905	4	6269	5	NULL	NULL	0	NULL	alpha5beta1	NULL		mediate	NULL				signal transduction	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_32_29863_s_292	12754207	1) uPA binds to uPAR,  2) uPAR then binds to alpha5beta1 in cis, and 3)  signal transduction is mediated through alpha5beta1  ( Fig. 8).	bind
21641	1	6269	7	NULL	NULL	NULL	NULL	uPA	GP		binds to					uPAR	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_32_29863_s_292	12754207	1) uPA binds to uPAR,  2) uPAR then binds to alpha5beta1 in cis, and 3)  signal transduction is mediated through alpha5beta1  ( Fig. 8).	bind
21642	2	6269	7	NULL	NULL	NULL	NULL	uPAR	GP		binds to					alpha5beta1	GP	cis			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_32_29863_s_292	12754207	1) uPA binds to uPAR,  2) uPAR then binds to alpha5beta1 in cis, and 3)  signal transduction is mediated through alpha5beta1  ( Fig. 8).	bind
21643	3	6269	7	NULL	NULL	NULL	NULL	signal transduction	Process		is mediated through					alpha5beta1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_32_29863_s_292	12754207	1) uPA binds to uPAR,  2) uPAR then binds to alpha5beta1 in cis, and 3)  signal transduction is mediated through alpha5beta1  ( Fig. 8).	bind
26375	4	6269	7	NULL	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_32_29863_s_292	12754207	1) uPA binds to uPAR,  2) uPAR then binds to alpha5beta1 in cis, and 3)  signal transduction is mediated through alpha5beta1  ( Fig. 8).	bind
16906	1	6270	5	NULL	NULL	0	NULL	Vx	NULL		bind	NULL					NULL		N1 site		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_21924_s_233	16754673	1) Vx bound to the N1 and V1 site is rapidly (within 10-20 min) convertible to Zx. 2) Vx bound to the L2 site is either slowly (within hours) or not convertible to Zx. 3) Vx bound to L1 (only in recombinant proteins) is not convertible to Zx.	bind
16907	2	6270	5	NULL	NULL	0	NULL	Vx	NULL		bind	NULL					NULL		V1 site		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_21924_s_233	16754673	1) Vx bound to the N1 and V1 site is rapidly (within 10-20 min) convertible to Zx. 2) Vx bound to the L2 site is either slowly (within hours) or not convertible to Zx. 3) Vx bound to L1 (only in recombinant proteins) is not convertible to Zx.	bind
16908	3	6270	5	NULL	NULL	0	NULL	statement 1	NULL		is convertible to	NULL	rapidly			Zx	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_21924_s_233	16754673	1) Vx bound to the N1 and V1 site is rapidly (within 10-20 min) convertible to Zx. 2) Vx bound to the L2 site is either slowly (within hours) or not convertible to Zx. 3) Vx bound to L1 (only in recombinant proteins) is not convertible to Zx.	bind
16909	4	6270	5	NULL	NULL	0	NULL	statement 2	NULL		is convertible to	NULL	rapidly			Zx	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_21924_s_233	16754673	1) Vx bound to the N1 and V1 site is rapidly (within 10-20 min) convertible to Zx. 2) Vx bound to the L2 site is either slowly (within hours) or not convertible to Zx. 3) Vx bound to L1 (only in recombinant proteins) is not convertible to Zx.	bind
16910	5	6270	5	NULL	NULL	0	NULL	Vx	NULL		bind	NULL					NULL		L2 site		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_21924_s_233	16754673	1) Vx bound to the N1 and V1 site is rapidly (within 10-20 min) convertible to Zx. 2) Vx bound to the L2 site is either slowly (within hours) or not convertible to Zx. 3) Vx bound to L1 (only in recombinant proteins) is not convertible to Zx.	bind
16911	6	6270	5	NULL	NULL	0	NULL	statement 5	NULL		is convertible to	NULL	slowly			Zx	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_21924_s_233	16754673	1) Vx bound to the N1 and V1 site is rapidly (within 10-20 min) convertible to Zx. 2) Vx bound to the L2 site is either slowly (within hours) or not convertible to Zx. 3) Vx bound to L1 (only in recombinant proteins) is not convertible to Zx.	bind
16912	7	6270	5	NULL	NULL	0	NULL	statement 5	NULL		is not convertible to	NULL				Zx	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_21924_s_233	16754673	1) Vx bound to the N1 and V1 site is rapidly (within 10-20 min) convertible to Zx. 2) Vx bound to the L2 site is either slowly (within hours) or not convertible to Zx. 3) Vx bound to L1 (only in recombinant proteins) is not convertible to Zx.	bind
16913	8	6270	5	NULL	NULL	0	NULL	Vx	NULL		bind	NULL	only				NULL	recombinant	L1		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_31_21924_s_233	16754673	1) Vx bound to the N1 and V1 site is rapidly (within 10-20 min) convertible to Zx. 2) Vx bound to the L2 site is either slowly (within hours) or not convertible to Zx. 3) Vx bound to L1 (only in recombinant proteins) is not convertible to Zx.	bind
16914	9	6270	5	NULL	NULL	0	NULL	statement 8	NULL		is not convertible to	NULL				Zx	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_21924_s_233	16754673	1) Vx bound to the N1 and V1 site is rapidly (within 10-20 min) convertible to Zx. 2) Vx bound to the L2 site is either slowly (within hours) or not convertible to Zx. 3) Vx bound to L1 (only in recombinant proteins) is not convertible to Zx.	bind
21644	1	6270	7	NULL	NULL	NULL	NULL	 Vx	Chemical		bind								N1 site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_31_21924_s_233	16754673	1) Vx bound to the N1 and V1 site is rapidly (within 10-20 min) convertible to Zx. 2) Vx bound to the L2 site is either slowly (within hours) or not convertible to Zx. 3) Vx bound to L1 (only in recombinant proteins) is not convertible to Zx.	bind
21645	2	6270	7	NULL	NULL	NULL	NULL	Vx	Chemical		bind								V1 site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_31_21924_s_233	16754673	1) Vx bound to the N1 and V1 site is rapidly (within 10-20 min) convertible to Zx. 2) Vx bound to the L2 site is either slowly (within hours) or not convertible to Zx. 3) Vx bound to L1 (only in recombinant proteins) is not convertible to Zx.	bind
21646	3	6270	7	NULL	NULL	NULL	NULL	statement 1	Process		converts to		rapidly			Zx	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_31_21924_s_233	16754673	1) Vx bound to the N1 and V1 site is rapidly (within 10-20 min) convertible to Zx. 2) Vx bound to the L2 site is either slowly (within hours) or not convertible to Zx. 3) Vx bound to L1 (only in recombinant proteins) is not convertible to Zx.	bind
21647	4	6270	7	NULL	NULL	NULL	NULL	Vx	Chemical		binds to								L2 site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_31_21924_s_233	16754673	1) Vx bound to the N1 and V1 site is rapidly (within 10-20 min) convertible to Zx. 2) Vx bound to the L2 site is either slowly (within hours) or not convertible to Zx. 3) Vx bound to L1 (only in recombinant proteins) is not convertible to Zx.	bind
21648	5	6270	7	NULL	NULL	NULL	NULL	statement 4	Process		is not converted to					Zx	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_31_21924_s_233	16754673	1) Vx bound to the N1 and V1 site is rapidly (within 10-20 min) convertible to Zx. 2) Vx bound to the L2 site is either slowly (within hours) or not convertible to Zx. 3) Vx bound to L1 (only in recombinant proteins) is not convertible to Zx.	bind
21649	6	6270	7	NULL	NULL	NULL	NULL	Vx	Chemical		bind		only					recombinant	L1 		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_31_21924_s_233	16754673	1) Vx bound to the N1 and V1 site is rapidly (within 10-20 min) convertible to Zx. 2) Vx bound to the L2 site is either slowly (within hours) or not convertible to Zx. 3) Vx bound to L1 (only in recombinant proteins) is not convertible to Zx.	bind
21650	7	6270	7	NULL	NULL	NULL	NULL	statement 6	Process		is not converted to					Zx	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_31_21924_s_233	16754673	1) Vx bound to the N1 and V1 site is rapidly (within 10-20 min) convertible to Zx. 2) Vx bound to the L2 site is either slowly (within hours) or not convertible to Zx. 3) Vx bound to L1 (only in recombinant proteins) is not convertible to Zx.	bind
21651	8	6270	7	NULL	NULL	NULL	NULL	statement 4	Process		converts to		slowly			Zx	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_31_21924_s_233	16754673	1) Vx bound to the N1 and V1 site is rapidly (within 10-20 min) convertible to Zx. 2) Vx bound to the L2 site is either slowly (within hours) or not convertible to Zx. 3) Vx bound to L1 (only in recombinant proteins) is not convertible to Zx.	bind
16915	1	6271	5	NULL	NULL	0	NULL	tropomyosin	NULL		bind	NULL				actin filaments	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_14_7836_s_135	7713874	1) We have demonstrated that  tropomyosin and troponin are actually bound to the actin filaments at  motility assay conditions.	bind
16916	2	6271	5	NULL	NULL	0	NULL	troponin	NULL		bind	NULL				actin filaments	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_14_7836_s_135	7713874	1) We have demonstrated that  tropomyosin and troponin are actually bound to the actin filaments at  motility assay conditions.	bind
21652	1	6271	7	NULL	NULL	NULL	NULL	tropomyosin	GP		bind					actin filaments	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_14_7836_s_135	7713874	1) We have demonstrated that  tropomyosin and troponin are actually bound to the actin filaments at  motility assay conditions.	bind
21653	2	6271	7	NULL	NULL	NULL	NULL	troponin 	GP		bind					actin filaments	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_14_7836_s_135	7713874	1) We have demonstrated that  tropomyosin and troponin are actually bound to the actin filaments at  motility assay conditions.	bind
16917	1	6272	5	10	NULL	0	NULL	PEA3			interact with					AP1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
16918	2	6272	5	10	NULL	0	NULL	SIF			bind					human immunodeficiency virus				tar element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
16919	3	6272	5	10	NULL	0	NULL	SIF			bind					UBP1				TATA box	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
54176	4	6272	5	10	NULL	0	NULL	C/EBP			regulates					cell		growth of;;differentiation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
54177	5	6272	5	10	NULL	0	NULL	PEA3			is					phorbol ester and serum					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
54178	6	6272	5	10	NULL	0	NULL	PEA3			is a type of					transcription factor					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
54179	7	6272	5	10	NULL	0	NULL	statement 1			plays a role in					SV40 gene		regulation of;;expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
54180	8	6272	5	10	NULL	0	NULL	SIF			is					c-sis and platelet derived growth factor					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
54181	9	6272	5	10	NULL	0	NULL	SIF			is a type of					transcription factor					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
54182	10	6272	5	10	NULL	0	NULL	PuF			is an inducer of					c-myc gene				promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
54183	11	6272	5	10	NULL	0	NULL	C/EBP			is					CCAAT enhancer binding protein					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
21688	1	6272	7	NULL	NULL	NULL	NULL	PEA3	Chemical		interacts with									 AP1	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
21690	2	6272	7	NULL	NULL	NULL	NULL	statement 1	Process		regulates					SV40	Organism	expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
21703	3	6272	7	NULL	NULL	NULL	NULL	PuF	GP		is a inducer of					c-myc gene	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
21705	4	6272	7	NULL	NULL	NULL	NULL	C/EBP	GP		regulates					cell 	Cell	growth of;; differentiation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
21707	5	6272	7	NULL	NULL	NULL	NULL	C/EBP	GP		is					CCAAT enhancer binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
21709	6	6272	7	NULL	NULL	NULL	NULL	SIF	GP		bind							human immunodeficiency virus		tar element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
21712	7	6272	7	NULL	NULL	NULL	NULL	SIF	GP		bind					UBP1	GP			TATA box	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
21714	8	6272	7	NULL	NULL	NULL	NULL	PEA3	Chemical		is					phorbol ester and serum	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
21715	9	6272	7	NULL	NULL	NULL	NULL	SIF	GP		is					c-sis and platelet derived growth factor 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
55044	10	6272	7	NULL	NULL	NULL	NULL	SIF	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
55045	11	6272	7	NULL	NULL	NULL	NULL	 PEA3	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31225_s_210	8537388	1), inducer of  c-myc  gene promoter ( PuF), CCAAT enhancer binding protein, a  regulator of cell growth and differentiation ( C/EBP), a  primary target of signal transduction induced by epidermal growth  factor, phorbol ester and serum ( PEA3), a transcription factor  that interacts with AP1 in the regulation of SV40 gene expression ( AP-4), activator of  c-fos  gene expression and  induced by  c-sis  and platelet derived growth factor ( SIF), a transcription factor that binds to human  immunodeficiency virus  tar  element and to the TATA box ( UBP1).	bind
16920	1	6273	5	10	NULL	0	NULL	NK cells	NULL	fetal	bind	NULL				Qa1b tetramers	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-immunol_162_12_10358137_s_5	10358137	1+Ly-49- cell lysates  contain CD94 protein and that a significant proportion of fetal NK cells  are bound by Qa1b tetramers.	bind
21719	1	6273	7	NULL	NULL	NULL	NULL	NK cells	Cell	fetal	bind					Qa1b tetramers	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-immunol_162_12_10358137_s_5	10358137	1+Ly-49- cell lysates  contain CD94 protein and that a significant proportion of fetal NK cells  are bound by Qa1b tetramers.	bind
21721	2	6273	7	NULL	NULL	NULL	NULL	Ly-49- cell lysates	Cell		contain					CD94 protein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-immunol_162_12_10358137_s_5	10358137	1+Ly-49- cell lysates  contain CD94 protein and that a significant proportion of fetal NK cells  are bound by Qa1b tetramers.	bind
16921	1	6274	5	10	NULL	0	NULL	thiazolidinediones	NULL		activate	NULL				PPARgamma	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
16922	2	6274	5	10	NULL	0	NULL	15d-PGJ2	NULL		activate	NULL				PPARgamma	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
16923	3	6274	5	NULL	NULL	0	NULL	15d-PGJ2	NULL		is	NULL				15-deoxy-delta12,14-prostaglandin J2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
16924	4	6274	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
16925	5	6274	5	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				retinoid X receptor	NULL	heterodimerization with			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
16926	6	6274	5	NULL	NULL	0	NULL	statement 2	NULL		results in	NULL				retinoid X receptor	NULL	heterodimerization with			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
16927	7	6274	5	NULL	NULL	0	NULL	statement 5	NULL		bind	NULL				target genes	NULL			PPRE	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
16928	8	6274	5	NULL	NULL	0	NULL	PPRE	NULL		is	NULL				PPAR response element	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
16929	9	6274	5	NULL	NULL	0	NULL	statement 6	NULL		bind	NULL				target genes	NULL			PPRE	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
45578	10	6274	5	10	NULL	0	NULL	thiazolidinediones	NULL		are type of	NULL				insulin-sensitizing agent	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
21739	1	6274	7	NULL	NULL	NULL	NULL	 antidiabetic ligand	Chemical		activates					PPARgamma	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
21741	2	6274	7	NULL	NULL	NULL	NULL	thiazolidinediones	Chemical		activates					PPARgamma	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
21742	3	6274	7	NULL	NULL	NULL	NULL	15d-PGJ2	Chemical		activates					PPARgamma	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
21747	4	6274	7	NULL	NULL	NULL	NULL	PPARgamma	GP	ligand activated	heterodimerizes					retinoid X receptor 	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
21750	5	6274	7	NULL	NULL	NULL	NULL	statement 1	Process		results in					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
21753	6	6274	7	NULL	NULL	NULL	NULL	statement 2	Process		results in					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
21757	7	6274	7	NULL	NULL	NULL	NULL	statement 3	Process		results in					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
21760	8	6274	7	NULL	NULL	NULL	NULL	statement 4	Process		bind									PPRE	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
21762	9	6274	7	NULL	NULL	NULL	NULL	15d-PGJ2	GP		is					15-deoxy-delta12,14-prostaglandin J2 	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
21763	10	6274	7	NULL	NULL	NULL	NULL	PPRE	GP		is					PPAR response element	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_16	12615657	1, 2 The activation of PPARgamma with a ligand, such as a class of antidiabetic, insulin-sensitizing agents known as thiazolidinediones, 3 or eicosanoid derivatives, including 15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2), 4 results in its heterodimerization with the retinoid X receptor and the binding of their complex to the PPAR response element (PPRE) of target genes.	bind
16930	1	6275	5	NULL	NULL	0	NULL	cGKIalpha	NULL		interact with	NULL	specifically	amino terminus		myosin phosphatase	NULL		myosin-binding subunit		NULL		0	NULL	NULL	NULL	gw60_circulationres_90_10_1080_s_25	12039797	1, 2, 25 Recent experiments have shown that the amino terminus of cGKIalpha interacts specifically with the myosin-binding subunit of myosin phosphatase, 12 whereas the amino terminus of cGKIbeta interacts specifically with inositol 1,4,5-trisphosphate receptor - associated cGMP kinase substrate (IRAG), a cGKI substrate protein.	bind
16931	2	6275	5	10	NULL	0	NULL	cGKIbeta 			interact with		specifically	amino terminus		IRAG					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_10_1080_s_25	12039797	1, 2, 25 Recent experiments have shown that the amino terminus of cGKIalpha interacts specifically with the myosin-binding subunit of myosin phosphatase, 12 whereas the amino terminus of cGKIbeta interacts specifically with inositol 1,4,5-trisphosphate receptor - associated cGMP kinase substrate (IRAG), a cGKI substrate protein.	bind
16932	3	6275	5	NULL	NULL	0	NULL	IRAG	NULL		is	NULL				1,4,5-trisphosphate receptor - associated cGMP kinase substrate	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_10_1080_s_25	12039797	1, 2, 25 Recent experiments have shown that the amino terminus of cGKIalpha interacts specifically with the myosin-binding subunit of myosin phosphatase, 12 whereas the amino terminus of cGKIbeta interacts specifically with inositol 1,4,5-trisphosphate receptor - associated cGMP kinase substrate (IRAG), a cGKI substrate protein.	bind
26090	4	6275	5	NULL	NULL	0	NULL	IRAG	NULL		is a type of	NULL				cGKI substrate protein	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_10_1080_s_25	12039797	1, 2, 25 Recent experiments have shown that the amino terminus of cGKIalpha interacts specifically with the myosin-binding subunit of myosin phosphatase, 12 whereas the amino terminus of cGKIbeta interacts specifically with inositol 1,4,5-trisphosphate receptor - associated cGMP kinase substrate (IRAG), a cGKI substrate protein.	bind
21771	1	6275	7	NULL	NULL	NULL	NULL	cGKIalpha	GP		interacts		specifically	amino terminus		myosin phosphatase	GP		myosin-binding subunit 		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_10_1080_s_25	12039797	1, 2, 25 Recent experiments have shown that the amino terminus of cGKIalpha interacts specifically with the myosin-binding subunit of myosin phosphatase, 12 whereas the amino terminus of cGKIbeta interacts specifically with inositol 1,4,5-trisphosphate receptor - associated cGMP kinase substrate (IRAG), a cGKI substrate protein.	bind
21773	2	6275	7	NULL	NULL	NULL	NULL	cGKIbeta	GP		interacts		specifically	amino terminus		IRAG	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_10_1080_s_25	12039797	1, 2, 25 Recent experiments have shown that the amino terminus of cGKIalpha interacts specifically with the myosin-binding subunit of myosin phosphatase, 12 whereas the amino terminus of cGKIbeta interacts specifically with inositol 1,4,5-trisphosphate receptor - associated cGMP kinase substrate (IRAG), a cGKI substrate protein.	bind
21774	3	6275	7	NULL	NULL	NULL	NULL	IRAG	GP		is					inositol 1,4,5-trisphosphate receptor - associated cGMP kinase substrate	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_10_1080_s_25	12039797	1, 2, 25 Recent experiments have shown that the amino terminus of cGKIalpha interacts specifically with the myosin-binding subunit of myosin phosphatase, 12 whereas the amino terminus of cGKIbeta interacts specifically with inositol 1,4,5-trisphosphate receptor - associated cGMP kinase substrate (IRAG), a cGKI substrate protein.	bind
21775	4	6275	7	NULL	NULL	NULL	NULL	IRAG	GP		is a type of					cGKI substrate protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_10_1080_s_25	12039797	1, 2, 25 Recent experiments have shown that the amino terminus of cGKIalpha interacts specifically with the myosin-binding subunit of myosin phosphatase, 12 whereas the amino terminus of cGKIbeta interacts specifically with inositol 1,4,5-trisphosphate receptor - associated cGMP kinase substrate (IRAG), a cGKI substrate protein.	bind
16933	1	6276	5	NULL	NULL	0	NULL	CCR3	NULL		bind	NULL				eotaxin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
16934	2	6276	5	NULL	NULL	0	NULL	CCR3	NULL		bind	NULL				RANTES	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
16935	3	6276	5	10	NULL	0	NULL	CCR3	NULL		bind	NULL				(MCP)-3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
16936	4	6276	5	NULL	NULL	0	NULL	CCR3	NULL		bind	NULL				MCP-4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
16937	5	6276	5	NULL	NULL	0	NULL	CCR3	NULL		bind	NULL				chemokines	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
16938	6	6276	5	NULL	NULL	0	NULL	CCR3	NULL		is expressed in	NULL				eosinophils	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
16939	7	6276	5	NULL	NULL	0	NULL	CCR3	NULL		is expressed in	NULL				basophils	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
16940	8	6276	5	NULL	NULL	0	NULL	CCR3	NULL		is expressed in	NULL				Th2 cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
16941	9	6276	5	NULL	NULL	0	NULL	Th2 cells	NULL		is	NULL				type 2 T helper cells	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
26091	10	6276	5	NULL	NULL	0	NULL	CCR3	NULL		is a type of	NULL				chemokine receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
45579	11	6276	5	10	NULL	0	NULL	MCP	NULL		is	NULL				monocyte chemotactic protein	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
21776	1	6276	7	NULL	NULL	NULL	NULL	CCR3	GP		binds					eotaxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
21777	2	6276	7	NULL	NULL	NULL	NULL	CCR3	GP		binds					RANTES	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
21779	3	6276	7	NULL	NULL	NULL	NULL	CCR3	GP		binds					MCP-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
21780	4	6276	7	NULL	NULL	NULL	NULL	CCR3	GP		binds					MCP-4	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
21781	5	6276	7	NULL	NULL	NULL	NULL	CCR3	GP		is expressed in					 eosinophils	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
21783	6	6276	7	NULL	NULL	NULL	NULL	CCR3	GP		is expressed in					basophils	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
21785	7	6276	7	NULL	NULL	NULL	NULL	CCR3	GP		is expressed in					Th2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
21786	8	6276	7	NULL	NULL	NULL	NULL	MCP	GP		is					monocyte chemotactic protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
21787	9	6276	7	NULL	NULL	NULL	NULL	Th2	Cell		is					type 2 T helper	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
26376	10	6276	7	NULL	NULL	NULL	NULL	CCR3	GP		is a type of					chemokine receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
26377	11	6276	7	NULL	NULL	NULL	NULL	CCR3	GP		bind					chemokines	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1195_s_25	10514402	1, 3  he chemokine receptor CCR3, which binds eotaxin, RANTES, monocyte chemotactic protein (MCP)-3, MCP-4, and some other chemokines, is expressed in human eosinophils, 4- 6  basophils, 7  and type 2 T helper (Th2) cells.	bind
16942	1	6277	5	NULL	NULL	0	NULL	ORC	NULL	Drosophila	bind	NULL	specifically				NULL			ACE3	NULL		NULL	NULL	NULL	NULL	gw70_nature_430_6997_372_s_247	15254542	1, 8 13 (2002) |  ChemPort |            Austin, R. J., Orr-Weaver, T. L. & Bell, S. P.  Drosophila ORC specifically binds to ACE3, an origin of DNA replication control element.	bind
16943	2	6277	5	NULL	NULL	0	NULL	ACE3	NULL		is origin of	NULL					NULL			DNA replication control element	NULL		NULL	NULL	NULL	NULL	gw70_nature_430_6997_372_s_247	15254542	1, 8 13 (2002) |  ChemPort |            Austin, R. J., Orr-Weaver, T. L. & Bell, S. P.  Drosophila ORC specifically binds to ACE3, an origin of DNA replication control element.	bind
21792	1	6277	7	NULL	NULL	NULL	NULL	ORC	GP	Drosophila	binds		specifically							ACE3	NULL		NULL	NULL	NULL	NULL	gw70_nature_430_6997_372_s_247	15254542	1, 8 13 (2002) |  ChemPort |            Austin, R. J., Orr-Weaver, T. L. & Bell, S. P.  Drosophila ORC specifically binds to ACE3, an origin of DNA replication control element.	bind
21794	2	6277	7	NULL	NULL	NULL	NULL	ACE3	GP		is origin of									DNA replication control element	NULL		NULL	NULL	NULL	NULL	gw70_nature_430_6997_372_s_247	15254542	1, 8 13 (2002) |  ChemPort |            Austin, R. J., Orr-Weaver, T. L. & Bell, S. P.  Drosophila ORC specifically binds to ACE3, an origin of DNA replication control element.	bind
16944	1	6279	5	NULL	NULL	0	NULL	FLAG-Plk	NULL	WT	bind	NULL				GST-C	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_4_1984_s_138	11854496	1, FLAG-Plk WT protein bound to GST-C; 2, FLAG-deltaC1-401 protein bound to GST-C; 3, FLAG-deltaC1-401 protein (T210D) bound to GST-C.	bind
16945	2	6279	5	NULL	NULL	0	NULL	FLAG-deltaC1-401 protein	NULL		bind	NULL				GST-C	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_4_1984_s_138	11854496	1, FLAG-Plk WT protein bound to GST-C; 2, FLAG-deltaC1-401 protein bound to GST-C; 3, FLAG-deltaC1-401 protein (T210D) bound to GST-C.	bind
16946	3	6279	5	NULL	NULL	0	NULL	FLAG-deltaC1-401 protein	NULL		bind	NULL		T210D		GST-C	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_4_1984_s_138	11854496	1, FLAG-Plk WT protein bound to GST-C; 2, FLAG-deltaC1-401 protein bound to GST-C; 3, FLAG-deltaC1-401 protein (T210D) bound to GST-C.	bind
21801	1	6279	7	NULL	NULL	NULL	NULL	FLAG-Plk protein	GP	WT	bind					GST-C	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_4_1984_s_138	11854496	1, FLAG-Plk WT protein bound to GST-C; 2, FLAG-deltaC1-401 protein bound to GST-C; 3, FLAG-deltaC1-401 protein (T210D) bound to GST-C.	bind
21803	2	6279	7	NULL	NULL	NULL	NULL	FLAG-deltaC1-401 protein	GP		bind					GST-C	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_4_1984_s_138	11854496	1, FLAG-Plk WT protein bound to GST-C; 2, FLAG-deltaC1-401 protein bound to GST-C; 3, FLAG-deltaC1-401 protein (T210D) bound to GST-C.	bind
21804	3	6279	7	NULL	NULL	NULL	NULL	FLAG-deltaC1-401 protein	GP		bind			 T210D		GST-C	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_4_1984_s_138	11854496	1, FLAG-Plk WT protein bound to GST-C; 2, FLAG-deltaC1-401 protein bound to GST-C; 3, FLAG-deltaC1-401 protein (T210D) bound to GST-C.	bind
16947	1	6280	5	10	NULL	0	NULL	FPP	NULL		bind	NULL				FTase	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_303_1_1_s_41	12646157	1, FPP (blue) bound to FTase (PDB number 1FT2).	bind
21807	1	6280	7	NULL	NULL	NULL	NULL	FPP	Chemical		bind					FTase	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_303_1_1_s_41	12646157	1, FPP (blue) bound to FTase (PDB number 1FT2).	bind
16948	1	6281	5	NULL	NULL	0	NULL	Mex67p	NULL		bind	NULL				GST-Nup116p	NULL		repeats		NULL		0	NULL	NULL	NULL	gw60_cellbiol_150_4_695_s_227	10952996	1, Protein standard; 2, recombinant Mex67p/His-Mtr2p complex, expressed in  E.  coli, and purified by Ni-NTA affinity, FPLC-MonoS, and gel filtration chromatography; 3, Mex67p and Mtr2p bound to GST-Nup116p repeats.	bind
16949	2	6281	5	NULL	NULL	0	NULL	Mtr2p	NULL		bind	NULL				GST-Nup116p	NULL		repeats		NULL		0	NULL	NULL	NULL	gw60_cellbiol_150_4_695_s_227	10952996	1, Protein standard; 2, recombinant Mex67p/His-Mtr2p complex, expressed in  E.  coli, and purified by Ni-NTA affinity, FPLC-MonoS, and gel filtration chromatography; 3, Mex67p and Mtr2p bound to GST-Nup116p repeats.	bind
21808	1	6281	7	NULL	NULL	NULL	NULL	Mex67p	GP		bind					GST-Nup116p	GP		repeats		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_4_695_s_227	10952996	1, Protein standard; 2, recombinant Mex67p/His-Mtr2p complex, expressed in  E.  coli, and purified by Ni-NTA affinity, FPLC-MonoS, and gel filtration chromatography; 3, Mex67p and Mtr2p bound to GST-Nup116p repeats.	bind
21809	2	6281	7	NULL	NULL	NULL	NULL	Mtr2p	GP		bind					GST-Nup116p	GP		repeats		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_4_695_s_227	10952996	1, Protein standard; 2, recombinant Mex67p/His-Mtr2p complex, expressed in  E.  coli, and purified by Ni-NTA affinity, FPLC-MonoS, and gel filtration chromatography; 3, Mex67p and Mtr2p bound to GST-Nup116p repeats.	bind
16950	1	6282	5	NULL	NULL	0	NULL	R7.1	NULL		bind	NULL					NULL		alphaL I domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_10590_s_173	11781316	1, R7.1, and clone 38 bind to the alphaL I domain ( 8,  10,  28).	bind
21813	1	6282	7	NULL	NULL	NULL	NULL	R7.1	GP		bind								alphaL I domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10590_s_173	11781316	1, R7.1, and clone 38 bind to the alphaL I domain ( 8,  10,  28).	bind
16951	1	6283	5	NULL	NULL	0	NULL	Sox2 protein	NULL		bind	NULL	individually			DNA	NULL			enhancer	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_23387_s_345	10801796	1, Sox2 or Oct-3 proteins bound individually to the enhancer DNA are relatively inactive.	bind
16952	2	6283	5	NULL	NULL	0	NULL	Oct-3 protein	NULL		bind	NULL	individually			DNA	NULL			enhancer	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_23387_s_345	10801796	1, Sox2 or Oct-3 proteins bound individually to the enhancer DNA are relatively inactive.	bind
16953	3	6283	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_30_23387_s_345	10801796	1, Sox2 or Oct-3 proteins bound individually to the enhancer DNA are relatively inactive.	bind
16954	4	6283	5	NULL	NULL	0	NULL	statement 1	NULL		is	NULL				inactive	NULL	relatively			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_30_23387_s_345	10801796	1, Sox2 or Oct-3 proteins bound individually to the enhancer DNA are relatively inactive.	bind
16955	5	6283	5	NULL	NULL	0	NULL	statement 2	NULL		is	NULL				inactive	NULL	relatively			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_30_23387_s_345	10801796	1, Sox2 or Oct-3 proteins bound individually to the enhancer DNA are relatively inactive.	bind
21816	1	6283	7	NULL	NULL	NULL	NULL	 Sox2 protein	GP		bind					DNA	NucleicAcid			enhancer	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_23387_s_345	10801796	1, Sox2 or Oct-3 proteins bound individually to the enhancer DNA are relatively inactive.	bind
21817	2	6283	7	NULL	NULL	NULL	NULL	Oct-3 protein	GP		bind					DNA	NucleicAcid			enhancer	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_23387_s_345	10801796	1, Sox2 or Oct-3 proteins bound individually to the enhancer DNA are relatively inactive.	bind
21818	3	6283	7	NULL	NULL	NULL	NULL	statement 1	Process		is					inactive	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_23387_s_345	10801796	1, Sox2 or Oct-3 proteins bound individually to the enhancer DNA are relatively inactive.	bind
21819	4	6283	7	NULL	NULL	NULL	NULL	statement 2	Process		is					inactive	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_23387_s_345	10801796	1, Sox2 or Oct-3 proteins bound individually to the enhancer DNA are relatively inactive.	bind
54184	5	6283	7	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_23387_s_345	10801796	1, Sox2 or Oct-3 proteins bound individually to the enhancer DNA are relatively inactive.	bind
19287	1	6284	5	NULL	NULL	0	NULL	A52R	NULL		is	NULL				virally derived vaccinia protein	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19288	2	6284	5	NULL	NULL	0	NULL	statement 1	NULL		acts as	NULL				dominant-negative form of MyD88	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19289	3	6284	5	NULL	NULL	0	NULL	Yop proteins	NULL	Yersinia	interferes with	NULL				MAP3K	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19290	4	6284	5	NULL	NULL	0	NULL	statement 3	NULL		prevents	NULL				IkappaBalpha	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19291	5	6284	5	NULL	NULL	0	NULL	Yop proteins	NULL	Yersinia	interferes with	NULL				IKKbeta	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19292	6	6284	5	NULL	NULL	0	NULL	statement 5	NULL		prevents	NULL				IkappaBalpha	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19293	7	6284	5	NULL	NULL	0	NULL	UPEC virulence factors	NULL		interferes with	NULL				MAP kinase	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19294	8	6284	5	NULL	NULL	0	NULL	measles virus	NULL		prevents	NULL				IkappaBalpha	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19295	9	6284	5	NULL	NULL	0	NULL	IkappaBalpha	NULL	phosphorylated	undergoes	NULL				ubiquitination	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19296	10	6284	5	NULL	NULL	0	NULL	Vpu protein	NULL	Salmonella	inhibit	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19297	11	6284	5	NULL	NULL	0	NULL	Vpu protein	NULL	HIV-1	inhibit	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19298	12	6284	5	NULL	NULL	0	NULL	orthopoxviruses	NULL		dephosphorylate	NULL				IkappaBalpha	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19299	13	6284	5	NULL	NULL	0	NULL	orthopoxviruses	NULL		inhibit	NULL				IkappaBalpha	NULL	degradation of phosphorylated			NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19300	14	6284	5	NULL	NULL	0	NULL	ASFV-derived protein	NULL		acts as	NULL				IkappaB-like molecule	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19301	15	6284	5	NULL	NULL	0	NULL	NF-kappaB	NULL		is translocated to	NULL				nucleus	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19302	16	6284	5	NULL	NULL	0	NULL	statement 14	NULL		inhibit	NULL				statement 15	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19303	17	6284	5	NULL	NULL	0	NULL	ZEBRA protein	NULL	EBV-derived	bind	NULL				p65	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19304	18	6284	5	NULL	NULL	0	NULL	soluble toxin	NULL	M. ulcerans	prevent	NULL	may			p65	NULL	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19305	19	6284	5	NULL	NULL	0	NULL	NF-kappaB	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19306	20	6284	5	NULL	NULL	0	NULL	soluble toxin	NULL	M. ulcerans	prevent	NULL	may			statement 19	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19307	21	6284	5	NULL	NULL	0	NULL	statement 18	NULL		is an alternative to	NULL				statement 20	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19308	22	6284	5	NULL	NULL	0	NULL		NULL	T. gondii	prevents	NULL				NF-kappaB	NULL	nuclear translocation of 			NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
19309	23	6284	5	NULL	NULL	0	NULL		NULL	S. mansoni 	disrupt	NULL				statement 19	NULL				NULL	in nucleus	0	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21883	1	6284	7	NULL	NULL	NULL	NULL	vaccinia protein	GP	virally derived 	acts as a			A52R		MyD88	GP	dominant-negative form of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21884	2	6284	7	NULL	NULL	NULL	NULL	Yop proteins	GP	Yersinia	interfere with					MAP3K	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21885	3	6284	7	NULL	NULL	NULL	NULL	Yop proteins	GP	Yersinia	interfere with					IKKbeta	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21886	4	6284	7	NULL	NULL	NULL	NULL	statement 2	Process		prevents					IkappaBalpha	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21887	5	6284	7	NULL	NULL	NULL	NULL	statement 3	Process		prevents					IkappaBalpha	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21888	7	6284	7	NULL	NULL	NULL	NULL	UPEC	GP	virulence factors	interfere with					MAP kinase	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21889	6	6284	7	NULL	NULL	NULL	NULL	statement 2	Process		occur along with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21890	8	6284	7	NULL	NULL	NULL	NULL	measles virus	Organism		prevents					IkappaBalpha	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21891	9	6284	7	NULL	NULL	NULL	NULL	Vpu protein	GP	Salmonella 	inhibits					IkappaBalpha	GP	ubiquitination of;; phosphorylated 			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21892	10	6284	7	NULL	NULL	NULL	NULL	HIV-1 Vpu protein	GP		inhibits					IkappaBalpha	GP	ubiquitination of;; phosphorylated 			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21893	11	6284	7	NULL	NULL	NULL	NULL	orthopoxviruses	Organism		dephosphorylate					IkappaBalpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21894	12	6284	7	NULL	NULL	NULL	NULL	orthopoxviruses	Organism		inhibit					phosphorylated protein	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21895	13	6284	7	NULL	NULL	NULL	NULL	statement 11	Process		is an alternative to					statement 12	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21896	14	6284	7	NULL	NULL	NULL	NULL	ASFV-derived protein 	GP		acts as an					IkappaB-like molecule 	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21897	15	6284	7	NULL	NULL	NULL	NULL	statement 14	Process		inhibit					NF-kappaB 	GP	translocation to nucleus			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21898	16	6284	7	NULL	NULL	NULL	NULL	ZEBRA protein 	GP	EBV-derived	binds to					p65	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21899	17	6284	7	NULL	NULL	NULL	NULL	soluble toxin	GP	M. ulcerans	prevent		may			p65	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21900	18	6284	7	NULL	NULL	NULL	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21901	19	6284	7	NULL	NULL	NULL	NULL	soluble toxin	GP	M.ulcerans	prevent					statement 18	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21902	20	6284	7	NULL	NULL	NULL	NULL	T. gondii	Organism		prevents					NF-kappaB	GP	nuclear translocation of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21903	21	6284	7	NULL	NULL	NULL	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL	nucleus	NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
21904	22	6284	7	NULL	NULL	NULL	NULL	S. mansoni	Organism		disrupts					statement 21	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3311_s_36	12065467	1, virally derived vaccinia protein, A52R, acts as a dominant-negative form of MyD88; 2,  Yersinia Yop proteins interfere with MAP3K and IKKbeta to prevent phosphorylation of IkappaBalpha and UPEC virulence factors interfere with MAP kinase activity; 3, measles virus prevents phosphorylation of IkappaBalpha; 4,  Salmonella and HIV-1 Vpu protein inhibit ubiquitination of phosphorylated IkappaBalpha; 5, orthopoxviruses can either dephosphorylate IkappaBalpha or inhibit degradation of the phosphorylated protein; 6, an ASFV-derived protein acts as an IkappaB-like molecule to inhibit NF-kappaB translocation to the nucleus; 7, EBV-derived ZEBRA protein binds to p65; 8, soluble toxin from  M. ulcerans may prevent phosphorylation of p65 and/or binding of NF-kappaB to DNA; 9,  T. gondii prevents nuclear translocation of NF-kappaB; 10,  S. mansoni disrupts NF-kappaB binding to DNA in the nucleus.	bind
16956	1	6286	5	NULL	NULL	0	NULL	FGF2	NULL		bind	NULL				FGFRs	NULL	cell-surface			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_14	14684627	1,2  Binding of FGF2 to cell-surface tyrosine kinase FGF receptors (FGFRs) triggers receptor dimerization and autophosphorylation of tyrosine residues, which act as docking sites for downstream proteins leading to cell response.	bind
16957	2	6286	5	NULL	NULL	0	NULL	FGFRs	NULL		is	NULL				FGF receptors	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_14	14684627	1,2  Binding of FGF2 to cell-surface tyrosine kinase FGF receptors (FGFRs) triggers receptor dimerization and autophosphorylation of tyrosine residues, which act as docking sites for downstream proteins leading to cell response.	bind
16958	3	6286	5	NULL	NULL	0	NULL	statement 1	NULL		trigger	NULL				receptor dimerization	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_14	14684627	1,2  Binding of FGF2 to cell-surface tyrosine kinase FGF receptors (FGFRs) triggers receptor dimerization and autophosphorylation of tyrosine residues, which act as docking sites for downstream proteins leading to cell response.	bind
16959	4	6286	5	NULL	NULL	0	NULL	statement 1	NULL		trigger	NULL				autophosphorylation	NULL			tyrosine residues	NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_14	14684627	1,2  Binding of FGF2 to cell-surface tyrosine kinase FGF receptors (FGFRs) triggers receptor dimerization and autophosphorylation of tyrosine residues, which act as docking sites for downstream proteins leading to cell response.	bind
16960	5	6286	5	NULL	NULL	0	NULL	statement 4	NULL		act as	NULL				docking sites	NULL	for downstream proteins			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_14	14684627	1,2  Binding of FGF2 to cell-surface tyrosine kinase FGF receptors (FGFRs) triggers receptor dimerization and autophosphorylation of tyrosine residues, which act as docking sites for downstream proteins leading to cell response.	bind
16961	6	6286	5	NULL	NULL	0	NULL	statement 5	NULL		leads to	NULL				cell response	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_14	14684627	1,2  Binding of FGF2 to cell-surface tyrosine kinase FGF receptors (FGFRs) triggers receptor dimerization and autophosphorylation of tyrosine residues, which act as docking sites for downstream proteins leading to cell response.	bind
21905	1	6286	7	NULL	NULL	NULL	NULL	FGF2	GP		bind					tyrosine kinase FGFRs	GP	cell-surface			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_14	14684627	1,2  Binding of FGF2 to cell-surface tyrosine kinase FGF receptors (FGFRs) triggers receptor dimerization and autophosphorylation of tyrosine residues, which act as docking sites for downstream proteins leading to cell response.	bind
21906	2	6286	7	NULL	NULL	NULL	NULL	statement 1	Process		triggers					receptor	GP	dimerzation of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_14	14684627	1,2  Binding of FGF2 to cell-surface tyrosine kinase FGF receptors (FGFRs) triggers receptor dimerization and autophosphorylation of tyrosine residues, which act as docking sites for downstream proteins leading to cell response.	bind
21908	3	6286	7	NULL	NULL	NULL	NULL	statement 1	Process		triggers					autophosphorylation	Process		tyrosine residues		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_14	14684627	1,2  Binding of FGF2 to cell-surface tyrosine kinase FGF receptors (FGFRs) triggers receptor dimerization and autophosphorylation of tyrosine residues, which act as docking sites for downstream proteins leading to cell response.	bind
21909	4	6286	7	NULL	NULL	NULL	NULL	statement 2	Process		occurs along with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_14	14684627	1,2  Binding of FGF2 to cell-surface tyrosine kinase FGF receptors (FGFRs) triggers receptor dimerization and autophosphorylation of tyrosine residues, which act as docking sites for downstream proteins leading to cell response.	bind
21910	5	6286	7	NULL	NULL	NULL	NULL	statement 4	Process		act as					downstream proteins	GP	docking site for			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_14	14684627	1,2  Binding of FGF2 to cell-surface tyrosine kinase FGF receptors (FGFRs) triggers receptor dimerization and autophosphorylation of tyrosine residues, which act as docking sites for downstream proteins leading to cell response.	bind
21911	6	6286	7	NULL	NULL	NULL	NULL	statement 5	Process		leads to					cell response	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_14	14684627	1,2  Binding of FGF2 to cell-surface tyrosine kinase FGF receptors (FGFRs) triggers receptor dimerization and autophosphorylation of tyrosine residues, which act as docking sites for downstream proteins leading to cell response.	bind
21914	7	6286	7	NULL	NULL	NULL	NULL	FGFRs	GP		is					FGF receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_14	14684627	1,2  Binding of FGF2 to cell-surface tyrosine kinase FGF receptors (FGFRs) triggers receptor dimerization and autophosphorylation of tyrosine residues, which act as docking sites for downstream proteins leading to cell response.	bind
16962	1	6287	5	NULL	NULL	0	NULL	eIF4E	NULL		interact with	NULL				eIF4G	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_225	14605021	1,2  eIF4E also interacts with eIF4G, a molecule that binds to other translation factors, including eIF4A and eIF3.	bind
16963	2	6287	5	NULL	NULL	0	NULL	eIF4G	NULL		bind	NULL				eIF4A	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_225	14605021	1,2  eIF4E also interacts with eIF4G, a molecule that binds to other translation factors, including eIF4A and eIF3.	bind
16964	3	6287	5	NULL	NULL	0	NULL	eIF4G	NULL		bind	NULL				eIF3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_225	14605021	1,2  eIF4E also interacts with eIF4G, a molecule that binds to other translation factors, including eIF4A and eIF3.	bind
26096	4	6287	5	NULL	NULL	0	NULL	eIF4A	NULL		is a type of	NULL				translation factor	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_225	14605021	1,2  eIF4E also interacts with eIF4G, a molecule that binds to other translation factors, including eIF4A and eIF3.	bind
26097	5	6287	5	NULL	NULL	0	NULL	eIF3	NULL		is a type of	NULL				translation factor	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_225	14605021	1,2  eIF4E also interacts with eIF4G, a molecule that binds to other translation factors, including eIF4A and eIF3.	bind
21915	1	6287	7	NULL	NULL	NULL	NULL	eIF4E	GP		interacts with					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_225	14605021	1,2  eIF4E also interacts with eIF4G, a molecule that binds to other translation factors, including eIF4A and eIF3.	bind
21916	2	6287	7	NULL	NULL	NULL	NULL	eIF4G	GP		binds					eIF4A	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_225	14605021	1,2  eIF4E also interacts with eIF4G, a molecule that binds to other translation factors, including eIF4A and eIF3.	bind
21917	3	6287	7	NULL	NULL	NULL	NULL	eIF4G	GP		binds					eIF3	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_225	14605021	1,2  eIF4E also interacts with eIF4G, a molecule that binds to other translation factors, including eIF4A and eIF3.	bind
26378	4	6287	7	NULL	NULL	NULL	NULL	eIF4A	GP		is a type of					translation factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_225	14605021	1,2  eIF4E also interacts with eIF4G, a molecule that binds to other translation factors, including eIF4A and eIF3.	bind
26379	5	6287	7	NULL	NULL	NULL	NULL	eIF3	GP		is a type of					translation factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_225	14605021	1,2  eIF4E also interacts with eIF4G, a molecule that binds to other translation factors, including eIF4A and eIF3.	bind
16965	1	6288	5	NULL	NULL	0	NULL	eIF4E	NULL		bind	NULL				7-methylguanosine triphosphate ("`cap"`) structure	NULL			5''-end of cytoplasmic mRNA	NULL		0	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_19	14605021	1,2  eIF4E binds to the 7-methylguanosine triphosphate ("`cap"`) structure at the 5''-end of cytoplasmic mRNA and interacts with eIF4G, a large scaffold protein that binds to other translation factors, including eIF4A and eIF3.	bind
16966	2	6288	5	NULL	NULL	0	NULL	eIF4E	NULL		interacts with	NULL				eIF4G	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_19	14605021	1,2  eIF4E binds to the 7-methylguanosine triphosphate ("`cap"`) structure at the 5''-end of cytoplasmic mRNA and interacts with eIF4G, a large scaffold protein that binds to other translation factors, including eIF4A and eIF3.	bind
16967	3	6288	5	NULL	NULL	0	NULL	eIF4G	NULL		bind	NULL				eIF4A	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_19	14605021	1,2  eIF4E binds to the 7-methylguanosine triphosphate ("`cap"`) structure at the 5''-end of cytoplasmic mRNA and interacts with eIF4G, a large scaffold protein that binds to other translation factors, including eIF4A and eIF3.	bind
16968	4	6288	5	NULL	NULL	0	NULL	eIF4G	NULL		bind	NULL				eIF3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_19	14605021	1,2  eIF4E binds to the 7-methylguanosine triphosphate ("`cap"`) structure at the 5''-end of cytoplasmic mRNA and interacts with eIF4G, a large scaffold protein that binds to other translation factors, including eIF4A and eIF3.	bind
26103	5	6288	5	NULL	NULL	0	NULL	eIF4G	NULL		is a type of	NULL				large scaffold protein	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_19	14605021	1,2  eIF4E binds to the 7-methylguanosine triphosphate ("`cap"`) structure at the 5''-end of cytoplasmic mRNA and interacts with eIF4G, a large scaffold protein that binds to other translation factors, including eIF4A and eIF3.	bind
26104	6	6288	5	NULL	NULL	0	NULL	eIF4A	NULL		is a type of	NULL				translation factor	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_19	14605021	1,2  eIF4E binds to the 7-methylguanosine triphosphate ("`cap"`) structure at the 5''-end of cytoplasmic mRNA and interacts with eIF4G, a large scaffold protein that binds to other translation factors, including eIF4A and eIF3.	bind
26106	7	6288	5	NULL	NULL	0	NULL	eIF3	NULL		is a type of	NULL				translation factor	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_19	14605021	1,2  eIF4E binds to the 7-methylguanosine triphosphate ("`cap"`) structure at the 5''-end of cytoplasmic mRNA and interacts with eIF4G, a large scaffold protein that binds to other translation factors, including eIF4A and eIF3.	bind
21920	1	6288	7	NULL	NULL	NULL	NULL	eIF4E	GP		binds to					7-methylguanosine triphosphate	Chemical			5''-end of cytoplasmic mRNA	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_19	14605021	1,2  eIF4E binds to the 7-methylguanosine triphosphate ("`cap"`) structure at the 5''-end of cytoplasmic mRNA and interacts with eIF4G, a large scaffold protein that binds to other translation factors, including eIF4A and eIF3.	bind
21930	2	6288	7	NULL	NULL	NULL	NULL	 eIF4E	GP		interact with					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_19	14605021	1,2  eIF4E binds to the 7-methylguanosine triphosphate ("`cap"`) structure at the 5''-end of cytoplasmic mRNA and interacts with eIF4G, a large scaffold protein that binds to other translation factors, including eIF4A and eIF3.	bind
21931	3	6288	7	NULL	NULL	NULL	NULL	eIF4G	GP		bind					eIF4A	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_19	14605021	1,2  eIF4E binds to the 7-methylguanosine triphosphate ("`cap"`) structure at the 5''-end of cytoplasmic mRNA and interacts with eIF4G, a large scaffold protein that binds to other translation factors, including eIF4A and eIF3.	bind
21932	4	6288	7	NULL	NULL	NULL	NULL	eIF4G	GP		bind					eIF3	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_19	14605021	1,2  eIF4E binds to the 7-methylguanosine triphosphate ("`cap"`) structure at the 5''-end of cytoplasmic mRNA and interacts with eIF4G, a large scaffold protein that binds to other translation factors, including eIF4A and eIF3.	bind
26380	6	6288	7	NULL	NULL	NULL	NULL	eIF4G	GP		is a type of					scaffold protein	GP	large			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_19	14605021	1,2  eIF4E binds to the 7-methylguanosine triphosphate ("`cap"`) structure at the 5''-end of cytoplasmic mRNA and interacts with eIF4G, a large scaffold protein that binds to other translation factors, including eIF4A and eIF3.	bind
26381	7	6288	7	NULL	NULL	NULL	NULL	eIF3	GP		is a type of					translation factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_19	14605021	1,2  eIF4E binds to the 7-methylguanosine triphosphate ("`cap"`) structure at the 5''-end of cytoplasmic mRNA and interacts with eIF4G, a large scaffold protein that binds to other translation factors, including eIF4A and eIF3.	bind
26382	8	6288	7	NULL	NULL	NULL	NULL	 eIF4A	GP		is a type of					translation factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_19	14605021	1,2  eIF4E binds to the 7-methylguanosine triphosphate ("`cap"`) structure at the 5''-end of cytoplasmic mRNA and interacts with eIF4G, a large scaffold protein that binds to other translation factors, including eIF4A and eIF3.	bind
16969	1	6289	5	10	NULL	0	NULL	heparin			bind					AT					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_18	15231514	1,2  In 1973, Rosenberg and Damus suggested that heparin binds the protease inhibitor antithrombin (AT), causing a conformational change within AT, accelerating its reaction with the protease thrombin and the formation of an active complex between protease and inhibitor.	bind
16970	2	6289	5	NULL	NULL	0	NULL	AT	NULL		is	NULL				antithrombin	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_18	15231514	1,2  In 1973, Rosenberg and Damus suggested that heparin binds the protease inhibitor antithrombin (AT), causing a conformational change within AT, accelerating its reaction with the protease thrombin and the formation of an active complex between protease and inhibitor.	bind
16971	3	6289	5	10	NULL	0	NULL	statement 1	NULL		causes	NULL				AT	NULL	conformational change within			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_18	15231514	1,2  In 1973, Rosenberg and Damus suggested that heparin binds the protease inhibitor antithrombin (AT), causing a conformational change within AT, accelerating its reaction with the protease thrombin and the formation of an active complex between protease and inhibitor.	bind
16972	4	6289	5	10	NULL	0	NULL	statement 3			accelerate					statement 9					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_18	15231514	1,2  In 1973, Rosenberg and Damus suggested that heparin binds the protease inhibitor antithrombin (AT), causing a conformational change within AT, accelerating its reaction with the protease thrombin and the formation of an active complex between protease and inhibitor.	bind
16973	5	6289	5	NULL	NULL	0	NULL	protease	NULL		forms complex with	NULL	active			inhibitor	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_18	15231514	1,2  In 1973, Rosenberg and Damus suggested that heparin binds the protease inhibitor antithrombin (AT), causing a conformational change within AT, accelerating its reaction with the protease thrombin and the formation of an active complex between protease and inhibitor.	bind
16974	6	6289	5	NULL	NULL	0	NULL	statement 3	NULL		accelerate	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_18	15231514	1,2  In 1973, Rosenberg and Damus suggested that heparin binds the protease inhibitor antithrombin (AT), causing a conformational change within AT, accelerating its reaction with the protease thrombin and the formation of an active complex between protease and inhibitor.	bind
54185	7	6289	5	10	NULL	0	NULL	antithrombin			is a type of					protease inhibitor					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_18	15231514	1,2  In 1973, Rosenberg and Damus suggested that heparin binds the protease inhibitor antithrombin (AT), causing a conformational change within AT, accelerating its reaction with the protease thrombin and the formation of an active complex between protease and inhibitor.	bind
54187	8	6289	5	10	NULL	0	NULL	thrombin			is a type of					protease					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_18	15231514	1,2  In 1973, Rosenberg and Damus suggested that heparin binds the protease inhibitor antithrombin (AT), causing a conformational change within AT, accelerating its reaction with the protease thrombin and the formation of an active complex between protease and inhibitor.	bind
54189	9	6289	5	10	NULL	0	NULL	AT			reacts with					thrombin					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_18	15231514	1,2  In 1973, Rosenberg and Damus suggested that heparin binds the protease inhibitor antithrombin (AT), causing a conformational change within AT, accelerating its reaction with the protease thrombin and the formation of an active complex between protease and inhibitor.	bind
21938	1	6289	7	NULL	NULL	NULL	NULL	heparin	GP		binds					AT	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_18	15231514	1,2  In 1973, Rosenberg and Damus suggested that heparin binds the protease inhibitor antithrombin (AT), causing a conformational change within AT, accelerating its reaction with the protease thrombin and the formation of an active complex between protease and inhibitor.	bind
21940	2	6289	7	NULL	NULL	NULL	NULL	statement 1	Process		cause					AT	GP	conformational change within			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_18	15231514	1,2  In 1973, Rosenberg and Damus suggested that heparin binds the protease inhibitor antithrombin (AT), causing a conformational change within AT, accelerating its reaction with the protease thrombin and the formation of an active complex between protease and inhibitor.	bind
21941	3	6289	7	NULL	NULL	NULL	NULL	AT	GP		reacts with					thrombin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_18	15231514	1,2  In 1973, Rosenberg and Damus suggested that heparin binds the protease inhibitor antithrombin (AT), causing a conformational change within AT, accelerating its reaction with the protease thrombin and the formation of an active complex between protease and inhibitor.	bind
21942	4	6289	7	NULL	NULL	NULL	NULL	statement 2	Process		accelerates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_18	15231514	1,2  In 1973, Rosenberg and Damus suggested that heparin binds the protease inhibitor antithrombin (AT), causing a conformational change within AT, accelerating its reaction with the protease thrombin and the formation of an active complex between protease and inhibitor.	bind
21943	5	6289	7	NULL	NULL	NULL	NULL	protease	GP		complex with					inhibitor	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_18	15231514	1,2  In 1973, Rosenberg and Damus suggested that heparin binds the protease inhibitor antithrombin (AT), causing a conformational change within AT, accelerating its reaction with the protease thrombin and the formation of an active complex between protease and inhibitor.	bind
21944	6	6289	7	NULL	NULL	NULL	NULL	statement 2	Process		accelerates					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_18	15231514	1,2  In 1973, Rosenberg and Damus suggested that heparin binds the protease inhibitor antithrombin (AT), causing a conformational change within AT, accelerating its reaction with the protease thrombin and the formation of an active complex between protease and inhibitor.	bind
21945	7	6289	7	NULL	NULL	NULL	NULL	At	GP		is					antithrombin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_18	15231514	1,2  In 1973, Rosenberg and Damus suggested that heparin binds the protease inhibitor antithrombin (AT), causing a conformational change within AT, accelerating its reaction with the protease thrombin and the formation of an active complex between protease and inhibitor.	bind
54186	8	6289	7	NULL	NULL	NULL	NULL	antithrombin	GP		is a type of					protease inhibitor	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_18	15231514	1,2  In 1973, Rosenberg and Damus suggested that heparin binds the protease inhibitor antithrombin (AT), causing a conformational change within AT, accelerating its reaction with the protease thrombin and the formation of an active complex between protease and inhibitor.	bind
54188	9	6289	7	NULL	NULL	NULL	NULL	thrombin	GP		is a type of					protease	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_18	15231514	1,2  In 1973, Rosenberg and Damus suggested that heparin binds the protease inhibitor antithrombin (AT), causing a conformational change within AT, accelerating its reaction with the protease thrombin and the formation of an active complex between protease and inhibitor.	bind
16975	1	6290	5	NULL	NULL	0	NULL	LXRalpha/RXRs heterodimers	NULL		bind	NULL					NULL			DR-4 - type sequence elements	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_3_622_s_16	15625283	1,2  LXRalpha/RXRs heterodimers bind to DR-4 - type sequence elements known as the LXR response element in their target genes.	bind
26111	2	6290	5	10	NULL	0	NULL	DR-4 - type sequence elements			is a type of									LXR response element	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_3_622_s_16	15625283	1,2  LXRalpha/RXRs heterodimers bind to DR-4 - type sequence elements known as the LXR response element in their target genes.	bind
21946	1	6290	7	NULL	NULL	NULL	NULL	LXRalpha/RXRs heterodimers	GP		binds to									DR-4 - type sequence elements	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_3_622_s_16	15625283	1,2  LXRalpha/RXRs heterodimers bind to DR-4 - type sequence elements known as the LXR response element in their target genes.	bind
21947	2	6290	7	NULL	NULL	NULL	NULL	DR-4 - type sequence elements	GP		is a type of									LXR response element	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_3_622_s_16	15625283	1,2  LXRalpha/RXRs heterodimers bind to DR-4 - type sequence elements known as the LXR response element in their target genes.	bind
16976	1	6291	5	NULL	NULL	0	NULL	versican core protein	NULL		bind	NULL		G1		HA	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_370_s_14	16385080	1,2  The amino-terminal globular domain (G1) of versican core protein binds to hyaluronan (HA) and affects cell adhesion, proliferation, and migration.	bind
16977	2	6291	5	NULL	NULL	0	NULL	HA	NULL		is	NULL				hyaluronan	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_370_s_14	16385080	1,2  The amino-terminal globular domain (G1) of versican core protein binds to hyaluronan (HA) and affects cell adhesion, proliferation, and migration.	bind
16978	3	6291	5	NULL	NULL	0	NULL	G1	NULL		is	NULL				amino-terminal globular domain	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_370_s_14	16385080	1,2  The amino-terminal globular domain (G1) of versican core protein binds to hyaluronan (HA) and affects cell adhesion, proliferation, and migration.	bind
16979	4	6291	5	NULL	NULL	0	NULL	statement 1	NULL		affect	NULL				cell adhesion	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_370_s_14	16385080	1,2  The amino-terminal globular domain (G1) of versican core protein binds to hyaluronan (HA) and affects cell adhesion, proliferation, and migration.	bind
16980	5	6291	5	NULL	NULL	0	NULL	statement 2	NULL		affect	NULL				proliferation	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_370_s_14	16385080	1,2  The amino-terminal globular domain (G1) of versican core protein binds to hyaluronan (HA) and affects cell adhesion, proliferation, and migration.	bind
16981	6	6291	5	NULL	NULL	0	NULL	statement 1	NULL		affect	NULL				migration	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_370_s_14	16385080	1,2  The amino-terminal globular domain (G1) of versican core protein binds to hyaluronan (HA) and affects cell adhesion, proliferation, and migration.	bind
21979	1	6291	7	NULL	NULL	NULL	NULL	versican core protein	GP		binds to			amino-terminal G1 domain		HA	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_370_s_14	16385080	1,2  The amino-terminal globular domain (G1) of versican core protein binds to hyaluronan (HA) and affects cell adhesion, proliferation, and migration.	bind
21980	2	6291	7	NULL	NULL	NULL	NULL	statement 1	Process		affects					cell adhesion	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_370_s_14	16385080	1,2  The amino-terminal globular domain (G1) of versican core protein binds to hyaluronan (HA) and affects cell adhesion, proliferation, and migration.	bind
21981	3	6291	7	NULL	NULL	NULL	NULL	statement 1	GP		affects					cell proliferation	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_370_s_14	16385080	1,2  The amino-terminal globular domain (G1) of versican core protein binds to hyaluronan (HA) and affects cell adhesion, proliferation, and migration.	bind
21982	4	6291	7	NULL	NULL	NULL	NULL	statement 1	GP		affects					cell migration	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_370_s_14	16385080	1,2  The amino-terminal globular domain (G1) of versican core protein binds to hyaluronan (HA) and affects cell adhesion, proliferation, and migration.	bind
21983	5	6291	7	NULL	NULL	NULL	NULL	G1	GP		is					globular domain	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_370_s_14	16385080	1,2  The amino-terminal globular domain (G1) of versican core protein binds to hyaluronan (HA) and affects cell adhesion, proliferation, and migration.	bind
21984	6	6291	7	NULL	NULL	NULL	NULL	HA	Chemical		is					hyaluronan	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_370_s_14	16385080	1,2  The amino-terminal globular domain (G1) of versican core protein binds to hyaluronan (HA) and affects cell adhesion, proliferation, and migration.	bind
16982	1	6292	5	NULL	NULL	0	NULL	biglycan proteoglycans	NULL	arterial	bind	NULL	avidly			apoB-containing lipoproteins	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2162_s_181	15345509	1,24,25   However, of particular relevance to this study are the recent observations that arterial biglycan proteoglycans avidly bind to apoB-containing and apoE-containing lipoproteins.	bind
16983	2	6292	5	NULL	NULL	0	NULL	biglycan proteoglycans	NULL	arterial	bind	NULL	avidly			apoE-containing lipoproteins	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2162_s_181	15345509	1,24,25   However, of particular relevance to this study are the recent observations that arterial biglycan proteoglycans avidly bind to apoB-containing and apoE-containing lipoproteins.	bind
21985	1	6292	7	NULL	NULL	NULL	NULL	biglycan proteoglycans	Chemical	arterial 	bind		avidly			apoB-containing lipoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2162_s_181	15345509	1,24,25   However, of particular relevance to this study are the recent observations that arterial biglycan proteoglycans avidly bind to apoB-containing and apoE-containing lipoproteins.	bind
21986	2	6292	7	NULL	NULL	NULL	NULL	biglycan proteoglycans	Chemical	arterial 	bind		avidly			apoE-containing lipoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2162_s_181	15345509	1,24,25   However, of particular relevance to this study are the recent observations that arterial biglycan proteoglycans avidly bind to apoB-containing and apoE-containing lipoproteins.	bind
16984	1	6293	5	10	NULL	0	NULL	1,25(OH)2D3			alters					EGFR membrane 		trafficking of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38965_s_32	12181310	1,25(OH)2D3 alters EGFR membrane trafficking, down-regulates EGFR-growth signaling, and impairs binding of nuclear EGFR to cognate DNA sequences, which in turn decreases its transcriptional activity on the cyclin D1 promoter.	bind
16985	2	6293	5	NULL	NULL	0	NULL	1,25(OH)2D3	NULL		down-regulate	NULL				EGFR-growth signaling	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_41_38965_s_32	12181310	1,25(OH)2D3 alters EGFR membrane trafficking, down-regulates EGFR-growth signaling, and impairs binding of nuclear EGFR to cognate DNA sequences, which in turn decreases its transcriptional activity on the cyclin D1 promoter.	bind
16986	3	6293	5	NULL	NULL	0	NULL	EGFR	NULL	nuclear	bind	NULL				cognate DNA sequences	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38965_s_32	12181310	1,25(OH)2D3 alters EGFR membrane trafficking, down-regulates EGFR-growth signaling, and impairs binding of nuclear EGFR to cognate DNA sequences, which in turn decreases its transcriptional activity on the cyclin D1 promoter.	bind
16987	4	6293	5	NULL	NULL	0	NULL	1,25(OH)2D3	NULL		impairs	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_41_38965_s_32	12181310	1,25(OH)2D3 alters EGFR membrane trafficking, down-regulates EGFR-growth signaling, and impairs binding of nuclear EGFR to cognate DNA sequences, which in turn decreases its transcriptional activity on the cyclin D1 promoter.	bind
16988	6	6293	5	NULL	NULL	0	NULL	statement 4	NULL		decrease	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38965_s_32	12181310	1,25(OH)2D3 alters EGFR membrane trafficking, down-regulates EGFR-growth signaling, and impairs binding of nuclear EGFR to cognate DNA sequences, which in turn decreases its transcriptional activity on the cyclin D1 promoter.	bind
16989	7	6293	5	NULL	NULL	0	NULL	statement 2	NULL		decrease	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38965_s_32	12181310	1,25(OH)2D3 alters EGFR membrane trafficking, down-regulates EGFR-growth signaling, and impairs binding of nuclear EGFR to cognate DNA sequences, which in turn decreases its transcriptional activity on the cyclin D1 promoter.	bind
16990	8	6293	5	NULL	NULL	0	NULL	statement 1	NULL		decrease	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38965_s_32	12181310	1,25(OH)2D3 alters EGFR membrane trafficking, down-regulates EGFR-growth signaling, and impairs binding of nuclear EGFR to cognate DNA sequences, which in turn decreases its transcriptional activity on the cyclin D1 promoter.	bind
26116	5	6293	5	NULL	NULL	0	NULL	1,25(OH)2D3	NULL		induces	NULL				cyclin D1	NULL	transcriptional activity of		promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_41_38965_s_32	12181310	1,25(OH)2D3 alters EGFR membrane trafficking, down-regulates EGFR-growth signaling, and impairs binding of nuclear EGFR to cognate DNA sequences, which in turn decreases its transcriptional activity on the cyclin D1 promoter.	bind
54201	9	6293	5	10	NULL	0	NULL	statement 4			decreases					cyclin D1		transcriptional activity of		promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_41_38965_s_32	12181310	1,25(OH)2D3 alters EGFR membrane trafficking, down-regulates EGFR-growth signaling, and impairs binding of nuclear EGFR to cognate DNA sequences, which in turn decreases its transcriptional activity on the cyclin D1 promoter.	bind
21987	1	6293	7	NULL	NULL	NULL	NULL	1,25(OH)2D3	Chemical		alters					 EGFR membrane	GP	trafficking of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38965_s_32	12181310	1,25(OH)2D3 alters EGFR membrane trafficking, down-regulates EGFR-growth signaling, and impairs binding of nuclear EGFR to cognate DNA sequences, which in turn decreases its transcriptional activity on the cyclin D1 promoter.	bind
21988	2	6293	7	NULL	NULL	NULL	NULL	1,25(OH)2D3	Chemical		downregulates					EGFR-growth signaling	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38965_s_32	12181310	1,25(OH)2D3 alters EGFR membrane trafficking, down-regulates EGFR-growth signaling, and impairs binding of nuclear EGFR to cognate DNA sequences, which in turn decreases its transcriptional activity on the cyclin D1 promoter.	bind
21989	3	6293	7	NULL	NULL	NULL	NULL	EGFR	GP	nuclear	binds					 cognate DNA sequences	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38965_s_32	12181310	1,25(OH)2D3 alters EGFR membrane trafficking, down-regulates EGFR-growth signaling, and impairs binding of nuclear EGFR to cognate DNA sequences, which in turn decreases its transcriptional activity on the cyclin D1 promoter.	bind
21990	4	6293	7	NULL	NULL	NULL	NULL	1,25(OH)2D3	Chemical		impairs					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38965_s_32	12181310	1,25(OH)2D3 alters EGFR membrane trafficking, down-regulates EGFR-growth signaling, and impairs binding of nuclear EGFR to cognate DNA sequences, which in turn decreases its transcriptional activity on the cyclin D1 promoter.	bind
21991	5	6293	7	NULL	NULL	NULL	NULL	statement 4	Process		decrease					cyclin D1	GP	transcriptional activity of		promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38965_s_32	12181310	1,25(OH)2D3 alters EGFR membrane trafficking, down-regulates EGFR-growth signaling, and impairs binding of nuclear EGFR to cognate DNA sequences, which in turn decreases its transcriptional activity on the cyclin D1 promoter.	bind
26387	6	6293	7	NULL	NULL	NULL	NULL	1,25(OH)2D3	Process		induce					cyclin D1	GP	transcriptional activity of		promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38965_s_32	12181310	1,25(OH)2D3 alters EGFR membrane trafficking, down-regulates EGFR-growth signaling, and impairs binding of nuclear EGFR to cognate DNA sequences, which in turn decreases its transcriptional activity on the cyclin D1 promoter.	bind
26388	7	6293	7	NULL	NULL	NULL	NULL	statement 1	Process		decrease					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38965_s_32	12181310	1,25(OH)2D3 alters EGFR membrane trafficking, down-regulates EGFR-growth signaling, and impairs binding of nuclear EGFR to cognate DNA sequences, which in turn decreases its transcriptional activity on the cyclin D1 promoter.	bind
26389	8	6293	7	NULL	NULL	NULL	NULL	statement 2	Process		decrease					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38965_s_32	12181310	1,25(OH)2D3 alters EGFR membrane trafficking, down-regulates EGFR-growth signaling, and impairs binding of nuclear EGFR to cognate DNA sequences, which in turn decreases its transcriptional activity on the cyclin D1 promoter.	bind
26390	9	6293	7	NULL	NULL	NULL	NULL	statement 4	Process		decrease					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38965_s_32	12181310	1,25(OH)2D3 alters EGFR membrane trafficking, down-regulates EGFR-growth signaling, and impairs binding of nuclear EGFR to cognate DNA sequences, which in turn decreases its transcriptional activity on the cyclin D1 promoter.	bind
16991	1	6294	5	NULL	NULL	0	NULL	1,25-(OH)2-D3	NULL		repress	NULL				IL-2 gene	NULL	expression of			NULL	in T lymphocytes	NULL	NULL	NULL	NULL	gw60_febslett_436_3_329_s_8	9801142	1,25-(OH)2-D3 has also been shown to repress IL-2 gene expression in T lymphocytes by inhibiting complex formation between nuclear factor of activated T cells (NFATp) and AP-1 at the NFAT binding site of the IL-2 promoter.	bind
16993	3	6294	5	NULL	NULL	0	NULL	NFATp	NULL		is	NULL				nuclear factor of activated T cells	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_436_3_329_s_8	9801142	1,25-(OH)2-D3 has also been shown to repress IL-2 gene expression in T lymphocytes by inhibiting complex formation between nuclear factor of activated T cells (NFATp) and AP-1 at the NFAT binding site of the IL-2 promoter.	bind
16995	5	6294	5	NULL	NULL	0	NULL	NFATp	NULL		forms complex with	NULL				AP-1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_436_3_329_s_8	9801142	1,25-(OH)2-D3 has also been shown to repress IL-2 gene expression in T lymphocytes by inhibiting complex formation between nuclear factor of activated T cells (NFATp) and AP-1 at the NFAT binding site of the IL-2 promoter.	bind
16996	7	6294	5	NULL	NULL	0	NULL	statement 1	NULL		occurs by	NULL				statement 5	NULL	inhibiting			NULL		NULL	NULL	NULL	NULL	gw60_febslett_436_3_329_s_8	9801142	1,25-(OH)2-D3 has also been shown to repress IL-2 gene expression in T lymphocytes by inhibiting complex formation between nuclear factor of activated T cells (NFATp) and AP-1 at the NFAT binding site of the IL-2 promoter.	bind
26121	6	6294	5	NULL	NULL	0	NULL	statement 5	NULL		occurs at	NULL				NFAT binding site of the IL-2 promoter	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_436_3_329_s_8	9801142	1,25-(OH)2-D3 has also been shown to repress IL-2 gene expression in T lymphocytes by inhibiting complex formation between nuclear factor of activated T cells (NFATp) and AP-1 at the NFAT binding site of the IL-2 promoter.	bind
21992	1	6294	7	NULL	NULL	NULL	NULL	1,25-(OH)2-D3	GP		repress					 IL-2 gene	GP	expression of			NULL	T lymphocytes	NULL	NULL	NULL	NULL	gw60_febslett_436_3_329_s_8	9801142	1,25-(OH)2-D3 has also been shown to repress IL-2 gene expression in T lymphocytes by inhibiting complex formation between nuclear factor of activated T cells (NFATp) and AP-1 at the NFAT binding site of the IL-2 promoter.	bind
21993	2	6294	7	NULL	NULL	NULL	NULL	NFATp	GP		complex with					AP-1 	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_436_3_329_s_8	9801142	1,25-(OH)2-D3 has also been shown to repress IL-2 gene expression in T lymphocytes by inhibiting complex formation between nuclear factor of activated T cells (NFATp) and AP-1 at the NFAT binding site of the IL-2 promoter.	bind
21994	3	6294	7	NULL	NULL	NULL	NULL	1,25-(OH)2-D3	Chemical		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_436_3_329_s_8	9801142	1,25-(OH)2-D3 has also been shown to repress IL-2 gene expression in T lymphocytes by inhibiting complex formation between nuclear factor of activated T cells (NFATp) and AP-1 at the NFAT binding site of the IL-2 promoter.	bind
21995	4	6294	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs upon					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_436_3_329_s_8	9801142	1,25-(OH)2-D3 has also been shown to repress IL-2 gene expression in T lymphocytes by inhibiting complex formation between nuclear factor of activated T cells (NFATp) and AP-1 at the NFAT binding site of the IL-2 promoter.	bind
21996	5	6294	7	NULL	NULL	NULL	NULL	NFATp	GP		is					nuclear factor of activated T cells	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_436_3_329_s_8	9801142	1,25-(OH)2-D3 has also been shown to repress IL-2 gene expression in T lymphocytes by inhibiting complex formation between nuclear factor of activated T cells (NFATp) and AP-1 at the NFAT binding site of the IL-2 promoter.	bind
26391	6	6294	7	NULL	NULL	NULL	NULL	statement 2	Process		occurs at					IL-2	GP			NFAT binding site promoter	NULL		NULL	NULL	NULL	NULL	gw60_febslett_436_3_329_s_8	9801142	1,25-(OH)2-D3 has also been shown to repress IL-2 gene expression in T lymphocytes by inhibiting complex formation between nuclear factor of activated T cells (NFATp) and AP-1 at the NFAT binding site of the IL-2 promoter.	bind
16997	1	6295	5	10	NULL	0	NULL	1,25-(OH)2D3			activates					VDR					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46862_s_16	12954644	1,25-(OH)2D3 activates the vitamin D receptor (VDR), a ligand-dependent transcription factor that binds  cis-acting DNA sequences known as vitamin D response elements ( ).	bind
16998	2	6295	5	NULL	NULL	0	NULL	VDR	NULL		is	NULL				vitamin D receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46862_s_16	12954644	1,25-(OH)2D3 activates the vitamin D receptor (VDR), a ligand-dependent transcription factor that binds  cis-acting DNA sequences known as vitamin D response elements ( ).	bind
16999	3	6295	5	10	NULL	0	NULL	VDR			bind									vitamin D response elements	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46862_s_16	12954644	1,25-(OH)2D3 activates the vitamin D receptor (VDR), a ligand-dependent transcription factor that binds  cis-acting DNA sequences known as vitamin D response elements ( ).	bind
45580	4	6295	5	10	NULL	0	NULL	VDR			is a type of					ligand-dependent transcription factor					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46862_s_16	12954644	1,25-(OH)2D3 activates the vitamin D receptor (VDR), a ligand-dependent transcription factor that binds  cis-acting DNA sequences known as vitamin D response elements ( ).	bind
54202	5	6295	5	10	NULL	0	NULL	vitamin D response elements			is a type of					cis-acting DNA sequences					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46862_s_16	12954644	1,25-(OH)2D3 activates the vitamin D receptor (VDR), a ligand-dependent transcription factor that binds  cis-acting DNA sequences known as vitamin D response elements ( ).	bind
21997	1	6295	7	NULL	NULL	NULL	NULL	1,25-(OH)2D3	Chemical		activates					VDR	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46862_s_16	12954644	1,25-(OH)2D3 activates the vitamin D receptor (VDR), a ligand-dependent transcription factor that binds  cis-acting DNA sequences known as vitamin D response elements ( ).	bind
21998	2	6295	7	NULL	NULL	NULL	NULL	VDR	GP		binds									vitamin D response elements	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46862_s_16	12954644	1,25-(OH)2D3 activates the vitamin D receptor (VDR), a ligand-dependent transcription factor that binds  cis-acting DNA sequences known as vitamin D response elements ( ).	bind
21999	3	6295	7	NULL	NULL	NULL	NULL	VDR	GP		is a type of					ligand-dependent transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46862_s_16	12954644	1,25-(OH)2D3 activates the vitamin D receptor (VDR), a ligand-dependent transcription factor that binds  cis-acting DNA sequences known as vitamin D response elements ( ).	bind
22000	4	6295	7	NULL	NULL	NULL	NULL	VDR	GP		is					vitamin D receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46862_s_16	12954644	1,25-(OH)2D3 activates the vitamin D receptor (VDR), a ligand-dependent transcription factor that binds  cis-acting DNA sequences known as vitamin D response elements ( ).	bind
54203	5	6295	7	NULL	NULL	NULL	NULL	vitamin D response elements	GP		is a type of					cis-acting DNA sequences	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46862_s_16	12954644	1,25-(OH)2D3 activates the vitamin D receptor (VDR), a ligand-dependent transcription factor that binds  cis-acting DNA sequences known as vitamin D response elements ( ).	bind
17000	1	6296	5	NULL	NULL	0	NULL	OSF2	NULL		bind	NULL				OSE2	NULL				NULL	primary osteoblasts	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_1_110_s_155	8995235	1,25-(OH)2D3 Treatment of Primary Osteoblasts Abolishes Binding of OSF2 to OSE2	bind
17001	2	6296	5	10	NULL	0	NULL	1,25-(OH)2D3	NULL		abolishes	NULL				statement 1	NULL				NULL	primary osteoblasts	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_1_110_s_155	8995235	1,25-(OH)2D3 Treatment of Primary Osteoblasts Abolishes Binding of OSF2 to OSE2	bind
22002	1	6296	7	NULL	NULL	NULL	NULL	OSF2	GP		bind					OSE2	GP				NULL	primary osteoblast	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_1_110_s_155	8995235	1,25-(OH)2D3 Treatment of Primary Osteoblasts Abolishes Binding of OSF2 to OSE2	bind
22003	2	6296	7	NULL	NULL	NULL	NULL	1,25-(OH)2D3	Chemical		abolishes					statement 1	Process				NULL	Primary Osteoblasts	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_1_110_s_155	8995235	1,25-(OH)2D3 Treatment of Primary Osteoblasts Abolishes Binding of OSF2 to OSE2	bind
19196	1	6297	5	NULL	NULL	0	NULL	1,25-D3	NULL		induce	NULL				CYP3A4	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_60_6_1399_s_7	11723248	1,25-D3 uses the vitamin D receptor to induce CYP3A4 because a) the vitamin D receptor (VDR)-retinoid X receptor (RXR) heterodimer binds specifically to the  CYP3A4 ER6; b) selective mutation of the  CYP3A4 ER6 disrupted the binding of VDR-RXR; and c) reporter constructs containing only three copies of the CYP3A4 ER6 linked to a TK-CAT reporter were activated by 1,25-D3 only in cells cotransfected with a human VDR expression plasmid.	bind
19197	2	6297	5	NULL	NULL	0	NULL	1,25-D3	NULL		uses	NULL				vitamin D receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_60_6_1399_s_7	11723248	1,25-D3 uses the vitamin D receptor to induce CYP3A4 because a) the vitamin D receptor (VDR)-retinoid X receptor (RXR) heterodimer binds specifically to the  CYP3A4 ER6; b) selective mutation of the  CYP3A4 ER6 disrupted the binding of VDR-RXR; and c) reporter constructs containing only three copies of the CYP3A4 ER6 linked to a TK-CAT reporter were activated by 1,25-D3 only in cells cotransfected with a human VDR expression plasmid.	bind
19198	3	6297	5	NULL	NULL	0	NULL	statement 2	NULL		is required for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_60_6_1399_s_7	11723248	1,25-D3 uses the vitamin D receptor to induce CYP3A4 because a) the vitamin D receptor (VDR)-retinoid X receptor (RXR) heterodimer binds specifically to the  CYP3A4 ER6; b) selective mutation of the  CYP3A4 ER6 disrupted the binding of VDR-RXR; and c) reporter constructs containing only three copies of the CYP3A4 ER6 linked to a TK-CAT reporter were activated by 1,25-D3 only in cells cotransfected with a human VDR expression plasmid.	bind
19200	4	6297	5	NULL	NULL	0	NULL	VDR-RXR heterodimer	NULL		is	NULL				vitamin D receptor-retinoid X receptor heterodimer	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_60_6_1399_s_7	11723248	1,25-D3 uses the vitamin D receptor to induce CYP3A4 because a) the vitamin D receptor (VDR)-retinoid X receptor (RXR) heterodimer binds specifically to the  CYP3A4 ER6; b) selective mutation of the  CYP3A4 ER6 disrupted the binding of VDR-RXR; and c) reporter constructs containing only three copies of the CYP3A4 ER6 linked to a TK-CAT reporter were activated by 1,25-D3 only in cells cotransfected with a human VDR expression plasmid.	bind
19205	5	6297	5	NULL	NULL	0	NULL	VDR-RXR heterodimer	NULL		bind	NULL	specifically			 CYP3A4	NULL			ER6	NULL		0	NULL	NULL	NULL	gw60_molpharmacol_60_6_1399_s_7	11723248	1,25-D3 uses the vitamin D receptor to induce CYP3A4 because a) the vitamin D receptor (VDR)-retinoid X receptor (RXR) heterodimer binds specifically to the  CYP3A4 ER6; b) selective mutation of the  CYP3A4 ER6 disrupted the binding of VDR-RXR; and c) reporter constructs containing only three copies of the CYP3A4 ER6 linked to a TK-CAT reporter were activated by 1,25-D3 only in cells cotransfected with a human VDR expression plasmid.	bind
19207	6	6297	5	NULL	NULL	0	NULL	CYP3A4	NULL	mutant	disrupt	NULL			ER6	VDR-RXR	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_60_6_1399_s_7	11723248	1,25-D3 uses the vitamin D receptor to induce CYP3A4 because a) the vitamin D receptor (VDR)-retinoid X receptor (RXR) heterodimer binds specifically to the  CYP3A4 ER6; b) selective mutation of the  CYP3A4 ER6 disrupted the binding of VDR-RXR; and c) reporter constructs containing only three copies of the CYP3A4 ER6 linked to a TK-CAT reporter were activated by 1,25-D3 only in cells cotransfected with a human VDR expression plasmid.	bind
19210	7	6297	5	NULL	NULL	0	NULL	1,25-D3	NULL		activate	NULL				CYP3A4	NULL			ER6	NULL	cells cotransfected with human VDR expression plasmid	NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1399_s_7	11723248	1,25-D3 uses the vitamin D receptor to induce CYP3A4 because a) the vitamin D receptor (VDR)-retinoid X receptor (RXR) heterodimer binds specifically to the  CYP3A4 ER6; b) selective mutation of the  CYP3A4 ER6 disrupted the binding of VDR-RXR; and c) reporter constructs containing only three copies of the CYP3A4 ER6 linked to a TK-CAT reporter were activated by 1,25-D3 only in cells cotransfected with a human VDR expression plasmid.	bind
22004	1	6297	7	NULL	NULL	NULL	NULL	1,25-D3 	Chemical		use					vitamin D receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1399_s_7	11723248	1,25-D3 uses the vitamin D receptor to induce CYP3A4 because a) the vitamin D receptor (VDR)-retinoid X receptor (RXR) heterodimer binds specifically to the  CYP3A4 ER6; b) selective mutation of the  CYP3A4 ER6 disrupted the binding of VDR-RXR; and c) reporter constructs containing only three copies of the CYP3A4 ER6 linked to a TK-CAT reporter were activated by 1,25-D3 only in cells cotransfected with a human VDR expression plasmid.	bind
22005	2	6297	7	NULL	NULL	NULL	NULL	statement 1	Process		induce					CYP3A4 	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1399_s_7	11723248	1,25-D3 uses the vitamin D receptor to induce CYP3A4 because a) the vitamin D receptor (VDR)-retinoid X receptor (RXR) heterodimer binds specifically to the  CYP3A4 ER6; b) selective mutation of the  CYP3A4 ER6 disrupted the binding of VDR-RXR; and c) reporter constructs containing only three copies of the CYP3A4 ER6 linked to a TK-CAT reporter were activated by 1,25-D3 only in cells cotransfected with a human VDR expression plasmid.	bind
22006	3	6297	7	NULL	NULL	NULL	NULL	VDR/RXR heterodimer	GP		binds		specifically			CYP3A4	GP			 ER6	NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1399_s_7	11723248	1,25-D3 uses the vitamin D receptor to induce CYP3A4 because a) the vitamin D receptor (VDR)-retinoid X receptor (RXR) heterodimer binds specifically to the  CYP3A4 ER6; b) selective mutation of the  CYP3A4 ER6 disrupted the binding of VDR-RXR; and c) reporter constructs containing only three copies of the CYP3A4 ER6 linked to a TK-CAT reporter were activated by 1,25-D3 only in cells cotransfected with a human VDR expression plasmid.	bind
22007	4	6297	7	NULL	NULL	NULL	NULL	VDR	GP		binds					RXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1399_s_7	11723248	1,25-D3 uses the vitamin D receptor to induce CYP3A4 because a) the vitamin D receptor (VDR)-retinoid X receptor (RXR) heterodimer binds specifically to the  CYP3A4 ER6; b) selective mutation of the  CYP3A4 ER6 disrupted the binding of VDR-RXR; and c) reporter constructs containing only three copies of the CYP3A4 ER6 linked to a TK-CAT reporter were activated by 1,25-D3 only in cells cotransfected with a human VDR expression plasmid.	bind
22008	5	6297	7	NULL	NULL	NULL	NULL	CYP3A4 	GP	mutation of	disrupts				ER6	statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1399_s_7	11723248	1,25-D3 uses the vitamin D receptor to induce CYP3A4 because a) the vitamin D receptor (VDR)-retinoid X receptor (RXR) heterodimer binds specifically to the  CYP3A4 ER6; b) selective mutation of the  CYP3A4 ER6 disrupted the binding of VDR-RXR; and c) reporter constructs containing only three copies of the CYP3A4 ER6 linked to a TK-CAT reporter were activated by 1,25-D3 only in cells cotransfected with a human VDR expression plasmid.	bind
22009	6	6297	7	NULL	NULL	NULL	NULL	VDR	GP		is					vitamin D receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1399_s_7	11723248	1,25-D3 uses the vitamin D receptor to induce CYP3A4 because a) the vitamin D receptor (VDR)-retinoid X receptor (RXR) heterodimer binds specifically to the  CYP3A4 ER6; b) selective mutation of the  CYP3A4 ER6 disrupted the binding of VDR-RXR; and c) reporter constructs containing only three copies of the CYP3A4 ER6 linked to a TK-CAT reporter were activated by 1,25-D3 only in cells cotransfected with a human VDR expression plasmid.	bind
22010	7	6297	7	NULL	NULL	NULL	NULL	RXR	GP		is					retinoid X receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1399_s_7	11723248	1,25-D3 uses the vitamin D receptor to induce CYP3A4 because a) the vitamin D receptor (VDR)-retinoid X receptor (RXR) heterodimer binds specifically to the  CYP3A4 ER6; b) selective mutation of the  CYP3A4 ER6 disrupted the binding of VDR-RXR; and c) reporter constructs containing only three copies of the CYP3A4 ER6 linked to a TK-CAT reporter were activated by 1,25-D3 only in cells cotransfected with a human VDR expression plasmid.	bind
17002	1	6298	5	NULL	NULL	0	NULL	1,25-Dihydroxyvitamin D3	NULL		activates	NULL				PLD	NULL				NULL	Caco-2 cells	0	NULL	NULL	NULL	gw60_jbiolchem_271_36_21767_s_512	8702973	1,25-Dihydroxyvitamin D3 but not TPA activates PLD in Caco-2 cells via pp60c-src and RhoA.	bind
17003	2	6298	5	NULL	NULL	0	NULL	statement 1	NULL		via	NULL				pp60c-src	NULL				NULL	Caco-2 cells	0	NULL	NULL	NULL	gw60_jbiolchem_271_36_21767_s_512	8702973	1,25-Dihydroxyvitamin D3 but not TPA activates PLD in Caco-2 cells via pp60c-src and RhoA.	bind
17004	3	6298	5	NULL	NULL	0	NULL	statement 1	NULL		via	NULL				RhoA	NULL				NULL	Caco-2 cells	0	NULL	NULL	NULL	gw60_jbiolchem_271_36_21767_s_512	8702973	1,25-Dihydroxyvitamin D3 but not TPA activates PLD in Caco-2 cells via pp60c-src and RhoA.	bind
17005	4	6298	5	NULL	NULL	0	NULL	TPA	NULL		does not activate	NULL				PLD	NULL				NULL	Caco-2 cells	0	NULL	NULL	NULL	gw60_jbiolchem_271_36_21767_s_512	8702973	1,25-Dihydroxyvitamin D3 but not TPA activates PLD in Caco-2 cells via pp60c-src and RhoA.	bind
22011	1	6298	7	NULL	NULL	NULL	NULL	1,25-Dihydroxyvitamin D3	Chemical		activates					PLD	GP				NULL	Caco-2 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_36_21767_s_512	8702973	1,25-Dihydroxyvitamin D3 but not TPA activates PLD in Caco-2 cells via pp60c-src and RhoA.	bind
22012	2	6298	7	NULL	NULL	NULL	NULL	TPA	Chemical		does not activate					PLD	GP				NULL	Caco-2 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_36_21767_s_512	8702973	1,25-Dihydroxyvitamin D3 but not TPA activates PLD in Caco-2 cells via pp60c-src and RhoA.	bind
22013	3	6298	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs via					pp60c-src	Process				NULL	Caco-2 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_36_21767_s_512	8702973	1,25-Dihydroxyvitamin D3 but not TPA activates PLD in Caco-2 cells via pp60c-src and RhoA.	bind
22014	4	6298	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs via					RhoA	GP				NULL	Caco-2 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_36_21767_s_512	8702973	1,25-Dihydroxyvitamin D3 but not TPA activates PLD in Caco-2 cells via pp60c-src and RhoA.	bind
17006	1	6299	5	NULL	NULL	0	NULL	1,25-Dihydroxyvitamin D3	NULL		stimulate	NULL				Caco-2	NULL	differentiation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5073_s_606	9710591	1,25-Dihydroxyvitamin D3 Stimulates Activator Protein-1-dependent Caco-2 Cell Differentiation.	bind
17007	2	6299	5	NULL	NULL	0	NULL	Caco-2	NULL	differentiation of	depends on	NULL				activator protein-1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5073_s_606	9710591	1,25-Dihydroxyvitamin D3 Stimulates Activator Protein-1-dependent Caco-2 Cell Differentiation.	bind
22015	1	6299	7	NULL	NULL	NULL	NULL	Caco-2 Cells 	Cell	differentiation of	depends on					Activator Protein-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5073_s_606	9710591	1,25-Dihydroxyvitamin D3 Stimulates Activator Protein-1-dependent Caco-2 Cell Differentiation.	bind
22016	1	6299	7	NULL	NULL	NULL	NULL	1,25-Dihydroxyvitamin D3	Chemical		stimulates					Caco-2 cells	Cell	differentiation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5073_s_606	9710591	1,25-Dihydroxyvitamin D3 Stimulates Activator Protein-1-dependent Caco-2 Cell Differentiation.	bind
17008	1	6300	5	NULL	NULL	0	NULL	1,25-VD	NULL		inhibit	NULL				NF-kappaB	NULL	activity of			NULL	human lymphocytes	0	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
17009	2	6300	5	NULL	NULL	0	NULL	1,25-VD	NULL		inhibit	NULL				NF-kappaB	NULL	activity of			NULL	human fibroblasts	0	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
17010	4	6300	5	NULL	NULL	0	NULL	statement 1	NULL		occurs by	NULL				statement 3	NULL	decreasing			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
17011	6	6300	5	NULL	NULL	0	NULL	statement 1	NULL		occurs by	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
17012	7	6300	5	NULL	NULL	0	NULL	statement 4	NULL		is an alternative to	NULL				statement 6	NULL				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
17013	8	6300	5	NULL	NULL	0	NULL	statement 2	NULL		occurs by	NULL				statement 3	NULL	decreasing			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
17014	9	6300	5	NULL	NULL	0	NULL	statement 2	NULL		occurs by	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
17015	10	6300	5	NULL	NULL	0	NULL	statement 8	NULL		is an alternative to	NULL				statement 9	NULL				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
46194	3	6300	5	NULL	NULL	0	NULL	NF-kappaB	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
46196	5	6300	5	NULL	NULL	0	NULL	1,25-VD	NULL		decreases	NULL				NF-kappaB precursor protein	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
22017	1	6300	7	NULL	NULL	NULL	NULL	1,25-VD	Chemical		inhibits					NF-kappaB 	GP	activity of human			NULL	human lymphocytes	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
22018	2	6300	7	NULL	NULL	NULL	NULL	1,25-VD	Chemical		inhibits					NF-kappaB	GP	activity of			NULL	fibroblasts	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
22019	3	6300	7	NULL	NULL	NULL	NULL	NF-kappaB 	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
22020	4	6300	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs upon					statement 3	Process	decreasing			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
22021	5	6300	7	NULL	NULL	NULL	NULL	statement 2	Process		occurs upon					statement 3	Process	decreasing			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
22022	7	6300	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs upon					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
22023	6	6300	7	NULL	NULL	NULL	NULL	1,25-VD	Chemical		decrease					NF-kappaB	GP	expression of precursor protein			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
22024	8	6300	7	NULL	NULL	NULL	NULL	statement 2	Process		occurs upon					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
22025	9	6300	7	NULL	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
22026	10	6300	7	NULL	NULL	NULL	NULL	statement 5	Process		is an alternative to					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_1_32_s_232	15987715	1,25-VD has been reported to inhibit NF-kappaB activity in human lymphocytes and fibroblasts by either decreasing NF-kappaB DNA binding capacity or decreasing the expression of its precursor protein ( , ).	bind
19310	1	6301	5	10	NULL	0	NULL	1,25-VD			reduce					p50		levels of			NULL	human lymphocytes	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	bind
19311	2	6301	5	10	NULL	0	NULL	1,25-VD			reduce					p105		levels of			NULL	human lymphocytes	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	bind
19312	3	6301	5	NULL	NULL	0	NULL	p105	NULL		is a type of	NULL				precursor of p50	NULL				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	bind
19313	4	6301	5	NULL	NULL	0	NULL	NF-kappaB	NULL		bind	NULL				IL-6	NULL			promoter	NULL	human lymphocytes	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	bind
19314	5	6301	5	NULL	NULL	0	NULL	PMA	NULL		induce	NULL				statement 4	NULL				NULL	human lymphocytes	0	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	bind
19315	6	6301	5	NULL	NULL	0	NULL	1,25-VD	NULL		decrease	NULL				statement 5	NULL				NULL	human lymphocytes	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	bind
22027	1	6301	7	NULL	NULL	NULL	NULL	1,25-VD	Chemical		reduce					p50	GP	levels of			NULL	human lymphocytes	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	bind
22028	2	6301	7	NULL	NULL	NULL	NULL	1,25-VD	Chemical		reduce					p105	GP	levels of			NULL	human lymphocytes	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	bind
22029	3	6301	7	NULL	NULL	NULL	NULL	NF-kappaB	GP		bind					 IL-6	GP			promoter	NULL	human lymphocytes	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	bind
22030	4	6301	7	NULL	NULL	NULL	NULL	PMA	Chemical		induce					statement 3	Process				NULL	human lymphocytes	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	bind
22031	5	6301	7	NULL	NULL	NULL	NULL	1,25-VD	Chemical		decrease					statement 4	Process				NULL	human lymphocytes	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	bind
29273	6	6301	7	NULL	NULL	NULL	NULL	p105	GP		is a type of					p50 precursor	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	bind
19316	1	6303	5	NULL	NULL	0	NULL	1,3-Propanediol dehydrogenase	NULL		require	NULL				NAD(H)	NULL	as a cofactor			NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_154_2_337_s_139	9311132	1,3-Propanediol dehydrogenase requires NAD(H) as a cofactor, but the highly conserved NAD(H) binding fingerprint pattern G-X-G-X-X-G  [ 27] was not present in the amino acid sequence.	bind
19317	2	6303	5	NULL	NULL	0	NULL		NULL	highly conserved	is not present in	NULL		NAD(H) binding fingerprint pattern G-X-G-X-X-G		1,3-Propanediol dehydrogenase	NULL	amino acid sequence of			NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_154_2_337_s_139	9311132	1,3-Propanediol dehydrogenase requires NAD(H) as a cofactor, but the highly conserved NAD(H) binding fingerprint pattern G-X-G-X-X-G  [ 27] was not present in the amino acid sequence.	bind
46201	3	6303	5	NULL	NULL	0	NULL	NAD(H)	NULL		bind	NULL					NULL	highly conserved		fingerprint pattern G-X-G-X-X-G	NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_154_2_337_s_139	9311132	1,3-Propanediol dehydrogenase requires NAD(H) as a cofactor, but the highly conserved NAD(H) binding fingerprint pattern G-X-G-X-X-G  [ 27] was not present in the amino acid sequence.	bind
22032	1	6303	7	NULL	NULL	NULL	NULL	1,3-Propanediol dehydrogenase	GP		requires					NAD(H)	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_154_2_337_s_139	9311132	1,3-Propanediol dehydrogenase requires NAD(H) as a cofactor, but the highly conserved NAD(H) binding fingerprint pattern G-X-G-X-X-G  [ 27] was not present in the amino acid sequence.	bind
22033	2	6303	7	NULL	NULL	NULL	NULL	NAD(H) 	Chemical		bind							highly conserved	fingerprint pattern G-X-G-X-X-G		NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_154_2_337_s_139	9311132	1,3-Propanediol dehydrogenase requires NAD(H) as a cofactor, but the highly conserved NAD(H) binding fingerprint pattern G-X-G-X-X-G  [ 27] was not present in the amino acid sequence.	bind
29276	3	6303	7	NULL	NULL	NULL	NULL	NADH	Chemical		is not present in			fingerprint pattern G-X-G-X-X-G 		1,3-Propanediol dehydrogenase	GP	amino acid sequence of			NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_154_2_337_s_139	9311132	1,3-Propanediol dehydrogenase requires NAD(H) as a cofactor, but the highly conserved NAD(H) binding fingerprint pattern G-X-G-X-X-G  [ 27] was not present in the amino acid sequence.	bind
67932	4	6303	7	NULL	NULL	0	NULL	NADH	Chemical		is a type of					cofactor	Chemical				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_154_2_337_s_139	9311132	1,3-Propanediol dehydrogenase requires NAD(H) as a cofactor, but the highly conserved NAD(H) binding fingerprint pattern G-X-G-X-X-G  [ 27] was not present in the amino acid sequence.	bind
19318	1	6304	5	NULL	NULL	0	NULL	1,4 Angiotensin II	NULL		bind	NULL				G protein - coupled receptors	NULL				NULL	on the surface of cardiomyocytes	0	NULL	NULL	NULL	gw70_circulation_110_6_718_s_24	15289381	1,4  Angiotensin II and endothelin-1 bind to G protein - coupled receptors on the surface of cardiomyocytes.	bind
19319	2	6304	5	NULL	NULL	0	NULL	endothelin-1	NULL		bind	NULL				G protein - coupled receptors	NULL				NULL	on the surface of cardiomyocytes	0	NULL	NULL	NULL	gw70_circulation_110_6_718_s_24	15289381	1,4  Angiotensin II and endothelin-1 bind to G protein - coupled receptors on the surface of cardiomyocytes.	bind
22034	1	6304	7	NULL	NULL	NULL	NULL	1,4 Angiotensin II	GP		bind					G protein - coupled receptors 	GP				NULL	on the surface of cardiomyocytes	NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_24	15289381	1,4  Angiotensin II and endothelin-1 bind to G protein - coupled receptors on the surface of cardiomyocytes.	bind
22035	2	6304	7	NULL	NULL	NULL	NULL	endothelin-1	GP		bind					G protein - coupled receptors 	GP				NULL	on the surface of cardiomyocytes	NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_24	15289381	1,4  Angiotensin II and endothelin-1 bind to G protein - coupled receptors on the surface of cardiomyocytes.	bind
19320	1	6306	5	NULL	NULL	0	NULL	BRG-1	NULL		bind	NULL	preferentially			RXR	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1180_s_167	15774904	1,9,22   On the contrary, BRG-1 preferentially binds and activates zinc finger proteins (including RXR and RAR), whereas brm activates factors with 2 ankyrin repeat proteins.	bind
19321	2	6306	5	NULL	NULL	0	NULL	BRG-1	NULL		activates	NULL	preferentially			RXR	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1180_s_167	15774904	1,9,22   On the contrary, BRG-1 preferentially binds and activates zinc finger proteins (including RXR and RAR), whereas brm activates factors with 2 ankyrin repeat proteins.	bind
19322	3	6306	5	NULL	NULL	0	NULL	BRG-1	NULL		bind	NULL	preferentially			RAR	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1180_s_167	15774904	1,9,22   On the contrary, BRG-1 preferentially binds and activates zinc finger proteins (including RXR and RAR), whereas brm activates factors with 2 ankyrin repeat proteins.	bind
19323	4	6306	5	NULL	NULL	0	NULL	BRG-1	NULL		activates	NULL	preferentially			RAR	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1180_s_167	15774904	1,9,22   On the contrary, BRG-1 preferentially binds and activates zinc finger proteins (including RXR and RAR), whereas brm activates factors with 2 ankyrin repeat proteins.	bind
19324	5	6306	5	NULL	NULL	0	NULL	statement 1	NULL		occurs along with	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1180_s_167	15774904	1,9,22   On the contrary, BRG-1 preferentially binds and activates zinc finger proteins (including RXR and RAR), whereas brm activates factors with 2 ankyrin repeat proteins.	bind
19325	6	6306	5	NULL	NULL	0	NULL	brm	NULL		activates	NULL				factors with 2 ankyrin repeat proteins	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1180_s_167	15774904	1,9,22   On the contrary, BRG-1 preferentially binds and activates zinc finger proteins (including RXR and RAR), whereas brm activates factors with 2 ankyrin repeat proteins.	bind
45581	7	6306	5	10	NULL	0	NULL	RXR	NULL		is a type of	NULL				zinc finger protein	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1180_s_167	15774904	1,9,22   On the contrary, BRG-1 preferentially binds and activates zinc finger proteins (including RXR and RAR), whereas brm activates factors with 2 ankyrin repeat proteins.	bind
45582	8	6306	5	10	NULL	0	NULL	RAR	NULL		is a type of	NULL				zinc finger protein	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1180_s_167	15774904	1,9,22   On the contrary, BRG-1 preferentially binds and activates zinc finger proteins (including RXR and RAR), whereas brm activates factors with 2 ankyrin repeat proteins.	bind
46202	9	6306	5	NULL	NULL	0	NULL	statement 3	NULL		occurs along with	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1180_s_167	15774904	1,9,22   On the contrary, BRG-1 preferentially binds and activates zinc finger proteins (including RXR and RAR), whereas brm activates factors with 2 ankyrin repeat proteins.	bind
22036	1	6306	7	NULL	NULL	NULL	NULL	BRG-1	GP		binds		preferentially			RXR	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1180_s_167	15774904	1,9,22   On the contrary, BRG-1 preferentially binds and activates zinc finger proteins (including RXR and RAR), whereas brm activates factors with 2 ankyrin repeat proteins.	bind
22037	2	6306	7	NULL	NULL	NULL	NULL	BRG-1	GP		activates		preferentially			RXR	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1180_s_167	15774904	1,9,22   On the contrary, BRG-1 preferentially binds and activates zinc finger proteins (including RXR and RAR), whereas brm activates factors with 2 ankyrin repeat proteins.	bind
22038	3	6306	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs along with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1180_s_167	15774904	1,9,22   On the contrary, BRG-1 preferentially binds and activates zinc finger proteins (including RXR and RAR), whereas brm activates factors with 2 ankyrin repeat proteins.	bind
22039	4	6306	7	NULL	NULL	NULL	NULL	BRG-1	GP		binds		preferentially			RAR	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1180_s_167	15774904	1,9,22   On the contrary, BRG-1 preferentially binds and activates zinc finger proteins (including RXR and RAR), whereas brm activates factors with 2 ankyrin repeat proteins.	bind
22040	5	6306	7	NULL	NULL	NULL	NULL	BRG-1	GP		activates		preferentially			RAR	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1180_s_167	15774904	1,9,22   On the contrary, BRG-1 preferentially binds and activates zinc finger proteins (including RXR and RAR), whereas brm activates factors with 2 ankyrin repeat proteins.	bind
22041	6	6306	7	NULL	NULL	NULL	NULL	statement 4	Process		occurs along with					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1180_s_167	15774904	1,9,22   On the contrary, BRG-1 preferentially binds and activates zinc finger proteins (including RXR and RAR), whereas brm activates factors with 2 ankyrin repeat proteins.	bind
22042	7	6306	7	NULL	NULL	NULL	NULL	brm	GP		activates					factors with 2 ankyrin repeat proteins	GP		\\		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1180_s_167	15774904	1,9,22   On the contrary, BRG-1 preferentially binds and activates zinc finger proteins (including RXR and RAR), whereas brm activates factors with 2 ankyrin repeat proteins.	bind
45583	8	6306	7	NULL	NULL	NULL	NULL	RXR	GP		is a type of					zinc finger protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1180_s_167	15774904	1,9,22   On the contrary, BRG-1 preferentially binds and activates zinc finger proteins (including RXR and RAR), whereas brm activates factors with 2 ankyrin repeat proteins.	bind
45584	9	6306	7	NULL	NULL	NULL	NULL	RAR	GP		is a type of					zinc finger protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1180_s_167	15774904	1,9,22   On the contrary, BRG-1 preferentially binds and activates zinc finger proteins (including RXR and RAR), whereas brm activates factors with 2 ankyrin repeat proteins.	bind
19326	1	6308	5	NULL	NULL	0	NULL	RPA	NULL		bind	NULL				DNA	NULL	cisplatin-damaged			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_72	12486030	1-4 and references therein), both RPA and XPC-hHR23B showed preferential binding to the cisplatin-damaged DNA over the nondamaged one, whereas the XPA-DNA interaction was observed only in the presence of excess amounts (Fig.  2 A).	bind
19327	2	6308	5	NULL	NULL	0	NULL	RPA	NULL		bind	NULL				DNA	NULL	undamaged			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_72	12486030	1-4 and references therein), both RPA and XPC-hHR23B showed preferential binding to the cisplatin-damaged DNA over the nondamaged one, whereas the XPA-DNA interaction was observed only in the presence of excess amounts (Fig.  2 A).	bind
19328	3	6308	5	NULL	NULL	0	NULL	statement 1	NULL		is prefered over	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_72	12486030	1-4 and references therein), both RPA and XPC-hHR23B showed preferential binding to the cisplatin-damaged DNA over the nondamaged one, whereas the XPA-DNA interaction was observed only in the presence of excess amounts (Fig.  2 A).	bind
19329	4	6308	5	NULL	NULL	0	NULL	XPC-hHR23B	NULL		bind	NULL				DNA	NULL	cisplatin-damaged			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_72	12486030	1-4 and references therein), both RPA and XPC-hHR23B showed preferential binding to the cisplatin-damaged DNA over the nondamaged one, whereas the XPA-DNA interaction was observed only in the presence of excess amounts (Fig.  2 A).	bind
19330	5	6308	5	NULL	NULL	0	NULL	XPC-hHR23B	NULL		bind	NULL				DNA	NULL	undamaged			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_72	12486030	1-4 and references therein), both RPA and XPC-hHR23B showed preferential binding to the cisplatin-damaged DNA over the nondamaged one, whereas the XPA-DNA interaction was observed only in the presence of excess amounts (Fig.  2 A).	bind
19331	6	6308	5	NULL	NULL	0	NULL	statement 4	NULL		is prefered over	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_72	12486030	1-4 and references therein), both RPA and XPC-hHR23B showed preferential binding to the cisplatin-damaged DNA over the nondamaged one, whereas the XPA-DNA interaction was observed only in the presence of excess amounts (Fig.  2 A).	bind
19332	7	6308	5	NULL	NULL	0	NULL	XPA	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_72	12486030	1-4 and references therein), both RPA and XPC-hHR23B showed preferential binding to the cisplatin-damaged DNA over the nondamaged one, whereas the XPA-DNA interaction was observed only in the presence of excess amounts (Fig.  2 A).	bind
22044	1	6308	7	NULL	NULL	NULL	NULL	 RPA	GP		binds		preferentially			DNA	NucleicAcid	cisplatin-damaged 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_72	12486030	1-4 and references therein), both RPA and XPC-hHR23B showed preferential binding to the cisplatin-damaged DNA over the nondamaged one, whereas the XPA-DNA interaction was observed only in the presence of excess amounts (Fig.  2 A).	bind
22045	2	6308	7	NULL	NULL	NULL	NULL	RPA	GP		bind					DNA	NucleicAcid	non damaged 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_72	12486030	1-4 and references therein), both RPA and XPC-hHR23B showed preferential binding to the cisplatin-damaged DNA over the nondamaged one, whereas the XPA-DNA interaction was observed only in the presence of excess amounts (Fig.  2 A).	bind
22046	3	6308	7	NULL	NULL	NULL	NULL	statement 1	Process		is preferred over					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_72	12486030	1-4 and references therein), both RPA and XPC-hHR23B showed preferential binding to the cisplatin-damaged DNA over the nondamaged one, whereas the XPA-DNA interaction was observed only in the presence of excess amounts (Fig.  2 A).	bind
22047	4	6308	7	NULL	NULL	NULL	NULL	XPC-hHR23B	GP		binds		preferentially			DNA	NucleicAcid	cisplatin-damaged 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_72	12486030	1-4 and references therein), both RPA and XPC-hHR23B showed preferential binding to the cisplatin-damaged DNA over the nondamaged one, whereas the XPA-DNA interaction was observed only in the presence of excess amounts (Fig.  2 A).	bind
22048	6	6308	7	NULL	NULL	NULL	NULL	statement 4	Process		is preferred over					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_72	12486030	1-4 and references therein), both RPA and XPC-hHR23B showed preferential binding to the cisplatin-damaged DNA over the nondamaged one, whereas the XPA-DNA interaction was observed only in the presence of excess amounts (Fig.  2 A).	bind
29284	5	6308	7	NULL	NULL	NULL	NULL	XPC-hHR23B	GP		binds					DNA	NucleicAcid	nondamaged			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_72	12486030	1-4 and references therein), both RPA and XPC-hHR23B showed preferential binding to the cisplatin-damaged DNA over the nondamaged one, whereas the XPA-DNA interaction was observed only in the presence of excess amounts (Fig.  2 A).	bind
29287	7	6308	7	NULL	NULL	NULL	NULL	XPA	GP		interacts with					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_72	12486030	1-4 and references therein), both RPA and XPC-hHR23B showed preferential binding to the cisplatin-damaged DNA over the nondamaged one, whereas the XPA-DNA interaction was observed only in the presence of excess amounts (Fig.  2 A).	bind
19333	1	6310	5	NULL	NULL	0	NULL	1-alpha,25-dihydroxyvitamin D3	NULL		inhibit	NULL				lung cancer cell line	NULL	growth of			NULL		0	NULL	NULL	NULL	gw60_jclininvest_103_12_1729_s_250	10377179	1-alpha,25-dihydroxyvitamin D3 and all-trans retinoic acid inhibit the growth of a lung cancer cell line.	bind
19334	2	6310	5	NULL	NULL	0	NULL	trans retinoic acid	NULL		inhibit	NULL				lung cancer cell line	NULL	growth of			NULL		0	NULL	NULL	NULL	gw60_jclininvest_103_12_1729_s_250	10377179	1-alpha,25-dihydroxyvitamin D3 and all-trans retinoic acid inhibit the growth of a lung cancer cell line.	bind
22049	1	6310	7	NULL	NULL	NULL	NULL	1-alpha,25-dihydroxyvitamin D3	Chemical		inhibit					lung cancer cell line	Cell	growth of 			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_103_12_1729_s_250	10377179	1-alpha,25-dihydroxyvitamin D3 and all-trans retinoic acid inhibit the growth of a lung cancer cell line.	bind
22050	2	6310	7	NULL	NULL	NULL	NULL	all-trans retinoic acid	Chemical		inhibit					lung cancer cell line	Cell	growth of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_103_12_1729_s_250	10377179	1-alpha,25-dihydroxyvitamin D3 and all-trans retinoic acid inhibit the growth of a lung cancer cell line.	bind
19377	1	6311	5	NULL	NULL	0	NULL	m-CPP	NULL		interacts with	NULL				neurotransmitter receptors	NULL				NULL	human brain	0	NULL	NULL	NULL	gw60_neuropharmacology_42_2_162_s_236	11804612	1-m-(chlorophenyl)piperazine (m-CPP) interactions with neurotransmitter receptors in the human brain.	bind
19378	2	6311	5	NULL	NULL	0	NULL	m-CPP	NULL		is	NULL				1-m-(chlorophenyl)piperazine	NULL				NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_42_2_162_s_236	11804612	1-m-(chlorophenyl)piperazine (m-CPP) interactions with neurotransmitter receptors in the human brain.	bind
22051	1	6311	7	NULL	NULL	NULL	NULL	m-CPP	Chemical		interacts with					neurotransmitter receptors	GP				NULL	human brain	NULL	NULL	NULL	NULL	gw60_neuropharmacology_42_2_162_s_236	11804612	1-m-(chlorophenyl)piperazine (m-CPP) interactions with neurotransmitter receptors in the human brain.	bind
22052	2	6311	7	NULL	NULL	NULL	NULL	m-CPP	Chemical		is					1-m-(chlorophenyl)piperazine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_42_2_162_s_236	11804612	1-m-(chlorophenyl)piperazine (m-CPP) interactions with neurotransmitter receptors in the human brain.	bind
19379	1	6312	5	10	NULL	0	NULL	PX-12			bind								Cys73 residue		NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_25_0_261_s_383	16011468	1-Methyl-propyl-2-imidazolozyl disulfide (PX-12), a TRX-1  inhibitor binding to the Cys73 residue, not only significantly potentiated the inhibitory  effect of cisplatin on pancreatic cancer ( 8) but also exhibited promising antitumor activities among a variety of tumor cell  lines both in vitro and in vivo ( 158).	bind
19380	2	6312	5	NULL	NULL	0	NULL	PX-12	NULL		is	NULL				1-Methyl-propyl-2-imidazolozyl disulfide	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevnutr_25_0_261_s_383	16011468	1-Methyl-propyl-2-imidazolozyl disulfide (PX-12), a TRX-1  inhibitor binding to the Cys73 residue, not only significantly potentiated the inhibitory  effect of cisplatin on pancreatic cancer ( 8) but also exhibited promising antitumor activities among a variety of tumor cell  lines both in vitro and in vivo ( 158).	bind
19381	3	6312	5	NULL	NULL	0	NULL	cisplatin	NULL		inhibit	NULL				pancreatic cancer	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevnutr_25_0_261_s_383	16011468	1-Methyl-propyl-2-imidazolozyl disulfide (PX-12), a TRX-1  inhibitor binding to the Cys73 residue, not only significantly potentiated the inhibitory  effect of cisplatin on pancreatic cancer ( 8) but also exhibited promising antitumor activities among a variety of tumor cell  lines both in vitro and in vivo ( 158).	bind
19382	4	6312	5	NULL	NULL	0	NULL	statement 1	NULL		potentiate	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevnutr_25_0_261_s_383	16011468	1-Methyl-propyl-2-imidazolozyl disulfide (PX-12), a TRX-1  inhibitor binding to the Cys73 residue, not only significantly potentiated the inhibitory  effect of cisplatin on pancreatic cancer ( 8) but also exhibited promising antitumor activities among a variety of tumor cell  lines both in vitro and in vivo ( 158).	bind
19383	5	6312	5	10	NULL	0	NULL	statement 1	NULL		exhibit	NULL				antitumor activities	NULL	promising			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_annurevnutr_25_0_261_s_383	16011468	1-Methyl-propyl-2-imidazolozyl disulfide (PX-12), a TRX-1  inhibitor binding to the Cys73 residue, not only significantly potentiated the inhibitory  effect of cisplatin on pancreatic cancer ( 8) but also exhibited promising antitumor activities among a variety of tumor cell  lines both in vitro and in vivo ( 158).	bind
19384	6	6312	5	10	NULL	0	NULL	statement 1	NULL		exhibit	NULL				antitumor activities	NULL	promising			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_annurevnutr_25_0_261_s_383	16011468	1-Methyl-propyl-2-imidazolozyl disulfide (PX-12), a TRX-1  inhibitor binding to the Cys73 residue, not only significantly potentiated the inhibitory  effect of cisplatin on pancreatic cancer ( 8) but also exhibited promising antitumor activities among a variety of tumor cell  lines both in vitro and in vivo ( 158).	bind
54204	7	6312	5	10	NULL	0	NULL	PX-12			is an inhibitor of					TRX-1					NULL		0	NULL	NULL	NULL	gw70_annurevnutr_25_0_261_s_383	16011468	1-Methyl-propyl-2-imidazolozyl disulfide (PX-12), a TRX-1  inhibitor binding to the Cys73 residue, not only significantly potentiated the inhibitory  effect of cisplatin on pancreatic cancer ( 8) but also exhibited promising antitumor activities among a variety of tumor cell  lines both in vitro and in vivo ( 158).	bind
22053	1	6312	7	NULL	NULL	NULL	NULL	PX-12	Chemical		bind								Cys73 residue		NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_25_0_261_s_383	16011468	1-Methyl-propyl-2-imidazolozyl disulfide (PX-12), a TRX-1  inhibitor binding to the Cys73 residue, not only significantly potentiated the inhibitory  effect of cisplatin on pancreatic cancer ( 8) but also exhibited promising antitumor activities among a variety of tumor cell  lines both in vitro and in vivo ( 158).	bind
22054	2	6312	7	NULL	NULL	NULL	NULL	PX-12	Chemical		is					1-Methyl-propyl-2-imidazolozyl disulfide	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_25_0_261_s_383	16011468	1-Methyl-propyl-2-imidazolozyl disulfide (PX-12), a TRX-1  inhibitor binding to the Cys73 residue, not only significantly potentiated the inhibitory  effect of cisplatin on pancreatic cancer ( 8) but also exhibited promising antitumor activities among a variety of tumor cell  lines both in vitro and in vivo ( 158).	bind
22055	3	6312	7	NULL	NULL	NULL	NULL	PX-12	Chemical		is an inhibitor of					TRX-1 	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_25_0_261_s_383	16011468	1-Methyl-propyl-2-imidazolozyl disulfide (PX-12), a TRX-1  inhibitor binding to the Cys73 residue, not only significantly potentiated the inhibitory  effect of cisplatin on pancreatic cancer ( 8) but also exhibited promising antitumor activities among a variety of tumor cell  lines both in vitro and in vivo ( 158).	bind
22056	4	6312	7	NULL	NULL	NULL	NULL	statement 1	Process		potentiate					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_25_0_261_s_383	16011468	1-Methyl-propyl-2-imidazolozyl disulfide (PX-12), a TRX-1  inhibitor binding to the Cys73 residue, not only significantly potentiated the inhibitory  effect of cisplatin on pancreatic cancer ( 8) but also exhibited promising antitumor activities among a variety of tumor cell  lines both in vitro and in vivo ( 158).	bind
22057	5	6312	7	NULL	NULL	NULL	NULL	PX-12	Chemical		activate					antitumor	Cell				NULL	invitro	NULL	NULL	NULL	NULL	gw70_annurevnutr_25_0_261_s_383	16011468	1-Methyl-propyl-2-imidazolozyl disulfide (PX-12), a TRX-1  inhibitor binding to the Cys73 residue, not only significantly potentiated the inhibitory  effect of cisplatin on pancreatic cancer ( 8) but also exhibited promising antitumor activities among a variety of tumor cell  lines both in vitro and in vivo ( 158).	bind
22058	6	6312	7	NULL	NULL	NULL	NULL	PX-12	Chemical		activate					antitumor	Cell				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_annurevnutr_25_0_261_s_383	16011468	1-Methyl-propyl-2-imidazolozyl disulfide (PX-12), a TRX-1  inhibitor binding to the Cys73 residue, not only significantly potentiated the inhibitory  effect of cisplatin on pancreatic cancer ( 8) but also exhibited promising antitumor activities among a variety of tumor cell  lines both in vitro and in vivo ( 158).	bind
54205	7	6312	7	NULL	NULL	NULL	NULL	cisplatin	Chemical		inhibits					pancreatic cancer	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_25_0_261_s_383	16011468	1-Methyl-propyl-2-imidazolozyl disulfide (PX-12), a TRX-1  inhibitor binding to the Cys73 residue, not only significantly potentiated the inhibitory  effect of cisplatin on pancreatic cancer ( 8) but also exhibited promising antitumor activities among a variety of tumor cell  lines both in vitro and in vivo ( 158).	bind
19385	1	6318	5	NULL	NULL	0	NULL	cyclophilins	NULL		bind	NULL				cyclosporin A	NULL	immunosuppressant			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_2_968_s_14	16260779	1.8 [EC]): the cyclophilins, which bind the immunosuppressant cyclosporin A, the FK506-binding proteins, and the parvulins.	bind
54206	2	6318	5	10	NULL	0	NULL	cyclophilins			bind					FK506-binding proteins					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_2_968_s_14	16260779	1.8 [EC]): the cyclophilins, which bind the immunosuppressant cyclosporin A, the FK506-binding proteins, and the parvulins.	bind
54207	3	6318	5	10	NULL	0	NULL	cyclophilins			bind					parvulins					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_2_968_s_14	16260779	1.8 [EC]): the cyclophilins, which bind the immunosuppressant cyclosporin A, the FK506-binding proteins, and the parvulins.	bind
22060	1	6318	7	NULL	NULL	NULL	NULL	cyclophilins	GP		bind					cyclosporin A	Chemical	immunosuppressant			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_2_968_s_14	16260779	1.8 [EC]): the cyclophilins, which bind the immunosuppressant cyclosporin A, the FK506-binding proteins, and the parvulins.	bind
22061	2	6318	7	NULL	NULL	NULL	NULL	cyclophilins	GP		bind					FK506-binding proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_2_968_s_14	16260779	1.8 [EC]): the cyclophilins, which bind the immunosuppressant cyclosporin A, the FK506-binding proteins, and the parvulins.	bind
22063	3	6318	7	NULL	NULL	NULL	NULL	cyclophilins	GP		bind					parvulins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_2_968_s_14	16260779	1.8 [EC]): the cyclophilins, which bind the immunosuppressant cyclosporin A, the FK506-binding proteins, and the parvulins.	bind
19386	1	6319	5	10	NULL	0	NULL	ColIb-P9 antisense Inc RNA	NULL		bind	NULL				RNA	NULL		5''-rUUGGCG-3'' motif in the loop sequence		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3145_s_285	11470871	10       Asano,K., Niimi,T., Yokoyama,S. and Mizobuchi,K. (1998) Structural basis for binding of the plasmid ColIb-P9 antisense Inc RNA to its target RNA with the 5''-rUUGGCG-3'' motif in the loop sequence.	bind
22071	1	6319	7	NULL	NULL	NULL	NULL	ColIb-P9 antisense Inc RNA	NucleicAcid		bind					RNA	NucleicAcid		5''-rUUGGCG-3'' motif in the loop sequence 		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3145_s_285	11470871	10       Asano,K., Niimi,T., Yokoyama,S. and Mizobuchi,K. (1998) Structural basis for binding of the plasmid ColIb-P9 antisense Inc RNA to its target RNA with the 5''-rUUGGCG-3'' motif in the loop sequence.	bind
19387	1	6320	5	NULL	NULL	0	NULL	GSK3beta	NULL		bind	NULL				APC-beta-catenin complex	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1410_s_290	11266540	10       Rubinfeld,B., Albert,I., Porfiri,E., Fiol,C., Munemitsu,S. and Polakis,P. (1996) Binding of GSK3beta to the APC-beta-catenin complex and regulation of complex assembly.	bind
19388	2	6320	5	NULL	NULL	0	NULL	GSK3beta	NULL		regulates	NULL				complex assembly	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1410_s_290	11266540	10       Rubinfeld,B., Albert,I., Porfiri,E., Fiol,C., Munemitsu,S. and Polakis,P. (1996) Binding of GSK3beta to the APC-beta-catenin complex and regulation of complex assembly.	bind
22072	1	6320	7	NULL	NULL	NULL	NULL	GSK3beta	GP		bind					APC-beta-catenin complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1410_s_290	11266540	10       Rubinfeld,B., Albert,I., Porfiri,E., Fiol,C., Munemitsu,S. and Polakis,P. (1996) Binding of GSK3beta to the APC-beta-catenin complex and regulation of complex assembly.	bind
29341	2	6320	7	NULL	NULL	NULL	NULL	GSK3beta	GP		regulates					complex assembly	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1410_s_290	11266540	10       Rubinfeld,B., Albert,I., Porfiri,E., Fiol,C., Munemitsu,S. and Polakis,P. (1996) Binding of GSK3beta to the APC-beta-catenin complex and regulation of complex assembly.	bind
19389	1	6321	5	NULL	NULL	0	NULL	GS1 strand-specific DNA binding complex	NULL		is enriched in	NULL				brain	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4433_s_256	11691931	10       Taira,E., Finkenstadt,P.M. and Baraban,J.M. (1998) Identification of translin and trax as components of the GS1 strand-specific DNA binding complex enriched in brain.	bind
19390	2	6321	5	NULL	NULL	0	NULL	translin	NULL		is a component of	NULL				GS1 strand-specific DNA binding complex	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4433_s_256	11691931	10       Taira,E., Finkenstadt,P.M. and Baraban,J.M. (1998) Identification of translin and trax as components of the GS1 strand-specific DNA binding complex enriched in brain.	bind
19391	3	6321	5	NULL	NULL	0	NULL	trax	NULL		is a component of	NULL				GS1 strand-specific DNA binding complex	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4433_s_256	11691931	10       Taira,E., Finkenstadt,P.M. and Baraban,J.M. (1998) Identification of translin and trax as components of the GS1 strand-specific DNA binding complex enriched in brain.	bind
22443	1	6321	7	NULL	NULL	NULL	NULL	translin	GP		is a component of					GS1 strand-specific DNA binding complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4433_s_256	11691931	10       Taira,E., Finkenstadt,P.M. and Baraban,J.M. (1998) Identification of translin and trax as components of the GS1 strand-specific DNA binding complex enriched in brain.	bind
22444	2	6321	7	NULL	NULL	NULL	NULL	trax	GP		is a component of					GS1 strand-specific DNA binding complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4433_s_256	11691931	10       Taira,E., Finkenstadt,P.M. and Baraban,J.M. (1998) Identification of translin and trax as components of the GS1 strand-specific DNA binding complex enriched in brain.	bind
29342	3	6321	7	NULL	NULL	NULL	NULL	GS1 strand-specific DNA binding complex	GP		is enriched in					brain	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4433_s_256	11691931	10       Taira,E., Finkenstadt,P.M. and Baraban,J.M. (1998) Identification of translin and trax as components of the GS1 strand-specific DNA binding complex enriched in brain.	bind
23060	1	6322	5	10	NULL	0	NULL	beta2GPI	NULL		target	NULL				APLAs	NULL				NULL	at the EC surface	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
23061	2	6322	5	10	NULL	0	NULL	beta2GPI-phospholipid complexes	NULL		target	NULL				APLAs	NULL				NULL	at the EC surface	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
23062	3	6322	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
23063	4	6322	5	NULL	NULL	0	NULL	MoAbs	NULL		up-regulates	NULL				adhesion molecule	NULL	expression of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
23064	5	6322	5	NULL	NULL	0	NULL	polyclonal anti-beta2GPI antibodies	NULL		up-regulates	NULL				adhesion molecule	NULL	expression of-			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
23065	6	6322	5	NULL	NULL	0	NULL	MoAbs	NULL		up-regulates	NULL				interleukin-6	NULL	secretion of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
23066	7	6322	5	NULL	NULL	0	NULL	polyclonal anti-beta2GPI antibodies	NULL		up-regulates	NULL				interleukin-6	NULL	secretion of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
23067	8	6322	5	NULL	NULL	0	NULL	statement 4	NULL		occurs after	NULL				EC	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
23068	9	6322	5	NULL	NULL	0	NULL	statement 5	NULL		occurs after	NULL				EC	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
23069	10	6322	5	NULL	NULL	0	NULL	statement 6	NULL		occurs after	NULL				EC	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
23070	11	6322	5	NULL	NULL	0	NULL	statement 7	NULL		occurs after	NULL				EC	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
23071	12	6322	5	NULL	NULL	0	NULL	monocytes	NULL		adhere to	NULL				ECs	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
23072	13	6322	5	NULL	NULL	0	NULL	MoAbs	NULL		induces	NULL				statement 12	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
23073	14	6322	5	NULL	NULL	0	NULL	polyclonal anti-beta2GPI antibodies	NULL		induces	NULL				statement 12	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
22445	1	6322	7	NULL	NULL	NULL	NULL	APLAs	GP		target					beta2GPI	GP				NULL	at the EC surface	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
22446	2	6322	7	NULL	NULL	NULL	NULL	APLAs	GP		target					beta2GPI-phospholipid complex	GP				NULL	at the EC surface	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
45648	3	6322	7	NULL	NULL	NULL	NULL	MoAbs	GP		upregulate					adhesion molecule	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
45649	4	6322	7	NULL	NULL	NULL	NULL	polyclonal anti-beta2GPI antibodies 	GP		upregulate					adhesion molecule	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
45650	5	6322	7	NULL	NULL	NULL	NULL	MoAbs	GP		upregulate					interleukin-6	GP	secretion of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
45651	6	6322	7	NULL	NULL	NULL	NULL	polyclonal anti-beta2GPI antibodies	GP		upregulate					interleukin-6	GP	secretion of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
45652	7	6322	7	NULL	NULL	NULL	NULL	statement 3	Process		occurs after					EC	CellComponent	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
45653	8	6322	7	NULL	NULL	NULL	NULL	statement 4	Process		occurs after					EC	CellComponent	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
45654	9	6322	7	NULL	NULL	NULL	NULL	statement 5	Process		occurs after					EC	CellComponent	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
45655	10	6322	7	NULL	NULL	NULL	NULL	statement 6	Process		occurs after					EC	CellComponent	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
45656	11	6322	7	NULL	NULL	NULL	NULL	monocytes	Cell		adhere to					ECs	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
45657	12	6322	7	NULL	NULL	NULL	NULL	MoAbs	GP		induce					statement 11	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
45658	13	6322	7	NULL	NULL	NULL	NULL	polyclonal anti-beta2GPI antibodies	GP		induce					statement 11	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
45659	14	6322	7	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_303	10669657	10  23 25 31  At the EC surface, beta2GPI or beta2GPI-phospholipid complexes were thought to be the main targets of APLAs, and it has been shown that both MoAbs and polyclonal anti-beta2GPI antibodies can upregulate adhesion molecule expression and interleukin-6 secretion after EC binding 24 32  and induce adherence of monocytes to ECs. 10 25  However, the binding of APLAs to the EC surface has never been clearly demonstrated and remains speculative in view of scarce evidence of the loss in membrane asymmetry.	bind
19392	1	6323	5	10	NULL	0	NULL	SLIGRL			is a type of					synthetic PAR-2 hexapeptide agonist					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_10_1054_s_35	10827135	10  Accordingly, the present study uses SLIGRL (a synthetic PAR-2 hexapeptide agonist, which activates PAR-2 but not PAR-1 10 ) to test the hypothesis that incremental responses to SFLLRN over thrombin are due to the copresence of PAR-1 and PAR-2.	bind
19393	2	6323	5	NULL	NULL	0	NULL	SLIGRL	NULL		activates	NULL				PAR-2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_10_1054_s_35	10827135	10  Accordingly, the present study uses SLIGRL (a synthetic PAR-2 hexapeptide agonist, which activates PAR-2 but not PAR-1 10 ) to test the hypothesis that incremental responses to SFLLRN over thrombin are due to the copresence of PAR-1 and PAR-2.	bind
19394	3	6323	5	NULL	NULL	0	NULL	SLIGRL	NULL		does not activate	NULL				PAR-1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_10_1054_s_35	10827135	10  Accordingly, the present study uses SLIGRL (a synthetic PAR-2 hexapeptide agonist, which activates PAR-2 but not PAR-1 10 ) to test the hypothesis that incremental responses to SFLLRN over thrombin are due to the copresence of PAR-1 and PAR-2.	bind
22454	1	6323	7	NULL	NULL	NULL	NULL	SLIGRL	Chemical		activates					PAR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_10_1054_s_35	10827135	10  Accordingly, the present study uses SLIGRL (a synthetic PAR-2 hexapeptide agonist, which activates PAR-2 but not PAR-1 10 ) to test the hypothesis that incremental responses to SFLLRN over thrombin are due to the copresence of PAR-1 and PAR-2.	bind
22455	2	6323	7	NULL	NULL	NULL	NULL	SLIGRL	Chemical		does not activate					PAR-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_10_1054_s_35	10827135	10  Accordingly, the present study uses SLIGRL (a synthetic PAR-2 hexapeptide agonist, which activates PAR-2 but not PAR-1 10 ) to test the hypothesis that incremental responses to SFLLRN over thrombin are due to the copresence of PAR-1 and PAR-2.	bind
22458	3	6323	7	NULL	NULL	NULL	NULL	 SLIGRL	Chemical		is a type of					synthetic PAR-2 hexapeptide agonist	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_10_1054_s_35	10827135	10  Accordingly, the present study uses SLIGRL (a synthetic PAR-2 hexapeptide agonist, which activates PAR-2 but not PAR-1 10 ) to test the hypothesis that incremental responses to SFLLRN over thrombin are due to the copresence of PAR-1 and PAR-2.	bind
22978	1	6324	5	NULL	NULL	0	NULL	c-Fosc-Jun	NULL		bind	NULL					NULL			LRE	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_158	9081693	10  Conservation of the 15-bp spacing between the proximal AP-1 site and the kappaB site in the human and murine TF promoters 53  suggested that this separation might optimize the functional interaction between c-Fosc-Jun and c-Relp65 bound to the LRE.	bind
22979	2	6324	5	NULL	NULL	0	NULL	c-Relp65	NULL		bind	NULL					NULL			LRE	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_158	9081693	10  Conservation of the 15-bp spacing between the proximal AP-1 site and the kappaB site in the human and murine TF promoters 53  suggested that this separation might optimize the functional interaction between c-Fosc-Jun and c-Relp65 bound to the LRE.	bind
22980	3	6324	5	NULL	NULL	0	NULL	statement 1	NULL		interacts with	NULL	functionally			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_158	9081693	10  Conservation of the 15-bp spacing between the proximal AP-1 site and the kappaB site in the human and murine TF promoters 53  suggested that this separation might optimize the functional interaction between c-Fosc-Jun and c-Relp65 bound to the LRE.	bind
22985	4	6324	5	NULL	NULL	0	NULL	TF	NULL	human	is seperated from	NULL			AP-1 site in promoter	TF	NULL	human		kappaB site in promoter	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_158	9081693	10  Conservation of the 15-bp spacing between the proximal AP-1 site and the kappaB site in the human and murine TF promoters 53  suggested that this separation might optimize the functional interaction between c-Fosc-Jun and c-Relp65 bound to the LRE.	bind
22986	5	6324	5	NULL	NULL	0	NULL	statement 4	NULL	conservation of	suggests	NULL				statement 3	NULL	optimization of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_158	9081693	10  Conservation of the 15-bp spacing between the proximal AP-1 site and the kappaB site in the human and murine TF promoters 53  suggested that this separation might optimize the functional interaction between c-Fosc-Jun and c-Relp65 bound to the LRE.	bind
22987	6	6324	5	NULL	NULL	0	NULL	TF	NULL	murine	is seperated from	NULL			AP-1 site in promoter	TF	NULL	murine		kappaB site in promoter	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_158	9081693	10  Conservation of the 15-bp spacing between the proximal AP-1 site and the kappaB site in the human and murine TF promoters 53  suggested that this separation might optimize the functional interaction between c-Fosc-Jun and c-Relp65 bound to the LRE.	bind
22988	7	6324	5	NULL	NULL	0	NULL	statement 6	NULL	conservation of	suggests	NULL				statement 3	NULL	optimization of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_158	9081693	10  Conservation of the 15-bp spacing between the proximal AP-1 site and the kappaB site in the human and murine TF promoters 53  suggested that this separation might optimize the functional interaction between c-Fosc-Jun and c-Relp65 bound to the LRE.	bind
22460	1	6324	7	NULL	NULL	NULL	NULL	c-Relp65	GP		bind									LRE	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_158	9081693	10  Conservation of the 15-bp spacing between the proximal AP-1 site and the kappaB site in the human and murine TF promoters 53  suggested that this separation might optimize the functional interaction between c-Fosc-Jun and c-Relp65 bound to the LRE.	bind
22461	2	6324	7	NULL	NULL	NULL	NULL	c-Fosc-Jun	GP		bind									LRE	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_158	9081693	10  Conservation of the 15-bp spacing between the proximal AP-1 site and the kappaB site in the human and murine TF promoters 53  suggested that this separation might optimize the functional interaction between c-Fosc-Jun and c-Relp65 bound to the LRE.	bind
22462	4	6324	7	NULL	NULL	NULL	NULL	TF	GP	human proximal	is separated from				 AP-1 site in promoter	TF	GP	human		kappaB site in promoter	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_158	9081693	10  Conservation of the 15-bp spacing between the proximal AP-1 site and the kappaB site in the human and murine TF promoters 53  suggested that this separation might optimize the functional interaction between c-Fosc-Jun and c-Relp65 bound to the LRE.	bind
22463	5	6324	7	NULL	NULL	NULL	NULL	statement 4	Process	conservation of	suggests					statement 3	Process	optimization of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_158	9081693	10  Conservation of the 15-bp spacing between the proximal AP-1 site and the kappaB site in the human and murine TF promoters 53  suggested that this separation might optimize the functional interaction between c-Fosc-Jun and c-Relp65 bound to the LRE.	bind
22464	6	6324	7	NULL	NULL	NULL	NULL	TF	GP	murine proximal	is separated from				 AP-1 site in promoter	TF	GP	murine		kappaB site in promoter	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_158	9081693	10  Conservation of the 15-bp spacing between the proximal AP-1 site and the kappaB site in the human and murine TF promoters 53  suggested that this separation might optimize the functional interaction between c-Fosc-Jun and c-Relp65 bound to the LRE.	bind
22465	7	6324	7	NULL	NULL	NULL	NULL	statement 6	Process	conservation of	suggests					statement 3	Process	optimization of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_158	9081693	10  Conservation of the 15-bp spacing between the proximal AP-1 site and the kappaB site in the human and murine TF promoters 53  suggested that this separation might optimize the functional interaction between c-Fosc-Jun and c-Relp65 bound to the LRE.	bind
29343	3	6324	7	NULL	NULL	NULL	NULL	statement 1	Process		functionally interacts with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_158	9081693	10  Conservation of the 15-bp spacing between the proximal AP-1 site and the kappaB site in the human and murine TF promoters 53  suggested that this separation might optimize the functional interaction between c-Fosc-Jun and c-Relp65 bound to the LRE.	bind
19395	1	6325	5	NULL	NULL	0	NULL	tissue factor	NULL	exposed	bind	NULL				factor VIIa	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_27	7586275	10  Exposed tissue factor binds to factor VIIa, an essential step in the initiation of the coagulation pathway.	bind
19396	2	6325	5	10	NULL	0	NULL	statement 1	NULL		leads to	NULL				coagulation pathway	NULL	initiation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_27	7586275	10  Exposed tissue factor binds to factor VIIa, an essential step in the initiation of the coagulation pathway.	bind
22466	1	6325	7	NULL	NULL	NULL	NULL	tissue factor	GP	exposed	binds to					factor VIIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_27	7586275	10  Exposed tissue factor binds to factor VIIa, an essential step in the initiation of the coagulation pathway.	bind
22467	2	6325	7	NULL	NULL	NULL	NULL	statement 1	Process		leads to					coagulation pathway	Process	initiation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_27	7586275	10  Exposed tissue factor binds to factor VIIa, an essential step in the initiation of the coagulation pathway.	bind
19405	1	6327	5	NULL	NULL	0	NULL	Heparin	NULL		used as	NULL	clinically			anticoagulant	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
19406	2	6327	5	NULL	NULL	0	NULL	acute venous thromboembolism	NULL	initial treatment of	require	NULL				Heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
19407	3	6327	5	NULL	NULL	0	NULL	unstable angina	NULL	treatment of	require	NULL				Heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
19408	4	6327	5	NULL	NULL	0	NULL	antithrombin	NULL		mediate	NULL				thrombin	NULL	inactivation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
19409	5	6327	5	NULL	NULL	0	NULL	Heparin	NULL		accelerate	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
19410	6	6327	5	NULL	NULL	0	NULL	antithrombin	NULL		mediate	NULL				FXa	NULL	inactivation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
19411	7	6327	5	NULL	NULL	0	NULL	Heparin	NULL		accelerate	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
19412	8	6327	5	NULL	NULL	0	NULL	antithrombin	NULL		mediate	NULL				FIXa	NULL	inactivation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
19413	9	6327	5	NULL	NULL	0	NULL	Heparin	NULL		accelerate	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
19414	10	6327	5	NULL	NULL	0	NULL	heparin cofactor II	NULL		bind	NULL				thrombin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
19415	11	6327	5	NULL	NULL	0	NULL	Heparin	NULL		accelerate	NULL				statement 10	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
22469	1	6327	7	NULL	NULL	NULL	NULL	antithrombin	GP		mediates					thrombin	GP	inactivation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
22470	2	6327	7	NULL	NULL	NULL	NULL	antithrombin	GP		mediates					FXa	GP	inactivation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
22471	3	6327	7	NULL	NULL	NULL	NULL	antithrombin	GP		mediates					FIXa	GP	inactivation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
22472	4	6327	7	NULL	NULL	NULL	NULL	Heparin	GP		accelerates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
22473	5	6327	7	NULL	NULL	NULL	NULL	Heparin	GP		accelerates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
22474	6	6327	7	NULL	NULL	NULL	NULL	Heparin	GP		accelerates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
22475	7	6327	7	NULL	NULL	NULL	NULL	heparin cofactor II	GP		bind					thrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
29386	8	6327	7	NULL	NULL	NULL	NULL	Heparin	GP		use as an					anticoagulant	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
29387	9	6327	7	NULL	NULL	NULL	NULL	Heparin	GP		is used in the					acute venous thromboembolism	MedicalFinding	initial treatment of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
29388	10	6327	7	NULL	NULL	NULL	NULL	Heparin	GP		is used in the 					unstable angina	MedicalFinding	initial treatment of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_44	10479670	10  Heparin has wide clinical use as an anticoagulant in the initial treatment of acute venous thromboembolism and unstable angina, 26 27  its main action being the acceleration of antithrombin-mediated inactivation of thrombin, FXa, and FIXa and the binding of thrombin by heparin cofactor II. 28 29	bind
19397	1	6328	5	10	NULL	0	NULL	apo(a)	NULL		bind	NULL				core protein of decorin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_6_707_s_208	10747008	10  In addition, apo(a) from Lp(a) binds to the core protein of decorin.	bind
45613	2	6328	5	10	NULL	0	NULL	apo(a)	NULL		is from	NULL				Lp(a)	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_6_707_s_208	10747008	10  In addition, apo(a) from Lp(a) binds to the core protein of decorin.	bind
22476	1	6328	7	NULL	NULL	NULL	NULL	apo(a)	GP		binds to					core protein of decorin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_6_707_s_208	10747008	10  In addition, apo(a) from Lp(a) binds to the core protein of decorin.	bind
22477	2	6328	7	NULL	NULL	NULL	NULL	apo(a)	GP		is from					Lp(a)	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_6_707_s_208	10747008	10  In addition, apo(a) from Lp(a) binds to the core protein of decorin.	bind
19398	1	6330	5	NULL	NULL	0	NULL	111In-VLDL	NULL		bind	NULL				basophils	NULL	human			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_1_17_s_239	7538422	10  In this study, 111In-VLDL bound to human basophils and mast cells and binding of VLDL to the LDL receptor were demonstrable.	bind
19399	2	6330	5	NULL	NULL	0	NULL	111In-VLDL	NULL		bind	NULL				mast cells	NULL	human			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_1_17_s_239	7538422	10  In this study, 111In-VLDL bound to human basophils and mast cells and binding of VLDL to the LDL receptor were demonstrable.	bind
19400	3	6330	5	NULL	NULL	0	NULL	VLDL	NULL		bind	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_1_17_s_239	7538422	10  In this study, 111In-VLDL bound to human basophils and mast cells and binding of VLDL to the LDL receptor were demonstrable.	bind
22478	1	6330	7	NULL	NULL	NULL	NULL	111In-VLDL	Chemical		bind					basophils	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_1_17_s_239	7538422	10  In this study, 111In-VLDL bound to human basophils and mast cells and binding of VLDL to the LDL receptor were demonstrable.	bind
22479	2	6330	7	NULL	NULL	NULL	NULL	111In-VLDL	Chemical		bind					mast cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_1_17_s_239	7538422	10  In this study, 111In-VLDL bound to human basophils and mast cells and binding of VLDL to the LDL receptor were demonstrable.	bind
22480	3	6330	7	NULL	NULL	NULL	NULL	VLDL	Chemical		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_1_17_s_239	7538422	10  In this study, 111In-VLDL bound to human basophils and mast cells and binding of VLDL to the LDL receptor were demonstrable.	bind
19401	1	6331	5	NULL	NULL	0	NULL		NULL	cleavage of	disrupts	NULL		70 amino acids from the C-terminus		apoA-I	NULL		HDL receptor - binding domain		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_1_210_s_197	10634820	10  Indeed, a limited proteolysis study showed that cleavage of 70 amino acids from the  C-terminus resulted in disruption of the HDL receptor - binding domain of apoA-I.	bind
22481	1	6331	7	NULL	NULL	NULL	NULL			cleavage of 	disrupts			70 amino acids  of C-terminus		apoA-I	GP		HDL receptor - binding domain		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_1_210_s_197	10634820	10  Indeed, a limited proteolysis study showed that cleavage of 70 amino acids from the  C-terminus resulted in disruption of the HDL receptor - binding domain of apoA-I.	bind
19402	1	6332	5	NULL	NULL	0	NULL	IP3	NULL		bind	NULL				IP3 receptor	NULL				NULL	on the membrane of SR	NULL	NULL	NULL	NULL	gw60_circulation_94_2_190_s_22	8674178	10  IP3 then binds to an IP3 receptor on the membrane of the SR to mobilize the stored calcium ions (Ca2+) from the SR into the cytosol.	bind
19403	2	6332	5	10	NULL	0	NULL	statement 1			mobilize					Ca2+		stored			NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_2_190_s_22	8674178	10  IP3 then binds to an IP3 receptor on the membrane of the SR to mobilize the stored calcium ions (Ca2+) from the SR into the cytosol.	bind
19404	3	6332	5	NULL	NULL	0	NULL	Ca2+	NULL		is	NULL				calcium ions	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_94_2_190_s_22	8674178	10  IP3 then binds to an IP3 receptor on the membrane of the SR to mobilize the stored calcium ions (Ca2+) from the SR into the cytosol.	bind
28691	4	6332	5	NULL	NULL	0	NULL	Ca2+	NULL	from SR	moves to	NULL				cytosol	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_94_2_190_s_22	8674178	10  IP3 then binds to an IP3 receptor on the membrane of the SR to mobilize the stored calcium ions (Ca2+) from the SR into the cytosol.	bind
22482	1	6332	7	NULL	NULL	NULL	NULL	IP3	Chemical		binds to					IP3 receptor	GP				NULL	membrane of the SR	NULL	NULL	NULL	NULL	gw60_circulation_94_2_190_s_22	8674178	10  IP3 then binds to an IP3 receptor on the membrane of the SR to mobilize the stored calcium ions (Ca2+) from the SR into the cytosol.	bind
22483	2	6332	7	NULL	NULL	NULL	NULL	statement 1	Process		mobilize					Ca2+	Chemical	stored			NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_2_190_s_22	8674178	10  IP3 then binds to an IP3 receptor on the membrane of the SR to mobilize the stored calcium ions (Ca2+) from the SR into the cytosol.	bind
22484	3	6332	7	NULL	NULL	NULL	NULL	Ca2+	Chemical	From SR	move to					cytosol	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_2_190_s_22	8674178	10  IP3 then binds to an IP3 receptor on the membrane of the SR to mobilize the stored calcium ions (Ca2+) from the SR into the cytosol.	bind
22485	4	6332	7	NULL	NULL	NULL	NULL	Ca2+	Chemical		is					calcium ions	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_2_190_s_22	8674178	10  IP3 then binds to an IP3 receptor on the membrane of the SR to mobilize the stored calcium ions (Ca2+) from the SR into the cytosol.	bind
19416	1	6334	5	NULL	NULL	0	NULL	GRB2	NULL		bind	NULL				Shc	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_79_6_1167_s_259	8943955	10  On the other hand, generally, GRB2 is known to bind Shc in response to insulin and subsequently activates the p21ras pathway, including MAP kinase and p90RSK, and association of GRB2 with IRS-1 is not a major pathway for activation of the p21ras pathway.	bind
19417	2	6334	5	NULL	NULL	0	NULL	statement 1	NULL		occurs in response to	NULL				insulin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_79_6_1167_s_259	8943955	10  On the other hand, generally, GRB2 is known to bind Shc in response to insulin and subsequently activates the p21ras pathway, including MAP kinase and p90RSK, and association of GRB2 with IRS-1 is not a major pathway for activation of the p21ras pathway.	bind
19418	3	6334	5	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL	subsequently			p21ras pathway	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_79_6_1167_s_259	8943955	10  On the other hand, generally, GRB2 is known to bind Shc in response to insulin and subsequently activates the p21ras pathway, including MAP kinase and p90RSK, and association of GRB2 with IRS-1 is not a major pathway for activation of the p21ras pathway.	bind
19419	4	6334	5	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL	subsequently			 MAP kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_79_6_1167_s_259	8943955	10  On the other hand, generally, GRB2 is known to bind Shc in response to insulin and subsequently activates the p21ras pathway, including MAP kinase and p90RSK, and association of GRB2 with IRS-1 is not a major pathway for activation of the p21ras pathway.	bind
19420	5	6334	5	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL	subsequently			p90RSK	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_79_6_1167_s_259	8943955	10  On the other hand, generally, GRB2 is known to bind Shc in response to insulin and subsequently activates the p21ras pathway, including MAP kinase and p90RSK, and association of GRB2 with IRS-1 is not a major pathway for activation of the p21ras pathway.	bind
19421	6	6334	5	NULL	NULL	0	NULL	GRB2	NULL		associates with	NULL				IRS-1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_79_6_1167_s_259	8943955	10  On the other hand, generally, GRB2 is known to bind Shc in response to insulin and subsequently activates the p21ras pathway, including MAP kinase and p90RSK, and association of GRB2 with IRS-1 is not a major pathway for activation of the p21ras pathway.	bind
19422	7	6334	5	NULL	NULL	0	NULL	statement 6	NULL		is not required for	NULL				p21ras pathway	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_6_1167_s_259	8943955	10  On the other hand, generally, GRB2 is known to bind Shc in response to insulin and subsequently activates the p21ras pathway, including MAP kinase and p90RSK, and association of GRB2 with IRS-1 is not a major pathway for activation of the p21ras pathway.	bind
22486	1	6334	7	NULL	NULL	NULL	NULL	 GRB2	GP		bind					Shc	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_6_1167_s_259	8943955	10  On the other hand, generally, GRB2 is known to bind Shc in response to insulin and subsequently activates the p21ras pathway, including MAP kinase and p90RSK, and association of GRB2 with IRS-1 is not a major pathway for activation of the p21ras pathway.	bind
22487	2	6334	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs in response to					insulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_6_1167_s_259	8943955	10  On the other hand, generally, GRB2 is known to bind Shc in response to insulin and subsequently activates the p21ras pathway, including MAP kinase and p90RSK, and association of GRB2 with IRS-1 is not a major pathway for activation of the p21ras pathway.	bind
22488	3	6334	7	NULL	NULL	NULL	NULL	statement 1	Process		activates		subsequently			p21ras pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_6_1167_s_259	8943955	10  On the other hand, generally, GRB2 is known to bind Shc in response to insulin and subsequently activates the p21ras pathway, including MAP kinase and p90RSK, and association of GRB2 with IRS-1 is not a major pathway for activation of the p21ras pathway.	bind
22489	4	6334	7	NULL	NULL	NULL	NULL	statement 1	Process		activates		subsequently			MAP kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_6_1167_s_259	8943955	10  On the other hand, generally, GRB2 is known to bind Shc in response to insulin and subsequently activates the p21ras pathway, including MAP kinase and p90RSK, and association of GRB2 with IRS-1 is not a major pathway for activation of the p21ras pathway.	bind
22490	5	6334	7	NULL	NULL	NULL	NULL	statement 1	Process		activates		subsequently			p90RSK	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_6_1167_s_259	8943955	10  On the other hand, generally, GRB2 is known to bind Shc in response to insulin and subsequently activates the p21ras pathway, including MAP kinase and p90RSK, and association of GRB2 with IRS-1 is not a major pathway for activation of the p21ras pathway.	bind
22491	6	6334	7	NULL	NULL	NULL	NULL	GRB2	GP		associate with					IRS-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_6_1167_s_259	8943955	10  On the other hand, generally, GRB2 is known to bind Shc in response to insulin and subsequently activates the p21ras pathway, including MAP kinase and p90RSK, and association of GRB2 with IRS-1 is not a major pathway for activation of the p21ras pathway.	bind
22492	7	6334	7	NULL	NULL	NULL	NULL	statement 6	Process		 is not required for					p21ras pathway	Process	 activation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_6_1167_s_259	8943955	10  On the other hand, generally, GRB2 is known to bind Shc in response to insulin and subsequently activates the p21ras pathway, including MAP kinase and p90RSK, and association of GRB2 with IRS-1 is not a major pathway for activation of the p21ras pathway.	bind
19423	1	6335	5	NULL	NULL	0	NULL	FXa	NULL		bind	NULL				TF	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_30	10479670	10  TFPI uses the tandem Kunitz-type domains in its structure to form a quaternary complex with FXa bound to TF .	bind
19424	2	6335	5	NULL	NULL	0	NULL	TFPI	NULL		bind	NULL		tandem Kunitz-type domains		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_30	10479670	10  TFPI uses the tandem Kunitz-type domains in its structure to form a quaternary complex with FXa bound to TF .	bind
28692	3	6335	5	NULL	NULL	0	NULL	statement 2	NULL		forms	NULL				quaternary complex	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_30	10479670	10  TFPI uses the tandem Kunitz-type domains in its structure to form a quaternary complex with FXa bound to TF .	bind
22493	1	6335	7	NULL	NULL	NULL	NULL	FXa	GP		bind					TF	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_30	10479670	10  TFPI uses the tandem Kunitz-type domains in its structure to form a quaternary complex with FXa bound to TF .	bind
22494	3	6335	7	NULL	NULL	NULL	NULL	statement 2	Process		forms					quaternary complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_30	10479670	10  TFPI uses the tandem Kunitz-type domains in its structure to form a quaternary complex with FXa bound to TF .	bind
22495	2	6335	7	NULL	NULL	NULL	NULL	TFPI	GP		bind			tandem Kunitz-type domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_30	10479670	10  TFPI uses the tandem Kunitz-type domains in its structure to form a quaternary complex with FXa bound to TF .	bind
19425	1	6336	5	NULL	NULL	0	NULL	follistatin	NULL		regulates	NULL				activin	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_circulationres_85_10_931_s_19	10559140	10  The activity of activin is regulated by follistatin, a 34-kDa glycoprotein, which binds activin with high affinity in equimolar complexes that are unable to bind and activate the activin receptors.	bind
19426	2	6336	5	NULL	NULL	0	NULL	follistatin	NULL		bind	NULL	high affinity			activin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_10_931_s_19	10559140	10  The activity of activin is regulated by follistatin, a 34-kDa glycoprotein, which binds activin with high affinity in equimolar complexes that are unable to bind and activate the activin receptors.	bind
19427	3	6336	5	NULL	NULL	0	NULL	statement 2	NULL		does not bind	NULL				activin receptors	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_10_931_s_19	10559140	10  The activity of activin is regulated by follistatin, a 34-kDa glycoprotein, which binds activin with high affinity in equimolar complexes that are unable to bind and activate the activin receptors.	bind
19428	4	6336	5	NULL	NULL	0	NULL	statement 2	NULL		does not activate	NULL				activin receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_10_931_s_19	10559140	10  The activity of activin is regulated by follistatin, a 34-kDa glycoprotein, which binds activin with high affinity in equimolar complexes that are unable to bind and activate the activin receptors.	bind
28693	5	6336	5	NULL	NULL	0	NULL	follistatin	NULL		is a type of	NULL				34-kDa glycoprotein	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_10_931_s_19	10559140	10  The activity of activin is regulated by follistatin, a 34-kDa glycoprotein, which binds activin with high affinity in equimolar complexes that are unable to bind and activate the activin receptors.	bind
22496	1	6336	7	NULL	NULL	NULL	NULL	follistatin	GP		binds		high affinity			activin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_10_931_s_19	10559140	10  The activity of activin is regulated by follistatin, a 34-kDa glycoprotein, which binds activin with high affinity in equimolar complexes that are unable to bind and activate the activin receptors.	bind
22497	2	6336	7	NULL	NULL	NULL	NULL	follistatin	GP		regulates					activin	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_10_931_s_19	10559140	10  The activity of activin is regulated by follistatin, a 34-kDa glycoprotein, which binds activin with high affinity in equimolar complexes that are unable to bind and activate the activin receptors.	bind
22498	3	6336	7	NULL	NULL	NULL	NULL	follistatin	GP		is a type of					34-kDa glycoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_10_931_s_19	10559140	10  The activity of activin is regulated by follistatin, a 34-kDa glycoprotein, which binds activin with high affinity in equimolar complexes that are unable to bind and activate the activin receptors.	bind
22499	4	6336	7	NULL	NULL	NULL	NULL	statement 1	Process		does not bind					activin receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_10_931_s_19	10559140	10  The activity of activin is regulated by follistatin, a 34-kDa glycoprotein, which binds activin with high affinity in equimolar complexes that are unable to bind and activate the activin receptors.	bind
22500	5	6336	7	NULL	NULL	NULL	NULL	statement 1	Process		does not activate					activin receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_10_931_s_19	10559140	10  The activity of activin is regulated by follistatin, a 34-kDa glycoprotein, which binds activin with high affinity in equimolar complexes that are unable to bind and activate the activin receptors.	bind
19429	1	6337	5	10	NULL	0	NULL	hirudin			bind					fibrinogen			recognition exosite		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_987_s_36	11375267	10  The exogenous leech - derived inhibitor hirudin also binds to the fibrinogen-recognition exosite and the active site to inhibit thrombin function 11  and is used clinically as a potent antithrombin.	bind
19430	2	6337	5	10	NULL	0	NULL	hirudin			bind					fibrinogen			active site		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_987_s_36	11375267	10  The exogenous leech - derived inhibitor hirudin also binds to the fibrinogen-recognition exosite and the active site to inhibit thrombin function 11  and is used clinically as a potent antithrombin.	bind
19431	3	6337	5	NULL	NULL	0	NULL	statement 1	NULL		inhibit	NULL				thrombin	NULL	function of			NULL		0	NULL	NULL	NULL	gw60_circulationres_88_10_987_s_36	11375267	10  The exogenous leech - derived inhibitor hirudin also binds to the fibrinogen-recognition exosite and the active site to inhibit thrombin function 11  and is used clinically as a potent antithrombin.	bind
19432	4	6337	5	NULL	NULL	0	NULL	statement 2	NULL		inhibit	NULL				thrombin	NULL	function of			NULL		0	NULL	NULL	NULL	gw60_circulationres_88_10_987_s_36	11375267	10  The exogenous leech - derived inhibitor hirudin also binds to the fibrinogen-recognition exosite and the active site to inhibit thrombin function 11  and is used clinically as a potent antithrombin.	bind
19433	5	6337	5	10	NULL	0	NULL	hirudin			is used as		clinically			antithrombin		potent			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_987_s_36	11375267	10  The exogenous leech - derived inhibitor hirudin also binds to the fibrinogen-recognition exosite and the active site to inhibit thrombin function 11  and is used clinically as a potent antithrombin.	bind
54208	5	6337	5	10	NULL	0	NULL	hirudin			is a type of					exogenous leech - derived inhibitor					NULL		0	NULL	NULL	NULL	gw60_circulationres_88_10_987_s_36	11375267	10  The exogenous leech - derived inhibitor hirudin also binds to the fibrinogen-recognition exosite and the active site to inhibit thrombin function 11  and is used clinically as a potent antithrombin.	bind
22501	1	6337	7	NULL	NULL	NULL	NULL	hirudin	GP		binds to					fibrinogen	GP		recognition exosite		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_987_s_36	11375267	10  The exogenous leech - derived inhibitor hirudin also binds to the fibrinogen-recognition exosite and the active site to inhibit thrombin function 11  and is used clinically as a potent antithrombin.	bind
22502	2	6337	7	NULL	NULL	NULL	NULL	hirudin	GP		binds to					fibrinogen	GP		active site		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_987_s_36	11375267	10  The exogenous leech - derived inhibitor hirudin also binds to the fibrinogen-recognition exosite and the active site to inhibit thrombin function 11  and is used clinically as a potent antithrombin.	bind
22503	3	6337	7	NULL	NULL	NULL	NULL	statement 1	Process		inhibit					thrombin	GP	function of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_987_s_36	11375267	10  The exogenous leech - derived inhibitor hirudin also binds to the fibrinogen-recognition exosite and the active site to inhibit thrombin function 11  and is used clinically as a potent antithrombin.	bind
22504	4	6337	7	NULL	NULL	NULL	NULL	statement 2	Process		inhibit					thrombin	GP	function of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_987_s_36	11375267	10  The exogenous leech - derived inhibitor hirudin also binds to the fibrinogen-recognition exosite and the active site to inhibit thrombin function 11  and is used clinically as a potent antithrombin.	bind
22505	5	6337	7	NULL	NULL	NULL	NULL	hirudin	GP		is used as		clinically			antithrombin	GP	potent			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_987_s_36	11375267	10  The exogenous leech - derived inhibitor hirudin also binds to the fibrinogen-recognition exosite and the active site to inhibit thrombin function 11  and is used clinically as a potent antithrombin.	bind
54209	6	6337	7	NULL	NULL	NULL	NULL	hirudin	GP		is a type of					exogenous leech - derived inhibitor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_987_s_36	11375267	10  The exogenous leech - derived inhibitor hirudin also binds to the fibrinogen-recognition exosite and the active site to inhibit thrombin function 11  and is used clinically as a potent antithrombin.	bind
19434	1	6338	5	NULL	NULL	0	NULL		NULL		bind	NULL		tryptophan-rich motif within the type 1 repeats		heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_13_1423_s_24	10500044	10  The peptides used in these assays included a tryptophan-rich motif within the type 1 repeats that binds to heparin.	bind
22506	1	6338	7	NULL	NULL	NULL	NULL				bind			tryptophan-rich motif within type 1 repeat		heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_13_1423_s_24	10500044	10  The peptides used in these assays included a tryptophan-rich motif within the type 1 repeats that binds to heparin.	bind
19435	1	6339	5	NULL	NULL	0	NULL	heparin	NULL		bind	NULL					NULL		I domain		NULL		0	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_158	10510057	10  Therefore, our data could be explained by binding of heparin to the I domain which may then cause steric hindrance of the binding of factor X to spatially distinct binding sites within Mac-1.	bind
19436	2	6339	5	NULL	NULL	0	NULL	factor X	NULL		bind	NULL				Mac-1	NULL	spatially distinct binding sites			NULL		0	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_158	10510057	10  Therefore, our data could be explained by binding of heparin to the I domain which may then cause steric hindrance of the binding of factor X to spatially distinct binding sites within Mac-1.	bind
19437	3	6339	5	NULL	NULL	0	NULL	statement 1	NULL		cause	NULL	may			statement 2	NULL	steric hindrance of			NULL		0	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_158	10510057	10  Therefore, our data could be explained by binding of heparin to the I domain which may then cause steric hindrance of the binding of factor X to spatially distinct binding sites within Mac-1.	bind
22507	1	6339	7	NULL	NULL	NULL	NULL	 heparin	GP		bind								I domain		NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_158	10510057	10  Therefore, our data could be explained by binding of heparin to the I domain which may then cause steric hindrance of the binding of factor X to spatially distinct binding sites within Mac-1.	bind
22508	2	6339	7	NULL	NULL	NULL	NULL	factor X	GP		bind					Mac-1	GP		spatially distinct binding site within		NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_158	10510057	10  Therefore, our data could be explained by binding of heparin to the I domain which may then cause steric hindrance of the binding of factor X to spatially distinct binding sites within Mac-1.	bind
22509	3	6339	7	NULL	NULL	NULL	NULL	statement 1	Process		cause		may			statement 2	Process	steric hindrance of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_158	10510057	10  Therefore, our data could be explained by binding of heparin to the I domain which may then cause steric hindrance of the binding of factor X to spatially distinct binding sites within Mac-1.	bind
19438	1	6340	5	10	NULL	0	NULL	PAI-1			bind					vitronectin					NULL	vascular smooth muscle cells	NULL	NULL	NULL	NULL	gw60_circulation_103_25_3105_s_25	11425776	10  This effect appears to be mediated by inhibition of plasmin formation and possibly by PAI-1 binding to vitronectin, thereby preventing its interaction with vitronectin receptors present on vascular smooth muscle cells.	bind
19439	2	6340	5	NULL	NULL	0	NULL	PAI-1	NULL		interacts with	NULL				vitronectin receptors	NULL				NULL	on vascular smooth muscle cells	NULL	NULL	NULL	NULL	gw60_circulation_103_25_3105_s_25	11425776	10  This effect appears to be mediated by inhibition of plasmin formation and possibly by PAI-1 binding to vitronectin, thereby preventing its interaction with vitronectin receptors present on vascular smooth muscle cells.	bind
28694	3	6340	5	10	NULL	0	NULL	statement 1			prevents					statement 2					NULL	vascular smooth muscle cells	NULL	NULL	NULL	NULL	gw60_circulation_103_25_3105_s_25	11425776	10  This effect appears to be mediated by inhibition of plasmin formation and possibly by PAI-1 binding to vitronectin, thereby preventing its interaction with vitronectin receptors present on vascular smooth muscle cells.	bind
22510	1	6340	7	NULL	NULL	NULL	NULL	 PAI-1	GP		bind					vitronectin	GP				NULL	vascular smooth muscle cells	NULL	NULL	NULL	NULL	gw60_circulation_103_25_3105_s_25	11425776	10  This effect appears to be mediated by inhibition of plasmin formation and possibly by PAI-1 binding to vitronectin, thereby preventing its interaction with vitronectin receptors present on vascular smooth muscle cells.	bind
22511	2	6340	7	NULL	NULL	NULL	NULL	PAI-1	GP		binds					vitronectin receptors	GP				NULL	vascular smooth muscle cells	NULL	NULL	NULL	NULL	gw60_circulation_103_25_3105_s_25	11425776	10  This effect appears to be mediated by inhibition of plasmin formation and possibly by PAI-1 binding to vitronectin, thereby preventing its interaction with vitronectin receptors present on vascular smooth muscle cells.	bind
22512	3	6340	7	NULL	NULL	NULL	NULL	statement 1	Process		prevents					statement 2	Process				NULL	vascular smooth muscle cells	NULL	NULL	NULL	NULL	gw60_circulation_103_25_3105_s_25	11425776	10  This effect appears to be mediated by inhibition of plasmin formation and possibly by PAI-1 binding to vitronectin, thereby preventing its interaction with vitronectin receptors present on vascular smooth muscle cells.	bind
19440	1	6342	5	NULL	NULL	0	NULL	osteonectin	NULL		bind	NULL				plasminogen	NULL				NULL	 in ECs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1852_s_29	10446063	10 11 12  Recently, it has been shown that osteonectin binds to plasminogen, 13 increases its activation and binding to collagen, 13  and induces the expression of type 1 plasminogen activator inhibitor in endothelial cells (ECs).	bind
19441	2	6342	5	NULL	NULL	0	NULL	osteonectin	NULL		increases	NULL				plasminogen	NULL	activation of			NULL	in ECs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1852_s_29	10446063	10 11 12  Recently, it has been shown that osteonectin binds to plasminogen, 13 increases its activation and binding to collagen, 13  and induces the expression of type 1 plasminogen activator inhibitor in endothelial cells (ECs).	bind
19442	3	6342	5	NULL	NULL	0	NULL	plasminogen	NULL		bind	NULL				collagen	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1852_s_29	10446063	10 11 12  Recently, it has been shown that osteonectin binds to plasminogen, 13 increases its activation and binding to collagen, 13  and induces the expression of type 1 plasminogen activator inhibitor in endothelial cells (ECs).	bind
19443	4	6342	5	NULL	NULL	0	NULL	osteonectin	NULL		increases	NULL				statement 3	NULL				NULL	in ECs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1852_s_29	10446063	10 11 12  Recently, it has been shown that osteonectin binds to plasminogen, 13 increases its activation and binding to collagen, 13  and induces the expression of type 1 plasminogen activator inhibitor in endothelial cells (ECs).	bind
19444	5	6342	5	NULL	NULL	0	NULL	osteonectin	NULL		induces	NULL				type 1 plasminogen activator inhibitor	NULL	expression of			NULL	in ECs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1852_s_29	10446063	10 11 12  Recently, it has been shown that osteonectin binds to plasminogen, 13 increases its activation and binding to collagen, 13  and induces the expression of type 1 plasminogen activator inhibitor in endothelial cells (ECs).	bind
28695	6	6342	5	NULL	NULL	0	NULL	ECs	NULL		is	NULL				endothelial cells	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1852_s_29	10446063	10 11 12  Recently, it has been shown that osteonectin binds to plasminogen, 13 increases its activation and binding to collagen, 13  and induces the expression of type 1 plasminogen activator inhibitor in endothelial cells (ECs).	bind
22513	1	6342	7	NULL	NULL	NULL	NULL	osteonectin	GP		binds to					plasminogen	GP				NULL	in ECs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1852_s_29	10446063	10 11 12  Recently, it has been shown that osteonectin binds to plasminogen, 13 increases its activation and binding to collagen, 13  and induces the expression of type 1 plasminogen activator inhibitor in endothelial cells (ECs).	bind
22514	2	6342	7	NULL	NULL	NULL	NULL	statement 1	Process		increases					plasminogen	GP	activation of			NULL	in ECs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1852_s_29	10446063	10 11 12  Recently, it has been shown that osteonectin binds to plasminogen, 13 increases its activation and binding to collagen, 13  and induces the expression of type 1 plasminogen activator inhibitor in endothelial cells (ECs).	bind
22515	3	6342	7	NULL	NULL	NULL	NULL	plasminogen	GP		binds to					collagen	GP				NULL	in ECs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1852_s_29	10446063	10 11 12  Recently, it has been shown that osteonectin binds to plasminogen, 13 increases its activation and binding to collagen, 13  and induces the expression of type 1 plasminogen activator inhibitor in endothelial cells (ECs).	bind
22516	4	6342	7	NULL	NULL	NULL	NULL	statement 1	Process		increases					statement 3	Process				NULL	in ECs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1852_s_29	10446063	10 11 12  Recently, it has been shown that osteonectin binds to plasminogen, 13 increases its activation and binding to collagen, 13  and induces the expression of type 1 plasminogen activator inhibitor in endothelial cells (ECs).	bind
22517	5	6342	7	NULL	NULL	NULL	NULL	osteonectin	GP		induces					type 1 plasminogen activator inhibitor	GP	expression of			NULL	in ECs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1852_s_29	10446063	10 11 12  Recently, it has been shown that osteonectin binds to plasminogen, 13 increases its activation and binding to collagen, 13  and induces the expression of type 1 plasminogen activator inhibitor in endothelial cells (ECs).	bind
22518	6	6342	7	NULL	NULL	NULL	NULL	ECs	Cell		is					Endothelial cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1852_s_29	10446063	10 11 12  Recently, it has been shown that osteonectin binds to plasminogen, 13 increases its activation and binding to collagen, 13  and induces the expression of type 1 plasminogen activator inhibitor in endothelial cells (ECs).	bind
22989	1	6344	5	NULL	NULL	0	NULL	GR	NULL	endogenous	bind	NULL					NULL			glucocorticoid-response element	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_33_30031_s_155	12039962	10 7M dexamethasone was added to activate the gene by the endogenous GR binding to the glucocorticoid-response element located from  333 to  319 of the promoter Ib sequence.	bind
22990	2	6344	5	10	NULL	0	NULL				is located from				glucocorticoid-response element					333 to 319 of promoter Ib sequence	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_30031_s_155	12039962	10 7M dexamethasone was added to activate the gene by the endogenous GR binding to the glucocorticoid-response element located from  333 to  319 of the promoter Ib sequence.	bind
22544	1	6344	7	NULL	NULL	NULL	NULL	GR	GP	endogenous	bind									glucocorticoid-response element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_30031_s_155	12039962	10 7M dexamethasone was added to activate the gene by the endogenous GR binding to the glucocorticoid-response element located from  333 to  319 of the promoter Ib sequence.	bind
22545	2	6344	7	NULL	NULL	0	NULL		NULL		located	NULL			glucocorticoid-response element		NULL			 from 333 to 319 of the promoter Ib sequence	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_33_30031_s_155	12039962	10 7M dexamethasone was added to activate the gene by the endogenous GR binding to the glucocorticoid-response element located from  333 to  319 of the promoter Ib sequence.	bind
22546	3	6344	7	NULL	NULL	NULL	NULL	dexamethasone	Chemical		activate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_30031_s_155	12039962	10 7M dexamethasone was added to activate the gene by the endogenous GR binding to the glucocorticoid-response element located from  333 to  319 of the promoter Ib sequence.	bind
19445	1	6345	5	NULL	NULL	0	NULL	AcrB	NULL		bind	NULL	directly			TolC	NULL				NULL		0	NULL	NULL	NULL	gw60_jantimicrobchemoth_52_2_176_s_84	12837741	10 According to the three-dimensional structure, AcrB directly binds to TolC.	bind
22549	1	6345	7	NULL	NULL	NULL	NULL	AcrB	GP		binds to		directly			TolC	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_52_2_176_s_84	12837741	10 According to the three-dimensional structure, AcrB directly binds to TolC.	bind
19477	1	6346	5	NULL	NULL	0	NULL	beta3 peptide	NULL	diphosphorylated	bind	NULL				myosin	NULL	purified			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_22_13878_s_172	9593734	10 mM phenylphosphate inhibited completely the binding of the diphosphorylated beta3 peptide to purified myosin in renatured blots (Fig.  4 C), indicating that the beta3-myosin interaction was phosphotyrosine-dependent under these binding conditions.	bind
19478	2	6346	5	NULL	NULL	0	NULL	phenylphosphate	NULL		inhibit	NULL	completely			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_22_13878_s_172	9593734	10 mM phenylphosphate inhibited completely the binding of the diphosphorylated beta3 peptide to purified myosin in renatured blots (Fig.  4 C), indicating that the beta3-myosin interaction was phosphotyrosine-dependent under these binding conditions.	bind
19479	3	6346	5	10	NULL	0	NULL	statement 1			is dependent on								phosphotyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_13878_s_172	9593734	10 mM phenylphosphate inhibited completely the binding of the diphosphorylated beta3 peptide to purified myosin in renatured blots (Fig.  4 C), indicating that the beta3-myosin interaction was phosphotyrosine-dependent under these binding conditions.	bind
19480	4	6346	5	NULL	NULL	0	NULL	statement 2	NULL		indicates	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_22_13878_s_172	9593734	10 mM phenylphosphate inhibited completely the binding of the diphosphorylated beta3 peptide to purified myosin in renatured blots (Fig.  4 C), indicating that the beta3-myosin interaction was phosphotyrosine-dependent under these binding conditions.	bind
22550	1	6346	7	NULL	NULL	NULL	NULL	  beta3 peptide	GP	diphosphorylated	binds					myosin	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_13878_s_172	9593734	10 mM phenylphosphate inhibited completely the binding of the diphosphorylated beta3 peptide to purified myosin in renatured blots (Fig.  4 C), indicating that the beta3-myosin interaction was phosphotyrosine-dependent under these binding conditions.	bind
22551	2	6346	7	NULL	NULL	NULL	NULL	statement 1	Process		depends on								phosphotyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_13878_s_172	9593734	10 mM phenylphosphate inhibited completely the binding of the diphosphorylated beta3 peptide to purified myosin in renatured blots (Fig.  4 C), indicating that the beta3-myosin interaction was phosphotyrosine-dependent under these binding conditions.	bind
22552	3	6346	7	NULL	NULL	NULL	NULL	phenylphosphate	Chemical		inhibits		completely			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_13878_s_172	9593734	10 mM phenylphosphate inhibited completely the binding of the diphosphorylated beta3 peptide to purified myosin in renatured blots (Fig.  4 C), indicating that the beta3-myosin interaction was phosphotyrosine-dependent under these binding conditions.	bind
29389	4	6346	7	NULL	NULL	NULL	NULL	statement 3	Process		indicates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_13878_s_172	9593734	10 mM phenylphosphate inhibited completely the binding of the diphosphorylated beta3 peptide to purified myosin in renatured blots (Fig.  4 C), indicating that the beta3-myosin interaction was phosphotyrosine-dependent under these binding conditions.	bind
19481	1	6351	5	NULL	NULL	0	NULL	Tel-2b	NULL		bind	NULL				E74 probe	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_12_9421_s_308	11108721	10 ng of wild-type competitor completely abolished binding of Tel-2b to the E74 probe.	bind
19482	2	6351	5	NULL	NULL	0	NULL	competitor	NULL	wild-type	abolishes	NULL	completely			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_12_9421_s_308	11108721	10 ng of wild-type competitor completely abolished binding of Tel-2b to the E74 probe.	bind
22553	1	6351	7	NULL	NULL	NULL	NULL	Tel-2b	GP		binds to					E74 probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_12_9421_s_308	11108721	10 ng of wild-type competitor completely abolished binding of Tel-2b to the E74 probe.	bind
22554	2	6351	7	NULL	NULL	NULL	NULL	competitor	GP	wild-type	abolish		completely			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_12_9421_s_308	11108721	10 ng of wild-type competitor completely abolished binding of Tel-2b to the E74 probe.	bind
19483	1	6352	5	NULL	NULL	0	NULL		NULL		bind	NULL		GST DH domain		Cdc42	NULL	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1624_s_185	12686614	10 nM GST DH and GST DHPH domains with and without adjacent SH3 domains were bound to recombinant Cdc42 (Figure  4C).	bind
19484	2	6352	5	NULL	NULL	0	NULL	statement 1	NULL		occurs with	NULL					NULL	adjacent	SH3 domains		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_4_1624_s_185	12686614	10 nM GST DH and GST DHPH domains with and without adjacent SH3 domains were bound to recombinant Cdc42 (Figure  4C).	bind
19485	3	6352	5	NULL	NULL	0	NULL	statement 1	NULL		occurs without	NULL					NULL	adjacent	SH3 domains		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_4_1624_s_185	12686614	10 nM GST DH and GST DHPH domains with and without adjacent SH3 domains were bound to recombinant Cdc42 (Figure  4C).	bind
19486	4	6352	5	NULL	NULL	0	NULL		NULL		bind	NULL		GST DHPH domain		Cdc42	NULL	recombinant			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_4_1624_s_185	12686614	10 nM GST DH and GST DHPH domains with and without adjacent SH3 domains were bound to recombinant Cdc42 (Figure  4C).	bind
19487	5	6352	5	NULL	NULL	0	NULL	statement 4	NULL		occurs with	NULL					NULL	adjacent	SH3 domains		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_4_1624_s_185	12686614	10 nM GST DH and GST DHPH domains with and without adjacent SH3 domains were bound to recombinant Cdc42 (Figure  4C).	bind
19488	6	6352	5	NULL	NULL	0	NULL	statement 4	NULL		occurs without	NULL					NULL	adjacent	SH3 domains		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_4_1624_s_185	12686614	10 nM GST DH and GST DHPH domains with and without adjacent SH3 domains were bound to recombinant Cdc42 (Figure  4C).	bind
22555	1	6352	7	NULL	NULL	NULL	NULL				bind			GST DH		Cdc42	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1624_s_185	12686614	10 nM GST DH and GST DHPH domains with and without adjacent SH3 domains were bound to recombinant Cdc42 (Figure  4C).	bind
22556	2	6352	7	NULL	NULL	NULL	NULL				bind			 GST DHPH		Cdc42	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1624_s_185	12686614	10 nM GST DH and GST DHPH domains with and without adjacent SH3 domains were bound to recombinant Cdc42 (Figure  4C).	bind
22557	3	6352	7	NULL	NULL	0	NULL		NULL		adjacent to	NULL		GST DH			NULL		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1624_s_185	12686614	10 nM GST DH and GST DHPH domains with and without adjacent SH3 domains were bound to recombinant Cdc42 (Figure  4C).	bind
22558	4	6352	7	NULL	NULL	0	NULL		NULL		adjacent to	NULL		GST DHPH			NULL		SH3 domain		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_4_1624_s_185	12686614	10 nM GST DH and GST DHPH domains with and without adjacent SH3 domains were bound to recombinant Cdc42 (Figure  4C).	bind
22559	5	6352	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1624_s_185	12686614	10 nM GST DH and GST DHPH domains with and without adjacent SH3 domains were bound to recombinant Cdc42 (Figure  4C).	bind
22560	6	6352	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs without					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1624_s_185	12686614	10 nM GST DH and GST DHPH domains with and without adjacent SH3 domains were bound to recombinant Cdc42 (Figure  4C).	bind
22561	7	6352	7	NULL	NULL	NULL	NULL	statement 2	Process		occurs with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1624_s_185	12686614	10 nM GST DH and GST DHPH domains with and without adjacent SH3 domains were bound to recombinant Cdc42 (Figure  4C).	bind
22562	8	6352	7	NULL	NULL	NULL	NULL	statement 2	Process		occurs without					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_4_1624_s_185	12686614	10 nM GST DH and GST DHPH domains with and without adjacent SH3 domains were bound to recombinant Cdc42 (Figure  4C).	bind
19489	1	6353	5	NULL	NULL	0	NULL	OHT-ER	NULL		bind	NULL				PI-9 ERU	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_6_5025_s_342	14617632	10 nM OHT induces PI-9 mRNA to levels  20% of those seen with MOX, and OHT-ER binds to the PI-9 ERU roughly 20% as well as MOX-ER.	bind
19490	2	6353	5	NULL	NULL	0	NULL	MOX-ER	NULL		bind	NULL				PI-9 ERU	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_6_5025_s_342	14617632	10 nM OHT induces PI-9 mRNA to levels  20% of those seen with MOX, and OHT-ER binds to the PI-9 ERU roughly 20% as well as MOX-ER.	bind
19491	3	6353	5	NULL	NULL	0	NULL	OHT	NULL		induces	NULL				PI-9 mRNA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_6_5025_s_342	14617632	10 nM OHT induces PI-9 mRNA to levels  20% of those seen with MOX, and OHT-ER binds to the PI-9 ERU roughly 20% as well as MOX-ER.	bind
19492	4	6353	5	10	NULL	0	NULL	MOX			induces					PI-9 mRNA					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_6_5025_s_342	14617632	10 nM OHT induces PI-9 mRNA to levels  20% of those seen with MOX, and OHT-ER binds to the PI-9 ERU roughly 20% as well as MOX-ER.	bind
22565	1	6353	7	NULL	NULL	NULL	NULL	 OHT	Chemical		induce					PI-9 mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_6_5025_s_342	14617632	10 nM OHT induces PI-9 mRNA to levels  20% of those seen with MOX, and OHT-ER binds to the PI-9 ERU roughly 20% as well as MOX-ER.	bind
22566	2	6353	7	NULL	NULL	NULL	NULL	MOX	Chemical		induce					PI-9 mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_6_5025_s_342	14617632	10 nM OHT induces PI-9 mRNA to levels  20% of those seen with MOX, and OHT-ER binds to the PI-9 ERU roughly 20% as well as MOX-ER.	bind
22567	3	6353	7	NULL	NULL	NULL	NULL	OHT-ER	Chemical		bind					PI-9 ERU	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_6_5025_s_342	14617632	10 nM OHT induces PI-9 mRNA to levels  20% of those seen with MOX, and OHT-ER binds to the PI-9 ERU roughly 20% as well as MOX-ER.	bind
22568	4	6353	7	NULL	NULL	NULL	NULL	MOX-ER	Chemical		bind					PI-9 ERU	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_6_5025_s_342	14617632	10 nM OHT induces PI-9 mRNA to levels  20% of those seen with MOX, and OHT-ER binds to the PI-9 ERU roughly 20% as well as MOX-ER.	bind
19494	1	6354	5	NULL	NULL	0	NULL	growth factors	NULL		promote	NULL				angiogenic function	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_462_s_214	11884291	10 Perlecan can bind growth factors that promote angiogenic and tumor growth functions.	bind
19495	2	6354	5	NULL	NULL	0	NULL	growth factors	NULL		promote	NULL				tumor growth function	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_462_s_214	11884291	10 Perlecan can bind growth factors that promote angiogenic and tumor growth functions.	bind
19496	3	6354	5	NULL	NULL	0	NULL	Perlecan	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_462_s_214	11884291	10 Perlecan can bind growth factors that promote angiogenic and tumor growth functions.	bind
19497	4	6354	5	NULL	NULL	0	NULL	Perlecan	NULL		bind	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_462_s_214	11884291	10 Perlecan can bind growth factors that promote angiogenic and tumor growth functions.	bind
22569	3	6354	7	NULL	NULL	NULL	NULL	Perlecan	Chemical		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_462_s_214	11884291	10 Perlecan can bind growth factors that promote angiogenic and tumor growth functions.	bind
22570	1	6354	7	NULL	NULL	NULL	NULL	growth factors	GP		promote					angiogenic function	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_462_s_214	11884291	10 Perlecan can bind growth factors that promote angiogenic and tumor growth functions.	bind
22571	2	6354	7	NULL	NULL	NULL	NULL	growth factors	GP		promote					tumor growth function	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_462_s_214	11884291	10 Perlecan can bind growth factors that promote angiogenic and tumor growth functions.	bind
29390	4	6354	7	NULL	NULL	NULL	NULL	Perlecan	Chemical		bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_462_s_214	11884291	10 Perlecan can bind growth factors that promote angiogenic and tumor growth functions.	bind
19498	1	6355	5	NULL	NULL	0	NULL	myosin	NULL		bind	NULL	weakly			actin	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20375_s_8	8702773	10 S cross-linked myosin weakly bound actin (dissociation constant > 500 muM) and did not move actin  in vitro.	bind
19499	2	6355	5	NULL	NULL	0	NULL	myosin	NULL		does not move	NULL				actin	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_271_34_20375_s_8	8702773	10 S cross-linked myosin weakly bound actin (dissociation constant > 500 muM) and did not move actin  in vitro.	bind
22572	1	6355	7	NULL	NULL	NULL	NULL	myosin	GP	S cross-linked	bind		weakly			actin	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20375_s_8	8702773	10 S cross-linked myosin weakly bound actin (dissociation constant > 500 muM) and did not move actin  in vitro.	bind
22573	2	6355	7	NULL	NULL	NULL	NULL	myosin	GP	S cross-linked	does not move					actin	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20375_s_8	8702773	10 S cross-linked myosin weakly bound actin (dissociation constant > 500 muM) and did not move actin  in vitro.	bind
19500	1	6356	5	10	NULL	0	NULL	nuclear protein			bind									NF-kappaB sequences	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1414_s_196	11557665	10 Similarly, LDL treatment appears to have little effect on the nuclear protein binding to the ICAM-1 - specific NF-kappaB sequences.	bind
19501	2	6356	5	10	NULL	0	NULL	LDL		treatment	effects		negligibly			statement 1					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1414_s_196	11557665	10 Similarly, LDL treatment appears to have little effect on the nuclear protein binding to the ICAM-1 - specific NF-kappaB sequences.	bind
54215	3	6356	5	10	NULL	0	NULL				is specific to				NF-kappaB sequences	ICAM-1					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1414_s_196	11557665	10 Similarly, LDL treatment appears to have little effect on the nuclear protein binding to the ICAM-1 - specific NF-kappaB sequences.	bind
22574	1	6356	7	NULL	NULL	NULL	NULL	nuclear protein	GP		bind									NF-kappaB sequence	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1414_s_196	11557665	10 Similarly, LDL treatment appears to have little effect on the nuclear protein binding to the ICAM-1 - specific NF-kappaB sequences.	bind
22575	2	6356	7	NULL	NULL	NULL	NULL				is specific to				NF-kappaB sequence	ICAM-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1414_s_196	11557665	10 Similarly, LDL treatment appears to have little effect on the nuclear protein binding to the ICAM-1 - specific NF-kappaB sequences.	bind
22576	3	6356	7	NULL	NULL	NULL	NULL	LDL	GP	treatment	effect		negligibly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1414_s_196	11557665	10 Similarly, LDL treatment appears to have little effect on the nuclear protein binding to the ICAM-1 - specific NF-kappaB sequences.	bind
19502	1	6357	5	NULL	NULL	0	NULL	Sp3	NULL		bind	NULL					NULL			GC box	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_168	12067897	10 Sp3 is bound to a GC box with an affinity and specificity comparable to those of Sp1 and, thereby, represses Sp1-mediated transcription.	bind
19503	3	6357	5	NULL	NULL	0	NULL	statement 1	NULL	affinity of	is comparable to	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_168	12067897	10 Sp3 is bound to a GC box with an affinity and specificity comparable to those of Sp1 and, thereby, represses Sp1-mediated transcription.	bind
19504	4	6357	5	NULL	NULL	0	NULL	statement 1	NULL	specificity of	is comparable to	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_168	12067897	10 Sp3 is bound to a GC box with an affinity and specificity comparable to those of Sp1 and, thereby, represses Sp1-mediated transcription.	bind
19505	5	6357	5	10	NULL	0	NULL	Sp1			mediate					transcription					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_168	12067897	10 Sp3 is bound to a GC box with an affinity and specificity comparable to those of Sp1 and, thereby, represses Sp1-mediated transcription.	bind
19506	6	6357	5	10	NULL	0	NULL	statement 1			repress					statement 5					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_168	12067897	10 Sp3 is bound to a GC box with an affinity and specificity comparable to those of Sp1 and, thereby, represses Sp1-mediated transcription.	bind
23074	2	6357	5	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL					NULL			GC box	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_168	12067897	10 Sp3 is bound to a GC box with an affinity and specificity comparable to those of Sp1 and, thereby, represses Sp1-mediated transcription.	bind
22577	1	6357	7	NULL	NULL	NULL	NULL	 Sp3	GP		bind									GC box	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_168	12067897	10 Sp3 is bound to a GC box with an affinity and specificity comparable to those of Sp1 and, thereby, represses Sp1-mediated transcription.	bind
22578	2	6357	7	NULL	NULL	NULL	NULL	Sp1	GP		bind									GC box	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_168	12067897	10 Sp3 is bound to a GC box with an affinity and specificity comparable to those of Sp1 and, thereby, represses Sp1-mediated transcription.	bind
22579	3	6357	7	NULL	NULL	NULL	NULL	statement 1	Process	affinity of	is comparable to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_168	12067897	10 Sp3 is bound to a GC box with an affinity and specificity comparable to those of Sp1 and, thereby, represses Sp1-mediated transcription.	bind
22580	5	6357	7	NULL	NULL	NULL	NULL	Sp1	GP		mediates					transcription	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_168	12067897	10 Sp3 is bound to a GC box with an affinity and specificity comparable to those of Sp1 and, thereby, represses Sp1-mediated transcription.	bind
22581	6	6357	7	NULL	NULL	NULL	NULL	statement 1	Process		repress					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_168	12067897	10 Sp3 is bound to a GC box with an affinity and specificity comparable to those of Sp1 and, thereby, represses Sp1-mediated transcription.	bind
22981	4	6357	7	NULL	NULL	NULL	NULL	statement 1	Process	specificity of	is comparable to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_168	12067897	10 Sp3 is bound to a GC box with an affinity and specificity comparable to those of Sp1 and, thereby, represses Sp1-mediated transcription.	bind
19507	1	6358	5	NULL	NULL	0	NULL	ERalpha	NULL		bind	NULL				target genes	NULL			estrogen-responsive promoters	NULL		0	NULL	NULL	NULL	gw60_circulation_105_22_2653_s_30	12045172	10 SRC-3 was recently shown to be associated with ERalpha bound to the estrogen-responsive promoters of target genes after estrogen treatment.	bind
19508	2	6358	5	NULL	NULL	0	NULL	SRC-3	NULL		is associated with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_22_2653_s_30	12045172	10 SRC-3 was recently shown to be associated with ERalpha bound to the estrogen-responsive promoters of target genes after estrogen treatment.	bind
19509	3	6358	5	NULL	NULL	0	NULL	statement 2	NULL		occurs after	NULL				estrogen	NULL	treatment			NULL		0	NULL	NULL	NULL	gw60_circulation_105_22_2653_s_30	12045172	10 SRC-3 was recently shown to be associated with ERalpha bound to the estrogen-responsive promoters of target genes after estrogen treatment.	bind
22634	1	6358	7	NULL	NULL	NULL	NULL	ERalpha 	GP		bind									estrogen-responsive promoter	NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_22_2653_s_30	12045172	10 SRC-3 was recently shown to be associated with ERalpha bound to the estrogen-responsive promoters of target genes after estrogen treatment.	bind
22635	3	6358	7	NULL	NULL	NULL	NULL	statement 2	Process		occurs after					estrogen	GP	treatment			NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_22_2653_s_30	12045172	10 SRC-3 was recently shown to be associated with ERalpha bound to the estrogen-responsive promoters of target genes after estrogen treatment.	bind
22636	2	6358	7	NULL	NULL	NULL	NULL	SRC-3	GP		associate with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_22_2653_s_30	12045172	10 SRC-3 was recently shown to be associated with ERalpha bound to the estrogen-responsive promoters of target genes after estrogen treatment.	bind
19510	1	6359	5	NULL	NULL	0	NULL	FKBP12.6	NULL		does not bind	NULL				RyR2	NULL	phosphorylated	serine-2808		NULL		0	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_26	14715536	10 These observations have led to the notions that FKBP12.6 cannot bind to serine-2808 phosphorylated RyR2 and that PKA phosphorylation physiologically regulates FKBP12.6-RyR2 interaction.	bind
19511	2	6359	5	10	NULL	0	NULL	PKA	NULL	phosphorylation	regulates	NULL	physiologically			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_26	14715536	10 These observations have led to the notions that FKBP12.6 cannot bind to serine-2808 phosphorylated RyR2 and that PKA phosphorylation physiologically regulates FKBP12.6-RyR2 interaction.	bind
22637	1	6359	7	NULL	NULL	NULL	NULL	FKBP12.6	GP		does not bind					RyR2	GP	phosphorylated	serine-2808		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_26	14715536	10 These observations have led to the notions that FKBP12.6 cannot bind to serine-2808 phosphorylated RyR2 and that PKA phosphorylation physiologically regulates FKBP12.6-RyR2 interaction.	bind
22638	2	6359	7	NULL	NULL	NULL	NULL	PKA	GP	phosphorylation of	regulates		physiologically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_26	14715536	10 These observations have led to the notions that FKBP12.6 cannot bind to serine-2808 phosphorylated RyR2 and that PKA phosphorylation physiologically regulates FKBP12.6-RyR2 interaction.	bind
19512	1	6361	5	NULL	NULL	0	NULL	FKBP12.6	NULL		bind	NULL				RyR2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_225	14715536	10 This is surprising, given our previous observation that a large region in RyR2 (residues 1937 to 4967) encompassing the serine-2808 phosphorylation site and the previously mapped FKBP12.6 binding site (residues 2427 through 2428) is not required for FKBP12.6 binding to RyR2.	bind
19513	2	6361	5	10	NULL	0	NULL	RyR2			encompass			\tresidues 1937 to 4967					serine-2808 phosphorylation site		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_225	14715536	10 This is surprising, given our previous observation that a large region in RyR2 (residues 1937 to 4967) encompassing the serine-2808 phosphorylation site and the previously mapped FKBP12.6 binding site (residues 2427 through 2428) is not required for FKBP12.6 binding to RyR2.	bind
19514	3	6361	5	10	NULL	0	NULL	RyR2			encompass			residues 2427 through 2428					FKBP12.6 binding site		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_225	14715536	10 This is surprising, given our previous observation that a large region in RyR2 (residues 1937 to 4967) encompassing the serine-2808 phosphorylation site and the previously mapped FKBP12.6 binding site (residues 2427 through 2428) is not required for FKBP12.6 binding to RyR2.	bind
19515	4	6361	5	NULL	NULL	0	NULL	statement 1	NULL		does not require	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_225	14715536	10 This is surprising, given our previous observation that a large region in RyR2 (residues 1937 to 4967) encompassing the serine-2808 phosphorylation site and the previously mapped FKBP12.6 binding site (residues 2427 through 2428) is not required for FKBP12.6 binding to RyR2.	bind
19516	5	6361	5	NULL	NULL	0	NULL	statement 1	NULL		does not require	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_225	14715536	10 This is surprising, given our previous observation that a large region in RyR2 (residues 1937 to 4967) encompassing the serine-2808 phosphorylation site and the previously mapped FKBP12.6 binding site (residues 2427 through 2428) is not required for FKBP12.6 binding to RyR2.	bind
22639	1	6361	7	NULL	NULL	NULL	NULL	FKBP12.6	GP		bind					RyR2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_225	14715536	10 This is surprising, given our previous observation that a large region in RyR2 (residues 1937 to 4967) encompassing the serine-2808 phosphorylation site and the previously mapped FKBP12.6 binding site (residues 2427 through 2428) is not required for FKBP12.6 binding to RyR2.	bind
22640	2	6361	7	NULL	NULL	NULL	NULL	RyR2	GP		encompass			residues 1937 to 4967					serine-2808 phosphorylation site		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_225	14715536	10 This is surprising, given our previous observation that a large region in RyR2 (residues 1937 to 4967) encompassing the serine-2808 phosphorylation site and the previously mapped FKBP12.6 binding site (residues 2427 through 2428) is not required for FKBP12.6 binding to RyR2.	bind
22641	3	6361	7	NULL	NULL	NULL	NULL	RyR2	GP		encompass			residues 2427 through 2428					FKBP12.6 binding site		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_225	14715536	10 This is surprising, given our previous observation that a large region in RyR2 (residues 1937 to 4967) encompassing the serine-2808 phosphorylation site and the previously mapped FKBP12.6 binding site (residues 2427 through 2428) is not required for FKBP12.6 binding to RyR2.	bind
22642	4	6361	7	NULL	NULL	NULL	NULL	statement 2	Process		is not required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_225	14715536	10 This is surprising, given our previous observation that a large region in RyR2 (residues 1937 to 4967) encompassing the serine-2808 phosphorylation site and the previously mapped FKBP12.6 binding site (residues 2427 through 2428) is not required for FKBP12.6 binding to RyR2.	bind
54216	5	6361	7	NULL	NULL	NULL	NULL	statement 3	Process		is not required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_225	14715536	10 This is surprising, given our previous observation that a large region in RyR2 (residues 1937 to 4967) encompassing the serine-2808 phosphorylation site and the previously mapped FKBP12.6 binding site (residues 2427 through 2428) is not required for FKBP12.6 binding to RyR2.	bind
19517	1	6362	5	NULL	NULL	0	NULL	VEGF	NULL		bind	NULL				VEGFR-1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_11_1443_s_22	15192038	10 VEGF binds to VEGFR-1 and VEGFR-2 and induces vasculogenesis, angiogenesis, and vascular permeability.	bind
19518	2	6362	5	NULL	NULL	0	NULL	VEGF	NULL		bind	NULL				VEGFR-2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_11_1443_s_22	15192038	10 VEGF binds to VEGFR-1 and VEGFR-2 and induces vasculogenesis, angiogenesis, and vascular permeability.	bind
19519	3	6362	5	NULL	NULL	0	NULL	VEGF	NULL		induces	NULL				vasculogenesis	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_11_1443_s_22	15192038	10 VEGF binds to VEGFR-1 and VEGFR-2 and induces vasculogenesis, angiogenesis, and vascular permeability.	bind
19520	4	6362	5	NULL	NULL	0	NULL	VEGF	NULL		induces	NULL				angiogenesis	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_11_1443_s_22	15192038	10 VEGF binds to VEGFR-1 and VEGFR-2 and induces vasculogenesis, angiogenesis, and vascular permeability.	bind
19521	5	6362	5	NULL	NULL	0	NULL	VEGF	NULL		induces	NULL				vascular permeability	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_11_1443_s_22	15192038	10 VEGF binds to VEGFR-1 and VEGFR-2 and induces vasculogenesis, angiogenesis, and vascular permeability.	bind
22643	1	6362	7	NULL	NULL	NULL	NULL	VEGF	GP		binds					 VEGFR-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1443_s_22	15192038	10 VEGF binds to VEGFR-1 and VEGFR-2 and induces vasculogenesis, angiogenesis, and vascular permeability.	bind
22644	2	6362	7	NULL	NULL	NULL	NULL	VEGF	GP		binds					VEGFR-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1443_s_22	15192038	10 VEGF binds to VEGFR-1 and VEGFR-2 and induces vasculogenesis, angiogenesis, and vascular permeability.	bind
22645	3	6362	7	NULL	NULL	NULL	NULL	statement 1	Process		induces					vasculogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1443_s_22	15192038	10 VEGF binds to VEGFR-1 and VEGFR-2 and induces vasculogenesis, angiogenesis, and vascular permeability.	bind
22646	4	6362	7	NULL	NULL	NULL	NULL	statement 1	Process		induces					angiogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1443_s_22	15192038	10 VEGF binds to VEGFR-1 and VEGFR-2 and induces vasculogenesis, angiogenesis, and vascular permeability.	bind
22647	5	6362	7	NULL	NULL	NULL	NULL	statement 1	Process		induces					vascular permeability	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1443_s_22	15192038	10 VEGF binds to VEGFR-1 and VEGFR-2 and induces vasculogenesis, angiogenesis, and vascular permeability.	bind
22648	6	6362	7	NULL	NULL	NULL	NULL	statement 2	Process		induces					vasculogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1443_s_22	15192038	10 VEGF binds to VEGFR-1 and VEGFR-2 and induces vasculogenesis, angiogenesis, and vascular permeability.	bind
22649	7	6362	7	NULL	NULL	NULL	NULL	statement 2	Process		induces					angiogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1443_s_22	15192038	10 VEGF binds to VEGFR-1 and VEGFR-2 and induces vasculogenesis, angiogenesis, and vascular permeability.	bind
22650	8	6362	7	NULL	NULL	NULL	NULL	statement 2	Process		induces					vascular permeability	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1443_s_22	15192038	10 VEGF binds to VEGFR-1 and VEGFR-2 and induces vasculogenesis, angiogenesis, and vascular permeability.	bind
19522	1	6363	5	NULL	NULL	0	NULL	[ H]LPS	NULL		bind	NULL	significantly			CD14	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_361_s_35	7529231	10%  human serum was required for  significant [ H]LPS binding to CD14.	bind
19523	2	6363	5	NULL	NULL	0	NULL	serum	NULL	human	is required for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_361_s_35	7529231	10%  human serum was required for  significant [ H]LPS binding to CD14.	bind
22651	1	6363	7	NULL	NULL	NULL	NULL	[ H]LPS	Chemical		bind					CD14	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_361_s_35	7529231	10%  human serum was required for  significant [ H]LPS binding to CD14.	bind
22652	2	6363	7	NULL	NULL	NULL	NULL	serum	OrganismPart	human	is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_361_s_35	7529231	10%  human serum was required for  significant [ H]LPS binding to CD14.	bind
19524	1	6364	5	NULL	NULL	0	NULL	betabeta receptor dimer	NULL		bind	NULL				PDGF-BB	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_6_1763_s_17	10362801	10, 11 The betabeta receptor dimer binds only PDGF-BB, the alphabeta receptor dimer binds PDGF-BB and PDGF-AB, and the alphaalpha receptor dimer binds all three types of PDGF dimers.	bind
19525	2	6364	5	NULL	NULL	0	NULL	alphabeta receptor dimer	NULL		bind	NULL				PDGF-BB	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_6_1763_s_17	10362801	10, 11 The betabeta receptor dimer binds only PDGF-BB, the alphabeta receptor dimer binds PDGF-BB and PDGF-AB, and the alphaalpha receptor dimer binds all three types of PDGF dimers.	bind
19526	3	6364	5	NULL	NULL	0	NULL	alphabeta receptor dimer	NULL		bind	NULL				PDGF-AB	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_6_1763_s_17	10362801	10, 11 The betabeta receptor dimer binds only PDGF-BB, the alphabeta receptor dimer binds PDGF-BB and PDGF-AB, and the alphaalpha receptor dimer binds all three types of PDGF dimers.	bind
19527	4	6364	5	10	NULL	0	NULL	alphaalpha receptor dimer	NULL		bind	NULL				PDGF-AB	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1763_s_17	10362801	10, 11 The betabeta receptor dimer binds only PDGF-BB, the alphabeta receptor dimer binds PDGF-BB and PDGF-AB, and the alphaalpha receptor dimer binds all three types of PDGF dimers.	bind
54217	5	6364	5	10	NULL	0	NULL	alphaalpha receptor dimer			bind					PDGF-BB					NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_6_1763_s_17	10362801	10, 11 The betabeta receptor dimer binds only PDGF-BB, the alphabeta receptor dimer binds PDGF-BB and PDGF-AB, and the alphaalpha receptor dimer binds all three types of PDGF dimers.	bind
22653	1	6364	7	NULL	NULL	NULL	NULL	betabeta receptor dimer	GP		binds					PDGF-BB	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1763_s_17	10362801	10, 11 The betabeta receptor dimer binds only PDGF-BB, the alphabeta receptor dimer binds PDGF-BB and PDGF-AB, and the alphaalpha receptor dimer binds all three types of PDGF dimers.	bind
22654	2	6364	7	NULL	NULL	NULL	NULL	alphabeta receptor dimer 	GP		binds					PDGF-BB	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1763_s_17	10362801	10, 11 The betabeta receptor dimer binds only PDGF-BB, the alphabeta receptor dimer binds PDGF-BB and PDGF-AB, and the alphaalpha receptor dimer binds all three types of PDGF dimers.	bind
22655	3	6364	7	NULL	NULL	NULL	NULL	alphabeta receptor dimer 	GP		binds					PDGF-AB	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1763_s_17	10362801	10, 11 The betabeta receptor dimer binds only PDGF-BB, the alphabeta receptor dimer binds PDGF-BB and PDGF-AB, and the alphaalpha receptor dimer binds all three types of PDGF dimers.	bind
22656	4	6364	7	NULL	NULL	NULL	NULL	alphaalpha receptor dimer	GP		binds					PDGF-BB	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1763_s_17	10362801	10, 11 The betabeta receptor dimer binds only PDGF-BB, the alphabeta receptor dimer binds PDGF-BB and PDGF-AB, and the alphaalpha receptor dimer binds all three types of PDGF dimers.	bind
22657	5	6364	7	NULL	NULL	NULL	NULL	alphaalpha receptor dimer	GP		binds					PDGF-AB	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1763_s_17	10362801	10, 11 The betabeta receptor dimer binds only PDGF-BB, the alphabeta receptor dimer binds PDGF-BB and PDGF-AB, and the alphaalpha receptor dimer binds all three types of PDGF dimers.	bind
23075	1	6365	5	NULL	NULL	0	NULL	cMyBP-C	NULL		undergoes	NULL				trimerization	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_9_1249_s_19	15059932	10,11  It has been proposed that cMyBP-C trimerizes to form a collar around the thick filament 2,3,7   with interdomain binding of C5 and C7 of one molecule to C8 and C10, respectively, of another.	bind
23076	2	6365	5	NULL	NULL	0	NULL	statement 1	NULL		forms	NULL				collar	NULL				NULL	around thick filament	0	NULL	NULL	NULL	gw70_circulationres_94_9_1249_s_19	15059932	10,11  It has been proposed that cMyBP-C trimerizes to form a collar around the thick filament 2,3,7   with interdomain binding of C5 and C7 of one molecule to C8 and C10, respectively, of another.	bind
23077	3	6365	5	NULL	NULL	0	NULL	myosin binding protein-C	NULL	interdomains of	bind	NULL		C5		myosin binding protein-C	NULL		C8		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1249_s_19	15059932	10,11  It has been proposed that cMyBP-C trimerizes to form a collar around the thick filament 2,3,7   with interdomain binding of C5 and C7 of one molecule to C8 and C10, respectively, of another.	bind
23078	4	6365	5	NULL	NULL	0	NULL	myosin binding protein-C	NULL	interdomains of	bind	NULL		C7		myosin binding protein-C	NULL		C10		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1249_s_19	15059932	10,11  It has been proposed that cMyBP-C trimerizes to form a collar around the thick filament 2,3,7   with interdomain binding of C5 and C7 of one molecule to C8 and C10, respectively, of another.	bind
22658	1	6365	7	NULL	NULL	NULL	NULL	cMyBP-C	GP		undergoes					trimerization	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1249_s_19	15059932	10,11  It has been proposed that cMyBP-C trimerizes to form a collar around the thick filament 2,3,7   with interdomain binding of C5 and C7 of one molecule to C8 and C10, respectively, of another.	bind
22659	3	6365	7	NULL	NULL	NULL	NULL	cMyBP-C	GP	interdomain	binds to			C5 		cMyBP-C	GP	interdomain	C8		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1249_s_19	15059932	10,11  It has been proposed that cMyBP-C trimerizes to form a collar around the thick filament 2,3,7   with interdomain binding of C5 and C7 of one molecule to C8 and C10, respectively, of another.	bind
22660	4	6365	7	NULL	NULL	NULL	NULL	cMyBP-C	GP	interdomain	binds to			C7		cMyBP-C	GP	interdomain	C10		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1249_s_19	15059932	10,11  It has been proposed that cMyBP-C trimerizes to form a collar around the thick filament 2,3,7   with interdomain binding of C5 and C7 of one molecule to C8 and C10, respectively, of another.	bind
29391	2	6365	7	NULL	NULL	NULL	NULL	statement 1	Process		forms					collar	OrganismPart				NULL	around thick filament	NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1249_s_19	15059932	10,11  It has been proposed that cMyBP-C trimerizes to form a collar around the thick filament 2,3,7   with interdomain binding of C5 and C7 of one molecule to C8 and C10, respectively, of another.	bind
19619	1	6370	5	NULL	NULL	0	NULL	estrogen receptor	NULL	human	bind	NULL					NULL			estrogen response element	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_597	11452016	100       Nardulli,A.M., Greene,G.L. and Shapiro,D.J. (1993) Human estrogen receptor bound to an estrogen response element bends DNA.	bind
19620	2	6370	5	NULL	NULL	0	NULL	statement 1	NULL		bends	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_597	11452016	100       Nardulli,A.M., Greene,G.L. and Shapiro,D.J. (1993) Human estrogen receptor bound to an estrogen response element bends DNA.	bind
22661	1	6370	7	NULL	NULL	NULL	NULL	estrogen receptor	GP	human	binds to									estrogen response element 	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_597	11452016	100       Nardulli,A.M., Greene,G.L. and Shapiro,D.J. (1993) Human estrogen receptor bound to an estrogen response element bends DNA.	bind
22662	2	6370	7	NULL	NULL	NULL	NULL	statement 1	Process		bends 					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_597	11452016	100       Nardulli,A.M., Greene,G.L. and Shapiro,D.J. (1993) Human estrogen receptor bound to an estrogen response element bends DNA.	bind
23079	1	6375	5	NULL	NULL	0	NULL	[3]ALDO	NULL		bind	NULL				surface	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_98_1_157_s_4	8690788	100 nM 8-Br-cGMP decreased  surface [3]ALDO binding by 42 plus-or-minus 4% but increased crypt  [3]ALDO binding by 52 plus-or-minus 16%.	bind
23080	2	6375	5	NULL	NULL	0	NULL	[3]ALDO	NULL		bind	NULL				crypt	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_98_1_157_s_4	8690788	100 nM 8-Br-cGMP decreased  surface [3]ALDO binding by 42 plus-or-minus 4% but increased crypt  [3]ALDO binding by 52 plus-or-minus 16%.	bind
28697	3	6375	5	NULL	NULL	0	NULL	8-Br-cGMP	NULL		decreases	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_1_157_s_4	8690788	100 nM 8-Br-cGMP decreased  surface [3]ALDO binding by 42 plus-or-minus 4% but increased crypt  [3]ALDO binding by 52 plus-or-minus 16%.	bind
28698	4	6375	5	NULL	NULL	0	NULL	8-Br-cGMP	NULL		increases	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_1_157_s_4	8690788	100 nM 8-Br-cGMP decreased  surface [3]ALDO binding by 42 plus-or-minus 4% but increased crypt  [3]ALDO binding by 52 plus-or-minus 16%.	bind
22713	1	6375	7	NULL	NULL	NULL	NULL	[3]ALDO	Chemical		bind					surface	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_98_1_157_s_4	8690788	100 nM 8-Br-cGMP decreased  surface [3]ALDO binding by 42 plus-or-minus 4% but increased crypt  [3]ALDO binding by 52 plus-or-minus 16%.	bind
22714	2	6375	7	NULL	NULL	NULL	NULL	 [3]ALDO	Chemical		bind					crypt	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_98_1_157_s_4	8690788	100 nM 8-Br-cGMP decreased  surface [3]ALDO binding by 42 plus-or-minus 4% but increased crypt  [3]ALDO binding by 52 plus-or-minus 16%.	bind
22715	3	6375	7	NULL	NULL	NULL	NULL	 8-Br-cGMP 	Chemical		decrease					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_98_1_157_s_4	8690788	100 nM 8-Br-cGMP decreased  surface [3]ALDO binding by 42 plus-or-minus 4% but increased crypt  [3]ALDO binding by 52 plus-or-minus 16%.	bind
22716	4	6375	7	NULL	NULL	NULL	NULL	 8-Br-cGMP 	Chemical		increase					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_98_1_157_s_4	8690788	100 nM 8-Br-cGMP decreased  surface [3]ALDO binding by 42 plus-or-minus 4% but increased crypt  [3]ALDO binding by 52 plus-or-minus 16%.	bind
19621	1	6378	5	10	NULL	0	NULL	Hsc70			bind					clathrin			heavy chain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_8439_s_227	10722678	100% complex indicates one Hsc70 bound per clathrin heavy chain in the reaction mixture.	bind
22718	1	6378	7	NULL	NULL	NULL	NULL	Hsc70	GP		bind					clathrin	GP		heavy chain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_8439_s_227	10722678	100% complex indicates one Hsc70 bound per clathrin heavy chain in the reaction mixture.	bind
19622	1	6379	5	NULL	NULL	0	NULL	[gamma-32]GTP	NULL		bind	NULL				Arf1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_11_10128_s_244	15644318	100% refers the amount of [gamma-32]GTP bound to Arf1 or RhoA in the absence of M9b-tail.	bind
19623	2	6379	5	NULL	NULL	0	NULL	statement 1	NULL		in the absence of	NULL				M9b-tail	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_11_10128_s_244	15644318	100% refers the amount of [gamma-32]GTP bound to Arf1 or RhoA in the absence of M9b-tail.	bind
19624	3	6379	5	NULL	NULL	0	NULL	[gamma-32]GTP	NULL		bind	NULL				RhoA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_11_10128_s_244	15644318	100% refers the amount of [gamma-32]GTP bound to Arf1 or RhoA in the absence of M9b-tail.	bind
19625	4	6379	5	NULL	NULL	0	NULL	statement 3	NULL		in the absence of	NULL				M9b-tail	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_11_10128_s_244	15644318	100% refers the amount of [gamma-32]GTP bound to Arf1 or RhoA in the absence of M9b-tail.	bind
19626	5	6379	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_11_10128_s_244	15644318	100% refers the amount of [gamma-32]GTP bound to Arf1 or RhoA in the absence of M9b-tail.	bind
22720	1	6379	7	NULL	NULL	NULL	NULL	[gamma-32]GTP 	Chemical		bind					Arf1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10128_s_244	15644318	100% refers the amount of [gamma-32]GTP bound to Arf1 or RhoA in the absence of M9b-tail.	bind
22722	2	6379	7	NULL	NULL	NULL	NULL	[gamma-32]GTP	Chemical		bind					RhoA 	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10128_s_244	15644318	100% refers the amount of [gamma-32]GTP bound to Arf1 or RhoA in the absence of M9b-tail.	bind
22723	3	6379	7	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10128_s_244	15644318	100% refers the amount of [gamma-32]GTP bound to Arf1 or RhoA in the absence of M9b-tail.	bind
22725	4	6379	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs in absence of					M9b-tail	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10128_s_244	15644318	100% refers the amount of [gamma-32]GTP bound to Arf1 or RhoA in the absence of M9b-tail.	bind
22726	5	6379	7	NULL	NULL	NULL	NULL	statement 2	Process		occurs in  absence of					M9b-tail	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10128_s_244	15644318	100% refers the amount of [gamma-32]GTP bound to Arf1 or RhoA in the absence of M9b-tail.	bind
19627	1	6380	5	NULL	NULL	0	NULL	VEGF	NULL		bind	NULL				alpha2M-MA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_26806_s_140	10862607	100% represents total VEGF bound to either alpha2M-MA or alpha2M-PPE.	bind
19628	2	6380	5	NULL	NULL	0	NULL	VEGF	NULL		bind	NULL				alpha2M-PPE	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_26806_s_140	10862607	100% represents total VEGF bound to either alpha2M-MA or alpha2M-PPE.	bind
19629	3	6380	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_26806_s_140	10862607	100% represents total VEGF bound to either alpha2M-MA or alpha2M-PPE.	bind
22732	1	6380	7	NULL	NULL	NULL	NULL	VEGF	GP		bind					alpha2M-MA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_35_26806_s_140	10862607	100% represents total VEGF bound to either alpha2M-MA or alpha2M-PPE.	bind
22733	2	6380	7	NULL	NULL	NULL	NULL	VEGF	GP		bind					alpha2M-PPE	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_35_26806_s_140	10862607	100% represents total VEGF bound to either alpha2M-MA or alpha2M-PPE.	bind
29394	3	6380	7	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_35_26806_s_140	10862607	100% represents total VEGF bound to either alpha2M-MA or alpha2M-PPE.	bind
19630	1	6381	5	NULL	NULL	0	NULL	HSP	NULL		bind	NULL				HIF-1beta/ARNT	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_1_15_s_188	15637304	100,101  HSP binding to HIF-1beta/ARNT acts as a chaperone, maintaining HIF-1alpha in a receptive state for signaling.	bind
19631	2	6381	5	NULL	NULL	0	NULL	statement 1	NULL		acts as	NULL				chaperone	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_1_15_s_188	15637304	100,101  HSP binding to HIF-1beta/ARNT acts as a chaperone, maintaining HIF-1alpha in a receptive state for signaling.	bind
19632	3	6381	5	10	NULL	0	NULL	HIF-1alpha	NULL		is maintained in	NULL				receptive state	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_1_15_s_188	15637304	100,101  HSP binding to HIF-1beta/ARNT acts as a chaperone, maintaining HIF-1alpha in a receptive state for signaling.	bind
19633	4	6381	5	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_1_15_s_188	15637304	100,101  HSP binding to HIF-1beta/ARNT acts as a chaperone, maintaining HIF-1alpha in a receptive state for signaling.	bind
22735	1	6381	7	NULL	NULL	NULL	NULL	HSP	GP		bind					HIF-1beta/ARNT	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_1_15_s_188	15637304	100,101  HSP binding to HIF-1beta/ARNT acts as a chaperone, maintaining HIF-1alpha in a receptive state for signaling.	bind
22736	2	6381	7	NULL	NULL	NULL	NULL	statement 1	Process		acts as a					chaperone	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_1_15_s_188	15637304	100,101  HSP binding to HIF-1beta/ARNT acts as a chaperone, maintaining HIF-1alpha in a receptive state for signaling.	bind
22737	3	6381	7	NULL	NULL	NULL	NULL	HIF-1 alpha	GP		is maintained at					receptive state	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_1_15_s_188	15637304	100,101  HSP binding to HIF-1beta/ARNT acts as a chaperone, maintaining HIF-1alpha in a receptive state for signaling.	bind
23081	1	6382	5	NULL	NULL	0	NULL	SR-BI	NULL		mediate	NULL				cholesterol efflux	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_150	11145929	102  However, SR-BI - mediated cholesterol efflux does not simply reflect the binding of HDL to cells, inasmuch as binding of HDL to CD36, which is another HDL binding scavenger receptor, does not facilitate cholesterol efflux.	bind
23082	2	6382	5	NULL	NULL	0	NULL	HDL	NULL		bind	NULL				cells	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_150	11145929	102  However, SR-BI - mediated cholesterol efflux does not simply reflect the binding of HDL to cells, inasmuch as binding of HDL to CD36, which is another HDL binding scavenger receptor, does not facilitate cholesterol efflux.	bind
23083	3	6382	5	NULL	NULL	0	NULL	statement 1	NULL		reflects	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_150	11145929	102  However, SR-BI - mediated cholesterol efflux does not simply reflect the binding of HDL to cells, inasmuch as binding of HDL to CD36, which is another HDL binding scavenger receptor, does not facilitate cholesterol efflux.	bind
23084	4	6382	5	NULL	NULL	0	NULL	HDL	NULL		bind	NULL				CD36	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_150	11145929	102  However, SR-BI - mediated cholesterol efflux does not simply reflect the binding of HDL to cells, inasmuch as binding of HDL to CD36, which is another HDL binding scavenger receptor, does not facilitate cholesterol efflux.	bind
23085	5	6382	5	NULL	NULL	0	NULL	CD36	NULL		is	NULL				HDL binding scavenger receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_150	11145929	102  However, SR-BI - mediated cholesterol efflux does not simply reflect the binding of HDL to cells, inasmuch as binding of HDL to CD36, which is another HDL binding scavenger receptor, does not facilitate cholesterol efflux.	bind
23086	6	6382	5	NULL	NULL	0	NULL	statement 4	NULL		does not facilitate	NULL				cholesterol efflux	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_150	11145929	102  However, SR-BI - mediated cholesterol efflux does not simply reflect the binding of HDL to cells, inasmuch as binding of HDL to CD36, which is another HDL binding scavenger receptor, does not facilitate cholesterol efflux.	bind
22738	1	6382	7	NULL	NULL	NULL	NULL	HDL	GP		bind					cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_150	11145929	102  However, SR-BI - mediated cholesterol efflux does not simply reflect the binding of HDL to cells, inasmuch as binding of HDL to CD36, which is another HDL binding scavenger receptor, does not facilitate cholesterol efflux.	bind
22739	2	6382	7	NULL	NULL	NULL	NULL	HDL	GP		bind					CD36	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_150	11145929	102  However, SR-BI - mediated cholesterol efflux does not simply reflect the binding of HDL to cells, inasmuch as binding of HDL to CD36, which is another HDL binding scavenger receptor, does not facilitate cholesterol efflux.	bind
22740	3	6382	7	NULL	NULL	NULL	NULL	SR-BI	Cell		mediates					cholesterol 	Chemical	efflux of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_150	11145929	102  However, SR-BI - mediated cholesterol efflux does not simply reflect the binding of HDL to cells, inasmuch as binding of HDL to CD36, which is another HDL binding scavenger receptor, does not facilitate cholesterol efflux.	bind
22743	4	6382	7	NULL	NULL	NULL	NULL	statement 3	Process		does not reflect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_150	11145929	102  However, SR-BI - mediated cholesterol efflux does not simply reflect the binding of HDL to cells, inasmuch as binding of HDL to CD36, which is another HDL binding scavenger receptor, does not facilitate cholesterol efflux.	bind
22745	5	6382	7	NULL	NULL	NULL	NULL	CD36	Cell		is					HDL binding scavenger receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_150	11145929	102  However, SR-BI - mediated cholesterol efflux does not simply reflect the binding of HDL to cells, inasmuch as binding of HDL to CD36, which is another HDL binding scavenger receptor, does not facilitate cholesterol efflux.	bind
22746	6	6382	7	NULL	NULL	NULL	NULL	statement 5	Process		does not facilitate					cholesterol	Chemical	efflux of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_150	11145929	102  However, SR-BI - mediated cholesterol efflux does not simply reflect the binding of HDL to cells, inasmuch as binding of HDL to CD36, which is another HDL binding scavenger receptor, does not facilitate cholesterol efflux.	bind
19634	1	6383	5	NULL	NULL	0	NULL	HDL	NULL		bind	NULL				SR-BI	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_151	11145929	103  Therefore, it has been suggested that binding of HDL to SR-BI facilitates the bidirectional flux between HDL and plasma membrane by reorganization of lipids within cholesterol- and caveolae-rich domains within the plasma membrane.	bind
19635	2	6383	5	NULL	NULL	0	NULL	statement 1	NULL		facilitates	NULL				bidirectional flux	NULL				NULL	between HDL and plasma membrane	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_151	11145929	103  Therefore, it has been suggested that binding of HDL to SR-BI facilitates the bidirectional flux between HDL and plasma membrane by reorganization of lipids within cholesterol- and caveolae-rich domains within the plasma membrane.	bind
19636	3	6383	5	NULL	NULL	0	NULL	lipids	NULL		are reorganized within	NULL					NULL		cholesterol-rich domains		NULL	within the plasma membrane	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_151	11145929	103  Therefore, it has been suggested that binding of HDL to SR-BI facilitates the bidirectional flux between HDL and plasma membrane by reorganization of lipids within cholesterol- and caveolae-rich domains within the plasma membrane.	bind
19637	4	6383	5	NULL	NULL	0	NULL	lipids	NULL		are reorganized within	NULL					NULL		caveolae-rich domains		NULL	within the plasma membrane	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_151	11145929	103  Therefore, it has been suggested that binding of HDL to SR-BI facilitates the bidirectional flux between HDL and plasma membrane by reorganization of lipids within cholesterol- and caveolae-rich domains within the plasma membrane.	bind
19638	5	6383	5	NULL	NULL	0	NULL	statement 3	NULL		is required for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_151	11145929	103  Therefore, it has been suggested that binding of HDL to SR-BI facilitates the bidirectional flux between HDL and plasma membrane by reorganization of lipids within cholesterol- and caveolae-rich domains within the plasma membrane.	bind
19639	6	6383	5	NULL	NULL	0	NULL	statement 4	NULL		is required for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_151	11145929	103  Therefore, it has been suggested that binding of HDL to SR-BI facilitates the bidirectional flux between HDL and plasma membrane by reorganization of lipids within cholesterol- and caveolae-rich domains within the plasma membrane.	bind
22747	1	6383	7	NULL	NULL	NULL	NULL	HDL	GP		bind					SR-BI	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_151	11145929	103  Therefore, it has been suggested that binding of HDL to SR-BI facilitates the bidirectional flux between HDL and plasma membrane by reorganization of lipids within cholesterol- and caveolae-rich domains within the plasma membrane.	bind
22749	2	6383	7	NULL	NULL	NULL	NULL	statement 1	Process		facilitate					bidirectional flux	Process				NULL	between HDL and plasma membrane 	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_151	11145929	103  Therefore, it has been suggested that binding of HDL to SR-BI facilitates the bidirectional flux between HDL and plasma membrane by reorganization of lipids within cholesterol- and caveolae-rich domains within the plasma membrane.	bind
22752	3	6383	7	NULL	NULL	NULL	NULL	lipids	Chemical		are reorganized within								cholesterol-rich domains		NULL	within the plasma membrane	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_151	11145929	103  Therefore, it has been suggested that binding of HDL to SR-BI facilitates the bidirectional flux between HDL and plasma membrane by reorganization of lipids within cholesterol- and caveolae-rich domains within the plasma membrane.	bind
22753	4	6383	7	NULL	NULL	NULL	NULL	lipids	Chemical		are reorganized within								caveolae-rich domains 		NULL	within the plasma membrane	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_151	11145929	103  Therefore, it has been suggested that binding of HDL to SR-BI facilitates the bidirectional flux between HDL and plasma membrane by reorganization of lipids within cholesterol- and caveolae-rich domains within the plasma membrane.	bind
45660	5	6383	7	NULL	NULL	NULL	NULL	statement 3	Process		is required for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_151	11145929	103  Therefore, it has been suggested that binding of HDL to SR-BI facilitates the bidirectional flux between HDL and plasma membrane by reorganization of lipids within cholesterol- and caveolae-rich domains within the plasma membrane.	bind
45661	6	6383	7	NULL	NULL	NULL	NULL	statement 4	Process		is required for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_13_s_151	11145929	103  Therefore, it has been suggested that binding of HDL to SR-BI facilitates the bidirectional flux between HDL and plasma membrane by reorganization of lipids within cholesterol- and caveolae-rich domains within the plasma membrane.	bind
19640	1	6384	5	NULL	NULL	0	NULL	c-Jun	NULL		bind	NULL	enhanced				NULL			AP-1 - binding sites	NULL	kidneys	0	NULL	NULL	NULL	gw60_circulationres_79_2_162_s_311	8755992	104  Such kidneys also display enhanced binding of c-Jun and ATF2 (both substrates for JNK/SAPKs 22  23 43 44 ) to AP-1 - binding sites and cAMP response elements.	bind
19641	2	6384	5	NULL	NULL	0	NULL	c-Jun	NULL		bind	NULL	enhanced				NULL			cAMP response elements	NULL	kidneys	NULL	NULL	NULL	NULL	gw60_circulationres_79_2_162_s_311	8755992	104  Such kidneys also display enhanced binding of c-Jun and ATF2 (both substrates for JNK/SAPKs 22  23 43 44 ) to AP-1 - binding sites and cAMP response elements.	bind
19642	3	6384	5	10	NULL	0	NULL	ATF2			bind		enhanced							AP-1 - binding sites	NULL	kidneys	NULL	NULL	NULL	NULL	gw60_circulationres_79_2_162_s_311	8755992	104  Such kidneys also display enhanced binding of c-Jun and ATF2 (both substrates for JNK/SAPKs 22  23 43 44 ) to AP-1 - binding sites and cAMP response elements.	bind
19643	4	6384	5	10	NULL	0	NULL	ATF2			bind		enhanced							cAMP response elements	NULL	kidneys	NULL	NULL	NULL	NULL	gw60_circulationres_79_2_162_s_311	8755992	104  Such kidneys also display enhanced binding of c-Jun and ATF2 (both substrates for JNK/SAPKs 22  23 43 44 ) to AP-1 - binding sites and cAMP response elements.	bind
19644	5	6384	5	NULL	NULL	0	NULL	c-Jun	NULL		is a substrate for	NULL				JNK/SAPKs	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_79_2_162_s_311	8755992	104  Such kidneys also display enhanced binding of c-Jun and ATF2 (both substrates for JNK/SAPKs 22  23 43 44 ) to AP-1 - binding sites and cAMP response elements.	bind
19645	6	6384	5	NULL	NULL	0	NULL	ATF2	NULL		is a substrate for	NULL				JNK/SAPKs	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_79_2_162_s_311	8755992	104  Such kidneys also display enhanced binding of c-Jun and ATF2 (both substrates for JNK/SAPKs 22  23 43 44 ) to AP-1 - binding sites and cAMP response elements.	bind
22756	1	6384	7	NULL	NULL	NULL	NULL	c-Jun	GP		bind									AP-1 - binding sites	NULL	kidneys	NULL	NULL	NULL	NULL	gw60_circulationres_79_2_162_s_311	8755992	104  Such kidneys also display enhanced binding of c-Jun and ATF2 (both substrates for JNK/SAPKs 22  23 43 44 ) to AP-1 - binding sites and cAMP response elements.	bind
22757	2	6384	7	NULL	NULL	NULL	NULL	ATF2	GP		bind									cAMP response element	NULL	kidneys	NULL	NULL	NULL	NULL	gw60_circulationres_79_2_162_s_311	8755992	104  Such kidneys also display enhanced binding of c-Jun and ATF2 (both substrates for JNK/SAPKs 22  23 43 44 ) to AP-1 - binding sites and cAMP response elements.	bind
22758	3	6384	7	NULL	NULL	NULL	NULL	c-Jun 	GP		is a substrate for					JNK/SAPKs	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_2_162_s_311	8755992	104  Such kidneys also display enhanced binding of c-Jun and ATF2 (both substrates for JNK/SAPKs 22  23 43 44 ) to AP-1 - binding sites and cAMP response elements.	bind
22759	4	6384	7	NULL	NULL	NULL	NULL	ATF2	GP		is a substrate for					JNK/SAPKs	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_2_162_s_311	8755992	104  Such kidneys also display enhanced binding of c-Jun and ATF2 (both substrates for JNK/SAPKs 22  23 43 44 ) to AP-1 - binding sites and cAMP response elements.	bind
54248	5	6384	7	NULL	NULL	NULL	NULL	c-Jun	GP		bind									cAMP response elements	NULL	kidneys	NULL	NULL	NULL	NULL	gw60_circulationres_79_2_162_s_311	8755992	104  Such kidneys also display enhanced binding of c-Jun and ATF2 (both substrates for JNK/SAPKs 22  23 43 44 ) to AP-1 - binding sites and cAMP response elements.	bind
54249	6	6384	7	NULL	NULL	NULL	NULL	ATF2	GP		bind									AP-1 - binding sites	NULL	kidneys	NULL	NULL	NULL	NULL	gw60_circulationres_79_2_162_s_311	8755992	104  Such kidneys also display enhanced binding of c-Jun and ATF2 (both substrates for JNK/SAPKs 22  23 43 44 ) to AP-1 - binding sites and cAMP response elements.	bind
19646	1	6386	5	NULL	NULL	0	NULL	MTP	NULL		bind	NULL				apoB	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_887_s_139	11397693	108  It has been recently reported that an MTP inhibitor (AGI-S17) blocked MTP-apoB binding and the secretion of apoB without interfering with MTP lipid transfer activity.	bind
19647	2	6386	5	NULL	NULL	0	NULL	AGI-S17	NULL		is a type of	NULL				MTP inhibitor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_887_s_139	11397693	108  It has been recently reported that an MTP inhibitor (AGI-S17) blocked MTP-apoB binding and the secretion of apoB without interfering with MTP lipid transfer activity.	bind
19648	3	6386	5	NULL	NULL	0	NULL	AGI-S17	NULL		blocks	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_887_s_139	11397693	108  It has been recently reported that an MTP inhibitor (AGI-S17) blocked MTP-apoB binding and the secretion of apoB without interfering with MTP lipid transfer activity.	bind
19649	4	6386	5	NULL	NULL	0	NULL	AGI-S17	NULL		blocks	NULL				apoB	NULL	secretion of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_887_s_139	11397693	108  It has been recently reported that an MTP inhibitor (AGI-S17) blocked MTP-apoB binding and the secretion of apoB without interfering with MTP lipid transfer activity.	bind
19650	6	6386	5	NULL	NULL	0	NULL	statement 4	NULL		does not interfere with	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_887_s_139	11397693	108  It has been recently reported that an MTP inhibitor (AGI-S17) blocked MTP-apoB binding and the secretion of apoB without interfering with MTP lipid transfer activity.	bind
28696	7	6386	5	NULL	NULL	0	NULL	statement 3	NULL		does not interfere with	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_887_s_139	11397693	108  It has been recently reported that an MTP inhibitor (AGI-S17) blocked MTP-apoB binding and the secretion of apoB without interfering with MTP lipid transfer activity.	bind
46203	5	6386	5	NULL	NULL	0	NULL	MTP	NULL		exhibits	NULL				lipid transfer activity	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_887_s_139	11397693	108  It has been recently reported that an MTP inhibitor (AGI-S17) blocked MTP-apoB binding and the secretion of apoB without interfering with MTP lipid transfer activity.	bind
22760	1	6386	7	NULL	NULL	NULL	NULL	MTP	GP		bind					apoB	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_887_s_139	11397693	108  It has been recently reported that an MTP inhibitor (AGI-S17) blocked MTP-apoB binding and the secretion of apoB without interfering with MTP lipid transfer activity.	bind
22761	2	6386	7	NULL	NULL	NULL	NULL	AGI-S17	Chemical		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_887_s_139	11397693	108  It has been recently reported that an MTP inhibitor (AGI-S17) blocked MTP-apoB binding and the secretion of apoB without interfering with MTP lipid transfer activity.	bind
22763	3	6386	7	NULL	NULL	NULL	NULL	AGI-S17	Chemical		blocks					apoB	Chemical	secretion of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_887_s_139	11397693	108  It has been recently reported that an MTP inhibitor (AGI-S17) blocked MTP-apoB binding and the secretion of apoB without interfering with MTP lipid transfer activity.	bind
22765	5	6386	7	NULL	NULL	NULL	NULL	statement 2	Process		does not interfere with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_887_s_139	11397693	108  It has been recently reported that an MTP inhibitor (AGI-S17) blocked MTP-apoB binding and the secretion of apoB without interfering with MTP lipid transfer activity.	bind
22766	6	6386	7	NULL	NULL	NULL	NULL	statement 3	Process		does not interfere with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_887_s_139	11397693	108  It has been recently reported that an MTP inhibitor (AGI-S17) blocked MTP-apoB binding and the secretion of apoB without interfering with MTP lipid transfer activity.	bind
29398	7	6386	7	NULL	NULL	NULL	NULL	AGI-S17	Chemical		is a type of					MTP inhibitor	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_887_s_139	11397693	108  It has been recently reported that an MTP inhibitor (AGI-S17) blocked MTP-apoB binding and the secretion of apoB without interfering with MTP lipid transfer activity.	bind
45662	4	6386	7	NULL	NULL	NULL	NULL	MTP	GP		exhibits					lipid transfer activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_887_s_139	11397693	108  It has been recently reported that an MTP inhibitor (AGI-S17) blocked MTP-apoB binding and the secretion of apoB without interfering with MTP lipid transfer activity.	bind
19651	1	6387	5	NULL	NULL	0	NULL	prothrombin	NULL		bind	NULL				GP IIb-IIIa	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_177	12231555	108 -  111 One group has suggested that prothrombin binding to GP IIb-IIIa may provide a pool of prothrombin for activation by the factor Xa/Va complex and that abciximab may decrease thrombin generation by blocking prothrombin binding.	bind
19652	2	6387	5	10	NULL	0	NULL	prothrombin			is activated by					factor Xa/Va complex					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_177	12231555	108 -  111 One group has suggested that prothrombin binding to GP IIb-IIIa may provide a pool of prothrombin for activation by the factor Xa/Va complex and that abciximab may decrease thrombin generation by blocking prothrombin binding.	bind
19653	3	6387	5	NULL	NULL	0	NULL	statement 1	NULL		lead to	NULL	may			statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_177	12231555	108 -  111 One group has suggested that prothrombin binding to GP IIb-IIIa may provide a pool of prothrombin for activation by the factor Xa/Va complex and that abciximab may decrease thrombin generation by blocking prothrombin binding.	bind
19654	4	6387	5	NULL	NULL	0	NULL	abciximab	NULL		blocks	NULL				prothrombin	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_177	12231555	108 -  111 One group has suggested that prothrombin binding to GP IIb-IIIa may provide a pool of prothrombin for activation by the factor Xa/Va complex and that abciximab may decrease thrombin generation by blocking prothrombin binding.	bind
19655	5	6387	5	NULL	NULL	0	NULL	abciximab	NULL		decrease	NULL	may			thrombin	NULL	generation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_177	12231555	108 -  111 One group has suggested that prothrombin binding to GP IIb-IIIa may provide a pool of prothrombin for activation by the factor Xa/Va complex and that abciximab may decrease thrombin generation by blocking prothrombin binding.	bind
19656	6	6387	5	NULL	NULL	0	NULL	statement 4	NULL		leads to	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_177	12231555	108 -  111 One group has suggested that prothrombin binding to GP IIb-IIIa may provide a pool of prothrombin for activation by the factor Xa/Va complex and that abciximab may decrease thrombin generation by blocking prothrombin binding.	bind
22767	1	6387	7	NULL	NULL	NULL	NULL	prothrombin	GP		bind					GP IIb-IIIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_177	12231555	108 -  111 One group has suggested that prothrombin binding to GP IIb-IIIa may provide a pool of prothrombin for activation by the factor Xa/Va complex and that abciximab may decrease thrombin generation by blocking prothrombin binding.	bind
22768	2	6387	7	NULL	NULL	NULL	NULL	factor Xa/Va complex	GP		activate					prothrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_177	12231555	108 -  111 One group has suggested that prothrombin binding to GP IIb-IIIa may provide a pool of prothrombin for activation by the factor Xa/Va complex and that abciximab may decrease thrombin generation by blocking prothrombin binding.	bind
22769	3	6387	7	NULL	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_177	12231555	108 -  111 One group has suggested that prothrombin binding to GP IIb-IIIa may provide a pool of prothrombin for activation by the factor Xa/Va complex and that abciximab may decrease thrombin generation by blocking prothrombin binding.	bind
22770	4	6387	7	NULL	NULL	NULL	NULL	abciximab	Chemical		blocks					prothrombin	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_177	12231555	108 -  111 One group has suggested that prothrombin binding to GP IIb-IIIa may provide a pool of prothrombin for activation by the factor Xa/Va complex and that abciximab may decrease thrombin generation by blocking prothrombin binding.	bind
22771	5	6387	7	NULL	NULL	NULL	NULL	abciximab	Chemical		decrease		may			thrombin	GP	generation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_177	12231555	108 -  111 One group has suggested that prothrombin binding to GP IIb-IIIa may provide a pool of prothrombin for activation by the factor Xa/Va complex and that abciximab may decrease thrombin generation by blocking prothrombin binding.	bind
22772	6	6387	7	NULL	NULL	NULL	NULL	statement 5	Process		occurs by					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_177	12231555	108 -  111 One group has suggested that prothrombin binding to GP IIb-IIIa may provide a pool of prothrombin for activation by the factor Xa/Va complex and that abciximab may decrease thrombin generation by blocking prothrombin binding.	bind
19657	1	6388	5	NULL	NULL	0	NULL	ferritin	NULL		bind	NULL					NULL		VL-domain		NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biochemistry-(mosc)_65_9_11042491_s_9	11042491	108 M(-1)) is similar to the affinity of  the full-length parental antibody F11 because when the immobilized VL-domain  was used, the binding constant of ferritin to the VL-domain was only 4-6-fold  lower than that in the case of F11 antibody.	bind
22773	1	6388	7	NULL	NULL	NULL	NULL	ferritin	GP		bind								VL-domain		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochemistry-(mosc)_65_9_11042491_s_9	11042491	108 M(-1)) is similar to the affinity of  the full-length parental antibody F11 because when the immobilized VL-domain  was used, the binding constant of ferritin to the VL-domain was only 4-6-fold  lower than that in the case of F11 antibody.	bind
19658	1	6390	5	NULL	NULL	0	NULL	transcription factor	NULL		bind	NULL				HER2	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4257_s_210	11691913	11       Noonberg,S.B., Scott,G.K., Hunt,C.A., Hogan,M.E. and Benz,C.C. (1994) Inhibition of transcription factor binding to the HER2 promoter by triplex-forming oligodeoxyribonucleotides.	bind
19659	2	6390	5	NULL	NULL	0	NULL	oligodeoxyribonucleotides	NULL	triplex-forming	inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4257_s_210	11691913	11       Noonberg,S.B., Scott,G.K., Hunt,C.A., Hogan,M.E. and Benz,C.C. (1994) Inhibition of transcription factor binding to the HER2 promoter by triplex-forming oligodeoxyribonucleotides.	bind
22775	1	6390	7	NULL	NULL	NULL	NULL	transcription factor	GP		bind					HER2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4257_s_210	11691913	11       Noonberg,S.B., Scott,G.K., Hunt,C.A., Hogan,M.E. and Benz,C.C. (1994) Inhibition of transcription factor binding to the HER2 promoter by triplex-forming oligodeoxyribonucleotides.	bind
22776	2	6390	7	NULL	NULL	NULL	NULL	oligodeoxyribonucleotides	NucleicAcid	triplex-forming	inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4257_s_210	11691913	11       Noonberg,S.B., Scott,G.K., Hunt,C.A., Hogan,M.E. and Benz,C.C. (1994) Inhibition of transcription factor binding to the HER2 promoter by triplex-forming oligodeoxyribonucleotides.	bind
19660	1	6391	5	NULL	NULL	0	NULL	DpnM DNA adenine methyltransferase	NULL	DpnII restriction system of Streptococcus pneumoniae	bind	NULL				S-adenosylmethionine	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3137_s_242	11470870	11       Tran,P.H., Korszun,Z.R., Cerritelli,S., Springhorn,S.S. and Lacks,S.A. (1998) Crystal structure of the  DpnM DNA adenine methyltransferase from the  DpnII restriction system of  Streptococcus pneumoniae bound to S-adenosylmethionine.	bind
22777	1	6391	7	NULL	NULL	NULL	NULL	DpnM DNA adenine methyltransferase	GP	streptococcus pneumoniae	bind					S-adenosylmethionine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3137_s_242	11470870	11       Tran,P.H., Korszun,Z.R., Cerritelli,S., Springhorn,S.S. and Lacks,S.A. (1998) Crystal structure of the  DpnM DNA adenine methyltransferase from the  DpnII restriction system of  Streptococcus pneumoniae bound to S-adenosylmethionine.	bind
22778	2	6391	7	NULL	NULL	NULL	NULL	DpnM DNA adenine methyltransferase	GP		is derived from					DpnII restriction system	GP	Streptococcus pneumoniae			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3137_s_242	11470870	11       Tran,P.H., Korszun,Z.R., Cerritelli,S., Springhorn,S.S. and Lacks,S.A. (1998) Crystal structure of the  DpnM DNA adenine methyltransferase from the  DpnII restriction system of  Streptococcus pneumoniae bound to S-adenosylmethionine.	bind
19661	1	6392	5	NULL	NULL	0	NULL	MDM2 protein	NULL		interacts with	NULL	specifically	central acidic domain		L5 protein	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
19662	2	6392	5	10	NULL	0	NULL	L5 protein			is a component of					large ribosomal subunit					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
19663	3	6392	5	NULL	NULL	0	NULL	L5 protein	NULL		is associated with	NULL				5s rRNA	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
19664	4	6392	5	NULL	NULL	0	NULL	MDM2	NULL		bind	NULL				TAFII250	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
19665	5	6392	5	NULL	NULL	0	NULL	statement 4	NULL		correlates with	NULL	positively			cyclin A	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
19666	6	6392	5	NULL	NULL	0	NULL	cyclin A	NULL		is	NULL				a regulator of cell cycle	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
54250	7	6392	5	10	NULL	0	NULL	MDM2 protein			function in		possibly			ribosome		biosynthesis of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
54251	8	6392	5	10	NULL	0	NULL	MDM2 protein			function in		possibly			translation		regulation of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
54252	9	6392	5	10	NULL	0	NULL	statement 1			suggests					statement 7					NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
54253	10	6392	5	10	NULL	0	NULL	statement 1			suggests					statement 8					NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
22779	1	6392	7	NULL	NULL	NULL	NULL	MDM2 protein	GP		interacts with		specifically	central acidic domain 		L5 protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
22780	2	6392	7	NULL	NULL	NULL	NULL	statement 1	Process		suggests					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
22781	3	6392	7	NULL	NULL	NULL	NULL	statement 1	Process		suggests					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
22783	4	6392	7	NULL	NULL	NULL	NULL	L5 protein	GP		is a component of					large ribosomal subunit	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
22784	5	6392	7	NULL	NULL	NULL	NULL	L5 protein	GP		associate with					5s rRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
22787	6	6392	7	NULL	NULL	NULL	NULL	MDM2	GP		bind					TAFII250	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
22795	7	6392	7	NULL	NULL	NULL	NULL	cyclin A	GP	activation of	regulates					cell cycle	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
22797	8	6392	7	NULL	NULL	NULL	NULL	statement 6	Process		correlates with		positively			statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
54254	9	6392	7	NULL	NULL	NULL	NULL	MDM2 protein	GP		function in		possibly			ribosome	CellComponent	biosynthesis of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
54255	10	6392	7	NULL	NULL	NULL	NULL	MDM2 protein	GP		function in		possibly			translation	Process	regulation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_587_s_21	10934161	11  A possible function of MDM2 protein in ribosome biosynthesis or in translational regulation is suggested by the specific interaction of the central acidic domain of the MDM2 protein with the L5 protein, a component of a large ribosomal subunit, which is itself associated with 5s rRNA. 12, 13  A positive correlation was found between MDM2 binding to TAFII250 and activation of cyclin A, a regulator of the cell cycle.	bind
19751	1	6393	5	10	NULL	0	NULL	cdc25A	NULL	ectopic expression of 	results in	NULL				cdc25A	NULL	higher levels of expression of 			NULL	VSM-myc cells	NULL	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_126	10205150	11  Ectopic expression of cdc25A resulted in higher levels of cdc25A expression in all clones of VSM-myc cells irrespective of their c-Myc expression.	bind
45618	2	6393	5	10	NULL	0	NULL	statement 1	NULL		is irrespective of	NULL				c-Myc	NULL	expression of			NULL		0	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_126	10205150	11  Ectopic expression of cdc25A resulted in higher levels of cdc25A expression in all clones of VSM-myc cells irrespective of their c-Myc expression.	bind
22828	1	6393	7	NULL	NULL	NULL	NULL	cdc25A	GP	Ectopic expression of	results in					cdc25A	GP	higher expression of			NULL	VSM-myc cells	NULL	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_126	10205150	11  Ectopic expression of cdc25A resulted in higher levels of cdc25A expression in all clones of VSM-myc cells irrespective of their c-Myc expression.	bind
22829	2	6393	7	NULL	NULL	NULL	NULL	statement 1	Process		is irrespective of					c-Myc	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_126	10205150	11  Ectopic expression of cdc25A resulted in higher levels of cdc25A expression in all clones of VSM-myc cells irrespective of their c-Myc expression.	bind
19752	1	6394	5	NULL	NULL	0	NULL	apo E	NULL		plays a role in	NULL	important			TG-rich lipoproteins	NULL	catabolism of 			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_29	7600129	11  Even if all studies suggest an important role for apo E in the catabolism of TG-rich lipoproteins and an inhibitory effect of lipids and C apolipoproteins for apo B binding to the LDL receptor, no one can definitively determine the individual effect of each factor.	bind
19753	2	6394	5	NULL	NULL	0	NULL	apo B	NULL		bind	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_29	7600129	11  Even if all studies suggest an important role for apo E in the catabolism of TG-rich lipoproteins and an inhibitory effect of lipids and C apolipoproteins for apo B binding to the LDL receptor, no one can definitively determine the individual effect of each factor.	bind
19754	3	6394	5	NULL	NULL	0	NULL	lipids	NULL		inhibit	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_29	7600129	11  Even if all studies suggest an important role for apo E in the catabolism of TG-rich lipoproteins and an inhibitory effect of lipids and C apolipoproteins for apo B binding to the LDL receptor, no one can definitively determine the individual effect of each factor.	bind
19755	4	6394	5	NULL	NULL	0	NULL	C apolipoproteins	NULL		inhibit	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_29	7600129	11  Even if all studies suggest an important role for apo E in the catabolism of TG-rich lipoproteins and an inhibitory effect of lipids and C apolipoproteins for apo B binding to the LDL receptor, no one can definitively determine the individual effect of each factor.	bind
22830	1	6394	7	NULL	NULL	NULL	NULL	apo E	GP		plays a role in		importantly			 TG-rich lipoproteins	GP	catabolism of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_29	7600129	11  Even if all studies suggest an important role for apo E in the catabolism of TG-rich lipoproteins and an inhibitory effect of lipids and C apolipoproteins for apo B binding to the LDL receptor, no one can definitively determine the individual effect of each factor.	bind
22831	2	6394	7	NULL	NULL	NULL	NULL	apo B	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_29	7600129	11  Even if all studies suggest an important role for apo E in the catabolism of TG-rich lipoproteins and an inhibitory effect of lipids and C apolipoproteins for apo B binding to the LDL receptor, no one can definitively determine the individual effect of each factor.	bind
22832	3	6394	7	NULL	NULL	NULL	NULL	lipids	Chemical		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_29	7600129	11  Even if all studies suggest an important role for apo E in the catabolism of TG-rich lipoproteins and an inhibitory effect of lipids and C apolipoproteins for apo B binding to the LDL receptor, no one can definitively determine the individual effect of each factor.	bind
22833	4	6394	7	NULL	NULL	NULL	NULL	C apolipoproteins	GP		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_29	7600129	11  Even if all studies suggest an important role for apo E in the catabolism of TG-rich lipoproteins and an inhibitory effect of lipids and C apolipoproteins for apo B binding to the LDL receptor, no one can definitively determine the individual effect of each factor.	bind
19756	1	6395	5	10	NULL	0	NULL	Sp1	NULL	porcine;; endothelial cells	bind	NULL				TF	NULL			oligonucleotide spanning two putative Sp1 sites in promoter	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_261	9081693	11  Furthermore, Sp1 from porcine endothelial cells bound to an oligonucleotide spanning two putative Sp1 sites in the porcine TF promoter, 11  one of which is equivalent to Sp1V.	bind
19757	2	6395	5	10	NULL	0	NULL	TF	NULL	porcine	is equivalent to	NULL			putative Sp1 site in promoter		NULL			Sp1V	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_261	9081693	11  Furthermore, Sp1 from porcine endothelial cells bound to an oligonucleotide spanning two putative Sp1 sites in the porcine TF promoter, 11  one of which is equivalent to Sp1V.	bind
22834	1	6395	7	NULL	NULL	NULL	NULL	Sp1	GP	porcine;; endothelial cells	bind					TF	GP	porcine		oligonucleotide spanning two putative Sp1 sites in the promoter	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_261	9081693	11  Furthermore, Sp1 from porcine endothelial cells bound to an oligonucleotide spanning two putative Sp1 sites in the porcine TF promoter, 11  one of which is equivalent to Sp1V.	bind
22836	2	6395	7	NULL	NULL	NULL	NULL	TF	GP	porcine	is equivalent to				putative Sp1 site in the promoter					Sp1V	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_261	9081693	11  Furthermore, Sp1 from porcine endothelial cells bound to an oligonucleotide spanning two putative Sp1 sites in the porcine TF promoter, 11  one of which is equivalent to Sp1V.	bind
19777	1	6397	5	NULL	NULL	0	NULL	VLDLR sequence	NULL	human	is similar to	NULL				vitellogenin receptor	NULL	chicken			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_407_s_32	8630667	11  In addition, the human VLDLR shares 84% of its sequence with the chicken vitellogenin receptor, 12  which also binds VLDL and is required for the delivery of nutrients to the developing avian oocyte.	bind
19778	2	6397	5	NULL	NULL	0	NULL	VLDLR	NULL	human	bind	NULL				VLDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_407_s_32	8630667	11  In addition, the human VLDLR shares 84% of its sequence with the chicken vitellogenin receptor, 12  which also binds VLDL and is required for the delivery of nutrients to the developing avian oocyte.	bind
19779	3	6397	5	NULL	NULL	0	NULL	VLDLR	NULL		is required for	NULL				nutrients	NULL	delivery of			NULL	to the developing avian oocyte	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_407_s_32	8630667	11  In addition, the human VLDLR shares 84% of its sequence with the chicken vitellogenin receptor, 12  which also binds VLDL and is required for the delivery of nutrients to the developing avian oocyte.	bind
22839	1	6397	7	NULL	NULL	NULL	NULL	VLDLR	GP	human	binds					VLDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_407_s_32	8630667	11  In addition, the human VLDLR shares 84% of its sequence with the chicken vitellogenin receptor, 12  which also binds VLDL and is required for the delivery of nutrients to the developing avian oocyte.	bind
22840	2	6397	7	NULL	NULL	NULL	NULL	statement 1	Process		is required for					nutrients	Chemical	delivery of 			NULL	developing avian oocyte	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_407_s_32	8630667	11  In addition, the human VLDLR shares 84% of its sequence with the chicken vitellogenin receptor, 12  which also binds VLDL and is required for the delivery of nutrients to the developing avian oocyte.	bind
29401	3	6397	7	NULL	NULL	NULL	NULL	VLDLR 	GP	human	is similar to					vitellogenin receptor	GP	chicken			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_407_s_32	8630667	11  In addition, the human VLDLR shares 84% of its sequence with the chicken vitellogenin receptor, 12  which also binds VLDL and is required for the delivery of nutrients to the developing avian oocyte.	bind
19798	1	6398	5	NULL	NULL	0	NULL	apo B	NULL		bind	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_158	7600129	11  LpB was radiolabeled, enriched with lipids, and then incubated with apolipoproteins CI, CII, CIII, and E. Preliminary studies indicated that free apolipoproteins did not interfere with apo B binding to the LDL receptor (V. Clavey, PR, et al, unpublished data, 1994), so we did not remove free apolipoproteins.	bind
19803	2	6398	5	NULL	NULL	0	NULL	apolipoproteins	NULL	free	does not interfere with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_158	7600129	11  LpB was radiolabeled, enriched with lipids, and then incubated with apolipoproteins CI, CII, CIII, and E. Preliminary studies indicated that free apolipoproteins did not interfere with apo B binding to the LDL receptor (V. Clavey, PR, et al, unpublished data, 1994), so we did not remove free apolipoproteins.	bind
22841	1	6398	7	NULL	NULL	NULL	NULL	apo B 	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_158	7600129	11  LpB was radiolabeled, enriched with lipids, and then incubated with apolipoproteins CI, CII, CIII, and E. Preliminary studies indicated that free apolipoproteins did not interfere with apo B binding to the LDL receptor (V. Clavey, PR, et al, unpublished data, 1994), so we did not remove free apolipoproteins.	bind
22842	2	6398	7	NULL	NULL	NULL	NULL	apolipoproteins 	GP	free 	does not interfere with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_158	7600129	11  LpB was radiolabeled, enriched with lipids, and then incubated with apolipoproteins CI, CII, CIII, and E. Preliminary studies indicated that free apolipoproteins did not interfere with apo B binding to the LDL receptor (V. Clavey, PR, et al, unpublished data, 1994), so we did not remove free apolipoproteins.	bind
19781	1	6399	5	NULL	NULL	0	NULL	caldesmon	NULL		bind	NULL				actin	NULL		low-affinity sites		NULL		0	NULL	NULL	NULL	gw60_circulationres_83_6_661_s_25	9742062	11  Numerous studies using in vitro reconstituted tropomyosin/actin/myosin complexes have shown that caldesmon binds actin at low- and high-affinity sites and that occupancy of the high-affinity site of actin is associated with a significant inhibition of actin-activated myosin ATPase activity.	bind
19782	2	6399	5	NULL	NULL	0	NULL	caldesmon	NULL		bind	NULL				actin	NULL		high-affinity sites		NULL		0	NULL	NULL	NULL	gw60_circulationres_83_6_661_s_25	9742062	11  Numerous studies using in vitro reconstituted tropomyosin/actin/myosin complexes have shown that caldesmon binds actin at low- and high-affinity sites and that occupancy of the high-affinity site of actin is associated with a significant inhibition of actin-activated myosin ATPase activity.	bind
19783	3	6399	5	10	NULL	0	NULL	actin	NULL		activates	NULL				myosin ATPase 	NULL	activity of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_6_661_s_25	9742062	11  Numerous studies using in vitro reconstituted tropomyosin/actin/myosin complexes have shown that caldesmon binds actin at low- and high-affinity sites and that occupancy of the high-affinity site of actin is associated with a significant inhibition of actin-activated myosin ATPase activity.	bind
19784	4	6399	5	NULL	NULL	0	NULL	actin	NULL	occupancy of	is associated with	NULL		high-affinity site		statement 3	NULL	significant inhibition of 			NULL		0	NULL	NULL	NULL	gw60_circulationres_83_6_661_s_25	9742062	11  Numerous studies using in vitro reconstituted tropomyosin/actin/myosin complexes have shown that caldesmon binds actin at low- and high-affinity sites and that occupancy of the high-affinity site of actin is associated with a significant inhibition of actin-activated myosin ATPase activity.	bind
22844	1	6399	7	NULL	NULL	NULL	NULL	caldesmon	GP		binds					actin	GP		low-affinity site		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_6_661_s_25	9742062	11  Numerous studies using in vitro reconstituted tropomyosin/actin/myosin complexes have shown that caldesmon binds actin at low- and high-affinity sites and that occupancy of the high-affinity site of actin is associated with a significant inhibition of actin-activated myosin ATPase activity.	bind
22845	2	6399	7	NULL	NULL	NULL	NULL	caldesmon	GP		binds					actin	GP		high-affinity site		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_6_661_s_25	9742062	11  Numerous studies using in vitro reconstituted tropomyosin/actin/myosin complexes have shown that caldesmon binds actin at low- and high-affinity sites and that occupancy of the high-affinity site of actin is associated with a significant inhibition of actin-activated myosin ATPase activity.	bind
22846	3	6399	7	NULL	NULL	NULL	NULL	actin	GP		activates					myosin ATPase 	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_6_661_s_25	9742062	11  Numerous studies using in vitro reconstituted tropomyosin/actin/myosin complexes have shown that caldesmon binds actin at low- and high-affinity sites and that occupancy of the high-affinity site of actin is associated with a significant inhibition of actin-activated myosin ATPase activity.	bind
22847	4	6399	7	NULL	NULL	NULL	NULL	actin	GP	occupancy	associate with			high-affinity site		statement 3	Process	inhibition of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_6_661_s_25	9742062	11  Numerous studies using in vitro reconstituted tropomyosin/actin/myosin complexes have shown that caldesmon binds actin at low- and high-affinity sites and that occupancy of the high-affinity site of actin is associated with a significant inhibition of actin-activated myosin ATPase activity.	bind
19780	1	6400	5	10	NULL	0	NULL	GAGs	NULL	highly sulfated	bind	NULL	high affinity			PDGF A isoform	NULL	long			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2897_s_214	9409273	11  Particularly highly sulfated GAGs bind the long PDGF A isoform with high affinity.	bind
22843	1	6400	7	NULL	NULL	NULL	NULL	GAGs	Chemical	highly sulfated	bind		high affinity			PDGF A isoform	GP	long			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2897_s_214	9409273	11  Particularly highly sulfated GAGs bind the long PDGF A isoform with high affinity.	bind
19804	1	6401	5	NULL	NULL	0	NULL	vWF	NULL		is	NULL				von Willebrand factor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_17_2045_s_24	11044418	11  Shear stress induces the binding of von Willebrand factor (vWF) to the GP Ib/IXV complex on platelets.	bind
19805	2	6401	5	NULL	NULL	0	NULL	vWF	NULL		bind	NULL				GP Ib/IXV complex	NULL				NULL	on platelets	0	NULL	NULL	NULL	gw60_circulation_102_17_2045_s_24	11044418	11  Shear stress induces the binding of von Willebrand factor (vWF) to the GP Ib/IXV complex on platelets.	bind
19928	3	6401	5	NULL	NULL	0	NULL	shear stress	NULL		induces	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_17_2045_s_24	11044418	11  Shear stress induces the binding of von Willebrand factor (vWF) to the GP Ib/IXV complex on platelets.	bind
22982	1	6401	7	NULL	NULL	NULL	NULL	vWF	GP		bind					GP Ib/IXV complex	GP				NULL	platelets	NULL	NULL	NULL	NULL	gw60_circulation_102_17_2045_s_24	11044418	11  Shear stress induces the binding of von Willebrand factor (vWF) to the GP Ib/IXV complex on platelets.	bind
22983	2	6401	7	NULL	NULL	NULL	NULL	shear stress	Process		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_17_2045_s_24	11044418	11  Shear stress induces the binding of von Willebrand factor (vWF) to the GP Ib/IXV complex on platelets.	bind
22984	3	6401	7	NULL	NULL	NULL	NULL	vWF	GP		is					von Willebrand factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_17_2045_s_24	11044418	11  Shear stress induces the binding of von Willebrand factor (vWF) to the GP Ib/IXV complex on platelets.	bind
19929	1	6402	5	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL				GPIIb/IIIa receptors	NULL	functional			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_12_2195_s_18	7489242	11  The binding of fibrinogen by functional GPIIb/IIIa receptors represents the final common step in platelet activation by all agonists.	bind
19930	2	6402	5	NULL	NULL	0	NULL	agonists	NULL		activates	NULL				platelets	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_12_2195_s_18	7489242	11  The binding of fibrinogen by functional GPIIb/IIIa receptors represents the final common step in platelet activation by all agonists.	bind
19931	3	6402	5	NULL	NULL	0	NULL	statement 1	NULL		is final step in	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_12_2195_s_18	7489242	11  The binding of fibrinogen by functional GPIIb/IIIa receptors represents the final common step in platelet activation by all agonists.	bind
22991	1	6402	7	NULL	NULL	NULL	NULL	fibrinogen	GP		bind					GPIIb/IIIa receptors	GP	functional			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_12_2195_s_18	7489242	11  The binding of fibrinogen by functional GPIIb/IIIa receptors represents the final common step in platelet activation by all agonists.	bind
22992	2	6402	7	NULL	NULL	NULL	NULL	agonists	Chemical		activates					platelet	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_12_2195_s_18	7489242	11  The binding of fibrinogen by functional GPIIb/IIIa receptors represents the final common step in platelet activation by all agonists.	bind
22993	3	6402	7	NULL	NULL	NULL	NULL	statement 1	Process		is final step in					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_12_2195_s_18	7489242	11  The binding of fibrinogen by functional GPIIb/IIIa receptors represents the final common step in platelet activation by all agonists.	bind
19933	1	6404	5	NULL	NULL	0	NULL	cell surface receptor	NULL		is linked to	NULL		transmembrane domain		tyrosine kinase	NULL	intracellular			NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_8_1927_s_20	8873670	11  The molecule has a cell surface receptor linked by a transmembrane domain to an intracellular tyrosine kinase; it binds to heparin, basement membrane, and heparan sulfate components of the extracellular matrix, providing a tissue depot of bFGF.	bind
22996	1	6404	7	NULL	NULL	NULL	NULL	cell surface receptor	GP		is linked to			transmembrane domain		tyrosine kinase	GP	intracellular			NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_8_1927_s_20	8873670	11  The molecule has a cell surface receptor linked by a transmembrane domain to an intracellular tyrosine kinase; it binds to heparin, basement membrane, and heparan sulfate components of the extracellular matrix, providing a tissue depot of bFGF.	bind
19936	1	6405	5	NULL	NULL	0	NULL	apo B	NULL		bind	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_128	7600129	11  The same experiment, performed without removal of free apolipoproteins, produced the same results, indicating that free apolipoproteins do not interfere with apo B binding to the LDL receptor (Fig 1  ).	bind
19937	2	6405	5	NULL	NULL	0	NULL	apolipoproteins	NULL	free	does not interfere with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_128	7600129	11  The same experiment, performed without removal of free apolipoproteins, produced the same results, indicating that free apolipoproteins do not interfere with apo B binding to the LDL receptor (Fig 1  ).	bind
23002	1	6405	7	NULL	NULL	NULL	NULL	 apo B	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_128	7600129	11  The same experiment, performed without removal of free apolipoproteins, produced the same results, indicating that free apolipoproteins do not interfere with apo B binding to the LDL receptor (Fig 1  ).	bind
23003	2	6405	7	NULL	NULL	NULL	NULL	apolipoproteins	GP	free	does not interfere with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_128	7600129	11  The same experiment, performed without removal of free apolipoproteins, produced the same results, indicating that free apolipoproteins do not interfere with apo B binding to the LDL receptor (Fig 1  ).	bind
19938	1	6406	5	NULL	NULL	0	NULL	SEK-1	NULL		bind	NULL				Ste5 homologues	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_6_947_s_46	8635244	11  Under this scenario, SEK-1, which could activate p38, never gains access to it because SEK-1 and p38 are bound to different Ste5 homologues.	bind
19939	2	6406	5	NULL	NULL	0	NULL	p38	NULL		bind	NULL				Ste5 homologues	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_6_947_s_46	8635244	11  Under this scenario, SEK-1, which could activate p38, never gains access to it because SEK-1 and p38 are bound to different Ste5 homologues.	bind
19940	3	6406	5	NULL	NULL	0	NULL	SEK-1	NULL		activate	NULL				p38	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_6_947_s_46	8635244	11  Under this scenario, SEK-1, which could activate p38, never gains access to it because SEK-1 and p38 are bound to different Ste5 homologues.	bind
19941	4	6406	5	NULL	NULL	0	NULL	SEK-1	NULL		does not gain access to	NULL				p38	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_6_947_s_46	8635244	11  Under this scenario, SEK-1, which could activate p38, never gains access to it because SEK-1 and p38 are bound to different Ste5 homologues.	bind
19942	5	6406	5	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_6_947_s_46	8635244	11  Under this scenario, SEK-1, which could activate p38, never gains access to it because SEK-1 and p38 are bound to different Ste5 homologues.	bind
19943	6	6406	5	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_6_947_s_46	8635244	11  Under this scenario, SEK-1, which could activate p38, never gains access to it because SEK-1 and p38 are bound to different Ste5 homologues.	bind
23004	1	6406	7	NULL	NULL	NULL	NULL	SEK-1	GP		bind					Ste5 homologue	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_6_947_s_46	8635244	11  Under this scenario, SEK-1, which could activate p38, never gains access to it because SEK-1 and p38 are bound to different Ste5 homologues.	bind
23005	2	6406	7	NULL	NULL	NULL	NULL	p38	GP		bind					Ste5 homologue	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_6_947_s_46	8635244	11  Under this scenario, SEK-1, which could activate p38, never gains access to it because SEK-1 and p38 are bound to different Ste5 homologues.	bind
23007	3	6406	7	NULL	NULL	NULL	NULL	SEK-1	GP		activate					p38	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_6_947_s_46	8635244	11  Under this scenario, SEK-1, which could activate p38, never gains access to it because SEK-1 and p38 are bound to different Ste5 homologues.	bind
30259	4	6406	7	NULL	NULL	NULL	NULL	SEK-1	GP		does not gain access to					p38	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_6_947_s_46	8635244	11  Under this scenario, SEK-1, which could activate p38, never gains access to it because SEK-1 and p38 are bound to different Ste5 homologues.	bind
30260	5	6406	7	NULL	NULL	NULL	NULL	statement 1	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_6_947_s_46	8635244	11  Under this scenario, SEK-1, which could activate p38, never gains access to it because SEK-1 and p38 are bound to different Ste5 homologues.	bind
30261	6	6406	7	NULL	NULL	NULL	NULL	statement 2	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_6_947_s_46	8635244	11  Under this scenario, SEK-1, which could activate p38, never gains access to it because SEK-1 and p38 are bound to different Ste5 homologues.	bind
19953	1	6407	5	NULL	NULL	0	NULL	Lp(a)	NULL		bind	NULL				lysine	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_656_s_25	8963723	11 12  Lp(a) also binds to lysine-Sepharose, 3  several cell types, including hepatocytes, 13 14  monocytes, 15  16 17  and endothelial cells, 18 19  and extracellular matrices 20  21  and matrix proteins.	bind
19954	2	6407	5	NULL	NULL	0	NULL	Lp(a)	NULL		bind	NULL				hepatocytes	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_656_s_25	8963723	11 12  Lp(a) also binds to lysine-Sepharose, 3  several cell types, including hepatocytes, 13 14  monocytes, 15  16 17  and endothelial cells, 18 19  and extracellular matrices 20  21  and matrix proteins.	bind
19955	3	6407	5	NULL	NULL	0	NULL	Lp(a)	NULL		bind	NULL				monocytes	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_656_s_25	8963723	11 12  Lp(a) also binds to lysine-Sepharose, 3  several cell types, including hepatocytes, 13 14  monocytes, 15  16 17  and endothelial cells, 18 19  and extracellular matrices 20  21  and matrix proteins.	bind
19956	4	6407	5	NULL	NULL	0	NULL	Lp(a)	NULL		bind	NULL				endothelial cells	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_656_s_25	8963723	11 12  Lp(a) also binds to lysine-Sepharose, 3  several cell types, including hepatocytes, 13 14  monocytes, 15  16 17  and endothelial cells, 18 19  and extracellular matrices 20  21  and matrix proteins.	bind
19957	5	6407	5	NULL	NULL	0	NULL	Lp(a)	NULL		bind	NULL				extracellular matrices	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_656_s_25	8963723	11 12  Lp(a) also binds to lysine-Sepharose, 3  several cell types, including hepatocytes, 13 14  monocytes, 15  16 17  and endothelial cells, 18 19  and extracellular matrices 20  21  and matrix proteins.	bind
19958	6	6407	5	NULL	NULL	0	NULL	Lp(a)	NULL		bind	NULL				matrix proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_656_s_25	8963723	11 12  Lp(a) also binds to lysine-Sepharose, 3  several cell types, including hepatocytes, 13 14  monocytes, 15  16 17  and endothelial cells, 18 19  and extracellular matrices 20  21  and matrix proteins.	bind
23008	1	6407	7	NULL	NULL	NULL	NULL	 Lp	GP		binds to					lysine-Sepharose	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_656_s_25	8963723	11 12  Lp(a) also binds to lysine-Sepharose, 3  several cell types, including hepatocytes, 13 14  monocytes, 15  16 17  and endothelial cells, 18 19  and extracellular matrices 20  21  and matrix proteins.	bind
23009	2	6407	7	NULL	NULL	NULL	NULL	Lp	GP		binds to					hepatocytes	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_656_s_25	8963723	11 12  Lp(a) also binds to lysine-Sepharose, 3  several cell types, including hepatocytes, 13 14  monocytes, 15  16 17  and endothelial cells, 18 19  and extracellular matrices 20  21  and matrix proteins.	bind
23010	3	6407	7	NULL	NULL	NULL	NULL	Lp	GP		binds to					monocytes	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_656_s_25	8963723	11 12  Lp(a) also binds to lysine-Sepharose, 3  several cell types, including hepatocytes, 13 14  monocytes, 15  16 17  and endothelial cells, 18 19  and extracellular matrices 20  21  and matrix proteins.	bind
23011	4	6407	7	NULL	NULL	NULL	NULL	Lp	GP		binds to					endothelial cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_656_s_25	8963723	11 12  Lp(a) also binds to lysine-Sepharose, 3  several cell types, including hepatocytes, 13 14  monocytes, 15  16 17  and endothelial cells, 18 19  and extracellular matrices 20  21  and matrix proteins.	bind
23012	5	6407	7	NULL	NULL	NULL	NULL	Lp	GP		binds to					extracellular matrices	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_656_s_25	8963723	11 12  Lp(a) also binds to lysine-Sepharose, 3  several cell types, including hepatocytes, 13 14  monocytes, 15  16 17  and endothelial cells, 18 19  and extracellular matrices 20  21  and matrix proteins.	bind
23013	6	6407	7	NULL	NULL	NULL	NULL	Lp	GP		binds to					matrix proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_656_s_25	8963723	11 12  Lp(a) also binds to lysine-Sepharose, 3  several cell types, including hepatocytes, 13 14  monocytes, 15  16 17  and endothelial cells, 18 19  and extracellular matrices 20  21  and matrix proteins.	bind
19944	1	6410	5	NULL	NULL	0	NULL	HB-EGF	NULL		bind	NULL				EGF-R	NULL				NULL	human SMCs	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1524_s_28	8977458	11 12 13  HB-EGF binds to the EGF-R of human 14  and bovine SMCs 15  and stimulates its phosphorylation.	bind
19945	2	6410	5	NULL	NULL	0	NULL	HB-EGF	NULL		bind	NULL				EGF-R	NULL				NULL	bovine SMCs	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1524_s_28	8977458	11 12 13  HB-EGF binds to the EGF-R of human 14  and bovine SMCs 15  and stimulates its phosphorylation.	bind
19946	3	6410	5	NULL	NULL	0	NULL	statement 1	NULL		stimulates	NULL				EGF-R	NULL	phosphorylation of			NULL	human SMCs	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1524_s_28	8977458	11 12 13  HB-EGF binds to the EGF-R of human 14  and bovine SMCs 15  and stimulates its phosphorylation.	bind
19947	4	6410	5	NULL	NULL	0	NULL	statement 2	NULL		stimulates	NULL				EGF-R	NULL	phosphorylation of			NULL	bovine SMCs	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1524_s_28	8977458	11 12 13  HB-EGF binds to the EGF-R of human 14  and bovine SMCs 15  and stimulates its phosphorylation.	bind
23015	1	6410	7	NULL	NULL	NULL	NULL	HB-EGF	GP		binds to					EGF-R	GP				NULL	human SMCs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1524_s_28	8977458	11 12 13  HB-EGF binds to the EGF-R of human 14  and bovine SMCs 15  and stimulates its phosphorylation.	bind
23016	2	6410	7	NULL	NULL	NULL	NULL	HB-EGF	GP		binds to					EGF-R	GP				NULL	bovine SMCs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1524_s_28	8977458	11 12 13  HB-EGF binds to the EGF-R of human 14  and bovine SMCs 15  and stimulates its phosphorylation.	bind
30262	3	6410	7	NULL	NULL	NULL	NULL	statement 1	Process		stimulates					EGF-R	GP	phosphorylation of			NULL	human SMCs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1524_s_28	8977458	11 12 13  HB-EGF binds to the EGF-R of human 14  and bovine SMCs 15  and stimulates its phosphorylation.	bind
30263	4	6410	7	NULL	NULL	NULL	NULL	statement 2	Process		stimulates					EGF-R	GP	phosphorylation of			NULL	bovine SMCs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1524_s_28	8977458	11 12 13  HB-EGF binds to the EGF-R of human 14  and bovine SMCs 15  and stimulates its phosphorylation.	bind
19948	1	6411	5	10	NULL	0	NULL	TPA			exists as					TPA		free;;active			NULL	in blood	NULL	NULL	NULL	NULL	gw60_circulation_96_3_761_s_16	9264480	11 12 13 14  TPA exists in several forms in blood, including free active TPA and TPA bound to PAI-1 and other inhibitors.	bind
19949	2	6411	5	NULL	NULL	0	NULL	TPA	NULL		bind	NULL				PAI-1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_3_761_s_16	9264480	11 12 13 14  TPA exists in several forms in blood, including free active TPA and TPA bound to PAI-1 and other inhibitors.	bind
19951	4	6411	5	NULL	NULL	0	NULL	TPA	NULL		exists as	NULL				statement 2	NULL				NULL	in blood	0	NULL	NULL	NULL	gw60_circulation_96_3_761_s_16	9264480	11 12 13 14  TPA exists in several forms in blood, including free active TPA and TPA bound to PAI-1 and other inhibitors.	bind
23017	1	6411	7	NULL	NULL	NULL	NULL	TPA 	GP		bind					PAI-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_3_761_s_16	9264480	11 12 13 14  TPA exists in several forms in blood, including free active TPA and TPA bound to PAI-1 and other inhibitors.	bind
54256	2	6411	7	NULL	NULL	NULL	NULL	TPA	GP		exists as					statement 1	Process				NULL	blood	NULL	NULL	NULL	NULL	gw60_circulation_96_3_761_s_16	9264480	11 12 13 14  TPA exists in several forms in blood, including free active TPA and TPA bound to PAI-1 and other inhibitors.	bind
54257	3	6411	7	NULL	NULL	NULL	NULL	TPA	GP		exists as					TPA	GP	free;;active			NULL	blood	NULL	NULL	NULL	NULL	gw60_circulation_96_3_761_s_16	9264480	11 12 13 14  TPA exists in several forms in blood, including free active TPA and TPA bound to PAI-1 and other inhibitors.	bind
19961	1	6412	5	NULL	NULL	0	NULL	apoB-100 	NULL		bind	NULL	strongly	LDL receptor - binding regions		GAGs	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_250	9012650	11 14  The data presented here and from other studies indicate that the LDL receptor - binding regions of apoB-100 are also the segments that bind GAGs most strongly.	bind
23018	1	6412	7	NULL	NULL	NULL	NULL	apoB-100	GP		bind		strongly	LDL receptor - binding region		GAGs	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_250	9012650	11 14  The data presented here and from other studies indicate that the LDL receptor - binding regions of apoB-100 are also the segments that bind GAGs most strongly.	bind
19962	1	6413	5	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL				GP IIb/IIIa receptors	NULL	activated			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_954_s_202	9633937	11 22 23 24  Phillips et al 25  studied binding of PAC1, an antibody that simulates fibrinogen binding to activated GP IIb/IIIa receptors, after ADP stimulation.	bind
19963	2	6413	5	NULL	NULL	0	NULL	PAC1 antibody	NULL		stimulates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_954_s_202	9633937	11 22 23 24  Phillips et al 25  studied binding of PAC1, an antibody that simulates fibrinogen binding to activated GP IIb/IIIa receptors, after ADP stimulation.	bind
19964	3	6413	5	NULL	NULL	0	NULL	ADP	NULL	stimulation	is required for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_954_s_202	9633937	11 22 23 24  Phillips et al 25  studied binding of PAC1, an antibody that simulates fibrinogen binding to activated GP IIb/IIIa receptors, after ADP stimulation.	bind
23019	1	6413	7	NULL	NULL	NULL	NULL	fibrinogen	GP		bind					GP IIb/IIIa receptors	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_954_s_202	9633937	11 22 23 24  Phillips et al 25  studied binding of PAC1, an antibody that simulates fibrinogen binding to activated GP IIb/IIIa receptors, after ADP stimulation.	bind
23020	2	6413	7	NULL	NULL	NULL	NULL	PAC1 antibody	GP		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_954_s_202	9633937	11 22 23 24  Phillips et al 25  studied binding of PAC1, an antibody that simulates fibrinogen binding to activated GP IIb/IIIa receptors, after ADP stimulation.	bind
23021	3	6413	7	NULL	NULL	NULL	NULL	statement 2	Process		occurs after					ADP	Chemical	stimulation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_954_s_202	9633937	11 22 23 24  Phillips et al 25  studied binding of PAC1, an antibody that simulates fibrinogen binding to activated GP IIb/IIIa receptors, after ADP stimulation.	bind
25765	1	6414	5	NULL	NULL	0	NULL	polypeptides	NULL	protein folding of newly synthesized	is essential for	NULL				oxidative metabolism	NULL	maintaining			NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25766	2	6414	5	NULL	NULL	0	NULL	statement 1	NULL		occurs after	NULL				myocyte	NULL	damage of			NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25767	3	6414	5	NULL	NULL	0	NULL	statement 1	NULL		is a function of	NULL	potential			molecular chaperones	NULL				NULL	in ischemic heart	NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25768	4	6414	5	NULL	NULL	0	NULL	mitochondria	NULL		is protected from	NULL				ROS	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25769	5	6414	5	NULL	NULL	0	NULL	statement 4	NULL		is a function of	NULL	potential			molecular chaperones	NULL				NULL	in ischemic heart	0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25770	6	6414	5	NULL	NULL	0	NULL	TNFalpha	NULL		is a type of	NULL				cytokines	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25771	7	6414	5	NULL	NULL	0	NULL	mitochondria	NULL		is protected from	NULL				cytokines	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25772	8	6414	5	NULL	NULL	0	NULL	statement 7	NULL		is a function of	NULL	potential			molecular chaperones	NULL				NULL	in ischemic heart	0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25773	9	6414	5	NULL	NULL	0	NULL	proteins	NULL	newly synthesized	undergoes	NULL				translocation	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25774	10	6414	5	NULL	NULL	0	NULL	statement 9	NULL		occurs during	NULL				organelle repair	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25775	11	6414	5	NULL	NULL	0	NULL	statement 10	NULL		is a function of	NULL	potential			molecular chaperones	NULL				NULL	in ischemic heart	0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25776	12	6414	5	NULL	NULL	0	NULL	molecular chaperones	NULL		repairs	NULL	potential			structural proteins	NULL	critical			NULL	in ischemic heart	0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25777	13	6414	5	10	NULL	0	NULL	statement 12			occurs after					statement 37					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25778	14	6414	5	NULL	NULL	0	NULL	molecular chaperones	NULL		recycles	NULL	potential			membrane vesicles	NULL				NULL	in ischemic heart	0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25779	15	6414	5	NULL	NULL	0	NULL	molecular chaperones	NULL		transports	NULL	potential			byproducts	NULL	potential toxic			NULL	in ischemic heart	0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25780	16	6414	5	NULL	NULL	0	NULL	proteasome	NULL		degrades	NULL				byproducts	NULL	potential toxic			NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25781	17	6414	5	NULL	NULL	0	NULL	pro - interleukin-1beta	NULL		is a type of	NULL				cytokines	NULL	proinflammatory			NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25782	18	6414	5	NULL	NULL	0	NULL	molecular chaperones	NULL		suppresses	NULL	potential			cytokines	NULL	proinflammatory			NULL	in ischemic heart	0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25783	19	6414	5	NULL	NULL	0	NULL	molecular chaperones	NULL		suppresses	NULL	potential			NADPH oxidase	NULL				NULL	in ischemic heart	0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25784	20	6414	5	NULL	NULL	0	NULL	statement 19	NULL		occurs by	NULL				heat shock response	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25785	21	6414	5	NULL	NULL	0	NULL	molecular chaperones	NULL		suppresses	NULL	potential			oxidative burst	NULL				NULL	in ischemic heart	0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25786	22	6414	5	NULL	NULL	0	NULL	statement 21	NULL		occurs by	NULL				heat shock response	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25787	23	6414	5	NULL	NULL	0	NULL	molecular chaperones	NULL		prevents	NULL	potential			apoptosis	NULL				NULL	in ischemic heart	0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25788	24	6414	5	NULL	NULL	0	NULL	Hsp60	NULL		bind	NULL				cytochrome c	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25789	25	6414	5	NULL	NULL	0	NULL	Hsp70	NULL		bind	NULL				cytosolic targets	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25790	26	6414	5	NULL	NULL	0	NULL	Hsp60	NULL		is a type of	NULL				mitochondrial chaperone	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25791	27	6414	5	NULL	NULL	0	NULL	Hsp70	NULL		is a type of	NULL				mitochondrial chaperone	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25792	28	6414	5	NULL	NULL	0	NULL	statement 23	NULL		occurs through	NULL				statement 24	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25793	29	6414	5	NULL	NULL	0	NULL	statement 23	NULL		occurs through	NULL				statement 25	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25794	30	6414	5	NULL	NULL	0	NULL	statement 28	NULL		is an alternative to	NULL				statement 29	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25795	31	6414	5	NULL	NULL	0	NULL	molecular chaperones	NULL		repairs	NULL	potential			ion channel	NULL				NULL	in ischemic heart	NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25796	32	6414	5	NULL	NULL	0	NULL	Hsp47 chaperone	NULL		synthesises	NULL	potential			collagen	NULL				NULL	in ischemic heart	NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25797	33	6414	5	10	NULL	0	NULL	statement 32			occurs for					reparative fibrosis					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
25798	34	6414	5	NULL	NULL	0	NULL	molecular chaperones	NULL		modulates	NULL	potential			ischemic injury	NULL	immune-mediated			NULL	in ischemic heart	0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
29967	35	6414	5	NULL	NULL	0	NULL	NO	NULL		is produced from	NULL				HSP	NULL	inducible synthesis of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
29968	36	6414	5	NULL	NULL	0	NULL	molecular chaperones	NULL		protect	NULL				statement 35	NULL				NULL	in ischemic heart	0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
55798	37	6414	5	10	NULL	0	NULL	ischemia			induces					cytoskeleton		alterations of \t\t\t			NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
23022	1	6414	7	NULL	NULL	NULL	NULL	polypeptide	GP	protein folding of newly synthesized	maintain					oxidative metabolism 	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
23023	6	6414	7	NULL	NULL	NULL	NULL	protein	GP	newly synthesized	undergoes					translocation	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
23028	10	6414	7	NULL	NULL	NULL	NULL	heat shock response	Process		suppress					NADPH oxidase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
23029	12	6414	7	NULL	NULL	NULL	NULL	Hsp60	GP		binds					cytochrome c	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
23030	13	6414	7	NULL	NULL	NULL	NULL	Hsp70	GP		bind					cytosolic targets	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
23031	15	6414	7	NULL	NULL	NULL	NULL	statement 14	Process		occur through					statement 12	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
23033	35	6414	7	NULL	NULL	NULL	NULL	statement 15	Process		is an alternative to					statement 16	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
23034	17	6414	7	NULL	NULL	NULL	NULL	Hsp47 chaperone	GP		synthesize					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
23035	18	6414	7	NULL	NULL	NULL	NULL	statement 17	Process		occurs for					reparative fibrosis 	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
23045	7	6414	7	NULL	NULL	NULL	NULL	ischemia	MedicalFinding		induce					cytoskeletal alterations	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
30835	3	6414	7	NULL	NULL	NULL	NULL	mitochondria 	CellComponent		is protected from					ROS	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
30836	4	6414	7	NULL	NULL	NULL	NULL	mitochondria 	CellComponent		is protected from					TNFalpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
30837	5	6414	7	NULL	NULL	NULL	NULL	TNFalpha	GP		is a type of					cytokine	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
30838	2	6414	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs after					myocyte	Cell	damage of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
30839	8	6414	7	NULL	NULL	NULL	NULL	molecular chaperones	GP		transports					potential toxic byproducts	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
30840	9	6414	7	NULL	NULL	NULL	NULL	toxic byproducts	GP		is degraded by					proteasome	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
30841	11	6414	7	NULL	NULL	NULL	NULL	heat shock response	Process		suppress					oxidative burst	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
30842	16	6414	7	NULL	NULL	NULL	NULL	statement 14	Process		occur through					statement 13	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
30843	19	6414	7	NULL	NULL	NULL	NULL	statement 1	Process		is a function of 		potentially			molecular chaperones	GP				NULL	in ischemic heart	NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
54323	20	6414	7	NULL	NULL	NULL	NULL	statement 3	Process		is a function of 		potentially			molecular chaperones	GP				NULL	in ischemic heart	NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
54324	21	6414	7	NULL	NULL	NULL	NULL	statement 4	Process		is a function of 		potentially			molecular chaperones	GP				NULL	in ischemic heart	NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
54325	22	6414	7	NULL	NULL	NULL	NULL	statement 6	Process		occur during					organelle repair	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
54326	23	6414	7	NULL	NULL	NULL	NULL	statement 6	Process		is a function of 		potentially			molecular chaperones	GP				NULL	in ischemic heart	NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
54327	24	6414	7	NULL	NULL	NULL	NULL	molecular chaperones	GP		repairs					critical structural proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
54328	25	6414	7	NULL	NULL	NULL	NULL	statement 24	Process		occurs after					statement 7	Process				NULL	in ischemic heart	NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
54329	26	6414	7	NULL	NULL	NULL	NULL	molecular chaperones	GP		recycle					membrane vesicles	CellComponent				NULL	in ischemic heart	NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
54336	27	6414	7	NULL	NULL	NULL	NULL	molecular chaperones	GP		suppress					pro - interleukin-1beta 	GP				NULL	in ischemic heart	NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
54338	28	6414	7	NULL	NULL	NULL	NULL	pro - interleukin-1beta 	GP		is a type of					proinflammatory cytokines	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
54341	29	6414	7	NULL	NULL	NULL	NULL	statement 10	Process		is a function of 		potentially			molecular chaperones	GP				NULL	in ischemic heart	NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
54344	30	6414	7	NULL	NULL	NULL	NULL	statement 11	Process		is a function of 		potentially			molecular chaperones	GP				NULL	in ischemic heart	NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
54345	31	6414	7	NULL	NULL	NULL	NULL	NO	Chemical		produced from					HSP	GP	inducible synthesis of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
54348	32	6414	7	NULL	NULL	NULL	NULL	molecular chaperones	GP		protects					statement 31	Process				NULL	in ischemic heart	NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
54349	33	6414	7	NULL	NULL	NULL	NULL	Hsp60 	GP		is a type of					mitochondrial chaperone	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
54350	34	6414	7	NULL	NULL	NULL	NULL	Hsp70	GP		is a type of					mitochondrial chaperone	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
54351	14	6414	7	NULL	NULL	NULL	NULL	molecular chaperones	GP		prevents					apoptosis	Process				NULL	in ischemic heart	NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
54353	36	6414	7	NULL	NULL	NULL	NULL	molecular chaperones	GP		repair					ion channel	CellComponent				NULL	in ischemic heart	NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
54354	37	6414	7	NULL	NULL	NULL	NULL	statement 17	Process		is a function of 		potentially			molecular chaperones	GP				NULL	in ischemic heart	NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
54363	38	6414	7	NULL	NULL	NULL	NULL	molecular chaperones	GP		modulates					 ischemic injury 	MedicalFinding	 immune-mediated			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_66	9686751	11 234 235  In physiological terms, potential functions for molecular chaperones in the ischemic heart include the following: protein folding of newly synthesized polypeptides essential for maintaining oxidative metabolism after myocyte damage (L), protection of mitochondria from ROS and cytokines such as TNFalpha 204 236  and translocation of newly synthesized proteins during organelle repair (M), repair of critical structural proteins after ischemia-induced cytoskeletal alterations (N), 237  recycling of membrane vesicles (Hsc70) (O), transport of potential toxic byproducts for degradation by the proteasome (P), 78 238 239  suppression of proinflammatory cytokines such as pro - interleukin-1beta (Q), 204 236 240  suppression of NADPH oxidase and the oxidative burst by the heat shock response (R), 241  protection by NO production from inducible synthesis of HSP expression (S), 61 242 243 244 245 246  prevention of apoptosis either through the mitochondrial chaperone Hsp60 binding of cytochrome  c and/or Hsp70 binding of cytosolic targets (T), 36 204  repair of ion channel (U), collagen synthesis by Hsp47 chaperone for reparative fibrosis (V), 180  and modulation of the immune-mediated ischemic injury (W).	bind
19959	1	6415	5	NULL	NULL	0	NULL	APLAs	NULL		bind	NULL	may			heparin-like glycosaminoglycans	NULL				NULL	on ECs	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_299	10669657	11 28  APLAs may bind to heparin-like glycosaminoglycans on ECs and thereby inhibit local antithrombin III activity.	bind
19960	2	6415	5	NULL	NULL	0	NULL	statement 1	NULL		inhibit	NULL				antithrombin III	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_299	10669657	11 28  APLAs may bind to heparin-like glycosaminoglycans on ECs and thereby inhibit local antithrombin III activity.	bind
23047	1	6415	7	NULL	NULL	NULL	NULL	APLAs	GP		bind		may			heparin-like glycosaminoglycans 	Chemical				NULL	on ECs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_299	10669657	11 28  APLAs may bind to heparin-like glycosaminoglycans on ECs and thereby inhibit local antithrombin III activity.	bind
23048	2	6415	7	NULL	NULL	NULL	NULL	statement 1	Process		inhibit					antithrombin III	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_563_s_299	10669657	11 28  APLAs may bind to heparin-like glycosaminoglycans on ECs and thereby inhibit local antithrombin III activity.	bind
29997	1	6417	5	NULL	NULL	0	NULL	T cells	NULL	activated	does not bind	NULL				CD40 construct	NULL	recombinant			NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_1_196_s_6	8550833	11 different mutations were found in DNA from all 13 patients whose activated T cells failed to bind a recombinant  CD40 construct.	bind
23049	1	6417	7	NULL	NULL	NULL	NULL	T cells	Cell	activated	does not bind					CD40 construct	Cell	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_1_196_s_6	8550833	11 different mutations were found in DNA from all 13 patients whose activated T cells failed to bind a recombinant  CD40 construct.	bind
19966	1	6418	5	NULL	NULL	0	NULL	RNA polymerase	NULL	Escherichia coli	bind	NULL				fork junction DNA	NULL			- 10 region of promoter	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2437_s_172	11410649	11 has also been used to examine the binding of  Escherichia coli RNA polymerase with the fork junction DNA containing the  - 10 region of the promoter ( 64).	bind
23050	1	6418	7	NULL	NULL	NULL	NULL	RNA polymerase	GP	Escherichia coli 	binds					fork junction DNA	NucleicAcid			 -10 region of the promoter	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2437_s_172	11410649	11 has also been used to examine the binding of  Escherichia coli RNA polymerase with the fork junction DNA containing the  - 10 region of the promoter ( 64).	bind
19967	1	6419	5	NULL	NULL	0	NULL	angiotensin II	NULL		does not bind	NULL				APJ	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_108_12_1432_s_30	12963638	11 However, angiotensin II does not bind to APJ.	bind
23051	1	6419	7	NULL	NULL	NULL	NULL	angiotensin II 	GP		does not bind					APJ	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_108_12_1432_s_30	12963638	11 However, angiotensin II does not bind to APJ.	bind
19968	1	6420	5	NULL	NULL	0	NULL	C pneumoniae	NULL	infection with	leads to	NULL				TF mRNA	NULL	increased			NULL		0	NULL	NULL	NULL	gw60_circulationres_92_4_394_s_165	12600889	11 In support, our data demonstrate that infection with  C pneumoniae leads to increased TF mRNA and protein that is associated with increased binding of Egr-1 to the SRR of the TF promoter and to the consensus Egr-1 sequence.	bind
20012	2	6420	5	NULL	NULL	0	NULL	Egr-1	NULL		bind	NULL				TF	NULL			SRR of promoter	NULL		0	NULL	NULL	NULL	gw60_circulationres_92_4_394_s_165	12600889	11 In support, our data demonstrate that infection with  C pneumoniae leads to increased TF mRNA and protein that is associated with increased binding of Egr-1 to the SRR of the TF promoter and to the consensus Egr-1 sequence.	bind
20013	3	6420	5	NULL	NULL	0	NULL	Egr-1	NULL		bind	NULL				Egr-1 sequence	NULL	consensus			NULL		0	NULL	NULL	NULL	gw60_circulationres_92_4_394_s_165	12600889	11 In support, our data demonstrate that infection with  C pneumoniae leads to increased TF mRNA and protein that is associated with increased binding of Egr-1 to the SRR of the TF promoter and to the consensus Egr-1 sequence.	bind
20014	4	6420	5	NULL	NULL	0	NULL	protein	NULL		associates with	NULL				statement 2	NULL	increased			NULL		0	NULL	NULL	NULL	gw60_circulationres_92_4_394_s_165	12600889	11 In support, our data demonstrate that infection with  C pneumoniae leads to increased TF mRNA and protein that is associated with increased binding of Egr-1 to the SRR of the TF promoter and to the consensus Egr-1 sequence.	bind
20015	5	6420	5	NULL	NULL	0	NULL	protein	NULL		associates with	NULL				statement 3	NULL	increased			NULL		0	NULL	NULL	NULL	gw60_circulationres_92_4_394_s_165	12600889	11 In support, our data demonstrate that infection with  C pneumoniae leads to increased TF mRNA and protein that is associated with increased binding of Egr-1 to the SRR of the TF promoter and to the consensus Egr-1 sequence.	bind
20016	6	6420	5	NULL	NULL	0	NULL	C pneumoniae	NULL	infection with	leads to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_4_394_s_165	12600889	11 In support, our data demonstrate that infection with  C pneumoniae leads to increased TF mRNA and protein that is associated with increased binding of Egr-1 to the SRR of the TF promoter and to the consensus Egr-1 sequence.	bind
20017	7	6420	5	NULL	NULL	0	NULL	C pneumoniae	NULL	infection with	leads to	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_4_394_s_165	12600889	11 In support, our data demonstrate that infection with  C pneumoniae leads to increased TF mRNA and protein that is associated with increased binding of Egr-1 to the SRR of the TF promoter and to the consensus Egr-1 sequence.	bind
23052	1	6420	7	NULL	NULL	NULL	NULL	C pneumoniae 	Organism		leads to					TF mRNA	NucleicAcid	increased			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_4_394_s_165	12600889	11 In support, our data demonstrate that infection with  C pneumoniae leads to increased TF mRNA and protein that is associated with increased binding of Egr-1 to the SRR of the TF promoter and to the consensus Egr-1 sequence.	bind
23053	2	6420	7	NULL	NULL	NULL	NULL	C pneumoniae 	Organism		leads to					TF protein	GP	increased			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_4_394_s_165	12600889	11 In support, our data demonstrate that infection with  C pneumoniae leads to increased TF mRNA and protein that is associated with increased binding of Egr-1 to the SRR of the TF promoter and to the consensus Egr-1 sequence.	bind
23054	3	6420	7	NULL	NULL	NULL	NULL	Egr-1	GP		bind					TF	GP			SRR in the promoter	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_4_394_s_165	12600889	11 In support, our data demonstrate that infection with  C pneumoniae leads to increased TF mRNA and protein that is associated with increased binding of Egr-1 to the SRR of the TF promoter and to the consensus Egr-1 sequence.	bind
23055	4	6420	7	NULL	NULL	NULL	NULL	Egr-1	GP		bind							consensus		Egr-1 sequence	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_4_394_s_165	12600889	11 In support, our data demonstrate that infection with  C pneumoniae leads to increased TF mRNA and protein that is associated with increased binding of Egr-1 to the SRR of the TF promoter and to the consensus Egr-1 sequence.	bind
23056	5	6420	7	NULL	NULL	NULL	NULL	statement 1	Process		increase					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_4_394_s_165	12600889	11 In support, our data demonstrate that infection with  C pneumoniae leads to increased TF mRNA and protein that is associated with increased binding of Egr-1 to the SRR of the TF promoter and to the consensus Egr-1 sequence.	bind
23057	6	6420	7	NULL	NULL	NULL	NULL	statement 1	Process		increase					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_4_394_s_165	12600889	11 In support, our data demonstrate that infection with  C pneumoniae leads to increased TF mRNA and protein that is associated with increased binding of Egr-1 to the SRR of the TF promoter and to the consensus Egr-1 sequence.	bind
23058	7	6420	7	NULL	NULL	NULL	NULL	statement 2	Process		increase					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_4_394_s_165	12600889	11 In support, our data demonstrate that infection with  C pneumoniae leads to increased TF mRNA and protein that is associated with increased binding of Egr-1 to the SRR of the TF promoter and to the consensus Egr-1 sequence.	bind
23059	8	6420	7	NULL	NULL	NULL	NULL	statement 2	Process		increase					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_4_394_s_165	12600889	11 In support, our data demonstrate that infection with  C pneumoniae leads to increased TF mRNA and protein that is associated with increased binding of Egr-1 to the SRR of the TF promoter and to the consensus Egr-1 sequence.	bind
20018	1	6421	5	NULL	NULL	0	NULL	TGF-beta1	NULL		is secreted in	NULL				inactive form	NULL	biologically			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1503_s_26	16690877	11 In vitro studies indicate that TGF-beta1 is secreted in a biologically inactive form in a complex with LAP. 11 Within the extracellular matrix, this precursor TGF-beta1 protein binds to latency TGF-binding protein (LTBP).	bind
20019	2	6421	5	NULL	NULL	0	NULL	statement 1	NULL		is in complex with	NULL				LAP	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1503_s_26	16690877	11 In vitro studies indicate that TGF-beta1 is secreted in a biologically inactive form in a complex with LAP. 11 Within the extracellular matrix, this precursor TGF-beta1 protein binds to latency TGF-binding protein (LTBP).	bind
20020	3	6421	5	NULL	NULL	0	NULL	TGF-beta1 protein	NULL	precursor	bind	NULL				LTBP	NULL				NULL	within the extracellular matrix	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1503_s_26	16690877	11 In vitro studies indicate that TGF-beta1 is secreted in a biologically inactive form in a complex with LAP. 11 Within the extracellular matrix, this precursor TGF-beta1 protein binds to latency TGF-binding protein (LTBP).	bind
20021	4	6421	5	NULL	NULL	0	NULL	LTBP	NULL		is	NULL				latency TGF-binding protein	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1503_s_26	16690877	11 In vitro studies indicate that TGF-beta1 is secreted in a biologically inactive form in a complex with LAP. 11 Within the extracellular matrix, this precursor TGF-beta1 protein binds to latency TGF-binding protein (LTBP).	bind
23087	1	6421	7	NULL	NULL	NULL	NULL	TGF-beta1	GP	inactive 	complex with					LAP	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1503_s_26	16690877	11 In vitro studies indicate that TGF-beta1 is secreted in a biologically inactive form in a complex with LAP. 11 Within the extracellular matrix, this precursor TGF-beta1 protein binds to latency TGF-binding protein (LTBP).	bind
23088	2	6421	7	NULL	NULL	NULL	NULL	TGF-beta1	GP		is secreted in					inactive form	Process	biologically			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1503_s_26	16690877	11 In vitro studies indicate that TGF-beta1 is secreted in a biologically inactive form in a complex with LAP. 11 Within the extracellular matrix, this precursor TGF-beta1 protein binds to latency TGF-binding protein (LTBP).	bind
23089	3	6421	7	NULL	NULL	NULL	NULL	TGF-beta1	GP	precursor 	binds to					LTBP	GP				NULL	extracellular matrix	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1503_s_26	16690877	11 In vitro studies indicate that TGF-beta1 is secreted in a biologically inactive form in a complex with LAP. 11 Within the extracellular matrix, this precursor TGF-beta1 protein binds to latency TGF-binding protein (LTBP).	bind
23090	4	6421	7	NULL	NULL	NULL	NULL	LTBP	GP		is					latency TGF-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1503_s_26	16690877	11 In vitro studies indicate that TGF-beta1 is secreted in a biologically inactive form in a complex with LAP. 11 Within the extracellular matrix, this precursor TGF-beta1 protein binds to latency TGF-binding protein (LTBP).	bind
20022	1	6422	5	NULL	NULL	0	NULL	Ang II	NULL		increases	NULL				Prx1	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_28	15016729	11 Moreover, we found that Ang II also increased expression of the  paired-related homeobox gene-1, (Prx1, formerly known as MHox or Phox), and that Prx1 markedly enhanced SRF binding to CArG B in the SM alpha-actin gene in EMSA. 11 Whereas these studies significantly advanced our understanding of mechanisms whereby Ang II could increase expression of multiple CArG-dependent SMC genes, there were several unresolved questions from these studies.	bind
20023	2	6422	5	NULL	NULL	0	NULL	Prx1	NULL		is	NULL				paired-related homeobox gene-1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_28	15016729	11 Moreover, we found that Ang II also increased expression of the  paired-related homeobox gene-1, (Prx1, formerly known as MHox or Phox), and that Prx1 markedly enhanced SRF binding to CArG B in the SM alpha-actin gene in EMSA. 11 Whereas these studies significantly advanced our understanding of mechanisms whereby Ang II could increase expression of multiple CArG-dependent SMC genes, there were several unresolved questions from these studies.	bind
20024	3	6422	5	NULL	NULL	0	NULL	Prx1	NULL		is formerly known as	NULL				MHox	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_28	15016729	11 Moreover, we found that Ang II also increased expression of the  paired-related homeobox gene-1, (Prx1, formerly known as MHox or Phox), and that Prx1 markedly enhanced SRF binding to CArG B in the SM alpha-actin gene in EMSA. 11 Whereas these studies significantly advanced our understanding of mechanisms whereby Ang II could increase expression of multiple CArG-dependent SMC genes, there were several unresolved questions from these studies.	bind
20025	4	6422	5	NULL	NULL	0	NULL	Prx1	NULL		is formerly known as	NULL				Phox	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_28	15016729	11 Moreover, we found that Ang II also increased expression of the  paired-related homeobox gene-1, (Prx1, formerly known as MHox or Phox), and that Prx1 markedly enhanced SRF binding to CArG B in the SM alpha-actin gene in EMSA. 11 Whereas these studies significantly advanced our understanding of mechanisms whereby Ang II could increase expression of multiple CArG-dependent SMC genes, there were several unresolved questions from these studies.	bind
20026	5	6422	5	NULL	NULL	0	NULL	statement 3	NULL		is an alternative to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_28	15016729	11 Moreover, we found that Ang II also increased expression of the  paired-related homeobox gene-1, (Prx1, formerly known as MHox or Phox), and that Prx1 markedly enhanced SRF binding to CArG B in the SM alpha-actin gene in EMSA. 11 Whereas these studies significantly advanced our understanding of mechanisms whereby Ang II could increase expression of multiple CArG-dependent SMC genes, there were several unresolved questions from these studies.	bind
20027	6	6422	5	NULL	NULL	0	NULL	SRF	NULL		bind	NULL				SM alpha-actin gene	NULL			CArG B	NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_28	15016729	11 Moreover, we found that Ang II also increased expression of the  paired-related homeobox gene-1, (Prx1, formerly known as MHox or Phox), and that Prx1 markedly enhanced SRF binding to CArG B in the SM alpha-actin gene in EMSA. 11 Whereas these studies significantly advanced our understanding of mechanisms whereby Ang II could increase expression of multiple CArG-dependent SMC genes, there were several unresolved questions from these studies.	bind
20028	7	6422	5	NULL	NULL	0	NULL	Prx1	NULL		enhances	NULL	markedly			statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_28	15016729	11 Moreover, we found that Ang II also increased expression of the  paired-related homeobox gene-1, (Prx1, formerly known as MHox or Phox), and that Prx1 markedly enhanced SRF binding to CArG B in the SM alpha-actin gene in EMSA. 11 Whereas these studies significantly advanced our understanding of mechanisms whereby Ang II could increase expression of multiple CArG-dependent SMC genes, there were several unresolved questions from these studies.	bind
20029	8	6422	5	10	NULL	0	NULL	Ang II	NULL		increases	NULL				SMC genes	NULL	expression of;; CArG-dependent			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_28	15016729	11 Moreover, we found that Ang II also increased expression of the  paired-related homeobox gene-1, (Prx1, formerly known as MHox or Phox), and that Prx1 markedly enhanced SRF binding to CArG B in the SM alpha-actin gene in EMSA. 11 Whereas these studies significantly advanced our understanding of mechanisms whereby Ang II could increase expression of multiple CArG-dependent SMC genes, there were several unresolved questions from these studies.	bind
23192	1	6422	7	NULL	NULL	NULL	NULL	Ang II 	GP		increase					Prx1	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_28	15016729	11 Moreover, we found that Ang II also increased expression of the  paired-related homeobox gene-1, (Prx1, formerly known as MHox or Phox), and that Prx1 markedly enhanced SRF binding to CArG B in the SM alpha-actin gene in EMSA. 11 Whereas these studies significantly advanced our understanding of mechanisms whereby Ang II could increase expression of multiple CArG-dependent SMC genes, there were several unresolved questions from these studies.	bind
23193	2	6422	7	NULL	NULL	NULL	NULL	SRF	GP		bind					SM alpha-actin gene	GP			CArG B	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_28	15016729	11 Moreover, we found that Ang II also increased expression of the  paired-related homeobox gene-1, (Prx1, formerly known as MHox or Phox), and that Prx1 markedly enhanced SRF binding to CArG B in the SM alpha-actin gene in EMSA. 11 Whereas these studies significantly advanced our understanding of mechanisms whereby Ang II could increase expression of multiple CArG-dependent SMC genes, there were several unresolved questions from these studies.	bind
23194	3	6422	7	NULL	NULL	NULL	NULL	Prx1	GP		enhance					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_28	15016729	11 Moreover, we found that Ang II also increased expression of the  paired-related homeobox gene-1, (Prx1, formerly known as MHox or Phox), and that Prx1 markedly enhanced SRF binding to CArG B in the SM alpha-actin gene in EMSA. 11 Whereas these studies significantly advanced our understanding of mechanisms whereby Ang II could increase expression of multiple CArG-dependent SMC genes, there were several unresolved questions from these studies.	bind
23195	4	6422	7	NULL	NULL	NULL	NULL	Ang II 	GP		increase					SMC genes	GP	expression of;;CArG-dependent 			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_28	15016729	11 Moreover, we found that Ang II also increased expression of the  paired-related homeobox gene-1, (Prx1, formerly known as MHox or Phox), and that Prx1 markedly enhanced SRF binding to CArG B in the SM alpha-actin gene in EMSA. 11 Whereas these studies significantly advanced our understanding of mechanisms whereby Ang II could increase expression of multiple CArG-dependent SMC genes, there were several unresolved questions from these studies.	bind
23196	5	6422	7	NULL	NULL	NULL	NULL	Prx1	GP		is					paired-related homeobox gene-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_28	15016729	11 Moreover, we found that Ang II also increased expression of the  paired-related homeobox gene-1, (Prx1, formerly known as MHox or Phox), and that Prx1 markedly enhanced SRF binding to CArG B in the SM alpha-actin gene in EMSA. 11 Whereas these studies significantly advanced our understanding of mechanisms whereby Ang II could increase expression of multiple CArG-dependent SMC genes, there were several unresolved questions from these studies.	bind
23197	6	6422	7	NULL	NULL	NULL	NULL	Prx1	GP		formerly known as					MHox	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_28	15016729	11 Moreover, we found that Ang II also increased expression of the  paired-related homeobox gene-1, (Prx1, formerly known as MHox or Phox), and that Prx1 markedly enhanced SRF binding to CArG B in the SM alpha-actin gene in EMSA. 11 Whereas these studies significantly advanced our understanding of mechanisms whereby Ang II could increase expression of multiple CArG-dependent SMC genes, there were several unresolved questions from these studies.	bind
23198	7	6422	7	NULL	NULL	NULL	NULL	Prx1	GP		formerly known as					Phox	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_28	15016729	11 Moreover, we found that Ang II also increased expression of the  paired-related homeobox gene-1, (Prx1, formerly known as MHox or Phox), and that Prx1 markedly enhanced SRF binding to CArG B in the SM alpha-actin gene in EMSA. 11 Whereas these studies significantly advanced our understanding of mechanisms whereby Ang II could increase expression of multiple CArG-dependent SMC genes, there were several unresolved questions from these studies.	bind
25972	1	6424	5	NULL	NULL	0	NULL	PGRMC1	NULL		bind	NULL				progesterone AOP2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_febslett_579_5_1089_s_193	15710396	11 Proteolysis and peptidolysis  1.37  Y12711 Rogesterone receptor membrane component 1 PGRMC1 Xq22-q24 Liver-rich protein that binds to progesterone  1.36  D14662 Anti-oxidant protein 2 AOP2 1q23.	bind
25974	2	6424	5	NULL	NULL	0	NULL	PGRMC1	NULL		is	NULL				progesterone receptor membrane component 1	NULL				NULL		0	NULL	NULL	NULL	gw70_febslett_579_5_1089_s_193	15710396	11 Proteolysis and peptidolysis  1.37  Y12711 Rogesterone receptor membrane component 1 PGRMC1 Xq22-q24 Liver-rich protein that binds to progesterone  1.36  D14662 Anti-oxidant protein 2 AOP2 1q23.	bind
25976	3	6424	5	NULL	NULL	0	NULL	AOP2	NULL		is	NULL				Anti-oxidant protein 2	NULL				NULL		0	NULL	NULL	NULL	gw70_febslett_579_5_1089_s_193	15710396	11 Proteolysis and peptidolysis  1.37  Y12711 Rogesterone receptor membrane component 1 PGRMC1 Xq22-q24 Liver-rich protein that binds to progesterone  1.36  D14662 Anti-oxidant protein 2 AOP2 1q23.	bind
23199	1	6424	7	NULL	NULL	NULL	NULL	PGRMC1	GP		binds to					progesterone AOP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_579_5_1089_s_193	15710396	11 Proteolysis and peptidolysis  1.37  Y12711 Rogesterone receptor membrane component 1 PGRMC1 Xq22-q24 Liver-rich protein that binds to progesterone  1.36  D14662 Anti-oxidant protein 2 AOP2 1q23.	bind
23200	2	6424	7	NULL	NULL	NULL	NULL	PGRMC1	GP		is					Rogesterone receptor membrane component 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_579_5_1089_s_193	15710396	11 Proteolysis and peptidolysis  1.37  Y12711 Rogesterone receptor membrane component 1 PGRMC1 Xq22-q24 Liver-rich protein that binds to progesterone  1.36  D14662 Anti-oxidant protein 2 AOP2 1q23.	bind
23201	3	6424	7	NULL	NULL	NULL	NULL	AOP2	GP		is					Anti-oxidant protein 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_579_5_1089_s_193	15710396	11 Proteolysis and peptidolysis  1.37  Y12711 Rogesterone receptor membrane component 1 PGRMC1 Xq22-q24 Liver-rich protein that binds to progesterone  1.36  D14662 Anti-oxidant protein 2 AOP2 1q23.	bind
20070	1	6425	5	NULL	NULL	0	NULL	Ang II	NULL	induced	increases	NULL				SM alpha-actin	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_185	15016729	11 Results thus support a model wherein Ang II-induced increases SM alpha-actin expression are mediated through Prx1-mediated increases in SRF binding to degenerate CArG elements and subsequent recruitment of myocardin and/or other SRF coactivators.	bind
20071	2	6425	5	NULL	NULL	0	NULL	SRF	NULL		bind	NULL					NULL	degenerate		CArG elements	NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_185	15016729	11 Results thus support a model wherein Ang II-induced increases SM alpha-actin expression are mediated through Prx1-mediated increases in SRF binding to degenerate CArG elements and subsequent recruitment of myocardin and/or other SRF coactivators.	bind
20072	3	6425	5	NULL	NULL	0	NULL	statement 2	NULL		recruits	NULL	subsequently			myocardin	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_185	15016729	11 Results thus support a model wherein Ang II-induced increases SM alpha-actin expression are mediated through Prx1-mediated increases in SRF binding to degenerate CArG elements and subsequent recruitment of myocardin and/or other SRF coactivators.	bind
20073	4	6425	5	NULL	NULL	0	NULL	statement 2	NULL		recruits	NULL	subsequently			SRF coactivators	NULL	other			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_185	15016729	11 Results thus support a model wherein Ang II-induced increases SM alpha-actin expression are mediated through Prx1-mediated increases in SRF binding to degenerate CArG elements and subsequent recruitment of myocardin and/or other SRF coactivators.	bind
20074	5	6425	5	NULL	NULL	0	NULL	Prx1	NULL		mediate	NULL				statement 2	NULL	increase in			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_185	15016729	11 Results thus support a model wherein Ang II-induced increases SM alpha-actin expression are mediated through Prx1-mediated increases in SRF binding to degenerate CArG elements and subsequent recruitment of myocardin and/or other SRF coactivators.	bind
20075	6	6425	5	NULL	NULL	0	NULL	Prx1	NULL		mediate	NULL				statement 3	NULL	increase in			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_185	15016729	11 Results thus support a model wherein Ang II-induced increases SM alpha-actin expression are mediated through Prx1-mediated increases in SRF binding to degenerate CArG elements and subsequent recruitment of myocardin and/or other SRF coactivators.	bind
20076	7	6425	5	NULL	NULL	0	NULL	Prx1	NULL		mediate	NULL				statement 4	NULL	increase in			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_185	15016729	11 Results thus support a model wherein Ang II-induced increases SM alpha-actin expression are mediated through Prx1-mediated increases in SRF binding to degenerate CArG elements and subsequent recruitment of myocardin and/or other SRF coactivators.	bind
20077	8	6425	5	NULL	NULL	0	NULL	statement 1	NULL		is mediated through	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_185	15016729	11 Results thus support a model wherein Ang II-induced increases SM alpha-actin expression are mediated through Prx1-mediated increases in SRF binding to degenerate CArG elements and subsequent recruitment of myocardin and/or other SRF coactivators.	bind
20078	9	6425	5	NULL	NULL	0	NULL	statement 1	NULL		is mediated through	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_185	15016729	11 Results thus support a model wherein Ang II-induced increases SM alpha-actin expression are mediated through Prx1-mediated increases in SRF binding to degenerate CArG elements and subsequent recruitment of myocardin and/or other SRF coactivators.	bind
20079	10	6425	5	NULL	NULL	0	NULL	statement 1	NULL		is mediated through	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_185	15016729	11 Results thus support a model wherein Ang II-induced increases SM alpha-actin expression are mediated through Prx1-mediated increases in SRF binding to degenerate CArG elements and subsequent recruitment of myocardin and/or other SRF coactivators.	bind
23202	1	6425	7	NULL	NULL	NULL	NULL	Ang II	GP	induced	increase					SM alpha-actin	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_185	15016729	11 Results thus support a model wherein Ang II-induced increases SM alpha-actin expression are mediated through Prx1-mediated increases in SRF binding to degenerate CArG elements and subsequent recruitment of myocardin and/or other SRF coactivators.	bind
23203	2	6425	7	NULL	NULL	NULL	NULL	 SRF	GP		bind									CArG elements 	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_185	15016729	11 Results thus support a model wherein Ang II-induced increases SM alpha-actin expression are mediated through Prx1-mediated increases in SRF binding to degenerate CArG elements and subsequent recruitment of myocardin and/or other SRF coactivators.	bind
23204	3	6425	7	NULL	NULL	NULL	NULL	statement 2	Process		degenerate									CArG elements 	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_185	15016729	11 Results thus support a model wherein Ang II-induced increases SM alpha-actin expression are mediated through Prx1-mediated increases in SRF binding to degenerate CArG elements and subsequent recruitment of myocardin and/or other SRF coactivators.	bind
23205	4	6425	7	NULL	NULL	NULL	NULL	Prx-1	GP		mediates					statement 2	Process	increase in			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_185	15016729	11 Results thus support a model wherein Ang II-induced increases SM alpha-actin expression are mediated through Prx1-mediated increases in SRF binding to degenerate CArG elements and subsequent recruitment of myocardin and/or other SRF coactivators.	bind
23206	5	6425	7	NULL	NULL	NULL	NULL	statement 2	Process		recruits					myocardin	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_185	15016729	11 Results thus support a model wherein Ang II-induced increases SM alpha-actin expression are mediated through Prx1-mediated increases in SRF binding to degenerate CArG elements and subsequent recruitment of myocardin and/or other SRF coactivators.	bind
23207	6	6425	7	NULL	NULL	NULL	NULL	statement 2	GP		recruits					SRF coactivators	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_185	15016729	11 Results thus support a model wherein Ang II-induced increases SM alpha-actin expression are mediated through Prx1-mediated increases in SRF binding to degenerate CArG elements and subsequent recruitment of myocardin and/or other SRF coactivators.	bind
23208	7	6425	7	NULL	NULL	NULL	NULL	statement 4	Process		mediates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_185	15016729	11 Results thus support a model wherein Ang II-induced increases SM alpha-actin expression are mediated through Prx1-mediated increases in SRF binding to degenerate CArG elements and subsequent recruitment of myocardin and/or other SRF coactivators.	bind
23209	8	6425	7	NULL	NULL	NULL	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1075_s_185	15016729	11 Results thus support a model wherein Ang II-induced increases SM alpha-actin expression are mediated through Prx1-mediated increases in SRF binding to degenerate CArG elements and subsequent recruitment of myocardin and/or other SRF coactivators.	bind
20032	1	6426	5	NULL	NULL	0	NULL	R-L3	NULL		bind	NULL				KCNQ1 channels	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_10_941_s_41	14576198	11 The mechanisms of R-L3 binding and modulation of KCNQ1 channels are not understood.	bind
20033	2	6426	5	NULL	NULL	0	NULL	R-L3	NULL		modulate	NULL				KCNQ1 channels	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_10_941_s_41	14576198	11 The mechanisms of R-L3 binding and modulation of KCNQ1 channels are not understood.	bind
23837	1	6426	7	NULL	NULL	NULL	NULL	R-L3	Chemical		bind					KCNQ1 channels	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_10_941_s_41	14576198	11 The mechanisms of R-L3 binding and modulation of KCNQ1 channels are not understood.	bind
23838	2	6426	7	NULL	NULL	NULL	NULL	R-L3	Chemical		modulates					KCNQ1 channels	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_10_941_s_41	14576198	11 The mechanisms of R-L3 binding and modulation of KCNQ1 channels are not understood.	bind
20080	1	6427	5	NULL	NULL	0	NULL	NFATc1	NULL		bind	NULL	sequence specific			bcl-2	NULL			NFAT site within promoter	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1492_s_186	15117818	11 The present study demonstrated that NFATc1 binds to the NFAT site within the bcl-2 promoter in a sequence-specific manner.	bind
23210	1	6427	7	NULL	NULL	NULL	NULL	NFATc1	GP		binds		sequence specific			bcl-2	GP			NFAT site within the promoter	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1492_s_186	15117818	11 The present study demonstrated that NFATc1 binds to the NFAT site within the bcl-2 promoter in a sequence-specific manner.	bind
20081	1	6428	5	NULL	NULL	0	NULL	ECSOD	NULL		bind	NULL		R213G		aortic endothelial cells	NULL	bovine			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_circulation_112_7_1047_s_161	16087794	11 Third, ECSODR213G binds to bovine aortic endothelial cells 50-fold less than ECSOD in vitro, as quantified by ELISA.	bind
20082	2	6428	5	NULL	NULL	0	NULL	ECSOD	NULL		bind	NULL				aortic endothelial cells	NULL	bovine			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_circulation_112_7_1047_s_161	16087794	11 Third, ECSODR213G binds to bovine aortic endothelial cells 50-fold less than ECSOD in vitro, as quantified by ELISA.	bind
20083	3	6428	5	NULL	NULL	0	NULL	statement 1	NULL		is lesser than	NULL				statement 2	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_circulation_112_7_1047_s_161	16087794	11 Third, ECSODR213G binds to bovine aortic endothelial cells 50-fold less than ECSOD in vitro, as quantified by ELISA.	bind
23212	1	6428	7	NULL	NULL	NULL	NULL	ECSOD	GP		binds to			R213G		aortic endothelial cells	Cell	bovine			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_circulation_112_7_1047_s_161	16087794	11 Third, ECSODR213G binds to bovine aortic endothelial cells 50-fold less than ECSOD in vitro, as quantified by ELISA.	bind
23213	2	6428	7	NULL	NULL	NULL	NULL	ECSOD	GP		binds					aortic endothelial cells	Cell	bovine			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_circulation_112_7_1047_s_161	16087794	11 Third, ECSODR213G binds to bovine aortic endothelial cells 50-fold less than ECSOD in vitro, as quantified by ELISA.	bind
23214	3	6428	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs less than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_7_1047_s_161	16087794	11 Third, ECSODR213G binds to bovine aortic endothelial cells 50-fold less than ECSOD in vitro, as quantified by ELISA.	bind
20084	1	6429	5	NULL	NULL	0	NULL	AT III	NULL		is	NULL				antithrombin III	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_4_1383_s_19	11583966	11, 12  In terms of anticoagulant factors, serum levels of antithrombin III (AT III), which binds and irreversibly inactivates a number of activated serine proteases, including thrombin, are reduced in patients with acute respiratory distress syndrome.	bind
20085	2	6429	5	NULL	NULL	0	NULL	AT III	NULL		bind	NULL				serine proteases	NULL	activated			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_4_1383_s_19	11583966	11, 12  In terms of anticoagulant factors, serum levels of antithrombin III (AT III), which binds and irreversibly inactivates a number of activated serine proteases, including thrombin, are reduced in patients with acute respiratory distress syndrome.	bind
20086	3	6429	5	NULL	NULL	0	NULL	AT III	NULL		bind	NULL				thrombin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_4_1383_s_19	11583966	11, 12  In terms of anticoagulant factors, serum levels of antithrombin III (AT III), which binds and irreversibly inactivates a number of activated serine proteases, including thrombin, are reduced in patients with acute respiratory distress syndrome.	bind
20087	4	6429	5	NULL	NULL	0	NULL	statement 2	NULL		inactivates	NULL	irreversibly			serine proteases	NULL	activated			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_4_1383_s_19	11583966	11, 12  In terms of anticoagulant factors, serum levels of antithrombin III (AT III), which binds and irreversibly inactivates a number of activated serine proteases, including thrombin, are reduced in patients with acute respiratory distress syndrome.	bind
20089	6	6429	5	NULL	NULL	0	NULL	AT III	NULL	serum levels of	is reduced in	NULL				acute respiratory distress syndrome	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_4_1383_s_19	11583966	11, 12  In terms of anticoagulant factors, serum levels of antithrombin III (AT III), which binds and irreversibly inactivates a number of activated serine proteases, including thrombin, are reduced in patients with acute respiratory distress syndrome.	bind
29999	5	6429	5	NULL	NULL	0	NULL	statement 3	NULL		inactivates	NULL	irreversibly			thrombin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_4_1383_s_19	11583966	11, 12  In terms of anticoagulant factors, serum levels of antithrombin III (AT III), which binds and irreversibly inactivates a number of activated serine proteases, including thrombin, are reduced in patients with acute respiratory distress syndrome.	bind
23215	1	6429	7	NULL	NULL	NULL	NULL	AT III	GP		binds					serine proteases	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_4_1383_s_19	11583966	11, 12  In terms of anticoagulant factors, serum levels of antithrombin III (AT III), which binds and irreversibly inactivates a number of activated serine proteases, including thrombin, are reduced in patients with acute respiratory distress syndrome.	bind
23216	2	6429	7	NULL	NULL	NULL	NULL	AT III	GP		binds					thrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_4_1383_s_19	11583966	11, 12  In terms of anticoagulant factors, serum levels of antithrombin III (AT III), which binds and irreversibly inactivates a number of activated serine proteases, including thrombin, are reduced in patients with acute respiratory distress syndrome.	bind
23217	3	6429	7	NULL	NULL	NULL	NULL	statement 1	Process		inactivates		irreversibly			serine proteases	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_4_1383_s_19	11583966	11, 12  In terms of anticoagulant factors, serum levels of antithrombin III (AT III), which binds and irreversibly inactivates a number of activated serine proteases, including thrombin, are reduced in patients with acute respiratory distress syndrome.	bind
23218	4	6429	7	NULL	NULL	NULL	NULL	statement 2	Process		inactivates					thrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_4_1383_s_19	11583966	11, 12  In terms of anticoagulant factors, serum levels of antithrombin III (AT III), which binds and irreversibly inactivates a number of activated serine proteases, including thrombin, are reduced in patients with acute respiratory distress syndrome.	bind
23219	5	6429	7	NULL	NULL	NULL	NULL	AT III	GP		is					antithrombin III	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_4_1383_s_19	11583966	11, 12  In terms of anticoagulant factors, serum levels of antithrombin III (AT III), which binds and irreversibly inactivates a number of activated serine proteases, including thrombin, are reduced in patients with acute respiratory distress syndrome.	bind
30689	6	6429	7	NULL	NULL	NULL	NULL	ATIII	GP	serum levels of 	is reduced in					acute respiratory distress syndrome	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_4_1383_s_19	11583966	11, 12  In terms of anticoagulant factors, serum levels of antithrombin III (AT III), which binds and irreversibly inactivates a number of activated serine proteases, including thrombin, are reduced in patients with acute respiratory distress syndrome.	bind
20136	1	6431	5	NULL	NULL	0	NULL	LPS	NULL		induces	NULL				cellular responses	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_179	12427659	11, 15, 27 It has been proposed that the cellular responses induced by LPS occur through the binding of LPS to CD14, with subsequent signal transduction via TLR4.	bind
20137	2	6431	5	NULL	NULL	0	NULL	LPS	NULL		bind	NULL				CD14	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_179	12427659	11, 15, 27 It has been proposed that the cellular responses induced by LPS occur through the binding of LPS to CD14, with subsequent signal transduction via TLR4.	bind
20138	3	6431	5	NULL	NULL	0	NULL	statement 1	NULL		occurs through	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_179	12427659	11, 15, 27 It has been proposed that the cellular responses induced by LPS occur through the binding of LPS to CD14, with subsequent signal transduction via TLR4.	bind
20139	4	6431	5	NULL	NULL	0	NULL	statement 3	NULL		occurs with	NULL	subsequently			signal transduction	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_179	12427659	11, 15, 27 It has been proposed that the cellular responses induced by LPS occur through the binding of LPS to CD14, with subsequent signal transduction via TLR4.	bind
20140	5	6431	5	NULL	NULL	0	NULL	statement 4	NULL		via	NULL				TLR4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_179	12427659	11, 15, 27 It has been proposed that the cellular responses induced by LPS occur through the binding of LPS to CD14, with subsequent signal transduction via TLR4.	bind
23220	1	6431	7	NULL	NULL	NULL	NULL	LPS	Chemical		bind					CD14	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_179	12427659	11, 15, 27 It has been proposed that the cellular responses induced by LPS occur through the binding of LPS to CD14, with subsequent signal transduction via TLR4.	bind
23221	2	6431	7	NULL	NULL	NULL	NULL	LPS	Chemical		induce					cellular response	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_179	12427659	11, 15, 27 It has been proposed that the cellular responses induced by LPS occur through the binding of LPS to CD14, with subsequent signal transduction via TLR4.	bind
23222	3	6431	7	NULL	NULL	NULL	NULL	statement 3	Process		occurs with					signal transduction	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_179	12427659	11, 15, 27 It has been proposed that the cellular responses induced by LPS occur through the binding of LPS to CD14, with subsequent signal transduction via TLR4.	bind
23223	4	6431	7	NULL	NULL	NULL	NULL	statement 3	Process		occurs via					TLR4	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_179	12427659	11, 15, 27 It has been proposed that the cellular responses induced by LPS occur through the binding of LPS to CD14, with subsequent signal transduction via TLR4.	bind
20141	1	6432	5	10	NULL	0	NULL				plays a role in		major		CRE	statement 8					NULL	osteoblasts	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1415_s_161	12231559	11, 16 Previous reports have indicated that CRE, CCAAT/enhancer binding protein-beta (same as NF-IL6), and activator protein-1 motifs play major roles in the shear stress induction of the COX-2 gene in osteoblasts, which is consistent with our results because of multiple binding activity of the CRE for CRE binding protein, CCAAT/enhancer binding proteins, and activator protein-1.	bind
20142	2	6432	5	10	NULL	0	NULL	CCAAT/enhancer binding protein-beta			is a synonym of					NF-IL6					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1415_s_161	12231559	11, 16 Previous reports have indicated that CRE, CCAAT/enhancer binding protein-beta (same as NF-IL6), and activator protein-1 motifs play major roles in the shear stress induction of the COX-2 gene in osteoblasts, which is consistent with our results because of multiple binding activity of the CRE for CRE binding protein, CCAAT/enhancer binding proteins, and activator protein-1.	bind
20143	3	6432	5	10	NULL	0	NULL	CCAAT/enhancer binding protein-beta			plays a role in		major			statement 8					NULL	osteoblasts	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1415_s_161	12231559	11, 16 Previous reports have indicated that CRE, CCAAT/enhancer binding protein-beta (same as NF-IL6), and activator protein-1 motifs play major roles in the shear stress induction of the COX-2 gene in osteoblasts, which is consistent with our results because of multiple binding activity of the CRE for CRE binding protein, CCAAT/enhancer binding proteins, and activator protein-1.	bind
20144	4	6432	5	10	NULL	0	NULL	activator protein-1			plays a role in		major			statement 8					NULL	osteoblasts	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1415_s_161	12231559	11, 16 Previous reports have indicated that CRE, CCAAT/enhancer binding protein-beta (same as NF-IL6), and activator protein-1 motifs play major roles in the shear stress induction of the COX-2 gene in osteoblasts, which is consistent with our results because of multiple binding activity of the CRE for CRE binding protein, CCAAT/enhancer binding proteins, and activator protein-1.	bind
20145	5	6432	5	NULL	NULL	0	NULL		NULL		bind	NULL			CRE	CRE binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1415_s_161	12231559	11, 16 Previous reports have indicated that CRE, CCAAT/enhancer binding protein-beta (same as NF-IL6), and activator protein-1 motifs play major roles in the shear stress induction of the COX-2 gene in osteoblasts, which is consistent with our results because of multiple binding activity of the CRE for CRE binding protein, CCAAT/enhancer binding proteins, and activator protein-1.	bind
20146	6	6432	5	NULL	NULL	0	NULL		NULL		bind	NULL			CRE	CCAAT/enhancer binding proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1415_s_161	12231559	11, 16 Previous reports have indicated that CRE, CCAAT/enhancer binding protein-beta (same as NF-IL6), and activator protein-1 motifs play major roles in the shear stress induction of the COX-2 gene in osteoblasts, which is consistent with our results because of multiple binding activity of the CRE for CRE binding protein, CCAAT/enhancer binding proteins, and activator protein-1.	bind
20147	7	6432	5	NULL	NULL	0	NULL		NULL		bind	NULL			CRE	activator protein-1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1415_s_161	12231559	11, 16 Previous reports have indicated that CRE, CCAAT/enhancer binding protein-beta (same as NF-IL6), and activator protein-1 motifs play major roles in the shear stress induction of the COX-2 gene in osteoblasts, which is consistent with our results because of multiple binding activity of the CRE for CRE binding protein, CCAAT/enhancer binding proteins, and activator protein-1.	bind
54258	8	6432	5	10	NULL	0	NULL	shear stress			induces					COX-2 gene					NULL	osteoblasts	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1415_s_161	12231559	11, 16 Previous reports have indicated that CRE, CCAAT/enhancer binding protein-beta (same as NF-IL6), and activator protein-1 motifs play major roles in the shear stress induction of the COX-2 gene in osteoblasts, which is consistent with our results because of multiple binding activity of the CRE for CRE binding protein, CCAAT/enhancer binding proteins, and activator protein-1.	bind
23340	1	6432	7	NULL	NULL	NULL	NULL	shear stress 	Process		induce					COX-2 gene	GP				NULL	in osteoblasts	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1415_s_161	12231559	11, 16 Previous reports have indicated that CRE, CCAAT/enhancer binding protein-beta (same as NF-IL6), and activator protein-1 motifs play major roles in the shear stress induction of the COX-2 gene in osteoblasts, which is consistent with our results because of multiple binding activity of the CRE for CRE binding protein, CCAAT/enhancer binding proteins, and activator protein-1.	bind
23342	2	6432	7	NULL	NULL	NULL	NULL				plays a role in		major		 CRE	statement 1	Process				NULL	osteoblasts	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1415_s_161	12231559	11, 16 Previous reports have indicated that CRE, CCAAT/enhancer binding protein-beta (same as NF-IL6), and activator protein-1 motifs play major roles in the shear stress induction of the COX-2 gene in osteoblasts, which is consistent with our results because of multiple binding activity of the CRE for CRE binding protein, CCAAT/enhancer binding proteins, and activator protein-1.	bind
23344	3	6432	7	NULL	NULL	NULL	NULL	CCAAT/enhancer binding protein-beta	GP		plays a role in		major			statement 1	Process				NULL	osteoblasts	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1415_s_161	12231559	11, 16 Previous reports have indicated that CRE, CCAAT/enhancer binding protein-beta (same as NF-IL6), and activator protein-1 motifs play major roles in the shear stress induction of the COX-2 gene in osteoblasts, which is consistent with our results because of multiple binding activity of the CRE for CRE binding protein, CCAAT/enhancer binding proteins, and activator protein-1.	bind
23348	4	6432	7	NULL	NULL	NULL	NULL	activator protein-1 motif	GP		plays a role in		major			statement 1	Process				NULL	osteoblasts	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1415_s_161	12231559	11, 16 Previous reports have indicated that CRE, CCAAT/enhancer binding protein-beta (same as NF-IL6), and activator protein-1 motifs play major roles in the shear stress induction of the COX-2 gene in osteoblasts, which is consistent with our results because of multiple binding activity of the CRE for CRE binding protein, CCAAT/enhancer binding proteins, and activator protein-1.	bind
23352	5	6432	7	NULL	NULL	NULL	NULL	CRE binding protein	GP		bind									CRE	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1415_s_161	12231559	11, 16 Previous reports have indicated that CRE, CCAAT/enhancer binding protein-beta (same as NF-IL6), and activator protein-1 motifs play major roles in the shear stress induction of the COX-2 gene in osteoblasts, which is consistent with our results because of multiple binding activity of the CRE for CRE binding protein, CCAAT/enhancer binding proteins, and activator protein-1.	bind
23355	6	6432	7	NULL	NULL	NULL	NULL	CCAAT/enhancer binding protein	GP		bind									CRE	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1415_s_161	12231559	11, 16 Previous reports have indicated that CRE, CCAAT/enhancer binding protein-beta (same as NF-IL6), and activator protein-1 motifs play major roles in the shear stress induction of the COX-2 gene in osteoblasts, which is consistent with our results because of multiple binding activity of the CRE for CRE binding protein, CCAAT/enhancer binding proteins, and activator protein-1.	bind
23357	7	6432	7	NULL	NULL	NULL	NULL	 activator protein-1	GP		bind									CRE	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1415_s_161	12231559	11, 16 Previous reports have indicated that CRE, CCAAT/enhancer binding protein-beta (same as NF-IL6), and activator protein-1 motifs play major roles in the shear stress induction of the COX-2 gene in osteoblasts, which is consistent with our results because of multiple binding activity of the CRE for CRE binding protein, CCAAT/enhancer binding proteins, and activator protein-1.	bind
23358	8	6432	7	NULL	NULL	NULL	NULL	CCAAT/enhancer binding protein-beta	GP		is a synonym of					NF-IL6	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1415_s_161	12231559	11, 16 Previous reports have indicated that CRE, CCAAT/enhancer binding protein-beta (same as NF-IL6), and activator protein-1 motifs play major roles in the shear stress induction of the COX-2 gene in osteoblasts, which is consistent with our results because of multiple binding activity of the CRE for CRE binding protein, CCAAT/enhancer binding proteins, and activator protein-1.	bind
20148	1	6433	5	NULL	NULL	0	NULL	Grb2	NULL		bind	NULL				Shc	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1759_s_228	10550332	11, 28, 29 Our data demonstrating increased binding of adapter protein Grb2 to Shc and to Sos indicate their involvement as mediators of receptor tyrosine kinase signaling via Ras during ulcer healing.	bind
20149	2	6433	5	NULL	NULL	0	NULL	Grb2	NULL		bind	NULL				Sos	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1759_s_228	10550332	11, 28, 29 Our data demonstrating increased binding of adapter protein Grb2 to Shc and to Sos indicate their involvement as mediators of receptor tyrosine kinase signaling via Ras during ulcer healing.	bind
20150	3	6433	5	NULL	NULL	0	NULL	Grb2	NULL		mediates	NULL				receptor tyrosine kinase signaling	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1759_s_228	10550332	11, 28, 29 Our data demonstrating increased binding of adapter protein Grb2 to Shc and to Sos indicate their involvement as mediators of receptor tyrosine kinase signaling via Ras during ulcer healing.	bind
20151	4	6433	5	NULL	NULL	0	NULL	statement 3	NULL		via	NULL				Ras	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1759_s_228	10550332	11, 28, 29 Our data demonstrating increased binding of adapter protein Grb2 to Shc and to Sos indicate their involvement as mediators of receptor tyrosine kinase signaling via Ras during ulcer healing.	bind
20152	5	6433	5	NULL	NULL	0	NULL	statement 1	NULL	increased	indicates	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_5_1759_s_228	10550332	11, 28, 29 Our data demonstrating increased binding of adapter protein Grb2 to Shc and to Sos indicate their involvement as mediators of receptor tyrosine kinase signaling via Ras during ulcer healing.	bind
20153	6	6433	5	NULL	NULL	0	NULL	statement 2	NULL	increased	indicates	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_5_1759_s_228	10550332	11, 28, 29 Our data demonstrating increased binding of adapter protein Grb2 to Shc and to Sos indicate their involvement as mediators of receptor tyrosine kinase signaling via Ras during ulcer healing.	bind
30019	7	6433	5	NULL	NULL	0	NULL	statement 3	NULL		occurs during	NULL				ulcer	NULL	healing of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_5_1759_s_228	10550332	11, 28, 29 Our data demonstrating increased binding of adapter protein Grb2 to Shc and to Sos indicate their involvement as mediators of receptor tyrosine kinase signaling via Ras during ulcer healing.	bind
30021	8	6433	5	NULL	NULL	0	NULL	Grb2	NULL		is a type of	NULL				adapter protein	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_5_1759_s_228	10550332	11, 28, 29 Our data demonstrating increased binding of adapter protein Grb2 to Shc and to Sos indicate their involvement as mediators of receptor tyrosine kinase signaling via Ras during ulcer healing.	bind
23361	1	6433	7	NULL	NULL	NULL	NULL	Grb2 	GP		bind					Shc	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1759_s_228	10550332	11, 28, 29 Our data demonstrating increased binding of adapter protein Grb2 to Shc and to Sos indicate their involvement as mediators of receptor tyrosine kinase signaling via Ras during ulcer healing.	bind
23362	2	6433	7	NULL	NULL	NULL	NULL	Grb2 	GP		bind					Sos	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1759_s_228	10550332	11, 28, 29 Our data demonstrating increased binding of adapter protein Grb2 to Shc and to Sos indicate their involvement as mediators of receptor tyrosine kinase signaling via Ras during ulcer healing.	bind
23363	3	6433	7	NULL	NULL	NULL	NULL	Grb2 	GP		mediates					tyrosine kinase signaling	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1759_s_228	10550332	11, 28, 29 Our data demonstrating increased binding of adapter protein Grb2 to Shc and to Sos indicate their involvement as mediators of receptor tyrosine kinase signaling via Ras during ulcer healing.	bind
23364	4	6433	7	NULL	NULL	NULL	NULL	statement 3	Process		occurs via					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1759_s_228	10550332	11, 28, 29 Our data demonstrating increased binding of adapter protein Grb2 to Shc and to Sos indicate their involvement as mediators of receptor tyrosine kinase signaling via Ras during ulcer healing.	bind
23365	5	6433	7	NULL	NULL	NULL	NULL	statement 3	Process		occur during					Ulcer 	MedicalFinding	healing of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1759_s_228	10550332	11, 28, 29 Our data demonstrating increased binding of adapter protein Grb2 to Shc and to Sos indicate their involvement as mediators of receptor tyrosine kinase signaling via Ras during ulcer healing.	bind
54259	6	6433	7	NULL	NULL	NULL	NULL	Grb2	GP		is a type of					adapter protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1759_s_228	10550332	11, 28, 29 Our data demonstrating increased binding of adapter protein Grb2 to Shc and to Sos indicate their involvement as mediators of receptor tyrosine kinase signaling via Ras during ulcer healing.	bind
20154	1	6434	5	NULL	NULL	0	NULL	FoxA1	NULL		bind	NULL					NULL			MMTV LTR	NULL		NULL	NULL	NULL	NULL	gw70_nature_435_7044_944_s_142	15959514	11, 281 285 (2000) |  PubMed |  ChemPort |            Holmqvist, P. H., Belikov, S., Zaret, K. S. & Wrange, O. FoxA1 binding to the  MMTV LTR modulates chromatin structure and transcription.	bind
20155	2	6434	5	NULL	NULL	0	NULL	statement 1	NULL		modulates	NULL				chromatin	NULL	structure of			NULL		0	NULL	NULL	NULL	gw70_nature_435_7044_944_s_142	15959514	11, 281 285 (2000) |  PubMed |  ChemPort |            Holmqvist, P. H., Belikov, S., Zaret, K. S. & Wrange, O. FoxA1 binding to the  MMTV LTR modulates chromatin structure and transcription.	bind
20156	3	6434	5	NULL	NULL	0	NULL	statement 1	NULL		modulates	NULL				transcription	NULL				NULL		0	NULL	NULL	NULL	gw70_nature_435_7044_944_s_142	15959514	11, 281 285 (2000) |  PubMed |  ChemPort |            Holmqvist, P. H., Belikov, S., Zaret, K. S. & Wrange, O. FoxA1 binding to the  MMTV LTR modulates chromatin structure and transcription.	bind
23366	1	6434	7	NULL	NULL	NULL	NULL	FoxA1	GP		binds to									MMTV LTR	NULL		NULL	NULL	NULL	NULL	gw70_nature_435_7044_944_s_142	15959514	11, 281 285 (2000) |  PubMed |  ChemPort |            Holmqvist, P. H., Belikov, S., Zaret, K. S. & Wrange, O. FoxA1 binding to the  MMTV LTR modulates chromatin structure and transcription.	bind
23367	2	6434	7	NULL	NULL	NULL	NULL	statement 1	Process		modulate					chromatin	Chromosome	structure of			NULL		NULL	NULL	NULL	NULL	gw70_nature_435_7044_944_s_142	15959514	11, 281 285 (2000) |  PubMed |  ChemPort |            Holmqvist, P. H., Belikov, S., Zaret, K. S. & Wrange, O. FoxA1 binding to the  MMTV LTR modulates chromatin structure and transcription.	bind
23368	3	6434	7	NULL	NULL	NULL	NULL	statement 1	Process		modulate					transcription	Process				NULL		NULL	NULL	NULL	NULL	gw70_nature_435_7044_944_s_142	15959514	11, 281 285 (2000) |  PubMed |  ChemPort |            Holmqvist, P. H., Belikov, S., Zaret, K. S. & Wrange, O. FoxA1 binding to the  MMTV LTR modulates chromatin structure and transcription.	bind
20157	1	6435	5	NULL	NULL	0	NULL	BNP	NULL		bind	NULL				natriuretic peptide receptor A	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_109_13_1680_s_39	15023890	11,12  Studies have established that BNP binds to the natriuretic peptide receptor A, which, via 3'',5''-cGMP, mediates its biological actions.	bind
20158	2	6435	5	NULL	NULL	0	NULL	statement 1	NULL		mediates	NULL				actions of BNP	NULL	biological			NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_13_1680_s_39	15023890	11,12  Studies have established that BNP binds to the natriuretic peptide receptor A, which, via 3'',5''-cGMP, mediates its biological actions.	bind
20159	3	6435	5	NULL	NULL	0	NULL	statement 2	NULL		via	NULL				3'',5''-cGMP	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_109_13_1680_s_39	15023890	11,12  Studies have established that BNP binds to the natriuretic peptide receptor A, which, via 3'',5''-cGMP, mediates its biological actions.	bind
23369	1	6435	7	NULL	NULL	NULL	NULL	BNP	GP		binds to					natriuretic peptide receptor A	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_13_1680_s_39	15023890	11,12  Studies have established that BNP binds to the natriuretic peptide receptor A, which, via 3'',5''-cGMP, mediates its biological actions.	bind
23370	2	6435	7	NULL	NULL	NULL	NULL	statement 1	Process		mediates					BNP	GP	actions of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_13_1680_s_39	15023890	11,12  Studies have established that BNP binds to the natriuretic peptide receptor A, which, via 3'',5''-cGMP, mediates its biological actions.	bind
23371	3	6435	7	NULL	NULL	NULL	NULL	statement 2	Process		occur via					3'',5''-cGMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_13_1680_s_39	15023890	11,12  Studies have established that BNP binds to the natriuretic peptide receptor A, which, via 3'',5''-cGMP, mediates its biological actions.	bind
20160	2	6436	5	NULL	NULL	0	NULL	statement 1	NULL	restimulation of	bind	NULL	may			Fas receptors	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_387_s_75	11159176	11- 14 On restimulation, membrane-bound Fas-L molecules may bind to Fas receptors, eg, by membrane folding, to trigger the death signaling cascade that causes the apoptotic suicide of the T cell.	bind
20161	3	6436	5	NULL	NULL	0	NULL	statement 2	NULL		occurs by	NULL				membrane folding	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_387_s_75	11159176	11- 14 On restimulation, membrane-bound Fas-L molecules may bind to Fas receptors, eg, by membrane folding, to trigger the death signaling cascade that causes the apoptotic suicide of the T cell.	bind
20162	4	6436	5	NULL	NULL	0	NULL	statement 3	NULL		triggers	NULL				death signaling cascade	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_387_s_75	11159176	11- 14 On restimulation, membrane-bound Fas-L molecules may bind to Fas receptors, eg, by membrane folding, to trigger the death signaling cascade that causes the apoptotic suicide of the T cell.	bind
20163	5	6436	5	NULL	NULL	0	NULL	death signaling cascade	NULL		causes	NULL				T cell	NULL	apoptosis of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_387_s_75	11159176	11- 14 On restimulation, membrane-bound Fas-L molecules may bind to Fas receptors, eg, by membrane folding, to trigger the death signaling cascade that causes the apoptotic suicide of the T cell.	bind
46189	1	6436	5	NULL	NULL	0	NULL	Fas-L molecules	NULL		bind	NULL				membrane	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_387_s_75	11159176	11- 14 On restimulation, membrane-bound Fas-L molecules may bind to Fas receptors, eg, by membrane folding, to trigger the death signaling cascade that causes the apoptotic suicide of the T cell.	bind
23372	2	6436	7	NULL	NULL	NULL	NULL	statement 1	Process		bind					Fas receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_387_s_75	11159176	11- 14 On restimulation, membrane-bound Fas-L molecules may bind to Fas receptors, eg, by membrane folding, to trigger the death signaling cascade that causes the apoptotic suicide of the T cell.	bind
23373	3	6436	7	NULL	NULL	NULL	NULL	statement 2	Process		occurs upon					restimulation	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_387_s_75	11159176	11- 14 On restimulation, membrane-bound Fas-L molecules may bind to Fas receptors, eg, by membrane folding, to trigger the death signaling cascade that causes the apoptotic suicide of the T cell.	bind
23374	4	6436	7	NULL	NULL	NULL	NULL	statement 2	Process		occurs by					membrane folding	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_387_s_75	11159176	11- 14 On restimulation, membrane-bound Fas-L molecules may bind to Fas receptors, eg, by membrane folding, to trigger the death signaling cascade that causes the apoptotic suicide of the T cell.	bind
23375	4	6436	7	NULL	NULL	NULL	NULL	statement 2	Process		trigger					death signaling cascade	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_387_s_75	11159176	11- 14 On restimulation, membrane-bound Fas-L molecules may bind to Fas receptors, eg, by membrane folding, to trigger the death signaling cascade that causes the apoptotic suicide of the T cell.	bind
23376	5	6436	7	NULL	NULL	NULL	NULL	statement 4	Process		leads to					T cell	Cell	apoptosis of  			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_387_s_75	11159176	11- 14 On restimulation, membrane-bound Fas-L molecules may bind to Fas receptors, eg, by membrane folding, to trigger the death signaling cascade that causes the apoptotic suicide of the T cell.	bind
45752	1	6436	7	NULL	NULL	NULL	NULL	Fas-L molecules	GP		bind					membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_387_s_75	11159176	11- 14 On restimulation, membrane-bound Fas-L molecules may bind to Fas receptors, eg, by membrane folding, to trigger the death signaling cascade that causes the apoptotic suicide of the T cell.	bind
20164	1	6437	5	NULL	NULL	0	NULL	XPC	NULL		bind	NULL				XPA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_121	12486030	11-13 and Fig.  3), it is possible that the binding of XPC (or RPA) to XPA may competitively exclude RPA (or XPC) from the complex.	bind
20165	2	6437	5	NULL	NULL	0	NULL	RPA	NULL		bind	NULL				XPA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_121	12486030	11-13 and Fig.  3), it is possible that the binding of XPC (or RPA) to XPA may competitively exclude RPA (or XPC) from the complex.	bind
20166	3	6437	5	NULL	NULL	0	NULL	statement 1	NULL		exclude	NULL	may;;competitively			RPA	NULL	from the complex			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_121	12486030	11-13 and Fig.  3), it is possible that the binding of XPC (or RPA) to XPA may competitively exclude RPA (or XPC) from the complex.	bind
20167	4	6437	5	NULL	NULL	0	NULL	statement 2	NULL		exclude	NULL	may;;competitively			XPC	NULL	from the complex			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_121	12486030	11-13 and Fig.  3), it is possible that the binding of XPC (or RPA) to XPA may competitively exclude RPA (or XPC) from the complex.	bind
23377	1	6437	7	NULL	NULL	NULL	NULL	XPC	GP		bind					XPA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_121	12486030	11-13 and Fig.  3), it is possible that the binding of XPC (or RPA) to XPA may competitively exclude RPA (or XPC) from the complex.	bind
23378	2	6437	7	NULL	NULL	NULL	NULL	RPA	GP		bind					XPA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_121	12486030	11-13 and Fig.  3), it is possible that the binding of XPC (or RPA) to XPA may competitively exclude RPA (or XPC) from the complex.	bind
23379	3	6437	7	NULL	NULL	NULL	NULL	statement 1	Process		exclude		may;;competitively			RPA	GP	from the complex			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_121	12486030	11-13 and Fig.  3), it is possible that the binding of XPC (or RPA) to XPA may competitively exclude RPA (or XPC) from the complex.	bind
23380	4	6437	7	NULL	NULL	NULL	NULL	statement 2	Process		exclude		may;;competitively			XPC	GP	from the complex			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_7476_s_121	12486030	11-13 and Fig.  3), it is possible that the binding of XPC (or RPA) to XPA may competitively exclude RPA (or XPC) from the complex.	bind
20168	1	6438	5	NULL	NULL	0	NULL	cadherin-like protein	NULL		bind	NULL				Cry1Aa	NULL				NULL	M. sexta	NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_30_11_1069_s_10	10989294	11.2), the exception being a cadherin-like protein which bound Cry1Aa in  M. sexta ( Valdamudi et al., 1995;   Francis and Bulla, 1997;   Keeton and Bulla, 1997).	bind
23381	1	6438	7	NULL	NULL	NULL	NULL	 cadherin-like protein	GP		bind					Cry1Aa	GP				NULL	M. sexta	NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_30_11_1069_s_10	10989294	11.2), the exception being a cadherin-like protein which bound Cry1Aa in  M. sexta ( Valdamudi et al., 1995;   Francis and Bulla, 1997;   Keeton and Bulla, 1997).	bind
20169	1	6440	5	NULL	NULL	0	NULL	Ag+	NULL		bind	NULL				metallothionein	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_35_44_8909290_s_1	8909290	111Cd NMR studies of the domain specificity of Ag+ and Cu+ binding to metallothionein..	bind
20170	2	6440	5	NULL	NULL	0	NULL	Cu+	NULL		bind	NULL				metallothionein	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_35_44_8909290_s_1	8909290	111Cd NMR studies of the domain specificity of Ag+ and Cu+ binding to metallothionein..	bind
23382	1	6440	7	NULL	NULL	NULL	NULL	Ag+	Chemical		bind					metallothionein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_35_44_8909290_s_1	8909290	111Cd NMR studies of the domain specificity of Ag+ and Cu+ binding to metallothionein..	bind
23383	2	6440	7	NULL	NULL	NULL	NULL	Cu+	Chemical		bind					metallothionein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_35_44_8909290_s_1	8909290	111Cd NMR studies of the domain specificity of Ag+ and Cu+ binding to metallothionein..	bind
20171	1	6441	5	NULL	NULL	0	NULL	ERalpha	NULL		bind	NULL	constitutively			PI3K	NULL		p85alpha subunit		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_123	12482819	113 Interestingly, ERalpha binds constitutively to the p85alpha subunit of PI3K and activates PI3K/Akt in an E2-independent manner, implicating a feed-forward mechanism of ERalpha activation.	bind
20172	2	6441	5	10	NULL	0	NULL	statement 1			activates					PI3K/Akt					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_123	12482819	113 Interestingly, ERalpha binds constitutively to the p85alpha subunit of PI3K and activates PI3K/Akt in an E2-independent manner, implicating a feed-forward mechanism of ERalpha activation.	bind
20173	3	6441	5	NULL	NULL	0	NULL	statement 2	NULL		is independent of	NULL				E2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_123	12482819	113 Interestingly, ERalpha binds constitutively to the p85alpha subunit of PI3K and activates PI3K/Akt in an E2-independent manner, implicating a feed-forward mechanism of ERalpha activation.	bind
20174	4	6441	5	NULL	NULL	0	NULL	statement 3	NULL		implicate	NULL				feed-forward mechanism of ERalpha	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_123	12482819	113 Interestingly, ERalpha binds constitutively to the p85alpha subunit of PI3K and activates PI3K/Akt in an E2-independent manner, implicating a feed-forward mechanism of ERalpha activation.	bind
23384	1	6441	7	NULL	NULL	NULL	NULL	ERalpha	GP		binds		constitutively			PI3K	GP		p85alpha subunit		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_123	12482819	113 Interestingly, ERalpha binds constitutively to the p85alpha subunit of PI3K and activates PI3K/Akt in an E2-independent manner, implicating a feed-forward mechanism of ERalpha activation.	bind
23385	2	6441	7	NULL	NULL	NULL	NULL	statement 1	Process		activates					PI3K/Akt	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_123	12482819	113 Interestingly, ERalpha binds constitutively to the p85alpha subunit of PI3K and activates PI3K/Akt in an E2-independent manner, implicating a feed-forward mechanism of ERalpha activation.	bind
23386	3	6441	7	NULL	NULL	NULL	NULL	statement 2	Process		is independent of					E2	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_123	12482819	113 Interestingly, ERalpha binds constitutively to the p85alpha subunit of PI3K and activates PI3K/Akt in an E2-independent manner, implicating a feed-forward mechanism of ERalpha activation.	bind
23387	4	6441	7	NULL	NULL	NULL	NULL	statement 2	Process		implicate					feed-forward mechanism ofER alpha	Process	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_123	12482819	113 Interestingly, ERalpha binds constitutively to the p85alpha subunit of PI3K and activates PI3K/Akt in an E2-independent manner, implicating a feed-forward mechanism of ERalpha activation.	bind
20175	1	6442	5	NULL	NULL	0	NULL	Cd(II)	NULL		bind	NULL				Suwannee River fulvic acid	NULL				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_ann-chim_95_7-8_16235791_s_1	16235791	113Cd NMR and fluorescence studies of multiple binding mechanisms of Cd(II) by the Suwannee River fulvic acid..	bind
23388	1	6442	7	NULL	NULL	NULL	NULL	Cd(II) 	Chemical		bind					Suwannee River fulvic acid	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_ann-chim_95_7-8_16235791_s_1	16235791	113Cd NMR and fluorescence studies of multiple binding mechanisms of Cd(II) by the Suwannee River fulvic acid..	bind
20176	1	6443	5	NULL	NULL	0	NULL		NULL	prebending	destabilizes	NULL			estrogen response element	estrogen receptor	NULL	binding of	DNA binding domain		NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_656	11452016	114       Kim,J., DeHaan,G., Nardulli,A.M. and Shapiro,D.J. (1997) Prebending the estrogen response element destabilized binding of the estrogen receptor DNA binding domain.	bind
23389	1	6443	7	NULL	NULL	NULL	NULL			Prebending	destabilize				estrogen response element	estrogen receptor 	GP	binding of	DNA binding domain		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_656	11452016	114       Kim,J., DeHaan,G., Nardulli,A.M. and Shapiro,D.J. (1997) Prebending the estrogen response element destabilized binding of the estrogen receptor DNA binding domain.	bind
23126	1	6444	5	10	NULL	0	NULL	1178T			bind		dramatically reduced			PI 3-kinase					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_49_29286_s_122	7493960	1178T ( 31) shows dramatically reduced binding  of PI 3-kinase, while Y250F ( 8,  9,  32) is  deficient in associating with SHC and thereby unable to initiate  signaling through Ras. NG59 ( 38) binds none of the molecules  characterized so far, 1387T (a truncated mutant protein lacking the  membrane anchor sequence) only binds PP2A( 39,  60) ,  and dl1015 associates with all cellular enzymes described so far, but  is unable to activate PI 3-kinase( 40,  41) .	bind
23127	2	6444	5	NULL	NULL	0	NULL		NULL		is deficient in associating with	NULL		Y250F		SHC	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_49_29286_s_122	7493960	1178T ( 31) shows dramatically reduced binding  of PI 3-kinase, while Y250F ( 8,  9,  32) is  deficient in associating with SHC and thereby unable to initiate  signaling through Ras. NG59 ( 38) binds none of the molecules  characterized so far, 1387T (a truncated mutant protein lacking the  membrane anchor sequence) only binds PP2A( 39,  60) ,  and dl1015 associates with all cellular enzymes described so far, but  is unable to activate PI 3-kinase( 40,  41) .	bind
23128	3	6444	5	10	NULL	0	NULL	statement 2	NULL		does not initiate	NULL				Ras	NULL	signaling through			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_49_29286_s_122	7493960	1178T ( 31) shows dramatically reduced binding  of PI 3-kinase, while Y250F ( 8,  9,  32) is  deficient in associating with SHC and thereby unable to initiate  signaling through Ras. NG59 ( 38) binds none of the molecules  characterized so far, 1387T (a truncated mutant protein lacking the  membrane anchor sequence) only binds PP2A( 39,  60) ,  and dl1015 associates with all cellular enzymes described so far, but  is unable to activate PI 3-kinase( 40,  41) .	bind
23129	4	6444	5	NULL	NULL	0	NULL	1387T	NULL		is	NULL				truncated mutant protein lacking the membrane anchor sequence	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_49_29286_s_122	7493960	1178T ( 31) shows dramatically reduced binding  of PI 3-kinase, while Y250F ( 8,  9,  32) is  deficient in associating with SHC and thereby unable to initiate  signaling through Ras. NG59 ( 38) binds none of the molecules  characterized so far, 1387T (a truncated mutant protein lacking the  membrane anchor sequence) only binds PP2A( 39,  60) ,  and dl1015 associates with all cellular enzymes described so far, but  is unable to activate PI 3-kinase( 40,  41) .	bind
23130	5	6444	5	NULL	NULL	0	NULL	1387T	NULL		bind	NULL	only			PP2A	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_49_29286_s_122	7493960	1178T ( 31) shows dramatically reduced binding  of PI 3-kinase, while Y250F ( 8,  9,  32) is  deficient in associating with SHC and thereby unable to initiate  signaling through Ras. NG59 ( 38) binds none of the molecules  characterized so far, 1387T (a truncated mutant protein lacking the  membrane anchor sequence) only binds PP2A( 39,  60) ,  and dl1015 associates with all cellular enzymes described so far, but  is unable to activate PI 3-kinase( 40,  41) .	bind
23131	6	6444	5	NULL	NULL	0	NULL	dl1015 	NULL		associates with	NULL				cellular enzymes	NULL	all			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_49_29286_s_122	7493960	1178T ( 31) shows dramatically reduced binding  of PI 3-kinase, while Y250F ( 8,  9,  32) is  deficient in associating with SHC and thereby unable to initiate  signaling through Ras. NG59 ( 38) binds none of the molecules  characterized so far, 1387T (a truncated mutant protein lacking the  membrane anchor sequence) only binds PP2A( 39,  60) ,  and dl1015 associates with all cellular enzymes described so far, but  is unable to activate PI 3-kinase( 40,  41) .	bind
23132	7	6444	5	NULL	NULL	0	NULL	dl1015	NULL		does not activate	NULL				PI 3-kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_49_29286_s_122	7493960	1178T ( 31) shows dramatically reduced binding  of PI 3-kinase, while Y250F ( 8,  9,  32) is  deficient in associating with SHC and thereby unable to initiate  signaling through Ras. NG59 ( 38) binds none of the molecules  characterized so far, 1387T (a truncated mutant protein lacking the  membrane anchor sequence) only binds PP2A( 39,  60) ,  and dl1015 associates with all cellular enzymes described so far, but  is unable to activate PI 3-kinase( 40,  41) .	bind
23133	8	6444	5	NULL	NULL	0	NULL	NG59	NULL		does not bind	NULL				characterized molecules	NULL	any			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_49_29286_s_122	7493960	1178T ( 31) shows dramatically reduced binding  of PI 3-kinase, while Y250F ( 8,  9,  32) is  deficient in associating with SHC and thereby unable to initiate  signaling through Ras. NG59 ( 38) binds none of the molecules  characterized so far, 1387T (a truncated mutant protein lacking the  membrane anchor sequence) only binds PP2A( 39,  60) ,  and dl1015 associates with all cellular enzymes described so far, but  is unable to activate PI 3-kinase( 40,  41) .	bind
23456	1	6444	7	NULL	NULL	NULL	NULL	1178T	NucleicAcid		bind		reduced			PI 3-kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_49_29286_s_122	7493960	1178T ( 31) shows dramatically reduced binding  of PI 3-kinase, while Y250F ( 8,  9,  32) is  deficient in associating with SHC and thereby unable to initiate  signaling through Ras. NG59 ( 38) binds none of the molecules  characterized so far, 1387T (a truncated mutant protein lacking the  membrane anchor sequence) only binds PP2A( 39,  60) ,  and dl1015 associates with all cellular enzymes described so far, but  is unable to activate PI 3-kinase( 40,  41) .	bind
23457	2	6444	7	NULL	NULL	NULL	NULL				is defecient in			Y250F		SHC	GP	associating with			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_49_29286_s_122	7493960	1178T ( 31) shows dramatically reduced binding  of PI 3-kinase, while Y250F ( 8,  9,  32) is  deficient in associating with SHC and thereby unable to initiate  signaling through Ras. NG59 ( 38) binds none of the molecules  characterized so far, 1387T (a truncated mutant protein lacking the  membrane anchor sequence) only binds PP2A( 39,  60) ,  and dl1015 associates with all cellular enzymes described so far, but  is unable to activate PI 3-kinase( 40,  41) .	bind
23458	3	6444	7	NULL	NULL	NULL	NULL	statement 2	Process		is unable to 					Ras	GP	initiate signaling through			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_49_29286_s_122	7493960	1178T ( 31) shows dramatically reduced binding  of PI 3-kinase, while Y250F ( 8,  9,  32) is  deficient in associating with SHC and thereby unable to initiate  signaling through Ras. NG59 ( 38) binds none of the molecules  characterized so far, 1387T (a truncated mutant protein lacking the  membrane anchor sequence) only binds PP2A( 39,  60) ,  and dl1015 associates with all cellular enzymes described so far, but  is unable to activate PI 3-kinase( 40,  41) .	bind
23459	4	6444	7	NULL	NULL	NULL	NULL	1387T	GP		binds					PP2A	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_49_29286_s_122	7493960	1178T ( 31) shows dramatically reduced binding  of PI 3-kinase, while Y250F ( 8,  9,  32) is  deficient in associating with SHC and thereby unable to initiate  signaling through Ras. NG59 ( 38) binds none of the molecules  characterized so far, 1387T (a truncated mutant protein lacking the  membrane anchor sequence) only binds PP2A( 39,  60) ,  and dl1015 associates with all cellular enzymes described so far, but  is unable to activate PI 3-kinase( 40,  41) .	bind
23460	5	6444	7	NULL	NULL	NULL	NULL	dl1015	NucleicAcid		associate with					cellular enzymes	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_49_29286_s_122	7493960	1178T ( 31) shows dramatically reduced binding  of PI 3-kinase, while Y250F ( 8,  9,  32) is  deficient in associating with SHC and thereby unable to initiate  signaling through Ras. NG59 ( 38) binds none of the molecules  characterized so far, 1387T (a truncated mutant protein lacking the  membrane anchor sequence) only binds PP2A( 39,  60) ,  and dl1015 associates with all cellular enzymes described so far, but  is unable to activate PI 3-kinase( 40,  41) .	bind
23461	6	6444	7	NULL	NULL	NULL	NULL	dl1015	NucleicAcid		is unable to activate					PI 3-kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_49_29286_s_122	7493960	1178T ( 31) shows dramatically reduced binding  of PI 3-kinase, while Y250F ( 8,  9,  32) is  deficient in associating with SHC and thereby unable to initiate  signaling through Ras. NG59 ( 38) binds none of the molecules  characterized so far, 1387T (a truncated mutant protein lacking the  membrane anchor sequence) only binds PP2A( 39,  60) ,  and dl1015 associates with all cellular enzymes described so far, but  is unable to activate PI 3-kinase( 40,  41) .	bind
23462	7	6444	7	NULL	NULL	NULL	NULL	1387T	GP		is a type of					truncated mutant protein lacking the membrane anchor sequence	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_49_29286_s_122	7493960	1178T ( 31) shows dramatically reduced binding  of PI 3-kinase, while Y250F ( 8,  9,  32) is  deficient in associating with SHC and thereby unable to initiate  signaling through Ras. NG59 ( 38) binds none of the molecules  characterized so far, 1387T (a truncated mutant protein lacking the  membrane anchor sequence) only binds PP2A( 39,  60) ,  and dl1015 associates with all cellular enzymes described so far, but  is unable to activate PI 3-kinase( 40,  41) .	bind
23108	1	6446	5	NULL	NULL	0	NULL	11F8	NULL		forms a complex with	NULL				histone	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23109	2	6446	5	NULL	NULL	0	NULL	9F11	NULL		forms a complex with	NULL				histone	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23110	3	6446	5	NULL	NULL	0	NULL	11F8	NULL		forms a complex with	NULL				ssDNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23111	4	6446	5	NULL	NULL	0	NULL	9F11	NULL		forms a complex with	NULL				ssDNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23112	5	6446	5	NULL	NULL	0	NULL	poly(dT)	NULL		bind	NULL				laminin	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23113	6	6446	5	NULL	NULL	0	NULL	poly(dT)	NULL		bind	NULL				collagen IV	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23116	7	6446	5	NULL	NULL	0	NULL	poly(dT)	NULL		does not bind	NULL				heparan sulfate	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23117	8	6446	5	NULL	NULL	0	NULL	poly(dT)	NULL		does not bind	NULL				fibronectin	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23118	9	6446	5	NULL	NULL	0	NULL	11F8	NULL		forms a complex with	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23119	10	6446	5	NULL	NULL	0	NULL	11F8	NULL		forms a complex with	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23120	11	6446	5	NULL	NULL	0	NULL	9F11	NULL		forms a complex with	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23121	12	6446	5	NULL	NULL	0	NULL	9F11	NULL		forms a complex with	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23122	13	6446	5	NULL	NULL	0	NULL	statement 3	NULL		is an alternative to	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23123	14	6446	5	NULL	NULL	0	NULL	statement 3	NULL		is an alternative to	NULL				statement 10	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23124	15	6446	5	NULL	NULL	0	NULL	statement 4	NULL		is an alternative to	NULL				statement 11	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23125	16	6446	5	NULL	NULL	0	NULL	statement 4	NULL		is an alternative to	NULL				statement 12	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23463	1	6446	7	NULL	NULL	NULL	NULL	11F8	NucleicAcid		complex with					histone	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23464	2	6446	7	NULL	NULL	NULL	NULL	 9F11	NucleicAcid		complex with					histone	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23465	3	6446	7	NULL	NULL	NULL	NULL	11F8	NucleicAcid		complex with					ssDNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23466	4	6446	7	NULL	NULL	NULL	NULL	9F11	NucleicAcid		complex with					ssDNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23467	5	6446	7	NULL	NULL	NULL	NULL	11F8	NucleicAcid		complex with					poly(dT)	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23468	6	6446	7	NULL	NULL	NULL	NULL	9F11	NucleicAcid		complex with					poly(dT)	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23469	7	6446	7	NULL	NULL	NULL	NULL	statement 1	Process		is simultaneously with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23470	8	6446	7	NULL	NULL	NULL	NULL	statement 2	Process		is simultaneously with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23471	9	6446	7	NULL	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23472	10	6446	7	NULL	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
23473	11	6446	7	NULL	NULL	NULL	NULL	statement 1	Process		binds to					laminin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
24391	12	6446	7	NULL	NULL	NULL	NULL	statement 2	Process		binds to					laminin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
24392	13	6446	7	NULL	NULL	NULL	NULL	statement 1	Process		binds to					collagen IV	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
24393	14	6446	7	NULL	NULL	NULL	NULL	statement 2	Process		binds to					collagen IV	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
24394	15	6446	7	NULL	NULL	NULL	NULL	statement 1	Process		does not bind					heparan sulfate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
24395	16	6446	7	NULL	NULL	NULL	NULL	statement 2	Process		does not bind					heparan sulfate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
24396	17	6446	7	NULL	NULL	NULL	NULL	statement 1	Process		does not bind					fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
24397	18	6446	7	NULL	NULL	NULL	NULL	statement 2	Process		does not bind					fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1748_s_202	8601641	11F8 and 9F11 both form complexes with histone and either ssDNA or poly(dT) that bind to laminin and collagen IV,  but not to heparan sulfate or fibronectin.	bind
20177	1	6447	5	10	NULL	0	NULL	spermine			bind					Z-DNA				d(m5CGm5CGm5CG)2	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_419_s_377	11788703	12       Banville,D.L., Feuerstein,B.G. and Shafer,R.H. (1991) 1H and 31P nuclear magnetic resonance studies of spermine binding to the Z-DNA form of d(m5CGm5CGm5CG)2: evidence for decreased spermine mobility.	bind
20178	2	6447	5	NULL	NULL	0	NULL	statement 1	NULL		is an evidence for	NULL				spermine	NULL	decreased mobility of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_419_s_377	11788703	12       Banville,D.L., Feuerstein,B.G. and Shafer,R.H. (1991) 1H and 31P nuclear magnetic resonance studies of spermine binding to the Z-DNA form of d(m5CGm5CGm5CG)2: evidence for decreased spermine mobility.	bind
23474	1	6447	7	NULL	NULL	NULL	NULL	spermine	GP		binds to					 Z-DNA	NucleicAcid			d(m5CGm5CGm5CG)2	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_419_s_377	11788703	12       Banville,D.L., Feuerstein,B.G. and Shafer,R.H. (1991) 1H and 31P nuclear magnetic resonance studies of spermine binding to the Z-DNA form of d(m5CGm5CGm5CG)2: evidence for decreased spermine mobility.	bind
20180	1	6450	5	NULL	NULL	0	NULL	TnI	NULL		moves away from	NULL				actin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_9_s_24	null	12  13  The calcium-dependent movement of TnI away from actin reveals a tropomyosin binding site, which results in movement of tropomyosin away from high-affinity myosin binding sites on actin.	bind
20181	3	6450	5	NULL	NULL	0	NULL	statement 1	NULL		reveals	NULL					NULL		tropomyosin binding site		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_9_s_24	null	12  13  The calcium-dependent movement of TnI away from actin reveals a tropomyosin binding site, which results in movement of tropomyosin away from high-affinity myosin binding sites on actin.	bind
20182	4	6450	5	NULL	NULL	0	NULL	tropomyosin	NULL		moves away from	NULL				actin	NULL	 high-affinity	myosin binding sites		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_9_s_24	null	12  13  The calcium-dependent movement of TnI away from actin reveals a tropomyosin binding site, which results in movement of tropomyosin away from high-affinity myosin binding sites on actin.	bind
20183	5	6450	5	NULL	NULL	0	NULL	statement 3	NULL		results in	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_9_s_24	null	12  13  The calcium-dependent movement of TnI away from actin reveals a tropomyosin binding site, which results in movement of tropomyosin away from high-affinity myosin binding sites on actin.	bind
30030	2	6450	5	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				calcium	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_1_9_s_24	null	12  13  The calcium-dependent movement of TnI away from actin reveals a tropomyosin binding site, which results in movement of tropomyosin away from high-affinity myosin binding sites on actin.	bind
23605	1	6450	7	NULL	NULL	NULL	NULL	TnI 	GP		move away from					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_9_s_24	null	12  13  The calcium-dependent movement of TnI away from actin reveals a tropomyosin binding site, which results in movement of tropomyosin away from high-affinity myosin binding sites on actin.	bind
23606	2	6450	7	NULL	NULL	NULL	NULL	statement 1	Process		is dependent on					calcium	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_9_s_24	null	12  13  The calcium-dependent movement of TnI away from actin reveals a tropomyosin binding site, which results in movement of tropomyosin away from high-affinity myosin binding sites on actin.	bind
23607	3	6450	7	NULL	NULL	NULL	NULL	statement 1	Process		reveals								tropomyosin binding site		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_9_s_24	null	12  13  The calcium-dependent movement of TnI away from actin reveals a tropomyosin binding site, which results in movement of tropomyosin away from high-affinity myosin binding sites on actin.	bind
23608	4	6450	7	NULL	NULL	NULL	NULL	tropomyosin	GP		move away from					actin	GP	high-affinity	myosin binding site		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_9_s_24	null	12  13  The calcium-dependent movement of TnI away from actin reveals a tropomyosin binding site, which results in movement of tropomyosin away from high-affinity myosin binding sites on actin.	bind
23609	5	6450	7	NULL	NULL	NULL	NULL	statement 3	Process		results in					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_9_s_24	null	12  13  The calcium-dependent movement of TnI away from actin reveals a tropomyosin binding site, which results in movement of tropomyosin away from high-affinity myosin binding sites on actin.	bind
20184	1	6451	5	NULL	NULL	0	NULL	tryp-VLDL	NULL		does not bind	NULL				LDL receptors	NULL	partially purified bovine			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_45	9633939	12  13 27  Functional loss of apoE was demonstrated by lack of binding of tryp-VLDL to partially purified bovine LDL receptors on ligand blots.	bind
20185	2	6451	5	NULL	NULL	0	NULL	statement 1	NULL		demonstrate	NULL				apoE	NULL	functional loss of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_45	9633939	12  13 27  Functional loss of apoE was demonstrated by lack of binding of tryp-VLDL to partially purified bovine LDL receptors on ligand blots.	bind
23610	1	6451	7	NULL	NULL	NULL	NULL	tryp-VLDL	GP		does not bind					LDL receptors	GP	partially purified bovine			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_45	9633939	12  13 27  Functional loss of apoE was demonstrated by lack of binding of tryp-VLDL to partially purified bovine LDL receptors on ligand blots.	bind
23611	2	6451	7	NULL	NULL	NULL	NULL	apoE	GP	functional loss of	demonstrate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_45	9633939	12  13 27  Functional loss of apoE was demonstrated by lack of binding of tryp-VLDL to partially purified bovine LDL receptors on ligand blots.	bind
20186	1	6452	5	NULL	NULL	0	NULL	vWF multimers	NULL	large	is adsorbed onto	NULL				collagen I 	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_28	7867173	12  Adhesion at elevated shear rates in our system is the result of the adsorption of large vWF multimers onto collagen I and the binding of platelet GPIb to the insolubilized vWF.	bind
20187	2	6452	5	10	NULL	0	NULL	GPIb		platelet	bind					vWF		insolubilized			NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_28	7867173	12  Adhesion at elevated shear rates in our system is the result of the adsorption of large vWF multimers onto collagen I and the binding of platelet GPIb to the insolubilized vWF.	bind
20188	3	6452	5	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				adhesion	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_28	7867173	12  Adhesion at elevated shear rates in our system is the result of the adsorption of large vWF multimers onto collagen I and the binding of platelet GPIb to the insolubilized vWF.	bind
20189	4	6452	5	NULL	NULL	0	NULL	statement 2	NULL		results in	NULL				adhesion	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_28	7867173	12  Adhesion at elevated shear rates in our system is the result of the adsorption of large vWF multimers onto collagen I and the binding of platelet GPIb to the insolubilized vWF.	bind
30031	5	6452	5	NULL	NULL	0	NULL	statement 3	NULL		occurs at	NULL				shear rates	NULL	elevated			NULL		0	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_28	7867173	12  Adhesion at elevated shear rates in our system is the result of the adsorption of large vWF multimers onto collagen I and the binding of platelet GPIb to the insolubilized vWF.	bind
30032	6	6452	5	NULL	NULL	0	NULL	statement 4	NULL		occurs at	NULL				shear rates	NULL	elevated			NULL		0	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_28	7867173	12  Adhesion at elevated shear rates in our system is the result of the adsorption of large vWF multimers onto collagen I and the binding of platelet GPIb to the insolubilized vWF.	bind
23612	1	6452	7	NULL	NULL	NULL	NULL	vWF multimers	GP	large	adsorb to					collagen I	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_28	7867173	12  Adhesion at elevated shear rates in our system is the result of the adsorption of large vWF multimers onto collagen I and the binding of platelet GPIb to the insolubilized vWF.	bind
23613	2	6452	7	NULL	NULL	NULL	NULL	GPIb	GP	platelet	bind					vWF	GP	insolubilized			NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_28	7867173	12  Adhesion at elevated shear rates in our system is the result of the adsorption of large vWF multimers onto collagen I and the binding of platelet GPIb to the insolubilized vWF.	bind
30844	3	6452	7	NULL	NULL	NULL	NULL	statement 1	Process		results in					adhesion	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_28	7867173	12  Adhesion at elevated shear rates in our system is the result of the adsorption of large vWF multimers onto collagen I and the binding of platelet GPIb to the insolubilized vWF.	bind
30845	4	6452	7	NULL	NULL	NULL	NULL	statement 2	Process		results in					adhesion	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_28	7867173	12  Adhesion at elevated shear rates in our system is the result of the adsorption of large vWF multimers onto collagen I and the binding of platelet GPIb to the insolubilized vWF.	bind
30846	5	6452	7	NULL	NULL	NULL	NULL	statement 3	Process		occurs at					shear rates	Process	elevated			NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_28	7867173	12  Adhesion at elevated shear rates in our system is the result of the adsorption of large vWF multimers onto collagen I and the binding of platelet GPIb to the insolubilized vWF.	bind
30847	6	6452	7	NULL	NULL	NULL	NULL	statement 4	Process		occurs at					shear rates	Process	elevated			NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1354_s_28	7867173	12  Adhesion at elevated shear rates in our system is the result of the adsorption of large vWF multimers onto collagen I and the binding of platelet GPIb to the insolubilized vWF.	bind
20190	1	6454	5	10	NULL	0	NULL	thrombomodulin	NULL		bind	NULL				thrombin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_12_1118_s_167	10082479	12  Another downregulated gene was thrombomodulin (-2.6-fold at 24 hours), an integral membrane glycoprotein that binds thrombin, the final enzyme of the procoagulant pathway 31 ; we confirmed by Northern analysis that thrombomodulin was downregulated 3.3 plus-or-minus 1.0-fold by cyclic deformation (Figure 6  ).	bind
20191	2	6454	5	10	NULL	0	NULL	thrombin			is final enzyme of					procoagulant pathway					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_12_1118_s_167	10082479	12  Another downregulated gene was thrombomodulin (-2.6-fold at 24 hours), an integral membrane glycoprotein that binds thrombin, the final enzyme of the procoagulant pathway 31 ; we confirmed by Northern analysis that thrombomodulin was downregulated 3.3 plus-or-minus 1.0-fold by cyclic deformation (Figure 6  ).	bind
20192	3	6454	5	NULL	NULL	0	NULL	thrombomodulin	NULL		is downregulated by	NULL				cyclic deformation	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_12_1118_s_167	10082479	12  Another downregulated gene was thrombomodulin (-2.6-fold at 24 hours), an integral membrane glycoprotein that binds thrombin, the final enzyme of the procoagulant pathway 31 ; we confirmed by Northern analysis that thrombomodulin was downregulated 3.3 plus-or-minus 1.0-fold by cyclic deformation (Figure 6  ).	bind
45619	4	6454	5	10	NULL	0	NULL	thrombomodulin	NULL		is a type of	NULL				integral membrane glycoprotein	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_12_1118_s_167	10082479	12  Another downregulated gene was thrombomodulin (-2.6-fold at 24 hours), an integral membrane glycoprotein that binds thrombin, the final enzyme of the procoagulant pathway 31 ; we confirmed by Northern analysis that thrombomodulin was downregulated 3.3 plus-or-minus 1.0-fold by cyclic deformation (Figure 6  ).	bind
23614	1	6454	7	NULL	NULL	NULL	NULL	thrombomodulin	GP		binds					thrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_12_1118_s_167	10082479	12  Another downregulated gene was thrombomodulin (-2.6-fold at 24 hours), an integral membrane glycoprotein that binds thrombin, the final enzyme of the procoagulant pathway 31 ; we confirmed by Northern analysis that thrombomodulin was downregulated 3.3 plus-or-minus 1.0-fold by cyclic deformation (Figure 6  ).	bind
23615	2	6454	7	NULL	NULL	NULL	NULL	thrombin	GP		is the final enzyme of					procoagulant pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_12_1118_s_167	10082479	12  Another downregulated gene was thrombomodulin (-2.6-fold at 24 hours), an integral membrane glycoprotein that binds thrombin, the final enzyme of the procoagulant pathway 31 ; we confirmed by Northern analysis that thrombomodulin was downregulated 3.3 plus-or-minus 1.0-fold by cyclic deformation (Figure 6  ).	bind
23616	3	6454	7	NULL	NULL	NULL	NULL	cyclic deformation 	Process		downregulates					thrombomodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_12_1118_s_167	10082479	12  Another downregulated gene was thrombomodulin (-2.6-fold at 24 hours), an integral membrane glycoprotein that binds thrombin, the final enzyme of the procoagulant pathway 31 ; we confirmed by Northern analysis that thrombomodulin was downregulated 3.3 plus-or-minus 1.0-fold by cyclic deformation (Figure 6  ).	bind
45620	4	6454	7	NULL	NULL	NULL	NULL	thrombomodulin	GP		is a type of					integral membrane glycoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_12_1118_s_167	10082479	12  Another downregulated gene was thrombomodulin (-2.6-fold at 24 hours), an integral membrane glycoprotein that binds thrombin, the final enzyme of the procoagulant pathway 31 ; we confirmed by Northern analysis that thrombomodulin was downregulated 3.3 plus-or-minus 1.0-fold by cyclic deformation (Figure 6  ).	bind
20193	1	6455	5	NULL	NULL	0	NULL	VLDL particles	NULL		bind	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1354_s_100	10323790	12  As both VLDL and LDL particles bind to the LDL receptor, whereas only VLDL enhances PAI-1 secretion from endothelial and liver cells in culture, the TG content of the lipoprotein particle might be important for the induction of PAI-1.	bind
20194	2	6455	5	NULL	NULL	0	NULL	LDL particles	NULL		bind	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1354_s_100	10323790	12  As both VLDL and LDL particles bind to the LDL receptor, whereas only VLDL enhances PAI-1 secretion from endothelial and liver cells in culture, the TG content of the lipoprotein particle might be important for the induction of PAI-1.	bind
20195	3	6455	5	NULL	NULL	0	NULL	VLDL	NULL		enhances	NULL	only			PAI-1	NULL	secretion of			NULL	from endothelial cells in culture	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1354_s_100	10323790	12  As both VLDL and LDL particles bind to the LDL receptor, whereas only VLDL enhances PAI-1 secretion from endothelial and liver cells in culture, the TG content of the lipoprotein particle might be important for the induction of PAI-1.	bind
20196	4	6455	5	NULL	NULL	0	NULL	VLDL	NULL		enhances	NULL	only			PAI-1	NULL	secretion of			NULL	from liver cells in culture	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1354_s_100	10323790	12  As both VLDL and LDL particles bind to the LDL receptor, whereas only VLDL enhances PAI-1 secretion from endothelial and liver cells in culture, the TG content of the lipoprotein particle might be important for the induction of PAI-1.	bind
20197	5	6455	5	NULL	NULL	0	NULL	lipoprotein particle	NULL	TG content of	is important for	NULL	might be			PAI-1	NULL	induction of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1354_s_100	10323790	12  As both VLDL and LDL particles bind to the LDL receptor, whereas only VLDL enhances PAI-1 secretion from endothelial and liver cells in culture, the TG content of the lipoprotein particle might be important for the induction of PAI-1.	bind
23617	1	6455	7	NULL	NULL	NULL	NULL	VLDL particles	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1354_s_100	10323790	12  As both VLDL and LDL particles bind to the LDL receptor, whereas only VLDL enhances PAI-1 secretion from endothelial and liver cells in culture, the TG content of the lipoprotein particle might be important for the induction of PAI-1.	bind
23618	2	6455	7	NULL	NULL	NULL	NULL	LDL particles	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1354_s_100	10323790	12  As both VLDL and LDL particles bind to the LDL receptor, whereas only VLDL enhances PAI-1 secretion from endothelial and liver cells in culture, the TG content of the lipoprotein particle might be important for the induction of PAI-1.	bind
23619	3	6455	7	NULL	NULL	NULL	NULL	VLDL	GP		enhance					PAI-1	GP	secretion of			NULL	from endothelial cells in culture	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1354_s_100	10323790	12  As both VLDL and LDL particles bind to the LDL receptor, whereas only VLDL enhances PAI-1 secretion from endothelial and liver cells in culture, the TG content of the lipoprotein particle might be important for the induction of PAI-1.	bind
23620	4	6455	7	NULL	NULL	NULL	NULL	VLDL	GP		enhance					PAI-1	GP	secretion of			NULL	liver cells in culture	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1354_s_100	10323790	12  As both VLDL and LDL particles bind to the LDL receptor, whereas only VLDL enhances PAI-1 secretion from endothelial and liver cells in culture, the TG content of the lipoprotein particle might be important for the induction of PAI-1.	bind
23621	5	6455	7	NULL	NULL	NULL	NULL	lipoprotein 	GP	TG content of	is important for					PAI-1	GP	induction of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1354_s_100	10323790	12  As both VLDL and LDL particles bind to the LDL receptor, whereas only VLDL enhances PAI-1 secretion from endothelial and liver cells in culture, the TG content of the lipoprotein particle might be important for the induction of PAI-1.	bind
20198	1	6456	5	NULL	NULL	0	NULL	p60c-Src	NULL		bind	NULL	weakly			Fak	NULL				NULL	in the myocardium of control rats	NULL	NULL	NULL	NULL	gw60_circulationres_87_7_558_s_95	11009560	12  Coimmunoprecipitation assays with anti-Fak and anti - c-Src antibodies showed only a weak binding of p60c-Src to Fak in the myocardium of control rats (Figure 4A  ).	bind
23623	1	6456	7	NULL	NULL	NULL	NULL	p60c-Src	GP		bind		weakly			Fak	GP				NULL	myocardium of control rats	NULL	NULL	NULL	NULL	gw60_circulationres_87_7_558_s_95	11009560	12  Coimmunoprecipitation assays with anti-Fak and anti - c-Src antibodies showed only a weak binding of p60c-Src to Fak in the myocardium of control rats (Figure 4A  ).	bind
20199	1	6457	5	NULL	NULL	0	NULL	CRP	NULL		is found within	NULL				endothelial vessel walls	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_97_5_425_s_78	9490235	12  Experimental work also suggests that CRP can be found within endothelial vessel walls, 13  that CRP avidly binds to human neutrophils, 14  and that CRP can induce complement activation.	bind
20200	2	6457	5	NULL	NULL	0	NULL	CRP	NULL		bind	NULL	avidly			neutrophils	NULL	human			NULL		0	NULL	NULL	NULL	gw60_circulation_97_5_425_s_78	9490235	12  Experimental work also suggests that CRP can be found within endothelial vessel walls, 13  that CRP avidly binds to human neutrophils, 14  and that CRP can induce complement activation.	bind
20201	3	6457	5	NULL	NULL	0	NULL	CRP	NULL		induces	NULL				complement	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_circulation_97_5_425_s_78	9490235	12  Experimental work also suggests that CRP can be found within endothelial vessel walls, 13  that CRP avidly binds to human neutrophils, 14  and that CRP can induce complement activation.	bind
23624	1	6457	7	NULL	NULL	NULL	NULL	CRP	GP		is found within					endothelial vessel walls	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_5_425_s_78	9490235	12  Experimental work also suggests that CRP can be found within endothelial vessel walls, 13  that CRP avidly binds to human neutrophils, 14  and that CRP can induce complement activation.	bind
23625	2	6457	7	NULL	NULL	NULL	NULL	CRP	GP		binds		avidly			neutrophils	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_5_425_s_78	9490235	12  Experimental work also suggests that CRP can be found within endothelial vessel walls, 13  that CRP avidly binds to human neutrophils, 14  and that CRP can induce complement activation.	bind
23626	3	6457	7	NULL	NULL	NULL	NULL	CRP	GP		induce					complement	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_5_425_s_78	9490235	12  Experimental work also suggests that CRP can be found within endothelial vessel walls, 13  that CRP avidly binds to human neutrophils, 14  and that CRP can induce complement activation.	bind
20202	1	6458	5	NULL	NULL	0	NULL	apoB	NULL		bind	NULL				LDLR	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_195	8640407	12  However, according to the direct binding assays in this study, we found no evidence for altered binding of apoB or apoE to the LDLR of pattern B subjects, consistent with recent evidence (J.K. Naggert et al, unpublished data, 1995) of the absence of functional mutations in the structural position of the LDLR gene in pattern B subjects.	bind
20203	2	6458	5	NULL	NULL	0	NULL	apoE	NULL		bind	NULL				LDLR	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_195	8640407	12  However, according to the direct binding assays in this study, we found no evidence for altered binding of apoB or apoE to the LDLR of pattern B subjects, consistent with recent evidence (J.K. Naggert et al, unpublished data, 1995) of the absence of functional mutations in the structural position of the LDLR gene in pattern B subjects.	bind
20204	3	6458	5	NULL	NULL	0	NULL	functional mutations	NULL		is absent in	NULL				LDLR gene	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_195	8640407	12  However, according to the direct binding assays in this study, we found no evidence for altered binding of apoB or apoE to the LDLR of pattern B subjects, consistent with recent evidence (J.K. Naggert et al, unpublished data, 1995) of the absence of functional mutations in the structural position of the LDLR gene in pattern B subjects.	bind
23633	1	6458	7	NULL	NULL	NULL	NULL	apoB	GP		bind					LDLR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_195	8640407	12  However, according to the direct binding assays in this study, we found no evidence for altered binding of apoB or apoE to the LDLR of pattern B subjects, consistent with recent evidence (J.K. Naggert et al, unpublished data, 1995) of the absence of functional mutations in the structural position of the LDLR gene in pattern B subjects.	bind
23634	2	6458	7	NULL	NULL	NULL	NULL	apoE	GP		bind					LDLR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_195	8640407	12  However, according to the direct binding assays in this study, we found no evidence for altered binding of apoB or apoE to the LDLR of pattern B subjects, consistent with recent evidence (J.K. Naggert et al, unpublished data, 1995) of the absence of functional mutations in the structural position of the LDLR gene in pattern B subjects.	bind
30857	3	6458	7	NULL	NULL	NULL	NULL	functional mutation	Process		is absent in					LDLR gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_195	8640407	12  However, according to the direct binding assays in this study, we found no evidence for altered binding of apoB or apoE to the LDLR of pattern B subjects, consistent with recent evidence (J.K. Naggert et al, unpublished data, 1995) of the absence of functional mutations in the structural position of the LDLR gene in pattern B subjects.	bind
20205	1	6459	5	NULL	NULL	0	NULL	CRP	NULL		bind	NULL	low affinity			FCgammaRI	NULL				NULL	on leukocytes	NULL	NULL	NULL	NULL	gw60_circulation_102_18_2165_s_83	11056086	12  In addition, recent studies 13  have shown that CRP can bind to receptor FCgammaRI (with low affinity) and FCgammaRII (with high affinity) on leukocytes.	bind
20206	2	6459	5	NULL	NULL	0	NULL	CRP	NULL		bind	NULL	high affinity			FCgammaRII	NULL				NULL	on leukocytes	NULL	NULL	NULL	NULL	gw60_circulation_102_18_2165_s_83	11056086	12  In addition, recent studies 13  have shown that CRP can bind to receptor FCgammaRI (with low affinity) and FCgammaRII (with high affinity) on leukocytes.	bind
30033	3	6459	5	NULL	NULL	0	NULL	FCgammaRI	NULL		is a type of	NULL				receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_18_2165_s_83	11056086	12  In addition, recent studies 13  have shown that CRP can bind to receptor FCgammaRI (with low affinity) and FCgammaRII (with high affinity) on leukocytes.	bind
30034	4	6459	5	NULL	NULL	0	NULL	FCgammaRII	NULL		is a type of	NULL				receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_18_2165_s_83	11056086	12  In addition, recent studies 13  have shown that CRP can bind to receptor FCgammaRI (with low affinity) and FCgammaRII (with high affinity) on leukocytes.	bind
23638	1	6459	7	NULL	NULL	NULL	NULL	CRP	GP		bind		low affinity			FCgammaRI	GP				NULL	leukocytes	NULL	NULL	NULL	NULL	gw60_circulation_102_18_2165_s_83	11056086	12  In addition, recent studies 13  have shown that CRP can bind to receptor FCgammaRI (with low affinity) and FCgammaRII (with high affinity) on leukocytes.	bind
23641	2	6459	7	NULL	NULL	NULL	NULL	CRP	GP		bind		high affinity			 FCgammaRII 	GP				NULL	leukocytes	NULL	NULL	NULL	NULL	gw60_circulation_102_18_2165_s_83	11056086	12  In addition, recent studies 13  have shown that CRP can bind to receptor FCgammaRI (with low affinity) and FCgammaRII (with high affinity) on leukocytes.	bind
30867	3	6459	7	NULL	NULL	NULL	NULL	FCgammaRI	GP		is a type of					receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2165_s_83	11056086	12  In addition, recent studies 13  have shown that CRP can bind to receptor FCgammaRI (with low affinity) and FCgammaRII (with high affinity) on leukocytes.	bind
30869	4	6459	7	NULL	NULL	NULL	NULL	FCgammaRII	GP		is a type of					receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2165_s_83	11056086	12  In addition, recent studies 13  have shown that CRP can bind to receptor FCgammaRI (with low affinity) and FCgammaRII (with high affinity) on leukocytes.	bind
20207	1	6460	5	10	NULL	0	NULL	Egr-1			bind					PDGF-A - chain				promoter	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_6_678_s_243	10189355	12  In these studies, the binding of Egr-1 to the PDGF-A - chain promoter was induced by shear stress, which displaced SP-1 from their overlapping recognition elements.	bind
20208	2	6460	5	NULL	NULL	0	NULL	shear stress	NULL		induces	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_6_678_s_243	10189355	12  In these studies, the binding of Egr-1 to the PDGF-A - chain promoter was induced by shear stress, which displaced SP-1 from their overlapping recognition elements.	bind
20209	3	6460	5	10	NULL	0	NULL	SP-1	NULL		is displaced from	NULL					NULL			overlapping recognition elements	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_6_678_s_243	10189355	12  In these studies, the binding of Egr-1 to the PDGF-A - chain promoter was induced by shear stress, which displaced SP-1 from their overlapping recognition elements.	bind
20210	4	6460	5	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_6_678_s_243	10189355	12  In these studies, the binding of Egr-1 to the PDGF-A - chain promoter was induced by shear stress, which displaced SP-1 from their overlapping recognition elements.	bind
23644	1	6460	7	NULL	NULL	NULL	NULL	Egr-1 	GP		bind					PDGF-A - chain	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_6_678_s_243	10189355	12  In these studies, the binding of Egr-1 to the PDGF-A - chain promoter was induced by shear stress, which displaced SP-1 from their overlapping recognition elements.	bind
23646	2	6460	7	NULL	NULL	NULL	NULL	shear stress	Process		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_6_678_s_243	10189355	12  In these studies, the binding of Egr-1 to the PDGF-A - chain promoter was induced by shear stress, which displaced SP-1 from their overlapping recognition elements.	bind
23651	3	6460	7	NULL	NULL	NULL	NULL	SP-1	GP		is displaced from									overlapping recognition elements	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_6_678_s_243	10189355	12  In these studies, the binding of Egr-1 to the PDGF-A - chain promoter was induced by shear stress, which displaced SP-1 from their overlapping recognition elements.	bind
30872	4	6460	7	NULL	NULL	NULL	NULL	statement 1	Process		results in					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_6_678_s_243	10189355	12  In these studies, the binding of Egr-1 to the PDGF-A - chain promoter was induced by shear stress, which displaced SP-1 from their overlapping recognition elements.	bind
20211	1	6461	5	NULL	NULL	0	NULL	IP-10	NULL		is a ligand for	NULL	major			CXCR3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_1053_s_222	11238053	12  IP-10 is a major ligand for CXCR3, suggesting its involvement in type 1 cell recruitment, whereas eotaxin and MDC bind preferentially CCR3 and CCR4, respectively, suggesting an activity on type 2 cells.	bind
20212	2	6461	5	NULL	NULL	0	NULL	 IP-10	NULL		is involved in	NULL				type 1 cell 	NULL	recruitment of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_1053_s_222	11238053	12  IP-10 is a major ligand for CXCR3, suggesting its involvement in type 1 cell recruitment, whereas eotaxin and MDC bind preferentially CCR3 and CCR4, respectively, suggesting an activity on type 2 cells.	bind
20213	3	6461	5	NULL	NULL	0	NULL	statement 1	NULL		suggests	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_1053_s_222	11238053	12  IP-10 is a major ligand for CXCR3, suggesting its involvement in type 1 cell recruitment, whereas eotaxin and MDC bind preferentially CCR3 and CCR4, respectively, suggesting an activity on type 2 cells.	bind
20215	4	6461	5	NULL	NULL	0	NULL	eotaxin	NULL		bind	NULL	preferentially			CCR3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_1053_s_222	11238053	12  IP-10 is a major ligand for CXCR3, suggesting its involvement in type 1 cell recruitment, whereas eotaxin and MDC bind preferentially CCR3 and CCR4, respectively, suggesting an activity on type 2 cells.	bind
20216	5	6461	5	NULL	NULL	0	NULL	MDC	NULL		bind	NULL	preferentially			CCR4	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_1053_s_222	11238053	12  IP-10 is a major ligand for CXCR3, suggesting its involvement in type 1 cell recruitment, whereas eotaxin and MDC bind preferentially CCR3 and CCR4, respectively, suggesting an activity on type 2 cells.	bind
20217	6	6461	5	NULL	NULL	0	NULL	statement 4	NULL		suggests	NULL				type 2 cells	NULL	activity on			NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_1053_s_222	11238053	12  IP-10 is a major ligand for CXCR3, suggesting its involvement in type 1 cell recruitment, whereas eotaxin and MDC bind preferentially CCR3 and CCR4, respectively, suggesting an activity on type 2 cells.	bind
20218	7	6461	5	NULL	NULL	0	NULL	statement 5	NULL		suggests	NULL				type 2 cells	NULL	activity on			NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_1053_s_222	11238053	12  IP-10 is a major ligand for CXCR3, suggesting its involvement in type 1 cell recruitment, whereas eotaxin and MDC bind preferentially CCR3 and CCR4, respectively, suggesting an activity on type 2 cells.	bind
23665	1	6461	7	NULL	NULL	NULL	NULL	IP-10	GP		is a ligand for					CXCR3	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_1053_s_222	11238053	12  IP-10 is a major ligand for CXCR3, suggesting its involvement in type 1 cell recruitment, whereas eotaxin and MDC bind preferentially CCR3 and CCR4, respectively, suggesting an activity on type 2 cells.	bind
23669	2	6461	7	NULL	NULL	NULL	NULL	statement 1	Process		involve in					type 1 cell 	Cell	recruitment of 			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_1053_s_222	11238053	12  IP-10 is a major ligand for CXCR3, suggesting its involvement in type 1 cell recruitment, whereas eotaxin and MDC bind preferentially CCR3 and CCR4, respectively, suggesting an activity on type 2 cells.	bind
23670	3	6461	7	NULL	NULL	NULL	NULL	eotaxin	GP		bind		preferentially			CCR3	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_1053_s_222	11238053	12  IP-10 is a major ligand for CXCR3, suggesting its involvement in type 1 cell recruitment, whereas eotaxin and MDC bind preferentially CCR3 and CCR4, respectively, suggesting an activity on type 2 cells.	bind
23671	4	6461	7	NULL	NULL	NULL	NULL	MDC	GP		bind		preferentially			CCR4	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_1053_s_222	11238053	12  IP-10 is a major ligand for CXCR3, suggesting its involvement in type 1 cell recruitment, whereas eotaxin and MDC bind preferentially CCR3 and CCR4, respectively, suggesting an activity on type 2 cells.	bind
23676	5	6461	7	NULL	NULL	NULL	NULL	statement 3	Process		suggests					type 2 cells	Cell	activity on			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_1053_s_222	11238053	12  IP-10 is a major ligand for CXCR3, suggesting its involvement in type 1 cell recruitment, whereas eotaxin and MDC bind preferentially CCR3 and CCR4, respectively, suggesting an activity on type 2 cells.	bind
23679	6	6461	7	NULL	NULL	NULL	NULL	statement 4	Process		suggests					type 2 cells	Cell	activity on			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_1053_s_222	11238053	12  IP-10 is a major ligand for CXCR3, suggesting its involvement in type 1 cell recruitment, whereas eotaxin and MDC bind preferentially CCR3 and CCR4, respectively, suggesting an activity on type 2 cells.	bind
30873	7	6461	7	NULL	NULL	NULL	NULL	statement 1	Process		suggests					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_1053_s_222	11238053	12  IP-10 is a major ligand for CXCR3, suggesting its involvement in type 1 cell recruitment, whereas eotaxin and MDC bind preferentially CCR3 and CCR4, respectively, suggesting an activity on type 2 cells.	bind
20219	1	6462	5	NULL	NULL	0	NULL	PAI-1	NULL		bind	NULL				vitronectin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2037_s_28	7583587	12  PAI-1 bound to vitronectin in the matrix is known to be a spreading factor for several cell types.	bind
30035	2	6462	5	NULL	NULL	0	NULL	statement 1	NULL		is a type of	NULL				spreading factor	NULL				NULL	several cell types	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2037_s_28	7583587	12  PAI-1 bound to vitronectin in the matrix is known to be a spreading factor for several cell types.	bind
23683	1	6462	7	NULL	NULL	NULL	NULL	PAI-1	GP		bind					vitronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2037_s_28	7583587	12  PAI-1 bound to vitronectin in the matrix is known to be a spreading factor for several cell types.	bind
23686	2	6462	7	NULL	NULL	NULL	NULL	statement 1	Process		is a type of					spreading factor	Process				NULL	several cell types	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2037_s_28	7583587	12  PAI-1 bound to vitronectin in the matrix is known to be a spreading factor for several cell types.	bind
20220	1	6463	5	NULL	NULL	0	NULL	SRF	NULL		bind	NULL					NULL			CArG A	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2049_s_158	10479645	12  Taken together, these data indicate that TGF-beta - induced increases in SRF binding to CArG A and B were much greater in SMCs than non-SMCs and that SRF binding activities are regulated in a cell-specific manner.	bind
20221	2	6463	5	NULL	NULL	0	NULL	SRF	NULL		bind	NULL					NULL			CArG B	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2049_s_158	10479645	12  Taken together, these data indicate that TGF-beta - induced increases in SRF binding to CArG A and B were much greater in SMCs than non-SMCs and that SRF binding activities are regulated in a cell-specific manner.	bind
20222	3	6463	5	NULL	NULL	0	NULL	TGF-beta	NULL	induced	increases	NULL				statement 1	NULL				NULL	in SMCs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2049_s_158	10479645	12  Taken together, these data indicate that TGF-beta - induced increases in SRF binding to CArG A and B were much greater in SMCs than non-SMCs and that SRF binding activities are regulated in a cell-specific manner.	bind
20223	4	6463	5	NULL	NULL	0	NULL	TGF-beta	NULL	induced	increases	NULL				statement 2	NULL				NULL	in SMCs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2049_s_158	10479645	12  Taken together, these data indicate that TGF-beta - induced increases in SRF binding to CArG A and B were much greater in SMCs than non-SMCs and that SRF binding activities are regulated in a cell-specific manner.	bind
20224	5	6463	5	NULL	NULL	0	NULL	TGF-beta	NULL	induced	increases	NULL				statement 1	NULL				NULL	in non-SMCs	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2049_s_158	10479645	12  Taken together, these data indicate that TGF-beta - induced increases in SRF binding to CArG A and B were much greater in SMCs than non-SMCs and that SRF binding activities are regulated in a cell-specific manner.	bind
20225	6	6463	5	NULL	NULL	0	NULL	TGF-beta	NULL	induced	increases	NULL				statement 2	NULL				NULL	in non-SMCs	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2049_s_158	10479645	12  Taken together, these data indicate that TGF-beta - induced increases in SRF binding to CArG A and B were much greater in SMCs than non-SMCs and that SRF binding activities are regulated in a cell-specific manner.	bind
20226	7	6463	5	NULL	NULL	0	NULL	statement 3	NULL		greater than	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2049_s_158	10479645	12  Taken together, these data indicate that TGF-beta - induced increases in SRF binding to CArG A and B were much greater in SMCs than non-SMCs and that SRF binding activities are regulated in a cell-specific manner.	bind
20227	8	6463	5	NULL	NULL	0	NULL	statement 4	NULL		greater than	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2049_s_158	10479645	12  Taken together, these data indicate that TGF-beta - induced increases in SRF binding to CArG A and B were much greater in SMCs than non-SMCs and that SRF binding activities are regulated in a cell-specific manner.	bind
20228	9	6463	5	NULL	NULL	0	NULL	SRF	NULL	binding activities	is regulated in	NULL				cell-specific manner	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2049_s_158	10479645	12  Taken together, these data indicate that TGF-beta - induced increases in SRF binding to CArG A and B were much greater in SMCs than non-SMCs and that SRF binding activities are regulated in a cell-specific manner.	bind
23688	1	6463	7	NULL	NULL	NULL	NULL	SRF	GP		bind									CArG A	NULL	SMCs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2049_s_158	10479645	12  Taken together, these data indicate that TGF-beta - induced increases in SRF binding to CArG A and B were much greater in SMCs than non-SMCs and that SRF binding activities are regulated in a cell-specific manner.	bind
23689	2	6463	7	NULL	NULL	NULL	NULL	SRF	GP		bind									CArG B	NULL	SMCs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2049_s_158	10479645	12  Taken together, these data indicate that TGF-beta - induced increases in SRF binding to CArG A and B were much greater in SMCs than non-SMCs and that SRF binding activities are regulated in a cell-specific manner.	bind
23690	3	6463	7	NULL	NULL	NULL	NULL	SRF	GP		bind									CArG A	NULL	non-SMCs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2049_s_158	10479645	12  Taken together, these data indicate that TGF-beta - induced increases in SRF binding to CArG A and B were much greater in SMCs than non-SMCs and that SRF binding activities are regulated in a cell-specific manner.	bind
23691	4	6463	7	NULL	NULL	NULL	NULL	SRF	GP		bind									CArG B	NULL	non-SMCs	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2049_s_158	10479645	12  Taken together, these data indicate that TGF-beta - induced increases in SRF binding to CArG A and B were much greater in SMCs than non-SMCs and that SRF binding activities are regulated in a cell-specific manner.	bind
23692	5	6463	7	NULL	NULL	NULL	NULL	TGF-beta	GP	induced	increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2049_s_158	10479645	12  Taken together, these data indicate that TGF-beta - induced increases in SRF binding to CArG A and B were much greater in SMCs than non-SMCs and that SRF binding activities are regulated in a cell-specific manner.	bind
23693	6	6463	7	NULL	NULL	NULL	NULL	TGF-beta	GP	induced	increase					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2049_s_158	10479645	12  Taken together, these data indicate that TGF-beta - induced increases in SRF binding to CArG A and B were much greater in SMCs than non-SMCs and that SRF binding activities are regulated in a cell-specific manner.	bind
23694	7	6463	7	NULL	NULL	NULL	NULL	TGF-beta	GP	induced	increase					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2049_s_158	10479645	12  Taken together, these data indicate that TGF-beta - induced increases in SRF binding to CArG A and B were much greater in SMCs than non-SMCs and that SRF binding activities are regulated in a cell-specific manner.	bind
23695	8	6463	7	NULL	NULL	NULL	NULL	TGF-beta	GP	induced	increase					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2049_s_158	10479645	12  Taken together, these data indicate that TGF-beta - induced increases in SRF binding to CArG A and B were much greater in SMCs than non-SMCs and that SRF binding activities are regulated in a cell-specific manner.	bind
23696	9	6463	7	NULL	NULL	NULL	NULL	statement 5	Process		is greater than					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2049_s_158	10479645	12  Taken together, these data indicate that TGF-beta - induced increases in SRF binding to CArG A and B were much greater in SMCs than non-SMCs and that SRF binding activities are regulated in a cell-specific manner.	bind
23697	10	6463	7	NULL	NULL	NULL	NULL	statement 6	Process		is greater than					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2049_s_158	10479645	12  Taken together, these data indicate that TGF-beta - induced increases in SRF binding to CArG A and B were much greater in SMCs than non-SMCs and that SRF binding activities are regulated in a cell-specific manner.	bind
20229	1	6464	5	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL				GP IIb/IIIa receptors	NULL				NULL	on activated platelets	0	NULL	NULL	NULL	gw60_circulation_98_8_813_s_172	9727553	12  The binding of fibrinogen to GP IIb/IIIa receptors on activated platelets represents the final common pathway for platelet aggregation.	bind
20230	2	6464	5	NULL	NULL	0	NULL	statement 1	NULL		represents	NULL				platelet aggregation	NULL	final common pathway for			NULL		0	NULL	NULL	NULL	gw60_circulation_98_8_813_s_172	9727553	12  The binding of fibrinogen to GP IIb/IIIa receptors on activated platelets represents the final common pathway for platelet aggregation.	bind
23698	1	6464	7	NULL	NULL	NULL	NULL	fibrinogen	GP		bind					GP IIb/IIIa receptors 	GP				NULL	activated platelets	NULL	NULL	NULL	NULL	gw60_circulation_98_8_813_s_172	9727553	12  The binding of fibrinogen to GP IIb/IIIa receptors on activated platelets represents the final common pathway for platelet aggregation.	bind
23699	2	6464	7	NULL	NULL	NULL	NULL	statement 1	Process		represent					platelet aggregation	Process	final common pathway for			NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_813_s_172	9727553	12  The binding of fibrinogen to GP IIb/IIIa receptors on activated platelets represents the final common pathway for platelet aggregation.	bind
20231	1	6465	5	10	NULL	0	NULL	CN-Cbl	NULL		is not 	NULL				Cbl	NULL	biologically active form of 			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_39	9351374	12 13  CN-Cbl is not the biologically active form of Cbl; CN-Cbl must be converted to aqCbl to become a precursor of the Cbl II that is bound by apo-methionine synthase (Fig 1  ).	bind
20232	2	6465	5	10	NULL	0	NULL	CN-Cbl	NULL		is converted to	NULL				aqCbl	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_39	9351374	12 13  CN-Cbl is not the biologically active form of Cbl; CN-Cbl must be converted to aqCbl to become a precursor of the Cbl II that is bound by apo-methionine synthase (Fig 1  ).	bind
20233	4	6465	5	10	NULL	0	NULL	aqCbl	NULL		becomes	NULL				statement 3	NULL	precursor of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_39	9351374	12 13  CN-Cbl is not the biologically active form of Cbl; CN-Cbl must be converted to aqCbl to become a precursor of the Cbl II that is bound by apo-methionine synthase (Fig 1  ).	bind
20234	3	6465	5	NULL	NULL	0	NULL	Cbl II	NULL		bind	NULL				apo-methionine synthase	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_39	9351374	12 13  CN-Cbl is not the biologically active form of Cbl; CN-Cbl must be converted to aqCbl to become a precursor of the Cbl II that is bound by apo-methionine synthase (Fig 1  ).	bind
23700	1	6465	7	NULL	NULL	NULL	NULL	CN-Cbl	Chemical		is not					Cbl	Chemical	biologically active form of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_39	9351374	12 13  CN-Cbl is not the biologically active form of Cbl; CN-Cbl must be converted to aqCbl to become a precursor of the Cbl II that is bound by apo-methionine synthase (Fig 1  ).	bind
23701	2	6465	7	NULL	NULL	NULL	NULL	CN-Cbl	Chemical		is converted to					aqCbl	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_39	9351374	12 13  CN-Cbl is not the biologically active form of Cbl; CN-Cbl must be converted to aqCbl to become a precursor of the Cbl II that is bound by apo-methionine synthase (Fig 1  ).	bind
23702	3	6465	7	NULL	NULL	NULL	NULL	statement 2	Process		is a precursor of					Cbl II	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_39	9351374	12 13  CN-Cbl is not the biologically active form of Cbl; CN-Cbl must be converted to aqCbl to become a precursor of the Cbl II that is bound by apo-methionine synthase (Fig 1  ).	bind
23703	4	6465	7	NULL	NULL	NULL	NULL	apo-methionine synthase	GP		bind					Cbl II	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_39	9351374	12 13  CN-Cbl is not the biologically active form of Cbl; CN-Cbl must be converted to aqCbl to become a precursor of the Cbl II that is bound by apo-methionine synthase (Fig 1  ).	bind
20235	1	6466	5	NULL	NULL	0	NULL	CETP	NULL		bind	NULL				HDL cholesteryl ester	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_18_2197_s_117	11056092	12 13 14  An amino acid substitution such as the present (resulting in loss of positive charge at this position) could therefore influence the binding of CETP to HDL cholesteryl ester and thereby indirectly affect the efficiency of the protein transferring cholesteryl ester out of HDL particles.	bind
20236	2	6466	5	10	NULL	0	NULL	amino acid		substitution	influence					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2197_s_117	11056092	12 13 14  An amino acid substitution such as the present (resulting in loss of positive charge at this position) could therefore influence the binding of CETP to HDL cholesteryl ester and thereby indirectly affect the efficiency of the protein transferring cholesteryl ester out of HDL particles.	bind
20237	4	6466	5	NULL	NULL	0	NULL	statement 2	NULL		affect	NULL	indirectly			statement 3	NULL	efficiency of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2197_s_117	11056092	12 13 14  An amino acid substitution such as the present (resulting in loss of positive charge at this position) could therefore influence the binding of CETP to HDL cholesteryl ester and thereby indirectly affect the efficiency of the protein transferring cholesteryl ester out of HDL particles.	bind
46190	3	6466	5	NULL	NULL	0	NULL	cholesteryl ester	NULL		is transferred out of	NULL				HDL particles	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_18_2197_s_117	11056092	12 13 14  An amino acid substitution such as the present (resulting in loss of positive charge at this position) could therefore influence the binding of CETP to HDL cholesteryl ester and thereby indirectly affect the efficiency of the protein transferring cholesteryl ester out of HDL particles.	bind
23704	1	6466	7	NULL	NULL	NULL	NULL	CETP 	GP		bind					HDL cholesteryl ester	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2197_s_117	11056092	12 13 14  An amino acid substitution such as the present (resulting in loss of positive charge at this position) could therefore influence the binding of CETP to HDL cholesteryl ester and thereby indirectly affect the efficiency of the protein transferring cholesteryl ester out of HDL particles.	bind
23705	2	6466	7	NULL	NULL	NULL	NULL	aminoacid	AminoAcid	substitution	influence					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2197_s_117	11056092	12 13 14  An amino acid substitution such as the present (resulting in loss of positive charge at this position) could therefore influence the binding of CETP to HDL cholesteryl ester and thereby indirectly affect the efficiency of the protein transferring cholesteryl ester out of HDL particles.	bind
23706	3	6466	7	NULL	NULL	NULL	NULL	cholesteryl ester	Chemical		is transferred out of					HDL particles	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2197_s_117	11056092	12 13 14  An amino acid substitution such as the present (resulting in loss of positive charge at this position) could therefore influence the binding of CETP to HDL cholesteryl ester and thereby indirectly affect the efficiency of the protein transferring cholesteryl ester out of HDL particles.	bind
45753	4	6466	7	NULL	NULL	NULL	NULL	statement 2	Process		affect 		indirectly			statement 3	Process	efficiency of protein of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2197_s_117	11056092	12 13 14  An amino acid substitution such as the present (resulting in loss of positive charge at this position) could therefore influence the binding of CETP to HDL cholesteryl ester and thereby indirectly affect the efficiency of the protein transferring cholesteryl ester out of HDL particles.	bind
20238	1	6467	5	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				Ral	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_108	11397694	12 15  Recently, a binding site for calmodulin on Ral has been detected, and calmodulin has been shown to enhance the binding of GTP to Ral. 23  24  We investigated whether thrombin-induced activation of Ral is affected by antagonists of calmodulin.	bind
20239	2	6467	5	NULL	NULL	0	NULL	calmodulin	NULL		enhances	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_108	11397694	12 15  Recently, a binding site for calmodulin on Ral has been detected, and calmodulin has been shown to enhance the binding of GTP to Ral. 23  24  We investigated whether thrombin-induced activation of Ral is affected by antagonists of calmodulin.	bind
45623	3	6467	5	10	NULL	0	NULL	thrombin	NULL		induce	NULL				Ral	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_108	11397694	12 15  Recently, a binding site for calmodulin on Ral has been detected, and calmodulin has been shown to enhance the binding of GTP to Ral. 23  24  We investigated whether thrombin-induced activation of Ral is affected by antagonists of calmodulin.	bind
23839	1	6467	7	NULL	NULL	NULL	NULL	GTP	Chemical		bind					Ral	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_108	11397694	12 15  Recently, a binding site for calmodulin on Ral has been detected, and calmodulin has been shown to enhance the binding of GTP to Ral. 23  24  We investigated whether thrombin-induced activation of Ral is affected by antagonists of calmodulin.	bind
23840	2	6467	7	NULL	NULL	NULL	NULL	calmodulin	GP		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_108	11397694	12 15  Recently, a binding site for calmodulin on Ral has been detected, and calmodulin has been shown to enhance the binding of GTP to Ral. 23  24  We investigated whether thrombin-induced activation of Ral is affected by antagonists of calmodulin.	bind
23841	3	6467	7	NULL	NULL	NULL	NULL	thrombin	GP		induce					Ral	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_108	11397694	12 15  Recently, a binding site for calmodulin on Ral has been detected, and calmodulin has been shown to enhance the binding of GTP to Ral. 23  24  We investigated whether thrombin-induced activation of Ral is affected by antagonists of calmodulin.	bind
23842	4	6467	7	NULL	NULL	NULL	NULL	Ral	GP		contain								calmodulin binding site		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_108	11397694	12 15  Recently, a binding site for calmodulin on Ral has been detected, and calmodulin has been shown to enhance the binding of GTP to Ral. 23  24  We investigated whether thrombin-induced activation of Ral is affected by antagonists of calmodulin.	bind
20240	1	6469	5	NULL	NULL	0	NULL	glucocorticoids	NULL		up-regulates	NULL				HDL-specific binding	NULL				NULL	rat hepatocytes	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_6_1143_s_213	9194766	12 57  Moreover, despite earlier published data showed that glucocorticoids can upregulate HDL-specific binding in rat hepatocytes, 58  in our experiments Dex had no effect on specific binding of HDL3 to cultured SMC (Table 6  ).	bind
20241	2	6469	5	NULL	NULL	0	NULL	HDL3	NULL		bind	NULL	specifically			SMC	NULL	cultured			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_6_1143_s_213	9194766	12 57  Moreover, despite earlier published data showed that glucocorticoids can upregulate HDL-specific binding in rat hepatocytes, 58  in our experiments Dex had no effect on specific binding of HDL3 to cultured SMC (Table 6  ).	bind
20242	3	6469	5	NULL	NULL	0	NULL	Dex	NULL		does not effect	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_6_1143_s_213	9194766	12 57  Moreover, despite earlier published data showed that glucocorticoids can upregulate HDL-specific binding in rat hepatocytes, 58  in our experiments Dex had no effect on specific binding of HDL3 to cultured SMC (Table 6  ).	bind
23844	1	6469	7	NULL	NULL	NULL	NULL	 glucocorticoids	Chemical		upregulate					HDL-specific binding	Process				NULL	rat hepatocytes	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_6_1143_s_213	9194766	12 57  Moreover, despite earlier published data showed that glucocorticoids can upregulate HDL-specific binding in rat hepatocytes, 58  in our experiments Dex had no effect on specific binding of HDL3 to cultured SMC (Table 6  ).	bind
23845	2	6469	7	NULL	NULL	NULL	NULL	HDL3	GP		bind					SMC	Cell	cultured 			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_6_1143_s_213	9194766	12 57  Moreover, despite earlier published data showed that glucocorticoids can upregulate HDL-specific binding in rat hepatocytes, 58  in our experiments Dex had no effect on specific binding of HDL3 to cultured SMC (Table 6  ).	bind
23846	3	6469	7	NULL	NULL	NULL	NULL	Dex	Chemical		does not effect					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_6_1143_s_213	9194766	12 57  Moreover, despite earlier published data showed that glucocorticoids can upregulate HDL-specific binding in rat hepatocytes, 58  in our experiments Dex had no effect on specific binding of HDL3 to cultured SMC (Table 6  ).	bind
20243	1	6471	5	NULL	NULL	0	NULL	E7	NULL		bind	NULL				Rb	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_162_6_1789_s_20	12759237	12 E7 binds to the retinoblastoma protein Rb, and disrupts the complex between Rb and the E2F transcription factor family, which controls the expression of genes involved in cell-cycle progression.	bind
20244	2	6471	5	NULL	NULL	0	NULL	Rb	NULL		is	NULL				retinoblastoma protein	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_162_6_1789_s_20	12759237	12 E7 binds to the retinoblastoma protein Rb, and disrupts the complex between Rb and the E2F transcription factor family, which controls the expression of genes involved in cell-cycle progression.	bind
20245	3	6471	5	NULL	NULL	0	NULL	Rb	NULL		complexes with	NULL				E2F transcription factor family	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_162_6_1789_s_20	12759237	12 E7 binds to the retinoblastoma protein Rb, and disrupts the complex between Rb and the E2F transcription factor family, which controls the expression of genes involved in cell-cycle progression.	bind
20246	4	6471	5	NULL	NULL	0	NULL	statement 1	NULL		disrupts	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_162_6_1789_s_20	12759237	12 E7 binds to the retinoblastoma protein Rb, and disrupts the complex between Rb and the E2F transcription factor family, which controls the expression of genes involved in cell-cycle progression.	bind
20247	5	6471	5	NULL	NULL	0	NULL	statement 4	NULL		controls	NULL				genes involved in cell-cycle progression	NULL	expression of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_162_6_1789_s_20	12759237	12 E7 binds to the retinoblastoma protein Rb, and disrupts the complex between Rb and the E2F transcription factor family, which controls the expression of genes involved in cell-cycle progression.	bind
23847	1	6471	7	NULL	NULL	NULL	NULL	E7	GP		binds to					Rb	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_6_1789_s_20	12759237	12 E7 binds to the retinoblastoma protein Rb, and disrupts the complex between Rb and the E2F transcription factor family, which controls the expression of genes involved in cell-cycle progression.	bind
23848	2	6471	7	NULL	NULL	NULL	NULL	Rb	GP		complex with					transcription factor family E2F	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_6_1789_s_20	12759237	12 E7 binds to the retinoblastoma protein Rb, and disrupts the complex between Rb and the E2F transcription factor family, which controls the expression of genes involved in cell-cycle progression.	bind
23849	3	6471	7	NULL	NULL	NULL	NULL	statement 1	Process		disrupts					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_6_1789_s_20	12759237	12 E7 binds to the retinoblastoma protein Rb, and disrupts the complex between Rb and the E2F transcription factor family, which controls the expression of genes involved in cell-cycle progression.	bind
23850	4	6471	7	NULL	NULL	NULL	NULL	E2F	GP		controls					genes involved in cell-cycle progression	GP	expression of 			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_6_1789_s_20	12759237	12 E7 binds to the retinoblastoma protein Rb, and disrupts the complex between Rb and the E2F transcription factor family, which controls the expression of genes involved in cell-cycle progression.	bind
30878	5	6471	7	NULL	NULL	NULL	NULL	Rb	GP		is					retinoblastoma protein 	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_6_1789_s_20	12759237	12 E7 binds to the retinoblastoma protein Rb, and disrupts the complex between Rb and the E2F transcription factor family, which controls the expression of genes involved in cell-cycle progression.	bind
20248	1	6472	5	NULL	NULL	0	NULL	Notch	NULL		mediate	NULL				SMA	NULL	upregulation of 			NULL		0	NULL	NULL	NULL	gw70_circulationres_98_12_1468_s_25	16741155	12 Here we demonstrate that Notch-mediated upregulation of SMA is directly dependent on the activation and binding of CSL to the SMA promoter.	bind
20249	2	6472	5	NULL	NULL	0	NULL	CSL	NULL		bind	NULL				SMA	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_circulationres_98_12_1468_s_25	16741155	12 Here we demonstrate that Notch-mediated upregulation of SMA is directly dependent on the activation and binding of CSL to the SMA promoter.	bind
20250	3	6472	5	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL	directly			CSL	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_circulationres_98_12_1468_s_25	16741155	12 Here we demonstrate that Notch-mediated upregulation of SMA is directly dependent on the activation and binding of CSL to the SMA promoter.	bind
20251	4	6472	5	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL	directly			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_12_1468_s_25	16741155	12 Here we demonstrate that Notch-mediated upregulation of SMA is directly dependent on the activation and binding of CSL to the SMA promoter.	bind
23851	1	6472	7	NULL	NULL	NULL	NULL	CSL 	GP		bind					SMA	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_12_1468_s_25	16741155	12 Here we demonstrate that Notch-mediated upregulation of SMA is directly dependent on the activation and binding of CSL to the SMA promoter.	bind
23852	2	6472	7	NULL	NULL	NULL	NULL	Notch	GP		mediates					SMA	GP	upregulation of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_12_1468_s_25	16741155	12 Here we demonstrate that Notch-mediated upregulation of SMA is directly dependent on the activation and binding of CSL to the SMA promoter.	bind
23853	3	6472	7	NULL	NULL	NULL	NULL	statement 2	Process		depends on		directly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_12_1468_s_25	16741155	12 Here we demonstrate that Notch-mediated upregulation of SMA is directly dependent on the activation and binding of CSL to the SMA promoter.	bind
23854	4	6472	7	NULL	NULL	NULL	NULL	statement 2	Process		depends on		directly			CSL	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_12_1468_s_25	16741155	12 Here we demonstrate that Notch-mediated upregulation of SMA is directly dependent on the activation and binding of CSL to the SMA promoter.	bind
20252	1	6473	5	NULL	NULL	0	NULL	SRF	NULL		bind	NULL				SMC marker genes	NULL			CArG regions	NULL		0	NULL	NULL	NULL	gw60_circulationres_92_8_856_s_197	12663482	12 However, on RA treatment, cells exhibited a number of histone modifications consistent with chromatin relaxation and SRF bound to CArG regions of SMC marker genes.	bind
20253	2	6473	5	NULL	NULL	0	NULL	histone	NULL	modification of	is consistent with	NULL				chromatin	NULL	relaxation of			NULL		0	NULL	NULL	NULL	gw60_circulationres_92_8_856_s_197	12663482	12 However, on RA treatment, cells exhibited a number of histone modifications consistent with chromatin relaxation and SRF bound to CArG regions of SMC marker genes.	bind
20254	3	6473	5	NULL	NULL	0	NULL	RA	NULL	treatment	exhibit	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_8_856_s_197	12663482	12 However, on RA treatment, cells exhibited a number of histone modifications consistent with chromatin relaxation and SRF bound to CArG regions of SMC marker genes.	bind
20255	4	6473	5	NULL	NULL	0	NULL	RA	NULL	treatment	exhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_8_856_s_197	12663482	12 However, on RA treatment, cells exhibited a number of histone modifications consistent with chromatin relaxation and SRF bound to CArG regions of SMC marker genes.	bind
23855	1	6473	7	NULL	NULL	NULL	NULL	SRF	GP		bind					SMC marker	GP			CArG regions	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_8_856_s_197	12663482	12 However, on RA treatment, cells exhibited a number of histone modifications consistent with chromatin relaxation and SRF bound to CArG regions of SMC marker genes.	bind
23856	2	6473	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs upon					RA 	Chemical	treatment with			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_8_856_s_197	12663482	12 However, on RA treatment, cells exhibited a number of histone modifications consistent with chromatin relaxation and SRF bound to CArG regions of SMC marker genes.	bind
23857	3	6473	7	NULL	NULL	NULL	NULL	cells	Cell	RA treated	exhibit					histone	GP	modifications of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_8_856_s_197	12663482	12 However, on RA treatment, cells exhibited a number of histone modifications consistent with chromatin relaxation and SRF bound to CArG regions of SMC marker genes.	bind
23858	4	6473	7	NULL	NULL	NULL	NULL	statement 3	Process		is consistent with					chromatin relaxation	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_8_856_s_197	12663482	12 However, on RA treatment, cells exhibited a number of histone modifications consistent with chromatin relaxation and SRF bound to CArG regions of SMC marker genes.	bind
20256	1	6474	5	NULL	NULL	0	NULL	P-selectin	NULL		bind	NULL				PSGL-1	NULL				NULL	on monocytes	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_1065_s_25	15705928	12 Importantly, binding of P-selectin to PSGL-1 on monocytes also induces the expression of tissue factor (TF), 2 the main initiator of coagulation in vivo.	bind
20257	2	6474	5	NULL	NULL	0	NULL	statement 1	NULL		induces	NULL				TF	NULL	expression of			NULL	in vivo	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_1065_s_25	15705928	12 Importantly, binding of P-selectin to PSGL-1 on monocytes also induces the expression of tissue factor (TF), 2 the main initiator of coagulation in vivo.	bind
20258	3	6474	5	NULL	NULL	0	NULL	TF	NULL		is	NULL				tissue factor	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_1065_s_25	15705928	12 Importantly, binding of P-selectin to PSGL-1 on monocytes also induces the expression of tissue factor (TF), 2 the main initiator of coagulation in vivo.	bind
20259	4	6474	5	NULL	NULL	0	NULL	TF	NULL		initiates	NULL				coagulation	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_1065_s_25	15705928	12 Importantly, binding of P-selectin to PSGL-1 on monocytes also induces the expression of tissue factor (TF), 2 the main initiator of coagulation in vivo.	bind
23859	1	6474	7	NULL	NULL	NULL	NULL	P-selectin	GP		bind					PSGL-1	GP				NULL	monocytes	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_1065_s_25	15705928	12 Importantly, binding of P-selectin to PSGL-1 on monocytes also induces the expression of tissue factor (TF), 2 the main initiator of coagulation in vivo.	bind
23860	2	6474	7	NULL	NULL	NULL	NULL	statement 1	Process		induce					TF	GP	expression of			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_1065_s_25	15705928	12 Importantly, binding of P-selectin to PSGL-1 on monocytes also induces the expression of tissue factor (TF), 2 the main initiator of coagulation in vivo.	bind
23861	3	6474	7	NULL	NULL	NULL	NULL	TF	GP		initiates					coagulation	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_1065_s_25	15705928	12 Importantly, binding of P-selectin to PSGL-1 on monocytes also induces the expression of tissue factor (TF), 2 the main initiator of coagulation in vivo.	bind
23862	4	6474	7	NULL	NULL	NULL	NULL	TF	GP		is					Tissue Factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_1065_s_25	15705928	12 Importantly, binding of P-selectin to PSGL-1 on monocytes also induces the expression of tissue factor (TF), 2 the main initiator of coagulation in vivo.	bind
20374	1	6475	5	NULL	NULL	0	NULL	mmLDL	NULL		bind	NULL				heat shock protein-60	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1085_s_46	15923538	12 In addition to mmLDL, TLR4 also binds heat shock protein-60, another antigenic protein implicated in atherosclerosis.	bind
20375	2	6475	5	NULL	NULL	0	NULL	TLR4	NULL		bind	NULL				heat shock protein-60	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1085_s_46	15923538	12 In addition to mmLDL, TLR4 also binds heat shock protein-60, another antigenic protein implicated in atherosclerosis.	bind
20376	3	6475	5	NULL	NULL	0	NULL	heat shock protein-60	NULL		is a type of	NULL				antigenic protein	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1085_s_46	15923538	12 In addition to mmLDL, TLR4 also binds heat shock protein-60, another antigenic protein implicated in atherosclerosis.	bind
20377	4	6475	5	NULL	NULL	0	NULL	heat shock protein-60	NULL		is implicated in	NULL				atherosclerosis	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1085_s_46	15923538	12 In addition to mmLDL, TLR4 also binds heat shock protein-60, another antigenic protein implicated in atherosclerosis.	bind
23863	1	6475	7	NULL	NULL	NULL	NULL	TLR4	GP		binds					mmLDL	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1085_s_46	15923538	12 In addition to mmLDL, TLR4 also binds heat shock protein-60, another antigenic protein implicated in atherosclerosis.	bind
23864	2	6475	7	NULL	NULL	NULL	NULL	TLR4	GP		bind					heat shock protein-60	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1085_s_46	15923538	12 In addition to mmLDL, TLR4 also binds heat shock protein-60, another antigenic protein implicated in atherosclerosis.	bind
23865	3	6475	7	NULL	NULL	NULL	NULL	heat shock protein-60	GP		implicated in					atherosclerosis	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1085_s_46	15923538	12 In addition to mmLDL, TLR4 also binds heat shock protein-60, another antigenic protein implicated in atherosclerosis.	bind
30885	4	6475	7	NULL	NULL	NULL	NULL	heat shock protein-60	GP		is a type of					antigenic protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1085_s_46	15923538	12 In addition to mmLDL, TLR4 also binds heat shock protein-60, another antigenic protein implicated in atherosclerosis.	bind
20378	1	6476	5	NULL	NULL	0	NULL	CCL5	NULL		bind	NULL				CCR5 receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_jantimicrobchemoth_53_6_895_s_23	15128728	12 Increased binding of CCL5 to its receptor CCR5 further decreases CCR5 surface density due to receptor internalization.	bind
20380	2	6476	5	NULL	NULL	0	NULL	statement 1	NULL	increased	decreases	NULL				CCR5	NULL	surface density of			NULL		0	NULL	NULL	NULL	gw70_jantimicrobchemoth_53_6_895_s_23	15128728	12 Increased binding of CCL5 to its receptor CCR5 further decreases CCR5 surface density due to receptor internalization.	bind
20381	3	6476	5	NULL	NULL	0	NULL	statement 2	NULL		occurs due to	NULL				receptor internalization	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_53_6_895_s_23	15128728	12 Increased binding of CCL5 to its receptor CCR5 further decreases CCR5 surface density due to receptor internalization.	bind
23866	1	6476	7	NULL	NULL	NULL	NULL	CCL5	GP		binds to					CCR5 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_53_6_895_s_23	15128728	12 Increased binding of CCL5 to its receptor CCR5 further decreases CCR5 surface density due to receptor internalization.	bind
23867	2	6476	7	NULL	NULL	NULL	NULL	statement 1	Process	increased	decrease					CCR5	GP	surface density			NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_53_6_895_s_23	15128728	12 Increased binding of CCL5 to its receptor CCR5 further decreases CCR5 surface density due to receptor internalization.	bind
23868	3	6476	7	NULL	NULL	NULL	NULL	statement 2	GP		occurs due to					receptor internalization	Process				NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_53_6_895_s_23	15128728	12 Increased binding of CCL5 to its receptor CCR5 further decreases CCR5 surface density due to receptor internalization.	bind
20382	1	6478	5	NULL	NULL	0	NULL	VEGF-C	NULL		undergoes	NULL				proteolytic processing	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_59	9665459	12 Proteolytic processing of VEGF-C generates several VEGF-C forms with increased activity toward VEGFR-3, but only the fully processed VEGF-C can bind to VEGFR-2.	bind
20383	2	6478	5	NULL	NULL	0	NULL	VEGF-C forms	NULL		shows increased activity towards	NULL				VEGFR-3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_59	9665459	12 Proteolytic processing of VEGF-C generates several VEGF-C forms with increased activity toward VEGFR-3, but only the fully processed VEGF-C can bind to VEGFR-2.	bind
20385	3	6478	5	NULL	NULL	0	NULL	statement 1	NULL		generates	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_59	9665459	12 Proteolytic processing of VEGF-C generates several VEGF-C forms with increased activity toward VEGFR-3, but only the fully processed VEGF-C can bind to VEGFR-2.	bind
20386	4	6478	5	NULL	NULL	0	NULL	VEGF-C	NULL	only fully processed	bind	NULL				VEGFR-2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_59	9665459	12 Proteolytic processing of VEGF-C generates several VEGF-C forms with increased activity toward VEGFR-3, but only the fully processed VEGF-C can bind to VEGFR-2.	bind
23869	1	6478	7	NULL	NULL	NULL	NULL	VEGF-C	GP	Proteolytic processing of	generates					VEGF-C forms	GP	several			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_59	9665459	12 Proteolytic processing of VEGF-C generates several VEGF-C forms with increased activity toward VEGFR-3, but only the fully processed VEGF-C can bind to VEGFR-2.	bind
23870	2	6478	7	NULL	NULL	NULL	NULL	VEGF-C forms	GP		shows					VEGFR-3	GP	increased activity towards			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_59	9665459	12 Proteolytic processing of VEGF-C generates several VEGF-C forms with increased activity toward VEGFR-3, but only the fully processed VEGF-C can bind to VEGFR-2.	bind
23871	3	6478	7	NULL	NULL	NULL	NULL	VEGF-C	GP	fully processed	bind					VEGFR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_59	9665459	12 Proteolytic processing of VEGF-C generates several VEGF-C forms with increased activity toward VEGFR-3, but only the fully processed VEGF-C can bind to VEGFR-2.	bind
20384	1	6479	5	NULL	NULL	0	NULL	E1A	NULL		bind	NULL	strongly			importin-alpha3	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_277_41_38755_s_41	12161448	12 S E1A binds strongly to importin-alpha3  in vitro, while Lys239 substitution mutations and acetylation of E1A by CBP abrogate this interaction.	bind
20387	2	6479	5	10	NULL	0	NULL	E1A		substitution mutations	abrogate			Lys239		statement 1					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38755_s_41	12161448	12 S E1A binds strongly to importin-alpha3  in vitro, while Lys239 substitution mutations and acetylation of E1A by CBP abrogate this interaction.	bind
20388	3	6479	5	NULL	NULL	0	NULL	CBP	NULL		acetylate	NULL				E1A	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_41_38755_s_41	12161448	12 S E1A binds strongly to importin-alpha3  in vitro, while Lys239 substitution mutations and acetylation of E1A by CBP abrogate this interaction.	bind
20389	4	6479	5	10	NULL	0	NULL	statement 3			abrogate					statement 1					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38755_s_41	12161448	12 S E1A binds strongly to importin-alpha3  in vitro, while Lys239 substitution mutations and acetylation of E1A by CBP abrogate this interaction.	bind
23872	1	6479	7	NULL	NULL	NULL	NULL	S E1A	GP		bind		strongly			importin-alpha3	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38755_s_41	12161448	12 S E1A binds strongly to importin-alpha3  in vitro, while Lys239 substitution mutations and acetylation of E1A by CBP abrogate this interaction.	bind
23873	2	6479	7	NULL	NULL	NULL	NULL	E1A	GP	substitution mutation	abrogates			Lys239		statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38755_s_41	12161448	12 S E1A binds strongly to importin-alpha3  in vitro, while Lys239 substitution mutations and acetylation of E1A by CBP abrogate this interaction.	bind
23874	3	6479	7	NULL	NULL	NULL	NULL	CBP	GP		acetylates					E1A	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38755_s_41	12161448	12 S E1A binds strongly to importin-alpha3  in vitro, while Lys239 substitution mutations and acetylation of E1A by CBP abrogate this interaction.	bind
23875	4	6479	7	NULL	NULL	NULL	NULL	statement 3	Process		abrogates					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38755_s_41	12161448	12 S E1A binds strongly to importin-alpha3  in vitro, while Lys239 substitution mutations and acetylation of E1A by CBP abrogate this interaction.	bind
20390	1	6480	5	NULL	NULL	0	NULL	keratinocytes	NULL	human	is treated with	NULL				arsenic	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
20391	2	6480	5	NULL	NULL	0	NULL	statement 1	NULL		induces	NULL				ornithine decarboxylase	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
20392	3	6480	5	NULL	NULL	0	NULL	statement 1	NULL		induces	NULL				growth factor	NULL	expression of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
20393	4	6480	5	10	NULL	0	NULL	AP-1	NULL		bind	NULL				DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
20394	5	6480	5	10	NULL	0	NULL	AP-2	NULL		bind	NULL				DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
20395	6	6480	5	NULL	NULL	0	NULL	statement 1	NULL		alters	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
20396	7	6480	5	NULL	NULL	0	NULL	statement 1	NULL		alters	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
20397	8	6480	5	10	NULL	0	NULL	AP-1	NULL		is involved in	NULL				proliferative events	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
20398	9	6480	5	10	NULL	0	NULL	AP-2	NULL		is involved in	NULL				proliferative events	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
45624	10	6480	5	10	NULL	0	NULL	AP1	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
45625	11	6480	5	10	NULL	0	NULL	AP2	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
23876	1	6480	7	NULL	NULL	NULL	NULL	keratinocytes	Cell	arsenic treated;;human	induce					ornithine decarboxylase	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
23877	2	6480	7	NULL	NULL	NULL	NULL	keratinocytes	Cell	arsenic treated;;human	induce					growth factor	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
23878	3	6480	7	NULL	NULL	NULL	NULL	AP-1	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
23879	4	6480	7	NULL	NULL	NULL	NULL	AP-2	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
23880	5	6480	7	NULL	NULL	NULL	NULL	keratinocytes	Cell	arsenic treated;;human	increase					cell proliferation	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
23881	6	6480	7	NULL	NULL	NULL	NULL	keratinocytes	Cell	arsenic treated;;human	alters					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
23882	7	6480	7	NULL	NULL	NULL	NULL	keratinocytes	Cell	arsenic treated;;human	alters					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
23887	8	6480	7	NULL	NULL	NULL	NULL	AP-1	GP		is involved in					proliferative events	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
23888	9	6480	7	NULL	NULL	NULL	NULL	AP-2	GP		is involved in					proliferative events	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
45626	10	6480	7	NULL	NULL	NULL	NULL	AP1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
45627	11	6480	7	NULL	NULL	NULL	NULL	AP2	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1775_s_20	9846968	12 Support exists that increased cell proliferation is a central event, as treatment of human keratinocytes with arsenic induces ornithine decarboxylase activity 13  and growth factor expression 14 as well as alters the DNA-binding activities of the AP-1 and AP-2 transcription factors, which are involved in proliferative events.	bind
20399	1	6481	5	NULL	NULL	0	NULL	CV-N	NULL		is	NULL				cyanovirin-N	NULL				NULL		0	NULL	NULL	NULL	gw70_jantimicrobchemoth_52_6_890_s_74	14613946	12 The cyanobacterial protein cyanovirin-N (CV-N) binds to gp120 via mannose moieties on individual N-linked glycans.	bind
20400	2	6481	5	NULL	NULL	0	NULL	CV-N	NULL	cyanobacterial protein	bind	NULL				gp120	NULL				NULL		0	NULL	NULL	NULL	gw70_jantimicrobchemoth_52_6_890_s_74	14613946	12 The cyanobacterial protein cyanovirin-N (CV-N) binds to gp120 via mannose moieties on individual N-linked glycans.	bind
20401	3	6481	5	NULL	NULL	0	NULL	statement 2	NULL		via	NULL				N-linked glycans	NULL	individual	mannose moieties		NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_52_6_890_s_74	14613946	12 The cyanobacterial protein cyanovirin-N (CV-N) binds to gp120 via mannose moieties on individual N-linked glycans.	bind
23889	1	6481	7	NULL	NULL	NULL	NULL	CV-N	GP	cyanobacterial protein	binds to					gp120	Gp				NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_52_6_890_s_74	14613946	12 The cyanobacterial protein cyanovirin-N (CV-N) binds to gp120 via mannose moieties on individual N-linked glycans.	bind
23890	2	6481	7	NULL	NULL	NULL	NULL	statement 1	Process		 via					N-linked glycans	Chemical		mannose moieties		NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_52_6_890_s_74	14613946	12 The cyanobacterial protein cyanovirin-N (CV-N) binds to gp120 via mannose moieties on individual N-linked glycans.	bind
23891	3	6481	7	NULL	NULL	NULL	NULL	CV-N	GP		is					cyanovirin-N	GP				NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_52_6_890_s_74	14613946	12 The cyanobacterial protein cyanovirin-N (CV-N) binds to gp120 via mannose moieties on individual N-linked glycans.	bind
20402	1	6483	5	NULL	NULL	0	NULL	IAP	NULL		bind	NULL				SHPS-1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_10_925_s_202	14563713	12 We have shown recently that when IAP binding to SHPS-1 is blocked, IGF-I - stimulated SHPS-1 phosphorylation is inhibited.	bind
20403	2	6483	5	NULL	NULL	0	NULL	IGF-I	NULL		stimulates	NULL				SHPS-1	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw70_circulationres_93_10_925_s_202	14563713	12 We have shown recently that when IAP binding to SHPS-1 is blocked, IGF-I - stimulated SHPS-1 phosphorylation is inhibited.	bind
20404	3	6483	5	NULL	NULL	0	NULL	statement 1	NULL	blocking of	leads to	NULL				statement 2	NULL	inhibition of			NULL		0	NULL	NULL	NULL	gw70_circulationres_93_10_925_s_202	14563713	12 We have shown recently that when IAP binding to SHPS-1 is blocked, IGF-I - stimulated SHPS-1 phosphorylation is inhibited.	bind
23892	1	6483	7	NULL	NULL	NULL	NULL	IAP 	GP		bind					SHPS-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_10_925_s_202	14563713	12 We have shown recently that when IAP binding to SHPS-1 is blocked, IGF-I - stimulated SHPS-1 phosphorylation is inhibited.	bind
23893	2	6483	7	NULL	NULL	NULL	NULL	IGF-I 	GP		stimulates					SHPS-1	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_10_925_s_202	14563713	12 We have shown recently that when IAP binding to SHPS-1 is blocked, IGF-I - stimulated SHPS-1 phosphorylation is inhibited.	bind
23894	3	6483	7	NULL	NULL	NULL	NULL	statement 1	Process	blocking	results in					statement 2	Process	inhibition of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_10_925_s_202	14563713	12 We have shown recently that when IAP binding to SHPS-1 is blocked, IGF-I - stimulated SHPS-1 phosphorylation is inhibited.	bind
20405	1	6485	5	NULL	NULL	0	NULL	PlA2 variant platelet	NULL		bind	NULL				fibrinogen	NULL	exogenous			NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_2_140_s_32	11447076	12, 13 Paradoxically, however, Goldschmidt-Clermont et al 14 showed that platelets with the  PlA2 variant bound less exogenous fibrinogen than did the  PlA1-homozygous platelets when stimulated with ADP.	bind
20406	2	6485	5	NULL	NULL	0	NULL	PlA1-homozygous platelets	NULL		bind	NULL				fibrinogen	NULL	exogenous			NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_2_140_s_32	11447076	12, 13 Paradoxically, however, Goldschmidt-Clermont et al 14 showed that platelets with the  PlA2 variant bound less exogenous fibrinogen than did the  PlA1-homozygous platelets when stimulated with ADP.	bind
20407	3	6485	5	NULL	NULL	0	NULL	statement 1	NULL		is lesser than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_104_2_140_s_32	11447076	12, 13 Paradoxically, however, Goldschmidt-Clermont et al 14 showed that platelets with the  PlA2 variant bound less exogenous fibrinogen than did the  PlA1-homozygous platelets when stimulated with ADP.	bind
20408	4	6485	5	NULL	NULL	0	NULL	statement 3	NULL		occurs on	NULL				ADP	NULL	stimulation with			NULL		0	NULL	NULL	NULL	gw60_circulation_104_2_140_s_32	11447076	12, 13 Paradoxically, however, Goldschmidt-Clermont et al 14 showed that platelets with the  PlA2 variant bound less exogenous fibrinogen than did the  PlA1-homozygous platelets when stimulated with ADP.	bind
23895	1	6485	7	NULL	NULL	NULL	NULL	PlA2 variant platelet	Cell		bind					fibrinogen	GP	exogenous			NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_2_140_s_32	11447076	12, 13 Paradoxically, however, Goldschmidt-Clermont et al 14 showed that platelets with the  PlA2 variant bound less exogenous fibrinogen than did the  PlA1-homozygous platelets when stimulated with ADP.	bind
23896	2	6485	7	NULL	NULL	NULL	NULL	PlA1-homozygous platelets	Cell		bind					fibrinogen	GP	exogenous			NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_2_140_s_32	11447076	12, 13 Paradoxically, however, Goldschmidt-Clermont et al 14 showed that platelets with the  PlA2 variant bound less exogenous fibrinogen than did the  PlA1-homozygous platelets when stimulated with ADP.	bind
23897	3	6485	7	NULL	NULL	NULL	NULL	statement 1	Process	binding of	is less than					statement 2	Process	binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_2_140_s_32	11447076	12, 13 Paradoxically, however, Goldschmidt-Clermont et al 14 showed that platelets with the  PlA2 variant bound less exogenous fibrinogen than did the  PlA1-homozygous platelets when stimulated with ADP.	bind
23898	4	6485	7	NULL	NULL	NULL	NULL	statement 3	Process		occurs when					ADP	Chemical	stimulated with			NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_2_140_s_32	11447076	12, 13 Paradoxically, however, Goldschmidt-Clermont et al 14 showed that platelets with the  PlA2 variant bound less exogenous fibrinogen than did the  PlA1-homozygous platelets when stimulated with ADP.	bind
20409	1	6486	5	10	NULL	0	NULL	ets			bind			DNA-binding domain						GGA(A/T) DNA sequence	NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_10_1411_s_31	12642363	12, 13 The ets family of transcription factors has a common DNA-binding domain that binds to a core GGA(A/T) DNA sequence.	bind
54268	2	6486	5	10	NULL	0	NULL	ets			is a type of					transcription factor					NULL		0	NULL	NULL	NULL	gw60_circulation_107_10_1411_s_31	12642363	12, 13 The ets family of transcription factors has a common DNA-binding domain that binds to a core GGA(A/T) DNA sequence.	bind
24058	1	6486	7	NULL	NULL	NULL	NULL	ets	GP		binds			DNA-binding domain						core GGA(A/T) DNA sequence	NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_10_1411_s_31	12642363	12, 13 The ets family of transcription factors has a common DNA-binding domain that binds to a core GGA(A/T) DNA sequence.	bind
30886	2	6486	7	NULL	NULL	NULL	NULL	ets	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_10_1411_s_31	12642363	12, 13 The ets family of transcription factors has a common DNA-binding domain that binds to a core GGA(A/T) DNA sequence.	bind
20411	1	6488	5	NULL	NULL	0	NULL	LRR	NULL		bind	NULL			cis-regulatory element	NF-kappaB	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
20412	2	6488	5	NULL	NULL	0	NULL	LRR	NULL		bind	NULL			cis-regulatory element	AP-1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
20413	3	6488	5	NULL	NULL	0	NULL	LPS	NULL		stimulates	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
20414	4	6488	5	NULL	NULL	0	NULL	LPS	NULL		stimulates	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
20415	5	6488	5	NULL	NULL	0	NULL	TNF-alpha	NULL		stimulates	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
20416	6	6488	5	NULL	NULL	0	NULL	TNF-alpha	NULL		stimulates	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
20417	7	6488	5	NULL	NULL	0	NULL	IL-1beta	NULL		stimulates	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
20418	8	6488	5	NULL	NULL	0	NULL	IL-1beta	NULL		stimulates	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
30264	9	6488	5	NULL	NULL	0	NULL	LPS	NULL		is a type of	NULL				inflammatory mediator	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
30265	10	6488	5	NULL	NULL	0	NULL	TNF-alpha	NULL		is a type of	NULL				inflammatory mediator	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
30266	11	6488	5	NULL	NULL	0	NULL	IL-1beta	NULL		is a type of	NULL				inflammatory mediator	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
24069	1	6488	7	NULL	NULL	NULL	NULL	LRR	GP		bind				cis-regulatory element 	NF-kappaB	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
24071	2	6488	7	NULL	NULL	NULL	NULL	LRR	GP		bind				cis-regulatory element 	AP-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
24073	3	6488	7	NULL	NULL	NULL	NULL	LPS	Chemical		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
24074	4	6488	7	NULL	NULL	NULL	NULL	TNF-alpha	GP		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
24078	5	6488	7	NULL	NULL	NULL	NULL	IL-1beta	GP		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
24079	6	6488	7	NULL	NULL	NULL	NULL	LPS	Chemical		stimulates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
24080	7	6488	7	NULL	NULL	NULL	NULL	TNF-alpha	GP		stimulates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
24081	8	6488	7	NULL	NULL	NULL	NULL	IL-1beta	GP		stimulates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
30887	9	6488	7	NULL	NULL	NULL	NULL	LPS	Chemical		is a type of					inflammatory mediator	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
30888	10	6488	7	NULL	NULL	NULL	NULL	TNF-alpha	GP		is a type of					inflammatory mediator	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
30889	11	6488	7	NULL	NULL	NULL	NULL	IL-1beta	GP		is a type of					inflammatory mediator	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_162	12600889	12, 19 The LRR contains the  cis-regulatory element for NF-kappaB and AP-1 binding on stimulation by inflammatory mediators such as LPS, TNF-alpha, or IL-1beta.	bind
20419	1	6489	5	NULL	NULL	0	NULL	VEGF	NULL		bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_56	9665459	12, 35, 36  Unlike some of the VEGF, VEGF-B, and PlGF isoforms, VEGF-C does not bind to heparin.	bind
20420	2	6489	5	NULL	NULL	0	NULL	VEGF-B	NULL		bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_56	9665459	12, 35, 36  Unlike some of the VEGF, VEGF-B, and PlGF isoforms, VEGF-C does not bind to heparin.	bind
20421	3	6489	5	NULL	NULL	0	NULL	PlGF isoforms	NULL		bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_56	9665459	12, 35, 36  Unlike some of the VEGF, VEGF-B, and PlGF isoforms, VEGF-C does not bind to heparin.	bind
20422	4	6489	5	NULL	NULL	0	NULL	VEGF-C	NULL		does not bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_56	9665459	12, 35, 36  Unlike some of the VEGF, VEGF-B, and PlGF isoforms, VEGF-C does not bind to heparin.	bind
24082	1	6489	7	NULL	NULL	NULL	NULL	VEGF-C	GP		does not bind					heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_56	9665459	12, 35, 36  Unlike some of the VEGF, VEGF-B, and PlGF isoforms, VEGF-C does not bind to heparin.	bind
24083	2	6489	7	NULL	NULL	NULL	NULL	VEGF	GP		bind					heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_56	9665459	12, 35, 36  Unlike some of the VEGF, VEGF-B, and PlGF isoforms, VEGF-C does not bind to heparin.	bind
24084	3	6489	7	NULL	NULL	NULL	NULL	VEGF-B	GP		bind					heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_56	9665459	12, 35, 36  Unlike some of the VEGF, VEGF-B, and PlGF isoforms, VEGF-C does not bind to heparin.	bind
24085	4	6489	7	NULL	NULL	NULL	NULL	PlGF isoform	GP		bind					heparin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_56	9665459	12, 35, 36  Unlike some of the VEGF, VEGF-B, and PlGF isoforms, VEGF-C does not bind to heparin.	bind
20423	1	6490	5	NULL	NULL	0	NULL	CRP	NULL		bind	NULL				LDL	NULL	oxidized			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_30	15692104	12,13  In addition, binding of CRP to oxidized LDL and degraded nonoxidized LDL transforms the acute-phase protein to an activator of the classical complement pathway.	bind
20424	2	6490	5	10	NULL	0	NULL	CRP	NULL		bind	NULL				LDL	NULL	degraded;; nonoxidized			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_30	15692104	12,13  In addition, binding of CRP to oxidized LDL and degraded nonoxidized LDL transforms the acute-phase protein to an activator of the classical complement pathway.	bind
20425	3	6490	5	NULL	NULL	0	NULL	acute-phase protein	NULL		is transformed to	NULL				classical complement pathway activator	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_30	15692104	12,13  In addition, binding of CRP to oxidized LDL and degraded nonoxidized LDL transforms the acute-phase protein to an activator of the classical complement pathway.	bind
20426	4	6490	5	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_30	15692104	12,13  In addition, binding of CRP to oxidized LDL and degraded nonoxidized LDL transforms the acute-phase protein to an activator of the classical complement pathway.	bind
20427	5	6490	5	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_30	15692104	12,13  In addition, binding of CRP to oxidized LDL and degraded nonoxidized LDL transforms the acute-phase protein to an activator of the classical complement pathway.	bind
24086	1	6490	7	NULL	NULL	NULL	NULL	CRP 	GP		bind					 LDL	GP	oxidized			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_30	15692104	12,13  In addition, binding of CRP to oxidized LDL and degraded nonoxidized LDL transforms the acute-phase protein to an activator of the classical complement pathway.	bind
24087	2	6490	7	NULL	NULL	NULL	NULL	CRP	GP		bind					LDL	GP	degraded;; nonoxidized			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_30	15692104	12,13  In addition, binding of CRP to oxidized LDL and degraded nonoxidized LDL transforms the acute-phase protein to an activator of the classical complement pathway.	bind
24088	3	6490	7	NULL	NULL	NULL	NULL	acute-phase protein	GP		become an					classical complement pathway activator	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_30	15692104	12,13  In addition, binding of CRP to oxidized LDL and degraded nonoxidized LDL transforms the acute-phase protein to an activator of the classical complement pathway.	bind
24089	4	6490	7	NULL	NULL	NULL	NULL	statement 1	Process		transform					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_30	15692104	12,13  In addition, binding of CRP to oxidized LDL and degraded nonoxidized LDL transforms the acute-phase protein to an activator of the classical complement pathway.	bind
24090	5	6490	7	NULL	NULL	NULL	NULL	statement 2	Process		transform					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_30	15692104	12,13  In addition, binding of CRP to oxidized LDL and degraded nonoxidized LDL transforms the acute-phase protein to an activator of the classical complement pathway.	bind
20428	1	6491	5	NULL	NULL	0	NULL	agonists	NULL		bind	NULL				G-protein - coupled receptors	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_7_630_s_26	12946946	12,13  Such agonists that bind to G-protein - coupled receptors produced contraction by increasing both the cytosolic Ca2+ concentration and the Ca2+ sensitivity of the contractile apparatus.	bind
20429	2	6491	5	NULL	NULL	0	NULL	statement 1	NULL		produces	NULL				contraction	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_7_630_s_26	12946946	12,13  Such agonists that bind to G-protein - coupled receptors produced contraction by increasing both the cytosolic Ca2+ concentration and the Ca2+ sensitivity of the contractile apparatus.	bind
20430	3	6491	5	NULL	NULL	0	NULL	Ca2+ 	NULL	increased cytosolic concentration of	leads to	NULL				statement 2	NULL				NULL	contractile apparatus	0	NULL	NULL	NULL	gw70_circulationres_93_7_630_s_26	12946946	12,13  Such agonists that bind to G-protein - coupled receptors produced contraction by increasing both the cytosolic Ca2+ concentration and the Ca2+ sensitivity of the contractile apparatus.	bind
20431	4	6491	5	NULL	NULL	0	NULL	Ca2+	NULL	increased sensitivity of	leads to	NULL				statement 2	NULL				NULL	contractile apparatus	NULL	NULL	NULL	NULL	gw70_circulationres_93_7_630_s_26	12946946	12,13  Such agonists that bind to G-protein - coupled receptors produced contraction by increasing both the cytosolic Ca2+ concentration and the Ca2+ sensitivity of the contractile apparatus.	bind
24091	2	6491	7	NULL	NULL	NULL	NULL	statement 1	Process		produce					contraction	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_7_630_s_26	12946946	12,13  Such agonists that bind to G-protein - coupled receptors produced contraction by increasing both the cytosolic Ca2+ concentration and the Ca2+ sensitivity of the contractile apparatus.	bind
24092	3	6491	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs by					Ca2+	Chemical	increased cytosolic concentration of 			NULL	contractile appartus	NULL	NULL	NULL	NULL	gw70_circulationres_93_7_630_s_26	12946946	12,13  Such agonists that bind to G-protein - coupled receptors produced contraction by increasing both the cytosolic Ca2+ concentration and the Ca2+ sensitivity of the contractile apparatus.	bind
24093	4	6491	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs by					Ca2+	Chemical	increased sensitivity of 			NULL	contractile appartus	NULL	NULL	NULL	NULL	gw70_circulationres_93_7_630_s_26	12946946	12,13  Such agonists that bind to G-protein - coupled receptors produced contraction by increasing both the cytosolic Ca2+ concentration and the Ca2+ sensitivity of the contractile apparatus.	bind
30901	1	6491	7	NULL	NULL	NULL	NULL	agonists	GP		bind					G-protein-coupled receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_7_630_s_26	12946946	12,13  Such agonists that bind to G-protein - coupled receptors produced contraction by increasing both the cytosolic Ca2+ concentration and the Ca2+ sensitivity of the contractile apparatus.	bind
20432	1	6492	5	NULL	NULL	0	NULL	FVII	NULL		bind	NULL	probably			TF	NULL	extravascular			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_41_s_66	16254201	12,13  Thus, FVII is probably bound to extravascular TF even in the absence of an injury, and the extravascular factors X and IX can be activated as they pass through the tissues.	bind
20433	2	6492	5	NULL	NULL	0	NULL	statement 1	NULL		in the absence of	NULL				injury	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_41_s_66	16254201	12,13  Thus, FVII is probably bound to extravascular TF even in the absence of an injury, and the extravascular factors X and IX can be activated as they pass through the tissues.	bind
20434	3	6492	5	10	NULL	0	NULL	extravascular factor X			pass through					tissues					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_41_s_66	16254201	12,13  Thus, FVII is probably bound to extravascular TF even in the absence of an injury, and the extravascular factors X and IX can be activated as they pass through the tissues.	bind
20435	4	6492	5	10	NULL	0	NULL	extravascular factor IX			pass through					tissues					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_41_s_66	16254201	12,13  Thus, FVII is probably bound to extravascular TF even in the absence of an injury, and the extravascular factors X and IX can be activated as they pass through the tissues.	bind
54269	5	6492	5	10	NULL	0	NULL	statement 3			activates					extravascular factors X					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_41_s_66	16254201	12,13  Thus, FVII is probably bound to extravascular TF even in the absence of an injury, and the extravascular factors X and IX can be activated as they pass through the tissues.	bind
54270	6	6492	5	10	NULL	0	NULL	statement 4			activates					extravascular factors IX					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_41_s_66	16254201	12,13  Thus, FVII is probably bound to extravascular TF even in the absence of an injury, and the extravascular factors X and IX can be activated as they pass through the tissues.	bind
24094	1	6492	7	NULL	NULL	NULL	NULL	FVII 	GP		bind		probably			TF	GP	extravascular			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_41_s_66	16254201	12,13  Thus, FVII is probably bound to extravascular TF even in the absence of an injury, and the extravascular factors X and IX can be activated as they pass through the tissues.	bind
24095	2	6492	7	NULL	NULL	NULL	NULL	statement 1	Process		in absence of					injury	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_41_s_66	16254201	12,13  Thus, FVII is probably bound to extravascular TF even in the absence of an injury, and the extravascular factors X and IX can be activated as they pass through the tissues.	bind
24096	3	6492	7	NULL	NULL	NULL	NULL	extravascular factor X	GP		pass through					tissues	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_41_s_66	16254201	12,13  Thus, FVII is probably bound to extravascular TF even in the absence of an injury, and the extravascular factors X and IX can be activated as they pass through the tissues.	bind
24097	4	6492	7	NULL	NULL	NULL	NULL	extravascular factor IX	GP		pass through					tissues	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_41_s_66	16254201	12,13  Thus, FVII is probably bound to extravascular TF even in the absence of an injury, and the extravascular factors X and IX can be activated as they pass through the tissues.	bind
54271	5	6492	7	NULL	NULL	NULL	NULL	statement 3	Process		activates					extravascular factors X	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_41_s_66	16254201	12,13  Thus, FVII is probably bound to extravascular TF even in the absence of an injury, and the extravascular factors X and IX can be activated as they pass through the tissues.	bind
54272	6	6492	7	NULL	NULL	NULL	NULL	statement 4	Process		activates					extravascular factors IX	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_41_s_66	16254201	12,13  Thus, FVII is probably bound to extravascular TF even in the absence of an injury, and the extravascular factors X and IX can be activated as they pass through the tissues.	bind
20436	1	6494	5	NULL	NULL	0	NULL	AP-1	NULL		bind	NULL				sPLA2-IIA	NULL	rat		promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_27_25830_s_196	15878884	12/15-LOX Enhances Binding of AP-1 to Rat sPLA2-IIA Promoter --	bind
20437	2	6494	5	NULL	NULL	0	NULL	LOX	NULL		enhances	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_27_25830_s_196	15878884	12/15-LOX Enhances Binding of AP-1 to Rat sPLA2-IIA Promoter --	bind
24098	1	6494	7	NULL	NULL	NULL	NULL	AP-1	GP		bind					sPLA2-IIA 	GP	rat		promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_27_25830_s_196	15878884	12/15-LOX Enhances Binding of AP-1 to Rat sPLA2-IIA Promoter --	bind
24099	2	6494	7	NULL	NULL	NULL	NULL	12/15-LOX	GP		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_27_25830_s_196	15878884	12/15-LOX Enhances Binding of AP-1 to Rat sPLA2-IIA Promoter --	bind
20438	1	6495	5	10	NULL	0	NULL	Bcl-xL	NULL	mutant	is defective for	NULL				Bax	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_154	15539639	120 Consistent with this model, a Bcl-xL mutant, which is defective for Bax and Bak binding but competent to bind tBid, is still cytoprotective.	bind
20439	2	6495	5	NULL	NULL	0	NULL	Bcl-xL	NULL	mutant	is defective for	NULL				Bak	NULL	binding of			NULL		0	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_154	15539639	120 Consistent with this model, a Bcl-xL mutant, which is defective for Bax and Bak binding but competent to bind tBid, is still cytoprotective.	bind
20440	3	6495	5	10	NULL	0	NULL	Bcl-xL		mutant	bind					tBid					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_154	15539639	120 Consistent with this model, a Bcl-xL mutant, which is defective for Bax and Bak binding but competent to bind tBid, is still cytoprotective.	bind
20441	4	6495	5	NULL	NULL	0	NULL	cytoprotective	NULL		is a characteristic of	NULL				Bcl-xL	NULL	mutant			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_154	15539639	120 Consistent with this model, a Bcl-xL mutant, which is defective for Bax and Bak binding but competent to bind tBid, is still cytoprotective.	bind
24100	1	6495	7	NULL	NULL	NULL	NULL	Bcl-xL	GP	mutant	defective in 					Bax	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_154	15539639	120 Consistent with this model, a Bcl-xL mutant, which is defective for Bax and Bak binding but competent to bind tBid, is still cytoprotective.	bind
24101	2	6495	7	NULL	NULL	NULL	NULL	Bcl-xL	GP	mutant	defective in 					Bak	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_154	15539639	120 Consistent with this model, a Bcl-xL mutant, which is defective for Bax and Bak binding but competent to bind tBid, is still cytoprotective.	bind
24102	3	6495	7	NULL	NULL	NULL	NULL	Bcl-xL	GP	mutant	bind					tBid	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_154	15539639	120 Consistent with this model, a Bcl-xL mutant, which is defective for Bax and Bak binding but competent to bind tBid, is still cytoprotective.	bind
24103	4	6495	7	NULL	NULL	NULL	NULL	cytoprotective	Process		is a characteristic of					Bcl-xL	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_154	15539639	120 Consistent with this model, a Bcl-xL mutant, which is defective for Bax and Bak binding but competent to bind tBid, is still cytoprotective.	bind
20446	1	6497	5	NULL	NULL	0	NULL	IgG1 mAb	NULL		bind	NULL	high affinity			GPI	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_10_3734_s_30	16505356	121 is an IgG1 mAb that binds GPI with high affinity ( Kd = 0.37 nM), and is arthritogenic when combined with other mAbs that recognize spaced epitopes on GPI ( ).	bind
24104	1	6497	7	NULL	NULL	NULL	NULL	 IgG1 mAb	GP		bind		high affinity			GPI	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_10_3734_s_30	16505356	121 is an IgG1 mAb that binds GPI with high affinity ( Kd = 0.37 nM), and is arthritogenic when combined with other mAbs that recognize spaced epitopes on GPI ( ).	bind
20451	1	6498	5	10	NULL	0	NULL	C/EBPdelta			acts as				APRE site in promoter					IL-6-inducible element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2108_s_420	9528783	121:731-738, 1997) have also identified the APRE site in the C/EBPdelta promoter as an IL-6-inducible element that binds Stat3.	bind
20452	2	6498	5	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				Stat3	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_2108_s_420	9528783	121:731-738, 1997) have also identified the APRE site in the C/EBPdelta promoter as an IL-6-inducible element that binds Stat3.	bind
24107	2	6498	7	NULL	NULL	NULL	NULL	statement 1	Process		binds					Stat3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2108_s_420	9528783	121:731-738, 1997) have also identified the APRE site in the C/EBPdelta promoter as an IL-6-inducible element that binds Stat3.	bind
24108	1	6498	7	NULL	NULL	NULL	NULL	C/EBPdelta	GP		acts as				APRE site in the promoter					 IL-6-inducible element 	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_2108_s_420	9528783	121:731-738, 1997) have also identified the APRE site in the C/EBPdelta promoter as an IL-6-inducible element that binds Stat3.	bind
20453	1	6499	5	NULL	NULL	0	NULL	sHSP60	NULL	human	bind	NULL				TLR4/CD14	NULL				NULL	in human mononuclear cells	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_10_1547_s_218	12377729	122 -  127 In human mononuclear cells, human sHSP60 binds to TLR4/CD14, leading to p38 MAPK activation, 122 whereas in smooth muscle and epithelial cells, chlamydial and human sHSP60 stimulates ERK42/44 activation.	bind
20454	2	6499	5	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				p38 MAPK	NULL	activation of			NULL	in human mononuclear cells	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_10_1547_s_218	12377729	122 -  127 In human mononuclear cells, human sHSP60 binds to TLR4/CD14, leading to p38 MAPK activation, 122 whereas in smooth muscle and epithelial cells, chlamydial and human sHSP60 stimulates ERK42/44 activation.	bind
20455	3	6499	5	NULL	NULL	0	NULL	sHSP60	NULL	chlamydial	stimulates	NULL				ERK42/44	NULL	activation of			NULL	in smooth muscle	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_10_1547_s_218	12377729	122 -  127 In human mononuclear cells, human sHSP60 binds to TLR4/CD14, leading to p38 MAPK activation, 122 whereas in smooth muscle and epithelial cells, chlamydial and human sHSP60 stimulates ERK42/44 activation.	bind
20457	4	6499	5	NULL	NULL	0	NULL	sHSP60	NULL	human	stimulates	NULL				ERK42/44	NULL	activation of			NULL	in smooth muscle	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_10_1547_s_218	12377729	122 -  127 In human mononuclear cells, human sHSP60 binds to TLR4/CD14, leading to p38 MAPK activation, 122 whereas in smooth muscle and epithelial cells, chlamydial and human sHSP60 stimulates ERK42/44 activation.	bind
20458	5	6499	5	NULL	NULL	0	NULL	sHSP60	NULL	chlamydial	stimulates	NULL				ERK42/44	NULL	activation of			NULL	in epithelial cells	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_10_1547_s_218	12377729	122 -  127 In human mononuclear cells, human sHSP60 binds to TLR4/CD14, leading to p38 MAPK activation, 122 whereas in smooth muscle and epithelial cells, chlamydial and human sHSP60 stimulates ERK42/44 activation.	bind
20459	6	6499	5	NULL	NULL	0	NULL	sHSP60	NULL	human	stimulates	NULL				ERK42/44	NULL	activation of			NULL	in epithelial cells	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_10_1547_s_218	12377729	122 -  127 In human mononuclear cells, human sHSP60 binds to TLR4/CD14, leading to p38 MAPK activation, 122 whereas in smooth muscle and epithelial cells, chlamydial and human sHSP60 stimulates ERK42/44 activation.	bind
24109	1	6499	7	NULL	NULL	NULL	NULL	sHSP60	GP	human 	bind					TLR4/CD14	Cell				NULL	human mononuclear cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_10_1547_s_218	12377729	122 -  127 In human mononuclear cells, human sHSP60 binds to TLR4/CD14, leading to p38 MAPK activation, 122 whereas in smooth muscle and epithelial cells, chlamydial and human sHSP60 stimulates ERK42/44 activation.	bind
24110	2	6499	7	NULL	NULL	NULL	NULL	statement 1	Process		leads to					p38 MAPK	GP	activation of			NULL	human mononuclear cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_10_1547_s_218	12377729	122 -  127 In human mononuclear cells, human sHSP60 binds to TLR4/CD14, leading to p38 MAPK activation, 122 whereas in smooth muscle and epithelial cells, chlamydial and human sHSP60 stimulates ERK42/44 activation.	bind
24111	3	6499	7	NULL	NULL	NULL	NULL	sHSP60	GP	human	stimulates					ERK42/44	GP	activation of			NULL	smooth muscle cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_10_1547_s_218	12377729	122 -  127 In human mononuclear cells, human sHSP60 binds to TLR4/CD14, leading to p38 MAPK activation, 122 whereas in smooth muscle and epithelial cells, chlamydial and human sHSP60 stimulates ERK42/44 activation.	bind
24112	4	6499	7	NULL	NULL	NULL	NULL	sHSP60	GP	human	stimulates					ERK42/44	GP	activation of			NULL	epithelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_10_1547_s_218	12377729	122 -  127 In human mononuclear cells, human sHSP60 binds to TLR4/CD14, leading to p38 MAPK activation, 122 whereas in smooth muscle and epithelial cells, chlamydial and human sHSP60 stimulates ERK42/44 activation.	bind
24113	5	6499	7	NULL	NULL	NULL	NULL	sHSP60	GP	chlamydial	stimulates					ERK42/44	GP	activation of			NULL	smooth muscle cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_10_1547_s_218	12377729	122 -  127 In human mononuclear cells, human sHSP60 binds to TLR4/CD14, leading to p38 MAPK activation, 122 whereas in smooth muscle and epithelial cells, chlamydial and human sHSP60 stimulates ERK42/44 activation.	bind
24114	6	6499	7	NULL	NULL	NULL	NULL	sHSP60	GP	chlamydial	stimulates					ERK42/44	GP	activation of			NULL	epithelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_10_1547_s_218	12377729	122 -  127 In human mononuclear cells, human sHSP60 binds to TLR4/CD14, leading to p38 MAPK activation, 122 whereas in smooth muscle and epithelial cells, chlamydial and human sHSP60 stimulates ERK42/44 activation.	bind
20460	1	6500	5	NULL	NULL	0	NULL	PBR gene	NULL	disruption	blocks	NULL				steroidogenesis	NULL				NULL	in Leydig cells	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1150_s_289	15130918	124 Many lines of experimental evidence have implicated this protein in mitochondrial cholesterol transport: PBR gene disruption in Leydig cells blocks steroidogenesis, PBR binds cholesterol with high affinity, bacteria expressing PBR take-up cholesterol, and PBR ligands stimulate steroidogenesis and 27-hydroxycholesterol formation.	bind
20461	2	6500	5	NULL	NULL	0	NULL	PBR	NULL		bind	NULL	high affinity			cholesterol	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1150_s_289	15130918	124 Many lines of experimental evidence have implicated this protein in mitochondrial cholesterol transport: PBR gene disruption in Leydig cells blocks steroidogenesis, PBR binds cholesterol with high affinity, bacteria expressing PBR take-up cholesterol, and PBR ligands stimulate steroidogenesis and 27-hydroxycholesterol formation.	bind
20462	3	6500	5	NULL	NULL	0	NULL	bacteria	NULL	expressing PBR	take-up	NULL				cholesterol	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1150_s_289	15130918	124 Many lines of experimental evidence have implicated this protein in mitochondrial cholesterol transport: PBR gene disruption in Leydig cells blocks steroidogenesis, PBR binds cholesterol with high affinity, bacteria expressing PBR take-up cholesterol, and PBR ligands stimulate steroidogenesis and 27-hydroxycholesterol formation.	bind
20463	4	6500	5	NULL	NULL	0	NULL	PBR ligands	NULL		stimulates	NULL				steroidogenesis	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1150_s_289	15130918	124 Many lines of experimental evidence have implicated this protein in mitochondrial cholesterol transport: PBR gene disruption in Leydig cells blocks steroidogenesis, PBR binds cholesterol with high affinity, bacteria expressing PBR take-up cholesterol, and PBR ligands stimulate steroidogenesis and 27-hydroxycholesterol formation.	bind
20464	5	6500	5	NULL	NULL	0	NULL	PBR ligands	NULL		stimulates	NULL				27-hydroxycholesterol	NULL	formation of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1150_s_289	15130918	124 Many lines of experimental evidence have implicated this protein in mitochondrial cholesterol transport: PBR gene disruption in Leydig cells blocks steroidogenesis, PBR binds cholesterol with high affinity, bacteria expressing PBR take-up cholesterol, and PBR ligands stimulate steroidogenesis and 27-hydroxycholesterol formation.	bind
24115	1	6500	7	NULL	NULL	NULL	NULL	PBR gene	GP	disruption in	blocks					steroidogenesis	Process				NULL	Leydig cells	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1150_s_289	15130918	124 Many lines of experimental evidence have implicated this protein in mitochondrial cholesterol transport: PBR gene disruption in Leydig cells blocks steroidogenesis, PBR binds cholesterol with high affinity, bacteria expressing PBR take-up cholesterol, and PBR ligands stimulate steroidogenesis and 27-hydroxycholesterol formation.	bind
24116	2	6500	7	NULL	NULL	NULL	NULL	PBR	GP		binds		high affinity			cholesterol	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1150_s_289	15130918	124 Many lines of experimental evidence have implicated this protein in mitochondrial cholesterol transport: PBR gene disruption in Leydig cells blocks steroidogenesis, PBR binds cholesterol with high affinity, bacteria expressing PBR take-up cholesterol, and PBR ligands stimulate steroidogenesis and 27-hydroxycholesterol formation.	bind
24117	3	6500	7	NULL	NULL	NULL	NULL	PBR	GP	bacteria expressing 	take-up					cholesterol	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1150_s_289	15130918	124 Many lines of experimental evidence have implicated this protein in mitochondrial cholesterol transport: PBR gene disruption in Leydig cells blocks steroidogenesis, PBR binds cholesterol with high affinity, bacteria expressing PBR take-up cholesterol, and PBR ligands stimulate steroidogenesis and 27-hydroxycholesterol formation.	bind
24118	4	6500	7	NULL	NULL	NULL	NULL	PBR ligands	GP		stimulate					steroidogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1150_s_289	15130918	124 Many lines of experimental evidence have implicated this protein in mitochondrial cholesterol transport: PBR gene disruption in Leydig cells blocks steroidogenesis, PBR binds cholesterol with high affinity, bacteria expressing PBR take-up cholesterol, and PBR ligands stimulate steroidogenesis and 27-hydroxycholesterol formation.	bind
24119	5	6500	7	NULL	NULL	NULL	NULL	PBR ligands	GP		stimulate					27-hydroxycholesterol	Chemical	formation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1150_s_289	15130918	124 Many lines of experimental evidence have implicated this protein in mitochondrial cholesterol transport: PBR gene disruption in Leydig cells blocks steroidogenesis, PBR binds cholesterol with high affinity, bacteria expressing PBR take-up cholesterol, and PBR ligands stimulate steroidogenesis and 27-hydroxycholesterol formation.	bind
20465	1	6502	5	10	NULL	0	NULL	CK18		I 125 labelled	bind					trypomastigote cells		T. cruzi			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_22_19382_s_202	11278913	125 I-CK18 binds to  T. cruzi trypomastigote cells.	bind
24178	1	6502	7	NULL	NULL	NULL	NULL	CK18	GP	I 125 labelled	binds to					trypomastigote cells	Cell	T. cruzi			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_22_19382_s_202	11278913	125 I-CK18 binds to  T. cruzi trypomastigote cells.	bind
20466	1	6503	5	NULL	NULL	0	NULL	125 I-hCG	NULL		bind	NULL				LH/CG Receptor	NULL	solubilized			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_22_13835_s_45	9593728	125 I-hCG Binding to Solubilized LH/CG Receptor-- Transfected cells were washed twice with ice-cold 150 mM NaCl and 20 mM HEPES, pH 7.4 (buffer A).	bind
24179	1	6503	7	NULL	NULL	NULL	NULL	125 I-hCG	GP		bind					LH/CG Receptor	GP	solubilized			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_13835_s_45	9593728	125 I-hCG Binding to Solubilized LH/CG Receptor-- Transfected cells were washed twice with ice-cold 150 mM NaCl and 20 mM HEPES, pH 7.4 (buffer A).	bind
20467	1	6505	5	NULL	NULL	0	NULL	Bowes melanoma cells	NULL		is transfected with	NULL				LIMPII cDNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_4855_s_146	9478926	125 I-TSP1 binds to Bowes melanoma cells transfected with LIMPII cDNA.	bind
20468	2	6505	5	NULL	NULL	0	NULL	125 I-TSP1	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_4855_s_146	9478926	125 I-TSP1 binds to Bowes melanoma cells transfected with LIMPII cDNA.	bind
24180	1	6505	7	NULL	NULL	NULL	NULL	Bowes melanoma cells	Cell		transfected with					LIMPII cDNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_9_4855_s_146	9478926	125 I-TSP1 binds to Bowes melanoma cells transfected with LIMPII cDNA.	bind
24181	2	6505	7	NULL	NULL	NULL	NULL	125 I-TSP1	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_9_4855_s_146	9478926	125 I-TSP1 binds to Bowes melanoma cells transfected with LIMPII cDNA.	bind
20469	1	6506	5	NULL	NULL	0	NULL	125 I-VEGF145	NULL		bind	NULL				np-2 receptors	NULL				NULL	on endothelial cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18040_s_152	10748121	125 I-VEGF145 binding differentiates between  np-2  and  np-1  receptors on endothelial cells and breast cancer cells.	bind
20470	2	6506	5	NULL	NULL	0	NULL	125 I-VEGF145	NULL		bind	NULL				np-1 receptors	NULL				NULL	on endothelial cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18040_s_152	10748121	125 I-VEGF145 binding differentiates between  np-2  and  np-1  receptors on endothelial cells and breast cancer cells.	bind
20471	3	6506	5	NULL	NULL	0	NULL	125 I-VEGF145	NULL		bind	NULL				np-2 receptors	NULL				NULL	on breast cancer cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18040_s_152	10748121	125 I-VEGF145 binding differentiates between  np-2  and  np-1  receptors on endothelial cells and breast cancer cells.	bind
20472	4	6506	5	NULL	NULL	0	NULL	125 I-VEGF145	NULL		bind	NULL				np-1 receptors	NULL				NULL	on breast cancer cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18040_s_152	10748121	125 I-VEGF145 binding differentiates between  np-2  and  np-1  receptors on endothelial cells and breast cancer cells.	bind
24182	1	6506	7	NULL	NULL	NULL	NULL	125 I-VEGF145	GP		bind					np-2 receptor	GP				NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18040_s_152	10748121	125 I-VEGF145 binding differentiates between  np-2  and  np-1  receptors on endothelial cells and breast cancer cells.	bind
24183	2	6506	7	NULL	NULL	NULL	NULL	125 I-VEGF145	GP		bind					np-1 receptor	GP				NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18040_s_152	10748121	125 I-VEGF145 binding differentiates between  np-2  and  np-1  receptors on endothelial cells and breast cancer cells.	bind
24184	3	6506	7	NULL	NULL	NULL	NULL	125 I-VEGF145	GP		bind					np-2 receptor	GP				NULL	breast cancer cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18040_s_152	10748121	125 I-VEGF145 binding differentiates between  np-2  and  np-1  receptors on endothelial cells and breast cancer cells.	bind
24185	4	6506	7	NULL	NULL	NULL	NULL	125 I-VEGF145	GP		bind					np-1 receptor	GP				NULL	breast cancer cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18040_s_152	10748121	125 I-VEGF145 binding differentiates between  np-2  and  np-1  receptors on endothelial cells and breast cancer cells.	bind
20476	1	6507	5	NULL	NULL	0	NULL	Hb	NULL		bind	NULL				BCE surface proteins	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_8_2528_s_172	12670977	125/CE and 65/CE, positive controls where IgG 125 and 65 were used  to neutralize Hb binding of the BCE surface proteins; 125/HA2 and 65/HA2, same assay  after rHA2-bound resin had been used to deplete rHA2-related IgG from IgG 125 and  65, resulting in a shift in the profile of the curves.	bind
30267	2	6507	5	NULL	NULL	0	NULL	IgG 125	NULL		neutralize	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_8_2528_s_172	12670977	125/CE and 65/CE, positive controls where IgG 125 and 65 were used  to neutralize Hb binding of the BCE surface proteins; 125/HA2 and 65/HA2, same assay  after rHA2-bound resin had been used to deplete rHA2-related IgG from IgG 125 and  65, resulting in a shift in the profile of the curves.	bind
30268	3	6507	5	NULL	NULL	0	NULL	IgG 65	NULL		neutralize	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_8_2528_s_172	12670977	125/CE and 65/CE, positive controls where IgG 125 and 65 were used  to neutralize Hb binding of the BCE surface proteins; 125/HA2 and 65/HA2, same assay  after rHA2-bound resin had been used to deplete rHA2-related IgG from IgG 125 and  65, resulting in a shift in the profile of the curves.	bind
24186	1	6507	7	NULL	NULL	NULL	NULL	Hb	GP		bind					BCE surface protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2528_s_172	12670977	125/CE and 65/CE, positive controls where IgG 125 and 65 were used  to neutralize Hb binding of the BCE surface proteins; 125/HA2 and 65/HA2, same assay  after rHA2-bound resin had been used to deplete rHA2-related IgG from IgG 125 and  65, resulting in a shift in the profile of the curves.	bind
24187	2	6507	7	NULL	NULL	NULL	NULL	IgG 125	GP		neutralize					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2528_s_172	12670977	125/CE and 65/CE, positive controls where IgG 125 and 65 were used  to neutralize Hb binding of the BCE surface proteins; 125/HA2 and 65/HA2, same assay  after rHA2-bound resin had been used to deplete rHA2-related IgG from IgG 125 and  65, resulting in a shift in the profile of the curves.	bind
24188	3	6507	7	NULL	NULL	NULL	NULL	IgG 65	GP		neutralize					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2528_s_172	12670977	125/CE and 65/CE, positive controls where IgG 125 and 65 were used  to neutralize Hb binding of the BCE surface proteins; 125/HA2 and 65/HA2, same assay  after rHA2-bound resin had been used to deplete rHA2-related IgG from IgG 125 and  65, resulting in a shift in the profile of the curves.	bind
20479	1	6509	5	NULL	NULL	0	NULL	pili	NULL	125I labeled	bind	NULL				CEPs	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_invest-ophthalmol-vis-sci_36_3_7890494_s_13	7890494	125I labeling of pili and a solid-phase  binding assay confirmed that pili bind to CEPs and, further, that binding  could be competitively inhibited by excess unlabeled pili and that the  receptors appeared saturable.	bind
20482	2	6509	5	NULL	NULL	0	NULL	pili	NULL	unlabeled	bind	NULL				CEPs	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_invest-ophthalmol-vis-sci_36_3_7890494_s_13	7890494	125I labeling of pili and a solid-phase  binding assay confirmed that pili bind to CEPs and, further, that binding  could be competitively inhibited by excess unlabeled pili and that the  receptors appeared saturable.	bind
20484	3	6509	5	NULL	NULL	0	NULL	statement 2	NULL		inhibits	NULL	competitively			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_invest-ophthalmol-vis-sci_36_3_7890494_s_13	7890494	125I labeling of pili and a solid-phase  binding assay confirmed that pili bind to CEPs and, further, that binding  could be competitively inhibited by excess unlabeled pili and that the  receptors appeared saturable.	bind
24189	1	6509	7	NULL	NULL	NULL	NULL	pili	OrganismPart	125I labeled	bind					CEPs	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_invest-ophthalmol-vis-sci_36_3_7890494_s_13	7890494	125I labeling of pili and a solid-phase  binding assay confirmed that pili bind to CEPs and, further, that binding  could be competitively inhibited by excess unlabeled pili and that the  receptors appeared saturable.	bind
24190	2	6509	7	NULL	NULL	NULL	NULL	pili	OrganismPart	unlabeled	bind					CEPs	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_invest-ophthalmol-vis-sci_36_3_7890494_s_13	7890494	125I labeling of pili and a solid-phase  binding assay confirmed that pili bind to CEPs and, further, that binding  could be competitively inhibited by excess unlabeled pili and that the  receptors appeared saturable.	bind
24191	3	6509	7	NULL	NULL	NULL	NULL	statement 2	Process		inhibits		competitively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_invest-ophthalmol-vis-sci_36_3_7890494_s_13	7890494	125I labeling of pili and a solid-phase  binding assay confirmed that pili bind to CEPs and, further, that binding  could be competitively inhibited by excess unlabeled pili and that the  receptors appeared saturable.	bind
20485	1	6510	5	NULL	NULL	0	NULL	125I- -Conotoxin	NULL		bind	NULL	specifically			cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_188_1_97_s_76	10867241	125I- -Conotoxin specifically bound to Tris-EDTA-permeabilized cells with saturation kinetics.	bind
24192	1	6510	7	NULL	NULL	NULL	NULL	125I- -Conotoxin	Chemical		bind		specifically			cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_188_1_97_s_76	10867241	125I- -Conotoxin specifically bound to Tris-EDTA-permeabilized cells with saturation kinetics.	bind
20486	1	6511	5	NULL	NULL	0	NULL	125I-Abeta	NULL		is cross-linked to	NULL	covalently			alpha2M-MA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_13338_s_101	11823454	125I-Abeta that was covalently cross-linked to alpha2M-MA (bound) and free 125I-Abeta (free), which includes free Abeta and Abeta that was bound to alpha2M-MA but not cross-linked, were quantitated by PhosphorImager analysis.	bind
24193	1	6511	7	NULL	NULL	NULL	NULL	125I-Abeta	GP		bind					alpha2M-MA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_13338_s_101	11823454	125I-Abeta that was covalently cross-linked to alpha2M-MA (bound) and free 125I-Abeta (free), which includes free Abeta and Abeta that was bound to alpha2M-MA but not cross-linked, were quantitated by PhosphorImager analysis.	bind
20489	1	6512	5	NULL	NULL	0	NULL	TIMP-2	NULL		bind	NULL				MMP 	NULL		active sites		NULL		NULL	NULL	NULL	NULL	gw60_cell_114_2_171_s_101	12887919	125I-Ala+TIMP-2 was utilized in these experiments to reduce potential background from TIMP-2 binding to MMP active sites  (Hoegy et al., 2001  ).	bind
24194	1	6512	7	NULL	NULL	NULL	NULL	 TIMP-2	GP		bind					MMP	GP		active site		NULL		NULL	NULL	NULL	NULL	gw60_cell_114_2_171_s_101	12887919	125I-Ala+TIMP-2 was utilized in these experiments to reduce potential background from TIMP-2 binding to MMP active sites  (Hoegy et al., 2001  ).	bind
20490	1	6513	5	NULL	NULL	0	NULL	125I-alpha-BGT	NULL		bind	NULL				neonatal muscle cells	NULL				NULL	in culture	NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_281_3_1463_s_63	9190884	125I-alpha-BGT binding to neonatal muscle cells in culture.	bind
24195	1	6513	7	NULL	NULL	NULL	NULL	125I-alpha-BGT	GP		binds to					neonatal muscle cells	Cell				NULL	in culture	NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_281_3_1463_s_63	9190884	125I-alpha-BGT binding to neonatal muscle cells in culture.	bind
20491	1	6514	5	NULL	NULL	0	NULL	125I-aminopeptidase	NULL		bind	NULL				Cry1Ab	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_5_2106_s_8	11976078	125I-aminopeptidase bound Cry1Ab to a limited extent but not the Cry1Ab domain I mutant Y153D or Cry1Ca.	bind
20492	2	6514	5	NULL	NULL	0	NULL	Cry1Ab	NULL	mutant	does not bind	NULL		domain I Y153D		125I-aminopeptidase	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_5_2106_s_8	11976078	125I-aminopeptidase bound Cry1Ab to a limited extent but not the Cry1Ab domain I mutant Y153D or Cry1Ca.	bind
20493	3	6514	5	NULL	NULL	0	NULL	Cry1Ca	NULL		does not bind	NULL				125I-aminopeptidase	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_5_2106_s_8	11976078	125I-aminopeptidase bound Cry1Ab to a limited extent but not the Cry1Ab domain I mutant Y153D or Cry1Ca.	bind
24196	1	6514	7	NULL	NULL	NULL	NULL	125I-aminopeptidase	GP		bind					Cry1Ab	GP				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_68_5_2106_s_8	11976078	125I-aminopeptidase bound Cry1Ab to a limited extent but not the Cry1Ab domain I mutant Y153D or Cry1Ca.	bind
24197	2	6514	7	NULL	NULL	NULL	NULL	125I-aminopeptidase	GP		does not bind					Cry1Ab	GP	mutant 	domain I Y153D		NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_68_5_2106_s_8	11976078	125I-aminopeptidase bound Cry1Ab to a limited extent but not the Cry1Ab domain I mutant Y153D or Cry1Ca.	bind
24198	3	6514	7	NULL	NULL	NULL	NULL	125I-aminopeptidase	GP		does not bind					Cry1Ca	GP				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_68_5_2106_s_8	11976078	125I-aminopeptidase bound Cry1Ab to a limited extent but not the Cry1Ab domain I mutant Y153D or Cry1Ca.	bind
24722	1	6515	5	NULL	NULL	0	NULL	125I-Ang IV	NULL		bind	NULL				MDBK	NULL	cell membranes of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24723	2	6515	5	NULL	NULL	0	NULL	losartan	NULL		is antagonist of	NULL				AT1 receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24724	3	6515	5	NULL	NULL	0	NULL	statement 1	NULL		is unaffected by	NULL				losartan	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24725	4	6515	5	NULL	NULL	0	NULL	PD 123177	NULL		is antagonist of	NULL				AT2 receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24726	5	6515	5	NULL	NULL	0	NULL	statement 1	NULL		is unaffected by	NULL				PD 123177	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24727	6	6515	5	NULL	NULL	0	NULL	Sar1,Thr8 Ang II	NULL		is antagonist of	NULL				AT1/AT2 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24728	7	6515	5	NULL	NULL	0	NULL	statement 1	NULL		is unaffected by	NULL				Sar1,Thr8 Ang II	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24729	8	6515	5	NULL	NULL	0	NULL	Sar1,Ile8 Ang II	NULL		is antagonist of	NULL				AT1/AT2 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24730	9	6515	5	NULL	NULL	0	NULL	statement 1	NULL		is unaffected by	NULL				Sar1,Ile8 Ang II	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24731	10	6515	5	NULL	NULL	0	NULL	D-Ala7 Ang(1-7)	NULL		is antagonist of	NULL	putative			Ang(1-7) receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24732	11	6515	5	NULL	NULL	0	NULL	statement 1	NULL		is unaffected by	NULL				D-Ala7 Ang(1-7)	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24733	12	6515	5	NULL	NULL	0	NULL	divalinal Ang IV 	NULL		is antagonist of	NULL	putative			AT4 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24734	13	6515	5	NULL	NULL	0	NULL	divalinal Ang IV 	NULL		bind	NULL					NULL		125I-Ang IV binding site		NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24735	14	6515	5	NULL	NULL	0	NULL	NleYI-6-hexamide	NULL		is antagonist of	NULL	putative			AT4 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24736	15	6515	5	NULL	NULL	0	NULL	NleYI-6-hexamide	NULL		bind	NULL					NULL		125I-Ang IV binding site		NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24737	16	6515	5	NULL	NULL	0	NULL	statement 13	NULL		competes with	NULL	high affinity			statement 15	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24199	1	6515	7	NULL	NULL	NULL	NULL	125I-Ang IV	GP		bind					MDBK	GP	cell membrane of			NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24200	3	6515	7	NULL	NULL	NULL	NULL	statement 1	Process		is unaffected by					losartan 	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24201	5	6515	7	NULL	NULL	NULL	NULL	statement 1	Process		is unaffected by					PD 123177	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24203	7	6515	7	NULL	NULL	NULL	NULL	statement 1	Process		is unaffected by					Sar1,Thr8 Ang II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
24204	8	6515	7	NULL	NULL	NULL	NULL	Sar1,Ile8 Ang II 	GP		is antagonist of					AT1/AT2 receptor 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
31336	2	6515	7	NULL	NULL	NULL	NULL	losartan 	Chemical		is  antagonist of					AT1 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
31337	4	6515	7	NULL	NULL	NULL	NULL	PD 123177	Chemical		is antagonist of					AT2 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
31338	6	6515	7	NULL	NULL	NULL	NULL	Sar1,Thr8 Ang II	GP		is antagonist of					AT1/AT2 receptor 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
31339	10	6515	7	NULL	NULL	NULL	NULL	D-Ala7 Ang(1-7)	GP		is antagonist of					putative Ang(1-7) receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
31340	12	6515	7	NULL	NULL	NULL	NULL	divalinal Ang IV	GP		is antagonist of					putative AT4 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
31341	13	6515	7	NULL	NULL	NULL	NULL	NleYI-6-hexamide	Chemical		is antagonist of					putative AT4 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
31342	9	6515	7	NULL	NULL	NULL	NULL	statement 1	Process		is unaffected by					Sar1,Ile8 Ang II 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
31343	11	6515	7	NULL	NULL	NULL	NULL	statement 1	Process		is unaffected by					D-Ala7 Ang(1-7) 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
31344	14	6515	7	NULL	NULL	NULL	NULL	divalinal Ang IV	GP		bind		high affinity			125I-Ang IV	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
31345	15	6515	7	NULL	NULL	NULL	NULL	NleYI-6-hexamide	Chemical		bind		high affinity			125I-Ang IV 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
31346	16	6515	7	NULL	NULL	NULL	NULL	statement 14	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
31347	17	6515	7	NULL	NULL	NULL	NULL	statement 15	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_1242_s_104	10565848	125I-Ang IV binding to MDBK cell membranes was largely unaffected by losartan (AT1 receptor antagonist), PD 123177 (AT2 receptor antagonist), Sar1,Thr8 Ang II and Sar1,Ile8 Ang II (both AT1/AT2 receptor antagonists), or D-Ala7 Ang(1-7) [putative Ang(1-7) receptor antagonist], whereas divalinal Ang IV and NleYI-6-hexamide (both putative AT4 receptor antagonists) competed with high affinity for the 125I-Ang IV binding site.	bind
20495	1	6516	5	NULL	NULL	0	NULL	125I-Anti-CK18 IgG	NULL		bind	NULL				HTC cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_45_28574_s_162	9353322	125I-Anti-CK18 IgG bound to HTC cells to a much greater extent than preimmune IgG, and comparable results were obtained with HepG2 cells.	bind
20496	2	6516	5	NULL	NULL	0	NULL	preimmune IgG	NULL		bind	NULL				HTC cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_45_28574_s_162	9353322	125I-Anti-CK18 IgG bound to HTC cells to a much greater extent than preimmune IgG, and comparable results were obtained with HepG2 cells.	bind
20497	3	6516	5	NULL	NULL	0	NULL	statement 1	NULL		greater than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_45_28574_s_162	9353322	125I-Anti-CK18 IgG bound to HTC cells to a much greater extent than preimmune IgG, and comparable results were obtained with HepG2 cells.	bind
20498	4	6516	5	NULL	NULL	0	NULL	125I-Anti-CK18 IgG	NULL		bind	NULL				HepG2 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_45_28574_s_162	9353322	125I-Anti-CK18 IgG bound to HTC cells to a much greater extent than preimmune IgG, and comparable results were obtained with HepG2 cells.	bind
20499	5	6516	5	NULL	NULL	0	NULL	preimmune IgG	NULL		bind	NULL				HepG2 cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_45_28574_s_162	9353322	125I-Anti-CK18 IgG bound to HTC cells to a much greater extent than preimmune IgG, and comparable results were obtained with HepG2 cells.	bind
20500	6	6516	5	NULL	NULL	0	NULL	statement 1	NULL		is comparable to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_45_28574_s_162	9353322	125I-Anti-CK18 IgG bound to HTC cells to a much greater extent than preimmune IgG, and comparable results were obtained with HepG2 cells.	bind
20501	7	6516	5	NULL	NULL	0	NULL	statement 2	NULL		is comparable to	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_45_28574_s_162	9353322	125I-Anti-CK18 IgG bound to HTC cells to a much greater extent than preimmune IgG, and comparable results were obtained with HepG2 cells.	bind
24207	1	6516	7	NULL	NULL	NULL	NULL	125I-Anti-CK18 IgG	GP		bind					 HTC cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_45_28574_s_162	9353322	125I-Anti-CK18 IgG bound to HTC cells to a much greater extent than preimmune IgG, and comparable results were obtained with HepG2 cells.	bind
24208	2	6516	7	NULL	NULL	NULL	NULL	preimmune IgG	GP		bind					HTC cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_45_28574_s_162	9353322	125I-Anti-CK18 IgG bound to HTC cells to a much greater extent than preimmune IgG, and comparable results were obtained with HepG2 cells.	bind
24209	3	6516	7	NULL	NULL	NULL	NULL	statement 1	Process		is greater than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_45_28574_s_162	9353322	125I-Anti-CK18 IgG bound to HTC cells to a much greater extent than preimmune IgG, and comparable results were obtained with HepG2 cells.	bind
24210	4	6516	7	NULL	NULL	NULL	NULL	125I-Anti-CK18 IgG	GP		bind					HepG2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_45_28574_s_162	9353322	125I-Anti-CK18 IgG bound to HTC cells to a much greater extent than preimmune IgG, and comparable results were obtained with HepG2 cells.	bind
31348	5	6516	7	NULL	NULL	NULL	NULL	preimmune IgG	GP		bind					HepG2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_45_28574_s_162	9353322	125I-Anti-CK18 IgG bound to HTC cells to a much greater extent than preimmune IgG, and comparable results were obtained with HepG2 cells.	bind
20502	1	6517	5	NULL	NULL	0	NULL	125I-b-FGF	NULL		bind	NULL				V3wt-Rg	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_4_2511_s_197	9891022	125I-b-FGF Binds V3wt-Rg but Not V3mut-Rg-- Previously we demonstrated that b-FGF can bind HS-modified CD44 produced in COS cells ( 4).	bind
20503	2	6517	5	NULL	NULL	0	NULL	125I-b-FGF	NULL		does not bind	NULL				V3mut-Rg	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_4_2511_s_197	9891022	125I-b-FGF Binds V3wt-Rg but Not V3mut-Rg-- Previously we demonstrated that b-FGF can bind HS-modified CD44 produced in COS cells ( 4).	bind
20504	3	6517	5	10	NULL	0	NULL	b-FGF	NULL		bind	NULL				CD44	NULL	HS-modified			NULL	COS cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_4_2511_s_197	9891022	125I-b-FGF Binds V3wt-Rg but Not V3mut-Rg-- Previously we demonstrated that b-FGF can bind HS-modified CD44 produced in COS cells ( 4).	bind
24217	1	6517	7	NULL	NULL	NULL	NULL	125I-b-FGF	GP		binds					V3-Rg 	GP	wt			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_4_2511_s_197	9891022	125I-b-FGF Binds V3wt-Rg but Not V3mut-Rg-- Previously we demonstrated that b-FGF can bind HS-modified CD44 produced in COS cells ( 4).	bind
24218	2	6517	7	NULL	NULL	NULL	NULL	125I-b-FGF	GP		does not bind					V3-Rg 	GP	mut			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_4_2511_s_197	9891022	125I-b-FGF Binds V3wt-Rg but Not V3mut-Rg-- Previously we demonstrated that b-FGF can bind HS-modified CD44 produced in COS cells ( 4).	bind
24219	3	6517	7	NULL	NULL	NULL	NULL	b-FGF	GP		bind					CD44	Cell	HS-modified			NULL	COS cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_4_2511_s_197	9891022	125I-b-FGF Binds V3wt-Rg but Not V3mut-Rg-- Previously we demonstrated that b-FGF can bind HS-modified CD44 produced in COS cells ( 4).	bind
20505	1	6518	5	NULL	NULL	0	NULL	125I-b-FGF	NULL		does not bind	NULL				V3mut-Rg	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_4_2511_s_201	9891022	125I-b-FGF did not bind to V3mut-Rg, confirming the requirement of HS for the interaction.	bind
24738	2	6518	5	NULL	NULL	0	NULL	HS	NULL		is required for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_4_2511_s_201	9891022	125I-b-FGF did not bind to V3mut-Rg, confirming the requirement of HS for the interaction.	bind
24739	3	6518	5	NULL	NULL	0	NULL	statement 1	NULL		confirms	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_4_2511_s_201	9891022	125I-b-FGF did not bind to V3mut-Rg, confirming the requirement of HS for the interaction.	bind
24220	1	6518	7	NULL	NULL	NULL	NULL	125I-b-FGF	GP		does not bind					V3mut-Rg	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_4_2511_s_201	9891022	125I-b-FGF did not bind to V3mut-Rg, confirming the requirement of HS for the interaction.	bind
24221	2	6518	7	NULL	NULL	NULL	NULL	HS	Chemical		is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_4_2511_s_201	9891022	125I-b-FGF did not bind to V3mut-Rg, confirming the requirement of HS for the interaction.	bind
45754	3	6518	7	NULL	NULL	NULL	NULL	statement 1	Process		confirms					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_4_2511_s_201	9891022	125I-b-FGF did not bind to V3mut-Rg, confirming the requirement of HS for the interaction.	bind
20510	1	6519	5	NULL	NULL	0	NULL	Botrocetin	NULL		bind	NULL				VWF	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_15_11044_s_51	10753907	125I-Botrocetin Binding Assays-- Botrocetin binding to VWF was assayed according to methods of Fujimura  et al. ( 15) as described previously ( 9).	bind
24222	1	6519	7	NULL	NULL	NULL	NULL	125I-Botrocetin	Chemical		bind					VWF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_15_11044_s_51	10753907	125I-Botrocetin Binding Assays-- Botrocetin binding to VWF was assayed according to methods of Fujimura  et al. ( 15) as described previously ( 9).	bind
20511	1	6520	5	10	NULL	0	NULL	pancreatic membranes	NULL	wild-type;; mouse	bind	NULL				CCK-8	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_103_3_383_s_169	9927499	125I-CCK-8 competition-binding experiments (Fig.  1 c) revealed that wild-type mouse pancreatic membranes bound CCK-8 with affinity in the nanomolar range: dissociation constant,  Kd = 0.18  plus-or-minus  0.03 nM (mean  plus-or-minus  SEM,  n = 3).	bind
24223	1	6520	7	NULL	NULL	NULL	NULL	pancreatic membranes	OrganismPart	wild-type;; mouse	bind					125I-CCK-8	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_103_3_383_s_169	9927499	125I-CCK-8 competition-binding experiments (Fig.  1 c) revealed that wild-type mouse pancreatic membranes bound CCK-8 with affinity in the nanomolar range: dissociation constant,  Kd = 0.18  plus-or-minus  0.03 nM (mean  plus-or-minus  SEM,  n = 3).	bind
20512	1	6522	5	NULL	NULL	0	NULL	125I-EGF	NULL		bind	NULL				ECD	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_10108_s_71	11796728	125I-EGF Binding to the ECD-- The binding constants of the ECD for EGF in the presence or absence of gangliosides were determined using the scintillation proximity assay (SPA) developed by Amersham Biosciences, Inc.	bind
24224	1	6522	7	NULL	NULL	NULL	NULL	125I-EGF	GP		bind								ECD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10108_s_71	11796728	125I-EGF Binding to the ECD-- The binding constants of the ECD for EGF in the presence or absence of gangliosides were determined using the scintillation proximity assay (SPA) developed by Amersham Biosciences, Inc.	bind
20513	1	6523	5	10	NULL	0	NULL	125I-F-heparin	NULL		bind	NULL	specifically			ATIII	NULL	recombinant;; native			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20935_s_141	8702852	125I-F-heparin bound to recombinant native ATIII specifically and saturably, as demonstrated by the effective competition for binding by unlabeled F-heparin.	bind
20514	2	6523	5	10	NULL	0	NULL	125I-F-heparin	NULL		bind	NULL	saturably			ATIII	NULL	recombinant;; native			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20935_s_141	8702852	125I-F-heparin bound to recombinant native ATIII specifically and saturably, as demonstrated by the effective competition for binding by unlabeled F-heparin.	bind
20515	3	6523	5	10	NULL	0	NULL	F-heparin	NULL	unlabeled	bind	NULL				ATIII	NULL	recombinant;; native			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20935_s_141	8702852	125I-F-heparin bound to recombinant native ATIII specifically and saturably, as demonstrated by the effective competition for binding by unlabeled F-heparin.	bind
20516	4	6523	5	NULL	NULL	0	NULL	statement 3	NULL		competes with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_34_20935_s_141	8702852	125I-F-heparin bound to recombinant native ATIII specifically and saturably, as demonstrated by the effective competition for binding by unlabeled F-heparin.	bind
24225	1	6523	7	NULL	NULL	NULL	NULL	125I-F-heparin	GP		bind		specifically			ATIII	GP	recombinant;; native			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20935_s_141	8702852	125I-F-heparin bound to recombinant native ATIII specifically and saturably, as demonstrated by the effective competition for binding by unlabeled F-heparin.	bind
24226	2	6523	7	NULL	NULL	NULL	NULL	F-heparin	GP	unlabeled	bind					ATIII 	GP	recombinant;; native			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20935_s_141	8702852	125I-F-heparin bound to recombinant native ATIII specifically and saturably, as demonstrated by the effective competition for binding by unlabeled F-heparin.	bind
24227	3	6523	7	NULL	NULL	NULL	NULL	125I-F-heparin 	GP		bind		saturably			ATIII	GP	recombinant;; native			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20935_s_141	8702852	125I-F-heparin bound to recombinant native ATIII specifically and saturably, as demonstrated by the effective competition for binding by unlabeled F-heparin.	bind
24228	4	6523	7	NULL	NULL	NULL	NULL	statement 2	Process		compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20935_s_141	8702852	125I-F-heparin bound to recombinant native ATIII specifically and saturably, as demonstrated by the effective competition for binding by unlabeled F-heparin.	bind
24229	5	6523	7	NULL	NULL	NULL	NULL	statement 2	Process		compete with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20935_s_141	8702852	125I-F-heparin bound to recombinant native ATIII specifically and saturably, as demonstrated by the effective competition for binding by unlabeled F-heparin.	bind
20517	1	6524	5	NULL	NULL	0	NULL	125I-factor Xa	NULL		bind	NULL				SMC monolayers	NULL	human			NULL		0	NULL	NULL	NULL	gw60_jclininvest_101_5_993_s_127	9486969	125I-factor Xa binding to human SMC monolayers.	bind
24230	1	6524	7	NULL	NULL	NULL	NULL	125I-factor Xa	GP		bind					SMC monolayers	OrganismPart	human			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_101_5_993_s_127	9486969	125I-factor Xa binding to human SMC monolayers.	bind
20518	1	6525	5	NULL	NULL	0	NULL	125I-HI-8	NULL		does not bind	NULL				UTI-BPs	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_134	11278581	125I-HI-8 failed to bind any of the UTI-BPs (data not shown), demonstrating that there was no indication that the C-domain of UTI was involved in binding of UTI to these UTI-BPs.	bind
20519	2	6525	5	NULL	NULL	0	NULL	UTI	NULL		bind	NULL				UTI-BPs	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_134	11278581	125I-HI-8 failed to bind any of the UTI-BPs (data not shown), demonstrating that there was no indication that the C-domain of UTI was involved in binding of UTI to these UTI-BPs.	bind
30269	3	6525	5	NULL	NULL	0	NULL	UTI	NULL		is not involved in	NULL		C domain		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_134	11278581	125I-HI-8 failed to bind any of the UTI-BPs (data not shown), demonstrating that there was no indication that the C-domain of UTI was involved in binding of UTI to these UTI-BPs.	bind
24231	1	6525	7	NULL	NULL	NULL	NULL	125I-HI-8	GP		does not bind					UTI-BPs	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_134	11278581	125I-HI-8 failed to bind any of the UTI-BPs (data not shown), demonstrating that there was no indication that the C-domain of UTI was involved in binding of UTI to these UTI-BPs.	bind
24232	2	6525	7	NULL	NULL	NULL	NULL	UTI	GP		bind					UTI-BPs	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_134	11278581	125I-HI-8 failed to bind any of the UTI-BPs (data not shown), demonstrating that there was no indication that the C-domain of UTI was involved in binding of UTI to these UTI-BPs.	bind
24233	3	6525	7	NULL	NULL	NULL	NULL	 UTI	GP		is not involved in			C-domain		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_134	11278581	125I-HI-8 failed to bind any of the UTI-BPs (data not shown), demonstrating that there was no indication that the C-domain of UTI was involved in binding of UTI to these UTI-BPs.	bind
20520	1	6526	5	NULL	NULL	0	NULL	125I-Hst 5	NULL		bind	NULL	saturably			SSA1/SSA2 strain	NULL	wild-type			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_31_28553_s_8	12761219	125I-Hst 5 binding assays showed saturable binding  ( K d = 2.57 x  10 - 6M) with the wild-type   SSA1/SSA2 strain; however, Hst 5 binding with the  delta ssa1ssa2 double mutant was reduced  ( K d = 1.25 x 10 - 6M).	bind
20521	2	6526	5	NULL	NULL	0	NULL	Hst 5	NULL		bind	NULL	reduced			delta ssa1ssa2	NULL	double mutant			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_31_28553_s_8	12761219	125I-Hst 5 binding assays showed saturable binding  ( K d = 2.57 x  10 - 6M) with the wild-type   SSA1/SSA2 strain; however, Hst 5 binding with the  delta ssa1ssa2 double mutant was reduced  ( K d = 1.25 x 10 - 6M).	bind
24398	1	6526	7	NULL	NULL	NULL	NULL	125I-Hst 5	GP		bind		saturably			SSA1/SSA2 strain	Organism	wild-type			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_31_28553_s_8	12761219	125I-Hst 5 binding assays showed saturable binding  ( K d = 2.57 x  10 - 6M) with the wild-type   SSA1/SSA2 strain; however, Hst 5 binding with the  delta ssa1ssa2 double mutant was reduced  ( K d = 1.25 x 10 - 6M).	bind
24399	2	6526	7	NULL	NULL	NULL	NULL	Hst 5	GP		bind		reduced			delta ssa1ssa2	Organism	double mutant			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_31_28553_s_8	12761219	125I-Hst 5 binding assays showed saturable binding  ( K d = 2.57 x  10 - 6M) with the wild-type   SSA1/SSA2 strain; however, Hst 5 binding with the  delta ssa1ssa2 double mutant was reduced  ( K d = 1.25 x 10 - 6M).	bind
20523	1	6527	5	NULL	NULL	0	NULL	anti-band 3 IgG	NULL	125I-labeled human	bind	NULL	specifically			band 3 glycoprotein	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-(tokyo)_119_4_8743563_s_3	8743563	125I-labeled  human anti-band 3 IgG specifically bound to band 3 glycoprotein and lactoferrin,  a glycoprotein that has poly-N-acetyllactosamine-type sugar chains like  band 3, on the polyvinylidene difluoride blotting membrane.	bind
20524	2	6527	5	NULL	NULL	0	NULL	anti-band 3 IgG	NULL	125I-labeled human	bind	NULL	specifically			lactoferrin	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-(tokyo)_119_4_8743563_s_3	8743563	125I-labeled  human anti-band 3 IgG specifically bound to band 3 glycoprotein and lactoferrin,  a glycoprotein that has poly-N-acetyllactosamine-type sugar chains like  band 3, on the polyvinylidene difluoride blotting membrane.	bind
20525	3	6527	5	NULL	NULL	0	NULL	lactoferrin	NULL		contains	NULL				poly-N-acetyllactosamine-type sugar chains	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-(tokyo)_119_4_8743563_s_3	8743563	125I-labeled  human anti-band 3 IgG specifically bound to band 3 glycoprotein and lactoferrin,  a glycoprotein that has poly-N-acetyllactosamine-type sugar chains like  band 3, on the polyvinylidene difluoride blotting membrane.	bind
30270	4	6527	5	NULL	NULL	0	NULL	lactoferrin	NULL		is a type of	NULL				glycoprotein	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-(tokyo)_119_4_8743563_s_3	8743563	125I-labeled  human anti-band 3 IgG specifically bound to band 3 glycoprotein and lactoferrin,  a glycoprotein that has poly-N-acetyllactosamine-type sugar chains like  band 3, on the polyvinylidene difluoride blotting membrane.	bind
24400	1	6527	7	NULL	NULL	NULL	NULL	anti-band 3 IgG	GP	125I-labeled human	bind		specifically			band 3 glycoprotein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-(tokyo)_119_4_8743563_s_3	8743563	125I-labeled  human anti-band 3 IgG specifically bound to band 3 glycoprotein and lactoferrin,  a glycoprotein that has poly-N-acetyllactosamine-type sugar chains like  band 3, on the polyvinylidene difluoride blotting membrane.	bind
24401	2	6527	7	NULL	NULL	NULL	NULL	anti-band 3 IgG	GP	125I-labeled human	bind		specifically			lactoferrin	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-(tokyo)_119_4_8743563_s_3	8743563	125I-labeled  human anti-band 3 IgG specifically bound to band 3 glycoprotein and lactoferrin,  a glycoprotein that has poly-N-acetyllactosamine-type sugar chains like  band 3, on the polyvinylidene difluoride blotting membrane.	bind
24402	3	6527	7	NULL	NULL	NULL	NULL	lactoferrin	GP		contains					poly-N-acetyllactosamine-type sugar chains	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-(tokyo)_119_4_8743563_s_3	8743563	125I-labeled  human anti-band 3 IgG specifically bound to band 3 glycoprotein and lactoferrin,  a glycoprotein that has poly-N-acetyllactosamine-type sugar chains like  band 3, on the polyvinylidene difluoride blotting membrane.	bind
31349	4	6527	7	NULL	NULL	NULL	NULL	lactoferrin	GP		is a type of					glycoprotein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-(tokyo)_119_4_8743563_s_3	8743563	125I-labeled  human anti-band 3 IgG specifically bound to band 3 glycoprotein and lactoferrin,  a glycoprotein that has poly-N-acetyllactosamine-type sugar chains like  band 3, on the polyvinylidene difluoride blotting membrane.	bind
20526	2	6528	5	NULL	NULL	0	NULL	statement 1	NULL		via	NULL				cell surface	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_3_376_s_68	10706585	125I-labeled AcLDL binding   ell surface binding of 125I-labeled AcLDL to MPM was measured as described by Nakagawara and Nathan  ( 33) and Brown et al.  ( 36) Briefly, cells were cultured as described above, in the presence or absence of 10 ng/ml of IL-4 for 96 h.	bind
20527	1	6528	5	NULL	NULL	0	NULL	AcLDL	NULL	125I-labeled	bind	NULL				MPM	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_3_376_s_68	10706585	125I-labeled AcLDL binding   ell surface binding of 125I-labeled AcLDL to MPM was measured as described by Nakagawara and Nathan  ( 33) and Brown et al.  ( 36) Briefly, cells were cultured as described above, in the presence or absence of 10 ng/ml of IL-4 for 96 h.	bind
24403	1	6528	7	NULL	NULL	NULL	NULL	AcLDL	GP	125I-labeled	bind					MPM	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_3_376_s_68	10706585	125I-labeled AcLDL binding   ell surface binding of 125I-labeled AcLDL to MPM was measured as described by Nakagawara and Nathan  ( 33) and Brown et al.  ( 36) Briefly, cells were cultured as described above, in the presence or absence of 10 ng/ml of IL-4 for 96 h.	bind
31350	2	6528	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs via					cell surface	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_3_376_s_68	10706585	125I-labeled AcLDL binding   ell surface binding of 125I-labeled AcLDL to MPM was measured as described by Nakagawara and Nathan  ( 33) and Brown et al.  ( 36) Briefly, cells were cultured as described above, in the presence or absence of 10 ng/ml of IL-4 for 96 h.	bind
20528	1	6529	5	NULL	NULL	0	NULL	ADA	NULL	125I-labeled	bind	NULL				Pg 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_20_20993_s_140	15016824	125I-labeled ADA also binds to Pg 2 electroblotted to a nitrocellulose membrane after electrophoresis ( Fig. 5,  inset, lane 2).	bind
24404	1	6529	7	NULL	NULL	NULL	NULL	ADA	GP	125I-labeled	bind					Pg2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_20_20993_s_140	15016824	125I-labeled ADA also binds to Pg 2 electroblotted to a nitrocellulose membrane after electrophoresis ( Fig. 5,  inset, lane 2).	bind
20529	1	6530	5	NULL	NULL	0	NULL	ankyrin-B	NULL	125I-Labeled	bind	NULL	saturable	C-terminal domain		GST-Hdj1/Hsp40	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_24_25798_s_167	15075330	125I-Labeled ankyrin-B C-terminal domain binds to GST-Hdj1/Hsp40 in a saturable manner with a  K d of 53 nM ( Fig. 6).	bind
24405	1	6530	7	NULL	NULL	NULL	NULL	ankyrin-B	GP	125I-Labeled	bind		saturably	C-terminal domain		GST-Hdj1/Hsp40 	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_24_25798_s_167	15075330	125I-Labeled ankyrin-B C-terminal domain binds to GST-Hdj1/Hsp40 in a saturable manner with a  K d of 53 nM ( Fig. 6).	bind
20530	1	6531	5	NULL	NULL	0	NULL	anti-Tac	NULL	125I-Labeled	bind	NULL				IL-2R/sorLA transfectants	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_25_22788_s_266	11294867	125I-Labeled anti-Tac bound to the IL-2R/sorLA transfectants at 4  degrees C but not to mock transfected cells (not shown).	bind
20531	2	6531	5	NULL	NULL	0	NULL	anti-Tac	NULL	125I-Labeled	does not bind	NULL				mock transfected cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_25_22788_s_266	11294867	125I-Labeled anti-Tac bound to the IL-2R/sorLA transfectants at 4  degrees C but not to mock transfected cells (not shown).	bind
24406	1	6531	7	NULL	NULL	NULL	NULL	anti-Tac	GP	125I-Labeled	bind					IL-2R/sorLA transfectants	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_22788_s_266	11294867	125I-Labeled anti-Tac bound to the IL-2R/sorLA transfectants at 4  degrees C but not to mock transfected cells (not shown).	bind
24407	2	6531	7	NULL	NULL	NULL	NULL	anti-Tac	GP	125I-labeled	does not bind					mock transfected cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_22788_s_266	11294867	125I-Labeled anti-Tac bound to the IL-2R/sorLA transfectants at 4  degrees C but not to mock transfected cells (not shown).	bind
20532	1	6532	5	NULL	NULL	0	NULL	B2	NULL	125I-labeled	bind	NULL	high affinity			TSHR	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_thyroid_15_7_16053383_s_5	16053383	125I-labeled B2 bound to the TSHR with high affinity  (2 x 10(10) L/mol) and patient serum TSHR autoantibodies inhibited labeled  B2 binding to the receptor in a similar way to inhibition of labeled TSH  binding (r = 0.75; n = 20).	bind
20534	2	6532	5	NULL	NULL	0	NULL	TSHR autoantibodies	NULL	patient serum	inhibit	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_thyroid_15_7_16053383_s_5	16053383	125I-labeled B2 bound to the TSHR with high affinity  (2 x 10(10) L/mol) and patient serum TSHR autoantibodies inhibited labeled  B2 binding to the receptor in a similar way to inhibition of labeled TSH  binding (r = 0.75; n = 20).	bind
20535	3	6532	5	NULL	NULL	0	NULL	TSHR autoantibodies	NULL	patient serum	inhibit	NULL				TSH 	NULL	labeled binding of			NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_thyroid_15_7_16053383_s_5	16053383	125I-labeled B2 bound to the TSHR with high affinity  (2 x 10(10) L/mol) and patient serum TSHR autoantibodies inhibited labeled  B2 binding to the receptor in a similar way to inhibition of labeled TSH  binding (r = 0.75; n = 20).	bind
20536	4	6532	5	NULL	NULL	0	NULL	statement 2	NULL		is similar to	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_thyroid_15_7_16053383_s_5	16053383	125I-labeled B2 bound to the TSHR with high affinity  (2 x 10(10) L/mol) and patient serum TSHR autoantibodies inhibited labeled  B2 binding to the receptor in a similar way to inhibition of labeled TSH  binding (r = 0.75; n = 20).	bind
24408	1	6532	7	NULL	NULL	NULL	NULL	B2	GP	125I-labeled	bind		high affinity			TSHR	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_thyroid_15_7_16053383_s_5	16053383	125I-labeled B2 bound to the TSHR with high affinity  (2 x 10(10) L/mol) and patient serum TSHR autoantibodies inhibited labeled  B2 binding to the receptor in a similar way to inhibition of labeled TSH  binding (r = 0.75; n = 20).	bind
24409	2	6532	7	NULL	NULL	NULL	NULL	TSHR autoantibodies 	GP	patient serum	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_thyroid_15_7_16053383_s_5	16053383	125I-labeled B2 bound to the TSHR with high affinity  (2 x 10(10) L/mol) and patient serum TSHR autoantibodies inhibited labeled  B2 binding to the receptor in a similar way to inhibition of labeled TSH  binding (r = 0.75; n = 20).	bind
24410	3	6532	7	NULL	NULL	NULL	NULL	TSHR autoantibodies	GP	patient serum	inhibits					TSH	GP	binding of			NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_thyroid_15_7_16053383_s_5	16053383	125I-labeled B2 bound to the TSHR with high affinity  (2 x 10(10) L/mol) and patient serum TSHR autoantibodies inhibited labeled  B2 binding to the receptor in a similar way to inhibition of labeled TSH  binding (r = 0.75; n = 20).	bind
24411	4	6532	7	NULL	NULL	NULL	NULL	statement 2	Process		is similar to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_thyroid_15_7_16053383_s_5	16053383	125I-labeled B2 bound to the TSHR with high affinity  (2 x 10(10) L/mol) and patient serum TSHR autoantibodies inhibited labeled  B2 binding to the receptor in a similar way to inhibition of labeled TSH  binding (r = 0.75; n = 20).	bind
20537	1	6533	5	10	NULL	0	NULL	B7 Ig		125I-labeled	bind					CHO cells		CD28-transfected			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-exp-med_173_3_1847722_s_6	1847722	125I-labeled B7 Ig bound to CD28-transfected Chinese  hamster ovary (CHO) cells, and to immobilized CD28 Ig with a Kd approximately  200 nM. B7 Ig also inhibited CD28-mediated cellular adhesion.	bind
20538	2	6533	5	NULL	NULL	0	NULL	CHO cells	NULL		is	NULL				Chinese hamster ovary cells	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-exp-med_173_3_1847722_s_6	1847722	125I-labeled B7 Ig bound to CD28-transfected Chinese  hamster ovary (CHO) cells, and to immobilized CD28 Ig with a Kd approximately  200 nM. B7 Ig also inhibited CD28-mediated cellular adhesion.	bind
20539	3	6533	5	NULL	NULL	0	NULL	B7 Ig	NULL	125I-labeled	bind	NULL				CD28 Ig	NULL	immobilized			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-exp-med_173_3_1847722_s_6	1847722	125I-labeled B7 Ig bound to CD28-transfected Chinese  hamster ovary (CHO) cells, and to immobilized CD28 Ig with a Kd approximately  200 nM. B7 Ig also inhibited CD28-mediated cellular adhesion.	bind
20540	4	6533	5	NULL	NULL	0	NULL	CD28	NULL		mediates	NULL				cellular adhesion	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-exp-med_173_3_1847722_s_6	1847722	125I-labeled B7 Ig bound to CD28-transfected Chinese  hamster ovary (CHO) cells, and to immobilized CD28 Ig with a Kd approximately  200 nM. B7 Ig also inhibited CD28-mediated cellular adhesion.	bind
30271	5	6533	5	NULL	NULL	0	NULL	B7 Ig	NULL		inhibits	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-exp-med_173_3_1847722_s_6	1847722	125I-labeled B7 Ig bound to CD28-transfected Chinese  hamster ovary (CHO) cells, and to immobilized CD28 Ig with a Kd approximately  200 nM. B7 Ig also inhibited CD28-mediated cellular adhesion.	bind
24413	1	6533	7	NULL	NULL	NULL	NULL	 B7 Ig 	GP	125I-labeled	binds to					CHO cells	Cell	CD28-transfected			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-exp-med_173_3_1847722_s_6	1847722	125I-labeled B7 Ig bound to CD28-transfected Chinese  hamster ovary (CHO) cells, and to immobilized CD28 Ig with a Kd approximately  200 nM. B7 Ig also inhibited CD28-mediated cellular adhesion.	bind
24414	2	6533	7	NULL	NULL	NULL	NULL	B7 Ig	GP	125I-labeled	binds to					CD28 Ig 	GP	immobilized			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-exp-med_173_3_1847722_s_6	1847722	125I-labeled B7 Ig bound to CD28-transfected Chinese  hamster ovary (CHO) cells, and to immobilized CD28 Ig with a Kd approximately  200 nM. B7 Ig also inhibited CD28-mediated cellular adhesion.	bind
24415	3	6533	7	NULL	NULL	NULL	NULL	CD28	Cell		mediates					cellular adhesion	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-exp-med_173_3_1847722_s_6	1847722	125I-labeled B7 Ig bound to CD28-transfected Chinese  hamster ovary (CHO) cells, and to immobilized CD28 Ig with a Kd approximately  200 nM. B7 Ig also inhibited CD28-mediated cellular adhesion.	bind
24416	4	6533	7	NULL	NULL	NULL	NULL	B7 Ig	GP		inhibits					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-exp-med_173_3_1847722_s_6	1847722	125I-labeled B7 Ig bound to CD28-transfected Chinese  hamster ovary (CHO) cells, and to immobilized CD28 Ig with a Kd approximately  200 nM. B7 Ig also inhibited CD28-mediated cellular adhesion.	bind
31351	5	6533	7	NULL	NULL	NULL	NULL	CHO	Cell		is					Chinese hamster ovary cells	Cell				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-exp-med_173_3_1847722_s_6	1847722	125I-labeled B7 Ig bound to CD28-transfected Chinese  hamster ovary (CHO) cells, and to immobilized CD28 Ig with a Kd approximately  200 nM. B7 Ig also inhibited CD28-mediated cellular adhesion.	bind
20541	1	6534	5	NULL	NULL	0	NULL	beta-glucuronidase	NULL	125I-Labeled	bind	NULL	specifically			IGF-IIPRs	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22358_s_209	9712856	125I-Labeled beta-glucuronidase specifically bound to the IGF-IIPRs was eluted by incubation for 1 h with 10 mM Man-6-P.	bind
24419	1	6534	7	NULL	NULL	NULL	NULL	beta-glucuronidase	GP	125I-Labeled 	bind		specifically			IGF-IIPRs	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_35_22358_s_209	9712856	125I-Labeled beta-glucuronidase specifically bound to the IGF-IIPRs was eluted by incubation for 1 h with 10 mM Man-6-P.	bind
20542	1	6535	5	NULL	NULL	0	NULL	BMP-7	NULL	125I-Labeled	bind	NULL				ROS 17/2	NULL				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_4_858_s_200	12927798	125I-Labeled BMP-7 binding to ROS 17/2.	bind
24420	1	6535	7	NULL	NULL	NULL	NULL	BMP-7	GP	125I-Labeled	binds to					ROS 17/2	Cell				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_4_858_s_200	12927798	125I-Labeled BMP-7 binding to ROS 17/2.	bind
20585	1	6536	5	10	NULL	0	NULL	HEK 293T cells	NULL	intact	express	NULL	transiently			GnRH-R constructs	NULL	wt;; catfish			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_6_1229_s_174	10570050	125I-Labeled cGnRH-II binding to intact HEK 293T cells transiently expressing wt or Ser-mutant catfish GnRH-R constructs was performed in the presence or absence of 10 6 M unlabeled cGnRH-II.	bind
20586	2	6536	5	10	NULL	0	NULL	HEK 293T cells	NULL	intact	express	NULL	transiently			GnRH-R constructs	NULL	mutant;; catfish	Ser		NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_6_1229_s_174	10570050	125I-Labeled cGnRH-II binding to intact HEK 293T cells transiently expressing wt or Ser-mutant catfish GnRH-R constructs was performed in the presence or absence of 10 6 M unlabeled cGnRH-II.	bind
20587	3	6536	5	NULL	NULL	0	NULL	cGnRH-II	NULL	125I-Labeled	bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_56_6_1229_s_174	10570050	125I-Labeled cGnRH-II binding to intact HEK 293T cells transiently expressing wt or Ser-mutant catfish GnRH-R constructs was performed in the presence or absence of 10 6 M unlabeled cGnRH-II.	bind
20588	4	6536	5	NULL	NULL	0	NULL	cGnRH-II	NULL	125I-Labeled	bind	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_56_6_1229_s_174	10570050	125I-Labeled cGnRH-II binding to intact HEK 293T cells transiently expressing wt or Ser-mutant catfish GnRH-R constructs was performed in the presence or absence of 10 6 M unlabeled cGnRH-II.	bind
20589	5	6536	5	NULL	NULL	0	NULL	statement 3	NULL		is an alternative to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_56_6_1229_s_174	10570050	125I-Labeled cGnRH-II binding to intact HEK 293T cells transiently expressing wt or Ser-mutant catfish GnRH-R constructs was performed in the presence or absence of 10 6 M unlabeled cGnRH-II.	bind
24476	1	6536	7	NULL	NULL	NULL	NULL	HEK 293T cells 	Cell	intact	express		transiently			GnRH-R constructs	GP	wt;; catfish			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_6_1229_s_174	10570050	125I-Labeled cGnRH-II binding to intact HEK 293T cells transiently expressing wt or Ser-mutant catfish GnRH-R constructs was performed in the presence or absence of 10 6 M unlabeled cGnRH-II.	bind
24477	2	6536	7	NULL	NULL	NULL	NULL	HEK 293T cells 	Cell	intact	express		transiently			GnRH-R constructs	GP	mutant;; catfish	Ser		NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_6_1229_s_174	10570050	125I-Labeled cGnRH-II binding to intact HEK 293T cells transiently expressing wt or Ser-mutant catfish GnRH-R constructs was performed in the presence or absence of 10 6 M unlabeled cGnRH-II.	bind
24478	3	6536	7	NULL	NULL	NULL	NULL	 cGnRH-II	GP	125I-Labeled	bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_6_1229_s_174	10570050	125I-Labeled cGnRH-II binding to intact HEK 293T cells transiently expressing wt or Ser-mutant catfish GnRH-R constructs was performed in the presence or absence of 10 6 M unlabeled cGnRH-II.	bind
24479	4	6536	7	NULL	NULL	NULL	NULL	cGnRH-II	GP	125I-labeled	bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_6_1229_s_174	10570050	125I-Labeled cGnRH-II binding to intact HEK 293T cells transiently expressing wt or Ser-mutant catfish GnRH-R constructs was performed in the presence or absence of 10 6 M unlabeled cGnRH-II.	bind
24480	5	6536	7	NULL	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_6_1229_s_174	10570050	125I-Labeled cGnRH-II binding to intact HEK 293T cells transiently expressing wt or Ser-mutant catfish GnRH-R constructs was performed in the presence or absence of 10 6 M unlabeled cGnRH-II.	bind
20574	1	6537	5	NULL	NULL	0	NULL	Cry1Ac	NULL	125I-labeled	bind	NULL	specifically			brush border membrane vesicles	NULL	E. insulana			NULL		0	NULL	NULL	NULL	abs-batch0580-0599_appl-environ-microbiol_72_1_16391075_s_12	16391075	125I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
20575	2	6537	5	NULL	NULL	0	NULL	Cry1Ab	NULL	125I-labeled	bind	NULL	specifically			brush border membrane vesicles	NULL	E. insulana			NULL		0	NULL	NULL	NULL	abs-batch0580-0599_appl-environ-microbiol_72_1_16391075_s_12	16391075	125I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
20576	3	6537	5	NULL	NULL	0	NULL	Cry1Ba	NULL	biotinylated	bind	NULL	specifically			brush border membrane vesicles	NULL	E. insulana			NULL		0	NULL	NULL	NULL	abs-batch0580-0599_appl-environ-microbiol_72_1_16391075_s_12	16391075	125I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
20577	4	6537	5	NULL	NULL	0	NULL	Cry1Ia	NULL	biotinylated	bind	NULL	specifically			brush border membrane vesicles	NULL	E. insulana			NULL		0	NULL	NULL	NULL	abs-batch0580-0599_appl-environ-microbiol_72_1_16391075_s_12	16391075	125I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
20578	5	6537	5	NULL	NULL	0	NULL	Cry9Ca	NULL	biotinylated	bind	NULL	specifically			brush border membrane vesicles	NULL	E. insulana			NULL		0	NULL	NULL	NULL	abs-batch0580-0599_appl-environ-microbiol_72_1_16391075_s_12	16391075	125I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
24481	1	6537	7	NULL	NULL	NULL	NULL	Cry1Ac 	GP	125I-labeled 	bind		specific			 brush border membrane vesicles	CellComponent	E. insulana			NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_appl-environ-microbiol_72_1_16391075_s_12	16391075	125I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
24482	2	6537	7	NULL	NULL	NULL	NULL	Cry1Ab	GP	125I-labeled	bind		specific			brush border membrane vesicles	CellComponent	E. insulana			NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_appl-environ-microbiol_72_1_16391075_s_12	16391075	125I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
24483	3	6537	7	NULL	NULL	NULL	NULL	Cry1Ba	GP	biotinylated	bind		specific			brush border membrane vesicles	CellComponent	E.insulana			NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_appl-environ-microbiol_72_1_16391075_s_12	16391075	125I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
24484	4	6537	7	NULL	NULL	NULL	NULL	Cry1Ia	GP	biotinylated	bind		specific			brush border membrane vesicles	CellComponent	E.insulana			NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_appl-environ-microbiol_72_1_16391075_s_12	16391075	125I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
24485	5	6537	7	NULL	NULL	NULL	NULL	Cry9Ca	GP	biotinylated	bind		specific			brush border membrane vesicles	CellComponent	E.insulana			NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_appl-environ-microbiol_72_1_16391075_s_12	16391075	125I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba,  Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane  vesicles from E. insulana.	bind
20634	1	6538	5	NULL	NULL	0	NULL	Cry1Ab	NULL	125I-labeled	bind	NULL	specifically			brush border membrane vesicles	NULL	E. insulana			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_1_437_s_12	16391075	125I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba, Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane vesicles from  E. insulana.	bind
20635	2	6538	5	NULL	NULL	0	NULL	Cry1Ac	NULL	125I-labeled	bind	NULL	specifically			brush border membrane vesicles	NULL	E. insulana			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_1_437_s_12	16391075	125I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba, Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane vesicles from  E. insulana.	bind
20636	3	6538	5	NULL	NULL	0	NULL	Cry1Ba	NULL	biotinylated	bind	NULL	specifically			brush border membrane vesicles	NULL	E. insulana			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_1_437_s_12	16391075	125I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba, Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane vesicles from  E. insulana.	bind
20637	4	6538	5	NULL	NULL	0	NULL	Cry1Ia	NULL	biotinylated	bind	NULL	specifically			brush border membrane vesicles	NULL	E. insulana			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_1_437_s_12	16391075	125I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba, Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane vesicles from  E. insulana.	bind
20638	5	6538	5	NULL	NULL	0	NULL	Cry9Ca	NULL	biotinylated	bind	NULL	specifically			brush border membrane vesicles	NULL	E. insulana			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_1_437_s_12	16391075	125I-labeled Cry1Ac and Cry1Ab and biotinylated Cry1Ba, Cry1Ia, and Cry9Ca showed specific binding to the brush border membrane vesicles from  E. insulana.	bind
20580	1	6539	5	NULL	NULL	0	NULL	DNT1-54	NULL	125I-labeled	bind	NULL				MC3T3-E1	NULL	DNT-susceptible			NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
20581	2	6539	5	NULL	NULL	0	NULL	DNT1-54	NULL	125I-labeled	bind	NULL				C3H10T1/2	NULL	DNT-susceptible			NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
20582	3	6539	5	NULL	NULL	0	NULL	DNT1-54	NULL	125I-labeled	bind	NULL				Swiss 3T3	NULL	DNT-susceptible			NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
20583	4	6539	5	NULL	NULL	0	NULL	DNT1-54	NULL	125I-labeled	bind	NULL				rat embryo fibroblasts	NULL	DNT-susceptible			NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
20584	5	6539	5	NULL	NULL	0	NULL	DNT1-54	NULL	125I-labeled	bind	NULL				NIH 3T3 cells	NULL	DNT-susceptible			NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
20639	6	6539	5	NULL	NULL	0	NULL	DNT1-54	NULL	125I-labeled	does not bind	NULL				COS7 cells	NULL	resistant			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
20640	7	6539	5	NULL	NULL	0	NULL	DNT1-54	NULL	125I-labeled	does not bind	NULL				BALB/3T3 cells	NULL	resistant			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
20641	8	6539	5	NULL	NULL	0	NULL	DNT1-54	NULL	125I-labeled	does not bind	NULL				L929 cells	NULL	resistant			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
20642	9	6539	5	NULL	NULL	0	NULL	DNT1-54	NULL	125I-labeled	does not bind	NULL				PAE cells	NULL	resistant			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
20643	10	6539	5	NULL	NULL	0	NULL	DNT1-54	NULL	125I-labeled	does not bind	NULL				K562 cells	NULL	resistant			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
20644	11	6539	5	NULL	NULL	0	NULL	sensitivity of cells	NULL	to DNT	is attributable to	NULL				unknown receptor	NULL	existence of			NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
24486	1	6539	7	NULL	NULL	NULL	NULL	DNT1-54 	GP	125I-labeled	bind					MC3T3-E1 cells	Cell	 DNT-susceptible			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
24487	2	6539	7	NULL	NULL	NULL	NULL	DNT1-54 	GP	125I-labeled	bind					C3H10T1/2 cells	Cell	DNT-susceptible			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
24488	3	6539	7	NULL	NULL	NULL	NULL	DNT1-54 	GP	125I-labeled	bind					Swiss 3T3 cells	Cell	DNT-susceptible			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
24489	4	6539	7	NULL	NULL	NULL	NULL	DNT1-54	GP	125I-labeled	bind					embryo fibroblasts	Cell	DNT-susceptible rat 			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
24490	5	6539	7	NULL	NULL	NULL	NULL	DNT1-54	GP	125I-labeled	bind					NIH 3T3 cells 	Cell	DNT-susceptible			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
24491	6	6539	7	NULL	NULL	NULL	NULL	DNT1-54 	GP	125I-labeled	does not bind					COS7 cells	Cell	DNT-resistant			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
24492	7	6539	7	NULL	NULL	NULL	NULL	DNT1-54	GP	125I-labeled	does not bind					BALB/3T3 cells	Cell	DNT-resistant			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
24493	8	6539	7	NULL	NULL	NULL	NULL	DNT1-54	GP	125I-labeled	does not bind					L929 cells	Cell	DNT-resistant			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
24494	9	6539	7	NULL	NULL	NULL	NULL	DNT1-54	GP	125I-labeled 	does not bind					PAE cells	Cell	DNT-resistant			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
24495	10	6539	7	NULL	NULL	NULL	NULL	DNT1-54	GP	125I-labeled	does not bind					K562 cells	Cell	DNT-resistant			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
24496	11	6539	7	NULL	NULL	NULL	NULL	statement 1	Process	DNT sensitivity in	indicate					unknown receptor	GP	existence of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
24497	12	6539	7	NULL	NULL	NULL	NULL	statement 2	Process	DNT sensitivity in	indicate					unknown receptor	GP	existence of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
24498	13	6539	7	NULL	NULL	NULL	NULL	statement 3	Process	DNT sensitivity in	indicate					unknown receptor	GP	existence of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
24500	14	6539	7	NULL	NULL	NULL	NULL	statement 4	Process	DNT sensitivity in	indicate					unknown receptor	GP	existence of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
31399	15	6539	7	NULL	NULL	NULL	NULL	statement 5	Process	DNT sensitivity in	indicate					unknown receptor	GP	existence of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
31400	16	6539	7	NULL	NULL	NULL	NULL	statement 6	Process	DNT sensitivity in	indicate					unknown receptor	GP	existence of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
31401	17	6539	7	NULL	NULL	NULL	NULL	statement 7	Process	DNT sensitivity in	indicate					unknown receptor	GP	existence of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
31402	18	6539	7	NULL	NULL	NULL	NULL	statement 8	Process	DNT sensitivity in	indicate					unknown receptor	GP	existence of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
31403	19	6539	7	NULL	NULL	NULL	NULL	statement 9	Process	DNT sensitivity in	indicate					unknown receptor	GP	existence of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
31404	20	6539	7	NULL	NULL	NULL	NULL	statement 10	Process	DNT sensitivity in	indicate					unknown receptor	GP	existence of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3427_s_160	12065482	125I-labeled DNT1-54 bound to the DNT-susceptible MC3T3-E1, C3H10T1/2, Swiss 3T3, rat embryo fibroblasts, and NIH 3T3 cells but not to the resistant COS7, BALB/3T3, L929, PAE, and K562 cells (Fig.  4D), indicating that the sensitivity of cells to DNT is attributable to the existence of an unknown receptor.	bind
20645	1	6540	5	NULL	NULL	0	NULL	flagellin	NULL	125I-labeled	bind	NULL				GM1	NULL	glycolipid			NULL	in vitro	0	NULL	NULL	NULL	gw60_infectimmun_66_1_43_s_9	9423837	125I-labeled flagellin bound to the glycolipids GM1 and GD1a and to asialoGM1 in an in vitro binding assay.	bind
20646	2	6540	5	NULL	NULL	0	NULL	flagellin	NULL	125I-labeled	bind	NULL				GD1a	NULL	glycolipid			NULL	in vitro	0	NULL	NULL	NULL	gw60_infectimmun_66_1_43_s_9	9423837	125I-labeled flagellin bound to the glycolipids GM1 and GD1a and to asialoGM1 in an in vitro binding assay.	bind
20647	3	6540	5	NULL	NULL	0	NULL	flagellin	NULL	125I-labeled	bind	NULL				asialoGM1	NULL	glycolipid			NULL	in vitro	0	NULL	NULL	NULL	gw60_infectimmun_66_1_43_s_9	9423837	125I-labeled flagellin bound to the glycolipids GM1 and GD1a and to asialoGM1 in an in vitro binding assay.	bind
24501	1	6540	7	NULL	NULL	NULL	NULL	flagellin	GP	125I-labeled	bind					GM1	Chemical	glycolipids			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_infectimmun_66_1_43_s_9	9423837	125I-labeled flagellin bound to the glycolipids GM1 and GD1a and to asialoGM1 in an in vitro binding assay.	bind
24502	2	6540	7	NULL	NULL	NULL	NULL	flagellin	GP	125I-labeled	bind					GD1a	Chemical	glycolipids			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_infectimmun_66_1_43_s_9	9423837	125I-labeled flagellin bound to the glycolipids GM1 and GD1a and to asialoGM1 in an in vitro binding assay.	bind
24503	3	6540	7	NULL	NULL	NULL	NULL	flagellin	GP	125I-labeled	bind					asialoGM1	Chemical	glycolipids			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_infectimmun_66_1_43_s_9	9423837	125I-labeled flagellin bound to the glycolipids GM1 and GD1a and to asialoGM1 in an in vitro binding assay.	bind
20649	1	6542	5	10	NULL	0	NULL	galanin		125I-labeled;;human	bind		saturably			GalR2 receptor		rat			NULL	COS-1 cells	NULL	NULL	NULL	NULL	gw60_molpharmacol_52_3_337_s_8	9281594	125I-Labeled human galanin binding to rat GalR2 receptor expressed in COS-1 cells was saturable ( Kd = 0.59 nM) and could be displaced by galanin, several galanin fragments, and chimeric peptides.	bind
20650	2	6542	5	NULL	NULL	0	NULL	galanin	NULL		displace	NULL				statement 1	NULL	ligand of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_3_337_s_8	9281594	125I-Labeled human galanin binding to rat GalR2 receptor expressed in COS-1 cells was saturable ( Kd = 0.59 nM) and could be displaced by galanin, several galanin fragments, and chimeric peptides.	bind
20651	4	6542	5	NULL	NULL	0	NULL	several galanin fragments	NULL		displace	NULL				statement 1	NULL	ligand of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_3_337_s_8	9281594	125I-Labeled human galanin binding to rat GalR2 receptor expressed in COS-1 cells was saturable ( Kd = 0.59 nM) and could be displaced by galanin, several galanin fragments, and chimeric peptides.	bind
20652	5	6542	5	NULL	NULL	0	NULL	chimeric peptides	NULL		displace	NULL				statement 1	NULL	ligand of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_3_337_s_8	9281594	125I-Labeled human galanin binding to rat GalR2 receptor expressed in COS-1 cells was saturable ( Kd = 0.59 nM) and could be displaced by galanin, several galanin fragments, and chimeric peptides.	bind
24504	1	6542	7	NULL	NULL	NULL	NULL	galanin	GP	125I-labeled;;human	binds to		saturably			GalR2 receptor	GP	rat			NULL	COS-1 cells	NULL	NULL	NULL	NULL	gw60_molpharmacol_52_3_337_s_8	9281594	125I-Labeled human galanin binding to rat GalR2 receptor expressed in COS-1 cells was saturable ( Kd = 0.59 nM) and could be displaced by galanin, several galanin fragments, and chimeric peptides.	bind
24506	2	6542	7	NULL	NULL	NULL	NULL	galanin	GP		displace					statement 1	Process	ligand of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_3_337_s_8	9281594	125I-Labeled human galanin binding to rat GalR2 receptor expressed in COS-1 cells was saturable ( Kd = 0.59 nM) and could be displaced by galanin, several galanin fragments, and chimeric peptides.	bind
24507	3	6542	7	NULL	NULL	NULL	NULL	galanin fragments	AminoAcid		displace					statement 1	Process	ligand of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_3_337_s_8	9281594	125I-Labeled human galanin binding to rat GalR2 receptor expressed in COS-1 cells was saturable ( Kd = 0.59 nM) and could be displaced by galanin, several galanin fragments, and chimeric peptides.	bind
31405	4	6542	7	NULL	NULL	NULL	NULL	galanin	GP	chimeric peptides	displace 					statement 1	Process	ligand of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_3_337_s_8	9281594	125I-Labeled human galanin binding to rat GalR2 receptor expressed in COS-1 cells was saturable ( Kd = 0.59 nM) and could be displaced by galanin, several galanin fragments, and chimeric peptides.	bind
20653	1	6543	5	10	NULL	0	NULL	NPW23		125I-labeled;;human	bind					GPR7		human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_39_35826_s_178	12130646	125I-Labeled human NPW23 bound both human GPR7 and GPR8 with nearly the same affinity.	bind
20654	2	6543	5	10	NULL	0	NULL	NPW23		125I-labeled;;human	bind					GPR8		human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_39_35826_s_178	12130646	125I-Labeled human NPW23 bound both human GPR7 and GPR8 with nearly the same affinity.	bind
20655	3	6543	5	NULL	NULL	0	NULL	statement 1	NULL		same affinity as	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_39_35826_s_178	12130646	125I-Labeled human NPW23 bound both human GPR7 and GPR8 with nearly the same affinity.	bind
24508	1	6543	7	NULL	NULL	NULL	NULL	NPW23	GP	125I-labeled;;human	bind					GPR7	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_39_35826_s_178	12130646	125I-Labeled human NPW23 bound both human GPR7 and GPR8 with nearly the same affinity.	bind
24509	2	6543	7	NULL	NULL	NULL	NULL	 NPW23	GP	125I-labeled;;human	bind					GPR8	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_39_35826_s_178	12130646	125I-Labeled human NPW23 bound both human GPR7 and GPR8 with nearly the same affinity.	bind
24510	3	6543	7	NULL	NULL	NULL	NULL	statement 1	Process		same affinity as					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_39_35826_s_178	12130646	125I-Labeled human NPW23 bound both human GPR7 and GPR8 with nearly the same affinity.	bind
20656	1	6544	5	NULL	NULL	0	NULL	JRFL gp120	NULL	125I-labeled	bind	NULL				HEK-293 cells	NULL	CCR5-transiently transfected			NULL		0	NULL	NULL	NULL	gw60_pnas_97_7_3388_s_43	10725362	125I-labeled JRFL gp120 was allowed to bind to CCR5-transiently transfected HEK-293 cells in Hepes binding buffer (50 nM Hepes, pH 7.4/5 nM MgCl2) with 0.5% BSA, alone or with 2D7 mAb ( 20), CCR5-02, or mIg.	bind
24511	1	6544	7	NULL	NULL	NULL	NULL	JRFL gp120	GP	125I-labeled	bind					HEK-293 cells	Cell	CCR5-transiently transfected			NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_7_3388_s_43	10725362	125I-labeled JRFL gp120 was allowed to bind to CCR5-transiently transfected HEK-293 cells in Hepes binding buffer (50 nM Hepes, pH 7.4/5 nM MgCl2) with 0.5% BSA, alone or with 2D7 mAb ( 20), CCR5-02, or mIg.	bind
20657	1	6546	5	NULL	NULL	0	NULL	MMP-9	NULL	125I-labeled	bind	NULL	specifically	C-domain		CS-1 melanoma cells	NULL	beta5 integrin-transfected			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_28_29589_s_296	15123665	125I-Labeled MMP-9 C domain showed a specific binding to beta5 integrin-transfected, but not to the untransfected CS-1 melanoma cells ( Fig. 6 A).	bind
20658	2	6546	5	10	NULL	0	NULL	MMP-9		125I-labeled	does not bind			C domain		CS-1 melanoma cells		untransfected			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_28_29589_s_296	15123665	125I-Labeled MMP-9 C domain showed a specific binding to beta5 integrin-transfected, but not to the untransfected CS-1 melanoma cells ( Fig. 6 A).	bind
24512	1	6546	7	NULL	NULL	NULL	NULL	MMP-9 	GP	125I-Labeled	bind		specific	C domain		CS-1 melanoma cells	Cell	beta5 integrin-transfected			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_28_29589_s_296	15123665	125I-Labeled MMP-9 C domain showed a specific binding to beta5 integrin-transfected, but not to the untransfected CS-1 melanoma cells ( Fig. 6 A).	bind
24513	2	6546	7	NULL	NULL	NULL	NULL	MMP-9	GP	125I-labeled	does not bind			C domain		CS-1 melanoma cells	Cell	untransfected			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_28_29589_s_296	15123665	125I-Labeled MMP-9 C domain showed a specific binding to beta5 integrin-transfected, but not to the untransfected CS-1 melanoma cells ( Fig. 6 A).	bind
20659	1	6547	5	NULL	NULL	0	NULL	neuroserpin	NULL	125I-labeled	bind	NULL	most effectively			LRP	NULL	purified			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50250_s_116	14522960	125I-Labeled neuroserpin binds most effectively to purified LRP after incubation with  tPA.	bind
20660	2	6547	5	NULL	NULL	0	NULL	tPA	NULL	incubation with	is required for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50250_s_116	14522960	125I-Labeled neuroserpin binds most effectively to purified LRP after incubation with  tPA.	bind
24514	1	6547	7	NULL	NULL	NULL	NULL	neuroserpin	GP	125I-Labeled	binds		effectively			LRP	GP	purified			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_50250_s_116	14522960	125I-Labeled neuroserpin binds most effectively to purified LRP after incubation with  tPA.	bind
24515	2	6547	7	NULL	NULL	NULL	NULL	statement 1	Process		occurs after					tPA	GP	incubation with			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_50250_s_116	14522960	125I-Labeled neuroserpin binds most effectively to purified LRP after incubation with  tPA.	bind
20661	1	6548	5	NULL	NULL	0	NULL	plasminogen	NULL	125I-labeled	does not bind	NULL				ATP synthase	NULL	recombinant	alpha-subunit 		NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_6_2811_s_179	10077593	125I-labeled plasminogen did not bind to the recombinant alpha-subunit ATP synthase (Fig.  7 E), but did bind to annexin II (Fig.  3 D).	bind
20662	2	6548	5	NULL	NULL	0	NULL	plasminogen	NULL	125I-labeled	bind	NULL				annexin II	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_6_2811_s_179	10077593	125I-labeled plasminogen did not bind to the recombinant alpha-subunit ATP synthase (Fig.  7 E), but did bind to annexin II (Fig.  3 D).	bind
24516	1	6548	7	NULL	NULL	NULL	NULL	plasminogen	GP	125I-labeled	does not bind					ATP synthase	GP	recombinant	alpha-subunit		NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_6_2811_s_179	10077593	125I-labeled plasminogen did not bind to the recombinant alpha-subunit ATP synthase (Fig.  7 E), but did bind to annexin II (Fig.  3 D).	bind
24517	2	6548	7	NULL	NULL	NULL	NULL	plasminogen	GP	125I-labeled	bind					annexin II 	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_6_2811_s_179	10077593	125I-labeled plasminogen did not bind to the recombinant alpha-subunit ATP synthase (Fig.  7 E), but did bind to annexin II (Fig.  3 D).	bind
20663	1	6549	5	NULL	NULL	0	NULL	plasminogen	NULL	125I-labeled	does not bind	NULL				p63	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_43_42679_s_199	12913003	125I-labeled plasminogen did not detect isolated p63 in ligand blotting experiments, and p63 did not bind to a plasminogen affinity matrix as detected either by immunoblotting or ligand blotting, although the plasminogen binding protein alpha-enolase ( ) was readily detected by both methods (data not shown).	bind
20664	2	6549	5	NULL	NULL	0	NULL	plasminogen	NULL	125I-labeled	bind	NULL				alpha-enolase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_43_42679_s_199	12913003	125I-labeled plasminogen did not detect isolated p63 in ligand blotting experiments, and p63 did not bind to a plasminogen affinity matrix as detected either by immunoblotting or ligand blotting, although the plasminogen binding protein alpha-enolase ( ) was readily detected by both methods (data not shown).	bind
24519	1	6549	7	NULL	NULL	NULL	NULL	p63	GP		does not bind					plasminogen 	GP	125I-labeled			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_43_42679_s_199	12913003	125I-labeled plasminogen did not detect isolated p63 in ligand blotting experiments, and p63 did not bind to a plasminogen affinity matrix as detected either by immunoblotting or ligand blotting, although the plasminogen binding protein alpha-enolase ( ) was readily detected by both methods (data not shown).	bind
31406	2	6549	7	NULL	NULL	NULL	NULL	plasminogen	GP	125I-labeled	bind					alpha-enolase	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_43_42679_s_199	12913003	125I-labeled plasminogen did not detect isolated p63 in ligand blotting experiments, and p63 did not bind to a plasminogen affinity matrix as detected either by immunoblotting or ligand blotting, although the plasminogen binding protein alpha-enolase ( ) was readily detected by both methods (data not shown).	bind
20665	1	6550	5	NULL	NULL	0	NULL	protein A	NULL	125I-labeled	bind	NULL				anti-phosphotyrosine antibodies	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_3_992_s_37	15240146	125I-labeled protein A bound to the anti-phosphotyrosine and anti-peptide antibodies  was detected by autoradiography using preflashed Kodak XAR film with Cronex Lightning  Plus intensifying screens at  80  degrees C for 12-48 h.	bind
20666	2	6550	5	NULL	NULL	0	NULL	protein A	NULL	125I-labeled	bind	NULL				anti-peptide antibodies	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_3_992_s_37	15240146	125I-labeled protein A bound to the anti-phosphotyrosine and anti-peptide antibodies  was detected by autoradiography using preflashed Kodak XAR film with Cronex Lightning  Plus intensifying screens at  80  degrees C for 12-48 h.	bind
24522	1	6550	7	NULL	NULL	NULL	NULL	protein A	GP	125I-labeled	bind					anti-phosphotyrosine antibody	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_3_992_s_37	15240146	125I-labeled protein A bound to the anti-phosphotyrosine and anti-peptide antibodies  was detected by autoradiography using preflashed Kodak XAR film with Cronex Lightning  Plus intensifying screens at  80  degrees C for 12-48 h.	bind
24523	2	6550	7	NULL	NULL	NULL	NULL	protein A	GP	125I-labeled	bind					anti-peptide antibodies	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_3_992_s_37	15240146	125I-labeled protein A bound to the anti-phosphotyrosine and anti-peptide antibodies  was detected by autoradiography using preflashed Kodak XAR film with Cronex Lightning  Plus intensifying screens at  80  degrees C for 12-48 h.	bind
20672	1	6553	5	NULL	NULL	0	NULL	SecA	NULL	125I-labeled	bind	NULL				IMVs	NULL	urea-washed			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2243_s_167	11914356	125I-labeled SecA (2 mug) was bound to 4 M urea-washed IMVs (5 mug of proteins in a final volume of 200 mul) at 0 degrees C for 30 min, and the complexes were isolated by centrifugation.	bind
24952	1	6553	7	NULL	NULL	NULL	NULL	SecA	GP	25I-labeled	bind					IMVs	CellComponent	urea washed			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_8_2243_s_167	11914356	125I-labeled SecA (2 mug) was bound to 4 M urea-washed IMVs (5 mug of proteins in a final volume of 200 mul) at 0 degrees C for 30 min, and the complexes were isolated by centrifugation.	bind
20673	1	6556	5	NULL	NULL	0	NULL	VEGF	NULL	125I-labeled	bind	NULL				NRP1	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_25_13_3045_s_278	16763549	125I-labeled VEGF binding to NRP1	bind
24959	1	6556	7	NULL	NULL	NULL	NULL	VEGF	GP	125I-labeled	binds to					NRP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_13_3045_s_278	16763549	125I-labeled VEGF binding to NRP1	bind
20674	1	6557	5	NULL	NULL	0	NULL	S8-SP11	NULL	125I-labeled	bind	NULL	specifically			S8 homozygote stigmatic microsomal membranes	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nature_413_6855_534_s_50	11586363	125I-labelled  S8-SP11 specifically binds the stigmatic microsomal membranes of the  S8 homozygote ( Fig. 3a).	bind
24962	1	6557	7	NULL	NULL	NULL	NULL	S8-SP11	GP	125I-labelled 	binds		specifically			S8 homozygote stigmatic microsomal membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_nature_413_6855_534_s_50	11586363	125I-labelled  S8-SP11 specifically binds the stigmatic microsomal membranes of the  S8 homozygote ( Fig. 3a).	bind
20675	1	6558	5	NULL	NULL	0	NULL	PK2	NULL		bind	NULL				PK-Rs	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1579_2_173_s_104	12427552	125I-labelled PK2 was used to determine the binding affinity of PK2 for two PK-Rs.	bind
24969	1	6558	7	NULL	NULL	NULL	NULL	PK2	GP		bind					PK-Rs	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1579_2_173_s_104	12427552	125I-labelled PK2 was used to determine the binding affinity of PK2 for two PK-Rs.	bind
20676	1	6559	5	NULL	NULL	0	NULL	sPLA2-X	NULL	125I-mouse	bind	NULL				PLA2R	NULL	mouse			NULL	COS-7 cells	0	NULL	NULL	NULL	gw60_febslett_478_1_187_s_123	10922494	125I-mouse sPLA2-X binding to mouse PLA2R expressed in COS-7 cells.	bind
24976	1	6559	7	NULL	NULL	NULL	NULL	sPLA2-X 	GP	125I-mouse	binds to					PLA2R	GP	mouse			NULL	COS-7 cells	NULL	NULL	NULL	NULL	gw60_febslett_478_1_187_s_123	10922494	125I-mouse sPLA2-X binding to mouse PLA2R expressed in COS-7 cells.	bind
20677	1	6560	5	NULL	NULL	0	NULL	125I-PDGF-BB	NULL		bind	NULL	specifically			HSC	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_30_28274_s_108	11346654	125I-PDGF-BB binding experiments showed that pretreatment with NAC for 24 h decreased the specific binding of PDGF-BB to HSC (Fig.  1 F).	bind
20678	2	6560	5	NULL	NULL	0	NULL	NAC	NULL	pretreatment with	decrease	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_30_28274_s_108	11346654	125I-PDGF-BB binding experiments showed that pretreatment with NAC for 24 h decreased the specific binding of PDGF-BB to HSC (Fig.  1 F).	bind
24979	1	6560	7	NULL	NULL	NULL	NULL	PDGF-BB	GP	125I	bind		specifically			HSC	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_30_28274_s_108	11346654	125I-PDGF-BB binding experiments showed that pretreatment with NAC for 24 h decreased the specific binding of PDGF-BB to HSC (Fig.  1 F).	bind
24982	2	6560	7	NULL	NULL	NULL	NULL	NAC	Chemical	pretreatment	decrease					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_30_28274_s_108	11346654	125I-PDGF-BB binding experiments showed that pretreatment with NAC for 24 h decreased the specific binding of PDGF-BB to HSC (Fig.  1 F).	bind
20679	1	6561	5	10	NULL	0	NULL	Polymeric IgA		125I	bind					FcalphaR molecules		transfected			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_11_7216_s_262	10066783	125I-Polymeric IgA was bound to transfected FcalphaR molecules and allowed to internalize for various periods in the presence or absence of primaquine.	bind
24986	1	6561	7	NULL	NULL	NULL	NULL	Polymeric IgA	GP	125I	binds					FcalphaR molecules	GP	transfected			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_11_7216_s_262	10066783	125I-Polymeric IgA was bound to transfected FcalphaR molecules and allowed to internalize for various periods in the presence or absence of primaquine.	bind
20680	1	6562	5	NULL	NULL	0	NULL	GalR3 receptor	NULL	rat	is expressed in	NULL				COS-7 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_8	9405385	125I-Porcine galanin binds the rat GalR3 receptor expressed in COS-7 cells with high affinity ( K d = 0.6 nM) and could be displaced by galanin and galanin fragments and galanin-chimeric peptides.	bind
20681	2	6562	5	NULL	NULL	0	NULL	galanin	NULL	125I-Porcine	bind	NULL	high affinity			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_8	9405385	125I-Porcine galanin binds the rat GalR3 receptor expressed in COS-7 cells with high affinity ( K d = 0.6 nM) and could be displaced by galanin and galanin fragments and galanin-chimeric peptides.	bind
20682	3	6562	5	10	NULL	0	NULL	galanin			bind					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_8	9405385	125I-Porcine galanin binds the rat GalR3 receptor expressed in COS-7 cells with high affinity ( K d = 0.6 nM) and could be displaced by galanin and galanin fragments and galanin-chimeric peptides.	bind
20683	4	6562	5	10	NULL	0	NULL	statement 3			displace					statement 2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_8	9405385	125I-Porcine galanin binds the rat GalR3 receptor expressed in COS-7 cells with high affinity ( K d = 0.6 nM) and could be displaced by galanin and galanin fragments and galanin-chimeric peptides.	bind
20684	5	6562	5	10	NULL	0	NULL	galanin fragments			bind					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_8	9405385	125I-Porcine galanin binds the rat GalR3 receptor expressed in COS-7 cells with high affinity ( K d = 0.6 nM) and could be displaced by galanin and galanin fragments and galanin-chimeric peptides.	bind
54423	6	6562	5	10	NULL	0	NULL	statement 5			displace					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_8	9405385	125I-Porcine galanin binds the rat GalR3 receptor expressed in COS-7 cells with high affinity ( K d = 0.6 nM) and could be displaced by galanin and galanin fragments and galanin-chimeric peptides.	bind
54424	7	6562	5	10	NULL	0	NULL	galanin-chimeric peptides			bind					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_8	9405385	125I-Porcine galanin binds the rat GalR3 receptor expressed in COS-7 cells with high affinity ( K d = 0.6 nM) and could be displaced by galanin and galanin fragments and galanin-chimeric peptides.	bind
54425	8	6562	5	10	NULL	0	NULL	statement 7			displace					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_8	9405385	125I-Porcine galanin binds the rat GalR3 receptor expressed in COS-7 cells with high affinity ( K d = 0.6 nM) and could be displaced by galanin and galanin fragments and galanin-chimeric peptides.	bind
24993	2	6562	7	NULL	NULL	NULL	NULL	galanin	GP	125I-Porcine	bind		high affinity			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_8	9405385	125I-Porcine galanin binds the rat GalR3 receptor expressed in COS-7 cells with high affinity ( K d = 0.6 nM) and could be displaced by galanin and galanin fragments and galanin-chimeric peptides.	bind
24995	3	6562	7	NULL	NULL	NULL	NULL	galanin	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_8	9405385	125I-Porcine galanin binds the rat GalR3 receptor expressed in COS-7 cells with high affinity ( K d = 0.6 nM) and could be displaced by galanin and galanin fragments and galanin-chimeric peptides.	bind
24996	4	6562	7	NULL	NULL	NULL	NULL	galanin fragments	AminoAcid		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_8	9405385	125I-Porcine galanin binds the rat GalR3 receptor expressed in COS-7 cells with high affinity ( K d = 0.6 nM) and could be displaced by galanin and galanin fragments and galanin-chimeric peptides.	bind
24998	5	6562	7	NULL	NULL	NULL	NULL	galanin-chimeric peptides	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_8	9405385	125I-Porcine galanin binds the rat GalR3 receptor expressed in COS-7 cells with high affinity ( K d = 0.6 nM) and could be displaced by galanin and galanin fragments and galanin-chimeric peptides.	bind
54667	1	6562	7	NULL	NULL	NULL	NULL	GalR3 receptor	GP	rat	expressed in					COS-7 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_8	9405385	125I-Porcine galanin binds the rat GalR3 receptor expressed in COS-7 cells with high affinity ( K d = 0.6 nM) and could be displaced by galanin and galanin fragments and galanin-chimeric peptides.	bind
54668	6	6562	7	NULL	NULL	NULL	NULL	statement 3	Process		displace					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_8	9405385	125I-Porcine galanin binds the rat GalR3 receptor expressed in COS-7 cells with high affinity ( K d = 0.6 nM) and could be displaced by galanin and galanin fragments and galanin-chimeric peptides.	bind
54669	7	6562	7	NULL	NULL	NULL	NULL	statement 4	Process		displace					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_8	9405385	125I-Porcine galanin binds the rat GalR3 receptor expressed in COS-7 cells with high affinity ( K d = 0.6 nM) and could be displaced by galanin and galanin fragments and galanin-chimeric peptides.	bind
54670	8	6562	7	NULL	NULL	NULL	NULL	statement 5	Process		displace					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_51_31949_s_8	9405385	125I-Porcine galanin binds the rat GalR3 receptor expressed in COS-7 cells with high affinity ( K d = 0.6 nM) and could be displaced by galanin and galanin fragments and galanin-chimeric peptides.	bind
20685	1	6563	5	NULL	NULL	0	NULL	CHO cells	NULL		is transfected with	NULL	stably			cDNA	NULL	rabbit 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_44_27217_s_81	8910290	125I-Porcine PYY specifically bound with high affinity ( K d = 50 pM) to membranes from CHO cells stably transfected with the rabbit cDNA.	bind
20686	2	6563	5	10	NULL	0	NULL	PYY		125I-Porcine	bind		specifically;;high affinity			statement 1		membranes from			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27217_s_81	8910290	125I-Porcine PYY specifically bound with high affinity ( K d = 50 pM) to membranes from CHO cells stably transfected with the rabbit cDNA.	bind
25003	1	6563	7	NULL	NULL	NULL	NULL	PYY	GP	125I-Porcine	bind		specifically;;high affinity			membranes	CellComponent	CHO cells			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27217_s_81	8910290	125I-Porcine PYY specifically bound with high affinity ( K d = 50 pM) to membranes from CHO cells stably transfected with the rabbit cDNA.	bind
25006	2	6563	7	NULL	NULL	NULL	NULL	CHO cells	Cell		transfected with		stably			cDNA	NucleicAcid	rabbit			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27217_s_81	8910290	125I-Porcine PYY specifically bound with high affinity ( K d = 50 pM) to membranes from CHO cells stably transfected with the rabbit cDNA.	bind
20687	1	6564	5	10	NULL	0	NULL	PSP-II		125I	bind		lesser extent			polysaccharide zymosan A					NULL		NULL	NULL	NULL	NULL	gw60_febslett_431_2_273_s_63	9708918	125I-PSP-II bound to a lesser extent to the polysaccharide zymosan A, no binding was observed to chondroitin-6-sulfate, and only trace binding to yeast invertase was deteced ( Fig. 1).	bind
20688	2	6564	5	10	NULL	0	NULL	PSP-II		125I	does not bind					chondroitin-6-sulfate					NULL		NULL	NULL	NULL	NULL	gw60_febslett_431_2_273_s_63	9708918	125I-PSP-II bound to a lesser extent to the polysaccharide zymosan A, no binding was observed to chondroitin-6-sulfate, and only trace binding to yeast invertase was deteced ( Fig. 1).	bind
20689	3	6564	5	10	NULL	0	NULL	PSP-II		125I	bind		trace			invertase		yeast			NULL		NULL	NULL	NULL	NULL	gw60_febslett_431_2_273_s_63	9708918	125I-PSP-II bound to a lesser extent to the polysaccharide zymosan A, no binding was observed to chondroitin-6-sulfate, and only trace binding to yeast invertase was deteced ( Fig. 1).	bind
25039	1	6564	7	NULL	NULL	NULL	NULL	PSP-II 	GP	125I	bind		less			zymosan A	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_431_2_273_s_63	9708918	125I-PSP-II bound to a lesser extent to the polysaccharide zymosan A, no binding was observed to chondroitin-6-sulfate, and only trace binding to yeast invertase was deteced ( Fig. 1).	bind
25040	2	6564	7	NULL	NULL	NULL	NULL	PSP-II 	GP	125I	does not bind					chondroitin-6-sulfate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_431_2_273_s_63	9708918	125I-PSP-II bound to a lesser extent to the polysaccharide zymosan A, no binding was observed to chondroitin-6-sulfate, and only trace binding to yeast invertase was deteced ( Fig. 1).	bind
25041	3	6564	7	NULL	NULL	NULL	NULL	PSP-II 	GP	125I	bind		trace			invertase	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw60_febslett_431_2_273_s_63	9708918	125I-PSP-II bound to a lesser extent to the polysaccharide zymosan A, no binding was observed to chondroitin-6-sulfate, and only trace binding to yeast invertase was deteced ( Fig. 1).	bind
67962	4	6564	7	NULL	NULL	0	NULL	zymosan A	Chemical		is a type of					polysaccharide	Chemical				NULL		0	NULL	NULL	NULL	gw60_febslett_431_2_273_s_63	9708918	125I-PSP-II bound to a lesser extent to the polysaccharide zymosan A, no binding was observed to chondroitin-6-sulfate, and only trace binding to yeast invertase was deteced ( Fig. 1).	bind
20690	1	6565	5	10	NULL	0	NULL	TGF-beta		125I	bind					malpha2M					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_40_24982_s_77	8798779	125I-TGF-beta binding to malpha2M was detected by autoradiography.	bind
25042	1	6565	7	NULL	NULL	NULL	NULL	TGF-beta	GP	125I	bind					malpha2M	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_40_24982_s_77	8798779	125I-TGF-beta binding to malpha2M was detected by autoradiography.	bind
20691	1	6566	5	NULL	NULL	0	NULL	125I-TGF-beta1	NULL		bind	NULL	low			TbetaR-II	NULL				NULL	CHO-K1 cells	0	NULL	NULL	NULL	abs-batch0680-0699_j-biol-chem_281_17_16492675_s_5	16492675	125I-TGF-beta1 affinity labeling analysis of cell-surface TGF-beta  receptors reveals that CHO-K1 and CHO-677 cells exhibit low (<1) and high  (>1) ratios of 125I-TGF-beta1 binding to TbetaR-II and TbetaR-I, respectively.	bind
20692	2	6566	5	10	NULL	0	NULL	125I-TGF-beta1	NULL		bind	NULL	low			TbetaR-I	NULL				NULL	CHO-K1 cells	NULL	NULL	NULL	NULL	abs-batch0680-0699_j-biol-chem_281_17_16492675_s_5	16492675	125I-TGF-beta1 affinity labeling analysis of cell-surface TGF-beta  receptors reveals that CHO-K1 and CHO-677 cells exhibit low (<1) and high  (>1) ratios of 125I-TGF-beta1 binding to TbetaR-II and TbetaR-I, respectively.	bind
20693	3	6566	5	10	NULL	0	NULL	125I-TGF-beta1	NULL		bind	NULL	high			TbetaR-II	NULL				NULL	CHO-677 cells	NULL	NULL	NULL	NULL	abs-batch0680-0699_j-biol-chem_281_17_16492675_s_5	16492675	125I-TGF-beta1 affinity labeling analysis of cell-surface TGF-beta  receptors reveals that CHO-K1 and CHO-677 cells exhibit low (<1) and high  (>1) ratios of 125I-TGF-beta1 binding to TbetaR-II and TbetaR-I, respectively.	bind
20694	4	6566	5	NULL	NULL	0	NULL	125I-TGF-beta1	NULL		bind	NULL	high			TbetaR-I	NULL				NULL	CHO-677 cells	NULL	NULL	NULL	NULL	abs-batch0680-0699_j-biol-chem_281_17_16492675_s_5	16492675	125I-TGF-beta1 affinity labeling analysis of cell-surface TGF-beta  receptors reveals that CHO-K1 and CHO-677 cells exhibit low (<1) and high  (>1) ratios of 125I-TGF-beta1 binding to TbetaR-II and TbetaR-I, respectively.	bind
25043	1	6566	7	NULL	NULL	NULL	NULL	125I-TGF-beta1	GP		bind		low			TbetaR-I	GP				NULL	CHO-K1 cells	NULL	NULL	NULL	NULL	abs-batch0680-0699_j-biol-chem_281_17_16492675_s_5	16492675	125I-TGF-beta1 affinity labeling analysis of cell-surface TGF-beta  receptors reveals that CHO-K1 and CHO-677 cells exhibit low (<1) and high  (>1) ratios of 125I-TGF-beta1 binding to TbetaR-II and TbetaR-I, respectively.	bind
25044	2	6566	7	NULL	NULL	NULL	NULL	125I-TGF-beta1	GP		bind		low			TbetaR-II	GP				NULL	CHO-K1 cells	NULL	NULL	NULL	NULL	abs-batch0680-0699_j-biol-chem_281_17_16492675_s_5	16492675	125I-TGF-beta1 affinity labeling analysis of cell-surface TGF-beta  receptors reveals that CHO-K1 and CHO-677 cells exhibit low (<1) and high  (>1) ratios of 125I-TGF-beta1 binding to TbetaR-II and TbetaR-I, respectively.	bind
45757	3	6566	7	NULL	NULL	NULL	NULL	125I-TGF-beta1	GP		bind		high			TbetaR-I	GP				NULL	CHO-677 cells	NULL	NULL	NULL	NULL	abs-batch0680-0699_j-biol-chem_281_17_16492675_s_5	16492675	125I-TGF-beta1 affinity labeling analysis of cell-surface TGF-beta  receptors reveals that CHO-K1 and CHO-677 cells exhibit low (<1) and high  (>1) ratios of 125I-TGF-beta1 binding to TbetaR-II and TbetaR-I, respectively.	bind
45758	4	6566	7	NULL	NULL	NULL	NULL	125I-TGF-beta1	GP		bind		high			TbetaR-II	GP				NULL	CHO-677 cells	NULL	NULL	NULL	NULL	abs-batch0680-0699_j-biol-chem_281_17_16492675_s_5	16492675	125I-TGF-beta1 affinity labeling analysis of cell-surface TGF-beta  receptors reveals that CHO-K1 and CHO-677 cells exhibit low (<1) and high  (>1) ratios of 125I-TGF-beta1 binding to TbetaR-II and TbetaR-I, respectively.	bind
20695	1	6568	5	NULL	NULL	0	NULL	TGF-beta1	NULL	125I	bind	NULL				malpha2M	NULL	purified			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_40_24982_s_150	8798779	125I-TGF-beta1 and 125I-TGF-beta2 bound to purified malpha2M and MUG, as determined by the BS3-rapid cross-linking method.	bind
20696	2	6568	5	NULL	NULL	0	NULL	TGF-beta2	NULL	125I	bind	NULL				malpha2M	NULL	purified			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_40_24982_s_150	8798779	125I-TGF-beta1 and 125I-TGF-beta2 bound to purified malpha2M and MUG, as determined by the BS3-rapid cross-linking method.	bind
20697	3	6568	5	NULL	NULL	0	NULL	TGF-beta1	NULL	125I	bind	NULL				MUG	NULL	purified			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_40_24982_s_150	8798779	125I-TGF-beta1 and 125I-TGF-beta2 bound to purified malpha2M and MUG, as determined by the BS3-rapid cross-linking method.	bind
20698	4	6568	5	NULL	NULL	0	NULL	TGF-beta2	NULL	125I	bind	NULL				MUG	NULL	purified			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_40_24982_s_150	8798779	125I-TGF-beta1 and 125I-TGF-beta2 bound to purified malpha2M and MUG, as determined by the BS3-rapid cross-linking method.	bind
25047	1	6568	7	NULL	NULL	NULL	NULL	TGF-beta1	GP	125I	bind					 malpha2M	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_40_24982_s_150	8798779	125I-TGF-beta1 and 125I-TGF-beta2 bound to purified malpha2M and MUG, as determined by the BS3-rapid cross-linking method.	bind
25048	2	6568	7	NULL	NULL	NULL	NULL	TGF-beta2	GP	125I	bind					malpha2M	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_40_24982_s_150	8798779	125I-TGF-beta1 and 125I-TGF-beta2 bound to purified malpha2M and MUG, as determined by the BS3-rapid cross-linking method.	bind
25049	3	6568	7	NULL	NULL	NULL	NULL	TGF-beta1	GP	125I	bind					MUG	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_40_24982_s_150	8798779	125I-TGF-beta1 and 125I-TGF-beta2 bound to purified malpha2M and MUG, as determined by the BS3-rapid cross-linking method.	bind
25050	4	6568	7	NULL	NULL	NULL	NULL	TGF-beta2	GP	125I	bind					MUG	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_40_24982_s_150	8798779	125I-TGF-beta1 and 125I-TGF-beta2 bound to purified malpha2M and MUG, as determined by the BS3-rapid cross-linking method.	bind
20699	1	6570	5	NULL	NULL	0	NULL	ZIF-1/ Glycodelin-A	NULL	125I	bind	NULL				sperm extracts	NULL	human			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_15_13570_s_248	12571233	125I-ZIF-1/ Glycodelin-A Binding to the Human Sperm Extracts-- Previous study using the same protocol for preparation of human sperm extracts suggested  that the isolated proteins contained mainly membrane proteins ( ).	bind
25052	1	6570	7	NULL	NULL	NULL	NULL	ZIF-1/ Glycodelin-A	GP	125I	bind					Sperm Extracts	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_15_13570_s_248	12571233	125I-ZIF-1/ Glycodelin-A Binding to the Human Sperm Extracts-- Previous study using the same protocol for preparation of human sperm extracts suggested  that the isolated proteins contained mainly membrane proteins ( ).	bind
20700	1	6573	5	NULL	NULL	0	NULL	ZIF-1/ Glycodelin-A	NULL	125I	bind	NULL				sperm extracts	NULL	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_13570_s_159	12571233	125I-ZIF-1/ Glycodelin-A Binding to the Human Sperm Extracts-- Sperm extracts was isolated as described ( 25).	bind
25053	1	6573	7	NULL	NULL	NULL	NULL	ZIF-1/ Glycodelin-A	GP	125I	bind					Sperm Extracts	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_13570_s_159	12571233	125I-ZIF-1/ Glycodelin-A Binding to the Human Sperm Extracts-- Sperm extracts was isolated as described ( 25).	bind
20701	1	6575	5	NULL	NULL	0	NULL	Sar-1, Ile-8Ang II	NULL	125I	bind	NULL	predominantly			AT1 receptor subtype	NULL				NULL	WT kidneys	NULL	NULL	NULL	NULL	gw60_pnas_100_14_8258_s_75	12829792	125I-[Sar-1,  Ile-8Ang II bound predominantly to the AT1 receptor subtype, in  both WT and  Mas-knockout kidneys  ( Fig. 1  A Center and   C), with low binding to the AT2 receptor  subtype ( Fig. 1  A Right and   C).	bind
20702	2	6575	5	NULL	NULL	0	NULL	Sar-1, Ile-8Ang II	NULL	125I	bind	NULL	predominantly			AT1 receptor subtype	NULL				NULL	Mas-knockout kidneys	NULL	NULL	NULL	NULL	gw60_pnas_100_14_8258_s_75	12829792	125I-[Sar-1,  Ile-8Ang II bound predominantly to the AT1 receptor subtype, in  both WT and  Mas-knockout kidneys  ( Fig. 1  A Center and   C), with low binding to the AT2 receptor  subtype ( Fig. 1  A Right and   C).	bind
20703	3	6575	5	NULL	NULL	0	NULL	Sar-1, Ile-8Ang II	NULL	125I	bind	NULL	low			AT2 receptor subtype	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_14_8258_s_75	12829792	125I-[Sar-1,  Ile-8Ang II bound predominantly to the AT1 receptor subtype, in  both WT and  Mas-knockout kidneys  ( Fig. 1  A Center and   C), with low binding to the AT2 receptor  subtype ( Fig. 1  A Right and   C).	bind
25055	1	6575	7	NULL	NULL	NULL	NULL	Sar-1, Ile-8Ang II	GP	125I	bind		predominantly			AT1 receptor subtype	GP				NULL	WT kidneys	NULL	NULL	NULL	NULL	gw60_pnas_100_14_8258_s_75	12829792	125I-[Sar-1,  Ile-8Ang II bound predominantly to the AT1 receptor subtype, in  both WT and  Mas-knockout kidneys  ( Fig. 1  A Center and   C), with low binding to the AT2 receptor  subtype ( Fig. 1  A Right and   C).	bind
25056	2	6575	7	NULL	NULL	NULL	NULL	Sar-1, Ile-8Ang II	GP	125I	bind		predominantly			AT1 receptor subtype	GP				NULL	Mas-knockout kidneys	NULL	NULL	NULL	NULL	gw60_pnas_100_14_8258_s_75	12829792	125I-[Sar-1,  Ile-8Ang II bound predominantly to the AT1 receptor subtype, in  both WT and  Mas-knockout kidneys  ( Fig. 1  A Center and   C), with low binding to the AT2 receptor  subtype ( Fig. 1  A Right and   C).	bind
25058	3	6575	7	NULL	NULL	NULL	NULL	Sar-1, Ile-8Ang II	GP	125I	bind		low			AT2 receptor subtype	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_14_8258_s_75	12829792	125I-[Sar-1,  Ile-8Ang II bound predominantly to the AT1 receptor subtype, in  both WT and  Mas-knockout kidneys  ( Fig. 1  A Center and   C), with low binding to the AT2 receptor  subtype ( Fig. 1  A Right and   C).	bind
20704	1	6576	5	NULL	NULL	0	NULL	125I-[Tyr3]MP	NULL		bind	NULL				HSR	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_57_6_1235_s_184	10825395	125I-[Tyr3]MP binding to HSR was inhibited by unlabeled [Tyr3]MP (0.1-500 muM) in a concentration-dependent manner at 0 degrees C under the same conditions for 45Ca2+ release experiments (data not shown).	bind
20705	2	6576	5	NULL	NULL	0	NULL	[Tyr3]MP	NULL	unlabeled	inhibit	NULL	concentration dependent			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_57_6_1235_s_184	10825395	125I-[Tyr3]MP binding to HSR was inhibited by unlabeled [Tyr3]MP (0.1-500 muM) in a concentration-dependent manner at 0 degrees C under the same conditions for 45Ca2+ release experiments (data not shown).	bind
25060	1	6576	7	NULL	NULL	NULL	NULL	[Tyr3]MP	Chemical	125I	bind					HSR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_57_6_1235_s_184	10825395	125I-[Tyr3]MP binding to HSR was inhibited by unlabeled [Tyr3]MP (0.1-500 muM) in a concentration-dependent manner at 0 degrees C under the same conditions for 45Ca2+ release experiments (data not shown).	bind
25062	2	6576	7	NULL	NULL	NULL	NULL	[Tyr3]MP	Chemical	unlabeled	inhibits		concentration-dependent			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_57_6_1235_s_184	10825395	125I-[Tyr3]MP binding to HSR was inhibited by unlabeled [Tyr3]MP (0.1-500 muM) in a concentration-dependent manner at 0 degrees C under the same conditions for 45Ca2+ release experiments (data not shown).	bind
20706	1	6577	5	NULL	NULL	0	NULL	[Tyr3]MP	NULL	125I	bind	NULL				HSR	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_57_6_1235_s_182	10825395	125I-[Tyr3]MP Binding to HSR.	bind
25066	1	6577	7	NULL	NULL	NULL	NULL	[Tyr3]MP	Chemical	125I	bind					HSR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_57_6_1235_s_182	10825395	125I-[Tyr3]MP Binding to HSR.	bind
20707	1	6578	5	NULL	NULL	0	NULL	VE-cadherin	NULL		bind	NULL				p120	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_294	16574915	126 - 128   Consequently, the binding of VE-cadherin to p120 and beta-catenin is disrupted, and a rapid internalization and degradation of VE-cadherin occurs via a clathrin-dependent pathway ( Figure 3).	bind
20708	2	6578	5	NULL	NULL	0	NULL	VE-cadherin	NULL		bind	NULL				beta-catenin	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_294	16574915	126 - 128   Consequently, the binding of VE-cadherin to p120 and beta-catenin is disrupted, and a rapid internalization and degradation of VE-cadherin occurs via a clathrin-dependent pathway ( Figure 3).	bind
20743	3	6578	5	NULL	NULL	0	NULL	VE-cadherin	NULL		undergoes	NULL				internalization	NULL	rapid			NULL		0	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_294	16574915	126 - 128   Consequently, the binding of VE-cadherin to p120 and beta-catenin is disrupted, and a rapid internalization and degradation of VE-cadherin occurs via a clathrin-dependent pathway ( Figure 3).	bind
20744	4	6578	5	NULL	NULL	0	NULL	statement 3	NULL		occurs via	NULL				clathrin-dependent pathway	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_294	16574915	126 - 128   Consequently, the binding of VE-cadherin to p120 and beta-catenin is disrupted, and a rapid internalization and degradation of VE-cadherin occurs via a clathrin-dependent pathway ( Figure 3).	bind
20745	5	6578	5	NULL	NULL	0	NULL	VE-cadherin	NULL		undergoes	NULL				degradation	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_294	16574915	126 - 128   Consequently, the binding of VE-cadherin to p120 and beta-catenin is disrupted, and a rapid internalization and degradation of VE-cadherin occurs via a clathrin-dependent pathway ( Figure 3).	bind
20746	6	6578	5	NULL	NULL	0	NULL	statement 5	NULL		occurs via	NULL				clathrin-dependent pathway	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_294	16574915	126 - 128   Consequently, the binding of VE-cadherin to p120 and beta-catenin is disrupted, and a rapid internalization and degradation of VE-cadherin occurs via a clathrin-dependent pathway ( Figure 3).	bind
25067	1	6578	7	NULL	NULL	NULL	NULL	VE-cadherin	GP		binds to					p120	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_294	16574915	126 - 128   Consequently, the binding of VE-cadherin to p120 and beta-catenin is disrupted, and a rapid internalization and degradation of VE-cadherin occurs via a clathrin-dependent pathway ( Figure 3).	bind
25068	2	6578	7	NULL	NULL	NULL	NULL	VE-cadherin	GP		binds to					beta-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_294	16574915	126 - 128   Consequently, the binding of VE-cadherin to p120 and beta-catenin is disrupted, and a rapid internalization and degradation of VE-cadherin occurs via a clathrin-dependent pathway ( Figure 3).	bind
25069	3	6578	7	NULL	NULL	NULL	NULL	statement 1	Process	disruption of	internalizes		rapidly			VE-cadherin	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_294	16574915	126 - 128   Consequently, the binding of VE-cadherin to p120 and beta-catenin is disrupted, and a rapid internalization and degradation of VE-cadherin occurs via a clathrin-dependent pathway ( Figure 3).	bind
25070	4	6578	7	NULL	NULL	NULL	NULL	VE-cadherin	GP	degradation of	occurs via					clathrin-dependent pathway	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_294	16574915	126 - 128   Consequently, the binding of VE-cadherin to p120 and beta-catenin is disrupted, and a rapid internalization and degradation of VE-cadherin occurs via a clathrin-dependent pathway ( Figure 3).	bind
25071	5	6578	7	NULL	NULL	NULL	NULL	statement 3	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_294	16574915	126 - 128   Consequently, the binding of VE-cadherin to p120 and beta-catenin is disrupted, and a rapid internalization and degradation of VE-cadherin occurs via a clathrin-dependent pathway ( Figure 3).	bind
25072	6	6578	7	NULL	NULL	NULL	NULL	statement 2	Process	disruption of	internalizes		rapidly			VE-cadherin	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_294	16574915	126 - 128   Consequently, the binding of VE-cadherin to p120 and beta-catenin is disrupted, and a rapid internalization and degradation of VE-cadherin occurs via a clathrin-dependent pathway ( Figure 3).	bind
25073	7	6578	7	NULL	NULL	NULL	NULL	statement 6	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_294	16574915	126 - 128   Consequently, the binding of VE-cadherin to p120 and beta-catenin is disrupted, and a rapid internalization and degradation of VE-cadherin occurs via a clathrin-dependent pathway ( Figure 3).	bind
20747	2	6579	5	NULL	NULL	0	NULL	TZDs	NULL		inhibit	NULL				LPS-inducible genes	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_230_s_160	14592855	126,127  Second, the doses of TZDs that exert maximal inhibitory effects on LPS-inducible genes are significantly higher than their binding affinity to PPARgamma.	bind
20748	1	6579	5	NULL	NULL	0	NULL	LPS-inducible genes	NULL		bind	NULL				PPARgamma	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_230_s_160	14592855	126,127  Second, the doses of TZDs that exert maximal inhibitory effects on LPS-inducible genes are significantly higher than their binding affinity to PPARgamma.	bind
30305	3	6579	5	NULL	NULL	0	NULL	statement 2	NULL		is higher than	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_230_s_160	14592855	126,127  Second, the doses of TZDs that exert maximal inhibitory effects on LPS-inducible genes are significantly higher than their binding affinity to PPARgamma.	bind
25075	1	6579	7	NULL	NULL	NULL	NULL	LPS-inducible genes	GP		bind					PPARgamma	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_230_s_160	14592855	126,127  Second, the doses of TZDs that exert maximal inhibitory effects on LPS-inducible genes are significantly higher than their binding affinity to PPARgamma.	bind
25077	2	6579	7	NULL	NULL	NULL	NULL	TZDs	Chemical		inhibits					LPS-inducible genes	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_230_s_160	14592855	126,127  Second, the doses of TZDs that exert maximal inhibitory effects on LPS-inducible genes are significantly higher than their binding affinity to PPARgamma.	bind
25078	3	6579	7	NULL	NULL	NULL	NULL	statement 2	Process		is higher than					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_230_s_160	14592855	126,127  Second, the doses of TZDs that exert maximal inhibitory effects on LPS-inducible genes are significantly higher than their binding affinity to PPARgamma.	bind
20749	1	6580	5	NULL	NULL	0	NULL	12CO	NULL		bind	NULL				Ch-CooA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_5_3269_s_115	15537640	12CO-bound Ch-CooA ( a), 13CO-bound Ch-CooA ( b), and the difference spectrum ( a -  b) ( c).	bind
20750	2	6580	5	NULL	NULL	0	NULL	13CO	NULL		bind	NULL				Ch-CooA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_5_3269_s_115	15537640	12CO-bound Ch-CooA ( a), 13CO-bound Ch-CooA ( b), and the difference spectrum ( a -  b) ( c).	bind
25080	1	6580	7	NULL	NULL	NULL	NULL	12CO	Chemical		bind					Ch-CooA	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_5_3269_s_115	15537640	12CO-bound Ch-CooA ( a), 13CO-bound Ch-CooA ( b), and the difference spectrum ( a -  b) ( c).	bind
25081	2	6580	7	NULL	NULL	NULL	NULL	13CO	Chemical		bind					Ch-CooA	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_5_3269_s_115	15537640	12CO-bound Ch-CooA ( a), 13CO-bound Ch-CooA ( b), and the difference spectrum ( a -  b) ( c).	bind
20751	1	6581	5	NULL	NULL	0	NULL	SDF-1	NULL		mediate	NULL				chemotactic responses	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_3_651_s_250	9348282	12G5 can partially inhibit SDF-1-mediated chemotactic responses, SDF-1-induced modulation of intracellular  calcium, and SDF-1 binding to CXCR4 ( 8,  30).	bind
20752	2	6581	5	NULL	NULL	0	NULL	12G5	NULL		inhibit	NULL	partially			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_3_651_s_250	9348282	12G5 can partially inhibit SDF-1-mediated chemotactic responses, SDF-1-induced modulation of intracellular  calcium, and SDF-1 binding to CXCR4 ( 8,  30).	bind
20753	3	6581	5	NULL	NULL	0	NULL	SDF-1	NULL		induces	NULL				intracellular calcium	NULL	modulation of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_3_651_s_250	9348282	12G5 can partially inhibit SDF-1-mediated chemotactic responses, SDF-1-induced modulation of intracellular  calcium, and SDF-1 binding to CXCR4 ( 8,  30).	bind
20754	4	6581	5	NULL	NULL	0	NULL	12G5	NULL		inhibit	NULL	partially			statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_3_651_s_250	9348282	12G5 can partially inhibit SDF-1-mediated chemotactic responses, SDF-1-induced modulation of intracellular  calcium, and SDF-1 binding to CXCR4 ( 8,  30).	bind
20755	5	6581	5	NULL	NULL	0	NULL	SDF-1	NULL		bind	NULL				CXCR4	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_3_651_s_250	9348282	12G5 can partially inhibit SDF-1-mediated chemotactic responses, SDF-1-induced modulation of intracellular  calcium, and SDF-1 binding to CXCR4 ( 8,  30).	bind
20756	6	6581	5	NULL	NULL	0	NULL	12G5	NULL		inhibit	NULL	partially			statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_3_651_s_250	9348282	12G5 can partially inhibit SDF-1-mediated chemotactic responses, SDF-1-induced modulation of intracellular  calcium, and SDF-1 binding to CXCR4 ( 8,  30).	bind
25092	1	6581	7	NULL	NULL	NULL	NULL	SDF-1	GP		mediates					chemotactic responses	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_139_3_651_s_250	9348282	12G5 can partially inhibit SDF-1-mediated chemotactic responses, SDF-1-induced modulation of intracellular  calcium, and SDF-1 binding to CXCR4 ( 8,  30).	bind
25093	2	6581	7	NULL	NULL	NULL	NULL	12G5	GP		inhibit		partially			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_139_3_651_s_250	9348282	12G5 can partially inhibit SDF-1-mediated chemotactic responses, SDF-1-induced modulation of intracellular  calcium, and SDF-1 binding to CXCR4 ( 8,  30).	bind
25094	3	6581	7	NULL	NULL	NULL	NULL	SDF-1	GP		induce					 calcium	Chemical	modulation of;; intracellular			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_139_3_651_s_250	9348282	12G5 can partially inhibit SDF-1-mediated chemotactic responses, SDF-1-induced modulation of intracellular  calcium, and SDF-1 binding to CXCR4 ( 8,  30).	bind
25095	4	6581	7	NULL	NULL	NULL	NULL	SDF-1	GP		bind					CXCR4	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_139_3_651_s_250	9348282	12G5 can partially inhibit SDF-1-mediated chemotactic responses, SDF-1-induced modulation of intracellular  calcium, and SDF-1 binding to CXCR4 ( 8,  30).	bind
31407	5	6581	7	NULL	NULL	NULL	NULL	12G5	GP		inhibit		partially			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_139_3_651_s_250	9348282	12G5 can partially inhibit SDF-1-mediated chemotactic responses, SDF-1-induced modulation of intracellular  calcium, and SDF-1 binding to CXCR4 ( 8,  30).	bind
31408	6	6581	7	NULL	NULL	NULL	NULL	12G5	GP		inhibit		partially			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_139_3_651_s_250	9348282	12G5 can partially inhibit SDF-1-mediated chemotactic responses, SDF-1-induced modulation of intracellular  calcium, and SDF-1 binding to CXCR4 ( 8,  30).	bind
20759	1	6582	5	NULL	NULL	0	NULL	1D4	NULL		bind	NULL				CXCR4-C9	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_5_3378_s_148	12433920	12G5 only recognizes conformationally intact CXCR4, whereas the 1D4 can bind all CXCR4-C9, regardless of conformation.	bind
20760	2	6582	5	NULL	NULL	0	NULL	12G5	NULL		recognizes	NULL				CXCR4	NULL	conformationally intact			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_5_3378_s_148	12433920	12G5 only recognizes conformationally intact CXCR4, whereas the 1D4 can bind all CXCR4-C9, regardless of conformation.	bind
30306	3	6582	5	NULL	NULL	0	NULL	statement 2	NULL		is regardless of	NULL				conformation	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_5_3378_s_148	12433920	12G5 only recognizes conformationally intact CXCR4, whereas the 1D4 can bind all CXCR4-C9, regardless of conformation.	bind
25096	1	6582	7	NULL	NULL	NULL	NULL	12G5	GP		recognizes					CXCR4	GP	conformationally intact			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_3378_s_148	12433920	12G5 only recognizes conformationally intact CXCR4, whereas the 1D4 can bind all CXCR4-C9, regardless of conformation.	bind
25097	2	6582	7	NULL	NULL	NULL	NULL	1D4	GP		bind					 CXCR4-C9	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_3378_s_148	12433920	12G5 only recognizes conformationally intact CXCR4, whereas the 1D4 can bind all CXCR4-C9, regardless of conformation.	bind
25098	3	6582	7	NULL	NULL	NULL	NULL	statement 2	Process		is regardless of					conformation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_3378_s_148	12433920	12G5 only recognizes conformationally intact CXCR4, whereas the 1D4 can bind all CXCR4-C9, regardless of conformation.	bind
20761	1	6583	5	NULL	NULL	0	NULL	TFIIB	NULL		bind	NULL				p300	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_171	10330164	12S E1A inhibits the binding of TFIIB to p300, while 13S E1A has no effect on the p300-TFIIB interaction.	bind
20762	2	6583	5	NULL	NULL	0	NULL	12S E1A	NULL		inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_171	10330164	12S E1A inhibits the binding of TFIIB to p300, while 13S E1A has no effect on the p300-TFIIB interaction.	bind
20763	3	6583	5	NULL	NULL	0	NULL	13S E1A	NULL		does not effect	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_171	10330164	12S E1A inhibits the binding of TFIIB to p300, while 13S E1A has no effect on the p300-TFIIB interaction.	bind
25099	1	6583	7	NULL	NULL	NULL	NULL	TFIIB	GP		bind					p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_171	10330164	12S E1A inhibits the binding of TFIIB to p300, while 13S E1A has no effect on the p300-TFIIB interaction.	bind
25100	2	6583	7	NULL	NULL	NULL	NULL	12S E1A	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_171	10330164	12S E1A inhibits the binding of TFIIB to p300, while 13S E1A has no effect on the p300-TFIIB interaction.	bind
25101	3	6583	7	NULL	NULL	NULL	NULL	13S E1A	GP		has no effect on					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_171	10330164	12S E1A inhibits the binding of TFIIB to p300, while 13S E1A has no effect on the p300-TFIIB interaction.	bind
20764	1	6584	5	NULL	NULL	0	NULL	DNA ligase IV	NULL		bind	NULL		motif located between BRCT domains		XRCC4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_23_4642_s_270	11095673	13       Grawunder,U., Zimmer,D. and Leiber,M.R. (1998) DNA ligase IV binds to XRCC4 via a motif located between rather than within its BRCT domains.	bind
25102	1	6584	7	NULL	NULL	NULL	NULL	DNA ligase IV	GP		binds to			motif between BRCT domain		XRCC4	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_23_4642_s_270	11095673	13       Grawunder,U., Zimmer,D. and Leiber,M.R. (1998) DNA ligase IV binds to XRCC4 via a motif located between rather than within its BRCT domains.	bind
20765	1	6585	5	NULL	NULL	0	NULL	H19 RNA	NULL		bind	NULL				IGF-II mRNA-binding protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_1_189_s_210	11125087	13       Runge,S., Nielsen,F.C., Nielsen,J., Lykke-Andersen,J., Wewer,U.M. and Christiansen,J. (2000) H19 RNA binds four molecules of IGF-II mRNA-binding protein.	bind
25103	1	6585	7	NULL	NULL	NULL	NULL	H19 RNA	NucleicAcid		binds					IGF-II mRNA-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_1_189_s_210	11125087	13       Runge,S., Nielsen,F.C., Nielsen,J., Lykke-Andersen,J., Wewer,U.M. and Christiansen,J. (2000) H19 RNA binds four molecules of IGF-II mRNA-binding protein.	bind
20766	1	6586	5	NULL	NULL	0	NULL	CNP	NULL		bind	NULL				NPR-B	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_96_7_2272_s_25	9337200	13  CNP binds to NPR-B, which contains guanylyl cyclase 14  and induces the production of cGMP.	bind
20767	2	6586	5	10	NULL	0	NULL	NPR-B			contains					guanylyl cyclase					NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_7_2272_s_25	9337200	13  CNP binds to NPR-B, which contains guanylyl cyclase 14  and induces the production of cGMP.	bind
20768	3	6586	5	NULL	NULL	0	NULL	NPR-B	NULL		induces	NULL				cGMP	NULL	production of			NULL		0	NULL	NULL	NULL	gw60_circulation_96_7_2272_s_25	9337200	13  CNP binds to NPR-B, which contains guanylyl cyclase 14  and induces the production of cGMP.	bind
25104	1	6586	7	NULL	NULL	NULL	NULL	CNP	GP		binds to					NPR-B	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_7_2272_s_25	9337200	13  CNP binds to NPR-B, which contains guanylyl cyclase 14  and induces the production of cGMP.	bind
25105	2	6586	7	NULL	NULL	NULL	NULL	NPR-B	GP		contains					guanylyl cyclase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_7_2272_s_25	9337200	13  CNP binds to NPR-B, which contains guanylyl cyclase 14  and induces the production of cGMP.	bind
25106	3	6586	7	NULL	NULL	NULL	NULL	statement 1	Process		induces					cGMP	Chemical	production of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_7_2272_s_25	9337200	13  CNP binds to NPR-B, which contains guanylyl cyclase 14  and induces the production of cGMP.	bind
20769	1	6587	5	NULL	NULL	0	NULL	 CT-1	NULL		bind	NULL				gp130-LIF receptor complex	NULL				NULL	in myocytes	0	NULL	NULL	NULL	gw60_circulationres_88_7_727_s_23	11304496	13  CT-1 binds to the gp130-LIF receptor complex in myocytes, activating the JAK-STAT pathway and inducing hypertrophic responses.	bind
20770	2	6587	5	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				JAK-STAT pathway	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_88_7_727_s_23	11304496	13  CT-1 binds to the gp130-LIF receptor complex in myocytes, activating the JAK-STAT pathway and inducing hypertrophic responses.	bind
20771	3	6587	5	NULL	NULL	0	NULL	statement 1	NULL		induces	NULL				hypertrophic responses	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_88_7_727_s_23	11304496	13  CT-1 binds to the gp130-LIF receptor complex in myocytes, activating the JAK-STAT pathway and inducing hypertrophic responses.	bind
25107	1	6587	7	NULL	NULL	NULL	NULL	CT-1	GP		binds to					gp130-LIF receptor complex	GP				NULL	myocytes	NULL	NULL	NULL	NULL	gw60_circulationres_88_7_727_s_23	11304496	13  CT-1 binds to the gp130-LIF receptor complex in myocytes, activating the JAK-STAT pathway and inducing hypertrophic responses.	bind
25108	2	6587	7	NULL	NULL	NULL	NULL	statement 1	Process		activates					JAK-STAT pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_7_727_s_23	11304496	13  CT-1 binds to the gp130-LIF receptor complex in myocytes, activating the JAK-STAT pathway and inducing hypertrophic responses.	bind
25109	3	6587	7	NULL	NULL	NULL	NULL	statement 1	Process		induce					hypertrophic responses	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_7_727_s_23	11304496	13  CT-1 binds to the gp130-LIF receptor complex in myocytes, activating the JAK-STAT pathway and inducing hypertrophic responses.	bind
20792	1	6588	5	NULL	NULL	0	NULL	FHC LDL	NULL		binding	NULL	defective			LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_137_s_31	8548414	13  In addition, the FHC LDL shows defective binding to the LDL receptor 21  and delayed plasma clearance 22  that seemed to be independent of the LDL receptor.	bind
20795	2	6588	5	NULL	NULL	0	NULL	FHC LDL	NULL		shows	NULL				plasma clearance	NULL	delayed			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_137_s_31	8548414	13  In addition, the FHC LDL shows defective binding to the LDL receptor 21  and delayed plasma clearance 22  that seemed to be independent of the LDL receptor.	bind
20796	3	6588	5	NULL	NULL	0	NULL	plasma clearance	NULL		is independent of	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_137_s_31	8548414	13  In addition, the FHC LDL shows defective binding to the LDL receptor 21  and delayed plasma clearance 22  that seemed to be independent of the LDL receptor.	bind
25110	1	6588	7	NULL	NULL	NULL	NULL	FHC LDL	GP		bind		defective			LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_137_s_31	8548414	13  In addition, the FHC LDL shows defective binding to the LDL receptor 21  and delayed plasma clearance 22  that seemed to be independent of the LDL receptor.	bind
25111	2	6588	7	NULL	NULL	NULL	NULL	FHC LDL	GP		shows					plasma clearance	Process	delayed			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_137_s_31	8548414	13  In addition, the FHC LDL shows defective binding to the LDL receptor 21  and delayed plasma clearance 22  that seemed to be independent of the LDL receptor.	bind
25112	3	6588	7	NULL	NULL	NULL	NULL	statement 2	Process		is independent of					LDL receptor	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_137_s_31	8548414	13  In addition, the FHC LDL shows defective binding to the LDL receptor 21  and delayed plasma clearance 22  that seemed to be independent of the LDL receptor.	bind
20783	1	6589	5	NULL	NULL	0	NULL	 NF-kappaB	NULL		is present as	NULL				heterodimer	NULL				NULL	in cytosol	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1116_s_199	10764682	13  NF-kappaB is present in cytosol as a heterodimer composed of NF-kappaB1 (P50) and Rel (P65) subunits bound to an inhibitor protein, I-kappaB.	bind
20785	2	6589	5	NULL	NULL	0	NULL	NF-kappaB	NULL		is composed of	NULL					NULL		P50 subunit		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1116_s_199	10764682	13  NF-kappaB is present in cytosol as a heterodimer composed of NF-kappaB1 (P50) and Rel (P65) subunits bound to an inhibitor protein, I-kappaB.	bind
20786	3	6589	5	10	NULL	0	NULL	p50 subunit			is					NF-kappaB1					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1116_s_199	10764682	13  NF-kappaB is present in cytosol as a heterodimer composed of NF-kappaB1 (P50) and Rel (P65) subunits bound to an inhibitor protein, I-kappaB.	bind
20788	4	6589	5	NULL	NULL	0	NULL	NF-kappaB	NULL		is composed of	NULL					NULL		p65 subunit		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1116_s_199	10764682	13  NF-kappaB is present in cytosol as a heterodimer composed of NF-kappaB1 (P50) and Rel (P65) subunits bound to an inhibitor protein, I-kappaB.	bind
20790	5	6589	5	10	NULL	0	NULL	p65 subunit			is					Rel					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1116_s_199	10764682	13  NF-kappaB is present in cytosol as a heterodimer composed of NF-kappaB1 (P50) and Rel (P65) subunits bound to an inhibitor protein, I-kappaB.	bind
20791	6	6589	5	NULL	NULL	0	NULL	NF-kappaB	NULL		bind	NULL				I-kappaB protein	NULL				NULL	in cytosol	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1116_s_199	10764682	13  NF-kappaB is present in cytosol as a heterodimer composed of NF-kappaB1 (P50) and Rel (P65) subunits bound to an inhibitor protein, I-kappaB.	bind
30307	7	6589	5	NULL	NULL	0	NULL	NF-kappa-B	NULL		is a type of	NULL				heterodimer	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1116_s_199	10764682	13  NF-kappaB is present in cytosol as a heterodimer composed of NF-kappaB1 (P50) and Rel (P65) subunits bound to an inhibitor protein, I-kappaB.	bind
30308	8	6589	5	NULL	NULL	0	NULL	I-kappaB	NULL		is a type of	NULL				inhibitor protein	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1116_s_199	10764682	13  NF-kappaB is present in cytosol as a heterodimer composed of NF-kappaB1 (P50) and Rel (P65) subunits bound to an inhibitor protein, I-kappaB.	bind
54453	9	6589	5	10	NULL	0	NULL	statement 2			occurs along with					statement 4					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1116_s_199	10764682	13  NF-kappaB is present in cytosol as a heterodimer composed of NF-kappaB1 (P50) and Rel (P65) subunits bound to an inhibitor protein, I-kappaB.	bind
25113	1	6589	7	NULL	NULL	NULL	NULL	NF-kappaB 	GP		is present in					cytosol	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1116_s_199	10764682	13  NF-kappaB is present in cytosol as a heterodimer composed of NF-kappaB1 (P50) and Rel (P65) subunits bound to an inhibitor protein, I-kappaB.	bind
25114	2	6589	7	NULL	NULL	NULL	NULL	NF-kappaB	GP		is composed of								P50 subunit		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1116_s_199	10764682	13  NF-kappaB is present in cytosol as a heterodimer composed of NF-kappaB1 (P50) and Rel (P65) subunits bound to an inhibitor protein, I-kappaB.	bind
25115	3	6589	7	NULL	NULL	NULL	NULL	NF-kappaB	GP		is composed of								P65 subunit		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1116_s_199	10764682	13  NF-kappaB is present in cytosol as a heterodimer composed of NF-kappaB1 (P50) and Rel (P65) subunits bound to an inhibitor protein, I-kappaB.	bind
25116	4	6589	7	NULL	NULL	NULL	NULL	NF-kappaB	GP		bind					 I-kappaB	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1116_s_199	10764682	13  NF-kappaB is present in cytosol as a heterodimer composed of NF-kappaB1 (P50) and Rel (P65) subunits bound to an inhibitor protein, I-kappaB.	bind
25117	5	6589	7	NULL	NULL	NULL	NULL	P50 subunit	GP		is					NF-kappaB1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1116_s_199	10764682	13  NF-kappaB is present in cytosol as a heterodimer composed of NF-kappaB1 (P50) and Rel (P65) subunits bound to an inhibitor protein, I-kappaB.	bind
25118	6	6589	7	NULL	NULL	NULL	NULL	P65 subunit	GP 		is					Rel	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1116_s_199	10764682	13  NF-kappaB is present in cytosol as a heterodimer composed of NF-kappaB1 (P50) and Rel (P65) subunits bound to an inhibitor protein, I-kappaB.	bind
32057	7	6589	7	NULL	NULL	NULL	NULL	NF-kappaB	GP		is a type of					heterodimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1116_s_199	10764682	13  NF-kappaB is present in cytosol as a heterodimer composed of NF-kappaB1 (P50) and Rel (P65) subunits bound to an inhibitor protein, I-kappaB.	bind
32058	8	6589	7	NULL	NULL	NULL	NULL	I-kappaB	GP		is a type of					inhibitor protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1116_s_199	10764682	13  NF-kappaB is present in cytosol as a heterodimer composed of NF-kappaB1 (P50) and Rel (P65) subunits bound to an inhibitor protein, I-kappaB.	bind
54454	9	6589	7	NULL	NULL	NULL	NULL	statement 2	Process		occurs along with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1116_s_199	10764682	13  NF-kappaB is present in cytosol as a heterodimer composed of NF-kappaB1 (P50) and Rel (P65) subunits bound to an inhibitor protein, I-kappaB.	bind
20779	1	6590	5	NULL	NULL	0	NULL	TRADD	NULL		bind	NULL		C-terminal portion		FADD	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_997_s_27	10702415	13  The C-terminal portion of TRADD binds the death domain-containing protein FADD, resulting in apoptosis.	bind
20781	2	6590	5	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				apoptosis	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_3_997_s_27	10702415	13  The C-terminal portion of TRADD binds the death domain-containing protein FADD, resulting in apoptosis.	bind
30309	3	6590	5	NULL	NULL	0	NULL	FADD	NULL		is a type of	NULL				death domain-containing protein	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_3_997_s_27	10702415	13  The C-terminal portion of TRADD binds the death domain-containing protein FADD, resulting in apoptosis.	bind
25119	1	6590	7	NULL	NULL	NULL	NULL	TRADD	GP		binds			C-terminal		FADD	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_997_s_27	10702415	13  The C-terminal portion of TRADD binds the death domain-containing protein FADD, resulting in apoptosis.	bind
25120	2	6590	7	NULL	NULL	NULL	NULL	statement 1	Process		results in					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_997_s_27	10702415	13  The C-terminal portion of TRADD binds the death domain-containing protein FADD, resulting in apoptosis.	bind
31441	3	6590	7	NULL	NULL	NULL	NULL	FADD	GP		is a type of					death domain-containing protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_997_s_27	10702415	13  The C-terminal portion of TRADD binds the death domain-containing protein FADD, resulting in apoptosis.	bind
20773	1	6591	5	NULL	NULL	0	NULL	decorin	NULL		bind	NULL				collagen	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_847_s_155	10195908	13  These experiments showed that when decorin was first allowed to bind to the collagen, binding of LDL to the decorin-collagen complex was >10 fold greaterR than to collagen alone.	bind
20774	2	6591	5	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				decorin-collagen complex	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_847_s_155	10195908	13  These experiments showed that when decorin was first allowed to bind to the collagen, binding of LDL to the decorin-collagen complex was >10 fold greaterR than to collagen alone.	bind
20775	3	6591	5	10	NULL	0	NULL	LDL	NULL		bind	NULL				collagen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_847_s_155	10195908	13  These experiments showed that when decorin was first allowed to bind to the collagen, binding of LDL to the decorin-collagen complex was >10 fold greaterR than to collagen alone.	bind
20776	4	6591	5	NULL	NULL	0	NULL	statement 2	NULL		greater than	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_847_s_155	10195908	13  These experiments showed that when decorin was first allowed to bind to the collagen, binding of LDL to the decorin-collagen complex was >10 fold greaterR than to collagen alone.	bind
20777	5	6591	5	NULL	NULL	0	NULL	statement 1	NULL		is required for	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_847_s_155	10195908	13  These experiments showed that when decorin was first allowed to bind to the collagen, binding of LDL to the decorin-collagen complex was >10 fold greaterR than to collagen alone.	bind
25121	1	6591	7	NULL	NULL	NULL	NULL	decorin 	GP		bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_847_s_155	10195908	13  These experiments showed that when decorin was first allowed to bind to the collagen, binding of LDL to the decorin-collagen complex was >10 fold greaterR than to collagen alone.	bind
25122	2	6591	7	NULL	NULL	NULL	NULL	LDL	GP		bind					decorin-collagen complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_847_s_155	10195908	13  These experiments showed that when decorin was first allowed to bind to the collagen, binding of LDL to the decorin-collagen complex was >10 fold greaterR than to collagen alone.	bind
25123	3	6591	7	NULL	NULL	NULL	NULL	LDL	GP		bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_847_s_155	10195908	13  These experiments showed that when decorin was first allowed to bind to the collagen, binding of LDL to the decorin-collagen complex was >10 fold greaterR than to collagen alone.	bind
25124	4	6591	7	NULL	NULL	NULL	NULL	statement 2	Process		is greater than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_847_s_155	10195908	13  These experiments showed that when decorin was first allowed to bind to the collagen, binding of LDL to the decorin-collagen complex was >10 fold greaterR than to collagen alone.	bind
20772	1	6592	5	10	NULL	0	NULL	thrombin			bind					hirudin-CD4					NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_24_2744_s_102	9851962	13  Thrombin binding to the hirudin-CD4 fusion protein was assessed after preincubation of the enzyme with either native hirudin, the tripeptide active site inhibitor PPACK, or a synthetic COOH-terminal hirudin dodecapeptide.	bind
54455	2	6592	5	10	NULL	0	NULL	hirudin-CD4			is a type of					fusion protein					NULL		0	NULL	NULL	NULL	gw60_circulation_98_24_2744_s_102	9851962	13  Thrombin binding to the hirudin-CD4 fusion protein was assessed after preincubation of the enzyme with either native hirudin, the tripeptide active site inhibitor PPACK, or a synthetic COOH-terminal hirudin dodecapeptide.	bind
25125	1	6592	7	NULL	NULL	NULL	NULL	Thrombin	GP		binds					hirudin-CD4	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_24_2744_s_102	9851962	13  Thrombin binding to the hirudin-CD4 fusion protein was assessed after preincubation of the enzyme with either native hirudin, the tripeptide active site inhibitor PPACK, or a synthetic COOH-terminal hirudin dodecapeptide.	bind
54456	2	6592	7	NULL	NULL	NULL	NULL	hirudin-CD4	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_24_2744_s_102	9851962	13  Thrombin binding to the hirudin-CD4 fusion protein was assessed after preincubation of the enzyme with either native hirudin, the tripeptide active site inhibitor PPACK, or a synthetic COOH-terminal hirudin dodecapeptide.	bind
20799	1	6593	5	NULL	NULL	0	NULL	TGF ligand	NULL		bind	NULL				type II receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_28	10934147	13  Type III receptor (also known as betaglycan) is a membrane-anchored proteoglycan that facilitates TGF ligand binding to the type II receptor.	bind
20800	2	6593	5	10	NULL	0	NULL	Type III receptor			is a synonym of					betaglycan					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_28	10934147	13  Type III receptor (also known as betaglycan) is a membrane-anchored proteoglycan that facilitates TGF ligand binding to the type II receptor.	bind
20801	3	6593	5	10	NULL	0	NULL	Type III receptor			facilitates					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_28	10934147	13  Type III receptor (also known as betaglycan) is a membrane-anchored proteoglycan that facilitates TGF ligand binding to the type II receptor.	bind
54457	4	6593	5	10	NULL	0	NULL	Type III receptor			is a type of					membrane-anchored proteoglycan					NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_28	10934147	13  Type III receptor (also known as betaglycan) is a membrane-anchored proteoglycan that facilitates TGF ligand binding to the type II receptor.	bind
25126	1	6593	7	NULL	NULL	NULL	NULL	 TGF ligand	GP		bind					type II receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_28	10934147	13  Type III receptor (also known as betaglycan) is a membrane-anchored proteoglycan that facilitates TGF ligand binding to the type II receptor.	bind
25127	2	6593	7	NULL	NULL	NULL	NULL	Type III receptor	GP		facilitates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_28	10934147	13  Type III receptor (also known as betaglycan) is a membrane-anchored proteoglycan that facilitates TGF ligand binding to the type II receptor.	bind
25128	3	6593	7	NULL	NULL	NULL	NULL	Type III receptor	GP		is 					betaglycan	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_28	10934147	13  Type III receptor (also known as betaglycan) is a membrane-anchored proteoglycan that facilitates TGF ligand binding to the type II receptor.	bind
54458	4	6593	7	NULL	NULL	NULL	NULL	Type III receptor	GP		is a type of					membrane-anchored proteoglycan	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_28	10934147	13  Type III receptor (also known as betaglycan) is a membrane-anchored proteoglycan that facilitates TGF ligand binding to the type II receptor.	bind
20805	1	6594	5	NULL	NULL	0	NULL	VEGF	NULL		bind	NULL				Flk-1	NULL				NULL	in endothelial cells	NULL	NULL	NULL	NULL	gw60_circulationres_85_2_192_s_36	10417401	13  VEGF binding to receptor tyrosinekinase  Flk-1 and Flt-1 14  expressed in endothelial cells is required for normal vascularization.	bind
20806	2	6594	5	NULL	NULL	0	NULL	VEGF	NULL		bind	NULL				Flt-1	NULL				NULL	in endothelial cells	NULL	NULL	NULL	NULL	gw60_circulationres_85_2_192_s_36	10417401	13  VEGF binding to receptor tyrosinekinase  Flk-1 and Flt-1 14  expressed in endothelial cells is required for normal vascularization.	bind
20807	3	6594	5	NULL	NULL	0	NULL	statement 1	NULL		is required for	NULL				normal vascularization	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_2_192_s_36	10417401	13  VEGF binding to receptor tyrosinekinase  Flk-1 and Flt-1 14  expressed in endothelial cells is required for normal vascularization.	bind
20809	4	6594	5	NULL	NULL	0	NULL	statement 2	NULL		is required for	NULL				normal vascularization	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_2_192_s_36	10417401	13  VEGF binding to receptor tyrosinekinase  Flk-1 and Flt-1 14  expressed in endothelial cells is required for normal vascularization.	bind
54459	5	6594	5	10	NULL	0	NULL	Flk-1			is a type of					receptor tyrosinekinase					NULL		0	NULL	NULL	NULL	gw60_circulationres_85_2_192_s_36	10417401	13  VEGF binding to receptor tyrosinekinase  Flk-1 and Flt-1 14  expressed in endothelial cells is required for normal vascularization.	bind
54460	6	6594	5	10	NULL	0	NULL	Flt-1			is a type of					receptor tyrosinekinase					NULL		0	NULL	NULL	NULL	gw60_circulationres_85_2_192_s_36	10417401	13  VEGF binding to receptor tyrosinekinase  Flk-1 and Flt-1 14  expressed in endothelial cells is required for normal vascularization.	bind
25129	1	6594	7	NULL	NULL	NULL	NULL	VEGF	GP		binds to					 Flk-1	GP				NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_circulationres_85_2_192_s_36	10417401	13  VEGF binding to receptor tyrosinekinase  Flk-1 and Flt-1 14  expressed in endothelial cells is required for normal vascularization.	bind
25130	2	6594	7	NULL	NULL	NULL	NULL	VEGF	GP		binds to					 Flt-1	GP				NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_circulationres_85_2_192_s_36	10417401	13  VEGF binding to receptor tyrosinekinase  Flk-1 and Flt-1 14  expressed in endothelial cells is required for normal vascularization.	bind
25131	3	6594	7	NULL	NULL	NULL	NULL	statement 1	Process		is required for					normal vascularization	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_2_192_s_36	10417401	13  VEGF binding to receptor tyrosinekinase  Flk-1 and Flt-1 14  expressed in endothelial cells is required for normal vascularization.	bind
25132	4	6594	7	NULL	NULL	NULL	NULL	statement 2	Process		is required for					normal vascularization	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_2_192_s_36	10417401	13  VEGF binding to receptor tyrosinekinase  Flk-1 and Flt-1 14  expressed in endothelial cells is required for normal vascularization.	bind
31442	5	6594	7	NULL	NULL	NULL	NULL	 Flk-1	GP		is a type of					receptor tyrosinekinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_2_192_s_36	10417401	13  VEGF binding to receptor tyrosinekinase  Flk-1 and Flt-1 14  expressed in endothelial cells is required for normal vascularization.	bind
31443	6	6594	7	NULL	NULL	NULL	NULL	Flt-1	GP		is a type of					receptor tyrosine kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_2_192_s_36	10417401	13  VEGF binding to receptor tyrosinekinase  Flk-1 and Flt-1 14  expressed in endothelial cells is required for normal vascularization.	bind
20808	1	6595	5	NULL	NULL	0	NULL	VEGF-D	NULL		is a ligand for	NULL				VEGFR-2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_74	9665459	13  VEGF-D is a ligand for both VEGFR-2 and VEGFR-3, but does not bind to the VEGFR-1.	bind
20810	2	6595	5	NULL	NULL	0	NULL	VEGF-D	NULL		is a ligand for	NULL				VEGFR-3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_74	9665459	13  VEGF-D is a ligand for both VEGFR-2 and VEGFR-3, but does not bind to the VEGFR-1.	bind
20811	3	6595	5	NULL	NULL	0	NULL	VEGF-D	NULL		does not bind	NULL				VEGFR-1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_74	9665459	13  VEGF-D is a ligand for both VEGFR-2 and VEGFR-3, but does not bind to the VEGFR-1.	bind
25135	1	6595	7	NULL	NULL	NULL	NULL	VEGF-D	GP		is a ligand for					VEGFR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_74	9665459	13  VEGF-D is a ligand for both VEGFR-2 and VEGFR-3, but does not bind to the VEGFR-1.	bind
25136	2	6595	7	NULL	NULL	NULL	NULL	VEGF-D	GP		is a ligand for					VEGFR-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_74	9665459	13  VEGF-D is a ligand for both VEGFR-2 and VEGFR-3, but does not bind to the VEGFR-1.	bind
25137	3	6595	7	NULL	NULL	NULL	NULL	VEGF-D	GP		does not bind					VEGFR-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_1_11_s_74	9665459	13  VEGF-D is a ligand for both VEGFR-2 and VEGFR-3, but does not bind to the VEGFR-1.	bind
20812	1	6597	5	NULL	NULL	0	NULL	LPS	NULL		bind	NULL				CD14	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_32	12427659	13 -  15 In vitro studies indicate that the strong proinflammatory response of monocyte/macrophages and neutrophils to LPS requires binding of LPS to CD14 and, at a minimum, TLR4/MD2 for signaling.	bind
20815	2	6597	5	NULL	NULL	0	NULL	LPS	NULL		induces	NULL				proinflammatory response	NULL	strong			NULL	monocyte/macrophages in vitro	NULL	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_32	12427659	13 -  15 In vitro studies indicate that the strong proinflammatory response of monocyte/macrophages and neutrophils to LPS requires binding of LPS to CD14 and, at a minimum, TLR4/MD2 for signaling.	bind
20816	3	6597	5	NULL	NULL	0	NULL	LPS	NULL		induces	NULL				proinflammatory response	NULL	strong			NULL	neutrophils in vitro	NULL	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_32	12427659	13 -  15 In vitro studies indicate that the strong proinflammatory response of monocyte/macrophages and neutrophils to LPS requires binding of LPS to CD14 and, at a minimum, TLR4/MD2 for signaling.	bind
20817	4	6597	5	NULL	NULL	0	NULL	statement 2	NULL		requires	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_32	12427659	13 -  15 In vitro studies indicate that the strong proinflammatory response of monocyte/macrophages and neutrophils to LPS requires binding of LPS to CD14 and, at a minimum, TLR4/MD2 for signaling.	bind
20818	5	6597	5	NULL	NULL	0	NULL	statement 3	NULL		requires	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_32	12427659	13 -  15 In vitro studies indicate that the strong proinflammatory response of monocyte/macrophages and neutrophils to LPS requires binding of LPS to CD14 and, at a minimum, TLR4/MD2 for signaling.	bind
20819	6	6597	5	10	NULL	0	NULL	statement 2			requires					TLR4/MD2		signaling of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_32	12427659	13 -  15 In vitro studies indicate that the strong proinflammatory response of monocyte/macrophages and neutrophils to LPS requires binding of LPS to CD14 and, at a minimum, TLR4/MD2 for signaling.	bind
20820	7	6597	5	10	NULL	0	NULL	statement 3			requires					TLR4/MD2		signaling of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_32	12427659	13 -  15 In vitro studies indicate that the strong proinflammatory response of monocyte/macrophages and neutrophils to LPS requires binding of LPS to CD14 and, at a minimum, TLR4/MD2 for signaling.	bind
25322	1	6597	7	NULL	NULL	NULL	NULL	LPS	Chemical		bind					CD14	Cell				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_32	12427659	13 -  15 In vitro studies indicate that the strong proinflammatory response of monocyte/macrophages and neutrophils to LPS requires binding of LPS to CD14 and, at a minimum, TLR4/MD2 for signaling.	bind
25323	3	6597	7	NULL	NULL	NULL	NULL	statement 2	Process		requires					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_32	12427659	13 -  15 In vitro studies indicate that the strong proinflammatory response of monocyte/macrophages and neutrophils to LPS requires binding of LPS to CD14 and, at a minimum, TLR4/MD2 for signaling.	bind
25324	5	6597	7	NULL	NULL	NULL	NULL	statement 4	Process		requires					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_32	12427659	13 -  15 In vitro studies indicate that the strong proinflammatory response of monocyte/macrophages and neutrophils to LPS requires binding of LPS to CD14 and, at a minimum, TLR4/MD2 for signaling.	bind
25325	6	6597	7	NULL	NULL	NULL	NULL	statement 2	Process		requires					TLR4/MD2 	GP	signaling of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_32	12427659	13 -  15 In vitro studies indicate that the strong proinflammatory response of monocyte/macrophages and neutrophils to LPS requires binding of LPS to CD14 and, at a minimum, TLR4/MD2 for signaling.	bind
25326	7	6597	7	NULL	NULL	NULL	NULL	statement 4	Process		requires					TLR4/MD2 	GP	signaling of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_32	12427659	13 -  15 In vitro studies indicate that the strong proinflammatory response of monocyte/macrophages and neutrophils to LPS requires binding of LPS to CD14 and, at a minimum, TLR4/MD2 for signaling.	bind
25327	2	6597	7	NULL	NULL	NULL	NULL	LPS	Chemical		induces		strong			proinflammatory response	Process				NULL	monocyte/macrophages, in vitro	NULL	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_32	12427659	13 -  15 In vitro studies indicate that the strong proinflammatory response of monocyte/macrophages and neutrophils to LPS requires binding of LPS to CD14 and, at a minimum, TLR4/MD2 for signaling.	bind
25328	4	6597	7	NULL	NULL	NULL	NULL	LPS	Chemical		induces		strong			proinflammatory response	Process				NULL	neutrophils, in vitro	NULL	NULL	NULL	NULL	gw60_circulation_106_20_2608_s_32	12427659	13 -  15 In vitro studies indicate that the strong proinflammatory response of monocyte/macrophages and neutrophils to LPS requires binding of LPS to CD14 and, at a minimum, TLR4/MD2 for signaling.	bind
20821	1	6598	5	10	NULL	0	NULL	GATA-6			bind					SM-MHC		rat;;conserved		GATA-like motif within promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_23	12615657	13 -  15 We have recently demonstrated that GATA-6 binds a conserved GATA-like motif within the rat SM-MHC promoter and activates this promoter in a sequence-specific manner.	bind
20823	2	6598	5	10	NULL	0	NULL	statement 1			activates		sequence specifically			SM-MHC 		rat		promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_23	12615657	13 -  15 We have recently demonstrated that GATA-6 binds a conserved GATA-like motif within the rat SM-MHC promoter and activates this promoter in a sequence-specific manner.	bind
25329	1	6598	7	NULL	NULL	NULL	NULL	GATA-6	GP		binds					SM-MHC	GP	rat;;conserved		GATA-like motif within the promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_23	12615657	13 -  15 We have recently demonstrated that GATA-6 binds a conserved GATA-like motif within the rat SM-MHC promoter and activates this promoter in a sequence-specific manner.	bind
25330	2	6598	7	NULL	NULL	NULL	NULL	statement 1	Process		activates		sequence specifically			SM-MHC	GP	rat		promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_404_s_23	12615657	13 -  15 We have recently demonstrated that GATA-6 binds a conserved GATA-like motif within the rat SM-MHC promoter and activates this promoter in a sequence-specific manner.	bind
20854	1	6599	5	NULL	NULL	0	NULL	platelet subpopulations	NULL		contains	NULL				FV	NULL	distinct levels of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_28	15653564	13 - 16    Previous studies have shown that the combination of convulxin, a GPVI agonist, and thrombin leads to 2 platelet subpopulations with distinct levels of alpha-granule factor V (FV), and this may be related to serotonin and fibrinogen binding.	bind
20856	2	6599	5	NULL	NULL	0	NULL	FV	NULL		is	NULL				alpha-granule factor V	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_28	15653564	13 - 16    Previous studies have shown that the combination of convulxin, a GPVI agonist, and thrombin leads to 2 platelet subpopulations with distinct levels of alpha-granule factor V (FV), and this may be related to serotonin and fibrinogen binding.	bind
20857	3	6599	5	NULL	NULL	0	NULL	convulxin	NULL		leads to	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_28	15653564	13 - 16    Previous studies have shown that the combination of convulxin, a GPVI agonist, and thrombin leads to 2 platelet subpopulations with distinct levels of alpha-granule factor V (FV), and this may be related to serotonin and fibrinogen binding.	bind
20858	4	6599	5	NULL	NULL	0	NULL	convulxin	NULL		is a type of	NULL				GPVI agonist	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_28	15653564	13 - 16    Previous studies have shown that the combination of convulxin, a GPVI agonist, and thrombin leads to 2 platelet subpopulations with distinct levels of alpha-granule factor V (FV), and this may be related to serotonin and fibrinogen binding.	bind
20859	5	6599	5	NULL	NULL	0	NULL	thrombin	NULL		leads to	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_28	15653564	13 - 16    Previous studies have shown that the combination of convulxin, a GPVI agonist, and thrombin leads to 2 platelet subpopulations with distinct levels of alpha-granule factor V (FV), and this may be related to serotonin and fibrinogen binding.	bind
20860	6	6599	5	10	NULL	0	NULL	statement 3			occurs in combination with					statement 5					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_28	15653564	13 - 16    Previous studies have shown that the combination of convulxin, a GPVI agonist, and thrombin leads to 2 platelet subpopulations with distinct levels of alpha-granule factor V (FV), and this may be related to serotonin and fibrinogen binding.	bind
20861	7	6599	5	10	NULL	0	NULL	statement 6			related to		may be			fibrinogen		binding of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_28	15653564	13 - 16    Previous studies have shown that the combination of convulxin, a GPVI agonist, and thrombin leads to 2 platelet subpopulations with distinct levels of alpha-granule factor V (FV), and this may be related to serotonin and fibrinogen binding.	bind
20866	8	6599	5	10	NULL	0	NULL	statement 6			related to		may be			serotonin		binding of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_28	15653564	13 - 16    Previous studies have shown that the combination of convulxin, a GPVI agonist, and thrombin leads to 2 platelet subpopulations with distinct levels of alpha-granule factor V (FV), and this may be related to serotonin and fibrinogen binding.	bind
25331	1	6599	7	NULL	NULL	NULL	NULL	Platelet subpopulations	Cell		contain					FV	GP	distinct levels of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_28	15653564	13 - 16    Previous studies have shown that the combination of convulxin, a GPVI agonist, and thrombin leads to 2 platelet subpopulations with distinct levels of alpha-granule factor V (FV), and this may be related to serotonin and fibrinogen binding.	bind
25332	4	6599	7	NULL	NULL	NULL	NULL	thrombin	GP		leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_28	15653564	13 - 16    Previous studies have shown that the combination of convulxin, a GPVI agonist, and thrombin leads to 2 platelet subpopulations with distinct levels of alpha-granule factor V (FV), and this may be related to serotonin and fibrinogen binding.	bind
25333	5	6599	7	NULL	NULL	NULL	NULL	statement 2	Process		occurs in combination with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_28	15653564	13 - 16    Previous studies have shown that the combination of convulxin, a GPVI agonist, and thrombin leads to 2 platelet subpopulations with distinct levels of alpha-granule factor V (FV), and this may be related to serotonin and fibrinogen binding.	bind
25334	6	6599	7	NULL	NULL	NULL	NULL	FV	GP		is					alpha-granule factor V	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_28	15653564	13 - 16    Previous studies have shown that the combination of convulxin, a GPVI agonist, and thrombin leads to 2 platelet subpopulations with distinct levels of alpha-granule factor V (FV), and this may be related to serotonin and fibrinogen binding.	bind
25336	7	6599	7	NULL	NULL	NULL	NULL	statement 5	Process		be related to		may			serotonin	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_28	15653564	13 - 16    Previous studies have shown that the combination of convulxin, a GPVI agonist, and thrombin leads to 2 platelet subpopulations with distinct levels of alpha-granule factor V (FV), and this may be related to serotonin and fibrinogen binding.	bind
25859	2	6599	7	NULL	NULL	NULL	NULL	convulxin	GP		leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_28	15653564	13 - 16    Previous studies have shown that the combination of convulxin, a GPVI agonist, and thrombin leads to 2 platelet subpopulations with distinct levels of alpha-granule factor V (FV), and this may be related to serotonin and fibrinogen binding.	bind
25860	3	6599	7	NULL	NULL	NULL	NULL	convulxin	GP		is a type of					GPVI agonist	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_28	15653564	13 - 16    Previous studies have shown that the combination of convulxin, a GPVI agonist, and thrombin leads to 2 platelet subpopulations with distinct levels of alpha-granule factor V (FV), and this may be related to serotonin and fibrinogen binding.	bind
25861	8	6599	7	NULL	NULL	NULL	NULL	statement 5	Process		be related to		may			fibrinogen	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_28	15653564	13 - 16    Previous studies have shown that the combination of convulxin, a GPVI agonist, and thrombin leads to 2 platelet subpopulations with distinct levels of alpha-granule factor V (FV), and this may be related to serotonin and fibrinogen binding.	bind
20825	1	6600	5	13	NULL	NULL	NULL	myosin subfragments	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_6_661_s_27	9742062	13 14  In support of this hypothesis was the finding that the binding of myosin subfragments to actin is enhanced in the presence of caldesmon.	bind
20826	2	6600	5	13	NULL	NULL	NULL	caldesmon	GP		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_6_661_s_27	9742062	13 14  In support of this hypothesis was the finding that the binding of myosin subfragments to actin is enhanced in the presence of caldesmon.	bind
67196	1	6600	5	13	NULL	NULL	NULL	myosin subfragments	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_6_661_s_27	9742062	13 14  In support of this hypothesis was the finding that the binding of myosin subfragments to actin is enhanced in the presence of caldesmon.	bind
25337	1	6600	7	NULL	NULL	NULL	NULL	myosin subfragments	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_6_661_s_27	9742062	13 14  In support of this hypothesis was the finding that the binding of myosin subfragments to actin is enhanced in the presence of caldesmon.	bind
25338	2	6600	7	13	NULL	NULL	NULL	caldesmon	GP		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_6_661_s_27	9742062	13 14  In support of this hypothesis was the finding that the binding of myosin subfragments to actin is enhanced in the presence of caldesmon.	bind
20869	1	6601	5	13	NULL	NULL	NULL	OPN	GP		bind		directly			collagen I	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
20870	2	6601	5	13	NULL	NULL	NULL	OPN	GP		interacts with					collagen II	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
20871	3	6601	5	13	NULL	NULL	NULL	OPN	GP		interacts with					collagen III	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
20872	4	6601	5	13	NULL	NULL	NULL	OPN	GP		interacts with					collagen IV	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
20873	5	6601	5	13	NULL	NULL	NULL	OPN	GP		interacts with					collagen V	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
20874	6	6601	5	13	NULL	NULL	NULL	OPN	GP		interacts with					fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
56119	7	6601	5	13	NULL	NULL	NULL	collagen	GP		is disorganized in					OPN	GP	mice lacking			NULL	models of skin incision/wound healing	NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
56120	8	6601	5	13	NULL	NULL	NULL	collagen	GP		is disorganized in					OPN	GP	mice lacking			NULL	obstructive uropathy	NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
56121	9	6601	5	13	NULL	NULL	NULL	collagen I	GP		decrease in					OPN	GP	mice lacking			NULL	models of skin incision/wound healing	NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
56122	10	6601	5	13	NULL	NULL	NULL	collagen	GP		decrease in					OPN	GP	mice lacking			NULL	obstructive uropathy	NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
18532	1	6601	6	13	NULL	NULL	NULL	OPN	GP		bind		directly			collagen I	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
18533	2	6601	6	13	NULL	NULL	NULL	OPN	GP		interacts with					collagen II	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
18534	3	6601	6	13	NULL	NULL	NULL	OPN	GP		interacts with					collagen III	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
18535	4	6601	6	13	NULL	NULL	NULL	OPN	GP		interacts with					collagen IV	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
18536	5	6601	6	13	NULL	NULL	NULL	OPN	GP		interacts with					collagen V	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
18537	6	6601	6	13	NULL	NULL	NULL	OPN	GP		interacts with					fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
56123	7	6601	6	13	NULL	NULL	NULL	collagen	GP		is disorganized in					OPN	GP	mice lacking			NULL	models of skin incision/wound healing	NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
56124	8	6601	6	13	NULL	NULL	NULL	collagen	GP		is disorganized in					OPN	GP	mice lacking			NULL	obstructive uropathy	NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
56125	9	6601	6	13	NULL	NULL	NULL	collagen I	GP		decrease in					OPN	GP	mice lacking			NULL	models of skin incision/wound healing	NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
56126	10	6601	6	13	NULL	NULL	NULL	collagen I	GP		decrease in					OPN	GP	mice lacking			NULL	obstructive uropathy	NULL	NULL	NULL	NULL	gw60_circulationres_88_10_1080_s_229	11375279	13 14  In the models of skin incision/wound healing and in obstructive uropathy, disorganization of collagen and decreases in collagen I content were observed in mice lacking OPN. 13 14  OPN can bind directly to collagen I and interacts with collagen II, III, IV, V, and fibronectin.	bind
18663	1	6602	6	13	NULL	NULL	NULL	NAD(H)	Chemical		bind					IDH2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_2_1204_s_215	11042198	13 and  14; summarized in Table  III) consistent with these designations of catalytic  versus regulatory function include ( a) substitutions for active site serine residues corresponding to bacterial Ser-113 that reduce catalytic activity (IDH2 S98A)  versus cooperativity and AMP activation (IDH1 S92A) and ( b) substitutions for adjacent residues corresponding to bacterial residues known to be important for cofactor specificity ( 25) that eliminate apparent binding of NAD(H) by IDH2 (D286A/I287A)  versus of AMP by IDH1 (D279A/I280A).	bind
18664	2	6602	6	13	NULL	NULL	NULL			substitution of	eliminates			D286A/I287A		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_2_1204_s_215	11042198	13 and  14; summarized in Table  III) consistent with these designations of catalytic  versus regulatory function include ( a) substitutions for active site serine residues corresponding to bacterial Ser-113 that reduce catalytic activity (IDH2 S98A)  versus cooperativity and AMP activation (IDH1 S92A) and ( b) substitutions for adjacent residues corresponding to bacterial residues known to be important for cofactor specificity ( 25) that eliminate apparent binding of NAD(H) by IDH2 (D286A/I287A)  versus of AMP by IDH1 (D279A/I280A).	bind
18740	3	6602	6	13	NULL	NULL	NULL	AMP	Chemical		bind					IDH1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_2_1204_s_215	11042198	13 and  14; summarized in Table  III) consistent with these designations of catalytic  versus regulatory function include ( a) substitutions for active site serine residues corresponding to bacterial Ser-113 that reduce catalytic activity (IDH2 S98A)  versus cooperativity and AMP activation (IDH1 S92A) and ( b) substitutions for adjacent residues corresponding to bacterial residues known to be important for cofactor specificity ( 25) that eliminate apparent binding of NAD(H) by IDH2 (D286A/I287A)  versus of AMP by IDH1 (D279A/I280A).	bind
18741	4	6602	6	13	NULL	NULL	NULL			substitution of	eliminates			D279A/I280A		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_2_1204_s_215	11042198	13 and  14; summarized in Table  III) consistent with these designations of catalytic  versus regulatory function include ( a) substitutions for active site serine residues corresponding to bacterial Ser-113 that reduce catalytic activity (IDH2 S98A)  versus cooperativity and AMP activation (IDH1 S92A) and ( b) substitutions for adjacent residues corresponding to bacterial residues known to be important for cofactor specificity ( 25) that eliminate apparent binding of NAD(H) by IDH2 (D286A/I287A)  versus of AMP by IDH1 (D279A/I280A).	bind
24750	1	6603	5	13	NULL	NULL	NULL	MyBP-C	GP		modulates					myosin crossbridges	CellComponent	range of movement of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_8_752_s_140	14500336	13 Based on these results, a model was proposed in which MyBP-C modulates the range of movement of myosin crossbridges, perhaps by tethering the crossbridges to the thick filament backbone, so that following MyBP-C extraction crossbridges are less constrained and the probability of myosin binding to actin is increased.	bind
24752	2	6603	5	13	NULL	NULL	NULL	myosin crossbridges	CellComponent		is tethered to					filament backbone	CellComponent	thick			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_8_752_s_140	14500336	13 Based on these results, a model was proposed in which MyBP-C modulates the range of movement of myosin crossbridges, perhaps by tethering the crossbridges to the thick filament backbone, so that following MyBP-C extraction crossbridges are less constrained and the probability of myosin binding to actin is increased.	bind
24753	3	6603	5	13	NULL	NULL	NULL	statement 1	Process		occurs by		perhaps			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_8_752_s_140	14500336	13 Based on these results, a model was proposed in which MyBP-C modulates the range of movement of myosin crossbridges, perhaps by tethering the crossbridges to the thick filament backbone, so that following MyBP-C extraction crossbridges are less constrained and the probability of myosin binding to actin is increased.	bind
24754	4	6603	5	13	NULL	NULL	NULL	MyBP-C	GP	extraction of	leads to					crossbridges	CellComponent	less constrained			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_8_752_s_140	14500336	13 Based on these results, a model was proposed in which MyBP-C modulates the range of movement of myosin crossbridges, perhaps by tethering the crossbridges to the thick filament backbone, so that following MyBP-C extraction crossbridges are less constrained and the probability of myosin binding to actin is increased.	bind
24755	5	6603	5	13	NULL	NULL	NULL	myosin	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_8_752_s_140	14500336	13 Based on these results, a model was proposed in which MyBP-C modulates the range of movement of myosin crossbridges, perhaps by tethering the crossbridges to the thick filament backbone, so that following MyBP-C extraction crossbridges are less constrained and the probability of myosin binding to actin is increased.	bind
24756	6	6603	5	13	NULL	NULL	NULL	MyBP-C	GP	extraction of	leads to					statement 5	Process	increased probability of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_8_752_s_140	14500336	13 Based on these results, a model was proposed in which MyBP-C modulates the range of movement of myosin crossbridges, perhaps by tethering the crossbridges to the thick filament backbone, so that following MyBP-C extraction crossbridges are less constrained and the probability of myosin binding to actin is increased.	bind
18541	1	6603	6	13	NULL	NULL	NULL	myosin	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_8_752_s_140	14500336	13 Based on these results, a model was proposed in which MyBP-C modulates the range of movement of myosin crossbridges, perhaps by tethering the crossbridges to the thick filament backbone, so that following MyBP-C extraction crossbridges are less constrained and the probability of myosin binding to actin is increased.	bind
30284	2	6603	6	13	NULL	NULL	NULL	MyBP-C	GP		modulates		may			myosin crossbridges	CellComponent	range of movement of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_8_752_s_140	14500336	13 Based on these results, a model was proposed in which MyBP-C modulates the range of movement of myosin crossbridges, perhaps by tethering the crossbridges to the thick filament backbone, so that following MyBP-C extraction crossbridges are less constrained and the probability of myosin binding to actin is increased.	bind
30285	3	6603	6	13	NULL	NULL	NULL	myosin crossbridges	CellComponent		are tethered to		perhaps			filament backbone	CellComponent	thick			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_8_752_s_140	14500336	13 Based on these results, a model was proposed in which MyBP-C modulates the range of movement of myosin crossbridges, perhaps by tethering the crossbridges to the thick filament backbone, so that following MyBP-C extraction crossbridges are less constrained and the probability of myosin binding to actin is increased.	bind
30286	4	6603	6	13	NULL	NULL	NULL	MyBP-C	GP		modulates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_8_752_s_140	14500336	13 Based on these results, a model was proposed in which MyBP-C modulates the range of movement of myosin crossbridges, perhaps by tethering the crossbridges to the thick filament backbone, so that following MyBP-C extraction crossbridges are less constrained and the probability of myosin binding to actin is increased.	bind
30311	5	6603	6	13	NULL	NULL	NULL	MyBP-C	GP	extraction of	leads to					crossbridges	CellComponent	less constrained			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_8_752_s_140	14500336	13 Based on these results, a model was proposed in which MyBP-C modulates the range of movement of myosin crossbridges, perhaps by tethering the crossbridges to the thick filament backbone, so that following MyBP-C extraction crossbridges are less constrained and the probability of myosin binding to actin is increased.	bind
56131	6	6603	6	13	NULL	NULL	NULL	MyBP-C	GP	extraction of	increase					statement 1	Process	probability of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_8_752_s_140	14500336	13 Based on these results, a model was proposed in which MyBP-C modulates the range of movement of myosin crossbridges, perhaps by tethering the crossbridges to the thick filament backbone, so that following MyBP-C extraction crossbridges are less constrained and the probability of myosin binding to actin is increased.	bind
24757	1	6604	5	13	NULL	NULL	NULL	PAI-1	GP	mutant	bind		normally			vitronectin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_365_s_157	15576638	13 In an experimental model of glomerulonephritis, intravenous administration of a mutant PAI-1 that binds vitronectin normally but lacks protease inhibitory activity, restored plasmin generation, and reduced matrix accumulation of collagen I, collagen III, fibronectin, and laminin.	bind
24758	2	6604	5	13	NULL	NULL	NULL	PAI-1	GP	mutant	lacks					protease inhibitory activity					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_365_s_157	15576638	13 In an experimental model of glomerulonephritis, intravenous administration of a mutant PAI-1 that binds vitronectin normally but lacks protease inhibitory activity, restored plasmin generation, and reduced matrix accumulation of collagen I, collagen III, fibronectin, and laminin.	bind
24759	3	6604	5	13	NULL	NULL	NULL	PAI-1	GP	mutant	restored					plasmin	GP	generation of			NULL	in an experimental model of glomerulonephritis	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_365_s_157	15576638	13 In an experimental model of glomerulonephritis, intravenous administration of a mutant PAI-1 that binds vitronectin normally but lacks protease inhibitory activity, restored plasmin generation, and reduced matrix accumulation of collagen I, collagen III, fibronectin, and laminin.	bind
24760	4	6604	5	13	NULL	NULL	NULL	PAI-1	GP	mutant	reduces					collagen I	GP	matrix accumulation of			NULL	in an experimental model of glomerulonephritis	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_365_s_157	15576638	13 In an experimental model of glomerulonephritis, intravenous administration of a mutant PAI-1 that binds vitronectin normally but lacks protease inhibitory activity, restored plasmin generation, and reduced matrix accumulation of collagen I, collagen III, fibronectin, and laminin.	bind
24761	5	6604	5	13	NULL	NULL	NULL	PAI-1	GP	mutant	reduces					collagen III	GP	matrix accumulation of			NULL	in an experimental model of glomerulonephritis	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_365_s_157	15576638	13 In an experimental model of glomerulonephritis, intravenous administration of a mutant PAI-1 that binds vitronectin normally but lacks protease inhibitory activity, restored plasmin generation, and reduced matrix accumulation of collagen I, collagen III, fibronectin, and laminin.	bind
24762	6	6604	5	13	NULL	NULL	NULL	PAI-1	GP	mutant	reduces					fibronectin	GP	matrix accumulation of			NULL	in an experimental model of glomerulonephritis	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_365_s_157	15576638	13 In an experimental model of glomerulonephritis, intravenous administration of a mutant PAI-1 that binds vitronectin normally but lacks protease inhibitory activity, restored plasmin generation, and reduced matrix accumulation of collagen I, collagen III, fibronectin, and laminin.	bind
24763	7	6604	5	13	NULL	NULL	NULL	PAI-1	GP	mutant	reduces					laminin	GP	matrix accumulation of			NULL	in an experimental model of glomerulonephritis	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_365_s_157	15576638	13 In an experimental model of glomerulonephritis, intravenous administration of a mutant PAI-1 that binds vitronectin normally but lacks protease inhibitory activity, restored plasmin generation, and reduced matrix accumulation of collagen I, collagen III, fibronectin, and laminin.	bind
18543	1	6604	6	13	NULL	NULL	NULL	PAI-1	GP	mutant	bind					vitronectin	GP				NULL	experimental model of glomerulonephritis	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_365_s_157	15576638	13 In an experimental model of glomerulonephritis, intravenous administration of a mutant PAI-1 that binds vitronectin normally but lacks protease inhibitory activity, restored plasmin generation, and reduced matrix accumulation of collagen I, collagen III, fibronectin, and laminin.	bind
18598	2	6604	6	13	NULL	NULL	NULL	PAI-1	GP	mutant	lacks					protease inhibitory activity					NULL	experimental model of glomerulonephritis	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_365_s_157	15576638	13 In an experimental model of glomerulonephritis, intravenous administration of a mutant PAI-1 that binds vitronectin normally but lacks protease inhibitory activity, restored plasmin generation, and reduced matrix accumulation of collagen I, collagen III, fibronectin, and laminin.	bind
18599	3	6604	6	13	NULL	NULL	NULL	PAI-1	GP	mutant	restored					plasmin	GP	generation of			NULL	experimental model of glomerulonephritis	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_365_s_157	15576638	13 In an experimental model of glomerulonephritis, intravenous administration of a mutant PAI-1 that binds vitronectin normally but lacks protease inhibitory activity, restored plasmin generation, and reduced matrix accumulation of collagen I, collagen III, fibronectin, and laminin.	bind
18600	4	6604	6	13	NULL	NULL	NULL	PAI-1	GP	mutant	reduced					collagen I	GP	matrix accumulation of 			NULL	experimental model of glomerulonephritis	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_365_s_157	15576638	13 In an experimental model of glomerulonephritis, intravenous administration of a mutant PAI-1 that binds vitronectin normally but lacks protease inhibitory activity, restored plasmin generation, and reduced matrix accumulation of collagen I, collagen III, fibronectin, and laminin.	bind
18601	5	6604	6	13	NULL	NULL	NULL	PAI-1	GP	mutant	reduced					collagen III	GP	matrix accumulation of			NULL	experimental model of glomerulonephritis	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_365_s_157	15576638	13 In an experimental model of glomerulonephritis, intravenous administration of a mutant PAI-1 that binds vitronectin normally but lacks protease inhibitory activity, restored plasmin generation, and reduced matrix accumulation of collagen I, collagen III, fibronectin, and laminin.	bind
18602	6	6604	6	13	NULL	NULL	NULL	PAI-1	GP	mutant	reduced					fibronectin	GP	matrix accumulation of			NULL	experimental model of glomerulonephritis	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_365_s_157	15576638	13 In an experimental model of glomerulonephritis, intravenous administration of a mutant PAI-1 that binds vitronectin normally but lacks protease inhibitory activity, restored plasmin generation, and reduced matrix accumulation of collagen I, collagen III, fibronectin, and laminin.	bind
18603	7	6604	6	13	NULL	NULL	NULL	PAI-1	GP	mutant	reduced					laminin	GP	matrix accumulation of			NULL	experimental model of glomerulonephritis	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_365_s_157	15576638	13 In an experimental model of glomerulonephritis, intravenous administration of a mutant PAI-1 that binds vitronectin normally but lacks protease inhibitory activity, restored plasmin generation, and reduced matrix accumulation of collagen I, collagen III, fibronectin, and laminin.	bind
20879	1	6605	5	13	NULL	NULL	NULL	apoA-I	GP	human	bind					lipid hydroperoxides	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1325_s_57	15831812	13 It was concluded that human apoA-I binds lipid hydroperoxides in such a manner that the lipid hydroperoxides can still participate in the formation of oxidized phospholipids if the apoA-I-lipid hydroperoxide complexes are not removed.	bind
20881	2	6605	5	13	NULL	NULL	NULL	lipid hydroperoxides	Chemical		participate in					oxidized phospholipids	Chemical	formation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1325_s_57	15831812	13 It was concluded that human apoA-I binds lipid hydroperoxides in such a manner that the lipid hydroperoxides can still participate in the formation of oxidized phospholipids if the apoA-I-lipid hydroperoxide complexes are not removed.	bind
20884	3	6605	5	13	NULL	NULL	NULL	statement 2	Process		on non removal of					apoA-I-lipid hydroperoxide complexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1325_s_57	15831812	13 It was concluded that human apoA-I binds lipid hydroperoxides in such a manner that the lipid hydroperoxides can still participate in the formation of oxidized phospholipids if the apoA-I-lipid hydroperoxide complexes are not removed.	bind
18604	1	6605	6	13	NULL	NULL	NULL	apoA-I	GP	human	bind					lipid hydroperoxides	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1325_s_57	15831812	13 It was concluded that human apoA-I binds lipid hydroperoxides in such a manner that the lipid hydroperoxides can still participate in the formation of oxidized phospholipids if the apoA-I-lipid hydroperoxide complexes are not removed.	bind
18605	2	6605	6	13	NULL	NULL	NULL	lipid hydroperoxides	Chemical		participate					oxidized phospholipids	Chemical	formation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1325_s_57	15831812	13 It was concluded that human apoA-I binds lipid hydroperoxides in such a manner that the lipid hydroperoxides can still participate in the formation of oxidized phospholipids if the apoA-I-lipid hydroperoxide complexes are not removed.	bind
18606	3	6605	6	13	NULL	NULL	NULL	statement 2	Process		occurs on nonremoval of					apoA-I-lipid hydroperoxide complexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1325_s_57	15831812	13 It was concluded that human apoA-I binds lipid hydroperoxides in such a manner that the lipid hydroperoxides can still participate in the formation of oxidized phospholipids if the apoA-I-lipid hydroperoxide complexes are not removed.	bind
20885	1	6606	5	13	NULL	NULL	NULL	plasma constituents	CellComponent		bind					PDGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_24_2893_s_161	12070119	13 Raines et al 29 reported the presence of plasma constituents, which have the capacity to bind to PDGF and inhibit the binding of PDGF to its cell-surface receptor.	bind
20886	2	6606	5	13	NULL	NULL	NULL	PDGF	GP		bind					cell-surface receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_24_2893_s_161	12070119	13 Raines et al 29 reported the presence of plasma constituents, which have the capacity to bind to PDGF and inhibit the binding of PDGF to its cell-surface receptor.	bind
20887	3	6606	5	13	NULL	NULL	NULL	plasma constituents	CellComponent		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_24_2893_s_161	12070119	13 Raines et al 29 reported the presence of plasma constituents, which have the capacity to bind to PDGF and inhibit the binding of PDGF to its cell-surface receptor.	bind
18607	1	6606	6	13	NULL	NULL	NULL	plasma constituents	CellComponent		bind					PDGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_24_2893_s_161	12070119	13 Raines et al 29 reported the presence of plasma constituents, which have the capacity to bind to PDGF and inhibit the binding of PDGF to its cell-surface receptor.	bind
18608	2	6606	6	13	NULL	NULL	NULL	PDGF	GP		bind					cell-surface receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_24_2893_s_161	12070119	13 Raines et al 29 reported the presence of plasma constituents, which have the capacity to bind to PDGF and inhibit the binding of PDGF to its cell-surface receptor.	bind
18609	3	6606	6	13	NULL	NULL	NULL	plasma constituents	CellComponent		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_24_2893_s_161	12070119	13 Raines et al 29 reported the presence of plasma constituents, which have the capacity to bind to PDGF and inhibit the binding of PDGF to its cell-surface receptor.	bind
20888	1	6607	5	13	NULL	NULL	NULL	vitronectin	GP	radiolabeled	bind					fibrin matrices	CellComponent	pre-formed			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_12_2679_s_164	16210568	13 The apparent binding affinity estimated by SPR ( KD of 0.26 mumol/L) is higher but consistent with that previously determined by solid-phase binding assay ( KD of  0.60 mumol/L) in which radiolabeled vitronectin was bound to pre-formed fibrin matrices.	bind
18610	1	6607	6	13	NULL	NULL	NULL	vitronectin	GP	radiolabeled	bind					fibrin matrices	CellComponent	pre-formed 			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_12_2679_s_164	16210568	13 The apparent binding affinity estimated by SPR ( KD of 0.26 mumol/L) is higher but consistent with that previously determined by solid-phase binding assay ( KD of  0.60 mumol/L) in which radiolabeled vitronectin was bound to pre-formed fibrin matrices.	bind
20889	1	6608	5	13	NULL	NULL	NULL	NFAT	GP		bind					calcineurin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_7_725_s_81	12663489	13 The VIVIT peptide was found to be 25 times more effective at inhibiting NFAT binding to calcineurin than a peptide spanning the naturally occurring calcineurin binding site of NFATc2.	bind
20890	2	6608	5	13	NULL	NULL	NULL	VIVIT peptide	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_7_725_s_81	12663489	13 The VIVIT peptide was found to be 25 times more effective at inhibiting NFAT binding to calcineurin than a peptide spanning the naturally occurring calcineurin binding site of NFATc2.	bind
20891	3	6608	5	13	NULL	NULL	NULL	peptide	GP	 naturally occurring 	inhibit			calcineurin binding site of NFATc2		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_7_725_s_81	12663489	13 The VIVIT peptide was found to be 25 times more effective at inhibiting NFAT binding to calcineurin than a peptide spanning the naturally occurring calcineurin binding site of NFATc2.	bind
20892	4	6608	5	13	NULL	NULL	NULL	statement 2	Process		more effective than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_7_725_s_81	12663489	13 The VIVIT peptide was found to be 25 times more effective at inhibiting NFAT binding to calcineurin than a peptide spanning the naturally occurring calcineurin binding site of NFATc2.	bind
18611	1	6608	6	13	NULL	NULL	NULL	NFAT	GP		bind					calcineurin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_7_725_s_81	12663489	13 The VIVIT peptide was found to be 25 times more effective at inhibiting NFAT binding to calcineurin than a peptide spanning the naturally occurring calcineurin binding site of NFATc2.	bind
18612	2	6608	6	13	NULL	NULL	NULL	VIVIT peptide	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_7_725_s_81	12663489	13 The VIVIT peptide was found to be 25 times more effective at inhibiting NFAT binding to calcineurin than a peptide spanning the naturally occurring calcineurin binding site of NFATc2.	bind
18613	3	6608	6	13	NULL	NULL	NULL	peptide	GP	naturally occuring	inhibits			calcineurin binding site of NFATc2		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_7_725_s_81	12663489	13 The VIVIT peptide was found to be 25 times more effective at inhibiting NFAT binding to calcineurin than a peptide spanning the naturally occurring calcineurin binding site of NFATc2.	bind
30283	4	6608	6	13	NULL	NULL	NULL	statement 2	Process		is more effective than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_7_725_s_81	12663489	13 The VIVIT peptide was found to be 25 times more effective at inhibiting NFAT binding to calcineurin than a peptide spanning the naturally occurring calcineurin binding site of NFATc2.	bind
20893	1	6609	5	13	NULL	NULL	NULL	Rad	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_8_1071_s_25	15710763	13 These interactions are enhanced by an increase in calcium influx and favor the inactive GDP-bound form of Rad.	bind
18614	1	6609	6	13	NULL	NULL	NULL	GDP	Chemical		bind					Rad	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_8_1071_s_25	15710763	13 These interactions are enhanced by an increase in calcium influx and favor the inactive GDP-bound form of Rad.	bind
20894	1	6610	5	13	NULL	NULL	NULL	monocytes	Cell	attached	is capable of					LDL	GP	uptake of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_684_s_135	14988094	13 To exclude that these cells are attached monocytes or macrophages, which are also capable for LDL uptake and lectin binding, 17,18  additional characterization is necessary.	bind
20899	2	6610	5	13	NULL	NULL	NULL	macrophages	Cell	attached	is capable of					LDL	GP	uptake of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_684_s_135	14988094	13 To exclude that these cells are attached monocytes or macrophages, which are also capable for LDL uptake and lectin binding, 17,18  additional characterization is necessary.	bind
20900	3	6610	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_684_s_135	14988094	13 To exclude that these cells are attached monocytes or macrophages, which are also capable for LDL uptake and lectin binding, 17,18  additional characterization is necessary.	bind
20901	4	6610	5	13	NULL	NULL	NULL	monocytes	Cell	attached	bind					lectin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_684_s_135	14988094	13 To exclude that these cells are attached monocytes or macrophages, which are also capable for LDL uptake and lectin binding, 17,18  additional characterization is necessary.	bind
20902	5	6610	5	13	NULL	NULL	NULL	macrophages	Cell	attached	bind					lectin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_684_s_135	14988094	13 To exclude that these cells are attached monocytes or macrophages, which are also capable for LDL uptake and lectin binding, 17,18  additional characterization is necessary.	bind
20903	6	6610	5	13	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_684_s_135	14988094	13 To exclude that these cells are attached monocytes or macrophages, which are also capable for LDL uptake and lectin binding, 17,18  additional characterization is necessary.	bind
18615	1	6610	6	13	NULL	NULL	NULL	monocytes	Cell	attached	are capable of					LDL	GP	uptake of 			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_684_s_135	14988094	13 To exclude that these cells are attached monocytes or macrophages, which are also capable for LDL uptake and lectin binding, 17,18  additional characterization is necessary.	bind
18616	2	6610	6	13	NULL	NULL	NULL	monocytes	Cell	attached	bind					lectin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_684_s_135	14988094	13 To exclude that these cells are attached monocytes or macrophages, which are also capable for LDL uptake and lectin binding, 17,18  additional characterization is necessary.	bind
18617	3	6610	6	13	NULL	NULL	NULL	macrophages	Cell	attached 	bind					lectin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_684_s_135	14988094	13 To exclude that these cells are attached monocytes or macrophages, which are also capable for LDL uptake and lectin binding, 17,18  additional characterization is necessary.	bind
18618	4	6610	6	13	NULL	NULL	NULL	macrophages	Cell	attached	are capable of					LDL 	GP	uptake of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_684_s_135	14988094	13 To exclude that these cells are attached monocytes or macrophages, which are also capable for LDL uptake and lectin binding, 17,18  additional characterization is necessary.	bind
30281	5	6610	6	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_684_s_135	14988094	13 To exclude that these cells are attached monocytes or macrophages, which are also capable for LDL uptake and lectin binding, 17,18  additional characterization is necessary.	bind
30282	6	6610	6	13	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_684_s_135	14988094	13 To exclude that these cells are attached monocytes or macrophages, which are also capable for LDL uptake and lectin binding, 17,18  additional characterization is necessary.	bind
20904	1	6611	5	13	NULL	NULL	NULL	TTP	GP		bind					TNF-alpha mRNA	NucleicAcid			AU-rich element in 3' untranslated region	NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_17_2631_s_32	15492321	13 TTP binds to the AU-rich element in the 3' untranslated region of TNF-alpha mRNA to destabilize the mRNA. STAT6 signaling has been reported to induce TTP in mast cells, which then reduces the expression of TNF-alpha.	bind
20905	2	6611	5	13	NULL	NULL	NULL	statement 1	Process		destabilize					TNF-alpha mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_17_2631_s_32	15492321	13 TTP binds to the AU-rich element in the 3' untranslated region of TNF-alpha mRNA to destabilize the mRNA. STAT6 signaling has been reported to induce TTP in mast cells, which then reduces the expression of TNF-alpha.	bind
20906	3	6611	5	13	NULL	NULL	NULL	STAT6 signaling	Process		induces					TTP	GP				NULL	in mast cells	NULL	NULL	NULL	NULL	gw70_circulation_110_17_2631_s_32	15492321	13 TTP binds to the AU-rich element in the 3' untranslated region of TNF-alpha mRNA to destabilize the mRNA. STAT6 signaling has been reported to induce TTP in mast cells, which then reduces the expression of TNF-alpha.	bind
20908	4	6611	5	13	NULL	NULL	NULL	statement 3	Process		reduces					TNF-alpha	GP	expression of 			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_17_2631_s_32	15492321	13 TTP binds to the AU-rich element in the 3' untranslated region of TNF-alpha mRNA to destabilize the mRNA. STAT6 signaling has been reported to induce TTP in mast cells, which then reduces the expression of TNF-alpha.	bind
18619	1	6611	6	13	NULL	NULL	NULL	TTP	GP		bind					TNF-alpha mRNA	NucleicAcid			AU-rich element in 3' untranslated region	NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_17_2631_s_32	15492321	13 TTP binds to the AU-rich element in the 3' untranslated region of TNF-alpha mRNA to destabilize the mRNA. STAT6 signaling has been reported to induce TTP in mast cells, which then reduces the expression of TNF-alpha.	bind
18620	2	6611	6	13	NULL	NULL	NULL	STAT6 signaling	Process		induce					TTP	GP				NULL	mast cells	NULL	NULL	NULL	NULL	gw70_circulation_110_17_2631_s_32	15492321	13 TTP binds to the AU-rich element in the 3' untranslated region of TNF-alpha mRNA to destabilize the mRNA. STAT6 signaling has been reported to induce TTP in mast cells, which then reduces the expression of TNF-alpha.	bind
18621	3	6611	6	13	NULL	NULL	NULL	STAT6 signaling	Process		reduces					TNF-alpha	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_17_2631_s_32	15492321	13 TTP binds to the AU-rich element in the 3' untranslated region of TNF-alpha mRNA to destabilize the mRNA. STAT6 signaling has been reported to induce TTP in mast cells, which then reduces the expression of TNF-alpha.	bind
18622	4	6611	6	13	NULL	NULL	NULL	statement 1	Process		destabilize					mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_17_2631_s_32	15492321	13 TTP binds to the AU-rich element in the 3' untranslated region of TNF-alpha mRNA to destabilize the mRNA. STAT6 signaling has been reported to induce TTP in mast cells, which then reduces the expression of TNF-alpha.	bind
21045	1	6612	5	13	NULL	NULL	NULL	CXCL1	GP	murine	is					 KC	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
21046	2	6612	5	13	NULL	NULL	NULL	CXCL1	GP	murine	mediate					cell adhesion	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
21047	3	6612	5	13	NULL	NULL	NULL	statement 2	Process		occurs through					CXCR2 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
21051	4	6612	5	13	NULL	NULL	NULL	CX3CL1	GP		induces					cell adhesion	Process	firm			NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
21052	5	6612	5	13	NULL	NULL	NULL	chemokine	GP		bind		directly			CX3CR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
21053	6	6612	5	13	NULL	NULL	NULL	statement 5	Process		mediates		uniquely			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
21054	7	6612	5	13	NULL	NULL	NULL	statement 4	Process		does not require					integrins	GP	upregulation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
21055	8	6612	5	13	NULL	NULL	NULL	statement 4	Process		does not require					integrins	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
21056	9	6612	5	13	NULL	NULL	NULL	CX3CL1	GP		mediate					leukocyte trafficking	Process	novel pathway for			NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
21057	10	6612	5	13	NULL	NULL	NULL	CX3CR1	GP		mediate					leukocyte trafficking	Process	novel pathway for			NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
21058	11	6612	5	13	NULL	NULL	NULL	statement 7	Process		suggests					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
21059	12	6612	5	13	NULL	NULL	NULL	statement 7	Process		suggests					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
21060	13	6612	5	13	NULL	NULL	NULL	statement 8	Process		suggests					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
21061	14	6612	5	13	NULL	NULL	NULL	statement 8	Process		suggests					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
56132	15	6612	5	13	NULL	NULL	NULL	KC	GP		is a type of					chemokine	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
18665	1	6612	6	13	NULL	NULL	NULL	KC	GP		bind		directly			CX3CR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
18666	2	6612	6	13	NULL	NULL	NULL	CX3CL1	GP		mediate					leukocyte trafficking	Process	novel pathway for 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
18667	3	6612	6	13	NULL	NULL	NULL	CX3CR1	GP		mediate					 leukocyte trafficking	Process	novel pathway for			NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
18668	4	6612	6	13	NULL	NULL	NULL	KC	GP		mediates					cell adhesion	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
18669	5	6612	6	13	NULL	NULL	NULL	statement 4	Process		occurs through					CXCR2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
18670	6	6612	6	13	NULL	NULL	NULL	CX3CL1	GP		induces					cell adhesion	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
18742	7	6612	6	13	NULL	NULL	NULL	KC	GP		is					murine CXCL1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
18743	8	6612	6	13	NULL	NULL	NULL	CXCR2 	GP		is					receptor for chemokine KC	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
18744	9	6612	6	13	NULL	NULL	NULL	statement 2	Process		occurs simultaneously with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
30312	10	6612	6	13	NULL	NULL	NULL	statement 1	Process		mediates					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
30313	11	6612	6	13	NULL	NULL	NULL	statement 10	Process		does not require					integrin	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
30314	12	6612	6	13	NULL	NULL	NULL	statement 10	Process		does not require					integrins	GP	upregulation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
56133	13	6612	6	13	NULL	NULL	NULL	KC	GP		is a type of					chemokine	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
56134	14	6612	6	13	NULL	NULL	NULL	statement 11	Process		suggest					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
56135	15	6612	6	13	NULL	NULL	NULL	statement 11	Process		suggest					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
56138	16	6612	6	13	NULL	NULL	NULL	statement 12	Process		suggest					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
56139	17	6612	6	13	NULL	NULL	NULL	statement 12	Process		suggest					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_7_1009_s_25	12600915	13, 14 In contrast to cell adhesion mediated by the chemokine KC (murine CXCL1) through its receptor CXCR2, the CX3CL1-induced firm adhesion is uniquely mediated by direct binding of the chemokine to CX3CR1 and does not require the upregulation and activation of integrins, suggesting that CX3CL1 and CX3CR1 mediate a novel pathway for leukocyte trafficking.	bind
20909	1	6613	5	13	NULL	NULL	NULL	CD30	GP		bind					TRAF1	GP		C-terminal region		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2029_s_21	10595933	13, 14 We and other investigators have demonstrated that CD30 binds to tumor necrosis factor receptor-associated factor (TRAF) proteins TRAF1, 2, and 5 in the C-terminal region.	bind
20910	2	6613	5	13	NULL	NULL	NULL	TRAF1	GP		is					tumor necrosis factor receptor-associated factor 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2029_s_21	10595933	13, 14 We and other investigators have demonstrated that CD30 binds to tumor necrosis factor receptor-associated factor (TRAF) proteins TRAF1, 2, and 5 in the C-terminal region.	bind
21062	3	6613	5	13	NULL	NULL	NULL	CD30	GP		bind					TRAF2	GP		C-terminal region		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2029_s_21	10595933	13, 14 We and other investigators have demonstrated that CD30 binds to tumor necrosis factor receptor-associated factor (TRAF) proteins TRAF1, 2, and 5 in the C-terminal region.	bind
21063	4	6613	5	13	NULL	NULL	NULL	TRAF2	GP		is					tumor necrosis factor receptor-associated factor 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2029_s_21	10595933	13, 14 We and other investigators have demonstrated that CD30 binds to tumor necrosis factor receptor-associated factor (TRAF) proteins TRAF1, 2, and 5 in the C-terminal region.	bind
21064	5	6613	5	13	NULL	NULL	NULL	CD30	GP		bind					TRAF5	GP		C-terminal region		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2029_s_21	10595933	13, 14 We and other investigators have demonstrated that CD30 binds to tumor necrosis factor receptor-associated factor (TRAF) proteins TRAF1, 2, and 5 in the C-terminal region.	bind
21065	6	6613	5	13	NULL	NULL	NULL	TRAF5	GP		is					tumor necrosis factor receptor-associated factor 5	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2029_s_21	10595933	13, 14 We and other investigators have demonstrated that CD30 binds to tumor necrosis factor receptor-associated factor (TRAF) proteins TRAF1, 2, and 5 in the C-terminal region.	bind
18623	1	6613	6	13	NULL	NULL	NULL	CD30	GP		bind					TRAF1	GP		C-terminal		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2029_s_21	10595933	13, 14 We and other investigators have demonstrated that CD30 binds to tumor necrosis factor receptor-associated factor (TRAF) proteins TRAF1, 2, and 5 in the C-terminal region.	bind
18624	2	6613	6	13	NULL	NULL	NULL	CD30	GP		bind					TRAF2	GP		C-terminal		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2029_s_21	10595933	13, 14 We and other investigators have demonstrated that CD30 binds to tumor necrosis factor receptor-associated factor (TRAF) proteins TRAF1, 2, and 5 in the C-terminal region.	bind
18625	3	6613	6	13	NULL	NULL	NULL	CD30	GP		bind					TRAF5	GP		C-terminal		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2029_s_21	10595933	13, 14 We and other investigators have demonstrated that CD30 binds to tumor necrosis factor receptor-associated factor (TRAF) proteins TRAF1, 2, and 5 in the C-terminal region.	bind
18626	4	6613	6	13	NULL	NULL	NULL	TRAF1	GP		is					tumor necrosis factor receptor-associated factor1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2029_s_21	10595933	13, 14 We and other investigators have demonstrated that CD30 binds to tumor necrosis factor receptor-associated factor (TRAF) proteins TRAF1, 2, and 5 in the C-terminal region.	bind
30279	5	6613	6	13	NULL	NULL	NULL	TRAF2	GP		is					tumor necrosis factor receptor-associated factor 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2029_s_21	10595933	13, 14 We and other investigators have demonstrated that CD30 binds to tumor necrosis factor receptor-associated factor (TRAF) proteins TRAF1, 2, and 5 in the C-terminal region.	bind
30280	6	6613	6	13	NULL	NULL	NULL	TRAF5	GP		is					tumor necrosis factor receptor-associated factor 5	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2029_s_21	10595933	13, 14 We and other investigators have demonstrated that CD30 binds to tumor necrosis factor receptor-associated factor (TRAF) proteins TRAF1, 2, and 5 in the C-terminal region.	bind
21112	1	6614	5	13	NULL	NULL	NULL	CD36	GP		is a type of					class B scavenger receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_98_s_34	14563650	13,14  In further support of this hypothesis, CD36 (a class B scavenger receptor that binds both native and modified LDL) is expressed in endothelial cells, has been localized to caveolae, and interacts with Cav-1.	bind
21113	2	6614	5	13	NULL	NULL	NULL	CD36	GP		bind					LDL	GP	native			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_98_s_34	14563650	13,14  In further support of this hypothesis, CD36 (a class B scavenger receptor that binds both native and modified LDL) is expressed in endothelial cells, has been localized to caveolae, and interacts with Cav-1.	bind
21114	3	6614	5	13	NULL	NULL	NULL	CD36	GP		bind					LDL	GP	modified			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_98_s_34	14563650	13,14  In further support of this hypothesis, CD36 (a class B scavenger receptor that binds both native and modified LDL) is expressed in endothelial cells, has been localized to caveolae, and interacts with Cav-1.	bind
21115	4	6614	5	13	NULL	NULL	NULL	CD36	GP		is expressed in					endothelial cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_98_s_34	14563650	13,14  In further support of this hypothesis, CD36 (a class B scavenger receptor that binds both native and modified LDL) is expressed in endothelial cells, has been localized to caveolae, and interacts with Cav-1.	bind
21116	5	6614	5	13	NULL	NULL	NULL	CD36	GP		is localized to					caveolae	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_98_s_34	14563650	13,14  In further support of this hypothesis, CD36 (a class B scavenger receptor that binds both native and modified LDL) is expressed in endothelial cells, has been localized to caveolae, and interacts with Cav-1.	bind
21117	6	6614	5	13	NULL	NULL	NULL	CD36	GP		interacts with					Cav-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_98_s_34	14563650	13,14  In further support of this hypothesis, CD36 (a class B scavenger receptor that binds both native and modified LDL) is expressed in endothelial cells, has been localized to caveolae, and interacts with Cav-1.	bind
18627	1	6614	6	13	NULL	NULL	NULL	CD36	GP		is a type of					a class B scavenger receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_98_s_34	14563650	13,14  In further support of this hypothesis, CD36 (a class B scavenger receptor that binds both native and modified LDL) is expressed in endothelial cells, has been localized to caveolae, and interacts with Cav-1.	bind
18628	2	6614	6	13	NULL	NULL	NULL	CD36	GP		bind					LDL	GP	native			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_98_s_34	14563650	13,14  In further support of this hypothesis, CD36 (a class B scavenger receptor that binds both native and modified LDL) is expressed in endothelial cells, has been localized to caveolae, and interacts with Cav-1.	bind
18629	3	6614	6	13	NULL	NULL	NULL	CD36	GP		bind					LDL	GP	modified			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_98_s_34	14563650	13,14  In further support of this hypothesis, CD36 (a class B scavenger receptor that binds both native and modified LDL) is expressed in endothelial cells, has been localized to caveolae, and interacts with Cav-1.	bind
18630	4	6614	6	13	NULL	NULL	NULL	CD36	GP		is expressed in					endothelial cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_98_s_34	14563650	13,14  In further support of this hypothesis, CD36 (a class B scavenger receptor that binds both native and modified LDL) is expressed in endothelial cells, has been localized to caveolae, and interacts with Cav-1.	bind
18631	5	6614	6	13	NULL	NULL	NULL	CD36	GP		has been localized to					caveolae	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_98_s_34	14563650	13,14  In further support of this hypothesis, CD36 (a class B scavenger receptor that binds both native and modified LDL) is expressed in endothelial cells, has been localized to caveolae, and interacts with Cav-1.	bind
18632	6	6614	6	13	NULL	NULL	NULL	CD36	GP		interacts with					Cav-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_98_s_34	14563650	13,14  In further support of this hypothesis, CD36 (a class B scavenger receptor that binds both native and modified LDL) is expressed in endothelial cells, has been localized to caveolae, and interacts with Cav-1.	bind
21118	1	6615	5	13	NULL	NULL	NULL	Rb	GP		bind					E2F1	GP				NULL	in nonproliferating cells	NULL	NULL	NULL	NULL	gw70_circulationres_93_10_932_s_25	14576193	13,14  In nonproliferating cells, Rb is bound to E2F1 and suppresses its transcriptional activity.	bind
21119	2	6615	5	13	NULL	NULL	NULL	Rb	GP		suppresses					E2F1	GP	transcriptional activity of			NULL	in nonproliferating cells	NULL	NULL	NULL	NULL	gw70_circulationres_93_10_932_s_25	14576193	13,14  In nonproliferating cells, Rb is bound to E2F1 and suppresses its transcriptional activity.	bind
18633	1	6615	6	13	NULL	NULL	NULL	Rb	GP		bind					E2F1	GP				NULL	nonproliferating cells	NULL	NULL	NULL	NULL	gw70_circulationres_93_10_932_s_25	14576193	13,14  In nonproliferating cells, Rb is bound to E2F1 and suppresses its transcriptional activity.	bind
18634	2	6615	6	13	NULL	NULL	NULL	Rb	GP		suppresses					E2F1	GP	transcriptional activity of			NULL	nonproliferating cells	NULL	NULL	NULL	NULL	gw70_circulationres_93_10_932_s_25	14576193	13,14  In nonproliferating cells, Rb is bound to E2F1 and suppresses its transcriptional activity.	bind
21120	1	6616	5	13	NULL	NULL	NULL	Grb2	GP		promotes					ras	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_32	15289381	13,14,19,20    Grb2 promotes the activation of ras via its interaction with the guanine nucleotide exchange factor SOS. 20,21  Finally, pressure overload may lead to the local release of growth factors that bind to cell surface receptor tyrosine kinases, which activate the ras cascade via Grb2 and SOS. 22	bind
21121	2	6616	5	13	NULL	NULL	NULL	Grb2	GP		interacts with					SOS	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_32	15289381	13,14,19,20    Grb2 promotes the activation of ras via its interaction with the guanine nucleotide exchange factor SOS. 20,21  Finally, pressure overload may lead to the local release of growth factors that bind to cell surface receptor tyrosine kinases, which activate the ras cascade via Grb2 and SOS. 22	bind
21122	3	6616	5	13	NULL	NULL	NULL	statement 1	Process		occurs via					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_32	15289381	13,14,19,20    Grb2 promotes the activation of ras via its interaction with the guanine nucleotide exchange factor SOS. 20,21  Finally, pressure overload may lead to the local release of growth factors that bind to cell surface receptor tyrosine kinases, which activate the ras cascade via Grb2 and SOS. 22	bind
21123	4	6616	5	13	NULL	NULL	NULL	pressure overload	ResearchActivity		lead to		may			growth factors	GP	local release of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_32	15289381	13,14,19,20    Grb2 promotes the activation of ras via its interaction with the guanine nucleotide exchange factor SOS. 20,21  Finally, pressure overload may lead to the local release of growth factors that bind to cell surface receptor tyrosine kinases, which activate the ras cascade via Grb2 and SOS. 22	bind
21124	5	6616	5	13	NULL	NULL	NULL	growth factors	GP		bind					receptor tyrosine kinases	GP	cell surface			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_32	15289381	13,14,19,20    Grb2 promotes the activation of ras via its interaction with the guanine nucleotide exchange factor SOS. 20,21  Finally, pressure overload may lead to the local release of growth factors that bind to cell surface receptor tyrosine kinases, which activate the ras cascade via Grb2 and SOS. 22	bind
21125	6	6616	5	13	NULL	NULL	NULL	receptor tyrosine kinases	GP	cell surface	activate					ras cascade	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_32	15289381	13,14,19,20    Grb2 promotes the activation of ras via its interaction with the guanine nucleotide exchange factor SOS. 20,21  Finally, pressure overload may lead to the local release of growth factors that bind to cell surface receptor tyrosine kinases, which activate the ras cascade via Grb2 and SOS. 22	bind
21126	7	6616	5	13	NULL	NULL	NULL	statement 6	Process		occurs via					Grb2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_32	15289381	13,14,19,20    Grb2 promotes the activation of ras via its interaction with the guanine nucleotide exchange factor SOS. 20,21  Finally, pressure overload may lead to the local release of growth factors that bind to cell surface receptor tyrosine kinases, which activate the ras cascade via Grb2 and SOS. 22	bind
21127	8	6616	5	13	NULL	NULL	NULL	statement 6	Process		occurs via					SOS	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_32	15289381	13,14,19,20    Grb2 promotes the activation of ras via its interaction with the guanine nucleotide exchange factor SOS. 20,21  Finally, pressure overload may lead to the local release of growth factors that bind to cell surface receptor tyrosine kinases, which activate the ras cascade via Grb2 and SOS. 22	bind
56176	9	6616	5	13	NULL	NULL	NULL	SOS	GP		is a type of					guanine nucleotide exchange factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_32	15289381	13,14,19,20    Grb2 promotes the activation of ras via its interaction with the guanine nucleotide exchange factor SOS. 20,21  Finally, pressure overload may lead to the local release of growth factors that bind to cell surface receptor tyrosine kinases, which activate the ras cascade via Grb2 and SOS. 22	bind
18635	1	6616	6	13	NULL	NULL	NULL	Grb2	GP		interacts with					SOS	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_32	15289381	13,14,19,20    Grb2 promotes the activation of ras via its interaction with the guanine nucleotide exchange factor SOS. 20,21  Finally, pressure overload may lead to the local release of growth factors that bind to cell surface receptor tyrosine kinases, which activate the ras cascade via Grb2 and SOS. 22	bind
18636	2	6616	6	13	NULL	NULL	NULL	Grb2	GP		promotes					Ras	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_32	15289381	13,14,19,20    Grb2 promotes the activation of ras via its interaction with the guanine nucleotide exchange factor SOS. 20,21  Finally, pressure overload may lead to the local release of growth factors that bind to cell surface receptor tyrosine kinases, which activate the ras cascade via Grb2 and SOS. 22	bind
18637	3	6616	6	13	NULL	NULL	NULL	statement 1	Process		occurs via					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_32	15289381	13,14,19,20    Grb2 promotes the activation of ras via its interaction with the guanine nucleotide exchange factor SOS. 20,21  Finally, pressure overload may lead to the local release of growth factors that bind to cell surface receptor tyrosine kinases, which activate the ras cascade via Grb2 and SOS. 22	bind
18638	4	6616	6	13	NULL	NULL	NULL	SOS	GP		is a type of					guanine nucleotide exchange factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_32	15289381	13,14,19,20    Grb2 promotes the activation of ras via its interaction with the guanine nucleotide exchange factor SOS. 20,21  Finally, pressure overload may lead to the local release of growth factors that bind to cell surface receptor tyrosine kinases, which activate the ras cascade via Grb2 and SOS. 22	bind
18639	5	6616	6	13	NULL	NULL	NULL	growth factor	GP		bind					 receptor tyrosine kinases	GP	cell surface			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_32	15289381	13,14,19,20    Grb2 promotes the activation of ras via its interaction with the guanine nucleotide exchange factor SOS. 20,21  Finally, pressure overload may lead to the local release of growth factors that bind to cell surface receptor tyrosine kinases, which activate the ras cascade via Grb2 and SOS. 22	bind
18640	6	6616	6	13	NULL	NULL	NULL	pressure overload	ResearchActivity		may lead to					growth factor	GP	release of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_32	15289381	13,14,19,20    Grb2 promotes the activation of ras via its interaction with the guanine nucleotide exchange factor SOS. 20,21  Finally, pressure overload may lead to the local release of growth factors that bind to cell surface receptor tyrosine kinases, which activate the ras cascade via Grb2 and SOS. 22	bind
18641	7	6616	6	13	NULL	NULL	NULL	 receptor tyrosine kinases	GP	cell surface	activate					ras cascade	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_32	15289381	13,14,19,20    Grb2 promotes the activation of ras via its interaction with the guanine nucleotide exchange factor SOS. 20,21  Finally, pressure overload may lead to the local release of growth factors that bind to cell surface receptor tyrosine kinases, which activate the ras cascade via Grb2 and SOS. 22	bind
18642	8	6616	6	13	NULL	NULL	NULL	statement 7	Process		occurs via					Grb2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_32	15289381	13,14,19,20    Grb2 promotes the activation of ras via its interaction with the guanine nucleotide exchange factor SOS. 20,21  Finally, pressure overload may lead to the local release of growth factors that bind to cell surface receptor tyrosine kinases, which activate the ras cascade via Grb2 and SOS. 22	bind
18643	9	6616	6	13	NULL	NULL	NULL	statement 7	Process		occurs via					SOS	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_6_718_s_32	15289381	13,14,19,20    Grb2 promotes the activation of ras via its interaction with the guanine nucleotide exchange factor SOS. 20,21  Finally, pressure overload may lead to the local release of growth factors that bind to cell surface receptor tyrosine kinases, which activate the ras cascade via Grb2 and SOS. 22	bind
21144	1	6617	5	13	NULL	NULL	NULL	VEGF	GP		mediate					chemotaxis	Process	endothelial			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1257_s_157	15920019	13,18,31   As has been previously reported, stable coexpression of Npn-1 and VEGFR2 enhanced VEGF-mediated endothelial chemotaxis, 19,43  and Npn-1 inhibition partially attenuated human pulmonary artery VEGF-mediated endothelial cell migration.	bind
21145	2	6617	5	13	NULL	NULL	NULL	Npn-1	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1257_s_157	15920019	13,18,31   As has been previously reported, stable coexpression of Npn-1 and VEGFR2 enhanced VEGF-mediated endothelial chemotaxis, 19,43  and Npn-1 inhibition partially attenuated human pulmonary artery VEGF-mediated endothelial cell migration.	bind
21146	5	6617	5	13	NULL	NULL	NULL	VEGF	GP		mediate					cell migration	Process	endothelial			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1257_s_157	15920019	13,18,31   As has been previously reported, stable coexpression of Npn-1 and VEGFR2 enhanced VEGF-mediated endothelial chemotaxis, 19,43  and Npn-1 inhibition partially attenuated human pulmonary artery VEGF-mediated endothelial cell migration.	bind
21147	6	6617	5	13	NULL	NULL	NULL	Npn-1	GP	inhibition	attenuates		partially			statement 3	Process				NULL	human pulmonary artery	NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1257_s_157	15920019	13,18,31   As has been previously reported, stable coexpression of Npn-1 and VEGFR2 enhanced VEGF-mediated endothelial chemotaxis, 19,43  and Npn-1 inhibition partially attenuated human pulmonary artery VEGF-mediated endothelial cell migration.	bind
56177	3	6617	5	13	NULL	NULL	NULL	VEGFR2	GP		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1257_s_157	15920019	13,18,31   As has been previously reported, stable coexpression of Npn-1 and VEGFR2 enhanced VEGF-mediated endothelial chemotaxis, 19,43  and Npn-1 inhibition partially attenuated human pulmonary artery VEGF-mediated endothelial cell migration.	bind
56178	4	6617	5	13	NULL	NULL	NULL	statement 2	Process		occur simultaneous with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1257_s_157	15920019	13,18,31   As has been previously reported, stable coexpression of Npn-1 and VEGFR2 enhanced VEGF-mediated endothelial chemotaxis, 19,43  and Npn-1 inhibition partially attenuated human pulmonary artery VEGF-mediated endothelial cell migration.	bind
18644	1	6617	6	13	NULL	NULL	NULL	VEGF	GP		mediates					 chemotaxis	Process	endothelial			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1257_s_157	15920019	13,18,31   As has been previously reported, stable coexpression of Npn-1 and VEGFR2 enhanced VEGF-mediated endothelial chemotaxis, 19,43  and Npn-1 inhibition partially attenuated human pulmonary artery VEGF-mediated endothelial cell migration.	bind
18645	2	6617	6	13	NULL	NULL	NULL	Npn-1	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1257_s_157	15920019	13,18,31   As has been previously reported, stable coexpression of Npn-1 and VEGFR2 enhanced VEGF-mediated endothelial chemotaxis, 19,43  and Npn-1 inhibition partially attenuated human pulmonary artery VEGF-mediated endothelial cell migration.	bind
18646	3	6617	6	13	NULL	NULL	NULL	VEGFR2	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1257_s_157	15920019	13,18,31   As has been previously reported, stable coexpression of Npn-1 and VEGFR2 enhanced VEGF-mediated endothelial chemotaxis, 19,43  and Npn-1 inhibition partially attenuated human pulmonary artery VEGF-mediated endothelial cell migration.	bind
18647	4	6617	6	13	NULL	NULL	NULL	statement 2	Process		occurs simultaneously with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1257_s_157	15920019	13,18,31   As has been previously reported, stable coexpression of Npn-1 and VEGFR2 enhanced VEGF-mediated endothelial chemotaxis, 19,43  and Npn-1 inhibition partially attenuated human pulmonary artery VEGF-mediated endothelial cell migration.	bind
18648	6	6617	6	13	NULL	NULL	NULL	Npn-1	GP	inhibition of	attenuates		partially			statement 5	Process				NULL	human pulmonary artery	NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1257_s_157	15920019	13,18,31   As has been previously reported, stable coexpression of Npn-1 and VEGFR2 enhanced VEGF-mediated endothelial chemotaxis, 19,43  and Npn-1 inhibition partially attenuated human pulmonary artery VEGF-mediated endothelial cell migration.	bind
56180	5	6617	6	13	NULL	NULL	NULL	VEGF	GP		mediate					cell migration	Process	endothelial			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1257_s_157	15920019	13,18,31   As has been previously reported, stable coexpression of Npn-1 and VEGFR2 enhanced VEGF-mediated endothelial chemotaxis, 19,43  and Npn-1 inhibition partially attenuated human pulmonary artery VEGF-mediated endothelial cell migration.	bind
21148	1	6618	5	13	NULL	NULL	NULL				is phosphorylated by		constitutively	Thr495		PKCs	GP				NULL	in endothelial cells	NULL	NULL	NULL	NULL	gw70_circulation_109_3_399_s_140	14707024	13,29,30   By contrast, Thr495 is constitutively phosphorylated by PKCs in the endothelial cells investigated to date, and it is a negative regulatory site, ie, phosphorylation causes a decrease in enzyme activity through interference with the binding of calmodulin to the calmodulin-binding domain.	bind
21150	2	6618	5	13	NULL	NULL	NULL	calmodulin	GP		bind								calmodulin-binding domain		NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_3_399_s_140	14707024	13,29,30   By contrast, Thr495 is constitutively phosphorylated by PKCs in the endothelial cells investigated to date, and it is a negative regulatory site, ie, phosphorylation causes a decrease in enzyme activity through interference with the binding of calmodulin to the calmodulin-binding domain.	bind
18649	1	6618	6	13	NULL	NULL	NULL				is phosphorylated 		constitutively	Thr495		PKC	GP				NULL	endothelial cells	NULL	NULL	NULL	NULL	gw70_circulation_109_3_399_s_140	14707024	13,29,30   By contrast, Thr495 is constitutively phosphorylated by PKCs in the endothelial cells investigated to date, and it is a negative regulatory site, ie, phosphorylation causes a decrease in enzyme activity through interference with the binding of calmodulin to the calmodulin-binding domain.	bind
18650	2	6618	6	13	NULL	NULL	NULL	calmodulin	GP		bind								calmodulin-binding domain		NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_3_399_s_140	14707024	13,29,30   By contrast, Thr495 is constitutively phosphorylated by PKCs in the endothelial cells investigated to date, and it is a negative regulatory site, ie, phosphorylation causes a decrease in enzyme activity through interference with the binding of calmodulin to the calmodulin-binding domain.	bind
21152	1	6619	5	13	NULL	NULL	NULL	13- cis-RA	Chemical		does not bind					retinoic acid receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_35008_s_245	9857033	13- cis-RA does not bind to retinoic acid receptors and is thought to act through its metabolites including ATRA ( 3).	bind
21153	2	6619	5	13	NULL	NULL	NULL	13-cis-RA	Chemical		act through		might			ATRA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_35008_s_245	9857033	13- cis-RA does not bind to retinoic acid receptors and is thought to act through its metabolites including ATRA ( 3).	bind
21154	3	6619	5	13	NULL	NULL	NULL	ATRA	Chemical		is a metabolite of					13- cis-RA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_35008_s_245	9857033	13- cis-RA does not bind to retinoic acid receptors and is thought to act through its metabolites including ATRA ( 3).	bind
18651	1	6619	6	13	NULL	NULL	NULL	13- cis-RA	Chemical		does not bind					retinoic acid receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_35008_s_245	9857033	13- cis-RA does not bind to retinoic acid receptors and is thought to act through its metabolites including ATRA ( 3).	bind
56182	3	6619	6	13	NULL	NULL	NULL	ATRA	Chemical		is a metabolite of					13- cis-RA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_35008_s_245	9857033	13- cis-RA does not bind to retinoic acid receptors and is thought to act through its metabolites including ATRA ( 3).	bind
56183	2	6619	6	13	NULL	NULL	NULL	13- cis-RA	Chemical		act through		might			ATRA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_35008_s_245	9857033	13- cis-RA does not bind to retinoic acid receptors and is thought to act through its metabolites including ATRA ( 3).	bind
21155	2	6620	5	13	NULL	NULL	NULL	statement 1	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7988_s_8	14662773	13-Mers containing these profilin-like segments bound actin in fluorescent anisotropy studies and competed with profilin for binding to actin.	bind
21156	3	6620	5	13	NULL	NULL	NULL	profilin	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7988_s_8	14662773	13-Mers containing these profilin-like segments bound actin in fluorescent anisotropy studies and competed with profilin for binding to actin.	bind
21157	4	6620	5	13	NULL	NULL	NULL	statement 2	Process		competes with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7988_s_8	14662773	13-Mers containing these profilin-like segments bound actin in fluorescent anisotropy studies and competed with profilin for binding to actin.	bind
44667	1	6620	5	13	NULL	NULL	NULL	13-Mers	GP		contain					profilin-like segments	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7988_s_8	14662773	13-Mers containing these profilin-like segments bound actin in fluorescent anisotropy studies and competed with profilin for binding to actin.	bind
18652	1	6620	6	13	NULL	NULL	NULL	profilin	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7988_s_8	14662773	13-Mers containing these profilin-like segments bound actin in fluorescent anisotropy studies and competed with profilin for binding to actin.	bind
18653	2	6620	6	13	NULL	NULL	NULL	13-Mers	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7988_s_8	14662773	13-Mers containing these profilin-like segments bound actin in fluorescent anisotropy studies and competed with profilin for binding to actin.	bind
18654	3	6620	6	13	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7988_s_8	14662773	13-Mers containing these profilin-like segments bound actin in fluorescent anisotropy studies and competed with profilin for binding to actin.	bind
56184	4	6620	6	13	NULL	NULL	NULL	13-Mers	GP		contain					profilin-like segments	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7988_s_8	14662773	13-Mers containing these profilin-like segments bound actin in fluorescent anisotropy studies and competed with profilin for binding to actin.	bind
21158	1	6621	5	13	NULL	NULL	NULL	CsA	Chemical	prophylactic administration of 	inhibit					cardiac hypertrophy	Process	development of			NULL	rat	NULL	NULL	NULL	NULL	gw60_circulationres_84_6_633_s_234	10189351	139  In addition, prophylactic administration of CsA inhibited the development of cardiac hypertrophy after suprarenal banding of the abdominal aorta in the rat.	bind
21159	2	6621	5	13	NULL	NULL	NULL	statement 1	Process		occurs after					 abdominal aorta	OrganismPart	suprarenal banding of			NULL	rat	NULL	NULL	NULL	NULL	gw60_circulationres_84_6_633_s_234	10189351	139  In addition, prophylactic administration of CsA inhibited the development of cardiac hypertrophy after suprarenal banding of the abdominal aorta in the rat.	bind
18655	1	6621	6	13	NULL	NULL	NULL	CsA	Chemical		inhibits					cardiac hypertrophy	Process	development of 			NULL	rat	NULL	NULL	NULL	NULL	gw60_circulationres_84_6_633_s_234	10189351	139  In addition, prophylactic administration of CsA inhibited the development of cardiac hypertrophy after suprarenal banding of the abdominal aorta in the rat.	bind
30278	2	6621	6	13	NULL	NULL	NULL	statement 1	Process		occurs after					abdominal aorta	OrganismPart	suprarenal banding of			NULL	rat	NULL	NULL	NULL	NULL	gw60_circulationres_84_6_633_s_234	10189351	139  In addition, prophylactic administration of CsA inhibited the development of cardiac hypertrophy after suprarenal banding of the abdominal aorta in the rat.	bind
21372	1	6622	5	13	NULL	NULL	NULL	SCP-2	GP		interacts with					fatty acid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_50_35425_s_125	10585412	13C Chemical Shifts of SCP-2 Bound Versus Unbound Fully Enriched [1318]Oleate-- Prior to using 13C-labeled fatty acids to determine if the cholesterol and fatty acid binding sites were the same or different, it was necessary to first characterize the interaction of fatty acid with SCP-2.	bind
18656	1	6622	6	13	NULL	NULL	NULL	fatty acid	Chemical		interacts with					SCP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_50_35425_s_125	10585412	13C Chemical Shifts of SCP-2 Bound Versus Unbound Fully Enriched [1318]Oleate-- Prior to using 13C-labeled fatty acids to determine if the cholesterol and fatty acid binding sites were the same or different, it was necessary to first characterize the interaction of fatty acid with SCP-2.	bind
21373	1	6623	5	13	NULL	NULL	NULL	palmitate	Chemical		bind					HSA	GP		domain III		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_50_17958_s_130	16330771	13C NMR spectra were obtained to study [13]palmitate binding to domain III of HSA.	bind
18657	1	6623	6	13	NULL	NULL	NULL	palmitate	Chemical		bind					HSA	GP		domain III		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_50_17958_s_130	16330771	13C NMR spectra were obtained to study [13]palmitate binding to domain III of HSA.	bind
21374	1	6624	5	13	NULL	NULL	NULL	XPA	GP		bind					RPA	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2635_s_271	11410673	14       Matsuda,T., Saijo,M., Kuraoka,I., Kobayashi,T., Nakatsu,Y., Nagai,A., Enjoji,T., Masutani,C., Sugasawa,K., Hanoaka,F. et al. (1995) DNA repair protein XPA binds replication protein A (RPA).	bind
21375	2	6624	5	13	NULL	NULL	NULL	RPA	GP		is					replication protein A	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2635_s_271	11410673	14       Matsuda,T., Saijo,M., Kuraoka,I., Kobayashi,T., Nakatsu,Y., Nagai,A., Enjoji,T., Masutani,C., Sugasawa,K., Hanoaka,F. et al. (1995) DNA repair protein XPA binds replication protein A (RPA).	bind
30310	3	6624	5	13	NULL	NULL	NULL	XPA	GP		is a type of					DNA repair protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2635_s_271	11410673	14       Matsuda,T., Saijo,M., Kuraoka,I., Kobayashi,T., Nakatsu,Y., Nagai,A., Enjoji,T., Masutani,C., Sugasawa,K., Hanoaka,F. et al. (1995) DNA repair protein XPA binds replication protein A (RPA).	bind
18658	1	6624	6	13	NULL	NULL	NULL	XPA	GP		bind					RPA	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2635_s_271	11410673	14       Matsuda,T., Saijo,M., Kuraoka,I., Kobayashi,T., Nakatsu,Y., Nagai,A., Enjoji,T., Masutani,C., Sugasawa,K., Hanoaka,F. et al. (1995) DNA repair protein XPA binds replication protein A (RPA).	bind
18659	2	6624	6	13	NULL	NULL	NULL	XPA	GP		is a type of					DNA repair protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2635_s_271	11410673	14       Matsuda,T., Saijo,M., Kuraoka,I., Kobayashi,T., Nakatsu,Y., Nagai,A., Enjoji,T., Masutani,C., Sugasawa,K., Hanoaka,F. et al. (1995) DNA repair protein XPA binds replication protein A (RPA).	bind
18660	3	6624	6	13	NULL	NULL	NULL	RPA	GP		is					replication protein A	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2635_s_271	11410673	14       Matsuda,T., Saijo,M., Kuraoka,I., Kobayashi,T., Nakatsu,Y., Nagai,A., Enjoji,T., Masutani,C., Sugasawa,K., Hanoaka,F. et al. (1995) DNA repair protein XPA binds replication protein A (RPA).	bind
21377	1	6625	5	13	NULL	NULL	NULL	Rap1p	GP		is					telomere binding protein	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2382_s_413	11376157	14       Ray,A. and Runge,K.W. (1998) The C-terminus of the major yeast telomere binding protein Rap1p enhances telomere formation.	bind
21378	2	6625	5	13	NULL	NULL	NULL	Rap1p	GP		enhances			C-terminus		telomere	NucleicAcid	formation of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2382_s_413	11376157	14       Ray,A. and Runge,K.W. (1998) The C-terminus of the major yeast telomere binding protein Rap1p enhances telomere formation.	bind
18661	1	6625	6	13	NULL	NULL	NULL	Rap1p	GP		is					telomere binding protein	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2382_s_413	11376157	14       Ray,A. and Runge,K.W. (1998) The C-terminus of the major yeast telomere binding protein Rap1p enhances telomere formation.	bind
18662	2	6625	6	13	NULL	NULL	NULL	Rap1p	GP		enhances			C-terminus		telomere	NucleicAcid	formation of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2382_s_413	11376157	14       Ray,A. and Runge,K.W. (1998) The C-terminus of the major yeast telomere binding protein Rap1p enhances telomere formation.	bind
21381	1	6626	5	13	NULL	NULL	NULL	Grb2	GP		bind					Fak	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_7_558_s_131	11009560	14  As shown in Figure 7A  , acute pressure overload increased the amount of Grb2 binding to Fak in parallel with activation of the Fak/c-Src complex.	bind
21383	2	6626	5	13	NULL	NULL	NULL	acute pressure overload	ResearchActivity		increases					statement 1	Process	amount of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_7_558_s_131	11009560	14  As shown in Figure 7A  , acute pressure overload increased the amount of Grb2 binding to Fak in parallel with activation of the Fak/c-Src complex.	bind
21385	3	6626	5	13	NULL	NULL	NULL	acute pressure overload	ResearchActivity		increases					Fak/c-Src complex	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_7_558_s_131	11009560	14  As shown in Figure 7A  , acute pressure overload increased the amount of Grb2 binding to Fak in parallel with activation of the Fak/c-Src complex.	bind
21387	4	6626	5	13	NULL	NULL	NULL	statement 2	Process		in parallel with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_7_558_s_131	11009560	14  As shown in Figure 7A  , acute pressure overload increased the amount of Grb2 binding to Fak in parallel with activation of the Fak/c-Src complex.	bind
18671	1	6626	6	13	NULL	NULL	NULL	Grb2	GP		bind					Fak	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_7_558_s_131	11009560	14  As shown in Figure 7A  , acute pressure overload increased the amount of Grb2 binding to Fak in parallel with activation of the Fak/c-Src complex.	bind
18672	2	6626	6	13	NULL	NULL	NULL	acute pressure overload	ResearchActivity		increased					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_7_558_s_131	11009560	14  As shown in Figure 7A  , acute pressure overload increased the amount of Grb2 binding to Fak in parallel with activation of the Fak/c-Src complex.	bind
18673	3	6626	6	13	NULL	NULL	NULL	acute pressure overload	ResearchActivity		increased					FAK/c-Src complex	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_7_558_s_131	11009560	14  As shown in Figure 7A  , acute pressure overload increased the amount of Grb2 binding to Fak in parallel with activation of the Fak/c-Src complex.	bind
30277	4	6626	6	13	NULL	NULL	NULL	statement 2	Process		in parallel with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_7_558_s_131	11009560	14  As shown in Figure 7A  , acute pressure overload increased the amount of Grb2 binding to Fak in parallel with activation of the Fak/c-Src complex.	bind
21391	1	6627	5	13	NULL	NULL	NULL	TRADD	GP		bind			N-terminal portion		TRAF-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_997_s_28	10702415	14  he N-terminal portion of TRADD binds the TNF receptor-associated factor 2 (TRAF-2), and other more recently identified proteins such as RIP, ultimately resulting in the activation of NF-kappaB.	bind
21392	2	6627	5	13	NULL	NULL	NULL	TRAF-2	GP		is					TNF receptor-associated factor 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_997_s_28	10702415	14  he N-terminal portion of TRADD binds the TNF receptor-associated factor 2 (TRAF-2), and other more recently identified proteins such as RIP, ultimately resulting in the activation of NF-kappaB.	bind
21393	3	6627	5	13	NULL	NULL	NULL	TRADD	GP		bind			N-terminal portion		RIP	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_997_s_28	10702415	14  he N-terminal portion of TRADD binds the TNF receptor-associated factor 2 (TRAF-2), and other more recently identified proteins such as RIP, ultimately resulting in the activation of NF-kappaB.	bind
21395	4	6627	5	13	NULL	NULL	NULL	statement 1	Process		results in					NF-kappaB	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_997_s_28	10702415	14  he N-terminal portion of TRADD binds the TNF receptor-associated factor 2 (TRAF-2), and other more recently identified proteins such as RIP, ultimately resulting in the activation of NF-kappaB.	bind
21396	5	6627	5	13	NULL	NULL	NULL	statement 3	Process		results in					NF-kappaB	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_997_s_28	10702415	14  he N-terminal portion of TRADD binds the TNF receptor-associated factor 2 (TRAF-2), and other more recently identified proteins such as RIP, ultimately resulting in the activation of NF-kappaB.	bind
18674	1	6627	6	13	NULL	NULL	NULL	TRADD	GP		bind			N terminal		TRAF-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_997_s_28	10702415	14  he N-terminal portion of TRADD binds the TNF receptor-associated factor 2 (TRAF-2), and other more recently identified proteins such as RIP, ultimately resulting in the activation of NF-kappaB.	bind
18675	2	6627	6	13	NULL	NULL	NULL	TRAF-2	GP		is					TNF receptor-associated factor 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_997_s_28	10702415	14  he N-terminal portion of TRADD binds the TNF receptor-associated factor 2 (TRAF-2), and other more recently identified proteins such as RIP, ultimately resulting in the activation of NF-kappaB.	bind
18676	3	6627	6	13	NULL	NULL	NULL	TRADD	GP		bind			N-terminal		RIP	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_997_s_28	10702415	14  he N-terminal portion of TRADD binds the TNF receptor-associated factor 2 (TRAF-2), and other more recently identified proteins such as RIP, ultimately resulting in the activation of NF-kappaB.	bind
18677	4	6627	6	13	NULL	NULL	NULL	statement 1	Process		results in					NF-kappaB	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_997_s_28	10702415	14  he N-terminal portion of TRADD binds the TNF receptor-associated factor 2 (TRAF-2), and other more recently identified proteins such as RIP, ultimately resulting in the activation of NF-kappaB.	bind
18678	5	6627	6	13	NULL	NULL	NULL	statement 3	Process		results in					NF-kappaB	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_997_s_28	10702415	14  he N-terminal portion of TRADD binds the TNF receptor-associated factor 2 (TRAF-2), and other more recently identified proteins such as RIP, ultimately resulting in the activation of NF-kappaB.	bind
21398	2	6628	5	13	NULL	NULL	NULL	sPLA2	GP		bind					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulationres_86_6_610_s_27	10746993	14  Later, they studied the binding of sPLA2 to collagen-associated proteoglycans in vitro and found that sPLA2 binds to the glycosaminoglycan chains of biglycan.	bind
21400	3	6628	5	13	NULL	NULL	NULL	sPLA2	GP		bind					biglycan	GP		glycosaminoglycan chains 		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulationres_86_6_610_s_27	10746993	14  Later, they studied the binding of sPLA2 to collagen-associated proteoglycans in vitro and found that sPLA2 binds to the glycosaminoglycan chains of biglycan.	bind
56200	1	6628	5	13	NULL	NULL	NULL	collagen	GP		associate with					proteoglycans	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_6_610_s_27	10746993	14  Later, they studied the binding of sPLA2 to collagen-associated proteoglycans in vitro and found that sPLA2 binds to the glycosaminoglycan chains of biglycan.	bind
18679	1	6628	6	13	NULL	NULL	NULL	sPLA2	GP		bind					biglycan	GP		glycosaminoglycan chains		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulationres_86_6_610_s_27	10746993	14  Later, they studied the binding of sPLA2 to collagen-associated proteoglycans in vitro and found that sPLA2 binds to the glycosaminoglycan chains of biglycan.	bind
56201	2	6628	6	13	NULL	NULL	NULL	collagen	GP		associate with					proteoglycans	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_6_610_s_27	10746993	14  Later, they studied the binding of sPLA2 to collagen-associated proteoglycans in vitro and found that sPLA2 binds to the glycosaminoglycan chains of biglycan.	bind
56203	3	6628	6	13	NULL	NULL	NULL	sPLA2	GP		bind					statement 2	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulationres_86_6_610_s_27	10746993	14  Later, they studied the binding of sPLA2 to collagen-associated proteoglycans in vitro and found that sPLA2 binds to the glycosaminoglycan chains of biglycan.	bind
21402	1	6629	5	13	NULL	NULL	NULL	 NT	GP		bind					TrkB	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_405_s_229	10027399	14  NT also bind to truncated TK- receptors, identified for TrkB and TrkC, 15- 18  which may function as dominant negative isoforms, 20  or immunoadhesins.	bind
21406	2	6629	5	13	NULL	NULL	NULL	NT	GP		bind					TrkC	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_405_s_229	10027399	14  NT also bind to truncated TK- receptors, identified for TrkB and TrkC, 15- 18  which may function as dominant negative isoforms, 20  or immunoadhesins.	bind
21409	3	6629	5	13	NULL	NULL	NULL	TrkB	GP		is					truncated TK- receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_405_s_229	10027399	14  NT also bind to truncated TK- receptors, identified for TrkB and TrkC, 15- 18  which may function as dominant negative isoforms, 20  or immunoadhesins.	bind
21410	4	6629	5	13	NULL	NULL	NULL	TrkC	GP		is					truncated TK- receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_405_s_229	10027399	14  NT also bind to truncated TK- receptors, identified for TrkB and TrkC, 15- 18  which may function as dominant negative isoforms, 20  or immunoadhesins.	bind
21411	5	6629	5	13	NULL	NULL	NULL	TrkB	GP		function as		may			dominant negative isoforms	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_405_s_229	10027399	14  NT also bind to truncated TK- receptors, identified for TrkB and TrkC, 15- 18  which may function as dominant negative isoforms, 20  or immunoadhesins.	bind
21412	6	6629	5	13	NULL	NULL	NULL	TrkC	GP		function as		may			dominant negative isoforms	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_405_s_229	10027399	14  NT also bind to truncated TK- receptors, identified for TrkB and TrkC, 15- 18  which may function as dominant negative isoforms, 20  or immunoadhesins.	bind
21413	7	6629	5	13	NULL	NULL	NULL	TrkB	GP		function as		may			immunoadhesins	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_405_s_229	10027399	14  NT also bind to truncated TK- receptors, identified for TrkB and TrkC, 15- 18  which may function as dominant negative isoforms, 20  or immunoadhesins.	bind
21415	8	6629	5	13	NULL	NULL	NULL	TrkC	GP		function as		may			immunoadhesins	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_405_s_229	10027399	14  NT also bind to truncated TK- receptors, identified for TrkB and TrkC, 15- 18  which may function as dominant negative isoforms, 20  or immunoadhesins.	bind
18680	1	6629	6	13	NULL	NULL	NULL	NT	GP		bind					TK-receptors	GP	truncated			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_405_s_229	10027399	14  NT also bind to truncated TK- receptors, identified for TrkB and TrkC, 15- 18  which may function as dominant negative isoforms, 20  or immunoadhesins.	bind
21419	1	6630	5	13	NULL	NULL	NULL	macrophages	Cell	human	bind					LDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_208	9012650	14  The GAG-induced alterations are associated with an increase in LDL binding and degradation by human monocyte - derived macrophages and smooth muscle cells.	bind
21422	2	6630	5	13	NULL	NULL	NULL	smooth muscle cells	Cell	human	bind					LDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_208	9012650	14  The GAG-induced alterations are associated with an increase in LDL binding and degradation by human monocyte - derived macrophages and smooth muscle cells.	bind
21425	3	6630	5	13	NULL	NULL	NULL	GAG-induced alterations	Process		is associated with					statement 1	Process	increase in			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_208	9012650	14  The GAG-induced alterations are associated with an increase in LDL binding and degradation by human monocyte - derived macrophages and smooth muscle cells.	bind
21426	4	6630	5	13	NULL	NULL	NULL	GAG-induced alterations	Process		is associated with					statement 2	Process	increase in			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_208	9012650	14  The GAG-induced alterations are associated with an increase in LDL binding and degradation by human monocyte - derived macrophages and smooth muscle cells.	bind
21427	5	6630	5	13	NULL	NULL	NULL	macrophages	Cell	human 	degrade					LDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_208	9012650	14  The GAG-induced alterations are associated with an increase in LDL binding and degradation by human monocyte - derived macrophages and smooth muscle cells.	bind
21430	6	6630	5	13	NULL	NULL	NULL	smooth muscle cells	Cell	human	degrade					LDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_208	9012650	14  The GAG-induced alterations are associated with an increase in LDL binding and degradation by human monocyte - derived macrophages and smooth muscle cells.	bind
21431	7	6630	5	13	NULL	NULL	NULL	GAG-induced alterations	Process		is associated with					statement 5	Process	increase in			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_208	9012650	14  The GAG-induced alterations are associated with an increase in LDL binding and degradation by human monocyte - derived macrophages and smooth muscle cells.	bind
21432	8	6630	5	13	NULL	NULL	NULL	GAG-induced alterations	Process		is associated with					statement 6	Process	increase in			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_208	9012650	14  The GAG-induced alterations are associated with an increase in LDL binding and degradation by human monocyte - derived macrophages and smooth muscle cells.	bind
56204	9	6630	5	13	NULL	NULL	NULL	macrophages	Cell		derived from					monocyte	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_208	9012650	14  The GAG-induced alterations are associated with an increase in LDL binding and degradation by human monocyte - derived macrophages and smooth muscle cells.	bind
18912	1	6630	6	13	NULL	NULL	NULL	 macrophages	Cell	human	bind					LDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_208	9012650	14  The GAG-induced alterations are associated with an increase in LDL binding and degradation by human monocyte - derived macrophages and smooth muscle cells.	bind
18913	2	6630	6	13	NULL	NULL	NULL	smooth muscle cells	Cell	human	bind					LDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_208	9012650	14  The GAG-induced alterations are associated with an increase in LDL binding and degradation by human monocyte - derived macrophages and smooth muscle cells.	bind
18942	3	6630	6	13	NULL	NULL	NULL	GAG-induced alterations	Process		increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_208	9012650	14  The GAG-induced alterations are associated with an increase in LDL binding and degradation by human monocyte - derived macrophages and smooth muscle cells.	bind
18943	4	6630	6	13	NULL	NULL	NULL	GAG-induced alterations	Process		increase					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_208	9012650	14  The GAG-induced alterations are associated with an increase in LDL binding and degradation by human monocyte - derived macrophages and smooth muscle cells.	bind
30315	5	6630	6	13	NULL	NULL	NULL	macrophages	Cell	human	degrade					LDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_208	9012650	14  The GAG-induced alterations are associated with an increase in LDL binding and degradation by human monocyte - derived macrophages and smooth muscle cells.	bind
30316	6	6630	6	13	NULL	NULL	NULL	smooth muscle cells	Cell	human	degrade					LDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_208	9012650	14  The GAG-induced alterations are associated with an increase in LDL binding and degradation by human monocyte - derived macrophages and smooth muscle cells.	bind
30317	7	6630	6	13	NULL	NULL	NULL	GAG-induced alterations	Process		increase					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_208	9012650	14  The GAG-induced alterations are associated with an increase in LDL binding and degradation by human monocyte - derived macrophages and smooth muscle cells.	bind
30318	8	6630	6	13	NULL	NULL	NULL	GAG-induced alterations	Process		increase					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_208	9012650	14  The GAG-induced alterations are associated with an increase in LDL binding and degradation by human monocyte - derived macrophages and smooth muscle cells.	bind
56205	9	6630	6	13	NULL	NULL	NULL	macrophages	Cell		derived from					monocyte	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_208	9012650	14  The GAG-induced alterations are associated with an increase in LDL binding and degradation by human monocyte - derived macrophages and smooth muscle cells.	bind
21433	1	6631	5	13	NULL	NULL	NULL	 coagulation factor VII	GP		bind					tissue factor	GP				NULL	exposed on the surfaces of infiltrating cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1143_s_176	10764685	14  The generation of thrombin is thought to be initiated by coagulation factor VII/VIIa bound to tissue factor, which is exposed on the surfaces of infiltrating cells.	bind
21434	2	6631	5	13	NULL	NULL	NULL	statement 1	Process		initiates					thrombin	GP	generation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1143_s_176	10764685	14  The generation of thrombin is thought to be initiated by coagulation factor VII/VIIa bound to tissue factor, which is exposed on the surfaces of infiltrating cells.	bind
56206	3	6631	5	13	NULL	NULL	NULL	coagulation factor VIIa	GP		bind					tissue factor	GP				NULL	exposed on the surfaces of infiltrating cells.	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1143_s_176	10764685	14  The generation of thrombin is thought to be initiated by coagulation factor VII/VIIa bound to tissue factor, which is exposed on the surfaces of infiltrating cells.	bind
56207	4	6631	5	13	NULL	NULL	NULL	statement 3	Process		initiates					thrombin	GP	generation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1143_s_176	10764685	14  The generation of thrombin is thought to be initiated by coagulation factor VII/VIIa bound to tissue factor, which is exposed on the surfaces of infiltrating cells.	bind
18681	1	6631	6	13	NULL	NULL	NULL	coagulation factor VII	GP		bind					tissue factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1143_s_176	10764685	14  The generation of thrombin is thought to be initiated by coagulation factor VII/VIIa bound to tissue factor, which is exposed on the surfaces of infiltrating cells.	bind
18683	2	6631	6	13	NULL	NULL	NULL	statement 1	Process		initiates					thrombin	GP	generation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1143_s_176	10764685	14  The generation of thrombin is thought to be initiated by coagulation factor VII/VIIa bound to tissue factor, which is exposed on the surfaces of infiltrating cells.	bind
18684	3	6631	6	13	NULL	NULL	NULL	tissue factor	GP		is exposed on					surfaces of infiltrating cells	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1143_s_176	10764685	14  The generation of thrombin is thought to be initiated by coagulation factor VII/VIIa bound to tissue factor, which is exposed on the surfaces of infiltrating cells.	bind
56208	4	6631	6	13	NULL	NULL	NULL	coagulation factor VIIa	GP		bind					tissue factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1143_s_176	10764685	14  The generation of thrombin is thought to be initiated by coagulation factor VII/VIIa bound to tissue factor, which is exposed on the surfaces of infiltrating cells.	bind
56209	5	6631	6	13	NULL	NULL	NULL	statement 4	Process		initiates					thrombin	GP	generation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1143_s_176	10764685	14  The generation of thrombin is thought to be initiated by coagulation factor VII/VIIa bound to tissue factor, which is exposed on the surfaces of infiltrating cells.	bind
21438	1	6632	5	13	NULL	NULL	NULL	von Willebrand factor	GP		bind					GP Ib	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_742_s_162	9727543	14 15  Previous work suggests that the mechanism of activation involves the binding of von Willebrand factor to GP Ib, followed by an increase in cytoplasmic ionized calcium, leading to activation of the GP IIb/IIa receptor, binding of fibrinogen to GP IIb/IIa, and finally aggregation of platelets.	bind
21440	2	6632	5	13	NULL	NULL	NULL	statement 1	Process		is followed by					ionized calcium	Chemical	increase in cytoplasmic			NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_742_s_162	9727543	14 15  Previous work suggests that the mechanism of activation involves the binding of von Willebrand factor to GP Ib, followed by an increase in cytoplasmic ionized calcium, leading to activation of the GP IIb/IIa receptor, binding of fibrinogen to GP IIb/IIa, and finally aggregation of platelets.	bind
21441	3	6632	5	13	NULL	NULL	NULL	statement 2	Process		leads to					GP IIb/IIa receptor	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_742_s_162	9727543	14 15  Previous work suggests that the mechanism of activation involves the binding of von Willebrand factor to GP Ib, followed by an increase in cytoplasmic ionized calcium, leading to activation of the GP IIb/IIa receptor, binding of fibrinogen to GP IIb/IIa, and finally aggregation of platelets.	bind
21442	4	6632	5	13	NULL	NULL	NULL	fibrinogen	GP		bind					GP IIb/IIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_742_s_162	9727543	14 15  Previous work suggests that the mechanism of activation involves the binding of von Willebrand factor to GP Ib, followed by an increase in cytoplasmic ionized calcium, leading to activation of the GP IIb/IIa receptor, binding of fibrinogen to GP IIb/IIa, and finally aggregation of platelets.	bind
21445	5	6632	5	13	NULL	NULL	NULL	statement 2	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_742_s_162	9727543	14 15  Previous work suggests that the mechanism of activation involves the binding of von Willebrand factor to GP Ib, followed by an increase in cytoplasmic ionized calcium, leading to activation of the GP IIb/IIa receptor, binding of fibrinogen to GP IIb/IIa, and finally aggregation of platelets.	bind
21446	6	6632	5	13	NULL	NULL	NULL	statement 2	Process		leads to		finally			platelets	Cell	aggregation of 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_742_s_162	9727543	14 15  Previous work suggests that the mechanism of activation involves the binding of von Willebrand factor to GP Ib, followed by an increase in cytoplasmic ionized calcium, leading to activation of the GP IIb/IIa receptor, binding of fibrinogen to GP IIb/IIa, and finally aggregation of platelets.	bind
18686	1	6632	6	13	NULL	NULL	NULL	von Willebrand factor 	GP		bind					GP Ib	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_742_s_162	9727543	14 15  Previous work suggests that the mechanism of activation involves the binding of von Willebrand factor to GP Ib, followed by an increase in cytoplasmic ionized calcium, leading to activation of the GP IIb/IIa receptor, binding of fibrinogen to GP IIb/IIa, and finally aggregation of platelets.	bind
18687	2	6632	6	13	NULL	NULL	NULL	fibrinogen	GP		bind					GP IIb/IIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_742_s_162	9727543	14 15  Previous work suggests that the mechanism of activation involves the binding of von Willebrand factor to GP Ib, followed by an increase in cytoplasmic ionized calcium, leading to activation of the GP IIb/IIa receptor, binding of fibrinogen to GP IIb/IIa, and finally aggregation of platelets.	bind
18688	3	6632	6	13	NULL	NULL	NULL	cytoplasmic ionized calcium	Chemical	increase in	leads to					GP IIb/IIa receptor	GP	activation of 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_742_s_162	9727543	14 15  Previous work suggests that the mechanism of activation involves the binding of von Willebrand factor to GP Ib, followed by an increase in cytoplasmic ionized calcium, leading to activation of the GP IIb/IIa receptor, binding of fibrinogen to GP IIb/IIa, and finally aggregation of platelets.	bind
18689	4	6632	6	13	NULL	NULL	NULL	statement 2	Process		leads to					aggregation of platelets	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_742_s_162	9727543	14 15  Previous work suggests that the mechanism of activation involves the binding of von Willebrand factor to GP Ib, followed by an increase in cytoplasmic ionized calcium, leading to activation of the GP IIb/IIa receptor, binding of fibrinogen to GP IIb/IIa, and finally aggregation of platelets.	bind
56210	5	6632	6	13	NULL	NULL	NULL	statement 1	Process		is followed by 					ionized calcium	Chemical	increase in cytoplasmic			NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_742_s_162	9727543	14 15  Previous work suggests that the mechanism of activation involves the binding of von Willebrand factor to GP Ib, followed by an increase in cytoplasmic ionized calcium, leading to activation of the GP IIb/IIa receptor, binding of fibrinogen to GP IIb/IIa, and finally aggregation of platelets.	bind
56211	6	6632	6	13	NULL	NULL	NULL	statement 5	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_742_s_162	9727543	14 15  Previous work suggests that the mechanism of activation involves the binding of von Willebrand factor to GP Ib, followed by an increase in cytoplasmic ionized calcium, leading to activation of the GP IIb/IIa receptor, binding of fibrinogen to GP IIb/IIa, and finally aggregation of platelets.	bind
21447	1	6633	5	13	NULL	NULL	NULL	LDL subfractions	GP		bind					LDLRs	GP				NULL	on fibroblasts	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_21	8640407	14 15 16 17 18  Swinkels et al 14  found no differences in the receptor binding of LDL subfractions to LDLRs on fibroblasts and HepG2 cells, but two other studies found that both buoyant ( d=1.024 to 1.037 g/mL) and dense ( d=1.036 to 1.047 g/mL) LDL subfractions had reduced binding affinity compared with medium-density LDL subfractions ( d=1.027 to 1.041 g/mL).	bind
21448	2	6633	5	13	NULL	NULL	NULL	LDL subfractions	GP		bind					LDLRs	GP				NULL	on HepG2 cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_21	8640407	14 15 16 17 18  Swinkels et al 14  found no differences in the receptor binding of LDL subfractions to LDLRs on fibroblasts and HepG2 cells, but two other studies found that both buoyant ( d=1.024 to 1.037 g/mL) and dense ( d=1.036 to 1.047 g/mL) LDL subfractions had reduced binding affinity compared with medium-density LDL subfractions ( d=1.027 to 1.041 g/mL).	bind
24765	3	6633	5	13	NULL	NULL	NULL	statement 1	Process	binding of	is not different from					statement 2	Process	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_21	8640407	14 15 16 17 18  Swinkels et al 14  found no differences in the receptor binding of LDL subfractions to LDLRs on fibroblasts and HepG2 cells, but two other studies found that both buoyant ( d=1.024 to 1.037 g/mL) and dense ( d=1.036 to 1.047 g/mL) LDL subfractions had reduced binding affinity compared with medium-density LDL subfractions ( d=1.027 to 1.041 g/mL).	bind
24766	4	6633	5	13	NULL	NULL	NULL	LDL subfractions	GP	buoyant	bind					LDLRs	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_21	8640407	14 15 16 17 18  Swinkels et al 14  found no differences in the receptor binding of LDL subfractions to LDLRs on fibroblasts and HepG2 cells, but two other studies found that both buoyant ( d=1.024 to 1.037 g/mL) and dense ( d=1.036 to 1.047 g/mL) LDL subfractions had reduced binding affinity compared with medium-density LDL subfractions ( d=1.027 to 1.041 g/mL).	bind
24769	5	6633	5	13	NULL	NULL	NULL	LDL subfractions	GP	dense	bind					LDLRs	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_21	8640407	14 15 16 17 18  Swinkels et al 14  found no differences in the receptor binding of LDL subfractions to LDLRs on fibroblasts and HepG2 cells, but two other studies found that both buoyant ( d=1.024 to 1.037 g/mL) and dense ( d=1.036 to 1.047 g/mL) LDL subfractions had reduced binding affinity compared with medium-density LDL subfractions ( d=1.027 to 1.041 g/mL).	bind
24772	6	6633	5	13	NULL	NULL	NULL	LDL subfractions	GP	medium-density	bind					LDLRs	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_21	8640407	14 15 16 17 18  Swinkels et al 14  found no differences in the receptor binding of LDL subfractions to LDLRs on fibroblasts and HepG2 cells, but two other studies found that both buoyant ( d=1.024 to 1.037 g/mL) and dense ( d=1.036 to 1.047 g/mL) LDL subfractions had reduced binding affinity compared with medium-density LDL subfractions ( d=1.027 to 1.041 g/mL).	bind
24773	7	6633	5	13	NULL	NULL	NULL	statement 4	Process		reduced affinity than					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_21	8640407	14 15 16 17 18  Swinkels et al 14  found no differences in the receptor binding of LDL subfractions to LDLRs on fibroblasts and HepG2 cells, but two other studies found that both buoyant ( d=1.024 to 1.037 g/mL) and dense ( d=1.036 to 1.047 g/mL) LDL subfractions had reduced binding affinity compared with medium-density LDL subfractions ( d=1.027 to 1.041 g/mL).	bind
24774	8	6633	5	13	NULL	NULL	NULL	statement 5	Process		reduced affinity than					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_21	8640407	14 15 16 17 18  Swinkels et al 14  found no differences in the receptor binding of LDL subfractions to LDLRs on fibroblasts and HepG2 cells, but two other studies found that both buoyant ( d=1.024 to 1.037 g/mL) and dense ( d=1.036 to 1.047 g/mL) LDL subfractions had reduced binding affinity compared with medium-density LDL subfractions ( d=1.027 to 1.041 g/mL).	bind
18708	1	6633	6	13	NULL	NULL	NULL	LDL subfraction	GP		bind					LDLR	GP				NULL	fibroblasts	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_21	8640407	14 15 16 17 18  Swinkels et al 14  found no differences in the receptor binding of LDL subfractions to LDLRs on fibroblasts and HepG2 cells, but two other studies found that both buoyant ( d=1.024 to 1.037 g/mL) and dense ( d=1.036 to 1.047 g/mL) LDL subfractions had reduced binding affinity compared with medium-density LDL subfractions ( d=1.027 to 1.041 g/mL).	bind
18709	2	6633	6	13	NULL	NULL	NULL	LDL subfraction	GP		bind					LDLR	GP				NULL	HepG2 cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_21	8640407	14 15 16 17 18  Swinkels et al 14  found no differences in the receptor binding of LDL subfractions to LDLRs on fibroblasts and HepG2 cells, but two other studies found that both buoyant ( d=1.024 to 1.037 g/mL) and dense ( d=1.036 to 1.047 g/mL) LDL subfractions had reduced binding affinity compared with medium-density LDL subfractions ( d=1.027 to 1.041 g/mL).	bind
18710	3	6633	6	13	NULL	NULL	NULL	LDL subfraction	GP	buoyant	bind					LDLR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_21	8640407	14 15 16 17 18  Swinkels et al 14  found no differences in the receptor binding of LDL subfractions to LDLRs on fibroblasts and HepG2 cells, but two other studies found that both buoyant ( d=1.024 to 1.037 g/mL) and dense ( d=1.036 to 1.047 g/mL) LDL subfractions had reduced binding affinity compared with medium-density LDL subfractions ( d=1.027 to 1.041 g/mL).	bind
18711	4	6633	6	13	NULL	NULL	NULL	LDL subfraction	GP	dense	bind					LDLR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_21	8640407	14 15 16 17 18  Swinkels et al 14  found no differences in the receptor binding of LDL subfractions to LDLRs on fibroblasts and HepG2 cells, but two other studies found that both buoyant ( d=1.024 to 1.037 g/mL) and dense ( d=1.036 to 1.047 g/mL) LDL subfractions had reduced binding affinity compared with medium-density LDL subfractions ( d=1.027 to 1.041 g/mL).	bind
30274	5	6633	6	13	NULL	NULL	NULL	LDL subfraction	GP	medium	bind					LDLR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_21	8640407	14 15 16 17 18  Swinkels et al 14  found no differences in the receptor binding of LDL subfractions to LDLRs on fibroblasts and HepG2 cells, but two other studies found that both buoyant ( d=1.024 to 1.037 g/mL) and dense ( d=1.036 to 1.047 g/mL) LDL subfractions had reduced binding affinity compared with medium-density LDL subfractions ( d=1.027 to 1.041 g/mL).	bind
30275	6	6633	6	13	NULL	NULL	NULL	statement 3	Process	affinity of	is reduced in comparision with					statement 5	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_21	8640407	14 15 16 17 18  Swinkels et al 14  found no differences in the receptor binding of LDL subfractions to LDLRs on fibroblasts and HepG2 cells, but two other studies found that both buoyant ( d=1.024 to 1.037 g/mL) and dense ( d=1.036 to 1.047 g/mL) LDL subfractions had reduced binding affinity compared with medium-density LDL subfractions ( d=1.027 to 1.041 g/mL).	bind
30276	7	6633	6	13	NULL	NULL	NULL	statement 4	Process	affinity of	is reduced in comparision with					statement 5	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_21	8640407	14 15 16 17 18  Swinkels et al 14  found no differences in the receptor binding of LDL subfractions to LDLRs on fibroblasts and HepG2 cells, but two other studies found that both buoyant ( d=1.024 to 1.037 g/mL) and dense ( d=1.036 to 1.047 g/mL) LDL subfractions had reduced binding affinity compared with medium-density LDL subfractions ( d=1.027 to 1.041 g/mL).	bind
56212	8	6633	6	13	NULL	NULL	NULL	statement 1	Process	binding of	is not different from					statement 2	Process	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_6_794_s_21	8640407	14 15 16 17 18  Swinkels et al 14  found no differences in the receptor binding of LDL subfractions to LDLRs on fibroblasts and HepG2 cells, but two other studies found that both buoyant ( d=1.024 to 1.037 g/mL) and dense ( d=1.036 to 1.047 g/mL) LDL subfractions had reduced binding affinity compared with medium-density LDL subfractions ( d=1.027 to 1.041 g/mL).	bind
21449	1	6634	5	13	NULL	NULL	NULL	CA-4	GP		bind					tubulin	GP		colchicine binding site		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_1097_s_151	11891206	14 Although the mechanism of action giving rise to this effect remains to be elucidated, it has been proposed that CA-4, which binds to the colchicine binding site of tubulin, elicits a shape change in the endothelial cells of tumor vessels that compromises the integrity of the lumenal monolayer.	bind
21450	2	6634	5	13	NULL	NULL	NULL	CA-4	GP		elicits					endothelial cells	Cell	shape change			NULL	of tumor vessels	NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_1097_s_151	11891206	14 Although the mechanism of action giving rise to this effect remains to be elucidated, it has been proposed that CA-4, which binds to the colchicine binding site of tubulin, elicits a shape change in the endothelial cells of tumor vessels that compromises the integrity of the lumenal monolayer.	bind
21451	3	6634	5	13	NULL	NULL	NULL	statement 2	Process		compromises					lumenal monolayer	OrganismPart	integrity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_1097_s_151	11891206	14 Although the mechanism of action giving rise to this effect remains to be elucidated, it has been proposed that CA-4, which binds to the colchicine binding site of tubulin, elicits a shape change in the endothelial cells of tumor vessels that compromises the integrity of the lumenal monolayer.	bind
18712	1	6634	6	13	NULL	NULL	NULL	CA-4	GP		bind					tubulin	GP		colchicine binding site		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_1097_s_151	11891206	14 Although the mechanism of action giving rise to this effect remains to be elucidated, it has been proposed that CA-4, which binds to the colchicine binding site of tubulin, elicits a shape change in the endothelial cells of tumor vessels that compromises the integrity of the lumenal monolayer.	bind
18713	2	6634	6	13	NULL	NULL	NULL	CA-4	GP		elicits					endothelial  cells	Cell	shape change of			NULL	tumour vessels	NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_1097_s_151	11891206	14 Although the mechanism of action giving rise to this effect remains to be elucidated, it has been proposed that CA-4, which binds to the colchicine binding site of tubulin, elicits a shape change in the endothelial cells of tumor vessels that compromises the integrity of the lumenal monolayer.	bind
18714	3	6634	6	13	NULL	NULL	NULL	statement 2	Process		compromises					lumenal monolayer	OrganismPart	integrity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_1097_s_151	11891206	14 Although the mechanism of action giving rise to this effect remains to be elucidated, it has been proposed that CA-4, which binds to the colchicine binding site of tubulin, elicits a shape change in the endothelial cells of tumor vessels that compromises the integrity of the lumenal monolayer.	bind
21452	1	6635	5	13	NULL	NULL	NULL	PS1	GP		associates with					E-cadherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_5_2381_s_62	11226248	14 and  22), our data show that PS1 associates with E-cadherin even when catenins are not bound to E-cadherin.	bind
21453	2	6635	5	13	NULL	NULL	NULL	catenins	GP		bind					E-cadherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_5_2381_s_62	11226248	14 and  22), our data show that PS1 associates with E-cadherin even when catenins are not bound to E-cadherin.	bind
21454	3	6635	5	13	NULL	NULL	NULL	statement 1	Process		in the absence of					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_5_2381_s_62	11226248	14 and  22), our data show that PS1 associates with E-cadherin even when catenins are not bound to E-cadherin.	bind
18715	1	6635	6	13	NULL	NULL	NULL	PS1	GP		associates with					E-cadherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_5_2381_s_62	11226248	14 and  22), our data show that PS1 associates with E-cadherin even when catenins are not bound to E-cadherin.	bind
18716	2	6635	6	13	NULL	NULL	NULL	catenin	GP		does not bind					E-cadherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_5_2381_s_62	11226248	14 and  22), our data show that PS1 associates with E-cadherin even when catenins are not bound to E-cadherin.	bind
18717	3	6635	6	13	NULL	NULL	NULL	statement 1	Process		occurs irrespective of					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_5_2381_s_62	11226248	14 and  22), our data show that PS1 associates with E-cadherin even when catenins are not bound to E-cadherin.	bind
21455	1	6636	5	13	NULL	NULL	NULL	laminin 5	GP		dimerizes with					laminin 6	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_2_459_s_18	11839566	14 Instead, laminin 5 forms a dimer with laminin 6 or 7 18  and binds to collagen VII. 19, 20  In addition, laminin 5 is synthesized as a 460-kd precursor that is extracellularly converted into tissular forms of 440- and 400-kd by enzymatic processing.	bind
21456	2	6636	5	13	NULL	NULL	NULL	laminin 5	GP		dimerizes with					laminin 7	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_2_459_s_18	11839566	14 Instead, laminin 5 forms a dimer with laminin 6 or 7 18  and binds to collagen VII. 19, 20  In addition, laminin 5 is synthesized as a 460-kd precursor that is extracellularly converted into tissular forms of 440- and 400-kd by enzymatic processing.	bind
21457	3	6636	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_2_459_s_18	11839566	14 Instead, laminin 5 forms a dimer with laminin 6 or 7 18  and binds to collagen VII. 19, 20  In addition, laminin 5 is synthesized as a 460-kd precursor that is extracellularly converted into tissular forms of 440- and 400-kd by enzymatic processing.	bind
21458	4	6636	5	13	NULL	NULL	NULL	laminin 5	GP		bind					collagen VII	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_2_459_s_18	11839566	14 Instead, laminin 5 forms a dimer with laminin 6 or 7 18  and binds to collagen VII. 19, 20  In addition, laminin 5 is synthesized as a 460-kd precursor that is extracellularly converted into tissular forms of 440- and 400-kd by enzymatic processing.	bind
21461	5	6636	5	13	NULL	NULL	NULL	laminin 5	GP	precursor	is converted into		extracellularly			tissular forms					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_2_459_s_18	11839566	14 Instead, laminin 5 forms a dimer with laminin 6 or 7 18  and binds to collagen VII. 19, 20  In addition, laminin 5 is synthesized as a 460-kd precursor that is extracellularly converted into tissular forms of 440- and 400-kd by enzymatic processing.	bind
21462	6	6636	5	13	NULL	NULL	NULL	enzymatic processing	Process		is required for					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_2_459_s_18	11839566	14 Instead, laminin 5 forms a dimer with laminin 6 or 7 18  and binds to collagen VII. 19, 20  In addition, laminin 5 is synthesized as a 460-kd precursor that is extracellularly converted into tissular forms of 440- and 400-kd by enzymatic processing.	bind
18718	1	6636	6	13	NULL	NULL	NULL	laminin 5	GP		forms a dimer with					laminin 6	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_2_459_s_18	11839566	14 Instead, laminin 5 forms a dimer with laminin 6 or 7 18  and binds to collagen VII. 19, 20  In addition, laminin 5 is synthesized as a 460-kd precursor that is extracellularly converted into tissular forms of 440- and 400-kd by enzymatic processing.	bind
18719	2	6636	6	13	NULL	NULL	NULL	laminin 5	GP		forms a dimer with					laminin 7	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_2_459_s_18	11839566	14 Instead, laminin 5 forms a dimer with laminin 6 or 7 18  and binds to collagen VII. 19, 20  In addition, laminin 5 is synthesized as a 460-kd precursor that is extracellularly converted into tissular forms of 440- and 400-kd by enzymatic processing.	bind
18720	3	6636	6	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_2_459_s_18	11839566	14 Instead, laminin 5 forms a dimer with laminin 6 or 7 18  and binds to collagen VII. 19, 20  In addition, laminin 5 is synthesized as a 460-kd precursor that is extracellularly converted into tissular forms of 440- and 400-kd by enzymatic processing.	bind
18721	4	6636	6	13	NULL	NULL	NULL	laminin 5	GP		bind					collagen VII	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_2_459_s_18	11839566	14 Instead, laminin 5 forms a dimer with laminin 6 or 7 18  and binds to collagen VII. 19, 20  In addition, laminin 5 is synthesized as a 460-kd precursor that is extracellularly converted into tissular forms of 440- and 400-kd by enzymatic processing.	bind
56213	5	6636	6	13	NULL	NULL	NULL	laminin 5	GP	precursor	coverted to		extracellularly			tissular forms					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_2_459_s_18	11839566	14 Instead, laminin 5 forms a dimer with laminin 6 or 7 18  and binds to collagen VII. 19, 20  In addition, laminin 5 is synthesized as a 460-kd precursor that is extracellularly converted into tissular forms of 440- and 400-kd by enzymatic processing.	bind
56214	6	6636	6	13	NULL	NULL	NULL	enzymatic processing	Process		is required for					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_2_459_s_18	11839566	14 Instead, laminin 5 forms a dimer with laminin 6 or 7 18  and binds to collagen VII. 19, 20  In addition, laminin 5 is synthesized as a 460-kd precursor that is extracellularly converted into tissular forms of 440- and 400-kd by enzymatic processing.	bind
21463	1	6637	5	13	NULL	NULL	NULL	Sp1	GP		bind									Sp1 motif	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1202_s_225	14593001	14 It has been proposed that Sp3 competes with Sp1 binding to the Sp1 motif and thus serves as negative regulator of Sp1 sites.	bind
21464	2	6637	5	13	NULL	NULL	NULL	Sp3	GP		bind									Sp1 motif	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1202_s_225	14593001	14 It has been proposed that Sp3 competes with Sp1 binding to the Sp1 motif and thus serves as negative regulator of Sp1 sites.	bind
21465	3	6637	5	13	NULL	NULL	NULL	statement 2	Process		competes with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1202_s_225	14593001	14 It has been proposed that Sp3 competes with Sp1 binding to the Sp1 motif and thus serves as negative regulator of Sp1 sites.	bind
21466	4	6637	5	13	NULL	NULL	NULL	Sp3	GP		regulates		negatively							Sp1 sites	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1202_s_225	14593001	14 It has been proposed that Sp3 competes with Sp1 binding to the Sp1 motif and thus serves as negative regulator of Sp1 sites.	bind
21467	5	6637	5	13	NULL	NULL	NULL	statement 3	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1202_s_225	14593001	14 It has been proposed that Sp3 competes with Sp1 binding to the Sp1 motif and thus serves as negative regulator of Sp1 sites.	bind
18722	1	6637	6	13	NULL	NULL	NULL	Sp1	GP		bind									Sp1 motif	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1202_s_225	14593001	14 It has been proposed that Sp3 competes with Sp1 binding to the Sp1 motif and thus serves as negative regulator of Sp1 sites.	bind
18723	2	6637	6	13	NULL	NULL	NULL	Sp3	GP		bind									Sp1 motif	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1202_s_225	14593001	14 It has been proposed that Sp3 competes with Sp1 binding to the Sp1 motif and thus serves as negative regulator of Sp1 sites.	bind
18724	3	6637	6	13	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1202_s_225	14593001	14 It has been proposed that Sp3 competes with Sp1 binding to the Sp1 motif and thus serves as negative regulator of Sp1 sites.	bind
18725	4	6637	6	13	NULL	NULL	NULL	Sp3	GP		regulates		negatively 							Sp1 sites	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1202_s_225	14593001	14 It has been proposed that Sp3 competes with Sp1 binding to the Sp1 motif and thus serves as negative regulator of Sp1 sites.	bind
30273	5	6637	6	13	NULL	NULL	NULL	statement 3	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1202_s_225	14593001	14 It has been proposed that Sp3 competes with Sp1 binding to the Sp1 motif and thus serves as negative regulator of Sp1 sites.	bind
21468	1	6638	5	13	NULL	NULL	NULL	CYP2C9	GP		increase					COX-2	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_321_s_170	15569819	14 Moreover, the CYP2C9-induced increase in COX-2 expression reported here also depends on an increase in the DNA binding of CREB to the COX-2 promoter.	bind
21469	2	6638	5	13	NULL	NULL	NULL	CREB	GP		bind					COX-2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_321_s_170	15569819	14 Moreover, the CYP2C9-induced increase in COX-2 expression reported here also depends on an increase in the DNA binding of CREB to the COX-2 promoter.	bind
21470	3	6638	5	13	NULL	NULL	NULL	statement 1	Process		depends upon					statement 2	Process	increase in			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_321_s_170	15569819	14 Moreover, the CYP2C9-induced increase in COX-2 expression reported here also depends on an increase in the DNA binding of CREB to the COX-2 promoter.	bind
18726	1	6638	6	13	NULL	NULL	NULL	CYP2C9	GP		increase					COX-2	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_321_s_170	15569819	14 Moreover, the CYP2C9-induced increase in COX-2 expression reported here also depends on an increase in the DNA binding of CREB to the COX-2 promoter.	bind
18727	2	6638	6	13	NULL	NULL	NULL	CREB	GP		bind					COX-2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_321_s_170	15569819	14 Moreover, the CYP2C9-induced increase in COX-2 expression reported here also depends on an increase in the DNA binding of CREB to the COX-2 promoter.	bind
30272	3	6638	6	13	NULL	NULL	NULL	statement 1	Process		depends on					statement 2	Process	increase in			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_321_s_170	15569819	14 Moreover, the CYP2C9-induced increase in COX-2 expression reported here also depends on an increase in the DNA binding of CREB to the COX-2 promoter.	bind
21471	1	6639	5	13	NULL	NULL	NULL	MR	GP		bind									glucocorticoid response elements	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_circulationres_96_6_643_s_35	15718497	14 MR binds in vitro to glucocorticoid and mineralocorticoid response elements in a ligand-dependent manner.	bind
21472	2	6639	5	13	NULL	NULL	NULL	statement 1	Process		is dependent on					ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_6_643_s_35	15718497	14 MR binds in vitro to glucocorticoid and mineralocorticoid response elements in a ligand-dependent manner.	bind
21473	3	6639	5	13	NULL	NULL	NULL	MR	GP		bind									mineralocorticoid response elements	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_circulationres_96_6_643_s_35	15718497	14 MR binds in vitro to glucocorticoid and mineralocorticoid response elements in a ligand-dependent manner.	bind
21474	4	6639	5	13	NULL	NULL	NULL	statement 3	Process		is dependent on					ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_6_643_s_35	15718497	14 MR binds in vitro to glucocorticoid and mineralocorticoid response elements in a ligand-dependent manner.	bind
18728	1	6639	6	13	NULL	NULL	NULL	MR	GP		bind									glucocorticoid responsive element	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_circulationres_96_6_643_s_35	15718497	14 MR binds in vitro to glucocorticoid and mineralocorticoid response elements in a ligand-dependent manner.	bind
18729	2	6639	6	13	NULL	NULL	NULL	MR	GP		bind									mineralocorticoid response element	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_circulationres_96_6_643_s_35	15718497	14 MR binds in vitro to glucocorticoid and mineralocorticoid response elements in a ligand-dependent manner.	bind
18730	3	6639	6	13	NULL	NULL	NULL	statement 1	Process		is dependent on					ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_6_643_s_35	15718497	14 MR binds in vitro to glucocorticoid and mineralocorticoid response elements in a ligand-dependent manner.	bind
18731	4	6639	6	13	NULL	NULL	NULL	statement 2	Process		is dependent on					ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_6_643_s_35	15718497	14 MR binds in vitro to glucocorticoid and mineralocorticoid response elements in a ligand-dependent manner.	bind
24775	1	6640	5	13	NULL	NULL	NULL	Flt-sel	GP		elicits		potently			PAE	Cell	migration of			NULL	in PAE cells transfected with an Flt-1 mutant receptor	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1934_s_191	11742867	14 Recently Gille et al 15 showed that Flt-sel could potently elicit PAE migration by using PAE cells transfected with an Flt-1 mutant receptor in which 3 amino acids of the juxtamembrane region were exchanged with KDR. 30 Finally, the lack of response to PLGF, a naturally occurring VEGF family member that selectively binds Flt-1, further substantiates the differential roles of KDR versus Flt-1 in endothelial tube formation.	bind
24776	2	6640	5	13	NULL	NULL	NULL	Flt-1 receptor	GP	mutant	is exchanged with			3 amino acids of the juxtamembrane region		KDR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1934_s_191	11742867	14 Recently Gille et al 15 showed that Flt-sel could potently elicit PAE migration by using PAE cells transfected with an Flt-1 mutant receptor in which 3 amino acids of the juxtamembrane region were exchanged with KDR. 30 Finally, the lack of response to PLGF, a naturally occurring VEGF family member that selectively binds Flt-1, further substantiates the differential roles of KDR versus Flt-1 in endothelial tube formation.	bind
24777	3	6640	5	13	NULL	NULL	NULL	PLGF	GP		is a member of					VEGF family	GP	naturally occurring			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1934_s_191	11742867	14 Recently Gille et al 15 showed that Flt-sel could potently elicit PAE migration by using PAE cells transfected with an Flt-1 mutant receptor in which 3 amino acids of the juxtamembrane region were exchanged with KDR. 30 Finally, the lack of response to PLGF, a naturally occurring VEGF family member that selectively binds Flt-1, further substantiates the differential roles of KDR versus Flt-1 in endothelial tube formation.	bind
24778	4	6640	5	13	NULL	NULL	NULL	PLGF	GP		bind		selectively			Flt-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1934_s_191	11742867	14 Recently Gille et al 15 showed that Flt-sel could potently elicit PAE migration by using PAE cells transfected with an Flt-1 mutant receptor in which 3 amino acids of the juxtamembrane region were exchanged with KDR. 30 Finally, the lack of response to PLGF, a naturally occurring VEGF family member that selectively binds Flt-1, further substantiates the differential roles of KDR versus Flt-1 in endothelial tube formation.	bind
24781	5	6640	5	13	NULL	NULL	NULL	KDR	GP		plays a role in		differential			endothelial tube	OrganismPart	formation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1934_s_191	11742867	14 Recently Gille et al 15 showed that Flt-sel could potently elicit PAE migration by using PAE cells transfected with an Flt-1 mutant receptor in which 3 amino acids of the juxtamembrane region were exchanged with KDR. 30 Finally, the lack of response to PLGF, a naturally occurring VEGF family member that selectively binds Flt-1, further substantiates the differential roles of KDR versus Flt-1 in endothelial tube formation.	bind
24782	6	6640	5	13	NULL	NULL	NULL	Flt-1	GP		plays a role in		differential			endothelial tube	OrganismPart	formation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1934_s_191	11742867	14 Recently Gille et al 15 showed that Flt-sel could potently elicit PAE migration by using PAE cells transfected with an Flt-1 mutant receptor in which 3 amino acids of the juxtamembrane region were exchanged with KDR. 30 Finally, the lack of response to PLGF, a naturally occurring VEGF family member that selectively binds Flt-1, further substantiates the differential roles of KDR versus Flt-1 in endothelial tube formation.	bind
24784	7	6640	5	13	NULL	NULL	NULL	PLGF	GP	lack of response to	substantiates					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1934_s_191	11742867	14 Recently Gille et al 15 showed that Flt-sel could potently elicit PAE migration by using PAE cells transfected with an Flt-1 mutant receptor in which 3 amino acids of the juxtamembrane region were exchanged with KDR. 30 Finally, the lack of response to PLGF, a naturally occurring VEGF family member that selectively binds Flt-1, further substantiates the differential roles of KDR versus Flt-1 in endothelial tube formation.	bind
24786	8	6640	5	13	NULL	NULL	NULL	PLGF	GP	lack of response to	substantiates					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1934_s_191	11742867	14 Recently Gille et al 15 showed that Flt-sel could potently elicit PAE migration by using PAE cells transfected with an Flt-1 mutant receptor in which 3 amino acids of the juxtamembrane region were exchanged with KDR. 30 Finally, the lack of response to PLGF, a naturally occurring VEGF family member that selectively binds Flt-1, further substantiates the differential roles of KDR versus Flt-1 in endothelial tube formation.	bind
18732	1	6640	6	13	NULL	NULL	NULL	Flt-sel	GP		elicit 		potentially			PAE	Cell	migration of			NULL	PAE cells transfected with an Flt-1 mutant receptor	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1934_s_191	11742867	14 Recently Gille et al 15 showed that Flt-sel could potently elicit PAE migration by using PAE cells transfected with an Flt-1 mutant receptor in which 3 amino acids of the juxtamembrane region were exchanged with KDR. 30 Finally, the lack of response to PLGF, a naturally occurring VEGF family member that selectively binds Flt-1, further substantiates the differential roles of KDR versus Flt-1 in endothelial tube formation.	bind
18733	2	6640	6	13	NULL	NULL	NULL	PLGF	GP		bind		selectively			Flt-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1934_s_191	11742867	14 Recently Gille et al 15 showed that Flt-sel could potently elicit PAE migration by using PAE cells transfected with an Flt-1 mutant receptor in which 3 amino acids of the juxtamembrane region were exchanged with KDR. 30 Finally, the lack of response to PLGF, a naturally occurring VEGF family member that selectively binds Flt-1, further substantiates the differential roles of KDR versus Flt-1 in endothelial tube formation.	bind
18734	3	6640	6	13	NULL	NULL	NULL	Flt-1	GP		plays a role in		differential			endothelial tube 	OrganismPart	formation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1934_s_191	11742867	14 Recently Gille et al 15 showed that Flt-sel could potently elicit PAE migration by using PAE cells transfected with an Flt-1 mutant receptor in which 3 amino acids of the juxtamembrane region were exchanged with KDR. 30 Finally, the lack of response to PLGF, a naturally occurring VEGF family member that selectively binds Flt-1, further substantiates the differential roles of KDR versus Flt-1 in endothelial tube formation.	bind
56215	4	6640	6	13	NULL	NULL	NULL	Flt-1 receptor	GP	mutant	exchanged with			3 amino acids of the juxtamembrane region		KDR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1934_s_191	11742867	14 Recently Gille et al 15 showed that Flt-sel could potently elicit PAE migration by using PAE cells transfected with an Flt-1 mutant receptor in which 3 amino acids of the juxtamembrane region were exchanged with KDR. 30 Finally, the lack of response to PLGF, a naturally occurring VEGF family member that selectively binds Flt-1, further substantiates the differential roles of KDR versus Flt-1 in endothelial tube formation.	bind
56216	5	6640	6	13	NULL	NULL	NULL	KDR	GP		play role in		differential			endothelial tube	OrganismPart	formation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1934_s_191	11742867	14 Recently Gille et al 15 showed that Flt-sel could potently elicit PAE migration by using PAE cells transfected with an Flt-1 mutant receptor in which 3 amino acids of the juxtamembrane region were exchanged with KDR. 30 Finally, the lack of response to PLGF, a naturally occurring VEGF family member that selectively binds Flt-1, further substantiates the differential roles of KDR versus Flt-1 in endothelial tube formation.	bind
56218	6	6640	6	13	NULL	NULL	NULL	PLGF	GP		is a member of					VEGF family	GP	naturally occurring			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1934_s_191	11742867	14 Recently Gille et al 15 showed that Flt-sel could potently elicit PAE migration by using PAE cells transfected with an Flt-1 mutant receptor in which 3 amino acids of the juxtamembrane region were exchanged with KDR. 30 Finally, the lack of response to PLGF, a naturally occurring VEGF family member that selectively binds Flt-1, further substantiates the differential roles of KDR versus Flt-1 in endothelial tube formation.	bind
56219	7	6640	6	13	NULL	NULL	NULL	PLGF	GP	lack of response to	substantiates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1934_s_191	11742867	14 Recently Gille et al 15 showed that Flt-sel could potently elicit PAE migration by using PAE cells transfected with an Flt-1 mutant receptor in which 3 amino acids of the juxtamembrane region were exchanged with KDR. 30 Finally, the lack of response to PLGF, a naturally occurring VEGF family member that selectively binds Flt-1, further substantiates the differential roles of KDR versus Flt-1 in endothelial tube formation.	bind
56220	8	6640	6	13	NULL	NULL	NULL	PLGF	GP	lack of response to	substantiates					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1934_s_191	11742867	14 Recently Gille et al 15 showed that Flt-sel could potently elicit PAE migration by using PAE cells transfected with an Flt-1 mutant receptor in which 3 amino acids of the juxtamembrane region were exchanged with KDR. 30 Finally, the lack of response to PLGF, a naturally occurring VEGF family member that selectively binds Flt-1, further substantiates the differential roles of KDR versus Flt-1 in endothelial tube formation.	bind
21475	1	6641	5	13	NULL	NULL	NULL	DDAH2	GP		bind		directly			PKA	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1419_s_29	16794231	14 Surprisingly, the mechanism is not via increased NO production, as had been previously assumed, but by the direct binding of DDAH2 to protein kinase A (PKA) and subsequent phosphorylation of the transcription factor Sp1.	bind
21476	2	6641	5	13	NULL	NULL	NULL	PKA	GP		is					protein kinase A	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1419_s_29	16794231	14 Surprisingly, the mechanism is not via increased NO production, as had been previously assumed, but by the direct binding of DDAH2 to protein kinase A (PKA) and subsequent phosphorylation of the transcription factor Sp1.	bind
21477	3	6641	5	13	NULL	NULL	NULL	statement 1	Process		phosphorylate		subsequently			Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1419_s_29	16794231	14 Surprisingly, the mechanism is not via increased NO production, as had been previously assumed, but by the direct binding of DDAH2 to protein kinase A (PKA) and subsequent phosphorylation of the transcription factor Sp1.	bind
30339	4	6641	5	13	NULL	NULL	NULL	Sp1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1419_s_29	16794231	14 Surprisingly, the mechanism is not via increased NO production, as had been previously assumed, but by the direct binding of DDAH2 to protein kinase A (PKA) and subsequent phosphorylation of the transcription factor Sp1.	bind
18735	1	6641	6	13	NULL	NULL	NULL	DDAH2	GP		bind		directly			PKA	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1419_s_29	16794231	14 Surprisingly, the mechanism is not via increased NO production, as had been previously assumed, but by the direct binding of DDAH2 to protein kinase A (PKA) and subsequent phosphorylation of the transcription factor Sp1.	bind
18736	2	6641	6	13	NULL	NULL	NULL	PKA	GP		is					protein kinase A	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1419_s_29	16794231	14 Surprisingly, the mechanism is not via increased NO production, as had been previously assumed, but by the direct binding of DDAH2 to protein kinase A (PKA) and subsequent phosphorylation of the transcription factor Sp1.	bind
18737	3	6641	6	13	NULL	NULL	NULL	statement 1	Process		phosphorylate					Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1419_s_29	16794231	14 Surprisingly, the mechanism is not via increased NO production, as had been previously assumed, but by the direct binding of DDAH2 to protein kinase A (PKA) and subsequent phosphorylation of the transcription factor Sp1.	bind
30458	4	6641	6	13	NULL	NULL	NULL	Sp1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1419_s_29	16794231	14 Surprisingly, the mechanism is not via increased NO production, as had been previously assumed, but by the direct binding of DDAH2 to protein kinase A (PKA) and subsequent phosphorylation of the transcription factor Sp1.	bind
21478	1	6642	5	13	NULL	NULL	NULL	syndecan-4	GP		bind		specifically	extracellular domain		foreskin fibroblasts	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_5_488_s_45	15774861	14 The extracellular domain of syndecan-4 binds specifically to human foreskin fibroblasts (IC50=10 - 8 M) and mouse aortic endothelial cells, as well as other cell types, whereas same-species syndecan family members did not efficiently compete with these interactions.	bind
21479	2	6642	5	13	NULL	NULL	NULL	syndecan-4	GP		bind		specifically	extracellular domain		aortic endothelial cells	Cell	mouse			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_5_488_s_45	15774861	14 The extracellular domain of syndecan-4 binds specifically to human foreskin fibroblasts (IC50=10 - 8 M) and mouse aortic endothelial cells, as well as other cell types, whereas same-species syndecan family members did not efficiently compete with these interactions.	bind
21480	3	6642	5	13	NULL	NULL	NULL	same-species syndecan family members	GP		does not compete with		efficiently			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_5_488_s_45	15774861	14 The extracellular domain of syndecan-4 binds specifically to human foreskin fibroblasts (IC50=10 - 8 M) and mouse aortic endothelial cells, as well as other cell types, whereas same-species syndecan family members did not efficiently compete with these interactions.	bind
21481	4	6642	5	13	NULL	NULL	NULL	same-species syndecan family members	GP		does not compete with		efficiently			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_5_488_s_45	15774861	14 The extracellular domain of syndecan-4 binds specifically to human foreskin fibroblasts (IC50=10 - 8 M) and mouse aortic endothelial cells, as well as other cell types, whereas same-species syndecan family members did not efficiently compete with these interactions.	bind
18738	1	6642	6	13	NULL	NULL	NULL	syndecan-4	GP		bind		specifically	extracellular domain		foreskin fibroblasts	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_5_488_s_45	15774861	14 The extracellular domain of syndecan-4 binds specifically to human foreskin fibroblasts (IC50=10 - 8 M) and mouse aortic endothelial cells, as well as other cell types, whereas same-species syndecan family members did not efficiently compete with these interactions.	bind
18739	2	6642	6	13	NULL	NULL	NULL	syndecan-4	GP		bind		specifically	extracellular domain		aortic endothelial cells	Cell	mouse			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_5_488_s_45	15774861	14 The extracellular domain of syndecan-4 binds specifically to human foreskin fibroblasts (IC50=10 - 8 M) and mouse aortic endothelial cells, as well as other cell types, whereas same-species syndecan family members did not efficiently compete with these interactions.	bind
30459	3	6642	6	13	NULL	NULL	NULL	same-species syndecan family members	GP		does not compete with		efficiently			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_5_488_s_45	15774861	14 The extracellular domain of syndecan-4 binds specifically to human foreskin fibroblasts (IC50=10 - 8 M) and mouse aortic endothelial cells, as well as other cell types, whereas same-species syndecan family members did not efficiently compete with these interactions.	bind
30460	4	6642	6	13	NULL	NULL	NULL	same-species syndecan family members	GP		does not compete with		efficiently			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_5_488_s_45	15774861	14 The extracellular domain of syndecan-4 binds specifically to human foreskin fibroblasts (IC50=10 - 8 M) and mouse aortic endothelial cells, as well as other cell types, whereas same-species syndecan family members did not efficiently compete with these interactions.	bind
24791	1	6643	5	13	NULL	NULL	NULL	L4 protein	GP		bind			region joining alpha3 and alpha2 helices		23S rRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_6_935_s_77	12039885	14 This region is located in a segment of the L4 protein joining two alpha-helices, designated alpha3 and alpha2, which is essential for the binding of this protein to 23S rRNA.	bind
31143	1	6643	6	13	NULL	NULL	NULL	L4 protein	GP		bind			region joining alpha3 and alpha2 helices		23S rRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_6_935_s_77	12039885	14 This region is located in a segment of the L4 protein joining two alpha-helices, designated alpha3 and alpha2, which is essential for the binding of this protein to 23S rRNA.	bind
21557	1	6645	5	13	NULL	NULL	NULL	HEB	GP		interacts with		possibly			SRF	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
21558	2	6645	5	13	NULL	NULL	NULL	E2-2	GP		interacts with		possibly			SRF	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
21559	3	6645	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
21565	5	6645	5	13	NULL	NULL	NULL	statement 1	Process		occurs through					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
21567	7	6645	5	13	NULL	NULL	NULL	statement 1	Process		occurs through					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
21568	8	6645	5	13	NULL	NULL	NULL	statement 5	Process		is an alternative to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
21570	9	6645	5	13	NULL	NULL	NULL	statement 2	Process		occurs through					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
21577	10	6645	5	13	NULL	NULL	NULL	statement 2	Process		occurs through					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
21578	11	6645	5	13	NULL	NULL	NULL	statement 9	Process		is an alternative to					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
21579	12	6645	5	13	NULL	NULL	NULL	SRF	GP		bind					CArG probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
30342	4	6645	5	13	NULL	NULL	NULL	ternary complex	GP	stable	forms on					CArG probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
30343	6	6645	5	13	NULL	NULL	NULL	ternary complex	GP	stable	forms on					E-box probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
18944	1	6645	6	13	NULL	NULL	NULL	HEB	GP		interacts with					SRF	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
18945	2	6645	6	13	NULL	NULL	NULL	E2-2	GP		interacts with					SRF	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
18946	3	6645	6	13	NULL	NULL	NULL	SRF	GP		bind									CArG probe	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
19047	4	6645	6	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
19048	6	6645	6	13	NULL	NULL	NULL	ternary complex	GP	stable	forms on					E-box probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
19049	7	6645	6	13	NULL	NULL	NULL	statement 1	Process		occurs through					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
30461	5	6645	6	13	NULL	NULL	NULL	ternary complex	GP	stable	forms on					CArG probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
30462	8	6645	6	13	NULL	NULL	NULL	statement 1	Process		occurs through					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
30463	9	6645	6	13	NULL	NULL	NULL	statement 2	Process		occurs through					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
56221	10	6645	6	13	NULL	NULL	NULL	statement 2	Process		occurs through					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
56222	11	6645	6	13	NULL	NULL	NULL	statement 7	Process		is an alternative to					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
56223	12	6645	6	13	NULL	NULL	NULL	statement 9	Process		is an alternative to					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_840_s_159	12663487	14 Using EMSAs, we investigated the possibility that HEB or E2-2 interacted with SRF (through the formation of a stable ternary complex on a CArG probe or E-box probe) or enhanced SRF binding to a CArG probe.	bind
21618	1	6646	5	13	NULL	NULL	NULL	Dpp	GP		is a type of					typical ABC transporter	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
21619	2	6646	5	13	NULL	NULL	NULL	statement 1	Process		is energized by					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
21620	3	6646	5	13	NULL	NULL	NULL	Opp	GP		is a type of					typical ABC transporter	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
21621	4	6646	5	13	NULL	NULL	NULL	statement 3	Process		is energized by					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
21623	5	6646	5	13	NULL	NULL	NULL	Dpp	GP		comprises					four membrane proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
21624	6	6646	5	13	NULL	NULL	NULL	Dpp	GP		comprises					DppA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
21625	7	6646	5	13	NULL	NULL	NULL	DppA	GP		is a type of					periplasmic peptide binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
21626	8	6646	5	13	NULL	NULL	NULL	Opp	GP		comprises					four membrane proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
21627	9	6646	5	13	NULL	NULL	NULL	Opp	GP		comprises					OppA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
21628	10	6646	5	13	NULL	NULL	NULL	OppA	GP		is a type of					periplasmic peptide binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
56228	11	6646	5	13	NULL	NULL	NULL	statement 5	Process		occur simultaneous with					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
56229	12	6646	5	13	NULL	NULL	NULL	statement 8	Process		occur simultaneous with					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
18749	1	6646	6	13	NULL	NULL	NULL	Dpp	GP		is a type of					ABC transporter	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
18750	2	6646	6	13	NULL	NULL	NULL	statement 1	Process		is energized by					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
18751	3	6646	6	13	NULL	NULL	NULL	Opp	GP		is a type of					ABC transporter	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
18752	4	6646	6	13	NULL	NULL	NULL	statement 3	Process		is energized by					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
30464	5	6646	6	13	NULL	NULL	NULL	Dpp	GP		comprises of					four membrane proteins 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
30465	6	6646	6	13	NULL	NULL	NULL	DppA	GP		is a type of					periplasmic peptide binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
30466	7	6646	6	13	NULL	NULL	NULL	Opp	GP		comprises of					four membrane proteins 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
30467	8	6646	6	13	NULL	NULL	NULL	OppA	GP		is a type of					periplasmic peptide binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
56224	9	6646	6	13	NULL	NULL	NULL	Dpp	GP		comprise of					DppA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
56225	10	6646	6	13	NULL	NULL	NULL	Opp	GP		comprise of					OppA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
56226	11	6646	6	13	NULL	NULL	NULL	statement 5	Process		occur simultaneous with					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
56227	12	6646	6	13	NULL	NULL	NULL	statement 7	Process		occur simultaneous with					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_51_4_821_s_32	12654735	14, 17 Dpp and Opp are typical ABC transporters energized by ATP; each comprises four membrane proteins plus a periplasmic peptide binding protein DppA or OppA, respectively.	bind
21630	1	6647	5	13	NULL	NULL	NULL	myosin light chain phosphatase	GP		is target of		major			Rho-kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_13_1545_s_70	11927519	14, 17 In that model, it was shown that inactivation of the myosin-binding subunit of myosin light chain phosphatase, which is a major target protein of Rho-kinase, was a primary mechanism whereby fasudil or Y27632 prevented coronary artery spasm.	bind
21631	2	6647	5	13	NULL	NULL	NULL	fasudil	Chemical		prevents					coronary artery spasm	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_13_1545_s_70	11927519	14, 17 In that model, it was shown that inactivation of the myosin-binding subunit of myosin light chain phosphatase, which is a major target protein of Rho-kinase, was a primary mechanism whereby fasudil or Y27632 prevented coronary artery spasm.	bind
21632	3	6647	5	13	NULL	NULL	NULL				prevents			Y27632		coronary artery spasm	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_13_1545_s_70	11927519	14, 17 In that model, it was shown that inactivation of the myosin-binding subunit of myosin light chain phosphatase, which is a major target protein of Rho-kinase, was a primary mechanism whereby fasudil or Y27632 prevented coronary artery spasm.	bind
21633	4	6647	5	13	NULL	NULL	NULL	myosin-binding subunit 	GP		is a subunit of					myosin light chain phosphatase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_13_1545_s_70	11927519	14, 17 In that model, it was shown that inactivation of the myosin-binding subunit of myosin light chain phosphatase, which is a major target protein of Rho-kinase, was a primary mechanism whereby fasudil or Y27632 prevented coronary artery spasm.	bind
21635	5	6647	5	13	NULL	NULL	NULL	statement 4	Process	inactivation of	mechanism for		primary			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_13_1545_s_70	11927519	14, 17 In that model, it was shown that inactivation of the myosin-binding subunit of myosin light chain phosphatase, which is a major target protein of Rho-kinase, was a primary mechanism whereby fasudil or Y27632 prevented coronary artery spasm.	bind
21636	6	6647	5	13	NULL	NULL	NULL	statement 4	Process	inactivation of	mechanism for		primary			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_13_1545_s_70	11927519	14, 17 In that model, it was shown that inactivation of the myosin-binding subunit of myosin light chain phosphatase, which is a major target protein of Rho-kinase, was a primary mechanism whereby fasudil or Y27632 prevented coronary artery spasm.	bind
18753	1	6647	6	13	NULL	NULL	NULL	fasudil	Chemical		prevents					coronary artery spasm	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_13_1545_s_70	11927519	14, 17 In that model, it was shown that inactivation of the myosin-binding subunit of myosin light chain phosphatase, which is a major target protein of Rho-kinase, was a primary mechanism whereby fasudil or Y27632 prevented coronary artery spasm.	bind
18754	2	6647	6	13	NULL	NULL	NULL				prevents			Y27632		coronary artery spasm	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_13_1545_s_70	11927519	14, 17 In that model, it was shown that inactivation of the myosin-binding subunit of myosin light chain phosphatase, which is a major target protein of Rho-kinase, was a primary mechanism whereby fasudil or Y27632 prevented coronary artery spasm.	bind
18755	4	6647	6	13	NULL	NULL	NULL	statement 3	Process	inactivation of	mechanism for		primary			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_13_1545_s_70	11927519	14, 17 In that model, it was shown that inactivation of the myosin-binding subunit of myosin light chain phosphatase, which is a major target protein of Rho-kinase, was a primary mechanism whereby fasudil or Y27632 prevented coronary artery spasm.	bind
18756	5	6647	6	13	NULL	NULL	NULL	statement 3	Process	inactivation of	mechanism for		primary			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_13_1545_s_70	11927519	14, 17 In that model, it was shown that inactivation of the myosin-binding subunit of myosin light chain phosphatase, which is a major target protein of Rho-kinase, was a primary mechanism whereby fasudil or Y27632 prevented coronary artery spasm.	bind
56230	3	6647	6	13	NULL	NULL	NULL	myosin-binding subunit	GP		is a subunit of					 myosin light chain phosphatase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_13_1545_s_70	11927519	14, 17 In that model, it was shown that inactivation of the myosin-binding subunit of myosin light chain phosphatase, which is a major target protein of Rho-kinase, was a primary mechanism whereby fasudil or Y27632 prevented coronary artery spasm.	bind
56231	6	6647	6	13	NULL	NULL	NULL	 myosin light chain phosphatase	GP		target protein of					Rho-kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_13_1545_s_70	11927519	14, 17 In that model, it was shown that inactivation of the myosin-binding subunit of myosin light chain phosphatase, which is a major target protein of Rho-kinase, was a primary mechanism whereby fasudil or Y27632 prevented coronary artery spasm.	bind
21637	1	6648	5	13	NULL	NULL	NULL	CXCR2	GP		bind					Gro-alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_753_s_284	10487833	14, 53 The CXCR2 also binds another member of the CXC chemokine superfamily, the chemokine growth- related oncogene alpha (synonymous with melanoma growth-stimulating activity) Gro-alpha, which is also known to act as an autocrine growth factor for melanoma.	bind
21654	2	6648	5	13	NULL	NULL	NULL	Gro-alpha	GP		is					chemokine growth- related oncogene alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_753_s_284	10487833	14, 53 The CXCR2 also binds another member of the CXC chemokine superfamily, the chemokine growth- related oncogene alpha (synonymous with melanoma growth-stimulating activity) Gro-alpha, which is also known to act as an autocrine growth factor for melanoma.	bind
21655	3	6648	5	13	NULL	NULL	NULL	chemokine growth- related oncogene alpha	GP		is synonymous with					melanoma growth-stimulating activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_753_s_284	10487833	14, 53 The CXCR2 also binds another member of the CXC chemokine superfamily, the chemokine growth- related oncogene alpha (synonymous with melanoma growth-stimulating activity) Gro-alpha, which is also known to act as an autocrine growth factor for melanoma.	bind
21656	4	6648	5	13	NULL	NULL	NULL	Gro-alpha	GP		acts as					autocrine growth factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_753_s_284	10487833	14, 53 The CXCR2 also binds another member of the CXC chemokine superfamily, the chemokine growth- related oncogene alpha (synonymous with melanoma growth-stimulating activity) Gro-alpha, which is also known to act as an autocrine growth factor for melanoma.	bind
44668	5	6648	5	13	NULL	NULL	NULL	statement 4	Process		occurs for					melanoma	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_753_s_284	10487833	14, 53 The CXCR2 also binds another member of the CXC chemokine superfamily, the chemokine growth- related oncogene alpha (synonymous with melanoma growth-stimulating activity) Gro-alpha, which is also known to act as an autocrine growth factor for melanoma.	bind
18757	1	6648	6	13	NULL	NULL	NULL	CXCR2	GP		bind					Gro-alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_753_s_284	10487833	14, 53 The CXCR2 also binds another member of the CXC chemokine superfamily, the chemokine growth- related oncogene alpha (synonymous with melanoma growth-stimulating activity) Gro-alpha, which is also known to act as an autocrine growth factor for melanoma.	bind
18758	2	6648	6	13	NULL	NULL	NULL	Gro-alpha	GP		is					chemokine growth- related oncogene alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_753_s_284	10487833	14, 53 The CXCR2 also binds another member of the CXC chemokine superfamily, the chemokine growth- related oncogene alpha (synonymous with melanoma growth-stimulating activity) Gro-alpha, which is also known to act as an autocrine growth factor for melanoma.	bind
18759	3	6648	6	13	NULL	NULL	NULL	Gro-alpha	GP		is synonymous with					melanoma growth-stimulating activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_753_s_284	10487833	14, 53 The CXCR2 also binds another member of the CXC chemokine superfamily, the chemokine growth- related oncogene alpha (synonymous with melanoma growth-stimulating activity) Gro-alpha, which is also known to act as an autocrine growth factor for melanoma.	bind
18760	4	6648	6	13	NULL	NULL	NULL	Gro-alpha	GP		acts as an					autocrine growth factor 	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_753_s_284	10487833	14, 53 The CXCR2 also binds another member of the CXC chemokine superfamily, the chemokine growth- related oncogene alpha (synonymous with melanoma growth-stimulating activity) Gro-alpha, which is also known to act as an autocrine growth factor for melanoma.	bind
56232	5	6648	6	13	NULL	NULL	NULL	statement 4	Process		occurs for					melanoma	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_753_s_284	10487833	14, 53 The CXCR2 also binds another member of the CXC chemokine superfamily, the chemokine growth- related oncogene alpha (synonymous with melanoma growth-stimulating activity) Gro-alpha, which is also known to act as an autocrine growth factor for melanoma.	bind
21657	1	6649	5	13	NULL	NULL	NULL	GTP	Chemical		bind		readily			tTG	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_10_1153_s_27	12702643	14,15  Both GTP and GDP readily bind tTG. 16 Distinct GTP binding and TG domains have been identified within Gh/tTG, 17 and the latter function may be negatively regulated by GTP binding.	bind
21658	2	6649	5	13	NULL	NULL	NULL	GDP	Chemical		bind		readily			tTG	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_10_1153_s_27	12702643	14,15  Both GTP and GDP readily bind tTG. 16 Distinct GTP binding and TG domains have been identified within Gh/tTG, 17 and the latter function may be negatively regulated by GTP binding.	bind
21659	3	6649	5	13	NULL	NULL	NULL	Gh/tTG	GP		contains							distinct	GTP binding domain		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_10_1153_s_27	12702643	14,15  Both GTP and GDP readily bind tTG. 16 Distinct GTP binding and TG domains have been identified within Gh/tTG, 17 and the latter function may be negatively regulated by GTP binding.	bind
21660	4	6649	5	13	NULL	NULL	NULL	Gh/tTG	GP		contains							distinct	TG domains		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_10_1153_s_27	12702643	14,15  Both GTP and GDP readily bind tTG. 16 Distinct GTP binding and TG domains have been identified within Gh/tTG, 17 and the latter function may be negatively regulated by GTP binding.	bind
18761	1	6649	6	13	NULL	NULL	NULL	GTP	Chemical		bind					tTG	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_10_1153_s_27	12702643	14,15  Both GTP and GDP readily bind tTG. 16 Distinct GTP binding and TG domains have been identified within Gh/tTG, 17 and the latter function may be negatively regulated by GTP binding.	bind
18762	2	6649	6	13	NULL	NULL	NULL	GDP	Chemical		bind					tTG	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_10_1153_s_27	12702643	14,15  Both GTP and GDP readily bind tTG. 16 Distinct GTP binding and TG domains have been identified within Gh/tTG, 17 and the latter function may be negatively regulated by GTP binding.	bind
30468	3	6649	6	13	NULL	NULL	NULL	Gh/tTG	GP		contain								GTP binding domain		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_10_1153_s_27	12702643	14,15  Both GTP and GDP readily bind tTG. 16 Distinct GTP binding and TG domains have been identified within Gh/tTG, 17 and the latter function may be negatively regulated by GTP binding.	bind
30469	4	6649	6	13	NULL	NULL	NULL	Gh/tTG	GP		contain								TG domain		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_10_1153_s_27	12702643	14,15  Both GTP and GDP readily bind tTG. 16 Distinct GTP binding and TG domains have been identified within Gh/tTG, 17 and the latter function may be negatively regulated by GTP binding.	bind
21661	1	6650	5	13	NULL	NULL	NULL	SRF	GP		bind									CArG elements (CC (A/T) 6-GG motif)	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_163	16397143	14,15,21,22    It activates transcription of a large subset of SMC marker genes by binding of SRF to CArG elements (CC (A/T) 6-GG motif) found in the promoters of these genes.	bind
21662	2	6650	5	13	NULL	NULL	NULL	SMC marker genes	GP	transcription of	is activated by					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_163	16397143	14,15,21,22    It activates transcription of a large subset of SMC marker genes by binding of SRF to CArG elements (CC (A/T) 6-GG motif) found in the promoters of these genes.	bind
18763	1	6650	6	13	NULL	NULL	NULL	SRF	GP		bind									CArG element	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_163	16397143	14,15,21,22    It activates transcription of a large subset of SMC marker genes by binding of SRF to CArG elements (CC (A/T) 6-GG motif) found in the promoters of these genes.	bind
31148	2	6650	6	13	NULL	NULL	NULL	statement 1	Process		activates					 SMC marker genes	GP	transcription of;;large subset of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_163	16397143	14,15,21,22    It activates transcription of a large subset of SMC marker genes by binding of SRF to CArG elements (CC (A/T) 6-GG motif) found in the promoters of these genes.	bind
21663	1	6651	5	13	NULL	NULL	NULL	Ear2	GP		bind					T3R	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_9_1033_s_210	12690040	14,17  Studies of T3R function suggest that Ear2 binds to T3R, preventing its binding to the TRE. 16 Ear2 is a member of COUP-TF family.	bind
21664	2	6651	5	13	NULL	NULL	NULL	T3R	GP		bind									TRE	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_9_1033_s_210	12690040	14,17  Studies of T3R function suggest that Ear2 binds to T3R, preventing its binding to the TRE. 16 Ear2 is a member of COUP-TF family.	bind
21665	3	6651	5	13	NULL	NULL	NULL	statement 1	Process		prevents					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_9_1033_s_210	12690040	14,17  Studies of T3R function suggest that Ear2 binds to T3R, preventing its binding to the TRE. 16 Ear2 is a member of COUP-TF family.	bind
21666	4	6651	5	13	NULL	NULL	NULL	Ear2	GP		is a member of					COUP-TF family	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_9_1033_s_210	12690040	14,17  Studies of T3R function suggest that Ear2 binds to T3R, preventing its binding to the TRE. 16 Ear2 is a member of COUP-TF family.	bind
18764	1	6651	6	13	NULL	NULL	NULL	Ear2	GP		bind					T3R	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_9_1033_s_210	12690040	14,17  Studies of T3R function suggest that Ear2 binds to T3R, preventing its binding to the TRE. 16 Ear2 is a member of COUP-TF family.	bind
18765	2	6651	6	13	NULL	NULL	NULL	T3R	GP		bind									TRE	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_9_1033_s_210	12690040	14,17  Studies of T3R function suggest that Ear2 binds to T3R, preventing its binding to the TRE. 16 Ear2 is a member of COUP-TF family.	bind
18766	3	6651	6	13	NULL	NULL	NULL	statement 1	Process		prevents					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_9_1033_s_210	12690040	14,17  Studies of T3R function suggest that Ear2 binds to T3R, preventing its binding to the TRE. 16 Ear2 is a member of COUP-TF family.	bind
18767	4	6651	6	13	NULL	NULL	NULL	Ear2	GP		is a member of					COUP-TF family	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_9_1033_s_210	12690040	14,17  Studies of T3R function suggest that Ear2 binds to T3R, preventing its binding to the TRE. 16 Ear2 is a member of COUP-TF family.	bind
21667	1	6652	5	13	NULL	NULL	NULL	14-3-3 zeta	GP		bind			amphipathic groove		Raf peptide	GP	phosphorylated			NULL		NULL	NULL	NULL	NULL	gw70_annurevplantbiol_50_0_277_s_671	null	14-3-3  zeta binds a phosphorylated Raf peptide and an unphosphorylated peptide via its conserved  amphipathic groove.	bind
21669	2	6652	5	13	NULL	NULL	NULL	14-3-3 zeta	GP		bind			amphipathic groove		peptide	GP	unphosphorylated			NULL		NULL	NULL	NULL	NULL	gw70_annurevplantbiol_50_0_277_s_671	null	14-3-3  zeta binds a phosphorylated Raf peptide and an unphosphorylated peptide via its conserved  amphipathic groove.	bind
18768	1	6652	6	13	NULL	NULL	NULL	14-3-3 zeta	GP		bind			amphipathic groove		Raf peptide	GP	phosphorylated			NULL		NULL	NULL	NULL	NULL	gw70_annurevplantbiol_50_0_277_s_671	null	14-3-3  zeta binds a phosphorylated Raf peptide and an unphosphorylated peptide via its conserved  amphipathic groove.	bind
18769	2	6652	6	13	NULL	NULL	NULL	14-3-3 zeta	GP		bind			amphipathic groove		peptide	GP	unphosphorylated			NULL		NULL	NULL	NULL	NULL	gw70_annurevplantbiol_50_0_277_s_671	null	14-3-3  zeta binds a phosphorylated Raf peptide and an unphosphorylated peptide via its conserved  amphipathic groove.	bind
21671	1	6653	5	13	NULL	NULL	NULL	14-3-3	GP		bind					tau	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18392_s_277	14970201	14-3-3 and tubulin share a common binding site on tau, and their binding to tau is mutually exclusive ( ), suggesting that 14-3-3 may regulate binding of tau to microtubules.	bind
21672	2	6653	5	13	NULL	NULL	NULL	tubulin	GP		bind					tau	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18392_s_277	14970201	14-3-3 and tubulin share a common binding site on tau, and their binding to tau is mutually exclusive ( ), suggesting that 14-3-3 may regulate binding of tau to microtubules.	bind
21673	3	6653	5	13	NULL	NULL	NULL	14-3-3	GP	binding site of	share with					tubulin	GP	binding site of			NULL	 Tau	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18392_s_277	14970201	14-3-3 and tubulin share a common binding site on tau, and their binding to tau is mutually exclusive ( ), suggesting that 14-3-3 may regulate binding of tau to microtubules.	bind
21674	4	6653	5	13	NULL	NULL	NULL	statement 1	Process		is mutually exclusive to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18392_s_277	14970201	14-3-3 and tubulin share a common binding site on tau, and their binding to tau is mutually exclusive ( ), suggesting that 14-3-3 may regulate binding of tau to microtubules.	bind
21675	5	6653	5	13	NULL	NULL	NULL	tau	GP		bind					microtubules	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18392_s_277	14970201	14-3-3 and tubulin share a common binding site on tau, and their binding to tau is mutually exclusive ( ), suggesting that 14-3-3 may regulate binding of tau to microtubules.	bind
21676	6	6653	5	13	NULL	NULL	NULL	14-3-3	GP		regulates		may			statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18392_s_277	14970201	14-3-3 and tubulin share a common binding site on tau, and their binding to tau is mutually exclusive ( ), suggesting that 14-3-3 may regulate binding of tau to microtubules.	bind
21677	7	6653	5	13	NULL	NULL	NULL	statement 4	Process		suggests					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18392_s_277	14970201	14-3-3 and tubulin share a common binding site on tau, and their binding to tau is mutually exclusive ( ), suggesting that 14-3-3 may regulate binding of tau to microtubules.	bind
18770	1	6653	6	NULL	NULL	0	NULL	14-3-3	NULL		bind	NULL				tau	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_18392_s_277	14970201	14-3-3 and tubulin share a common binding site on tau, and their binding to tau is mutually exclusive ( ), suggesting that 14-3-3 may regulate binding of tau to microtubules.	bind
18771	2	6653	6	NULL	NULL	0	NULL	tubulin	NULL		bind	NULL				tau	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_18392_s_277	14970201	14-3-3 and tubulin share a common binding site on tau, and their binding to tau is mutually exclusive ( ), suggesting that 14-3-3 may regulate binding of tau to microtubules.	bind
18772	3	6653	6	NULL	NULL	0	NULL	statement 1	NULL		is independent of	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_18392_s_277	14970201	14-3-3 and tubulin share a common binding site on tau, and their binding to tau is mutually exclusive ( ), suggesting that 14-3-3 may regulate binding of tau to microtubules.	bind
18773	4	6653	6	NULL	NULL	0	NULL	tau	NULL		bind	NULL				microtubules	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_18392_s_277	14970201	14-3-3 and tubulin share a common binding site on tau, and their binding to tau is mutually exclusive ( ), suggesting that 14-3-3 may regulate binding of tau to microtubules.	bind
18774	5	6653	6	NULL	NULL	0	NULL	14-3-3	NULL		regulate	NULL	may			statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_18392_s_277	14970201	14-3-3 and tubulin share a common binding site on tau, and their binding to tau is mutually exclusive ( ), suggesting that 14-3-3 may regulate binding of tau to microtubules.	bind
56308	6	6653	6	10	NULL	0	NULL	14-3-3		binding site of	share with					tubulin		binding site of			NULL	Tau	0	NULL	NULL	NULL	gw70_jbiolchem_279_18_18392_s_277	14970201	14-3-3 and tubulin share a common binding site on tau, and their binding to tau is mutually exclusive ( ), suggesting that 14-3-3 may regulate binding of tau to microtubules.	bind
56309	7	6653	6	10	NULL	0	NULL	statement 3			suggest					statement 5					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_18392_s_277	14970201	14-3-3 and tubulin share a common binding site on tau, and their binding to tau is mutually exclusive ( ), suggesting that 14-3-3 may regulate binding of tau to microtubules.	bind
21678	1	6659	5	13	NULL	NULL	NULL	14-3-3 zeta	GP		bind					Bcr	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_46_28882_s_36	9360956	14-3-3 zeta also binds to Bcr, but is not phosphorylated ( 19).	bind
21679	2	6659	5	13	NULL	NULL	NULL	14-3-3 zeta	GP		does not undergo					phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_46_28882_s_36	9360956	14-3-3 zeta also binds to Bcr, but is not phosphorylated ( 19).	bind
18775	1	6659	6	NULL	NULL	0	NULL	14-3-3 zeta	NULL	unphosphorylated	bind	NULL				Bcr	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_46_28882_s_36	9360956	14-3-3 zeta also binds to Bcr, but is not phosphorylated ( 19).	bind
21680	1	6660	5	13	NULL	NULL	NULL	Nedd4-2	GP		bind					alpha-ENaC	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_24_16323_s_197	16613846	14-3-3beta knockdown reverses the aldosterone-induced decrease in Nedd4-2 binding to alpha-ENaC.	bind
21681	2	6660	5	13	NULL	NULL	NULL	aldosterone	Chemical	induction of	decreases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_24_16323_s_197	16613846	14-3-3beta knockdown reverses the aldosterone-induced decrease in Nedd4-2 binding to alpha-ENaC.	bind
21682	3	6660	5	13	NULL	NULL	NULL	14-3-3beta	GP	knockdown of	reverses					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_24_16323_s_197	16613846	14-3-3beta knockdown reverses the aldosterone-induced decrease in Nedd4-2 binding to alpha-ENaC.	bind
18776	1	6660	6	NULL	NULL	0	NULL	Nedd4-2	NULL		bind	NULL				alpha-ENaC	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_24_16323_s_197	16613846	14-3-3beta knockdown reverses the aldosterone-induced decrease in Nedd4-2 binding to alpha-ENaC.	bind
18777	2	6660	6	NULL	NULL	0	NULL	aldosterone	NULL		decreases	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_24_16323_s_197	16613846	14-3-3beta knockdown reverses the aldosterone-induced decrease in Nedd4-2 binding to alpha-ENaC.	bind
18778	3	6660	6	NULL	NULL	0	NULL	14-3-3beta	NULL	knockdown of	reverses	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_24_16323_s_197	16613846	14-3-3beta knockdown reverses the aldosterone-induced decrease in Nedd4-2 binding to alpha-ENaC.	bind
21683	1	6663	5	13	NULL	NULL	NULL	14C-ADP	Chemical		bind					platelet membranes	CellComponent	normal human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_311	9108793	14C-ADP binding to normal human and thrombasthenic platelet membranes: study of the dissociation of the nucleotide from its receptors.	bind
21684	2	6663	5	13	NULL	NULL	NULL	14C-ADP	Chemical		bind					platelet membranes	CellComponent	thrombasthenic			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_311	9108793	14C-ADP binding to normal human and thrombasthenic platelet membranes: study of the dissociation of the nucleotide from its receptors.	bind
18779	1	6663	6	NULL	NULL	0	NULL	14C-ADP	NULL		bind	NULL				platelet membrane	NULL	normal human			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_311	9108793	14C-ADP binding to normal human and thrombasthenic platelet membranes: study of the dissociation of the nucleotide from its receptors.	bind
18780	2	6663	6	NULL	NULL	0	NULL	14C-ADP	NULL		bind	NULL				platelet membrane	NULL	thrombasthenic			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_311	9108793	14C-ADP binding to normal human and thrombasthenic platelet membranes: study of the dissociation of the nucleotide from its receptors.	bind
21685	1	6665	5	13	NULL	NULL	NULL	DpnM DNA adenine methyltransferase	GP	DpnII restriction system of Streptococcus pneumoniae	bind					S-adenosylmethionine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1491_s_434	11266551	15       Tran,P.H., Korszun,Z.R., Cerritelli,S., Springhorn,S.S. and Lacks,S.A. (1998) Crystal structure of the  DpnM DNA adenine methyltransferase from the  DpnII restriction system of  Streptococcus pneumoniae bound to  S-adenosylmethionine.	bind
18781	1	6665	6	NULL	NULL	0	NULL	DpnM DNA adenine methyltransferase	NULL	streptococcus pneumoniae	bind	NULL				S-adenosylmethionine	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1491_s_434	11266551	15       Tran,P.H., Korszun,Z.R., Cerritelli,S., Springhorn,S.S. and Lacks,S.A. (1998) Crystal structure of the  DpnM DNA adenine methyltransferase from the  DpnII restriction system of  Streptococcus pneumoniae bound to  S-adenosylmethionine.	bind
21686	1	6666	5	13	NULL	NULL	NULL	VEGF-C	GP		bind					VEGFR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_7_s_23	10880369	15  A proteolytically processed form of VEGF-C can also bind to VEGFR-2, which is expressed in both blood and lymphatic vessel endothelia.	bind
21687	2	6666	5	13	NULL	NULL	NULL	VEGF-C	GP		is processed					proteolytically	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_7_s_23	10880369	15  A proteolytically processed form of VEGF-C can also bind to VEGFR-2, which is expressed in both blood and lymphatic vessel endothelia.	bind
30344	3	6666	5	13	NULL	NULL	NULL	VEGFR-2	GP		is expressed in					blood vessel endothelia	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_7_s_23	10880369	15  A proteolytically processed form of VEGF-C can also bind to VEGFR-2, which is expressed in both blood and lymphatic vessel endothelia.	bind
30345	4	6666	5	13	NULL	NULL	NULL	VEGFR-2	GP		is expressed in					lymphatic vessel endothelia	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_7_s_23	10880369	15  A proteolytically processed form of VEGF-C can also bind to VEGFR-2, which is expressed in both blood and lymphatic vessel endothelia.	bind
18782	1	6666	6	NULL	NULL	0	NULL	VEGF-C	NULL		bind	NULL				VEGFR-2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_7_s_23	10880369	15  A proteolytically processed form of VEGF-C can also bind to VEGFR-2, which is expressed in both blood and lymphatic vessel endothelia.	bind
18783	2	6666	6	10	NULL	0	NULL	VEGFR-2			expressed in					blood vessel endothelia					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_7_s_23	10880369	15  A proteolytically processed form of VEGF-C can also bind to VEGFR-2, which is expressed in both blood and lymphatic vessel endothelia.	bind
18784	3	6666	6	10	NULL	0	NULL	VEGFR-2			expressed in					lymphatic vessel endothelia					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_7_s_23	10880369	15  A proteolytically processed form of VEGF-C can also bind to VEGFR-2, which is expressed in both blood and lymphatic vessel endothelia.	bind
32786	4	6666	6	NULL	NULL	0	NULL	VEGF-C	NULL		is processed 	NULL				proteolytically	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_1_7_s_23	10880369	15  A proteolytically processed form of VEGF-C can also bind to VEGFR-2, which is expressed in both blood and lymphatic vessel endothelia.	bind
21689	1	6667	5	13	NULL	NULL	NULL	EPCR	GP		bind		specifically			protein C	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3633_s_29	9396465	15  EPCR binds specifically to either protein C or APC. 15  Binding of protein C to EPCR promotes protein C activation 17  and blocks APC anticoagulant activity.	bind
21691	2	6667	5	13	NULL	NULL	NULL	EPCR	GP		bind		specifically			APC	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3633_s_29	9396465	15  EPCR binds specifically to either protein C or APC. 15  Binding of protein C to EPCR promotes protein C activation 17  and blocks APC anticoagulant activity.	bind
21692	3	6667	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3633_s_29	9396465	15  EPCR binds specifically to either protein C or APC. 15  Binding of protein C to EPCR promotes protein C activation 17  and blocks APC anticoagulant activity.	bind
21693	4	6667	5	13	NULL	NULL	NULL	statement 1	Process		promote					protein C	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3633_s_29	9396465	15  EPCR binds specifically to either protein C or APC. 15  Binding of protein C to EPCR promotes protein C activation 17  and blocks APC anticoagulant activity.	bind
21694	5	6667	5	13	NULL	NULL	NULL	statement 1	Process		blocks					APC	GP	anticoagulant activity of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3633_s_29	9396465	15  EPCR binds specifically to either protein C or APC. 15  Binding of protein C to EPCR promotes protein C activation 17  and blocks APC anticoagulant activity.	bind
18785	1	6667	6	NULL	NULL	0	NULL	EPCR	NULL		bind	NULL	specifically			protein C	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3633_s_29	9396465	15  EPCR binds specifically to either protein C or APC. 15  Binding of protein C to EPCR promotes protein C activation 17  and blocks APC anticoagulant activity.	bind
18786	2	6667	6	NULL	NULL	0	NULL	EPCR	NULL		bind	NULL	specifically			APC	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_96_10_3633_s_29	9396465	15  EPCR binds specifically to either protein C or APC. 15  Binding of protein C to EPCR promotes protein C activation 17  and blocks APC anticoagulant activity.	bind
18787	3	6667	6	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_96_10_3633_s_29	9396465	15  EPCR binds specifically to either protein C or APC. 15  Binding of protein C to EPCR promotes protein C activation 17  and blocks APC anticoagulant activity.	bind
18788	4	6667	6	NULL	NULL	0	NULL	statement 1	NULL		promotes	NULL				protein C	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_circulation_96_10_3633_s_29	9396465	15  EPCR binds specifically to either protein C or APC. 15  Binding of protein C to EPCR promotes protein C activation 17  and blocks APC anticoagulant activity.	bind
18790	5	6667	6	10	NULL	0	NULL	statement 1			blocks					APC		anticoagulant activity of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3633_s_29	9396465	15  EPCR binds specifically to either protein C or APC. 15  Binding of protein C to EPCR promotes protein C activation 17  and blocks APC anticoagulant activity.	bind
21695	1	6668	5	13	NULL	NULL	NULL	sPLA2	GP		bind					decorin	GP		core protein		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulationres_86_6_610_s_28	10746993	15  In this issue of  Circulation Research, the investigation group reports that sPLA2 can bind to both the core protein and the glycosaminoglycan chains of decorin in vitro.	bind
21696	2	6668	5	13	NULL	NULL	NULL	sPLA2	GP		bind					decorin	GP		glycosaminoglycan chains		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulationres_86_6_610_s_28	10746993	15  In this issue of  Circulation Research, the investigation group reports that sPLA2 can bind to both the core protein and the glycosaminoglycan chains of decorin in vitro.	bind
18791	1	6668	6	NULL	NULL	0	NULL	sPLA2	NULL		bind	NULL				decorin	NULL		core protein		NULL	in vitro	0	NULL	NULL	NULL	gw60_circulationres_86_6_610_s_28	10746993	15  In this issue of  Circulation Research, the investigation group reports that sPLA2 can bind to both the core protein and the glycosaminoglycan chains of decorin in vitro.	bind
18792	2	6668	6	NULL	NULL	0	NULL	sPLA2	NULL		bind	NULL				decorin	NULL		glycosaminoglycan chains		NULL	in vitro	0	NULL	NULL	NULL	gw60_circulationres_86_6_610_s_28	10746993	15  In this issue of  Circulation Research, the investigation group reports that sPLA2 can bind to both the core protein and the glycosaminoglycan chains of decorin in vitro.	bind
21697	1	6669	5	13	NULL	NULL	NULL	CTL cells	Cell		recognizes					susceptible target cell	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1805_s_23	10362805	15  In this pathway, the recognition and tight binding of a susceptible target cell by a CTL or NK cell induces the release of electron-dense cytoplasmic granules by the effector cells.	bind
21698	2	6669	5	13	NULL	NULL	NULL	NK cells	Cell		recognizes					susceptible target cell	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1805_s_23	10362805	15  In this pathway, the recognition and tight binding of a susceptible target cell by a CTL or NK cell induces the release of electron-dense cytoplasmic granules by the effector cells.	bind
21699	3	6669	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1805_s_23	10362805	15  In this pathway, the recognition and tight binding of a susceptible target cell by a CTL or NK cell induces the release of electron-dense cytoplasmic granules by the effector cells.	bind
21700	4	6669	5	13	NULL	NULL	NULL	CTL cells	Cell		bind		tightly			susceptible target cell	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1805_s_23	10362805	15  In this pathway, the recognition and tight binding of a susceptible target cell by a CTL or NK cell induces the release of electron-dense cytoplasmic granules by the effector cells.	bind
21701	5	6669	5	13	NULL	NULL	NULL	NK cells	Cell		bind		tightly			susceptible target cell	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1805_s_23	10362805	15  In this pathway, the recognition and tight binding of a susceptible target cell by a CTL or NK cell induces the release of electron-dense cytoplasmic granules by the effector cells.	bind
21702	6	6669	5	13	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1805_s_23	10362805	15  In this pathway, the recognition and tight binding of a susceptible target cell by a CTL or NK cell induces the release of electron-dense cytoplasmic granules by the effector cells.	bind
21704	7	6669	5	13	NULL	NULL	NULL	effector cells	Cell		release					electron-dense cytoplasmic granules	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1805_s_23	10362805	15  In this pathway, the recognition and tight binding of a susceptible target cell by a CTL or NK cell induces the release of electron-dense cytoplasmic granules by the effector cells.	bind
21706	8	6669	5	13	NULL	NULL	NULL	statement 3	Process		induces					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1805_s_23	10362805	15  In this pathway, the recognition and tight binding of a susceptible target cell by a CTL or NK cell induces the release of electron-dense cytoplasmic granules by the effector cells.	bind
21708	9	6669	5	13	NULL	NULL	NULL	statement 6	Process		induces					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1805_s_23	10362805	15  In this pathway, the recognition and tight binding of a susceptible target cell by a CTL or NK cell induces the release of electron-dense cytoplasmic granules by the effector cells.	bind
18947	1	6669	6	10	NULL	0	NULL	CTL			bind		tightly			susceptible target cell					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1805_s_23	10362805	15  In this pathway, the recognition and tight binding of a susceptible target cell by a CTL or NK cell induces the release of electron-dense cytoplasmic granules by the effector cells.	bind
18948	2	6669	6	10	NULL	0	NULL	NK cell			bind		tightly			susceptible target cell					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1805_s_23	10362805	15  In this pathway, the recognition and tight binding of a susceptible target cell by a CTL or NK cell induces the release of electron-dense cytoplasmic granules by the effector cells.	bind
18968	4	6669	6	10	NULL	0	NULL	CTL			recognizes					susceptible target cell					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1805_s_23	10362805	15  In this pathway, the recognition and tight binding of a susceptible target cell by a CTL or NK cell induces the release of electron-dense cytoplasmic granules by the effector cells.	bind
18970	5	6669	6	10	NULL	0	NULL	NK cells			recognizes					susceptible target cell					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1805_s_23	10362805	15  In this pathway, the recognition and tight binding of a susceptible target cell by a CTL or NK cell induces the release of electron-dense cytoplasmic granules by the effector cells.	bind
19050	6	6669	6	10	NULL	0	NULL	statement 1			is an alternative to					statement 2					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1805_s_23	10362805	15  In this pathway, the recognition and tight binding of a susceptible target cell by a CTL or NK cell induces the release of electron-dense cytoplasmic granules by the effector cells.	bind
56336	3	6669	6	10	NULL	0	NULL	effector cells			release					 electron-dense cytoplasmic granules					NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_6_1805_s_23	10362805	15  In this pathway, the recognition and tight binding of a susceptible target cell by a CTL or NK cell induces the release of electron-dense cytoplasmic granules by the effector cells.	bind
56337	7	6669	6	10	NULL	0	NULL	statement 4			is an alternative to					statement 5					NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_6_1805_s_23	10362805	15  In this pathway, the recognition and tight binding of a susceptible target cell by a CTL or NK cell induces the release of electron-dense cytoplasmic granules by the effector cells.	bind
56338	8	6669	6	10	NULL	0	NULL	statement 6			induces					statement 3					NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_6_1805_s_23	10362805	15  In this pathway, the recognition and tight binding of a susceptible target cell by a CTL or NK cell induces the release of electron-dense cytoplasmic granules by the effector cells.	bind
56339	9	6669	6	10	NULL	0	NULL	statement 7			induces					statement 3					NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_6_1805_s_23	10362805	15  In this pathway, the recognition and tight binding of a susceptible target cell by a CTL or NK cell induces the release of electron-dense cytoplasmic granules by the effector cells.	bind
21710	1	6670	5	13	NULL	NULL	NULL	MS1 cells	Cell		bind					VEGF 165	GP	radio-iodinated			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_4_1469_s_84	10751370	15  MS1 and SVR cells were found to bind radio-iodinated VEGF 165, yielding a band consistent with the combined molecular weight of VEGF and VEGFR-2 after cross-linking (data not shown).	bind
21711	2	6670	5	13	NULL	NULL	NULL	SVR cells	Cell		bind					VEGF 165	GP	radio-iodinated			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_4_1469_s_84	10751370	15  MS1 and SVR cells were found to bind radio-iodinated VEGF 165, yielding a band consistent with the combined molecular weight of VEGF and VEGFR-2 after cross-linking (data not shown).	bind
18793	1	6670	6	NULL	NULL	0	NULL	MS1	NULL		bind	NULL				VEGF 165	NULL	radio-iodinated			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_4_1469_s_84	10751370	15  MS1 and SVR cells were found to bind radio-iodinated VEGF 165, yielding a band consistent with the combined molecular weight of VEGF and VEGFR-2 after cross-linking (data not shown).	bind
18794	2	6670	6	NULL	NULL	0	NULL	SVR cells	NULL		bind	NULL				VEGF 165	NULL	radio-iodinated			NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_4_1469_s_84	10751370	15  MS1 and SVR cells were found to bind radio-iodinated VEGF 165, yielding a band consistent with the combined molecular weight of VEGF and VEGFR-2 after cross-linking (data not shown).	bind
21713	1	6671	5	13	NULL	NULL	NULL	tuberin	GP		bind			59-amino-acid motif in C-terminus		rabaptin-5	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_10_1069_s_34	10827137	15  Other studies identified a 59-amino-acid motif located at the C-terminus of tuberin that binds to rabaptin-5.	bind
18795	1	6671	6	NULL	NULL	0	NULL	tuberin	NULL		bind	NULL		59-amino-acid motif at C-terminus		rabaptin-5	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_10_1069_s_34	10827137	15  Other studies identified a 59-amino-acid motif located at the C-terminus of tuberin that binds to rabaptin-5.	bind
21716	1	6672	5	13	NULL	NULL	NULL	PrPL	GP		is					ligand of PrPC	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_111	11073804	15  They hypothesized two putative molecules; one is a ligand of PrPC (PrPL) eliciting a signal necessary for the survival of neurons, and the other is protein pi that binds to PrPL with lower affinity but also capable of generating the survival signal.	bind
21717	2	6672	5	13	NULL	NULL	NULL	PrPL	GP		signals for					neuronal survival	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_111	11073804	15  They hypothesized two putative molecules; one is a ligand of PrPC (PrPL) eliciting a signal necessary for the survival of neurons, and the other is protein pi that binds to PrPL with lower affinity but also capable of generating the survival signal.	bind
21718	3	6672	5	13	NULL	NULL	NULL	protein pi	GP		bind		low affinity			PrPL	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_111	11073804	15  They hypothesized two putative molecules; one is a ligand of PrPC (PrPL) eliciting a signal necessary for the survival of neurons, and the other is protein pi that binds to PrPL with lower affinity but also capable of generating the survival signal.	bind
21720	4	6672	5	13	NULL	NULL	NULL	protein pi	GP		generates					survival signal	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_111	11073804	15  They hypothesized two putative molecules; one is a ligand of PrPC (PrPL) eliciting a signal necessary for the survival of neurons, and the other is protein pi that binds to PrPL with lower affinity but also capable of generating the survival signal.	bind
18796	1	6672	6	NULL	NULL	0	NULL	protein pi	NULL		bind	NULL	low affinity			PrPL	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_111	11073804	15  They hypothesized two putative molecules; one is a ligand of PrPC (PrPL) eliciting a signal necessary for the survival of neurons, and the other is protein pi that binds to PrPL with lower affinity but also capable of generating the survival signal.	bind
18797	2	6672	6	NULL	NULL	0	NULL	PrPL	NULL		is	NULL				ligand of PrPC	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_111	11073804	15  They hypothesized two putative molecules; one is a ligand of PrPC (PrPL) eliciting a signal necessary for the survival of neurons, and the other is protein pi that binds to PrPL with lower affinity but also capable of generating the survival signal.	bind
18798	3	6672	6	NULL	NULL	0	NULL	PrPL	NULL		plays a role in	NULL				neuron survival	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_111	11073804	15  They hypothesized two putative molecules; one is a ligand of PrPC (PrPL) eliciting a signal necessary for the survival of neurons, and the other is protein pi that binds to PrPL with lower affinity but also capable of generating the survival signal.	bind
18799	4	6672	6	10	NULL	0	NULL	protein pi			play a role in					 survival signal					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_111	11073804	15  They hypothesized two putative molecules; one is a ligand of PrPC (PrPL) eliciting a signal necessary for the survival of neurons, and the other is protein pi that binds to PrPL with lower affinity but also capable of generating the survival signal.	bind
21722	1	6673	5	13	NULL	NULL	NULL	SV40 LT antigen	GP		bind					p53	GP	wild-type			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_973_s_102	10764661	15  Those studies also established that SV40 LT antigen binds to wild-type p53 and extends its half-life.	bind
21723	2	6673	5	13	NULL	NULL	NULL	statement 1	Process		extends					p53	GP	half life of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_973_s_102	10764661	15  Those studies also established that SV40 LT antigen binds to wild-type p53 and extends its half-life.	bind
18800	1	6673	6	NULL	NULL	0	NULL	SV40 LT antigen	NULL		bind	NULL				p53	NULL	wild type			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_973_s_102	10764661	15  Those studies also established that SV40 LT antigen binds to wild-type p53 and extends its half-life.	bind
31149	2	6673	6	10	NULL	0	NULL	statement 1			extends					p53 		half life of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_973_s_102	10764661	15  Those studies also established that SV40 LT antigen binds to wild-type p53 and extends its half-life.	bind
21724	1	6674	5	13	NULL	NULL	NULL	SV40 LT antigen	GP		bind					p53	GP	wild-type			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_3_636_s_105	10712385	15  Those studies have also established that SV40 LT antigen binds to wild-type p53 and extends its half-life.	bind
21725	2	6674	5	13	NULL	NULL	NULL	SV40 LT antigen	GP		extends					p53	GP	half life of wild-type			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_3_636_s_105	10712385	15  Those studies have also established that SV40 LT antigen binds to wild-type p53 and extends its half-life.	bind
21726	1	6675	5	13	NULL	NULL	NULL	annexin V	GP		bind					 phospholipid	Chemical	anionic			NULL	on platelets	NULL	NULL	NULL	NULL	gw60_circulation_96_7_2339_s_32	9337209	15  We have shown previously that annexin V binds to anionic phospholipid on platelets and blocks the binding of factors Xa and Va to platelets.	bind
21727	2	6675	5	13	NULL	NULL	NULL	factor Xa	GP		bind					platelets	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_7_2339_s_32	9337209	15  We have shown previously that annexin V binds to anionic phospholipid on platelets and blocks the binding of factors Xa and Va to platelets.	bind
21728	3	6675	5	13	NULL	NULL	NULL	factor Va	GP		bind					platelets	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_7_2339_s_32	9337209	15  We have shown previously that annexin V binds to anionic phospholipid on platelets and blocks the binding of factors Xa and Va to platelets.	bind
21729	4	6675	5	13	NULL	NULL	NULL	statement 1	Process		blocks					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_7_2339_s_32	9337209	15  We have shown previously that annexin V binds to anionic phospholipid on platelets and blocks the binding of factors Xa and Va to platelets.	bind
21730	5	6675	5	13	NULL	NULL	NULL	statement 1	Process		blocks					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_7_2339_s_32	9337209	15  We have shown previously that annexin V binds to anionic phospholipid on platelets and blocks the binding of factors Xa and Va to platelets.	bind
18801	1	6675	6	NULL	NULL	0	NULL	annexin V	NULL		bind	NULL				phospholipids	NULL	anionic			NULL	platelets	0	NULL	NULL	NULL	gw60_circulation_96_7_2339_s_32	9337209	15  We have shown previously that annexin V binds to anionic phospholipid on platelets and blocks the binding of factors Xa and Va to platelets.	bind
18802	2	6675	6	NULL	NULL	0	NULL	factor Xa	NULL		bind	NULL				platelets	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_96_7_2339_s_32	9337209	15  We have shown previously that annexin V binds to anionic phospholipid on platelets and blocks the binding of factors Xa and Va to platelets.	bind
18803	3	6675	6	NULL	NULL	0	NULL	factor Va	NULL		bind	NULL				platelets	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_96_7_2339_s_32	9337209	15  We have shown previously that annexin V binds to anionic phospholipid on platelets and blocks the binding of factors Xa and Va to platelets.	bind
18804	4	6675	6	NULL	NULL	0	NULL	statement 1	NULL		blocks	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_96_7_2339_s_32	9337209	15  We have shown previously that annexin V binds to anionic phospholipid on platelets and blocks the binding of factors Xa and Va to platelets.	bind
18805	5	6675	6	NULL	NULL	0	NULL	statement 1	NULL		blocks	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_96_7_2339_s_32	9337209	15  We have shown previously that annexin V binds to anionic phospholipid on platelets and blocks the binding of factors Xa and Va to platelets.	bind
24797	1	6676	5	13	NULL	NULL	NULL	F1F0-ATPase	GP	natural inhibitor of	bind					F1F0-ATPase	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
24798	2	6676	5	13	NULL	NULL	NULL	statement 1	Process		inhibit					glycolytic ATP	Chemical	breakdown of 			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
24799	3	6676	5	13	NULL	NULL	NULL	ischemia	MedicalFinding		leads to					ATP	Chemical	preferential decrease in cytosolic			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
24800	4	6676	5	13	NULL	NULL	NULL	ischemia	MedicalFinding		leads to					ATP	Chemical	preferential decrease in mitochondrial			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
24801	5	6676	5	13	NULL	NULL	NULL	anoxia	MedicalFinding		leads to					ATP	Chemical	preferential decrease in cytosolic			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
24802	6	6676	5	13	NULL	NULL	NULL	anoxia	MedicalFinding		leads to					ATP	Chemical	preferential decrease in mitochondrial			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
24803	7	6676	5	13	NULL	NULL	NULL	cells	Cell		regulates		may			ADP/ATP	Chemical	mitochondrial;;exchange of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
24805	8	6676	5	13	NULL	NULL	NULL	statement 3	Process		suggests					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
24806	9	6676	5	13	NULL	NULL	NULL	statement 4	Process		suggests					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
24807	10	6676	5	13	NULL	NULL	NULL	statement 5	Process		suggests					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
24808	11	6676	5	13	NULL	NULL	NULL	statement 6	Process		suggests					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
56350	12	6676	5	13	NULL	NULL	NULL	statement 1	Process		occur during					ischemia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
56351	13	6676	5	13	NULL	NULL	NULL	statement 7	Process		occur during					ischemia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
18987	1	6676	6	10	NULL	0	NULL	F1F0-ATPase		natural inhibitor of	bind					F1F0-ATPase					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
18988	2	6676	6	NULL	NULL	0	NULL	statement 1	NULL		occurs during	NULL				ischemia	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
18991	3	6676	6	NULL	NULL	0	NULL	statement 1	NULL		inhibit	NULL				glycolytic ATP	NULL	breakdown of 			NULL		0	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
56340	4	6676	6	10	NULL	0	NULL	 ischemia 			lead to					ATP		preferential decrease in cytosolic			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
56341	5	6676	6	10	NULL	0	NULL	ischemia			lead to					ATP		preferential decrease in mitochondrial			NULL		0	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
56342	6	6676	6	10	NULL	0	NULL	anoxia 			lead to					ATP		preferential decrease in cytosolic			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
56343	7	6676	6	10	NULL	0	NULL	anoxia 			lead to					ATP		preferential decrease in mitochondrial			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
56344	8	6676	6	10	NULL	0	NULL	cells			regulate		may			ADP/ATP		mitochondrial;;exchange of			NULL		0	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
56345	9	6676	6	10	NULL	0	NULL	statement 8			occur during					ischemia					NULL		0	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
56346	10	6676	6	10	NULL	0	NULL	statement 4			suggest					statement 8					NULL		0	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
56347	11	6676	6	10	NULL	0	NULL	statement 5			suggest					statement 8					NULL		0	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
56348	12	6676	6	10	NULL	0	NULL	statement 6			suggest					statement 8					NULL		0	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
56349	13	6676	6	10	NULL	0	NULL	statement 7			suggest					statement 8					NULL		0	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_29	15345651	15 - 19     In fact, many cells contain a natural inhibitor of the F1F0-ATPase, which binds the F1F0-ATPase during ischemia to inhibit breakdown of glycolytic ATP. 20 There are also data showing that ischemia and anoxia lead to a preferential decrease in cytosolic versus mitochondrial ATP, 21,22  suggesting that cells may regulate mitochondrial ADP/ATP exchange during ischemia.	bind
21731	1	6677	5	13	NULL	NULL	NULL	Endoglin	GP		does not bind					TGF-beta1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2546_s_38	11116051	15 16  Endoglin alone does not bind TGF-beta1 or -beta3 but requires the presence of TbetaR-II.	bind
21732	2	6677	5	13	NULL	NULL	NULL	Endoglin	GP		does not bind					TGF-beta3	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2546_s_38	11116051	15 16  Endoglin alone does not bind TGF-beta1 or -beta3 but requires the presence of TbetaR-II.	bind
21733	3	6677	5	13	NULL	NULL	NULL	Endoglin	GP		bind					TGF-beta1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2546_s_38	11116051	15 16  Endoglin alone does not bind TGF-beta1 or -beta3 but requires the presence of TbetaR-II.	bind
21734	4	6677	5	13	NULL	NULL	NULL	statement 3	Process		in the presence of					TbetaR-II	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2546_s_38	11116051	15 16  Endoglin alone does not bind TGF-beta1 or -beta3 but requires the presence of TbetaR-II.	bind
21735	5	6677	5	13	NULL	NULL	NULL	Endoglin	GP		bind					TGF-beta3	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2546_s_38	11116051	15 16  Endoglin alone does not bind TGF-beta1 or -beta3 but requires the presence of TbetaR-II.	bind
21736	6	6677	5	13	NULL	NULL	NULL	statement 5	Process		in the presence of					TbetaR-II	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2546_s_38	11116051	15 16  Endoglin alone does not bind TGF-beta1 or -beta3 but requires the presence of TbetaR-II.	bind
18806	1	6677	6	NULL	NULL	0	NULL	Endoglin	NULL		bind	NULL				TGF-beta1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2546_s_38	11116051	15 16  Endoglin alone does not bind TGF-beta1 or -beta3 but requires the presence of TbetaR-II.	bind
18807	2	6677	6	NULL	NULL	0	NULL	Endoglin	NULL		bind	NULL				TGF-beta3	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2546_s_38	11116051	15 16  Endoglin alone does not bind TGF-beta1 or -beta3 but requires the presence of TbetaR-II.	bind
18808	3	6677	6	NULL	NULL	0	NULL	statement 1	NULL		occurs in presence of	NULL	only			TbetaR-II	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2546_s_38	11116051	15 16  Endoglin alone does not bind TGF-beta1 or -beta3 but requires the presence of TbetaR-II.	bind
18809	4	6677	6	NULL	NULL	0	NULL	statement 2	NULL		occurs in presence of	NULL	only			TbetaR-II	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2546_s_38	11116051	15 16  Endoglin alone does not bind TGF-beta1 or -beta3 but requires the presence of TbetaR-II.	bind
21737	1	6678	5	13	NULL	NULL	NULL	Heparin	Chemical		bind		avidly			smooth muscle cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_6_1143_s_209	7586227	15 17  Heparin avidly binds to smooth muscle cells and extracellular structures.	bind
21738	2	6678	5	13	NULL	NULL	NULL	Heparin	Chemical		bind		avidly			extracellular structures	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_6_1143_s_209	7586227	15 17  Heparin avidly binds to smooth muscle cells and extracellular structures.	bind
18810	1	6678	6	NULL	NULL	0	NULL	heparin	NULL		bind	NULL	avidly			smooth muscle cells	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_77_6_1143_s_209	7586227	15 17  Heparin avidly binds to smooth muscle cells and extracellular structures.	bind
18811	2	6678	6	NULL	NULL	0	NULL	heparin	NULL		bind	NULL	avidly			extracellular structures	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_77_6_1143_s_209	7586227	15 17  Heparin avidly binds to smooth muscle cells and extracellular structures.	bind
21740	1	6681	5	13	NULL	NULL	NULL	SREBP-2	GP		bind		exclusively			squalene synthase	NucleicAcid	human		SRE 5''-TCCACCCCAC-3''	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2358_s_156	15486308	15 Conversely, it has also been suggested that differences in the first 2 5' nucleotides of the LDL-receptor SRE-1 could explain the exclusive binding of SREBP-2 to the human squalene synthase SRE (8/10) 5''-TCCACCCCAC-3''.	bind
21743	2	6681	5	13	NULL	NULL	NULL	LDL-receptor	GP	differences of	explains				SRE-1 nucleotides	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2358_s_156	15486308	15 Conversely, it has also been suggested that differences in the first 2 5' nucleotides of the LDL-receptor SRE-1 could explain the exclusive binding of SREBP-2 to the human squalene synthase SRE (8/10) 5''-TCCACCCCAC-3''.	bind
18812	1	6681	6	NULL	NULL	0	NULL	SREBP-2	NULL		bind	NULL	exclusively			squalene synthase	NULL	human		SRE (8/10)-TCCACCCCAC	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2358_s_156	15486308	15 Conversely, it has also been suggested that differences in the first 2 5' nucleotides of the LDL-receptor SRE-1 could explain the exclusive binding of SREBP-2 to the human squalene synthase SRE (8/10) 5''-TCCACCCCAC-3''.	bind
30470	2	6681	6	NULL	NULL	0	NULL	LDL receptor	NULL	difference of	explains	NULL			SRE-1 nucleotides	statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2358_s_156	15486308	15 Conversely, it has also been suggested that differences in the first 2 5' nucleotides of the LDL-receptor SRE-1 could explain the exclusive binding of SREBP-2 to the human squalene synthase SRE (8/10) 5''-TCCACCCCAC-3''.	bind
21744	1	6682	5	13	NULL	NULL	NULL	DDAH1	GP		bind					NF1	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1419_s_33	16794231	15 DDAH1 binding to NF1 promoted the phosphorylation of NF1 by PKA at specific residues within the cysteine/serine rich domain.	bind
21745	2	6682	5	13	NULL	NULL	NULL	PKA	GP		phosphorylates					NF1	GP		specific residues within the  cysteine/serine rich domain		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1419_s_33	16794231	15 DDAH1 binding to NF1 promoted the phosphorylation of NF1 by PKA at specific residues within the cysteine/serine rich domain.	bind
21746	3	6682	5	13	NULL	NULL	NULL	statement 1	Process		promote					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1419_s_33	16794231	15 DDAH1 binding to NF1 promoted the phosphorylation of NF1 by PKA at specific residues within the cysteine/serine rich domain.	bind
18813	1	6682	6	NULL	NULL	0	NULL	DDAH1	NULL		bind	NULL				NF1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1419_s_33	16794231	15 DDAH1 binding to NF1 promoted the phosphorylation of NF1 by PKA at specific residues within the cysteine/serine rich domain.	bind
18814	2	6682	6	NULL	NULL	0	NULL	PKA	NULL		phosphorylates	NULL				NF1	NULL		specific residues within the cysteine/serine rich domain		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1419_s_33	16794231	15 DDAH1 binding to NF1 promoted the phosphorylation of NF1 by PKA at specific residues within the cysteine/serine rich domain.	bind
18815	3	6682	6	NULL	NULL	0	NULL	statement 1	NULL		promotes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1419_s_33	16794231	15 DDAH1 binding to NF1 promoted the phosphorylation of NF1 by PKA at specific residues within the cysteine/serine rich domain.	bind
21748	1	6683	5	13	NULL	NULL	NULL	fibrinogen	GP		bind					GPIIb-IIIa	GP	activated			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_1_252_s_171	15514209	15 Despite a larger number of heterozygotes and homozygotes for the minor haplotype in our study, we did not detect any effect of this variant on fibrinogen binding to activated GPIIb-IIIa.	bind
18816	1	6683	6	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL				GPIIb-IIIa	NULL	activated			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_1_252_s_171	15514209	15 Despite a larger number of heterozygotes and homozygotes for the minor haplotype in our study, we did not detect any effect of this variant on fibrinogen binding to activated GPIIb-IIIa.	bind
21749	1	6684	5	13	NULL	NULL	NULL	CKIs	GP		is					cyclin-dependent kinase inhibitors	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_511_s_33	14726409	15 Furthermore, cell cycle progression is regulated by the expression of cyclin-dependent kinase inhibitors (CKIs) such as p27kip1 and p21waf, which bind to CDKs and prevent their activation 14,15	bind
21751	2	6684	5	13	NULL	NULL	NULL	p27kip1	GP		is a type of					CKIs	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_511_s_33	14726409	15 Furthermore, cell cycle progression is regulated by the expression of cyclin-dependent kinase inhibitors (CKIs) such as p27kip1 and p21waf, which bind to CDKs and prevent their activation 14,15	bind
21752	3	6684	5	13	NULL	NULL	NULL	p21waf	GP		is a type of					CKIs	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_511_s_33	14726409	15 Furthermore, cell cycle progression is regulated by the expression of cyclin-dependent kinase inhibitors (CKIs) such as p27kip1 and p21waf, which bind to CDKs and prevent their activation 14,15	bind
21754	4	6684	5	13	NULL	NULL	NULL	p27kip1	GP		bind					CDKs	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_511_s_33	14726409	15 Furthermore, cell cycle progression is regulated by the expression of cyclin-dependent kinase inhibitors (CKIs) such as p27kip1 and p21waf, which bind to CDKs and prevent their activation 14,15	bind
21755	5	6684	5	13	NULL	NULL	NULL	statement 4	Process		prevents					CDKs	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_511_s_33	14726409	15 Furthermore, cell cycle progression is regulated by the expression of cyclin-dependent kinase inhibitors (CKIs) such as p27kip1 and p21waf, which bind to CDKs and prevent their activation 14,15	bind
21756	6	6684	5	13	NULL	NULL	NULL	p21waf	GP		bind					CDKs	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_511_s_33	14726409	15 Furthermore, cell cycle progression is regulated by the expression of cyclin-dependent kinase inhibitors (CKIs) such as p27kip1 and p21waf, which bind to CDKs and prevent their activation 14,15	bind
21758	7	6684	5	13	NULL	NULL	NULL	statement 6	Process		prevents					CDKs	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_511_s_33	14726409	15 Furthermore, cell cycle progression is regulated by the expression of cyclin-dependent kinase inhibitors (CKIs) such as p27kip1 and p21waf, which bind to CDKs and prevent their activation 14,15	bind
21759	8	6684	5	13	NULL	NULL	NULL	CKIs	GP	expression of	regulates					cell cycle 	Process	progression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_511_s_33	14726409	15 Furthermore, cell cycle progression is regulated by the expression of cyclin-dependent kinase inhibitors (CKIs) such as p27kip1 and p21waf, which bind to CDKs and prevent their activation 14,15	bind
18817	1	6684	6	NULL	NULL	0	NULL	p27kip1	NULL		bind	NULL				CDK	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_511_s_33	14726409	15 Furthermore, cell cycle progression is regulated by the expression of cyclin-dependent kinase inhibitors (CKIs) such as p27kip1 and p21waf, which bind to CDKs and prevent their activation 14,15	bind
18818	2	6684	6	NULL	NULL	0	NULL	p21waf	NULL		bind	NULL				CDK	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_511_s_33	14726409	15 Furthermore, cell cycle progression is regulated by the expression of cyclin-dependent kinase inhibitors (CKIs) such as p27kip1 and p21waf, which bind to CDKs and prevent their activation 14,15	bind
18819	3	6684	6	NULL	NULL	0	NULL	p27kip1	NULL		is a type of	NULL				CKI	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_511_s_33	14726409	15 Furthermore, cell cycle progression is regulated by the expression of cyclin-dependent kinase inhibitors (CKIs) such as p27kip1 and p21waf, which bind to CDKs and prevent their activation 14,15	bind
18820	4	6684	6	NULL	NULL	0	NULL	CKI	NULL		is	NULL				cyclin dependent kinase inhibitors	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_511_s_33	14726409	15 Furthermore, cell cycle progression is regulated by the expression of cyclin-dependent kinase inhibitors (CKIs) such as p27kip1 and p21waf, which bind to CDKs and prevent their activation 14,15	bind
18821	5	6684	6	NULL	NULL	0	NULL	p21waf1	NULL		is a type of	NULL				CKI	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_511_s_33	14726409	15 Furthermore, cell cycle progression is regulated by the expression of cyclin-dependent kinase inhibitors (CKIs) such as p27kip1 and p21waf, which bind to CDKs and prevent their activation 14,15	bind
18822	6	6684	6	NULL	NULL	0	NULL	p27kip1	NULL		regulates	NULL				cell cycle 	NULL	progression of 			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_511_s_33	14726409	15 Furthermore, cell cycle progression is regulated by the expression of cyclin-dependent kinase inhibitors (CKIs) such as p27kip1 and p21waf, which bind to CDKs and prevent their activation 14,15	bind
18823	7	6684	6	NULL	NULL	0	NULL	p21waf1	NULL		regulates	NULL				cell cycle 	NULL	progression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_511_s_33	14726409	15 Furthermore, cell cycle progression is regulated by the expression of cyclin-dependent kinase inhibitors (CKIs) such as p27kip1 and p21waf, which bind to CDKs and prevent their activation 14,15	bind
30471	8	6684	6	NULL	NULL	0	NULL	statement 1	NULL		prevents	NULL				CDK	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_511_s_33	14726409	15 Furthermore, cell cycle progression is regulated by the expression of cyclin-dependent kinase inhibitors (CKIs) such as p27kip1 and p21waf, which bind to CDKs and prevent their activation 14,15	bind
30472	9	6684	6	NULL	NULL	0	NULL	statement 2	NULL		prevents	NULL				CDK	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_511_s_33	14726409	15 Furthermore, cell cycle progression is regulated by the expression of cyclin-dependent kinase inhibitors (CKIs) such as p27kip1 and p21waf, which bind to CDKs and prevent their activation 14,15	bind
21761	1	6685	5	13	NULL	NULL	NULL	Grp78	GP		bind		transiently			proteins	GP	newly synthesized			NULL	ER	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_3_571_s_31	15618547	15 Grp78 binds transiently to newly synthesized proteins in the ER and more permanently to misfolded unglycosylated proteins whose transport from the ER is blocked.	bind
21764	2	6685	5	13	NULL	NULL	NULL	Grp78	GP		bind		permanently			proteins	GP	misfolded;;unglycosylated			NULL	ER	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_3_571_s_31	15618547	15 Grp78 binds transiently to newly synthesized proteins in the ER and more permanently to misfolded unglycosylated proteins whose transport from the ER is blocked.	bind
18824	1	6685	6	10	NULL	0	NULL	Grp78	NULL		bind	NULL	transiently			 proteins	NULL	newly synthesized			NULL	ER	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_3_571_s_31	15618547	15 Grp78 binds transiently to newly synthesized proteins in the ER and more permanently to misfolded unglycosylated proteins whose transport from the ER is blocked.	bind
18825	2	6685	6	10	NULL	0	NULL	Grp78			bind		permanently			protein		misfolded;;unglycosylated			NULL	ER	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_3_571_s_31	15618547	15 Grp78 binds transiently to newly synthesized proteins in the ER and more permanently to misfolded unglycosylated proteins whose transport from the ER is blocked.	bind
21765	1	6686	5	13	NULL	NULL	NULL	HSPGs	GP		bind					bFGF	GP				NULL	 pericellular matrix	NULL	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
21766	2	6686	5	13	NULL	NULL	NULL	Heparin	Chemical		bind					bFGF	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
21767	3	6686	5	13	NULL	NULL	NULL	statement 2	Process		competes with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
21768	4	6686	5	13	NULL	NULL	NULL	Heparin	Chemical		inhibit					FGF	Process	signalling of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
21769	5	6686	5	13	NULL	NULL	NULL	statement 3	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
21770	6	6686	5	13	NULL	NULL	NULL	bFGF	GP		released from					cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
21772	7	6686	5	13	NULL	NULL	NULL	statement 6	Process		occurs after stimulation with					thrombin	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
21782	9	6686	5	13	NULL	NULL	NULL	statement 7	Process		occurs along with					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
44669	8	6686	5	13	NULL	NULL	NULL	statement 6	Process		occurs after stimulation with					FXa	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
56353	10	6686	5	13	NULL	NULL	NULL	statement 1	Process		occurs after					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
18826	1	6686	6	NULL	NULL	0	NULL	HSPG	NULL		bind	NULL				bFGF	NULL				NULL	pericellular matrix	NULL	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
18827	2	6686	6	NULL	NULL	0	NULL	heparin	NULL		bind	NULL				bFGF	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
18828	3	6686	6	NULL	NULL	0	NULL	statement 1	NULL		competes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
18861	4	6686	6	10	NULL	0	NULL	heparin			inhibits					FGF 		signaling of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
18862	5	6686	6	NULL	NULL	0	NULL	statement 4	NULL		occurs by	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
18863	6	6686	6	NULL	NULL	0	NULL	bFGF	NULL		released from	NULL				cells	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
18864	7	6686	6	NULL	NULL	0	NULL	statement 6	NULL		occurs after stimulation with	NULL				thrombin	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
18865	8	6686	6	NULL	NULL	0	NULL	statement 6	NULL		occurs after stimulation with	NULL				FXa	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
56352	9	6686	6	10	NULL	0	NULL	statement 7			occur along with					statement 8					NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
56354	10	6686	6	10	NULL	0	NULL	statement 1			occurs after					statement 9					NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_340_s_152	14670838	15 Heparin inhibits FGF signaling by competing with HSPGs for binding bFGF. 15,28  Our data suggest that bFGF is released from the cells after stimulation with thrombin and FXa and binds to HSPGs in the pericellular matrix ( Figures 4A and 5   ).	bind
22925	1	6687	5	13	NULL	NULL	NULL	ADP-P2y12	GP		activates					type 1B PI3-K	GP				NULL	in human platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_2_417_s_30	16339499	15 In human platelets, the role of type 1B PI3-K is less well understood, because although being activated by ADP-P2y12 contact, it appears under negative control by ADP-P2y1 binding and activation of Src and PKC. 10,16	bind
24809	2	6687	5	13	NULL	NULL	NULL	ADP-P2y1	GP	binding of	controls		negatively			type 1B PI3-K	GP				NULL	in human platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_2_417_s_30	16339499	15 In human platelets, the role of type 1B PI3-K is less well understood, because although being activated by ADP-P2y12 contact, it appears under negative control by ADP-P2y1 binding and activation of Src and PKC. 10,16	bind
24810	3	6687	5	13	NULL	NULL	NULL	Src	GP	activation of	controls		negatively			type 1B PI3-K	GP				NULL	in human platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_2_417_s_30	16339499	15 In human platelets, the role of type 1B PI3-K is less well understood, because although being activated by ADP-P2y12 contact, it appears under negative control by ADP-P2y1 binding and activation of Src and PKC. 10,16	bind
24811	4	6687	5	13	NULL	NULL	NULL	PKC	GP	activation of	controls		negatively			type 1B PI3-K	GP				NULL	in human platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_2_417_s_30	16339499	15 In human platelets, the role of type 1B PI3-K is less well understood, because although being activated by ADP-P2y12 contact, it appears under negative control by ADP-P2y1 binding and activation of Src and PKC. 10,16	bind
18866	1	6687	6	NULL	NULL	0	NULL	type 1B PI3-K	NULL		is activated by	NULL				ADP-P2y12	NULL				NULL	human platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_2_417_s_30	16339499	15 In human platelets, the role of type 1B PI3-K is less well understood, because although being activated by ADP-P2y12 contact, it appears under negative control by ADP-P2y1 binding and activation of Src and PKC. 10,16	bind
18867	2	6687	6	NULL	NULL	0	NULL	ADP-P2y12	NULL	binding of	controls	NULL	negatively 			type 1B PI3-K	NULL				NULL	human platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_2_417_s_30	16339499	15 In human platelets, the role of type 1B PI3-K is less well understood, because although being activated by ADP-P2y12 contact, it appears under negative control by ADP-P2y1 binding and activation of Src and PKC. 10,16	bind
18868	3	6687	6	NULL	NULL	0	NULL	ADP-P2y12	NULL	binding of	controls	NULL	negatively			src	NULL	activation of			NULL	human platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_2_417_s_30	16339499	15 In human platelets, the role of type 1B PI3-K is less well understood, because although being activated by ADP-P2y12 contact, it appears under negative control by ADP-P2y1 binding and activation of Src and PKC. 10,16	bind
18869	4	6687	6	NULL	NULL	0	NULL	ADP-P2y12	NULL	binding of	controls	NULL	negatively			PKC	NULL	activation of			NULL	human platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_2_417_s_30	16339499	15 In human platelets, the role of type 1B PI3-K is less well understood, because although being activated by ADP-P2y12 contact, it appears under negative control by ADP-P2y1 binding and activation of Src and PKC. 10,16	bind
21788	1	6691	5	13	NULL	NULL	NULL	MyBP-C 	GP		bind					actin	GP				NULL	in solution	NULL	NULL	NULL	NULL	gw70_circulationres_93_8_752_s_133	14500336	15 MyBP-C also binds actin and regulated thin filaments in solution, and the latter is Ca2+ dependent.	bind
21789	2	6691	5	13	NULL	NULL	NULL	MyBP-C 	GP		bind					thin filaments	CellComponent	regulated			NULL	in solution	NULL	NULL	NULL	NULL	gw70_circulationres_93_8_752_s_133	14500336	15 MyBP-C also binds actin and regulated thin filaments in solution, and the latter is Ca2+ dependent.	bind
21790	3	6691	5	13	NULL	NULL	NULL	statement 2	Process		is dependent on					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_8_752_s_133	14500336	15 MyBP-C also binds actin and regulated thin filaments in solution, and the latter is Ca2+ dependent.	bind
18871	1	6691	6	10	NULL	0	NULL	MyBP-C			bind					actin					NULL	in solution	NULL	NULL	NULL	NULL	gw70_circulationres_93_8_752_s_133	14500336	15 MyBP-C also binds actin and regulated thin filaments in solution, and the latter is Ca2+ dependent.	bind
18872	2	6691	6	NULL	NULL	0	NULL	MyBP-C	NULL		regulates	NULL				thin filaments	NULL				NULL	in solution	0	NULL	NULL	NULL	gw70_circulationres_93_8_752_s_133	14500336	15 MyBP-C also binds actin and regulated thin filaments in solution, and the latter is Ca2+ dependent.	bind
18873	3	6691	6	NULL	NULL	0	NULL	statement 2	NULL		is dependent on	NULL				calcium	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_8_752_s_133	14500336	15 MyBP-C also binds actin and regulated thin filaments in solution, and the latter is Ca2+ dependent.	bind
21791	1	6692	5	13	NULL	NULL	NULL	Skp1	GP		bind					cdk2/cyclin A complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1217_s_165	15117732	15 Skp1 binds the cdk2/cyclin A complex and regulates the cell cycle by the timely destruction of numerous regulatory proteins such as cyclins.	bind
21793	2	6692	5	13	NULL	NULL	NULL	Skp1	GP		regulates					cell cycle	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1217_s_165	15117732	15 Skp1 binds the cdk2/cyclin A complex and regulates the cell cycle by the timely destruction of numerous regulatory proteins such as cyclins.	bind
21795	3	6692	5	13	NULL	NULL	NULL	Skp1	GP		destroys					regulatory proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1217_s_165	15117732	15 Skp1 binds the cdk2/cyclin A complex and regulates the cell cycle by the timely destruction of numerous regulatory proteins such as cyclins.	bind
21796	4	6692	5	13	NULL	NULL	NULL	statement 3	Process		is mechanism of					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1217_s_165	15117732	15 Skp1 binds the cdk2/cyclin A complex and regulates the cell cycle by the timely destruction of numerous regulatory proteins such as cyclins.	bind
18874	1	6692	6	NULL	NULL	0	NULL	Skp1	NULL		bind	NULL				cdk2/cyclin A complex	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1217_s_165	15117732	15 Skp1 binds the cdk2/cyclin A complex and regulates the cell cycle by the timely destruction of numerous regulatory proteins such as cyclins.	bind
18875	2	6692	6	NULL	NULL	0	NULL	Skp1	NULL		regulates	NULL				cell cycle	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1217_s_165	15117732	15 Skp1 binds the cdk2/cyclin A complex and regulates the cell cycle by the timely destruction of numerous regulatory proteins such as cyclins.	bind
30473	3	6692	6	NULL	NULL	0	NULL	Skp1	NULL		destroys	NULL				regulatory proteins	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1217_s_165	15117732	15 Skp1 binds the cdk2/cyclin A complex and regulates the cell cycle by the timely destruction of numerous regulatory proteins such as cyclins.	bind
30474	4	6692	6	NULL	NULL	0	NULL	statement 3	NULL		is the mechanism for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1217_s_165	15117732	15 Skp1 binds the cdk2/cyclin A complex and regulates the cell cycle by the timely destruction of numerous regulatory proteins such as cyclins.	bind
21797	1	6693	5	13	NULL	NULL	NULL	BS-1 lectin	GP	biotin-labeled 	bind					luminal surface of endothelial cells	Cell				NULL	 ear skin from wild-type mice	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2108_s_94	15345507	15 The architecture of the microvasculature was examined in whole-mount preparations of ear skin from wild-type and beta3-null mice in which vessels were visualized with biotin-labeled BS-1 lectin, which binds to the luminal surface of endothelial cells.	bind
21798	2	6693	5	13	NULL	NULL	NULL	BS-1 lectin	GP	biotin-labeled 	bind					luminal surface of endothelial cells	Cell				NULL	ear skin from beta3-null mice	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2108_s_94	15345507	15 The architecture of the microvasculature was examined in whole-mount preparations of ear skin from wild-type and beta3-null mice in which vessels were visualized with biotin-labeled BS-1 lectin, which binds to the luminal surface of endothelial cells.	bind
18879	1	6693	6	10	NULL	0	NULL	BS-1 lectin		biotin-labeled	bind					luminal surface of endothelial cells					NULL	ear skin from wild type mice	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2108_s_94	15345507	15 The architecture of the microvasculature was examined in whole-mount preparations of ear skin from wild-type and beta3-null mice in which vessels were visualized with biotin-labeled BS-1 lectin, which binds to the luminal surface of endothelial cells.	bind
18880	2	6693	6	10	NULL	0	NULL	BS-1 lectin		biotin-labeled	bind					luminal surface of endothelial cells					NULL	ear skin from beta3-null mice	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2108_s_94	15345507	15 The architecture of the microvasculature was examined in whole-mount preparations of ear skin from wild-type and beta3-null mice in which vessels were visualized with biotin-labeled BS-1 lectin, which binds to the luminal surface of endothelial cells.	bind
21799	1	6694	5	13	NULL	NULL	NULL	E-cadherin	GP		is different from			p120ctn binding site		E-cadherin	GP		beta- catenin/plakoglobin binding site		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_787_s_21	10487836	15 The p120ctn binding site in E-cadherin is different from the beta- catenin/plakoglobin binding site and p120ctn does not bind to alpha-catenin.	bind
21800	2	6694	5	13	NULL	NULL	NULL	p120ctn	GP		does not bind					alpha-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_787_s_21	10487836	15 The p120ctn binding site in E-cadherin is different from the beta- catenin/plakoglobin binding site and p120ctn does not bind to alpha-catenin.	bind
18882	1	6694	6	NULL	NULL	0	NULL	p120ctn	NULL		does not bind	NULL				alpha-catenin	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_3_787_s_21	10487836	15 The p120ctn binding site in E-cadherin is different from the beta- catenin/plakoglobin binding site and p120ctn does not bind to alpha-catenin.	bind
30533	2	6694	6	10	NULL	0	NULL	E-cadherin			is different from			p120ctn binding site		E-cadherin			beta- catenin/plakoglobin binding site		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_787_s_21	10487836	15 The p120ctn binding site in E-cadherin is different from the beta- catenin/plakoglobin binding site and p120ctn does not bind to alpha-catenin.	bind
21802	1	6696	5	13	NULL	NULL	NULL	CRP	GP		bind					FcgammaRI	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_21_2566_s_151	15136507	15 We found that blocking binding of CRP to FcgammaRI abolished the positive regulatory effect of CRP on monocyte CCR2 expression.	bind
21805	2	6696	5	13	NULL	NULL	NULL	CRP	GP		regulates		positive			CCR2	GP	expression of			NULL	monocyte	NULL	NULL	NULL	NULL	gw70_circulation_109_21_2566_s_151	15136507	15 We found that blocking binding of CRP to FcgammaRI abolished the positive regulatory effect of CRP on monocyte CCR2 expression.	bind
21806	3	6696	5	13	NULL	NULL	NULL	statement 1	Process	blocking of	abolishes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_21_2566_s_151	15136507	15 We found that blocking binding of CRP to FcgammaRI abolished the positive regulatory effect of CRP on monocyte CCR2 expression.	bind
18906	1	6696	6	NULL	NULL	0	NULL	CRP	NULL		bind	NULL				FcgammaRI	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_109_21_2566_s_151	15136507	15 We found that blocking binding of CRP to FcgammaRI abolished the positive regulatory effect of CRP on monocyte CCR2 expression.	bind
18908	2	6696	6	NULL	NULL	0	NULL	CRP	NULL		regulates	NULL	positively			CCR2 	NULL	expression of			NULL	monocytes	NULL	NULL	NULL	NULL	gw70_circulation_109_21_2566_s_151	15136507	15 We found that blocking binding of CRP to FcgammaRI abolished the positive regulatory effect of CRP on monocyte CCR2 expression.	bind
18910	3	6696	6	NULL	NULL	0	NULL	statement 1	NULL	blocking of	abolishes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_109_21_2566_s_151	15136507	15 We found that blocking binding of CRP to FcgammaRI abolished the positive regulatory effect of CRP on monocyte CCR2 expression.	bind
21824	1	6697	5	13	NULL	NULL	NULL	P. aeruginosa	Organism		induces					MUC2	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_4_1475_s_268	12368220	15, 16  MUC2 transcription induced by  P. aeruginosa was mediated by the binding of NF-kappaB (p55 and p65 subunits) to this kappaB site.	bind
21825	2	6697	5	13	NULL	NULL	NULL	NF-kappaB	GP		bind									kappaB site	NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_4_1475_s_268	12368220	15, 16  MUC2 transcription induced by  P. aeruginosa was mediated by the binding of NF-kappaB (p55 and p65 subunits) to this kappaB site.	bind
21826	3	6697	5	13	NULL	NULL	NULL	NF-kappaB	GP		consists of					p55 subunit	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_4_1475_s_268	12368220	15, 16  MUC2 transcription induced by  P. aeruginosa was mediated by the binding of NF-kappaB (p55 and p65 subunits) to this kappaB site.	bind
21827	4	6697	5	13	NULL	NULL	NULL	NF-kappaB	GP		consists of					p65 subunit	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_4_1475_s_268	12368220	15, 16  MUC2 transcription induced by  P. aeruginosa was mediated by the binding of NF-kappaB (p55 and p65 subunits) to this kappaB site.	bind
21828	5	6697	5	13	NULL	NULL	NULL	statement 2	Process		mediate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_4_1475_s_268	12368220	15, 16  MUC2 transcription induced by  P. aeruginosa was mediated by the binding of NF-kappaB (p55 and p65 subunits) to this kappaB site.	bind
19000	1	6697	6	NULL	NULL	0	NULL	MUC2	NULL	transcription of	is induced by	NULL				P. aeruginosa	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_4_1475_s_268	12368220	15, 16  MUC2 transcription induced by  P. aeruginosa was mediated by the binding of NF-kappaB (p55 and p65 subunits) to this kappaB site.	bind
19004	2	6697	6	NULL	NULL	0	NULL	NF-kappaB	NULL		bind	NULL					NULL			kappaB site	NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_4_1475_s_268	12368220	15, 16  MUC2 transcription induced by  P. aeruginosa was mediated by the binding of NF-kappaB (p55 and p65 subunits) to this kappaB site.	bind
19005	3	6697	6	NULL	NULL	0	NULL	statement 1	NULL		is mediated by	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_4_1475_s_268	12368220	15, 16  MUC2 transcription induced by  P. aeruginosa was mediated by the binding of NF-kappaB (p55 and p65 subunits) to this kappaB site.	bind
56355	4	6697	6	10	NULL	0	NULL	NF-kappaB			consist of					p55 subunit					NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_4_1475_s_268	12368220	15, 16  MUC2 transcription induced by  P. aeruginosa was mediated by the binding of NF-kappaB (p55 and p65 subunits) to this kappaB site.	bind
56356	5	6697	6	10	NULL	0	NULL	NF-kappaB			consist of					p65 subunit					NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_4_1475_s_268	12368220	15, 16  MUC2 transcription induced by  P. aeruginosa was mediated by the binding of NF-kappaB (p55 and p65 subunits) to this kappaB site.	bind
21829	1	6698	5	13	NULL	NULL	NULL				upstream of				kappaB-binding site	MUC2 gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_4_1475_s_267	12368220	15, 16, 41  The kappaB-binding site exists upstream of the MUC2 gene, which can bind to a transcription factor, nuclear factor (NF)-kappaB.	bind
21830	2	6698	5	13	NULL	NULL	NULL	MUC2 gene	GP		bind				kappaB-binding site	NF-kappaB	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_4_1475_s_267	12368220	15, 16, 41  The kappaB-binding site exists upstream of the MUC2 gene, which can bind to a transcription factor, nuclear factor (NF)-kappaB.	bind
21831	3	6698	5	13	NULL	NULL	NULL	NF-kappaB	GP		is					nuclear factor-kappaB	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_4_1475_s_267	12368220	15, 16, 41  The kappaB-binding site exists upstream of the MUC2 gene, which can bind to a transcription factor, nuclear factor (NF)-kappaB.	bind
19008	1	6698	6	NULL	NULL	0	NULL	NF-kappaB	NULL		bind	NULL				MUC2 gene	NULL			kappaB-binding site	NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_4_1475_s_267	12368220	15, 16, 41  The kappaB-binding site exists upstream of the MUC2 gene, which can bind to a transcription factor, nuclear factor (NF)-kappaB.	bind
30534	2	6698	6	NULL	NULL	0	NULL		NULL		exists	NULL			kappaB-binding site	MUC2 gene	NULL	upstream of 			NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_4_1475_s_267	12368220	15, 16, 41  The kappaB-binding site exists upstream of the MUC2 gene, which can bind to a transcription factor, nuclear factor (NF)-kappaB.	bind
30535	3	6698	6	NULL	NULL	0	NULL	NF-kappaB	NULL		is	NULL				nuclear factor-kappaB	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_4_1475_s_267	12368220	15, 16, 41  The kappaB-binding site exists upstream of the MUC2 gene, which can bind to a transcription factor, nuclear factor (NF)-kappaB.	bind
21832	1	6699	5	13	NULL	NULL	NULL	XIP	GP	exogenous	bind		avidly			PIP2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_1_91_s_177	15550690	15,16  Because exogenous XIP also avidly binds to PIP2, 15 it may be speculated that differences in the native membrane content of PIP2 between cardiac myocytes, HEK, and A549 cells may also account for the different inhibitory efficacy of XIP in these cells.	bind
19009	1	6699	6	NULL	NULL	0	NULL	XIP	NULL	exogenous	bind	NULL	avidly			PIP2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_1_91_s_177	15550690	15,16  Because exogenous XIP also avidly binds to PIP2, 15 it may be speculated that differences in the native membrane content of PIP2 between cardiac myocytes, HEK, and A549 cells may also account for the different inhibitory efficacy of XIP in these cells.	bind
21833	1	6700	5	13	NULL	NULL	NULL	decorin	GP		bind					TGF-beta 17	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_3_869_s_17	12937128	15,16  It is well established that decorin binds to TGF-beta 17  and inhibits its biological activity in a number of cell types, including rat aortic SMCs. 16  However, it is not known whether decorin may also exert its regulatory effects by interacting with and modulating the activity of PDGF, another prominent growth factor involved in arterial repair.	bind
21834	2	6700	5	13	NULL	NULL	NULL	statement 1	Process		inhibit					TGF-beta 17	GP	biological activity of			NULL	in a number of cell types, including rat aortic SMCs	NULL	NULL	NULL	NULL	gw60_amjpathol_163_3_869_s_17	12937128	15,16  It is well established that decorin binds to TGF-beta 17  and inhibits its biological activity in a number of cell types, including rat aortic SMCs. 16  However, it is not known whether decorin may also exert its regulatory effects by interacting with and modulating the activity of PDGF, another prominent growth factor involved in arterial repair.	bind
19051	1	6700	6	NULL	NULL	0	NULL	decorin	NULL		bind	NULL				TGF-beta17	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_163_3_869_s_17	12937128	15,16  It is well established that decorin binds to TGF-beta 17  and inhibits its biological activity in a number of cell types, including rat aortic SMCs. 16  However, it is not known whether decorin may also exert its regulatory effects by interacting with and modulating the activity of PDGF, another prominent growth factor involved in arterial repair.	bind
19052	2	6700	6	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				TGF-beta17	NULL	biological activity of			NULL	rat aortic SMCs	NULL	NULL	NULL	NULL	gw60_amjpathol_163_3_869_s_17	12937128	15,16  It is well established that decorin binds to TGF-beta 17  and inhibits its biological activity in a number of cell types, including rat aortic SMCs. 16  However, it is not known whether decorin may also exert its regulatory effects by interacting with and modulating the activity of PDGF, another prominent growth factor involved in arterial repair.	bind
21835	1	6701	5	13	NULL	NULL	NULL	p65 NF-kappaB	GP		bind					ICAM-1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_41_s_132	14551154	15,37  PKC-delta was also implicated in thrombin-mediated induction of p65 NF-kappaB binding to the ICAM-1 promoter.	bind
21836	2	6701	5	13	NULL	NULL	NULL	statement 1	Process	induction of	is mediated by					thrombin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_41_s_132	14551154	15,37  PKC-delta was also implicated in thrombin-mediated induction of p65 NF-kappaB binding to the ICAM-1 promoter.	bind
21837	3	6701	5	13	NULL	NULL	NULL	PKC-delta	GP		is implicated in					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_41_s_132	14551154	15,37  PKC-delta was also implicated in thrombin-mediated induction of p65 NF-kappaB binding to the ICAM-1 promoter.	bind
19088	1	6701	6	NULL	NULL	0	NULL	p65 NF-kappaB	NULL		bind	NULL				ICAM-1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_41_s_132	14551154	15,37  PKC-delta was also implicated in thrombin-mediated induction of p65 NF-kappaB binding to the ICAM-1 promoter.	bind
19089	2	6701	6	NULL	NULL	0	NULL	thrombin	NULL		mediates	NULL				statement 1	NULL	induction of 			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_41_s_132	14551154	15,37  PKC-delta was also implicated in thrombin-mediated induction of p65 NF-kappaB binding to the ICAM-1 promoter.	bind
56458	3	6701	6	10	NULL	0	NULL	PKC-delta			is implicated in					statement 2					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_41_s_132	14551154	15,37  PKC-delta was also implicated in thrombin-mediated induction of p65 NF-kappaB binding to the ICAM-1 promoter.	bind
21838	1	6702	5	13	NULL	NULL	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_16_10863_s_330	10196163	15-Deoxy-Delta 12,14-prostaglandin J2 Inhibition of NF-kappa B-DNA Binding through Covalent Modification of the p50 Subunit.	bind
21839	2	6702	5	13	NULL	NULL	NULL	15-Deoxy-Delta 12,14-prostaglandin J2	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_16_10863_s_330	10196163	15-Deoxy-Delta 12,14-prostaglandin J2 Inhibition of NF-kappa B-DNA Binding through Covalent Modification of the p50 Subunit.	bind
21840	3	6702	5	13	NULL	NULL	NULL	statement 2	Process		occurs through					p50 Subunit	GP	covalent modification of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_16_10863_s_330	10196163	15-Deoxy-Delta 12,14-prostaglandin J2 Inhibition of NF-kappa B-DNA Binding through Covalent Modification of the p50 Subunit.	bind
19090	1	6702	6	NULL	NULL	0	NULL	NF-kappaB	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_16_10863_s_330	10196163	15-Deoxy-Delta 12,14-prostaglandin J2 Inhibition of NF-kappa B-DNA Binding through Covalent Modification of the p50 Subunit.	bind
19091	2	6702	6	NULL	NULL	0	NULL	15-Deoxy-Delta 12,14-prostaglandin J2	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_16_10863_s_330	10196163	15-Deoxy-Delta 12,14-prostaglandin J2 Inhibition of NF-kappa B-DNA Binding through Covalent Modification of the p50 Subunit.	bind
19152	3	6702	6	NULL	NULL	0	NULL	statement 2	NULL		occurs via	NULL				p50 subuit	NULL	covalent modification of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_16_10863_s_330	10196163	15-Deoxy-Delta 12,14-prostaglandin J2 Inhibition of NF-kappa B-DNA Binding through Covalent Modification of the p50 Subunit.	bind
21848	1	6704	5	13	NULL	NULL	NULL	15-deoxy-delta12,14-PGJ2	Chemical		is					PGD2 metabolite	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_137_8_1163_s_205	12466225	15-deoxy-delta12,14-PGJ2 is another PGD2 metabolite which preferentially binds CRTH2 over DP with 89 fold selectivity.	bind
21849	2	6704	5	13	NULL	NULL	NULL	15-deoxy-delta12,14-PGJ2	Chemical		bind		preferentially			CRTH2	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_137_8_1163_s_205	12466225	15-deoxy-delta12,14-PGJ2 is another PGD2 metabolite which preferentially binds CRTH2 over DP with 89 fold selectivity.	bind
21851	3	6704	5	13	NULL	NULL	NULL	15-deoxy-delta12,14-PGJ2	Chemical		bind					DP	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_137_8_1163_s_205	12466225	15-deoxy-delta12,14-PGJ2 is another PGD2 metabolite which preferentially binds CRTH2 over DP with 89 fold selectivity.	bind
21852	4	6704	5	13	NULL	NULL	NULL	statement 2	Process		is prefered over					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_137_8_1163_s_205	12466225	15-deoxy-delta12,14-PGJ2 is another PGD2 metabolite which preferentially binds CRTH2 over DP with 89 fold selectivity.	bind
19153	1	6704	6	NULL	NULL	0	NULL	15-deoxy-delta12,14-PGJ2	NULL		is	NULL				PGD2 metabolite	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_137_8_1163_s_205	12466225	15-deoxy-delta12,14-PGJ2 is another PGD2 metabolite which preferentially binds CRTH2 over DP with 89 fold selectivity.	bind
19173	2	6704	6	NULL	NULL	0	NULL	15-deoxy-delta12,14-PGJ2	NULL		bind	NULL	preferentially			CRTH2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_137_8_1163_s_205	12466225	15-deoxy-delta12,14-PGJ2 is another PGD2 metabolite which preferentially binds CRTH2 over DP with 89 fold selectivity.	bind
19174	3	6704	6	NULL	NULL	0	NULL	15-deoxy-delta12,14-PGJ2	NULL		bind	NULL				DP	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_137_8_1163_s_205	12466225	15-deoxy-delta12,14-PGJ2 is another PGD2 metabolite which preferentially binds CRTH2 over DP with 89 fold selectivity.	bind
19175	4	6704	6	NULL	NULL	0	NULL	statement 2	NULL		is more preferential than	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_137_8_1163_s_205	12466225	15-deoxy-delta12,14-PGJ2 is another PGD2 metabolite which preferentially binds CRTH2 over DP with 89 fold selectivity.	bind
21861	1	6706	5	13	NULL	NULL	NULL	15/7	GP		enhances					cell adhesion	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_48_28740_s_289	7499396	15/7 Enhances Cell Adhesion by Stabilizing an Active  Conformation of beta  Integrin15/7  promoted THP-1 cell binding to beta   integrin ligands, even  though the cells did not express a significant level of the 15/7  epitope ( Fig. 5).	bind
21862	2	6706	5	13	NULL	NULL	NULL	15/7	GP		stabilizes					beta Integrin	GP	active conformation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_48_28740_s_289	7499396	15/7 Enhances Cell Adhesion by Stabilizing an Active  Conformation of beta  Integrin15/7  promoted THP-1 cell binding to beta   integrin ligands, even  though the cells did not express a significant level of the 15/7  epitope ( Fig. 5).	bind
21863	3	6706	5	13	NULL	NULL	NULL	statement 2	Process		leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_48_28740_s_289	7499396	15/7 Enhances Cell Adhesion by Stabilizing an Active  Conformation of beta  Integrin15/7  promoted THP-1 cell binding to beta   integrin ligands, even  though the cells did not express a significant level of the 15/7  epitope ( Fig. 5).	bind
21864	4	6706	5	13	NULL	NULL	NULL	THP-1 cell	Cell		bind					beta integrin ligands	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_48_28740_s_289	7499396	15/7 Enhances Cell Adhesion by Stabilizing an Active  Conformation of beta  Integrin15/7  promoted THP-1 cell binding to beta   integrin ligands, even  though the cells did not express a significant level of the 15/7  epitope ( Fig. 5).	bind
21865	5	6706	5	13	NULL	NULL	NULL	15/7	GP		promote					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_48_28740_s_289	7499396	15/7 Enhances Cell Adhesion by Stabilizing an Active  Conformation of beta  Integrin15/7  promoted THP-1 cell binding to beta   integrin ligands, even  though the cells did not express a significant level of the 15/7  epitope ( Fig. 5).	bind
56462	6	6706	5	13	NULL	NULL	NULL	THP-1 cell 	Cell		does not express					15/7 epitope	GP	significant level of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_48_28740_s_289	7499396	15/7 Enhances Cell Adhesion by Stabilizing an Active  Conformation of beta  Integrin15/7  promoted THP-1 cell binding to beta   integrin ligands, even  though the cells did not express a significant level of the 15/7  epitope ( Fig. 5).	bind
19446	1	6706	6	NULL	NULL	0	NULL	THP-1 cell	NULL		bind	NULL				beta integrin ligands	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_48_28740_s_289	7499396	15/7 Enhances Cell Adhesion by Stabilizing an Active  Conformation of beta  Integrin15/7  promoted THP-1 cell binding to beta   integrin ligands, even  though the cells did not express a significant level of the 15/7  epitope ( Fig. 5).	bind
19447	2	6706	6	10	NULL	0	NULL	15/7			promotes					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_48_28740_s_289	7499396	15/7 Enhances Cell Adhesion by Stabilizing an Active  Conformation of beta  Integrin15/7  promoted THP-1 cell binding to beta   integrin ligands, even  though the cells did not express a significant level of the 15/7  epitope ( Fig. 5).	bind
19448	3	6706	6	10	NULL	0	NULL	THP-1 cells			does not express					15/7 epitope		significant level of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_48_28740_s_289	7499396	15/7 Enhances Cell Adhesion by Stabilizing an Active  Conformation of beta  Integrin15/7  promoted THP-1 cell binding to beta   integrin ligands, even  though the cells did not express a significant level of the 15/7  epitope ( Fig. 5).	bind
56459	4	6706	6	10	NULL	0	NULL	15/7			enhance					cell adhesion					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_48_28740_s_289	7499396	15/7 Enhances Cell Adhesion by Stabilizing an Active  Conformation of beta  Integrin15/7  promoted THP-1 cell binding to beta   integrin ligands, even  though the cells did not express a significant level of the 15/7  epitope ( Fig. 5).	bind
56460	5	6706	6	10	NULL	0	NULL	15/7			stabilize					beta Integrin		active conformation of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_48_28740_s_289	7499396	15/7 Enhances Cell Adhesion by Stabilizing an Active  Conformation of beta  Integrin15/7  promoted THP-1 cell binding to beta   integrin ligands, even  though the cells did not express a significant level of the 15/7  epitope ( Fig. 5).	bind
56461	6	6706	6	10	NULL	0	NULL	statement 1			occur by					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_48_28740_s_289	7499396	15/7 Enhances Cell Adhesion by Stabilizing an Active  Conformation of beta  Integrin15/7  promoted THP-1 cell binding to beta   integrin ligands, even  though the cells did not express a significant level of the 15/7  epitope ( Fig. 5).	bind
21866	1	6708	5	13	NULL	NULL	NULL	H4	GP	acetylation	occurs at					 eotaxin	GP			promoter	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
21867	2	6708	5	13	NULL	NULL	NULL	TNFalpha	GP		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
21868	3	6708	5	13	NULL	NULL	NULL	15d-PGJ(2)	Chemical		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
21869	4	6708	5	13	NULL	NULL	NULL	fluticasone	Chemical		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
21870	5	6708	5	13	NULL	NULL	NULL	salmeterol	Chemical		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
21871	6	6708	5	13	NULL	NULL	NULL	NF-kappaB p65	GP		bind					eotaxin	GP			promoter	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
21872	7	6708	5	13	NULL	NULL	NULL	15d-PGJ(2)	Chemical		inhibit					statement 6	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
21873	8	6708	5	13	NULL	NULL	NULL	fluticasone	Chemical		inhibit					statement 6	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
21874	9	6708	5	13	NULL	NULL	NULL	salmeterol	Chemical		inhibit					statement 6	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
21875	10	6708	5	13	NULL	NULL	NULL	PPARgamma	GP		associates with					eotaxin	GP			promoter	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
21876	11	6708	5	13	NULL	NULL	NULL	15d-PGJ(2)	Chemical		induces					statement 10	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
21877	12	6708	5	13	NULL	NULL	NULL	fluticasone	Chemical		induces					statement 10	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
21878	13	6708	5	13	NULL	NULL	NULL	salmeterol	Chemical		induces					statement 10	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
21879	14	6708	5	13	NULL	NULL	NULL	GR	GP		associates with					eotaxin	GP			promoter	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
21880	15	6708	5	13	NULL	NULL	NULL	15d-PGJ(2)	Chemical		induces					statement 14	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
21881	16	6708	5	13	NULL	NULL	NULL	fluticasone	Chemical		induces					statement 14	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
21882	17	6708	5	13	NULL	NULL	NULL	salmeterol	Chemical		induces					statement 14	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
19449	1	6708	6	NULL	NULL	0	NULL	NF-kappaB p65	NULL		bind	NULL				eotaxin	NULL			promoter	NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
19450	2	6708	6	NULL	NULL	0	NULL	histone H4	NULL		acetylated at	NULL				eotaxin	NULL			promoter	NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
19451	3	6708	6	NULL	NULL	0	NULL	TNF-alpha	NULL		induces	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
19452	4	6708	6	NULL	NULL	0	NULL	PPARgamma	NULL		associates with	NULL				eotaxin 	NULL			promoter	NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
19453	5	6708	6	NULL	NULL	0	NULL	GR	NULL		associates with	NULL				eotaxin	NULL			promoter	NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
19454	6	6708	6	NULL	NULL	0	NULL	15d-PGJ(2)	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
19455	7	6708	6	NULL	NULL	0	NULL	15d-PGJ(2)	NULL		inhibits	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
19456	8	6708	6	NULL	NULL	0	NULL	15d-PGJ(2)	NULL		induces	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
19457	9	6708	6	NULL	NULL	0	NULL	15d-PGJ(2)	NULL		induces	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
19458	10	6708	6	NULL	NULL	0	NULL	fluticasone	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
19459	11	6708	6	NULL	NULL	0	NULL	fluticasone	NULL		inhibits	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
19460	12	6708	6	NULL	NULL	0	NULL	fluticasone	NULL		induces	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
19461	13	6708	6	NULL	NULL	0	NULL	fluticasone	NULL		induces	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
19462	14	6708	6	NULL	NULL	0	NULL	salmeterol	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
19463	15	6708	6	NULL	NULL	0	NULL	salmeterol	NULL		inhibits	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
19464	16	6708	6	NULL	NULL	0	NULL	salmeterol	NULL		induces	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
19465	17	6708	6	NULL	NULL	0	NULL	salmeterol	NULL		induces	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_280_4_15531761_s_8	15531761	15d-PGJ(2), fluticasone, and  salmeterol all inhibited TNFalpha-induced histone H4 acetylation at the  eotaxin promoter and NF-kappaB p65 binding to the eotaxin promoter and  induced PPARgamma and GR association with the eotaxin promoter, as analyzed  by chromatin immunoprecipitation assay.	bind
21844	1	6709	5	13	NULL	NULL	NULL	p300	GP		bind					PPARgamma	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_9_3057_s_204	11287611	15d-PGJ2 enhanced binding of p300 to PPARgamma and reduced binding to c-Fos.	bind
21845	2	6709	5	13	NULL	NULL	NULL	15d-PGJ2	Chemical		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_9_3057_s_204	11287611	15d-PGJ2 enhanced binding of p300 to PPARgamma and reduced binding to c-Fos.	bind
21846	3	6709	5	13	NULL	NULL	NULL	p300	GP		bind					c-Fos	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_9_3057_s_204	11287611	15d-PGJ2 enhanced binding of p300 to PPARgamma and reduced binding to c-Fos.	bind
21847	4	6709	5	13	NULL	NULL	NULL	15d-PGJ2	Chemical		reduces					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_9_3057_s_204	11287611	15d-PGJ2 enhanced binding of p300 to PPARgamma and reduced binding to c-Fos.	bind
19177	1	6709	6	NULL	NULL	0	NULL	p300	NULL		bind	NULL				PPARgamma	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_9_3057_s_204	11287611	15d-PGJ2 enhanced binding of p300 to PPARgamma and reduced binding to c-Fos.	bind
19178	2	6709	6	NULL	NULL	0	NULL	p300	NULL		bind	NULL				c-Fos	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_9_3057_s_204	11287611	15d-PGJ2 enhanced binding of p300 to PPARgamma and reduced binding to c-Fos.	bind
19179	3	6709	6	NULL	NULL	0	NULL	15d-PGJ2	NULL		enhanced	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_9_3057_s_204	11287611	15d-PGJ2 enhanced binding of p300 to PPARgamma and reduced binding to c-Fos.	bind
19180	4	6709	6	NULL	NULL	0	NULL	15d-PGJ2	NULL		reduced	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_9_3057_s_204	11287611	15d-PGJ2 enhanced binding of p300 to PPARgamma and reduced binding to c-Fos.	bind
22116	1	6711	5	13	NULL	NULL	NULL	Tbeta4	GP		bind			Leu		G-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_22_23637_s_198	15039431	15N HSQC spectra of [15]AA Tbeta4 (where AA is Leu, Thr, or Lys) bound to G-actin are shown in  Fig. 3 B. Resonances obtained for the selectively labeled Tbeta4 perfectly superimposed those obtained for the uniformly labeled protein.	bind
22117	2	6711	5	13	NULL	NULL	NULL	Tbeta4	GP		bind			Thr		G-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_22_23637_s_198	15039431	15N HSQC spectra of [15]AA Tbeta4 (where AA is Leu, Thr, or Lys) bound to G-actin are shown in  Fig. 3 B. Resonances obtained for the selectively labeled Tbeta4 perfectly superimposed those obtained for the uniformly labeled protein.	bind
22118	3	6711	5	13	NULL	NULL	NULL	Tbeta4	GP		bind			Lys		G-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_22_23637_s_198	15039431	15N HSQC spectra of [15]AA Tbeta4 (where AA is Leu, Thr, or Lys) bound to G-actin are shown in  Fig. 3 B. Resonances obtained for the selectively labeled Tbeta4 perfectly superimposed those obtained for the uniformly labeled protein.	bind
19181	1	6711	6	NULL	NULL	0	NULL	Tbeta4	NULL		bind	NULL		Leu		G-actin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_22_23637_s_198	15039431	15N HSQC spectra of [15]AA Tbeta4 (where AA is Leu, Thr, or Lys) bound to G-actin are shown in  Fig. 3 B. Resonances obtained for the selectively labeled Tbeta4 perfectly superimposed those obtained for the uniformly labeled protein.	bind
19182	2	6711	6	NULL	NULL	0	NULL	Tbeta4	NULL		bind	NULL		Thr		G-actin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_22_23637_s_198	15039431	15N HSQC spectra of [15]AA Tbeta4 (where AA is Leu, Thr, or Lys) bound to G-actin are shown in  Fig. 3 B. Resonances obtained for the selectively labeled Tbeta4 perfectly superimposed those obtained for the uniformly labeled protein.	bind
19183	3	6711	6	NULL	NULL	0	NULL	Tbeta4	NULL		bind	NULL		Lys		G-actin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_22_23637_s_198	15039431	15N HSQC spectra of [15]AA Tbeta4 (where AA is Leu, Thr, or Lys) bound to G-actin are shown in  Fig. 3 B. Resonances obtained for the selectively labeled Tbeta4 perfectly superimposed those obtained for the uniformly labeled protein.	bind
22119	1	6712	5	13	NULL	NULL	NULL	cTnC	GP	Ca2+ saturated	bind					cTnI	GP		1-80		NULL		NULL	NULL	NULL	NULL	gw60_febslett_469_2_168_s_142	10713265	15{1} heteronuclear NOE values for Ca2+ saturated [15N, 2]cTnC bound to cTnI(1-80)	bind
19184	1	6712	6	10	NULL	0	NULL	cTnC	NULL	Ca2+ saturated	bind	NULL				cTnI	NULL		1-80		NULL		NULL	NULL	NULL	NULL	gw60_febslett_469_2_168_s_142	10713265	15{1} heteronuclear NOE values for Ca2+ saturated [15N, 2]cTnC bound to cTnI(1-80)	bind
22120	1	6714	5	13	NULL	NULL	NULL	CBF1	GP		belongs to					helix - loophelix protein family	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1054_s_247	11222754	16       Cai,M. and Davis,R.W. (1990) Yeast centromere binding protein CBF1, of the  - helix - loophelix protein family, is required for chromosome stability and methionine prototrophy.	bind
22121	2	6714	5	13	NULL	NULL	NULL	CBF1	GP		is					Yeast centromere binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1054_s_247	11222754	16       Cai,M. and Davis,R.W. (1990) Yeast centromere binding protein CBF1, of the  - helix - loophelix protein family, is required for chromosome stability and methionine prototrophy.	bind
22122	3	6714	5	13	NULL	NULL	NULL	CBF1	GP		is required for					chromosome	Chromosome	stability of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1054_s_247	11222754	16       Cai,M. and Davis,R.W. (1990) Yeast centromere binding protein CBF1, of the  - helix - loophelix protein family, is required for chromosome stability and methionine prototrophy.	bind
22123	4	6714	5	13	NULL	NULL	NULL	CBF1	GP		is required for					methionine prototrophy	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1054_s_247	11222754	16       Cai,M. and Davis,R.W. (1990) Yeast centromere binding protein CBF1, of the  - helix - loophelix protein family, is required for chromosome stability and methionine prototrophy.	bind
19185	1	6714	6	NULL	NULL	0	NULL	CBF1	NULL		is	NULL				centromere binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1054_s_247	11222754	16       Cai,M. and Davis,R.W. (1990) Yeast centromere binding protein CBF1, of the  - helix - loophelix protein family, is required for chromosome stability and methionine prototrophy.	bind
19186	2	6714	6	NULL	NULL	0	NULL	CBF1	NULL	yeast	is a member of	NULL				helix - loophelix protein family	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1054_s_247	11222754	16       Cai,M. and Davis,R.W. (1990) Yeast centromere binding protein CBF1, of the  - helix - loophelix protein family, is required for chromosome stability and methionine prototrophy.	bind
19187	3	6714	6	10	NULL	0	NULL	CBF1		yeast	is required for					chromosome 		stability of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1054_s_247	11222754	16       Cai,M. and Davis,R.W. (1990) Yeast centromere binding protein CBF1, of the  - helix - loophelix protein family, is required for chromosome stability and methionine prototrophy.	bind
19188	4	6714	6	NULL	NULL	0	NULL	CBF1	NULL	yeast	is required for	NULL				methionine prototrophy	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1054_s_247	11222754	16       Cai,M. and Davis,R.W. (1990) Yeast centromere binding protein CBF1, of the  - helix - loophelix protein family, is required for chromosome stability and methionine prototrophy.	bind
22124	1	6715	5	13	NULL	NULL	NULL	HAP1	GP		bind		dramatically;;assymetrically			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_10_2181_s_237	11353088	16       King,D.A., Zhang,L., Guarente,L. and Marmorstein,R. (1999) Structure of a HAP1 - DNA complex reveals dramatically asymmetric DNA binding by a homodimeric protein.	bind
56497	2	6715	5	13	NULL	NULL	NULL	HAP1	GP		is a type of					homodimeric protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_10_2181_s_237	11353088	16       King,D.A., Zhang,L., Guarente,L. and Marmorstein,R. (1999) Structure of a HAP1 - DNA complex reveals dramatically asymmetric DNA binding by a homodimeric protein.	bind
19189	1	6715	6	10	NULL	0	NULL	HAP1			bind		dramatically;;assymetrically			DNA					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_10_2181_s_237	11353088	16       King,D.A., Zhang,L., Guarente,L. and Marmorstein,R. (1999) Structure of a HAP1 - DNA complex reveals dramatically asymmetric DNA binding by a homodimeric protein.	bind
56498	2	6715	6	10	NULL	0	NULL	HAP1			is a type of					homodimeric protein					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_10_2181_s_237	11353088	16       King,D.A., Zhang,L., Guarente,L. and Marmorstein,R. (1999) Structure of a HAP1 - DNA complex reveals dramatically asymmetric DNA binding by a homodimeric protein.	bind
22125	1	6716	5	13	NULL	NULL	NULL	RPA	GP		is					Replication Protein A	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_23_4634_s_289	11095672	16       Patrick,S.M. and Turchi,J.J. (1999) Replication Protein A (RPA) Binding to Duplex Cisplatin-Damaged DNA Is Mediated Through the Generation of Single-Stranded DNA.  J. Biol.	bind
22126	2	6716	5	13	NULL	NULL	NULL	RPA	GP		bind					duplex DNA	NucleicAcid	cisplatin-damaged			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_23_4634_s_289	11095672	16       Patrick,S.M. and Turchi,J.J. (1999) Replication Protein A (RPA) Binding to Duplex Cisplatin-Damaged DNA Is Mediated Through the Generation of Single-Stranded DNA.  J. Biol.	bind
22127	3	6716	5	13	NULL	NULL	NULL	single-stranded DNA	NucleicAcid	generation of	mediate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_23_4634_s_289	11095672	16       Patrick,S.M. and Turchi,J.J. (1999) Replication Protein A (RPA) Binding to Duplex Cisplatin-Damaged DNA Is Mediated Through the Generation of Single-Stranded DNA.  J. Biol.	bind
19190	1	6716	6	NULL	NULL	0	NULL	Replication Protein A	NULL		is	NULL				RPA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_23_4634_s_289	11095672	16       Patrick,S.M. and Turchi,J.J. (1999) Replication Protein A (RPA) Binding to Duplex Cisplatin-Damaged DNA Is Mediated Through the Generation of Single-Stranded DNA.  J. Biol.	bind
19192	2	6716	6	NULL	NULL	0	NULL	RPA	NULL		bind	NULL				duplex DNA	NULL	Cisplatin-Damaged			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_23_4634_s_289	11095672	16       Patrick,S.M. and Turchi,J.J. (1999) Replication Protein A (RPA) Binding to Duplex Cisplatin-Damaged DNA Is Mediated Through the Generation of Single-Stranded DNA.  J. Biol.	bind
19193	3	6716	6	NULL	NULL	0	NULL	statement 2	NULL		is mediated through	NULL				single-stranded DNA	NULL	generation of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_23_4634_s_289	11095672	16       Patrick,S.M. and Turchi,J.J. (1999) Replication Protein A (RPA) Binding to Duplex Cisplatin-Damaged DNA Is Mediated Through the Generation of Single-Stranded DNA.  J. Biol.	bind
22128	1	6717	5	13	NULL	NULL	NULL	U1A	GP		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3841_s_262	11557816	16       Rimmele,M.E. and Belasco,J.G. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
22129	2	6717	5	13	NULL	NULL	NULL	U2B	GP		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3841_s_262	11557816	16       Rimmele,M.E. and Belasco,J.G. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
44678	3	6717	5	13	NULL	NULL	NULL	U1A	GP		is a type of					spliceosomal protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3841_s_262	11557816	16       Rimmele,M.E. and Belasco,J.G. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
44679	4	6717	5	13	NULL	NULL	NULL	U2B	GP		is a type of					spliceosomal protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3841_s_262	11557816	16       Rimmele,M.E. and Belasco,J.G. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
56501	5	6717	5	13	NULL	NULL	NULL	U2A	GP		is a type of					ancillary protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3841_s_262	11557816	16       Rimmele,M.E. and Belasco,J.G. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
19194	1	6717	6	10	NULL	0	NULL	U1A			is a type of					spliceosomal protein					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3841_s_262	11557816	16       Rimmele,M.E. and Belasco,J.G. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
19195	2	6717	6	10	NULL	0	NULL	U2B			is a type of					spliceosomal protein					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3841_s_262	11557816	16       Rimmele,M.E. and Belasco,J.G. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
19199	3	6717	6	10	NULL	0	NULL	U2A			is a type of					ancillary protein					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3841_s_262	11557816	16       Rimmele,M.E. and Belasco,J.G. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
44680	4	6717	6	10	NULL	0	NULL	U1A	NULL		bind	NULL				RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3841_s_262	11557816	16       Rimmele,M.E. and Belasco,J.G. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
44682	5	6717	6	10	NULL	0	NULL	U2B	NULL		bind	NULL				RNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3841_s_262	11557816	16       Rimmele,M.E. and Belasco,J.G. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
22130	1	6718	5	13	NULL	NULL	NULL	DNA	NucleicAcid		bind		noncovalently			bis(1,10-phenanthroline)copper	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4856_s_288	11121476	16       Veal,J.M., Merchant,K. and Rill,R.L. (1991) Noncovalent DNA binding of bis(1,10-phenanthroline)copper	bind
19201	1	6718	6	10	NULL	0	NULL	bis(1,10-phenanthroline)copper			bind		noncovalently			DNA					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4856_s_288	11121476	16       Veal,J.M., Merchant,K. and Rill,R.L. (1991) Noncovalent DNA binding of bis(1,10-phenanthroline)copper	bind
22131	1	6719	5	13	NULL	NULL	NULL	Lp(a)	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_129_s_25	8548413	16  17  Because it is an apoB-100 - containing particle, Lp(a) binds to the LDL receptor.	bind
44683	2	6719	5	13	NULL	NULL	NULL	Lp(a)	GP		contains					apoB-100	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_129_s_25	8548413	16  17  Because it is an apoB-100 - containing particle, Lp(a) binds to the LDL receptor.	bind
19202	1	6719	6	NULL	NULL	0	NULL	Lp(a)	NULL		bind	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_129_s_25	8548413	16  17  Because it is an apoB-100 - containing particle, Lp(a) binds to the LDL receptor.	bind
56503	2	6719	6	10	NULL	0	NULL	Lp(a)			contains					apoB-100					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_129_s_25	8548413	16  17  Because it is an apoB-100 - containing particle, Lp(a) binds to the LDL receptor.	bind
22132	1	6720	5	13	NULL	NULL	NULL	GP IIb/IIIa antagonists	Chemical	most	bind					GP IIb/IIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_4_437_s_33	10421606	16  Because most GP IIb/IIIa antagonists bind to GP IIb/IIa, irrespective of its state of activation, these antagonists inhibit the GP IIb/IIa receptor functions on unstimulated platelets.	bind
22133	2	6720	5	13	NULL	NULL	NULL	GP IIb/IIIa antagonists	Chemical		inhibit					GP IIb/IIa receptor	GP	function of			NULL	on unstimulated platelets	NULL	NULL	NULL	NULL	gw60_circulation_100_4_437_s_33	10421606	16  Because most GP IIb/IIIa antagonists bind to GP IIb/IIa, irrespective of its state of activation, these antagonists inhibit the GP IIb/IIa receptor functions on unstimulated platelets.	bind
56505	3	6720	5	13	NULL	NULL	NULL	statement 1	Process		occurs irrespective of					activation state	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_4_437_s_33	10421606	16  Because most GP IIb/IIIa antagonists bind to GP IIb/IIa, irrespective of its state of activation, these antagonists inhibit the GP IIb/IIa receptor functions on unstimulated platelets.	bind
19203	1	6720	6	NULL	NULL	0	NULL	GP IIb/IIIa antagonists	NULL		bind	NULL				GP IIb/IIa	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_4_437_s_33	10421606	16  Because most GP IIb/IIIa antagonists bind to GP IIb/IIa, irrespective of its state of activation, these antagonists inhibit the GP IIb/IIa receptor functions on unstimulated platelets.	bind
19204	2	6720	6	10	NULL	0	NULL	statement 1			occurs irrespective of					 activation state					NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_4_437_s_33	10421606	16  Because most GP IIb/IIIa antagonists bind to GP IIb/IIa, irrespective of its state of activation, these antagonists inhibit the GP IIb/IIa receptor functions on unstimulated platelets.	bind
19206	3	6720	6	10	NULL	0	NULL	GP IIb/IIIa antagonists			inhibit					GP IIb/IIa receptor		function of			NULL	unstimulated platelets	NULL	NULL	NULL	NULL	gw60_circulation_100_4_437_s_33	10421606	16  Because most GP IIb/IIIa antagonists bind to GP IIb/IIa, irrespective of its state of activation, these antagonists inhibit the GP IIb/IIa receptor functions on unstimulated platelets.	bind
22134	1	6721	5	13	NULL	NULL	NULL	GATA-3	GP		is a type of					GATA family of transcription factors	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_6_1945_s_140	12057898	16  GATA-3 belongs to the GATA family of transcription factors, which bind to the consensus sequence (A/T)GATA(A/G) and to the related motifs CGATGG and (T/A)GAT(T/A)(A/G).	bind
22135	2	6721	5	13	NULL	NULL	NULL	GATA-3	GP		bind							consensus sequence		(A/T)GATA(A/G)	NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_6_1945_s_140	12057898	16  GATA-3 belongs to the GATA family of transcription factors, which bind to the consensus sequence (A/T)GATA(A/G) and to the related motifs CGATGG and (T/A)GAT(T/A)(A/G).	bind
22136	3	6721	5	13	NULL	NULL	NULL	GATA-3	GP		bind									CGATGG	NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_6_1945_s_140	12057898	16  GATA-3 belongs to the GATA family of transcription factors, which bind to the consensus sequence (A/T)GATA(A/G) and to the related motifs CGATGG and (T/A)GAT(T/A)(A/G).	bind
22137	4	6721	5	13	NULL	NULL	NULL	GATA-3	GP		bind									(T/A)GAT(T/A)(A/G)	NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_6_1945_s_140	12057898	16  GATA-3 belongs to the GATA family of transcription factors, which bind to the consensus sequence (A/T)GATA(A/G) and to the related motifs CGATGG and (T/A)GAT(T/A)(A/G).	bind
19208	1	6721	6	10	NULL	0	NULL	GATA-3	NULL		is a type of	NULL				GATA family of transcription factors	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_6_1945_s_140	12057898	16  GATA-3 belongs to the GATA family of transcription factors, which bind to the consensus sequence (A/T)GATA(A/G) and to the related motifs CGATGG and (T/A)GAT(T/A)(A/G).	bind
19209	2	6721	6	10	NULL	0	NULL	GATA-3			bind							consensus sequence		(A/T)GATA(A/G)	NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_6_1945_s_140	12057898	16  GATA-3 belongs to the GATA family of transcription factors, which bind to the consensus sequence (A/T)GATA(A/G) and to the related motifs CGATGG and (T/A)GAT(T/A)(A/G).	bind
19211	3	6721	6	NULL	NULL	0	NULL	GATA-3	NULL		bind	NULL					NULL			CGATGG	NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_6_1945_s_140	12057898	16  GATA-3 belongs to the GATA family of transcription factors, which bind to the consensus sequence (A/T)GATA(A/G) and to the related motifs CGATGG and (T/A)GAT(T/A)(A/G).	bind
19212	4	6721	6	NULL	NULL	0	NULL	GATA-3	NULL		bind	NULL					NULL			(T/A)GAT(T/A)(A/G)	NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_6_1945_s_140	12057898	16  GATA-3 belongs to the GATA family of transcription factors, which bind to the consensus sequence (A/T)GATA(A/G) and to the related motifs CGATGG and (T/A)GAT(T/A)(A/G).	bind
22138	1	6722	5	13	NULL	NULL	NULL	PAI-1	GP		inhibit					cell migration	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_4_597_s_163	11157728	16  In addition, PAI-1 can inhibit cell migration by interfering with the binding of uPA receptor to vitronectin, independent of its function as a PAI. 39  These data suggest that alterations in the expression of PA system components may modulate intimal thickening via plasmin-dependent and plasmin-independent mechanisms.	bind
22139	2	6722	5	13	NULL	NULL	NULL	uPA receptor	GP		bind					vitronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_4_597_s_163	11157728	16  In addition, PAI-1 can inhibit cell migration by interfering with the binding of uPA receptor to vitronectin, independent of its function as a PAI. 39  These data suggest that alterations in the expression of PA system components may modulate intimal thickening via plasmin-dependent and plasmin-independent mechanisms.	bind
22140	3	6722	5	13	NULL	NULL	NULL	PAI-1	GP		interferes with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_4_597_s_163	11157728	16  In addition, PAI-1 can inhibit cell migration by interfering with the binding of uPA receptor to vitronectin, independent of its function as a PAI. 39  These data suggest that alterations in the expression of PA system components may modulate intimal thickening via plasmin-dependent and plasmin-independent mechanisms.	bind
22141	4	6722	5	13	NULL	NULL	NULL	statement 3	Process		leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_4_597_s_163	11157728	16  In addition, PAI-1 can inhibit cell migration by interfering with the binding of uPA receptor to vitronectin, independent of its function as a PAI. 39  These data suggest that alterations in the expression of PA system components may modulate intimal thickening via plasmin-dependent and plasmin-independent mechanisms.	bind
22142	5	6722	5	13	NULL	NULL	NULL	statement 4	Process		is independent of					PAI	GP	function of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_4_597_s_163	11157728	16  In addition, PAI-1 can inhibit cell migration by interfering with the binding of uPA receptor to vitronectin, independent of its function as a PAI. 39  These data suggest that alterations in the expression of PA system components may modulate intimal thickening via plasmin-dependent and plasmin-independent mechanisms.	bind
22143	6	6722	5	13	NULL	NULL	NULL	PA system components	GP	alterations in the expression of	modulates					intimal thickening	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_4_597_s_163	11157728	16  In addition, PAI-1 can inhibit cell migration by interfering with the binding of uPA receptor to vitronectin, independent of its function as a PAI. 39  These data suggest that alterations in the expression of PA system components may modulate intimal thickening via plasmin-dependent and plasmin-independent mechanisms.	bind
22144	7	6722	5	13	NULL	NULL	NULL	statement 6	Process		via					plasmin-dependent mechanism	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_4_597_s_163	11157728	16  In addition, PAI-1 can inhibit cell migration by interfering with the binding of uPA receptor to vitronectin, independent of its function as a PAI. 39  These data suggest that alterations in the expression of PA system components may modulate intimal thickening via plasmin-dependent and plasmin-independent mechanisms.	bind
22145	8	6722	5	13	NULL	NULL	NULL	statement 6	Process		via					plasmin-independent mechanism	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_4_597_s_163	11157728	16  In addition, PAI-1 can inhibit cell migration by interfering with the binding of uPA receptor to vitronectin, independent of its function as a PAI. 39  These data suggest that alterations in the expression of PA system components may modulate intimal thickening via plasmin-dependent and plasmin-independent mechanisms.	bind
19213	1	6722	6	NULL	NULL	0	NULL	uPA receptor	NULL		bind	NULL				vitronectin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_4_597_s_163	11157728	16  In addition, PAI-1 can inhibit cell migration by interfering with the binding of uPA receptor to vitronectin, independent of its function as a PAI. 39  These data suggest that alterations in the expression of PA system components may modulate intimal thickening via plasmin-dependent and plasmin-independent mechanisms.	bind
19214	2	6722	6	NULL	NULL	0	NULL	PAI-1	NULL		inhibit	NULL				cell migration	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_4_597_s_163	11157728	16  In addition, PAI-1 can inhibit cell migration by interfering with the binding of uPA receptor to vitronectin, independent of its function as a PAI. 39  These data suggest that alterations in the expression of PA system components may modulate intimal thickening via plasmin-dependent and plasmin-independent mechanisms.	bind
19235	3	6722	6	NULL	NULL	0	NULL	statement 2	NULL		occurs via	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_4_597_s_163	11157728	16  In addition, PAI-1 can inhibit cell migration by interfering with the binding of uPA receptor to vitronectin, independent of its function as a PAI. 39  These data suggest that alterations in the expression of PA system components may modulate intimal thickening via plasmin-dependent and plasmin-independent mechanisms.	bind
19236	4	6722	6	NULL	NULL	0	NULL	PA system components	NULL	alterations in	modulate	NULL	may			intimal thickening	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_4_597_s_163	11157728	16  In addition, PAI-1 can inhibit cell migration by interfering with the binding of uPA receptor to vitronectin, independent of its function as a PAI. 39  These data suggest that alterations in the expression of PA system components may modulate intimal thickening via plasmin-dependent and plasmin-independent mechanisms.	bind
56519	5	6722	6	10	NULL	0	NULL	statement 3			is independent of					PAI		function of			NULL		0	NULL	NULL	NULL	gw60_circulation_103_4_597_s_163	11157728	16  In addition, PAI-1 can inhibit cell migration by interfering with the binding of uPA receptor to vitronectin, independent of its function as a PAI. 39  These data suggest that alterations in the expression of PA system components may modulate intimal thickening via plasmin-dependent and plasmin-independent mechanisms.	bind
56520	6	6722	6	10	NULL	0	NULL	statement 4			via					plasmin-dependent mechanism					NULL		0	NULL	NULL	NULL	gw60_circulation_103_4_597_s_163	11157728	16  In addition, PAI-1 can inhibit cell migration by interfering with the binding of uPA receptor to vitronectin, independent of its function as a PAI. 39  These data suggest that alterations in the expression of PA system components may modulate intimal thickening via plasmin-dependent and plasmin-independent mechanisms.	bind
56521	7	6722	6	10	NULL	0	NULL	statement 4			via					plasmin-independent mechanism					NULL		0	NULL	NULL	NULL	gw60_circulation_103_4_597_s_163	11157728	16  In addition, PAI-1 can inhibit cell migration by interfering with the binding of uPA receptor to vitronectin, independent of its function as a PAI. 39  These data suggest that alterations in the expression of PA system components may modulate intimal thickening via plasmin-dependent and plasmin-independent mechanisms.	bind
22146	1	6723	5	13	NULL	NULL	NULL	LPS	Chemical		bind					CD14	GP	soluble			NULL	 in serum	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_465_s_28	9102164	16  Recent evidence suggests that such activation occurs via LPS binding to soluble CD14 present in serum, with the resulting complex then binding to a cellular receptor.	bind
22147	2	6723	5	13	NULL	NULL	NULL	statement 1	Process		bind					cellular receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_465_s_28	9102164	16  Recent evidence suggests that such activation occurs via LPS binding to soluble CD14 present in serum, with the resulting complex then binding to a cellular receptor.	bind
22148	3	6723	5	13	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_465_s_28	9102164	16  Recent evidence suggests that such activation occurs via LPS binding to soluble CD14 present in serum, with the resulting complex then binding to a cellular receptor.	bind
19237	1	6723	6	10	NULL	0	NULL	LPS			bind					CD14		soluble			NULL	serum	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_465_s_28	9102164	16  Recent evidence suggests that such activation occurs via LPS binding to soluble CD14 present in serum, with the resulting complex then binding to a cellular receptor.	bind
56522	2	6723	6	10	NULL	0	NULL	statement 1			bind					cellular receptor					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_465_s_28	9102164	16  Recent evidence suggests that such activation occurs via LPS binding to soluble CD14 present in serum, with the resulting complex then binding to a cellular receptor.	bind
56523	3	6723	6	10	NULL	0	NULL	statement 1			leads to					statement 2					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_465_s_28	9102164	16  Recent evidence suggests that such activation occurs via LPS binding to soluble CD14 present in serum, with the resulting complex then binding to a cellular receptor.	bind
22149	1	6724	5	13	NULL	NULL	NULL	HL-60 cells	Cell		bind					platelet monolayers	Cell	thrombin-activated;;mouse			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_11_1124_s_42	9831707	16  RMP-1 inhibits binding of HL-60 cells to thrombin-activated mouse platelet monolayers and recombinant murine P-selectin.	bind
22150	2	6724	5	13	NULL	NULL	NULL	RMP-1	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_11_1124_s_42	9831707	16  RMP-1 inhibits binding of HL-60 cells to thrombin-activated mouse platelet monolayers and recombinant murine P-selectin.	bind
22151	3	6724	5	13	NULL	NULL	NULL	HL-60 cells	Cell		bind					P-selectin	GP	recombinant;;murine			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_11_1124_s_42	9831707	16  RMP-1 inhibits binding of HL-60 cells to thrombin-activated mouse platelet monolayers and recombinant murine P-selectin.	bind
22152	4	6724	5	13	NULL	NULL	NULL	RMP-1	GP		inhibit					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_11_1124_s_42	9831707	16  RMP-1 inhibits binding of HL-60 cells to thrombin-activated mouse platelet monolayers and recombinant murine P-selectin.	bind
19238	1	6724	6	10	NULL	0	NULL	HL-60 cells			bind					platelet monolayers		thrombin activated;;mouse			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_11_1124_s_42	9831707	16  RMP-1 inhibits binding of HL-60 cells to thrombin-activated mouse platelet monolayers and recombinant murine P-selectin.	bind
19239	2	6724	6	10	NULL	0	NULL	HL-60 cells			bind					P-selectin		recombinant;;murine			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_11_1124_s_42	9831707	16  RMP-1 inhibits binding of HL-60 cells to thrombin-activated mouse platelet monolayers and recombinant murine P-selectin.	bind
19240	3	6724	6	NULL	NULL	0	NULL	RMP-1	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_11_1124_s_42	9831707	16  RMP-1 inhibits binding of HL-60 cells to thrombin-activated mouse platelet monolayers and recombinant murine P-selectin.	bind
19241	4	6724	6	NULL	NULL	0	NULL	RMP-1	NULL		inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_11_1124_s_42	9831707	16  RMP-1 inhibits binding of HL-60 cells to thrombin-activated mouse platelet monolayers and recombinant murine P-selectin.	bind
22153	1	6725	5	13	NULL	NULL	NULL	TGF-betaR1	GP		is a type of					cell surface type I receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_109_s_22	11438459	16  TGF-beta1 signaling is transduced via cell surface type I and type II receptors (TGF-betaR1 and TGF-betaR2): TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 that activates intracellular signaling cascades.	bind
22154	2	6725	5	13	NULL	NULL	NULL	TGF-betaR2	GP		is a type of					cell surface type II receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_109_s_22	11438459	16  TGF-beta1 signaling is transduced via cell surface type I and type II receptors (TGF-betaR1 and TGF-betaR2): TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 that activates intracellular signaling cascades.	bind
22155	3	6725	5	13	NULL	NULL	NULL	TGF-beta1	Process	signalling	is transduced via					TGF-betaR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_109_s_22	11438459	16  TGF-beta1 signaling is transduced via cell surface type I and type II receptors (TGF-betaR1 and TGF-betaR2): TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 that activates intracellular signaling cascades.	bind
22156	4	6725	5	13	NULL	NULL	NULL	TGF-beta1	Process	signalling	is transduced via					TGF-betaR2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_109_s_22	11438459	16  TGF-beta1 signaling is transduced via cell surface type I and type II receptors (TGF-betaR1 and TGF-betaR2): TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 that activates intracellular signaling cascades.	bind
22157	5	6725	5	13	NULL	NULL	NULL	TGF-betaR2	GP		bind					ligand	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_109_s_22	11438459	16  TGF-beta1 signaling is transduced via cell surface type I and type II receptors (TGF-betaR1 and TGF-betaR2): TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 that activates intracellular signaling cascades.	bind
22158	6	6725	5	13	NULL	NULL	NULL	TGF-betaR2	GP		forms a complex with					TGF-betaR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_109_s_22	11438459	16  TGF-beta1 signaling is transduced via cell surface type I and type II receptors (TGF-betaR1 and TGF-betaR2): TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 that activates intracellular signaling cascades.	bind
22159	7	6725	5	13	NULL	NULL	NULL	TGF-betaR1	GP		activates					intracellular signaling cascades	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_109_s_22	11438459	16  TGF-beta1 signaling is transduced via cell surface type I and type II receptors (TGF-betaR1 and TGF-betaR2): TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 that activates intracellular signaling cascades.	bind
19466	1	6725	6	10	NULL	0	NULL	TGF-betaR1			transduces					TGF-beta1 		signaling of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_109_s_22	11438459	16  TGF-beta1 signaling is transduced via cell surface type I and type II receptors (TGF-betaR1 and TGF-betaR2): TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 that activates intracellular signaling cascades.	bind
19467	2	6725	6	10	NULL	0	NULL	TGF-betaR2			transduces					TGF-beta1 		signaling of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_109_s_22	11438459	16  TGF-beta1 signaling is transduced via cell surface type I and type II receptors (TGF-betaR1 and TGF-betaR2): TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 that activates intracellular signaling cascades.	bind
19468	3	6725	6	NULL	NULL	0	NULL	TGF-betaR2	NULL		bind	NULL				ligand	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_1_109_s_22	11438459	16  TGF-beta1 signaling is transduced via cell surface type I and type II receptors (TGF-betaR1 and TGF-betaR2): TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 that activates intracellular signaling cascades.	bind
19469	4	6725	6	NULL	NULL	0	NULL	statement 3	NULL		forms a complex with	NULL				TGF-betaR1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_1_109_s_22	11438459	16  TGF-beta1 signaling is transduced via cell surface type I and type II receptors (TGF-betaR1 and TGF-betaR2): TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 that activates intracellular signaling cascades.	bind
19470	5	6725	6	NULL	NULL	0	NULL	statement 4	NULL		activates	NULL				intracellular signaling cascades	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_1_109_s_22	11438459	16  TGF-beta1 signaling is transduced via cell surface type I and type II receptors (TGF-betaR1 and TGF-betaR2): TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 that activates intracellular signaling cascades.	bind
56524	6	6725	6	10	NULL	0	NULL	TGF-betaR1			is a type of					cell surface type I receptor					NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_1_109_s_22	11438459	16  TGF-beta1 signaling is transduced via cell surface type I and type II receptors (TGF-betaR1 and TGF-betaR2): TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 that activates intracellular signaling cascades.	bind
56525	7	6725	6	10	NULL	0	NULL	TGF-betaR2			is a type of					cell surface type II receptor					NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_1_109_s_22	11438459	16  TGF-beta1 signaling is transduced via cell surface type I and type II receptors (TGF-betaR1 and TGF-betaR2): TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 that activates intracellular signaling cascades.	bind
22241	1	6726	5	13	NULL	NULL	NULL	heparin	Chemical		bind		non-specifically			plasma proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_1_118_s_33	8994426	16  These observations may explain why the anticoagulant response, as measured by anti-Xa levels, is more predictable for LMWH than for UFH. 14  We also demonstrated that the extent of nonspecific binding of heparin to plasma proteins is dependent on the molecular weight of the heparin chains, with the longer chains exhibiting the most nonspecific binding.	bind
22242	3	6726	5	13	NULL	NULL	NULL	statement 2	Process		is greater than					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_1_118_s_33	8994426	16  These observations may explain why the anticoagulant response, as measured by anti-Xa levels, is more predictable for LMWH than for UFH. 14  We also demonstrated that the extent of nonspecific binding of heparin to plasma proteins is dependent on the molecular weight of the heparin chains, with the longer chains exhibiting the most nonspecific binding.	bind
22243	2	6726	5	13	NULL	NULL	NULL	heparin	Chemical	longer chains of	bind		non-specifically			plasma proteins	GP	 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_1_118_s_33	8994426	16  These observations may explain why the anticoagulant response, as measured by anti-Xa levels, is more predictable for LMWH than for UFH. 14  We also demonstrated that the extent of nonspecific binding of heparin to plasma proteins is dependent on the molecular weight of the heparin chains, with the longer chains exhibiting the most nonspecific binding.	bind
58590	4	6726	5	13	NULL	NULL	NULL	statement 1	Process		depends on					heparin	Chemical	molecular weight of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_1_118_s_33	8994426	16  These observations may explain why the anticoagulant response, as measured by anti-Xa levels, is more predictable for LMWH than for UFH. 14  We also demonstrated that the extent of nonspecific binding of heparin to plasma proteins is dependent on the molecular weight of the heparin chains, with the longer chains exhibiting the most nonspecific binding.	bind
19242	1	6726	6	NULL	NULL	0	NULL	heparin	NULL		bind	NULL	non-specifically			plasma proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_95_1_118_s_33	8994426	16  These observations may explain why the anticoagulant response, as measured by anti-Xa levels, is more predictable for LMWH than for UFH. 14  We also demonstrated that the extent of nonspecific binding of heparin to plasma proteins is dependent on the molecular weight of the heparin chains, with the longer chains exhibiting the most nonspecific binding.	bind
19243	4	6726	6	10	NULL	0	NULL	statement 1			is dependent on					heparin chains		molecular weight of 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_1_118_s_33	8994426	16  These observations may explain why the anticoagulant response, as measured by anti-Xa levels, is more predictable for LMWH than for UFH. 14  We also demonstrated that the extent of nonspecific binding of heparin to plasma proteins is dependent on the molecular weight of the heparin chains, with the longer chains exhibiting the most nonspecific binding.	bind
56526	2	6726	6	10	NULL	0	NULL	heparin		longer chains of	bind		non-specifically			plasma proteins					NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_1_118_s_33	8994426	16  These observations may explain why the anticoagulant response, as measured by anti-Xa levels, is more predictable for LMWH than for UFH. 14  We also demonstrated that the extent of nonspecific binding of heparin to plasma proteins is dependent on the molecular weight of the heparin chains, with the longer chains exhibiting the most nonspecific binding.	bind
58591	3	6726	6	10	NULL	0	NULL	statement 2			is greater than					statement 1					NULL		0	NULL	NULL	NULL	gw60_circulation_95_1_118_s_33	8994426	16  These observations may explain why the anticoagulant response, as measured by anti-Xa levels, is more predictable for LMWH than for UFH. 14  We also demonstrated that the extent of nonspecific binding of heparin to plasma proteins is dependent on the molecular weight of the heparin chains, with the longer chains exhibiting the most nonspecific binding.	bind
22244	1	6727	5	13	NULL	NULL	NULL	TFPI	GP	 125I-labeled;; heparin-releasable	bind					LDL/VLDL	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_879_s_183	7600119	16  This hypothesis has been supported by animal studies by Novotny et al, 12  who demonstrated that exogenously added 125I-labeled heparin-releasable TFPI can bind LDL/VLDL and HDL in vivo.	bind
22246	2	6727	5	13	NULL	NULL	NULL	TFPI	GP	 125I-labeled;; heparin-releasable	bind					HDL	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_879_s_183	7600119	16  This hypothesis has been supported by animal studies by Novotny et al, 12  who demonstrated that exogenously added 125I-labeled heparin-releasable TFPI can bind LDL/VLDL and HDL in vivo.	bind
19244	1	6727	6	10	NULL	0	NULL	TFPI	NULL	125I-labeled;;heparin-releasable	bind	NULL				LDL/VLDL	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_879_s_183	7600119	16  This hypothesis has been supported by animal studies by Novotny et al, 12  who demonstrated that exogenously added 125I-labeled heparin-releasable TFPI can bind LDL/VLDL and HDL in vivo.	bind
19245	2	6727	6	10	NULL	0	NULL	TFPI	NULL	125I-labeled;; heparin-releasable	bind	NULL				HDL	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_879_s_183	7600119	16  This hypothesis has been supported by animal studies by Novotny et al, 12  who demonstrated that exogenously added 125I-labeled heparin-releasable TFPI can bind LDL/VLDL and HDL in vivo.	bind
22251	1	6728	5	13	NULL	NULL	NULL	FXa	GP		bind								second Kunitz-type domain		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2055_s_24	7583589	16  Thus, binding of FXa by the second Kunitz-type domain potentiates inhibition of the TF-FVIIa complex by the first Kunitz-type domain.	bind
22252	2	6728	5	13	NULL	NULL	NULL				inhibit			first Kunitz-type domain		TF-FVIIa complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2055_s_24	7583589	16  Thus, binding of FXa by the second Kunitz-type domain potentiates inhibition of the TF-FVIIa complex by the first Kunitz-type domain.	bind
22253	3	6728	5	13	NULL	NULL	NULL	statement 1	Process		potentiate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2055_s_24	7583589	16  Thus, binding of FXa by the second Kunitz-type domain potentiates inhibition of the TF-FVIIa complex by the first Kunitz-type domain.	bind
19246	1	6728	6	NULL	NULL	0	NULL	FXa	NULL		bind	NULL					NULL		Kunitz-type domain		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2055_s_24	7583589	16  Thus, binding of FXa by the second Kunitz-type domain potentiates inhibition of the TF-FVIIa complex by the first Kunitz-type domain.	bind
19471	2	6728	6	NULL	NULL	0	NULL	statement 1	NULL		potentiates	NULL				TF-FVIIa complex	NULL	inhibition of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2055_s_24	7583589	16  Thus, binding of FXa by the second Kunitz-type domain potentiates inhibition of the TF-FVIIa complex by the first Kunitz-type domain.	bind
19472	3	6728	6	NULL	NULL	0	NULL	statement 2	NULL		occurs via	NULL					NULL	first	Kunitz-type domain		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2055_s_24	7583589	16  Thus, binding of FXa by the second Kunitz-type domain potentiates inhibition of the TF-FVIIa complex by the first Kunitz-type domain.	bind
22255	1	6729	5	13	NULL	NULL	NULL	MBL	GP		bind		may			CK1	GP		head region		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_1045_s_267	11549596	16  Thus, MBL may bind the CK1 head and/or tail region(s) after endothelial oxidative stress.	bind
22256	2	6729	5	13	NULL	NULL	NULL	MBL	GP		bind		may			CK1	GP		tail region		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_1045_s_267	11549596	16  Thus, MBL may bind the CK1 head and/or tail region(s) after endothelial oxidative stress.	bind
22257	3	6729	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_1045_s_267	11549596	16  Thus, MBL may bind the CK1 head and/or tail region(s) after endothelial oxidative stress.	bind
22258	4	6729	5	13	NULL	NULL	NULL	statement 1	Process		occurs after					oxidative stress	Process	endothelial			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_1045_s_267	11549596	16  Thus, MBL may bind the CK1 head and/or tail region(s) after endothelial oxidative stress.	bind
22260	5	6729	5	13	NULL	NULL	NULL	statement 2	Process		occurs after					oxidative stress	Process	endothelial			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_1045_s_267	11549596	16  Thus, MBL may bind the CK1 head and/or tail region(s) after endothelial oxidative stress.	bind
19247	1	6729	6	NULL	NULL	0	NULL	MBL	NULL		bind	NULL	may			CK1	NULL		head region		NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_1045_s_267	11549596	16  Thus, MBL may bind the CK1 head and/or tail region(s) after endothelial oxidative stress.	bind
19248	2	6729	6	NULL	NULL	0	NULL	MBL	NULL		bind	NULL	may			CK1	NULL		tail region		NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_1045_s_267	11549596	16  Thus, MBL may bind the CK1 head and/or tail region(s) after endothelial oxidative stress.	bind
19249	3	6729	6	NULL	NULL	0	NULL	statement 1	NULL		occurs after	NULL				oxidative stress 	NULL	endothelial			NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_1045_s_267	11549596	16  Thus, MBL may bind the CK1 head and/or tail region(s) after endothelial oxidative stress.	bind
19250	4	6729	6	NULL	NULL	0	NULL	statement 2	NULL		occurs after	NULL				oxidative stress	NULL	endothelial			NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_1045_s_267	11549596	16  Thus, MBL may bind the CK1 head and/or tail region(s) after endothelial oxidative stress.	bind
19251	5	6729	6	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_1045_s_267	11549596	16  Thus, MBL may bind the CK1 head and/or tail region(s) after endothelial oxidative stress.	bind
22262	1	6730	5	13	NULL	NULL	NULL	Trx	GP	oxidized form	does not bind			intramolecular disulfide between C32 and C35		ASK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_33	12089063	16 -  18 The oxidized form (intramolecular disulfide between C32 and C35) or redox-inactive form (the double-mutation at catalytic sites C32 and C35) of Trx does not bind to ASK1.	bind
22263	2	6730	5	13	NULL	NULL	NULL	Trx	GP	redox-inactive form;;double-mutant	does not bind			catalytic sites C32 and C35		ASK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_33	12089063	16 -  18 The oxidized form (intramolecular disulfide between C32 and C35) or redox-inactive form (the double-mutation at catalytic sites C32 and C35) of Trx does not bind to ASK1.	bind
19252	1	6730	6	NULL	NULL	0	NULL	Trx	NULL	oxidized form	does not bind	NULL		intramolecular disulfide between C32 and C35		ASK1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_33	12089063	16 -  18 The oxidized form (intramolecular disulfide between C32 and C35) or redox-inactive form (the double-mutation at catalytic sites C32 and C35) of Trx does not bind to ASK1.	bind
19253	2	6730	6	10	NULL	0	NULL	Trx		redox-inactive form;;double mutants	does not bind			catalytic sites C32 and C35		ASK1					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_33	12089063	16 -  18 The oxidized form (intramolecular disulfide between C32 and C35) or redox-inactive form (the double-mutation at catalytic sites C32 and C35) of Trx does not bind to ASK1.	bind
22265	1	6731	5	13	NULL	NULL	NULL	VWF	GP		bind					GPIb-IX-V	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2131_s_26	14500287	16 - 18   Here also VWF binds to its platelet membrane receptor, GPIb-IX-V, establishing a transient bond that slows down platelets and thus facilitates their activation.	bind
22267	3	6731	5	13	NULL	NULL	NULL	statement 1	Process		slows down					platelets	Cell				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2131_s_26	14500287	16 - 18   Here also VWF binds to its platelet membrane receptor, GPIb-IX-V, establishing a transient bond that slows down platelets and thus facilitates their activation.	bind
22268	4	6731	5	13	NULL	NULL	NULL	statement 3	Process		facilitates					platelets	Cell	activation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2131_s_26	14500287	16 - 18   Here also VWF binds to its platelet membrane receptor, GPIb-IX-V, establishing a transient bond that slows down platelets and thus facilitates their activation.	bind
56527	2	6731	5	13	NULL	NULL	NULL	GPIb-IX-V	GP		is a type of					platelet membrane receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2131_s_26	14500287	16 - 18   Here also VWF binds to its platelet membrane receptor, GPIb-IX-V, establishing a transient bond that slows down platelets and thus facilitates their activation.	bind
19254	1	6731	6	NULL	NULL	0	NULL	VWF	NULL		bind	NULL				GPIb-IX-V	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2131_s_26	14500287	16 - 18   Here also VWF binds to its platelet membrane receptor, GPIb-IX-V, establishing a transient bond that slows down platelets and thus facilitates their activation.	bind
19255	2	6731	6	10	NULL	0	NULL	GPIb-IX-V			is a type of					platelet membrane receptor					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2131_s_26	14500287	16 - 18   Here also VWF binds to its platelet membrane receptor, GPIb-IX-V, establishing a transient bond that slows down platelets and thus facilitates their activation.	bind
19256	4	6731	6	10	NULL	0	NULL	statement 3			facilitate					platelets		activation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2131_s_26	14500287	16 - 18   Here also VWF binds to its platelet membrane receptor, GPIb-IX-V, establishing a transient bond that slows down platelets and thus facilitates their activation.	bind
19257	3	6731	6	10	NULL	0	NULL	statement 1			slows down					platelets					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2131_s_26	14500287	16 - 18   Here also VWF binds to its platelet membrane receptor, GPIb-IX-V, establishing a transient bond that slows down platelets and thus facilitates their activation.	bind
22270	1	6732	5	13	NULL	NULL	NULL	apoB	GP		bind		covalently	cysteine residue		apo(a)	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2219_s_34	15345512	16 - 18   Notably, the cysteine residue in apoB involved in the covalent bond between apoB and apo(a) is close to the postulated LDL receptor-binding region of apoB.	bind
22278	2	6732	5	13	NULL	NULL	NULL	statement 1	Process		is close to					apoB	GP		LDL receptor-binding region		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2219_s_34	15345512	16 - 18   Notably, the cysteine residue in apoB involved in the covalent bond between apoB and apo(a) is close to the postulated LDL receptor-binding region of apoB.	bind
19335	1	6732	6	10	NULL	0	NULL	apoB			bind		covalently	cysteine residue		apo(a)					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2219_s_34	15345512	16 - 18   Notably, the cysteine residue in apoB involved in the covalent bond between apoB and apo(a) is close to the postulated LDL receptor-binding region of apoB.	bind
56528	2	6732	6	10	NULL	0	NULL	statement 1			is close to					apoB			LDL receptor-binding region of 		NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2219_s_34	15345512	16 - 18   Notably, the cysteine residue in apoB involved in the covalent bond between apoB and apo(a) is close to the postulated LDL receptor-binding region of apoB.	bind
22279	1	6733	5	13	NULL	NULL	NULL	HB-EGF	GP	soluble	bind					HSPG	GP				NULL	on the surface of SMCs	NULL	NULL	NULL	NULL	gw70_circulation_108_21_2679_s_147	14623816	16 - 19    Because most of the soluble HB-EGF binds to HSPG on the surface of SMCs, 20 membrane-associated soluble HB-EGF reflects the amount of HB-EGF shedding.	bind
19336	1	6733	6	NULL	NULL	0	NULL	HB-EGF	NULL	soluble	bind	NULL				HSPG	NULL				NULL	surface of SMCs	0	NULL	NULL	NULL	gw70_circulation_108_21_2679_s_147	14623816	16 - 19    Because most of the soluble HB-EGF binds to HSPG on the surface of SMCs, 20 membrane-associated soluble HB-EGF reflects the amount of HB-EGF shedding.	bind
22281	1	6734	5	13	NULL	NULL	NULL	PI3-K	GP		bind			p85 regulatory subunit of		IRS-1 variant	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_3_399_s_127	14707024	16 - 20     Thus, it has been demonstrated that the presence of the Gly Arg change at codon 972-IRS-1 causes a specific defect in binding of the p85 regulatory subunit of PI3-K to the IRS-1 variant.	bind
22284	2	6734	5	13	NULL	NULL	NULL			change of	occurs at			Gly Arg		IRS-1	GP			codon 972	NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_3_399_s_127	14707024	16 - 20     Thus, it has been demonstrated that the presence of the Gly Arg change at codon 972-IRS-1 causes a specific defect in binding of the p85 regulatory subunit of PI3-K to the IRS-1 variant.	bind
22285	3	6734	5	13	NULL	NULL	NULL	statement 2	Process		causes					statement 1	Process	specific defect in			NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_3_399_s_127	14707024	16 - 20     Thus, it has been demonstrated that the presence of the Gly Arg change at codon 972-IRS-1 causes a specific defect in binding of the p85 regulatory subunit of PI3-K to the IRS-1 variant.	bind
19337	1	6734	6	NULL	NULL	0	NULL	PI3-K 	NULL		bind	NULL		p85 regulatory subunit		IRS-1 variant	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_109_3_399_s_127	14707024	16 - 20     Thus, it has been demonstrated that the presence of the Gly Arg change at codon 972-IRS-1 causes a specific defect in binding of the p85 regulatory subunit of PI3-K to the IRS-1 variant.	bind
19338	2	6734	6	NULL	NULL	0	NULL	IRS-1	NULL		causes	NULL		Gly Arg change at codon 972		statement 1	NULL	defect in 			NULL		0	NULL	NULL	NULL	gw70_circulation_109_3_399_s_127	14707024	16 - 20     Thus, it has been demonstrated that the presence of the Gly Arg change at codon 972-IRS-1 causes a specific defect in binding of the p85 regulatory subunit of PI3-K to the IRS-1 variant.	bind
22286	1	6736	5	13	NULL	NULL	NULL	ryanodine	Chemical		bind					SR release channel	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_12_1192_s_31	null	16 17  Furthermore, McCall et al 15  found that BayK increased binding of ryanodine to the SR release channel, but only under conditions in which sarcolemmal-SR junctions may be expected to be intact (ie, not after physical disruption).	bind
22287	2	6736	5	13	NULL	NULL	NULL	BayK	Chemical		increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_12_1192_s_31	null	16 17  Furthermore, McCall et al 15  found that BayK increased binding of ryanodine to the SR release channel, but only under conditions in which sarcolemmal-SR junctions may be expected to be intact (ie, not after physical disruption).	bind
22288	3	6736	5	13	NULL	NULL	NULL	statement 2	Process		occurs in		only			sarcolemmal-SR junctions	OrganismPart	intact			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_12_1192_s_31	null	16 17  Furthermore, McCall et al 15  found that BayK increased binding of ryanodine to the SR release channel, but only under conditions in which sarcolemmal-SR junctions may be expected to be intact (ie, not after physical disruption).	bind
19340	1	6736	6	NULL	NULL	0	NULL	ryanodine	NULL		bind	NULL				SR release channel	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_12_1192_s_31	null	16 17  Furthermore, McCall et al 15  found that BayK increased binding of ryanodine to the SR release channel, but only under conditions in which sarcolemmal-SR junctions may be expected to be intact (ie, not after physical disruption).	bind
19341	2	6736	6	NULL	NULL	0	NULL	BayK	NULL		increases	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_12_1192_s_31	null	16 17  Furthermore, McCall et al 15  found that BayK increased binding of ryanodine to the SR release channel, but only under conditions in which sarcolemmal-SR junctions may be expected to be intact (ie, not after physical disruption).	bind
19342	3	6736	6	NULL	NULL	0	NULL	statement 2	NULL		occurs in presence of	NULL	only			intact sarcolemmal-SR junctions	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_12_1192_s_31	null	16 17  Furthermore, McCall et al 15  found that BayK increased binding of ryanodine to the SR release channel, but only under conditions in which sarcolemmal-SR junctions may be expected to be intact (ie, not after physical disruption).	bind
22295	1	6737	5	13	NULL	NULL	NULL	heparan sulfate	Chemical		is required for					FGF-2 receptor	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_9_981_s_173	10468530	16 17  In addition, heparin can substitute for heparan sulfate as a required factor for FGF-2 receptor binding and may separately bind FGF to cells and facilitate internalization.	bind
22297	2	6737	5	13	NULL	NULL	NULL	heparin	Chemical		is required for					FGF-2 receptor	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_9_981_s_173	10468530	16 17  In addition, heparin can substitute for heparan sulfate as a required factor for FGF-2 receptor binding and may separately bind FGF to cells and facilitate internalization.	bind
22298	3	6737	5	13	NULL	NULL	NULL	statement 2	Process		substitutes for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_9_981_s_173	10468530	16 17  In addition, heparin can substitute for heparan sulfate as a required factor for FGF-2 receptor binding and may separately bind FGF to cells and facilitate internalization.	bind
22300	4	6737	5	13	NULL	NULL	NULL	FGF	GP		binds to					cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_9_981_s_173	10468530	16 17  In addition, heparin can substitute for heparan sulfate as a required factor for FGF-2 receptor binding and may separately bind FGF to cells and facilitate internalization.	bind
22302	6	6737	5	13	NULL	NULL	NULL	statement 5	Process		facilitates					internalization	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_9_981_s_173	10468530	16 17  In addition, heparin can substitute for heparan sulfate as a required factor for FGF-2 receptor binding and may separately bind FGF to cells and facilitate internalization.	bind
44684	5	6737	5	13	NULL	NULL	NULL	heparin	Chemical		bind		may;;separately			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_9_981_s_173	10468530	16 17  In addition, heparin can substitute for heparan sulfate as a required factor for FGF-2 receptor binding and may separately bind FGF to cells and facilitate internalization.	bind
19473	1	6737	6	NULL	NULL	0	NULL	heparan sulfate	NULL		is required for	NULL				FGF-2 receptor	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_circulation_100_9_981_s_173	10468530	16 17  In addition, heparin can substitute for heparan sulfate as a required factor for FGF-2 receptor binding and may separately bind FGF to cells and facilitate internalization.	bind
19475	2	6737	6	10	NULL	0	NULL	FGF			bind		may			cells					NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_9_981_s_173	10468530	16 17  In addition, heparin can substitute for heparan sulfate as a required factor for FGF-2 receptor binding and may separately bind FGF to cells and facilitate internalization.	bind
19476	3	6737	6	10	NULL	0	NULL	heparin			bind		may;;separately			statement 2					NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_9_981_s_173	10468530	16 17  In addition, heparin can substitute for heparan sulfate as a required factor for FGF-2 receptor binding and may separately bind FGF to cells and facilitate internalization.	bind
56529	4	6737	6	10	NULL	0	NULL	heparin			is required for					FGF-2 receptor		binding of			NULL		0	NULL	NULL	NULL	gw60_circulation_100_9_981_s_173	10468530	16 17  In addition, heparin can substitute for heparan sulfate as a required factor for FGF-2 receptor binding and may separately bind FGF to cells and facilitate internalization.	bind
56530	5	6737	6	10	NULL	0	NULL	statement 2			substitutes for					statement 1					NULL		0	NULL	NULL	NULL	gw60_circulation_100_9_981_s_173	10468530	16 17  In addition, heparin can substitute for heparan sulfate as a required factor for FGF-2 receptor binding and may separately bind FGF to cells and facilitate internalization.	bind
56531	6	6737	6	10	NULL	0	NULL	statement 3			facilitate					internalization					NULL		0	NULL	NULL	NULL	gw60_circulation_100_9_981_s_173	10468530	16 17  In addition, heparin can substitute for heparan sulfate as a required factor for FGF-2 receptor binding and may separately bind FGF to cells and facilitate internalization.	bind
22301	1	6738	5	13	NULL	NULL	NULL	vWF	GP		bind					GPIb	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_64_s_34	8548428	16 17  There is evidence that the binding of vWF to GPIb induced by botrocetin is localized elsewhere within the disulfide-bonded loop.	bind
22303	2	6738	5	13	NULL	NULL	NULL	botrocetin	Chemical		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_64_s_34	8548428	16 17  There is evidence that the binding of vWF to GPIb induced by botrocetin is localized elsewhere within the disulfide-bonded loop.	bind
22305	3	6738	5	13	NULL	NULL	NULL	statement 2	Process		is localized within					disulfide-bonded loop	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_64_s_34	8548428	16 17  There is evidence that the binding of vWF to GPIb induced by botrocetin is localized elsewhere within the disulfide-bonded loop.	bind
19343	1	6738	6	NULL	NULL	0	NULL	vWF	NULL		bind	NULL				GPIb	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_64_s_34	8548428	16 17  There is evidence that the binding of vWF to GPIb induced by botrocetin is localized elsewhere within the disulfide-bonded loop.	bind
19344	2	6738	6	NULL	NULL	0	NULL	botrocetin	NULL		induces	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_64_s_34	8548428	16 17  There is evidence that the binding of vWF to GPIb induced by botrocetin is localized elsewhere within the disulfide-bonded loop.	bind
56532	3	6738	6	10	NULL	0	NULL	statement 2			is localized within					disulfide-bonded loop					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_64_s_34	8548428	16 17  There is evidence that the binding of vWF to GPIb induced by botrocetin is localized elsewhere within the disulfide-bonded loop.	bind
22306	1	6739	5	13	NULL	NULL	NULL	VEGF-C	GP		bind					VEGFR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_11_992_s_25	10571529	16 17  VEGF-C and VEGF-D bind both VEGFR-2 and VEGFR-3/Flt4 and constitute a subgroup within the VEGF family characterized by N- and C-terminal extensions flanking the VEGF homology domain.	bind
22307	2	6739	5	13	NULL	NULL	NULL	VEGF-C	GP		bind					VEGFR-3/Flt4	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_11_992_s_25	10571529	16 17  VEGF-C and VEGF-D bind both VEGFR-2 and VEGFR-3/Flt4 and constitute a subgroup within the VEGF family characterized by N- and C-terminal extensions flanking the VEGF homology domain.	bind
22308	3	6739	5	13	NULL	NULL	NULL	VEGF-D	GP		bind					VEGFR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_11_992_s_25	10571529	16 17  VEGF-C and VEGF-D bind both VEGFR-2 and VEGFR-3/Flt4 and constitute a subgroup within the VEGF family characterized by N- and C-terminal extensions flanking the VEGF homology domain.	bind
22309	4	6739	5	13	NULL	NULL	NULL	VEGF-D	GP		bind					VEGFR-3/Flt4	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_11_992_s_25	10571529	16 17  VEGF-C and VEGF-D bind both VEGFR-2 and VEGFR-3/Flt4 and constitute a subgroup within the VEGF family characterized by N- and C-terminal extensions flanking the VEGF homology domain.	bind
22310	5	6739	5	13	NULL	NULL	NULL	VEGF-C	GP		constitutes					VEGF family	GP	a subgroup within			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_11_992_s_25	10571529	16 17  VEGF-C and VEGF-D bind both VEGFR-2 and VEGFR-3/Flt4 and constitute a subgroup within the VEGF family characterized by N- and C-terminal extensions flanking the VEGF homology domain.	bind
22311	6	6739	5	13	NULL	NULL	NULL	VEGF-D	GP		constitutes					VEGF family	GP	a subgroup within			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_11_992_s_25	10571529	16 17  VEGF-C and VEGF-D bind both VEGFR-2 and VEGFR-3/Flt4 and constitute a subgroup within the VEGF family characterized by N- and C-terminal extensions flanking the VEGF homology domain.	bind
22313	7	6739	5	13	NULL	NULL	NULL	statement 5	GP		is characterized by								N-terminal extension flanking VEGF homology domain		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_11_992_s_25	10571529	16 17  VEGF-C and VEGF-D bind both VEGFR-2 and VEGFR-3/Flt4 and constitute a subgroup within the VEGF family characterized by N- and C-terminal extensions flanking the VEGF homology domain.	bind
22314	8	6739	5	13	NULL	NULL	NULL	statement 6	GP		is characterized by								C-terminal extension flanking VEGF homology domain		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_11_992_s_25	10571529	16 17  VEGF-C and VEGF-D bind both VEGFR-2 and VEGFR-3/Flt4 and constitute a subgroup within the VEGF family characterized by N- and C-terminal extensions flanking the VEGF homology domain.	bind
19345	1	6739	6	10	NULL	0	NULL	VEGF-C			bind					VEGFR-2					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_11_992_s_25	10571529	16 17  VEGF-C and VEGF-D bind both VEGFR-2 and VEGFR-3/Flt4 and constitute a subgroup within the VEGF family characterized by N- and C-terminal extensions flanking the VEGF homology domain.	bind
19346	2	6739	6	NULL	NULL	0	NULL	VEGF-C	NULL		bind	NULL				VEGFR-3/Flt4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_11_992_s_25	10571529	16 17  VEGF-C and VEGF-D bind both VEGFR-2 and VEGFR-3/Flt4 and constitute a subgroup within the VEGF family characterized by N- and C-terminal extensions flanking the VEGF homology domain.	bind
19347	3	6739	6	NULL	NULL	0	NULL	VEGF-D	NULL		bind	NULL				VEGFR-2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_11_992_s_25	10571529	16 17  VEGF-C and VEGF-D bind both VEGFR-2 and VEGFR-3/Flt4 and constitute a subgroup within the VEGF family characterized by N- and C-terminal extensions flanking the VEGF homology domain.	bind
19348	4	6739	6	NULL	NULL	0	NULL	VEGF-D	NULL		bind	NULL				VEGFR-3/Flt4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_11_992_s_25	10571529	16 17  VEGF-C and VEGF-D bind both VEGFR-2 and VEGFR-3/Flt4 and constitute a subgroup within the VEGF family characterized by N- and C-terminal extensions flanking the VEGF homology domain.	bind
56533	5	6739	6	10	NULL	0	NULL	VEGF-C			constitute					VEGF family		a subgroup within			NULL		0	NULL	NULL	NULL	gw60_circulationres_85_11_992_s_25	10571529	16 17  VEGF-C and VEGF-D bind both VEGFR-2 and VEGFR-3/Flt4 and constitute a subgroup within the VEGF family characterized by N- and C-terminal extensions flanking the VEGF homology domain.	bind
56534	6	6739	6	10	NULL	0	NULL	VEGF-D			constitute					VEGF family		a subgroup within			NULL		0	NULL	NULL	NULL	gw60_circulationres_85_11_992_s_25	10571529	16 17  VEGF-C and VEGF-D bind both VEGFR-2 and VEGFR-3/Flt4 and constitute a subgroup within the VEGF family characterized by N- and C-terminal extensions flanking the VEGF homology domain.	bind
56535	7	6739	6	10	NULL	0	NULL	statement 5			characterized by								N-terminal extension flanking the VEGF homology domain		NULL		0	NULL	NULL	NULL	gw60_circulationres_85_11_992_s_25	10571529	16 17  VEGF-C and VEGF-D bind both VEGFR-2 and VEGFR-3/Flt4 and constitute a subgroup within the VEGF family characterized by N- and C-terminal extensions flanking the VEGF homology domain.	bind
56536	8	6739	6	10	NULL	0	NULL	statement 6			characterized by								C-terminal extension flanking the VEGF homology domain		NULL		0	NULL	NULL	NULL	gw60_circulationres_85_11_992_s_25	10571529	16 17  VEGF-C and VEGF-D bind both VEGFR-2 and VEGFR-3/Flt4 and constitute a subgroup within the VEGF family characterized by N- and C-terminal extensions flanking the VEGF homology domain.	bind
24818	1	6741	5	13	NULL	NULL	NULL	receptor-associated kinases	GP	of JAK family	bind					AT1 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_6_1053_s_188	7586216	16 17 38 39  The fact that the receptor-associated kinases of the JAK family bind to the AT1 receptor and phosphorylate the STAT family of transcription factors 36  suggests that the long-term effects of Ang II on gene expression may resemble those of tyrosine kinase - coupled receptors, such as the PDGF receptor, and classic cytokine receptors, such as the interleukin and interferon receptors.	bind
24819	2	6741	5	13	NULL	NULL	NULL	statement 1	Process		phosphorylates					STAT family of transcription factors	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_6_1053_s_188	7586216	16 17 38 39  The fact that the receptor-associated kinases of the JAK family bind to the AT1 receptor and phosphorylate the STAT family of transcription factors 36  suggests that the long-term effects of Ang II on gene expression may resemble those of tyrosine kinase - coupled receptors, such as the PDGF receptor, and classic cytokine receptors, such as the interleukin and interferon receptors.	bind
19350	1	6741	6	NULL	NULL	0	NULL	receptor-associated kinases 	NULL	JAK family	bind	NULL				AT1 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_77_6_1053_s_188	7586216	16 17 38 39  The fact that the receptor-associated kinases of the JAK family bind to the AT1 receptor and phosphorylate the STAT family of transcription factors 36  suggests that the long-term effects of Ang II on gene expression may resemble those of tyrosine kinase - coupled receptors, such as the PDGF receptor, and classic cytokine receptors, such as the interleukin and interferon receptors.	bind
19351	2	6741	6	10	NULL	0	NULL	statement 1			phosphorylates					STAT family of transcription factors					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_6_1053_s_188	7586216	16 17 38 39  The fact that the receptor-associated kinases of the JAK family bind to the AT1 receptor and phosphorylate the STAT family of transcription factors 36  suggests that the long-term effects of Ang II on gene expression may resemble those of tyrosine kinase - coupled receptors, such as the PDGF receptor, and classic cytokine receptors, such as the interleukin and interferon receptors.	bind
22315	1	6742	5	13	NULL	NULL	NULL	aldosterone	Chemical		bind					MR	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_6_643_s_37	15718497	16 Aldosterone and cortisol bind to human MR with equal affinity.	bind
22323	2	6742	5	13	NULL	NULL	NULL	cortisol	Chemical		bind					MR	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_6_643_s_37	15718497	16 Aldosterone and cortisol bind to human MR with equal affinity.	bind
22325	3	6742	5	13	NULL	NULL	NULL	statement 1	Process		same affinity as					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_6_643_s_37	15718497	16 Aldosterone and cortisol bind to human MR with equal affinity.	bind
19352	1	6742	6	NULL	NULL	0	NULL	aldosterone	NULL		bind	NULL				MR	NULL	human			NULL		0	NULL	NULL	NULL	gw70_circulationres_96_6_643_s_37	15718497	16 Aldosterone and cortisol bind to human MR with equal affinity.	bind
19353	2	6742	6	NULL	NULL	0	NULL	cortisol	NULL		bind	NULL				MR	NULL	human			NULL		0	NULL	NULL	NULL	gw70_circulationres_96_6_643_s_37	15718497	16 Aldosterone and cortisol bind to human MR with equal affinity.	bind
19354	3	6742	6	NULL	NULL	0	NULL	statement 1	NULL		has equal affinity as	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_6_643_s_37	15718497	16 Aldosterone and cortisol bind to human MR with equal affinity.	bind
22324	1	6743	5	13	NULL	NULL	NULL	antibody JTC4	GP		bind					PC	GP		catalytic domain		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_865_s_37	12663483	16 Antibody JTC4 binds to the catalytic domain of PC, and its binding to the PC catalytic domain is decreased significantly after reduction.	bind
22328	2	6743	5	13	NULL	NULL	NULL	statement 1	Process		decrease after		significantly			reduction	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_865_s_37	12663483	16 Antibody JTC4 binds to the catalytic domain of PC, and its binding to the PC catalytic domain is decreased significantly after reduction.	bind
19355	1	6743	6	NULL	NULL	0	NULL	JTC4 antibody	NULL		bind	NULL				PC	NULL		catalytic domain		NULL		0	NULL	NULL	NULL	gw70_circulationres_92_8_865_s_37	12663483	16 Antibody JTC4 binds to the catalytic domain of PC, and its binding to the PC catalytic domain is decreased significantly after reduction.	bind
56537	2	6743	6	10	NULL	0	NULL	statement 1			decrease after		significantly			reduction					NULL		0	NULL	NULL	NULL	gw70_circulationres_92_8_865_s_37	12663483	16 Antibody JTC4 binds to the catalytic domain of PC, and its binding to the PC catalytic domain is decreased significantly after reduction.	bind
22330	1	6744	5	13	NULL	NULL	NULL	group V sPLA2	GP	human	bind					PC membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_762_s_32	14962950	16 Binding studies using phosphatidylcholine (PC)-coated hydrophobic beads demonstrate that human group V sPLA2 binds PC membranes more than 50-times more tightly than human group IIa sPLA2.	bind
22332	2	6744	5	13	NULL	NULL	NULL	group IIa sPLA2	GP	human	bind					PC membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_762_s_32	14962950	16 Binding studies using phosphatidylcholine (PC)-coated hydrophobic beads demonstrate that human group V sPLA2 binds PC membranes more than 50-times more tightly than human group IIa sPLA2.	bind
22338	3	6744	5	13	NULL	NULL	NULL	statement 1	Process		more tightly than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_762_s_32	14962950	16 Binding studies using phosphatidylcholine (PC)-coated hydrophobic beads demonstrate that human group V sPLA2 binds PC membranes more than 50-times more tightly than human group IIa sPLA2.	bind
19356	1	6744	6	NULL	NULL	0	NULL	group V sPLA2 	NULL	human	bind	NULL				PC membranes	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_762_s_32	14962950	16 Binding studies using phosphatidylcholine (PC)-coated hydrophobic beads demonstrate that human group V sPLA2 binds PC membranes more than 50-times more tightly than human group IIa sPLA2.	bind
19357	2	6744	6	NULL	NULL	0	NULL	group IIa sPLA2	NULL	human	bind	NULL				PC membranes	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_762_s_32	14962950	16 Binding studies using phosphatidylcholine (PC)-coated hydrophobic beads demonstrate that human group V sPLA2 binds PC membranes more than 50-times more tightly than human group IIa sPLA2.	bind
19358	3	6744	6	NULL	NULL	0	NULL	statement 1	NULL		is stronger than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_762_s_32	14962950	16 Binding studies using phosphatidylcholine (PC)-coated hydrophobic beads demonstrate that human group V sPLA2 binds PC membranes more than 50-times more tightly than human group IIa sPLA2.	bind
22335	1	6745	5	13	NULL	NULL	NULL	Lp-PLA2 plasma isoform	GP		bind					LDL	GP				NULL	in bloodstream	NULL	NULL	NULL	NULL	gw70_circulation_110_14_1903_s_30	15451783	16 In the bloodstream, two thirds of the Lp-PLA2 plasma isoform circulates primarily bound to LDL; the other third is distributed between HDL and VLDL. 17	bind
22336	2	6745	5	13	NULL	NULL	NULL	statement 1	Process		circulates in					blood stream	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_14_1903_s_30	15451783	16 In the bloodstream, two thirds of the Lp-PLA2 plasma isoform circulates primarily bound to LDL; the other third is distributed between HDL and VLDL. 17	bind
19359	1	6745	6	10	NULL	0	NULL	Lp-PLA2 plasma isoform			bind					LDL					NULL	blood stream	NULL	NULL	NULL	NULL	gw70_circulation_110_14_1903_s_30	15451783	16 In the bloodstream, two thirds of the Lp-PLA2 plasma isoform circulates primarily bound to LDL; the other third is distributed between HDL and VLDL. 17	bind
22339	1	6746	5	13	NULL	NULL	NULL	Trx	GP	single mutation at	bind			catalytic site Trx-C32S		ASK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_257	12089063	16 Our data show that the single mutation of Trx at the catalytic site (Trx-C32S or Trx-C35S) can bind to ASK1, suggesting that the redox activity is not required for the association of Trx with ASK1.	bind
22340	2	6746	5	13	NULL	NULL	NULL	Trx	GP	single mutation at	bind			catalytic site Trx-C35S		ASK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_257	12089063	16 Our data show that the single mutation of Trx at the catalytic site (Trx-C32S or Trx-C35S) can bind to ASK1, suggesting that the redox activity is not required for the association of Trx with ASK1.	bind
22341	3	6746	5	13	NULL	NULL	NULL	Trx	GP		associates with					ASK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_257	12089063	16 Our data show that the single mutation of Trx at the catalytic site (Trx-C32S or Trx-C35S) can bind to ASK1, suggesting that the redox activity is not required for the association of Trx with ASK1.	bind
22342	4	6746	5	13	NULL	NULL	NULL	redox activity	Process		is not required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_257	12089063	16 Our data show that the single mutation of Trx at the catalytic site (Trx-C32S or Trx-C35S) can bind to ASK1, suggesting that the redox activity is not required for the association of Trx with ASK1.	bind
56538	5	6746	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_257	12089063	16 Our data show that the single mutation of Trx at the catalytic site (Trx-C32S or Trx-C35S) can bind to ASK1, suggesting that the redox activity is not required for the association of Trx with ASK1.	bind
19360	1	6746	6	10	NULL	0	NULL	Trx		single mutant	bind			catalytic site Trx-C32S		ASK1					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_257	12089063	16 Our data show that the single mutation of Trx at the catalytic site (Trx-C32S or Trx-C35S) can bind to ASK1, suggesting that the redox activity is not required for the association of Trx with ASK1.	bind
19361	2	6746	6	10	NULL	0	NULL	Trx		single mutant	bind			catalytic site Trx-C35S		ASK1					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_257	12089063	16 Our data show that the single mutation of Trx at the catalytic site (Trx-C32S or Trx-C35S) can bind to ASK1, suggesting that the redox activity is not required for the association of Trx with ASK1.	bind
19362	3	6746	6	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_257	12089063	16 Our data show that the single mutation of Trx at the catalytic site (Trx-C32S or Trx-C35S) can bind to ASK1, suggesting that the redox activity is not required for the association of Trx with ASK1.	bind
19363	4	6746	6	NULL	NULL	0	NULL	Trx	NULL	redox activity of	is not required for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_257	12089063	16 Our data show that the single mutation of Trx at the catalytic site (Trx-C32S or Trx-C35S) can bind to ASK1, suggesting that the redox activity is not required for the association of Trx with ASK1.	bind
19364	5	6746	6	NULL	NULL	0	NULL	Trx	NULL	redox activity of	is not required for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_257	12089063	16 Our data show that the single mutation of Trx at the catalytic site (Trx-C32S or Trx-C35S) can bind to ASK1, suggesting that the redox activity is not required for the association of Trx with ASK1.	bind
22343	1	6747	5	13	NULL	NULL	NULL	APOA5	GP		is					apolipoprotein A-V	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1985_s_38	15976322	16 Recently USF1 was also shown to stimulate apolipoprotein A-V ( APOA5) promoter activity in an insulin-dependent manner, demonstrated by the reduced binding of USF1 to the  APOA5 promoter in the presence of insulin.	bind
22344	2	6747	5	13	NULL	NULL	NULL	USF1	GP		bind					APOA5	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1985_s_38	15976322	16 Recently USF1 was also shown to stimulate apolipoprotein A-V ( APOA5) promoter activity in an insulin-dependent manner, demonstrated by the reduced binding of USF1 to the  APOA5 promoter in the presence of insulin.	bind
22345	3	6747	5	13	NULL	NULL	NULL	insulin	GP		reduces					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1985_s_38	15976322	16 Recently USF1 was also shown to stimulate apolipoprotein A-V ( APOA5) promoter activity in an insulin-dependent manner, demonstrated by the reduced binding of USF1 to the  APOA5 promoter in the presence of insulin.	bind
22346	4	6747	5	13	NULL	NULL	NULL	USF1	GP		stimulates					APOA5	GP	activity of		promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1985_s_38	15976322	16 Recently USF1 was also shown to stimulate apolipoprotein A-V ( APOA5) promoter activity in an insulin-dependent manner, demonstrated by the reduced binding of USF1 to the  APOA5 promoter in the presence of insulin.	bind
22347	5	6747	5	13	NULL	NULL	NULL	statement 4	Process		is dependent on					insulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1985_s_38	15976322	16 Recently USF1 was also shown to stimulate apolipoprotein A-V ( APOA5) promoter activity in an insulin-dependent manner, demonstrated by the reduced binding of USF1 to the  APOA5 promoter in the presence of insulin.	bind
19365	1	6747	6	NULL	NULL	0	NULL	USF1	NULL		bind	NULL				APOA5	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1985_s_38	15976322	16 Recently USF1 was also shown to stimulate apolipoprotein A-V ( APOA5) promoter activity in an insulin-dependent manner, demonstrated by the reduced binding of USF1 to the  APOA5 promoter in the presence of insulin.	bind
19366	2	6747	6	NULL	NULL	0	NULL	APOA5	NULL		is	NULL				apolipoprotein A-V	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1985_s_38	15976322	16 Recently USF1 was also shown to stimulate apolipoprotein A-V ( APOA5) promoter activity in an insulin-dependent manner, demonstrated by the reduced binding of USF1 to the  APOA5 promoter in the presence of insulin.	bind
19367	3	6747	6	10	NULL	0	NULL	insulin			reduces					statement 1					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1985_s_38	15976322	16 Recently USF1 was also shown to stimulate apolipoprotein A-V ( APOA5) promoter activity in an insulin-dependent manner, demonstrated by the reduced binding of USF1 to the  APOA5 promoter in the presence of insulin.	bind
56539	4	6747	6	10	NULL	0	NULL	USF1			stimulate					APOA5		activity of		promoter	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1985_s_38	15976322	16 Recently USF1 was also shown to stimulate apolipoprotein A-V ( APOA5) promoter activity in an insulin-dependent manner, demonstrated by the reduced binding of USF1 to the  APOA5 promoter in the presence of insulin.	bind
56540	5	6747	6	10	NULL	0	NULL	statement 4			depends on					insulin					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1985_s_38	15976322	16 Recently USF1 was also shown to stimulate apolipoprotein A-V ( APOA5) promoter activity in an insulin-dependent manner, demonstrated by the reduced binding of USF1 to the  APOA5 promoter in the presence of insulin.	bind
22348	1	6748	5	13	NULL	NULL	NULL	L22 protein	GP		bind		primarily			23S rRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_52_3_345_s_303	12917252	16 The L22 protein binds primarily to the 23S rRNA.	bind
19368	1	6748	6	NULL	NULL	0	NULL	L22 protein	NULL		bind	NULL	primarily			23S rRNA	NULL				NULL		0	NULL	NULL	NULL	gw70_jantimicrobchemoth_52_3_345_s_303	12917252	16 The L22 protein binds primarily to the 23S rRNA.	bind
22350	1	6749	5	13	NULL	NULL	NULL	PDGF-BB	GP		bind					R-1 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_15_1830_s_92	11956127	16 There were no differences in PDGF-BB binding to R-1, R-2, and C-1 cells or the levels of immunoreactive PDGF-beta receptor among these cells ( Figure 3A).	bind
22351	2	6749	5	13	NULL	NULL	NULL	PDGF-BB	GP		bind					R-2 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_15_1830_s_92	11956127	16 There were no differences in PDGF-BB binding to R-1, R-2, and C-1 cells or the levels of immunoreactive PDGF-beta receptor among these cells ( Figure 3A).	bind
22352	3	6749	5	13	NULL	NULL	NULL	PDGF-BB	GP		bind					C-1 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_15_1830_s_92	11956127	16 There were no differences in PDGF-BB binding to R-1, R-2, and C-1 cells or the levels of immunoreactive PDGF-beta receptor among these cells ( Figure 3A).	bind
19369	1	6749	6	NULL	NULL	0	NULL	PDGF-BB	NULL		bind	NULL				R-1 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_15_1830_s_92	11956127	16 There were no differences in PDGF-BB binding to R-1, R-2, and C-1 cells or the levels of immunoreactive PDGF-beta receptor among these cells ( Figure 3A).	bind
19370	2	6749	6	NULL	NULL	0	NULL	PDGF-BB	NULL		bind	NULL				R-2 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_15_1830_s_92	11956127	16 There were no differences in PDGF-BB binding to R-1, R-2, and C-1 cells or the levels of immunoreactive PDGF-beta receptor among these cells ( Figure 3A).	bind
19371	3	6749	6	NULL	NULL	0	NULL	PDGF-BB	NULL		bind	NULL				C-1 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_15_1830_s_92	11956127	16 There were no differences in PDGF-BB binding to R-1, R-2, and C-1 cells or the levels of immunoreactive PDGF-beta receptor among these cells ( Figure 3A).	bind
22353	1	6750	5	13	NULL	NULL	NULL	TIMPs	GP		bind					MMPs	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_9_1166_s_31	15723986	16 TIMPs bind to MMPs in a 1:1 ratio, thereby preventing continued proteolytic activity.	bind
22354	2	6750	5	13	NULL	NULL	NULL	statement 1	Process		prevents					proteolytic activity	Process	continued			NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_9_1166_s_31	15723986	16 TIMPs bind to MMPs in a 1:1 ratio, thereby preventing continued proteolytic activity.	bind
19372	1	6750	6	NULL	NULL	0	NULL	TIMP	NULL		bind	NULL				MMP	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_111_9_1166_s_31	15723986	16 TIMPs bind to MMPs in a 1:1 ratio, thereby preventing continued proteolytic activity.	bind
56541	2	6750	6	10	NULL	0	NULL	statement 1			prevents					proteolytic activity		continued			NULL		0	NULL	NULL	NULL	gw70_circulation_111_9_1166_s_31	15723986	16 TIMPs bind to MMPs in a 1:1 ratio, thereby preventing continued proteolytic activity.	bind
22355	1	6751	5	13	NULL	NULL	NULL	fibrinogen	GP		bind					GP IIb/IIa receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1720_s_30	15242858	16 VASP phosphorylation correlates closely with inhibition of fibrinogen binding to the GP IIb/IIa receptor.	bind
22356	2	6751	5	13	NULL	NULL	NULL	VASP	GP	phosphorylation	correlates with		closely			statement 1	Process	inhibition of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1720_s_30	15242858	16 VASP phosphorylation correlates closely with inhibition of fibrinogen binding to the GP IIb/IIa receptor.	bind
19373	1	6751	6	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL				GP IIb/IIa receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1720_s_30	15242858	16 VASP phosphorylation correlates closely with inhibition of fibrinogen binding to the GP IIb/IIa receptor.	bind
19374	2	6751	6	NULL	NULL	0	NULL	VASP	NULL	phosphorylation of	correlates with	NULL				statement 1	NULL	inhibition of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1720_s_30	15242858	16 VASP phosphorylation correlates closely with inhibition of fibrinogen binding to the GP IIb/IIa receptor.	bind
22357	1	6753	5	13	NULL	NULL	NULL	growth factor	GP		bind					receptor tyrosine kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_3_899_s_15	10079268	16, 17  It is believed that the initial events involve binding of growth factor to a receptor tyrosine kinase and receptor oligomerization.	bind
22358	2	6753	5	13	NULL	NULL	NULL	statement 1	Process		leads to					receptor 	GP	oligomerization of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_3_899_s_15	10079268	16, 17  It is believed that the initial events involve binding of growth factor to a receptor tyrosine kinase and receptor oligomerization.	bind
19375	1	6753	6	NULL	NULL	0	NULL	growth factor	NULL		bind	NULL				receptor tyrosine kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_3_899_s_15	10079268	16, 17  It is believed that the initial events involve binding of growth factor to a receptor tyrosine kinase and receptor oligomerization.	bind
56542	2	6753	6	10	NULL	0	NULL	statement 1			leads to					receptor		oligomerization of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_3_899_s_15	10079268	16, 17  It is believed that the initial events involve binding of growth factor to a receptor tyrosine kinase and receptor oligomerization.	bind
22359	1	6754	5	13	NULL	NULL	NULL	IL-6	GP	murine	does not bind					IL-6R	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_2_639_s_20	9708822	16, 17  Transgenic mice expressing the human sIL-6R do not develop any specific morphological changes, because murine IL-6 does not bind to the human IL-6R.	bind
19376	1	6754	6	NULL	NULL	0	NULL	IL-6	NULL	murine	does not bind	NULL				IL-6R	NULL	human			NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_2_639_s_20	9708822	16, 17  Transgenic mice expressing the human sIL-6R do not develop any specific morphological changes, because murine IL-6 does not bind to the human IL-6R.	bind
22360	1	6755	5	13	NULL	NULL	NULL	alpha1	GP		bind			I domain		type II collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1779_s_20	12000729	16, 17 Thus, although alpha1 I domain can bind type II collagen and the alpha1 integrin can probably transduce signals from type II collagen, it is likely that adhesion to type II collagen of structural importance is mediated by alpha2beta1.	bind
22361	2	6755	5	13	NULL	NULL	NULL	alpha1 integrin	GP		transduce		probably			type II collagen	GP	signals from			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1779_s_20	12000729	16, 17 Thus, although alpha1 I domain can bind type II collagen and the alpha1 integrin can probably transduce signals from type II collagen, it is likely that adhesion to type II collagen of structural importance is mediated by alpha2beta1.	bind
22362	3	6755	5	13	NULL	NULL	NULL	type II collagen	GP	adhesion to	is mediated by					alpha2beta1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1779_s_20	12000729	16, 17 Thus, although alpha1 I domain can bind type II collagen and the alpha1 integrin can probably transduce signals from type II collagen, it is likely that adhesion to type II collagen of structural importance is mediated by alpha2beta1.	bind
19528	1	6755	6	10	NULL	0	NULL	alpha1			bind			 I domain		type II collagen					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1779_s_20	12000729	16, 17 Thus, although alpha1 I domain can bind type II collagen and the alpha1 integrin can probably transduce signals from type II collagen, it is likely that adhesion to type II collagen of structural importance is mediated by alpha2beta1.	bind
19529	2	6755	6	NULL	NULL	0	NULL	alpha2beta1	NULL		mediates	NULL				type II collagen	NULL	adhesion to			NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1779_s_20	12000729	16, 17 Thus, although alpha1 I domain can bind type II collagen and the alpha1 integrin can probably transduce signals from type II collagen, it is likely that adhesion to type II collagen of structural importance is mediated by alpha2beta1.	bind
19530	3	6755	6	NULL	NULL	0	NULL	alpha1 integrin	NULL		transduce	NULL	probably			type II collagen	NULL	signals from			NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1779_s_20	12000729	16, 17 Thus, although alpha1 I domain can bind type II collagen and the alpha1 integrin can probably transduce signals from type II collagen, it is likely that adhesion to type II collagen of structural importance is mediated by alpha2beta1.	bind
22363	1	6756	5	13	NULL	NULL	NULL	ALK	GP		interacts with					PLC-gamma	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_3_875_s_187	12213716	16, 19, 20  Further, the interaction between ALK and PLC-gamma has been shown to be essential because mutation of the ALK residue responsible for PLC-gamma binding eliminates the transforming potential of NPM-ALK.	bind
22364	3	6756	5	13	NULL	NULL	NULL	statement 2	Process		eliminates					NPM-ALK	GP	transforming potential of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_3_875_s_187	12213716	16, 19, 20  Further, the interaction between ALK and PLC-gamma has been shown to be essential because mutation of the ALK residue responsible for PLC-gamma binding eliminates the transforming potential of NPM-ALK.	bind
44688	2	6756	5	13	NULL	NULL	NULL			mutation of	responsible for			ALK residue		PLC-gamma	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_3_875_s_187	12213716	16, 19, 20  Further, the interaction between ALK and PLC-gamma has been shown to be essential because mutation of the ALK residue responsible for PLC-gamma binding eliminates the transforming potential of NPM-ALK.	bind
19531	1	6756	6	NULL	NULL	0	NULL	ALK	NULL		interacts with	NULL				PLC-gamma	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_3_875_s_187	12213716	16, 19, 20  Further, the interaction between ALK and PLC-gamma has been shown to be essential because mutation of the ALK residue responsible for PLC-gamma binding eliminates the transforming potential of NPM-ALK.	bind
19532	2	6756	6	10	NULL	0	NULL	ALK		mutant	responsible for					PLC-gamma		binding of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_3_875_s_187	12213716	16, 19, 20  Further, the interaction between ALK and PLC-gamma has been shown to be essential because mutation of the ALK residue responsible for PLC-gamma binding eliminates the transforming potential of NPM-ALK.	bind
56543	3	6756	6	10	NULL	0	NULL	statement 2			eliminates					NPM-ALK		transforming potential of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_3_875_s_187	12213716	16, 19, 20  Further, the interaction between ALK and PLC-gamma has been shown to be essential because mutation of the ALK residue responsible for PLC-gamma binding eliminates the transforming potential of NPM-ALK.	bind
22365	1	6757	5	13	NULL	NULL	NULL	P300	GP		bind					transactivator-DNA complex	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_23_2760_s_160	12057991	16, 25 In this study, we provide direct evidence for P300 binding to transactivator-DNA complex.	bind
19533	1	6757	6	NULL	NULL	0	NULL	p300	NULL		bind	NULL	directly			transactivator-DNA complex	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_23_2760_s_160	12057991	16, 25 In this study, we provide direct evidence for P300 binding to transactivator-DNA complex.	bind
22366	1	6758	5	13	NULL	NULL	NULL	apoptotic protease-activating factor 1	GP		bind					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_nature_442_7098_39_s_228	16823444	16, 48-62 (2004) |  Article |  PubMed |  ISI |  ChemPort |    iedl, S. J. ,  Li, W. ,  Chao, Y. ,  Schwarzenbacher, [[ R.  &  Shi ]], Y.  Structure  of the apoptotic protease-activating factor 1 bound to ADP.	bind
19534	1	6758	6	10	NULL	0	NULL	apoptotic protease-activating factor 1	NULL		bind	NULL				ADP	NULL				NULL		NULL	NULL	NULL	NULL	gw70_nature_442_7098_39_s_228	16823444	16, 48-62 (2004) |  Article |  PubMed |  ISI |  ChemPort |    iedl, S. J. ,  Li, W. ,  Chao, Y. ,  Schwarzenbacher, [[ R.  &  Shi ]], Y.  Structure  of the apoptotic protease-activating factor 1 bound to ADP.	bind
22367	1	6760	5	13	NULL	NULL	NULL	Hip	GP		bind					Hsc70	GP		ATPase domain		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_100	9686751	166 247 248  After Hsp40 is released, Hip binds to the ATPase domain of Hsc70 (E), stimulates its activity, and then remains bound to stabilize the ADP-Hsc70-substrate complex, suggesting that it may play a role in the transport of substrates within cells (F).	bind
22368	2	6760	5	13	NULL	NULL	NULL	statement 1	Process		occurs after					Hsp40	GP	release of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_100	9686751	166 247 248  After Hsp40 is released, Hip binds to the ATPase domain of Hsc70 (E), stimulates its activity, and then remains bound to stabilize the ADP-Hsc70-substrate complex, suggesting that it may play a role in the transport of substrates within cells (F).	bind
22369	3	6760	5	13	NULL	NULL	NULL	statement 1	Process		stimulates					Hsc70	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_100	9686751	166 247 248  After Hsp40 is released, Hip binds to the ATPase domain of Hsc70 (E), stimulates its activity, and then remains bound to stabilize the ADP-Hsc70-substrate complex, suggesting that it may play a role in the transport of substrates within cells (F).	bind
22370	4	6760	5	13	NULL	NULL	NULL	Hip	GP		remains					Hsc70	GP	bound to			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_100	9686751	166 247 248  After Hsp40 is released, Hip binds to the ATPase domain of Hsc70 (E), stimulates its activity, and then remains bound to stabilize the ADP-Hsc70-substrate complex, suggesting that it may play a role in the transport of substrates within cells (F).	bind
22371	5	6760	5	13	NULL	NULL	NULL	statement 4	Process		stabilizes					ADP-Hsc70-substrate complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_100	9686751	166 247 248  After Hsp40 is released, Hip binds to the ATPase domain of Hsc70 (E), stimulates its activity, and then remains bound to stabilize the ADP-Hsc70-substrate complex, suggesting that it may play a role in the transport of substrates within cells (F).	bind
22372	6	6760	5	13	NULL	NULL	NULL	statement 5	Process		plays a role in		may			substrates	GP	transport of			NULL	within cells	NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_100	9686751	166 247 248  After Hsp40 is released, Hip binds to the ATPase domain of Hsc70 (E), stimulates its activity, and then remains bound to stabilize the ADP-Hsc70-substrate complex, suggesting that it may play a role in the transport of substrates within cells (F).	bind
19535	1	6760	6	NULL	NULL	0	NULL	Hip	NULL		bind	NULL				Hsc70	NULL		ATPase domain		NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_100	9686751	166 247 248  After Hsp40 is released, Hip binds to the ATPase domain of Hsc70 (E), stimulates its activity, and then remains bound to stabilize the ADP-Hsc70-substrate complex, suggesting that it may play a role in the transport of substrates within cells (F).	bind
19536	2	6760	6	10	NULL	0	NULL	statement 1			occurs after 		release of			Hsp40					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_100	9686751	166 247 248  After Hsp40 is released, Hip binds to the ATPase domain of Hsc70 (E), stimulates its activity, and then remains bound to stabilize the ADP-Hsc70-substrate complex, suggesting that it may play a role in the transport of substrates within cells (F).	bind
19537	3	6760	6	NULL	NULL	0	NULL	Hip	NULL		stimulates 	NULL				Hsc70	NULL	activity of 			NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_100	9686751	166 247 248  After Hsp40 is released, Hip binds to the ATPase domain of Hsc70 (E), stimulates its activity, and then remains bound to stabilize the ADP-Hsc70-substrate complex, suggesting that it may play a role in the transport of substrates within cells (F).	bind
19538	4	6760	6	NULL	NULL	0	NULL	ADP	NULL		forms a complex with	NULL				Hsc70	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_100	9686751	166 247 248  After Hsp40 is released, Hip binds to the ATPase domain of Hsc70 (E), stimulates its activity, and then remains bound to stabilize the ADP-Hsc70-substrate complex, suggesting that it may play a role in the transport of substrates within cells (F).	bind
19539	5	6760	6	NULL	NULL	0	NULL	Hip	NULL		stabilizes	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_100	9686751	166 247 248  After Hsp40 is released, Hip binds to the ATPase domain of Hsc70 (E), stimulates its activity, and then remains bound to stabilize the ADP-Hsc70-substrate complex, suggesting that it may play a role in the transport of substrates within cells (F).	bind
19540	6	6760	6	NULL	NULL	0	NULL	Hip	NULL		plays a role in	NULL	may			substrates	NULL	transport of 			NULL	cells	0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_100	9686751	166 247 248  After Hsp40 is released, Hip binds to the ATPase domain of Hsc70 (E), stimulates its activity, and then remains bound to stabilize the ADP-Hsc70-substrate complex, suggesting that it may play a role in the transport of substrates within cells (F).	bind
23224	1	6761	5	13	NULL	NULL	NULL	XPG	GP		bind					PCNA	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1341_s_359	11239001	17       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
23225	2	6761	5	13	NULL	NULL	NULL	XPG	GP		is a type of					DNA repair endonuclease	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1341_s_359	11239001	17       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
23226	3	6761	5	13	NULL	NULL	NULL	PCNA	GP		is					proliferating cell nuclear antigen	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1341_s_359	11239001	17       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
23227	4	6761	5	13	NULL	NULL	NULL	XPG	GP		share					FEN-1	GP	sequence elements with	PCNA-binding regions		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1341_s_359	11239001	17       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
23228	5	6761	5	13	NULL	NULL	NULL	XPG	GP		share					p21	GP	sequence elements with			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1341_s_359	11239001	17       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
23230	6	6761	5	13	NULL	NULL	NULL	p21	GP		is a type of					cyclin-dependent kinase inhibitor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1341_s_359	11239001	17       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
19541	1	6761	6	10	NULL	0	NULL	XPG	NULL		is a type of	NULL				DNA repair endonuclease	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1341_s_359	11239001	17       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
19542	2	6761	6	NULL	NULL	0	NULL	XPG	NULL		bind	NULL				PCNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1341_s_359	11239001	17       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
19543	3	6761	6	NULL	NULL	0	NULL	PCNA	NULL		is	NULL				proliferating cell nuclear antigen	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1341_s_359	11239001	17       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
56544	4	6761	6	10	NULL	0	NULL	XPG			shares					FEN-1		sequence elements with	PCNA-binding region		NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1341_s_359	11239001	17       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
56545	5	6761	6	10	NULL	0	NULL	XPG			shares					p21		sequence elements with			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1341_s_359	11239001	17       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
56546	6	6761	6	10	NULL	0	NULL	p21			is a type of					cyclin-dependent kinase inhibitor					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1341_s_359	11239001	17       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
23231	1	6763	5	13	NULL	NULL	NULL	Cu2+	Chemical		bind					LDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3338_s_35	9409331	17  19  Subsequent studies have shown that Cu2+ binds to LDL 20 21  22  and that LDL can reduce Cu2+ to Cu1+.	bind
23232	2	6763	5	13	NULL	NULL	NULL	Cu2+	Chemical		is reduced to					Cu1+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3338_s_35	9409331	17  19  Subsequent studies have shown that Cu2+ binds to LDL 20 21  22  and that LDL can reduce Cu2+ to Cu1+.	bind
23233	3	6763	5	13	NULL	NULL	NULL	LDL	GP		is required for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3338_s_35	9409331	17  19  Subsequent studies have shown that Cu2+ binds to LDL 20 21  22  and that LDL can reduce Cu2+ to Cu1+.	bind
19546	1	6763	6	NULL	NULL	0	NULL	Cu2+	NULL		bind	NULL				LDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3338_s_35	9409331	17  19  Subsequent studies have shown that Cu2+ binds to LDL 20 21  22  and that LDL can reduce Cu2+ to Cu1+.	bind
19547	2	6763	6	NULL	NULL	0	NULL	Cu2+	NULL		reduced to	NULL				Cu1+	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3338_s_35	9409331	17  19  Subsequent studies have shown that Cu2+ binds to LDL 20 21  22  and that LDL can reduce Cu2+ to Cu1+.	bind
19548	3	6763	6	NULL	NULL	0	NULL	statement 2	NULL		occurs by	NULL				LDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3338_s_35	9409331	17  19  Subsequent studies have shown that Cu2+ binds to LDL 20 21  22  and that LDL can reduce Cu2+ to Cu1+.	bind
23234	1	6764	5	13	NULL	NULL	NULL	vWF	GP		is changed to			RDDS		vWF	GP		RGGS		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_6_1661_s_43	10845886	17  Arg-Gly-Gly-Ser (RGGS)-vWF, in which Asp (D)-1746 has been changed to Gly (G), has virtually no binding to thrombin-stimulated platelets, indicating that the interaction of this vWF with alphaIIb-beta3 is defective.	bind
23235	2	6764	5	13	NULL	NULL	NULL	statement 1	GP		does not bind					platelets	Cell	thrombin-stimulated			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_6_1661_s_43	10845886	17  Arg-Gly-Gly-Ser (RGGS)-vWF, in which Asp (D)-1746 has been changed to Gly (G), has virtually no binding to thrombin-stimulated platelets, indicating that the interaction of this vWF with alphaIIb-beta3 is defective.	bind
23236	3	6764	5	13	NULL	NULL	NULL	vWF	GP		interacts with					alphaIIb-beta3	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_6_1661_s_43	10845886	17  Arg-Gly-Gly-Ser (RGGS)-vWF, in which Asp (D)-1746 has been changed to Gly (G), has virtually no binding to thrombin-stimulated platelets, indicating that the interaction of this vWF with alphaIIb-beta3 is defective.	bind
23237	4	6764	5	13	NULL	NULL	NULL	statement 2	Process		indicates					statement 3	Process	defective			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_6_1661_s_43	10845886	17  Arg-Gly-Gly-Ser (RGGS)-vWF, in which Asp (D)-1746 has been changed to Gly (G), has virtually no binding to thrombin-stimulated platelets, indicating that the interaction of this vWF with alphaIIb-beta3 is defective.	bind
19818	2	6764	6	10	NULL	0	NULL	statement 1			does not bind					platelets		thrombin-stimulated			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_6_1661_s_43	10845886	17  Arg-Gly-Gly-Ser (RGGS)-vWF, in which Asp (D)-1746 has been changed to Gly (G), has virtually no binding to thrombin-stimulated platelets, indicating that the interaction of this vWF with alphaIIb-beta3 is defective.	bind
19819	3	6764	6	10	NULL	0	NULL	vWF 			 interact with					alphaIIb-beta3					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_6_1661_s_43	10845886	17  Arg-Gly-Gly-Ser (RGGS)-vWF, in which Asp (D)-1746 has been changed to Gly (G), has virtually no binding to thrombin-stimulated platelets, indicating that the interaction of this vWF with alphaIIb-beta3 is defective.	bind
19820	4	6764	6	10	NULL	0	NULL	statement 2			indicates					statement 3		defective			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_6_1661_s_43	10845886	17  Arg-Gly-Gly-Ser (RGGS)-vWF, in which Asp (D)-1746 has been changed to Gly (G), has virtually no binding to thrombin-stimulated platelets, indicating that the interaction of this vWF with alphaIIb-beta3 is defective.	bind
56547	1	6764	6	10	NULL	0	NULL	vWF			is changed to			RDDS		vWF			RGGS		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_6_1661_s_43	10845886	17  Arg-Gly-Gly-Ser (RGGS)-vWF, in which Asp (D)-1746 has been changed to Gly (G), has virtually no binding to thrombin-stimulated platelets, indicating that the interaction of this vWF with alphaIIb-beta3 is defective.	bind
23238	1	6765	5	13	NULL	NULL	NULL	anti-hsp65/60 Abs	GP	serum	bind		high affinity			GroEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_536_s_151	9102173	17  As a consequence of this and because serum anti-hsp65/60 Abs also exhibit a high binding capacity to GroEL, the corresponding areas of Ab binding on the three-dimensional GroEL structure may be of interest.	bind
19549	1	6765	6	NULL	NULL	0	NULL	anti-hsp65/60 Abs	NULL	serum	bind	NULL	high affinity			GroEL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_536_s_151	9102173	17  As a consequence of this and because serum anti-hsp65/60 Abs also exhibit a high binding capacity to GroEL, the corresponding areas of Ab binding on the three-dimensional GroEL structure may be of interest.	bind
23239	1	6766	5	13	NULL	NULL	NULL	perlecan	GP		bind			core protein		Abeta 	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2115_s_21	10595940	17  Because perlecan can bind to both Abeta and the amyloid precursor protein (betaPP) through its core protein or GAG moieties, 18- 21  this molecule may play a significant role in amyloid formation in Alzheimer s disease, eg, by affecting the processing of betaPP or by determining the localization of Abeta deposition at sites where perlecan is produced.	bind
23244	2	6766	5	13	NULL	NULL	NULL	perlecan	GP		bind			GAG moieties		Abeta	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2115_s_21	10595940	17  Because perlecan can bind to both Abeta and the amyloid precursor protein (betaPP) through its core protein or GAG moieties, 18- 21  this molecule may play a significant role in amyloid formation in Alzheimer s disease, eg, by affecting the processing of betaPP or by determining the localization of Abeta deposition at sites where perlecan is produced.	bind
23245	3	6766	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2115_s_21	10595940	17  Because perlecan can bind to both Abeta and the amyloid precursor protein (betaPP) through its core protein or GAG moieties, 18- 21  this molecule may play a significant role in amyloid formation in Alzheimer s disease, eg, by affecting the processing of betaPP or by determining the localization of Abeta deposition at sites where perlecan is produced.	bind
23246	4	6766	5	13	NULL	NULL	NULL	betaPP	GP		is a type of					amyloid precursor protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2115_s_21	10595940	17  Because perlecan can bind to both Abeta and the amyloid precursor protein (betaPP) through its core protein or GAG moieties, 18- 21  this molecule may play a significant role in amyloid formation in Alzheimer s disease, eg, by affecting the processing of betaPP or by determining the localization of Abeta deposition at sites where perlecan is produced.	bind
23247	5	6766	5	13	NULL	NULL	NULL	perlecan	GP		bind			core protein		betaPP	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2115_s_21	10595940	17  Because perlecan can bind to both Abeta and the amyloid precursor protein (betaPP) through its core protein or GAG moieties, 18- 21  this molecule may play a significant role in amyloid formation in Alzheimer s disease, eg, by affecting the processing of betaPP or by determining the localization of Abeta deposition at sites where perlecan is produced.	bind
23248	6	6766	5	13	NULL	NULL	NULL	perlecan	GP		bind			GAG moieties		betaPP	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2115_s_21	10595940	17  Because perlecan can bind to both Abeta and the amyloid precursor protein (betaPP) through its core protein or GAG moieties, 18- 21  this molecule may play a significant role in amyloid formation in Alzheimer s disease, eg, by affecting the processing of betaPP or by determining the localization of Abeta deposition at sites where perlecan is produced.	bind
23249	7	6766	5	13	NULL	NULL	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2115_s_21	10595940	17  Because perlecan can bind to both Abeta and the amyloid precursor protein (betaPP) through its core protein or GAG moieties, 18- 21  this molecule may play a significant role in amyloid formation in Alzheimer s disease, eg, by affecting the processing of betaPP or by determining the localization of Abeta deposition at sites where perlecan is produced.	bind
23250	8	6766	5	13	NULL	NULL	NULL	perlecan	GP		plays a role in		may;;significant			amyloid	GP	formation of			NULL	in Alzheimer s disease	NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2115_s_21	10595940	17  Because perlecan can bind to both Abeta and the amyloid precursor protein (betaPP) through its core protein or GAG moieties, 18- 21  this molecule may play a significant role in amyloid formation in Alzheimer s disease, eg, by affecting the processing of betaPP or by determining the localization of Abeta deposition at sites where perlecan is produced.	bind
23251	9	6766	5	13	NULL	NULL	NULL	perlecan	GP		affect					betaPP	GP	processing of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2115_s_21	10595940	17  Because perlecan can bind to both Abeta and the amyloid precursor protein (betaPP) through its core protein or GAG moieties, 18- 21  this molecule may play a significant role in amyloid formation in Alzheimer s disease, eg, by affecting the processing of betaPP or by determining the localization of Abeta deposition at sites where perlecan is produced.	bind
19550	1	6766	6	NULL	NULL	0	NULL	perlecan	NULL		bind	NULL		GAG moeity		Abeta	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2115_s_21	10595940	17  Because perlecan can bind to both Abeta and the amyloid precursor protein (betaPP) through its core protein or GAG moieties, 18- 21  this molecule may play a significant role in amyloid formation in Alzheimer s disease, eg, by affecting the processing of betaPP or by determining the localization of Abeta deposition at sites where perlecan is produced.	bind
19551	2	6766	6	NULL	NULL	0	NULL	perlecan	NULL		bind	NULL		GAG moeity		betaPP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2115_s_21	10595940	17  Because perlecan can bind to both Abeta and the amyloid precursor protein (betaPP) through its core protein or GAG moieties, 18- 21  this molecule may play a significant role in amyloid formation in Alzheimer s disease, eg, by affecting the processing of betaPP or by determining the localization of Abeta deposition at sites where perlecan is produced.	bind
19552	3	6766	6	10	NULL	0	NULL	betaPP			is a type of					amyloid precursor protein					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2115_s_21	10595940	17  Because perlecan can bind to both Abeta and the amyloid precursor protein (betaPP) through its core protein or GAG moieties, 18- 21  this molecule may play a significant role in amyloid formation in Alzheimer s disease, eg, by affecting the processing of betaPP or by determining the localization of Abeta deposition at sites where perlecan is produced.	bind
19553	4	6766	6	10	NULL	0	NULL	perlecan			play a role in		may			amyloid 		formation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2115_s_21	10595940	17  Because perlecan can bind to both Abeta and the amyloid precursor protein (betaPP) through its core protein or GAG moieties, 18- 21  this molecule may play a significant role in amyloid formation in Alzheimer s disease, eg, by affecting the processing of betaPP or by determining the localization of Abeta deposition at sites where perlecan is produced.	bind
19554	5	6766	6	NULL	NULL	0	NULL	statement 4	NULL		occurs in	NULL				Alzheimer s disease	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_6_2115_s_21	10595940	17  Because perlecan can bind to both Abeta and the amyloid precursor protein (betaPP) through its core protein or GAG moieties, 18- 21  this molecule may play a significant role in amyloid formation in Alzheimer s disease, eg, by affecting the processing of betaPP or by determining the localization of Abeta deposition at sites where perlecan is produced.	bind
56548	6	6766	6	10	NULL	0	NULL	perlecan			bind			core protein		Abeta					NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_6_2115_s_21	10595940	17  Because perlecan can bind to both Abeta and the amyloid precursor protein (betaPP) through its core protein or GAG moieties, 18- 21  this molecule may play a significant role in amyloid formation in Alzheimer s disease, eg, by affecting the processing of betaPP or by determining the localization of Abeta deposition at sites where perlecan is produced.	bind
56549	7	6766	6	10	NULL	0	NULL	perlecan			bind			core protein		betaPP					NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_6_2115_s_21	10595940	17  Because perlecan can bind to both Abeta and the amyloid precursor protein (betaPP) through its core protein or GAG moieties, 18- 21  this molecule may play a significant role in amyloid formation in Alzheimer s disease, eg, by affecting the processing of betaPP or by determining the localization of Abeta deposition at sites where perlecan is produced.	bind
56550	8	6766	6	10	NULL	0	NULL	statement 1			is an alternative to					statement 6					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2115_s_21	10595940	17  Because perlecan can bind to both Abeta and the amyloid precursor protein (betaPP) through its core protein or GAG moieties, 18- 21  this molecule may play a significant role in amyloid formation in Alzheimer s disease, eg, by affecting the processing of betaPP or by determining the localization of Abeta deposition at sites where perlecan is produced.	bind
56551	9	6766	6	10	NULL	0	NULL	statement 2			is an alternative to					statement 7					NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_6_2115_s_21	10595940	17  Because perlecan can bind to both Abeta and the amyloid precursor protein (betaPP) through its core protein or GAG moieties, 18- 21  this molecule may play a significant role in amyloid formation in Alzheimer s disease, eg, by affecting the processing of betaPP or by determining the localization of Abeta deposition at sites where perlecan is produced.	bind
57601	10	6766	6	10	NULL	0	NULL	perlecan			affects					betaPP		processing of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_6_2115_s_21	10595940	17  Because perlecan can bind to both Abeta and the amyloid precursor protein (betaPP) through its core protein or GAG moieties, 18- 21  this molecule may play a significant role in amyloid formation in Alzheimer s disease, eg, by affecting the processing of betaPP or by determining the localization of Abeta deposition at sites where perlecan is produced.	bind
23240	1	6767	5	13	NULL	NULL	NULL	FGF-2	GP		bind					tyrosine kinase receptor(s)	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_3_293_s_37	10679481	17  Binding of FGF-2 to its tyrosine kinase receptor(s) initiates a signal transduction cascade that has been shown to activate both the MAPK and PKC pathways in cardiomyocytes.	bind
23241	2	6767	5	13	NULL	NULL	NULL	statement 1	Process		initiates					signal transduction cascade	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_3_293_s_37	10679481	17  Binding of FGF-2 to its tyrosine kinase receptor(s) initiates a signal transduction cascade that has been shown to activate both the MAPK and PKC pathways in cardiomyocytes.	bind
23242	3	6767	5	13	NULL	NULL	NULL	statement 2	Process		activates					MAPK pathway	Process				NULL	in cardiomyocytes	NULL	NULL	NULL	NULL	gw60_circulationres_86_3_293_s_37	10679481	17  Binding of FGF-2 to its tyrosine kinase receptor(s) initiates a signal transduction cascade that has been shown to activate both the MAPK and PKC pathways in cardiomyocytes.	bind
23243	4	6767	5	13	NULL	NULL	NULL	statement 2	Process		activates					PKC pathway	Process				NULL	in cardiomyocytes	NULL	NULL	NULL	NULL	gw60_circulationres_86_3_293_s_37	10679481	17  Binding of FGF-2 to its tyrosine kinase receptor(s) initiates a signal transduction cascade that has been shown to activate both the MAPK and PKC pathways in cardiomyocytes.	bind
19555	1	6767	6	NULL	NULL	0	NULL	FGF-2	NULL		bind	NULL				tyrosine kinase receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_3_293_s_37	10679481	17  Binding of FGF-2 to its tyrosine kinase receptor(s) initiates a signal transduction cascade that has been shown to activate both the MAPK and PKC pathways in cardiomyocytes.	bind
19556	2	6767	6	NULL	NULL	0	NULL	statement 1	NULL		initiates	NULL				signal transduction cascade	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_3_293_s_37	10679481	17  Binding of FGF-2 to its tyrosine kinase receptor(s) initiates a signal transduction cascade that has been shown to activate both the MAPK and PKC pathways in cardiomyocytes.	bind
19557	3	6767	6	NULL	NULL	0	NULL	statement 2	NULL		activate	NULL				MAPK pathway	NULL				NULL	cardiomyocytes	0	NULL	NULL	NULL	gw60_circulationres_86_3_293_s_37	10679481	17  Binding of FGF-2 to its tyrosine kinase receptor(s) initiates a signal transduction cascade that has been shown to activate both the MAPK and PKC pathways in cardiomyocytes.	bind
19558	4	6767	6	NULL	NULL	0	NULL	statement 2	NULL		activate	NULL				PKC pathway	NULL				NULL	cardiomyocytes	0	NULL	NULL	NULL	gw60_circulationres_86_3_293_s_37	10679481	17  Binding of FGF-2 to its tyrosine kinase receptor(s) initiates a signal transduction cascade that has been shown to activate both the MAPK and PKC pathways in cardiomyocytes.	bind
19559	1	6768	6	NULL	NULL	0	NULL	hyaluronan	NULL		bind	NULL				CD44	NULL	soluble			NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_6_2159_s_74	10854236	17  Binding of hyaluronan to the soluble CD44 transfectants and their adhesion to a hyaluronan substratum were shown previously to be reduced compared to wild-type TA3/St cells and vector controls.	bind
19560	2	6768	6	NULL	NULL	0	NULL	hyaluronan	NULL		adhers to	NULL				hyaluronan substratum	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_6_2159_s_74	10854236	17  Binding of hyaluronan to the soluble CD44 transfectants and their adhesion to a hyaluronan substratum were shown previously to be reduced compared to wild-type TA3/St cells and vector controls.	bind
23256	1	6769	5	13	NULL	NULL	NULL	(LIF) receptor	GP		is					leukemia inhibitory factor receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_10_1116_s_27	10477538	17  CT-1 binds to the leukemia inhibitory factor (LIF) receptor/gp130 heterodimer and activates both mitogen-activated protein kinase and Janus kinase signal transducers and activators of transcription (STAT) signaling pathways.	bind
23257	3	6769	5	13	NULL	NULL	NULL	CT-1	GP		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_10_1116_s_27	10477538	17  CT-1 binds to the leukemia inhibitory factor (LIF) receptor/gp130 heterodimer and activates both mitogen-activated protein kinase and Janus kinase signal transducers and activators of transcription (STAT) signaling pathways.	bind
23258	4	6769	5	13	NULL	NULL	NULL	statement 3	Process		activates					mitogen-activated protein kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_10_1116_s_27	10477538	17  CT-1 binds to the leukemia inhibitory factor (LIF) receptor/gp130 heterodimer and activates both mitogen-activated protein kinase and Janus kinase signal transducers and activators of transcription (STAT) signaling pathways.	bind
23259	5	6769	5	13	NULL	NULL	NULL	statement 3	Process		activates					Janus kinase signal transducers	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_10_1116_s_27	10477538	17  CT-1 binds to the leukemia inhibitory factor (LIF) receptor/gp130 heterodimer and activates both mitogen-activated protein kinase and Janus kinase signal transducers and activators of transcription (STAT) signaling pathways.	bind
23260	6	6769	5	13	NULL	NULL	NULL	CT-1	GP		activates					transcription (STAT) signaling pathways	GP	activators of 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_10_1116_s_27	10477538	17  CT-1 binds to the leukemia inhibitory factor (LIF) receptor/gp130 heterodimer and activates both mitogen-activated protein kinase and Janus kinase signal transducers and activators of transcription (STAT) signaling pathways.	bind
56552	2	6769	5	13	NULL	NULL	NULL	LIF receptor	GP		heterodimerize with					gp130	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_10_1116_s_27	10477538	17  CT-1 binds to the leukemia inhibitory factor (LIF) receptor/gp130 heterodimer and activates both mitogen-activated protein kinase and Janus kinase signal transducers and activators of transcription (STAT) signaling pathways.	bind
19561	1	6769	6	10	NULL	0	NULL	LIF			heterodimerize with					gp130					NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_10_1116_s_27	10477538	17  CT-1 binds to the leukemia inhibitory factor (LIF) receptor/gp130 heterodimer and activates both mitogen-activated protein kinase and Janus kinase signal transducers and activators of transcription (STAT) signaling pathways.	bind
19562	2	6769	6	NULL	NULL	0	NULL	LIF	NULL		is	NULL				leukemia inhibitory factor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_10_1116_s_27	10477538	17  CT-1 binds to the leukemia inhibitory factor (LIF) receptor/gp130 heterodimer and activates both mitogen-activated protein kinase and Janus kinase signal transducers and activators of transcription (STAT) signaling pathways.	bind
19563	3	6769	6	10	NULL	0	NULL	CT-1			binds to					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_10_1116_s_27	10477538	17  CT-1 binds to the leukemia inhibitory factor (LIF) receptor/gp130 heterodimer and activates both mitogen-activated protein kinase and Janus kinase signal transducers and activators of transcription (STAT) signaling pathways.	bind
19564	4	6769	6	10	NULL	0	NULL	statement 3			activates					mitogen-activated protein kinase 					NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_10_1116_s_27	10477538	17  CT-1 binds to the leukemia inhibitory factor (LIF) receptor/gp130 heterodimer and activates both mitogen-activated protein kinase and Janus kinase signal transducers and activators of transcription (STAT) signaling pathways.	bind
19565	5	6769	6	10	NULL	0	NULL	statement 3			activates					Janus kinase signal transducers					NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_10_1116_s_27	10477538	17  CT-1 binds to the leukemia inhibitory factor (LIF) receptor/gp130 heterodimer and activates both mitogen-activated protein kinase and Janus kinase signal transducers and activators of transcription (STAT) signaling pathways.	bind
56553	6	6769	6	10	NULL	0	NULL	statement 3			activates					transcription (STAT) signaling pathways		activators of 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_10_1116_s_27	10477538	17  CT-1 binds to the leukemia inhibitory factor (LIF) receptor/gp130 heterodimer and activates both mitogen-activated protein kinase and Janus kinase signal transducers and activators of transcription (STAT) signaling pathways.	bind
23262	1	6771	5	13	NULL	NULL	NULL	cGMP	Chemical	increased levels of	induce					calcium ion 	Chemical	decrease in;; intracellular concentration of			NULL	in platelets	NULL	NULL	NULL	NULL	gw60_circulation_97_15_1481_s_139	9576429	17  Increased cGMP levels in platelets can induce a decrease in intracellular calcium ion concentration, which may contribute to an inhibition of fibrinogen binding to the GP IIb/IIa receptor on the surface of the platelet membrane, which mediates platelet aggregation.	bind
23263	2	6771	5	13	NULL	NULL	NULL	fibrinogen	GP		bind					GP IIb/IIa receptor	GP				NULL	on the surface of the platelet membrane	NULL	NULL	NULL	NULL	gw60_circulation_97_15_1481_s_139	9576429	17  Increased cGMP levels in platelets can induce a decrease in intracellular calcium ion concentration, which may contribute to an inhibition of fibrinogen binding to the GP IIb/IIa receptor on the surface of the platelet membrane, which mediates platelet aggregation.	bind
23264	3	6771	5	13	NULL	NULL	NULL	statement 2	Process		mediate					platelets	Cell	aggregation of 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_15_1481_s_139	9576429	17  Increased cGMP levels in platelets can induce a decrease in intracellular calcium ion concentration, which may contribute to an inhibition of fibrinogen binding to the GP IIb/IIa receptor on the surface of the platelet membrane, which mediates platelet aggregation.	bind
23265	4	6771	5	13	NULL	NULL	NULL	statement 1	Process		contribute to		may			statement 2	Process	inhibition of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_15_1481_s_139	9576429	17  Increased cGMP levels in platelets can induce a decrease in intracellular calcium ion concentration, which may contribute to an inhibition of fibrinogen binding to the GP IIb/IIa receptor on the surface of the platelet membrane, which mediates platelet aggregation.	bind
19572	1	6771	6	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL				GP IIb/IIa receptor	NULL				NULL	surface of the platelet membrane	0	NULL	NULL	NULL	gw60_circulation_97_15_1481_s_139	9576429	17  Increased cGMP levels in platelets can induce a decrease in intracellular calcium ion concentration, which may contribute to an inhibition of fibrinogen binding to the GP IIb/IIa receptor on the surface of the platelet membrane, which mediates platelet aggregation.	bind
19573	2	6771	6	10	NULL	0	NULL	statement 1			mediates					platelets		aggregation of 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_15_1481_s_139	9576429	17  Increased cGMP levels in platelets can induce a decrease in intracellular calcium ion concentration, which may contribute to an inhibition of fibrinogen binding to the GP IIb/IIa receptor on the surface of the platelet membrane, which mediates platelet aggregation.	bind
19574	3	6771	6	10	NULL	0	NULL	cGMP 		increased levels of	induce					calcium ion 		decrease in;; intracellular concentration of			NULL	platelets	NULL	NULL	NULL	NULL	gw60_circulation_97_15_1481_s_139	9576429	17  Increased cGMP levels in platelets can induce a decrease in intracellular calcium ion concentration, which may contribute to an inhibition of fibrinogen binding to the GP IIb/IIa receptor on the surface of the platelet membrane, which mediates platelet aggregation.	bind
19575	4	6771	6	10	NULL	0	NULL	statement 3			contribute to		may			statement 1		inhibition of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_15_1481_s_139	9576429	17  Increased cGMP levels in platelets can induce a decrease in intracellular calcium ion concentration, which may contribute to an inhibition of fibrinogen binding to the GP IIb/IIa receptor on the surface of the platelet membrane, which mediates platelet aggregation.	bind
28342	1	6772	5	13	NULL	NULL	NULL	B cells	Cell	sensitized	bind					HLA-DR molecules	GP	specific			NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_786_s_143	9727549	17  Similar patterns of progressive intramolecular and intermolecular HLA-DR epitope spreading can be detected in heart transplantation recipients developing accelerated transplantation-related CAD. 18  This diversification of the immune response has been postulated to be driven by sensitized B cells that bind soluble HLA-DR molecules by using specific surface Ig receptors, endocytose these molecules, and subsequently present multiple HLA-DR allopeptides to CD4 T cells.	bind
28345	2	6772	5	13	NULL	NULL	NULL	statement 1	Process		uses					Ig receptors	GP	specific;;surface			NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_786_s_143	9727549	17  Similar patterns of progressive intramolecular and intermolecular HLA-DR epitope spreading can be detected in heart transplantation recipients developing accelerated transplantation-related CAD. 18  This diversification of the immune response has been postulated to be driven by sensitized B cells that bind soluble HLA-DR molecules by using specific surface Ig receptors, endocytose these molecules, and subsequently present multiple HLA-DR allopeptides to CD4 T cells.	bind
28347	3	6772	5	13	NULL	NULL	NULL	statement 1	Process		undergoes					endocytosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_786_s_143	9727549	17  Similar patterns of progressive intramolecular and intermolecular HLA-DR epitope spreading can be detected in heart transplantation recipients developing accelerated transplantation-related CAD. 18  This diversification of the immune response has been postulated to be driven by sensitized B cells that bind soluble HLA-DR molecules by using specific surface Ig receptors, endocytose these molecules, and subsequently present multiple HLA-DR allopeptides to CD4 T cells.	bind
28348	4	6772	5	13	NULL	NULL	NULL	HLA-DR allopeptides	GP	multiple	is presented to		subsequently			CD4 T cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_786_s_143	9727549	17  Similar patterns of progressive intramolecular and intermolecular HLA-DR epitope spreading can be detected in heart transplantation recipients developing accelerated transplantation-related CAD. 18  This diversification of the immune response has been postulated to be driven by sensitized B cells that bind soluble HLA-DR molecules by using specific surface Ig receptors, endocytose these molecules, and subsequently present multiple HLA-DR allopeptides to CD4 T cells.	bind
19821	1	6772	6	NULL	NULL	0	NULL	B cells	NULL	sensitized	bind	NULL				HLA-DR molecules	NULL	soluble			NULL		0	NULL	NULL	NULL	gw60_circulation_98_8_786_s_143	9727549	17  Similar patterns of progressive intramolecular and intermolecular HLA-DR epitope spreading can be detected in heart transplantation recipients developing accelerated transplantation-related CAD. 18  This diversification of the immune response has been postulated to be driven by sensitized B cells that bind soluble HLA-DR molecules by using specific surface Ig receptors, endocytose these molecules, and subsequently present multiple HLA-DR allopeptides to CD4 T cells.	bind
19822	2	6772	6	10	NULL	0	NULL	statement 1			occurs by					 Ig receptors		specific;;surface			NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_786_s_143	9727549	17  Similar patterns of progressive intramolecular and intermolecular HLA-DR epitope spreading can be detected in heart transplantation recipients developing accelerated transplantation-related CAD. 18  This diversification of the immune response has been postulated to be driven by sensitized B cells that bind soluble HLA-DR molecules by using specific surface Ig receptors, endocytose these molecules, and subsequently present multiple HLA-DR allopeptides to CD4 T cells.	bind
19823	4	6772	6	10	NULL	0	NULL	HLA-DR allopeptides			presented to					CD4 T cells					NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_786_s_143	9727549	17  Similar patterns of progressive intramolecular and intermolecular HLA-DR epitope spreading can be detected in heart transplantation recipients developing accelerated transplantation-related CAD. 18  This diversification of the immune response has been postulated to be driven by sensitized B cells that bind soluble HLA-DR molecules by using specific surface Ig receptors, endocytose these molecules, and subsequently present multiple HLA-DR allopeptides to CD4 T cells.	bind
19824	3	6772	6	10	NULL	0	NULL	statement 1			undergoes					endocytosis					NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_8_786_s_143	9727549	17  Similar patterns of progressive intramolecular and intermolecular HLA-DR epitope spreading can be detected in heart transplantation recipients developing accelerated transplantation-related CAD. 18  This diversification of the immune response has been postulated to be driven by sensitized B cells that bind soluble HLA-DR molecules by using specific surface Ig receptors, endocytose these molecules, and subsequently present multiple HLA-DR allopeptides to CD4 T cells.	bind
23266	1	6773	5	13	NULL	NULL	NULL	Raf-1	GP		bind					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_7_1159_s_116	11451745	17  The Raf-1 - bound Ras was increased by LDL exposure (see Figure 3B  ).	bind
23267	2	6773	5	13	NULL	NULL	NULL	LDL	GP	exposure	increases					Ras	GP	Raf-1 - bound			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_7_1159_s_116	11451745	17  The Raf-1 - bound Ras was increased by LDL exposure (see Figure 3B  ).	bind
19576	1	6773	6	NULL	NULL	0	NULL	Raf-1	NULL		bind	NULL				Ras	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_7_1159_s_116	11451745	17  The Raf-1 - bound Ras was increased by LDL exposure (see Figure 3B  ).	bind
19577	2	6773	6	NULL	NULL	0	NULL	statement 1	NULL		is increased by	NULL				LDL	NULL	exposure to			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_7_1159_s_116	11451745	17  The Raf-1 - bound Ras was increased by LDL exposure (see Figure 3B  ).	bind
23268	1	6774	5	13	NULL	NULL	NULL	LDL	GP		bind					PG	GP	arterial			NULL	in LNG group	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1216_s_187	9261249	17  Together these results suggest that a likely explanation for the increased binding of LDL to arterial PG in the LNG group is related to the increased apo E content.	bind
23269	2	6774	5	13	NULL	NULL	NULL	statement 1	Process	increased	is related to					apo E	GP	increased content of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1216_s_187	9261249	17  Together these results suggest that a likely explanation for the increased binding of LDL to arterial PG in the LNG group is related to the increased apo E content.	bind
19578	1	6774	6	10	NULL	0	NULL	LDL			bind					PG		arterial			NULL	LNG group	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1216_s_187	9261249	17  Together these results suggest that a likely explanation for the increased binding of LDL to arterial PG in the LNG group is related to the increased apo E content.	bind
19579	2	6774	6	10	NULL	0	NULL	statement 1			is related to					apoE 		increased content of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1216_s_187	9261249	17  Together these results suggest that a likely explanation for the increased binding of LDL to arterial PG in the LNG group is related to the increased apo E content.	bind
23271	1	6775	5	13	NULL	NULL	NULL	EC	Cell		express					growth factors	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_26	16690881	17 - 19   Ang1 induces EC to express growth factors, such as endothelial-derived heparin binding EGF-like growth factor (HB-EGF) 20 and serotonin, 21 that recruit pericytes and SMC to form support for newly formed vessels.	bind
23273	2	6775	5	13	NULL	NULL	NULL	growth factors	GP		includes					HB-EGF	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_26	16690881	17 - 19   Ang1 induces EC to express growth factors, such as endothelial-derived heparin binding EGF-like growth factor (HB-EGF) 20 and serotonin, 21 that recruit pericytes and SMC to form support for newly formed vessels.	bind
23274	3	6775	5	13	NULL	NULL	NULL	HB-EGF	GP		is					endothelial-derived heparin binding EGF-like growth factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_26	16690881	17 - 19   Ang1 induces EC to express growth factors, such as endothelial-derived heparin binding EGF-like growth factor (HB-EGF) 20 and serotonin, 21 that recruit pericytes and SMC to form support for newly formed vessels.	bind
23275	4	6775	5	13	NULL	NULL	NULL	growth factors	GP		includes					serotonin	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_26	16690881	17 - 19   Ang1 induces EC to express growth factors, such as endothelial-derived heparin binding EGF-like growth factor (HB-EGF) 20 and serotonin, 21 that recruit pericytes and SMC to form support for newly formed vessels.	bind
23276	5	6775	5	13	NULL	NULL	NULL	Ang1	GP		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_26	16690881	17 - 19   Ang1 induces EC to express growth factors, such as endothelial-derived heparin binding EGF-like growth factor (HB-EGF) 20 and serotonin, 21 that recruit pericytes and SMC to form support for newly formed vessels.	bind
23277	6	6775	5	13	NULL	NULL	NULL	serotonin	GP		recruits					pericytes	Cell				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_26	16690881	17 - 19   Ang1 induces EC to express growth factors, such as endothelial-derived heparin binding EGF-like growth factor (HB-EGF) 20 and serotonin, 21 that recruit pericytes and SMC to form support for newly formed vessels.	bind
23278	7	6775	5	13	NULL	NULL	NULL	serotonin	GP		recruits					SMC	Cell				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_26	16690881	17 - 19   Ang1 induces EC to express growth factors, such as endothelial-derived heparin binding EGF-like growth factor (HB-EGF) 20 and serotonin, 21 that recruit pericytes and SMC to form support for newly formed vessels.	bind
23279	8	6775	5	13	NULL	NULL	NULL	statement 6	Process		form support for					vessels	OrganismPart	newly formed			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_26	16690881	17 - 19   Ang1 induces EC to express growth factors, such as endothelial-derived heparin binding EGF-like growth factor (HB-EGF) 20 and serotonin, 21 that recruit pericytes and SMC to form support for newly formed vessels.	bind
23280	9	6775	5	13	NULL	NULL	NULL	statement 7	Process		form support for					vessels	OrganismPart	newly formed			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_26	16690881	17 - 19   Ang1 induces EC to express growth factors, such as endothelial-derived heparin binding EGF-like growth factor (HB-EGF) 20 and serotonin, 21 that recruit pericytes and SMC to form support for newly formed vessels.	bind
19580	1	6775	6	NULL	NULL	0	NULL	EC	NULL		express	NULL				HB-EGF	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_26	16690881	17 - 19   Ang1 induces EC to express growth factors, such as endothelial-derived heparin binding EGF-like growth factor (HB-EGF) 20 and serotonin, 21 that recruit pericytes and SMC to form support for newly formed vessels.	bind
19581	2	6775	6	NULL	NULL	0	NULL	HB-EGF	NULL		is	NULL				heparin binding EGF-like growth factor	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_26	16690881	17 - 19   Ang1 induces EC to express growth factors, such as endothelial-derived heparin binding EGF-like growth factor (HB-EGF) 20 and serotonin, 21 that recruit pericytes and SMC to form support for newly formed vessels.	bind
19582	3	6775	6	NULL	NULL	0	NULL	Ang1	NULL		induces	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_26	16690881	17 - 19   Ang1 induces EC to express growth factors, such as endothelial-derived heparin binding EGF-like growth factor (HB-EGF) 20 and serotonin, 21 that recruit pericytes and SMC to form support for newly formed vessels.	bind
19583	6	6775	6	10	NULL	0	NULL	statement 4			form support for					 vessels		newly formed			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_26	16690881	17 - 19   Ang1 induces EC to express growth factors, such as endothelial-derived heparin binding EGF-like growth factor (HB-EGF) 20 and serotonin, 21 that recruit pericytes and SMC to form support for newly formed vessels.	bind
19584	7	6775	6	10	NULL	0	NULL	statement 5			forms support for					 vessels		newly formed			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_26	16690881	17 - 19   Ang1 induces EC to express growth factors, such as endothelial-derived heparin binding EGF-like growth factor (HB-EGF) 20 and serotonin, 21 that recruit pericytes and SMC to form support for newly formed vessels.	bind
19585	4	6775	6	10	NULL	0	NULL	serotonin			recruit					pericytes					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_26	16690881	17 - 19   Ang1 induces EC to express growth factors, such as endothelial-derived heparin binding EGF-like growth factor (HB-EGF) 20 and serotonin, 21 that recruit pericytes and SMC to form support for newly formed vessels.	bind
19586	5	6775	6	10	NULL	0	NULL	serotonin			recruit					SMC					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_26	16690881	17 - 19   Ang1 induces EC to express growth factors, such as endothelial-derived heparin binding EGF-like growth factor (HB-EGF) 20 and serotonin, 21 that recruit pericytes and SMC to form support for newly formed vessels.	bind
56554	8	6775	6	10	NULL	0	NULL	HB-EGF			is a type of					growth factor					NULL		0	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_26	16690881	17 - 19   Ang1 induces EC to express growth factors, such as endothelial-derived heparin binding EGF-like growth factor (HB-EGF) 20 and serotonin, 21 that recruit pericytes and SMC to form support for newly formed vessels.	bind
56555	9	6775	6	10	NULL	0	NULL	serotonin			is a type of					growth factor					NULL		0	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_26	16690881	17 - 19   Ang1 induces EC to express growth factors, such as endothelial-derived heparin binding EGF-like growth factor (HB-EGF) 20 and serotonin, 21 that recruit pericytes and SMC to form support for newly formed vessels.	bind
23283	1	6776	5	13	NULL	NULL	NULL	myocardial ischemia	MedicalFinding		leads to					Mgi	Chemical	increase in			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_3_975_s_36	9264509	17 18  During myocardial ischemia, Mgi increases with degradation of ATP, which binds most Mgi. 19 20 21 22  Increased Mgi levels could be harmful to cardiac cells if they are compensated for by Mg2+ efflux through Na+-Mg2+ countertransport, which in turn would promote excess cellular Ca2+ gain through Na+-Ca2+ exchange.	bind
23284	2	6776	5	13	NULL	NULL	NULL	statement 1	Process		occurs with					ATP	Chemical	degradation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_3_975_s_36	9264509	17 18  During myocardial ischemia, Mgi increases with degradation of ATP, which binds most Mgi. 19 20 21 22  Increased Mgi levels could be harmful to cardiac cells if they are compensated for by Mg2+ efflux through Na+-Mg2+ countertransport, which in turn would promote excess cellular Ca2+ gain through Na+-Ca2+ exchange.	bind
23285	3	6776	5	13	NULL	NULL	NULL	ATP	Chemical		bind					Mgi	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_3_975_s_36	9264509	17 18  During myocardial ischemia, Mgi increases with degradation of ATP, which binds most Mgi. 19 20 21 22  Increased Mgi levels could be harmful to cardiac cells if they are compensated for by Mg2+ efflux through Na+-Mg2+ countertransport, which in turn would promote excess cellular Ca2+ gain through Na+-Ca2+ exchange.	bind
23286	4	6776	5	13	NULL	NULL	NULL	Mgi	Chemical	increased levels of	is harmful for		could be			cardiac cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_3_975_s_36	9264509	17 18  During myocardial ischemia, Mgi increases with degradation of ATP, which binds most Mgi. 19 20 21 22  Increased Mgi levels could be harmful to cardiac cells if they are compensated for by Mg2+ efflux through Na+-Mg2+ countertransport, which in turn would promote excess cellular Ca2+ gain through Na+-Ca2+ exchange.	bind
23287	5	6776	5	13	NULL	NULL	NULL	statement 4	Process		occurs when					Mg2+ 	Chemical	compensated for by efflux of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_3_975_s_36	9264509	17 18  During myocardial ischemia, Mgi increases with degradation of ATP, which binds most Mgi. 19 20 21 22  Increased Mgi levels could be harmful to cardiac cells if they are compensated for by Mg2+ efflux through Na+-Mg2+ countertransport, which in turn would promote excess cellular Ca2+ gain through Na+-Ca2+ exchange.	bind
23288	6	6776	5	13	NULL	NULL	NULL	Mg2+ efflux	Process		occurs through					Na+-Mg2+ 	Process	countertransport of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_3_975_s_36	9264509	17 18  During myocardial ischemia, Mgi increases with degradation of ATP, which binds most Mgi. 19 20 21 22  Increased Mgi levels could be harmful to cardiac cells if they are compensated for by Mg2+ efflux through Na+-Mg2+ countertransport, which in turn would promote excess cellular Ca2+ gain through Na+-Ca2+ exchange.	bind
23289	7	6776	5	13	NULL	NULL	NULL	statement 5	Process		promotes					Ca2+	Chemical	excess cellular gain of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_3_975_s_36	9264509	17 18  During myocardial ischemia, Mgi increases with degradation of ATP, which binds most Mgi. 19 20 21 22  Increased Mgi levels could be harmful to cardiac cells if they are compensated for by Mg2+ efflux through Na+-Mg2+ countertransport, which in turn would promote excess cellular Ca2+ gain through Na+-Ca2+ exchange.	bind
23291	8	6776	5	13	NULL	NULL	NULL	statement 7	Process		occurs through					Na+-Ca2+ 	Chemical	exchange of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_3_975_s_36	9264509	17 18  During myocardial ischemia, Mgi increases with degradation of ATP, which binds most Mgi. 19 20 21 22  Increased Mgi levels could be harmful to cardiac cells if they are compensated for by Mg2+ efflux through Na+-Mg2+ countertransport, which in turn would promote excess cellular Ca2+ gain through Na+-Ca2+ exchange.	bind
19825	1	6776	6	NULL	NULL	0	NULL	Mgi	NULL		increases with	NULL				ATP	NULL	degradation of			NULL		0	NULL	NULL	NULL	gw60_circulation_96_3_975_s_36	9264509	17 18  During myocardial ischemia, Mgi increases with degradation of ATP, which binds most Mgi. 19 20 21 22  Increased Mgi levels could be harmful to cardiac cells if they are compensated for by Mg2+ efflux through Na+-Mg2+ countertransport, which in turn would promote excess cellular Ca2+ gain through Na+-Ca2+ exchange.	bind
19826	2	6776	6	NULL	NULL	0	NULL	statement 1	NULL		occurs during	NULL				myocardial ischemia	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_96_3_975_s_36	9264509	17 18  During myocardial ischemia, Mgi increases with degradation of ATP, which binds most Mgi. 19 20 21 22  Increased Mgi levels could be harmful to cardiac cells if they are compensated for by Mg2+ efflux through Na+-Mg2+ countertransport, which in turn would promote excess cellular Ca2+ gain through Na+-Ca2+ exchange.	bind
20098	3	6776	6	NULL	NULL	0	NULL	Mgi	NULL		bind	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_96_3_975_s_36	9264509	17 18  During myocardial ischemia, Mgi increases with degradation of ATP, which binds most Mgi. 19 20 21 22  Increased Mgi levels could be harmful to cardiac cells if they are compensated for by Mg2+ efflux through Na+-Mg2+ countertransport, which in turn would promote excess cellular Ca2+ gain through Na+-Ca2+ exchange.	bind
56556	4	6776	6	10	NULL	0	NULL	Mgi 		increased levels of	harmful for		could be			cardiac cells					NULL		0	NULL	NULL	NULL	gw60_circulation_96_3_975_s_36	9264509	17 18  During myocardial ischemia, Mgi increases with degradation of ATP, which binds most Mgi. 19 20 21 22  Increased Mgi levels could be harmful to cardiac cells if they are compensated for by Mg2+ efflux through Na+-Mg2+ countertransport, which in turn would promote excess cellular Ca2+ gain through Na+-Ca2+ exchange.	bind
56557	5	6776	6	10	NULL	0	NULL	statement 4			occurs when					Mg2+		compensated for by efflux of			NULL		0	NULL	NULL	NULL	gw60_circulation_96_3_975_s_36	9264509	17 18  During myocardial ischemia, Mgi increases with degradation of ATP, which binds most Mgi. 19 20 21 22  Increased Mgi levels could be harmful to cardiac cells if they are compensated for by Mg2+ efflux through Na+-Mg2+ countertransport, which in turn would promote excess cellular Ca2+ gain through Na+-Ca2+ exchange.	bind
56558	6	6776	6	10	NULL	0	NULL	Mg2+		efflux of	occur through					Na+-Mg2+ 		countertransport of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_3_975_s_36	9264509	17 18  During myocardial ischemia, Mgi increases with degradation of ATP, which binds most Mgi. 19 20 21 22  Increased Mgi levels could be harmful to cardiac cells if they are compensated for by Mg2+ efflux through Na+-Mg2+ countertransport, which in turn would promote excess cellular Ca2+ gain through Na+-Ca2+ exchange.	bind
56559	7	6776	6	10	NULL	0	NULL	statement 5			promotes					Ca2+		excess cellular gain of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_3_975_s_36	9264509	17 18  During myocardial ischemia, Mgi increases with degradation of ATP, which binds most Mgi. 19 20 21 22  Increased Mgi levels could be harmful to cardiac cells if they are compensated for by Mg2+ efflux through Na+-Mg2+ countertransport, which in turn would promote excess cellular Ca2+ gain through Na+-Ca2+ exchange.	bind
56560	8	6776	6	10	NULL	0	NULL	statement 7			occur through					Na+-Ca2+		exchange of			NULL		0	NULL	NULL	NULL	gw60_circulation_96_3_975_s_36	9264509	17 18  During myocardial ischemia, Mgi increases with degradation of ATP, which binds most Mgi. 19 20 21 22  Increased Mgi levels could be harmful to cardiac cells if they are compensated for by Mg2+ efflux through Na+-Mg2+ countertransport, which in turn would promote excess cellular Ca2+ gain through Na+-Ca2+ exchange.	bind
23292	1	6777	5	13	NULL	NULL	NULL	NOS1	GP		bind			latch domain		calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_15	8781470	17 18  In NOS1 and NOS3, physiological concentrations of Ca2+ in cells regulate the binding of calmodulin to the "`latch domain,"` thereby initiating electron transfer from the flavins to the heme moieties.	bind
23293	2	6777	5	13	NULL	NULL	NULL	NOS3	GP		bind			latch domain		calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_15	8781470	17 18  In NOS1 and NOS3, physiological concentrations of Ca2+ in cells regulate the binding of calmodulin to the "`latch domain,"` thereby initiating electron transfer from the flavins to the heme moieties.	bind
23294	3	6777	5	13	NULL	NULL	NULL	Ca2+	Chemical	physiological concentrations of	regulates					statement 1	Process				NULL	in cells	NULL	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_15	8781470	17 18  In NOS1 and NOS3, physiological concentrations of Ca2+ in cells regulate the binding of calmodulin to the "`latch domain,"` thereby initiating electron transfer from the flavins to the heme moieties.	bind
23297	4	6777	5	13	NULL	NULL	NULL	ca2+	Chemical	physiological concentrations of	regulates					statement 2	Process				NULL	in cells	NULL	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_15	8781470	17 18  In NOS1 and NOS3, physiological concentrations of Ca2+ in cells regulate the binding of calmodulin to the "`latch domain,"` thereby initiating electron transfer from the flavins to the heme moieties.	bind
23298	5	6777	5	13	NULL	NULL	NULL	flavins	Chemical	electrons from	transferred to					heme moieties	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_15	8781470	17 18  In NOS1 and NOS3, physiological concentrations of Ca2+ in cells regulate the binding of calmodulin to the "`latch domain,"` thereby initiating electron transfer from the flavins to the heme moieties.	bind
23299	6	6777	5	13	NULL	NULL	NULL	statement 3	Process		initiates					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_15	8781470	17 18  In NOS1 and NOS3, physiological concentrations of Ca2+ in cells regulate the binding of calmodulin to the "`latch domain,"` thereby initiating electron transfer from the flavins to the heme moieties.	bind
56561	7	6777	5	13	NULL	NULL	NULL	statement 4	Process		initiates					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_15	8781470	17 18  In NOS1 and NOS3, physiological concentrations of Ca2+ in cells regulate the binding of calmodulin to the "`latch domain,"` thereby initiating electron transfer from the flavins to the heme moieties.	bind
19587	1	6777	6	10	NULL	0	NULL	calmodulin			bind					NOS1			latch domain		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_15	8781470	17 18  In NOS1 and NOS3, physiological concentrations of Ca2+ in cells regulate the binding of calmodulin to the "`latch domain,"` thereby initiating electron transfer from the flavins to the heme moieties.	bind
19588	2	6777	6	10	NULL	0	NULL	Calmodulin			bind					NOS3			latch domain		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_15	8781470	17 18  In NOS1 and NOS3, physiological concentrations of Ca2+ in cells regulate the binding of calmodulin to the "`latch domain,"` thereby initiating electron transfer from the flavins to the heme moieties.	bind
19589	3	6777	6	NULL	NULL	0	NULL	Ca2+	NULL	physiological concentrations of	regulates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_15	8781470	17 18  In NOS1 and NOS3, physiological concentrations of Ca2+ in cells regulate the binding of calmodulin to the "`latch domain,"` thereby initiating electron transfer from the flavins to the heme moieties.	bind
19590	4	6777	6	NULL	NULL	0	NULL	Ca2+	NULL	physiological concentrations of	regulates	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_15	8781470	17 18  In NOS1 and NOS3, physiological concentrations of Ca2+ in cells regulate the binding of calmodulin to the "`latch domain,"` thereby initiating electron transfer from the flavins to the heme moieties.	bind
19591	5	6777	6	10	NULL	0	NULL	flavins		electron from	transferred to					heme moieties					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_15	8781470	17 18  In NOS1 and NOS3, physiological concentrations of Ca2+ in cells regulate the binding of calmodulin to the "`latch domain,"` thereby initiating electron transfer from the flavins to the heme moieties.	bind
19592	6	6777	6	10	NULL	0	NULL	statement 3			initiates					statement 5					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_15	8781470	17 18  In NOS1 and NOS3, physiological concentrations of Ca2+ in cells regulate the binding of calmodulin to the "`latch domain,"` thereby initiating electron transfer from the flavins to the heme moieties.	bind
19593	7	6777	6	10	NULL	0	NULL	statement 4			initiates					statement 5					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_15	8781470	17 18  In NOS1 and NOS3, physiological concentrations of Ca2+ in cells regulate the binding of calmodulin to the "`latch domain,"` thereby initiating electron transfer from the flavins to the heme moieties.	bind
23319	1	6778	5	13	NULL	NULL	NULL	osteopontin	GP		regulate		may			vascular calcification	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_2_166_s_37	9933248	17 18 19  These data suggest that osteopontin might be an important regulator of vascular calcification.	bind
19594	1	6778	6	NULL	NULL	0	NULL	osteopontin	NULL		regulates	NULL	may			vascular calcification	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_2_166_s_37	9933248	17 18 19  These data suggest that osteopontin might be an important regulator of vascular calcification.	bind
23321	1	6779	5	13	NULL	NULL	NULL	E1A gene product	GP	adenovirus	bind					RB	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_184	10205150	17 18 29 47 48 49  The adenovirus E1A gene product binds to RB, which releases E2F, and E1A-induced apoptosis is dependent on E2F.	bind
23322	2	6779	5	13	NULL	NULL	NULL	RB	GP		release					E2F	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_184	10205150	17 18 29 47 48 49  The adenovirus E1A gene product binds to RB, which releases E2F, and E1A-induced apoptosis is dependent on E2F.	bind
23324	4	6779	5	13	NULL	NULL	NULL	statement 3	Process		is dependent on					E2F	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_184	10205150	17 18 29 47 48 49  The adenovirus E1A gene product binds to RB, which releases E2F, and E1A-induced apoptosis is dependent on E2F.	bind
44689	3	6779	5	13	NULL	NULL	NULL	E1A	GP		induce					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_184	10205150	17 18 29 47 48 49  The adenovirus E1A gene product binds to RB, which releases E2F, and E1A-induced apoptosis is dependent on E2F.	bind
19595	1	6779	6	NULL	NULL	0	NULL	E1A gene product	NULL	Adenovirus	bind	NULL				RB	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_184	10205150	17 18 29 47 48 49  The adenovirus E1A gene product binds to RB, which releases E2F, and E1A-induced apoptosis is dependent on E2F.	bind
19596	2	6779	6	NULL	NULL	0	NULL	RB	NULL		releases	NULL				E2F	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_184	10205150	17 18 29 47 48 49  The adenovirus E1A gene product binds to RB, which releases E2F, and E1A-induced apoptosis is dependent on E2F.	bind
19597	4	6779	6	10	NULL	0	NULL	statement 3	NULL		is dependent on	NULL				E2F	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_184	10205150	17 18 29 47 48 49  The adenovirus E1A gene product binds to RB, which releases E2F, and E1A-induced apoptosis is dependent on E2F.	bind
44690	3	6779	6	10	NULL	0	NULL	E1A	NULL		induce	NULL				apoptosis	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_184	10205150	17 18 29 47 48 49  The adenovirus E1A gene product binds to RB, which releases E2F, and E1A-induced apoptosis is dependent on E2F.	bind
23326	1	6780	5	13	NULL	NULL	NULL	FVII 	GP		bind					TG-rich particles	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_8_1539_s_122	9301633	17 21  The correlation between FVIIc and lipoproteins may be explained by the binding of FVII to TG-rich particles.	bind
19598	1	6780	6	NULL	NULL	0	NULL	FVII	NULL		bind	NULL				TG-rich particles	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_8_1539_s_122	9301633	17 21  The correlation between FVIIc and lipoproteins may be explained by the binding of FVII to TG-rich particles.	bind
28356	1	6781	5	13	NULL	NULL	NULL	apolipoprotein	GP		mediate					lipid efflux	Process	defect in			NULL	in Tangier cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1813_s_181	9327782	17 27 38 39  The lack of acceptor specificity in the apolipoprotein-mediated lipid efflux defect in Tangier cells makes it less likely that a defect in the binding of apoA-I to Tangier cells 11  is the mechanism for the decreased lipid efflux.	bind
28358	2	6781	5	13	NULL	NULL	NULL	acceptor specificity	Process		is absent in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1813_s_181	9327782	17 27 38 39  The lack of acceptor specificity in the apolipoprotein-mediated lipid efflux defect in Tangier cells makes it less likely that a defect in the binding of apoA-I to Tangier cells 11  is the mechanism for the decreased lipid efflux.	bind
28359	3	6781	5	13	NULL	NULL	NULL	apoA-I	GP		bind					Tangier cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1813_s_181	9327782	17 27 38 39  The lack of acceptor specificity in the apolipoprotein-mediated lipid efflux defect in Tangier cells makes it less likely that a defect in the binding of apoA-I to Tangier cells 11  is the mechanism for the decreased lipid efflux.	bind
28362	4	6781	5	13	NULL	NULL	NULL	statement 3	Process	defect in	decreases					lipid efflux	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1813_s_181	9327782	17 27 38 39  The lack of acceptor specificity in the apolipoprotein-mediated lipid efflux defect in Tangier cells makes it less likely that a defect in the binding of apoA-I to Tangier cells 11  is the mechanism for the decreased lipid efflux.	bind
19599	1	6781	6	NULL	NULL	0	NULL	apoA-I	NULL		bind	NULL				Tangier cells	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1813_s_181	9327782	17 27 38 39  The lack of acceptor specificity in the apolipoprotein-mediated lipid efflux defect in Tangier cells makes it less likely that a defect in the binding of apoA-I to Tangier cells 11  is the mechanism for the decreased lipid efflux.	bind
19600	3	6781	6	10	NULL	0	NULL	acceptor specificity	NULL		lacks in	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1813_s_181	9327782	17 27 38 39  The lack of acceptor specificity in the apolipoprotein-mediated lipid efflux defect in Tangier cells makes it less likely that a defect in the binding of apoA-I to Tangier cells 11  is the mechanism for the decreased lipid efflux.	bind
44692	2	6781	6	10	NULL	0	NULL	apolipoprotein	NULL		mediates	NULL				lipid efflux	NULL	defect in			NULL	Tangier cells	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1813_s_181	9327782	17 27 38 39  The lack of acceptor specificity in the apolipoprotein-mediated lipid efflux defect in Tangier cells makes it less likely that a defect in the binding of apoA-I to Tangier cells 11  is the mechanism for the decreased lipid efflux.	bind
44693	4	6781	6	10	NULL	0	NULL	statement 1	NULL	defect in	decrease	NULL				lipid efflux	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1813_s_181	9327782	17 27 38 39  The lack of acceptor specificity in the apolipoprotein-mediated lipid efflux defect in Tangier cells makes it less likely that a defect in the binding of apoA-I to Tangier cells 11  is the mechanism for the decreased lipid efflux.	bind
23328	1	6782	5	13	NULL	NULL	NULL	nuclear protein	GP		bind					NF-kappaB-3'	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_295_s_266	9710122	17 34  35  Our results have shown that HMG I(Y) protein facilitates nuclear protein binding with NF-kappaB-3' and with TATA box elements.	bind
23329	2	6782	5	13	NULL	NULL	NULL	HMG I(Y) protein	GP		facilitates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_295_s_266	9710122	17 34  35  Our results have shown that HMG I(Y) protein facilitates nuclear protein binding with NF-kappaB-3' and with TATA box elements.	bind
23330	3	6782	5	13	NULL	NULL	NULL	nuclear protein	GP		bind									TATA box elements	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_295_s_266	9710122	17 34  35  Our results have shown that HMG I(Y) protein facilitates nuclear protein binding with NF-kappaB-3' and with TATA box elements.	bind
23331	4	6782	5	13	NULL	NULL	NULL	HMG I(Y) protein	GP		facilitates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_295_s_266	9710122	17 34  35  Our results have shown that HMG I(Y) protein facilitates nuclear protein binding with NF-kappaB-3' and with TATA box elements.	bind
19827	1	6782	6	NULL	NULL	0	NULL	nuclear protein	NULL		bind	NULL					NULL			NF-kappaB-3' element	NULL		0	NULL	NULL	NULL	gw60_circulationres_83_3_295_s_266	9710122	17 34  35  Our results have shown that HMG I(Y) protein facilitates nuclear protein binding with NF-kappaB-3' and with TATA box elements.	bind
19828	2	6782	6	NULL	NULL	0	NULL	Nuclear protein	NULL		bind	NULL					NULL			TATA box	NULL		0	NULL	NULL	NULL	gw60_circulationres_83_3_295_s_266	9710122	17 34  35  Our results have shown that HMG I(Y) protein facilitates nuclear protein binding with NF-kappaB-3' and with TATA box elements.	bind
19829	3	6782	6	NULL	NULL	0	NULL	HMG I(Y) protein	NULL		facilitates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_3_295_s_266	9710122	17 34  35  Our results have shown that HMG I(Y) protein facilitates nuclear protein binding with NF-kappaB-3' and with TATA box elements.	bind
19830	4	6782	6	NULL	NULL	0	NULL	HMG I(Y) protein	NULL		facilitates	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_3_295_s_266	9710122	17 34  35  Our results have shown that HMG I(Y) protein facilitates nuclear protein binding with NF-kappaB-3' and with TATA box elements.	bind
23332	1	6783	5	13	NULL	NULL	NULL	Atorvastatin	Chemical		inhibit					ethinyl estradiol	Chemical	metabolism of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_1_32_s_112	12515739	17 Atorvastatin has previously been shown to inhibit the metabolism of only a few substrates, such as ethinyl estradiol, 19 which binds CYP3A4  30-fold less tightly than atorvastatin lactone and is also present in vivo at low concentrations.	bind
23333	2	6783	5	13	NULL	NULL	NULL	ethinyl estradiol	Chemical		bind					CYP3A4	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_1_32_s_112	12515739	17 Atorvastatin has previously been shown to inhibit the metabolism of only a few substrates, such as ethinyl estradiol, 19 which binds CYP3A4  30-fold less tightly than atorvastatin lactone and is also present in vivo at low concentrations.	bind
23334	3	6783	5	13	NULL	NULL	NULL	ethinyl estradiol	Chemical		bind					atorvastatin lactone	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_1_32_s_112	12515739	17 Atorvastatin has previously been shown to inhibit the metabolism of only a few substrates, such as ethinyl estradiol, 19 which binds CYP3A4  30-fold less tightly than atorvastatin lactone and is also present in vivo at low concentrations.	bind
23335	4	6783	5	13	NULL	NULL	NULL	statement 2	Process		less tightly than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_1_32_s_112	12515739	17 Atorvastatin has previously been shown to inhibit the metabolism of only a few substrates, such as ethinyl estradiol, 19 which binds CYP3A4  30-fold less tightly than atorvastatin lactone and is also present in vivo at low concentrations.	bind
19602	1	6783	6	NULL	NULL	0	NULL	ethinyl estradiol	NULL		bind	NULL				CYP3A4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_107_1_32_s_112	12515739	17 Atorvastatin has previously been shown to inhibit the metabolism of only a few substrates, such as ethinyl estradiol, 19 which binds CYP3A4  30-fold less tightly than atorvastatin lactone and is also present in vivo at low concentrations.	bind
19603	2	6783	6	NULL	NULL	0	NULL	atorvastatin lactone	NULL		bind	NULL				CYP3A4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_107_1_32_s_112	12515739	17 Atorvastatin has previously been shown to inhibit the metabolism of only a few substrates, such as ethinyl estradiol, 19 which binds CYP3A4  30-fold less tightly than atorvastatin lactone and is also present in vivo at low concentrations.	bind
19604	3	6783	6	NULL	NULL	0	NULL	statement 2	NULL		is less as compared to	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_107_1_32_s_112	12515739	17 Atorvastatin has previously been shown to inhibit the metabolism of only a few substrates, such as ethinyl estradiol, 19 which binds CYP3A4  30-fold less tightly than atorvastatin lactone and is also present in vivo at low concentrations.	bind
19605	4	6783	6	NULL	NULL	0	NULL	Atorvastatin	NULL		inhibits	NULL				ethinyl estradiol	NULL	metabolism of 			NULL		0	NULL	NULL	NULL	gw60_circulation_107_1_32_s_112	12515739	17 Atorvastatin has previously been shown to inhibit the metabolism of only a few substrates, such as ethinyl estradiol, 19 which binds CYP3A4  30-fold less tightly than atorvastatin lactone and is also present in vivo at low concentrations.	bind
23390	1	6784	5	13	NULL	NULL	NULL	CD40L	GP		bind					CD40 receptor	GP				NULL	on the surface of endothelial cells	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23391	2	6784	5	13	NULL	NULL	NULL	CD40L	GP		bind					CD40 receptor	GP				NULL	on the surface of smooth muscle cells	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23392	3	6784	5	13	NULL	NULL	NULL	CD40L	GP		bind					CD40 receptor	GP				NULL	on the surface of macrophages	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23393	4	6784	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23394	5	6784	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23395	6	6784	5	13	NULL	NULL	NULL	statement 1	Process		triggers					cytokines	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23396	7	6784	5	13	NULL	NULL	NULL	statement 1	Process		triggers					chemokines	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23397	8	6784	5	13	NULL	NULL	NULL	statement 1	Process		triggers					growth factors	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23398	9	6784	5	13	NULL	NULL	NULL	statement 1	Process		triggers					matrix metalloproteinases	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23399	10	6784	5	13	NULL	NULL	NULL	statement 1	Process		triggers					adhesion molecules	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23400	11	6784	5	13	NULL	NULL	NULL	statement 1	Process		triggers					procoagulants	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23401	12	6784	5	13	NULL	NULL	NULL	statement 2	Process		triggers					cytokines	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23402	13	6784	5	13	NULL	NULL	NULL	statement 2	Process		triggers					chemokines	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23403	14	6784	5	13	NULL	NULL	NULL	statement 2	Process		triggers					growth factors	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23404	15	6784	5	13	NULL	NULL	NULL	statement 2	Process		triggers					matrix metalloproteinases	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23405	16	6784	5	13	NULL	NULL	NULL	statement 2	Process		triggers					adhesion molecules	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23406	17	6784	5	13	NULL	NULL	NULL	statement 2	Process		triggers					procoagulants	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23407	18	6784	5	13	NULL	NULL	NULL	statement 3	Process		triggers					cytokines	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23408	19	6784	5	13	NULL	NULL	NULL	statement 3	Process		triggers					chemokines	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23409	20	6784	5	13	NULL	NULL	NULL	statement 3	Process		triggers					growth factors	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23410	21	6784	5	13	NULL	NULL	NULL	statement 3	Process		triggers					matrix metalloproteinases	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23411	22	6784	5	13	NULL	NULL	NULL	statement 3	Process		triggers					adhesion molecules	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23412	23	6784	5	13	NULL	NULL	NULL	statement 3	Process		triggers					procoagulants	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23413	24	6784	5	13	NULL	NULL	NULL	statement 6	Process		elaborate					inflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23414	25	6784	5	13	NULL	NULL	NULL	statement 7	Process		elaborate					inflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23415	26	6784	5	13	NULL	NULL	NULL	statement 8	Process		elaborate					inflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23416	27	6784	5	13	NULL	NULL	NULL	statement 9	Process		elaborate					inflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23417	28	6784	5	13	NULL	NULL	NULL	statement 10	Process		elaborate					inflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23418	29	6784	5	13	NULL	NULL	NULL	statement 11	Process		elaborate					inflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23419	30	6784	5	13	NULL	NULL	NULL	statement 12	Process		elaborate					inflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23420	31	6784	5	13	NULL	NULL	NULL	statement 13	Process		elaborate					inflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23421	32	6784	5	13	NULL	NULL	NULL	statement 14	Process		elaborate					inflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23422	33	6784	5	13	NULL	NULL	NULL	statement 15	Process		elaborate					inflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23423	34	6784	5	13	NULL	NULL	NULL	statement 16	Process		elaborate					inflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23424	35	6784	5	13	NULL	NULL	NULL	statement 17	Process		elaborate					inflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23425	36	6784	5	13	NULL	NULL	NULL	statement 18	Process		elaborate					inflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23426	37	6784	5	13	NULL	NULL	NULL	statement 19	Process		elaborate					inflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23427	38	6784	5	13	NULL	NULL	NULL	statement 20	Process		elaborate					inflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23428	39	6784	5	13	NULL	NULL	NULL	statement 21	Process		elaborate					inflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23429	40	6784	5	13	NULL	NULL	NULL	statement 22	Process		elaborate					inflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23430	41	6784	5	13	NULL	NULL	NULL	statement 23	Process		elaborate					inflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
19606	1	6784	6	NULL	NULL	0	NULL	CD40L	NULL		bind	NULL				CD40 receptor	NULL				NULL	surface of endothelial cells	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
19669	2	6784	6	NULL	NULL	0	NULL	CD40L	NULL		bind	NULL				CD40 receptor	NULL				NULL	surface of smooth muscle cells	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
19670	3	6784	6	NULL	NULL	0	NULL	CD40L	NULL		bind	NULL				CD40 receptor	NULL				NULL	surface of macrophages	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
19671	4	6784	6	NULL	NULL	0	NULL	statement 1	NULL		triggers	NULL				cytokines	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
20099	5	6784	6	NULL	NULL	0	NULL	statement 2	NULL		triggers	NULL				cytokines	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
20100	6	6784	6	NULL	NULL	0	NULL	statement 3	NULL		triggers	NULL				cytokines	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
20101	7	6784	6	NULL	NULL	0	NULL	statement 1	NULL		triggers	NULL				chemokines	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
20102	8	6784	6	NULL	NULL	0	NULL	statement 2	NULL		triggers	NULL				chemokines	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
20103	9	6784	6	NULL	NULL	0	NULL	statement 3	NULL		triggers	NULL				chemokines	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
20104	10	6784	6	NULL	NULL	0	NULL	statement 1	NULL		triggers	NULL				growth factors	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
20105	11	6784	6	NULL	NULL	0	NULL	statement 2	NULL		triggers	NULL				growth factors	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
20106	12	6784	6	NULL	NULL	0	NULL	statement 3	NULL		triggers	NULL				growth factors	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
20107	13	6784	6	NULL	NULL	0	NULL	statement 1	NULL		triggers	NULL				matrix metalloproteinases	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
20108	14	6784	6	NULL	NULL	0	NULL	statement 2	NULL		triggers	NULL				matrix metalloproteinases	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
20109	15	6784	6	NULL	NULL	0	NULL	statement 3	NULL		triggers	NULL				matrix metalloproteinases	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
20110	16	6784	6	NULL	NULL	0	NULL	statement 1	NULL		triggers	NULL				adhesion molecules	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
20111	17	6784	6	NULL	NULL	0	NULL	statement 2	NULL		triggers	NULL				adhesion molecules	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
20112	18	6784	6	NULL	NULL	0	NULL	statement 3	NULL		triggers	NULL				adhesion molecules	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
20113	19	6784	6	NULL	NULL	0	NULL	statement 1	NULL		triggers	NULL				procoagulants	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
20114	20	6784	6	NULL	NULL	0	NULL	statement 2	NULL		triggers	NULL				procoagulants	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
20115	21	6784	6	NULL	NULL	0	NULL	statement 3	NULL		triggers	NULL				procoagulants	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1088_s_20	15923539	17 Binding of CD40L to the CD40 receptor on the surface of endothelial cells, smooth muscle cells, or macrophages triggers the expression of cytokines, chemokines, growth factors, matrix metalloproteinases, adhesion molecules, and procoagulants, all of which elaborate the inflammatory response.	bind
23432	1	6785	5	13	NULL	NULL	NULL	self-associative interaction	Process		influence					ROCKs	GP	kinase activity of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
23433	2	6785	5	13	NULL	NULL	NULL	oligomerization (dimerization)	Process		influence					ROCKs	GP	kinase activity of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
23434	3	6785	5	13	NULL	NULL	NULL	ROCKs	GP		has affinity for					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
23435	4	6785	5	13	NULL	NULL	NULL	statement 3	Process	regulation of	leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
23436	5	6785	5	13	NULL	NULL	NULL	statement 3	Process	regulation of	leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
23438	6	6785	5	13	NULL	NULL	NULL	RhoA	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
23439	7	6785	5	13	NULL	NULL	NULL	statement 6	Process	active 	bind								RBD		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
23440	8	6785	5	13	NULL	NULL	NULL	statement 7	Process		stimulates					ROCKs	GP	phosphotransferase activity of 			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
23441	9	6785	5	13	NULL	NULL	NULL	ROCKs	GP		interacts with			catalytic C-terminal region		ROCKs	GP		inhibitory C-terminal region		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
23442	10	6785	5	13	NULL	NULL	NULL	statement 9	Process	disruption of	leads to					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
19672	1	6785	6	NULL	NULL	0	NULL	oligomerization (dimerization)	NULL		influences	NULL				ROCKs	NULL	kinase activity of			NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
19673	2	6785	6	NULL	NULL	0	NULL	ROCK	NULL		has affinity for	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
19674	4	6785	6	10	NULL	0	NULL	statement 3	NULL	active 	bind	NULL					NULL		RBD		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
19675	5	6785	6	10	NULL	0	NULL	statement 4	NULL		stimulates	NULL				ROCKs	NULL	phosphotransferase activity of 			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
19676	6	6785	6	10	NULL	0	NULL	ROCK	NULL		interacts with	NULL		catalytic region		ROCK	NULL	inhibitory	C-terminal region		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
19677	7	6785	6	10	NULL	0	NULL	statement 4	NULL		disrupts	NULL				statement 6	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
44695	3	6785	6	10	NULL	0	NULL	GTP	NULL		bind	NULL				RhoA	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
56562	8	6785	6	10	NULL	0	NULL	self-associative interaction			influence					ROCKs		kinase activity of			NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
56563	9	6785	6	10	NULL	0	NULL	statement 2		regulation of	leads to					statement 1					NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
56564	10	6785	6	10	NULL	0	NULL	statement 2		regulation of	leads to					statement 8					NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_322_s_48	16484628	17 In addition to this self-associative interaction, oligomerization (dimerization) also influences the kinase activity of ROCKs by regulating its affinity for ATP. 18 Binding of active GTP-bound form of RhoA to RBD stimulates the phosphotransferase activity of ROCKs by disrupting the interaction between the catalytic and the inhibitory C-terminal region of the enzyme ( Figure 2).	bind
23443	1	6786	5	13	NULL	NULL	NULL	sCD40L	GP		promote					platelets	Cell	aggregation of;;human			NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
23444	2	6786	5	13	NULL	NULL	NULL	statement 1	Process		under conditions of					shear		high			NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
23445	3	6786	5	13	NULL	NULL	NULL	sCD40L	GP		promote					platelets	Cell	aggregation of;;mouse			NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
23446	4	6786	5	13	NULL	NULL	NULL	statement 3	Process		under conditions of					shear		high			NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
23447	5	6786	5	13	NULL	NULL	NULL	sCD40L	GP		bind					GP IIb/IIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
23448	6	6786	5	13	NULL	NULL	NULL	statement 5	Process		results in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
23449	7	6786	5	13	NULL	NULL	NULL	statement 5	Process		results in					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
23450	8	6786	5	13	NULL	NULL	NULL	sCD40L	GP		is agonist of					platelet	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
23475	9	6786	5	13	NULL	NULL	NULL	sCD40L	GP		is necessary for					thrombi stability	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
23476	10	6786	5	13	NULL	NULL	NULL	statement 9	Process		under conditions of					arterial shear					NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
19678	1	6786	6	NULL	NULL	0	NULL	sCD40L	NULL		bind	NULL				GP IIb/IIa	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
19679	2	6786	6	10	NULL	0	NULL	sCD40L			promotes					platelets		aggregation of;;human			NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
19680	3	6786	6	10	NULL	0	NULL	sCD40L			promotes					platelets		aggregation of;;mouse			NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
19681	4	6786	6	NULL	NULL	0	NULL	statement 2	NULL		occurs under conditions of	NULL				shear	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
19682	5	6786	6	NULL	NULL	0	NULL	statement 3	NULL		occurs under conditions of	NULL				shear	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
19683	6	6786	6	10	NULL	0	NULL	sCD40L			is agonist of					platelet					NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
19684	7	6786	6	NULL	NULL	0	NULL	sCD40L	NULL		is necessary for	NULL				thrombi stability	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
19685	8	6786	6	NULL	NULL	0	NULL	statement 7	NULL		occurs under conditions of	NULL				arterial shear	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
56565	9	6786	6	10	NULL	0	NULL	statement 1			result in					statement 2					NULL		0	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
56566	10	6786	6	10	NULL	0	NULL	statement 1			result in					statement 3					NULL		0	NULL	NULL	NULL	gw60_circulation_105_24_2849_s_146	12070112	17 In addition, sCD40L has been shown to promote the aggregation of human or mouse platelets under conditions of high shear, an activity that results from sCD40L binding to GP IIb/IIa. 17 Thus, sCD40L appears to be a platelet agonist and necessary for thrombi stability under conditions of arterial shear.	bind
23477	1	6788	5	13	NULL	NULL	NULL	SMC	Cell	degenerate	limits				CArG box 	SRF	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_82	16614312	17 Our laboratory has provided evidence that this degenerate SMC CArG box serves to limit SRF binding, thereby restricting expression of SMC markers to cells that express high levels of SRF and/or cells like SMCs that have evolved mechanisms to enhance SRF binding to degenerate CArGs, ie, a SMC-selective transcriptional SRF cofactor.	bind
23478	2	6788	5	13	NULL	NULL	NULL	statement 1	Process		restricts					SMC markers	GP	expression of			NULL	cells expressing high levels of SRF	NULL	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_82	16614312	17 Our laboratory has provided evidence that this degenerate SMC CArG box serves to limit SRF binding, thereby restricting expression of SMC markers to cells that express high levels of SRF and/or cells like SMCs that have evolved mechanisms to enhance SRF binding to degenerate CArGs, ie, a SMC-selective transcriptional SRF cofactor.	bind
28366	3	6788	5	13	NULL	NULL	NULL	statement 1	Process		restricts					SMC markers	GP	expression of			NULL	SMCs	NULL	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_82	16614312	17 Our laboratory has provided evidence that this degenerate SMC CArG box serves to limit SRF binding, thereby restricting expression of SMC markers to cells that express high levels of SRF and/or cells like SMCs that have evolved mechanisms to enhance SRF binding to degenerate CArGs, ie, a SMC-selective transcriptional SRF cofactor.	bind
28367	4	6788	5	13	NULL	NULL	NULL	SRF	GP	binding of	degenerates									CArGs	NULL	SMCs	NULL	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_82	16614312	17 Our laboratory has provided evidence that this degenerate SMC CArG box serves to limit SRF binding, thereby restricting expression of SMC markers to cells that express high levels of SRF and/or cells like SMCs that have evolved mechanisms to enhance SRF binding to degenerate CArGs, ie, a SMC-selective transcriptional SRF cofactor.	bind
28371	5	6788	5	13	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_82	16614312	17 Our laboratory has provided evidence that this degenerate SMC CArG box serves to limit SRF binding, thereby restricting expression of SMC markers to cells that express high levels of SRF and/or cells like SMCs that have evolved mechanisms to enhance SRF binding to degenerate CArGs, ie, a SMC-selective transcriptional SRF cofactor.	bind
19831	1	6788	6	10	NULL	0	NULL			degenerate	limits				CArG box	SRF		binding of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_82	16614312	17 Our laboratory has provided evidence that this degenerate SMC CArG box serves to limit SRF binding, thereby restricting expression of SMC markers to cells that express high levels of SRF and/or cells like SMCs that have evolved mechanisms to enhance SRF binding to degenerate CArGs, ie, a SMC-selective transcriptional SRF cofactor.	bind
20116	2	6788	6	10	NULL	0	NULL	statement 1			restricts					SMC markers		expression of			NULL	cells expressing high levels of SRF	NULL	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_82	16614312	17 Our laboratory has provided evidence that this degenerate SMC CArG box serves to limit SRF binding, thereby restricting expression of SMC markers to cells that express high levels of SRF and/or cells like SMCs that have evolved mechanisms to enhance SRF binding to degenerate CArGs, ie, a SMC-selective transcriptional SRF cofactor.	bind
44696	3	6788	6	10	NULL	0	NULL	statement 1			restricts					SMC markers		expression of			NULL	SMCs	NULL	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_82	16614312	17 Our laboratory has provided evidence that this degenerate SMC CArG box serves to limit SRF binding, thereby restricting expression of SMC markers to cells that express high levels of SRF and/or cells like SMCs that have evolved mechanisms to enhance SRF binding to degenerate CArGs, ie, a SMC-selective transcriptional SRF cofactor.	bind
57785	5	6788	6	10	NULL	0	NULL	statement 2			is an alternative to					statement 3					NULL		0	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_82	16614312	17 Our laboratory has provided evidence that this degenerate SMC CArG box serves to limit SRF binding, thereby restricting expression of SMC markers to cells that express high levels of SRF and/or cells like SMCs that have evolved mechanisms to enhance SRF binding to degenerate CArGs, ie, a SMC-selective transcriptional SRF cofactor.	bind
57786	4	6788	6	10	NULL	0	NULL	SRF		binding of	degenerates									CArGs	NULL	SMCs	NULL	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_82	16614312	17 Our laboratory has provided evidence that this degenerate SMC CArG box serves to limit SRF binding, thereby restricting expression of SMC markers to cells that express high levels of SRF and/or cells like SMCs that have evolved mechanisms to enhance SRF binding to degenerate CArGs, ie, a SMC-selective transcriptional SRF cofactor.	bind
23479	1	6789	5	13	NULL	NULL	NULL	ST2	GP		does not bind					interleukin-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_5_721_s_101	12578875	17 Subsequently, a membrane-anchored receptor form of ST2 was identified, 18 consisting of an extracellular domain identical to ST2, a transmembrane domain, and an intracellular domain, all with homology to the interleukin-1 receptor, although ST2 does not bind interleukin-1.	bind
23480	2	6789	5	13	NULL	NULL	NULL	ST2 receptor	GP	membrane-anchored 	homologous to					interleukin-1 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_5_721_s_101	12578875	17 Subsequently, a membrane-anchored receptor form of ST2 was identified, 18 consisting of an extracellular domain identical to ST2, a transmembrane domain, and an intracellular domain, all with homology to the interleukin-1 receptor, although ST2 does not bind interleukin-1.	bind
56569	3	6789	5	13	NULL	NULL	NULL	ST2 receptor	GP	membrane-anchored	consist of								 extracellular domain		NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_5_721_s_101	12578875	17 Subsequently, a membrane-anchored receptor form of ST2 was identified, 18 consisting of an extracellular domain identical to ST2, a transmembrane domain, and an intracellular domain, all with homology to the interleukin-1 receptor, although ST2 does not bind interleukin-1.	bind
56570	4	6789	5	13	NULL	NULL	NULL	ST2 receptor	GP	membrane-anchored	consist of								transmembrane domain		NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_5_721_s_101	12578875	17 Subsequently, a membrane-anchored receptor form of ST2 was identified, 18 consisting of an extracellular domain identical to ST2, a transmembrane domain, and an intracellular domain, all with homology to the interleukin-1 receptor, although ST2 does not bind interleukin-1.	bind
56572	5	6789	5	13	NULL	NULL	NULL	ST2 receptor	GP	membrane-anchored	consist of								intracellular domain		NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_5_721_s_101	12578875	17 Subsequently, a membrane-anchored receptor form of ST2 was identified, 18 consisting of an extracellular domain identical to ST2, a transmembrane domain, and an intracellular domain, all with homology to the interleukin-1 receptor, although ST2 does not bind interleukin-1.	bind
19832	1	6789	6	NULL	NULL	0	NULL	ST2	NULL		does not bind	NULL				interleukin-1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_107_5_721_s_101	12578875	17 Subsequently, a membrane-anchored receptor form of ST2 was identified, 18 consisting of an extracellular domain identical to ST2, a transmembrane domain, and an intracellular domain, all with homology to the interleukin-1 receptor, although ST2 does not bind interleukin-1.	bind
19833	2	6789	6	NULL	NULL	0	NULL	ST2 receptor	NULL	membrane-anchored	consists of	NULL					NULL		extracellular domain		NULL		0	NULL	NULL	NULL	gw60_circulation_107_5_721_s_101	12578875	17 Subsequently, a membrane-anchored receptor form of ST2 was identified, 18 consisting of an extracellular domain identical to ST2, a transmembrane domain, and an intracellular domain, all with homology to the interleukin-1 receptor, although ST2 does not bind interleukin-1.	bind
19834	3	6789	6	NULL	NULL	0	NULL	ST2 receptor	NULL	membrane-anchored	consists of	NULL					NULL		transmembrane domain		NULL		0	NULL	NULL	NULL	gw60_circulation_107_5_721_s_101	12578875	17 Subsequently, a membrane-anchored receptor form of ST2 was identified, 18 consisting of an extracellular domain identical to ST2, a transmembrane domain, and an intracellular domain, all with homology to the interleukin-1 receptor, although ST2 does not bind interleukin-1.	bind
19835	4	6789	6	NULL	NULL	0	NULL	ST2 receptor	NULL	membrane-anchored	consists of	NULL					NULL		intracellular domain		NULL		0	NULL	NULL	NULL	gw60_circulation_107_5_721_s_101	12578875	17 Subsequently, a membrane-anchored receptor form of ST2 was identified, 18 consisting of an extracellular domain identical to ST2, a transmembrane domain, and an intracellular domain, all with homology to the interleukin-1 receptor, although ST2 does not bind interleukin-1.	bind
56568	5	6789	6	10	NULL	0	NULL	ST2 receptor		membrane-anchored	is homologous to					 interleukin-1 receptor					NULL		0	NULL	NULL	NULL	gw60_circulation_107_5_721_s_101	12578875	17 Subsequently, a membrane-anchored receptor form of ST2 was identified, 18 consisting of an extracellular domain identical to ST2, a transmembrane domain, and an intracellular domain, all with homology to the interleukin-1 receptor, although ST2 does not bind interleukin-1.	bind
23481	1	6790	5	13	NULL	NULL	NULL	fibrinogen	GP		acts as								serotonin binding sites		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_192	15653564	17 Subsequently, it was postulated that fibrinogen and thrombospondin act as serotonin binding sites to anchor serotonin derivatized - platelet FV on the surface of platelets stimulated by thrombin plus convulxin.	bind
23482	2	6790	5	13	NULL	NULL	NULL	thrombospondin	GP		acts as								serotonin binding sites		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_192	15653564	17 Subsequently, it was postulated that fibrinogen and thrombospondin act as serotonin binding sites to anchor serotonin derivatized - platelet FV on the surface of platelets stimulated by thrombin plus convulxin.	bind
23483	3	6790	5	13	NULL	NULL	NULL	statement 1	GP		anchor					platelet FV	GP	serotonin derivatized			NULL	on the surface of platelets stimulated by thrombin plus convulxin	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_192	15653564	17 Subsequently, it was postulated that fibrinogen and thrombospondin act as serotonin binding sites to anchor serotonin derivatized - platelet FV on the surface of platelets stimulated by thrombin plus convulxin.	bind
23484	4	6790	5	13	NULL	NULL	NULL	statement 2	GP		anchor					platelet FV	GP	serotonin derivatized			NULL	on the surface of platelets stimulated by thrombin plus convulxin	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_192	15653564	17 Subsequently, it was postulated that fibrinogen and thrombospondin act as serotonin binding sites to anchor serotonin derivatized - platelet FV on the surface of platelets stimulated by thrombin plus convulxin.	bind
19836	1	6790	6	NULL	NULL	0	NULL	fibrinogen	NULL		acts as	NULL					NULL		serotonin binding sites		NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_192	15653564	17 Subsequently, it was postulated that fibrinogen and thrombospondin act as serotonin binding sites to anchor serotonin derivatized - platelet FV on the surface of platelets stimulated by thrombin plus convulxin.	bind
19837	2	6790	6	NULL	NULL	0	NULL	thrombospondin	NULL		acts as	NULL					NULL		serotonin binding sites		NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_192	15653564	17 Subsequently, it was postulated that fibrinogen and thrombospondin act as serotonin binding sites to anchor serotonin derivatized - platelet FV on the surface of platelets stimulated by thrombin plus convulxin.	bind
19838	3	6790	6	NULL	NULL	0	NULL	platelet FV	NULL	serotonin derivatized	anchored on	NULL				surface of platelets	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_192	15653564	17 Subsequently, it was postulated that fibrinogen and thrombospondin act as serotonin binding sites to anchor serotonin derivatized - platelet FV on the surface of platelets stimulated by thrombin plus convulxin.	bind
19839	4	6790	6	NULL	NULL	0	NULL	statement 1	NULL		anchor	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_192	15653564	17 Subsequently, it was postulated that fibrinogen and thrombospondin act as serotonin binding sites to anchor serotonin derivatized - platelet FV on the surface of platelets stimulated by thrombin plus convulxin.	bind
19840	5	6790	6	NULL	NULL	0	NULL	statement 2	NULL		anchor	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_192	15653564	17 Subsequently, it was postulated that fibrinogen and thrombospondin act as serotonin binding sites to anchor serotonin derivatized - platelet FV on the surface of platelets stimulated by thrombin plus convulxin.	bind
19841	6	6790	6	NULL	NULL	0	NULL	statement 3	NULL		stimulated by	NULL				thrombin plus convulxin	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_861_s_192	15653564	17 Subsequently, it was postulated that fibrinogen and thrombospondin act as serotonin binding sites to anchor serotonin derivatized - platelet FV on the surface of platelets stimulated by thrombin plus convulxin.	bind
23487	1	6791	5	13	NULL	NULL	NULL	SRF	GP		bind									CArG boxes	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_75	16614312	17 The general paradigm is that expression of CArG-dependent SMC differentiation genes requires SRF binding to CArG boxes to drive transcription.	bind
23488	3	6791	5	13	NULL	NULL	NULL	statement 2	Process		requires					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_75	16614312	17 The general paradigm is that expression of CArG-dependent SMC differentiation genes requires SRF binding to CArG boxes to drive transcription.	bind
23489	4	6791	5	13	NULL	NULL	NULL	statement 3	Process		drives					transcription	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_75	16614312	17 The general paradigm is that expression of CArG-dependent SMC differentiation genes requires SRF binding to CArG boxes to drive transcription.	bind
44697	2	6791	5	13	NULL	NULL	NULL	SMC differentiation genes	GP		depends on					CArG	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_75	16614312	17 The general paradigm is that expression of CArG-dependent SMC differentiation genes requires SRF binding to CArG boxes to drive transcription.	bind
19686	1	6791	6	NULL	NULL	0	NULL	SRF	NULL		bind	NULL					NULL			CArG box	NULL		0	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_75	16614312	17 The general paradigm is that expression of CArG-dependent SMC differentiation genes requires SRF binding to CArG boxes to drive transcription.	bind
19687	3	6791	6	10	NULL	0	NULL	statement 2	NULL		requires	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_75	16614312	17 The general paradigm is that expression of CArG-dependent SMC differentiation genes requires SRF binding to CArG boxes to drive transcription.	bind
44698	2	6791	6	10	NULL	0	NULL	SMC differentiation genes	NULL		depends on	NULL				CArG	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_75	16614312	17 The general paradigm is that expression of CArG-dependent SMC differentiation genes requires SRF binding to CArG boxes to drive transcription.	bind
56573	4	6791	6	10	NULL	0	NULL	statement 3			drives					transcription					NULL		0	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_75	16614312	17 The general paradigm is that expression of CArG-dependent SMC differentiation genes requires SRF binding to CArG boxes to drive transcription.	bind
45616	1	6792	5	13	NULL	NULL	NULL	RhoA	GP		interacts with					nuclear trafficking machinery	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_108_7_876_s_189	12874183	17 The interaction between RhoA and this nuclear trafficking machinery or ERK binding/scaffolding proteins to functionally compartmentalize ERK within the cell is not known.	bind
45617	2	6792	5	13	NULL	NULL	NULL	RhoA	GP		interacts with					ERK binding/scaffolding proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_108_7_876_s_189	12874183	17 The interaction between RhoA and this nuclear trafficking machinery or ERK binding/scaffolding proteins to functionally compartmentalize ERK within the cell is not known.	bind
19843	2	6792	6	NULL	NULL	0	NULL	RhoA	NULL		interacts with	NULL				ERK binding/scaffolding proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_108_7_876_s_189	12874183	17 The interaction between RhoA and this nuclear trafficking machinery or ERK binding/scaffolding proteins to functionally compartmentalize ERK within the cell is not known.	bind
44833	1	6792	6	10	NULL	0	NULL	RhoA	NULL		interact with	NULL				\tnuclear trafficking machinery	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_108_7_876_s_189	12874183	17 The interaction between RhoA and this nuclear trafficking machinery or ERK binding/scaffolding proteins to functionally compartmentalize ERK within the cell is not known.	bind
23490	1	6793	5	13	NULL	NULL	NULL	apoA-I	GP		bind		directly			ABCA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_32	12738681	17 These findings led us to suggest that apoA-I directly binds ABCA1 to form a complex that is required for ABCA1-facilitated cellular cholesterol and phospholipid efflux.	bind
23491	2	6793	5	13	NULL	NULL	NULL	 ABCA1	GP		facilitate					cellular cholesterol efflux	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_32	12738681	17 These findings led us to suggest that apoA-I directly binds ABCA1 to form a complex that is required for ABCA1-facilitated cellular cholesterol and phospholipid efflux.	bind
23492	4	6793	5	13	NULL	NULL	NULL	statement 1	Process		is required for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_32	12738681	17 These findings led us to suggest that apoA-I directly binds ABCA1 to form a complex that is required for ABCA1-facilitated cellular cholesterol and phospholipid efflux.	bind
44699	3	6793	5	13	NULL	NULL	NULL	ABCA1	GP		facilitate					phospholipid efflux	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_32	12738681	17 These findings led us to suggest that apoA-I directly binds ABCA1 to form a complex that is required for ABCA1-facilitated cellular cholesterol and phospholipid efflux.	bind
44700	5	6793	5	13	NULL	NULL	NULL	statement 1	Process		is required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_32	12738681	17 These findings led us to suggest that apoA-I directly binds ABCA1 to form a complex that is required for ABCA1-facilitated cellular cholesterol and phospholipid efflux.	bind
19688	1	6793	6	NULL	NULL	0	NULL	apoA-I	NULL		bind	NULL	directly			ABCA1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_32	12738681	17 These findings led us to suggest that apoA-I directly binds ABCA1 to form a complex that is required for ABCA1-facilitated cellular cholesterol and phospholipid efflux.	bind
19689	2	6793	6	NULL	NULL	0	NULL	ABCA-1	NULL		facilitate	NULL				cellular cholesterol efflux	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_32	12738681	17 These findings led us to suggest that apoA-I directly binds ABCA1 to form a complex that is required for ABCA1-facilitated cellular cholesterol and phospholipid efflux.	bind
19690	3	6793	6	NULL	NULL	0	NULL	ABCA-1	NULL		facilitate	NULL				phospholipid efflux	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_32	12738681	17 These findings led us to suggest that apoA-I directly binds ABCA1 to form a complex that is required for ABCA1-facilitated cellular cholesterol and phospholipid efflux.	bind
19691	4	6793	6	NULL	NULL	0	NULL	statement 1	NULL		is required for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_32	12738681	17 These findings led us to suggest that apoA-I directly binds ABCA1 to form a complex that is required for ABCA1-facilitated cellular cholesterol and phospholipid efflux.	bind
19692	5	6793	6	NULL	NULL	0	NULL	statement 1	NULL		is required for	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_32	12738681	17 These findings led us to suggest that apoA-I directly binds ABCA1 to form a complex that is required for ABCA1-facilitated cellular cholesterol and phospholipid efflux.	bind
28374	1	6794	5	13	NULL	NULL	NULL	oxLDL	GP		bind					FcgammaRII-B2	GP	murine			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3248_s_188	9409319	17 Thus, amino acid sequence differences in the IgG ligand-binding sites between both receptors could explain the discrepancy in oxLDL binding between murine FcgammaRII-B2 and human FcgammaRIIA.	bind
28375	2	6794	5	13	NULL	NULL	NULL	oxLDL	GP		bind					FcgammaRIIA	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3248_s_188	9409319	17 Thus, amino acid sequence differences in the IgG ligand-binding sites between both receptors could explain the discrepancy in oxLDL binding between murine FcgammaRII-B2 and human FcgammaRIIA.	bind
28376	3	6794	5	13	NULL	NULL	NULL	statement 1	Process		is discrepant to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3248_s_188	9409319	17 Thus, amino acid sequence differences in the IgG ligand-binding sites between both receptors could explain the discrepancy in oxLDL binding between murine FcgammaRII-B2 and human FcgammaRIIA.	bind
28377	4	6794	5	13	NULL	NULL	NULL	FcgammaRII-B2	GP	amino acid sequence of murine	differs from			IgG ligand-binding sites		FcgammaRIIA	GP	amino acid sequence of human	IgG ligand-binding sites		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3248_s_188	9409319	17 Thus, amino acid sequence differences in the IgG ligand-binding sites between both receptors could explain the discrepancy in oxLDL binding between murine FcgammaRII-B2 and human FcgammaRIIA.	bind
28378	5	6794	5	13	NULL	NULL	NULL	statement 4	Process		explains					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3248_s_188	9409319	17 Thus, amino acid sequence differences in the IgG ligand-binding sites between both receptors could explain the discrepancy in oxLDL binding between murine FcgammaRII-B2 and human FcgammaRIIA.	bind
19693	1	6794	6	NULL	NULL	0	NULL	oxLDL	NULL		bind	NULL				FcgammaRII-B2	NULL	murine			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3248_s_188	9409319	17 Thus, amino acid sequence differences in the IgG ligand-binding sites between both receptors could explain the discrepancy in oxLDL binding between murine FcgammaRII-B2 and human FcgammaRIIA.	bind
19694	2	6794	6	NULL	NULL	0	NULL	oxLDL	NULL		bind	NULL				FcgammaRIIA	NULL	human			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3248_s_188	9409319	17 Thus, amino acid sequence differences in the IgG ligand-binding sites between both receptors could explain the discrepancy in oxLDL binding between murine FcgammaRII-B2 and human FcgammaRIIA.	bind
56574	3	6794	6	10	NULL	0	NULL	statement 1			discrepant to					statement 2					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3248_s_188	9409319	17 Thus, amino acid sequence differences in the IgG ligand-binding sites between both receptors could explain the discrepancy in oxLDL binding between murine FcgammaRII-B2 and human FcgammaRIIA.	bind
56575	4	6794	6	10	NULL	0	NULL	FcgammaRII-B2		amino acid sequence of murine	differs from			 IgG ligand-binding sites		FcgammaRIIA		amino acid sequence of human	IgG ligand-binding sites		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3248_s_188	9409319	17 Thus, amino acid sequence differences in the IgG ligand-binding sites between both receptors could explain the discrepancy in oxLDL binding between murine FcgammaRII-B2 and human FcgammaRIIA.	bind
56576	5	6794	6	10	NULL	0	NULL	statement 4			explains					statement 3					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3248_s_188	9409319	17 Thus, amino acid sequence differences in the IgG ligand-binding sites between both receptors could explain the discrepancy in oxLDL binding between murine FcgammaRII-B2 and human FcgammaRIIA.	bind
23495	1	6795	5	13	NULL	NULL	NULL	Tie2	GP		bind					Dok-R	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_6_630_s_27	12609966	17 Tie2 binding with Dok-R mediates the effects of the receptor on endothelial migration.	bind
23496	2	6795	5	13	NULL	NULL	NULL	statement 1	Process		mediates					endothelial migration	Process	effects on			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_6_630_s_27	12609966	17 Tie2 binding with Dok-R mediates the effects of the receptor on endothelial migration.	bind
19695	1	6795	6	NULL	NULL	0	NULL	Tie2	NULL		bind	NULL				Dok-R	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_6_630_s_27	12609966	17 Tie2 binding with Dok-R mediates the effects of the receptor on endothelial migration.	bind
19696	2	6795	6	NULL	NULL	0	NULL	statement 1	NULL		mediates	NULL				endothelial migration	NULL	effects on			NULL		0	NULL	NULL	NULL	gw60_circulationres_92_6_630_s_27	12609966	17 Tie2 binding with Dok-R mediates the effects of the receptor on endothelial migration.	bind
23497	1	6796	5	13	NULL	NULL	NULL	FAK	GP		mediate					ERK	GP	downstream activation of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_34391_s_257	12110680	17,  18,  31,  43), the beta4-mCLCA1-triggered, FAK-mediated downstream activation of ERK is closely associated with increased rates of proliferation and BrdUrd incorporation of B16-F10 cells bound to mCLCA1-coated dishes as well as the clonal growth of tumor cells bound to BAEC monolayers that constitutively express bCLCA2 ( 5).	bind
23498	2	6796	5	13	NULL	NULL	NULL	beta4-mCLCA1	GP		triggers					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_34391_s_257	12110680	17,  18,  31,  43), the beta4-mCLCA1-triggered, FAK-mediated downstream activation of ERK is closely associated with increased rates of proliferation and BrdUrd incorporation of B16-F10 cells bound to mCLCA1-coated dishes as well as the clonal growth of tumor cells bound to BAEC monolayers that constitutively express bCLCA2 ( 5).	bind
23499	3	6796	5	13	NULL	NULL	NULL	statement 2	Process		is associated with		closely			B16-F10 cells 	Cell	increased rates of proliferation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_34391_s_257	12110680	17,  18,  31,  43), the beta4-mCLCA1-triggered, FAK-mediated downstream activation of ERK is closely associated with increased rates of proliferation and BrdUrd incorporation of B16-F10 cells bound to mCLCA1-coated dishes as well as the clonal growth of tumor cells bound to BAEC monolayers that constitutively express bCLCA2 ( 5).	bind
23500	4	6796	5	13	NULL	NULL	NULL	statement 2	Process		is associated with		closely			B16-F10 cells	Cell	BrdUrd incorporation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_34391_s_257	12110680	17,  18,  31,  43), the beta4-mCLCA1-triggered, FAK-mediated downstream activation of ERK is closely associated with increased rates of proliferation and BrdUrd incorporation of B16-F10 cells bound to mCLCA1-coated dishes as well as the clonal growth of tumor cells bound to BAEC monolayers that constitutively express bCLCA2 ( 5).	bind
23501	5	6796	5	13	NULL	NULL	NULL	BAEC monolayers	Cell		express		constitutively			bCLCA2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_34391_s_257	12110680	17,  18,  31,  43), the beta4-mCLCA1-triggered, FAK-mediated downstream activation of ERK is closely associated with increased rates of proliferation and BrdUrd incorporation of B16-F10 cells bound to mCLCA1-coated dishes as well as the clonal growth of tumor cells bound to BAEC monolayers that constitutively express bCLCA2 ( 5).	bind
23502	6	6796	5	13	NULL	NULL	NULL	tumor cells	Cell		bind					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_34391_s_257	12110680	17,  18,  31,  43), the beta4-mCLCA1-triggered, FAK-mediated downstream activation of ERK is closely associated with increased rates of proliferation and BrdUrd incorporation of B16-F10 cells bound to mCLCA1-coated dishes as well as the clonal growth of tumor cells bound to BAEC monolayers that constitutively express bCLCA2 ( 5).	bind
23503	7	6796	5	13	NULL	NULL	NULL	statement 2	Process		is associated with		closely			statement 6	Process	clonal growth of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_34391_s_257	12110680	17,  18,  31,  43), the beta4-mCLCA1-triggered, FAK-mediated downstream activation of ERK is closely associated with increased rates of proliferation and BrdUrd incorporation of B16-F10 cells bound to mCLCA1-coated dishes as well as the clonal growth of tumor cells bound to BAEC monolayers that constitutively express bCLCA2 ( 5).	bind
19844	1	6796	6	NULL	NULL	0	NULL	BAEC monolayers	NULL		express	NULL	constitutively			bCLCA2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_37_34391_s_257	12110680	17,  18,  31,  43), the beta4-mCLCA1-triggered, FAK-mediated downstream activation of ERK is closely associated with increased rates of proliferation and BrdUrd incorporation of B16-F10 cells bound to mCLCA1-coated dishes as well as the clonal growth of tumor cells bound to BAEC monolayers that constitutively express bCLCA2 ( 5).	bind
19845	2	6796	6	NULL	NULL	0	NULL	tumor cells	NULL		bind	NULL				BAEC monolayers	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_37_34391_s_257	12110680	17,  18,  31,  43), the beta4-mCLCA1-triggered, FAK-mediated downstream activation of ERK is closely associated with increased rates of proliferation and BrdUrd incorporation of B16-F10 cells bound to mCLCA1-coated dishes as well as the clonal growth of tumor cells bound to BAEC monolayers that constitutively express bCLCA2 ( 5).	bind
19846	3	6796	6	NULL	NULL	0	NULL	FAK	NULL		mediates	NULL				ERK	NULL	downstream activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_37_34391_s_257	12110680	17,  18,  31,  43), the beta4-mCLCA1-triggered, FAK-mediated downstream activation of ERK is closely associated with increased rates of proliferation and BrdUrd incorporation of B16-F10 cells bound to mCLCA1-coated dishes as well as the clonal growth of tumor cells bound to BAEC monolayers that constitutively express bCLCA2 ( 5).	bind
19847	6	6796	6	10	NULL	0	NULL	statement 4			is associated with					B16-F10 cells 		increased rate of proliferation			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_34391_s_257	12110680	17,  18,  31,  43), the beta4-mCLCA1-triggered, FAK-mediated downstream activation of ERK is closely associated with increased rates of proliferation and BrdUrd incorporation of B16-F10 cells bound to mCLCA1-coated dishes as well as the clonal growth of tumor cells bound to BAEC monolayers that constitutively express bCLCA2 ( 5).	bind
19848	5	6796	6	10	NULL	0	NULL	statement 4			is associated with					statement 2		clonal growth of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_34391_s_257	12110680	17,  18,  31,  43), the beta4-mCLCA1-triggered, FAK-mediated downstream activation of ERK is closely associated with increased rates of proliferation and BrdUrd incorporation of B16-F10 cells bound to mCLCA1-coated dishes as well as the clonal growth of tumor cells bound to BAEC monolayers that constitutively express bCLCA2 ( 5).	bind
20300	4	6796	6	10	NULL	0	NULL	beta4-mCLCA1			triggers					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_34391_s_257	12110680	17,  18,  31,  43), the beta4-mCLCA1-triggered, FAK-mediated downstream activation of ERK is closely associated with increased rates of proliferation and BrdUrd incorporation of B16-F10 cells bound to mCLCA1-coated dishes as well as the clonal growth of tumor cells bound to BAEC monolayers that constitutively express bCLCA2 ( 5).	bind
56577	7	6796	6	10	NULL	0	NULL	statement 4			associated with		closely			B16-F10 cells 		BrdUrd incorporation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_37_34391_s_257	12110680	17,  18,  31,  43), the beta4-mCLCA1-triggered, FAK-mediated downstream activation of ERK is closely associated with increased rates of proliferation and BrdUrd incorporation of B16-F10 cells bound to mCLCA1-coated dishes as well as the clonal growth of tumor cells bound to BAEC monolayers that constitutively express bCLCA2 ( 5).	bind
23504	1	6797	5	13	NULL	NULL	NULL	VEGF	GP		bind					VEGFR-2/Flk1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1124_s_217	15044320	17,18  In physiological angiogenesis, the net levels of VEGF binding to VEGFR-2/Flk1 are regulated by competing levels of VEGFR-1/Flt1, thereby preventing aberrant activation of VEGFR-2/Flk1.	bind
23505	2	6797	5	13	NULL	NULL	NULL	VEGF	GP		bind					VEGFR-1/Flt1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1124_s_217	15044320	17,18  In physiological angiogenesis, the net levels of VEGF binding to VEGFR-2/Flk1 are regulated by competing levels of VEGFR-1/Flt1, thereby preventing aberrant activation of VEGFR-2/Flk1.	bind
23506	3	6797	5	13	NULL	NULL	NULL	statement 2	Process		competes with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1124_s_217	15044320	17,18  In physiological angiogenesis, the net levels of VEGF binding to VEGFR-2/Flk1 are regulated by competing levels of VEGFR-1/Flt1, thereby preventing aberrant activation of VEGFR-2/Flk1.	bind
23507	4	6797	5	13	NULL	NULL	NULL	statement 1	Process	levels of	is regulated by					statement 3	Process				NULL	in physiological angiogenesis	NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1124_s_217	15044320	17,18  In physiological angiogenesis, the net levels of VEGF binding to VEGFR-2/Flk1 are regulated by competing levels of VEGFR-1/Flt1, thereby preventing aberrant activation of VEGFR-2/Flk1.	bind
23508	5	6797	5	13	NULL	NULL	NULL	statement 4	Process		prevents					VEGFR-2/Flk1	GP	aberrant activation of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1124_s_217	15044320	17,18  In physiological angiogenesis, the net levels of VEGF binding to VEGFR-2/Flk1 are regulated by competing levels of VEGFR-1/Flt1, thereby preventing aberrant activation of VEGFR-2/Flk1.	bind
19849	1	6797	6	NULL	NULL	0	NULL	VEGF	NULL		bind	NULL				VEGFR-2/Flk1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1124_s_217	15044320	17,18  In physiological angiogenesis, the net levels of VEGF binding to VEGFR-2/Flk1 are regulated by competing levels of VEGFR-1/Flt1, thereby preventing aberrant activation of VEGFR-2/Flk1.	bind
19850	2	6797	6	10	NULL	0	NULL	VEGF			bind					VEGFR-1/Flt1					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1124_s_217	15044320	17,18  In physiological angiogenesis, the net levels of VEGF binding to VEGFR-2/Flk1 are regulated by competing levels of VEGFR-1/Flt1, thereby preventing aberrant activation of VEGFR-2/Flk1.	bind
56578	3	6797	6	10	NULL	0	NULL	statement 2			compete with					statement 3					NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1124_s_217	15044320	17,18  In physiological angiogenesis, the net levels of VEGF binding to VEGFR-2/Flk1 are regulated by competing levels of VEGFR-1/Flt1, thereby preventing aberrant activation of VEGFR-2/Flk1.	bind
56579	4	6797	6	10	NULL	0	NULL	statement 3			regulates					statement 1		levels of			NULL	physiological angiogenesis	NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1124_s_217	15044320	17,18  In physiological angiogenesis, the net levels of VEGF binding to VEGFR-2/Flk1 are regulated by competing levels of VEGFR-1/Flt1, thereby preventing aberrant activation of VEGFR-2/Flk1.	bind
56580	5	6797	6	10	NULL	0	NULL	statement 4			prevents					VEGFR-2/Flk1		aberrant activation of			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1124_s_217	15044320	17,18  In physiological angiogenesis, the net levels of VEGF binding to VEGFR-2/Flk1 are regulated by competing levels of VEGFR-1/Flt1, thereby preventing aberrant activation of VEGFR-2/Flk1.	bind
23509	1	6798	5	13	NULL	NULL	NULL	MCP-1	GP	mutant	bind					CCR2 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_534_s_34	14739122	17,18  This mutant MCP-1 binds to its receptor CCR2 and blocks MCP-1 - mediated monocyte chemotaxis.	bind
23510	2	6798	5	13	NULL	NULL	NULL	MCP-1	GP		mediate					monocyte chemotaxis	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_534_s_34	14739122	17,18  This mutant MCP-1 binds to its receptor CCR2 and blocks MCP-1 - mediated monocyte chemotaxis.	bind
23511	3	6798	5	13	NULL	NULL	NULL	statement 1	Process		blocks					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_534_s_34	14739122	17,18  This mutant MCP-1 binds to its receptor CCR2 and blocks MCP-1 - mediated monocyte chemotaxis.	bind
19697	1	6798	6	NULL	NULL	0	NULL	MCP-1	NULL	mutant	bind	NULL				CCR2 receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_534_s_34	14739122	17,18  This mutant MCP-1 binds to its receptor CCR2 and blocks MCP-1 - mediated monocyte chemotaxis.	bind
19698	2	6798	6	NULL	NULL	0	NULL	MCP-1	NULL		mediates	NULL				monocyte chemotaxis	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_534_s_34	14739122	17,18  This mutant MCP-1 binds to its receptor CCR2 and blocks MCP-1 - mediated monocyte chemotaxis.	bind
19699	3	6798	6	NULL	NULL	0	NULL	statement 1	NULL		blocks	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_534_s_34	14739122	17,18  This mutant MCP-1 binds to its receptor CCR2 and blocks MCP-1 - mediated monocyte chemotaxis.	bind
23512	1	6799	5	13	NULL	NULL	NULL	Stat3	GP	activation	is dependent on					Rac1	GP				NULL	 in epidermal growth factor - stimulated COS-1 cells	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1395_s_149	15860735	17,19  Stat3 activation has been shown to be Rac1 dependent in epidermal growth factor - stimulated COS-1 cells, 20 attributed to direct binding of Rac1 to Stat3 or indirect enhancement of ROS production by Rac1.	bind
23513	2	6799	5	13	NULL	NULL	NULL	Rac1	GP		bind		directly			Stat3	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1395_s_149	15860735	17,19  Stat3 activation has been shown to be Rac1 dependent in epidermal growth factor - stimulated COS-1 cells, 20 attributed to direct binding of Rac1 to Stat3 or indirect enhancement of ROS production by Rac1.	bind
23514	3	6799	5	13	NULL	NULL	NULL	statement 1	Process		is attributed to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1395_s_149	15860735	17,19  Stat3 activation has been shown to be Rac1 dependent in epidermal growth factor - stimulated COS-1 cells, 20 attributed to direct binding of Rac1 to Stat3 or indirect enhancement of ROS production by Rac1.	bind
23515	4	6799	5	13	NULL	NULL	NULL	Rac1	GP		enhances		indirectly			ROS	Chemical	production of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1395_s_149	15860735	17,19  Stat3 activation has been shown to be Rac1 dependent in epidermal growth factor - stimulated COS-1 cells, 20 attributed to direct binding of Rac1 to Stat3 or indirect enhancement of ROS production by Rac1.	bind
23516	5	6799	5	13	NULL	NULL	NULL	statement 1	Process		is attributed to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1395_s_149	15860735	17,19  Stat3 activation has been shown to be Rac1 dependent in epidermal growth factor - stimulated COS-1 cells, 20 attributed to direct binding of Rac1 to Stat3 or indirect enhancement of ROS production by Rac1.	bind
19851	1	6799	6	NULL	NULL	0	NULL	Stat3	NULL	activation of	is dependent on	NULL				Rac1	NULL				NULL	epidermal growth factor - stimulated COS-1 cells	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1395_s_149	15860735	17,19  Stat3 activation has been shown to be Rac1 dependent in epidermal growth factor - stimulated COS-1 cells, 20 attributed to direct binding of Rac1 to Stat3 or indirect enhancement of ROS production by Rac1.	bind
19852	2	6799	6	NULL	NULL	0	NULL	Rac1	NULL		bind	NULL	directly			Stat3	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1395_s_149	15860735	17,19  Stat3 activation has been shown to be Rac1 dependent in epidermal growth factor - stimulated COS-1 cells, 20 attributed to direct binding of Rac1 to Stat3 or indirect enhancement of ROS production by Rac1.	bind
19853	3	6799	6	NULL	NULL	0	NULL	Rac1	NULL		enhances	NULL	indirectly			ROS	NULL	production of 			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1395_s_149	15860735	17,19  Stat3 activation has been shown to be Rac1 dependent in epidermal growth factor - stimulated COS-1 cells, 20 attributed to direct binding of Rac1 to Stat3 or indirect enhancement of ROS production by Rac1.	bind
56581	4	6799	6	10	NULL	0	NULL	statement 1			attributed to					statement 2					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1395_s_149	15860735	17,19  Stat3 activation has been shown to be Rac1 dependent in epidermal growth factor - stimulated COS-1 cells, 20 attributed to direct binding of Rac1 to Stat3 or indirect enhancement of ROS production by Rac1.	bind
56582	5	6799	6	10	NULL	0	NULL	statement 1			attributed to					statement 3					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1395_s_149	15860735	17,19  Stat3 activation has been shown to be Rac1 dependent in epidermal growth factor - stimulated COS-1 cells, 20 attributed to direct binding of Rac1 to Stat3 or indirect enhancement of ROS production by Rac1.	bind
23517	1	6800	5	13	NULL	NULL	NULL	calmodulin	GP		bind					eNOS	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2238_s_30	15486309	17,20  Furthermore, Hsp90 may mediate eNOS phosphorylation through regulating calmodulin binding to eNOS and Akt. 18,19,21	bind
23518	2	6800	5	13	NULL	NULL	NULL	calmodulin	GP		bind					Akt	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2238_s_30	15486309	17,20  Furthermore, Hsp90 may mediate eNOS phosphorylation through regulating calmodulin binding to eNOS and Akt. 18,19,21	bind
23519	3	6800	5	13	NULL	NULL	NULL	Hsp90	GP		regulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2238_s_30	15486309	17,20  Furthermore, Hsp90 may mediate eNOS phosphorylation through regulating calmodulin binding to eNOS and Akt. 18,19,21	bind
23520	4	6800	5	13	NULL	NULL	NULL	Hsp90	GP		regulates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2238_s_30	15486309	17,20  Furthermore, Hsp90 may mediate eNOS phosphorylation through regulating calmodulin binding to eNOS and Akt. 18,19,21	bind
23521	5	6800	5	13	NULL	NULL	NULL	Hsp90	GP		mediate		may			eNOS	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2238_s_30	15486309	17,20  Furthermore, Hsp90 may mediate eNOS phosphorylation through regulating calmodulin binding to eNOS and Akt. 18,19,21	bind
23522	6	6800	5	13	NULL	NULL	NULL	statement 5	Process		occurs through					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2238_s_30	15486309	17,20  Furthermore, Hsp90 may mediate eNOS phosphorylation through regulating calmodulin binding to eNOS and Akt. 18,19,21	bind
23523	7	6800	5	13	NULL	NULL	NULL	statement 5	Process		occurs through					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2238_s_30	15486309	17,20  Furthermore, Hsp90 may mediate eNOS phosphorylation through regulating calmodulin binding to eNOS and Akt. 18,19,21	bind
19700	1	6800	6	NULL	NULL	0	NULL	Calmodulin	NULL		bind	NULL				eNOS	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2238_s_30	15486309	17,20  Furthermore, Hsp90 may mediate eNOS phosphorylation through regulating calmodulin binding to eNOS and Akt. 18,19,21	bind
19701	2	6800	6	NULL	NULL	0	NULL	Calmodulin	NULL		bind	NULL				Akt	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2238_s_30	15486309	17,20  Furthermore, Hsp90 may mediate eNOS phosphorylation through regulating calmodulin binding to eNOS and Akt. 18,19,21	bind
19702	3	6800	6	NULL	NULL	0	NULL	Hsp90	NULL		mediate	NULL	may			eNOS	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2238_s_30	15486309	17,20  Furthermore, Hsp90 may mediate eNOS phosphorylation through regulating calmodulin binding to eNOS and Akt. 18,19,21	bind
19703	4	6800	6	NULL	NULL	0	NULL	Hsp90	NULL		regulate	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2238_s_30	15486309	17,20  Furthermore, Hsp90 may mediate eNOS phosphorylation through regulating calmodulin binding to eNOS and Akt. 18,19,21	bind
19704	5	6800	6	NULL	NULL	0	NULL	Hsp90	NULL		regulate	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2238_s_30	15486309	17,20  Furthermore, Hsp90 may mediate eNOS phosphorylation through regulating calmodulin binding to eNOS and Akt. 18,19,21	bind
19705	6	6800	6	NULL	NULL	0	NULL	statement 3	NULL		occurs through	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2238_s_30	15486309	17,20  Furthermore, Hsp90 may mediate eNOS phosphorylation through regulating calmodulin binding to eNOS and Akt. 18,19,21	bind
19706	7	6800	6	NULL	NULL	0	NULL	statement 3	NULL		occurs through	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2238_s_30	15486309	17,20  Furthermore, Hsp90 may mediate eNOS phosphorylation through regulating calmodulin binding to eNOS and Akt. 18,19,21	bind
23524	1	6801	5	13	NULL	NULL	NULL	FrzA/sFRP-1	GP		bind					Wnt	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1299_s_29	15920021	17,22  We and others have shown that FrzA/sFRP-1 binds Wnt to prevent it from accessing its cell-surface receptor Frizzled, and that it blocks the canonical Wnt pathway as measured by cytosolic accumulation of beta-catenin in endothelial cells (ECs).	bind
23525	2	6801	5	13	NULL	NULL	NULL	Wnt	GP		access					Frizzled	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1299_s_29	15920021	17,22  We and others have shown that FrzA/sFRP-1 binds Wnt to prevent it from accessing its cell-surface receptor Frizzled, and that it blocks the canonical Wnt pathway as measured by cytosolic accumulation of beta-catenin in endothelial cells (ECs).	bind
23526	3	6801	5	13	NULL	NULL	NULL	statement 1	Process		prevents					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1299_s_29	15920021	17,22  We and others have shown that FrzA/sFRP-1 binds Wnt to prevent it from accessing its cell-surface receptor Frizzled, and that it blocks the canonical Wnt pathway as measured by cytosolic accumulation of beta-catenin in endothelial cells (ECs).	bind
23527	4	6801	5	13	NULL	NULL	NULL	statement 3	Process		blocks					 Wnt pathway	Process	canonical			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1299_s_29	15920021	17,22  We and others have shown that FrzA/sFRP-1 binds Wnt to prevent it from accessing its cell-surface receptor Frizzled, and that it blocks the canonical Wnt pathway as measured by cytosolic accumulation of beta-catenin in endothelial cells (ECs).	bind
56583	5	6801	5	13	NULL	NULL	NULL	Frizzled	GP		is a type of					cell-surface receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1299_s_29	15920021	17,22  We and others have shown that FrzA/sFRP-1 binds Wnt to prevent it from accessing its cell-surface receptor Frizzled, and that it blocks the canonical Wnt pathway as measured by cytosolic accumulation of beta-catenin in endothelial cells (ECs).	bind
19707	1	6801	6	NULL	NULL	0	NULL	FrzA/sFRP-1	NULL		bind	NULL				Wnt	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_12_1299_s_29	15920021	17,22  We and others have shown that FrzA/sFRP-1 binds Wnt to prevent it from accessing its cell-surface receptor Frizzled, and that it blocks the canonical Wnt pathway as measured by cytosolic accumulation of beta-catenin in endothelial cells (ECs).	bind
19708	2	6801	6	NULL	NULL	0	NULL	FrzA/sFRP-1	NULL		blocks	NULL				Wnt pathway	NULL	canonical			NULL		0	NULL	NULL	NULL	gw70_circulationres_96_12_1299_s_29	15920021	17,22  We and others have shown that FrzA/sFRP-1 binds Wnt to prevent it from accessing its cell-surface receptor Frizzled, and that it blocks the canonical Wnt pathway as measured by cytosolic accumulation of beta-catenin in endothelial cells (ECs).	bind
19709	3	6801	6	NULL	NULL	0	NULL	Wnt	NULL		access	NULL				Frizzled	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_12_1299_s_29	15920021	17,22  We and others have shown that FrzA/sFRP-1 binds Wnt to prevent it from accessing its cell-surface receptor Frizzled, and that it blocks the canonical Wnt pathway as measured by cytosolic accumulation of beta-catenin in endothelial cells (ECs).	bind
19710	4	6801	6	10	NULL	0	NULL	frizzled			is a type of					cell-surface receptor					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1299_s_29	15920021	17,22  We and others have shown that FrzA/sFRP-1 binds Wnt to prevent it from accessing its cell-surface receptor Frizzled, and that it blocks the canonical Wnt pathway as measured by cytosolic accumulation of beta-catenin in endothelial cells (ECs).	bind
19711	5	6801	6	NULL	NULL	0	NULL	statement 1	NULL		prevents	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_12_1299_s_29	15920021	17,22  We and others have shown that FrzA/sFRP-1 binds Wnt to prevent it from accessing its cell-surface receptor Frizzled, and that it blocks the canonical Wnt pathway as measured by cytosolic accumulation of beta-catenin in endothelial cells (ECs).	bind
23529	1	6802	5	13	NULL	NULL	NULL	sPLA2-IIA proteins	GP		does not bind					proteoglycans	GP	mutant b3E			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1161_s_224	15802623	17,33  Our results using cell supernatant containing sPLA2-IIA proteins unable to bind proteoglycans (mutant b3E) demonstrated the involvement of proteoglycan interactions in the induction of sPLA2-IIA gene transcription.	bind
23530	2	6802	5	13	NULL	NULL	NULL	proteoglycan	GP	interactions	is involved in					sPLA2-IIA gene	GP	induction of;;transcription of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1161_s_224	15802623	17,33  Our results using cell supernatant containing sPLA2-IIA proteins unable to bind proteoglycans (mutant b3E) demonstrated the involvement of proteoglycan interactions in the induction of sPLA2-IIA gene transcription.	bind
23532	3	6802	5	13	NULL	NULL	NULL	statement 1	Process		demonstrate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1161_s_224	15802623	17,33  Our results using cell supernatant containing sPLA2-IIA proteins unable to bind proteoglycans (mutant b3E) demonstrated the involvement of proteoglycan interactions in the induction of sPLA2-IIA gene transcription.	bind
19712	1	6802	6	10	NULL	0	NULL	sPLA2-IIA protein	NULL		does not bind	NULL				proteoglycans	NULL	mutant b3E			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1161_s_224	15802623	17,33  Our results using cell supernatant containing sPLA2-IIA proteins unable to bind proteoglycans (mutant b3E) demonstrated the involvement of proteoglycan interactions in the induction of sPLA2-IIA gene transcription.	bind
19713	2	6802	6	10	NULL	0	NULL	proteoglycan 		interactions	plays a role in					sPLA2-IIA gene		induction of;;transcription of 			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1161_s_224	15802623	17,33  Our results using cell supernatant containing sPLA2-IIA proteins unable to bind proteoglycans (mutant b3E) demonstrated the involvement of proteoglycan interactions in the induction of sPLA2-IIA gene transcription.	bind
56584	3	6802	6	10	NULL	0	NULL	statement 1			demonstrate					statement 2					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1161_s_224	15802623	17,33  Our results using cell supernatant containing sPLA2-IIA proteins unable to bind proteoglycans (mutant b3E) demonstrated the involvement of proteoglycan interactions in the induction of sPLA2-IIA gene transcription.	bind
23531	1	6803	5	13	NULL	NULL	NULL	LRP-1B	GP		is similar to					LRP-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1246_s_100	16574889	17,68 - 70    LRP-1B is the giant family member that is most similar to LRP-1; it also binds to the PDGF beta-receptor and modulates receptor-mediated signaling in SMCs. 23 These findings suggest that SMC migration might be regulated by the time-restricted expression of LRs, which determines the outcome of PDGF beta-receptor -  and uPA receptor - mediated signaling.	bind
23533	2	6803	5	13	NULL	NULL	NULL	LRP-1B	GP		bind					PDGF beta-receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1246_s_100	16574889	17,68 - 70    LRP-1B is the giant family member that is most similar to LRP-1; it also binds to the PDGF beta-receptor and modulates receptor-mediated signaling in SMCs. 23 These findings suggest that SMC migration might be regulated by the time-restricted expression of LRs, which determines the outcome of PDGF beta-receptor -  and uPA receptor - mediated signaling.	bind
23534	3	6803	5	13	NULL	NULL	NULL	LRP-1B	GP		modulates					receptor-mediated signaling	Process				NULL	in SMCs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1246_s_100	16574889	17,68 - 70    LRP-1B is the giant family member that is most similar to LRP-1; it also binds to the PDGF beta-receptor and modulates receptor-mediated signaling in SMCs. 23 These findings suggest that SMC migration might be regulated by the time-restricted expression of LRs, which determines the outcome of PDGF beta-receptor -  and uPA receptor - mediated signaling.	bind
23535	5	6803	5	13	NULL	NULL	NULL	statement 4	Process		determines					PDGF beta-receptor mediated signaling	Process	outcome of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1246_s_100	16574889	17,68 - 70    LRP-1B is the giant family member that is most similar to LRP-1; it also binds to the PDGF beta-receptor and modulates receptor-mediated signaling in SMCs. 23 These findings suggest that SMC migration might be regulated by the time-restricted expression of LRs, which determines the outcome of PDGF beta-receptor -  and uPA receptor - mediated signaling.	bind
23536	6	6803	5	13	NULL	NULL	NULL	statement 4	Process		determines					uPA receptor mediated signaling	Process	outcome of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1246_s_100	16574889	17,68 - 70    LRP-1B is the giant family member that is most similar to LRP-1; it also binds to the PDGF beta-receptor and modulates receptor-mediated signaling in SMCs. 23 These findings suggest that SMC migration might be regulated by the time-restricted expression of LRs, which determines the outcome of PDGF beta-receptor -  and uPA receptor - mediated signaling.	bind
56586	4	6803	5	13	NULL	NULL	NULL	LRs	GP	time-restricted expression of	regulates					SMC	Cell	migration of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1246_s_100	16574889	17,68 - 70    LRP-1B is the giant family member that is most similar to LRP-1; it also binds to the PDGF beta-receptor and modulates receptor-mediated signaling in SMCs. 23 These findings suggest that SMC migration might be regulated by the time-restricted expression of LRs, which determines the outcome of PDGF beta-receptor -  and uPA receptor - mediated signaling.	bind
19714	1	6803	6	NULL	NULL	0	NULL	LRP-1B	NULL		bind	NULL				PDGF beta-receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1246_s_100	16574889	17,68 - 70    LRP-1B is the giant family member that is most similar to LRP-1; it also binds to the PDGF beta-receptor and modulates receptor-mediated signaling in SMCs. 23 These findings suggest that SMC migration might be regulated by the time-restricted expression of LRs, which determines the outcome of PDGF beta-receptor -  and uPA receptor - mediated signaling.	bind
19715	2	6803	6	NULL	NULL	0	NULL	LRP-1B	NULL		modulates	NULL				receptor mediated signaling	NULL				NULL	SMC	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1246_s_100	16574889	17,68 - 70    LRP-1B is the giant family member that is most similar to LRP-1; it also binds to the PDGF beta-receptor and modulates receptor-mediated signaling in SMCs. 23 These findings suggest that SMC migration might be regulated by the time-restricted expression of LRs, which determines the outcome of PDGF beta-receptor -  and uPA receptor - mediated signaling.	bind
19716	3	6803	6	NULL	NULL	0	NULL	LRs	NULL	time dependent expression of	regulates	NULL				SMC	NULL	migration of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1246_s_100	16574889	17,68 - 70    LRP-1B is the giant family member that is most similar to LRP-1; it also binds to the PDGF beta-receptor and modulates receptor-mediated signaling in SMCs. 23 These findings suggest that SMC migration might be regulated by the time-restricted expression of LRs, which determines the outcome of PDGF beta-receptor -  and uPA receptor - mediated signaling.	bind
56585	4	6803	6	10	NULL	0	NULL	LRP-1B			is similar to					LRP-1					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1246_s_100	16574889	17,68 - 70    LRP-1B is the giant family member that is most similar to LRP-1; it also binds to the PDGF beta-receptor and modulates receptor-mediated signaling in SMCs. 23 These findings suggest that SMC migration might be regulated by the time-restricted expression of LRs, which determines the outcome of PDGF beta-receptor -  and uPA receptor - mediated signaling.	bind
56587	5	6803	6	10	NULL	0	NULL	statement 3			determines					PDGF beta-receptor mediated signaling		outcome of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1246_s_100	16574889	17,68 - 70    LRP-1B is the giant family member that is most similar to LRP-1; it also binds to the PDGF beta-receptor and modulates receptor-mediated signaling in SMCs. 23 These findings suggest that SMC migration might be regulated by the time-restricted expression of LRs, which determines the outcome of PDGF beta-receptor -  and uPA receptor - mediated signaling.	bind
56588	6	6803	6	10	NULL	0	NULL	statement 3			determines					uPA receptor - mediated signaling		outcome of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1246_s_100	16574889	17,68 - 70    LRP-1B is the giant family member that is most similar to LRP-1; it also binds to the PDGF beta-receptor and modulates receptor-mediated signaling in SMCs. 23 These findings suggest that SMC migration might be regulated by the time-restricted expression of LRs, which determines the outcome of PDGF beta-receptor -  and uPA receptor - mediated signaling.	bind
23537	1	6804	5	13	NULL	NULL	NULL	FasL	GP		bind					Fas protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1785_s_129	10362803	17- 19  Binding of FasL to Fas protein induces trimerization of Fas protein and FADD/MORT-1 and Daxx, the adapter proteins of Fas, bind to the trimerized Fas cytoplasmic region (death domain).	bind
23538	2	6804	5	13	NULL	NULL	NULL	statement 1	Process		induce					Fas protein	GP	trimerization of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1785_s_129	10362803	17- 19  Binding of FasL to Fas protein induces trimerization of Fas protein and FADD/MORT-1 and Daxx, the adapter proteins of Fas, bind to the trimerized Fas cytoplasmic region (death domain).	bind
23539	3	6804	5	13	NULL	NULL	NULL	FADD/MORT-1	GP		is a type of					Fas	GP	adapter protein of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1785_s_129	10362803	17- 19  Binding of FasL to Fas protein induces trimerization of Fas protein and FADD/MORT-1 and Daxx, the adapter proteins of Fas, bind to the trimerized Fas cytoplasmic region (death domain).	bind
23540	4	6804	5	13	NULL	NULL	NULL	Daxx	GP		is a type of					Fas	GP	adapter protein of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1785_s_129	10362803	17- 19  Binding of FasL to Fas protein induces trimerization of Fas protein and FADD/MORT-1 and Daxx, the adapter proteins of Fas, bind to the trimerized Fas cytoplasmic region (death domain).	bind
56589	5	6804	5	13	NULL	NULL	NULL	statement 3	GP		bind					Fas	GP	trimerized	cytoplasmic region (death domain)		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1785_s_129	10362803	17- 19  Binding of FasL to Fas protein induces trimerization of Fas protein and FADD/MORT-1 and Daxx, the adapter proteins of Fas, bind to the trimerized Fas cytoplasmic region (death domain).	bind
56590	6	6804	5	13	NULL	NULL	NULL	statement 4	GP		bind					Fas	GP	trimerized	cytoplasmic region (death domain)		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1785_s_129	10362803	17- 19  Binding of FasL to Fas protein induces trimerization of Fas protein and FADD/MORT-1 and Daxx, the adapter proteins of Fas, bind to the trimerized Fas cytoplasmic region (death domain).	bind
19717	1	6804	6	NULL	NULL	0	NULL	FasL	NULL		bind	NULL				Fas protein	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_6_1785_s_129	10362803	17- 19  Binding of FasL to Fas protein induces trimerization of Fas protein and FADD/MORT-1 and Daxx, the adapter proteins of Fas, bind to the trimerized Fas cytoplasmic region (death domain).	bind
19718	2	6804	6	NULL	NULL	0	NULL	statement 1	NULL		induces	NULL				Fas protein	NULL	trimerization of 			NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_6_1785_s_129	10362803	17- 19  Binding of FasL to Fas protein induces trimerization of Fas protein and FADD/MORT-1 and Daxx, the adapter proteins of Fas, bind to the trimerized Fas cytoplasmic region (death domain).	bind
19719	3	6804	6	10	NULL	0	NULL	FADD/MORT-1	NULL		is a type of	NULL				adapter protein of Fas	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1785_s_129	10362803	17- 19  Binding of FasL to Fas protein induces trimerization of Fas protein and FADD/MORT-1 and Daxx, the adapter proteins of Fas, bind to the trimerized Fas cytoplasmic region (death domain).	bind
19720	4	6804	6	10	NULL	0	NULL	Daxx	NULL		is a type of	NULL				adapter protein of Fas	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1785_s_129	10362803	17- 19  Binding of FasL to Fas protein induces trimerization of Fas protein and FADD/MORT-1 and Daxx, the adapter proteins of Fas, bind to the trimerized Fas cytoplasmic region (death domain).	bind
19721	5	6804	6	NULL	NULL	0	NULL	statement 3	NULL		bind	NULL				Fas	NULL	trimerized	cytoplasmic region (death domain)		NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_6_1785_s_129	10362803	17- 19  Binding of FasL to Fas protein induces trimerization of Fas protein and FADD/MORT-1 and Daxx, the adapter proteins of Fas, bind to the trimerized Fas cytoplasmic region (death domain).	bind
19722	6	6804	6	NULL	NULL	0	NULL	statement 4	NULL		bind	NULL				Fas	NULL	trimerized	cytoplasmic region (death domain)		NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_6_1785_s_129	10362803	17- 19  Binding of FasL to Fas protein induces trimerization of Fas protein and FADD/MORT-1 and Daxx, the adapter proteins of Fas, bind to the trimerized Fas cytoplasmic region (death domain).	bind
23541	1	6805	5	13	NULL	NULL	NULL	Hsp47	GP		bind		transiently			collagen type I	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_219	9686751	176  Hsp47 binds transiently to collagen types I to IV and avidly to denatured collagen substrates; thus, its role in procollagen processing and transport seems firmly established.	bind
23542	2	6805	5	13	NULL	NULL	NULL	Hsp47	GP		bind		transiently			collagen type II	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_219	9686751	176  Hsp47 binds transiently to collagen types I to IV and avidly to denatured collagen substrates; thus, its role in procollagen processing and transport seems firmly established.	bind
23543	3	6805	5	13	NULL	NULL	NULL	Hsp47	GP		bind		transiently			collagen type III	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_219	9686751	176  Hsp47 binds transiently to collagen types I to IV and avidly to denatured collagen substrates; thus, its role in procollagen processing and transport seems firmly established.	bind
23544	4	6805	5	13	NULL	NULL	NULL	Hsp47	GP		bind		transiently			collagen type IV	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_219	9686751	176  Hsp47 binds transiently to collagen types I to IV and avidly to denatured collagen substrates; thus, its role in procollagen processing and transport seems firmly established.	bind
23545	5	6805	5	13	NULL	NULL	NULL	Hsp47	GP		bind		avidly			collagen substrates	GP	denatured			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_219	9686751	176  Hsp47 binds transiently to collagen types I to IV and avidly to denatured collagen substrates; thus, its role in procollagen processing and transport seems firmly established.	bind
23546	6	6805	5	13	NULL	NULL	NULL	Hsp47	GP		plays a role in					procollagen	GP	 processing of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_219	9686751	176  Hsp47 binds transiently to collagen types I to IV and avidly to denatured collagen substrates; thus, its role in procollagen processing and transport seems firmly established.	bind
23547	7	6805	5	13	NULL	NULL	NULL	Hsp47	GP		plays a role in					procollagen 	GP	transport of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_219	9686751	176  Hsp47 binds transiently to collagen types I to IV and avidly to denatured collagen substrates; thus, its role in procollagen processing and transport seems firmly established.	bind
19723	1	6805	6	NULL	NULL	0	NULL	Hsp47	NULL		bind	NULL	transiently			collagen type I	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_219	9686751	176  Hsp47 binds transiently to collagen types I to IV and avidly to denatured collagen substrates; thus, its role in procollagen processing and transport seems firmly established.	bind
19724	2	6805	6	NULL	NULL	0	NULL	Hsp47	NULL		bind	NULL	transiently			collagen type IV	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_219	9686751	176  Hsp47 binds transiently to collagen types I to IV and avidly to denatured collagen substrates; thus, its role in procollagen processing and transport seems firmly established.	bind
19725	3	6805	6	NULL	NULL	0	NULL	Hsp47	NULL		bind	NULL	avidly			collagen substrates	NULL	denatured			NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_219	9686751	176  Hsp47 binds transiently to collagen types I to IV and avidly to denatured collagen substrates; thus, its role in procollagen processing and transport seems firmly established.	bind
19726	4	6805	6	10	NULL	0	NULL	Hsp47			plays a role in					procollagen 		processing of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_219	9686751	176  Hsp47 binds transiently to collagen types I to IV and avidly to denatured collagen substrates; thus, its role in procollagen processing and transport seems firmly established.	bind
19727	5	6805	6	10	NULL	0	NULL	Hsp47			plays a role in					procollagen		 transport of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_219	9686751	176  Hsp47 binds transiently to collagen types I to IV and avidly to denatured collagen substrates; thus, its role in procollagen processing and transport seems firmly established.	bind
56591	6	6805	6	10	NULL	0	NULL	Hsp47			bind		transiently			collagen type II					NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_219	9686751	176  Hsp47 binds transiently to collagen types I to IV and avidly to denatured collagen substrates; thus, its role in procollagen processing and transport seems firmly established.	bind
56592	7	6805	6	10	NULL	0	NULL	Hsp47			bind		transiently			collagen type III					NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_117_s_219	9686751	176  Hsp47 binds transiently to collagen types I to IV and avidly to denatured collagen substrates; thus, its role in procollagen processing and transport seems firmly established.	bind
23548	1	6806	5	13	NULL	NULL	NULL	TRL	GP		bind					macrophage membrane-binding proteins	GP	specific			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_230	10521378	177 178  This effect may be due to apoE-independent binding of TRL to specific macrophage membrane-binding proteins 179 180  or may be the result of cellular recognition and uptake of oxidized remnant lipoproteins.	bind
23549	2	6806	5	13	NULL	NULL	NULL	statement 1	Process		is independent of					apoE	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_230	10521378	177 178  This effect may be due to apoE-independent binding of TRL to specific macrophage membrane-binding proteins 179 180  or may be the result of cellular recognition and uptake of oxidized remnant lipoproteins.	bind
19728	1	6806	6	NULL	NULL	0	NULL	TRL	NULL		bind	NULL				macrophage membrane-binding proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_230	10521378	177 178  This effect may be due to apoE-independent binding of TRL to specific macrophage membrane-binding proteins 179 180  or may be the result of cellular recognition and uptake of oxidized remnant lipoproteins.	bind
19729	2	6806	6	NULL	NULL	0	NULL	statement 1	NULL		is independent of	NULL				apoE	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_230	10521378	177 178  This effect may be due to apoE-independent binding of TRL to specific macrophage membrane-binding proteins 179 180  or may be the result of cellular recognition and uptake of oxidized remnant lipoproteins.	bind
23550	1	6807	5	13	NULL	NULL	NULL	mAKAP	GP		bind					PKA	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_99_8_816_s_183	17038651	178 This latter complex is interesting because mAKAP not only binds PKA and PDE4D3 but also Epac1 and extracellular signal-regulated kinase 5 (ERK5).	bind
23551	2	6807	5	13	NULL	NULL	NULL	mAKAP	GP		bind					PDE4D3	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_99_8_816_s_183	17038651	178 This latter complex is interesting because mAKAP not only binds PKA and PDE4D3 but also Epac1 and extracellular signal-regulated kinase 5 (ERK5).	bind
23552	3	6807	5	13	NULL	NULL	NULL	mAKAP	GP		bind					Epac1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_99_8_816_s_183	17038651	178 This latter complex is interesting because mAKAP not only binds PKA and PDE4D3 but also Epac1 and extracellular signal-regulated kinase 5 (ERK5).	bind
23553	4	6807	5	13	NULL	NULL	NULL	mAKAP	GP		bind					ERK5	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_99_8_816_s_183	17038651	178 This latter complex is interesting because mAKAP not only binds PKA and PDE4D3 but also Epac1 and extracellular signal-regulated kinase 5 (ERK5).	bind
23554	5	6807	5	13	NULL	NULL	NULL	ERK5	GP		is					extracellular signal-regulated kinase 5	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_99_8_816_s_183	17038651	178 This latter complex is interesting because mAKAP not only binds PKA and PDE4D3 but also Epac1 and extracellular signal-regulated kinase 5 (ERK5).	bind
19730	1	6807	6	NULL	NULL	0	NULL	mAKAP	NULL		bind	NULL				PKA	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_99_8_816_s_183	17038651	178 This latter complex is interesting because mAKAP not only binds PKA and PDE4D3 but also Epac1 and extracellular signal-regulated kinase 5 (ERK5).	bind
19731	2	6807	6	NULL	NULL	0	NULL	mAKAP	NULL		bind	NULL				PDE4D3	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_99_8_816_s_183	17038651	178 This latter complex is interesting because mAKAP not only binds PKA and PDE4D3 but also Epac1 and extracellular signal-regulated kinase 5 (ERK5).	bind
19732	3	6807	6	NULL	NULL	0	NULL	mAKAP	NULL		bind	NULL				Epac1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_99_8_816_s_183	17038651	178 This latter complex is interesting because mAKAP not only binds PKA and PDE4D3 but also Epac1 and extracellular signal-regulated kinase 5 (ERK5).	bind
19733	4	6807	6	NULL	NULL	0	NULL	mAKAP	NULL		bind	NULL				ERK5	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_99_8_816_s_183	17038651	178 This latter complex is interesting because mAKAP not only binds PKA and PDE4D3 but also Epac1 and extracellular signal-regulated kinase 5 (ERK5).	bind
19734	5	6807	6	NULL	NULL	0	NULL	ERK5	NULL		is	NULL				extracellular signal-regulated kinase 5	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_99_8_816_s_183	17038651	178 This latter complex is interesting because mAKAP not only binds PKA and PDE4D3 but also Epac1 and extracellular signal-regulated kinase 5 (ERK5).	bind
23627	1	6808	5	13	NULL	NULL	NULL	ER	GP		bind					PI-9	GP			ERU	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_6_5025_s_167	14617632	17beta -Estradiol and Moxestrol Induce Similar Binding of ER to the PI-9 ERU and to the pS2 ERE --	bind
23628	2	6808	5	13	NULL	NULL	NULL	ER	GP		bind					pS2	GP			ERE	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_6_5025_s_167	14617632	17beta -Estradiol and Moxestrol Induce Similar Binding of ER to the PI-9 ERU and to the pS2 ERE --	bind
19735	1	6808	6	10	NULL	0	NULL	ER			bind					PI-9 				ERU	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_6_5025_s_167	14617632	17beta -Estradiol and Moxestrol Induce Similar Binding of ER to the PI-9 ERU and to the pS2 ERE --	bind
19736	2	6808	6	NULL	NULL	0	NULL	ER	NULL		bind	NULL				pS2	NULL			ERE	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_6_5025_s_167	14617632	17beta -Estradiol and Moxestrol Induce Similar Binding of ER to the PI-9 ERU and to the pS2 ERE --	bind
23639	1	6809	5	13	NULL	NULL	NULL	Ah receptor complex	GP		bind									AhRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3430_s_254	9920887	17beta-Estradiol reduced Ah receptor complex binding to AhRE. ECC-1 cells were exposed to TCDD ( T) (10 nM) and 17beta-estradiol ( E2) (10 nM) alone or in combination, or with solvent alone (0.1% Me2SO ( DMSO)), for 1 h, after which nuclear protein extracts were prepared.	bind
23640	2	6809	5	13	NULL	NULL	NULL	17beta-Estradiol	Chemical		reduces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3430_s_254	9920887	17beta-Estradiol reduced Ah receptor complex binding to AhRE. ECC-1 cells were exposed to TCDD ( T) (10 nM) and 17beta-estradiol ( E2) (10 nM) alone or in combination, or with solvent alone (0.1% Me2SO ( DMSO)), for 1 h, after which nuclear protein extracts were prepared.	bind
19737	1	6809	6	NULL	NULL	0	NULL	Ah receptor complex	NULL		bind	NULL					NULL			AhRE	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3430_s_254	9920887	17beta-Estradiol reduced Ah receptor complex binding to AhRE. ECC-1 cells were exposed to TCDD ( T) (10 nM) and 17beta-estradiol ( E2) (10 nM) alone or in combination, or with solvent alone (0.1% Me2SO ( DMSO)), for 1 h, after which nuclear protein extracts were prepared.	bind
19738	2	6809	6	NULL	NULL	0	NULL	17beta-Estradiol	NULL		reduces	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3430_s_254	9920887	17beta-Estradiol reduced Ah receptor complex binding to AhRE. ECC-1 cells were exposed to TCDD ( T) (10 nM) and 17beta-estradiol ( E2) (10 nM) alone or in combination, or with solvent alone (0.1% Me2SO ( DMSO)), for 1 h, after which nuclear protein extracts were prepared.	bind
23652	1	6811	5	13	NULL	NULL	NULL	binuclear zinc AlcR activator	GP		bind		specifically			DNA	NucleicAcid				NULL	in Aspergillus nidulans	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_10_2181_s_247	11353088	18       Nikolaev,I., Lenouvel,F. and Felenbok,B. (1999) Unique DNA binding specificity of the binuclear zinc AlcR activator of the ethanol utilization pathway in  Aspergillus nidulans.	bind
44701	2	6811	5	13	NULL	NULL	NULL	binuclear zinc AlcR activator	GP		belongs to					ethanol utilization pathway	Process				NULL	Aspergillus nidulans	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_10_2181_s_247	11353088	18       Nikolaev,I., Lenouvel,F. and Felenbok,B. (1999) Unique DNA binding specificity of the binuclear zinc AlcR activator of the ethanol utilization pathway in  Aspergillus nidulans.	bind
19739	1	6811	6	10	NULL	0	NULL	binuclear zinc AlcR activator 			bind					DNA					NULL	Aspergillus nidulans	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_10_2181_s_247	11353088	18       Nikolaev,I., Lenouvel,F. and Felenbok,B. (1999) Unique DNA binding specificity of the binuclear zinc AlcR activator of the ethanol utilization pathway in  Aspergillus nidulans.	bind
56593	2	6811	6	10	NULL	0	NULL	binuclear zinc AlcR activator			belongs to					ethanol utilization pathway					NULL	Aspergillus nidulans	0	NULL	NULL	NULL	gw60_nucleicacidsres_29_10_2181_s_247	11353088	18       Nikolaev,I., Lenouvel,F. and Felenbok,B. (1999) Unique DNA binding specificity of the binuclear zinc AlcR activator of the ethanol utilization pathway in  Aspergillus nidulans.	bind
23658	1	6813	5	13	NULL	NULL	NULL	DNA	NucleicAcid	nucleosomal	regulates					Hat1 acetyltransferase	GP	human	core-histone-binding subunit		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3131_s_239	11470869	18       Verreault,A., Kaufman,P.D., Kobayashi,R. and Stillman,B. (1998) Nucleosomal DNA regulates the core-histone-binding subunit of the human Hat1 acetyltransferase.	bind
19740	1	6813	6	10	NULL	0	NULL	 DNA		Nucleosomal	regulates					Hat1 acetyltransferase		human	core-histone-binding subunit		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3131_s_239	11470869	18       Verreault,A., Kaufman,P.D., Kobayashi,R. and Stillman,B. (1998) Nucleosomal DNA regulates the core-histone-binding subunit of the human Hat1 acetyltransferase.	bind
23675	1	6814	5	13	NULL	NULL	NULL	Megalin/gp330	GP		bind					plasminogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
23678	2	6814	5	13	NULL	NULL	NULL	Lp(a)	GP		bind		might			megalin/gp330	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
23681	3	6814	5	13	NULL	NULL	NULL	statement 2	Process		occurs by					apoB100	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
23682	4	6814	5	13	NULL	NULL	NULL	statement 2	Process		occurs by					apo(a)	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
23684	5	6814	5	13	NULL	NULL	NULL	statement 3	Process		occurs simulataneous with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
23685	6	6814	5	13	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
23687	7	6814	5	13	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
56594	8	6814	5	13	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
56595	9	6814	5	13	NULL	NULL	NULL	Megalin/gp330	GP		is a member of					LDLR gene family	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
56596	10	6814	5	13	NULL	NULL	NULL	plasminogen	GP		is homologous to					apo(a) 	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
19741	1	6814	6	10	NULL	0	NULL	Megalin/gp330			bind					 plasminogen					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
19742	2	6814	6	NULL	NULL	0	NULL	Megalin/gp330	NULL		is a member of	NULL				LDLR gene family	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
19743	3	6814	6	NULL	NULL	0	NULL	Lp(a)	NULL		bind	NULL	may			megalin/gp330	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
19744	4	6814	6	NULL	NULL	0	NULL	statement 3	NULL		occurs by	NULL				apoB100	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
19745	5	6814	6	NULL	NULL	0	NULL	statement 3	NULL		occurs by	NULL				apo(a)	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
19746	6	6814	6	NULL	NULL	0	NULL	statement 4	NULL		is an alternative to	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
56597	7	6814	6	10	NULL	0	NULL	statement 4			occur simulataneous with					statement 5					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
56598	8	6814	6	10	NULL	0	NULL	statement 4			is an alternative to					statement 7					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
56599	9	6814	6	10	NULL	0	NULL	statement 5			is an alternative to					statement 7					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
56600	10	6814	6	10	NULL	0	NULL	plasminogen			is homologous to					apo(a) 					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_248	10073957	18  19 20 21 22 23 24 25  Megalin/gp330 is known to be the only member of the  LDLR gene family to bind the apo(a) homologue plasminogen, 33 36  thus suggesting that Lp(a) might bind to megalin/gp330 by either apoB100, apo(a), or both apolipoproteins.	bind
23719	1	6815	5	13	NULL	NULL	NULL	TSP1	GP		bind					TGF-beta1	GP	latent			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_4_1255_s_33	11583953	18  Based on the identified interaction sites between TSP1 and TGF-beta1 it has been suggested that TSP1 and TSP2 may compete for binding to latent TGF-beta1, but only binding of TSP1 would lead to its activation.	bind
23720	2	6815	5	13	NULL	NULL	NULL	TSP2	GP		bind					TGF-beta1	GP	latent			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_4_1255_s_33	11583953	18  Based on the identified interaction sites between TSP1 and TGF-beta1 it has been suggested that TSP1 and TSP2 may compete for binding to latent TGF-beta1, but only binding of TSP1 would lead to its activation.	bind
23721	3	6815	5	13	NULL	NULL	NULL	statement 1	Process		competes with		may			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_4_1255_s_33	11583953	18  Based on the identified interaction sites between TSP1 and TGF-beta1 it has been suggested that TSP1 and TSP2 may compete for binding to latent TGF-beta1, but only binding of TSP1 would lead to its activation.	bind
23722	4	6815	5	13	NULL	NULL	NULL	statement 1	Process		leads to					TGF-beta1	GP	activation of latent			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_4_1255_s_33	11583953	18  Based on the identified interaction sites between TSP1 and TGF-beta1 it has been suggested that TSP1 and TSP2 may compete for binding to latent TGF-beta1, but only binding of TSP1 would lead to its activation.	bind
19747	1	6815	6	NULL	NULL	0	NULL	TSP1	NULL		bind	NULL				TGF-beta1	NULL	latent			NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_4_1255_s_33	11583953	18  Based on the identified interaction sites between TSP1 and TGF-beta1 it has been suggested that TSP1 and TSP2 may compete for binding to latent TGF-beta1, but only binding of TSP1 would lead to its activation.	bind
19748	2	6815	6	NULL	NULL	0	NULL	TSP2	NULL		bind	NULL				TGF-beta1	NULL	latent			NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_4_1255_s_33	11583953	18  Based on the identified interaction sites between TSP1 and TGF-beta1 it has been suggested that TSP1 and TSP2 may compete for binding to latent TGF-beta1, but only binding of TSP1 would lead to its activation.	bind
19749	3	6815	6	NULL	NULL	0	NULL	statement 1	NULL		competes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_4_1255_s_33	11583953	18  Based on the identified interaction sites between TSP1 and TGF-beta1 it has been suggested that TSP1 and TSP2 may compete for binding to latent TGF-beta1, but only binding of TSP1 would lead to its activation.	bind
19750	4	6815	6	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				TGF-beta1	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_4_1255_s_33	11583953	18  Based on the identified interaction sites between TSP1 and TGF-beta1 it has been suggested that TSP1 and TSP2 may compete for binding to latent TGF-beta1, but only binding of TSP1 would lead to its activation.	bind
23723	1	6816	5	13	NULL	NULL	NULL				lowers		greatly	Tyr-13 point mutations		monocyte chemoattractant protein-1 receptor	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_2_591_s_28	10433951	18  Consistent with the concept that tyrosine is important in binding to receptor, point mutations of Tyr-13 greatly lowered monocyte chemoattractant protein-1 receptor binding and activity, 19 and changing Tyr-28 to aspartate essentially abolished the monocyte chemoattractant activity of monocyte chemoattractant protein-1.	bind
23724	3	6816	5	10	NULL	0	NULL				is changed to			Tyr-28					aspartate		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_2_591_s_28	10433951	18  Consistent with the concept that tyrosine is important in binding to receptor, point mutations of Tyr-13 greatly lowered monocyte chemoattractant protein-1 receptor binding and activity, 19 and changing Tyr-28 to aspartate essentially abolished the monocyte chemoattractant activity of monocyte chemoattractant protein-1.	bind
23725	5	6816	5	13	NULL	NULL	NULL	statement 3	Process		abolishes					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_2_591_s_28	10433951	18  Consistent with the concept that tyrosine is important in binding to receptor, point mutations of Tyr-13 greatly lowered monocyte chemoattractant protein-1 receptor binding and activity, 19 and changing Tyr-28 to aspartate essentially abolished the monocyte chemoattractant activity of monocyte chemoattractant protein-1.	bind
23728	2	6816	5	13	NULL	NULL	NULL				lowers		greatly	Tyr-13 point mutations		monocyte chemoattractant protein-1 receptor	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_2_591_s_28	10433951	18  Consistent with the concept that tyrosine is important in binding to receptor, point mutations of Tyr-13 greatly lowered monocyte chemoattractant protein-1 receptor binding and activity, 19 and changing Tyr-28 to aspartate essentially abolished the monocyte chemoattractant activity of monocyte chemoattractant protein-1.	bind
58592	4	6816	5	13	NULL	NULL	NULL	monocyte chemoattractant protein-1	GP		activates					monocyte chemoattractant	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_2_591_s_28	10433951	18  Consistent with the concept that tyrosine is important in binding to receptor, point mutations of Tyr-13 greatly lowered monocyte chemoattractant protein-1 receptor binding and activity, 19 and changing Tyr-28 to aspartate essentially abolished the monocyte chemoattractant activity of monocyte chemoattractant protein-1.	bind
19854	1	6816	6	10	NULL	0	NULL				lowers		greatly	Tyr-13 point mutations		monocyte chemoattractant protein-1 receptor		binding of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_2_591_s_28	10433951	18  Consistent with the concept that tyrosine is important in binding to receptor, point mutations of Tyr-13 greatly lowered monocyte chemoattractant protein-1 receptor binding and activity, 19 and changing Tyr-28 to aspartate essentially abolished the monocyte chemoattractant activity of monocyte chemoattractant protein-1.	bind
19855	2	6816	6	10	NULL	0	NULL				lowers		greatly	Tyr-13 point mutations		monocyte chemoattractant protein-1 receptor		activity of 			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_2_591_s_28	10433951	18  Consistent with the concept that tyrosine is important in binding to receptor, point mutations of Tyr-13 greatly lowered monocyte chemoattractant protein-1 receptor binding and activity, 19 and changing Tyr-28 to aspartate essentially abolished the monocyte chemoattractant activity of monocyte chemoattractant protein-1.	bind
19856	3	6816	6	NULL	NULL	0	NULL		NULL		is changed to	NULL		Tyr-28			NULL		Aspartate		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_2_591_s_28	10433951	18  Consistent with the concept that tyrosine is important in binding to receptor, point mutations of Tyr-13 greatly lowered monocyte chemoattractant protein-1 receptor binding and activity, 19 and changing Tyr-28 to aspartate essentially abolished the monocyte chemoattractant activity of monocyte chemoattractant protein-1.	bind
19857	4	6816	6	10	NULL	0	NULL	monocyte chemoattractant protein-1			activates					monocyte chemoattractant					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_2_591_s_28	10433951	18  Consistent with the concept that tyrosine is important in binding to receptor, point mutations of Tyr-13 greatly lowered monocyte chemoattractant protein-1 receptor binding and activity, 19 and changing Tyr-28 to aspartate essentially abolished the monocyte chemoattractant activity of monocyte chemoattractant protein-1.	bind
19858	5	6816	6	NULL	NULL	0	NULL	statement 3	NULL		abolishes	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_2_591_s_28	10433951	18  Consistent with the concept that tyrosine is important in binding to receptor, point mutations of Tyr-13 greatly lowered monocyte chemoattractant protein-1 receptor binding and activity, 19 and changing Tyr-28 to aspartate essentially abolished the monocyte chemoattractant activity of monocyte chemoattractant protein-1.	bind
23726	1	6817	5	13	NULL	NULL	NULL			point mutations of	lowered		greatly	Tyr-13		monocyte chemoattractant protein-1 receptor	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_2_591_s_227	10433951	18  Consistent with the concept that tyrosine is important in binding to receptor, Steitz et al 19  reported that point mutations of Tyr-13 greatly lowered monocyte chemoattractant protein-1 receptor binding and activity.	bind
23727	2	6817	5	13	NULL	NULL	NULL			point mutations of	lowered		greatly	Tyr-13		monocyte chemoattractant protein-1 receptor	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_2_591_s_227	10433951	18  Consistent with the concept that tyrosine is important in binding to receptor, Steitz et al 19  reported that point mutations of Tyr-13 greatly lowered monocyte chemoattractant protein-1 receptor binding and activity.	bind
19760	1	6817	6	13	NULL	NULL	NULL	tyrosine	AminoAcid		is important for					receptor	GP	binding to			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_2_591_s_227	10433951	18  Consistent with the concept that tyrosine is important in binding to receptor, Steitz et al 19  reported that point mutations of Tyr-13 greatly lowered monocyte chemoattractant protein-1 receptor binding and activity.	bind
19761	2	6817	6	NULL	NULL	0	NULL		NULL	point mutation	lowered	NULL		Tyr-13		monocyte chemoattractant protein-1 receptor	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_2_591_s_227	10433951	18  Consistent with the concept that tyrosine is important in binding to receptor, Steitz et al 19  reported that point mutations of Tyr-13 greatly lowered monocyte chemoattractant protein-1 receptor binding and activity.	bind
19762	3	6817	6	NULL	NULL	0	NULL		NULL	point mutation	lowered	NULL		Tyr-13		monocyte chemoattractant protein-1 receptor	NULL	activity of 			NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_2_591_s_227	10433951	18  Consistent with the concept that tyrosine is important in binding to receptor, Steitz et al 19  reported that point mutations of Tyr-13 greatly lowered monocyte chemoattractant protein-1 receptor binding and activity.	bind
23729	1	6818	5	13	NULL	NULL	NULL	FN	GP		bind					ECs	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1544_s_154	8977460	18  Furthermore, heparin failed to inhibit binding of FN to ECs (Fig 8B  ), even though concentration-dependent binding of FN to ECs was demonstrated (Fig 8A  ).	bind
23730	2	6818	5	13	NULL	NULL	NULL	heparin	Chemical		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1544_s_154	8977460	18  Furthermore, heparin failed to inhibit binding of FN to ECs (Fig 8B  ), even though concentration-dependent binding of FN to ECs was demonstrated (Fig 8A  ).	bind
44702	3	6818	5	13	NULL	NULL	NULL	statement 1	Process		depends on					concentration	QuantityOrMeasure				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1544_s_154	8977460	18  Furthermore, heparin failed to inhibit binding of FN to ECs (Fig 8B  ), even though concentration-dependent binding of FN to ECs was demonstrated (Fig 8A  ).	bind
19763	1	6818	6	NULL	NULL	0	NULL	FN	NULL		bind	NULL				EC	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1544_s_154	8977460	18  Furthermore, heparin failed to inhibit binding of FN to ECs (Fig 8B  ), even though concentration-dependent binding of FN to ECs was demonstrated (Fig 8A  ).	bind
19764	2	6818	6	NULL	NULL	0	NULL	heparin	NULL		does not inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1544_s_154	8977460	18  Furthermore, heparin failed to inhibit binding of FN to ECs (Fig 8B  ), even though concentration-dependent binding of FN to ECs was demonstrated (Fig 8A  ).	bind
19766	3	6818	6	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				concentration	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1544_s_154	8977460	18  Furthermore, heparin failed to inhibit binding of FN to ECs (Fig 8B  ), even though concentration-dependent binding of FN to ECs was demonstrated (Fig 8A  ).	bind
23731	1	6819	5	13	NULL	NULL	NULL	antibodies	GP		bind		specifically			gelB	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
23732	2	6819	5	13	NULL	NULL	NULL	TIMP-1	GP		bind		specifically			gelB	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
23733	3	6819	5	13	NULL	NULL	NULL	statement 1	Process		disrupt		directly			cell-cell interactions	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
23734	4	6819	5	13	NULL	NULL	NULL	statement 1	Process		disrupt		indirectly			cell-cell interactions	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
23735	5	6819	5	13	NULL	NULL	NULL	statement 2	Process		disrupt		directly			cell-cell interactions	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
23736	6	6819	5	13	NULL	NULL	NULL	statement 2	Process		disrupt		indirectly			cell-cell interactions	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
23737	7	6819	5	13	NULL	NULL	NULL	statement 1	Process		disrupt		directly			cell-matrix interactions	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
23738	8	6819	5	13	NULL	NULL	NULL	statement 1	Process		disrupt		indirectly			cell-matrix interactions	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
23739	9	6819	5	13	NULL	NULL	NULL	statement 2	Process		disrupt		directly			cell-matrix interactions	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
23740	10	6819	5	13	NULL	NULL	NULL	statement 2	Process		disrupt		indirectly			cell-matrix interactions	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
23741	11	6819	5	13	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
23742	12	6819	5	13	NULL	NULL	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
23743	13	6819	5	13	NULL	NULL	NULL	statement 7	Process		is an alternative to					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
23744	14	6819	5	13	NULL	NULL	NULL	statement 9	Process		is an alternative to					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
56603	15	6819	5	13	NULL	NULL	NULL	cell-cell interactions	Process		are necessary for					branching morphogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
56604	16	6819	5	13	NULL	NULL	NULL	cell-matrix interactions	Process		are necessary for					branching morphogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
19767	1	6819	6	NULL	NULL	0	NULL	antibodies	NULL		bind	NULL	specifically			gelB	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
19768	2	6819	6	NULL	NULL	0	NULL	TIMP-1	NULL		bind	NULL	specifically			gelB	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
19769	3	6819	6	NULL	NULL	0	NULL	cell-cell interactions	NULL		are necessary for	NULL				branching morphogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
19770	4	6819	6	NULL	NULL	0	NULL	cell-matrix interactions	NULL		are necessary for	NULL				branching morphogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
19771	5	6819	6	NULL	NULL	0	NULL	statement 1	NULL		disrupts	NULL				cell-cell interactions	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
19772	6	6819	6	NULL	NULL	0	NULL	statement 2	NULL		disrupts	NULL				cell-matrix interactions	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_1_303_s_218	10880400	18  In the studies of Lelongt et al, 8  the antibodies and TIMP-1 which bind specifically to gelB may somehow, either directly or indirectly, disrupt cell-cell or cell-matrix interactions that are necessary for branching morphogenesis.	bind
23745	1	6820	5	13	NULL	NULL	NULL	JNK	GP		bind					c-Jun	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_227_s_23	9484987	18  On the other hand, JNK binds to c-Jun to specifically phosphorylate Ser-63 and -73 at the  N-terminal of c-Jun, 19  a major component of AP-1 transcriptional complex.	bind
23746	2	6820	5	13	NULL	NULL	NULL	statement 1	GP		phosphorylates		specifically			c-Jun	GP		Ser-63 at N-terminal		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_227_s_23	9484987	18  On the other hand, JNK binds to c-Jun to specifically phosphorylate Ser-63 and -73 at the  N-terminal of c-Jun, 19  a major component of AP-1 transcriptional complex.	bind
23747	3	6820	5	13	NULL	NULL	NULL	statement 1	GP		phosphorylates		specifically			c-Jun	GP		Ser-73 at N-terminal		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_227_s_23	9484987	18  On the other hand, JNK binds to c-Jun to specifically phosphorylate Ser-63 and -73 at the  N-terminal of c-Jun, 19  a major component of AP-1 transcriptional complex.	bind
23748	4	6820	5	13	NULL	NULL	NULL	statement 1	GP		is a component of		major			AP-1 transcriptional complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_227_s_23	9484987	18  On the other hand, JNK binds to c-Jun to specifically phosphorylate Ser-63 and -73 at the  N-terminal of c-Jun, 19  a major component of AP-1 transcriptional complex.	bind
56605	5	6820	5	13	NULL	NULL	NULL	statement 2	Process		occur simulataneous with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_227_s_23	9484987	18  On the other hand, JNK binds to c-Jun to specifically phosphorylate Ser-63 and -73 at the  N-terminal of c-Jun, 19  a major component of AP-1 transcriptional complex.	bind
19859	1	6820	6	NULL	NULL	0	NULL	JNK	NULL		bind	NULL				c-Jun	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_227_s_23	9484987	18  On the other hand, JNK binds to c-Jun to specifically phosphorylate Ser-63 and -73 at the  N-terminal of c-Jun, 19  a major component of AP-1 transcriptional complex.	bind
19860	2	6820	6	10	NULL	0	NULL	statement 1			phosphorylates		specifically			c-Jun			ser-63 at the N-terminal		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_227_s_23	9484987	18  On the other hand, JNK binds to c-Jun to specifically phosphorylate Ser-63 and -73 at the  N-terminal of c-Jun, 19  a major component of AP-1 transcriptional complex.	bind
19861	3	6820	6	10	NULL	0	NULL	statement 1			phosphorylates		specifically			c-Jun			Ser-73 at the N-terminal		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_227_s_23	9484987	18  On the other hand, JNK binds to c-Jun to specifically phosphorylate Ser-63 and -73 at the  N-terminal of c-Jun, 19  a major component of AP-1 transcriptional complex.	bind
19862	4	6820	6	NULL	NULL	0	NULL	c-Jun	NULL		is a major component of	NULL				AP-1 transcriptional complex	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_227_s_23	9484987	18  On the other hand, JNK binds to c-Jun to specifically phosphorylate Ser-63 and -73 at the  N-terminal of c-Jun, 19  a major component of AP-1 transcriptional complex.	bind
20118	5	6820	6	NULL	NULL	0	NULL	statement 2	NULL		occurs simultaneously with	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_227_s_23	9484987	18  On the other hand, JNK binds to c-Jun to specifically phosphorylate Ser-63 and -73 at the  N-terminal of c-Jun, 19  a major component of AP-1 transcriptional complex.	bind
23749	1	6821	5	13	NULL	NULL	NULL	TAFIa	GP		bind		reduced affinity			plasminogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2511_s_93	11116046	18  TAFIa exhibits at least a 10-fold reduced affinity for plasminogen, suggesting that binding to plasminogen is facilitated through the activation peptide, although the physiological role for the interaction has not been elucidated.	bind
23751	2	6821	5	13	NULL	NULL	NULL	statement 1	Process		is facilitated through					activation peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2511_s_93	11116046	18  TAFIa exhibits at least a 10-fold reduced affinity for plasminogen, suggesting that binding to plasminogen is facilitated through the activation peptide, although the physiological role for the interaction has not been elucidated.	bind
23752	3	6821	5	13	NULL	NULL	NULL	statement 1	Process		suggests					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2511_s_93	11116046	18  TAFIa exhibits at least a 10-fold reduced affinity for plasminogen, suggesting that binding to plasminogen is facilitated through the activation peptide, although the physiological role for the interaction has not been elucidated.	bind
19774	1	6821	6	NULL	NULL	0	NULL	TAFIa	NULL		bind	NULL	reduced affinity			plasminogen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2511_s_93	11116046	18  TAFIa exhibits at least a 10-fold reduced affinity for plasminogen, suggesting that binding to plasminogen is facilitated through the activation peptide, although the physiological role for the interaction has not been elucidated.	bind
19776	2	6821	6	NULL	NULL	0	NULL	statement 1	NULL		is facilitated through	NULL				activation peptide	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2511_s_93	11116046	18  TAFIa exhibits at least a 10-fold reduced affinity for plasminogen, suggesting that binding to plasminogen is facilitated through the activation peptide, although the physiological role for the interaction has not been elucidated.	bind
56606	3	6821	6	10	NULL	0	NULL	statement 1			suggests					statement 2					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2511_s_93	11116046	18  TAFIa exhibits at least a 10-fold reduced affinity for plasminogen, suggesting that binding to plasminogen is facilitated through the activation peptide, although the physiological role for the interaction has not been elucidated.	bind
23753	1	6822	5	13	NULL	NULL	NULL	myosin	GP		bind		weakly			actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_2_439_s_115	7614728	18  The hydrolysis step is believed to occur while the myosin is weakly bound to actin (ie, when the myosin rapidly attaches and detaches from actin).	bind
23754	2	6822	5	13	NULL	NULL	NULL	statement 1	Process		leads to					hydrolysis	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_2_439_s_115	7614728	18  The hydrolysis step is believed to occur while the myosin is weakly bound to actin (ie, when the myosin rapidly attaches and detaches from actin).	bind
19785	1	6822	6	NULL	NULL	0	NULL	myosin	NULL		bind	NULL	weakly			actin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_77_2_439_s_115	7614728	18  The hydrolysis step is believed to occur while the myosin is weakly bound to actin (ie, when the myosin rapidly attaches and detaches from actin).	bind
19786	2	6822	6	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				hydrolysis	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_77_2_439_s_115	7614728	18  The hydrolysis step is believed to occur while the myosin is weakly bound to actin (ie, when the myosin rapidly attaches and detaches from actin).	bind
23755	1	6823	5	13	NULL	NULL	NULL	apo(a)	GP		bind								lysine		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_575_s_210	10669658	18  The mechanism by which Lp(a) may favor the atherothrombotic process may be related to the lysine-binding properties of apo(a).	bind
23756	2	6823	5	13	NULL	NULL	NULL	Lp(a)	GP		favor		may			atherothrombosis	MedicalFinding	process of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_575_s_210	10669658	18  The mechanism by which Lp(a) may favor the atherothrombotic process may be related to the lysine-binding properties of apo(a).	bind
23757	3	6823	5	13	NULL	NULL	NULL	statement 2	Process	mechanism of	related to		may be			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_575_s_210	10669658	18  The mechanism by which Lp(a) may favor the atherothrombotic process may be related to the lysine-binding properties of apo(a).	bind
19787	1	6823	6	NULL	NULL	0	NULL	apo(a)	NULL		bind	NULL				lysine	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_575_s_210	10669658	18  The mechanism by which Lp(a) may favor the atherothrombotic process may be related to the lysine-binding properties of apo(a).	bind
19788	2	6823	6	10	NULL	0	NULL	Lp(a)			favour					atherothrombosis		process of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_575_s_210	10669658	18  The mechanism by which Lp(a) may favor the atherothrombotic process may be related to the lysine-binding properties of apo(a).	bind
19789	3	6823	6	10	NULL	0	NULL	statement 2			related to		may be			statement 1					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_575_s_210	10669658	18  The mechanism by which Lp(a) may favor the atherothrombotic process may be related to the lysine-binding properties of apo(a).	bind
23758	1	6824	5	13	NULL	NULL	NULL	CsA	Chemical		bind					immunophilin proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_20_2431_s_157	10821822	18  The significant biological effects in common to both CsA and FK506, which each bind different immunophilin proteins, have been attributed to their ability to inhibit calcineurin.	bind
23759	2	6824	5	13	NULL	NULL	NULL	FK506	Chemical		bind					immunophilin proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_20_2431_s_157	10821822	18  The significant biological effects in common to both CsA and FK506, which each bind different immunophilin proteins, have been attributed to their ability to inhibit calcineurin.	bind
23760	3	6824	5	13	NULL	NULL	NULL	CsA	Chemical		inhibit					calcineurin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_20_2431_s_157	10821822	18  The significant biological effects in common to both CsA and FK506, which each bind different immunophilin proteins, have been attributed to their ability to inhibit calcineurin.	bind
23761	4	6824	5	13	NULL	NULL	NULL	FK506	Chemical		inhibit					calcineurin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_20_2431_s_157	10821822	18  The significant biological effects in common to both CsA and FK506, which each bind different immunophilin proteins, have been attributed to their ability to inhibit calcineurin.	bind
23762	5	6824	5	13	NULL	NULL	NULL	statement 1	Process		is attributed to					statement 3	Process	ability of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_20_2431_s_157	10821822	18  The significant biological effects in common to both CsA and FK506, which each bind different immunophilin proteins, have been attributed to their ability to inhibit calcineurin.	bind
23763	6	6824	5	13	NULL	NULL	NULL	statement 2	Process		is attributed to					statement 4	Process	ability of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_20_2431_s_157	10821822	18  The significant biological effects in common to both CsA and FK506, which each bind different immunophilin proteins, have been attributed to their ability to inhibit calcineurin.	bind
19790	1	6824	6	NULL	NULL	0	NULL	CsA	NULL		inhibit	NULL				calcineurin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_101_20_2431_s_157	10821822	18  The significant biological effects in common to both CsA and FK506, which each bind different immunophilin proteins, have been attributed to their ability to inhibit calcineurin.	bind
19791	2	6824	6	NULL	NULL	0	NULL	CsA	NULL		bind	NULL				immunophilin proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_101_20_2431_s_157	10821822	18  The significant biological effects in common to both CsA and FK506, which each bind different immunophilin proteins, have been attributed to their ability to inhibit calcineurin.	bind
19792	3	6824	6	NULL	NULL	0	NULL	FK506	NULL		bind	NULL				immunophilin proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_101_20_2431_s_157	10821822	18  The significant biological effects in common to both CsA and FK506, which each bind different immunophilin proteins, have been attributed to their ability to inhibit calcineurin.	bind
19793	4	6824	6	NULL	NULL	0	NULL	FK506	NULL		inhibit	NULL				calcineurin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_101_20_2431_s_157	10821822	18  The significant biological effects in common to both CsA and FK506, which each bind different immunophilin proteins, have been attributed to their ability to inhibit calcineurin.	bind
56607	5	6824	6	10	NULL	0	NULL	statement 2			is attributed to					statement 1		ability of			NULL		0	NULL	NULL	NULL	gw60_circulation_101_20_2431_s_157	10821822	18  The significant biological effects in common to both CsA and FK506, which each bind different immunophilin proteins, have been attributed to their ability to inhibit calcineurin.	bind
56608	6	6824	6	10	NULL	0	NULL	statement 3			is attributed to					statement 4		ability of			NULL		0	NULL	NULL	NULL	gw60_circulation_101_20_2431_s_157	10821822	18  The significant biological effects in common to both CsA and FK506, which each bind different immunophilin proteins, have been attributed to their ability to inhibit calcineurin.	bind
23764	1	6825	5	13	NULL	NULL	NULL	FGF-1	GP		bind		may			FGFR-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_7_854_s_145	12176960	18 -  21 FGF-1 may bind to 4 FGF receptors, termed FGFR-1, -2, -3, and -4.	bind
23765	2	6825	5	13	NULL	NULL	NULL	FGF-1	GP		bind		may			FGFR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_7_854_s_145	12176960	18 -  21 FGF-1 may bind to 4 FGF receptors, termed FGFR-1, -2, -3, and -4.	bind
23766	3	6825	5	13	NULL	NULL	NULL	FGF-1	GP		bind		may			FGFR-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_7_854_s_145	12176960	18 -  21 FGF-1 may bind to 4 FGF receptors, termed FGFR-1, -2, -3, and -4.	bind
23767	4	6825	5	13	NULL	NULL	NULL	FGF-1	GP		bind		may			FGFR-4	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_7_854_s_145	12176960	18 -  21 FGF-1 may bind to 4 FGF receptors, termed FGFR-1, -2, -3, and -4.	bind
19794	1	6825	6	NULL	NULL	0	NULL	FGF-1	NULL		bind	NULL	may			FGFR-1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_7_854_s_145	12176960	18 -  21 FGF-1 may bind to 4 FGF receptors, termed FGFR-1, -2, -3, and -4.	bind
19795	2	6825	6	NULL	NULL	0	NULL	FGF-1	NULL		bind	NULL	may			FGFR-2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_7_854_s_145	12176960	18 -  21 FGF-1 may bind to 4 FGF receptors, termed FGFR-1, -2, -3, and -4.	bind
19796	3	6825	6	NULL	NULL	0	NULL	FGF-1	NULL		bind	NULL	may			FGFR-3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_7_854_s_145	12176960	18 -  21 FGF-1 may bind to 4 FGF receptors, termed FGFR-1, -2, -3, and -4.	bind
19797	4	6825	6	NULL	NULL	0	NULL	FGF-1	NULL		bind	NULL	may			FGFR-4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_7_854_s_145	12176960	18 -  21 FGF-1 may bind to 4 FGF receptors, termed FGFR-1, -2, -3, and -4.	bind
23768	1	6826	5	13	NULL	NULL	NULL	LTIP	GP		is					lipid transfer inhibitor protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
23769	2	6826	5	13	NULL	NULL	NULL	LTIP	GP		is characterized as					acidic glycoprotein	GP	unique			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
23770	3	6826	5	13	NULL	NULL	NULL	LTIP	GP		suppresses					LTP	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
23771	4	6826	5	13	NULL	NULL	NULL	LTP	GP		bind					lipoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
23772	5	6826	5	13	NULL	NULL	NULL	LTIP	GP		disrupt					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
23774	6	6826	5	13	NULL	NULL	NULL	statement 3	Process		correlates with		directly			statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
23775	7	6826	5	13	NULL	NULL	NULL	LTIP	GP		inhibit					LTP	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
23776	8	6826	5	13	NULL	NULL	NULL	LTIP	GP		interacts with					lipoprotein	GP	surface			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
23777	9	6826	5	13	NULL	NULL	NULL	transfer protein	GP		interacts with					lipoprotein	GP	surface			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
23778	10	6826	5	13	NULL	NULL	NULL	statement 8	Process		competes with					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
23779	11	6826	5	13	NULL	NULL	NULL	statement 6	Process		suggests					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
23780	12	6826	5	13	NULL	NULL	NULL	statement 7	Process		occurs by					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
19799	1	6826	6	NULL	NULL	0	NULL	LTIP	NULL		is	NULL				lipid transfer inhibitor protein	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
19800	2	6826	6	NULL	NULL	0	NULL	LTIP	NULL		is characterized as	NULL				acidic glycoprotein	NULL	unique 			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
19801	3	6826	6	NULL	NULL	0	NULL	LTIP	NULL		suppress	NULL				LTP 	NULL	activity of 			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
19802	4	6826	6	NULL	NULL	0	NULL	LTP	NULL		bind	NULL				lipoprotein	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
19806	5	6826	6	NULL	NULL	0	NULL	LTIP	NULL		disrupts	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
19807	6	6826	6	10	NULL	0	NULL	LTIP			inhibit					LTP					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
19808	7	6826	6	10	NULL	0	NULL	statement 3			correlates with		directly			statement 4					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
56609	8	6826	6	10	NULL	0	NULL	LTIP			interacts with					lipoprotein		surface			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
56610	9	6826	6	10	NULL	0	NULL	transfer protein			interacts with					lipoprotein		surface			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
56611	10	6826	6	10	NULL	0	NULL	statement 8			compete with					statement 9					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
56612	11	6826	6	10	NULL	0	NULL	statement 7			suggests					statement 6					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
56613	12	6826	6	10	NULL	0	NULL	statement 6			occur by					statement 10					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1716_s_28	9327768	18 - 20 This protein, termed lipid transfer inhibitor protein (LTIP), is characterized as a unique acidic glycoprotein with a molecular weight ranging from 29 000 to 35 000.18,19 Although the mechanism of LTIP is not well understood, binding studies have demonstrated a direct correlation between the suppression of LTP activity by LTIP and the disruption of LTP-lipoprotein binding by this protein,21 suggesting that LTIP inhibits LTP by competing with the transfer protein for the interaction with lipoprotein surface.	bind
23935	1	6827	5	13	NULL	NULL	NULL	EGFR	GP	activated	recruits					Grb2	GP		SH2 domain		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_65	16574915	18 Activated EGFR recruits the SH2 domain - containing signaling molecule Grb2 ( Growth factor  receptor -  binding protein  2) that, in turn, mediates the binding of EGFR to the E3 ubiquitin ligase c-Cbl to start the cascade of events leading to internalization and degradation.	bind
23936	2	6827	5	13	NULL	NULL	NULL	Grb2	GP		is					Growth factor receptor - binding protein 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_65	16574915	18 Activated EGFR recruits the SH2 domain - containing signaling molecule Grb2 ( Growth factor  receptor -  binding protein  2) that, in turn, mediates the binding of EGFR to the E3 ubiquitin ligase c-Cbl to start the cascade of events leading to internalization and degradation.	bind
23937	3	6827	5	13	NULL	NULL	NULL	EGFR	GP		bind					c-Cbl	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_65	16574915	18 Activated EGFR recruits the SH2 domain - containing signaling molecule Grb2 ( Growth factor  receptor -  binding protein  2) that, in turn, mediates the binding of EGFR to the E3 ubiquitin ligase c-Cbl to start the cascade of events leading to internalization and degradation.	bind
23938	4	6827	5	13	NULL	NULL	NULL	statement 1	Process		mediates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_65	16574915	18 Activated EGFR recruits the SH2 domain - containing signaling molecule Grb2 ( Growth factor  receptor -  binding protein  2) that, in turn, mediates the binding of EGFR to the E3 ubiquitin ligase c-Cbl to start the cascade of events leading to internalization and degradation.	bind
23939	5	6827	5	13	NULL	NULL	NULL	statement 3	Process		starts					internalization	Process	cascade of events leading to			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_65	16574915	18 Activated EGFR recruits the SH2 domain - containing signaling molecule Grb2 ( Growth factor  receptor -  binding protein  2) that, in turn, mediates the binding of EGFR to the E3 ubiquitin ligase c-Cbl to start the cascade of events leading to internalization and degradation.	bind
23940	6	6827	5	13	NULL	NULL	NULL	statement 3	Process		starts					degradation	Process	cascade of events leading to			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_65	16574915	18 Activated EGFR recruits the SH2 domain - containing signaling molecule Grb2 ( Growth factor  receptor -  binding protein  2) that, in turn, mediates the binding of EGFR to the E3 ubiquitin ligase c-Cbl to start the cascade of events leading to internalization and degradation.	bind
56614	7	6827	5	13	NULL	NULL	NULL	c-Cbl	GP		is a type of					E3 ubiquitin ligase	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_65	16574915	18 Activated EGFR recruits the SH2 domain - containing signaling molecule Grb2 ( Growth factor  receptor -  binding protein  2) that, in turn, mediates the binding of EGFR to the E3 ubiquitin ligase c-Cbl to start the cascade of events leading to internalization and degradation.	bind
19809	1	6827	6	NULL	NULL	0	NULL	EGFR	NULL	activated	recruits	NULL				Grb2	NULL		SH2 domain		NULL		0	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_65	16574915	18 Activated EGFR recruits the SH2 domain - containing signaling molecule Grb2 ( Growth factor  receptor -  binding protein  2) that, in turn, mediates the binding of EGFR to the E3 ubiquitin ligase c-Cbl to start the cascade of events leading to internalization and degradation.	bind
19810	2	6827	6	NULL	NULL	0	NULL	Grb2	NULL		is	NULL				Growth factor receptor - binding protein 2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_65	16574915	18 Activated EGFR recruits the SH2 domain - containing signaling molecule Grb2 ( Growth factor  receptor -  binding protein  2) that, in turn, mediates the binding of EGFR to the E3 ubiquitin ligase c-Cbl to start the cascade of events leading to internalization and degradation.	bind
19811	3	6827	6	NULL	NULL	0	NULL	EGFR	NULL		bind	NULL				c-Cbl	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_65	16574915	18 Activated EGFR recruits the SH2 domain - containing signaling molecule Grb2 ( Growth factor  receptor -  binding protein  2) that, in turn, mediates the binding of EGFR to the E3 ubiquitin ligase c-Cbl to start the cascade of events leading to internalization and degradation.	bind
19812	4	6827	6	10	NULL	0	NULL	c-Cbl			is a type of					E3 ubiquitin ligase					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_65	16574915	18 Activated EGFR recruits the SH2 domain - containing signaling molecule Grb2 ( Growth factor  receptor -  binding protein  2) that, in turn, mediates the binding of EGFR to the E3 ubiquitin ligase c-Cbl to start the cascade of events leading to internalization and degradation.	bind
19813	5	6827	6	10	NULL	0	NULL	statement 1			mediates					statement 3					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_65	16574915	18 Activated EGFR recruits the SH2 domain - containing signaling molecule Grb2 ( Growth factor  receptor -  binding protein  2) that, in turn, mediates the binding of EGFR to the E3 ubiquitin ligase c-Cbl to start the cascade of events leading to internalization and degradation.	bind
56615	6	6827	6	10	NULL	0	NULL	statement 3			starts					internalization		cascade of events leading to			NULL		0	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_65	16574915	18 Activated EGFR recruits the SH2 domain - containing signaling molecule Grb2 ( Growth factor  receptor -  binding protein  2) that, in turn, mediates the binding of EGFR to the E3 ubiquitin ligase c-Cbl to start the cascade of events leading to internalization and degradation.	bind
56616	7	6827	6	10	NULL	0	NULL	statement 3			starts					degradation		cascade of events leading to			NULL		0	NULL	NULL	NULL	gw70_circulationres_98_6_743_s_65	16574915	18 Activated EGFR recruits the SH2 domain - containing signaling molecule Grb2 ( Growth factor  receptor -  binding protein  2) that, in turn, mediates the binding of EGFR to the E3 ubiquitin ligase c-Cbl to start the cascade of events leading to internalization and degradation.	bind
23941	1	6828	5	13	NULL	NULL	NULL	factor Xa	GP		bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3320_s_220	10652320	18 and  35), most likely, a similar number of ionic contacts participate in the binding of factor Xa to heparin.	bind
23942	2	6828	5	13	NULL	NULL	NULL	ionic contacts	Process		participate in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3320_s_220	10652320	18 and  35), most likely, a similar number of ionic contacts participate in the binding of factor Xa to heparin.	bind
19814	1	6828	6	NULL	NULL	0	NULL	factor Xa	NULL		bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3320_s_220	10652320	18 and  35), most likely, a similar number of ionic contacts participate in the binding of factor Xa to heparin.	bind
19815	2	6828	6	NULL	NULL	0	NULL	ionic contacts	NULL		participate in	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3320_s_220	10652320	18 and  35), most likely, a similar number of ionic contacts participate in the binding of factor Xa to heparin.	bind
23943	1	6829	5	13	NULL	NULL	NULL	FasL	GP		bind					Fas	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_1_102_s_176	15499040	18 Binding of FasL to Fas in many cells leads to apoptosis of the Fas-bearing cell through mechanisms involving activation of caspases, particularly caspase-8.	bind
23944	2	6829	5	13	NULL	NULL	NULL	statement 1	Process		leads to					Fas-bearing cell	Cell	apoptosis of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_1_102_s_176	15499040	18 Binding of FasL to Fas in many cells leads to apoptosis of the Fas-bearing cell through mechanisms involving activation of caspases, particularly caspase-8.	bind
23945	3	6829	5	13	NULL	NULL	NULL	statement 2	Process		occurs through					caspases	GP	mechanisms involving activation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_1_102_s_176	15499040	18 Binding of FasL to Fas in many cells leads to apoptosis of the Fas-bearing cell through mechanisms involving activation of caspases, particularly caspase-8.	bind
23946	4	6829	5	13	NULL	NULL	NULL	statement 2	Process		occurs through		particularly			caspase-8	GP	mechanisms involving activation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_1_102_s_176	15499040	18 Binding of FasL to Fas in many cells leads to apoptosis of the Fas-bearing cell through mechanisms involving activation of caspases, particularly caspase-8.	bind
19863	1	6829	6	NULL	NULL	0	NULL	FasL	NULL		bind	NULL				Fas	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_1_102_s_176	15499040	18 Binding of FasL to Fas in many cells leads to apoptosis of the Fas-bearing cell through mechanisms involving activation of caspases, particularly caspase-8.	bind
19864	2	6829	6	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				Fas-bearing cell	NULL	apoptosis of 			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_1_102_s_176	15499040	18 Binding of FasL to Fas in many cells leads to apoptosis of the Fas-bearing cell through mechanisms involving activation of caspases, particularly caspase-8.	bind
19865	3	6829	6	NULL	NULL	0	NULL	statement 2	NULL		occurs via	NULL				caspases	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_1_102_s_176	15499040	18 Binding of FasL to Fas in many cells leads to apoptosis of the Fas-bearing cell through mechanisms involving activation of caspases, particularly caspase-8.	bind
56617	4	6829	6	10	NULL	0	NULL	statement 2			occur through		particularly			caspase-8		activation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_1_102_s_176	15499040	18 Binding of FasL to Fas in many cells leads to apoptosis of the Fas-bearing cell through mechanisms involving activation of caspases, particularly caspase-8.	bind
23947	1	6830	5	13	NULL	NULL	NULL	srGAP1	GP		bind					Cdc42	GP				NULL	in HEK cells expressing Robo1	NULL	NULL	NULL	NULL	gw70_circulationres_98_4_480_s_231	16439689	18 In HEK cells expressing Robo1, srGAP1 binds to Cdc42 and RhoA. 18 However, srGAPs neither bind to nor regulate Rac1, 18 and therefore they are unlikely to provide a direct link between Robo and Rac1 in VSMCs.	bind
23948	2	6830	5	13	NULL	NULL	NULL	srGAP1	GP		bind					RhoA	GP				NULL	in HEK cells expressing Robo1	NULL	NULL	NULL	NULL	gw70_circulationres_98_4_480_s_231	16439689	18 In HEK cells expressing Robo1, srGAP1 binds to Cdc42 and RhoA. 18 However, srGAPs neither bind to nor regulate Rac1, 18 and therefore they are unlikely to provide a direct link between Robo and Rac1 in VSMCs.	bind
23949	3	6830	5	13	NULL	NULL	NULL	srGAPs	GP		does not bind					Rac1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_4_480_s_231	16439689	18 In HEK cells expressing Robo1, srGAP1 binds to Cdc42 and RhoA. 18 However, srGAPs neither bind to nor regulate Rac1, 18 and therefore they are unlikely to provide a direct link between Robo and Rac1 in VSMCs.	bind
23950	4	6830	5	13	NULL	NULL	NULL	srGAPs	GP		does not regulate					Rac1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_4_480_s_231	16439689	18 In HEK cells expressing Robo1, srGAP1 binds to Cdc42 and RhoA. 18 However, srGAPs neither bind to nor regulate Rac1, 18 and therefore they are unlikely to provide a direct link between Robo and Rac1 in VSMCs.	bind
19866	1	6830	6	NULL	NULL	0	NULL	srGAP1	NULL		bind	NULL				Cdc42	NULL				NULL	statement 3	NULL	NULL	NULL	NULL	gw70_circulationres_98_4_480_s_231	16439689	18 In HEK cells expressing Robo1, srGAP1 binds to Cdc42 and RhoA. 18 However, srGAPs neither bind to nor regulate Rac1, 18 and therefore they are unlikely to provide a direct link between Robo and Rac1 in VSMCs.	bind
19867	2	6830	6	NULL	NULL	0	NULL	srGAP1	NULL		bind	NULL				RhoA	NULL				NULL	statement 3	NULL	NULL	NULL	NULL	gw70_circulationres_98_4_480_s_231	16439689	18 In HEK cells expressing Robo1, srGAP1 binds to Cdc42 and RhoA. 18 However, srGAPs neither bind to nor regulate Rac1, 18 and therefore they are unlikely to provide a direct link between Robo and Rac1 in VSMCs.	bind
19868	3	6830	6	NULL	NULL	0	NULL	HEK cells	NULL		express	NULL				Robo1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_4_480_s_231	16439689	18 In HEK cells expressing Robo1, srGAP1 binds to Cdc42 and RhoA. 18 However, srGAPs neither bind to nor regulate Rac1, 18 and therefore they are unlikely to provide a direct link between Robo and Rac1 in VSMCs.	bind
19869	4	6830	6	NULL	NULL	0	NULL	srGAP	NULL		does not bind	NULL				Rac1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_4_480_s_231	16439689	18 In HEK cells expressing Robo1, srGAP1 binds to Cdc42 and RhoA. 18 However, srGAPs neither bind to nor regulate Rac1, 18 and therefore they are unlikely to provide a direct link between Robo and Rac1 in VSMCs.	bind
19870	5	6830	6	NULL	NULL	0	NULL	srGAP	NULL		does not regulate	NULL				Rac1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_4_480_s_231	16439689	18 In HEK cells expressing Robo1, srGAP1 binds to Cdc42 and RhoA. 18 However, srGAPs neither bind to nor regulate Rac1, 18 and therefore they are unlikely to provide a direct link between Robo and Rac1 in VSMCs.	bind
23952	1	6832	5	13	NULL	NULL	NULL	neuregulins	GP	locally produced	promote					cardiac myocytes	Cell	survival of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_1_93_s_173	11772882	18 Locally produced neuregulins promote survival and growth of cardiac myocytes via ErbB2 and B4 receptors, which also bind heparin-binding epidermal growth factor - like factor.	bind
23953	2	6832	5	13	NULL	NULL	NULL	statement 1	Process		via					ErbB2 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_1_93_s_173	11772882	18 Locally produced neuregulins promote survival and growth of cardiac myocytes via ErbB2 and B4 receptors, which also bind heparin-binding epidermal growth factor - like factor.	bind
23955	3	6832	5	13	NULL	NULL	NULL	statement 1	Process		via					ErbB4 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_1_93_s_173	11772882	18 Locally produced neuregulins promote survival and growth of cardiac myocytes via ErbB2 and B4 receptors, which also bind heparin-binding epidermal growth factor - like factor.	bind
23956	4	6832	5	13	NULL	NULL	NULL	neuregulins	GP	locally produced	promote					cardiac myocytes	Cell	growth of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_1_93_s_173	11772882	18 Locally produced neuregulins promote survival and growth of cardiac myocytes via ErbB2 and B4 receptors, which also bind heparin-binding epidermal growth factor - like factor.	bind
23957	5	6832	5	13	NULL	NULL	NULL	statement 4	Process		via					ErbB2 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_1_93_s_173	11772882	18 Locally produced neuregulins promote survival and growth of cardiac myocytes via ErbB2 and B4 receptors, which also bind heparin-binding epidermal growth factor - like factor.	bind
23959	6	6832	5	13	NULL	NULL	NULL	statement 4	Process		via					ErbB4 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_1_93_s_173	11772882	18 Locally produced neuregulins promote survival and growth of cardiac myocytes via ErbB2 and B4 receptors, which also bind heparin-binding epidermal growth factor - like factor.	bind
23960	7	6832	5	13	NULL	NULL	NULL	neuregulins	GP	locally produced	bind					epidermal growth factor - like factor	GP	heparin-binding			NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_1_93_s_173	11772882	18 Locally produced neuregulins promote survival and growth of cardiac myocytes via ErbB2 and B4 receptors, which also bind heparin-binding epidermal growth factor - like factor.	bind
19871	1	6832	6	NULL	NULL	0	NULL	neuregulins	NULL	locally produced	bind	NULL				heparin-binding epidermal growth factor - like factor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_1_93_s_173	11772882	18 Locally produced neuregulins promote survival and growth of cardiac myocytes via ErbB2 and B4 receptors, which also bind heparin-binding epidermal growth factor - like factor.	bind
19872	2	6832	6	NULL	NULL	0	NULL	neuregulins	NULL		promotes	NULL				cardiac myocytes	NULL	survival of 			NULL		0	NULL	NULL	NULL	gw60_circulation_105_1_93_s_173	11772882	18 Locally produced neuregulins promote survival and growth of cardiac myocytes via ErbB2 and B4 receptors, which also bind heparin-binding epidermal growth factor - like factor.	bind
19873	3	6832	6	NULL	NULL	0	NULL	neuregulins	NULL		promotes	NULL				cardiac myocytes	NULL	growth of 			NULL		0	NULL	NULL	NULL	gw60_circulation_105_1_93_s_173	11772882	18 Locally produced neuregulins promote survival and growth of cardiac myocytes via ErbB2 and B4 receptors, which also bind heparin-binding epidermal growth factor - like factor.	bind
19874	4	6832	6	NULL	NULL	0	NULL	statement 2	NULL		occurs via	NULL				ErbB2 receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_1_93_s_173	11772882	18 Locally produced neuregulins promote survival and growth of cardiac myocytes via ErbB2 and B4 receptors, which also bind heparin-binding epidermal growth factor - like factor.	bind
19875	5	6832	6	NULL	NULL	0	NULL	statement 3	NULL		occurs via	NULL				ErbB4 receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_1_93_s_173	11772882	18 Locally produced neuregulins promote survival and growth of cardiac myocytes via ErbB2 and B4 receptors, which also bind heparin-binding epidermal growth factor - like factor.	bind
56618	6	6832	6	10	NULL	0	NULL	statement 2			via					ErbB4 receptor					NULL		0	NULL	NULL	NULL	gw60_circulation_105_1_93_s_173	11772882	18 Locally produced neuregulins promote survival and growth of cardiac myocytes via ErbB2 and B4 receptors, which also bind heparin-binding epidermal growth factor - like factor.	bind
56619	7	6832	6	10	NULL	0	NULL	statement 3			via					ErbB2 receptor					NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_1_93_s_173	11772882	18 Locally produced neuregulins promote survival and growth of cardiac myocytes via ErbB2 and B4 receptors, which also bind heparin-binding epidermal growth factor - like factor.	bind
23962	1	6833	5	13	NULL	NULL	NULL	TGF-betaR2	GP		bind					ligand	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1633_s_29	11073823	18 TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 which activates intracellular signaling cascades.	bind
23963	2	6833	5	13	NULL	NULL	NULL	statement 1	GP		forms a complex with					TGF-betaR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1633_s_29	11073823	18 TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 which activates intracellular signaling cascades.	bind
23964	3	6833	5	13	NULL	NULL	NULL	statement 2	Process		activates					intracellular signaling cascades	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1633_s_29	11073823	18 TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 which activates intracellular signaling cascades.	bind
19876	2	6833	6	10	NULL	0	NULL	statement 1			forms a complex with					TGF-betaR1					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1633_s_29	11073823	18 TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 which activates intracellular signaling cascades.	bind
19877	3	6833	6	10	NULL	0	NULL	statement 2			activates					intracellular signaling cascades					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1633_s_29	11073823	18 TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 which activates intracellular signaling cascades.	bind
56620	1	6833	6	10	NULL	0	NULL	TGF-betaR2			bind					ligand					NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_5_1633_s_29	11073823	18 TGF-betaR2 binds the ligand and forms a complex with TGF-betaR1 which activates intracellular signaling cascades.	bind
23965	1	6834	5	13	NULL	NULL	NULL	NorR	GP		bind					norA	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_54_2_364_s_39	15231765	18 The binding of NorR to the  norA promoter is modified in an  arlS -  strain such that increased  norA expression is observed; however, overexpression of  norR in an  arlS+ background also results in increased  norA expression.	bind
23966	2	6834	5	13	NULL	NULL	NULL	NorR	GP	overexpression of	results in					norA	GP	increased expression of			NULL	in an arlS+ background	NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_54_2_364_s_39	15231765	18 The binding of NorR to the  norA promoter is modified in an  arlS -  strain such that increased  norA expression is observed; however, overexpression of  norR in an  arlS+ background also results in increased  norA expression.	bind
56621	3	6834	5	13	NULL	NULL	NULL	statement 1	Process		increases					norA	GP	expression of			NULL	arlS - strain	NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_54_2_364_s_39	15231765	18 The binding of NorR to the  norA promoter is modified in an  arlS -  strain such that increased  norA expression is observed; however, overexpression of  norR in an  arlS+ background also results in increased  norA expression.	bind
19878	1	6834	6	NULL	NULL	0	NULL	NorR	NULL		bind	NULL				norA	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jantimicrobchemoth_54_2_364_s_39	15231765	18 The binding of NorR to the  norA promoter is modified in an  arlS -  strain such that increased  norA expression is observed; however, overexpression of  norR in an  arlS+ background also results in increased  norA expression.	bind
19879	2	6834	6	NULL	NULL	0	NULL	statement 1	NULL		increases	NULL				norA	NULL	expression of 			NULL	arlS - strain 	0	NULL	NULL	NULL	gw70_jantimicrobchemoth_54_2_364_s_39	15231765	18 The binding of NorR to the  norA promoter is modified in an  arlS -  strain such that increased  norA expression is observed; however, overexpression of  norR in an  arlS+ background also results in increased  norA expression.	bind
19880	3	6834	6	10	NULL	0	NULL	norR		overexpression of	results in					norA expression		increased expression of			NULL	arlS+ background	NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_54_2_364_s_39	15231765	18 The binding of NorR to the  norA promoter is modified in an  arlS -  strain such that increased  norA expression is observed; however, overexpression of  norR in an  arlS+ background also results in increased  norA expression.	bind
23967	1	6835	5	13	NULL	NULL	NULL	VEGF	GP		bind					VEGFR2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_6_692_s_194	12609969	18 The binding of VEGF to VEGFR2 elicits activation of signaling cascades that trigger the biological effects of VEGF.	bind
23968	2	6835	5	13	NULL	NULL	NULL	statement 1	Process		elicits					signaling cascades	Process	activation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_6_692_s_194	12609969	18 The binding of VEGF to VEGFR2 elicits activation of signaling cascades that trigger the biological effects of VEGF.	bind
23969	3	6835	5	13	NULL	NULL	NULL	statement 2	Process		triggers					VEGF	GP	biological effects of 			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_6_692_s_194	12609969	18 The binding of VEGF to VEGFR2 elicits activation of signaling cascades that trigger the biological effects of VEGF.	bind
19881	1	6835	6	NULL	NULL	0	NULL	VEGF	NULL		bind	NULL				VEGFR2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_6_692_s_194	12609969	18 The binding of VEGF to VEGFR2 elicits activation of signaling cascades that trigger the biological effects of VEGF.	bind
19882	2	6835	6	NULL	NULL	0	NULL	statement 1	NULL		elicits	NULL				signaling cascades	NULL	activation of 			NULL		0	NULL	NULL	NULL	gw60_circulationres_92_6_692_s_194	12609969	18 The binding of VEGF to VEGFR2 elicits activation of signaling cascades that trigger the biological effects of VEGF.	bind
19883	3	6835	6	NULL	NULL	0	NULL	statement 2	NULL		trigger	NULL				VEGF	NULL	biological effects of 			NULL		0	NULL	NULL	NULL	gw60_circulationres_92_6_692_s_194	12609969	18 The binding of VEGF to VEGFR2 elicits activation of signaling cascades that trigger the biological effects of VEGF.	bind
23970	1	6836	5	13	NULL	NULL	NULL	EGF-R	GP		bind		initially			caveolin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
23971	2	6836	5	13	NULL	NULL	NULL	Ang II	GP	stimulation	disrupt					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
23972	3	6836	5	13	NULL	NULL	NULL	statement 2	Process		is an essential step in					EGF-R	GP	transactivation of			NULL	in VSMCs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
23973	4	6836	5	13	NULL	NULL	NULL	Rac1	GP		is recruited into					caveolae/lipid rafts	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
23974	5	6836	5	13	NULL	NULL	NULL	Ang II	GP		stimulates					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
23975	6	6836	5	13	NULL	NULL	NULL	Rac1	GP		associates with					caveolin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
23976	7	6836	5	13	NULL	NULL	NULL	Ang II	GP		stimulates					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
23977	8	6836	5	13	NULL	NULL	NULL	statement 5	Process		is required for		may be			NAD(P)H oxidase	GP	activation of Nox-based			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
23978	9	6836	5	13	NULL	NULL	NULL	statement 7	Process		is required for		may be			NAD(P)H oxidase	GP	activation of Nox-based			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
23979	10	6836	5	13	NULL	NULL	NULL	statement 5	Process		is required for		may be			signaling events	Process	downstream ROS-dependent			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
23980	11	6836	5	13	NULL	NULL	NULL	statement 7	Process		is required for		may be			signaling events	Process	downstream ROS-dependent			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
23981	12	6836	5	13	NULL	NULL	NULL	signaling events	Process	downstream ROS-dependent 	includes					EGF-R	GP	transactivation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
19884	1	6836	6	NULL	NULL	0	NULL	EGF-R	NULL		bind	NULL				caveolin	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
19885	2	6836	6	NULL	NULL	0	NULL	statement 1	NULL		is disrupted by	NULL				Ang II	NULL	stimulation of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
19886	3	6836	6	NULL	NULL	0	NULL	statement 1	NULL		is essential step for	NULL				EGF-R	NULL	transactivation of			NULL	VSMC	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
19887	4	6836	6	NULL	NULL	0	NULL	Rac1	NULL		is recruited into	NULL				caveolae/lipid rafts	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
19888	5	6836	6	NULL	NULL	0	NULL	statement 4	NULL		is stimulated by	NULL				Ang II	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
19889	6	6836	6	NULL	NULL	0	NULL	Rac1	NULL		associates	NULL				caveolin	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
19890	7	6836	6	10	NULL	0	NULL	statement 5			be required for		may			 NAD(P)H oxidase		activation of Nox-based			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
19891	8	6836	6	10	NULL	0	NULL	statement 5			be required for		may			signaling events		downstream ROS-dependent			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
56622	9	6836	6	10	NULL	0	NULL	Ang II			stimulates					statement 6					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
56623	10	6836	6	10	NULL	0	NULL	statement 9			be required for		may			NAD(P)H oxidase		activation of Nox-based			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
56624	11	6836	6	10	NULL	0	NULL	statement 9			be required for		may			signaling events		downstream ROS-dependent 			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
56625	12	6836	6	10	NULL	0	NULL	signaling events		ROS-dependent 	include					EGF-R		transactivation of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1223_s_137	15142861	18 We also reported that EGF-R initially binds caveolin, but this association is disrupted by Ang II stimulation, which is an essential step in transactivation of EGF-R in VSMCs. 3 Thus, Ang II - stimulated recruitment of Rac1 into caveolae/lipid rafts and association with caveolin may be required for activation of Nox-based NAD(P)H oxidase and downstream ROS-dependent signaling events such as EGF-R transactivation.	bind
23982	1	6837	5	13	NULL	NULL	NULL	CD36 	GP	expression of	function as					TSP-1 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_841_s_315	10487979	18, 19  No previous report has demonstrated that CD36 binds TGF-beta1, but CD36 expression functions as a receptor for TSP-1, 43  collagen, 43  and a ligand exposed on the surface of erythrocytes infected with the parasite  Plasmodium falciparum.	bind
23983	2	6837	5	13	NULL	NULL	NULL	CD36	GP	expression of	function as					collagen receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_841_s_315	10487979	18, 19  No previous report has demonstrated that CD36 binds TGF-beta1, but CD36 expression functions as a receptor for TSP-1, 43  collagen, 43  and a ligand exposed on the surface of erythrocytes infected with the parasite  Plasmodium falciparum.	bind
23984	3	6837	5	13	NULL	NULL	NULL	CD36	GP	expression of	function as					ligand receptor	GP				NULL	surface of erythrocytes infected with the parasite Plasmodium falciparum	NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_841_s_315	10487979	18, 19  No previous report has demonstrated that CD36 binds TGF-beta1, but CD36 expression functions as a receptor for TSP-1, 43  collagen, 43  and a ligand exposed on the surface of erythrocytes infected with the parasite  Plasmodium falciparum.	bind
19892	1	6837	6	NULL	NULL	0	NULL	CD36	NULL	expression of	functions as 	NULL				TSP-1 receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_841_s_315	10487979	18, 19  No previous report has demonstrated that CD36 binds TGF-beta1, but CD36 expression functions as a receptor for TSP-1, 43  collagen, 43  and a ligand exposed on the surface of erythrocytes infected with the parasite  Plasmodium falciparum.	bind
20292	2	6837	6	NULL	NULL	0	NULL	CD36	NULL	expression of	functions as 	NULL				collagen receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_841_s_315	10487979	18, 19  No previous report has demonstrated that CD36 binds TGF-beta1, but CD36 expression functions as a receptor for TSP-1, 43  collagen, 43  and a ligand exposed on the surface of erythrocytes infected with the parasite  Plasmodium falciparum.	bind
20294	3	6837	6	NULL	NULL	0	NULL	CD36	NULL	expression of	functions as a 	NULL				ligand receptor	NULL				NULL	surface of erythrocytes infected with the parasite Plasmodium falciparum	NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_841_s_315	10487979	18, 19  No previous report has demonstrated that CD36 binds TGF-beta1, but CD36 expression functions as a receptor for TSP-1, 43  collagen, 43  and a ligand exposed on the surface of erythrocytes infected with the parasite  Plasmodium falciparum.	bind
23986	1	6838	5	13	NULL	NULL	NULL	VEGF	GP		bind					Flt-1	GP				NULL	vascular endothelial cells	NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_103_s_21	10880381	18, 19  VEGF binds to two type III tyrosine kinase receptors on vascular endothelial cells, Flt-1 and KDR/Flk-1.	bind
23987	2	6838	5	13	NULL	NULL	NULL	VEGF	GP		bind					KDR/Flk-1	GP				NULL	vascular endothelial cells	NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_103_s_21	10880381	18, 19  VEGF binds to two type III tyrosine kinase receptors on vascular endothelial cells, Flt-1 and KDR/Flk-1.	bind
30346	3	6838	5	13	NULL	NULL	NULL	Flt-1	GP		is a type of					type III tyrosine kinase receptors 	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_103_s_21	10880381	18, 19  VEGF binds to two type III tyrosine kinase receptors on vascular endothelial cells, Flt-1 and KDR/Flk-1.	bind
30347	4	6838	5	13	NULL	NULL	NULL	KDR/Flk-1	GP		is a type of					type III tyrosine kinase receptors 	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_103_s_21	10880381	18, 19  VEGF binds to two type III tyrosine kinase receptors on vascular endothelial cells, Flt-1 and KDR/Flk-1.	bind
19893	1	6838	6	NULL	NULL	0	NULL	VEGF	NULL		bind	NULL				Flt-1	NULL				NULL	vascular endothelial cells	NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_103_s_21	10880381	18, 19  VEGF binds to two type III tyrosine kinase receptors on vascular endothelial cells, Flt-1 and KDR/Flk-1.	bind
19894	2	6838	6	NULL	NULL	0	NULL	VEGF	NULL		bind	NULL				KDR/Flk-1	NULL				NULL	vascular endothelial cells	0	NULL	NULL	NULL	gw60_amjpathol_157_1_103_s_21	10880381	18, 19  VEGF binds to two type III tyrosine kinase receptors on vascular endothelial cells, Flt-1 and KDR/Flk-1.	bind
19895	3	6838	6	NULL	NULL	0	NULL	Flt-1	NULL		is a type of	NULL				type III tyrosine kinase receptors	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_103_s_21	10880381	18, 19  VEGF binds to two type III tyrosine kinase receptors on vascular endothelial cells, Flt-1 and KDR/Flk-1.	bind
19897	4	6838	6	NULL	NULL	0	NULL	KDR/Flk-1	NULL		is a type of	NULL				type III tyrosine kinase receptors	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_103_s_21	10880381	18, 19  VEGF binds to two type III tyrosine kinase receptors on vascular endothelial cells, Flt-1 and KDR/Flk-1.	bind
23988	1	6839	5	13	NULL	NULL	NULL	CD36	GP		bind					TSP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_841_s_151	10487979	18, 19  We next determined if the CD36 binding of TSP-1 is required for the posttranslational processing and activation of L-TGF- beta1.	bind
19898	1	6839	6	NULL	NULL	0	NULL	CD36	NULL		bind	NULL				TSP-1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_3_841_s_151	10487979	18, 19  We next determined if the CD36 binding of TSP-1 is required for the posttranslational processing and activation of L-TGF- beta1.	bind
23992	4	6840	5	13	NULL	NULL	NULL	statement 3	Process		enhances					actin filaments	GP	polymerization of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_12_1296_s_25	12775580	18,19  By inducing cofilin phosphorylation, Rho abolishes the actin-binding activity of cofilin, thereby enhancing the polymerization of actin filaments.	bind
30348	1	6840	5	13	NULL	NULL	NULL	Rho	GP		induces					cofilin	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_12_1296_s_25	12775580	18,19  By inducing cofilin phosphorylation, Rho abolishes the actin-binding activity of cofilin, thereby enhancing the polymerization of actin filaments.	bind
30349	2	6840	5	13	NULL	NULL	NULL	cofilin	GP		activates					actin-binding	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_12_1296_s_25	12775580	18,19  By inducing cofilin phosphorylation, Rho abolishes the actin-binding activity of cofilin, thereby enhancing the polymerization of actin filaments.	bind
30350	3	6840	5	13	NULL	NULL	NULL	statement 1	Process		abolishes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_12_1296_s_25	12775580	18,19  By inducing cofilin phosphorylation, Rho abolishes the actin-binding activity of cofilin, thereby enhancing the polymerization of actin filaments.	bind
19899	1	6840	6	NULL	NULL	0	NULL	Rho	NULL		induces	NULL				cofilin	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_circulationres_92_12_1296_s_25	12775580	18,19  By inducing cofilin phosphorylation, Rho abolishes the actin-binding activity of cofilin, thereby enhancing the polymerization of actin filaments.	bind
19900	2	6840	6	10	NULL	0	NULL	Cofilin			activates					actin-binding					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_12_1296_s_25	12775580	18,19  By inducing cofilin phosphorylation, Rho abolishes the actin-binding activity of cofilin, thereby enhancing the polymerization of actin filaments.	bind
19901	3	6840	6	NULL	NULL	0	NULL	statement 1	NULL		abolishes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_12_1296_s_25	12775580	18,19  By inducing cofilin phosphorylation, Rho abolishes the actin-binding activity of cofilin, thereby enhancing the polymerization of actin filaments.	bind
19902	4	6840	6	NULL	NULL	0	NULL	statement 3	NULL		enhances	NULL				actin filaments	NULL	polymerization of 			NULL		0	NULL	NULL	NULL	gw60_circulationres_92_12_1296_s_25	12775580	18,19  By inducing cofilin phosphorylation, Rho abolishes the actin-binding activity of cofilin, thereby enhancing the polymerization of actin filaments.	bind
23993	1	6842	5	13	NULL	NULL	NULL	PKCalpha	GP		bind					syndecan-4	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_7_674_s_31	16141413	18,19 alpha-Actinin may compete with PKCalpha for binding to syndecan-4 because the increased association of phorbol 12-myristate 13-acetate - activated PKCalpha with syndecan-4 is accompanied by decreased alpha-actinin binding to syndecan-4.	bind
23994	2	6842	5	13	NULL	NULL	NULL	alpha-Actinin	GP		bind					syndecan-4	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_7_674_s_31	16141413	18,19 alpha-Actinin may compete with PKCalpha for binding to syndecan-4 because the increased association of phorbol 12-myristate 13-acetate - activated PKCalpha with syndecan-4 is accompanied by decreased alpha-actinin binding to syndecan-4.	bind
23995	3	6842	5	13	NULL	NULL	NULL	statement 2	Process		competes with		may			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_7_674_s_31	16141413	18,19 alpha-Actinin may compete with PKCalpha for binding to syndecan-4 because the increased association of phorbol 12-myristate 13-acetate - activated PKCalpha with syndecan-4 is accompanied by decreased alpha-actinin binding to syndecan-4.	bind
23996	4	6842	5	13	NULL	NULL	NULL	phorbol 12-myristate 13-acetate	Chemical		activates					PKCalpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_7_674_s_31	16141413	18,19 alpha-Actinin may compete with PKCalpha for binding to syndecan-4 because the increased association of phorbol 12-myristate 13-acetate - activated PKCalpha with syndecan-4 is accompanied by decreased alpha-actinin binding to syndecan-4.	bind
23997	5	6842	5	13	NULL	NULL	NULL	statement 4	Process		associates with					syndecan-4	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_7_674_s_31	16141413	18,19 alpha-Actinin may compete with PKCalpha for binding to syndecan-4 because the increased association of phorbol 12-myristate 13-acetate - activated PKCalpha with syndecan-4 is accompanied by decreased alpha-actinin binding to syndecan-4.	bind
23998	6	6842	5	13	NULL	NULL	NULL	statement 5	Process	increased	is accompanied by					statement 2	Process	decreased			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_7_674_s_31	16141413	18,19 alpha-Actinin may compete with PKCalpha for binding to syndecan-4 because the increased association of phorbol 12-myristate 13-acetate - activated PKCalpha with syndecan-4 is accompanied by decreased alpha-actinin binding to syndecan-4.	bind
19903	1	6842	6	NULL	NULL	0	NULL	PKCalpha	NULL		bind	NULL				syndecan-4	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_7_674_s_31	16141413	18,19 alpha-Actinin may compete with PKCalpha for binding to syndecan-4 because the increased association of phorbol 12-myristate 13-acetate - activated PKCalpha with syndecan-4 is accompanied by decreased alpha-actinin binding to syndecan-4.	bind
19904	2	6842	6	NULL	NULL	0	NULL	alpha-Actinin	NULL		bind	NULL				syndecan-4	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_7_674_s_31	16141413	18,19 alpha-Actinin may compete with PKCalpha for binding to syndecan-4 because the increased association of phorbol 12-myristate 13-acetate - activated PKCalpha with syndecan-4 is accompanied by decreased alpha-actinin binding to syndecan-4.	bind
19905	3	6842	6	NULL	NULL	0	NULL	statement 1	NULL		competes	NULL	may			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_7_674_s_31	16141413	18,19 alpha-Actinin may compete with PKCalpha for binding to syndecan-4 because the increased association of phorbol 12-myristate 13-acetate - activated PKCalpha with syndecan-4 is accompanied by decreased alpha-actinin binding to syndecan-4.	bind
19906	4	6842	6	10	NULL	0	NULL	PKCalpha		activated	associate with					syndecan-4					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_7_674_s_31	16141413	18,19 alpha-Actinin may compete with PKCalpha for binding to syndecan-4 because the increased association of phorbol 12-myristate 13-acetate - activated PKCalpha with syndecan-4 is accompanied by decreased alpha-actinin binding to syndecan-4.	bind
19907	5	6842	6	NULL	NULL	0	NULL	statement 4	NULL	increase in	leads to	NULL				statement 2	NULL	decrease in			NULL		0	NULL	NULL	NULL	gw70_circulationres_97_7_674_s_31	16141413	18,19 alpha-Actinin may compete with PKCalpha for binding to syndecan-4 because the increased association of phorbol 12-myristate 13-acetate - activated PKCalpha with syndecan-4 is accompanied by decreased alpha-actinin binding to syndecan-4.	bind
30287	6	6842	6	NULL	NULL	0	NULL	phorbol 12-myristate 13-acetate	NULL		activates	NULL				PKCalpha	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_7_674_s_31	16141413	18,19 alpha-Actinin may compete with PKCalpha for binding to syndecan-4 because the increased association of phorbol 12-myristate 13-acetate - activated PKCalpha with syndecan-4 is accompanied by decreased alpha-actinin binding to syndecan-4.	bind
23999	1	6843	5	13	NULL	NULL	NULL	HDL	GP		bind					SR-BI	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_712_s_91	12615688	18,31  There is a half-maximal efflux at low concentrations of HDL (<30 mug protein/mL) that is similar to the Kd for HDL binding to SR-BI.	bind
19908	1	6843	6	NULL	NULL	0	NULL	HDL	NULL		bind	NULL				SR-BI	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_712_s_91	12615688	18,31  There is a half-maximal efflux at low concentrations of HDL (<30 mug protein/mL) that is similar to the Kd for HDL binding to SR-BI.	bind
24001	1	6844	5	13	NULL	NULL	NULL	I-LPL	GP		bind					LDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_14_8081_s_154	7713910	181 nM  unlabeled LDL inhibited  the binding of  I-LPL to LDL-coated plates by  approximately 50%  in both control and delipidated plates.	bind
24002	2	6844	5	13	NULL	NULL	NULL	LDL	GP	unlabeled	inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_14_8081_s_154	7713910	181 nM  unlabeled LDL inhibited  the binding of  I-LPL to LDL-coated plates by  approximately 50%  in both control and delipidated plates.	bind
19909	1	6844	6	NULL	NULL	0	NULL	I-LPL	NULL		bind	NULL				LDL	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_14_8081_s_154	7713910	181 nM  unlabeled LDL inhibited  the binding of  I-LPL to LDL-coated plates by  approximately 50%  in both control and delipidated plates.	bind
19910	2	6844	6	NULL	NULL	0	NULL	LDL	NULL	unlabeled	inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_14_8081_s_154	7713910	181 nM  unlabeled LDL inhibited  the binding of  I-LPL to LDL-coated plates by  approximately 50%  in both control and delipidated plates.	bind
24003	1	6845	5	13	NULL	NULL	NULL	luteinizing hormone beta gene	GP	rat	bind				upstream region	estrogen receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_941	11452016	184       Shupnik,M.A., Weinmann,C.M., Notides,A.C. and Chin,W.W. (1989) An upstream region of the rat luteinizing hormone beta gene binds estrogen receptor and confers estrogen responsiveness.	bind
24004	2	6845	5	13	NULL	NULL	NULL	luteinizing hormone beta gene	GP	rat	confers				upstream region	estrogen responsiveness	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_941	11452016	184       Shupnik,M.A., Weinmann,C.M., Notides,A.C. and Chin,W.W. (1989) An upstream region of the rat luteinizing hormone beta gene binds estrogen receptor and confers estrogen responsiveness.	bind
19911	1	6845	6	NULL	NULL	0	NULL	luteinizing hormone beta gene	NULL	rat	bind	NULL			upstream region	estrogen receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_941	11452016	184       Shupnik,M.A., Weinmann,C.M., Notides,A.C. and Chin,W.W. (1989) An upstream region of the rat luteinizing hormone beta gene binds estrogen receptor and confers estrogen responsiveness.	bind
19912	2	6845	6	NULL	NULL	0	NULL	statement 1	NULL		confers	NULL				estrogen responsiveness	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_941	11452016	184       Shupnik,M.A., Weinmann,C.M., Notides,A.C. and Chin,W.W. (1989) An upstream region of the rat luteinizing hormone beta gene binds estrogen receptor and confers estrogen responsiveness.	bind
24005	1	6847	5	13	NULL	NULL	NULL	platelet glycoprotein Ibbeta	GP	mutation in	results in				GATA binding site of promoter	Bernard-Soulier syndrome	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_1_312_s_182	11125123	19       Ludlow,L.B., Schick,B.P., Budarf,M.L., Driscoll,D.A., Zackai,E.H., Cohen,A. and Konkle,B.A. (1996) Identification of a mutation in a GATA binding site of the platelet glycoprotein Ibbeta promoter resulting in the Bernard-Soulier syndrome.	bind
19913	1	6847	6	NULL	NULL	0	NULL	platelet glycoprotein Ibbeta	NULL	mutant	results in	NULL			GATA binding site of the promoter	Bernard-Soulier syndrome	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_1_312_s_182	11125123	19       Ludlow,L.B., Schick,B.P., Budarf,M.L., Driscoll,D.A., Zackai,E.H., Cohen,A. and Konkle,B.A. (1996) Identification of a mutation in a GATA binding site of the platelet glycoprotein Ibbeta promoter resulting in the Bernard-Soulier syndrome.	bind
24006	1	6848	5	13	NULL	NULL	NULL	Ral 	GP		bind					GTP	Chemical	activated			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_32	11397694	19  Activated GTP-bound Ral binds to RLIP76 (or Ral binding protein), an effector molecule that possesses GTPase activity for cdc42 and Rac, suggesting a link between the activation of Ral and rearrangement of the cytoskeleton.	bind
24007	2	6848	5	13	NULL	NULL	NULL	statement 1	GP		bind					RLIP76	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_32	11397694	19  Activated GTP-bound Ral binds to RLIP76 (or Ral binding protein), an effector molecule that possesses GTPase activity for cdc42 and Rac, suggesting a link between the activation of Ral and rearrangement of the cytoskeleton.	bind
24008	3	6848	5	13	NULL	NULL	NULL	RLIP76	GP		possesses					cdc42 GTPase activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_32	11397694	19  Activated GTP-bound Ral binds to RLIP76 (or Ral binding protein), an effector molecule that possesses GTPase activity for cdc42 and Rac, suggesting a link between the activation of Ral and rearrangement of the cytoskeleton.	bind
24009	4	6848	5	13	NULL	NULL	NULL	RLIP76	GP		possesses					Rac GTPase activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_32	11397694	19  Activated GTP-bound Ral binds to RLIP76 (or Ral binding protein), an effector molecule that possesses GTPase activity for cdc42 and Rac, suggesting a link between the activation of Ral and rearrangement of the cytoskeleton.	bind
24010	5	6848	5	13	NULL	NULL	NULL	Ral	GP	activation of	is linked to					cytoskeleton	CellComponent	rearrangement of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_32	11397694	19  Activated GTP-bound Ral binds to RLIP76 (or Ral binding protein), an effector molecule that possesses GTPase activity for cdc42 and Rac, suggesting a link between the activation of Ral and rearrangement of the cytoskeleton.	bind
24011	6	6848	5	13	NULL	NULL	NULL	statement 3	Process		suggests					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_32	11397694	19  Activated GTP-bound Ral binds to RLIP76 (or Ral binding protein), an effector molecule that possesses GTPase activity for cdc42 and Rac, suggesting a link between the activation of Ral and rearrangement of the cytoskeleton.	bind
24012	7	6848	5	13	NULL	NULL	NULL	statement 4	Process		suggests					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_32	11397694	19  Activated GTP-bound Ral binds to RLIP76 (or Ral binding protein), an effector molecule that possesses GTPase activity for cdc42 and Rac, suggesting a link between the activation of Ral and rearrangement of the cytoskeleton.	bind
30351	8	6848	5	13	NULL	NULL	NULL	RLIP76	GP		is a type of					effector molecule	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_32	11397694	19  Activated GTP-bound Ral binds to RLIP76 (or Ral binding protein), an effector molecule that possesses GTPase activity for cdc42 and Rac, suggesting a link between the activation of Ral and rearrangement of the cytoskeleton.	bind
56630	9	6848	5	13	NULL	NULL	NULL	RLIP76	GP		is a type of					Ral binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_32	11397694	19  Activated GTP-bound Ral binds to RLIP76 (or Ral binding protein), an effector molecule that possesses GTPase activity for cdc42 and Rac, suggesting a link between the activation of Ral and rearrangement of the cytoskeleton.	bind
19914	1	6848	6	NULL	NULL	0	NULL	Ral	NULL		bind	NULL				GTP	NULL	activated			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_32	11397694	19  Activated GTP-bound Ral binds to RLIP76 (or Ral binding protein), an effector molecule that possesses GTPase activity for cdc42 and Rac, suggesting a link between the activation of Ral and rearrangement of the cytoskeleton.	bind
19915	2	6848	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				RLIP76	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_32	11397694	19  Activated GTP-bound Ral binds to RLIP76 (or Ral binding protein), an effector molecule that possesses GTPase activity for cdc42 and Rac, suggesting a link between the activation of Ral and rearrangement of the cytoskeleton.	bind
19916	3	6848	6	NULL	NULL	0	NULL	RLIP76	NULL		is a type of	NULL				Ral binding protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_32	11397694	19  Activated GTP-bound Ral binds to RLIP76 (or Ral binding protein), an effector molecule that possesses GTPase activity for cdc42 and Rac, suggesting a link between the activation of Ral and rearrangement of the cytoskeleton.	bind
19917	4	6848	6	NULL	NULL	0	NULL	RLIP76	NULL		possesses	NULL				GTPase activity	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_32	11397694	19  Activated GTP-bound Ral binds to RLIP76 (or Ral binding protein), an effector molecule that possesses GTPase activity for cdc42 and Rac, suggesting a link between the activation of Ral and rearrangement of the cytoskeleton.	bind
19918	5	6848	6	NULL	NULL	0	NULL	statement 4	NULL		occurs for	NULL				cdc42 GTPase activity	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_32	11397694	19  Activated GTP-bound Ral binds to RLIP76 (or Ral binding protein), an effector molecule that possesses GTPase activity for cdc42 and Rac, suggesting a link between the activation of Ral and rearrangement of the cytoskeleton.	bind
19919	6	6848	6	NULL	NULL	0	NULL	statement 4	NULL		occurs for	NULL				Rac GTPase activity	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_32	11397694	19  Activated GTP-bound Ral binds to RLIP76 (or Ral binding protein), an effector molecule that possesses GTPase activity for cdc42 and Rac, suggesting a link between the activation of Ral and rearrangement of the cytoskeleton.	bind
30288	7	6848	6	NULL	NULL	0	NULL	RLIP76	NULL		is a type of	NULL				effector molecule	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_32	11397694	19  Activated GTP-bound Ral binds to RLIP76 (or Ral binding protein), an effector molecule that possesses GTPase activity for cdc42 and Rac, suggesting a link between the activation of Ral and rearrangement of the cytoskeleton.	bind
56631	8	6848	6	10	NULL	0	NULL	Ral		activation of	is linked to					cytoskeleton		rearrangement of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_32	11397694	19  Activated GTP-bound Ral binds to RLIP76 (or Ral binding protein), an effector molecule that possesses GTPase activity for cdc42 and Rac, suggesting a link between the activation of Ral and rearrangement of the cytoskeleton.	bind
56632	9	6848	6	10	NULL	0	NULL	statement 5			suggests					statement 8					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_32	11397694	19  Activated GTP-bound Ral binds to RLIP76 (or Ral binding protein), an effector molecule that possesses GTPase activity for cdc42 and Rac, suggesting a link between the activation of Ral and rearrangement of the cytoskeleton.	bind
56633	10	6848	6	10	NULL	0	NULL	statement 6			suggests					statement 8					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_32	11397694	19  Activated GTP-bound Ral binds to RLIP76 (or Ral binding protein), an effector molecule that possesses GTPase activity for cdc42 and Rac, suggesting a link between the activation of Ral and rearrangement of the cytoskeleton.	bind
30352	1	6849	5	13	NULL	NULL	NULL	TNF-alpha	GP		bind					55kd membrane receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1839_s_180	9846974	19  As a trimeric complex, TNF-alpha binds to the two demonstrated membrane receptors of 55kd and 75kd.	bind
30353	2	6849	5	13	NULL	NULL	NULL	TNF-alpha	GP		bind					75kd membrane receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1839_s_180	9846974	19  As a trimeric complex, TNF-alpha binds to the two demonstrated membrane receptors of 55kd and 75kd.	bind
30354	3	6849	5	13	NULL	NULL	NULL	statement 1	GP		forms complex with					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1839_s_180	9846974	19  As a trimeric complex, TNF-alpha binds to the two demonstrated membrane receptors of 55kd and 75kd.	bind
19920	1	6849	6	NULL	NULL	0	NULL	TNF-alpha	NULL		bind	NULL				55kd membrane receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_6_1839_s_180	9846974	19  As a trimeric complex, TNF-alpha binds to the two demonstrated membrane receptors of 55kd and 75kd.	bind
19921	2	6849	6	NULL	NULL	0	NULL	TNF-alpha	NULL		bind	NULL				75kd membrane receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_6_1839_s_180	9846974	19  As a trimeric complex, TNF-alpha binds to the two demonstrated membrane receptors of 55kd and 75kd.	bind
19922	3	6849	6	NULL	NULL	0	NULL	statement 1	NULL		forms complex with	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1839_s_180	9846974	19  As a trimeric complex, TNF-alpha binds to the two demonstrated membrane receptors of 55kd and 75kd.	bind
24014	1	6850	5	13	NULL	NULL	NULL	CKIs	GP		bind					CDK  complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_119_s_18	9916926	19  CKIs bind to cyclin/cyclin-dependent kinase (CDK) complexes, consequently blocking progression through the cell cycle.	bind
24015	2	6850	5	13	NULL	NULL	NULL	CDK  complexes	GP		is					cyclin/cyclin-dependent kinase complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_119_s_18	9916926	19  CKIs bind to cyclin/cyclin-dependent kinase (CDK) complexes, consequently blocking progression through the cell cycle.	bind
24016	3	6850	5	13	NULL	NULL	NULL	statement 1	Process		blocks					cell cycle	Process	progression through			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_119_s_18	9916926	19  CKIs bind to cyclin/cyclin-dependent kinase (CDK) complexes, consequently blocking progression through the cell cycle.	bind
19923	1	6850	6	NULL	NULL	0	NULL	CKI	NULL		bind	NULL				CDK complexes	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_1_119_s_18	9916926	19  CKIs bind to cyclin/cyclin-dependent kinase (CDK) complexes, consequently blocking progression through the cell cycle.	bind
19924	2	6850	6	NULL	NULL	0	NULL	CDK	NULL		is	NULL				cyclin/cyclin-dependent kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_1_119_s_18	9916926	19  CKIs bind to cyclin/cyclin-dependent kinase (CDK) complexes, consequently blocking progression through the cell cycle.	bind
30289	3	6850	6	NULL	NULL	0	NULL	statement 1	NULL		blocks	NULL				cell cycle	NULL	progression through			NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_1_119_s_18	9916926	19  CKIs bind to cyclin/cyclin-dependent kinase (CDK) complexes, consequently blocking progression through the cell cycle.	bind
24017	1	6851	5	13	NULL	NULL	NULL	angiotensin II	GP		bind					AT1 receptors	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_103_6_904_s_72	11171802	19  In vitro, losartan competes with the binding of angiotensin II to AT1 receptors; the concentration that inhibits 50% of the binding of angiotensin II (IC50) is 20 nmol/L. Losartan has a major active metabolite, EXP 3174.	bind
24018	2	6851	5	13	NULL	NULL	NULL	losartan	Chemical		bind					AT1 receptors	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_103_6_904_s_72	11171802	19  In vitro, losartan competes with the binding of angiotensin II to AT1 receptors; the concentration that inhibits 50% of the binding of angiotensin II (IC50) is 20 nmol/L. Losartan has a major active metabolite, EXP 3174.	bind
24019	3	6851	5	13	NULL	NULL	NULL	statement 2	Process		competes with					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_103_6_904_s_72	11171802	19  In vitro, losartan competes with the binding of angiotensin II to AT1 receptors; the concentration that inhibits 50% of the binding of angiotensin II (IC50) is 20 nmol/L. Losartan has a major active metabolite, EXP 3174.	bind
24020	4	6851	5	13	NULL	NULL	NULL	EXP 3174	Chemical		is a metabolite of		major active			losartan	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_6_904_s_72	11171802	19  In vitro, losartan competes with the binding of angiotensin II to AT1 receptors; the concentration that inhibits 50% of the binding of angiotensin II (IC50) is 20 nmol/L. Losartan has a major active metabolite, EXP 3174.	bind
19925	1	6851	6	NULL	NULL	0	NULL	angiotensin II	NULL		bind	NULL				AT1 receptor	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_103_6_904_s_72	11171802	19  In vitro, losartan competes with the binding of angiotensin II to AT1 receptors; the concentration that inhibits 50% of the binding of angiotensin II (IC50) is 20 nmol/L. Losartan has a major active metabolite, EXP 3174.	bind
19926	2	6851	6	NULL	NULL	0	NULL	losartan	NULL		bind	NULL				AT1 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_6_904_s_72	11171802	19  In vitro, losartan competes with the binding of angiotensin II to AT1 receptors; the concentration that inhibits 50% of the binding of angiotensin II (IC50) is 20 nmol/L. Losartan has a major active metabolite, EXP 3174.	bind
19927	3	6851	6	NULL	NULL	0	NULL	statement 1	NULL		competes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_6_904_s_72	11171802	19  In vitro, losartan competes with the binding of angiotensin II to AT1 receptors; the concentration that inhibits 50% of the binding of angiotensin II (IC50) is 20 nmol/L. Losartan has a major active metabolite, EXP 3174.	bind
19932	4	6851	6	NULL	NULL	0	NULL	EXP 3174	NULL		is an active metabolite for	NULL				Losartan	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_6_904_s_72	11171802	19  In vitro, losartan competes with the binding of angiotensin II to AT1 receptors; the concentration that inhibits 50% of the binding of angiotensin II (IC50) is 20 nmol/L. Losartan has a major active metabolite, EXP 3174.	bind
24243	1	6852	5	13	NULL	NULL	NULL	Ang-2	GP		is antagonist of					Ang-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_6_2077_s_252	10854229	19  It has been proposed that Ang-2, the Ang-1 antagonist that binds to Tie-2 and blocks Ang-1-induced Tie-2 phosphorylation, could be an important pro-angiogenic factor, in that by interrupting the stabilizing Ang-1 signal it might promote a process of vessel wall disassembly that would allow endothelial cells to respond to angiogenic inducers.	bind
24244	2	6852	5	13	NULL	NULL	NULL	Ang-2	GP		bind					Tie-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_6_2077_s_252	10854229	19  It has been proposed that Ang-2, the Ang-1 antagonist that binds to Tie-2 and blocks Ang-1-induced Tie-2 phosphorylation, could be an important pro-angiogenic factor, in that by interrupting the stabilizing Ang-1 signal it might promote a process of vessel wall disassembly that would allow endothelial cells to respond to angiogenic inducers.	bind
24245	3	6852	5	13	NULL	NULL	NULL	Ang-1	GP		induces					Tie-2	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_6_2077_s_252	10854229	19  It has been proposed that Ang-2, the Ang-1 antagonist that binds to Tie-2 and blocks Ang-1-induced Tie-2 phosphorylation, could be an important pro-angiogenic factor, in that by interrupting the stabilizing Ang-1 signal it might promote a process of vessel wall disassembly that would allow endothelial cells to respond to angiogenic inducers.	bind
24246	4	6852	5	13	NULL	NULL	NULL	statement 2	Process		blocks					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_6_2077_s_252	10854229	19  It has been proposed that Ang-2, the Ang-1 antagonist that binds to Tie-2 and blocks Ang-1-induced Tie-2 phosphorylation, could be an important pro-angiogenic factor, in that by interrupting the stabilizing Ang-1 signal it might promote a process of vessel wall disassembly that would allow endothelial cells to respond to angiogenic inducers.	bind
24247	5	6852	5	13	NULL	NULL	NULL	Ang-2	GP		interrupts					Ang-1	GP	stabilizing signal of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_6_2077_s_252	10854229	19  It has been proposed that Ang-2, the Ang-1 antagonist that binds to Tie-2 and blocks Ang-1-induced Tie-2 phosphorylation, could be an important pro-angiogenic factor, in that by interrupting the stabilizing Ang-1 signal it might promote a process of vessel wall disassembly that would allow endothelial cells to respond to angiogenic inducers.	bind
24248	6	6852	5	13	NULL	NULL	NULL	statement 5	Process		promote		might			vessel wall disassembly	Process	process of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_6_2077_s_252	10854229	19  It has been proposed that Ang-2, the Ang-1 antagonist that binds to Tie-2 and blocks Ang-1-induced Tie-2 phosphorylation, could be an important pro-angiogenic factor, in that by interrupting the stabilizing Ang-1 signal it might promote a process of vessel wall disassembly that would allow endothelial cells to respond to angiogenic inducers.	bind
24249	7	6852	5	13	NULL	NULL	NULL	endothelial cells	Cell		responds to					angiogenic inducers	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_6_2077_s_252	10854229	19  It has been proposed that Ang-2, the Ang-1 antagonist that binds to Tie-2 and blocks Ang-1-induced Tie-2 phosphorylation, could be an important pro-angiogenic factor, in that by interrupting the stabilizing Ang-1 signal it might promote a process of vessel wall disassembly that would allow endothelial cells to respond to angiogenic inducers.	bind
24250	8	6852	5	13	NULL	NULL	NULL	statement 6	Process		allows					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_6_2077_s_252	10854229	19  It has been proposed that Ang-2, the Ang-1 antagonist that binds to Tie-2 and blocks Ang-1-induced Tie-2 phosphorylation, could be an important pro-angiogenic factor, in that by interrupting the stabilizing Ang-1 signal it might promote a process of vessel wall disassembly that would allow endothelial cells to respond to angiogenic inducers.	bind
24251	9	6852	5	13	NULL	NULL	NULL	Ang-2	GP		is a type of					pro-angiogenic factor	GP	 important			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_6_2077_s_252	10854229	19  It has been proposed that Ang-2, the Ang-1 antagonist that binds to Tie-2 and blocks Ang-1-induced Tie-2 phosphorylation, could be an important pro-angiogenic factor, in that by interrupting the stabilizing Ang-1 signal it might promote a process of vessel wall disassembly that would allow endothelial cells to respond to angiogenic inducers.	bind
19935	1	6852	6	NULL	NULL	0	NULL	Ang-2	NULL		bind	NULL				Tie-2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_6_2077_s_252	10854229	19  It has been proposed that Ang-2, the Ang-1 antagonist that binds to Tie-2 and blocks Ang-1-induced Tie-2 phosphorylation, could be an important pro-angiogenic factor, in that by interrupting the stabilizing Ang-1 signal it might promote a process of vessel wall disassembly that would allow endothelial cells to respond to angiogenic inducers.	bind
19971	2	6852	6	10	NULL	0	NULL	Ang-2			is antagonist of					Ang-1					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_6_2077_s_252	10854229	19  It has been proposed that Ang-2, the Ang-1 antagonist that binds to Tie-2 and blocks Ang-1-induced Tie-2 phosphorylation, could be an important pro-angiogenic factor, in that by interrupting the stabilizing Ang-1 signal it might promote a process of vessel wall disassembly that would allow endothelial cells to respond to angiogenic inducers.	bind
19972	3	6852	6	NULL	NULL	0	NULL	Ang-1	NULL		induces	NULL				Tie-2	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_6_2077_s_252	10854229	19  It has been proposed that Ang-2, the Ang-1 antagonist that binds to Tie-2 and blocks Ang-1-induced Tie-2 phosphorylation, could be an important pro-angiogenic factor, in that by interrupting the stabilizing Ang-1 signal it might promote a process of vessel wall disassembly that would allow endothelial cells to respond to angiogenic inducers.	bind
19973	4	6852	6	NULL	NULL	0	NULL	Ang-2	NULL		blocks	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_6_2077_s_252	10854229	19  It has been proposed that Ang-2, the Ang-1 antagonist that binds to Tie-2 and blocks Ang-1-induced Tie-2 phosphorylation, could be an important pro-angiogenic factor, in that by interrupting the stabilizing Ang-1 signal it might promote a process of vessel wall disassembly that would allow endothelial cells to respond to angiogenic inducers.	bind
19974	5	6852	6	10	NULL	0	NULL	Ang-2			is a type of					pro-angiogenic factor					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_6_2077_s_252	10854229	19  It has been proposed that Ang-2, the Ang-1 antagonist that binds to Tie-2 and blocks Ang-1-induced Tie-2 phosphorylation, could be an important pro-angiogenic factor, in that by interrupting the stabilizing Ang-1 signal it might promote a process of vessel wall disassembly that would allow endothelial cells to respond to angiogenic inducers.	bind
19975	6	6852	6	NULL	NULL	0	NULL	Ang-2	NULL		promote	NULL	might			vessel wall disassembly	NULL	process of 			NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_6_2077_s_252	10854229	19  It has been proposed that Ang-2, the Ang-1 antagonist that binds to Tie-2 and blocks Ang-1-induced Tie-2 phosphorylation, could be an important pro-angiogenic factor, in that by interrupting the stabilizing Ang-1 signal it might promote a process of vessel wall disassembly that would allow endothelial cells to respond to angiogenic inducers.	bind
19976	7	6852	6	NULL	NULL	0	NULL	endothelial cells	NULL		respond to	NULL				angiogenic inducers	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_6_2077_s_252	10854229	19  It has been proposed that Ang-2, the Ang-1 antagonist that binds to Tie-2 and blocks Ang-1-induced Tie-2 phosphorylation, could be an important pro-angiogenic factor, in that by interrupting the stabilizing Ang-1 signal it might promote a process of vessel wall disassembly that would allow endothelial cells to respond to angiogenic inducers.	bind
19977	8	6852	6	NULL	NULL	0	NULL	statement 6	NULL		allow	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_6_2077_s_252	10854229	19  It has been proposed that Ang-2, the Ang-1 antagonist that binds to Tie-2 and blocks Ang-1-induced Tie-2 phosphorylation, could be an important pro-angiogenic factor, in that by interrupting the stabilizing Ang-1 signal it might promote a process of vessel wall disassembly that would allow endothelial cells to respond to angiogenic inducers.	bind
56634	9	6852	6	10	NULL	0	NULL	Ang-2			interrupts 					Ang-1		stabilizing signal of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_6_2077_s_252	10854229	19  It has been proposed that Ang-2, the Ang-1 antagonist that binds to Tie-2 and blocks Ang-1-induced Tie-2 phosphorylation, could be an important pro-angiogenic factor, in that by interrupting the stabilizing Ang-1 signal it might promote a process of vessel wall disassembly that would allow endothelial cells to respond to angiogenic inducers.	bind
56635	1	6853	5	13	NULL	NULL	NULL	actin monomer-binding proteins	GP		bind					 monomeric actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_869_s_258	11891186	19  They were then identified as actin monomer-binding proteins 20, 21  that bind monomeric actin (G-actin) and disturb the assembly of filamentous actin (F-actin).	bind
56636	2	6853	5	13	NULL	NULL	NULL	actin monomer-binding proteins	GP		disturb					filamentous actin	GP	 assembly of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_869_s_258	11891186	19  They were then identified as actin monomer-binding proteins 20, 21  that bind monomeric actin (G-actin) and disturb the assembly of filamentous actin (F-actin).	bind
56637	3	6853	5	13	NULL	NULL	NULL	G-actin	GP		is a type of					monomeric actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_869_s_258	11891186	19  They were then identified as actin monomer-binding proteins 20, 21  that bind monomeric actin (G-actin) and disturb the assembly of filamentous actin (F-actin).	bind
56638	4	6853	5	13	NULL	NULL	NULL	F-actin	GP		is a type of					filamentous actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_869_s_258	11891186	19  They were then identified as actin monomer-binding proteins 20, 21  that bind monomeric actin (G-actin) and disturb the assembly of filamentous actin (F-actin).	bind
19978	1	6853	6	NULL	NULL	0	NULL	actin monomer-binding proteins	NULL		bind	NULL				monomeric actin	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_3_869_s_258	11891186	19  They were then identified as actin monomer-binding proteins 20, 21  that bind monomeric actin (G-actin) and disturb the assembly of filamentous actin (F-actin).	bind
19979	2	6853	6	NULL	NULL	0	NULL	actin monomer-binding proteins	NULL		disturb	NULL				filamentous actin	NULL	assembly of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_3_869_s_258	11891186	19  They were then identified as actin monomer-binding proteins 20, 21  that bind monomeric actin (G-actin) and disturb the assembly of filamentous actin (F-actin).	bind
19980	3	6853	6	10	NULL	0	NULL	G-actin	NULL		is a type of	NULL				monomeric actin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_869_s_258	11891186	19  They were then identified as actin monomer-binding proteins 20, 21  that bind monomeric actin (G-actin) and disturb the assembly of filamentous actin (F-actin).	bind
19981	4	6853	6	10	NULL	0	NULL	F-actin	NULL		is a type of	NULL				filamentous actin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_869_s_258	11891186	19  They were then identified as actin monomer-binding proteins 20, 21  that bind monomeric actin (G-actin) and disturb the assembly of filamentous actin (F-actin).	bind
24252	1	6854	5	13	NULL	NULL	NULL	Tie-2	GP		is					 receptor tyrosine kinase	GP	endothelium-specific			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_3_799_s_144	12213707	19  Tie-2 is an endothelium-specific receptor tyrosine kinase, which binds to angiopoietin-1 and -2.	bind
24253	2	6854	5	13	NULL	NULL	NULL	Tie-2	GP		bind					angiopoietin-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_3_799_s_144	12213707	19  Tie-2 is an endothelium-specific receptor tyrosine kinase, which binds to angiopoietin-1 and -2.	bind
24254	3	6854	5	13	NULL	NULL	NULL	Tie-2	GP		bind					angiopoietin-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_3_799_s_144	12213707	19  Tie-2 is an endothelium-specific receptor tyrosine kinase, which binds to angiopoietin-1 and -2.	bind
19982	1	6854	6	NULL	NULL	0	NULL	Tie-2	NULL		bind	NULL				angiopoietin-1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_3_799_s_144	12213707	19  Tie-2 is an endothelium-specific receptor tyrosine kinase, which binds to angiopoietin-1 and -2.	bind
19983	2	6854	6	NULL	NULL	0	NULL	Tie-2	NULL		bind	NULL				angiopoietin-2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_3_799_s_144	12213707	19  Tie-2 is an endothelium-specific receptor tyrosine kinase, which binds to angiopoietin-1 and -2.	bind
19985	3	6854	6	NULL	NULL	0	NULL	Tie-2	NULL		is	NULL				receptor tyrosine kinase	NULL	endothelium specific			NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_3_799_s_144	12213707	19  Tie-2 is an endothelium-specific receptor tyrosine kinase, which binds to angiopoietin-1 and -2.	bind
24255	1	6855	5	13	NULL	NULL	NULL	monocytes	Cell	human	express					FcRgammaIIa	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_975_s_36	15044210	19 - 22    Human monocytes express FcRgammaIIa or CD32, which binds CRP with high affinity and has been described as putative CRP-receptor 23 and FcRgammaI or CD64, which binds CRP with lower affinity.	bind
24256	2	6855	5	13	NULL	NULL	NULL	FcRgammaIIa 	GP		is					CD32	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_975_s_36	15044210	19 - 22    Human monocytes express FcRgammaIIa or CD32, which binds CRP with high affinity and has been described as putative CRP-receptor 23 and FcRgammaI or CD64, which binds CRP with lower affinity.	bind
24258	3	6855	5	13	NULL	NULL	NULL	FcRgammaIIa	GP		bind		high affinity			CRP	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_975_s_36	15044210	19 - 22    Human monocytes express FcRgammaIIa or CD32, which binds CRP with high affinity and has been described as putative CRP-receptor 23 and FcRgammaI or CD64, which binds CRP with lower affinity.	bind
24259	5	6855	5	13	NULL	NULL	NULL	FcRgammaIIa	GP		is described as					CRP-receptor	GP	putative			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_975_s_36	15044210	19 - 22    Human monocytes express FcRgammaIIa or CD32, which binds CRP with high affinity and has been described as putative CRP-receptor 23 and FcRgammaI or CD64, which binds CRP with lower affinity.	bind
24260	6	6855	5	13	NULL	NULL	NULL	monocytes	Cell	human	express					FcRgammaI	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_975_s_36	15044210	19 - 22    Human monocytes express FcRgammaIIa or CD32, which binds CRP with high affinity and has been described as putative CRP-receptor 23 and FcRgammaI or CD64, which binds CRP with lower affinity.	bind
24261	7	6855	5	13	NULL	NULL	NULL	FcRgammaI	GP		is					CD64	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_975_s_36	15044210	19 - 22    Human monocytes express FcRgammaIIa or CD32, which binds CRP with high affinity and has been described as putative CRP-receptor 23 and FcRgammaI or CD64, which binds CRP with lower affinity.	bind
24262	4	6855	5	13	NULL	NULL	NULL	FcRgammaI	GP		bind		low affinity			CRP	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_975_s_36	15044210	19 - 22    Human monocytes express FcRgammaIIa or CD32, which binds CRP with high affinity and has been described as putative CRP-receptor 23 and FcRgammaI or CD64, which binds CRP with lower affinity.	bind
19986	1	6855	6	NULL	NULL	0	NULL	monocytes	NULL	human	express	NULL				FcRgammaIIa	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_975_s_36	15044210	19 - 22    Human monocytes express FcRgammaIIa or CD32, which binds CRP with high affinity and has been described as putative CRP-receptor 23 and FcRgammaI or CD64, which binds CRP with lower affinity.	bind
19988	2	6855	6	NULL	NULL	0	NULL	FcRgammaIIa	NULL		is	NULL				CD32	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_975_s_36	15044210	19 - 22    Human monocytes express FcRgammaIIa or CD32, which binds CRP with high affinity and has been described as putative CRP-receptor 23 and FcRgammaI or CD64, which binds CRP with lower affinity.	bind
19989	3	6855	6	NULL	NULL	0	NULL	FcRgammaIIa	NULL		bind	NULL	high affinity			CRP	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_975_s_36	15044210	19 - 22    Human monocytes express FcRgammaIIa or CD32, which binds CRP with high affinity and has been described as putative CRP-receptor 23 and FcRgammaI or CD64, which binds CRP with lower affinity.	bind
20295	4	6855	6	10	NULL	0	NULL	FcRgammaIIa			is described as					 CRP-receptor		putative			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_975_s_36	15044210	19 - 22    Human monocytes express FcRgammaIIa or CD32, which binds CRP with high affinity and has been described as putative CRP-receptor 23 and FcRgammaI or CD64, which binds CRP with lower affinity.	bind
20296	5	6855	6	NULL	NULL	0	NULL	FcRgammaI	NULL		bind	NULL	low affinity			CRP	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_975_s_36	15044210	19 - 22    Human monocytes express FcRgammaIIa or CD32, which binds CRP with high affinity and has been described as putative CRP-receptor 23 and FcRgammaI or CD64, which binds CRP with lower affinity.	bind
20297	6	6855	6	NULL	NULL	0	NULL	FcRgammaI	NULL		is	NULL				CD64	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_975_s_36	15044210	19 - 22    Human monocytes express FcRgammaIIa or CD32, which binds CRP with high affinity and has been described as putative CRP-receptor 23 and FcRgammaI or CD64, which binds CRP with lower affinity.	bind
56639	7	6855	6	10	NULL	0	NULL	monocytes		human	express					FcRgammaI					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_975_s_36	15044210	19 - 22    Human monocytes express FcRgammaIIa or CD32, which binds CRP with high affinity and has been described as putative CRP-receptor 23 and FcRgammaI or CD64, which binds CRP with lower affinity.	bind
24263	1	6856	5	13	NULL	NULL	NULL	egr-1	GP	activated	bind					PDGF-A	GP	proximal		promoter	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_996_s_36	10195928	19 20  Activated  egr-1 binds to the proximal PDGF-A promoter by displacing  sp-1 from their overlapping recognition element, and the  egr-1 binding site has been identified as a cis-element for the induction of PDGF-A by fluid shear.	bind
24264	2	6856	5	13	NULL	NULL	NULL	sp-1	GP		is displaced from							overlapping		recognition element	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_996_s_36	10195928	19 20  Activated  egr-1 binds to the proximal PDGF-A promoter by displacing  sp-1 from their overlapping recognition element, and the  egr-1 binding site has been identified as a cis-element for the induction of PDGF-A by fluid shear.	bind
24265	3	6856	5	13	NULL	NULL	NULL	statement 1	Process		occurs by					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_996_s_36	10195928	19 20  Activated  egr-1 binds to the proximal PDGF-A promoter by displacing  sp-1 from their overlapping recognition element, and the  egr-1 binding site has been identified as a cis-element for the induction of PDGF-A by fluid shear.	bind
24266	5	6856	5	NULL	NULL	0	NULL		NULL		has been identified as	NULL			egr-1 binding site		NULL			cis-element	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_996_s_36	10195928	19 20  Activated  egr-1 binds to the proximal PDGF-A promoter by displacing  sp-1 from their overlapping recognition element, and the  egr-1 binding site has been identified as a cis-element for the induction of PDGF-A by fluid shear.	bind
24267	4	6856	5	13	NULL	NULL	NULL	PDGF-A	GP		is induced by					fluid shear					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_996_s_36	10195928	19 20  Activated  egr-1 binds to the proximal PDGF-A promoter by displacing  sp-1 from their overlapping recognition element, and the  egr-1 binding site has been identified as a cis-element for the induction of PDGF-A by fluid shear.	bind
24268	6	6856	5	13	NULL	NULL	NULL	statement 5	Process		is required for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_996_s_36	10195928	19 20  Activated  egr-1 binds to the proximal PDGF-A promoter by displacing  sp-1 from their overlapping recognition element, and the  egr-1 binding site has been identified as a cis-element for the induction of PDGF-A by fluid shear.	bind
19990	1	6856	6	NULL	NULL	0	NULL	egr-1	NULL	activated	bind	NULL				PDGF-A	NULL	proximal		promoter	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_996_s_36	10195928	19 20  Activated  egr-1 binds to the proximal PDGF-A promoter by displacing  sp-1 from their overlapping recognition element, and the  egr-1 binding site has been identified as a cis-element for the induction of PDGF-A by fluid shear.	bind
19991	2	6856	6	NULL	NULL	0	NULL		NULL		induces	NULL			egr-1 binding site	PDGF-A	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_996_s_36	10195928	19 20  Activated  egr-1 binds to the proximal PDGF-A promoter by displacing  sp-1 from their overlapping recognition element, and the  egr-1 binding site has been identified as a cis-element for the induction of PDGF-A by fluid shear.	bind
19992	3	6856	6	NULL	NULL	0	NULL	statement 2	NULL		occurs by	NULL				fluid shear	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_996_s_36	10195928	19 20  Activated  egr-1 binds to the proximal PDGF-A promoter by displacing  sp-1 from their overlapping recognition element, and the  egr-1 binding site has been identified as a cis-element for the induction of PDGF-A by fluid shear.	bind
20757	4	6856	6	NULL	NULL	0	NULL	egr-1	NULL		displaces	NULL				Sp1	NULL	overlapping 		recognition element	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_996_s_36	10195928	19 20  Activated  egr-1 binds to the proximal PDGF-A promoter by displacing  sp-1 from their overlapping recognition element, and the  egr-1 binding site has been identified as a cis-element for the induction of PDGF-A by fluid shear.	bind
20758	5	6856	6	NULL	NULL	0	NULL	statement 1	NULL		occurs by	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_996_s_36	10195928	19 20  Activated  egr-1 binds to the proximal PDGF-A promoter by displacing  sp-1 from their overlapping recognition element, and the  egr-1 binding site has been identified as a cis-element for the induction of PDGF-A by fluid shear.	bind
56640	6	6856	6	10	NULL	0	NULL				has been identified as			 egr-1 binding site						cis-element	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_4_996_s_36	10195928	19 20  Activated  egr-1 binds to the proximal PDGF-A promoter by displacing  sp-1 from their overlapping recognition element, and the  egr-1 binding site has been identified as a cis-element for the induction of PDGF-A by fluid shear.	bind
24269	1	6858	5	13	NULL	NULL	NULL	TF	GP		is a type of					integral membrane glycoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_520_s_35	9102171	19 22  TF is an integral membrane glycoprotein, which binds to factor VII(a).	bind
24270	2	6858	5	13	NULL	NULL	NULL	TF	GP		bind					factor VII	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_520_s_35	9102171	19 22  TF is an integral membrane glycoprotein, which binds to factor VII(a).	bind
19995	1	6858	6	NULL	NULL	0	NULL	TF	NULL		bind	NULL				factor VII	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_520_s_35	9102171	19 22  TF is an integral membrane glycoprotein, which binds to factor VII(a).	bind
19996	2	6858	6	10	NULL	0	NULL	TF	NULL		is a type of	NULL				integral membrane glycoprotein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_520_s_35	9102171	19 22  TF is an integral membrane glycoprotein, which binds to factor VII(a).	bind
24271	1	6859	5	13	NULL	NULL	NULL	Hdlq19 gene	GP		code for		may			plasma phospholipid transfer protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_161_s_133	14592847	19 A candidate gene for  Hdlq19 is the gene ( Pltp; cM 93.0) coding for plasma phospholipid transfer protein, which is bound to HDL and mediates the net transfer and exchange of phospholipids among different lipoproteins and participates in the transformation of larger HDL3 into smaller HDL2.	bind
24272	2	6859	5	13	NULL	NULL	NULL	statement 1	GP		bind					HDL	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_161_s_133	14592847	19 A candidate gene for  Hdlq19 is the gene ( Pltp; cM 93.0) coding for plasma phospholipid transfer protein, which is bound to HDL and mediates the net transfer and exchange of phospholipids among different lipoproteins and participates in the transformation of larger HDL3 into smaller HDL2.	bind
24273	3	6859	5	13	NULL	NULL	NULL	statement 2	Process		mediate					phospholipids	Chemical	net transfer of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_161_s_133	14592847	19 A candidate gene for  Hdlq19 is the gene ( Pltp; cM 93.0) coding for plasma phospholipid transfer protein, which is bound to HDL and mediates the net transfer and exchange of phospholipids among different lipoproteins and participates in the transformation of larger HDL3 into smaller HDL2.	bind
24274	4	6859	5	13	NULL	NULL	NULL	statement 2	Process		mediate					phospholipids	Chemical	exchange of 			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_161_s_133	14592847	19 A candidate gene for  Hdlq19 is the gene ( Pltp; cM 93.0) coding for plasma phospholipid transfer protein, which is bound to HDL and mediates the net transfer and exchange of phospholipids among different lipoproteins and participates in the transformation of larger HDL3 into smaller HDL2.	bind
24275	5	6859	5	13	NULL	NULL	NULL	HDL3	GP	larger	is transformed to					HDL2	GP	smaller			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_161_s_133	14592847	19 A candidate gene for  Hdlq19 is the gene ( Pltp; cM 93.0) coding for plasma phospholipid transfer protein, which is bound to HDL and mediates the net transfer and exchange of phospholipids among different lipoproteins and participates in the transformation of larger HDL3 into smaller HDL2.	bind
24276	6	6859	5	13	NULL	NULL	NULL	statement 2	Process		participates in					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_161_s_133	14592847	19 A candidate gene for  Hdlq19 is the gene ( Pltp; cM 93.0) coding for plasma phospholipid transfer protein, which is bound to HDL and mediates the net transfer and exchange of phospholipids among different lipoproteins and participates in the transformation of larger HDL3 into smaller HDL2.	bind
19997	1	6859	6	NULL	NULL	0	NULL	Hdlq19 gene	NULL		codes for	NULL				plasma phospholipid transfer protein	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_161_s_133	14592847	19 A candidate gene for  Hdlq19 is the gene ( Pltp; cM 93.0) coding for plasma phospholipid transfer protein, which is bound to HDL and mediates the net transfer and exchange of phospholipids among different lipoproteins and participates in the transformation of larger HDL3 into smaller HDL2.	bind
19998	2	6859	6	NULL	NULL	0	NULL	plasma phospholipid transfer protein	NULL		bind	NULL				HDL	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_161_s_133	14592847	19 A candidate gene for  Hdlq19 is the gene ( Pltp; cM 93.0) coding for plasma phospholipid transfer protein, which is bound to HDL and mediates the net transfer and exchange of phospholipids among different lipoproteins and participates in the transformation of larger HDL3 into smaller HDL2.	bind
19999	3	6859	6	NULL	NULL	0	NULL	statement 2	NULL		mediates	NULL				phospholipids	NULL	transfer of 			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_161_s_133	14592847	19 A candidate gene for  Hdlq19 is the gene ( Pltp; cM 93.0) coding for plasma phospholipid transfer protein, which is bound to HDL and mediates the net transfer and exchange of phospholipids among different lipoproteins and participates in the transformation of larger HDL3 into smaller HDL2.	bind
20000	4	6859	6	NULL	NULL	0	NULL	statement 2	NULL		mediates	NULL				phospholipids	NULL	exchange of 			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_161_s_133	14592847	19 A candidate gene for  Hdlq19 is the gene ( Pltp; cM 93.0) coding for plasma phospholipid transfer protein, which is bound to HDL and mediates the net transfer and exchange of phospholipids among different lipoproteins and participates in the transformation of larger HDL3 into smaller HDL2.	bind
20001	5	6859	6	NULL	NULL	0	NULL	HDL3	NULL		transformed into	NULL				HDL2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_161_s_133	14592847	19 A candidate gene for  Hdlq19 is the gene ( Pltp; cM 93.0) coding for plasma phospholipid transfer protein, which is bound to HDL and mediates the net transfer and exchange of phospholipids among different lipoproteins and participates in the transformation of larger HDL3 into smaller HDL2.	bind
56641	6	6859	6	10	NULL	0	NULL	statement 2			participate in					statement 5					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_161_s_133	14592847	19 A candidate gene for  Hdlq19 is the gene ( Pltp; cM 93.0) coding for plasma phospholipid transfer protein, which is bound to HDL and mediates the net transfer and exchange of phospholipids among different lipoproteins and participates in the transformation of larger HDL3 into smaller HDL2.	bind
24277	1	6860	5	13	NULL	NULL	NULL	IRS-1	GP		bind					IR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_988_s_160	12689920	19 Another possibility is that IRS-1 binds to IR with a higher affinity compared with IRS-2 or Shc 20,21  and therefore is a preferential substrate for IR. IRS-2 or Shc may become important only in the absence of IRS-1.	bind
24278	2	6860	5	13	NULL	NULL	NULL	IRS-2	GP		bind					IR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_988_s_160	12689920	19 Another possibility is that IRS-1 binds to IR with a higher affinity compared with IRS-2 or Shc 20,21  and therefore is a preferential substrate for IR. IRS-2 or Shc may become important only in the absence of IRS-1.	bind
24279	3	6860	5	13	NULL	NULL	NULL	Shc	GP		bind					IR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_988_s_160	12689920	19 Another possibility is that IRS-1 binds to IR with a higher affinity compared with IRS-2 or Shc 20,21  and therefore is a preferential substrate for IR. IRS-2 or Shc may become important only in the absence of IRS-1.	bind
24280	4	6860	5	13	NULL	NULL	NULL	statement 1	Process		has high affinity than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_988_s_160	12689920	19 Another possibility is that IRS-1 binds to IR with a higher affinity compared with IRS-2 or Shc 20,21  and therefore is a preferential substrate for IR. IRS-2 or Shc may become important only in the absence of IRS-1.	bind
24281	5	6860	5	13	NULL	NULL	NULL	statement 1	Process		has high affinity than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_988_s_160	12689920	19 Another possibility is that IRS-1 binds to IR with a higher affinity compared with IRS-2 or Shc 20,21  and therefore is a preferential substrate for IR. IRS-2 or Shc may become important only in the absence of IRS-1.	bind
24282	6	6860	5	13	NULL	NULL	NULL	IRS-1	GP		is a substrate for		preferential			IR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_988_s_160	12689920	19 Another possibility is that IRS-1 binds to IR with a higher affinity compared with IRS-2 or Shc 20,21  and therefore is a preferential substrate for IR. IRS-2 or Shc may become important only in the absence of IRS-1.	bind
24283	7	6860	5	13	NULL	NULL	NULL	IRS-2	GP		become important		may only			IRS-1	GP	in the absence of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_988_s_160	12689920	19 Another possibility is that IRS-1 binds to IR with a higher affinity compared with IRS-2 or Shc 20,21  and therefore is a preferential substrate for IR. IRS-2 or Shc may become important only in the absence of IRS-1.	bind
24284	8	6860	5	13	NULL	NULL	NULL	Shc	GP		become important		may only			IRS-1	GP	in the absence of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_988_s_160	12689920	19 Another possibility is that IRS-1 binds to IR with a higher affinity compared with IRS-2 or Shc 20,21  and therefore is a preferential substrate for IR. IRS-2 or Shc may become important only in the absence of IRS-1.	bind
20003	1	6860	6	10	NULL	0	NULL	IRS-1			bind					IR					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_988_s_160	12689920	19 Another possibility is that IRS-1 binds to IR with a higher affinity compared with IRS-2 or Shc 20,21  and therefore is a preferential substrate for IR. IRS-2 or Shc may become important only in the absence of IRS-1.	bind
20004	2	6860	6	NULL	NULL	0	NULL	IRS-2	NULL		bind	NULL				IR	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_988_s_160	12689920	19 Another possibility is that IRS-1 binds to IR with a higher affinity compared with IRS-2 or Shc 20,21  and therefore is a preferential substrate for IR. IRS-2 or Shc may become important only in the absence of IRS-1.	bind
20005	3	6860	6	NULL	NULL	0	NULL	Shc	NULL		bind	NULL				IR	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_988_s_160	12689920	19 Another possibility is that IRS-1 binds to IR with a higher affinity compared with IRS-2 or Shc 20,21  and therefore is a preferential substrate for IR. IRS-2 or Shc may become important only in the absence of IRS-1.	bind
56642	4	6860	6	10	NULL	0	NULL	statement 1			higher affinity than					statement 2					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_988_s_160	12689920	19 Another possibility is that IRS-1 binds to IR with a higher affinity compared with IRS-2 or Shc 20,21  and therefore is a preferential substrate for IR. IRS-2 or Shc may become important only in the absence of IRS-1.	bind
56643	5	6860	6	10	NULL	0	NULL	statement 1			higher affinity than					statement 3					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_988_s_160	12689920	19 Another possibility is that IRS-1 binds to IR with a higher affinity compared with IRS-2 or Shc 20,21  and therefore is a preferential substrate for IR. IRS-2 or Shc may become important only in the absence of IRS-1.	bind
56644	6	6860	6	10	NULL	0	NULL	 IRS-1			is substrate for		preferential			IR					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_988_s_160	12689920	19 Another possibility is that IRS-1 binds to IR with a higher affinity compared with IRS-2 or Shc 20,21  and therefore is a preferential substrate for IR. IRS-2 or Shc may become important only in the absence of IRS-1.	bind
56645	7	6860	6	10	NULL	0	NULL	IRS-2			become  important 		may			IRS-1		in the absence of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_988_s_160	12689920	19 Another possibility is that IRS-1 binds to IR with a higher affinity compared with IRS-2 or Shc 20,21  and therefore is a preferential substrate for IR. IRS-2 or Shc may become important only in the absence of IRS-1.	bind
56646	8	6860	6	10	NULL	0	NULL	Shc			become important 		may			IRS-1		in the absence of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_988_s_160	12689920	19 Another possibility is that IRS-1 binds to IR with a higher affinity compared with IRS-2 or Shc 20,21  and therefore is a preferential substrate for IR. IRS-2 or Shc may become important only in the absence of IRS-1.	bind
24285	1	6861	5	13	NULL	NULL	NULL	FKBP12.6	GP		bind					RyR	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1213_s_47	16339492	19 Furthermore, FKBP12.6 binding to RyR is not affected during catecholamine stimulation that results in arrhythmias in a mouse model of catecholamine-induced ventricular tachycardia, 20,21  a genetic disorder of hypersensitive RyR Ca2+ release.	bind
24286	2	6861	5	13	NULL	NULL	NULL	statement 1	Process		is not affected during					catecholamine	Chemical	stimulation			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1213_s_47	16339492	19 Furthermore, FKBP12.6 binding to RyR is not affected during catecholamine stimulation that results in arrhythmias in a mouse model of catecholamine-induced ventricular tachycardia, 20,21  a genetic disorder of hypersensitive RyR Ca2+ release.	bind
24287	3	6861	5	13	NULL	NULL	NULL	catecholamine	Chemical	stimulation with	results in					arrhythmias	MedicalFinding				NULL	 in a mouse model of catecholamine-induced ventricular tachycardia	NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1213_s_47	16339492	19 Furthermore, FKBP12.6 binding to RyR is not affected during catecholamine stimulation that results in arrhythmias in a mouse model of catecholamine-induced ventricular tachycardia, 20,21  a genetic disorder of hypersensitive RyR Ca2+ release.	bind
56647	4	6861	5	13	NULL	NULL	NULL	ventricular tachycardia	MedicalFinding	catecholamine-induced	genetic disorder of					hypersensitive RyR Ca2+ release	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1213_s_47	16339492	19 Furthermore, FKBP12.6 binding to RyR is not affected during catecholamine stimulation that results in arrhythmias in a mouse model of catecholamine-induced ventricular tachycardia, 20,21  a genetic disorder of hypersensitive RyR Ca2+ release.	bind
20006	1	6861	6	NULL	NULL	0	NULL	FKBP12.6	NULL		bind	NULL				RyR	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_12_1213_s_47	16339492	19 Furthermore, FKBP12.6 binding to RyR is not affected during catecholamine stimulation that results in arrhythmias in a mouse model of catecholamine-induced ventricular tachycardia, 20,21  a genetic disorder of hypersensitive RyR Ca2+ release.	bind
20007	2	6861	6	NULL	NULL	0	NULL	statement 1	NULL		is not affected during	NULL				catecholamine	NULL	stimulation by 			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1213_s_47	16339492	19 Furthermore, FKBP12.6 binding to RyR is not affected during catecholamine stimulation that results in arrhythmias in a mouse model of catecholamine-induced ventricular tachycardia, 20,21  a genetic disorder of hypersensitive RyR Ca2+ release.	bind
20298	3	6861	6	NULL	NULL	0	NULL	catecholamine	NULL	stimulation by	results in	NULL				arrhythmias	NULL				NULL	mouse model	NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1213_s_47	16339492	19 Furthermore, FKBP12.6 binding to RyR is not affected during catecholamine stimulation that results in arrhythmias in a mouse model of catecholamine-induced ventricular tachycardia, 20,21  a genetic disorder of hypersensitive RyR Ca2+ release.	bind
20299	4	6861	6	10	NULL	0	NULL	ventricular tachycardia		catecholamine-induced	is a genetic disorder of					hypersensitive RyR Ca2+ release					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1213_s_47	16339492	19 Furthermore, FKBP12.6 binding to RyR is not affected during catecholamine stimulation that results in arrhythmias in a mouse model of catecholamine-induced ventricular tachycardia, 20,21  a genetic disorder of hypersensitive RyR Ca2+ release.	bind
24288	1	6862	5	13	NULL	NULL	NULL	hsp90	GP		bind					Akt	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_8_866_s_112	11988487	19 In cells, the binding of hsp90 to Akt prevents dephosphorylation of threonine 308 by reducing PP2A-mediated dephosphorylation.	bind
24289	2	6862	5	13	NULL	NULL	NULL	statement 1	Process		prevents							dephosphorylation of	threonine 308		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_8_866_s_112	11988487	19 In cells, the binding of hsp90 to Akt prevents dephosphorylation of threonine 308 by reducing PP2A-mediated dephosphorylation.	bind
24290	4	6862	5	13	NULL	NULL	NULL	statement 2	Process		occurs by reducing					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_8_866_s_112	11988487	19 In cells, the binding of hsp90 to Akt prevents dephosphorylation of threonine 308 by reducing PP2A-mediated dephosphorylation.	bind
44704	3	6862	5	13	NULL	NULL	NULL	PP2A	GP		mediates					dephosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_8_866_s_112	11988487	19 In cells, the binding of hsp90 to Akt prevents dephosphorylation of threonine 308 by reducing PP2A-mediated dephosphorylation.	bind
20008	1	6862	6	NULL	NULL	0	NULL	hsp90	NULL		bind	NULL				Akt	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_8_866_s_112	11988487	19 In cells, the binding of hsp90 to Akt prevents dephosphorylation of threonine 308 by reducing PP2A-mediated dephosphorylation.	bind
20009	2	6862	6	10	NULL	0	NULL	statement 1			prevents							dephosphorylation of	threonine 308		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_8_866_s_112	11988487	19 In cells, the binding of hsp90 to Akt prevents dephosphorylation of threonine 308 by reducing PP2A-mediated dephosphorylation.	bind
20010	4	6862	6	10	NULL	0	NULL	statement 2			occurs by reducing					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_8_866_s_112	11988487	19 In cells, the binding of hsp90 to Akt prevents dephosphorylation of threonine 308 by reducing PP2A-mediated dephosphorylation.	bind
56648	3	6862	6	10	NULL	0	NULL	PP2A			mediates					dephosphorylation					NULL		0	NULL	NULL	NULL	gw60_circulationres_90_8_866_s_112	11988487	19 In cells, the binding of hsp90 to Akt prevents dephosphorylation of threonine 308 by reducing PP2A-mediated dephosphorylation.	bind
24292	1	6863	5	13	NULL	NULL	NULL	ER transcript	NucleicAcid	short	is expressed in					mice	Organism				NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_1_120_s_171	12515753	19 In these mice, a short ER transcript is expressed that encodes an  N-terminal truncated, mutant ER that binds estrogen but possesses significantly reduced estrogen-dependent transcriptional activity compared with that of the wild-type ER, 20 resulting in the same functional domain changes as our findings with ERalpha-46 in human endothelial cells.	bind
24293	2	6863	5	13	NULL	NULL	NULL	statement 1	GP		encodes					ER	GP	truncated;;mutant 	N-terminal		NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_1_120_s_171	12515753	19 In these mice, a short ER transcript is expressed that encodes an  N-terminal truncated, mutant ER that binds estrogen but possesses significantly reduced estrogen-dependent transcriptional activity compared with that of the wild-type ER, 20 resulting in the same functional domain changes as our findings with ERalpha-46 in human endothelial cells.	bind
24294	3	6863	5	13	NULL	NULL	NULL	statement 2	GP		bind					estrogen	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_1_120_s_171	12515753	19 In these mice, a short ER transcript is expressed that encodes an  N-terminal truncated, mutant ER that binds estrogen but possesses significantly reduced estrogen-dependent transcriptional activity compared with that of the wild-type ER, 20 resulting in the same functional domain changes as our findings with ERalpha-46 in human endothelial cells.	bind
24295	4	6863	5	13	NULL	NULL	NULL	statement 2	GP		possesses		significantly			transcriptional activity	Process	estrogen-dependent			NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_1_120_s_171	12515753	19 In these mice, a short ER transcript is expressed that encodes an  N-terminal truncated, mutant ER that binds estrogen but possesses significantly reduced estrogen-dependent transcriptional activity compared with that of the wild-type ER, 20 resulting in the same functional domain changes as our findings with ERalpha-46 in human endothelial cells.	bind
24296	5	6863	5	13	NULL	NULL	NULL	ER	GP	wild-type	possesses					transcriptional activity 	Process	estrogen-dependent			NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_1_120_s_171	12515753	19 In these mice, a short ER transcript is expressed that encodes an  N-terminal truncated, mutant ER that binds estrogen but possesses significantly reduced estrogen-dependent transcriptional activity compared with that of the wild-type ER, 20 resulting in the same functional domain changes as our findings with ERalpha-46 in human endothelial cells.	bind
24297	6	6863	5	13	NULL	NULL	NULL	statement 4	Process		is reduced than					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_1_120_s_171	12515753	19 In these mice, a short ER transcript is expressed that encodes an  N-terminal truncated, mutant ER that binds estrogen but possesses significantly reduced estrogen-dependent transcriptional activity compared with that of the wild-type ER, 20 resulting in the same functional domain changes as our findings with ERalpha-46 in human endothelial cells.	bind
24298	7	6863	5	13	NULL	NULL	NULL	statement 6	Process		results in					functional domain changes	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_1_120_s_171	12515753	19 In these mice, a short ER transcript is expressed that encodes an  N-terminal truncated, mutant ER that binds estrogen but possesses significantly reduced estrogen-dependent transcriptional activity compared with that of the wild-type ER, 20 resulting in the same functional domain changes as our findings with ERalpha-46 in human endothelial cells.	bind
20041	2	6863	6	10	NULL	0	NULL	statement 1			bind					estrogen					NULL	mice	NULL	NULL	NULL	NULL	gw70_circulation_107_1_120_s_171	12515753	19 In these mice, a short ER transcript is expressed that encodes an  N-terminal truncated, mutant ER that binds estrogen but possesses significantly reduced estrogen-dependent transcriptional activity compared with that of the wild-type ER, 20 resulting in the same functional domain changes as our findings with ERalpha-46 in human endothelial cells.	bind
20042	3	6863	6	10	NULL	0	NULL	statement 2			possesses 					 transcriptional activity		estrogen-dependent			NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_1_120_s_171	12515753	19 In these mice, a short ER transcript is expressed that encodes an  N-terminal truncated, mutant ER that binds estrogen but possesses significantly reduced estrogen-dependent transcriptional activity compared with that of the wild-type ER, 20 resulting in the same functional domain changes as our findings with ERalpha-46 in human endothelial cells.	bind
20043	4	6863	6	10	NULL	0	NULL	ER		wild-type	possesses					transcriptional activity		estrogen-dependent			NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_1_120_s_171	12515753	19 In these mice, a short ER transcript is expressed that encodes an  N-terminal truncated, mutant ER that binds estrogen but possesses significantly reduced estrogen-dependent transcriptional activity compared with that of the wild-type ER, 20 resulting in the same functional domain changes as our findings with ERalpha-46 in human endothelial cells.	bind
20044	5	6863	6	10	NULL	0	NULL	statement 2			is reduced than		significantly			statement 3					NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_1_120_s_171	12515753	19 In these mice, a short ER transcript is expressed that encodes an  N-terminal truncated, mutant ER that binds estrogen but possesses significantly reduced estrogen-dependent transcriptional activity compared with that of the wild-type ER, 20 resulting in the same functional domain changes as our findings with ERalpha-46 in human endothelial cells.	bind
56649	1	6863	6	10	NULL	0	NULL	ER transcript		short	encode					ErbB2 receptor		mutant;;truncated	N-terminal		NULL	mice	NULL	NULL	NULL	NULL	gw70_circulation_107_1_120_s_171	12515753	19 In these mice, a short ER transcript is expressed that encodes an  N-terminal truncated, mutant ER that binds estrogen but possesses significantly reduced estrogen-dependent transcriptional activity compared with that of the wild-type ER, 20 resulting in the same functional domain changes as our findings with ERalpha-46 in human endothelial cells.	bind
56650	6	6863	6	10	NULL	0	NULL	statement 5			results in					functional domain changes					NULL		0	NULL	NULL	NULL	gw70_circulation_107_1_120_s_171	12515753	19 In these mice, a short ER transcript is expressed that encodes an  N-terminal truncated, mutant ER that binds estrogen but possesses significantly reduced estrogen-dependent transcriptional activity compared with that of the wild-type ER, 20 resulting in the same functional domain changes as our findings with ERalpha-46 in human endothelial cells.	bind
24299	1	6864	5	13	NULL	NULL	NULL	alpha-actinin	GP		bind					syndecan-4	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_7_674_s_243	16141413	19 Increased alpha-actinin binding to syndecan-4 may decrease cell motility, similar to the effect of overexpression of alpha-actinin.	bind
24300	2	6864	5	13	NULL	NULL	NULL	statement 1	Process	increased	decrease		may			cell motility	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_7_674_s_243	16141413	19 Increased alpha-actinin binding to syndecan-4 may decrease cell motility, similar to the effect of overexpression of alpha-actinin.	bind
24301	3	6864	5	13	NULL	NULL	NULL	alpha-actinin	GP	effect of overexpression of	is similar to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_7_674_s_243	16141413	19 Increased alpha-actinin binding to syndecan-4 may decrease cell motility, similar to the effect of overexpression of alpha-actinin.	bind
20011	1	6864	6	NULL	NULL	0	NULL	alpha-Actinin	NULL		bind	NULL				syndecan-4	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_7_674_s_243	16141413	19 Increased alpha-actinin binding to syndecan-4 may decrease cell motility, similar to the effect of overexpression of alpha-actinin.	bind
20045	2	6864	6	NULL	NULL	0	NULL	statement 1	NULL	increased	decrease	NULL	may			cell motility	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_7_674_s_243	16141413	19 Increased alpha-actinin binding to syndecan-4 may decrease cell motility, similar to the effect of overexpression of alpha-actinin.	bind
20046	3	6864	6	NULL	NULL	0	NULL	alpha-Actinin	NULL	overexpression of	decrease	NULL	may			cell motility	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_7_674_s_243	16141413	19 Increased alpha-actinin binding to syndecan-4 may decrease cell motility, similar to the effect of overexpression of alpha-actinin.	bind
24302	1	6866	5	13	NULL	NULL	NULL	Src	GP	activated	bind					PYK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
24303	2	6866	5	13	NULL	NULL	NULL	statement 1	Process		phosphorylates		may			PYK2	GP		Tyr579		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
24304	3	6866	5	13	NULL	NULL	NULL	statement 1	Process		phosphorylates		may			PYK2	GP		Tyr580		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
24305	4	6866	5	13	NULL	NULL	NULL	statement 1	Process		phosphorylates		may			PYK2	GP		Tyr881		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
24306	5	6866	5	13	NULL	NULL	NULL	Grb2	GP		is a type of					an adaptor protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
24307	6	6866	5	13	NULL	NULL	NULL	Grb2	GP		bind					PYK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
24308	7	6866	5	13	NULL	NULL	NULL	statement 2	Process		promote					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
24309	8	6866	5	13	NULL	NULL	NULL	statement 3	Process		promote					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
24310	9	6866	5	13	NULL	NULL	NULL	statement 4	Process		promote					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
24311	10	6866	5	13	NULL	NULL	NULL	statement 2	Process		enhances					PYK2	GP	kinase activity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
24312	11	6866	5	13	NULL	NULL	NULL	statement 3	Process		enhances					PYK2	GP	kinase activity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
24313	12	6866	5	13	NULL	NULL	NULL	statement 4	Process		enhances					PYK2	GP	kinase activity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
20047	1	6866	6	NULL	NULL	0	NULL	Src	NULL	activated	bind	NULL				PYK2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
20048	2	6866	6	NULL	NULL	0	NULL	Src	NULL	activated	phosphorylate	NULL	may			PYK2	NULL		Tyr579		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
20049	3	6866	6	NULL	NULL	0	NULL	Src	NULL	activated	phosphorylate	NULL	may			PYK2	NULL		Tyr580		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
20050	4	6866	6	NULL	NULL	0	NULL	Src	NULL	activated	phosphorylate	NULL	may			PYK2	NULL		Tyr881		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
20051	5	6866	6	NULL	NULL	0	NULL	Grb2	NULL		bind	NULL				PYK2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
20052	6	6866	6	10	NULL	0	NULL	Grb2	NULL		is a type of	NULL				adaptor protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
20053	7	6866	6	NULL	NULL	0	NULL	statement 2	NULL		promotes	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
20054	8	6866	6	NULL	NULL	0	NULL	statement 3	NULL		promotes	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
20055	9	6866	6	NULL	NULL	0	NULL	statement 4	NULL		promotes	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
20056	10	6866	6	NULL	NULL	0	NULL	statement 2	NULL		enhances	NULL				PYK2	NULL	kinase activity of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
20057	11	6866	6	NULL	NULL	0	NULL	statement 3	NULL		enhances	NULL				PYK2	NULL	kinase activity of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
20058	12	6866	6	NULL	NULL	0	NULL	statement 4	NULL		enhances	NULL				PYK2	NULL	kinase activity of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_11_1790_s_33	12426206	19 The activated Src bound to PYK2 may phosphorylate PYK2 at Tyr579, Tyr580, and Tyr881, which promotes Grb2 (an adaptor protein) binding to PYK2 and enhances PYK2 kinase activity.	bind
24314	1	6867	5	13	NULL	NULL	NULL	TIMP-3	GP		bind		high affinity			ECM 20	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_754_s_39	15681295	19 The high binding affinity of TIMP-3 to ECM 20 offers a further advantage, potentially retaining and concentrating TIMP-3 in the area around the stent struts and limiting its spread to the uninjured media.	bind
24315	2	6867	5	13	NULL	NULL	NULL	statement 1	Process		retains					TIMP-3	GP				NULL	in the area around stent struts	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_754_s_39	15681295	19 The high binding affinity of TIMP-3 to ECM 20 offers a further advantage, potentially retaining and concentrating TIMP-3 in the area around the stent struts and limiting its spread to the uninjured media.	bind
24316	3	6867	5	13	NULL	NULL	NULL	statement 1	Process		concentrates					TIMP-3	GP				NULL	in the area around stent struts	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_754_s_39	15681295	19 The high binding affinity of TIMP-3 to ECM 20 offers a further advantage, potentially retaining and concentrating TIMP-3 in the area around the stent struts and limiting its spread to the uninjured media.	bind
24317	4	6867	5	13	NULL	NULL	NULL	statement 1	Process		limits					TIMP-3	GP	spreading of			NULL	to uninjured media	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_754_s_39	15681295	19 The high binding affinity of TIMP-3 to ECM 20 offers a further advantage, potentially retaining and concentrating TIMP-3 in the area around the stent struts and limiting its spread to the uninjured media.	bind
20059	1	6867	6	NULL	NULL	0	NULL	TIMP-3	NULL		bind	NULL	high affinity			ECM 20	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_754_s_39	15681295	19 The high binding affinity of TIMP-3 to ECM 20 offers a further advantage, potentially retaining and concentrating TIMP-3 in the area around the stent struts and limiting its spread to the uninjured media.	bind
30290	2	6867	6	NULL	NULL	0	NULL	statement 1	NULL		retains	NULL				TIMP-3	NULL				NULL	in the area around stent struts	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_754_s_39	15681295	19 The high binding affinity of TIMP-3 to ECM 20 offers a further advantage, potentially retaining and concentrating TIMP-3 in the area around the stent struts and limiting its spread to the uninjured media.	bind
30291	3	6867	6	NULL	NULL	0	NULL	statement 1	NULL		concentrates	NULL				TIMP-3	NULL				NULL	in the area around stent struts	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_754_s_39	15681295	19 The high binding affinity of TIMP-3 to ECM 20 offers a further advantage, potentially retaining and concentrating TIMP-3 in the area around the stent struts and limiting its spread to the uninjured media.	bind
30292	4	6867	6	NULL	NULL	0	NULL	statement 1	NULL		limits	NULL				TIMP-3	NULL	spreading of			NULL	to uninjured media	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_754_s_39	15681295	19 The high binding affinity of TIMP-3 to ECM 20 offers a further advantage, potentially retaining and concentrating TIMP-3 in the area around the stent struts and limiting its spread to the uninjured media.	bind
24318	1	6868	5	13	NULL	NULL	NULL	CDR3	GP		bind					THP	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_5_1859_s_185	11337384	19, 20, 45  It is therefore interesting that CDR3 binds THP, although there are similarities in this region among many kappa and lambda light chains.	bind
20060	1	6868	6	NULL	NULL	0	NULL	CDR3	NULL		bind	NULL				THP	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_5_1859_s_185	11337384	19, 20, 45  It is therefore interesting that CDR3 binds THP, although there are similarities in this region among many kappa and lambda light chains.	bind
24319	1	6869	5	13	NULL	NULL	NULL	decorin	GP		regulates					collagen assembly	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
24320	2	6869	5	13	NULL	NULL	NULL	decorin	GP		bind					TGF-beta1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
24321	3	6869	5	13	NULL	NULL	NULL	decorin	GP		bind					TGF-beta2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
24322	4	6869	5	13	NULL	NULL	NULL	decorin	GP		bind					TGF-beta3	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
24323	5	6869	5	13	NULL	NULL	NULL	biglycan	GP		regulates					collagen assembly	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
24324	6	6869	5	13	NULL	NULL	NULL	biglycan	GP		bind					TGF-beta1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
24325	7	6869	5	13	NULL	NULL	NULL	biglycan	GP		bind					TGF-beta2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
24326	8	6869	5	13	NULL	NULL	NULL	biglycan	GP		bind					TGF-beta3	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
24327	9	6869	5	13	NULL	NULL	NULL	fibromodulin	GP		regulates					collagen assembly	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
24328	10	6869	5	13	NULL	NULL	NULL	fibromodulin	GP		bind					TGF-beta1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
24329	11	6869	5	13	NULL	NULL	NULL	fibromodulin	GP		bind					TGF-beta2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
24330	12	6869	5	13	NULL	NULL	NULL	fibromodulin 	GP		bind					TGF-beta3	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
24331	13	6869	5	13	NULL	NULL	NULL	fibromodulin 	GP		affinity for		greatest			TGF-beta1 precursor	GP	latent			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
20061	1	6869	6	NULL	NULL	0	NULL	decorin	NULL		bind	NULL				TGF-beta1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
20062	2	6869	6	NULL	NULL	0	NULL	decorin	NULL		bind	NULL				TGF-beta2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
20063	3	6869	6	NULL	NULL	0	NULL	decorin	NULL		bind	NULL				TGF-beta3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
20064	4	6869	6	NULL	NULL	0	NULL	biglycan	NULL		bind	NULL				TGF-beta1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
20065	5	6869	6	NULL	NULL	0	NULL	biglycan	NULL		bind	NULL				TGF-beta2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
20066	6	6869	6	NULL	NULL	0	NULL	biglycan	NULL		bind	NULL				TGF-beta3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
20067	7	6869	6	NULL	NULL	0	NULL	fibromodulin	NULL		bind	NULL	high affinity			TGF-beta1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
20068	8	6869	6	NULL	NULL	0	NULL	fibromodulin	NULL		bind	NULL				TGF-beta2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
20069	9	6869	6	NULL	NULL	0	NULL	fibromodulin	NULL		bind	NULL				TGF-beta3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
30293	10	6869	6	NULL	NULL	0	NULL	decorin	NULL		regulate	NULL				collagen assembly	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
30294	11	6869	6	NULL	NULL	0	NULL	biglycan	NULL		regulate	NULL				collagen assembly	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
30295	12	6869	6	NULL	NULL	0	NULL	fibromodulin	NULL		regulate	NULL				collagen assembly	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
56651	13	6869	6	10	NULL	0	NULL	fibromodulin			affinity for		greatest 			TGF-beta1 precursor		latent			NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_2_423_s_293	10934147	19, 36, 37  Besides regulating collagen assembly, decorin, biglycan, and fibromodulin can all bind TGF-beta1, -beta2, and -beta3, with fibromodulin exhibiting the greatest affinity for TGF-beta1, as well as the latent TGF-beta1 precursor.	bind
24333	1	6870	5	13	NULL	NULL	NULL	HLA-G	GP		bind					ILT2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_71_s_182	11438456	19, [[ 20  This inhibition ]] is mediated by the binding of HLA-G to various inhibitory NKRs such as ILT2, ILT4, p49, and KIR2DL4.	bind
30355	2	6870	5	13	NULL	NULL	NULL	HLA-G	GP		bind					ILT4	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_71_s_182	11438456	19, [[ 20  This inhibition ]] is mediated by the binding of HLA-G to various inhibitory NKRs such as ILT2, ILT4, p49, and KIR2DL4.	bind
30356	3	6870	5	13	NULL	NULL	NULL	HLA-G	GP		bind					p49	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_71_s_182	11438456	19, [[ 20  This inhibition ]] is mediated by the binding of HLA-G to various inhibitory NKRs such as ILT2, ILT4, p49, and KIR2DL4.	bind
30357	4	6870	5	13	NULL	NULL	NULL	HLA-G	GP		bind					KIR2DL4	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_71_s_182	11438456	19, [[ 20  This inhibition ]] is mediated by the binding of HLA-G to various inhibitory NKRs such as ILT2, ILT4, p49, and KIR2DL4.	bind
56652	5	6870	5	13	NULL	NULL	NULL	ILT2	GP		is a type of					inhibitory NKR	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_71_s_182	11438456	19, [[ 20  This inhibition ]] is mediated by the binding of HLA-G to various inhibitory NKRs such as ILT2, ILT4, p49, and KIR2DL4.	bind
56653	6	6870	5	13	NULL	NULL	NULL	ILT4	GP		is a type of					inhibitory NKR	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_71_s_182	11438456	19, [[ 20  This inhibition ]] is mediated by the binding of HLA-G to various inhibitory NKRs such as ILT2, ILT4, p49, and KIR2DL4.	bind
56654	7	6870	5	13	NULL	NULL	NULL	p49	GP		is a type of					inhibitory NKR	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_71_s_182	11438456	19, [[ 20  This inhibition ]] is mediated by the binding of HLA-G to various inhibitory NKRs such as ILT2, ILT4, p49, and KIR2DL4.	bind
56655	8	6870	5	13	NULL	NULL	NULL	KIR2DL4	GP		is a type of					inhibitory NKR	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_71_s_182	11438456	19, [[ 20  This inhibition ]] is mediated by the binding of HLA-G to various inhibitory NKRs such as ILT2, ILT4, p49, and KIR2DL4.	bind
20119	1	6870	6	10	NULL	0	NULL	HLA-G			bind					ILT2					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_71_s_182	11438456	19, [[ 20  This inhibition ]] is mediated by the binding of HLA-G to various inhibitory NKRs such as ILT2, ILT4, p49, and KIR2DL4.	bind
20120	2	6870	6	10	NULL	0	NULL	HLA-G			bind					ILT4					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_71_s_182	11438456	19, [[ 20  This inhibition ]] is mediated by the binding of HLA-G to various inhibitory NKRs such as ILT2, ILT4, p49, and KIR2DL4.	bind
20121	3	6870	6	10	NULL	0	NULL	HLA-G			bind					p49 					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_71_s_182	11438456	19, [[ 20  This inhibition ]] is mediated by the binding of HLA-G to various inhibitory NKRs such as ILT2, ILT4, p49, and KIR2DL4.	bind
20122	4	6870	6	10	NULL	0	NULL	HLA-G			bind					KIR2DL4					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_71_s_182	11438456	19, [[ 20  This inhibition ]] is mediated by the binding of HLA-G to various inhibitory NKRs such as ILT2, ILT4, p49, and KIR2DL4.	bind
56656	5	6870	6	10	NULL	0	NULL	ILT2			is a type of					 inhibitory NKR					NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_1_71_s_182	11438456	19, [[ 20  This inhibition ]] is mediated by the binding of HLA-G to various inhibitory NKRs such as ILT2, ILT4, p49, and KIR2DL4.	bind
56657	6	6870	6	10	NULL	0	NULL	ILT4			is a type of					inhibitory NKR					NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_1_71_s_182	11438456	19, [[ 20  This inhibition ]] is mediated by the binding of HLA-G to various inhibitory NKRs such as ILT2, ILT4, p49, and KIR2DL4.	bind
56658	7	6870	6	10	NULL	0	NULL	p49			is a type of					inhibitory NKR					NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_1_71_s_182	11438456	19, [[ 20  This inhibition ]] is mediated by the binding of HLA-G to various inhibitory NKRs such as ILT2, ILT4, p49, and KIR2DL4.	bind
56659	8	6870	6	10	NULL	0	NULL	KIR2DL4			is a type of					inhibitory NKR					NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_1_71_s_182	11438456	19, [[ 20  This inhibition ]] is mediated by the binding of HLA-G to various inhibitory NKRs such as ILT2, ILT4, p49, and KIR2DL4.	bind
24338	1	6871	5	13	NULL	NULL	NULL	PAK	GP		is					p21-activated kinase	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1041_s_26	15016733	19,20  GIT proteins bind to p21-activated kinase (PAK), the downstream effector of Cdc42 and Rac, and a guanine nucleotide exchange factor termed PAK interacting exchange factor (PIX).	bind
24339	2	6871	5	13	NULL	NULL	NULL	GIT proteins	GP		bind					PAK	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1041_s_26	15016733	19,20  GIT proteins bind to p21-activated kinase (PAK), the downstream effector of Cdc42 and Rac, and a guanine nucleotide exchange factor termed PAK interacting exchange factor (PIX).	bind
24340	3	6871	5	13	NULL	NULL	NULL	PAK	GP		is a type of					downstream effector of Cdc42	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1041_s_26	15016733	19,20  GIT proteins bind to p21-activated kinase (PAK), the downstream effector of Cdc42 and Rac, and a guanine nucleotide exchange factor termed PAK interacting exchange factor (PIX).	bind
24341	4	6871	5	13	NULL	NULL	NULL	PAK	GP		is a type of					downstream effector of Rac	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1041_s_26	15016733	19,20  GIT proteins bind to p21-activated kinase (PAK), the downstream effector of Cdc42 and Rac, and a guanine nucleotide exchange factor termed PAK interacting exchange factor (PIX).	bind
24342	5	6871	5	13	NULL	NULL	NULL	PIX	GP		is					PAK interacting exchange factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1041_s_26	15016733	19,20  GIT proteins bind to p21-activated kinase (PAK), the downstream effector of Cdc42 and Rac, and a guanine nucleotide exchange factor termed PAK interacting exchange factor (PIX).	bind
24343	6	6871	5	13	NULL	NULL	NULL	GIT proteins	GP		bind					PIX	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1041_s_26	15016733	19,20  GIT proteins bind to p21-activated kinase (PAK), the downstream effector of Cdc42 and Rac, and a guanine nucleotide exchange factor termed PAK interacting exchange factor (PIX).	bind
44708	7	6871	5	13	NULL	NULL	NULL	PIX	GP		is a type of					guanine nucleotide exchange factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1041_s_26	15016733	19,20  GIT proteins bind to p21-activated kinase (PAK), the downstream effector of Cdc42 and Rac, and a guanine nucleotide exchange factor termed PAK interacting exchange factor (PIX).	bind
20123	1	6871	6	NULL	NULL	0	NULL	GIT protein	NULL		bind	NULL				PAK	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1041_s_26	15016733	19,20  GIT proteins bind to p21-activated kinase (PAK), the downstream effector of Cdc42 and Rac, and a guanine nucleotide exchange factor termed PAK interacting exchange factor (PIX).	bind
20124	2	6871	6	NULL	NULL	0	NULL	PAK	NULL		is	NULL				p21-activated kinase	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1041_s_26	15016733	19,20  GIT proteins bind to p21-activated kinase (PAK), the downstream effector of Cdc42 and Rac, and a guanine nucleotide exchange factor termed PAK interacting exchange factor (PIX).	bind
20125	3	6871	6	NULL	NULL	0	NULL	GIT protein	NULL		bind	NULL				PIX	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1041_s_26	15016733	19,20  GIT proteins bind to p21-activated kinase (PAK), the downstream effector of Cdc42 and Rac, and a guanine nucleotide exchange factor termed PAK interacting exchange factor (PIX).	bind
20126	4	6871	6	NULL	NULL	0	NULL	PIX	NULL		is	NULL				PAK interacting exchange factor	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1041_s_26	15016733	19,20  GIT proteins bind to p21-activated kinase (PAK), the downstream effector of Cdc42 and Rac, and a guanine nucleotide exchange factor termed PAK interacting exchange factor (PIX).	bind
20127	5	6871	6	NULL	NULL	0	NULL	PIX	NULL		is a type of	NULL				guanine nucleotide exchange factor	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1041_s_26	15016733	19,20  GIT proteins bind to p21-activated kinase (PAK), the downstream effector of Cdc42 and Rac, and a guanine nucleotide exchange factor termed PAK interacting exchange factor (PIX).	bind
20128	6	6871	6	NULL	NULL	0	NULL	PAK	NULL		is a type of	NULL				downstream effector of Cdc42	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1041_s_26	15016733	19,20  GIT proteins bind to p21-activated kinase (PAK), the downstream effector of Cdc42 and Rac, and a guanine nucleotide exchange factor termed PAK interacting exchange factor (PIX).	bind
20129	7	6871	6	NULL	NULL	0	NULL	PAK	NULL		is a type of	NULL				downstream effector of Rac	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1041_s_26	15016733	19,20  GIT proteins bind to p21-activated kinase (PAK), the downstream effector of Cdc42 and Rac, and a guanine nucleotide exchange factor termed PAK interacting exchange factor (PIX).	bind
24344	1	6872	5	13	NULL	NULL	NULL	AT1	GP		bind					Ang II	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_9_965_s_38	15831814	19,20  Two main subtypes, AT1 and AT2 that bind mainly to Ang II and Ang III, have been cloned and extensively studied.	bind
24345	2	6872	5	13	NULL	NULL	NULL	AT2	GP		bind					Ang III	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_9_965_s_38	15831814	19,20  Two main subtypes, AT1 and AT2 that bind mainly to Ang II and Ang III, have been cloned and extensively studied.	bind
24346	3	6872	5	13	NULL	NULL	NULL	AT1	GP		bind					Ang III	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_9_965_s_38	15831814	19,20  Two main subtypes, AT1 and AT2 that bind mainly to Ang II and Ang III, have been cloned and extensively studied.	bind
24347	4	6872	5	13	NULL	NULL	NULL	AT2	GP		bind					Ang II	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_9_965_s_38	15831814	19,20  Two main subtypes, AT1 and AT2 that bind mainly to Ang II and Ang III, have been cloned and extensively studied.	bind
20130	1	6872	6	NULL	NULL	0	NULL	AT1	NULL		bind	NULL				Ang II	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_9_965_s_38	15831814	19,20  Two main subtypes, AT1 and AT2 that bind mainly to Ang II and Ang III, have been cloned and extensively studied.	bind
20131	2	6872	6	NULL	NULL	0	NULL	AT1	NULL		bind	NULL				Ang III	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_9_965_s_38	15831814	19,20  Two main subtypes, AT1 and AT2 that bind mainly to Ang II and Ang III, have been cloned and extensively studied.	bind
20132	3	6872	6	NULL	NULL	0	NULL	AT2	NULL		bind	NULL				Ang II	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_9_965_s_38	15831814	19,20  Two main subtypes, AT1 and AT2 that bind mainly to Ang II and Ang III, have been cloned and extensively studied.	bind
20133	4	6872	6	NULL	NULL	0	NULL	AT2	NULL		bind	NULL				Ang III	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_9_965_s_38	15831814	19,20  Two main subtypes, AT1 and AT2 that bind mainly to Ang II and Ang III, have been cloned and extensively studied.	bind
24589	1	6873	5	13	NULL	NULL	NULL	decorin	GP		bind					hydroxyapatite	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2391_s_35	15472131	19,23  Furthermore, decorin binds hydroxyapatite 24 and is localized to the newly developing fetal bone matrix at all stages of bone formation and within the matrix of resting nonarticular cartilage.	bind
24590	2	6873	5	13	NULL	NULL	NULL	statement 1	GP		is localized to					bone matrix	OrganismPart	newly developing fetal			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2391_s_35	15472131	19,23  Furthermore, decorin binds hydroxyapatite 24 and is localized to the newly developing fetal bone matrix at all stages of bone formation and within the matrix of resting nonarticular cartilage.	bind
24591	4	6873	5	13	NULL	NULL	NULL	statement 1	GP		is localized within					resting nonarticular cartilage	OrganismPart	matrix of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2391_s_35	15472131	19,23  Furthermore, decorin binds hydroxyapatite 24 and is localized to the newly developing fetal bone matrix at all stages of bone formation and within the matrix of resting nonarticular cartilage.	bind
30358	3	6873	5	13	NULL	NULL	NULL	statement 2	Process		occurs at					bone formation	Process	all stages of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2391_s_35	15472131	19,23  Furthermore, decorin binds hydroxyapatite 24 and is localized to the newly developing fetal bone matrix at all stages of bone formation and within the matrix of resting nonarticular cartilage.	bind
20134	1	6873	6	NULL	NULL	0	NULL	decorin	NULL		bind	NULL				hydroxyapatite	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2391_s_35	15472131	19,23  Furthermore, decorin binds hydroxyapatite 24 and is localized to the newly developing fetal bone matrix at all stages of bone formation and within the matrix of resting nonarticular cartilage.	bind
20135	2	6873	6	NULL	NULL	0	NULL	decorin	NULL		localized to	NULL				bone matrix	NULL	newly developing fetal			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2391_s_35	15472131	19,23  Furthermore, decorin binds hydroxyapatite 24 and is localized to the newly developing fetal bone matrix at all stages of bone formation and within the matrix of resting nonarticular cartilage.	bind
20262	3	6873	6	10	NULL	0	NULL	statement 2			occurs at					 bone formation		all stages of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2391_s_35	15472131	19,23  Furthermore, decorin binds hydroxyapatite 24 and is localized to the newly developing fetal bone matrix at all stages of bone formation and within the matrix of resting nonarticular cartilage.	bind
20263	4	6873	6	10	NULL	0	NULL	decorin			localized within					resting nonarticular cartilage		matrix of 			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2391_s_35	15472131	19,23  Furthermore, decorin binds hydroxyapatite 24 and is localized to the newly developing fetal bone matrix at all stages of bone formation and within the matrix of resting nonarticular cartilage.	bind
24592	1	6875	5	13	NULL	NULL	NULL	nerve growth factor receptor	GP		modulates					MAP kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_1060	10688641	1992. ras mediates nerve growth factor receptor modulation of three signal-transducing protein kinases: MAP kinase, Raf-1, and RSK.	bind
24593	2	6875	5	13	NULL	NULL	NULL	nerve growth factor receptor	GP		modulates					Raf-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_1060	10688641	1992. ras mediates nerve growth factor receptor modulation of three signal-transducing protein kinases: MAP kinase, Raf-1, and RSK.	bind
24594	3	6875	5	13	NULL	NULL	NULL	nerve growth factor receptor	GP		modulates					RSK	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_1060	10688641	1992. ras mediates nerve growth factor receptor modulation of three signal-transducing protein kinases: MAP kinase, Raf-1, and RSK.	bind
24595	4	6875	5	13	NULL	NULL	NULL	ras	GP		mediates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_1060	10688641	1992. ras mediates nerve growth factor receptor modulation of three signal-transducing protein kinases: MAP kinase, Raf-1, and RSK.	bind
24596	5	6875	5	13	NULL	NULL	NULL	ras	GP		mediates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_1060	10688641	1992. ras mediates nerve growth factor receptor modulation of three signal-transducing protein kinases: MAP kinase, Raf-1, and RSK.	bind
24597	6	6875	5	13	NULL	NULL	NULL	ras	GP		mediates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_1060	10688641	1992. ras mediates nerve growth factor receptor modulation of three signal-transducing protein kinases: MAP kinase, Raf-1, and RSK.	bind
30359	7	6875	5	13	NULL	NULL	NULL	MAP kinase	GP		is a type of					signal-transducing protein kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_1060	10688641	1992. ras mediates nerve growth factor receptor modulation of three signal-transducing protein kinases: MAP kinase, Raf-1, and RSK.	bind
30360	8	6875	5	13	NULL	NULL	NULL	Raf-1	GP		is a type of					signal-transducing protein kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_1060	10688641	1992. ras mediates nerve growth factor receptor modulation of three signal-transducing protein kinases: MAP kinase, Raf-1, and RSK.	bind
30361	9	6875	5	13	NULL	NULL	NULL	RSK	GP		is a type of					signal-transducing protein kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_1060	10688641	1992. ras mediates nerve growth factor receptor modulation of three signal-transducing protein kinases: MAP kinase, Raf-1, and RSK.	bind
20264	1	6875	6	NULL	NULL	0	NULL	nerve growth factor receptor	NULL		modulates	NULL				MAP kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_1060	10688641	1992. ras mediates nerve growth factor receptor modulation of three signal-transducing protein kinases: MAP kinase, Raf-1, and RSK.	bind
20265	2	6875	6	NULL	NULL	0	NULL	nerve growth factor receptor	NULL		modulates	NULL				Raf-1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_1060	10688641	1992. ras mediates nerve growth factor receptor modulation of three signal-transducing protein kinases: MAP kinase, Raf-1, and RSK.	bind
20266	3	6875	6	NULL	NULL	0	NULL	nerve growth factor receptor	NULL		modulates	NULL				RSK	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_1060	10688641	1992. ras mediates nerve growth factor receptor modulation of three signal-transducing protein kinases: MAP kinase, Raf-1, and RSK.	bind
20267	4	6875	6	NULL	NULL	0	NULL	ras	NULL		mediates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_1060	10688641	1992. ras mediates nerve growth factor receptor modulation of three signal-transducing protein kinases: MAP kinase, Raf-1, and RSK.	bind
20268	5	6875	6	NULL	NULL	0	NULL	ras	NULL		mediates	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_1060	10688641	1992. ras mediates nerve growth factor receptor modulation of three signal-transducing protein kinases: MAP kinase, Raf-1, and RSK.	bind
20269	6	6875	6	NULL	NULL	0	NULL	ras	NULL		mediates	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_1060	10688641	1992. ras mediates nerve growth factor receptor modulation of three signal-transducing protein kinases: MAP kinase, Raf-1, and RSK.	bind
20270	7	6875	6	NULL	NULL	0	NULL	MAP kinase	NULL		is a type of	NULL				signal-transducing protein kinase	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_1060	10688641	1992. ras mediates nerve growth factor receptor modulation of three signal-transducing protein kinases: MAP kinase, Raf-1, and RSK.	bind
20271	8	6875	6	NULL	NULL	0	NULL	Raf-1	NULL		is a type of	NULL				signal-transducing protein kinase	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_1060	10688641	1992. ras mediates nerve growth factor receptor modulation of three signal-transducing protein kinases: MAP kinase, Raf-1, and RSK.	bind
20272	9	6875	6	NULL	NULL	0	NULL	RSK	NULL		is a type of	NULL				signal-transducing protein kinase	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_1931_s_1060	10688641	1992. ras mediates nerve growth factor receptor modulation of three signal-transducing protein kinases: MAP kinase, Raf-1, and RSK.	bind
24599	1	6878	5	13	NULL	NULL	NULL	OCI-5/glypican-3	GP	rat	bind					fibroblast growth factor-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_6_1407_s_493	9628896	1997. OCI-5/rat glypican-3 binds to fibroblast  growth factor-2 but not to insulin-like growth factor-2.	bind
24600	2	6878	5	13	NULL	NULL	NULL	OCI-5/glypican-3	GP	rat	does not bind					insulin-like growth factor-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_6_1407_s_493	9628896	1997. OCI-5/rat glypican-3 binds to fibroblast  growth factor-2 but not to insulin-like growth factor-2.	bind
20273	1	6878	6	NULL	NULL	0	NULL	OCI-5/glypican-3	NULL	Rat	bind	NULL				fibroblast growth factor-2	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_141_6_1407_s_493	9628896	1997. OCI-5/rat glypican-3 binds to fibroblast  growth factor-2 but not to insulin-like growth factor-2.	bind
20274	2	6878	6	NULL	NULL	0	NULL	OCI-5/glypican-3	NULL	rat	does not bind	NULL				insulin-like growth factor-2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_6_1407_s_493	9628896	1997. OCI-5/rat glypican-3 binds to fibroblast  growth factor-2 but not to insulin-like growth factor-2.	bind
24601	1	6879	5	13	NULL	NULL	NULL	arginine	AminoAcid		bind					ArgRS	GP	tRNA-free;;E. coli			NULL		NULL	NULL	NULL	NULL	gw60_febslett_547_1_197_s_110	12860413	19F NMR data at present illustrate that the 4-F-Trp162 resonance frequency is affected by the binding of arginine to tRNA-free  E. coli ArgRS, therefore suggesting that the local structure of Trp162 is involved in arginine binding.	bind
56660	2	6879	5	13	NULL	NULL	NULL				is involved in			Trp162		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_547_1_197_s_110	12860413	19F NMR data at present illustrate that the 4-F-Trp162 resonance frequency is affected by the binding of arginine to tRNA-free  E. coli ArgRS, therefore suggesting that the local structure of Trp162 is involved in arginine binding.	bind
20277	1	6879	6	10	NULL	0	NULL	arginine			bind					 ArgRS		tRNA-free;;E. coli			NULL		NULL	NULL	NULL	NULL	gw60_febslett_547_1_197_s_110	12860413	19F NMR data at present illustrate that the 4-F-Trp162 resonance frequency is affected by the binding of arginine to tRNA-free  E. coli ArgRS, therefore suggesting that the local structure of Trp162 is involved in arginine binding.	bind
20278	2	6879	6	NULL	NULL	0	NULL		NULL		is involved in	NULL		Trp162		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_547_1_197_s_110	12860413	19F NMR data at present illustrate that the 4-F-Trp162 resonance frequency is affected by the binding of arginine to tRNA-free  E. coli ArgRS, therefore suggesting that the local structure of Trp162 is involved in arginine binding.	bind
24605	1	6880	5	13	NULL	NULL	NULL	isoflurane	Chemical		bind		stereoselective			serum albumin	GP	bovine			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_127_1_131_s_385	10369465	19F nuclear magnetic resonance investigation of stereoselective binding of isoflurane to bovine serum albumin.	bind
20279	1	6880	6	NULL	NULL	0	NULL	isoflurane	NULL		bind	NULL	stereoselectively			serum albumin	NULL	bovine			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_127_1_131_s_385	10369465	19F nuclear magnetic resonance investigation of stereoselective binding of isoflurane to bovine serum albumin.	bind
24606	1	6882	5	13	NULL	NULL	NULL	1alpha,25(OH)2D3	Chemical		stimulates					MAP kinase	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_4_2199_s_192	12417593	1alpha,25(OH)2D3 stimulation of MAP kinase tyrosine phosphorylation ( P) is suppressed by antibody inhibition of Raf-1.	bind
24607	3	6882	5	13	NULL	NULL	NULL	statement 2	Process		suppresses					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_4_2199_s_192	12417593	1alpha,25(OH)2D3 stimulation of MAP kinase tyrosine phosphorylation ( P) is suppressed by antibody inhibition of Raf-1.	bind
44829	2	6882	5	13	NULL	NULL	NULL	antibody	GP		inhibit					Raf-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_4_2199_s_192	12417593	1alpha,25(OH)2D3 stimulation of MAP kinase tyrosine phosphorylation ( P) is suppressed by antibody inhibition of Raf-1.	bind
44830	4	6882	5	13	NULL	NULL	NULL	P	Process		is					phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_4_2199_s_192	12417593	1alpha,25(OH)2D3 stimulation of MAP kinase tyrosine phosphorylation ( P) is suppressed by antibody inhibition of Raf-1.	bind
20280	1	6882	6	NULL	NULL	0	NULL	1alpha,25(OH)2D3	NULL		stimulates	NULL				MAP kinase	NULL	phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_4_2199_s_192	12417593	1alpha,25(OH)2D3 stimulation of MAP kinase tyrosine phosphorylation ( P) is suppressed by antibody inhibition of Raf-1.	bind
20281	2	6882	6	10	NULL	0	NULL	antibody	NULL		inhibits	NULL				Raf-1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_4_2199_s_192	12417593	1alpha,25(OH)2D3 stimulation of MAP kinase tyrosine phosphorylation ( P) is suppressed by antibody inhibition of Raf-1.	bind
20282	3	6882	6	NULL	NULL	0	NULL	P	NULL		is	NULL				phosphorylation	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_4_2199_s_192	12417593	1alpha,25(OH)2D3 stimulation of MAP kinase tyrosine phosphorylation ( P) is suppressed by antibody inhibition of Raf-1.	bind
44820	4	6882	6	10	NULL	0	NULL	statement 2	NULL		suppress	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_4_2199_s_192	12417593	1alpha,25(OH)2D3 stimulation of MAP kinase tyrosine phosphorylation ( P) is suppressed by antibody inhibition of Raf-1.	bind
24608	1	6884	5	13	NULL	NULL	NULL	1alpha,25(OH)2D3	Chemical		induces					Raf-1	GP	phosphorylation of	serine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_4_2199_s_118	12417593	1alpha,25(OH)2D3-induced serine phosphorylation ( P) of Raf-1 is suppressed by Ras inhibitor peptide.	bind
24609	2	6884	5	13	NULL	NULL	NULL	Ras inhibitor peptide	GP		suppresses					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_4_2199_s_118	12417593	1alpha,25(OH)2D3-induced serine phosphorylation ( P) of Raf-1 is suppressed by Ras inhibitor peptide.	bind
20283	1	6884	6	NULL	NULL	0	NULL	1alpha,25(OH)2D3	NULL		induce	NULL				Raf-1	NULL	phosphorylation of	Serine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_4_2199_s_118	12417593	1alpha,25(OH)2D3-induced serine phosphorylation ( P) of Raf-1 is suppressed by Ras inhibitor peptide.	bind
20284	2	6884	6	NULL	NULL	0	NULL	statement 1	NULL		is suppressed by	NULL				Ras inhibitor peptide	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_4_2199_s_118	12417593	1alpha,25(OH)2D3-induced serine phosphorylation ( P) of Raf-1 is suppressed by Ras inhibitor peptide.	bind
24610	1	6885	5	13	NULL	NULL	NULL	nucleotide	NucleicAcid		bind					Gialpha	GP	purified			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_26_27567_s_176	15096500	1b and GPR peptides derived from AGS4/G18.1b, PCP2, RapIGAPII,  and  C. elegans GPR-1/2 on nucleotide binding to purified Gialpha and Goalpha A, GTPgammaS binding to Gialpha (100 nM) was measured in the presence of increasing concentrations of GST, GST-AGS4/G18.	bind
24611	2	6885	5	13	NULL	NULL	NULL	GTPgammaS	Chemical		bind					Gialpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_26_27567_s_176	15096500	1b and GPR peptides derived from AGS4/G18.1b, PCP2, RapIGAPII,  and  C. elegans GPR-1/2 on nucleotide binding to purified Gialpha and Goalpha A, GTPgammaS binding to Gialpha (100 nM) was measured in the presence of increasing concentrations of GST, GST-AGS4/G18.	bind
30362	3	6885	5	13	NULL	NULL	NULL	nucleotide	NucleicAcid		bind					Goalpha A	GP	purified			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_26_27567_s_176	15096500	1b and GPR peptides derived from AGS4/G18.1b, PCP2, RapIGAPII,  and  C. elegans GPR-1/2 on nucleotide binding to purified Gialpha and Goalpha A, GTPgammaS binding to Gialpha (100 nM) was measured in the presence of increasing concentrations of GST, GST-AGS4/G18.	bind
20323	1	6885	6	NULL	NULL	0	NULL	nucleotide	NULL		bind	NULL				Gialpha	NULL	purified			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_26_27567_s_176	15096500	1b and GPR peptides derived from AGS4/G18.1b, PCP2, RapIGAPII,  and  C. elegans GPR-1/2 on nucleotide binding to purified Gialpha and Goalpha A, GTPgammaS binding to Gialpha (100 nM) was measured in the presence of increasing concentrations of GST, GST-AGS4/G18.	bind
20324	2	6885	6	NULL	NULL	0	NULL	nucleotide	NULL		bind	NULL				Goalpha A	NULL	purified			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_26_27567_s_176	15096500	1b and GPR peptides derived from AGS4/G18.1b, PCP2, RapIGAPII,  and  C. elegans GPR-1/2 on nucleotide binding to purified Gialpha and Goalpha A, GTPgammaS binding to Gialpha (100 nM) was measured in the presence of increasing concentrations of GST, GST-AGS4/G18.	bind
20325	3	6885	6	NULL	NULL	0	NULL	GTPgammaS	NULL		bind	NULL				Gialpha	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_26_27567_s_176	15096500	1b and GPR peptides derived from AGS4/G18.1b, PCP2, RapIGAPII,  and  C. elegans GPR-1/2 on nucleotide binding to purified Gialpha and Goalpha A, GTPgammaS binding to Gialpha (100 nM) was measured in the presence of increasing concentrations of GST, GST-AGS4/G18.	bind
24612	1	6887	5	13	NULL	NULL	NULL	1D6	GP		does not bind					peptide iB-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_1_380_s_12	9423886	1D6 did not bind peptide iB-1 but rather bound a second inhibitory epitope called iB-2.	bind
24613	2	6887	5	13	NULL	NULL	NULL	1D6	GP		bind					iB-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_1_380_s_12	9423886	1D6 did not bind peptide iB-1 but rather bound a second inhibitory epitope called iB-2.	bind
30363	3	6887	5	13	NULL	NULL	NULL	iB-2	GP		is a type of					inhibitory epitope	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_1_380_s_12	9423886	1D6 did not bind peptide iB-1 but rather bound a second inhibitory epitope called iB-2.	bind
20326	1	6887	6	10	NULL	0	NULL	1D6			does not bind					peptide iB-1					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_1_380_s_12	9423886	1D6 did not bind peptide iB-1 but rather bound a second inhibitory epitope called iB-2.	bind
20327	2	6887	6	NULL	NULL	0	NULL	1D6	NULL		bind	NULL				iB2 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_1_380_s_12	9423886	1D6 did not bind peptide iB-1 but rather bound a second inhibitory epitope called iB-2.	bind
30296	3	6887	6	NULL	NULL	0	NULL	iB2	NULL		is a type of	NULL				inhibitory epitope	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_1_380_s_12	9423886	1D6 did not bind peptide iB-1 but rather bound a second inhibitory epitope called iB-2.	bind
24614	1	6888	5	13	NULL	NULL	NULL	LDL receptor	GP		bind					apoE	GP	epitope of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_29	11557678	1D7 binds to the LDL receptor - binding epitope of apoE 15 and would therefore bind lipoproteins that had apoE in a metabolically active conformation.	bind
24615	2	6888	5	13	NULL	NULL	NULL	1D7	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_29	11557678	1D7 binds to the LDL receptor - binding epitope of apoE 15 and would therefore bind lipoproteins that had apoE in a metabolically active conformation.	bind
24616	3	6888	5	13	NULL	NULL	NULL	lipoproteins	GP		contain					apoE	GP	metabolically active conformation			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_29	11557678	1D7 binds to the LDL receptor - binding epitope of apoE 15 and would therefore bind lipoproteins that had apoE in a metabolically active conformation.	bind
24617	4	6888	5	13	NULL	NULL	NULL	1D7	GP		bind					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_29	11557678	1D7 binds to the LDL receptor - binding epitope of apoE 15 and would therefore bind lipoproteins that had apoE in a metabolically active conformation.	bind
24618	5	6888	5	13	NULL	NULL	NULL	statement 2	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_29	11557678	1D7 binds to the LDL receptor - binding epitope of apoE 15 and would therefore bind lipoproteins that had apoE in a metabolically active conformation.	bind
20328	1	6888	6	10	NULL	0	NULL	LDL receptor			bind					 apoE		epitope of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_29	11557678	1D7 binds to the LDL receptor - binding epitope of apoE 15 and would therefore bind lipoproteins that had apoE in a metabolically active conformation.	bind
20329	2	6888	6	NULL	NULL	0	NULL	1D7	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_29	11557678	1D7 binds to the LDL receptor - binding epitope of apoE 15 and would therefore bind lipoproteins that had apoE in a metabolically active conformation.	bind
20731	3	6888	6	NULL	NULL	0	NULL	lipoproteins	NULL		contain	NULL				apoE	NULL	metabolically active conformation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_29	11557678	1D7 binds to the LDL receptor - binding epitope of apoE 15 and would therefore bind lipoproteins that had apoE in a metabolically active conformation.	bind
20732	4	6888	6	NULL	NULL	0	NULL	1D7	NULL		bind	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_29	11557678	1D7 binds to the LDL receptor - binding epitope of apoE 15 and would therefore bind lipoproteins that had apoE in a metabolically active conformation.	bind
56661	5	6888	6	10	NULL	0	NULL	statement 2			leads to					statement 4					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_29	11557678	1D7 binds to the LDL receptor - binding epitope of apoE 15 and would therefore bind lipoproteins that had apoE in a metabolically active conformation.	bind
24619	1	6890	5	13	NULL	NULL	NULL	VCAM-1	GP		bind					very late activation antibody-4	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_723_s_64	9598830	1G11, provided by Dr Dorian Haskard (Hammersmith Hospital, London) is an anti - VCAM-1 monoclonal antibody that blocks VCAM-1 binding to very late activation antibody-4.	bind
24620	2	6890	5	13	NULL	NULL	NULL	1G11	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_723_s_64	9598830	1G11, provided by Dr Dorian Haskard (Hammersmith Hospital, London) is an anti - VCAM-1 monoclonal antibody that blocks VCAM-1 binding to very late activation antibody-4.	bind
30364	3	6890	5	13	NULL	NULL	NULL	1G11	GP		is a type of					anti - VCAM-1 monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_723_s_64	9598830	1G11, provided by Dr Dorian Haskard (Hammersmith Hospital, London) is an anti - VCAM-1 monoclonal antibody that blocks VCAM-1 binding to very late activation antibody-4.	bind
20330	1	6890	6	NULL	NULL	0	NULL	1G11	NULL		is a type of	NULL				anti - VCAM-1 monoclonal antibody 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_723_s_64	9598830	1G11, provided by Dr Dorian Haskard (Hammersmith Hospital, London) is an anti - VCAM-1 monoclonal antibody that blocks VCAM-1 binding to very late activation antibody-4.	bind
20331	2	6890	6	NULL	NULL	0	NULL	VCAM-1	NULL		bind	NULL				very late activation antibody-4	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_723_s_64	9598830	1G11, provided by Dr Dorian Haskard (Hammersmith Hospital, London) is an anti - VCAM-1 monoclonal antibody that blocks VCAM-1 binding to very late activation antibody-4.	bind
20332	3	6890	6	NULL	NULL	0	NULL	1G11	NULL		blocks	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_723_s_64	9598830	1G11, provided by Dr Dorian Haskard (Hammersmith Hospital, London) is an anti - VCAM-1 monoclonal antibody that blocks VCAM-1 binding to very late activation antibody-4.	bind
24621	1	6891	5	13	NULL	NULL	NULL	SCN	Chemical		bind					HRP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_17_11049_s_35	9110998	1H and 15N NMR studies indicate that SCN  binds to HRP away from the distal histidine, near the heme methyl C1H3 and C18H3 with the  K d value of 158  plus-or-minus  19 mM and the binding is facilitated by protonation of an acid group with p K a 4.0 ( 38,  39).	bind
24622	2	6891	5	13	NULL	NULL	NULL	statement 1	Process		is facilitated by					acid group	Chemical	protonation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_17_11049_s_35	9110998	1H and 15N NMR studies indicate that SCN  binds to HRP away from the distal histidine, near the heme methyl C1H3 and C18H3 with the  K d value of 158  plus-or-minus  19 mM and the binding is facilitated by protonation of an acid group with p K a 4.0 ( 38,  39).	bind
30365	3	6891	5	13	NULL	NULL	NULL	statement 1	Process		occurs away from					HRP	GP	distal	histidine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_17_11049_s_35	9110998	1H and 15N NMR studies indicate that SCN  binds to HRP away from the distal histidine, near the heme methyl C1H3 and C18H3 with the  K d value of 158  plus-or-minus  19 mM and the binding is facilitated by protonation of an acid group with p K a 4.0 ( 38,  39).	bind
30366	4	6891	5	13	NULL	NULL	NULL	statement 1	Process		occurs near					HRP	GP		heme methyl  C1H3		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_17_11049_s_35	9110998	1H and 15N NMR studies indicate that SCN  binds to HRP away from the distal histidine, near the heme methyl C1H3 and C18H3 with the  K d value of 158  plus-or-minus  19 mM and the binding is facilitated by protonation of an acid group with p K a 4.0 ( 38,  39).	bind
30367	5	6891	5	13	NULL	NULL	NULL	statement 1	Process		occurs near					HRP	GP		heme methyl C18H3		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_17_11049_s_35	9110998	1H and 15N NMR studies indicate that SCN  binds to HRP away from the distal histidine, near the heme methyl C1H3 and C18H3 with the  K d value of 158  plus-or-minus  19 mM and the binding is facilitated by protonation of an acid group with p K a 4.0 ( 38,  39).	bind
20333	1	6891	6	NULL	NULL	0	NULL	SCN	NULL		bind	NULL				HRP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_17_11049_s_35	9110998	1H and 15N NMR studies indicate that SCN  binds to HRP away from the distal histidine, near the heme methyl C1H3 and C18H3 with the  K d value of 158  plus-or-minus  19 mM and the binding is facilitated by protonation of an acid group with p K a 4.0 ( 38,  39).	bind
20733	2	6891	6	10	NULL	0	NULL	statement 1			occurs away from					HRP		 distal	histidine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_17_11049_s_35	9110998	1H and 15N NMR studies indicate that SCN  binds to HRP away from the distal histidine, near the heme methyl C1H3 and C18H3 with the  K d value of 158  plus-or-minus  19 mM and the binding is facilitated by protonation of an acid group with p K a 4.0 ( 38,  39).	bind
20734	3	6891	6	NULL	NULL	0	NULL	statement 1	NULL		occurs near	NULL				HRP	NULL		heme methyl C1H3		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_17_11049_s_35	9110998	1H and 15N NMR studies indicate that SCN  binds to HRP away from the distal histidine, near the heme methyl C1H3 and C18H3 with the  K d value of 158  plus-or-minus  19 mM and the binding is facilitated by protonation of an acid group with p K a 4.0 ( 38,  39).	bind
20735	4	6891	6	NULL	NULL	0	NULL	statement 1	NULL		occurs near	NULL				HRP	NULL		heme methyl C18H3		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_17_11049_s_35	9110998	1H and 15N NMR studies indicate that SCN  binds to HRP away from the distal histidine, near the heme methyl C1H3 and C18H3 with the  K d value of 158  plus-or-minus  19 mM and the binding is facilitated by protonation of an acid group with p K a 4.0 ( 38,  39).	bind
56662	5	6891	6	10	NULL	0	NULL	statement 1			is facilitated by					acid group		protonation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_17_11049_s_35	9110998	1H and 15N NMR studies indicate that SCN  binds to HRP away from the distal histidine, near the heme methyl C1H3 and C18H3 with the  K d value of 158  plus-or-minus  19 mM and the binding is facilitated by protonation of an acid group with p K a 4.0 ( 38,  39).	bind
24623	1	6892	5	13	NULL	NULL	NULL	LMB	Chemical		bind					N-acetyl-L-cysteine methyl ester	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_16_9112_s_6	10430904	1H NMR analysis showed that LMB bound  N-acetyl-L-cysteine methyl ester through a Michael-type addition, consistent with the idea that LMB binds covalently via its alpha,beta-unsaturated delta-lactone to the sulfhydryl group of Cys-529.	bind
24624	2	6892	5	13	NULL	NULL	NULL	statement 1	Process		occurs through					Michael-type addition	ResearchActivity				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_16_9112_s_6	10430904	1H NMR analysis showed that LMB bound  N-acetyl-L-cysteine methyl ester through a Michael-type addition, consistent with the idea that LMB binds covalently via its alpha,beta-unsaturated delta-lactone to the sulfhydryl group of Cys-529.	bind
30368	3	6892	5	13	NULL	NULL	NULL	LMB	Chemical		bind		covalently	alpha,beta-unsaturated delta-lactone					sulfhydryl group of Cys-529		NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_16_9112_s_6	10430904	1H NMR analysis showed that LMB bound  N-acetyl-L-cysteine methyl ester through a Michael-type addition, consistent with the idea that LMB binds covalently via its alpha,beta-unsaturated delta-lactone to the sulfhydryl group of Cys-529.	bind
20357	1	6892	6	NULL	NULL	0	NULL	LMB	NULL		bind	NULL				N-acetyl-L-cysteine methyl ester	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_16_9112_s_6	10430904	1H NMR analysis showed that LMB bound  N-acetyl-L-cysteine methyl ester through a Michael-type addition, consistent with the idea that LMB binds covalently via its alpha,beta-unsaturated delta-lactone to the sulfhydryl group of Cys-529.	bind
20358	2	6892	6	NULL	NULL	0	NULL	LMB	NULL		bind	NULL	covalently	alpha,beta-unsaturated delta-lactone			NULL		sulfhydryl group of Cys-529		NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_16_9112_s_6	10430904	1H NMR analysis showed that LMB bound  N-acetyl-L-cysteine methyl ester through a Michael-type addition, consistent with the idea that LMB binds covalently via its alpha,beta-unsaturated delta-lactone to the sulfhydryl group of Cys-529.	bind
30297	3	6892	6	NULL	NULL	0	NULL	statement 1	NULL		occurs through	NULL				Michael-type addition	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_16_9112_s_6	10430904	1H NMR analysis showed that LMB bound  N-acetyl-L-cysteine methyl ester through a Michael-type addition, consistent with the idea that LMB binds covalently via its alpha,beta-unsaturated delta-lactone to the sulfhydryl group of Cys-529.	bind
24826	1	6893	5	13	NULL	NULL	NULL	Vpr1 - 40	GP		possesses					helical structure	GP		between residues 17 - 32		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_44_43188_s_6	12881523	1H NMR data indicate Vpr1 - 40 possesses helical structure between residues 17 - 32, and for the first time, this helix, which is bound by proline residues, was observed even in aqueous solution devoid of any detergent supplements.	bind
24827	2	6893	5	13	NULL	NULL	NULL	statement 1	GP		bind								proline residues		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_44_43188_s_6	12881523	1H NMR data indicate Vpr1 - 40 possesses helical structure between residues 17 - 32, and for the first time, this helix, which is bound by proline residues, was observed even in aqueous solution devoid of any detergent supplements.	bind
20361	1	6893	6	NULL	NULL	0	NULL	Vpr1-40	NULL		possesses	NULL				helical structure	NULL		between residues 17 - 32		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_44_43188_s_6	12881523	1H NMR data indicate Vpr1 - 40 possesses helical structure between residues 17 - 32, and for the first time, this helix, which is bound by proline residues, was observed even in aqueous solution devoid of any detergent supplements.	bind
20362	2	6893	6	10	NULL	0	NULL	statement 1			bind								proline residues		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_44_43188_s_6	12881523	1H NMR data indicate Vpr1 - 40 possesses helical structure between residues 17 - 32, and for the first time, this helix, which is bound by proline residues, was observed even in aqueous solution devoid of any detergent supplements.	bind
24828	1	6895	5	13	NULL	NULL	NULL	Pex14p	GP		bind								SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_5_1007_s_107	12453410	1H,15N correlation NMR spectra are shown for the uncomplexed (black) and the simultaneously Pex14p and Pex5p bound SH3 domain.	bind
24829	2	6895	5	13	NULL	NULL	NULL	Pex5p	GP		bind								SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_5_1007_s_107	12453410	1H,15N correlation NMR spectra are shown for the uncomplexed (black) and the simultaneously Pex14p and Pex5p bound SH3 domain.	bind
24830	3	6895	5	13	NULL	NULL	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_5_1007_s_107	12453410	1H,15N correlation NMR spectra are shown for the uncomplexed (black) and the simultaneously Pex14p and Pex5p bound SH3 domain.	bind
20363	1	6895	6	NULL	NULL	0	NULL	Pex14p	NULL		bind	NULL					NULL		SH3 domain		NULL		0	NULL	NULL	NULL	gw60_molcell_10_5_1007_s_107	12453410	1H,15N correlation NMR spectra are shown for the uncomplexed (black) and the simultaneously Pex14p and Pex5p bound SH3 domain.	bind
20364	2	6895	6	NULL	NULL	0	NULL	Pex5p	NULL		bind	NULL					NULL		SH3 domain		NULL		0	NULL	NULL	NULL	gw60_molcell_10_5_1007_s_107	12453410	1H,15N correlation NMR spectra are shown for the uncomplexed (black) and the simultaneously Pex14p and Pex5p bound SH3 domain.	bind
30298	3	6895	6	NULL	NULL	0	NULL	statement 1	NULL		occurs simultaneously with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_10_5_1007_s_107	12453410	1H,15N correlation NMR spectra are shown for the uncomplexed (black) and the simultaneously Pex14p and Pex5p bound SH3 domain.	bind
24831	2	6896	5	13	NULL	NULL	NULL	[15N,2]cTnC	GP	Ca2+-saturated	bind					cTnI-AllP	GP		1-211		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_1_703_s_249	15507454	1H-15N correlation spectra of Ca2+-saturated [15N,2]cTnC bound to cTnI-WT-(1-211), cTnI-AllP-(1-211), or cTnI-PP-(1-211).	bind
24832	1	6896	5	13	NULL	NULL	NULL	[15N,2]cTnC	GP	Ca2+-saturated	bind					cTnI	GP	WT	1-211		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_1_703_s_249	15507454	1H-15N correlation spectra of Ca2+-saturated [15N,2]cTnC bound to cTnI-WT-(1-211), cTnI-AllP-(1-211), or cTnI-PP-(1-211).	bind
24833	3	6896	5	13	NULL	NULL	NULL	[15N,2]cTnC	GP	Ca2+-saturated	bind					cTnI-PP	GP		1-211		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_1_703_s_249	15507454	1H-15N correlation spectra of Ca2+-saturated [15N,2]cTnC bound to cTnI-WT-(1-211), cTnI-AllP-(1-211), or cTnI-PP-(1-211).	bind
20365	1	6896	6	10	NULL	0	NULL	[15N,2]cTnC		Ca2+ saturated	bind					cTnI		WT	1-211		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_1_703_s_249	15507454	1H-15N correlation spectra of Ca2+-saturated [15N,2]cTnC bound to cTnI-WT-(1-211), cTnI-AllP-(1-211), or cTnI-PP-(1-211).	bind
20366	2	6896	6	10	NULL	0	NULL	[15N,2]cTnC		Ca2+ saturated	bind					cTnI-AllP			1-211		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_1_703_s_249	15507454	1H-15N correlation spectra of Ca2+-saturated [15N,2]cTnC bound to cTnI-WT-(1-211), cTnI-AllP-(1-211), or cTnI-PP-(1-211).	bind
20367	3	6896	6	10	NULL	0	NULL	[15N,2]cTnC		Ca2+ saturated	bind					cTnI-PP			1-211		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_1_703_s_249	15507454	1H-15N correlation spectra of Ca2+-saturated [15N,2]cTnC bound to cTnI-WT-(1-211), cTnI-AllP-(1-211), or cTnI-PP-(1-211).	bind
24834	1	6897	5	13	NULL	NULL	NULL		GP		bind			C2A domain		syntaxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_18_1_133_s_56	9010211	1H-15N HSQC Cross-Peak Shifts Map the Region of the C2A Domain That Binds to Syntaxin	bind
20368	1	6897	6	NULL	NULL	0	NULL		NULL		bind	NULL		C2A domain		Syntaxin	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_18_1_133_s_56	9010211	1H-15N HSQC Cross-Peak Shifts Map the Region of the C2A Domain That Binds to Syntaxin	bind
24835	1	6898	5	13	NULL	NULL	NULL	complexin	GP		bind					SNARE Complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_33_3_397_s_50	11832227	1H-15N TROSY-HSQC Spectra Reveal the Region of Complexin that Binds to the SNARE Complex	bind
20369	1	6898	6	NULL	NULL	0	NULL	Complexin	NULL		bind	NULL				SNARE complex	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_33_3_397_s_50	11832227	1H-15N TROSY-HSQC Spectra Reveal the Region of Complexin that Binds to the SNARE Complex	bind
24836	1	6899	5	13	NULL	NULL	NULL	tau	GP		bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_17_9503_s_196	10449722	1H-NMR studies suggest that the flexibility of tau can be changed, as shown by the fact that half of the methyl-containing residues of tau become immobilized on tau binding to tubulin ( 25).	bind
24837	2	6899	5	13	NULL	NULL	NULL	tau	GP		become			methyl residues		immobilized	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_17_9503_s_196	10449722	1H-NMR studies suggest that the flexibility of tau can be changed, as shown by the fact that half of the methyl-containing residues of tau become immobilized on tau binding to tubulin ( 25).	bind
24838	4	6899	5	13	NULL	NULL	NULL	statement 2	Process		suggests					tau	GP	change in flexibility of 			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_17_9503_s_196	10449722	1H-NMR studies suggest that the flexibility of tau can be changed, as shown by the fact that half of the methyl-containing residues of tau become immobilized on tau binding to tubulin ( 25).	bind
30369	3	6899	5	13	NULL	NULL	NULL	statement 2	Process		occurs on					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_17_9503_s_196	10449722	1H-NMR studies suggest that the flexibility of tau can be changed, as shown by the fact that half of the methyl-containing residues of tau become immobilized on tau binding to tubulin ( 25).	bind
20370	1	6899	6	NULL	NULL	0	NULL	tau	NULL		bind	NULL				tubulin	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9503_s_196	10449722	1H-NMR studies suggest that the flexibility of tau can be changed, as shown by the fact that half of the methyl-containing residues of tau become immobilized on tau binding to tubulin ( 25).	bind
20371	2	6899	6	NULL	NULL	0	NULL	tau	NULL		become	NULL		methyl residues		immobilized	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9503_s_196	10449722	1H-NMR studies suggest that the flexibility of tau can be changed, as shown by the fact that half of the methyl-containing residues of tau become immobilized on tau binding to tubulin ( 25).	bind
20372	3	6899	6	NULL	NULL	0	NULL	statement 2	NULL		occurs during	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9503_s_196	10449722	1H-NMR studies suggest that the flexibility of tau can be changed, as shown by the fact that half of the methyl-containing residues of tau become immobilized on tau binding to tubulin ( 25).	bind
56663	4	6899	6	10	NULL	0	NULL	statement 2			suggests					tau		change in flexibility of			NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9503_s_196	10449722	1H-NMR studies suggest that the flexibility of tau can be changed, as shown by the fact that half of the methyl-containing residues of tau become immobilized on tau binding to tubulin ( 25).	bind
20442	1	6900	6	NULL	NULL	0	NULL	S100B	NULL		bind	NULL				GST-alphaC28 pellet fraction	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_14_14382_s_198	14736868	1st lane, 2.5 muM S100B alone;  2nd lane, concentration of S100B bound in the 6 muM GST-alphaC28 pellet fraction;  3rd lane, nonspecific binding of S100B to glutathione-Sepharose resin alone;  4th lane, concentration of S100B bound in the 22 muM Affi-alphaC28 pellet fraction;  5th lane, nonspecific binding of S100B to Affi-Geltm resin alone.	bind
20444	2	6900	6	NULL	NULL	0	NULL	S100B	NULL		bind	NULL				Affi-alphaC28 pellet fraction	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_14382_s_198	14736868	1st lane, 2.5 muM S100B alone;  2nd lane, concentration of S100B bound in the 6 muM GST-alphaC28 pellet fraction;  3rd lane, nonspecific binding of S100B to glutathione-Sepharose resin alone;  4th lane, concentration of S100B bound in the 22 muM Affi-alphaC28 pellet fraction;  5th lane, nonspecific binding of S100B to Affi-Geltm resin alone.	bind
24840	1	6901	5	13	NULL	NULL	NULL	[CL3] RNA	NucleicAcid		bind					RNase III	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_9_2381_s_274	12711683	1[CL3] RNA binds RNase III in a manner distinct from that of a competent substrate.	bind
24841	2	6901	5	13	NULL	NULL	NULL	statement 1	Process		distinct from that of					competent substrate	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_9_2381_s_274	12711683	1[CL3] RNA binds RNase III in a manner distinct from that of a competent substrate.	bind
20447	1	6901	6	10	NULL	0	NULL	[CL3] RNA			bind					RNase III					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_9_2381_s_274	12711683	1[CL3] RNA binds RNase III in a manner distinct from that of a competent substrate.	bind
56705	2	6901	6	10	NULL	0	NULL	statement 1			distinct from that of					competent substrate					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_9_2381_s_274	12711683	1[CL3] RNA binds RNase III in a manner distinct from that of a competent substrate.	bind
24842	1	6902	5	13	NULL	NULL	NULL	[CL3] RNA	NucleicAcid		bind					RNase III	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_9_2381_s_290	12711683	1[CL3] RNA binds RNase III in the same manner as R1.1 RNA.	bind
24843	2	6902	5	13	NULL	NULL	NULL	R1.1 RNA	NucleicAcid		bind					RNase III	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_9_2381_s_290	12711683	1[CL3] RNA binds RNase III in the same manner as R1.1 RNA.	bind
24844	3	6902	5	13	NULL	NULL	NULL	statement 1	Process		same manner as					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_9_2381_s_290	12711683	1[CL3] RNA binds RNase III in the same manner as R1.1 RNA.	bind
20448	1	6902	6	NULL	NULL	0	NULL	RNA	NULL		bind	NULL				RNase III	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_9_2381_s_290	12711683	1[CL3] RNA binds RNase III in the same manner as R1.1 RNA.	bind
20449	2	6902	6	NULL	NULL	0	NULL	R1.1 RNA	NULL		bind	NULL				RNase III	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_9_2381_s_290	12711683	1[CL3] RNA binds RNase III in the same manner as R1.1 RNA.	bind
20450	3	6902	6	NULL	NULL	0	NULL	statement 1	NULL		occurs in the same manner as	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_9_2381_s_290	12711683	1[CL3] RNA binds RNase III in the same manner as R1.1 RNA.	bind
24848	1	6904	5	13	NULL	NULL	NULL	[CL3] RNA	NucleicAcid		is a variant of					 Class II R1.1 RNA	NucleicAcid	binding-competent;;cleavage-resistant			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_9_2381_s_238	12711683	1[CL3] RNA: a binding-competent, cleavage-resistant Class II R1.1 RNA variant   el shift assays revealed that none of the Class II R1.1 RNA variants are detectably bound by RNase III (data not shown), with one exception.	bind
24849	2	6904	5	13	NULL	NULL	NULL	Class II R1.1 RNA variants	NucleicAcid		does not bind					RNase III	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_9_2381_s_238	12711683	1[CL3] RNA: a binding-competent, cleavage-resistant Class II R1.1 RNA variant   el shift assays revealed that none of the Class II R1.1 RNA variants are detectably bound by RNase III (data not shown), with one exception.	bind
20456	1	6904	6	NULL	NULL	0	NULL	Class II R1.1 RNA variants	NULL		does not bind	NULL	detectably			RNase III	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_9_2381_s_238	12711683	1[CL3] RNA: a binding-competent, cleavage-resistant Class II R1.1 RNA variant   el shift assays revealed that none of the Class II R1.1 RNA variants are detectably bound by RNase III (data not shown), with one exception.	bind
30299	2	6904	6	NULL	NULL	0	NULL	[CL3] RNA	NULL		is a variant of	NULL				Class II R1.1 RNA	NULL	binding-competent;; cleavage-resistant			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_9_2381_s_238	12711683	1[CL3] RNA: a binding-competent, cleavage-resistant Class II R1.1 RNA variant   el shift assays revealed that none of the Class II R1.1 RNA variants are detectably bound by RNase III (data not shown), with one exception.	bind
24853	1	6906	5	13	NULL	NULL	NULL	 RNA	NucleicAcid		bind		efficiently			RNase III	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_25_13437_s_78	9391043	1[WC] RNA efficiently binds the RNase III mutant, the poorly cleaved substrates exhibit greatly weakened or undetectable binding (Fig.  3 A).	bind
20473	1	6906	6	NULL	NULL	0	NULL	RNA	NULL		bind	NULL	efficiently			RNase III	NULL	mutant			NULL		0	NULL	NULL	NULL	gw60_pnas_94_25_13437_s_78	9391043	1[WC] RNA efficiently binds the RNase III mutant, the poorly cleaved substrates exhibit greatly weakened or undetectable binding (Fig.  3 A).	bind
24854	1	6907	5	13	NULL	NULL	NULL	bacteriophage T5 5'' - 3' exonuclease	GP		bind		structure-specific			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2772_s_257	11433022	2       Garforth,S.J. and Sayers,J.R. (1997) Structure-specific DNA binding by bacteriophage T5 5'' - 3' exonuclease.	bind
20474	1	6907	6	10	NULL	0	NULL	bacteriophage T5 5'' - 3' exonuclease	NULL		bind	NULL	Structure-specific			DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2772_s_257	11433022	2       Garforth,S.J. and Sayers,J.R. (1997) Structure-specific DNA binding by bacteriophage T5 5'' - 3' exonuclease.	bind
24855	1	6909	5	13	NULL	NULL	NULL	telomerase	GP	yeast	bind			est1 subunit		tlc1 telomerase RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2268_s_252	11376145	2       Zhou,J., Hidaka,K. and Futcher,B. (2000) The est1 subunit of yeast telomerase binds the tlc1 telomerase RNA.	bind
20475	1	6909	6	NULL	NULL	0	NULL	Telomerase	NULL	yeast	bind	NULL		est1 subunit		tlc1 telomerase RNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2268_s_252	11376145	2       Zhou,J., Hidaka,K. and Futcher,B. (2000) The est1 subunit of yeast telomerase binds the tlc1 telomerase RNA.	bind
24856	1	6910	5	13	NULL	NULL	NULL	PAI-1	GP		bind					vitronectin	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5112_s_343	9030577	2    In order to test for potential disruption of the PAI-1.vitronectin complex at the higher ionic strengths achieved in the quenching experiment, salt effects on the interaction were determined by comparing the binding of PAI-1 to immobilized vitronectin at 0.15 and 2 M NaCl.	bind
24857	2	6910	5	13	NULL	NULL	NULL	higher ionic strengths	QuantityOrMeasure		disrupts		potential			PAI-1.vitronectin complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5112_s_343	9030577	2    In order to test for potential disruption of the PAI-1.vitronectin complex at the higher ionic strengths achieved in the quenching experiment, salt effects on the interaction were determined by comparing the binding of PAI-1 to immobilized vitronectin at 0.15 and 2 M NaCl.	bind
20477	1	6910	6	NULL	NULL	0	NULL	PAI	NULL		forms a complex with	NULL				vitronectin	NULL	immobilized			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_5112_s_343	9030577	2    In order to test for potential disruption of the PAI-1.vitronectin complex at the higher ionic strengths achieved in the quenching experiment, salt effects on the interaction were determined by comparing the binding of PAI-1 to immobilized vitronectin at 0.15 and 2 M NaCl.	bind
20478	2	6910	6	10	NULL	0	NULL	PAI-1.vitronectin complex 			is disrupted at					ionic strength		higher			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5112_s_343	9030577	2    In order to test for potential disruption of the PAI-1.vitronectin complex at the higher ionic strengths achieved in the quenching experiment, salt effects on the interaction were determined by comparing the binding of PAI-1 to immobilized vitronectin at 0.15 and 2 M NaCl.	bind
24858	1	6915	5	13	NULL	NULL	NULL	iCpG DNA	NucleicAcid		bind					TLR9	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22563_s_276	12695520	2  Although there is no formal demonstration that either CpG DNA or iCpG DNA  directly binds to TLR9, and the precise molecular mechanism by which iCpG DNA  blocks activity of CpG DNA has not been revealed, these previous studies  suggest that iCpG DNA may compete with CpG DNA for binding to TLR9.	bind
24859	2	6915	5	13	NULL	NULL	NULL	CpG DNA	NucleicAcid		bind					TLR9	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22563_s_276	12695520	2  Although there is no formal demonstration that either CpG DNA or iCpG DNA  directly binds to TLR9, and the precise molecular mechanism by which iCpG DNA  blocks activity of CpG DNA has not been revealed, these previous studies  suggest that iCpG DNA may compete with CpG DNA for binding to TLR9.	bind
24860	3	6915	5	13	NULL	NULL	NULL	statement 1	Process		competes with		may			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22563_s_276	12695520	2  Although there is no formal demonstration that either CpG DNA or iCpG DNA  directly binds to TLR9, and the precise molecular mechanism by which iCpG DNA  blocks activity of CpG DNA has not been revealed, these previous studies  suggest that iCpG DNA may compete with CpG DNA for binding to TLR9.	bind
24861	4	6915	5	13	NULL	NULL	NULL	iCpG DNA	NucleicAcid		blocks					CpG DNA	NucleicAcid	activity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22563_s_276	12695520	2  Although there is no formal demonstration that either CpG DNA or iCpG DNA  directly binds to TLR9, and the precise molecular mechanism by which iCpG DNA  blocks activity of CpG DNA has not been revealed, these previous studies  suggest that iCpG DNA may compete with CpG DNA for binding to TLR9.	bind
20480	1	6915	6	NULL	NULL	0	NULL	iCpG DNA	NULL		bind	NULL	directly			TLR9	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22563_s_276	12695520	2  Although there is no formal demonstration that either CpG DNA or iCpG DNA  directly binds to TLR9, and the precise molecular mechanism by which iCpG DNA  blocks activity of CpG DNA has not been revealed, these previous studies  suggest that iCpG DNA may compete with CpG DNA for binding to TLR9.	bind
20481	2	6915	6	NULL	NULL	0	NULL	CpG DNA	NULL		bind	NULL	directly			TLR9	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22563_s_276	12695520	2  Although there is no formal demonstration that either CpG DNA or iCpG DNA  directly binds to TLR9, and the precise molecular mechanism by which iCpG DNA  blocks activity of CpG DNA has not been revealed, these previous studies  suggest that iCpG DNA may compete with CpG DNA for binding to TLR9.	bind
20483	3	6915	6	NULL	NULL	0	NULL	statement 1	NULL		compete	NULL	may			statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22563_s_276	12695520	2  Although there is no formal demonstration that either CpG DNA or iCpG DNA  directly binds to TLR9, and the precise molecular mechanism by which iCpG DNA  blocks activity of CpG DNA has not been revealed, these previous studies  suggest that iCpG DNA may compete with CpG DNA for binding to TLR9.	bind
20509	4	6915	6	NULL	NULL	0	NULL	iCpG DNA	NULL		blocks	NULL				CpG DNA	NULL	activity of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22563_s_276	12695520	2  Although there is no formal demonstration that either CpG DNA or iCpG DNA  directly binds to TLR9, and the precise molecular mechanism by which iCpG DNA  blocks activity of CpG DNA has not been revealed, these previous studies  suggest that iCpG DNA may compete with CpG DNA for binding to TLR9.	bind
24862	1	6916	5	13	NULL	NULL	NULL	GP IIb/IIa	GP		interacts with					GP Ib/vWF	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_7_1124_s_20	9672073	2  GP IIb/IIa exists in an inactive state on resting platelets, but GP Ib/vWF interaction results in a conformational change within GP IIb/IIa, which then binds fibrinogen and vWF, resulting in platelet aggregation.	bind
24863	2	6916	5	13	NULL	NULL	NULL	statement 1	Process		results in					GP IIb/IIa	GP	conformational change within			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_7_1124_s_20	9672073	2  GP IIb/IIa exists in an inactive state on resting platelets, but GP Ib/vWF interaction results in a conformational change within GP IIb/IIa, which then binds fibrinogen and vWF, resulting in platelet aggregation.	bind
24864	3	6916	5	13	NULL	NULL	NULL	statement 2	GP		bind					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_7_1124_s_20	9672073	2  GP IIb/IIa exists in an inactive state on resting platelets, but GP Ib/vWF interaction results in a conformational change within GP IIb/IIa, which then binds fibrinogen and vWF, resulting in platelet aggregation.	bind
24865	4	6916	5	13	NULL	NULL	NULL	statement 2	GP		bind					vWF	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_7_1124_s_20	9672073	2  GP IIb/IIa exists in an inactive state on resting platelets, but GP Ib/vWF interaction results in a conformational change within GP IIb/IIa, which then binds fibrinogen and vWF, resulting in platelet aggregation.	bind
24866	5	6916	5	13	NULL	NULL	NULL	statement 3	Process		results in					platelet	Cell	aggregation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_7_1124_s_20	9672073	2  GP IIb/IIa exists in an inactive state on resting platelets, but GP Ib/vWF interaction results in a conformational change within GP IIb/IIa, which then binds fibrinogen and vWF, resulting in platelet aggregation.	bind
24867	6	6916	5	13	NULL	NULL	NULL	statement 4	Process		results in					platelet	Cell	aggregation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_7_1124_s_20	9672073	2  GP IIb/IIa exists in an inactive state on resting platelets, but GP Ib/vWF interaction results in a conformational change within GP IIb/IIa, which then binds fibrinogen and vWF, resulting in platelet aggregation.	bind
20543	1	6916	6	10	NULL	0	NULL	GP IIb/IIa	NULL		interacts with	NULL				GP Ib/vWF	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_7_1124_s_20	9672073	2  GP IIb/IIa exists in an inactive state on resting platelets, but GP Ib/vWF interaction results in a conformational change within GP IIb/IIa, which then binds fibrinogen and vWF, resulting in platelet aggregation.	bind
20544	2	6916	6	10	NULL	0	NULL	statement 1	NULL		results in	NULL				GP IIb/IIa	NULL	conformational change within			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_7_1124_s_20	9672073	2  GP IIb/IIa exists in an inactive state on resting platelets, but GP Ib/vWF interaction results in a conformational change within GP IIb/IIa, which then binds fibrinogen and vWF, resulting in platelet aggregation.	bind
20545	3	6916	6	10	NULL	0	NULL	statement 2	NULL		bind	NULL				vWF	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_7_1124_s_20	9672073	2  GP IIb/IIa exists in an inactive state on resting platelets, but GP Ib/vWF interaction results in a conformational change within GP IIb/IIa, which then binds fibrinogen and vWF, resulting in platelet aggregation.	bind
20546	4	6916	6	10	NULL	0	NULL	statement 2	NULL		bind	NULL				fibrinogen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_7_1124_s_20	9672073	2  GP IIb/IIa exists in an inactive state on resting platelets, but GP Ib/vWF interaction results in a conformational change within GP IIb/IIa, which then binds fibrinogen and vWF, resulting in platelet aggregation.	bind
20547	5	6916	6	10	NULL	0	NULL	statement 3	NULL		results in	NULL				platelet	NULL	aggregation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_7_1124_s_20	9672073	2  GP IIb/IIa exists in an inactive state on resting platelets, but GP Ib/vWF interaction results in a conformational change within GP IIb/IIa, which then binds fibrinogen and vWF, resulting in platelet aggregation.	bind
20548	6	6916	6	10	NULL	0	NULL	statement 4	NULL		results in	NULL				platelet	NULL	aggregation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_7_1124_s_20	9672073	2  GP IIb/IIa exists in an inactive state on resting platelets, but GP Ib/vWF interaction results in a conformational change within GP IIb/IIa, which then binds fibrinogen and vWF, resulting in platelet aggregation.	bind
24868	1	6917	5	13	NULL	NULL	NULL	Hsp47	GP		is					Heatshockprotein 47	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_11_1229_s_25	10725279	2  Heatshockprotein   47 (Hsp47) is a heat shock - inducible glycoprotein that binds nascent type I procollagen chains as they translocate into the endoplasmic reticulum.	bind
24869	2	6917	5	13	NULL	NULL	NULL	Hsp47	GP		bind					type I procollagen chains 	GP	nascent			NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_11_1229_s_25	10725279	2  Heatshockprotein   47 (Hsp47) is a heat shock - inducible glycoprotein that binds nascent type I procollagen chains as they translocate into the endoplasmic reticulum.	bind
24870	3	6917	5	13	NULL	NULL	NULL	type I procollagen chains 	GP	nascent	translocates into					endoplasmic reticulum	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_11_1229_s_25	10725279	2  Heatshockprotein   47 (Hsp47) is a heat shock - inducible glycoprotein that binds nascent type I procollagen chains as they translocate into the endoplasmic reticulum.	bind
24871	4	6917	5	13	NULL	NULL	NULL	statement 2	Process		occurs when					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_11_1229_s_25	10725279	2  Heatshockprotein   47 (Hsp47) is a heat shock - inducible glycoprotein that binds nascent type I procollagen chains as they translocate into the endoplasmic reticulum.	bind
30372	5	6917	5	13	NULL	NULL	NULL	Hsp47	GP		is a type of					heat shock-inducible glycoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_11_1229_s_25	10725279	2  Heatshockprotein   47 (Hsp47) is a heat shock - inducible glycoprotein that binds nascent type I procollagen chains as they translocate into the endoplasmic reticulum.	bind
20549	1	6917	6	10	NULL	0	NULL	Hsp47			is					Heatshockprotein 47					NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_11_1229_s_25	10725279	2  Heatshockprotein   47 (Hsp47) is a heat shock - inducible glycoprotein that binds nascent type I procollagen chains as they translocate into the endoplasmic reticulum.	bind
20550	2	6917	6	10	NULL	0	NULL	 type I procollagen chains		nascent	translocate into					endoplasmic reticulum					NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_11_1229_s_25	10725279	2  Heatshockprotein   47 (Hsp47) is a heat shock - inducible glycoprotein that binds nascent type I procollagen chains as they translocate into the endoplasmic reticulum.	bind
20551	3	6917	6	10	NULL	0	NULL	Hsp47			bind					 type I procollagen chains		nascent			NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_11_1229_s_25	10725279	2  Heatshockprotein   47 (Hsp47) is a heat shock - inducible glycoprotein that binds nascent type I procollagen chains as they translocate into the endoplasmic reticulum.	bind
20552	4	6917	6	NULL	NULL	0	NULL	Hsp47	NULL		is a type of	NULL				heat shock-inducible glycoprotein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_11_1229_s_25	10725279	2  Heatshockprotein   47 (Hsp47) is a heat shock - inducible glycoprotein that binds nascent type I procollagen chains as they translocate into the endoplasmic reticulum.	bind
56707	5	6917	6	10	NULL	0	NULL	statement 3			occurs upon					statement 2					NULL		0	NULL	NULL	NULL	gw60_circulation_101_11_1229_s_25	10725279	2  Heatshockprotein   47 (Hsp47) is a heat shock - inducible glycoprotein that binds nascent type I procollagen chains as they translocate into the endoplasmic reticulum.	bind
24872	1	6918	5	13	NULL	NULL	NULL	ANPR molecules	GP		occurs in					hh-dimer configuration	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_6115_s_252	14600147	2  In the ANP-bound complex structure, two ANPR molecules occur in the hh-dimer configuration, sandwiching one molecule of ANP.	bind
24873	2	6918	5	13	NULL	NULL	NULL	statement 1	GP		sandwich					 ANP	GP	one molecule of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_6115_s_252	14600147	2  In the ANP-bound complex structure, two ANPR molecules occur in the hh-dimer configuration, sandwiching one molecule of ANP.	bind
24874	3	6918	5	13	NULL	NULL	NULL	ANP-bound complex structure	GP		contains					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_6115_s_252	14600147	2  In the ANP-bound complex structure, two ANPR molecules occur in the hh-dimer configuration, sandwiching one molecule of ANP.	bind
56708	4	6918	5	13	NULL	NULL	NULL	statement 1	GP		occur in					ANP-bound complex structure	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_6115_s_252	14600147	2  In the ANP-bound complex structure, two ANPR molecules occur in the hh-dimer configuration, sandwiching one molecule of ANP.	bind
20553	1	6918	6	NULL	NULL	0	NULL	ANPR molecules	NULL		occur in	NULL				hh-dimer configuration	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_6115_s_252	14600147	2  In the ANP-bound complex structure, two ANPR molecules occur in the hh-dimer configuration, sandwiching one molecule of ANP.	bind
20554	2	6918	6	NULL	NULL	0	NULL	statement 1	NULL		occurs in	NULL				ANP-bound complex structure	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_6115_s_252	14600147	2  In the ANP-bound complex structure, two ANPR molecules occur in the hh-dimer configuration, sandwiching one molecule of ANP.	bind
20555	3	6918	6	10	NULL	0	NULL	ANPR molecules			sandwich					ANP		one molecule of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_6115_s_252	14600147	2  In the ANP-bound complex structure, two ANPR molecules occur in the hh-dimer configuration, sandwiching one molecule of ANP.	bind
20556	4	6918	6	10	NULL	0	NULL	ANP-bound complex structure			contains					statement 2					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_6115_s_252	14600147	2  In the ANP-bound complex structure, two ANPR molecules occur in the hh-dimer configuration, sandwiching one molecule of ANP.	bind
24875	1	6919	5	13	NULL	NULL	NULL	IP3	Chemical		bind					IP3 receptors	GP	specific			NULL	in smooth muscle cell	NULL	NULL	NULL	NULL	gw60_circulationres_84_5_536_s_15	10082475	2  IP3 binds to specific IP3 receptors in the smooth muscle cell, which produces a release of Ca2+ from the intracellular stores.	bind
24876	3	6919	5	13	NULL	NULL	NULL	statement 1	Process		produces					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_5_536_s_15	10082475	2  IP3 binds to specific IP3 receptors in the smooth muscle cell, which produces a release of Ca2+ from the intracellular stores.	bind
44744	2	6919	5	13	NULL	NULL	NULL	Ca2+	Chemical		released from					intracellular stores	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_5_536_s_15	10082475	2  IP3 binds to specific IP3 receptors in the smooth muscle cell, which produces a release of Ca2+ from the intracellular stores.	bind
20557	1	6919	6	NULL	NULL	0	NULL	IP3	NULL		bind	NULL				IP3 receptors	NULL	specific			NULL	smooth muscle cell	NULL	NULL	NULL	NULL	gw60_circulationres_84_5_536_s_15	10082475	2  IP3 binds to specific IP3 receptors in the smooth muscle cell, which produces a release of Ca2+ from the intracellular stores.	bind
20558	2	6919	6	NULL	NULL	0	NULL	Ca2+	NULL		released from	NULL				intracellular stores	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_5_536_s_15	10082475	2  IP3 binds to specific IP3 receptors in the smooth muscle cell, which produces a release of Ca2+ from the intracellular stores.	bind
20559	3	6919	6	NULL	NULL	0	NULL	statement 1	NULL		produces	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_5_536_s_15	10082475	2  IP3 binds to specific IP3 receptors in the smooth muscle cell, which produces a release of Ca2+ from the intracellular stores.	bind
24877	1	6920	5	13	NULL	NULL	NULL	DCoH/PCD molecules	GP		bind					HNF1 dimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_6_2021_s_13	11395380	2  It has been shown that two DCoH/PCD molecules bind to a HNF1 dimer forming a transcriptionally active heterotetrameric complex.	bind
24878	2	6920	5	13	NULL	NULL	NULL	statement 1	GP		forms					heterotetrameric complex	GP	transcriptionally active			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_6_2021_s_13	11395380	2  It has been shown that two DCoH/PCD molecules bind to a HNF1 dimer forming a transcriptionally active heterotetrameric complex.	bind
20560	1	6920	6	NULL	NULL	0	NULL	DcoH/PCD molecules	NULL		bind	NULL				HNF1 dimer	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_6_2021_s_13	11395380	2  It has been shown that two DCoH/PCD molecules bind to a HNF1 dimer forming a transcriptionally active heterotetrameric complex.	bind
20561	2	6920	6	NULL	NULL	0	NULL	statement 1	NULL		forms a 	NULL				heterotetrameric complex	NULL	transcriptionally active 			NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_6_2021_s_13	11395380	2  It has been shown that two DCoH/PCD molecules bind to a HNF1 dimer forming a transcriptionally active heterotetrameric complex.	bind
24879	1	6921	5	13	NULL	NULL	NULL	fibrinogen	GP		bind					GP IIb/IIa receptor	GP	activated form 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_9_1013_s_19	10704169	2  Platelet aggregation is mediated through the binding of fibrinogen or von Willebrand factor (vWF) to the activated form of the platelet glycoprotein (GP) IIb/IIa (integrin alphaIIbbeta3) receptor.	bind
24880	2	6921	5	13	NULL	NULL	NULL	GP	GP		is					platelet glycoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_9_1013_s_19	10704169	2  Platelet aggregation is mediated through the binding of fibrinogen or von Willebrand factor (vWF) to the activated form of the platelet glycoprotein (GP) IIb/IIa (integrin alphaIIbbeta3) receptor.	bind
24960	3	6921	5	13	NULL	NULL	NULL	platelet	Process	aggregation of	is mediated through					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_9_1013_s_19	10704169	2  Platelet aggregation is mediated through the binding of fibrinogen or von Willebrand factor (vWF) to the activated form of the platelet glycoprotein (GP) IIb/IIa (integrin alphaIIbbeta3) receptor.	bind
24961	4	6921	5	13	NULL	NULL	NULL	vWF	GP		is					von Willebrand factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_9_1013_s_19	10704169	2  Platelet aggregation is mediated through the binding of fibrinogen or von Willebrand factor (vWF) to the activated form of the platelet glycoprotein (GP) IIb/IIa (integrin alphaIIbbeta3) receptor.	bind
24963	5	6921	5	13	NULL	NULL	NULL	vWF	GP		bind					GP IIb/IIa receptor	GP	activated form			NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_9_1013_s_19	10704169	2  Platelet aggregation is mediated through the binding of fibrinogen or von Willebrand factor (vWF) to the activated form of the platelet glycoprotein (GP) IIb/IIa (integrin alphaIIbbeta3) receptor.	bind
24964	6	6921	5	13	NULL	NULL	NULL	platelet	Process	aggregation of	is mediated through					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_9_1013_s_19	10704169	2  Platelet aggregation is mediated through the binding of fibrinogen or von Willebrand factor (vWF) to the activated form of the platelet glycoprotein (GP) IIb/IIa (integrin alphaIIbbeta3) receptor.	bind
24965	7	6921	5	13	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_9_1013_s_19	10704169	2  Platelet aggregation is mediated through the binding of fibrinogen or von Willebrand factor (vWF) to the activated form of the platelet glycoprotein (GP) IIb/IIa (integrin alphaIIbbeta3) receptor.	bind
56713	8	6921	5	13	NULL	NULL	NULL	IIb/IIa	GP		is					integrin alphaIIbbeta3	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_9_1013_s_19	10704169	2  Platelet aggregation is mediated through the binding of fibrinogen or von Willebrand factor (vWF) to the activated form of the platelet glycoprotein (GP) IIb/IIa (integrin alphaIIbbeta3) receptor.	bind
20562	1	6921	6	NULL	NULL	0	NULL	vWF	NULL		is	NULL				von Willebrand factor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_101_9_1013_s_19	10704169	2  Platelet aggregation is mediated through the binding of fibrinogen or von Willebrand factor (vWF) to the activated form of the platelet glycoprotein (GP) IIb/IIa (integrin alphaIIbbeta3) receptor.	bind
20563	2	6921	6	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL				GP IIb/IIa receptor	NULL	activated form			NULL		0	NULL	NULL	NULL	gw60_circulation_101_9_1013_s_19	10704169	2  Platelet aggregation is mediated through the binding of fibrinogen or von Willebrand factor (vWF) to the activated form of the platelet glycoprotein (GP) IIb/IIa (integrin alphaIIbbeta3) receptor.	bind
20564	3	6921	6	NULL	NULL	0	NULL	vWF	NULL		bind	NULL				GP IIb/IIa receptor	NULL	activated form			NULL		0	NULL	NULL	NULL	gw60_circulation_101_9_1013_s_19	10704169	2  Platelet aggregation is mediated through the binding of fibrinogen or von Willebrand factor (vWF) to the activated form of the platelet glycoprotein (GP) IIb/IIa (integrin alphaIIbbeta3) receptor.	bind
20566	8	6921	6	10	NULL	0	NULL	GP			is					platelet glycoprotein					NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_9_1013_s_19	10704169	2  Platelet aggregation is mediated through the binding of fibrinogen or von Willebrand factor (vWF) to the activated form of the platelet glycoprotein (GP) IIb/IIa (integrin alphaIIbbeta3) receptor.	bind
20567	6	6921	6	10	NULL	0	NULL	 IIb/IIa			is					integrin alphaIIbbeta3					NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_9_1013_s_19	10704169	2  Platelet aggregation is mediated through the binding of fibrinogen or von Willebrand factor (vWF) to the activated form of the platelet glycoprotein (GP) IIb/IIa (integrin alphaIIbbeta3) receptor.	bind
56709	4	6921	6	10	NULL	0	NULL	platelet		aggregation of	is mediated through					statement 2					NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_9_1013_s_19	10704169	2  Platelet aggregation is mediated through the binding of fibrinogen or von Willebrand factor (vWF) to the activated form of the platelet glycoprotein (GP) IIb/IIa (integrin alphaIIbbeta3) receptor.	bind
56710	5	6921	6	10	NULL	0	NULL	platelet		aggregation of	is mediated through					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_9_1013_s_19	10704169	2  Platelet aggregation is mediated through the binding of fibrinogen or von Willebrand factor (vWF) to the activated form of the platelet glycoprotein (GP) IIb/IIa (integrin alphaIIbbeta3) receptor.	bind
56712	7	6921	6	10	NULL	0	NULL	statement 4			is an alternative to					statement 5					NULL		0	NULL	NULL	NULL	gw60_circulation_101_9_1013_s_19	10704169	2  Platelet aggregation is mediated through the binding of fibrinogen or von Willebrand factor (vWF) to the activated form of the platelet glycoprotein (GP) IIb/IIa (integrin alphaIIbbeta3) receptor.	bind
24966	1	6922	5	13	NULL	NULL	NULL				overlaps				cryptic element	PDGF-B	GP			Sp1 site in promoter	NULL	in cells exposed to PMA	NULL	NULL	NULL	NULL	gw60_circulationres_81_4_457_s_29	9314825	2  Similar strategies later revealed that Egr-1 binds to a cryptic element overlapping the Sp1 site in the PDGF-B promoter in cells exposed to PMA. 9	bind
24967	2	6922	5	13	NULL	NULL	NULL	Egr-1	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_81_4_457_s_29	9314825	2  Similar strategies later revealed that Egr-1 binds to a cryptic element overlapping the Sp1 site in the PDGF-B promoter in cells exposed to PMA. 9	bind
20568	2	6922	6	10	NULL	0	NULL	Egr-1			bind					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_81_4_457_s_29	9314825	2  Similar strategies later revealed that Egr-1 binds to a cryptic element overlapping the Sp1 site in the PDGF-B promoter in cells exposed to PMA. 9	bind
56714	1	6922	6	10	NULL	0	NULL				overlaps				cryptic element	PDGF-B				Sp1 site in promoter	NULL	cells exposed to PMA	0	NULL	NULL	NULL	gw60_circulationres_81_4_457_s_29	9314825	2  Similar strategies later revealed that Egr-1 binds to a cryptic element overlapping the Sp1 site in the PDGF-B promoter in cells exposed to PMA. 9	bind
24968	2	6923	5	13	NULL	NULL	NULL	hydrophobic contact	Process		stabilize			Phe96A-Phe96B		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_6115_s_277	14600147	2  The hydrophobic contact Phe96A-Phe96B remains and apparently contributes to stabilizing the ANP-bound activated complex.	bind
44709	1	6923	5	13	NULL	NULL	NULL	ANP	GP		bind					activated complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_6115_s_277	14600147	2  The hydrophobic contact Phe96A-Phe96B remains and apparently contributes to stabilizing the ANP-bound activated complex.	bind
20590	2	6923	6	10	NULL	0	NULL	hydrophobic contact	NULL		stabilize	NULL		Phe96A-Phe96B		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_6115_s_277	14600147	2  The hydrophobic contact Phe96A-Phe96B remains and apparently contributes to stabilizing the ANP-bound activated complex.	bind
44710	1	6923	6	10	NULL	0	NULL	ANP	NULL		bind	NULL				activated complex	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_6115_s_277	14600147	2  The hydrophobic contact Phe96A-Phe96B remains and apparently contributes to stabilizing the ANP-bound activated complex.	bind
24970	1	6924	5	13	NULL	NULL	NULL	RTs	GP	dNTP utilization efficiency of	contributes to					host cell specificity	Process				NULL	retroviruses	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12190_s_262	15644314	2  These combined findings support the idea that the dNTP utilization efficiency and dNTP binding affinity of RTs contribute to the host cell specificity of retroviruses.	bind
24971	2	6924	5	13	NULL	NULL	NULL	RTs	GP	dNTP binding affinity of	contributes to					host cell specificity	Process				NULL	retroviruses	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12190_s_262	15644314	2  These combined findings support the idea that the dNTP utilization efficiency and dNTP binding affinity of RTs contribute to the host cell specificity of retroviruses.	bind
20591	1	6924	6	10	NULL	0	NULL	RTs		dNTP utilization efficiency of	contribute to					host cell specificity					NULL	retroviruses	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12190_s_262	15644314	2  These combined findings support the idea that the dNTP utilization efficiency and dNTP binding affinity of RTs contribute to the host cell specificity of retroviruses.	bind
20592	2	6924	6	10	NULL	0	NULL	RTs		 dNTP binding affinity of	contribute to					host cell specificity					NULL	retroviruses	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12190_s_262	15644314	2  These combined findings support the idea that the dNTP utilization efficiency and dNTP binding affinity of RTs contribute to the host cell specificity of retroviruses.	bind
24972	1	6925	5	13	NULL	NULL	NULL	tissue factor	GP		bind					factor VII/VIIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_22_2651_s_19	10840019	2  Tissue factor binds factor VII/VIIa, and the TF:VIIa complex can proteolytically activate factor X, which in turn activates thrombin and generates fibrin.	bind
24973	2	6925	5	13	NULL	NULL	NULL	TF:VIIa complex	GP		activates		proteolytically			factor X	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_22_2651_s_19	10840019	2  Tissue factor binds factor VII/VIIa, and the TF:VIIa complex can proteolytically activate factor X, which in turn activates thrombin and generates fibrin.	bind
24974	3	6925	5	13	NULL	NULL	NULL	factor X	GP	activated	activates					thrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_22_2651_s_19	10840019	2  Tissue factor binds factor VII/VIIa, and the TF:VIIa complex can proteolytically activate factor X, which in turn activates thrombin and generates fibrin.	bind
24975	4	6925	5	13	NULL	NULL	NULL	statement 3	Process		generates					fibrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_22_2651_s_19	10840019	2  Tissue factor binds factor VII/VIIa, and the TF:VIIa complex can proteolytically activate factor X, which in turn activates thrombin and generates fibrin.	bind
20593	1	6925	6	NULL	NULL	0	NULL	Tissue factor	NULL		bind	NULL				factor VII/VIIa	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_101_22_2651_s_19	10840019	2  Tissue factor binds factor VII/VIIa, and the TF:VIIa complex can proteolytically activate factor X, which in turn activates thrombin and generates fibrin.	bind
20594	2	6925	6	10	NULL	0	NULL	TF:VIIa complex			activate		proteolytically			factor X					NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_22_2651_s_19	10840019	2  Tissue factor binds factor VII/VIIa, and the TF:VIIa complex can proteolytically activate factor X, which in turn activates thrombin and generates fibrin.	bind
20595	3	6925	6	NULL	NULL	0	NULL	factor X	NULL	activated	activates	NULL				thrombin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_101_22_2651_s_19	10840019	2  Tissue factor binds factor VII/VIIa, and the TF:VIIa complex can proteolytically activate factor X, which in turn activates thrombin and generates fibrin.	bind
20596	4	6925	6	NULL	NULL	0	NULL	statement 3	NULL		generates	NULL				fibrin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_101_22_2651_s_19	10840019	2  Tissue factor binds factor VII/VIIa, and the TF:VIIa complex can proteolytically activate factor X, which in turn activates thrombin and generates fibrin.	bind
25145	1	6926	5	13	NULL	NULL	NULL	CREB	GP		bind									AP-1 site 	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10647_s_306	9553127	2 (iii) Whether CREB or ATF-1 binds to the AP-1 site in a gel shift, this protein was not phosphorylated in response to PTH, since anti-phospho-CREB antibody did not cause a supershift (Fig.  7), whereas we know this antibody will supershift PTH-induced phosphorylated CREB bound to a cyclic AMP-response element in the c- fos gene ( 24).	bind
25146	2	6926	5	13	NULL	NULL	NULL	CREB	GP	PTH-induced phosphorylated	bind					c- fos gene	GP			cyclic AMP-response element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10647_s_306	9553127	2 (iii) Whether CREB or ATF-1 binds to the AP-1 site in a gel shift, this protein was not phosphorylated in response to PTH, since anti-phospho-CREB antibody did not cause a supershift (Fig.  7), whereas we know this antibody will supershift PTH-induced phosphorylated CREB bound to a cyclic AMP-response element in the c- fos gene ( 24).	bind
25147	3	6926	5	13	NULL	NULL	NULL	ATF-1	GP		bind									AP-1 site 	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10647_s_306	9553127	2 (iii) Whether CREB or ATF-1 binds to the AP-1 site in a gel shift, this protein was not phosphorylated in response to PTH, since anti-phospho-CREB antibody did not cause a supershift (Fig.  7), whereas we know this antibody will supershift PTH-induced phosphorylated CREB bound to a cyclic AMP-response element in the c- fos gene ( 24).	bind
20597	1	6926	6	NULL	NULL	0	NULL	CREB	NULL		bind	NULL					NULL			AP-1 site	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_17_10647_s_306	9553127	2 (iii) Whether CREB or ATF-1 binds to the AP-1 site in a gel shift, this protein was not phosphorylated in response to PTH, since anti-phospho-CREB antibody did not cause a supershift (Fig.  7), whereas we know this antibody will supershift PTH-induced phosphorylated CREB bound to a cyclic AMP-response element in the c- fos gene ( 24).	bind
20598	2	6926	6	NULL	NULL	0	NULL	ATF-1	NULL		bind	NULL					NULL			AP-1 site	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_17_10647_s_306	9553127	2 (iii) Whether CREB or ATF-1 binds to the AP-1 site in a gel shift, this protein was not phosphorylated in response to PTH, since anti-phospho-CREB antibody did not cause a supershift (Fig.  7), whereas we know this antibody will supershift PTH-induced phosphorylated CREB bound to a cyclic AMP-response element in the c- fos gene ( 24).	bind
20736	3	6926	6	NULL	NULL	0	NULL	CREB	NULL	PTH-induced phosphorylated	bind	NULL				c-fos gene	NULL			cyclic AMP-response element	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_17_10647_s_306	9553127	2 (iii) Whether CREB or ATF-1 binds to the AP-1 site in a gel shift, this protein was not phosphorylated in response to PTH, since anti-phospho-CREB antibody did not cause a supershift (Fig.  7), whereas we know this antibody will supershift PTH-induced phosphorylated CREB bound to a cyclic AMP-response element in the c- fos gene ( 24).	bind
25148	1	6927	5	13	NULL	NULL	NULL	fibrinogen	GP	circulating	bind					GP IIb/IIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_4_399_s_19	11468200	2 -  6 These agents block the binding of circulating fibrinogen and von Willebrand factor to GP IIb/IIa, preventing the cross-linking of platelets necessary for aggregation and thrombosis.	bind
25149	2	6927	5	13	NULL	NULL	NULL	von Willebrand factor	GP		bind					GP IIb/IIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_4_399_s_19	11468200	2 -  6 These agents block the binding of circulating fibrinogen and von Willebrand factor to GP IIb/IIa, preventing the cross-linking of platelets necessary for aggregation and thrombosis.	bind
25150	3	6927	5	13	NULL	NULL	NULL	platelets	Cell		is necessary for					aggregation	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_4_399_s_19	11468200	2 -  6 These agents block the binding of circulating fibrinogen and von Willebrand factor to GP IIb/IIa, preventing the cross-linking of platelets necessary for aggregation and thrombosis.	bind
25151	4	6927	5	13	NULL	NULL	NULL	platelets	Cell		is necessary for					thrombosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_4_399_s_19	11468200	2 -  6 These agents block the binding of circulating fibrinogen and von Willebrand factor to GP IIb/IIa, preventing the cross-linking of platelets necessary for aggregation and thrombosis.	bind
25152	5	6927	5	13	NULL	NULL	NULL	statement 1	Process	blocking of	prevents					statement 3	Process	cross-linking of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_4_399_s_19	11468200	2 -  6 These agents block the binding of circulating fibrinogen and von Willebrand factor to GP IIb/IIa, preventing the cross-linking of platelets necessary for aggregation and thrombosis.	bind
25153	6	6927	5	13	NULL	NULL	NULL	statement 1	Process	blocking of	prevents					statement 4	Process	cross-linking of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_4_399_s_19	11468200	2 -  6 These agents block the binding of circulating fibrinogen and von Willebrand factor to GP IIb/IIa, preventing the cross-linking of platelets necessary for aggregation and thrombosis.	bind
25154	7	6927	5	13	NULL	NULL	NULL	statement 2	Process	blocking of	prevents					statement 3	Process	cross-linking of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_4_399_s_19	11468200	2 -  6 These agents block the binding of circulating fibrinogen and von Willebrand factor to GP IIb/IIa, preventing the cross-linking of platelets necessary for aggregation and thrombosis.	bind
25155	8	6927	5	13	NULL	NULL	NULL	statement 2	Process	blocking of	prevents					statement 4	Process	cross-linking of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_4_399_s_19	11468200	2 -  6 These agents block the binding of circulating fibrinogen and von Willebrand factor to GP IIb/IIa, preventing the cross-linking of platelets necessary for aggregation and thrombosis.	bind
20599	1	6927	6	NULL	NULL	0	NULL	fibrinogen	NULL	circulating	bind	NULL				GP IIb/IIa	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_104_4_399_s_19	11468200	2 -  6 These agents block the binding of circulating fibrinogen and von Willebrand factor to GP IIb/IIa, preventing the cross-linking of platelets necessary for aggregation and thrombosis.	bind
20600	2	6927	6	NULL	NULL	0	NULL	von Willebrand factor	NULL		bind	NULL				GP IIb/IIa	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_104_4_399_s_19	11468200	2 -  6 These agents block the binding of circulating fibrinogen and von Willebrand factor to GP IIb/IIa, preventing the cross-linking of platelets necessary for aggregation and thrombosis.	bind
30675	3	6927	6	NULL	NULL	0	NULL	platelets	NULL		is necessary for	NULL				aggregation	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_104_4_399_s_19	11468200	2 -  6 These agents block the binding of circulating fibrinogen and von Willebrand factor to GP IIb/IIa, preventing the cross-linking of platelets necessary for aggregation and thrombosis.	bind
30676	4	6927	6	NULL	NULL	0	NULL	platelets	NULL		is necessary for	NULL				thrombosis	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_104_4_399_s_19	11468200	2 -  6 These agents block the binding of circulating fibrinogen and von Willebrand factor to GP IIb/IIa, preventing the cross-linking of platelets necessary for aggregation and thrombosis.	bind
30677	5	6927	6	NULL	NULL	0	NULL	statement 1	NULL	blocking of	prevents	NULL				statement 3	NULL	cross-linking of			NULL		0	NULL	NULL	NULL	gw60_circulation_104_4_399_s_19	11468200	2 -  6 These agents block the binding of circulating fibrinogen and von Willebrand factor to GP IIb/IIa, preventing the cross-linking of platelets necessary for aggregation and thrombosis.	bind
30678	6	6927	6	NULL	NULL	0	NULL	statement 1	NULL	blocking of	prevents	NULL				statement 4	NULL	cross-linking of			NULL		0	NULL	NULL	NULL	gw60_circulation_104_4_399_s_19	11468200	2 -  6 These agents block the binding of circulating fibrinogen and von Willebrand factor to GP IIb/IIa, preventing the cross-linking of platelets necessary for aggregation and thrombosis.	bind
30679	7	6927	6	NULL	NULL	0	NULL	statement 2	NULL	blocking of	prevents	NULL				statement 3	NULL	cross-linking of			NULL		0	NULL	NULL	NULL	gw60_circulation_104_4_399_s_19	11468200	2 -  6 These agents block the binding of circulating fibrinogen and von Willebrand factor to GP IIb/IIa, preventing the cross-linking of platelets necessary for aggregation and thrombosis.	bind
30680	8	6927	6	NULL	NULL	0	NULL	statement 2	NULL	blocking of	prevents	NULL				statement 4	NULL	cross-linking of			NULL		0	NULL	NULL	NULL	gw60_circulation_104_4_399_s_19	11468200	2 -  6 These agents block the binding of circulating fibrinogen and von Willebrand factor to GP IIb/IIa, preventing the cross-linking of platelets necessary for aggregation and thrombosis.	bind
25156	1	6928	5	13	NULL	NULL	NULL	GEFs	GP		is					guanine nucleotide exchange factors	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
25157	2	6928	5	13	NULL	NULL	NULL	Epac proteins	GP		bind					cAMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
25158	3	6928	5	13	NULL	NULL	NULL	Epac proteins	GP		bind					PKA	GP		regulatory subunit		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
25159	4	6928	5	13	NULL	NULL	NULL	statement 2	Process		similar affinity as					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
25160	5	6928	5	13	NULL	NULL	NULL	Epac proteins	GP		function as					GEFs	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
25161	6	6928	5	13	NULL	NULL	NULL	statement 5	GP		occurs for					Rap1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
25162	7	6928	5	13	NULL	NULL	NULL	statement 5	GP		occurs for					Rap2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
25163	8	6928	5	13	NULL	NULL	NULL	Epac proteins	GP		is activated by		directly			cAMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
25164	9	6928	5	13	NULL	NULL	NULL	statement 8	Process		is independent of					PKA	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
44750	10	6928	5	13	NULL	NULL	NULL	Rap1	GP		is a type of					Ras-like small GTPases	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
44751	11	6928	5	13	NULL	NULL	NULL	Rap2	GP		is a type of					Ras-like small GTPases	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
20601	1	6928	6	10	NULL	0	NULL	Epac proteins			is a type of					GEF					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
20602	2	6928	6	NULL	NULL	0	NULL	GEF	NULL		is	NULL				guanine nucleotide exchange factor	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
20603	3	6928	6	NULL	NULL	0	NULL	Epac proteins	NULL		bind	NULL				cAMP	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
20604	4	6928	6	NULL	NULL	0	NULL	PKA	NULL		bind	NULL		regulatory subunit		cAMP	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
20605	5	6928	6	NULL	NULL	0	NULL	statement 3	NULL		is of similar affinity as	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
20606	6	6928	6	NULL	NULL	0	NULL	cAMP	NULL		activates	NULL	directly			Epac proteins	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
20607	7	6928	6	NULL	NULL	0	NULL	statement 6	NULL		is independent of	NULL				PKA	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
20608	8	6928	6	NULL	NULL	0	NULL	statement 1	NULL		occurs for	NULL				Rap1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
20609	9	6928	6	NULL	NULL	0	NULL	statement 1	NULL		occurs for	NULL				Rap2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
20610	10	6928	6	10	NULL	0	NULL	Rap1	NULL		is a type of	NULL				Ras-like small GTPases	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
20611	11	6928	6	10	NULL	0	NULL	Rap2	NULL		is a type of	NULL				Ras-like small GTPases	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_12_1296_s_16	16269655	2 - 4   Epac proteins are guanine nucleotide exchange factors (GEFs) that bind cAMP with affinities similar to that of the regulatory subunit of PKA. 2,3  They have been shown to function as GEFs for the Ras-like small GTPases Rap1 and Rap2 and are directly activated by cAMP in a PKA independent manner.	bind
25165	1	6929	5	13	NULL	NULL	NULL	PDGF	GP		bind		selectively	A chain		alpha PDGFR	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_787_s_21	15061151	2 - 4   The PDGF A and C chains selectively bind alpha PDGFR, whereas PDGF D preferentially binds beta PDGFR and PDGF B displays similar affinity for both receptors.	bind
25166	2	6929	5	13	NULL	NULL	NULL	PDGF	GP		bind		selectively	C chain		alpha PDGFR	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_787_s_21	15061151	2 - 4   The PDGF A and C chains selectively bind alpha PDGFR, whereas PDGF D preferentially binds beta PDGFR and PDGF B displays similar affinity for both receptors.	bind
25167	3	6929	5	13	NULL	NULL	NULL	PDGF	GP		bind		preferentially	D chain		beta PDGFR	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_787_s_21	15061151	2 - 4   The PDGF A and C chains selectively bind alpha PDGFR, whereas PDGF D preferentially binds beta PDGFR and PDGF B displays similar affinity for both receptors.	bind
25168	4	6929	5	13	NULL	NULL	NULL	PDGF	GP		bind			B chain		alpha PDGFR	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_787_s_21	15061151	2 - 4   The PDGF A and C chains selectively bind alpha PDGFR, whereas PDGF D preferentially binds beta PDGFR and PDGF B displays similar affinity for both receptors.	bind
25169	5	6929	5	13	NULL	NULL	NULL	PDGF	GP		bind			B chain		beta PDGFR	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_787_s_21	15061151	2 - 4   The PDGF A and C chains selectively bind alpha PDGFR, whereas PDGF D preferentially binds beta PDGFR and PDGF B displays similar affinity for both receptors.	bind
25170	6	6929	5	13	NULL	NULL	NULL	statement 4	Process		similar affinity as					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_787_s_21	15061151	2 - 4   The PDGF A and C chains selectively bind alpha PDGFR, whereas PDGF D preferentially binds beta PDGFR and PDGF B displays similar affinity for both receptors.	bind
20612	1	6929	6	NULL	NULL	0	NULL	PDGF	NULL		bind	NULL	selectively	A chain		alpha PDGFR	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_787_s_21	15061151	2 - 4   The PDGF A and C chains selectively bind alpha PDGFR, whereas PDGF D preferentially binds beta PDGFR and PDGF B displays similar affinity for both receptors.	bind
20613	2	6929	6	NULL	NULL	0	NULL	PDGF	NULL		bind	NULL	selectively	C chain		alpha PDGFR	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_787_s_21	15061151	2 - 4   The PDGF A and C chains selectively bind alpha PDGFR, whereas PDGF D preferentially binds beta PDGFR and PDGF B displays similar affinity for both receptors.	bind
20614	3	6929	6	NULL	NULL	0	NULL	PDGF	NULL		bind	NULL	preferentially	D chain		beta PDGFR	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_787_s_21	15061151	2 - 4   The PDGF A and C chains selectively bind alpha PDGFR, whereas PDGF D preferentially binds beta PDGFR and PDGF B displays similar affinity for both receptors.	bind
20615	4	6929	6	NULL	NULL	0	NULL	PDGF	NULL		bind	NULL		B chain		alpha PDGFR	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_787_s_21	15061151	2 - 4   The PDGF A and C chains selectively bind alpha PDGFR, whereas PDGF D preferentially binds beta PDGFR and PDGF B displays similar affinity for both receptors.	bind
20616	5	6929	6	NULL	NULL	0	NULL	PDGF 	NULL		bind	NULL		B chain		beta PDGFR	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_787_s_21	15061151	2 - 4   The PDGF A and C chains selectively bind alpha PDGFR, whereas PDGF D preferentially binds beta PDGFR and PDGF B displays similar affinity for both receptors.	bind
20617	6	6929	6	NULL	NULL	0	NULL	statement 4	NULL		has equal affinity as	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_787_s_21	15061151	2 - 4   The PDGF A and C chains selectively bind alpha PDGFR, whereas PDGF D preferentially binds beta PDGFR and PDGF B displays similar affinity for both receptors.	bind
25171	1	6930	5	13	NULL	NULL	NULL	Cx43	GP		bind					c-Src	GP	constitutively active			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_2_215_s_19	14699011	2 - 5    Recent studies show that this association is potentially interlinked, because binding of Cx43 to constitutively active c-Src is correlated with a decrease in the Cx43/ZO-1 interaction.	bind
25172	3	6930	5	13	NULL	NULL	NULL	statement 1	Process		correlates with					statement 2	Process	decrease in			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_2_215_s_19	14699011	2 - 5    Recent studies show that this association is potentially interlinked, because binding of Cx43 to constitutively active c-Src is correlated with a decrease in the Cx43/ZO-1 interaction.	bind
31485	2	6930	5	13	NULL	NULL	NULL	Cx43	GP		interacts with					ZO-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_2_215_s_19	14699011	2 - 5    Recent studies show that this association is potentially interlinked, because binding of Cx43 to constitutively active c-Src is correlated with a decrease in the Cx43/ZO-1 interaction.	bind
20618	1	6930	6	NULL	NULL	0	NULL	Cx43	NULL		bind	NULL				c-Src	NULL	constitutively active			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_2_215_s_19	14699011	2 - 5    Recent studies show that this association is potentially interlinked, because binding of Cx43 to constitutively active c-Src is correlated with a decrease in the Cx43/ZO-1 interaction.	bind
20619	2	6930	6	NULL	NULL	0	NULL	Cx43	NULL		interacts with	NULL				ZO-1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_2_215_s_19	14699011	2 - 5    Recent studies show that this association is potentially interlinked, because binding of Cx43 to constitutively active c-Src is correlated with a decrease in the Cx43/ZO-1 interaction.	bind
20620	3	6930	6	NULL	NULL	0	NULL	statement 1	NULL		correlates with	NULL				statement 2	NULL	decrease in			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_2_215_s_19	14699011	2 - 5    Recent studies show that this association is potentially interlinked, because binding of Cx43 to constitutively active c-Src is correlated with a decrease in the Cx43/ZO-1 interaction.	bind
25173	1	6931	5	13	NULL	NULL	NULL	2 -F-arabino-FAD	GP		bind		very tightly			apo-glucose oxidase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_33_19915_s_225	8702705	2 -F-arabino-FAD binds very tightly to apo-glucose oxidase with quenching of the fluorescence and changes in the lambdamax from 372 and 444 nm to 376 and 454 nm.	bind
20621	1	6931	6	NULL	NULL	0	NULL	F-arabino-FAD	NULL		bind	NULL	very tightly			apo-glucose oxidase 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_33_19915_s_225	8702705	2 -F-arabino-FAD binds very tightly to apo-glucose oxidase with quenching of the fluorescence and changes in the lambdamax from 372 and 444 nm to 376 and 454 nm.	bind
25174	1	6933	5	13	NULL	NULL	NULL	LIFR	GP		is					LIF-specific receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_7_787_s_19	10764413	2 3  LIF binds to a receptor complex consisting of a LIF-specific receptor (LIFR) and the signal transducer gp130.	bind
25175	2	6933	5	13	NULL	NULL	NULL	LIFR	GP		is in complex with					gp130	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_7_787_s_19	10764413	2 3  LIF binds to a receptor complex consisting of a LIF-specific receptor (LIFR) and the signal transducer gp130.	bind
25176	3	6933	5	13	NULL	NULL	NULL	LIF	GP		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_7_787_s_19	10764413	2 3  LIF binds to a receptor complex consisting of a LIF-specific receptor (LIFR) and the signal transducer gp130.	bind
31486	4	6933	5	13	NULL	NULL	NULL	gp130	GP		is a type of					signal transducer	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_7_787_s_19	10764413	2 3  LIF binds to a receptor complex consisting of a LIF-specific receptor (LIFR) and the signal transducer gp130.	bind
20622	1	6933	6	NULL	NULL	0	NULL	LIF-specifc receptor	NULL		forms a complex with	NULL				gp130	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_7_787_s_19	10764413	2 3  LIF binds to a receptor complex consisting of a LIF-specific receptor (LIFR) and the signal transducer gp130.	bind
20623	2	6933	6	NULL	NULL	0	NULL	LIFR	NULL		is	NULL				LIF-specific receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_7_787_s_19	10764413	2 3  LIF binds to a receptor complex consisting of a LIF-specific receptor (LIFR) and the signal transducer gp130.	bind
20624	3	6933	6	NULL	NULL	0	NULL	gp130	NULL		is a type of	NULL				signal transducer	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_7_787_s_19	10764413	2 3  LIF binds to a receptor complex consisting of a LIF-specific receptor (LIFR) and the signal transducer gp130.	bind
20626	4	6933	6	NULL	NULL	0	NULL	LIF	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_7_787_s_19	10764413	2 3  LIF binds to a receptor complex consisting of a LIF-specific receptor (LIFR) and the signal transducer gp130.	bind
25177	1	6934	5	13	NULL	NULL	NULL	Ang II	GP		bind					AT1 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_81_4_550_s_17	9314836	2 3  Nonetheless, binding of Ang II to the AT1 receptor elicits many of the same cellular events induced by mitogens such as PDGF and EGF.	bind
25178	3	6934	5	13	NULL	NULL	NULL	statement 1	Process		elicits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_81_4_550_s_17	9314836	2 3  Nonetheless, binding of Ang II to the AT1 receptor elicits many of the same cellular events induced by mitogens such as PDGF and EGF.	bind
25179	2	6934	5	13	NULL	NULL	NULL	PDGF	GP		induce					cellular events	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_81_4_550_s_17	9314836	2 3  Nonetheless, binding of Ang II to the AT1 receptor elicits many of the same cellular events induced by mitogens such as PDGF and EGF.	bind
25181	4	6934	5	13	NULL	NULL	NULL	EGF	GP		induce					cellular events	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_81_4_550_s_17	9314836	2 3  Nonetheless, binding of Ang II to the AT1 receptor elicits many of the same cellular events induced by mitogens such as PDGF and EGF.	bind
31487	6	6934	5	13	NULL	NULL	NULL	PDGF	GP		is a type of					mitogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_81_4_550_s_17	9314836	2 3  Nonetheless, binding of Ang II to the AT1 receptor elicits many of the same cellular events induced by mitogens such as PDGF and EGF.	bind
31488	7	6934	5	13	NULL	NULL	NULL	EGF	GP		is a type of					mitogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_81_4_550_s_17	9314836	2 3  Nonetheless, binding of Ang II to the AT1 receptor elicits many of the same cellular events induced by mitogens such as PDGF and EGF.	bind
44752	5	6934	5	13	NULL	NULL	NULL	statement 1	Process		elicits					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_81_4_550_s_17	9314836	2 3  Nonetheless, binding of Ang II to the AT1 receptor elicits many of the same cellular events induced by mitogens such as PDGF and EGF.	bind
20627	1	6934	6	NULL	NULL	0	NULL	Ang II	NULL		bind	NULL				AT1 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_81_4_550_s_17	9314836	2 3  Nonetheless, binding of Ang II to the AT1 receptor elicits many of the same cellular events induced by mitogens such as PDGF and EGF.	bind
21255	2	6934	6	NULL	NULL	0	NULL	PDGF	NULL		induce	NULL				cellular events	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_81_4_550_s_17	9314836	2 3  Nonetheless, binding of Ang II to the AT1 receptor elicits many of the same cellular events induced by mitogens such as PDGF and EGF.	bind
21256	3	6934	6	NULL	NULL	0	NULL	EGF	NULL		induce	NULL				cellular events	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_81_4_550_s_17	9314836	2 3  Nonetheless, binding of Ang II to the AT1 receptor elicits many of the same cellular events induced by mitogens such as PDGF and EGF.	bind
21257	4	6934	6	NULL	NULL	0	NULL	statement 1	NULL		elicits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_81_4_550_s_17	9314836	2 3  Nonetheless, binding of Ang II to the AT1 receptor elicits many of the same cellular events induced by mitogens such as PDGF and EGF.	bind
21258	5	6934	6	NULL	NULL	0	NULL	statement 1	NULL		elicits	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_81_4_550_s_17	9314836	2 3  Nonetheless, binding of Ang II to the AT1 receptor elicits many of the same cellular events induced by mitogens such as PDGF and EGF.	bind
30681	6	6934	6	NULL	NULL	0	NULL	PDGF	NULL		is a type of	NULL				mitogen	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_81_4_550_s_17	9314836	2 3  Nonetheless, binding of Ang II to the AT1 receptor elicits many of the same cellular events induced by mitogens such as PDGF and EGF.	bind
30682	7	6934	6	NULL	NULL	0	NULL	EGF	NULL		is a type of	NULL				mitogen	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_81_4_550_s_17	9314836	2 3  Nonetheless, binding of Ang II to the AT1 receptor elicits many of the same cellular events induced by mitogens such as PDGF and EGF.	bind
25183	1	6935	5	13	NULL	NULL	NULL	VIIa	GP		bind					TF	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_11_1333_s_15	8911271	2 3 4 5 6  VIIa bound to TF initiates blood coagulation by activating factors IX and X, 7 8 9  a process already observed in the 1960s by Josso and Prou-Wartelle 10  and Nossel.	bind
25184	2	6935	5	13	NULL	NULL	NULL	statement 1	Process		initiates					blood coagulation	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_11_1333_s_15	8911271	2 3 4 5 6  VIIa bound to TF initiates blood coagulation by activating factors IX and X, 7 8 9  a process already observed in the 1960s by Josso and Prou-Wartelle 10  and Nossel.	bind
25185	3	6935	5	13	NULL	NULL	NULL	statement 2	Process		occurs by					factor IX	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_11_1333_s_15	8911271	2 3 4 5 6  VIIa bound to TF initiates blood coagulation by activating factors IX and X, 7 8 9  a process already observed in the 1960s by Josso and Prou-Wartelle 10  and Nossel.	bind
25186	4	6935	5	13	NULL	NULL	NULL	statement 2	Process		occurs by					factor X	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_11_1333_s_15	8911271	2 3 4 5 6  VIIa bound to TF initiates blood coagulation by activating factors IX and X, 7 8 9  a process already observed in the 1960s by Josso and Prou-Wartelle 10  and Nossel.	bind
20628	1	6935	6	NULL	NULL	0	NULL	VIIa	NULL		bind	NULL				TF	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_11_1333_s_15	8911271	2 3 4 5 6  VIIa bound to TF initiates blood coagulation by activating factors IX and X, 7 8 9  a process already observed in the 1960s by Josso and Prou-Wartelle 10  and Nossel.	bind
20629	2	6935	6	NULL	NULL	0	NULL	statement 1	NULL		initiates	NULL				blood coagulation	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_11_1333_s_15	8911271	2 3 4 5 6  VIIa bound to TF initiates blood coagulation by activating factors IX and X, 7 8 9  a process already observed in the 1960s by Josso and Prou-Wartelle 10  and Nossel.	bind
20630	3	6935	6	NULL	NULL	0	NULL	statement 2	NULL		occurs by	NULL				factor IX	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_11_1333_s_15	8911271	2 3 4 5 6  VIIa bound to TF initiates blood coagulation by activating factors IX and X, 7 8 9  a process already observed in the 1960s by Josso and Prou-Wartelle 10  and Nossel.	bind
20631	4	6935	6	NULL	NULL	0	NULL	statement 2	NULL		occurs by	NULL				factor X	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_11_1333_s_15	8911271	2 3 4 5 6  VIIa bound to TF initiates blood coagulation by activating factors IX and X, 7 8 9  a process already observed in the 1960s by Josso and Prou-Wartelle 10  and Nossel.	bind
25187	1	6936	5	13	NULL	NULL	NULL	cTnT	GP		bind		high affinity	NH2-terminal half		actin-Tm	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_5_471_s_146	9734469	2 3 42  As illustrated in Figure 2   and based largely on studies with fsTnT, it is apparent that both the NH2- and COOH-terminal halves of cTnT bind to actin-Tm with high affinity.	bind
25188	2	6936	5	13	NULL	NULL	NULL	cTnT	GP		bind		high affinity	COOH-terminal half		actin-Tm	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_5_471_s_146	9734469	2 3 42  As illustrated in Figure 2   and based largely on studies with fsTnT, it is apparent that both the NH2- and COOH-terminal halves of cTnT bind to actin-Tm with high affinity.	bind
20632	1	6936	6	NULL	NULL	0	NULL	cTnT	NULL		bind	NULL	high affinity	NH2 terminus		actin-Tm	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_5_471_s_146	9734469	2 3 42  As illustrated in Figure 2   and based largely on studies with fsTnT, it is apparent that both the NH2- and COOH-terminal halves of cTnT bind to actin-Tm with high affinity.	bind
20633	2	6936	6	NULL	NULL	0	NULL	cTnT	NULL		bind	NULL	high affinity	COOH terminus		actin-Tm	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_5_471_s_146	9734469	2 3 42  As illustrated in Figure 2   and based largely on studies with fsTnT, it is apparent that both the NH2- and COOH-terminal halves of cTnT bind to actin-Tm with high affinity.	bind
25189	2	6937	5	13	NULL	NULL	NULL	fumonisin B1	Chemical	fungal	inhibits		highly specific			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12587_s_181	11801602	2 A key enzyme in this pathway is CoA-dependent ceramide synthase, and fumonisin B1 is a highly specific fungal inhibitor of this enzyme ( 57,  58).	bind
44795	1	6937	5	13	NULL	NULL	NULL	ceramide synthase	GP		depends on					CoA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12587_s_181	11801602	2 A key enzyme in this pathway is CoA-dependent ceramide synthase, and fumonisin B1 is a highly specific fungal inhibitor of this enzyme ( 57,  58).	bind
20709	2	6937	6	10	NULL	0	NULL	fumonisin B1	NULL	fungal	inhibits	NULL	specifically			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12587_s_181	11801602	2 A key enzyme in this pathway is CoA-dependent ceramide synthase, and fumonisin B1 is a highly specific fungal inhibitor of this enzyme ( 57,  58).	bind
44796	1	6937	6	10	NULL	0	NULL	ceramide synthase	NULL		depends on	NULL				CoA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12587_s_181	11801602	2 A key enzyme in this pathway is CoA-dependent ceramide synthase, and fumonisin B1 is a highly specific fungal inhibitor of this enzyme ( 57,  58).	bind
25190	1	6938	5	13	NULL	NULL	NULL	CHF protein	GP		bind					B- myb	GP			DRS	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_39015_s_289	12147683	2 A protein (CHF) that can bind the B- myb DRS has been purified ( 41); however, evidence that this binding correlates with the sequence requirements for transcriptional corepression is lacking.	bind
56717	2	6938	5	13	NULL	NULL	NULL	statement 1	Process		does not correlate					transcriptional corepression	Process	sequence requirements of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_39015_s_289	12147683	2 A protein (CHF) that can bind the B- myb DRS has been purified ( 41); however, evidence that this binding correlates with the sequence requirements for transcriptional corepression is lacking.	bind
20710	1	6938	6	NULL	NULL	0	NULL	CHF protein	NULL		bind	NULL				B-myb	NULL			DRS	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_41_39015_s_289	12147683	2 A protein (CHF) that can bind the B- myb DRS has been purified ( 41); however, evidence that this binding correlates with the sequence requirements for transcriptional corepression is lacking.	bind
20711	2	6938	6	NULL	NULL	0	NULL	statement 1	NULL		does not correlate	NULL				transcriptional corepression	NULL	sequence requirements of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_41_39015_s_289	12147683	2 A protein (CHF) that can bind the B- myb DRS has been purified ( 41); however, evidence that this binding correlates with the sequence requirements for transcriptional corepression is lacking.	bind
25191	1	6939	5	13	NULL	NULL	NULL	TNFR2	GP		contains			carboxyl-terminal region		T2bs-C	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31572_s_268	16020544	2 A recent study indicated that the same carboxyl-terminal region of TNFR2 that contains T2bs-C binds to the protein tyrosine kinase Etk/mx in endothelial cells ( ).	bind
25192	2	6939	5	13	NULL	NULL	NULL	statement 1	GP		bind					Etk/mx	GP				NULL	in endothelial cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31572_s_268	16020544	2 A recent study indicated that the same carboxyl-terminal region of TNFR2 that contains T2bs-C binds to the protein tyrosine kinase Etk/mx in endothelial cells ( ).	bind
31489	3	6939	5	13	NULL	NULL	NULL	Etk/mx	GP		is a type of					protein tyrosine kinase	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31572_s_268	16020544	2 A recent study indicated that the same carboxyl-terminal region of TNFR2 that contains T2bs-C binds to the protein tyrosine kinase Etk/mx in endothelial cells ( ).	bind
20712	1	6939	6	NULL	NULL	0	NULL	TNFR2	NULL		contains	NULL		carboxyl-terminal region		T2bs-C	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_36_31572_s_268	16020544	2 A recent study indicated that the same carboxyl-terminal region of TNFR2 that contains T2bs-C binds to the protein tyrosine kinase Etk/mx in endothelial cells ( ).	bind
20713	2	6939	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				Etk/mx	NULL				NULL	endothelial cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31572_s_268	16020544	2 A recent study indicated that the same carboxyl-terminal region of TNFR2 that contains T2bs-C binds to the protein tyrosine kinase Etk/mx in endothelial cells ( ).	bind
20714	3	6939	6	NULL	NULL	0	NULL	Etk/mx	NULL		is a type of	NULL				protein tyrosine kinase	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31572_s_268	16020544	2 A recent study indicated that the same carboxyl-terminal region of TNFR2 that contains T2bs-C binds to the protein tyrosine kinase Etk/mx in endothelial cells ( ).	bind
25193	1	6940	5	NULL	NULL	0	NULL		NULL		interacts with	NULL		tryptophan		
\n	NULL		tryptophan		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20337_s_305	10764747	2 A tryptophan-tryptophan interaction may also be involved in mAb 16 binding to the alpha5 subunit because the second CDR loop of the light chain of mAb 16 contains a tryptophan residue (L. Burrows, A. P. Mould, and M. J. Humphries, unpublished results).	bind
25194	2	6940	5	13	NULL	NULL	NULL	mAb 16	GP		bind								alpha5 subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20337_s_305	10764747	2 A tryptophan-tryptophan interaction may also be involved in mAb 16 binding to the alpha5 subunit because the second CDR loop of the light chain of mAb 16 contains a tryptophan residue (L. Burrows, A. P. Mould, and M. J. Humphries, unpublished results).	bind
25195	3	6940	5	13	NULL	NULL	NULL	statement 1	Process		be involved in		may			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20337_s_305	10764747	2 A tryptophan-tryptophan interaction may also be involved in mAb 16 binding to the alpha5 subunit because the second CDR loop of the light chain of mAb 16 contains a tryptophan residue (L. Burrows, A. P. Mould, and M. J. Humphries, unpublished results).	bind
25196	4	6940	5	13	NULL	NULL	NULL	mAb 16	GP		contains			second CDR loop of light chain					tryptophan residue		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20337_s_305	10764747	2 A tryptophan-tryptophan interaction may also be involved in mAb 16 binding to the alpha5 subunit because the second CDR loop of the light chain of mAb 16 contains a tryptophan residue (L. Burrows, A. P. Mould, and M. J. Humphries, unpublished results).	bind
25197	5	6940	5	13	NULL	NULL	NULL	statement 4	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20337_s_305	10764747	2 A tryptophan-tryptophan interaction may also be involved in mAb 16 binding to the alpha5 subunit because the second CDR loop of the light chain of mAb 16 contains a tryptophan residue (L. Burrows, A. P. Mould, and M. J. Humphries, unpublished results).	bind
20715	1	6940	6	NULL	NULL	0	NULL	mAb 16	NULL		bind	NULL				alpha5 subunit	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20337_s_305	10764747	2 A tryptophan-tryptophan interaction may also be involved in mAb 16 binding to the alpha5 subunit because the second CDR loop of the light chain of mAb 16 contains a tryptophan residue (L. Burrows, A. P. Mould, and M. J. Humphries, unpublished results).	bind
20716	2	6940	6	10	NULL	0	NULL				interacts with			tryptophan					tryptophan		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20337_s_305	10764747	2 A tryptophan-tryptophan interaction may also be involved in mAb 16 binding to the alpha5 subunit because the second CDR loop of the light chain of mAb 16 contains a tryptophan residue (L. Burrows, A. P. Mould, and M. J. Humphries, unpublished results).	bind
20717	3	6940	6	10	NULL	0	NULL	statement 2			 be involved in		may			statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20337_s_305	10764747	2 A tryptophan-tryptophan interaction may also be involved in mAb 16 binding to the alpha5 subunit because the second CDR loop of the light chain of mAb 16 contains a tryptophan residue (L. Burrows, A. P. Mould, and M. J. Humphries, unpublished results).	bind
20718	4	6940	6	10	NULL	0	NULL	mAb16 	NULL		contains 	NULL		second CDR loop of light chain			NULL		tryptophan residue		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20337_s_305	10764747	2 A tryptophan-tryptophan interaction may also be involved in mAb 16 binding to the alpha5 subunit because the second CDR loop of the light chain of mAb 16 contains a tryptophan residue (L. Burrows, A. P. Mould, and M. J. Humphries, unpublished results).	bind
20719	5	6940	6	NULL	NULL	0	NULL	statement 3	NULL		is because of	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20337_s_305	10764747	2 A tryptophan-tryptophan interaction may also be involved in mAb 16 binding to the alpha5 subunit because the second CDR loop of the light chain of mAb 16 contains a tryptophan residue (L. Burrows, A. P. Mould, and M. J. Humphries, unpublished results).	bind
25198	1	6941	5	13	NULL	NULL	NULL	HSF	GP		bind					HSF targets	NucleicAcid	identified			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5169_s_67	14612437	2 According to the previously published mRNA expression data ( ), the large majority of the identified HSF targets that are bound by HSF  in vivo are induced by heat shock.	bind
25199	2	6941	5	13	NULL	NULL	NULL	heat shock	ResearchActivity		induces					statement 1	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5169_s_67	14612437	2 According to the previously published mRNA expression data ( ), the large majority of the identified HSF targets that are bound by HSF  in vivo are induced by heat shock.	bind
20720	1	6941	6	10	NULL	0	NULL	HSF			bind					 HSF targets		identified			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5169_s_67	14612437	2 According to the previously published mRNA expression data ( ), the large majority of the identified HSF targets that are bound by HSF  in vivo are induced by heat shock.	bind
20721	2	6941	6	NULL	NULL	0	NULL	heat shock	NULL		induces	NULL				statement 1	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5169_s_67	14612437	2 According to the previously published mRNA expression data ( ), the large majority of the identified HSF targets that are bound by HSF  in vivo are induced by heat shock.	bind
25200	1	6942	5	13	NULL	NULL	NULL	mPER3	GP		bind					mPER1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_45921_s_40	11591712	2 Additionally, mPER3 binding to mPER1 or mPER2 has been shown to contribute to nuclear localization of the heterodimer ( 19).	bind
25201	2	6942	5	13	NULL	NULL	NULL	mPER3	GP		bind					mPER2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_45921_s_40	11591712	2 Additionally, mPER3 binding to mPER1 or mPER2 has been shown to contribute to nuclear localization of the heterodimer ( 19).	bind
25202	3	6942	5	13	NULL	NULL	NULL	statement 1	Process		is localized to					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_45921_s_40	11591712	2 Additionally, mPER3 binding to mPER1 or mPER2 has been shown to contribute to nuclear localization of the heterodimer ( 19).	bind
25203	4	6942	5	13	NULL	NULL	NULL	statement 1	Process		contributes to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_45921_s_40	11591712	2 Additionally, mPER3 binding to mPER1 or mPER2 has been shown to contribute to nuclear localization of the heterodimer ( 19).	bind
25204	5	6942	5	13	NULL	NULL	NULL	statement 2	Process		is localized to					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_45921_s_40	11591712	2 Additionally, mPER3 binding to mPER1 or mPER2 has been shown to contribute to nuclear localization of the heterodimer ( 19).	bind
25205	6	6942	5	13	NULL	NULL	NULL	statement 2	Process		contributes to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_45921_s_40	11591712	2 Additionally, mPER3 binding to mPER1 or mPER2 has been shown to contribute to nuclear localization of the heterodimer ( 19).	bind
20722	1	6942	6	NULL	NULL	0	NULL	mPER3	NULL		bind	NULL				mPER1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_49_45921_s_40	11591712	2 Additionally, mPER3 binding to mPER1 or mPER2 has been shown to contribute to nuclear localization of the heterodimer ( 19).	bind
20723	2	6942	6	NULL	NULL	0	NULL	mPER3	NULL		bind	NULL				mPER2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_49_45921_s_40	11591712	2 Additionally, mPER3 binding to mPER1 or mPER2 has been shown to contribute to nuclear localization of the heterodimer ( 19).	bind
20724	3	6942	6	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_49_45921_s_40	11591712	2 Additionally, mPER3 binding to mPER1 or mPER2 has been shown to contribute to nuclear localization of the heterodimer ( 19).	bind
20725	4	6942	6	NULL	NULL	0	NULL	statement 1	NULL		localizes to	NULL				nucleus	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_45921_s_40	11591712	2 Additionally, mPER3 binding to mPER1 or mPER2 has been shown to contribute to nuclear localization of the heterodimer ( 19).	bind
20726	5	6942	6	NULL	NULL	0	NULL	statement 1	NULL		contribute to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_49_45921_s_40	11591712	2 Additionally, mPER3 binding to mPER1 or mPER2 has been shown to contribute to nuclear localization of the heterodimer ( 19).	bind
20727	7	6942	6	10	NULL	0	NULL	statement 2			contribute to					statement 6					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_45921_s_40	11591712	2 Additionally, mPER3 binding to mPER1 or mPER2 has been shown to contribute to nuclear localization of the heterodimer ( 19).	bind
31180	6	6942	6	10	NULL	0	NULL	statement 2			localizes to					nucleus					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_45921_s_40	11591712	2 Additionally, mPER3 binding to mPER1 or mPER2 has been shown to contribute to nuclear localization of the heterodimer ( 19).	bind
56718	7	6942	6	10	NULL	0	NULL	statement 1			is an alternative to					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_49_45921_s_40	11591712	2 Additionally, mPER3 binding to mPER1 or mPER2 has been shown to contribute to nuclear localization of the heterodimer ( 19).	bind
25206	1	6943	5	13	NULL	NULL	NULL	GR	GP		bind		intrinsically rapidly							GRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_43_39885_s_184	11518712	2 Additionally, we show that GR binding to a GRE is intrinsically rapid but can be altered by association with accessory factors.	bind
25207	3	6943	5	13	NULL	NULL	NULL	statement 2	Process		alters					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_43_39885_s_184	11518712	2 Additionally, we show that GR binding to a GRE is intrinsically rapid but can be altered by association with accessory factors.	bind
31490	2	6943	5	13	NULL	NULL	NULL	statement 1	Process		associate with					accessory factors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_43_39885_s_184	11518712	2 Additionally, we show that GR binding to a GRE is intrinsically rapid but can be altered by association with accessory factors.	bind
20728	1	6943	6	13	NULL	NULL	NULL	GR	GP		bind		intrinsically rapidly							GRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_43_39885_s_184	11518712	2 Additionally, we show that GR binding to a GRE is intrinsically rapid but can be altered by association with accessory factors.	bind
30683	2	6943	6	NULL	NULL	0	NULL	statement 1	NULL		associates with	NULL				accessory factors	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_43_39885_s_184	11518712	2 Additionally, we show that GR binding to a GRE is intrinsically rapid but can be altered by association with accessory factors.	bind
30684	3	6943	6	NULL	NULL	0	NULL	statement 2	NULL		alters	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_43_39885_s_184	11518712	2 Additionally, we show that GR binding to a GRE is intrinsically rapid but can be altered by association with accessory factors.	bind
25208	1	6944	5	13	NULL	NULL	NULL	ADP	Chemical		bind					DnaK	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_12_6643_s_401	9506960	2 ADP and Pi bind to DnaK with  K d values of 0.13 and 0.45 muM, respectively ( 19).	bind
25209	2	6944	5	13	NULL	NULL	NULL	Pi	Chemical		bind					DnaK	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_12_6643_s_401	9506960	2 ADP and Pi bind to DnaK with  K d values of 0.13 and 0.45 muM, respectively ( 19).	bind
20729	1	6944	6	NULL	NULL	0	NULL	ADP	NULL		bind	NULL				DnaK	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_12_6643_s_401	9506960	2 ADP and Pi bind to DnaK with  K d values of 0.13 and 0.45 muM, respectively ( 19).	bind
20730	2	6944	6	NULL	NULL	0	NULL	Pi	NULL		bind	NULL				DnaK	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_12_6643_s_401	9506960	2 ADP and Pi bind to DnaK with  K d values of 0.13 and 0.45 muM, respectively ( 19).	bind
25210	1	6945	5	13	NULL	NULL	NULL	actin-binding proteins	GP		bind		selectively			ATP-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_48_33827_s_174	10567336	2 Although no direct evidence exists for different structures of actin depending on bound nucleotide, it is remarkable that a number of actin-binding proteins display selective binding to either ATP- or ADP-actin.	bind
25211	2	6945	5	13	NULL	NULL	NULL	actin-binding proteins	GP		bind		selectively			ADP-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_48_33827_s_174	10567336	2 Although no direct evidence exists for different structures of actin depending on bound nucleotide, it is remarkable that a number of actin-binding proteins display selective binding to either ATP- or ADP-actin.	bind
25212	3	6945	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_48_33827_s_174	10567336	2 Although no direct evidence exists for different structures of actin depending on bound nucleotide, it is remarkable that a number of actin-binding proteins display selective binding to either ATP- or ADP-actin.	bind
20778	1	6945	6	NULL	NULL	0	NULL	actin-binding proteins	NULL		bind	NULL	selectively			ATP-actin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_48_33827_s_174	10567336	2 Although no direct evidence exists for different structures of actin depending on bound nucleotide, it is remarkable that a number of actin-binding proteins display selective binding to either ATP- or ADP-actin.	bind
20780	2	6945	6	NULL	NULL	0	NULL	actin-binding proteins	NULL		bind	NULL	selectively			ADP-actin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_48_33827_s_174	10567336	2 Although no direct evidence exists for different structures of actin depending on bound nucleotide, it is remarkable that a number of actin-binding proteins display selective binding to either ATP- or ADP-actin.	bind
56719	3	6945	6	10	NULL	0	NULL	statement 1			is an alternative to					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_48_33827_s_174	10567336	2 Although no direct evidence exists for different structures of actin depending on bound nucleotide, it is remarkable that a number of actin-binding proteins display selective binding to either ATP- or ADP-actin.	bind
25213	1	6947	5	13	NULL	NULL	NULL	HMG-1 peptide	GP		bind		preferentially			supercoiled DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_46_35699_s_214	10962007	2 Although transitional relieving the torsional stress in the supercoiled plasmid (without changing the linking number) by the AB didomain is not excluded (see Ref.  11), the extent of contribution of gel retardation to the "`topoisomer-like"` ladder by preferential binding of the HMG-1 peptide to supercoiled DNA (Fig.  7 c and also Ref.  21) awaits further investigation (see "`Discussion"`).	bind
20784	1	6947	6	10	NULL	0	NULL	HMG-1 peptide	NULL		bind	NULL	preferentially			supercoiled DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_46_35699_s_214	10962007	2 Although transitional relieving the torsional stress in the supercoiled plasmid (without changing the linking number) by the AB didomain is not excluded (see Ref.  11), the extent of contribution of gel retardation to the "`topoisomer-like"` ladder by preferential binding of the HMG-1 peptide to supercoiled DNA (Fig.  7 c and also Ref.  21) awaits further investigation (see "`Discussion"`).	bind
25214	1	6948	5	13	NULL	NULL	NULL	factor Xa	GP		bind		cooperatively			EPR-1	GP	vascular cell			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8340_s_150	9079657	2 Altogether, these data suggest a cooperative model of factor Xa binding to vascular cell EPR-1, potentially involving an initial Gla-dependent contact stabilized by an high affinity recognition of the inter-EGF sequence 83-88, and followed by an as yet unidentified step of local proteolysis by cell surface-bound factor Xa for downstream signal transduction events and effector responses ( 19).	bind
28379	2	6948	5	13	NULL	NULL	NULL	statement 1	Process		involve		potentially			Gla-dependent contact	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8340_s_150	9079657	2 Altogether, these data suggest a cooperative model of factor Xa binding to vascular cell EPR-1, potentially involving an initial Gla-dependent contact stabilized by an high affinity recognition of the inter-EGF sequence 83-88, and followed by an as yet unidentified step of local proteolysis by cell surface-bound factor Xa for downstream signal transduction events and effector responses ( 19).	bind
28380	3	6948	5	13	NULL	NULL	NULL	Gla-dependent contact	Process		is stabilized by							high affinity recognition of	inter-EGF sequence		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8340_s_150	9079657	2 Altogether, these data suggest a cooperative model of factor Xa binding to vascular cell EPR-1, potentially involving an initial Gla-dependent contact stabilized by an high affinity recognition of the inter-EGF sequence 83-88, and followed by an as yet unidentified step of local proteolysis by cell surface-bound factor Xa for downstream signal transduction events and effector responses ( 19).	bind
28381	4	6948	5	13	NULL	NULL	NULL	statement 2	Process		is followed by					local proteolysis	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8340_s_150	9079657	2 Altogether, these data suggest a cooperative model of factor Xa binding to vascular cell EPR-1, potentially involving an initial Gla-dependent contact stabilized by an high affinity recognition of the inter-EGF sequence 83-88, and followed by an as yet unidentified step of local proteolysis by cell surface-bound factor Xa for downstream signal transduction events and effector responses ( 19).	bind
28383	6	6948	5	13	NULL	NULL	NULL	statement 5	Process		is required for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8340_s_150	9079657	2 Altogether, these data suggest a cooperative model of factor Xa binding to vascular cell EPR-1, potentially involving an initial Gla-dependent contact stabilized by an high affinity recognition of the inter-EGF sequence 83-88, and followed by an as yet unidentified step of local proteolysis by cell surface-bound factor Xa for downstream signal transduction events and effector responses ( 19).	bind
28391	7	6948	5	13	NULL	NULL	NULL	statement 4	Process		leads to					signal transduction events	Process	downstream			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8340_s_150	9079657	2 Altogether, these data suggest a cooperative model of factor Xa binding to vascular cell EPR-1, potentially involving an initial Gla-dependent contact stabilized by an high affinity recognition of the inter-EGF sequence 83-88, and followed by an as yet unidentified step of local proteolysis by cell surface-bound factor Xa for downstream signal transduction events and effector responses ( 19).	bind
28394	8	6948	5	13	NULL	NULL	NULL	statement 4	Process		leads to					effector responses	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8340_s_150	9079657	2 Altogether, these data suggest a cooperative model of factor Xa binding to vascular cell EPR-1, potentially involving an initial Gla-dependent contact stabilized by an high affinity recognition of the inter-EGF sequence 83-88, and followed by an as yet unidentified step of local proteolysis by cell surface-bound factor Xa for downstream signal transduction events and effector responses ( 19).	bind
44797	5	6948	5	13	NULL	NULL	NULL	factor Xa	GP		bind					cell surface	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8340_s_150	9079657	2 Altogether, these data suggest a cooperative model of factor Xa binding to vascular cell EPR-1, potentially involving an initial Gla-dependent contact stabilized by an high affinity recognition of the inter-EGF sequence 83-88, and followed by an as yet unidentified step of local proteolysis by cell surface-bound factor Xa for downstream signal transduction events and effector responses ( 19).	bind
20787	1	6948	6	13	NULL	NULL	NULL	factor Xa	GP		bind					EPR-1	GP	vascular cell			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8340_s_150	9079657	2 Altogether, these data suggest a cooperative model of factor Xa binding to vascular cell EPR-1, potentially involving an initial Gla-dependent contact stabilized by an high affinity recognition of the inter-EGF sequence 83-88, and followed by an as yet unidentified step of local proteolysis by cell surface-bound factor Xa for downstream signal transduction events and effector responses ( 19).	bind
21185	5	6948	6	10	NULL	0	NULL	statement 3			followed by					local proteolysis					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8340_s_150	9079657	2 Altogether, these data suggest a cooperative model of factor Xa binding to vascular cell EPR-1, potentially involving an initial Gla-dependent contact stabilized by an high affinity recognition of the inter-EGF sequence 83-88, and followed by an as yet unidentified step of local proteolysis by cell surface-bound factor Xa for downstream signal transduction events and effector responses ( 19).	bind
21551	3	6948	6	NULL	NULL	0	NULL	Gla dependent contact	NULL		is involved in	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_13_8340_s_150	9079657	2 Altogether, these data suggest a cooperative model of factor Xa binding to vascular cell EPR-1, potentially involving an initial Gla-dependent contact stabilized by an high affinity recognition of the inter-EGF sequence 83-88, and followed by an as yet unidentified step of local proteolysis by cell surface-bound factor Xa for downstream signal transduction events and effector responses ( 19).	bind
21552	4	6948	6	10	NULL	0	NULL	statement 3			is stabilized by							high affinity recognition of	inter-EGF sequence 83-88		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8340_s_150	9079657	2 Altogether, these data suggest a cooperative model of factor Xa binding to vascular cell EPR-1, potentially involving an initial Gla-dependent contact stabilized by an high affinity recognition of the inter-EGF sequence 83-88, and followed by an as yet unidentified step of local proteolysis by cell surface-bound factor Xa for downstream signal transduction events and effector responses ( 19).	bind
21553	6	6948	6	10	NULL	0	NULL	statement 2			is required for					statement 5					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8340_s_150	9079657	2 Altogether, these data suggest a cooperative model of factor Xa binding to vascular cell EPR-1, potentially involving an initial Gla-dependent contact stabilized by an high affinity recognition of the inter-EGF sequence 83-88, and followed by an as yet unidentified step of local proteolysis by cell surface-bound factor Xa for downstream signal transduction events and effector responses ( 19).	bind
44798	2	6948	6	10	NULL	0	NULL	factor Xa	NULL		bind	NULL				cell surface	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_13_8340_s_150	9079657	2 Altogether, these data suggest a cooperative model of factor Xa binding to vascular cell EPR-1, potentially involving an initial Gla-dependent contact stabilized by an high affinity recognition of the inter-EGF sequence 83-88, and followed by an as yet unidentified step of local proteolysis by cell surface-bound factor Xa for downstream signal transduction events and effector responses ( 19).	bind
56790	7	6948	6	10	NULL	0	NULL	statement 5			lead to					signal transduction events		downstream			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_13_8340_s_150	9079657	2 Altogether, these data suggest a cooperative model of factor Xa binding to vascular cell EPR-1, potentially involving an initial Gla-dependent contact stabilized by an high affinity recognition of the inter-EGF sequence 83-88, and followed by an as yet unidentified step of local proteolysis by cell surface-bound factor Xa for downstream signal transduction events and effector responses ( 19).	bind
56791	8	6948	6	10	NULL	0	NULL	statement 5			lead to					effector responses					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_13_8340_s_150	9079657	2 Altogether, these data suggest a cooperative model of factor Xa binding to vascular cell EPR-1, potentially involving an initial Gla-dependent contact stabilized by an high affinity recognition of the inter-EGF sequence 83-88, and followed by an as yet unidentified step of local proteolysis by cell surface-bound factor Xa for downstream signal transduction events and effector responses ( 19).	bind
25215	1	6949	5	13	NULL	NULL	NULL	Gal80p	GP		undergoes					dimerization	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13485_s_20	16524886	2 An inhibitory protein Gal80p dimerizes and binds to nuclear Gal4p in the absence of galactose, preventing recruitment of activator proteins by Gal4p and effectively repressing gene expression.	bind
25216	2	6949	5	13	NULL	NULL	NULL	statement 1	GP		bind					Gal4p	GP	nuclear			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13485_s_20	16524886	2 An inhibitory protein Gal80p dimerizes and binds to nuclear Gal4p in the absence of galactose, preventing recruitment of activator proteins by Gal4p and effectively repressing gene expression.	bind
25217	3	6949	5	13	NULL	NULL	NULL	statement 2	Process		in the absence of					galactose	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13485_s_20	16524886	2 An inhibitory protein Gal80p dimerizes and binds to nuclear Gal4p in the absence of galactose, preventing recruitment of activator proteins by Gal4p and effectively repressing gene expression.	bind
25218	4	6949	5	13	NULL	NULL	NULL	Gal4p	GP		recruits					activator proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13485_s_20	16524886	2 An inhibitory protein Gal80p dimerizes and binds to nuclear Gal4p in the absence of galactose, preventing recruitment of activator proteins by Gal4p and effectively repressing gene expression.	bind
25219	5	6949	5	13	NULL	NULL	NULL	statement 3	Process		prevents					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13485_s_20	16524886	2 An inhibitory protein Gal80p dimerizes and binds to nuclear Gal4p in the absence of galactose, preventing recruitment of activator proteins by Gal4p and effectively repressing gene expression.	bind
25220	6	6949	5	13	NULL	NULL	NULL	statement 3	Process		represses		effectively			gene expression	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13485_s_20	16524886	2 An inhibitory protein Gal80p dimerizes and binds to nuclear Gal4p in the absence of galactose, preventing recruitment of activator proteins by Gal4p and effectively repressing gene expression.	bind
44799	7	6949	5	13	NULL	NULL	NULL	Gal80p	GP		is a type of					inhibitory protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13485_s_20	16524886	2 An inhibitory protein Gal80p dimerizes and binds to nuclear Gal4p in the absence of galactose, preventing recruitment of activator proteins by Gal4p and effectively repressing gene expression.	bind
20789	2	6949	6	10	NULL	0	NULL	statement 1			bind					Gal4p		nuclear			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13485_s_20	16524886	2 An inhibitory protein Gal80p dimerizes and binds to nuclear Gal4p in the absence of galactose, preventing recruitment of activator proteins by Gal4p and effectively repressing gene expression.	bind
20911	1	6949	6	10	NULL	0	NULL	Gal80p			bind					Gal80p					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13485_s_20	16524886	2 An inhibitory protein Gal80p dimerizes and binds to nuclear Gal4p in the absence of galactose, preventing recruitment of activator proteins by Gal4p and effectively repressing gene expression.	bind
20912	3	6949	6	10	NULL	0	NULL	statement 2			occurs in absence of					galactose					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13485_s_20	16524886	2 An inhibitory protein Gal80p dimerizes and binds to nuclear Gal4p in the absence of galactose, preventing recruitment of activator proteins by Gal4p and effectively repressing gene expression.	bind
20914	4	6949	6	10	NULL	0	NULL	Gal4p			recruits					activator proteins					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13485_s_20	16524886	2 An inhibitory protein Gal80p dimerizes and binds to nuclear Gal4p in the absence of galactose, preventing recruitment of activator proteins by Gal4p and effectively repressing gene expression.	bind
20916	5	6949	6	10	NULL	0	NULL	statement 2			prevents					statement 4					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13485_s_20	16524886	2 An inhibitory protein Gal80p dimerizes and binds to nuclear Gal4p in the absence of galactose, preventing recruitment of activator proteins by Gal4p and effectively repressing gene expression.	bind
20924	6	6949	6	10	NULL	0	NULL	statement 2			repress		effectively			gene expression					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13485_s_20	16524886	2 An inhibitory protein Gal80p dimerizes and binds to nuclear Gal4p in the absence of galactose, preventing recruitment of activator proteins by Gal4p and effectively repressing gene expression.	bind
44800	7	6949	6	10	NULL	0	NULL	Ga180p			is a type of					inhibitory protein					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13485_s_20	16524886	2 An inhibitory protein Gal80p dimerizes and binds to nuclear Gal4p in the absence of galactose, preventing recruitment of activator proteins by Gal4p and effectively repressing gene expression.	bind
25221	1	6950	5	13	NULL	NULL	NULL	Grb2	GP		bind					TrkA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18225_s_134	10748052	2 and  19) providing further evidence that Grb2 binds to TrkA independently of Shc/FRS-2.	bind
25222	2	6950	5	13	NULL	NULL	NULL	statement 1	Process		is independent of					Shc/FRS-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18225_s_134	10748052	2 and  19) providing further evidence that Grb2 binds to TrkA independently of Shc/FRS-2.	bind
20928	1	6950	6	NULL	NULL	0	NULL	Grb2	NULL		bind	NULL				TrkA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_24_18225_s_134	10748052	2 and  19) providing further evidence that Grb2 binds to TrkA independently of Shc/FRS-2.	bind
20929	2	6950	6	NULL	NULL	0	NULL	statement 1	NULL		is independent of	NULL				Shc/FRS-2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_24_18225_s_134	10748052	2 and  19) providing further evidence that Grb2 binds to TrkA independently of Shc/FRS-2.	bind
25226	1	6952	5	13	NULL	NULL	NULL	octasccharides	Chemical	3H- labeled	bind					FGF-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_33_30744_s_90	11406624	2 Approximately 25% of the 3H-labeled octasaccharides derived from intestinal HS bound to the FGF-1 column at physiological ionic strength.	bind
31491	2	6952	5	13	NULL	NULL	NULL	octasaccharides	Chemical	3H-labeled	derived from					HS	Chemical	intestinal			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_33_30744_s_90	11406624	2 Approximately 25% of the 3H-labeled octasaccharides derived from intestinal HS bound to the FGF-1 column at physiological ionic strength.	bind
31492	3	6952	5	13	NULL	NULL	NULL	statement 1	Process		occurs at					physiological ionic strength	QuantityOrMeasure				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_33_30744_s_90	11406624	2 Approximately 25% of the 3H-labeled octasaccharides derived from intestinal HS bound to the FGF-1 column at physiological ionic strength.	bind
20932	1	6952	6	10	NULL	0	NULL	octasaccharides		3H-labeled	derived from					 HS		intestinal			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_33_30744_s_90	11406624	2 Approximately 25% of the 3H-labeled octasaccharides derived from intestinal HS bound to the FGF-1 column at physiological ionic strength.	bind
20933	2	6952	6	NULL	NULL	0	NULL	octasaccharides	NULL	3H-labeled	bind	NULL				FGF-1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_33_30744_s_90	11406624	2 Approximately 25% of the 3H-labeled octasaccharides derived from intestinal HS bound to the FGF-1 column at physiological ionic strength.	bind
20947	3	6952	6	10	NULL	0	NULL	statement 2			occurs at					physiological ionic strength					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_33_30744_s_90	11406624	2 Approximately 25% of the 3H-labeled octasaccharides derived from intestinal HS bound to the FGF-1 column at physiological ionic strength.	bind
25227	1	6954	5	13	NULL	NULL	NULL	GST-GRK5 	GP		bind			1-200		calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_29_18273_s_203	9218466	2 As expected, the 1-200- and 20-39-containing GST-GRK5 fusion proteins bound to calmodulin, whereas the 98-136 and 50-200 fusions did not.	bind
31496	2	6954	5	13	NULL	NULL	NULL	GST-GRK5 	GP		bind			20-39		calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_29_18273_s_203	9218466	2 As expected, the 1-200- and 20-39-containing GST-GRK5 fusion proteins bound to calmodulin, whereas the 98-136 and 50-200 fusions did not.	bind
31497	3	6954	5	13	NULL	NULL	NULL	GST-GRK5 	GP		does not bind			98-136		calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_29_18273_s_203	9218466	2 As expected, the 1-200- and 20-39-containing GST-GRK5 fusion proteins bound to calmodulin, whereas the 98-136 and 50-200 fusions did not.	bind
31499	4	6954	5	13	NULL	NULL	NULL	GST-GRK5 	GP		does not bind			50-200		calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_29_18273_s_203	9218466	2 As expected, the 1-200- and 20-39-containing GST-GRK5 fusion proteins bound to calmodulin, whereas the 98-136 and 50-200 fusions did not.	bind
44801	5	6954	5	13	NULL	NULL	NULL	GST-GRK5	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_29_18273_s_203	9218466	2 As expected, the 1-200- and 20-39-containing GST-GRK5 fusion proteins bound to calmodulin, whereas the 98-136 and 50-200 fusions did not.	bind
20948	1	6954	6	10	NULL	0	NULL	GST-GRK5 	NULL		bind	NULL		1-200		calmodulin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_29_18273_s_203	9218466	2 As expected, the 1-200- and 20-39-containing GST-GRK5 fusion proteins bound to calmodulin, whereas the 98-136 and 50-200 fusions did not.	bind
20949	2	6954	6	10	NULL	0	NULL	GST-GRK5	NULL		bind	NULL		20-39		calmodulin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_29_18273_s_203	9218466	2 As expected, the 1-200- and 20-39-containing GST-GRK5 fusion proteins bound to calmodulin, whereas the 98-136 and 50-200 fusions did not.	bind
20950	3	6954	6	10	NULL	0	NULL	GST-GRK5	NULL		does not bind	NULL		98-136		calmodulin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_29_18273_s_203	9218466	2 As expected, the 1-200- and 20-39-containing GST-GRK5 fusion proteins bound to calmodulin, whereas the 98-136 and 50-200 fusions did not.	bind
20951	4	6954	6	10	NULL	0	NULL	GST-GRK5 	NULL		does not bind	NULL		50-200		calmodulin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_29_18273_s_203	9218466	2 As expected, the 1-200- and 20-39-containing GST-GRK5 fusion proteins bound to calmodulin, whereas the 98-136 and 50-200 fusions did not.	bind
44802	5	6954	6	10	NULL	0	NULL	GST-GRK5	NULL		is a type of	NULL				fusion protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_29_18273_s_203	9218466	2 As expected, the 1-200- and 20-39-containing GST-GRK5 fusion proteins bound to calmodulin, whereas the 98-136 and 50-200 fusions did not.	bind
25228	1	6955	5	13	NULL	NULL	NULL	Vps21p	GP		bind			S21N		GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_15284_s_126	10329739	2 As shown in Fig.  1 B, Vps21p-S21N bound substantially more GDP (26 pmol) than GTP (<2 pmol).	bind
25229	2	6955	5	13	NULL	NULL	NULL	Vps21p	GP		bind			S21N		GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_15284_s_126	10329739	2 As shown in Fig.  1 B, Vps21p-S21N bound substantially more GDP (26 pmol) than GTP (<2 pmol).	bind
25230	3	6955	5	13	NULL	NULL	NULL	statement 1	Process		more than		substantially			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_15284_s_126	10329739	2 As shown in Fig.  1 B, Vps21p-S21N bound substantially more GDP (26 pmol) than GTP (<2 pmol).	bind
20952	1	6955	6	NULL	NULL	0	NULL	Vps21p	NULL		bind	NULL		S21N		GDP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_15284_s_126	10329739	2 As shown in Fig.  1 B, Vps21p-S21N bound substantially more GDP (26 pmol) than GTP (<2 pmol).	bind
20953	2	6955	6	NULL	NULL	0	NULL	Vps21p	NULL		bind	NULL		S21N		GTP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_15284_s_126	10329739	2 As shown in Fig.  1 B, Vps21p-S21N bound substantially more GDP (26 pmol) than GTP (<2 pmol).	bind
20954	3	6955	6	10	NULL	0	NULL	statement 1			is more than		substantially			statement 2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_15284_s_126	10329739	2 As shown in Fig.  1 B, Vps21p-S21N bound substantially more GDP (26 pmol) than GTP (<2 pmol).	bind
25231	1	6956	5	13	NULL	NULL	NULL	TGF-beta1	GP		bind					TbetaRII	GP	soluble			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_48_30656_s_87	8940041	2 As shown in Fig.  1, TGF-beta1 binds soluble TbetaRII at all of the different coating concentrations, whereas under the same conditions, the binding of TGF-beta2 is detectable only at the highest coating concentration of TbetaRII (100 ng/well).	bind
25232	2	6956	5	13	NULL	NULL	NULL	TGF-beta2	GP		bind					TbetaRII	GP	soluble			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_48_30656_s_87	8940041	2 As shown in Fig.  1, TGF-beta1 binds soluble TbetaRII at all of the different coating concentrations, whereas under the same conditions, the binding of TGF-beta2 is detectable only at the highest coating concentration of TbetaRII (100 ng/well).	bind
20955	1	6956	6	NULL	NULL	0	NULL	TGF-beta1	NULL		bind	NULL				TbetaRII	NULL	soluble			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_48_30656_s_87	8940041	2 As shown in Fig.  1, TGF-beta1 binds soluble TbetaRII at all of the different coating concentrations, whereas under the same conditions, the binding of TGF-beta2 is detectable only at the highest coating concentration of TbetaRII (100 ng/well).	bind
30685	2	6956	6	NULL	NULL	0	NULL	TGF-beta2	NULL		bind	NULL				TbetaRII	NULL	soluble			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_48_30656_s_87	8940041	2 As shown in Fig.  1, TGF-beta1 binds soluble TbetaRII at all of the different coating concentrations, whereas under the same conditions, the binding of TGF-beta2 is detectable only at the highest coating concentration of TbetaRII (100 ng/well).	bind
25234	1	6957	5	13	NULL	NULL	NULL	Csk	GP	purified	bind					Syk	GP	endogenous			NULL	DT40 whole-cell extracts	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_27_17209_s_158	9202044	2 As shown in Fig.  5 B, purified Csk, Lyn, and Btk bound to the endogenous Syk from the DT40 whole-cell extracts, while a control His6-tagged protein (NF-AT-His6, a T-cell-specific transcription factor) did not.	bind
25235	2	6957	5	13	NULL	NULL	NULL	Lyn	GP	purified	bind					Syk	GP	endogenous			NULL	DT40 whole-cell extracts	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_27_17209_s_158	9202044	2 As shown in Fig.  5 B, purified Csk, Lyn, and Btk bound to the endogenous Syk from the DT40 whole-cell extracts, while a control His6-tagged protein (NF-AT-His6, a T-cell-specific transcription factor) did not.	bind
25236	3	6957	5	13	NULL	NULL	NULL	Btk	GP	purified	bind					Syk	GP	endogenous			NULL	DT40 whole-cell extracts	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_27_17209_s_158	9202044	2 As shown in Fig.  5 B, purified Csk, Lyn, and Btk bound to the endogenous Syk from the DT40 whole-cell extracts, while a control His6-tagged protein (NF-AT-His6, a T-cell-specific transcription factor) did not.	bind
25237	4	6957	5	13	NULL	NULL	NULL	NF-AT-His6	GP		does not bind					Syk	GP	endogenous			NULL	DT40 whole-cell extracts	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_27_17209_s_158	9202044	2 As shown in Fig.  5 B, purified Csk, Lyn, and Btk bound to the endogenous Syk from the DT40 whole-cell extracts, while a control His6-tagged protein (NF-AT-His6, a T-cell-specific transcription factor) did not.	bind
31501	5	6957	5	13	NULL	NULL	NULL	NF-AT-His6	GP		is a type of					T-cell-specific transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_27_17209_s_158	9202044	2 As shown in Fig.  5 B, purified Csk, Lyn, and Btk bound to the endogenous Syk from the DT40 whole-cell extracts, while a control His6-tagged protein (NF-AT-His6, a T-cell-specific transcription factor) did not.	bind
20956	1	6957	6	NULL	NULL	0	NULL	Csk	NULL	purified	bind	NULL				Syk	NULL	endogenous			NULL	DT40 whole-cell extracts	0	NULL	NULL	NULL	gw60_jbiolchem_272_27_17209_s_158	9202044	2 As shown in Fig.  5 B, purified Csk, Lyn, and Btk bound to the endogenous Syk from the DT40 whole-cell extracts, while a control His6-tagged protein (NF-AT-His6, a T-cell-specific transcription factor) did not.	bind
20957	2	6957	6	NULL	NULL	0	NULL	Lyn	NULL	purified	bind	NULL				Syk	NULL	endogenous			NULL	DT40 whole-cell extracts	0	NULL	NULL	NULL	gw60_jbiolchem_272_27_17209_s_158	9202044	2 As shown in Fig.  5 B, purified Csk, Lyn, and Btk bound to the endogenous Syk from the DT40 whole-cell extracts, while a control His6-tagged protein (NF-AT-His6, a T-cell-specific transcription factor) did not.	bind
20958	3	6957	6	NULL	NULL	0	NULL	Btk	NULL	purified	bind	NULL				Syk	NULL	endogenous			NULL	DT40 whole-cell extracts	0	NULL	NULL	NULL	gw60_jbiolchem_272_27_17209_s_158	9202044	2 As shown in Fig.  5 B, purified Csk, Lyn, and Btk bound to the endogenous Syk from the DT40 whole-cell extracts, while a control His6-tagged protein (NF-AT-His6, a T-cell-specific transcription factor) did not.	bind
20959	4	6957	6	NULL	NULL	0	NULL	NF-AT-His6	NULL		is a type of	NULL				T-cell-specific transcription factor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_27_17209_s_158	9202044	2 As shown in Fig.  5 B, purified Csk, Lyn, and Btk bound to the endogenous Syk from the DT40 whole-cell extracts, while a control His6-tagged protein (NF-AT-His6, a T-cell-specific transcription factor) did not.	bind
20960	5	6957	6	NULL	NULL	0	NULL	NF-AT-His6	NULL		does not bind	NULL				Syk	NULL	endogenous			NULL	DT40 whole-cell extracts	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_27_17209_s_158	9202044	2 As shown in Fig.  5 B, purified Csk, Lyn, and Btk bound to the endogenous Syk from the DT40 whole-cell extracts, while a control His6-tagged protein (NF-AT-His6, a T-cell-specific transcription factor) did not.	bind
25238	1	6958	5	13	NULL	NULL	NULL	Rab7	GP		bind					REP-1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_52_48637_s_224	11675392	2 At low concentrations of components, when the dissociation rates govern the kinetics, binding of Rab7 to REP-1 and the second prenylation step would become rate-limiting (Scheme  1).	bind
20961	1	6958	6	NULL	NULL	0	NULL	Rab7	NULL		bind	NULL				REP-1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_52_48637_s_224	11675392	2 At low concentrations of components, when the dissociation rates govern the kinetics, binding of Rab7 to REP-1 and the second prenylation step would become rate-limiting (Scheme  1).	bind
25241	1	6959	5	13	NULL	NULL	NULL	hRAD51 NPF	GP		bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_29_30385_s_298	15123651	2 Based on its ADP ATP exchange activity, these observations suggest that hXRCC2 promotes the ATP-bound form of the hRAD51 NPF.	bind
25242	2	6959	5	13	NULL	NULL	NULL	hXRCC2	GP		promotes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_29_30385_s_298	15123651	2 Based on its ADP ATP exchange activity, these observations suggest that hXRCC2 promotes the ATP-bound form of the hRAD51 NPF.	bind
20962	1	6959	6	NULL	NULL	0	NULL	hRAD51 NPF	NULL		bind	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_29_30385_s_298	15123651	2 Based on its ADP ATP exchange activity, these observations suggest that hXRCC2 promotes the ATP-bound form of the hRAD51 NPF.	bind
20963	2	6959	6	NULL	NULL	0	NULL	hXRCC2	NULL		promotes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_29_30385_s_298	15123651	2 Based on its ADP ATP exchange activity, these observations suggest that hXRCC2 promotes the ATP-bound form of the hRAD51 NPF.	bind
25243	1	6960	5	13	NULL	NULL	NULL	eIF4E	GP	mutations in	effects		differentially			eIF4G	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_27	10409688	2 Based on the findings that mutations in eIF4E have differential effects on the binding of eIF4G and Caf20p, it has been suggested that the interactions of eIF4G and the 4E-BPs with eIF4E are not limited to the eIF4E binding peptide ( 19).	bind
25244	2	6960	5	13	NULL	NULL	NULL	eIF4E	GP	mutations in	effects		differentially			Caf20p	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_27	10409688	2 Based on the findings that mutations in eIF4E have differential effects on the binding of eIF4G and Caf20p, it has been suggested that the interactions of eIF4G and the 4E-BPs with eIF4E are not limited to the eIF4E binding peptide ( 19).	bind
25245	3	6960	5	13	NULL	NULL	NULL	eIF4G	GP		interacts with					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_27	10409688	2 Based on the findings that mutations in eIF4E have differential effects on the binding of eIF4G and Caf20p, it has been suggested that the interactions of eIF4G and the 4E-BPs with eIF4E are not limited to the eIF4E binding peptide ( 19).	bind
25246	4	6960	5	13	NULL	NULL	NULL	statement 3	Process		is not limited to					eIF4E binding peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_27	10409688	2 Based on the findings that mutations in eIF4E have differential effects on the binding of eIF4G and Caf20p, it has been suggested that the interactions of eIF4G and the 4E-BPs with eIF4E are not limited to the eIF4E binding peptide ( 19).	bind
25247	5	6960	5	13	NULL	NULL	NULL	4E-BPs	GP		interacts with					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_27	10409688	2 Based on the findings that mutations in eIF4E have differential effects on the binding of eIF4G and Caf20p, it has been suggested that the interactions of eIF4G and the 4E-BPs with eIF4E are not limited to the eIF4E binding peptide ( 19).	bind
25248	6	6960	5	13	NULL	NULL	NULL	statement 5	Process		is not limited to					eIF4E binding peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_27	10409688	2 Based on the findings that mutations in eIF4E have differential effects on the binding of eIF4G and Caf20p, it has been suggested that the interactions of eIF4G and the 4E-BPs with eIF4E are not limited to the eIF4E binding peptide ( 19).	bind
20965	1	6960	6	10	NULL	0	NULL	eIF4E		mutations in	effects		differentially			eIF4G		binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_27	10409688	2 Based on the findings that mutations in eIF4E have differential effects on the binding of eIF4G and Caf20p, it has been suggested that the interactions of eIF4G and the 4E-BPs with eIF4E are not limited to the eIF4E binding peptide ( 19).	bind
20966	2	6960	6	10	NULL	0	NULL	eIF4E		mutations in	effect		differentially			Caf20p		binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_27	10409688	2 Based on the findings that mutations in eIF4E have differential effects on the binding of eIF4G and Caf20p, it has been suggested that the interactions of eIF4G and the 4E-BPs with eIF4E are not limited to the eIF4E binding peptide ( 19).	bind
20967	3	6960	6	NULL	NULL	0	NULL	eIF4G	NULL		interacts with	NULL				eIF4E	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_27	10409688	2 Based on the findings that mutations in eIF4E have differential effects on the binding of eIF4G and Caf20p, it has been suggested that the interactions of eIF4G and the 4E-BPs with eIF4E are not limited to the eIF4E binding peptide ( 19).	bind
20968	4	6960	6	NULL	NULL	0	NULL	4E-BP	NULL		interacts with	NULL				eIF4E	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_27	10409688	2 Based on the findings that mutations in eIF4E have differential effects on the binding of eIF4G and Caf20p, it has been suggested that the interactions of eIF4G and the 4E-BPs with eIF4E are not limited to the eIF4E binding peptide ( 19).	bind
20969	5	6960	6	NULL	NULL	0	NULL	statement 3	NULL		is not limited to	NULL				eIF4E binding peptide	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_27	10409688	2 Based on the findings that mutations in eIF4E have differential effects on the binding of eIF4G and Caf20p, it has been suggested that the interactions of eIF4G and the 4E-BPs with eIF4E are not limited to the eIF4E binding peptide ( 19).	bind
20970	6	6960	6	NULL	NULL	0	NULL	statement 4	NULL		is not limited to	NULL				eIF4E binding peptide	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_27	10409688	2 Based on the findings that mutations in eIF4E have differential effects on the binding of eIF4G and Caf20p, it has been suggested that the interactions of eIF4G and the 4E-BPs with eIF4E are not limited to the eIF4E binding peptide ( 19).	bind
25249	1	6961	5	13	NULL	NULL	NULL	Rtg2p	GP		does not bind					Rtg1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19801_s_159	9242640	2 Based on two-hybrid analysis carried out in the current study, we conclude that Rtg2p neither binds to Rtg1p or Rtg3p nor is required for the  direct interaction of these transcription factors with each other.	bind
25250	2	6961	5	13	NULL	NULL	NULL	Rtg2p	GP		does not bind					Rtg3p	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19801_s_159	9242640	2 Based on two-hybrid analysis carried out in the current study, we conclude that Rtg2p neither binds to Rtg1p or Rtg3p nor is required for the  direct interaction of these transcription factors with each other.	bind
25252	3	6961	5	13	NULL	NULL	NULL	Rtg1p	GP		interacts with		directly			Rtg3p	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19801_s_159	9242640	2 Based on two-hybrid analysis carried out in the current study, we conclude that Rtg2p neither binds to Rtg1p or Rtg3p nor is required for the  direct interaction of these transcription factors with each other.	bind
25253	4	6961	5	13	NULL	NULL	NULL	Rtg2p	GP		is not required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19801_s_159	9242640	2 Based on two-hybrid analysis carried out in the current study, we conclude that Rtg2p neither binds to Rtg1p or Rtg3p nor is required for the  direct interaction of these transcription factors with each other.	bind
31506	5	6961	5	13	NULL	NULL	NULL	Rtg2p	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19801_s_159	9242640	2 Based on two-hybrid analysis carried out in the current study, we conclude that Rtg2p neither binds to Rtg1p or Rtg3p nor is required for the  direct interaction of these transcription factors with each other.	bind
31507	6	6961	5	13	NULL	NULL	NULL	Rtg1p	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19801_s_159	9242640	2 Based on two-hybrid analysis carried out in the current study, we conclude that Rtg2p neither binds to Rtg1p or Rtg3p nor is required for the  direct interaction of these transcription factors with each other.	bind
31508	7	6961	5	13	NULL	NULL	NULL	Rtg3p	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19801_s_159	9242640	2 Based on two-hybrid analysis carried out in the current study, we conclude that Rtg2p neither binds to Rtg1p or Rtg3p nor is required for the  direct interaction of these transcription factors with each other.	bind
20971	1	6961	6	NULL	NULL	0	NULL	Rtg2p	NULL		does not bind	NULL				Rtg1p	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_32_19801_s_159	9242640	2 Based on two-hybrid analysis carried out in the current study, we conclude that Rtg2p neither binds to Rtg1p or Rtg3p nor is required for the  direct interaction of these transcription factors with each other.	bind
20972	2	6961	6	NULL	NULL	0	NULL	Rtg2p	NULL		does not bind	NULL				Rtg3p	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_32_19801_s_159	9242640	2 Based on two-hybrid analysis carried out in the current study, we conclude that Rtg2p neither binds to Rtg1p or Rtg3p nor is required for the  direct interaction of these transcription factors with each other.	bind
20973	3	6961	6	NULL	NULL	0	NULL	Rtg1p 	NULL		interacts with	NULL	directly			Rtg3p	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19801_s_159	9242640	2 Based on two-hybrid analysis carried out in the current study, we conclude that Rtg2p neither binds to Rtg1p or Rtg3p nor is required for the  direct interaction of these transcription factors with each other.	bind
20974	4	6961	6	NULL	NULL	0	NULL	Rtg2p	NULL		is not required for	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_32_19801_s_159	9242640	2 Based on two-hybrid analysis carried out in the current study, we conclude that Rtg2p neither binds to Rtg1p or Rtg3p nor is required for the  direct interaction of these transcription factors with each other.	bind
30686	5	6961	6	NULL	NULL	0	NULL	Rtg1p	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_32_19801_s_159	9242640	2 Based on two-hybrid analysis carried out in the current study, we conclude that Rtg2p neither binds to Rtg1p or Rtg3p nor is required for the  direct interaction of these transcription factors with each other.	bind
30687	6	6961	6	NULL	NULL	0	NULL	Rtg2p	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_32_19801_s_159	9242640	2 Based on two-hybrid analysis carried out in the current study, we conclude that Rtg2p neither binds to Rtg1p or Rtg3p nor is required for the  direct interaction of these transcription factors with each other.	bind
30688	7	6961	6	NULL	NULL	0	NULL	Rtg3p	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_32_19801_s_159	9242640	2 Based on two-hybrid analysis carried out in the current study, we conclude that Rtg2p neither binds to Rtg1p or Rtg3p nor is required for the  direct interaction of these transcription factors with each other.	bind
25254	1	6962	5	13	NULL	NULL	NULL	DnaB	GP		bind		stably			prepriming complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34255_s_207	9852089	2 Because a similar mechanism is likely to occur at  oriC, we conclude that the defect of the N-terminal deletions in Form 1* formation is in promoting the stable binding of DnaB to the prepriming complex.	bind
31509	2	6962	5	13	NULL	NULL	NULL	Form 1* formation	Process		promote			N-terminal deletion defects		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34255_s_207	9852089	2 Because a similar mechanism is likely to occur at  oriC, we conclude that the defect of the N-terminal deletions in Form 1* formation is in promoting the stable binding of DnaB to the prepriming complex.	bind
20975	1	6962	6	10	NULL	0	NULL	DnaB			bind		stably			prepriming complex					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34255_s_207	9852089	2 Because a similar mechanism is likely to occur at  oriC, we conclude that the defect of the N-terminal deletions in Form 1* formation is in promoting the stable binding of DnaB to the prepriming complex.	bind
21186	2	6962	6	10	NULL	0	NULL	Form 1* formation	NULL		promotes	NULL		N-terminal deletion defects		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34255_s_207	9852089	2 Because a similar mechanism is likely to occur at  oriC, we conclude that the defect of the N-terminal deletions in Form 1* formation is in promoting the stable binding of DnaB to the prepriming complex.	bind
25255	1	6963	5	13	NULL	NULL	NULL	eRF3	GP		interacts with					PAN deadenylase	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_312	15337765	2 Because eRF3 interacts with PAN deadenylase, the GDP-bound form of eRF3 might recruit PAN after translation termination to mediate poly	bind
25256	3	6963	5	13	NULL	NULL	NULL	statement 2	GP		recruits		might			PAN	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_312	15337765	2 Because eRF3 interacts with PAN deadenylase, the GDP-bound form of eRF3 might recruit PAN after translation termination to mediate poly	bind
25257	4	6963	5	13	NULL	NULL	NULL	statement 3	Process		occurs after					translation	Process	termination of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_312	15337765	2 Because eRF3 interacts with PAN deadenylase, the GDP-bound form of eRF3 might recruit PAN after translation termination to mediate poly	bind
31510	2	6963	5	13	NULL	NULL	NULL	eRF3	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_312	15337765	2 Because eRF3 interacts with PAN deadenylase, the GDP-bound form of eRF3 might recruit PAN after translation termination to mediate poly	bind
20976	1	6963	6	NULL	NULL	0	NULL	eRF3	NULL		interacts with	NULL				PAN deadenylase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_312	15337765	2 Because eRF3 interacts with PAN deadenylase, the GDP-bound form of eRF3 might recruit PAN after translation termination to mediate poly	bind
20977	2	6963	6	NULL	NULL	0	NULL	eRF3	NULL		bind	NULL				GDP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_312	15337765	2 Because eRF3 interacts with PAN deadenylase, the GDP-bound form of eRF3 might recruit PAN after translation termination to mediate poly	bind
20978	3	6963	6	NULL	NULL	0	NULL	statement 2	NULL		recruit	NULL	might			PAN 	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_312	15337765	2 Because eRF3 interacts with PAN deadenylase, the GDP-bound form of eRF3 might recruit PAN after translation termination to mediate poly	bind
20979	4	6963	6	NULL	NULL	0	NULL	statement 3	NULL		occurs after	NULL				translation	NULL	termination of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_44_45693_s_312	15337765	2 Because eRF3 interacts with PAN deadenylase, the GDP-bound form of eRF3 might recruit PAN after translation termination to mediate poly	bind
25477	1	6964	5	NULL	NULL	0	NULL		NULL		is associated with	NULL	covalently	amino-terminal			NULL	basic	middle rod domains		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_50_35375_s_166	10585405	2 Because the amino-terminal and basic middle rod domains must be covalently associated to stabilize F-actin ( 35) and utrophin lacks the middle rod domain actin binding activity of dystrophin (Figs.  5 and 6), we hypothesize that utrophin may lack the filament-stabilizing activity of dystrophin.	bind
25478	2	6964	5	13	NULL	NULL	NULL	statement 1	Process		stabilizes					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_50_35375_s_166	10585405	2 Because the amino-terminal and basic middle rod domains must be covalently associated to stabilize F-actin ( 35) and utrophin lacks the middle rod domain actin binding activity of dystrophin (Figs.  5 and 6), we hypothesize that utrophin may lack the filament-stabilizing activity of dystrophin.	bind
25479	3	6964	5	13	NULL	NULL	NULL	utrophin	GP		lacks					dystrophin	GP	actin binding activity of	middle rod domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_50_35375_s_166	10585405	2 Because the amino-terminal and basic middle rod domains must be covalently associated to stabilize F-actin ( 35) and utrophin lacks the middle rod domain actin binding activity of dystrophin (Figs.  5 and 6), we hypothesize that utrophin may lack the filament-stabilizing activity of dystrophin.	bind
25480	4	6964	5	13	NULL	NULL	NULL	utrophin	GP		lack		may			dystrophin	GP	filament-stabilizing activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_50_35375_s_166	10585405	2 Because the amino-terminal and basic middle rod domains must be covalently associated to stabilize F-actin ( 35) and utrophin lacks the middle rod domain actin binding activity of dystrophin (Figs.  5 and 6), we hypothesize that utrophin may lack the filament-stabilizing activity of dystrophin.	bind
25481	5	6964	5	13	NULL	NULL	NULL	statement 3	Process		suggests					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_50_35375_s_166	10585405	2 Because the amino-terminal and basic middle rod domains must be covalently associated to stabilize F-actin ( 35) and utrophin lacks the middle rod domain actin binding activity of dystrophin (Figs.  5 and 6), we hypothesize that utrophin may lack the filament-stabilizing activity of dystrophin.	bind
21187	1	6964	6	NULL	NULL	0	NULL		NULL		associate	NULL	covalently	amino terminal			NULL	basic	middle rod domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_50_35375_s_166	10585405	2 Because the amino-terminal and basic middle rod domains must be covalently associated to stabilize F-actin ( 35) and utrophin lacks the middle rod domain actin binding activity of dystrophin (Figs.  5 and 6), we hypothesize that utrophin may lack the filament-stabilizing activity of dystrophin.	bind
21188	2	6964	6	NULL	NULL	0	NULL	statement 1	NULL		stabilize	NULL				F-actin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_50_35375_s_166	10585405	2 Because the amino-terminal and basic middle rod domains must be covalently associated to stabilize F-actin ( 35) and utrophin lacks the middle rod domain actin binding activity of dystrophin (Figs.  5 and 6), we hypothesize that utrophin may lack the filament-stabilizing activity of dystrophin.	bind
21189	3	6964	6	10	NULL	0	NULL	Utrophin			lack					dystrophin		actin binding activity of 	 middle rod domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_50_35375_s_166	10585405	2 Because the amino-terminal and basic middle rod domains must be covalently associated to stabilize F-actin ( 35) and utrophin lacks the middle rod domain actin binding activity of dystrophin (Figs.  5 and 6), we hypothesize that utrophin may lack the filament-stabilizing activity of dystrophin.	bind
21190	5	6964	6	10	NULL	0	NULL	statement 3			suggest					statement 4					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_50_35375_s_166	10585405	2 Because the amino-terminal and basic middle rod domains must be covalently associated to stabilize F-actin ( 35) and utrophin lacks the middle rod domain actin binding activity of dystrophin (Figs.  5 and 6), we hypothesize that utrophin may lack the filament-stabilizing activity of dystrophin.	bind
21192	4	6964	6	10	NULL	0	NULL	Utrophin			lack		may			dystrophin		filament-stabilizing activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_50_35375_s_166	10585405	2 Because the amino-terminal and basic middle rod domains must be covalently associated to stabilize F-actin ( 35) and utrophin lacks the middle rod domain actin binding activity of dystrophin (Figs.  5 and 6), we hypothesize that utrophin may lack the filament-stabilizing activity of dystrophin.	bind
25482	1	6965	5	13	NULL	NULL	NULL	SRF	GP		plays a role in					cell proliferation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
25483	2	6965	5	13	NULL	NULL	NULL	SRF	GP		plays a role in					vascular smooth muscle-specific genes	Process	expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
25487	3	6965	5	10	NULL	0	NULL				is rich in				 CArG box				adenine residues		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
25488	4	6965	5	10	NULL	0	NULL				is rich in				CArG box				thymine residues		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
25489	5	6965	5	13	NULL	NULL	NULL	HMG-I proteins	GP		bind		may							CArG box	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
25490	6	6965	5	13	NULL	NULL	NULL	SRF	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
25491	7	6965	5	13	NULL	NULL	NULL	statement 6	Process		activates					transcription	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
25492	8	6965	5	13	NULL	NULL	NULL	statement 5	Process		affect		may			statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
25493	9	6965	5	13	NULL	NULL	NULL	statement 5	Process		affect		may			statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
26126	10	6965	5	13	NULL	NULL	NULL	statement 3	Process		occurs simultaneously with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
56792	11	6965	5	13	NULL	NULL	NULL	CArG box	NucleicAcid		is a type of					DNA-binding element	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
20980	1	6965	6	NULL	NULL	0	NULL	SRF	NULL		plays a role in	NULL				cell proliferation	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
20981	2	6965	6	NULL	NULL	0	NULL	SRF	NULL		plays a role in	NULL				vascular smooth muscle-specific genes	NULL	expression of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
20982	3	6965	6	NULL	NULL	0	NULL	HMG-I proteins	NULL		bind	NULL	may				NULL			CArG box	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
20983	4	6965	6	NULL	NULL	0	NULL		NULL		is rich in	NULL			CArG box	adenine residues	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
20984	5	6965	6	NULL	NULL	0	NULL		NULL		is rich in	NULL			CArG box	thymine residues	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
20985	6	6965	6	NULL	NULL	0	NULL	SRF	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
20986	7	6965	6	NULL	NULL	0	NULL	SRF	NULL		activate	NULL				transcription	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
20987	8	6965	6	NULL	NULL	0	NULL	HMG-I proteins	NULL		affect	NULL	may			statement 6	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
20988	9	6965	6	NULL	NULL	0	NULL	HMG-I proteins	NULL		affect	NULL	may			statement 7	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
25534	10	6965	6	NULL	NULL	0	NULL	statement 4	NULL		occurs simultaneously with	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
56793	11	6965	6	10	NULL	0	NULL	CArG box			is a type of					DNA-binding element					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9755_s_44	9545312	2 Because the role of SRF in cell proliferation and expression of vascular smooth muscle-specific genes is well established, and its DNA-binding element (the CArG box) is rich in adenine and thymine residues, we hypothesized that HMG-I proteins may bind to the CArG box and affect the ability of SRF to bind to DNA and activate transcription.	bind
25499	1	6966	5	13	NULL	NULL	NULL	rhotekin protein	GP	human homologue of	associates with		preferentially			RhoC	GP	mutated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_43_33962_s_123	10940294	2 Besides these artifactual constructs, two different clones corresponded to a cDNA encoding the human homologue of rhotekin, which was originally identified as a protein preferentially associating with a mutated form of RhoC that mimicked the GTP-bound form of this small GTPase ( 25).	bind
31514	2	6966	5	13	NULL	NULL	NULL	RhoC	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_43_33962_s_123	10940294	2 Besides these artifactual constructs, two different clones corresponded to a cDNA encoding the human homologue of rhotekin, which was originally identified as a protein preferentially associating with a mutated form of RhoC that mimicked the GTP-bound form of this small GTPase ( 25).	bind
31515	3	6966	5	13	NULL	NULL	NULL	statement 1	Process		mimics					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_43_33962_s_123	10940294	2 Besides these artifactual constructs, two different clones corresponded to a cDNA encoding the human homologue of rhotekin, which was originally identified as a protein preferentially associating with a mutated form of RhoC that mimicked the GTP-bound form of this small GTPase ( 25).	bind
32234	4	6966	5	13	NULL	NULL	NULL	RhoC	GP		is a type of					small GTPase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_43_33962_s_123	10940294	2 Besides these artifactual constructs, two different clones corresponded to a cDNA encoding the human homologue of rhotekin, which was originally identified as a protein preferentially associating with a mutated form of RhoC that mimicked the GTP-bound form of this small GTPase ( 25).	bind
21193	1	6966	6	10	NULL	0	NULL	rhotekin		human homologue of	associate		preferentially			RhoC		mutant			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_43_33962_s_123	10940294	2 Besides these artifactual constructs, two different clones corresponded to a cDNA encoding the human homologue of rhotekin, which was originally identified as a protein preferentially associating with a mutated form of RhoC that mimicked the GTP-bound form of this small GTPase ( 25).	bind
21194	2	6966	6	10	NULL	0	NULL	RhoC			is a type of					small GTPase					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_43_33962_s_123	10940294	2 Besides these artifactual constructs, two different clones corresponded to a cDNA encoding the human homologue of rhotekin, which was originally identified as a protein preferentially associating with a mutated form of RhoC that mimicked the GTP-bound form of this small GTPase ( 25).	bind
21195	3	6966	6	NULL	NULL	0	NULL	RhoC	NULL		bind	NULL				GTP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_43_33962_s_123	10940294	2 Besides these artifactual constructs, two different clones corresponded to a cDNA encoding the human homologue of rhotekin, which was originally identified as a protein preferentially associating with a mutated form of RhoC that mimicked the GTP-bound form of this small GTPase ( 25).	bind
21196	4	6966	6	NULL	NULL	0	NULL	statement 1	NULL		mimicks	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_43_33962_s_123	10940294	2 Besides these artifactual constructs, two different clones corresponded to a cDNA encoding the human homologue of rhotekin, which was originally identified as a protein preferentially associating with a mutated form of RhoC that mimicked the GTP-bound form of this small GTPase ( 25).	bind
25500	1	6967	5	13	NULL	NULL	NULL	Bet1p	GP		bind		directly			Sec24p	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_26_27225_s_250	15123693	2 Bet1p also binds directly to Sec24p, and its COPII binding motif is occluded when assembled into SNARE complexes, suggesting that Bet1p is also packaged into COPII vesicles in a free form ( ).	bind
25501	2	6967	5	13	NULL	NULL	NULL	Bet1p	GP		is occluded when			COPII binding motif		SNARE complexes	GP	assembled into			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_26_27225_s_250	15123693	2 Bet1p also binds directly to Sec24p, and its COPII binding motif is occluded when assembled into SNARE complexes, suggesting that Bet1p is also packaged into COPII vesicles in a free form ( ).	bind
25502	3	6967	5	13	NULL	NULL	NULL	Bet1p	GP	free form	is packaged into					COPII vesicles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_26_27225_s_250	15123693	2 Bet1p also binds directly to Sec24p, and its COPII binding motif is occluded when assembled into SNARE complexes, suggesting that Bet1p is also packaged into COPII vesicles in a free form ( ).	bind
25503	4	6967	5	13	NULL	NULL	NULL	statement 2	Process		suggests					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_26_27225_s_250	15123693	2 Bet1p also binds directly to Sec24p, and its COPII binding motif is occluded when assembled into SNARE complexes, suggesting that Bet1p is also packaged into COPII vesicles in a free form ( ).	bind
20989	1	6967	6	NULL	NULL	0	NULL	Bet1p	NULL		bind	NULL	directly			Sec24p	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_26_27225_s_250	15123693	2 Bet1p also binds directly to Sec24p, and its COPII binding motif is occluded when assembled into SNARE complexes, suggesting that Bet1p is also packaged into COPII vesicles in a free form ( ).	bind
20990	2	6967	6	NULL	NULL	0	NULL	Bet1p	NULL		is occluded when	NULL		COPII binding motif		SNARE complexs	NULL	assembled into			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_26_27225_s_250	15123693	2 Bet1p also binds directly to Sec24p, and its COPII binding motif is occluded when assembled into SNARE complexes, suggesting that Bet1p is also packaged into COPII vesicles in a free form ( ).	bind
20991	3	6967	6	NULL	NULL	0	NULL	Bet1p	NULL	free form	packaged into	NULL				COPII vesicles	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_26_27225_s_250	15123693	2 Bet1p also binds directly to Sec24p, and its COPII binding motif is occluded when assembled into SNARE complexes, suggesting that Bet1p is also packaged into COPII vesicles in a free form ( ).	bind
30690	4	6967	6	NULL	NULL	0	NULL	statement 2	NULL		suggests	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_26_27225_s_250	15123693	2 Bet1p also binds directly to Sec24p, and its COPII binding motif is occluded when assembled into SNARE complexes, suggesting that Bet1p is also packaged into COPII vesicles in a free form ( ).	bind
25504	1	6968	5	13	NULL	NULL	NULL	Bla g 2	GP		is not expressed in					P. americana	Organism				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_33_20907_s_142	9252418	2 Bla g 2 and Bla g 4 are not expressed in  P. americana and recent results showed that  P. americana extracts did not inhibit IgE Ab binding to Bla g 5 in RIA ( 12,  13).	bind
25505	2	6968	5	13	NULL	NULL	NULL	Bla g 4	GP		is not expressed in					P. americana	Organism				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_33_20907_s_142	9252418	2 Bla g 2 and Bla g 4 are not expressed in  P. americana and recent results showed that  P. americana extracts did not inhibit IgE Ab binding to Bla g 5 in RIA ( 12,  13).	bind
25506	3	6968	5	13	NULL	NULL	NULL	IgE Ab	GP		bind					Bla g 5	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_33_20907_s_142	9252418	2 Bla g 2 and Bla g 4 are not expressed in  P. americana and recent results showed that  P. americana extracts did not inhibit IgE Ab binding to Bla g 5 in RIA ( 12,  13).	bind
25507	4	6968	5	13	NULL	NULL	NULL	P. americana extracts	Cell		does not inhibit					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_33_20907_s_142	9252418	2 Bla g 2 and Bla g 4 are not expressed in  P. americana and recent results showed that  P. americana extracts did not inhibit IgE Ab binding to Bla g 5 in RIA ( 12,  13).	bind
20992	1	6968	6	NULL	NULL	0	NULL	Bla g2	NULL		is not expressed in	NULL				P. americana	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_33_20907_s_142	9252418	2 Bla g 2 and Bla g 4 are not expressed in  P. americana and recent results showed that  P. americana extracts did not inhibit IgE Ab binding to Bla g 5 in RIA ( 12,  13).	bind
20993	2	6968	6	NULL	NULL	0	NULL	Bla g4	NULL		is not expressed in	NULL				P. americana	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_33_20907_s_142	9252418	2 Bla g 2 and Bla g 4 are not expressed in  P. americana and recent results showed that  P. americana extracts did not inhibit IgE Ab binding to Bla g 5 in RIA ( 12,  13).	bind
20994	3	6968	6	NULL	NULL	0	NULL	IgE Ab	NULL		bind	NULL				Bla g5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_33_20907_s_142	9252418	2 Bla g 2 and Bla g 4 are not expressed in  P. americana and recent results showed that  P. americana extracts did not inhibit IgE Ab binding to Bla g 5 in RIA ( 12,  13).	bind
20995	4	6968	6	NULL	NULL	0	NULL	P. americana extracts	NULL		did not inhibit	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_33_20907_s_142	9252418	2 Bla g 2 and Bla g 4 are not expressed in  P. americana and recent results showed that  P. americana extracts did not inhibit IgE Ab binding to Bla g 5 in RIA ( 12,  13).	bind
25508	1	6970	5	13	NULL	NULL	NULL	nuclear receptor superfamily members	GP		is a class of					transcription factors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_1_663_s_20	8995310	2 Both steroid hormones and RA are triggers of ligand-dependent activation of their respective receptors, which are members of the nuclear receptor superfamily, a class of transcription factors that specifically bind to  cis-elements in the regulatory regions of given genes ( 15).	bind
25509	2	6970	5	13	NULL	NULL	NULL	nuclear receptor superfamily members	GP		bind					genes	GP			 cis-elements in the regulatory regions	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_1_663_s_20	8995310	2 Both steroid hormones and RA are triggers of ligand-dependent activation of their respective receptors, which are members of the nuclear receptor superfamily, a class of transcription factors that specifically bind to  cis-elements in the regulatory regions of given genes ( 15).	bind
31516	3	6970	5	13	NULL	NULL	NULL	steroid hormones	Chemical		triggers					nuclear receptor superfamily members	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_1_663_s_20	8995310	2 Both steroid hormones and RA are triggers of ligand-dependent activation of their respective receptors, which are members of the nuclear receptor superfamily, a class of transcription factors that specifically bind to  cis-elements in the regulatory regions of given genes ( 15).	bind
31517	4	6970	5	13	NULL	NULL	NULL	statement 3	Process		is dependent on					ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_1_663_s_20	8995310	2 Both steroid hormones and RA are triggers of ligand-dependent activation of their respective receptors, which are members of the nuclear receptor superfamily, a class of transcription factors that specifically bind to  cis-elements in the regulatory regions of given genes ( 15).	bind
56794	5	6970	5	13	NULL	NULL	NULL	RA	Chemical		triggers					nuclear receptor superfamily member	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_1_663_s_20	8995310	2 Both steroid hormones and RA are triggers of ligand-dependent activation of their respective receptors, which are members of the nuclear receptor superfamily, a class of transcription factors that specifically bind to  cis-elements in the regulatory regions of given genes ( 15).	bind
56795	6	6970	5	13	NULL	NULL	NULL	statement 5	Process		is dependent on					ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_1_663_s_20	8995310	2 Both steroid hormones and RA are triggers of ligand-dependent activation of their respective receptors, which are members of the nuclear receptor superfamily, a class of transcription factors that specifically bind to  cis-elements in the regulatory regions of given genes ( 15).	bind
21197	1	6970	6	10	NULL	0	NULL	nuclear receptor superfamily		members of	is a class of					transcription factors					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_1_663_s_20	8995310	2 Both steroid hormones and RA are triggers of ligand-dependent activation of their respective receptors, which are members of the nuclear receptor superfamily, a class of transcription factors that specifically bind to  cis-elements in the regulatory regions of given genes ( 15).	bind
21198	2	6970	6	NULL	NULL	0	NULL	transcription factors	NULL		bind	NULL	specifically			gene	NULL			cis-elements in the regulatory region	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_1_663_s_20	8995310	2 Both steroid hormones and RA are triggers of ligand-dependent activation of their respective receptors, which are members of the nuclear receptor superfamily, a class of transcription factors that specifically bind to  cis-elements in the regulatory regions of given genes ( 15).	bind
21199	3	6970	6	NULL	NULL	0	NULL	steroid hormone	NULL		triggers	NULL				members of nuclear receptor superfamily	NULL	activation of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_1_663_s_20	8995310	2 Both steroid hormones and RA are triggers of ligand-dependent activation of their respective receptors, which are members of the nuclear receptor superfamily, a class of transcription factors that specifically bind to  cis-elements in the regulatory regions of given genes ( 15).	bind
21200	4	6970	6	NULL	NULL	0	NULL	RA	NULL		triggers	NULL				members of nuclear receptor superfamily	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_1_663_s_20	8995310	2 Both steroid hormones and RA are triggers of ligand-dependent activation of their respective receptors, which are members of the nuclear receptor superfamily, a class of transcription factors that specifically bind to  cis-elements in the regulatory regions of given genes ( 15).	bind
21201	5	6970	6	NULL	NULL	0	NULL	statement 3	NULL		is dependent on	NULL				ligand	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_1_663_s_20	8995310	2 Both steroid hormones and RA are triggers of ligand-dependent activation of their respective receptors, which are members of the nuclear receptor superfamily, a class of transcription factors that specifically bind to  cis-elements in the regulatory regions of given genes ( 15).	bind
21212	6	6970	6	NULL	NULL	0	NULL	statement 4	NULL		is dependent on	NULL				ligand	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_1_663_s_20	8995310	2 Both steroid hormones and RA are triggers of ligand-dependent activation of their respective receptors, which are members of the nuclear receptor superfamily, a class of transcription factors that specifically bind to  cis-elements in the regulatory regions of given genes ( 15).	bind
25516	1	6971	5	13	NULL	NULL	NULL	CC-G24	GP		bind		specifically			bFcgamma2R	GP				NULL	in bovine neutrophils	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_51_47794_s_69	11641395	2 CC-G24 bound specifically to bFcgamma2R expressed at high levels on bovine neutrophils (Fig.  1,  panel A).	bind
31518	2	6971	5	13	NULL	NULL	NULL	bFcgamma2R	GP	high levels of	expressed on					neutrophils	Cell	bovine			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_51_47794_s_69	11641395	2 CC-G24 bound specifically to bFcgamma2R expressed at high levels on bovine neutrophils (Fig.  1,  panel A).	bind
20996	1	6971	6	10	NULL	0	NULL	bFcgamma2R		high levels of	expressed on					neutrophils		bovine			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_51_47794_s_69	11641395	2 CC-G24 bound specifically to bFcgamma2R expressed at high levels on bovine neutrophils (Fig.  1,  panel A).	bind
20997	2	6971	6	10	NULL	0	NULL	CC-G24			bind		specifically			bFcgamma2R					NULL	bovine neutrophils	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_51_47794_s_69	11641395	2 CC-G24 bound specifically to bFcgamma2R expressed at high levels on bovine neutrophils (Fig.  1,  panel A).	bind
28988	1	6972	5	13	NULL	NULL	NULL	RPs mRNAs	NucleicAcid	change of levels of	does not change		significantly			Rap1p	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13235_s_253	10224082	2 Conditions that produce changes in the levels of mRNAs encoding RPs do not significantly change the levels of expression of Rap1p ( 16), or change the binding affinities of Rap1p and Abf1p ( 12,  14,  16).	bind
28989	2	6972	5	13	NULL	NULL	NULL	RPs mRNAs	NucleicAcid	change of levels of	does not change					Rap1p	GP	binding affinities of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13235_s_253	10224082	2 Conditions that produce changes in the levels of mRNAs encoding RPs do not significantly change the levels of expression of Rap1p ( 16), or change the binding affinities of Rap1p and Abf1p ( 12,  14,  16).	bind
28990	3	6972	5	13	NULL	NULL	NULL	RPs mRNAs	NucleicAcid	change of levels of	does not change					Abf1p	GP	binding affinities of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13235_s_253	10224082	2 Conditions that produce changes in the levels of mRNAs encoding RPs do not significantly change the levels of expression of Rap1p ( 16), or change the binding affinities of Rap1p and Abf1p ( 12,  14,  16).	bind
20998	1	6972	6	13	NULL	NULL	NULL	RPs mRNAs	NucleicAcid	change of levels of 	does not change		significantly			Rap1p	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13235_s_253	10224082	2 Conditions that produce changes in the levels of mRNAs encoding RPs do not significantly change the levels of expression of Rap1p ( 16), or change the binding affinities of Rap1p and Abf1p ( 12,  14,  16).	bind
30691	2	6972	6	10	NULL	0	NULL	RPs mRNAs	NULL	change of levels of	does not change	NULL				Rap1p	NULL	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13235_s_253	10224082	2 Conditions that produce changes in the levels of mRNAs encoding RPs do not significantly change the levels of expression of Rap1p ( 16), or change the binding affinities of Rap1p and Abf1p ( 12,  14,  16).	bind
30692	3	6972	6	10	NULL	0	NULL	RPs mRNAs	NULL	change of levels of	does not change	NULL				Abf1p	NULL	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13235_s_253	10224082	2 Conditions that produce changes in the levels of mRNAs encoding RPs do not significantly change the levels of expression of Rap1p ( 16), or change the binding affinities of Rap1p and Abf1p ( 12,  14,  16).	bind
25517	1	6973	5	13	NULL	NULL	NULL	paxillin	GP		associates with					PTP-PEST	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_22736_s_226	10781578	2 Consequently, our data suggest that alpha4 can bind simultaneously to paxillin that is associated with PTP-PEST or FAK.	bind
25518	2	6973	5	13	NULL	NULL	NULL	paxillin	GP		associate with					FAK	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_22736_s_226	10781578	2 Consequently, our data suggest that alpha4 can bind simultaneously to paxillin that is associated with PTP-PEST or FAK.	bind
25519	3	6973	5	13	NULL	NULL	NULL	alpha4	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_22736_s_226	10781578	2 Consequently, our data suggest that alpha4 can bind simultaneously to paxillin that is associated with PTP-PEST or FAK.	bind
25520	4	6973	5	13	NULL	NULL	NULL	alpha4	GP		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_22736_s_226	10781578	2 Consequently, our data suggest that alpha4 can bind simultaneously to paxillin that is associated with PTP-PEST or FAK.	bind
25521	5	6973	5	13	NULL	NULL	NULL	statement 3	Process		occurs simultaneously with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_22736_s_226	10781578	2 Consequently, our data suggest that alpha4 can bind simultaneously to paxillin that is associated with PTP-PEST or FAK.	bind
56796	6	6973	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_22736_s_226	10781578	2 Consequently, our data suggest that alpha4 can bind simultaneously to paxillin that is associated with PTP-PEST or FAK.	bind
20999	1	6973	6	NULL	NULL	0	NULL	paxillin	NULL		is associated with	NULL				PTP-PEST	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_30_22736_s_226	10781578	2 Consequently, our data suggest that alpha4 can bind simultaneously to paxillin that is associated with PTP-PEST or FAK.	bind
21000	2	6973	6	NULL	NULL	0	NULL	Paxillin	NULL		is associated with	NULL				FAK	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_30_22736_s_226	10781578	2 Consequently, our data suggest that alpha4 can bind simultaneously to paxillin that is associated with PTP-PEST or FAK.	bind
21001	3	6973	6	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_30_22736_s_226	10781578	2 Consequently, our data suggest that alpha4 can bind simultaneously to paxillin that is associated with PTP-PEST or FAK.	bind
21002	4	6973	6	NULL	NULL	0	NULL	alpha4	NULL		bind	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_22736_s_226	10781578	2 Consequently, our data suggest that alpha4 can bind simultaneously to paxillin that is associated with PTP-PEST or FAK.	bind
21003	5	6973	6	NULL	NULL	0	NULL	alpha4	NULL		bind	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_22736_s_226	10781578	2 Consequently, our data suggest that alpha4 can bind simultaneously to paxillin that is associated with PTP-PEST or FAK.	bind
30695	6	6973	6	NULL	NULL	0	NULL	statement 4	NULL		occurs simultaneously with	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_30_22736_s_226	10781578	2 Consequently, our data suggest that alpha4 can bind simultaneously to paxillin that is associated with PTP-PEST or FAK.	bind
25522	1	6974	5	13	NULL	NULL	NULL	CrkL	GP		bind		constitutively			C3G guanine nucleotide exchange factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30630_s_294	9804835	2 CrkL constitutively binds the C3G guanine nucleotide exchange factor ( 15,  34), which has been implicated in activation of the Rap1 GTPase ( 35) and the c-Jun N-terminal kinase ( 36).	bind
25523	2	6974	5	13	NULL	NULL	NULL	C3G guanine nucleotide exchange factor	GP		is implicated in					Rap1 GTPase	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30630_s_294	9804835	2 CrkL constitutively binds the C3G guanine nucleotide exchange factor ( 15,  34), which has been implicated in activation of the Rap1 GTPase ( 35) and the c-Jun N-terminal kinase ( 36).	bind
25525	3	6974	5	13	NULL	NULL	NULL	C3G guanine nucleotide exchange factor	GP		is implicated in					c-Jun N-terminal kinase	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30630_s_294	9804835	2 CrkL constitutively binds the C3G guanine nucleotide exchange factor ( 15,  34), which has been implicated in activation of the Rap1 GTPase ( 35) and the c-Jun N-terminal kinase ( 36).	bind
21004	1	6974	6	NULL	NULL	0	NULL	CrkL	NULL		bind	NULL	constitutively			C3G guanine nucleotide exchange factor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_46_30630_s_294	9804835	2 CrkL constitutively binds the C3G guanine nucleotide exchange factor ( 15,  34), which has been implicated in activation of the Rap1 GTPase ( 35) and the c-Jun N-terminal kinase ( 36).	bind
21005	2	6974	6	NULL	NULL	0	NULL	C3G guanine nucleotide exchange factor	NULL		is involved in	NULL				Rap1 GTPase	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30630_s_294	9804835	2 CrkL constitutively binds the C3G guanine nucleotide exchange factor ( 15,  34), which has been implicated in activation of the Rap1 GTPase ( 35) and the c-Jun N-terminal kinase ( 36).	bind
21006	3	6974	6	NULL	NULL	0	NULL	C3G guanine nucleotide exchange factor	NULL		is involved in	NULL				c-Jun N-terminal kinase	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_46_30630_s_294	9804835	2 CrkL constitutively binds the C3G guanine nucleotide exchange factor ( 15,  34), which has been implicated in activation of the Rap1 GTPase ( 35) and the c-Jun N-terminal kinase ( 36).	bind
25527	1	6975	5	13	NULL	NULL	NULL			deletion of	results in				CREB/cAMP-response element modulator protein binding site	enhancer activity	NucleicAcid	complete loss of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_35_32489_s_252	11432851	2 Deletion or mutation of the CREB/cAMP-response element modulator protein binding site results in complete loss of enhancer activity.	bind
25528	2	6975	5	13	NULL	NULL	NULL			mutation of	results in				CREB/cAMP-response element modulator protein binding site	enhancer activity	NucleicAcid	complete loss of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_35_32489_s_252	11432851	2 Deletion or mutation of the CREB/cAMP-response element modulator protein binding site results in complete loss of enhancer activity.	bind
25529	3	6975	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_35_32489_s_252	11432851	2 Deletion or mutation of the CREB/cAMP-response element modulator protein binding site results in complete loss of enhancer activity.	bind
21229	1	6975	6	NULL	NULL	0	NULL		NULL	deletion of	results in	NULL			CREB/cAMP-response element modulator protein binding site	enhancer activity	NULL	complete loss of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32489_s_252	11432851	2 Deletion or mutation of the CREB/cAMP-response element modulator protein binding site results in complete loss of enhancer activity.	bind
30711	2	6975	6	NULL	NULL	0	NULL		NULL	mutation of	results in	NULL			CREB/cAMP-response element modulator protein binding site	enhancer activity	NULL	complete loss of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32489_s_252	11432851	2 Deletion or mutation of the CREB/cAMP-response element modulator protein binding site results in complete loss of enhancer activity.	bind
56797	3	6975	6	10	NULL	0	NULL	statement 1			is an alternative to					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32489_s_252	11432851	2 Deletion or mutation of the CREB/cAMP-response element modulator protein binding site results in complete loss of enhancer activity.	bind
25530	1	6976	5	13	NULL	NULL	NULL	Cya-RalF	GP		is delivered into					host cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_2_1392_s_84	15520000	2 Delivery of a Cya-RalF fusion protein into host cells results in calmodulin binding to the adenylate cyclase enzyme, resulting in the production of cAMP.	bind
25531	2	6976	5	13	NULL	NULL	NULL	calmodulin	GP		bind					adenylate cyclase enzyme	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_2_1392_s_84	15520000	2 Delivery of a Cya-RalF fusion protein into host cells results in calmodulin binding to the adenylate cyclase enzyme, resulting in the production of cAMP.	bind
25532	3	6976	5	13	NULL	NULL	NULL	statement 1	Process		results in					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_2_1392_s_84	15520000	2 Delivery of a Cya-RalF fusion protein into host cells results in calmodulin binding to the adenylate cyclase enzyme, resulting in the production of cAMP.	bind
25533	4	6976	5	13	NULL	NULL	NULL	statement 3	Process		results in					cAMP	Chemical	production of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_2_1392_s_84	15520000	2 Delivery of a Cya-RalF fusion protein into host cells results in calmodulin binding to the adenylate cyclase enzyme, resulting in the production of cAMP.	bind
44812	5	6976	5	13	NULL	NULL	NULL	Cya-RalF	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_2_1392_s_84	15520000	2 Delivery of a Cya-RalF fusion protein into host cells results in calmodulin binding to the adenylate cyclase enzyme, resulting in the production of cAMP.	bind
21027	1	6976	6	NULL	NULL	0	NULL	Calmodulin	NULL		bind	NULL				adenylate cyclase enzyme	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_2_1392_s_84	15520000	2 Delivery of a Cya-RalF fusion protein into host cells results in calmodulin binding to the adenylate cyclase enzyme, resulting in the production of cAMP.	bind
21028	2	6976	6	10	NULL	0	NULL	Cya-RalF	NULL	delivery of	into	NULL				host cells	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_2_1392_s_84	15520000	2 Delivery of a Cya-RalF fusion protein into host cells results in calmodulin binding to the adenylate cyclase enzyme, resulting in the production of cAMP.	bind
21029	3	6976	6	NULL	NULL	0	NULL	statement 2	NULL		results in	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_2_1392_s_84	15520000	2 Delivery of a Cya-RalF fusion protein into host cells results in calmodulin binding to the adenylate cyclase enzyme, resulting in the production of cAMP.	bind
21030	4	6976	6	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				cAMP	NULL	production of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_2_1392_s_84	15520000	2 Delivery of a Cya-RalF fusion protein into host cells results in calmodulin binding to the adenylate cyclase enzyme, resulting in the production of cAMP.	bind
44816	5	6976	6	10	NULL	0	NULL	Cya-RalF	NULL		is a type of	NULL				fusion protein	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_2_1392_s_84	15520000	2 Delivery of a Cya-RalF fusion protein into host cells results in calmodulin binding to the adenylate cyclase enzyme, resulting in the production of cAMP.	bind
25752	1	6977	5	13	NULL	NULL	NULL	ATP	Chemical		bind					Arp2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_50_46689_s_135	11598103	2 Detailed balance, however, implies that if the affinity of ATP for Arp2 is enhanced by WA, a structural change of the WA.Arp2 complex, linked to enhanced interaction of WA with Arp2, must accompany ATP binding to Arp2.	bind
25753	2	6977	5	13	NULL	NULL	NULL	WA	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_50_46689_s_135	11598103	2 Detailed balance, however, implies that if the affinity of ATP for Arp2 is enhanced by WA, a structural change of the WA.Arp2 complex, linked to enhanced interaction of WA with Arp2, must accompany ATP binding to Arp2.	bind
25754	3	6977	5	13	NULL	NULL	NULL	statement 2	Process		leads to					WA.Arp2 complex	GP	structural change of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_50_46689_s_135	11598103	2 Detailed balance, however, implies that if the affinity of ATP for Arp2 is enhanced by WA, a structural change of the WA.Arp2 complex, linked to enhanced interaction of WA with Arp2, must accompany ATP binding to Arp2.	bind
25755	4	6977	5	13	NULL	NULL	NULL	WA	GP		interacts with					Arp2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_50_46689_s_135	11598103	2 Detailed balance, however, implies that if the affinity of ATP for Arp2 is enhanced by WA, a structural change of the WA.Arp2 complex, linked to enhanced interaction of WA with Arp2, must accompany ATP binding to Arp2.	bind
25756	5	6977	5	13	NULL	NULL	NULL	statement 3	Process		is linked to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_50_46689_s_135	11598103	2 Detailed balance, however, implies that if the affinity of ATP for Arp2 is enhanced by WA, a structural change of the WA.Arp2 complex, linked to enhanced interaction of WA with Arp2, must accompany ATP binding to Arp2.	bind
25758	6	6977	5	13	NULL	NULL	NULL	statement 1	Process		accompanies					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_50_46689_s_135	11598103	2 Detailed balance, however, implies that if the affinity of ATP for Arp2 is enhanced by WA, a structural change of the WA.Arp2 complex, linked to enhanced interaction of WA with Arp2, must accompany ATP binding to Arp2.	bind
21031	1	6977	6	10	NULL	0	NULL	ATP			bind					Arp2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_50_46689_s_135	11598103	2 Detailed balance, however, implies that if the affinity of ATP for Arp2 is enhanced by WA, a structural change of the WA.Arp2 complex, linked to enhanced interaction of WA with Arp2, must accompany ATP binding to Arp2.	bind
21222	2	6977	6	NULL	NULL	0	NULL	WA	NULL		enhances	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_50_46689_s_135	11598103	2 Detailed balance, however, implies that if the affinity of ATP for Arp2 is enhanced by WA, a structural change of the WA.Arp2 complex, linked to enhanced interaction of WA with Arp2, must accompany ATP binding to Arp2.	bind
21224	3	6977	6	NULL	NULL	0	NULL	WA	NULL		interacts with	NULL				Arp2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_50_46689_s_135	11598103	2 Detailed balance, however, implies that if the affinity of ATP for Arp2 is enhanced by WA, a structural change of the WA.Arp2 complex, linked to enhanced interaction of WA with Arp2, must accompany ATP binding to Arp2.	bind
21228	4	6977	6	10	NULL	0	NULL	statement 1			accompanies					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_50_46689_s_135	11598103	2 Detailed balance, however, implies that if the affinity of ATP for Arp2 is enhanced by WA, a structural change of the WA.Arp2 complex, linked to enhanced interaction of WA with Arp2, must accompany ATP binding to Arp2.	bind
56898	5	6977	6	10	NULL	0	NULL	statement 2			leads to					WA.Arp2 complex		structural change of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_50_46689_s_135	11598103	2 Detailed balance, however, implies that if the affinity of ATP for Arp2 is enhanced by WA, a structural change of the WA.Arp2 complex, linked to enhanced interaction of WA with Arp2, must accompany ATP binding to Arp2.	bind
56899	6	6977	6	10	NULL	0	NULL	statement 5			is linked to					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_50_46689_s_135	11598103	2 Detailed balance, however, implies that if the affinity of ATP for Arp2 is enhanced by WA, a structural change of the WA.Arp2 complex, linked to enhanced interaction of WA with Arp2, must accompany ATP binding to Arp2.	bind
25760	1	6979	5	13	NULL	NULL	NULL	d[Cha(4)]AVP	Chemical		bind					hV(1b) receptors	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_br-j-pharmacol_146_5_16158071_s_5	16158071	2 d[Cha(4)]AVP bound to hV(1b) receptors and hOT receptors  with pK(i) values of 9.68+/-0.06 and 7.68+/-0.09, respectively.	bind
25761	2	6979	5	13	NULL	NULL	NULL	d[Cha(4)]AVP	Chemical		bind					hOT receptors	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_br-j-pharmacol_146_5_16158071_s_5	16158071	2 d[Cha(4)]AVP bound to hV(1b) receptors and hOT receptors  with pK(i) values of 9.68+/-0.06 and 7.68+/-0.09, respectively.	bind
21032	1	6979	6	10	NULL	0	NULL	d[Cha(4)]AVP			bind					hV(1b) receptors					NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_br-j-pharmacol_146_5_16158071_s_5	16158071	2 d[Cha(4)]AVP bound to hV(1b) receptors and hOT receptors  with pK(i) values of 9.68+/-0.06 and 7.68+/-0.09, respectively.	bind
21033	2	6979	6	10	NULL	0	NULL	d[Cha(4)]AVP			bind					hOT receptors					NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_br-j-pharmacol_146_5_16158071_s_5	16158071	2 d[Cha(4)]AVP bound to hV(1b) receptors and hOT receptors  with pK(i) values of 9.68+/-0.06 and 7.68+/-0.09, respectively.	bind
25762	1	6980	5	13	NULL	NULL	NULL	E3BP	GP		contains								inner domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6361_s_29	9045657	2 E3BP is also composed of three linker-connected domains (an inner domain that binds to the I domain of E2, an E3-binding domain, and a lipoyl domain) ( 3,  4,  13,  27).	bind
25763	2	6980	5	13	NULL	NULL	NULL	E3BP	GP		bind			inner domain		E2	GP		I domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6361_s_29	9045657	2 E3BP is also composed of three linker-connected domains (an inner domain that binds to the I domain of E2, an E3-binding domain, and a lipoyl domain) ( 3,  4,  13,  27).	bind
31519	3	6980	5	13	NULL	NULL	NULL	E3BP	GP		contains								E3-binding domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6361_s_29	9045657	2 E3BP is also composed of three linker-connected domains (an inner domain that binds to the I domain of E2, an E3-binding domain, and a lipoyl domain) ( 3,  4,  13,  27).	bind
31520	4	6980	5	13	NULL	NULL	NULL	E3BP	GP		contains								lipoyl domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6361_s_29	9045657	2 E3BP is also composed of three linker-connected domains (an inner domain that binds to the I domain of E2, an E3-binding domain, and a lipoyl domain) ( 3,  4,  13,  27).	bind
21034	1	6980	6	NULL	NULL	0	NULL	E3BP	NULL		contains	NULL					NULL		inner domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_10_6361_s_29	9045657	2 E3BP is also composed of three linker-connected domains (an inner domain that binds to the I domain of E2, an E3-binding domain, and a lipoyl domain) ( 3,  4,  13,  27).	bind
21035	2	6980	6	NULL	NULL	0	NULL	E3BP	NULL		contains	NULL					NULL		E3-binding domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_10_6361_s_29	9045657	2 E3BP is also composed of three linker-connected domains (an inner domain that binds to the I domain of E2, an E3-binding domain, and a lipoyl domain) ( 3,  4,  13,  27).	bind
21036	3	6980	6	NULL	NULL	0	NULL	E3BP	NULL		contains	NULL					NULL		lipoyl domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_10_6361_s_29	9045657	2 E3BP is also composed of three linker-connected domains (an inner domain that binds to the I domain of E2, an E3-binding domain, and a lipoyl domain) ( 3,  4,  13,  27).	bind
21037	4	6980	6	NULL	NULL	0	NULL	E3BP	NULL		bind	NULL		inner domain		E2	NULL		I domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_10_6361_s_29	9045657	2 E3BP is also composed of three linker-connected domains (an inner domain that binds to the I domain of E2, an E3-binding domain, and a lipoyl domain) ( 3,  4,  13,  27).	bind
25799	1	6981	5	13	NULL	NULL	NULL	Golgi p180	GP		bind					Cdc42	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_35_22537_s_105	9712880	2 Finally, similar to the cytosolic IQGAPs ( 21), binding of Golgi p180 to Cdc42 was competed by the p21-activated kinase, a putative target for Cdc42, but not by the Cdc42-GAP (data not shown).	bind
25800	2	6981	5	13	NULL	NULL	NULL	p21-activated kinase	GP		bind					Cdc42	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_35_22537_s_105	9712880	2 Finally, similar to the cytosolic IQGAPs ( 21), binding of Golgi p180 to Cdc42 was competed by the p21-activated kinase, a putative target for Cdc42, but not by the Cdc42-GAP (data not shown).	bind
25801	3	6981	5	13	NULL	NULL	NULL	statement 2	Process		competes with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_35_22537_s_105	9712880	2 Finally, similar to the cytosolic IQGAPs ( 21), binding of Golgi p180 to Cdc42 was competed by the p21-activated kinase, a putative target for Cdc42, but not by the Cdc42-GAP (data not shown).	bind
25802	4	6981	5	13	NULL	NULL	NULL	p21-activated kinase	GP		is target for		putative			Cdc42	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_35_22537_s_105	9712880	2 Finally, similar to the cytosolic IQGAPs ( 21), binding of Golgi p180 to Cdc42 was competed by the p21-activated kinase, a putative target for Cdc42, but not by the Cdc42-GAP (data not shown).	bind
25803	5	6981	5	13	NULL	NULL	NULL	p21-activated kinase	GP		is not target for					Cdc42-GAP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_35_22537_s_105	9712880	2 Finally, similar to the cytosolic IQGAPs ( 21), binding of Golgi p180 to Cdc42 was competed by the p21-activated kinase, a putative target for Cdc42, but not by the Cdc42-GAP (data not shown).	bind
21038	1	6981	6	NULL	NULL	0	NULL	golgi p180	NULL		bind	NULL				Cdc42	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22537_s_105	9712880	2 Finally, similar to the cytosolic IQGAPs ( 21), binding of Golgi p180 to Cdc42 was competed by the p21-activated kinase, a putative target for Cdc42, but not by the Cdc42-GAP (data not shown).	bind
21039	2	6981	6	NULL	NULL	0	NULL	p21-activated kinase	NULL		bind	NULL				Cdc42	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22537_s_105	9712880	2 Finally, similar to the cytosolic IQGAPs ( 21), binding of Golgi p180 to Cdc42 was competed by the p21-activated kinase, a putative target for Cdc42, but not by the Cdc42-GAP (data not shown).	bind
21040	3	6981	6	NULL	NULL	0	NULL	statement 1	NULL		competes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22537_s_105	9712880	2 Finally, similar to the cytosolic IQGAPs ( 21), binding of Golgi p180 to Cdc42 was competed by the p21-activated kinase, a putative target for Cdc42, but not by the Cdc42-GAP (data not shown).	bind
30714	4	6981	6	NULL	NULL	0	NULL	p21-activated kinase	NULL		is a target for	NULL	putative			Cdc42	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22537_s_105	9712880	2 Finally, similar to the cytosolic IQGAPs ( 21), binding of Golgi p180 to Cdc42 was competed by the p21-activated kinase, a putative target for Cdc42, but not by the Cdc42-GAP (data not shown).	bind
56900	5	6981	6	10	NULL	0	NULL	p21-activated kinase			is not target for					Cdc42-GAP					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22537_s_105	9712880	2 Finally, similar to the cytosolic IQGAPs ( 21), binding of Golgi p180 to Cdc42 was competed by the p21-activated kinase, a putative target for Cdc42, but not by the Cdc42-GAP (data not shown).	bind
25804	1	6982	5	13	NULL	NULL	NULL	gamma complex	GP		bind					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_12_10033_s_196	12519754	2 Following ATP hydrolysis, the ADP-bound form of gamma complex rapidly releases DNA.	bind
25805	2	6982	5	13	NULL	NULL	NULL	statement 1	Process		release		rapidly			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_12_10033_s_196	12519754	2 Following ATP hydrolysis, the ADP-bound form of gamma complex rapidly releases DNA.	bind
25806	3	6982	5	13	NULL	NULL	NULL	statement 2	Process		occurs following					ATP	Chemical	hydrolysis of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_12_10033_s_196	12519754	2 Following ATP hydrolysis, the ADP-bound form of gamma complex rapidly releases DNA.	bind
21041	1	6982	6	NULL	NULL	0	NULL	ADP	NULL		bind	NULL				gamma complex	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_12_10033_s_196	12519754	2 Following ATP hydrolysis, the ADP-bound form of gamma complex rapidly releases DNA.	bind
21042	2	6982	6	NULL	NULL	0	NULL	statement 1	NULL		releases	NULL	rapidly			DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_12_10033_s_196	12519754	2 Following ATP hydrolysis, the ADP-bound form of gamma complex rapidly releases DNA.	bind
21043	3	6982	6	NULL	NULL	0	NULL	statement 2	NULL		occurs following	NULL				ATP	NULL	hydrolysis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_12_10033_s_196	12519754	2 Following ATP hydrolysis, the ADP-bound form of gamma complex rapidly releases DNA.	bind
25807	1	6984	5	13	NULL	NULL	NULL	C6PS molecules	Chemical		bind					FVa	GP	bovine			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_29765_s_35	12045194	2 Four C6PS molecules also bind to bovine FVa to induce conformational and functional changes ( 10).	bind
25808	2	6984	5	13	NULL	NULL	NULL	statement 1	Process		induces					FVa 	GP	conformational change of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_29765_s_35	12045194	2 Four C6PS molecules also bind to bovine FVa to induce conformational and functional changes ( 10).	bind
25809	3	6984	5	13	NULL	NULL	NULL	statement 1	Process		induces					FVa	GP	functional change of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_29765_s_35	12045194	2 Four C6PS molecules also bind to bovine FVa to induce conformational and functional changes ( 10).	bind
21044	1	6984	6	NULL	NULL	0	NULL	C6PS molecules	NULL		bind	NULL				FVa	NULL	bovine			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_33_29765_s_35	12045194	2 Four C6PS molecules also bind to bovine FVa to induce conformational and functional changes ( 10).	bind
31181	2	6984	6	NULL	NULL	0	NULL	statement 1	NULL		induces	NULL				FVa	NULL	functional changes of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_33_29765_s_35	12045194	2 Four C6PS molecules also bind to bovine FVa to induce conformational and functional changes ( 10).	bind
31182	3	6984	6	NULL	NULL	0	NULL	statement 1	NULL		induces	NULL				FVa	NULL	conformational changes of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_33_29765_s_35	12045194	2 Four C6PS molecules also bind to bovine FVa to induce conformational and functional changes ( 10).	bind
28991	1	6985	5	13	NULL	NULL	NULL	YAF fraction	GP		is derived from					HeLa cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
28992	2	6985	5	13	NULL	NULL	NULL	statement 1	GP		contains					HMG-I(Y)-like activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
31526	3	6985	5	13	NULL	NULL	NULL	statement 1	Cell		interacts with		specifically			IFN-beta	GP			HMG-I(Y) DNA-binding site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
31527	4	6985	5	13	NULL	NULL	NULL	statement 1	Cell		resistant to					denaturation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
31528	5	6985	5	13	NULL	NULL	NULL	statement 1	Process		losses					DNA binding activity	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
31529	6	6985	5	13	NULL	NULL	NULL	statement 5	Process		occurs following					elevated temperature		exposure to			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
31531	7	6985	5	13	NULL	NULL	NULL	IFN-beta	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
31532	8	6985	5	13	NULL	NULL	NULL	poly(dI-dC) DNA	NucleicAcid		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
56909	9	6985	5	13	NULL	NULL	NULL	alpha-HMG-I antibodies	GP	specific	bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
56910	10	6985	5	13	NULL	NULL	NULL	statement 8	Process		compete with					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
56911	11	6985	5	13	NULL	NULL	NULL	statement 9	Process		compete with					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
56912	12	6985	5	13	NULL	NULL	NULL	YAF fraction	GP		is soluble in					perchloric acid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
21230	1	6985	6	NULL	NULL	0	NULL	YAF fractions	NULL		contains	NULL				HMG-I(Y)-like activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
21247	2	6985	6	NULL	NULL	0	NULL	YAF fraction	NULL		bind	NULL				IFN-beta	NULL			HMG-I(Y) DNA-binding site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
21248	3	6985	6	NULL	NULL	0	NULL	YAF fraction	NULL		is soluble in	NULL				perchloric acid	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
21249	4	6985	6	NULL	NULL	0	NULL	YAF fraction	NULL		is resistant to	NULL				denaturation	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
21250	5	6985	6	10	NULL	0	NULL	YAF fraction			loses					DNA binding activity					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
21251	6	6985	6	10	NULL	0	NULL	statement 5			upon exposure to					elevated temperature					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
21253	7	6985	6	10	NULL	0	NULL	 IFN-beta			bind					DNA					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
56904	8	6985	6	10	NULL	0	NULL	poly(dI-dC) DNA			bind					DNA					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
56905	9	6985	6	10	NULL	0	NULL	alpha-HMG-I antibodies		specific	bind					DNA					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
56906	10	6985	6	10	NULL	0	NULL	statement 8			compete with					statement 7					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
56907	11	6985	6	10	NULL	0	NULL	statement 9			compete with					statement 7					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
56908	12	6985	6	10	NULL	0	NULL	YAF fraction			derived from					HeLa cells					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30880_s_130	9388234	2 Further biochemical analyses have suggested the YAF fraction derived from a variety of cell types ( e.g. HeLa) contains an HMG-I(Y)-like activity as defined by specific interaction with a known IFN-beta HMG-I(Y) DNA-binding site, solubility in 5% perchloric acid, resistance to denaturation and loss of DNA binding activity following exposure to elevated temperature ( e.g. 65  degrees C), and competition of IFN-beta DNA binding activity by poly(dI-dC) DNA and specific alpha-HMG-I antibodies (Fig.  1).	bind
31521	1	6986	5	13	NULL	NULL	NULL	occludin	GP		bind		may			TJ-scaffolding proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49644_s_203	14512431	2 Further experiments are needed to investigate the regulation and binding affinity between occludin and the different TJ-scaffolding proteins.	bind
21048	1	6986	6	NULL	NULL	0	NULL	occludin	NULL		bind	NULL	may			TJ-scaffolding proteins	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49644_s_203	14512431	2 Further experiments are needed to investigate the regulation and binding affinity between occludin and the different TJ-scaffolding proteins.	bind
31522	1	6987	5	13	NULL	NULL	NULL	FRP/Frzb	GP		bind					Wnt	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_27_19465_s_280	10383463	2 Further studies will be required to determine whether Sk/Dkk binds Wnt, like FRP/Frzb and Cerberus, or antagonizes Wnt signaling indirectly through an independent inhibitory pathway.	bind
31523	2	6987	5	13	NULL	NULL	NULL	Cerberus	GP		bind					Wnt	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_27_19465_s_280	10383463	2 Further studies will be required to determine whether Sk/Dkk binds Wnt, like FRP/Frzb and Cerberus, or antagonizes Wnt signaling indirectly through an independent inhibitory pathway.	bind
21049	1	6987	6	NULL	NULL	0	NULL	FRP/Frzb	NULL		bind	NULL				Wnt	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_27_19465_s_280	10383463	2 Further studies will be required to determine whether Sk/Dkk binds Wnt, like FRP/Frzb and Cerberus, or antagonizes Wnt signaling indirectly through an independent inhibitory pathway.	bind
21050	2	6987	6	NULL	NULL	0	NULL	Cerberus	NULL		bind	NULL				Wnt	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_27_19465_s_280	10383463	2 Further studies will be required to determine whether Sk/Dkk binds Wnt, like FRP/Frzb and Cerberus, or antagonizes Wnt signaling indirectly through an independent inhibitory pathway.	bind
25810	1	6988	5	13	NULL	NULL	NULL	ProRS	GP	archaeal-type T. thermophilus	bind					cysteine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_38_34749_s_177	12130658	2 Further support is derived from suggestions based on a modeling experiment that the archaeal-type  T. thermophilus ProRS could also bind cysteine ( 35).	bind
21109	1	6988	6	NULL	NULL	0	NULL	 ProRS	NULL	archaeal-type T. thermophilus	bind	NULL				cysteine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_38_34749_s_177	12130658	2 Further support is derived from suggestions based on a modeling experiment that the archaeal-type  T. thermophilus ProRS could also bind cysteine ( 35).	bind
25811	1	6989	5	13	NULL	NULL	NULL	p68	GP		bind					p180	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20541_s_184	11927598	2 Furthermore, binding of p68 to p180 induces a conformational change in the latter polypeptide ( 51).	bind
25812	2	6989	5	13	NULL	NULL	NULL	statement 1	Process		induces					p180	GP	conformational change in			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20541_s_184	11927598	2 Furthermore, binding of p68 to p180 induces a conformational change in the latter polypeptide ( 51).	bind
21128	1	6989	6	NULL	NULL	0	NULL	p68	NULL		bind	NULL				p180	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_23_20541_s_184	11927598	2 Furthermore, binding of p68 to p180 induces a conformational change in the latter polypeptide ( 51).	bind
21160	2	6989	6	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL				p180	NULL	conformational change of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20541_s_184	11927598	2 Furthermore, binding of p68 to p180 induces a conformational change in the latter polypeptide ( 51).	bind
25813	1	6990	5	13	NULL	NULL	NULL	PAI-1	GP		does not bind								heparin-binding domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5112_s_220	9030577	2 Furthermore, these data indicate that PAI-1 does not bind to the heparin-binding domain, as that would alter the quenching behavior of the coumarin probe.	bind
25814	2	6990	5	13	NULL	NULL	NULL				alter			heparin-binding domain		coumarin probe	NucleicAcid	quenching behaviour of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5112_s_220	9030577	2 Furthermore, these data indicate that PAI-1 does not bind to the heparin-binding domain, as that would alter the quenching behavior of the coumarin probe.	bind
58593	3	6990	5	13	NULL	NULL	NULL	statement 1	Process		does not alter					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5112_s_220	9030577	2 Furthermore, these data indicate that PAI-1 does not bind to the heparin-binding domain, as that would alter the quenching behavior of the coumarin probe.	bind
21161	1	6990	6	NULL	NULL	0	NULL	PAI-1	NULL		does not bind	NULL					NULL		heparin binding domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_5112_s_220	9030577	2 Furthermore, these data indicate that PAI-1 does not bind to the heparin-binding domain, as that would alter the quenching behavior of the coumarin probe.	bind
21162	2	6990	6	10	NULL	0	NULL				alter			heparin-binding domain		coumarin probe		quenching behavior of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5112_s_220	9030577	2 Furthermore, these data indicate that PAI-1 does not bind to the heparin-binding domain, as that would alter the quenching behavior of the coumarin probe.	bind
21163	3	6990	6	NULL	NULL	0	NULL	statement 1	NULL		does not alter	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_5112_s_220	9030577	2 Furthermore, these data indicate that PAI-1 does not bind to the heparin-binding domain, as that would alter the quenching behavior of the coumarin probe.	bind
25815	1	6991	5	13	NULL	NULL	NULL	E2	GP		bind					RSP5	GP	S. cerevisiae			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_21_13548_s_52	9153201	2 Furthermore, we show that a different subfamily of structurally related E2s bind to the  S. cerevisiae Hect protein RSP5 ( 17,  23).	bind
25816	2	6991	5	13	NULL	NULL	NULL	RSP5	GP		is a type of					Hect protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_21_13548_s_52	9153201	2 Furthermore, we show that a different subfamily of structurally related E2s bind to the  S. cerevisiae Hect protein RSP5 ( 17,  23).	bind
21164	1	6991	6	10	NULL	0	NULL	E2	NULL		bind	NULL				RSP5	NULL	S. cerevisiae 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_21_13548_s_52	9153201	2 Furthermore, we show that a different subfamily of structurally related E2s bind to the  S. cerevisiae Hect protein RSP5 ( 17,  23).	bind
44822	2	6991	6	10	NULL	0	NULL	RSP5	NULL		is a type of	NULL				hect protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_21_13548_s_52	9153201	2 Furthermore, we show that a different subfamily of structurally related E2s bind to the  S. cerevisiae Hect protein RSP5 ( 17,  23).	bind
25817	1	6992	5	13	NULL	NULL	NULL	GCK	GP		associates with					TRAF6.3	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_9_5259_s_135	10026130	2 GCK can also associate  in vivo with TRAF6.3 The CT extensions (Fig.  1) are required for the binding of GCK and GCKR to TRAF2 ( 46).	bind
25818	2	6992	5	13	NULL	NULL	NULL	GCK	GP		bind					TRAF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_9_5259_s_135	10026130	2 GCK can also associate  in vivo with TRAF6.3 The CT extensions (Fig.  1) are required for the binding of GCK and GCKR to TRAF2 ( 46).	bind
25819	3	6992	5	13	NULL	NULL	NULL				is required for			CT extensions		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_9_5259_s_135	10026130	2 GCK can also associate  in vivo with TRAF6.3 The CT extensions (Fig.  1) are required for the binding of GCK and GCKR to TRAF2 ( 46).	bind
25820	4	6992	5	13	NULL	NULL	NULL	GCKR	GP		bind					TRAF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_9_5259_s_135	10026130	2 GCK can also associate  in vivo with TRAF6.3 The CT extensions (Fig.  1) are required for the binding of GCK and GCKR to TRAF2 ( 46).	bind
25821	5	6992	5	13	NULL	NULL	NULL				is required for			CT extensions		statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_9_5259_s_135	10026130	2 GCK can also associate  in vivo with TRAF6.3 The CT extensions (Fig.  1) are required for the binding of GCK and GCKR to TRAF2 ( 46).	bind
21165	1	6992	6	NULL	NULL	0	NULL	GCK	NULL		associate	NULL				TRAF6.3	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5259_s_135	10026130	2 GCK can also associate  in vivo with TRAF6.3 The CT extensions (Fig.  1) are required for the binding of GCK and GCKR to TRAF2 ( 46).	bind
21166	2	6992	6	10	NULL	0	NULL	GCK			bind					TRAF2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_9_5259_s_135	10026130	2 GCK can also associate  in vivo with TRAF6.3 The CT extensions (Fig.  1) are required for the binding of GCK and GCKR to TRAF2 ( 46).	bind
21167	3	6992	6	10	NULL	0	NULL	GCKR			bind					TRAF2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_9_5259_s_135	10026130	2 GCK can also associate  in vivo with TRAF6.3 The CT extensions (Fig.  1) are required for the binding of GCK and GCKR to TRAF2 ( 46).	bind
21168	4	6992	6	NULL	NULL	0	NULL	statement 2	NULL		requires	NULL					NULL		CT extensions		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5259_s_135	10026130	2 GCK can also associate  in vivo with TRAF6.3 The CT extensions (Fig.  1) are required for the binding of GCK and GCKR to TRAF2 ( 46).	bind
21169	5	6992	6	NULL	NULL	0	NULL	statement 3	NULL		requires	NULL					NULL		CT extensions		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5259_s_135	10026130	2 GCK can also associate  in vivo with TRAF6.3 The CT extensions (Fig.  1) are required for the binding of GCK and GCKR to TRAF2 ( 46).	bind
25822	1	6993	5	13	NULL	NULL	NULL	capping enzyme	GP	mammalian	bind			triphosphatase domain		Spt5	GP	mammalian			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_334	11893740	2 Given that the individual triphosphatase and guanylyltransferase domains of mammalian capping enzyme bind  in vitro to mammalian Spt5 ( 13), our results suggest that the structural basis for the Spt5-capping enzyme interaction is distinct in fission yeast  versus mammals.	bind
25824	2	6993	5	13	NULL	NULL	NULL	capping enzyme	GP	mammalian	bind			guanylyltransferase domain		Spt5	GP	mammalian			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_334	11893740	2 Given that the individual triphosphatase and guanylyltransferase domains of mammalian capping enzyme bind  in vitro to mammalian Spt5 ( 13), our results suggest that the structural basis for the Spt5-capping enzyme interaction is distinct in fission yeast  versus mammals.	bind
25825	3	6993	5	13	NULL	NULL	NULL	Spt5	GP	fission yeast	bind					capping enzyme	GP	fission yeast			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_334	11893740	2 Given that the individual triphosphatase and guanylyltransferase domains of mammalian capping enzyme bind  in vitro to mammalian Spt5 ( 13), our results suggest that the structural basis for the Spt5-capping enzyme interaction is distinct in fission yeast  versus mammals.	bind
21170	1	6993	6	NULL	NULL	0	NULL	capping enzyme	NULL	mammalian	bind	NULL		triphosphatase domain		Spt5	NULL	mammalian			NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_334	11893740	2 Given that the individual triphosphatase and guanylyltransferase domains of mammalian capping enzyme bind  in vitro to mammalian Spt5 ( 13), our results suggest that the structural basis for the Spt5-capping enzyme interaction is distinct in fission yeast  versus mammals.	bind
21171	2	6993	6	NULL	NULL	0	NULL	capping enzyme	NULL	mammalian	bind	NULL		guanylyltransferase domain		Spt5	NULL	mammalian			NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_334	11893740	2 Given that the individual triphosphatase and guanylyltransferase domains of mammalian capping enzyme bind  in vitro to mammalian Spt5 ( 13), our results suggest that the structural basis for the Spt5-capping enzyme interaction is distinct in fission yeast  versus mammals.	bind
44846	3	6993	6	10	NULL	0	NULL	Spt5	NULL	fission yeast	bind	NULL				capping enzyme	NULL	fission yeast			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_334	11893740	2 Given that the individual triphosphatase and guanylyltransferase domains of mammalian capping enzyme bind  in vitro to mammalian Spt5 ( 13), our results suggest that the structural basis for the Spt5-capping enzyme interaction is distinct in fission yeast  versus mammals.	bind
25828	1	6994	5	13	NULL	NULL	NULL	snRNP	GP		bind					pre-mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17333_s_276	9211871	2 Given the known order of snRNP binding to the pre-mRNA during spliceosome assembly (for reviews, see Refs.	bind
25829	2	6994	5	13	NULL	NULL	NULL	statement 1	Process		occurs during					spliceosome		assembly of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17333_s_276	9211871	2 Given the known order of snRNP binding to the pre-mRNA during spliceosome assembly (for reviews, see Refs.	bind
21172	1	6994	6	NULL	NULL	0	NULL	snRNP	NULL		bind	NULL				pre-mRNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_28_17333_s_276	9211871	2 Given the known order of snRNP binding to the pre-mRNA during spliceosome assembly (for reviews, see Refs.	bind
21173	2	6994	6	10	NULL	0	NULL	statement 1			occurs during					spliceosome 		assembly of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17333_s_276	9211871	2 Given the known order of snRNP binding to the pre-mRNA during spliceosome assembly (for reviews, see Refs.	bind
25830	1	6995	5	13	NULL	NULL	NULL	ERp57	GP		bind		non-specifically			CRT	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_29686_s_310	12052826	2 Given these solubility changes, we considered the possibility that Zn2+-dependent ERp57 binding to CRT and CNX is nonspecific.	bind
25831	2	6995	5	13	NULL	NULL	NULL	statement 1	Process		is dependent on					Zn2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_29686_s_310	12052826	2 Given these solubility changes, we considered the possibility that Zn2+-dependent ERp57 binding to CRT and CNX is nonspecific.	bind
25833	3	6995	5	13	NULL	NULL	NULL	ERp57	GP		bind		non-specifically			CNX	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_29686_s_310	12052826	2 Given these solubility changes, we considered the possibility that Zn2+-dependent ERp57 binding to CRT and CNX is nonspecific.	bind
25834	4	6995	5	13	NULL	NULL	NULL	statement 3	Process		is dependent on					Zn2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_29686_s_310	12052826	2 Given these solubility changes, we considered the possibility that Zn2+-dependent ERp57 binding to CRT and CNX is nonspecific.	bind
21174	1	6995	6	NULL	NULL	0	NULL	ERp57	NULL		bind	NULL	non-specifically			CRT	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_33_29686_s_310	12052826	2 Given these solubility changes, we considered the possibility that Zn2+-dependent ERp57 binding to CRT and CNX is nonspecific.	bind
21175	2	6995	6	NULL	NULL	0	NULL	ERp57	NULL		bind	NULL	non-specifically			CNX	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_33_29686_s_310	12052826	2 Given these solubility changes, we considered the possibility that Zn2+-dependent ERp57 binding to CRT and CNX is nonspecific.	bind
21176	3	6995	6	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				Zn2+	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_33_29686_s_310	12052826	2 Given these solubility changes, we considered the possibility that Zn2+-dependent ERp57 binding to CRT and CNX is nonspecific.	bind
21177	4	6995	6	NULL	NULL	0	NULL	statement 2	NULL		is dependent on	NULL				Zn2+	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_33_29686_s_310	12052826	2 Given these solubility changes, we considered the possibility that Zn2+-dependent ERp57 binding to CRT and CNX is nonspecific.	bind
26407	1	6996	5	13	NULL	NULL	NULL	ROKalpha binding domain antibody	GP		activates					ROKalpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12680_s_173	11815607	2 h after incubation with the individual antibodies, the filter was subjected to RhoA binding with GST-RhoAV14 loaded with [gamma-32]GTP before exposing to x-ray film for 2 h.  B, ROKalpha binding domain antibody activates ROKalpha.	bind
21178	1	6996	6	NULL	NULL	0	NULL	antiROKalpha binding domain antibody	NULL		activates	NULL				ROKalpha	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12680_s_173	11815607	2 h after incubation with the individual antibodies, the filter was subjected to RhoA binding with GST-RhoAV14 loaded with [gamma-32]GTP before exposing to x-ray film for 2 h.  B, ROKalpha binding domain antibody activates ROKalpha.	bind
26408	1	6997	5	13	NULL	NULL	NULL	heparin	Chemical		bind					BPIs	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2149_s_128	8999916	2 Heparin Binding of the BPIs, LBPs, and Fusion Proteins Is Dependent on the N-terminal LPS Binding Domain	bind
26409	2	6997	5	13	NULL	NULL	NULL	statement 1	Process		is dependent on								N-terminal LPS binding domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2149_s_128	8999916	2 Heparin Binding of the BPIs, LBPs, and Fusion Proteins Is Dependent on the N-terminal LPS Binding Domain	bind
26410	3	6997	5	13	NULL	NULL	NULL	heparin	Chemical		bind					LBPs	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2149_s_128	8999916	2 Heparin Binding of the BPIs, LBPs, and Fusion Proteins Is Dependent on the N-terminal LPS Binding Domain	bind
26411	4	6997	5	13	NULL	NULL	NULL	statement 3	Process		is dependent on								N-terminal LPS binding domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2149_s_128	8999916	2 Heparin Binding of the BPIs, LBPs, and Fusion Proteins Is Dependent on the N-terminal LPS Binding Domain	bind
21179	1	6997	6	NULL	NULL	0	NULL	Heparin	NULL		bind	NULL				BPIs	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_4_2149_s_128	8999916	2 Heparin Binding of the BPIs, LBPs, and Fusion Proteins Is Dependent on the N-terminal LPS Binding Domain	bind
21180	2	6997	6	NULL	NULL	0	NULL	heparin	NULL		bind	NULL				LBPs	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_4_2149_s_128	8999916	2 Heparin Binding of the BPIs, LBPs, and Fusion Proteins Is Dependent on the N-terminal LPS Binding Domain	bind
21182	3	6997	6	10	NULL	0	NULL	statement 1			is dependent on								N-terminal LPS Binding Domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2149_s_128	8999916	2 Heparin Binding of the BPIs, LBPs, and Fusion Proteins Is Dependent on the N-terminal LPS Binding Domain	bind
21183	4	6997	6	10	NULL	0	NULL	statement 2			is dependent on								N-terminal LPS Binding Domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2149_s_128	8999916	2 Heparin Binding of the BPIs, LBPs, and Fusion Proteins Is Dependent on the N-terminal LPS Binding Domain	bind
26412	1	6999	5	13	NULL	NULL	NULL	TSP2	GP		bind					pro-MMP2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_11_8403_s_95	11113133	2 However, as revealed by a gelatinolytic assay with soluble [3]gelatin as a substrate, the binding of TSP2 to pro-MMP2 did not inhibit its activation by APMA (Fig.  2).	bind
26413	2	6999	5	13	NULL	NULL	NULL	pro-MMP2	GP		is activated by					APMA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_11_8403_s_95	11113133	2 However, as revealed by a gelatinolytic assay with soluble [3]gelatin as a substrate, the binding of TSP2 to pro-MMP2 did not inhibit its activation by APMA (Fig.  2).	bind
26414	3	6999	5	13	NULL	NULL	NULL	statement 1	Process		does not inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_11_8403_s_95	11113133	2 However, as revealed by a gelatinolytic assay with soluble [3]gelatin as a substrate, the binding of TSP2 to pro-MMP2 did not inhibit its activation by APMA (Fig.  2).	bind
21259	1	6999	6	NULL	NULL	0	NULL	TSP2	NULL		bind	NULL				pro-MMP2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_11_8403_s_95	11113133	2 However, as revealed by a gelatinolytic assay with soluble [3]gelatin as a substrate, the binding of TSP2 to pro-MMP2 did not inhibit its activation by APMA (Fig.  2).	bind
21260	2	6999	6	10	NULL	0	NULL	APMA			activates					pro-MMP2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_11_8403_s_95	11113133	2 However, as revealed by a gelatinolytic assay with soluble [3]gelatin as a substrate, the binding of TSP2 to pro-MMP2 did not inhibit its activation by APMA (Fig.  2).	bind
21261	3	6999	6	10	NULL	0	NULL	statement 1			does not inhibit					statement 2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_11_8403_s_95	11113133	2 However, as revealed by a gelatinolytic assay with soluble [3]gelatin as a substrate, the binding of TSP2 to pro-MMP2 did not inhibit its activation by APMA (Fig.  2).	bind
26415	1	7000	5	13	NULL	NULL	NULL	MDM2	GP		inhibit					MyoD	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( ),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
26416	2	7000	5	13	NULL	NULL	NULL	MDM2	GP		bind					Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( ),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
26417	3	7000	5	13	NULL	NULL	NULL	MDM2	GP		bind					pRb	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( ),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
26418	4	7000	5	13	NULL	NULL	NULL	MDM2	GP		target for		potentially			pRb	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( ),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
26419	5	7000	5	13	NULL	NULL	NULL	MDM2	GP		target for		potentially			Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( ),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
31524	6	7000	5	13	NULL	NULL	NULL	statement 4	Process		inhibits					pRb	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( ),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
31525	7	7000	5	13	NULL	NULL	NULL	statement 5	Process		inhibits					Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( ),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
21262	1	7000	6	NULL	NULL	0	NULL	MDM2	NULL		inhibits	NULL				MyoD	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( ),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
21263	2	7000	6	NULL	NULL	0	NULL	MDM2	NULL		bind	NULL				Sp1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( ),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
21264	3	7000	6	NULL	NULL	0	NULL	MDM2	NULL		bind	NULL				pRb	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( ),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
21265	4	7000	6	NULL	NULL	0	NULL	MDM2	NULL		target for	NULL	potentially			pRb	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( ),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
21266	5	7000	6	NULL	NULL	0	NULL	statement 4	NULL		inhibit	NULL				pRb	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( ),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
30720	6	7000	6	NULL	NULL	0	NULL	MDM2	NULL		target for	NULL	potentially			Sp1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( ),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
30721	7	7000	6	NULL	NULL	0	NULL	statement 6	NULL		inhibits	NULL				Sp1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( ),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
25374	1	7001	7	13	NULL	NULL	NULL	MDM2	GP		binds					Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( 2),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
25375	2	7001	7	13	NULL	NULL	NULL	MDM2	GP		binds					pRb	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( 2),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
25376	3	7001	7	13	NULL	NULL	NULL	MDM2	GP		inhibits					MyoD	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( 2),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
25377	4	7001	7	13	NULL	NULL	NULL	MDM2	GP		target for		potentially			pRb	GP	 inhibition of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( 2),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
25378	5	7001	7	13	NULL	NULL	NULL	MDM2	GP		target for		potentially			Sp1	GP	inhibition of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( 2),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
53255	6	7001	7	13	NULL	NULL	NULL	statement 4	Process		inhibits					pRb	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( 2),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
53256	7	7001	7	13	NULL	NULL	NULL	statement 5	Process		inhibits					Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_25_22615_s_113	12702724	2 However, because the region of MDM2 that inhibits MyoD  binds to both Sp1 and pRb ( 2),  these observations suggest that pRb and/or Sp1 were potential targets for MDM2  inhibition.	bind
22160	1	7003	6	13	NULL	NULL	NULL	DNA-PK	GP		phosphorylates					Ku	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_7848_s_274	10075677	2 However, Ku cannot be ruled out as a key target of p460 for its entry into DNA since (i) the consequence on IR sensitivity of mutations in Ku80 DNA-PK phosphorylation sites has not been evaluated yet, (ii) the intrinsic Ku DNA-dependent ATPase activity has been reported to be greatly stimulated when Ku was phosphorylated by DNA-PK ( 23), which could in turn modify its putative helicase activity, (iii) Ku molecules bound to a DNA-PK activating DNA fragment are indeed in a phosphorylated form under kinase permissive conditions.	bind
22162	3	7003	6	13	NULL	NULL	NULL	Ku	GP	ATPase activity of	is dependent on					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_7848_s_274	10075677	2 However, Ku cannot be ruled out as a key target of p460 for its entry into DNA since (i) the consequence on IR sensitivity of mutations in Ku80 DNA-PK phosphorylation sites has not been evaluated yet, (ii) the intrinsic Ku DNA-dependent ATPase activity has been reported to be greatly stimulated when Ku was phosphorylated by DNA-PK ( 23), which could in turn modify its putative helicase activity, (iii) Ku molecules bound to a DNA-PK activating DNA fragment are indeed in a phosphorylated form under kinase permissive conditions.	bind
22163	4	7003	6	13	NULL	NULL	NULL	statement 1	Process		stimulates					Ku	GP	intrinsic;;ATPase activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_7848_s_274	10075677	2 However, Ku cannot be ruled out as a key target of p460 for its entry into DNA since (i) the consequence on IR sensitivity of mutations in Ku80 DNA-PK phosphorylation sites has not been evaluated yet, (ii) the intrinsic Ku DNA-dependent ATPase activity has been reported to be greatly stimulated when Ku was phosphorylated by DNA-PK ( 23), which could in turn modify its putative helicase activity, (iii) Ku molecules bound to a DNA-PK activating DNA fragment are indeed in a phosphorylated form under kinase permissive conditions.	bind
22165	6	7003	6	13	NULL	NULL	NULL	statement 1	Process		modifies					Ku	GP	putative;;helicase activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_7848_s_274	10075677	2 However, Ku cannot be ruled out as a key target of p460 for its entry into DNA since (i) the consequence on IR sensitivity of mutations in Ku80 DNA-PK phosphorylation sites has not been evaluated yet, (ii) the intrinsic Ku DNA-dependent ATPase activity has been reported to be greatly stimulated when Ku was phosphorylated by DNA-PK ( 23), which could in turn modify its putative helicase activity, (iii) Ku molecules bound to a DNA-PK activating DNA fragment are indeed in a phosphorylated form under kinase permissive conditions.	bind
22166	7	7003	6	13	NULL	NULL	NULL	Ku molecules	GP	phosphorylated	bind					DNA-PK	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_7848_s_274	10075677	2 However, Ku cannot be ruled out as a key target of p460 for its entry into DNA since (i) the consequence on IR sensitivity of mutations in Ku80 DNA-PK phosphorylation sites has not been evaluated yet, (ii) the intrinsic Ku DNA-dependent ATPase activity has been reported to be greatly stimulated when Ku was phosphorylated by DNA-PK ( 23), which could in turn modify its putative helicase activity, (iii) Ku molecules bound to a DNA-PK activating DNA fragment are indeed in a phosphorylated form under kinase permissive conditions.	bind
22167	8	7003	6	13	NULL	NULL	NULL	statement 7	Process		activates					DNA fragment	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_7848_s_274	10075677	2 However, Ku cannot be ruled out as a key target of p460 for its entry into DNA since (i) the consequence on IR sensitivity of mutations in Ku80 DNA-PK phosphorylation sites has not been evaluated yet, (ii) the intrinsic Ku DNA-dependent ATPase activity has been reported to be greatly stimulated when Ku was phosphorylated by DNA-PK ( 23), which could in turn modify its putative helicase activity, (iii) Ku molecules bound to a DNA-PK activating DNA fragment are indeed in a phosphorylated form under kinase permissive conditions.	bind
25379	1	7003	7	NULL	NULL	0	NULL	DNA-PK 	NULL		phosphorylate	NULL				Ku	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_12_7848_s_274	10075677	2 However, Ku cannot be ruled out as a key target of p460 for its entry into DNA since (i) the consequence on IR sensitivity of mutations in Ku80 DNA-PK phosphorylation sites has not been evaluated yet, (ii) the intrinsic Ku DNA-dependent ATPase activity has been reported to be greatly stimulated when Ku was phosphorylated by DNA-PK ( 23), which could in turn modify its putative helicase activity, (iii) Ku molecules bound to a DNA-PK activating DNA fragment are indeed in a phosphorylated form under kinase permissive conditions.	bind
25380	2	7003	7	10	NULL	0	NULL	statement 1	NULL		stimulates	NULL				Ku	NULL	intrinsic;;ATPase activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_7848_s_274	10075677	2 However, Ku cannot be ruled out as a key target of p460 for its entry into DNA since (i) the consequence on IR sensitivity of mutations in Ku80 DNA-PK phosphorylation sites has not been evaluated yet, (ii) the intrinsic Ku DNA-dependent ATPase activity has been reported to be greatly stimulated when Ku was phosphorylated by DNA-PK ( 23), which could in turn modify its putative helicase activity, (iii) Ku molecules bound to a DNA-PK activating DNA fragment are indeed in a phosphorylated form under kinase permissive conditions.	bind
25381	4	7003	7	10	NULL	0	NULL	statement 1	NULL		modifies	NULL				Ku	NULL	putative;;helicase activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_7848_s_274	10075677	2 However, Ku cannot be ruled out as a key target of p460 for its entry into DNA since (i) the consequence on IR sensitivity of mutations in Ku80 DNA-PK phosphorylation sites has not been evaluated yet, (ii) the intrinsic Ku DNA-dependent ATPase activity has been reported to be greatly stimulated when Ku was phosphorylated by DNA-PK ( 23), which could in turn modify its putative helicase activity, (iii) Ku molecules bound to a DNA-PK activating DNA fragment are indeed in a phosphorylated form under kinase permissive conditions.	bind
25382	5	7003	7	10	NULL	0	NULL	Ku molecules	NULL	phosphorylated	bind	NULL				DNA-PK	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_7848_s_274	10075677	2 However, Ku cannot be ruled out as a key target of p460 for its entry into DNA since (i) the consequence on IR sensitivity of mutations in Ku80 DNA-PK phosphorylation sites has not been evaluated yet, (ii) the intrinsic Ku DNA-dependent ATPase activity has been reported to be greatly stimulated when Ku was phosphorylated by DNA-PK ( 23), which could in turn modify its putative helicase activity, (iii) Ku molecules bound to a DNA-PK activating DNA fragment are indeed in a phosphorylated form under kinase permissive conditions.	bind
25383	7	7003	7	10	NULL	0	NULL	statement 5	NULL		occurs under	NULL				kinase permissive condition	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_7848_s_274	10075677	2 However, Ku cannot be ruled out as a key target of p460 for its entry into DNA since (i) the consequence on IR sensitivity of mutations in Ku80 DNA-PK phosphorylation sites has not been evaluated yet, (ii) the intrinsic Ku DNA-dependent ATPase activity has been reported to be greatly stimulated when Ku was phosphorylated by DNA-PK ( 23), which could in turn modify its putative helicase activity, (iii) Ku molecules bound to a DNA-PK activating DNA fragment are indeed in a phosphorylated form under kinase permissive conditions.	bind
46413	6	7003	7	10	NULL	0	NULL	statement 5	NULL		activates	NULL				DNA fragment	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_12_7848_s_274	10075677	2 However, Ku cannot be ruled out as a key target of p460 for its entry into DNA since (i) the consequence on IR sensitivity of mutations in Ku80 DNA-PK phosphorylation sites has not been evaluated yet, (ii) the intrinsic Ku DNA-dependent ATPase activity has been reported to be greatly stimulated when Ku was phosphorylated by DNA-PK ( 23), which could in turn modify its putative helicase activity, (iii) Ku molecules bound to a DNA-PK activating DNA fragment are indeed in a phosphorylated form under kinase permissive conditions.	bind
53257	8	7003	7	10	NULL	0	NULL	Ku	NULL	ATPase activity of	is dependent on	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_12_7848_s_274	10075677	2 However, Ku cannot be ruled out as a key target of p460 for its entry into DNA since (i) the consequence on IR sensitivity of mutations in Ku80 DNA-PK phosphorylation sites has not been evaluated yet, (ii) the intrinsic Ku DNA-dependent ATPase activity has been reported to be greatly stimulated when Ku was phosphorylated by DNA-PK ( 23), which could in turn modify its putative helicase activity, (iii) Ku molecules bound to a DNA-PK activating DNA fragment are indeed in a phosphorylated form under kinase permissive conditions.	bind
21267	1	7004	6	13	NULL	NULL	NULL	Ku	GP		bind									C3H-NRE1 microcircles	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_9_5647_s_112	9038175	2 However, over several repetitions of the binding assay, Ku binding to C3H-NRE1 microcircles was consistently about 4-fold lower than binding to the GR-NRE1 microcircles.	bind
21268	2	7004	6	13	NULL	NULL	NULL	Ku	GP		bind									GR-NRE1 microcircles	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_9_5647_s_112	9038175	2 However, over several repetitions of the binding assay, Ku binding to C3H-NRE1 microcircles was consistently about 4-fold lower than binding to the GR-NRE1 microcircles.	bind
21269	3	7004	6	13	NULL	NULL	NULL	statement 1	Process		is lower than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_9_5647_s_112	9038175	2 However, over several repetitions of the binding assay, Ku binding to C3H-NRE1 microcircles was consistently about 4-fold lower than binding to the GR-NRE1 microcircles.	bind
25384	1	7004	7	10	NULL	0	NULL	Ku	NULL		binds to	NULL					NULL			C3H-NRE1 microcircles	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_9_5647_s_112	9038175	2 However, over several repetitions of the binding assay, Ku binding to C3H-NRE1 microcircles was consistently about 4-fold lower than binding to the GR-NRE1 microcircles.	bind
25385	2	7004	7	10	NULL	0	NULL	Ku	NULL		binds to	NULL					NULL			GR-NRE1 microcircles	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_9_5647_s_112	9038175	2 However, over several repetitions of the binding assay, Ku binding to C3H-NRE1 microcircles was consistently about 4-fold lower than binding to the GR-NRE1 microcircles.	bind
25386	3	7004	7	NULL	NULL	0	NULL	statement 1	NULL		is lower than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_9_5647_s_112	9038175	2 However, over several repetitions of the binding assay, Ku binding to C3H-NRE1 microcircles was consistently about 4-fold lower than binding to the GR-NRE1 microcircles.	bind
21270	1	7005	6	13	NULL	NULL	NULL	myosin	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_1_668_s_19	16186114	2 However, these myosin-ligand complexes promote an open switch II conformation of myosin (compared with the closed switch II conformation of M-ADP-Pi) (  -  ) and may also change the mechanism of myosin binding to actin.	bind
21271	2	7005	6	13	NULL	NULL	NULL	myosin-ligand complexes	GP		promote					myosin	GP	open switch II conformation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_1_668_s_19	16186114	2 However, these myosin-ligand complexes promote an open switch II conformation of myosin (compared with the closed switch II conformation of M-ADP-Pi) (  -  ) and may also change the mechanism of myosin binding to actin.	bind
21273	4	7005	6	13	NULL	NULL	NULL	myosin-ligand complexes	GP		change		may			statement 1	Process	mechanism of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_1_668_s_19	16186114	2 However, these myosin-ligand complexes promote an open switch II conformation of myosin (compared with the closed switch II conformation of M-ADP-Pi) (  -  ) and may also change the mechanism of myosin binding to actin.	bind
25387	1	7005	7	NULL	NULL	0	NULL	myosin	NULL		bind	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_668_s_19	16186114	2 However, these myosin-ligand complexes promote an open switch II conformation of myosin (compared with the closed switch II conformation of M-ADP-Pi) (  -  ) and may also change the mechanism of myosin binding to actin.	bind
25388	2	7005	7	NULL	NULL	0	NULL	myosin-ligand complexes	NULL		promote	NULL				myosin	NULL	open switch II conformation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_668_s_19	16186114	2 However, these myosin-ligand complexes promote an open switch II conformation of myosin (compared with the closed switch II conformation of M-ADP-Pi) (  -  ) and may also change the mechanism of myosin binding to actin.	bind
25390	3	7005	7	NULL	NULL	0	NULL	myosin-ligand complexes	NULL		change	NULL	may			statement 1	NULL	mechanism of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_668_s_19	16186114	2 However, these myosin-ligand complexes promote an open switch II conformation of myosin (compared with the closed switch II conformation of M-ADP-Pi) (  -  ) and may also change the mechanism of myosin binding to actin.	bind
21274	1	7006	6	13	NULL	NULL	NULL	X11L molecule	GP		bind					APP	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49448_s_272	12972431	2 However, we cannot rule out the possibility that more than one X11L molecule is bound to APP because both X11s could form homo- and/or heterodimers when the respective proteins were overexpressed in cells.	bind
21275	2	7006	6	13	NULL	NULL	NULL	X11L molecule	GP		bind					X11L molecule	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49448_s_272	12972431	2 However, we cannot rule out the possibility that more than one X11L molecule is bound to APP because both X11s could form homo- and/or heterodimers when the respective proteins were overexpressed in cells.	bind
53259	3	7006	6	13	NULL	NULL	NULL	statement 1	Process		forms					heterodimer	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49448_s_272	12972431	2 However, we cannot rule out the possibility that more than one X11L molecule is bound to APP because both X11s could form homo- and/or heterodimers when the respective proteins were overexpressed in cells.	bind
53260	4	7006	6	13	NULL	NULL	NULL	statement 2	Process		forms					homodimer	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49448_s_272	12972431	2 However, we cannot rule out the possibility that more than one X11L molecule is bound to APP because both X11s could form homo- and/or heterodimers when the respective proteins were overexpressed in cells.	bind
25391	1	7006	7	NULL	NULL	0	NULL	X11L molecule	NULL		bind	NULL				APP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49448_s_272	12972431	2 However, we cannot rule out the possibility that more than one X11L molecule is bound to APP because both X11s could form homo- and/or heterodimers when the respective proteins were overexpressed in cells.	bind
25392	2	7006	7	10	NULL	0	NULL	X11 molecule	NULL		bind	NULL				X11 molecule	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49448_s_272	12972431	2 However, we cannot rule out the possibility that more than one X11L molecule is bound to APP because both X11s could form homo- and/or heterodimers when the respective proteins were overexpressed in cells.	bind
25393	3	7006	7	10	NULL	0	NULL	statement 1	NULL		form	NULL				heterodimer	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49448_s_272	12972431	2 However, we cannot rule out the possibility that more than one X11L molecule is bound to APP because both X11s could form homo- and/or heterodimers when the respective proteins were overexpressed in cells.	bind
53258	4	7006	7	10	NULL	0	NULL	statement 2	NULL		forms	NULL				homodimer	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49448_s_272	12972431	2 However, we cannot rule out the possibility that more than one X11L molecule is bound to APP because both X11s could form homo- and/or heterodimers when the respective proteins were overexpressed in cells.	bind
21276	1	7007	6	13	NULL	NULL	NULL	BMP-2	GP		bind					BMPR-II 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_35_21345_s_40	8702914	2 Human BMPR-II was recently cloned, and it was shown that BMP-2, BMP-4, and OP-1/BMP-7 bound to BMPR-II and transduced signals in combination with certain type I receptors after forming heteromeric complexes ( 35,  36,  37).	bind
21277	2	7007	6	13	NULL	NULL	NULL	BMP-4	GP		bind					BMPR-II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_35_21345_s_40	8702914	2 Human BMPR-II was recently cloned, and it was shown that BMP-2, BMP-4, and OP-1/BMP-7 bound to BMPR-II and transduced signals in combination with certain type I receptors after forming heteromeric complexes ( 35,  36,  37).	bind
21278	3	7007	6	13	NULL	NULL	NULL	OP-1/BMP-7	GP		bind					BMPR-II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_35_21345_s_40	8702914	2 Human BMPR-II was recently cloned, and it was shown that BMP-2, BMP-4, and OP-1/BMP-7 bound to BMPR-II and transduced signals in combination with certain type I receptors after forming heteromeric complexes ( 35,  36,  37).	bind
25394	1	7007	7	13	NULL	NULL	NULL	BMP-2	GP		bind					BMPR-II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_35_21345_s_40	8702914	2 Human BMPR-II was recently cloned, and it was shown that BMP-2, BMP-4, and OP-1/BMP-7 bound to BMPR-II and transduced signals in combination with certain type I receptors after forming heteromeric complexes ( 35,  36,  37).	bind
25395	2	7007	7	13	NULL	NULL	NULL	BMP-4	GP		bind					BMPR-II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_35_21345_s_40	8702914	2 Human BMPR-II was recently cloned, and it was shown that BMP-2, BMP-4, and OP-1/BMP-7 bound to BMPR-II and transduced signals in combination with certain type I receptors after forming heteromeric complexes ( 35,  36,  37).	bind
25396	3	7007	7	13	NULL	NULL	NULL	OP-1/BMP-7	GP		bind					BMPR-II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_35_21345_s_40	8702914	2 Human BMPR-II was recently cloned, and it was shown that BMP-2, BMP-4, and OP-1/BMP-7 bound to BMPR-II and transduced signals in combination with certain type I receptors after forming heteromeric complexes ( 35,  36,  37).	bind
25400	8	7007	7	13	NULL	NULL	NULL	statement 5	GP		transduce					signals	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_35_21345_s_40	8702914	2 Human BMPR-II was recently cloned, and it was shown that BMP-2, BMP-4, and OP-1/BMP-7 bound to BMPR-II and transduced signals in combination with certain type I receptors after forming heteromeric complexes ( 35,  36,  37).	bind
25401	9	7007	7	13	NULL	NULL	NULL	statement 6	GP		transduce					signals	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_35_21345_s_40	8702914	2 Human BMPR-II was recently cloned, and it was shown that BMP-2, BMP-4, and OP-1/BMP-7 bound to BMPR-II and transduced signals in combination with certain type I receptors after forming heteromeric complexes ( 35,  36,  37).	bind
25402	7	7007	7	13	NULL	NULL	NULL	statement 4	GP		transduce					signals	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_35_21345_s_40	8702914	2 Human BMPR-II was recently cloned, and it was shown that BMP-2, BMP-4, and OP-1/BMP-7 bound to BMPR-II and transduced signals in combination with certain type I receptors after forming heteromeric complexes ( 35,  36,  37).	bind
53261	4	7007	7	13	NULL	NULL	NULL	statement 1	GP		complex with					type I receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_35_21345_s_40	8702914	2 Human BMPR-II was recently cloned, and it was shown that BMP-2, BMP-4, and OP-1/BMP-7 bound to BMPR-II and transduced signals in combination with certain type I receptors after forming heteromeric complexes ( 35,  36,  37).	bind
53262	5	7007	7	13	NULL	NULL	NULL	statement 2	GP		complex with					type I receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_35_21345_s_40	8702914	2 Human BMPR-II was recently cloned, and it was shown that BMP-2, BMP-4, and OP-1/BMP-7 bound to BMPR-II and transduced signals in combination with certain type I receptors after forming heteromeric complexes ( 35,  36,  37).	bind
53263	6	7007	7	13	NULL	NULL	NULL	statement 3	GP		complex with					type I receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_35_21345_s_40	8702914	2 Human BMPR-II was recently cloned, and it was shown that BMP-2, BMP-4, and OP-1/BMP-7 bound to BMPR-II and transduced signals in combination with certain type I receptors after forming heteromeric complexes ( 35,  36,  37).	bind
21279	1	7008	6	13	NULL	NULL	NULL	HuR	GP		is expressed in					HeLa cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_41_39470_s_39	12882963	2 HuR, which is expressed in HeLa cells ( ), also binds the p38 MAPK-responsive COX-2 and TNF AREs (  -  ).	bind
21280	2	7008	6	13	NULL	NULL	NULL	HuR	GP		bind					COX-2	GP	p38 MAPK-responsive			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_41_39470_s_39	12882963	2 HuR, which is expressed in HeLa cells ( ), also binds the p38 MAPK-responsive COX-2 and TNF AREs (  -  ).	bind
21281	3	7008	6	13	NULL	NULL	NULL	HuR	GP		bind					TNF	NucleicAcid			ARE	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_41_39470_s_39	12882963	2 HuR, which is expressed in HeLa cells ( ), also binds the p38 MAPK-responsive COX-2 and TNF AREs (  -  ).	bind
25403	2	7008	7	10	NULL	0	NULL	HuR	NULL		binds	NULL				COX-2	NULL	p38 MAPK-responsive			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_41_39470_s_39	12882963	2 HuR, which is expressed in HeLa cells ( ), also binds the p38 MAPK-responsive COX-2 and TNF AREs (  -  ).	bind
25404	3	7008	7	10	NULL	0	NULL	HuR	NULL		binds	NULL				TNF	NULL			ARE	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_41_39470_s_39	12882963	2 HuR, which is expressed in HeLa cells ( ), also binds the p38 MAPK-responsive COX-2 and TNF AREs (  -  ).	bind
46414	1	7008	7	10	NULL	0	NULL	HuR	NULL		is expressed in	NULL				HeLa cells	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_41_39470_s_39	12882963	2 HuR, which is expressed in HeLa cells ( ), also binds the p38 MAPK-responsive COX-2 and TNF AREs (  -  ).	bind
21282	1	7009	6	13	NULL	NULL	NULL	Fe2+	Chemical		bind					membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_23_16213_s_310	10347176	2 If a fraction of added Fe2+ is bound to the membranes, ascorbate, etc., the true binding affinity of Fe2+ will be higher than the calculated affinity, but the relative difference in Rb+-  versus Na+-containing media will remain.	bind
21283	2	7009	6	13	NULL	NULL	NULL	Fe2+	Chemical		bind					ascorbate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_23_16213_s_310	10347176	2 If a fraction of added Fe2+ is bound to the membranes, ascorbate, etc., the true binding affinity of Fe2+ will be higher than the calculated affinity, but the relative difference in Rb+-  versus Na+-containing media will remain.	bind
25405	1	7009	7	NULL	NULL	0	NULL	Fe2+	NULL		binds	NULL				membranes	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_23_16213_s_310	10347176	2 If a fraction of added Fe2+ is bound to the membranes, ascorbate, etc., the true binding affinity of Fe2+ will be higher than the calculated affinity, but the relative difference in Rb+-  versus Na+-containing media will remain.	bind
25406	2	7009	7	NULL	NULL	0	NULL	Fe2+	NULL		binds	NULL				ascorbate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_23_16213_s_310	10347176	2 If a fraction of added Fe2+ is bound to the membranes, ascorbate, etc., the true binding affinity of Fe2+ will be higher than the calculated affinity, but the relative difference in Rb+-  versus Na+-containing media will remain.	bind
23094	1	7010	6	13	NULL	NULL	NULL	hnRNP E1	GP		bind					FR mRNA	NucleicAcid			C/U-rich cis-element	NULL	megaloblastic erythroid precursors	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41510_s_290	11527973	2 If similar mechanisms are operative during erythroid development, (folate deficiency-induced) homocysteine-mediated augmentation of binding of hnRNP E1 to C/U-rich  cis-elements in mRNAs of FR, 15-lipoxygenase, and alpha-globin should result in coordinated up-regulation of FR and alpha-globin but down-regulation of 15-lipoxygenase in megaloblastic erythroid precursors.	bind
23095	2	7010	6	13	NULL	NULL	NULL	hnRNP E1	GP		bind					15-lipoxygenase mRNA	NucleicAcid			C/U-rich cis-element	NULL	megaloblastic erythroid precursors	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41510_s_290	11527973	2 If similar mechanisms are operative during erythroid development, (folate deficiency-induced) homocysteine-mediated augmentation of binding of hnRNP E1 to C/U-rich  cis-elements in mRNAs of FR, 15-lipoxygenase, and alpha-globin should result in coordinated up-regulation of FR and alpha-globin but down-regulation of 15-lipoxygenase in megaloblastic erythroid precursors.	bind
23096	3	7010	6	13	NULL	NULL	NULL	hnRNP E1	GP		bind					alpha-globin mRNA	NucleicAcid			C/U-rich cis-element	NULL	megaloblastic erythroid precursors	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41510_s_290	11527973	2 If similar mechanisms are operative during erythroid development, (folate deficiency-induced) homocysteine-mediated augmentation of binding of hnRNP E1 to C/U-rich  cis-elements in mRNAs of FR, 15-lipoxygenase, and alpha-globin should result in coordinated up-regulation of FR and alpha-globin but down-regulation of 15-lipoxygenase in megaloblastic erythroid precursors.	bind
23097	4	7010	6	13	NULL	NULL	NULL	homocysteine	AminoAcid		augments					statement 1	Process				NULL	megaloblastic erythroid precursors	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41510_s_290	11527973	2 If similar mechanisms are operative during erythroid development, (folate deficiency-induced) homocysteine-mediated augmentation of binding of hnRNP E1 to C/U-rich  cis-elements in mRNAs of FR, 15-lipoxygenase, and alpha-globin should result in coordinated up-regulation of FR and alpha-globin but down-regulation of 15-lipoxygenase in megaloblastic erythroid precursors.	bind
23098	5	7010	6	13	NULL	NULL	NULL	homocysteine	AminoAcid		augments					statement 2	Process				NULL	megaloblastic erythroid precursors	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41510_s_290	11527973	2 If similar mechanisms are operative during erythroid development, (folate deficiency-induced) homocysteine-mediated augmentation of binding of hnRNP E1 to C/U-rich  cis-elements in mRNAs of FR, 15-lipoxygenase, and alpha-globin should result in coordinated up-regulation of FR and alpha-globin but down-regulation of 15-lipoxygenase in megaloblastic erythroid precursors.	bind
23099	6	7010	6	13	NULL	NULL	NULL	homocysteine	AminoAcid		augments					statement 3	Process				NULL	megaloblastic erythroid precursors	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41510_s_290	11527973	2 If similar mechanisms are operative during erythroid development, (folate deficiency-induced) homocysteine-mediated augmentation of binding of hnRNP E1 to C/U-rich  cis-elements in mRNAs of FR, 15-lipoxygenase, and alpha-globin should result in coordinated up-regulation of FR and alpha-globin but down-regulation of 15-lipoxygenase in megaloblastic erythroid precursors.	bind
23100	7	7010	6	13	NULL	NULL	NULL	statement 4	Process		upregulates					FR	GP				NULL	megaloblastic erythroid precursors	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41510_s_290	11527973	2 If similar mechanisms are operative during erythroid development, (folate deficiency-induced) homocysteine-mediated augmentation of binding of hnRNP E1 to C/U-rich  cis-elements in mRNAs of FR, 15-lipoxygenase, and alpha-globin should result in coordinated up-regulation of FR and alpha-globin but down-regulation of 15-lipoxygenase in megaloblastic erythroid precursors.	bind
23101	8	7010	6	13	NULL	NULL	NULL	statement 6	Process		upregulates					alpha-globin 	GP				NULL	megaloblastic erythroid precursors	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41510_s_290	11527973	2 If similar mechanisms are operative during erythroid development, (folate deficiency-induced) homocysteine-mediated augmentation of binding of hnRNP E1 to C/U-rich  cis-elements in mRNAs of FR, 15-lipoxygenase, and alpha-globin should result in coordinated up-regulation of FR and alpha-globin but down-regulation of 15-lipoxygenase in megaloblastic erythroid precursors.	bind
23102	9	7010	6	13	NULL	NULL	NULL	statement 5	Process		downregulates					15-lipoxygenase 	GP				NULL	megaloblastic erythroid precursors	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41510_s_290	11527973	2 If similar mechanisms are operative during erythroid development, (folate deficiency-induced) homocysteine-mediated augmentation of binding of hnRNP E1 to C/U-rich  cis-elements in mRNAs of FR, 15-lipoxygenase, and alpha-globin should result in coordinated up-regulation of FR and alpha-globin but down-regulation of 15-lipoxygenase in megaloblastic erythroid precursors.	bind
25407	1	7010	7	10	NULL	0	NULL	hnRNP E1 	NULL		binds	NULL				FR mRNA	NULL			C/U-rich cis-elements	NULL	megaloblastic erythroid precursors	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41510_s_290	11527973	2 If similar mechanisms are operative during erythroid development, (folate deficiency-induced) homocysteine-mediated augmentation of binding of hnRNP E1 to C/U-rich  cis-elements in mRNAs of FR, 15-lipoxygenase, and alpha-globin should result in coordinated up-regulation of FR and alpha-globin but down-regulation of 15-lipoxygenase in megaloblastic erythroid precursors.	bind
25408	2	7010	7	10	NULL	0	NULL	hnRNP E1 	NULL		bind	NULL				15-lipoxygenase mRNA	NULL			C/U-rich cis-elements	NULL	megaloblastic erythroid precursors	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41510_s_290	11527973	2 If similar mechanisms are operative during erythroid development, (folate deficiency-induced) homocysteine-mediated augmentation of binding of hnRNP E1 to C/U-rich  cis-elements in mRNAs of FR, 15-lipoxygenase, and alpha-globin should result in coordinated up-regulation of FR and alpha-globin but down-regulation of 15-lipoxygenase in megaloblastic erythroid precursors.	bind
25409	3	7010	7	10	NULL	0	NULL	hnRNP E1 	NULL		binds	NULL				alpha-globin mRNA	NULL			C/U-rich cis-elements	NULL	megaloblastic erythroid precursors	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41510_s_290	11527973	2 If similar mechanisms are operative during erythroid development, (folate deficiency-induced) homocysteine-mediated augmentation of binding of hnRNP E1 to C/U-rich  cis-elements in mRNAs of FR, 15-lipoxygenase, and alpha-globin should result in coordinated up-regulation of FR and alpha-globin but down-regulation of 15-lipoxygenase in megaloblastic erythroid precursors.	bind
25410	4	7010	7	10	NULL	0	NULL	homocysteine	NULL		augments	NULL				statement 1	NULL				NULL	megaloblastic erythroid precursors	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41510_s_290	11527973	2 If similar mechanisms are operative during erythroid development, (folate deficiency-induced) homocysteine-mediated augmentation of binding of hnRNP E1 to C/U-rich  cis-elements in mRNAs of FR, 15-lipoxygenase, and alpha-globin should result in coordinated up-regulation of FR and alpha-globin but down-regulation of 15-lipoxygenase in megaloblastic erythroid precursors.	bind
25411	5	7010	7	10	NULL	0	NULL	homocysteine	NULL		augments	NULL				statement 2	NULL				NULL	megaloblastic erythroid precursors	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41510_s_290	11527973	2 If similar mechanisms are operative during erythroid development, (folate deficiency-induced) homocysteine-mediated augmentation of binding of hnRNP E1 to C/U-rich  cis-elements in mRNAs of FR, 15-lipoxygenase, and alpha-globin should result in coordinated up-regulation of FR and alpha-globin but down-regulation of 15-lipoxygenase in megaloblastic erythroid precursors.	bind
25412	6	7010	7	10	NULL	0	NULL	homocysteine	NULL		augments	NULL				statement 3	NULL				NULL	megaloblastic erythroid precursors	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41510_s_290	11527973	2 If similar mechanisms are operative during erythroid development, (folate deficiency-induced) homocysteine-mediated augmentation of binding of hnRNP E1 to C/U-rich  cis-elements in mRNAs of FR, 15-lipoxygenase, and alpha-globin should result in coordinated up-regulation of FR and alpha-globin but down-regulation of 15-lipoxygenase in megaloblastic erythroid precursors.	bind
25413	7	7010	7	10	NULL	0	NULL	statement 1	NULL		upregulates	NULL				FR	NULL				NULL	megaloblastic erythroid precursors	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41510_s_290	11527973	2 If similar mechanisms are operative during erythroid development, (folate deficiency-induced) homocysteine-mediated augmentation of binding of hnRNP E1 to C/U-rich  cis-elements in mRNAs of FR, 15-lipoxygenase, and alpha-globin should result in coordinated up-regulation of FR and alpha-globin but down-regulation of 15-lipoxygenase in megaloblastic erythroid precursors.	bind
25414	8	7010	7	10	NULL	0	NULL	statement 3	NULL		upregulates	NULL				alpha-globin	NULL				NULL	megaloblastic erythroid precursors	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41510_s_290	11527973	2 If similar mechanisms are operative during erythroid development, (folate deficiency-induced) homocysteine-mediated augmentation of binding of hnRNP E1 to C/U-rich  cis-elements in mRNAs of FR, 15-lipoxygenase, and alpha-globin should result in coordinated up-regulation of FR and alpha-globin but down-regulation of 15-lipoxygenase in megaloblastic erythroid precursors.	bind
25415	9	7010	7	10	NULL	0	NULL	statement 2	NULL		upregulates	NULL				15-lipoxygenase	NULL				NULL	megaloblastic erythroid precursors	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41510_s_290	11527973	2 If similar mechanisms are operative during erythroid development, (folate deficiency-induced) homocysteine-mediated augmentation of binding of hnRNP E1 to C/U-rich  cis-elements in mRNAs of FR, 15-lipoxygenase, and alpha-globin should result in coordinated up-regulation of FR and alpha-globin but down-regulation of 15-lipoxygenase in megaloblastic erythroid precursors.	bind
21284	1	7011	6	13	NULL	NULL	NULL	SREBP-1c	GP		does not bind		cooperatively			S14	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_37_34419_s_173	11448969	2 If the  in vitro EMSA is a reflection of the binding of these two factors to the S14 promoter  in vivo, then our results indicate that SREBP-1c and NF-Y do not bind cooperatively to the S14 promoter.	bind
21285	2	7011	6	13	NULL	NULL	NULL	NF-Y	GP		does not bind		cooperatively			S14	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_37_34419_s_173	11448969	2 If the  in vitro EMSA is a reflection of the binding of these two factors to the S14 promoter  in vivo, then our results indicate that SREBP-1c and NF-Y do not bind cooperatively to the S14 promoter.	bind
25416	1	7011	7	NULL	NULL	0	NULL	SREBP-1c	NULL		does not bind	NULL	cooperatively			S14	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_37_34419_s_173	11448969	2 If the  in vitro EMSA is a reflection of the binding of these two factors to the S14 promoter  in vivo, then our results indicate that SREBP-1c and NF-Y do not bind cooperatively to the S14 promoter.	bind
25417	2	7011	7	NULL	NULL	0	NULL	NF-Y 	NULL		does not bind	NULL	cooperatively			S14	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_37_34419_s_173	11448969	2 If the  in vitro EMSA is a reflection of the binding of these two factors to the S14 promoter  in vivo, then our results indicate that SREBP-1c and NF-Y do not bind cooperatively to the S14 promoter.	bind
21287	1	7012	6	13	NULL	NULL	NULL	Rap1A	GP		bind								CRR		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_18_11702_s_66	9115221	2 In a striking contrast, Rap1A bound to CRR yielded stronger signal than that to RBD under the same condition, indicating that it has the ability to bind equally to RBD and to CRR (see also Fig.  1 A).	bind
21288	2	7012	6	13	NULL	NULL	NULL	Rap1A	GP		bind								RBD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_18_11702_s_66	9115221	2 In a striking contrast, Rap1A bound to CRR yielded stronger signal than that to RBD under the same condition, indicating that it has the ability to bind equally to RBD and to CRR (see also Fig.  1 A).	bind
21289	3	7012	6	13	NULL	NULL	NULL	statement 1	Process		has equal affinity as					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_18_11702_s_66	9115221	2 In a striking contrast, Rap1A bound to CRR yielded stronger signal than that to RBD under the same condition, indicating that it has the ability to bind equally to RBD and to CRR (see also Fig.  1 A).	bind
25418	1	7012	7	NULL	NULL	0	NULL	Rap1A 	NULL		bind	NULL					NULL		CRR		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_18_11702_s_66	9115221	2 In a striking contrast, Rap1A bound to CRR yielded stronger signal than that to RBD under the same condition, indicating that it has the ability to bind equally to RBD and to CRR (see also Fig.  1 A).	bind
25419	2	7012	7	NULL	NULL	0	NULL	Rap1A 	NULL		bind	NULL					NULL		RBD		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_18_11702_s_66	9115221	2 In a striking contrast, Rap1A bound to CRR yielded stronger signal than that to RBD under the same condition, indicating that it has the ability to bind equally to RBD and to CRR (see also Fig.  1 A).	bind
25420	3	7012	7	10	NULL	0	NULL	statement 1	NULL		has equal affinity as	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_18_11702_s_66	9115221	2 In a striking contrast, Rap1A bound to CRR yielded stronger signal than that to RBD under the same condition, indicating that it has the ability to bind equally to RBD and to CRR (see also Fig.  1 A).	bind
21290	1	7013	6	13	NULL	NULL	NULL	HP1	GP		bind		specifically	chromo-domain		H3	AminoAcid	methylated	lysine 9		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25309_s_259	11316813	2 In accordance with this idea, several groups showed most recently that the chromo-domain of HP1 could bind specifically to methylated lysine 9 of H3 ( 36-38).	bind
25422	1	7013	7	NULL	NULL	0	NULL	HP1	NULL		bind	NULL	specifically	 chromo-domain		H3	NULL	methylated	 lysine 9		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_27_25309_s_259	11316813	2 In accordance with this idea, several groups showed most recently that the chromo-domain of HP1 could bind specifically to methylated lysine 9 of H3 ( 36-38).	bind
21291	1	7014	6	13	NULL	NULL	NULL	IRE1	GP		bind					TRAF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35867_s_283	11447214	2 In accordance with this, JNK was activated by ER stress through binding of IRE1 to TRAF2 ( 29), an adaptor protein that couples plasma membrane receptors to the activation of JNK.	bind
21292	2	7014	6	13	NULL	NULL	NULL	ER stress	Process		activates					JNK	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35867_s_283	11447214	2 In accordance with this, JNK was activated by ER stress through binding of IRE1 to TRAF2 ( 29), an adaptor protein that couples plasma membrane receptors to the activation of JNK.	bind
21293	3	7014	6	13	NULL	NULL	NULL	statement 2	Process		occurs through					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35867_s_283	11447214	2 In accordance with this, JNK was activated by ER stress through binding of IRE1 to TRAF2 ( 29), an adaptor protein that couples plasma membrane receptors to the activation of JNK.	bind
27016	4	7014	6	13	NULL	NULL	NULL	IRE1	GP		is a type of					plasma membrane receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35867_s_283	11447214	2 In accordance with this, JNK was activated by ER stress through binding of IRE1 to TRAF2 ( 29), an adaptor protein that couples plasma membrane receptors to the activation of JNK.	bind
27017	5	7014	6	13	NULL	NULL	NULL	TRAF2	GP		is a type of					adaptor protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35867_s_283	11447214	2 In accordance with this, JNK was activated by ER stress through binding of IRE1 to TRAF2 ( 29), an adaptor protein that couples plasma membrane receptors to the activation of JNK.	bind
25423	1	7014	7	NULL	NULL	0	NULL	 IRE1	NULL		bind	NULL				TRAF2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35867_s_283	11447214	2 In accordance with this, JNK was activated by ER stress through binding of IRE1 to TRAF2 ( 29), an adaptor protein that couples plasma membrane receptors to the activation of JNK.	bind
25424	2	7014	7	NULL	NULL	0	NULL	plasma membrane receptors	NULL		activates	NULL				JNK	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35867_s_283	11447214	2 In accordance with this, JNK was activated by ER stress through binding of IRE1 to TRAF2 ( 29), an adaptor protein that couples plasma membrane receptors to the activation of JNK.	bind
25425	3	7014	7	NULL	NULL	0	NULL	TRAF2	NULL		couples	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35867_s_283	11447214	2 In accordance with this, JNK was activated by ER stress through binding of IRE1 to TRAF2 ( 29), an adaptor protein that couples plasma membrane receptors to the activation of JNK.	bind
25426	4	7014	7	NULL	NULL	0	NULL	ER stress	NULL		activates	NULL				JNK	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_38_35867_s_283	11447214	2 In accordance with this, JNK was activated by ER stress through binding of IRE1 to TRAF2 ( 29), an adaptor protein that couples plasma membrane receptors to the activation of JNK.	bind
25427	5	7014	7	NULL	NULL	0	NULL	statement 4	NULL		occurs through	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_38_35867_s_283	11447214	2 In accordance with this, JNK was activated by ER stress through binding of IRE1 to TRAF2 ( 29), an adaptor protein that couples plasma membrane receptors to the activation of JNK.	bind
28017	6	7014	7	NULL	NULL	0	NULL	TRAF2	NULL		is a type of	NULL				adaptor protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_38_35867_s_283	11447214	2 In accordance with this, JNK was activated by ER stress through binding of IRE1 to TRAF2 ( 29), an adaptor protein that couples plasma membrane receptors to the activation of JNK.	bind
46415	7	7014	7	10	NULL	0	NULL	IRE1	NULL		is a type of	NULL				\tplasma membrane receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_38_35867_s_283	11447214	2 In accordance with this, JNK was activated by ER stress through binding of IRE1 to TRAF2 ( 29), an adaptor protein that couples plasma membrane receptors to the activation of JNK.	bind
21294	1	7015	6	13	NULL	NULL	NULL	LCE	GP	mouse	possesses				promoter			potential		SREBP binding sequence (TCATGCCAG)	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_48_45358_s_290	11567032	2 In addition, analysis of the mouse LCE promoter sequence identified in the Celera data base revealed a potential SREBP binding sequence (TCATGCCAG) located 364 base pairs upstream of exon 1 of the gene.	bind
25862	1	7015	7	NULL	NULL	0	NULL	LCE	NULL	mouse	contains	NULL			promoter		NULL	potential		SREBP binding sequence (TCATGCCAG)	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_48_45358_s_290	11567032	2 In addition, analysis of the mouse LCE promoter sequence identified in the Celera data base revealed a potential SREBP binding sequence (TCATGCCAG) located 364 base pairs upstream of exon 1 of the gene.	bind
21295	1	7016	6	13	NULL	NULL	NULL	HeLa nuclear protein extract	GP		contains					GATA-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_36_22076_s_145	8703016	2 In addition, HeLa nuclear protein extract, which contains GATA-2, but not GATA-1 ( 29), did not bind either the normal or patient oligonucleotide, but did bind to Sp1 as a control.	bind
21296	2	7016	6	13	NULL	NULL	NULL	HeLa nuclear protein extract	GP		does not contain					GATA-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_36_22076_s_145	8703016	2 In addition, HeLa nuclear protein extract, which contains GATA-2, but not GATA-1 ( 29), did not bind either the normal or patient oligonucleotide, but did bind to Sp1 as a control.	bind
21299	3	7016	6	13	NULL	NULL	NULL	HeLa nuclear protein extract	GP		bind					Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_36_22076_s_145	8703016	2 In addition, HeLa nuclear protein extract, which contains GATA-2, but not GATA-1 ( 29), did not bind either the normal or patient oligonucleotide, but did bind to Sp1 as a control.	bind
25428	1	7016	7	NULL	NULL	0	NULL	HeLa nuclear protein extract	NULL		contains	NULL				GATA-2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_36_22076_s_145	8703016	2 In addition, HeLa nuclear protein extract, which contains GATA-2, but not GATA-1 ( 29), did not bind either the normal or patient oligonucleotide, but did bind to Sp1 as a control.	bind
25429	2	7016	7	NULL	NULL	0	NULL	HeLa nuclear protein extract	NULL		does not contain	NULL				GATA-1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_36_22076_s_145	8703016	2 In addition, HeLa nuclear protein extract, which contains GATA-2, but not GATA-1 ( 29), did not bind either the normal or patient oligonucleotide, but did bind to Sp1 as a control.	bind
25432	3	7016	7	NULL	NULL	0	NULL	HeLa nuclear protein extract	NULL		binds	NULL				Sp1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_36_22076_s_145	8703016	2 In addition, HeLa nuclear protein extract, which contains GATA-2, but not GATA-1 ( 29), did not bind either the normal or patient oligonucleotide, but did bind to Sp1 as a control.	bind
21300	1	7017	6	13	NULL	NULL	NULL	FGF-1	GP		bind		high affinity			FGFR2 IIIb	GP	soluble			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2444_s_269	11714710	2 In addition, high affinity binding of both FGF-1 and FGF-7 to soluble FGFR2 IIIb is not dependent on heparin, whereas efficient binding to the native receptor requires heparin ( 19,  50).	bind
21301	2	7017	6	13	NULL	NULL	NULL	FGF-7	GP		bind		high affinity			FGFR2 IIIb	GP	soluble			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2444_s_269	11714710	2 In addition, high affinity binding of both FGF-1 and FGF-7 to soluble FGFR2 IIIb is not dependent on heparin, whereas efficient binding to the native receptor requires heparin ( 19,  50).	bind
21302	3	7017	6	13	NULL	NULL	NULL	statement 1	Process		is not dependent on					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2444_s_269	11714710	2 In addition, high affinity binding of both FGF-1 and FGF-7 to soluble FGFR2 IIIb is not dependent on heparin, whereas efficient binding to the native receptor requires heparin ( 19,  50).	bind
21303	4	7017	6	13	NULL	NULL	NULL	statement 2	Process		is not dependent on					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2444_s_269	11714710	2 In addition, high affinity binding of both FGF-1 and FGF-7 to soluble FGFR2 IIIb is not dependent on heparin, whereas efficient binding to the native receptor requires heparin ( 19,  50).	bind
21304	5	7017	6	13	NULL	NULL	NULL	FGF-1	GP		bind		efficiently			receptor	GP	native			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2444_s_269	11714710	2 In addition, high affinity binding of both FGF-1 and FGF-7 to soluble FGFR2 IIIb is not dependent on heparin, whereas efficient binding to the native receptor requires heparin ( 19,  50).	bind
27018	6	7017	6	13	NULL	NULL	NULL	FGF-7	GP		bind		efficiently			receptor	GP	native			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2444_s_269	11714710	2 In addition, high affinity binding of both FGF-1 and FGF-7 to soluble FGFR2 IIIb is not dependent on heparin, whereas efficient binding to the native receptor requires heparin ( 19,  50).	bind
27019	7	7017	6	13	NULL	NULL	NULL	statement 5	Process		requires					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2444_s_269	11714710	2 In addition, high affinity binding of both FGF-1 and FGF-7 to soluble FGFR2 IIIb is not dependent on heparin, whereas efficient binding to the native receptor requires heparin ( 19,  50).	bind
27020	8	7017	6	13	NULL	NULL	NULL	statement 6	Process		requires					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2444_s_269	11714710	2 In addition, high affinity binding of both FGF-1 and FGF-7 to soluble FGFR2 IIIb is not dependent on heparin, whereas efficient binding to the native receptor requires heparin ( 19,  50).	bind
25433	1	7017	7	NULL	NULL	0	NULL	FGF-1	NULL		bind	NULL	high affinity			FGFR2 IIIb 	NULL	soluble			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2444_s_269	11714710	2 In addition, high affinity binding of both FGF-1 and FGF-7 to soluble FGFR2 IIIb is not dependent on heparin, whereas efficient binding to the native receptor requires heparin ( 19,  50).	bind
25434	2	7017	7	NULL	NULL	0	NULL	FGF-7	NULL		bind	NULL	high affinity			FGFR2 IIIb	NULL	soluble			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2444_s_269	11714710	2 In addition, high affinity binding of both FGF-1 and FGF-7 to soluble FGFR2 IIIb is not dependent on heparin, whereas efficient binding to the native receptor requires heparin ( 19,  50).	bind
25435	3	7017	7	NULL	NULL	0	NULL	statement 1	NULL		does not depend on	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2444_s_269	11714710	2 In addition, high affinity binding of both FGF-1 and FGF-7 to soluble FGFR2 IIIb is not dependent on heparin, whereas efficient binding to the native receptor requires heparin ( 19,  50).	bind
25436	4	7017	7	NULL	NULL	0	NULL	statement 2	NULL		does not depend on	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2444_s_269	11714710	2 In addition, high affinity binding of both FGF-1 and FGF-7 to soluble FGFR2 IIIb is not dependent on heparin, whereas efficient binding to the native receptor requires heparin ( 19,  50).	bind
25437	5	7017	7	NULL	NULL	0	NULL	FGF-1	NULL		bind	NULL				FGFR2 IIIb	NULL	native receptor			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2444_s_269	11714710	2 In addition, high affinity binding of both FGF-1 and FGF-7 to soluble FGFR2 IIIb is not dependent on heparin, whereas efficient binding to the native receptor requires heparin ( 19,  50).	bind
25438	6	7017	7	NULL	NULL	0	NULL	FGF-7	NULL		bind	NULL				FGFR2 IIIb	NULL	native receptor			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2444_s_269	11714710	2 In addition, high affinity binding of both FGF-1 and FGF-7 to soluble FGFR2 IIIb is not dependent on heparin, whereas efficient binding to the native receptor requires heparin ( 19,  50).	bind
25439	7	7017	7	NULL	NULL	0	NULL	statement 5	NULL		requires	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2444_s_269	11714710	2 In addition, high affinity binding of both FGF-1 and FGF-7 to soluble FGFR2 IIIb is not dependent on heparin, whereas efficient binding to the native receptor requires heparin ( 19,  50).	bind
25440	8	7017	7	NULL	NULL	0	NULL	statement 6	NULL		requires	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2444_s_269	11714710	2 In addition, high affinity binding of both FGF-1 and FGF-7 to soluble FGFR2 IIIb is not dependent on heparin, whereas efficient binding to the native receptor requires heparin ( 19,  50).	bind
21306	1	7018	6	13	NULL	NULL	NULL	thrombin	GP		bind					thrombomodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_45_28168_s_265	8910432	2 In addition, the binding of thrombin to thrombomodulin fixes the active site of the otherwise soluble enzyme at a specific height above the membrane surface ( 12).	bind
25441	1	7018	7	NULL	NULL	0	NULL	thrombin	NULL		bind	NULL				thrombomodulin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_45_28168_s_265	8910432	2 In addition, the binding of thrombin to thrombomodulin fixes the active site of the otherwise soluble enzyme at a specific height above the membrane surface ( 12).	bind
21308	1	7019	6	13	NULL	NULL	NULL	ficolin	GP	recombinant;;wild-type	does not bind					GlcNAc	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_6534_s_174	14660572	2 In addition, we are unable to explain why the majority of recombinant wild-type ficolin did not bind the GlcNAc column.	bind
25442	1	7019	7	10	NULL	0	NULL	ficolin	NULL	recombinant;;wild-type	does not bind	NULL				GlcNAc column	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_6534_s_174	14660572	2 In addition, we are unable to explain why the majority of recombinant wild-type ficolin did not bind the GlcNAc column.	bind
21309	1	7020	6	13	NULL	NULL	NULL	tsf: su coat proteins	GP		bind					GroEL	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17473_s_350	14764588	2 In agreement with the  in vitro results presented here, our recent  in vivo experiments also show that not only is a higher percentage of  tsf: su coat proteins bound to GroEL than their  tsf parents, but the  tsf: su coat proteins actually induce GroEL expression as compared with the induced GroEL levels for the  tsf coat proteins.	bind
21310	2	7020	6	13	NULL	NULL	NULL	tsf	GP		bind					GroEL	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17473_s_350	14764588	2 In agreement with the  in vitro results presented here, our recent  in vivo experiments also show that not only is a higher percentage of  tsf: su coat proteins bound to GroEL than their  tsf parents, but the  tsf: su coat proteins actually induce GroEL expression as compared with the induced GroEL levels for the  tsf coat proteins.	bind
21311	3	7020	6	13	NULL	NULL	NULL	statement 1	GP	affinity of	is higher than					statement 2	GP	affinity of			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17473_s_350	14764588	2 In agreement with the  in vitro results presented here, our recent  in vivo experiments also show that not only is a higher percentage of  tsf: su coat proteins bound to GroEL than their  tsf parents, but the  tsf: su coat proteins actually induce GroEL expression as compared with the induced GroEL levels for the  tsf coat proteins.	bind
21312	4	7020	6	13	NULL	NULL	NULL	tsf: su coat proteins	GP		induce					GroEL	GP	expression of			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17473_s_350	14764588	2 In agreement with the  in vitro results presented here, our recent  in vivo experiments also show that not only is a higher percentage of  tsf: su coat proteins bound to GroEL than their  tsf parents, but the  tsf: su coat proteins actually induce GroEL expression as compared with the induced GroEL levels for the  tsf coat proteins.	bind
25443	1	7020	7	NULL	NULL	0	NULL	tsf: su coat proteins	NULL		bind	NULL				GroEL	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17473_s_350	14764588	2 In agreement with the  in vitro results presented here, our recent  in vivo experiments also show that not only is a higher percentage of  tsf: su coat proteins bound to GroEL than their  tsf parents, but the  tsf: su coat proteins actually induce GroEL expression as compared with the induced GroEL levels for the  tsf coat proteins.	bind
25444	2	7020	7	NULL	NULL	0	NULL	tsf	NULL		bind	NULL				GroEL	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17473_s_350	14764588	2 In agreement with the  in vitro results presented here, our recent  in vivo experiments also show that not only is a higher percentage of  tsf: su coat proteins bound to GroEL than their  tsf parents, but the  tsf: su coat proteins actually induce GroEL expression as compared with the induced GroEL levels for the  tsf coat proteins.	bind
25445	3	7020	7	10	NULL	0	NULL	statement 1	NULL	affinity of	is greater than	NULL				statement 2	NULL	affinity of			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17473_s_350	14764588	2 In agreement with the  in vitro results presented here, our recent  in vivo experiments also show that not only is a higher percentage of  tsf: su coat proteins bound to GroEL than their  tsf parents, but the  tsf: su coat proteins actually induce GroEL expression as compared with the induced GroEL levels for the  tsf coat proteins.	bind
25446	4	7020	7	10	NULL	0	NULL	 tsf: su coat proteins 	NULL		induce	NULL				GroEL	NULL	expression of			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17473_s_350	14764588	2 In agreement with the  in vitro results presented here, our recent  in vivo experiments also show that not only is a higher percentage of  tsf: su coat proteins bound to GroEL than their  tsf parents, but the  tsf: su coat proteins actually induce GroEL expression as compared with the induced GroEL levels for the  tsf coat proteins.	bind
21313	1	7021	6	13	NULL	NULL	NULL	integrin	GP		adopts			I-domain				classic	dinucleotide binding fold		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25162_s_25	9312128	2 In all cases, the integrin I-domain adopts the classic "`dinucleotide binding"` fold with a central hydrophobic parallel beta-sheet, flanked on two sides by amphipathic helices ( 10).	bind
21314	2	7021	6	13	NULL	NULL	NULL	integrin	GP	classic	contains			dinucleotide binding fold				central hydrophobic parallel	beta sheet		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25162_s_25	9312128	2 In all cases, the integrin I-domain adopts the classic "`dinucleotide binding"` fold with a central hydrophobic parallel beta-sheet, flanked on two sides by amphipathic helices ( 10).	bind
21315	3	7021	6	13	NULL	NULL	NULL	integrin	GP	classic	is flanked by			dinucleotide binding fold					amphipathic helices		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25162_s_25	9312128	2 In all cases, the integrin I-domain adopts the classic "`dinucleotide binding"` fold with a central hydrophobic parallel beta-sheet, flanked on two sides by amphipathic helices ( 10).	bind
25447	1	7021	7	NULL	NULL	0	NULL	integrin	NULL		adopts	NULL		 I-domain			NULL	classic	dinucleotide binding fold		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25162_s_25	9312128	2 In all cases, the integrin I-domain adopts the classic "`dinucleotide binding"` fold with a central hydrophobic parallel beta-sheet, flanked on two sides by amphipathic helices ( 10).	bind
25448	2	7021	7	10	NULL	0	NULL	integrin	NULL	classic	contain	NULL		dinucleotide binding fold			NULL	 central hydrophobic parallel	beta-sheet		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25162_s_25	9312128	2 In all cases, the integrin I-domain adopts the classic "`dinucleotide binding"` fold with a central hydrophobic parallel beta-sheet, flanked on two sides by amphipathic helices ( 10).	bind
25449	3	7021	7	10	NULL	0	NULL	integrin	NULL	classic	flanked by	NULL		dinucleotide binding fold			NULL		amphipathic helices		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25162_s_25	9312128	2 In all cases, the integrin I-domain adopts the classic "`dinucleotide binding"` fold with a central hydrophobic parallel beta-sheet, flanked on two sides by amphipathic helices ( 10).	bind
21316	1	7022	6	13	NULL	NULL	NULL	PTPD1	GP		bind								PH domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41124_s_278	11013262	2 In consideration of the molecular mechanism regulating Etk activity, it is likely that the binding of PTPD1 to the PH domain dissociates the intramolecular interaction between the PH domain and other subdomains of Etk, leading to Etk in an open conformation and kinase-active state.	bind
21317	2	7022	6	13	NULL	NULL	NULL	Etk	GP		interacts with		intramolecularly	PH domain		Etk	GP		subdomains		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41124_s_278	11013262	2 In consideration of the molecular mechanism regulating Etk activity, it is likely that the binding of PTPD1 to the PH domain dissociates the intramolecular interaction between the PH domain and other subdomains of Etk, leading to Etk in an open conformation and kinase-active state.	bind
21318	3	7022	6	13	NULL	NULL	NULL	statement 1	Process		dissociates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41124_s_278	11013262	2 In consideration of the molecular mechanism regulating Etk activity, it is likely that the binding of PTPD1 to the PH domain dissociates the intramolecular interaction between the PH domain and other subdomains of Etk, leading to Etk in an open conformation and kinase-active state.	bind
21319	4	7022	6	13	NULL	NULL	NULL	statement 3	Process		leads to					Etk	GP	open conformation of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41124_s_278	11013262	2 In consideration of the molecular mechanism regulating Etk activity, it is likely that the binding of PTPD1 to the PH domain dissociates the intramolecular interaction between the PH domain and other subdomains of Etk, leading to Etk in an open conformation and kinase-active state.	bind
25450	1	7022	7	NULL	NULL	0	NULL	PTPD1	NULL		bind	NULL				Etk	NULL		PH domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41124_s_278	11013262	2 In consideration of the molecular mechanism regulating Etk activity, it is likely that the binding of PTPD1 to the PH domain dissociates the intramolecular interaction between the PH domain and other subdomains of Etk, leading to Etk in an open conformation and kinase-active state.	bind
25451	2	7022	7	10	NULL	0	NULL	Etk	NULL		interacts with	NULL	intramolecular	PH domain		Etk	NULL		subdomains		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41124_s_278	11013262	2 In consideration of the molecular mechanism regulating Etk activity, it is likely that the binding of PTPD1 to the PH domain dissociates the intramolecular interaction between the PH domain and other subdomains of Etk, leading to Etk in an open conformation and kinase-active state.	bind
25452	3	7022	7	NULL	NULL	0	NULL	statement 1	NULL		dissociates	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41124_s_278	11013262	2 In consideration of the molecular mechanism regulating Etk activity, it is likely that the binding of PTPD1 to the PH domain dissociates the intramolecular interaction between the PH domain and other subdomains of Etk, leading to Etk in an open conformation and kinase-active state.	bind
25453	4	7022	7	NULL	NULL	0	NULL	statement 3	NULL		leads to	NULL				Etk	NULL	open conformation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41124_s_278	11013262	2 In consideration of the molecular mechanism regulating Etk activity, it is likely that the binding of PTPD1 to the PH domain dissociates the intramolecular interaction between the PH domain and other subdomains of Etk, leading to Etk in an open conformation and kinase-active state.	bind
25454	5	7022	7	NULL	NULL	0	NULL	statement 3	NULL		leads to	NULL				Etk	NULL	kinase-active state of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41124_s_278	11013262	2 In consideration of the molecular mechanism regulating Etk activity, it is likely that the binding of PTPD1 to the PH domain dissociates the intramolecular interaction between the PH domain and other subdomains of Etk, leading to Etk in an open conformation and kinase-active state.	bind
21320	1	7023	6	13	NULL	NULL	NULL	TARC receptor	GP	T cell	specific for		highly			TARC	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_35_21514_s_240	8702936	2 In contrast to other known CC chemokine receptors that usually bind more than one chemokine, the TARC receptor on T cells appears to be highly specific for TARC.	bind
21321	2	7023	6	13	NULL	NULL	NULL	CC chemokine receptors	GP		bind					chemokine	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_35_21514_s_240	8702936	2 In contrast to other known CC chemokine receptors that usually bind more than one chemokine, the TARC receptor on T cells appears to be highly specific for TARC.	bind
25455	1	7023	7	NULL	NULL	0	NULL	CC chemokine receptors	NULL		bind	NULL				chemokine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_35_21514_s_240	8702936	2 In contrast to other known CC chemokine receptors that usually bind more than one chemokine, the TARC receptor on T cells appears to be highly specific for TARC.	bind
25456	2	7023	7	10	NULL	0	NULL	TARC receptor	NULL	T cells	specific for	NULL	highly			TARC	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_35_21514_s_240	8702936	2 In contrast to other known CC chemokine receptors that usually bind more than one chemokine, the TARC receptor on T cells appears to be highly specific for TARC.	bind
21322	1	7024	6	13	NULL	NULL	NULL	paxillin fragment	GP	expression of	failed to bind								alpha 4 tail		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20887_s_208	11919182	2 In contrast, expression of a fragment of paxillin that failed to bind to the alpha4 tail, P(Met1-Lys125), did not inhibit cell migration on fibrinogen (Fig.  7 A, left panel).	bind
21323	2	7024	6	13	NULL	NULL	NULL	fibrinogen	GP		did not inhibit			P(Met1-Lys125)		cell migration	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20887_s_208	11919182	2 In contrast, expression of a fragment of paxillin that failed to bind to the alpha4 tail, P(Met1-Lys125), did not inhibit cell migration on fibrinogen (Fig.  7 A, left panel).	bind
25457	1	7024	7	NULL	NULL	0	NULL	 paxillin fragment	NULL		does not bind	NULL					NULL		  alpha4 tail		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_23_20887_s_208	11919182	2 In contrast, expression of a fragment of paxillin that failed to bind to the alpha4 tail, P(Met1-Lys125), did not inhibit cell migration on fibrinogen (Fig.  7 A, left panel).	bind
25458	2	7024	7	NULL	NULL	0	NULL	paxillin fragment	NULL		does not bind	NULL					NULL		P(Met1-Lys125)		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_23_20887_s_208	11919182	2 In contrast, expression of a fragment of paxillin that failed to bind to the alpha4 tail, P(Met1-Lys125), did not inhibit cell migration on fibrinogen (Fig.  7 A, left panel).	bind
25459	3	7024	7	NULL	NULL	0	NULL	paxillin fragment	NULL		does not inhibit	NULL				fibrinogen	NULL	cell migration on			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20887_s_208	11919182	2 In contrast, expression of a fragment of paxillin that failed to bind to the alpha4 tail, P(Met1-Lys125), did not inhibit cell migration on fibrinogen (Fig.  7 A, left panel).	bind
21324	1	7025	6	13	NULL	NULL	NULL	CD151	GP		associates with					CD9	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
21325	2	7025	6	13	NULL	NULL	NULL	CD151	GP		associates with					CD81	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
21326	3	7025	6	13	NULL	NULL	NULL	alpha3beta1	GP		associates with					CD9	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
21327	4	7025	6	13	NULL	NULL	NULL	alpha3beta1	GP		associates with					CD81	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
21328	5	7025	6	13	NULL	NULL	NULL	alpha6beta1	GP		associates with					CD9	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
21329	6	7025	6	13	NULL	NULL	NULL	alpha6beta1	GP		associates with					CD81	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
21330	7	7025	6	13	NULL	NULL	NULL	EWI-2	GP		does not associate with					alpha 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
21331	8	7025	6	13	NULL	NULL	NULL	EWI-2	GP		does not associate with					alpha3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
21332	9	7025	6	13	NULL	NULL	NULL	EWI-2	GP		does not associate with					alpha6	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
21333	10	7025	6	13	NULL	NULL	NULL	EWI-2	GP		does not associate with					beta1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
21334	11	7025	6	13	NULL	NULL	NULL	EWI-2	GP		does not associate with					CD151	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
21335	12	7025	6	13	NULL	NULL	NULL	EWI-F	GP		does not associate with					alpha2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
21336	13	7025	6	13	NULL	NULL	NULL	EWI-F	GP		does not associate with					alpha3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
21337	14	7025	6	13	NULL	NULL	NULL	EWI-F	GP		does not associate with					alpha6	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
21338	15	7025	6	13	NULL	NULL	NULL	EWI-F	GP		does not associate with					beta1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
21339	16	7025	6	13	NULL	NULL	NULL	EWI-F	GP		does not associate with					CD151	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
25460	1	7025	7	NULL	NULL	0	NULL	CD151	NULL		associate with	NULL				CD9	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
25461	2	7025	7	NULL	NULL	0	NULL	alpha3beta1	NULL		associate with	NULL				CD9	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
25462	3	7025	7	NULL	NULL	0	NULL	alpha6beta1 	NULL		associate with	NULL				CD9	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
25463	4	7025	7	NULL	NULL	0	NULL	CD151	NULL		associate with	NULL				CD81	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
25464	5	7025	7	NULL	NULL	0	NULL	alpha3beta1	NULL		associate with	NULL				CD81	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
25465	6	7025	7	NULL	NULL	0	NULL	alpha6beta1	NULL		associate with	NULL				CD81	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
25466	7	7025	7	NULL	NULL	0	NULL	EWI-2	NULL		does not associate with	NULL				alpha2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
25467	8	7025	7	NULL	NULL	0	NULL	EWI-2	NULL		does not associate with	NULL				alpha3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
25468	9	7025	7	NULL	NULL	0	NULL	EWI-2	NULL		does not associate with	NULL				alpha6	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
25469	10	7025	7	NULL	NULL	0	NULL	EWI-2	NULL		does not associate with	NULL				beta1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
25470	11	7025	7	NULL	NULL	0	NULL	EWI-2	NULL		does not associate with	NULL				CD151	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
25471	12	7025	7	NULL	NULL	0	NULL	EWI-F	NULL		does not associate with	NULL				alpha2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
25472	13	7025	7	NULL	NULL	0	NULL	EWI-F	NULL		does not associate with	NULL				alpha3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
25473	14	7025	7	NULL	NULL	0	NULL	EWI-F	NULL		does not associate with	NULL				alpha6	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
25474	15	7025	7	NULL	NULL	0	NULL	EWI-F	NULL		does not associate with	NULL				beta1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
25475	16	7025	7	NULL	NULL	0	NULL	EWI-F	NULL		does not associate with	NULL				CD151	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40545_s_296	11504738	2 In contrast, the 293 cellular environment seems to lack an extensive "`tetraspan web"` such that CD151, alpha3beta1, and alpha6beta1 associated with CD9 and CD81 only at a very low stoichiometry ( 30)), and no EWI-2 or EWI-F association with alpha2, alpha3, alpha6, beta1, or CD151 could be detected (Ref.  30 and Fig.  4).	bind
21340	1	7026	6	13	NULL	NULL	NULL	apoA-I	GP		does not bind		significantly			ECM	CellComponent				NULL	efflux-impaired U937 macrophages	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_31318_s_297	12050168	2 In contrast, we have been unable to demonstrate significant binding of apoA-I to the ECM of efflux-impaired U937 macrophages or fibroblasts (Fig.  1).	bind
21341	2	7026	6	13	NULL	NULL	NULL	Apo A-I	GP		does not bind		significantly			ECM	CellComponent				NULL	efflux-impaired U937 fibroblasts	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_31318_s_297	12050168	2 In contrast, we have been unable to demonstrate significant binding of apoA-I to the ECM of efflux-impaired U937 macrophages or fibroblasts (Fig.  1).	bind
25596	1	7026	7	NULL	NULL	0	NULL	apoA-I 	NULL		does not bind	NULL	significantly			 ECM 	NULL				NULL	efflux-impaired U937 macrophages	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_31318_s_297	12050168	2 In contrast, we have been unable to demonstrate significant binding of apoA-I to the ECM of efflux-impaired U937 macrophages or fibroblasts (Fig.  1).	bind
25597	2	7026	7	NULL	NULL	0	NULL	apoA-I	NULL		does not bind	NULL	significantly			ECM	NULL				NULL	efflux-impaired U937 fibroblasts	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_31318_s_297	12050168	2 In contrast, we have been unable to demonstrate significant binding of apoA-I to the ECM of efflux-impaired U937 macrophages or fibroblasts (Fig.  1).	bind
22168	1	7027	6	13	NULL	NULL	NULL	glypican	GP		bind					Abeta	GP	fibrillar 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31617_s_216	9395501	2 In future, we plan to use ACE both to refine the characterization of the heparin-binding conformation of Abeta as well as to more thoroughly characterize the binding of intact HSPGs such as glypican and perlecan to fibrillar and nonfibrillar Abeta.	bind
22169	2	7027	6	13	NULL	NULL	NULL	perlecan	GP		bind					Abeta	GP	nonfibrillar			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31617_s_216	9395501	2 In future, we plan to use ACE both to refine the characterization of the heparin-binding conformation of Abeta as well as to more thoroughly characterize the binding of intact HSPGs such as glypican and perlecan to fibrillar and nonfibrillar Abeta.	bind
22170	3	7027	6	13	NULL	NULL	NULL	Abeta	GP		bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31617_s_216	9395501	2 In future, we plan to use ACE both to refine the characterization of the heparin-binding conformation of Abeta as well as to more thoroughly characterize the binding of intact HSPGs such as glypican and perlecan to fibrillar and nonfibrillar Abeta.	bind
27021	4	7027	6	13	NULL	NULL	NULL	glypican	GP		is a type of					HSPG	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31617_s_216	9395501	2 In future, we plan to use ACE both to refine the characterization of the heparin-binding conformation of Abeta as well as to more thoroughly characterize the binding of intact HSPGs such as glypican and perlecan to fibrillar and nonfibrillar Abeta.	bind
27022	5	7027	6	13	NULL	NULL	NULL	perlecan	GP		is a type of					HSPG	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31617_s_216	9395501	2 In future, we plan to use ACE both to refine the characterization of the heparin-binding conformation of Abeta as well as to more thoroughly characterize the binding of intact HSPGs such as glypican and perlecan to fibrillar and nonfibrillar Abeta.	bind
53264	6	7027	6	13	NULL	NULL	NULL	glypican	GP		bind					Abeta	GP	nonfibrillar			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31617_s_216	9395501	2 In future, we plan to use ACE both to refine the characterization of the heparin-binding conformation of Abeta as well as to more thoroughly characterize the binding of intact HSPGs such as glypican and perlecan to fibrillar and nonfibrillar Abeta.	bind
53265	7	7027	6	13	NULL	NULL	NULL	perlecan	GP		bind					Abeta	GP	fibrillar			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31617_s_216	9395501	2 In future, we plan to use ACE both to refine the characterization of the heparin-binding conformation of Abeta as well as to more thoroughly characterize the binding of intact HSPGs such as glypican and perlecan to fibrillar and nonfibrillar Abeta.	bind
25598	1	7027	7	10	NULL	0	NULL	glypican	NULL		bind	NULL				Abeta	NULL	fibrillar			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31617_s_216	9395501	2 In future, we plan to use ACE both to refine the characterization of the heparin-binding conformation of Abeta as well as to more thoroughly characterize the binding of intact HSPGs such as glypican and perlecan to fibrillar and nonfibrillar Abeta.	bind
25599	2	7027	7	10	NULL	0	NULL	 perlecan	NULL		bind	NULL				Abeta	NULL	fibrillar			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31617_s_216	9395501	2 In future, we plan to use ACE both to refine the characterization of the heparin-binding conformation of Abeta as well as to more thoroughly characterize the binding of intact HSPGs such as glypican and perlecan to fibrillar and nonfibrillar Abeta.	bind
25600	3	7027	7	10	NULL	0	NULL	glypican	NULL		bind	NULL				Abeta	NULL	nonfibrillar			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31617_s_216	9395501	2 In future, we plan to use ACE both to refine the characterization of the heparin-binding conformation of Abeta as well as to more thoroughly characterize the binding of intact HSPGs such as glypican and perlecan to fibrillar and nonfibrillar Abeta.	bind
25601	4	7027	7	10	NULL	0	NULL	Perlecan	NULL		bind	NULL				Abeta	NULL	nonfibrillar			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31617_s_216	9395501	2 In future, we plan to use ACE both to refine the characterization of the heparin-binding conformation of Abeta as well as to more thoroughly characterize the binding of intact HSPGs such as glypican and perlecan to fibrillar and nonfibrillar Abeta.	bind
25602	5	7027	7	NULL	NULL	0	NULL	glypican	NULL		is a type of	NULL				HSPG	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31617_s_216	9395501	2 In future, we plan to use ACE both to refine the characterization of the heparin-binding conformation of Abeta as well as to more thoroughly characterize the binding of intact HSPGs such as glypican and perlecan to fibrillar and nonfibrillar Abeta.	bind
25603	6	7027	7	NULL	NULL	0	NULL	Perlecan	NULL		is a type of	NULL				HSPG	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31617_s_216	9395501	2 In future, we plan to use ACE both to refine the characterization of the heparin-binding conformation of Abeta as well as to more thoroughly characterize the binding of intact HSPGs such as glypican and perlecan to fibrillar and nonfibrillar Abeta.	bind
53266	7	7027	7	10	NULL	0	NULL	Abeta	NULL		bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31617_s_216	9395501	2 In future, we plan to use ACE both to refine the characterization of the heparin-binding conformation of Abeta as well as to more thoroughly characterize the binding of intact HSPGs such as glypican and perlecan to fibrillar and nonfibrillar Abeta.	bind
21342	1	7028	6	13	NULL	NULL	NULL	Cdc42p	AminoAcid		is mutated to			Tyr-40		Cdc42p	AminoAcid		Cys		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7176_s_155	11113154	2 In particular, mutation of Tyr-40 to Cys created a version of Cdc42p largely unable to bind the Cdc42/Rac-interactive binding motif ( 42) common to several effectors ( 43).	bind
21343	2	7028	6	13	NULL	NULL	NULL	Cdc42p	AminoAcid		does not bind			Cys					Cdc42/Rac-interactive binding motif		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7176_s_155	11113154	2 In particular, mutation of Tyr-40 to Cys created a version of Cdc42p largely unable to bind the Cdc42/Rac-interactive binding motif ( 42) common to several effectors ( 43).	bind
25604	1	7028	7	NULL	NULL	0	NULL	Cdc42p	NULL		mutated to	NULL		Tyr-40		Cdc42p	NULL		Cys		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_10_7176_s_155	11113154	2 In particular, mutation of Tyr-40 to Cys created a version of Cdc42p largely unable to bind the Cdc42/Rac-interactive binding motif ( 42) common to several effectors ( 43).	bind
25605	2	7028	7	NULL	NULL	0	NULL	Cdc42p	NULL		does not bind	NULL		Cys			NULL		Cdc42/Rac-interactive binding motif		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_10_7176_s_155	11113154	2 In particular, mutation of Tyr-40 to Cys created a version of Cdc42p largely unable to bind the Cdc42/Rac-interactive binding motif ( 42) common to several effectors ( 43).	bind
21344	1	7029	6	13	NULL	NULL	NULL	MEK	GP	nematode	bind					TAO1	GP	mammalian			NULL		NULL	NULL	NULL	NULL	gw60_gene_279_2_137_s_218	11733138	2 in TAO1-HA immune complexes as well as the converse, indicating that the nematode MEK binds to mammalian TAO1 when the two proteins are co-expressed (  Fig. 8B).	bind
25607	2	7029	7	NULL	NULL	0	NULL	MEK	NULL	nematode	binds	NULL				 TAO1	NULL	mammalian			NULL		NULL	NULL	NULL	NULL	gw60_gene_279_2_137_s_218	11733138	2 in TAO1-HA immune complexes as well as the converse, indicating that the nematode MEK binds to mammalian TAO1 when the two proteins are co-expressed (  Fig. 8B).	bind
21345	1	7030	6	13	NULL	NULL	NULL	cADP	Chemical		bind					ribose	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17739_s_155	8663443	2 In the latter cells, positive results ( 16,  39) have been questioned because of a possible competition of cADP-ribose binding by ATP ( 13,  17,  18).	bind
21346	2	7030	6	13	NULL	NULL	NULL	ATP	Chemical		bind					ribose	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17739_s_155	8663443	2 In the latter cells, positive results ( 16,  39) have been questioned because of a possible competition of cADP-ribose binding by ATP ( 13,  17,  18).	bind
21347	3	7030	6	13	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17739_s_155	8663443	2 In the latter cells, positive results ( 16,  39) have been questioned because of a possible competition of cADP-ribose binding by ATP ( 13,  17,  18).	bind
25608	1	7030	7	NULL	NULL	0	NULL	cADP	NULL		bind	NULL				ribose	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17739_s_155	8663443	2 In the latter cells, positive results ( 16,  39) have been questioned because of a possible competition of cADP-ribose binding by ATP ( 13,  17,  18).	bind
28022	2	7030	7	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				ribose	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17739_s_155	8663443	2 In the latter cells, positive results ( 16,  39) have been questioned because of a possible competition of cADP-ribose binding by ATP ( 13,  17,  18).	bind
28023	3	7030	7	NULL	NULL	0	NULL	statement 1	NULL		competes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17739_s_155	8663443	2 In the latter cells, positive results ( 16,  39) have been questioned because of a possible competition of cADP-ribose binding by ATP ( 13,  17,  18).	bind
21348	1	7032	6	13	NULL	NULL	NULL	GST-FinO protein	GP	purified	bind					FinP RNA	NucleicAcid	radiolabeled			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_15_10356_s_69	10187824	2 In the present study, the relative equilibrium association constants for GST-FinO binding to FinP variants were determined by performing gel-shift assays in which radiolabeled RNA was combined with increasing amounts of purified GST-FinO protein.	bind
25611	1	7032	7	10	NULL	0	NULL	GST-FinO protein	NULL	Purified	bind	NULL				FinP RNA	NULL	radiolabeled			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_15_10356_s_69	10187824	2 In the present study, the relative equilibrium association constants for GST-FinO binding to FinP variants were determined by performing gel-shift assays in which radiolabeled RNA was combined with increasing amounts of purified GST-FinO protein.	bind
21349	1	7033	6	13	NULL	NULL	NULL	MEKK1	GP		bind					Axin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_38_39366_s_266	15262978	2 In the present study, we found that like glycogen synthase kinase-3beta and casein kinase Ialpha/epsilon, Ccd1 binding competes against MEKK1 binding to Axin.	bind
21350	2	7033	6	13	NULL	NULL	NULL	Ccd1	GP		bind					Axin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_38_39366_s_266	15262978	2 In the present study, we found that like glycogen synthase kinase-3beta and casein kinase Ialpha/epsilon, Ccd1 binding competes against MEKK1 binding to Axin.	bind
21351	3	7033	6	13	NULL	NULL	NULL	statement 2	Process		competes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_38_39366_s_266	15262978	2 In the present study, we found that like glycogen synthase kinase-3beta and casein kinase Ialpha/epsilon, Ccd1 binding competes against MEKK1 binding to Axin.	bind
21352	4	7033	6	13	NULL	NULL	NULL	glycogen synthase kinase-3beta	GP		bind					Axin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_38_39366_s_266	15262978	2 In the present study, we found that like glycogen synthase kinase-3beta and casein kinase Ialpha/epsilon, Ccd1 binding competes against MEKK1 binding to Axin.	bind
21353	5	7033	6	13	NULL	NULL	NULL	statement 4	Process		competes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_38_39366_s_266	15262978	2 In the present study, we found that like glycogen synthase kinase-3beta and casein kinase Ialpha/epsilon, Ccd1 binding competes against MEKK1 binding to Axin.	bind
21354	6	7033	6	13	NULL	NULL	NULL	casein kinase Ialpha/epsilon	GP		bind					Axin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_38_39366_s_266	15262978	2 In the present study, we found that like glycogen synthase kinase-3beta and casein kinase Ialpha/epsilon, Ccd1 binding competes against MEKK1 binding to Axin.	bind
21355	7	7033	6	13	NULL	NULL	NULL	statement 6	Process		competes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_38_39366_s_266	15262978	2 In the present study, we found that like glycogen synthase kinase-3beta and casein kinase Ialpha/epsilon, Ccd1 binding competes against MEKK1 binding to Axin.	bind
25612	1	7033	7	NULL	NULL	0	NULL	MEKK1	NULL		bind	NULL				Axin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_38_39366_s_266	15262978	2 In the present study, we found that like glycogen synthase kinase-3beta and casein kinase Ialpha/epsilon, Ccd1 binding competes against MEKK1 binding to Axin.	bind
25613	2	7033	7	NULL	NULL	0	NULL	Ccd1	NULL		bind	NULL				Axin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_38_39366_s_266	15262978	2 In the present study, we found that like glycogen synthase kinase-3beta and casein kinase Ialpha/epsilon, Ccd1 binding competes against MEKK1 binding to Axin.	bind
25614	3	7033	7	NULL	NULL	0	NULL	statement 2	NULL		compete with	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_38_39366_s_266	15262978	2 In the present study, we found that like glycogen synthase kinase-3beta and casein kinase Ialpha/epsilon, Ccd1 binding competes against MEKK1 binding to Axin.	bind
25615	4	7033	7	NULL	NULL	0	NULL	glycogen synthase kinase-3beta	NULL		bind	NULL				Axin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_38_39366_s_266	15262978	2 In the present study, we found that like glycogen synthase kinase-3beta and casein kinase Ialpha/epsilon, Ccd1 binding competes against MEKK1 binding to Axin.	bind
25616	5	7033	7	NULL	NULL	0	NULL	casein kinase Ialpha/epsilon	NULL		bind	NULL				Axin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_38_39366_s_266	15262978	2 In the present study, we found that like glycogen synthase kinase-3beta and casein kinase Ialpha/epsilon, Ccd1 binding competes against MEKK1 binding to Axin.	bind
25617	6	7033	7	NULL	NULL	0	NULL	statement 4	NULL		compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_38_39366_s_266	15262978	2 In the present study, we found that like glycogen synthase kinase-3beta and casein kinase Ialpha/epsilon, Ccd1 binding competes against MEKK1 binding to Axin.	bind
25618	7	7033	7	NULL	NULL	0	NULL	statement 5	NULL		compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_38_39366_s_266	15262978	2 In the present study, we found that like glycogen synthase kinase-3beta and casein kinase Ialpha/epsilon, Ccd1 binding competes against MEKK1 binding to Axin.	bind
21356	1	7034	6	13	NULL	NULL	NULL	p65	GP		is translocated to					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_21_2707_s_19	12438297	2 In the stable trimeric complex of p65, p105/50, and IkappaB, IkappaB prevents nuclear translocation and DNA binding of p65 by masking its nuclear localization signal.	bind
21357	2	7034	6	13	NULL	NULL	NULL	p65	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_21_2707_s_19	12438297	2 In the stable trimeric complex of p65, p105/50, and IkappaB, IkappaB prevents nuclear translocation and DNA binding of p65 by masking its nuclear localization signal.	bind
21358	3	7034	6	13	NULL	NULL	NULL	IkappaB	GP		prevents					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_21_2707_s_19	12438297	2 In the stable trimeric complex of p65, p105/50, and IkappaB, IkappaB prevents nuclear translocation and DNA binding of p65 by masking its nuclear localization signal.	bind
21359	4	7034	6	13	NULL	NULL	NULL	IkappaB	GP		prevents					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_21_2707_s_19	12438297	2 In the stable trimeric complex of p65, p105/50, and IkappaB, IkappaB prevents nuclear translocation and DNA binding of p65 by masking its nuclear localization signal.	bind
21360	5	7034	6	13	NULL	NULL	NULL	IkappaB	GP		mask					p65	GP		 nuclear localization signal		NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_21_2707_s_19	12438297	2 In the stable trimeric complex of p65, p105/50, and IkappaB, IkappaB prevents nuclear translocation and DNA binding of p65 by masking its nuclear localization signal.	bind
46613	6	7034	6	13	NULL	NULL	NULL	p65	GP		complex with					p105/50	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_21_2707_s_19	12438297	2 In the stable trimeric complex of p65, p105/50, and IkappaB, IkappaB prevents nuclear translocation and DNA binding of p65 by masking its nuclear localization signal.	bind
46614	7	7034	6	13	NULL	NULL	NULL	IkappaB	GP		complex with					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_21_2707_s_19	12438297	2 In the stable trimeric complex of p65, p105/50, and IkappaB, IkappaB prevents nuclear translocation and DNA binding of p65 by masking its nuclear localization signal.	bind
53267	8	7034	6	13	NULL	NULL	NULL	statement 5	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_21_2707_s_19	12438297	2 In the stable trimeric complex of p65, p105/50, and IkappaB, IkappaB prevents nuclear translocation and DNA binding of p65 by masking its nuclear localization signal.	bind
25619	1	7034	7	NULL	NULL	0	NULL	p65	NULL		complex with	NULL				p105/50	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_21_2707_s_19	12438297	2 In the stable trimeric complex of p65, p105/50, and IkappaB, IkappaB prevents nuclear translocation and DNA binding of p65 by masking its nuclear localization signal.	bind
25620	2	7034	7	NULL	NULL	0	NULL	 IkappaB	NULL		forms trimeric complex with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_21_2707_s_19	12438297	2 In the stable trimeric complex of p65, p105/50, and IkappaB, IkappaB prevents nuclear translocation and DNA binding of p65 by masking its nuclear localization signal.	bind
25621	3	7034	7	10	NULL	0	NULL	IkappaB	NULL		prevents	NULL				statement 7	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_21_2707_s_19	12438297	2 In the stable trimeric complex of p65, p105/50, and IkappaB, IkappaB prevents nuclear translocation and DNA binding of p65 by masking its nuclear localization signal.	bind
25622	4	7034	7	NULL	NULL	0	NULL	p65	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_21_2707_s_19	12438297	2 In the stable trimeric complex of p65, p105/50, and IkappaB, IkappaB prevents nuclear translocation and DNA binding of p65 by masking its nuclear localization signal.	bind
25623	5	7034	7	NULL	NULL	0	NULL	IkappaB	NULL		prevents	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_21_2707_s_19	12438297	2 In the stable trimeric complex of p65, p105/50, and IkappaB, IkappaB prevents nuclear translocation and DNA binding of p65 by masking its nuclear localization signal.	bind
25624	6	7034	7	10	NULL	0	NULL	IkappaB	NULL		masks	NULL				p65	NULL		nuclear localization signal		NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_21_2707_s_19	12438297	2 In the stable trimeric complex of p65, p105/50, and IkappaB, IkappaB prevents nuclear translocation and DNA binding of p65 by masking its nuclear localization signal.	bind
53268	7	7034	7	10	NULL	0	NULL	p65	NULL		is translocated to	NULL				nucleus	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_21_2707_s_19	12438297	2 In the stable trimeric complex of p65, p105/50, and IkappaB, IkappaB prevents nuclear translocation and DNA binding of p65 by masking its nuclear localization signal.	bind
53269	8	7034	7	10	NULL	0	NULL	statement 6	NULL		leads to	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_21_2707_s_19	12438297	2 In the stable trimeric complex of p65, p105/50, and IkappaB, IkappaB prevents nuclear translocation and DNA binding of p65 by masking its nuclear localization signal.	bind
21361	1	7035	6	13	NULL	NULL	NULL	AKAP9-LIZ fragment	GP		bind					InsP3R1 SII splice variants	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_19375_s_172	14982933	2 In these experiments we found that AKAP9-LIZ fragment binds to both InsP3R1 SII splice variants, but not to the InsP3R2 or InsP3R3 isoforms ( Fig. 4 B).	bind
21362	2	7035	6	13	NULL	NULL	NULL	AKAP9-LIZ fragment	GP		does not bind					InsP3R2 isoforms	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_19375_s_172	14982933	2 In these experiments we found that AKAP9-LIZ fragment binds to both InsP3R1 SII splice variants, but not to the InsP3R2 or InsP3R3 isoforms ( Fig. 4 B).	bind
21363	3	7035	6	13	NULL	NULL	NULL	AKAP9-LIZ fragment	GP		does not bind					InsP3R3 isoform	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_19375_s_172	14982933	2 In these experiments we found that AKAP9-LIZ fragment binds to both InsP3R1 SII splice variants, but not to the InsP3R2 or InsP3R3 isoforms ( Fig. 4 B).	bind
25625	1	7035	7	NULL	NULL	0	NULL	KAP9-LIZ fragment	NULL		binds	NULL				InsP3R1 SII splice variant	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_19375_s_172	14982933	2 In these experiments we found that AKAP9-LIZ fragment binds to both InsP3R1 SII splice variants, but not to the InsP3R2 or InsP3R3 isoforms ( Fig. 4 B).	bind
25626	2	7035	7	NULL	NULL	0	NULL	AKAP9-LIZ fragment	NULL		does not bind	NULL				InsP3R2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_19375_s_172	14982933	2 In these experiments we found that AKAP9-LIZ fragment binds to both InsP3R1 SII splice variants, but not to the InsP3R2 or InsP3R3 isoforms ( Fig. 4 B).	bind
25627	3	7035	7	NULL	NULL	0	NULL	AKAP9-LIZ fragment	NULL		does not bind	NULL				InsP3R3 isoforms	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_19375_s_172	14982933	2 In these experiments we found that AKAP9-LIZ fragment binds to both InsP3R1 SII splice variants, but not to the InsP3R2 or InsP3R3 isoforms ( Fig. 4 B).	bind
21364	1	7036	6	13	NULL	NULL	NULL	Ral-A	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14525_s_27	10329639	2 In this study we report the effect of Ca2+/calmodulin on GTP binding activity of Ral-A.	bind
25628	1	7036	7	NULL	NULL	0	NULL	GTP 	NULL		bind	NULL				Ral-A	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_14525_s_27	10329639	2 In this study we report the effect of Ca2+/calmodulin on GTP binding activity of Ral-A.	bind
22171	1	7037	6	13	NULL	NULL	NULL	proteoglycans	GP		bind		may					high affinity	heparin binding domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18932_s_185	9228073	2 Interactions between cell-surface receptors such as proteoglycans, which may bind the high affinity heparin-binding domain, and either of these integrins must, therefore, occur between separated portions of the FN molecule.	bind
22172	2	7037	6	13	NULL	NULL	NULL	proteoglycans	GP		bind					integrins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18932_s_185	9228073	2 Interactions between cell-surface receptors such as proteoglycans, which may bind the high affinity heparin-binding domain, and either of these integrins must, therefore, occur between separated portions of the FN molecule.	bind
23103	3	7037	6	13	NULL	NULL	NULL	proteoglycans	GP		is a type of					cell surface receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18932_s_185	9228073	2 Interactions between cell-surface receptors such as proteoglycans, which may bind the high affinity heparin-binding domain, and either of these integrins must, therefore, occur between separated portions of the FN molecule.	bind
25857	4	7037	6	13	NULL	NULL	NULL	integrins	GP		occur between					FN molecule	GP	separated portions of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18932_s_185	9228073	2 Interactions between cell-surface receptors such as proteoglycans, which may bind the high affinity heparin-binding domain, and either of these integrins must, therefore, occur between separated portions of the FN molecule.	bind
25858	5	7037	6	13	NULL	NULL	NULL	statement 2	Process		occurs via					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18932_s_185	9228073	2 Interactions between cell-surface receptors such as proteoglycans, which may bind the high affinity heparin-binding domain, and either of these integrins must, therefore, occur between separated portions of the FN molecule.	bind
25629	1	7037	7	NULL	NULL	0	NULL	proteoglycans	NULL		bind	NULL	may				NULL	high affinity	heparin-binding domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18932_s_185	9228073	2 Interactions between cell-surface receptors such as proteoglycans, which may bind the high affinity heparin-binding domain, and either of these integrins must, therefore, occur between separated portions of the FN molecule.	bind
25630	2	7037	7	NULL	NULL	0	NULL	proteoglycans	NULL		bind	NULL				integrins	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18932_s_185	9228073	2 Interactions between cell-surface receptors such as proteoglycans, which may bind the high affinity heparin-binding domain, and either of these integrins must, therefore, occur between separated portions of the FN molecule.	bind
25631	3	7037	7	NULL	NULL	0	NULL	statement 2	NULL		occur between	NULL				FN molecule	NULL	separated portions of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18932_s_185	9228073	2 Interactions between cell-surface receptors such as proteoglycans, which may bind the high affinity heparin-binding domain, and either of these integrins must, therefore, occur between separated portions of the FN molecule.	bind
25880	4	7037	7	10	NULL	0	NULL	proteoglycans	NULL		is a type of	NULL				cell-surface receptors	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18932_s_185	9228073	2 Interactions between cell-surface receptors such as proteoglycans, which may bind the high affinity heparin-binding domain, and either of these integrins must, therefore, occur between separated portions of the FN molecule.	bind
22173	1	7038	6	13	NULL	NULL	NULL	clones RD	NucleicAcid		bind		selectively			albumin	GP	rat			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_38_35035_s_247	12119302	2 Interestingly, SA08, a matured sequence derived from libraries patterned after the sequence of the multispecies binding clone RB, inhibited the binding of clones RD and BA, which selectively bound rat and rabbit albumin, respectively.	bind
22174	2	7038	6	13	NULL	NULL	NULL	clones BA	NucleicAcid		bind		selectively			albumin	GP	rabbit			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_38_35035_s_247	12119302	2 Interestingly, SA08, a matured sequence derived from libraries patterned after the sequence of the multispecies binding clone RB, inhibited the binding of clones RD and BA, which selectively bound rat and rabbit albumin, respectively.	bind
22175	3	7038	6	13	NULL	NULL	NULL	SA08	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_38_35035_s_247	12119302	2 Interestingly, SA08, a matured sequence derived from libraries patterned after the sequence of the multispecies binding clone RB, inhibited the binding of clones RD and BA, which selectively bound rat and rabbit albumin, respectively.	bind
22176	4	7038	6	13	NULL	NULL	NULL	SA08	GP		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_38_35035_s_247	12119302	2 Interestingly, SA08, a matured sequence derived from libraries patterned after the sequence of the multispecies binding clone RB, inhibited the binding of clones RD and BA, which selectively bound rat and rabbit albumin, respectively.	bind
25632	1	7038	7	NULL	NULL	0	NULL	clones RD	NULL		bind	NULL	selectively			albumin	NULL	rat			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_38_35035_s_247	12119302	2 Interestingly, SA08, a matured sequence derived from libraries patterned after the sequence of the multispecies binding clone RB, inhibited the binding of clones RD and BA, which selectively bound rat and rabbit albumin, respectively.	bind
25633	2	7038	7	NULL	NULL	0	NULL	clones BA	NULL		bind	NULL	selectively			albumin	NULL	rabbit			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_38_35035_s_247	12119302	2 Interestingly, SA08, a matured sequence derived from libraries patterned after the sequence of the multispecies binding clone RB, inhibited the binding of clones RD and BA, which selectively bound rat and rabbit albumin, respectively.	bind
25634	3	7038	7	NULL	NULL	0	NULL	SA08	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_38_35035_s_247	12119302	2 Interestingly, SA08, a matured sequence derived from libraries patterned after the sequence of the multispecies binding clone RB, inhibited the binding of clones RD and BA, which selectively bound rat and rabbit albumin, respectively.	bind
25635	4	7038	7	NULL	NULL	0	NULL	SA08	NULL		inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_38_35035_s_247	12119302	2 Interestingly, SA08, a matured sequence derived from libraries patterned after the sequence of the multispecies binding clone RB, inhibited the binding of clones RD and BA, which selectively bound rat and rabbit albumin, respectively.	bind
21365	1	7039	6	13	NULL	NULL	NULL	Ce-MAN1	GP		bind					BAF	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_14_13863_s_217	15681850	2 It is noteworthy that the SRV motif is also present in domain D, shared by Ce-MAN1 (data not shown) and human MAN1 (see Figs.  1 and  2 A), which might account for the binding of Ce-MAN1 to BAF.	bind
21366	2	7039	6	13	NULL	NULL	NULL				is shared by			SRV motif		MAN1	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_14_13863_s_217	15681850	2 It is noteworthy that the SRV motif is also present in domain D, shared by Ce-MAN1 (data not shown) and human MAN1 (see Figs.  1 and  2 A), which might account for the binding of Ce-MAN1 to BAF.	bind
27023	3	7039	6	13	NULL	NULL	NULL				is present in			SRV motif					domain D		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_14_13863_s_217	15681850	2 It is noteworthy that the SRV motif is also present in domain D, shared by Ce-MAN1 (data not shown) and human MAN1 (see Figs.  1 and  2 A), which might account for the binding of Ce-MAN1 to BAF.	bind
27024	4	7039	6	13	NULL	NULL	NULL				is shared by			SRV motif		Ce-MAN1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_14_13863_s_217	15681850	2 It is noteworthy that the SRV motif is also present in domain D, shared by Ce-MAN1 (data not shown) and human MAN1 (see Figs.  1 and  2 A), which might account for the binding of Ce-MAN1 to BAF.	bind
25636	1	7039	7	NULL	NULL	0	NULL	Ce-MAN1	NULL		bind	NULL				BAF	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_14_13863_s_217	15681850	2 It is noteworthy that the SRV motif is also present in domain D, shared by Ce-MAN1 (data not shown) and human MAN1 (see Figs.  1 and  2 A), which might account for the binding of Ce-MAN1 to BAF.	bind
25666	2	7039	7	NULL	NULL	0	NULL		NULL		is present in	NULL		SRV motif			NULL		domain D		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_14_13863_s_217	15681850	2 It is noteworthy that the SRV motif is also present in domain D, shared by Ce-MAN1 (data not shown) and human MAN1 (see Figs.  1 and  2 A), which might account for the binding of Ce-MAN1 to BAF.	bind
25667	3	7039	7	NULL	NULL	0	NULL		NULL		is shared by	NULL		SRV motif		Ce-MAN1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_14_13863_s_217	15681850	2 It is noteworthy that the SRV motif is also present in domain D, shared by Ce-MAN1 (data not shown) and human MAN1 (see Figs.  1 and  2 A), which might account for the binding of Ce-MAN1 to BAF.	bind
25668	4	7039	7	NULL	NULL	0	NULL		NULL		is shared by	NULL		SRV motif		MAN1	NULL	human			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_14_13863_s_217	15681850	2 It is noteworthy that the SRV motif is also present in domain D, shared by Ce-MAN1 (data not shown) and human MAN1 (see Figs.  1 and  2 A), which might account for the binding of Ce-MAN1 to BAF.	bind
21367	1	7040	6	13	NULL	NULL	NULL	p120ctn protein	GP	mutant	bind					E-cadherin polypeptides	GP	nonfunctional			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21409_s_245	10409703	2 It is therefore conceivable that these mutant p120ctn proteins bound to the nonfunctional E-cadherin polypeptides could function as dominant-positive (activating) mutants through facilitating dimerization of the mutant E-cadherin.	bind
27025	2	7040	6	13	NULL	NULL	NULL	statement 1	GP		functions as					dominant-positive (activating) mutants	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21409_s_245	10409703	2 It is therefore conceivable that these mutant p120ctn proteins bound to the nonfunctional E-cadherin polypeptides could function as dominant-positive (activating) mutants through facilitating dimerization of the mutant E-cadherin.	bind
27026	3	7040	6	13	NULL	NULL	NULL	statement 1	GP		dimerize					E-cadherin	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21409_s_245	10409703	2 It is therefore conceivable that these mutant p120ctn proteins bound to the nonfunctional E-cadherin polypeptides could function as dominant-positive (activating) mutants through facilitating dimerization of the mutant E-cadherin.	bind
25637	1	7040	7	NULL	NULL	0	NULL	p120ctn protein	NULL	mutant	bind	NULL				E-cadherin polypeptide	NULL	nonfunctional			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21409_s_245	10409703	2 It is therefore conceivable that these mutant p120ctn proteins bound to the nonfunctional E-cadherin polypeptides could function as dominant-positive (activating) mutants through facilitating dimerization of the mutant E-cadherin.	bind
25638	2	7040	7	NULL	NULL	0	NULL	statement 1	NULL		function as	NULL				dominant-positive mutant	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21409_s_245	10409703	2 It is therefore conceivable that these mutant p120ctn proteins bound to the nonfunctional E-cadherin polypeptides could function as dominant-positive (activating) mutants through facilitating dimerization of the mutant E-cadherin.	bind
25639	3	7040	7	NULL	NULL	0	NULL	statement 1	NULL		dimerize	NULL				E-cadherin	NULL	mutant			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21409_s_245	10409703	2 It is therefore conceivable that these mutant p120ctn proteins bound to the nonfunctional E-cadherin polypeptides could function as dominant-positive (activating) mutants through facilitating dimerization of the mutant E-cadherin.	bind
21379	1	7041	6	13	NULL	NULL	NULL	Fas ligand	GP		bind					Fas	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2354_s_144	8999945	2 It is thus possible that apoptosis of spermatogenic cells is induced by the binding of Fas ligand to Fas through interaction between Sertoli cells and spermatogenic cells.	bind
21380	2	7041	6	13	NULL	NULL	NULL	Sertoli cells	Cell		interacts with					spermatogenic cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2354_s_144	8999945	2 It is thus possible that apoptosis of spermatogenic cells is induced by the binding of Fas ligand to Fas through interaction between Sertoli cells and spermatogenic cells.	bind
21384	3	7041	6	13	NULL	NULL	NULL	statement 1	Process		occurs through					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2354_s_144	8999945	2 It is thus possible that apoptosis of spermatogenic cells is induced by the binding of Fas ligand to Fas through interaction between Sertoli cells and spermatogenic cells.	bind
21389	4	7041	6	13	NULL	NULL	NULL	spermatogenic cells	Cell	apoptosis of	is induced by					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2354_s_144	8999945	2 It is thus possible that apoptosis of spermatogenic cells is induced by the binding of Fas ligand to Fas through interaction between Sertoli cells and spermatogenic cells.	bind
25669	1	7041	7	NULL	NULL	0	NULL	Fas ligand	NULL		bind	NULL				Fas	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_4_2354_s_144	8999945	2 It is thus possible that apoptosis of spermatogenic cells is induced by the binding of Fas ligand to Fas through interaction between Sertoli cells and spermatogenic cells.	bind
25670	2	7041	7	NULL	NULL	0	NULL	Sertoli cells	NULL		interacts with	NULL				spermatogenic cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_4_2354_s_144	8999945	2 It is thus possible that apoptosis of spermatogenic cells is induced by the binding of Fas ligand to Fas through interaction between Sertoli cells and spermatogenic cells.	bind
25675	3	7041	7	NULL	NULL	0	NULL	statement 1	NULL		occurs through	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_4_2354_s_144	8999945	2 It is thus possible that apoptosis of spermatogenic cells is induced by the binding of Fas ligand to Fas through interaction between Sertoli cells and spermatogenic cells.	bind
25676	4	7041	7	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL				spermatogenic cells	NULL	apoptosis of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_4_2354_s_144	8999945	2 It is thus possible that apoptosis of spermatogenic cells is induced by the binding of Fas ligand to Fas through interaction between Sertoli cells and spermatogenic cells.	bind
21405	1	7042	6	13	NULL	NULL	NULL	p53	GP		bind		may			EGFR	NucleicAcid			p53RE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_41717_s_284	11546792	2 It is, therefore, possible to speculate that binding affinity of p53 and TAp63gamma to the EGFRp53RE is above and below detection at our level, respectively.	bind
21407	2	7042	6	13	NULL	NULL	NULL	TAp63gamma	GP		bind		may			EGFR	NucleicAcid			p53RE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_41717_s_284	11546792	2 It is, therefore, possible to speculate that binding affinity of p53 and TAp63gamma to the EGFRp53RE is above and below detection at our level, respectively.	bind
25688	1	7042	7	NULL	NULL	0	NULL	p53	NULL		bind	NULL	may			EGFR	NULL			p53RE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_41717_s_284	11546792	2 It is, therefore, possible to speculate that binding affinity of p53 and TAp63gamma to the EGFRp53RE is above and below detection at our level, respectively.	bind
25691	2	7042	7	NULL	NULL	0	NULL	TAp63gamma	NULL		bind	NULL	may			EGFR	NULL			p53RE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_41717_s_284	11546792	2 It is, therefore, possible to speculate that binding affinity of p53 and TAp63gamma to the EGFRp53RE is above and below detection at our level, respectively.	bind
21421	1	7043	6	13	NULL	NULL	NULL	PKG	GP		bind					MBS	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_1_597_s_184	14530290	2 It should be noted that all of the constructs of PKG used by Surks  et al. ( ) containing the LZ also contained the coiled-coil domain, and mutations that disrupted the coiled-coil domain of PKGI inhibited binding of PKG and the MBS.	bind
21424	2	7043	6	13	NULL	NULL	NULL	PKGI	GP	mutant	inhibits			coiled coil domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_1_597_s_184	14530290	2 It should be noted that all of the constructs of PKG used by Surks  et al. ( ) containing the LZ also contained the coiled-coil domain, and mutations that disrupted the coiled-coil domain of PKGI inhibited binding of PKG and the MBS.	bind
25692	1	7043	7	NULL	NULL	0	NULL	PKG	NULL		bind	NULL				MBS	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_1_597_s_184	14530290	2 It should be noted that all of the constructs of PKG used by Surks  et al. ( ) containing the LZ also contained the coiled-coil domain, and mutations that disrupted the coiled-coil domain of PKGI inhibited binding of PKG and the MBS.	bind
25696	2	7043	7	NULL	NULL	0	NULL	PKGI	NULL	mutant	inhibits	NULL		coiled-coil domain		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_1_597_s_184	14530290	2 It should be noted that all of the constructs of PKG used by Surks  et al. ( ) containing the LZ also contained the coiled-coil domain, and mutations that disrupted the coiled-coil domain of PKGI inhibited binding of PKG and the MBS.	bind
21429	1	7044	6	13	NULL	NULL	NULL	h-rhotekin	GP		bind					Rho	GP	active			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_43_33962_s_143	10940294	2 It was also verified that h-rhotekin indeed binds to the active form of Rho.	bind
25697	1	7044	7	NULL	NULL	0	NULL	h-rhotekin	NULL		binds to	NULL				Rho	NULL	active			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_43_33962_s_143	10940294	2 It was also verified that h-rhotekin indeed binds to the active form of Rho.	bind
22177	1	7045	6	13	NULL	NULL	NULL	PDP1c	GP	alone	does not interact		directly			Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_361	11842080	2 ITC studies indicate that neither PDP1c nor L2, alone, directly interact with <100 muM Ca2+ and ITC, analytical ultracentrifugation, and other studies indicate L2 and PDP1c bind each in forming a tight Ca2+ binding site ( Kd < 3 muM); similar complex formation by PDP1 is enhanced by Mg2+ (A. Turkan, Y. Hiromasa, and T. E. Roche, manuscript in preparation).	bind
22178	2	7045	6	13	NULL	NULL	NULL	L2	GP	alone	does not interact		directly			Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_361	11842080	2 ITC studies indicate that neither PDP1c nor L2, alone, directly interact with <100 muM Ca2+ and ITC, analytical ultracentrifugation, and other studies indicate L2 and PDP1c bind each in forming a tight Ca2+ binding site ( Kd < 3 muM); similar complex formation by PDP1 is enhanced by Mg2+ (A. Turkan, Y. Hiromasa, and T. E. Roche, manuscript in preparation).	bind
22179	3	7045	6	13	NULL	NULL	NULL	PDP1c	GP		bind					L2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_361	11842080	2 ITC studies indicate that neither PDP1c nor L2, alone, directly interact with <100 muM Ca2+ and ITC, analytical ultracentrifugation, and other studies indicate L2 and PDP1c bind each in forming a tight Ca2+ binding site ( Kd < 3 muM); similar complex formation by PDP1 is enhanced by Mg2+ (A. Turkan, Y. Hiromasa, and T. E. Roche, manuscript in preparation).	bind
22180	4	7045	6	13	NULL	NULL	NULL	statement 3	Process		forms a								Ca2+ binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_361	11842080	2 ITC studies indicate that neither PDP1c nor L2, alone, directly interact with <100 muM Ca2+ and ITC, analytical ultracentrifugation, and other studies indicate L2 and PDP1c bind each in forming a tight Ca2+ binding site ( Kd < 3 muM); similar complex formation by PDP1 is enhanced by Mg2+ (A. Turkan, Y. Hiromasa, and T. E. Roche, manuscript in preparation).	bind
22181	5	7045	6	13	NULL	NULL	NULL	PDP1	GP	complex formation by	is enhanced by					Mg2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_361	11842080	2 ITC studies indicate that neither PDP1c nor L2, alone, directly interact with <100 muM Ca2+ and ITC, analytical ultracentrifugation, and other studies indicate L2 and PDP1c bind each in forming a tight Ca2+ binding site ( Kd < 3 muM); similar complex formation by PDP1 is enhanced by Mg2+ (A. Turkan, Y. Hiromasa, and T. E. Roche, manuscript in preparation).	bind
53302	6	7045	6	13	NULL	NULL	NULL	PDP1c	GP	alone	does not bind		directly			ITC	ResearchActivity				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_361	11842080	2 ITC studies indicate that neither PDP1c nor L2, alone, directly interact with <100 muM Ca2+ and ITC, analytical ultracentrifugation, and other studies indicate L2 and PDP1c bind each in forming a tight Ca2+ binding site ( Kd < 3 muM); similar complex formation by PDP1 is enhanced by Mg2+ (A. Turkan, Y. Hiromasa, and T. E. Roche, manuscript in preparation).	bind
53303	7	7045	6	13	NULL	NULL	NULL	L2	GP	alone	does not bind		directly			ITC	ResearchActivity				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_361	11842080	2 ITC studies indicate that neither PDP1c nor L2, alone, directly interact with <100 muM Ca2+ and ITC, analytical ultracentrifugation, and other studies indicate L2 and PDP1c bind each in forming a tight Ca2+ binding site ( Kd < 3 muM); similar complex formation by PDP1 is enhanced by Mg2+ (A. Turkan, Y. Hiromasa, and T. E. Roche, manuscript in preparation).	bind
25698	1	7045	7	10	NULL	0	NULL	PDP1c 	NULL	alone	does not interact with	NULL	directly			Ca2+	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_361	11842080	2 ITC studies indicate that neither PDP1c nor L2, alone, directly interact with <100 muM Ca2+ and ITC, analytical ultracentrifugation, and other studies indicate L2 and PDP1c bind each in forming a tight Ca2+ binding site ( Kd < 3 muM); similar complex formation by PDP1 is enhanced by Mg2+ (A. Turkan, Y. Hiromasa, and T. E. Roche, manuscript in preparation).	bind
25699	2	7045	7	10	NULL	0	NULL	L2	NULL	alone	does not interact with	NULL	directly			Ca2+	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_361	11842080	2 ITC studies indicate that neither PDP1c nor L2, alone, directly interact with <100 muM Ca2+ and ITC, analytical ultracentrifugation, and other studies indicate L2 and PDP1c bind each in forming a tight Ca2+ binding site ( Kd < 3 muM); similar complex formation by PDP1 is enhanced by Mg2+ (A. Turkan, Y. Hiromasa, and T. E. Roche, manuscript in preparation).	bind
25701	3	7045	7	10	NULL	0	NULL	PDP1c 	NULL	alone	does not interact with	NULL	directly			ITC	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_361	11842080	2 ITC studies indicate that neither PDP1c nor L2, alone, directly interact with <100 muM Ca2+ and ITC, analytical ultracentrifugation, and other studies indicate L2 and PDP1c bind each in forming a tight Ca2+ binding site ( Kd < 3 muM); similar complex formation by PDP1 is enhanced by Mg2+ (A. Turkan, Y. Hiromasa, and T. E. Roche, manuscript in preparation).	bind
25702	4	7045	7	10	NULL	0	NULL	L2	NULL	alone	does not interact with	NULL	directly			ITC	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_361	11842080	2 ITC studies indicate that neither PDP1c nor L2, alone, directly interact with <100 muM Ca2+ and ITC, analytical ultracentrifugation, and other studies indicate L2 and PDP1c bind each in forming a tight Ca2+ binding site ( Kd < 3 muM); similar complex formation by PDP1 is enhanced by Mg2+ (A. Turkan, Y. Hiromasa, and T. E. Roche, manuscript in preparation).	bind
25703	5	7045	7	NULL	NULL	0	NULL	L2	NULL		bind	NULL				PDP1c 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_361	11842080	2 ITC studies indicate that neither PDP1c nor L2, alone, directly interact with <100 muM Ca2+ and ITC, analytical ultracentrifugation, and other studies indicate L2 and PDP1c bind each in forming a tight Ca2+ binding site ( Kd < 3 muM); similar complex formation by PDP1 is enhanced by Mg2+ (A. Turkan, Y. Hiromasa, and T. E. Roche, manuscript in preparation).	bind
25704	6	7045	7	NULL	NULL	0	NULL	statement 5	NULL		forms	NULL				Ca2+	NULL	tight binding site for			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_361	11842080	2 ITC studies indicate that neither PDP1c nor L2, alone, directly interact with <100 muM Ca2+ and ITC, analytical ultracentrifugation, and other studies indicate L2 and PDP1c bind each in forming a tight Ca2+ binding site ( Kd < 3 muM); similar complex formation by PDP1 is enhanced by Mg2+ (A. Turkan, Y. Hiromasa, and T. E. Roche, manuscript in preparation).	bind
25705	7	7045	7	10	NULL	0	NULL	Mg2+	NULL		enhance	NULL				PDP1	NULL	complex formation by			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_361	11842080	2 ITC studies indicate that neither PDP1c nor L2, alone, directly interact with <100 muM Ca2+ and ITC, analytical ultracentrifugation, and other studies indicate L2 and PDP1c bind each in forming a tight Ca2+ binding site ( Kd < 3 muM); similar complex formation by PDP1 is enhanced by Mg2+ (A. Turkan, Y. Hiromasa, and T. E. Roche, manuscript in preparation).	bind
21435	1	7046	6	13	NULL	NULL	NULL	AP-1	GP		exhibits					TF binding activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8558_s_119	9079686	2 Likewise, forskolin partially suppressed TF binding activities of AP-1 and NUR-77 induced by alphaCD3 (Fig.  2 B).	bind
21436	2	7046	6	13	NULL	NULL	NULL	NUR-77	GP		exhibits					TF binding activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8558_s_119	9079686	2 Likewise, forskolin partially suppressed TF binding activities of AP-1 and NUR-77 induced by alphaCD3 (Fig.  2 B).	bind
21437	3	7046	6	13	NULL	NULL	NULL	alphaCD3	GP		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8558_s_119	9079686	2 Likewise, forskolin partially suppressed TF binding activities of AP-1 and NUR-77 induced by alphaCD3 (Fig.  2 B).	bind
21439	4	7046	6	13	NULL	NULL	NULL	alphaCD3	GP		induces					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8558_s_119	9079686	2 Likewise, forskolin partially suppressed TF binding activities of AP-1 and NUR-77 induced by alphaCD3 (Fig.  2 B).	bind
21443	5	7046	6	13	NULL	NULL	NULL	forskolin	Chemical		suppress		partially			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8558_s_119	9079686	2 Likewise, forskolin partially suppressed TF binding activities of AP-1 and NUR-77 induced by alphaCD3 (Fig.  2 B).	bind
21444	6	7046	6	13	NULL	NULL	NULL	forskolin	Chemical		suppress		partially			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8558_s_119	9079686	2 Likewise, forskolin partially suppressed TF binding activities of AP-1 and NUR-77 induced by alphaCD3 (Fig.  2 B).	bind
25706	2	7046	7	10	NULL	0	NULL	alphaCD3	NULL		induce	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8558_s_119	9079686	2 Likewise, forskolin partially suppressed TF binding activities of AP-1 and NUR-77 induced by alphaCD3 (Fig.  2 B).	bind
25707	4	7046	7	10	NULL	0	NULL	alphaCD3	NULL		induce	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8558_s_119	9079686	2 Likewise, forskolin partially suppressed TF binding activities of AP-1 and NUR-77 induced by alphaCD3 (Fig.  2 B).	bind
25708	5	7046	7	10	NULL	0	NULL	forskolin	NULL		suppress	NULL	partially			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8558_s_119	9079686	2 Likewise, forskolin partially suppressed TF binding activities of AP-1 and NUR-77 induced by alphaCD3 (Fig.  2 B).	bind
25709	6	7046	7	10	NULL	0	NULL	forskolin	NULL		suppress	NULL	partially			statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8558_s_119	9079686	2 Likewise, forskolin partially suppressed TF binding activities of AP-1 and NUR-77 induced by alphaCD3 (Fig.  2 B).	bind
46416	1	7046	7	10	NULL	0	NULL	AP-1	NULL		exhibits	NULL				TF binding activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_13_8558_s_119	9079686	2 Likewise, forskolin partially suppressed TF binding activities of AP-1 and NUR-77 induced by alphaCD3 (Fig.  2 B).	bind
46417	3	7046	7	10	NULL	0	NULL	NUR-77	NULL		exhibits	NULL				TF binding activity	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8558_s_119	9079686	2 Likewise, forskolin partially suppressed TF binding activities of AP-1 and NUR-77 induced by alphaCD3 (Fig.  2 B).	bind
21554	1	7047	6	13	NULL	NULL	NULL	RasGRP1.2	GP		is localized in					endoplasmic reticulum	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_33465_s_309	12782630	2 Likewise, treatment of cells with a phospholipase Cgamma chemical inhibitor  does not abolish the reticular distribution of RasGRP1.2 Based on  those results, we surmise that the localization of RasGRP1 in the endoplasmic  reticulum is helped by the binding of the RasGRP1 ZF to a docking protein  present in that subcellular compartment.	bind
21555	2	7047	6	13	NULL	NULL	NULL	RasGRP1	GP		bind			ZF		docking protein	GP				NULL	subcellular compartment	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_33465_s_309	12782630	2 Likewise, treatment of cells with a phospholipase Cgamma chemical inhibitor  does not abolish the reticular distribution of RasGRP1.2 Based on  those results, we surmise that the localization of RasGRP1 in the endoplasmic  reticulum is helped by the binding of the RasGRP1 ZF to a docking protein  present in that subcellular compartment.	bind
21556	3	7047	6	13	NULL	NULL	NULL	phospholipase Cgamma	GP		does not abolish					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_33465_s_309	12782630	2 Likewise, treatment of cells with a phospholipase Cgamma chemical inhibitor  does not abolish the reticular distribution of RasGRP1.2 Based on  those results, we surmise that the localization of RasGRP1 in the endoplasmic  reticulum is helped by the binding of the RasGRP1 ZF to a docking protein  present in that subcellular compartment.	bind
46418	4	7047	6	13	NULL	NULL	NULL	\tphospholipase Cgamma	GP		is a type of					chemical inhibitor					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_33465_s_309	12782630	2 Likewise, treatment of cells with a phospholipase Cgamma chemical inhibitor  does not abolish the reticular distribution of RasGRP1.2 Based on  those results, we surmise that the localization of RasGRP1 in the endoplasmic  reticulum is helped by the binding of the RasGRP1 ZF to a docking protein  present in that subcellular compartment.	bind
25710	2	7047	7	10	NULL	0	NULL	phospholipase Cgamma 	NULL		does not abolish	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_33465_s_309	12782630	2 Likewise, treatment of cells with a phospholipase Cgamma chemical inhibitor  does not abolish the reticular distribution of RasGRP1.2 Based on  those results, we surmise that the localization of RasGRP1 in the endoplasmic  reticulum is helped by the binding of the RasGRP1 ZF to a docking protein  present in that subcellular compartment.	bind
25711	3	7047	7	10	NULL	0	NULL	RasGRP1	NULL		bind	NULL		ZF		docking protein	NULL				NULL	subcellular compartment	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_33465_s_309	12782630	2 Likewise, treatment of cells with a phospholipase Cgamma chemical inhibitor  does not abolish the reticular distribution of RasGRP1.2 Based on  those results, we surmise that the localization of RasGRP1 in the endoplasmic  reticulum is helped by the binding of the RasGRP1 ZF to a docking protein  present in that subcellular compartment.	bind
25713	4	7047	7	10	NULL	0	NULL	statement 3	NULL		helps	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_33465_s_309	12782630	2 Likewise, treatment of cells with a phospholipase Cgamma chemical inhibitor  does not abolish the reticular distribution of RasGRP1.2 Based on  those results, we surmise that the localization of RasGRP1 in the endoplasmic  reticulum is helped by the binding of the RasGRP1 ZF to a docking protein  present in that subcellular compartment.	bind
46419	1	7047	7	10	NULL	0	NULL	RasGRP1	NULL		is localized in	NULL				endoplasmic reticulum	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_33465_s_309	12782630	2 Likewise, treatment of cells with a phospholipase Cgamma chemical inhibitor  does not abolish the reticular distribution of RasGRP1.2 Based on  those results, we surmise that the localization of RasGRP1 in the endoplasmic  reticulum is helped by the binding of the RasGRP1 ZF to a docking protein  present in that subcellular compartment.	bind
21560	1	7048	6	13	NULL	NULL	NULL	ACP	GP		bind					Glycerol	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_1_194_s_63	12409302	2 M glycerol, suggesting that ACP binds glycerol.	bind
25715	1	7048	7	NULL	NULL	0	NULL	ACP	NULL		binds	NULL				glycerol	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_1_194_s_63	12409302	2 M glycerol, suggesting that ACP binds glycerol.	bind
21561	1	7049	6	13	NULL	NULL	NULL	mAb 1E5	GP		bind		specifically			BP230	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9711_s_44	9545306	2 mAb 1E5 binds specifically to BP230.	bind
25716	1	7049	7	NULL	NULL	0	NULL	mAb 1E5	NULL		bind	NULL	specifically			BP230	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9711_s_44	9545306	2 mAb 1E5 binds specifically to BP230.	bind
21562	1	7050	6	13	NULL	NULL	NULL	CD4	GP		bind					mAb	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_508_1_67_s_113	11707270	2 mAb demonstrating CD4 binding ability	bind
25882	1	7050	7	NULL	NULL	0	NULL	mAb	NULL		binds	NULL				CD4	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_508_1_67_s_113	11707270	2 mAb demonstrating CD4 binding ability	bind
21563	1	7051	6	13	NULL	NULL	NULL	nonO	GP		contain		may			CA enzymatic activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_16044_s_136	10821857	2 mM acetazolamide completely prevented the binding of both nonO and CA II to the column, suggesting that the binding properties of nonO and CA II are quite similar and that nonO may also contain CA enzymatic activity.	bind
21571	2	7051	6	13	NULL	NULL	NULL	nonO	GP	binding properties of	are quite similar to					CA II	GP	binding properties of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_16044_s_136	10821857	2 mM acetazolamide completely prevented the binding of both nonO and CA II to the column, suggesting that the binding properties of nonO and CA II are quite similar and that nonO may also contain CA enzymatic activity.	bind
25717	1	7051	7	NULL	NULL	0	NULL	nonO	NULL		contain	NULL	may			CA enzymatic activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_16044_s_136	10821857	2 mM acetazolamide completely prevented the binding of both nonO and CA II to the column, suggesting that the binding properties of nonO and CA II are quite similar and that nonO may also contain CA enzymatic activity.	bind
25881	2	7051	7	NULL	NULL	0	NULL	nonO	NULL	 binding properties of 	are quite similar to	NULL				CA II	NULL	binding properties of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_16044_s_136	10821857	2 mM acetazolamide completely prevented the binding of both nonO and CA II to the column, suggesting that the binding properties of nonO and CA II are quite similar and that nonO may also contain CA enzymatic activity.	bind
21574	1	7053	6	13	NULL	NULL	NULL	calmodulin	GP	biotinylated	bind					Ral-A	GP	renatured			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_25_16002_s_229	9188503	2 Moreover, biotinylated calmodulin overlay experiments have shown that biotinylated calmodulin binds to renatured Ral-A in a Ca2+-dependent manner, confirming our finding that Ral-A is a calmodulin-binding protein.	bind
21575	2	7053	6	13	NULL	NULL	NULL	statement 1	Process		is dependent on					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_25_16002_s_229	9188503	2 Moreover, biotinylated calmodulin overlay experiments have shown that biotinylated calmodulin binds to renatured Ral-A in a Ca2+-dependent manner, confirming our finding that Ral-A is a calmodulin-binding protein.	bind
21576	3	7053	6	13	NULL	NULL	NULL	Ral-A	GP		is a type of					calmodulin-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_25_16002_s_229	9188503	2 Moreover, biotinylated calmodulin overlay experiments have shown that biotinylated calmodulin binds to renatured Ral-A in a Ca2+-dependent manner, confirming our finding that Ral-A is a calmodulin-binding protein.	bind
25719	1	7053	7	NULL	NULL	0	NULL	calmodulin	NULL	biotinylated	binds to	NULL				Ral-A	NULL	renatured 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_25_16002_s_229	9188503	2 Moreover, biotinylated calmodulin overlay experiments have shown that biotinylated calmodulin binds to renatured Ral-A in a Ca2+-dependent manner, confirming our finding that Ral-A is a calmodulin-binding protein.	bind
25720	2	7053	7	NULL	NULL	0	NULL	statement 1	NULL		depends on	NULL				Ca2+	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_25_16002_s_229	9188503	2 Moreover, biotinylated calmodulin overlay experiments have shown that biotinylated calmodulin binds to renatured Ral-A in a Ca2+-dependent manner, confirming our finding that Ral-A is a calmodulin-binding protein.	bind
25721	3	7053	7	NULL	NULL	0	NULL	Ral-A	NULL		is a type of	NULL				calmodulin-binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_25_16002_s_229	9188503	2 Moreover, biotinylated calmodulin overlay experiments have shown that biotinylated calmodulin binds to renatured Ral-A in a Ca2+-dependent manner, confirming our finding that Ral-A is a calmodulin-binding protein.	bind
22182	1	7058	6	13	NULL	NULL	NULL	caldesmon	GP		is located between		primarily	myosin binding domain					residues 25 and 53		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3213_s_234	10652307	2 MY27C binds less strongly2 and was less potent and less effective in the present study, consistent with the myosin binding domain of caldesmon being primarily located between residues 25 and 53, but also, to a lesser extent, extending to the N terminus.	bind
22183	2	7058	6	13	NULL	NULL	NULL	caldesmon	GP		is extended to 			myosin binding domain					N-terminus		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3213_s_234	10652307	2 MY27C binds less strongly2 and was less potent and less effective in the present study, consistent with the myosin binding domain of caldesmon being primarily located between residues 25 and 53, but also, to a lesser extent, extending to the N terminus.	bind
21591	1	7059	6	13	NULL	NULL	NULL	scuPA	GP		forms a complex with					sDI	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5348_s_171	9030610	2 Nevertheless, the observation that complexes composed of scuPA and sDI, sDII-DIII, or full-length suPAR bind to LMTK  cells to the same extent provides additional support for the involvement of urokinase in this interaction.	bind
21592	2	7059	6	13	NULL	NULL	NULL	statement 1	GP		forms a complex with					sDII-DIII	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5348_s_171	9030610	2 Nevertheless, the observation that complexes composed of scuPA and sDI, sDII-DIII, or full-length suPAR bind to LMTK  cells to the same extent provides additional support for the involvement of urokinase in this interaction.	bind
21593	3	7059	6	13	NULL	NULL	NULL	statement 1	GP		forms a complex with					suPAR	GP	full length			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5348_s_171	9030610	2 Nevertheless, the observation that complexes composed of scuPA and sDI, sDII-DIII, or full-length suPAR bind to LMTK  cells to the same extent provides additional support for the involvement of urokinase in this interaction.	bind
21594	4	7059	6	13	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5348_s_171	9030610	2 Nevertheless, the observation that complexes composed of scuPA and sDI, sDII-DIII, or full-length suPAR bind to LMTK  cells to the same extent provides additional support for the involvement of urokinase in this interaction.	bind
21595	5	7059	6	13	NULL	NULL	NULL	statement 3	GP		bind					LMTK cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5348_s_171	9030610	2 Nevertheless, the observation that complexes composed of scuPA and sDI, sDII-DIII, or full-length suPAR bind to LMTK  cells to the same extent provides additional support for the involvement of urokinase in this interaction.	bind
22184	6	7059	6	13	NULL	NULL	NULL	statement 2	GP		bind					LMTK cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5348_s_171	9030610	2 Nevertheless, the observation that complexes composed of scuPA and sDI, sDII-DIII, or full-length suPAR bind to LMTK  cells to the same extent provides additional support for the involvement of urokinase in this interaction.	bind
22185	7	7059	6	13	NULL	NULL	NULL	urokinase	GP		is involved in					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5348_s_171	9030610	2 Nevertheless, the observation that complexes composed of scuPA and sDI, sDII-DIII, or full-length suPAR bind to LMTK  cells to the same extent provides additional support for the involvement of urokinase in this interaction.	bind
22186	8	7059	6	13	NULL	NULL	NULL	urokinase	GP		is involved in					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5348_s_171	9030610	2 Nevertheless, the observation that complexes composed of scuPA and sDI, sDII-DIII, or full-length suPAR bind to LMTK  cells to the same extent provides additional support for the involvement of urokinase in this interaction.	bind
25885	1	7059	7	NULL	NULL	0	NULL	scuPA	NULL		forms complex with	NULL				sDI	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_5348_s_171	9030610	2 Nevertheless, the observation that complexes composed of scuPA and sDI, sDII-DIII, or full-length suPAR bind to LMTK  cells to the same extent provides additional support for the involvement of urokinase in this interaction.	bind
25886	2	7059	7	NULL	NULL	0	NULL	statement 1			forms complex with					sDII-DIII					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5348_s_171	9030610	2 Nevertheless, the observation that complexes composed of scuPA and sDI, sDII-DIII, or full-length suPAR bind to LMTK  cells to the same extent provides additional support for the involvement of urokinase in this interaction.	bind
25887	3	7059	7	NULL	NULL	0	NULL	statement 1			forms complex with					suPAR		full-length			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5348_s_171	9030610	2 Nevertheless, the observation that complexes composed of scuPA and sDI, sDII-DIII, or full-length suPAR bind to LMTK  cells to the same extent provides additional support for the involvement of urokinase in this interaction.	bind
25888	4	7059	7	NULL	NULL	0	NULL	statement 2			bind					LMTK cells					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5348_s_171	9030610	2 Nevertheless, the observation that complexes composed of scuPA and sDI, sDII-DIII, or full-length suPAR bind to LMTK  cells to the same extent provides additional support for the involvement of urokinase in this interaction.	bind
25889	5	7059	7	NULL	NULL	0	NULL	statement 3			bind					LMTK cells					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5348_s_171	9030610	2 Nevertheless, the observation that complexes composed of scuPA and sDI, sDII-DIII, or full-length suPAR bind to LMTK  cells to the same extent provides additional support for the involvement of urokinase in this interaction.	bind
25890	6	7059	7	NULL	NULL	0	NULL	statement 2			is an alternative to					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5348_s_171	9030610	2 Nevertheless, the observation that complexes composed of scuPA and sDI, sDII-DIII, or full-length suPAR bind to LMTK  cells to the same extent provides additional support for the involvement of urokinase in this interaction.	bind
25891	7	7059	7	NULL	NULL	0	NULL	urokinase			is involved in					statement 4					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5348_s_171	9030610	2 Nevertheless, the observation that complexes composed of scuPA and sDI, sDII-DIII, or full-length suPAR bind to LMTK  cells to the same extent provides additional support for the involvement of urokinase in this interaction.	bind
25892	8	7059	7	NULL	NULL	0	NULL	urokinase			is involved in					statement 5					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5348_s_171	9030610	2 Nevertheless, the observation that complexes composed of scuPA and sDI, sDII-DIII, or full-length suPAR bind to LMTK  cells to the same extent provides additional support for the involvement of urokinase in this interaction.	bind
21598	1	7060	6	13	NULL	NULL	NULL	TRAF	GP		bind					CD40	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19777_s_124	9242637	2 NF-kappaB activation is also a major function associated with TRAF binding to TNF receptor family members including CD40.	bind
21599	2	7060	6	13	NULL	NULL	NULL	CD40	GP		is a type of					TNF receptor family members	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19777_s_124	9242637	2 NF-kappaB activation is also a major function associated with TRAF binding to TNF receptor family members including CD40.	bind
21601	3	7060	6	13	NULL	NULL	NULL	NF-kappaB 	GP	activation of	is associated with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19777_s_124	9242637	2 NF-kappaB activation is also a major function associated with TRAF binding to TNF receptor family members including CD40.	bind
25897	1	7060	7	NULL	NULL	0	NULL	TRAF	NULL		bind	NULL				CD40	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_32_19777_s_124	9242637	2 NF-kappaB activation is also a major function associated with TRAF binding to TNF receptor family members including CD40.	bind
25898	2	7060	7	NULL	NULL	0	NULL	CD40	NULL		is a type of	NULL				 TNF receptor family	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_32_19777_s_124	9242637	2 NF-kappaB activation is also a major function associated with TRAF binding to TNF receptor family members including CD40.	bind
25899	3	7060	7	10	NULL	0	NULL	NF-kappaB	NULL	activation of	is associated with	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19777_s_124	9242637	2 NF-kappaB activation is also a major function associated with TRAF binding to TNF receptor family members including CD40.	bind
21810	1	7062	6	13	NULL	NULL	NULL	GRP-R	GP		bind					bombesin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17405_s_16	9211882	2 Notably, GRP-R, NMB-R, and bb4 all bind bombesin with affinities in the nanomolar range, whereas BRS-3 binds bombesin with much lower affinity (>10 muM).	bind
21811	2	7062	6	13	NULL	NULL	NULL	NMB-R	GP		bind					bombesin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17405_s_16	9211882	2 Notably, GRP-R, NMB-R, and bb4 all bind bombesin with affinities in the nanomolar range, whereas BRS-3 binds bombesin with much lower affinity (>10 muM).	bind
21812	3	7062	6	13	NULL	NULL	NULL	bb4	GP		bind					bombesin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17405_s_16	9211882	2 Notably, GRP-R, NMB-R, and bb4 all bind bombesin with affinities in the nanomolar range, whereas BRS-3 binds bombesin with much lower affinity (>10 muM).	bind
21814	4	7062	6	13	NULL	NULL	NULL	BRS-3	GP		bind		low affinity			bombesin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17405_s_16	9211882	2 Notably, GRP-R, NMB-R, and bb4 all bind bombesin with affinities in the nanomolar range, whereas BRS-3 binds bombesin with much lower affinity (>10 muM).	bind
25900	1	7062	7	NULL	NULL	0	NULL	GRP-R	NULL		bind	NULL				bombesin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_28_17405_s_16	9211882	2 Notably, GRP-R, NMB-R, and bb4 all bind bombesin with affinities in the nanomolar range, whereas BRS-3 binds bombesin with much lower affinity (>10 muM).	bind
25901	2	7062	7	NULL	NULL	0	NULL	NMB-R	NULL		bind	NULL				bombesin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_28_17405_s_16	9211882	2 Notably, GRP-R, NMB-R, and bb4 all bind bombesin with affinities in the nanomolar range, whereas BRS-3 binds bombesin with much lower affinity (>10 muM).	bind
25902	3	7062	7	NULL	NULL	0	NULL	bb4	NULL		bind	NULL				bombesin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_28_17405_s_16	9211882	2 Notably, GRP-R, NMB-R, and bb4 all bind bombesin with affinities in the nanomolar range, whereas BRS-3 binds bombesin with much lower affinity (>10 muM).	bind
25903	4	7062	7	NULL	NULL	0	NULL	BRS-3	NULL		bind	NULL	low affinity			bombesin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_28_17405_s_16	9211882	2 Notably, GRP-R, NMB-R, and bb4 all bind bombesin with affinities in the nanomolar range, whereas BRS-3 binds bombesin with much lower affinity (>10 muM).	bind
21820	1	7063	6	13	NULL	NULL	NULL	IgE	GP		bind					fast omega-gliadin	Chemical				NULL	sera of patients with WDEIA	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_13_12135_s_141	14699123	2 of the 15 patients with WDEIA (patients 11 and 13) had no specific IgE bound to these epitopes ( Fig. 5), although their sera had IgE bound to fast omega-gliadin.	bind
25904	1	7063	7	10	NULL	0	NULL	IgE	NULL		bind	NULL				fast omega-gliadin	NULL				NULL	sera of patients with WDEIA	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_13_12135_s_141	14699123	2 of the 15 patients with WDEIA (patients 11 and 13) had no specific IgE bound to these epitopes ( Fig. 5), although their sera had IgE bound to fast omega-gliadin.	bind
21821	1	7064	6	13	NULL	NULL	NULL	MCP-1	GP		bind					CCR2	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_969_s_19	12067906	2 One of the chemoattractants implicated in the early atherogenesis is monocyte chemoattractant protein-1 (MCP-1), which binds to C-C chemokine receptor 2 (CCR2).	bind
21822	2	7064	6	13	NULL	NULL	NULL	MCP-1	GP		is					monocyte chemoattractant protein-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_969_s_19	12067906	2 One of the chemoattractants implicated in the early atherogenesis is monocyte chemoattractant protein-1 (MCP-1), which binds to C-C chemokine receptor 2 (CCR2).	bind
21823	3	7064	6	13	NULL	NULL	NULL	CCR2	GP		is					C-C chemokine receptor 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_969_s_19	12067906	2 One of the chemoattractants implicated in the early atherogenesis is monocyte chemoattractant protein-1 (MCP-1), which binds to C-C chemokine receptor 2 (CCR2).	bind
25905	1	7064	7	NULL	NULL	0	NULL	MCP-1	NULL		binds to	NULL				CCR2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_969_s_19	12067906	2 One of the chemoattractants implicated in the early atherogenesis is monocyte chemoattractant protein-1 (MCP-1), which binds to C-C chemokine receptor 2 (CCR2).	bind
25906	2	7064	7	NULL	NULL	0	NULL	MCP-1	NULL		is	NULL				monocyte chemoattractant protein-1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_969_s_19	12067906	2 One of the chemoattractants implicated in the early atherogenesis is monocyte chemoattractant protein-1 (MCP-1), which binds to C-C chemokine receptor 2 (CCR2).	bind
25907	3	7064	7	NULL	NULL	0	NULL	CCR2	NULL		is	NULL				C-C chemokine receptor 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_969_s_19	12067906	2 One of the chemoattractants implicated in the early atherogenesis is monocyte chemoattractant protein-1 (MCP-1), which binds to C-C chemokine receptor 2 (CCR2).	bind
21907	1	7065	6	13	NULL	NULL	NULL	eIF4G1	GP		bind		directly			eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_150	10409688	2 Our protease protection data implied that a greater portion of eIF4G1 is directly bound to eIF4E than had been previously supposed and/or that the eIF4E binding domain of eIF4G1 forms a folded structure when the eIF4E binding peptide binds to eIF4E.	bind
21912	2	7065	6	13	NULL	NULL	NULL	eIF4G1	GP		forms a			eIF4E binding domain		folded structure	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_150	10409688	2 Our protease protection data implied that a greater portion of eIF4G1 is directly bound to eIF4E than had been previously supposed and/or that the eIF4E binding domain of eIF4G1 forms a folded structure when the eIF4E binding peptide binds to eIF4E.	bind
21913	3	7065	6	13	NULL	NULL	NULL	eIF4E binding peptide	GP		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_150	10409688	2 Our protease protection data implied that a greater portion of eIF4G1 is directly bound to eIF4E than had been previously supposed and/or that the eIF4E binding domain of eIF4G1 forms a folded structure when the eIF4E binding peptide binds to eIF4E.	bind
53304	4	7065	6	13	NULL	NULL	NULL	statement 3	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_150	10409688	2 Our protease protection data implied that a greater portion of eIF4G1 is directly bound to eIF4E than had been previously supposed and/or that the eIF4E binding domain of eIF4G1 forms a folded structure when the eIF4E binding peptide binds to eIF4E.	bind
25908	1	7065	7	NULL	NULL	0	NULL	eIF4G1	NULL		binds	NULL	directly			eIF4E	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_150	10409688	2 Our protease protection data implied that a greater portion of eIF4G1 is directly bound to eIF4E than had been previously supposed and/or that the eIF4E binding domain of eIF4G1 forms a folded structure when the eIF4E binding peptide binds to eIF4E.	bind
25909	2	7065	7	NULL	NULL	0	NULL	eIF4G1	NULL		forms a	NULL		eIF4E binding domain 		folded structure	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_150	10409688	2 Our protease protection data implied that a greater portion of eIF4G1 is directly bound to eIF4E than had been previously supposed and/or that the eIF4E binding domain of eIF4G1 forms a folded structure when the eIF4E binding peptide binds to eIF4E.	bind
25910	3	7065	7	NULL	NULL	0	NULL	eIF4E binding peptide	NULL		binds to	NULL				eIF4E	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_150	10409688	2 Our protease protection data implied that a greater portion of eIF4G1 is directly bound to eIF4E than had been previously supposed and/or that the eIF4E binding domain of eIF4G1 forms a folded structure when the eIF4E binding peptide binds to eIF4E.	bind
25911	4	7065	7	NULL	NULL	0	NULL	statement 2	NULL		occurs upon	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21297_s_150	10409688	2 Our protease protection data implied that a greater portion of eIF4G1 is directly bound to eIF4E than had been previously supposed and/or that the eIF4E binding domain of eIF4G1 forms a folded structure when the eIF4E binding peptide binds to eIF4E.	bind
21918	1	7066	6	13	NULL	NULL	NULL	GG	NucleicAcid		does not bind		directly			Ras-GRF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_41_38029_s_225	11500499	2 Overall these results suggest that GG does not bind directly to Ras-GRF2.	bind
25912	1	7066	7	NULL	NULL	0	NULL	 GG	NULL		does not bind	NULL	directly			Ras-GRF2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_41_38029_s_225	11500499	2 Overall these results suggest that GG does not bind directly to Ras-GRF2.	bind
21919	1	7067	6	13	NULL	NULL	NULL	p53	GP		does not bind			His-175		SCS	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_41_25468_s_95	8810317	2 p53(His-175) did not bind to SCS either; however, its generally weaker binding to the other sites makes this observation less significant.	bind
25913	1	7067	7	NULL	NULL	0	NULL	p53	NULL		does not bind	NULL		His-175		SCS	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_41_25468_s_95	8810317	2 p53(His-175) did not bind to SCS either; however, its generally weaker binding to the other sites makes this observation less significant.	bind
21921	1	7069	6	13	NULL	NULL	NULL	F-actin	GP		bind					spinophilin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_2_1186_s_313	12417592	2 Phosphorylation of spinophilin may disrupt one of these sites, reducing the number of actin molecules bound to spinophilin without perturbing the binding affinity of spinophilin for F-actin.	bind
21922	2	7069	6	13	NULL	NULL	NULL	spinophilin	GP	phosphorylation of	reduces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_2_1186_s_313	12417592	2 Phosphorylation of spinophilin may disrupt one of these sites, reducing the number of actin molecules bound to spinophilin without perturbing the binding affinity of spinophilin for F-actin.	bind
21923	3	7069	6	13	NULL	NULL	NULL	spinophilin	GP	phosphorylation of	does not affect					spinophilin	GP	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_2_1186_s_313	12417592	2 Phosphorylation of spinophilin may disrupt one of these sites, reducing the number of actin molecules bound to spinophilin without perturbing the binding affinity of spinophilin for F-actin.	bind
25917	1	7069	7	NULL	NULL	0	NULL	spinophilin	NULL		bind	NULL				F-actin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_2_1186_s_313	12417592	2 Phosphorylation of spinophilin may disrupt one of these sites, reducing the number of actin molecules bound to spinophilin without perturbing the binding affinity of spinophilin for F-actin.	bind
25918	2	7069	7	NULL	NULL	0	NULL	spinophilin	NULL	Phosphorylation of	does not perturb	NULL				statement 1	NULL	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_2_1186_s_313	12417592	2 Phosphorylation of spinophilin may disrupt one of these sites, reducing the number of actin molecules bound to spinophilin without perturbing the binding affinity of spinophilin for F-actin.	bind
25919	3	7069	7	NULL	NULL	0	NULL	spinophilin	NULL	phosphorylation of	reduce	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_2_1186_s_313	12417592	2 Phosphorylation of spinophilin may disrupt one of these sites, reducing the number of actin molecules bound to spinophilin without perturbing the binding affinity of spinophilin for F-actin.	bind
21924	1	7070	6	13	NULL	NULL	NULL	cisplatin	Chemical		bind		rapidly			plasma proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_5_1193_s_316	8636430	2 Previous studies have demonstrated that the large  majority of cisplatin is bound rapidly by plasma proteins, including albumin ( 62).	bind
21925	2	7070	6	13	NULL	NULL	NULL	cisplatin	Chemical		bind					albumin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_5_1193_s_316	8636430	2 Previous studies have demonstrated that the large  majority of cisplatin is bound rapidly by plasma proteins, including albumin ( 62).	bind
27027	3	7070	6	13	NULL	NULL	NULL	albumin	GP		is a type of					plasma protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_5_1193_s_316	8636430	2 Previous studies have demonstrated that the large  majority of cisplatin is bound rapidly by plasma proteins, including albumin ( 62).	bind
25920	1	7070	7	NULL	NULL	0	NULL	cisplatin	NULL		binds	NULL	rapidly			albumin	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_5_1193_s_316	8636430	2 Previous studies have demonstrated that the large  majority of cisplatin is bound rapidly by plasma proteins, including albumin ( 62).	bind
25921	2	7070	7	NULL	NULL	0	NULL	albumin	NULL		is a type of	NULL				plasma protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_5_1193_s_316	8636430	2 Previous studies have demonstrated that the large  majority of cisplatin is bound rapidly by plasma proteins, including albumin ( 62).	bind
30062	3	7070	7	NULL	NULL	0	NULL	cisplatin	NULL		bind	NULL				plasma proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_5_1193_s_316	8636430	2 Previous studies have demonstrated that the large  majority of cisplatin is bound rapidly by plasma proteins, including albumin ( 62).	bind
21926	1	7071	6	13	NULL	NULL	NULL	Axin	GP		bind					beta-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_4_2399_s_76	10644691	2 Previously, it had been shown that Axin binds beta-catenin to regulate its abundance ( 9).	bind
21927	2	7071	6	13	NULL	NULL	NULL	statement 1	Process		regulates					beta-catenin	GP	abundance of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_4_2399_s_76	10644691	2 Previously, it had been shown that Axin binds beta-catenin to regulate its abundance ( 9).	bind
25922	1	7071	7	NULL	NULL	0	NULL	Axin	NULL		binds	NULL				beta-catenin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_4_2399_s_76	10644691	2 Previously, it had been shown that Axin binds beta-catenin to regulate its abundance ( 9).	bind
25923	2	7071	7	NULL	NULL	0	NULL	statement 1	NULL		regulate 	NULL				beta-catenin	NULL	abundance of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_4_2399_s_76	10644691	2 Previously, it had been shown that Axin binds beta-catenin to regulate its abundance ( 9).	bind
21928	1	7072	6	13	NULL	NULL	NULL	JNK	GP		bind					growth factor receptor binding protein 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_38_23304_s_139	8798530	2 Recent studies suggest that JNK binds to growth factor receptor binding protein 2 ( 11), the adapter protein that links tyrosine kinase receptors to the SOS protein, which, in turn, activates p21 ras by promoting GTP/GDP exchange.	bind
21929	2	7072	6	13	NULL	NULL	NULL	tyrosine kinase receptors	GP		linked to					SOS protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_38_23304_s_139	8798530	2 Recent studies suggest that JNK binds to growth factor receptor binding protein 2 ( 11), the adapter protein that links tyrosine kinase receptors to the SOS protein, which, in turn, activates p21 ras by promoting GTP/GDP exchange.	bind
21933	3	7072	6	13	NULL	NULL	NULL	growth factor receptor binding protein 2	GP		plays a role in					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_38_23304_s_139	8798530	2 Recent studies suggest that JNK binds to growth factor receptor binding protein 2 ( 11), the adapter protein that links tyrosine kinase receptors to the SOS protein, which, in turn, activates p21 ras by promoting GTP/GDP exchange.	bind
21935	4	7072	6	13	NULL	NULL	NULL	statement 2	Process		activates					p21 ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_38_23304_s_139	8798530	2 Recent studies suggest that JNK binds to growth factor receptor binding protein 2 ( 11), the adapter protein that links tyrosine kinase receptors to the SOS protein, which, in turn, activates p21 ras by promoting GTP/GDP exchange.	bind
21936	5	7072	6	13	NULL	NULL	NULL	statement 4	Process		occurs by					GTP/GDP exchange	Process	promoting 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_38_23304_s_139	8798530	2 Recent studies suggest that JNK binds to growth factor receptor binding protein 2 ( 11), the adapter protein that links tyrosine kinase receptors to the SOS protein, which, in turn, activates p21 ras by promoting GTP/GDP exchange.	bind
27028	6	7072	6	13	NULL	NULL	NULL	growth factor receptor binding protein 2	GP		is a type of					adapter protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_38_23304_s_139	8798530	2 Recent studies suggest that JNK binds to growth factor receptor binding protein 2 ( 11), the adapter protein that links tyrosine kinase receptors to the SOS protein, which, in turn, activates p21 ras by promoting GTP/GDP exchange.	bind
25924	1	7072	7	NULL	NULL	0	NULL	 JNK	NULL		binds to	NULL				growth factor receptor binding protein 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_38_23304_s_139	8798530	2 Recent studies suggest that JNK binds to growth factor receptor binding protein 2 ( 11), the adapter protein that links tyrosine kinase receptors to the SOS protein, which, in turn, activates p21 ras by promoting GTP/GDP exchange.	bind
25925	2	7072	7	NULL	NULL	0	NULL	growth factor receptor binding protein 2	NULL		is a type of	NULL				adaptor protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_38_23304_s_139	8798530	2 Recent studies suggest that JNK binds to growth factor receptor binding protein 2 ( 11), the adapter protein that links tyrosine kinase receptors to the SOS protein, which, in turn, activates p21 ras by promoting GTP/GDP exchange.	bind
25926	3	7072	7	10	NULL	0	NULL	tyrosine kinase receptors	NULL		is linked to	NULL				SOS protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_38_23304_s_139	8798530	2 Recent studies suggest that JNK binds to growth factor receptor binding protein 2 ( 11), the adapter protein that links tyrosine kinase receptors to the SOS protein, which, in turn, activates p21 ras by promoting GTP/GDP exchange.	bind
25927	4	7072	7	10	NULL	0	NULL	growth factor receptor binding protein 2	NULL		plays a role in	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_38_23304_s_139	8798530	2 Recent studies suggest that JNK binds to growth factor receptor binding protein 2 ( 11), the adapter protein that links tyrosine kinase receptors to the SOS protein, which, in turn, activates p21 ras by promoting GTP/GDP exchange.	bind
25928	5	7072	7	NULL	NULL	0	NULL	statement 3	NULL		activates	NULL				p21ras	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_38_23304_s_139	8798530	2 Recent studies suggest that JNK binds to growth factor receptor binding protein 2 ( 11), the adapter protein that links tyrosine kinase receptors to the SOS protein, which, in turn, activates p21 ras by promoting GTP/GDP exchange.	bind
25929	6	7072	7	10	NULL	0	NULL	statement 5	NULL		occurs by	NULL				GTP/GDP exchange	NULL	promoting			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_38_23304_s_139	8798530	2 Recent studies suggest that JNK binds to growth factor receptor binding protein 2 ( 11), the adapter protein that links tyrosine kinase receptors to the SOS protein, which, in turn, activates p21 ras by promoting GTP/GDP exchange.	bind
22188	1	7073	6	13	NULL	NULL	NULL	gp41	GP		assembles onto					gp32-ssDNA complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_33_20198_s_33	8702746	2 Second, gp59-dependent assembly of gp41 onto gp32-ssDNA complexes, as measured by activation of the helicase's ssDNA-stimulated nucleotidase activity, is inhibited by excess free gp32, suggesting that gp59 must contact ssDNA-bound gp32 molecules in order to promote helicase-ssDNA assembly (Morrical  et al., 1994  ).	bind
22189	2	7073	6	13	NULL	NULL	NULL	statement 1	Process		is dependent on					gp59	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_33_20198_s_33	8702746	2 Second, gp59-dependent assembly of gp41 onto gp32-ssDNA complexes, as measured by activation of the helicase's ssDNA-stimulated nucleotidase activity, is inhibited by excess free gp32, suggesting that gp59 must contact ssDNA-bound gp32 molecules in order to promote helicase-ssDNA assembly (Morrical  et al., 1994  ).	bind
22190	3	7073	6	13	NULL	NULL	NULL	ssDNA	NucleicAcid		stimulates					nucleotidase 	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_33_20198_s_33	8702746	2 Second, gp59-dependent assembly of gp41 onto gp32-ssDNA complexes, as measured by activation of the helicase's ssDNA-stimulated nucleotidase activity, is inhibited by excess free gp32, suggesting that gp59 must contact ssDNA-bound gp32 molecules in order to promote helicase-ssDNA assembly (Morrical  et al., 1994  ).	bind
22191	4	7073	6	13	NULL	NULL	NULL	gp32	GP	excess of	inhibits					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_33_20198_s_33	8702746	2 Second, gp59-dependent assembly of gp41 onto gp32-ssDNA complexes, as measured by activation of the helicase's ssDNA-stimulated nucleotidase activity, is inhibited by excess free gp32, suggesting that gp59 must contact ssDNA-bound gp32 molecules in order to promote helicase-ssDNA assembly (Morrical  et al., 1994  ).	bind
22192	5	7073	6	13	NULL	NULL	NULL	gp59	GP		promote					helicase-ssDNA 	GP	assembly of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_33_20198_s_33	8702746	2 Second, gp59-dependent assembly of gp41 onto gp32-ssDNA complexes, as measured by activation of the helicase's ssDNA-stimulated nucleotidase activity, is inhibited by excess free gp32, suggesting that gp59 must contact ssDNA-bound gp32 molecules in order to promote helicase-ssDNA assembly (Morrical  et al., 1994  ).	bind
22193	6	7073	6	13	NULL	NULL	NULL	gp39	GP		contact		must			statement 8	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_33_20198_s_33	8702746	2 Second, gp59-dependent assembly of gp41 onto gp32-ssDNA complexes, as measured by activation of the helicase's ssDNA-stimulated nucleotidase activity, is inhibited by excess free gp32, suggesting that gp59 must contact ssDNA-bound gp32 molecules in order to promote helicase-ssDNA assembly (Morrical  et al., 1994  ).	bind
22194	7	7073	6	13	NULL	NULL	NULL	statement 5	Process		promote					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_33_20198_s_33	8702746	2 Second, gp59-dependent assembly of gp41 onto gp32-ssDNA complexes, as measured by activation of the helicase's ssDNA-stimulated nucleotidase activity, is inhibited by excess free gp32, suggesting that gp59 must contact ssDNA-bound gp32 molecules in order to promote helicase-ssDNA assembly (Morrical  et al., 1994  ).	bind
46420	8	7073	6	13	NULL	NULL	NULL	ssDNA	NucleicAcid		bind					gp32 molecules	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_33_20198_s_33	8702746	2 Second, gp59-dependent assembly of gp41 onto gp32-ssDNA complexes, as measured by activation of the helicase's ssDNA-stimulated nucleotidase activity, is inhibited by excess free gp32, suggesting that gp59 must contact ssDNA-bound gp32 molecules in order to promote helicase-ssDNA assembly (Morrical  et al., 1994  ).	bind
25930	1	7073	7	NULL	NULL	0	NULL	gp41	NULL		assemble onto	NULL				gp32-ssDNA complex	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_33_20198_s_33	8702746	2 Second, gp59-dependent assembly of gp41 onto gp32-ssDNA complexes, as measured by activation of the helicase's ssDNA-stimulated nucleotidase activity, is inhibited by excess free gp32, suggesting that gp59 must contact ssDNA-bound gp32 molecules in order to promote helicase-ssDNA assembly (Morrical  et al., 1994  ).	bind
25931	2	7073	7	NULL	NULL	0	NULL	statement 1	NULL		depends on	NULL				gp59	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_33_20198_s_33	8702746	2 Second, gp59-dependent assembly of gp41 onto gp32-ssDNA complexes, as measured by activation of the helicase's ssDNA-stimulated nucleotidase activity, is inhibited by excess free gp32, suggesting that gp59 must contact ssDNA-bound gp32 molecules in order to promote helicase-ssDNA assembly (Morrical  et al., 1994  ).	bind
25932	3	7073	7	NULL	NULL	0	NULL	gp32	NULL	excess of	inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_33_20198_s_33	8702746	2 Second, gp59-dependent assembly of gp41 onto gp32-ssDNA complexes, as measured by activation of the helicase's ssDNA-stimulated nucleotidase activity, is inhibited by excess free gp32, suggesting that gp59 must contact ssDNA-bound gp32 molecules in order to promote helicase-ssDNA assembly (Morrical  et al., 1994  ).	bind
25933	4	7073	7	10	NULL	0	NULL	gp59	NULL		contact	NULL	must			statement 8	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_33_20198_s_33	8702746	2 Second, gp59-dependent assembly of gp41 onto gp32-ssDNA complexes, as measured by activation of the helicase's ssDNA-stimulated nucleotidase activity, is inhibited by excess free gp32, suggesting that gp59 must contact ssDNA-bound gp32 molecules in order to promote helicase-ssDNA assembly (Morrical  et al., 1994  ).	bind
25934	5	7073	7	NULL	NULL	0	NULL	statement 3	NULL		suggests	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_33_20198_s_33	8702746	2 Second, gp59-dependent assembly of gp41 onto gp32-ssDNA complexes, as measured by activation of the helicase's ssDNA-stimulated nucleotidase activity, is inhibited by excess free gp32, suggesting that gp59 must contact ssDNA-bound gp32 molecules in order to promote helicase-ssDNA assembly (Morrical  et al., 1994  ).	bind
25935	6	7073	7	NULL	NULL	0	NULL	statement 4	NULL		promote	NULL				helicase-ssDNA 	NULL	assembly of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_33_20198_s_33	8702746	2 Second, gp59-dependent assembly of gp41 onto gp32-ssDNA complexes, as measured by activation of the helicase's ssDNA-stimulated nucleotidase activity, is inhibited by excess free gp32, suggesting that gp59 must contact ssDNA-bound gp32 molecules in order to promote helicase-ssDNA assembly (Morrical  et al., 1994  ).	bind
28025	7	7073	7	NULL	NULL	0	NULL	ssDNA	NULL		stimulates	NULL				nucleotidase	NULL	activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_33_20198_s_33	8702746	2 Second, gp59-dependent assembly of gp41 onto gp32-ssDNA complexes, as measured by activation of the helicase's ssDNA-stimulated nucleotidase activity, is inhibited by excess free gp32, suggesting that gp59 must contact ssDNA-bound gp32 molecules in order to promote helicase-ssDNA assembly (Morrical  et al., 1994  ).	bind
46421	8	7073	7	10	NULL	0	NULL	ssDNA	NULL		bind	NULL				gp32 molecules	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_33_20198_s_33	8702746	2 Second, gp59-dependent assembly of gp41 onto gp32-ssDNA complexes, as measured by activation of the helicase's ssDNA-stimulated nucleotidase activity, is inhibited by excess free gp32, suggesting that gp59 must contact ssDNA-bound gp32 molecules in order to promote helicase-ssDNA assembly (Morrical  et al., 1994  ).	bind
21939	1	7074	6	13	NULL	NULL	NULL	Serine/arginine-rich proteins	GP		is a type of					RNA transactivating factors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_2_910_s_253	9422749	2 Serine/arginine-rich (SR) proteins and pyrimidine tract-binding protein are known RNA transactivating factors that bind to these  cis-elements and affect exon inclusion and 5  splice selection ( 21).	bind
21948	2	7074	6	13	NULL	NULL	NULL	pyrimidine tract-binding protein	GP		is a type of					RNA transactivating factors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_2_910_s_253	9422749	2 Serine/arginine-rich (SR) proteins and pyrimidine tract-binding protein are known RNA transactivating factors that bind to these  cis-elements and affect exon inclusion and 5  splice selection ( 21).	bind
21949	3	7074	6	13	NULL	NULL	NULL	Serine/arginine-rich proteins	GP		is 					SR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_2_910_s_253	9422749	2 Serine/arginine-rich (SR) proteins and pyrimidine tract-binding protein are known RNA transactivating factors that bind to these  cis-elements and affect exon inclusion and 5  splice selection ( 21).	bind
21950	4	7074	6	13	NULL	NULL	NULL	statement 1	GP		bind									cis-elements	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_2_910_s_253	9422749	2 Serine/arginine-rich (SR) proteins and pyrimidine tract-binding protein are known RNA transactivating factors that bind to these  cis-elements and affect exon inclusion and 5  splice selection ( 21).	bind
21951	5	7074	6	13	NULL	NULL	NULL	statement 4	Process		affect					exon inclusion	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_2_910_s_253	9422749	2 Serine/arginine-rich (SR) proteins and pyrimidine tract-binding protein are known RNA transactivating factors that bind to these  cis-elements and affect exon inclusion and 5  splice selection ( 21).	bind
21952	6	7074	6	13	NULL	NULL	NULL	statement 4	Process		affect					splice selection	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_2_910_s_253	9422749	2 Serine/arginine-rich (SR) proteins and pyrimidine tract-binding protein are known RNA transactivating factors that bind to these  cis-elements and affect exon inclusion and 5  splice selection ( 21).	bind
21953	7	7074	6	13	NULL	NULL	NULL	statement 2	GP		bind									cis-elements	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_2_910_s_253	9422749	2 Serine/arginine-rich (SR) proteins and pyrimidine tract-binding protein are known RNA transactivating factors that bind to these  cis-elements and affect exon inclusion and 5  splice selection ( 21).	bind
21954	8	7074	6	13	NULL	NULL	NULL	statement 7	Process		affect					exon inclusion	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_2_910_s_253	9422749	2 Serine/arginine-rich (SR) proteins and pyrimidine tract-binding protein are known RNA transactivating factors that bind to these  cis-elements and affect exon inclusion and 5  splice selection ( 21).	bind
21955	9	7074	6	13	NULL	NULL	NULL	statement 7	Process		affect					splice selection	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_2_910_s_253	9422749	2 Serine/arginine-rich (SR) proteins and pyrimidine tract-binding protein are known RNA transactivating factors that bind to these  cis-elements and affect exon inclusion and 5  splice selection ( 21).	bind
25936	1	7074	7	NULL	NULL	0	NULL	SR protein	NULL		is a type of	NULL				RNA transactivating factors	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_2_910_s_253	9422749	2 Serine/arginine-rich (SR) proteins and pyrimidine tract-binding protein are known RNA transactivating factors that bind to these  cis-elements and affect exon inclusion and 5  splice selection ( 21).	bind
25937	2	7074	7	NULL	NULL	0	NULL	pyrimidine tract-binding protein	NULL		is a type of	NULL				RNA transactivating factors	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_2_910_s_253	9422749	2 Serine/arginine-rich (SR) proteins and pyrimidine tract-binding protein are known RNA transactivating factors that bind to these  cis-elements and affect exon inclusion and 5  splice selection ( 21).	bind
25938	3	7074	7	NULL	NULL	0	NULL	SR protein	NULL		bind	NULL					NULL			cis-elements	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_2_910_s_253	9422749	2 Serine/arginine-rich (SR) proteins and pyrimidine tract-binding protein are known RNA transactivating factors that bind to these  cis-elements and affect exon inclusion and 5  splice selection ( 21).	bind
25939	4	7074	7	NULL	NULL	0	NULL	pyrimidine tract-binding protein	NULL		bind	NULL					NULL			cis-elements	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_2_910_s_253	9422749	2 Serine/arginine-rich (SR) proteins and pyrimidine tract-binding protein are known RNA transactivating factors that bind to these  cis-elements and affect exon inclusion and 5  splice selection ( 21).	bind
25940	5	7074	7	NULL	NULL	0	NULL	statement 3	NULL		affect	NULL				exon inclusion	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_2_910_s_253	9422749	2 Serine/arginine-rich (SR) proteins and pyrimidine tract-binding protein are known RNA transactivating factors that bind to these  cis-elements and affect exon inclusion and 5  splice selection ( 21).	bind
25941	6	7074	7	NULL	NULL	0	NULL	statement 3	NULL		affect	NULL				splice selection 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_2_910_s_253	9422749	2 Serine/arginine-rich (SR) proteins and pyrimidine tract-binding protein are known RNA transactivating factors that bind to these  cis-elements and affect exon inclusion and 5  splice selection ( 21).	bind
25942	7	7074	7	NULL	NULL	0	NULL	statement 4	NULL		affect	NULL				exon inclusion	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_2_910_s_253	9422749	2 Serine/arginine-rich (SR) proteins and pyrimidine tract-binding protein are known RNA transactivating factors that bind to these  cis-elements and affect exon inclusion and 5  splice selection ( 21).	bind
25943	8	7074	7	NULL	NULL	0	NULL	statement 4	NULL		affect	NULL				splice selection	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_2_910_s_253	9422749	2 Serine/arginine-rich (SR) proteins and pyrimidine tract-binding protein are known RNA transactivating factors that bind to these  cis-elements and affect exon inclusion and 5  splice selection ( 21).	bind
22195	1	7075	6	13	NULL	NULL	NULL	rGPBP	GP		bind					protein	GP	human;;recombinant	alpha1 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
22196	2	7075	6	13	NULL	NULL	NULL	rGPBP	GP		bind			delta26		protein	GP	human;;recombinant	alpha1 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
22197	3	7075	6	13	NULL	NULL	NULL	rGPBP	GP		bind					protein	GP	human;;recombinant	alpha5(IV)NC1 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
22198	4	7075	6	13	NULL	NULL	NULL	rGPBP	GP		bind			delta26		protein	GP	human;;recombinant	alpha5(IV)NC1 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
22199	5	7075	6	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
22200	6	7075	6	13	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
22201	7	7075	6	13	NULL	NULL	NULL	rGPBP	GP		does not bind					protein	GP	human;;recombinant	alpha2 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
22202	8	7075	6	13	NULL	NULL	NULL	rGPBP	GP		does not bind					protein	GP	human;;recombinant	alpha4 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
22203	9	7075	6	13	NULL	NULL	NULL	rGPBP	GP		does not bind					protein	GP	human;;recombinant	alpha6(IV)NC1 		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
22204	10	7075	6	13	NULL	NULL	NULL	rGPBP	GP		does not bind			delta26		protein	GP	human;;recombinant	alpha2 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
22205	11	7075	6	13	NULL	NULL	NULL	rGPBP	GP		does not bind			delta26		protein	GP	human;;recombinant	alpha4 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
22206	12	7075	6	13	NULL	NULL	NULL	rGPBP	GP		does not bind			delta26		protein	GP	human;;recombinant	alpha6(IV)NC1		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
25946	1	7075	7	10	NULL	0	NULL	rGPBP	NULL		bind	NULL				proteins	NULL	human;;highly homologous;;recombinant	alpha1 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
25947	2	7075	7	10	NULL	0	NULL	rGPBP	NULL		bind	NULL				proteins	NULL	human;;highly homologous;;recombinant	alpha5(IV)NC1 domains		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
28472	3	7075	7	10	NULL	0	NULL	 rGPBP	NULL		bind	NULL		delta26		proteins	NULL	human;;highly homologous;;recombinant	alpha1 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
28473	4	7075	7	10	NULL	0	NULL	 rGPBP	NULL		bind	NULL		delta26		proteins	NULL	human;;highly homologous;;recombinant	alpha5(IV)NC1 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
28474	5	7075	7	10	NULL	0	NULL	rGPBP	NULL		does not bind	NULL				protein	NULL	human;;recombinant	alpha2 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
28475	6	7075	7	10	NULL	0	NULL	rGPBP	NULL		does not bind	NULL				protein	NULL	human;;recombinant	alpha4 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
28476	7	7075	7	10	NULL	0	NULL	rGPBP	NULL		does not bind	NULL				protein	NULL	human;;recombinant	alpha6(IV)NC1 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
30063	8	7075	7	10	NULL	0	NULL	 rGPBP	NULL		does not bind	NULL		delta26		protein	NULL	human;;recombinant	alpha2 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
30064	9	7075	7	10	NULL	0	NULL	rGPBP	NULL		does not bind	NULL		delta26		protein	NULL	human;;recombinant	alpha4 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
30065	10	7075	7	10	NULL	0	NULL	rGPBP	NULL		does not bind	NULL		delta26		protein	NULL	human;;recombinant	alpha6(IV)NC1 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40392_s_265	11007769	2 Similar pattern to that shown in Fig.  3 D was obtained when assessing the binding of rGPBP or rGPBPdelta26 to recombinant proteins representing the human highly homologous alpha1 and alpha5(IV)NC1 domains; however, no significant material bound to the recombinant material representing the alpha2-, alpha4 , and alpha6(IV)NC1 counterparts.	bind
21956	1	7076	6	13	NULL	NULL	NULL	SF-1	GP		interacts with					p300	GP		amino terminal region		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_8_4585_s_189	9468515	2 Similar to other nuclear receptors, SF-1 interacts with the amino-terminal region of p300; however, SF-1 also binds p300 at the carboxyl-terminal region, which have been shown to interact with several transcription factors including SRC-1 ( 50).	bind
21957	2	7076	6	13	NULL	NULL	NULL	SF-1	GP		bind					p300	GP		carboxyl-terminal region		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_8_4585_s_189	9468515	2 Similar to other nuclear receptors, SF-1 interacts with the amino-terminal region of p300; however, SF-1 also binds p300 at the carboxyl-terminal region, which have been shown to interact with several transcription factors including SRC-1 ( 50).	bind
21958	3	7076	6	13	NULL	NULL	NULL	p300	GP		interact with			carboxyl-terminal region		SRC-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_8_4585_s_189	9468515	2 Similar to other nuclear receptors, SF-1 interacts with the amino-terminal region of p300; however, SF-1 also binds p300 at the carboxyl-terminal region, which have been shown to interact with several transcription factors including SRC-1 ( 50).	bind
27029	4	7076	6	13	NULL	NULL	NULL	SRC-1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_8_4585_s_189	9468515	2 Similar to other nuclear receptors, SF-1 interacts with the amino-terminal region of p300; however, SF-1 also binds p300 at the carboxyl-terminal region, which have been shown to interact with several transcription factors including SRC-1 ( 50).	bind
25948	1	7076	7	NULL	NULL	0	NULL	SF-1 	NULL		interacts with	NULL				p300	NULL		 amino-terminal		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_8_4585_s_189	9468515	2 Similar to other nuclear receptors, SF-1 interacts with the amino-terminal region of p300; however, SF-1 also binds p300 at the carboxyl-terminal region, which have been shown to interact with several transcription factors including SRC-1 ( 50).	bind
25949	2	7076	7	10	NULL	0	NULL	 SF-1	NULL		bind	NULL				p300	NULL		carboxyl-terminal region		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_8_4585_s_189	9468515	2 Similar to other nuclear receptors, SF-1 interacts with the amino-terminal region of p300; however, SF-1 also binds p300 at the carboxyl-terminal region, which have been shown to interact with several transcription factors including SRC-1 ( 50).	bind
25950	3	7076	7	NULL	NULL	0	NULL	p300	NULL		interacts with	NULL		carboxyl-terminal region		SRC-1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_8_4585_s_189	9468515	2 Similar to other nuclear receptors, SF-1 interacts with the amino-terminal region of p300; however, SF-1 also binds p300 at the carboxyl-terminal region, which have been shown to interact with several transcription factors including SRC-1 ( 50).	bind
28477	4	7076	7	NULL	NULL	0	NULL	SRC-1	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_8_4585_s_189	9468515	2 Similar to other nuclear receptors, SF-1 interacts with the amino-terminal region of p300; however, SF-1 also binds p300 at the carboxyl-terminal region, which have been shown to interact with several transcription factors including SRC-1 ( 50).	bind
21959	1	7077	6	13	NULL	NULL	NULL	SEMA3A/Sema3A	GP		bind					neuropilin-1 receptor	GP	endothelial			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39647_s_227	10993894	2 Similarly, binding of the well known guidance signal SEMA3A/Sema3A to the endothelial neuropilin-1 receptor, which mediates repulsive signals, also leads to a reduced cell motility ( 41).	bind
21960	2	7077	6	13	NULL	NULL	NULL	statement 1	Process		mediates					repulsive signals	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39647_s_227	10993894	2 Similarly, binding of the well known guidance signal SEMA3A/Sema3A to the endothelial neuropilin-1 receptor, which mediates repulsive signals, also leads to a reduced cell motility ( 41).	bind
21961	3	7077	6	13	NULL	NULL	NULL	statement 1	Process		leads to					cell motility	Process	reduced			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39647_s_227	10993894	2 Similarly, binding of the well known guidance signal SEMA3A/Sema3A to the endothelial neuropilin-1 receptor, which mediates repulsive signals, also leads to a reduced cell motility ( 41).	bind
25951	1	7077	7	NULL	NULL	0	NULL	 SEMA3A/Sema3A 	NULL		binds to	NULL				neuropilin-1 receptor	NULL	endothelial			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39647_s_227	10993894	2 Similarly, binding of the well known guidance signal SEMA3A/Sema3A to the endothelial neuropilin-1 receptor, which mediates repulsive signals, also leads to a reduced cell motility ( 41).	bind
25952	2	7077	7	NULL	NULL	0	NULL	statement 1	NULL		mediates	NULL				repulsive signals	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39647_s_227	10993894	2 Similarly, binding of the well known guidance signal SEMA3A/Sema3A to the endothelial neuropilin-1 receptor, which mediates repulsive signals, also leads to a reduced cell motility ( 41).	bind
25953	3	7077	7	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				cell motility	NULL	reduced			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39647_s_227	10993894	2 Similarly, binding of the well known guidance signal SEMA3A/Sema3A to the endothelial neuropilin-1 receptor, which mediates repulsive signals, also leads to a reduced cell motility ( 41).	bind
21962	1	7078	6	13	NULL	NULL	NULL	aminopeptidases	GP	Manduca sexta	bind					Cry1A toxins	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13863_s_16	11836242	2 Similarly, in  Manduca sexta and  Bombyx mori, aminopeptidases and the cadherin-like proteins bind Cry1A toxins as well ( 10-14).	bind
21963	2	7078	6	13	NULL	NULL	NULL	aminopeptidases	GP	bombyx mori	bind					Cry1A toxins	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13863_s_16	11836242	2 Similarly, in  Manduca sexta and  Bombyx mori, aminopeptidases and the cadherin-like proteins bind Cry1A toxins as well ( 10-14).	bind
21964	3	7078	6	13	NULL	NULL	NULL	cadherin-like proteins	GP	Manduca sexta	bind					Cry1A toxins	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13863_s_16	11836242	2 Similarly, in  Manduca sexta and  Bombyx mori, aminopeptidases and the cadherin-like proteins bind Cry1A toxins as well ( 10-14).	bind
21965	4	7078	6	13	NULL	NULL	NULL	cadherin-like proteins	GP	bombyx mori	bind					Cry1A toxins	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13863_s_16	11836242	2 Similarly, in  Manduca sexta and  Bombyx mori, aminopeptidases and the cadherin-like proteins bind Cry1A toxins as well ( 10-14).	bind
25954	1	7078	7	NULL	NULL	0	NULL	aminopeptidases	NULL	Manduca sexta 	bind	NULL				Cry1A toxins	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13863_s_16	11836242	2 Similarly, in  Manduca sexta and  Bombyx mori, aminopeptidases and the cadherin-like proteins bind Cry1A toxins as well ( 10-14).	bind
25955	2	7078	7	NULL	NULL	0	NULL	aminopeptidases 	NULL	Bombyx mori	bind	NULL				Cry1A toxins	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13863_s_16	11836242	2 Similarly, in  Manduca sexta and  Bombyx mori, aminopeptidases and the cadherin-like proteins bind Cry1A toxins as well ( 10-14).	bind
25956	3	7078	7	NULL	NULL	0	NULL	cadherin-like proteins	NULL	Manduca sexta	bind	NULL				Cry1A toxins	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13863_s_16	11836242	2 Similarly, in  Manduca sexta and  Bombyx mori, aminopeptidases and the cadherin-like proteins bind Cry1A toxins as well ( 10-14).	bind
25957	4	7078	7	NULL	NULL	0	NULL	 cadherin-like proteins	NULL	Bombyx mori	bind	NULL				Cry1A toxins	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13863_s_16	11836242	2 Similarly, in  Manduca sexta and  Bombyx mori, aminopeptidases and the cadherin-like proteins bind Cry1A toxins as well ( 10-14).	bind
21966	1	7079	6	13	NULL	NULL	NULL	syndecan-4	GP		bind					PIP2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10624_s_34	9553124	2 Since syndecan-4 can bind PIP2 and activate PKC, we investigated whether PIP2 and syndecan-4 act synergistically to activate PKC, representing an alternative pathway to those previously described.	bind
21967	2	7079	6	13	NULL	NULL	NULL	statement 1	Process		activate					PKC	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10624_s_34	9553124	2 Since syndecan-4 can bind PIP2 and activate PKC, we investigated whether PIP2 and syndecan-4 act synergistically to activate PKC, representing an alternative pathway to those previously described.	bind
25958	1	7079	7	NULL	NULL	0	NULL	syndecan-4	NULL		bind	NULL				 PIP2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_17_10624_s_34	9553124	2 Since syndecan-4 can bind PIP2 and activate PKC, we investigated whether PIP2 and syndecan-4 act synergistically to activate PKC, representing an alternative pathway to those previously described.	bind
25959	2	7079	7	NULL	NULL	0	NULL	statement 1	NULL		activate	NULL				PKC	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_17_10624_s_34	9553124	2 Since syndecan-4 can bind PIP2 and activate PKC, we investigated whether PIP2 and syndecan-4 act synergistically to activate PKC, representing an alternative pathway to those previously described.	bind
21968	1	7080	6	13	NULL	NULL	NULL	His6-sCD4	GP		bind					PDP-CB1	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_508_1_67_s_24	11707270	2 specifically displaced the binding of His6-sCD4 to PDPs CB1 and CB8, indicating that anti-CD4 PDPs recognize an epitope on the CD4 molecule closely related or similar to that identified for the 13B8.	bind
21969	2	7080	6	13	NULL	NULL	NULL	His6-sCD4	GP		bind					PDP-CB8	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_508_1_67_s_24	11707270	2 specifically displaced the binding of His6-sCD4 to PDPs CB1 and CB8, indicating that anti-CD4 PDPs recognize an epitope on the CD4 molecule closely related or similar to that identified for the 13B8.	bind
21970	3	7080	6	13	NULL	NULL	NULL	anti-CD4 PDP	GP		recognize					CD4 molecule epitope	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_508_1_67_s_24	11707270	2 specifically displaced the binding of His6-sCD4 to PDPs CB1 and CB8, indicating that anti-CD4 PDPs recognize an epitope on the CD4 molecule closely related or similar to that identified for the 13B8.	bind
25973	1	7080	7	NULL	NULL	0	NULL	His6-sCD4	NULL		bind	NULL				PDPs CB1 	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_508_1_67_s_24	11707270	2 specifically displaced the binding of His6-sCD4 to PDPs CB1 and CB8, indicating that anti-CD4 PDPs recognize an epitope on the CD4 molecule closely related or similar to that identified for the 13B8.	bind
25975	2	7080	7	NULL	NULL	0	NULL	His6-sCD4 	NULL		bind	NULL				PDPs CB8	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_508_1_67_s_24	11707270	2 specifically displaced the binding of His6-sCD4 to PDPs CB1 and CB8, indicating that anti-CD4 PDPs recognize an epitope on the CD4 molecule closely related or similar to that identified for the 13B8.	bind
25977	3	7080	7	NULL	NULL	0	NULL	anti-CD4 PDPs	NULL		recognize	NULL				CD4 molecule epitope	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_508_1_67_s_24	11707270	2 specifically displaced the binding of His6-sCD4 to PDPs CB1 and CB8, indicating that anti-CD4 PDPs recognize an epitope on the CD4 molecule closely related or similar to that identified for the 13B8.	bind
25978	4	7080	7	NULL	NULL	0	NULL	CD4 molecule epitope	NULL		is similar to	NULL				13B8	NULL	identified for			NULL		NULL	NULL	NULL	NULL	gw60_febslett_508_1_67_s_24	11707270	2 specifically displaced the binding of His6-sCD4 to PDPs CB1 and CB8, indicating that anti-CD4 PDPs recognize an epitope on the CD4 molecule closely related or similar to that identified for the 13B8.	bind
21971	1	7082	6	13	NULL	NULL	NULL	ProX	GP		bind		high affinity;;specificity			GB	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_46_48270_s_42	15308642	2 Substrate binding assays with radiolabeled glycine betaine and competition experiments with other compatible solutes revealed that ProX binds both GB and PB with high affinity and specificity at room temperature with an apparent  KD of 60 and 50 nM, respectively.	bind
21972	2	7082	6	13	NULL	NULL	NULL	ProX	GP		bind		high affinity;; specificity			PB	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_46_48270_s_42	15308642	2 Substrate binding assays with radiolabeled glycine betaine and competition experiments with other compatible solutes revealed that ProX binds both GB and PB with high affinity and specificity at room temperature with an apparent  KD of 60 and 50 nM, respectively.	bind
25987	1	7082	7	NULL	NULL	0	NULL	ProX	NULL		binds	NULL	high affinity;;specificity			GB	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_46_48270_s_42	15308642	2 Substrate binding assays with radiolabeled glycine betaine and competition experiments with other compatible solutes revealed that ProX binds both GB and PB with high affinity and specificity at room temperature with an apparent  KD of 60 and 50 nM, respectively.	bind
25988	2	7082	7	NULL	NULL	0	NULL	Prox	NULL		binds	NULL	high affinity;;specificity			PB	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_46_48270_s_42	15308642	2 Substrate binding assays with radiolabeled glycine betaine and competition experiments with other compatible solutes revealed that ProX binds both GB and PB with high affinity and specificity at room temperature with an apparent  KD of 60 and 50 nM, respectively.	bind
21973	1	7083	6	13	NULL	NULL	NULL	Rad3 protein	GP		bind		directly			SSL2/Rad25	GP				NULL	yeast	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_43_33260_s_211	10924514	2 Such interactions have also been reported in the yeast in which Rad3 protein binds directly to both SSL2/Rad25 and SSL1 proteins ( 33).	bind
21974	2	7083	6	13	NULL	NULL	NULL	Rad3 protein	GP		bind		directly			SSL1 protein	GP				NULL	yeast	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_43_33260_s_211	10924514	2 Such interactions have also been reported in the yeast in which Rad3 protein binds directly to both SSL2/Rad25 and SSL1 proteins ( 33).	bind
25990	1	7083	7	NULL	NULL	0	NULL	Rad3 protein	NULL		binds	NULL	directly			SSL2/Rad25	NULL				NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_275_43_33260_s_211	10924514	2 Such interactions have also been reported in the yeast in which Rad3 protein binds directly to both SSL2/Rad25 and SSL1 proteins ( 33).	bind
25992	2	7083	7	NULL	NULL	0	NULL	Rad3 protein	NULL		binds	NULL	directly			SSL1 proteins	NULL				NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_275_43_33260_s_211	10924514	2 Such interactions have also been reported in the yeast in which Rad3 protein binds directly to both SSL2/Rad25 and SSL1 proteins ( 33).	bind
22207	1	7084	6	13	NULL	NULL	NULL	SV-150	GP		is composed of								amino acids 150-186		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27182_s_169	9765238	2 SV-150, composed of amino acids 150-186, is an elongated version of the biologically inactive SV-163 peptide ( 32) that inhibits virus-mediated erythrocyte hemolysis at doses ~50% that of SV-473.2 SV-269 is a leucine zipper motif which specifically binds Sendai virions and inhibits virus-mediated hemolysis ( 43).	bind
22208	2	7084	6	13	NULL	NULL	NULL	SV150	GP		is an elongated version of					SV163 peptide	GP	biologically inactive			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27182_s_169	9765238	2 SV-150, composed of amino acids 150-186, is an elongated version of the biologically inactive SV-163 peptide ( 32) that inhibits virus-mediated erythrocyte hemolysis at doses ~50% that of SV-473.2 SV-269 is a leucine zipper motif which specifically binds Sendai virions and inhibits virus-mediated hemolysis ( 43).	bind
22209	3	7084	6	13	NULL	NULL	NULL	SV-163 peptide	GP		inhibits					erythrocyte hemolysis	MedicalFinding	virus mediated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27182_s_169	9765238	2 SV-150, composed of amino acids 150-186, is an elongated version of the biologically inactive SV-163 peptide ( 32) that inhibits virus-mediated erythrocyte hemolysis at doses ~50% that of SV-473.2 SV-269 is a leucine zipper motif which specifically binds Sendai virions and inhibits virus-mediated hemolysis ( 43).	bind
22210	4	7084	6	13	NULL	NULL	NULL	SV-269	GP		is a type of					leucine zipper motif	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27182_s_169	9765238	2 SV-150, composed of amino acids 150-186, is an elongated version of the biologically inactive SV-163 peptide ( 32) that inhibits virus-mediated erythrocyte hemolysis at doses ~50% that of SV-473.2 SV-269 is a leucine zipper motif which specifically binds Sendai virions and inhibits virus-mediated hemolysis ( 43).	bind
22211	5	7084	6	13	NULL	NULL	NULL	statement 4	GP		bind		specifically			Sendai virions	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27182_s_169	9765238	2 SV-150, composed of amino acids 150-186, is an elongated version of the biologically inactive SV-163 peptide ( 32) that inhibits virus-mediated erythrocyte hemolysis at doses ~50% that of SV-473.2 SV-269 is a leucine zipper motif which specifically binds Sendai virions and inhibits virus-mediated hemolysis ( 43).	bind
22212	6	7084	6	13	NULL	NULL	NULL	statement 4	Process		inhibits					hemolysis	MedicalFinding	virus mediated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27182_s_169	9765238	2 SV-150, composed of amino acids 150-186, is an elongated version of the biologically inactive SV-163 peptide ( 32) that inhibits virus-mediated erythrocyte hemolysis at doses ~50% that of SV-473.2 SV-269 is a leucine zipper motif which specifically binds Sendai virions and inhibits virus-mediated hemolysis ( 43).	bind
25994	1	7084	7	10	NULL	0	NULL	SV-150	NULL		is composed of	NULL					NULL		amino acids 150-186		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27182_s_169	9765238	2 SV-150, composed of amino acids 150-186, is an elongated version of the biologically inactive SV-163 peptide ( 32) that inhibits virus-mediated erythrocyte hemolysis at doses ~50% that of SV-473.2 SV-269 is a leucine zipper motif which specifically binds Sendai virions and inhibits virus-mediated hemolysis ( 43).	bind
25995	2	7084	7	NULL	NULL	0	NULL	SV-150	NULL		is an elongated version of	NULL				SV-163 peptide	NULL	biologically inactive			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27182_s_169	9765238	2 SV-150, composed of amino acids 150-186, is an elongated version of the biologically inactive SV-163 peptide ( 32) that inhibits virus-mediated erythrocyte hemolysis at doses ~50% that of SV-473.2 SV-269 is a leucine zipper motif which specifically binds Sendai virions and inhibits virus-mediated hemolysis ( 43).	bind
25996	3	7084	7	NULL	NULL	0	NULL	virus	NULL		mediates	NULL				erythrocyte hemolysis 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27182_s_169	9765238	2 SV-150, composed of amino acids 150-186, is an elongated version of the biologically inactive SV-163 peptide ( 32) that inhibits virus-mediated erythrocyte hemolysis at doses ~50% that of SV-473.2 SV-269 is a leucine zipper motif which specifically binds Sendai virions and inhibits virus-mediated hemolysis ( 43).	bind
25997	4	7084	7	NULL	NULL	0	NULL	SV-150	NULL		inhibits	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27182_s_169	9765238	2 SV-150, composed of amino acids 150-186, is an elongated version of the biologically inactive SV-163 peptide ( 32) that inhibits virus-mediated erythrocyte hemolysis at doses ~50% that of SV-473.2 SV-269 is a leucine zipper motif which specifically binds Sendai virions and inhibits virus-mediated hemolysis ( 43).	bind
25998	5	7084	7	NULL	NULL	0	NULL	SV-473	NULL		inhibits	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27182_s_169	9765238	2 SV-150, composed of amino acids 150-186, is an elongated version of the biologically inactive SV-163 peptide ( 32) that inhibits virus-mediated erythrocyte hemolysis at doses ~50% that of SV-473.2 SV-269 is a leucine zipper motif which specifically binds Sendai virions and inhibits virus-mediated hemolysis ( 43).	bind
25999	6	7084	7	NULL	NULL	0	NULL	statement 4	NULL	efficiency of	is greater than	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27182_s_169	9765238	2 SV-150, composed of amino acids 150-186, is an elongated version of the biologically inactive SV-163 peptide ( 32) that inhibits virus-mediated erythrocyte hemolysis at doses ~50% that of SV-473.2 SV-269 is a leucine zipper motif which specifically binds Sendai virions and inhibits virus-mediated hemolysis ( 43).	bind
26000	7	7084	7	10	NULL	0	NULL	SV-269	NULL		is a type of	NULL				leucine zipper motif	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27182_s_169	9765238	2 SV-150, composed of amino acids 150-186, is an elongated version of the biologically inactive SV-163 peptide ( 32) that inhibits virus-mediated erythrocyte hemolysis at doses ~50% that of SV-473.2 SV-269 is a leucine zipper motif which specifically binds Sendai virions and inhibits virus-mediated hemolysis ( 43).	bind
26001	8	7084	7	10	NULL	0	NULL	statement 7	NULL		binds	NULL	specifically			Sendai virions	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27182_s_169	9765238	2 SV-150, composed of amino acids 150-186, is an elongated version of the biologically inactive SV-163 peptide ( 32) that inhibits virus-mediated erythrocyte hemolysis at doses ~50% that of SV-473.2 SV-269 is a leucine zipper motif which specifically binds Sendai virions and inhibits virus-mediated hemolysis ( 43).	bind
26002	9	7084	7	NULL	NULL	0	NULL	virus	NULL		mediates	NULL				hemolysis	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27182_s_169	9765238	2 SV-150, composed of amino acids 150-186, is an elongated version of the biologically inactive SV-163 peptide ( 32) that inhibits virus-mediated erythrocyte hemolysis at doses ~50% that of SV-473.2 SV-269 is a leucine zipper motif which specifically binds Sendai virions and inhibits virus-mediated hemolysis ( 43).	bind
26003	10	7084	7	NULL	NULL	0	NULL	statement 8	NULL		inhibits	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27182_s_169	9765238	2 SV-150, composed of amino acids 150-186, is an elongated version of the biologically inactive SV-163 peptide ( 32) that inhibits virus-mediated erythrocyte hemolysis at doses ~50% that of SV-473.2 SV-269 is a leucine zipper motif which specifically binds Sendai virions and inhibits virus-mediated hemolysis ( 43).	bind
21975	1	7086	6	13	NULL	NULL	NULL	A6c134 TCR	GP		bind					HLA A2 antigen	Chemical		LLF-GYPVYV		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_3_1882_s_245	15531581	2 The A6c134 TCR binds to HLA A2-LLF-GYPVYV antigen with a half-life of 3900s and can stain cells pulsed with as little as 10 - 8M antigen.	bind
26009	1	7086	7	10	NULL	0	NULL	A6c134 TCR	NULL		binds to	NULL				HLA A2 antigen	NULL		LLF-GYPVYV		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_3_1882_s_245	15531581	2 The A6c134 TCR binds to HLA A2-LLF-GYPVYV antigen with a half-life of 3900s and can stain cells pulsed with as little as 10 - 8M antigen.	bind
21976	1	7093	6	13	NULL	NULL	NULL	Prs a 1	GP		form		may	chitin binding motif		IgE epitope	GP	cross-reactive			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_43_28091_s_217	9774427	2 The amino acid sequence similarity between the major latex allergen hevein and the N-terminal portion of Prs a 1 suggests that the chitin-binding motif of Prs a 1 may form an important cross-reactive IgE epitope.	bind
21977	2	7093	6	13	NULL	NULL	NULL	hevein	GP	amino acid sequence of	is similar to					Prs a 1 	GP		N-terminal portion		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_43_28091_s_217	9774427	2 The amino acid sequence similarity between the major latex allergen hevein and the N-terminal portion of Prs a 1 suggests that the chitin-binding motif of Prs a 1 may form an important cross-reactive IgE epitope.	bind
46439	3	7093	6	10	NULL	0	NULL	hevein	NULL		is a type of	NULL				latex allergen	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_43_28091_s_217	9774427	2 The amino acid sequence similarity between the major latex allergen hevein and the N-terminal portion of Prs a 1 suggests that the chitin-binding motif of Prs a 1 may form an important cross-reactive IgE epitope.	bind
26011	1	7093	7	NULL	NULL	0	NULL	Prs a 1	NULL		forms	NULL		chitin-binding motif 		IgE epitope	NULL	cross-reactive 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_43_28091_s_217	9774427	2 The amino acid sequence similarity between the major latex allergen hevein and the N-terminal portion of Prs a 1 suggests that the chitin-binding motif of Prs a 1 may form an important cross-reactive IgE epitope.	bind
21978	1	7094	6	13	NULL	NULL	NULL	gp59	GP		bind					statement 6	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_49839_s_27	14500719	2 The binding of gp59 to gp32 coated DNA facilitates the loading of a hexameric helicase with the lagging DNA strand passing through the center of a complex of the helicase and gp59 ( ).	bind
22213	2	7094	6	13	NULL	NULL	NULL	hexameric helicase	GP		forms a complex with					gp59	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_49839_s_27	14500719	2 The binding of gp59 to gp32 coated DNA facilitates the loading of a hexameric helicase with the lagging DNA strand passing through the center of a complex of the helicase and gp59 ( ).	bind
22214	3	7094	6	13	NULL	NULL	NULL	lagging DNA strand	NucleicAcid		passes through					statement 2	Process	center of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_49839_s_27	14500719	2 The binding of gp59 to gp32 coated DNA facilitates the loading of a hexameric helicase with the lagging DNA strand passing through the center of a complex of the helicase and gp59 ( ).	bind
22215	4	7094	6	13	NULL	NULL	NULL	statement 1	Process		facilitates					hexameric helicase	GP	loading of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_49839_s_27	14500719	2 The binding of gp59 to gp32 coated DNA facilitates the loading of a hexameric helicase with the lagging DNA strand passing through the center of a complex of the helicase and gp59 ( ).	bind
22216	5	7094	6	13	NULL	NULL	NULL	statement 1	Process		facilitates					statement 3	Process	loading of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_49839_s_27	14500719	2 The binding of gp59 to gp32 coated DNA facilitates the loading of a hexameric helicase with the lagging DNA strand passing through the center of a complex of the helicase and gp59 ( ).	bind
46440	6	7094	6	13	NULL	NULL	NULL	DNA	NucleicAcid		is coated with					gp32	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_49839_s_27	14500719	2 The binding of gp59 to gp32 coated DNA facilitates the loading of a hexameric helicase with the lagging DNA strand passing through the center of a complex of the helicase and gp59 ( ).	bind
26012	1	7094	7	10	NULL	0	NULL	gp59	NULL		binds	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_49839_s_27	14500719	2 The binding of gp59 to gp32 coated DNA facilitates the loading of a hexameric helicase with the lagging DNA strand passing through the center of a complex of the helicase and gp59 ( ).	bind
26013	2	7094	7	NULL	NULL	0	NULL	statement 1	NULL		facilitate	NULL				hexameric helicase	NULL	loading of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_49839_s_27	14500719	2 The binding of gp59 to gp32 coated DNA facilitates the loading of a hexameric helicase with the lagging DNA strand passing through the center of a complex of the helicase and gp59 ( ).	bind
26014	4	7094	7	NULL	NULL	0	NULL	lagging DNA strand	NULL		pass through 	NULL				statement 3	NULL	the center of the complex of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_49839_s_27	14500719	2 The binding of gp59 to gp32 coated DNA facilitates the loading of a hexameric helicase with the lagging DNA strand passing through the center of a complex of the helicase and gp59 ( ).	bind
26015	3	7094	7	NULL	NULL	0	NULL	gp59	NULL		complex with	NULL				helicase	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_49839_s_27	14500719	2 The binding of gp59 to gp32 coated DNA facilitates the loading of a hexameric helicase with the lagging DNA strand passing through the center of a complex of the helicase and gp59 ( ).	bind
46441	5	7094	7	10	NULL	0	NULL	DNA	NULL		is coated with	NULL				gp32	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_49839_s_27	14500719	2 The binding of gp59 to gp32 coated DNA facilitates the loading of a hexameric helicase with the lagging DNA strand passing through the center of a complex of the helicase and gp59 ( ).	bind
22059	1	7095	6	13	NULL	NULL	NULL	polyubiquitin	GP		bind					p97 complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_37_34774_s_274	12813030	2 The binding of polyubiquitin to the p97 complex is also  consistent with it being the immediate downstream component.	bind
26016	1	7095	7	NULL	NULL	0	NULL	polyubiquitin	NULL		binds	NULL				p97 complex	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_34774_s_274	12813030	2 The binding of polyubiquitin to the p97 complex is also  consistent with it being the immediate downstream component.	bind
22062	1	7096	6	13	NULL	NULL	NULL				bind			rC domain		fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_7473_s_226	9054449	2 The binding of rC domain to fibronectin and potentially to heparan sulfate proteoglycans reveals additional extracellular or pericellular matrix components that may serve as anchors to sequester gelatinase A in tissues and to the cell surface.	bind
22064	2	7096	6	13	NULL	NULL	NULL				bind		potentially	rC domain		heparan sulfate proteoglycans	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_7473_s_226	9054449	2 The binding of rC domain to fibronectin and potentially to heparan sulfate proteoglycans reveals additional extracellular or pericellular matrix components that may serve as anchors to sequester gelatinase A in tissues and to the cell surface.	bind
22217	3	7096	6	13	NULL	NULL	NULL	gelatinase A	GP		sequestered in					tissues	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_7473_s_226	9054449	2 The binding of rC domain to fibronectin and potentially to heparan sulfate proteoglycans reveals additional extracellular or pericellular matrix components that may serve as anchors to sequester gelatinase A in tissues and to the cell surface.	bind
22218	4	7096	6	13	NULL	NULL	NULL	gelatinase A	GP		sequestered to					cell surface	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_7473_s_226	9054449	2 The binding of rC domain to fibronectin and potentially to heparan sulfate proteoglycans reveals additional extracellular or pericellular matrix components that may serve as anchors to sequester gelatinase A in tissues and to the cell surface.	bind
22219	5	7096	6	13	NULL	NULL	NULL	extracellular matrix components	CellComponent		serve as anchors for		may			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_7473_s_226	9054449	2 The binding of rC domain to fibronectin and potentially to heparan sulfate proteoglycans reveals additional extracellular or pericellular matrix components that may serve as anchors to sequester gelatinase A in tissues and to the cell surface.	bind
22220	6	7096	6	NULL	NULL	0	NULL	pericellular matrix components	NULL		serve as anchors for	NULL	may			statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_11_7473_s_226	9054449	2 The binding of rC domain to fibronectin and potentially to heparan sulfate proteoglycans reveals additional extracellular or pericellular matrix components that may serve as anchors to sequester gelatinase A in tissues and to the cell surface.	bind
22221	7	7096	6	NULL	NULL	0	NULL	extracellular matrix components	NULL		serve as anchors for	NULL	may			statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_11_7473_s_226	9054449	2 The binding of rC domain to fibronectin and potentially to heparan sulfate proteoglycans reveals additional extracellular or pericellular matrix components that may serve as anchors to sequester gelatinase A in tissues and to the cell surface.	bind
22222	8	7096	6	NULL	NULL	0	NULL	pericellular matrix components	NULL		serve as anchors for	NULL	may			statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_11_7473_s_226	9054449	2 The binding of rC domain to fibronectin and potentially to heparan sulfate proteoglycans reveals additional extracellular or pericellular matrix components that may serve as anchors to sequester gelatinase A in tissues and to the cell surface.	bind
26017	1	7096	7	NULL	NULL	0	NULL		NULL		binds	NULL		rC domain		fibronectin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_11_7473_s_226	9054449	2 The binding of rC domain to fibronectin and potentially to heparan sulfate proteoglycans reveals additional extracellular or pericellular matrix components that may serve as anchors to sequester gelatinase A in tissues and to the cell surface.	bind
26018	2	7096	7	NULL	NULL	0	NULL		NULL		bind	NULL	potentially	rC domain		heparan sulfate proteoglycans 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_11_7473_s_226	9054449	2 The binding of rC domain to fibronectin and potentially to heparan sulfate proteoglycans reveals additional extracellular or pericellular matrix components that may serve as anchors to sequester gelatinase A in tissues and to the cell surface.	bind
26019	3	7096	7	NULL	NULL	0	NULL	gelatinase A 			sequestered in					tissues					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_7473_s_226	9054449	2 The binding of rC domain to fibronectin and potentially to heparan sulfate proteoglycans reveals additional extracellular or pericellular matrix components that may serve as anchors to sequester gelatinase A in tissues and to the cell surface.	bind
26020	4	7096	7	NULL	NULL	0	NULL	gelatinase A			sequestered in					cell surface					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_7473_s_226	9054449	2 The binding of rC domain to fibronectin and potentially to heparan sulfate proteoglycans reveals additional extracellular or pericellular matrix components that may serve as anchors to sequester gelatinase A in tissues and to the cell surface.	bind
26021	5	7096	7	NULL	NULL	0	NULL	extracellular matrix components			serve as anchor to		may			statement 3					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_7473_s_226	9054449	2 The binding of rC domain to fibronectin and potentially to heparan sulfate proteoglycans reveals additional extracellular or pericellular matrix components that may serve as anchors to sequester gelatinase A in tissues and to the cell surface.	bind
26022	6	7096	7	NULL	NULL	0	NULL	extracellular matrix components			serve as anchor to		may			statement 4					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_7473_s_226	9054449	2 The binding of rC domain to fibronectin and potentially to heparan sulfate proteoglycans reveals additional extracellular or pericellular matrix components that may serve as anchors to sequester gelatinase A in tissues and to the cell surface.	bind
26023	7	7096	7	NULL	NULL	0	NULL	pericellular matrix components			serve as anchor to		may			statement 3					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_7473_s_226	9054449	2 The binding of rC domain to fibronectin and potentially to heparan sulfate proteoglycans reveals additional extracellular or pericellular matrix components that may serve as anchors to sequester gelatinase A in tissues and to the cell surface.	bind
26024	8	7096	7	10	NULL	0	NULL	pericellular matrix components			serve as anchor to		may			statement 4					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_7473_s_226	9054449	2 The binding of rC domain to fibronectin and potentially to heparan sulfate proteoglycans reveals additional extracellular or pericellular matrix components that may serve as anchors to sequester gelatinase A in tissues and to the cell surface.	bind
22065	1	7097	6	13	NULL	NULL	NULL	Wnt ligands	GP		bind					cell-surface receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_3_1381_s_12	16293629	2 The binding of Wnt ligands to cell-surface receptors leads to the activation of the intracellular protein Dishevelled.	bind
22066	2	7097	6	13	NULL	NULL	NULL	statement 1	Process		leads to					Dishevelled	GP	activation of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_3_1381_s_12	16293629	2 The binding of Wnt ligands to cell-surface receptors leads to the activation of the intracellular protein Dishevelled.	bind
46442	3	7097	6	13	NULL	NULL	NULL	Dishevelled	GP		is a type of					intracellular protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_3_1381_s_12	16293629	2 The binding of Wnt ligands to cell-surface receptors leads to the activation of the intracellular protein Dishevelled.	bind
26025	1	7097	7	NULL	NULL	0	NULL	Wnt ligands	NULL		binds	NULL				cell-surface receptors	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1381_s_12	16293629	2 The binding of Wnt ligands to cell-surface receptors leads to the activation of the intracellular protein Dishevelled.	bind
26026	2	7097	7	10	NULL	0	NULL	statement 1	NULL		leads to	NULL				Dishevelled	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_3_1381_s_12	16293629	2 The binding of Wnt ligands to cell-surface receptors leads to the activation of the intracellular protein Dishevelled.	bind
46443	3	7097	7	10	NULL	0	NULL	Dishevelled	NULL		is a type of	NULL				intracellular protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1381_s_12	16293629	2 The binding of Wnt ligands to cell-surface receptors leads to the activation of the intracellular protein Dishevelled.	bind
22067	1	7098	6	13	NULL	NULL	NULL				bind				CArG box element	SRF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1511_s_260	9430690	2 The CArG box element is known to bind to SRF or related factors; however, the precise role of SRF transcription factors in smooth muscle-specific gene expression remains to be explored.	bind
22069	2	7098	6	13	NULL	NULL	NULL	SRF	GP		plays a role in		may			smooth muscle-specific gene 	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1511_s_260	9430690	2 The CArG box element is known to bind to SRF or related factors; however, the precise role of SRF transcription factors in smooth muscle-specific gene expression remains to be explored.	bind
27030	3	7098	6	13	NULL	NULL	NULL	SRF	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1511_s_260	9430690	2 The CArG box element is known to bind to SRF or related factors; however, the precise role of SRF transcription factors in smooth muscle-specific gene expression remains to be explored.	bind
26027	1	7098	7	NULL	NULL	0	NULL		NULL		binds to	NULL			CArG box element	SRF	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1511_s_260	9430690	2 The CArG box element is known to bind to SRF or related factors; however, the precise role of SRF transcription factors in smooth muscle-specific gene expression remains to be explored.	bind
26028	2	7098	7	NULL	NULL	0	NULL	SRF	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1511_s_260	9430690	2 The CArG box element is known to bind to SRF or related factors; however, the precise role of SRF transcription factors in smooth muscle-specific gene expression remains to be explored.	bind
28506	3	7098	7	10	NULL	0	NULL	SRF	NULL		plays a role in	NULL	may			smooth muscle-specific gene 	NULL	expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1511_s_260	9430690	2 The CArG box element is known to bind to SRF or related factors; however, the precise role of SRF transcription factors in smooth muscle-specific gene expression remains to be explored.	bind
22070	1	7100	6	13	NULL	NULL	NULL	NapC	GP		bind					hemes	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_44_28785_s_145	9786877	2 The combined approach of UV-visible, EPR, MCD, and redox potentiometry provides unambiguous evidence that NapC binds four hemes, all of which are low spin and  bis-His-ligated in the ferric state.	bind
26033	1	7100	7	NULL	NULL	0	NULL	NapC	NULL		binds	NULL				heme	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_44_28785_s_145	9786877	2 The combined approach of UV-visible, EPR, MCD, and redox potentiometry provides unambiguous evidence that NapC binds four hemes, all of which are low spin and  bis-His-ligated in the ferric state.	bind
22073	1	7101	6	13	NULL	NULL	NULL	insulin	GP		bind				CRE	winged helix-like proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_29_18499_s_247	9660819	2 The cross-competition between the insulin CRE and G3B indicates that the winged helix-like proteins binding to the insulin CRE are the same as those binding to domain B of the G3 enhancer element of the glucagon gene.	bind
22074	2	7101	6	13	NULL	NULL	NULL	glucagon gene	GP		bind				domain B of G3 enhancer	winged helix-like proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_29_18499_s_247	9660819	2 The cross-competition between the insulin CRE and G3B indicates that the winged helix-like proteins binding to the insulin CRE are the same as those binding to domain B of the G3 enhancer element of the glucagon gene.	bind
27031	3	7101	6	13	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_29_18499_s_247	9660819	2 The cross-competition between the insulin CRE and G3B indicates that the winged helix-like proteins binding to the insulin CRE are the same as those binding to domain B of the G3 enhancer element of the glucagon gene.	bind
26035	1	7101	7	NULL	NULL	0	NULL	winged helix-like proteins	NULL		bind	NULL				insulin	NULL			CRE	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_29_18499_s_247	9660819	2 The cross-competition between the insulin CRE and G3B indicates that the winged helix-like proteins binding to the insulin CRE are the same as those binding to domain B of the G3 enhancer element of the glucagon gene.	bind
26036	2	7101	7	NULL	NULL	0	NULL	winged helix-like proteins	NULL		bind	NULL				glucagon gene	NULL			domain B of G3 enhancer	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_29_18499_s_247	9660819	2 The cross-competition between the insulin CRE and G3B indicates that the winged helix-like proteins binding to the insulin CRE are the same as those binding to domain B of the G3 enhancer element of the glucagon gene.	bind
26037	3	7101	7	10	NULL	0	NULL	statement 1	NULL		competes with	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_29_18499_s_247	9660819	2 The cross-competition between the insulin CRE and G3B indicates that the winged helix-like proteins binding to the insulin CRE are the same as those binding to domain B of the G3 enhancer element of the glucagon gene.	bind
22075	1	7103	6	13	NULL	NULL	NULL	Rgt1	GP		does not bind					HXT1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_12_10322_s_110	12527758	2 The data obtained with the ChIP assay indicate that Rgt1 does not bind to the  HXT1 promoter in response to glucose and that it activates  HXT1 gene expression probably by an indirect mechanism.	bind
22076	2	7103	6	13	NULL	NULL	NULL	statement 1	Process		occurs in response to					glucose	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_12_10322_s_110	12527758	2 The data obtained with the ChIP assay indicate that Rgt1 does not bind to the  HXT1 promoter in response to glucose and that it activates  HXT1 gene expression probably by an indirect mechanism.	bind
22077	3	7103	6	13	NULL	NULL	NULL	Rgt1	GP		activates					HXT1	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_12_10322_s_110	12527758	2 The data obtained with the ChIP assay indicate that Rgt1 does not bind to the  HXT1 promoter in response to glucose and that it activates  HXT1 gene expression probably by an indirect mechanism.	bind
26038	1	7103	7	NULL	NULL	0	NULL	Rgt1	NULL		does not bind	NULL				HXT1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10322_s_110	12527758	2 The data obtained with the ChIP assay indicate that Rgt1 does not bind to the  HXT1 promoter in response to glucose and that it activates  HXT1 gene expression probably by an indirect mechanism.	bind
26039	2	7103	7	NULL	NULL	0	NULL	statement 1	NULL		in response to	NULL				glucose	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10322_s_110	12527758	2 The data obtained with the ChIP assay indicate that Rgt1 does not bind to the  HXT1 promoter in response to glucose and that it activates  HXT1 gene expression probably by an indirect mechanism.	bind
26040	3	7103	7	NULL	NULL	0	NULL	Rgt1	NULL		activates	NULL				HXT1 gene	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10322_s_110	12527758	2 The data obtained with the ChIP assay indicate that Rgt1 does not bind to the  HXT1 promoter in response to glucose and that it activates  HXT1 gene expression probably by an indirect mechanism.	bind
22078	1	7104	6	13	NULL	NULL	NULL	IGFBP-7	GP		bind					IGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_48_30322_s_99	8939990	2 The failure to demonstrate IGFBP-7 binding of IGF by conventional Western ligand blotting methods may be attributable to the loss of structural integrity under denaturing conditions, since binding was observed when blotting was performed with non-denaturing gels.	bind
26041	1	7104	7	NULL	NULL	0	NULL	IGF	NULL		bind	NULL				IGFBP-7	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_48_30322_s_99	8939990	2 The failure to demonstrate IGFBP-7 binding of IGF by conventional Western ligand blotting methods may be attributable to the loss of structural integrity under denaturing conditions, since binding was observed when blotting was performed with non-denaturing gels.	bind
22079	1	7106	6	13	NULL	NULL	NULL	Cbl	GP	phosphorylated	bind			tyrosine		Hck	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_19_14615_s_150	10799548	2 The filter was reprobed with anti-phosphotyrosine antibodies in order to determine if tyrosine-phosphorylated Cbl binds the SH3 domain of Hck in preference to the SH2.	bind
27032	2	7106	6	13	NULL	NULL	NULL	Cbl	GP	phosphorylated	bind			tyrosine		Hck	GP		SH2 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_19_14615_s_150	10799548	2 The filter was reprobed with anti-phosphotyrosine antibodies in order to determine if tyrosine-phosphorylated Cbl binds the SH3 domain of Hck in preference to the SH2.	bind
46444	3	7106	6	13	NULL	NULL	NULL	statement 2	Process		is preferred over					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_19_14615_s_150	10799548	2 The filter was reprobed with anti-phosphotyrosine antibodies in order to determine if tyrosine-phosphorylated Cbl binds the SH3 domain of Hck in preference to the SH2.	bind
26049	1	7106	7	NULL	NULL	0	NULL	Cbl	NULL	phosphorylated	binds	NULL		tyrosine		Hck	NULL		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_19_14615_s_150	10799548	2 The filter was reprobed with anti-phosphotyrosine antibodies in order to determine if tyrosine-phosphorylated Cbl binds the SH3 domain of Hck in preference to the SH2.	bind
26051	2	7106	7	NULL	NULL	0	NULL	Cbl	NULL	phosphorylated	binds	NULL		tyrosine		Hck	NULL		SH2 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_19_14615_s_150	10799548	2 The filter was reprobed with anti-phosphotyrosine antibodies in order to determine if tyrosine-phosphorylated Cbl binds the SH3 domain of Hck in preference to the SH2.	bind
26054	3	7106	7	NULL	NULL	0	NULL	statement 2	NULL		is preferred than	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_19_14615_s_150	10799548	2 The filter was reprobed with anti-phosphotyrosine antibodies in order to determine if tyrosine-phosphorylated Cbl binds the SH3 domain of Hck in preference to the SH2.	bind
22080	1	7107	6	13	NULL	NULL	NULL	nuclear protein	GP	transport of	is regulated at 		differentially			NLS recognition step	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_42_26375_s_196	9334211	2 The findings herein suggest that nuclear protein transport is differentially regulated at the NLS recognition step through the expression level and/or the controls of NLS binding specificities of NLS receptors in various cells, which, in turn, may lead to the regulation of development or cell differentiation.	bind
22081	2	7107	6	13	NULL	NULL	NULL	NLS receptor	GP		bind					NLS	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_42_26375_s_196	9334211	2 The findings herein suggest that nuclear protein transport is differentially regulated at the NLS recognition step through the expression level and/or the controls of NLS binding specificities of NLS receptors in various cells, which, in turn, may lead to the regulation of development or cell differentiation.	bind
22082	3	7107	6	13	NULL	NULL	NULL	statement 1	Process		occurs by					statement 2	Process	control of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_42_26375_s_196	9334211	2 The findings herein suggest that nuclear protein transport is differentially regulated at the NLS recognition step through the expression level and/or the controls of NLS binding specificities of NLS receptors in various cells, which, in turn, may lead to the regulation of development or cell differentiation.	bind
22083	4	7107	6	13	NULL	NULL	NULL	statement 3	Process		lead to		may			development	Process	regulation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_42_26375_s_196	9334211	2 The findings herein suggest that nuclear protein transport is differentially regulated at the NLS recognition step through the expression level and/or the controls of NLS binding specificities of NLS receptors in various cells, which, in turn, may lead to the regulation of development or cell differentiation.	bind
22084	5	7107	6	13	NULL	NULL	NULL	statement 3	Process		lead to 		may			cell differentiation	Process	regulation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_42_26375_s_196	9334211	2 The findings herein suggest that nuclear protein transport is differentially regulated at the NLS recognition step through the expression level and/or the controls of NLS binding specificities of NLS receptors in various cells, which, in turn, may lead to the regulation of development or cell differentiation.	bind
26055	1	7107	7	NULL	NULL	0	NULL	nuclear protein 	NULL	transport of	regulated at	NULL	differentially			NLS recognition step	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_42_26375_s_196	9334211	2 The findings herein suggest that nuclear protein transport is differentially regulated at the NLS recognition step through the expression level and/or the controls of NLS binding specificities of NLS receptors in various cells, which, in turn, may lead to the regulation of development or cell differentiation.	bind
26057	3	7107	7	10	NULL	0	NULL	NLS	NULL		bind	NULL				NLS receptors	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_42_26375_s_196	9334211	2 The findings herein suggest that nuclear protein transport is differentially regulated at the NLS recognition step through the expression level and/or the controls of NLS binding specificities of NLS receptors in various cells, which, in turn, may lead to the regulation of development or cell differentiation.	bind
26058	4	7107	7	NULL	NULL	0	NULL	statement 1	NULL		occurs through	NULL				statement 3	NULL	control of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_42_26375_s_196	9334211	2 The findings herein suggest that nuclear protein transport is differentially regulated at the NLS recognition step through the expression level and/or the controls of NLS binding specificities of NLS receptors in various cells, which, in turn, may lead to the regulation of development or cell differentiation.	bind
26059	5	7107	7	NULL	NULL	0	NULL	statement 3	NULL		lead to	NULL	may			development	NULL	regulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_42_26375_s_196	9334211	2 The findings herein suggest that nuclear protein transport is differentially regulated at the NLS recognition step through the expression level and/or the controls of NLS binding specificities of NLS receptors in various cells, which, in turn, may lead to the regulation of development or cell differentiation.	bind
26060	6	7107	7	NULL	NULL	0	NULL	statement 3	NULL		lead to	NULL	may			cell differentiation	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_42_26375_s_196	9334211	2 The findings herein suggest that nuclear protein transport is differentially regulated at the NLS recognition step through the expression level and/or the controls of NLS binding specificities of NLS receptors in various cells, which, in turn, may lead to the regulation of development or cell differentiation.	bind
22085	1	7108	6	13	NULL	NULL	NULL	heme	Chemical		bind					CYP4A protein	GP		glutamic acid residue on the I-helix		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12755_s_23	11821421	2 The heme is bound to the CYP4A proteins via a conserved glutamic acid residue on the I-helix of the protein ( 16).	bind
26061	1	7108	7	NULL	NULL	0	NULL	 heme	NULL		binds	NULL				CYP4A proteins	NULL		glutamic acid residue on the I-helix of		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12755_s_23	11821421	2 The heme is bound to the CYP4A proteins via a conserved glutamic acid residue on the I-helix of the protein ( 16).	bind
22086	1	7109	6	13	NULL	NULL	NULL	pro-IAPP peptide	GP		bind			N-terminal		heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_20_16611_s_136	11145957	2 The heparin binding activity of the N-terminal pro-IAPP peptide therefore does not depend upon any conformational change induced by formation of the disulfide bond.	bind
22087	2	7109	6	13	NULL	NULL	NULL	disulfide bond	Process	formation of	induces					conformational change	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_20_16611_s_136	11145957	2 The heparin binding activity of the N-terminal pro-IAPP peptide therefore does not depend upon any conformational change induced by formation of the disulfide bond.	bind
22088	3	7109	6	13	NULL	NULL	NULL	statement 1	Process		does not depend upon					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_20_16611_s_136	11145957	2 The heparin binding activity of the N-terminal pro-IAPP peptide therefore does not depend upon any conformational change induced by formation of the disulfide bond.	bind
26063	1	7109	7	NULL	NULL	0	NULL	pro-IAPP peptide	NULL		binds	NULL		N-terminal		heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_20_16611_s_136	11145957	2 The heparin binding activity of the N-terminal pro-IAPP peptide therefore does not depend upon any conformational change induced by formation of the disulfide bond.	bind
26064	2	7109	7	NULL	NULL	0	NULL	disulfide bond	NULL	 formation of	induce	NULL				conformational change	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_20_16611_s_136	11145957	2 The heparin binding activity of the N-terminal pro-IAPP peptide therefore does not depend upon any conformational change induced by formation of the disulfide bond.	bind
26065	3	7109	7	NULL	NULL	0	NULL	statement 1	NULL		does not depend on	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_20_16611_s_136	11145957	2 The heparin binding activity of the N-terminal pro-IAPP peptide therefore does not depend upon any conformational change induced by formation of the disulfide bond.	bind
22089	1	7110	6	13	NULL	NULL	NULL	TGF-beta1	GP	125I	bind					TGF-beta receptors	GP				NULL	mink lung epithelial cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_33_20572_s_35	9252371	2 The IC50 values of TGF-beta1 and TGF-beta3 peptide antagonists for inhibiting 125I-TGF-beta1 (0.1 nM) binding to TGF-beta receptors in mink lung epithelial cells are ~1-2 and ~20-30 muM, respectively.	bind
22090	2	7110	6	13	NULL	NULL	NULL	TGF-beta1 peptide antagonist	Chemical		inhibit					statement 1	Process				NULL	mink lung epithelial cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_33_20572_s_35	9252371	2 The IC50 values of TGF-beta1 and TGF-beta3 peptide antagonists for inhibiting 125I-TGF-beta1 (0.1 nM) binding to TGF-beta receptors in mink lung epithelial cells are ~1-2 and ~20-30 muM, respectively.	bind
22091	3	7110	6	13	NULL	NULL	NULL	TGF-beta3 peptide antagonist	Chemical		inhibit					statement 1	Process				NULL	mink lung epithelial cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_33_20572_s_35	9252371	2 The IC50 values of TGF-beta1 and TGF-beta3 peptide antagonists for inhibiting 125I-TGF-beta1 (0.1 nM) binding to TGF-beta receptors in mink lung epithelial cells are ~1-2 and ~20-30 muM, respectively.	bind
26066	1	7110	7	NULL	NULL	0	NULL	TGF-beta1 	NULL	125I	bind	NULL				TGF-beta receptors	NULL				NULL	mink lung epithelial cells	0	NULL	NULL	NULL	gw60_jbiolchem_272_33_20572_s_35	9252371	2 The IC50 values of TGF-beta1 and TGF-beta3 peptide antagonists for inhibiting 125I-TGF-beta1 (0.1 nM) binding to TGF-beta receptors in mink lung epithelial cells are ~1-2 and ~20-30 muM, respectively.	bind
26067	2	7110	7	10	NULL	0	NULL	TGF-beta1 peptide antagonist	NULL		inhibits	NULL				statement 1	NULL				NULL	mink lung epithelial cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_33_20572_s_35	9252371	2 The IC50 values of TGF-beta1 and TGF-beta3 peptide antagonists for inhibiting 125I-TGF-beta1 (0.1 nM) binding to TGF-beta receptors in mink lung epithelial cells are ~1-2 and ~20-30 muM, respectively.	bind
26068	3	7110	7	10	NULL	0	NULL	TGF-beta3 peptide antagonist	NULL		inhibits	NULL				statement 1	NULL				NULL	mink lung epithelial cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_33_20572_s_35	9252371	2 The IC50 values of TGF-beta1 and TGF-beta3 peptide antagonists for inhibiting 125I-TGF-beta1 (0.1 nM) binding to TGF-beta receptors in mink lung epithelial cells are ~1-2 and ~20-30 muM, respectively.	bind
22092	1	7111	6	13	NULL	NULL	NULL	hypertonicity			increases					TonEBP	GP	activity of 			NULL	HeLa cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_20615_s_208	9685419	2 The increase in TonEBP activity in HeLa cells in response to hypertonicity (Fig.  4) predicts that there should be a parallel increase in binding of TonEBP to the SMIT TonEs.	bind
22093	2	7111	6	13	NULL	NULL	NULL	TonEBP	GP		bind					SMIT TonE	GP				NULL	HeLa cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_20615_s_208	9685419	2 The increase in TonEBP activity in HeLa cells in response to hypertonicity (Fig.  4) predicts that there should be a parallel increase in binding of TonEBP to the SMIT TonEs.	bind
22094	3	7111	6	13	NULL	NULL	NULL	statement 1	Process		increases		may;;partially			statement 2	Process				NULL	HeLa cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_20615_s_208	9685419	2 The increase in TonEBP activity in HeLa cells in response to hypertonicity (Fig.  4) predicts that there should be a parallel increase in binding of TonEBP to the SMIT TonEs.	bind
26069	1	7111	7	10	NULL	0	NULL	TonEBP	NULL		binds	NULL				SMIT TonEs	NULL				NULL	HeLa cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_20615_s_208	9685419	2 The increase in TonEBP activity in HeLa cells in response to hypertonicity (Fig.  4) predicts that there should be a parallel increase in binding of TonEBP to the SMIT TonEs.	bind
26070	2	7111	7	NULL	NULL	0	NULL	hypertonicity 	NULL		increase	NULL				TonEBP	NULL	activity of			NULL	HeLa cells	0	NULL	NULL	NULL	gw60_jbiolchem_273_32_20615_s_208	9685419	2 The increase in TonEBP activity in HeLa cells in response to hypertonicity (Fig.  4) predicts that there should be a parallel increase in binding of TonEBP to the SMIT TonEs.	bind
26071	3	7111	7	10	NULL	0	NULL	statement 1	NULL		increases	NULL	may;;partially			statement 1	NULL				NULL	HeLa cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_20615_s_208	9685419	2 The increase in TonEBP activity in HeLa cells in response to hypertonicity (Fig.  4) predicts that there should be a parallel increase in binding of TonEBP to the SMIT TonEs.	bind
22095	1	7112	6	13	NULL	NULL	NULL	apoACP	GP		bind			S36T		AcpS	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_959_s_250	10625633	2 The introduction of the gamma-CH3 in S36T apoACP blocked the conversion of this protein to the holo form, but the binding of S36T apoACP by AcpS may induce an allosteric change in the homodimeric enzyme that relieves substrate inhibition by apoACP.	bind
22096	2	7112	6	13	NULL	NULL	NULL	statement 1	Process		induce		may			homodimeric enzyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_959_s_250	10625633	2 The introduction of the gamma-CH3 in S36T apoACP blocked the conversion of this protein to the holo form, but the binding of S36T apoACP by AcpS may induce an allosteric change in the homodimeric enzyme that relieves substrate inhibition by apoACP.	bind
22225	3	7112	6	13	NULL	NULL	NULL				introduced to			gamma-CH3		apoACP	GP		S36T		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_959_s_250	10625633	2 The introduction of the gamma-CH3 in S36T apoACP blocked the conversion of this protein to the holo form, but the binding of S36T apoACP by AcpS may induce an allosteric change in the homodimeric enzyme that relieves substrate inhibition by apoACP.	bind
22226	4	7112	6	13	NULL	NULL	NULL	apoACP	GP		converted to					holo form	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_959_s_250	10625633	2 The introduction of the gamma-CH3 in S36T apoACP blocked the conversion of this protein to the holo form, but the binding of S36T apoACP by AcpS may induce an allosteric change in the homodimeric enzyme that relieves substrate inhibition by apoACP.	bind
22227	5	7112	6	13	NULL	NULL	NULL	statement 3	Process		blocks 					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_959_s_250	10625633	2 The introduction of the gamma-CH3 in S36T apoACP blocked the conversion of this protein to the holo form, but the binding of S36T apoACP by AcpS may induce an allosteric change in the homodimeric enzyme that relieves substrate inhibition by apoACP.	bind
22228	6	7112	6	13	NULL	NULL	NULL	statement 2	Process		relieves					apoACP	GP	substrate inhibition by			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_959_s_250	10625633	2 The introduction of the gamma-CH3 in S36T apoACP blocked the conversion of this protein to the holo form, but the binding of S36T apoACP by AcpS may induce an allosteric change in the homodimeric enzyme that relieves substrate inhibition by apoACP.	bind
27033	7	7112	6	13	NULL	NULL	NULL	apoACP	GP		inhibits					homodimeric enzyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_959_s_250	10625633	2 The introduction of the gamma-CH3 in S36T apoACP blocked the conversion of this protein to the holo form, but the binding of S36T apoACP by AcpS may induce an allosteric change in the homodimeric enzyme that relieves substrate inhibition by apoACP.	bind
27034	8	7112	6	13	NULL	NULL	NULL	statement 4	Process		relieves					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_959_s_250	10625633	2 The introduction of the gamma-CH3 in S36T apoACP blocked the conversion of this protein to the holo form, but the binding of S36T apoACP by AcpS may induce an allosteric change in the homodimeric enzyme that relieves substrate inhibition by apoACP.	bind
26072	1	7112	7	10	NULL	0	NULL		NULL		added to	NULL		gamma-CH3		apoACP	NULL		S36T		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_959_s_250	10625633	2 The introduction of the gamma-CH3 in S36T apoACP blocked the conversion of this protein to the holo form, but the binding of S36T apoACP by AcpS may induce an allosteric change in the homodimeric enzyme that relieves substrate inhibition by apoACP.	bind
26073	2	7112	7	10	NULL	0	NULL	statement 1	NULL		blocks	NULL				statement 7	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_959_s_250	10625633	2 The introduction of the gamma-CH3 in S36T apoACP blocked the conversion of this protein to the holo form, but the binding of S36T apoACP by AcpS may induce an allosteric change in the homodimeric enzyme that relieves substrate inhibition by apoACP.	bind
26074	3	7112	7	10	NULL	0	NULL	AcpS	NULL		bind	NULL				apoACP	NULL		S36T		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_959_s_250	10625633	2 The introduction of the gamma-CH3 in S36T apoACP blocked the conversion of this protein to the holo form, but the binding of S36T apoACP by AcpS may induce an allosteric change in the homodimeric enzyme that relieves substrate inhibition by apoACP.	bind
26075	4	7112	7	NULL	NULL	0	NULL	statement 3	NULL		induce	NULL				homodimeric enzyme	NULL	allosteric change in			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_2_959_s_250	10625633	2 The introduction of the gamma-CH3 in S36T apoACP blocked the conversion of this protein to the holo form, but the binding of S36T apoACP by AcpS may induce an allosteric change in the homodimeric enzyme that relieves substrate inhibition by apoACP.	bind
26076	5	7112	7	NULL	NULL	0	NULL	apoACP	NULL		inhibits	NULL				homodimeric enzyme	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_959_s_250	10625633	2 The introduction of the gamma-CH3 in S36T apoACP blocked the conversion of this protein to the holo form, but the binding of S36T apoACP by AcpS may induce an allosteric change in the homodimeric enzyme that relieves substrate inhibition by apoACP.	bind
28513	6	7112	7	NULL	NULL	0	NULL	statement 4	NULL		relieves	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_2_959_s_250	10625633	2 The introduction of the gamma-CH3 in S36T apoACP blocked the conversion of this protein to the holo form, but the binding of S36T apoACP by AcpS may induce an allosteric change in the homodimeric enzyme that relieves substrate inhibition by apoACP.	bind
46445	7	7112	7	10	NULL	0	NULL	apoACP	NULL		is converted to	NULL				holo form	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_2_959_s_250	10625633	2 The introduction of the gamma-CH3 in S36T apoACP blocked the conversion of this protein to the holo form, but the binding of S36T apoACP by AcpS may induce an allosteric change in the homodimeric enzyme that relieves substrate inhibition by apoACP.	bind
22097	1	7113	6	13	NULL	NULL	NULL	H3	GP		is methylated in			Lys 9		G9a / ES cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_17_14996_s_107	12586828	2 The level of H3 Lys-9 methylation of the PWS-IC in  G9a /  ES cells is reduced to ~30% of that observed in  G9a +/+ ES cells.	bind
22098	2	7113	6	13	NULL	NULL	NULL	H3	GP		is methylated in			Lys-9		G9a +/+ ES cells.	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_17_14996_s_107	12586828	2 The level of H3 Lys-9 methylation of the PWS-IC in  G9a /  ES cells is reduced to ~30% of that observed in  G9a +/+ ES cells.	bind
26138	3	7113	6	13	NULL	NULL	NULL	statement 1	Process	level of	is less than					statement 2	Process	level of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_17_14996_s_107	12586828	2 The level of H3 Lys-9 methylation of the PWS-IC in  G9a /  ES cells is reduced to ~30% of that observed in  G9a +/+ ES cells.	bind
26321	1	7113	7	NULL	NULL	0	NULL	H3	NULL		is methylated in	NULL		Lys-9		G9a / ES cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_17_14996_s_107	12586828	2 The level of H3 Lys-9 methylation of the PWS-IC in  G9a /  ES cells is reduced to ~30% of that observed in  G9a +/+ ES cells.	bind
26326	2	7113	7	NULL	NULL	0	NULL	H3	NULL		is methylated in	NULL		Lys-9		G9a +/+ ES cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_17_14996_s_107	12586828	2 The level of H3 Lys-9 methylation of the PWS-IC in  G9a /  ES cells is reduced to ~30% of that observed in  G9a +/+ ES cells.	bind
26327	3	7113	7	NULL	NULL	0	NULL	statement 1	NULL	levels of	is less than	NULL				statement 2	NULL	levels of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_17_14996_s_107	12586828	2 The level of H3 Lys-9 methylation of the PWS-IC in  G9a /  ES cells is reduced to ~30% of that observed in  G9a +/+ ES cells.	bind
22229	1	7114	6	13	NULL	NULL	NULL	alpha3beta1 integrin	GP	melanoma cell	bind					alpha1(IV)	GP		531-543		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_16_14321_s_21	12574156	2 The melanoma cell alpha3beta1 integrin binds to alpha1(IV)531-543 ( ,  ,  ).	bind
26079	1	7114	7	NULL	NULL	0	NULL	alpha3beta1 integrin	NULL	melanoma cell	binds to	NULL				 alpha1(IV)	NULL		531-543		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_16_14321_s_21	12574156	2 The melanoma cell alpha3beta1 integrin binds to alpha1(IV)531-543 ( ,  ,  ).	bind
22468	1	7115	6	13	NULL	NULL	NULL	4E-BP1	GP		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_32779_s_151	9407052	2 The observation that overexpression of a phosphorylation-resistant mutant of eIF2alpha reduces the extent of inhibition of protein synthesis seen during heat shock supports this idea ( 62,  63), although the fact that such protection was only partial is consistent with the hypothesis that other distinct mechanisms ( e.g. the enhanced binding of 4E-BP1 to eIF4E) may also operate to reduce translation rates under this condition.	bind
23104	2	7115	6	13	NULL	NULL	NULL	eIF2alpha	GP	overexpression of;;phosphorylation-resistant mutant of	reduces					protein synthesis	Process	inhibiton of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_32779_s_151	9407052	2 The observation that overexpression of a phosphorylation-resistant mutant of eIF2alpha reduces the extent of inhibition of protein synthesis seen during heat shock supports this idea ( 62,  63), although the fact that such protection was only partial is consistent with the hypothesis that other distinct mechanisms ( e.g. the enhanced binding of 4E-BP1 to eIF4E) may also operate to reduce translation rates under this condition.	bind
26080	1	7115	7	10	NULL	0	NULL	eIF2alpha	NULL	overexpression of;;phosphorylation-resistant mutant of	reduces	NULL				protein synthesis	NULL	inhibition of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_32779_s_151	9407052	2 The observation that overexpression of a phosphorylation-resistant mutant of eIF2alpha reduces the extent of inhibition of protein synthesis seen during heat shock supports this idea ( 62,  63), although the fact that such protection was only partial is consistent with the hypothesis that other distinct mechanisms ( e.g. the enhanced binding of 4E-BP1 to eIF4E) may also operate to reduce translation rates under this condition.	bind
26081	2	7115	7	NULL	NULL	0	NULL	4E-BP1	NULL		bind	NULL				eIF4E	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_32779_s_151	9407052	2 The observation that overexpression of a phosphorylation-resistant mutant of eIF2alpha reduces the extent of inhibition of protein synthesis seen during heat shock supports this idea ( 62,  63), although the fact that such protection was only partial is consistent with the hypothesis that other distinct mechanisms ( e.g. the enhanced binding of 4E-BP1 to eIF4E) may also operate to reduce translation rates under this condition.	bind
22230	1	7116	6	13	NULL	NULL	NULL	p50 homodimer	GP		bind		weakly			IkappaBalpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29840_s_134	10882738	2 The p50 homodimer binds IkappaBalpha weakly with an equilibrium dissociation constant of 218 nM.	bind
26082	1	7116	7	NULL	NULL	0	NULL	p50 homodimer	NULL		binds	NULL	weakly			IkappaBalpha	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29840_s_134	10882738	2 The p50 homodimer binds IkappaBalpha weakly with an equilibrium dissociation constant of 218 nM.	bind
22231	1	7117	6	13	NULL	NULL	NULL	NifX	GP		bind					FeMo-co	Chemical	finished			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_19_15968_s_239	11279153	2 The partial transfer of radio label from 55Fe-NifX to apodinitrogenase suggested that 55Fe-NifX is comprised of a mixture of either NifX bound to finished FeMo-co or to NifX bound to a FeMo-co precursor that is yet to be completed.	bind
22232	2	7117	6	13	NULL	NULL	NULL	NifX	GP		bind					FeMo-co precursor	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_19_15968_s_239	11279153	2 The partial transfer of radio label from 55Fe-NifX to apodinitrogenase suggested that 55Fe-NifX is comprised of a mixture of either NifX bound to finished FeMo-co or to NifX bound to a FeMo-co precursor that is yet to be completed.	bind
22233	3	7117	6	13	NULL	NULL	NULL	55Fe-NifX	GP		comprises of 					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_19_15968_s_239	11279153	2 The partial transfer of radio label from 55Fe-NifX to apodinitrogenase suggested that 55Fe-NifX is comprised of a mixture of either NifX bound to finished FeMo-co or to NifX bound to a FeMo-co precursor that is yet to be completed.	bind
22234	4	7117	6	13	NULL	NULL	NULL	55Fe-NifX	GP		comprises of					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_19_15968_s_239	11279153	2 The partial transfer of radio label from 55Fe-NifX to apodinitrogenase suggested that 55Fe-NifX is comprised of a mixture of either NifX bound to finished FeMo-co or to NifX bound to a FeMo-co precursor that is yet to be completed.	bind
26083	1	7117	7	NULL	NULL	0	NULL	NifX	NULL		bind	NULL				FeMo-co 	NULL	finished			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_19_15968_s_239	11279153	2 The partial transfer of radio label from 55Fe-NifX to apodinitrogenase suggested that 55Fe-NifX is comprised of a mixture of either NifX bound to finished FeMo-co or to NifX bound to a FeMo-co precursor that is yet to be completed.	bind
26084	2	7117	7	NULL	NULL	0	NULL	NifX	NULL		bind	NULL				FeMo-co precursor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_19_15968_s_239	11279153	2 The partial transfer of radio label from 55Fe-NifX to apodinitrogenase suggested that 55Fe-NifX is comprised of a mixture of either NifX bound to finished FeMo-co or to NifX bound to a FeMo-co precursor that is yet to be completed.	bind
26085	3	7117	7	NULL	NULL	0	NULL	55Fe-NifX	NULL		comprises of	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_19_15968_s_239	11279153	2 The partial transfer of radio label from 55Fe-NifX to apodinitrogenase suggested that 55Fe-NifX is comprised of a mixture of either NifX bound to finished FeMo-co or to NifX bound to a FeMo-co precursor that is yet to be completed.	bind
26086	4	7117	7	NULL	NULL	0	NULL	55Fe-NifX	NULL		comprises of	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_19_15968_s_239	11279153	2 The partial transfer of radio label from 55Fe-NifX to apodinitrogenase suggested that 55Fe-NifX is comprised of a mixture of either NifX bound to finished FeMo-co or to NifX bound to a FeMo-co precursor that is yet to be completed.	bind
22519	1	7118	6	13	NULL	NULL	NULL	heat shock			induces					hsp90beta gene	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_51143_s_200	14532285	2 The specificity of PKC-epsilon on heat shock-induced expression of the  hsp90beta gene is further supported by the fact that neither CA-PKC-alpha nor DN-PKC-alpha affected the promoter activity of the  hsp90beta gene in response to heat shock, suggesting that heat shock-induced expression of the  hsp90beta gene is regulated by a PKC-epsilon-dependent mechanism.	bind
22520	2	7118	6	13	NULL	NULL	NULL	statement 1	Process		is dependent on					PKC-epsilon	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_51143_s_200	14532285	2 The specificity of PKC-epsilon on heat shock-induced expression of the  hsp90beta gene is further supported by the fact that neither CA-PKC-alpha nor DN-PKC-alpha affected the promoter activity of the  hsp90beta gene in response to heat shock, suggesting that heat shock-induced expression of the  hsp90beta gene is regulated by a PKC-epsilon-dependent mechanism.	bind
22521	3	7118	6	13	NULL	NULL	NULL	CA-PKC-alpha	GP		does not affect					hsp90beta gene	GP	promoter activity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_51143_s_200	14532285	2 The specificity of PKC-epsilon on heat shock-induced expression of the  hsp90beta gene is further supported by the fact that neither CA-PKC-alpha nor DN-PKC-alpha affected the promoter activity of the  hsp90beta gene in response to heat shock, suggesting that heat shock-induced expression of the  hsp90beta gene is regulated by a PKC-epsilon-dependent mechanism.	bind
22522	4	7118	6	13	NULL	NULL	NULL	DN-PKC-alpha	GP		does not affect					hsp90beta gene	GP	promoter activity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_51143_s_200	14532285	2 The specificity of PKC-epsilon on heat shock-induced expression of the  hsp90beta gene is further supported by the fact that neither CA-PKC-alpha nor DN-PKC-alpha affected the promoter activity of the  hsp90beta gene in response to heat shock, suggesting that heat shock-induced expression of the  hsp90beta gene is regulated by a PKC-epsilon-dependent mechanism.	bind
53356	5	7118	6	13	NULL	NULL	NULL	statement 3	Process		occurs in response to					heat shock 					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_51143_s_200	14532285	2 The specificity of PKC-epsilon on heat shock-induced expression of the  hsp90beta gene is further supported by the fact that neither CA-PKC-alpha nor DN-PKC-alpha affected the promoter activity of the  hsp90beta gene in response to heat shock, suggesting that heat shock-induced expression of the  hsp90beta gene is regulated by a PKC-epsilon-dependent mechanism.	bind
53357	6	7118	6	13	NULL	NULL	NULL	statement 4	Process		occurs in response to					heat shock 					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_51143_s_200	14532285	2 The specificity of PKC-epsilon on heat shock-induced expression of the  hsp90beta gene is further supported by the fact that neither CA-PKC-alpha nor DN-PKC-alpha affected the promoter activity of the  hsp90beta gene in response to heat shock, suggesting that heat shock-induced expression of the  hsp90beta gene is regulated by a PKC-epsilon-dependent mechanism.	bind
26545	1	7118	7	10	NULL	0	NULL	CA-PKC-alpha	NULL		does not affect	NULL				hsp90beta	NULL	promoter activity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_51143_s_200	14532285	2 The specificity of PKC-epsilon on heat shock-induced expression of the  hsp90beta gene is further supported by the fact that neither CA-PKC-alpha nor DN-PKC-alpha affected the promoter activity of the  hsp90beta gene in response to heat shock, suggesting that heat shock-induced expression of the  hsp90beta gene is regulated by a PKC-epsilon-dependent mechanism.	bind
26546	2	7118	7	10	NULL	0	NULL	DN-PKC-alpha	NULL		does not affect	NULL				hsp90beta	NULL	promoter activity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_51143_s_200	14532285	2 The specificity of PKC-epsilon on heat shock-induced expression of the  hsp90beta gene is further supported by the fact that neither CA-PKC-alpha nor DN-PKC-alpha affected the promoter activity of the  hsp90beta gene in response to heat shock, suggesting that heat shock-induced expression of the  hsp90beta gene is regulated by a PKC-epsilon-dependent mechanism.	bind
26547	3	7118	7	NULL	NULL	0	NULL	statement 1	NULL		occurs in response to	NULL				heat shock 	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_51_51143_s_200	14532285	2 The specificity of PKC-epsilon on heat shock-induced expression of the  hsp90beta gene is further supported by the fact that neither CA-PKC-alpha nor DN-PKC-alpha affected the promoter activity of the  hsp90beta gene in response to heat shock, suggesting that heat shock-induced expression of the  hsp90beta gene is regulated by a PKC-epsilon-dependent mechanism.	bind
26548	4	7118	7	NULL	NULL	0	NULL	statement 2	NULL		occurs in response to	NULL				heat shock	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_51_51143_s_200	14532285	2 The specificity of PKC-epsilon on heat shock-induced expression of the  hsp90beta gene is further supported by the fact that neither CA-PKC-alpha nor DN-PKC-alpha affected the promoter activity of the  hsp90beta gene in response to heat shock, suggesting that heat shock-induced expression of the  hsp90beta gene is regulated by a PKC-epsilon-dependent mechanism.	bind
26549	5	7118	7	NULL	NULL	0	NULL	heat shock	NULL		induce	NULL				hsp90beta gene	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_51_51143_s_200	14532285	2 The specificity of PKC-epsilon on heat shock-induced expression of the  hsp90beta gene is further supported by the fact that neither CA-PKC-alpha nor DN-PKC-alpha affected the promoter activity of the  hsp90beta gene in response to heat shock, suggesting that heat shock-induced expression of the  hsp90beta gene is regulated by a PKC-epsilon-dependent mechanism.	bind
26550	6	7118	7	NULL	NULL	0	NULL	PKC-epsilon-dependent mechanism	NULL		regulates	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_51_51143_s_200	14532285	2 The specificity of PKC-epsilon on heat shock-induced expression of the  hsp90beta gene is further supported by the fact that neither CA-PKC-alpha nor DN-PKC-alpha affected the promoter activity of the  hsp90beta gene in response to heat shock, suggesting that heat shock-induced expression of the  hsp90beta gene is regulated by a PKC-epsilon-dependent mechanism.	bind
22235	1	7119	6	13	NULL	NULL	NULL	ATP	Chemical		bind								NBD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29407_s_27	10893239	2 The structure of the ATP-binding subunit of the bacterial histidine transporter (HisP) provides a model for the binding of ATP to an NBD ( 9).	bind
26551	1	7119	7	NULL	NULL	0	NULL	ATP	NULL		bind	NULL					NULL		NBD		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29407_s_27	10893239	2 The structure of the ATP-binding subunit of the bacterial histidine transporter (HisP) provides a model for the binding of ATP to an NBD ( 9).	bind
22236	1	7120	6	13	NULL	NULL	NULL	CNX	GP		bind					glycoproteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_12_8623_s_172	11254652	2 The term "`lectin-like chaperone"` was originally introduced into the literature when the binding of CNX and CRT to glycoproteins was known to require specific oligosaccharide-dependent interactions, but the lectin activities for CNX and CRT remained to be demonstrated.	bind
22237	2	7120	6	13	NULL	NULL	NULL	CRT	GP		bind					glycoproteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_12_8623_s_172	11254652	2 The term "`lectin-like chaperone"` was originally introduced into the literature when the binding of CNX and CRT to glycoproteins was known to require specific oligosaccharide-dependent interactions, but the lectin activities for CNX and CRT remained to be demonstrated.	bind
22239	3	7120	6	13	NULL	NULL	NULL	statement 1	Process		require					oligosaccharide-dependent interactions	Process	specific			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_12_8623_s_172	11254652	2 The term "`lectin-like chaperone"` was originally introduced into the literature when the binding of CNX and CRT to glycoproteins was known to require specific oligosaccharide-dependent interactions, but the lectin activities for CNX and CRT remained to be demonstrated.	bind
22240	4	7120	6	13	NULL	NULL	NULL	statement 2	Process		require					oligosaccharide-dependent interactions	Process	specific			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_12_8623_s_172	11254652	2 The term "`lectin-like chaperone"` was originally introduced into the literature when the binding of CNX and CRT to glycoproteins was known to require specific oligosaccharide-dependent interactions, but the lectin activities for CNX and CRT remained to be demonstrated.	bind
26552	1	7120	7	NULL	NULL	0	NULL	CNX	NULL		bind	NULL				glycoproteins	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_12_8623_s_172	11254652	2 The term "`lectin-like chaperone"` was originally introduced into the literature when the binding of CNX and CRT to glycoproteins was known to require specific oligosaccharide-dependent interactions, but the lectin activities for CNX and CRT remained to be demonstrated.	bind
26553	2	7120	7	NULL	NULL	0	NULL	CRT	NULL		bind	NULL				glycoproteins	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_12_8623_s_172	11254652	2 The term "`lectin-like chaperone"` was originally introduced into the literature when the binding of CNX and CRT to glycoproteins was known to require specific oligosaccharide-dependent interactions, but the lectin activities for CNX and CRT remained to be demonstrated.	bind
26554	3	7120	7	NULL	NULL	0	NULL	statement 1	NULL		require	NULL				oligosaccharide-dependent interactions	NULL	specific			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_12_8623_s_172	11254652	2 The term "`lectin-like chaperone"` was originally introduced into the literature when the binding of CNX and CRT to glycoproteins was known to require specific oligosaccharide-dependent interactions, but the lectin activities for CNX and CRT remained to be demonstrated.	bind
26555	4	7120	7	NULL	NULL	0	NULL	statement 2	NULL		require	NULL				oligosaccharide-dependent interactions	NULL	specific			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_12_8623_s_172	11254652	2 The term "`lectin-like chaperone"` was originally introduced into the literature when the binding of CNX and CRT to glycoproteins was known to require specific oligosaccharide-dependent interactions, but the lectin activities for CNX and CRT remained to be demonstrated.	bind
22245	1	7121	6	13	NULL	NULL	NULL	Par6	GP	Drosophila	bind		directly			Patj	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_40_41557_s_169	15292221	2 There are also recent reports that the  Drosophila Par6 can bind directly to Patj (previously called Dlt) ( ), which is a binding partner for Pals1, and that Par6C can bind directly to the C terminus of Crb3 ( ), which is also a binding partner for Pals1.	bind
22249	2	7121	6	13	NULL	NULL	NULL	PatJ	GP		is 					Dlt	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_40_41557_s_169	15292221	2 There are also recent reports that the  Drosophila Par6 can bind directly to Patj (previously called Dlt) ( ), which is a binding partner for Pals1, and that Par6C can bind directly to the C terminus of Crb3 ( ), which is also a binding partner for Pals1.	bind
22254	3	7121	6	13	NULL	NULL	NULL	Patj	GP		bind					Pals1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_40_41557_s_169	15292221	2 There are also recent reports that the  Drosophila Par6 can bind directly to Patj (previously called Dlt) ( ), which is a binding partner for Pals1, and that Par6C can bind directly to the C terminus of Crb3 ( ), which is also a binding partner for Pals1.	bind
22259	4	7121	6	13	NULL	NULL	NULL	Par6C	GP		bind		directly			Crb3	GP		C terminus		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_40_41557_s_169	15292221	2 There are also recent reports that the  Drosophila Par6 can bind directly to Patj (previously called Dlt) ( ), which is a binding partner for Pals1, and that Par6C can bind directly to the C terminus of Crb3 ( ), which is also a binding partner for Pals1.	bind
22261	5	7121	6	13	NULL	NULL	NULL	Pals1	GP		bind					Crb3	GP		C terminus		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_40_41557_s_169	15292221	2 There are also recent reports that the  Drosophila Par6 can bind directly to Patj (previously called Dlt) ( ), which is a binding partner for Pals1, and that Par6C can bind directly to the C terminus of Crb3 ( ), which is also a binding partner for Pals1.	bind
26556	1	7121	7	NULL	NULL	0	NULL	Par6	NULL	Drosophila 	bind	NULL	directly			Patj	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_40_41557_s_169	15292221	2 There are also recent reports that the  Drosophila Par6 can bind directly to Patj (previously called Dlt) ( ), which is a binding partner for Pals1, and that Par6C can bind directly to the C terminus of Crb3 ( ), which is also a binding partner for Pals1.	bind
26557	2	7121	7	NULL	NULL	0	NULL	Patj	NULL		is	NULL				Dlt	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_40_41557_s_169	15292221	2 There are also recent reports that the  Drosophila Par6 can bind directly to Patj (previously called Dlt) ( ), which is a binding partner for Pals1, and that Par6C can bind directly to the C terminus of Crb3 ( ), which is also a binding partner for Pals1.	bind
26558	3	7121	7	NULL	NULL	0	NULL	Pals1	NULL		bind	NULL				Patj	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_40_41557_s_169	15292221	2 There are also recent reports that the  Drosophila Par6 can bind directly to Patj (previously called Dlt) ( ), which is a binding partner for Pals1, and that Par6C can bind directly to the C terminus of Crb3 ( ), which is also a binding partner for Pals1.	bind
26559	4	7121	7	NULL	NULL	0	NULL	Par6C	NULL		bind	NULL	directly			Crb3	NULL		C terminus		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_40_41557_s_169	15292221	2 There are also recent reports that the  Drosophila Par6 can bind directly to Patj (previously called Dlt) ( ), which is a binding partner for Pals1, and that Par6C can bind directly to the C terminus of Crb3 ( ), which is also a binding partner for Pals1.	bind
26560	5	7121	7	10	NULL	0	NULL	Pals1	NULL		bind	NULL				Crb3	NULL		C terminus		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_40_41557_s_169	15292221	2 There are also recent reports that the  Drosophila Par6 can bind directly to Patj (previously called Dlt) ( ), which is a binding partner for Pals1, and that Par6C can bind directly to the C terminus of Crb3 ( ), which is also a binding partner for Pals1.	bind
22269	1	7122	6	13	NULL	NULL	NULL	myosin phosphatase	GP		is a substrate for			regulatory myosin-binding subunit		PKG	GP				NULL	smooth muscle cell	NULL	NULL	NULL	NULL	gw60_circulationres_93_4_280_s_50	12933699	2 There are several specific physiological substrates for PKG in smooth muscle including the regulatory myosin-binding subunit of myosin phosphatase, 3 calcium-activated maxi K+ (BKCa) channels, 4 and IRAG (IP3 receptor associated cGMP kinase substrate).	bind
22271	2	7122	6	13	NULL	NULL	NULL	BKCa channels	GP		is a substrate for					PKG	GP				NULL	smooth muscle cell	NULL	NULL	NULL	NULL	gw60_circulationres_93_4_280_s_50	12933699	2 There are several specific physiological substrates for PKG in smooth muscle including the regulatory myosin-binding subunit of myosin phosphatase, 3 calcium-activated maxi K+ (BKCa) channels, 4 and IRAG (IP3 receptor associated cGMP kinase substrate).	bind
22272	3	7122	6	13	NULL	NULL	NULL	BKCa	GP		is					calcium-activated maxi K+ channels	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_280_s_50	12933699	2 There are several specific physiological substrates for PKG in smooth muscle including the regulatory myosin-binding subunit of myosin phosphatase, 3 calcium-activated maxi K+ (BKCa) channels, 4 and IRAG (IP3 receptor associated cGMP kinase substrate).	bind
22273	4	7122	6	13	NULL	NULL	NULL	IRAG	GP		is a substrate for					PKG	GP				NULL	smooth muscle cell	NULL	NULL	NULL	NULL	gw60_circulationres_93_4_280_s_50	12933699	2 There are several specific physiological substrates for PKG in smooth muscle including the regulatory myosin-binding subunit of myosin phosphatase, 3 calcium-activated maxi K+ (BKCa) channels, 4 and IRAG (IP3 receptor associated cGMP kinase substrate).	bind
22274	5	7122	6	13	NULL	NULL	NULL	IRAG	GP		is					IP3 receptor associated cGMP kinase substrate	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_280_s_50	12933699	2 There are several specific physiological substrates for PKG in smooth muscle including the regulatory myosin-binding subunit of myosin phosphatase, 3 calcium-activated maxi K+ (BKCa) channels, 4 and IRAG (IP3 receptor associated cGMP kinase substrate).	bind
37877	6	7122	6	13	NULL	NULL	NULL	IRAG	GP		is a type of					specific physiological substrate for PKG	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_280_s_50	12933699	2 There are several specific physiological substrates for PKG in smooth muscle including the regulatory myosin-binding subunit of myosin phosphatase, 3 calcium-activated maxi K+ (BKCa) channels, 4 and IRAG (IP3 receptor associated cGMP kinase substrate).	bind
37878	7	7122	6	13	NULL	NULL	NULL	myosin phosphatase	GP		is a type of					specific physiological substrate for PKG	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_280_s_50	12933699	2 There are several specific physiological substrates for PKG in smooth muscle including the regulatory myosin-binding subunit of myosin phosphatase, 3 calcium-activated maxi K+ (BKCa) channels, 4 and IRAG (IP3 receptor associated cGMP kinase substrate).	bind
37879	8	7122	6	13	NULL	NULL	NULL	BKCa channels	GP		is a type of					specific physiological substrate for PKG	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_280_s_50	12933699	2 There are several specific physiological substrates for PKG in smooth muscle including the regulatory myosin-binding subunit of myosin phosphatase, 3 calcium-activated maxi K+ (BKCa) channels, 4 and IRAG (IP3 receptor associated cGMP kinase substrate).	bind
26561	1	7122	7	NULL	NULL	0	NULL	myosin phosphatase	NULL		is a substrate of	NULL		regulatory myosin-binding subunit		PKG	NULL				NULL	smooth muscle	NULL	NULL	NULL	NULL	gw60_circulationres_93_4_280_s_50	12933699	2 There are several specific physiological substrates for PKG in smooth muscle including the regulatory myosin-binding subunit of myosin phosphatase, 3 calcium-activated maxi K+ (BKCa) channels, 4 and IRAG (IP3 receptor associated cGMP kinase substrate).	bind
26562	2	7122	7	NULL	NULL	0	NULL	BKCa	NULL		is a substrate of	NULL				PKG	NULL				NULL	smooth muscle	NULL	NULL	NULL	NULL	gw60_circulationres_93_4_280_s_50	12933699	2 There are several specific physiological substrates for PKG in smooth muscle including the regulatory myosin-binding subunit of myosin phosphatase, 3 calcium-activated maxi K+ (BKCa) channels, 4 and IRAG (IP3 receptor associated cGMP kinase substrate).	bind
26563	3	7122	7	NULL	NULL	0	NULL	IRAG	NULL		is a substrate of	NULL				PKG	NULL				NULL	smooth muscle	NULL	NULL	NULL	NULL	gw60_circulationres_93_4_280_s_50	12933699	2 There are several specific physiological substrates for PKG in smooth muscle including the regulatory myosin-binding subunit of myosin phosphatase, 3 calcium-activated maxi K+ (BKCa) channels, 4 and IRAG (IP3 receptor associated cGMP kinase substrate).	bind
26564	4	7122	7	NULL	NULL	0	NULL	BKCa	NULL		is	NULL				calcium-activated maxi K+ channels	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_4_280_s_50	12933699	2 There are several specific physiological substrates for PKG in smooth muscle including the regulatory myosin-binding subunit of myosin phosphatase, 3 calcium-activated maxi K+ (BKCa) channels, 4 and IRAG (IP3 receptor associated cGMP kinase substrate).	bind
26565	5	7122	7	NULL	NULL	0	NULL	IRAG	NULL		is	NULL				IP3 receptor associated cGMP kinase substrate	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_4_280_s_50	12933699	2 There are several specific physiological substrates for PKG in smooth muscle including the regulatory myosin-binding subunit of myosin phosphatase, 3 calcium-activated maxi K+ (BKCa) channels, 4 and IRAG (IP3 receptor associated cGMP kinase substrate).	bind
46446	6	7122	7	10	NULL	0	NULL	IRAG	NULL		is a type of	NULL				\tspecific physiological substrate for PKG	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_4_280_s_50	12933699	2 There are several specific physiological substrates for PKG in smooth muscle including the regulatory myosin-binding subunit of myosin phosphatase, 3 calcium-activated maxi K+ (BKCa) channels, 4 and IRAG (IP3 receptor associated cGMP kinase substrate).	bind
46447	7	7122	7	10	NULL	0	NULL	myosin phosphatase	NULL		is a type of	NULL				\tspecific physiological substrate for PKG	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_4_280_s_50	12933699	2 There are several specific physiological substrates for PKG in smooth muscle including the regulatory myosin-binding subunit of myosin phosphatase, 3 calcium-activated maxi K+ (BKCa) channels, 4 and IRAG (IP3 receptor associated cGMP kinase substrate).	bind
46448	8	7122	7	10	NULL	0	NULL	BKCa channels	NULL		is a type of	NULL				specific physiological substrate for PKG	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_4_280_s_50	12933699	2 There are several specific physiological substrates for PKG in smooth muscle including the regulatory myosin-binding subunit of myosin phosphatase, 3 calcium-activated maxi K+ (BKCa) channels, 4 and IRAG (IP3 receptor associated cGMP kinase substrate).	bind
22282	1	7124	6	13	NULL	NULL	NULL	target proteins	GP		do not contain								(K/R) XTQT motif		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_14059_s_249	11148209	2 Therefore, it is perhaps not surprising that DLC8 can bind a number of other target proteins, even though these proteins do not contain a (K/R) XTQT motif.	bind
22283	2	7124	6	13	NULL	NULL	NULL	DLC8	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_14059_s_249	11148209	2 Therefore, it is perhaps not surprising that DLC8 can bind a number of other target proteins, even though these proteins do not contain a (K/R) XTQT motif.	bind
26567	1	7124	7	NULL	NULL	0	NULL	protein	NULL		does not contain	NULL					NULL		(K/R) XTQT motif		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_14059_s_249	11148209	2 Therefore, it is perhaps not surprising that DLC8 can bind a number of other target proteins, even though these proteins do not contain a (K/R) XTQT motif.	bind
26568	2	7124	7	NULL	NULL	0	NULL	DLC8	NULL		bind	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_14059_s_249	11148209	2 Therefore, it is perhaps not surprising that DLC8 can bind a number of other target proteins, even though these proteins do not contain a (K/R) XTQT motif.	bind
22289	1	7125	6	13	NULL	NULL	NULL	gentamicin	Chemical		bind					megalin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_1_618_s_163	11700326	2 Therefore, the antagonist is largely ineffective in blocking gentamicin binding to megalin.	bind
26569	1	7125	7	NULL	NULL	0	NULL	gentamicin	NULL		bind	NULL				megalin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_1_618_s_163	11700326	2 Therefore, the antagonist is largely ineffective in blocking gentamicin binding to megalin.	bind
22290	1	7126	6	13	NULL	NULL	NULL	histone H3	GP		bind					NF-I	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1645_s_180	10636857	2 Therefore, the binding of histone H3 by NF-I may be the key step by which this transcription factor overcomes chromatin repression on both promoters and replication origins.	bind
22291	2	7126	6	13	NULL	NULL	NULL	NF-I 	GP		overcomes					chromatin	CellComponent	repression of		promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1645_s_180	10636857	2 Therefore, the binding of histone H3 by NF-I may be the key step by which this transcription factor overcomes chromatin repression on both promoters and replication origins.	bind
22292	3	7126	6	13	NULL	NULL	NULL	NF-I	GP		overcomes					chromatin	CellComponent	repression of		replication origins	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1645_s_180	10636857	2 Therefore, the binding of histone H3 by NF-I may be the key step by which this transcription factor overcomes chromatin repression on both promoters and replication origins.	bind
37406	4	7126	6	13	NULL	NULL	NULL	statement 1	Process		leads to		may			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1645_s_180	10636857	2 Therefore, the binding of histone H3 by NF-I may be the key step by which this transcription factor overcomes chromatin repression on both promoters and replication origins.	bind
37407	5	7126	6	13	NULL	NULL	NULL	statement 1	Process		leads to		may			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1645_s_180	10636857	2 Therefore, the binding of histone H3 by NF-I may be the key step by which this transcription factor overcomes chromatin repression on both promoters and replication origins.	bind
53358	6	7126	6	13	NULL	NULL	NULL	NF-I	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1645_s_180	10636857	2 Therefore, the binding of histone H3 by NF-I may be the key step by which this transcription factor overcomes chromatin repression on both promoters and replication origins.	bind
26571	1	7126	7	NULL	NULL	0	NULL	NF-I	NULL		bind	NULL				histone H3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_3_1645_s_180	10636857	2 Therefore, the binding of histone H3 by NF-I may be the key step by which this transcription factor overcomes chromatin repression on both promoters and replication origins.	bind
26572	2	7126	7	10	NULL	0	NULL	NF-I	NULL		overcomes	NULL				chromatin	NULL	repression of		promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1645_s_180	10636857	2 Therefore, the binding of histone H3 by NF-I may be the key step by which this transcription factor overcomes chromatin repression on both promoters and replication origins.	bind
26573	3	7126	7	10	NULL	0	NULL	NF-I	NULL		overcomes	NULL				chromatin	NULL	repression of		replication origin	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1645_s_180	10636857	2 Therefore, the binding of histone H3 by NF-I may be the key step by which this transcription factor overcomes chromatin repression on both promoters and replication origins.	bind
26574	4	7126	7	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_3_1645_s_180	10636857	2 Therefore, the binding of histone H3 by NF-I may be the key step by which this transcription factor overcomes chromatin repression on both promoters and replication origins.	bind
26575	5	7126	7	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_3_1645_s_180	10636857	2 Therefore, the binding of histone H3 by NF-I may be the key step by which this transcription factor overcomes chromatin repression on both promoters and replication origins.	bind
53359	6	7126	7	10	NULL	0	NULL	NF-I	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_3_1645_s_180	10636857	2 Therefore, the binding of histone H3 by NF-I may be the key step by which this transcription factor overcomes chromatin repression on both promoters and replication origins.	bind
37408	1	7127	6	13	NULL	NULL	NULL	LARG-RhoA complex 	GP	changes in	reflect			P loop		GTPase	GP	plasticity of	active site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_47352_s_328	15331592	2 Therefore, the novel changes we observe in the P loop and the purine-binding pocket of the LARG-RhoA complex ( Fig. 5) probably reflect the natural plasticity of the GTPase active site when nucleotides are absent, rather than an active exchange mechanism exerted by the LARG DH domain.	bind
37409	2	7127	6	13	NULL	NULL	NULL	LARG-RhoA complex	GP	changes in	reflect			purine binding pocket		GTPase	GP	plasticity of	active site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_47352_s_328	15331592	2 Therefore, the novel changes we observe in the P loop and the purine-binding pocket of the LARG-RhoA complex ( Fig. 5) probably reflect the natural plasticity of the GTPase active site when nucleotides are absent, rather than an active exchange mechanism exerted by the LARG DH domain.	bind
37410	3	7127	6	13	NULL	NULL	NULL	statement 1	Process		occurs in absence of					nucleotides	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_47352_s_328	15331592	2 Therefore, the novel changes we observe in the P loop and the purine-binding pocket of the LARG-RhoA complex ( Fig. 5) probably reflect the natural plasticity of the GTPase active site when nucleotides are absent, rather than an active exchange mechanism exerted by the LARG DH domain.	bind
37411	4	7127	6	13	NULL	NULL	NULL	statement 2	Process		occurs in absence of					nucleotides	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_47352_s_328	15331592	2 Therefore, the novel changes we observe in the P loop and the purine-binding pocket of the LARG-RhoA complex ( Fig. 5) probably reflect the natural plasticity of the GTPase active site when nucleotides are absent, rather than an active exchange mechanism exerted by the LARG DH domain.	bind
26576	1	7127	7	NULL	NULL	0	NULL	LARG-RhoA complex	NULL	novel changes in	reflect	NULL		P loop		GTPase 	NULL	natural plasticity of	active site 		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_47352_s_328	15331592	2 Therefore, the novel changes we observe in the P loop and the purine-binding pocket of the LARG-RhoA complex ( Fig. 5) probably reflect the natural plasticity of the GTPase active site when nucleotides are absent, rather than an active exchange mechanism exerted by the LARG DH domain.	bind
26577	2	7127	7	NULL	NULL	0	NULL	 LARG-RhoA complex	NULL	novel changes in	reflect	NULL		 purine-binding pocket		GTPase 	NULL	natural plasticity of	active site 		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_45_47352_s_328	15331592	2 Therefore, the novel changes we observe in the P loop and the purine-binding pocket of the LARG-RhoA complex ( Fig. 5) probably reflect the natural plasticity of the GTPase active site when nucleotides are absent, rather than an active exchange mechanism exerted by the LARG DH domain.	bind
26578	3	7127	7	NULL	NULL	0	NULL	statement 1	NULL		in absence of	NULL				nucleotides	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_45_47352_s_328	15331592	2 Therefore, the novel changes we observe in the P loop and the purine-binding pocket of the LARG-RhoA complex ( Fig. 5) probably reflect the natural plasticity of the GTPase active site when nucleotides are absent, rather than an active exchange mechanism exerted by the LARG DH domain.	bind
26579	4	7127	7	NULL	NULL	0	NULL	statement 2	NULL		in absence of	NULL				nucleotides	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_45_47352_s_328	15331592	2 Therefore, the novel changes we observe in the P loop and the purine-binding pocket of the LARG-RhoA complex ( Fig. 5) probably reflect the natural plasticity of the GTPase active site when nucleotides are absent, rather than an active exchange mechanism exerted by the LARG DH domain.	bind
22296	1	7129	6	13	NULL	NULL	NULL				bind		directly	last seven amino acids of NR2 subunit		SAP90	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_35_21622_s_172	8702950	2 These data are similar to the recent findings, which suggested that the last seven amino acids of the NR2 subunit bind directly to SAP90 (Kornau  et al., 1995  ).	bind
26580	1	7129	7	NULL	NULL	0	NULL		NULL		bind	NULL	directly	last seven amino acids of  NR2 subunit		SAP90	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_35_21622_s_172	8702950	2 These data are similar to the recent findings, which suggested that the last seven amino acids of the NR2 subunit bind directly to SAP90 (Kornau  et al., 1995  ).	bind
22299	1	7130	6	13	NULL	NULL	NULL	CBP/p300	GP		bind					Py large T	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_36_33533_s_229	11438528	2 These findings indicate that CBP/p300 binding by Py large T is essential for virus growth.	bind
37417	2	7130	6	13	NULL	NULL	NULL	statement 1	Process		is essential for					virus growth	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_36_33533_s_229	11438528	2 These findings indicate that CBP/p300 binding by Py large T is essential for virus growth.	bind
26581	1	7130	7	NULL	NULL	0	NULL	Py large T	NULL		bind	NULL				CBP/p300	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_36_33533_s_229	11438528	2 These findings indicate that CBP/p300 binding by Py large T is essential for virus growth.	bind
26582	2	7130	7	NULL	NULL	0	NULL	statement 1	NULL		is essential for	NULL				virus growth	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_36_33533_s_229	11438528	2 These findings indicate that CBP/p300 binding by Py large T is essential for virus growth.	bind
22304	1	7131	6	13	NULL	NULL	NULL	heme	Chemical		bind					CBS	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_1_16_s_98	11042162	2 These findings indicate that under these conditions the heme groups that were bound to CBS had been completely released.	bind
26583	1	7131	7	NULL	NULL	0	NULL	heme groups	NULL		bind	NULL				CBS	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_16_s_98	11042162	2 These findings indicate that under these conditions the heme groups that were bound to CBS had been completely released.	bind
22312	1	7133	6	13	NULL	NULL	NULL	C/EBPdelta	GP		bind					HS3D	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31793_s_194	9395525	2 These results are now explained with the identification of C/EBPdelta as the nuclear protein binding to HS3D.	bind
37418	2	7133	6	13	NULL	NULL	NULL	C/EBPdelta	GP		is a type of					nuclear protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31793_s_194	9395525	2 These results are now explained with the identification of C/EBPdelta as the nuclear protein binding to HS3D.	bind
26584	1	7133	7	NULL	NULL	0	NULL	C/EBPdelta	NULL		bind	NULL				HS3D	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31793_s_194	9395525	2 These results are now explained with the identification of C/EBPdelta as the nuclear protein binding to HS3D.	bind
26585	2	7133	7	NULL	NULL	0	NULL	C/EBPdelta	NULL		is a type of	NULL				nuclear protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31793_s_194	9395525	2 These results are now explained with the identification of C/EBPdelta as the nuclear protein binding to HS3D.	bind
22523	1	7134	6	13	NULL	NULL	NULL	vinculin	GP		bind		may			beta-catenin	GP		vinculin binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_9078_s_202	9535896	2 These results raise the possibility that vinculin may bind beta-catenin with a lower affinity than does alpha-catenin or to a site on beta-catenin distinct from the alpha-catenin binding site that is sensitive to tyrosine phosphorylation.	bind
22524	2	7134	6	13	NULL	NULL	NULL	vinculin	GP		bind					beta-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_9078_s_202	9535896	2 These results raise the possibility that vinculin may bind beta-catenin with a lower affinity than does alpha-catenin or to a site on beta-catenin distinct from the alpha-catenin binding site that is sensitive to tyrosine phosphorylation.	bind
22525	3	7134	6	13	NULL	NULL	NULL	statement 1	Process		lower affinity than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_9078_s_202	9535896	2 These results raise the possibility that vinculin may bind beta-catenin with a lower affinity than does alpha-catenin or to a site on beta-catenin distinct from the alpha-catenin binding site that is sensitive to tyrosine phosphorylation.	bind
22526	4	7134	6	13	NULL	NULL	NULL	beta-catenin	GP		is sensitive to			vinculin binding site		phosphorylation	Process		tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_9078_s_202	9535896	2 These results raise the possibility that vinculin may bind beta-catenin with a lower affinity than does alpha-catenin or to a site on beta-catenin distinct from the alpha-catenin binding site that is sensitive to tyrosine phosphorylation.	bind
26586	1	7134	7	NULL	NULL	0	NULL	vinculin	NULL		bind	NULL	may			beta-catenin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_9078_s_202	9535896	2 These results raise the possibility that vinculin may bind beta-catenin with a lower affinity than does alpha-catenin or to a site on beta-catenin distinct from the alpha-catenin binding site that is sensitive to tyrosine phosphorylation.	bind
26587	2	7134	7	NULL	NULL	0	NULL	vinculin	NULL		bind	NULL				alpha-catenin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_15_9078_s_202	9535896	2 These results raise the possibility that vinculin may bind beta-catenin with a lower affinity than does alpha-catenin or to a site on beta-catenin distinct from the alpha-catenin binding site that is sensitive to tyrosine phosphorylation.	bind
26588	3	7134	7	10	NULL	0	NULL	statement 1	NULL		lower affinity than	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_9078_s_202	9535896	2 These results raise the possibility that vinculin may bind beta-catenin with a lower affinity than does alpha-catenin or to a site on beta-catenin distinct from the alpha-catenin binding site that is sensitive to tyrosine phosphorylation.	bind
26589	4	7134	7	NULL	NULL	0	NULL	statement 1	NULL		is distinct from	NULL		binding site of		statement 2	NULL		binding site of		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_9078_s_202	9535896	2 These results raise the possibility that vinculin may bind beta-catenin with a lower affinity than does alpha-catenin or to a site on beta-catenin distinct from the alpha-catenin binding site that is sensitive to tyrosine phosphorylation.	bind
26590	5	7134	7	NULL	NULL	0	NULL	beta-catenin	NULL		is sensitive to	NULL		binding site		tyrosine phosphorylation	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_9078_s_202	9535896	2 These results raise the possibility that vinculin may bind beta-catenin with a lower affinity than does alpha-catenin or to a site on beta-catenin distinct from the alpha-catenin binding site that is sensitive to tyrosine phosphorylation.	bind
22316	1	7136	6	13	NULL	NULL	NULL	MT1 MMP	GP	active	bind			deltaTM 		heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_2_871_s_321	9422744	2 This domain appears to be responsible for the binding of active deltaTM MT1 MMP to heparin.	bind
26591	1	7136	7	NULL	NULL	0	NULL	 MT1 MMP	NULL	active	bind	NULL		deltaTM		heparin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_2_871_s_321	9422744	2 This domain appears to be responsible for the binding of active deltaTM MT1 MMP to heparin.	bind
22317	1	7137	6	13	NULL	NULL	NULL	RIP140	GP		bind		efficiently			AhR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_32_22155_s_205	10428779	2 This is also consistent with the fact that RIP140 can bind efficiently to AhR without its LBD (Fig.  2).	bind
22318	2	7137	6	13	NULL	NULL	NULL	statement 1	Process		occur in the absence of					RIP140	GP		LBD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_32_22155_s_205	10428779	2 This is also consistent with the fact that RIP140 can bind efficiently to AhR without its LBD (Fig.  2).	bind
26592	1	7137	7	NULL	NULL	0	NULL	RIP140	NULL		bind	NULL	efficiently			AhR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_32_22155_s_205	10428779	2 This is also consistent with the fact that RIP140 can bind efficiently to AhR without its LBD (Fig.  2).	bind
26593	2	7137	7	NULL	NULL	0	NULL	statement 1	NULL		occur without	NULL				AhR	NULL		LBD		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_32_22155_s_205	10428779	2 This is also consistent with the fact that RIP140 can bind efficiently to AhR without its LBD (Fig.  2).	bind
22319	1	7138	6	13	NULL	NULL	NULL	gliotoxin	Chemical		bind		covalently						Cys-282		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_33_25202_s_164	10827185	2 This movement may be induced by covalent binding of gliotoxin to Cys-282.	bind
26594	1	7138	7	NULL	NULL	0	NULL	gliotoxin	NULL		bind	NULL	covalently				NULL		Cys-282		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_33_25202_s_164	10827185	2 This movement may be induced by covalent binding of gliotoxin to Cys-282.	bind
22320	1	7139	6	13	NULL	NULL	NULL	Sp1	GP		bind					E2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25976_s_202	9325332	2 This observation and the immunoprecipitation/Western blot data presented above suggest a model in which Sp1 and Sp3 bind E2 and Puralpha binds E1 with Sp1 participating in protein-protein interactions with both Sp3 and Puralpha (Fig.  6).	bind
22321	2	7139	6	13	NULL	NULL	NULL	Sp3	GP		bind					E2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25976_s_202	9325332	2 This observation and the immunoprecipitation/Western blot data presented above suggest a model in which Sp1 and Sp3 bind E2 and Puralpha binds E1 with Sp1 participating in protein-protein interactions with both Sp3 and Puralpha (Fig.  6).	bind
22322	3	7139	6	13	NULL	NULL	NULL	Puralpha	GP		bind					E1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25976_s_202	9325332	2 This observation and the immunoprecipitation/Western blot data presented above suggest a model in which Sp1 and Sp3 bind E2 and Puralpha binds E1 with Sp1 participating in protein-protein interactions with both Sp3 and Puralpha (Fig.  6).	bind
22527	4	7139	6	13	NULL	NULL	NULL	Sp1	GP		interacts with					Sp3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25976_s_202	9325332	2 This observation and the immunoprecipitation/Western blot data presented above suggest a model in which Sp1 and Sp3 bind E2 and Puralpha binds E1 with Sp1 participating in protein-protein interactions with both Sp3 and Puralpha (Fig.  6).	bind
22528	5	7139	6	13	NULL	NULL	NULL	Sp1	GP		interacts with					Puralpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25976_s_202	9325332	2 This observation and the immunoprecipitation/Western blot data presented above suggest a model in which Sp1 and Sp3 bind E2 and Puralpha binds E1 with Sp1 participating in protein-protein interactions with both Sp3 and Puralpha (Fig.  6).	bind
26595	1	7139	7	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				E2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_41_25976_s_202	9325332	2 This observation and the immunoprecipitation/Western blot data presented above suggest a model in which Sp1 and Sp3 bind E2 and Puralpha binds E1 with Sp1 participating in protein-protein interactions with both Sp3 and Puralpha (Fig.  6).	bind
26596	2	7139	7	NULL	NULL	0	NULL	Sp3	NULL		bind	NULL				E2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_41_25976_s_202	9325332	2 This observation and the immunoprecipitation/Western blot data presented above suggest a model in which Sp1 and Sp3 bind E2 and Puralpha binds E1 with Sp1 participating in protein-protein interactions with both Sp3 and Puralpha (Fig.  6).	bind
26597	3	7139	7	NULL	NULL	0	NULL	Puralpha	NULL		binds	NULL				E1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_41_25976_s_202	9325332	2 This observation and the immunoprecipitation/Western blot data presented above suggest a model in which Sp1 and Sp3 bind E2 and Puralpha binds E1 with Sp1 participating in protein-protein interactions with both Sp3 and Puralpha (Fig.  6).	bind
26598	4	7139	7	NULL	NULL	0	NULL	 Sp1	NULL		bind	NULL				Sp3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_41_25976_s_202	9325332	2 This observation and the immunoprecipitation/Western blot data presented above suggest a model in which Sp1 and Sp3 bind E2 and Puralpha binds E1 with Sp1 participating in protein-protein interactions with both Sp3 and Puralpha (Fig.  6).	bind
26599	5	7139	7	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				Puralpha	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_41_25976_s_202	9325332	2 This observation and the immunoprecipitation/Western blot data presented above suggest a model in which Sp1 and Sp3 bind E2 and Puralpha binds E1 with Sp1 participating in protein-protein interactions with both Sp3 and Puralpha (Fig.  6).	bind
22326	1	7140	6	13	NULL	NULL	NULL	GEF-H1	GP		bind					Rho	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34954_s_174	9857026	2 This observation can be rationalized by the fact that GEF-H1 binds to Rho and Rac independently of their nucleotide binding status (Fig.  6) and therefore remains bound to RhoA-GTP even after the GDP/GTP exchange is accomplished.	bind
22327	2	7140	6	13	NULL	NULL	NULL	GEF-H1	GP		bind					Rac	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34954_s_174	9857026	2 This observation can be rationalized by the fact that GEF-H1 binds to Rho and Rac independently of their nucleotide binding status (Fig.  6) and therefore remains bound to RhoA-GTP even after the GDP/GTP exchange is accomplished.	bind
22329	3	7140	6	13	NULL	NULL	NULL	statement 1	Process		is independent of					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34954_s_174	9857026	2 This observation can be rationalized by the fact that GEF-H1 binds to Rho and Rac independently of their nucleotide binding status (Fig.  6) and therefore remains bound to RhoA-GTP even after the GDP/GTP exchange is accomplished.	bind
22331	4	7140	6	13	NULL	NULL	NULL	statement 2	Process		is independent of					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34954_s_174	9857026	2 This observation can be rationalized by the fact that GEF-H1 binds to Rho and Rac independently of their nucleotide binding status (Fig.  6) and therefore remains bound to RhoA-GTP even after the GDP/GTP exchange is accomplished.	bind
22333	5	7140	6	13	NULL	NULL	NULL	GEF-H1	GP		bind					RhoA-GTP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34954_s_174	9857026	2 This observation can be rationalized by the fact that GEF-H1 binds to Rho and Rac independently of their nucleotide binding status (Fig.  6) and therefore remains bound to RhoA-GTP even after the GDP/GTP exchange is accomplished.	bind
22334	6	7140	6	13	NULL	NULL	NULL	statement 5	Process		occurs after					GDP/GTP 	Process	exchange of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34954_s_174	9857026	2 This observation can be rationalized by the fact that GEF-H1 binds to Rho and Rac independently of their nucleotide binding status (Fig.  6) and therefore remains bound to RhoA-GTP even after the GDP/GTP exchange is accomplished.	bind
55796	7	7140	6	13	NULL	NULL	NULL	Rho	GP		bind					nucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34954_s_174	9857026	2 This observation can be rationalized by the fact that GEF-H1 binds to Rho and Rac independently of their nucleotide binding status (Fig.  6) and therefore remains bound to RhoA-GTP even after the GDP/GTP exchange is accomplished.	bind
55797	8	7140	6	13	NULL	NULL	NULL	Rac	GP		bind					nucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34954_s_174	9857026	2 This observation can be rationalized by the fact that GEF-H1 binds to Rho and Rac independently of their nucleotide binding status (Fig.  6) and therefore remains bound to RhoA-GTP even after the GDP/GTP exchange is accomplished.	bind
26600	3	7140	7	NULL	NULL	0	NULL	GEF-H1			bind					Rho					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34954_s_174	9857026	2 This observation can be rationalized by the fact that GEF-H1 binds to Rho and Rac independently of their nucleotide binding status (Fig.  6) and therefore remains bound to RhoA-GTP even after the GDP/GTP exchange is accomplished.	bind
26601	4	7140	7	NULL	NULL	0	NULL	GEF-H1			bind					Rac					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34954_s_174	9857026	2 This observation can be rationalized by the fact that GEF-H1 binds to Rho and Rac independently of their nucleotide binding status (Fig.  6) and therefore remains bound to RhoA-GTP even after the GDP/GTP exchange is accomplished.	bind
26602	4	7140	7	NULL	NULL	0	NULL	statement 3			is independent of					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34954_s_174	9857026	2 This observation can be rationalized by the fact that GEF-H1 binds to Rho and Rac independently of their nucleotide binding status (Fig.  6) and therefore remains bound to RhoA-GTP even after the GDP/GTP exchange is accomplished.	bind
26603	6	7140	7	NULL	NULL	0	NULL	statement 4			is independent of					statement 2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34954_s_174	9857026	2 This observation can be rationalized by the fact that GEF-H1 binds to Rho and Rac independently of their nucleotide binding status (Fig.  6) and therefore remains bound to RhoA-GTP even after the GDP/GTP exchange is accomplished.	bind
26604	7	7140	7	NULL	NULL	0	NULL	GEF-H1			bind					RhoA-GTP					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34954_s_174	9857026	2 This observation can be rationalized by the fact that GEF-H1 binds to Rho and Rac independently of their nucleotide binding status (Fig.  6) and therefore remains bound to RhoA-GTP even after the GDP/GTP exchange is accomplished.	bind
26606	8	7140	7	NULL	NULL	0	NULL	statement 7			occurs after					GDP/GTP		exchange of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34954_s_174	9857026	2 This observation can be rationalized by the fact that GEF-H1 binds to Rho and Rac independently of their nucleotide binding status (Fig.  6) and therefore remains bound to RhoA-GTP even after the GDP/GTP exchange is accomplished.	bind
54626	1	7140	7	NULL	NULL	0	NULL	Rho			bind					nucleotide					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34954_s_174	9857026	2 This observation can be rationalized by the fact that GEF-H1 binds to Rho and Rac independently of their nucleotide binding status (Fig.  6) and therefore remains bound to RhoA-GTP even after the GDP/GTP exchange is accomplished.	bind
54627	2	7140	7	NULL	NULL	0	NULL	Rac			bind					nucleotide					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34954_s_174	9857026	2 This observation can be rationalized by the fact that GEF-H1 binds to Rho and Rac independently of their nucleotide binding status (Fig.  6) and therefore remains bound to RhoA-GTP even after the GDP/GTP exchange is accomplished.	bind
22529	1	7141	6	13	NULL	NULL	NULL	HSP70	GP		activates					TLR2 transfected cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_15107_s_186	11842086	2 This question needs to be addressed by analyzing whether inhibition of endocytosis differentially affects HSP70-driven activation of TLR2-transfected  versus TLR4 plus MD-2-transfected cells.	bind
22530	2	7141	6	13	NULL	NULL	NULL	HSP70	GP		activates					TLR4 plus MD-2-transfected cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_15107_s_186	11842086	2 This question needs to be addressed by analyzing whether inhibition of endocytosis differentially affects HSP70-driven activation of TLR2-transfected  versus TLR4 plus MD-2-transfected cells.	bind
26628	1	7141	7	NULL	NULL	0	NULL	HSP70	NULL		activates	NULL				TLR2-transfected cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_17_15107_s_186	11842086	2 This question needs to be addressed by analyzing whether inhibition of endocytosis differentially affects HSP70-driven activation of TLR2-transfected  versus TLR4 plus MD-2-transfected cells.	bind
26629	2	7141	7	NULL	NULL	0	NULL	HSP70	NULL		activates	NULL				TLR4 plus MD-2-transfected cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_15107_s_186	11842086	2 This question needs to be addressed by analyzing whether inhibition of endocytosis differentially affects HSP70-driven activation of TLR2-transfected  versus TLR4 plus MD-2-transfected cells.	bind
22373	1	7142	6	13	NULL	NULL	NULL	HDL	GP		bind		might;;directly			CD36	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_41_26338_s_124	9756864	2 This raised the possibility that, as is the case with the other well characterized class B scavenger receptor SR-BI, HDL might bind directly to CD36.	bind
22374	2	7142	6	13	NULL	NULL	NULL	SR-BI	GP		is a type of					class B scavenger receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_41_26338_s_124	9756864	2 This raised the possibility that, as is the case with the other well characterized class B scavenger receptor SR-BI, HDL might bind directly to CD36.	bind
37421	3	7142	6	13	NULL	NULL	NULL	SR-BI	GP		bind		directly			CD36	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_41_26338_s_124	9756864	2 This raised the possibility that, as is the case with the other well characterized class B scavenger receptor SR-BI, HDL might bind directly to CD36.	bind
26630	1	7142	7	NULL	NULL	0	NULL	SR-BI	NULL		bind	NULL	directly			CD36	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_41_26338_s_124	9756864	2 This raised the possibility that, as is the case with the other well characterized class B scavenger receptor SR-BI, HDL might bind directly to CD36.	bind
26631	2	7142	7	NULL	NULL	0	NULL	HDL	NULL		bind	NULL	might;;directly			CD36	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_41_26338_s_124	9756864	2 This raised the possibility that, as is the case with the other well characterized class B scavenger receptor SR-BI, HDL might bind directly to CD36.	bind
26632	3	7142	7	NULL	NULL	0	NULL	SR-BI	NULL		is a type of	NULL				class B scavenger receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_41_26338_s_124	9756864	2 This raised the possibility that, as is the case with the other well characterized class B scavenger receptor SR-BI, HDL might bind directly to CD36.	bind
22375	1	7143	6	13	NULL	NULL	NULL	CDH1 gene	GP		encode 				exon 6	NLS	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_14_12530_s_148	12560341	2 This raises the possibility that exons 6 and 7 of the  CDH1 gene could encode an NLS.	bind
22376	2	7143	6	13	NULL	NULL	NULL	CDH1 gene	GP		encode				exon 7	NLS	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_14_12530_s_148	12560341	2 This raises the possibility that exons 6 and 7 of the  CDH1 gene could encode an NLS.	bind
26633	1	7143	7	NULL	NULL	0	NULL	CDH1 gene	NULL		encode	NULL			exon 6	NLS	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_14_12530_s_148	12560341	2 This raises the possibility that exons 6 and 7 of the  CDH1 gene could encode an NLS.	bind
26634	2	7143	7	NULL	NULL	0	NULL	CDH1 gene	NULL		encode	NULL			exon 7	NLS	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_14_12530_s_148	12560341	2 This raises the possibility that exons 6 and 7 of the  CDH1 gene could encode an NLS.	bind
22377	1	7144	6	13	NULL	NULL	NULL	Cl	Chemical	oxygen-linked	bind					Hb	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39048_s_166	10984477	2 This Root effect fish Hb is fully responsive to phosphates but has a blocked alpha-N terminus and thus lacks one of the residues of importance in oxygen-linked Cl  binding to human Hb ( 52).	bind
22378	2	7144	6	13	NULL	NULL	NULL	Hb	GP	fish	is responsive to		fully			phosphates	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39048_s_166	10984477	2 This Root effect fish Hb is fully responsive to phosphates but has a blocked alpha-N terminus and thus lacks one of the residues of importance in oxygen-linked Cl  binding to human Hb ( 52).	bind
22379	3	7144	6	13	NULL	NULL	NULL	Hb	GP	fish	contains							blocked	alpha-N terminus		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39048_s_166	10984477	2 This Root effect fish Hb is fully responsive to phosphates but has a blocked alpha-N terminus and thus lacks one of the residues of importance in oxygen-linked Cl  binding to human Hb ( 52).	bind
26635	1	7144	7	NULL	NULL	0	NULL	 Cl	NULL	oxygen-linked	bind	NULL				Hb	NULL	human			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39048_s_166	10984477	2 This Root effect fish Hb is fully responsive to phosphates but has a blocked alpha-N terminus and thus lacks one of the residues of importance in oxygen-linked Cl  binding to human Hb ( 52).	bind
26636	2	7144	7	10	NULL	0	NULL	Hb	NULL	fish	is responsive to	NULL	fully			phosphates	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39048_s_166	10984477	2 This Root effect fish Hb is fully responsive to phosphates but has a blocked alpha-N terminus and thus lacks one of the residues of importance in oxygen-linked Cl  binding to human Hb ( 52).	bind
26637	3	7144	7	10	NULL	0	NULL	Hb	NULL	fish	contains	NULL					NULL	blocked	alpha-N terminus		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39048_s_166	10984477	2 This Root effect fish Hb is fully responsive to phosphates but has a blocked alpha-N terminus and thus lacks one of the residues of importance in oxygen-linked Cl  binding to human Hb ( 52).	bind
26638	4	7144	7	NULL	NULL	0	NULL	Hb	NULL	fish	lacks	NULL				statement 1	NULL	residues for			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39048_s_166	10984477	2 This Root effect fish Hb is fully responsive to phosphates but has a blocked alpha-N terminus and thus lacks one of the residues of importance in oxygen-linked Cl  binding to human Hb ( 52).	bind
22380	1	7145	6	13	NULL	NULL	NULL	IRS-1	GP		bind		might	Tyr- X-X-Met motifs		PI 3 kinase	GP				NULL	insulin sensitive tissues	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_45_28677_s_123	8910502	2 Thus in insulin-sensitive tissues, Tyr- X-X-Met motifs other than Tyr-460, -608, -939, and -987 of IRS-1 might bind and activate PI 3-kinase in response to insulin.	bind
22381	2	7145	6	13	NULL	NULL	NULL	statement 1	Process		activate		might			PI 3 kinase	GP				NULL	insulin sensitive tissues	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_45_28677_s_123	8910502	2 Thus in insulin-sensitive tissues, Tyr- X-X-Met motifs other than Tyr-460, -608, -939, and -987 of IRS-1 might bind and activate PI 3-kinase in response to insulin.	bind
22382	3	7145	6	13	NULL	NULL	NULL	statement 2	Process		occurs in response to					insulin	GP				NULL	insulin sensitive tissues	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_45_28677_s_123	8910502	2 Thus in insulin-sensitive tissues, Tyr- X-X-Met motifs other than Tyr-460, -608, -939, and -987 of IRS-1 might bind and activate PI 3-kinase in response to insulin.	bind
22383	4	7145	6	13	NULL	NULL	NULL	IRS-1	GP		does not bind			Tyr-460		PI 3 kinase	GP				NULL	insulin sensitive tissues	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_45_28677_s_123	8910502	2 Thus in insulin-sensitive tissues, Tyr- X-X-Met motifs other than Tyr-460, -608, -939, and -987 of IRS-1 might bind and activate PI 3-kinase in response to insulin.	bind
22384	5	7145	6	13	NULL	NULL	NULL	IRS-1	GP		does not bind			Tyr-608		PI 3 kinase	GP				NULL	insulin sensitive tissues	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_45_28677_s_123	8910502	2 Thus in insulin-sensitive tissues, Tyr- X-X-Met motifs other than Tyr-460, -608, -939, and -987 of IRS-1 might bind and activate PI 3-kinase in response to insulin.	bind
22385	6	7145	6	13	NULL	NULL	NULL	IRS-1	GP		does not bind			Tyr-939		PI 3 kinase	GP				NULL	insulin sensitive tissues	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_45_28677_s_123	8910502	2 Thus in insulin-sensitive tissues, Tyr- X-X-Met motifs other than Tyr-460, -608, -939, and -987 of IRS-1 might bind and activate PI 3-kinase in response to insulin.	bind
22386	7	7145	6	13	NULL	NULL	NULL	IRS-1	GP		does not bind			Tyr-987		PI 3 kinase	GP				NULL	insulin sensitive tissues	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_45_28677_s_123	8910502	2 Thus in insulin-sensitive tissues, Tyr- X-X-Met motifs other than Tyr-460, -608, -939, and -987 of IRS-1 might bind and activate PI 3-kinase in response to insulin.	bind
26639	1	7145	7	10	NULL	0	NULL	IRS-1	NULL		bind	NULL	might	Tyr- X-X-Met motif		PI 3-kinase	NULL				NULL	insulin-sensitive tissues	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_45_28677_s_123	8910502	2 Thus in insulin-sensitive tissues, Tyr- X-X-Met motifs other than Tyr-460, -608, -939, and -987 of IRS-1 might bind and activate PI 3-kinase in response to insulin.	bind
26646	2	7145	7	10	NULL	0	NULL	statement 1	NULL		activate	NULL	might			PI 3-kinase	NULL				NULL	insulin-sensitive tissues	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_45_28677_s_123	8910502	2 Thus in insulin-sensitive tissues, Tyr- X-X-Met motifs other than Tyr-460, -608, -939, and -987 of IRS-1 might bind and activate PI 3-kinase in response to insulin.	bind
26650	3	7145	7	NULL	NULL	0	NULL	IRS-1	NULL		does not bind	NULL		 Tyr-460		PI 3-kinase	NULL				NULL	insulin-sensitive tissues	0	NULL	NULL	NULL	gw60_jbiolchem_271_45_28677_s_123	8910502	2 Thus in insulin-sensitive tissues, Tyr- X-X-Met motifs other than Tyr-460, -608, -939, and -987 of IRS-1 might bind and activate PI 3-kinase in response to insulin.	bind
26663	4	7145	7	NULL	NULL	0	NULL	 IRS-1 	NULL		does not bind	NULL		Tyr-608		PI 3-kinase	NULL				NULL	 insulin-sensitive tissues	0	NULL	NULL	NULL	gw60_jbiolchem_271_45_28677_s_123	8910502	2 Thus in insulin-sensitive tissues, Tyr- X-X-Met motifs other than Tyr-460, -608, -939, and -987 of IRS-1 might bind and activate PI 3-kinase in response to insulin.	bind
26669	5	7145	7	NULL	NULL	0	NULL	IRS-1	NULL		does not bind	NULL		Tyr-939		PI 3-kinase	NULL				NULL	insulin-sensitive tissues	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_45_28677_s_123	8910502	2 Thus in insulin-sensitive tissues, Tyr- X-X-Met motifs other than Tyr-460, -608, -939, and -987 of IRS-1 might bind and activate PI 3-kinase in response to insulin.	bind
26671	6	7145	7	NULL	NULL	0	NULL	IRS-1	NULL		does not bind	NULL		Tyr-987		PI 3-kinase	NULL				NULL	insulin-sensitive tissues	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_45_28677_s_123	8910502	2 Thus in insulin-sensitive tissues, Tyr- X-X-Met motifs other than Tyr-460, -608, -939, and -987 of IRS-1 might bind and activate PI 3-kinase in response to insulin.	bind
26673	7	7145	7	NULL	NULL	0	NULL	statement 2	NULL		occurs in response to	NULL				insulin	NULL				NULL	insulin-sensitive tissues	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_45_28677_s_123	8910502	2 Thus in insulin-sensitive tissues, Tyr- X-X-Met motifs other than Tyr-460, -608, -939, and -987 of IRS-1 might bind and activate PI 3-kinase in response to insulin.	bind
22387	1	7146	6	13	NULL	NULL	NULL	Bud6	GP		stimulates					formin	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28023_s_276	15923184	2 Thus, all detectable binding and stimulation of formin activity by Bud6 is specific to Bni1 and not Bnr1.	bind
22388	2	7146	6	13	NULL	NULL	NULL	statement 1	Process		is specific to					Bni1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28023_s_276	15923184	2 Thus, all detectable binding and stimulation of formin activity by Bud6 is specific to Bni1 and not Bnr1.	bind
22389	3	7146	6	13	NULL	NULL	NULL	statement 1	Process		is not specific to					Bnr1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28023_s_276	15923184	2 Thus, all detectable binding and stimulation of formin activity by Bud6 is specific to Bni1 and not Bnr1.	bind
26686	1	7146	7	NULL	NULL	0	NULL	Bud6	NULL		stimulates	NULL				formin	NULL	activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_30_28023_s_276	15923184	2 Thus, all detectable binding and stimulation of formin activity by Bud6 is specific to Bni1 and not Bnr1.	bind
26687	2	7146	7	10	NULL	0	NULL	statement 1			is specific to					Bni1					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28023_s_276	15923184	2 Thus, all detectable binding and stimulation of formin activity by Bud6 is specific to Bni1 and not Bnr1.	bind
26688	3	7146	7	NULL	NULL	0	NULL	statement 1	NULL		is not specific to	NULL				Bnr1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_30_28023_s_276	15923184	2 Thus, all detectable binding and stimulation of formin activity by Bud6 is specific to Bni1 and not Bnr1.	bind
22390	1	7147	6	13	NULL	NULL	NULL	HNF4	GP		bind								HNF4 binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_30_19339_s_41	9668124	2 Thus, although some of our results agreed with that reported by Waltz  et al. ( 17), we could not explain tissue-specific expression of MSP mRNA simply by the binding of HNF-4 to the previously reported HNF-4-binding site.	bind
22391	2	7147	6	13	NULL	NULL	NULL	MSP mRNA	NucleicAcid		is specific to					tissue	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_30_19339_s_41	9668124	2 Thus, although some of our results agreed with that reported by Waltz  et al. ( 17), we could not explain tissue-specific expression of MSP mRNA simply by the binding of HNF-4 to the previously reported HNF-4-binding site.	bind
26689	1	7147	7	NULL	NULL	0	NULL	HNF-4 	NULL		bind	NULL					NULL		HNF-4-binding site		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_30_19339_s_41	9668124	2 Thus, although some of our results agreed with that reported by Waltz  et al. ( 17), we could not explain tissue-specific expression of MSP mRNA simply by the binding of HNF-4 to the previously reported HNF-4-binding site.	bind
37491	2	7147	7	NULL	NULL	0	NULL	MSP mRNA	NULL		is specific to	NULL				tissue	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_30_19339_s_41	9668124	2 Thus, although some of our results agreed with that reported by Waltz  et al. ( 17), we could not explain tissue-specific expression of MSP mRNA simply by the binding of HNF-4 to the previously reported HNF-4-binding site.	bind
22392	1	7148	6	13	NULL	NULL	NULL	RecA protein	GP		bind		directly			dsDNA substrate	NucleicAcid	linear			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_17_11063_s_132	9111000	2 Thus, any effect of direct RecA protein binding to the linear dsDNA substrate (prior to its involvement in DNA strand exchange) can be neglected on the time scale used in these reactions.	bind
22393	2	7148	6	13	NULL	NULL	NULL	RecA protein	GP		is involved in					DNA strand exchange	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_17_11063_s_132	9111000	2 Thus, any effect of direct RecA protein binding to the linear dsDNA substrate (prior to its involvement in DNA strand exchange) can be neglected on the time scale used in these reactions.	bind
26690	1	7148	7	NULL	NULL	0	NULL	RecA protein	NULL		bind	NULL	directly			dsDNA substrate	NULL	linear			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_17_11063_s_132	9111000	2 Thus, any effect of direct RecA protein binding to the linear dsDNA substrate (prior to its involvement in DNA strand exchange) can be neglected on the time scale used in these reactions.	bind
37492	2	7148	7	NULL	NULL	0	NULL	RecA protein	NULL		is involved in	NULL				DNA strand exchange	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_17_11063_s_132	9111000	2 Thus, any effect of direct RecA protein binding to the linear dsDNA substrate (prior to its involvement in DNA strand exchange) can be neglected on the time scale used in these reactions.	bind
22394	1	7149	6	13	NULL	NULL	NULL	MEKK1	GP		bind		stably			GCK	GP	free	CTD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_35_22681_s_205	9712898	2 Thus, MEKK1 binds most stably to the free GCK-CTD; binding of GCK to full-length GCK, while detectable, is less avid, and kinase-inactive GCK binds MEKK1 less stably than does wild type GCK.	bind
22395	2	7149	6	13	NULL	NULL	NULL	GCK	GP		bind					GCK	GP	full length			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_35_22681_s_205	9712898	2 Thus, MEKK1 binds most stably to the free GCK-CTD; binding of GCK to full-length GCK, while detectable, is less avid, and kinase-inactive GCK binds MEKK1 less stably than does wild type GCK.	bind
22396	3	7149	6	13	NULL	NULL	NULL	GCK	GP	kinase inactive	bind					MEKK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_35_22681_s_205	9712898	2 Thus, MEKK1 binds most stably to the free GCK-CTD; binding of GCK to full-length GCK, while detectable, is less avid, and kinase-inactive GCK binds MEKK1 less stably than does wild type GCK.	bind
22397	4	7149	6	13	NULL	NULL	NULL	statement 3	Process		is less stable than					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_35_22681_s_205	9712898	2 Thus, MEKK1 binds most stably to the free GCK-CTD; binding of GCK to full-length GCK, while detectable, is less avid, and kinase-inactive GCK binds MEKK1 less stably than does wild type GCK.	bind
37424	5	7149	6	13	NULL	NULL	NULL	GCK	GP	wild type	bind					MEKK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_35_22681_s_205	9712898	2 Thus, MEKK1 binds most stably to the free GCK-CTD; binding of GCK to full-length GCK, while detectable, is less avid, and kinase-inactive GCK binds MEKK1 less stably than does wild type GCK.	bind
26691	1	7149	7	NULL	NULL	0	NULL	MEKK1	NULL		bind	NULL	stably			GCK	NULL	free	CTD		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22681_s_205	9712898	2 Thus, MEKK1 binds most stably to the free GCK-CTD; binding of GCK to full-length GCK, while detectable, is less avid, and kinase-inactive GCK binds MEKK1 less stably than does wild type GCK.	bind
26692	2	7149	7	NULL	NULL	0	NULL	GCK 	NULL		bind	NULL				GCK	NULL	full-length			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22681_s_205	9712898	2 Thus, MEKK1 binds most stably to the free GCK-CTD; binding of GCK to full-length GCK, while detectable, is less avid, and kinase-inactive GCK binds MEKK1 less stably than does wild type GCK.	bind
26693	3	7149	7	NULL	NULL	0	NULL	GCK	NULL	kinase-inactive	binds	NULL				MEKK1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22681_s_205	9712898	2 Thus, MEKK1 binds most stably to the free GCK-CTD; binding of GCK to full-length GCK, while detectable, is less avid, and kinase-inactive GCK binds MEKK1 less stably than does wild type GCK.	bind
26694	4	7149	7	NULL	NULL	0	NULL	GCK	NULL	wild type	binds	NULL				MEKK1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22681_s_205	9712898	2 Thus, MEKK1 binds most stably to the free GCK-CTD; binding of GCK to full-length GCK, while detectable, is less avid, and kinase-inactive GCK binds MEKK1 less stably than does wild type GCK.	bind
26695	5	7149	7	10	NULL	0	NULL	statement 3	NULL		 less stable than	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_35_22681_s_205	9712898	2 Thus, MEKK1 binds most stably to the free GCK-CTD; binding of GCK to full-length GCK, while detectable, is less avid, and kinase-inactive GCK binds MEKK1 less stably than does wild type GCK.	bind
22398	1	7150	6	13	NULL	NULL	NULL	decorin	GP		bind					collagen type I	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_29_18404_s_132	9218483	2 Thus, primarily ionic interactions appear to be responsible for the binding between decorin and type I collagen.	bind
22399	2	7150	6	13	NULL	NULL	NULL	ionic interactions	Process		is responsible for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_29_18404_s_132	9218483	2 Thus, primarily ionic interactions appear to be responsible for the binding between decorin and type I collagen.	bind
26696	1	7150	7	NULL	NULL	0	NULL	decorin	NULL		bind	NULL				type I collagen	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_29_18404_s_132	9218483	2 Thus, primarily ionic interactions appear to be responsible for the binding between decorin and type I collagen.	bind
26697	2	7150	7	NULL	NULL	0	NULL	ionic interactions	NULL		is responsible for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_29_18404_s_132	9218483	2 Thus, primarily ionic interactions appear to be responsible for the binding between decorin and type I collagen.	bind
22400	1	7151	6	13	NULL	NULL	NULL	Tat	GP		interacts with					microtubules	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_46_48197_s_275	15331610	2 Thus, the difference in the speed of apoptosis could be due to the efficiency with which Tat interacts with microtubules, and the  in vitro data presented here show that Ug05RP bound to tubulin with a higher affinity compared with Ug11LTS.	bind
22401	2	7151	6	13	NULL	NULL	NULL	Ug05RP	GP		bind					tubulin	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_46_48197_s_275	15331610	2 Thus, the difference in the speed of apoptosis could be due to the efficiency with which Tat interacts with microtubules, and the  in vitro data presented here show that Ug05RP bound to tubulin with a higher affinity compared with Ug11LTS.	bind
22402	3	7151	6	13	NULL	NULL	NULL	Ug11LTS	GP		bind					tubulin	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_46_48197_s_275	15331610	2 Thus, the difference in the speed of apoptosis could be due to the efficiency with which Tat interacts with microtubules, and the  in vitro data presented here show that Ug05RP bound to tubulin with a higher affinity compared with Ug11LTS.	bind
22403	4	7151	6	13	NULL	NULL	NULL	statement 2	Process		is higher than					statement 3	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_46_48197_s_275	15331610	2 Thus, the difference in the speed of apoptosis could be due to the efficiency with which Tat interacts with microtubules, and the  in vitro data presented here show that Ug05RP bound to tubulin with a higher affinity compared with Ug11LTS.	bind
22404	5	7151	6	13	NULL	NULL	NULL	statement 1	Process	efficiency of	change					apoptosis	Process	speed of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_46_48197_s_275	15331610	2 Thus, the difference in the speed of apoptosis could be due to the efficiency with which Tat interacts with microtubules, and the  in vitro data presented here show that Ug05RP bound to tubulin with a higher affinity compared with Ug11LTS.	bind
26698	1	7151	7	NULL	NULL	0	NULL	Tat	NULL		interacts with	NULL				microtubules	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_46_48197_s_275	15331610	2 Thus, the difference in the speed of apoptosis could be due to the efficiency with which Tat interacts with microtubules, and the  in vitro data presented here show that Ug05RP bound to tubulin with a higher affinity compared with Ug11LTS.	bind
26699	2	7151	7	NULL	NULL	0	NULL	Ug05RP	NULL		bind	NULL	high affinity			tubulin	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_46_48197_s_275	15331610	2 Thus, the difference in the speed of apoptosis could be due to the efficiency with which Tat interacts with microtubules, and the  in vitro data presented here show that Ug05RP bound to tubulin with a higher affinity compared with Ug11LTS.	bind
26700	3	7151	7	NULL	NULL	0	NULL	Ug11LTS	NULL		bind	NULL				tubulin	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_46_48197_s_275	15331610	2 Thus, the difference in the speed of apoptosis could be due to the efficiency with which Tat interacts with microtubules, and the  in vitro data presented here show that Ug05RP bound to tubulin with a higher affinity compared with Ug11LTS.	bind
26701	4	7151	7	10	NULL	0	NULL	statement 2	NULL		is higher than	NULL				statement 3	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_46_48197_s_275	15331610	2 Thus, the difference in the speed of apoptosis could be due to the efficiency with which Tat interacts with microtubules, and the  in vitro data presented here show that Ug05RP bound to tubulin with a higher affinity compared with Ug11LTS.	bind
37493	5	7151	7	NULL	NULL	0	NULL	statement 1	NULL	efficiency of	change	NULL				apoptosis	NULL	speed of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_46_48197_s_275	15331610	2 Thus, the difference in the speed of apoptosis could be due to the efficiency with which Tat interacts with microtubules, and the  in vitro data presented here show that Ug05RP bound to tubulin with a higher affinity compared with Ug11LTS.	bind
22405	1	7152	6	13	NULL	NULL	NULL	megalin	GP		bind					Tg	GP	intact			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_43_30377_s_356	10521414	2 Thus, the inhibition produced by the antibody against Tg peptide 1 on megalin binding to intact Tg may be explained by a steric effect.	bind
22406	2	7152	6	13	NULL	NULL	NULL	Tg peptide 1 antibody	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_43_30377_s_356	10521414	2 Thus, the inhibition produced by the antibody against Tg peptide 1 on megalin binding to intact Tg may be explained by a steric effect.	bind
37425	3	7152	6	13	NULL	NULL	NULL	steric effect	Process		cause		may			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_43_30377_s_356	10521414	2 Thus, the inhibition produced by the antibody against Tg peptide 1 on megalin binding to intact Tg may be explained by a steric effect.	bind
26702	1	7152	7	NULL	NULL	0	NULL	 megalin	NULL		bind	NULL				Tg	NULL	intact			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_43_30377_s_356	10521414	2 Thus, the inhibition produced by the antibody against Tg peptide 1 on megalin binding to intact Tg may be explained by a steric effect.	bind
26703	2	7152	7	NULL	NULL	0	NULL	Tg peptide 1 antibody	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_43_30377_s_356	10521414	2 Thus, the inhibition produced by the antibody against Tg peptide 1 on megalin binding to intact Tg may be explained by a steric effect.	bind
26704	3	7152	7	NULL	NULL	0	NULL	steric effect	NULL		cause	NULL	may			statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_43_30377_s_356	10521414	2 Thus, the inhibition produced by the antibody against Tg peptide 1 on megalin binding to intact Tg may be explained by a steric effect.	bind
22407	1	7153	6	13	NULL	NULL	NULL	ConA	GP		bind					insulin receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_12_7833_s_218	9065448	2 Thus, the stimulation of ALPase is not mediated by the binding of ConA to insulin receptors.	bind
22408	2	7153	6	13	NULL	NULL	NULL	ALPase	GP	stimulation of	is not mediated by					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_12_7833_s_218	9065448	2 Thus, the stimulation of ALPase is not mediated by the binding of ConA to insulin receptors.	bind
26705	1	7153	7	NULL	NULL	0	NULL	ConA	NULL		bind	NULL				insulin receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_12_7833_s_218	9065448	2 Thus, the stimulation of ALPase is not mediated by the binding of ConA to insulin receptors.	bind
26706	2	7153	7	NULL	NULL	0	NULL	statement 1	NULL		does not mediate	NULL				ALPase	NULL	stimulation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_12_7833_s_218	9065448	2 Thus, the stimulation of ALPase is not mediated by the binding of ConA to insulin receptors.	bind
22409	1	7154	6	13	NULL	NULL	NULL	CtBP	GP		bind					nNOS	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_51_48262_s_232	11590170	2 Thus, we believe that the binding of CtBP to nNOS plays a role in protein localization rather than regulation of enzymatic activity, suggesting a novel role for nNOS as a targeting molecule.	bind
22410	2	7154	6	13	NULL	NULL	NULL	statement 1	Process		plays a role in					protein localization	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_51_48262_s_232	11590170	2 Thus, we believe that the binding of CtBP to nNOS plays a role in protein localization rather than regulation of enzymatic activity, suggesting a novel role for nNOS as a targeting molecule.	bind
22411	3	7154	6	13	NULL	NULL	NULL	statement 1	Process		does not play a role in					enzymatic activity	Process	regulation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_51_48262_s_232	11590170	2 Thus, we believe that the binding of CtBP to nNOS plays a role in protein localization rather than regulation of enzymatic activity, suggesting a novel role for nNOS as a targeting molecule.	bind
22412	4	7154	6	13	NULL	NULL	NULL	nNOS	GP		acts as a 					targeting molecule	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_51_48262_s_232	11590170	2 Thus, we believe that the binding of CtBP to nNOS plays a role in protein localization rather than regulation of enzymatic activity, suggesting a novel role for nNOS as a targeting molecule.	bind
26707	1	7154	7	NULL	NULL	0	NULL	CtBP	NULL		bind	NULL				nNOS	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_48262_s_232	11590170	2 Thus, we believe that the binding of CtBP to nNOS plays a role in protein localization rather than regulation of enzymatic activity, suggesting a novel role for nNOS as a targeting molecule.	bind
26708	2	7154	7	NULL	NULL	0	NULL	statement 1	NULL		plays a role in	NULL				protein localization	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_48262_s_232	11590170	2 Thus, we believe that the binding of CtBP to nNOS plays a role in protein localization rather than regulation of enzymatic activity, suggesting a novel role for nNOS as a targeting molecule.	bind
53360	3	7154	7	10	NULL	0	NULL	statement 1	NULL		does not play a role in	NULL				enzymatic activity	NULL	regulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_48262_s_232	11590170	2 Thus, we believe that the binding of CtBP to nNOS plays a role in protein localization rather than regulation of enzymatic activity, suggesting a novel role for nNOS as a targeting molecule.	bind
53361	4	7154	7	10	NULL	0	NULL	nNOS	NULL		acts as	NULL				targeting molecule	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_48262_s_232	11590170	2 Thus, we believe that the binding of CtBP to nNOS plays a role in protein localization rather than regulation of enzymatic activity, suggesting a novel role for nNOS as a targeting molecule.	bind
22413	1	7155	6	13	NULL	NULL	NULL	TM	GP		bind					thrombin	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_1_41_s_20	12522119	2 TM binds thrombin and alters its active site specificity to facilitate proteolytic activation of protein C, a potent inhibitor of the coagulation cascade.	bind
22414	3	7155	6	13	NULL	NULL	NULL	statement 2	Process		facilitates					protein C	GP	proteolytic activation of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_1_41_s_20	12522119	2 TM binds thrombin and alters its active site specificity to facilitate proteolytic activation of protein C, a potent inhibitor of the coagulation cascade.	bind
22415	4	7155	6	13	NULL	NULL	NULL	Protein C	GP		is an inhibitor of		potent			coagulation cascade	Process	inhibitor of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_1_41_s_20	12522119	2 TM binds thrombin and alters its active site specificity to facilitate proteolytic activation of protein C, a potent inhibitor of the coagulation cascade.	bind
22416	2	7155	6	13	NULL	NULL	NULL	statement 1	Process		alters					thrombin	GP	specificity of 	active site		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_1_41_s_20	12522119	2 TM binds thrombin and alters its active site specificity to facilitate proteolytic activation of protein C, a potent inhibitor of the coagulation cascade.	bind
26713	1	7155	7	NULL	NULL	0	NULL	TM	NULL		binds	NULL				thrombin	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_92_1_41_s_20	12522119	2 TM binds thrombin and alters its active site specificity to facilitate proteolytic activation of protein C, a potent inhibitor of the coagulation cascade.	bind
26716	2	7155	7	NULL	NULL	0	NULL	statement 1	NULL		alter	NULL				thrombin	NULL	specificity of	active site		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_1_41_s_20	12522119	2 TM binds thrombin and alters its active site specificity to facilitate proteolytic activation of protein C, a potent inhibitor of the coagulation cascade.	bind
26718	3	7155	7	NULL	NULL	0	NULL	statement 2	NULL		facilitate	NULL				protein C	NULL	proteolytic activation of			NULL		0	NULL	NULL	NULL	gw70_circulationres_92_1_41_s_20	12522119	2 TM binds thrombin and alters its active site specificity to facilitate proteolytic activation of protein C, a potent inhibitor of the coagulation cascade.	bind
26721	4	7155	7	10	NULL	0	NULL	protein C	NULL		is an inhibitor of	NULL	potent			coagulation cascade	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_1_41_s_20	12522119	2 TM binds thrombin and alters its active site specificity to facilitate proteolytic activation of protein C, a potent inhibitor of the coagulation cascade.	bind
22417	1	7156	6	13	NULL	NULL	NULL	rHSF-1	GP		bind					IL1B	GP			promoter fragments	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_40_24874_s_34	8926278	2 To analyze the binding of rHSF-1 to  IL1B promoter fragments, probes were labeled by end filling with Klenow fragment using [32]dCTP at 6,000 Ci/mmol (DuPont NEN) to an activity of 100,000 cpm/ng and incubated (0.2 ng each) with rHSF-1 (0.7 mug), poly(DI.	bind
26722	1	7156	7	10	NULL	0	NULL	rHSF-1	NULL		bind	NULL				IL1B	NULL			promoter fragments	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_40_24874_s_34	8926278	2 To analyze the binding of rHSF-1 to  IL1B promoter fragments, probes were labeled by end filling with Klenow fragment using [32]dCTP at 6,000 Ci/mmol (DuPont NEN) to an activity of 100,000 cpm/ng and incubated (0.2 ng each) with rHSF-1 (0.7 mug), poly(DI.	bind
22418	1	7157	6	13	NULL	NULL	NULL	CB1	GP		bind					His6-sCD4	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_508_1_67_s_168	11707270	2 to displace the binding of PDPs CB1 and CB8 to His6-sCD4 was studied by using an ELISA inhibition assay.	bind
22419	2	7157	6	13	NULL	NULL	NULL	CB8	GP		bind					His6-sCD4	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_508_1_67_s_168	11707270	2 to displace the binding of PDPs CB1 and CB8 to His6-sCD4 was studied by using an ELISA inhibition assay.	bind
37426	3	7157	6	13	NULL	NULL	NULL	CB1	GP		is a type of					PDP	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_508_1_67_s_168	11707270	2 to displace the binding of PDPs CB1 and CB8 to His6-sCD4 was studied by using an ELISA inhibition assay.	bind
37427	4	7157	6	13	NULL	NULL	NULL	CB8	GP		is a type of					PDP	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_508_1_67_s_168	11707270	2 to displace the binding of PDPs CB1 and CB8 to His6-sCD4 was studied by using an ELISA inhibition assay.	bind
26723	1	7157	7	NULL	NULL	0	NULL	 CB1	NULL		bind	NULL				His6-sCD4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_508_1_67_s_168	11707270	2 to displace the binding of PDPs CB1 and CB8 to His6-sCD4 was studied by using an ELISA inhibition assay.	bind
26725	2	7157	7	NULL	NULL	0	NULL	 CB8	NULL		bind	NULL				His6-sCD4 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_508_1_67_s_168	11707270	2 to displace the binding of PDPs CB1 and CB8 to His6-sCD4 was studied by using an ELISA inhibition assay.	bind
37494	3	7157	7	NULL	NULL	0	NULL	CB1	NULL		is a type of	NULL				PDPs	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_508_1_67_s_168	11707270	2 to displace the binding of PDPs CB1 and CB8 to His6-sCD4 was studied by using an ELISA inhibition assay.	bind
37495	4	7157	7	NULL	NULL	0	NULL	CB8	NULL		is a type of	NULL				PDPs	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_508_1_67_s_168	11707270	2 to displace the binding of PDPs CB1 and CB8 to His6-sCD4 was studied by using an ELISA inhibition assay.	bind
22420	1	7159	6	13	NULL	NULL	NULL	integrin	GP		mediates					Raf-1	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27268_s_69	9765250	2 To more directly address the question of whether interaction with Ras is required for integrin-mediated activation of Raf-1, cells were transiently transfected with plasmids encoding either wild-type Raf (Raf-WT) or a mutant allele containing an arginine to leucine substitution at position 89, within the Ras binding domain (Raf-R89L) ( 25).	bind
26729	1	7159	7	NULL	NULL	0	NULL	 integrin	NULL		mediates	NULL				Raf-1	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27268_s_69	9765250	2 To more directly address the question of whether interaction with Ras is required for integrin-mediated activation of Raf-1, cells were transiently transfected with plasmids encoding either wild-type Raf (Raf-WT) or a mutant allele containing an arginine to leucine substitution at position 89, within the Ras binding domain (Raf-R89L) ( 25).	bind
22421	1	7160	6	13	NULL	NULL	NULL	TRP	GP		does not bind					DNA	NucleicAcid			TATA	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_122_s_239	10617594	2 TRP does not bind to TATA-DNA but does interact with general transcription factors TFIIA and TFIIB.	bind
22422	2	7160	6	13	NULL	NULL	NULL	TRP	GP		interacts with					TFIIA 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_122_s_239	10617594	2 TRP does not bind to TATA-DNA but does interact with general transcription factors TFIIA and TFIIB.	bind
22423	3	7160	6	13	NULL	NULL	NULL	TRP	GP		interacts with					TFIIB	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_122_s_239	10617594	2 TRP does not bind to TATA-DNA but does interact with general transcription factors TFIIA and TFIIB.	bind
37428	4	7160	6	13	NULL	NULL	NULL	TFIIA	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_122_s_239	10617594	2 TRP does not bind to TATA-DNA but does interact with general transcription factors TFIIA and TFIIB.	bind
37429	5	7160	6	13	NULL	NULL	NULL	TFIIB	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_122_s_239	10617594	2 TRP does not bind to TATA-DNA but does interact with general transcription factors TFIIA and TFIIB.	bind
26731	1	7160	7	NULL	NULL	0	NULL	TRP	NULL		does not bind	NULL				 DNA	NULL			TATA	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_1_122_s_239	10617594	2 TRP does not bind to TATA-DNA but does interact with general transcription factors TFIIA and TFIIB.	bind
26732	2	7160	7	NULL	NULL	0	NULL	TRP	NULL		interacts with	NULL				TFIIA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_1_122_s_239	10617594	2 TRP does not bind to TATA-DNA but does interact with general transcription factors TFIIA and TFIIB.	bind
26733	3	7160	7	NULL	NULL	0	NULL	TRP	NULL		interacts with	NULL				TFIIB	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_1_122_s_239	10617594	2 TRP does not bind to TATA-DNA but does interact with general transcription factors TFIIA and TFIIB.	bind
26734	4	7160	7	NULL	NULL	0	NULL	TFIIA	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_1_122_s_239	10617594	2 TRP does not bind to TATA-DNA but does interact with general transcription factors TFIIA and TFIIB.	bind
26735	5	7160	7	NULL	NULL	0	NULL	TFIIB	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_1_122_s_239	10617594	2 TRP does not bind to TATA-DNA but does interact with general transcription factors TFIIA and TFIIB.	bind
22424	1	7161	6	13	NULL	NULL	NULL	GDP	Chemical		bind					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_8_4392_s_26	9468490	2 Two GAPs, NF1 and RasGAP, form stable complexes with the GDP-bound form of Ras in the presence of aluminum fluoride, indicating that it also mimics the transition state of GTP hydrolysis in low molecular weight GTP-binding proteins.	bind
22425	2	7161	6	13	NULL	NULL	NULL	NF1	GP		form stable complex with					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_8_4392_s_26	9468490	2 Two GAPs, NF1 and RasGAP, form stable complexes with the GDP-bound form of Ras in the presence of aluminum fluoride, indicating that it also mimics the transition state of GTP hydrolysis in low molecular weight GTP-binding proteins.	bind
22426	3	7161	6	13	NULL	NULL	NULL	RasGAP	GP		form stable complex with					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_8_4392_s_26	9468490	2 Two GAPs, NF1 and RasGAP, form stable complexes with the GDP-bound form of Ras in the presence of aluminum fluoride, indicating that it also mimics the transition state of GTP hydrolysis in low molecular weight GTP-binding proteins.	bind
22427	4	7161	6	13	NULL	NULL	NULL	statement 2	Process		occurs in presence of					aluminium fluoride	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_8_4392_s_26	9468490	2 Two GAPs, NF1 and RasGAP, form stable complexes with the GDP-bound form of Ras in the presence of aluminum fluoride, indicating that it also mimics the transition state of GTP hydrolysis in low molecular weight GTP-binding proteins.	bind
22428	5	7161	6	13	NULL	NULL	NULL	statement 3	Process		occurs in presence of					aluminium fluoride	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_8_4392_s_26	9468490	2 Two GAPs, NF1 and RasGAP, form stable complexes with the GDP-bound form of Ras in the presence of aluminum fluoride, indicating that it also mimics the transition state of GTP hydrolysis in low molecular weight GTP-binding proteins.	bind
26920	1	7161	7	10	NULL	0	NULL	NF1	NULL		forms stable complex with	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_8_4392_s_26	9468490	2 Two GAPs, NF1 and RasGAP, form stable complexes with the GDP-bound form of Ras in the presence of aluminum fluoride, indicating that it also mimics the transition state of GTP hydrolysis in low molecular weight GTP-binding proteins.	bind
26921	2	7161	7	NULL	NULL	0	NULL	RasGAP	NULL		forms stable complex with	NULL				GDP-bound Ras	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_8_4392_s_26	9468490	2 Two GAPs, NF1 and RasGAP, form stable complexes with the GDP-bound form of Ras in the presence of aluminum fluoride, indicating that it also mimics the transition state of GTP hydrolysis in low molecular weight GTP-binding proteins.	bind
26922	3	7161	7	NULL	NULL	0	NULL	statement 1	NULL		in presence of	NULL				aluminum fluoride	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_8_4392_s_26	9468490	2 Two GAPs, NF1 and RasGAP, form stable complexes with the GDP-bound form of Ras in the presence of aluminum fluoride, indicating that it also mimics the transition state of GTP hydrolysis in low molecular weight GTP-binding proteins.	bind
26923	4	7161	7	NULL	NULL	0	NULL	statement 2	NULL		in presence of	NULL				aluminum fluoride	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_8_4392_s_26	9468490	2 Two GAPs, NF1 and RasGAP, form stable complexes with the GDP-bound form of Ras in the presence of aluminum fluoride, indicating that it also mimics the transition state of GTP hydrolysis in low molecular weight GTP-binding proteins.	bind
46449	5	7161	7	10	NULL	0	NULL	GDP	NULL		bind	NULL				Ras	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_8_4392_s_26	9468490	2 Two GAPs, NF1 and RasGAP, form stable complexes with the GDP-bound form of Ras in the presence of aluminum fluoride, indicating that it also mimics the transition state of GTP hydrolysis in low molecular weight GTP-binding proteins.	bind
22531	1	7162	6	13	NULL	NULL	NULL	CBD23 construct	GP	mutant	does not bind			W316A/W374A		gelatin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_43336_s_222	15292230	2 Using a CBD23 construct with the tryptophan mutations W316A/W374A that no longerR binds gelatin nor blocks MMP-2 gelatinolytic and collagenolytic activities in competition experiments, we specifically confirmed the importance of the collagen binding properties of the CBD in collagen and gelatin cleavage by MMP-2.	bind
22532	2	7162	6	13	NULL	NULL	NULL	MMP-2	GP		cleaves					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_43336_s_222	15292230	2 Using a CBD23 construct with the tryptophan mutations W316A/W374A that no longerR binds gelatin nor blocks MMP-2 gelatinolytic and collagenolytic activities in competition experiments, we specifically confirmed the importance of the collagen binding properties of the CBD in collagen and gelatin cleavage by MMP-2.	bind
22533	3	7162	6	13	NULL	NULL	NULL	MMP-2	GP		cleaves					gelatin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_43336_s_222	15292230	2 Using a CBD23 construct with the tryptophan mutations W316A/W374A that no longerR binds gelatin nor blocks MMP-2 gelatinolytic and collagenolytic activities in competition experiments, we specifically confirmed the importance of the collagen binding properties of the CBD in collagen and gelatin cleavage by MMP-2.	bind
22534	4	7162	6	13	NULL	NULL	NULL	CBD23 construct	GP	mutant	does not block			W316A/W374A		MMP-2	GP	gelatinolytic activity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_43336_s_222	15292230	2 Using a CBD23 construct with the tryptophan mutations W316A/W374A that no longerR binds gelatin nor blocks MMP-2 gelatinolytic and collagenolytic activities in competition experiments, we specifically confirmed the importance of the collagen binding properties of the CBD in collagen and gelatin cleavage by MMP-2.	bind
22535	5	7162	6	13	NULL	NULL	NULL	CBD23 construct	GP	mutant	does not block			W316A/W374A		MMP-2	GP	collagenolytic activity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_43336_s_222	15292230	2 Using a CBD23 construct with the tryptophan mutations W316A/W374A that no longerR binds gelatin nor blocks MMP-2 gelatinolytic and collagenolytic activities in competition experiments, we specifically confirmed the importance of the collagen binding properties of the CBD in collagen and gelatin cleavage by MMP-2.	bind
22536	6	7162	6	13	NULL	NULL	NULL				bind			CBD		collagen	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_43336_s_222	15292230	2 Using a CBD23 construct with the tryptophan mutations W316A/W374A that no longerR binds gelatin nor blocks MMP-2 gelatinolytic and collagenolytic activities in competition experiments, we specifically confirmed the importance of the collagen binding properties of the CBD in collagen and gelatin cleavage by MMP-2.	bind
22537	7	7162	6	13	NULL	NULL	NULL	statement 6	Process		plays a role in					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_43336_s_222	15292230	2 Using a CBD23 construct with the tryptophan mutations W316A/W374A that no longerR binds gelatin nor blocks MMP-2 gelatinolytic and collagenolytic activities in competition experiments, we specifically confirmed the importance of the collagen binding properties of the CBD in collagen and gelatin cleavage by MMP-2.	bind
22538	8	7162	6	13	NULL	NULL	NULL	statement 6	Process		plays a role in					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_43336_s_222	15292230	2 Using a CBD23 construct with the tryptophan mutations W316A/W374A that no longerR binds gelatin nor blocks MMP-2 gelatinolytic and collagenolytic activities in competition experiments, we specifically confirmed the importance of the collagen binding properties of the CBD in collagen and gelatin cleavage by MMP-2.	bind
26926	1	7162	7	NULL	NULL	0	NULL	CBD	NULL		binds	NULL				collagen	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_41_43336_s_222	15292230	2 Using a CBD23 construct with the tryptophan mutations W316A/W374A that no longerR binds gelatin nor blocks MMP-2 gelatinolytic and collagenolytic activities in competition experiments, we specifically confirmed the importance of the collagen binding properties of the CBD in collagen and gelatin cleavage by MMP-2.	bind
26927	2	7162	7	NULL	NULL	0	NULL	MMP-2	NULL		cleaves	NULL				gelatin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_41_43336_s_222	15292230	2 Using a CBD23 construct with the tryptophan mutations W316A/W374A that no longerR binds gelatin nor blocks MMP-2 gelatinolytic and collagenolytic activities in competition experiments, we specifically confirmed the importance of the collagen binding properties of the CBD in collagen and gelatin cleavage by MMP-2.	bind
27857	3	7162	7	NULL	NULL	0	NULL	 CBD23 construct	NULL	mutant	does not bind	NULL		W316A/W374A		gelatin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_41_43336_s_222	15292230	2 Using a CBD23 construct with the tryptophan mutations W316A/W374A that no longerR binds gelatin nor blocks MMP-2 gelatinolytic and collagenolytic activities in competition experiments, we specifically confirmed the importance of the collagen binding properties of the CBD in collagen and gelatin cleavage by MMP-2.	bind
27858	5	7162	7	10	NULL	0	NULL	CBD23 construct	NULL	mutant	does not block	NULL		W316A/W374A		MMP-2	NULL	gelatinolytic activity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_43336_s_222	15292230	2 Using a CBD23 construct with the tryptophan mutations W316A/W374A that no longerR binds gelatin nor blocks MMP-2 gelatinolytic and collagenolytic activities in competition experiments, we specifically confirmed the importance of the collagen binding properties of the CBD in collagen and gelatin cleavage by MMP-2.	bind
27859	7	7162	7	10	NULL	0	NULL	CBD23 construct	NULL	mutant	does not block	NULL		W316A/W374A		MMP-2	NULL	collagenolytic activity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_43336_s_222	15292230	2 Using a CBD23 construct with the tryptophan mutations W316A/W374A that no longerR binds gelatin nor blocks MMP-2 gelatinolytic and collagenolytic activities in competition experiments, we specifically confirmed the importance of the collagen binding properties of the CBD in collagen and gelatin cleavage by MMP-2.	bind
37587	4	7162	7	10	NULL	0	NULL	MMP-2	NULL		cleaves	NULL				collagen	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_43336_s_222	15292230	2 Using a CBD23 construct with the tryptophan mutations W316A/W374A that no longerR binds gelatin nor blocks MMP-2 gelatinolytic and collagenolytic activities in competition experiments, we specifically confirmed the importance of the collagen binding properties of the CBD in collagen and gelatin cleavage by MMP-2.	bind
37588	6	7162	7	10	NULL	0	NULL	statement 1	NULL		plays a role in	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_43336_s_222	15292230	2 Using a CBD23 construct with the tryptophan mutations W316A/W374A that no longerR binds gelatin nor blocks MMP-2 gelatinolytic and collagenolytic activities in competition experiments, we specifically confirmed the importance of the collagen binding properties of the CBD in collagen and gelatin cleavage by MMP-2.	bind
53362	8	7162	7	10	NULL	0	NULL	statement 1	NULL		plays a role in	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_41_43336_s_222	15292230	2 Using a CBD23 construct with the tryptophan mutations W316A/W374A that no longerR binds gelatin nor blocks MMP-2 gelatinolytic and collagenolytic activities in competition experiments, we specifically confirmed the importance of the collagen binding properties of the CBD in collagen and gelatin cleavage by MMP-2.	bind
22429	1	7163	6	13	NULL	NULL	NULL	GTP	Chemical		bind					Rho	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_38_23022_s_26	8798490	2 Using the two hybrid system, we also isolated another molecule showing binding to GTP-bound forms of Rho and Rac.	bind
22430	2	7163	6	13	NULL	NULL	NULL	GTP	Chemical		bind					Rac	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_38_23022_s_26	8798490	2 Using the two hybrid system, we also isolated another molecule showing binding to GTP-bound forms of Rho and Rac.	bind
26928	1	7163	7	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				Rho	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_38_23022_s_26	8798490	2 Using the two hybrid system, we also isolated another molecule showing binding to GTP-bound forms of Rho and Rac.	bind
26929	2	7163	7	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				Rac	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_38_23022_s_26	8798490	2 Using the two hybrid system, we also isolated another molecule showing binding to GTP-bound forms of Rho and Rac.	bind
22431	1	7165	6	13	NULL	NULL	NULL	ETO-1 protein	GP	arabidopsis	bind			BTB domain		CUL3a	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_19_18810_s_61	15749712	2 Wang  et al. ( ) provided further support with the discovery that the  Arabidopsis ethylene  overproducer (ETO)-1 protein contains a BTB domain that binds CUL3a.	bind
22432	2	7165	6	13	NULL	NULL	NULL	ETO-1	GP		is					ethylene overproducer 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_19_18810_s_61	15749712	2 Wang  et al. ( ) provided further support with the discovery that the  Arabidopsis ethylene  overproducer (ETO)-1 protein contains a BTB domain that binds CUL3a.	bind
26930	1	7165	7	NULL	NULL	0	NULL	ETO-1 protein 	NULL	Arabidopsis	binds	NULL		BTB domain		CUL3a	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_19_18810_s_61	15749712	2 Wang  et al. ( ) provided further support with the discovery that the  Arabidopsis ethylene  overproducer (ETO)-1 protein contains a BTB domain that binds CUL3a.	bind
26931	2	7165	7	NULL	NULL	0	NULL	ETO-1 protein	NULL		is	NULL				ethylene overproducer-1 protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_19_18810_s_61	15749712	2 Wang  et al. ( ) provided further support with the discovery that the  Arabidopsis ethylene  overproducer (ETO)-1 protein contains a BTB domain that binds CUL3a.	bind
22433	1	7166	6	13	NULL	NULL	NULL	Cox17	GP		exist within a					binuclear thiolate center	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_37582_s_237	10970896	2 We had proposed that the two Cu(I) ions bound to Cox17 purified as a GST fusion exist within a binuclear thiolate center with either four or five thiolate ligands ( 14).	bind
22434	2	7166	6	13	NULL	NULL	NULL	Cu(I) ions	Chemical		bind					Cox17	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_37582_s_237	10970896	2 We had proposed that the two Cu(I) ions bound to Cox17 purified as a GST fusion exist within a binuclear thiolate center with either four or five thiolate ligands ( 14).	bind
37430	3	7166	6	13	NULL	NULL	NULL	Cox17	GP		contains					thiolate ligands	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_37582_s_237	10970896	2 We had proposed that the two Cu(I) ions bound to Cox17 purified as a GST fusion exist within a binuclear thiolate center with either four or five thiolate ligands ( 14).	bind
46450	4	7166	6	13	NULL	NULL	NULL	Cox17	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_37582_s_237	10970896	2 We had proposed that the two Cu(I) ions bound to Cox17 purified as a GST fusion exist within a binuclear thiolate center with either four or five thiolate ligands ( 14).	bind
26932	1	7166	7	10	NULL	0	NULL	Cu(I) ions	NULL		bind	NULL				Cox17	NULL	purified 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_37582_s_237	10970896	2 We had proposed that the two Cu(I) ions bound to Cox17 purified as a GST fusion exist within a binuclear thiolate center with either four or five thiolate ligands ( 14).	bind
26933	2	7166	7	NULL	NULL	0	NULL	 Cox17	NULL		exist within	NULL				binuclear thiolate center	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_48_37582_s_237	10970896	2 We had proposed that the two Cu(I) ions bound to Cox17 purified as a GST fusion exist within a binuclear thiolate center with either four or five thiolate ligands ( 14).	bind
26934	3	7166	7	NULL	NULL	0	NULL	Cox17	NULL		contains	NULL				thiolate ligands	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_48_37582_s_237	10970896	2 We had proposed that the two Cu(I) ions bound to Cox17 purified as a GST fusion exist within a binuclear thiolate center with either four or five thiolate ligands ( 14).	bind
46451	4	7166	7	10	NULL	0	NULL	Cox17	NULL		is a type of	NULL				GST fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_48_37582_s_237	10970896	2 We had proposed that the two Cu(I) ions bound to Cox17 purified as a GST fusion exist within a binuclear thiolate center with either four or five thiolate ligands ( 14).	bind
22435	1	7167	6	13	NULL	NULL	NULL	hnRNP C	GP		bind									29-base instability element 	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_2_1119_s_295	11042220	2 We have proposed that the stable phase was a consequence of hnRNP C binding to the 29-base instability element that prevented RNase attack.	bind
22436	2	7167	6	13	NULL	NULL	NULL	statement 1	Process		prevents					RNase attack	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_2_1119_s_295	11042220	2 We have proposed that the stable phase was a consequence of hnRNP C binding to the 29-base instability element that prevented RNase attack.	bind
26935	1	7167	7	NULL	NULL	0	NULL	hnRNP C	NULL		bind	NULL					NULL			29-base instability element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_2_1119_s_295	11042220	2 We have proposed that the stable phase was a consequence of hnRNP C binding to the 29-base instability element that prevented RNase attack.	bind
26936	2	7167	7	NULL	NULL	0	NULL	statement 1	NULL		prevents	NULL				RNase attack	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_2_1119_s_295	11042220	2 We have proposed that the stable phase was a consequence of hnRNP C binding to the 29-base instability element that prevented RNase attack.	bind
22437	1	7168	6	13	NULL	NULL	NULL	LDL	GP		bind					LRP	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_15_13350_s_180	12566436	2 We show here that binding of LDL to LRP is also required for 12/15 -lipoxygenasetranslocation (Fig.  3).	bind
22438	2	7168	6	13	NULL	NULL	NULL	statement 1	Process		is required for					12/15 -lipoxygenase	GP	translocation of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_15_13350_s_180	12566436	2 We show here that binding of LDL to LRP is also required for 12/15 -lipoxygenasetranslocation (Fig.  3).	bind
26937	1	7168	7	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				LRP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_15_13350_s_180	12566436	2 We show here that binding of LDL to LRP is also required for 12/15 -lipoxygenasetranslocation (Fig.  3).	bind
26938	2	7168	7	NULL	NULL	0	NULL	statement 1	NULL		is required for	NULL				12/15 -lipoxygenase	NULL	translocation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_15_13350_s_180	12566436	2 We show here that binding of LDL to LRP is also required for 12/15 -lipoxygenasetranslocation (Fig.  3).	bind
37434	2	7169	6	13	NULL	NULL	NULL	Galphaq	GP		interacts with			Q209L		statement 1	GP				NULL	cultured cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_6050_s_217	12427730	2 We thus used this assay to examine interactions between Galphaq-Q209L and a Galphaq binding-defective mutant of GRK2 in cultured cells (Fig.  4).	bind
46452	1	7169	6	13	NULL	NULL	NULL	GRK2	GP	defective mutant	bind					Galphaq	GP				NULL	cultured cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_6050_s_217	12427730	2 We thus used this assay to examine interactions between Galphaq-Q209L and a Galphaq binding-defective mutant of GRK2 in cultured cells (Fig.  4).	bind
26939	2	7169	7	10	NULL	0	NULL	Galphaq	NULL		interacts with	NULL		Q209L		statement 1	NULL				NULL	cultured cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_6050_s_217	12427730	2 We thus used this assay to examine interactions between Galphaq-Q209L and a Galphaq binding-defective mutant of GRK2 in cultured cells (Fig.  4).	bind
46453	1	7169	7	10	NULL	0	NULL	GRK2	NULL	defective mutant	bind	NULL				Galphaq	NULL				NULL	cultured cells	0	NULL	NULL	NULL	gw70_jbiolchem_278_8_6050_s_217	12427730	2 We thus used this assay to examine interactions between Galphaq-Q209L and a Galphaq binding-defective mutant of GRK2 in cultured cells (Fig.  4).	bind
22439	1	7170	6	13	NULL	NULL	NULL	Diva	GP		interacts with					Apaf-1	GP				NULL	mammalian cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_49_32479_s_185	9829980	2 We verified the interaction between Diva and Apaf-1 in mammalian cells and tested whether Diva might block the binding of Bcl-XL to Apaf-1, because Bcl-XL can also interact with Apaf-1 ( 10,  11).	bind
22440	2	7170	6	13	NULL	NULL	NULL	Bcl-XL	GP		interacts with					Apaf1	GP				NULL	mammalian cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_49_32479_s_185	9829980	2 We verified the interaction between Diva and Apaf-1 in mammalian cells and tested whether Diva might block the binding of Bcl-XL to Apaf-1, because Bcl-XL can also interact with Apaf-1 ( 10,  11).	bind
46454	3	7170	6	13	NULL	NULL	NULL	Diva	GP		block		may			statement 2	Process				NULL	mammalian cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_49_32479_s_185	9829980	2 We verified the interaction between Diva and Apaf-1 in mammalian cells and tested whether Diva might block the binding of Bcl-XL to Apaf-1, because Bcl-XL can also interact with Apaf-1 ( 10,  11).	bind
26940	1	7170	7	NULL	NULL	0	NULL	 Diva	NULL		interacts with	NULL				Apaf-1	NULL				NULL	mammalian cells	0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32479_s_185	9829980	2 We verified the interaction between Diva and Apaf-1 in mammalian cells and tested whether Diva might block the binding of Bcl-XL to Apaf-1, because Bcl-XL can also interact with Apaf-1 ( 10,  11).	bind
26941	2	7170	7	NULL	NULL	0	NULL	 Bcl-XL	NULL		interacts with	NULL				Apaf-1 	NULL				NULL	mammalian cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_49_32479_s_185	9829980	2 We verified the interaction between Diva and Apaf-1 in mammalian cells and tested whether Diva might block the binding of Bcl-XL to Apaf-1, because Bcl-XL can also interact with Apaf-1 ( 10,  11).	bind
26942	3	7170	7	NULL	NULL	0	NULL	Diva	NULL		block	NULL	may			statement 2	NULL				NULL	mammalian cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_49_32479_s_185	9829980	2 We verified the interaction between Diva and Apaf-1 in mammalian cells and tested whether Diva might block the binding of Bcl-XL to Apaf-1, because Bcl-XL can also interact with Apaf-1 ( 10,  11).	bind
22441	1	7171	6	13	NULL	NULL	NULL	Grb7	GP		bind		specifically	SH2 domain		erbB2	GP				NULL	lysates of control cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_13_7717_s_153	9516479	2 Western blot analysis using specific antibodies revealed that the Grb7 SH2 domain specifically bound erbB2 and erbB3 from lysates of control cells, presumably because of the basal phosphorylation of these erbB receptors observed in ZR-75-1 cells ( 45), but this interaction was increased significantly when lysates from heregulin-stimulated cells were used (Fig.  3 A).	bind
22442	2	7171	6	13	NULL	NULL	NULL	Grb7	GP		bind		specifically	SH2 domain		erbB3	GP				NULL	lysates of control cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_13_7717_s_153	9516479	2 Western blot analysis using specific antibodies revealed that the Grb7 SH2 domain specifically bound erbB2 and erbB3 from lysates of control cells, presumably because of the basal phosphorylation of these erbB receptors observed in ZR-75-1 cells ( 45), but this interaction was increased significantly when lysates from heregulin-stimulated cells were used (Fig.  3 A).	bind
22539	3	7171	6	13	NULL	NULL	NULL	erbB receptors	GP	basal phosphorylation of 	cause		presumably			statement 1	Process				NULL	ZR-75-1 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_13_7717_s_153	9516479	2 Western blot analysis using specific antibodies revealed that the Grb7 SH2 domain specifically bound erbB2 and erbB3 from lysates of control cells, presumably because of the basal phosphorylation of these erbB receptors observed in ZR-75-1 cells ( 45), but this interaction was increased significantly when lysates from heregulin-stimulated cells were used (Fig.  3 A).	bind
22540	4	7171	6	13	NULL	NULL	NULL	erbB receptors	GP	basal phosphorylation of 	cause		presumably			statement 2	Process				NULL	ZR-75-1 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_13_7717_s_153	9516479	2 Western blot analysis using specific antibodies revealed that the Grb7 SH2 domain specifically bound erbB2 and erbB3 from lysates of control cells, presumably because of the basal phosphorylation of these erbB receptors observed in ZR-75-1 cells ( 45), but this interaction was increased significantly when lysates from heregulin-stimulated cells were used (Fig.  3 A).	bind
22541	5	7171	6	13	NULL	NULL	NULL	Grb7	GP		bind		specifically	SH2 domain		erbB2 receptors	GP				NULL	lysates from heregulin-stimulated cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_13_7717_s_153	9516479	2 Western blot analysis using specific antibodies revealed that the Grb7 SH2 domain specifically bound erbB2 and erbB3 from lysates of control cells, presumably because of the basal phosphorylation of these erbB receptors observed in ZR-75-1 cells ( 45), but this interaction was increased significantly when lysates from heregulin-stimulated cells were used (Fig.  3 A).	bind
22542	6	7171	6	13	NULL	NULL	NULL	Grb7	GP		bind		specifically	SH2 domain		erbB3 receptor	GP				NULL	lysates from heregulin-stimulated cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_13_7717_s_153	9516479	2 Western blot analysis using specific antibodies revealed that the Grb7 SH2 domain specifically bound erbB2 and erbB3 from lysates of control cells, presumably because of the basal phosphorylation of these erbB receptors observed in ZR-75-1 cells ( 45), but this interaction was increased significantly when lysates from heregulin-stimulated cells were used (Fig.  3 A).	bind
22543	7	7171	6	13	NULL	NULL	NULL	statement 5	Process		is increased as compared to		significantly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_13_7717_s_153	9516479	2 Western blot analysis using specific antibodies revealed that the Grb7 SH2 domain specifically bound erbB2 and erbB3 from lysates of control cells, presumably because of the basal phosphorylation of these erbB receptors observed in ZR-75-1 cells ( 45), but this interaction was increased significantly when lysates from heregulin-stimulated cells were used (Fig.  3 A).	bind
46808	8	7171	6	13	NULL	NULL	NULL	statement 6	Process		is increased as compared to		significantly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_13_7717_s_153	9516479	2 Western blot analysis using specific antibodies revealed that the Grb7 SH2 domain specifically bound erbB2 and erbB3 from lysates of control cells, presumably because of the basal phosphorylation of these erbB receptors observed in ZR-75-1 cells ( 45), but this interaction was increased significantly when lysates from heregulin-stimulated cells were used (Fig.  3 A).	bind
26943	1	7171	7	10	NULL	0	NULL	Grb7 	NULL		bind	NULL	specifically	SH2 domain		erbB2 	NULL				NULL	lysates of control cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_13_7717_s_153	9516479	2 Western blot analysis using specific antibodies revealed that the Grb7 SH2 domain specifically bound erbB2 and erbB3 from lysates of control cells, presumably because of the basal phosphorylation of these erbB receptors observed in ZR-75-1 cells ( 45), but this interaction was increased significantly when lysates from heregulin-stimulated cells were used (Fig.  3 A).	bind
26944	2	7171	7	10	NULL	0	NULL	Grb7	NULL		bind	NULL	specifically	SH2 domain		erbB3	NULL				NULL	lysates of control cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_13_7717_s_153	9516479	2 Western blot analysis using specific antibodies revealed that the Grb7 SH2 domain specifically bound erbB2 and erbB3 from lysates of control cells, presumably because of the basal phosphorylation of these erbB receptors observed in ZR-75-1 cells ( 45), but this interaction was increased significantly when lysates from heregulin-stimulated cells were used (Fig.  3 A).	bind
26945	3	7171	7	10	NULL	0	NULL	statement 1			because of		presumably			erbB receptors 		basal phosphorylation of			NULL	ZR-75-1 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_13_7717_s_153	9516479	2 Western blot analysis using specific antibodies revealed that the Grb7 SH2 domain specifically bound erbB2 and erbB3 from lysates of control cells, presumably because of the basal phosphorylation of these erbB receptors observed in ZR-75-1 cells ( 45), but this interaction was increased significantly when lysates from heregulin-stimulated cells were used (Fig.  3 A).	bind
26947	4	7171	7	10	NULL	0	NULL	statement 2			because of		presumably			erbB receptors		basal phosphorylation of			NULL	ZR-75-1 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_13_7717_s_153	9516479	2 Western blot analysis using specific antibodies revealed that the Grb7 SH2 domain specifically bound erbB2 and erbB3 from lysates of control cells, presumably because of the basal phosphorylation of these erbB receptors observed in ZR-75-1 cells ( 45), but this interaction was increased significantly when lysates from heregulin-stimulated cells were used (Fig.  3 A).	bind
26948	6	7171	7	NULL	NULL	0	NULL	Grb7			bind			SH2 domain		erbB3					NULL	heregulin-stimulated cells 	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_13_7717_s_153	9516479	2 Western blot analysis using specific antibodies revealed that the Grb7 SH2 domain specifically bound erbB2 and erbB3 from lysates of control cells, presumably because of the basal phosphorylation of these erbB receptors observed in ZR-75-1 cells ( 45), but this interaction was increased significantly when lysates from heregulin-stimulated cells were used (Fig.  3 A).	bind
54109	5	7171	7	NULL	NULL	0	NULL	Grb7			bind			SH2 domain		erbB2					NULL	 heregulin-stimulated cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_13_7717_s_153	9516479	2 Western blot analysis using specific antibodies revealed that the Grb7 SH2 domain specifically bound erbB2 and erbB3 from lysates of control cells, presumably because of the basal phosphorylation of these erbB receptors observed in ZR-75-1 cells ( 45), but this interaction was increased significantly when lysates from heregulin-stimulated cells were used (Fig.  3 A).	bind
54110	7	7171	7	NULL	NULL	0	NULL	statement 5		binding of	is higher than					statement 1		binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_13_7717_s_153	9516479	2 Western blot analysis using specific antibodies revealed that the Grb7 SH2 domain specifically bound erbB2 and erbB3 from lysates of control cells, presumably because of the basal phosphorylation of these erbB receptors observed in ZR-75-1 cells ( 45), but this interaction was increased significantly when lysates from heregulin-stimulated cells were used (Fig.  3 A).	bind
54111	8	7171	7	NULL	NULL	0	NULL	statement 6		binding of	is higher than					statement 2		binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_13_7717_s_153	9516479	2 Western blot analysis using specific antibodies revealed that the Grb7 SH2 domain specifically bound erbB2 and erbB3 from lysates of control cells, presumably because of the basal phosphorylation of these erbB receptors observed in ZR-75-1 cells ( 45), but this interaction was increased significantly when lysates from heregulin-stimulated cells were used (Fig.  3 A).	bind
22915	1	7172	6	13	NULL	NULL	NULL	Elongin C	GP	mutant	does not bind			Ala92-94		VHL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_43_27444_s_103	9341197	2 When the same Elongin C alanine-scanning mutants were tested for their abilities to bind the VHL protein using the TSK DEAE-NPR binding assay, we observed that the Elongin C mutants defective in VHL binding (C(Ala92-94), C(Ala104-105), and C(Ala110-112)) were a subset of those Elongin C alanine-scanning mutants shown previously to be defective in activation of Elongin A; we identified no Elongin C mutations that interfered with VHL binding but not the activation of Elongin A.	bind
22916	2	7172	6	13	NULL	NULL	NULL	elongin C	GP	mutant	does not bind			Ala104-105		VHL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_43_27444_s_103	9341197	2 When the same Elongin C alanine-scanning mutants were tested for their abilities to bind the VHL protein using the TSK DEAE-NPR binding assay, we observed that the Elongin C mutants defective in VHL binding (C(Ala92-94), C(Ala104-105), and C(Ala110-112)) were a subset of those Elongin C alanine-scanning mutants shown previously to be defective in activation of Elongin A; we identified no Elongin C mutations that interfered with VHL binding but not the activation of Elongin A.	bind
22917	3	7172	6	13	NULL	NULL	NULL	Elongin C	GP	mutant	does not bind			Ala110-112		VHL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_43_27444_s_103	9341197	2 When the same Elongin C alanine-scanning mutants were tested for their abilities to bind the VHL protein using the TSK DEAE-NPR binding assay, we observed that the Elongin C mutants defective in VHL binding (C(Ala92-94), C(Ala104-105), and C(Ala110-112)) were a subset of those Elongin C alanine-scanning mutants shown previously to be defective in activation of Elongin A; we identified no Elongin C mutations that interfered with VHL binding but not the activation of Elongin A.	bind
22918	4	7172	6	13	NULL	NULL	NULL	Elongin C	GP	mutant	is defective in			Ala92-94		elongin A	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_43_27444_s_103	9341197	2 When the same Elongin C alanine-scanning mutants were tested for their abilities to bind the VHL protein using the TSK DEAE-NPR binding assay, we observed that the Elongin C mutants defective in VHL binding (C(Ala92-94), C(Ala104-105), and C(Ala110-112)) were a subset of those Elongin C alanine-scanning mutants shown previously to be defective in activation of Elongin A; we identified no Elongin C mutations that interfered with VHL binding but not the activation of Elongin A.	bind
22919	5	7172	6	13	NULL	NULL	NULL	Elongin C	GP	mutant	is defective in			Ala104-105		elongin A	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_43_27444_s_103	9341197	2 When the same Elongin C alanine-scanning mutants were tested for their abilities to bind the VHL protein using the TSK DEAE-NPR binding assay, we observed that the Elongin C mutants defective in VHL binding (C(Ala92-94), C(Ala104-105), and C(Ala110-112)) were a subset of those Elongin C alanine-scanning mutants shown previously to be defective in activation of Elongin A; we identified no Elongin C mutations that interfered with VHL binding but not the activation of Elongin A.	bind
22920	6	7172	6	13	NULL	NULL	NULL	Elongin C	GP	mutant	is defective in			Ala110-112		elongin A	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_43_27444_s_103	9341197	2 When the same Elongin C alanine-scanning mutants were tested for their abilities to bind the VHL protein using the TSK DEAE-NPR binding assay, we observed that the Elongin C mutants defective in VHL binding (C(Ala92-94), C(Ala104-105), and C(Ala110-112)) were a subset of those Elongin C alanine-scanning mutants shown previously to be defective in activation of Elongin A; we identified no Elongin C mutations that interfered with VHL binding but not the activation of Elongin A.	bind
27860	1	7172	7	NULL	NULL	0	NULL	Elongin C	NULL	mutant	does not bind	NULL		C(Ala92-94)		VHL	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_43_27444_s_103	9341197	2 When the same Elongin C alanine-scanning mutants were tested for their abilities to bind the VHL protein using the TSK DEAE-NPR binding assay, we observed that the Elongin C mutants defective in VHL binding (C(Ala92-94), C(Ala104-105), and C(Ala110-112)) were a subset of those Elongin C alanine-scanning mutants shown previously to be defective in activation of Elongin A; we identified no Elongin C mutations that interfered with VHL binding but not the activation of Elongin A.	bind
27861	2	7172	7	NULL	NULL	0	NULL	Elongin C	NULL	mutant	does not bind	NULL		C(Ala104-105)		VHL	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_43_27444_s_103	9341197	2 When the same Elongin C alanine-scanning mutants were tested for their abilities to bind the VHL protein using the TSK DEAE-NPR binding assay, we observed that the Elongin C mutants defective in VHL binding (C(Ala92-94), C(Ala104-105), and C(Ala110-112)) were a subset of those Elongin C alanine-scanning mutants shown previously to be defective in activation of Elongin A; we identified no Elongin C mutations that interfered with VHL binding but not the activation of Elongin A.	bind
27862	3	7172	7	NULL	NULL	0	NULL	Elongin C	NULL	mutant	does not bind	NULL		C(Ala110-112)		VHL	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_43_27444_s_103	9341197	2 When the same Elongin C alanine-scanning mutants were tested for their abilities to bind the VHL protein using the TSK DEAE-NPR binding assay, we observed that the Elongin C mutants defective in VHL binding (C(Ala92-94), C(Ala104-105), and C(Ala110-112)) were a subset of those Elongin C alanine-scanning mutants shown previously to be defective in activation of Elongin A; we identified no Elongin C mutations that interfered with VHL binding but not the activation of Elongin A.	bind
27863	4	7172	7	NULL	NULL	0	NULL	Elongin C	NULL	mutant	does not activate	NULL		C(Ala92-94)		Elongin A	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_43_27444_s_103	9341197	2 When the same Elongin C alanine-scanning mutants were tested for their abilities to bind the VHL protein using the TSK DEAE-NPR binding assay, we observed that the Elongin C mutants defective in VHL binding (C(Ala92-94), C(Ala104-105), and C(Ala110-112)) were a subset of those Elongin C alanine-scanning mutants shown previously to be defective in activation of Elongin A; we identified no Elongin C mutations that interfered with VHL binding but not the activation of Elongin A.	bind
27864	5	7172	7	NULL	NULL	0	NULL	Elongin C	NULL	mutant	does not activate	NULL		C(Ala104-105)		Elongin A	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_43_27444_s_103	9341197	2 When the same Elongin C alanine-scanning mutants were tested for their abilities to bind the VHL protein using the TSK DEAE-NPR binding assay, we observed that the Elongin C mutants defective in VHL binding (C(Ala92-94), C(Ala104-105), and C(Ala110-112)) were a subset of those Elongin C alanine-scanning mutants shown previously to be defective in activation of Elongin A; we identified no Elongin C mutations that interfered with VHL binding but not the activation of Elongin A.	bind
27865	6	7172	7	NULL	NULL	0	NULL	Elongin C	NULL	mutant	does not activate	NULL		C(Ala110-112)		Elongin A	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_43_27444_s_103	9341197	2 When the same Elongin C alanine-scanning mutants were tested for their abilities to bind the VHL protein using the TSK DEAE-NPR binding assay, we observed that the Elongin C mutants defective in VHL binding (C(Ala92-94), C(Ala104-105), and C(Ala110-112)) were a subset of those Elongin C alanine-scanning mutants shown previously to be defective in activation of Elongin A; we identified no Elongin C mutations that interfered with VHL binding but not the activation of Elongin A.	bind
22547	1	7173	6	13	NULL	NULL	NULL	TRAF2	GP		bind					T2bs-C	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31572_s_270	16020544	2 Whereas this indicates that Etk/mx is not the intermediary protein for the binding of TRAF2 to T2bs-C, the fact that Etk/mx can bind to T2bs-C indicates that TRAF2 may be indirectly recruited to T2bs-C by a protein with homology to Etk/Bmx.	bind
22548	2	7173	6	13	NULL	NULL	NULL	Etk/mx	GP		bind					T2bs-C	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31572_s_270	16020544	2 Whereas this indicates that Etk/mx is not the intermediary protein for the binding of TRAF2 to T2bs-C, the fact that Etk/mx can bind to T2bs-C indicates that TRAF2 may be indirectly recruited to T2bs-C by a protein with homology to Etk/Bmx.	bind
22582	3	7173	6	13	NULL	NULL	NULL	TRAF2	GP		is recruited to		indirectly			T2bs-C	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31572_s_270	16020544	2 Whereas this indicates that Etk/mx is not the intermediary protein for the binding of TRAF2 to T2bs-C, the fact that Etk/mx can bind to T2bs-C indicates that TRAF2 may be indirectly recruited to T2bs-C by a protein with homology to Etk/Bmx.	bind
22583	4	7173	6	13	NULL	NULL	NULL	statement 3	Process		occurs by					Etk/Bmx homologous protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31572_s_270	16020544	2 Whereas this indicates that Etk/mx is not the intermediary protein for the binding of TRAF2 to T2bs-C, the fact that Etk/mx can bind to T2bs-C indicates that TRAF2 may be indirectly recruited to T2bs-C by a protein with homology to Etk/Bmx.	bind
26957	1	7173	7	NULL	NULL	0	NULL	 TRAF2 	NULL		bind	NULL				 T2bs-C	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_36_31572_s_270	16020544	2 Whereas this indicates that Etk/mx is not the intermediary protein for the binding of TRAF2 to T2bs-C, the fact that Etk/mx can bind to T2bs-C indicates that TRAF2 may be indirectly recruited to T2bs-C by a protein with homology to Etk/Bmx.	bind
26958	2	7173	7	NULL	NULL	0	NULL	Etk/mx	NULL		bind	NULL				T2bs-C 	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_36_31572_s_270	16020544	2 Whereas this indicates that Etk/mx is not the intermediary protein for the binding of TRAF2 to T2bs-C, the fact that Etk/mx can bind to T2bs-C indicates that TRAF2 may be indirectly recruited to T2bs-C by a protein with homology to Etk/Bmx.	bind
26959	3	7173	7	NULL	NULL	0	NULL	 TRAF2	NULL		recruited to	NULL	indirectly			T2bs-C	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_36_31572_s_270	16020544	2 Whereas this indicates that Etk/mx is not the intermediary protein for the binding of TRAF2 to T2bs-C, the fact that Etk/mx can bind to T2bs-C indicates that TRAF2 may be indirectly recruited to T2bs-C by a protein with homology to Etk/Bmx.	bind
26960	4	7173	7	NULL	NULL	0	NULL	statement 3	NULL		occurs by a	NULL				Etk/Bmx homologous protein	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31572_s_270	16020544	2 Whereas this indicates that Etk/mx is not the intermediary protein for the binding of TRAF2 to T2bs-C, the fact that Etk/mx can bind to T2bs-C indicates that TRAF2 may be indirectly recruited to T2bs-C by a protein with homology to Etk/Bmx.	bind
26961	5	7173	7	NULL	NULL	0	NULL	Etk/mx	NULL		is not an	NULL				intermediary protein	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31572_s_270	16020544	2 Whereas this indicates that Etk/mx is not the intermediary protein for the binding of TRAF2 to T2bs-C, the fact that Etk/mx can bind to T2bs-C indicates that TRAF2 may be indirectly recruited to T2bs-C by a protein with homology to Etk/Bmx.	bind
37600	6	7173	7	NULL	NULL	0	NULL	statement 1	NULL		does not occur through	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_36_31572_s_270	16020544	2 Whereas this indicates that Etk/mx is not the intermediary protein for the binding of TRAF2 to T2bs-C, the fact that Etk/mx can bind to T2bs-C indicates that TRAF2 may be indirectly recruited to T2bs-C by a protein with homology to Etk/Bmx.	bind
22584	1	7174	6	13	NULL	NULL	NULL	CD36	GP		expressed in					COS cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_41_26338_s_128	9756864	2 While this manuscript was in preparation, Calvo  et al. ( 64) reported their independent observation that HDL binds to CD36 expressed in COS and Sf9 cells.	bind
22585	2	7174	6	13	NULL	NULL	NULL	CD36	GP		expressed in					Sf9 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_41_26338_s_128	9756864	2 While this manuscript was in preparation, Calvo  et al. ( 64) reported their independent observation that HDL binds to CD36 expressed in COS and Sf9 cells.	bind
22586	3	7174	6	13	NULL	NULL	NULL	HDL	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_41_26338_s_128	9756864	2 While this manuscript was in preparation, Calvo  et al. ( 64) reported their independent observation that HDL binds to CD36 expressed in COS and Sf9 cells.	bind
22587	4	7174	6	13	NULL	NULL	NULL	HDL	GP		bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_41_26338_s_128	9756864	2 While this manuscript was in preparation, Calvo  et al. ( 64) reported their independent observation that HDL binds to CD36 expressed in COS and Sf9 cells.	bind
26962	2	7174	7	NULL	NULL	0	NULL	HDL	NULL		binds to	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_41_26338_s_128	9756864	2 While this manuscript was in preparation, Calvo  et al. ( 64) reported their independent observation that HDL binds to CD36 expressed in COS and Sf9 cells.	bind
26963	1	7174	7	NULL	NULL	0	NULL	CD36	NULL		expressed in	NULL				COS cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_41_26338_s_128	9756864	2 While this manuscript was in preparation, Calvo  et al. ( 64) reported their independent observation that HDL binds to CD36 expressed in COS and Sf9 cells.	bind
37601	3	7174	7	NULL	NULL	0	NULL	CD36	NULL		expressed in	NULL				Sf9 cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_41_26338_s_128	9756864	2 While this manuscript was in preparation, Calvo  et al. ( 64) reported their independent observation that HDL binds to CD36 expressed in COS and Sf9 cells.	bind
37602	4	7174	7	NULL	NULL	0	NULL	HDL	NULL		binds to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_41_26338_s_128	9756864	2 While this manuscript was in preparation, Calvo  et al. ( 64) reported their independent observation that HDL binds to CD36 expressed in COS and Sf9 cells.	bind
22588	1	7175	6	13	NULL	NULL	NULL	DnaA protein	GP		bind					dnaA	G			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23017_s_18	9287298	2 With an  in vivo assay that measured the binding of DnaA protein to the  dnaA promoter region of a  dnaA promoter- lacZ fusion, encoding amino acid substitutions within the C-terminal 89 residues or lacking C-terminal coding sequence were unable to repress expression.	bind
26964	1	7175	7	10	NULL	0	NULL	DnaA protein	NULL		bind	NULL				dnaA	NULL			promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23017_s_18	9287298	2 With an  in vivo assay that measured the binding of DnaA protein to the  dnaA promoter region of a  dnaA promoter- lacZ fusion, encoding amino acid substitutions within the C-terminal 89 residues or lacking C-terminal coding sequence were unable to repress expression.	bind
22589	1	7176	6	13	NULL	NULL	NULL	secYEG	GP		bind					SecA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13769_s_211	14722060	2 With the experimentally determined  koff value (4 x 10-3 s-1), the apparent  Kd values for MANT-ADP and MANT-ATP binding to the SecYEG-bound SecA correspond to 21 and 59 nM, respectively.	bind
22590	2	7176	6	13	NULL	NULL	NULL	mant-ADP	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13769_s_211	14722060	2 With the experimentally determined  koff value (4 x 10-3 s-1), the apparent  Kd values for MANT-ADP and MANT-ATP binding to the SecYEG-bound SecA correspond to 21 and 59 nM, respectively.	bind
22591	3	7176	6	13	NULL	NULL	NULL	mant-ATP	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13769_s_211	14722060	2 With the experimentally determined  koff value (4 x 10-3 s-1), the apparent  Kd values for MANT-ADP and MANT-ATP binding to the SecYEG-bound SecA correspond to 21 and 59 nM, respectively.	bind
26965	2	7176	7	10	NULL	0	NULL	MANT-ADP	NULL		bind	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13769_s_211	14722060	2 With the experimentally determined  koff value (4 x 10-3 s-1), the apparent  Kd values for MANT-ADP and MANT-ATP binding to the SecYEG-bound SecA correspond to 21 and 59 nM, respectively.	bind
26966	3	7176	7	10	NULL	0	NULL	MANT-ATP	NULL		bind	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13769_s_211	14722060	2 With the experimentally determined  koff value (4 x 10-3 s-1), the apparent  Kd values for MANT-ADP and MANT-ATP binding to the SecYEG-bound SecA correspond to 21 and 59 nM, respectively.	bind
46455	1	7176	7	10	NULL	0	NULL	SecYEG	NULL		bind	NULL				SecA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_14_13769_s_211	14722060	2 With the experimentally determined  koff value (4 x 10-3 s-1), the apparent  Kd values for MANT-ADP and MANT-ATP binding to the SecYEG-bound SecA correspond to 21 and 59 nM, respectively.	bind
22592	1	7177	6	13	NULL	NULL	NULL				bind			RCC1-like domains		GTP-binding proteins	GP	small			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_20_12148_s_212	9575161	2 WW domains have been implicated in the binding of peptides containing PY and PY-like domains (Ref.  32, and references therein), and it is suggested that RCC1-like domains bind small GTP-binding proteins ( 23).	bind
22593	2	7177	6	13	NULL	NULL	NULL				plays a role in			WW domain		peptides 	GP	binding of	PY domain		NULL	 	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_20_12148_s_212	9575161	2 WW domains have been implicated in the binding of peptides containing PY and PY-like domains (Ref.  32, and references therein), and it is suggested that RCC1-like domains bind small GTP-binding proteins ( 23).	bind
22594	3	7177	6	13	NULL	NULL	NULL				plays a role in			WW domain		peptides	GP	binding of	PY-like domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_20_12148_s_212	9575161	2 WW domains have been implicated in the binding of peptides containing PY and PY-like domains (Ref.  32, and references therein), and it is suggested that RCC1-like domains bind small GTP-binding proteins ( 23).	bind
26967	1	7177	7	10	NULL	0	NULL		NULL		plays a role in	NULL		 WW domains		peptides	NULL	binding of	PY domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_20_12148_s_212	9575161	2 WW domains have been implicated in the binding of peptides containing PY and PY-like domains (Ref.  32, and references therein), and it is suggested that RCC1-like domains bind small GTP-binding proteins ( 23).	bind
26968	2	7177	7	10	NULL	0	NULL		NULL		plays a role in	NULL		WW domains		peptides	NULL	binding of	PY-like domains		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_20_12148_s_212	9575161	2 WW domains have been implicated in the binding of peptides containing PY and PY-like domains (Ref.  32, and references therein), and it is suggested that RCC1-like domains bind small GTP-binding proteins ( 23).	bind
26969	3	7177	7	NULL	NULL	0	NULL		NULL		bind	NULL		RCC1-like domains		GTP-binding proteins	NULL	small			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_20_12148_s_212	9575161	2 WW domains have been implicated in the binding of peptides containing PY and PY-like domains (Ref.  32, and references therein), and it is suggested that RCC1-like domains bind small GTP-binding proteins ( 23).	bind
22595	1	7179	6	13	NULL	NULL	NULL	EF	GP		bind					AC toxins	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_19_19955_s_50	14981084	2''-d-3''-ANT-ATP fluorescence increases upon binding of the EF and ACT activator calmodulin to the AC toxins ( ,  ).	bind
22596	2	7179	6	13	NULL	NULL	NULL	calmodulin	GP		bind					AC toxins	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_19_19955_s_50	14981084	2''-d-3''-ANT-ATP fluorescence increases upon binding of the EF and ACT activator calmodulin to the AC toxins ( ,  ).	bind
46456	3	7179	6	13	NULL	NULL	NULL	calmodulin	GP		is a type of					ACT activator	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_19_19955_s_50	14981084	2''-d-3''-ANT-ATP fluorescence increases upon binding of the EF and ACT activator calmodulin to the AC toxins ( ,  ).	bind
26970	1	7179	7	NULL	NULL	0	NULL	EF	NULL		bind	NULL				AC toxins	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_19_19955_s_50	14981084	2''-d-3''-ANT-ATP fluorescence increases upon binding of the EF and ACT activator calmodulin to the AC toxins ( ,  ).	bind
26971	2	7179	7	NULL	NULL	0	NULL	calmodulin	NULL		bind	NULL				AC toxins	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_19_19955_s_50	14981084	2''-d-3''-ANT-ATP fluorescence increases upon binding of the EF and ACT activator calmodulin to the AC toxins ( ,  ).	bind
26972	3	7179	7	NULL	NULL	0	NULL	calmodulin	NULL		is a type of	NULL				ACT activator	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_19_19955_s_50	14981084	2''-d-3''-ANT-ATP fluorescence increases upon binding of the EF and ACT activator calmodulin to the AC toxins ( ,  ).	bind
22597	1	7180	6	13	NULL	NULL	NULL	mammalian membrane	CellComponent		bind					AC	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_12_11513_s_153	15649897	2''-substituted nucleotides and nucleosides also inhibit mammalian membrane-bound AC in a mixed competitive manner ( ).	bind
22598	2	7180	6	13	NULL	NULL	NULL	nucleotides	NucleicAcid	substituted	bind					AC	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_12_11513_s_153	15649897	2''-substituted nucleotides and nucleosides also inhibit mammalian membrane-bound AC in a mixed competitive manner ( ).	bind
22599	3	7180	6	13	NULL	NULL	NULL	nucleosides	GP	substituted	bind					AC	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_12_11513_s_153	15649897	2''-substituted nucleotides and nucleosides also inhibit mammalian membrane-bound AC in a mixed competitive manner ( ).	bind
22600	4	7180	6	13	NULL	NULL	NULL	statement 2	Process		inhibit		competitively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_12_11513_s_153	15649897	2''-substituted nucleotides and nucleosides also inhibit mammalian membrane-bound AC in a mixed competitive manner ( ).	bind
22601	5	7180	6	13	NULL	NULL	NULL	statement 3	Process		inhibit		competitively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_12_11513_s_153	15649897	2''-substituted nucleotides and nucleosides also inhibit mammalian membrane-bound AC in a mixed competitive manner ( ).	bind
26975	2	7180	7	10	NULL	0	NULL	nucleotides	NULL	2''-substituted	bind	NULL				AC	NULL	 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_12_11513_s_153	15649897	2''-substituted nucleotides and nucleosides also inhibit mammalian membrane-bound AC in a mixed competitive manner ( ).	bind
26976	3	7180	7	10	NULL	0	NULL	nucleosides 	NULL	2''-substituted	bind	NULL				AC	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_12_11513_s_153	15649897	2''-substituted nucleotides and nucleosides also inhibit mammalian membrane-bound AC in a mixed competitive manner ( ).	bind
37619	1	7180	7	NULL	NULL	0	NULL	mammalian membrane	NULL		bind	NULL				AC	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_12_11513_s_153	15649897	2''-substituted nucleotides and nucleosides also inhibit mammalian membrane-bound AC in a mixed competitive manner ( ).	bind
37620	4	7180	7	NULL	NULL	0	NULL	statement 2	NULL		inhibit	NULL	competitively			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_12_11513_s_153	15649897	2''-substituted nucleotides and nucleosides also inhibit mammalian membrane-bound AC in a mixed competitive manner ( ).	bind
37621	5	7180	7	NULL	NULL	0	NULL	statement 3	NULL		inhibit	NULL	competitively			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_12_11513_s_153	15649897	2''-substituted nucleotides and nucleosides also inhibit mammalian membrane-bound AC in a mixed competitive manner ( ).	bind
22602	1	7181	6	13	NULL	NULL	NULL	GTPgamma35S	GP		bind					Galphaq	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_55_2_339_s_274	9927627	2) A marked degree of constitutive activity is detectable for both the A293E and D142A mutants also in a membrane assay (in which desensitization should not occur) measuring receptor-mediated stimulation of GTPgamma35S binding to Galphaq (our unpublished results).	bind
22603	2	7181	6	13	NULL	NULL	NULL	statement 1	Process	stimulation of	is mediated through					receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_55_2_339_s_274	9927627	2) A marked degree of constitutive activity is detectable for both the A293E and D142A mutants also in a membrane assay (in which desensitization should not occur) measuring receptor-mediated stimulation of GTPgamma35S binding to Galphaq (our unpublished results).	bind
26977	1	7181	7	NULL	NULL	0	NULL	GTPgamma35S	NULL		bind	NULL				Galphaq	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_55_2_339_s_274	9927627	2) A marked degree of constitutive activity is detectable for both the A293E and D142A mutants also in a membrane assay (in which desensitization should not occur) measuring receptor-mediated stimulation of GTPgamma35S binding to Galphaq (our unpublished results).	bind
26978	2	7181	7	NULL	NULL	0	NULL	receptor	NULL		mediates	NULL				statement 1	NULL	stimulation of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_55_2_339_s_274	9927627	2) A marked degree of constitutive activity is detectable for both the A293E and D142A mutants also in a membrane assay (in which desensitization should not occur) measuring receptor-mediated stimulation of GTPgamma35S binding to Galphaq (our unpublished results).	bind
22604	1	7182	6	13	NULL	NULL	NULL	S3 dimer	GP		bind					LPS micelle	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_50150_s_276	15328339	2) At the initial low ratio of S3:LPS, binding of the S3 dimer to LPS micelle occurs via electrostatic and hydrophobic interactions.	bind
22605	2	7182	6	13	NULL	NULL	NULL	statement 1	Process		occurs via					electrostatic interactions	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_50150_s_276	15328339	2) At the initial low ratio of S3:LPS, binding of the S3 dimer to LPS micelle occurs via electrostatic and hydrophobic interactions.	bind
22606	3	7182	6	13	NULL	NULL	NULL	statement 1	Process		occurs via					hydrophobic interactions	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_50150_s_276	15328339	2) At the initial low ratio of S3:LPS, binding of the S3 dimer to LPS micelle occurs via electrostatic and hydrophobic interactions.	bind
26979	1	7182	7	NULL	NULL	0	NULL	 S3 dimer	NULL		bind	NULL				LPS micelle	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50150_s_276	15328339	2) At the initial low ratio of S3:LPS, binding of the S3 dimer to LPS micelle occurs via electrostatic and hydrophobic interactions.	bind
26980	2	7182	7	NULL	NULL	0	NULL	statement 1	NULL		occurs via	NULL				electrostatic interaction	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50150_s_276	15328339	2) At the initial low ratio of S3:LPS, binding of the S3 dimer to LPS micelle occurs via electrostatic and hydrophobic interactions.	bind
26981	3	7182	7	NULL	NULL	0	NULL	statement 1	NULL		occurs via	NULL				hydrophobic interaction	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_50150_s_276	15328339	2) At the initial low ratio of S3:LPS, binding of the S3 dimer to LPS micelle occurs via electrostatic and hydrophobic interactions.	bind
22607	1	7183	6	13	NULL	NULL	NULL	NCoR	GP		bind					TR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30175_s_225	9804773	2) Both NCoR and SRC-1 do not bind simultaneously to TR, suggesting at least two discreet steps are necessary for transactivation.	bind
22608	2	7183	6	13	NULL	NULL	NULL	SRC-1	GP		bind					TR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30175_s_225	9804773	2) Both NCoR and SRC-1 do not bind simultaneously to TR, suggesting at least two discreet steps are necessary for transactivation.	bind
22609	3	7183	6	13	NULL	NULL	NULL	statement 1	Process		does not occur simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30175_s_225	9804773	2) Both NCoR and SRC-1 do not bind simultaneously to TR, suggesting at least two discreet steps are necessary for transactivation.	bind
26982	1	7183	7	NULL	NULL	0	NULL	NCoR	NULL		bind	NULL				TR	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30175_s_225	9804773	2) Both NCoR and SRC-1 do not bind simultaneously to TR, suggesting at least two discreet steps are necessary for transactivation.	bind
26983	2	7183	7	NULL	NULL	0	NULL	SRC-1	NULL		 bind	NULL				TR	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30175_s_225	9804773	2) Both NCoR and SRC-1 do not bind simultaneously to TR, suggesting at least two discreet steps are necessary for transactivation.	bind
37622	3	7183	7	NULL	NULL	0	NULL	statement 1	NULL		does not occur simulataneous with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_46_30175_s_225	9804773	2) Both NCoR and SRC-1 do not bind simultaneously to TR, suggesting at least two discreet steps are necessary for transactivation.	bind
22610	1	7184	6	13	NULL	NULL	NULL	BRMS1	GP		bind			delta204-246		HDAC1.RpAp46/48	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
22611	2	7184	6	13	NULL	NULL	NULL	BRMS1	GP	full length	bind					HDAC1.RpAp46/48	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
22612	3	7184	6	13	NULL	NULL	NULL	statement 1	Process		is less than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
22613	4	7184	6	13	NULL	NULL	NULL	BRMS1	GP		bind			delta204-246		mSin3A	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
22614	5	7184	6	13	NULL	NULL	NULL	BRMS1	GP		bind			delta204-246		mSin3B	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
22615	6	7184	6	13	NULL	NULL	NULL	BRMS1	GP		bind			delta204-246		SAP30	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
22616	7	7184	6	13	NULL	NULL	NULL	BRMS1	GP		bind			delta204-246		HDAC2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
22617	8	7184	6	13	NULL	NULL	NULL	BRMS1	GP		bind			delta204-246		RBP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
22618	9	7184	6	13	NULL	NULL	NULL	BRMS1	GP	full length	bind					mSin3A	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
22619	10	7184	6	13	NULL	NULL	NULL	BRMS1	GP	full length	bind					mSin3B	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
22620	11	7184	6	13	NULL	NULL	NULL	BRMS1	GP	full length	bind					SAP30	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
22621	12	7184	6	13	NULL	NULL	NULL	BRMS1	GP	full length	bind					RBP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
22622	13	7184	6	13	NULL	NULL	NULL	BRMS1	GP	full length	bind					HDAC2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
22623	14	7184	6	13	NULL	NULL	NULL	statement 4	Process		is as effective as					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
22624	15	7184	6	13	NULL	NULL	NULL	statement 5	Process		is as effective as					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
22625	16	7184	6	13	NULL	NULL	NULL	statement 6	Process		is as effective as					statement 11	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
22626	17	7184	6	13	NULL	NULL	NULL	statement 7	Process		is as effective as					statement 13	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
22627	18	7184	6	13	NULL	NULL	NULL	statement 8	Process		is as effective as					statement 12	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
26984	1	7184	7	NULL	NULL	0	NULL	BRMS1	NULL		bind	NULL	less effectively	delta204-246		HDAC1.RpAp46/48	NULL		core subunit		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
26985	2	7184	7	NULL	NULL	0	NULL	BRMS1	NULL	full-length	bind	NULL				HDAC1.RpAp46/48	NULL		core subunit		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
26986	3	7184	7	10	NULL	0	NULL	statement 1	NULL		is less than	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
26987	4	7184	7	NULL	NULL	0	NULL	BRMS1	NULL		binds	NULL		delta204-246		mSin3A	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
26988	5	7184	7	NULL	NULL	0	NULL	BRMS1	NULL		binds	NULL		delta204-246		mSin3B	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
26989	6	7184	7	NULL	NULL	0	NULL	BRMS1	NULL		binds	NULL		delta204-246		SAP30	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
26990	7	7184	7	NULL	NULL	0	NULL	BRMS1	NULL		binds 	NULL		delta204-246		HDAC2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
26991	8	7184	7	NULL	NULL	0	NULL	BRMS1	NULL		binds	NULL		delta204-246		RBP1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
37623	9	7184	7	NULL	NULL	0	NULL	BRMS1	NULL	full-length	binds	NULL				mSin3A	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
37625	10	7184	7	NULL	NULL	0	NULL	statement 4	NULL		is as effective as	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
37626	11	7184	7	NULL	NULL	0	NULL	BRMS1	NULL	full-length	bind	NULL				mSin3B	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
37627	12	7184	7	NULL	NULL	0	NULL	statement 5	NULL		is as effective as	NULL				statement 11	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
37628	13	7184	7	NULL	NULL	0	NULL	BRMS1	NULL	full-length	bind	NULL				SAP30	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
37629	14	7184	7	NULL	NULL	0	NULL	statement 6	NULL		is as effective as	NULL				statement 13	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
37630	15	7184	7	NULL	NULL	0	NULL	BRMS1	NULL	full-length	bind	NULL				HDAC2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
37631	16	7184	7	NULL	NULL	0	NULL	statement 7	NULL		is as effective as	NULL				statement 15	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
37632	17	7184	7	NULL	NULL	0	NULL	BRMS1	NULL	full-length	bind	NULL				RBP1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
37633	18	7184	7	NULL	NULL	0	NULL	statement 8	NULL		is as effective as	NULL				statement 17	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_2_1562_s_312	14581478	2) BRMS1 has distinct binding site(s) for the HDAC1.RbAp46/48 core subunit as compared with the rest of the complex (mSin3A, mSin3B, SAP30, HDAC2, and RBP1) as demonstrated by BRMS1(delta204-246) binding less effectively to HDAC1.RpAp46/48 than does full-length BRMS1; in contrast, BRMS1(delta204-246) binds the remaining complex components as effectively ( Fig. 4).	bind
22628	1	7186	6	13	NULL	NULL	NULL				bind			Domain Ia		LRP/alpha2MR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7566_s_39	10713063	2) Domain Ia binds to LRP/alpha2MR and is internalized via endosomes to the transreticular Golgi ( 27).	bind
22629	2	7186	6	13	NULL	NULL	NULL				is internalized to			Domain Ia		transreticular Golgi	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7566_s_39	10713063	2) Domain Ia binds to LRP/alpha2MR and is internalized via endosomes to the transreticular Golgi ( 27).	bind
22630	3	7186	6	13	NULL	NULL	NULL	statement 2	Process		occurs via					endosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7566_s_39	10713063	2) Domain Ia binds to LRP/alpha2MR and is internalized via endosomes to the transreticular Golgi ( 27).	bind
26994	1	7186	7	NULL	NULL	0	NULL		NULL		bind	NULL		Domain Ia 		LRP/alpha2MR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_11_7566_s_39	10713063	2) Domain Ia binds to LRP/alpha2MR and is internalized via endosomes to the transreticular Golgi ( 27).	bind
26995	2	7186	7	NULL	NULL	0	NULL		NULL		is internalized to	NULL		Domain Ia 		transreticular Golgi	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7566_s_39	10713063	2) Domain Ia binds to LRP/alpha2MR and is internalized via endosomes to the transreticular Golgi ( 27).	bind
26996	3	7186	7	NULL	NULL	0	NULL	statement 2	NULL		occurs via	NULL				endosomes	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_11_7566_s_39	10713063	2) Domain Ia binds to LRP/alpha2MR and is internalized via endosomes to the transreticular Golgi ( 27).	bind
22631	1	7187	6	13	NULL	NULL	NULL	E2F	GP		bind					DHFR-E2F oligonucleotide	NucleicAcid	hamster			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_2_1218_s_211	8557653	2) E2F binds to the hamster DHFR-E2F  oligonucleotide only in the presence of salmon sperm DNA but not with  poly(dI-dC) as carrier DNA ( Fig. 7,  lanes 7- 11).	bind
22632	2	7187	6	13	NULL	NULL	NULL	statement 1	Process		occurs in presence of		only			sperm DNA	NucleicAcid	salmon			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_2_1218_s_211	8557653	2) E2F binds to the hamster DHFR-E2F  oligonucleotide only in the presence of salmon sperm DNA but not with  poly(dI-dC) as carrier DNA ( Fig. 7,  lanes 7- 11).	bind
22633	3	7187	6	13	NULL	NULL	NULL	statement 1	Process		occurs in absence of					poly(dI-dC)	NucleicAcid	carrier DNA			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_2_1218_s_211	8557653	2) E2F binds to the hamster DHFR-E2F  oligonucleotide only in the presence of salmon sperm DNA but not with  poly(dI-dC) as carrier DNA ( Fig. 7,  lanes 7- 11).	bind
26997	1	7187	7	NULL	NULL	0	NULL	 E2F	NULL		binds to	NULL				DHFR-E2F oligonucleotide	NULL	hamster			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_2_1218_s_211	8557653	2) E2F binds to the hamster DHFR-E2F  oligonucleotide only in the presence of salmon sperm DNA but not with  poly(dI-dC) as carrier DNA ( Fig. 7,  lanes 7- 11).	bind
26998	2	7187	7	NULL	NULL	0	NULL	statement 1	NULL		in presence of	NULL				sperm DNA	NULL	salmon			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_2_1218_s_211	8557653	2) E2F binds to the hamster DHFR-E2F  oligonucleotide only in the presence of salmon sperm DNA but not with  poly(dI-dC) as carrier DNA ( Fig. 7,  lanes 7- 11).	bind
26999	3	7187	7	NULL	NULL	0	NULL	statement 1	NULL		does not occur with	NULL				poly(dI-dC)	NULL	carrier DNA			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_2_1218_s_211	8557653	2) E2F binds to the hamster DHFR-E2F  oligonucleotide only in the presence of salmon sperm DNA but not with  poly(dI-dC) as carrier DNA ( Fig. 7,  lanes 7- 11).	bind
22663	1	7188	6	13	NULL	NULL	NULL	iNOS	GP		encompasses				promoter					HIF-1 binding site	NULL	ANA-1 macrophages	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_18_12236_s_178	9115299	2) encompassing the HIF-1 binding site of the iNOS promoter in ANA-1 macrophages.	bind
27000	1	7188	7	NULL	NULL	0	NULL	 iNOS	NULL		contains	NULL			promoter		NULL			HIF-1 binding site	NULL	ANA-1 macrophages	0	NULL	NULL	NULL	gw60_jbiolchem_272_18_12236_s_178	9115299	2) encompassing the HIF-1 binding site of the iNOS promoter in ANA-1 macrophages.	bind
22664	1	7189	6	13	NULL	NULL	NULL	FGF-2	GP		bind		directly			TSP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2449_s_37	9398667	2) FGF-2 binds directly to TSP (Taraboletti  et al., 1997  ) and may interact also with other adhesive proteins including FN, laminin, and collagen (Feige  et al., 1989  ).	bind
22665	2	7189	6	13	NULL	NULL	NULL	FGF-2	GP		interact with		may			FN	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2449_s_37	9398667	2) FGF-2 binds directly to TSP (Taraboletti  et al., 1997  ) and may interact also with other adhesive proteins including FN, laminin, and collagen (Feige  et al., 1989  ).	bind
22666	3	7189	6	13	NULL	NULL	NULL	FGF-2	GP		interact with		may			laminin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2449_s_37	9398667	2) FGF-2 binds directly to TSP (Taraboletti  et al., 1997  ) and may interact also with other adhesive proteins including FN, laminin, and collagen (Feige  et al., 1989  ).	bind
22667	4	7189	6	13	NULL	NULL	NULL	FGF-2	GP		interact with		may			collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2449_s_37	9398667	2) FGF-2 binds directly to TSP (Taraboletti  et al., 1997  ) and may interact also with other adhesive proteins including FN, laminin, and collagen (Feige  et al., 1989  ).	bind
37431	5	7189	6	13	NULL	NULL	NULL	FN	GP		is a type of					adhesive protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2449_s_37	9398667	2) FGF-2 binds directly to TSP (Taraboletti  et al., 1997  ) and may interact also with other adhesive proteins including FN, laminin, and collagen (Feige  et al., 1989  ).	bind
37432	6	7189	6	13	NULL	NULL	NULL	laminin	GP		is a type of					adhesive protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2449_s_37	9398667	2) FGF-2 binds directly to TSP (Taraboletti  et al., 1997  ) and may interact also with other adhesive proteins including FN, laminin, and collagen (Feige  et al., 1989  ).	bind
37433	7	7189	6	13	NULL	NULL	NULL	collagen	GP		is a type of					adhesive protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_8_12_2449_s_37	9398667	2) FGF-2 binds directly to TSP (Taraboletti  et al., 1997  ) and may interact also with other adhesive proteins including FN, laminin, and collagen (Feige  et al., 1989  ).	bind
27001	1	7189	7	NULL	NULL	0	NULL	FGF-2	NULL		binds	NULL	directly			TSP	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_8_12_2449_s_37	9398667	2) FGF-2 binds directly to TSP (Taraboletti  et al., 1997  ) and may interact also with other adhesive proteins including FN, laminin, and collagen (Feige  et al., 1989  ).	bind
27002	2	7189	7	NULL	NULL	0	NULL	FGF-2	NULL		interact with	NULL	may			FN	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_8_12_2449_s_37	9398667	2) FGF-2 binds directly to TSP (Taraboletti  et al., 1997  ) and may interact also with other adhesive proteins including FN, laminin, and collagen (Feige  et al., 1989  ).	bind
27003	3	7189	7	NULL	NULL	0	NULL	FGF-2	NULL		interact with	NULL	may			laminin	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_8_12_2449_s_37	9398667	2) FGF-2 binds directly to TSP (Taraboletti  et al., 1997  ) and may interact also with other adhesive proteins including FN, laminin, and collagen (Feige  et al., 1989  ).	bind
27004	4	7189	7	NULL	NULL	0	NULL	FGF-2	NULL		interact with	NULL	may			collagen	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_8_12_2449_s_37	9398667	2) FGF-2 binds directly to TSP (Taraboletti  et al., 1997  ) and may interact also with other adhesive proteins including FN, laminin, and collagen (Feige  et al., 1989  ).	bind
27005	5	7189	7	NULL	NULL	0	NULL	FN	NULL		is a type of	NULL				adhesive protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_8_12_2449_s_37	9398667	2) FGF-2 binds directly to TSP (Taraboletti  et al., 1997  ) and may interact also with other adhesive proteins including FN, laminin, and collagen (Feige  et al., 1989  ).	bind
27006	6	7189	7	NULL	NULL	0	NULL	laminin	NULL		is a type of	NULL				adhesive protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_8_12_2449_s_37	9398667	2) FGF-2 binds directly to TSP (Taraboletti  et al., 1997  ) and may interact also with other adhesive proteins including FN, laminin, and collagen (Feige  et al., 1989  ).	bind
27007	7	7189	7	NULL	NULL	0	NULL	collagen	NULL		is a type of	NULL				adhesive protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_8_12_2449_s_37	9398667	2) FGF-2 binds directly to TSP (Taraboletti  et al., 1997  ) and may interact also with other adhesive proteins including FN, laminin, and collagen (Feige  et al., 1989  ).	bind
22668	1	7190	6	13	NULL	NULL	NULL	FXI	GP		bind		directly			GPIbalpha fragment	GP		His1 - Glu282		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_47_49323_s_179	15375170	2) FXI binds directly to the GPIbalpha fragment His1 - Glu282 and to glycocalicin with almost identical affinity ( Kd of  10 nM) in the presence of ZnCl2 ( Fig. 2).	bind
22669	2	7190	6	13	NULL	NULL	NULL	FXI	GP		bind		directly			glycocalicin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_47_49323_s_179	15375170	2) FXI binds directly to the GPIbalpha fragment His1 - Glu282 and to glycocalicin with almost identical affinity ( Kd of  10 nM) in the presence of ZnCl2 ( Fig. 2).	bind
22670	3	7190	6	13	NULL	NULL	NULL	statement 1	Process		has equal affinity as					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_47_49323_s_179	15375170	2) FXI binds directly to the GPIbalpha fragment His1 - Glu282 and to glycocalicin with almost identical affinity ( Kd of  10 nM) in the presence of ZnCl2 ( Fig. 2).	bind
22671	4	7190	6	13	NULL	NULL	NULL	statement 1	Process		occurs in presence of					ZnCl2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_47_49323_s_179	15375170	2) FXI binds directly to the GPIbalpha fragment His1 - Glu282 and to glycocalicin with almost identical affinity ( Kd of  10 nM) in the presence of ZnCl2 ( Fig. 2).	bind
22672	5	7190	6	13	NULL	NULL	NULL	statement 2	Process		occurs in presence of					ZnCl2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_47_49323_s_179	15375170	2) FXI binds directly to the GPIbalpha fragment His1 - Glu282 and to glycocalicin with almost identical affinity ( Kd of  10 nM) in the presence of ZnCl2 ( Fig. 2).	bind
27008	1	7190	7	NULL	NULL	0	NULL	FXI 	NULL		binds	NULL	directly			GPIbalpha fragment	NULL		His1 - Glu282		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_49323_s_179	15375170	2) FXI binds directly to the GPIbalpha fragment His1 - Glu282 and to glycocalicin with almost identical affinity ( Kd of  10 nM) in the presence of ZnCl2 ( Fig. 2).	bind
27009	2	7190	7	NULL	NULL	0	NULL	FXI	NULL		binds	NULL	directly			glycocalicin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_49323_s_179	15375170	2) FXI binds directly to the GPIbalpha fragment His1 - Glu282 and to glycocalicin with almost identical affinity ( Kd of  10 nM) in the presence of ZnCl2 ( Fig. 2).	bind
27010	3	7190	7	NULL	NULL	0	NULL	statement 1	NULL	affinity of	is identical to	NULL				statement 2	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_49323_s_179	15375170	2) FXI binds directly to the GPIbalpha fragment His1 - Glu282 and to glycocalicin with almost identical affinity ( Kd of  10 nM) in the presence of ZnCl2 ( Fig. 2).	bind
27011	4	7190	7	NULL	NULL	0	NULL	statement 1	NULL		in presence of	NULL				ZnCl2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_49323_s_179	15375170	2) FXI binds directly to the GPIbalpha fragment His1 - Glu282 and to glycocalicin with almost identical affinity ( Kd of  10 nM) in the presence of ZnCl2 ( Fig. 2).	bind
27012	5	7190	7	NULL	NULL	0	NULL	statement 2	NULL		in presence of	NULL				ZnCl2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_49323_s_179	15375170	2) FXI binds directly to the GPIbalpha fragment His1 - Glu282 and to glycocalicin with almost identical affinity ( Kd of  10 nM) in the presence of ZnCl2 ( Fig. 2).	bind
22673	1	7191	6	13	NULL	NULL	NULL	mAb 60.11	GP		bind					gC1qR	GP		NH2-terminal site residues 76 - 93		NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_106_10_1239_s_211	11086025	2) have been used for this study: mAb 60.11 binds to an NH2-terminal site spanning amino acid residues 76 - 93 of gC1qR, and mAb 74.5.	bind
22674	2	7191	6	13	NULL	NULL	NULL	mAb 60.11	GP		bind					mAb 74.5	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_106_10_1239_s_211	11086025	2) have been used for this study: mAb 60.11 binds to an NH2-terminal site spanning amino acid residues 76 - 93 of gC1qR, and mAb 74.5.	bind
27579	1	7191	7	NULL	NULL	0	NULL	 mAb 60.11	NULL		binds to	NULL				gC1qR	NULL		NH2-terminal site residues 76 - 93		NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_106_10_1239_s_211	11086025	2) have been used for this study: mAb 60.11 binds to an NH2-terminal site spanning amino acid residues 76 - 93 of gC1qR, and mAb 74.5.	bind
27581	2	7191	7	NULL	NULL	0	NULL	mAb 60.11 	NULL		binds to	NULL				mAb 74.5	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_106_10_1239_s_211	11086025	2) have been used for this study: mAb 60.11 binds to an NH2-terminal site spanning amino acid residues 76 - 93 of gC1qR, and mAb 74.5.	bind
22675	1	7192	6	13	NULL	NULL	NULL	heparin	Chemical		bind					flXa	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_32_23066_s_227	16766524	2) Heparin binding to fIXa in part counteracts the steric protection provided by Lys98.	bind
22676	2	7192	6	13	NULL	NULL	NULL	statement 1	Process		counteracts 							steric protection provided by	Lys98		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_32_23066_s_227	16766524	2) Heparin binding to fIXa in part counteracts the steric protection provided by Lys98.	bind
27587	1	7192	7	NULL	NULL	0	NULL	Heparin 	NULL		binds to	NULL				fIXa	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23066_s_227	16766524	2) Heparin binding to fIXa in part counteracts the steric protection provided by Lys98.	bind
27588	2	7192	7	NULL	NULL	0	NULL	statement 1	NULL		counteracts	NULL					NULL	steric protection by	Lys98		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_32_23066_s_227	16766524	2) Heparin binding to fIXa in part counteracts the steric protection provided by Lys98.	bind
22677	1	7193	6	13	NULL	NULL	NULL	SP-B21 T cells	Cell	hIL-4-responsive;;human	bind					hIL-4	GP		Y124D		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_23_13869_s_90	7775445	2) hIL-4-responsive human SP-B21  T cells bind hIL-4.Y124D at this same affinity, but bind hIL-4   100-fold more avidly.	bind
22678	2	7193	6	13	NULL	NULL	NULL	SP-B21 T cells	Cell	hIL-4-responsive;;human	bind					hIL-4	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_23_13869_s_90	7775445	2) hIL-4-responsive human SP-B21  T cells bind hIL-4.Y124D at this same affinity, but bind hIL-4   100-fold more avidly.	bind
22921	3	7193	6	13	NULL	NULL	NULL	statement 2	Process		is more avid than					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_23_13869_s_90	7775445	2) hIL-4-responsive human SP-B21  T cells bind hIL-4.Y124D at this same affinity, but bind hIL-4   100-fold more avidly.	bind
27591	1	7193	7	10	NULL	0	NULL	 SP-B21 T cells	NULL	hIL-4-responsive;;human	bind	NULL				hIL-4	NULL		Y124D		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_23_13869_s_90	7775445	2) hIL-4-responsive human SP-B21  T cells bind hIL-4.Y124D at this same affinity, but bind hIL-4   100-fold more avidly.	bind
27592	2	7193	7	10	NULL	0	NULL	SP-B21 T cells	NULL	hIL-4-responsive;;human	bind	NULL	avidly			hIL-4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_23_13869_s_90	7775445	2) hIL-4-responsive human SP-B21  T cells bind hIL-4.Y124D at this same affinity, but bind hIL-4   100-fold more avidly.	bind
27593	3	7193	7	10	NULL	0	NULL	statement 2	NULL		is more avid than	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_23_13869_s_90	7775445	2) hIL-4-responsive human SP-B21  T cells bind hIL-4.Y124D at this same affinity, but bind hIL-4   100-fold more avidly.	bind
22679	1	7194	6	13	NULL	NULL	NULL	GTPgammaS	Chemical		bind					Gq/11	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_59_4_886_s_36	11259634	2) M1 muscarinic receptors facilitate [35]GTPgammaS binding to Gq/11 and Gi/o proteins (Lazareno and Birdsall 1993  ; DeLapp et al., 1999  ).	bind
22680	2	7194	6	13	NULL	NULL	NULL	GTPgammaS	Chemical		bind					Gi/o proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_59_4_886_s_36	11259634	2) M1 muscarinic receptors facilitate [35]GTPgammaS binding to Gq/11 and Gi/o proteins (Lazareno and Birdsall 1993  ; DeLapp et al., 1999  ).	bind
22681	3	7194	6	13	NULL	NULL	NULL	M1 muscarinic receptors	GP		facilitate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_59_4_886_s_36	11259634	2) M1 muscarinic receptors facilitate [35]GTPgammaS binding to Gq/11 and Gi/o proteins (Lazareno and Birdsall 1993  ; DeLapp et al., 1999  ).	bind
22682	4	7194	6	13	NULL	NULL	NULL	M1 muscarinic receptors	GP		facilitate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_59_4_886_s_36	11259634	2) M1 muscarinic receptors facilitate [35]GTPgammaS binding to Gq/11 and Gi/o proteins (Lazareno and Birdsall 1993  ; DeLapp et al., 1999  ).	bind
27594	1	7194	7	10	NULL	0	NULL	GTPgammaS	NULL		bind	NULL				Gq/11 protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_59_4_886_s_36	11259634	2) M1 muscarinic receptors facilitate [35]GTPgammaS binding to Gq/11 and Gi/o proteins (Lazareno and Birdsall 1993  ; DeLapp et al., 1999  ).	bind
27595	2	7194	7	10	NULL	0	NULL	GTPgammaS	NULL		bind	NULL				Gi/o protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_59_4_886_s_36	11259634	2) M1 muscarinic receptors facilitate [35]GTPgammaS binding to Gq/11 and Gi/o proteins (Lazareno and Birdsall 1993  ; DeLapp et al., 1999  ).	bind
27596	3	7194	7	NULL	NULL	0	NULL	M1 muscarinic receptors	NULL		facilitate	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_59_4_886_s_36	11259634	2) M1 muscarinic receptors facilitate [35]GTPgammaS binding to Gq/11 and Gi/o proteins (Lazareno and Birdsall 1993  ; DeLapp et al., 1999  ).	bind
27597	4	7194	7	NULL	NULL	0	NULL	M1 muscarinic receptors	NULL		facilitate	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_59_4_886_s_36	11259634	2) M1 muscarinic receptors facilitate [35]GTPgammaS binding to Gq/11 and Gi/o proteins (Lazareno and Birdsall 1993  ; DeLapp et al., 1999  ).	bind
22683	1	7195	6	13	NULL	NULL	NULL	TM1	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_14039_s_309	14722123	2) Modification of the N terminus decreases TM1 binding to actin which allows cofilin-mediated cytoskeletal disorganization.	bind
22684	2	7195	6	13	NULL	NULL	NULL			modification of	decreases			N terminus		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_14039_s_309	14722123	2) Modification of the N terminus decreases TM1 binding to actin which allows cofilin-mediated cytoskeletal disorganization.	bind
22685	3	7195	6	13	NULL	NULL	NULL	cofilin	GP		mediates					cytoskeletal disorganization	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_14039_s_309	14722123	2) Modification of the N terminus decreases TM1 binding to actin which allows cofilin-mediated cytoskeletal disorganization.	bind
22686	4	7195	6	13	NULL	NULL	NULL	statement 1	Process		allows					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_14039_s_309	14722123	2) Modification of the N terminus decreases TM1 binding to actin which allows cofilin-mediated cytoskeletal disorganization.	bind
27598	1	7195	7	NULL	NULL	0	NULL	TM1 	NULL		binds to	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_14_14039_s_309	14722123	2) Modification of the N terminus decreases TM1 binding to actin which allows cofilin-mediated cytoskeletal disorganization.	bind
27599	2	7195	7	NULL	NULL	0	NULL		NULL	modification of	decreases	NULL		N terminus		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_14_14039_s_309	14722123	2) Modification of the N terminus decreases TM1 binding to actin which allows cofilin-mediated cytoskeletal disorganization.	bind
27600	3	7195	7	NULL	NULL	0	NULL	cofilin	NULL		mediates	NULL				cytoskeletal disorganization	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_14_14039_s_309	14722123	2) Modification of the N terminus decreases TM1 binding to actin which allows cofilin-mediated cytoskeletal disorganization.	bind
27601	4	7195	7	NULL	NULL	0	NULL	statement 2	NULL		allows	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_14_14039_s_309	14722123	2) Modification of the N terminus decreases TM1 binding to actin which allows cofilin-mediated cytoskeletal disorganization.	bind
22926	1	7196	6	13	NULL	NULL	NULL	mannitol	Chemical		bind								C domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_16_12756_s_24	11278734	2) Modification or mutagenesis of the phosphorylation site in the B domain as well as removal of the cytoplasmic domains changes the mannitol binding kinetics of the C domain ( 11,  12).	bind
22927	2	7196	6	13	NULL	NULL	NULL			mutagenesis of	changes			phosphorylation site in the B domain		statement 1	Process	kinetics of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_16_12756_s_24	11278734	2) Modification or mutagenesis of the phosphorylation site in the B domain as well as removal of the cytoplasmic domains changes the mannitol binding kinetics of the C domain ( 11,  12).	bind
22928	3	7196	6	13	NULL	NULL	NULL			removal of	changes			cytoplasmic domain		statement 1	Process	kinetics of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_16_12756_s_24	11278734	2) Modification or mutagenesis of the phosphorylation site in the B domain as well as removal of the cytoplasmic domains changes the mannitol binding kinetics of the C domain ( 11,  12).	bind
27602	1	7196	7	NULL	NULL	0	NULL	mannitol	NULL		binds	NULL					NULL		C domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_16_12756_s_24	11278734	2) Modification or mutagenesis of the phosphorylation site in the B domain as well as removal of the cytoplasmic domains changes the mannitol binding kinetics of the C domain ( 11,  12).	bind
27603	2	7196	7	NULL	NULL	0	NULL		NULL	mutation of	changes	NULL		 B domain phosphorylation site		statement 1	NULL	binding kinetics of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_16_12756_s_24	11278734	2) Modification or mutagenesis of the phosphorylation site in the B domain as well as removal of the cytoplasmic domains changes the mannitol binding kinetics of the C domain ( 11,  12).	bind
27604	3	7196	7	NULL	NULL	0	NULL		NULL	removal of	changes	NULL		cytoplasmic domain		statement 1	NULL	binding kinetics of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_16_12756_s_24	11278734	2) Modification or mutagenesis of the phosphorylation site in the B domain as well as removal of the cytoplasmic domains changes the mannitol binding kinetics of the C domain ( 11,  12).	bind
22687	1	7197	6	13	NULL	NULL	NULL	fibrinogen	GP		bind					Rap1b	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25715_s_181	11994301	2) Modulation of fibrinogen binding by Rap1b appears to be due primarily to effects on alphaIIbbeta3 affinity.	bind
22688	2	7197	6	13	NULL	NULL	NULL	alphaIIbbeta3	GP	affinity of	effects					statement 1	Process	 modulation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25715_s_181	11994301	2) Modulation of fibrinogen binding by Rap1b appears to be due primarily to effects on alphaIIbbeta3 affinity.	bind
27605	1	7197	7	NULL	NULL	0	NULL	Rap1b	NULL		bind	NULL				fibrinogen	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_28_25715_s_181	11994301	2) Modulation of fibrinogen binding by Rap1b appears to be due primarily to effects on alphaIIbbeta3 affinity.	bind
27606	2	7197	7	NULL	NULL	0	NULL	alphaIIbbeta3	NULL	affinity of	effects	NULL				statement 1	NULL	modulation  of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25715_s_181	11994301	2) Modulation of fibrinogen binding by Rap1b appears to be due primarily to effects on alphaIIbbeta3 affinity.	bind
22689	1	7198	6	13	NULL	NULL	NULL	Monoclonal antibodies	GP		are specific for					Stat1	GP		SH2 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27954_s_244	8910398	2) Monoclonal antibodies specific for the Stat1 SH2 domain block binding of purified latent Stat1 to the tyrosine-phosphorylated IFNgamma receptor docking site ( 24,  25).	bind
22690	2	7198	6	13	NULL	NULL	NULL	Stat1	GP	purified latent	bind					IFNgamma receptor 	GP		tyrosine-phosphorylated docking site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27954_s_244	8910398	2) Monoclonal antibodies specific for the Stat1 SH2 domain block binding of purified latent Stat1 to the tyrosine-phosphorylated IFNgamma receptor docking site ( 24,  25).	bind
22691	3	7198	6	13	NULL	NULL	NULL	statement 1	Process		block					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27954_s_244	8910398	2) Monoclonal antibodies specific for the Stat1 SH2 domain block binding of purified latent Stat1 to the tyrosine-phosphorylated IFNgamma receptor docking site ( 24,  25).	bind
27607	1	7198	7	NULL	NULL	0	NULL	Stat1	NULL	purified latent	bind	NULL				 IFNgamma receptor	NULL		tyrosine-phosphorylated docking site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27954_s_244	8910398	2) Monoclonal antibodies specific for the Stat1 SH2 domain block binding of purified latent Stat1 to the tyrosine-phosphorylated IFNgamma receptor docking site ( 24,  25).	bind
27608	3	7198	7	NULL	NULL	0	NULL	statement 2	NULL		block	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27954_s_244	8910398	2) Monoclonal antibodies specific for the Stat1 SH2 domain block binding of purified latent Stat1 to the tyrosine-phosphorylated IFNgamma receptor docking site ( 24,  25).	bind
37634	2	7198	7	NULL	NULL	0	NULL	Monoclonal antibodies	NULL		are specific for	NULL				Stat1	NULL		SH2 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27954_s_244	8910398	2) Monoclonal antibodies specific for the Stat1 SH2 domain block binding of purified latent Stat1 to the tyrosine-phosphorylated IFNgamma receptor docking site ( 24,  25).	bind
22692	1	7199	6	13	NULL	NULL	NULL	GRK1	GP		bind								PDEdelta		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_1_407_s_236	14561760	2) Mutations in the C AAX box motif-disabling prenylation eliminate the binding of GRK1 to PDEdelta, suggesting that for some interacting partners the lipid attachment is essential.	bind
22693	2	7199	6	13	NULL	NULL	NULL			mutant	disable				C AAX box motif	prenylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_1_407_s_236	14561760	2) Mutations in the C AAX box motif-disabling prenylation eliminate the binding of GRK1 to PDEdelta, suggesting that for some interacting partners the lipid attachment is essential.	bind
22694	3	7199	6	13	NULL	NULL	NULL	statement 2	Process		eliminate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_1_407_s_236	14561760	2) Mutations in the C AAX box motif-disabling prenylation eliminate the binding of GRK1 to PDEdelta, suggesting that for some interacting partners the lipid attachment is essential.	bind
27609	1	7199	7	NULL	NULL	0	NULL	GRK1	NULL		bind	NULL					NULL		PDEdelta		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_1_407_s_236	14561760	2) Mutations in the C AAX box motif-disabling prenylation eliminate the binding of GRK1 to PDEdelta, suggesting that for some interacting partners the lipid attachment is essential.	bind
27610	2	7199	7	10	NULL	0	NULL		NULL	mutant	disables	NULL			C AAX box motif	prenylation	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_1_407_s_236	14561760	2) Mutations in the C AAX box motif-disabling prenylation eliminate the binding of GRK1 to PDEdelta, suggesting that for some interacting partners the lipid attachment is essential.	bind
27611	3	7199	7	10	NULL	0	NULL	statement 2	NULL		eliminate	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_1_407_s_236	14561760	2) Mutations in the C AAX box motif-disabling prenylation eliminate the binding of GRK1 to PDEdelta, suggesting that for some interacting partners the lipid attachment is essential.	bind
22695	1	7200	6	13	NULL	NULL	NULL	N1	GP		bind					ANS	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_13_7448_s_74	9516443	2) Only N1 binds with ANS and ATP.	bind
22696	2	7200	6	13	NULL	NULL	NULL	N1	GP		bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_13_7448_s_74	9516443	2) Only N1 binds with ANS and ATP.	bind
27612	1	7200	7	NULL	NULL	0	NULL	N1	NULL		binds	NULL				ANS	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_13_7448_s_74	9516443	2) Only N1 binds with ANS and ATP.	bind
27613	2	7200	7	NULL	NULL	0	NULL	N1	NULL		binds	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_13_7448_s_74	9516443	2) Only N1 binds with ANS and ATP.	bind
22697	2	7201	6	13	NULL	NULL	NULL	p47 phox	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_311	11733522	2) p47 phox binds not only to the proline-rich region located at residues 151-160 in the C-terminal cytosolic part of p22 phox but also to a domain, consisting of residues 51-63, located on a loop exposed to the cytosol.	bind
22698	3	7201	6	13	NULL	NULL	NULL	p47 phox	GP		bind					p22 phox	GP		residues 51-63		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_311	11733522	2) p47 phox binds not only to the proline-rich region located at residues 151-160 in the C-terminal cytosolic part of p22 phox but also to a domain, consisting of residues 51-63, located on a loop exposed to the cytosol.	bind
46490	1	7201	6	13	NULL	NULL	NULL	p22 phox	GP		is located in			proline-rich region		p22 phox	GP		residues 151-160 in C-terminal cytosolic part		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_311	11733522	2) p47 phox binds not only to the proline-rich region located at residues 151-160 in the C-terminal cytosolic part of p22 phox but also to a domain, consisting of residues 51-63, located on a loop exposed to the cytosol.	bind
46491	4	7201	6	13	NULL	NULL	NULL	loop	GP		is exposed to					cytosol	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_311	11733522	2) p47 phox binds not only to the proline-rich region located at residues 151-160 in the C-terminal cytosolic part of p22 phox but also to a domain, consisting of residues 51-63, located on a loop exposed to the cytosol.	bind
46492	5	7201	6	13	NULL	NULL	NULL	p22 phox	GP		is located on			residues 51-63		statement 4	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_311	11733522	2) p47 phox binds not only to the proline-rich region located at residues 151-160 in the C-terminal cytosolic part of p22 phox but also to a domain, consisting of residues 51-63, located on a loop exposed to the cytosol.	bind
27614	2	7201	7	10	NULL	0	NULL	p47 phox	NULL		bind	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_311	11733522	2) p47 phox binds not only to the proline-rich region located at residues 151-160 in the C-terminal cytosolic part of p22 phox but also to a domain, consisting of residues 51-63, located on a loop exposed to the cytosol.	bind
27615	3	7201	7	10	NULL	0	NULL	p47 phox	NULL		bind	NULL				p22 phox 	NULL		residues 51-63		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_311	11733522	2) p47 phox binds not only to the proline-rich region located at residues 151-160 in the C-terminal cytosolic part of p22 phox but also to a domain, consisting of residues 51-63, located on a loop exposed to the cytosol.	bind
46493	1	7201	7	10	NULL	0	NULL	p22 phox	NULL		is located in	NULL		proline-rich region		p22 phox	NULL		residues 151-160 in C-terminal cytosolic part		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_311	11733522	2) p47 phox binds not only to the proline-rich region located at residues 151-160 in the C-terminal cytosolic part of p22 phox but also to a domain, consisting of residues 51-63, located on a loop exposed to the cytosol.	bind
46494	4	7201	7	10	NULL	0	NULL	loop	NULL		is exposed to	NULL				cytosol	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_311	11733522	2) p47 phox binds not only to the proline-rich region located at residues 151-160 in the C-terminal cytosolic part of p22 phox but also to a domain, consisting of residues 51-63, located on a loop exposed to the cytosol.	bind
46495	5	7201	7	10	NULL	0	NULL	p22 phox	NULL		is located on	NULL		residues 51-63		statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_311	11733522	2) p47 phox binds not only to the proline-rich region located at residues 151-160 in the C-terminal cytosolic part of p22 phox but also to a domain, consisting of residues 51-63, located on a loop exposed to the cytosol.	bind
22699	1	7204	6	13	NULL	NULL	NULL	TFPI	GP		bind					hepatoma cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_25873_s_29	8824219	2) Protamine, which competes for HSPG-binding sites, inhibits TFPI binding to hepatoma cells and prolongs the half-life of 125I-TFPI in mice ( 19).	bind
22700	2	7204	6	13	NULL	NULL	NULL	Protamine	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_25873_s_29	8824219	2) Protamine, which competes for HSPG-binding sites, inhibits TFPI binding to hepatoma cells and prolongs the half-life of 125I-TFPI in mice ( 19).	bind
22701	3	7204	6	13	NULL	NULL	NULL	Protamine	GP		competes for								HSPG binding sites		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_25873_s_29	8824219	2) Protamine, which competes for HSPG-binding sites, inhibits TFPI binding to hepatoma cells and prolongs the half-life of 125I-TFPI in mice ( 19).	bind
53363	4	7204	6	13	NULL	NULL	NULL	Protamine	GP		prolonges					125I-TFPI	GP	half-life of;;mice			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_25873_s_29	8824219	2) Protamine, which competes for HSPG-binding sites, inhibits TFPI binding to hepatoma cells and prolongs the half-life of 125I-TFPI in mice ( 19).	bind
27616	1	7204	7	NULL	NULL	0	NULL	TFPI	NULL		bind	NULL				hepatoma cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_42_25873_s_29	8824219	2) Protamine, which competes for HSPG-binding sites, inhibits TFPI binding to hepatoma cells and prolongs the half-life of 125I-TFPI in mice ( 19).	bind
27617	2	7204	7	NULL	NULL	0	NULL	Protamine	NULL		competes for	NULL					NULL		HSPG-binding sites		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_25873_s_29	8824219	2) Protamine, which competes for HSPG-binding sites, inhibits TFPI binding to hepatoma cells and prolongs the half-life of 125I-TFPI in mice ( 19).	bind
27618	3	7204	7	NULL	NULL	0	NULL	Protamine	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_42_25873_s_29	8824219	2) Protamine, which competes for HSPG-binding sites, inhibits TFPI binding to hepatoma cells and prolongs the half-life of 125I-TFPI in mice ( 19).	bind
27619	4	7204	7	10	NULL	0	NULL	Protamine	NULL		prolongs	NULL				125I-TFPI	NULL	half-life of;;mice			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_25873_s_29	8824219	2) Protamine, which competes for HSPG-binding sites, inhibits TFPI binding to hepatoma cells and prolongs the half-life of 125I-TFPI in mice ( 19).	bind
22702	1	7205	6	13	NULL	NULL	NULL	PAFAH-45	GP		bind			WD40 repeats		beta-adrenergic receptor kinase	GP		PH domain		NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biochem-biophys-res-commun_209_2_7733932_s_5	7733932	2) Protein constructs expressing all 7 WD40 repeats of PAFAH-45  but lacking the N-terminal non WD40 region also bind PH domains of beta-adrenergic  receptor kinase, beta-spectrin, TecIIa and dynamin but with a differing  hierarchy of affinities than that seen with G beta.	bind
22703	2	7205	6	13	NULL	NULL	NULL	PAFAH-45	GP		bind			WD40 repeats		beta-spectrin	GP		PH domain		NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biochem-biophys-res-commun_209_2_7733932_s_5	7733932	2) Protein constructs expressing all 7 WD40 repeats of PAFAH-45  but lacking the N-terminal non WD40 region also bind PH domains of beta-adrenergic  receptor kinase, beta-spectrin, TecIIa and dynamin but with a differing  hierarchy of affinities than that seen with G beta.	bind
22704	3	7205	6	13	NULL	NULL	NULL	PAFAH-45	GP		bind			WD40 repeats		TecIIa	GP		PH domain		NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biochem-biophys-res-commun_209_2_7733932_s_5	7733932	2) Protein constructs expressing all 7 WD40 repeats of PAFAH-45  but lacking the N-terminal non WD40 region also bind PH domains of beta-adrenergic  receptor kinase, beta-spectrin, TecIIa and dynamin but with a differing  hierarchy of affinities than that seen with G beta.	bind
22705	4	7205	6	13	NULL	NULL	NULL	PAFAH-45	GP		bind			WD40 repeats		Dynamin	GP		PH domain		NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biochem-biophys-res-commun_209_2_7733932_s_5	7733932	2) Protein constructs expressing all 7 WD40 repeats of PAFAH-45  but lacking the N-terminal non WD40 region also bind PH domains of beta-adrenergic  receptor kinase, beta-spectrin, TecIIa and dynamin but with a differing  hierarchy of affinities than that seen with G beta.	bind
23107	5	7205	6	13	NULL	NULL	NULL	PAFAH-45	GP		bind			WD40 repeats		G beta	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biochem-biophys-res-commun_209_2_7733932_s_5	7733932	2) Protein constructs expressing all 7 WD40 repeats of PAFAH-45  but lacking the N-terminal non WD40 region also bind PH domains of beta-adrenergic  receptor kinase, beta-spectrin, TecIIa and dynamin but with a differing  hierarchy of affinities than that seen with G beta.	bind
53364	6	7205	6	13	NULL	NULL	NULL	PAFAH-45	GP		lacks								N-terminal non WD40 region		NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biochem-biophys-res-commun_209_2_7733932_s_5	7733932	2) Protein constructs expressing all 7 WD40 repeats of PAFAH-45  but lacking the N-terminal non WD40 region also bind PH domains of beta-adrenergic  receptor kinase, beta-spectrin, TecIIa and dynamin but with a differing  hierarchy of affinities than that seen with G beta.	bind
27620	1	7205	7	NULL	NULL	0	NULL	PAFAH-45	NULL		bind	NULL		WD40 repeat		beta-adrenergic receptor kinase	NULL		PH domain		NULL		0	NULL	NULL	NULL	abs-batch0517-0529_biochem-biophys-res-commun_209_2_7733932_s_5	7733932	2) Protein constructs expressing all 7 WD40 repeats of PAFAH-45  but lacking the N-terminal non WD40 region also bind PH domains of beta-adrenergic  receptor kinase, beta-spectrin, TecIIa and dynamin but with a differing  hierarchy of affinities than that seen with G beta.	bind
27621	2	7205	7	NULL	NULL	0	NULL	PAFAH-45	NULL		bind	NULL		WD40 repeat		beta-spectrin	NULL		PH domain		NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biochem-biophys-res-commun_209_2_7733932_s_5	7733932	2) Protein constructs expressing all 7 WD40 repeats of PAFAH-45  but lacking the N-terminal non WD40 region also bind PH domains of beta-adrenergic  receptor kinase, beta-spectrin, TecIIa and dynamin but with a differing  hierarchy of affinities than that seen with G beta.	bind
27622	3	7205	7	NULL	NULL	0	NULL	PAFAH-45	NULL		bind	NULL		WD40 repeat		TecIIa	NULL		PH domain		NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biochem-biophys-res-commun_209_2_7733932_s_5	7733932	2) Protein constructs expressing all 7 WD40 repeats of PAFAH-45  but lacking the N-terminal non WD40 region also bind PH domains of beta-adrenergic  receptor kinase, beta-spectrin, TecIIa and dynamin but with a differing  hierarchy of affinities than that seen with G beta.	bind
27623	4	7205	7	NULL	NULL	0	NULL	PAFAH-45	NULL		bind	NULL		WD40 repeat		dynamin	NULL		PH domain		NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biochem-biophys-res-commun_209_2_7733932_s_5	7733932	2) Protein constructs expressing all 7 WD40 repeats of PAFAH-45  but lacking the N-terminal non WD40 region also bind PH domains of beta-adrenergic  receptor kinase, beta-spectrin, TecIIa and dynamin but with a differing  hierarchy of affinities than that seen with G beta.	bind
27624	5	7205	7	NULL	NULL	0	NULL	PAFAH-45	NULL		bind	NULL		WD40 repeat		Gbeta	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_biochem-biophys-res-commun_209_2_7733932_s_5	7733932	2) Protein constructs expressing all 7 WD40 repeats of PAFAH-45  but lacking the N-terminal non WD40 region also bind PH domains of beta-adrenergic  receptor kinase, beta-spectrin, TecIIa and dynamin but with a differing  hierarchy of affinities than that seen with G beta.	bind
27625	6	7205	7	NULL	NULL	0	NULL	PAFAH-45	NULL		lacks	NULL					NULL		N-terminal non WD40 region		NULL		0	NULL	NULL	NULL	abs-batch0517-0529_biochem-biophys-res-commun_209_2_7733932_s_5	7733932	2) Protein constructs expressing all 7 WD40 repeats of PAFAH-45  but lacking the N-terminal non WD40 region also bind PH domains of beta-adrenergic  receptor kinase, beta-spectrin, TecIIa and dynamin but with a differing  hierarchy of affinities than that seen with G beta.	bind
22706	1	7206	6	13	NULL	NULL	NULL	RAP74	GP		bind					RAP30	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_20_11703_s_207	8662660	2) RAP74 could bind RAP30 to block the TFIIB binding site on  RAP30.	bind
22707	2	7206	6	13	NULL	NULL	NULL	statement 1	Process		block					RAP30	GP		TFIIB binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_20_11703_s_207	8662660	2) RAP74 could bind RAP30 to block the TFIIB binding site on  RAP30.	bind
27626	1	7206	7	NULL	NULL	0	NULL	RAP74	NULL		bind	NULL				RAP30	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_20_11703_s_207	8662660	2) RAP74 could bind RAP30 to block the TFIIB binding site on  RAP30.	bind
27627	2	7206	7	NULL	NULL	0	NULL	statement 1	NULL		block	NULL				RAP30	NULL		TFIIB binding site		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_20_11703_s_207	8662660	2) RAP74 could bind RAP30 to block the TFIIB binding site on  RAP30.	bind
22708	1	7207	6	13	NULL	NULL	NULL	ATP	Chemical		bind					DnaK	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_157	8626401	2) The  exogenous P   inhibits both ATP hydrolysis and DnaK  conformational change but does not influence the binding of ATP to DnaK  (this paper).	bind
22709	2	7207	6	13	NULL	NULL	NULL	exogenous P	Chemical		inhibits					ATP	Chemical	hydrolysis of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_157	8626401	2) The  exogenous P   inhibits both ATP hydrolysis and DnaK  conformational change but does not influence the binding of ATP to DnaK  (this paper).	bind
22710	3	7207	6	13	NULL	NULL	NULL	exogenous P	Chemical		inhibits					DnaK	GP	conformational change of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_157	8626401	2) The  exogenous P   inhibits both ATP hydrolysis and DnaK  conformational change but does not influence the binding of ATP to DnaK  (this paper).	bind
53365	4	7207	6	13	NULL	NULL	NULL	exogenous P	Chemical		does not influence					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_157	8626401	2) The  exogenous P   inhibits both ATP hydrolysis and DnaK  conformational change but does not influence the binding of ATP to DnaK  (this paper).	bind
27628	1	7207	7	NULL	NULL	0	NULL	ATP  	NULL		bind	NULL				DnaK	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_157	8626401	2) The  exogenous P   inhibits both ATP hydrolysis and DnaK  conformational change but does not influence the binding of ATP to DnaK  (this paper).	bind
27629	2	7207	7	NULL	NULL	0	NULL	exogenous P	NULL		inhibits	NULL				ATP	NULL	hydrolysis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_157	8626401	2) The  exogenous P   inhibits both ATP hydrolysis and DnaK  conformational change but does not influence the binding of ATP to DnaK  (this paper).	bind
27630	3	7207	7	NULL	NULL	0	NULL	exogenous P	NULL		inhibits	NULL				DnaK	NULL	conformational change of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_157	8626401	2) The  exogenous P   inhibits both ATP hydrolysis and DnaK  conformational change but does not influence the binding of ATP to DnaK  (this paper).	bind
27631	4	7207	7	NULL	NULL	0	NULL	exogenous P	NULL		does not influence	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_157	8626401	2) The  exogenous P   inhibits both ATP hydrolysis and DnaK  conformational change but does not influence the binding of ATP to DnaK  (this paper).	bind
22711	1	7208	6	13	NULL	NULL	NULL	Stat3	GP		bind					pY XXQ-containing peptides	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18967_s_27	14966128	2) The +3 Gln is required for binding of Stat3 to pY XXQ-containing peptides.	bind
22712	2	7208	6	13	NULL	NULL	NULL	Gln	AminoAcid		is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18967_s_27	14966128	2) The +3 Gln is required for binding of Stat3 to pY XXQ-containing peptides.	bind
27632	1	7208	7	10	NULL	0	NULL	 Stat3	NULL		bind	NULL				pY XXQ-containing peptides	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18967_s_27	14966128	2) The +3 Gln is required for binding of Stat3 to pY XXQ-containing peptides.	bind
27633	2	7208	7	NULL	NULL	0	NULL	Gln	NULL		is required for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_18967_s_27	14966128	2) The +3 Gln is required for binding of Stat3 to pY XXQ-containing peptides.	bind
22717	1	7209	6	13	NULL	NULL	NULL	TSG101/Vps23p	GP		bind			C-terminal region		VPS28/Vps28p	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_34_36059_s_33	15218037	2) The C-terminal region of TSG101/Vps23p binds VPS28/Vps28p ( ,  ,  ).	bind
27634	1	7209	7	NULL	NULL	0	NULL	TSG101/Vps23p	NULL		binds	NULL		C-terminal region		 VPS28/Vps28p	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_34_36059_s_33	15218037	2) The C-terminal region of TSG101/Vps23p binds VPS28/Vps28p ( ,  ,  ).	bind
22719	1	7210	6	13	NULL	NULL	NULL	Cu(I)	Chemical	binding of	signals					APP	GP	processing of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_19_17401_s_172	12611883	2) The Cu(I) binding signals APP processing or proteolytic breakdown via the non-amyloidogenic route ( 21,  22).	bind
22721	2	7210	6	13	NULL	NULL	NULL	Cu(I)	Chemical	binding of	signals					APP	GP	proteolytic breakdown of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_19_17401_s_172	12611883	2) The Cu(I) binding signals APP processing or proteolytic breakdown via the non-amyloidogenic route ( 21,  22).	bind
22724	3	7210	6	13	NULL	NULL	NULL	statement 2	Process		occurs by					non-amyloidogenic route	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_19_17401_s_172	12611883	2) The Cu(I) binding signals APP processing or proteolytic breakdown via the non-amyloidogenic route ( 21,  22).	bind
27635	1	7210	7	NULL	NULL	0	NULL	Cu(I)	NULL	binding of	signals	NULL				APP	NULL	processing of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_17401_s_172	12611883	2) The Cu(I) binding signals APP processing or proteolytic breakdown via the non-amyloidogenic route ( 21,  22).	bind
27636	2	7210	7	10	NULL	0	NULL	Cu(I)	NULL	binding of	signals	NULL				APP	NULL	proteolytic breakdown of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_19_17401_s_172	12611883	2) The Cu(I) binding signals APP processing or proteolytic breakdown via the non-amyloidogenic route ( 21,  22).	bind
46496	3	7210	7	10	NULL	0	NULL	statement 2	NULL		via	NULL				non-amyloidogenic route	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_17401_s_172	12611883	2) The Cu(I) binding signals APP processing or proteolytic breakdown via the non-amyloidogenic route ( 21,  22).	bind
22727	1	7211	6	13	NULL	NULL	NULL	GAT	GP		is					GGA and Tom1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_7105_s_17	14660606	2) The GAT ( GGA  and  Tom1) domain interacts with a GTP-bound form of the small GTPase ADP-ribosylation factor (ARF) and is responsible for association of GGAs with TGN membranes ( - ).	bind
22728	2	7211	6	13	NULL	NULL	NULL	GTP	Chemical		bind					ARF	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_7105_s_17	14660606	2) The GAT ( GGA  and  Tom1) domain interacts with a GTP-bound form of the small GTPase ADP-ribosylation factor (ARF) and is responsible for association of GGAs with TGN membranes ( - ).	bind
22729	3	7211	6	13	NULL	NULL	NULL	ARF	GP		is					ADP-ribosylation factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_7105_s_17	14660606	2) The GAT ( GGA  and  Tom1) domain interacts with a GTP-bound form of the small GTPase ADP-ribosylation factor (ARF) and is responsible for association of GGAs with TGN membranes ( - ).	bind
22730	4	7211	6	13	NULL	NULL	NULL				interacts with			GAT domain		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_7105_s_17	14660606	2) The GAT ( GGA  and  Tom1) domain interacts with a GTP-bound form of the small GTPase ADP-ribosylation factor (ARF) and is responsible for association of GGAs with TGN membranes ( - ).	bind
22731	5	7211	6	13	NULL	NULL	NULL	GGAs	GP		associate with					TGN membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_7105_s_17	14660606	2) The GAT ( GGA  and  Tom1) domain interacts with a GTP-bound form of the small GTPase ADP-ribosylation factor (ARF) and is responsible for association of GGAs with TGN membranes ( - ).	bind
22734	6	7211	6	13	NULL	NULL	NULL				is responsible for			GAT domain		statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_7105_s_17	14660606	2) The GAT ( GGA  and  Tom1) domain interacts with a GTP-bound form of the small GTPase ADP-ribosylation factor (ARF) and is responsible for association of GGAs with TGN membranes ( - ).	bind
46499	7	7211	6	13	NULL	NULL	NULL	ARF	GP		is a type of					small GTPases	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_7105_s_17	14660606	2) The GAT ( GGA  and  Tom1) domain interacts with a GTP-bound form of the small GTPase ADP-ribosylation factor (ARF) and is responsible for association of GGAs with TGN membranes ( - ).	bind
27637	1	7211	7	13	NULL	NULL	NULL				interacts with			GAT domain		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_7105_s_17	14660606	2) The GAT ( GGA  and  Tom1) domain interacts with a GTP-bound form of the small GTPase ADP-ribosylation factor (ARF) and is responsible for association of GGAs with TGN membranes ( - ).	bind
27638	2	7211	7	NULL	NULL	0	NULL		NULL		consist of	NULL		GAT domain			NULL		GGA and Tom1 domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_7105_s_17	14660606	2) The GAT ( GGA  and  Tom1) domain interacts with a GTP-bound form of the small GTPase ADP-ribosylation factor (ARF) and is responsible for association of GGAs with TGN membranes ( - ).	bind
27639	3	7211	7	NULL	NULL	0	NULL		NULL		associate with	NULL		GGA		TGN membranes	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_7105_s_17	14660606	2) The GAT ( GGA  and  Tom1) domain interacts with a GTP-bound form of the small GTPase ADP-ribosylation factor (ARF) and is responsible for association of GGAs with TGN membranes ( - ).	bind
27640	4	7211	7	NULL	NULL	0	NULL		NULL		is responsible for	NULL		GAT domain		statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_7105_s_17	14660606	2) The GAT ( GGA  and  Tom1) domain interacts with a GTP-bound form of the small GTPase ADP-ribosylation factor (ARF) and is responsible for association of GGAs with TGN membranes ( - ).	bind
27641	5	7211	7	NULL	NULL	0	NULL	ARF	NULL		is	NULL				ADP-ribosylation factor	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_7105_s_17	14660606	2) The GAT ( GGA  and  Tom1) domain interacts with a GTP-bound form of the small GTPase ADP-ribosylation factor (ARF) and is responsible for association of GGAs with TGN membranes ( - ).	bind
46497	6	7211	7	10	NULL	0	NULL	GTP	NULL		bind	NULL				ARF	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_7105_s_17	14660606	2) The GAT ( GGA  and  Tom1) domain interacts with a GTP-bound form of the small GTPase ADP-ribosylation factor (ARF) and is responsible for association of GGAs with TGN membranes ( - ).	bind
46498	7	7211	7	10	NULL	0	NULL	ARF	NULL		is a type of	NULL				small GTPase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_7105_s_17	14660606	2) The GAT ( GGA  and  Tom1) domain interacts with a GTP-bound form of the small GTPase ADP-ribosylation factor (ARF) and is responsible for association of GGAs with TGN membranes ( - ).	bind
22741	1	7212	6	13	NULL	NULL	NULL	hnRNP M4	GP	rat	expressed in					E.coli	Organism				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_33_31067_s_266	11406629	2) The rat hnRNP M4 fusion protein expressed in  E. coli binds CEA and this interaction is a Ca2+-dependent process (Fig.  5).	bind
22742	2	7212	6	13	NULL	NULL	NULL	statement 1	GP		bind					CEA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_33_31067_s_266	11406629	2) The rat hnRNP M4 fusion protein expressed in  E. coli binds CEA and this interaction is a Ca2+-dependent process (Fig.  5).	bind
22744	3	7212	6	13	NULL	NULL	NULL	statement 2	Process		is dependent on					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_33_31067_s_266	11406629	2) The rat hnRNP M4 fusion protein expressed in  E. coli binds CEA and this interaction is a Ca2+-dependent process (Fig.  5).	bind
46500	3	7212	6	13	NULL	NULL	NULL	hnRNP M4	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_33_31067_s_266	11406629	2) The rat hnRNP M4 fusion protein expressed in  E. coli binds CEA and this interaction is a Ca2+-dependent process (Fig.  5).	bind
27642	1	7212	7	10	NULL	0	NULL	hnRNP M4	NULL	rat	binds	NULL				CEA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_33_31067_s_266	11406629	2) The rat hnRNP M4 fusion protein expressed in  E. coli binds CEA and this interaction is a Ca2+-dependent process (Fig.  5).	bind
27643	2	7212	7	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				Ca2+	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_33_31067_s_266	11406629	2) The rat hnRNP M4 fusion protein expressed in  E. coli binds CEA and this interaction is a Ca2+-dependent process (Fig.  5).	bind
46501	3	7212	7	10	NULL	0	NULL	hnRNP M4	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_33_31067_s_266	11406629	2) The rat hnRNP M4 fusion protein expressed in  E. coli binds CEA and this interaction is a Ca2+-dependent process (Fig.  5).	bind
22748	1	7213	6	13	NULL	NULL	NULL	S4GGnM-R	GP		bind					ligand	GP	soluble	terminal S4GGnM		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_23_14629_s_141	9169424	2) The S4GGnM-R is able to bind soluble ligands terminating with S4GGnM as well as ligands with terminal Man or Fuc in the PEG precipitation assay, whereas the Man-R will bind ligands with terminal Man or Fuc but not those with terminal S4GGnM in the same assay.	bind
22751	2	7213	6	13	NULL	NULL	NULL	S4GGnM-R	GP		bind					ligand	Chemical	soluble	terminal Fuc		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_23_14629_s_141	9169424	2) The S4GGnM-R is able to bind soluble ligands terminating with S4GGnM as well as ligands with terminal Man or Fuc in the PEG precipitation assay, whereas the Man-R will bind ligands with terminal Man or Fuc but not those with terminal S4GGnM in the same assay.	bind
22929	3	7213	6	13	NULL	NULL	NULL	S4GGnM-R	GP		bind					ligand	Chemical	soluble	terminal Man		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_23_14629_s_141	9169424	2) The S4GGnM-R is able to bind soluble ligands terminating with S4GGnM as well as ligands with terminal Man or Fuc in the PEG precipitation assay, whereas the Man-R will bind ligands with terminal Man or Fuc but not those with terminal S4GGnM in the same assay.	bind
22930	4	7213	6	13	NULL	NULL	NULL	ManR	GP		bind					ligand	Chemical	soluble	terminal Man		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_23_14629_s_141	9169424	2) The S4GGnM-R is able to bind soluble ligands terminating with S4GGnM as well as ligands with terminal Man or Fuc in the PEG precipitation assay, whereas the Man-R will bind ligands with terminal Man or Fuc but not those with terminal S4GGnM in the same assay.	bind
22931	5	7213	6	13	NULL	NULL	NULL	ManR	GP		bind					ligand	Chemical	soluble	terminal Fuc		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_23_14629_s_141	9169424	2) The S4GGnM-R is able to bind soluble ligands terminating with S4GGnM as well as ligands with terminal Man or Fuc in the PEG precipitation assay, whereas the Man-R will bind ligands with terminal Man or Fuc but not those with terminal S4GGnM in the same assay.	bind
22932	6	7213	6	13	NULL	NULL	NULL	ManR	GP		does not bind					ligand	Chemical	soluble	terminal S4GGnM		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_23_14629_s_141	9169424	2) The S4GGnM-R is able to bind soluble ligands terminating with S4GGnM as well as ligands with terminal Man or Fuc in the PEG precipitation assay, whereas the Man-R will bind ligands with terminal Man or Fuc but not those with terminal S4GGnM in the same assay.	bind
27644	1	7213	7	10	NULL	0	NULL	S4GGnM-R	NULL		bind	NULL				ligand	NULL	soluble	terminal S4GGnM		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_23_14629_s_141	9169424	2) The S4GGnM-R is able to bind soluble ligands terminating with S4GGnM as well as ligands with terminal Man or Fuc in the PEG precipitation assay, whereas the Man-R will bind ligands with terminal Man or Fuc but not those with terminal S4GGnM in the same assay.	bind
27645	2	7213	7	10	NULL	0	NULL	S4GGnM-R	NULL		bind	NULL				ligand	NULL	soluble	terminal Man		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_23_14629_s_141	9169424	2) The S4GGnM-R is able to bind soluble ligands terminating with S4GGnM as well as ligands with terminal Man or Fuc in the PEG precipitation assay, whereas the Man-R will bind ligands with terminal Man or Fuc but not those with terminal S4GGnM in the same assay.	bind
27646	3	7213	7	10	NULL	0	NULL	S4GGnM-R	NULL		binds	NULL				ligand	NULL	soluble	terminal Fuc		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_23_14629_s_141	9169424	2) The S4GGnM-R is able to bind soluble ligands terminating with S4GGnM as well as ligands with terminal Man or Fuc in the PEG precipitation assay, whereas the Man-R will bind ligands with terminal Man or Fuc but not those with terminal S4GGnM in the same assay.	bind
27647	4	7213	7	10	NULL	0	NULL	 Man-R	NULL		bind	NULL				ligand	NULL	soluble	terminal Man		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_23_14629_s_141	9169424	2) The S4GGnM-R is able to bind soluble ligands terminating with S4GGnM as well as ligands with terminal Man or Fuc in the PEG precipitation assay, whereas the Man-R will bind ligands with terminal Man or Fuc but not those with terminal S4GGnM in the same assay.	bind
27648	5	7213	7	10	NULL	0	NULL	Man-R	NULL		bind	NULL				ligand	NULL	soluble	terminal Fuc		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_23_14629_s_141	9169424	2) The S4GGnM-R is able to bind soluble ligands terminating with S4GGnM as well as ligands with terminal Man or Fuc in the PEG precipitation assay, whereas the Man-R will bind ligands with terminal Man or Fuc but not those with terminal S4GGnM in the same assay.	bind
27649	6	7213	7	10	NULL	0	NULL	Man-R	NULL		does not bind	NULL				ligand	NULL	soluble	terminal S4GGnM		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_23_14629_s_141	9169424	2) The S4GGnM-R is able to bind soluble ligands terminating with S4GGnM as well as ligands with terminal Man or Fuc in the PEG precipitation assay, whereas the Man-R will bind ligands with terminal Man or Fuc but not those with terminal S4GGnM in the same assay.	bind
22755	1	7214	6	13	NULL	NULL	NULL	GST-hTom70	GP	mutant	bind			N267		Mcl-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_9_3952_s_187	16822835	2) The Tom70 mutant containing the N-terminal three TPR domains as in GST-hTom70N267 bound to Mcl-1 with an affinity that was much higher than the mutant without this N-terminal region ( Figure 7B).	bind
22762	2	7214	6	13	NULL	NULL	NULL	GST-hTom70	GP	mutant	bind					Mcl-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_9_3952_s_187	16822835	2) The Tom70 mutant containing the N-terminal three TPR domains as in GST-hTom70N267 bound to Mcl-1 with an affinity that was much higher than the mutant without this N-terminal region ( Figure 7B).	bind
22764	3	7214	6	13	NULL	NULL	NULL	statement 1	Process		higher affinity than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_9_3952_s_187	16822835	2) The Tom70 mutant containing the N-terminal three TPR domains as in GST-hTom70N267 bound to Mcl-1 with an affinity that was much higher than the mutant without this N-terminal region ( Figure 7B).	bind
53366	4	7214	6	13	NULL	NULL	NULL	Tom70	GP	mutant	contains								N-terminal three TPR domains		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_9_3952_s_187	16822835	2) The Tom70 mutant containing the N-terminal three TPR domains as in GST-hTom70N267 bound to Mcl-1 with an affinity that was much higher than the mutant without this N-terminal region ( Figure 7B).	bind
27650	1	7214	7	NULL	NULL	0	NULL	GST-hTom70	NULL	mutant	bind	NULL		N267		Mcl-1	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_9_3952_s_187	16822835	2) The Tom70 mutant containing the N-terminal three TPR domains as in GST-hTom70N267 bound to Mcl-1 with an affinity that was much higher than the mutant without this N-terminal region ( Figure 7B).	bind
27651	2	7214	7	NULL	NULL	0	NULL	Tom70	NULL	mutant	contains	NULL					NULL		N-terminal three TPR domains		NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_9_3952_s_187	16822835	2) The Tom70 mutant containing the N-terminal three TPR domains as in GST-hTom70N267 bound to Mcl-1 with an affinity that was much higher than the mutant without this N-terminal region ( Figure 7B).	bind
27654	3	7214	7	NULL	NULL	0	NULL	Tom70	NULL	mutant lacking	bind	NULL		 N-terminal TPR domain		Mcl-1 	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_9_3952_s_187	16822835	2) The Tom70 mutant containing the N-terminal three TPR domains as in GST-hTom70N267 bound to Mcl-1 with an affinity that was much higher than the mutant without this N-terminal region ( Figure 7B).	bind
27656	4	7214	7	10	NULL	0	NULL	statement 1	NULL		higher affinity than	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_9_3952_s_187	16822835	2) The Tom70 mutant containing the N-terminal three TPR domains as in GST-hTom70N267 bound to Mcl-1 with an affinity that was much higher than the mutant without this N-terminal region ( Figure 7B).	bind
22782	1	7216	6	13	NULL	NULL	NULL				bind			Tyr(P)527					SH2 domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_33_23776_s_280	16790421	2) Tyr(P)527 binds to the SH2 domain.	bind
27661	1	7216	7	NULL	NULL	0	NULL		NULL		binds to	NULL		Tyr(P)527			NULL		SH2 domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_33_23776_s_280	16790421	2) Tyr(P)527 binds to the SH2 domain.	bind
22785	1	7217	6	13	NULL	NULL	NULL	VPAC1 receptor	GP		bind					vasoactive intestinal polypeptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
22786	2	7217	6	13	NULL	NULL	NULL	VPAC1 receptor	GP		bind					PACAP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
22788	3	7217	6	13	NULL	NULL	NULL	VPAC2 receptor	GP		bind					vasoactive intestinal polypeptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
22789	4	7217	6	13	NULL	NULL	NULL	VPAC2 receptor	GP		bind					PACAP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
22790	5	7217	6	13	NULL	NULL	NULL	VPAC1 receptor	GP		activates		exclusively			adenylate cyclase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
22791	6	7217	6	13	NULL	NULL	NULL	VPAC2 receptor	GP		activate		exclusively			adenylate cyclase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
22792	7	7217	6	13	NULL	NULL	NULL	VPAC1 receptor	GP		is found in					lung	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
22793	8	7217	6	13	NULL	NULL	NULL	VPAC1 receptor	GP		is found in					liver	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
22794	9	7217	6	13	NULL	NULL	NULL	VPAC1 receptor	GP		is found in					prostate gland	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
22796	10	7217	6	13	NULL	NULL	NULL	VPAC1 receptor	GP		is found in					seminal vesicle	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
22798	11	7217	6	13	NULL	NULL	NULL	VPAC2 receptor	GP		is found in					lung	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
22799	12	7217	6	13	NULL	NULL	NULL	VPAC2 receptor	GP		is found in					liver	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
22800	13	7217	6	13	NULL	NULL	NULL	VPAC2 receptor	GP		is found in					prostate gland	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
22801	14	7217	6	13	NULL	NULL	NULL	VPAC2 receptor	GP		is found in					seminal vesicle	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
27662	1	7217	7	10	NULL	0	NULL	VPAC1 receptors	NULL		bind	NULL				vasoactive intestinal polypeptide	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
27663	2	7217	7	10	NULL	0	NULL	VPAC2 receptors	NULL		bind	NULL				vasoactive intestinal polypeptide	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
27664	3	7217	7	10	NULL	0	NULL	VPAC1 receptors	NULL		bind	NULL				PACAP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
27666	4	7217	7	10	NULL	0	NULL	VPAC2 receptors	NULL		bind	NULL				PACAP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
27668	5	7217	7	10	NULL	0	NULL	VPAC1 receptor			activate		exclusively			adenylate cyclase					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
27669	6	7217	7	10	NULL	0	NULL	VPAC2 receptor			activate		exclusively			adenylate cyclase					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
27670	7	7217	7	10	NULL	0	NULL	VPAC1 receptor			is found in					lung					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
27672	8	7217	7	10	NULL	0	NULL	VPAC1 receptor			is found in					liver					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
54112	9	7217	7	10	NULL	0	NULL	VPAC1 receptor			is found in					prostate gland					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
54113	10	7217	7	10	NULL	0	NULL	VPAC1 receptor			is found in					seminal vesicles					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
54114	11	7217	7	10	NULL	0	NULL	VPAC2 receptor			is found in					lung					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
54115	12	7217	7	10	NULL	0	NULL	VPAC2 receptor			is found in					liver					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
54116	13	7217	7	10	NULL	0	NULL	VPAC2 receptor			is found in					prostate gland					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
54117	14	7217	7	10	NULL	0	NULL	VPAC2 receptor			is found in					seminal vesicles					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_26_23562_s_31	11320087	2) VPAC1 and VPAC2 receptors, which bind both vasoactive intestinal polypeptide and PACAP but activate almost exclusively adenylate cyclase ( 19-21) and have been found in lung, liver, prostate gland, and seminal vesicles.	bind
22933	1	7221	6	13	NULL	NULL	NULL	apoB gene	GP		increase				LDLR binding region	LDL cholesterol	Chemical	levels of 			NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_34_0_233_s_110	11092828	2), in familial hypercholesterolemia,  and the LDLR binding region of the apo B gene (chromosome 2p23-p24), in familial  defective apo B100, have both been shown to increase LDL cholesterol levels and risk  of coronary heart disease ( 34,  40,  47,  67,  85,  101).	bind
22934	2	7221	6	13	NULL	NULL	NULL	statement 1	Process		occurs in					familial hypercholesterolemia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_34_0_233_s_110	11092828	2), in familial hypercholesterolemia,  and the LDLR binding region of the apo B gene (chromosome 2p23-p24), in familial  defective apo B100, have both been shown to increase LDL cholesterol levels and risk  of coronary heart disease ( 34,  40,  47,  67,  85,  101).	bind
22935	3	7221	6	13	NULL	NULL	NULL	apoB-100	GP	defective	increases					LDL cholesterol	Chemical	levels of			NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_34_0_233_s_110	11092828	2), in familial hypercholesterolemia,  and the LDLR binding region of the apo B gene (chromosome 2p23-p24), in familial  defective apo B100, have both been shown to increase LDL cholesterol levels and risk  of coronary heart disease ( 34,  40,  47,  67,  85,  101).	bind
22936	4	7221	6	13	NULL	NULL	NULL	statement 3	Process		occurs in					familial hypercholesterolemia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_34_0_233_s_110	11092828	2), in familial hypercholesterolemia,  and the LDLR binding region of the apo B gene (chromosome 2p23-p24), in familial  defective apo B100, have both been shown to increase LDL cholesterol levels and risk  of coronary heart disease ( 34,  40,  47,  67,  85,  101).	bind
22937	5	7221	6	13	NULL	NULL	NULL	apoB gene	GP		increases				LDLR binding region	coronary heart disease	MedicalFinding	risk of			NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_34_0_233_s_110	11092828	2), in familial hypercholesterolemia,  and the LDLR binding region of the apo B gene (chromosome 2p23-p24), in familial  defective apo B100, have both been shown to increase LDL cholesterol levels and risk  of coronary heart disease ( 34,  40,  47,  67,  85,  101).	bind
22938	6	7221	6	13	NULL	NULL	NULL	apoB-100	GP	defective	increases					coronary heart disease	MedicalFinding	risk of			NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_34_0_233_s_110	11092828	2), in familial hypercholesterolemia,  and the LDLR binding region of the apo B gene (chromosome 2p23-p24), in familial  defective apo B100, have both been shown to increase LDL cholesterol levels and risk  of coronary heart disease ( 34,  40,  47,  67,  85,  101).	bind
27853	1	7221	7	NULL	NULL	0	NULL	apoB gene	NULL		increase	NULL			LDLR binding region 	LDL cholesterol	NULL	levels of			NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_34_0_233_s_110	11092828	2), in familial hypercholesterolemia,  and the LDLR binding region of the apo B gene (chromosome 2p23-p24), in familial  defective apo B100, have both been shown to increase LDL cholesterol levels and risk  of coronary heart disease ( 34,  40,  47,  67,  85,  101).	bind
27854	2	7221	7	NULL	NULL	0	NULL	 apo B100	NULL	familial defective	increase	NULL				LDL cholesterol	NULL	levels of			NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_34_0_233_s_110	11092828	2), in familial hypercholesterolemia,  and the LDLR binding region of the apo B gene (chromosome 2p23-p24), in familial  defective apo B100, have both been shown to increase LDL cholesterol levels and risk  of coronary heart disease ( 34,  40,  47,  67,  85,  101).	bind
27855	3	7221	7	NULL	NULL	0	NULL	statement 1	NULL		increase	NULL				coronary heart disease	NULL	risk of			NULL		0	NULL	NULL	NULL	gw70_annurevgenet_34_0_233_s_110	11092828	2), in familial hypercholesterolemia,  and the LDLR binding region of the apo B gene (chromosome 2p23-p24), in familial  defective apo B100, have both been shown to increase LDL cholesterol levels and risk  of coronary heart disease ( 34,  40,  47,  67,  85,  101).	bind
27856	4	7221	7	NULL	NULL	0	NULL	statement 2	NULL		increase	NULL				coronary heart disease	NULL	risk of			NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_34_0_233_s_110	11092828	2), in familial hypercholesterolemia,  and the LDLR binding region of the apo B gene (chromosome 2p23-p24), in familial  defective apo B100, have both been shown to increase LDL cholesterol levels and risk  of coronary heart disease ( 34,  40,  47,  67,  85,  101).	bind
27866	5	7221	7	NULL	NULL	0	NULL	statement 1	NULL		occurs in	NULL				familial hypercholesterolemia	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevgenet_34_0_233_s_110	11092828	2), in familial hypercholesterolemia,  and the LDLR binding region of the apo B gene (chromosome 2p23-p24), in familial  defective apo B100, have both been shown to increase LDL cholesterol levels and risk  of coronary heart disease ( 34,  40,  47,  67,  85,  101).	bind
22803	1	7224	6	13	NULL	NULL	NULL	AGS3	GP		bind		preferentially			Galpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_43_33193_s_22	10969064	2, 3 AGS3 preferentially binds to Galpha in the presence of GDP ( 1).	bind
22804	2	7224	6	13	NULL	NULL	NULL	statement 1	Process		occurs in presence of					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_43_33193_s_22	10969064	2, 3 AGS3 preferentially binds to Galpha in the presence of GDP ( 1).	bind
27679	1	7224	7	NULL	NULL	0	NULL	AGS3	NULL		binds	NULL	preferentially			Galpha	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_43_33193_s_22	10969064	2, 3 AGS3 preferentially binds to Galpha in the presence of GDP ( 1).	bind
27680	2	7224	7	NULL	NULL	0	NULL	statement 1	NULL		in presence of	NULL				GDP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_43_33193_s_22	10969064	2, 3 AGS3 preferentially binds to Galpha in the presence of GDP ( 1).	bind
22805	1	7225	6	13	NULL	NULL	NULL	emerin	GP		bind					multiple transcription factors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_6969_s_239	12493765	2, 3 We therefore suggest that EDMD disease results from the combined loss of emerin binding to multiple transcription factors, some of which may be more "`important"` than others in maintaining the function of a specific tissue.	bind
22806	2	7225	6	13	NULL	NULL	NULL	statement 1	Process	combined loss of	results in					EDMD disease	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_6969_s_239	12493765	2, 3 We therefore suggest that EDMD disease results from the combined loss of emerin binding to multiple transcription factors, some of which may be more "`important"` than others in maintaining the function of a specific tissue.	bind
27681	1	7225	7	NULL	NULL	0	NULL	emerin	NULL		bind	NULL				multiple transcription factors	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_6969_s_239	12493765	2, 3 We therefore suggest that EDMD disease results from the combined loss of emerin binding to multiple transcription factors, some of which may be more "`important"` than others in maintaining the function of a specific tissue.	bind
53627	2	7225	7	10	NULL	0	NULL	statement 1	NULL	combined loss of	results in	NULL				EDMD disease	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_6969_s_239	12493765	2, 3 We therefore suggest that EDMD disease results from the combined loss of emerin binding to multiple transcription factors, some of which may be more "`important"` than others in maintaining the function of a specific tissue.	bind
22807	1	7226	6	13	NULL	NULL	NULL	SHP2	GP		bind			SH2 domain		tyrosine kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1081_s_103	12117720	2, 3, 14 SHP2 binds to tyrosine kinases via its SH2 domains and is activated by phosphorylation of its tyrosine residue.	bind
22808	2	7226	6	13	NULL	NULL	NULL	SHP2	GP		is activated by					SHP2	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1081_s_103	12117720	2, 3, 14 SHP2 binds to tyrosine kinases via its SH2 domains and is activated by phosphorylation of its tyrosine residue.	bind
27682	1	7226	7	10	NULL	0	NULL	 SHP2	NULL		binds	NULL		SH2 domain		tyrosine kinase	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1081_s_103	12117720	2, 3, 14 SHP2 binds to tyrosine kinases via its SH2 domains and is activated by phosphorylation of its tyrosine residue.	bind
27683	2	7226	7	NULL	NULL	0	NULL		NULL	phosphorylation of	activates	NULL		tyrosine residue		tyrosine kinase	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1081_s_103	12117720	2, 3, 14 SHP2 binds to tyrosine kinases via its SH2 domains and is activated by phosphorylation of its tyrosine residue.	bind
22809	1	7227	6	13	NULL	NULL	NULL	statement 3	GP		interacts with		electrostatically			statement 4	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_50150_s_266	15328339	2, at the initial low ratio of S3:LPS, binding of S3 dimer to LPS occurs via ( a) electrostatic interactions between the positively charged amino acid residues near  the N termini of S3 dimer and the negatively charged bisphosphate head groups of  the lipid A moiety of LPS and ( b) hydrophobic interactions between the C termini of S3 dimer and the acyl chains of  lipid A.	bind
22939	2	7227	6	13	NULL	NULL	NULL	S3 dimer	GP		interacts with		hydrophobically 	C termini		LPS	Chemical		acyl chains of lipid A		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_50150_s_266	15328339	2, at the initial low ratio of S3:LPS, binding of S3 dimer to LPS occurs via ( a) electrostatic interactions between the positively charged amino acid residues near  the N termini of S3 dimer and the negatively charged bisphosphate head groups of  the lipid A moiety of LPS and ( b) hydrophobic interactions between the C termini of S3 dimer and the acyl chains of  lipid A.	bind
53628	3	7227	6	13	NULL	NULL	NULL	S3 dimer	GP	positively charged amino acid	resides near					S3 dimer	GP		N termini		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_50150_s_266	15328339	2, at the initial low ratio of S3:LPS, binding of S3 dimer to LPS occurs via ( a) electrostatic interactions between the positively charged amino acid residues near  the N termini of S3 dimer and the negatively charged bisphosphate head groups of  the lipid A moiety of LPS and ( b) hydrophobic interactions between the C termini of S3 dimer and the acyl chains of  lipid A.	bind
53629	4	7227	6	13	NULL	NULL	NULL	LPS	Chemical		contains			lipid A moiety					negatively charged bisphosphate head groups		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_50150_s_266	15328339	2, at the initial low ratio of S3:LPS, binding of S3 dimer to LPS occurs via ( a) electrostatic interactions between the positively charged amino acid residues near  the N termini of S3 dimer and the negatively charged bisphosphate head groups of  the lipid A moiety of LPS and ( b) hydrophobic interactions between the C termini of S3 dimer and the acyl chains of  lipid A.	bind
27684	1	7227	7	NULL	NULL	0	NULL	S3 dimer	NULL		binds	NULL				LPS	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50150_s_266	15328339	2, at the initial low ratio of S3:LPS, binding of S3 dimer to LPS occurs via ( a) electrostatic interactions between the positively charged amino acid residues near  the N termini of S3 dimer and the negatively charged bisphosphate head groups of  the lipid A moiety of LPS and ( b) hydrophobic interactions between the C termini of S3 dimer and the acyl chains of  lipid A.	bind
27685	2	7227	7	10	NULL	0	NULL	statement 5	NULL		interacts with	NULL	electrostatically			statement 6	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_50150_s_266	15328339	2, at the initial low ratio of S3:LPS, binding of S3 dimer to LPS occurs via ( a) electrostatic interactions between the positively charged amino acid residues near  the N termini of S3 dimer and the negatively charged bisphosphate head groups of  the lipid A moiety of LPS and ( b) hydrophobic interactions between the C termini of S3 dimer and the acyl chains of  lipid A.	bind
27686	3	7227	7	NULL	NULL	0	NULL	statement 1	NULL		occurs via	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50150_s_266	15328339	2, at the initial low ratio of S3:LPS, binding of S3 dimer to LPS occurs via ( a) electrostatic interactions between the positively charged amino acid residues near  the N termini of S3 dimer and the negatively charged bisphosphate head groups of  the lipid A moiety of LPS and ( b) hydrophobic interactions between the C termini of S3 dimer and the acyl chains of  lipid A.	bind
27687	4	7227	7	10	NULL	0	NULL	S3 dimer	NULL		interacts with	NULL	hydrophobically	C termini of		lipid A	NULL		acyl chains of		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_50150_s_266	15328339	2, at the initial low ratio of S3:LPS, binding of S3 dimer to LPS occurs via ( a) electrostatic interactions between the positively charged amino acid residues near  the N termini of S3 dimer and the negatively charged bisphosphate head groups of  the lipid A moiety of LPS and ( b) hydrophobic interactions between the C termini of S3 dimer and the acyl chains of  lipid A.	bind
53630	5	7227	7	10	NULL	0	NULL	S3 dimer	NULL	\tpositively charged amino acid 	resides near	NULL				S3 dimer	NULL		N termini		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50150_s_266	15328339	2, at the initial low ratio of S3:LPS, binding of S3 dimer to LPS occurs via ( a) electrostatic interactions between the positively charged amino acid residues near  the N termini of S3 dimer and the negatively charged bisphosphate head groups of  the lipid A moiety of LPS and ( b) hydrophobic interactions between the C termini of S3 dimer and the acyl chains of  lipid A.	bind
53631	6	7227	7	10	NULL	0	NULL	LPS	NULL		contains	NULL		lipid A moiety			NULL		negatively charged bisphosphate head groups		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50150_s_266	15328339	2, at the initial low ratio of S3:LPS, binding of S3 dimer to LPS occurs via ( a) electrostatic interactions between the positively charged amino acid residues near  the N termini of S3 dimer and the negatively charged bisphosphate head groups of  the lipid A moiety of LPS and ( b) hydrophobic interactions between the C termini of S3 dimer and the acyl chains of  lipid A.	bind
22810	1	7228	6	13	NULL	NULL	NULL	ATP	Chemical		bind					P2X receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_20_23_8868_s_240	11102496	2, ATP binds to the P2X receptor resulting in the opening of a nonspecific ion channel.	bind
22811	2	7228	6	13	NULL	NULL	NULL	statement 1	Process		results in					nonspecific ion channel	Process	opening of 			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_20_23_8868_s_240	11102496	2, ATP binds to the P2X receptor resulting in the opening of a nonspecific ion channel.	bind
27688	1	7228	7	NULL	NULL	0	NULL	ATP 	NULL		binds to	NULL				P2X receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_23_8868_s_240	11102496	2, ATP binds to the P2X receptor resulting in the opening of a nonspecific ion channel.	bind
27689	2	7228	7	10	NULL	0	NULL	statement 1	NULL		results in	NULL				nonspecific ion channel	NULL	opening of			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_20_23_8868_s_240	11102496	2, ATP binds to the P2X receptor resulting in the opening of a nonspecific ion channel.	bind
22812	1	7229	6	13	NULL	NULL	NULL	heparin	Chemical	biotin-labeled	bind					Tg	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12898_s_210	10212279	2, binding of biotin-labeled heparin to Tg-coated wells in the presence of 500 units/ml of unlabeled heparin.	bind
22813	2	7229	6	13	NULL	NULL	NULL	statement 1	Process		occurs in presence of					heparin	Chemical	unlabeled			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12898_s_210	10212279	2, binding of biotin-labeled heparin to Tg-coated wells in the presence of 500 units/ml of unlabeled heparin.	bind
27690	1	7229	7	10	NULL	0	NULL	heparin	NULL	biotin-labeled 	binds to	NULL				Tg	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12898_s_210	10212279	2, binding of biotin-labeled heparin to Tg-coated wells in the presence of 500 units/ml of unlabeled heparin.	bind
27691	2	7229	7	NULL	NULL	0	NULL	statement 1	NULL		in presence of	NULL				heparin	NULL	unlabeled			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_18_12898_s_210	10212279	2, binding of biotin-labeled heparin to Tg-coated wells in the presence of 500 units/ml of unlabeled heparin.	bind
22814	1	7230	6	13	NULL	NULL	NULL	Rifampin	Chemical		bind					RNAP	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14925_s_130	15466710	2, Certain mutations (asterisks) on the  rpoB gene diminish the binding of rifampin to RNAP, making bacteria resistant in the presence  of rifampin.	bind
22815	2	7230	6	13	NULL	NULL	NULL	rpoB gene	GP	mutant	diminish					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14925_s_130	15466710	2, Certain mutations (asterisks) on the  rpoB gene diminish the binding of rifampin to RNAP, making bacteria resistant in the presence  of rifampin.	bind
22816	3	7230	6	13	NULL	NULL	NULL	statement 1	Process		make					resistant bacteria	Organism				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14925_s_130	15466710	2, Certain mutations (asterisks) on the  rpoB gene diminish the binding of rifampin to RNAP, making bacteria resistant in the presence  of rifampin.	bind
22817	4	7230	6	13	NULL	NULL	NULL	statement 3	Process		occurs in presence of					rifampin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_41_14925_s_130	15466710	2, Certain mutations (asterisks) on the  rpoB gene diminish the binding of rifampin to RNAP, making bacteria resistant in the presence  of rifampin.	bind
27692	1	7230	7	NULL	NULL	0	NULL	rifampin	NULL		bind	NULL				RNAP	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_41_14925_s_130	15466710	2, Certain mutations (asterisks) on the  rpoB gene diminish the binding of rifampin to RNAP, making bacteria resistant in the presence  of rifampin.	bind
27693	2	7230	7	NULL	NULL	0	NULL	 rpoB gene	NULL	mutant	diminish	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_41_14925_s_130	15466710	2, Certain mutations (asterisks) on the  rpoB gene diminish the binding of rifampin to RNAP, making bacteria resistant in the presence  of rifampin.	bind
27694	3	7230	7	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				bacteria	NULL	resistance of			NULL		0	NULL	NULL	NULL	gw70_pnas_101_41_14925_s_130	15466710	2, Certain mutations (asterisks) on the  rpoB gene diminish the binding of rifampin to RNAP, making bacteria resistant in the presence  of rifampin.	bind
27695	4	7230	7	NULL	NULL	0	NULL	statement 3	NULL		in the presence of	NULL				rifampin	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_41_14925_s_130	15466710	2, Certain mutations (asterisks) on the  rpoB gene diminish the binding of rifampin to RNAP, making bacteria resistant in the presence  of rifampin.	bind
22818	1	7231	6	13	NULL	NULL	NULL	Tau	GP		bind					MT surface	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30335_s_337	10869348	2, initial binding of Tau to the MT surface (first phase of binding), accompanied by a conformational change.	bind
27872	1	7231	7	NULL	NULL	0	NULL	Tau 	NULL		bind	NULL				MT surface	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_39_30335_s_337	10869348	2, initial binding of Tau to the MT surface (first phase of binding), accompanied by a conformational change.	bind
27873	2	7231	7	NULL	NULL	0	NULL	conformational change	NULL		accompanies	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_39_30335_s_337	10869348	2, initial binding of Tau to the MT surface (first phase of binding), accompanied by a conformational change.	bind
22819	1	7232	6	13	NULL	NULL	NULL	Hb:Hp ligand	GP		bind					CD163	GP				NULL	human monocyte-macrophages isolated in vitro	NULL	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_163	14656926	2,19 - 22     In this study we demonstrate for the first time that Hb:Hp ligand binding to CD163 on human monocyte-macrophages isolated in vitro and in vivo elicits a direct antiinflammatory effect via the secretion of IL-10.	bind
22940	2	7232	6	13	NULL	NULL	NULL	Hb:Hp ligand	GP		bind					CD163	GP				NULL	human monocyte-macrophages isolated in vivo	NULL	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_163	14656926	2,19 - 22     In this study we demonstrate for the first time that Hb:Hp ligand binding to CD163 on human monocyte-macrophages isolated in vitro and in vivo elicits a direct antiinflammatory effect via the secretion of IL-10.	bind
22941	3	7232	6	13	NULL	NULL	NULL	statement 1	Process		elicits					antiinflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_163	14656926	2,19 - 22     In this study we demonstrate for the first time that Hb:Hp ligand binding to CD163 on human monocyte-macrophages isolated in vitro and in vivo elicits a direct antiinflammatory effect via the secretion of IL-10.	bind
22942	4	7232	6	13	NULL	NULL	NULL	statement 2	Process		elicits					antiinflammatory response	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_163	14656926	2,19 - 22     In this study we demonstrate for the first time that Hb:Hp ligand binding to CD163 on human monocyte-macrophages isolated in vitro and in vivo elicits a direct antiinflammatory effect via the secretion of IL-10.	bind
22943	5	7232	6	13	NULL	NULL	NULL	statement 3	Process		occurs via					IL-10	GP	secretion of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_163	14656926	2,19 - 22     In this study we demonstrate for the first time that Hb:Hp ligand binding to CD163 on human monocyte-macrophages isolated in vitro and in vivo elicits a direct antiinflammatory effect via the secretion of IL-10.	bind
22944	6	7232	6	13	NULL	NULL	NULL	statement 4	Process		occurs via					IL-10	GP	secretion of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_163	14656926	2,19 - 22     In this study we demonstrate for the first time that Hb:Hp ligand binding to CD163 on human monocyte-macrophages isolated in vitro and in vivo elicits a direct antiinflammatory effect via the secretion of IL-10.	bind
27875	1	7232	7	NULL	NULL	0	NULL	Hb:Hp ligand	NULL		bind	NULL				CD163	NULL	human			NULL	monocyte-macrophages in vitro	NULL	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_163	14656926	2,19 - 22     In this study we demonstrate for the first time that Hb:Hp ligand binding to CD163 on human monocyte-macrophages isolated in vitro and in vivo elicits a direct antiinflammatory effect via the secretion of IL-10.	bind
27876	2	7232	7	NULL	NULL	0	NULL	Hb:Hp ligand	NULL		bind	NULL				CD163	NULL	human			NULL	 monocyte-macrophages in vivo	NULL	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_163	14656926	2,19 - 22     In this study we demonstrate for the first time that Hb:Hp ligand binding to CD163 on human monocyte-macrophages isolated in vitro and in vivo elicits a direct antiinflammatory effect via the secretion of IL-10.	bind
27879	3	7232	7	NULL	NULL	0	NULL	statement 1	NULL		elicits	NULL				antiinflammatory effect 	NULL	direct			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_163	14656926	2,19 - 22     In this study we demonstrate for the first time that Hb:Hp ligand binding to CD163 on human monocyte-macrophages isolated in vitro and in vivo elicits a direct antiinflammatory effect via the secretion of IL-10.	bind
27880	4	7232	7	NULL	NULL	0	NULL	statement 2	NULL		elicits	NULL				antiinflammatory effect 	NULL	direct			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_163	14656926	2,19 - 22     In this study we demonstrate for the first time that Hb:Hp ligand binding to CD163 on human monocyte-macrophages isolated in vitro and in vivo elicits a direct antiinflammatory effect via the secretion of IL-10.	bind
27882	5	7232	7	NULL	NULL	0	NULL	statement 3	NULL		occurs via	NULL				IL-10	NULL	secretion of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_163	14656926	2,19 - 22     In this study we demonstrate for the first time that Hb:Hp ligand binding to CD163 on human monocyte-macrophages isolated in vitro and in vivo elicits a direct antiinflammatory effect via the secretion of IL-10.	bind
27883	6	7232	7	NULL	NULL	0	NULL	statement 4	NULL		occurs via	NULL				IL-10	NULL	secretion of			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_163	14656926	2,19 - 22     In this study we demonstrate for the first time that Hb:Hp ligand binding to CD163 on human monocyte-macrophages isolated in vitro and in vivo elicits a direct antiinflammatory effect via the secretion of IL-10.	bind
22820	1	7233	6	13	NULL	NULL	NULL	cholesterol	Chemical		bind					(apo)B-containing lipoproteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1972_s_25	15994445	2,3  In FLD, plasma LCAT is either absent or completely lacks catalytic activity; in FED, the mutant LCAT lacks activity on HDL lipids but esterifies cholesterol bound to apolipoprotein (apo)B-containing lipoproteins.	bind
22945	2	7233	6	13	NULL	NULL	NULL	plasma LCAT	GP		completely lacks					catalytic activity	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1972_s_25	15994445	2,3  In FLD, plasma LCAT is either absent or completely lacks catalytic activity; in FED, the mutant LCAT lacks activity on HDL lipids but esterifies cholesterol bound to apolipoprotein (apo)B-containing lipoproteins.	bind
22946	3	7233	6	13	NULL	NULL	NULL	statement 2	Process		occurs in					FLD	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1972_s_25	15994445	2,3  In FLD, plasma LCAT is either absent or completely lacks catalytic activity; in FED, the mutant LCAT lacks activity on HDL lipids but esterifies cholesterol bound to apolipoprotein (apo)B-containing lipoproteins.	bind
22947	4	7233	6	13	NULL	NULL	NULL	LCAT	GP	mutant	lacks activity on					HDL lipids	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1972_s_25	15994445	2,3  In FLD, plasma LCAT is either absent or completely lacks catalytic activity; in FED, the mutant LCAT lacks activity on HDL lipids but esterifies cholesterol bound to apolipoprotein (apo)B-containing lipoproteins.	bind
22948	5	7233	6	13	NULL	NULL	NULL	LCAT	GP	mutant	esterifies					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1972_s_25	15994445	2,3  In FLD, plasma LCAT is either absent or completely lacks catalytic activity; in FED, the mutant LCAT lacks activity on HDL lipids but esterifies cholesterol bound to apolipoprotein (apo)B-containing lipoproteins.	bind
22949	6	7233	6	13	NULL	NULL	NULL	statement 4	Process		occurs in					FED	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1972_s_25	15994445	2,3  In FLD, plasma LCAT is either absent or completely lacks catalytic activity; in FED, the mutant LCAT lacks activity on HDL lipids but esterifies cholesterol bound to apolipoprotein (apo)B-containing lipoproteins.	bind
22950	7	7233	6	13	NULL	NULL	NULL	statement 5	Process		occurs in					FED	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1972_s_25	15994445	2,3  In FLD, plasma LCAT is either absent or completely lacks catalytic activity; in FED, the mutant LCAT lacks activity on HDL lipids but esterifies cholesterol bound to apolipoprotein (apo)B-containing lipoproteins.	bind
27887	1	7233	7	NULL	NULL	0	NULL	LCAT	NULL		lacks 	NULL				catalytic activity	NULL				NULL	FLD	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1972_s_25	15994445	2,3  In FLD, plasma LCAT is either absent or completely lacks catalytic activity; in FED, the mutant LCAT lacks activity on HDL lipids but esterifies cholesterol bound to apolipoprotein (apo)B-containing lipoproteins.	bind
27888	2	7233	7	NULL	NULL	0	NULL	LCAT	NULL	mutant	lacks	NULL				HDL lipids	NULL	activity on			NULL	FED	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1972_s_25	15994445	2,3  In FLD, plasma LCAT is either absent or completely lacks catalytic activity; in FED, the mutant LCAT lacks activity on HDL lipids but esterifies cholesterol bound to apolipoprotein (apo)B-containing lipoproteins.	bind
27889	3	7233	7	NULL	NULL	0	NULL	cholesterol 	NULL		bind	NULL				(apo)B-containing lipoproteins	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1972_s_25	15994445	2,3  In FLD, plasma LCAT is either absent or completely lacks catalytic activity; in FED, the mutant LCAT lacks activity on HDL lipids but esterifies cholesterol bound to apolipoprotein (apo)B-containing lipoproteins.	bind
27890	4	7233	7	NULL	NULL	0	NULL	LCAT	NULL	mutant	esterifies	NULL				statement 3	NULL				NULL	FED	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1972_s_25	15994445	2,3  In FLD, plasma LCAT is either absent or completely lacks catalytic activity; in FED, the mutant LCAT lacks activity on HDL lipids but esterifies cholesterol bound to apolipoprotein (apo)B-containing lipoproteins.	bind
22821	1	7235	6	13	NULL	NULL	NULL	TCDD	Chemical		bind					Ah-R	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_1_30_s_2	9224809	2,3,7,8-Tetrachlorodibenzo-  p-dioxin (TCDD) binds and activates the aryl hydrocarbon receptor (Ah-R), an endogenous transcription factor that is expressed in the thymus.	bind
22822	2	7235	6	13	NULL	NULL	NULL	TCDD	Chemical		is					2,3,7,8-Tetrachlorodibenzo- p-dioxin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_1_30_s_2	9224809	2,3,7,8-Tetrachlorodibenzo-  p-dioxin (TCDD) binds and activates the aryl hydrocarbon receptor (Ah-R), an endogenous transcription factor that is expressed in the thymus.	bind
22823	3	7235	6	13	NULL	NULL	NULL	Ah-R	GP		is					aryl hydrocarbon receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_1_30_s_2	9224809	2,3,7,8-Tetrachlorodibenzo-  p-dioxin (TCDD) binds and activates the aryl hydrocarbon receptor (Ah-R), an endogenous transcription factor that is expressed in the thymus.	bind
22824	4	7235	6	13	NULL	NULL	NULL	Ah-R	GP		is a type of					transcription factor	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_1_30_s_2	9224809	2,3,7,8-Tetrachlorodibenzo-  p-dioxin (TCDD) binds and activates the aryl hydrocarbon receptor (Ah-R), an endogenous transcription factor that is expressed in the thymus.	bind
22825	5	7235	6	13	NULL	NULL	NULL	Ah-R	GP		is expressed in					thymus	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_1_30_s_2	9224809	2,3,7,8-Tetrachlorodibenzo-  p-dioxin (TCDD) binds and activates the aryl hydrocarbon receptor (Ah-R), an endogenous transcription factor that is expressed in the thymus.	bind
53632	6	7235	6	13	NULL	NULL	NULL	statement 1	Process		activates					Ah-R	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_1_30_s_2	9224809	2,3,7,8-Tetrachlorodibenzo-  p-dioxin (TCDD) binds and activates the aryl hydrocarbon receptor (Ah-R), an endogenous transcription factor that is expressed in the thymus.	bind
27892	1	7235	7	NULL	NULL	0	NULL	TCDD	NULL		binds	NULL				Ah-R	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_1_30_s_2	9224809	2,3,7,8-Tetrachlorodibenzo-  p-dioxin (TCDD) binds and activates the aryl hydrocarbon receptor (Ah-R), an endogenous transcription factor that is expressed in the thymus.	bind
27893	2	7235	7	10	NULL	0	NULL	statement 1	NULL		activates	NULL				Ah-R	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_1_30_s_2	9224809	2,3,7,8-Tetrachlorodibenzo-  p-dioxin (TCDD) binds and activates the aryl hydrocarbon receptor (Ah-R), an endogenous transcription factor that is expressed in the thymus.	bind
27895	3	7235	7	NULL	NULL	0	NULL	Ah-R	NULL		is a type of	NULL				transcription factor	NULL	endogenous			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_1_30_s_2	9224809	2,3,7,8-Tetrachlorodibenzo-  p-dioxin (TCDD) binds and activates the aryl hydrocarbon receptor (Ah-R), an endogenous transcription factor that is expressed in the thymus.	bind
27897	4	7235	7	NULL	NULL	0	NULL	Ah-R	NULL		is expressed in	NULL				thymus	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_1_30_s_2	9224809	2,3,7,8-Tetrachlorodibenzo-  p-dioxin (TCDD) binds and activates the aryl hydrocarbon receptor (Ah-R), an endogenous transcription factor that is expressed in the thymus.	bind
27898	5	7235	7	NULL	NULL	0	NULL	TCDD	NULL		is	NULL				2,3,7,8-Tetrachlorodibenzo- p-dioxin	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_1_30_s_2	9224809	2,3,7,8-Tetrachlorodibenzo-  p-dioxin (TCDD) binds and activates the aryl hydrocarbon receptor (Ah-R), an endogenous transcription factor that is expressed in the thymus.	bind
27900	6	7235	7	NULL	NULL	0	NULL	Ah-R	NULL		is	NULL				aryl hydrocarbon receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_1_30_s_2	9224809	2,3,7,8-Tetrachlorodibenzo-  p-dioxin (TCDD) binds and activates the aryl hydrocarbon receptor (Ah-R), an endogenous transcription factor that is expressed in the thymus.	bind
22826	1	7237	6	13	NULL	NULL	NULL	DFA	Chemical		does not bind					hCyp-18	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_505_1_191_s_105	11557067	2,4-Difluoroaniline (DFA) did not bind hCyp-18.	bind
22827	2	7237	6	13	NULL	NULL	NULL	DFA	Chemical		is					2,4-Difluoroaniline 	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_505_1_191_s_105	11557067	2,4-Difluoroaniline (DFA) did not bind hCyp-18.	bind
27904	1	7237	7	NULL	NULL	0	NULL	DFA	NULL		does not bind	NULL				hCyp-18	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_505_1_191_s_105	11557067	2,4-Difluoroaniline (DFA) did not bind hCyp-18.	bind
27905	2	7237	7	NULL	NULL	0	NULL	DFA	NULL		is	NULL				2,4-Difluoroaniline	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_505_1_191_s_105	11557067	2,4-Difluoroaniline (DFA) did not bind hCyp-18.	bind
22951	1	7238	6	13	NULL	NULL	NULL	guanylate cyclase C receptor	GP		is					GC-C	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_6_2169_s_13	12466132	2- 4  Once elaborated into the intestinal lumen, guanylin, another similar mammalian peptide, uroguanylin, and STa can all bind to the receptor guanylate cyclase C (GC-C), located on the enterocyte brush border membrane.	bind
22952	2	7238	6	13	NULL	NULL	NULL	GC-C	GP		is located on					enterocyte brush border membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_6_2169_s_13	12466132	2- 4  Once elaborated into the intestinal lumen, guanylin, another similar mammalian peptide, uroguanylin, and STa can all bind to the receptor guanylate cyclase C (GC-C), located on the enterocyte brush border membrane.	bind
22953	3	7238	6	13	NULL	NULL	NULL	guanylin	GP		bind					GC-C	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_6_2169_s_13	12466132	2- 4  Once elaborated into the intestinal lumen, guanylin, another similar mammalian peptide, uroguanylin, and STa can all bind to the receptor guanylate cyclase C (GC-C), located on the enterocyte brush border membrane.	bind
22954	4	7238	6	13	NULL	NULL	NULL	uroguanylin	GP		bind					GC-C	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_6_2169_s_13	12466132	2- 4  Once elaborated into the intestinal lumen, guanylin, another similar mammalian peptide, uroguanylin, and STa can all bind to the receptor guanylate cyclase C (GC-C), located on the enterocyte brush border membrane.	bind
22955	5	7238	6	13	NULL	NULL	NULL	STa	GP		bind					GC-C	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_6_2169_s_13	12466132	2- 4  Once elaborated into the intestinal lumen, guanylin, another similar mammalian peptide, uroguanylin, and STa can all bind to the receptor guanylate cyclase C (GC-C), located on the enterocyte brush border membrane.	bind
27914	1	7238	7	NULL	NULL	0	NULL	guanylin	NULL		bind	NULL				GC-C receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_6_2169_s_13	12466132	2- 4  Once elaborated into the intestinal lumen, guanylin, another similar mammalian peptide, uroguanylin, and STa can all bind to the receptor guanylate cyclase C (GC-C), located on the enterocyte brush border membrane.	bind
27915	2	7238	7	NULL	NULL	0	NULL	uroguanylin	NULL		bind	NULL				receptor GC-C	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_6_2169_s_13	12466132	2- 4  Once elaborated into the intestinal lumen, guanylin, another similar mammalian peptide, uroguanylin, and STa can all bind to the receptor guanylate cyclase C (GC-C), located on the enterocyte brush border membrane.	bind
27916	3	7238	7	NULL	NULL	0	NULL	STa	NULL		bind	NULL				GC-C receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_6_2169_s_13	12466132	2- 4  Once elaborated into the intestinal lumen, guanylin, another similar mammalian peptide, uroguanylin, and STa can all bind to the receptor guanylate cyclase C (GC-C), located on the enterocyte brush border membrane.	bind
27917	4	7238	7	NULL	NULL	0	NULL	GC-C receptor	NULL		is located on the	NULL				enterocyte brush border membrane	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_6_2169_s_13	12466132	2- 4  Once elaborated into the intestinal lumen, guanylin, another similar mammalian peptide, uroguanylin, and STa can all bind to the receptor guanylate cyclase C (GC-C), located on the enterocyte brush border membrane.	bind
27918	5	7238	7	NULL	NULL	0	NULL	GC-C	NULL		is	NULL				guanylate cyclase C	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_6_2169_s_13	12466132	2- 4  Once elaborated into the intestinal lumen, guanylin, another similar mammalian peptide, uroguanylin, and STa can all bind to the receptor guanylate cyclase C (GC-C), located on the enterocyte brush border membrane.	bind
22848	1	7240	6	13	NULL	NULL	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL	H4-II-E overproducing H9 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_1_413_s_210	11020383	2-AAF Activates NF-kappaB DNA Binding through Generating ROS-- Since mdr1b is a NF-kappaB-regulated gene and NF-kappaB is an important oxidative stress responder, we then compared 2-AAF induced NF-kappaB DNA binding activity in H4-II-E (Fig.  8 A) and GSH overproducing H9 cells (Fig.  8 B).	bind
22849	2	7240	6	13	NULL	NULL	NULL	AAF	Chemical		activates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_1_413_s_210	11020383	2-AAF Activates NF-kappaB DNA Binding through Generating ROS-- Since mdr1b is a NF-kappaB-regulated gene and NF-kappaB is an important oxidative stress responder, we then compared 2-AAF induced NF-kappaB DNA binding activity in H4-II-E (Fig.  8 A) and GSH overproducing H9 cells (Fig.  8 B).	bind
22850	3	7240	6	13	NULL	NULL	NULL	statement 1	Process		occurs through					ROS	GP	generation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_1_413_s_210	11020383	2-AAF Activates NF-kappaB DNA Binding through Generating ROS-- Since mdr1b is a NF-kappaB-regulated gene and NF-kappaB is an important oxidative stress responder, we then compared 2-AAF induced NF-kappaB DNA binding activity in H4-II-E (Fig.  8 A) and GSH overproducing H9 cells (Fig.  8 B).	bind
22851	4	7240	6	13	NULL	NULL	NULL	mdr1b gene	GP		is regulated by					NF-kappaB	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_1_413_s_210	11020383	2-AAF Activates NF-kappaB DNA Binding through Generating ROS-- Since mdr1b is a NF-kappaB-regulated gene and NF-kappaB is an important oxidative stress responder, we then compared 2-AAF induced NF-kappaB DNA binding activity in H4-II-E (Fig.  8 A) and GSH overproducing H9 cells (Fig.  8 B).	bind
22852	5	7240	6	13	NULL	NULL	NULL	NF-kappaB	GP		responds to					oxidative stress	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_1_413_s_210	11020383	2-AAF Activates NF-kappaB DNA Binding through Generating ROS-- Since mdr1b is a NF-kappaB-regulated gene and NF-kappaB is an important oxidative stress responder, we then compared 2-AAF induced NF-kappaB DNA binding activity in H4-II-E (Fig.  8 A) and GSH overproducing H9 cells (Fig.  8 B).	bind
22853	6	7240	6	13	NULL	NULL	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL	GSH overproducing H9 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_1_413_s_210	11020383	2-AAF Activates NF-kappaB DNA Binding through Generating ROS-- Since mdr1b is a NF-kappaB-regulated gene and NF-kappaB is an important oxidative stress responder, we then compared 2-AAF induced NF-kappaB DNA binding activity in H4-II-E (Fig.  8 A) and GSH overproducing H9 cells (Fig.  8 B).	bind
22854	7	7240	6	13	NULL	NULL	NULL	AAF	Chemical		activates					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_1_413_s_210	11020383	2-AAF Activates NF-kappaB DNA Binding through Generating ROS-- Since mdr1b is a NF-kappaB-regulated gene and NF-kappaB is an important oxidative stress responder, we then compared 2-AAF induced NF-kappaB DNA binding activity in H4-II-E (Fig.  8 A) and GSH overproducing H9 cells (Fig.  8 B).	bind
53633	8	7240	6	13	NULL	NULL	NULL	AAF	Chemical		activates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_1_413_s_210	11020383	2-AAF Activates NF-kappaB DNA Binding through Generating ROS-- Since mdr1b is a NF-kappaB-regulated gene and NF-kappaB is an important oxidative stress responder, we then compared 2-AAF induced NF-kappaB DNA binding activity in H4-II-E (Fig.  8 A) and GSH overproducing H9 cells (Fig.  8 B).	bind
27919	1	7240	7	NULL	NULL	0	NULL	NF-kappaB	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_413_s_210	11020383	2-AAF Activates NF-kappaB DNA Binding through Generating ROS-- Since mdr1b is a NF-kappaB-regulated gene and NF-kappaB is an important oxidative stress responder, we then compared 2-AAF induced NF-kappaB DNA binding activity in H4-II-E (Fig.  8 A) and GSH overproducing H9 cells (Fig.  8 B).	bind
27920	2	7240	7	NULL	NULL	0	NULL	AAF	NULL		activates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_413_s_210	11020383	2-AAF Activates NF-kappaB DNA Binding through Generating ROS-- Since mdr1b is a NF-kappaB-regulated gene and NF-kappaB is an important oxidative stress responder, we then compared 2-AAF induced NF-kappaB DNA binding activity in H4-II-E (Fig.  8 A) and GSH overproducing H9 cells (Fig.  8 B).	bind
27921	3	7240	7	NULL	NULL	0	NULL	statement 2	NULL		occurs through	NULL				ROS	NULL	generating			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_413_s_210	11020383	2-AAF Activates NF-kappaB DNA Binding through Generating ROS-- Since mdr1b is a NF-kappaB-regulated gene and NF-kappaB is an important oxidative stress responder, we then compared 2-AAF induced NF-kappaB DNA binding activity in H4-II-E (Fig.  8 A) and GSH overproducing H9 cells (Fig.  8 B).	bind
27922	4	7240	7	NULL	NULL	0	NULL	NF-kappaB	NULL		regulates	NULL				 mdr1b gene	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_413_s_210	11020383	2-AAF Activates NF-kappaB DNA Binding through Generating ROS-- Since mdr1b is a NF-kappaB-regulated gene and NF-kappaB is an important oxidative stress responder, we then compared 2-AAF induced NF-kappaB DNA binding activity in H4-II-E (Fig.  8 A) and GSH overproducing H9 cells (Fig.  8 B).	bind
27923	5	7240	7	NULL	NULL	0	NULL	NF-kappaB	NULL		responds to	NULL				oxidative stress	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_413_s_210	11020383	2-AAF Activates NF-kappaB DNA Binding through Generating ROS-- Since mdr1b is a NF-kappaB-regulated gene and NF-kappaB is an important oxidative stress responder, we then compared 2-AAF induced NF-kappaB DNA binding activity in H4-II-E (Fig.  8 A) and GSH overproducing H9 cells (Fig.  8 B).	bind
27924	6	7240	7	NULL	NULL	0	NULL	AAF	NULL		induce	NULL				statement 1	NULL				NULL	H4-II-E overproducing H9 cells	0	NULL	NULL	NULL	gw60_jbiolchem_276_1_413_s_210	11020383	2-AAF Activates NF-kappaB DNA Binding through Generating ROS-- Since mdr1b is a NF-kappaB-regulated gene and NF-kappaB is an important oxidative stress responder, we then compared 2-AAF induced NF-kappaB DNA binding activity in H4-II-E (Fig.  8 A) and GSH overproducing H9 cells (Fig.  8 B).	bind
27925	7	7240	7	NULL	NULL	0	NULL	AAF	NULL		induce	NULL				statement 1	NULL				NULL	GSH overproducing H9 cells	0	NULL	NULL	NULL	gw60_jbiolchem_276_1_413_s_210	11020383	2-AAF Activates NF-kappaB DNA Binding through Generating ROS-- Since mdr1b is a NF-kappaB-regulated gene and NF-kappaB is an important oxidative stress responder, we then compared 2-AAF induced NF-kappaB DNA binding activity in H4-II-E (Fig.  8 A) and GSH overproducing H9 cells (Fig.  8 B).	bind
22855	1	7241	6	13	NULL	NULL	NULL	2-Acetoxyamino-6-methyldipyrido imidazole	Chemical		bind		covalently			DNA	NucleicAcid			guanine residues	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-biophys-res-commun_116_3_6651841_s_2	6651841	2-Acetoxyamino-6-methyldipyrido[1,2-a:3'',2''-d]imidazole binds covalently  to the 8 position of guanine residues in DNA.	bind
27926	1	7241	7	NULL	NULL	0	NULL	2-Acetoxyamino-6-methyldipyrido[1,2-a:3'',2''-d]imidazole	NULL		binds	NULL	covalently			DNA	NULL			guanine residues	NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biochem-biophys-res-commun_116_3_6651841_s_2	6651841	2-Acetoxyamino-6-methyldipyrido[1,2-a:3'',2''-d]imidazole binds covalently  to the 8 position of guanine residues in DNA.	bind
22856	1	7242	6	13	NULL	NULL	NULL	GTP	Chemical		bind					Rho	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_40_0_459_s_108	10836144	2-Adrenergic receptor stimulation increased [32]GTP binding to Rho and decreased [32]GDP-Rho binding in preadipocytes ( 52).	bind
22857	2	7242	6	13	NULL	NULL	NULL	Adrenergic receptor	GP	stimulation of	increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_40_0_459_s_108	10836144	2-Adrenergic receptor stimulation increased [32]GTP binding to Rho and decreased [32]GDP-Rho binding in preadipocytes ( 52).	bind
22858	3	7242	6	13	NULL	NULL	NULL	GDP	Chemical		bind					Rho	GP				NULL	preadipocytes	NULL	NULL	NULL	NULL	gw70_annurevpharmacol_40_0_459_s_108	10836144	2-Adrenergic receptor stimulation increased [32]GTP binding to Rho and decreased [32]GDP-Rho binding in preadipocytes ( 52).	bind
22859	4	7242	6	13	NULL	NULL	NULL	Adrenergic receptor	GP	stimulation of	decreases					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_40_0_459_s_108	10836144	2-Adrenergic receptor stimulation increased [32]GTP binding to Rho and decreased [32]GDP-Rho binding in preadipocytes ( 52).	bind
27927	1	7242	7	10	NULL	0	NULL	GTP	NULL		bind	NULL				Rho	NULL				NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_40_0_459_s_108	10836144	2-Adrenergic receptor stimulation increased [32]GTP binding to Rho and decreased [32]GDP-Rho binding in preadipocytes ( 52).	bind
27928	2	7242	7	NULL	NULL	0	NULL	Adrenergic receptor	NULL	stimulation of	increase	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevpharmacol_40_0_459_s_108	10836144	2-Adrenergic receptor stimulation increased [32]GTP binding to Rho and decreased [32]GDP-Rho binding in preadipocytes ( 52).	bind
27929	3	7242	7	NULL	NULL	0	NULL	Adrenergic receptor	NULL	stimulation of	decrease	NULL				statement 1	NULL				NULL	preadipocytes	0	NULL	NULL	NULL	gw70_annurevpharmacol_40_0_459_s_108	10836144	2-Adrenergic receptor stimulation increased [32]GTP binding to Rho and decreased [32]GDP-Rho binding in preadipocytes ( 52).	bind
22860	1	7243	6	13	NULL	NULL	NULL	PPARgamma	GP		bind					PPAR	NucleicAcid			response element	NULL	activated Jurkat T cells	NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16611855_s_10	16611855	2-AG treatment  also induced PPARgamma binding to a PPAR response element in activated  Jurkat T cells.	bind
22861	2	7243	6	13	NULL	NULL	NULL	AG	Chemical	treatment with	induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16611855_s_10	16611855	2-AG treatment  also induced PPARgamma binding to a PPAR response element in activated  Jurkat T cells.	bind
27930	1	7243	7	NULL	NULL	0	NULL	 PPARgamma	NULL		bind	NULL				PPAR	NULL			 response element	NULL	activated Jurkat T cells	0	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16611855_s_10	16611855	2-AG treatment  also induced PPARgamma binding to a PPAR response element in activated  Jurkat T cells.	bind
27931	2	7243	7	10	NULL	0	NULL	AG	NULL	treatment	induce	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16611855_s_10	16611855	2-AG treatment  also induced PPARgamma binding to a PPAR response element in activated  Jurkat T cells.	bind
22862	1	7245	6	13	NULL	NULL	NULL	2-Chloro- cis,cis-muconate	Chemical		bind		high affinity			muconate cycloisomerase	GP	P. putida			NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_9_3290_s_205	9726873	2-Chloro- cis,cis-muconate binds to the  P. putida muconate cycloisomerase with a relatively high affinity but with a low  kcat (Table  3).	bind
27932	1	7245	7	NULL	NULL	0	NULL	2-Chloro- cis,cis-muconate	NULL		binds	NULL	high affinity			 muconate cycloisomerase	NULL	P. putida			NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_9_3290_s_205	9726873	2-Chloro- cis,cis-muconate binds to the  P. putida muconate cycloisomerase with a relatively high affinity but with a low  kcat (Table  3).	bind
22863	1	7246	6	13	NULL	NULL	NULL	2-Ketoglutarate	Chemical	C-labeled	bind					PII	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_30_17797_s_209	7629080	2-Ketoglutarate and ATP Bind to PII In order to  determine the target for 2-ketoglutarate, we used  C-labeled 2-ketoglutarate to measure directly the binding  of 2-ketoglutarate to the individual signal transduction components  (NRI, NRII, PII, and UTase/UR).	bind
22864	2	7246	6	13	NULL	NULL	NULL	ATP	Chemical		bind					PII	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_30_17797_s_209	7629080	2-Ketoglutarate and ATP Bind to PII In order to  determine the target for 2-ketoglutarate, we used  C-labeled 2-ketoglutarate to measure directly the binding  of 2-ketoglutarate to the individual signal transduction components  (NRI, NRII, PII, and UTase/UR).	bind
22865	3	7246	6	13	NULL	NULL	NULL	2-ketoglutarate	Chemical	C-labeled	bind					NRI	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_30_17797_s_209	7629080	2-Ketoglutarate and ATP Bind to PII In order to  determine the target for 2-ketoglutarate, we used  C-labeled 2-ketoglutarate to measure directly the binding  of 2-ketoglutarate to the individual signal transduction components  (NRI, NRII, PII, and UTase/UR).	bind
22866	4	7246	6	13	NULL	NULL	NULL	2-Ketoglutarate	Chemical	C-labeled	bind					NRII	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_30_17797_s_209	7629080	2-Ketoglutarate and ATP Bind to PII In order to  determine the target for 2-ketoglutarate, we used  C-labeled 2-ketoglutarate to measure directly the binding  of 2-ketoglutarate to the individual signal transduction components  (NRI, NRII, PII, and UTase/UR).	bind
22867	5	7246	6	13	NULL	NULL	NULL	2-Ketoglutarate	Chemical	C-labeled	bind					UTase/UR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_30_17797_s_209	7629080	2-Ketoglutarate and ATP Bind to PII In order to  determine the target for 2-ketoglutarate, we used  C-labeled 2-ketoglutarate to measure directly the binding  of 2-ketoglutarate to the individual signal transduction components  (NRI, NRII, PII, and UTase/UR).	bind
27933	1	7246	7	NULL	NULL	0	NULL	2-Ketoglutarate	NULL	C-labeled	bind	NULL				PII	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_30_17797_s_209	7629080	2-Ketoglutarate and ATP Bind to PII In order to  determine the target for 2-ketoglutarate, we used  C-labeled 2-ketoglutarate to measure directly the binding  of 2-ketoglutarate to the individual signal transduction components  (NRI, NRII, PII, and UTase/UR).	bind
27934	2	7246	7	NULL	NULL	0	NULL	 ATP	NULL		bind	NULL				PII	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_30_17797_s_209	7629080	2-Ketoglutarate and ATP Bind to PII In order to  determine the target for 2-ketoglutarate, we used  C-labeled 2-ketoglutarate to measure directly the binding  of 2-ketoglutarate to the individual signal transduction components  (NRI, NRII, PII, and UTase/UR).	bind
27936	4	7246	7	NULL	NULL	0	NULL	2-ketoglutarate	NULL	C-labeled	bind	NULL				NRI	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_30_17797_s_209	7629080	2-Ketoglutarate and ATP Bind to PII In order to  determine the target for 2-ketoglutarate, we used  C-labeled 2-ketoglutarate to measure directly the binding  of 2-ketoglutarate to the individual signal transduction components  (NRI, NRII, PII, and UTase/UR).	bind
27937	5	7246	7	NULL	NULL	0	NULL	2-ketoglutarate	NULL	C-labeled	bind	NULL				NRII	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_30_17797_s_209	7629080	2-Ketoglutarate and ATP Bind to PII In order to  determine the target for 2-ketoglutarate, we used  C-labeled 2-ketoglutarate to measure directly the binding  of 2-ketoglutarate to the individual signal transduction components  (NRI, NRII, PII, and UTase/UR).	bind
27938	6	7246	7	NULL	NULL	0	NULL	2-ketoglutarate	NULL	C-labeled	bind	NULL				UTase/UR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_30_17797_s_209	7629080	2-Ketoglutarate and ATP Bind to PII In order to  determine the target for 2-ketoglutarate, we used  C-labeled 2-ketoglutarate to measure directly the binding  of 2-ketoglutarate to the individual signal transduction components  (NRI, NRII, PII, and UTase/UR).	bind
22868	1	7247	6	13	NULL	NULL	NULL	2-Oxoglutarate	Chemical		bind					PII	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2582_s_22	12670983	2-Oxoglutarate and ATP bind to PII in a synergistic manner ( ), stimulating the phosphorylation of  Synechococcus elongatus strain PCC 7942 PII at Ser 49 ( ,  ).	bind
22869	2	7247	6	13	NULL	NULL	NULL	ATP	Chemical		bind					PII	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2582_s_22	12670983	2-Oxoglutarate and ATP bind to PII in a synergistic manner ( ), stimulating the phosphorylation of  Synechococcus elongatus strain PCC 7942 PII at Ser 49 ( ,  ).	bind
22870	3	7247	6	13	NULL	NULL	NULL	statement 1	Process		acts synergistically with 					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2582_s_22	12670983	2-Oxoglutarate and ATP bind to PII in a synergistic manner ( ), stimulating the phosphorylation of  Synechococcus elongatus strain PCC 7942 PII at Ser 49 ( ,  ).	bind
22871	4	7247	6	13	NULL	NULL	NULL	statement 1	Process		stimulates					PCC 7942 PII	GP	phosphorylation of	Ser 49		NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2582_s_22	12670983	2-Oxoglutarate and ATP bind to PII in a synergistic manner ( ), stimulating the phosphorylation of  Synechococcus elongatus strain PCC 7942 PII at Ser 49 ( ,  ).	bind
22872	5	7247	6	13	NULL	NULL	NULL	statement 2	Process		stimulates					PCC 7942 PII	GP	phosphorylation of	Ser 49		NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2582_s_22	12670983	2-Oxoglutarate and ATP bind to PII in a synergistic manner ( ), stimulating the phosphorylation of  Synechococcus elongatus strain PCC 7942 PII at Ser 49 ( ,  ).	bind
46502	6	7247	6	13	NULL	NULL	NULL	PCC 7942 PII	Organism		is a strain of					Synechococcus elongatus	Organism				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2582_s_22	12670983	2-Oxoglutarate and ATP bind to PII in a synergistic manner ( ), stimulating the phosphorylation of  Synechococcus elongatus strain PCC 7942 PII at Ser 49 ( ,  ).	bind
27939	1	7247	7	NULL	NULL	0	NULL	2-Oxoglutarate	NULL		bind	NULL				PII	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_8_2582_s_22	12670983	2-Oxoglutarate and ATP bind to PII in a synergistic manner ( ), stimulating the phosphorylation of  Synechococcus elongatus strain PCC 7942 PII at Ser 49 ( ,  ).	bind
27940	2	7247	7	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				PII	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_8_2582_s_22	12670983	2-Oxoglutarate and ATP bind to PII in a synergistic manner ( ), stimulating the phosphorylation of  Synechococcus elongatus strain PCC 7942 PII at Ser 49 ( ,  ).	bind
27941	3	7247	7	NULL	NULL	0	NULL	statement 1	NULL		synergistically occur with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_8_2582_s_22	12670983	2-Oxoglutarate and ATP bind to PII in a synergistic manner ( ), stimulating the phosphorylation of  Synechococcus elongatus strain PCC 7942 PII at Ser 49 ( ,  ).	bind
27942	4	7247	7	10	NULL	0	NULL	statement 3	NULL		stimulate	NULL				PCC 7942 PII	NULL	phosphorylation of	Ser 49		NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2582_s_22	12670983	2-Oxoglutarate and ATP bind to PII in a synergistic manner ( ), stimulating the phosphorylation of  Synechococcus elongatus strain PCC 7942 PII at Ser 49 ( ,  ).	bind
46503	5	7247	7	10	NULL	0	NULL	PCC 7942 PII	NULL		is a strain of	NULL				Synechococcus elongatus	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_8_2582_s_22	12670983	2-Oxoglutarate and ATP bind to PII in a synergistic manner ( ), stimulating the phosphorylation of  Synechococcus elongatus strain PCC 7942 PII at Ser 49 ( ,  ).	bind
22873	1	7249	6	13	NULL	NULL	NULL	PipX	GP		forms a complex with					NtcA	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_2_16796668_s_8	16796668	2-Oxoglutarate favours complex formation  between PipX and NtcA, but impairs binding to PII, suggesting that partner  swapping between these nitrogen regulators is driven by the 2-oxoglutarate  concentration.	bind
22874	2	7249	6	13	NULL	NULL	NULL	2-Oxoglutarate	Chemical		favours					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_2_16796668_s_8	16796668	2-Oxoglutarate favours complex formation  between PipX and NtcA, but impairs binding to PII, suggesting that partner  swapping between these nitrogen regulators is driven by the 2-oxoglutarate  concentration.	bind
22875	3	7249	6	13	NULL	NULL	NULL	PipX	GP		bind					PII	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_2_16796668_s_8	16796668	2-Oxoglutarate favours complex formation  between PipX and NtcA, but impairs binding to PII, suggesting that partner  swapping between these nitrogen regulators is driven by the 2-oxoglutarate  concentration.	bind
22876	4	7249	6	13	NULL	NULL	NULL	2-Oxoglutarate	Chemical		impairs					PII	GP	binding to			NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_2_16796668_s_8	16796668	2-Oxoglutarate favours complex formation  between PipX and NtcA, but impairs binding to PII, suggesting that partner  swapping between these nitrogen regulators is driven by the 2-oxoglutarate  concentration.	bind
46504	5	7249	6	13	NULL	NULL	NULL	PipX	GP		is a type of					nitrogen regulator	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_2_16796668_s_8	16796668	2-Oxoglutarate favours complex formation  between PipX and NtcA, but impairs binding to PII, suggesting that partner  swapping between these nitrogen regulators is driven by the 2-oxoglutarate  concentration.	bind
46505	6	7249	6	13	NULL	NULL	NULL	NtcA	GP		is a type of					nitrogen regulator	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_2_16796668_s_8	16796668	2-Oxoglutarate favours complex formation  between PipX and NtcA, but impairs binding to PII, suggesting that partner  swapping between these nitrogen regulators is driven by the 2-oxoglutarate  concentration.	bind
27943	1	7249	7	NULL	NULL	0	NULL	PipX	NULL		forms complex with	NULL				NtcA	NULL				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_2_16796668_s_8	16796668	2-Oxoglutarate favours complex formation  between PipX and NtcA, but impairs binding to PII, suggesting that partner  swapping between these nitrogen regulators is driven by the 2-oxoglutarate  concentration.	bind
27944	2	7249	7	NULL	NULL	0	NULL	2-Oxoglutarate	NULL		favours	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_2_16796668_s_8	16796668	2-Oxoglutarate favours complex formation  between PipX and NtcA, but impairs binding to PII, suggesting that partner  swapping between these nitrogen regulators is driven by the 2-oxoglutarate  concentration.	bind
27945	3	7249	7	NULL	NULL	0	NULL	2-Oxoglutarate	NULL		impairs	NULL				PII	NULL	binding to			NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_2_16796668_s_8	16796668	2-Oxoglutarate favours complex formation  between PipX and NtcA, but impairs binding to PII, suggesting that partner  swapping between these nitrogen regulators is driven by the 2-oxoglutarate  concentration.	bind
27946	4	7249	7	NULL	NULL	0	NULL	2-Oxoglutarate	NULL		swaps	NULL				PipX	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_2_16796668_s_8	16796668	2-Oxoglutarate favours complex formation  between PipX and NtcA, but impairs binding to PII, suggesting that partner  swapping between these nitrogen regulators is driven by the 2-oxoglutarate  concentration.	bind
27947	5	7249	7	NULL	NULL	0	NULL	2-Oxoglutarate	NULL		swaps	NULL				NtcA	NULL				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_2_16796668_s_8	16796668	2-Oxoglutarate favours complex formation  between PipX and NtcA, but impairs binding to PII, suggesting that partner  swapping between these nitrogen regulators is driven by the 2-oxoglutarate  concentration.	bind
27948	6	7249	7	NULL	NULL	0	NULL	PipX	NULL		is a type of	NULL				nitrogen regulator	NULL				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_2_16796668_s_8	16796668	2-Oxoglutarate favours complex formation  between PipX and NtcA, but impairs binding to PII, suggesting that partner  swapping between these nitrogen regulators is driven by the 2-oxoglutarate  concentration.	bind
27949	7	7249	7	NULL	NULL	0	NULL	NtcA	NULL		is a type of	NULL				nitrogen regulator	NULL				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_2_16796668_s_8	16796668	2-Oxoglutarate favours complex formation  between PipX and NtcA, but impairs binding to PII, suggesting that partner  swapping between these nitrogen regulators is driven by the 2-oxoglutarate  concentration.	bind
22877	1	7250	6	13	NULL	NULL	NULL	q12	Chromosome		bind									CpG regions	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_18_6913_s_22	16624877	2-q12 and SP1 binding to CpG regions appears to be important for basal transcription ( ).	bind
22878	2	7250	6	13	NULL	NULL	NULL	Sp1	GP		bind									CpG regions	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_18_6913_s_22	16624877	2-q12 and SP1 binding to CpG regions appears to be important for basal transcription ( ).	bind
22879	3	7250	6	13	NULL	NULL	NULL	statement 1	Process		is important for					basal transcription	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_18_6913_s_22	16624877	2-q12 and SP1 binding to CpG regions appears to be important for basal transcription ( ).	bind
22880	4	7250	6	13	NULL	NULL	NULL	statement 2	Process		is important for					basal transcription	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_18_6913_s_22	16624877	2-q12 and SP1 binding to CpG regions appears to be important for basal transcription ( ).	bind
27950	1	7250	7	NULL	NULL	0	NULL	2-q12	NULL		bind	NULL					NULL			CpG region	NULL		0	NULL	NULL	NULL	gw70_pnas_103_18_6913_s_22	16624877	2-q12 and SP1 binding to CpG regions appears to be important for basal transcription ( ).	bind
27951	2	7250	7	NULL	NULL	0	NULL	SP1	NULL		bind	NULL					NULL			CpG region	NULL		0	NULL	NULL	NULL	gw70_pnas_103_18_6913_s_22	16624877	2-q12 and SP1 binding to CpG regions appears to be important for basal transcription ( ).	bind
27952	3	7250	7	NULL	NULL	0	NULL	statement 1	NULL		is important for	NULL				basal transcription	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_18_6913_s_22	16624877	2-q12 and SP1 binding to CpG regions appears to be important for basal transcription ( ).	bind
27953	4	7250	7	NULL	NULL	0	NULL	statement 2	NULL		is important for	NULL				basal transcription	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_18_6913_s_22	16624877	2-q12 and SP1 binding to CpG regions appears to be important for basal transcription ( ).	bind
22881	1	7252	6	13	NULL	NULL	NULL	salicylhydroxamic acid	Chemical		bind					myeloperoxidase	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_annurevbiophysbiomol_32_0_183_s_473	12574066	2.3  Ang  resolution X-ray crystal structure of the bisubstrate  analogue inhibitor salicylhydroxamic acid bound to human myeloperoxidase: a model  for a prereaction complex with hydroperoxide.	bind
46506	2	7252	6	13	NULL	NULL	NULL	salicylhydroxamic acid	Chemical		is a type of					bisubstrate analogue inhibitor	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiophysbiomol_32_0_183_s_473	12574066	2.3  Ang  resolution X-ray crystal structure of the bisubstrate  analogue inhibitor salicylhydroxamic acid bound to human myeloperoxidase: a model  for a prereaction complex with hydroperoxide.	bind
27954	1	7252	7	NULL	NULL	0	NULL	salicylhydroxamic acid	NULL		bind	NULL				 myeloperoxidase	NULL	human			NULL		0	NULL	NULL	NULL	gw70_annurevbiophysbiomol_32_0_183_s_473	12574066	2.3  Ang  resolution X-ray crystal structure of the bisubstrate  analogue inhibitor salicylhydroxamic acid bound to human myeloperoxidase: a model  for a prereaction complex with hydroperoxide.	bind
27955	2	7252	7	NULL	NULL	0	NULL	salicylhydroxamic acid	NULL		is a type of	NULL				bisubstrate analogue inhibitor 	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevbiophysbiomol_32_0_183_s_473	12574066	2.3  Ang  resolution X-ray crystal structure of the bisubstrate  analogue inhibitor salicylhydroxamic acid bound to human myeloperoxidase: a model  for a prereaction complex with hydroperoxide.	bind
22882	1	7253	6	13	NULL	NULL	NULL	flavosemiquinone	Chemical		is					FSQ	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_31_46_1445874_s_3	1445874	2.3)  are modified by the product pyruvate, which binds to the flavosemiquinone  (FSQ) form of the prosthetic flavin and decreases the thermodynamic driving  force for electron transfer from FSQ to heme.	bind
22883	2	7253	6	13	NULL	NULL	NULL	pyruvate	Chemical		bind					prosthetic flavin	Chemical	FSQ form of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_31_46_1445874_s_3	1445874	2.3)  are modified by the product pyruvate, which binds to the flavosemiquinone  (FSQ) form of the prosthetic flavin and decreases the thermodynamic driving  force for electron transfer from FSQ to heme.	bind
22956	3	7253	6	13	NULL	NULL	NULL	electron	Chemical		transfered to					heme	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_31_46_1445874_s_3	1445874	2.3)  are modified by the product pyruvate, which binds to the flavosemiquinone  (FSQ) form of the prosthetic flavin and decreases the thermodynamic driving  force for electron transfer from FSQ to heme.	bind
22957	4	7253	6	13	NULL	NULL	NULL	pyruvate	Chemical		decreases					statement 7	Process	thermodynamic driving force of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_31_46_1445874_s_3	1445874	2.3)  are modified by the product pyruvate, which binds to the flavosemiquinone  (FSQ) form of the prosthetic flavin and decreases the thermodynamic driving  force for electron transfer from FSQ to heme.	bind
53637	6	7253	6	13	NULL	NULL	NULL	electron	Chemical		is transfered from					FSQ	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_31_46_1445874_s_3	1445874	2.3)  are modified by the product pyruvate, which binds to the flavosemiquinone  (FSQ) form of the prosthetic flavin and decreases the thermodynamic driving  force for electron transfer from FSQ to heme.	bind
53638	7	7253	6	13	NULL	NULL	NULL	statement 3	Process		occurs simultaneously with					statement 6	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_31_46_1445874_s_3	1445874	2.3)  are modified by the product pyruvate, which binds to the flavosemiquinone  (FSQ) form of the prosthetic flavin and decreases the thermodynamic driving  force for electron transfer from FSQ to heme.	bind
27956	1	7253	7	NULL	NULL	0	NULL	pyruvate	NULL		binds to	NULL				prosthetic flavin	NULL	FSQ form of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_31_46_1445874_s_3	1445874	2.3)  are modified by the product pyruvate, which binds to the flavosemiquinone  (FSQ) form of the prosthetic flavin and decreases the thermodynamic driving  force for electron transfer from FSQ to heme.	bind
27957	2	7253	7	10	NULL	0	NULL	electron	NULL		is transfered from	NULL				FSQ	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_31_46_1445874_s_3	1445874	2.3)  are modified by the product pyruvate, which binds to the flavosemiquinone  (FSQ) form of the prosthetic flavin and decreases the thermodynamic driving  force for electron transfer from FSQ to heme.	bind
27958	3	7253	7	10	NULL	0	NULL	pyruvate	NULL		decrease	NULL				statement 6	NULL	thermodynamic driving force of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_31_46_1445874_s_3	1445874	2.3)  are modified by the product pyruvate, which binds to the flavosemiquinone  (FSQ) form of the prosthetic flavin and decreases the thermodynamic driving  force for electron transfer from FSQ to heme.	bind
53636	4	7253	7	10	NULL	0	NULL	FSQ	NULL		is	NULL				flavosemiquinone	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_31_46_1445874_s_3	1445874	2.3)  are modified by the product pyruvate, which binds to the flavosemiquinone  (FSQ) form of the prosthetic flavin and decreases the thermodynamic driving  force for electron transfer from FSQ to heme.	bind
53639	5	7253	7	10	NULL	0	NULL	electron	NULL		is transfered to	NULL				heme	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_31_46_1445874_s_3	1445874	2.3)  are modified by the product pyruvate, which binds to the flavosemiquinone  (FSQ) form of the prosthetic flavin and decreases the thermodynamic driving  force for electron transfer from FSQ to heme.	bind
53640	6	7253	7	10	NULL	0	NULL	statement 2	NULL		occurs simultaneously with	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_31_46_1445874_s_3	1445874	2.3)  are modified by the product pyruvate, which binds to the flavosemiquinone  (FSQ) form of the prosthetic flavin and decreases the thermodynamic driving  force for electron transfer from FSQ to heme.	bind
22884	1	7255	6	13	NULL	NULL	NULL	Ase1p	GP		bind					MT	CellComponent	taxol-stabilized			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_160_4_517_s_115	12591913	2.5 mug of (BV)Ase1p was bound to Taxol-stabilized  MTs as in  Fig. 3 A (s, supernatant; p, pellet).	bind
27959	1	7255	7	NULL	NULL	0	NULL	Ase1p	NULL		bind	NULL				MTs	NULL	 Taxol-stabilized 			NULL		0	NULL	NULL	NULL	gw70_cellbiol_160_4_517_s_115	12591913	2.5 mug of (BV)Ase1p was bound to Taxol-stabilized  MTs as in  Fig. 3 A (s, supernatant; p, pellet).	bind
22885	1	7258	6	13	NULL	NULL	NULL	Sp1 	GP		bind					DNA	NucleicAcid			GC box	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4920_s_294	11812820	20       Kuwahara,J., Yonezawa,A., Futamura,M. and Sugiura,Y. (1993) Binding of transcription factor Sp1 to GC box DNA revealed by footprinting analysis: different contact of three zinc fingers and sequence recognition mode.	bind
46507	2	7258	6	13	NULL	NULL	NULL	Sp1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4920_s_294	11812820	20       Kuwahara,J., Yonezawa,A., Futamura,M. and Sugiura,Y. (1993) Binding of transcription factor Sp1 to GC box DNA revealed by footprinting analysis: different contact of three zinc fingers and sequence recognition mode.	bind
27960	1	7258	7	10	NULL	0	NULL	 Sp1	NULL		bind	NULL				DNA	NULL			GC box	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4920_s_294	11812820	20       Kuwahara,J., Yonezawa,A., Futamura,M. and Sugiura,Y. (1993) Binding of transcription factor Sp1 to GC box DNA revealed by footprinting analysis: different contact of three zinc fingers and sequence recognition mode.	bind
46509	2	7258	7	10	NULL	0	NULL	Sp1	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4920_s_294	11812820	20       Kuwahara,J., Yonezawa,A., Futamura,M. and Sugiura,Y. (1993) Binding of transcription factor Sp1 to GC box DNA revealed by footprinting analysis: different contact of three zinc fingers and sequence recognition mode.	bind
22886	1	7259	6	13	NULL	NULL	NULL	Mot3	GP		bind					Ty	NucleicAcid	Saccharomyces cerevisiae		long terminal repeat (delta)	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_799_s_357	11160904	20       Madison,J.M., Dudley,A.M. and Winston,F. (1998) Identification and analysis of Mot3, a zinc finger protein that binds to the retrotransposon Ty long terminal repeat (delta) in  Saccharomyces cerevisiae.	bind
46510	2	7259	6	13	NULL	NULL	NULL	Mot3	GP		is a type of					zinc finger protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_799_s_357	11160904	20       Madison,J.M., Dudley,A.M. and Winston,F. (1998) Identification and analysis of Mot3, a zinc finger protein that binds to the retrotransposon Ty long terminal repeat (delta) in  Saccharomyces cerevisiae.	bind
46511	3	7259	6	13	NULL	NULL	NULL	Ty	NucleicAcid		is a type of					retrotransposon	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_799_s_357	11160904	20       Madison,J.M., Dudley,A.M. and Winston,F. (1998) Identification and analysis of Mot3, a zinc finger protein that binds to the retrotransposon Ty long terminal repeat (delta) in  Saccharomyces cerevisiae.	bind
27961	1	7259	7	10	NULL	0	NULL	Mot3	NULL		binds to	NULL				Ty	NULL	Saccharomyces cerevisiae		long terminal repeat (delta)	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_799_s_357	11160904	20       Madison,J.M., Dudley,A.M. and Winston,F. (1998) Identification and analysis of Mot3, a zinc finger protein that binds to the retrotransposon Ty long terminal repeat (delta) in  Saccharomyces cerevisiae.	bind
27962	2	7259	7	NULL	NULL	0	NULL	Mot3	NULL		is a type of	NULL				zinc finger protein	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_799_s_357	11160904	20       Madison,J.M., Dudley,A.M. and Winston,F. (1998) Identification and analysis of Mot3, a zinc finger protein that binds to the retrotransposon Ty long terminal repeat (delta) in  Saccharomyces cerevisiae.	bind
27963	3	7259	7	10	NULL	0	NULL	Ty	NULL		is a type of	NULL				retrotransposon	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_799_s_357	11160904	20       Madison,J.M., Dudley,A.M. and Winston,F. (1998) Identification and analysis of Mot3, a zinc finger protein that binds to the retrotransposon Ty long terminal repeat (delta) in  Saccharomyces cerevisiae.	bind
22887	1	7260	6	13	NULL	NULL	NULL	L5	GP	Xenopus laevis	bind					5S rRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2510_s_288	11410658	20       Wormington,W.M. (1989) Developmental expression and 5S rRNA-binding activity of  Xenopus laevis ribosomal protein L5.	bind
46512	2	7260	6	13	NULL	NULL	NULL	L5	GP		is a type of					ribosomal protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2510_s_288	11410658	20       Wormington,W.M. (1989) Developmental expression and 5S rRNA-binding activity of  Xenopus laevis ribosomal protein L5.	bind
27964	1	7260	7	NULL	NULL	0	NULL	5S rRNA	NULL		bind	NULL				L5	NULL	Xenopus laevis			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2510_s_288	11410658	20       Wormington,W.M. (1989) Developmental expression and 5S rRNA-binding activity of  Xenopus laevis ribosomal protein L5.	bind
27965	2	7260	7	NULL	NULL	0	NULL	L5	NULL		is a type of	NULL				ribosomal protein	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2510_s_288	11410658	20       Wormington,W.M. (1989) Developmental expression and 5S rRNA-binding activity of  Xenopus laevis ribosomal protein L5.	bind
22888	1	7261	6	13	NULL	NULL	NULL	factor VIIa	GP		bind					tissue factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_21_2555_s_125	11382723	20  23  This mechanism may also explain why the plasma level of recombinant factor VIIa required for adequate hemostatic efficiency far exceeds the  Kd for binding of factor VIIa to tissue factor.	bind
22889	2	7261	6	13	NULL	NULL	NULL	factor VIIa	GP	recombinant	required for					hemostatic efficiency	Process	adequate 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_21_2555_s_125	11382723	20  23  This mechanism may also explain why the plasma level of recombinant factor VIIa required for adequate hemostatic efficiency far exceeds the  Kd for binding of factor VIIa to tissue factor.	bind
27966	1	7261	7	10	NULL	0	NULL	factor VIIa	NULL		bind	NULL				tissue factor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_21_2555_s_125	11382723	20  23  This mechanism may also explain why the plasma level of recombinant factor VIIa required for adequate hemostatic efficiency far exceeds the  Kd for binding of factor VIIa to tissue factor.	bind
27967	2	7261	7	10	NULL	0	NULL	factor VIIa	NULL	recombinant	is required for	NULL				hemostatic efficiency	NULL	adequate			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_21_2555_s_125	11382723	20  23  This mechanism may also explain why the plasma level of recombinant factor VIIa required for adequate hemostatic efficiency far exceeds the  Kd for binding of factor VIIa to tissue factor.	bind
22890	1	7262	6	13	NULL	NULL	NULL	TGF-alpha	GP		bind					EGF-R	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_4_1307_s_158	10751356	20  Following inhalation of asbestos by rats, transforming growth factor-alpha (TGF-alpha), which can bind EGF-R, is also up-regulated with corresponding increases in cellular proliferation within developing asbestotic lesions.	bind
22891	2	7262	6	13	NULL	NULL	NULL	TGF-alpha	GP		is					transforming growth factor-alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_4_1307_s_158	10751356	20  Following inhalation of asbestos by rats, transforming growth factor-alpha (TGF-alpha), which can bind EGF-R, is also up-regulated with corresponding increases in cellular proliferation within developing asbestotic lesions.	bind
22892	3	7262	6	13	NULL	NULL	NULL	TGF-alpha	GP		is upregulated with					cellular proliferation	Process	increase in			NULL	developing asbestotic lesions	NULL	NULL	NULL	NULL	gw60_amjpathol_156_4_1307_s_158	10751356	20  Following inhalation of asbestos by rats, transforming growth factor-alpha (TGF-alpha), which can bind EGF-R, is also up-regulated with corresponding increases in cellular proliferation within developing asbestotic lesions.	bind
53643	4	7262	6	13	NULL	NULL	NULL	asbestos	Chemical		upregulates					TGF-alpha	GP				NULL	rats	NULL	NULL	NULL	NULL	gw60_amjpathol_156_4_1307_s_158	10751356	20  Following inhalation of asbestos by rats, transforming growth factor-alpha (TGF-alpha), which can bind EGF-R, is also up-regulated with corresponding increases in cellular proliferation within developing asbestotic lesions.	bind
27968	1	7262	7	NULL	NULL	0	NULL	TGF-alpha	NULL		bind	NULL				EGF-R	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_4_1307_s_158	10751356	20  Following inhalation of asbestos by rats, transforming growth factor-alpha (TGF-alpha), which can bind EGF-R, is also up-regulated with corresponding increases in cellular proliferation within developing asbestotic lesions.	bind
27969	2	7262	7	10	NULL	0	NULL	asbestos	NULL		upregulates	NULL				TGF-alpha	NULL				NULL	rats	NULL	NULL	NULL	NULL	gw60_amjpathol_156_4_1307_s_158	10751356	20  Following inhalation of asbestos by rats, transforming growth factor-alpha (TGF-alpha), which can bind EGF-R, is also up-regulated with corresponding increases in cellular proliferation within developing asbestotic lesions.	bind
27970	3	7262	7	10	NULL	0	NULL	TGF-alpha	NULL		is upregulated with	NULL				cellular proliferation	NULL	increase in			NULL	developing asbestotic lesions	NULL	NULL	NULL	NULL	gw60_amjpathol_156_4_1307_s_158	10751356	20  Following inhalation of asbestos by rats, transforming growth factor-alpha (TGF-alpha), which can bind EGF-R, is also up-regulated with corresponding increases in cellular proliferation within developing asbestotic lesions.	bind
27971	4	7262	7	NULL	NULL	0	NULL	TGF-alpha	NULL		is	NULL				transforming growth factor-alpha	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_4_1307_s_158	10751356	20  Following inhalation of asbestos by rats, transforming growth factor-alpha (TGF-alpha), which can bind EGF-R, is also up-regulated with corresponding increases in cellular proliferation within developing asbestotic lesions.	bind
22893	1	7263	6	13	NULL	NULL	NULL	EC-SOD	GP	subtype of	is bound to					endothelium	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_19_2264_s_152	10811593	20  Heparin specifically binds the subtype of EC-SOD (type C) that is bound to the endothelium.	bind
22894	2	7263	6	13	NULL	NULL	NULL	heparin	Chemical		bind		specifically			statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_19_2264_s_152	10811593	20  Heparin specifically binds the subtype of EC-SOD (type C) that is bound to the endothelium.	bind
27972	1	7263	7	NULL	NULL	0	NULL	EC-SOD	NULL	subtype of	bind	NULL				 endothelium	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_19_2264_s_152	10811593	20  Heparin specifically binds the subtype of EC-SOD (type C) that is bound to the endothelium.	bind
27973	2	7263	7	NULL	NULL	0	NULL	Heparin 	NULL		binds	NULL	specifically			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_19_2264_s_152	10811593	20  Heparin specifically binds the subtype of EC-SOD (type C) that is bound to the endothelium.	bind
22895	1	7264	6	13	NULL	NULL	NULL	polyclonal anti - c-Src antibody	GP	rabbit	bind					protein A	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_8_672_s_75	10521240	20  Immunoprecipitates prepared with rabbit polyclonal anti - c-Src antibody bound to protein A - Sepharose beads were incubated for 10 minutes at 30 degrees C with an assay buffer containing (in mmol/L) Tris-HCl (pH 7.2) 100, MgCl2 125, MnCl2 25, EGTA 2, Na2VO4 0.25, and DTT 2, and 125 mumol/L cold ATP and 10 muCi of [gamma-32]ATP.	bind
27974	1	7264	7	NULL	NULL	0	NULL	  polyclonal anti - c-Src antibody	NULL	rabbit	bind	NULL				protein A	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_8_672_s_75	10521240	20  Immunoprecipitates prepared with rabbit polyclonal anti - c-Src antibody bound to protein A - Sepharose beads were incubated for 10 minutes at 30 degrees C with an assay buffer containing (in mmol/L) Tris-HCl (pH 7.2) 100, MgCl2 125, MnCl2 25, EGTA 2, Na2VO4 0.25, and DTT 2, and 125 mumol/L cold ATP and 10 muCi of [gamma-32]ATP.	bind
22896	1	7265	6	13	NULL	NULL	NULL	alpha2beta1 integrin	GP		bind					collagen	GP	native			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_5_1489_s_92	10793060	20  In addition, the alpha2beta1 integrin which binds native collagen showed minimal binding to denatured collagen.	bind
22897	2	7265	6	13	NULL	NULL	NULL	alpha2beta1 integrin	GP		bind		minimally			collagen	GP	denatured			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_5_1489_s_92	10793060	20  In addition, the alpha2beta1 integrin which binds native collagen showed minimal binding to denatured collagen.	bind
27975	1	7265	7	NULL	NULL	0	NULL	alpha2beta1 integrin	NULL		binds	NULL				collagen	NULL	native			NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_5_1489_s_92	10793060	20  In addition, the alpha2beta1 integrin which binds native collagen showed minimal binding to denatured collagen.	bind
27976	2	7265	7	NULL	NULL	0	NULL	alpha2beta1 integrin	NULL		binds	NULL	minimally			collagen	NULL	denatured			NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_5_1489_s_92	10793060	20  In addition, the alpha2beta1 integrin which binds native collagen showed minimal binding to denatured collagen.	bind
22898	1	7266	6	13	NULL	NULL	NULL	Rnd1	GP		bind		constitutively			GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_3_173_s_50	10926864	20  Rnd1 is constitutively bound to GTP and able to block Ca2+ sensitization by RhoA.	bind
22899	2	7266	6	13	NULL	NULL	NULL	RhoA	GP		plays a role in					Ca2+	Chemical	sensitization of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_3_173_s_50	10926864	20  Rnd1 is constitutively bound to GTP and able to block Ca2+ sensitization by RhoA.	bind
22900	3	7266	6	13	NULL	NULL	NULL	Rnd1	GP		block					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_3_173_s_50	10926864	20  Rnd1 is constitutively bound to GTP and able to block Ca2+ sensitization by RhoA.	bind
27977	1	7266	7	NULL	NULL	0	NULL	Rnd1 	NULL		binds	NULL	constitutively			GTP	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_3_173_s_50	10926864	20  Rnd1 is constitutively bound to GTP and able to block Ca2+ sensitization by RhoA.	bind
27978	2	7266	7	NULL	NULL	0	NULL	RhoA	NULL		sensitize	NULL				Ca2+	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_3_173_s_50	10926864	20  Rnd1 is constitutively bound to GTP and able to block Ca2+ sensitization by RhoA.	bind
27979	3	7266	7	NULL	NULL	0	NULL	statement 1	NULL		block	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_3_173_s_50	10926864	20  Rnd1 is constitutively bound to GTP and able to block Ca2+ sensitization by RhoA.	bind
22901	1	7267	6	13	NULL	NULL	NULL	hypoxia	MedicalFinding		increases					Egr-1	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2029_s_87	10479642	20  Studies are in progress to trace the sequence of events increasing Egr-1 activation in hypoxia, and preliminary results indicate that oxygen deprivation enhances de novo Egr-1 synthesis and that this is driven by binding of ternary complex factor to ets/SRE sites in the Egr-1 promoter.	bind
22902	2	7267	6	13	NULL	NULL	NULL	oxygen 	Chemical	deprivation of	enhances					Egr-1	GP	de novo synthesis of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2029_s_87	10479642	20  Studies are in progress to trace the sequence of events increasing Egr-1 activation in hypoxia, and preliminary results indicate that oxygen deprivation enhances de novo Egr-1 synthesis and that this is driven by binding of ternary complex factor to ets/SRE sites in the Egr-1 promoter.	bind
22903	3	7267	6	13	NULL	NULL	NULL	ternary complex factor	GP		bind					Egr-1 	GP			ets/SRE sites of the promoter	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2029_s_87	10479642	20  Studies are in progress to trace the sequence of events increasing Egr-1 activation in hypoxia, and preliminary results indicate that oxygen deprivation enhances de novo Egr-1 synthesis and that this is driven by binding of ternary complex factor to ets/SRE sites in the Egr-1 promoter.	bind
27980	1	7267	7	NULL	NULL	0	NULL	oxygen	NULL	deprivation of	enhance	NULL				Egr-1	NULL	de novo synthesis of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2029_s_87	10479642	20  Studies are in progress to trace the sequence of events increasing Egr-1 activation in hypoxia, and preliminary results indicate that oxygen deprivation enhances de novo Egr-1 synthesis and that this is driven by binding of ternary complex factor to ets/SRE sites in the Egr-1 promoter.	bind
27981	2	7267	7	NULL	NULL	0	NULL	ternary complex factor 	NULL		bind	NULL				 Egr-1	NULL			ets/SRE sites in the promoter	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2029_s_87	10479642	20  Studies are in progress to trace the sequence of events increasing Egr-1 activation in hypoxia, and preliminary results indicate that oxygen deprivation enhances de novo Egr-1 synthesis and that this is driven by binding of ternary complex factor to ets/SRE sites in the Egr-1 promoter.	bind
27982	3	7267	7	NULL	NULL	0	NULL	statement 2	NULL		drives	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2029_s_87	10479642	20  Studies are in progress to trace the sequence of events increasing Egr-1 activation in hypoxia, and preliminary results indicate that oxygen deprivation enhances de novo Egr-1 synthesis and that this is driven by binding of ternary complex factor to ets/SRE sites in the Egr-1 promoter.	bind
22904	1	7268	6	13	NULL	NULL	NULL	FXa	GP		bind					TF	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_5_1362_s_34	10807755	20  TFPI uses the tandem Kunitz-type domains in its structure to form a quaternary complex with FXa bound to TF .	bind
22905	2	7268	6	13	NULL	NULL	NULL	TFPI	GP		form a quaternary complex with			tandem Kunitz-type domains		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_5_1362_s_34	10807755	20  TFPI uses the tandem Kunitz-type domains in its structure to form a quaternary complex with FXa bound to TF .	bind
27983	1	7268	7	NULL	NULL	0	NULL	FXa 	NULL		bind	NULL				TF	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_5_1362_s_34	10807755	20  TFPI uses the tandem Kunitz-type domains in its structure to form a quaternary complex with FXa bound to TF .	bind
27984	2	7268	7	NULL	NULL	0	NULL	TFPI	NULL		form quaternary complex with	NULL		tandem Kunitz-type domain		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_5_1362_s_34	10807755	20  TFPI uses the tandem Kunitz-type domains in its structure to form a quaternary complex with FXa bound to TF .	bind
22906	1	7269	6	13	NULL	NULL	NULL	fibrinogen	GP		bind					glycoprotein IIb/IIa complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_36	9437193	20 21  Binding of fibrinogen to the glycoprotein IIb/IIa complex appears to be the final common pathway for platelet aggregation.	bind
22907	2	7269	6	13	NULL	NULL	NULL	statement 1	Process		is needed for					platelet aggregation	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_36	9437193	20 21  Binding of fibrinogen to the glycoprotein IIb/IIa complex appears to be the final common pathway for platelet aggregation.	bind
27985	1	7269	7	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL				glycoprotein IIb/IIa complex	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_36	9437193	20 21  Binding of fibrinogen to the glycoprotein IIb/IIa complex appears to be the final common pathway for platelet aggregation.	bind
27986	2	7269	7	NULL	NULL	0	NULL	statement 1	NULL		is the pathway for	NULL				platelet aggregation	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_36	9437193	20 21  Binding of fibrinogen to the glycoprotein IIb/IIa complex appears to be the final common pathway for platelet aggregation.	bind
22908	1	7270	6	13	NULL	NULL	NULL	heparin	Chemical		bind					thrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_10_1158_s_189	10715263	20 21  Heparin binds to various other partners besides thrombin and is thereby inhibited.	bind
27987	1	7270	7	NULL	NULL	0	NULL	Heparin	NULL		binds to	NULL				thrombin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_101_10_1158_s_189	10715263	20 21  Heparin binds to various other partners besides thrombin and is thereby inhibited.	bind
27988	2	7270	7	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				thrombin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_101_10_1158_s_189	10715263	20 21  Heparin binds to various other partners besides thrombin and is thereby inhibited.	bind
22909	1	7271	6	13	NULL	NULL	NULL	heparin/HS	Chemical		bind					bFGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_7_1853_s_22	9107173	20 21 22  Polyaromatic heparin-mimicking anionic molecules compete with heparin/HS for bFGF binding and hence inhibit bFGF receptor binding and mitogenic activity.	bind
22910	2	7271	6	13	NULL	NULL	NULL	Polyaromatic heparin-mimicking anionic molecules	Chemical		bind					bFGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_7_1853_s_22	9107173	20 21 22  Polyaromatic heparin-mimicking anionic molecules compete with heparin/HS for bFGF binding and hence inhibit bFGF receptor binding and mitogenic activity.	bind
22911	3	7271	6	13	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_7_1853_s_22	9107173	20 21 22  Polyaromatic heparin-mimicking anionic molecules compete with heparin/HS for bFGF binding and hence inhibit bFGF receptor binding and mitogenic activity.	bind
22913	5	7271	6	13	NULL	NULL	NULL	statement 3	Process		inhibits					bFGF receptor	GP	mitogenic activity of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_7_1853_s_22	9107173	20 21 22  Polyaromatic heparin-mimicking anionic molecules compete with heparin/HS for bFGF binding and hence inhibit bFGF receptor binding and mitogenic activity.	bind
22914	6	7271	6	13	NULL	NULL	NULL	statement 3	Process		inhibits					bFGF receptor	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_7_1853_s_22	9107173	20 21 22  Polyaromatic heparin-mimicking anionic molecules compete with heparin/HS for bFGF binding and hence inhibit bFGF receptor binding and mitogenic activity.	bind
27989	1	7271	7	NULL	NULL	0	NULL	heparin/HS	NULL		bind	NULL				bFGF	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_95_7_1853_s_22	9107173	20 21 22  Polyaromatic heparin-mimicking anionic molecules compete with heparin/HS for bFGF binding and hence inhibit bFGF receptor binding and mitogenic activity.	bind
27990	2	7271	7	NULL	NULL	0	NULL	Polyaromatic heparin-mimicking anionic molecules	NULL		bind	NULL				bFGF	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_95_7_1853_s_22	9107173	20 21 22  Polyaromatic heparin-mimicking anionic molecules compete with heparin/HS for bFGF binding and hence inhibit bFGF receptor binding and mitogenic activity.	bind
27991	3	7271	7	NULL	NULL	0	NULL	statement 1	NULL		compete with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_95_7_1853_s_22	9107173	20 21 22  Polyaromatic heparin-mimicking anionic molecules compete with heparin/HS for bFGF binding and hence inhibit bFGF receptor binding and mitogenic activity.	bind
27992	4	7271	7	NULL	NULL	0	NULL	statement 2	NULL		inhibit	NULL				bFGF receptor	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_circulation_95_7_1853_s_22	9107173	20 21 22  Polyaromatic heparin-mimicking anionic molecules compete with heparin/HS for bFGF binding and hence inhibit bFGF receptor binding and mitogenic activity.	bind
27993	5	7271	7	NULL	NULL	0	NULL	statement 2	NULL		inhibit	NULL				bFGF receptor	NULL	mitogenic activity of			NULL		0	NULL	NULL	NULL	gw60_circulation_95_7_1853_s_22	9107173	20 21 22  Polyaromatic heparin-mimicking anionic molecules compete with heparin/HS for bFGF binding and hence inhibit bFGF receptor binding and mitogenic activity.	bind
22959	1	7272	6	13	NULL	NULL	NULL	tryp-VLDL	GP		bind		high affinity;;specificity			macrophage receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_200	9633939	20 21 22  The tryp-VLDL bound with high affinity and specificity to this macrophage receptor and MBP 200, 235 and failed to bind to the LDL receptor.	bind
22960	2	7272	6	13	NULL	NULL	NULL	tryp-VLDL	GP		bind		high affinity;;specificity			MBP 200	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_200	9633939	20 21 22  The tryp-VLDL bound with high affinity and specificity to this macrophage receptor and MBP 200, 235 and failed to bind to the LDL receptor.	bind
22961	3	7272	6	13	NULL	NULL	NULL	tryp-VLDL	GP		bind		high affinity;;specificity			MBP 235	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_200	9633939	20 21 22  The tryp-VLDL bound with high affinity and specificity to this macrophage receptor and MBP 200, 235 and failed to bind to the LDL receptor.	bind
22962	4	7272	6	13	NULL	NULL	NULL	tryp-VLDL	GP		does not bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_200	9633939	20 21 22  The tryp-VLDL bound with high affinity and specificity to this macrophage receptor and MBP 200, 235 and failed to bind to the LDL receptor.	bind
27994	1	7272	7	NULL	NULL	0	NULL	tryp-VLDL	NULL		bind	NULL	high affinity;;specificity			macrophage receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_200	9633939	20 21 22  The tryp-VLDL bound with high affinity and specificity to this macrophage receptor and MBP 200, 235 and failed to bind to the LDL receptor.	bind
27995	2	7272	7	NULL	NULL	0	NULL	tryp-VLDL	NULL		bind	NULL	high affinity;;specificity			MBP 200	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_200	9633939	20 21 22  The tryp-VLDL bound with high affinity and specificity to this macrophage receptor and MBP 200, 235 and failed to bind to the LDL receptor.	bind
27996	3	7272	7	NULL	NULL	0	NULL	tryp-VLDL	NULL		bind	NULL	high affinity;;specificity			MBP 235	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_200	9633939	20 21 22  The tryp-VLDL bound with high affinity and specificity to this macrophage receptor and MBP 200, 235 and failed to bind to the LDL receptor.	bind
27997	4	7272	7	NULL	NULL	0	NULL	tryp-VLDL	NULL		does not bind	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_200	9633939	20 21 22  The tryp-VLDL bound with high affinity and specificity to this macrophage receptor and MBP 200, 235 and failed to bind to the LDL receptor.	bind
22963	1	7273	6	13	NULL	NULL	NULL	ets proteins	GP		bind					GGA core	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_585_s_159	10669659	20 21 32  The  ets proteins are members of a large family with a conserved 84 - amino acid sequence (the  ets domain) allowing their binding to the GGA core as monomers.	bind
22964	2	7273	6	13	NULL	NULL	NULL	ets protein members	GP		have conserved 								ETS domain		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_585_s_159	10669659	20 21 32  The  ets proteins are members of a large family with a conserved 84 - amino acid sequence (the  ets domain) allowing their binding to the GGA core as monomers.	bind
46518	3	7273	6	13	NULL	NULL	NULL	GGA core	NucleicAcid		occur as					monomers	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_585_s_159	10669659	20 21 32  The  ets proteins are members of a large family with a conserved 84 - amino acid sequence (the  ets domain) allowing their binding to the GGA core as monomers.	bind
27998	1	7273	7	NULL	NULL	0	NULL	ets protein	NULL		bind	NULL				GGA core	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_585_s_159	10669659	20 21 32  The  ets proteins are members of a large family with a conserved 84 - amino acid sequence (the  ets domain) allowing their binding to the GGA core as monomers.	bind
27999	2	7273	7	NULL	NULL	0	NULL	ets protein	NULL		are members of	NULL					NULL		ets domain family		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_585_s_159	10669659	20 21 32  The  ets proteins are members of a large family with a conserved 84 - amino acid sequence (the  ets domain) allowing their binding to the GGA core as monomers.	bind
28000	3	7273	7	NULL	NULL	0	NULL	ets domain	NULL		contains	NULL					NULL		conserved 84 - amino acid sequence		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_585_s_159	10669659	20 21 32  The  ets proteins are members of a large family with a conserved 84 - amino acid sequence (the  ets domain) allowing their binding to the GGA core as monomers.	bind
28001	4	7273	7	NULL	NULL	0	NULL	statement 1	NULL		occur as	NULL				monomers	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_585_s_159	10669659	20 21 32  The  ets proteins are members of a large family with a conserved 84 - amino acid sequence (the  ets domain) allowing their binding to the GGA core as monomers.	bind
22965	1	7274	6	13	NULL	NULL	NULL	Sp1	GP		bind									repeat 3	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_7_1777_s_221	10894816	20 35  A further difference between OM and IL-6 is that only IL-6 directly enhances the binding of Sp1 and Sp3 to repeat 3, whereas OM does not directly upregulate Sp1 binding activity.	bind
22966	2	7274	6	13	NULL	NULL	NULL	Sp3	GP		bind									repeat 3	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_7_1777_s_221	10894816	20 35  A further difference between OM and IL-6 is that only IL-6 directly enhances the binding of Sp1 and Sp3 to repeat 3, whereas OM does not directly upregulate Sp1 binding activity.	bind
22967	3	7274	6	13	NULL	NULL	NULL	IL-6	GP		enhances		directly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_7_1777_s_221	10894816	20 35  A further difference between OM and IL-6 is that only IL-6 directly enhances the binding of Sp1 and Sp3 to repeat 3, whereas OM does not directly upregulate Sp1 binding activity.	bind
22968	4	7274	6	13	NULL	NULL	NULL	IL-6	GP		enhances		directly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_7_1777_s_221	10894816	20 35  A further difference between OM and IL-6 is that only IL-6 directly enhances the binding of Sp1 and Sp3 to repeat 3, whereas OM does not directly upregulate Sp1 binding activity.	bind
22969	5	7274	6	13	NULL	NULL	NULL	OM	GP		does not upregulate		directly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_7_1777_s_221	10894816	20 35  A further difference between OM and IL-6 is that only IL-6 directly enhances the binding of Sp1 and Sp3 to repeat 3, whereas OM does not directly upregulate Sp1 binding activity.	bind
28002	1	7274	7	10	NULL	0	NULL	Sp1			bind									repeat 3	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_7_1777_s_221	10894816	20 35  A further difference between OM and IL-6 is that only IL-6 directly enhances the binding of Sp1 and Sp3 to repeat 3, whereas OM does not directly upregulate Sp1 binding activity.	bind
28003	2	7274	7	10	NULL	0	NULL	Sp3			bind									repeat 3	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_7_1777_s_221	10894816	20 35  A further difference between OM and IL-6 is that only IL-6 directly enhances the binding of Sp1 and Sp3 to repeat 3, whereas OM does not directly upregulate Sp1 binding activity.	bind
28004	3	7274	7	NULL	NULL	0	NULL	 IL-6	NULL		enhance	NULL	directly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_7_1777_s_221	10894816	20 35  A further difference between OM and IL-6 is that only IL-6 directly enhances the binding of Sp1 and Sp3 to repeat 3, whereas OM does not directly upregulate Sp1 binding activity.	bind
28005	4	7274	7	NULL	NULL	0	NULL	IL-6	NULL		enhance	NULL	directly			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_7_1777_s_221	10894816	20 35  A further difference between OM and IL-6 is that only IL-6 directly enhances the binding of Sp1 and Sp3 to repeat 3, whereas OM does not directly upregulate Sp1 binding activity.	bind
28006	5	7274	7	NULL	NULL	0	NULL	OM	NULL		does not upregulate	NULL	directly			Sp1	NULL	binding activity of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_7_1777_s_221	10894816	20 35  A further difference between OM and IL-6 is that only IL-6 directly enhances the binding of Sp1 and Sp3 to repeat 3, whereas OM does not directly upregulate Sp1 binding activity.	bind
22970	1	7275	6	13	NULL	NULL	NULL	endothelin-1	GP		is					ET-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
22971	2	7275	6	13	NULL	NULL	NULL	angiotensin II	GP		is					Ang II	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
22972	3	7275	6	13	NULL	NULL	NULL	ET-1	GP		bind					GPCR	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
22973	4	7275	6	13	NULL	NULL	NULL	Ang II	GP		bind					GPCR	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
22974	5	7275	6	13	NULL	NULL	NULL	statement 3	Process		induce					cardiomyocyte size	Cell	increase in			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
22975	6	7275	6	13	NULL	NULL	NULL	statement 4	Process		induce					cardiomyocyte size	Cell	increase in			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
22976	7	7275	6	13	NULL	NULL	NULL	statement 5	Process		results from					myofibrils	Cell	addition of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
22977	8	7275	6	13	NULL	NULL	NULL	statement 6	Process		results from					myofibrils	Cell	addition of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
46519	9	7275	6	13	NULL	NULL	NULL	ET-1	GP		is a type of					Adrenergic agonist	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
46520	10	7275	6	13	NULL	NULL	NULL	Ang II	GP		is a type of					Adrenergic agonist	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
28007	1	7275	7	NULL	NULL	0	NULL	ET-1	NULL		bind	NULL				GPCR	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
28008	2	7275	7	NULL	NULL	0	NULL	Ang II 	NULL		bind	NULL				GPCR	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
28009	3	7275	7	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL				cardiomyocyte size	NULL	increase in			NULL		0	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
28010	4	7275	7	10	NULL	0	NULL	statement 2			induce					cardiomyocyte size		increase in			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
28011	5	7275	7	NULL	NULL	0	NULL	ET-1	NULL		is a type of	NULL				Adrenergic agonists	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
28012	6	7275	7	NULL	NULL	0	NULL	Ang II 	NULL		is a type of	NULL				Adrenergic agonists	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
28013	7	7275	7	NULL	NULL	0	NULL	ET-1	NULL		is	NULL				 endothelin-1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
28014	8	7275	7	NULL	NULL	0	NULL	Ang II	NULL		is	NULL				angiotensin II	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
53652	9	7275	7	10	NULL	0	NULL	statement 3			results from					myofibrils		addition of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
53653	10	7275	7	10	NULL	0	NULL	statement 4			results from					myofibrils 		addition of			NULL		0	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_37	12855672	20 Adrenergic agonists, endothelin-1 (ET-1), and angiotensin II (Ang II) binding to GPCR induce a rather uniform increase in cardiomyocyte size, resulting from the addition of myofibrils in parallel.	bind
23707	1	7276	6	13	NULL	NULL	NULL	fibrils 	CellComponent		is formed by					Abeta	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
23708	2	7276	6	13	NULL	NULL	NULL	beta-pleated sheet	GP	formation of	occurs in					statement 1	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
23709	3	7276	6	13	NULL	NULL	NULL	tau	GP	hyperphosphorylated	substrate for		may be			BSB	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
23710	4	7276	6	13	NULL	NULL	NULL	alpha-synuclein	GP		substrate for		may be			THIOS	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
53655	5	7276	6	13	NULL	NULL	NULL	tau	GP	hyperphosphorylated	substrate for		may be			BSB	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
53656	6	7276	6	13	NULL	NULL	NULL	alpha-synuclein	GP		substrate for		may be			THIOS	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
53657	7	7276	6	13	NULL	NULL	NULL	BSB	Chemical		bind					lesions	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
53658	8	7276	6	13	NULL	NULL	NULL	THIOS	Chemical		bind					lesions	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
53659	9	7276	6	13	NULL	NULL	NULL	statement 7	Process	differences in	causes					beta-pleated sheet	GP	variations in;;structure of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
53660	10	7276	6	13	NULL	NULL	NULL	statement 8	Process	differences in	causes					beta-pleated sheet	GP	variations in;;structure of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
28573	1	7276	7	10	NULL	0	NULL	fibrils			is formed by					Abeta					NULL	 	NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
28574	2	7276	7	10	NULL	0	NULL	 tau		hyperphosphorylated	 substrate for		may be			BSB		binding of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
28575	3	7276	7	10	NULL	0	NULL	alpha-synuclein			substrate for		may be			BSB		binding of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
28576	4	7276	7	10	NULL	0	NULL	tau		hyperphosphorylated	substrate for		may be			THIOS		binding of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
28577	5	7276	7	10	NULL	0	NULL	alpha-synuclein			substrate for		may be			THIOS		binding of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
28578	6	7276	7	NULL	NULL	0	NULL	BSB	NULL		bind	NULL				lesions	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
28579	7	7276	7	NULL	NULL	0	NULL	THIOS	NULL		bind	NULL				lesions	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
28585	8	7276	7	10	NULL	0	NULL	statement 6		differences in	cause					beta-pleated sheet		variations in;;structure of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
28586	9	7276	7	10	NULL	0	NULL	statement 7		differences in	cause					beta-pleated sheet		variations in;;structure of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
53654	10	7276	7	10	NULL	0	NULL	beta-pleated sheet		formation of	occurs in					statement 1					NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_128	11549586	20 Although the beta-pleated sheet formation occurring in the fibrils formed by Abeta, hyperphosphorylated tau, as well as alpha-synuclein may be the substrate for BSB and THIOS binding, minor variations in the beta-pleated sheet structures in the lesions described may account for the differences observed in the binding of BSB and THIOS to these lesions.	bind
23134	1	7277	6	13	NULL	NULL	NULL	HSF	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_24489_s_79	7592665	20 mM  salicylate  induced HSF DNA binding comparable to a 42  degrees C heat shock,  while lower concentrations produced less HSF DNA binding in a  dose-dependent fashion.	bind
23135	2	7277	6	13	NULL	NULL	NULL	salicylate	Chemical		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_24489_s_79	7592665	20 mM  salicylate  induced HSF DNA binding comparable to a 42  degrees C heat shock,  while lower concentrations produced less HSF DNA binding in a  dose-dependent fashion.	bind
53661	3	7277	6	13	NULL	NULL	NULL	heat shock			induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_24489_s_79	7592665	20 mM  salicylate  induced HSF DNA binding comparable to a 42  degrees C heat shock,  while lower concentrations produced less HSF DNA binding in a  dose-dependent fashion.	bind
53662	4	7277	6	13	NULL	NULL	NULL	statement 2	Process		is comparable to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_24489_s_79	7592665	20 mM  salicylate  induced HSF DNA binding comparable to a 42  degrees C heat shock,  while lower concentrations produced less HSF DNA binding in a  dose-dependent fashion.	bind
28587	1	7277	7	NULL	NULL	0	NULL	HSF	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_41_24489_s_79	7592665	20 mM  salicylate  induced HSF DNA binding comparable to a 42  degrees C heat shock,  while lower concentrations produced less HSF DNA binding in a  dose-dependent fashion.	bind
28588	2	7277	7	NULL	NULL	0	NULL	salicylate	NULL		induce	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_41_24489_s_79	7592665	20 mM  salicylate  induced HSF DNA binding comparable to a 42  degrees C heat shock,  while lower concentrations produced less HSF DNA binding in a  dose-dependent fashion.	bind
28589	3	7277	7	NULL	NULL	0	NULL	heat shock	NULL		induce	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_41_24489_s_79	7592665	20 mM  salicylate  induced HSF DNA binding comparable to a 42  degrees C heat shock,  while lower concentrations produced less HSF DNA binding in a  dose-dependent fashion.	bind
28590	4	7277	7	10	NULL	0	NULL	statement 2			is comparable to					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_24489_s_79	7592665	20 mM  salicylate  induced HSF DNA binding comparable to a 42  degrees C heat shock,  while lower concentrations produced less HSF DNA binding in a  dose-dependent fashion.	bind
23136	1	7280	6	13	NULL	NULL	NULL	p65	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33508_s_181	9837931	20 muM helenalin completely impaired both p65 DNA binding as well as TNF-alpha stimulated NF-kappaB activity.	bind
23137	2	7280	6	13	NULL	NULL	NULL	helenalin	Chemical		impairs		completely			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33508_s_181	9837931	20 muM helenalin completely impaired both p65 DNA binding as well as TNF-alpha stimulated NF-kappaB activity.	bind
23138	3	7280	6	13	NULL	NULL	NULL	TNF-alpha	GP		stimulates					NF-kappaB activity	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33508_s_181	9837931	20 muM helenalin completely impaired both p65 DNA binding as well as TNF-alpha stimulated NF-kappaB activity.	bind
23139	4	7280	6	13	NULL	NULL	NULL	helenalin	Chemical		inhibits		completely			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33508_s_181	9837931	20 muM helenalin completely impaired both p65 DNA binding as well as TNF-alpha stimulated NF-kappaB activity.	bind
28591	1	7280	7	NULL	NULL	0	NULL	 p65	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_50_33508_s_181	9837931	20 muM helenalin completely impaired both p65 DNA binding as well as TNF-alpha stimulated NF-kappaB activity.	bind
28592	2	7280	7	NULL	NULL	0	NULL	helenalin	NULL		impairs	NULL	completely			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33508_s_181	9837931	20 muM helenalin completely impaired both p65 DNA binding as well as TNF-alpha stimulated NF-kappaB activity.	bind
28593	3	7280	7	NULL	NULL	0	NULL	 TNF-alpha	NULL		stimulate	NULL				NF-kappaB	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_50_33508_s_181	9837931	20 muM helenalin completely impaired both p65 DNA binding as well as TNF-alpha stimulated NF-kappaB activity.	bind
28594	4	7280	7	NULL	NULL	0	NULL	helenalin	NULL		impairs	NULL	completely			statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_50_33508_s_181	9837931	20 muM helenalin completely impaired both p65 DNA binding as well as TNF-alpha stimulated NF-kappaB activity.	bind
23140	1	7281	6	13	NULL	NULL	NULL	NF-kappaB	GP		activates					transcription	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_10_1585_s_164	11597930	20 Neither has been demonstrated to have a transcription-enhancing property; in fact, activated glucocorticoid responsive element mediates the downregulation of NF-kappaB-activated transcription by interfering with the binding of NF-kappaB p65 to its  cis-element 30 or by directly interfering with transactivation of the NF-kappaB p65 subunit.	bind
23141	2	7281	6	13	NULL	NULL	NULL			activated	mediates				glucocorticoid responsive element	statement 1	Process	downregulation of 			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_10_1585_s_164	11597930	20 Neither has been demonstrated to have a transcription-enhancing property; in fact, activated glucocorticoid responsive element mediates the downregulation of NF-kappaB-activated transcription by interfering with the binding of NF-kappaB p65 to its  cis-element 30 or by directly interfering with transactivation of the NF-kappaB p65 subunit.	bind
23142	3	7281	6	13	NULL	NULL	NULL	NF-kappaB p65	GP		bind									cis-element	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_10_1585_s_164	11597930	20 Neither has been demonstrated to have a transcription-enhancing property; in fact, activated glucocorticoid responsive element mediates the downregulation of NF-kappaB-activated transcription by interfering with the binding of NF-kappaB p65 to its  cis-element 30 or by directly interfering with transactivation of the NF-kappaB p65 subunit.	bind
23143	4	7281	6	13	NULL	NULL	NULL			activated	interfere				glucocorticoid responsive element	statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_10_1585_s_164	11597930	20 Neither has been demonstrated to have a transcription-enhancing property; in fact, activated glucocorticoid responsive element mediates the downregulation of NF-kappaB-activated transcription by interfering with the binding of NF-kappaB p65 to its  cis-element 30 or by directly interfering with transactivation of the NF-kappaB p65 subunit.	bind
23144	5	7281	6	13	NULL	NULL	NULL			activated	interfere		directly		glucocorticoid responsive element	NF-kappaB p65 subunit	GP	transactivation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_10_1585_s_164	11597930	20 Neither has been demonstrated to have a transcription-enhancing property; in fact, activated glucocorticoid responsive element mediates the downregulation of NF-kappaB-activated transcription by interfering with the binding of NF-kappaB p65 to its  cis-element 30 or by directly interfering with transactivation of the NF-kappaB p65 subunit.	bind
23145	6	7281	6	13	NULL	NULL	NULL	statement 2	Process		occurs via					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_10_1585_s_164	11597930	20 Neither has been demonstrated to have a transcription-enhancing property; in fact, activated glucocorticoid responsive element mediates the downregulation of NF-kappaB-activated transcription by interfering with the binding of NF-kappaB p65 to its  cis-element 30 or by directly interfering with transactivation of the NF-kappaB p65 subunit.	bind
53663	7	7281	6	13	NULL	NULL	NULL	statement 2	Process		occur via					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_10_1585_s_164	11597930	20 Neither has been demonstrated to have a transcription-enhancing property; in fact, activated glucocorticoid responsive element mediates the downregulation of NF-kappaB-activated transcription by interfering with the binding of NF-kappaB p65 to its  cis-element 30 or by directly interfering with transactivation of the NF-kappaB p65 subunit.	bind
53664	8	7281	6	13	NULL	NULL	NULL	statement 6	Process		is an alternative to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_10_1585_s_164	11597930	20 Neither has been demonstrated to have a transcription-enhancing property; in fact, activated glucocorticoid responsive element mediates the downregulation of NF-kappaB-activated transcription by interfering with the binding of NF-kappaB p65 to its  cis-element 30 or by directly interfering with transactivation of the NF-kappaB p65 subunit.	bind
28595	1	7281	7	NULL	NULL	0	NULL	NF-kappaB	NULL		activates	NULL				transcription 	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_10_1585_s_164	11597930	20 Neither has been demonstrated to have a transcription-enhancing property; in fact, activated glucocorticoid responsive element mediates the downregulation of NF-kappaB-activated transcription by interfering with the binding of NF-kappaB p65 to its  cis-element 30 or by directly interfering with transactivation of the NF-kappaB p65 subunit.	bind
28596	2	7281	7	NULL	NULL	0	NULL		NULL	activated	mediates	NULL			glucocorticoid responsive element	statement 1	NULL	downregulation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_10_1585_s_164	11597930	20 Neither has been demonstrated to have a transcription-enhancing property; in fact, activated glucocorticoid responsive element mediates the downregulation of NF-kappaB-activated transcription by interfering with the binding of NF-kappaB p65 to its  cis-element 30 or by directly interfering with transactivation of the NF-kappaB p65 subunit.	bind
28597	3	7281	7	10	NULL	0	NULL	NF-kappaB p65			bind									cis-element	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_10_1585_s_164	11597930	20 Neither has been demonstrated to have a transcription-enhancing property; in fact, activated glucocorticoid responsive element mediates the downregulation of NF-kappaB-activated transcription by interfering with the binding of NF-kappaB p65 to its  cis-element 30 or by directly interfering with transactivation of the NF-kappaB p65 subunit.	bind
28598	4	7281	7	10	NULL	0	NULL			activated	interferes with				glucocorticoid responsive element	statement 3					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_10_1585_s_164	11597930	20 Neither has been demonstrated to have a transcription-enhancing property; in fact, activated glucocorticoid responsive element mediates the downregulation of NF-kappaB-activated transcription by interfering with the binding of NF-kappaB p65 to its  cis-element 30 or by directly interfering with transactivation of the NF-kappaB p65 subunit.	bind
28599	5	7281	7	10	NULL	0	NULL			activated	interferes with				glucocorticoid responsive element	NF-kappaB p65 subunit		transactivation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_10_1585_s_164	11597930	20 Neither has been demonstrated to have a transcription-enhancing property; in fact, activated glucocorticoid responsive element mediates the downregulation of NF-kappaB-activated transcription by interfering with the binding of NF-kappaB p65 to its  cis-element 30 or by directly interfering with transactivation of the NF-kappaB p65 subunit.	bind
28600	6	7281	7	NULL	NULL	0	NULL	statement 2	NULL		occurs by	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_10_1585_s_164	11597930	20 Neither has been demonstrated to have a transcription-enhancing property; in fact, activated glucocorticoid responsive element mediates the downregulation of NF-kappaB-activated transcription by interfering with the binding of NF-kappaB p65 to its  cis-element 30 or by directly interfering with transactivation of the NF-kappaB p65 subunit.	bind
28601	7	7281	7	NULL	NULL	0	NULL	statement 2	NULL		occurs by	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_10_1585_s_164	11597930	20 Neither has been demonstrated to have a transcription-enhancing property; in fact, activated glucocorticoid responsive element mediates the downregulation of NF-kappaB-activated transcription by interfering with the binding of NF-kappaB p65 to its  cis-element 30 or by directly interfering with transactivation of the NF-kappaB p65 subunit.	bind
28602	8	7281	7	NULL	NULL	0	NULL	statement 6	NULL		is an alternative to	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_10_1585_s_164	11597930	20 Neither has been demonstrated to have a transcription-enhancing property; in fact, activated glucocorticoid responsive element mediates the downregulation of NF-kappaB-activated transcription by interfering with the binding of NF-kappaB p65 to its  cis-element 30 or by directly interfering with transactivation of the NF-kappaB p65 subunit.	bind
23146	1	7282	6	13	NULL	NULL	NULL	SCH 23390	Chemical		bind					serotonin 5-HT2 receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_80_4_1187_s_61	9284070	20 nM mianserin was also included to block binding of SCH 23390 to serotonin 5-HT2 receptors for which SCH 23390 has some affinity and which develop early in the rat.	bind
23147	2	7282	6	13	NULL	NULL	NULL	mianserin	Chemical		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_80_4_1187_s_61	9284070	20 nM mianserin was also included to block binding of SCH 23390 to serotonin 5-HT2 receptors for which SCH 23390 has some affinity and which develop early in the rat.	bind
28603	1	7282	7	NULL	NULL	0	NULL	SCH 23390	NULL		bind	NULL				serotonin 5-HT2 receptors	NULL	rat			NULL		0	NULL	NULL	NULL	gw60_neuroscience_80_4_1187_s_61	9284070	20 nM mianserin was also included to block binding of SCH 23390 to serotonin 5-HT2 receptors for which SCH 23390 has some affinity and which develop early in the rat.	bind
28604	2	7282	7	NULL	NULL	0	NULL	mianserin	NULL		blocks	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_neuroscience_80_4_1187_s_61	9284070	20 nM mianserin was also included to block binding of SCH 23390 to serotonin 5-HT2 receptors for which SCH 23390 has some affinity and which develop early in the rat.	bind
23148	1	7283	6	13	NULL	NULL	NULL	eIF2	GP		bind					met-tRNAmet	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_7_926_s_237	15001529	20 One of the critical steps controlling initiation of protein translation is the binding of eukaryotic translation initiation factor 2 (eIF2) to the activated initiator tRNA (met-tRNAmet) and subsequent formation of a ternary complex that binds to the 40S ribosomal subunit.	bind
23149	2	7283	6	13	NULL	NULL	NULL	eIF2	GP		is					eukaryotic translation initiation factor 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_7_926_s_237	15001529	20 One of the critical steps controlling initiation of protein translation is the binding of eukaryotic translation initiation factor 2 (eIF2) to the activated initiator tRNA (met-tRNAmet) and subsequent formation of a ternary complex that binds to the 40S ribosomal subunit.	bind
23150	3	7283	6	13	NULL	NULL	NULL	met-tRNAmet	NucleicAcid		is					activated initiator tRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_7_926_s_237	15001529	20 One of the critical steps controlling initiation of protein translation is the binding of eukaryotic translation initiation factor 2 (eIF2) to the activated initiator tRNA (met-tRNAmet) and subsequent formation of a ternary complex that binds to the 40S ribosomal subunit.	bind
23151	4	7283	6	13	NULL	NULL	NULL	protein translation	Process	initiation of	is controlled by					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_7_926_s_237	15001529	20 One of the critical steps controlling initiation of protein translation is the binding of eukaryotic translation initiation factor 2 (eIF2) to the activated initiator tRNA (met-tRNAmet) and subsequent formation of a ternary complex that binds to the 40S ribosomal subunit.	bind
23152	5	7283	6	13	NULL	NULL	NULL	ternary complex	GP		bind					40S ribosomal subunit	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_7_926_s_237	15001529	20 One of the critical steps controlling initiation of protein translation is the binding of eukaryotic translation initiation factor 2 (eIF2) to the activated initiator tRNA (met-tRNAmet) and subsequent formation of a ternary complex that binds to the 40S ribosomal subunit.	bind
28606	1	7283	7	NULL	NULL	0	NULL	eIF2	NULL		bind	NULL				met-tRNAmet	NULL	activated			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_7_926_s_237	15001529	20 One of the critical steps controlling initiation of protein translation is the binding of eukaryotic translation initiation factor 2 (eIF2) to the activated initiator tRNA (met-tRNAmet) and subsequent formation of a ternary complex that binds to the 40S ribosomal subunit.	bind
28607	2	7283	7	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				ternary complex	NULL	formation of			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_7_926_s_237	15001529	20 One of the critical steps controlling initiation of protein translation is the binding of eukaryotic translation initiation factor 2 (eIF2) to the activated initiator tRNA (met-tRNAmet) and subsequent formation of a ternary complex that binds to the 40S ribosomal subunit.	bind
28608	3	7283	7	NULL	NULL	0	NULL	ternary complex	NULL		binds to	NULL				40S ribosomal subunit	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_7_926_s_237	15001529	20 One of the critical steps controlling initiation of protein translation is the binding of eukaryotic translation initiation factor 2 (eIF2) to the activated initiator tRNA (met-tRNAmet) and subsequent formation of a ternary complex that binds to the 40S ribosomal subunit.	bind
28609	4	7283	7	NULL	NULL	0	NULL	statement 1	NULL		controls	NULL				protein translation	NULL	initiation of			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_7_926_s_237	15001529	20 One of the critical steps controlling initiation of protein translation is the binding of eukaryotic translation initiation factor 2 (eIF2) to the activated initiator tRNA (met-tRNAmet) and subsequent formation of a ternary complex that binds to the 40S ribosomal subunit.	bind
28610	5	7283	7	NULL	NULL	0	NULL	eIF2	NULL		is	NULL				eukaryotic translation initiation factor 2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_7_926_s_237	15001529	20 One of the critical steps controlling initiation of protein translation is the binding of eukaryotic translation initiation factor 2 (eIF2) to the activated initiator tRNA (met-tRNAmet) and subsequent formation of a ternary complex that binds to the 40S ribosomal subunit.	bind
28611	6	7283	7	NULL	NULL	0	NULL	met-tRNAmet	NULL		is	NULL				initiator tRNA	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_7_926_s_237	15001529	20 One of the critical steps controlling initiation of protein translation is the binding of eukaryotic translation initiation factor 2 (eIF2) to the activated initiator tRNA (met-tRNAmet) and subsequent formation of a ternary complex that binds to the 40S ribosomal subunit.	bind
23153	1	7284	6	13	NULL	NULL	NULL	calmodulin	GP		bind					KCNQ1 protein	GP		\tC terminus calmodulin binding motif		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_8_979_s_19	16645144	20 Potential calmodulin binding motifs are found in the KCNQ1 C terminus: accordingly, both the Pongs-Attali group 12 and the Pitt group 13 postulated that calmodulin would bind to the KCNQ1 protein and modulate current amplitude (perhaps even calcium sensitivity).	bind
23154	2	7284	6	13	NULL	NULL	NULL	statement 1	Process		modulate					current amplitude	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_8_979_s_19	16645144	20 Potential calmodulin binding motifs are found in the KCNQ1 C terminus: accordingly, both the Pongs-Attali group 12 and the Pitt group 13 postulated that calmodulin would bind to the KCNQ1 protein and modulate current amplitude (perhaps even calcium sensitivity).	bind
23155	3	7284	6	13	NULL	NULL	NULL	statement 1	Process		modulate		may			calcium sensitivity	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_8_979_s_19	16645144	20 Potential calmodulin binding motifs are found in the KCNQ1 C terminus: accordingly, both the Pongs-Attali group 12 and the Pitt group 13 postulated that calmodulin would bind to the KCNQ1 protein and modulate current amplitude (perhaps even calcium sensitivity).	bind
28612	1	7284	7	NULL	NULL	0	NULL	 calmodulin 	NULL		bind	NULL				KCNQ1 protein	NULL		C terminus calmodulin binding motif		NULL		0	NULL	NULL	NULL	gw70_circulationres_98_8_979_s_19	16645144	20 Potential calmodulin binding motifs are found in the KCNQ1 C terminus: accordingly, both the Pongs-Attali group 12 and the Pitt group 13 postulated that calmodulin would bind to the KCNQ1 protein and modulate current amplitude (perhaps even calcium sensitivity).	bind
28613	2	7284	7	NULL	NULL	0	NULL	statement 1	NULL		modulate	NULL				current amplitude	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_8_979_s_19	16645144	20 Potential calmodulin binding motifs are found in the KCNQ1 C terminus: accordingly, both the Pongs-Attali group 12 and the Pitt group 13 postulated that calmodulin would bind to the KCNQ1 protein and modulate current amplitude (perhaps even calcium sensitivity).	bind
28614	3	7284	7	10	NULL	0	NULL	statement 1			modulate		may			calcium sensitivity					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_8_979_s_19	16645144	20 Potential calmodulin binding motifs are found in the KCNQ1 C terminus: accordingly, both the Pongs-Attali group 12 and the Pitt group 13 postulated that calmodulin would bind to the KCNQ1 protein and modulate current amplitude (perhaps even calcium sensitivity).	bind
23156	1	7285	6	13	NULL	NULL	NULL	caveolin protein	GP		bind					cholesterol	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_9_1528_s_31	12907462	20 The protein caveolin binds cholesterol and stabilizes caveolae.	bind
23157	2	7285	6	13	NULL	NULL	NULL	statement 1	Process		stabilizes					caveolae	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_9_1528_s_31	12907462	20 The protein caveolin binds cholesterol and stabilizes caveolae.	bind
28615	1	7285	7	NULL	NULL	0	NULL	caveolin	NULL		binds	NULL				cholesterol	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_9_1528_s_31	12907462	20 The protein caveolin binds cholesterol and stabilizes caveolae.	bind
28616	2	7285	7	NULL	NULL	0	NULL	statement 1	NULL		stabilize	NULL				caveolae	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_9_1528_s_31	12907462	20 The protein caveolin binds cholesterol and stabilizes caveolae.	bind
23158	1	7286	6	13	NULL	NULL	NULL	Cx43	GP		bind			terminal 5 amino acids (DDLEI)		ZO-1	GP		second PDZ domain		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_3_317_s_39	11861421	20 Together this work has shown that the terminal 5 amino acids (DDLEI) of Cx43 bind the second PDZ domain of ZO-1 and that this interaction may be regulated by src-tyrosine phosphorylation of Cx43.	bind
23159	2	7286	6	13	NULL	NULL	NULL	src	GP		phosphorylates					Cx43	GP		tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_3_317_s_39	11861421	20 Together this work has shown that the terminal 5 amino acids (DDLEI) of Cx43 bind the second PDZ domain of ZO-1 and that this interaction may be regulated by src-tyrosine phosphorylation of Cx43.	bind
23160	3	7286	6	13	NULL	NULL	NULL	statement 2	Process		regulate		may			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_3_317_s_39	11861421	20 Together this work has shown that the terminal 5 amino acids (DDLEI) of Cx43 bind the second PDZ domain of ZO-1 and that this interaction may be regulated by src-tyrosine phosphorylation of Cx43.	bind
28731	1	7286	7	NULL	NULL	0	NULL	Cx43	NULL		bind	NULL		DDLEI		 ZO-1	NULL		PDZ domain		NULL		0	NULL	NULL	NULL	gw60_circulationres_90_3_317_s_39	11861421	20 Together this work has shown that the terminal 5 amino acids (DDLEI) of Cx43 bind the second PDZ domain of ZO-1 and that this interaction may be regulated by src-tyrosine phosphorylation of Cx43.	bind
28732	2	7286	7	NULL	NULL	0	NULL	src	NULL		phosphorylates	NULL				Cx43	NULL		tyrosine		NULL		0	NULL	NULL	NULL	gw60_circulationres_90_3_317_s_39	11861421	20 Together this work has shown that the terminal 5 amino acids (DDLEI) of Cx43 bind the second PDZ domain of ZO-1 and that this interaction may be regulated by src-tyrosine phosphorylation of Cx43.	bind
28733	3	7286	7	NULL	NULL	0	NULL	statement 2	NULL		regulates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_3_317_s_39	11861421	20 Together this work has shown that the terminal 5 amino acids (DDLEI) of Cx43 bind the second PDZ domain of ZO-1 and that this interaction may be regulated by src-tyrosine phosphorylation of Cx43.	bind
23161	1	7287	6	13	NULL	NULL	NULL	RPTPalpha	GP	phosphorylated	bind			tyrosyl		Grb2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_43_41677_s_187	12923167	20% of RPTPalpha is phosphorylated constitutively on Tyr-789 and, like Shp2, tyrosyl-phosphorylated RPTPalpha binds Grb2 ( ,  ).	bind
23162	2	7287	6	13	NULL	NULL	NULL	Shp2	GP	phosphorylated	bind			tyrosyl		Grb2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_43_41677_s_187	12923167	20% of RPTPalpha is phosphorylated constitutively on Tyr-789 and, like Shp2, tyrosyl-phosphorylated RPTPalpha binds Grb2 ( ,  ).	bind
23163	3	7287	6	13	NULL	NULL	NULL	RPTPalpha	GP		is phosphorylated		constitutively						Tyr-789		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_43_41677_s_187	12923167	20% of RPTPalpha is phosphorylated constitutively on Tyr-789 and, like Shp2, tyrosyl-phosphorylated RPTPalpha binds Grb2 ( ,  ).	bind
28734	1	7287	7	NULL	NULL	0	NULL	RPTPalpha	NULL	phosphorylated	binds	NULL		Tyr-789		Grb2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_43_41677_s_187	12923167	20% of RPTPalpha is phosphorylated constitutively on Tyr-789 and, like Shp2, tyrosyl-phosphorylated RPTPalpha binds Grb2 ( ,  ).	bind
28735	2	7287	7	NULL	NULL	0	NULL	RPTPalpha	NULL		phosphorylated 	NULL	constitutively				NULL		Tyr-789		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_43_41677_s_187	12923167	20% of RPTPalpha is phosphorylated constitutively on Tyr-789 and, like Shp2, tyrosyl-phosphorylated RPTPalpha binds Grb2 ( ,  ).	bind
28736	3	7287	7	NULL	NULL	0	NULL	Shp2	NULL	phosphorylated	binds	NULL		tyrosine		Grb2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_43_41677_s_187	12923167	20% of RPTPalpha is phosphorylated constitutively on Tyr-789 and, like Shp2, tyrosyl-phosphorylated RPTPalpha binds Grb2 ( ,  ).	bind
23164	1	7288	6	13	NULL	NULL	NULL	p300	GP		bind					NF-kappaB	GP		RelA (p65) subunit		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_297_s_138	10880399	20, 21  p300 also binds to the RelA (p65) subunit of NF-kappaB and has been shown to be necessary for NF-kappaB-mediated gene transcription.	bind
23165	2	7288	6	13	NULL	NULL	NULL	NF-kappaB	GP		mediates					gene transcription	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_297_s_138	10880399	20, 21  p300 also binds to the RelA (p65) subunit of NF-kappaB and has been shown to be necessary for NF-kappaB-mediated gene transcription.	bind
23166	3	7288	6	13	NULL	NULL	NULL	p300	GP		is necessary for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_297_s_138	10880399	20, 21  p300 also binds to the RelA (p65) subunit of NF-kappaB and has been shown to be necessary for NF-kappaB-mediated gene transcription.	bind
28737	1	7288	7	NULL	NULL	0	NULL	p300	NULL		binds	NULL				NF-kappaB	NULL		RelA (p65) subunit 		NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_1_297_s_138	10880399	20, 21  p300 also binds to the RelA (p65) subunit of NF-kappaB and has been shown to be necessary for NF-kappaB-mediated gene transcription.	bind
28738	2	7288	7	NULL	NULL	0	NULL	NF-kappaB	NULL		mediates	NULL				gene transcription	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_1_297_s_138	10880399	20, 21  p300 also binds to the RelA (p65) subunit of NF-kappaB and has been shown to be necessary for NF-kappaB-mediated gene transcription.	bind
28739	3	7288	7	NULL	NULL	0	NULL	statement 1	NULL		necessary for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_1_297_s_138	10880399	20, 21  p300 also binds to the RelA (p65) subunit of NF-kappaB and has been shown to be necessary for NF-kappaB-mediated gene transcription.	bind
23167	1	7289	6	13	NULL	NULL	NULL	PDGF-B	GP		bind					HSPG	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_6_512_s_190	16166562	20,107  Binding of PDGF-B to HSPG is most likely needed for localizing secreted PDGF-B in close vicinity to endothelial cells, where it promotes the recognition of PDGFB -  by PDGFR-beta - expressing cells ( Figure 5).	bind
23168	2	7289	6	13	NULL	NULL	NULL	PDGF-B	GP		is localized to					endothelial cells	Cell	close vicinity to			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_6_512_s_190	16166562	20,107  Binding of PDGF-B to HSPG is most likely needed for localizing secreted PDGF-B in close vicinity to endothelial cells, where it promotes the recognition of PDGFB -  by PDGFR-beta - expressing cells ( Figure 5).	bind
23169	3	7289	6	13	NULL	NULL	NULL	statement 1	Process		is needed for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_6_512_s_190	16166562	20,107  Binding of PDGF-B to HSPG is most likely needed for localizing secreted PDGF-B in close vicinity to endothelial cells, where it promotes the recognition of PDGFB -  by PDGFR-beta - expressing cells ( Figure 5).	bind
23170	4	7289	6	13	NULL	NULL	NULL	PDGFR-beta - expressing cells	Cell		recognize					PDGFB	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_6_512_s_190	16166562	20,107  Binding of PDGF-B to HSPG is most likely needed for localizing secreted PDGF-B in close vicinity to endothelial cells, where it promotes the recognition of PDGFB -  by PDGFR-beta - expressing cells ( Figure 5).	bind
23171	5	7289	6	13	NULL	NULL	NULL	PDGF-B	GP		promotes					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_6_512_s_190	16166562	20,107  Binding of PDGF-B to HSPG is most likely needed for localizing secreted PDGF-B in close vicinity to endothelial cells, where it promotes the recognition of PDGFB -  by PDGFR-beta - expressing cells ( Figure 5).	bind
28740	1	7289	7	NULL	NULL	0	NULL	PDGF-B	NULL		bind	NULL				HSPG	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_6_512_s_190	16166562	20,107  Binding of PDGF-B to HSPG is most likely needed for localizing secreted PDGF-B in close vicinity to endothelial cells, where it promotes the recognition of PDGFB -  by PDGFR-beta - expressing cells ( Figure 5).	bind
28741	2	7289	7	NULL	NULL	0	NULL	statement 1	NULL		localize	NULL				PDGF-B	NULL	 secreted 			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_6_512_s_190	16166562	20,107  Binding of PDGF-B to HSPG is most likely needed for localizing secreted PDGF-B in close vicinity to endothelial cells, where it promotes the recognition of PDGFB -  by PDGFR-beta - expressing cells ( Figure 5).	bind
28742	3	7289	7	NULL	NULL	0	NULL	PDGF-B	NULL		is in close vicinity to	NULL				endothelial cells	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_6_512_s_190	16166562	20,107  Binding of PDGF-B to HSPG is most likely needed for localizing secreted PDGF-B in close vicinity to endothelial cells, where it promotes the recognition of PDGFB -  by PDGFR-beta - expressing cells ( Figure 5).	bind
28743	4	7289	7	NULL	NULL	0	NULL	PDGFR-beta - expressing cells	NULL		recognize	NULL				PDGFB	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_6_512_s_190	16166562	20,107  Binding of PDGF-B to HSPG is most likely needed for localizing secreted PDGF-B in close vicinity to endothelial cells, where it promotes the recognition of PDGFB -  by PDGFR-beta - expressing cells ( Figure 5).	bind
28744	5	7289	7	NULL	NULL	0	NULL	statement 3	NULL		promotes	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_6_512_s_190	16166562	20,107  Binding of PDGF-B to HSPG is most likely needed for localizing secreted PDGF-B in close vicinity to endothelial cells, where it promotes the recognition of PDGFB -  by PDGFR-beta - expressing cells ( Figure 5).	bind
23172	1	7290	6	13	NULL	NULL	NULL	glargine	Chemical		has affinity for					IGF-1 receptor	GP				NULL	osteosarcoma cells expressing predominantly IGF-1 receptor	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_325_s_142	14684428	20,21  In osteosarcoma cells expressing predominantly IGF-1 receptors 10 and baby hamster kidney cells overexpressing the human IGF-1 receptor, 10 the affinity of glargine for the IGF-1 receptor is 6- to 8-times higher than that of human insulin, whereas glargine and human insulin bind similarly to cultured human skeletal muscle cells.	bind
23173	2	7290	6	13	NULL	NULL	NULL	glargine	Chemical		has affinity for					IGF-1 receptor	GP				NULL	baby hamster kidney cells overexpressing the human IGF-1 receptor	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_325_s_142	14684428	20,21  In osteosarcoma cells expressing predominantly IGF-1 receptors 10 and baby hamster kidney cells overexpressing the human IGF-1 receptor, 10 the affinity of glargine for the IGF-1 receptor is 6- to 8-times higher than that of human insulin, whereas glargine and human insulin bind similarly to cultured human skeletal muscle cells.	bind
23174	3	7290	6	13	NULL	NULL	NULL	insulin	GP	human	has affinity for					IGF-1 receptor	GP				NULL	osteosarcoma cells expressing predominantly IGF-1 receptor	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_325_s_142	14684428	20,21  In osteosarcoma cells expressing predominantly IGF-1 receptors 10 and baby hamster kidney cells overexpressing the human IGF-1 receptor, 10 the affinity of glargine for the IGF-1 receptor is 6- to 8-times higher than that of human insulin, whereas glargine and human insulin bind similarly to cultured human skeletal muscle cells.	bind
23175	4	7290	6	13	NULL	NULL	NULL	insulin	GP	human	has affinity for					IGF-1 receptor	GP				NULL	baby hamster kidney cells overexpressing the human IGF-1 receptor	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_325_s_142	14684428	20,21  In osteosarcoma cells expressing predominantly IGF-1 receptors 10 and baby hamster kidney cells overexpressing the human IGF-1 receptor, 10 the affinity of glargine for the IGF-1 receptor is 6- to 8-times higher than that of human insulin, whereas glargine and human insulin bind similarly to cultured human skeletal muscle cells.	bind
23176	5	7290	6	13	NULL	NULL	NULL	statement 2	Process	affinity of	is higher than					statement 4	Process	affinity of 			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_325_s_142	14684428	20,21  In osteosarcoma cells expressing predominantly IGF-1 receptors 10 and baby hamster kidney cells overexpressing the human IGF-1 receptor, 10 the affinity of glargine for the IGF-1 receptor is 6- to 8-times higher than that of human insulin, whereas glargine and human insulin bind similarly to cultured human skeletal muscle cells.	bind
23177	6	7290	6	13	NULL	NULL	NULL	glargine	Chemical		bind					IGF-1 receptor	GP				NULL	cultured human skeletal muscle cells	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_325_s_142	14684428	20,21  In osteosarcoma cells expressing predominantly IGF-1 receptors 10 and baby hamster kidney cells overexpressing the human IGF-1 receptor, 10 the affinity of glargine for the IGF-1 receptor is 6- to 8-times higher than that of human insulin, whereas glargine and human insulin bind similarly to cultured human skeletal muscle cells.	bind
46809	7	7290	6	13	NULL	NULL	NULL	statement 1	Process	affinity of	is higher than					statement 3	Process	affinity of 			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_325_s_142	14684428	20,21  In osteosarcoma cells expressing predominantly IGF-1 receptors 10 and baby hamster kidney cells overexpressing the human IGF-1 receptor, 10 the affinity of glargine for the IGF-1 receptor is 6- to 8-times higher than that of human insulin, whereas glargine and human insulin bind similarly to cultured human skeletal muscle cells.	bind
46810	8	7290	6	13	NULL	NULL	NULL	insulin	GP	human	bind					IGF-1 receptor	GP				NULL	cultured human skeletal muscle cells	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_325_s_142	14684428	20,21  In osteosarcoma cells expressing predominantly IGF-1 receptors 10 and baby hamster kidney cells overexpressing the human IGF-1 receptor, 10 the affinity of glargine for the IGF-1 receptor is 6- to 8-times higher than that of human insulin, whereas glargine and human insulin bind similarly to cultured human skeletal muscle cells.	bind
46811	9	7290	6	13	NULL	NULL	NULL	statement 6	Process	affinity of	is similar to					statement 8	Process	affinity of 			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_325_s_142	14684428	20,21  In osteosarcoma cells expressing predominantly IGF-1 receptors 10 and baby hamster kidney cells overexpressing the human IGF-1 receptor, 10 the affinity of glargine for the IGF-1 receptor is 6- to 8-times higher than that of human insulin, whereas glargine and human insulin bind similarly to cultured human skeletal muscle cells.	bind
28745	1	7290	7	NULL	NULL	0	NULL	glargine	NULL		has affinity for	NULL				IGF-1 receptor	NULL				NULL	osteosarcoma cells expressing predominantly IGF-1 receptor	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_325_s_142	14684428	20,21  In osteosarcoma cells expressing predominantly IGF-1 receptors 10 and baby hamster kidney cells overexpressing the human IGF-1 receptor, 10 the affinity of glargine for the IGF-1 receptor is 6- to 8-times higher than that of human insulin, whereas glargine and human insulin bind similarly to cultured human skeletal muscle cells.	bind
28746	2	7290	7	NULL	NULL	0	NULL	glargine	NULL		has affinity for	NULL				IGF-1 receptor	NULL				NULL	baby hamster kidney cells overexpressing the human IGF-1 receptor	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_325_s_142	14684428	20,21  In osteosarcoma cells expressing predominantly IGF-1 receptors 10 and baby hamster kidney cells overexpressing the human IGF-1 receptor, 10 the affinity of glargine for the IGF-1 receptor is 6- to 8-times higher than that of human insulin, whereas glargine and human insulin bind similarly to cultured human skeletal muscle cells.	bind
28747	3	7290	7	NULL	NULL	0	NULL	insulin	NULL	human	has affinity for	NULL				IGF-1 receptor	NULL				NULL	osteosarcoma cells expressing predominantly IGF-1 receptor	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_325_s_142	14684428	20,21  In osteosarcoma cells expressing predominantly IGF-1 receptors 10 and baby hamster kidney cells overexpressing the human IGF-1 receptor, 10 the affinity of glargine for the IGF-1 receptor is 6- to 8-times higher than that of human insulin, whereas glargine and human insulin bind similarly to cultured human skeletal muscle cells.	bind
28748	4	7290	7	NULL	NULL	0	NULL	insulin	NULL	human	has affinity for	NULL				IGF-1 receptor	NULL				NULL	baby hamster kidney cells overexpressing the human IGF-1 receptor	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_325_s_142	14684428	20,21  In osteosarcoma cells expressing predominantly IGF-1 receptors 10 and baby hamster kidney cells overexpressing the human IGF-1 receptor, 10 the affinity of glargine for the IGF-1 receptor is 6- to 8-times higher than that of human insulin, whereas glargine and human insulin bind similarly to cultured human skeletal muscle cells.	bind
28749	5	7290	7	NULL	NULL	0	NULL	statement 1	NULL	affinity of	is higher than	NULL				statement 3	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_325_s_142	14684428	20,21  In osteosarcoma cells expressing predominantly IGF-1 receptors 10 and baby hamster kidney cells overexpressing the human IGF-1 receptor, 10 the affinity of glargine for the IGF-1 receptor is 6- to 8-times higher than that of human insulin, whereas glargine and human insulin bind similarly to cultured human skeletal muscle cells.	bind
28750	6	7290	7	NULL	NULL	0	NULL	statement 2	NULL	affinity of	is higher than	NULL				statement 4	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_325_s_142	14684428	20,21  In osteosarcoma cells expressing predominantly IGF-1 receptors 10 and baby hamster kidney cells overexpressing the human IGF-1 receptor, 10 the affinity of glargine for the IGF-1 receptor is 6- to 8-times higher than that of human insulin, whereas glargine and human insulin bind similarly to cultured human skeletal muscle cells.	bind
28751	7	7290	7	NULL	NULL	0	NULL	glargine	NULL		bind	NULL				IGF-1 receptor	NULL				NULL	cultured human skeletal muscle cells	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_325_s_142	14684428	20,21  In osteosarcoma cells expressing predominantly IGF-1 receptors 10 and baby hamster kidney cells overexpressing the human IGF-1 receptor, 10 the affinity of glargine for the IGF-1 receptor is 6- to 8-times higher than that of human insulin, whereas glargine and human insulin bind similarly to cultured human skeletal muscle cells.	bind
28752	8	7290	7	NULL	NULL	0	NULL	insulin	NULL	human	bind	NULL				IGF-1 receptor	NULL				NULL	cultured human skeletal muscle cells	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_325_s_142	14684428	20,21  In osteosarcoma cells expressing predominantly IGF-1 receptors 10 and baby hamster kidney cells overexpressing the human IGF-1 receptor, 10 the affinity of glargine for the IGF-1 receptor is 6- to 8-times higher than that of human insulin, whereas glargine and human insulin bind similarly to cultured human skeletal muscle cells.	bind
28753	9	7290	7	NULL	NULL	0	NULL	statement 7	NULL		is similar to	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_325_s_142	14684428	20,21  In osteosarcoma cells expressing predominantly IGF-1 receptors 10 and baby hamster kidney cells overexpressing the human IGF-1 receptor, 10 the affinity of glargine for the IGF-1 receptor is 6- to 8-times higher than that of human insulin, whereas glargine and human insulin bind similarly to cultured human skeletal muscle cells.	bind
23178	1	7293	6	13	NULL	NULL	NULL	DRIP Coactivator Complex	GP		bind					vitamin D3 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_2_507_s_672	9430642	20-Epi Analogues of 1,25-Dihydroxyvitamin D3 Are Highly Potent Inducers of DRIP Coactivator Complex Binding to the Vitamin D3 Receptor.	bind
23179	2	7293	6	13	NULL	NULL	NULL	Epi Analogues of 1,25-Dihydroxyvitamin D3	Chemical		induces		highly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_2_507_s_672	9430642	20-Epi Analogues of 1,25-Dihydroxyvitamin D3 Are Highly Potent Inducers of DRIP Coactivator Complex Binding to the Vitamin D3 Receptor.	bind
28754	1	7293	7	NULL	NULL	0	NULL	DRIP Coactivator Complex	NULL		bind	NULL				Vitamin D3 Receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_17_2_507_s_672	9430642	20-Epi Analogues of 1,25-Dihydroxyvitamin D3 Are Highly Potent Inducers of DRIP Coactivator Complex Binding to the Vitamin D3 Receptor.	bind
28755	2	7293	7	10	NULL	0	NULL	Epi Analogues of 1,25-Dihydroxyvitamin D3	NULL		inducers  of	NULL	highly potent			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_2_507_s_672	9430642	20-Epi Analogues of 1,25-Dihydroxyvitamin D3 Are Highly Potent Inducers of DRIP Coactivator Complex Binding to the Vitamin D3 Receptor.	bind
23180	1	7296	6	13	NULL	NULL	NULL	CCh	Chemical		bind					M2 mAChR	GP				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_312_1_382_s_184	15333678	200-fold reciprocal reduction in ligand affinity when both CCh and gallamine bound to the M2 mAChR at the same time.	bind
23181	2	7296	6	13	NULL	NULL	NULL	gallamine	Chemical		bind					M2 mAChR	GP				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_312_1_382_s_184	15333678	200-fold reciprocal reduction in ligand affinity when both CCh and gallamine bound to the M2 mAChR at the same time.	bind
23182	3	7296	6	13	NULL	NULL	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_312_1_382_s_184	15333678	200-fold reciprocal reduction in ligand affinity when both CCh and gallamine bound to the M2 mAChR at the same time.	bind
28756	1	7296	7	NULL	NULL	0	NULL	CCh	NULL		bind	NULL				M2 mAChR	NULL				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_312_1_382_s_184	15333678	200-fold reciprocal reduction in ligand affinity when both CCh and gallamine bound to the M2 mAChR at the same time.	bind
28757	2	7296	7	NULL	NULL	0	NULL	gallamine	NULL		bind	NULL				M2 mAChR	NULL				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_312_1_382_s_184	15333678	200-fold reciprocal reduction in ligand affinity when both CCh and gallamine bound to the M2 mAChR at the same time.	bind
28758	3	7296	7	NULL	NULL	0	NULL	statement 1	NULL		occurs simultaneous with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_312_1_382_s_184	15333678	200-fold reciprocal reduction in ligand affinity when both CCh and gallamine bound to the M2 mAChR at the same time.	bind
23183	1	7299	6	13	NULL	NULL	NULL	Mac-2 antigen	Chemical		is					lectin	GP	galactoside specific			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3595_s_319	11522829	21       Cherayil,B.J., Weiner,S.J. and Pillai,S. (1989) The Mac-2 antigen is a galactoside specific lectin that binds IgE.	bind
23184	2	7299	6	13	NULL	NULL	NULL	Mac-2 antigen	Chemical		bind					IgE	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3595_s_319	11522829	21       Cherayil,B.J., Weiner,S.J. and Pillai,S. (1989) The Mac-2 antigen is a galactoside specific lectin that binds IgE.	bind
28759	1	7299	7	NULL	NULL	0	NULL	Mac-2 antigen	NULL		binds	NULL				IgE	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3595_s_319	11522829	21       Cherayil,B.J., Weiner,S.J. and Pillai,S. (1989) The Mac-2 antigen is a galactoside specific lectin that binds IgE.	bind
28760	2	7299	7	NULL	NULL	0	NULL	Mac-2 antigen	NULL		is a type of	NULL				galactoside specific lectin	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3595_s_319	11522829	21       Cherayil,B.J., Weiner,S.J. and Pillai,S. (1989) The Mac-2 antigen is a galactoside specific lectin that binds IgE.	bind
23185	1	7300	6	13	NULL	NULL	NULL	tRNALys molecule	NucleicAcid		plays a role in					reverse transcription	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2757_s_315	11433020	21       Das,A.T., Klaver,B. and Berkhout,B. (1997) Sequence variation of the HIV primer binding site suggests the use of an alternative tRNALys molecule in reverse transcription.	bind
23186	2	7300	6	13	NULL	NULL	NULL	HIV 	NucleicAcid	sequence variation of 	suggests				primer binding site	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2757_s_315	11433020	21       Das,A.T., Klaver,B. and Berkhout,B. (1997) Sequence variation of the HIV primer binding site suggests the use of an alternative tRNALys molecule in reverse transcription.	bind
28761	1	7300	7	NULL	NULL	0	NULL	tRNALys molecule	NULL		is involved in	NULL				reverse transcription	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2757_s_315	11433020	21       Das,A.T., Klaver,B. and Berkhout,B. (1997) Sequence variation of the HIV primer binding site suggests the use of an alternative tRNALys molecule in reverse transcription.	bind
54469	2	7300	7	10	NULL	0	NULL	HIV		sequence variation of 	suggest				primer binding site	statement 1					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2757_s_315	11433020	21       Das,A.T., Klaver,B. and Berkhout,B. (1997) Sequence variation of the HIV primer binding site suggests the use of an alternative tRNALys molecule in reverse transcription.	bind
26420	1	7302	5	13	NULL	NULL	NULL	spermine	Chemical		bind					B-DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_5121_s_285	11812845	21       Tari,L.W. and Secco,A.S. (1995) Base-pair opening and spermine binding B-DNA features displayed in the crystal structure of a gal operon fragment: implications for protein-DNA recognition.	bind
28762	1	7302	7	NULL	NULL	0	NULL	spermine	NULL		bind	NULL				B-DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_5121_s_285	11812845	21       Tari,L.W. and Secco,A.S. (1995) Base-pair opening and spermine binding B-DNA features displayed in the crystal structure of a gal operon fragment: implications for protein-DNA recognition.	bind
26421	1	7303	5	13	NULL	NULL	NULL	GP Ib/VIX	GP		bind					vWF	GP		A1 domain		NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_4_437_s_50	10421606	21  GP Ib/VIX binding to the A1 domain is facilitated when vWF becomes activated either by its binding to collagen on vessel walls or by conditions of high shear.	bind
26422	2	7303	5	13	NULL	NULL	NULL	vWF	GP		bind					collagen	GP				NULL	on vessel walls	NULL	NULL	NULL	NULL	gw60_circulation_100_4_437_s_50	10421606	21  GP Ib/VIX binding to the A1 domain is facilitated when vWF becomes activated either by its binding to collagen on vessel walls or by conditions of high shear.	bind
26423	3	7303	5	13	NULL	NULL	NULL	statement 2	Process		activates					vWF	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_4_437_s_50	10421606	21  GP Ib/VIX binding to the A1 domain is facilitated when vWF becomes activated either by its binding to collagen on vessel walls or by conditions of high shear.	bind
26424	4	7303	5	13	NULL	NULL	NULL	shear		high	activates					vWF	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_4_437_s_50	10421606	21  GP Ib/VIX binding to the A1 domain is facilitated when vWF becomes activated either by its binding to collagen on vessel walls or by conditions of high shear.	bind
26425	5	7303	5	13	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_4_437_s_50	10421606	21  GP Ib/VIX binding to the A1 domain is facilitated when vWF becomes activated either by its binding to collagen on vessel walls or by conditions of high shear.	bind
26426	6	7303	5	13	NULL	NULL	NULL	statement 3	Process		facilitates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_4_437_s_50	10421606	21  GP Ib/VIX binding to the A1 domain is facilitated when vWF becomes activated either by its binding to collagen on vessel walls or by conditions of high shear.	bind
26427	7	7303	5	13	NULL	NULL	NULL	statement 4	Process		facilitates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_4_437_s_50	10421606	21  GP Ib/VIX binding to the A1 domain is facilitated when vWF becomes activated either by its binding to collagen on vessel walls or by conditions of high shear.	bind
28763	1	7303	7	10	NULL	0	NULL	GP Ib/VIX			binds to					vWF			A1 domain		NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_4_437_s_50	10421606	21  GP Ib/VIX binding to the A1 domain is facilitated when vWF becomes activated either by its binding to collagen on vessel walls or by conditions of high shear.	bind
28764	2	7303	7	NULL	NULL	0	NULL	vWF	NULL		bind	NULL				collagen	NULL				NULL	vessel walls	0	NULL	NULL	NULL	gw60_circulation_100_4_437_s_50	10421606	21  GP Ib/VIX binding to the A1 domain is facilitated when vWF becomes activated either by its binding to collagen on vessel walls or by conditions of high shear.	bind
28765	3	7303	7	NULL	NULL	0	NULL	statement 2	NULL		activates	NULL				vWF	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_4_437_s_50	10421606	21  GP Ib/VIX binding to the A1 domain is facilitated when vWF becomes activated either by its binding to collagen on vessel walls or by conditions of high shear.	bind
28766	4	7303	7	10	NULL	0	NULL	shear		high	activates					vWF					NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_4_437_s_50	10421606	21  GP Ib/VIX binding to the A1 domain is facilitated when vWF becomes activated either by its binding to collagen on vessel walls or by conditions of high shear.	bind
28767	5	7303	7	NULL	NULL	0	NULL	statement 3	NULL		facilitates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_4_437_s_50	10421606	21  GP Ib/VIX binding to the A1 domain is facilitated when vWF becomes activated either by its binding to collagen on vessel walls or by conditions of high shear.	bind
28768	6	7303	7	NULL	NULL	0	NULL	statement 4	NULL		facilitates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_4_437_s_50	10421606	21  GP Ib/VIX binding to the A1 domain is facilitated when vWF becomes activated either by its binding to collagen on vessel walls or by conditions of high shear.	bind
54470	7	7303	7	10	NULL	0	NULL	statement 3			is an alternative to					statement 4					NULL		0	NULL	NULL	NULL	gw60_circulation_100_4_437_s_50	10421606	21  GP Ib/VIX binding to the A1 domain is facilitated when vWF becomes activated either by its binding to collagen on vessel walls or by conditions of high shear.	bind
26428	1	7305	5	13	NULL	NULL	NULL	WGA	GP		bind					endothelial cells	Cell	luminal surface of			NULL	in arterioles	NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
26429	2	7305	5	13	NULL	NULL	NULL	WGA	GP		bind					endothelial cells	Cell	luminal surface of			NULL	in capillaries	NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
26430	3	7305	5	13	NULL	NULL	NULL	statement 1	Process		occurs in					tracheal vessels	OrganismPart				NULL	in pathogen-free C3H mice	NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
26431	4	7305	5	13	NULL	NULL	NULL	statement 1	Process		occurs in					tracheal vessels	OrganismPart				NULL	in pathogen-free C57BL/6 mice	NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
26432	5	7305	5	13	NULL	NULL	NULL	statement 2	Process		occurs in					tracheal vessels	OrganismPart				NULL	in pathogen-free C3H mice	NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
26433	6	7305	5	13	NULL	NULL	NULL	statement 2	Process		occurs in					tracheal vessels	OrganismPart				NULL	in pathogen-free C57BL/6 mice	NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
26434	7	7305	5	13	NULL	NULL	NULL	WGA	GP		bind		weakly			endothelial cells	Cell	luminal surface of			NULL	in venules	NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
26435	8	7305	5	13	NULL	NULL	NULL	statement 7	Process		occurs in					tracheal vessels	OrganismPart				NULL	in pathogen-free C3H mice	NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
26436	9	7305	5	13	NULL	NULL	NULL	statement 7	Process		occurs in					tracheal vessels	OrganismPart				NULL	in pathogen-free C57BL/6 mice	NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
28769	1	7305	7	NULL	NULL	0	NULL	WGA			bind					endothelial cells 		luminal surface of 			NULL	arterioles	NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
28770	2	7305	7	NULL	NULL	0	NULL	WGA			bind					endothelial cells 		luminal surface of 			NULL	capillaries	NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
28771	3	7305	7	NULL	NULL	0	NULL	WGA			bind		weakly			endothelial cells		luminal surface of 			NULL	venules	NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
28772	4	7305	7	NULL	NULL	0	NULL	WGA			does not bind					endothelial cells		luminal surface of			NULL	venules	NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
28773	5	7305	7	NULL	NULL	0	NULL	statement 1			occur in					 pathogen-free C3H mice		tracheal vessels of 			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
28774	6	7305	7	NULL	NULL	0	NULL	statement 1			occur in					  C57BL/6 mice		tracheal vessels of 			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
28775	7	7305	7	NULL	NULL	0	NULL	statement 2			occur in					pathogen-free C3H mice		tracheal vessels of 			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
28776	8	7305	7	NULL	NULL	0	NULL	statement 2			occur in					C57BL/6 mice		tracheal vessels of 			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
54671	9	7305	7	NULL	NULL	0	NULL	statement 3			occur in					pathogen-free C3H mice		tracheal vessels of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
54672	10	7305	7	NULL	NULL	0	NULL	statement 3			occur in					C57BL/6 mice		tracheal vessels of 			NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
54673	11	7305	7	NULL	NULL	0	NULL	statement 4			occur in					pathogen-free C3H mice		tracheal vessels of 			NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
54674	12	7305	7	NULL	NULL	0	NULL	statement 4			occur in					C57BL/6 mice		tracheal vessels of 			NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
54675	13	7305	7	NULL	NULL	0	NULL	statement 3			is an alternative to					statement 4					NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_4_1099_s_215	9777941	21  In tracheal vessels of pathogen-free C3H and C57BL/6 mice, WGA bound to the luminal surface of endothelial cells in arterioles and capillaries but bound weakly or not at all in venules (Figure 8A)   .	bind
26437	1	7306	5	13	NULL	NULL	NULL	VCAM-1 immunoglobulin	GP		bind					peripheral T cells	Cell	resting 			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_723_s_237	9598830	21  Jakubowski et al 39  reported that there was little binding of VCAM-1 immunoglobulin to resting peripheral T cells even at a concentration of 100 mug/mL, whereas VCAM-1 immunoglobulin at a concentration as low as 0.03 mug/mL bound to T cells stimulated with MnCl2.	bind
26438	2	7306	5	13	NULL	NULL	NULL	T cells	Cell		is stimulated with					MnCl2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_723_s_237	9598830	21  Jakubowski et al 39  reported that there was little binding of VCAM-1 immunoglobulin to resting peripheral T cells even at a concentration of 100 mug/mL, whereas VCAM-1 immunoglobulin at a concentration as low as 0.03 mug/mL bound to T cells stimulated with MnCl2.	bind
26439	3	7306	5	13	NULL	NULL	NULL	VCAM-1 immunoglobulin	GP		bind					statement 2	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_723_s_237	9598830	21  Jakubowski et al 39  reported that there was little binding of VCAM-1 immunoglobulin to resting peripheral T cells even at a concentration of 100 mug/mL, whereas VCAM-1 immunoglobulin at a concentration as low as 0.03 mug/mL bound to T cells stimulated with MnCl2.	bind
28777	1	7306	7	NULL	NULL	0	NULL	VCAM-1 immunoglobulin	NULL		bind	NULL	less			peripheral T cells	NULL	resting			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_723_s_237	9598830	21  Jakubowski et al 39  reported that there was little binding of VCAM-1 immunoglobulin to resting peripheral T cells even at a concentration of 100 mug/mL, whereas VCAM-1 immunoglobulin at a concentration as low as 0.03 mug/mL bound to T cells stimulated with MnCl2.	bind
28778	2	7306	7	NULL	NULL	0	NULL	Mncl2	NULL		stimulates	NULL				T cells	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_723_s_237	9598830	21  Jakubowski et al 39  reported that there was little binding of VCAM-1 immunoglobulin to resting peripheral T cells even at a concentration of 100 mug/mL, whereas VCAM-1 immunoglobulin at a concentration as low as 0.03 mug/mL bound to T cells stimulated with MnCl2.	bind
28779	3	7306	7	NULL	NULL	0	NULL	VCAM-1 immunoglobulin	NULL		bind	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_723_s_237	9598830	21  Jakubowski et al 39  reported that there was little binding of VCAM-1 immunoglobulin to resting peripheral T cells even at a concentration of 100 mug/mL, whereas VCAM-1 immunoglobulin at a concentration as low as 0.03 mug/mL bound to T cells stimulated with MnCl2.	bind
28993	1	7307	5	13	NULL	NULL	NULL	ASA	Chemical		blocks					cyclooxygenase	GP	platelet			NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
28994	2	7307	5	13	NULL	NULL	NULL	ASA	Chemical		blocks					thromboxane A2	Chemical	production of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
28995	3	7307	5	13	NULL	NULL	NULL	statement 1	Process		does not inhibit					cytosolic Ca2+	Chemical	mobilization of 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
28996	4	7307	5	13	NULL	NULL	NULL	statement 2	Process		does not inhibit					cytosolic Ca2+	Chemical	mobilization of 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
28997	5	7307	5	13	NULL	NULL	NULL	shear stress			induce					aggregation	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
28998	6	7307	5	13	NULL	NULL	NULL	statement 1	Process		does not inhibit					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
28999	7	7307	5	13	NULL	NULL	NULL	statement 2	Process		does not inhibit					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
29000	8	7307	5	13	NULL	NULL	NULL	vWF	GP	plasma	bind					GPIb	GP	platelet			NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
29001	9	7307	5	13	NULL	NULL	NULL	shear stress		high levels of	induces		may			statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
29002	10	7307	5	13	NULL	NULL	NULL	shear stress		high levels of	increases					cytosolic Ca2+	Chemical	platelet			NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
29003	11	7307	5	13	NULL	NULL	NULL	shear stress		high levels of	increases					platelets	Cell	aggregation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
29004	12	7307	5	13	NULL	NULL	NULL	vWF	GP		bind					GPIIb-IIIa complex	GP	platelet			NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
29005	13	7307	5	13	NULL	NULL	NULL	statement 12	Process		potentiate					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
29006	14	7307	5	13	NULL	NULL	NULL	statement 12	Process		potentiate					statement 11	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
28780	1	7307	7	10	NULL	0	NULL	ASA			blocks					cyclooxygenase		production of;;platelet			NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
28781	2	7307	7	NULL	NULL	0	NULL	ASA	NULL		blocks	NULL				thromboxane A2	NULL	production of			NULL		0	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
28782	3	7307	7	10	NULL	0	NULL	statement 1	NULL		does not inhibit	NULL				cytosolic Ca2+	NULL	mobilization of 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
28783	4	7307	7	10	NULL	0	NULL	statement 2	NULL		does not inhibit	NULL				cytosolic Ca2+	NULL	mobilization of 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
28784	5	7307	7	10	NULL	0	NULL	statement 1			does not inhibit					statement 14					NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
28785	6	7307	7	10	NULL	0	NULL	statement 2			does not inhibit					statement 14					NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
28786	7	7307	7	NULL	NULL	0	NULL	vWF	NULL	plasma	bind	NULL				GPIb	NULL	platelet			NULL		0	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
28787	8	7307	7	NULL	NULL	0	NULL	shear stress	NULL	high levels of	induce	NULL	may			statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
28788	9	7307	7	10	NULL	0	NULL	shear stress	NULL	high levels of	increase	NULL				cytosolic Ca2+	NULL	platelet 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
28789	10	7307	7	NULL	NULL	0	NULL	shear stress	NULL	high levels of	increase	NULL				platelet aggregation	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
28790	11	7307	7	NULL	NULL	0	NULL	vWF	NULL		bind	NULL				GPIIb-IIIa complex	NULL	platelet			NULL		0	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
28791	12	7307	7	NULL	NULL	0	NULL	statement 11	NULL		potentiates	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
28792	13	7307	7	NULL	NULL	0	NULL	statement 11	NULL		potentiates	NULL				statement 10	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
54471	14	7307	7	10	NULL	0	NULL	shear stress			induce					aggregation					NULL		0	NULL	NULL	NULL	gw60_circulation_93_6_1201_s_129	8653842	21  The aggregation response to shear forces generated in a cone and plate viscometer showed that neither the mobilization of cytosolic Ca2+ nor the aggregation response to shear stress was inhibited by blocking the platelet cyclooxygenase and thromboxane A2 production with ASA. 22  These results suggest that the high levels of shear stress (>30 dyne/cm2) may have induced plasma vWF to bind to platelet GPIb and caused an increase in platelet cytosolic Ca2+ and platelet aggregation, both of which are potentiated by the vWF binding to the platelet GPIIb-IIIa complex.	bind
26440	1	7308	5	13	NULL	NULL	NULL	factor VIIa	GP		bind					TF	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_409_s_259	9081698	21  The second is the inhibition of factor Xa - catalyzed back activation to VIIa of factor VII molecules bound to TF.	bind
26441	2	7308	5	13	NULL	NULL	NULL	factor Xa	GP	inhibition of	catalyzes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_409_s_259	9081698	21  The second is the inhibition of factor Xa - catalyzed back activation to VIIa of factor VII molecules bound to TF.	bind
28793	1	7308	7	NULL	NULL	0	NULL	factor VIIa	NULL		bind	NULL				TF	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_409_s_259	9081698	21  The second is the inhibition of factor Xa - catalyzed back activation to VIIa of factor VII molecules bound to TF.	bind
28794	2	7308	7	10	NULL	0	NULL	factor Xa	NULL	inhibition of	catalyzes	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_409_s_259	9081698	21  The second is the inhibition of factor Xa - catalyzed back activation to VIIa of factor VII molecules bound to TF.	bind
28795	3	7308	7	NULL	NULL	0	NULL	factor VIIa	NULL		is a type of	NULL				factor VII	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_409_s_259	9081698	21  The second is the inhibition of factor Xa - catalyzed back activation to VIIa of factor VII molecules bound to TF.	bind
26442	1	7309	5	13	NULL	NULL	NULL	ECM	CellComponent		bind					TIMP-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_3_296_s_176	10645926	21  Under these circumstances, ECM binding of TIMP-3 may become saturated by overexpression, resulting in the generation of local levels of a soluble form of TIMP-3.	bind
26443	2	7309	5	13	NULL	NULL	NULL	TIMP-3	GP	overexpression of	saturates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_3_296_s_176	10645926	21  Under these circumstances, ECM binding of TIMP-3 may become saturated by overexpression, resulting in the generation of local levels of a soluble form of TIMP-3.	bind
26444	3	7309	5	13	NULL	NULL	NULL	statement 2	Process		generates					TIMP-3	GP	soluble forms of 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_3_296_s_176	10645926	21  Under these circumstances, ECM binding of TIMP-3 may become saturated by overexpression, resulting in the generation of local levels of a soluble form of TIMP-3.	bind
28796	1	7309	7	13	NULL	NULL	NULL	ECM	CellComponent		bind					TIMP-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_3_296_s_176	10645926	21  Under these circumstances, ECM binding of TIMP-3 may become saturated by overexpression, resulting in the generation of local levels of a soluble form of TIMP-3.	bind
28797	3	7309	7	10	NULL	0	NULL	statement 2	NULL		generates	NULL				TIMP-3	NULL	soluble form of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_3_296_s_176	10645926	21  Under these circumstances, ECM binding of TIMP-3 may become saturated by overexpression, resulting in the generation of local levels of a soluble form of TIMP-3.	bind
46546	2	7309	7	10	NULL	0	NULL	TIMP-3	NULL	overexpression of	saturates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_101_3_296_s_176	10645926	21  Under these circumstances, ECM binding of TIMP-3 may become saturated by overexpression, resulting in the generation of local levels of a soluble form of TIMP-3.	bind
26445	1	7310	5	13	NULL	NULL	NULL	mAb anti-C3-9	GP		is a type of					capture antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3542_s_82	9396453	21 - 23 Briefly, C3b/c was measured with mAb anti-C3-9 as capture antibody, which binds to C3b, iC3b, C3c, as well as iC3 (C3b-like C3).	bind
26446	2	7310	5	13	NULL	NULL	NULL	mAb anti-C3-9	GP		bind					C3b	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3542_s_82	9396453	21 - 23 Briefly, C3b/c was measured with mAb anti-C3-9 as capture antibody, which binds to C3b, iC3b, C3c, as well as iC3 (C3b-like C3).	bind
26447	3	7310	5	13	NULL	NULL	NULL	mAb anti-C3-9	GP		bind					iC3b	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3542_s_82	9396453	21 - 23 Briefly, C3b/c was measured with mAb anti-C3-9 as capture antibody, which binds to C3b, iC3b, C3c, as well as iC3 (C3b-like C3).	bind
26448	4	7310	5	13	NULL	NULL	NULL	mAb anti-C3-9	GP		bind					C3c	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3542_s_82	9396453	21 - 23 Briefly, C3b/c was measured with mAb anti-C3-9 as capture antibody, which binds to C3b, iC3b, C3c, as well as iC3 (C3b-like C3).	bind
26449	5	7310	5	13	NULL	NULL	NULL	mAb anti-C3-9	GP		bind					iC3	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3542_s_82	9396453	21 - 23 Briefly, C3b/c was measured with mAb anti-C3-9 as capture antibody, which binds to C3b, iC3b, C3c, as well as iC3 (C3b-like C3).	bind
26450	6	7310	5	13	NULL	NULL	NULL	iC3	GP		is					C3b-like C3	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3542_s_82	9396453	21 - 23 Briefly, C3b/c was measured with mAb anti-C3-9 as capture antibody, which binds to C3b, iC3b, C3c, as well as iC3 (C3b-like C3).	bind
28798	1	7310	7	10	NULL	0	NULL	 mAb anti-C3-9			binds to					C3b					NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3542_s_82	9396453	21 - 23 Briefly, C3b/c was measured with mAb anti-C3-9 as capture antibody, which binds to C3b, iC3b, C3c, as well as iC3 (C3b-like C3).	bind
28799	2	7310	7	10	NULL	0	NULL	 mAb anti-C3-9			bind					iC3b					NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3542_s_82	9396453	21 - 23 Briefly, C3b/c was measured with mAb anti-C3-9 as capture antibody, which binds to C3b, iC3b, C3c, as well as iC3 (C3b-like C3).	bind
28800	3	7310	7	10	NULL	0	NULL	mAb anti-C3-9			bind					C3c					NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3542_s_82	9396453	21 - 23 Briefly, C3b/c was measured with mAb anti-C3-9 as capture antibody, which binds to C3b, iC3b, C3c, as well as iC3 (C3b-like C3).	bind
28801	4	7310	7	10	NULL	0	NULL	mAb anti-C3-9			bind					iC3					NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3542_s_82	9396453	21 - 23 Briefly, C3b/c was measured with mAb anti-C3-9 as capture antibody, which binds to C3b, iC3b, C3c, as well as iC3 (C3b-like C3).	bind
28802	5	7310	7	10	NULL	0	NULL	iC3			is					C3b-like C3					NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3542_s_82	9396453	21 - 23 Briefly, C3b/c was measured with mAb anti-C3-9 as capture antibody, which binds to C3b, iC3b, C3c, as well as iC3 (C3b-like C3).	bind
54792	6	7310	7	10	NULL	0	NULL	mAb anti-C3-9			is a type of					capture antibody					NULL		0	NULL	NULL	NULL	gw60_circulation_96_10_3542_s_82	9396453	21 - 23 Briefly, C3b/c was measured with mAb anti-C3-9 as capture antibody, which binds to C3b, iC3b, C3c, as well as iC3 (C3b-like C3).	bind
26451	1	7311	5	13	NULL	NULL	NULL	ATF2 homodimer	GP		recognizes;;binds							specific		ATF/CRE motifs	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_42	16497991	21 Although ATF2 recognizes and binds specific ATF/CRE motifs as a homo- or heterodimer in the same fashion as CREB, the differential role of ATF2 and CREB remains largely uncharacterized.	bind
26453	2	7311	5	13	NULL	NULL	NULL	ATF2 heterodimer	GP		recognizes;;binds							specific		ATF/CRE motifs	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_42	16497991	21 Although ATF2 recognizes and binds specific ATF/CRE motifs as a homo- or heterodimer in the same fashion as CREB, the differential role of ATF2 and CREB remains largely uncharacterized.	bind
26455	3	7311	5	13	NULL	NULL	NULL	CREB homodimer	GP		recognizes;;binds							specific		ATF/CRE motifs	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_42	16497991	21 Although ATF2 recognizes and binds specific ATF/CRE motifs as a homo- or heterodimer in the same fashion as CREB, the differential role of ATF2 and CREB remains largely uncharacterized.	bind
26457	4	7311	5	13	NULL	NULL	NULL	CREB heterodimer	GP		recognizes;;binds							specific		ATF/CRE motifs	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_42	16497991	21 Although ATF2 recognizes and binds specific ATF/CRE motifs as a homo- or heterodimer in the same fashion as CREB, the differential role of ATF2 and CREB remains largely uncharacterized.	bind
26458	5	7311	5	13	NULL	NULL	NULL	statement 3	Process		same manner as					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_42	16497991	21 Although ATF2 recognizes and binds specific ATF/CRE motifs as a homo- or heterodimer in the same fashion as CREB, the differential role of ATF2 and CREB remains largely uncharacterized.	bind
26459	6	7311	5	13	NULL	NULL	NULL	statement 4	Process		same manner as					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_42	16497991	21 Although ATF2 recognizes and binds specific ATF/CRE motifs as a homo- or heterodimer in the same fashion as CREB, the differential role of ATF2 and CREB remains largely uncharacterized.	bind
28803	1	7311	7	NULL	NULL	0	NULL	ATF2 homodimer	NULL		recognizes	NULL					NULL			ATF/CRE motifs 	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_42	16497991	21 Although ATF2 recognizes and binds specific ATF/CRE motifs as a homo- or heterodimer in the same fashion as CREB, the differential role of ATF2 and CREB remains largely uncharacterized.	bind
28804	2	7311	7	NULL	NULL	0	NULL	ATF2 heterodimer	NULL		recognizes	NULL					NULL			ATF/CRE motifs 	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_42	16497991	21 Although ATF2 recognizes and binds specific ATF/CRE motifs as a homo- or heterodimer in the same fashion as CREB, the differential role of ATF2 and CREB remains largely uncharacterized.	bind
28805	6	7311	7	NULL	NULL	0	NULL	statement 1	NULL		same as	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_42	16497991	21 Although ATF2 recognizes and binds specific ATF/CRE motifs as a homo- or heterodimer in the same fashion as CREB, the differential role of ATF2 and CREB remains largely uncharacterized.	bind
28806	7	7311	7	NULL	NULL	0	NULL	statement 2	NULL		same as	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_42	16497991	21 Although ATF2 recognizes and binds specific ATF/CRE motifs as a homo- or heterodimer in the same fashion as CREB, the differential role of ATF2 and CREB remains largely uncharacterized.	bind
28807	5	7311	7	NULL	NULL	0	NULL	CREB	NULL		bind	NULL					NULL			ATF/CRE motifs 	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_42	16497991	21 Although ATF2 recognizes and binds specific ATF/CRE motifs as a homo- or heterodimer in the same fashion as CREB, the differential role of ATF2 and CREB remains largely uncharacterized.	bind
46597	3	7311	7	NULL	NULL	0	NULL	ATF2 homodimer	NULL		bind	NULL					NULL			 ATF/CRE motifs	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_42	16497991	21 Although ATF2 recognizes and binds specific ATF/CRE motifs as a homo- or heterodimer in the same fashion as CREB, the differential role of ATF2 and CREB remains largely uncharacterized.	bind
46598	4	7311	7	NULL	NULL	0	NULL	ATF2 heterodimer	NULL		bind	NULL					NULL			ATF/CRE motifs 	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_42	16497991	21 Although ATF2 recognizes and binds specific ATF/CRE motifs as a homo- or heterodimer in the same fashion as CREB, the differential role of ATF2 and CREB remains largely uncharacterized.	bind
46599	8	7311	7	NULL	NULL	0	NULL	statement 3	NULL		same as	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_42	16497991	21 Although ATF2 recognizes and binds specific ATF/CRE motifs as a homo- or heterodimer in the same fashion as CREB, the differential role of ATF2 and CREB remains largely uncharacterized.	bind
46600	9	7311	7	NULL	NULL	0	NULL	statement 4	NULL		same as	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_42	16497991	21 Although ATF2 recognizes and binds specific ATF/CRE motifs as a homo- or heterodimer in the same fashion as CREB, the differential role of ATF2 and CREB remains largely uncharacterized.	bind
26460	1	7312	5	13	NULL	NULL	NULL	Ras	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_23_2955_s_160	12782568	21 Binding of  Ras to GTP results in the activation of  Raf kinase, which then phosphorylates MEK triggering the sequential phosphorylation of the MAPK module.	bind
26461	2	7312	5	13	NULL	NULL	NULL	statement 1	Process		results in					Raf kinase	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_23_2955_s_160	12782568	21 Binding of  Ras to GTP results in the activation of  Raf kinase, which then phosphorylates MEK triggering the sequential phosphorylation of the MAPK module.	bind
26462	3	7312	5	13	NULL	NULL	NULL	Raf kinase	GP	activated	phosphorylates					MEK	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_23_2955_s_160	12782568	21 Binding of  Ras to GTP results in the activation of  Raf kinase, which then phosphorylates MEK triggering the sequential phosphorylation of the MAPK module.	bind
26463	4	7312	5	13	NULL	NULL	NULL	statement 3	Process		triggers					MAPK module	Process	sequential phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_23_2955_s_160	12782568	21 Binding of  Ras to GTP results in the activation of  Raf kinase, which then phosphorylates MEK triggering the sequential phosphorylation of the MAPK module.	bind
28808	1	7312	7	NULL	NULL	0	NULL	Ras	NULL		binds	NULL				GTP	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_107_23_2955_s_160	12782568	21 Binding of  Ras to GTP results in the activation of  Raf kinase, which then phosphorylates MEK triggering the sequential phosphorylation of the MAPK module.	bind
28809	2	7312	7	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				Raf kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_107_23_2955_s_160	12782568	21 Binding of  Ras to GTP results in the activation of  Raf kinase, which then phosphorylates MEK triggering the sequential phosphorylation of the MAPK module.	bind
28810	3	7312	7	NULL	NULL	0	NULL	Raf kinase	NULL	activated 	phosphorylates	NULL				MEK	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_107_23_2955_s_160	12782568	21 Binding of  Ras to GTP results in the activation of  Raf kinase, which then phosphorylates MEK triggering the sequential phosphorylation of the MAPK module.	bind
28811	4	7312	7	NULL	NULL	0	NULL	statement 3	NULL		triggers	NULL				MAPK module	NULL	 sequential phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_circulation_107_23_2955_s_160	12782568	21 Binding of  Ras to GTP results in the activation of  Raf kinase, which then phosphorylates MEK triggering the sequential phosphorylation of the MAPK module.	bind
26464	1	7313	5	13	NULL	NULL	NULL	lipoprotein	GP		interacts with					APG	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2507_s_29	9409221	21 It is predictable that such therapy affects lipoprotein-APG interaction, and it has recently been shown that drugs can reduce total LDL binding with APG.	bind
26465	2	7313	5	13	NULL	NULL	NULL	LDL	GP		bind					APG	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2507_s_29	9409221	21 It is predictable that such therapy affects lipoprotein-APG interaction, and it has recently been shown that drugs can reduce total LDL binding with APG.	bind
26466	3	7313	5	13	NULL	NULL	NULL	drugs	Chemical		reduces					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2507_s_29	9409221	21 It is predictable that such therapy affects lipoprotein-APG interaction, and it has recently been shown that drugs can reduce total LDL binding with APG.	bind
28812	1	7313	7	NULL	NULL	0	NULL	lipoprotein	NULL		interacts with	NULL				APG	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2507_s_29	9409221	21 It is predictable that such therapy affects lipoprotein-APG interaction, and it has recently been shown that drugs can reduce total LDL binding with APG.	bind
28813	2	7313	7	NULL	NULL	0	NULL	total LDL	NULL		bind	NULL				APG	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2507_s_29	9409221	21 It is predictable that such therapy affects lipoprotein-APG interaction, and it has recently been shown that drugs can reduce total LDL binding with APG.	bind
28814	3	7313	7	NULL	NULL	0	NULL	drugs	NULL		reduce	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2507_s_29	9409221	21 It is predictable that such therapy affects lipoprotein-APG interaction, and it has recently been shown that drugs can reduce total LDL binding with APG.	bind
26467	1	7314	5	13	NULL	NULL	NULL	TRL particles	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_105	12231568	21 More specifically, apoC-I inhibits apoE-mediated binding of TRL particles to the LDL receptor and to the LDL receptor-like protein.	bind
26468	2	7314	5	13	NULL	NULL	NULL	apoE	GP		mediates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_105	12231568	21 More specifically, apoC-I inhibits apoE-mediated binding of TRL particles to the LDL receptor and to the LDL receptor-like protein.	bind
26469	3	7314	5	13	NULL	NULL	NULL	apoC-I	GP		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_105	12231568	21 More specifically, apoC-I inhibits apoE-mediated binding of TRL particles to the LDL receptor and to the LDL receptor-like protein.	bind
26470	4	7314	5	13	NULL	NULL	NULL	TRL particles	GP		bind					LDL receptor-like protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_105	12231568	21 More specifically, apoC-I inhibits apoE-mediated binding of TRL particles to the LDL receptor and to the LDL receptor-like protein.	bind
26471	5	7314	5	13	NULL	NULL	NULL	apoE	GP		mediates					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_105	12231568	21 More specifically, apoC-I inhibits apoE-mediated binding of TRL particles to the LDL receptor and to the LDL receptor-like protein.	bind
26472	6	7314	5	13	NULL	NULL	NULL	apoC-I	GP		inhibit					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_105	12231568	21 More specifically, apoC-I inhibits apoE-mediated binding of TRL particles to the LDL receptor and to the LDL receptor-like protein.	bind
28815	1	7314	7	NULL	NULL	0	NULL	TRL particles	NULL		bind	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_105	12231568	21 More specifically, apoC-I inhibits apoE-mediated binding of TRL particles to the LDL receptor and to the LDL receptor-like protein.	bind
28816	2	7314	7	NULL	NULL	0	NULL	TRL particles	NULL		bind	NULL				LDL receptor-like protein	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_105	12231568	21 More specifically, apoC-I inhibits apoE-mediated binding of TRL particles to the LDL receptor and to the LDL receptor-like protein.	bind
28817	3	7314	7	NULL	NULL	0	NULL	apoE	NULL		mediates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_105	12231568	21 More specifically, apoC-I inhibits apoE-mediated binding of TRL particles to the LDL receptor and to the LDL receptor-like protein.	bind
28818	4	7314	7	NULL	NULL	0	NULL	apoE	NULL		mediates	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_105	12231568	21 More specifically, apoC-I inhibits apoE-mediated binding of TRL particles to the LDL receptor and to the LDL receptor-like protein.	bind
28819	5	7314	7	NULL	NULL	0	NULL	apoC-I 	NULL		inhibits	NULL	specifically			statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_105	12231568	21 More specifically, apoC-I inhibits apoE-mediated binding of TRL particles to the LDL receptor and to the LDL receptor-like protein.	bind
28820	6	7314	7	NULL	NULL	0	NULL	apoC-I 	NULL		inhibits	NULL	specifically			statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_105	12231568	21 More specifically, apoC-I inhibits apoE-mediated binding of TRL particles to the LDL receptor and to the LDL receptor-like protein.	bind
26473	1	7315	5	13	NULL	NULL	NULL	PPAR-alpha	GP	activated	bind					AP-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_7_904_s_172	14967736	21 Therefore, it is considered that activated PPAR-alpha binds to AP-1 or its cofactor and that AP-1 is prevented from binding to the cis-elements of the promoter region, which results in impairment of ET-1 gene induction.	bind
26474	2	7315	5	13	NULL	NULL	NULL	PPAR-alpha	GP	activated	bind					AP-1 cofactor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_7_904_s_172	14967736	21 Therefore, it is considered that activated PPAR-alpha binds to AP-1 or its cofactor and that AP-1 is prevented from binding to the cis-elements of the promoter region, which results in impairment of ET-1 gene induction.	bind
26475	3	7315	5	13	NULL	NULL	NULL	AP-1	GP		bind									cis-elements of promoter region	NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_7_904_s_172	14967736	21 Therefore, it is considered that activated PPAR-alpha binds to AP-1 or its cofactor and that AP-1 is prevented from binding to the cis-elements of the promoter region, which results in impairment of ET-1 gene induction.	bind
26476	4	7315	5	13	NULL	NULL	NULL	statement 1	Process		prevents					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_7_904_s_172	14967736	21 Therefore, it is considered that activated PPAR-alpha binds to AP-1 or its cofactor and that AP-1 is prevented from binding to the cis-elements of the promoter region, which results in impairment of ET-1 gene induction.	bind
54472	5	7315	5	13	NULL	NULL	NULL	statement 2	Process		prevents					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_7_904_s_172	14967736	21 Therefore, it is considered that activated PPAR-alpha binds to AP-1 or its cofactor and that AP-1 is prevented from binding to the cis-elements of the promoter region, which results in impairment of ET-1 gene induction.	bind
54473	7	7315	5	13	NULL	NULL	NULL	statement 4	Process		impairs					ET-1 gene	GP	induction of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_7_904_s_172	14967736	21 Therefore, it is considered that activated PPAR-alpha binds to AP-1 or its cofactor and that AP-1 is prevented from binding to the cis-elements of the promoter region, which results in impairment of ET-1 gene induction.	bind
54474	8	7315	5	13	NULL	NULL	NULL	statement 5	Process		impairs					ET-1 gene	GP	induction of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_7_904_s_172	14967736	21 Therefore, it is considered that activated PPAR-alpha binds to AP-1 or its cofactor and that AP-1 is prevented from binding to the cis-elements of the promoter region, which results in impairment of ET-1 gene induction.	bind
28821	1	7315	7	NULL	NULL	0	NULL	PPAR-alpha	NULL	activated	binds to	NULL				AP-1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_109_7_904_s_172	14967736	21 Therefore, it is considered that activated PPAR-alpha binds to AP-1 or its cofactor and that AP-1 is prevented from binding to the cis-elements of the promoter region, which results in impairment of ET-1 gene induction.	bind
28822	2	7315	7	NULL	NULL	0	NULL	PPAR-alpha	NULL	activated	binds	NULL				AP-1 cofactor	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_109_7_904_s_172	14967736	21 Therefore, it is considered that activated PPAR-alpha binds to AP-1 or its cofactor and that AP-1 is prevented from binding to the cis-elements of the promoter region, which results in impairment of ET-1 gene induction.	bind
28823	3	7315	7	NULL	NULL	0	NULL	AP-1	NULL		bind	NULL					NULL	cis-elements of the promoter			NULL		0	NULL	NULL	NULL	gw70_circulation_109_7_904_s_172	14967736	21 Therefore, it is considered that activated PPAR-alpha binds to AP-1 or its cofactor and that AP-1 is prevented from binding to the cis-elements of the promoter region, which results in impairment of ET-1 gene induction.	bind
28824	4	7315	7	NULL	NULL	0	NULL	statement 1	NULL		prevents	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_109_7_904_s_172	14967736	21 Therefore, it is considered that activated PPAR-alpha binds to AP-1 or its cofactor and that AP-1 is prevented from binding to the cis-elements of the promoter region, which results in impairment of ET-1 gene induction.	bind
28825	5	7315	7	NULL	NULL	0	NULL	statement 2	NULL		prevents	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_109_7_904_s_172	14967736	21 Therefore, it is considered that activated PPAR-alpha binds to AP-1 or its cofactor and that AP-1 is prevented from binding to the cis-elements of the promoter region, which results in impairment of ET-1 gene induction.	bind
28826	6	7315	7	NULL	NULL	0	NULL	statement 4	NULL		impairs	NULL				ET-1 gene	NULL	induction of			NULL		0	NULL	NULL	NULL	gw70_circulation_109_7_904_s_172	14967736	21 Therefore, it is considered that activated PPAR-alpha binds to AP-1 or its cofactor and that AP-1 is prevented from binding to the cis-elements of the promoter region, which results in impairment of ET-1 gene induction.	bind
28827	7	7315	7	NULL	NULL	0	NULL	statement 5	NULL		impairs	NULL				ET-1 gene	NULL	induction of			NULL		0	NULL	NULL	NULL	gw70_circulation_109_7_904_s_172	14967736	21 Therefore, it is considered that activated PPAR-alpha binds to AP-1 or its cofactor and that AP-1 is prevented from binding to the cis-elements of the promoter region, which results in impairment of ET-1 gene induction.	bind
26477	1	7316	5	13	NULL	NULL	NULL	Cdk inhibitors	GP		regulates					Cyclin-Cdk	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1511_s_27	10550307	21, 22 Cyclin-Cdk activity is, in turn, regulated by Cdk inhibitors, which bind the Cdk-cyclin complexes, inhibit their activity, and block cell cycle progression.	bind
26478	2	7316	5	13	NULL	NULL	NULL	Cdk inhibitors	GP		bind					Cdk-cyclin complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1511_s_27	10550307	21, 22 Cyclin-Cdk activity is, in turn, regulated by Cdk inhibitors, which bind the Cdk-cyclin complexes, inhibit their activity, and block cell cycle progression.	bind
26479	3	7316	5	13	NULL	NULL	NULL	statement 2	Process		inhibit					Cdk-cyclin complexes	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1511_s_27	10550307	21, 22 Cyclin-Cdk activity is, in turn, regulated by Cdk inhibitors, which bind the Cdk-cyclin complexes, inhibit their activity, and block cell cycle progression.	bind
26480	4	7316	5	13	NULL	NULL	NULL	statement 3	Process		blocks					cell cycle progression	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1511_s_27	10550307	21, 22 Cyclin-Cdk activity is, in turn, regulated by Cdk inhibitors, which bind the Cdk-cyclin complexes, inhibit their activity, and block cell cycle progression.	bind
29086	1	7316	7	NULL	NULL	0	NULL	Cdk inhibitors	NULL		regulate	NULL				Cyclin-Cdk	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_5_1511_s_27	10550307	21, 22 Cyclin-Cdk activity is, in turn, regulated by Cdk inhibitors, which bind the Cdk-cyclin complexes, inhibit their activity, and block cell cycle progression.	bind
29087	2	7316	7	NULL	NULL	0	NULL	Cdk inhibitors	NULL		bind	NULL				Cdk-cyclin complexes	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_5_1511_s_27	10550307	21, 22 Cyclin-Cdk activity is, in turn, regulated by Cdk inhibitors, which bind the Cdk-cyclin complexes, inhibit their activity, and block cell cycle progression.	bind
29088	3	7316	7	NULL	NULL	0	NULL	statement 2	NULL		inhibit 	NULL				Cdk-cyclin complexes	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_5_1511_s_27	10550307	21, 22 Cyclin-Cdk activity is, in turn, regulated by Cdk inhibitors, which bind the Cdk-cyclin complexes, inhibit their activity, and block cell cycle progression.	bind
29089	4	7316	7	NULL	NULL	0	NULL	statement 3	NULL		block	NULL				cell cycle progression	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_5_1511_s_27	10550307	21, 22 Cyclin-Cdk activity is, in turn, regulated by Cdk inhibitors, which bind the Cdk-cyclin complexes, inhibit their activity, and block cell cycle progression.	bind
26481	1	7317	5	13	NULL	NULL	NULL	Hdm2	GP		bind					p53	GP				NULL	in HL tissue samples	NULL	NULL	NULL	NULL	gw60_amjpathol_160_2_569_s_199	11839577	21, 29  The observations from this study of HL tissue samples and cell lines show that, in parallel with the absence of these Hdm2/p14ARF complexes, p53 is bound by Hdm2, which under different circumstances has been shown to inactivate the ability of p53 to induce the expression of p53-transactivated genes.	bind
26482	2	7317	5	13	NULL	NULL	NULL	p53 	GP		induces					p53-transactivated genes	Process	expression of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_2_569_s_199	11839577	21, 29  The observations from this study of HL tissue samples and cell lines show that, in parallel with the absence of these Hdm2/p14ARF complexes, p53 is bound by Hdm2, which under different circumstances has been shown to inactivate the ability of p53 to induce the expression of p53-transactivated genes.	bind
26483	3	7317	5	13	NULL	NULL	NULL	statement 1	Process		inactivates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_2_569_s_199	11839577	21, 29  The observations from this study of HL tissue samples and cell lines show that, in parallel with the absence of these Hdm2/p14ARF complexes, p53 is bound by Hdm2, which under different circumstances has been shown to inactivate the ability of p53 to induce the expression of p53-transactivated genes.	bind
29090	1	7317	7	NULL	NULL	0	NULL	Hdm2	NULL		bind	NULL				p53	NULL				NULL	HL tissue samples	0	NULL	NULL	NULL	gw60_amjpathol_160_2_569_s_199	11839577	21, 29  The observations from this study of HL tissue samples and cell lines show that, in parallel with the absence of these Hdm2/p14ARF complexes, p53 is bound by Hdm2, which under different circumstances has been shown to inactivate the ability of p53 to induce the expression of p53-transactivated genes.	bind
29091	2	7317	7	NULL	NULL	0	NULL	statement 1	NULL		in absence of	NULL				Hdm2/p14ARF complexes	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_2_569_s_199	11839577	21, 29  The observations from this study of HL tissue samples and cell lines show that, in parallel with the absence of these Hdm2/p14ARF complexes, p53 is bound by Hdm2, which under different circumstances has been shown to inactivate the ability of p53 to induce the expression of p53-transactivated genes.	bind
29092	3	7317	7	NULL	NULL	0	NULL	p53	NULL		induce	NULL				p53-transactivated genes	NULL	expression of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_2_569_s_199	11839577	21, 29  The observations from this study of HL tissue samples and cell lines show that, in parallel with the absence of these Hdm2/p14ARF complexes, p53 is bound by Hdm2, which under different circumstances has been shown to inactivate the ability of p53 to induce the expression of p53-transactivated genes.	bind
29093	4	7317	7	NULL	NULL	0	NULL	Hdm2	NULL		inactivate	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_2_569_s_199	11839577	21, 29  The observations from this study of HL tissue samples and cell lines show that, in parallel with the absence of these Hdm2/p14ARF complexes, p53 is bound by Hdm2, which under different circumstances has been shown to inactivate the ability of p53 to induce the expression of p53-transactivated genes.	bind
26640	1	7318	5	13	NULL	NULL	NULL	HuR	GP		is a type of					ubiquitous mRNA binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_11_1034_s_209	14645134	21,24,81,86,87,140      Stability of sGC-alpha1 mRNA is regulated by the ubiquitous mRNA binding protein HuR, which binds to AU-rich elements in the 3''-untranslated region (UTR) and increases mRNA half-life; cGMP-elevating agents decrease expression and RNA binding of HuR, thereby destabilizing sGC-alpha1 mRNA.	bind
26641	2	7318	5	13	NULL	NULL	NULL	sGC-alpha1 mRNA	NucleicAcid	stability of	is regulated by					HuR	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_11_1034_s_209	14645134	21,24,81,86,87,140      Stability of sGC-alpha1 mRNA is regulated by the ubiquitous mRNA binding protein HuR, which binds to AU-rich elements in the 3''-untranslated region (UTR) and increases mRNA half-life; cGMP-elevating agents decrease expression and RNA binding of HuR, thereby destabilizing sGC-alpha1 mRNA.	bind
26642	3	7318	5	13	NULL	NULL	NULL	HuR	GP		bind									AU-rich elements in 3''-untranslated region	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_11_1034_s_209	14645134	21,24,81,86,87,140      Stability of sGC-alpha1 mRNA is regulated by the ubiquitous mRNA binding protein HuR, which binds to AU-rich elements in the 3''-untranslated region (UTR) and increases mRNA half-life; cGMP-elevating agents decrease expression and RNA binding of HuR, thereby destabilizing sGC-alpha1 mRNA.	bind
26643	4	7318	5	13	NULL	NULL	NULL	statement 3	Process		increases					mRNA	NucleicAcid	half life of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_11_1034_s_209	14645134	21,24,81,86,87,140      Stability of sGC-alpha1 mRNA is regulated by the ubiquitous mRNA binding protein HuR, which binds to AU-rich elements in the 3''-untranslated region (UTR) and increases mRNA half-life; cGMP-elevating agents decrease expression and RNA binding of HuR, thereby destabilizing sGC-alpha1 mRNA.	bind
26644	5	7318	5	13	NULL	NULL	NULL	cGMP-elevating agents	Chemical		decreases					HuR	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_11_1034_s_209	14645134	21,24,81,86,87,140      Stability of sGC-alpha1 mRNA is regulated by the ubiquitous mRNA binding protein HuR, which binds to AU-rich elements in the 3''-untranslated region (UTR) and increases mRNA half-life; cGMP-elevating agents decrease expression and RNA binding of HuR, thereby destabilizing sGC-alpha1 mRNA.	bind
26645	6	7318	5	13	NULL	NULL	NULL	HuR	GP		bind					RNA	NucleicAcid	RNA binding of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_11_1034_s_209	14645134	21,24,81,86,87,140      Stability of sGC-alpha1 mRNA is regulated by the ubiquitous mRNA binding protein HuR, which binds to AU-rich elements in the 3''-untranslated region (UTR) and increases mRNA half-life; cGMP-elevating agents decrease expression and RNA binding of HuR, thereby destabilizing sGC-alpha1 mRNA.	bind
26647	7	7318	5	13	NULL	NULL	NULL	statement 5	Process		destabilizes					sGC-alpha1 mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_11_1034_s_209	14645134	21,24,81,86,87,140      Stability of sGC-alpha1 mRNA is regulated by the ubiquitous mRNA binding protein HuR, which binds to AU-rich elements in the 3''-untranslated region (UTR) and increases mRNA half-life; cGMP-elevating agents decrease expression and RNA binding of HuR, thereby destabilizing sGC-alpha1 mRNA.	bind
26648	8	7318	5	13	NULL	NULL	NULL	statement 6	Process		destabilizes					sGC-alpha1 mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_11_1034_s_209	14645134	21,24,81,86,87,140      Stability of sGC-alpha1 mRNA is regulated by the ubiquitous mRNA binding protein HuR, which binds to AU-rich elements in the 3''-untranslated region (UTR) and increases mRNA half-life; cGMP-elevating agents decrease expression and RNA binding of HuR, thereby destabilizing sGC-alpha1 mRNA.	bind
46554	9	7318	5	13	NULL	NULL	NULL	cGMP-elevating agents	Chemical		decreases					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_11_1034_s_209	14645134	21,24,81,86,87,140      Stability of sGC-alpha1 mRNA is regulated by the ubiquitous mRNA binding protein HuR, which binds to AU-rich elements in the 3''-untranslated region (UTR) and increases mRNA half-life; cGMP-elevating agents decrease expression and RNA binding of HuR, thereby destabilizing sGC-alpha1 mRNA.	bind
29094	1	7318	7	NULL	NULL	0	NULL	HuR	NULL		regulates	NULL				sGC-alpha1 mRNA	NULL	 stability of			NULL		0	NULL	NULL	NULL	gw70_circulationres_93_11_1034_s_209	14645134	21,24,81,86,87,140      Stability of sGC-alpha1 mRNA is regulated by the ubiquitous mRNA binding protein HuR, which binds to AU-rich elements in the 3''-untranslated region (UTR) and increases mRNA half-life; cGMP-elevating agents decrease expression and RNA binding of HuR, thereby destabilizing sGC-alpha1 mRNA.	bind
29095	2	7318	7	10	NULL	0	NULL	HuR			is a type of					ubiquitous mRNA binding protein					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_11_1034_s_209	14645134	21,24,81,86,87,140      Stability of sGC-alpha1 mRNA is regulated by the ubiquitous mRNA binding protein HuR, which binds to AU-rich elements in the 3''-untranslated region (UTR) and increases mRNA half-life; cGMP-elevating agents decrease expression and RNA binding of HuR, thereby destabilizing sGC-alpha1 mRNA.	bind
29096	3	7318	7	10	NULL	0	NULL	HuR	NULL		binds	NULL					NULL			AU-rich elements in 3'' UTR	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_11_1034_s_209	14645134	21,24,81,86,87,140      Stability of sGC-alpha1 mRNA is regulated by the ubiquitous mRNA binding protein HuR, which binds to AU-rich elements in the 3''-untranslated region (UTR) and increases mRNA half-life; cGMP-elevating agents decrease expression and RNA binding of HuR, thereby destabilizing sGC-alpha1 mRNA.	bind
29097	4	7318	7	NULL	NULL	0	NULL	statement 3	NULL		increases	NULL				mRNA 	NULL	half-life of 			NULL		0	NULL	NULL	NULL	gw70_circulationres_93_11_1034_s_209	14645134	21,24,81,86,87,140      Stability of sGC-alpha1 mRNA is regulated by the ubiquitous mRNA binding protein HuR, which binds to AU-rich elements in the 3''-untranslated region (UTR) and increases mRNA half-life; cGMP-elevating agents decrease expression and RNA binding of HuR, thereby destabilizing sGC-alpha1 mRNA.	bind
29098	5	7318	7	NULL	NULL	0	NULL	HuR	NULL		bind	NULL				RNA	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_11_1034_s_209	14645134	21,24,81,86,87,140      Stability of sGC-alpha1 mRNA is regulated by the ubiquitous mRNA binding protein HuR, which binds to AU-rich elements in the 3''-untranslated region (UTR) and increases mRNA half-life; cGMP-elevating agents decrease expression and RNA binding of HuR, thereby destabilizing sGC-alpha1 mRNA.	bind
29099	6	7318	7	NULL	NULL	0	NULL	cGMP-elevating agents	NULL		decrease	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_11_1034_s_209	14645134	21,24,81,86,87,140      Stability of sGC-alpha1 mRNA is regulated by the ubiquitous mRNA binding protein HuR, which binds to AU-rich elements in the 3''-untranslated region (UTR) and increases mRNA half-life; cGMP-elevating agents decrease expression and RNA binding of HuR, thereby destabilizing sGC-alpha1 mRNA.	bind
29100	7	7318	7	NULL	NULL	0	NULL	cGMP-elevating agents	NULL		decrease	NULL				RNA	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_circulationres_93_11_1034_s_209	14645134	21,24,81,86,87,140      Stability of sGC-alpha1 mRNA is regulated by the ubiquitous mRNA binding protein HuR, which binds to AU-rich elements in the 3''-untranslated region (UTR) and increases mRNA half-life; cGMP-elevating agents decrease expression and RNA binding of HuR, thereby destabilizing sGC-alpha1 mRNA.	bind
29101	8	7318	7	NULL	NULL	0	NULL	statement 6	NULL		destabilize	NULL				sGC-alpha1 mRNA	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_11_1034_s_209	14645134	21,24,81,86,87,140      Stability of sGC-alpha1 mRNA is regulated by the ubiquitous mRNA binding protein HuR, which binds to AU-rich elements in the 3''-untranslated region (UTR) and increases mRNA half-life; cGMP-elevating agents decrease expression and RNA binding of HuR, thereby destabilizing sGC-alpha1 mRNA.	bind
29102	9	7318	7	NULL	NULL	0	NULL	statement 7	NULL		destabilize	NULL				sGC-alpha1 mRNA	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_11_1034_s_209	14645134	21,24,81,86,87,140      Stability of sGC-alpha1 mRNA is regulated by the ubiquitous mRNA binding protein HuR, which binds to AU-rich elements in the 3''-untranslated region (UTR) and increases mRNA half-life; cGMP-elevating agents decrease expression and RNA binding of HuR, thereby destabilizing sGC-alpha1 mRNA.	bind
26484	1	7319	5	13	NULL	NULL	NULL	ribosomal protein L5	GP	xenopus	bind					5S rRNA	NucleicAcid	oocyte			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2510_s_296	11410658	22       Scripture,J.B. and Huber,P.W. (1996) Analysis of the binding of  Xenopus ribosomal protein L5 to oocyte 5S rRNA.	bind
29103	1	7319	7	NULL	NULL	0	NULL	ribosomal protein L5	NULL	Xenopus	bind	NULL				5S rRNA	NULL	oocyte			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2510_s_296	11410658	22       Scripture,J.B. and Huber,P.W. (1996) Analysis of the binding of  Xenopus ribosomal protein L5 to oocyte 5S rRNA.	bind
26649	1	7320	5	13	NULL	NULL	NULL	LDL particles	GP		bind		abnormally			LDL receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_4_517_s_133	8624773	22  23  Second, our investigations have shown that patients having LDL particles that bind abnormally to LDL receptors and are slowly removed exhibit LDL particles that are enriched with cholesterol.	bind
26651	2	7320	5	13	NULL	NULL	NULL	LDL particles	GP		is enriched with					cholesterol	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_4_517_s_133	8624773	22  23  Second, our investigations have shown that patients having LDL particles that bind abnormally to LDL receptors and are slowly removed exhibit LDL particles that are enriched with cholesterol.	bind
26652	3	7320	5	13	NULL	NULL	NULL	statement 1	Process		exhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_4_517_s_133	8624773	22  23  Second, our investigations have shown that patients having LDL particles that bind abnormally to LDL receptors and are slowly removed exhibit LDL particles that are enriched with cholesterol.	bind
29104	1	7320	7	NULL	NULL	0	NULL	LDL particles	NULL		bind	NULL	abnormally			LDL receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_4_517_s_133	8624773	22  23  Second, our investigations have shown that patients having LDL particles that bind abnormally to LDL receptors and are slowly removed exhibit LDL particles that are enriched with cholesterol.	bind
29105	2	7320	7	10	NULL	0	NULL	LDL particles	NULL		are enriched with	NULL				cholesterol	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_4_517_s_133	8624773	22  23  Second, our investigations have shown that patients having LDL particles that bind abnormally to LDL receptors and are slowly removed exhibit LDL particles that are enriched with cholesterol.	bind
46555	3	7320	7	10	NULL	0	NULL	statement 1	NULL		exhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_4_517_s_133	8624773	22  23  Second, our investigations have shown that patients having LDL particles that bind abnormally to LDL receptors and are slowly removed exhibit LDL particles that are enriched with cholesterol.	bind
26653	1	7325	5	13	NULL	NULL	NULL	LPL	GP		induces					TNFalpha	GP	production of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_6_1405_s_157	10364070	22  Our results, which show that heparinase treatment of human monocytes totally inhibits LPL-induced TNFalpha production, demonstrate that LPL binding to the monocytic cell surface HSPG is required for its effect on TNFalpha production.	bind
26654	2	7325	5	13	NULL	NULL	NULL	heparinase	GP	treatment	inhibit		totally			statement 1	Process				NULL	human monocytes	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_6_1405_s_157	10364070	22  Our results, which show that heparinase treatment of human monocytes totally inhibits LPL-induced TNFalpha production, demonstrate that LPL binding to the monocytic cell surface HSPG is required for its effect on TNFalpha production.	bind
26655	3	7325	5	13	NULL	NULL	NULL	LPL	GP		bind					HSPG	GP	monocytic cell surface 			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_6_1405_s_157	10364070	22  Our results, which show that heparinase treatment of human monocytes totally inhibits LPL-induced TNFalpha production, demonstrate that LPL binding to the monocytic cell surface HSPG is required for its effect on TNFalpha production.	bind
26656	4	7325	5	13	NULL	NULL	NULL	statement 3	Process		is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_6_1405_s_157	10364070	22  Our results, which show that heparinase treatment of human monocytes totally inhibits LPL-induced TNFalpha production, demonstrate that LPL binding to the monocytic cell surface HSPG is required for its effect on TNFalpha production.	bind
29106	1	7325	7	NULL	NULL	0	NULL	LPL	NULL		induce	NULL				TNFalpha	NULL	production of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_6_1405_s_157	10364070	22  Our results, which show that heparinase treatment of human monocytes totally inhibits LPL-induced TNFalpha production, demonstrate that LPL binding to the monocytic cell surface HSPG is required for its effect on TNFalpha production.	bind
29107	2	7325	7	10	NULL	0	NULL	heparinise		treatment	inhibit		totally			statement 1					NULL	human monocytes	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_6_1405_s_157	10364070	22  Our results, which show that heparinase treatment of human monocytes totally inhibits LPL-induced TNFalpha production, demonstrate that LPL binding to the monocytic cell surface HSPG is required for its effect on TNFalpha production.	bind
29108	3	7325	7	NULL	NULL	0	NULL	LPL	NULL		bind	NULL				HSPG	NULL	monocytic cell surface			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_6_1405_s_157	10364070	22  Our results, which show that heparinase treatment of human monocytes totally inhibits LPL-induced TNFalpha production, demonstrate that LPL binding to the monocytic cell surface HSPG is required for its effect on TNFalpha production.	bind
29109	4	7325	7	NULL	NULL	0	NULL	statement 3	NULL		is required for	NULL				TNFalpha	NULL	production of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_6_1405_s_157	10364070	22  Our results, which show that heparinase treatment of human monocytes totally inhibits LPL-induced TNFalpha production, demonstrate that LPL binding to the monocytic cell surface HSPG is required for its effect on TNFalpha production.	bind
26657	1	7326	5	13	NULL	NULL	NULL			wt	bind			kringle IV-10		PM-fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_392_s_197	8630665	22  Our work now shows that the individual wt kringle IV-10 also binds to PM-fibrinogen via two components, one LBS mediated and another LBS independent.	bind
26659	2	7326	5	13	NULL	NULL	NULL	statement 1	Process		is mediated by								LBS		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_392_s_197	8630665	22  Our work now shows that the individual wt kringle IV-10 also binds to PM-fibrinogen via two components, one LBS mediated and another LBS independent.	bind
26660	3	7326	5	13	NULL	NULL	NULL	statement 1	Process		is independent of								LBS		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_392_s_197	8630665	22  Our work now shows that the individual wt kringle IV-10 also binds to PM-fibrinogen via two components, one LBS mediated and another LBS independent.	bind
29110	1	7326	7	10	NULL	0	NULL		NULL	wt	binds to	NULL		kringle IV-10		PM-fibrinogen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_392_s_197	8630665	22  Our work now shows that the individual wt kringle IV-10 also binds to PM-fibrinogen via two components, one LBS mediated and another LBS independent.	bind
29111	2	7326	7	10	NULL	0	NULL				mediates			LBS		statement 1					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_392_s_197	8630665	22  Our work now shows that the individual wt kringle IV-10 also binds to PM-fibrinogen via two components, one LBS mediated and another LBS independent.	bind
29112	3	7326	7	10	NULL	0	NULL	statement 1			independent of								LBS		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_392_s_197	8630665	22  Our work now shows that the individual wt kringle IV-10 also binds to PM-fibrinogen via two components, one LBS mediated and another LBS independent.	bind
26666	1	7328	5	13	NULL	NULL	NULL	growth factors	GP		bind					tyrosine kinase receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1157_s_235	9777947	22  The results of our experiments therefore indicate that stimulation of U-373 MG glioblastoma cells by various growth factors binding to tyrosine kinase receptors leads to a less differentiated phenotype.	bind
26667	2	7328	5	13	NULL	NULL	NULL	statement 1	Process		stimulates					U-373 MG	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1157_s_235	9777947	22  The results of our experiments therefore indicate that stimulation of U-373 MG glioblastoma cells by various growth factors binding to tyrosine kinase receptors leads to a less differentiated phenotype.	bind
26668	3	7328	5	13	NULL	NULL	NULL	statement 2	Process		leads to					phenotype	Cell	less differentiated			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1157_s_235	9777947	22  The results of our experiments therefore indicate that stimulation of U-373 MG glioblastoma cells by various growth factors binding to tyrosine kinase receptors leads to a less differentiated phenotype.	bind
54475	4	7328	5	13	NULL	NULL	NULL	U-373 MG 	Cell		is a type of					glioblastoma cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1157_s_235	9777947	22  The results of our experiments therefore indicate that stimulation of U-373 MG glioblastoma cells by various growth factors binding to tyrosine kinase receptors leads to a less differentiated phenotype.	bind
29114	1	7328	7	NULL	NULL	0	NULL	growth factors 	NULL		binds to	NULL				tyrosine kinase receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_4_1157_s_235	9777947	22  The results of our experiments therefore indicate that stimulation of U-373 MG glioblastoma cells by various growth factors binding to tyrosine kinase receptors leads to a less differentiated phenotype.	bind
29115	2	7328	7	10	NULL	0	NULL	growth factors			stimulate					U-373 MG					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1157_s_235	9777947	22  The results of our experiments therefore indicate that stimulation of U-373 MG glioblastoma cells by various growth factors binding to tyrosine kinase receptors leads to a less differentiated phenotype.	bind
29116	3	7328	7	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				phenotype	NULL	less differentiated			NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_4_1157_s_235	9777947	22  The results of our experiments therefore indicate that stimulation of U-373 MG glioblastoma cells by various growth factors binding to tyrosine kinase receptors leads to a less differentiated phenotype.	bind
54476	4	7328	7	10	NULL	0	NULL	U-373 MG			is a type of					glioblastoma cells					NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_4_1157_s_235	9777947	22  The results of our experiments therefore indicate that stimulation of U-373 MG glioblastoma cells by various growth factors binding to tyrosine kinase receptors leads to a less differentiated phenotype.	bind
26670	1	7329	5	13	NULL	NULL	NULL	warfarin	Chemical		inhibit					mesangial cell 	warfarin	proliferation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_4_1423_s_17	11290560	22  These two inhibitors exert their activities in different ways; warfarin inhibits mesangial cell proliferation possibly by inhibiting gamma-carboxylation of Gas6, whereas Axl-Fc blocks the binding of Gas6 to the cell surface Axl by scavenging Gas6.	bind
26672	2	7329	5	13	NULL	NULL	NULL	warfarin	Chemical		inhibit					Gas6	GP	carboxylation of	gamma		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_4_1423_s_17	11290560	22  These two inhibitors exert their activities in different ways; warfarin inhibits mesangial cell proliferation possibly by inhibiting gamma-carboxylation of Gas6, whereas Axl-Fc blocks the binding of Gas6 to the cell surface Axl by scavenging Gas6.	bind
26675	3	7329	5	13	NULL	NULL	NULL	statement 2	Process		leads to		possibly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_4_1423_s_17	11290560	22  These two inhibitors exert their activities in different ways; warfarin inhibits mesangial cell proliferation possibly by inhibiting gamma-carboxylation of Gas6, whereas Axl-Fc blocks the binding of Gas6 to the cell surface Axl by scavenging Gas6.	bind
26676	4	7329	5	13	NULL	NULL	NULL	Gas6	GP		bind					Axl	GP	cell surface			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_4_1423_s_17	11290560	22  These two inhibitors exert their activities in different ways; warfarin inhibits mesangial cell proliferation possibly by inhibiting gamma-carboxylation of Gas6, whereas Axl-Fc blocks the binding of Gas6 to the cell surface Axl by scavenging Gas6.	bind
26677	5	7329	5	13	NULL	NULL	NULL	Axl-Fc	GP		blocks					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_4_1423_s_17	11290560	22  These two inhibitors exert their activities in different ways; warfarin inhibits mesangial cell proliferation possibly by inhibiting gamma-carboxylation of Gas6, whereas Axl-Fc blocks the binding of Gas6 to the cell surface Axl by scavenging Gas6.	bind
26678	6	7329	5	13	NULL	NULL	NULL	Axl-Fc	GP		scavenges					Gas6	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_4_1423_s_17	11290560	22  These two inhibitors exert their activities in different ways; warfarin inhibits mesangial cell proliferation possibly by inhibiting gamma-carboxylation of Gas6, whereas Axl-Fc blocks the binding of Gas6 to the cell surface Axl by scavenging Gas6.	bind
26679	7	7329	5	13	NULL	NULL	NULL	statement 6	Process		leads to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_4_1423_s_17	11290560	22  These two inhibitors exert their activities in different ways; warfarin inhibits mesangial cell proliferation possibly by inhibiting gamma-carboxylation of Gas6, whereas Axl-Fc blocks the binding of Gas6 to the cell surface Axl by scavenging Gas6.	bind
29117	1	7329	7	10	NULL	0	NULL	 warfarin			inhibits					mesangial cell 		proliferation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_4_1423_s_17	11290560	22  These two inhibitors exert their activities in different ways; warfarin inhibits mesangial cell proliferation possibly by inhibiting gamma-carboxylation of Gas6, whereas Axl-Fc blocks the binding of Gas6 to the cell surface Axl by scavenging Gas6.	bind
29118	2	7329	7	10	NULL	0	NULL	statement 1			occur by		may			Gas6		 inhibition of;;carboxylation of	gamma		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_4_1423_s_17	11290560	22  These two inhibitors exert their activities in different ways; warfarin inhibits mesangial cell proliferation possibly by inhibiting gamma-carboxylation of Gas6, whereas Axl-Fc blocks the binding of Gas6 to the cell surface Axl by scavenging Gas6.	bind
29119	3	7329	7	NULL	NULL	0	NULL	Gas6	NULL		bind	NULL				 Axl	NULL	cell surface			NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_4_1423_s_17	11290560	22  These two inhibitors exert their activities in different ways; warfarin inhibits mesangial cell proliferation possibly by inhibiting gamma-carboxylation of Gas6, whereas Axl-Fc blocks the binding of Gas6 to the cell surface Axl by scavenging Gas6.	bind
29120	4	7329	7	NULL	NULL	0	NULL	Axl-Fc	NULL		blocks	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_4_1423_s_17	11290560	22  These two inhibitors exert their activities in different ways; warfarin inhibits mesangial cell proliferation possibly by inhibiting gamma-carboxylation of Gas6, whereas Axl-Fc blocks the binding of Gas6 to the cell surface Axl by scavenging Gas6.	bind
29121	5	7329	7	NULL	NULL	0	NULL	statement 3	NULL		occurs by	NULL				Gas6	NULL	scavenging			NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_4_1423_s_17	11290560	22  These two inhibitors exert their activities in different ways; warfarin inhibits mesangial cell proliferation possibly by inhibiting gamma-carboxylation of Gas6, whereas Axl-Fc blocks the binding of Gas6 to the cell surface Axl by scavenging Gas6.	bind
26680	1	7330	5	13	NULL	NULL	NULL	anti-LIBS1	GP	binding of	indicates					fibrinogen receptor	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_3_279_s_88	8759067	22  Thus, anti-LIBS1 binding indicates fibrinogen receptor activity.	bind
29122	1	7330	7	NULL	NULL	0	NULL	anti-LIBS1	NULL	binding of	indicates	NULL				fibrinogen receptor	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_circulation_94_3_279_s_88	8759067	22  Thus, anti-LIBS1 binding indicates fibrinogen receptor activity.	bind
26786	1	7332	5	13	NULL	NULL	NULL	tissue factor	GP		bind					factor VII	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
26787	2	7332	5	13	NULL	NULL	NULL	blood	OrganismPart	exposure to	leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
26788	3	7332	5	13	NULL	NULL	NULL	tissue factor	GP		bind					factor VIIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
26789	4	7332	5	13	NULL	NULL	NULL	blood	OrganismPart	exposure to	leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
26790	5	7332	5	13	NULL	NULL	NULL	statement 1	Process		assembles					tissue factor - factor VIIa complex	GP	functional			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
26791	6	7332	5	13	NULL	NULL	NULL	statement 3	Process		assembles					tissue factor - factor VIIa complex	GP	functional			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
26792	7	7332	5	13	NULL	NULL	NULL	statement 5	Process		activates					factor IX	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
26793	8	7332	5	13	NULL	NULL	NULL	statement 5	Process		activates					factor X	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
26794	9	7332	5	13	NULL	NULL	NULL	statement 6	Process		activates					factor IX	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
26795	10	7332	5	13	NULL	NULL	NULL	statement 6	Process		activates					factor X	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
26796	11	7332	5	13	NULL	NULL	NULL	prothrombin	GP		is converted to					thrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
26797	12	7332	5	10	NULL	0	NULL	factor Xa	NULL		is required for	NULL				statement 11	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
26798	13	7332	5	10	NULL	0	NULL	cofactor Va	NULL		is required for	NULL				statement 11	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
46572	14	7332	5	13	NULL	NULL	NULL	Factor Xa	Process		is assembled on					cell surfaces	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
46573	15	7332	5	10	NULL	0	NULL	cofactor Va	NULL		is assembled on	NULL				cell surface	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
29151	1	7332	7	NULL	NULL	0	NULL	 tissue factor	NULL		binds	NULL				factors VII	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
29153	2	7332	7	NULL	NULL	0	NULL	tissue factor	NULL		binds	NULL				factor VIIa	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
29155	3	7332	7	NULL	NULL	0	NULL	statement 1	NULL		occurs when	NULL				blood 	NULL	exposed to			NULL		0	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
29156	4	7332	7	NULL	NULL	0	NULL	statement 2	NULL		occurs when	NULL				blood	NULL	exposed to			NULL		0	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
29158	5	7332	7	NULL	NULL	0	NULL	statement 1	NULL		assembles 	NULL				tissue factor - factor VIIa complex	NULL	 functional			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
29161	6	7332	7	NULL	NULL	0	NULL	statement 2	NULL		assembles 	NULL				tissue factor - factor VIIa complex	NULL	functional			NULL		0	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
29162	7	7332	7	NULL	NULL	0	NULL	statement 5	NULL		activates	NULL				 factors IX	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
29163	8	7332	7	NULL	NULL	0	NULL	statement 6	NULL		activates	NULL				factor IX	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
29164	9	7332	7	NULL	NULL	0	NULL	statement 5	NULL		activates	NULL				factor X	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
29165	10	7332	7	NULL	NULL	0	NULL	statement 6	NULL		activates	NULL				factor X	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
29166	11	7332	7	NULL	NULL	0	NULL	Factor Xa	NULL		assemble on	NULL				cell surface	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
29169	12	7332	7	NULL	NULL	0	NULL	cofactor Va	NULL		assemble on	NULL				cell surface	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
29173	13	7332	7	NULL	NULL	0	NULL	prothrombin	NULL		converts to	NULL				thrombin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
29175	14	7332	7	NULL	NULL	0	NULL	statement 11	NULL		converts 	NULL				statement 13	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
29178	15	7332	7	NULL	NULL	0	NULL	statement 12	NULL		converts	NULL				statement 13	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_11_3323_s_24	7586321	22  When exposed to blood, tissue factor binds factors VII and VIIa, resulting in assembly of the functional tissue factor - factor VIIa complex, which in turn activates factors IX and X. 23 24  Factor Xa and its cofactor Va assembled on cell surfaces then convert prothrombin to thrombin.	bind
26799	1	7333	5	13	NULL	NULL	NULL	HSBP1	GP		is					hsp binding factor 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_8_1012_s_27	11864934	22 A second mechanism involves an interaction between hsp binding factor 1 (HSBP1) with the active trimeric form of HSF1 and hsp70, thereby inhibiting the capacity of HSF1 to bind to DNA. 23	bind
26800	2	7333	5	13	NULL	NULL	NULL	HSBP1	GP		interacts with					HSF1	GP	active trimeric form of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_8_1012_s_27	11864934	22 A second mechanism involves an interaction between hsp binding factor 1 (HSBP1) with the active trimeric form of HSF1 and hsp70, thereby inhibiting the capacity of HSF1 to bind to DNA. 23	bind
26801	3	7333	5	13	NULL	NULL	NULL	HSBP1	GP		interacts with					hsp70	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_8_1012_s_27	11864934	22 A second mechanism involves an interaction between hsp binding factor 1 (HSBP1) with the active trimeric form of HSF1 and hsp70, thereby inhibiting the capacity of HSF1 to bind to DNA. 23	bind
26802	4	7333	5	13	NULL	NULL	NULL	HSF1	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_8_1012_s_27	11864934	22 A second mechanism involves an interaction between hsp binding factor 1 (HSBP1) with the active trimeric form of HSF1 and hsp70, thereby inhibiting the capacity of HSF1 to bind to DNA. 23	bind
26803	5	7333	5	13	NULL	NULL	NULL	statement 2	Process		inhibit					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_8_1012_s_27	11864934	22 A second mechanism involves an interaction between hsp binding factor 1 (HSBP1) with the active trimeric form of HSF1 and hsp70, thereby inhibiting the capacity of HSF1 to bind to DNA. 23	bind
26804	6	7333	5	13	NULL	NULL	NULL	statement 3	Process		inhibit					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_8_1012_s_27	11864934	22 A second mechanism involves an interaction between hsp binding factor 1 (HSBP1) with the active trimeric form of HSF1 and hsp70, thereby inhibiting the capacity of HSF1 to bind to DNA. 23	bind
29182	1	7333	7	NULL	NULL	0	NULL	HSBP1	NULL		interacts with	NULL				HSF1	NULL	active trimeric form of			NULL		0	NULL	NULL	NULL	gw60_circulation_105_8_1012_s_27	11864934	22 A second mechanism involves an interaction between hsp binding factor 1 (HSBP1) with the active trimeric form of HSF1 and hsp70, thereby inhibiting the capacity of HSF1 to bind to DNA. 23	bind
29183	2	7333	7	NULL	NULL	0	NULL	HSBP1	NULL		interacts with	NULL				hsp70	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_8_1012_s_27	11864934	22 A second mechanism involves an interaction between hsp binding factor 1 (HSBP1) with the active trimeric form of HSF1 and hsp70, thereby inhibiting the capacity of HSF1 to bind to DNA. 23	bind
29184	3	7333	7	NULL	NULL	0	NULL	HSF1	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_8_1012_s_27	11864934	22 A second mechanism involves an interaction between hsp binding factor 1 (HSBP1) with the active trimeric form of HSF1 and hsp70, thereby inhibiting the capacity of HSF1 to bind to DNA. 23	bind
29185	4	7333	7	NULL	NULL	0	NULL	statement 1	NULL		inhibit	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_8_1012_s_27	11864934	22 A second mechanism involves an interaction between hsp binding factor 1 (HSBP1) with the active trimeric form of HSF1 and hsp70, thereby inhibiting the capacity of HSF1 to bind to DNA. 23	bind
29186	5	7333	7	NULL	NULL	0	NULL	statement 2	NULL		inhibit	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_8_1012_s_27	11864934	22 A second mechanism involves an interaction between hsp binding factor 1 (HSBP1) with the active trimeric form of HSF1 and hsp70, thereby inhibiting the capacity of HSF1 to bind to DNA. 23	bind
29223	6	7333	7	NULL	NULL	0	NULL	HSBP1	NULL		is	NULL				hsp binding factor 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_8_1012_s_27	11864934	22 A second mechanism involves an interaction between hsp binding factor 1 (HSBP1) with the active trimeric form of HSF1 and hsp70, thereby inhibiting the capacity of HSF1 to bind to DNA. 23	bind
26805	1	7334	5	13	NULL	NULL	NULL	Rac1	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_3_276_s_29	15217908	22 Although originally posited to be a GAP based on its amino acid sequence similarity to Ras-GAP, subsequent in vitro analysis revealed that IQGAP1 binds to active (GTP-bound) Rac1, which in turn inhibits its intrinsic GTPase activity, thereby increasing active Rac1.	bind
26806	2	7334	5	13	NULL	NULL	NULL	IQGAP1	GP		bind					statement 1	Process	active			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_circulationres_95_3_276_s_29	15217908	22 Although originally posited to be a GAP based on its amino acid sequence similarity to Ras-GAP, subsequent in vitro analysis revealed that IQGAP1 binds to active (GTP-bound) Rac1, which in turn inhibits its intrinsic GTPase activity, thereby increasing active Rac1.	bind
26807	3	7334	5	13	NULL	NULL	NULL	statement 2	Process		inhibit					GTPase 	GP	intrinsic activity of			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_circulationres_95_3_276_s_29	15217908	22 Although originally posited to be a GAP based on its amino acid sequence similarity to Ras-GAP, subsequent in vitro analysis revealed that IQGAP1 binds to active (GTP-bound) Rac1, which in turn inhibits its intrinsic GTPase activity, thereby increasing active Rac1.	bind
26808	4	7334	5	13	NULL	NULL	NULL	statement 3	Process		increases					Rac1	GP	active			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_circulationres_95_3_276_s_29	15217908	22 Although originally posited to be a GAP based on its amino acid sequence similarity to Ras-GAP, subsequent in vitro analysis revealed that IQGAP1 binds to active (GTP-bound) Rac1, which in turn inhibits its intrinsic GTPase activity, thereby increasing active Rac1.	bind
29187	1	7334	7	10	NULL	0	NULL	GTP			binds to					Rac1					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_3_276_s_29	15217908	22 Although originally posited to be a GAP based on its amino acid sequence similarity to Ras-GAP, subsequent in vitro analysis revealed that IQGAP1 binds to active (GTP-bound) Rac1, which in turn inhibits its intrinsic GTPase activity, thereby increasing active Rac1.	bind
29188	2	7334	7	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				GTPase	NULL	intrinsic activity of			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_circulationres_95_3_276_s_29	15217908	22 Although originally posited to be a GAP based on its amino acid sequence similarity to Ras-GAP, subsequent in vitro analysis revealed that IQGAP1 binds to active (GTP-bound) Rac1, which in turn inhibits its intrinsic GTPase activity, thereby increasing active Rac1.	bind
29189	3	7334	7	NULL	NULL	0	NULL	statement 2	NULL		increase	NULL				Rac1	NULL	active			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_circulationres_95_3_276_s_29	15217908	22 Although originally posited to be a GAP based on its amino acid sequence similarity to Ras-GAP, subsequent in vitro analysis revealed that IQGAP1 binds to active (GTP-bound) Rac1, which in turn inhibits its intrinsic GTPase activity, thereby increasing active Rac1.	bind
46574	4	7334	7	10	NULL	0	NULL	IQGAP1			bind					statement 1					NULL	in vitro	NULL	NULL	NULL	NULL	gw70_circulationres_95_3_276_s_29	15217908	22 Although originally posited to be a GAP based on its amino acid sequence similarity to Ras-GAP, subsequent in vitro analysis revealed that IQGAP1 binds to active (GTP-bound) Rac1, which in turn inhibits its intrinsic GTPase activity, thereby increasing active Rac1.	bind
26809	1	7335	5	13	NULL	NULL	NULL	LDLR	GP		bind					apoE	GP	newly synthesized			NULL	in macrophages	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_91_s_161	12969990	22 Although the role of LDLR in these processes has not been addressed, LDLR is known to bind to newly synthesized apoE in macrophages and limits its secretion.	bind
26810	2	7335	5	13	NULL	NULL	NULL	statement 1	Process		limits					apoE	GP	secretion of			NULL	macrophages	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_91_s_161	12969990	22 Although the role of LDLR in these processes has not been addressed, LDLR is known to bind to newly synthesized apoE in macrophages and limits its secretion.	bind
29190	1	7335	7	NULL	NULL	0	NULL	 LDLR 	NULL		binds	NULL				apoE	NULL	newly synthesized			NULL	macrophages	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_91_s_161	12969990	22 Although the role of LDLR in these processes has not been addressed, LDLR is known to bind to newly synthesized apoE in macrophages and limits its secretion.	bind
29191	2	7335	7	10	NULL	0	NULL	statement 1			limits					apoE		secretion of			NULL	macrophages	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_91_s_161	12969990	22 Although the role of LDLR in these processes has not been addressed, LDLR is known to bind to newly synthesized apoE in macrophages and limits its secretion.	bind
26811	1	7336	5	13	NULL	NULL	NULL				plays a role in				CArG elements	SRF	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1596_s_154	15231515	22 It is also possible that subtle difference in DNA sequences within the CArG elements may play a role in determining not only SRF binding, 26 but also subsequent recruitment of myocardin.	bind
26812	2	7336	5	13	NULL	NULL	NULL				plays a role in				CArG elements	myocardin	GP	recruitment of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1596_s_154	15231515	22 It is also possible that subtle difference in DNA sequences within the CArG elements may play a role in determining not only SRF binding, 26 but also subsequent recruitment of myocardin.	bind
29192	1	7336	7	NULL	NULL	0	NULL		NULL		plays a role in	NULL			 CArG elements	SRF	NULL	binding of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1596_s_154	15231515	22 It is also possible that subtle difference in DNA sequences within the CArG elements may play a role in determining not only SRF binding, 26 but also subsequent recruitment of myocardin.	bind
29193	2	7336	7	NULL	NULL	0	NULL		NULL		plays a role in	NULL			CArG elements	myocardin	NULL	recruitment of 			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1596_s_154	15231515	22 It is also possible that subtle difference in DNA sequences within the CArG elements may play a role in determining not only SRF binding, 26 but also subsequent recruitment of myocardin.	bind
26813	1	7337	5	13	NULL	NULL	NULL	PTX3	GP		bind					FGF2	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1837_s_33	16020751	22 Moreover, PTX3 binds FGF2 and inhibits its angiogenic activity on endothelial cells.	bind
26814	2	7337	5	13	NULL	NULL	NULL	FGF2	GP		exhibits					angiogenic activity	Process				NULL	on endothelial cells	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1837_s_33	16020751	22 Moreover, PTX3 binds FGF2 and inhibits its angiogenic activity on endothelial cells.	bind
46575	3	7337	5	13	NULL	NULL	NULL	statement 1	Process		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1837_s_33	16020751	22 Moreover, PTX3 binds FGF2 and inhibits its angiogenic activity on endothelial cells.	bind
29194	1	7337	7	NULL	NULL	0	NULL	PTX3	NULL		binds	NULL				FGF2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1837_s_33	16020751	22 Moreover, PTX3 binds FGF2 and inhibits its angiogenic activity on endothelial cells.	bind
29195	2	7337	7	10	NULL	0	NULL	FGF2	NULL		exhibits	NULL				angiogenic activity	NULL				NULL	endothelial cells	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1837_s_33	16020751	22 Moreover, PTX3 binds FGF2 and inhibits its angiogenic activity on endothelial cells.	bind
46576	3	7337	7	10	NULL	0	NULL	statement 1	NULL		inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_9_1837_s_33	16020751	22 Moreover, PTX3 binds FGF2 and inhibits its angiogenic activity on endothelial cells.	bind
26815	1	7338	5	13	NULL	NULL	NULL	PKC	GP	activation of	cause		might			insulin resistance	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_28_s_42	16239592	22 The activation of PKC might cause insulin resistance by ultimately inducing serine/tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1) sites, thereby inhibiting IRS-1 binding and activation of phosphoinositol 3-kinase.	bind
26816	2	7338	5	13	NULL	NULL	NULL	IRS-1	GP		is					insulin receptor substrate 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_28_s_42	16239592	22 The activation of PKC might cause insulin resistance by ultimately inducing serine/tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1) sites, thereby inhibiting IRS-1 binding and activation of phosphoinositol 3-kinase.	bind
26817	3	7338	5	13	NULL	NULL	NULL	statement 1	Process		induces					IRS-1	GP	phosphorylation of	serine/tyrosine		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_28_s_42	16239592	22 The activation of PKC might cause insulin resistance by ultimately inducing serine/tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1) sites, thereby inhibiting IRS-1 binding and activation of phosphoinositol 3-kinase.	bind
26818	4	7338	5	13	NULL	NULL	NULL	statement 3	Process		inhibit					IRS-1	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_28_s_42	16239592	22 The activation of PKC might cause insulin resistance by ultimately inducing serine/tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1) sites, thereby inhibiting IRS-1 binding and activation of phosphoinositol 3-kinase.	bind
26819	5	7338	5	13	NULL	NULL	NULL	statement 3	Process		inhibit					phosphoinositol 3-kinase	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_28_s_42	16239592	22 The activation of PKC might cause insulin resistance by ultimately inducing serine/tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1) sites, thereby inhibiting IRS-1 binding and activation of phosphoinositol 3-kinase.	bind
29196	1	7338	7	NULL	NULL	0	NULL	PKC	NULL	activation of	cause	NULL				insulin resistance	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_28_s_42	16239592	22 The activation of PKC might cause insulin resistance by ultimately inducing serine/tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1) sites, thereby inhibiting IRS-1 binding and activation of phosphoinositol 3-kinase.	bind
29197	2	7338	7	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL				IRS-1	NULL	phosphorylation of	serine/tyrosine sites		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_28_s_42	16239592	22 The activation of PKC might cause insulin resistance by ultimately inducing serine/tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1) sites, thereby inhibiting IRS-1 binding and activation of phosphoinositol 3-kinase.	bind
29198	3	7338	7	10	NULL	0	NULL	IRS-1			is					insulin receptor substrate 1					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_28_s_42	16239592	22 The activation of PKC might cause insulin resistance by ultimately inducing serine/tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1) sites, thereby inhibiting IRS-1 binding and activation of phosphoinositol 3-kinase.	bind
29199	4	7338	7	NULL	NULL	0	NULL	statement 2	NULL		activates	NULL				phosphoinositol 3-kinase	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_28_s_42	16239592	22 The activation of PKC might cause insulin resistance by ultimately inducing serine/tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1) sites, thereby inhibiting IRS-1 binding and activation of phosphoinositol 3-kinase.	bind
29200	5	7338	7	NULL	NULL	0	NULL	statement 2	NULL		inhibits	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_28_s_42	16239592	22 The activation of PKC might cause insulin resistance by ultimately inducing serine/tyrosine phosphorylation of insulin receptor substrate 1 (IRS-1) sites, thereby inhibiting IRS-1 binding and activation of phosphoinositol 3-kinase.	bind
26820	1	7339	5	13	NULL	NULL	NULL	heparin	Chemical		decrease		may			RLP-SMC	Process	interaction of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_108_21_2679_s_152	14623816	22 Thus, heparin and heparitinase may not only decrease RLP-SMC interaction but also interfere with the binding of soluble HB-EGF generated by RLPs to EGF receptor.	bind
26821	2	7339	5	13	NULL	NULL	NULL	heparitinase	GP		decreases		may			RLP-SMC	Process	interaction of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_108_21_2679_s_152	14623816	22 Thus, heparin and heparitinase may not only decrease RLP-SMC interaction but also interfere with the binding of soluble HB-EGF generated by RLPs to EGF receptor.	bind
26822	3	7339	5	13	NULL	NULL	NULL	HB-EGF	GP	soluble	is generated by					RLPs	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_108_21_2679_s_152	14623816	22 Thus, heparin and heparitinase may not only decrease RLP-SMC interaction but also interfere with the binding of soluble HB-EGF generated by RLPs to EGF receptor.	bind
26823	4	7339	5	13	NULL	NULL	NULL	statement 3	GP		bind					EGF receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_108_21_2679_s_152	14623816	22 Thus, heparin and heparitinase may not only decrease RLP-SMC interaction but also interfere with the binding of soluble HB-EGF generated by RLPs to EGF receptor.	bind
26824	5	7339	5	13	NULL	NULL	NULL	heparin	Chemical		interferes with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_108_21_2679_s_152	14623816	22 Thus, heparin and heparitinase may not only decrease RLP-SMC interaction but also interfere with the binding of soluble HB-EGF generated by RLPs to EGF receptor.	bind
26825	6	7339	5	13	NULL	NULL	NULL	heparitinase	GP		interferes with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_108_21_2679_s_152	14623816	22 Thus, heparin and heparitinase may not only decrease RLP-SMC interaction but also interfere with the binding of soluble HB-EGF generated by RLPs to EGF receptor.	bind
29201	1	7339	7	NULL	NULL	0	NULL	RLP	NULL		interacts with	NULL				SMC	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_108_21_2679_s_152	14623816	22 Thus, heparin and heparitinase may not only decrease RLP-SMC interaction but also interfere with the binding of soluble HB-EGF generated by RLPs to EGF receptor.	bind
29202	2	7339	7	NULL	NULL	0	NULL	HB-EGF	NULL	soluble	binds to	NULL				EGF receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_108_21_2679_s_152	14623816	22 Thus, heparin and heparitinase may not only decrease RLP-SMC interaction but also interfere with the binding of soluble HB-EGF generated by RLPs to EGF receptor.	bind
29203	3	7339	7	NULL	NULL	0	NULL	heparin	NULL		decrease	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulation_108_21_2679_s_152	14623816	22 Thus, heparin and heparitinase may not only decrease RLP-SMC interaction but also interfere with the binding of soluble HB-EGF generated by RLPs to EGF receptor.	bind
29204	4	7339	7	NULL	NULL	0	NULL	heparitinase	NULL		decrease	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulation_108_21_2679_s_152	14623816	22 Thus, heparin and heparitinase may not only decrease RLP-SMC interaction but also interfere with the binding of soluble HB-EGF generated by RLPs to EGF receptor.	bind
29205	5	7339	7	NULL	NULL	0	NULL	heparin	NULL		interferes with	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulation_108_21_2679_s_152	14623816	22 Thus, heparin and heparitinase may not only decrease RLP-SMC interaction but also interfere with the binding of soluble HB-EGF generated by RLPs to EGF receptor.	bind
29206	6	7339	7	NULL	NULL	0	NULL	heparitinase	NULL		interferes with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_108_21_2679_s_152	14623816	22 Thus, heparin and heparitinase may not only decrease RLP-SMC interaction but also interfere with the binding of soluble HB-EGF generated by RLPs to EGF receptor.	bind
29207	7	7339	7	NULL	NULL	0	NULL	RLP	NULL		generates	NULL				HB-EGF	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_108_21_2679_s_152	14623816	22 Thus, heparin and heparitinase may not only decrease RLP-SMC interaction but also interfere with the binding of soluble HB-EGF generated by RLPs to EGF receptor.	bind
26826	1	7340	5	13	NULL	NULL	NULL	elastin	GP		mediate					calcification	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_6_1981_s_143	11733347	22 With respect to elastin-mediated calcification, both MMP-2 and MMP-9 are known to bind insoluble elastin, 8  and each have been shown to be actively involved in elastin degradation.	bind
26827	2	7340	5	13	NULL	NULL	NULL	MMP-2	GP		bind					elastin	GP	insoluble			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_6_1981_s_143	11733347	22 With respect to elastin-mediated calcification, both MMP-2 and MMP-9 are known to bind insoluble elastin, 8  and each have been shown to be actively involved in elastin degradation.	bind
26828	3	7340	5	13	NULL	NULL	NULL	MMP-9	GP		bind					elastin	GP	insoluble			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_6_1981_s_143	11733347	22 With respect to elastin-mediated calcification, both MMP-2 and MMP-9 are known to bind insoluble elastin, 8  and each have been shown to be actively involved in elastin degradation.	bind
26829	4	7340	5	13	NULL	NULL	NULL	MMP-2	GP		is involved in		actively			elastin	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_6_1981_s_143	11733347	22 With respect to elastin-mediated calcification, both MMP-2 and MMP-9 are known to bind insoluble elastin, 8  and each have been shown to be actively involved in elastin degradation.	bind
26830	5	7340	5	13	NULL	NULL	NULL	MMP-9	GP		is involved in		actively			elastin	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_6_1981_s_143	11733347	22 With respect to elastin-mediated calcification, both MMP-2 and MMP-9 are known to bind insoluble elastin, 8  and each have been shown to be actively involved in elastin degradation.	bind
29208	1	7340	7	NULL	NULL	0	NULL	MMP-2	NULL		bind	NULL				elastin	NULL	insoluble			NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_6_1981_s_143	11733347	22 With respect to elastin-mediated calcification, both MMP-2 and MMP-9 are known to bind insoluble elastin, 8  and each have been shown to be actively involved in elastin degradation.	bind
29209	2	7340	7	NULL	NULL	0	NULL	MMP-9	NULL		bind	NULL				elastin	NULL	insoluble			NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_6_1981_s_143	11733347	22 With respect to elastin-mediated calcification, both MMP-2 and MMP-9 are known to bind insoluble elastin, 8  and each have been shown to be actively involved in elastin degradation.	bind
29210	3	7340	7	NULL	NULL	0	NULL	MMP-2	NULL		involved in	NULL	actively			elastin	NULL	degradation of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_6_1981_s_143	11733347	22 With respect to elastin-mediated calcification, both MMP-2 and MMP-9 are known to bind insoluble elastin, 8  and each have been shown to be actively involved in elastin degradation.	bind
29211	4	7340	7	NULL	NULL	0	NULL	MMP-9	NULL		 involved in	NULL	actively			elastin	NULL	degradation of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_6_1981_s_143	11733347	22 With respect to elastin-mediated calcification, both MMP-2 and MMP-9 are known to bind insoluble elastin, 8  and each have been shown to be actively involved in elastin degradation.	bind
29212	5	7340	7	NULL	NULL	0	NULL	elastin	NULL		mediates	NULL				calcification	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_6_1981_s_143	11733347	22 With respect to elastin-mediated calcification, both MMP-2 and MMP-9 are known to bind insoluble elastin, 8  and each have been shown to be actively involved in elastin degradation.	bind
26831	1	7341	5	13	NULL	NULL	NULL	NO	Chemical	low levels of	is implicated in					lymphocyte	Cell	activation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_905_s_16	11891189	22, 23 Low levels of NO have also been implicated in lymphocyte activation and proliferation, increasing TNF-alpha production, nuclear factor-kappaB binding activity, and enhancing tyrosine kinase p56 activity.	bind
26832	2	7341	5	13	NULL	NULL	NULL	NO	Chemical	low levels of	is implicated in					lymphocyte	Cell	proliferation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_905_s_16	11891189	22, 23 Low levels of NO have also been implicated in lymphocyte activation and proliferation, increasing TNF-alpha production, nuclear factor-kappaB binding activity, and enhancing tyrosine kinase p56 activity.	bind
26833	3	7341	5	13	NULL	NULL	NULL	NO	Chemical	low levels of	is implicated in					TNF-alpha	GP	increasing production of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_905_s_16	11891189	22, 23 Low levels of NO have also been implicated in lymphocyte activation and proliferation, increasing TNF-alpha production, nuclear factor-kappaB binding activity, and enhancing tyrosine kinase p56 activity.	bind
26834	4	7341	5	13	NULL	NULL	NULL	NO	Chemical	low levels of	is implicated in					nuclear factor-kappaB	GP	binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_905_s_16	11891189	22, 23 Low levels of NO have also been implicated in lymphocyte activation and proliferation, increasing TNF-alpha production, nuclear factor-kappaB binding activity, and enhancing tyrosine kinase p56 activity.	bind
26835	5	7341	5	13	NULL	NULL	NULL	NO	Chemical	low levels of	is implicated in					tyrosine kinase p56	GP	enhancing activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_905_s_16	11891189	22, 23 Low levels of NO have also been implicated in lymphocyte activation and proliferation, increasing TNF-alpha production, nuclear factor-kappaB binding activity, and enhancing tyrosine kinase p56 activity.	bind
29213	1	7341	7	NULL	NULL	0	NULL	NO	NULL	low levels of	is implicated in	NULL				lymphocyte	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_905_s_16	11891189	22, 23 Low levels of NO have also been implicated in lymphocyte activation and proliferation, increasing TNF-alpha production, nuclear factor-kappaB binding activity, and enhancing tyrosine kinase p56 activity.	bind
29214	2	7341	7	NULL	NULL	0	NULL	NO	NULL	low levels of	implicated in	NULL				lymphocyte	NULL	proliferation of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_3_905_s_16	11891189	22, 23 Low levels of NO have also been implicated in lymphocyte activation and proliferation, increasing TNF-alpha production, nuclear factor-kappaB binding activity, and enhancing tyrosine kinase p56 activity.	bind
29215	3	7341	7	NULL	NULL	0	NULL	NO	NULL	low levels of	increase	NULL				TNF-alpha	NULL	production of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_3_905_s_16	11891189	22, 23 Low levels of NO have also been implicated in lymphocyte activation and proliferation, increasing TNF-alpha production, nuclear factor-kappaB binding activity, and enhancing tyrosine kinase p56 activity.	bind
29216	4	7341	7	NULL	NULL	0	NULL	NO	NULL	low levels of	increase	NULL				 nuclear factor-kappaB	NULL	binding activity of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_3_905_s_16	11891189	22, 23 Low levels of NO have also been implicated in lymphocyte activation and proliferation, increasing TNF-alpha production, nuclear factor-kappaB binding activity, and enhancing tyrosine kinase p56 activity.	bind
29217	5	7341	7	NULL	NULL	0	NULL	NO	NULL	low levels of	enhance	NULL				tyrosine kinase p56 	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_3_905_s_16	11891189	22, 23 Low levels of NO have also been implicated in lymphocyte activation and proliferation, increasing TNF-alpha production, nuclear factor-kappaB binding activity, and enhancing tyrosine kinase p56 activity.	bind
26836	1	7343	5	13	NULL	NULL	NULL	IFN-gammaR	GP		is					IFN-gamma receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1549_s_26	10329607	22- 27  However, it is still unresolved whether IFN-gamma, which binds to the IFN-gamma receptor (IFN-gammaR), and/or TNF-alpha, which binds to the TNFR1 in its soluble form 28  and to the TNFR2 in its membranous form, 29  are crucial for the activation of cerebral endothelium, microglia, and astrocytes  in vivo.	bind
26837	2	7343	5	13	NULL	NULL	NULL	IFN-gamma	GP		bind					IFN-gammaR	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1549_s_26	10329607	22- 27  However, it is still unresolved whether IFN-gamma, which binds to the IFN-gamma receptor (IFN-gammaR), and/or TNF-alpha, which binds to the TNFR1 in its soluble form 28  and to the TNFR2 in its membranous form, 29  are crucial for the activation of cerebral endothelium, microglia, and astrocytes  in vivo.	bind
26838	3	7343	5	13	NULL	NULL	NULL	TNF-alpha	GP		bind					TNFR1	GP	soluble			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1549_s_26	10329607	22- 27  However, it is still unresolved whether IFN-gamma, which binds to the IFN-gamma receptor (IFN-gammaR), and/or TNF-alpha, which binds to the TNFR1 in its soluble form 28  and to the TNFR2 in its membranous form, 29  are crucial for the activation of cerebral endothelium, microglia, and astrocytes  in vivo.	bind
26839	4	7343	5	13	NULL	NULL	NULL	TNF-alpha	GP		bind					TNFR2	GP	membranous form			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1549_s_26	10329607	22- 27  However, it is still unresolved whether IFN-gamma, which binds to the IFN-gamma receptor (IFN-gammaR), and/or TNF-alpha, which binds to the TNFR1 in its soluble form 28  and to the TNFR2 in its membranous form, 29  are crucial for the activation of cerebral endothelium, microglia, and astrocytes  in vivo.	bind
29219	1	7343	7	NULL	NULL	0	NULL	IFN-gamma	NULL		binds to	NULL				IFN-gammaR	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_5_1549_s_26	10329607	22- 27  However, it is still unresolved whether IFN-gamma, which binds to the IFN-gamma receptor (IFN-gammaR), and/or TNF-alpha, which binds to the TNFR1 in its soluble form 28  and to the TNFR2 in its membranous form, 29  are crucial for the activation of cerebral endothelium, microglia, and astrocytes  in vivo.	bind
29220	2	7343	7	NULL	NULL	0	NULL	TNF-alpha	NULL		binds to	NULL				TNFR1	NULL	soluble form			NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_5_1549_s_26	10329607	22- 27  However, it is still unresolved whether IFN-gamma, which binds to the IFN-gamma receptor (IFN-gammaR), and/or TNF-alpha, which binds to the TNFR1 in its soluble form 28  and to the TNFR2 in its membranous form, 29  are crucial for the activation of cerebral endothelium, microglia, and astrocytes  in vivo.	bind
29221	3	7343	7	NULL	NULL	0	NULL	TNF-alpha	NULL		binds to	NULL				TNFR2	NULL	membranous form			NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_5_1549_s_26	10329607	22- 27  However, it is still unresolved whether IFN-gamma, which binds to the IFN-gamma receptor (IFN-gammaR), and/or TNF-alpha, which binds to the TNFR1 in its soluble form 28  and to the TNFR2 in its membranous form, 29  are crucial for the activation of cerebral endothelium, microglia, and astrocytes  in vivo.	bind
29222	4	7343	7	NULL	NULL	0	NULL	IFN-gammaR	NULL		is	NULL				IFN-gamma receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_5_1549_s_26	10329607	22- 27  However, it is still unresolved whether IFN-gamma, which binds to the IFN-gamma receptor (IFN-gammaR), and/or TNF-alpha, which binds to the TNFR1 in its soluble form 28  and to the TNFR2 in its membranous form, 29  are crucial for the activation of cerebral endothelium, microglia, and astrocytes  in vivo.	bind
26840	1	7344	5	13	NULL	NULL	NULL	HLA-E leader sequence	GP		does not bind			MVDGTLLLL		HLA-E	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_currbiol_8_1_1_s_90	9427624	221 cells at 26 degrees C in the presence of exogenous added peptides: MVDGTLLLL from HLA-E leader sequence which is not capable of binding to HLA-E  in vitro and VMAPRTVLL from HLA-B 0801 which can bind to HLA-E.	bind
26841	2	7344	5	13	NULL	NULL	NULL	HLA-B 0801	GP		bind			VMAPRTVLL		HLA-E	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_1_1_s_90	9427624	221 cells at 26 degrees C in the presence of exogenous added peptides: MVDGTLLLL from HLA-E leader sequence which is not capable of binding to HLA-E  in vitro and VMAPRTVLL from HLA-B 0801 which can bind to HLA-E.	bind
29224	1	7344	7	NULL	NULL	0	NULL	HLA-E leader sequence	NULL		does not bind	NULL		MVDGTLLLL		HLA-E	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_currbiol_8_1_1_s_90	9427624	221 cells at 26 degrees C in the presence of exogenous added peptides: MVDGTLLLL from HLA-E leader sequence which is not capable of binding to HLA-E  in vitro and VMAPRTVLL from HLA-B 0801 which can bind to HLA-E.	bind
29225	2	7344	7	NULL	NULL	0	NULL	HLA-B 0801	NULL		binds to	NULL		VMAPRTVLL 		HLA-E	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_8_1_1_s_90	9427624	221 cells at 26 degrees C in the presence of exogenous added peptides: MVDGTLLLL from HLA-E leader sequence which is not capable of binding to HLA-E  in vitro and VMAPRTVLL from HLA-B 0801 which can bind to HLA-E.	bind
26842	1	7345	5	13	NULL	NULL	NULL	HLA-A 0201	GP		bind			leader sequence peptide		HLA-E	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_1_1_s_107	9427624	221 cells transfected with HLA-A 0201, whose leader sequence peptide binds to HLA-E  [25]  .	bind
29226	1	7345	7	NULL	NULL	0	NULL	HLA-A 0201	NULL		binds to	NULL		leader sequence peptide		HLA-E	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_8_1_1_s_107	9427624	221 cells transfected with HLA-A 0201, whose leader sequence peptide binds to HLA-E  [25]  .	bind
26844	1	7346	5	13	NULL	NULL	NULL				bind			ralpha2I domain		collagen type I	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3513_s_277	9920897	229ox peptide inhibits ralpha2I domain binding to collagens type I and IV and to laminin-1.	bind
26845	2	7346	5	13	NULL	NULL	NULL				bind			ralpha2I domain		collagen type IV	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3513_s_277	9920897	229ox peptide inhibits ralpha2I domain binding to collagens type I and IV and to laminin-1.	bind
26846	3	7346	5	13	NULL	NULL	NULL				bind			ralpha2I domain		laminin-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3513_s_277	9920897	229ox peptide inhibits ralpha2I domain binding to collagens type I and IV and to laminin-1.	bind
26847	4	7346	5	13	NULL	NULL	NULL	229ox peptide	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3513_s_277	9920897	229ox peptide inhibits ralpha2I domain binding to collagens type I and IV and to laminin-1.	bind
26848	5	7346	5	13	NULL	NULL	NULL	229ox peptide	GP		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3513_s_277	9920897	229ox peptide inhibits ralpha2I domain binding to collagens type I and IV and to laminin-1.	bind
26849	6	7346	5	13	NULL	NULL	NULL	229ox peptide	GP		inhibit					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3513_s_277	9920897	229ox peptide inhibits ralpha2I domain binding to collagens type I and IV and to laminin-1.	bind
29227	1	7346	7	NULL	NULL	0	NULL		NULL		binds to	NULL		ralpha2I domain		collagen type I	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3513_s_277	9920897	229ox peptide inhibits ralpha2I domain binding to collagens type I and IV and to laminin-1.	bind
29228	2	7346	7	NULL	NULL	0	NULL		NULL		binds to	NULL		ralpha2I domain		collagen type IV	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3513_s_277	9920897	229ox peptide inhibits ralpha2I domain binding to collagens type I and IV and to laminin-1.	bind
29229	3	7346	7	NULL	NULL	0	NULL		NULL		binds to	NULL		ralpha2I domain		laminin-1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3513_s_277	9920897	229ox peptide inhibits ralpha2I domain binding to collagens type I and IV and to laminin-1.	bind
29230	4	7346	7	NULL	NULL	0	NULL	ox peptide	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3513_s_277	9920897	229ox peptide inhibits ralpha2I domain binding to collagens type I and IV and to laminin-1.	bind
29231	5	7346	7	NULL	NULL	0	NULL	ox peptide	NULL		inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3513_s_277	9920897	229ox peptide inhibits ralpha2I domain binding to collagens type I and IV and to laminin-1.	bind
29232	6	7346	7	NULL	NULL	0	NULL	ox peptide	NULL		inhibits	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3513_s_277	9920897	229ox peptide inhibits ralpha2I domain binding to collagens type I and IV and to laminin-1.	bind
26850	1	7347	5	13	NULL	NULL	NULL	snR10	NucleicAcid		is a type of					small nucleolar RNAs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_264	11160879	23       Bagni,C. and Lapeyre,B. (1998) Gar1p binds to the small nucleolar RNAs snR10 and snR30 in vitro through a nontypical RNA binding element.	bind
26851	2	7347	5	13	NULL	NULL	NULL	snR30	NucleicAcid		is a type of					small nucleolar RNAs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_264	11160879	23       Bagni,C. and Lapeyre,B. (1998) Gar1p binds to the small nucleolar RNAs snR10 and snR30 in vitro through a nontypical RNA binding element.	bind
26852	3	7347	5	13	NULL	NULL	NULL	Gar1p	GP		bind			nontypical RNA binding element		snR10	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_264	11160879	23       Bagni,C. and Lapeyre,B. (1998) Gar1p binds to the small nucleolar RNAs snR10 and snR30 in vitro through a nontypical RNA binding element.	bind
26853	4	7347	5	13	NULL	NULL	NULL	Gar1p	GP		bind			nontypical RNA binding element		snR30	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_264	11160879	23       Bagni,C. and Lapeyre,B. (1998) Gar1p binds to the small nucleolar RNAs snR10 and snR30 in vitro through a nontypical RNA binding element.	bind
29233	1	7347	7	NULL	NULL	0	NULL	Gar1p	NULL		binds to	NULL				snR10	NULL		nontypical RNA binding element		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_264	11160879	23       Bagni,C. and Lapeyre,B. (1998) Gar1p binds to the small nucleolar RNAs snR10 and snR30 in vitro through a nontypical RNA binding element.	bind
29234	2	7347	7	NULL	NULL	0	NULL	Gar1p	NULL		binds to	NULL				snR30	NULL		nontypical RNA binding element		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_264	11160879	23       Bagni,C. and Lapeyre,B. (1998) Gar1p binds to the small nucleolar RNAs snR10 and snR30 in vitro through a nontypical RNA binding element.	bind
29235	3	7347	7	NULL	NULL	0	NULL	snR10	NULL		is a type of	NULL				small nucleolar RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_264	11160879	23       Bagni,C. and Lapeyre,B. (1998) Gar1p binds to the small nucleolar RNAs snR10 and snR30 in vitro through a nontypical RNA binding element.	bind
29236	4	7347	7	NULL	NULL	0	NULL	snR30	NULL		is a type of	NULL				small nucleolar RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_264	11160879	23       Bagni,C. and Lapeyre,B. (1998) Gar1p binds to the small nucleolar RNAs snR10 and snR30 in vitro through a nontypical RNA binding element.	bind
26854	1	7348	5	13	NULL	NULL	NULL	Ral	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_35	11397694	23  Binding to calmodulin enhances GTP binding to Ral 2- to 3-fold.	bind
26855	2	7348	5	13	NULL	NULL	NULL	calmodulin	GP	binding to	enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_35	11397694	23  Binding to calmodulin enhances GTP binding to Ral 2- to 3-fold.	bind
29237	1	7348	7	NULL	NULL	0	NULL	GTP	NULL		binds	NULL				Ral	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_35	11397694	23  Binding to calmodulin enhances GTP binding to Ral 2- to 3-fold.	bind
29238	2	7348	7	NULL	NULL	0	NULL	calmodulin	NULL	binding to	enhances	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_899_s_35	11397694	23  Binding to calmodulin enhances GTP binding to Ral 2- to 3-fold.	bind
26856	1	7349	5	13	NULL	NULL	NULL	CD80	GP		bind					CTLA4	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_977_s_175	11238045	23  CD80 and CD86 also bind CTLA4, an Ig superfamily member with homology to CD28, which delivers a negative signal to activated T cells.	bind
26857	2	7349	5	13	NULL	NULL	NULL	CD86	GP		bind					CTLA4	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_977_s_175	11238045	23  CD80 and CD86 also bind CTLA4, an Ig superfamily member with homology to CD28, which delivers a negative signal to activated T cells.	bind
26858	3	7349	5	13	NULL	NULL	NULL	CTLA4	GP		is a member of					Ig superfamily	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_977_s_175	11238045	23  CD80 and CD86 also bind CTLA4, an Ig superfamily member with homology to CD28, which delivers a negative signal to activated T cells.	bind
26859	4	7349	5	13	NULL	NULL	NULL	CTLA4	GP		is homologous to					CD28	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_977_s_175	11238045	23  CD80 and CD86 also bind CTLA4, an Ig superfamily member with homology to CD28, which delivers a negative signal to activated T cells.	bind
26860	5	7349	5	13	NULL	NULL	NULL	CTLA4	GP		delivers					T cells	Cell	negative signal to activated			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_977_s_175	11238045	23  CD80 and CD86 also bind CTLA4, an Ig superfamily member with homology to CD28, which delivers a negative signal to activated T cells.	bind
29239	1	7349	7	NULL	NULL	0	NULL	CD80	NULL		bind	NULL				CTLA4	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_977_s_175	11238045	23  CD80 and CD86 also bind CTLA4, an Ig superfamily member with homology to CD28, which delivers a negative signal to activated T cells.	bind
29240	2	7349	7	NULL	NULL	0	NULL	CD86	NULL		bind	NULL				CTLA4	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_977_s_175	11238045	23  CD80 and CD86 also bind CTLA4, an Ig superfamily member with homology to CD28, which delivers a negative signal to activated T cells.	bind
29241	3	7349	7	10	NULL	0	NULL	CTLA4			is a member of					Ig superfamily					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_977_s_175	11238045	23  CD80 and CD86 also bind CTLA4, an Ig superfamily member with homology to CD28, which delivers a negative signal to activated T cells.	bind
29242	4	7349	7	NULL	NULL	0	NULL	CTLA4	NULL		is homologous to	NULL				CD28	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_977_s_175	11238045	23  CD80 and CD86 also bind CTLA4, an Ig superfamily member with homology to CD28, which delivers a negative signal to activated T cells.	bind
29243	5	7349	7	NULL	NULL	0	NULL	CTLA4	NULL		delivers	NULL				T cells	NULL	negative signal to activated			NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_977_s_175	11238045	23  CD80 and CD86 also bind CTLA4, an Ig superfamily member with homology to CD28, which delivers a negative signal to activated T cells.	bind
26861	1	7350	5	13	NULL	NULL	NULL	FK506	Chemical		is more potent than					CsA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_24_2449_s_148	10595959	23  FK506 is 10 to 100 times more potent than CsA. 24  FK506 binds to FK506 binding protein (FKBP), and the FK506/FKBP complex inhibits calcineurin.	bind
26862	2	7350	5	13	NULL	NULL	NULL	FKBP	GP		is					FK506 binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_24_2449_s_148	10595959	23  FK506 is 10 to 100 times more potent than CsA. 24  FK506 binds to FK506 binding protein (FKBP), and the FK506/FKBP complex inhibits calcineurin.	bind
26863	3	7350	5	13	NULL	NULL	NULL	FK506	Chemical		bind					FKBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_24_2449_s_148	10595959	23  FK506 is 10 to 100 times more potent than CsA. 24  FK506 binds to FK506 binding protein (FKBP), and the FK506/FKBP complex inhibits calcineurin.	bind
26864	4	7350	5	13	NULL	NULL	NULL	FK506/FKBP complex	GP		inhibit					calcineurin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_24_2449_s_148	10595959	23  FK506 is 10 to 100 times more potent than CsA. 24  FK506 binds to FK506 binding protein (FKBP), and the FK506/FKBP complex inhibits calcineurin.	bind
29244	1	7350	7	NULL	NULL	0	NULL	FK506	NULL		is more potent than	NULL				CsA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_24_2449_s_148	10595959	23  FK506 is 10 to 100 times more potent than CsA. 24  FK506 binds to FK506 binding protein (FKBP), and the FK506/FKBP complex inhibits calcineurin.	bind
29245	2	7350	7	NULL	NULL	0	NULL	 FK506	NULL		binds	NULL				FKBP	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_24_2449_s_148	10595959	23  FK506 is 10 to 100 times more potent than CsA. 24  FK506 binds to FK506 binding protein (FKBP), and the FK506/FKBP complex inhibits calcineurin.	bind
29246	3	7350	7	NULL	NULL	0	NULL	FK506/FKBP complex	NULL		inhibits	NULL				calcineurin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_24_2449_s_148	10595959	23  FK506 is 10 to 100 times more potent than CsA. 24  FK506 binds to FK506 binding protein (FKBP), and the FK506/FKBP complex inhibits calcineurin.	bind
29247	4	7350	7	NULL	NULL	0	NULL	FKBP	NULL		is	NULL				FK506 binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_24_2449_s_148	10595959	23  FK506 is 10 to 100 times more potent than CsA. 24  FK506 binds to FK506 binding protein (FKBP), and the FK506/FKBP complex inhibits calcineurin.	bind
26865	2	7351	5	13	NULL	NULL	NULL	IL-13Ralpha2	GP		is inhibitor of		potent			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_5_1475_s_105	12707030	23  IL-13Ralpha2 acts as a potent inhibitor of IL-13 binding to its cell surface receptor leading to the initial suggestion 24  and later demonstration 26,27 that it modulates the effects of IL-13  in vivo.	bind
26866	1	7351	5	13	NULL	NULL	NULL	IL-13	GP		bind					cell surface receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_5_1475_s_105	12707030	23  IL-13Ralpha2 acts as a potent inhibitor of IL-13 binding to its cell surface receptor leading to the initial suggestion 24  and later demonstration 26,27 that it modulates the effects of IL-13  in vivo.	bind
26867	3	7351	5	13	NULL	NULL	NULL	IL-13Ralpha2	GP		modulates					IL-13	GP	effects of			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_amjpathol_162_5_1475_s_105	12707030	23  IL-13Ralpha2 acts as a potent inhibitor of IL-13 binding to its cell surface receptor leading to the initial suggestion 24  and later demonstration 26,27 that it modulates the effects of IL-13  in vivo.	bind
29248	1	7351	7	NULL	NULL	0	NULL	IL-13	NULL		binds to	NULL				cell surface receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_162_5_1475_s_105	12707030	23  IL-13Ralpha2 acts as a potent inhibitor of IL-13 binding to its cell surface receptor leading to the initial suggestion 24  and later demonstration 26,27 that it modulates the effects of IL-13  in vivo.	bind
29249	2	7351	7	NULL	NULL	0	NULL	IL-13Ralpha2	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_162_5_1475_s_105	12707030	23  IL-13Ralpha2 acts as a potent inhibitor of IL-13 binding to its cell surface receptor leading to the initial suggestion 24  and later demonstration 26,27 that it modulates the effects of IL-13  in vivo.	bind
29250	3	7351	7	NULL	NULL	0	NULL	IL-13Ralpha2	NULL		modulates	NULL				IL-13	NULL	effects of			NULL	in vivo	0	NULL	NULL	NULL	gw60_amjpathol_162_5_1475_s_105	12707030	23  IL-13Ralpha2 acts as a potent inhibitor of IL-13 binding to its cell surface receptor leading to the initial suggestion 24  and later demonstration 26,27 that it modulates the effects of IL-13  in vivo.	bind
26868	1	7352	5	13	NULL	NULL	NULL	PAI-1	GP		is inhibitor of					serpin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_6_1095_s_45	7586221	23  PAI-1 is a serpin inhibitor that endogenously binds and inactivates plasminogen activators such as TPA and UPA.	bind
26869	2	7352	5	13	NULL	NULL	NULL	TPA	GP		is a type of					plasminogen activator	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_6_1095_s_45	7586221	23  PAI-1 is a serpin inhibitor that endogenously binds and inactivates plasminogen activators such as TPA and UPA.	bind
26870	3	7352	5	13	NULL	NULL	NULL	UPA	GP		is a type of					plasminogen activator	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_6_1095_s_45	7586221	23  PAI-1 is a serpin inhibitor that endogenously binds and inactivates plasminogen activators such as TPA and UPA.	bind
26871	4	7352	5	13	NULL	NULL	NULL	PAI-1	GP		bind		endogenously			TPA	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_6_1095_s_45	7586221	23  PAI-1 is a serpin inhibitor that endogenously binds and inactivates plasminogen activators such as TPA and UPA.	bind
26872	5	7352	5	13	NULL	NULL	NULL	PAI-1	GP		inactivates		endogenously			TPA	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_6_1095_s_45	7586221	23  PAI-1 is a serpin inhibitor that endogenously binds and inactivates plasminogen activators such as TPA and UPA.	bind
26873	6	7352	5	13	NULL	NULL	NULL	PAI-1	GP		bind		endogenously			UPA	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_6_1095_s_45	7586221	23  PAI-1 is a serpin inhibitor that endogenously binds and inactivates plasminogen activators such as TPA and UPA.	bind
26874	7	7352	5	13	NULL	NULL	NULL	PAI-1	GP		inactivates		endogenously			UPA	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_6_1095_s_45	7586221	23  PAI-1 is a serpin inhibitor that endogenously binds and inactivates plasminogen activators such as TPA and UPA.	bind
29251	1	7352	7	NULL	NULL	0	NULL	PAI-1	NULL		is a type of	NULL				serpin inhibitor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_77_6_1095_s_45	7586221	23  PAI-1 is a serpin inhibitor that endogenously binds and inactivates plasminogen activators such as TPA and UPA.	bind
29252	2	7352	7	NULL	NULL	0	NULL	PAI-1	NULL		binds	NULL	endogenously			TPA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_6_1095_s_45	7586221	23  PAI-1 is a serpin inhibitor that endogenously binds and inactivates plasminogen activators such as TPA and UPA.	bind
29253	3	7352	7	NULL	NULL	0	NULL	PAI-1	NULL		binds 	NULL	endogenously			UPA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_6_1095_s_45	7586221	23  PAI-1 is a serpin inhibitor that endogenously binds and inactivates plasminogen activators such as TPA and UPA.	bind
29254	4	7352	7	10	NULL	0	NULL	PAI-1			inactivates		endogenously			TPA					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_6_1095_s_45	7586221	23  PAI-1 is a serpin inhibitor that endogenously binds and inactivates plasminogen activators such as TPA and UPA.	bind
29255	5	7352	7	10	NULL	0	NULL	PAI-1			inactivates		endogenously			UPA					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_6_1095_s_45	7586221	23  PAI-1 is a serpin inhibitor that endogenously binds and inactivates plasminogen activators such as TPA and UPA.	bind
29256	6	7352	7	NULL	NULL	0	NULL	TPA	NULL		is a type of	NULL				plasminogen activator	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_77_6_1095_s_45	7586221	23  PAI-1 is a serpin inhibitor that endogenously binds and inactivates plasminogen activators such as TPA and UPA.	bind
29257	7	7352	7	NULL	NULL	0	NULL	uPA	NULL		is a type of	NULL				plasminogen activator	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_77_6_1095_s_45	7586221	23  PAI-1 is a serpin inhibitor that endogenously binds and inactivates plasminogen activators such as TPA and UPA.	bind
26875	1	7353	5	13	NULL	NULL	NULL	KDR	GP		bind					bFGF	GP				NULL	KS cells	NULL	NULL	NULL	NULL	gw60_amjpathol_156_4_1381_s_119	10751362	23  Supernatants from KS cells, 27  which contain bFGF and VEGF, and Tat, which binds the VEGF receptor KDR, 28 strongly induce angiogenesis.	bind
26876	2	7353	5	13	NULL	NULL	NULL	KDR	GP		bind					VEGF	GP				NULL	KS cells	NULL	NULL	NULL	NULL	gw60_amjpathol_156_4_1381_s_119	10751362	23  Supernatants from KS cells, 27  which contain bFGF and VEGF, and Tat, which binds the VEGF receptor KDR, 28 strongly induce angiogenesis.	bind
26918	3	7353	5	13	NULL	NULL	NULL	KDR	GP		is a type of					VEGF receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_4_1381_s_119	10751362	23  Supernatants from KS cells, 27  which contain bFGF and VEGF, and Tat, which binds the VEGF receptor KDR, 28 strongly induce angiogenesis.	bind
26919	4	7353	5	13	NULL	NULL	NULL	Tat	GP		bind					KDR	GP				NULL	KS cells	NULL	NULL	NULL	NULL	gw60_amjpathol_156_4_1381_s_119	10751362	23  Supernatants from KS cells, 27  which contain bFGF and VEGF, and Tat, which binds the VEGF receptor KDR, 28 strongly induce angiogenesis.	bind
27039	5	7353	5	13	NULL	NULL	NULL	statement 1	Process		induces		strongly			angiogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_4_1381_s_119	10751362	23  Supernatants from KS cells, 27  which contain bFGF and VEGF, and Tat, which binds the VEGF receptor KDR, 28 strongly induce angiogenesis.	bind
27040	6	7353	5	13	NULL	NULL	NULL	statement 2	Process		induces		strongly			angiogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_4_1381_s_119	10751362	23  Supernatants from KS cells, 27  which contain bFGF and VEGF, and Tat, which binds the VEGF receptor KDR, 28 strongly induce angiogenesis.	bind
27041	7	7353	5	13	NULL	NULL	NULL	statement 4	Process		induces		strongly			angiogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_4_1381_s_119	10751362	23  Supernatants from KS cells, 27  which contain bFGF and VEGF, and Tat, which binds the VEGF receptor KDR, 28 strongly induce angiogenesis.	bind
29258	1	7353	7	NULL	NULL	0	NULL	bFGF	NULL		binds	NULL				KDR	NULL				NULL	KS cells	NULL	NULL	NULL	NULL	gw60_amjpathol_156_4_1381_s_119	10751362	23  Supernatants from KS cells, 27  which contain bFGF and VEGF, and Tat, which binds the VEGF receptor KDR, 28 strongly induce angiogenesis.	bind
29259	2	7353	7	NULL	NULL	0	NULL	VEGF	NULL		binds	NULL				KDR	NULL				NULL	KS cells	NULL	NULL	NULL	NULL	gw60_amjpathol_156_4_1381_s_119	10751362	23  Supernatants from KS cells, 27  which contain bFGF and VEGF, and Tat, which binds the VEGF receptor KDR, 28 strongly induce angiogenesis.	bind
29260	3	7353	7	NULL	NULL	0	NULL	Tat	NULL		binds	NULL				KDR	NULL				NULL	KS cells	NULL	NULL	NULL	NULL	gw60_amjpathol_156_4_1381_s_119	10751362	23  Supernatants from KS cells, 27  which contain bFGF and VEGF, and Tat, which binds the VEGF receptor KDR, 28 strongly induce angiogenesis.	bind
29261	4	7353	7	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL	strongly			angiogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_4_1381_s_119	10751362	23  Supernatants from KS cells, 27  which contain bFGF and VEGF, and Tat, which binds the VEGF receptor KDR, 28 strongly induce angiogenesis.	bind
29262	5	7353	7	NULL	NULL	0	NULL	statement 2	NULL		induce	NULL	strongly			angiogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_4_1381_s_119	10751362	23  Supernatants from KS cells, 27  which contain bFGF and VEGF, and Tat, which binds the VEGF receptor KDR, 28 strongly induce angiogenesis.	bind
29263	6	7353	7	NULL	NULL	0	NULL	statement 3	NULL		induce	NULL	strongly			angiogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_4_1381_s_119	10751362	23  Supernatants from KS cells, 27  which contain bFGF and VEGF, and Tat, which binds the VEGF receptor KDR, 28 strongly induce angiogenesis.	bind
29265	7	7353	7	NULL	NULL	0	NULL	KDR	NULL		is a type of	NULL				VEGF receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_4_1381_s_119	10751362	23  Supernatants from KS cells, 27  which contain bFGF and VEGF, and Tat, which binds the VEGF receptor KDR, 28 strongly induce angiogenesis.	bind
27042	1	7354	5	13	NULL	NULL	NULL	FGF ligand	GP	binding of	requires							different	structural motifs within HS chains		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_17	11786412	23  The HS-binding regions of FGF ligand and RTK require different structural motifs within the HS chains for binding.	bind
27044	3	7354	5	13	NULL	NULL	NULL	RTK	GP	binding of	requires								structural motifs within HS chains		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_17	11786412	23  The HS-binding regions of FGF ligand and RTK require different structural motifs within the HS chains for binding.	bind
29271	1	7354	7	10	NULL	0	NULL	FGF ligand 	NULL	binding of	requires	NULL					NULL		structural motifs within the HS chains		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_17	11786412	23  The HS-binding regions of FGF ligand and RTK require different structural motifs within the HS chains for binding.	bind
29272	2	7354	7	10	NULL	0	NULL	RTK	NULL	binding of	requires	NULL					NULL		structural motifs within the HS chains		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_17	11786412	23  The HS-binding regions of FGF ligand and RTK require different structural motifs within the HS chains for binding.	bind
27047	1	7356	5	13	NULL	NULL	NULL	Src	GP		bind					PDGF beta-receptor	GP	autophosphorylated	phosphotyrosine residue 579		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_1_12_s_34	10400906	23 24  Activation occurs by the binding of  Src to the autophosphorylated PDGF beta-receptor at phosphotyrosine residues 579 and 581.	bind
27048	2	7356	5	13	NULL	NULL	NULL	statement 1	Process		leads to					activation	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_1_12_s_34	10400906	23 24  Activation occurs by the binding of  Src to the autophosphorylated PDGF beta-receptor at phosphotyrosine residues 579 and 581.	bind
27049	3	7356	5	13	NULL	NULL	NULL	Src	GP		bind					PDGF beta-receptor	GP	autophosphorylated	phosphotyrosine residue 581		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_1_12_s_34	10400906	23 24  Activation occurs by the binding of  Src to the autophosphorylated PDGF beta-receptor at phosphotyrosine residues 579 and 581.	bind
27050	4	7356	5	13	NULL	NULL	NULL	statement 3	Process		leads to					activation	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_1_12_s_34	10400906	23 24  Activation occurs by the binding of  Src to the autophosphorylated PDGF beta-receptor at phosphotyrosine residues 579 and 581.	bind
29344	1	7356	7	NULL	NULL	0	NULL	Src	NULL		binds	NULL				PDGF beta-receptor	NULL	autophosphorylated	phosphotyrosine residues 579 		NULL		0	NULL	NULL	NULL	gw60_circulationres_85_1_12_s_34	10400906	23 24  Activation occurs by the binding of  Src to the autophosphorylated PDGF beta-receptor at phosphotyrosine residues 579 and 581.	bind
29345	2	7356	7	NULL	NULL	0	NULL	Src	NULL		binds	NULL				PDGF beta-receptor	NULL	autophosphorylated	phosphotyrosine residues 581		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_1_12_s_34	10400906	23 24  Activation occurs by the binding of  Src to the autophosphorylated PDGF beta-receptor at phosphotyrosine residues 579 and 581.	bind
29346	3	7356	7	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				activation	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_1_12_s_34	10400906	23 24  Activation occurs by the binding of  Src to the autophosphorylated PDGF beta-receptor at phosphotyrosine residues 579 and 581.	bind
29347	4	7356	7	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				activation	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_1_12_s_34	10400906	23 24  Activation occurs by the binding of  Src to the autophosphorylated PDGF beta-receptor at phosphotyrosine residues 579 and 581.	bind
27051	1	7357	5	13	NULL	NULL	NULL	prothrombin	GP		bind		may			VLDLs	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_32	9445253	23 24 25  It is still unknown whether vitamin K - dependent proteins interact with TGRLP in vivo, although prothrombin and factor Xa may bind to VLDLs in vitro, partially through a calcium-dependent association.	bind
27052	2	7357	5	13	NULL	NULL	NULL	factor Xa	GP		bind		may			VLDLs	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_32	9445253	23 24 25  It is still unknown whether vitamin K - dependent proteins interact with TGRLP in vivo, although prothrombin and factor Xa may bind to VLDLs in vitro, partially through a calcium-dependent association.	bind
27053	3	7357	5	13	NULL	NULL	NULL	statement 1	Process		is dependent on		partially			calcium	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_32	9445253	23 24 25  It is still unknown whether vitamin K - dependent proteins interact with TGRLP in vivo, although prothrombin and factor Xa may bind to VLDLs in vitro, partially through a calcium-dependent association.	bind
27054	4	7357	5	13	NULL	NULL	NULL	statement 2	Process		is dependent on		partially			calcium	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_32	9445253	23 24 25  It is still unknown whether vitamin K - dependent proteins interact with TGRLP in vivo, although prothrombin and factor Xa may bind to VLDLs in vitro, partially through a calcium-dependent association.	bind
29348	1	7357	7	NULL	NULL	0	NULL	prothrombin	NULL		bind	NULL	may			VLDL	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_32	9445253	23 24 25  It is still unknown whether vitamin K - dependent proteins interact with TGRLP in vivo, although prothrombin and factor Xa may bind to VLDLs in vitro, partially through a calcium-dependent association.	bind
29349	2	7357	7	NULL	NULL	0	NULL	factor Xa	NULL		bind	NULL	may			VLDL	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_32	9445253	23 24 25  It is still unknown whether vitamin K - dependent proteins interact with TGRLP in vivo, although prothrombin and factor Xa may bind to VLDLs in vitro, partially through a calcium-dependent association.	bind
29350	3	7357	7	10	NULL	0	NULL	statement 1	NULL		is dependent on	NULL	partially			calcium	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_32	9445253	23 24 25  It is still unknown whether vitamin K - dependent proteins interact with TGRLP in vivo, although prothrombin and factor Xa may bind to VLDLs in vitro, partially through a calcium-dependent association.	bind
29351	4	7357	7	10	NULL	0	NULL	statement 2	NULL		is dependent on	NULL	partially			calcium	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_32	9445253	23 24 25  It is still unknown whether vitamin K - dependent proteins interact with TGRLP in vivo, although prothrombin and factor Xa may bind to VLDLs in vitro, partially through a calcium-dependent association.	bind
27056	1	7360	5	13	NULL	NULL	NULL	HDLs	GP	apoA-II - enriched	bind					SR-BI	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_4_638_s_91	11950703	23 However, although apoA-II - enriched HDLs bind to human SR-BI with higher affinity than apoA-I - rich HDLs, they display a lower capacity to deliver cholesteryl esters to human adrenal cells.	bind
27057	2	7360	5	13	NULL	NULL	NULL	HDLs	GP	apoA-I - rich	bind					SR-BI	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_4_638_s_91	11950703	23 However, although apoA-II - enriched HDLs bind to human SR-BI with higher affinity than apoA-I - rich HDLs, they display a lower capacity to deliver cholesteryl esters to human adrenal cells.	bind
27058	3	7360	5	13	NULL	NULL	NULL	statement 1	Process		has high affinity than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_4_638_s_91	11950703	23 However, although apoA-II - enriched HDLs bind to human SR-BI with higher affinity than apoA-I - rich HDLs, they display a lower capacity to deliver cholesteryl esters to human adrenal cells.	bind
27067	4	7360	5	13	NULL	NULL	NULL	cholesteryl esters	Chemical		is delivered to					adrenal cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_4_638_s_91	11950703	23 However, although apoA-II - enriched HDLs bind to human SR-BI with higher affinity than apoA-I - rich HDLs, they display a lower capacity to deliver cholesteryl esters to human adrenal cells.	bind
27070	5	7360	5	13	NULL	NULL	NULL	HDLs	GP	apoA-II - enriched	display					statement 4	Process	lower capacity to			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_4_638_s_91	11950703	23 However, although apoA-II - enriched HDLs bind to human SR-BI with higher affinity than apoA-I - rich HDLs, they display a lower capacity to deliver cholesteryl esters to human adrenal cells.	bind
29353	1	7360	7	NULL	NULL	0	NULL	HDLs	NULL	apoA-II - enriched	binds to	NULL				SR-BI 	NULL	human			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_4_638_s_91	11950703	23 However, although apoA-II - enriched HDLs bind to human SR-BI with higher affinity than apoA-I - rich HDLs, they display a lower capacity to deliver cholesteryl esters to human adrenal cells.	bind
29354	2	7360	7	NULL	NULL	0	NULL	HDLs	NULL	apoA-I - rich	binds to	NULL				SR-BI	NULL	human			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_4_638_s_91	11950703	23 However, although apoA-II - enriched HDLs bind to human SR-BI with higher affinity than apoA-I - rich HDLs, they display a lower capacity to deliver cholesteryl esters to human adrenal cells.	bind
29355	3	7360	7	NULL	NULL	0	NULL	statement 1	NULL		higher affinity than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_4_638_s_91	11950703	23 However, although apoA-II - enriched HDLs bind to human SR-BI with higher affinity than apoA-I - rich HDLs, they display a lower capacity to deliver cholesteryl esters to human adrenal cells.	bind
29357	4	7360	7	NULL	NULL	0	NULL	 cholesteryl esters	NULL		is delivered to	NULL				adrenal cells	NULL	human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_4_638_s_91	11950703	23 However, although apoA-II - enriched HDLs bind to human SR-BI with higher affinity than apoA-I - rich HDLs, they display a lower capacity to deliver cholesteryl esters to human adrenal cells.	bind
29358	5	7360	7	NULL	NULL	0	NULL	HDLs	NULL	apoA-II - enriched	displays 	NULL				statement 4	NULL	a lower capacity to			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_4_638_s_91	11950703	23 However, although apoA-II - enriched HDLs bind to human SR-BI with higher affinity than apoA-I - rich HDLs, they display a lower capacity to deliver cholesteryl esters to human adrenal cells.	bind
29359	1	7361	7	NULL	NULL	0	NULL	HSP90 	NULL		binds to	NULL				PM-eNOS	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_23	16627819	23 Interestingly, the authors also observed that there was significantly more HSP90 (but not caveolin-1) bound to the PM-eNOS versus the Golgi-eNOS.	bind
29360	2	7361	7	NULL	NULL	0	NULL	HSP90	NULL		binds to	NULL				Golgi-eNOS	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_23	16627819	23 Interestingly, the authors also observed that there was significantly more HSP90 (but not caveolin-1) bound to the PM-eNOS versus the Golgi-eNOS.	bind
29361	3	7361	7	NULL	NULL	0	NULL	caveolin-1	NULL		does not bind	NULL				PM-eNOS	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_23	16627819	23 Interestingly, the authors also observed that there was significantly more HSP90 (but not caveolin-1) bound to the PM-eNOS versus the Golgi-eNOS.	bind
29362	4	7361	7	NULL	NULL	0	NULL	caveolin-1	NULL		does not bind	NULL				Golgi-eNOS	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_23	16627819	23 Interestingly, the authors also observed that there was significantly more HSP90 (but not caveolin-1) bound to the PM-eNOS versus the Golgi-eNOS.	bind
27089	1	7362	5	13	NULL	NULL	NULL	LDL receptor	GP		contains									SRE in promoter	NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_24_3104_s_24	12473559	23 LDL receptor, like other genes involved in lipid metabolism, contains the consensus sterol regulatory elements (SRE) in the promoter, allowing its regulation through SRE-1 binding proteins (SREBPs).	bind
27090	2	7362	5	13	NULL	NULL	NULL	SRE	GP		is					sterol regulatory elements	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_24_3104_s_24	12473559	23 LDL receptor, like other genes involved in lipid metabolism, contains the consensus sterol regulatory elements (SRE) in the promoter, allowing its regulation through SRE-1 binding proteins (SREBPs).	bind
27091	3	7362	5	13	NULL	NULL	NULL	statement 1	GP		allows					SREBPs	GP	regulation through			NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_24_3104_s_24	12473559	23 LDL receptor, like other genes involved in lipid metabolism, contains the consensus sterol regulatory elements (SRE) in the promoter, allowing its regulation through SRE-1 binding proteins (SREBPs).	bind
27092	4	7362	5	13	NULL	NULL	NULL	SREBPs	GP		is					SRE-1 binding proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_24_3104_s_24	12473559	23 LDL receptor, like other genes involved in lipid metabolism, contains the consensus sterol regulatory elements (SRE) in the promoter, allowing its regulation through SRE-1 binding proteins (SREBPs).	bind
29363	1	7362	7	NULL	NULL	0	NULL	LDL receptor gene	NULL		is involved in	NULL				lipid metabolism	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_24_3104_s_24	12473559	23 LDL receptor, like other genes involved in lipid metabolism, contains the consensus sterol regulatory elements (SRE) in the promoter, allowing its regulation through SRE-1 binding proteins (SREBPs).	bind
29364	2	7362	7	NULL	NULL	0	NULL	LDL receptor gene	NULL		contains	NULL					NULL	consensus		SRE in the promoter	NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_24_3104_s_24	12473559	23 LDL receptor, like other genes involved in lipid metabolism, contains the consensus sterol regulatory elements (SRE) in the promoter, allowing its regulation through SRE-1 binding proteins (SREBPs).	bind
29365	3	7362	7	NULL	NULL	0	NULL	LDL receptor gene	NULL		regulates through	NULL				SREBPs	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_24_3104_s_24	12473559	23 LDL receptor, like other genes involved in lipid metabolism, contains the consensus sterol regulatory elements (SRE) in the promoter, allowing its regulation through SRE-1 binding proteins (SREBPs).	bind
29366	4	7362	7	NULL	NULL	0	NULL	SRE	NULL		is	NULL				sterol regulatory elements	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_24_3104_s_24	12473559	23 LDL receptor, like other genes involved in lipid metabolism, contains the consensus sterol regulatory elements (SRE) in the promoter, allowing its regulation through SRE-1 binding proteins (SREBPs).	bind
29367	5	7362	7	NULL	NULL	0	NULL	SREBPs	NULL		is	NULL				SRE-1 binding proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_24_3104_s_24	12473559	23 LDL receptor, like other genes involved in lipid metabolism, contains the consensus sterol regulatory elements (SRE) in the promoter, allowing its regulation through SRE-1 binding proteins (SREBPs).	bind
27093	1	7363	5	13	NULL	NULL	NULL	LXR	GP		is a type of					nuclear hormone receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_116	15178557	23 LXR is a nuclear hormone receptor that binds oxysterols and activates its target genes, such as  CYP7A encoding the rate-limiting enzyme in the conversion of cholesterol to bile acids by dimerizing with retinoid X receptor (RXR).	bind
27094	2	7363	5	13	NULL	NULL	NULL	LXR	GP		bind					oxysterols	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_116	15178557	23 LXR is a nuclear hormone receptor that binds oxysterols and activates its target genes, such as  CYP7A encoding the rate-limiting enzyme in the conversion of cholesterol to bile acids by dimerizing with retinoid X receptor (RXR).	bind
27095	3	7363	5	13	NULL	NULL	NULL	statement 2	Process		activates					CYP7A	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_116	15178557	23 LXR is a nuclear hormone receptor that binds oxysterols and activates its target genes, such as  CYP7A encoding the rate-limiting enzyme in the conversion of cholesterol to bile acids by dimerizing with retinoid X receptor (RXR).	bind
27096	4	7363	5	13	NULL	NULL	NULL	CYP7A	GP		is a type of					LXR target genes	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_116	15178557	23 LXR is a nuclear hormone receptor that binds oxysterols and activates its target genes, such as  CYP7A encoding the rate-limiting enzyme in the conversion of cholesterol to bile acids by dimerizing with retinoid X receptor (RXR).	bind
27097	5	7363	5	13	NULL	NULL	NULL	cholesterol	Chemical		is converted to					bile acids	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_116	15178557	23 LXR is a nuclear hormone receptor that binds oxysterols and activates its target genes, such as  CYP7A encoding the rate-limiting enzyme in the conversion of cholesterol to bile acids by dimerizing with retinoid X receptor (RXR).	bind
27098	6	7363	5	13	NULL	NULL	NULL	LXR	GP		dimerizes with					RXR	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_116	15178557	23 LXR is a nuclear hormone receptor that binds oxysterols and activates its target genes, such as  CYP7A encoding the rate-limiting enzyme in the conversion of cholesterol to bile acids by dimerizing with retinoid X receptor (RXR).	bind
27099	7	7363	5	13	NULL	NULL	NULL	RXR	GP		is					retinoid X receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_116	15178557	23 LXR is a nuclear hormone receptor that binds oxysterols and activates its target genes, such as  CYP7A encoding the rate-limiting enzyme in the conversion of cholesterol to bile acids by dimerizing with retinoid X receptor (RXR).	bind
27100	8	7363	5	13	NULL	NULL	NULL	CYP7A	GP		encodes					rate-limiting enzyme	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_116	15178557	23 LXR is a nuclear hormone receptor that binds oxysterols and activates its target genes, such as  CYP7A encoding the rate-limiting enzyme in the conversion of cholesterol to bile acids by dimerizing with retinoid X receptor (RXR).	bind
27101	9	7363	5	13	NULL	NULL	NULL	statement 8	Process		plays a role in					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_116	15178557	23 LXR is a nuclear hormone receptor that binds oxysterols and activates its target genes, such as  CYP7A encoding the rate-limiting enzyme in the conversion of cholesterol to bile acids by dimerizing with retinoid X receptor (RXR).	bind
29368	1	7363	7	NULL	NULL	0	NULL	LXR	NULL		binds	NULL				oxysterols	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_116	15178557	23 LXR is a nuclear hormone receptor that binds oxysterols and activates its target genes, such as  CYP7A encoding the rate-limiting enzyme in the conversion of cholesterol to bile acids by dimerizing with retinoid X receptor (RXR).	bind
29369	2	7363	7	NULL	NULL	0	NULL	LXR	NULL		activates	NULL				CYP7A genes	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_116	15178557	23 LXR is a nuclear hormone receptor that binds oxysterols and activates its target genes, such as  CYP7A encoding the rate-limiting enzyme in the conversion of cholesterol to bile acids by dimerizing with retinoid X receptor (RXR).	bind
29370	3	7363	7	NULL	NULL	0	NULL	CYP7A	NULL		encodes	NULL				rate-limiting enzyme	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_116	15178557	23 LXR is a nuclear hormone receptor that binds oxysterols and activates its target genes, such as  CYP7A encoding the rate-limiting enzyme in the conversion of cholesterol to bile acids by dimerizing with retinoid X receptor (RXR).	bind
29371	4	7363	7	NULL	NULL	0	NULL	cholesterol	NULL		dimerizes with	NULL				RXR	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_116	15178557	23 LXR is a nuclear hormone receptor that binds oxysterols and activates its target genes, such as  CYP7A encoding the rate-limiting enzyme in the conversion of cholesterol to bile acids by dimerizing with retinoid X receptor (RXR).	bind
29372	5	7363	7	NULL	NULL	0	NULL	cholesterol	NULL		converts to	NULL				bile acids	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_116	15178557	23 LXR is a nuclear hormone receptor that binds oxysterols and activates its target genes, such as  CYP7A encoding the rate-limiting enzyme in the conversion of cholesterol to bile acids by dimerizing with retinoid X receptor (RXR).	bind
29373	6	7363	7	NULL	NULL	0	NULL	rate-limiting enzyme	NULL		is involved in	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_116	15178557	23 LXR is a nuclear hormone receptor that binds oxysterols and activates its target genes, such as  CYP7A encoding the rate-limiting enzyme in the conversion of cholesterol to bile acids by dimerizing with retinoid X receptor (RXR).	bind
29374	7	7363	7	NULL	NULL	0	NULL	LXR	NULL		is a type of	NULL				nuclear hormone receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_116	15178557	23 LXR is a nuclear hormone receptor that binds oxysterols and activates its target genes, such as  CYP7A encoding the rate-limiting enzyme in the conversion of cholesterol to bile acids by dimerizing with retinoid X receptor (RXR).	bind
29375	8	7363	7	NULL	NULL	0	NULL	RXR	NULL		is	NULL				retinoid X receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_116	15178557	23 LXR is a nuclear hormone receptor that binds oxysterols and activates its target genes, such as  CYP7A encoding the rate-limiting enzyme in the conversion of cholesterol to bile acids by dimerizing with retinoid X receptor (RXR).	bind
27140	1	7364	5	13	NULL	NULL	NULL	apoA-I	GP		bind		likely			PS	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_38	12738681	23 The authors suggested that apoA-I is likely bound to phosphatidylserine (PS) that is presented to the exofacial leaflet by the "`floppase"` activity of ABCA1 because PS levels on the exofacial leaflet are increased by ABCA1 expression.	bind
27141	2	7364	5	13	NULL	NULL	NULL	PS	Chemical		is					phosphatidylserine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_38	12738681	23 The authors suggested that apoA-I is likely bound to phosphatidylserine (PS) that is presented to the exofacial leaflet by the "`floppase"` activity of ABCA1 because PS levels on the exofacial leaflet are increased by ABCA1 expression.	bind
27142	3	7364	5	13	NULL	NULL	NULL	PS	Chemical		is presented to					exofacial leaflet					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_38	12738681	23 The authors suggested that apoA-I is likely bound to phosphatidylserine (PS) that is presented to the exofacial leaflet by the "`floppase"` activity of ABCA1 because PS levels on the exofacial leaflet are increased by ABCA1 expression.	bind
27143	4	7364	5	13	NULL	NULL	NULL	ABCA1	GP		exhibits					floppase activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_38	12738681	23 The authors suggested that apoA-I is likely bound to phosphatidylserine (PS) that is presented to the exofacial leaflet by the "`floppase"` activity of ABCA1 because PS levels on the exofacial leaflet are increased by ABCA1 expression.	bind
27144	5	7364	5	13	NULL	NULL	NULL	PS	Chemical	levels of	is increased by					ABCA1	GP	expression of			NULL	exofacial leaflet	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_38	12738681	23 The authors suggested that apoA-I is likely bound to phosphatidylserine (PS) that is presented to the exofacial leaflet by the "`floppase"` activity of ABCA1 because PS levels on the exofacial leaflet are increased by ABCA1 expression.	bind
46589	6	7364	5	13	NULL	NULL	NULL	statement 3	Process		occurs by					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_38	12738681	23 The authors suggested that apoA-I is likely bound to phosphatidylserine (PS) that is presented to the exofacial leaflet by the "`floppase"` activity of ABCA1 because PS levels on the exofacial leaflet are increased by ABCA1 expression.	bind
29376	1	7364	7	NULL	NULL	0	NULL	apoA-I	NULL		bind	NULL				PS	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_38	12738681	23 The authors suggested that apoA-I is likely bound to phosphatidylserine (PS) that is presented to the exofacial leaflet by the "`floppase"` activity of ABCA1 because PS levels on the exofacial leaflet are increased by ABCA1 expression.	bind
29377	2	7364	7	10	NULL	0	NULL	PS			is presented to					 exofacial leaflet					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_38	12738681	23 The authors suggested that apoA-I is likely bound to phosphatidylserine (PS) that is presented to the exofacial leaflet by the "`floppase"` activity of ABCA1 because PS levels on the exofacial leaflet are increased by ABCA1 expression.	bind
29378	3	7364	7	10	NULL	0	NULL	ABCA1	NULL		exhibits	NULL				floppase activity	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_38	12738681	23 The authors suggested that apoA-I is likely bound to phosphatidylserine (PS) that is presented to the exofacial leaflet by the "`floppase"` activity of ABCA1 because PS levels on the exofacial leaflet are increased by ABCA1 expression.	bind
29379	4	7364	7	10	NULL	0	NULL	ABCA1 expression			increase					PS 		levels of			NULL	exofacial leaflet	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_38	12738681	23 The authors suggested that apoA-I is likely bound to phosphatidylserine (PS) that is presented to the exofacial leaflet by the "`floppase"` activity of ABCA1 because PS levels on the exofacial leaflet are increased by ABCA1 expression.	bind
29380	5	7364	7	NULL	NULL	0	NULL	statement 3	NULL		because of	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_38	12738681	23 The authors suggested that apoA-I is likely bound to phosphatidylserine (PS) that is presented to the exofacial leaflet by the "`floppase"` activity of ABCA1 because PS levels on the exofacial leaflet are increased by ABCA1 expression.	bind
29381	6	7364	7	NULL	NULL	0	NULL	PS	NULL		is	NULL				phosphatidylserine	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_38	12738681	23 The authors suggested that apoA-I is likely bound to phosphatidylserine (PS) that is presented to the exofacial leaflet by the "`floppase"` activity of ABCA1 because PS levels on the exofacial leaflet are increased by ABCA1 expression.	bind
46590	7	7364	7	10	NULL	0	NULL	statement 3	NULL		occurs because of	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_38	12738681	23 The authors suggested that apoA-I is likely bound to phosphatidylserine (PS) that is presented to the exofacial leaflet by the "`floppase"` activity of ABCA1 because PS levels on the exofacial leaflet are increased by ABCA1 expression.	bind
27145	1	7365	5	13	NULL	NULL	NULL	CRP	GP		bind					LDL	GP	oxidized			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
27146	2	7365	5	13	NULL	NULL	NULL	annexin	GP		bind					LDL	GP	oxidized			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
27147	4	7365	5	13	NULL	NULL	NULL	statement 3	Process		competes with		effectively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
27148	5	7365	5	13	NULL	NULL	NULL	statement 3	Process		competes with		effectively			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
27149	6	7365	5	13	NULL	NULL	NULL	4E6	GP		does not compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
27150	7	7365	5	13	NULL	NULL	NULL	4E6	GP		does not compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
27151	8	7365	5	13	NULL	NULL	NULL	polyclonal antibodies to apoB	GP		does not compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
27152	9	7365	5	13	NULL	NULL	NULL	polyclonal antibodies to apoB	GP		does not compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
27153	10	7365	5	13	NULL	NULL	NULL	oxidized phospholipids	Chemical	choline head group of	is present in					LDL	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
27155	11	7365	5	13	NULL	NULL	NULL	CRP	GP		bind					statement 10	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
27157	12	7365	5	13	NULL	NULL	NULL	annexin	GP		bind					statement 10	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
27159	13	7365	5	13	NULL	NULL	NULL	apoB	GP	specific sequences of	is not essential for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
27160	14	7365	5	13	NULL	NULL	NULL	apoB	GP	specific sequences of	is not essential for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
27161	3	7365	5	13	NULL	NULL	NULL	DLH3	GP		bind					LDL	GP	oxidized			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
29410	1	7365	7	NULL	NULL	0	NULL	 CRP	NULL		bind	NULL				LDL	NULL	oxidized	choline head group 		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
29411	2	7365	7	NULL	NULL	0	NULL	annexin 	NULL		bind	NULL				LDL	NULL	oxidized	choline head group 		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
29412	3	7365	7	NULL	NULL	0	NULL	DLH3	NULL		bind	NULL				LDL	NULL	oxidized			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
29413	4	7365	7	NULL	NULL	0	NULL	statement 3	NULL		compete with	NULL	effectively			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
29414	5	7365	7	NULL	NULL	0	NULL	statement 3	NULL		compete with	NULL	effectively			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
29415	6	7365	7	NULL	NULL	0	NULL	4E6	NULL		does not compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
29416	7	7365	7	NULL	NULL	0	NULL	4E6	NULL		does not compete with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
29417	8	7365	7	NULL	NULL	0	NULL	polyclonal antibodies apoB	NULL		does not compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
29418	9	7365	7	NULL	NULL	0	NULL	polyclonal antibodies apoB	NULL		does not compete with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
29419	10	7365	7	NULL	NULL	0	NULL	apoB	NULL	specific sequences of 	is not required for	NULL				LDL	NULL	binding to			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_126	15692104	23 We found that DLH3, but not 4E6 and polyclonal antibodies to apoB, effectively competes with CRP and annexin binding to oxidized LDL, suggesting that both ligands bind to the choline head group of oxidized phospholipids present in the LDL and that specific sequences of the apoB were not essential.	bind
27172	1	7366	5	13	NULL	NULL	NULL	CREB	GP	phosphorylated	bind						NucleicAcid			CRE sites	NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_17_2088_s_174	11673351	23, 24, 34 A functional relevance for CREB-dependent transcription in the heart derives from studies in human failing and nonfailing heart samples, where binding of phosphorylated CREB to CRE sites has been demonstrated.	bind
29420	1	7366	7	NULL	NULL	0	NULL	CREB	NULL	phosphorylated	binds to	NULL					NULL			CRE sites	NULL		0	NULL	NULL	NULL	gw60_circulation_104_17_2088_s_174	11673351	23, 24, 34 A functional relevance for CREB-dependent transcription in the heart derives from studies in human failing and nonfailing heart samples, where binding of phosphorylated CREB to CRE sites has been demonstrated.	bind
27173	1	7367	5	13	NULL	NULL	NULL	CREB	GP		bind					Rac1 gene	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1634_s_163	15242860	23,24  Our data also indicated that CREB phosphorylation did not increase CREB binding to Rac1 gene promoter.	bind
27174	2	7367	5	13	NULL	NULL	NULL	CREB	GP	phosphorylation	does not increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1634_s_163	15242860	23,24  Our data also indicated that CREB phosphorylation did not increase CREB binding to Rac1 gene promoter.	bind
29421	1	7367	7	NULL	NULL	0	NULL	CREB 	NULL		bind	NULL				Rac1 gene	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1634_s_163	15242860	23,24  Our data also indicated that CREB phosphorylation did not increase CREB binding to Rac1 gene promoter.	bind
29422	2	7367	7	NULL	NULL	0	NULL	CREB	NULL	phosphorylation of	does not increase	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1634_s_163	15242860	23,24  Our data also indicated that CREB phosphorylation did not increase CREB binding to Rac1 gene promoter.	bind
27175	1	7368	5	13	NULL	NULL	NULL	EphB4	GP		bind		specifically			ephrin-B2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_17_2210_s_225	15851594	23,24  Whereas EphB4 showed specific binding to ephrin-B2 with its essential role for vascular development, 22,24  EphB3 and EphB2 show less specific binding to ephrin-B2 without their critical role for vascular development.	bind
27176	2	7368	5	13	NULL	NULL	NULL	EphB4	GP		plays a role in		essential			vascular development	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_17_2210_s_225	15851594	23,24  Whereas EphB4 showed specific binding to ephrin-B2 with its essential role for vascular development, 22,24  EphB3 and EphB2 show less specific binding to ephrin-B2 without their critical role for vascular development.	bind
27177	3	7368	5	13	NULL	NULL	NULL	EphB3	GP		bind		less specific			ephrin-B2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_17_2210_s_225	15851594	23,24  Whereas EphB4 showed specific binding to ephrin-B2 with its essential role for vascular development, 22,24  EphB3 and EphB2 show less specific binding to ephrin-B2 without their critical role for vascular development.	bind
27178	4	7368	5	13	NULL	NULL	NULL	EphB3	GP		does not play a role in		critical			vascular development	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_17_2210_s_225	15851594	23,24  Whereas EphB4 showed specific binding to ephrin-B2 with its essential role for vascular development, 22,24  EphB3 and EphB2 show less specific binding to ephrin-B2 without their critical role for vascular development.	bind
27179	5	7368	5	13	NULL	NULL	NULL	EphB2	GP		bind		less specific			ephrin-B2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_17_2210_s_225	15851594	23,24  Whereas EphB4 showed specific binding to ephrin-B2 with its essential role for vascular development, 22,24  EphB3 and EphB2 show less specific binding to ephrin-B2 without their critical role for vascular development.	bind
27180	6	7368	5	13	NULL	NULL	NULL	EphB2	GP		does not play a role in		critical			vascular development	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_17_2210_s_225	15851594	23,24  Whereas EphB4 showed specific binding to ephrin-B2 with its essential role for vascular development, 22,24  EphB3 and EphB2 show less specific binding to ephrin-B2 without their critical role for vascular development.	bind
29423	1	7368	7	NULL	NULL	0	NULL	EphB4	NULL		binds	NULL	specifically			ephrin-B2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_111_17_2210_s_225	15851594	23,24  Whereas EphB4 showed specific binding to ephrin-B2 with its essential role for vascular development, 22,24  EphB3 and EphB2 show less specific binding to ephrin-B2 without their critical role for vascular development.	bind
29424	2	7368	7	10	NULL	0	NULL	statement 1			plays a role in		essential			vascular development					NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_17_2210_s_225	15851594	23,24  Whereas EphB4 showed specific binding to ephrin-B2 with its essential role for vascular development, 22,24  EphB3 and EphB2 show less specific binding to ephrin-B2 without their critical role for vascular development.	bind
29425	3	7368	7	NULL	NULL	0	NULL	EphB3	NULL		binds	NULL	less specific			 ephrin-B2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_111_17_2210_s_225	15851594	23,24  Whereas EphB4 showed specific binding to ephrin-B2 with its essential role for vascular development, 22,24  EphB3 and EphB2 show less specific binding to ephrin-B2 without their critical role for vascular development.	bind
29426	4	7368	7	NULL	NULL	0	NULL	 EphB2	NULL		bind	NULL	less specific			ephrin-B2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_111_17_2210_s_225	15851594	23,24  Whereas EphB4 showed specific binding to ephrin-B2 with its essential role for vascular development, 22,24  EphB3 and EphB2 show less specific binding to ephrin-B2 without their critical role for vascular development.	bind
29427	5	7368	7	NULL	NULL	0	NULL	statement 3	NULL		does not play a role in	NULL				vascular development	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_111_17_2210_s_225	15851594	23,24  Whereas EphB4 showed specific binding to ephrin-B2 with its essential role for vascular development, 22,24  EphB3 and EphB2 show less specific binding to ephrin-B2 without their critical role for vascular development.	bind
29428	6	7368	7	NULL	NULL	0	NULL	statement 4	NULL		does not play a role in	NULL				vascular development	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_111_17_2210_s_225	15851594	23,24  Whereas EphB4 showed specific binding to ephrin-B2 with its essential role for vascular development, 22,24  EphB3 and EphB2 show less specific binding to ephrin-B2 without their critical role for vascular development.	bind
27195	1	7369	5	13	NULL	NULL	NULL	apoA-I	GP		bind								W590S		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_55	12738681	23,32  The moderate increase in apoA-I binding to W590S may imply that dissociation of apoA-I from ABCA1 could be facilitated by lipid efflux to apolipoproteins bound to ABCA1 and is consistent with the earlier finding that ABCA1 binds apoA-I but not HDL3.	bind
27196	2	7369	5	13	NULL	NULL	NULL	apoA-I	GP		dissociates from					ABCA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_55	12738681	23,32  The moderate increase in apoA-I binding to W590S may imply that dissociation of apoA-I from ABCA1 could be facilitated by lipid efflux to apolipoproteins bound to ABCA1 and is consistent with the earlier finding that ABCA1 binds apoA-I but not HDL3.	bind
27197	3	7369	5	13	NULL	NULL	NULL	apolipoproteins	GP		bind					ABCA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_55	12738681	23,32  The moderate increase in apoA-I binding to W590S may imply that dissociation of apoA-I from ABCA1 could be facilitated by lipid efflux to apolipoproteins bound to ABCA1 and is consistent with the earlier finding that ABCA1 binds apoA-I but not HDL3.	bind
27198	4	7369	5	13	NULL	NULL	NULL	statement 2	Process		is facilitated by					statement 3	Process	lipid efflux to			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_55	12738681	23,32  The moderate increase in apoA-I binding to W590S may imply that dissociation of apoA-I from ABCA1 could be facilitated by lipid efflux to apolipoproteins bound to ABCA1 and is consistent with the earlier finding that ABCA1 binds apoA-I but not HDL3.	bind
27199	5	7369	5	13	NULL	NULL	NULL	statement 1	Process	moderate increase in	imply		may			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_55	12738681	23,32  The moderate increase in apoA-I binding to W590S may imply that dissociation of apoA-I from ABCA1 could be facilitated by lipid efflux to apolipoproteins bound to ABCA1 and is consistent with the earlier finding that ABCA1 binds apoA-I but not HDL3.	bind
27200	6	7369	5	13	NULL	NULL	NULL	ABCA1	GP		bind					apoA-I	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_55	12738681	23,32  The moderate increase in apoA-I binding to W590S may imply that dissociation of apoA-I from ABCA1 could be facilitated by lipid efflux to apolipoproteins bound to ABCA1 and is consistent with the earlier finding that ABCA1 binds apoA-I but not HDL3.	bind
27201	7	7369	5	13	NULL	NULL	NULL	ABCA1	GP		does not bind					HDL3	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_55	12738681	23,32  The moderate increase in apoA-I binding to W590S may imply that dissociation of apoA-I from ABCA1 could be facilitated by lipid efflux to apolipoproteins bound to ABCA1 and is consistent with the earlier finding that ABCA1 binds apoA-I but not HDL3.	bind
29429	1	7369	7	NULL	NULL	0	NULL	apoA-I	NULL		binds to	NULL					NULL		W590S 		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_55	12738681	23,32  The moderate increase in apoA-I binding to W590S may imply that dissociation of apoA-I from ABCA1 could be facilitated by lipid efflux to apolipoproteins bound to ABCA1 and is consistent with the earlier finding that ABCA1 binds apoA-I but not HDL3.	bind
29430	2	7369	7	NULL	NULL	0	NULL	apoA-I	NULL		dissociates from	NULL				ABCA1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_55	12738681	23,32  The moderate increase in apoA-I binding to W590S may imply that dissociation of apoA-I from ABCA1 could be facilitated by lipid efflux to apolipoproteins bound to ABCA1 and is consistent with the earlier finding that ABCA1 binds apoA-I but not HDL3.	bind
29431	3	7369	7	NULL	NULL	0	NULL	statement 1	NULL	increase in	imply	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_55	12738681	23,32  The moderate increase in apoA-I binding to W590S may imply that dissociation of apoA-I from ABCA1 could be facilitated by lipid efflux to apolipoproteins bound to ABCA1 and is consistent with the earlier finding that ABCA1 binds apoA-I but not HDL3.	bind
29432	4	7369	7	NULL	NULL	0	NULL	apolipoproteins	NULL		bind	NULL				ABCA1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_55	12738681	23,32  The moderate increase in apoA-I binding to W590S may imply that dissociation of apoA-I from ABCA1 could be facilitated by lipid efflux to apolipoproteins bound to ABCA1 and is consistent with the earlier finding that ABCA1 binds apoA-I but not HDL3.	bind
29433	5	7369	7	NULL	NULL	0	NULL	statement 4	NULL	lipid efflux to	facilitate	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_55	12738681	23,32  The moderate increase in apoA-I binding to W590S may imply that dissociation of apoA-I from ABCA1 could be facilitated by lipid efflux to apolipoproteins bound to ABCA1 and is consistent with the earlier finding that ABCA1 binds apoA-I but not HDL3.	bind
29434	6	7369	7	NULL	NULL	0	NULL	ABCA1	NULL		binds	NULL				apoA-I	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_55	12738681	23,32  The moderate increase in apoA-I binding to W590S may imply that dissociation of apoA-I from ABCA1 could be facilitated by lipid efflux to apolipoproteins bound to ABCA1 and is consistent with the earlier finding that ABCA1 binds apoA-I but not HDL3.	bind
29435	7	7369	7	NULL	NULL	0	NULL	ABCA1	NULL		does not bind	NULL				HDL3	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_55	12738681	23,32  The moderate increase in apoA-I binding to W590S may imply that dissociation of apoA-I from ABCA1 could be facilitated by lipid efflux to apolipoproteins bound to ABCA1 and is consistent with the earlier finding that ABCA1 binds apoA-I but not HDL3.	bind
27202	1	7370	5	13	NULL	NULL	NULL	VN	GP	surface-bound serum-derived	bind					uPAR	GP				NULL	 cells cultured in serum-containing medium	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2251_s_155	15458976	23,38  When cultured in serum-containing medium, cells may have surface-bound serum-derived VN that binds uPAR and Mac-1, thereby influencing cell adhesion.	bind
27203	2	7370	5	13	NULL	NULL	NULL	statement 1	Process		influence					cell adhesion	Process				NULL	cells cultured in serum-containing medium	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2251_s_155	15458976	23,38  When cultured in serum-containing medium, cells may have surface-bound serum-derived VN that binds uPAR and Mac-1, thereby influencing cell adhesion.	bind
27204	3	7370	5	13	NULL	NULL	NULL	VN	GP	surface-bound serum-derived	bind					Mac-1	GP				NULL	cells cultured in serum-containing medium	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2251_s_155	15458976	23,38  When cultured in serum-containing medium, cells may have surface-bound serum-derived VN that binds uPAR and Mac-1, thereby influencing cell adhesion.	bind
27205	4	7370	5	13	NULL	NULL	NULL	statement 2	Process		influence					cell adhesion	Process				NULL	cells cultured in serum-containing medium	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2251_s_155	15458976	23,38  When cultured in serum-containing medium, cells may have surface-bound serum-derived VN that binds uPAR and Mac-1, thereby influencing cell adhesion.	bind
29436	1	7370	7	NULL	NULL	0	NULL	VN	NULL	surface-bound serum-derived	binds	NULL				uPAR	NULL				NULL	serum-containing medium	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2251_s_155	15458976	23,38  When cultured in serum-containing medium, cells may have surface-bound serum-derived VN that binds uPAR and Mac-1, thereby influencing cell adhesion.	bind
29437	2	7370	7	NULL	NULL	0	NULL	VN	NULL	surface-bound serum-derived	binds	NULL				Mac-1	NULL				NULL	serum-containing medium	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2251_s_155	15458976	23,38  When cultured in serum-containing medium, cells may have surface-bound serum-derived VN that binds uPAR and Mac-1, thereby influencing cell adhesion.	bind
29438	3	7370	7	10	NULL	0	NULL	statement 1			influence					cell adhesion					NULL	serum-containing medium	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2251_s_155	15458976	23,38  When cultured in serum-containing medium, cells may have surface-bound serum-derived VN that binds uPAR and Mac-1, thereby influencing cell adhesion.	bind
29439	4	7370	7	10	NULL	0	NULL	statement 2			influence					cell adhesion					NULL	serum-containing medium	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2251_s_155	15458976	23,38  When cultured in serum-containing medium, cells may have surface-bound serum-derived VN that binds uPAR and Mac-1, thereby influencing cell adhesion.	bind
27206	1	7372	5	13	NULL	NULL	NULL	dystrophin	GP		bind			N-terminus		actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_9_1256_s_143	11238270	24  At the N-terminus, dystrophin binds to actin.	bind
29440	1	7372	7	NULL	NULL	0	NULL	dystrophin	NULL		binds to	NULL		N-terminus		actin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_9_1256_s_143	11238270	24  At the N-terminus, dystrophin binds to actin.	bind
27207	1	7373	5	13	NULL	NULL	NULL	p27	GP		bind			69-amino-acid amino-terminal inhibitory domain		cyclin A-CDK2	GP	phosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_313_s_36	10027389	24  Examination of the crystal structure of the 69-amino-acid amino-terminal inhibitory domain of p27 bound to the phosphorylated cyclin A-CDK2 showed that p27 binding causes large conformational changes in and around the catalytic cleft of CDK2 24  and that p27 has separate binding sites on the cyclin and CDK subunits.	bind
27208	2	7373	5	13	NULL	NULL	NULL	statement 1	Process		results in					CDK2	GP	large conformational changes in and around	catalytic cleft		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_313_s_36	10027389	24  Examination of the crystal structure of the 69-amino-acid amino-terminal inhibitory domain of p27 bound to the phosphorylated cyclin A-CDK2 showed that p27 binding causes large conformational changes in and around the catalytic cleft of CDK2 24  and that p27 has separate binding sites on the cyclin and CDK subunits.	bind
27209	3	7373	5	13	NULL	NULL	NULL	p27	GP		contains					cyclin	GP		binding site		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_313_s_36	10027389	24  Examination of the crystal structure of the 69-amino-acid amino-terminal inhibitory domain of p27 bound to the phosphorylated cyclin A-CDK2 showed that p27 binding causes large conformational changes in and around the catalytic cleft of CDK2 24  and that p27 has separate binding sites on the cyclin and CDK subunits.	bind
27210	4	7373	5	13	NULL	NULL	NULL	p27	GP		contains					CDK subunits	GP		binding site		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_313_s_36	10027389	24  Examination of the crystal structure of the 69-amino-acid amino-terminal inhibitory domain of p27 bound to the phosphorylated cyclin A-CDK2 showed that p27 binding causes large conformational changes in and around the catalytic cleft of CDK2 24  and that p27 has separate binding sites on the cyclin and CDK subunits.	bind
29441	1	7373	7	NULL	NULL	0	NULL	p27	NULL		bind	NULL		69-amino-acid amino-terminal inhibitory domain 		cyclin A-CDK2 	NULL	phosphorylated			NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_2_313_s_36	10027389	24  Examination of the crystal structure of the 69-amino-acid amino-terminal inhibitory domain of p27 bound to the phosphorylated cyclin A-CDK2 showed that p27 binding causes large conformational changes in and around the catalytic cleft of CDK2 24  and that p27 has separate binding sites on the cyclin and CDK subunits.	bind
29442	2	7373	7	NULL	NULL	0	NULL	statement 1	NULL		cause	NULL				CDK2	NULL	conformational changes in and around	catalytic cleft		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_313_s_36	10027389	24  Examination of the crystal structure of the 69-amino-acid amino-terminal inhibitory domain of p27 bound to the phosphorylated cyclin A-CDK2 showed that p27 binding causes large conformational changes in and around the catalytic cleft of CDK2 24  and that p27 has separate binding sites on the cyclin and CDK subunits.	bind
29443	3	7373	7	NULL	NULL	0	NULL	cyclin	NULL		contains	NULL				p27	NULL		binding site		NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_2_313_s_36	10027389	24  Examination of the crystal structure of the 69-amino-acid amino-terminal inhibitory domain of p27 bound to the phosphorylated cyclin A-CDK2 showed that p27 binding causes large conformational changes in and around the catalytic cleft of CDK2 24  and that p27 has separate binding sites on the cyclin and CDK subunits.	bind
29444	4	7373	7	NULL	NULL	0	NULL	CDK subunits	NULL		contains	NULL				p27	NULL		binding site		NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_2_313_s_36	10027389	24  Examination of the crystal structure of the 69-amino-acid amino-terminal inhibitory domain of p27 bound to the phosphorylated cyclin A-CDK2 showed that p27 binding causes large conformational changes in and around the catalytic cleft of CDK2 24  and that p27 has separate binding sites on the cyclin and CDK subunits.	bind
27211	1	7374	5	13	NULL	NULL	NULL	FK506	Chemical		bind					FKBP	GP				NULL	in cardiomyocytes	NULL	NULL	NULL	NULL	gw60_circulation_100_24_2449_s_149	10595959	24  In cardiomyocytes, it has been reported that FK506 binds to FKBP and opens the ryanodine receptor, resulting in an increase in intracellular calcium concentration.	bind
27212	2	7374	5	13	NULL	NULL	NULL	statement 1	Process		opens					ryanodine receptor	GP				NULL	cardiomyocytes	NULL	NULL	NULL	NULL	gw60_circulation_100_24_2449_s_149	10595959	24  In cardiomyocytes, it has been reported that FK506 binds to FKBP and opens the ryanodine receptor, resulting in an increase in intracellular calcium concentration.	bind
27213	3	7374	5	13	NULL	NULL	NULL	statement 2	Process		results in					calcium concentration	Chemical	increase in intracellular			NULL	cardiomyocytes	NULL	NULL	NULL	NULL	gw60_circulation_100_24_2449_s_149	10595959	24  In cardiomyocytes, it has been reported that FK506 binds to FKBP and opens the ryanodine receptor, resulting in an increase in intracellular calcium concentration.	bind
29445	1	7374	7	NULL	NULL	0	NULL	FK506	NULL		binds to	NULL				FKBP	NULL				NULL	cardiomyocytes	NULL	NULL	NULL	NULL	gw60_circulation_100_24_2449_s_149	10595959	24  In cardiomyocytes, it has been reported that FK506 binds to FKBP and opens the ryanodine receptor, resulting in an increase in intracellular calcium concentration.	bind
29446	2	7374	7	NULL	NULL	0	NULL	statement 1	NULL		opens	NULL				ryanodine receptor	NULL				NULL	cardiomyocytes	0	NULL	NULL	NULL	gw60_circulation_100_24_2449_s_149	10595959	24  In cardiomyocytes, it has been reported that FK506 binds to FKBP and opens the ryanodine receptor, resulting in an increase in intracellular calcium concentration.	bind
29447	3	7374	7	NULL	NULL	0	NULL	statement 2	NULL		increase	NULL				calcium	NULL	intracellular concentration of			NULL	cardiomyocytes	NULL	NULL	NULL	NULL	gw60_circulation_100_24_2449_s_149	10595959	24  In cardiomyocytes, it has been reported that FK506 binds to FKBP and opens the ryanodine receptor, resulting in an increase in intracellular calcium concentration.	bind
27214	1	7375	5	13	NULL	NULL	NULL	LDL particles	GP		bind					mast cell granule remnants	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2047_s_144	7583588	24  Moreover, a specific mechanism that increases the strength of binding between LDL particles and mast cell granule remnants was recently discovered.	bind
29448	1	7375	7	NULL	NULL	0	NULL	 LDL particles	NULL		bind	NULL				 mast cell granule remnants	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2047_s_144	7583588	24  Moreover, a specific mechanism that increases the strength of binding between LDL particles and mast cell granule remnants was recently discovered.	bind
27215	1	7376	5	13	NULL	NULL	NULL	IgG	GP		bind					MDA-LDL antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_18_2277_s_43	11342477	24  The amount of IgG bound to the MDA-LDL antigen was detected with alkaline phosphatase - labeled anti-mouse IgG.	bind
29449	1	7376	7	NULL	NULL	0	NULL	IgG	NULL		bind	NULL				MDA-LDL antigen	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_18_2277_s_43	11342477	24  The amount of IgG bound to the MDA-LDL antigen was detected with alkaline phosphatase - labeled anti-mouse IgG.	bind
27216	1	7377	5	13	NULL	NULL	NULL	IL-1R1	GP		is					IL-1 receptor 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
27217	2	7377	5	13	NULL	NULL	NULL	 IL-1	GP		bind					IL-1R1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
27218	3	7377	5	13	NULL	NULL	NULL	IL-1	GP		bind					accessory protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
27219	4	7377	5	13	NULL	NULL	NULL	statement 2	Process		triggers					signal transduction	Process	intracellular			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
27220	5	7377	5	13	NULL	NULL	NULL	statement 3	Process		triggers					signal transduction	Process	intracellular			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
27221	6	7377	5	13	NULL	NULL	NULL	statement 4 & 5	Process		activates					vasoactive substances	GP	synthesis of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
27222	7	7377	5	13	NULL	NULL	NULL	statement 4 & 5	Process		activates					growth factors	GP	synthesis of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
27223	8	7377	5	13	NULL	NULL	NULL	statement 4 & 5	Process		activates					cytokines	GP	synthesis of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
27224	9	7377	5	13	NULL	NULL	NULL	chemokines	GP		attract					monocyte-derived cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
27225	10	7377	5	13	NULL	NULL	NULL	statement 2	Process		increases					adhesion molecules	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
27226	11	7377	5	13	NULL	NULL	NULL	statement 3	Process		increases					adhesion molecules	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
27227	12	7377	5	13	NULL	NULL	NULL	statement 2	Process		increases					statement 9	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
27228	13	7377	5	13	NULL	NULL	NULL	statement 3	Process		increases					statement 9	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
27229	14	7377	5	13	NULL	NULL	NULL	statement 2	Process		enhances					diapedesis	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
27230	15	7377	5	13	NULL	NULL	NULL	statement 3	Process		enhances					diapedesis	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
29450	1	7377	7	NULL	NULL	0	NULL	 IL-1	NULL		bind	NULL				IL-1R1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
29451	2	7377	7	NULL	NULL	0	NULL	IL-1	NULL		binds	NULL				IL-1R1 accessory protein	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
29452	3	7377	7	NULL	NULL	0	NULL	statement 1	NULL		triggers	NULL				signal transduction	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
29453	4	7377	7	NULL	NULL	0	NULL	statement 2	NULL		triggers	NULL				signal transduction	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
29454	5	7377	7	NULL	NULL	0	NULL	statement 3	NULL		activates	NULL				vasoactive substances	NULL	synthesis of			NULL		0	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
29455	6	7377	7	NULL	NULL	0	NULL	statement 4	NULL		activates	NULL				vasoactive substances	NULL	synthesis of			NULL		0	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
29456	7	7377	7	NULL	NULL	0	NULL	statement 3	NULL		activates	NULL				growth factors	NULL	synthesis of			NULL		0	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
29457	8	7377	7	NULL	NULL	0	NULL	statement 4	NULL		activates	NULL				growth factors	NULL	synthesis of			NULL		0	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
29458	9	7377	7	NULL	NULL	0	NULL	statement 3	NULL		activates	NULL				cytokines	NULL	synthesis of			NULL		0	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
29459	10	7377	7	NULL	NULL	0	NULL	statement 4	NULL		activates	NULL				cytokines	NULL	synthesis of			NULL		0	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
29460	11	7377	7	NULL	NULL	0	NULL	statement 3	NULL		increase	NULL				vascular adhesion molecules	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
29461	12	7377	7	NULL	NULL	0	NULL	statement 4	NULL		increase	NULL				vascular adhesion molecules	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
29464	13	7377	7	NULL	NULL	0	NULL	statement 3	NULL		increase	NULL				chemokines	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
29465	14	7377	7	NULL	NULL	0	NULL	statement 4	NULL		increase	NULL				chemokines	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
29466	15	7377	7	NULL	NULL	0	NULL	chemokines	NULL		attract	NULL				monocyte-derived cells	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
29467	16	7377	7	NULL	NULL	0	NULL	statement 15	NULL		enhance	NULL				diapedesis	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
29468	17	7377	7	NULL	NULL	0	NULL	chemokines	NULL		stimulate	NULL				monocyte-derived cells	NULL	proliferation of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
29469	18	7377	7	NULL	NULL	0	NULL	chemokines	NULL		stimulate	NULL				monocyte-derived cells	NULL	differentiation of			NULL		0	NULL	NULL	NULL	gw70_circulation_110_12_1678_s_31	15353494	24 - 26   IL-1 binding to the IL-1 receptor 1 (IL-1R1) and its accessory protein triggers intracellular signal transduction to activate the synthesis of vasoactive substances, growth factors, and cytokines, as well as increases the expression of vascular adhesion molecules and chemokines that attract monocyte-derived cells, enhance diapedesis, and stimulate their proliferation and differentiation.	bind
27231	1	7378	5	13	NULL	NULL	NULL	TNF-alpha 	GP		combines with					IFN-gamma	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_2_227_s_136	11156857	24 25 26  For example, the combination of TNF-alpha and IFN-gamma activates the human class I MHC promoter synergistically, and this induction requires the binding of both NF-kappaB and IRF-1 to the class I MHC promoter.	bind
27232	2	7378	5	13	NULL	NULL	NULL	NF-kappaB	GP		bind					class I MHC	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_2_227_s_136	11156857	24 25 26  For example, the combination of TNF-alpha and IFN-gamma activates the human class I MHC promoter synergistically, and this induction requires the binding of both NF-kappaB and IRF-1 to the class I MHC promoter.	bind
27233	3	7378	5	13	NULL	NULL	NULL	IRF-1	GP		bind					class I MHC	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_2_227_s_136	11156857	24 25 26  For example, the combination of TNF-alpha and IFN-gamma activates the human class I MHC promoter synergistically, and this induction requires the binding of both NF-kappaB and IRF-1 to the class I MHC promoter.	bind
27234	4	7378	5	13	NULL	NULL	NULL	statement 1	Process		requires					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_2_227_s_136	11156857	24 25 26  For example, the combination of TNF-alpha and IFN-gamma activates the human class I MHC promoter synergistically, and this induction requires the binding of both NF-kappaB and IRF-1 to the class I MHC promoter.	bind
27235	5	7378	5	13	NULL	NULL	NULL	statement 1	Process		requires					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_2_227_s_136	11156857	24 25 26  For example, the combination of TNF-alpha and IFN-gamma activates the human class I MHC promoter synergistically, and this induction requires the binding of both NF-kappaB and IRF-1 to the class I MHC promoter.	bind
46602	6	7378	5	13	NULL	NULL	NULL	statement 1	Process		activates					class I MHC	GP	human		promoter	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_2_227_s_136	11156857	24 25 26  For example, the combination of TNF-alpha and IFN-gamma activates the human class I MHC promoter synergistically, and this induction requires the binding of both NF-kappaB and IRF-1 to the class I MHC promoter.	bind
29471	1	7378	7	NULL	NULL	0	NULL	TNF-alpha	NULL		combines with	NULL				IFN-gamma	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_2_227_s_136	11156857	24 25 26  For example, the combination of TNF-alpha and IFN-gamma activates the human class I MHC promoter synergistically, and this induction requires the binding of both NF-kappaB and IRF-1 to the class I MHC promoter.	bind
29472	2	7378	7	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				class I MHC	NULL	human		promoter	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_2_227_s_136	11156857	24 25 26  For example, the combination of TNF-alpha and IFN-gamma activates the human class I MHC promoter synergistically, and this induction requires the binding of both NF-kappaB and IRF-1 to the class I MHC promoter.	bind
29478	3	7378	7	NULL	NULL	0	NULL	statement 2	NULL		occurs synergistically with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_2_227_s_136	11156857	24 25 26  For example, the combination of TNF-alpha and IFN-gamma activates the human class I MHC promoter synergistically, and this induction requires the binding of both NF-kappaB and IRF-1 to the class I MHC promoter.	bind
29479	4	7378	7	NULL	NULL	0	NULL	NF-kappaB 	NULL		binds to	NULL				class I MHC	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_2_227_s_136	11156857	24 25 26  For example, the combination of TNF-alpha and IFN-gamma activates the human class I MHC promoter synergistically, and this induction requires the binding of both NF-kappaB and IRF-1 to the class I MHC promoter.	bind
29480	5	7378	7	NULL	NULL	0	NULL	IRF-1	NULL		binds to	NULL				class I MHC	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_2_227_s_136	11156857	24 25 26  For example, the combination of TNF-alpha and IFN-gamma activates the human class I MHC promoter synergistically, and this induction requires the binding of both NF-kappaB and IRF-1 to the class I MHC promoter.	bind
29481	6	7378	7	NULL	NULL	0	NULL	statement 3	NULL		requires	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_2_227_s_136	11156857	24 25 26  For example, the combination of TNF-alpha and IFN-gamma activates the human class I MHC promoter synergistically, and this induction requires the binding of both NF-kappaB and IRF-1 to the class I MHC promoter.	bind
29482	7	7378	7	NULL	NULL	0	NULL	statement 3	NULL		requires	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_2_227_s_136	11156857	24 25 26  For example, the combination of TNF-alpha and IFN-gamma activates the human class I MHC promoter synergistically, and this induction requires the binding of both NF-kappaB and IRF-1 to the class I MHC promoter.	bind
27236	1	7380	5	13	NULL	NULL	NULL				bind		strongly		palindromic CRE	CREB	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
27237	2	7380	5	13	NULL	NULL	NULL				bind		strongly		palindromic CRE	ATF1	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
27238	3	7380	5	13	NULL	NULL	NULL				bind		strongly		palindromic CRE	ATF2	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
27239	4	7380	5	13	NULL	NULL	NULL				bind		strongly		palindromic CRE	c-Jun	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
27240	5	7380	5	13	NULL	NULL	NULL	CREB	GP		is a member of					bZIP family	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
27241	6	7380	5	13	NULL	NULL	NULL	ATF1	GP		is a member of					bZIP family	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
27242	7	7380	5	13	NULL	NULL	NULL	ATF2	GP		is a member of					bZIP family	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
27243	8	7380	5	13	NULL	NULL	NULL	c-Jun	GP		is a member of					bZIP family	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
27244	9	7380	5	13	NULL	NULL	NULL			variant	bind		predominantly		CRE	ATF2	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
27245	10	7380	5	13	NULL	NULL	NULL			variant	bind		predominantly		CRE	c-Jun	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
29483	1	7380	7	NULL	NULL	0	NULL	 	NULL		bind	NULL	strongly		palindromic CRE	CREB	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
29484	2	7380	7	NULL	NULL	0	NULL		NULL		bind	NULL	strongly		palindromic CRE	ATF1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
29485	3	7380	7	NULL	NULL	0	NULL		NULL		bind	NULL	strongly		palindromic CRE	ATF2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
29486	4	7380	7	NULL	NULL	0	NULL		NULL		bind	NULL	strongly		palindromic CRE	c-Jun	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
29487	5	7380	7	NULL	NULL	0	NULL		NULL		bind	NULL			variant CRE	ATF2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
29488	6	7380	7	NULL	NULL	0	NULL		NULL		bind	NULL			variant CRE	c-Jun	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
29489	7	7380	7	NULL	NULL	0	NULL	CREB	NULL		belongs to	NULL				bZIP family	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
29490	8	7380	7	NULL	NULL	0	NULL	ATF1	NULL		belongs to	NULL				bZIP family	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
29491	9	7380	7	NULL	NULL	0	NULL	ATF2	NULL		belongs to	NULL				bZIP family	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
29492	10	7380	7	NULL	NULL	0	NULL	c-Jun	NULL		belongs to	NULL				bZIP family	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_1036_s_157	16497991	24 Although palindromic CRE bind strongly to several members of the bZIP family, including CREB, ATF1, ATF2, and c-Jun, variant CRE binds to predominantly ATF2 and c-Jun.	bind
27246	1	7381	5	13	NULL	NULL	NULL	SRF	GP		bind					SMalpha-actin	GP			CArG containing regions of promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2328_s_190	16151017	24 Although the authors did not find the effect of KLF4 on SRF - DNA binding in EMSA, they observed that overexpression of KLF4 was associated with reduction in SRF binding to CArG containing regions of SMalpha-actin promoter.	bind
27247	2	7381	5	13	NULL	NULL	NULL	KLF4	GP	overexpression of	reduces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2328_s_190	16151017	24 Although the authors did not find the effect of KLF4 on SRF - DNA binding in EMSA, they observed that overexpression of KLF4 was associated with reduction in SRF binding to CArG containing regions of SMalpha-actin promoter.	bind
29493	1	7381	7	NULL	NULL	0	NULL	SRF	NULL		binds	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2328_s_190	16151017	24 Although the authors did not find the effect of KLF4 on SRF - DNA binding in EMSA, they observed that overexpression of KLF4 was associated with reduction in SRF binding to CArG containing regions of SMalpha-actin promoter.	bind
29494	2	7381	7	10	NULL	0	NULL	SRF 	NULL		binds to	NULL				SMalpha-actin	NULL			CArG containing regions of promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2328_s_190	16151017	24 Although the authors did not find the effect of KLF4 on SRF - DNA binding in EMSA, they observed that overexpression of KLF4 was associated with reduction in SRF binding to CArG containing regions of SMalpha-actin promoter.	bind
29495	3	7381	7	NULL	NULL	0	NULL	KLF4	NULL	overexpression	reduce	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2328_s_190	16151017	24 Although the authors did not find the effect of KLF4 on SRF - DNA binding in EMSA, they observed that overexpression of KLF4 was associated with reduction in SRF binding to CArG containing regions of SMalpha-actin promoter.	bind
27248	1	7382	5	13	NULL	NULL	NULL	 iron protoporphyrin IX	Chemical		attached to		covalently			FixL	GP		histidine residue		NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_6_2995_s_29	11248020	24 and  25); ( ii) iron protoporphyrin IX covalently attached to a histidine residue in FixL (sensor protein in  Rhizobium nitrogen fixation pathway; ref.  26); ( iii) flavin adenine dinucleotide noncovalently bound to nitrogen fixation regulatory protein L and  Escherichia coli aerotaxis sensor ( 27-29); and ( iv) FMN noncovalently bound to phototropin ( 9,  12).	bind
27249	2	7382	5	13	NULL	NULL	NULL	FixL	GP		is a type of					sensor protein	GP	Rhizobium nitrogen fixation pathway			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_6_2995_s_29	11248020	24 and  25); ( ii) iron protoporphyrin IX covalently attached to a histidine residue in FixL (sensor protein in  Rhizobium nitrogen fixation pathway; ref.  26); ( iii) flavin adenine dinucleotide noncovalently bound to nitrogen fixation regulatory protein L and  Escherichia coli aerotaxis sensor ( 27-29); and ( iv) FMN noncovalently bound to phototropin ( 9,  12).	bind
27250	3	7382	5	13	NULL	NULL	NULL	flavin adenine dinucleotide	Chemical		bind		noncovalently			nitrogen fixation regulatory protein L	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_6_2995_s_29	11248020	24 and  25); ( ii) iron protoporphyrin IX covalently attached to a histidine residue in FixL (sensor protein in  Rhizobium nitrogen fixation pathway; ref.  26); ( iii) flavin adenine dinucleotide noncovalently bound to nitrogen fixation regulatory protein L and  Escherichia coli aerotaxis sensor ( 27-29); and ( iv) FMN noncovalently bound to phototropin ( 9,  12).	bind
27251	4	7382	5	13	NULL	NULL	NULL	flavin adenine dinucleotide	Chemical		bind		noncovalently			aerotaxis sensor		Escherichia coli			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_6_2995_s_29	11248020	24 and  25); ( ii) iron protoporphyrin IX covalently attached to a histidine residue in FixL (sensor protein in  Rhizobium nitrogen fixation pathway; ref.  26); ( iii) flavin adenine dinucleotide noncovalently bound to nitrogen fixation regulatory protein L and  Escherichia coli aerotaxis sensor ( 27-29); and ( iv) FMN noncovalently bound to phototropin ( 9,  12).	bind
27252	5	7382	5	13	NULL	NULL	NULL	FMN	Chemical		bind		noncovalently			phototropin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_6_2995_s_29	11248020	24 and  25); ( ii) iron protoporphyrin IX covalently attached to a histidine residue in FixL (sensor protein in  Rhizobium nitrogen fixation pathway; ref.  26); ( iii) flavin adenine dinucleotide noncovalently bound to nitrogen fixation regulatory protein L and  Escherichia coli aerotaxis sensor ( 27-29); and ( iv) FMN noncovalently bound to phototropin ( 9,  12).	bind
29496	1	7382	7	NULL	NULL	0	NULL	iron protoporphyrin IX 	NULL		binds	NULL	covalently			FixL	NULL		histidine residue		NULL		0	NULL	NULL	NULL	gw60_pnas_98_6_2995_s_29	11248020	24 and  25); ( ii) iron protoporphyrin IX covalently attached to a histidine residue in FixL (sensor protein in  Rhizobium nitrogen fixation pathway; ref.  26); ( iii) flavin adenine dinucleotide noncovalently bound to nitrogen fixation regulatory protein L and  Escherichia coli aerotaxis sensor ( 27-29); and ( iv) FMN noncovalently bound to phototropin ( 9,  12).	bind
29497	2	7382	7	NULL	NULL	0	NULL	FixL	NULL		is a type of	NULL				sensor protein	NULL	Rhizobium nitrogen fixation pathway			NULL		0	NULL	NULL	NULL	gw60_pnas_98_6_2995_s_29	11248020	24 and  25); ( ii) iron protoporphyrin IX covalently attached to a histidine residue in FixL (sensor protein in  Rhizobium nitrogen fixation pathway; ref.  26); ( iii) flavin adenine dinucleotide noncovalently bound to nitrogen fixation regulatory protein L and  Escherichia coli aerotaxis sensor ( 27-29); and ( iv) FMN noncovalently bound to phototropin ( 9,  12).	bind
29498	3	7382	7	NULL	NULL	0	NULL	flavin adenine dinucleotide 	NULL		bind	NULL	noncovalently			nitrogen fixation regulatory protein L	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_98_6_2995_s_29	11248020	24 and  25); ( ii) iron protoporphyrin IX covalently attached to a histidine residue in FixL (sensor protein in  Rhizobium nitrogen fixation pathway; ref.  26); ( iii) flavin adenine dinucleotide noncovalently bound to nitrogen fixation regulatory protein L and  Escherichia coli aerotaxis sensor ( 27-29); and ( iv) FMN noncovalently bound to phototropin ( 9,  12).	bind
29499	4	7382	7	NULL	NULL	0	NULL	flavin adenine dinucleotide 	NULL		bind	NULL	noncovalently			aerotaxis sensor	NULL	Escherichia coli 			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_6_2995_s_29	11248020	24 and  25); ( ii) iron protoporphyrin IX covalently attached to a histidine residue in FixL (sensor protein in  Rhizobium nitrogen fixation pathway; ref.  26); ( iii) flavin adenine dinucleotide noncovalently bound to nitrogen fixation regulatory protein L and  Escherichia coli aerotaxis sensor ( 27-29); and ( iv) FMN noncovalently bound to phototropin ( 9,  12).	bind
29500	5	7382	7	NULL	NULL	0	NULL	FMN	NULL		bind	NULL	noncovalently			phototropin	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_98_6_2995_s_29	11248020	24 and  25); ( ii) iron protoporphyrin IX covalently attached to a histidine residue in FixL (sensor protein in  Rhizobium nitrogen fixation pathway; ref.  26); ( iii) flavin adenine dinucleotide noncovalently bound to nitrogen fixation regulatory protein L and  Escherichia coli aerotaxis sensor ( 27-29); and ( iv) FMN noncovalently bound to phototropin ( 9,  12).	bind
27253	1	7383	5	13	NULL	NULL	NULL	VLDL E+	GP		transfered to					VLDL E-	GP	nascent			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_141	11557678	24 Another source of the apoE on VLDL could be from VLDL E+ transferring to nascent VLDL E-, although not so extensively as to produce a donor VLDL particle that no longerR binds to the anti-apoE column.	bind
27254	2	7383	5	13	NULL	NULL	NULL	statement 1	Process		is a source of					apoE	GP				NULL	VLDL	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_141	11557678	24 Another source of the apoE on VLDL could be from VLDL E+ transferring to nascent VLDL E-, although not so extensively as to produce a donor VLDL particle that no longerR binds to the anti-apoE column.	bind
29501	1	7383	7	NULL	NULL	0	NULL	VLDL E+	NULL		transfer to	NULL				VLDL E	NULL	nascent			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_141	11557678	24 Another source of the apoE on VLDL could be from VLDL E+ transferring to nascent VLDL E-, although not so extensively as to produce a donor VLDL particle that no longerR binds to the anti-apoE column.	bind
29503	2	7383	7	10	NULL	0	NULL	apoE VLDL			is from					statement 1					NULL	VLDL	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_141	11557678	24 Another source of the apoE on VLDL could be from VLDL E+ transferring to nascent VLDL E-, although not so extensively as to produce a donor VLDL particle that no longerR binds to the anti-apoE column.	bind
27336	1	7385	5	13	NULL	NULL	NULL	HBP/vigilin	GP		is associated with					t-RNA-protein complexes	GP	cytoplasmic			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2350_s_222	9409201	24 HBP/vigilin has also been found to be associated with cytoplasmic t-RNA-protein complexes isolated from human liver cells21 and from  Xenopus liver bound to vitellogenin mRNA.22 HBP/vigilin has also been reported to contain a functional nuclear localization sequence and to be present in the nucleus.	bind
27338	2	7385	5	13	NULL	NULL	NULL	t-RNA-protein complexes	GP	cytoplasmic	is isolated from					liver cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2350_s_222	9409201	24 HBP/vigilin has also been found to be associated with cytoplasmic t-RNA-protein complexes isolated from human liver cells21 and from  Xenopus liver bound to vitellogenin mRNA.22 HBP/vigilin has also been reported to contain a functional nuclear localization sequence and to be present in the nucleus.	bind
27341	3	7385	5	13	NULL	NULL	NULL	HBP/vigilin	GP		bind					vitellogenin mRNA	NucleicAcid				NULL	Xenopus liver	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2350_s_222	9409201	24 HBP/vigilin has also been found to be associated with cytoplasmic t-RNA-protein complexes isolated from human liver cells21 and from  Xenopus liver bound to vitellogenin mRNA.22 HBP/vigilin has also been reported to contain a functional nuclear localization sequence and to be present in the nucleus.	bind
27343	4	7385	5	13	NULL	NULL	NULL	HBP/vigilin	GP		contains							functional	nuclear localization sequence		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2350_s_222	9409201	24 HBP/vigilin has also been found to be associated with cytoplasmic t-RNA-protein complexes isolated from human liver cells21 and from  Xenopus liver bound to vitellogenin mRNA.22 HBP/vigilin has also been reported to contain a functional nuclear localization sequence and to be present in the nucleus.	bind
27344	5	7385	5	13	NULL	NULL	NULL	HBP/vigilin	GP		is present in					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2350_s_222	9409201	24 HBP/vigilin has also been found to be associated with cytoplasmic t-RNA-protein complexes isolated from human liver cells21 and from  Xenopus liver bound to vitellogenin mRNA.22 HBP/vigilin has also been reported to contain a functional nuclear localization sequence and to be present in the nucleus.	bind
29506	1	7385	7	NULL	NULL	0	NULL	HBP/vigilin	NULL		associate with	NULL				 t-RNA-protein complexes 	NULL	cytoplasmic			NULL	human liver cells	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2350_s_222	9409201	24 HBP/vigilin has also been found to be associated with cytoplasmic t-RNA-protein complexes isolated from human liver cells21 and from  Xenopus liver bound to vitellogenin mRNA.22 HBP/vigilin has also been reported to contain a functional nuclear localization sequence and to be present in the nucleus.	bind
29507	2	7385	7	NULL	NULL	0	NULL	Xenopus liver	NULL		binds to	NULL				vitellogenin mRNA	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2350_s_222	9409201	24 HBP/vigilin has also been found to be associated with cytoplasmic t-RNA-protein complexes isolated from human liver cells21 and from  Xenopus liver bound to vitellogenin mRNA.22 HBP/vigilin has also been reported to contain a functional nuclear localization sequence and to be present in the nucleus.	bind
29508	3	7385	7	NULL	NULL	0	NULL	HBP/vigilin	NULL		associate with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2350_s_222	9409201	24 HBP/vigilin has also been found to be associated with cytoplasmic t-RNA-protein complexes isolated from human liver cells21 and from  Xenopus liver bound to vitellogenin mRNA.22 HBP/vigilin has also been reported to contain a functional nuclear localization sequence and to be present in the nucleus.	bind
29509	4	7385	7	NULL	NULL	0	NULL	HBP/vigilin	NULL		contains	NULL				functional nuclear localization sequence	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2350_s_222	9409201	24 HBP/vigilin has also been found to be associated with cytoplasmic t-RNA-protein complexes isolated from human liver cells21 and from  Xenopus liver bound to vitellogenin mRNA.22 HBP/vigilin has also been reported to contain a functional nuclear localization sequence and to be present in the nucleus.	bind
29510	5	7385	7	NULL	NULL	0	NULL	HBP/vigilin	NULL		is present in the 	NULL				nucleus	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2350_s_222	9409201	24 HBP/vigilin has also been found to be associated with cytoplasmic t-RNA-protein complexes isolated from human liver cells21 and from  Xenopus liver bound to vitellogenin mRNA.22 HBP/vigilin has also been reported to contain a functional nuclear localization sequence and to be present in the nucleus.	bind
27346	1	7386	5	13	NULL	NULL	NULL	Hp	GP		is found in		normally			serum	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_11_1193_s_214	12750308	24 Hp is normally found in serum in a >400 molar excess compared with free Hb, 25 and therefore all intravascular free Hb will be rapidly bound by Hp, preventing Hb-induced oxidation.	bind
27348	2	7386	5	13	NULL	NULL	NULL	Hb	GP	free	is found in					serum	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_11_1193_s_214	12750308	24 Hp is normally found in serum in a >400 molar excess compared with free Hb, 25 and therefore all intravascular free Hb will be rapidly bound by Hp, preventing Hb-induced oxidation.	bind
27349	3	7386	5	13	NULL	NULL	NULL	statement 1	GP		is more abundant than					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_11_1193_s_214	12750308	24 Hp is normally found in serum in a >400 molar excess compared with free Hb, 25 and therefore all intravascular free Hb will be rapidly bound by Hp, preventing Hb-induced oxidation.	bind
27350	4	7386	5	13	NULL	NULL	NULL	Hb	GP	intravascular free	bind		rapidly			Hp	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_11_1193_s_214	12750308	24 Hp is normally found in serum in a >400 molar excess compared with free Hb, 25 and therefore all intravascular free Hb will be rapidly bound by Hp, preventing Hb-induced oxidation.	bind
27351	5	7386	5	13	NULL	NULL	NULL	Hb	GP		induces					oxidation	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_11_1193_s_214	12750308	24 Hp is normally found in serum in a >400 molar excess compared with free Hb, 25 and therefore all intravascular free Hb will be rapidly bound by Hp, preventing Hb-induced oxidation.	bind
54484	6	7386	5	13	NULL	NULL	NULL	statement 4	Process		prevents					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_11_1193_s_214	12750308	24 Hp is normally found in serum in a >400 molar excess compared with free Hb, 25 and therefore all intravascular free Hb will be rapidly bound by Hp, preventing Hb-induced oxidation.	bind
29511	1	7386	7	10	NULL	0	NULL	Hp			is found in		normally			serum					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_11_1193_s_214	12750308	24 Hp is normally found in serum in a >400 molar excess compared with free Hb, 25 and therefore all intravascular free Hb will be rapidly bound by Hp, preventing Hb-induced oxidation.	bind
29512	2	7386	7	NULL	NULL	0	NULL	Hp	NULL		bind	NULL	rapidly			Hb	NULL	intravascular free			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_11_1193_s_214	12750308	24 Hp is normally found in serum in a >400 molar excess compared with free Hb, 25 and therefore all intravascular free Hb will be rapidly bound by Hp, preventing Hb-induced oxidation.	bind
29513	3	7386	7	NULL	NULL	0	NULL	Hb	NULL		induce	NULL				oxidation	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_11_1193_s_214	12750308	24 Hp is normally found in serum in a >400 molar excess compared with free Hb, 25 and therefore all intravascular free Hb will be rapidly bound by Hp, preventing Hb-induced oxidation.	bind
29514	4	7386	7	NULL	NULL	0	NULL	statement 2	NULL		prevents	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_11_1193_s_214	12750308	24 Hp is normally found in serum in a >400 molar excess compared with free Hb, 25 and therefore all intravascular free Hb will be rapidly bound by Hp, preventing Hb-induced oxidation.	bind
54485	5	7386	7	10	NULL	0	NULL	Hb		free	is found in					serum					NULL		0	NULL	NULL	NULL	gw60_circulationres_92_11_1193_s_214	12750308	24 Hp is normally found in serum in a >400 molar excess compared with free Hb, 25 and therefore all intravascular free Hb will be rapidly bound by Hp, preventing Hb-induced oxidation.	bind
54486	6	7386	7	10	NULL	0	NULL	statement 1			is more abundant than					statement 2					NULL		0	NULL	NULL	NULL	gw60_circulationres_92_11_1193_s_214	12750308	24 Hp is normally found in serum in a >400 molar excess compared with free Hb, 25 and therefore all intravascular free Hb will be rapidly bound by Hp, preventing Hb-induced oxidation.	bind
27356	1	7387	5	13	NULL	NULL	NULL	PPRE	NucleicAcid		is					PPAR response elements	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_546_s_32	10073956	24 Once activated, PPARgamma binds to the PPAR response elements (PPRE) in the promotor region of target genes.	bind
27358	2	7387	5	13	NULL	NULL	NULL	PPARgamma	GP	activated	bind					target genes	GP			PPRE in promoter	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_546_s_32	10073956	24 Once activated, PPARgamma binds to the PPAR response elements (PPRE) in the promotor region of target genes.	bind
29613	1	7387	7	10	NULL	0	NULL	PPARgamma		activated	binds to					target gene				PPRE in promoter	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_546_s_32	10073956	24 Once activated, PPARgamma binds to the PPAR response elements (PPRE) in the promotor region of target genes.	bind
29614	2	7387	7	NULL	NULL	0	NULL	PPRE	NULL		is	NULL				PPAR response elements	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_546_s_32	10073956	24 Once activated, PPARgamma binds to the PPAR response elements (PPRE) in the promotor region of target genes.	bind
27359	1	7388	5	13	NULL	NULL	NULL	SRE-1	NucleicAcid		bind					SREBP-1a	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_24_3104_s_25	12473559	24 SRE-1 can bind 3 different transcription factors: SREBP-1a, SREBP-1c, and SREBP-2.	bind
27360	2	7388	5	13	NULL	NULL	NULL	SRE-1	NucleicAcid		bind					SREBP-1c	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_24_3104_s_25	12473559	24 SRE-1 can bind 3 different transcription factors: SREBP-1a, SREBP-1c, and SREBP-2.	bind
27361	3	7388	5	13	NULL	NULL	NULL	SRE-1	NucleicAcid		bind					SREBP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_24_3104_s_25	12473559	24 SRE-1 can bind 3 different transcription factors: SREBP-1a, SREBP-1c, and SREBP-2.	bind
29615	1	7388	7	NULL	NULL	0	NULL	 SRE-1	NULL		bind	NULL				SREBP-1a	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_24_3104_s_25	12473559	24 SRE-1 can bind 3 different transcription factors: SREBP-1a, SREBP-1c, and SREBP-2.	bind
29616	2	7388	7	NULL	NULL	0	NULL	SRE-1	NULL		bind	NULL				 SREBP-1c	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_24_3104_s_25	12473559	24 SRE-1 can bind 3 different transcription factors: SREBP-1a, SREBP-1c, and SREBP-2.	bind
29617	3	7388	7	NULL	NULL	0	NULL	SRE-1	NULL		bind	NULL				SREBP-2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_24_3104_s_25	12473559	24 SRE-1 can bind 3 different transcription factors: SREBP-1a, SREBP-1c, and SREBP-2.	bind
27363	1	7389	5	13	NULL	NULL	NULL	synthetic peptides	GP		contains					9 contiguous arginine residues	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_61	15231514	24 Synthetic peptides containing 9 contiguous arginine residues bind heparin with affinity similar to that of heparin-binding proteins.	bind
27364	2	7389	5	13	NULL	NULL	NULL	statement 1	GP		bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_61	15231514	24 Synthetic peptides containing 9 contiguous arginine residues bind heparin with affinity similar to that of heparin-binding proteins.	bind
27365	3	7389	5	13	NULL	NULL	NULL	statement 1	GP		bind					heparin-binding proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_61	15231514	24 Synthetic peptides containing 9 contiguous arginine residues bind heparin with affinity similar to that of heparin-binding proteins.	bind
27367	4	7389	5	13	NULL	NULL	NULL	statement 2	Process		similar affinity as					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_61	15231514	24 Synthetic peptides containing 9 contiguous arginine residues bind heparin with affinity similar to that of heparin-binding proteins.	bind
29618	2	7389	7	10	NULL	0	NULL	statement 1	NULL		bind	NULL				heparin	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_61	15231514	24 Synthetic peptides containing 9 contiguous arginine residues bind heparin with affinity similar to that of heparin-binding proteins.	bind
29619	3	7389	7	10	NULL	0	NULL	statement 1	NULL		bind	NULL				heparin-binding proteins	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_61	15231514	24 Synthetic peptides containing 9 contiguous arginine residues bind heparin with affinity similar to that of heparin-binding proteins.	bind
46603	1	7389	7	10	NULL	0	NULL	sythetic peptides 	NULL		contain	NULL				9 contiguous arginine residues	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_61	15231514	24 Synthetic peptides containing 9 contiguous arginine residues bind heparin with affinity similar to that of heparin-binding proteins.	bind
46604	4	7389	7	10	NULL	0	NULL	statement 2	NULL		is similar to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_61	15231514	24 Synthetic peptides containing 9 contiguous arginine residues bind heparin with affinity similar to that of heparin-binding proteins.	bind
27369	1	7390	5	13	NULL	NULL	NULL	P300	GP		bind									CRE/E-box complex	NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_23_2760_s_125	12057991	24 We determined P300 binding to the CRE/E-box complex.	bind
29620	1	7390	7	NULL	NULL	0	NULL	P300	NULL		binds to	NULL					NULL			CRE/E-box complex	NULL		0	NULL	NULL	NULL	gw60_circulation_105_23_2760_s_125	12057991	24 We determined P300 binding to the CRE/E-box complex.	bind
27373	1	7391	5	13	NULL	NULL	NULL	GFP-FRNK	GP		bind		competitively	C-terminal FAT sequence		paxillin	GP				NULL	NRVMs overexpressing GFP-FRNK	NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1282_s_219	12089066	24 We now show that in NRVMs overexpressing GFP-FRNK, FAK was displaced from focal adhesions, which was likely the result of competitive binding of GFP-FRNK to paxillin and other cytoskeletal proteins via its identical C-terminal FAT sequence.	bind
27375	2	7391	5	13	NULL	NULL	NULL	GFP-FRNK	GP		bind		competitively	C-terminal FAT sequence		cytoskeletal proteins	GP				NULL	NRVMs overexpressing GFP-FRNK	NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1282_s_219	12089066	24 We now show that in NRVMs overexpressing GFP-FRNK, FAK was displaced from focal adhesions, which was likely the result of competitive binding of GFP-FRNK to paxillin and other cytoskeletal proteins via its identical C-terminal FAT sequence.	bind
27379	3	7391	5	13	NULL	NULL	NULL	FAK	GP		is displaced from					focal adhesions	CellComponent				NULL	NRVMs overexpressing GFP-FRNK	NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1282_s_219	12089066	24 We now show that in NRVMs overexpressing GFP-FRNK, FAK was displaced from focal adhesions, which was likely the result of competitive binding of GFP-FRNK to paxillin and other cytoskeletal proteins via its identical C-terminal FAT sequence.	bind
27386	4	7391	5	13	NULL	NULL	NULL	statement 1	Process		results in		likely			statement 3	Process				NULL	NRVMs overexpressing GFP-FRNK	NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1282_s_219	12089066	24 We now show that in NRVMs overexpressing GFP-FRNK, FAK was displaced from focal adhesions, which was likely the result of competitive binding of GFP-FRNK to paxillin and other cytoskeletal proteins via its identical C-terminal FAT sequence.	bind
27388	5	7391	5	13	NULL	NULL	NULL	statement 2	Process		results in		likely			statement 3	Process				NULL	NRVMs overexpressing GFP-FRNK	NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1282_s_219	12089066	24 We now show that in NRVMs overexpressing GFP-FRNK, FAK was displaced from focal adhesions, which was likely the result of competitive binding of GFP-FRNK to paxillin and other cytoskeletal proteins via its identical C-terminal FAT sequence.	bind
29621	1	7391	7	NULL	NULL	0	NULL	 GFP-FRNK	NULL		bind	NULL		C-terminal FAT sequence		 paxillin	NULL				NULL	NRVMs overexpressing GFP-FRNK	NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1282_s_219	12089066	24 We now show that in NRVMs overexpressing GFP-FRNK, FAK was displaced from focal adhesions, which was likely the result of competitive binding of GFP-FRNK to paxillin and other cytoskeletal proteins via its identical C-terminal FAT sequence.	bind
29622	2	7391	7	NULL	NULL	0	NULL	GFP-FRNK	NULL		bind	NULL		C-terminal FAT sequence		cytoskeletal proteins	NULL				NULL	NRVMs overexpressing GFP-FRNK	NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1282_s_219	12089066	24 We now show that in NRVMs overexpressing GFP-FRNK, FAK was displaced from focal adhesions, which was likely the result of competitive binding of GFP-FRNK to paxillin and other cytoskeletal proteins via its identical C-terminal FAT sequence.	bind
29623	3	7391	7	10	NULL	0	NULL	FAK			displaced from					focal adhesions					NULL	NRVMs overexpressing GFP-FRNK	NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1282_s_219	12089066	24 We now show that in NRVMs overexpressing GFP-FRNK, FAK was displaced from focal adhesions, which was likely the result of competitive binding of GFP-FRNK to paxillin and other cytoskeletal proteins via its identical C-terminal FAT sequence.	bind
29624	4	7391	7	10	NULL	0	NULL	statement 1			leads to					statement 3					NULL	NRVMs overexpressing GFP-FRNK	NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1282_s_219	12089066	24 We now show that in NRVMs overexpressing GFP-FRNK, FAK was displaced from focal adhesions, which was likely the result of competitive binding of GFP-FRNK to paxillin and other cytoskeletal proteins via its identical C-terminal FAT sequence.	bind
29625	5	7391	7	10	NULL	0	NULL	statement 2			leads to					statement 3					NULL	NRVMs overexpressing GFP-FRNK	NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1282_s_219	12089066	24 We now show that in NRVMs overexpressing GFP-FRNK, FAK was displaced from focal adhesions, which was likely the result of competitive binding of GFP-FRNK to paxillin and other cytoskeletal proteins via its identical C-terminal FAT sequence.	bind
27394	1	7392	5	13	NULL	NULL	NULL	CD40L	GP		is					CD40 ligand	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_229_s_21	9916937	24, 25  CD40 binds CD40 ligand (CD40L, also referred to as gp39 or TRAP), a cell surface molecule until recently considered restricted to activated CD4+ T cells.	bind
27396	2	7392	5	13	NULL	NULL	NULL	CD40L	GP		is a synonym of					gp39	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_229_s_21	9916937	24, 25  CD40 binds CD40 ligand (CD40L, also referred to as gp39 or TRAP), a cell surface molecule until recently considered restricted to activated CD4+ T cells.	bind
27397	3	7392	5	13	NULL	NULL	NULL	CD40L	GP		is a synonym of					TRAP	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_229_s_21	9916937	24, 25  CD40 binds CD40 ligand (CD40L, also referred to as gp39 or TRAP), a cell surface molecule until recently considered restricted to activated CD4+ T cells.	bind
27398	4	7392	5	13	NULL	NULL	NULL	statement 2	GP		is an alternative to					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_229_s_21	9916937	24, 25  CD40 binds CD40 ligand (CD40L, also referred to as gp39 or TRAP), a cell surface molecule until recently considered restricted to activated CD4+ T cells.	bind
27400	5	7392	5	13	NULL	NULL	NULL	 CD40	GP		bind					CD40L	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_229_s_21	9916937	24, 25  CD40 binds CD40 ligand (CD40L, also referred to as gp39 or TRAP), a cell surface molecule until recently considered restricted to activated CD4+ T cells.	bind
27401	6	7392	5	13	NULL	NULL	NULL	CD40L	GP		is a type of					cell surface molecule	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_229_s_21	9916937	24, 25  CD40 binds CD40 ligand (CD40L, also referred to as gp39 or TRAP), a cell surface molecule until recently considered restricted to activated CD4+ T cells.	bind
27402	7	7392	5	13	NULL	NULL	NULL	CD40L	GP		is restricted to					CD4+ T cells	Cell	activated			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_229_s_21	9916937	24, 25  CD40 binds CD40 ligand (CD40L, also referred to as gp39 or TRAP), a cell surface molecule until recently considered restricted to activated CD4+ T cells.	bind
29626	1	7392	7	NULL	NULL	0	NULL	CD40 	NULL		binds	NULL				CD40L	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_1_229_s_21	9916937	24, 25  CD40 binds CD40 ligand (CD40L, also referred to as gp39 or TRAP), a cell surface molecule until recently considered restricted to activated CD4+ T cells.	bind
29627	2	7392	7	NULL	NULL	0	NULL	CD40L	NULL		is	NULL				CD40 ligand	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_1_229_s_21	9916937	24, 25  CD40 binds CD40 ligand (CD40L, also referred to as gp39 or TRAP), a cell surface molecule until recently considered restricted to activated CD4+ T cells.	bind
29628	3	7392	7	10	NULL	0	NULL	CD40			is a synonym of					gp39					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_229_s_21	9916937	24, 25  CD40 binds CD40 ligand (CD40L, also referred to as gp39 or TRAP), a cell surface molecule until recently considered restricted to activated CD4+ T cells.	bind
29629	4	7392	7	10	NULL	0	NULL	CD40L			is a synonym of					TRAP					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_229_s_21	9916937	24, 25  CD40 binds CD40 ligand (CD40L, also referred to as gp39 or TRAP), a cell surface molecule until recently considered restricted to activated CD4+ T cells.	bind
29630	5	7392	7	NULL	NULL	0	NULL	CD40L 	NULL		is a type of	NULL				cell surface molecule	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_1_229_s_21	9916937	24, 25  CD40 binds CD40 ligand (CD40L, also referred to as gp39 or TRAP), a cell surface molecule until recently considered restricted to activated CD4+ T cells.	bind
29631	6	7392	7	NULL	NULL	0	NULL	CD40L	NULL		is restricted to	NULL				CD4+ T cells	NULL	activated			NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_1_229_s_21	9916937	24, 25  CD40 binds CD40 ligand (CD40L, also referred to as gp39 or TRAP), a cell surface molecule until recently considered restricted to activated CD4+ T cells.	bind
27405	1	7393	5	13	NULL	NULL	NULL	FAP-1	GP		promote		may			Fas resistance	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_4_1335_s_224	11290551	24, 25  In addition, whereas FAP-1 may promote Fas resistance in some cell types, deletion of the C-terminal FAP-1-binding region of Fas did not alter its ability to induce apoptosis in murine lymphoid cell lines, implying that the relative importance of FAP-1 as an inhibitor of Fas-induced apoptosis may be dependent on cell context.	bind
27407	2	7393	5	13	NULL	NULL	NULL				is deleted from			C-terminal FAP-1-binding region		Fas	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_4_1335_s_224	11290551	24, 25  In addition, whereas FAP-1 may promote Fas resistance in some cell types, deletion of the C-terminal FAP-1-binding region of Fas did not alter its ability to induce apoptosis in murine lymphoid cell lines, implying that the relative importance of FAP-1 as an inhibitor of Fas-induced apoptosis may be dependent on cell context.	bind
27409	3	7393	5	13	NULL	NULL	NULL	Fas	GP		induces					apoptosis	Process				NULL	in murine lymphoid cell lines	NULL	NULL	NULL	NULL	gw60_amjpathol_158_4_1335_s_224	11290551	24, 25  In addition, whereas FAP-1 may promote Fas resistance in some cell types, deletion of the C-terminal FAP-1-binding region of Fas did not alter its ability to induce apoptosis in murine lymphoid cell lines, implying that the relative importance of FAP-1 as an inhibitor of Fas-induced apoptosis may be dependent on cell context.	bind
27410	4	7393	5	13	NULL	NULL	NULL	statement 2	Process		does not alter					statement 3	Process	ability of			NULL	in murine lymphoid cell lines	NULL	NULL	NULL	NULL	gw60_amjpathol_158_4_1335_s_224	11290551	24, 25  In addition, whereas FAP-1 may promote Fas resistance in some cell types, deletion of the C-terminal FAP-1-binding region of Fas did not alter its ability to induce apoptosis in murine lymphoid cell lines, implying that the relative importance of FAP-1 as an inhibitor of Fas-induced apoptosis may be dependent on cell context.	bind
27411	5	7393	5	13	NULL	NULL	NULL	FAP-1	GP		is inhibitor of					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_4_1335_s_224	11290551	24, 25  In addition, whereas FAP-1 may promote Fas resistance in some cell types, deletion of the C-terminal FAP-1-binding region of Fas did not alter its ability to induce apoptosis in murine lymphoid cell lines, implying that the relative importance of FAP-1 as an inhibitor of Fas-induced apoptosis may be dependent on cell context.	bind
27412	6	7393	5	13	NULL	NULL	NULL	statement 5	Process	importance of	is dependent on					cell context	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_4_1335_s_224	11290551	24, 25  In addition, whereas FAP-1 may promote Fas resistance in some cell types, deletion of the C-terminal FAP-1-binding region of Fas did not alter its ability to induce apoptosis in murine lymphoid cell lines, implying that the relative importance of FAP-1 as an inhibitor of Fas-induced apoptosis may be dependent on cell context.	bind
27413	7	7393	5	13	NULL	NULL	NULL	statement 4	Process		imply					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_4_1335_s_224	11290551	24, 25  In addition, whereas FAP-1 may promote Fas resistance in some cell types, deletion of the C-terminal FAP-1-binding region of Fas did not alter its ability to induce apoptosis in murine lymphoid cell lines, implying that the relative importance of FAP-1 as an inhibitor of Fas-induced apoptosis may be dependent on cell context.	bind
29632	1	7393	7	NULL	NULL	0	NULL	FAP-1	NULL		promote	NULL	may			Fas resistance	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_4_1335_s_224	11290551	24, 25  In addition, whereas FAP-1 may promote Fas resistance in some cell types, deletion of the C-terminal FAP-1-binding region of Fas did not alter its ability to induce apoptosis in murine lymphoid cell lines, implying that the relative importance of FAP-1 as an inhibitor of Fas-induced apoptosis may be dependent on cell context.	bind
29633	2	7393	7	NULL	NULL	0	NULL	Fas	NULL	deletion of	does not alter	NULL		C-terminal FAP-1-binding region		apoptosis	NULL	its ability to induce			NULL	murine lymphoid cell lines	NULL	NULL	NULL	NULL	gw60_amjpathol_158_4_1335_s_224	11290551	24, 25  In addition, whereas FAP-1 may promote Fas resistance in some cell types, deletion of the C-terminal FAP-1-binding region of Fas did not alter its ability to induce apoptosis in murine lymphoid cell lines, implying that the relative importance of FAP-1 as an inhibitor of Fas-induced apoptosis may be dependent on cell context.	bind
29634	3	7393	7	NULL	NULL	0	NULL	 Fas	NULL		induce	NULL				apoptosis	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_4_1335_s_224	11290551	24, 25  In addition, whereas FAP-1 may promote Fas resistance in some cell types, deletion of the C-terminal FAP-1-binding region of Fas did not alter its ability to induce apoptosis in murine lymphoid cell lines, implying that the relative importance of FAP-1 as an inhibitor of Fas-induced apoptosis may be dependent on cell context.	bind
29635	4	7393	7	NULL	NULL	0	NULL	 FAP-1	NULL		inhibits	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_4_1335_s_224	11290551	24, 25  In addition, whereas FAP-1 may promote Fas resistance in some cell types, deletion of the C-terminal FAP-1-binding region of Fas did not alter its ability to induce apoptosis in murine lymphoid cell lines, implying that the relative importance of FAP-1 as an inhibitor of Fas-induced apoptosis may be dependent on cell context.	bind
29636	5	7393	7	NULL	NULL	0	NULL	statement 4	NULL		depends on	NULL				cell context	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_4_1335_s_224	11290551	24, 25  In addition, whereas FAP-1 may promote Fas resistance in some cell types, deletion of the C-terminal FAP-1-binding region of Fas did not alter its ability to induce apoptosis in murine lymphoid cell lines, implying that the relative importance of FAP-1 as an inhibitor of Fas-induced apoptosis may be dependent on cell context.	bind
27414	1	7394	5	13	NULL	NULL	NULL	insulin receptor	GP		bind		high affinity			insulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_5_1905_s_282	11696451	24, 25  The insulin receptor demonstrates high-affinity binding to insulin and lower affinity binding to IGF-1, whereas the IGF-1 receptor binds IGF-1 (and IGF-2) with a higher affinity than it does insulin.	bind
27415	2	7394	5	13	NULL	NULL	NULL	insulin receptor	GP		bind		low affinity			IGF-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_5_1905_s_282	11696451	24, 25  The insulin receptor demonstrates high-affinity binding to insulin and lower affinity binding to IGF-1, whereas the IGF-1 receptor binds IGF-1 (and IGF-2) with a higher affinity than it does insulin.	bind
27416	3	7394	5	13	NULL	NULL	NULL	IGF-1 receptor	GP		bind					IGF-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_5_1905_s_282	11696451	24, 25  The insulin receptor demonstrates high-affinity binding to insulin and lower affinity binding to IGF-1, whereas the IGF-1 receptor binds IGF-1 (and IGF-2) with a higher affinity than it does insulin.	bind
27417	4	7394	5	13	NULL	NULL	NULL	IGF-1 receptor	GP		bind					IGF-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_5_1905_s_282	11696451	24, 25  The insulin receptor demonstrates high-affinity binding to insulin and lower affinity binding to IGF-1, whereas the IGF-1 receptor binds IGF-1 (and IGF-2) with a higher affinity than it does insulin.	bind
27418	5	7394	5	13	NULL	NULL	NULL	IGF-1 receptor	GP		bind					insulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_5_1905_s_282	11696451	24, 25  The insulin receptor demonstrates high-affinity binding to insulin and lower affinity binding to IGF-1, whereas the IGF-1 receptor binds IGF-1 (and IGF-2) with a higher affinity than it does insulin.	bind
27419	6	7394	5	13	NULL	NULL	NULL	statement 3	Process		has high affinity than					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_5_1905_s_282	11696451	24, 25  The insulin receptor demonstrates high-affinity binding to insulin and lower affinity binding to IGF-1, whereas the IGF-1 receptor binds IGF-1 (and IGF-2) with a higher affinity than it does insulin.	bind
27420	7	7394	5	13	NULL	NULL	NULL	statement 4	Process		has high affinity than					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_5_1905_s_282	11696451	24, 25  The insulin receptor demonstrates high-affinity binding to insulin and lower affinity binding to IGF-1, whereas the IGF-1 receptor binds IGF-1 (and IGF-2) with a higher affinity than it does insulin.	bind
29637	1	7394	7	NULL	NULL	0	NULL	insulin receptor	NULL		bind	NULL	high-affinity			insulin	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_5_1905_s_282	11696451	24, 25  The insulin receptor demonstrates high-affinity binding to insulin and lower affinity binding to IGF-1, whereas the IGF-1 receptor binds IGF-1 (and IGF-2) with a higher affinity than it does insulin.	bind
29638	2	7394	7	NULL	NULL	0	NULL	insulin receptor	NULL		bind	NULL	low affinity			IGF-1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_5_1905_s_282	11696451	24, 25  The insulin receptor demonstrates high-affinity binding to insulin and lower affinity binding to IGF-1, whereas the IGF-1 receptor binds IGF-1 (and IGF-2) with a higher affinity than it does insulin.	bind
29639	3	7394	7	NULL	NULL	0	NULL	IGF-1 receptor	NULL		binds	NULL				IGF-1 	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_5_1905_s_282	11696451	24, 25  The insulin receptor demonstrates high-affinity binding to insulin and lower affinity binding to IGF-1, whereas the IGF-1 receptor binds IGF-1 (and IGF-2) with a higher affinity than it does insulin.	bind
29640	4	7394	7	NULL	NULL	0	NULL	IGF-1 receptor	NULL		binds	NULL				IGF-2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_5_1905_s_282	11696451	24, 25  The insulin receptor demonstrates high-affinity binding to insulin and lower affinity binding to IGF-1, whereas the IGF-1 receptor binds IGF-1 (and IGF-2) with a higher affinity than it does insulin.	bind
29641	5	7394	7	NULL	NULL	0	NULL	IGF-1 receptor	NULL		bind	NULL				insulin	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_5_1905_s_282	11696451	24, 25  The insulin receptor demonstrates high-affinity binding to insulin and lower affinity binding to IGF-1, whereas the IGF-1 receptor binds IGF-1 (and IGF-2) with a higher affinity than it does insulin.	bind
29642	6	7394	7	NULL	NULL	0	NULL	statement 3	NULL		has higher affinity than	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_5_1905_s_282	11696451	24, 25  The insulin receptor demonstrates high-affinity binding to insulin and lower affinity binding to IGF-1, whereas the IGF-1 receptor binds IGF-1 (and IGF-2) with a higher affinity than it does insulin.	bind
29643	7	7394	7	NULL	NULL	0	NULL	statement 4	NULL		has higher affinity than	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_5_1905_s_282	11696451	24, 25  The insulin receptor demonstrates high-affinity binding to insulin and lower affinity binding to IGF-1, whereas the IGF-1 receptor binds IGF-1 (and IGF-2) with a higher affinity than it does insulin.	bind
27421	1	7395	5	13	NULL	NULL	NULL	ATP	Chemical		is hydrolysed to					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_3_279_s_220	11485979	24, 25 After hydrolysis of ATP to ADP, cytochrome  c binds to Apaf-1, promoting its multimerization from a monomeric form to a large complex.	bind
27422	2	7395	5	13	NULL	NULL	NULL	cytochrome c	GP		bind					Apaf-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_3_279_s_220	11485979	24, 25 After hydrolysis of ATP to ADP, cytochrome  c binds to Apaf-1, promoting its multimerization from a monomeric form to a large complex.	bind
27423	3	7395	5	13	NULL	NULL	NULL	statement 2	Process		occurs after					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_3_279_s_220	11485979	24, 25 After hydrolysis of ATP to ADP, cytochrome  c binds to Apaf-1, promoting its multimerization from a monomeric form to a large complex.	bind
27424	4	7395	5	13	NULL	NULL	NULL	Apaf-1 monomer	GP		multimerize to					large complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_3_279_s_220	11485979	24, 25 After hydrolysis of ATP to ADP, cytochrome  c binds to Apaf-1, promoting its multimerization from a monomeric form to a large complex.	bind
27425	5	7395	5	13	NULL	NULL	NULL	statement 2	Process		promote					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_3_279_s_220	11485979	24, 25 After hydrolysis of ATP to ADP, cytochrome  c binds to Apaf-1, promoting its multimerization from a monomeric form to a large complex.	bind
29644	1	7395	7	NULL	NULL	0	NULL	cytochrome c	NULL		binds to	NULL				Apaf-1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_89_3_279_s_220	11485979	24, 25 After hydrolysis of ATP to ADP, cytochrome  c binds to Apaf-1, promoting its multimerization from a monomeric form to a large complex.	bind
29645	2	7395	7	NULL	NULL	0	NULL	ATP	NULL		hydrolysed to	NULL				ADP	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_89_3_279_s_220	11485979	24, 25 After hydrolysis of ATP to ADP, cytochrome  c binds to Apaf-1, promoting its multimerization from a monomeric form to a large complex.	bind
29646	3	7395	7	NULL	NULL	0	NULL	statement 1	NULL		occurs after	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_89_3_279_s_220	11485979	24, 25 After hydrolysis of ATP to ADP, cytochrome  c binds to Apaf-1, promoting its multimerization from a monomeric form to a large complex.	bind
29647	4	7395	7	10	NULL	0	NULL	Apaf-1 monomer			multimerizes to					large complex					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_3_279_s_220	11485979	24, 25 After hydrolysis of ATP to ADP, cytochrome  c binds to Apaf-1, promoting its multimerization from a monomeric form to a large complex.	bind
29648	5	7395	7	NULL	NULL	0	NULL	statement 1	NULL		promotes	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_89_3_279_s_220	11485979	24, 25 After hydrolysis of ATP to ADP, cytochrome  c binds to Apaf-1, promoting its multimerization from a monomeric form to a large complex.	bind
27426	1	7396	5	13	NULL	NULL	NULL	apoA-I	GP		bind					integral membrane protein	GP				NULL	in ABCA1-expressing cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_40	12738681	24,25  Using a fluorescence photobleaching technique, this study also suggested that apoA-I bound to an integral membrane protein in ABCA1-expressing cells.	bind
29649	1	7396	7	NULL	NULL	0	NULL	apoA-I	NULL		bind	NULL				integral membrane protein	NULL				NULL	ABCA1-expressing cells	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_40	12738681	24,25  Using a fluorescence photobleaching technique, this study also suggested that apoA-I bound to an integral membrane protein in ABCA1-expressing cells.	bind
27427	1	7397	5	13	NULL	NULL	NULL	ETF	GP		bind					p53	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_23777_s_233	10446138	243R Is Required for the Binding of both ETF and E2F to the p53 Promoter-- Both E1a proteins, 243R and 289R, are transcriptional activators; however, they are thought to bring about activation by different mechanisms ( 38,  77,  80).	bind
27428	2	7397	5	13	NULL	NULL	NULL	E2F	GP		bind					p53	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_23777_s_233	10446138	243R Is Required for the Binding of both ETF and E2F to the p53 Promoter-- Both E1a proteins, 243R and 289R, are transcriptional activators; however, they are thought to bring about activation by different mechanisms ( 38,  77,  80).	bind
27429	3	7397	5	13	NULL	NULL	NULL	243R	GP		is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_23777_s_233	10446138	243R Is Required for the Binding of both ETF and E2F to the p53 Promoter-- Both E1a proteins, 243R and 289R, are transcriptional activators; however, they are thought to bring about activation by different mechanisms ( 38,  77,  80).	bind
27430	4	7397	5	13	NULL	NULL	NULL	243R	GP		is required for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_23777_s_233	10446138	243R Is Required for the Binding of both ETF and E2F to the p53 Promoter-- Both E1a proteins, 243R and 289R, are transcriptional activators; however, they are thought to bring about activation by different mechanisms ( 38,  77,  80).	bind
27431	5	7397	5	13	NULL	NULL	NULL	243R	GP		is a type of					E1a proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_23777_s_233	10446138	243R Is Required for the Binding of both ETF and E2F to the p53 Promoter-- Both E1a proteins, 243R and 289R, are transcriptional activators; however, they are thought to bring about activation by different mechanisms ( 38,  77,  80).	bind
27432	6	7397	5	13	NULL	NULL	NULL	289R	GP		is a type of					E1a proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_23777_s_233	10446138	243R Is Required for the Binding of both ETF and E2F to the p53 Promoter-- Both E1a proteins, 243R and 289R, are transcriptional activators; however, they are thought to bring about activation by different mechanisms ( 38,  77,  80).	bind
27433	7	7397	5	13	NULL	NULL	NULL	243R	GP		function as					transcriptional activator	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_23777_s_233	10446138	243R Is Required for the Binding of both ETF and E2F to the p53 Promoter-- Both E1a proteins, 243R and 289R, are transcriptional activators; however, they are thought to bring about activation by different mechanisms ( 38,  77,  80).	bind
27434	8	7397	5	13	NULL	NULL	NULL	289R	GP		function as					transcriptional activator	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_23777_s_233	10446138	243R Is Required for the Binding of both ETF and E2F to the p53 Promoter-- Both E1a proteins, 243R and 289R, are transcriptional activators; however, they are thought to bring about activation by different mechanisms ( 38,  77,  80).	bind
27435	9	7397	5	13	NULL	NULL	NULL	243R	GP	mechanism of activation by	differs from					289R	GP	mechanism of activation by			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_23777_s_233	10446138	243R Is Required for the Binding of both ETF and E2F to the p53 Promoter-- Both E1a proteins, 243R and 289R, are transcriptional activators; however, they are thought to bring about activation by different mechanisms ( 38,  77,  80).	bind
29650	1	7397	7	NULL	NULL	0	NULL	ETF	NULL		bind	NULL				p53	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_34_23777_s_233	10446138	243R Is Required for the Binding of both ETF and E2F to the p53 Promoter-- Both E1a proteins, 243R and 289R, are transcriptional activators; however, they are thought to bring about activation by different mechanisms ( 38,  77,  80).	bind
29651	2	7397	7	NULL	NULL	0	NULL	E2F	NULL		bind	NULL				p53	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_34_23777_s_233	10446138	243R Is Required for the Binding of both ETF and E2F to the p53 Promoter-- Both E1a proteins, 243R and 289R, are transcriptional activators; however, they are thought to bring about activation by different mechanisms ( 38,  77,  80).	bind
29652	3	7397	7	NULL	NULL	0	NULL	243R	NULL		is required for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_34_23777_s_233	10446138	243R Is Required for the Binding of both ETF and E2F to the p53 Promoter-- Both E1a proteins, 243R and 289R, are transcriptional activators; however, they are thought to bring about activation by different mechanisms ( 38,  77,  80).	bind
29653	4	7397	7	NULL	NULL	0	NULL	243R	NULL		is required for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_34_23777_s_233	10446138	243R Is Required for the Binding of both ETF and E2F to the p53 Promoter-- Both E1a proteins, 243R and 289R, are transcriptional activators; however, they are thought to bring about activation by different mechanisms ( 38,  77,  80).	bind
29654	5	7397	7	NULL	NULL	0	NULL	243R	NULL		is a type of	NULL				transcriptional activator	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_23777_s_233	10446138	243R Is Required for the Binding of both ETF and E2F to the p53 Promoter-- Both E1a proteins, 243R and 289R, are transcriptional activators; however, they are thought to bring about activation by different mechanisms ( 38,  77,  80).	bind
29655	6	7397	7	NULL	NULL	0	NULL	289R	NULL		is a type of	NULL				transcriptional activator	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_34_23777_s_233	10446138	243R Is Required for the Binding of both ETF and E2F to the p53 Promoter-- Both E1a proteins, 243R and 289R, are transcriptional activators; however, they are thought to bring about activation by different mechanisms ( 38,  77,  80).	bind
29656	7	7397	7	NULL	NULL	0	NULL	243R	NULL		is a type of	NULL				E1a protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_34_23777_s_233	10446138	243R Is Required for the Binding of both ETF and E2F to the p53 Promoter-- Both E1a proteins, 243R and 289R, are transcriptional activators; however, they are thought to bring about activation by different mechanisms ( 38,  77,  80).	bind
29657	8	7397	7	NULL	NULL	0	NULL	289R	NULL		is a type of	NULL				E1a protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_34_23777_s_233	10446138	243R Is Required for the Binding of both ETF and E2F to the p53 Promoter-- Both E1a proteins, 243R and 289R, are transcriptional activators; however, they are thought to bring about activation by different mechanisms ( 38,  77,  80).	bind
27436	1	7398	5	13	NULL	NULL	NULL	24p3	GP		bind		specifically			statement 15	Cell				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
27437	2	7398	5	13	NULL	NULL	NULL	24p3	GP		bind		specifically			32D	Cell				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
27438	3	7398	5	13	NULL	NULL	NULL	24p3	GP		bind		specifically			HT-2	Cell	murine			NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
27439	4	7398	5	13	NULL	NULL	NULL	32D	Cell		is a type of					leukocytic cell lines	Cell				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
27440	5	7398	5	13	NULL	NULL	NULL	HT-2	Cell	murine	is a type of					leukocytic cell lines	Cell				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
27441	6	7398	5	13	NULL	NULL	NULL	32D	Cell		is susceptible to					statement 14	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
27442	7	7398	5	13	NULL	NULL	NULL	HT-2	Cell	murine	is susceptible to					statement 14	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
27443	8	7398	5	13	NULL	NULL	NULL	NIH 3T3	Cell	murine	is a type of					nonhematopoietic cell lines	Cell				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
27444	9	7398	5	13	NULL	NULL	NULL	COS-7	Cell		is a type of					nonhematopoietic cell lines	Cell				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
27445	10	7398	5	13	NULL	NULL	NULL	24p3	GP		does not bind					NIH 3T3	Cell	murine			NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
27446	11	7398	5	13	NULL	NULL	NULL	24p3	GP		does not bind					COS-7	Cell				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
27447	12	7398	5	13	NULL	NULL	NULL	NIH 3T3	Cell	murine	is resistant to					apoptosis	Process	24p3-mediated			NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
27448	13	7398	5	13	NULL	NULL	NULL	COS-7	Cell		is resistant to					apoptosis	Process	24p3-mediated			NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
54487	14	7398	5	13	NULL	NULL	NULL	24p3	GP		mediates					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
54488	15	7398	5	13	NULL	NULL	NULL	\tprimary bone marrow cells	Cell		is dependent on					IL-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
29658	1	7398	7	10	NULL	0	NULL	24p3			bind		specifically			statement 15					NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
29659	2	7398	7	NULL	NULL	0	NULL	24p3	NULL		bind	NULL	specifically			32D	NULL				NULL		0	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
29660	3	7398	7	NULL	NULL	0	NULL	24p3	NULL		bind	NULL	specifically			HT-2	NULL	murine			NULL		0	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
29661	4	7398	7	NULL	NULL	0	NULL	24p3	NULL		mediates	NULL				apoptosis	NULL				NULL		0	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
29662	5	7398	7	NULL	NULL	0	NULL	32D	NULL		is susceptible to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
29663	6	7398	7	NULL	NULL	0	NULL	HT-2	NULL	murine	is susceptible to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
29664	7	7398	7	NULL	NULL	0	NULL	24p3	NULL		does not bind	NULL				NIH 3T3 	NULL	murine			NULL		0	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
29665	8	7398	7	NULL	NULL	0	NULL	24p3d	NULL		does not bind	NULL				COS-7 	NULL				NULL		0	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
29666	9	7398	7	NULL	NULL	0	NULL	NIH 3T3 	NULL	murine	is resistant to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
29667	10	7398	7	NULL	NULL	0	NULL	COS-7	NULL		is resistant to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
29668	11	7398	7	NULL	NULL	0	NULL	32D	NULL		is a type of	NULL				leukocytic cell line	NULL				NULL		0	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
29669	12	7398	7	NULL	NULL	0	NULL	HT-2	NULL	murine	is a type of	NULL				leukocytic cell line	NULL				NULL		0	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
29670	13	7398	7	NULL	NULL	0	NULL	NIH 3T3	NULL	murine	is a type of	NULL				 nonhematopoietic cell line	NULL				NULL		0	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
29671	14	7398	7	NULL	NULL	0	NULL	 COS-7	NULL		is a type of	NULL				nonhematopoietic cell line	NULL				NULL		0	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
54489	15	7398	7	10	NULL	0	NULL	primary bone marrow cells			is dependent on					IL-3					NULL		0	NULL	NULL	NULL	gw60_science_293_5531_829_s_102	11486081	24p3 also bound specifically to IL-3-dependent primary bone marrow cells and to other leukocytic cell lines, such as 32D and murine HT-2, which are susceptible to 24p3-mediated apoptosis but not to nonhematopoietic cell lines, such as murine NIH 3T3 and COS-7, which are resistant.	bind
27449	1	7399	5	13	NULL	NULL	NULL	Smad3	GP		bind		directly			plasminogen activator inhibitor-type 1 gene	GP	human		TGF-beta-inducible elements in promoter	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_515_s_342	11788714	25       Dennler,S., Itoh,S., Vivien,D., ten Dijke,P., Huet,S. and Gauthier,J.-M. (1998) Direct binding of Smad3 and Smad4 to critical TGF-beta-inducible elements in the promoter of human plasminogen activator inhibitor-type 1 gene.	bind
27451	2	7399	5	13	NULL	NULL	NULL	Smad4	GP		bind		directly			plasminogen activator inhibitor-type 1 gene	GP	human		TGF-beta-inducible elements in promoter	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_515_s_342	11788714	25       Dennler,S., Itoh,S., Vivien,D., ten Dijke,P., Huet,S. and Gauthier,J.-M. (1998) Direct binding of Smad3 and Smad4 to critical TGF-beta-inducible elements in the promoter of human plasminogen activator inhibitor-type 1 gene.	bind
29672	1	7399	7	NULL	NULL	0	NULL	Smad3 	NULL		bind	NULL	directly			plasminogen activator inhibitor-type 1 gene	NULL	human		TGF-beta-inducible elements in the promoter of	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_515_s_342	11788714	25       Dennler,S., Itoh,S., Vivien,D., ten Dijke,P., Huet,S. and Gauthier,J.-M. (1998) Direct binding of Smad3 and Smad4 to critical TGF-beta-inducible elements in the promoter of human plasminogen activator inhibitor-type 1 gene.	bind
29673	2	7399	7	NULL	NULL	0	NULL	Smad4	NULL		bind	NULL	directly			plasminogen activator inhibitor-type 1 gene	NULL	human		TGF-beta-inducible elements in the promoter of	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_515_s_342	11788714	25       Dennler,S., Itoh,S., Vivien,D., ten Dijke,P., Huet,S. and Gauthier,J.-M. (1998) Direct binding of Smad3 and Smad4 to critical TGF-beta-inducible elements in the promoter of human plasminogen activator inhibitor-type 1 gene.	bind
27452	1	7400	5	13	NULL	NULL	NULL	p53	GP		bind		sequence-specific			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4994_s_321	11812829	25       Gu,W. and Roeder,R.G. (1997) Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.	bind
27453	2	7400	5	13	NULL	NULL	NULL	p53	GP		udergoes			C-terminal domain		acetylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4994_s_321	11812829	25       Gu,W. and Roeder,R.G. (1997) Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.	bind
27454	3	7400	5	13	NULL	NULL	NULL	statement 2	Process		activates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4994_s_321	11812829	25       Gu,W. and Roeder,R.G. (1997) Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.	bind
29674	1	7400	7	10	NULL	0	NULL	p53			undergoes			C-terminal domain		acetylation					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4994_s_321	11812829	25       Gu,W. and Roeder,R.G. (1997) Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.	bind
29675	2	7400	7	10	NULL	0	NULL	statement 1			activates					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4994_s_321	11812829	25       Gu,W. and Roeder,R.G. (1997) Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.	bind
54490	3	7400	7	10	NULL	0	NULL	p53			bind		sequence specifically			DNA					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4994_s_321	11812829	25       Gu,W. and Roeder,R.G. (1997) Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.	bind
27455	1	7401	5	13	NULL	NULL	NULL	nuclear proteins	GP		bind					pre-mRNA	NucleicAcid			r(UUAG/G)	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2268_s_334	11376145	25       Ishikawa,F., Matunis,M.J., Dreyfuss,G. and Cech,T.R. (1993) Nuclear proteins that bind the pre-mRNA 3' splice site sequence r(UUAG/G) and the human telomeric DNA sequence d(TTAGGG)n.  Mol.	bind
27456	2	7401	5	13	NULL	NULL	NULL	r(UUAG/G)	NucleicAcid		is a type of					3' splice site sequence	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2268_s_334	11376145	25       Ishikawa,F., Matunis,M.J., Dreyfuss,G. and Cech,T.R. (1993) Nuclear proteins that bind the pre-mRNA 3' splice site sequence r(UUAG/G) and the human telomeric DNA sequence d(TTAGGG)n.  Mol.	bind
27457	3	7401	5	13	NULL	NULL	NULL	nuclear proteins	GP		bind							human		d(TTAGGG)n	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2268_s_334	11376145	25       Ishikawa,F., Matunis,M.J., Dreyfuss,G. and Cech,T.R. (1993) Nuclear proteins that bind the pre-mRNA 3' splice site sequence r(UUAG/G) and the human telomeric DNA sequence d(TTAGGG)n.  Mol.	bind
27458	4	7401	5	13	NULL	NULL	NULL	d(TTAGGG)n	NucleicAcid		is a type of					telomeric DNA sequence	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2268_s_334	11376145	25       Ishikawa,F., Matunis,M.J., Dreyfuss,G. and Cech,T.R. (1993) Nuclear proteins that bind the pre-mRNA 3' splice site sequence r(UUAG/G) and the human telomeric DNA sequence d(TTAGGG)n.  Mol.	bind
29676	1	7401	7	10	NULL	0	NULL	Nuclear proteins			bind					pre-mRNA			r(UUAG/G)		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2268_s_334	11376145	25       Ishikawa,F., Matunis,M.J., Dreyfuss,G. and Cech,T.R. (1993) Nuclear proteins that bind the pre-mRNA 3' splice site sequence r(UUAG/G) and the human telomeric DNA sequence d(TTAGGG)n.  Mol.	bind
29677	2	7401	7	10	NULL	0	NULL	Nuclear proteins 			bind							human		d(TTAGGG)	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2268_s_334	11376145	25       Ishikawa,F., Matunis,M.J., Dreyfuss,G. and Cech,T.R. (1993) Nuclear proteins that bind the pre-mRNA 3' splice site sequence r(UUAG/G) and the human telomeric DNA sequence d(TTAGGG)n.  Mol.	bind
54499	3	7401	7	10	NULL	0	NULL	d(TTAGGG)n			is a type of					telomeric DNA sequence					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2268_s_334	11376145	25       Ishikawa,F., Matunis,M.J., Dreyfuss,G. and Cech,T.R. (1993) Nuclear proteins that bind the pre-mRNA 3' splice site sequence r(UUAG/G) and the human telomeric DNA sequence d(TTAGGG)n.  Mol.	bind
54500	5	7401	7	10	NULL	0	NULL	r(UUAG/G)			is a type of					3' splice site sequence					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2268_s_334	11376145	25       Ishikawa,F., Matunis,M.J., Dreyfuss,G. and Cech,T.R. (1993) Nuclear proteins that bind the pre-mRNA 3' splice site sequence r(UUAG/G) and the human telomeric DNA sequence d(TTAGGG)n.  Mol.	bind
27463	1	7404	5	13	NULL	NULL	NULL	Rb	GP	active	bind					E2Fs	GP				NULL	repressor complex	NULL	NULL	NULL	NULL	gw60_amjpathol_157_6_1795_s_155	11106551	25  Active Rb is normally bound to E2Fs in a repressor complex.	bind
29679	1	7404	7	NULL	NULL	0	NULL	Rb	NULL	active	bind	NULL				E2Fs	NULL				NULL	repressor complex	0	NULL	NULL	NULL	gw60_amjpathol_157_6_1795_s_155	11106551	25  Active Rb is normally bound to E2Fs in a repressor complex.	bind
27698	1	7405	5	NULL	NULL	0	NULL		NULL		stabilizes	NULL		Arginine 3500			NULL	clusters of amino acids	3147 to 3157		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_153	7583549	25  Arginine 3500 is suggested to stabilize two clusters of amino acids (3147 to 3157 and 3359 to 3367) that have been assumed to ensure the binding of the apoB to the LDL receptor.	bind
27699	2	7405	5	NULL	NULL	0	NULL		NULL		stabilizes	NULL		Arginine 3500			NULL	clusters of amino acids	3359 to 3367		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_153	7583549	25  Arginine 3500 is suggested to stabilize two clusters of amino acids (3147 to 3157 and 3359 to 3367) that have been assumed to ensure the binding of the apoB to the LDL receptor.	bind
27700	3	7405	5	13	NULL	NULL	NULL	apoB	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_153	7583549	25  Arginine 3500 is suggested to stabilize two clusters of amino acids (3147 to 3157 and 3359 to 3367) that have been assumed to ensure the binding of the apoB to the LDL receptor.	bind
27701	4	7405	5	13	NULL	NULL	NULL	statement 1	Process		ensure					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_153	7583549	25  Arginine 3500 is suggested to stabilize two clusters of amino acids (3147 to 3157 and 3359 to 3367) that have been assumed to ensure the binding of the apoB to the LDL receptor.	bind
27702	5	7405	5	13	NULL	NULL	NULL	statement 2	Process		ensure					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_153	7583549	25  Arginine 3500 is suggested to stabilize two clusters of amino acids (3147 to 3157 and 3359 to 3367) that have been assumed to ensure the binding of the apoB to the LDL receptor.	bind
29680	1	7405	7	NULL	NULL	0	NULL	apoB	NULL		bind	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_153	7583549	25  Arginine 3500 is suggested to stabilize two clusters of amino acids (3147 to 3157 and 3359 to 3367) that have been assumed to ensure the binding of the apoB to the LDL receptor.	bind
29681	2	7405	7	NULL	NULL	0	NULL		NULL		stabilize	NULL		Arginine 3500			NULL		aminoacids 3147 to 3157		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_153	7583549	25  Arginine 3500 is suggested to stabilize two clusters of amino acids (3147 to 3157 and 3359 to 3367) that have been assumed to ensure the binding of the apoB to the LDL receptor.	bind
29682	3	7405	7	NULL	NULL	0	NULL		NULL		stabilize	NULL		Arginine 3500			NULL		aminoacids 3359 to 3367		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_153	7583549	25  Arginine 3500 is suggested to stabilize two clusters of amino acids (3147 to 3157 and 3359 to 3367) that have been assumed to ensure the binding of the apoB to the LDL receptor.	bind
29683	4	7405	7	NULL	NULL	0	NULL	statement 2	NULL		ensures	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_153	7583549	25  Arginine 3500 is suggested to stabilize two clusters of amino acids (3147 to 3157 and 3359 to 3367) that have been assumed to ensure the binding of the apoB to the LDL receptor.	bind
29684	5	7405	7	NULL	NULL	0	NULL	statement 3	NULL		ensures	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_153	7583549	25  Arginine 3500 is suggested to stabilize two clusters of amino acids (3147 to 3157 and 3359 to 3367) that have been assumed to ensure the binding of the apoB to the LDL receptor.	bind
27703	1	7406	5	13	NULL	NULL	NULL	ADP	Chemical		bind					CMK 11-5 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_190	9108793	25  In addition, neither GDP nor adenosine competed significantly with the binding of ADP to CMK 11-5 cells, indicating the absence of other purinergic receptors.	bind
27704	2	7406	5	13	NULL	NULL	NULL	GDP	Chemical		does not compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_190	9108793	25  In addition, neither GDP nor adenosine competed significantly with the binding of ADP to CMK 11-5 cells, indicating the absence of other purinergic receptors.	bind
27705	3	7406	5	13	NULL	NULL	NULL	adenosine	Chemical		does not compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_190	9108793	25  In addition, neither GDP nor adenosine competed significantly with the binding of ADP to CMK 11-5 cells, indicating the absence of other purinergic receptors.	bind
27706	4	7406	5	13	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_190	9108793	25  In addition, neither GDP nor adenosine competed significantly with the binding of ADP to CMK 11-5 cells, indicating the absence of other purinergic receptors.	bind
27707	5	7406	5	13	NULL	NULL	NULL	statement 2	Process		indicates					purinergic receptors	GP	absence of other			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_190	9108793	25  In addition, neither GDP nor adenosine competed significantly with the binding of ADP to CMK 11-5 cells, indicating the absence of other purinergic receptors.	bind
27708	6	7406	5	13	NULL	NULL	NULL	statement 3	Process		indicates					purinergic receptors	GP	absence of other			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_190	9108793	25  In addition, neither GDP nor adenosine competed significantly with the binding of ADP to CMK 11-5 cells, indicating the absence of other purinergic receptors.	bind
29685	1	7406	7	NULL	NULL	0	NULL	ADP	NULL		binds	NULL				CMK 11-5 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_190	9108793	25  In addition, neither GDP nor adenosine competed significantly with the binding of ADP to CMK 11-5 cells, indicating the absence of other purinergic receptors.	bind
29686	2	7406	7	NULL	NULL	0	NULL	GDP	NULL		does not compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_190	9108793	25  In addition, neither GDP nor adenosine competed significantly with the binding of ADP to CMK 11-5 cells, indicating the absence of other purinergic receptors.	bind
29687	3	7406	7	NULL	NULL	0	NULL	adenosine	NULL		does not compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_190	9108793	25  In addition, neither GDP nor adenosine competed significantly with the binding of ADP to CMK 11-5 cells, indicating the absence of other purinergic receptors.	bind
29688	4	7406	7	NULL	NULL	0	NULL	statement 2	NULL		indicate	NULL				purinergic receptors	NULL	absence of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_190	9108793	25  In addition, neither GDP nor adenosine competed significantly with the binding of ADP to CMK 11-5 cells, indicating the absence of other purinergic receptors.	bind
29689	5	7406	7	NULL	NULL	0	NULL	statement 3	NULL		indicate	NULL				purinergic receptors	NULL	absence of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_190	9108793	25  In addition, neither GDP nor adenosine competed significantly with the binding of ADP to CMK 11-5 cells, indicating the absence of other purinergic receptors.	bind
27709	1	7407	5	13	NULL	NULL	NULL	PAF-acetylhydrolase	GP		inactivates					PAF	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_4_787_s_61	9054729	25  PAF is inactivated by PAF-acetylhydrolase, an enzyme that circulates bound to LDL.	bind
27710	2	7407	5	13	NULL	NULL	NULL	PAF-acetylhydrolase	GP		bind					LDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_4_787_s_61	9054729	25  PAF is inactivated by PAF-acetylhydrolase, an enzyme that circulates bound to LDL.	bind
29690	1	7407	7	NULL	NULL	0	NULL	PAF-acetylhydrolase	NULL		inactivates	NULL				PAF	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_95_4_787_s_61	9054729	25  PAF is inactivated by PAF-acetylhydrolase, an enzyme that circulates bound to LDL.	bind
29691	2	7407	7	NULL	NULL	0	NULL	PAF-acetylhydrolase	NULL		bind	NULL				LDL	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_95_4_787_s_61	9054729	25  PAF is inactivated by PAF-acetylhydrolase, an enzyme that circulates bound to LDL.	bind
29692	3	7407	7	NULL	NULL	0	NULL	PAF-acetylhydrolase	NULL		is a type of	NULL				enzyme	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_95_4_787_s_61	9054729	25  PAF is inactivated by PAF-acetylhydrolase, an enzyme that circulates bound to LDL.	bind
27711	1	7408	5	13	NULL	NULL	NULL	apoB-100	GP		is a component of					LDL	GP	granule-bound			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2047_s_145	7583588	25  When the apoB-100 component of granule-bound LDL is proteolyzed by granule chymase, the LDL particles become unstable and fuse, and the fused particles bind more tightly to the granule remnant heparin proteoglycans.	bind
27712	2	7408	5	13	NULL	NULL	NULL	statement 1	GP		is proteolyzed by					granule chymase	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2047_s_145	7583588	25  When the apoB-100 component of granule-bound LDL is proteolyzed by granule chymase, the LDL particles become unstable and fuse, and the fused particles bind more tightly to the granule remnant heparin proteoglycans.	bind
27713	3	7408	5	13	NULL	NULL	NULL	statement 2	Process		leads to					LDL particles	GP	unstable			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2047_s_145	7583588	25  When the apoB-100 component of granule-bound LDL is proteolyzed by granule chymase, the LDL particles become unstable and fuse, and the fused particles bind more tightly to the granule remnant heparin proteoglycans.	bind
27714	4	7408	5	13	NULL	NULL	NULL	statement 3	Process		results in					LDL particles	GP	fusion of;;unstable			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2047_s_145	7583588	25  When the apoB-100 component of granule-bound LDL is proteolyzed by granule chymase, the LDL particles become unstable and fuse, and the fused particles bind more tightly to the granule remnant heparin proteoglycans.	bind
27715	5	7408	5	13	NULL	NULL	NULL	LDL particles	GP	fused	bind		tightly			heparin proteoglycans	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2047_s_145	7583588	25  When the apoB-100 component of granule-bound LDL is proteolyzed by granule chymase, the LDL particles become unstable and fuse, and the fused particles bind more tightly to the granule remnant heparin proteoglycans.	bind
54501	6	7408	5	13	NULL	NULL	NULL	heparin proteoglycans \t	GP		is a type of					granule remnant	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2047_s_145	7583588	25  When the apoB-100 component of granule-bound LDL is proteolyzed by granule chymase, the LDL particles become unstable and fuse, and the fused particles bind more tightly to the granule remnant heparin proteoglycans.	bind
29706	1	7408	7	NULL	NULL	0	NULL	granule	NULL	apoB-100	bind	NULL				LDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2047_s_145	7583588	25  When the apoB-100 component of granule-bound LDL is proteolyzed by granule chymase, the LDL particles become unstable and fuse, and the fused particles bind more tightly to the granule remnant heparin proteoglycans.	bind
29707	2	7408	7	NULL	NULL	0	NULL	granule chymase	NULL		proteolyze	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2047_s_145	7583588	25  When the apoB-100 component of granule-bound LDL is proteolyzed by granule chymase, the LDL particles become unstable and fuse, and the fused particles bind more tightly to the granule remnant heparin proteoglycans.	bind
29710	3	7408	7	NULL	NULL	0	NULL	LDL particles	NULL		become	NULL				unstable	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2047_s_145	7583588	25  When the apoB-100 component of granule-bound LDL is proteolyzed by granule chymase, the LDL particles become unstable and fuse, and the fused particles bind more tightly to the granule remnant heparin proteoglycans.	bind
29712	4	7408	7	NULL	NULL	0	NULL	statement 3	NULL		leads to	NULL				LDL particles	NULL	fusion of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2047_s_145	7583588	25  When the apoB-100 component of granule-bound LDL is proteolyzed by granule chymase, the LDL particles become unstable and fuse, and the fused particles bind more tightly to the granule remnant heparin proteoglycans.	bind
29713	5	7408	7	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2047_s_145	7583588	25  When the apoB-100 component of granule-bound LDL is proteolyzed by granule chymase, the LDL particles become unstable and fuse, and the fused particles bind more tightly to the granule remnant heparin proteoglycans.	bind
29715	6	7408	7	NULL	NULL	0	NULL	LDL	NULL	fused particles	bind	NULL	tightly			heparin proteoglycans	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2047_s_145	7583588	25  When the apoB-100 component of granule-bound LDL is proteolyzed by granule chymase, the LDL particles become unstable and fuse, and the fused particles bind more tightly to the granule remnant heparin proteoglycans.	bind
29716	7	7408	7	NULL	NULL	0	NULL	heparin proteoglycans	NULL		is a type of	NULL				granule remnant	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_11_2047_s_145	7583588	25  When the apoB-100 component of granule-bound LDL is proteolyzed by granule chymase, the LDL particles become unstable and fuse, and the fused particles bind more tightly to the granule remnant heparin proteoglycans.	bind
27716	1	7409	5	13	NULL	NULL	NULL	uPAR	GP	recombinant	bind					vitronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_41	9848876	25 26  Recombinant uPAR binds vitronectin, and this binding is augmented by the addition of uPA.	bind
27717	2	7409	5	13	NULL	NULL	NULL	uPA	GP		augments					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_41	9848876	25 26  Recombinant uPAR binds vitronectin, and this binding is augmented by the addition of uPA.	bind
29854	1	7409	7	NULL	NULL	0	NULL	uPAR	NULL	recombinant	binds	NULL				vitronectin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_41	9848876	25 26  Recombinant uPAR binds vitronectin, and this binding is augmented by the addition of uPA.	bind
29855	2	7409	7	NULL	NULL	0	NULL	uPA	NULL		augments	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_41	9848876	25 26  Recombinant uPAR binds vitronectin, and this binding is augmented by the addition of uPA.	bind
29604	1	7410	5	13	NULL	NULL	NULL	Glanzmann's thrombasthenic platelets	Cell		lack					GP IIb/IIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
29605	2	7410	5	13	NULL	NULL	NULL	statement 1	Cell		bind					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
29606	3	7410	5	13	NULL	NULL	NULL	statement 1	Cell		bind					ATP-alpha-S	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
29607	4	7410	5	13	NULL	NULL	NULL	ADP	Chemical		induces					Ca2+ influx	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
29608	5	7410	5	13	NULL	NULL	NULL	statement 4	Process		occurs in					statement 1	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
29609	6	7410	5	13	NULL	NULL	NULL	platelet	Cell	shape change in	occurs in					statement 1	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
29610	7	7410	5	13	NULL	NULL	NULL	cAMP	Chemical	inhibition of	occurs in					statement 1	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
29611	8	7410	5	13	NULL	NULL	NULL	thromboxane B2	Chemical	ability to synthesize	is reduced in					statement 1	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
29856	1	7410	7	10	NULL	0	NULL	Glanzmann's thrombasthenic platelets	NULL		bind	NULL				ADP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
29857	2	7410	7	10	NULL	0	NULL	Glanzmann's thrombasthenic platelets	NULL		bind	NULL				ATP-alpha-S	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
29858	3	7410	7	NULL	NULL	0	NULL	statement 1	NULL		in absence of	NULL				GP IIb/IIa	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
29859	4	7410	7	NULL	NULL	0	NULL	statement 2	NULL		in absence of	NULL				GP IIb/IIa	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
29860	5	7410	7	NULL	NULL	0	NULL	ADP	NULL	normal	induce	NULL				Ca2+	NULL	influx of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
29861	6	7410	7	NULL	NULL	0	NULL	ADP	NULL	normal	change	NULL				platelet shape	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
29862	7	7410	7	NULL	NULL	0	NULL	ADP	NULL	normal	inhibits	NULL				cAMP	NULL	levels of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
29863	8	7410	7	NULL	NULL	0	NULL	platelets	NULL	control	bind	NULL				ADP	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
29864	9	7410	7	NULL	NULL	0	NULL	platelets	NULL	normal	bind	NULL				ATP-alpha-S	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
29866	10	7410	7	NULL	NULL	0	NULL	statement 1	NULL		is similar to	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
29867	11	7410	7	NULL	NULL	0	NULL	statement 2	NULL		is similar to	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
29868	12	7410	7	NULL	NULL	0	NULL	ADP	NULL	normal	reduce	NULL				thromboxane B2	NULL	synthesis of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_4_769_s_34	9108793	25 26 27  Glanzmann's thrombasthenic platelets, despite the absence of GP IIb/IIa, show binding of ADP and ATP-alpha-S similar to that of control platelets, normal ADP-induced Ca2+ influx, platelet shape change, and inhibition of cAMP levels, 28 29 30  although their ability to synthesize thromboxane B2 is reduced.	bind
27718	1	7411	5	13	NULL	NULL	NULL	IRF-1	GP	competitive binding of	plays a role in		critical			growth	Process	determining			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_233_s_173	10666420	25 26 27 47 48 49 50  Recently, competitive binding of IRF-1 and IRF-2 was reported to play a critical role in determining growth, transformation, and apoptosis of cells.	bind
27719	2	7411	5	13	NULL	NULL	NULL	IRF-2	GP	competitive binding of	plays a role in		critical			growth	Process	determining			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_233_s_173	10666420	25 26 27 47 48 49 50  Recently, competitive binding of IRF-1 and IRF-2 was reported to play a critical role in determining growth, transformation, and apoptosis of cells.	bind
27720	3	7411	5	13	NULL	NULL	NULL	IRF-1	GP	competitive binding of	plays a role in		critical			transformation	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_233_s_173	10666420	25 26 27 47 48 49 50  Recently, competitive binding of IRF-1 and IRF-2 was reported to play a critical role in determining growth, transformation, and apoptosis of cells.	bind
27721	4	7411	5	13	NULL	NULL	NULL	IRF-2	GP	competitive binding of	plays a role in		critical			transformation	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_233_s_173	10666420	25 26 27 47 48 49 50  Recently, competitive binding of IRF-1 and IRF-2 was reported to play a critical role in determining growth, transformation, and apoptosis of cells.	bind
27722	5	7411	5	13	NULL	NULL	NULL	IRF-1	GP	competitive binding of	plays a role in		critical			apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_233_s_173	10666420	25 26 27 47 48 49 50  Recently, competitive binding of IRF-1 and IRF-2 was reported to play a critical role in determining growth, transformation, and apoptosis of cells.	bind
27723	6	7411	5	13	NULL	NULL	NULL	IRF-2	GP	competitive binding of	plays a role in		critical			apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_233_s_173	10666420	25 26 27 47 48 49 50  Recently, competitive binding of IRF-1 and IRF-2 was reported to play a critical role in determining growth, transformation, and apoptosis of cells.	bind
29871	1	7411	7	10	NULL	0	NULL	IRF-1	NULL	competitive binding of	plays a role in	NULL	critical			growth	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_233_s_173	10666420	25 26 27 47 48 49 50  Recently, competitive binding of IRF-1 and IRF-2 was reported to play a critical role in determining growth, transformation, and apoptosis of cells.	bind
29873	2	7411	7	10	NULL	0	NULL	IRF-1	NULL	competitive binding of	plays a role in	NULL	critical			transformation	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_233_s_173	10666420	25 26 27 47 48 49 50  Recently, competitive binding of IRF-1 and IRF-2 was reported to play a critical role in determining growth, transformation, and apoptosis of cells.	bind
29875	3	7411	7	10	NULL	0	NULL	IRF-1	NULL	competitive binding of	plays a role in	NULL	critical			apoptosis of cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_233_s_173	10666420	25 26 27 47 48 49 50  Recently, competitive binding of IRF-1 and IRF-2 was reported to play a critical role in determining growth, transformation, and apoptosis of cells.	bind
29877	4	7411	7	10	NULL	0	NULL	IRF-2	NULL	competitive binding of	plays a role in	NULL	critical			growth	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_233_s_173	10666420	25 26 27 47 48 49 50  Recently, competitive binding of IRF-1 and IRF-2 was reported to play a critical role in determining growth, transformation, and apoptosis of cells.	bind
29878	5	7411	7	10	NULL	0	NULL	IRF-2	NULL	competitive binding of	plays a role in	NULL	critical			transformation	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_233_s_173	10666420	25 26 27 47 48 49 50  Recently, competitive binding of IRF-1 and IRF-2 was reported to play a critical role in determining growth, transformation, and apoptosis of cells.	bind
29879	6	7411	7	10	NULL	0	NULL	IRF-2	NULL	competitive binding of	plays a role in	NULL	critical			apoptosis of cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_233_s_173	10666420	25 26 27 47 48 49 50  Recently, competitive binding of IRF-1 and IRF-2 was reported to play a critical role in determining growth, transformation, and apoptosis of cells.	bind
27724	1	7412	5	13	NULL	NULL	NULL	Lp(a)	GP		bind		weakly			LDLR	GP				NULL	yolk sac cell line 1461	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_262	10073957	25 62 63 However, because the yolk sac cell line 1461 was shown to express slightly higher amounts of LDLR than did control cells (Figure 1B  ), it was essential to make sure that the weak Lp(a) binding to the LDLR was of negligible influence within the assay system used in this study.	bind
29884	1	7412	7	10	NULL	0	NULL	Lp(a)	NULL		bind	NULL	weakly			LDLR	NULL				NULL	 yolk sac cell line 1461	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_552_s_262	10073957	25 62 63 However, because the yolk sac cell line 1461 was shown to express slightly higher amounts of LDLR than did control cells (Figure 1B  ), it was essential to make sure that the weak Lp(a) binding to the LDLR was of negligible influence within the assay system used in this study.	bind
27728	1	7413	5	13	NULL	NULL	NULL	ANP	GP		bind					NPR-A receptors	GP				NULL	on adipocytes	NULL	NULL	NULL	NULL	gw70_circulation_109_5_594_s_131	14769680	25 Investigators have demonstrated that binding of ANP to NPR-A receptors on adipocytes induces lipolysis.	bind
27729	2	7413	5	13	NULL	NULL	NULL	statement 1	Process		induces					lipolysis	Process				NULL	adipocytes	NULL	NULL	NULL	NULL	gw70_circulation_109_5_594_s_131	14769680	25 Investigators have demonstrated that binding of ANP to NPR-A receptors on adipocytes induces lipolysis.	bind
29888	1	7413	7	NULL	NULL	0	NULL	ANP	NULL		bind	NULL				NPR-A receptors	NULL				NULL	adipocytes	0	NULL	NULL	NULL	gw70_circulation_109_5_594_s_131	14769680	25 Investigators have demonstrated that binding of ANP to NPR-A receptors on adipocytes induces lipolysis.	bind
29891	2	7413	7	10	NULL	0	NULL	statement 1			induces					lipolysis					NULL	adipocytes	NULL	NULL	NULL	NULL	gw70_circulation_109_5_594_s_131	14769680	25 Investigators have demonstrated that binding of ANP to NPR-A receptors on adipocytes induces lipolysis.	bind
29009	1	7414	5	13	NULL	NULL	NULL	external signals	Process		is linked to					nuclear responses	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29010	2	7414	5	13	NULL	NULL	NULL	MAPKs	GP		is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29011	3	7414	5	13	NULL	NULL	NULL	growth factor	GP		bind					RTK	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29012	4	7414	5	13	NULL	NULL	NULL	growth factor	GP		bind					GPCR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29013	5	7414	5	13	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29014	6	7414	5	13	NULL	NULL	NULL	statement 3	Process		leads to					gene	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29015	7	7414	5	13	NULL	NULL	NULL	MAPKs	GP		is required for					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29016	8	7414	5	13	NULL	NULL	NULL	statement 4	Process		leads to					gene	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29017	9	7414	5	13	NULL	NULL	NULL	MAPKs	GP		is required for					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29515	10	7414	5	13	NULL	NULL	NULL	GPCRs	GP		is coupled to					Galphaq	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29516	11	7414	5	13	NULL	NULL	NULL	GPCRs	GP		is coupled to					Galphai	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29517	12	7414	5	13	NULL	NULL	NULL	statement 10	Process	activation of	triggers					Ras	GP	action of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29518	13	7414	5	13	NULL	NULL	NULL	statement 12	Process		occurs during					MAPK signal transduction	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
30123	14	7414	5	13	NULL	NULL	NULL	statement 11	Process	activation of	triggers					Ras	GP	action of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
30124	15	7414	5	13	NULL	NULL	NULL	statement 14	Process		occurs during					MAPK signal transduction	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
30125	16	7414	5	13	NULL	NULL	NULL	GPCRs	GP	stimulation of	induces		rapidly			Shc	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
30126	17	7414	5	13	NULL	NULL	NULL	Shc	GP		bind					Grb2	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
30127	18	7414	5	13	NULL	NULL	NULL	GPCRs	GP	stimulation of	induces		rapidly			statement 17	Process	formation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
30128	19	7414	5	13	NULL	NULL	NULL	GPCR	GP		is coupled to					Ras	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
30129	20	7414	5	13	NULL	NULL	NULL	RTK	GP		is coupled to					Ras	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
30130	21	7414	5	13	NULL	NULL	NULL	statement 16	Process		is required for					statement 19	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
30131	22	7414	5	13	NULL	NULL	NULL	statement 16	Process		is required for					statement 20	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
30132	23	7414	5	13	NULL	NULL	NULL	statement 18	Process		is required for					statement 19	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
30133	24	7414	5	13	NULL	NULL	NULL	statement 18	Process		is required for					statement 20	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
30134	25	7414	5	13	NULL	NULL	NULL	lysophosphatidic acid receptor	GP		is a type of					GPCRs	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
30135	26	7414	5	13	NULL	NULL	NULL	thyroid-releasing hormone receptor	GP		is a type of					GPCRs	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
30136	27	7414	5	13	NULL	NULL	NULL	endothelin-1 receptor	GP		is a type of					GPCRs	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
30137	28	7414	5	13	NULL	NULL	NULL	bradykinin receptor	GP		is a type of					GPCRs	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29893	1	7414	7	NULL	NULL	0	NULL	growth factor	NULL		bind	NULL				RTK	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29894	2	7414	7	NULL	NULL	0	NULL	growth factor	NULL		bind	NULL				GPCR	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29895	3	7414	7	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29896	4	7414	7	NULL	NULL	0	NULL	MAPKs	NULL		link	NULL				gene expression	NULL	external signals to			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29898	5	7414	7	NULL	NULL	0	NULL	statement 4	NULL		in response to	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29899	6	7414	7	NULL	NULL	0	NULL	statement 4	NULL		in response to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29901	7	7414	7	10	NULL	0	NULL	Galphaq		activation of	triggers					Ras		action of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29902	8	7414	7	10	NULL	0	NULL	Galphai-coupled GPCRs		activation of	triggers					Ras		action of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29905	9	7414	7	NULL	NULL	0	NULL	lysophosphatidic acid receptor	NULL		induce	NULL	rapidly			Shc	NULL	phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29906	10	7414	7	NULL	NULL	0	NULL	thyroid-releasing hormone receptor	NULL		induce	NULL	rapidly			Shc	NULL	phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29907	11	7414	7	NULL	NULL	0	NULL	endothelin-1 receptor	NULL		induce	NULL	rapidly			Shc	NULL	phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29908	12	7414	7	NULL	NULL	0	NULL	bradykinin receptor	NULL		induce	NULL	rapidly			Shc	NULL	phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29909	13	7414	7	NULL	NULL	0	NULL	lysophosphatidic acid receptor	NULL		induce	NULL	rapidly			Shc-Grb2 complexes	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29910	14	7414	7	NULL	NULL	0	NULL	thyroid-releasing hormone receptor	NULL		induce	NULL	rapidly			Shc-Grb2 complexes	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29911	15	7414	7	NULL	NULL	0	NULL	endothelin-1 receptor	NULL		induce	NULL	rapidly			Shc-Grb2 complexes	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29912	16	7414	7	NULL	NULL	0	NULL	bradykinin receptor	NULL		induce	NULL	rapidly			Shc-Grb2 complexes	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29913	18	7414	7	NULL	NULL	0	NULL	statement 17	NULL		activates	NULL				Ras	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29914	17	7414	7	NULL	NULL	0	NULL	GPCR	NULL		couple with	NULL				RTK	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29915	19	7414	7	NULL	NULL	0	NULL	lysophosphatidic acid receptor	NULL		is a type of	NULL				GPCR	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29916	20	7414	7	NULL	NULL	0	NULL	thyroid-releasing hormone receptor	NULL		is a type of	NULL				GPCR	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29917	21	7414	7	NULL	NULL	0	NULL	endothelin-1 receptor	NULL		is a type of	NULL				GPCR	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
29918	22	7414	7	NULL	NULL	0	NULL	bradykinin receptor	NULL		is a type of	NULL				GPCR	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_994_s_175	12714438	25 MAPKs link external signals to nuclear responses, such as gene expression in response to growth factor binding to either RTK or GPCR. 26,27  The action of Ras in MAPK signal transduction is triggered by activation of Galphaq- or Galphai-coupled GPCRs. 25,28  Stimulation of various GPCRs, such as those for lysophosphatidic acid, 29 thyroid-releasing hormone, 30 endothelin-1, 31 and bradykinin, 32 rapidly induce tyrosine phosphorylation of Shc and formation of Shc-Grb2 complexes, steps that couple both GPCR and RTK to Ras activation.	bind
27730	1	7417	5	13	NULL	NULL	NULL	TNF-alpha	GP		promote					ICAM-1	GP	clustering of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1089_s_234	12714560	25 These results collectively point to an important role of TNF-alpha in promoting ICAM-1 clustering, and the increased binding activity of cell surface ICAM-1 to PMN.	bind
27731	2	7417	5	13	NULL	NULL	NULL	ICAM-1	GP	cell surface	bind					PMN	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1089_s_234	12714560	25 These results collectively point to an important role of TNF-alpha in promoting ICAM-1 clustering, and the increased binding activity of cell surface ICAM-1 to PMN.	bind
27732	3	7417	5	13	NULL	NULL	NULL	TNF-alpha	GP		increases					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1089_s_234	12714560	25 These results collectively point to an important role of TNF-alpha in promoting ICAM-1 clustering, and the increased binding activity of cell surface ICAM-1 to PMN.	bind
29919	1	7417	7	NULL	NULL	0	NULL	TNF-alpha	NULL		promote	NULL				ICAM-1	NULL	clustering of			NULL		0	NULL	NULL	NULL	gw60_circulationres_92_10_1089_s_234	12714560	25 These results collectively point to an important role of TNF-alpha in promoting ICAM-1 clustering, and the increased binding activity of cell surface ICAM-1 to PMN.	bind
29920	2	7417	7	NULL	NULL	0	NULL	ICAM-1	NULL	cell surface	binds	NULL				PMN	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_10_1089_s_234	12714560	25 These results collectively point to an important role of TNF-alpha in promoting ICAM-1 clustering, and the increased binding activity of cell surface ICAM-1 to PMN.	bind
29921	3	7417	7	NULL	NULL	0	NULL	TNF-alpha	NULL		increase	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_10_1089_s_234	12714560	25 These results collectively point to an important role of TNF-alpha in promoting ICAM-1 clustering, and the increased binding activity of cell surface ICAM-1 to PMN.	bind
27733	1	7418	5	13	NULL	NULL	NULL	heparin-binding proteins	GP		bind					HS	Chemical				NULL	in biological systems	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_65	15231514	25 This finding is in accordance with the observation that heparin-binding proteins usually bind HS in biological systems.	bind
29922	1	7418	7	NULL	NULL	0	NULL	heparin-binding proteins	NULL		bind	NULL				HS	NULL				NULL	biological systems	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1549_s_65	15231514	25 This finding is in accordance with the observation that heparin-binding proteins usually bind HS in biological systems.	bind
27734	1	7419	5	13	NULL	NULL	NULL	tau 1	GP		bind					MTs	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1649_s_56	10362789	25 To see the tau bound to MTs, the cells were fixed with cold methanol to wash [[ away cytosolic tau. 26  With ]] this fixation protocol, tau 1 immunoreactivity was almost completely colocalized with MTs (Figure 1, c and d)   .	bind
29923	1	7419	7	NULL	NULL	0	NULL	tau 	NULL		bind	NULL				MTs	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_6_1649_s_56	10362789	25 To see the tau bound to MTs, the cells were fixed with cold methanol to wash [[ away cytosolic tau. 26  With ]] this fixation protocol, tau 1 immunoreactivity was almost completely colocalized with MTs (Figure 1, c and d)   .	bind
27735	1	7420	5	13	NULL	NULL	NULL	Mnk1	GP		bind					ERK2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_257	14605021	25 Whereas Mnk1 binds both ERK2 and p38 MAPK, Mnk2 interacts strongly only with ERK2.	bind
27736	2	7420	5	13	NULL	NULL	NULL	Mnk1	GP		bind					p38 MAPK	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_257	14605021	25 Whereas Mnk1 binds both ERK2 and p38 MAPK, Mnk2 interacts strongly only with ERK2.	bind
27737	3	7420	5	13	NULL	NULL	NULL	Mnk2	GP		interacts with		strongly			ERK2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_257	14605021	25 Whereas Mnk1 binds both ERK2 and p38 MAPK, Mnk2 interacts strongly only with ERK2.	bind
29924	1	7420	7	NULL	NULL	0	NULL	Mnk1	NULL		binds	NULL				ERK2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_257	14605021	25 Whereas Mnk1 binds both ERK2 and p38 MAPK, Mnk2 interacts strongly only with ERK2.	bind
29925	2	7420	7	NULL	NULL	0	NULL	Mnk1	NULL		binds	NULL				p38 MAPK	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_257	14605021	25 Whereas Mnk1 binds both ERK2 and p38 MAPK, Mnk2 interacts strongly only with ERK2.	bind
29926	3	7420	7	NULL	NULL	0	NULL	Mnk2	NULL		interacts	NULL	strongly			ERK2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_12_1218_s_257	14605021	25 Whereas Mnk1 binds both ERK2 and p38 MAPK, Mnk2 interacts strongly only with ERK2.	bind
27738	1	7422	5	13	NULL	NULL	NULL	aldosterone	Chemical		bind					MR	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_27	12756192	25) The binding of aldosterone to the MR results in dissociation of the ligand-activated MR from a multiprotein complex containing molecular chaperones, translocation into the nucleus, and binding to hormone response elements in the regulatory region of target gene promoters.	bind
27739	2	7422	5	13	NULL	NULL	NULL	MR	GP	ligand-activated	froms multiprotein complex with					molecular chaperones	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_27	12756192	25) The binding of aldosterone to the MR results in dissociation of the ligand-activated MR from a multiprotein complex containing molecular chaperones, translocation into the nucleus, and binding to hormone response elements in the regulatory region of target gene promoters.	bind
27740	3	7422	5	13	NULL	NULL	NULL	statement 1	Process		results in					statement 2	Process	dissociation of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_27	12756192	25) The binding of aldosterone to the MR results in dissociation of the ligand-activated MR from a multiprotein complex containing molecular chaperones, translocation into the nucleus, and binding to hormone response elements in the regulatory region of target gene promoters.	bind
27741	4	7422	5	13	NULL	NULL	NULL	MR	GP		is translocated to					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_27	12756192	25) The binding of aldosterone to the MR results in dissociation of the ligand-activated MR from a multiprotein complex containing molecular chaperones, translocation into the nucleus, and binding to hormone response elements in the regulatory region of target gene promoters.	bind
27742	5	7422	5	13	NULL	NULL	NULL	statement 1	Process		results in					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_27	12756192	25) The binding of aldosterone to the MR results in dissociation of the ligand-activated MR from a multiprotein complex containing molecular chaperones, translocation into the nucleus, and binding to hormone response elements in the regulatory region of target gene promoters.	bind
27743	6	7422	5	13	NULL	NULL	NULL	MR	GP		bind					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_27	12756192	25) The binding of aldosterone to the MR results in dissociation of the ligand-activated MR from a multiprotein complex containing molecular chaperones, translocation into the nucleus, and binding to hormone response elements in the regulatory region of target gene promoters.	bind
27744	7	7422	5	13	NULL	NULL	NULL	statement 1	Process		results in					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_27	12756192	25) The binding of aldosterone to the MR results in dissociation of the ligand-activated MR from a multiprotein complex containing molecular chaperones, translocation into the nucleus, and binding to hormone response elements in the regulatory region of target gene promoters.	bind
54503	8	7422	5	13	NULL	NULL	NULL	target gene	NucleicAcid		resides in				hormone response elements	target gene	NucleicAcid			regulatory region of promoter	NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_27	12756192	25) The binding of aldosterone to the MR results in dissociation of the ligand-activated MR from a multiprotein complex containing molecular chaperones, translocation into the nucleus, and binding to hormone response elements in the regulatory region of target gene promoters.	bind
29927	1	7422	7	NULL	NULL	0	NULL	aldosterone	NULL		bind	NULL				MR	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_27	12756192	25) The binding of aldosterone to the MR results in dissociation of the ligand-activated MR from a multiprotein complex containing molecular chaperones, translocation into the nucleus, and binding to hormone response elements in the regulatory region of target gene promoters.	bind
29928	2	7422	7	10	NULL	0	NULL	MR	NULL	ligand-activated	forms multiprotein complex with	NULL				molecular chaperones	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_27	12756192	25) The binding of aldosterone to the MR results in dissociation of the ligand-activated MR from a multiprotein complex containing molecular chaperones, translocation into the nucleus, and binding to hormone response elements in the regulatory region of target gene promoters.	bind
29929	3	7422	7	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_27	12756192	25) The binding of aldosterone to the MR results in dissociation of the ligand-activated MR from a multiprotein complex containing molecular chaperones, translocation into the nucleus, and binding to hormone response elements in the regulatory region of target gene promoters.	bind
29930	4	7422	7	10	NULL	0	NULL	MR			is translocated to					nucleus					NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_27	12756192	25) The binding of aldosterone to the MR results in dissociation of the ligand-activated MR from a multiprotein complex containing molecular chaperones, translocation into the nucleus, and binding to hormone response elements in the regulatory region of target gene promoters.	bind
29931	5	7422	7	10	NULL	0	NULL	statement 1			bind					statement 7					NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_27	12756192	25) The binding of aldosterone to the MR results in dissociation of the ligand-activated MR from a multiprotein complex containing molecular chaperones, translocation into the nucleus, and binding to hormone response elements in the regulatory region of target gene promoters.	bind
54502	6	7422	7	10	NULL	0	NULL	statement 1			results in					statement 4					NULL		0	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_27	12756192	25) The binding of aldosterone to the MR results in dissociation of the ligand-activated MR from a multiprotein complex containing molecular chaperones, translocation into the nucleus, and binding to hormone response elements in the regulatory region of target gene promoters.	bind
54504	7	7422	7	10	NULL	0	NULL	target gene			resides in				hormone response elements	target gene				regulatory region of promoter	NULL		0	NULL	NULL	NULL	gw70_circulation_107_19_2512_s_27	12756192	25) The binding of aldosterone to the MR results in dissociation of the ligand-activated MR from a multiprotein complex containing molecular chaperones, translocation into the nucleus, and binding to hormone response elements in the regulatory region of target gene promoters.	bind
27745	1	7424	5	13	NULL	NULL	NULL	AP-2	GP		bind		may			statement 6	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_6_682_s_195	11934836	25, 38 These along with other factors (such as AP-2, CRE, ER, GATA-1, and SP-1) may bind onto  cis elements of known consensus sequences on the human eNOS promoter.	bind
27746	2	7424	5	13	NULL	NULL	NULL	CRE	GP		bind		may			statement 6	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_6_682_s_195	11934836	25, 38 These along with other factors (such as AP-2, CRE, ER, GATA-1, and SP-1) may bind onto  cis elements of known consensus sequences on the human eNOS promoter.	bind
27747	3	7424	5	13	NULL	NULL	NULL	ER	GP		bind		may			statement 6	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_6_682_s_195	11934836	25, 38 These along with other factors (such as AP-2, CRE, ER, GATA-1, and SP-1) may bind onto  cis elements of known consensus sequences on the human eNOS promoter.	bind
27748	4	7424	5	13	NULL	NULL	NULL	GATA-1	GP		bind		may			statement 6	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_6_682_s_195	11934836	25, 38 These along with other factors (such as AP-2, CRE, ER, GATA-1, and SP-1) may bind onto  cis elements of known consensus sequences on the human eNOS promoter.	bind
27749	5	7424	5	13	NULL	NULL	NULL	SP-1	GP		bind		may			statement 6	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_6_682_s_195	11934836	25, 38 These along with other factors (such as AP-2, CRE, ER, GATA-1, and SP-1) may bind onto  cis elements of known consensus sequences on the human eNOS promoter.	bind
54508	6	7424	5	13	NULL	NULL	NULL				is present on				cis elements	eNOS	NucleicAcid	human		promoter	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_6_682_s_195	11934836	25, 38 These along with other factors (such as AP-2, CRE, ER, GATA-1, and SP-1) may bind onto  cis elements of known consensus sequences on the human eNOS promoter.	bind
29938	1	7424	7	10	NULL	0	NULL	AP-2			bind		may			statement 6					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_6_682_s_195	11934836	25, 38 These along with other factors (such as AP-2, CRE, ER, GATA-1, and SP-1) may bind onto  cis elements of known consensus sequences on the human eNOS promoter.	bind
29939	2	7424	7	10	NULL	0	NULL	 CRE			bind		may			statement 6					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_6_682_s_195	11934836	25, 38 These along with other factors (such as AP-2, CRE, ER, GATA-1, and SP-1) may bind onto  cis elements of known consensus sequences on the human eNOS promoter.	bind
29940	3	7424	7	10	NULL	0	NULL	ER			bind		may			statement 6					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_6_682_s_195	11934836	25, 38 These along with other factors (such as AP-2, CRE, ER, GATA-1, and SP-1) may bind onto  cis elements of known consensus sequences on the human eNOS promoter.	bind
29941	4	7424	7	10	NULL	0	NULL	GATA-1			bind		may			statement 6					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_6_682_s_195	11934836	25, 38 These along with other factors (such as AP-2, CRE, ER, GATA-1, and SP-1) may bind onto  cis elements of known consensus sequences on the human eNOS promoter.	bind
29942	5	7424	7	10	NULL	0	NULL	SP-1			bind		may			statement 6					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_6_682_s_195	11934836	25, 38 These along with other factors (such as AP-2, CRE, ER, GATA-1, and SP-1) may bind onto  cis elements of known consensus sequences on the human eNOS promoter.	bind
54509	6	7424	7	10	NULL	0	NULL				is present on				cis elements	eNOS		human		promoter	NULL		0	NULL	NULL	NULL	gw60_circulationres_90_6_682_s_195	11934836	25, 38 These along with other factors (such as AP-2, CRE, ER, GATA-1, and SP-1) may bind onto  cis elements of known consensus sequences on the human eNOS promoter.	bind
27750	1	7425	5	13	NULL	NULL	NULL	cytochrome C	GP		enters into					cytosol	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2178_s_26	14551153	25,26  On entry into the cytosol, cytochrome C binds the caspase-activating protein Apaf-1, stimulating its binding to procaspase 9 and activating caspase networks that trigger apoptosis.	bind
27751	2	7425	5	13	NULL	NULL	NULL	cytochrome C	GP		bind					Apaf-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2178_s_26	14551153	25,26  On entry into the cytosol, cytochrome C binds the caspase-activating protein Apaf-1, stimulating its binding to procaspase 9 and activating caspase networks that trigger apoptosis.	bind
27752	3	7425	5	13	NULL	NULL	NULL	Apaf-1	GP		is a type of					caspase-activating protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2178_s_26	14551153	25,26  On entry into the cytosol, cytochrome C binds the caspase-activating protein Apaf-1, stimulating its binding to procaspase 9 and activating caspase networks that trigger apoptosis.	bind
27753	4	7425	5	13	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2178_s_26	14551153	25,26  On entry into the cytosol, cytochrome C binds the caspase-activating protein Apaf-1, stimulating its binding to procaspase 9 and activating caspase networks that trigger apoptosis.	bind
27754	5	7425	5	13	NULL	NULL	NULL	Apaf-1	GP		bind					procaspase 9	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2178_s_26	14551153	25,26  On entry into the cytosol, cytochrome C binds the caspase-activating protein Apaf-1, stimulating its binding to procaspase 9 and activating caspase networks that trigger apoptosis.	bind
27755	6	7425	5	13	NULL	NULL	NULL	statement 2	Process		stimulates					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2178_s_26	14551153	25,26  On entry into the cytosol, cytochrome C binds the caspase-activating protein Apaf-1, stimulating its binding to procaspase 9 and activating caspase networks that trigger apoptosis.	bind
27756	7	7425	5	13	NULL	NULL	NULL	statement 6	Process		activates					caspase networks	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2178_s_26	14551153	25,26  On entry into the cytosol, cytochrome C binds the caspase-activating protein Apaf-1, stimulating its binding to procaspase 9 and activating caspase networks that trigger apoptosis.	bind
27757	8	7425	5	13	NULL	NULL	NULL	statement 7	Process		triggers					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2178_s_26	14551153	25,26  On entry into the cytosol, cytochrome C binds the caspase-activating protein Apaf-1, stimulating its binding to procaspase 9 and activating caspase networks that trigger apoptosis.	bind
29943	1	7425	7	NULL	NULL	0	NULL	 cytochrome C	NULL		binds	NULL				Apaf-1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2178_s_26	14551153	25,26  On entry into the cytosol, cytochrome C binds the caspase-activating protein Apaf-1, stimulating its binding to procaspase 9 and activating caspase networks that trigger apoptosis.	bind
29944	2	7425	7	NULL	NULL	0	NULL	statement 1	NULL		occurs upon	NULL				cytosol	NULL	entry into the			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2178_s_26	14551153	25,26  On entry into the cytosol, cytochrome C binds the caspase-activating protein Apaf-1, stimulating its binding to procaspase 9 and activating caspase networks that trigger apoptosis.	bind
29945	3	7425	7	NULL	NULL	0	NULL	Apaf-1	NULL		is a type of	NULL				caspase-activating protein	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2178_s_26	14551153	25,26  On entry into the cytosol, cytochrome C binds the caspase-activating protein Apaf-1, stimulating its binding to procaspase 9 and activating caspase networks that trigger apoptosis.	bind
29946	4	7425	7	NULL	NULL	0	NULL	cytochrome C	NULL		binds	NULL				procaspase 9	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2178_s_26	14551153	25,26  On entry into the cytosol, cytochrome C binds the caspase-activating protein Apaf-1, stimulating its binding to procaspase 9 and activating caspase networks that trigger apoptosis.	bind
29947	5	7425	7	NULL	NULL	0	NULL	statement 1	NULL		stimulates	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2178_s_26	14551153	25,26  On entry into the cytosol, cytochrome C binds the caspase-activating protein Apaf-1, stimulating its binding to procaspase 9 and activating caspase networks that trigger apoptosis.	bind
29948	6	7425	7	NULL	NULL	0	NULL	statement 5	NULL		activate	NULL				caspase networks	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2178_s_26	14551153	25,26  On entry into the cytosol, cytochrome C binds the caspase-activating protein Apaf-1, stimulating its binding to procaspase 9 and activating caspase networks that trigger apoptosis.	bind
29949	7	7425	7	NULL	NULL	0	NULL	statement 6	NULL		trigger	NULL				apoptosis	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2178_s_26	14551153	25,26  On entry into the cytosol, cytochrome C binds the caspase-activating protein Apaf-1, stimulating its binding to procaspase 9 and activating caspase networks that trigger apoptosis.	bind
27758	1	7426	5	13	NULL	NULL	NULL	25-Dx	GP		is a variant of					IZA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_316_1_448_s_19	16234411	25-Dx is a variant of IZA (Min et al., 2004 ), suggesting that it binds to heme, and we show in the present study that Hpr6 binds to heme.	bind
27759	2	7426	5	13	NULL	NULL	NULL	25-Dx	GP		bind					heme	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_316_1_448_s_19	16234411	25-Dx is a variant of IZA (Min et al., 2004 ), suggesting that it binds to heme, and we show in the present study that Hpr6 binds to heme.	bind
27760	3	7426	5	13	NULL	NULL	NULL	statement 1	Process		suggests					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_316_1_448_s_19	16234411	25-Dx is a variant of IZA (Min et al., 2004 ), suggesting that it binds to heme, and we show in the present study that Hpr6 binds to heme.	bind
27761	4	7426	5	13	NULL	NULL	NULL	Hpr6	GP		bind					heme	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_316_1_448_s_19	16234411	25-Dx is a variant of IZA (Min et al., 2004 ), suggesting that it binds to heme, and we show in the present study that Hpr6 binds to heme.	bind
29950	1	7426	7	NULL	NULL	0	NULL	25-Dx	NULL		is a variant of	NULL				IZA	NULL				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_316_1_448_s_19	16234411	25-Dx is a variant of IZA (Min et al., 2004 ), suggesting that it binds to heme, and we show in the present study that Hpr6 binds to heme.	bind
29951	2	7426	7	NULL	NULL	0	NULL	25-Dx	NULL		binds to	NULL				heme	NULL				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_316_1_448_s_19	16234411	25-Dx is a variant of IZA (Min et al., 2004 ), suggesting that it binds to heme, and we show in the present study that Hpr6 binds to heme.	bind
29952	3	7426	7	NULL	NULL	0	NULL	Hpr6	NULL		binds to	NULL				heme	NULL				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_316_1_448_s_19	16234411	25-Dx is a variant of IZA (Min et al., 2004 ), suggesting that it binds to heme, and we show in the present study that Hpr6 binds to heme.	bind
27762	1	7427	5	13	NULL	NULL	NULL	Sp1	GP		is a type of					transcription facor	GP				NULL		NULL	NULL	NULL	NULL	gw60_atherosclerosis_158_1_61_s_202	11500175	25-hydroxycholesterol and Oxidized LDL increased the binding of the transcription facors Sp1 and Sp3 to the TNF-  promoter	bind
27763	2	7427	5	13	NULL	NULL	NULL	Sp3	GP		is a type of					transcription facor	GP				NULL		NULL	NULL	NULL	NULL	gw60_atherosclerosis_158_1_61_s_202	11500175	25-hydroxycholesterol and Oxidized LDL increased the binding of the transcription facors Sp1 and Sp3 to the TNF-  promoter	bind
27764	3	7427	5	13	NULL	NULL	NULL	Sp1	GP		bind					TNF	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_atherosclerosis_158_1_61_s_202	11500175	25-hydroxycholesterol and Oxidized LDL increased the binding of the transcription facors Sp1 and Sp3 to the TNF-  promoter	bind
27765	4	7427	5	13	NULL	NULL	NULL	Sp3	GP		bind					TNF	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_atherosclerosis_158_1_61_s_202	11500175	25-hydroxycholesterol and Oxidized LDL increased the binding of the transcription facors Sp1 and Sp3 to the TNF-  promoter	bind
27766	5	7427	5	13	NULL	NULL	NULL	25-hydroxycholesterol	Chemical		increases					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_atherosclerosis_158_1_61_s_202	11500175	25-hydroxycholesterol and Oxidized LDL increased the binding of the transcription facors Sp1 and Sp3 to the TNF-  promoter	bind
27767	6	7427	5	13	NULL	NULL	NULL	25-hydroxycholesterol	Chemical		increases					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_atherosclerosis_158_1_61_s_202	11500175	25-hydroxycholesterol and Oxidized LDL increased the binding of the transcription facors Sp1 and Sp3 to the TNF-  promoter	bind
27768	7	7427	5	13	NULL	NULL	NULL	LDL	GP	oxidized	increases					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_atherosclerosis_158_1_61_s_202	11500175	25-hydroxycholesterol and Oxidized LDL increased the binding of the transcription facors Sp1 and Sp3 to the TNF-  promoter	bind
27769	8	7427	5	13	NULL	NULL	NULL	LDL	GP	oxidized	increases					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_atherosclerosis_158_1_61_s_202	11500175	25-hydroxycholesterol and Oxidized LDL increased the binding of the transcription facors Sp1 and Sp3 to the TNF-  promoter	bind
29953	1	7427	7	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				TNF	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_atherosclerosis_158_1_61_s_202	11500175	25-hydroxycholesterol and Oxidized LDL increased the binding of the transcription facors Sp1 and Sp3 to the TNF-  promoter	bind
29954	2	7427	7	NULL	NULL	0	NULL	Sp3	NULL		bind	NULL				TNF	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_atherosclerosis_158_1_61_s_202	11500175	25-hydroxycholesterol and Oxidized LDL increased the binding of the transcription facors Sp1 and Sp3 to the TNF-  promoter	bind
29955	3	7427	7	NULL	NULL	0	NULL	25-hydroxycholesterol	NULL		increase	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_atherosclerosis_158_1_61_s_202	11500175	25-hydroxycholesterol and Oxidized LDL increased the binding of the transcription facors Sp1 and Sp3 to the TNF-  promoter	bind
29956	4	7427	7	NULL	NULL	0	NULL	LDL	NULL	Oxidized	increase	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_atherosclerosis_158_1_61_s_202	11500175	25-hydroxycholesterol and Oxidized LDL increased the binding of the transcription facors Sp1 and Sp3 to the TNF-  promoter	bind
29957	5	7427	7	NULL	NULL	0	NULL	25-hydroxycholesterol	NULL		increase	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_atherosclerosis_158_1_61_s_202	11500175	25-hydroxycholesterol and Oxidized LDL increased the binding of the transcription facors Sp1 and Sp3 to the TNF-  promoter	bind
29958	6	7427	7	NULL	NULL	0	NULL	LDL	NULL	Oxidized	increase	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_atherosclerosis_158_1_61_s_202	11500175	25-hydroxycholesterol and Oxidized LDL increased the binding of the transcription facors Sp1 and Sp3 to the TNF-  promoter	bind
29959	7	7427	7	NULL	NULL	0	NULL	Sp1	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_atherosclerosis_158_1_61_s_202	11500175	25-hydroxycholesterol and Oxidized LDL increased the binding of the transcription facors Sp1 and Sp3 to the TNF-  promoter	bind
29960	8	7427	7	NULL	NULL	0	NULL	Sp3	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_atherosclerosis_158_1_61_s_202	11500175	25-hydroxycholesterol and Oxidized LDL increased the binding of the transcription facors Sp1 and Sp3 to the TNF-  promoter	bind
27770	1	7432	5	13	NULL	NULL	NULL				regulates				SBE	SM22alpha	GP	activity of		promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_circulationres_97_10_983_s_172	16224064	25a,26  In this report, we show that SBE is another critical element regulating SM22alpha promoter activity in vivo, and Smad3 binds to the SBE in response to TGF-beta1 stimulation.	bind
27771	2	7432	5	13	NULL	NULL	NULL	Smad3	GP		bind									SBE	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_10_983_s_172	16224064	25a,26  In this report, we show that SBE is another critical element regulating SM22alpha promoter activity in vivo, and Smad3 binds to the SBE in response to TGF-beta1 stimulation.	bind
27772	3	7432	5	13	NULL	NULL	NULL	TGF-beta1	GP	stimulation	leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_10_983_s_172	16224064	25a,26  In this report, we show that SBE is another critical element regulating SM22alpha promoter activity in vivo, and Smad3 binds to the SBE in response to TGF-beta1 stimulation.	bind
29961	1	7432	7	10	NULL	0	NULL				regulates				SBE	SM22alpha		activity of		promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_circulationres_97_10_983_s_172	16224064	25a,26  In this report, we show that SBE is another critical element regulating SM22alpha promoter activity in vivo, and Smad3 binds to the SBE in response to TGF-beta1 stimulation.	bind
29962	2	7432	7	NULL	NULL	0	NULL	Smad3	NULL		binds to	NULL					NULL			SBE	NULL		0	NULL	NULL	NULL	gw70_circulationres_97_10_983_s_172	16224064	25a,26  In this report, we show that SBE is another critical element regulating SM22alpha promoter activity in vivo, and Smad3 binds to the SBE in response to TGF-beta1 stimulation.	bind
29963	3	7432	7	NULL	NULL	0	NULL	statement 2	NULL		occurs upon	NULL				TGF-beta1	NULL	stimulation of			NULL		0	NULL	NULL	NULL	gw70_circulationres_97_10_983_s_172	16224064	25a,26  In this report, we show that SBE is another critical element regulating SM22alpha promoter activity in vivo, and Smad3 binds to the SBE in response to TGF-beta1 stimulation.	bind
27773	1	7433	5	13	NULL	NULL	NULL	plasmid ColIb-P9 antisense Inc RNA	NucleicAcid		bind					target RNA	NucleicAcid			5''-rUUGGCG-3'' motif in loop sequence	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1034_s_412	11222752	26       Asano,K., Niimi,T., Yokoyama,S. and Mizobuchi,K. (1998) Structural basis for binding of the plasmid ColIb-P9 antisense Inc RNA to its target RNA with the 5''-rUUGGCG-3'' motif in the loop sequence.	bind
29964	1	7433	7	10	NULL	0	NULL	plasmid ColIb-P9 ColIb-P9 antisense Inc RNA			binds					RNA				5''-rUUGGCG-3'' motif in the loop sequence	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1034_s_412	11222752	26       Asano,K., Niimi,T., Yokoyama,S. and Mizobuchi,K. (1998) Structural basis for binding of the plasmid ColIb-P9 antisense Inc RNA to its target RNA with the 5''-rUUGGCG-3'' motif in the loop sequence.	bind
27774	1	7434	5	13	NULL	NULL	NULL	PKR	GP		bind		specifically			RNA	NucleicAcid	delta agent genomic			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2535_s_295	11410661	26       Circle,D.A., Neel,O.D., Robertson,H.D., Clarke,P.A. and Mathews,M.B. (1997) Surprising specificity of PKR binding to delta agent genomic RNA.	bind
29966	1	7434	7	10	NULL	0	NULL	PKR			binds					RNA		delta agent genomic			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2535_s_295	11410661	26       Circle,D.A., Neel,O.D., Robertson,H.D., Clarke,P.A. and Mathews,M.B. (1997) Surprising specificity of PKR binding to delta agent genomic RNA.	bind
27775	1	7435	5	13	NULL	NULL	NULL	MyEF-2	GP		bind					MBP	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3197_s_335	10954586	26       Muralidharan,V., Tretiakova,A., Steplewski,A., Haas,S., Amini,S., Johnson,E. and Khalili,K. (1997) Evidence for inhibition of MyEF-2 binding to MBP promoter by MEF-1/Puralpha.	bind
27776	2	7435	5	13	NULL	NULL	NULL	MEF-1/Puralpha	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3197_s_335	10954586	26       Muralidharan,V., Tretiakova,A., Steplewski,A., Haas,S., Amini,S., Johnson,E. and Khalili,K. (1997) Evidence for inhibition of MyEF-2 binding to MBP promoter by MEF-1/Puralpha.	bind
29969	1	7435	7	NULL	NULL	0	NULL	MyEF-2	NULL		bind	NULL				MBP	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3197_s_335	10954586	26       Muralidharan,V., Tretiakova,A., Steplewski,A., Haas,S., Amini,S., Johnson,E. and Khalili,K. (1997) Evidence for inhibition of MyEF-2 binding to MBP promoter by MEF-1/Puralpha.	bind
29970	2	7435	7	NULL	NULL	0	NULL	MEF-1/Puralpha	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3197_s_335	10954586	26       Muralidharan,V., Tretiakova,A., Steplewski,A., Haas,S., Amini,S., Johnson,E. and Khalili,K. (1997) Evidence for inhibition of MyEF-2 binding to MBP promoter by MEF-1/Puralpha.	bind
27777	1	7436	5	13	NULL	NULL	NULL	CUG-binding protein	GP		bind		specifically							UG dinucleotide repeats	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2766_s_267	11433021	26       Takahashi,N., Sasagawa,N., Suzuki,K. and Ishiura,S. (2000) The CUG-binding protein binds specifically to UG dinucleotide repeats in a yeast three-hybrid system.	bind
29971	1	7436	7	10	NULL	0	NULL	CUG-binding protein	NULL		binds	NULL	specifically				NULL			UG dinucleotide repeats	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2766_s_267	11433021	26       Takahashi,N., Sasagawa,N., Suzuki,K. and Ishiura,S. (2000) The CUG-binding protein binds specifically to UG dinucleotide repeats in a yeast three-hybrid system.	bind
27778	1	7437	5	13	NULL	NULL	NULL	early growth response protein	GP		bind					statement 4	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_652_s_372	11160886	26       Yan,Y.-X., Nakagawa,H., Lees,M.-H. and Rustig,A.K. (1997) Transforming growth factor-alpha enhances cyclin D1 transcription through the binding of early growth response protein to a cis-regulatory element in the cyclin D1 promoter.	bind
27779	2	7437	5	13	NULL	NULL	NULL	Transforming growth factor-alpha	GP		enhances					cyclin D1	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_652_s_372	11160886	26       Yan,Y.-X., Nakagawa,H., Lees,M.-H. and Rustig,A.K. (1997) Transforming growth factor-alpha enhances cyclin D1 transcription through the binding of early growth response protein to a cis-regulatory element in the cyclin D1 promoter.	bind
27780	3	7437	5	13	NULL	NULL	NULL	statement 2	Process		occurs through					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_652_s_372	11160886	26       Yan,Y.-X., Nakagawa,H., Lees,M.-H. and Rustig,A.K. (1997) Transforming growth factor-alpha enhances cyclin D1 transcription through the binding of early growth response protein to a cis-regulatory element in the cyclin D1 promoter.	bind
54510	4	7437	5	13	NULL	NULL	NULL				is present in				cis-regulatory element	cyclin D1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_652_s_372	11160886	26       Yan,Y.-X., Nakagawa,H., Lees,M.-H. and Rustig,A.K. (1997) Transforming growth factor-alpha enhances cyclin D1 transcription through the binding of early growth response protein to a cis-regulatory element in the cyclin D1 promoter.	bind
29972	1	7437	7	10	NULL	0	NULL	early growth response protein			bind					statement 4					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_652_s_372	11160886	26       Yan,Y.-X., Nakagawa,H., Lees,M.-H. and Rustig,A.K. (1997) Transforming growth factor-alpha enhances cyclin D1 transcription through the binding of early growth response protein to a cis-regulatory element in the cyclin D1 promoter.	bind
29973	2	7437	7	NULL	NULL	0	NULL	Transforming growth factor-alpha	NULL		enhances	NULL				 cyclin D1	NULL	transcription of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_652_s_372	11160886	26       Yan,Y.-X., Nakagawa,H., Lees,M.-H. and Rustig,A.K. (1997) Transforming growth factor-alpha enhances cyclin D1 transcription through the binding of early growth response protein to a cis-regulatory element in the cyclin D1 promoter.	bind
29974	3	7437	7	NULL	NULL	0	NULL	statement 2	NULL		occurs through	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_652_s_372	11160886	26       Yan,Y.-X., Nakagawa,H., Lees,M.-H. and Rustig,A.K. (1997) Transforming growth factor-alpha enhances cyclin D1 transcription through the binding of early growth response protein to a cis-regulatory element in the cyclin D1 promoter.	bind
54512	4	7437	7	10	NULL	0	NULL				is present in				cis-regulatory element	cyclin D1				promoter	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_652_s_372	11160886	26       Yan,Y.-X., Nakagawa,H., Lees,M.-H. and Rustig,A.K. (1997) Transforming growth factor-alpha enhances cyclin D1 transcription through the binding of early growth response protein to a cis-regulatory element in the cyclin D1 promoter.	bind
27781	1	7438	5	13	NULL	NULL	NULL	Ang II	GP		bind					AT1 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_10_2297_s_133	11031218	26  31  Because candesartan reduces maximal Ang II binding to the AT1 receptor, whereas losartan causes a rightward shift in the Ang II dose response without reducing maximal Ang II binding, 31  it is likely that the partial reduction of Ang II - induced PAI-1 expression by losartan 9  was due to incomplete antagonism of the AT1 receptor.	bind
30138	2	7438	5	13	NULL	NULL	NULL	candesartan	Chemical		reduces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_10_2297_s_133	11031218	26  31  Because candesartan reduces maximal Ang II binding to the AT1 receptor, whereas losartan causes a rightward shift in the Ang II dose response without reducing maximal Ang II binding, 31  it is likely that the partial reduction of Ang II - induced PAI-1 expression by losartan 9  was due to incomplete antagonism of the AT1 receptor.	bind
30140	4	7438	5	13	NULL	NULL	NULL	losartan	Chemical		does not reduce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_10_2297_s_133	11031218	26  31  Because candesartan reduces maximal Ang II binding to the AT1 receptor, whereas losartan causes a rightward shift in the Ang II dose response without reducing maximal Ang II binding, 31  it is likely that the partial reduction of Ang II - induced PAI-1 expression by losartan 9  was due to incomplete antagonism of the AT1 receptor.	bind
30141	5	7438	5	13	NULL	NULL	NULL	Ang II	GP		induces					PAI-1	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_10_2297_s_133	11031218	26  31  Because candesartan reduces maximal Ang II binding to the AT1 receptor, whereas losartan causes a rightward shift in the Ang II dose response without reducing maximal Ang II binding, 31  it is likely that the partial reduction of Ang II - induced PAI-1 expression by losartan 9  was due to incomplete antagonism of the AT1 receptor.	bind
30142	6	7438	5	13	NULL	NULL	NULL	losartan 9	Chemical		reduces		partially			statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_10_2297_s_133	11031218	26  31  Because candesartan reduces maximal Ang II binding to the AT1 receptor, whereas losartan causes a rightward shift in the Ang II dose response without reducing maximal Ang II binding, 31  it is likely that the partial reduction of Ang II - induced PAI-1 expression by losartan 9  was due to incomplete antagonism of the AT1 receptor.	bind
30143	7	7438	5	13	NULL	NULL	NULL	AT1 receptor	GP	incomplete antagonism of	leads to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_10_2297_s_133	11031218	26  31  Because candesartan reduces maximal Ang II binding to the AT1 receptor, whereas losartan causes a rightward shift in the Ang II dose response without reducing maximal Ang II binding, 31  it is likely that the partial reduction of Ang II - induced PAI-1 expression by losartan 9  was due to incomplete antagonism of the AT1 receptor.	bind
29975	1	7438	7	NULL	NULL	0	NULL	 Ang II	NULL		bind	NULL				AT1 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_10_2297_s_133	11031218	26  31  Because candesartan reduces maximal Ang II binding to the AT1 receptor, whereas losartan causes a rightward shift in the Ang II dose response without reducing maximal Ang II binding, 31  it is likely that the partial reduction of Ang II - induced PAI-1 expression by losartan 9  was due to incomplete antagonism of the AT1 receptor.	bind
29976	2	7438	7	NULL	NULL	0	NULL	candesartan	NULL		reduces	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_10_2297_s_133	11031218	26  31  Because candesartan reduces maximal Ang II binding to the AT1 receptor, whereas losartan causes a rightward shift in the Ang II dose response without reducing maximal Ang II binding, 31  it is likely that the partial reduction of Ang II - induced PAI-1 expression by losartan 9  was due to incomplete antagonism of the AT1 receptor.	bind
29977	3	7438	7	NULL	NULL	0	NULL	losartan	NULL		does not reduce	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_10_2297_s_133	11031218	26  31  Because candesartan reduces maximal Ang II binding to the AT1 receptor, whereas losartan causes a rightward shift in the Ang II dose response without reducing maximal Ang II binding, 31  it is likely that the partial reduction of Ang II - induced PAI-1 expression by losartan 9  was due to incomplete antagonism of the AT1 receptor.	bind
29978	4	7438	7	NULL	NULL	0	NULL	Ang II	NULL		induce	NULL				 PAI-1 	NULL	expression of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_10_2297_s_133	11031218	26  31  Because candesartan reduces maximal Ang II binding to the AT1 receptor, whereas losartan causes a rightward shift in the Ang II dose response without reducing maximal Ang II binding, 31  it is likely that the partial reduction of Ang II - induced PAI-1 expression by losartan 9  was due to incomplete antagonism of the AT1 receptor.	bind
29979	5	7438	7	NULL	NULL	0	NULL	losartan	NULL		reduce	NULL	partially			statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_10_2297_s_133	11031218	26  31  Because candesartan reduces maximal Ang II binding to the AT1 receptor, whereas losartan causes a rightward shift in the Ang II dose response without reducing maximal Ang II binding, 31  it is likely that the partial reduction of Ang II - induced PAI-1 expression by losartan 9  was due to incomplete antagonism of the AT1 receptor.	bind
29980	6	7438	7	NULL	NULL	0	NULL	statement 5	NULL		is due to	NULL				AT1 receptor	NULL	incomplete antagonism of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_10_2297_s_133	11031218	26  31  Because candesartan reduces maximal Ang II binding to the AT1 receptor, whereas losartan causes a rightward shift in the Ang II dose response without reducing maximal Ang II binding, 31  it is likely that the partial reduction of Ang II - induced PAI-1 expression by losartan 9  was due to incomplete antagonism of the AT1 receptor.	bind
27782	1	7439	5	13	NULL	NULL	NULL	PBL	Cell		bind					smooth muscle cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_1953_s_251	10595925	26  A 50% reduction of PBL binding to smooth muscle cells with these antibodies was observed.	bind
29981	1	7439	7	NULL	NULL	0	NULL	PBL	NULL		bind	NULL				smooth muscle cells	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_6_1953_s_251	10595925	26  A 50% reduction of PBL binding to smooth muscle cells with these antibodies was observed.	bind
27783	1	7440	5	13	NULL	NULL	NULL	VLA-4	GP		bind					FN	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_2_153_s_38	10904000	26  An alternative interpretation of these results 25  is that the VCAM-1 and FN binding sites may indeed be identical, but the binding affinity of VLA-4 for FN could be lower.	bind
29982	1	7440	7	NULL	NULL	0	NULL	VLA-4	NULL		bind	NULL				FN	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_2_153_s_38	10904000	26  An alternative interpretation of these results 25  is that the VCAM-1 and FN binding sites may indeed be identical, but the binding affinity of VLA-4 for FN could be lower.	bind
27784	1	7441	5	13	NULL	NULL	NULL	ELAM-1	GP		bind					neutrophils	Cell		carbohydrate containing moiety		NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_2_403_s_142	7805244	26  ELAM-1 binds to a carbohydrate containing moiety (sialyl Lewisx structure) on neutrophils, while ICAM-1 binds to the heterodimeric B2 integrins (CD11a/CD18 and CD11b/CD18).	bind
27785	2	7441	5	13	NULL	NULL	NULL	ICAM-1	GP		bind					CD11a/CD18	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_2_403_s_142	7805244	26  ELAM-1 binds to a carbohydrate containing moiety (sialyl Lewisx structure) on neutrophils, while ICAM-1 binds to the heterodimeric B2 integrins (CD11a/CD18 and CD11b/CD18).	bind
27786	3	7441	5	13	NULL	NULL	NULL	ICAM-1	GP		bind					CD11b/CD18	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_2_403_s_142	7805244	26  ELAM-1 binds to a carbohydrate containing moiety (sialyl Lewisx structure) on neutrophils, while ICAM-1 binds to the heterodimeric B2 integrins (CD11a/CD18 and CD11b/CD18).	bind
27787	4	7441	5	13	NULL	NULL	NULL	CD11b/CD18	GP		is a type of					heterodimeric B2 integrins	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_2_403_s_142	7805244	26  ELAM-1 binds to a carbohydrate containing moiety (sialyl Lewisx structure) on neutrophils, while ICAM-1 binds to the heterodimeric B2 integrins (CD11a/CD18 and CD11b/CD18).	bind
27788	5	7441	5	13	NULL	NULL	NULL	CD11a/CD18	GP		is a type of					heterodimeric B2 integrins	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_2_403_s_142	7805244	26  ELAM-1 binds to a carbohydrate containing moiety (sialyl Lewisx structure) on neutrophils, while ICAM-1 binds to the heterodimeric B2 integrins (CD11a/CD18 and CD11b/CD18).	bind
29984	1	7441	7	NULL	NULL	0	NULL	ELAM-1	NULL		binds to	NULL				neutrophils	NULL		carbohydrate containing moiety		NULL		0	NULL	NULL	NULL	gw60_circulation_91_2_403_s_142	7805244	26  ELAM-1 binds to a carbohydrate containing moiety (sialyl Lewisx structure) on neutrophils, while ICAM-1 binds to the heterodimeric B2 integrins (CD11a/CD18 and CD11b/CD18).	bind
29985	2	7441	7	10	NULL	0	NULL	ICAM-1 			binds to					CD11a/CD18					NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_2_403_s_142	7805244	26  ELAM-1 binds to a carbohydrate containing moiety (sialyl Lewisx structure) on neutrophils, while ICAM-1 binds to the heterodimeric B2 integrins (CD11a/CD18 and CD11b/CD18).	bind
54513	3	7441	7	10	NULL	0	NULL	ICAM-1			bind					CD11b/CD18					NULL		0	NULL	NULL	NULL	gw60_circulation_91_2_403_s_142	7805244	26  ELAM-1 binds to a carbohydrate containing moiety (sialyl Lewisx structure) on neutrophils, while ICAM-1 binds to the heterodimeric B2 integrins (CD11a/CD18 and CD11b/CD18).	bind
54514	4	7441	7	10	NULL	0	NULL	CD11b/CD18			is a type of					heterodimeric B2 integrins					NULL		0	NULL	NULL	NULL	gw60_circulation_91_2_403_s_142	7805244	26  ELAM-1 binds to a carbohydrate containing moiety (sialyl Lewisx structure) on neutrophils, while ICAM-1 binds to the heterodimeric B2 integrins (CD11a/CD18 and CD11b/CD18).	bind
54515	5	7441	7	10	NULL	0	NULL	CD11a/CD18			is a type of					heterodimeric B2 integrins					NULL		0	NULL	NULL	NULL	gw60_circulation_91_2_403_s_142	7805244	26  ELAM-1 binds to a carbohydrate containing moiety (sialyl Lewisx structure) on neutrophils, while ICAM-1 binds to the heterodimeric B2 integrins (CD11a/CD18 and CD11b/CD18).	bind
27789	1	7442	5	13	NULL	NULL	NULL	synthetic agonist of retinoic acid	Chemical		bind		selectively			RXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_1_4_s_77	8925567	26  Further analysis using synthetic agonists of retinoic acid, which selectively bind to RXR or RAR, were used in  trans-activation transient transfection assays, demonstrating that RAR/RXR heterodimers mediate suppression of alpha-adrenergic receptor-dependent hypertrophy.	bind
27790	2	7442	5	13	NULL	NULL	NULL	synthetic agonist of retinoic acid	Chemical		bind		selectively			RAR	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_1_4_s_77	8925567	26  Further analysis using synthetic agonists of retinoic acid, which selectively bind to RXR or RAR, were used in  trans-activation transient transfection assays, demonstrating that RAR/RXR heterodimers mediate suppression of alpha-adrenergic receptor-dependent hypertrophy.	bind
27791	3	7442	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_1_4_s_77	8925567	26  Further analysis using synthetic agonists of retinoic acid, which selectively bind to RXR or RAR, were used in  trans-activation transient transfection assays, demonstrating that RAR/RXR heterodimers mediate suppression of alpha-adrenergic receptor-dependent hypertrophy.	bind
27792	4	7442	5	13	NULL	NULL	NULL	RAR/RXR heterodimers	GP		mediate					hypertrophy	Process	suppression of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_1_4_s_77	8925567	26  Further analysis using synthetic agonists of retinoic acid, which selectively bind to RXR or RAR, were used in  trans-activation transient transfection assays, demonstrating that RAR/RXR heterodimers mediate suppression of alpha-adrenergic receptor-dependent hypertrophy.	bind
27793	5	7442	5	13	NULL	NULL	NULL	hypertrophy	Process		is dependent on					alpha-adrenergic receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_1_4_s_77	8925567	26  Further analysis using synthetic agonists of retinoic acid, which selectively bind to RXR or RAR, were used in  trans-activation transient transfection assays, demonstrating that RAR/RXR heterodimers mediate suppression of alpha-adrenergic receptor-dependent hypertrophy.	bind
29986	1	7442	7	10	NULL	0	NULL	synthetic agonist of retinoic acid			bind		selectively			RXR					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_1_4_s_77	8925567	26  Further analysis using synthetic agonists of retinoic acid, which selectively bind to RXR or RAR, were used in  trans-activation transient transfection assays, demonstrating that RAR/RXR heterodimers mediate suppression of alpha-adrenergic receptor-dependent hypertrophy.	bind
29987	2	7442	7	10	NULL	0	NULL	synthetic agonist of retinoic acid			bind		selectively			RAR					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_1_4_s_77	8925567	26  Further analysis using synthetic agonists of retinoic acid, which selectively bind to RXR or RAR, were used in  trans-activation transient transfection assays, demonstrating that RAR/RXR heterodimers mediate suppression of alpha-adrenergic receptor-dependent hypertrophy.	bind
29988	3	7442	7	10	NULL	0	NULL	RAR/RXR heterodimers			mediate					hypertrophy		suppression of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_1_4_s_77	8925567	26  Further analysis using synthetic agonists of retinoic acid, which selectively bind to RXR or RAR, were used in  trans-activation transient transfection assays, demonstrating that RAR/RXR heterodimers mediate suppression of alpha-adrenergic receptor-dependent hypertrophy.	bind
54516	4	7442	7	10	NULL	0	NULL	hypertrophy			is dependent on					alpha-adrenergic receptor					NULL		0	NULL	NULL	NULL	gw60_circulationres_79_1_4_s_77	8925567	26  Further analysis using synthetic agonists of retinoic acid, which selectively bind to RXR or RAR, were used in  trans-activation transient transfection assays, demonstrating that RAR/RXR heterodimers mediate suppression of alpha-adrenergic receptor-dependent hypertrophy.	bind
54517	5	7442	7	10	NULL	0	NULL	statement 1			is an alternative to					statement 2					NULL		0	NULL	NULL	NULL	gw60_circulationres_79_1_4_s_77	8925567	26  Further analysis using synthetic agonists of retinoic acid, which selectively bind to RXR or RAR, were used in  trans-activation transient transfection assays, demonstrating that RAR/RXR heterodimers mediate suppression of alpha-adrenergic receptor-dependent hypertrophy.	bind
27794	1	7443	5	13	NULL	NULL	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_82_5_576_s_238	9529162	26  In contrast, cells subjected to more severe hypoxia (0% O2 for 1 to 6 hours) exhibited time-dependent increases in the DNA binding activities of both NF-kappaB and AP-1 as shown by gel shift analysis (Figs 7A   and 7B  ).	bind
27795	2	7443	5	13	NULL	NULL	NULL	AP-1	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_82_5_576_s_238	9529162	26  In contrast, cells subjected to more severe hypoxia (0% O2 for 1 to 6 hours) exhibited time-dependent increases in the DNA binding activities of both NF-kappaB and AP-1 as shown by gel shift analysis (Figs 7A   and 7B  ).	bind
29989	1	7443	7	NULL	NULL	0	NULL	NF-kappaB	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_82_5_576_s_238	9529162	26  In contrast, cells subjected to more severe hypoxia (0% O2 for 1 to 6 hours) exhibited time-dependent increases in the DNA binding activities of both NF-kappaB and AP-1 as shown by gel shift analysis (Figs 7A   and 7B  ).	bind
29990	2	7443	7	NULL	NULL	0	NULL	AP-1	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_82_5_576_s_238	9529162	26  In contrast, cells subjected to more severe hypoxia (0% O2 for 1 to 6 hours) exhibited time-dependent increases in the DNA binding activities of both NF-kappaB and AP-1 as shown by gel shift analysis (Figs 7A   and 7B  ).	bind
28033	1	7444	5	13	NULL	NULL	NULL	protein(s)	GP		bind					ecNOS	GP	putative		NF-1 binding site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_8_1255_s_218	7543000	26  In gel mobility shift assays, a polyclonal antibody against CTF/NF-1 crossreacted with the protein(s) bound to the putative NF-1 binding site of the ecNOS promoter, whereas they had low affinity for consensus NF-1 oligonucleotides.	bind
28034	2	7444	5	13	NULL	NULL	NULL	CTF/NF-1 polyclonal antibody	GP		crossreacts with					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_8_1255_s_218	7543000	26  In gel mobility shift assays, a polyclonal antibody against CTF/NF-1 crossreacted with the protein(s) bound to the putative NF-1 binding site of the ecNOS promoter, whereas they had low affinity for consensus NF-1 oligonucleotides.	bind
28035	3	7444	5	13	NULL	NULL	NULL	CTF/NF-1 polyclonal antibody	GP		bind		low affinity			NF-1 oligonucleotides	NucleicAcid	consensus			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_8_1255_s_218	7543000	26  In gel mobility shift assays, a polyclonal antibody against CTF/NF-1 crossreacted with the protein(s) bound to the putative NF-1 binding site of the ecNOS promoter, whereas they had low affinity for consensus NF-1 oligonucleotides.	bind
29991	1	7444	7	10	NULL	0	NULL	 proteins			bind					ecNOS		putative		NF-1 binding site in promoter	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_8_1255_s_218	7543000	26  In gel mobility shift assays, a polyclonal antibody against CTF/NF-1 crossreacted with the protein(s) bound to the putative NF-1 binding site of the ecNOS promoter, whereas they had low affinity for consensus NF-1 oligonucleotides.	bind
29992	2	7444	7	NULL	NULL	0	NULL	CTF/NF-1 polyclonal antibody	NULL		crossreacts with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_8_1255_s_218	7543000	26  In gel mobility shift assays, a polyclonal antibody against CTF/NF-1 crossreacted with the protein(s) bound to the putative NF-1 binding site of the ecNOS promoter, whereas they had low affinity for consensus NF-1 oligonucleotides.	bind
29993	3	7444	7	NULL	NULL	0	NULL	CTF/NF-1 polyclonal antibody	NULL		bind	NULL	low affinity			 NF-1 oligonucleotides	NULL	consensus			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_8_1255_s_218	7543000	26  In gel mobility shift assays, a polyclonal antibody against CTF/NF-1 crossreacted with the protein(s) bound to the putative NF-1 binding site of the ecNOS promoter, whereas they had low affinity for consensus NF-1 oligonucleotides.	bind
28036	1	7445	5	13	NULL	NULL	NULL	prothrombin	GP		bind					CMs	CellComponent	native;;chyle			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_139	9445253	26  In our previous studies, we examined binding of prothrombin to native chyle CMs, which contain more phospholipids and a higher proportion of phosphatidylethanolamine in the polar surface coat 49  than the particles that have been exposed to plasma or lipoprotein lipase.	bind
28037	2	7445	5	13	NULL	NULL	NULL	CMs	CellComponent	native;;chyle	contains					phospholipids	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_139	9445253	26  In our previous studies, we examined binding of prothrombin to native chyle CMs, which contain more phospholipids and a higher proportion of phosphatidylethanolamine in the polar surface coat 49  than the particles that have been exposed to plasma or lipoprotein lipase.	bind
28038	3	7445	5	13	NULL	NULL	NULL	CMs	CellComponent	native;;chyle	contains					phosphatidylethanolamine	Chemical	higher proportion of			NULL	polar surface coat	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_139	9445253	26  In our previous studies, we examined binding of prothrombin to native chyle CMs, which contain more phospholipids and a higher proportion of phosphatidylethanolamine in the polar surface coat 49  than the particles that have been exposed to plasma or lipoprotein lipase.	bind
29994	1	7445	7	10	NULL	0	NULL	prothrombin			binds					CMs		native;;chyle			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_139	9445253	26  In our previous studies, we examined binding of prothrombin to native chyle CMs, which contain more phospholipids and a higher proportion of phosphatidylethanolamine in the polar surface coat 49  than the particles that have been exposed to plasma or lipoprotein lipase.	bind
29995	2	7445	7	10	NULL	0	NULL	CMs		native;;chyle	contains					phospholipids					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_139	9445253	26  In our previous studies, we examined binding of prothrombin to native chyle CMs, which contain more phospholipids and a higher proportion of phosphatidylethanolamine in the polar surface coat 49  than the particles that have been exposed to plasma or lipoprotein lipase.	bind
29996	3	7445	7	10	NULL	0	NULL	CMs		native;;chyle	contains					phosphatidylethanolamine 					NULL	polar surface coat	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_139	9445253	26  In our previous studies, we examined binding of prothrombin to native chyle CMs, which contain more phospholipids and a higher proportion of phosphatidylethanolamine in the polar surface coat 49  than the particles that have been exposed to plasma or lipoprotein lipase.	bind
30113	1	7446	5	13	NULL	NULL	NULL	thrombin	GP		bind					clot					NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_7_681_s_134	9495304	26  The superior antithrombotic efficacy of specific thrombin inhibition over heparin appears to be due to several mechanisms, including better inhibition of catalytically active clot-bound thrombin, 27  28  lack of natural inhibitors against hirudin but present against heparin, 29  30  and high affinity for platelet thrombin receptor by r-hirudin, which can displace thrombin bound to platelet receptor.	bind
30114	8	7446	5	13	NULL	NULL	NULL	statement 1	Process	inhibition of;;catalytically active	results in					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_7_681_s_134	9495304	26  The superior antithrombotic efficacy of specific thrombin inhibition over heparin appears to be due to several mechanisms, including better inhibition of catalytically active clot-bound thrombin, 27  28  lack of natural inhibitors against hirudin but present against heparin, 29  30  and high affinity for platelet thrombin receptor by r-hirudin, which can displace thrombin bound to platelet receptor.	bind
30115	3	7446	5	13	NULL	NULL	NULL	inhibitors	Chemical	natural	is present against					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_7_681_s_134	9495304	26  The superior antithrombotic efficacy of specific thrombin inhibition over heparin appears to be due to several mechanisms, including better inhibition of catalytically active clot-bound thrombin, 27  28  lack of natural inhibitors against hirudin but present against heparin, 29  30  and high affinity for platelet thrombin receptor by r-hirudin, which can displace thrombin bound to platelet receptor.	bind
30117	5	7446	5	13	NULL	NULL	NULL	r-hirudin	GP		bind		high affinity			platelet thrombin receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_7_681_s_134	9495304	26  The superior antithrombotic efficacy of specific thrombin inhibition over heparin appears to be due to several mechanisms, including better inhibition of catalytically active clot-bound thrombin, 27  28  lack of natural inhibitors against hirudin but present against heparin, 29  30  and high affinity for platelet thrombin receptor by r-hirudin, which can displace thrombin bound to platelet receptor.	bind
30118	6	7446	5	13	NULL	NULL	NULL	thrombin	GP		bind					platelet receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_7_681_s_134	9495304	26  The superior antithrombotic efficacy of specific thrombin inhibition over heparin appears to be due to several mechanisms, including better inhibition of catalytically active clot-bound thrombin, 27  28  lack of natural inhibitors against hirudin but present against heparin, 29  30  and high affinity for platelet thrombin receptor by r-hirudin, which can displace thrombin bound to platelet receptor.	bind
30119	7	7446	5	13	NULL	NULL	NULL	statement 5	Process		displaces					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_7_681_s_134	9495304	26  The superior antithrombotic efficacy of specific thrombin inhibition over heparin appears to be due to several mechanisms, including better inhibition of catalytically active clot-bound thrombin, 27  28  lack of natural inhibitors against hirudin but present against heparin, 29  30  and high affinity for platelet thrombin receptor by r-hirudin, which can displace thrombin bound to platelet receptor.	bind
30122	2	7446	5	13	NULL	NULL	NULL	thrombin	GP	antithrombotic efficacy of;;inhibition of	is superior to					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_7_681_s_134	9495304	26  The superior antithrombotic efficacy of specific thrombin inhibition over heparin appears to be due to several mechanisms, including better inhibition of catalytically active clot-bound thrombin, 27  28  lack of natural inhibitors against hirudin but present against heparin, 29  30  and high affinity for platelet thrombin receptor by r-hirudin, which can displace thrombin bound to platelet receptor.	bind
54518	4	7446	5	13	NULL	NULL	NULL	statement 3	Process		results in					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_7_681_s_134	9495304	26  The superior antithrombotic efficacy of specific thrombin inhibition over heparin appears to be due to several mechanisms, including better inhibition of catalytically active clot-bound thrombin, 27  28  lack of natural inhibitors against hirudin but present against heparin, 29  30  and high affinity for platelet thrombin receptor by r-hirudin, which can displace thrombin bound to platelet receptor.	bind
54519	9	7446	5	13	NULL	NULL	NULL	statement 5	Process		results in					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_7_681_s_134	9495304	26  The superior antithrombotic efficacy of specific thrombin inhibition over heparin appears to be due to several mechanisms, including better inhibition of catalytically active clot-bound thrombin, 27  28  lack of natural inhibitors against hirudin but present against heparin, 29  30  and high affinity for platelet thrombin receptor by r-hirudin, which can displace thrombin bound to platelet receptor.	bind
29998	1	7446	7	NULL	NULL	0	NULL	thrombin 	NULL		bind	NULL				platelet receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_97_7_681_s_134	9495304	26  The superior antithrombotic efficacy of specific thrombin inhibition over heparin appears to be due to several mechanisms, including better inhibition of catalytically active clot-bound thrombin, 27  28  lack of natural inhibitors against hirudin but present against heparin, 29  30  and high affinity for platelet thrombin receptor by r-hirudin, which can displace thrombin bound to platelet receptor.	bind
30000	2	7446	7	NULL	NULL	0	NULL	 r-hirudin	NULL		high affinity for	NULL				platelet thrombin receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_97_7_681_s_134	9495304	26  The superior antithrombotic efficacy of specific thrombin inhibition over heparin appears to be due to several mechanisms, including better inhibition of catalytically active clot-bound thrombin, 27  28  lack of natural inhibitors against hirudin but present against heparin, 29  30  and high affinity for platelet thrombin receptor by r-hirudin, which can displace thrombin bound to platelet receptor.	bind
30001	3	7446	7	NULL	NULL	0	NULL	statement 2	NULL		displace	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_97_7_681_s_134	9495304	26  The superior antithrombotic efficacy of specific thrombin inhibition over heparin appears to be due to several mechanisms, including better inhibition of catalytically active clot-bound thrombin, 27  28  lack of natural inhibitors against hirudin but present against heparin, 29  30  and high affinity for platelet thrombin receptor by r-hirudin, which can displace thrombin bound to platelet receptor.	bind
30002	4	7446	7	10	NULL	0	NULL	thrombin		antithrombotic efficacy of;;inhibition of	is superior over					heparin					NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_7_681_s_134	9495304	26  The superior antithrombotic efficacy of specific thrombin inhibition over heparin appears to be due to several mechanisms, including better inhibition of catalytically active clot-bound thrombin, 27  28  lack of natural inhibitors against hirudin but present against heparin, 29  30  and high affinity for platelet thrombin receptor by r-hirudin, which can displace thrombin bound to platelet receptor.	bind
30003	5	7446	7	NULL	NULL	0	NULL	thrombin	NULL		bind	NULL				clot	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_7_681_s_134	9495304	26  The superior antithrombotic efficacy of specific thrombin inhibition over heparin appears to be due to several mechanisms, including better inhibition of catalytically active clot-bound thrombin, 27  28  lack of natural inhibitors against hirudin but present against heparin, 29  30  and high affinity for platelet thrombin receptor by r-hirudin, which can displace thrombin bound to platelet receptor.	bind
30004	6	7446	7	10	NULL	0	NULL	statement 4			is due to					statement 5		inhibition of;;catalytically active			NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_7_681_s_134	9495304	26  The superior antithrombotic efficacy of specific thrombin inhibition over heparin appears to be due to several mechanisms, including better inhibition of catalytically active clot-bound thrombin, 27  28  lack of natural inhibitors against hirudin but present against heparin, 29  30  and high affinity for platelet thrombin receptor by r-hirudin, which can displace thrombin bound to platelet receptor.	bind
30005	7	7446	7	NULL	NULL	0	NULL	hirudin	NULL		lacks	NULL				natural inhibitors	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_97_7_681_s_134	9495304	26  The superior antithrombotic efficacy of specific thrombin inhibition over heparin appears to be due to several mechanisms, including better inhibition of catalytically active clot-bound thrombin, 27  28  lack of natural inhibitors against hirudin but present against heparin, 29  30  and high affinity for platelet thrombin receptor by r-hirudin, which can displace thrombin bound to platelet receptor.	bind
30006	8	7446	7	NULL	NULL	0	NULL	statement 4	NULL		is due to	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_97_7_681_s_134	9495304	26  The superior antithrombotic efficacy of specific thrombin inhibition over heparin appears to be due to several mechanisms, including better inhibition of catalytically active clot-bound thrombin, 27  28  lack of natural inhibitors against hirudin but present against heparin, 29  30  and high affinity for platelet thrombin receptor by r-hirudin, which can displace thrombin bound to platelet receptor.	bind
30007	9	7446	7	NULL	NULL	0	NULL	statement 4	NULL		is due to	NULL				heparin	NULL	natural inhibitors against			NULL		0	NULL	NULL	NULL	gw60_circulation_97_7_681_s_134	9495304	26  The superior antithrombotic efficacy of specific thrombin inhibition over heparin appears to be due to several mechanisms, including better inhibition of catalytically active clot-bound thrombin, 27  28  lack of natural inhibitors against hirudin but present against heparin, 29  30  and high affinity for platelet thrombin receptor by r-hirudin, which can displace thrombin bound to platelet receptor.	bind
30008	10	7446	7	NULL	NULL	0	NULL	statement 4	NULL		is due to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_97_7_681_s_134	9495304	26  The superior antithrombotic efficacy of specific thrombin inhibition over heparin appears to be due to several mechanisms, including better inhibition of catalytically active clot-bound thrombin, 27  28  lack of natural inhibitors against hirudin but present against heparin, 29  30  and high affinity for platelet thrombin receptor by r-hirudin, which can displace thrombin bound to platelet receptor.	bind
28040	1	7447	5	13	NULL	NULL	NULL	anti-apo(a) antibody	GP		bind					THP-1 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2036_s_146	9351369	26  The y axis represents the amount of anti-apo(a) antibody bound to THP-1 cells or fibrin.	bind
28041	2	7447	5	13	NULL	NULL	NULL	anti-apo(a) antibody	GP		bind					fibrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2036_s_146	9351369	26  The y axis represents the amount of anti-apo(a) antibody bound to THP-1 cells or fibrin.	bind
30009	1	7447	7	NULL	NULL	0	NULL	anti-apo(a) antibody	NULL		bind	NULL				THP-1 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2036_s_146	9351369	26  The y axis represents the amount of anti-apo(a) antibody bound to THP-1 cells or fibrin.	bind
30010	2	7447	7	NULL	NULL	0	NULL	anti-apo(a) antibody	NULL		bind	NULL				fibrin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2036_s_146	9351369	26  The y axis represents the amount of anti-apo(a) antibody bound to THP-1 cells or fibrin.	bind
28042	1	7448	5	13	NULL	NULL	NULL	TIMP-3	GP		is secreted from					locally infected cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_3_296_s_168	10645926	26  TIMP-3 secreted from locally infected cells therefore binds tightly to the ECM surrounding cells at the luminal surface and in the upper media, but not substantially within the ECM of distant sites.	bind
28043	2	7448	5	13	NULL	NULL	NULL	statement 1	GP		bind					ECM surrounding cells	Cell				NULL	luminal surface, upper media	NULL	NULL	NULL	NULL	gw60_circulation_101_3_296_s_168	10645926	26  TIMP-3 secreted from locally infected cells therefore binds tightly to the ECM surrounding cells at the luminal surface and in the upper media, but not substantially within the ECM of distant sites.	bind
28044	3	7448	5	13	NULL	NULL	NULL	statement 1	GP		does not bind		substantially			ECM	CellComponent	distant sites			NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_3_296_s_168	10645926	26  TIMP-3 secreted from locally infected cells therefore binds tightly to the ECM surrounding cells at the luminal surface and in the upper media, but not substantially within the ECM of distant sites.	bind
30012	1	7448	7	NULL	NULL	0	NULL	TIMP-3	NULL		is secreted from	NULL				locally infected cells	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_101_3_296_s_168	10645926	26  TIMP-3 secreted from locally infected cells therefore binds tightly to the ECM surrounding cells at the luminal surface and in the upper media, but not substantially within the ECM of distant sites.	bind
30013	2	7448	7	10	NULL	0	NULL	TIMP-3			binds		tightly			ECM surrounding cells					NULL	luminal surface, upper media	NULL	NULL	NULL	NULL	gw60_circulation_101_3_296_s_168	10645926	26  TIMP-3 secreted from locally infected cells therefore binds tightly to the ECM surrounding cells at the luminal surface and in the upper media, but not substantially within the ECM of distant sites.	bind
30016	5	7448	7	10	NULL	0	NULL	TIMP-3			does not bind					ECM		distant site			NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_3_296_s_168	10645926	26  TIMP-3 secreted from locally infected cells therefore binds tightly to the ECM surrounding cells at the luminal surface and in the upper media, but not substantially within the ECM of distant sites.	bind
28045	1	7449	5	13	NULL	NULL	NULL	factor VIIa	GP		bind					tissue factor	GP				NULL	rabbit atherosclerotic model	NULL	NULL	NULL	NULL	gw60_circulation_94_12_3098_s_117	8989115	26 27  Blockage of factor VIIa binding to tissue factor as well as the use of recombinant tissue factor pathway inhibitor reduced angiographic restenosis and decreased neointimal hyperplasia in the rabbit atherosclerotic model.	bind
28046	2	7449	5	13	NULL	NULL	NULL	statement 1	Process	blockage of	reduces					angiographic restenosis	MedicalFinding				NULL	in  rabbit atherosclerotic model	NULL	NULL	NULL	NULL	gw60_circulation_94_12_3098_s_117	8989115	26 27  Blockage of factor VIIa binding to tissue factor as well as the use of recombinant tissue factor pathway inhibitor reduced angiographic restenosis and decreased neointimal hyperplasia in the rabbit atherosclerotic model.	bind
28047	3	7449	5	13	NULL	NULL	NULL	statement 1	Process	blockage of	decrease					hyperplasia	MedicalFinding	neointimal			NULL	in  rabbit atherosclerotic model	NULL	NULL	NULL	NULL	gw60_circulation_94_12_3098_s_117	8989115	26 27  Blockage of factor VIIa binding to tissue factor as well as the use of recombinant tissue factor pathway inhibitor reduced angiographic restenosis and decreased neointimal hyperplasia in the rabbit atherosclerotic model.	bind
28048	4	7449	5	13	NULL	NULL	NULL	tissue factor pathway inhibitor	GP	recombinant	reduces					angiographic restenosis	MedicalFinding				NULL	in  rabbit atherosclerotic model	NULL	NULL	NULL	NULL	gw60_circulation_94_12_3098_s_117	8989115	26 27  Blockage of factor VIIa binding to tissue factor as well as the use of recombinant tissue factor pathway inhibitor reduced angiographic restenosis and decreased neointimal hyperplasia in the rabbit atherosclerotic model.	bind
28049	5	7449	5	13	NULL	NULL	NULL	tissue factor pathway inhibitor	GP	recombinant	decrease					hyperplasia	MedicalFinding	neointimal			NULL	in  rabbit atherosclerotic model	NULL	NULL	NULL	NULL	gw60_circulation_94_12_3098_s_117	8989115	26 27  Blockage of factor VIIa binding to tissue factor as well as the use of recombinant tissue factor pathway inhibitor reduced angiographic restenosis and decreased neointimal hyperplasia in the rabbit atherosclerotic model.	bind
30017	1	7449	7	10	NULL	0	NULL	factor VIIa			bind					tissue factor					NULL	rabbit atherosclerotic model	NULL	NULL	NULL	NULL	gw60_circulation_94_12_3098_s_117	8989115	26 27  Blockage of factor VIIa binding to tissue factor as well as the use of recombinant tissue factor pathway inhibitor reduced angiographic restenosis and decreased neointimal hyperplasia in the rabbit atherosclerotic model.	bind
30018	2	7449	7	10	NULL	0	NULL	tissue factor pathway inhibitor		recombinant	reduce					angiographic restenosis					NULL	rabbit atherosclerotic model	NULL	NULL	NULL	NULL	gw60_circulation_94_12_3098_s_117	8989115	26 27  Blockage of factor VIIa binding to tissue factor as well as the use of recombinant tissue factor pathway inhibitor reduced angiographic restenosis and decreased neointimal hyperplasia in the rabbit atherosclerotic model.	bind
30020	3	7449	7	NULL	NULL	0	NULL	tissue factor pathway inhibitor	NULL	recombinant	decrease	NULL				neointimal hyperplasia 	NULL				NULL	 rabbit atherosclerotic model	0	NULL	NULL	NULL	gw60_circulation_94_12_3098_s_117	8989115	26 27  Blockage of factor VIIa binding to tissue factor as well as the use of recombinant tissue factor pathway inhibitor reduced angiographic restenosis and decreased neointimal hyperplasia in the rabbit atherosclerotic model.	bind
30022	4	7449	7	10	NULL	0	NULL	statement 1		blockage of	reduce					angiographic restenosis					NULL	rabbit atherosclerotic model	NULL	NULL	NULL	NULL	gw60_circulation_94_12_3098_s_117	8989115	26 27  Blockage of factor VIIa binding to tissue factor as well as the use of recombinant tissue factor pathway inhibitor reduced angiographic restenosis and decreased neointimal hyperplasia in the rabbit atherosclerotic model.	bind
30023	5	7449	7	NULL	NULL	0	NULL	statement 1	NULL	blockage of	decrease	NULL				neointimal hyperplasia 	NULL				NULL	rabbit atherosclerotic model	0	NULL	NULL	NULL	gw60_circulation_94_12_3098_s_117	8989115	26 27  Blockage of factor VIIa binding to tissue factor as well as the use of recombinant tissue factor pathway inhibitor reduced angiographic restenosis and decreased neointimal hyperplasia in the rabbit atherosclerotic model.	bind
28050	1	7450	5	13	NULL	NULL	NULL	von Willebrand factor	GP		bind					platelet gpIb	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1331_s_143	9261264	26 27  Shear stress-induced von Willebrand factor binding to platelet gpIb has been found to initiate calcium influx 28 29  and activation of protein kinase C, 30  both of which are known to trigger platelet secretion.	bind
28051	2	7450	5	13	NULL	NULL	NULL	shear stress			induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1331_s_143	9261264	26 27  Shear stress-induced von Willebrand factor binding to platelet gpIb has been found to initiate calcium influx 28 29  and activation of protein kinase C, 30  both of which are known to trigger platelet secretion.	bind
28052	3	7450	5	13	NULL	NULL	NULL	statement 2	Process		initiates					calcium influx	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1331_s_143	9261264	26 27  Shear stress-induced von Willebrand factor binding to platelet gpIb has been found to initiate calcium influx 28 29  and activation of protein kinase C, 30  both of which are known to trigger platelet secretion.	bind
28053	4	7450	5	13	NULL	NULL	NULL	statement 2	Process		activates					protein kinase C	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1331_s_143	9261264	26 27  Shear stress-induced von Willebrand factor binding to platelet gpIb has been found to initiate calcium influx 28 29  and activation of protein kinase C, 30  both of which are known to trigger platelet secretion.	bind
28054	5	7450	5	13	NULL	NULL	NULL	statement 3	Process		triggers					platelet	Cell	secretion of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1331_s_143	9261264	26 27  Shear stress-induced von Willebrand factor binding to platelet gpIb has been found to initiate calcium influx 28 29  and activation of protein kinase C, 30  both of which are known to trigger platelet secretion.	bind
28055	6	7450	5	13	NULL	NULL	NULL	statement 4	Process		triggers					platelet	Cell	secretion of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1331_s_143	9261264	26 27  Shear stress-induced von Willebrand factor binding to platelet gpIb has been found to initiate calcium influx 28 29  and activation of protein kinase C, 30  both of which are known to trigger platelet secretion.	bind
30024	1	7450	7	NULL	NULL	0	NULL	Shear stress	NULL		induce	NULL				von Willebrand factor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1331_s_143	9261264	26 27  Shear stress-induced von Willebrand factor binding to platelet gpIb has been found to initiate calcium influx 28 29  and activation of protein kinase C, 30  both of which are known to trigger platelet secretion.	bind
30025	2	7450	7	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				platelet gpIb	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1331_s_143	9261264	26 27  Shear stress-induced von Willebrand factor binding to platelet gpIb has been found to initiate calcium influx 28 29  and activation of protein kinase C, 30  both of which are known to trigger platelet secretion.	bind
30026	3	7450	7	NULL	NULL	0	NULL	statement 2	NULL		initiate	NULL				calcium influx	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1331_s_143	9261264	26 27  Shear stress-induced von Willebrand factor binding to platelet gpIb has been found to initiate calcium influx 28 29  and activation of protein kinase C, 30  both of which are known to trigger platelet secretion.	bind
30027	4	7450	7	NULL	NULL	0	NULL	statement 2	NULL		activates	NULL				protein kinase C	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1331_s_143	9261264	26 27  Shear stress-induced von Willebrand factor binding to platelet gpIb has been found to initiate calcium influx 28 29  and activation of protein kinase C, 30  both of which are known to trigger platelet secretion.	bind
30028	5	7450	7	10	NULL	0	NULL	statement 3			trigger					platelet		secretion of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1331_s_143	9261264	26 27  Shear stress-induced von Willebrand factor binding to platelet gpIb has been found to initiate calcium influx 28 29  and activation of protein kinase C, 30  both of which are known to trigger platelet secretion.	bind
30029	6	7450	7	10	NULL	0	NULL	statement 4			trigger					platelet		secretion of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1331_s_143	9261264	26 27  Shear stress-induced von Willebrand factor binding to platelet gpIb has been found to initiate calcium influx 28 29  and activation of protein kinase C, 30  both of which are known to trigger platelet secretion.	bind
28056	1	7451	5	13	NULL	NULL	NULL	AT1-R antagonists	Chemical		increases					Ang II	GP	circulating levels of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_11_3954_s_247	9403620	26 27 28 29  Because circulating Ang II levels are increased by treatment with AT1-R antagonists 45  and Ang II preferentially binds to cardiac AT2-R, AT2-R - mediated actions are expected to be further activated under these pathological conditions.	bind
28057	2	7451	5	13	NULL	NULL	NULL	Ang II	GP		bind		preferentially			AT2-R	GP	cardiac			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_11_3954_s_247	9403620	26 27 28 29  Because circulating Ang II levels are increased by treatment with AT1-R antagonists 45  and Ang II preferentially binds to cardiac AT2-R, AT2-R - mediated actions are expected to be further activated under these pathological conditions.	bind
30036	1	7451	7	NULL	NULL	0	NULL	AT1-R antagonists	NULL		increase	NULL				AngII	NULL	circulating levels of 			NULL		0	NULL	NULL	NULL	gw60_circulation_96_11_3954_s_247	9403620	26 27 28 29  Because circulating Ang II levels are increased by treatment with AT1-R antagonists 45  and Ang II preferentially binds to cardiac AT2-R, AT2-R - mediated actions are expected to be further activated under these pathological conditions.	bind
30037	2	7451	7	NULL	NULL	0	NULL	 Ang II 	NULL		binds	NULL	preferentially			AT2-R	NULL	cardiac			NULL		0	NULL	NULL	NULL	gw60_circulation_96_11_3954_s_247	9403620	26 27 28 29  Because circulating Ang II levels are increased by treatment with AT1-R antagonists 45  and Ang II preferentially binds to cardiac AT2-R, AT2-R - mediated actions are expected to be further activated under these pathological conditions.	bind
28058	1	7452	5	13	NULL	NULL	NULL	E1A	GP		bind					pocket protein	GP				NULL	in cardiac muscle	NULL	NULL	NULL	NULL	gw60_circulationres_85_4_319_s_33	10455060	26 29 30  Forced expression of E2F-1, the prototype for E2F proteins that are the best understood endogenous occupants of the "`pocket,"` was sufficient by itself to reproduce the effect of pocket protein binding by E1A on G1 exit in cardiac muscle, 26  27  a finding also seen in other cell backgrounds.	bind
28059	3	7452	5	13	NULL	NULL	NULL	E2F-1	GP		reproduce		sufficiently			statement 1	Process	effect of 			NULL	in cardiac muscle	NULL	NULL	NULL	NULL	gw60_circulationres_85_4_319_s_33	10455060	26 29 30  Forced expression of E2F-1, the prototype for E2F proteins that are the best understood endogenous occupants of the "`pocket,"` was sufficient by itself to reproduce the effect of pocket protein binding by E1A on G1 exit in cardiac muscle, 26  27  a finding also seen in other cell backgrounds.	bind
28060	2	7452	5	13	NULL	NULL	NULL	statement 1	Process		occurs in					G1 exit	Process				NULL	in cardiac muscle	NULL	NULL	NULL	NULL	gw60_circulationres_85_4_319_s_33	10455060	26 29 30  Forced expression of E2F-1, the prototype for E2F proteins that are the best understood endogenous occupants of the "`pocket,"` was sufficient by itself to reproduce the effect of pocket protein binding by E1A on G1 exit in cardiac muscle, 26  27  a finding also seen in other cell backgrounds.	bind
28061	4	7452	5	13	NULL	NULL	NULL	E2F-1	GP		is a prototype for					E2F proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_4_319_s_33	10455060	26 29 30  Forced expression of E2F-1, the prototype for E2F proteins that are the best understood endogenous occupants of the "`pocket,"` was sufficient by itself to reproduce the effect of pocket protein binding by E1A on G1 exit in cardiac muscle, 26  27  a finding also seen in other cell backgrounds.	bind
28062	5	7452	5	13	NULL	NULL	NULL	E2F proteins	GP		occupants of		endogenous			pocket	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_4_319_s_33	10455060	26 29 30  Forced expression of E2F-1, the prototype for E2F proteins that are the best understood endogenous occupants of the "`pocket,"` was sufficient by itself to reproduce the effect of pocket protein binding by E1A on G1 exit in cardiac muscle, 26  27  a finding also seen in other cell backgrounds.	bind
30067	1	7452	7	NULL	NULL	0	NULL	E1A	NULL		bind	NULL				pocket proteins	NULL				NULL	cardiac muscle	NULL	NULL	NULL	NULL	gw60_circulationres_85_4_319_s_33	10455060	26 29 30  Forced expression of E2F-1, the prototype for E2F proteins that are the best understood endogenous occupants of the "`pocket,"` was sufficient by itself to reproduce the effect of pocket protein binding by E1A on G1 exit in cardiac muscle, 26  27  a finding also seen in other cell backgrounds.	bind
30068	2	7452	7	NULL	NULL	0	NULL	statement 1	NULL		occurs upon	NULL				G1 	NULL	exit of			NULL	cardiac muscle	NULL	NULL	NULL	NULL	gw60_circulationres_85_4_319_s_33	10455060	26 29 30  Forced expression of E2F-1, the prototype for E2F proteins that are the best understood endogenous occupants of the "`pocket,"` was sufficient by itself to reproduce the effect of pocket protein binding by E1A on G1 exit in cardiac muscle, 26  27  a finding also seen in other cell backgrounds.	bind
30069	3	7452	7	NULL	NULL	0	NULL	E2F-1	NULL		is a prototype for	NULL				E2F proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_4_319_s_33	10455060	26 29 30  Forced expression of E2F-1, the prototype for E2F proteins that are the best understood endogenous occupants of the "`pocket,"` was sufficient by itself to reproduce the effect of pocket protein binding by E1A on G1 exit in cardiac muscle, 26  27  a finding also seen in other cell backgrounds.	bind
30070	4	7452	7	10	NULL	0	NULL	E2F proteins			occupants of		endogenous			pocket					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_4_319_s_33	10455060	26 29 30  Forced expression of E2F-1, the prototype for E2F proteins that are the best understood endogenous occupants of the "`pocket,"` was sufficient by itself to reproduce the effect of pocket protein binding by E1A on G1 exit in cardiac muscle, 26  27  a finding also seen in other cell backgrounds.	bind
30475	5	7452	7	NULL	NULL	0	NULL	E2F-1	NULL		bind	NULL				pocket proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_4_319_s_33	10455060	26 29 30  Forced expression of E2F-1, the prototype for E2F proteins that are the best understood endogenous occupants of the "`pocket,"` was sufficient by itself to reproduce the effect of pocket protein binding by E1A on G1 exit in cardiac muscle, 26  27  a finding also seen in other cell backgrounds.	bind
28063	1	7453	5	13	NULL	NULL	NULL	HSP90	GP		bind					eNOS	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
28064	2	7453	5	13	NULL	NULL	NULL	statement 1	Process		occurs in response to					VEGF	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
28065	3	7453	5	13	NULL	NULL	NULL	statement 1	Process		occurs in response to					fluid shear stress					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
28066	4	7453	5	13	NULL	NULL	NULL	statement 2	Process		increases					eNOS	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
28067	5	7453	5	13	NULL	NULL	NULL	statement 3	Process		increases					eNOS	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
28068	6	7453	5	13	NULL	NULL	NULL	caveolin-1	GP		is displaced from					eNOS	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
28069	7	7453	5	13	NULL	NULL	NULL	CaM	GP		induces					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
28070	8	7453	5	13	NULL	NULL	NULL	statement 4	Process		occurs by					statement 7	Process	facilitating			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
28071	9	7453	5	13	NULL	NULL	NULL	statement 5	Process		occurs by					statement 7	Process	facilitating			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
28072	10	7453	5	13	NULL	NULL	NULL	caveolin-1	GP		interacts with					eNOS	GP	PM			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
28073	11	7453	5	13	NULL	NULL	NULL	caveolin-1	GP		interacts with					Golgi-PM	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
30039	1	7453	7	NULL	NULL	0	NULL	HSP90	NULL		bind	NULL				eNOS	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
30040	2	7453	7	NULL	NULL	0	NULL	statement 1	NULL		in response to	NULL				VEGF	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
30041	5	7453	7	NULL	NULL	0	NULL	statement 1			increase					eNOS		activity of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
30042	7	7453	7	10	NULL	0	NULL	CaM			induce					statement 6					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
30043	6	7453	7	NULL	NULL	0	NULL	caveolin-1			displaced from					eNOS		endogenous			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
30044	8	7453	7	10	NULL	0	NULL	statement 5			occur by					statement 7		facilitating			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
30045	9	7453	7	NULL	NULL	0	NULL	caveolin-1 			interacts with					eNOS		PM			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
30046	10	7453	7	10	NULL	0	NULL	caveolin-1			interacts with					Golgi-PM					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
54676	3	7453	7	NULL	NULL	0	NULL	statement 1			in response to					fluid shear stress					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
54677	4	7453	7	NULL	NULL	0	NULL	statement 2			occur along with					statement 3					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_5_959_s_26	16627819	26 Although binding of HSP90 to eNOS in response to VEGF and fluid shear stress increases eNOS activity by facilitating CaM-induced displacement of caveolin-1 from endogenous eNOS, 27 it remains unclear whether there is any change in caveolin-1 interaction with the PM eNOS versus the Golgi-PM in response to agonists.	bind
28074	1	7454	5	13	NULL	NULL	NULL	SUR2B	GP		bind			NBD2		ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_5_554_s_202	11909819	26 Because it was reported that NBD2 of SUR2B exhibits higherR binding capability to ADP than that of SUR2A 27 and because the primary function of Walker-A loop is to bind nucleotides, it seems likely that the difference between SUR2A and SUR2B in the binding property of ADP to their NBD2 may be one of the most possible candidates.	bind
28075	2	7454	5	13	NULL	NULL	NULL	SUR2A	GP		bind			NBD2		ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_5_554_s_202	11909819	26 Because it was reported that NBD2 of SUR2B exhibits higherR binding capability to ADP than that of SUR2A 27 and because the primary function of Walker-A loop is to bind nucleotides, it seems likely that the difference between SUR2A and SUR2B in the binding property of ADP to their NBD2 may be one of the most possible candidates.	bind
28076	3	7454	5	13	NULL	NULL	NULL	statement 1	GP		higher binding capability than					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_5_554_s_202	11909819	26 Because it was reported that NBD2 of SUR2B exhibits higherR binding capability to ADP than that of SUR2A 27 and because the primary function of Walker-A loop is to bind nucleotides, it seems likely that the difference between SUR2A and SUR2B in the binding property of ADP to their NBD2 may be one of the most possible candidates.	bind
28077	4	7454	5	13	NULL	NULL	NULL				bind			Walker-A loop		nucleotides	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_5_554_s_202	11909819	26 Because it was reported that NBD2 of SUR2B exhibits higherR binding capability to ADP than that of SUR2A 27 and because the primary function of Walker-A loop is to bind nucleotides, it seems likely that the difference between SUR2A and SUR2B in the binding property of ADP to their NBD2 may be one of the most possible candidates.	bind
30047	1	7454	7	NULL	NULL	0	NULL	SUR2B	NULL		bind	NULL		NBD2		ADP	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_5_554_s_202	11909819	26 Because it was reported that NBD2 of SUR2B exhibits higherR binding capability to ADP than that of SUR2A 27 and because the primary function of Walker-A loop is to bind nucleotides, it seems likely that the difference between SUR2A and SUR2B in the binding property of ADP to their NBD2 may be one of the most possible candidates.	bind
30048	2	7454	7	10	NULL	0	NULL	SUR2A	NULL		bind	NULL		NBD2		ADP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_5_554_s_202	11909819	26 Because it was reported that NBD2 of SUR2B exhibits higherR binding capability to ADP than that of SUR2A 27 and because the primary function of Walker-A loop is to bind nucleotides, it seems likely that the difference between SUR2A and SUR2B in the binding property of ADP to their NBD2 may be one of the most possible candidates.	bind
30049	3	7454	7	NULL	NULL	0	NULL	statement 1	NULL		higher affinity than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_5_554_s_202	11909819	26 Because it was reported that NBD2 of SUR2B exhibits higherR binding capability to ADP than that of SUR2A 27 and because the primary function of Walker-A loop is to bind nucleotides, it seems likely that the difference between SUR2A and SUR2B in the binding property of ADP to their NBD2 may be one of the most possible candidates.	bind
30050	4	7454	7	NULL	NULL	0	NULL		NULL		bind	NULL		Walker-A loop		nucleotides	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_5_554_s_202	11909819	26 Because it was reported that NBD2 of SUR2B exhibits higherR binding capability to ADP than that of SUR2A 27 and because the primary function of Walker-A loop is to bind nucleotides, it seems likely that the difference between SUR2A and SUR2B in the binding property of ADP to their NBD2 may be one of the most possible candidates.	bind
28078	1	7455	5	13	NULL	NULL	NULL	procaspase-9	GP		bind					Apaf-1	GP				NULL	in cytosol	NULL	NULL	NULL	NULL	gw60_circulationres_89_3_279_s_108	11485979	26 By immunoprecipitation of myocyte proteins with Apaf-1 antibody and subsequent exposure of the immunoprecipitated proteins to anti - procaspase-9 and Western blot, the fraction of procaspase-9 bound to Apaf-1 was detected in the cytosol ( Figure 3D).	bind
30051	1	7455	7	NULL	NULL	0	NULL	procaspase-9	NULL		bind	NULL				Apaf-1	NULL				NULL	cytosol	0	NULL	NULL	NULL	gw60_circulationres_89_3_279_s_108	11485979	26 By immunoprecipitation of myocyte proteins with Apaf-1 antibody and subsequent exposure of the immunoprecipitated proteins to anti - procaspase-9 and Western blot, the fraction of procaspase-9 bound to Apaf-1 was detected in the cytosol ( Figure 3D).	bind
28079	1	7456	5	13	NULL	NULL	NULL	ricin lectin	GP	rhodamine-labeled	bind		weakly			luminal surface	OrganismPart	endothelial			NULL	in untreated vessels	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2108_s_108	15345507	26 In untreated vessels, rhodamine-labeled ricin lectin binding to the endothelial luminal surface was weak and uniform in both genotypes (data not shown).	bind
30052	1	7456	7	10	NULL	0	NULL	ricin lectin	NULL	rhodamine-labeled	bind	NULL	weakly			 luminal surface	NULL	endothelial			NULL	untreated vessels	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2108_s_108	15345507	26 In untreated vessels, rhodamine-labeled ricin lectin binding to the endothelial luminal surface was weak and uniform in both genotypes (data not shown).	bind
28080	1	7457	5	13	NULL	NULL	NULL	C4BPbeta+ isoform molecules	GP		bind					PS	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_508_s_106	12615682	26 In vivo, all C4BPbeta+ isoform molecules circulate bound to PS.	bind
30053	1	7457	7	NULL	NULL	0	NULL	C4BPbeta+ isoform molecules	NULL		bind	NULL				PS	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_508_s_106	12615682	26 In vivo, all C4BPbeta+ isoform molecules circulate bound to PS.	bind
28081	1	7458	5	13	NULL	NULL	NULL	KIAA1437	GP		bind					k-ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_19_2467_s_157	12742993	26 KIAA1437 binds k-ras, where k-ras - deficient mice develop a thin ventricular wall and die until term.	bind
28082	2	7458	5	13	NULL	NULL	NULL	k-ras	GP	mice deficient in	develop					ventricular wall	OrganismPart	thin			NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_19_2467_s_157	12742993	26 KIAA1437 binds k-ras, where k-ras - deficient mice develop a thin ventricular wall and die until term.	bind
30055	1	7458	7	NULL	NULL	0	NULL	KIAA1437	NULL		binds	NULL				k-ras	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_107_19_2467_s_157	12742993	26 KIAA1437 binds k-ras, where k-ras - deficient mice develop a thin ventricular wall and die until term.	bind
30056	2	7458	7	10	NULL	0	NULL	k-ras - 		mice deficient in	develop					ventricular wall		thin			NULL		NULL	NULL	NULL	NULL	gw60_circulation_107_19_2467_s_157	12742993	26 KIAA1437 binds k-ras, where k-ras - deficient mice develop a thin ventricular wall and die until term.	bind
29897	1	7459	5	13	NULL	NULL	NULL	TRL	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_805_s_115	12006394	26 The E2 allele is also known to demonstrate impaired TRL binding by the LDL receptor 27 and more recently, has been shown to be associated with impaired lipoprotein lipase - mediated lipolysis of TRLs. 28 The greatest increase in LDL cholesterol associated with the L162V polymorphism ( Figure 1) was seen in carriers of the E2 allele and the smallest in those with the E4 allele.	bind
29900	2	7459	5	13	NULL	NULL	NULL	E2 allele	GP		impairs					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_805_s_115	12006394	26 The E2 allele is also known to demonstrate impaired TRL binding by the LDL receptor 27 and more recently, has been shown to be associated with impaired lipoprotein lipase - mediated lipolysis of TRLs. 28 The greatest increase in LDL cholesterol associated with the L162V polymorphism ( Figure 1) was seen in carriers of the E2 allele and the smallest in those with the E4 allele.	bind
29903	3	7459	5	13	NULL	NULL	NULL	lipoprotein lipase	GP		mediate					TRLs	GP	lipolysis of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_805_s_115	12006394	26 The E2 allele is also known to demonstrate impaired TRL binding by the LDL receptor 27 and more recently, has been shown to be associated with impaired lipoprotein lipase - mediated lipolysis of TRLs. 28 The greatest increase in LDL cholesterol associated with the L162V polymorphism ( Figure 1) was seen in carriers of the E2 allele and the smallest in those with the E4 allele.	bind
29904	4	7459	5	13	NULL	NULL	NULL	E2 allele	GP		is associtaed with					statement 3	Process	impaired			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_805_s_115	12006394	26 The E2 allele is also known to demonstrate impaired TRL binding by the LDL receptor 27 and more recently, has been shown to be associated with impaired lipoprotein lipase - mediated lipolysis of TRLs. 28 The greatest increase in LDL cholesterol associated with the L162V polymorphism ( Figure 1) was seen in carriers of the E2 allele and the smallest in those with the E4 allele.	bind
29932	5	7459	5	13	NULL	NULL	NULL	LDL cholesterol	Chemical	increase in	is associtaed with					L162V polymorphism	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_805_s_115	12006394	26 The E2 allele is also known to demonstrate impaired TRL binding by the LDL receptor 27 and more recently, has been shown to be associated with impaired lipoprotein lipase - mediated lipolysis of TRLs. 28 The greatest increase in LDL cholesterol associated with the L162V polymorphism ( Figure 1) was seen in carriers of the E2 allele and the smallest in those with the E4 allele.	bind
29933	6	7459	5	13	NULL	NULL	NULL	statement 5	Process		is seen in					E2 allele	GP	carriers of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_805_s_115	12006394	26 The E2 allele is also known to demonstrate impaired TRL binding by the LDL receptor 27 and more recently, has been shown to be associated with impaired lipoprotein lipase - mediated lipolysis of TRLs. 28 The greatest increase in LDL cholesterol associated with the L162V polymorphism ( Figure 1) was seen in carriers of the E2 allele and the smallest in those with the E4 allele.	bind
29934	7	7459	5	13	NULL	NULL	NULL	statement 5	Process		is seen in					E4 allele	GP	carriers of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_805_s_115	12006394	26 The E2 allele is also known to demonstrate impaired TRL binding by the LDL receptor 27 and more recently, has been shown to be associated with impaired lipoprotein lipase - mediated lipolysis of TRLs. 28 The greatest increase in LDL cholesterol associated with the L162V polymorphism ( Figure 1) was seen in carriers of the E2 allele and the smallest in those with the E4 allele.	bind
30058	1	7459	7	NULL	NULL	0	NULL	LDL receptor	NULL		bind	NULL				TRL	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_805_s_115	12006394	26 The E2 allele is also known to demonstrate impaired TRL binding by the LDL receptor 27 and more recently, has been shown to be associated with impaired lipoprotein lipase - mediated lipolysis of TRLs. 28 The greatest increase in LDL cholesterol associated with the L162V polymorphism ( Figure 1) was seen in carriers of the E2 allele and the smallest in those with the E4 allele.	bind
30059	2	7459	7	NULL	NULL	0	NULL	E2 allele	NULL		impairs	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_805_s_115	12006394	26 The E2 allele is also known to demonstrate impaired TRL binding by the LDL receptor 27 and more recently, has been shown to be associated with impaired lipoprotein lipase - mediated lipolysis of TRLs. 28 The greatest increase in LDL cholesterol associated with the L162V polymorphism ( Figure 1) was seen in carriers of the E2 allele and the smallest in those with the E4 allele.	bind
30060	3	7459	7	NULL	NULL	0	NULL	lipoprotein lipase	NULL		mediates	NULL				TRLs	NULL	lipolysis of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_805_s_115	12006394	26 The E2 allele is also known to demonstrate impaired TRL binding by the LDL receptor 27 and more recently, has been shown to be associated with impaired lipoprotein lipase - mediated lipolysis of TRLs. 28 The greatest increase in LDL cholesterol associated with the L162V polymorphism ( Figure 1) was seen in carriers of the E2 allele and the smallest in those with the E4 allele.	bind
30476	4	7459	7	NULL	NULL	0	NULL	E2 allele	NULL		impairs	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_805_s_115	12006394	26 The E2 allele is also known to demonstrate impaired TRL binding by the LDL receptor 27 and more recently, has been shown to be associated with impaired lipoprotein lipase - mediated lipolysis of TRLs. 28 The greatest increase in LDL cholesterol associated with the L162V polymorphism ( Figure 1) was seen in carriers of the E2 allele and the smallest in those with the E4 allele.	bind
30477	5	7459	7	NULL	NULL	0	NULL	LDL cholesterol 	NULL	increase in	is associated with	NULL				polymorph	NULL		L162V		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_805_s_115	12006394	26 The E2 allele is also known to demonstrate impaired TRL binding by the LDL receptor 27 and more recently, has been shown to be associated with impaired lipoprotein lipase - mediated lipolysis of TRLs. 28 The greatest increase in LDL cholesterol associated with the L162V polymorphism ( Figure 1) was seen in carriers of the E2 allele and the smallest in those with the E4 allele.	bind
30478	6	7459	7	10	NULL	0	NULL	statement 5			is seen in 					E2 allele		carriers of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_805_s_115	12006394	26 The E2 allele is also known to demonstrate impaired TRL binding by the LDL receptor 27 and more recently, has been shown to be associated with impaired lipoprotein lipase - mediated lipolysis of TRLs. 28 The greatest increase in LDL cholesterol associated with the L162V polymorphism ( Figure 1) was seen in carriers of the E2 allele and the smallest in those with the E4 allele.	bind
30479	7	7459	7	10	NULL	0	NULL	statement 5			is seen in 					E4 allele		carriers of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_805_s_115	12006394	26 The E2 allele is also known to demonstrate impaired TRL binding by the LDL receptor 27 and more recently, has been shown to be associated with impaired lipoprotein lipase - mediated lipolysis of TRLs. 28 The greatest increase in LDL cholesterol associated with the L162V polymorphism ( Figure 1) was seen in carriers of the E2 allele and the smallest in those with the E4 allele.	bind
30480	8	7459	7	NULL	NULL	0	NULL	statement 7	NULL	increase in	is less than	NULL				statement 6	NULL	increase in			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_805_s_115	12006394	26 The E2 allele is also known to demonstrate impaired TRL binding by the LDL receptor 27 and more recently, has been shown to be associated with impaired lipoprotein lipase - mediated lipolysis of TRLs. 28 The greatest increase in LDL cholesterol associated with the L162V polymorphism ( Figure 1) was seen in carriers of the E2 allele and the smallest in those with the E4 allele.	bind
30144	1	7460	5	13	NULL	NULL	NULL	MYPT1	GP		bind		strong			PP1c	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulationres_90_5_546_s_181	11909818	26 Thus, in vitro, the binding of MYPT1 and PP1c is relatively strong.	bind
30071	1	7460	7	NULL	NULL	0	NULL	MYPT1	NULL		bind	NULL	strongly			PP1c	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_circulationres_90_5_546_s_181	11909818	26 Thus, in vitro, the binding of MYPT1 and PP1c is relatively strong.	bind
28085	1	7461	5	13	NULL	NULL	NULL	VWF	GP		does not bind					rHPA-2a	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_117	12775575	26 Whereas no binding of VWF to either rHPA-2a or rHPA-2b could be observed in the absence of ristocetin (not shown), both dose dependently interacted with VWF in the presence of 1500 mug/mL ristocetin ( Figure 3A) with a Kd,app of, respectively, 0.69 plus-or-minus 0.06 and 0.67 plus-or-minus 0.03 nmol/L (mean plus-or-minus SE) ( P=0.80), showing no statistical difference in VWF interaction at this ristocetin concentration.	bind
28086	2	7461	5	13	NULL	NULL	NULL	VWF	GP		does not bind					rHPA-2b	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_117	12775575	26 Whereas no binding of VWF to either rHPA-2a or rHPA-2b could be observed in the absence of ristocetin (not shown), both dose dependently interacted with VWF in the presence of 1500 mug/mL ristocetin ( Figure 3A) with a Kd,app of, respectively, 0.69 plus-or-minus 0.06 and 0.67 plus-or-minus 0.03 nmol/L (mean plus-or-minus SE) ( P=0.80), showing no statistical difference in VWF interaction at this ristocetin concentration.	bind
28087	3	7461	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_117	12775575	26 Whereas no binding of VWF to either rHPA-2a or rHPA-2b could be observed in the absence of ristocetin (not shown), both dose dependently interacted with VWF in the presence of 1500 mug/mL ristocetin ( Figure 3A) with a Kd,app of, respectively, 0.69 plus-or-minus 0.06 and 0.67 plus-or-minus 0.03 nmol/L (mean plus-or-minus SE) ( P=0.80), showing no statistical difference in VWF interaction at this ristocetin concentration.	bind
28088	4	7461	5	13	NULL	NULL	NULL	statement 1	Process		in the absence of					ristocetin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_117	12775575	26 Whereas no binding of VWF to either rHPA-2a or rHPA-2b could be observed in the absence of ristocetin (not shown), both dose dependently interacted with VWF in the presence of 1500 mug/mL ristocetin ( Figure 3A) with a Kd,app of, respectively, 0.69 plus-or-minus 0.06 and 0.67 plus-or-minus 0.03 nmol/L (mean plus-or-minus SE) ( P=0.80), showing no statistical difference in VWF interaction at this ristocetin concentration.	bind
28089	5	7461	5	13	NULL	NULL	NULL	statement 2	Process		in the absence of					ristocetin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_117	12775575	26 Whereas no binding of VWF to either rHPA-2a or rHPA-2b could be observed in the absence of ristocetin (not shown), both dose dependently interacted with VWF in the presence of 1500 mug/mL ristocetin ( Figure 3A) with a Kd,app of, respectively, 0.69 plus-or-minus 0.06 and 0.67 plus-or-minus 0.03 nmol/L (mean plus-or-minus SE) ( P=0.80), showing no statistical difference in VWF interaction at this ristocetin concentration.	bind
28090	6	7461	5	13	NULL	NULL	NULL	rHPA-2a	GP		interacts with		dose dependently			VWF	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_117	12775575	26 Whereas no binding of VWF to either rHPA-2a or rHPA-2b could be observed in the absence of ristocetin (not shown), both dose dependently interacted with VWF in the presence of 1500 mug/mL ristocetin ( Figure 3A) with a Kd,app of, respectively, 0.69 plus-or-minus 0.06 and 0.67 plus-or-minus 0.03 nmol/L (mean plus-or-minus SE) ( P=0.80), showing no statistical difference in VWF interaction at this ristocetin concentration.	bind
28091	7	7461	5	13	NULL	NULL	NULL	statement 6	Process		in the presence of					ristocetin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_117	12775575	26 Whereas no binding of VWF to either rHPA-2a or rHPA-2b could be observed in the absence of ristocetin (not shown), both dose dependently interacted with VWF in the presence of 1500 mug/mL ristocetin ( Figure 3A) with a Kd,app of, respectively, 0.69 plus-or-minus 0.06 and 0.67 plus-or-minus 0.03 nmol/L (mean plus-or-minus SE) ( P=0.80), showing no statistical difference in VWF interaction at this ristocetin concentration.	bind
28092	8	7461	5	13	NULL	NULL	NULL	rHPA-2b	GP		interacts with		dose dependently			VWF	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_117	12775575	26 Whereas no binding of VWF to either rHPA-2a or rHPA-2b could be observed in the absence of ristocetin (not shown), both dose dependently interacted with VWF in the presence of 1500 mug/mL ristocetin ( Figure 3A) with a Kd,app of, respectively, 0.69 plus-or-minus 0.06 and 0.67 plus-or-minus 0.03 nmol/L (mean plus-or-minus SE) ( P=0.80), showing no statistical difference in VWF interaction at this ristocetin concentration.	bind
28093	9	7461	5	13	NULL	NULL	NULL	statement 8	Process		in the presence of					ristocetin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_117	12775575	26 Whereas no binding of VWF to either rHPA-2a or rHPA-2b could be observed in the absence of ristocetin (not shown), both dose dependently interacted with VWF in the presence of 1500 mug/mL ristocetin ( Figure 3A) with a Kd,app of, respectively, 0.69 plus-or-minus 0.06 and 0.67 plus-or-minus 0.03 nmol/L (mean plus-or-minus SE) ( P=0.80), showing no statistical difference in VWF interaction at this ristocetin concentration.	bind
30072	1	7461	7	NULL	NULL	0	NULL	VWF	NULL		does not bind	NULL				rHPA-2a	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_117	12775575	26 Whereas no binding of VWF to either rHPA-2a or rHPA-2b could be observed in the absence of ristocetin (not shown), both dose dependently interacted with VWF in the presence of 1500 mug/mL ristocetin ( Figure 3A) with a Kd,app of, respectively, 0.69 plus-or-minus 0.06 and 0.67 plus-or-minus 0.03 nmol/L (mean plus-or-minus SE) ( P=0.80), showing no statistical difference in VWF interaction at this ristocetin concentration.	bind
30073	2	7461	7	NULL	NULL	0	NULL	VWF	NULL		does not bind	NULL				rHPA-2b	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_117	12775575	26 Whereas no binding of VWF to either rHPA-2a or rHPA-2b could be observed in the absence of ristocetin (not shown), both dose dependently interacted with VWF in the presence of 1500 mug/mL ristocetin ( Figure 3A) with a Kd,app of, respectively, 0.69 plus-or-minus 0.06 and 0.67 plus-or-minus 0.03 nmol/L (mean plus-or-minus SE) ( P=0.80), showing no statistical difference in VWF interaction at this ristocetin concentration.	bind
30074	3	7461	7	NULL	NULL	0	NULL	statement 1	NULL		in absence of	NULL				ristocetin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_117	12775575	26 Whereas no binding of VWF to either rHPA-2a or rHPA-2b could be observed in the absence of ristocetin (not shown), both dose dependently interacted with VWF in the presence of 1500 mug/mL ristocetin ( Figure 3A) with a Kd,app of, respectively, 0.69 plus-or-minus 0.06 and 0.67 plus-or-minus 0.03 nmol/L (mean plus-or-minus SE) ( P=0.80), showing no statistical difference in VWF interaction at this ristocetin concentration.	bind
30075	4	7461	7	NULL	NULL	0	NULL	statement 2	NULL		in absence of	NULL				ristocetin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_117	12775575	26 Whereas no binding of VWF to either rHPA-2a or rHPA-2b could be observed in the absence of ristocetin (not shown), both dose dependently interacted with VWF in the presence of 1500 mug/mL ristocetin ( Figure 3A) with a Kd,app of, respectively, 0.69 plus-or-minus 0.06 and 0.67 plus-or-minus 0.03 nmol/L (mean plus-or-minus SE) ( P=0.80), showing no statistical difference in VWF interaction at this ristocetin concentration.	bind
30076	5	7461	7	NULL	NULL	0	NULL	VWF	NULL		interacts with	NULL	dose-dependently			rHPA-2a	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_117	12775575	26 Whereas no binding of VWF to either rHPA-2a or rHPA-2b could be observed in the absence of ristocetin (not shown), both dose dependently interacted with VWF in the presence of 1500 mug/mL ristocetin ( Figure 3A) with a Kd,app of, respectively, 0.69 plus-or-minus 0.06 and 0.67 plus-or-minus 0.03 nmol/L (mean plus-or-minus SE) ( P=0.80), showing no statistical difference in VWF interaction at this ristocetin concentration.	bind
30077	6	7461	7	NULL	NULL	0	NULL	VWF	NULL		interacts with	NULL	dose-dependently			rHPA-2b 	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_117	12775575	26 Whereas no binding of VWF to either rHPA-2a or rHPA-2b could be observed in the absence of ristocetin (not shown), both dose dependently interacted with VWF in the presence of 1500 mug/mL ristocetin ( Figure 3A) with a Kd,app of, respectively, 0.69 plus-or-minus 0.06 and 0.67 plus-or-minus 0.03 nmol/L (mean plus-or-minus SE) ( P=0.80), showing no statistical difference in VWF interaction at this ristocetin concentration.	bind
30078	7	7461	7	NULL	NULL	0	NULL	statement 5	NULL		in presence of	NULL				ristocetin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_117	12775575	26 Whereas no binding of VWF to either rHPA-2a or rHPA-2b could be observed in the absence of ristocetin (not shown), both dose dependently interacted with VWF in the presence of 1500 mug/mL ristocetin ( Figure 3A) with a Kd,app of, respectively, 0.69 plus-or-minus 0.06 and 0.67 plus-or-minus 0.03 nmol/L (mean plus-or-minus SE) ( P=0.80), showing no statistical difference in VWF interaction at this ristocetin concentration.	bind
30079	8	7461	7	NULL	NULL	0	NULL	statement 6	NULL		in presence of	NULL				ristocetin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_117	12775575	26 Whereas no binding of VWF to either rHPA-2a or rHPA-2b could be observed in the absence of ristocetin (not shown), both dose dependently interacted with VWF in the presence of 1500 mug/mL ristocetin ( Figure 3A) with a Kd,app of, respectively, 0.69 plus-or-minus 0.06 and 0.67 plus-or-minus 0.03 nmol/L (mean plus-or-minus SE) ( P=0.80), showing no statistical difference in VWF interaction at this ristocetin concentration.	bind
54520	9	7461	7	10	NULL	0	NULL	statement 1			is an alternative to					statement 2					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_117	12775575	26 Whereas no binding of VWF to either rHPA-2a or rHPA-2b could be observed in the absence of ristocetin (not shown), both dose dependently interacted with VWF in the presence of 1500 mug/mL ristocetin ( Figure 3A) with a Kd,app of, respectively, 0.69 plus-or-minus 0.06 and 0.67 plus-or-minus 0.03 nmol/L (mean plus-or-minus SE) ( P=0.80), showing no statistical difference in VWF interaction at this ristocetin concentration.	bind
28084	1	7462	5	13	NULL	NULL	NULL	p62	GP		bind					ubiquitin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1701_s_189	10362795	26, 27  This was unexpected in view of the ubiquitin-binding capacity of normal p62.	bind
30080	1	7462	7	NULL	NULL	0	NULL	ubiquitin	NULL		bind	NULL				p62	NULL	normal			NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_6_1701_s_189	10362795	26, 27  This was unexpected in view of the ubiquitin-binding capacity of normal p62.	bind
28083	1	7463	5	13	NULL	NULL	NULL	virus	Organism		bind		effectively			PC coating	Chemical	positively charged			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_754_s_191	15681295	26,27  We confirmed effective in vitro virus binding to the positively charged PC coating.	bind
30081	1	7463	7	NULL	NULL	0	NULL	 virus	NULL		binds	NULL	effectively			PC coating	NULL	positively charged			NULL	in vitro	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_754_s_191	15681295	26,27  We confirmed effective in vitro virus binding to the positively charged PC coating.	bind
28094	1	7464	5	13	NULL	NULL	NULL	CREB	GP		bind					NOR-1	GP	close to transcription initiation point of		CRE sites	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_697_s_170	14962944	26,37  By EMSA, we show that CREB binds to the CRE sites close to the transcription initiation point of NOR-1.	bind
30082	1	7464	7	10	NULL	0	NULL	CREB	NULL		bind	NULL				NOR-1	NULL	close to the transcription initiation point		CRE site	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_697_s_170	14962944	26,37  By EMSA, we show that CREB binds to the CRE sites close to the transcription initiation point of NOR-1.	bind
28095	1	7466	5	13	NULL	NULL	NULL	26iC	GP		is a type of					murine monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_187	9784544	26iC is a murine monoclonal antibody which also binds CD14 but does not block CD14-mediated activation by LPS.	bind
28096	2	7466	5	13	NULL	NULL	NULL	26iC	GP		bind					CD14	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_187	9784544	26iC is a murine monoclonal antibody which also binds CD14 but does not block CD14-mediated activation by LPS.	bind
28097	3	7466	5	13	NULL	NULL	NULL	LPS	Chemical		mediate					CD14	GP	activation			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_187	9784544	26iC is a murine monoclonal antibody which also binds CD14 but does not block CD14-mediated activation by LPS.	bind
28098	4	7466	5	13	NULL	NULL	NULL	26iC	GP		does not block					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_187	9784544	26iC is a murine monoclonal antibody which also binds CD14 but does not block CD14-mediated activation by LPS.	bind
30085	1	7466	7	10	NULL	0	NULL	26iC	NULL	murine	binds	NULL				CD14	NULL				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_187	9784544	26iC is a murine monoclonal antibody which also binds CD14 but does not block CD14-mediated activation by LPS.	bind
30086	2	7466	7	NULL	NULL	0	NULL	LPS 	NULL		mediates	NULL				CD14	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_187	9784544	26iC is a murine monoclonal antibody which also binds CD14 but does not block CD14-mediated activation by LPS.	bind
30087	3	7466	7	10	NULL	0	NULL	26iC		murine	does not block					statement 2					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_187	9784544	26iC is a murine monoclonal antibody which also binds CD14 but does not block CD14-mediated activation by LPS.	bind
46615	4	7466	7	10	NULL	0	NULL	26iC	NULL		is a type of	NULL				monoclonal antibody	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_187	9784544	26iC is a murine monoclonal antibody which also binds CD14 but does not block CD14-mediated activation by LPS.	bind
28102	1	7468	5	13	NULL	NULL	NULL	Ibbeta 	GP	mutation of	results in				GATA binding site of promoter	Bernard-Soulier syndrome	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_1_284_s_191	11125114	27       Ludlow,L.B., Schick,B.P., Budarf,M.L., Driscoll,D.A., Zackai,E.H., Cohen,A. and Konkle,B.A. (1996) Identification of a mutation in a GATA binding site of the platelet glycoprotein Ibbeta promoter resulting in the Bernard-Soulier syndrome.	bind
28103	2	7468	5	13	NULL	NULL	NULL	Ibbeta 	GP		is a type of					platelet glycoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_1_284_s_191	11125114	27       Ludlow,L.B., Schick,B.P., Budarf,M.L., Driscoll,D.A., Zackai,E.H., Cohen,A. and Konkle,B.A. (1996) Identification of a mutation in a GATA binding site of the platelet glycoprotein Ibbeta promoter resulting in the Bernard-Soulier syndrome.	bind
30088	1	7468	7	10	NULL	0	NULL	Ibbeta 	NULL	mutation of 	results in	NULL			GATA binding site of promoter	Bernard-Soulier syndrome	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_1_284_s_191	11125114	27       Ludlow,L.B., Schick,B.P., Budarf,M.L., Driscoll,D.A., Zackai,E.H., Cohen,A. and Konkle,B.A. (1996) Identification of a mutation in a GATA binding site of the platelet glycoprotein Ibbeta promoter resulting in the Bernard-Soulier syndrome.	bind
46616	2	7468	7	10	NULL	0	NULL	Ibbeta	NULL		is a type of	NULL				platelet glycoprotein	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_1_284_s_191	11125114	27       Ludlow,L.B., Schick,B.P., Budarf,M.L., Driscoll,D.A., Zackai,E.H., Cohen,A. and Konkle,B.A. (1996) Identification of a mutation in a GATA binding site of the platelet glycoprotein Ibbeta promoter resulting in the Bernard-Soulier syndrome.	bind
28104	1	7470	5	13	NULL	NULL	NULL	c-Myc	GP		bind		differentially			DNA	NucleicAcid	nucleosomal			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3520_s_350	11522821	27       Wechsler,D.S., Papoulas,O., Dang,C.V. and Kingston,R.E. (1994) Differential binding of c-Myc and Max to nucleosomal DNA.	bind
28105	2	7470	5	13	NULL	NULL	NULL	Max	GP		bind		differentially			DNA	NucleicAcid	nucleosomal			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3520_s_350	11522821	27       Wechsler,D.S., Papoulas,O., Dang,C.V. and Kingston,R.E. (1994) Differential binding of c-Myc and Max to nucleosomal DNA.	bind
30089	1	7470	7	10	NULL	0	NULL	c-Myc	NULL		binds to	NULL	differentially			DNA	NULL	nucleosomal			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3520_s_350	11522821	27       Wechsler,D.S., Papoulas,O., Dang,C.V. and Kingston,R.E. (1994) Differential binding of c-Myc and Max to nucleosomal DNA.	bind
30090	2	7470	7	10	NULL	0	NULL	Max	NULL		binds to	NULL	differentially			DNA	NULL	nucleosomal			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3520_s_350	11522821	27       Wechsler,D.S., Papoulas,O., Dang,C.V. and Kingston,R.E. (1994) Differential binding of c-Myc and Max to nucleosomal DNA.	bind
28099	1	7471	5	13	NULL	NULL	NULL	3H-PGI2	Chemical		bind					PGI2 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2066_s_158	9351373	27  Also the binding of 3H-PGI2 to the PGI2 receptor could be displaced by unlabeled PGE1.	bind
28100	2	7471	5	13	NULL	NULL	NULL	PGE1	Chemical	unlabeled	bind					PGI2 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2066_s_158	9351373	27  Also the binding of 3H-PGI2 to the PGI2 receptor could be displaced by unlabeled PGE1.	bind
28101	3	7471	5	13	NULL	NULL	NULL	statement 2	Process		displaces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2066_s_158	9351373	27  Also the binding of 3H-PGI2 to the PGI2 receptor could be displaced by unlabeled PGE1.	bind
30092	1	7471	7	NULL	NULL	0	NULL	3H-PGI2	NULL		binds to	NULL				PGI2 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2066_s_158	9351373	27  Also the binding of 3H-PGI2 to the PGI2 receptor could be displaced by unlabeled PGE1.	bind
30093	2	7471	7	NULL	NULL	0	NULL	PGE1	NULL	unlabeled	binds to	NULL				PGI2 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2066_s_158	9351373	27  Also the binding of 3H-PGI2 to the PGI2 receptor could be displaced by unlabeled PGE1.	bind
30094	3	7471	7	NULL	NULL	0	NULL	statement 2	NULL		displace	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2066_s_158	9351373	27  Also the binding of 3H-PGI2 to the PGI2 receptor could be displaced by unlabeled PGE1.	bind
28108	1	7472	5	13	NULL	NULL	NULL	hsp90	GP	binding of	is associated with					eNOS	GP	stimulation of;; activity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2045_s_170	10978247	27  Binding of hsp90 is associated with stimulation of eNOS activity, 27  and enhanced binding of hsp90 to eNOS also appears to be involved in the estrogen receptor - mediated activation of eNOS.	bind
28109	2	7472	5	13	NULL	NULL	NULL	hsp90	GP		bind					eNOS	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2045_s_170	10978247	27  Binding of hsp90 is associated with stimulation of eNOS activity, 27  and enhanced binding of hsp90 to eNOS also appears to be involved in the estrogen receptor - mediated activation of eNOS.	bind
28110	3	7472	5	13	NULL	NULL	NULL	estrogen receptor	GP		mediate					eNOS	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2045_s_170	10978247	27  Binding of hsp90 is associated with stimulation of eNOS activity, 27  and enhanced binding of hsp90 to eNOS also appears to be involved in the estrogen receptor - mediated activation of eNOS.	bind
28111	4	7472	5	13	NULL	NULL	NULL	statement 2	Process		is involved in					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2045_s_170	10978247	27  Binding of hsp90 is associated with stimulation of eNOS activity, 27  and enhanced binding of hsp90 to eNOS also appears to be involved in the estrogen receptor - mediated activation of eNOS.	bind
30095	1	7472	7	10	NULL	0	NULL	hsp90		binding of	is associated with					eNOS		stimulation of;; activity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2045_s_170	10978247	27  Binding of hsp90 is associated with stimulation of eNOS activity, 27  and enhanced binding of hsp90 to eNOS also appears to be involved in the estrogen receptor - mediated activation of eNOS.	bind
30096	2	7472	7	NULL	NULL	0	NULL	hsp90	NULL		binding to	NULL	enhanced			eNOS	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2045_s_170	10978247	27  Binding of hsp90 is associated with stimulation of eNOS activity, 27  and enhanced binding of hsp90 to eNOS also appears to be involved in the estrogen receptor - mediated activation of eNOS.	bind
30097	3	7472	7	NULL	NULL	0	NULL	 estrogen receptor	NULL		mediates	NULL				eNOS	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2045_s_170	10978247	27  Binding of hsp90 is associated with stimulation of eNOS activity, 27  and enhanced binding of hsp90 to eNOS also appears to be involved in the estrogen receptor - mediated activation of eNOS.	bind
30098	4	7472	7	NULL	NULL	0	NULL	statement 2	NULL		is involved in	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2045_s_170	10978247	27  Binding of hsp90 is associated with stimulation of eNOS activity, 27  and enhanced binding of hsp90 to eNOS also appears to be involved in the estrogen receptor - mediated activation of eNOS.	bind
28112	1	7473	5	13	NULL	NULL	NULL	profilin	GP		bind					VASP	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_127	10978248	27  Binding of profilin to VASP could provide a means for the local accumulation of polymerization-competent G-actin, which, in the presence of nucleating activity, can lead to filament assembly and membrane ruffling.	bind
28113	2	7473	5	13	NULL	NULL	NULL	statement 1	Process		accumulates					G-actin	GP	polymerization-competent			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_127	10978248	27  Binding of profilin to VASP could provide a means for the local accumulation of polymerization-competent G-actin, which, in the presence of nucleating activity, can lead to filament assembly and membrane ruffling.	bind
28114	3	7473	5	13	NULL	NULL	NULL	G-actin	GP		leads to					filament 	CellComponent	assembly of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_127	10978248	27  Binding of profilin to VASP could provide a means for the local accumulation of polymerization-competent G-actin, which, in the presence of nucleating activity, can lead to filament assembly and membrane ruffling.	bind
28115	4	7473	5	13	NULL	NULL	NULL	statement 3	Process		in the presence of					nucleating activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_127	10978248	27  Binding of profilin to VASP could provide a means for the local accumulation of polymerization-competent G-actin, which, in the presence of nucleating activity, can lead to filament assembly and membrane ruffling.	bind
28116	5	7473	5	13	NULL	NULL	NULL	statement 2	Process		leads to					membrane ruffling	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_127	10978248	27  Binding of profilin to VASP could provide a means for the local accumulation of polymerization-competent G-actin, which, in the presence of nucleating activity, can lead to filament assembly and membrane ruffling.	bind
28117	6	7473	5	13	NULL	NULL	NULL	statement 5	Process		in the presence of					nucleating activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_127	10978248	27  Binding of profilin to VASP could provide a means for the local accumulation of polymerization-competent G-actin, which, in the presence of nucleating activity, can lead to filament assembly and membrane ruffling.	bind
30099	1	7473	7	NULL	NULL	0	NULL	 profilin	NULL		bind	NULL				VASP	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_127	10978248	27  Binding of profilin to VASP could provide a means for the local accumulation of polymerization-competent G-actin, which, in the presence of nucleating activity, can lead to filament assembly and membrane ruffling.	bind
30100	2	7473	7	NULL	NULL	0	NULL	statement 1	NULL		accumulates	NULL	locally			G-actin	NULL	polymerization-competent			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_127	10978248	27  Binding of profilin to VASP could provide a means for the local accumulation of polymerization-competent G-actin, which, in the presence of nucleating activity, can lead to filament assembly and membrane ruffling.	bind
30101	3	7473	7	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				filament 	NULL	assembly of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_127	10978248	27  Binding of profilin to VASP could provide a means for the local accumulation of polymerization-competent G-actin, which, in the presence of nucleating activity, can lead to filament assembly and membrane ruffling.	bind
30102	4	7473	7	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				membrane ruffling	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_127	10978248	27  Binding of profilin to VASP could provide a means for the local accumulation of polymerization-competent G-actin, which, in the presence of nucleating activity, can lead to filament assembly and membrane ruffling.	bind
30103	5	7473	7	NULL	NULL	0	NULL	statement 3	NULL		in presence of	NULL				nucleating activity	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_127	10978248	27  Binding of profilin to VASP could provide a means for the local accumulation of polymerization-competent G-actin, which, in the presence of nucleating activity, can lead to filament assembly and membrane ruffling.	bind
30104	6	7473	7	NULL	NULL	0	NULL	statement 4	NULL		in presence of	NULL				nucleating activity	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_127	10978248	27  Binding of profilin to VASP could provide a means for the local accumulation of polymerization-competent G-actin, which, in the presence of nucleating activity, can lead to filament assembly and membrane ruffling.	bind
28118	1	7474	5	13	NULL	NULL	NULL	NETA	Chemical		interacts with					progesterone receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_902_s_136	9633929	27  In addition, the progestogenic effect of NETA is mediated via interaction of NETA with the progesterone receptor, 27  whereas other studies in the rabbit uterus have shown that MPA does not bind to the estrogen receptor.	bind
28119	2	7474	5	13	NULL	NULL	NULL	NETA	Chemical	progestogenic effect of	is mediated via					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_902_s_136	9633929	27  In addition, the progestogenic effect of NETA is mediated via interaction of NETA with the progesterone receptor, 27  whereas other studies in the rabbit uterus have shown that MPA does not bind to the estrogen receptor.	bind
28120	3	7474	5	13	NULL	NULL	NULL	MPA	Chemical		does not bind					estrogen receptor	GP				NULL	in rabbit uterus	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_902_s_136	9633929	27  In addition, the progestogenic effect of NETA is mediated via interaction of NETA with the progesterone receptor, 27  whereas other studies in the rabbit uterus have shown that MPA does not bind to the estrogen receptor.	bind
30105	1	7474	7	NULL	NULL	0	NULL	NETA	NULL		interacts with	NULL				progesterone receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_902_s_136	9633929	27  In addition, the progestogenic effect of NETA is mediated via interaction of NETA with the progesterone receptor, 27  whereas other studies in the rabbit uterus have shown that MPA does not bind to the estrogen receptor.	bind
30106	2	7474	7	NULL	NULL	0	NULL	statement 1	NULL		mediates	NULL				NETA	NULL	progestogenic effect of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_902_s_136	9633929	27  In addition, the progestogenic effect of NETA is mediated via interaction of NETA with the progesterone receptor, 27  whereas other studies in the rabbit uterus have shown that MPA does not bind to the estrogen receptor.	bind
30107	3	7474	7	NULL	NULL	0	NULL	MPA	NULL		does not bind	NULL				estrogen receptor 	NULL				NULL	rabbit uterus	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_902_s_136	9633929	27  In addition, the progestogenic effect of NETA is mediated via interaction of NETA with the progesterone receptor, 27  whereas other studies in the rabbit uterus have shown that MPA does not bind to the estrogen receptor.	bind
28121	1	7475	5	13	NULL	NULL	NULL	E2F-4	GP		bind					pRb2/p130	GP				NULL	G0/G1 phases in primary mouse fibroblasts	NULL	NULL	NULL	NULL	gw60_circulationres_85_11_1032_s_171	10571534	27  The main form of E2F detected in the G0/G1 phases in primary mouse fibroblasts is E2F-4 bound to pRb2/p130, which is then replaced by p107/E2F-4 complexes in late G1.	bind
28122	2	7475	5	13	NULL	NULL	NULL	E2F-4	GP		bind					p107/E2F-4 complexes	GP				NULL	late G1	NULL	NULL	NULL	NULL	gw60_circulationres_85_11_1032_s_171	10571534	27  The main form of E2F detected in the G0/G1 phases in primary mouse fibroblasts is E2F-4 bound to pRb2/p130, which is then replaced by p107/E2F-4 complexes in late G1.	bind
28123	3	7475	5	13	NULL	NULL	NULL	statement 2	Process		replaces					statement 1	Process				NULL	late G1	NULL	NULL	NULL	NULL	gw60_circulationres_85_11_1032_s_171	10571534	27  The main form of E2F detected in the G0/G1 phases in primary mouse fibroblasts is E2F-4 bound to pRb2/p130, which is then replaced by p107/E2F-4 complexes in late G1.	bind
30108	1	7475	7	NULL	NULL	0	NULL	E2F-4	NULL		bind	NULL				 pRb2/p130	NULL				NULL	G0/G1 phases in primary mouse fibroblasts	0	NULL	NULL	NULL	gw60_circulationres_85_11_1032_s_171	10571534	27  The main form of E2F detected in the G0/G1 phases in primary mouse fibroblasts is E2F-4 bound to pRb2/p130, which is then replaced by p107/E2F-4 complexes in late G1.	bind
30109	2	7475	7	NULL	NULL	0	NULL	E2F-4	NULL		bind	NULL				p107/E2F-4 complexes	NULL				NULL	late G1	NULL	NULL	NULL	NULL	gw60_circulationres_85_11_1032_s_171	10571534	27  The main form of E2F detected in the G0/G1 phases in primary mouse fibroblasts is E2F-4 bound to pRb2/p130, which is then replaced by p107/E2F-4 complexes in late G1.	bind
30110	3	7475	7	NULL	NULL	0	NULL	statement 2	NULL		replace	NULL				statement 1	NULL				NULL	late G1	0	NULL	NULL	NULL	gw60_circulationres_85_11_1032_s_171	10571534	27  The main form of E2F detected in the G0/G1 phases in primary mouse fibroblasts is E2F-4 bound to pRb2/p130, which is then replaced by p107/E2F-4 complexes in late G1.	bind
28126	1	7476	5	13	NULL	NULL	NULL			motif	is present within			WS YGVTI W		erbB1/EGFR	GP		kinase domain		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_35	10381889	27  The motif  WS YGVTI W within the kinase domain of erbB1/EGFR has been shown to be responsible for binding of this receptor tyrosine kinase to caveolins.	bind
28127	2	7476	5	13	NULL	NULL	NULL	erbB1/EGFR	GP		bind					caveolins	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_35	10381889	27  The motif  WS YGVTI W within the kinase domain of erbB1/EGFR has been shown to be responsible for binding of this receptor tyrosine kinase to caveolins.	bind
28128	3	7476	5	13	NULL	NULL	NULL	statement 1	Process		is responsible for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_35	10381889	27  The motif  WS YGVTI W within the kinase domain of erbB1/EGFR has been shown to be responsible for binding of this receptor tyrosine kinase to caveolins.	bind
28129	4	7476	5	13	NULL	NULL	NULL	erbB1/EGFR	GP		is a type of					receptor tyrosine kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_35	10381889	27  The motif  WS YGVTI W within the kinase domain of erbB1/EGFR has been shown to be responsible for binding of this receptor tyrosine kinase to caveolins.	bind
30111	1	7476	7	NULL	NULL	0	NULL		NULL		is present within	NULL		 WS YGVTI W 		erbB1/EGFR	NULL		kinase domain		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_35	10381889	27  The motif  WS YGVTI W within the kinase domain of erbB1/EGFR has been shown to be responsible for binding of this receptor tyrosine kinase to caveolins.	bind
30112	2	7476	7	NULL	NULL	0	NULL	erbB1/EGFR	NULL		bind	NULL				caveolins	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_35	10381889	27  The motif  WS YGVTI W within the kinase domain of erbB1/EGFR has been shown to be responsible for binding of this receptor tyrosine kinase to caveolins.	bind
46618	3	7476	7	NULL	NULL	0	NULL	statement 1	NULL		is responsible for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_35	10381889	27  The motif  WS YGVTI W within the kinase domain of erbB1/EGFR has been shown to be responsible for binding of this receptor tyrosine kinase to caveolins.	bind
46619	4	7476	7	NULL	NULL	0	NULL	 erbB1/EGFR	NULL		is a type of	NULL				receptor tyrosine kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_35	10381889	27  The motif  WS YGVTI W within the kinase domain of erbB1/EGFR has been shown to be responsible for binding of this receptor tyrosine kinase to caveolins.	bind
28130	1	7477	5	13	NULL	NULL	NULL				coordinate			paired cysteine residues		zinc sulfate	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_9_1282_s_227	11238274	27  This region contains paired cysteine residues that coordinate binding of a zinc sulfate, which in turn seems to be critical in maintaining the integrity of tetrahydrobiopterin binding.	bind
28131	2	7477	5	13	NULL	NULL	NULL	statement 1	Process		maintains		critical			tetrahydrobiopterin	Chemical	integrity of;;binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_9_1282_s_227	11238274	27  This region contains paired cysteine residues that coordinate binding of a zinc sulfate, which in turn seems to be critical in maintaining the integrity of tetrahydrobiopterin binding.	bind
30156	1	7477	7	10	NULL	0	NULL				coordinates			paired cysteine residues		zinc sulfate		binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_9_1282_s_227	11238274	27  This region contains paired cysteine residues that coordinate binding of a zinc sulfate, which in turn seems to be critical in maintaining the integrity of tetrahydrobiopterin binding.	bind
30157	2	7477	7	10	NULL	0	NULL	statement 1			maintains					tetrahydrobiopterin		integrity of;;binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_9_1282_s_227	11238274	27  This region contains paired cysteine residues that coordinate binding of a zinc sulfate, which in turn seems to be critical in maintaining the integrity of tetrahydrobiopterin binding.	bind
28132	1	7478	5	13	NULL	NULL	NULL	beta2-glycoprotein I	GP		bind					cardiolipin	Chemical	oxidized			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_108_s_113	11145941	27  We also assessed another potential cross-reactivity, which is caused by beta2-glycoprotein I binding to oxidized cardiolipin 50 ; therefore, some anti-phospholipid antibodies could react with beta2-glycoprotein I rather than oxidized phospholipids.	bind
28133	2	7478	5	13	NULL	NULL	NULL	anti-phospholipid antibodies	GP		reacts with					beta2-glycoprotein I	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_108_s_113	11145941	27  We also assessed another potential cross-reactivity, which is caused by beta2-glycoprotein I binding to oxidized cardiolipin 50 ; therefore, some anti-phospholipid antibodies could react with beta2-glycoprotein I rather than oxidized phospholipids.	bind
28134	3	7478	5	13	NULL	NULL	NULL	anti-phospholipid antibodies	GP		does not react with					phospholipids	Chemical	oxidized			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_108_s_113	11145941	27  We also assessed another potential cross-reactivity, which is caused by beta2-glycoprotein I binding to oxidized cardiolipin 50 ; therefore, some anti-phospholipid antibodies could react with beta2-glycoprotein I rather than oxidized phospholipids.	bind
30158	1	7478	7	NULL	NULL	0	NULL	beta2-glycoprotein I	NULL		bind	NULL				cardiolipin 50	NULL	oxidized			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_108_s_113	11145941	27  We also assessed another potential cross-reactivity, which is caused by beta2-glycoprotein I binding to oxidized cardiolipin 50 ; therefore, some anti-phospholipid antibodies could react with beta2-glycoprotein I rather than oxidized phospholipids.	bind
30159	2	7478	7	NULL	NULL	0	NULL	anti-phospholipid antibodies	NULL		react with	NULL				beta2-glycoprotein I	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_108_s_113	11145941	27  We also assessed another potential cross-reactivity, which is caused by beta2-glycoprotein I binding to oxidized cardiolipin 50 ; therefore, some anti-phospholipid antibodies could react with beta2-glycoprotein I rather than oxidized phospholipids.	bind
30160	3	7478	7	10	NULL	0	NULL	anti-phospholipid antibodies			does not react with					phospholipids		oxidized			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_1_108_s_113	11145941	27  We also assessed another potential cross-reactivity, which is caused by beta2-glycoprotein I binding to oxidized cardiolipin 50 ; therefore, some anti-phospholipid antibodies could react with beta2-glycoprotein I rather than oxidized phospholipids.	bind
28135	1	7479	5	13	NULL	NULL	NULL	Lp(a)	GP	levels of plasma	decline during					sepsis	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1137_s_120	10764684	27 31  In the present study, plasma concentrations of free apo(a), which comprises apo(a) fragments and full-length apo(a) not bound to LDL particles, and urinary apo(a) levels remained unchanged during the study period, indicating that the decline in plasma Lp(a) levels during sepsis and burns was probably not due to accelerated fragmentation of apo(a) in plasma.	bind
28136	2	7479	5	13	NULL	NULL	NULL	Lp(a)	GP	levels of plasma	decline during					burns	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1137_s_120	10764684	27 31  In the present study, plasma concentrations of free apo(a), which comprises apo(a) fragments and full-length apo(a) not bound to LDL particles, and urinary apo(a) levels remained unchanged during the study period, indicating that the decline in plasma Lp(a) levels during sepsis and burns was probably not due to accelerated fragmentation of apo(a) in plasma.	bind
28137	3	7479	5	13	NULL	NULL	NULL	apo(a)	GP	accelerated fragmentation of	does not cause		probably			statement 1	Process				NULL	in plasma	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1137_s_120	10764684	27 31  In the present study, plasma concentrations of free apo(a), which comprises apo(a) fragments and full-length apo(a) not bound to LDL particles, and urinary apo(a) levels remained unchanged during the study period, indicating that the decline in plasma Lp(a) levels during sepsis and burns was probably not due to accelerated fragmentation of apo(a) in plasma.	bind
28138	4	7479	5	13	NULL	NULL	NULL	apo(a)	GP	accelerated fragmentation of	does not cause		probably			statement 2	Process				NULL	in plasma	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1137_s_120	10764684	27 31  In the present study, plasma concentrations of free apo(a), which comprises apo(a) fragments and full-length apo(a) not bound to LDL particles, and urinary apo(a) levels remained unchanged during the study period, indicating that the decline in plasma Lp(a) levels during sepsis and burns was probably not due to accelerated fragmentation of apo(a) in plasma.	bind
30162	1	7479	7	NULL	NULL	0	NULL	apo(a)	NULL		does not bind	NULL				LDL particles	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1137_s_120	10764684	27 31  In the present study, plasma concentrations of free apo(a), which comprises apo(a) fragments and full-length apo(a) not bound to LDL particles, and urinary apo(a) levels remained unchanged during the study period, indicating that the decline in plasma Lp(a) levels during sepsis and burns was probably not due to accelerated fragmentation of apo(a) in plasma.	bind
30165	2	7479	7	10	NULL	0	NULL	apo(a)			undergoes					fragmentation		accelerated			NULL	plasma	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1137_s_120	10764684	27 31  In the present study, plasma concentrations of free apo(a), which comprises apo(a) fragments and full-length apo(a) not bound to LDL particles, and urinary apo(a) levels remained unchanged during the study period, indicating that the decline in plasma Lp(a) levels during sepsis and burns was probably not due to accelerated fragmentation of apo(a) in plasma.	bind
30166	3	7479	7	10	NULL	0	NULL	Lp(a)		plasma levels of	decline during					sepsis					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1137_s_120	10764684	27 31  In the present study, plasma concentrations of free apo(a), which comprises apo(a) fragments and full-length apo(a) not bound to LDL particles, and urinary apo(a) levels remained unchanged during the study period, indicating that the decline in plasma Lp(a) levels during sepsis and burns was probably not due to accelerated fragmentation of apo(a) in plasma.	bind
30167	4	7479	7	10	NULL	0	NULL	Lp(a)		plasma levels of	decline during					burns					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1137_s_120	10764684	27 31  In the present study, plasma concentrations of free apo(a), which comprises apo(a) fragments and full-length apo(a) not bound to LDL particles, and urinary apo(a) levels remained unchanged during the study period, indicating that the decline in plasma Lp(a) levels during sepsis and burns was probably not due to accelerated fragmentation of apo(a) in plasma.	bind
30168	5	7479	7	10	NULL	0	NULL	statement 3			is not due to		probably			statement 2					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1137_s_120	10764684	27 31  In the present study, plasma concentrations of free apo(a), which comprises apo(a) fragments and full-length apo(a) not bound to LDL particles, and urinary apo(a) levels remained unchanged during the study period, indicating that the decline in plasma Lp(a) levels during sepsis and burns was probably not due to accelerated fragmentation of apo(a) in plasma.	bind
30169	6	7479	7	10	NULL	0	NULL	statement 4			is not due to		probably			statement 2					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_4_1137_s_120	10764684	27 31  In the present study, plasma concentrations of free apo(a), which comprises apo(a) fragments and full-length apo(a) not bound to LDL particles, and urinary apo(a) levels remained unchanged during the study period, indicating that the decline in plasma Lp(a) levels during sepsis and burns was probably not due to accelerated fragmentation of apo(a) in plasma.	bind
28139	1	7480	5	13	NULL	NULL	NULL	HSP27	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_2_192_s_167	15976317	27 As well as binding to actin, HSP27 also binds to the intermediate filament vimentin.	bind
28140	2	7480	5	13	NULL	NULL	NULL	HSP27	GP		bind					vimentin	GP	intermediate filament			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_2_192_s_167	15976317	27 As well as binding to actin, HSP27 also binds to the intermediate filament vimentin.	bind
30170	1	7480	7	NULL	NULL	0	NULL	HSP27	NULL		binds to	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_2_192_s_167	15976317	27 As well as binding to actin, HSP27 also binds to the intermediate filament vimentin.	bind
30171	2	7480	7	NULL	NULL	0	NULL	HSP27	NULL		binds to	NULL				 vimentin	NULL	intermediate filament			NULL		0	NULL	NULL	NULL	gw70_circulationres_97_2_192_s_167	15976317	27 As well as binding to actin, HSP27 also binds to the intermediate filament vimentin.	bind
28141	1	7483	5	13	NULL	NULL	NULL	SRF	GP		bind									CArG box	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1602_s_213	15242862	27 Further investigation of the molecular basis for enhancement of the binding of SRF to CArG box by Hex will provide the clue for the understanding of the context-dependent and signal-responsive regulation of phenotypic modulation of vascular SMC.	bind
46617	2	7483	5	13	NULL	NULL	NULL	Hex	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1602_s_213	15242862	27 Further investigation of the molecular basis for enhancement of the binding of SRF to CArG box by Hex will provide the clue for the understanding of the context-dependent and signal-responsive regulation of phenotypic modulation of vascular SMC.	bind
30172	1	7483	7	NULL	NULL	0	NULL	 SRF	NULL		binds to	NULL					NULL			CArG box 	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1602_s_213	15242862	27 Further investigation of the molecular basis for enhancement of the binding of SRF to CArG box by Hex will provide the clue for the understanding of the context-dependent and signal-responsive regulation of phenotypic modulation of vascular SMC.	bind
54521	2	7483	7	10	NULL	0	NULL	Hex			enhances					statement 1					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1602_s_213	15242862	27 Further investigation of the molecular basis for enhancement of the binding of SRF to CArG box by Hex will provide the clue for the understanding of the context-dependent and signal-responsive regulation of phenotypic modulation of vascular SMC.	bind
28143	1	7484	5	13	NULL	NULL	NULL	LpL	GP		function within		potential			arterial wall	OrganismPart	mouse			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_179	12089072	27 LpL also could potentially function within the mouse arterial wall to facilitate non - proteoglycan-mediated HDL3-E binding, because LpL may bind to HDL through lipophilic interactions that are independent of apo E. 28	bind
28144	2	7484	5	13	NULL	NULL	NULL	non - proteoglycan	GP		mediates					HDL3-E	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_179	12089072	27 LpL also could potentially function within the mouse arterial wall to facilitate non - proteoglycan-mediated HDL3-E binding, because LpL may bind to HDL through lipophilic interactions that are independent of apo E. 28	bind
28145	3	7484	5	13	NULL	NULL	NULL	LpL	GP		bind		may			HDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_179	12089072	27 LpL also could potentially function within the mouse arterial wall to facilitate non - proteoglycan-mediated HDL3-E binding, because LpL may bind to HDL through lipophilic interactions that are independent of apo E. 28	bind
28146	4	7484	5	13	NULL	NULL	NULL	lipophilic interactions	Process		is independent of					apo E	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_179	12089072	27 LpL also could potentially function within the mouse arterial wall to facilitate non - proteoglycan-mediated HDL3-E binding, because LpL may bind to HDL through lipophilic interactions that are independent of apo E. 28	bind
28147	5	7484	5	13	NULL	NULL	NULL	statement 3	Process		occurs through					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_179	12089072	27 LpL also could potentially function within the mouse arterial wall to facilitate non - proteoglycan-mediated HDL3-E binding, because LpL may bind to HDL through lipophilic interactions that are independent of apo E. 28	bind
30177	1	7484	7	NULL	NULL	0	NULL	 LpL	NULL		bind	NULL	may			HDL	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_179	12089072	27 LpL also could potentially function within the mouse arterial wall to facilitate non - proteoglycan-mediated HDL3-E binding, because LpL may bind to HDL through lipophilic interactions that are independent of apo E. 28	bind
30178	2	7484	7	NULL	NULL	0	NULL	statement 1	NULL		occurs through	NULL				lipophilic interactions	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_179	12089072	27 LpL also could potentially function within the mouse arterial wall to facilitate non - proteoglycan-mediated HDL3-E binding, because LpL may bind to HDL through lipophilic interactions that are independent of apo E. 28	bind
30179	3	7484	7	NULL	NULL	0	NULL	statement 1	NULL		is independent of	NULL				apo E	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_179	12089072	27 LpL also could potentially function within the mouse arterial wall to facilitate non - proteoglycan-mediated HDL3-E binding, because LpL may bind to HDL through lipophilic interactions that are independent of apo E. 28	bind
30180	4	7484	7	NULL	NULL	0	NULL	LpL	NULL		function within	NULL	potentially			arterial wall 	NULL	mouse			NULL		0	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_179	12089072	27 LpL also could potentially function within the mouse arterial wall to facilitate non - proteoglycan-mediated HDL3-E binding, because LpL may bind to HDL through lipophilic interactions that are independent of apo E. 28	bind
30181	5	7484	7	NULL	NULL	0	NULL	non - proteoglycan	NULL		mediates	NULL				HDL3-E	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_179	12089072	27 LpL also could potentially function within the mouse arterial wall to facilitate non - proteoglycan-mediated HDL3-E binding, because LpL may bind to HDL through lipophilic interactions that are independent of apo E. 28	bind
30182	6	7484	7	NULL	NULL	0	NULL	statement 4	NULL		facilitate	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_179	12089072	27 LpL also could potentially function within the mouse arterial wall to facilitate non - proteoglycan-mediated HDL3-E binding, because LpL may bind to HDL through lipophilic interactions that are independent of apo E. 28	bind
30183	7	7484	7	NULL	NULL	0	NULL	statement 6	NULL		is because of 	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_179	12089072	27 LpL also could potentially function within the mouse arterial wall to facilitate non - proteoglycan-mediated HDL3-E binding, because LpL may bind to HDL through lipophilic interactions that are independent of apo E. 28	bind
28148	1	7485	5	13	NULL	NULL	NULL	NFATc1	GP		bind			Rel homology domain		DNA	NucleicAcid			consensus sequence	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1492_s_185	15117818	27 NFATc1 - NFATc4 bind the consensus DNA sequence through a Rel homology domain, and all 4 of these factors are expressed in cardiac myocytes.	bind
46685	2	7485	5	13	NULL	NULL	NULL	NFATc2	GP		bind			Rel homology domain		DNA	NucleicAcid			consensus sequence	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1492_s_185	15117818	27 NFATc1 - NFATc4 bind the consensus DNA sequence through a Rel homology domain, and all 4 of these factors are expressed in cardiac myocytes.	bind
46686	3	7485	5	13	NULL	NULL	NULL	NFATc3	GP		bind			Rel homology domain		DNA	NucleicAcid			consensus sequence	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1492_s_185	15117818	27 NFATc1 - NFATc4 bind the consensus DNA sequence through a Rel homology domain, and all 4 of these factors are expressed in cardiac myocytes.	bind
46687	4	7485	5	13	NULL	NULL	NULL	NFATc4	GP		bind			Rel homology domain		DNA	NucleicAcid			consensus sequence	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1492_s_185	15117818	27 NFATc1 - NFATc4 bind the consensus DNA sequence through a Rel homology domain, and all 4 of these factors are expressed in cardiac myocytes.	bind
46688	5	7485	5	13	NULL	NULL	NULL	NFATc1	GP		is expressed in					cardiac myocytes	Cell				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1492_s_185	15117818	27 NFATc1 - NFATc4 bind the consensus DNA sequence through a Rel homology domain, and all 4 of these factors are expressed in cardiac myocytes.	bind
46689	6	7485	5	13	NULL	NULL	NULL	NFATc2	GP		is expressed in					cardiac myocytes	Cell				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1492_s_185	15117818	27 NFATc1 - NFATc4 bind the consensus DNA sequence through a Rel homology domain, and all 4 of these factors are expressed in cardiac myocytes.	bind
46690	7	7485	5	13	NULL	NULL	NULL	NFATc3	GP		is expressed in					cardiac myocytes	Cell				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1492_s_185	15117818	27 NFATc1 - NFATc4 bind the consensus DNA sequence through a Rel homology domain, and all 4 of these factors are expressed in cardiac myocytes.	bind
46691	8	7485	5	13	NULL	NULL	NULL	NFATc4	GP		is expressed in					cardiac myocytes	Cell				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1492_s_185	15117818	27 NFATc1 - NFATc4 bind the consensus DNA sequence through a Rel homology domain, and all 4 of these factors are expressed in cardiac myocytes.	bind
30184	1	7485	7	NULL	NULL	0	NULL	NFATc1	NULL		bind	NULL		Rel homology domain		DNA	NULL			consensus sequence	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1492_s_185	15117818	27 NFATc1 - NFATc4 bind the consensus DNA sequence through a Rel homology domain, and all 4 of these factors are expressed in cardiac myocytes.	bind
30185	2	7485	7	NULL	NULL	0	NULL	NFATc2	NULL		bind	NULL		Rel homology domain		DNA	NULL			consensus sequence	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1492_s_185	15117818	27 NFATc1 - NFATc4 bind the consensus DNA sequence through a Rel homology domain, and all 4 of these factors are expressed in cardiac myocytes.	bind
30186	3	7485	7	NULL	NULL	0	NULL	NFATc3	NULL		bind	NULL		Rel homology domain		DNA	NULL			consensus sequence	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1492_s_185	15117818	27 NFATc1 - NFATc4 bind the consensus DNA sequence through a Rel homology domain, and all 4 of these factors are expressed in cardiac myocytes.	bind
30187	4	7485	7	NULL	NULL	0	NULL	NFATc4	NULL		bind	NULL		Rel homology domain		DNA	NULL			consensus sequence	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1492_s_185	15117818	27 NFATc1 - NFATc4 bind the consensus DNA sequence through a Rel homology domain, and all 4 of these factors are expressed in cardiac myocytes.	bind
30188	5	7485	7	NULL	NULL	0	NULL	NFATc1	NULL		is expressed in	NULL				cardiac myocytes	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_11_1492_s_185	15117818	27 NFATc1 - NFATc4 bind the consensus DNA sequence through a Rel homology domain, and all 4 of these factors are expressed in cardiac myocytes.	bind
30189	6	7485	7	NULL	NULL	0	NULL	NFATc2	NULL		is expressed in	NULL				cardiac myocytes	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_11_1492_s_185	15117818	27 NFATc1 - NFATc4 bind the consensus DNA sequence through a Rel homology domain, and all 4 of these factors are expressed in cardiac myocytes.	bind
30190	7	7485	7	NULL	NULL	0	NULL	NFATc3	NULL		is expressed in	NULL				cardiac myocytes	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_11_1492_s_185	15117818	27 NFATc1 - NFATc4 bind the consensus DNA sequence through a Rel homology domain, and all 4 of these factors are expressed in cardiac myocytes.	bind
30191	8	7485	7	NULL	NULL	0	NULL	NFATc4	NULL		is expressed in	NULL				cardiac myocytes	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_11_1492_s_185	15117818	27 NFATc1 - NFATc4 bind the consensus DNA sequence through a Rel homology domain, and all 4 of these factors are expressed in cardiac myocytes.	bind
28149	1	7486	5	13	NULL	NULL	NULL	PKCzeta atypical isoform	GP		prevents					IkappaBalpha	GP	degradation of			NULL	in TNF-stimulated endothelial cells	NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1130_s_194	12714566	27 Rahman et al, 27 using a dominant-negative approach, were able to demonstrate in TNF-stimulated endothelial cells that the atypical isoform PKCzeta was able to prevent IkappaBalpha degradation and NF-kappaB binding to the ICAM-1 promoter.	bind
28150	2	7486	5	13	NULL	NULL	NULL	NF-kappaB	GP		bind					ICAM-1	GP			promoter	NULL	TNF-stimulated endothelial cells	NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1130_s_194	12714566	27 Rahman et al, 27 using a dominant-negative approach, were able to demonstrate in TNF-stimulated endothelial cells that the atypical isoform PKCzeta was able to prevent IkappaBalpha degradation and NF-kappaB binding to the ICAM-1 promoter.	bind
28151	3	7486	5	13	NULL	NULL	NULL	PKCzeta atypical isoform	GP		prevents					statement 2	Process				NULL	TNF-stimulated endothelial cells	NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1130_s_194	12714566	27 Rahman et al, 27 using a dominant-negative approach, were able to demonstrate in TNF-stimulated endothelial cells that the atypical isoform PKCzeta was able to prevent IkappaBalpha degradation and NF-kappaB binding to the ICAM-1 promoter.	bind
30192	1	7486	7	10	NULL	0	NULL	NF-kappaB			binds to					ICAM-1				promoter	NULL	TNF-stimulated endothelial cells	NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1130_s_194	12714566	27 Rahman et al, 27 using a dominant-negative approach, were able to demonstrate in TNF-stimulated endothelial cells that the atypical isoform PKCzeta was able to prevent IkappaBalpha degradation and NF-kappaB binding to the ICAM-1 promoter.	bind
30194	2	7486	7	10	NULL	0	NULL	PKCzeta atypical isoform			prevent					IkappaBalpha 		degradation of			NULL	TNF-stimulated endothelial cells	NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1130_s_194	12714566	27 Rahman et al, 27 using a dominant-negative approach, were able to demonstrate in TNF-stimulated endothelial cells that the atypical isoform PKCzeta was able to prevent IkappaBalpha degradation and NF-kappaB binding to the ICAM-1 promoter.	bind
30195	3	7486	7	10	NULL	0	NULL	PKCzeta atypical isoform			prevents					statement 1					NULL	TNF-stimulated endothelial cells	NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1130_s_194	12714566	27 Rahman et al, 27 using a dominant-negative approach, were able to demonstrate in TNF-stimulated endothelial cells that the atypical isoform PKCzeta was able to prevent IkappaBalpha degradation and NF-kappaB binding to the ICAM-1 promoter.	bind
28152	1	7487	5	13	NULL	NULL	NULL	WT1	GP		represses					PAX2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_181_s_44	9916932	27 Repression of  PAX2 by WT1 has been demonstrated  in vitro by the binding of WT1 to  PAX2 regulatory sequences and by cotransfection assays using CAT reporter constructs under the control of  PAX2 regulatory sequences showing WT1-dependent transcriptional repression.	bind
28153	2	7487	5	13	NULL	NULL	NULL	WT1	GP		bind					PAX2	GP			regulatory sequences	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_181_s_44	9916932	27 Repression of  PAX2 by WT1 has been demonstrated  in vitro by the binding of WT1 to  PAX2 regulatory sequences and by cotransfection assays using CAT reporter constructs under the control of  PAX2 regulatory sequences showing WT1-dependent transcriptional repression.	bind
28154	3	7487	5	13	NULL	NULL	NULL	statement 2	Process		leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_181_s_44	9916932	27 Repression of  PAX2 by WT1 has been demonstrated  in vitro by the binding of WT1 to  PAX2 regulatory sequences and by cotransfection assays using CAT reporter constructs under the control of  PAX2 regulatory sequences showing WT1-dependent transcriptional repression.	bind
30196	1	7487	7	NULL	NULL	0	NULL	WT1	NULL		bind	NULL				PAX2	NULL			regulatory sequences	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_181_s_44	9916932	27 Repression of  PAX2 by WT1 has been demonstrated  in vitro by the binding of WT1 to  PAX2 regulatory sequences and by cotransfection assays using CAT reporter constructs under the control of  PAX2 regulatory sequences showing WT1-dependent transcriptional repression.	bind
30197	2	7487	7	NULL	NULL	0	NULL	statement 1	NULL		repress	NULL				PAX2	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_amjpathol_154_1_181_s_44	9916932	27 Repression of  PAX2 by WT1 has been demonstrated  in vitro by the binding of WT1 to  PAX2 regulatory sequences and by cotransfection assays using CAT reporter constructs under the control of  PAX2 regulatory sequences showing WT1-dependent transcriptional repression.	bind
30198	3	7487	7	NULL	NULL	0	NULL	transcription	NULL	repression of	depends on	NULL				WT1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_1_181_s_44	9916932	27 Repression of  PAX2 by WT1 has been demonstrated  in vitro by the binding of WT1 to  PAX2 regulatory sequences and by cotransfection assays using CAT reporter constructs under the control of  PAX2 regulatory sequences showing WT1-dependent transcriptional repression.	bind
30199	4	7487	7	NULL	NULL	0	NULL	PAX2	NULL	control of	show	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_1_181_s_44	9916932	27 Repression of  PAX2 by WT1 has been demonstrated  in vitro by the binding of WT1 to  PAX2 regulatory sequences and by cotransfection assays using CAT reporter constructs under the control of  PAX2 regulatory sequences showing WT1-dependent transcriptional repression.	bind
28155	1	7488	5	13	NULL	NULL	NULL	DNA	NucleicAcid	adenovirus	bind					VCAM-1+ cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_2_238_s_98	11156859	27 There was  3-fold more adenovirus DNA bound to VCAM-1+ cells (2.7 plus-or-minus 0.8, n=3) than to parental NIH 3T3 cells (1 plus-or-minus 0, n=3; Figure 5  ).	bind
28156	2	7488	5	13	NULL	NULL	NULL	DNA	NucleicAcid	adenovirus	bind					NIH 3T3 cells	Cell	parental			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_2_238_s_98	11156859	27 There was  3-fold more adenovirus DNA bound to VCAM-1+ cells (2.7 plus-or-minus 0.8, n=3) than to parental NIH 3T3 cells (1 plus-or-minus 0, n=3; Figure 5  ).	bind
28157	3	7488	5	13	NULL	NULL	NULL	statement 1	Process	binding of	is more than					statement 2	Process	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_2_238_s_98	11156859	27 There was  3-fold more adenovirus DNA bound to VCAM-1+ cells (2.7 plus-or-minus 0.8, n=3) than to parental NIH 3T3 cells (1 plus-or-minus 0, n=3; Figure 5  ).	bind
30200	1	7488	7	NULL	NULL	0	NULL	DNA	NULL	adenovirus 	bind	NULL				VCAM-1+ cells	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_2_238_s_98	11156859	27 There was  3-fold more adenovirus DNA bound to VCAM-1+ cells (2.7 plus-or-minus 0.8, n=3) than to parental NIH 3T3 cells (1 plus-or-minus 0, n=3; Figure 5  ).	bind
30201	2	7488	7	NULL	NULL	0	NULL	DNA	NULL	adenovirus 	bind	NULL				NIH 3T3 cells	NULL	parental			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_2_238_s_98	11156859	27 There was  3-fold more adenovirus DNA bound to VCAM-1+ cells (2.7 plus-or-minus 0.8, n=3) than to parental NIH 3T3 cells (1 plus-or-minus 0, n=3; Figure 5  ).	bind
30202	3	7488	7	10	NULL	0	NULL	statement 1	NULL	binding of	is greater than	NULL				statement 2	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_2_238_s_98	11156859	27 There was  3-fold more adenovirus DNA bound to VCAM-1+ cells (2.7 plus-or-minus 0.8, n=3) than to parental NIH 3T3 cells (1 plus-or-minus 0, n=3; Figure 5  ).	bind
28158	1	7489	5	13	NULL	NULL	NULL	apoA-I	GP		bind		directly			ABCA1	GP				NULL	at the cell surface	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_53	12738681	27 These findings have been confirmed independently 30,31  and strongly suggested that apoA-I directly binds ABCA1 at the cell surface without requiring the ability of ABCA1 to mediate lipid efflux.	bind
28159	2	7489	5	13	NULL	NULL	NULL	ABCA1	GP		mediate					lipid efflux	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_53	12738681	27 These findings have been confirmed independently 30,31  and strongly suggested that apoA-I directly binds ABCA1 at the cell surface without requiring the ability of ABCA1 to mediate lipid efflux.	bind
28160	3	7489	5	13	NULL	NULL	NULL	statement 1	Process		does not require					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_53	12738681	27 These findings have been confirmed independently 30,31  and strongly suggested that apoA-I directly binds ABCA1 at the cell surface without requiring the ability of ABCA1 to mediate lipid efflux.	bind
30203	1	7489	7	NULL	NULL	0	NULL	apoA-I 	NULL		binds	NULL	directly			ABCA1	NULL				NULL	cell surface	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_53	12738681	27 These findings have been confirmed independently 30,31  and strongly suggested that apoA-I directly binds ABCA1 at the cell surface without requiring the ability of ABCA1 to mediate lipid efflux.	bind
30204	2	7489	7	NULL	NULL	0	NULL	ABCA1	NULL		mediate	NULL				lipid efflux	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_53	12738681	27 These findings have been confirmed independently 30,31  and strongly suggested that apoA-I directly binds ABCA1 at the cell surface without requiring the ability of ABCA1 to mediate lipid efflux.	bind
30205	3	7489	7	NULL	NULL	0	NULL	statement 1	NULL		does not require	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_53	12738681	27 These findings have been confirmed independently 30,31  and strongly suggested that apoA-I directly binds ABCA1 at the cell surface without requiring the ability of ABCA1 to mediate lipid efflux.	bind
28161	1	7490	5	13	NULL	NULL	NULL	MecI	GP	purified	bind					DNA bla	NucleicAcid			135bp operator containing inter blaZ - blaR1 sequence	NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_108	11266408	27 To investigate by the same technique whether or not there are differences between the sites on the  bla operators that are bound by MecI and BlaI, the purified proteins were bound to the 135 bp DNA  bla operator probe, which contains the inter  blaZ - blaR1 sequence.	bind
28162	2	7490	5	13	NULL	NULL	NULL	BlaI	GP	purified	bind					DNA bla	NucleicAcid			135bp operator containing inter blaZ - blaR1 sequence	NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_108	11266408	27 To investigate by the same technique whether or not there are differences between the sites on the  bla operators that are bound by MecI and BlaI, the purified proteins were bound to the 135 bp DNA  bla operator probe, which contains the inter  blaZ - blaR1 sequence.	bind
30206	1	7490	7	10	NULL	0	NULL	MecI	NULL	purified	bind	NULL				DNA bla	NULL			135bp operator containing inter blaZ - blaR1 sequence	NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_108	11266408	27 To investigate by the same technique whether or not there are differences between the sites on the  bla operators that are bound by MecI and BlaI, the purified proteins were bound to the 135 bp DNA  bla operator probe, which contains the inter  blaZ - blaR1 sequence.	bind
30207	2	7490	7	10	NULL	0	NULL	BlaI	NULL	purified	bind	NULL				DNA bla	NULL			135bp operator containing inter blaZ - blaR1 sequence	NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_108	11266408	27 To investigate by the same technique whether or not there are differences between the sites on the  bla operators that are bound by MecI and BlaI, the purified proteins were bound to the 135 bp DNA  bla operator probe, which contains the inter  blaZ - blaR1 sequence.	bind
28163	1	7491	5	13	NULL	NULL	NULL	TNF-alpha	GP		bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_12	12000736	27, 28 It is well recognized that TNF-alpha binds to ECM proteins, including collagen, fibronectin, and laminin, 31- 33  which constitute the main matrix components of epiretinal membranes.	bind
28164	2	7491	5	13	NULL	NULL	NULL	TNF-alpha	GP		bind					fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_12	12000736	27, 28 It is well recognized that TNF-alpha binds to ECM proteins, including collagen, fibronectin, and laminin, 31- 33  which constitute the main matrix components of epiretinal membranes.	bind
28165	3	7491	5	13	NULL	NULL	NULL	TNF-alpha	GP		bind					laminin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_12	12000736	27, 28 It is well recognized that TNF-alpha binds to ECM proteins, including collagen, fibronectin, and laminin, 31- 33  which constitute the main matrix components of epiretinal membranes.	bind
28166	4	7491	5	13	NULL	NULL	NULL	collagen	GP		is a type of					ECM proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_12	12000736	27, 28 It is well recognized that TNF-alpha binds to ECM proteins, including collagen, fibronectin, and laminin, 31- 33  which constitute the main matrix components of epiretinal membranes.	bind
28167	5	7491	5	13	NULL	NULL	NULL	fibronectin	GP		is a type of					ECM proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_12	12000736	27, 28 It is well recognized that TNF-alpha binds to ECM proteins, including collagen, fibronectin, and laminin, 31- 33  which constitute the main matrix components of epiretinal membranes.	bind
28168	6	7491	5	13	NULL	NULL	NULL	laminin	GP		is a type of					ECM proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_12	12000736	27, 28 It is well recognized that TNF-alpha binds to ECM proteins, including collagen, fibronectin, and laminin, 31- 33  which constitute the main matrix components of epiretinal membranes.	bind
28169	7	7491	5	13	NULL	NULL	NULL	collagen	GP		constitutes					epiretinal membranes	OrganismPart	main matrix components of 			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_12	12000736	27, 28 It is well recognized that TNF-alpha binds to ECM proteins, including collagen, fibronectin, and laminin, 31- 33  which constitute the main matrix components of epiretinal membranes.	bind
28170	8	7491	5	13	NULL	NULL	NULL	fibronectin	GP		constitutes					epiretinal membranes	OrganismPart	main matrix components of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_12	12000736	27, 28 It is well recognized that TNF-alpha binds to ECM proteins, including collagen, fibronectin, and laminin, 31- 33  which constitute the main matrix components of epiretinal membranes.	bind
28171	9	7491	5	13	NULL	NULL	NULL	laminin	GP		constitutes					epiretinal membranes	OrganismPart	main matrix components of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_12	12000736	27, 28 It is well recognized that TNF-alpha binds to ECM proteins, including collagen, fibronectin, and laminin, 31- 33  which constitute the main matrix components of epiretinal membranes.	bind
30208	1	7491	7	NULL	NULL	0	NULL	TNF-alpha	NULL		bind	NULL				collagen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_12	12000736	27, 28 It is well recognized that TNF-alpha binds to ECM proteins, including collagen, fibronectin, and laminin, 31- 33  which constitute the main matrix components of epiretinal membranes.	bind
30209	2	7491	7	NULL	NULL	0	NULL	TNF-alpha	NULL		bind	NULL				fibronectin	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_12	12000736	27, 28 It is well recognized that TNF-alpha binds to ECM proteins, including collagen, fibronectin, and laminin, 31- 33  which constitute the main matrix components of epiretinal membranes.	bind
30210	3	7491	7	NULL	NULL	0	NULL	TNF-alpha	NULL		bind	NULL				laminin	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_12	12000736	27, 28 It is well recognized that TNF-alpha binds to ECM proteins, including collagen, fibronectin, and laminin, 31- 33  which constitute the main matrix components of epiretinal membranes.	bind
30211	4	7491	7	NULL	NULL	0	NULL	collagen	NULL		is a type of	NULL				ECM protein	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_12	12000736	27, 28 It is well recognized that TNF-alpha binds to ECM proteins, including collagen, fibronectin, and laminin, 31- 33  which constitute the main matrix components of epiretinal membranes.	bind
30212	5	7491	7	NULL	NULL	0	NULL	fibronectin	NULL		is a type of	NULL				ECM protein	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_12	12000736	27, 28 It is well recognized that TNF-alpha binds to ECM proteins, including collagen, fibronectin, and laminin, 31- 33  which constitute the main matrix components of epiretinal membranes.	bind
30213	6	7491	7	NULL	NULL	0	NULL	laminin	NULL		is a type of	NULL				ECM protein	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_12	12000736	27, 28 It is well recognized that TNF-alpha binds to ECM proteins, including collagen, fibronectin, and laminin, 31- 33  which constitute the main matrix components of epiretinal membranes.	bind
30214	7	7491	7	NULL	NULL	0	NULL	collagen	NULL		constitute 	NULL				epiretinal membrane	NULL	main matrix component of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_12	12000736	27, 28 It is well recognized that TNF-alpha binds to ECM proteins, including collagen, fibronectin, and laminin, 31- 33  which constitute the main matrix components of epiretinal membranes.	bind
30215	8	7491	7	NULL	NULL	0	NULL	fibronectin	NULL		constitute 	NULL				epiretinal membrane	NULL	main matrix component of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_12	12000736	27, 28 It is well recognized that TNF-alpha binds to ECM proteins, including collagen, fibronectin, and laminin, 31- 33  which constitute the main matrix components of epiretinal membranes.	bind
30216	9	7491	7	NULL	NULL	0	NULL	laminin	NULL		constitute 	NULL				epiretinal membrane	NULL	main matrix component of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_12	12000736	27, 28 It is well recognized that TNF-alpha binds to ECM proteins, including collagen, fibronectin, and laminin, 31- 33  which constitute the main matrix components of epiretinal membranes.	bind
30145	1	7492	5	13	NULL	NULL	NULL	plasma gammaA/gamma'' fibrinogen	GP	levels of	is a marker for					arterial thrombosis	MedicalFinding	activity of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30146	2	7492	5	13	NULL	NULL	NULL	fibrinogen gamma'' chain	GP		bind		less			glycoprotein IIb/IIa	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30147	3	7492	5	13	NULL	NULL	NULL	glycoprotein IIb/IIa	GP		is a type of					platelet fibrinogen receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30148	4	7492	5	13	NULL	NULL	NULL	fibrin 	GP	architecture	interacts with					plasma gammaA/gamma'' fibrinogen	GP	levels of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30149	5	7492	5	13	NULL	NULL	NULL	fibrin	GP	architecture	interacts with					factor XIIIa polymorphism	GP		Val34Leu		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30150	6	7492	5	13	NULL	NULL	NULL	statement 4	Process		affects					fibrin network	CellComponent	physical properties of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30151	7	7492	5	13	NULL	NULL	NULL	statement 5	Process		affects					fibrin network	CellComponent	physical properties of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30152	8	7492	5	13	NULL	NULL	NULL	statement 4	Process		affects					platelet	Cell	deposition of			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30153	9	7492	5	13	NULL	NULL	NULL	statement 5	Process		affects					platelet	Cell	deposition of			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30154	10	7492	5	13	NULL	NULL	NULL	statement 4	Process		confers					myocardial infarction	Process	protective effect on occurrence of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30155	11	7492	5	13	NULL	NULL	NULL	myocardial infarction	Process		confers					myocardial infarction	Process	protective effect on occurrence of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30217	1	7492	7	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL	less	gamma chain		fibrinogen receptor	NULL	platelet			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30218	2	7492	7	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL	less	gamma chain		glycoprotein IIb/IIa	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30219	3	7492	7	NULL	NULL	0	NULL	 gammaA/gamma'' fibrinogen levels	NULL	plasma	is a marker of	NULL				arterial thrombotic activity	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30220	4	7492	7	NULL	NULL	0	NULL	fibrin architecture	NULL	interaction between	affect	NULL				fibrin network	NULL	physical property of			NULL	in vitro	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30221	5	7492	7	NULL	NULL	0	NULL	gammaA/gamma'' fibrinogen level	NULL	plasma	affect	NULL				fibrin network	NULL	physical property of			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30222	6	7492	7	NULL	NULL	0	NULL	factor XIIIa	NULL	polymorphic	affect	NULL		Val34Leu		fibrin network	NULL	physical property of			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30223	7	7492	7	NULL	NULL	0	NULL	fibrin architecture	NULL	interaction between	affect	NULL				platelet deposition	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30224	8	7492	7	NULL	NULL	0	NULL	 gammaA/gamma'' fibrinogen level	NULL	plasma	affect	NULL				platelet deposition	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30225	9	7492	7	NULL	NULL	0	NULL	factor XIIIa	NULL	polymorphic	affect	NULL		Val34Leu		platelet deposition	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30226	10	7492	7	NULL	NULL	0	NULL	fibrin architecture	NULL	interaction between	effect	NULL				myocardial infarction	NULL	the occurence of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30227	11	7492	7	NULL	NULL	0	NULL	gammaA/gamma'' fibrinogen level	NULL	plasma	effect	NULL				myocardial infarction	NULL	the occurence of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
30228	12	7492	7	NULL	NULL	0	NULL	factor XIIIa	NULL	polymorphic	effect	NULL		Val34Leu		myocardial infarction	NULL	occurence of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_382_s_154	14656741	27,28  This issue is especially relevant given the fact that plasma gammaA/gamma'' fibrinogen levels are a marker of arterial thrombotic activity, and also given that fibrinogen gamma'' chain displays much less binding to the platelet fibrinogen receptor, glycoprotein IIb/IIa. 17,29  Finally, other issues are the interaction between fibrin architecture and the plasma gammaA/gamma'' fibrinogen level, as well as the factor XIIIa Val34Leu polymorphism, which affects both the physical properties of the fibrin network and platelet deposition in vitro and confers a protective effect on subjects for the occurrence of myocardial infarction.	bind
28172	1	7493	5	13	NULL	NULL	NULL	TIMPs	GP	activated	bind					MMPs	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_4_716_s_83	16469948	27,28  TIMPs bind activated MMPs to form equimolar complexes.	bind
28173	2	7493	5	13	NULL	NULL	NULL	statement 1	Process		forms					equimolar complexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_4_716_s_83	16469948	27,28  TIMPs bind activated MMPs to form equimolar complexes.	bind
30229	1	7493	7	NULL	NULL	0	NULL	TIMPs	NULL		bind	NULL				MMPs	NULL	activated			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_4_716_s_83	16469948	27,28  TIMPs bind activated MMPs to form equimolar complexes.	bind
30230	2	7493	7	NULL	NULL	0	NULL	statement 1	NULL		form	NULL				equimolar complexes	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_4_716_s_83	16469948	27,28  TIMPs bind activated MMPs to form equimolar complexes.	bind
28174	1	7494	5	13	NULL	NULL	NULL	VH4-34 gene	GP		is found in		virtually			cold agglutinin disease	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_253_s_160	11438472	27- 32  Interestingly, the  VH4-34 gene is found in virtually all cases of cold agglutinin disease 33- 35 and the red blood cell I/i antigens bind to the FR1 domain of Ig.	bind
28175	2	7494	5	13	NULL	NULL	NULL	I/i antigens	Chemical	red blood cell	bind					Ig	GP		FR1 domain		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_253_s_160	11438472	27- 32  Interestingly, the  VH4-34 gene is found in virtually all cases of cold agglutinin disease 33- 35 and the red blood cell I/i antigens bind to the FR1 domain of Ig.	bind
30231	1	7494	7	NULL	NULL	0	NULL	VH4-34 gene	NULL		is found in	NULL				cold agglutinin disease	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_1_253_s_160	11438472	27- 32  Interestingly, the  VH4-34 gene is found in virtually all cases of cold agglutinin disease 33- 35 and the red blood cell I/i antigens bind to the FR1 domain of Ig.	bind
30232	2	7494	7	NULL	NULL	0	NULL	 I/i antigens	NULL	 red blood cell 	bind	NULL				Ig	NULL		FR1 domain		NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_1_253_s_160	11438472	27- 32  Interestingly, the  VH4-34 gene is found in virtually all cases of cold agglutinin disease 33- 35 and the red blood cell I/i antigens bind to the FR1 domain of Ig.	bind
28176	1	7495	5	13	NULL	NULL	NULL	Poly (rC) binding protein 2	GP		forms a ternary complex with					poliovirus RNA	NucleicAcid		5''- terminal sequences		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2427_s_399	11376162	28       Parsley,T.B., Towner,J.S., Blyn,L.B., Ehrenfeld,E. and Semler,B.L. (1997) Poly (rC) binding protein 2 forms a ternary complex with the 5''- terminal sequences of poliovirus RNA and the viral 3CD proteinase .	bind
28177	2	7495	5	13	NULL	NULL	NULL	Poly (rC) binding protein 2	GP		forms a ternary complex with					viral 3CD proteinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2427_s_399	11376162	28       Parsley,T.B., Towner,J.S., Blyn,L.B., Ehrenfeld,E. and Semler,B.L. (1997) Poly (rC) binding protein 2 forms a ternary complex with the 5''- terminal sequences of poliovirus RNA and the viral 3CD proteinase .	bind
30233	1	7495	7	NULL	NULL	0	NULL	Poly (rC) binding protein 2	NULL		forms a ternary complex with	NULL				poliovirus RNA	NULL		 5''- terminal sequences of		NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2427_s_399	11376162	28       Parsley,T.B., Towner,J.S., Blyn,L.B., Ehrenfeld,E. and Semler,B.L. (1997) Poly (rC) binding protein 2 forms a ternary complex with the 5''- terminal sequences of poliovirus RNA and the viral 3CD proteinase .	bind
30234	2	7495	7	NULL	NULL	0	NULL	Poly (rC) binding protein 2	NULL		forms a ternary complex with	NULL				viral 3CD proteinase	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2427_s_399	11376162	28       Parsley,T.B., Towner,J.S., Blyn,L.B., Ehrenfeld,E. and Semler,B.L. (1997) Poly (rC) binding protein 2 forms a ternary complex with the 5''- terminal sequences of poliovirus RNA and the viral 3CD proteinase .	bind
28178	1	7496	5	13	NULL	NULL	NULL	Flt-1	GP		undergoes					phosphorylation	Process	minimal	tyrosine		NULL	transfected cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_5_765_s_128	11348872	28  Flt-1 shows minimal tyrosine phosphorylation in response to VEGF, and binding of VEGF does not lead to significant biological roles in transfected cells.	bind
28179	2	7496	5	13	NULL	NULL	NULL	statement 1	Process		occurs in response to					VEGF	GP				NULL	transfected cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_5_765_s_128	11348872	28  Flt-1 shows minimal tyrosine phosphorylation in response to VEGF, and binding of VEGF does not lead to significant biological roles in transfected cells.	bind
28180	3	7496	5	13	NULL	NULL	NULL	VEGF	GP	binding of	does not lead to					biological roles	Process	significant			NULL	in transfected cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_5_765_s_128	11348872	28  Flt-1 shows minimal tyrosine phosphorylation in response to VEGF, and binding of VEGF does not lead to significant biological roles in transfected cells.	bind
30235	1	7496	7	10	NULL	0	NULL	Flt-1	NULL		undergoes	NULL				phosphorylation	NULL	minimal	tyrosine		NULL	transfected cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_5_765_s_128	11348872	28  Flt-1 shows minimal tyrosine phosphorylation in response to VEGF, and binding of VEGF does not lead to significant biological roles in transfected cells.	bind
30236	2	7496	7	NULL	NULL	0	NULL	statement 1	NULL		in response to	NULL				VEGF	NULL				NULL	transfected cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_5_765_s_128	11348872	28  Flt-1 shows minimal tyrosine phosphorylation in response to VEGF, and binding of VEGF does not lead to significant biological roles in transfected cells.	bind
30237	3	7496	7	NULL	NULL	0	NULL	Flt-1	NULL		bind	NULL				VEGF	NULL				NULL	transfected cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_5_765_s_128	11348872	28  Flt-1 shows minimal tyrosine phosphorylation in response to VEGF, and binding of VEGF does not lead to significant biological roles in transfected cells.	bind
30238	4	7496	7	NULL	NULL	0	NULL	statement 3	NULL		does not lead to	NULL				biological role	NULL	significant			NULL	transfected cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_5_765_s_128	11348872	28  Flt-1 shows minimal tyrosine phosphorylation in response to VEGF, and binding of VEGF does not lead to significant biological roles in transfected cells.	bind
28181	1	7497	5	13	NULL	NULL	NULL	insulin	GP		causes					smooth muscle cell	Cell	proliferation of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_91_3_831_s_180	7828312	28  In vitro, insulin has been shown to cause smooth muscle cell proliferation 29 ; stimulate LDL binding to smooth muscle cells, 30  fibroblasts, 31  and monocytes 32 ; and stimulate cholesterol synthesis in monocytes.	bind
28182	2	7497	5	13	NULL	NULL	NULL	LDL	GP		bind					smooth muscle cells	Cell				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_91_3_831_s_180	7828312	28  In vitro, insulin has been shown to cause smooth muscle cell proliferation 29 ; stimulate LDL binding to smooth muscle cells, 30  fibroblasts, 31  and monocytes 32 ; and stimulate cholesterol synthesis in monocytes.	bind
28183	3	7497	5	13	NULL	NULL	NULL	insulin	GP		stimulates					statement 2	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_91_3_831_s_180	7828312	28  In vitro, insulin has been shown to cause smooth muscle cell proliferation 29 ; stimulate LDL binding to smooth muscle cells, 30  fibroblasts, 31  and monocytes 32 ; and stimulate cholesterol synthesis in monocytes.	bind
28184	4	7497	5	13	NULL	NULL	NULL	LDL	GP		bind					fibroblasts	Cell				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_91_3_831_s_180	7828312	28  In vitro, insulin has been shown to cause smooth muscle cell proliferation 29 ; stimulate LDL binding to smooth muscle cells, 30  fibroblasts, 31  and monocytes 32 ; and stimulate cholesterol synthesis in monocytes.	bind
28185	5	7497	5	13	NULL	NULL	NULL	insulin	GP		stimulates					statement 4	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_91_3_831_s_180	7828312	28  In vitro, insulin has been shown to cause smooth muscle cell proliferation 29 ; stimulate LDL binding to smooth muscle cells, 30  fibroblasts, 31  and monocytes 32 ; and stimulate cholesterol synthesis in monocytes.	bind
28186	6	7497	5	13	NULL	NULL	NULL	LDL	GP		bind					monocytes	Cell				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_91_3_831_s_180	7828312	28  In vitro, insulin has been shown to cause smooth muscle cell proliferation 29 ; stimulate LDL binding to smooth muscle cells, 30  fibroblasts, 31  and monocytes 32 ; and stimulate cholesterol synthesis in monocytes.	bind
28187	7	7497	5	13	NULL	NULL	NULL	insulin	GP		stimulates					statement 6	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_91_3_831_s_180	7828312	28  In vitro, insulin has been shown to cause smooth muscle cell proliferation 29 ; stimulate LDL binding to smooth muscle cells, 30  fibroblasts, 31  and monocytes 32 ; and stimulate cholesterol synthesis in monocytes.	bind
28188	7	7497	5	13	NULL	NULL	NULL	insulin	GP		stimulates					statement 6	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_91_3_831_s_180	7828312	28  In vitro, insulin has been shown to cause smooth muscle cell proliferation 29 ; stimulate LDL binding to smooth muscle cells, 30  fibroblasts, 31  and monocytes 32 ; and stimulate cholesterol synthesis in monocytes.	bind
28189	8	7497	5	13	NULL	NULL	NULL	insulin	GP		stimulates					cholesterol	Chemical	synthesis of			NULL	in vitro, in monocytes	NULL	NULL	NULL	NULL	gw60_circulation_91_3_831_s_180	7828312	28  In vitro, insulin has been shown to cause smooth muscle cell proliferation 29 ; stimulate LDL binding to smooth muscle cells, 30  fibroblasts, 31  and monocytes 32 ; and stimulate cholesterol synthesis in monocytes.	bind
30239	1	7497	7	NULL	NULL	0	NULL	insulin	NULL		cause	NULL				smooth muscle cell proliferation	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_circulation_91_3_831_s_180	7828312	28  In vitro, insulin has been shown to cause smooth muscle cell proliferation 29 ; stimulate LDL binding to smooth muscle cells, 30  fibroblasts, 31  and monocytes 32 ; and stimulate cholesterol synthesis in monocytes.	bind
30240	2	7497	7	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				smooth muscle cells	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_91_3_831_s_180	7828312	28  In vitro, insulin has been shown to cause smooth muscle cell proliferation 29 ; stimulate LDL binding to smooth muscle cells, 30  fibroblasts, 31  and monocytes 32 ; and stimulate cholesterol synthesis in monocytes.	bind
30241	3	7497	7	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				fibroblasts	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_circulation_91_3_831_s_180	7828312	28  In vitro, insulin has been shown to cause smooth muscle cell proliferation 29 ; stimulate LDL binding to smooth muscle cells, 30  fibroblasts, 31  and monocytes 32 ; and stimulate cholesterol synthesis in monocytes.	bind
30242	4	7497	7	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				monocytes	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_91_3_831_s_180	7828312	28  In vitro, insulin has been shown to cause smooth muscle cell proliferation 29 ; stimulate LDL binding to smooth muscle cells, 30  fibroblasts, 31  and monocytes 32 ; and stimulate cholesterol synthesis in monocytes.	bind
30243	5	7497	7	NULL	NULL	0	NULL	insulin	NULL		stimulate	NULL				statement 2	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_circulation_91_3_831_s_180	7828312	28  In vitro, insulin has been shown to cause smooth muscle cell proliferation 29 ; stimulate LDL binding to smooth muscle cells, 30  fibroblasts, 31  and monocytes 32 ; and stimulate cholesterol synthesis in monocytes.	bind
30244	6	7497	7	NULL	NULL	0	NULL	insulin	NULL		stimulate	NULL				statement 3	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_circulation_91_3_831_s_180	7828312	28  In vitro, insulin has been shown to cause smooth muscle cell proliferation 29 ; stimulate LDL binding to smooth muscle cells, 30  fibroblasts, 31  and monocytes 32 ; and stimulate cholesterol synthesis in monocytes.	bind
30245	7	7497	7	NULL	NULL	0	NULL	insulin	NULL		stimulate	NULL				statement 4	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_91_3_831_s_180	7828312	28  In vitro, insulin has been shown to cause smooth muscle cell proliferation 29 ; stimulate LDL binding to smooth muscle cells, 30  fibroblasts, 31  and monocytes 32 ; and stimulate cholesterol synthesis in monocytes.	bind
30246	8	7497	7	10	NULL	0	NULL	insulin			stimulate					cholesterol		synthesis of			NULL	monocytes, in vitro	NULL	NULL	NULL	NULL	gw60_circulation_91_3_831_s_180	7828312	28  In vitro, insulin has been shown to cause smooth muscle cell proliferation 29 ; stimulate LDL binding to smooth muscle cells, 30  fibroblasts, 31  and monocytes 32 ; and stimulate cholesterol synthesis in monocytes.	bind
28225	1	7498	5	13	NULL	NULL	NULL	activator protein-1	GP		bind									DNA binding sites	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_1_244_s_197	10634825	28  Our previous study showed that lysoPC was capable of stimulating the binding of activator protein-1 and nuclear factor-kappaB to the DNA binding sites.	bind
28226	2	7498	5	13	NULL	NULL	NULL	nuclear factor-kappaB	GP		bind									DNA binding sites	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_1_244_s_197	10634825	28  Our previous study showed that lysoPC was capable of stimulating the binding of activator protein-1 and nuclear factor-kappaB to the DNA binding sites.	bind
28227	3	7498	5	13	NULL	NULL	NULL	lysoPC	Chemical		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_1_244_s_197	10634825	28  Our previous study showed that lysoPC was capable of stimulating the binding of activator protein-1 and nuclear factor-kappaB to the DNA binding sites.	bind
28228	4	7498	5	13	NULL	NULL	NULL	lysoPC	Chemical		stimulates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_1_244_s_197	10634825	28  Our previous study showed that lysoPC was capable of stimulating the binding of activator protein-1 and nuclear factor-kappaB to the DNA binding sites.	bind
30247	1	7498	7	10	NULL	0	NULL	activator protein-1			bind									DNA binding site	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_1_244_s_197	10634825	28  Our previous study showed that lysoPC was capable of stimulating the binding of activator protein-1 and nuclear factor-kappaB to the DNA binding sites.	bind
30248	2	7498	7	10	NULL	0	NULL	nuclear factor-kappaB			bind									DNA binding site	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_1_244_s_197	10634825	28  Our previous study showed that lysoPC was capable of stimulating the binding of activator protein-1 and nuclear factor-kappaB to the DNA binding sites.	bind
30249	3	7498	7	NULL	NULL	0	NULL	 lysoPC	NULL		stimulate	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_1_244_s_197	10634825	28  Our previous study showed that lysoPC was capable of stimulating the binding of activator protein-1 and nuclear factor-kappaB to the DNA binding sites.	bind
30250	4	7498	7	NULL	NULL	0	NULL	lysoPC	NULL		stimulate	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_1_244_s_197	10634825	28  Our previous study showed that lysoPC was capable of stimulating the binding of activator protein-1 and nuclear factor-kappaB to the DNA binding sites.	bind
28223	1	7499	5	13	NULL	NULL	NULL	proteins	GP	extracted from HTC rat hepatoma cells	bind					Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2696_s_184	11116074	28  Proteins extracted from HTC rat hepatoma cells bind to Sp1 and CTF/NF-1 - like binding sites in the rat PAI-1 regulatory region.	bind
28224	2	7499	5	13	NULL	NULL	NULL	proteins	GP	extracted from HTC rat hepatoma cells	bind					PAI-1	GP	rat		CTF/NF-1 - like binding sites in regulatory region	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2696_s_184	11116074	28  Proteins extracted from HTC rat hepatoma cells bind to Sp1 and CTF/NF-1 - like binding sites in the rat PAI-1 regulatory region.	bind
30251	1	7499	7	NULL	NULL	0	NULL	hepatoma cells	NULL	HTC rat	bind	NULL				 Sp1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2696_s_184	11116074	28  Proteins extracted from HTC rat hepatoma cells bind to Sp1 and CTF/NF-1 - like binding sites in the rat PAI-1 regulatory region.	bind
30252	2	7499	7	NULL	NULL	0	NULL	hepatoma cells	NULL	HTC rat	bind	NULL				PAI-1	NULL	rat		CTF/NF-1 - like binding sites in the regulatory region	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_12_2696_s_184	11116074	28  Proteins extracted from HTC rat hepatoma cells bind to Sp1 and CTF/NF-1 - like binding sites in the rat PAI-1 regulatory region.	bind
28203	1	7500	5	13	NULL	NULL	NULL	endothelial cell growth factor	GP		bind					FGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_1_178_s_203	9888881	28  Similar observations have been made by Nanberg et al 29  for another endothelial cell growth factor which binds to a tyrosine kinase receptor, namely FGF.	bind
28209	2	7500	5	13	NULL	NULL	NULL	FGF	GP		is a type of					tyrosine kinase receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_1_178_s_203	9888881	28  Similar observations have been made by Nanberg et al 29  for another endothelial cell growth factor which binds to a tyrosine kinase receptor, namely FGF.	bind
30253	1	7500	7	NULL	NULL	0	NULL	endothelial cell growth factor	NULL		binds	NULL				FGF	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_1_178_s_203	9888881	28  Similar observations have been made by Nanberg et al 29  for another endothelial cell growth factor which binds to a tyrosine kinase receptor, namely FGF.	bind
30254	2	7500	7	NULL	NULL	0	NULL	FGF	NULL		is a type of	NULL				tyrosine kinase receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_1_178_s_203	9888881	28  Similar observations have been made by Nanberg et al 29  for another endothelial cell growth factor which binds to a tyrosine kinase receptor, namely FGF.	bind
29869	1	7502	5	13	NULL	NULL	NULL	apoE	GP	neuronal	bind		may;;potentially			Abeta	GP				NULL	intraneuronally	NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
29870	2	7502	5	13	NULL	NULL	NULL	apoE	GP	astrocyte-generated	bind		may;;potentially			Abeta	GP				NULL	intraneuronally	NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
29872	3	7502	5	13	NULL	NULL	NULL	apoE	GP	neuronal	bind		may;;potentially			Abeta	GP				NULL	extracellularly 	NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
29874	4	7502	5	13	NULL	NULL	NULL	apoE	GP	astrocyte-generated	bind		may;;potentially			Abeta	GP				NULL	extracellularly	NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
29876	5	7502	5	13	NULL	NULL	NULL	statement 1	Process		leads to					neurons	Cell	internalization of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
29880	6	7502	5	13	NULL	NULL	NULL	statement 2	Process		leads to					neurons	Cell	internalization of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
29881	7	7502	5	13	NULL	NULL	NULL	statement 3	Process		leads to					neurons	Cell	internalization of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
29882	8	7502	5	13	NULL	NULL	NULL	statement 4	Process		leads to					neurons	Cell	internalization of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
29883	9	7502	5	13	NULL	NULL	NULL	Abeta	GP	accumulation of	leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
29885	10	7502	5	13	NULL	NULL	NULL	Abeta	GP	accumulation of	leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
29886	11	7502	5	13	NULL	NULL	NULL	Abeta	GP	accumulation of	leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
29887	12	7502	5	13	NULL	NULL	NULL	Abeta	GP	accumulation of	leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
29889	13	7502	5	13	NULL	NULL	NULL	neuronal dysfunction	MedicalFinding		leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
29890	14	7502	5	13	NULL	NULL	NULL	neuronal dysfunction	MedicalFinding		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
29892	18	7502	5	13	NULL	NULL	NULL	apoE	GP	increased immunoreactivity of	is observed in					statement 17	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
54522	15	7502	5	13	NULL	NULL	NULL	neuronal dysfunction	MedicalFinding		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
54523	16	7502	5	13	NULL	NULL	NULL	neuronal dysfunction	MedicalFinding		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
54524	17	7502	5	13	NULL	NULL	NULL	neurons	Cell		immunoreactive to					Abeta42	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
30481	1	7502	7	NULL	NULL	0	NULL	apoE	NULL	neuronal	bind	NULL	may;;potentially			Abeta	NULL				NULL	intraneuronal	NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
30482	2	7502	7	NULL	NULL	0	NULL	apoE	NULL	astrocyte-generated 	bind	NULL	may;;potentially			Abeta	NULL				NULL	intraneuronal	NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
30483	3	7502	7	NULL	NULL	0	NULL	apoE	NULL	neuronal	bind	NULL	may;;potentially			Abeta	NULL				NULL	extracellular	0	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
30484	4	7502	7	NULL	NULL	0	NULL	apoE	NULL	astrocyte-generated 	bind	NULL	may;;potentially			Abeta	NULL				NULL	extracellular	0	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
30485	5	7502	7	10	NULL	0	NULL	statement 1			leads to					neurons		internalization of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
30486	6	7502	7	10	NULL	0	NULL	statement 2			leads to					neurons		internalization of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
30487	7	7502	7	10	NULL	0	NULL	statement 3			leads to					neurons		internalization of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
30488	8	7502	7	10	NULL	0	NULL	statement 4			leads to					neurons		internalization of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
30489	9	7502	7	NULL	NULL	0	NULL	statement 1	NULL		occurs with	NULL				Abeta	NULL	accumulation of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
30490	10	7502	7	NULL	NULL	0	NULL	statement 2	NULL		occurs with	NULL				Abeta	NULL	accumulation of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
30491	11	7502	7	NULL	NULL	0	NULL	statement 3	NULL		occurs with	NULL				Abeta	NULL	accumulation of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
30492	12	7502	7	NULL	NULL	0	NULL	statement 4	NULL		occurs with	NULL				Abeta	NULL	accumulation of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
30493	13	7502	7	NULL	NULL	0	NULL	statement 1	NULL		occurs upon	NULL				neuronal dysfunction	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
30494	14	7502	7	NULL	NULL	0	NULL	statement 2	NULL		occurs upon	NULL				neuronal dysfunction	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
30495	15	7502	7	NULL	NULL	0	NULL	statement 3	NULL		occurs upon	NULL				neuronal dysfunction	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
30496	16	7502	7	NULL	NULL	0	NULL	statement 4	NULL		occurs upon	NULL				neuronal dysfunction	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
30497	17	7502	7	10	NULL	0	NULL	neurons			immunoreactive to					Abeta42					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
54525	18	7502	7	10	NULL	0	NULL	apoE		increased immunoreactivity of	is observed in					statement 17					NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_1_15_s_159	10623648	28  With Abeta accumulation and neuronal dysfunction, neuronal or astrocyte-generated apoE may potentially bind to Abeta intraneuronally and/or extracellularly with subsequent neuronal internalization, explaining the observation of apparent increased apoE immunoreactivity in Abeta42 immunoreactive neurons.	bind
28229	1	7503	5	13	NULL	NULL	NULL	HB-EGF	GP		bind					EGFR	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_11_2778_s_27	8941102	28 29 30  When HB-EGF binds to an EGFR, it induces EGFR autophosphorylation and exerts various biological activities such as cell proliferation and migration.	bind
28230	2	7503	5	13	NULL	NULL	NULL	statement 1	Process		induces					EGFR	GP	autophosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_11_2778_s_27	8941102	28 29 30  When HB-EGF binds to an EGFR, it induces EGFR autophosphorylation and exerts various biological activities such as cell proliferation and migration.	bind
28231	3	7503	5	13	NULL	NULL	NULL	statement 1	Process		exerts					cell proliferation	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_11_2778_s_27	8941102	28 29 30  When HB-EGF binds to an EGFR, it induces EGFR autophosphorylation and exerts various biological activities such as cell proliferation and migration.	bind
28232	4	7503	5	13	NULL	NULL	NULL	statement 1	Process		exerts					cell migration	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_11_2778_s_27	8941102	28 29 30  When HB-EGF binds to an EGFR, it induces EGFR autophosphorylation and exerts various biological activities such as cell proliferation and migration.	bind
30498	1	7503	7	NULL	NULL	0	NULL	HB-EGF	NULL		binds	NULL				EGFR	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_94_11_2778_s_27	8941102	28 29 30  When HB-EGF binds to an EGFR, it induces EGFR autophosphorylation and exerts various biological activities such as cell proliferation and migration.	bind
30499	2	7503	7	NULL	NULL	0	NULL	statement 1	NULL		induces	NULL				EGFR	NULL	autophosphorylation of			NULL		0	NULL	NULL	NULL	gw60_circulation_94_11_2778_s_27	8941102	28 29 30  When HB-EGF binds to an EGFR, it induces EGFR autophosphorylation and exerts various biological activities such as cell proliferation and migration.	bind
30500	3	7503	7	NULL	NULL	0	NULL	statement 2	NULL		exerts	NULL				cell proliferation	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_94_11_2778_s_27	8941102	28 29 30  When HB-EGF binds to an EGFR, it induces EGFR autophosphorylation and exerts various biological activities such as cell proliferation and migration.	bind
30501	4	7503	7	NULL	NULL	0	NULL	statement 2	NULL		exerts	NULL				cell migration	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_94_11_2778_s_27	8941102	28 29 30  When HB-EGF binds to an EGFR, it induces EGFR autophosphorylation and exerts various biological activities such as cell proliferation and migration.	bind
28233	1	7506	5	13	NULL	NULL	NULL	Ang-4	GP		bind					Tie-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_7_664_s_37	12958144	28 Ang-4 binds to Tie-2 as an agonist, although its precise function has not been documented.	bind
28234	2	7506	5	13	NULL	NULL	NULL	Ang-4	GP		is an agonist of					Tie-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_7_664_s_37	12958144	28 Ang-4 binds to Tie-2 as an agonist, although its precise function has not been documented.	bind
30502	1	7506	7	NULL	NULL	0	NULL	Ang-4	NULL		binds to	NULL				Tie-2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_7_664_s_37	12958144	28 Ang-4 binds to Tie-2 as an agonist, although its precise function has not been documented.	bind
30503	2	7506	7	10	NULL	0	NULL	Ang-4			is an agonist of					Tie-2					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_7_664_s_37	12958144	28 Ang-4 binds to Tie-2 as an agonist, although its precise function has not been documented.	bind
28235	1	7507	5	13	NULL	NULL	NULL	Src	GP		bind		weakly			Fak	GP				NULL	in the myocardium of control rats	NULL	NULL	NULL	NULL	gw70_circulationres_96_1_73_s_89	15576648	28 Coimmunoprecipitation assays with anti-Fak and anti-c-Src antibodies showed only a weak binding of Src to Fak in the myocardium of control rats ( Figure 1D and 1E).	bind
30504	1	7507	7	NULL	NULL	0	NULL	Src	NULL		binds	NULL	weakly			Fak	NULL				NULL	myocardium of  rats	0	NULL	NULL	NULL	gw70_circulationres_96_1_73_s_89	15576648	28 Coimmunoprecipitation assays with anti-Fak and anti-c-Src antibodies showed only a weak binding of Src to Fak in the myocardium of control rats ( Figure 1D and 1E).	bind
28236	1	7508	5	13	NULL	NULL	NULL	PTX3	GP		bind					leukemia Jurkat T cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_782_s_152	12006390	28 Recently, it has been reported that PTX3 binds to human leukemia Jurkat T cells.	bind
30505	1	7508	7	NULL	NULL	0	NULL	PTX3	NULL		binds to	NULL				leukemia Jurkat T cells	NULL	human 			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_782_s_152	12006390	28 Recently, it has been reported that PTX3 binds to human leukemia Jurkat T cells.	bind
28237	1	7509	5	13	NULL	NULL	NULL	cGMP	Chemical	receptor-generated	bind					cGK	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_2_269_s_171	14718400	28 Receptor-generated cGMP binds to cGK, which is thought to mediate the principal biological functions of cGMP.	bind
28238	2	7509	5	13	NULL	NULL	NULL	statement 1	Process		mediate					cGMP	Chemical	biological functions of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_2_269_s_171	14718400	28 Receptor-generated cGMP binds to cGK, which is thought to mediate the principal biological functions of cGMP.	bind
30506	1	7509	7	NULL	NULL	0	NULL	cGMP	NULL	 Receptor-generated	binds	NULL				cGK	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_109_2_269_s_171	14718400	28 Receptor-generated cGMP binds to cGK, which is thought to mediate the principal biological functions of cGMP.	bind
30507	2	7509	7	NULL	NULL	0	NULL	cGK	NULL		mediates	NULL				cGMP	NULL	biological functions of			NULL		0	NULL	NULL	NULL	gw70_circulation_109_2_269_s_171	14718400	28 Receptor-generated cGMP binds to cGK, which is thought to mediate the principal biological functions of cGMP.	bind
28239	1	7510	5	13	NULL	NULL	NULL	synaptotagmin	GP		bind			C2B domain		phosphoinositides	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1152_s_77	12738684	28 The C2B domain of synaptotagmin binds PIP2 preferentially to other phosphoinositides after exposure to Ca2+.	bind
28240	2	7510	5	13	NULL	NULL	NULL	synaptotagmin	GP		bind			C2B domain		PIP2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1152_s_77	12738684	28 The C2B domain of synaptotagmin binds PIP2 preferentially to other phosphoinositides after exposure to Ca2+.	bind
28241	3	7510	5	13	NULL	NULL	NULL	statement 1	Process		is preferred over					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1152_s_77	12738684	28 The C2B domain of synaptotagmin binds PIP2 preferentially to other phosphoinositides after exposure to Ca2+.	bind
46673	4	7510	5	13	NULL	NULL	NULL	statement 4	Process		occurs after					Ca2+	Chemical	exposure to			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1152_s_77	12738684	28 The C2B domain of synaptotagmin binds PIP2 preferentially to other phosphoinositides after exposure to Ca2+.	bind
30508	1	7510	7	10	NULL	0	NULL	synaptotagmin			binds			C2B domain		PIP2					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1152_s_77	12738684	28 The C2B domain of synaptotagmin binds PIP2 preferentially to other phosphoinositides after exposure to Ca2+.	bind
30509	2	7510	7	NULL	NULL	0	NULL	Synaptotagmin	NULL		binds	NULL		C2B domain		phosphoinositides	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1152_s_77	12738684	28 The C2B domain of synaptotagmin binds PIP2 preferentially to other phosphoinositides after exposure to Ca2+.	bind
30510	3	7510	7	NULL	NULL	0	NULL	statement 1	NULL	binding of	is preferred than	NULL				statement 2	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1152_s_77	12738684	28 The C2B domain of synaptotagmin binds PIP2 preferentially to other phosphoinositides after exposure to Ca2+.	bind
30511	4	7510	7	NULL	NULL	0	NULL	statement 1	NULL		occurs after	NULL				Ca2+	NULL	exposure to			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1152_s_77	12738684	28 The C2B domain of synaptotagmin binds PIP2 preferentially to other phosphoinositides after exposure to Ca2+.	bind
30512	5	7510	7	NULL	NULL	0	NULL	statement 2	NULL		occurs after	NULL				Ca2+	NULL	exposure to			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1152_s_77	12738684	28 The C2B domain of synaptotagmin binds PIP2 preferentially to other phosphoinositides after exposure to Ca2+.	bind
31554	1	7511	5	13	NULL	NULL	NULL	cMyBP-C	GP		is homologus to			N-terminus		ELC-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_10_1290_s_170	16614305	28 The N-terminal homology of cMyBP-C with ELC-1 raises the possibility that the pro/ala-rich sequence of the C0C1 domain could, by interfering with these interactions between ELC-1 and the S1 heads, free some of the heads and increase their flexibility, thereby promoting the binding of S1 to actin.	bind
31555	2	7511	5	13	NULL	NULL	NULL	ELC-1	GP		interacts with								S1 heads		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_10_1290_s_170	16614305	28 The N-terminal homology of cMyBP-C with ELC-1 raises the possibility that the pro/ala-rich sequence of the C0C1 domain could, by interfering with these interactions between ELC-1 and the S1 heads, free some of the heads and increase their flexibility, thereby promoting the binding of S1 to actin.	bind
31556	3	7511	5	13	NULL	NULL	NULL				bind			S1		actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_10_1290_s_170	16614305	28 The N-terminal homology of cMyBP-C with ELC-1 raises the possibility that the pro/ala-rich sequence of the C0C1 domain could, by interfering with these interactions between ELC-1 and the S1 heads, free some of the heads and increase their flexibility, thereby promoting the binding of S1 to actin.	bind
31557	4	7511	5	13	NULL	NULL	NULL	cMyBP-C	GP		contains			C0C1 domain		cMyBP-C	GP		pro/ala-rich sequence		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_10_1290_s_170	16614305	28 The N-terminal homology of cMyBP-C with ELC-1 raises the possibility that the pro/ala-rich sequence of the C0C1 domain could, by interfering with these interactions between ELC-1 and the S1 heads, free some of the heads and increase their flexibility, thereby promoting the binding of S1 to actin.	bind
31558	5	7511	5	13	NULL	NULL	NULL	statement 4	Process		interfere with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_10_1290_s_170	16614305	28 The N-terminal homology of cMyBP-C with ELC-1 raises the possibility that the pro/ala-rich sequence of the C0C1 domain could, by interfering with these interactions between ELC-1 and the S1 heads, free some of the heads and increase their flexibility, thereby promoting the binding of S1 to actin.	bind
31559	6	7511	5	13	NULL	NULL	NULL	statement 5	Process		promote					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_10_1290_s_170	16614305	28 The N-terminal homology of cMyBP-C with ELC-1 raises the possibility that the pro/ala-rich sequence of the C0C1 domain could, by interfering with these interactions between ELC-1 and the S1 heads, free some of the heads and increase their flexibility, thereby promoting the binding of S1 to actin.	bind
54564	7	7511	5	13	NULL	NULL	NULL	statement 5	Process		free								S1 heads		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_10_1290_s_170	16614305	28 The N-terminal homology of cMyBP-C with ELC-1 raises the possibility that the pro/ala-rich sequence of the C0C1 domain could, by interfering with these interactions between ELC-1 and the S1 heads, free some of the heads and increase their flexibility, thereby promoting the binding of S1 to actin.	bind
54565	8	7511	5	13	NULL	NULL	NULL	statement 5	Process		increases							flexibility of	S1 heads		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_10_1290_s_170	16614305	28 The N-terminal homology of cMyBP-C with ELC-1 raises the possibility that the pro/ala-rich sequence of the C0C1 domain could, by interfering with these interactions between ELC-1 and the S1 heads, free some of the heads and increase their flexibility, thereby promoting the binding of S1 to actin.	bind
30513	1	7511	7	10	NULL	0	NULL	ELC-1			interacts with								S1 heads		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_10_1290_s_170	16614305	28 The N-terminal homology of cMyBP-C with ELC-1 raises the possibility that the pro/ala-rich sequence of the C0C1 domain could, by interfering with these interactions between ELC-1 and the S1 heads, free some of the heads and increase their flexibility, thereby promoting the binding of S1 to actin.	bind
30514	2	7511	7	NULL	NULL	0	NULL	cMyBP-C 	NULL		is homologous to	NULL		N-terminal 		ELC-1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_10_1290_s_170	16614305	28 The N-terminal homology of cMyBP-C with ELC-1 raises the possibility that the pro/ala-rich sequence of the C0C1 domain could, by interfering with these interactions between ELC-1 and the S1 heads, free some of the heads and increase their flexibility, thereby promoting the binding of S1 to actin.	bind
30515	3	7511	7	NULL	NULL	0	NULL	cMyBP-C	NULL		interfere with	NULL	may	pro/ala-rich sequence of the C0C1 domain		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_10_1290_s_170	16614305	28 The N-terminal homology of cMyBP-C with ELC-1 raises the possibility that the pro/ala-rich sequence of the C0C1 domain could, by interfering with these interactions between ELC-1 and the S1 heads, free some of the heads and increase their flexibility, thereby promoting the binding of S1 to actin.	bind
30516	4	7511	7	10	NULL	0	NULL	statement 3			free								S1 heads		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_10_1290_s_170	16614305	28 The N-terminal homology of cMyBP-C with ELC-1 raises the possibility that the pro/ala-rich sequence of the C0C1 domain could, by interfering with these interactions between ELC-1 and the S1 heads, free some of the heads and increase their flexibility, thereby promoting the binding of S1 to actin.	bind
30517	5	7511	7	10	NULL	0	NULL	statement 3			increase							flexibility of	S1 heads		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_10_1290_s_170	16614305	28 The N-terminal homology of cMyBP-C with ELC-1 raises the possibility that the pro/ala-rich sequence of the C0C1 domain could, by interfering with these interactions between ELC-1 and the S1 heads, free some of the heads and increase their flexibility, thereby promoting the binding of S1 to actin.	bind
30518	6	7511	7	NULL	NULL	0	NULL	S1	NULL		binds	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_10_1290_s_170	16614305	28 The N-terminal homology of cMyBP-C with ELC-1 raises the possibility that the pro/ala-rich sequence of the C0C1 domain could, by interfering with these interactions between ELC-1 and the S1 heads, free some of the heads and increase their flexibility, thereby promoting the binding of S1 to actin.	bind
30519	7	7511	7	NULL	NULL	0	NULL	statement 5	NULL		promotes	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_10_1290_s_170	16614305	28 The N-terminal homology of cMyBP-C with ELC-1 raises the possibility that the pro/ala-rich sequence of the C0C1 domain could, by interfering with these interactions between ELC-1 and the S1 heads, free some of the heads and increase their flexibility, thereby promoting the binding of S1 to actin.	bind
28242	1	7512	5	13	NULL	NULL	NULL	acute phase SAA	GP	murine	bind					RAGE	GP	cell surface			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_561_s_257	11485914	28, 29 In addition, it was recently shown that murine acute phase SAA and murine AA fibril proteins bind to a cell surface receptor of advanced glycation end products (RAGE), which is a signal transduction receptor and does not lead to the internalization of SAA/AA fibril proteins.	bind
28243	2	7512	5	13	NULL	NULL	NULL	RAGE	GP		is					receptor of advanced glycation end products	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_561_s_257	11485914	28, 29 In addition, it was recently shown that murine acute phase SAA and murine AA fibril proteins bind to a cell surface receptor of advanced glycation end products (RAGE), which is a signal transduction receptor and does not lead to the internalization of SAA/AA fibril proteins.	bind
28244	3	7512	5	13	NULL	NULL	NULL	AA fibril proteins	GP	murine	bind					RAGE	GP	cell surface			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_561_s_257	11485914	28, 29 In addition, it was recently shown that murine acute phase SAA and murine AA fibril proteins bind to a cell surface receptor of advanced glycation end products (RAGE), which is a signal transduction receptor and does not lead to the internalization of SAA/AA fibril proteins.	bind
28245	4	7512	5	13	NULL	NULL	NULL	RAGE	GP		is a type of					signal transduction receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_561_s_257	11485914	28, 29 In addition, it was recently shown that murine acute phase SAA and murine AA fibril proteins bind to a cell surface receptor of advanced glycation end products (RAGE), which is a signal transduction receptor and does not lead to the internalization of SAA/AA fibril proteins.	bind
28246	5	7512	5	13	NULL	NULL	NULL	statement 1	Process		does not lead to					SAA/AA fibril proteins	GP	internalization of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_561_s_257	11485914	28, 29 In addition, it was recently shown that murine acute phase SAA and murine AA fibril proteins bind to a cell surface receptor of advanced glycation end products (RAGE), which is a signal transduction receptor and does not lead to the internalization of SAA/AA fibril proteins.	bind
28247	6	7512	5	13	NULL	NULL	NULL	statement 3	Process		does not lead to					SAA/AA fibril proteins	GP	internalization of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_561_s_257	11485914	28, 29 In addition, it was recently shown that murine acute phase SAA and murine AA fibril proteins bind to a cell surface receptor of advanced glycation end products (RAGE), which is a signal transduction receptor and does not lead to the internalization of SAA/AA fibril proteins.	bind
30520	1	7512	7	NULL	NULL	0	NULL	acute phase SAA proteins	NULL	murine 	bind	NULL				RAGE	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_561_s_257	11485914	28, 29 In addition, it was recently shown that murine acute phase SAA and murine AA fibril proteins bind to a cell surface receptor of advanced glycation end products (RAGE), which is a signal transduction receptor and does not lead to the internalization of SAA/AA fibril proteins.	bind
30521	2	7512	7	NULL	NULL	0	NULL	AA fibril proteins	NULL	murine	bind	NULL				RAGE	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_2_561_s_257	11485914	28, 29 In addition, it was recently shown that murine acute phase SAA and murine AA fibril proteins bind to a cell surface receptor of advanced glycation end products (RAGE), which is a signal transduction receptor and does not lead to the internalization of SAA/AA fibril proteins.	bind
30522	3	7512	7	NULL	NULL	0	NULL	RAGE	NULL		is	NULL				cell surface receptor of advanced glycation end products	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_2_561_s_257	11485914	28, 29 In addition, it was recently shown that murine acute phase SAA and murine AA fibril proteins bind to a cell surface receptor of advanced glycation end products (RAGE), which is a signal transduction receptor and does not lead to the internalization of SAA/AA fibril proteins.	bind
30523	4	7512	7	NULL	NULL	0	NULL	RAGE	NULL		is a type of	NULL				signal transduction receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_2_561_s_257	11485914	28, 29 In addition, it was recently shown that murine acute phase SAA and murine AA fibril proteins bind to a cell surface receptor of advanced glycation end products (RAGE), which is a signal transduction receptor and does not lead to the internalization of SAA/AA fibril proteins.	bind
30524	5	7512	7	NULL	NULL	0	NULL	statement 1	NULL		does not lead to	NULL				SAA/AA fibril proteins	NULL	internalization of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_2_561_s_257	11485914	28, 29 In addition, it was recently shown that murine acute phase SAA and murine AA fibril proteins bind to a cell surface receptor of advanced glycation end products (RAGE), which is a signal transduction receptor and does not lead to the internalization of SAA/AA fibril proteins.	bind
30525	6	7512	7	NULL	NULL	0	NULL	statement 2	NULL		does not lead to	NULL				SAA/AA fibril proteins	NULL	internalization of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_2_561_s_257	11485914	28, 29 In addition, it was recently shown that murine acute phase SAA and murine AA fibril proteins bind to a cell surface receptor of advanced glycation end products (RAGE), which is a signal transduction receptor and does not lead to the internalization of SAA/AA fibril proteins.	bind
31560	1	7513	5	13	NULL	NULL	NULL	PMEA	Chemical		is delivered to		selectively			macrophages	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_6_819_s_29	11389114	28, 29 In order to increase the selective delivery of PMEA to macrophages, a compound consisting of two molecules of PMEA bound together {di (P1,P2)[2-(adenin-9-yl)ethoxymethyl]phosphonate} (Bis-PMEA) was synthesized and encapsulated into autologous erythrocytes modified to increase their recognition and phagocytosis by human macrophages.	bind
30527	1	7513	7	10	NULL	0	NULL	PMEA			is delivered to		selectively			macrophages					NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_6_819_s_29	11389114	28, 29 In order to increase the selective delivery of PMEA to macrophages, a compound consisting of two molecules of PMEA bound together {di (P1,P2)[2-(adenin-9-yl)ethoxymethyl]phosphonate} (Bis-PMEA) was synthesized and encapsulated into autologous erythrocytes modified to increase their recognition and phagocytosis by human macrophages.	bind
28248	1	7514	5	13	NULL	NULL	NULL	gp91 phox	GP		bind					p47 phox	GP				NULL	in human neutrophils	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_776_s_32	12637340	28,29  In human neutrophils, small peptide sequences of gp91 phox, which are involved in the binding of gp91 phox to p47 phox, inhibit O2.	bind
28249	2	7514	5	13	NULL	NULL	NULL	gp91 phox	GP	small peptide sequences of	is involved in					statement 1	Process				NULL	in human neutrophils	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_776_s_32	12637340	28,29  In human neutrophils, small peptide sequences of gp91 phox, which are involved in the binding of gp91 phox to p47 phox, inhibit O2.	bind
28250	3	7514	5	13	NULL	NULL	NULL	gp91 phox	GP	small peptide sequences of	inhibit					O2	Chemical				NULL	in human neutrophils	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_776_s_32	12637340	28,29  In human neutrophils, small peptide sequences of gp91 phox, which are involved in the binding of gp91 phox to p47 phox, inhibit O2.	bind
30542	1	7514	7	NULL	NULL	0	NULL	gp91 phox	NULL		bind	NULL				p47phox	NULL				NULL	human neutrophils	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_776_s_32	12637340	28,29  In human neutrophils, small peptide sequences of gp91 phox, which are involved in the binding of gp91 phox to p47 phox, inhibit O2.	bind
30543	2	7514	7	10	NULL	0	NULL	gp91 phox		 small peptide sequences of	is involved in					statement 1					NULL	human neutrophils	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_776_s_32	12637340	28,29  In human neutrophils, small peptide sequences of gp91 phox, which are involved in the binding of gp91 phox to p47 phox, inhibit O2.	bind
30544	3	7514	7	10	NULL	0	NULL	gp91 phox	NULL	small peptide sequences of	inhibit	NULL				O2	NULL				NULL	human neutrophils	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_776_s_32	12637340	28,29  In human neutrophils, small peptide sequences of gp91 phox, which are involved in the binding of gp91 phox to p47 phox, inhibit O2.	bind
28251	1	7515	5	13	NULL	NULL	NULL	Nebulin	GP	sequence of	is similar to					nebulette	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
46654	2	7515	5	13	NULL	NULL	NULL	Nebulin	GP		contains								nebulin repeats		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
46674	3	7515	5	13	NULL	NULL	NULL	Nebulin	GP		contains								linker domain		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
46675	4	7515	5	13	NULL	NULL	NULL	Nebulin	GP		contains								C-terminal SH3		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
46676	5	7515	5	13	NULL	NULL	NULL	nebulin repeats	GP		contains								35 residue repeats		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
46677	6	7515	5	13	NULL	NULL	NULL	nebulette	GP		contains								nebulin repeats		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
46678	7	7515	5	13	NULL	NULL	NULL	nebulette	GP		contains								linker domain		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
46679	8	7515	5	13	NULL	NULL	NULL	nebulette	GP		contains								C-terminal SH3		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
46680	9	7515	5	13	NULL	NULL	NULL	nebulette	GP		bind			\tC-terminal SH3 domain		alpha-actinin	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
46681	10	7515	5	13	NULL	NULL	NULL	Nebulin	GP		bind			\tC-terminal SH3 domain		alpha-actinin	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
30545	1	7515	7	NULL	NULL	0	NULL	Nebulin 	NULL	sequence of	is similar to	NULL				nebulette	NULL	sequence of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
30546	2	7515	7	NULL	NULL	0	NULL	Nebulin	NULL		contains	NULL					NULL		nebulin repeats		NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
30547	3	7515	7	NULL	NULL	0	NULL	Nebulin	NULL		contains	NULL					NULL		linker domain		NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
30548	4	7515	7	NULL	NULL	0	NULL	Nebulin			contains								 C-terminal SH3 domain		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
30549	5	7515	7	NULL	NULL	0	NULL	Nebulin			bind			C-terminal SH3 domain		alpha-actinin					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
30553	6	7515	7	NULL	NULL	0	NULL	nebulin repeats	NULL		contains	NULL					NULL		35 residue repeats 		NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
30554	7	7515	7	NULL	NULL	0	NULL	SH3	NULL		is	NULL				 Src homology 3 	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
54818	8	7515	7	NULL	NULL	0	NULL	nebulette			contains					nebulin repeats					NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
54819	9	7515	7	NULL	NULL	0	NULL	nebulette			contains					 linker domain					NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
54820	10	7515	7	NULL	NULL	0	NULL	nebulette			contains								C-terminal SH3 domain		NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
54821	11	7515	7	NULL	NULL	0	NULL	nebulette			bind			C-terminal SH3 domain		alpha-actinin					NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_66	14976140	28,33  Nebulin and nebulette share sequence similarities and contain 35 residue repeats (nebulin repeats), a linker domain, and a C-terminal Src homology 3 (SH3) domain that also binds to alpha-actinin.	bind
28252	1	7516	5	13	NULL	NULL	NULL	LPS	Chemical		bind					TLR4	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21129_s_204	11274165	28C5 blocks  LPS  binding to TLR4 and MD-2.	bind
28253	2	7516	5	13	NULL	NULL	NULL	28C5	Chemical		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21129_s_204	11274165	28C5 blocks  LPS  binding to TLR4 and MD-2.	bind
28254	3	7516	5	13	NULL	NULL	NULL	LPS	Chemical		bind					MD-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21129_s_204	11274165	28C5 blocks  LPS  binding to TLR4 and MD-2.	bind
28255	4	7516	5	13	NULL	NULL	NULL	28C5	Chemical		blocks					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21129_s_204	11274165	28C5 blocks  LPS  binding to TLR4 and MD-2.	bind
28258	3	7516	5	13	NULL	NULL	NULL	MY-4	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21129_s_204	11274165	28C5 blocks  LPS  binding to TLR4 and MD-2.	bind
30570	1	7516	7	NULL	NULL	0	NULL	LPS	NULL		binds to	NULL				TLR4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_24_21129_s_204	11274165	28C5 blocks  LPS  binding to TLR4 and MD-2.	bind
30571	2	7516	7	NULL	NULL	0	NULL	LPS	NULL		binds to	NULL				MD-2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_24_21129_s_204	11274165	28C5 blocks  LPS  binding to TLR4 and MD-2.	bind
30573	3	7516	7	NULL	NULL	0	NULL	28C5	NULL		blocks	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_24_21129_s_204	11274165	28C5 blocks  LPS  binding to TLR4 and MD-2.	bind
30574	4	7516	7	NULL	NULL	0	NULL	28C5	NULL		blocks	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_24_21129_s_204	11274165	28C5 blocks  LPS  binding to TLR4 and MD-2.	bind
28256	1	7517	5	13	NULL	NULL	NULL	CD14	GP		bind					LPS	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3144_s_110	10652298	28C5, MY-4, and 60bca have been shown to inhibit CD14 binding to LPS ( 10,  26).	bind
28257	2	7517	5	13	NULL	NULL	NULL	28C5	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3144_s_110	10652298	28C5, MY-4, and 60bca have been shown to inhibit CD14 binding to LPS ( 10,  26).	bind
28259	4	7517	5	13	NULL	NULL	NULL	60bca	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3144_s_110	10652298	28C5, MY-4, and 60bca have been shown to inhibit CD14 binding to LPS ( 10,  26).	bind
30580	1	7517	7	NULL	NULL	0	NULL	CD14	NULL		binds to	NULL				LPS	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3144_s_110	10652298	28C5, MY-4, and 60bca have been shown to inhibit CD14 binding to LPS ( 10,  26).	bind
30581	2	7517	7	NULL	NULL	0	NULL	28C5	NULL		inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3144_s_110	10652298	28C5, MY-4, and 60bca have been shown to inhibit CD14 binding to LPS ( 10,  26).	bind
30582	3	7517	7	NULL	NULL	0	NULL	MY-4	NULL		inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3144_s_110	10652298	28C5, MY-4, and 60bca have been shown to inhibit CD14 binding to LPS ( 10,  26).	bind
30583	4	7517	7	NULL	NULL	0	NULL	60bca	NULL		inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3144_s_110	10652298	28C5, MY-4, and 60bca have been shown to inhibit CD14 binding to LPS ( 10,  26).	bind
28260	1	7518	5	13	NULL	NULL	NULL	spermine molecule	Chemical		bind					Z-DNA	NucleicAcid			minor groove	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_419_s_441	11788703	29       Bancroft,D., Williams,L.D., Rich,A. and Egli,M. (1994) The  low-temperature crystal structure of the pure-spermine form of Z-DNA reveals binding of a spermine molecule in the minor groove.	bind
28261	2	7518	5	13	NULL	NULL	NULL	statement 1	Process		occurs in					low-temperature					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_419_s_441	11788703	29       Bancroft,D., Williams,L.D., Rich,A. and Egli,M. (1994) The  low-temperature crystal structure of the pure-spermine form of Z-DNA reveals binding of a spermine molecule in the minor groove.	bind
30585	1	7518	7	NULL	NULL	0	NULL	 spermine molecule	NULL	pure	binds to	NULL				Z-DNA	NULL			minor groove	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_419_s_441	11788703	29       Bancroft,D., Williams,L.D., Rich,A. and Egli,M. (1994) The  low-temperature crystal structure of the pure-spermine form of Z-DNA reveals binding of a spermine molecule in the minor groove.	bind
28398	1	7519	5	13	NULL	NULL	NULL	Sos1	GP	human	is a type of					guanine nucleotide exchange factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1300_s_345	11238996	29       Chardin,P., Camonis,J.H., Gale,N.W., van Aelst,L., Schlessinger,J., Wigler,M.H. and Bar-Sagi,D. (1993) Human Sos1: a guanine nucleotide exchange factor for Ras that binds to Grb2.	bind
30438	2	7519	5	13	NULL	NULL	NULL	Sos1	GP	human	bind					Grb2	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1300_s_345	11238996	29       Chardin,P., Camonis,J.H., Gale,N.W., van Aelst,L., Schlessinger,J., Wigler,M.H. and Bar-Sagi,D. (1993) Human Sos1: a guanine nucleotide exchange factor for Ras that binds to Grb2.	bind
30586	1	7519	7	NULL	NULL	0	NULL	Sos1	NULL	human	binds to	NULL				Grb2	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1300_s_345	11238996	29       Chardin,P., Camonis,J.H., Gale,N.W., van Aelst,L., Schlessinger,J., Wigler,M.H. and Bar-Sagi,D. (1993) Human Sos1: a guanine nucleotide exchange factor for Ras that binds to Grb2.	bind
30587	2	7519	7	NULL	NULL	0	NULL	Sos1	NULL	human	is a type of	NULL				guanine nucleotide exchange factor for Ras	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1300_s_345	11238996	29       Chardin,P., Camonis,J.H., Gale,N.W., van Aelst,L., Schlessinger,J., Wigler,M.H. and Bar-Sagi,D. (1993) Human Sos1: a guanine nucleotide exchange factor for Ras that binds to Grb2.	bind
28400	1	7520	5	13	NULL	NULL	NULL	WT1	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4865_s_326	11121477	29       Hamilton,T.B., Borel,F. and Romaniuk,P.J. (1998) Comparison of the DNA binding characteristics of the related zinc finger proteins WT1 and EGR1.	bind
28401	2	7520	5	13	NULL	NULL	NULL	EGR1	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4865_s_326	11121477	29       Hamilton,T.B., Borel,F. and Romaniuk,P.J. (1998) Comparison of the DNA binding characteristics of the related zinc finger proteins WT1 and EGR1.	bind
28402	3	7520	5	13	NULL	NULL	NULL	EGR1	GP		is a type of					zinc finger proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4865_s_326	11121477	29       Hamilton,T.B., Borel,F. and Romaniuk,P.J. (1998) Comparison of the DNA binding characteristics of the related zinc finger proteins WT1 and EGR1.	bind
28403	4	7520	5	13	NULL	NULL	NULL	WT1	GP		is a type of					zinc finger proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4865_s_326	11121477	29       Hamilton,T.B., Borel,F. and Romaniuk,P.J. (1998) Comparison of the DNA binding characteristics of the related zinc finger proteins WT1 and EGR1.	bind
30592	1	7520	7	NULL	NULL	0	NULL	WT1	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4865_s_326	11121477	29       Hamilton,T.B., Borel,F. and Romaniuk,P.J. (1998) Comparison of the DNA binding characteristics of the related zinc finger proteins WT1 and EGR1.	bind
30593	2	7520	7	NULL	NULL	0	NULL	EGR1	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4865_s_326	11121477	29       Hamilton,T.B., Borel,F. and Romaniuk,P.J. (1998) Comparison of the DNA binding characteristics of the related zinc finger proteins WT1 and EGR1.	bind
30594	3	7520	7	NULL	NULL	0	NULL	WT1	NULL		is a type of	NULL				zinc finger protein	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4865_s_326	11121477	29       Hamilton,T.B., Borel,F. and Romaniuk,P.J. (1998) Comparison of the DNA binding characteristics of the related zinc finger proteins WT1 and EGR1.	bind
30595	4	7520	7	NULL	NULL	0	NULL	EGR1	NULL		is a type of	NULL				zinc finger protein	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4865_s_326	11121477	29       Hamilton,T.B., Borel,F. and Romaniuk,P.J. (1998) Comparison of the DNA binding characteristics of the related zinc finger proteins WT1 and EGR1.	bind
28404	1	7521	5	13	NULL	NULL	NULL	Pur factor	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3197_s_348	10954586	29       Herault,Y., Chatelain,G., Brum,G. and Michel,D. (1995) RNA-dependent DNA binding activity of the Pur factor, potentially involved in DNA replication and gene transcription.	bind
28407	2	7521	5	13	NULL	NULL	NULL	statement 1	Process		is dependent on					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3197_s_348	10954586	29       Herault,Y., Chatelain,G., Brum,G. and Michel,D. (1995) RNA-dependent DNA binding activity of the Pur factor, potentially involved in DNA replication and gene transcription.	bind
28410	3	7521	5	13	NULL	NULL	NULL	statement 1	Process		is involved in		potentially			DNA	NucleicAcid	replication of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3197_s_348	10954586	29       Herault,Y., Chatelain,G., Brum,G. and Michel,D. (1995) RNA-dependent DNA binding activity of the Pur factor, potentially involved in DNA replication and gene transcription.	bind
54531	4	7521	5	13	NULL	NULL	NULL	statement 1	Process		is involved in		potentially			gene	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3197_s_348	10954586	29       Herault,Y., Chatelain,G., Brum,G. and Michel,D. (1995) RNA-dependent DNA binding activity of the Pur factor, potentially involved in DNA replication and gene transcription.	bind
30597	1	7521	7	NULL	NULL	0	NULL	Pur factor	NULL		binds	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3197_s_348	10954586	29       Herault,Y., Chatelain,G., Brum,G. and Michel,D. (1995) RNA-dependent DNA binding activity of the Pur factor, potentially involved in DNA replication and gene transcription.	bind
30598	2	7521	7	NULL	NULL	0	NULL	statement 1	NULL		depends on	NULL				RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3197_s_348	10954586	29       Herault,Y., Chatelain,G., Brum,G. and Michel,D. (1995) RNA-dependent DNA binding activity of the Pur factor, potentially involved in DNA replication and gene transcription.	bind
30599	3	7521	7	10	NULL	0	NULL	statement 1			is involved in		potentially			DNA		replication of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3197_s_348	10954586	29       Herault,Y., Chatelain,G., Brum,G. and Michel,D. (1995) RNA-dependent DNA binding activity of the Pur factor, potentially involved in DNA replication and gene transcription.	bind
30600	4	7521	7	10	NULL	0	NULL	statement 1			is involved in		potentially			gene		transcription of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_17_3197_s_348	10954586	29       Herault,Y., Chatelain,G., Brum,G. and Michel,D. (1995) RNA-dependent DNA binding activity of the Pur factor, potentially involved in DNA replication and gene transcription.	bind
28413	1	7522	5	13	NULL	NULL	NULL	nuclear proteins	GP		bind							cauliflower mosaic virus		35S truncated promoter	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_775_s_283	11809891	29       Prat,S., Willmitzer,L. and Sanchez-Serrano,J.J. (1989) Nuclear proteins binding to a cauliflower mosaic virus 35S truncated promoter.	bind
30632	1	7522	7	NULL	NULL	0	NULL	Nuclear proteins	NULL		binds to	NULL					NULL	cauliflower mosaic virus		35S truncated promoter	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_775_s_283	11809891	29       Prat,S., Willmitzer,L. and Sanchez-Serrano,J.J. (1989) Nuclear proteins binding to a cauliflower mosaic virus 35S truncated promoter.	bind
28414	1	7523	5	13	NULL	NULL	NULL	NGFI-A	GP		bind		specifically			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4920_s_330	11812820	29       Swirnoff,A.H. and Milbrandt,J. (1995) DNA-binding specificity of NGFI-A and related zinc finger transcription factors.	bind
30633	1	7523	7	10	NULL	0	NULL	NGFI-A 			bind		specifically			DNA					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4920_s_330	11812820	29       Swirnoff,A.H. and Milbrandt,J. (1995) DNA-binding specificity of NGFI-A and related zinc finger transcription factors.	bind
28415	1	7524	5	13	NULL	NULL	NULL	TFIIIA	GP		bind					class III genes	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_767_s_355	11160900	29       Van Dyke,M.W. and Roeder,R.G. (1987) Novobiocin interferes with the binding of transcription factors TFIIIA and TFIIIC to the promoters of class III genes.	bind
28416	2	7524	5	13	NULL	NULL	NULL	TFIIIC	GP		bind					class III genes	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_767_s_355	11160900	29       Van Dyke,M.W. and Roeder,R.G. (1987) Novobiocin interferes with the binding of transcription factors TFIIIA and TFIIIC to the promoters of class III genes.	bind
28417	3	7524	5	13	NULL	NULL	NULL	TFIIIA	GP		is a type of					transcription facor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_767_s_355	11160900	29       Van Dyke,M.W. and Roeder,R.G. (1987) Novobiocin interferes with the binding of transcription factors TFIIIA and TFIIIC to the promoters of class III genes.	bind
28418	4	7524	5	13	NULL	NULL	NULL	TFIIIC	GP		is a type of					transcription facor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_767_s_355	11160900	29       Van Dyke,M.W. and Roeder,R.G. (1987) Novobiocin interferes with the binding of transcription factors TFIIIA and TFIIIC to the promoters of class III genes.	bind
28419	5	7524	5	13	NULL	NULL	NULL	novobiocin	Chemical		interferes with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_767_s_355	11160900	29       Van Dyke,M.W. and Roeder,R.G. (1987) Novobiocin interferes with the binding of transcription factors TFIIIA and TFIIIC to the promoters of class III genes.	bind
28420	6	7524	5	13	NULL	NULL	NULL	novobiocin	Chemical		interferes with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_767_s_355	11160900	29       Van Dyke,M.W. and Roeder,R.G. (1987) Novobiocin interferes with the binding of transcription factors TFIIIA and TFIIIC to the promoters of class III genes.	bind
30635	1	7524	7	NULL	NULL	0	NULL	TFIIIA	NULL		binds	NULL				class III genes	NULL			promoters of	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_767_s_355	11160900	29       Van Dyke,M.W. and Roeder,R.G. (1987) Novobiocin interferes with the binding of transcription factors TFIIIA and TFIIIC to the promoters of class III genes.	bind
30636	2	7524	7	NULL	NULL	0	NULL	TFIIIC	NULL		binds	NULL				class III genes	NULL			promoters of	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_767_s_355	11160900	29       Van Dyke,M.W. and Roeder,R.G. (1987) Novobiocin interferes with the binding of transcription factors TFIIIA and TFIIIC to the promoters of class III genes.	bind
30637	3	7524	7	NULL	NULL	0	NULL	Novobiocin	NULL		interferes with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_767_s_355	11160900	29       Van Dyke,M.W. and Roeder,R.G. (1987) Novobiocin interferes with the binding of transcription factors TFIIIA and TFIIIC to the promoters of class III genes.	bind
30638	4	7524	7	NULL	NULL	0	NULL	Novobiocin	NULL		interferes with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_767_s_355	11160900	29       Van Dyke,M.W. and Roeder,R.G. (1987) Novobiocin interferes with the binding of transcription factors TFIIIA and TFIIIC to the promoters of class III genes.	bind
30639	5	7524	7	NULL	NULL	0	NULL	TFIIIA	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_767_s_355	11160900	29       Van Dyke,M.W. and Roeder,R.G. (1987) Novobiocin interferes with the binding of transcription factors TFIIIA and TFIIIC to the promoters of class III genes.	bind
30640	6	7524	7	NULL	NULL	0	NULL	TFIIIC	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_767_s_355	11160900	29       Van Dyke,M.W. and Roeder,R.G. (1987) Novobiocin interferes with the binding of transcription factors TFIIIA and TFIIIC to the promoters of class III genes.	bind
28422	1	7525	5	13	NULL	NULL	NULL	thrombin	GP		interacts with					TM	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_520_s_204	9102171	29  Alternatively, the anti-TM antibody may specifically alter the cofactor protein C function of TM by blocking the interaction between thrombin and TM, since the primary thrombin binding site of TM is thought to be composed of the fifth and sixth epidermal growth factor homology regions.	bind
28424	2	7525	5	13	NULL	NULL	NULL	TM	GP		contains					cofactor protein C function	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_520_s_204	9102171	29  Alternatively, the anti-TM antibody may specifically alter the cofactor protein C function of TM by blocking the interaction between thrombin and TM, since the primary thrombin binding site of TM is thought to be composed of the fifth and sixth epidermal growth factor homology regions.	bind
28425	3	7525	5	13	NULL	NULL	NULL	anti-TM antibody	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_520_s_204	9102171	29  Alternatively, the anti-TM antibody may specifically alter the cofactor protein C function of TM by blocking the interaction between thrombin and TM, since the primary thrombin binding site of TM is thought to be composed of the fifth and sixth epidermal growth factor homology regions.	bind
28428	4	7525	5	13	NULL	NULL	NULL	statement 3	Process		alters		may;;specifically			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_520_s_204	9102171	29  Alternatively, the anti-TM antibody may specifically alter the cofactor protein C function of TM by blocking the interaction between thrombin and TM, since the primary thrombin binding site of TM is thought to be composed of the fifth and sixth epidermal growth factor homology regions.	bind
28429	5	7525	5	13	NULL	NULL	NULL	TM	GP	primary	is composed of			thrombin binding site					fifth epidermal growth factor homology region		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_520_s_204	9102171	29  Alternatively, the anti-TM antibody may specifically alter the cofactor protein C function of TM by blocking the interaction between thrombin and TM, since the primary thrombin binding site of TM is thought to be composed of the fifth and sixth epidermal growth factor homology regions.	bind
46655	6	7525	5	13	NULL	NULL	NULL	TM	GP	primary	is composed of			thrombin binding site					sixth epidermal growth factor homology regions		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_520_s_204	9102171	29  Alternatively, the anti-TM antibody may specifically alter the cofactor protein C function of TM by blocking the interaction between thrombin and TM, since the primary thrombin binding site of TM is thought to be composed of the fifth and sixth epidermal growth factor homology regions.	bind
30644	1	7525	7	10	NULL	0	NULL	 anti-TM antibody			alter		specifically			statement 6					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_520_s_204	9102171	29  Alternatively, the anti-TM antibody may specifically alter the cofactor protein C function of TM by blocking the interaction between thrombin and TM, since the primary thrombin binding site of TM is thought to be composed of the fifth and sixth epidermal growth factor homology regions.	bind
30647	2	7525	7	NULL	NULL	0	NULL	thrombin	NULL		interacts with	NULL				TM	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_520_s_204	9102171	29  Alternatively, the anti-TM antibody may specifically alter the cofactor protein C function of TM by blocking the interaction between thrombin and TM, since the primary thrombin binding site of TM is thought to be composed of the fifth and sixth epidermal growth factor homology regions.	bind
30649	3	7525	7	NULL	NULL	0	NULL	statement 1	NULL		occurs by blocking	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_520_s_204	9102171	29  Alternatively, the anti-TM antibody may specifically alter the cofactor protein C function of TM by blocking the interaction between thrombin and TM, since the primary thrombin binding site of TM is thought to be composed of the fifth and sixth epidermal growth factor homology regions.	bind
30650	4	7525	7	10	NULL	0	NULL	TM	NULL	primary	is composed of	NULL		thrombin binding site			NULL		fifth epidermal growth factor homology region		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_520_s_204	9102171	29  Alternatively, the anti-TM antibody may specifically alter the cofactor protein C function of TM by blocking the interaction between thrombin and TM, since the primary thrombin binding site of TM is thought to be composed of the fifth and sixth epidermal growth factor homology regions.	bind
30652	5	7525	7	10	NULL	0	NULL	TM	NULL	primary	is composed of	NULL		thrombin binding site			NULL		 sixth epidermal growth factor homology region		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_520_s_204	9102171	29  Alternatively, the anti-TM antibody may specifically alter the cofactor protein C function of TM by blocking the interaction between thrombin and TM, since the primary thrombin binding site of TM is thought to be composed of the fifth and sixth epidermal growth factor homology regions.	bind
54532	6	7525	7	10	NULL	0	NULL	TM			contains					cofactor protein C function					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_3_520_s_204	9102171	29  Alternatively, the anti-TM antibody may specifically alter the cofactor protein C function of TM by blocking the interaction between thrombin and TM, since the primary thrombin binding site of TM is thought to be composed of the fifth and sixth epidermal growth factor homology regions.	bind
28431	1	7526	5	13	NULL	NULL	NULL	AT1 receptor	GP		is a type of					G protein - coupled receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_6_1053_s_168	7586216	29  Although the AT1 receptor is a typical G protein - coupled receptor in that it lacks tyrosine kinase activity, many proteins are rapidly tyrosine-phosphorylated when Ang II binds to the AT1 receptor.	bind
28433	2	7526	5	13	NULL	NULL	NULL	AT1 receptor	GP		lacks					tyrosine kinase activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_6_1053_s_168	7586216	29  Although the AT1 receptor is a typical G protein - coupled receptor in that it lacks tyrosine kinase activity, many proteins are rapidly tyrosine-phosphorylated when Ang II binds to the AT1 receptor.	bind
28435	3	7526	5	13	NULL	NULL	NULL	Ang II	GP		bind					AT1 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_6_1053_s_168	7586216	29  Although the AT1 receptor is a typical G protein - coupled receptor in that it lacks tyrosine kinase activity, many proteins are rapidly tyrosine-phosphorylated when Ang II binds to the AT1 receptor.	bind
30666	1	7526	7	NULL	NULL	0	NULL	Ang II	NULL		binds to	NULL				AT1 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_77_6_1053_s_168	7586216	29  Although the AT1 receptor is a typical G protein - coupled receptor in that it lacks tyrosine kinase activity, many proteins are rapidly tyrosine-phosphorylated when Ang II binds to the AT1 receptor.	bind
30668	3	7526	7	NULL	NULL	0	NULL	 AT1 receptor	NULL		is a type of	NULL				G protein - coupled receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_77_6_1053_s_168	7586216	29  Although the AT1 receptor is a typical G protein - coupled receptor in that it lacks tyrosine kinase activity, many proteins are rapidly tyrosine-phosphorylated when Ang II binds to the AT1 receptor.	bind
30669	4	7526	7	NULL	NULL	0	NULL	AT1 receptor	NULL		lacks	NULL				tyrosine kinase activity	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_77_6_1053_s_168	7586216	29  Although the AT1 receptor is a typical G protein - coupled receptor in that it lacks tyrosine kinase activity, many proteins are rapidly tyrosine-phosphorylated when Ang II binds to the AT1 receptor.	bind
28444	1	7527	5	13	NULL	NULL	NULL	Plg	GP		bind					Plg receptors	GP	surface			NULL	on endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_3_433_s_149	11231925	29  Lp(a) also interferes with Plg binding to the surface Plg receptors on endothelial cells.	bind
28445	2	7527	5	13	NULL	NULL	NULL	Lp(a)	GP		interferes with					statement 1	Process				NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_3_433_s_149	11231925	29  Lp(a) also interferes with Plg binding to the surface Plg receptors on endothelial cells.	bind
30670	1	7527	7	10	NULL	0	NULL	Plg			binds					Plg receptors		surface			NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_3_433_s_149	11231925	29  Lp(a) also interferes with Plg binding to the surface Plg receptors on endothelial cells.	bind
30671	2	7527	7	10	NULL	0	NULL	 Lp(a)			interferes with					statement 1					NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_3_433_s_149	11231925	29  Lp(a) also interferes with Plg binding to the surface Plg receptors on endothelial cells.	bind
28447	1	7528	5	13	NULL	NULL	NULL	mAb C-7	GP		bind					apoB/E receptor	GP				NULL	in human cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_101	9012650	29  mAb C-7, which binds to the apoB/E receptor in human cells, was used for binding competition studies.	bind
30672	1	7528	7	10	NULL	0	NULL	 mAb C-7	NULL		binds to	NULL				apoB/E receptor	NULL				NULL	human cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_101	9012650	29  mAb C-7, which binds to the apoB/E receptor in human cells, was used for binding competition studies.	bind
28450	1	7530	5	13	NULL	NULL	NULL	fibrinogen	GP		bind					platelet GPIIb/IIIa receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2535_s_170	10521384	29  XV459 has been shown to be a competitive inhibitor with high affinity for inhibiting fibrinogen binding to platelet GPIIb/IIIa receptors.	bind
28451	2	7530	5	13	NULL	NULL	NULL	XV459	Chemical		is a type of					competitive inhibitor	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2535_s_170	10521384	29  XV459 has been shown to be a competitive inhibitor with high affinity for inhibiting fibrinogen binding to platelet GPIIb/IIIa receptors.	bind
28453	3	7530	5	13	NULL	NULL	NULL	XV459	Chemical		inhibit		high affinity			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2535_s_170	10521384	29  XV459 has been shown to be a competitive inhibitor with high affinity for inhibiting fibrinogen binding to platelet GPIIb/IIIa receptors.	bind
30673	1	7530	7	NULL	NULL	0	NULL	fibrinogen	NULL		binds to	NULL				platelet GPIIb/IIIa receptors	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2535_s_170	10521384	29  XV459 has been shown to be a competitive inhibitor with high affinity for inhibiting fibrinogen binding to platelet GPIIb/IIIa receptors.	bind
30674	2	7530	7	10	NULL	0	NULL	XV459	NULL		inhibits	NULL	high affinity			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2535_s_170	10521384	29  XV459 has been shown to be a competitive inhibitor with high affinity for inhibiting fibrinogen binding to platelet GPIIb/IIIa receptors.	bind
54533	3	7530	7	10	NULL	0	NULL	XV459			is a type of					competitive inhibitor					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2535_s_170	10521384	29  XV459 has been shown to be a competitive inhibitor with high affinity for inhibiting fibrinogen binding to platelet GPIIb/IIIa receptors.	bind
28455	1	7531	5	13	NULL	NULL	NULL	ECSODR213G	GP		bind					collagen type I	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_7_1047_s_181	16087794	29 Despite the difference in the degree of binding observed previously 29 and in the present study, which may have resulted from different methods of detection, both studies indicate that ECSODR213G indeed binds to collagen type I.	bind
30915	1	7531	7	NULL	NULL	0	NULL	ECSODR213G	NULL		binds to	NULL				collagen type I	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_112_7_1047_s_181	16087794	29 Despite the difference in the degree of binding observed previously 29 and in the present study, which may have resulted from different methods of detection, both studies indicate that ECSODR213G indeed binds to collagen type I.	bind
28469	1	7532	5	13	NULL	NULL	NULL	VLDL	GP		bind					VLDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_117	12231568	29 In consideration of the repeated observation that apoC-I interferes with the binding of VLDL to the VLDL receptor (apoE mediated) but not with the binding of VLDL to the LDL receptor (apoB-100 mediated), 30 the mechanism of the protection against obesity in the setting of high levels of apoC-I and in the setting of absent VLDL receptor could be similar.	bind
28470	3	7532	5	13	NULL	NULL	NULL	apoC-I	GP		interferes with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_117	12231568	29 In consideration of the repeated observation that apoC-I interferes with the binding of VLDL to the VLDL receptor (apoE mediated) but not with the binding of VLDL to the LDL receptor (apoB-100 mediated), 30 the mechanism of the protection against obesity in the setting of high levels of apoC-I and in the setting of absent VLDL receptor could be similar.	bind
28471	2	7532	5	13	NULL	NULL	NULL	apoE	GP		mediate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_117	12231568	29 In consideration of the repeated observation that apoC-I interferes with the binding of VLDL to the VLDL receptor (apoE mediated) but not with the binding of VLDL to the LDL receptor (apoB-100 mediated), 30 the mechanism of the protection against obesity in the setting of high levels of apoC-I and in the setting of absent VLDL receptor could be similar.	bind
28478	4	7532	5	13	NULL	NULL	NULL	apoB-100	GP		mediate					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_117	12231568	29 In consideration of the repeated observation that apoC-I interferes with the binding of VLDL to the VLDL receptor (apoE mediated) but not with the binding of VLDL to the LDL receptor (apoB-100 mediated), 30 the mechanism of the protection against obesity in the setting of high levels of apoC-I and in the setting of absent VLDL receptor could be similar.	bind
28479	5	7532	5	13	NULL	NULL	NULL	apoC-I	GP		does not interfere with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_117	12231568	29 In consideration of the repeated observation that apoC-I interferes with the binding of VLDL to the VLDL receptor (apoE mediated) but not with the binding of VLDL to the LDL receptor (apoB-100 mediated), 30 the mechanism of the protection against obesity in the setting of high levels of apoC-I and in the setting of absent VLDL receptor could be similar.	bind
54540	6	7532	5	13	NULL	NULL	NULL	VLDL	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_117	12231568	29 In consideration of the repeated observation that apoC-I interferes with the binding of VLDL to the VLDL receptor (apoE mediated) but not with the binding of VLDL to the LDL receptor (apoB-100 mediated), 30 the mechanism of the protection against obesity in the setting of high levels of apoC-I and in the setting of absent VLDL receptor could be similar.	bind
30917	1	7532	7	NULL	NULL	0	NULL	VLDL	NULL		binds	NULL				VLDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_117	12231568	29 In consideration of the repeated observation that apoC-I interferes with the binding of VLDL to the VLDL receptor (apoE mediated) but not with the binding of VLDL to the LDL receptor (apoB-100 mediated), 30 the mechanism of the protection against obesity in the setting of high levels of apoC-I and in the setting of absent VLDL receptor could be similar.	bind
30918	2	7532	7	NULL	NULL	0	NULL	apoE	NULL		mediates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_117	12231568	29 In consideration of the repeated observation that apoC-I interferes with the binding of VLDL to the VLDL receptor (apoE mediated) but not with the binding of VLDL to the LDL receptor (apoB-100 mediated), 30 the mechanism of the protection against obesity in the setting of high levels of apoC-I and in the setting of absent VLDL receptor could be similar.	bind
30919	3	7532	7	NULL	NULL	0	NULL	apoC-I	NULL		interferes with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_117	12231568	29 In consideration of the repeated observation that apoC-I interferes with the binding of VLDL to the VLDL receptor (apoE mediated) but not with the binding of VLDL to the LDL receptor (apoB-100 mediated), 30 the mechanism of the protection against obesity in the setting of high levels of apoC-I and in the setting of absent VLDL receptor could be similar.	bind
30920	4	7532	7	NULL	NULL	0	NULL	VLDL	NULL		binds	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_117	12231568	29 In consideration of the repeated observation that apoC-I interferes with the binding of VLDL to the VLDL receptor (apoE mediated) but not with the binding of VLDL to the LDL receptor (apoB-100 mediated), 30 the mechanism of the protection against obesity in the setting of high levels of apoC-I and in the setting of absent VLDL receptor could be similar.	bind
30922	5	7532	7	NULL	NULL	0	NULL	apoB-100	NULL		mediates	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_117	12231568	29 In consideration of the repeated observation that apoC-I interferes with the binding of VLDL to the VLDL receptor (apoE mediated) but not with the binding of VLDL to the LDL receptor (apoB-100 mediated), 30 the mechanism of the protection against obesity in the setting of high levels of apoC-I and in the setting of absent VLDL receptor could be similar.	bind
30924	6	7532	7	NULL	NULL	0	NULL	apoC-I 	NULL		does not interfere with	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1470_s_117	12231568	29 In consideration of the repeated observation that apoC-I interferes with the binding of VLDL to the VLDL receptor (apoE mediated) but not with the binding of VLDL to the LDL receptor (apoB-100 mediated), 30 the mechanism of the protection against obesity in the setting of high levels of apoC-I and in the setting of absent VLDL receptor could be similar.	bind
28465	1	7534	5	13	NULL	NULL	NULL			deletion of	inhibit				promoter region with AP-1-like site	bFGF	GP	effect of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_855_s_188	12006402	29 In the present study, deletion of the promoter region containing an AP-1-like site inhibited the effect of bFGF, and EMSA suggested that fenofibric acid did not inhibit nuclear translocation or DNA binding of the Ets-1-like transcription factor to the PAI-1 promoter.	bind
28466	2	7534	5	13	NULL	NULL	NULL	fenofibric acid	Chemical		does not inhibit					nuclear translocation	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_855_s_188	12006402	29 In the present study, deletion of the promoter region containing an AP-1-like site inhibited the effect of bFGF, and EMSA suggested that fenofibric acid did not inhibit nuclear translocation or DNA binding of the Ets-1-like transcription factor to the PAI-1 promoter.	bind
28467	3	7534	5	13	NULL	NULL	NULL	Ets-1-like transcription factor	GP		bind					PAI-1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_855_s_188	12006402	29 In the present study, deletion of the promoter region containing an AP-1-like site inhibited the effect of bFGF, and EMSA suggested that fenofibric acid did not inhibit nuclear translocation or DNA binding of the Ets-1-like transcription factor to the PAI-1 promoter.	bind
28468	4	7534	5	13	NULL	NULL	NULL	fenofibric acid	Chemical		does not inhibit					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_855_s_188	12006402	29 In the present study, deletion of the promoter region containing an AP-1-like site inhibited the effect of bFGF, and EMSA suggested that fenofibric acid did not inhibit nuclear translocation or DNA binding of the Ets-1-like transcription factor to the PAI-1 promoter.	bind
30927	1	7534	7	NULL	NULL	0	NULL		NULL	deletion of	inhibits	NULL			AP-1-like site promoter region	bFGF	NULL	effect of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_855_s_188	12006402	29 In the present study, deletion of the promoter region containing an AP-1-like site inhibited the effect of bFGF, and EMSA suggested that fenofibric acid did not inhibit nuclear translocation or DNA binding of the Ets-1-like transcription factor to the PAI-1 promoter.	bind
30928	2	7534	7	NULL	NULL	0	NULL	Ets-1-like transcription factor 	NULL		bind	NULL				PAI-1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_855_s_188	12006402	29 In the present study, deletion of the promoter region containing an AP-1-like site inhibited the effect of bFGF, and EMSA suggested that fenofibric acid did not inhibit nuclear translocation or DNA binding of the Ets-1-like transcription factor to the PAI-1 promoter.	bind
30929	3	7534	7	NULL	NULL	0	NULL	fenofibric acid	NULL		does not inhibit	NULL				statement 2	NULL	nuclear translocation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_855_s_188	12006402	29 In the present study, deletion of the promoter region containing an AP-1-like site inhibited the effect of bFGF, and EMSA suggested that fenofibric acid did not inhibit nuclear translocation or DNA binding of the Ets-1-like transcription factor to the PAI-1 promoter.	bind
30930	4	7534	7	NULL	NULL	0	NULL	fenofibric acid	NULL		does not inhibit	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_5_855_s_188	12006402	29 In the present study, deletion of the promoter region containing an AP-1-like site inhibited the effect of bFGF, and EMSA suggested that fenofibric acid did not inhibit nuclear translocation or DNA binding of the Ets-1-like transcription factor to the PAI-1 promoter.	bind
31549	1	7535	5	13	NULL	NULL	NULL	TNF-alpha	GP	soluble	associates with					p75 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_3_933_s_165	12598326	29 The fast association/dissociation kinetics of soluble TNF-alpha with the p75 receptor is thought to create an increase in the local concentration of the cytokine in the proximity of the cell membrane, thus potentially augmenting soluble TNF-alpha binding to the p55 receptor.	bind
31550	2	7535	5	13	NULL	NULL	NULL	TNF-alpha	GP	soluble	dissociates with					p75 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_3_933_s_165	12598326	29 The fast association/dissociation kinetics of soluble TNF-alpha with the p75 receptor is thought to create an increase in the local concentration of the cytokine in the proximity of the cell membrane, thus potentially augmenting soluble TNF-alpha binding to the p55 receptor.	bind
31551	3	7535	5	13	NULL	NULL	NULL	statement 6	Process	kinetics of	increases					cytokine	GP	local concentration of			NULL	proximity of cell membrane	NULL	NULL	NULL	NULL	gw60_amjpathol_162_3_933_s_165	12598326	29 The fast association/dissociation kinetics of soluble TNF-alpha with the p75 receptor is thought to create an increase in the local concentration of the cytokine in the proximity of the cell membrane, thus potentially augmenting soluble TNF-alpha binding to the p55 receptor.	bind
31552	4	7535	5	13	NULL	NULL	NULL	TNF-alpha	GP		bind					p55 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_3_933_s_165	12598326	29 The fast association/dissociation kinetics of soluble TNF-alpha with the p75 receptor is thought to create an increase in the local concentration of the cytokine in the proximity of the cell membrane, thus potentially augmenting soluble TNF-alpha binding to the p55 receptor.	bind
31553	5	7535	5	13	NULL	NULL	NULL	statement 3	Process		augments		potentially			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_3_933_s_165	12598326	29 The fast association/dissociation kinetics of soluble TNF-alpha with the p75 receptor is thought to create an increase in the local concentration of the cytokine in the proximity of the cell membrane, thus potentially augmenting soluble TNF-alpha binding to the p55 receptor.	bind
54541	6	7535	5	13	NULL	NULL	NULL	statement 1	Process		occurs along with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_3_933_s_165	12598326	29 The fast association/dissociation kinetics of soluble TNF-alpha with the p75 receptor is thought to create an increase in the local concentration of the cytokine in the proximity of the cell membrane, thus potentially augmenting soluble TNF-alpha binding to the p55 receptor.	bind
30934	1	7535	7	NULL	NULL	0	NULL	TNF-alpha	NULL	soluble	associate with	NULL				p75 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_162_3_933_s_165	12598326	29 The fast association/dissociation kinetics of soluble TNF-alpha with the p75 receptor is thought to create an increase in the local concentration of the cytokine in the proximity of the cell membrane, thus potentially augmenting soluble TNF-alpha binding to the p55 receptor.	bind
30935	3	7535	7	10	NULL	0	NULL	statement 6		kinetics of	increase					cytokine		local concentration of			NULL	proximity of cell membrane	NULL	NULL	NULL	NULL	gw60_amjpathol_162_3_933_s_165	12598326	29 The fast association/dissociation kinetics of soluble TNF-alpha with the p75 receptor is thought to create an increase in the local concentration of the cytokine in the proximity of the cell membrane, thus potentially augmenting soluble TNF-alpha binding to the p55 receptor.	bind
30937	2	7535	7	10	NULL	0	NULL	TNF-alpha		soluble	dissociates with					p75 receptor					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_3_933_s_165	12598326	29 The fast association/dissociation kinetics of soluble TNF-alpha with the p75 receptor is thought to create an increase in the local concentration of the cytokine in the proximity of the cell membrane, thus potentially augmenting soluble TNF-alpha binding to the p55 receptor.	bind
30941	4	7535	7	NULL	NULL	0	NULL	TNF-alpha	NULL	soluble	binds	NULL				p55 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_162_3_933_s_165	12598326	29 The fast association/dissociation kinetics of soluble TNF-alpha with the p75 receptor is thought to create an increase in the local concentration of the cytokine in the proximity of the cell membrane, thus potentially augmenting soluble TNF-alpha binding to the p55 receptor.	bind
30943	5	7535	7	NULL	NULL	0	NULL	statement 2	NULL		augments	NULL	potentially			statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_3_933_s_165	12598326	29 The fast association/dissociation kinetics of soluble TNF-alpha with the p75 receptor is thought to create an increase in the local concentration of the cytokine in the proximity of the cell membrane, thus potentially augmenting soluble TNF-alpha binding to the p55 receptor.	bind
54542	6	7535	7	10	NULL	0	NULL	statement 1			occurs along with					statement 2					NULL		0	NULL	NULL	NULL	gw60_amjpathol_162_3_933_s_165	12598326	29 The fast association/dissociation kinetics of soluble TNF-alpha with the p75 receptor is thought to create an increase in the local concentration of the cytokine in the proximity of the cell membrane, thus potentially augmenting soluble TNF-alpha binding to the p55 receptor.	bind
28482	1	7536	5	13	NULL	NULL	NULL	estrogen	Chemical	consensus sites for	is present in					betaine homocysteine methyltransferase gene	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_301_s_142	14699020	29 The presence of consensus sites for steroid hormones, including estrogen and androgen binding sites, in the human betaine homocysteine methyltransferase gene 30 may represent a molecular basis of sex steroid effects on plasma betaine.	bind
28483	2	7536	5	13	NULL	NULL	NULL	androgen	Chemical	consensus sites for	is present in					betaine homocysteine methyltransferase gene	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_301_s_142	14699020	29 The presence of consensus sites for steroid hormones, including estrogen and androgen binding sites, in the human betaine homocysteine methyltransferase gene 30 may represent a molecular basis of sex steroid effects on plasma betaine.	bind
28484	3	7536	5	13	NULL	NULL	NULL	estrogen	Chemical		is a type of					steroid hormone	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_301_s_142	14699020	29 The presence of consensus sites for steroid hormones, including estrogen and androgen binding sites, in the human betaine homocysteine methyltransferase gene 30 may represent a molecular basis of sex steroid effects on plasma betaine.	bind
28485	4	7536	5	13	NULL	NULL	NULL	androgen	Chemical		is a type of					steroid hormone	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_301_s_142	14699020	29 The presence of consensus sites for steroid hormones, including estrogen and androgen binding sites, in the human betaine homocysteine methyltransferase gene 30 may represent a molecular basis of sex steroid effects on plasma betaine.	bind
28486	5	7536	5	13	NULL	NULL	NULL	sex steroid	Chemical		effects					betaine	Chemical	plasma			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_301_s_142	14699020	29 The presence of consensus sites for steroid hormones, including estrogen and androgen binding sites, in the human betaine homocysteine methyltransferase gene 30 may represent a molecular basis of sex steroid effects on plasma betaine.	bind
28487	6	7536	5	13	NULL	NULL	NULL	statement 1	Process		represents		may			statement 5	Process	molecular basis of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_301_s_142	14699020	29 The presence of consensus sites for steroid hormones, including estrogen and androgen binding sites, in the human betaine homocysteine methyltransferase gene 30 may represent a molecular basis of sex steroid effects on plasma betaine.	bind
28488	7	7536	5	13	NULL	NULL	NULL	statement 2	Process		represents		may			statement 5	Process	molecular basis of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_301_s_142	14699020	29 The presence of consensus sites for steroid hormones, including estrogen and androgen binding sites, in the human betaine homocysteine methyltransferase gene 30 may represent a molecular basis of sex steroid effects on plasma betaine.	bind
30946	1	7536	7	NULL	NULL	0	NULL	betaine homocysteine methyltransferase gene	NULL	human	consist of	NULL					NULL			estrogen binding site	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_301_s_142	14699020	29 The presence of consensus sites for steroid hormones, including estrogen and androgen binding sites, in the human betaine homocysteine methyltransferase gene 30 may represent a molecular basis of sex steroid effects on plasma betaine.	bind
30947	2	7536	7	NULL	NULL	0	NULL	betaine homocysteine methyltransferase gene	NULL	human	consist of	NULL					NULL			androgen binding site	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_301_s_142	14699020	29 The presence of consensus sites for steroid hormones, including estrogen and androgen binding sites, in the human betaine homocysteine methyltransferase gene 30 may represent a molecular basis of sex steroid effects on plasma betaine.	bind
30954	3	7536	7	10	NULL	0	NULL	sex steroid			affects					betaine		plasma			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_301_s_142	14699020	29 The presence of consensus sites for steroid hormones, including estrogen and androgen binding sites, in the human betaine homocysteine methyltransferase gene 30 may represent a molecular basis of sex steroid effects on plasma betaine.	bind
30955	5	7536	7	10	NULL	0	NULL	statement 1	NULL		represents	NULL				statement 3	NULL	molecular basis of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_301_s_142	14699020	29 The presence of consensus sites for steroid hormones, including estrogen and androgen binding sites, in the human betaine homocysteine methyltransferase gene 30 may represent a molecular basis of sex steroid effects on plasma betaine.	bind
46656	4	7536	7	10	NULL	0	NULL	statement 2	NULL		represents	NULL				statement 3	NULL	molecular basis of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_301_s_142	14699020	29 The presence of consensus sites for steroid hormones, including estrogen and androgen binding sites, in the human betaine homocysteine methyltransferase gene 30 may represent a molecular basis of sex steroid effects on plasma betaine.	bind
54543	6	7536	7	10	NULL	0	NULL	estrogen			is a type of					steroid hormone					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_301_s_142	14699020	29 The presence of consensus sites for steroid hormones, including estrogen and androgen binding sites, in the human betaine homocysteine methyltransferase gene 30 may represent a molecular basis of sex steroid effects on plasma betaine.	bind
54544	7	7536	7	10	NULL	0	NULL	androgen			is a type of					steroid hormone					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_2_301_s_142	14699020	29 The presence of consensus sites for steroid hormones, including estrogen and androgen binding sites, in the human betaine homocysteine methyltransferase gene 30 may represent a molecular basis of sex steroid effects on plasma betaine.	bind
28489	1	7537	5	13	NULL	NULL	NULL	c-Src	GP		bind		specifically;;directly	SH2 domain		EGFR	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_8335_s_267	10075741	29,  49, and  50) demonstrate that the c-Src SH2 domain can bind activated EGFR specifically and directly, suggesting that recruitment of other tyrosine kinases is not necessary to mediate the phosphorylation of Tyr845.	bind
28490	2	7537	5	13	NULL	NULL	NULL	tyrosine kinases	GP	recruitment of 	is not necessary to							mediate phosphorylation of 	Tyr845		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_8335_s_267	10075741	29,  49, and  50) demonstrate that the c-Src SH2 domain can bind activated EGFR specifically and directly, suggesting that recruitment of other tyrosine kinases is not necessary to mediate the phosphorylation of Tyr845.	bind
30957	1	7537	7	NULL	NULL	0	NULL	c-Src	NULL		bind	NULL	directly;;specifically	SH2 domain		EGFR	NULL	activated			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_12_8335_s_267	10075741	29,  49, and  50) demonstrate that the c-Src SH2 domain can bind activated EGFR specifically and directly, suggesting that recruitment of other tyrosine kinases is not necessary to mediate the phosphorylation of Tyr845.	bind
30959	2	7537	7	NULL	NULL	0	NULL	tyrosine kinases	NULL	recruitment of	does not mediate	NULL					NULL	phosphorylation of	Tyr845		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_12_8335_s_267	10075741	29,  49, and  50) demonstrate that the c-Src SH2 domain can bind activated EGFR specifically and directly, suggesting that recruitment of other tyrosine kinases is not necessary to mediate the phosphorylation of Tyr845.	bind
30962	3	7537	7	NULL	NULL	0	NULL	statement 1	NULL		suggests	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_12_8335_s_267	10075741	29,  49, and  50) demonstrate that the c-Src SH2 domain can bind activated EGFR specifically and directly, suggesting that recruitment of other tyrosine kinases is not necessary to mediate the phosphorylation of Tyr845.	bind
28491	1	7538	5	13	NULL	NULL	NULL	c-src	GP		bind					SHP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1367_s_23	10329590	29, 30, 34  hosphorylation of these tyrosine residues mediates binding of c-src and the phosphatase SHP-2, which have been implicated in mediating a variety of signaling events.	bind
28492	2	7538	5	13	NULL	NULL	NULL	SHP-2	GP		is a type of					phosphatase	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1367_s_23	10329590	29, 30, 34  hosphorylation of these tyrosine residues mediates binding of c-src and the phosphatase SHP-2, which have been implicated in mediating a variety of signaling events.	bind
28493	3	7538	5	13	NULL	NULL	NULL			phosphorylation of	mediate			tyrosine residues		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1367_s_23	10329590	29, 30, 34  hosphorylation of these tyrosine residues mediates binding of c-src and the phosphatase SHP-2, which have been implicated in mediating a variety of signaling events.	bind
28494	4	7538	5	13	NULL	NULL	NULL	statement 1	Process		mediate					signaling events	Process	variety of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1367_s_23	10329590	29, 30, 34  hosphorylation of these tyrosine residues mediates binding of c-src and the phosphatase SHP-2, which have been implicated in mediating a variety of signaling events.	bind
30967	1	7538	7	NULL	NULL	0	NULL	 c-src	NULL		bind	NULL				SHP-2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_5_1367_s_23	10329590	29, 30, 34  hosphorylation of these tyrosine residues mediates binding of c-src and the phosphatase SHP-2, which have been implicated in mediating a variety of signaling events.	bind
30969	2	7538	7	NULL	NULL	0	NULL		NULL	phosphorylation of	mediates	NULL		tyrosine residues		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_5_1367_s_23	10329590	29, 30, 34  hosphorylation of these tyrosine residues mediates binding of c-src and the phosphatase SHP-2, which have been implicated in mediating a variety of signaling events.	bind
30970	3	7538	7	NULL	NULL	0	NULL	SHP-2	NULL		is a type of	NULL				phosphatase	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_5_1367_s_23	10329590	29, 30, 34  hosphorylation of these tyrosine residues mediates binding of c-src and the phosphatase SHP-2, which have been implicated in mediating a variety of signaling events.	bind
30972	4	7538	7	NULL	NULL	0	NULL	statement 1	NULL		mediates	NULL				signaling events	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_5_1367_s_23	10329590	29, 30, 34  hosphorylation of these tyrosine residues mediates binding of c-src and the phosphatase SHP-2, which have been implicated in mediating a variety of signaling events.	bind
28495	1	7539	5	13	NULL	NULL	NULL	C/EBPbeta	GP		bind					CRP	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_904_s_77	15731497	29,30  p50 enhanced and stabilized the binding of C/EBPbeta to the CRP promoter and p50 and C/EBPbeta binding sites in the promoter were necessary for full induction of the gene.	bind
28496	2	7539	5	13	NULL	NULL	NULL	p50	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_904_s_77	15731497	29,30  p50 enhanced and stabilized the binding of C/EBPbeta to the CRP promoter and p50 and C/EBPbeta binding sites in the promoter were necessary for full induction of the gene.	bind
28497	3	7539	5	13	NULL	NULL	NULL	p50	GP		stabilizes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_904_s_77	15731497	29,30  p50 enhanced and stabilized the binding of C/EBPbeta to the CRP promoter and p50 and C/EBPbeta binding sites in the promoter were necessary for full induction of the gene.	bind
28498	4	7539	5	13	NULL	NULL	NULL	CRP	GP		is necessary for				C/EBPbeta binding sites in promoter	CRP gene	GP	full induction of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_904_s_77	15731497	29,30  p50 enhanced and stabilized the binding of C/EBPbeta to the CRP promoter and p50 and C/EBPbeta binding sites in the promoter were necessary for full induction of the gene.	bind
28499	5	7539	5	13	NULL	NULL	NULL	CRP	GP		is necessary for				p50 binding sites in promoter	CRP gene	GP	full induction of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_904_s_77	15731497	29,30  p50 enhanced and stabilized the binding of C/EBPbeta to the CRP promoter and p50 and C/EBPbeta binding sites in the promoter were necessary for full induction of the gene.	bind
30975	1	7539	7	NULL	NULL	0	NULL	C/EBPbeta	NULL		binds to	NULL				CRP 	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_904_s_77	15731497	29,30  p50 enhanced and stabilized the binding of C/EBPbeta to the CRP promoter and p50 and C/EBPbeta binding sites in the promoter were necessary for full induction of the gene.	bind
30976	2	7539	7	NULL	NULL	0	NULL	p50	NULL		enhance	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_904_s_77	15731497	29,30  p50 enhanced and stabilized the binding of C/EBPbeta to the CRP promoter and p50 and C/EBPbeta binding sites in the promoter were necessary for full induction of the gene.	bind
30977	3	7539	7	NULL	NULL	0	NULL	p50	NULL		stabilize	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_904_s_77	15731497	29,30  p50 enhanced and stabilized the binding of C/EBPbeta to the CRP promoter and p50 and C/EBPbeta binding sites in the promoter were necessary for full induction of the gene.	bind
30978	4	7539	7	NULL	NULL	0	NULL		NULL		is necessary for	NULL			p50 binding site	CRP gene	NULL	full induction of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_904_s_77	15731497	29,30  p50 enhanced and stabilized the binding of C/EBPbeta to the CRP promoter and p50 and C/EBPbeta binding sites in the promoter were necessary for full induction of the gene.	bind
30979	5	7539	7	NULL	NULL	0	NULL		NULL		is necessary for	NULL			C/EBPbeta binding site	CRP gene	NULL	full induction of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_904_s_77	15731497	29,30  p50 enhanced and stabilized the binding of C/EBPbeta to the CRP promoter and p50 and C/EBPbeta binding sites in the promoter were necessary for full induction of the gene.	bind
28500	1	7540	5	13	NULL	NULL	NULL	annexin V	GP		bind					PS	Chemical				NULL	on the surface of a Ca2+ ionophore-stimulated cell	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_456_s_61	16397140	29,32 - 35     Furthermore, the binding of annexin V to PS on the surface of a Ca2+ ionophore-stimulated cell inhibits the expression of decrypted TF PCA. 23 Therefore, the loss of PS asymmetry appears to be connected to the process of TF decryption.	bind
28501	2	7540	5	13	NULL	NULL	NULL	statement 1	Process		inhibit					TF PCA	Process	expression of;;decrypted			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_456_s_61	16397140	29,32 - 35     Furthermore, the binding of annexin V to PS on the surface of a Ca2+ ionophore-stimulated cell inhibits the expression of decrypted TF PCA. 23 Therefore, the loss of PS asymmetry appears to be connected to the process of TF decryption.	bind
28502	3	7540	5	13	NULL	NULL	NULL	PS asymmetry	Process	loss of	is connected to		appears			TF decryption	Process	process of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_456_s_61	16397140	29,32 - 35     Furthermore, the binding of annexin V to PS on the surface of a Ca2+ ionophore-stimulated cell inhibits the expression of decrypted TF PCA. 23 Therefore, the loss of PS asymmetry appears to be connected to the process of TF decryption.	bind
30980	1	7540	7	NULL	NULL	0	NULL	annexin V	NULL		binds to	NULL				PS	NULL				NULL	surface of a Ca2+ ionophore-stimulated cell	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_456_s_61	16397140	29,32 - 35     Furthermore, the binding of annexin V to PS on the surface of a Ca2+ ionophore-stimulated cell inhibits the expression of decrypted TF PCA. 23 Therefore, the loss of PS asymmetry appears to be connected to the process of TF decryption.	bind
30981	2	7540	7	NULL	NULL	0	NULL	Ca2+ ionophore	NULL		stimulates	NULL				cell	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_456_s_61	16397140	29,32 - 35     Furthermore, the binding of annexin V to PS on the surface of a Ca2+ ionophore-stimulated cell inhibits the expression of decrypted TF PCA. 23 Therefore, the loss of PS asymmetry appears to be connected to the process of TF decryption.	bind
30982	3	7540	7	10	NULL	0	NULL	statement 1			inhibits					TF PCA		expression of;;decrypted			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_456_s_61	16397140	29,32 - 35     Furthermore, the binding of annexin V to PS on the surface of a Ca2+ ionophore-stimulated cell inhibits the expression of decrypted TF PCA. 23 Therefore, the loss of PS asymmetry appears to be connected to the process of TF decryption.	bind
30984	4	7540	7	NULL	NULL	0	NULL	PS asymmetry	NULL	loss of	is connected to	NULL				TF decryption	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_456_s_61	16397140	29,32 - 35     Furthermore, the binding of annexin V to PS on the surface of a Ca2+ ionophore-stimulated cell inhibits the expression of decrypted TF PCA. 23 Therefore, the loss of PS asymmetry appears to be connected to the process of TF decryption.	bind
28503	1	7541	5	13	NULL	NULL	NULL				bind		high affinity	nebulin repeats		actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_67	14976140	29,34  The nebulin repeats bind actin with high affinity, but there is also evidence that nebulette motifs bind troponin T and tropomyosin.	bind
28504	2	7541	5	13	NULL	NULL	NULL				bind			nebulette motifs		troponin T	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_67	14976140	29,34  The nebulin repeats bind actin with high affinity, but there is also evidence that nebulette motifs bind troponin T and tropomyosin.	bind
28505	3	7541	5	13	NULL	NULL	NULL				bind			nebulette motifs		tropomyosin	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_67	14976140	29,34  The nebulin repeats bind actin with high affinity, but there is also evidence that nebulette motifs bind troponin T and tropomyosin.	bind
30985	1	7541	7	NULL	NULL	0	NULL		NULL		bind	NULL	high affinity	nebulin repeats		actin	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_67	14976140	29,34  The nebulin repeats bind actin with high affinity, but there is also evidence that nebulette motifs bind troponin T and tropomyosin.	bind
30986	2	7541	7	NULL	NULL	0	NULL		NULL		bind	NULL		nebulette motifs		troponin T	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_67	14976140	29,34  The nebulin repeats bind actin with high affinity, but there is also evidence that nebulette motifs bind troponin T and tropomyosin.	bind
30987	3	7541	7	NULL	NULL	0	NULL		NULL		bind	NULL		nebulette motifs		tropomyosin	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_67	14976140	29,34  The nebulin repeats bind actin with high affinity, but there is also evidence that nebulette motifs bind troponin T and tropomyosin.	bind
28507	1	7542	5	13	NULL	NULL	NULL	Platelet P-selectin	GP		bind					PSGL-1	GP				NULL	on neutrophils	NULL	NULL	NULL	NULL	gw70_circulation_110_17_2713_s_200	15492312	29,40  Platelet P-selectin binding to PSGL-1 on neutrophils mediates initial tethering, followed by their firm adhesion dependent on CD11b/CD18 (Mac-1) binding to GPIbalpha 41 and/or junctional adhesion molecule-3.	bind
28508	2	7542	5	13	NULL	NULL	NULL	statement 1	Process		mediate					tethering	Process	initial			NULL	neutrophils	NULL	NULL	NULL	NULL	gw70_circulation_110_17_2713_s_200	15492312	29,40  Platelet P-selectin binding to PSGL-1 on neutrophils mediates initial tethering, followed by their firm adhesion dependent on CD11b/CD18 (Mac-1) binding to GPIbalpha 41 and/or junctional adhesion molecule-3.	bind
28509	3	7542	5	13	NULL	NULL	NULL	Mac-1	GP		is					CD11b/CD18	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_17_2713_s_200	15492312	29,40  Platelet P-selectin binding to PSGL-1 on neutrophils mediates initial tethering, followed by their firm adhesion dependent on CD11b/CD18 (Mac-1) binding to GPIbalpha 41 and/or junctional adhesion molecule-3.	bind
28510	4	7542	5	13	NULL	NULL	NULL	Mac-1	GP		bind					GPIbalpha 41	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_17_2713_s_200	15492312	29,40  Platelet P-selectin binding to PSGL-1 on neutrophils mediates initial tethering, followed by their firm adhesion dependent on CD11b/CD18 (Mac-1) binding to GPIbalpha 41 and/or junctional adhesion molecule-3.	bind
28511	5	7542	5	13	NULL	NULL	NULL	Mac-1	GP		bind					junctional adhesion molecule-3	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_17_2713_s_200	15492312	29,40  Platelet P-selectin binding to PSGL-1 on neutrophils mediates initial tethering, followed by their firm adhesion dependent on CD11b/CD18 (Mac-1) binding to GPIbalpha 41 and/or junctional adhesion molecule-3.	bind
28512	6	7542	5	13	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_17_2713_s_200	15492312	29,40  Platelet P-selectin binding to PSGL-1 on neutrophils mediates initial tethering, followed by their firm adhesion dependent on CD11b/CD18 (Mac-1) binding to GPIbalpha 41 and/or junctional adhesion molecule-3.	bind
28514	7	7542	5	13	NULL	NULL	NULL	statement 1	Process		is followed by					adhesion	Process	firm			NULL	neutrophils	NULL	NULL	NULL	NULL	gw70_circulation_110_17_2713_s_200	15492312	29,40  Platelet P-selectin binding to PSGL-1 on neutrophils mediates initial tethering, followed by their firm adhesion dependent on CD11b/CD18 (Mac-1) binding to GPIbalpha 41 and/or junctional adhesion molecule-3.	bind
28515	8	7542	5	13	NULL	NULL	NULL	adhesion	Process	firm	is dependent on					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_17_2713_s_200	15492312	29,40  Platelet P-selectin binding to PSGL-1 on neutrophils mediates initial tethering, followed by their firm adhesion dependent on CD11b/CD18 (Mac-1) binding to GPIbalpha 41 and/or junctional adhesion molecule-3.	bind
28516	9	7542	5	13	NULL	NULL	NULL	adhesion	Process	firm	is dependent on					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_17_2713_s_200	15492312	29,40  Platelet P-selectin binding to PSGL-1 on neutrophils mediates initial tethering, followed by their firm adhesion dependent on CD11b/CD18 (Mac-1) binding to GPIbalpha 41 and/or junctional adhesion molecule-3.	bind
28517	10	7542	5	13	NULL	NULL	NULL	statement 8	Process		is an alternative to					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_17_2713_s_200	15492312	29,40  Platelet P-selectin binding to PSGL-1 on neutrophils mediates initial tethering, followed by their firm adhesion dependent on CD11b/CD18 (Mac-1) binding to GPIbalpha 41 and/or junctional adhesion molecule-3.	bind
30990	1	7542	7	NULL	NULL	0	NULL	Platelet P-selectin	NULL		binds	NULL				PSGL-1 	NULL				NULL	neutrophils	0	NULL	NULL	NULL	gw70_circulation_110_17_2713_s_200	15492312	29,40  Platelet P-selectin binding to PSGL-1 on neutrophils mediates initial tethering, followed by their firm adhesion dependent on CD11b/CD18 (Mac-1) binding to GPIbalpha 41 and/or junctional adhesion molecule-3.	bind
30993	2	7542	7	NULL	NULL	0	NULL	statement 1	NULL		mediates	NULL				initial tethering	NULL				NULL	neutrophils	NULL	NULL	NULL	NULL	gw70_circulation_110_17_2713_s_200	15492312	29,40  Platelet P-selectin binding to PSGL-1 on neutrophils mediates initial tethering, followed by their firm adhesion dependent on CD11b/CD18 (Mac-1) binding to GPIbalpha 41 and/or junctional adhesion molecule-3.	bind
30995	3	7542	7	NULL	NULL	0	NULL	CD11b/CD18 (Mac-1)	NULL		binds to	NULL				GPIbalpha 41 	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_110_17_2713_s_200	15492312	29,40  Platelet P-selectin binding to PSGL-1 on neutrophils mediates initial tethering, followed by their firm adhesion dependent on CD11b/CD18 (Mac-1) binding to GPIbalpha 41 and/or junctional adhesion molecule-3.	bind
30997	4	7542	7	NULL	NULL	0	NULL	CD11b/CD18 (Mac-1)	NULL		binds to	NULL				junctional adhesion molecule-3	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_110_17_2713_s_200	15492312	29,40  Platelet P-selectin binding to PSGL-1 on neutrophils mediates initial tethering, followed by their firm adhesion dependent on CD11b/CD18 (Mac-1) binding to GPIbalpha 41 and/or junctional adhesion molecule-3.	bind
31000	5	7542	7	NULL	NULL	0	NULL	statement 3	NULL		is an alternative to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_110_17_2713_s_200	15492312	29,40  Platelet P-selectin binding to PSGL-1 on neutrophils mediates initial tethering, followed by their firm adhesion dependent on CD11b/CD18 (Mac-1) binding to GPIbalpha 41 and/or junctional adhesion molecule-3.	bind
31003	6	7542	7	10	NULL	0	NULL	statement 1			mediates					adhesion		firm			NULL	neutrophils	NULL	NULL	NULL	NULL	gw70_circulation_110_17_2713_s_200	15492312	29,40  Platelet P-selectin binding to PSGL-1 on neutrophils mediates initial tethering, followed by their firm adhesion dependent on CD11b/CD18 (Mac-1) binding to GPIbalpha 41 and/or junctional adhesion molecule-3.	bind
31004	7	7542	7	NULL	NULL	0	NULL	statement 6	NULL		depends on	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_110_17_2713_s_200	15492312	29,40  Platelet P-selectin binding to PSGL-1 on neutrophils mediates initial tethering, followed by their firm adhesion dependent on CD11b/CD18 (Mac-1) binding to GPIbalpha 41 and/or junctional adhesion molecule-3.	bind
31006	8	7542	7	NULL	NULL	0	NULL	statement 6	NULL		depends on	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_110_17_2713_s_200	15492312	29,40  Platelet P-selectin binding to PSGL-1 on neutrophils mediates initial tethering, followed by their firm adhesion dependent on CD11b/CD18 (Mac-1) binding to GPIbalpha 41 and/or junctional adhesion molecule-3.	bind
28520	1	7545	5	13	NULL	NULL	NULL	CTx PnIB	GP		bind					surface receptors	GP				NULL	HEK cells transfected with high affinity alpha7/5HT-3 cDNA	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_7_4889_s_135	10671525	293 HEK cells were transfected with high affinity alpha7/5HT-3 (see text) and mutant alpha7/5HT-3 subunit cDNAs, and binding of CTx PnIB to the resulting surface receptors was determined as described under	bind
31037	1	7545	7	NULL	NULL	0	NULL	CTx PnIB	NULL		bind	NULL				surface receptor	NULL				NULL	HEK cells transfected with high affinity alpha7/5HT-3 cDNA	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_7_4889_s_135	10671525	293 HEK cells were transfected with high affinity alpha7/5HT-3 (see text) and mutant alpha7/5HT-3 subunit cDNAs, and binding of CTx PnIB to the resulting surface receptors was determined as described under	bind
28523	1	7546	5	13	NULL	NULL	NULL	CTx ImI	GP		bind					surface receptors	GP				NULL	HEK cells transfected with high affinity alpha7/5HT-3 cDNA	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_28_19517_s_111	10391883	293 HEK cells were transfected with wild-type and mutant alpha7/5HT-3 subunit cDNAs and binding of CTx ImI to the resulting surface receptors was determined as described under	bind
31040	1	7546	7	NULL	NULL	0	NULL	CTx ImI 	NULL		bind	NULL				surface receptor	NULL				NULL	HEK cells transfected with wild-type alpha7/5HT-3 subunit cDNA	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_28_19517_s_111	10391883	293 HEK cells were transfected with wild-type and mutant alpha7/5HT-3 subunit cDNAs and binding of CTx ImI to the resulting surface receptors was determined as described under	bind
28524	1	7549	5	13	NULL	NULL	NULL	guanine nucleotides	NucleicAcid		bind					G proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_20020_s_81	10777492	293T cells expressing GST-tagged G proteins and GEFs were labeled with 32Pi, and guanine nucleotides bound to G proteins were analyzed by TLC.	bind
31047	1	7549	7	10	NULL	0	NULL	guanine nucleotides			bind					G proteins					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_20020_s_81	10777492	293T cells expressing GST-tagged G proteins and GEFs were labeled with 32Pi, and guanine nucleotides bound to G proteins were analyzed by TLC.	bind
28526	1	7556	5	13	NULL	NULL	NULL	alphaLacidbeta2base	GP		bind		lesser extent			ICAM-1	GP				NULL	293T transfectants	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_14642_s_235	11279101	293T transfectants that expressed alphaLacidbeta2base showed little binding to ICAM-1, whereas cells expressing wild-type alphaLbeta2 strongly bound to ICAM-1.	bind
28528	2	7556	5	13	NULL	NULL	NULL	alphaLbeta2	GP	wild-type	bind		strongly			ICAM-1	GP				NULL	293T transfectants	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_14642_s_235	11279101	293T transfectants that expressed alphaLacidbeta2base showed little binding to ICAM-1, whereas cells expressing wild-type alphaLbeta2 strongly bound to ICAM-1.	bind
31048	1	7556	7	NULL	NULL	0	NULL	alphaLacidbeta2base	NULL		bind	NULL	less			ICAM-1	NULL				NULL	293T transfectants	0	NULL	NULL	NULL	gw60_jbiolchem_276_18_14642_s_235	11279101	293T transfectants that expressed alphaLacidbeta2base showed little binding to ICAM-1, whereas cells expressing wild-type alphaLbeta2 strongly bound to ICAM-1.	bind
31049	2	7556	7	10	NULL	0	NULL	alphaLbeta2		wild-type	bind		strongly			ICAM-1					NULL	293T transfectants	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_14642_s_235	11279101	293T transfectants that expressed alphaLacidbeta2base showed little binding to ICAM-1, whereas cells expressing wild-type alphaLbeta2 strongly bound to ICAM-1.	bind
28529	1	7557	5	13	NULL	NULL	NULL	MDM2	GP		bind					ARF peptide	GP		N-terminal		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40583_s_219	11507088	2A10 inhibits the binding between MDM2 and an ARF N-terminal peptide  in vitro ( 8).	bind
28530	2	7557	5	13	NULL	NULL	NULL	2A10	GP		inhibit					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40583_s_219	11507088	2A10 inhibits the binding between MDM2 and an ARF N-terminal peptide  in vitro ( 8).	bind
31050	1	7557	7	NULL	NULL	0	NULL	MDM2	NULL		bind	NULL				ARF peptide	NULL		N-terminal		NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40583_s_219	11507088	2A10 inhibits the binding between MDM2 and an ARF N-terminal peptide  in vitro ( 8).	bind
31051	2	7557	7	10	NULL	0	NULL	2A10			inhibits					statement 1					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40583_s_219	11507088	2A10 inhibits the binding between MDM2 and an ARF N-terminal peptide  in vitro ( 8).	bind
28531	1	7559	5	13	NULL	NULL	NULL	2B4	GP		bind					CD48	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-immunol_170_10_12734329_s_3	12734329	2B4 binds to CD48 and activates NK cytotoxicity, but its function on CD8(+)  T cells is not clear.	bind
28532	2	7559	5	13	NULL	NULL	NULL	statement 1	Process		activates					NK cytotoxicity	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-immunol_170_10_12734329_s_3	12734329	2B4 binds to CD48 and activates NK cytotoxicity, but its function on CD8(+)  T cells is not clear.	bind
31052	1	7559	7	NULL	NULL	0	NULL	2B4	NULL		binds to	NULL				CD48	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-immunol_170_10_12734329_s_3	12734329	2B4 binds to CD48 and activates NK cytotoxicity, but its function on CD8(+)  T cells is not clear.	bind
31053	2	7559	7	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				NK cytotoxicity	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-immunol_170_10_12734329_s_3	12734329	2B4 binds to CD48 and activates NK cytotoxicity, but its function on CD8(+)  T cells is not clear.	bind
28533	1	7560	5	13	NULL	NULL	NULL	lipoproteins	GP		bind					LDLR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_10_7109_s_30	10702278	2E8 is a monoclonal antibody (mAb) that binds to apoE and prevents apoE-mediated binding of lipoproteins to the LDLR.	bind
28534	2	7560	5	13	NULL	NULL	NULL	apoE	GP		mediate					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_10_7109_s_30	10702278	2E8 is a monoclonal antibody (mAb) that binds to apoE and prevents apoE-mediated binding of lipoproteins to the LDLR.	bind
28535	3	7560	5	13	NULL	NULL	NULL	2E8	GP		is a type of					mAb	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_10_7109_s_30	10702278	2E8 is a monoclonal antibody (mAb) that binds to apoE and prevents apoE-mediated binding of lipoproteins to the LDLR.	bind
28536	4	7560	5	13	NULL	NULL	NULL	mAb	GP		is					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_10_7109_s_30	10702278	2E8 is a monoclonal antibody (mAb) that binds to apoE and prevents apoE-mediated binding of lipoproteins to the LDLR.	bind
28537	5	7560	5	13	NULL	NULL	NULL	2E8	GP		bind					apoE	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_10_7109_s_30	10702278	2E8 is a monoclonal antibody (mAb) that binds to apoE and prevents apoE-mediated binding of lipoproteins to the LDLR.	bind
28538	6	7560	5	13	NULL	NULL	NULL	statement 5	Process		prevents					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_10_7109_s_30	10702278	2E8 is a monoclonal antibody (mAb) that binds to apoE and prevents apoE-mediated binding of lipoproteins to the LDLR.	bind
31054	1	7560	7	NULL	NULL	0	NULL	2E8	NULL		binds to	NULL				apoE	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_7109_s_30	10702278	2E8 is a monoclonal antibody (mAb) that binds to apoE and prevents apoE-mediated binding of lipoproteins to the LDLR.	bind
31055	2	7560	7	NULL	NULL	0	NULL	2E8	NULL		is a type of	NULL				mAb	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_7109_s_30	10702278	2E8 is a monoclonal antibody (mAb) that binds to apoE and prevents apoE-mediated binding of lipoproteins to the LDLR.	bind
31056	3	7560	7	NULL	NULL	0	NULL	mAb	NULL		is	NULL				monoclonal antibody	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_7109_s_30	10702278	2E8 is a monoclonal antibody (mAb) that binds to apoE and prevents apoE-mediated binding of lipoproteins to the LDLR.	bind
31057	4	7560	7	NULL	NULL	0	NULL	lipoproteins	NULL		bind	NULL				LDLR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_7109_s_30	10702278	2E8 is a monoclonal antibody (mAb) that binds to apoE and prevents apoE-mediated binding of lipoproteins to the LDLR.	bind
31058	5	7560	7	NULL	NULL	0	NULL	apoE	NULL		mediates	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_7109_s_30	10702278	2E8 is a monoclonal antibody (mAb) that binds to apoE and prevents apoE-mediated binding of lipoproteins to the LDLR.	bind
31059	6	7560	7	NULL	NULL	0	NULL	statement 1	NULL		prevents	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_7109_s_30	10702278	2E8 is a monoclonal antibody (mAb) that binds to apoE and prevents apoE-mediated binding of lipoproteins to the LDLR.	bind
28539	1	7561	5	13	NULL	NULL	NULL	2M	GP		bind					growth factor	GP				NULL	AD-DD plasma samples	NULL	NULL	NULL	NULL	gw70_neurobioldis_14_3_504_s_132	14678766	2M in the other AD-DD plasma samples bound growth factor equivalently to the  2M in the II plasma samples.	bind
28540	2	7561	5	13	NULL	NULL	NULL	2M	GP		bind					growth factor	GP				NULL	II plasma samples	NULL	NULL	NULL	NULL	gw70_neurobioldis_14_3_504_s_132	14678766	2M in the other AD-DD plasma samples bound growth factor equivalently to the  2M in the II plasma samples.	bind
28541	3	7561	5	13	NULL	NULL	NULL	statement 1	Process		is equivalent to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_neurobioldis_14_3_504_s_132	14678766	2M in the other AD-DD plasma samples bound growth factor equivalently to the  2M in the II plasma samples.	bind
31060	1	7561	7	10	NULL	0	NULL	2M			bind					growth factor					NULL	AD-DD plasma samples	NULL	NULL	NULL	NULL	gw70_neurobioldis_14_3_504_s_132	14678766	2M in the other AD-DD plasma samples bound growth factor equivalently to the  2M in the II plasma samples.	bind
54559	2	7561	7	10	NULL	0	NULL	2M			bind					growth factor					NULL	II plasma samples	0	NULL	NULL	NULL	gw70_neurobioldis_14_3_504_s_132	14678766	2M in the other AD-DD plasma samples bound growth factor equivalently to the  2M in the II plasma samples.	bind
54560	3	7561	7	10	NULL	0	NULL	statement 1			is equivalent to					statement 2					NULL		0	NULL	NULL	NULL	gw70_neurobioldis_14_3_504_s_132	14678766	2M in the other AD-DD plasma samples bound growth factor equivalently to the  2M in the II plasma samples.	bind
28542	1	7562	5	13	NULL	NULL	NULL	2ME2	Chemical		bind					tubulin	GP		colchicine binding site		NULL		NULL	NULL	NULL	NULL	gw60_cancercell_3_4_363_s_128	12726862	2ME2 has been shown to bind to the colchicine binding site of tubulin  (D'Amato et al., 1994  ) and to depolymerize microtubules in endothelial  (Fotsis et al., 1994  ) as well as in tumor cells  (Aizu-Yokota et al., 1995  ), resulting in mitotic arrest and cell death.	bind
28543	2	7562	5	13	NULL	NULL	NULL	2ME2	Chemical		depolymerize					microtubules	CellComponent				NULL	in endothelial cells	NULL	NULL	NULL	NULL	gw60_cancercell_3_4_363_s_128	12726862	2ME2 has been shown to bind to the colchicine binding site of tubulin  (D'Amato et al., 1994  ) and to depolymerize microtubules in endothelial  (Fotsis et al., 1994  ) as well as in tumor cells  (Aizu-Yokota et al., 1995  ), resulting in mitotic arrest and cell death.	bind
28544	3	7562	5	13	NULL	NULL	NULL	2ME2	Chemical		depolymerize					microtubules	CellComponent				NULL	in tumor cells 	NULL	NULL	NULL	NULL	gw60_cancercell_3_4_363_s_128	12726862	2ME2 has been shown to bind to the colchicine binding site of tubulin  (D'Amato et al., 1994  ) and to depolymerize microtubules in endothelial  (Fotsis et al., 1994  ) as well as in tumor cells  (Aizu-Yokota et al., 1995  ), resulting in mitotic arrest and cell death.	bind
28546	4	7562	5	13	NULL	NULL	NULL	statement 2	Process		results in					mitotic arrest	Process				NULL		NULL	NULL	NULL	NULL	gw60_cancercell_3_4_363_s_128	12726862	2ME2 has been shown to bind to the colchicine binding site of tubulin  (D'Amato et al., 1994  ) and to depolymerize microtubules in endothelial  (Fotsis et al., 1994  ) as well as in tumor cells  (Aizu-Yokota et al., 1995  ), resulting in mitotic arrest and cell death.	bind
28547	5	7562	5	13	NULL	NULL	NULL	statement 2	Process		results in					cell death	Process				NULL		NULL	NULL	NULL	NULL	gw60_cancercell_3_4_363_s_128	12726862	2ME2 has been shown to bind to the colchicine binding site of tubulin  (D'Amato et al., 1994  ) and to depolymerize microtubules in endothelial  (Fotsis et al., 1994  ) as well as in tumor cells  (Aizu-Yokota et al., 1995  ), resulting in mitotic arrest and cell death.	bind
28548	6	7562	5	13	NULL	NULL	NULL	statement 3	Process		results in					mitotic arrest	Process				NULL		NULL	NULL	NULL	NULL	gw60_cancercell_3_4_363_s_128	12726862	2ME2 has been shown to bind to the colchicine binding site of tubulin  (D'Amato et al., 1994  ) and to depolymerize microtubules in endothelial  (Fotsis et al., 1994  ) as well as in tumor cells  (Aizu-Yokota et al., 1995  ), resulting in mitotic arrest and cell death.	bind
28549	7	7562	5	13	NULL	NULL	NULL	statement 3	Process		results in					cell death	Process				NULL		NULL	NULL	NULL	NULL	gw60_cancercell_3_4_363_s_128	12726862	2ME2 has been shown to bind to the colchicine binding site of tubulin  (D'Amato et al., 1994  ) and to depolymerize microtubules in endothelial  (Fotsis et al., 1994  ) as well as in tumor cells  (Aizu-Yokota et al., 1995  ), resulting in mitotic arrest and cell death.	bind
31061	1	7562	7	NULL	NULL	0	NULL	ME2	NULL		bind	NULL				tubulin	NULL		colchicine binding site		NULL		0	NULL	NULL	NULL	gw60_cancercell_3_4_363_s_128	12726862	2ME2 has been shown to bind to the colchicine binding site of tubulin  (D'Amato et al., 1994  ) and to depolymerize microtubules in endothelial  (Fotsis et al., 1994  ) as well as in tumor cells  (Aizu-Yokota et al., 1995  ), resulting in mitotic arrest and cell death.	bind
31062	2	7562	7	NULL	NULL	0	NULL	statement 1	NULL		depolymerize	NULL				microtubules	NULL				NULL	endothelial cells	0	NULL	NULL	NULL	gw60_cancercell_3_4_363_s_128	12726862	2ME2 has been shown to bind to the colchicine binding site of tubulin  (D'Amato et al., 1994  ) and to depolymerize microtubules in endothelial  (Fotsis et al., 1994  ) as well as in tumor cells  (Aizu-Yokota et al., 1995  ), resulting in mitotic arrest and cell death.	bind
31063	3	7562	7	NULL	NULL	0	NULL	statement 1	NULL		depolymerize	NULL				microtubules	NULL				NULL	tumor cells	0	NULL	NULL	NULL	gw60_cancercell_3_4_363_s_128	12726862	2ME2 has been shown to bind to the colchicine binding site of tubulin  (D'Amato et al., 1994  ) and to depolymerize microtubules in endothelial  (Fotsis et al., 1994  ) as well as in tumor cells  (Aizu-Yokota et al., 1995  ), resulting in mitotic arrest and cell death.	bind
31064	4	7562	7	NULL	NULL	0	NULL	statement 2	NULL		results in	NULL				mitotic arrest	NULL				NULL		0	NULL	NULL	NULL	gw60_cancercell_3_4_363_s_128	12726862	2ME2 has been shown to bind to the colchicine binding site of tubulin  (D'Amato et al., 1994  ) and to depolymerize microtubules in endothelial  (Fotsis et al., 1994  ) as well as in tumor cells  (Aizu-Yokota et al., 1995  ), resulting in mitotic arrest and cell death.	bind
31065	5	7562	7	NULL	NULL	0	NULL	statement 3	NULL		results in	NULL				mitotic arrest	NULL				NULL		0	NULL	NULL	NULL	gw60_cancercell_3_4_363_s_128	12726862	2ME2 has been shown to bind to the colchicine binding site of tubulin  (D'Amato et al., 1994  ) and to depolymerize microtubules in endothelial  (Fotsis et al., 1994  ) as well as in tumor cells  (Aizu-Yokota et al., 1995  ), resulting in mitotic arrest and cell death.	bind
31066	6	7562	7	NULL	NULL	0	NULL	statement 4	NULL		leads to	NULL				cell death	NULL				NULL		0	NULL	NULL	NULL	gw60_cancercell_3_4_363_s_128	12726862	2ME2 has been shown to bind to the colchicine binding site of tubulin  (D'Amato et al., 1994  ) and to depolymerize microtubules in endothelial  (Fotsis et al., 1994  ) as well as in tumor cells  (Aizu-Yokota et al., 1995  ), resulting in mitotic arrest and cell death.	bind
31067	7	7562	7	NULL	NULL	0	NULL	statement 5	NULL		leads to	NULL				cell death	NULL				NULL		0	NULL	NULL	NULL	gw60_cancercell_3_4_363_s_128	12726862	2ME2 has been shown to bind to the colchicine binding site of tubulin  (D'Amato et al., 1994  ) and to depolymerize microtubules in endothelial  (Fotsis et al., 1994  ) as well as in tumor cells  (Aizu-Yokota et al., 1995  ), resulting in mitotic arrest and cell death.	bind
28551	1	7563	5	13	NULL	NULL	NULL	NrpR	GP		bind					DNA	NucleicAcid			operator	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_7_5236_s_184	15590692	2OG inhibits binding of NrpR to operator DNA.	bind
28552	2	7563	5	13	NULL	NULL	NULL	2OG	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_7_5236_s_184	15590692	2OG inhibits binding of NrpR to operator DNA.	bind
31068	1	7563	7	NULL	NULL	0	NULL	NrpR	NULL		bind	NULL				DNA	NULL			operator	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_7_5236_s_184	15590692	2OG inhibits binding of NrpR to operator DNA.	bind
31069	2	7563	7	NULL	NULL	0	NULL	OG	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_7_5236_s_184	15590692	2OG inhibits binding of NrpR to operator DNA.	bind
28553	1	7564	5	13	NULL	NULL	NULL	2xTK49	NucleicAcid		bind		specifically		PPE	hnRNP L	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6303_s_262	16024770	2xTK49 PPE specifically binds only hnRNP L.	bind
31070	1	7564	7	10	NULL	0	NULL	TK49 	NULL		binds	NULL	specifically		PPE	hnRNP L	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6303_s_262	16024770	2xTK49 PPE specifically binds only hnRNP L.	bind
28554	1	7565	5	13	NULL	NULL	NULL	RNA	NucleicAcid	multisite binding of	occurs during					 c- src neural-specific splicing	Process	regulation of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_456_s_139	11788707	3       Chou,M.Y., Underwood,J.G., Nikolic,J., Luu,M.H. and Black,D.L. (2000) Multisite RNA binding and release of polypyrimidine tract binding protein during the regulation of c- src neural-specific splicing.	bind
28555	2	7565	5	13	NULL	NULL	NULL	polypyrimidine tract binding protein	Process	release of	occurs during					c- src neural-specific splicing	Process	regulation of 			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_456_s_139	11788707	3       Chou,M.Y., Underwood,J.G., Nikolic,J., Luu,M.H. and Black,D.L. (2000) Multisite RNA binding and release of polypyrimidine tract binding protein during the regulation of c- src neural-specific splicing.	bind
31121	1	7565	7	10	NULL	0	NULL	RNA		multisite binding of	occurs during 					c- src neural-specific splicing		regulation of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_456_s_139	11788707	3       Chou,M.Y., Underwood,J.G., Nikolic,J., Luu,M.H. and Black,D.L. (2000) Multisite RNA binding and release of polypyrimidine tract binding protein during the regulation of c- src neural-specific splicing.	bind
31123	2	7565	7	NULL	NULL	0	NULL	polypyrimidine tract binding protein 	NULL	release of	occurs during	NULL				c- src neural-specific splicing	NULL	regulation of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_456_s_139	11788707	3       Chou,M.Y., Underwood,J.G., Nikolic,J., Luu,M.H. and Black,D.L. (2000) Multisite RNA binding and release of polypyrimidine tract binding protein during the regulation of c- src neural-specific splicing.	bind
28556	1	7566	5	13	NULL	NULL	NULL	Raf	GP		bind					GST-Ras-GTP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_40_23681_s_289	7559537	3    at  >50-fold molar excess to Raf does not inhibit the binding of Raf to  GST-Ras-GTP ( Fig. 6,  upper panel,  lanes 1  and  2).	bind
31124	1	7566	7	NULL	NULL	0	NULL	Raf 	NULL		bind	NULL				GST-Ras-GTP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_40_23681_s_289	7559537	3    at  >50-fold molar excess to Raf does not inhibit the binding of Raf to  GST-Ras-GTP ( Fig. 6,  upper panel,  lanes 1  and  2).	bind
28558	1	7568	5	13	NULL	NULL	NULL	XRE	GP		bind					AHR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31845_s_342	9395531	3   This relatively mild effect of oxidation on XRE binding of the AHR.	bind
31132	1	7568	7	NULL	NULL	0	NULL	XRE	NULL		bind	NULL				AHR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31845_s_342	9395531	3   This relatively mild effect of oxidation on XRE binding of the AHR.	bind
28657	1	7569	5	13	NULL	NULL	NULL	dystrophin	GP		bind					actin filaments	GP		amino terminus		NULL	cytoplasmic side of the oligomeric complex	NULL	NULL	NULL	NULL	gw60_amjpathol_153_5_1623_s_12	9811355	3  At the cytoplasmic side of the oligomeric complex, dystrophin binds actin filaments along its amino terminus and spectrin-like rod domain.	bind
28658	2	7569	5	13	NULL	NULL	NULL	dystrophin	GP		bind					actin filaments	GP		spectrin-like rod domain		NULL	cytoplasmic side of the oligomeric complex	NULL	NULL	NULL	NULL	gw60_amjpathol_153_5_1623_s_12	9811355	3  At the cytoplasmic side of the oligomeric complex, dystrophin binds actin filaments along its amino terminus and spectrin-like rod domain.	bind
31138	1	7569	7	10	NULL	0	NULL	dystrophin	NULL		binds	NULL				actin filaments	NULL		amino terminus		NULL	cytoplasmic side of the oligomeric complex	NULL	NULL	NULL	NULL	gw60_amjpathol_153_5_1623_s_12	9811355	3  At the cytoplasmic side of the oligomeric complex, dystrophin binds actin filaments along its amino terminus and spectrin-like rod domain.	bind
31139	2	7569	7	NULL	NULL	0	NULL	dystrophin	NULL		binds	NULL				actin filaments	NULL		spectrin-like rod domain		NULL	cytoplasmic side of the oligomeric complex	NULL	NULL	NULL	NULL	gw60_amjpathol_153_5_1623_s_12	9811355	3  At the cytoplasmic side of the oligomeric complex, dystrophin binds actin filaments along its amino terminus and spectrin-like rod domain.	bind
28661	1	7570	5	13	NULL	NULL	NULL	apoB100 gene	GP	point mutation	causes					FDB	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_802_s_28	10073989	3  FDB is a genetic disorder caused by point mutations in the gene encoding for apoB100 that reduces the binding ability of LDL particles to the LDLR; as a consequence, LDL removal is reduced, and affected individuals develop high plasma cholesterol concentrations.	bind
28662	2	7570	5	13	NULL	NULL	NULL	FDB	MedicalFinding		is a type of					genetic disorder	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_802_s_28	10073989	3  FDB is a genetic disorder caused by point mutations in the gene encoding for apoB100 that reduces the binding ability of LDL particles to the LDLR; as a consequence, LDL removal is reduced, and affected individuals develop high plasma cholesterol concentrations.	bind
28663	3	7570	5	13	NULL	NULL	NULL	LDL particles	GP		bind					LDLR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_802_s_28	10073989	3  FDB is a genetic disorder caused by point mutations in the gene encoding for apoB100 that reduces the binding ability of LDL particles to the LDLR; as a consequence, LDL removal is reduced, and affected individuals develop high plasma cholesterol concentrations.	bind
28664	4	7570	5	13	NULL	NULL	NULL	apoB100 gene	GP	point mutation	reduces					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_802_s_28	10073989	3  FDB is a genetic disorder caused by point mutations in the gene encoding for apoB100 that reduces the binding ability of LDL particles to the LDLR; as a consequence, LDL removal is reduced, and affected individuals develop high plasma cholesterol concentrations.	bind
28665	5	7570	5	13	NULL	NULL	NULL	statement 4	Process		leads to					LDL	GP	reduced removal of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_802_s_28	10073989	3  FDB is a genetic disorder caused by point mutations in the gene encoding for apoB100 that reduces the binding ability of LDL particles to the LDLR; as a consequence, LDL removal is reduced, and affected individuals develop high plasma cholesterol concentrations.	bind
28666	6	7570	5	13	NULL	NULL	NULL	statement 5	Process		leads to					plasma cholesterol	Chemical	high concentration of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_802_s_28	10073989	3  FDB is a genetic disorder caused by point mutations in the gene encoding for apoB100 that reduces the binding ability of LDL particles to the LDLR; as a consequence, LDL removal is reduced, and affected individuals develop high plasma cholesterol concentrations.	bind
31141	1	7570	7	NULL	NULL	0	NULL	FDB	NULL		is a type of	NULL				genetic disorder	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_802_s_28	10073989	3  FDB is a genetic disorder caused by point mutations in the gene encoding for apoB100 that reduces the binding ability of LDL particles to the LDLR; as a consequence, LDL removal is reduced, and affected individuals develop high plasma cholesterol concentrations.	bind
31142	2	7570	7	NULL	NULL	0	NULL	apoB100 gene	NULL	point mutation 	cause	NULL				FDB	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_802_s_28	10073989	3  FDB is a genetic disorder caused by point mutations in the gene encoding for apoB100 that reduces the binding ability of LDL particles to the LDLR; as a consequence, LDL removal is reduced, and affected individuals develop high plasma cholesterol concentrations.	bind
31144	3	7570	7	NULL	NULL	0	NULL	LDL particles	NULL		bind	NULL				LDLR	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_802_s_28	10073989	3  FDB is a genetic disorder caused by point mutations in the gene encoding for apoB100 that reduces the binding ability of LDL particles to the LDLR; as a consequence, LDL removal is reduced, and affected individuals develop high plasma cholesterol concentrations.	bind
31145	4	7570	7	NULL	NULL	0	NULL	apoB100 gene	NULL	point mutation	reduces	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_802_s_28	10073989	3  FDB is a genetic disorder caused by point mutations in the gene encoding for apoB100 that reduces the binding ability of LDL particles to the LDLR; as a consequence, LDL removal is reduced, and affected individuals develop high plasma cholesterol concentrations.	bind
31146	5	7570	7	NULL	NULL	0	NULL	statement 4	NULL		reduce	NULL				LDL	NULL	removal of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_802_s_28	10073989	3  FDB is a genetic disorder caused by point mutations in the gene encoding for apoB100 that reduces the binding ability of LDL particles to the LDLR; as a consequence, LDL removal is reduced, and affected individuals develop high plasma cholesterol concentrations.	bind
31147	6	7570	7	NULL	NULL	0	NULL	statement 5	NULL		leads to	NULL				plasma cholesterol	NULL	high concentration of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_802_s_28	10073989	3  FDB is a genetic disorder caused by point mutations in the gene encoding for apoB100 that reduces the binding ability of LDL particles to the LDLR; as a consequence, LDL removal is reduced, and affected individuals develop high plasma cholesterol concentrations.	bind
28667	1	7572	5	13	NULL	NULL	NULL	SUR1	GP		bind			NBD1		ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_10_873_s_122	11073882	3  It was shown that SUR1 binds ATP at NBD1 and ADP at NBD2.	bind
28668	2	7572	5	13	NULL	NULL	NULL	SUR1	GP		bind			NBD2		ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_10_873_s_122	11073882	3  It was shown that SUR1 binds ATP at NBD1 and ADP at NBD2.	bind
31195	1	7572	7	NULL	NULL	0	NULL	SUR1 	NULL		binds	NULL		NBD1		ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_10_873_s_122	11073882	3  It was shown that SUR1 binds ATP at NBD1 and ADP at NBD2.	bind
31196	2	7572	7	NULL	NULL	0	NULL	SUR1 	NULL		bind	NULL		NBD2		ADP	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_10_873_s_122	11073882	3  It was shown that SUR1 binds ATP at NBD1 and ADP at NBD2.	bind
28671	1	7574	5	13	NULL	NULL	NULL	fibrinogen	GP		bind					GPIIb-IIIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2127_s_16	10595941	3  Subsequent binding of fibrinogen to GPIIb-IIIa promotes platelet aggregation and formation of an effective hemostatic plug at intermediate shear rates.	bind
28672	2	7574	5	13	NULL	NULL	NULL	statement 1	Process		promotes					platelet aggregation	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2127_s_16	10595941	3  Subsequent binding of fibrinogen to GPIIb-IIIa promotes platelet aggregation and formation of an effective hemostatic plug at intermediate shear rates.	bind
28673	3	7574	5	13	NULL	NULL	NULL	statement 1	Process		forms					hemostatic plug					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2127_s_16	10595941	3  Subsequent binding of fibrinogen to GPIIb-IIIa promotes platelet aggregation and formation of an effective hemostatic plug at intermediate shear rates.	bind
28674	4	7574	5	13	NULL	NULL	NULL	statement 3	Process		occurs at					shear rates		intermediate			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2127_s_16	10595941	3  Subsequent binding of fibrinogen to GPIIb-IIIa promotes platelet aggregation and formation of an effective hemostatic plug at intermediate shear rates.	bind
31197	1	7574	7	NULL	NULL	0	NULL	fibrinogen	NULL		binds to	NULL				GPIIb-IIIa	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_6_2127_s_16	10595941	3  Subsequent binding of fibrinogen to GPIIb-IIIa promotes platelet aggregation and formation of an effective hemostatic plug at intermediate shear rates.	bind
31198	2	7574	7	NULL	NULL	0	NULL	statement 1	NULL		promotes	NULL				platelet aggregation	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_6_2127_s_16	10595941	3  Subsequent binding of fibrinogen to GPIIb-IIIa promotes platelet aggregation and formation of an effective hemostatic plug at intermediate shear rates.	bind
31199	3	7574	7	NULL	NULL	0	NULL	statement 1	NULL		forms	NULL				hemostatic plug 	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_6_2127_s_16	10595941	3  Subsequent binding of fibrinogen to GPIIb-IIIa promotes platelet aggregation and formation of an effective hemostatic plug at intermediate shear rates.	bind
28675	1	7575	5	13	NULL	NULL	NULL	TRs	GP		regulate					alpha-MHC gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_6_700_s_149	10747007	3  The alpha-MHC gene is transcriptionally regulated by TRs, which bind to a positive TRE in the promoter of the gene.	bind
28676	2	7575	5	13	NULL	NULL	NULL	TRs	GP		bind					alpha-MHC gene	GP			positive TRE in the promoter	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_6_700_s_149	10747007	3  The alpha-MHC gene is transcriptionally regulated by TRs, which bind to a positive TRE in the promoter of the gene.	bind
31200	1	7575	7	NULL	NULL	0	NULL	TRs	NULL		bind	NULL				alpha-MHC gene	NULL			positive TRE in the promoter	NULL		0	NULL	NULL	NULL	gw60_circulationres_86_6_700_s_149	10747007	3  The alpha-MHC gene is transcriptionally regulated by TRs, which bind to a positive TRE in the promoter of the gene.	bind
31201	2	7575	7	NULL	NULL	0	NULL	TRs	NULL		regulate	NULL				alpha-MHC gene	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_6_700_s_149	10747007	3  The alpha-MHC gene is transcriptionally regulated by TRs, which bind to a positive TRE in the promoter of the gene.	bind
28677	1	7576	5	13	NULL	NULL	NULL	thrombin	GP		bind					TM	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_10_1292_s_22	8857927	3  Thus, binding of thrombin to TM induces a negative feedback loop that stops the coagulation.	bind
28678	2	7576	5	13	NULL	NULL	NULL	statement 1	Process		induces					negative feedback loop	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_10_1292_s_22	8857927	3  Thus, binding of thrombin to TM induces a negative feedback loop that stops the coagulation.	bind
28679	3	7576	5	13	NULL	NULL	NULL	statement 2	Process		stops					coagulation	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_10_1292_s_22	8857927	3  Thus, binding of thrombin to TM induces a negative feedback loop that stops the coagulation.	bind
31202	1	7576	7	NULL	NULL	0	NULL	thrombin	NULL		binds	NULL				TM	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_10_1292_s_22	8857927	3  Thus, binding of thrombin to TM induces a negative feedback loop that stops the coagulation.	bind
31203	2	7576	7	NULL	NULL	0	NULL	statement 1	NULL		induces	NULL				negative feedback loop	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_10_1292_s_22	8857927	3  Thus, binding of thrombin to TM induces a negative feedback loop that stops the coagulation.	bind
31204	3	7576	7	NULL	NULL	0	NULL	statement 2	NULL		stops	NULL				coagulation	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_10_1292_s_22	8857927	3  Thus, binding of thrombin to TM induces a negative feedback loop that stops the coagulation.	bind
28680	1	7578	5	13	NULL	NULL	NULL	LDL	GP	very early form of oxidized 	bind					CD14	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_27	15718493	3 - 5   We demonstrated recently that a very early form of oxidized LDL, minimally modified LDL (mmLDL), binds to the LPS receptor CD14 and stimulates macrophage spreading and actin polymerization.	bind
28681	2	7578	5	13	NULL	NULL	NULL	CD14	GP		is a type of					LPS receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_27	15718493	3 - 5   We demonstrated recently that a very early form of oxidized LDL, minimally modified LDL (mmLDL), binds to the LPS receptor CD14 and stimulates macrophage spreading and actin polymerization.	bind
28682	3	7578	5	13	NULL	NULL	NULL	mmLDL	GP		is					minimally modified LDL	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_27	15718493	3 - 5   We demonstrated recently that a very early form of oxidized LDL, minimally modified LDL (mmLDL), binds to the LPS receptor CD14 and stimulates macrophage spreading and actin polymerization.	bind
28683	4	7578	5	13	NULL	NULL	NULL	mmLDL	GP		bind					CD14	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_27	15718493	3 - 5   We demonstrated recently that a very early form of oxidized LDL, minimally modified LDL (mmLDL), binds to the LPS receptor CD14 and stimulates macrophage spreading and actin polymerization.	bind
28684	5	7578	5	13	NULL	NULL	NULL	statement 1	Process		stimulates					macrophage	Cell	spreading of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_27	15718493	3 - 5   We demonstrated recently that a very early form of oxidized LDL, minimally modified LDL (mmLDL), binds to the LPS receptor CD14 and stimulates macrophage spreading and actin polymerization.	bind
28685	6	7578	5	13	NULL	NULL	NULL	statement 4	Process		stimulates					macrophage	Cell	spreading of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_27	15718493	3 - 5   We demonstrated recently that a very early form of oxidized LDL, minimally modified LDL (mmLDL), binds to the LPS receptor CD14 and stimulates macrophage spreading and actin polymerization.	bind
28686	7	7578	5	13	NULL	NULL	NULL	statement 1	Process		stimulates					actin	GP	polymerization of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_27	15718493	3 - 5   We demonstrated recently that a very early form of oxidized LDL, minimally modified LDL (mmLDL), binds to the LPS receptor CD14 and stimulates macrophage spreading and actin polymerization.	bind
28687	8	7578	5	13	NULL	NULL	NULL	statement 4	Process		stimulates					actin	GP	polymerization of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_27	15718493	3 - 5   We demonstrated recently that a very early form of oxidized LDL, minimally modified LDL (mmLDL), binds to the LPS receptor CD14 and stimulates macrophage spreading and actin polymerization.	bind
31205	1	7578	7	10	NULL	0	NULL	LDL		early form of oxidized	binds to					CD14					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_27	15718493	3 - 5   We demonstrated recently that a very early form of oxidized LDL, minimally modified LDL (mmLDL), binds to the LPS receptor CD14 and stimulates macrophage spreading and actin polymerization.	bind
31206	2	7578	7	NULL	NULL	0	NULL	mmLDL	NULL		binds to	NULL				CD14	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_27	15718493	3 - 5   We demonstrated recently that a very early form of oxidized LDL, minimally modified LDL (mmLDL), binds to the LPS receptor CD14 and stimulates macrophage spreading and actin polymerization.	bind
31207	3	7578	7	10	NULL	0	NULL	statement 1			stimulate					macrophage		spreading of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_27	15718493	3 - 5   We demonstrated recently that a very early form of oxidized LDL, minimally modified LDL (mmLDL), binds to the LPS receptor CD14 and stimulates macrophage spreading and actin polymerization.	bind
31208	4	7578	7	10	NULL	0	NULL	statement 2			stimulate					macrophage		spreading of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_27	15718493	3 - 5   We demonstrated recently that a very early form of oxidized LDL, minimally modified LDL (mmLDL), binds to the LPS receptor CD14 and stimulates macrophage spreading and actin polymerization.	bind
31209	5	7578	7	NULL	NULL	0	NULL	statement 1	NULL		stimulate	NULL				actin	NULL	polymerization of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_27	15718493	3 - 5   We demonstrated recently that a very early form of oxidized LDL, minimally modified LDL (mmLDL), binds to the LPS receptor CD14 and stimulates macrophage spreading and actin polymerization.	bind
31210	6	7578	7	NULL	NULL	0	NULL	statement 2	NULL		stimulate	NULL				actin	NULL	polymerization of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_27	15718493	3 - 5   We demonstrated recently that a very early form of oxidized LDL, minimally modified LDL (mmLDL), binds to the LPS receptor CD14 and stimulates macrophage spreading and actin polymerization.	bind
31211	7	7578	7	NULL	NULL	0	NULL	CD14	NULL		is a type of	NULL				LPS receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_27	15718493	3 - 5   We demonstrated recently that a very early form of oxidized LDL, minimally modified LDL (mmLDL), binds to the LPS receptor CD14 and stimulates macrophage spreading and actin polymerization.	bind
31212	8	7578	7	NULL	NULL	0	NULL	mmLDL	NULL		is	NULL				minimally modified LDL	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_27	15718493	3 - 5   We demonstrated recently that a very early form of oxidized LDL, minimally modified LDL (mmLDL), binds to the LPS receptor CD14 and stimulates macrophage spreading and actin polymerization.	bind
28688	1	7579	5	13	NULL	NULL	NULL	TBPS	Chemical		bind					GABAA receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_813_2_343_s_165	9838187	3 -hydroxy steroids are known to inhibit [35]TBPS binding to GABAA receptors with IC50 values in the nanomolar range [ 15,  17], therefore in the present study we wanted to verify that steroid-inhibition of [3]GHB binding was not mediated by GABAA receptors.	bind
28689	2	7579	5	13	NULL	NULL	NULL	3 -hydroxy steroids	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_brainres_813_2_343_s_165	9838187	3 -hydroxy steroids are known to inhibit [35]TBPS binding to GABAA receptors with IC50 values in the nanomolar range [ 15,  17], therefore in the present study we wanted to verify that steroid-inhibition of [3]GHB binding was not mediated by GABAA receptors.	bind
31213	1	7579	7	10	NULL	0	NULL	TBPS			bind					GABAA receptors					NULL		NULL	NULL	NULL	NULL	gw60_brainres_813_2_343_s_165	9838187	3 -hydroxy steroids are known to inhibit [35]TBPS binding to GABAA receptors with IC50 values in the nanomolar range [ 15,  17], therefore in the present study we wanted to verify that steroid-inhibition of [3]GHB binding was not mediated by GABAA receptors.	bind
31214	2	7579	7	NULL	NULL	0	NULL	3 -hydroxy steroids	NULL		inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_brainres_813_2_343_s_165	9838187	3 -hydroxy steroids are known to inhibit [35]TBPS binding to GABAA receptors with IC50 values in the nanomolar range [ 15,  17], therefore in the present study we wanted to verify that steroid-inhibition of [3]GHB binding was not mediated by GABAA receptors.	bind
28699	1	7580	5	13	NULL	NULL	NULL	angiotensin II	GP		elicits					smooth muscle	OrganismPart	contractions of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
28700	2	7580	5	13	NULL	NULL	NULL	noradrenaline	Chemical		elicits					smooth muscle	OrganismPart	contractions of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
28701	3	7580	5	13	NULL	NULL	NULL	angiotensin II	GP		is a type of					agonist	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
28702	4	7580	5	13	NULL	NULL	NULL	noradrenaline	Chemical		is a type of					agonist	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
28703	5	7580	5	13	NULL	NULL	NULL	angiotensin II	GP		stimulates					G protein - linked receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
28704	6	7580	5	13	NULL	NULL	NULL	noradrenaline	Chemical		stimulates					G protein - linked receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
28705	7	7580	5	13	NULL	NULL	NULL	PTKs	GP	unidentified	mediate		partly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
28706	8	7580	5	13	NULL	NULL	NULL	PTKs	GP	unidentified	mediate		partly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
28707	9	7580	5	13	NULL	NULL	NULL	orthovanadate	Chemical		blocks					tyrosine phosphatases	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
28708	10	7580	5	13	NULL	NULL	NULL	orthovanadate	Chemical		induces					smooth muscle	OrganismPart	contractions of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
28709	11	7580	5	13	NULL	NULL	NULL	orthovanadate	Chemical		phosphorylates					cellular proteins	GP	unidentified	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
28710	12	7580	5	13	NULL	NULL	NULL	growth factors	GP		bind					receptor tyrosine kinases	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
28711	13	7580	5	13	NULL	NULL	NULL	statement 12	Process		causes					tension development	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
54561	14	7580	5	13	NULL	NULL	NULL	statement 10	Process		occurs in parallel with					statement 11	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
31217	1	7580	7	NULL	NULL	0	NULL	angiotensin II	NULL		elicits	NULL				smooth muscle contractions	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
31218	2	7580	7	NULL	NULL	0	NULL	noradrenaline	NULL		elicits	NULL				smooth muscle contractions	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
31219	3	7580	7	NULL	NULL	0	NULL	angiotensin II 	NULL		stimulate	NULL				G protein - linked receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
31220	4	7580	7	NULL	NULL	0	NULL	noradrenaline	NULL		stimulate	NULL				G protein - linked receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
31221	5	7580	7	NULL	NULL	0	NULL	unidentified PTKs	NULL		mediates	NULL	partly			statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
31222	6	7580	7	NULL	NULL	0	NULL	unidentified PTKs	NULL		mediates	NULL	partly			statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
31223	7	7580	7	NULL	NULL	0	NULL	orthovanadate	NULL		blocks	NULL				tyrosine phosphatases	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
31224	8	7580	7	NULL	NULL	0	NULL	statement 7	NULL		induces	NULL				smooth muscle contraction	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
31225	9	7580	7	NULL	NULL	0	NULL	orthovanadate	NULL		phosphorylates	NULL				unidentified cellular proteins	NULL		tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
31226	10	7580	7	NULL	NULL	0	NULL	statement 8	NULL		occurs in parallel with	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
31227	11	7580	7	NULL	NULL	0	NULL	growth factors	NULL		bind	NULL				 receptor tyrosine kinases	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
31228	12	7580	7	NULL	NULL	0	NULL	statement 11	NULL		cause	NULL				tension development	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
31234	13	7580	7	NULL	NULL	0	NULL	angiotensin II	NULL		is a type of	NULL				agonist	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
31235	14	7580	7	NULL	NULL	0	NULL	noradrenaline	NULL		is a type of	NULL				agonist	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_76_2_310_s_144	7834843	3 21  A number of recent reports have suggested that contractions of smooth muscle elicited by agonists such as angiotensin II and noradrenaline, which stimulate G protein - linked receptors, are mediated in part by as-yet-unidentified PTKs. 5  6  It is also the case that orthovanadate, which blocks tyrosine phosphatases, induces smooth muscle contraction in parallel with tyrosine phosphorylation of as-yet-unidentified cellular proteins 20  and that several growth factors that are known to bind to receptor tyrosine kinases cause tension development.	bind
28712	1	7581	5	13	NULL	NULL	NULL	fibrinogen	GP		bind					GPIIb-IIIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_621_s_20	8963718	3 4 5  6  Binding of fibrinogen to GPIIb-IIIa is mediated through amino acid sequences present in regions of the alpha and gamma chains of the fibrinogen macromolecule.	bind
28713	2	7581	5	13	NULL	NULL	NULL	statement 1	Process		is mediated through					fibrinogen macromolecule	GP		alpha chains amino acid		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_621_s_20	8963718	3 4 5  6  Binding of fibrinogen to GPIIb-IIIa is mediated through amino acid sequences present in regions of the alpha and gamma chains of the fibrinogen macromolecule.	bind
28714	3	7581	5	13	NULL	NULL	NULL	statement 1	Process		is mediated through					fibrinogen macromolecule	GP		gamma chain amino acid		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_621_s_20	8963718	3 4 5  6  Binding of fibrinogen to GPIIb-IIIa is mediated through amino acid sequences present in regions of the alpha and gamma chains of the fibrinogen macromolecule.	bind
31229	1	7581	7	10	NULL	0	NULL	fibrinogen	NULL		bind	NULL				GPIIb-IIIa	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_621_s_20	8963718	3 4 5  6  Binding of fibrinogen to GPIIb-IIIa is mediated through amino acid sequences present in regions of the alpha and gamma chains of the fibrinogen macromolecule.	bind
31230	2	7581	7	10	NULL	0	NULL	statement 1	NULL		is mediated through	NULL				fibrinogen macromolecule	NULL		alpha chains amino acid		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_621_s_20	8963718	3 4 5  6  Binding of fibrinogen to GPIIb-IIIa is mediated through amino acid sequences present in regions of the alpha and gamma chains of the fibrinogen macromolecule.	bind
46657	3	7581	7	10	NULL	0	NULL	statement 1	NULL		is mediated through	NULL				fibrinogen macromolecule	NULL		gamma chain amino acid		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_621_s_20	8963718	3 4 5  6  Binding of fibrinogen to GPIIb-IIIa is mediated through amino acid sequences present in regions of the alpha and gamma chains of the fibrinogen macromolecule.	bind
28690	1	7582	5	13	NULL	NULL	NULL	Ang II	GP		bind					AT1s	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_8_710_s_17	11029408	3 4 5  Binding of Ang II to AT1s activates several signaling pathways implicated in regulating cellular growth.	bind
28715	2	7582	5	13	NULL	NULL	NULL	statement 1	Process		activates					signaling pathways	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_8_710_s_17	11029408	3 4 5  Binding of Ang II to AT1s activates several signaling pathways implicated in regulating cellular growth.	bind
46658	3	7582	5	13	NULL	NULL	NULL	statement 2	Process		implicated in					cellular growth	Process	regulation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_8_710_s_17	11029408	3 4 5  Binding of Ang II to AT1s activates several signaling pathways implicated in regulating cellular growth.	bind
31231	1	7582	7	NULL	NULL	0	NULL	Ang II	NULL		bind	NULL				AT1s	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_8_710_s_17	11029408	3 4 5  Binding of Ang II to AT1s activates several signaling pathways implicated in regulating cellular growth.	bind
31232	2	7582	7	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				signaling pathways	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_8_710_s_17	11029408	3 4 5  Binding of Ang II to AT1s activates several signaling pathways implicated in regulating cellular growth.	bind
31233	3	7582	7	NULL	NULL	0	NULL	statement 2	NULL		implicated in	NULL				cellular growth	NULL	regulation of			NULL		0	NULL	NULL	NULL	gw60_circulationres_87_8_710_s_17	11029408	3 4 5  Binding of Ang II to AT1s activates several signaling pathways implicated in regulating cellular growth.	bind
28716	1	7584	5	13	NULL	NULL	NULL	c7E3	GP		is a type of					monoclonal IgG Fab antibody fragment	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_5_906_s_21	8790024	3 4 5 6  The currently available parenteral GP IIb/IIa receptor antagonist is a monoclonal IgG Fab antibody fragment (c7E3, abciximab [ReoPro] Centocor, Inc) that binds the GP IIb/IIa receptor with high affinity, resulting in a long biological half-life.	bind
28717	2	7584	5	13	NULL	NULL	NULL	c7E3	GP		is antagonist of					GP IIb/IIa receptor	GP	parenteral			NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_5_906_s_21	8790024	3 4 5 6  The currently available parenteral GP IIb/IIa receptor antagonist is a monoclonal IgG Fab antibody fragment (c7E3, abciximab [ReoPro] Centocor, Inc) that binds the GP IIb/IIa receptor with high affinity, resulting in a long biological half-life.	bind
28718	3	7584	5	13	NULL	NULL	NULL	c7E3	GP		bind		high affinity			GP IIb/IIa receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_5_906_s_21	8790024	3 4 5 6  The currently available parenteral GP IIb/IIa receptor antagonist is a monoclonal IgG Fab antibody fragment (c7E3, abciximab [ReoPro] Centocor, Inc) that binds the GP IIb/IIa receptor with high affinity, resulting in a long biological half-life.	bind
28719	4	7584	5	13	NULL	NULL	NULL	statement 3	Process		results in					biological half-life	Process	long			NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_5_906_s_21	8790024	3 4 5 6  The currently available parenteral GP IIb/IIa receptor antagonist is a monoclonal IgG Fab antibody fragment (c7E3, abciximab [ReoPro] Centocor, Inc) that binds the GP IIb/IIa receptor with high affinity, resulting in a long biological half-life.	bind
31236	1	7584	7	NULL	NULL	0	NULL	c7E3	NULL		binds	NULL	high affinity			GP IIb/IIa receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_5_906_s_21	8790024	3 4 5 6  The currently available parenteral GP IIb/IIa receptor antagonist is a monoclonal IgG Fab antibody fragment (c7E3, abciximab [ReoPro] Centocor, Inc) that binds the GP IIb/IIa receptor with high affinity, resulting in a long biological half-life.	bind
31237	2	7584	7	NULL	NULL	0	NULL	c7E3	NULL		is a type of	NULL				monoclonal IgG Fab antibody fragment	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_5_906_s_21	8790024	3 4 5 6  The currently available parenteral GP IIb/IIa receptor antagonist is a monoclonal IgG Fab antibody fragment (c7E3, abciximab [ReoPro] Centocor, Inc) that binds the GP IIb/IIa receptor with high affinity, resulting in a long biological half-life.	bind
31238	4	7584	7	10	NULL	0	NULL	statement 1			results in					biological half-life		 long			NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_5_906_s_21	8790024	3 4 5 6  The currently available parenteral GP IIb/IIa receptor antagonist is a monoclonal IgG Fab antibody fragment (c7E3, abciximab [ReoPro] Centocor, Inc) that binds the GP IIb/IIa receptor with high affinity, resulting in a long biological half-life.	bind
46724	3	7584	7	10	NULL	0	NULL	c7E3	NULL		is antagonist of	NULL				 GP IIb/IIa receptor 	NULL	parenteral			NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_5_906_s_21	8790024	3 4 5 6  The currently available parenteral GP IIb/IIa receptor antagonist is a monoclonal IgG Fab antibody fragment (c7E3, abciximab [ReoPro] Centocor, Inc) that binds the GP IIb/IIa receptor with high affinity, resulting in a long biological half-life.	bind
28720	1	7585	5	13	NULL	NULL	NULL				bind			L2 domain		E1a kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6361_s_34	9045657	3 4 The L2 domain binds the E1a kinase ( 30) and the E1b phosphatase ( 31).	bind
28721	2	7585	5	13	NULL	NULL	NULL				bind			L2 domain		E1b phosphatase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6361_s_34	9045657	3 4 The L2 domain binds the E1a kinase ( 30) and the E1b phosphatase ( 31).	bind
31239	1	7585	7	NULL	NULL	0	NULL		NULL		binds	NULL		L2 domain		E1a kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_10_6361_s_34	9045657	3 4 The L2 domain binds the E1a kinase ( 30) and the E1b phosphatase ( 31).	bind
31240	2	7585	7	NULL	NULL	0	NULL		NULL		binds	NULL		L2 domain		E1b phosphatase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_10_6361_s_34	9045657	3 4 The L2 domain binds the E1a kinase ( 30) and the E1b phosphatase ( 31).	bind
28722	1	7586	5	13	NULL	NULL	NULL	apoA-I	GP		bind					phospholipids	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1426_s_22	15845909	3 4F is an apoA-I mimetic peptide that binds phospholipids similar to apoA-I.	bind
28723	2	7586	5	13	NULL	NULL	NULL	4F	GP		is a type of					apoA-I mimetic peptide	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1426_s_22	15845909	3 4F is an apoA-I mimetic peptide that binds phospholipids similar to apoA-I.	bind
28724	3	7586	5	13	NULL	NULL	NULL	4F	GP		bind					phospholipids	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1426_s_22	15845909	3 4F is an apoA-I mimetic peptide that binds phospholipids similar to apoA-I.	bind
31241	1	7586	7	NULL	NULL	0	NULL	 4F	NULL		binds	NULL				phospholipids	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1426_s_22	15845909	3 4F is an apoA-I mimetic peptide that binds phospholipids similar to apoA-I.	bind
31242	2	7586	7	NULL	NULL	0	NULL	 4F	NULL		binds	NULL				apoA-I	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1426_s_22	15845909	3 4F is an apoA-I mimetic peptide that binds phospholipids similar to apoA-I.	bind
31243	3	7586	7	NULL	NULL	0	NULL	4F 	NULL		is a type of	NULL				apoA-I mimetic peptide	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1426_s_22	15845909	3 4F is an apoA-I mimetic peptide that binds phospholipids similar to apoA-I.	bind
28726	1	7587	5	13	NULL	NULL	NULL	apo B	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_2_505_s_66	7805256	3 8  The resulting amino acid substitution disrupts apo B binding to the LDL receptor, impairing LDL uptake.	bind
28727	2	7587	5	13	NULL	NULL	NULL	amino acid substitution	Process		disrupts					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_2_505_s_66	7805256	3 8  The resulting amino acid substitution disrupts apo B binding to the LDL receptor, impairing LDL uptake.	bind
28728	3	7587	5	13	NULL	NULL	NULL	statement 2	Process		impairs					LDL	GP	uptake of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_2_505_s_66	7805256	3 8  The resulting amino acid substitution disrupts apo B binding to the LDL receptor, impairing LDL uptake.	bind
31244	1	7587	7	NULL	NULL	0	NULL	apo B	NULL		bind	NULL				LDL receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_2_505_s_66	7805256	3 8  The resulting amino acid substitution disrupts apo B binding to the LDL receptor, impairing LDL uptake.	bind
31245	2	7587	7	NULL	NULL	0	NULL	aminoacid substitution	NULL		disrupts	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_2_505_s_66	7805256	3 8  The resulting amino acid substitution disrupts apo B binding to the LDL receptor, impairing LDL uptake.	bind
31246	3	7587	7	NULL	NULL	0	NULL	statement 1	NULL		impairs	NULL				LDL	NULL	uptake of			NULL		0	NULL	NULL	NULL	gw60_circulation_91_2_505_s_66	7805256	3 8  The resulting amino acid substitution disrupts apo B binding to the LDL receptor, impairing LDL uptake.	bind
28729	1	7588	5	13	NULL	NULL	NULL	MutY	GP		bind		differentially	G116D		DNA	NucleicAcid	A/G-containing			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24138_s_170	8798653	3 a result consistent with the differential binding of MutY(G116D) with A/G- and A/GO-containing DNA.	bind
28730	2	7588	5	13	NULL	NULL	NULL	MutY	GP		bind		differentially	G116D		DNA	NucleicAcid	A/GO-containing			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24138_s_170	8798653	3 a result consistent with the differential binding of MutY(G116D) with A/G- and A/GO-containing DNA.	bind
31247	1	7588	7	10	NULL	0	NULL	MutY			bind		differentially	G116D		DNA		A/G containing			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24138_s_170	8798653	3 a result consistent with the differential binding of MutY(G116D) with A/G- and A/GO-containing DNA.	bind
31248	2	7588	7	10	NULL	0	NULL	MutY			bind		differentially	G116D		DNA		A/GO-containing			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24138_s_170	8798653	3 a result consistent with the differential binding of MutY(G116D) with A/G- and A/GO-containing DNA.	bind
29042	2	7589	5	13	NULL	NULL	NULL	MHC class I molecules	GP	viral	bind					MHC class I receptor	GP	viral			NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_2_5_521_s_215	10865197	3 A,B.  Cis-binding of the viral MHC class I molecules with its receptor may lead to inhibition of NK cell stimulatory cytokines, preventing NK cell recruitment and activation.	bind
29043	3	7589	5	13	NULL	NULL	NULL	statement 1	Process		prevents					NK cell	Cell	recruitment of			NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_2_5_521_s_215	10865197	3 A,B.  Cis-binding of the viral MHC class I molecules with its receptor may lead to inhibition of NK cell stimulatory cytokines, preventing NK cell recruitment and activation.	bind
29044	4	7589	5	13	NULL	NULL	NULL	statement 1	Process		prevents					NK cell	Cell	activation of			NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_2_5_521_s_215	10865197	3 A,B.  Cis-binding of the viral MHC class I molecules with its receptor may lead to inhibition of NK cell stimulatory cytokines, preventing NK cell recruitment and activation.	bind
46659	1	7589	5	13	NULL	NULL	NULL	NK cells	Cell		stimulate					cytokines	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_2_5_521_s_215	10865197	3 A,B.  Cis-binding of the viral MHC class I molecules with its receptor may lead to inhibition of NK cell stimulatory cytokines, preventing NK cell recruitment and activation.	bind
46660	5	7589	5	13	NULL	NULL	NULL	statement 2	Process		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_2_5_521_s_215	10865197	3 A,B.  Cis-binding of the viral MHC class I molecules with its receptor may lead to inhibition of NK cell stimulatory cytokines, preventing NK cell recruitment and activation.	bind
31249	1	7589	7	10	NULL	0	NULL	MHC class I molecules 		viral	bind					MHC class I  receptor					NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_2_5_521_s_215	10865197	3 A,B.  Cis-binding of the viral MHC class I molecules with its receptor may lead to inhibition of NK cell stimulatory cytokines, preventing NK cell recruitment and activation.	bind
31250	2	7589	7	NULL	NULL	0	NULL	NK cells	NULL		stimulate	NULL				cytokines	NULL				NULL		0	NULL	NULL	NULL	gw60_microbesinfect_2_5_521_s_215	10865197	3 A,B.  Cis-binding of the viral MHC class I molecules with its receptor may lead to inhibition of NK cell stimulatory cytokines, preventing NK cell recruitment and activation.	bind
31251	3	7589	7	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_microbesinfect_2_5_521_s_215	10865197	3 A,B.  Cis-binding of the viral MHC class I molecules with its receptor may lead to inhibition of NK cell stimulatory cytokines, preventing NK cell recruitment and activation.	bind
31252	4	7589	7	NULL	NULL	0	NULL	statement 2	NULL		prevents	NULL				NK cell	NULL	recruitment of 			NULL		0	NULL	NULL	NULL	gw60_microbesinfect_2_5_521_s_215	10865197	3 A,B.  Cis-binding of the viral MHC class I molecules with its receptor may lead to inhibition of NK cell stimulatory cytokines, preventing NK cell recruitment and activation.	bind
31253	5	7589	7	NULL	NULL	0	NULL	statement 2	NULL		prevents	NULL				NK cell	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_microbesinfect_2_5_521_s_215	10865197	3 A,B.  Cis-binding of the viral MHC class I molecules with its receptor may lead to inhibition of NK cell stimulatory cytokines, preventing NK cell recruitment and activation.	bind
29045	1	7590	5	13	NULL	NULL	NULL	caspase-3	GP		is processed by					oligomeric Apaf-1-caspase-9 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_8461_s_211	10722681	3 Active caspase-3 not bound to the Apaf-1 complex appears to represent caspase-3 that is processed by the oligomeric Apaf-1-caspase-9 complex and subsequently released from the complex ( 14,  23).	bind
29046	2	7590	5	13	NULL	NULL	NULL	caspase-3	GP	active	is not bound to					Apaf-1 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_8461_s_211	10722681	3 Active caspase-3 not bound to the Apaf-1 complex appears to represent caspase-3 that is processed by the oligomeric Apaf-1-caspase-9 complex and subsequently released from the complex ( 14,  23).	bind
29047	3	7590	5	13	NULL	NULL	NULL	statement 2	Process		represents		appears to			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_8461_s_211	10722681	3 Active caspase-3 not bound to the Apaf-1 complex appears to represent caspase-3 that is processed by the oligomeric Apaf-1-caspase-9 complex and subsequently released from the complex ( 14,  23).	bind
29048	4	7590	5	13	NULL	NULL	NULL	caspase-3	GP		is released from		subsequently			oligomeric Apaf-1-caspase-9 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_8461_s_211	10722681	3 Active caspase-3 not bound to the Apaf-1 complex appears to represent caspase-3 that is processed by the oligomeric Apaf-1-caspase-9 complex and subsequently released from the complex ( 14,  23).	bind
31254	1	7590	7	NULL	NULL	0	NULL	caspase-3	NULL	active	does not bind	NULL				Apaf-1 complex	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_12_8461_s_211	10722681	3 Active caspase-3 not bound to the Apaf-1 complex appears to represent caspase-3 that is processed by the oligomeric Apaf-1-caspase-9 complex and subsequently released from the complex ( 14,  23).	bind
31255	2	7590	7	NULL	NULL	0	NULL	oligomeric Apaf-1-caspase-9 complex	NULL		process	NULL				caspase-3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_12_8461_s_211	10722681	3 Active caspase-3 not bound to the Apaf-1 complex appears to represent caspase-3 that is processed by the oligomeric Apaf-1-caspase-9 complex and subsequently released from the complex ( 14,  23).	bind
31256	3	7590	7	NULL	NULL	0	NULL	statement 1	NULL		represent	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_12_8461_s_211	10722681	3 Active caspase-3 not bound to the Apaf-1 complex appears to represent caspase-3 that is processed by the oligomeric Apaf-1-caspase-9 complex and subsequently released from the complex ( 14,  23).	bind
31257	4	7590	7	10	NULL	0	NULL	caspase-3			is released from		subsequently			statement 2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_8461_s_211	10722681	3 Active caspase-3 not bound to the Apaf-1 complex appears to represent caspase-3 that is processed by the oligomeric Apaf-1-caspase-9 complex and subsequently released from the complex ( 14,  23).	bind
29049	1	7591	5	13	NULL	NULL	NULL	FVII/VIIa	GP		is					plasma factor VII/VIIa	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
29050	2	7591	5	13	NULL	NULL	NULL	FVII/VIIa	GP		bind					TF	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
29051	3	7591	5	13	NULL	NULL	NULL	statement 2	GP		forms					TF:FVIIa complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
29052	4	7591	5	13	NULL	NULL	NULL	statement 3	Process		occurs after					vessel injury	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
29053	5	7591	5	13	NULL	NULL	NULL	statement 3	Process		activates					FX	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
29054	6	7591	5	13	NULL	NULL	NULL	statement 3	Process		activates					FIX	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
29055	7	7591	5	13	NULL	NULL	NULL	statement 5	Process		leads to					thrombin	GP	generation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
29056	8	7591	5	13	NULL	NULL	NULL	statement 5	Process		leads to					fibrin	GP	deposition of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
29057	9	7591	5	13	NULL	NULL	NULL	statement 5	Process		leads to					platelet	Cell	activation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
29058	10	7591	5	13	NULL	NULL	NULL	statement 6	Process		leads to					thrombin	GP	generation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
29059	11	7591	5	13	NULL	NULL	NULL	statement 6	Process		leads to					fibrin	GP	deposition of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
29060	12	7591	5	13	NULL	NULL	NULL	statement 6	Process		leads to					platelet	Cell	activation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
31258	1	7591	7	NULL	NULL	0	NULL	FVII/VIIa	NULL		bind	NULL				TF	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
31259	2	7591	7	NULL	NULL	0	NULL	statement 1	NULL		forms	NULL				TF:FVIIa complex	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
31260	3	7591	7	NULL	NULL	0	NULL	statement 1	NULL		occurs after	NULL				vessel injury	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
31261	4	7591	7	NULL	NULL	0	NULL	statement 2	NULL		activates	NULL				FX	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
31262	5	7591	7	NULL	NULL	0	NULL	statement 2	NULL		activates	NULL				FIX	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
31263	6	7591	7	NULL	NULL	0	NULL	statement 4	NULL		leads to	NULL				thrombin	NULL	generation of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
31264	7	7591	7	NULL	NULL	0	NULL	statement 5	NULL		leads to	NULL				thrombin	NULL	generation of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
31265	8	7591	7	NULL	NULL	0	NULL	statement 4	NULL		leads to	NULL				fibrin	NULL	deposition of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
31266	9	7591	7	NULL	NULL	0	NULL	statement 5	NULL		leads to	NULL				fibrin	NULL	deposition of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
31267	10	7591	7	NULL	NULL	0	NULL	statement 4	NULL		leads to	NULL				platelet 	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
31268	11	7591	7	NULL	NULL	0	NULL	statement 5	NULL		leads to	NULL				platelet	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
31269	12	7591	7	NULL	NULL	0	NULL	FVII/VIIa	NULL		is	NULL				plasma factor VII/VIIa	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_3_555_s_23	16385085	3 After vessel injury, plasma factor VII/VIIa (FVII/VIIa) binds to TF to form a TF:FVIIa complex, which activates FX and FIX, leading to thrombin generation, fibrin deposition, and platelet activation.	bind
29061	1	7592	5	13	NULL	NULL	NULL	Raf	GP	baculoviral;; recombinant	bind					GST-14.3.3 fusion protein	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_40_23681_s_183	7559537	3 already bound to the baculoviral  recombinant Raf-1 polypeptide, such Raf preparations bind  in vitro  to a GST-14.3.3    fusion protein but not to GST alone ( Fig. 3,  upper panel,  lanes 1  and  2); preincubation of Raf with cleaved, purified  E. coli  recombinant 14.3.	bind
31270	1	7592	7	10	NULL	0	NULL	Raf-1 polypeptide	NULL	baculoviral;; recombinant	bind	NULL				GST-14.3.3 fusion protein	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_40_23681_s_183	7559537	3 already bound to the baculoviral  recombinant Raf-1 polypeptide, such Raf preparations bind  in vitro  to a GST-14.3.3    fusion protein but not to GST alone ( Fig. 3,  upper panel,  lanes 1  and  2); preincubation of Raf with cleaved, purified  E. coli  recombinant 14.3.	bind
29063	1	7593	5	13	NULL	NULL	NULL	procaspase-8	GP		bind					TRADD	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
29064	3	7593	5	13	NULL	NULL	NULL	regulatory molecules	GP		blocks		physically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
29065	2	7593	5	13	NULL	NULL	NULL	FADD	GP		bind					TRADD	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
29066	4	7593	5	13	NULL	NULL	NULL	regulatory molecules	GP		blocks		physically			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
29067	5	7593	5	13	NULL	NULL	NULL	TRAF2	GP		bind					TRADD	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
29068	6	7593	5	13	NULL	NULL	NULL	RIP	GP		bind					TRADD	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
29069	7	7593	5	13	NULL	NULL	NULL	statement 5	Process	enhancing	inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
29070	8	7593	5	13	NULL	NULL	NULL	statement 5	Process	enhancing	inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
29071	9	7593	5	13	NULL	NULL	NULL	statement 6	Process	enhancing	inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
29072	10	7593	5	13	NULL	NULL	NULL	statement 6	Process	enhancing	inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
31300	1	7593	7	NULL	NULL	0	NULL	FADD	NULL		bind	NULL				TRADD	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
31301	2	7593	7	NULL	NULL	0	NULL	procaspase-8	NULL		bind	NULL				TRADD	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
31302	3	7593	7	10	NULL	0	NULL	regulatory molecules			block		physically			statement 1					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
31303	4	7593	7	10	NULL	0	NULL	regulatory molecules			block		physically			statement 2					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
31304	5	7593	7	NULL	NULL	0	NULL	TRAF2	NULL		bind	NULL				TRADD	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
31305	6	7593	7	NULL	NULL	0	NULL	RIP	NULL		bind	NULL				TRADD	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
31306	7	7593	7	NULL	NULL	0	NULL	statement 5	NULL	enhancement of	inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
31307	8	7593	7	NULL	NULL	0	NULL	statement 5	NULL	enhancement of	inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
31308	9	7593	7	NULL	NULL	0	NULL	statement 6	NULL	enhancement of	inhibits	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
31309	10	7593	7	NULL	NULL	0	NULL	statement 6	NULL	enhancement of	inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_40_39251_s_212	12882979	3 Alternatively, mechanisms to inhibit FADD and procaspase-8 binding to TRADD may exist, either by regulatory molecules physically blocking this association or preferentially enhancing the TRAF2 and RIP binding to TRADD.	bind
29833	1	7594	5	13	NULL	NULL	NULL	Arix	GP		bind					DB1	GP			enhancer	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_4_2911_s_351	10644760	3 Alternatively, the binding of Arix to the DB1 enhancer may provide a favorable environment for the recruitment of Fos-Jun heterodimers to the CRE/AP1 site following PKA stimulation.	bind
29834	2	7594	5	13	NULL	NULL	NULL	Fos-Jun heterodimers	GP		is recruited to									CRE/AP1 site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_4_2911_s_351	10644760	3 Alternatively, the binding of Arix to the DB1 enhancer may provide a favorable environment for the recruitment of Fos-Jun heterodimers to the CRE/AP1 site following PKA stimulation.	bind
29835	3	7594	5	13	NULL	NULL	NULL	statement 2	Process		occurs following					PKA	GP	stimulation with			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_4_2911_s_351	10644760	3 Alternatively, the binding of Arix to the DB1 enhancer may provide a favorable environment for the recruitment of Fos-Jun heterodimers to the CRE/AP1 site following PKA stimulation.	bind
29836	4	7594	5	13	NULL	NULL	NULL	statement 1	Process		provide		may			statement 3	Process	favorable environment for			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_4_2911_s_351	10644760	3 Alternatively, the binding of Arix to the DB1 enhancer may provide a favorable environment for the recruitment of Fos-Jun heterodimers to the CRE/AP1 site following PKA stimulation.	bind
31310	1	7594	7	NULL	NULL	0	NULL	 Arix	NULL		bind	NULL				DB1	NULL			enhancer	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_4_2911_s_351	10644760	3 Alternatively, the binding of Arix to the DB1 enhancer may provide a favorable environment for the recruitment of Fos-Jun heterodimers to the CRE/AP1 site following PKA stimulation.	bind
31311	2	7594	7	10	NULL	0	NULL	Fos-Jun heterodimers 			is recruited to									CRE/AP1 site 	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_4_2911_s_351	10644760	3 Alternatively, the binding of Arix to the DB1 enhancer may provide a favorable environment for the recruitment of Fos-Jun heterodimers to the CRE/AP1 site following PKA stimulation.	bind
31312	3	7594	7	NULL	NULL	0	NULL	statement 2	NULL		occurs upon	NULL				PKA	NULL	stimulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_4_2911_s_351	10644760	3 Alternatively, the binding of Arix to the DB1 enhancer may provide a favorable environment for the recruitment of Fos-Jun heterodimers to the CRE/AP1 site following PKA stimulation.	bind
31313	4	7594	7	NULL	NULL	0	NULL	statement 1	NULL		favor	NULL	may			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_4_2911_s_351	10644760	3 Alternatively, the binding of Arix to the DB1 enhancer may provide a favorable environment for the recruitment of Fos-Jun heterodimers to the CRE/AP1 site following PKA stimulation.	bind
29073	1	7595	5	13	NULL	NULL	NULL	SP-A	GP		bind		directly			TLR4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_31_21771_s_322	16754682	3 Although further experiments are required, we speculate that the physiological meaning of the direct binding of SP-A to TLR4 may be to modulate the subsequent structural changes of TLR4 initiated by LPS binding to MD-2.	bind
29074	2	7595	5	13	NULL	NULL	NULL	LPS	Chemical		bind					MD-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_31_21771_s_322	16754682	3 Although further experiments are required, we speculate that the physiological meaning of the direct binding of SP-A to TLR4 may be to modulate the subsequent structural changes of TLR4 initiated by LPS binding to MD-2.	bind
29075	3	7595	5	13	NULL	NULL	NULL	TLR4	GP	structural changes of	is initiated by					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_31_21771_s_322	16754682	3 Although further experiments are required, we speculate that the physiological meaning of the direct binding of SP-A to TLR4 may be to modulate the subsequent structural changes of TLR4 initiated by LPS binding to MD-2.	bind
29076	4	7595	5	13	NULL	NULL	NULL	statement 1	Process		modulate		may			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_31_21771_s_322	16754682	3 Although further experiments are required, we speculate that the physiological meaning of the direct binding of SP-A to TLR4 may be to modulate the subsequent structural changes of TLR4 initiated by LPS binding to MD-2.	bind
31314	1	7595	7	NULL	NULL	0	NULL	 SP-A	NULL		bind	NULL				TLR4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_21771_s_322	16754682	3 Although further experiments are required, we speculate that the physiological meaning of the direct binding of SP-A to TLR4 may be to modulate the subsequent structural changes of TLR4 initiated by LPS binding to MD-2.	bind
31315	2	7595	7	NULL	NULL	0	NULL	LPS	NULL		bind	NULL				MD-2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_21771_s_322	16754682	3 Although further experiments are required, we speculate that the physiological meaning of the direct binding of SP-A to TLR4 may be to modulate the subsequent structural changes of TLR4 initiated by LPS binding to MD-2.	bind
31316	3	7595	7	NULL	NULL	0	NULL	statement 2	NULL		initiate	NULL				TLR4	NULL	structural changes of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_21771_s_322	16754682	3 Although further experiments are required, we speculate that the physiological meaning of the direct binding of SP-A to TLR4 may be to modulate the subsequent structural changes of TLR4 initiated by LPS binding to MD-2.	bind
31317	4	7595	7	NULL	NULL	0	NULL	statement 1	NULL		modulate	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_21771_s_322	16754682	3 Although further experiments are required, we speculate that the physiological meaning of the direct binding of SP-A to TLR4 may be to modulate the subsequent structural changes of TLR4 initiated by LPS binding to MD-2.	bind
54562	1	7596	5	13	NULL	NULL	NULL				bind			CUT domain		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_5319_s_21	16371359	3 Although this structure showed similarity to those of the POU-specific domains of POU-homologous proteins ( ,  ), the DNA-binding mechanism of the CUT domain is yet unknown.	bind
31318	1	7596	7	NULL	NULL	0	NULL		NULL		bind	NULL		CUT domain		DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_8_5319_s_21	16371359	3 Although this structure showed similarity to those of the POU-specific domains of POU-homologous proteins ( ,  ), the DNA-binding mechanism of the CUT domain is yet unknown.	bind
29077	2	7598	5	13	NULL	NULL	NULL	statement 1	GP		bind					Galpha(GDP)	GP	inactive			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_38071_s_11	16129667	3 An agonist-activated GPCR (R*) binds to the inactive Galpha(GDP).	bind
54563	1	7598	5	13	NULL	NULL	NULL	agonist	Chemical		activates					GPCR (R*)	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_38071_s_11	16129667	3 An agonist-activated GPCR (R*) binds to the inactive Galpha(GDP).	bind
31320	1	7598	7	NULL	NULL	0	NULL	agonist	NULL		activates	NULL				GPCR (R*)	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_45_38071_s_11	16129667	3 An agonist-activated GPCR (R*) binds to the inactive Galpha(GDP).	bind
31321	2	7598	7	NULL	NULL	0	NULL	statement 1	NULL		binds to	NULL				Galpha(GDP)	NULL	inactive			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_45_38071_s_11	16129667	3 An agonist-activated GPCR (R*) binds to the inactive Galpha(GDP).	bind
29079	1	7599	5	13	NULL	NULL	NULL	SHBG	GP		does not bind					C4BP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_23_14658_s_44	9169428	3 and  4) bind to human C4BP with about the same affinity, whereas the homologous proteins SHBG (26% identical to the SHBG-like domain of human protein S; see Ref.  38) and growth arrest-specific protein 6 (Gas 6) (44% identical to human protein S; see Ref.  39) do not show any detectable binding to C4BP.	bind
29080	2	7599	5	13	NULL	NULL	NULL	Gas 6	GP		is					growth arrest-specific protein 6	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_23_14658_s_44	9169428	3 and  4) bind to human C4BP with about the same affinity, whereas the homologous proteins SHBG (26% identical to the SHBG-like domain of human protein S; see Ref.  38) and growth arrest-specific protein 6 (Gas 6) (44% identical to human protein S; see Ref.  39) do not show any detectable binding to C4BP.	bind
29081	3	7599	5	13	NULL	NULL	NULL	Gas 6	GP		does not bind					C4BP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_23_14658_s_44	9169428	3 and  4) bind to human C4BP with about the same affinity, whereas the homologous proteins SHBG (26% identical to the SHBG-like domain of human protein S; see Ref.  38) and growth arrest-specific protein 6 (Gas 6) (44% identical to human protein S; see Ref.  39) do not show any detectable binding to C4BP.	bind
46665	4	7599	5	13	NULL	NULL	NULL	SHBG	GP		is similar to					protein S	GP	human	SHBG-like domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_23_14658_s_44	9169428	3 and  4) bind to human C4BP with about the same affinity, whereas the homologous proteins SHBG (26% identical to the SHBG-like domain of human protein S; see Ref.  38) and growth arrest-specific protein 6 (Gas 6) (44% identical to human protein S; see Ref.  39) do not show any detectable binding to C4BP.	bind
46666	5	7599	5	13	NULL	NULL	NULL	Gas 6	GP		is similar to					protein S	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_23_14658_s_44	9169428	3 and  4) bind to human C4BP with about the same affinity, whereas the homologous proteins SHBG (26% identical to the SHBG-like domain of human protein S; see Ref.  38) and growth arrest-specific protein 6 (Gas 6) (44% identical to human protein S; see Ref.  39) do not show any detectable binding to C4BP.	bind
31322	1	7599	7	NULL	NULL	0	NULL	SHBG	NULL		is identical to	NULL				protein S	NULL	human	SHBG-like domain 		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_23_14658_s_44	9169428	3 and  4) bind to human C4BP with about the same affinity, whereas the homologous proteins SHBG (26% identical to the SHBG-like domain of human protein S; see Ref.  38) and growth arrest-specific protein 6 (Gas 6) (44% identical to human protein S; see Ref.  39) do not show any detectable binding to C4BP.	bind
31323	2	7599	7	NULL	NULL	0	NULL	Gas 6	NULL		is identical to	NULL				protein S	NULL	human			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_23_14658_s_44	9169428	3 and  4) bind to human C4BP with about the same affinity, whereas the homologous proteins SHBG (26% identical to the SHBG-like domain of human protein S; see Ref.  38) and growth arrest-specific protein 6 (Gas 6) (44% identical to human protein S; see Ref.  39) do not show any detectable binding to C4BP.	bind
31324	3	7599	7	NULL	NULL	0	NULL	SHBG	NULL		does not bind	NULL				C4BP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_23_14658_s_44	9169428	3 and  4) bind to human C4BP with about the same affinity, whereas the homologous proteins SHBG (26% identical to the SHBG-like domain of human protein S; see Ref.  38) and growth arrest-specific protein 6 (Gas 6) (44% identical to human protein S; see Ref.  39) do not show any detectable binding to C4BP.	bind
31325	4	7599	7	NULL	NULL	0	NULL	Gas 6	NULL		does not bind	NULL				C4BP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_23_14658_s_44	9169428	3 and  4) bind to human C4BP with about the same affinity, whereas the homologous proteins SHBG (26% identical to the SHBG-like domain of human protein S; see Ref.  38) and growth arrest-specific protein 6 (Gas 6) (44% identical to human protein S; see Ref.  39) do not show any detectable binding to C4BP.	bind
31326	5	7599	7	NULL	NULL	0	NULL	Gas 6	NULL		is	NULL				growth arrest-specific protein 6 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_23_14658_s_44	9169428	3 and  4) bind to human C4BP with about the same affinity, whereas the homologous proteins SHBG (26% identical to the SHBG-like domain of human protein S; see Ref.  38) and growth arrest-specific protein 6 (Gas 6) (44% identical to human protein S; see Ref.  39) do not show any detectable binding to C4BP.	bind
29082	1	7600	5	13	NULL	NULL	NULL	anti-N antibodies	GP		bind					ez1-586	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_20088_s_192	9242682	3 Anti-N and anti-C antibodies bound both ez1-586 and ez1-333.	bind
29083	2	7600	5	13	NULL	NULL	NULL	anti-N antibodies	GP		bind					ez1-333	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_20088_s_192	9242682	3 Anti-N and anti-C antibodies bound both ez1-586 and ez1-333.	bind
29084	3	7600	5	13	NULL	NULL	NULL	anti-C antibodies	GP		bind					ez1-586	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_20088_s_192	9242682	3 Anti-N and anti-C antibodies bound both ez1-586 and ez1-333.	bind
29085	4	7600	5	13	NULL	NULL	NULL	anti-C antibodies	GP		bind					ez1-333	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_20088_s_192	9242682	3 Anti-N and anti-C antibodies bound both ez1-586 and ez1-333.	bind
31327	1	7600	7	NULL	NULL	0	NULL	Anti-N antibody	NULL		bind	NULL				 ez1-586	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_32_20088_s_192	9242682	3 Anti-N and anti-C antibodies bound both ez1-586 and ez1-333.	bind
31328	2	7600	7	NULL	NULL	0	NULL	anti-C antibody	NULL		bind	NULL				ez1-333	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_32_20088_s_192	9242682	3 Anti-N and anti-C antibodies bound both ez1-586 and ez1-333.	bind
46586	3	7600	7	10	NULL	0	NULL	anti-C antibody	NULL		bind	NULL				ez1-586	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_20088_s_192	9242682	3 Anti-N and anti-C antibodies bound both ez1-586 and ez1-333.	bind
46587	1	7600	7	10	NULL	0	NULL	Anti-N antibody	NULL		bind	NULL				 ez1-333	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_32_20088_s_192	9242682	3 Anti-N and anti-C antibodies bound both ez1-586 and ez1-333.	bind
29123	1	7601	5	13	NULL	NULL	NULL	TNFalpha	GP		bind					membrane receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_23_13333_s_212	8662837	3 As the protective capabilities of M-T2 correlate with its ability to inhibit binding of TNFalpha to membrane receptors, we conclude that M-T2 inhibits the cytolytic activities of TNFalpha by physically preventing TNFalpha from associating with its cognate TNF membrane receptors.	bind
29124	2	7601	5	13	NULL	NULL	NULL	M-T2	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_23_13333_s_212	8662837	3 As the protective capabilities of M-T2 correlate with its ability to inhibit binding of TNFalpha to membrane receptors, we conclude that M-T2 inhibits the cytolytic activities of TNFalpha by physically preventing TNFalpha from associating with its cognate TNF membrane receptors.	bind
29125	3	7601	5	13	NULL	NULL	NULL	TNFalpha	GP		associates with					TNF membrane receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_23_13333_s_212	8662837	3 As the protective capabilities of M-T2 correlate with its ability to inhibit binding of TNFalpha to membrane receptors, we conclude that M-T2 inhibits the cytolytic activities of TNFalpha by physically preventing TNFalpha from associating with its cognate TNF membrane receptors.	bind
29126	4	7601	5	13	NULL	NULL	NULL	M-T2	GP		prevents		physically			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_23_13333_s_212	8662837	3 As the protective capabilities of M-T2 correlate with its ability to inhibit binding of TNFalpha to membrane receptors, we conclude that M-T2 inhibits the cytolytic activities of TNFalpha by physically preventing TNFalpha from associating with its cognate TNF membrane receptors.	bind
29127	5	7601	5	13	NULL	NULL	NULL	TNFalpha	GP		exhibits					cytolytic activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_23_13333_s_212	8662837	3 As the protective capabilities of M-T2 correlate with its ability to inhibit binding of TNFalpha to membrane receptors, we conclude that M-T2 inhibits the cytolytic activities of TNFalpha by physically preventing TNFalpha from associating with its cognate TNF membrane receptors.	bind
46653	6	7601	5	13	NULL	NULL	NULL	M-T2	GP		inhibits					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_23_13333_s_212	8662837	3 As the protective capabilities of M-T2 correlate with its ability to inhibit binding of TNFalpha to membrane receptors, we conclude that M-T2 inhibits the cytolytic activities of TNFalpha by physically preventing TNFalpha from associating with its cognate TNF membrane receptors.	bind
23187	1	7601	6	NULL	NULL	0	NULL	TNFalpha	NULL		bind	NULL				membrane receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_23_13333_s_212	8662837	3 As the protective capabilities of M-T2 correlate with its ability to inhibit binding of TNFalpha to membrane receptors, we conclude that M-T2 inhibits the cytolytic activities of TNFalpha by physically preventing TNFalpha from associating with its cognate TNF membrane receptors.	bind
23188	2	7601	6	NULL	NULL	0	NULL	M-T2 	NULL		inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_23_13333_s_212	8662837	3 As the protective capabilities of M-T2 correlate with its ability to inhibit binding of TNFalpha to membrane receptors, we conclude that M-T2 inhibits the cytolytic activities of TNFalpha by physically preventing TNFalpha from associating with its cognate TNF membrane receptors.	bind
23189	3	7601	6	NULL	NULL	0	NULL	TNFalpha	NULL		exhibit	NULL				cytolytic activities	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_23_13333_s_212	8662837	3 As the protective capabilities of M-T2 correlate with its ability to inhibit binding of TNFalpha to membrane receptors, we conclude that M-T2 inhibits the cytolytic activities of TNFalpha by physically preventing TNFalpha from associating with its cognate TNF membrane receptors.	bind
23190	4	7601	6	NULL	NULL	0	NULL	M-T2	NULL		inhibit	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_23_13333_s_212	8662837	3 As the protective capabilities of M-T2 correlate with its ability to inhibit binding of TNFalpha to membrane receptors, we conclude that M-T2 inhibits the cytolytic activities of TNFalpha by physically preventing TNFalpha from associating with its cognate TNF membrane receptors.	bind
23191	5	7601	6	NULL	NULL	0	NULL	TNFalpha	NULL		associate with	NULL				TNF membrane receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_23_13333_s_212	8662837	3 As the protective capabilities of M-T2 correlate with its ability to inhibit binding of TNFalpha to membrane receptors, we conclude that M-T2 inhibits the cytolytic activities of TNFalpha by physically preventing TNFalpha from associating with its cognate TNF membrane receptors.	bind
23270	6	7601	6	NULL	NULL	0	NULL	M-T2	NULL		inhibits	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_23_13333_s_212	8662837	3 As the protective capabilities of M-T2 correlate with its ability to inhibit binding of TNFalpha to membrane receptors, we conclude that M-T2 inhibits the cytolytic activities of TNFalpha by physically preventing TNFalpha from associating with its cognate TNF membrane receptors.	bind
29129	1	7602	5	13	NULL	NULL	NULL	p130Cas	GP		bind		consistently	SH3 domain		PTP1B	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_49_31290_s_86	8940134	3 As the SH3 domain derived from p130Cas consistently bound more PTP1B than any other SH3 domain tested  in vitro (as assessed by densitometry of immunoblots), we investigated this interaction in more detail.	bind
23272	1	7602	6	NULL	NULL	0	NULL	p130Cas	NULL		bind	NULL	consistently	SH3 domain		PTP1B	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_271_49_31290_s_86	8940134	3 As the SH3 domain derived from p130Cas consistently bound more PTP1B than any other SH3 domain tested  in vitro (as assessed by densitometry of immunoblots), we investigated this interaction in more detail.	bind
29130	1	7604	5	13	NULL	NULL	NULL	vitronectin	GP		bind					fibrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_19788_s_29	10764803	3 Based on these observations, we hypothesized that fibrin-bound vitronectin supports PAI-1 binding.	bind
29132	2	7604	5	13	NULL	NULL	NULL	statement 1	Process		supports					PAI-1	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_19788_s_29	10764803	3 Based on these observations, we hypothesized that fibrin-bound vitronectin supports PAI-1 binding.	bind
23281	1	7604	6	NULL	NULL	0	NULL	fibrin	NULL		bind	NULL				vitronectin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_26_19788_s_29	10764803	3 Based on these observations, we hypothesized that fibrin-bound vitronectin supports PAI-1 binding.	bind
23282	2	7604	6	NULL	NULL	0	NULL	statement 1	NULL		supports	NULL				PAI-1	NULL	binding of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_26_19788_s_29	10764803	3 Based on these observations, we hypothesized that fibrin-bound vitronectin supports PAI-1 binding.	bind
29133	1	7605	5	13	NULL	NULL	NULL	IMP	Chemical		bind					synthetase	GP		GTP pocket		NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_30_26779_s_271	12004071	3 Because IMP concentrations in exhaustively exercised muscle rise to 3.6 mM ( 12), the binding of IMP to the GTP pocket of the synthetase may occur  in vivo under these conditions.	bind
29136	2	7605	5	13	NULL	NULL	NULL	IMP	Chemical		rise in					muscle	OrganismPart	exhaustively exercised			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_30_26779_s_271	12004071	3 Because IMP concentrations in exhaustively exercised muscle rise to 3.6 mM ( 12), the binding of IMP to the GTP pocket of the synthetase may occur  in vivo under these conditions.	bind
23290	1	7605	6	NULL	NULL	0	NULL	IMP	NULL		bind	NULL	may			synthetase	NULL		GTP pocket		NULL	in vivo	0	NULL	NULL	NULL	gw60_jbiolchem_277_30_26779_s_271	12004071	3 Because IMP concentrations in exhaustively exercised muscle rise to 3.6 mM ( 12), the binding of IMP to the GTP pocket of the synthetase may occur  in vivo under these conditions.	bind
29137	1	7606	5	13	NULL	NULL	NULL	rigor myosin	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_8_982_s_54	15302786	3 Before each experiment, myosin (200 mug/mL), equimolar actin, and 1 mmol/L ATP are centrifuged (320 000 g; 20 minutes) to remove noncycling, rigor myosin bound to actin.	bind
23295	1	7606	6	NULL	NULL	0	NULL	rigor myosin	NULL		bind	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_110_8_982_s_54	15302786	3 Before each experiment, myosin (200 mug/mL), equimolar actin, and 1 mmol/L ATP are centrifuged (320 000 g; 20 minutes) to remove noncycling, rigor myosin bound to actin.	bind
29138	1	7607	5	13	NULL	NULL	NULL	Rac isoforms	GP		bind					p67 phox	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18834_s_166	9228059	3 Binding of Rac isoforms to p67 phox has been demonstrated using p67 phox (or a p67 phox-GST fusion protein) immobilized on glutathione beads ( 46) or on a nitrocellulose filter ( 48,  60) and also by yeast two-hybrid analysis ( 49).	bind
23296	1	7607	6	NULL	NULL	0	NULL	Rac isoforms	NULL		bind	NULL				p67 phox	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_30_18834_s_166	9228059	3 Binding of Rac isoforms to p67 phox has been demonstrated using p67 phox (or a p67 phox-GST fusion protein) immobilized on glutathione beads ( 46) or on a nitrocellulose filter ( 48,  60) and also by yeast two-hybrid analysis ( 49).	bind
29141	1	7609	5	13	NULL	NULL	NULL	Rsp5p	GP		is a type of			WW domains					type I WW domains		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_28_25974_s_251	11356856	3 Chang  et al. ( 58) showed that Rsp5p WW domains are type I WW domains that bind preferentially to PP XY-containing ligands.	bind
29147	2	7609	5	13	NULL	NULL	NULL	statement 1	GP		bind		preferentially			PP XY-containing ligands	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_28_25974_s_251	11356856	3 Chang  et al. ( 58) showed that Rsp5p WW domains are type I WW domains that bind preferentially to PP XY-containing ligands.	bind
23300	1	7609	6	10	NULL	0	NULL	Rsp5p	NULL		is a type of	NULL		WW domain			NULL		type I WW domains		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_28_25974_s_251	11356856	3 Chang  et al. ( 58) showed that Rsp5p WW domains are type I WW domains that bind preferentially to PP XY-containing ligands.	bind
23301	2	7609	6	NULL	NULL	0	NULL	Rsp5p	NULL		bind	NULL	preferentially	WW domain		PP-XY containing ligands	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_28_25974_s_251	11356856	3 Chang  et al. ( 58) showed that Rsp5p WW domains are type I WW domains that bind preferentially to PP XY-containing ligands.	bind
29150	1	7610	5	13	NULL	NULL	NULL	MyHC	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_18_2276_s_11	15883223	3 Consequently, MyHC binds to actin, hydrolyzes ATP to adenosine diphosphate (ADP) and inorganic phosphate, and displaces the actin filament.	bind
29157	2	7610	5	13	NULL	NULL	NULL	ATP	Chemical		is hydrolysed to					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_18_2276_s_11	15883223	3 Consequently, MyHC binds to actin, hydrolyzes ATP to adenosine diphosphate (ADP) and inorganic phosphate, and displaces the actin filament.	bind
29159	3	7610	5	13	NULL	NULL	NULL	statement 2	Process		displaces					actin filament	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_18_2276_s_11	15883223	3 Consequently, MyHC binds to actin, hydrolyzes ATP to adenosine diphosphate (ADP) and inorganic phosphate, and displaces the actin filament.	bind
29160	4	7610	5	13	NULL	NULL	NULL	ADP	Chemical		is					adenosine diphosphate	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_18_2276_s_11	15883223	3 Consequently, MyHC binds to actin, hydrolyzes ATP to adenosine diphosphate (ADP) and inorganic phosphate, and displaces the actin filament.	bind
55525	5	7610	5	13	NULL	NULL	NULL	ATP	Chemical		is hydrolyzed to					inorganic phosphate	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_18_2276_s_11	15883223	3 Consequently, MyHC binds to actin, hydrolyzes ATP to adenosine diphosphate (ADP) and inorganic phosphate, and displaces the actin filament.	bind
55526	6	7610	5	13	NULL	NULL	NULL	statement 2	Process		occurs along with					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_18_2276_s_11	15883223	3 Consequently, MyHC binds to actin, hydrolyzes ATP to adenosine diphosphate (ADP) and inorganic phosphate, and displaces the actin filament.	bind
23302	1	7610	6	NULL	NULL	0	NULL	MyHC	NULL		bind	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_111_18_2276_s_11	15883223	3 Consequently, MyHC binds to actin, hydrolyzes ATP to adenosine diphosphate (ADP) and inorganic phosphate, and displaces the actin filament.	bind
23303	2	7610	6	NULL	NULL	0	NULL	MyHC	NULL		displaces 	NULL				actin filament	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_111_18_2276_s_11	15883223	3 Consequently, MyHC binds to actin, hydrolyzes ATP to adenosine diphosphate (ADP) and inorganic phosphate, and displaces the actin filament.	bind
23304	3	7610	6	10	NULL	0	NULL	ATP			hydrolyzed to					ADP					NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_18_2276_s_11	15883223	3 Consequently, MyHC binds to actin, hydrolyzes ATP to adenosine diphosphate (ADP) and inorganic phosphate, and displaces the actin filament.	bind
23305	4	7610	6	NULL	NULL	0	NULL	MyHC	NULL		plays a role in	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_111_18_2276_s_11	15883223	3 Consequently, MyHC binds to actin, hydrolyzes ATP to adenosine diphosphate (ADP) and inorganic phosphate, and displaces the actin filament.	bind
46601	5	7610	6	10	NULL	0	NULL	ADP	NULL		is	NULL				adenosine diphosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_111_18_2276_s_11	15883223	3 Consequently, MyHC binds to actin, hydrolyzes ATP to adenosine diphosphate (ADP) and inorganic phosphate, and displaces the actin filament.	bind
55527	6	7610	6	10	NULL	0	NULL	ATP			is hydrolyzed to					inorganic phosphate					NULL		0	NULL	NULL	NULL	gw70_circulation_111_18_2276_s_11	15883223	3 Consequently, MyHC binds to actin, hydrolyzes ATP to adenosine diphosphate (ADP) and inorganic phosphate, and displaces the actin filament.	bind
55528	7	7610	6	10	NULL	0	NULL	statement 3			occurs along with					statement 6					NULL		0	NULL	NULL	NULL	gw70_circulation_111_18_2276_s_11	15883223	3 Consequently, MyHC binds to actin, hydrolyzes ATP to adenosine diphosphate (ADP) and inorganic phosphate, and displaces the actin filament.	bind
30415	1	7611	5	13	NULL	NULL	NULL	oligo FP4	NucleicAcid		bind					nuclear protein	GP	J774 cells			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_8331_s_141	10722663	3 Consistent with the footprinting experiments (Fig.  2), oligo FP4 binds a nuclear protein (band F) only from J774 cells.	bind
23306	1	7611	6	10	NULL	0	NULL	oligo FP4			bind					nuclear protein 		J774 cells			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_8331_s_141	10722663	3 Consistent with the footprinting experiments (Fig.  2), oligo FP4 binds a nuclear protein (band F) only from J774 cells.	bind
30416	1	7612	5	13	NULL	NULL	NULL	CT-1	GP		bind					gp130	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_2_128_s_23	11834704	3 CT-1 binds to glycoprotein130 (gp130) and the leukemia inhibitory factor (LIF) receptor, a component of the gp130 receptor.	bind
30417	2	7612	5	13	NULL	NULL	NULL	gp130	GP		is					glycoprotein130	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_2_128_s_23	11834704	3 CT-1 binds to glycoprotein130 (gp130) and the leukemia inhibitory factor (LIF) receptor, a component of the gp130 receptor.	bind
30418	3	7612	5	13	NULL	NULL	NULL	CT-1	GP		bind					LIF receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_2_128_s_23	11834704	3 CT-1 binds to glycoprotein130 (gp130) and the leukemia inhibitory factor (LIF) receptor, a component of the gp130 receptor.	bind
30419	4	7612	5	13	NULL	NULL	NULL	LIF receptor	GP		is					leukemia inhibitory factor receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_2_128_s_23	11834704	3 CT-1 binds to glycoprotein130 (gp130) and the leukemia inhibitory factor (LIF) receptor, a component of the gp130 receptor.	bind
30420	5	7612	5	13	NULL	NULL	NULL	LIF receptor	GP		is a component of					gp130 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_2_128_s_23	11834704	3 CT-1 binds to glycoprotein130 (gp130) and the leukemia inhibitory factor (LIF) receptor, a component of the gp130 receptor.	bind
23307	1	7612	6	NULL	NULL	0	NULL	CT-1	NULL		bind	NULL				gp130	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_2_128_s_23	11834704	3 CT-1 binds to glycoprotein130 (gp130) and the leukemia inhibitory factor (LIF) receptor, a component of the gp130 receptor.	bind
23308	2	7612	6	NULL	NULL	0	NULL	gp130	NULL		is	NULL				glycoprotein130	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_2_128_s_23	11834704	3 CT-1 binds to glycoprotein130 (gp130) and the leukemia inhibitory factor (LIF) receptor, a component of the gp130 receptor.	bind
23309	3	7612	6	NULL	NULL	0	NULL	CT-1	NULL		bind	NULL				LIF receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_2_128_s_23	11834704	3 CT-1 binds to glycoprotein130 (gp130) and the leukemia inhibitory factor (LIF) receptor, a component of the gp130 receptor.	bind
23310	4	7612	6	NULL	NULL	0	NULL	LIF	NULL		is	NULL				leukemia inhibitory factor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_2_128_s_23	11834704	3 CT-1 binds to glycoprotein130 (gp130) and the leukemia inhibitory factor (LIF) receptor, a component of the gp130 receptor.	bind
23311	5	7612	6	NULL	NULL	0	NULL	LIF receptor	NULL		is a component of	NULL				gp130 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_2_128_s_23	11834704	3 CT-1 binds to glycoprotein130 (gp130) and the leukemia inhibitory factor (LIF) receptor, a component of the gp130 receptor.	bind
30421	1	7613	5	13	NULL	NULL	NULL	Myc-Raf	GP		bind					GST-14.3.3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_40_23681_s_267	7559537	3 dimerization, inasmuch as the Myc-Raf  bound to GST-14.3.3 (1-180) ( Fig. 5 C,  middle panel,  lane 5), which dimerizes quite  well with Myc-14.3.3 ( Fig. 5 B,  bottom panel,  lane 5), also lacks detectable  kinase activity ( Fig. 5 C,  bottom panel,  lane 5).	bind
30422	2	7613	5	13	NULL	NULL	NULL	GST-14.3.3	GP		dimerizes with					Myc-14.3.3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_40_23681_s_267	7559537	3 dimerization, inasmuch as the Myc-Raf  bound to GST-14.3.3 (1-180) ( Fig. 5 C,  middle panel,  lane 5), which dimerizes quite  well with Myc-14.3.3 ( Fig. 5 B,  bottom panel,  lane 5), also lacks detectable  kinase activity ( Fig. 5 C,  bottom panel,  lane 5).	bind
30423	3	7613	5	13	NULL	NULL	NULL	GST-14.3.3	GP		lacks					kinase activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_40_23681_s_267	7559537	3 dimerization, inasmuch as the Myc-Raf  bound to GST-14.3.3 (1-180) ( Fig. 5 C,  middle panel,  lane 5), which dimerizes quite  well with Myc-14.3.3 ( Fig. 5 B,  bottom panel,  lane 5), also lacks detectable  kinase activity ( Fig. 5 C,  bottom panel,  lane 5).	bind
23312	1	7613	6	NULL	NULL	0	NULL	Myc-Raf	NULL		bind	NULL				GST-14.3.3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_40_23681_s_267	7559537	3 dimerization, inasmuch as the Myc-Raf  bound to GST-14.3.3 (1-180) ( Fig. 5 C,  middle panel,  lane 5), which dimerizes quite  well with Myc-14.3.3 ( Fig. 5 B,  bottom panel,  lane 5), also lacks detectable  kinase activity ( Fig. 5 C,  bottom panel,  lane 5).	bind
23313	2	7613	6	10	NULL	0	NULL	GST-14.3.3	NULL		dimerizes  with	NULL				Myc-14.3.3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_40_23681_s_267	7559537	3 dimerization, inasmuch as the Myc-Raf  bound to GST-14.3.3 (1-180) ( Fig. 5 C,  middle panel,  lane 5), which dimerizes quite  well with Myc-14.3.3 ( Fig. 5 B,  bottom panel,  lane 5), also lacks detectable  kinase activity ( Fig. 5 C,  bottom panel,  lane 5).	bind
23314	3	7613	6	10	NULL	0	NULL	GST-14.3.3	NULL		lacks	NULL				kinase activity	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_40_23681_s_267	7559537	3 dimerization, inasmuch as the Myc-Raf  bound to GST-14.3.3 (1-180) ( Fig. 5 C,  middle panel,  lane 5), which dimerizes quite  well with Myc-14.3.3 ( Fig. 5 B,  bottom panel,  lane 5), also lacks detectable  kinase activity ( Fig. 5 C,  bottom panel,  lane 5).	bind
30424	1	7614	5	13	NULL	NULL	NULL	Hb	GP	free	bind					Hp	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_16	14656926	3 During intravascular hemolysis, free Hb binds to the plasma protein Hp, and Hb:Hp complexes are formed.	bind
30425	2	7614	5	13	NULL	NULL	NULL	Hp	GP		is a type of					plasma protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_16	14656926	3 During intravascular hemolysis, free Hb binds to the plasma protein Hp, and Hb:Hp complexes are formed.	bind
30426	3	7614	5	13	NULL	NULL	NULL	statement 1	Process		forms					Hb:Hp complexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_16	14656926	3 During intravascular hemolysis, free Hb binds to the plasma protein Hp, and Hb:Hp complexes are formed.	bind
30427	4	7614	5	13	NULL	NULL	NULL	statement 1	Process		occurs during					intravascular hemolysis	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_16	14656926	3 During intravascular hemolysis, free Hb binds to the plasma protein Hp, and Hb:Hp complexes are formed.	bind
23315	1	7614	6	10	NULL	0	NULL	Hb		free	bind					Hp					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_16	14656926	3 During intravascular hemolysis, free Hb binds to the plasma protein Hp, and Hb:Hp complexes are formed.	bind
23316	2	7614	6	NULL	NULL	0	NULL	statement 1	NULL		occurs during	NULL				intravascular hemolysis	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_16	14656926	3 During intravascular hemolysis, free Hb binds to the plasma protein Hp, and Hb:Hp complexes are formed.	bind
23317	3	7614	6	NULL	NULL	0	NULL	statement 1	NULL		forms	NULL				Hb:Hp complexes	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_16	14656926	3 During intravascular hemolysis, free Hb binds to the plasma protein Hp, and Hb:Hp complexes are formed.	bind
55529	4	7614	6	10	NULL	0	NULL	Hp			is a type of					plasma protein					NULL		0	NULL	NULL	NULL	gw70_circulationres_94_1_119_s_16	14656926	3 During intravascular hemolysis, free Hb binds to the plasma protein Hp, and Hb:Hp complexes are formed.	bind
30428	1	7615	5	13	NULL	NULL	NULL	Hsp90alpha constructs	GP	recombinant;;chicken	bind			C-terminal		ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_9_7066_s_132	11751878	3 Finally, although we analyzed the binding of rat Hsp90 (beta), Marcu  et al. ( 20) could detect a C-terminal ATP binding by studying ATP-Sepharose binding of recombinant chicken Hsp90alpha constructs.	bind
23318	1	7615	6	10	NULL	0	NULL	Hsp90alpha constructs	NULL	recombinant;;chicken	bind	NULL		C-terminal		ATP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_9_7066_s_132	11751878	3 Finally, although we analyzed the binding of rat Hsp90 (beta), Marcu  et al. ( 20) could detect a C-terminal ATP binding by studying ATP-Sepharose binding of recombinant chicken Hsp90alpha constructs.	bind
30429	1	7616	5	13	NULL	NULL	NULL	MC2R	GP		is a type of					adrenocortical receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23000_s_212	9287296	3 Finally, it is interesting to note that the MC2R, the adrenocortical receptor which only binds the melanocortin ACTH, contains yet a third aspartic acid residue in this region (equivalent to position 118 in hMC1R).	bind
30430	2	7616	5	13	NULL	NULL	NULL	MC2R	GP		bind					ACTH	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23000_s_212	9287296	3 Finally, it is interesting to note that the MC2R, the adrenocortical receptor which only binds the melanocortin ACTH, contains yet a third aspartic acid residue in this region (equivalent to position 118 in hMC1R).	bind
30431	3	7616	5	13	NULL	NULL	NULL	ACTH	GP		is a type of					melanocortin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23000_s_212	9287296	3 Finally, it is interesting to note that the MC2R, the adrenocortical receptor which only binds the melanocortin ACTH, contains yet a third aspartic acid residue in this region (equivalent to position 118 in hMC1R).	bind
30432	4	7616	5	13	NULL	NULL	NULL	MC2R	GP		contains								aspartic acid residue		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23000_s_212	9287296	3 Finally, it is interesting to note that the MC2R, the adrenocortical receptor which only binds the melanocortin ACTH, contains yet a third aspartic acid residue in this region (equivalent to position 118 in hMC1R).	bind
30433	5	7616	5	13	NULL	NULL	NULL	statement 4	AminoAcid		is equivalent to					hMC1R	GP		position 118		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23000_s_212	9287296	3 Finally, it is interesting to note that the MC2R, the adrenocortical receptor which only binds the melanocortin ACTH, contains yet a third aspartic acid residue in this region (equivalent to position 118 in hMC1R).	bind
23323	1	7616	6	10	NULL	0	NULL	MC2R	NULL		bind	NULL				ACTH	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23000_s_212	9287296	3 Finally, it is interesting to note that the MC2R, the adrenocortical receptor which only binds the melanocortin ACTH, contains yet a third aspartic acid residue in this region (equivalent to position 118 in hMC1R).	bind
23325	2	7616	6	10	NULL	0	NULL	MC2R	NULL		contains	NULL					NULL		aspartic acid residue		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23000_s_212	9287296	3 Finally, it is interesting to note that the MC2R, the adrenocortical receptor which only binds the melanocortin ACTH, contains yet a third aspartic acid residue in this region (equivalent to position 118 in hMC1R).	bind
23337	3	7616	6	10	NULL	0	NULL	MC2R	NULL		is equivalent to	NULL		aspartic acid residue		hMC1R	NULL		position 118		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23000_s_212	9287296	3 Finally, it is interesting to note that the MC2R, the adrenocortical receptor which only binds the melanocortin ACTH, contains yet a third aspartic acid residue in this region (equivalent to position 118 in hMC1R).	bind
46620	4	7616	6	10	NULL	0	NULL	MC2R	NULL		is a type of	NULL				adrenocortical receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_37_23000_s_212	9287296	3 Finally, it is interesting to note that the MC2R, the adrenocortical receptor which only binds the melanocortin ACTH, contains yet a third aspartic acid residue in this region (equivalent to position 118 in hMC1R).	bind
46621	5	7616	6	10	NULL	0	NULL	ACTH	NULL		is a type of	NULL				melanocortin 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_37_23000_s_212	9287296	3 Finally, it is interesting to note that the MC2R, the adrenocortical receptor which only binds the melanocortin ACTH, contains yet a third aspartic acid residue in this region (equivalent to position 118 in hMC1R).	bind
30434	1	7617	5	13	NULL	NULL	NULL	RhoA proteins	GP	stably expressed;;phosphomimetic	bind					Rhotekin	GP		RBD domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_21_19023_s_291	12654918	3 Further,  stably expressed phosphomimetic RhoA proteins bound the RBD domain of the Rho  effector Rhotekin ( Fig.  8 B).	bind
30435	2	7617	5	13	NULL	NULL	NULL	Rhotekin 	GP		is a type of					Rho effector	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_21_19023_s_291	12654918	3 Further,  stably expressed phosphomimetic RhoA proteins bound the RBD domain of the Rho  effector Rhotekin ( Fig.  8 B).	bind
23338	1	7617	6	10	NULL	0	NULL	RhoA protein	NULL	stably expressed;;phosphomimetic 	bind	NULL				Rhotekin	NULL		RBD domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_21_19023_s_291	12654918	3 Further,  stably expressed phosphomimetic RhoA proteins bound the RBD domain of the Rho  effector Rhotekin ( Fig.  8 B).	bind
46622	2	7617	6	10	NULL	0	NULL	Rhotekin	NULL		is a type of	NULL				Rho effector	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_21_19023_s_291	12654918	3 Further,  stably expressed phosphomimetic RhoA proteins bound the RBD domain of the Rho  effector Rhotekin ( Fig.  8 B).	bind
30436	1	7618	5	13	NULL	NULL	NULL	HR1a/HR1b	GP		bind					RhoA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2698_s_204	9446575	3 Furthermore, overlapping oligopeptides based upon RhoA covering the entire predicted binding regions for HR1a and HR1b (residues 1-100) are neither able to interact directly nor able to compete for HR1a/HR1b binding to RhoA, indicating that the sites of interaction on RhoA are sensitive to conformational constraints.	bind
23711	1	7618	6	10	NULL	0	NULL	HR1a/HR1b			bind					RhoA					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2698_s_204	9446575	3 Furthermore, overlapping oligopeptides based upon RhoA covering the entire predicted binding regions for HR1a and HR1b (residues 1-100) are neither able to interact directly nor able to compete for HR1a/HR1b binding to RhoA, indicating that the sites of interaction on RhoA are sensitive to conformational constraints.	bind
46623	1	7619	5	13	NULL	NULL	NULL	genomic DNA sequences	NucleicAcid		bind					SATB1	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_17_11463_s_224	9111059	3 Genomic DNA sequences that are bound to SATB1  in vivo have recently been characterized based on cross-linking techniques.	bind
23339	1	7619	6	10	NULL	0	NULL	genomic DNA sequences	NULL		bind	NULL				SATB1	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_17_11463_s_224	9111059	3 Genomic DNA sequences that are bound to SATB1  in vivo have recently been characterized based on cross-linking techniques.	bind
30439	1	7620	5	13	NULL	NULL	NULL	Git2	GP		is homologous to		highly			p95PKL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_8_6037_s_312	11096073	3 Git2 is highly homologous to p95PKL; and we indeed detected ternary complexes of paxillin alpha/Git2/betaPIX, and Git2/betaPIX/PAK3.2 However, since paxillin alpha itself can bind to PAK3, we could not properly assess whether or not these four proteins make the tetra-protein complex in a linear configuration.	bind
30440	2	7620	5	13	NULL	NULL	NULL	paxillin alpha	GP		bind					PAK3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_8_6037_s_312	11096073	3 Git2 is highly homologous to p95PKL; and we indeed detected ternary complexes of paxillin alpha/Git2/betaPIX, and Git2/betaPIX/PAK3.2 However, since paxillin alpha itself can bind to PAK3, we could not properly assess whether or not these four proteins make the tetra-protein complex in a linear configuration.	bind
23713	1	7620	6	NULL	NULL	0	NULL	Git2	NULL		is homologous to	NULL	highly			p95PKL	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_8_6037_s_312	11096073	3 Git2 is highly homologous to p95PKL; and we indeed detected ternary complexes of paxillin alpha/Git2/betaPIX, and Git2/betaPIX/PAK3.2 However, since paxillin alpha itself can bind to PAK3, we could not properly assess whether or not these four proteins make the tetra-protein complex in a linear configuration.	bind
23714	2	7620	6	NULL	NULL	0	NULL	paxillin alpha	NULL		bind	NULL				PAK3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_8_6037_s_312	11096073	3 Git2 is highly homologous to p95PKL; and we indeed detected ternary complexes of paxillin alpha/Git2/betaPIX, and Git2/betaPIX/PAK3.2 However, since paxillin alpha itself can bind to PAK3, we could not properly assess whether or not these four proteins make the tetra-protein complex in a linear configuration.	bind
30441	1	7621	5	13	NULL	NULL	NULL	ADP	Chemical		bind					Pgp	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_46518_s_314	15326176	3 Given the very low turnover rate evident for mutant E552A/S528A in  Fig. 6 B the fact that ADP was bound to Pgp might seem surprising.	bind
23341	1	7621	6	NULL	NULL	0	NULL	ADP	NULL		bind	NULL				Pgp	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_45_46518_s_314	15326176	3 Given the very low turnover rate evident for mutant E552A/S528A in  Fig. 6 B the fact that ADP was bound to Pgp might seem surprising.	bind
23343	2	7621	6	10	NULL	0	NULL		NULL	mutant	exhibits	NULL		E552A/S528A		low turnover rate	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_46518_s_314	15326176	3 Given the very low turnover rate evident for mutant E552A/S528A in  Fig. 6 B the fact that ADP was bound to Pgp might seem surprising.	bind
30442	1	7622	5	13	NULL	NULL	NULL	bZIP protein	GP		bind									ABA-responsive elements	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1689_s_162	11704678	3 However, bZIP protein binding to ABA-responsive elements is independent of VP1/PvAlf and dependent on ABA  in vivo ( 33,  43,  67).	bind
30443	2	7622	5	13	NULL	NULL	NULL	statement 1	Process		is independent of					VP1/PvAlf	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1689_s_162	11704678	3 However, bZIP protein binding to ABA-responsive elements is independent of VP1/PvAlf and dependent on ABA  in vivo ( 33,  43,  67).	bind
30444	3	7622	5	13	NULL	NULL	NULL	statement 1	Process		is dependent on					ABA	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1689_s_162	11704678	3 However, bZIP protein binding to ABA-responsive elements is independent of VP1/PvAlf and dependent on ABA  in vivo ( 33,  43,  67).	bind
23345	1	7622	6	10	NULL	0	NULL	bZIP protein			bind									ABA-responsive elements	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1689_s_162	11704678	3 However, bZIP protein binding to ABA-responsive elements is independent of VP1/PvAlf and dependent on ABA  in vivo ( 33,  43,  67).	bind
23346	2	7622	6	NULL	NULL	0	NULL	statement 1	NULL		is independent of	NULL				VP1/PvAlf	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_jbiolchem_277_3_1689_s_162	11704678	3 However, bZIP protein binding to ABA-responsive elements is independent of VP1/PvAlf and dependent on ABA  in vivo ( 33,  43,  67).	bind
23347	3	7622	6	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				ABA	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_jbiolchem_277_3_1689_s_162	11704678	3 However, bZIP protein binding to ABA-responsive elements is independent of VP1/PvAlf and dependent on ABA  in vivo ( 33,  43,  67).	bind
30528	1	7623	5	13	NULL	NULL	NULL	SSB protein	GP		bind					32-mer oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_23874_s_284	8798618	3 In addition, LexA S119A repressor did not change the binding affinity of SSB protein for a 32-mer oligonucleotide or affect the apparent site size of SSB protein tetramers bound to epsilonM13 DNA.3 Therefore, there is no experimental support for proposal two.	bind
30530	2	7623	5	13	NULL	NULL	NULL	LexA repressor	GP		does not change			S119A		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_23874_s_284	8798618	3 In addition, LexA S119A repressor did not change the binding affinity of SSB protein for a 32-mer oligonucleotide or affect the apparent site size of SSB protein tetramers bound to epsilonM13 DNA.3 Therefore, there is no experimental support for proposal two.	bind
30532	3	7623	5	13	NULL	NULL	NULL	SSB protein tetramers	GP		bind					epsilonM13 DNA.3	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_23874_s_284	8798618	3 In addition, LexA S119A repressor did not change the binding affinity of SSB protein for a 32-mer oligonucleotide or affect the apparent site size of SSB protein tetramers bound to epsilonM13 DNA.3 Therefore, there is no experimental support for proposal two.	bind
30537	4	7623	5	13	NULL	NULL	NULL	LexA repressor	GP		does not affect			S119A		statement 3	Process	apparent site size of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_23874_s_284	8798618	3 In addition, LexA S119A repressor did not change the binding affinity of SSB protein for a 32-mer oligonucleotide or affect the apparent site size of SSB protein tetramers bound to epsilonM13 DNA.3 Therefore, there is no experimental support for proposal two.	bind
23349	1	7623	6	NULL	NULL	0	NULL	SSB protein	NULL		bind	NULL				32-mer oligonucleotide	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_39_23874_s_284	8798618	3 In addition, LexA S119A repressor did not change the binding affinity of SSB protein for a 32-mer oligonucleotide or affect the apparent site size of SSB protein tetramers bound to epsilonM13 DNA.3 Therefore, there is no experimental support for proposal two.	bind
23350	2	7623	6	10	NULL	0	NULL	LexA repressor	NULL		does not change	NULL		S119A		statement 1	NULL	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_23874_s_284	8798618	3 In addition, LexA S119A repressor did not change the binding affinity of SSB protein for a 32-mer oligonucleotide or affect the apparent site size of SSB protein tetramers bound to epsilonM13 DNA.3 Therefore, there is no experimental support for proposal two.	bind
23351	3	7623	6	NULL	NULL	0	NULL	SSB protein tetramers	NULL		bind	NULL				epsilonM13 DNA.3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_39_23874_s_284	8798618	3 In addition, LexA S119A repressor did not change the binding affinity of SSB protein for a 32-mer oligonucleotide or affect the apparent site size of SSB protein tetramers bound to epsilonM13 DNA.3 Therefore, there is no experimental support for proposal two.	bind
46624	4	7623	6	10	NULL	0	NULL	LexA repressor	NULL		does not change	NULL		S119A		statement 3	NULL	apparent site size of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_39_23874_s_284	8798618	3 In addition, LexA S119A repressor did not change the binding affinity of SSB protein for a 32-mer oligonucleotide or affect the apparent site size of SSB protein tetramers bound to epsilonM13 DNA.3 Therefore, there is no experimental support for proposal two.	bind
30539	1	7624	5	13	NULL	NULL	NULL	PP14	GP		bind					alpha2-macroglobulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_16_14059_s_194	12556471	3 In addition, PP14 binds to the large serum carrier protein alpha2-macroglobulin, which potentiates the T cell inhibitory activity of PP14 ( ).	bind
30540	2	7624	5	13	NULL	NULL	NULL	alpha2-macroglobulin	GP		is a type of					large serum carrier protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_16_14059_s_194	12556471	3 In addition, PP14 binds to the large serum carrier protein alpha2-macroglobulin, which potentiates the T cell inhibitory activity of PP14 ( ).	bind
30541	4	7624	5	13	NULL	NULL	NULL	alpha2-macroglobulin	GP		potentiates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_16_14059_s_194	12556471	3 In addition, PP14 binds to the large serum carrier protein alpha2-macroglobulin, which potentiates the T cell inhibitory activity of PP14 ( ).	bind
46625	3	7624	5	13	NULL	NULL	NULL	PP14	GP		inhibit					T cell	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_16_14059_s_194	12556471	3 In addition, PP14 binds to the large serum carrier protein alpha2-macroglobulin, which potentiates the T cell inhibitory activity of PP14 ( ).	bind
23353	1	7624	6	10	NULL	0	NULL	PP14	NULL		bind	NULL				 alpha2-macroglobulin	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_16_14059_s_194	12556471	3 In addition, PP14 binds to the large serum carrier protein alpha2-macroglobulin, which potentiates the T cell inhibitory activity of PP14 ( ).	bind
23354	2	7624	6	10	NULL	0	NULL	alpha2-macroglobulin	NULL		is a type of	NULL				large serum carrier protein	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_16_14059_s_194	12556471	3 In addition, PP14 binds to the large serum carrier protein alpha2-macroglobulin, which potentiates the T cell inhibitory activity of PP14 ( ).	bind
23356	4	7624	6	10	NULL	0	NULL	 alpha2-macroglobulin	NULL		potentiates	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_16_14059_s_194	12556471	3 In addition, PP14 binds to the large serum carrier protein alpha2-macroglobulin, which potentiates the T cell inhibitory activity of PP14 ( ).	bind
46626	3	7624	6	10	NULL	0	NULL	PP14	NULL		inhibit	NULL				T cell	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_16_14059_s_194	12556471	3 In addition, PP14 binds to the large serum carrier protein alpha2-macroglobulin, which potentiates the T cell inhibitory activity of PP14 ( ).	bind
30551	1	7626	5	13	NULL	NULL	NULL	iNOS	GP	purified	bind		high affinity			iNOS monomers	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_1_295_s_268	11689556	3 In addition, spectral binding experiments with purified iNOS confirm high affinity binding to iNOS monomers ( K s < =50 nM) but low affinity binding to iNOS dimers ( K s > 10 muM).	bind
30552	2	7626	5	13	NULL	NULL	NULL	iNOS	GP	purified	bind		low affinity			iNOS dimers	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_1_295_s_268	11689556	3 In addition, spectral binding experiments with purified iNOS confirm high affinity binding to iNOS monomers ( K s < =50 nM) but low affinity binding to iNOS dimers ( K s > 10 muM).	bind
23359	1	7626	6	NULL	NULL	0	NULL	iNOS	NULL	purified	bind	NULL	high affinity			iNOS monomers	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_1_295_s_268	11689556	3 In addition, spectral binding experiments with purified iNOS confirm high affinity binding to iNOS monomers ( K s < =50 nM) but low affinity binding to iNOS dimers ( K s > 10 muM).	bind
23360	2	7626	6	NULL	NULL	0	NULL	iNOS	NULL	purified	bind	NULL	low affinity			iNOS dimers	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_1_295_s_268	11689556	3 In addition, spectral binding experiments with purified iNOS confirm high affinity binding to iNOS monomers ( K s < =50 nM) but low affinity binding to iNOS dimers ( K s > 10 muM).	bind
30557	1	7628	5	13	NULL	NULL	NULL	PD180970	Chemical		inhibit					Src	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24935_s_337	10823829	3 Inhibition of Src or JAKs by PD180970 or AG490, respectively, results in inactivation of Stat3 DNA binding activity and growth inhibition of these breast cancer cells.	bind
30558	2	7628	5	13	NULL	NULL	NULL	AG490	Chemical		inhibit					JAK	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24935_s_337	10823829	3 Inhibition of Src or JAKs by PD180970 or AG490, respectively, results in inactivation of Stat3 DNA binding activity and growth inhibition of these breast cancer cells.	bind
30560	3	7628	5	13	NULL	NULL	NULL	Stat3	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24935_s_337	10823829	3 Inhibition of Src or JAKs by PD180970 or AG490, respectively, results in inactivation of Stat3 DNA binding activity and growth inhibition of these breast cancer cells.	bind
30561	4	7628	5	13	NULL	NULL	NULL	statement 1	Process		inactivates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24935_s_337	10823829	3 Inhibition of Src or JAKs by PD180970 or AG490, respectively, results in inactivation of Stat3 DNA binding activity and growth inhibition of these breast cancer cells.	bind
30562	5	7628	5	13	NULL	NULL	NULL	statement 2	Process		inactivates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24935_s_337	10823829	3 Inhibition of Src or JAKs by PD180970 or AG490, respectively, results in inactivation of Stat3 DNA binding activity and growth inhibition of these breast cancer cells.	bind
30564	6	7628	5	13	NULL	NULL	NULL	statement 1	Process		inhibits					breast cancer cells	Cell	growth of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24935_s_337	10823829	3 Inhibition of Src or JAKs by PD180970 or AG490, respectively, results in inactivation of Stat3 DNA binding activity and growth inhibition of these breast cancer cells.	bind
30565	7	7628	5	13	NULL	NULL	NULL	statement 2 	Process		inhibits					breast cancer cells	Cell	growth of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24935_s_337	10823829	3 Inhibition of Src or JAKs by PD180970 or AG490, respectively, results in inactivation of Stat3 DNA binding activity and growth inhibition of these breast cancer cells.	bind
23715	1	7628	6	NULL	NULL	0	NULL	PD180970	NULL		inhibits	NULL				Src	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24935_s_337	10823829	3 Inhibition of Src or JAKs by PD180970 or AG490, respectively, results in inactivation of Stat3 DNA binding activity and growth inhibition of these breast cancer cells.	bind
23716	2	7628	6	NULL	NULL	0	NULL	AG490	NULL		inhibit	NULL				JAK	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24935_s_337	10823829	3 Inhibition of Src or JAKs by PD180970 or AG490, respectively, results in inactivation of Stat3 DNA binding activity and growth inhibition of these breast cancer cells.	bind
23717	4	7628	6	10	NULL	0	NULL	statement 1	NULL		inactivate	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24935_s_337	10823829	3 Inhibition of Src or JAKs by PD180970 or AG490, respectively, results in inactivation of Stat3 DNA binding activity and growth inhibition of these breast cancer cells.	bind
23718	5	7628	6	10	NULL	0	NULL	statement 2	NULL		inactivate	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24935_s_337	10823829	3 Inhibition of Src or JAKs by PD180970 or AG490, respectively, results in inactivation of Stat3 DNA binding activity and growth inhibition of these breast cancer cells.	bind
46627	3	7628	6	10	NULL	0	NULL	Stat3	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24935_s_337	10823829	3 Inhibition of Src or JAKs by PD180970 or AG490, respectively, results in inactivation of Stat3 DNA binding activity and growth inhibition of these breast cancer cells.	bind
46628	6	7628	6	10	NULL	0	NULL	statement 1	NULL		inhibit	NULL				breast cancer cells	NULL	growth of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24935_s_337	10823829	3 Inhibition of Src or JAKs by PD180970 or AG490, respectively, results in inactivation of Stat3 DNA binding activity and growth inhibition of these breast cancer cells.	bind
46629	7	7628	6	10	NULL	0	NULL	statement 2	NULL		inhibit	NULL				breast cancer cells	NULL	growth of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24935_s_337	10823829	3 Inhibition of Src or JAKs by PD180970 or AG490, respectively, results in inactivation of Stat3 DNA binding activity and growth inhibition of these breast cancer cells.	bind
30578	1	7629	5	13	NULL	NULL	NULL	GTP gammaS	GP		bind		high-affinity			G alpha	GP		i3 subunits		NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1077_s_8	12684263	3 Isotopic dilution experiments ([35]GTP gammaS  versus GTP gammaS) revealed high-affinity [35]GTP gammaS binding to G alphai3 subunits in the absence of receptor ligands indicating constitutive activity.	bind
30579	2	7629	5	13	NULL	NULL	NULL	statement 1	Process		in the absence of					receptor ligands	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1077_s_8	12684263	3 Isotopic dilution experiments ([35]GTP gammaS  versus GTP gammaS) revealed high-affinity [35]GTP gammaS binding to G alphai3 subunits in the absence of receptor ligands indicating constitutive activity.	bind
23493	1	7629	6	10	NULL	0	NULL	GTP gammaS	NULL		bind	NULL	high affinity			G alpha	NULL		i3 subunits		NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1077_s_8	12684263	3 Isotopic dilution experiments ([35]GTP gammaS  versus GTP gammaS) revealed high-affinity [35]GTP gammaS binding to G alphai3 subunits in the absence of receptor ligands indicating constitutive activity.	bind
23494	2	7629	6	NULL	NULL	0	NULL	statement 1	NULL		occurs in absence of	NULL				receptor ligands	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1077_s_8	12684263	3 Isotopic dilution experiments ([35]GTP gammaS  versus GTP gammaS) revealed high-affinity [35]GTP gammaS binding to G alphai3 subunits in the absence of receptor ligands indicating constitutive activity.	bind
30584	1	7630	5	13	NULL	NULL	NULL	AGL15	GP		bind					DTA3	GP			regulatory regions	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_30_28154_s_271	12743119	3 It  seems likely that co-factors are involved in binding of AGL15 to  DTA3  regulatory regions  in vivo.	bind
30606	2	7630	5	13	NULL	NULL	NULL	co-factors	Chemical		involved in					statement 1	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_30_28154_s_271	12743119	3 It  seems likely that co-factors are involved in binding of AGL15 to  DTA3  regulatory regions  in vivo.	bind
23555	1	7630	6	NULL	NULL	0	NULL	AGL15	NULL		bind	NULL				DTA3	NULL			regulatory region	NULL	in vivo	0	NULL	NULL	NULL	gw70_jbiolchem_278_30_28154_s_271	12743119	3 It  seems likely that co-factors are involved in binding of AGL15 to  DTA3  regulatory regions  in vivo.	bind
23556	2	7630	6	10	NULL	0	NULL	co-factors			are involved in					statement 1					NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_30_28154_s_271	12743119	3 It  seems likely that co-factors are involved in binding of AGL15 to  DTA3  regulatory regions  in vivo.	bind
30615	1	7631	5	13	NULL	NULL	NULL	Mx1	GP		bind					GTP	Chemical				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_45_32071_s_242	10542240	3 It has been previously demonstrated by  in vitro studies that the GTP binding activity of Mx1 or MxA protein is sufficient to exert antiviral activity ( 12).	bind
30616	2	7631	5	13	NULL	NULL	NULL	MxA protein	GP		bind					GTP	Chemical				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_45_32071_s_242	10542240	3 It has been previously demonstrated by  in vitro studies that the GTP binding activity of Mx1 or MxA protein is sufficient to exert antiviral activity ( 12).	bind
46630	3	7631	5	13	NULL	NULL	NULL	statement 1	Process		is sufficient for					antiviral activity	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_45_32071_s_242	10542240	3 It has been previously demonstrated by  in vitro studies that the GTP binding activity of Mx1 or MxA protein is sufficient to exert antiviral activity ( 12).	bind
46631	4	7631	5	13	NULL	NULL	NULL	statement 2	Process		is sufficient for					antiviral activity	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_45_32071_s_242	10542240	3 It has been previously demonstrated by  in vitro studies that the GTP binding activity of Mx1 or MxA protein is sufficient to exert antiviral activity ( 12).	bind
23557	1	7631	6	NULL	NULL	0	NULL	Mx1	NULL		bind	NULL				GTP	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_45_32071_s_242	10542240	3 It has been previously demonstrated by  in vitro studies that the GTP binding activity of Mx1 or MxA protein is sufficient to exert antiviral activity ( 12).	bind
23558	2	7631	6	NULL	NULL	0	NULL	MxA protein	NULL		bind	NULL				GTP	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_274_45_32071_s_242	10542240	3 It has been previously demonstrated by  in vitro studies that the GTP binding activity of Mx1 or MxA protein is sufficient to exert antiviral activity ( 12).	bind
23559	3	7631	6	10	NULL	0	NULL	statement 1			is sufficient for					antiviral activity					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_45_32071_s_242	10542240	3 It has been previously demonstrated by  in vitro studies that the GTP binding activity of Mx1 or MxA protein is sufficient to exert antiviral activity ( 12).	bind
23560	4	7631	6	10	NULL	0	NULL	statement 2			is sufficient for					antiviral activity					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_45_32071_s_242	10542240	3 It has been previously demonstrated by  in vitro studies that the GTP binding activity of Mx1 or MxA protein is sufficient to exert antiviral activity ( 12).	bind
30625	1	7632	5	13	NULL	NULL	NULL	1-(bromomethyl)phenanthrene	Chemical		does not bind		efficiently			AAC(6'')-Ii	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_12873_s_206	12566434	3 Its inability to inactivate AAC(6'')-Ii could be because 1-(bromomethyl)phenanthrene can not efficiently bind to AAC(6'')-Ii or because AAC(6'')-Ii lacks an appropriate active site residue to serve as the nucleophile in the reaction.	bind
30626	2	7632	5	13	NULL	NULL	NULL	AAC(6'')-Ii	GP		lacks								active site residue		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_12873_s_206	12566434	3 Its inability to inactivate AAC(6'')-Ii could be because 1-(bromomethyl)phenanthrene can not efficiently bind to AAC(6'')-Ii or because AAC(6'')-Ii lacks an appropriate active site residue to serve as the nucleophile in the reaction.	bind
30628	3	7632	5	13	NULL	NULL	NULL	AAC(6'')-Ii	GP		serve as			active site residue		nucleophile	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_12873_s_206	12566434	3 Its inability to inactivate AAC(6'')-Ii could be because 1-(bromomethyl)phenanthrene can not efficiently bind to AAC(6'')-Ii or because AAC(6'')-Ii lacks an appropriate active site residue to serve as the nucleophile in the reaction.	bind
23561	1	7632	6	10	NULL	0	NULL	1-(bromomethyl)phenanthrene	NULL		does not bind	NULL	efficiently			AAC(6'')-Ii	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_12873_s_206	12566434	3 Its inability to inactivate AAC(6'')-Ii could be because 1-(bromomethyl)phenanthrene can not efficiently bind to AAC(6'')-Ii or because AAC(6'')-Ii lacks an appropriate active site residue to serve as the nucleophile in the reaction.	bind
23562	2	7632	6	10	NULL	0	NULL	AAC(6'')-Ii	NULL		lacks	NULL					NULL		active site residue		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_12873_s_206	12566434	3 Its inability to inactivate AAC(6'')-Ii could be because 1-(bromomethyl)phenanthrene can not efficiently bind to AAC(6'')-Ii or because AAC(6'')-Ii lacks an appropriate active site residue to serve as the nucleophile in the reaction.	bind
55530	3	7632	6	10	NULL	0	NULL	AAC(6'')-Ii			serves as			active site residue		nucleophile					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_15_12873_s_206	12566434	3 Its inability to inactivate AAC(6'')-Ii could be because 1-(bromomethyl)phenanthrene can not efficiently bind to AAC(6'')-Ii or because AAC(6'')-Ii lacks an appropriate active site residue to serve as the nucleophile in the reaction.	bind
30641	1	7633	5	13	NULL	NULL	NULL	gankyrin	GP		bind					Rb	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_12_10668_s_229	12525503	3 MAGE-A4 did not reduce the binding of gankyrin to Rb, S6, or Cdk4.	bind
30642	2	7633	5	13	NULL	NULL	NULL	gankyrin	GP		bind					S6	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_12_10668_s_229	12525503	3 MAGE-A4 did not reduce the binding of gankyrin to Rb, S6, or Cdk4.	bind
30643	3	7633	5	13	NULL	NULL	NULL	gankyrin	GP		bind					Cdk4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_12_10668_s_229	12525503	3 MAGE-A4 did not reduce the binding of gankyrin to Rb, S6, or Cdk4.	bind
30645	4	7633	5	13	NULL	NULL	NULL	statement 1	Process		is alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_12_10668_s_229	12525503	3 MAGE-A4 did not reduce the binding of gankyrin to Rb, S6, or Cdk4.	bind
30646	5	7633	5	13	NULL	NULL	NULL	statement 1	Process		is alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_12_10668_s_229	12525503	3 MAGE-A4 did not reduce the binding of gankyrin to Rb, S6, or Cdk4.	bind
30648	6	7633	5	13	NULL	NULL	NULL	MAGE-A4	GP		does not reduce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_12_10668_s_229	12525503	3 MAGE-A4 did not reduce the binding of gankyrin to Rb, S6, or Cdk4.	bind
30651	7	7633	5	13	NULL	NULL	NULL	MAGE-A4	GP		does not reduce					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_12_10668_s_229	12525503	3 MAGE-A4 did not reduce the binding of gankyrin to Rb, S6, or Cdk4.	bind
30653	8	7633	5	13	NULL	NULL	NULL	MAGE-A4	GP		does not reduce					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_12_10668_s_229	12525503	3 MAGE-A4 did not reduce the binding of gankyrin to Rb, S6, or Cdk4.	bind
23563	1	7633	6	NULL	NULL	0	NULL	gankyrin	NULL		bind	NULL				Rb	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10668_s_229	12525503	3 MAGE-A4 did not reduce the binding of gankyrin to Rb, S6, or Cdk4.	bind
23564	2	7633	6	NULL	NULL	0	NULL	gankyrin	NULL		bind	NULL				S6	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10668_s_229	12525503	3 MAGE-A4 did not reduce the binding of gankyrin to Rb, S6, or Cdk4.	bind
23565	3	7633	6	NULL	NULL	0	NULL	gankyrin	NULL		bind	NULL				Cdk4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10668_s_229	12525503	3 MAGE-A4 did not reduce the binding of gankyrin to Rb, S6, or Cdk4.	bind
23566	4	7633	6	NULL	NULL	0	NULL	MAGE-A4	NULL		did not reduce	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10668_s_229	12525503	3 MAGE-A4 did not reduce the binding of gankyrin to Rb, S6, or Cdk4.	bind
23567	5	7633	6	NULL	NULL	0	NULL	MAGE-A4	NULL		did not reduce	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10668_s_229	12525503	3 MAGE-A4 did not reduce the binding of gankyrin to Rb, S6, or Cdk4.	bind
23568	6	7633	6	NULL	NULL	0	NULL	MAGE-A4	NULL		did not reduce	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10668_s_229	12525503	3 MAGE-A4 did not reduce the binding of gankyrin to Rb, S6, or Cdk4.	bind
46632	7	7633	6	10	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10668_s_229	12525503	3 MAGE-A4 did not reduce the binding of gankyrin to Rb, S6, or Cdk4.	bind
46633	8	7633	6	10	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10668_s_229	12525503	3 MAGE-A4 did not reduce the binding of gankyrin to Rb, S6, or Cdk4.	bind
30693	1	7634	5	13	NULL	NULL	NULL	karyopherin beta	GP		bind					C-Nup1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_31_19538_s_91	9235958	3 Most importantly, when karyopherin alpha and RanGAP were added together, karyopherin beta binding to C-Nup1 was restored ( lane 5).	bind
30694	2	7634	5	13	NULL	NULL	NULL	karyopherin alpha 	GP		is added together with					RanGAP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_31_19538_s_91	9235958	3 Most importantly, when karyopherin alpha and RanGAP were added together, karyopherin beta binding to C-Nup1 was restored ( lane 5).	bind
46634	3	7634	5	13	NULL	NULL	NULL	statement 2	Process		restores					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_31_19538_s_91	9235958	3 Most importantly, when karyopherin alpha and RanGAP were added together, karyopherin beta binding to C-Nup1 was restored ( lane 5).	bind
23569	1	7634	6	NULL	NULL	0	NULL	karyopherin beta	NULL		bind	NULL				C-Nup1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_31_19538_s_91	9235958	3 Most importantly, when karyopherin alpha and RanGAP were added together, karyopherin beta binding to C-Nup1 was restored ( lane 5).	bind
23570	2	7634	6	NULL	NULL	0	NULL	karyopherin alpha	NULL		is added together with	NULL				RanGAP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_31_19538_s_91	9235958	3 Most importantly, when karyopherin alpha and RanGAP were added together, karyopherin beta binding to C-Nup1 was restored ( lane 5).	bind
23571	3	7634	6	NULL	NULL	0	NULL	statement 2	NULL		restores	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_31_19538_s_91	9235958	3 Most importantly, when karyopherin alpha and RanGAP were added together, karyopherin beta binding to C-Nup1 was restored ( lane 5).	bind
30697	1	7639	5	13	NULL	NULL	NULL	ISP	GP		bind					complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_13_12951_s_272	14718526	3 Mutation to aspartate may increase the stability of binding of the ISP to the complex.	bind
30698	2	7639	5	13	NULL	NULL	NULL	aspartate	Chemical	mutation to	increase		may			statement 1	Process	stability of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_13_12951_s_272	14718526	3 Mutation to aspartate may increase the stability of binding of the ISP to the complex.	bind
23572	1	7639	6	NULL	NULL	0	NULL	ISP	NULL		bind	NULL				complex	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12951_s_272	14718526	3 Mutation to aspartate may increase the stability of binding of the ISP to the complex.	bind
23573	2	7639	6	NULL	NULL	0	NULL	aspartate	NULL	mutant	increase	NULL	may			statement 1	NULL	stability of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12951_s_272	14718526	3 Mutation to aspartate may increase the stability of binding of the ISP to the complex.	bind
30832	2	7641	5	13	NULL	NULL	NULL	F-actin	GP		does not mediate					alpha-actinin	GP	recruitment of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13410_s_281	10224105	3 Nevertheless, in the case of zyxin, we can rule out the possibility that alpha-actinin recruitment is primarily due to an indirect association mediated by F-actin ( 18) or some other protein(s): a deletion, which is confined to a short zyxin peptide motif that has been positively identified as an alpha-actinin binding site in a parallel  in vitro assay, virtually abolishes alpha-actinin recruitment in the targeting assay and alpha-actinin binding to GST-zyxin fusion proteins in blot overlays  in vitro.	bind
30833	3	7641	5	13	NULL	NULL	NULL	zyxin peptide	GP		is identified as			short motif					alpha-actinin binding site		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13410_s_281	10224105	3 Nevertheless, in the case of zyxin, we can rule out the possibility that alpha-actinin recruitment is primarily due to an indirect association mediated by F-actin ( 18) or some other protein(s): a deletion, which is confined to a short zyxin peptide motif that has been positively identified as an alpha-actinin binding site in a parallel  in vitro assay, virtually abolishes alpha-actinin recruitment in the targeting assay and alpha-actinin binding to GST-zyxin fusion proteins in blot overlays  in vitro.	bind
32235	4	7641	5	13	NULL	NULL	NULL	statement 3	GP	deletion of	abolishes					alpha-actinin	GP	recruitment of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13410_s_281	10224105	3 Nevertheless, in the case of zyxin, we can rule out the possibility that alpha-actinin recruitment is primarily due to an indirect association mediated by F-actin ( 18) or some other protein(s): a deletion, which is confined to a short zyxin peptide motif that has been positively identified as an alpha-actinin binding site in a parallel  in vitro assay, virtually abolishes alpha-actinin recruitment in the targeting assay and alpha-actinin binding to GST-zyxin fusion proteins in blot overlays  in vitro.	bind
32236	5	7641	5	13	NULL	NULL	NULL	alpha-actinin	GP		bind					GST-zyxin fusion proteins	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13410_s_281	10224105	3 Nevertheless, in the case of zyxin, we can rule out the possibility that alpha-actinin recruitment is primarily due to an indirect association mediated by F-actin ( 18) or some other protein(s): a deletion, which is confined to a short zyxin peptide motif that has been positively identified as an alpha-actinin binding site in a parallel  in vitro assay, virtually abolishes alpha-actinin recruitment in the targeting assay and alpha-actinin binding to GST-zyxin fusion proteins in blot overlays  in vitro.	bind
32237	6	7641	5	13	NULL	NULL	NULL	statement 3	GP	deletion of	abolishes					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13410_s_281	10224105	3 Nevertheless, in the case of zyxin, we can rule out the possibility that alpha-actinin recruitment is primarily due to an indirect association mediated by F-actin ( 18) or some other protein(s): a deletion, which is confined to a short zyxin peptide motif that has been positively identified as an alpha-actinin binding site in a parallel  in vitro assay, virtually abolishes alpha-actinin recruitment in the targeting assay and alpha-actinin binding to GST-zyxin fusion proteins in blot overlays  in vitro.	bind
23781	1	7641	6	NULL	NULL	0	NULL	alpha-actinin	NULL		bind	NULL				GST-zyxin fusion protein	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_274_19_13410_s_281	10224105	3 Nevertheless, in the case of zyxin, we can rule out the possibility that alpha-actinin recruitment is primarily due to an indirect association mediated by F-actin ( 18) or some other protein(s): a deletion, which is confined to a short zyxin peptide motif that has been positively identified as an alpha-actinin binding site in a parallel  in vitro assay, virtually abolishes alpha-actinin recruitment in the targeting assay and alpha-actinin binding to GST-zyxin fusion proteins in blot overlays  in vitro.	bind
46888	2	7641	6	NULL	NULL	0	NULL	zyxin peptide motif	NULL	deletion of	abolishes	NULL				alpha-actinin	NULL	recruitment of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_19_13410_s_281	10224105	3 Nevertheless, in the case of zyxin, we can rule out the possibility that alpha-actinin recruitment is primarily due to an indirect association mediated by F-actin ( 18) or some other protein(s): a deletion, which is confined to a short zyxin peptide motif that has been positively identified as an alpha-actinin binding site in a parallel  in vitro assay, virtually abolishes alpha-actinin recruitment in the targeting assay and alpha-actinin binding to GST-zyxin fusion proteins in blot overlays  in vitro.	bind
46889	3	7641	6	NULL	NULL	0	NULL	zyxin peptide motif	NULL	deletion of	abolishes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_19_13410_s_281	10224105	3 Nevertheless, in the case of zyxin, we can rule out the possibility that alpha-actinin recruitment is primarily due to an indirect association mediated by F-actin ( 18) or some other protein(s): a deletion, which is confined to a short zyxin peptide motif that has been positively identified as an alpha-actinin binding site in a parallel  in vitro assay, virtually abolishes alpha-actinin recruitment in the targeting assay and alpha-actinin binding to GST-zyxin fusion proteins in blot overlays  in vitro.	bind
30699	1	7642	5	13	NULL	NULL	NULL	dN-Occ	GP		bind		nonspecific			protein A/G-IgG	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49644_s_277	14512431	3 Nonspecific binding of dN-Occ to protein A/G-IgG (GFAP antibody) did occur at a level of about 50% of the maximal specific binding, but was not concentration-dependent.	bind
30700	2	7642	5	13	NULL	NULL	NULL	protein A/G-IgG	GP		is a type of					GFAP antibody	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49644_s_277	14512431	3 Nonspecific binding of dN-Occ to protein A/G-IgG (GFAP antibody) did occur at a level of about 50% of the maximal specific binding, but was not concentration-dependent.	bind
30701	3	7642	5	13	NULL	NULL	NULL	statement 1	Process		is not dependent on					concentration					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49644_s_277	14512431	3 Nonspecific binding of dN-Occ to protein A/G-IgG (GFAP antibody) did occur at a level of about 50% of the maximal specific binding, but was not concentration-dependent.	bind
23574	1	7642	6	NULL	NULL	0	NULL	dN-Occ	NULL		bind	NULL	non-specifically			protein A/G-IgG	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49644_s_277	14512431	3 Nonspecific binding of dN-Occ to protein A/G-IgG (GFAP antibody) did occur at a level of about 50% of the maximal specific binding, but was not concentration-dependent.	bind
23575	2	7642	6	NULL	NULL	0	NULL	statement 1	NULL		is not dependent on	NULL				concentration	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49644_s_277	14512431	3 Nonspecific binding of dN-Occ to protein A/G-IgG (GFAP antibody) did occur at a level of about 50% of the maximal specific binding, but was not concentration-dependent.	bind
46635	3	7642	6	10	NULL	0	NULL	protein A/G-IgG	NULL		is a type of	NULL				GFAP antibody	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49644_s_277	14512431	3 Nonspecific binding of dN-Occ to protein A/G-IgG (GFAP antibody) did occur at a level of about 50% of the maximal specific binding, but was not concentration-dependent.	bind
30702	1	7643	5	13	NULL	NULL	NULL	ATP	Chemical		bind					ORC-5A	GP		Orc5p		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_185	12966094	3 One possible explanation is that in ORC-5A, the lack of ATP binding to Orc5p inhibits the ATP binding to Orc1p, thus inhibiting the ORC binding to origin DNA and leaving the entire complex sensitive to protein degradation.	bind
30703	2	7643	5	13	NULL	NULL	NULL	ATP	Chemical		bind					ORC-5A	GP		Orc1p		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_185	12966094	3 One possible explanation is that in ORC-5A, the lack of ATP binding to Orc5p inhibits the ATP binding to Orc1p, thus inhibiting the ORC binding to origin DNA and leaving the entire complex sensitive to protein degradation.	bind
30704	3	7643	5	13	NULL	NULL	NULL	statement 1	Process	lack of	inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_185	12966094	3 One possible explanation is that in ORC-5A, the lack of ATP binding to Orc5p inhibits the ATP binding to Orc1p, thus inhibiting the ORC binding to origin DNA and leaving the entire complex sensitive to protein degradation.	bind
30705	4	7643	5	13	NULL	NULL	NULL	ORC	GP		bind					origin DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_185	12966094	3 One possible explanation is that in ORC-5A, the lack of ATP binding to Orc5p inhibits the ATP binding to Orc1p, thus inhibiting the ORC binding to origin DNA and leaving the entire complex sensitive to protein degradation.	bind
30706	5	7643	5	13	NULL	NULL	NULL	statement 3	Process		inhibits					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_185	12966094	3 One possible explanation is that in ORC-5A, the lack of ATP binding to Orc5p inhibits the ATP binding to Orc1p, thus inhibiting the ORC binding to origin DNA and leaving the entire complex sensitive to protein degradation.	bind
30707	6	7643	5	13	NULL	NULL	NULL	statement 1	Process		is sensitive to					protein degradation	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_185	12966094	3 One possible explanation is that in ORC-5A, the lack of ATP binding to Orc5p inhibits the ATP binding to Orc1p, thus inhibiting the ORC binding to origin DNA and leaving the entire complex sensitive to protein degradation.	bind
30708	7	7643	5	13	NULL	NULL	NULL	statement 2	Process		is sensitive to					protein degradation	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_185	12966094	3 One possible explanation is that in ORC-5A, the lack of ATP binding to Orc5p inhibits the ATP binding to Orc1p, thus inhibiting the ORC binding to origin DNA and leaving the entire complex sensitive to protein degradation.	bind
30709	8	7643	5	13	NULL	NULL	NULL	statement 5	Process		leads to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_185	12966094	3 One possible explanation is that in ORC-5A, the lack of ATP binding to Orc5p inhibits the ATP binding to Orc1p, thus inhibiting the ORC binding to origin DNA and leaving the entire complex sensitive to protein degradation.	bind
30710	9	7643	5	13	NULL	NULL	NULL	statement 5	Process		leads to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_185	12966094	3 One possible explanation is that in ORC-5A, the lack of ATP binding to Orc5p inhibits the ATP binding to Orc1p, thus inhibiting the ORC binding to origin DNA and leaving the entire complex sensitive to protein degradation.	bind
23576	1	7643	6	10	NULL	0	NULL	ATP			bind					ORC-5A			Orc5p		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_185	12966094	3 One possible explanation is that in ORC-5A, the lack of ATP binding to Orc5p inhibits the ATP binding to Orc1p, thus inhibiting the ORC binding to origin DNA and leaving the entire complex sensitive to protein degradation.	bind
23577	2	7643	6	10	NULL	0	NULL	ATP			bind					ORC-5A			Orc1p		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_185	12966094	3 One possible explanation is that in ORC-5A, the lack of ATP binding to Orc5p inhibits the ATP binding to Orc1p, thus inhibiting the ORC binding to origin DNA and leaving the entire complex sensitive to protein degradation.	bind
23578	3	7643	6	NULL	NULL	0	NULL	ORC	NULL		bind	NULL				origin DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_185	12966094	3 One possible explanation is that in ORC-5A, the lack of ATP binding to Orc5p inhibits the ATP binding to Orc1p, thus inhibiting the ORC binding to origin DNA and leaving the entire complex sensitive to protein degradation.	bind
23579	4	7643	6	NULL	NULL	0	NULL	statement 1	NULL	lack of	inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_185	12966094	3 One possible explanation is that in ORC-5A, the lack of ATP binding to Orc5p inhibits the ATP binding to Orc1p, thus inhibiting the ORC binding to origin DNA and leaving the entire complex sensitive to protein degradation.	bind
23580	5	7643	6	NULL	NULL	0	NULL	statement 4	NULL		inhibits	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_185	12966094	3 One possible explanation is that in ORC-5A, the lack of ATP binding to Orc5p inhibits the ATP binding to Orc1p, thus inhibiting the ORC binding to origin DNA and leaving the entire complex sensitive to protein degradation.	bind
23581	6	7643	6	10	NULL	0	NULL	statement 1			is sensitive to					protein degradation					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_185	12966094	3 One possible explanation is that in ORC-5A, the lack of ATP binding to Orc5p inhibits the ATP binding to Orc1p, thus inhibiting the ORC binding to origin DNA and leaving the entire complex sensitive to protein degradation.	bind
55531	7	7643	6	10	NULL	0	NULL	statement 2			is sensitive to					protein degradation					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_185	12966094	3 One possible explanation is that in ORC-5A, the lack of ATP binding to Orc5p inhibits the ATP binding to Orc1p, thus inhibiting the ORC binding to origin DNA and leaving the entire complex sensitive to protein degradation.	bind
55532	8	7643	6	10	NULL	0	NULL	statement 5			leads to					statement 6					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_185	12966094	3 One possible explanation is that in ORC-5A, the lack of ATP binding to Orc5p inhibits the ATP binding to Orc1p, thus inhibiting the ORC binding to origin DNA and leaving the entire complex sensitive to protein degradation.	bind
55533	9	7643	6	10	NULL	0	NULL	statement 6			leads to					statement 7					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46440_s_185	12966094	3 One possible explanation is that in ORC-5A, the lack of ATP binding to Orc5p inhibits the ATP binding to Orc1p, thus inhibiting the ORC binding to origin DNA and leaving the entire complex sensitive to protein degradation.	bind
30712	1	7644	5	13	NULL	NULL	NULL	TIM10 complex	GP		function as					chaperone	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_39_36100_s_323	12138093	3 Our working hypothesis for the role of the 70-kDa TIM10 complex in this mechanism is that (i) it functions purely as a chaperone protecting AAC from aggregation; (ii) it remains stable as a heterohexamer; and (iii) passage of AAC onto the TIM22 complex for proper insertion is mediated by direct binding of AAC to the TIM22 complex accompanied by allosteric release of AAC from the TIM10 complex.	bind
30713	2	7644	5	13	NULL	NULL	NULL	statement 1	Process		protects					AAC	GP	aggregation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_39_36100_s_323	12138093	3 Our working hypothesis for the role of the 70-kDa TIM10 complex in this mechanism is that (i) it functions purely as a chaperone protecting AAC from aggregation; (ii) it remains stable as a heterohexamer; and (iii) passage of AAC onto the TIM22 complex for proper insertion is mediated by direct binding of AAC to the TIM22 complex accompanied by allosteric release of AAC from the TIM10 complex.	bind
30715	3	7644	5	13	NULL	NULL	NULL	TIM10 complex heterohexamer	GP		remains					stable					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_39_36100_s_323	12138093	3 Our working hypothesis for the role of the 70-kDa TIM10 complex in this mechanism is that (i) it functions purely as a chaperone protecting AAC from aggregation; (ii) it remains stable as a heterohexamer; and (iii) passage of AAC onto the TIM22 complex for proper insertion is mediated by direct binding of AAC to the TIM22 complex accompanied by allosteric release of AAC from the TIM10 complex.	bind
30716	4	7644	5	13	NULL	NULL	NULL	AAC	GP		bind		directly			TIM22 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_39_36100_s_323	12138093	3 Our working hypothesis for the role of the 70-kDa TIM10 complex in this mechanism is that (i) it functions purely as a chaperone protecting AAC from aggregation; (ii) it remains stable as a heterohexamer; and (iii) passage of AAC onto the TIM22 complex for proper insertion is mediated by direct binding of AAC to the TIM22 complex accompanied by allosteric release of AAC from the TIM10 complex.	bind
30717	5	7644	5	13	NULL	NULL	NULL	AAC	GP		is released from		allosterically			TIM10 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_39_36100_s_323	12138093	3 Our working hypothesis for the role of the 70-kDa TIM10 complex in this mechanism is that (i) it functions purely as a chaperone protecting AAC from aggregation; (ii) it remains stable as a heterohexamer; and (iii) passage of AAC onto the TIM22 complex for proper insertion is mediated by direct binding of AAC to the TIM22 complex accompanied by allosteric release of AAC from the TIM10 complex.	bind
30718	6	7644	5	13	NULL	NULL	NULL	statement 4	Process		is accompanied by					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_39_36100_s_323	12138093	3 Our working hypothesis for the role of the 70-kDa TIM10 complex in this mechanism is that (i) it functions purely as a chaperone protecting AAC from aggregation; (ii) it remains stable as a heterohexamer; and (iii) passage of AAC onto the TIM22 complex for proper insertion is mediated by direct binding of AAC to the TIM22 complex accompanied by allosteric release of AAC from the TIM10 complex.	bind
30719	7	7644	5	13	NULL	NULL	NULL	AAC	GP		is passed onto					TIM22 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_39_36100_s_323	12138093	3 Our working hypothesis for the role of the 70-kDa TIM10 complex in this mechanism is that (i) it functions purely as a chaperone protecting AAC from aggregation; (ii) it remains stable as a heterohexamer; and (iii) passage of AAC onto the TIM22 complex for proper insertion is mediated by direct binding of AAC to the TIM22 complex accompanied by allosteric release of AAC from the TIM10 complex.	bind
30722	8	7644	5	13	NULL	NULL	NULL	statement 6	Process		mediate					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_39_36100_s_323	12138093	3 Our working hypothesis for the role of the 70-kDa TIM10 complex in this mechanism is that (i) it functions purely as a chaperone protecting AAC from aggregation; (ii) it remains stable as a heterohexamer; and (iii) passage of AAC onto the TIM22 complex for proper insertion is mediated by direct binding of AAC to the TIM22 complex accompanied by allosteric release of AAC from the TIM10 complex.	bind
23782	1	7644	6	NULL	NULL	0	NULL	TIM10 complex	NULL		functions as 	NULL				chaperone	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_39_36100_s_323	12138093	3 Our working hypothesis for the role of the 70-kDa TIM10 complex in this mechanism is that (i) it functions purely as a chaperone protecting AAC from aggregation; (ii) it remains stable as a heterohexamer; and (iii) passage of AAC onto the TIM22 complex for proper insertion is mediated by direct binding of AAC to the TIM22 complex accompanied by allosteric release of AAC from the TIM10 complex.	bind
23783	2	7644	6	NULL	NULL	0	NULL	statement 1	NULL		protects	NULL				AAC	NULL	aggregation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_39_36100_s_323	12138093	3 Our working hypothesis for the role of the 70-kDa TIM10 complex in this mechanism is that (i) it functions purely as a chaperone protecting AAC from aggregation; (ii) it remains stable as a heterohexamer; and (iii) passage of AAC onto the TIM22 complex for proper insertion is mediated by direct binding of AAC to the TIM22 complex accompanied by allosteric release of AAC from the TIM10 complex.	bind
23784	3	7644	6	NULL	NULL	0	NULL	TIM10 complex	NULL		remains stable as a 	NULL				heterohexamer	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_39_36100_s_323	12138093	3 Our working hypothesis for the role of the 70-kDa TIM10 complex in this mechanism is that (i) it functions purely as a chaperone protecting AAC from aggregation; (ii) it remains stable as a heterohexamer; and (iii) passage of AAC onto the TIM22 complex for proper insertion is mediated by direct binding of AAC to the TIM22 complex accompanied by allosteric release of AAC from the TIM10 complex.	bind
23785	4	7644	6	NULL	NULL	0	NULL	AAC	NULL		bind	NULL	directly			TIM22 complex	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_39_36100_s_323	12138093	3 Our working hypothesis for the role of the 70-kDa TIM10 complex in this mechanism is that (i) it functions purely as a chaperone protecting AAC from aggregation; (ii) it remains stable as a heterohexamer; and (iii) passage of AAC onto the TIM22 complex for proper insertion is mediated by direct binding of AAC to the TIM22 complex accompanied by allosteric release of AAC from the TIM10 complex.	bind
23786	5	7644	6	NULL	NULL	0	NULL	AAC	NULL		moves to	NULL				TIM22 complex	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_39_36100_s_323	12138093	3 Our working hypothesis for the role of the 70-kDa TIM10 complex in this mechanism is that (i) it functions purely as a chaperone protecting AAC from aggregation; (ii) it remains stable as a heterohexamer; and (iii) passage of AAC onto the TIM22 complex for proper insertion is mediated by direct binding of AAC to the TIM22 complex accompanied by allosteric release of AAC from the TIM10 complex.	bind
23787	6	7644	6	NULL	NULL	0	NULL	statement 5	NULL		is mediated by	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_39_36100_s_323	12138093	3 Our working hypothesis for the role of the 70-kDa TIM10 complex in this mechanism is that (i) it functions purely as a chaperone protecting AAC from aggregation; (ii) it remains stable as a heterohexamer; and (iii) passage of AAC onto the TIM22 complex for proper insertion is mediated by direct binding of AAC to the TIM22 complex accompanied by allosteric release of AAC from the TIM10 complex.	bind
23788	7	7644	6	10	NULL	0	NULL	AAC	NULL		released from	NULL	allosterically			TIM10 complex	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_39_36100_s_323	12138093	3 Our working hypothesis for the role of the 70-kDa TIM10 complex in this mechanism is that (i) it functions purely as a chaperone protecting AAC from aggregation; (ii) it remains stable as a heterohexamer; and (iii) passage of AAC onto the TIM22 complex for proper insertion is mediated by direct binding of AAC to the TIM22 complex accompanied by allosteric release of AAC from the TIM10 complex.	bind
23789	8	7644	6	NULL	NULL	0	NULL	statement 4	NULL		is accompanied by	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_39_36100_s_323	12138093	3 Our working hypothesis for the role of the 70-kDa TIM10 complex in this mechanism is that (i) it functions purely as a chaperone protecting AAC from aggregation; (ii) it remains stable as a heterohexamer; and (iii) passage of AAC onto the TIM22 complex for proper insertion is mediated by direct binding of AAC to the TIM22 complex accompanied by allosteric release of AAC from the TIM10 complex.	bind
30723	1	7645	5	13	NULL	NULL	NULL	PDX-1	GP		bind									A1 elements	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_18_11986_s_133	9115263	3 PDX-1 Is the Predominant beta Cell Activity Binding to the A1 and A2 Elements	bind
30724	2	7645	5	13	NULL	NULL	NULL	PDX-1	GP		bind									A2 elements	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_18_11986_s_133	9115263	3 PDX-1 Is the Predominant beta Cell Activity Binding to the A1 and A2 Elements	bind
46636	3	7645	5	13	NULL	NULL	NULL	PDX-1	GP		exhibit					beta cell activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_18_11986_s_133	9115263	3 PDX-1 Is the Predominant beta Cell Activity Binding to the A1 and A2 Elements	bind
23582	1	7645	6	NULL	NULL	0	NULL	PDX-1	NULL		bind	NULL					NULL			A1 element	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_18_11986_s_133	9115263	3 PDX-1 Is the Predominant beta Cell Activity Binding to the A1 and A2 Elements	bind
23583	2	7645	6	NULL	NULL	0	NULL	PDX-1	NULL		bind	NULL					NULL			A2 element	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_18_11986_s_133	9115263	3 PDX-1 Is the Predominant beta Cell Activity Binding to the A1 and A2 Elements	bind
23584	3	7645	6	NULL	NULL	0	NULL	PDX-1	NULL		exhibits	NULL				beta cell activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_18_11986_s_133	9115263	3 PDX-1 Is the Predominant beta Cell Activity Binding to the A1 and A2 Elements	bind
30729	1	7647	5	13	NULL	NULL	NULL	Sp1	GP		bind					MDR1	GP			GC element within promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_4_2979_s_142	10644769	3 Previous studies have shown that Sp1 binds to a GC element within the MDR1 promoter and is required for basal expression in a number of cell lines ( 28,  29,  49).	bind
30730	2	7647	5	13	NULL	NULL	NULL	Sp1	GP		is required for					basal expression	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_4_2979_s_142	10644769	3 Previous studies have shown that Sp1 binds to a GC element within the MDR1 promoter and is required for basal expression in a number of cell lines ( 28,  29,  49).	bind
23585	1	7647	6	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				MDR1	NULL			GC element of the promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_4_2979_s_142	10644769	3 Previous studies have shown that Sp1 binds to a GC element within the MDR1 promoter and is required for basal expression in a number of cell lines ( 28,  29,  49).	bind
23586	2	7647	6	NULL	NULL	0	NULL	Sp1	NULL		is required for	NULL				basal expression	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_4_2979_s_142	10644769	3 Previous studies have shown that Sp1 binds to a GC element within the MDR1 promoter and is required for basal expression in a number of cell lines ( 28,  29,  49).	bind
30733	1	7648	5	13	NULL	NULL	NULL	AMP	Chemical		bind					GS	GP	E. coli			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_39_33298_s_180	16055443	3 Previous studies on the binding of AMP to  E. coli GS found a binding constant of 125 muM and a stoichiometry of 1 mol of AMP/mol of subunit ( ).	bind
23587	1	7648	6	NULL	NULL	0	NULL	AMP	NULL		bind	NULL				GS	NULL	E.coli			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_39_33298_s_180	16055443	3 Previous studies on the binding of AMP to  E. coli GS found a binding constant of 125 muM and a stoichiometry of 1 mol of AMP/mol of subunit ( ).	bind
30731	1	7649	5	13	NULL	NULL	NULL	Rad24p protein	GP		bind					Cdc25p	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_20_5483_s_231	11032815	3 protein Rad24p binds to Cdc25p after Chk1 phosphorylation ( Lopez-Girona   et al., 1999).	bind
30732	2	7649	5	13	NULL	NULL	NULL	statement 1	Process		occurs after					Chk1	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_20_5483_s_231	11032815	3 protein Rad24p binds to Cdc25p after Chk1 phosphorylation ( Lopez-Girona   et al., 1999).	bind
23588	1	7649	6	NULL	NULL	0	NULL	Rad24p protein	NULL		bind	NULL				Cdc25p	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_19_20_5483_s_231	11032815	3 protein Rad24p binds to Cdc25p after Chk1 phosphorylation ( Lopez-Girona   et al., 1999).	bind
23589	2	7649	6	NULL	NULL	0	NULL	statement 1	NULL		occurs after	NULL				Chk1	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_embo_19_20_5483_s_231	11032815	3 protein Rad24p binds to Cdc25p after Chk1 phosphorylation ( Lopez-Girona   et al., 1999).	bind
30734	1	7651	5	13	NULL	NULL	NULL	tapasin	GP		bind			interchain disulfide bond		ERp57	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_47_44838_s_226	12239218	3 Recently it has been shown that tapasin binds to ERp57 via an interchain disulfide bond, and cooperates with ERp57 in forming the correct disulfide bonds in the class I heavy chain ( 49).	bind
30735	2	7651	5	13	NULL	NULL	NULL	ERp57	GP		forms					disulfide bonds	GP	correct			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_47_44838_s_226	12239218	3 Recently it has been shown that tapasin binds to ERp57 via an interchain disulfide bond, and cooperates with ERp57 in forming the correct disulfide bonds in the class I heavy chain ( 49).	bind
30736	3	7651	5	13	NULL	NULL	NULL	statement 2	Process		occurs in					class I heavy chain	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_47_44838_s_226	12239218	3 Recently it has been shown that tapasin binds to ERp57 via an interchain disulfide bond, and cooperates with ERp57 in forming the correct disulfide bonds in the class I heavy chain ( 49).	bind
30737	4	7651	5	13	NULL	NULL	NULL	tapasin	GP		cooperates with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_47_44838_s_226	12239218	3 Recently it has been shown that tapasin binds to ERp57 via an interchain disulfide bond, and cooperates with ERp57 in forming the correct disulfide bonds in the class I heavy chain ( 49).	bind
23590	1	7651	6	NULL	NULL	0	NULL	tapasin	NULL		bind	NULL		interchain disulfide bond		ERp57	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_47_44838_s_226	12239218	3 Recently it has been shown that tapasin binds to ERp57 via an interchain disulfide bond, and cooperates with ERp57 in forming the correct disulfide bonds in the class I heavy chain ( 49).	bind
23591	2	7651	6	NULL	NULL	0	NULL	tapasin	NULL		cooperates with	NULL				ERp57	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_47_44838_s_226	12239218	3 Recently it has been shown that tapasin binds to ERp57 via an interchain disulfide bond, and cooperates with ERp57 in forming the correct disulfide bonds in the class I heavy chain ( 49).	bind
23592	3	7651	6	NULL	NULL	0	NULL	statement 2	NULL		forms	NULL				class I heavy chain	NULL	correct	disulfide bonds		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_47_44838_s_226	12239218	3 Recently it has been shown that tapasin binds to ERp57 via an interchain disulfide bond, and cooperates with ERp57 in forming the correct disulfide bonds in the class I heavy chain ( 49).	bind
30739	2	7652	5	13	NULL	NULL	NULL	testosterone	GP		does not result in					spin shift	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_14_9127_s_329	16467307	3 Recently, Roberts  et al. ( ) used EPR binding studies with high concentrations of P450 3A4 to suggest that the first bound molecule of testosterone does not result in a spin shift and, hence, cannot be detected by absorbance.	bind
23593	1	7652	6	NULL	NULL	0	NULL	testosterone molecule	NULL		does not result in	NULL				spin shift	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_14_9127_s_329	16467307	3 Recently, Roberts  et al. ( ) used EPR binding studies with high concentrations of P450 3A4 to suggest that the first bound molecule of testosterone does not result in a spin shift and, hence, cannot be detected by absorbance.	bind
30740	1	7653	5	13	NULL	NULL	NULL	RLI1	GP		bind					eIF2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7452_s_28	16421098	3 RLI1 binds to the eukaryotic initiation factors eIF2 and eIF5 and forms part of the pre-initiation complex required for the translation of mRNA in yeast.	bind
30741	2	7653	5	13	NULL	NULL	NULL	RLI1	GP		bind					eIF5	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7452_s_28	16421098	3 RLI1 binds to the eukaryotic initiation factors eIF2 and eIF5 and forms part of the pre-initiation complex required for the translation of mRNA in yeast.	bind
30742	3	7653	5	13	NULL	NULL	NULL	eIF2	GP		is a type of					eukaryotic initiation factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7452_s_28	16421098	3 RLI1 binds to the eukaryotic initiation factors eIF2 and eIF5 and forms part of the pre-initiation complex required for the translation of mRNA in yeast.	bind
30743	4	7653	5	13	NULL	NULL	NULL	eIF5	GP		is a type of					eukaryotic initiation factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7452_s_28	16421098	3 RLI1 binds to the eukaryotic initiation factors eIF2 and eIF5 and forms part of the pre-initiation complex required for the translation of mRNA in yeast.	bind
30744	5	7653	5	13	NULL	NULL	NULL	statement 1	Process		forms					pre-initiation complex 	GP	part of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7452_s_28	16421098	3 RLI1 binds to the eukaryotic initiation factors eIF2 and eIF5 and forms part of the pre-initiation complex required for the translation of mRNA in yeast.	bind
30745	6	7653	5	13	NULL	NULL	NULL	statement 2	Process		forms					pre-initiation complex 	GP	part of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7452_s_28	16421098	3 RLI1 binds to the eukaryotic initiation factors eIF2 and eIF5 and forms part of the pre-initiation complex required for the translation of mRNA in yeast.	bind
30746	7	7653	5	13	NULL	NULL	NULL	pre-initiation complex	GP		required for					mRNA	NucleicAcid	translation of			NULL	in yeast	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7452_s_28	16421098	3 RLI1 binds to the eukaryotic initiation factors eIF2 and eIF5 and forms part of the pre-initiation complex required for the translation of mRNA in yeast.	bind
23594	1	7653	6	NULL	NULL	0	NULL	RLI 1	NULL		bind	NULL				eIF2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7452_s_28	16421098	3 RLI1 binds to the eukaryotic initiation factors eIF2 and eIF5 and forms part of the pre-initiation complex required for the translation of mRNA in yeast.	bind
23595	2	7653	6	NULL	NULL	0	NULL	RLI 1	NULL		bind	NULL				eIF5	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7452_s_28	16421098	3 RLI1 binds to the eukaryotic initiation factors eIF2 and eIF5 and forms part of the pre-initiation complex required for the translation of mRNA in yeast.	bind
23596	3	7653	6	10	NULL	0	NULL	eIF2	NULL		is a type of	NULL				eukaryotic initiation factor	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7452_s_28	16421098	3 RLI1 binds to the eukaryotic initiation factors eIF2 and eIF5 and forms part of the pre-initiation complex required for the translation of mRNA in yeast.	bind
23597	4	7653	6	10	NULL	0	NULL	eIF5	NULL		is a type of	NULL				eukaryotic initiation factor	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7452_s_28	16421098	3 RLI1 binds to the eukaryotic initiation factors eIF2 and eIF5 and forms part of the pre-initiation complex required for the translation of mRNA in yeast.	bind
23598	5	7653	6	NULL	NULL	0	NULL	pre-initiation complex	NULL		is required for	NULL				mRNA	NULL	translation of			NULL	yeast	0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7452_s_28	16421098	3 RLI1 binds to the eukaryotic initiation factors eIF2 and eIF5 and forms part of the pre-initiation complex required for the translation of mRNA in yeast.	bind
46637	6	7653	6	10	NULL	0	NULL	statement 1	NULL		forms	NULL				pre-initiation complex 	NULL	part of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7452_s_28	16421098	3 RLI1 binds to the eukaryotic initiation factors eIF2 and eIF5 and forms part of the pre-initiation complex required for the translation of mRNA in yeast.	bind
46638	7	7653	6	10	NULL	0	NULL	statement 2	NULL		forms	NULL				pre-initiation complex 	NULL	part of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7452_s_28	16421098	3 RLI1 binds to the eukaryotic initiation factors eIF2 and eIF5 and forms part of the pre-initiation complex required for the translation of mRNA in yeast.	bind
30747	1	7654	5	13	NULL	NULL	NULL	RyR1	GP		bind					FKBP12	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34813_s_230	9857007	3 RyR1 and RyR3 can bind both FKBP12 and FKBP12.6.	bind
30748	2	7654	5	13	NULL	NULL	NULL	RyR1	GP		bind					FKBP12.6	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34813_s_230	9857007	3 RyR1 and RyR3 can bind both FKBP12 and FKBP12.6.	bind
30749	3	7654	5	13	NULL	NULL	NULL	RyR3	GP		bind					FKBP12	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34813_s_230	9857007	3 RyR1 and RyR3 can bind both FKBP12 and FKBP12.6.	bind
30750	4	7654	5	13	NULL	NULL	NULL	RyR3	GP		bind					FKBP12.6	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34813_s_230	9857007	3 RyR1 and RyR3 can bind both FKBP12 and FKBP12.6.	bind
23599	1	7654	6	13	NULL	NULL	NULL	RyR1	GP		bind					FKBP12	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34813_s_230	9857007	3 RyR1 and RyR3 can bind both FKBP12 and FKBP12.6.	bind
23600	2	7654	6	NULL	NULL	0	NULL	RyR1	NULL		bind	NULL				FKBP12.6	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34813_s_230	9857007	3 RyR1 and RyR3 can bind both FKBP12 and FKBP12.6.	bind
23601	3	7654	6	NULL	NULL	0	NULL	RyR3	NULL		bind	NULL				FKBP12	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34813_s_230	9857007	3 RyR1 and RyR3 can bind both FKBP12 and FKBP12.6.	bind
23602	4	7654	6	NULL	NULL	0	NULL	RyR3	NULL		bind	NULL				FKBP12.6	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34813_s_230	9857007	3 RyR1 and RyR3 can bind both FKBP12 and FKBP12.6.	bind
30751	1	7655	5	13	NULL	NULL	NULL	SNQ2	GP		encodes for					multidrug ATP-binding cassette transporter	GP	yeast plasma membrane			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_1511_s_147	10625705	3 SNQ2 encodes for a multidrug ATP-binding cassette transporter of the yeast plasma membrane ( 44,  45).	bind
23603	1	7655	6	10	NULL	0	NULL	SNQ2			encodes for					multidrug ATP-binding cassette transporter		yeast plasma membrane			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_1511_s_147	10625705	3 SNQ2 encodes for a multidrug ATP-binding cassette transporter of the yeast plasma membrane ( 44,  45).	bind
30752	1	7656	5	NULL	NULL	0	NULL		NULL		narrows	NULL		bulky helix alphaC in the alpha2I domain			NULL		collagen binding groove		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3348_s_272	10652324	3 Still, it could be speculated that the bulky helix alphaC in the alpha2I domain narrows the collagen binding groove and may actually disturb the binding of type IV collagen, which contains interrupted sequences between triple helices and is therefore less compact than type I collagen.	bind
30753	2	7656	5	13	NULL	NULL	NULL	statement 1	Process		disturbs					type IV collagen	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3348_s_272	10652324	3 Still, it could be speculated that the bulky helix alphaC in the alpha2I domain narrows the collagen binding groove and may actually disturb the binding of type IV collagen, which contains interrupted sequences between triple helices and is therefore less compact than type I collagen.	bind
30754	3	7656	5	13	NULL	NULL	NULL	type IV collagen	GP		contains								interrupted sequences between triple helices		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3348_s_272	10652324	3 Still, it could be speculated that the bulky helix alphaC in the alpha2I domain narrows the collagen binding groove and may actually disturb the binding of type IV collagen, which contains interrupted sequences between triple helices and is therefore less compact than type I collagen.	bind
30755	4	7656	5	13	NULL	NULL	NULL	type IV collagen	GP		less compact than					type I collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3348_s_272	10652324	3 Still, it could be speculated that the bulky helix alphaC in the alpha2I domain narrows the collagen binding groove and may actually disturb the binding of type IV collagen, which contains interrupted sequences between triple helices and is therefore less compact than type I collagen.	bind
55534	5	7656	5	13	NULL	NULL	NULL	statement 4	Process		is due to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3348_s_272	10652324	3 Still, it could be speculated that the bulky helix alphaC in the alpha2I domain narrows the collagen binding groove and may actually disturb the binding of type IV collagen, which contains interrupted sequences between triple helices and is therefore less compact than type I collagen.	bind
23622	1	7656	6	NULL	NULL	0	NULL		NULL		disturb	NULL	may	helix alphaC in the alpha2I domain		type IV collagen	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3348_s_272	10652324	3 Still, it could be speculated that the bulky helix alphaC in the alpha2I domain narrows the collagen binding groove and may actually disturb the binding of type IV collagen, which contains interrupted sequences between triple helices and is therefore less compact than type I collagen.	bind
23635	2	7656	6	NULL	NULL	0	NULL	type IV collagen	NULL		contains	NULL					NULL		interrupted sequences between triple helices 		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3348_s_272	10652324	3 Still, it could be speculated that the bulky helix alphaC in the alpha2I domain narrows the collagen binding groove and may actually disturb the binding of type IV collagen, which contains interrupted sequences between triple helices and is therefore less compact than type I collagen.	bind
23636	3	7656	6	NULL	NULL	0	NULL	type IV collagen	NULL		is less compact than	NULL				type I collagen	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3348_s_272	10652324	3 Still, it could be speculated that the bulky helix alphaC in the alpha2I domain narrows the collagen binding groove and may actually disturb the binding of type IV collagen, which contains interrupted sequences between triple helices and is therefore less compact than type I collagen.	bind
23637	4	7656	6	NULL	NULL	0	NULL	statement 3	NULL		is due to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3348_s_272	10652324	3 Still, it could be speculated that the bulky helix alphaC in the alpha2I domain narrows the collagen binding groove and may actually disturb the binding of type IV collagen, which contains interrupted sequences between triple helices and is therefore less compact than type I collagen.	bind
23642	5	7656	6	NULL	NULL	0	NULL		NULL		narrows the	NULL		helix alphaC in the alpha2I domain			NULL		collagen binding groove		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3348_s_272	10652324	3 Still, it could be speculated that the bulky helix alphaC in the alpha2I domain narrows the collagen binding groove and may actually disturb the binding of type IV collagen, which contains interrupted sequences between triple helices and is therefore less compact than type I collagen.	bind
30756	1	7657	5	13	NULL	NULL	NULL	Galphai1	GP		associates with					RGS4	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1269_s_111	9430654	3 Superposition of the structure of Galphai1 associated with RGS4 on that of Galphas associated with adenylyl cyclase suggests that the interaction of an RGS protein with a G protein alpha subunit would not block binding of a Galpha protein to adenylyl cyclase.	bind
30757	2	7657	5	13	NULL	NULL	NULL	Galphas	GP		associates with					adenylyl cyclase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1269_s_111	9430654	3 Superposition of the structure of Galphai1 associated with RGS4 on that of Galphas associated with adenylyl cyclase suggests that the interaction of an RGS protein with a G protein alpha subunit would not block binding of a Galpha protein to adenylyl cyclase.	bind
30758	3	7657	5	13	NULL	NULL	NULL	RGS protein	GP		interacts with					G protein	GP		alpha subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1269_s_111	9430654	3 Superposition of the structure of Galphai1 associated with RGS4 on that of Galphas associated with adenylyl cyclase suggests that the interaction of an RGS protein with a G protein alpha subunit would not block binding of a Galpha protein to adenylyl cyclase.	bind
30759	4	7657	5	13	NULL	NULL	NULL	Galpha protein	GP		bind					adenylyl cyclase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1269_s_111	9430654	3 Superposition of the structure of Galphai1 associated with RGS4 on that of Galphas associated with adenylyl cyclase suggests that the interaction of an RGS protein with a G protein alpha subunit would not block binding of a Galpha protein to adenylyl cyclase.	bind
30760	5	7657	5	13	NULL	NULL	NULL	statement 3	Process		does not block					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1269_s_111	9430654	3 Superposition of the structure of Galphai1 associated with RGS4 on that of Galphas associated with adenylyl cyclase suggests that the interaction of an RGS protein with a G protein alpha subunit would not block binding of a Galpha protein to adenylyl cyclase.	bind
23790	1	7657	6	10	NULL	0	NULL	RGS protein	NULL		interacts with	NULL				G protein 	NULL		alpha subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1269_s_111	9430654	3 Superposition of the structure of Galphai1 associated with RGS4 on that of Galphas associated with adenylyl cyclase suggests that the interaction of an RGS protein with a G protein alpha subunit would not block binding of a Galpha protein to adenylyl cyclase.	bind
23791	2	7657	6	NULL	NULL	0	NULL	Galpha protein	NULL		bind	NULL				adenylyl cyclase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1269_s_111	9430654	3 Superposition of the structure of Galphai1 associated with RGS4 on that of Galphas associated with adenylyl cyclase suggests that the interaction of an RGS protein with a G protein alpha subunit would not block binding of a Galpha protein to adenylyl cyclase.	bind
23792	3	7657	6	10	NULL	0	NULL	statement 1	NULL		does not block	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1269_s_111	9430654	3 Superposition of the structure of Galphai1 associated with RGS4 on that of Galphas associated with adenylyl cyclase suggests that the interaction of an RGS protein with a G protein alpha subunit would not block binding of a Galpha protein to adenylyl cyclase.	bind
24573	4	7657	6	NULL	NULL	0	NULL	Galphai1	NULL		associates with	NULL				RGS4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1269_s_111	9430654	3 Superposition of the structure of Galphai1 associated with RGS4 on that of Galphas associated with adenylyl cyclase suggests that the interaction of an RGS protein with a G protein alpha subunit would not block binding of a Galpha protein to adenylyl cyclase.	bind
46639	5	7657	6	10	NULL	0	NULL	Galphas	NULL		associate with	NULL				adenylyl cyclase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1269_s_111	9430654	3 Superposition of the structure of Galphai1 associated with RGS4 on that of Galphas associated with adenylyl cyclase suggests that the interaction of an RGS protein with a G protein alpha subunit would not block binding of a Galpha protein to adenylyl cyclase.	bind
30761	1	7659	5	13	NULL	NULL	NULL	Eps8	GP		bind					Etk	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41124_s_283	11013262	3 The binding of Eps8 to Etk also increases the kinase activity of Etk.	bind
30762	2	7659	5	13	NULL	NULL	NULL	statement 1	Process		increase					Etk	GP	kinase activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41124_s_283	11013262	3 The binding of Eps8 to Etk also increases the kinase activity of Etk.	bind
23643	1	7659	6	NULL	NULL	0	NULL	Eps8	NULL		bind	NULL				Etk	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41124_s_283	11013262	3 The binding of Eps8 to Etk also increases the kinase activity of Etk.	bind
23645	2	7659	6	NULL	NULL	0	NULL	statement 1	NULL		increases	NULL				Etk	NULL	kinase activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41124_s_283	11013262	3 The binding of Eps8 to Etk also increases the kinase activity of Etk.	bind
30763	1	7660	5	13	NULL	NULL	NULL	TrfA protein	GP		bind					RK2	GP			iterons at minimal origin of replication	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_20173_s_71	9242693	3 The binding of the TrfA protein to the iterons at the minimal RK2 origin of replication has been characterized in detail ( 25,  26,  37,  40); however, little is known about the nature of binding of the DnaA protein to  oriV.	bind
46640	2	7660	5	13	NULL	NULL	NULL	DnaA protein	GP		bind					oriV	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_20173_s_71	9242693	3 The binding of the TrfA protein to the iterons at the minimal RK2 origin of replication has been characterized in detail ( 25,  26,  37,  40); however, little is known about the nature of binding of the DnaA protein to  oriV.	bind
23647	1	7660	6	10	NULL	0	NULL	TrfA protein	NULL		bind	NULL				RK2	NULL			iterons at minimal  origin of replication	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_20173_s_71	9242693	3 The binding of the TrfA protein to the iterons at the minimal RK2 origin of replication has been characterized in detail ( 25,  26,  37,  40); however, little is known about the nature of binding of the DnaA protein to  oriV.	bind
23648	2	7660	6	NULL	NULL	0	NULL	DnaA protein	NULL		bind	NULL				oriV	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_32_20173_s_71	9242693	3 The binding of the TrfA protein to the iterons at the minimal RK2 origin of replication has been characterized in detail ( 25,  26,  37,  40); however, little is known about the nature of binding of the DnaA protein to  oriV.	bind
30764	1	7662	5	13	NULL	NULL	NULL	pemphigus antibody	GP		targets					alpha9	GP	keratinocyte			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
30765	2	7662	5	13	NULL	NULL	NULL	PV IgG	GP		bind					cell surface	CellComponent	keratinocyte			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
30766	3	7662	5	13	NULL	NULL	NULL	statement 2	Process		elicits					Ca2+ influx	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
30767	4	7662	5	13	NULL	NULL	NULL	Ca2+ influx	Process		is a type of					nicotinic-like effects	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
30768	5	7662	5	13	NULL	NULL	NULL	statement 2	Process		elicits					phospholipase C	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
30769	6	7662	5	13	NULL	NULL	NULL	statement 2	Process		elicits					inositol 1,4,5-trisphosphate	Chemical	production of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
30770	7	7662	5	13	NULL	NULL	NULL	statement 2	Process		elicits					Ca2+	Chemical	rapid transient increase of intracellular			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
30771	8	7662	5	13	NULL	NULL	NULL	statement 2	Process		elicits					cAMP/cGMP ratios	Chemical	changes in intracellular			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
30772	9	7662	5	13	NULL	NULL	NULL	statement 2	Process		elicits					protein kinase C	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
30773	10	7662	5	13	NULL	NULL	NULL	protein kinase C	GP	activated	 translocates from					cytosol	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
30774	12	7662	5	13	NULL	NULL	NULL	phospholipase C	GP	activation of	is a type of					muscarinic-like effects	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
30775	13	7662	5	13	NULL	NULL	NULL	inositol 1,4,5-trisphosphate	Chemical	production of	is a type of					muscarinic-like effects	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
30776	14	7662	5	13	NULL	NULL	NULL	Ca2+	Chemical	rapid transient increase of intracellular	is a type of					muscarinic-like effects	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
30777	15	7662	5	13	NULL	NULL	NULL	cAMP/cGMP ratios	Chemical	changes in intracellular	is a type of					muscarinic-like effects	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
30778	16	7662	5	13	NULL	NULL	NULL	protein kinase C	GP	activation of	is a type of					muscarinic-like effects	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
30779	17	7662	5	13	NULL	NULL	NULL	protein kinase C	GP	translocation of	is a type of					muscarinic-like effects	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
46641	11	7662	5	13	NULL	NULL	NULL	protein kinase C	GP		translocates to					particulate/cytoskeletal fractions	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
23649	1	7662	6	NULL	NULL	0	NULL	pemphigus antibody	NULL		targets	NULL				keratinocyte alpha9	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
23650	2	7662	6	NULL	NULL	0	NULL	PV IgG	NULL		bind	NULL				keratinocyte cell surface	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
23653	3	7662	6	NULL	NULL	0	NULL	statement 2	NULL		elicits	NULL				nicotinic-like effects	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
23654	4	7662	6	NULL	NULL	0	NULL	statement 2	NULL		elicits	NULL				muscarinic-like effects	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
23655	5	7662	6	10	NULL	0	NULL	Ca2+ influx	NULL		is a type of	NULL				nicotinic-like effect	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
23656	6	7662	6	10	NULL	0	NULL	phospholipase C	NULL	activation of 	is a type of	NULL				muscarinic-like effect	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
23657	7	7662	6	10	NULL	0	NULL	inositol 1,4,5-trisphosphate	NULL	production of	is a type of	NULL				muscarinic-like effect	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
23659	8	7662	6	10	NULL	0	NULL	intracellular Ca2+	NULL	transient increase of	is a type of	NULL				muscarinic-like effect	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
23660	9	7662	6	10	NULL	0	NULL	intracellular cAMP/cGMP ratio	NULL	changes in	is a type of	NULL				muscarinic-like effect	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
23661	11	7662	6	10	NULL	0	NULL	protein kinase C	NULL		 translocates to	NULL				particulate/cytoskeletal fraction	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
23662	12	7662	6	10	NULL	0	NULL	statement 10	NULL		is a type of	NULL				muscarinic-like effect	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
23663	13	7662	6	10	NULL	0	NULL	protein kinase C	NULL	activation of	is a type of	NULL				muscarinic-like effect	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
46642	10	7662	6	10	NULL	0	NULL	protein kinase C	NULL		translocates from	NULL				 cytosol	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_4_1377_s_262	11021840	3 The fact that keratinocyte alpha9 is targeted by pemphigus antibody is also in keeping with the notion that the biochemical events elicited because of PV IgG binding to the keratinocyte cell surface include both the nicotinic-like effects (ie, Ca2+ influx) and the muscarinic-like effects (ie, activation of phospholipase C, production of inositol 1,4,5-trisphosphate, rapid transient increase of intracellular Ca2+, changes in the intracellular cAMP/cGMP ratios, and activation and translocation of protein kinase C from the cytosol to the particulate/cytoskeletal fractions).	bind
30780	1	7663	5	13	NULL	NULL	NULL	p185deltaC	GP		stimulates					cell migration	Process	spontaneous			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_31_28954_s_235	11387320	3 The finding that p185deltaC is capable of stimulating spontaneous cell migration and inducing CML-like disease in BMT mice is consistent with the results reported by other investigators that the direct binding of Crkl to Bcr-Abl is not required for Bcr-Abl transformation ( 42).	bind
30781	2	7663	5	13	NULL	NULL	NULL	p185deltaC	GP		induces					CML-like disease	MedicalFinding				NULL	in BMT mice	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_31_28954_s_235	11387320	3 The finding that p185deltaC is capable of stimulating spontaneous cell migration and inducing CML-like disease in BMT mice is consistent with the results reported by other investigators that the direct binding of Crkl to Bcr-Abl is not required for Bcr-Abl transformation ( 42).	bind
30782	3	7663	5	13	NULL	NULL	NULL	Crkl	GP		bind		directly			Bcr-Abl	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_31_28954_s_235	11387320	3 The finding that p185deltaC is capable of stimulating spontaneous cell migration and inducing CML-like disease in BMT mice is consistent with the results reported by other investigators that the direct binding of Crkl to Bcr-Abl is not required for Bcr-Abl transformation ( 42).	bind
30783	4	7663	5	13	NULL	NULL	NULL	statement 3	Process		is not required for					Bcr-Abl	GP	 transformation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_31_28954_s_235	11387320	3 The finding that p185deltaC is capable of stimulating spontaneous cell migration and inducing CML-like disease in BMT mice is consistent with the results reported by other investigators that the direct binding of Crkl to Bcr-Abl is not required for Bcr-Abl transformation ( 42).	bind
23664	1	7663	6	NULL	NULL	0	NULL	p185deltaC	NULL		stimulates	NULL				cell migration	NULL	spontaneous			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_31_28954_s_235	11387320	3 The finding that p185deltaC is capable of stimulating spontaneous cell migration and inducing CML-like disease in BMT mice is consistent with the results reported by other investigators that the direct binding of Crkl to Bcr-Abl is not required for Bcr-Abl transformation ( 42).	bind
23666	2	7663	6	NULL	NULL	0	NULL	p185deltaC	NULL		induce	NULL				CML-like disease	NULL				NULL	BMT mice	0	NULL	NULL	NULL	gw60_jbiolchem_276_31_28954_s_235	11387320	3 The finding that p185deltaC is capable of stimulating spontaneous cell migration and inducing CML-like disease in BMT mice is consistent with the results reported by other investigators that the direct binding of Crkl to Bcr-Abl is not required for Bcr-Abl transformation ( 42).	bind
23667	3	7663	6	NULL	NULL	0	NULL	Crkl	NULL		bind	NULL	directly			Bcr-Abl	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_31_28954_s_235	11387320	3 The finding that p185deltaC is capable of stimulating spontaneous cell migration and inducing CML-like disease in BMT mice is consistent with the results reported by other investigators that the direct binding of Crkl to Bcr-Abl is not required for Bcr-Abl transformation ( 42).	bind
23668	4	7663	6	NULL	NULL	0	NULL	statement 3	NULL		is not required for	NULL				Bcr-Abl	NULL	transformation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_31_28954_s_235	11387320	3 The finding that p185deltaC is capable of stimulating spontaneous cell migration and inducing CML-like disease in BMT mice is consistent with the results reported by other investigators that the direct binding of Crkl to Bcr-Abl is not required for Bcr-Abl transformation ( 42).	bind
30784	1	7664	5	13	NULL	NULL	NULL	galectins	GP		bind		specifically			beta-galactoside derivatives	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1601_s_15	10329612	3 The first class comprises a family of small molecular mass proteins named galectins that specifically bind to beta-galactoside derivatives in a calcium-independent manner.	bind
30785	2	7664	5	13	NULL	NULL	NULL	statement 1	Process		is independent of					calcium	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1601_s_15	10329612	3 The first class comprises a family of small molecular mass proteins named galectins that specifically bind to beta-galactoside derivatives in a calcium-independent manner.	bind
30786	3	7664	5	13	NULL	NULL	NULL	galectins	GP		is a type of					small molecular mass proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1601_s_15	10329612	3 The first class comprises a family of small molecular mass proteins named galectins that specifically bind to beta-galactoside derivatives in a calcium-independent manner.	bind
23672	1	7664	6	NULL	NULL	0	NULL	galectins	NULL		bind	NULL	specifically			beta-galactoside derivatives	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_5_1601_s_15	10329612	3 The first class comprises a family of small molecular mass proteins named galectins that specifically bind to beta-galactoside derivatives in a calcium-independent manner.	bind
23673	2	7664	6	10	NULL	0	NULL	galectins	NULL		is a type of	NULL				small molecular mass proteins	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1601_s_15	10329612	3 The first class comprises a family of small molecular mass proteins named galectins that specifically bind to beta-galactoside derivatives in a calcium-independent manner.	bind
23674	3	7664	6	NULL	NULL	0	NULL	statement 1	NULL		is independent of	NULL				calcium	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_5_1601_s_15	10329612	3 The first class comprises a family of small molecular mass proteins named galectins that specifically bind to beta-galactoside derivatives in a calcium-independent manner.	bind
30787	1	7665	5	13	NULL	NULL	NULL	Fra-2	GP		is a type of					Fos-related antigen	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_17991_s_281	10747965	3 The Fos-related antigen, Fra-2, that can bind to the PF1 site ( 19) was also tested for its ability to regulate  p53 promoter activity.	bind
30788	2	7665	5	13	NULL	NULL	NULL	Fra-2	GP		bind									PF1 site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_17991_s_281	10747965	3 The Fos-related antigen, Fra-2, that can bind to the PF1 site ( 19) was also tested for its ability to regulate  p53 promoter activity.	bind
23677	1	7665	6	NULL	NULL	0	NULL	Fra-2	NULL		bind	NULL					NULL			PF1 site	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_24_17991_s_281	10747965	3 The Fos-related antigen, Fra-2, that can bind to the PF1 site ( 19) was also tested for its ability to regulate  p53 promoter activity.	bind
23680	2	7665	6	10	NULL	0	NULL	Fra-2	NULL		is a type of	NULL				Fos-related antigen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_17991_s_281	10747965	3 The Fos-related antigen, Fra-2, that can bind to the PF1 site ( 19) was also tested for its ability to regulate  p53 promoter activity.	bind
30789	1	7668	5	13	NULL	NULL	NULL	NF-kappaB	GP		bind					TAFII105alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_48_44963_s_185	11567023	3 The proximity of these domains raised the possibility that NF-kappaB binding and nuclear export protein binding with TAFII105alpha may be mutually exclusive.	bind
30790	2	7668	5	13	NULL	NULL	NULL	nuclear export protein	GP		bind					TAFII105alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_48_44963_s_185	11567023	3 The proximity of these domains raised the possibility that NF-kappaB binding and nuclear export protein binding with TAFII105alpha may be mutually exclusive.	bind
30791	3	7668	5	13	NULL	NULL	NULL	statement 1	Process		is mutually exclusive to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_48_44963_s_185	11567023	3 The proximity of these domains raised the possibility that NF-kappaB binding and nuclear export protein binding with TAFII105alpha may be mutually exclusive.	bind
23794	1	7668	6	NULL	NULL	0	NULL	NF-kappaB	NULL		bind	NULL				TAFII105alpha	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_48_44963_s_185	11567023	3 The proximity of these domains raised the possibility that NF-kappaB binding and nuclear export protein binding with TAFII105alpha may be mutually exclusive.	bind
23795	2	7668	6	NULL	NULL	0	NULL	nuclear export protein	NULL		bind	NULL				TAFII105alpha	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_48_44963_s_185	11567023	3 The proximity of these domains raised the possibility that NF-kappaB binding and nuclear export protein binding with TAFII105alpha may be mutually exclusive.	bind
23796	3	7668	6	NULL	NULL	0	NULL	statement 1	NULL		is independent of	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_48_44963_s_185	11567023	3 The proximity of these domains raised the possibility that NF-kappaB binding and nuclear export protein binding with TAFII105alpha may be mutually exclusive.	bind
30792	1	7669	5	13	NULL	NULL	NULL	ATP	Chemical		does not stabilize					TAP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14632_s_196	10329656	3 The reason for the lack of TAP stabilization by ATP reported by Russ ( 21) is less evident; it is possible that Triton or Nonidet P-40-solubilized TAP proteins bind ATP with reduced affinity allowing for labeling with photoreactive ATP analogues, but not stabilization of TAP structure.	bind
30793	2	7669	5	13	NULL	NULL	NULL	TAP proteins	GP	solubilized	bind		low affinity			ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14632_s_196	10329656	3 The reason for the lack of TAP stabilization by ATP reported by Russ ( 21) is less evident; it is possible that Triton or Nonidet P-40-solubilized TAP proteins bind ATP with reduced affinity allowing for labeling with photoreactive ATP analogues, but not stabilization of TAP structure.	bind
23797	1	7669	6	10	NULL	0	NULL	TAP protein	NULL	solubilized	bind	NULL	low affinity			ATP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14632_s_196	10329656	3 The reason for the lack of TAP stabilization by ATP reported by Russ ( 21) is less evident; it is possible that Triton or Nonidet P-40-solubilized TAP proteins bind ATP with reduced affinity allowing for labeling with photoreactive ATP analogues, but not stabilization of TAP structure.	bind
23798	2	7669	6	NULL	NULL	0	NULL	statement 1	NULL		does not stabilize	NULL				TAP	NULL	structure of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_14632_s_196	10329656	3 The reason for the lack of TAP stabilization by ATP reported by Russ ( 21) is less evident; it is possible that Triton or Nonidet P-40-solubilized TAP proteins bind ATP with reduced affinity allowing for labeling with photoreactive ATP analogues, but not stabilization of TAP structure.	bind
30794	1	7670	5	13	NULL	NULL	NULL	PDK	GP		bind								GST-lipoyl domains		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15773_s_383	10748134	3 The use of commercially available thrombin preparations to remove His tags from the PDKs caused problems in subsequent studies analyzing PDK binding to GST-lipoyl domains  .	bind
23799	1	7670	6	NULL	NULL	0	NULL	PDK	NULL		bind	NULL					NULL		GST-lipoyl domains		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15773_s_383	10748134	3 The use of commercially available thrombin preparations to remove His tags from the PDKs caused problems in subsequent studies analyzing PDK binding to GST-lipoyl domains  .	bind
30795	1	7671	5	13	NULL	NULL	NULL	EIIIA segment	GP		bind					alpha4beta1	GP				NULL	in MOLT-3 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14467_s_260	11839764	3 Therefore it is of interest that we observe (Fig.  6) that the interaction of EIIIA segment with alpha4beta1 in MOLT-3 cells increases phosphorylation of p44/42 MAP kinase.	bind
30796	2	7671	5	13	NULL	NULL	NULL	statement 1	Process		increases					p44/42 MAP kinase	GP	phosphorylation of			NULL	MOLT-3 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14467_s_260	11839764	3 Therefore it is of interest that we observe (Fig.  6) that the interaction of EIIIA segment with alpha4beta1 in MOLT-3 cells increases phosphorylation of p44/42 MAP kinase.	bind
23800	1	7671	6	NULL	NULL	0	NULL	EIIIA segment	NULL		bind	NULL				alpha4beta1	NULL				NULL	MOLT-3 cells	0	NULL	NULL	NULL	gw60_jbiolchem_277_17_14467_s_260	11839764	3 Therefore it is of interest that we observe (Fig.  6) that the interaction of EIIIA segment with alpha4beta1 in MOLT-3 cells increases phosphorylation of p44/42 MAP kinase.	bind
23801	2	7671	6	10	NULL	0	NULL	statement 1			increases					p44/42 MAP kinase		phosphorylation of			NULL	MOLT-3 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14467_s_260	11839764	3 Therefore it is of interest that we observe (Fig.  6) that the interaction of EIIIA segment with alpha4beta1 in MOLT-3 cells increases phosphorylation of p44/42 MAP kinase.	bind
30797	1	7672	5	13	NULL	NULL	NULL	NFkappaB	GP		regulates		may;;negatively			ISG	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_17_11678_s_162	16517601	3 Therefore, NFkappaB may negatively regulate ISG expression by directly or indirectly inhibiting the promoter binding of co-activators of ISG expression.	bind
30825	2	7672	5	13	NULL	NULL	NULL	co-activators	GP		bind					ISG	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_17_11678_s_162	16517601	3 Therefore, NFkappaB may negatively regulate ISG expression by directly or indirectly inhibiting the promoter binding of co-activators of ISG expression.	bind
30826	3	7672	5	13	NULL	NULL	NULL	NFkappaB	GP		inhibit		directly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_17_11678_s_162	16517601	3 Therefore, NFkappaB may negatively regulate ISG expression by directly or indirectly inhibiting the promoter binding of co-activators of ISG expression.	bind
30827	4	7672	5	13	NULL	NULL	NULL	NFkappaB	GP		inhibit		indirectly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_17_11678_s_162	16517601	3 Therefore, NFkappaB may negatively regulate ISG expression by directly or indirectly inhibiting the promoter binding of co-activators of ISG expression.	bind
30828	5	7672	5	13	NULL	NULL	NULL	statement 3	Process		is alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_17_11678_s_162	16517601	3 Therefore, NFkappaB may negatively regulate ISG expression by directly or indirectly inhibiting the promoter binding of co-activators of ISG expression.	bind
30829	6	7672	5	13	NULL	NULL	NULL	statement 3	Process		leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_17_11678_s_162	16517601	3 Therefore, NFkappaB may negatively regulate ISG expression by directly or indirectly inhibiting the promoter binding of co-activators of ISG expression.	bind
30830	7	7672	5	13	NULL	NULL	NULL	statement 4	Process		leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_17_11678_s_162	16517601	3 Therefore, NFkappaB may negatively regulate ISG expression by directly or indirectly inhibiting the promoter binding of co-activators of ISG expression.	bind
23802	1	7672	6	10	NULL	0	NULL	NFkappaB	NULL		 regulate	NULL	may;;negatively			ISG	NULL	expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_17_11678_s_162	16517601	3 Therefore, NFkappaB may negatively regulate ISG expression by directly or indirectly inhibiting the promoter binding of co-activators of ISG expression.	bind
23803	2	7672	6	NULL	NULL	0	NULL	co-activators	NULL		bind	NULL				ISG	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_17_11678_s_162	16517601	3 Therefore, NFkappaB may negatively regulate ISG expression by directly or indirectly inhibiting the promoter binding of co-activators of ISG expression.	bind
23804	3	7672	6	10	NULL	0	NULL	NF-kappaB	NULL		inhibits	NULL	directly			statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_17_11678_s_162	16517601	3 Therefore, NFkappaB may negatively regulate ISG expression by directly or indirectly inhibiting the promoter binding of co-activators of ISG expression.	bind
46643	4	7672	6	10	NULL	0	NULL	NFkappaB	NULL		inhibit	NULL	indirectly			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_17_11678_s_162	16517601	3 Therefore, NFkappaB may negatively regulate ISG expression by directly or indirectly inhibiting the promoter binding of co-activators of ISG expression.	bind
46644	5	7672	6	10	NULL	0	NULL	statement 3	NULL		is an alternative to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_17_11678_s_162	16517601	3 Therefore, NFkappaB may negatively regulate ISG expression by directly or indirectly inhibiting the promoter binding of co-activators of ISG expression.	bind
46645	6	7672	6	10	NULL	0	NULL	statement 3	NULL		leads to	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_17_11678_s_162	16517601	3 Therefore, NFkappaB may negatively regulate ISG expression by directly or indirectly inhibiting the promoter binding of co-activators of ISG expression.	bind
46646	7	7672	6	10	NULL	0	NULL	statement 4	NULL		leads to	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_17_11678_s_162	16517601	3 Therefore, NFkappaB may negatively regulate ISG expression by directly or indirectly inhibiting the promoter binding of co-activators of ISG expression.	bind
30798	1	7673	5	13	NULL	NULL	NULL	profilin	GP		bind					EVL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_46_36143_s_177	10945997	3 Therefore, we used profilin IIa to identify sequences through which profilin binds to EVL.	bind
23805	1	7673	6	NULL	NULL	0	NULL	profilin	NULL		bind	NULL				EVL	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_46_36143_s_177	10945997	3 Therefore, we used profilin IIa to identify sequences through which profilin binds to EVL.	bind
30799	1	7674	5	13	NULL	NULL	NULL	CRP	GP	native	bind					CD32	GP				NULL	on human neutrophils	NULL	NULL	NULL	NULL	gw70_circulationres_97_7_609_s_59	16195483	3 These authors have previously shown that native CRP binds to CD32, one of the Fc receptors, whereas mCRP binds to CD16, another Fc receptor isoform, on human neutrophils and exerting opposite function.	bind
30800	2	7674	5	13	NULL	NULL	NULL	CD32	GP		is a type of					Fc receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_7_609_s_59	16195483	3 These authors have previously shown that native CRP binds to CD32, one of the Fc receptors, whereas mCRP binds to CD16, another Fc receptor isoform, on human neutrophils and exerting opposite function.	bind
30801	3	7674	5	13	NULL	NULL	NULL	mCRP	GP		bind					CD16	GP				NULL	on human neutrophils	NULL	NULL	NULL	NULL	gw70_circulationres_97_7_609_s_59	16195483	3 These authors have previously shown that native CRP binds to CD32, one of the Fc receptors, whereas mCRP binds to CD16, another Fc receptor isoform, on human neutrophils and exerting opposite function.	bind
30802	4	7674	5	13	NULL	NULL	NULL	CD16	GP		is a type of					Fc receptor isoform	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_7_609_s_59	16195483	3 These authors have previously shown that native CRP binds to CD32, one of the Fc receptors, whereas mCRP binds to CD16, another Fc receptor isoform, on human neutrophils and exerting opposite function.	bind
30803	5	7674	5	13	NULL	NULL	NULL	statement 1 	Process		exert opposite funtion to					statement 3	Process				NULL	human neutrophils	NULL	NULL	NULL	NULL	gw70_circulationres_97_7_609_s_59	16195483	3 These authors have previously shown that native CRP binds to CD32, one of the Fc receptors, whereas mCRP binds to CD16, another Fc receptor isoform, on human neutrophils and exerting opposite function.	bind
23806	1	7674	6	10	NULL	0	NULL	CRP	NULL	native	bind	NULL				CD32	NULL				NULL	human neutrophils	NULL	NULL	NULL	NULL	gw70_circulationres_97_7_609_s_59	16195483	3 These authors have previously shown that native CRP binds to CD32, one of the Fc receptors, whereas mCRP binds to CD16, another Fc receptor isoform, on human neutrophils and exerting opposite function.	bind
23807	2	7674	6	10	NULL	0	NULL	mCRP	NULL		bind	NULL				CD16	NULL				NULL	human neutrophils	NULL	NULL	NULL	NULL	gw70_circulationres_97_7_609_s_59	16195483	3 These authors have previously shown that native CRP binds to CD32, one of the Fc receptors, whereas mCRP binds to CD16, another Fc receptor isoform, on human neutrophils and exerting opposite function.	bind
46647	3	7674	6	10	NULL	0	NULL	CD32	NULL		is a type of	NULL				Fc receptors	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_7_609_s_59	16195483	3 These authors have previously shown that native CRP binds to CD32, one of the Fc receptors, whereas mCRP binds to CD16, another Fc receptor isoform, on human neutrophils and exerting opposite function.	bind
46648	4	7674	6	10	NULL	0	NULL	CD16	NULL		is a type of	NULL				Fc receptor isoform	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_7_609_s_59	16195483	3 These authors have previously shown that native CRP binds to CD32, one of the Fc receptors, whereas mCRP binds to CD16, another Fc receptor isoform, on human neutrophils and exerting opposite function.	bind
46649	5	7674	6	10	NULL	0	NULL	statement 1			exert opposite funtion to					statement 2					NULL	human neutrophils	NULL	NULL	NULL	NULL	gw70_circulationres_97_7_609_s_59	16195483	3 These authors have previously shown that native CRP binds to CD32, one of the Fc receptors, whereas mCRP binds to CD16, another Fc receptor isoform, on human neutrophils and exerting opposite function.	bind
30804	1	7675	5	13	NULL	NULL	NULL	alpha1	GP		bind			 A-domain		collagen IV	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12311_s_200	9139675	3 These techniques produced  K D values in the range of 1-5 nM, which is in good agreement with the figures obtained for alpha1 A-domain binding to collagen IV (6-34 nM;	bind
23808	1	7675	6	NULL	NULL	0	NULL	alpha1	NULL		bind	NULL		A domain		collagen IV	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_19_12311_s_200	9139675	3 These techniques produced  K D values in the range of 1-5 nM, which is in good agreement with the figures obtained for alpha1 A-domain binding to collagen IV (6-34 nM;	bind
30805	1	7676	5	13	NULL	NULL	NULL	NK-3	GP		bind					DNA	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_25875_s_115	9748262	3 This effect may simply result from the enhancement of NK-3 DNA binding activity by HIPK2 that was seen in the  in vitro binding assays (Fig.  3).	bind
30806	2	7676	5	13	NULL	NULL	NULL	HIPK2	GP		enhances					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_25875_s_115	9748262	3 This effect may simply result from the enhancement of NK-3 DNA binding activity by HIPK2 that was seen in the  in vitro binding assays (Fig.  3).	bind
23809	1	7676	6	NULL	NULL	0	NULL	NK-3	NULL		bind	NULL				DNA	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_25875_s_115	9748262	3 This effect may simply result from the enhancement of NK-3 DNA binding activity by HIPK2 that was seen in the  in vitro binding assays (Fig.  3).	bind
23810	2	7676	6	10	NULL	0	NULL	HIPK2	NULL		enhances	NULL				statement 1	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_25875_s_115	9748262	3 This effect may simply result from the enhancement of NK-3 DNA binding activity by HIPK2 that was seen in the  in vitro binding assays (Fig.  3).	bind
30807	1	7677	5	13	NULL	NULL	NULL	PTB	GP		bind								UCUU motif within uridine-rich element region		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_21_22166_s_352	15010470	3 This feature does not allow testing by a mutational approach to know whether this downstream site is implicated in the repression of exon 9A9'', but it suggests a new model of regulation in which binding of PTB to the UCUU motif present within the uridine-rich element region could preclude CstF-64 binding.	bind
30808	2	7677	5	13	NULL	NULL	NULL	statement 1	Process		preclude					CstF-64	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_21_22166_s_352	15010470	3 This feature does not allow testing by a mutational approach to know whether this downstream site is implicated in the repression of exon 9A9'', but it suggests a new model of regulation in which binding of PTB to the UCUU motif present within the uridine-rich element region could preclude CstF-64 binding.	bind
23811	1	7677	6	10	NULL	0	NULL	PTB	NULL		bind	NULL					NULL		UCUU motif within uridine-rich element region		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_21_22166_s_352	15010470	3 This feature does not allow testing by a mutational approach to know whether this downstream site is implicated in the repression of exon 9A9'', but it suggests a new model of regulation in which binding of PTB to the UCUU motif present within the uridine-rich element region could preclude CstF-64 binding.	bind
46650	2	7677	6	10	NULL	0	NULL	statement 1	NULL		preclude	NULL				CstF-64	NULL	binding of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_21_22166_s_352	15010470	3 This feature does not allow testing by a mutational approach to know whether this downstream site is implicated in the repression of exon 9A9'', but it suggests a new model of regulation in which binding of PTB to the UCUU motif present within the uridine-rich element region could preclude CstF-64 binding.	bind
30809	1	7678	5	13	NULL	NULL	NULL	LRP	GP		is					LDL receptor-related protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1669_s_25	15178567	3 This implicates an endocytic step in selective uptake and prompted us to examine the role of the LDL receptor-related protein (LRP) 4 in selective uptake, particularly because the LRP binds to apolipoprotein E (apoE), lipoprotein lipase, and hepatic lipase, and these molecules have been shown to facilitate selective uptake.	bind
30810	2	7678	5	13	NULL	NULL	NULL	LRP	GP		bind					apoE	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1669_s_25	15178567	3 This implicates an endocytic step in selective uptake and prompted us to examine the role of the LDL receptor-related protein (LRP) 4 in selective uptake, particularly because the LRP binds to apolipoprotein E (apoE), lipoprotein lipase, and hepatic lipase, and these molecules have been shown to facilitate selective uptake.	bind
30811	3	7678	5	13	NULL	NULL	NULL	apoE	GP		is					apolipoprotein E	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1669_s_25	15178567	3 This implicates an endocytic step in selective uptake and prompted us to examine the role of the LDL receptor-related protein (LRP) 4 in selective uptake, particularly because the LRP binds to apolipoprotein E (apoE), lipoprotein lipase, and hepatic lipase, and these molecules have been shown to facilitate selective uptake.	bind
30812	4	7678	5	13	NULL	NULL	NULL	LRP	GP		bind					lipoprotein lipase	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1669_s_25	15178567	3 This implicates an endocytic step in selective uptake and prompted us to examine the role of the LDL receptor-related protein (LRP) 4 in selective uptake, particularly because the LRP binds to apolipoprotein E (apoE), lipoprotein lipase, and hepatic lipase, and these molecules have been shown to facilitate selective uptake.	bind
30813	5	7678	5	13	NULL	NULL	NULL	LRP	GP		bind					hepatic lipase	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1669_s_25	15178567	3 This implicates an endocytic step in selective uptake and prompted us to examine the role of the LDL receptor-related protein (LRP) 4 in selective uptake, particularly because the LRP binds to apolipoprotein E (apoE), lipoprotein lipase, and hepatic lipase, and these molecules have been shown to facilitate selective uptake.	bind
30814	6	7678	5	13	NULL	NULL	NULL	apoE	GP		facilitate					selective uptake	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1669_s_25	15178567	3 This implicates an endocytic step in selective uptake and prompted us to examine the role of the LDL receptor-related protein (LRP) 4 in selective uptake, particularly because the LRP binds to apolipoprotein E (apoE), lipoprotein lipase, and hepatic lipase, and these molecules have been shown to facilitate selective uptake.	bind
30815	7	7678	5	13	NULL	NULL	NULL	lipoprotein lipase	GP		facilitate					selective uptake	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1669_s_25	15178567	3 This implicates an endocytic step in selective uptake and prompted us to examine the role of the LDL receptor-related protein (LRP) 4 in selective uptake, particularly because the LRP binds to apolipoprotein E (apoE), lipoprotein lipase, and hepatic lipase, and these molecules have been shown to facilitate selective uptake.	bind
30816	8	7678	5	13	NULL	NULL	NULL	hepatic lipase	GP		facilitate					selective uptake	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1669_s_25	15178567	3 This implicates an endocytic step in selective uptake and prompted us to examine the role of the LDL receptor-related protein (LRP) 4 in selective uptake, particularly because the LRP binds to apolipoprotein E (apoE), lipoprotein lipase, and hepatic lipase, and these molecules have been shown to facilitate selective uptake.	bind
30817	9	7678	5	13	NULL	NULL	NULL	LRP	GP		plays a role in					selective uptake	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1669_s_25	15178567	3 This implicates an endocytic step in selective uptake and prompted us to examine the role of the LDL receptor-related protein (LRP) 4 in selective uptake, particularly because the LRP binds to apolipoprotein E (apoE), lipoprotein lipase, and hepatic lipase, and these molecules have been shown to facilitate selective uptake.	bind
23812	1	7678	6	NULL	NULL	0	NULL	LRP	NULL		is	NULL				LDL receptor-related protein	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1669_s_25	15178567	3 This implicates an endocytic step in selective uptake and prompted us to examine the role of the LDL receptor-related protein (LRP) 4 in selective uptake, particularly because the LRP binds to apolipoprotein E (apoE), lipoprotein lipase, and hepatic lipase, and these molecules have been shown to facilitate selective uptake.	bind
23813	2	7678	6	NULL	NULL	0	NULL	LRP	NULL		bind	NULL				apoE	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1669_s_25	15178567	3 This implicates an endocytic step in selective uptake and prompted us to examine the role of the LDL receptor-related protein (LRP) 4 in selective uptake, particularly because the LRP binds to apolipoprotein E (apoE), lipoprotein lipase, and hepatic lipase, and these molecules have been shown to facilitate selective uptake.	bind
23814	3	7678	6	NULL	NULL	0	NULL	apoE	NULL		is	NULL				apolipoprotein E	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1669_s_25	15178567	3 This implicates an endocytic step in selective uptake and prompted us to examine the role of the LDL receptor-related protein (LRP) 4 in selective uptake, particularly because the LRP binds to apolipoprotein E (apoE), lipoprotein lipase, and hepatic lipase, and these molecules have been shown to facilitate selective uptake.	bind
23815	4	7678	6	NULL	NULL	0	NULL	LRP	NULL		bind	NULL				lipoprotein lipase	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1669_s_25	15178567	3 This implicates an endocytic step in selective uptake and prompted us to examine the role of the LDL receptor-related protein (LRP) 4 in selective uptake, particularly because the LRP binds to apolipoprotein E (apoE), lipoprotein lipase, and hepatic lipase, and these molecules have been shown to facilitate selective uptake.	bind
23816	5	7678	6	NULL	NULL	0	NULL	LRP	NULL		bind	NULL				hepatic lipase	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1669_s_25	15178567	3 This implicates an endocytic step in selective uptake and prompted us to examine the role of the LDL receptor-related protein (LRP) 4 in selective uptake, particularly because the LRP binds to apolipoprotein E (apoE), lipoprotein lipase, and hepatic lipase, and these molecules have been shown to facilitate selective uptake.	bind
23817	6	7678	6	NULL	NULL	0	NULL	apoE	NULL		facilitate	NULL				selective uptake	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1669_s_25	15178567	3 This implicates an endocytic step in selective uptake and prompted us to examine the role of the LDL receptor-related protein (LRP) 4 in selective uptake, particularly because the LRP binds to apolipoprotein E (apoE), lipoprotein lipase, and hepatic lipase, and these molecules have been shown to facilitate selective uptake.	bind
23818	7	7678	6	NULL	NULL	0	NULL	lipoprotein lipase	NULL		facilitate	NULL				selective uptake	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1669_s_25	15178567	3 This implicates an endocytic step in selective uptake and prompted us to examine the role of the LDL receptor-related protein (LRP) 4 in selective uptake, particularly because the LRP binds to apolipoprotein E (apoE), lipoprotein lipase, and hepatic lipase, and these molecules have been shown to facilitate selective uptake.	bind
23819	8	7678	6	NULL	NULL	0	NULL	hepatic lipase	NULL		facilitate	NULL				selective uptake	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1669_s_25	15178567	3 This implicates an endocytic step in selective uptake and prompted us to examine the role of the LDL receptor-related protein (LRP) 4 in selective uptake, particularly because the LRP binds to apolipoprotein E (apoE), lipoprotein lipase, and hepatic lipase, and these molecules have been shown to facilitate selective uptake.	bind
46651	9	7678	6	10	NULL	0	NULL	LRP	NULL		plays a role in	NULL				selective uptake	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1669_s_25	15178567	3 This implicates an endocytic step in selective uptake and prompted us to examine the role of the LDL receptor-related protein (LRP) 4 in selective uptake, particularly because the LRP binds to apolipoprotein E (apoE), lipoprotein lipase, and hepatic lipase, and these molecules have been shown to facilitate selective uptake.	bind
30818	1	7679	5	13	NULL	NULL	NULL	fibrinogen	GP	bivalent	bind					(GP) IIb/IIa complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_17_2725_s_19	16246969	3 Thrombus forms as platelets aggregate via the binding of bivalent fibrinogen to the glycoprotein (GP) IIb/IIa complex.	bind
30819	2	7679	5	13	NULL	NULL	NULL	(GP) IIb/IIa complex	GP		is					glycoprotein IIb/IIa complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_17_2725_s_19	16246969	3 Thrombus forms as platelets aggregate via the binding of bivalent fibrinogen to the glycoprotein (GP) IIb/IIa complex.	bind
30820	3	7679	5	13	NULL	NULL	NULL	thrombus			forms					platelets aggregate	Cell				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_17_2725_s_19	16246969	3 Thrombus forms as platelets aggregate via the binding of bivalent fibrinogen to the glycoprotein (GP) IIb/IIa complex.	bind
30821	4	7679	5	13	NULL	NULL	NULL	statement 3	Process		via					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_17_2725_s_19	16246969	3 Thrombus forms as platelets aggregate via the binding of bivalent fibrinogen to the glycoprotein (GP) IIb/IIa complex.	bind
23820	1	7679	6	NULL	NULL	0	NULL	fibrinogen	NULL	bivalent	bind	NULL				GP IIb/IIa complex	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_112_17_2725_s_19	16246969	3 Thrombus forms as platelets aggregate via the binding of bivalent fibrinogen to the glycoprotein (GP) IIb/IIa complex.	bind
23821	2	7679	6	NULL	NULL	0	NULL	GP	NULL		is	NULL				glycoprotein	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_112_17_2725_s_19	16246969	3 Thrombus forms as platelets aggregate via the binding of bivalent fibrinogen to the glycoprotein (GP) IIb/IIa complex.	bind
23822	3	7679	6	NULL	NULL	0	NULL	thrombus	NULL		forms as	NULL				platelets aggregate	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_112_17_2725_s_19	16246969	3 Thrombus forms as platelets aggregate via the binding of bivalent fibrinogen to the glycoprotein (GP) IIb/IIa complex.	bind
23823	4	7679	6	NULL	NULL	0	NULL	statement 3	NULL		occurs via	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_112_17_2725_s_19	16246969	3 Thrombus forms as platelets aggregate via the binding of bivalent fibrinogen to the glycoprotein (GP) IIb/IIa complex.	bind
30822	1	7680	5	13	NULL	NULL	NULL	IP6	GP		functions as		possibly			classic signaling molecule	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_47_36575_s_319	10960485	3 Thus, it remains possible that IP6 functions as a classic signaling molecule that directly binds an effector protein in the mRNA export machinery.	bind
30823	2	7680	5	13	NULL	NULL	NULL	IP6	GP		bind		directly			effector protein	GP				NULL	mRNA export machinery	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_47_36575_s_319	10960485	3 Thus, it remains possible that IP6 functions as a classic signaling molecule that directly binds an effector protein in the mRNA export machinery.	bind
23824	1	7680	6	NULL	NULL	0	NULL	IP6	NULL		bind	NULL	directly			effector protein	NULL				NULL	mRNA export machinery	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_47_36575_s_319	10960485	3 Thus, it remains possible that IP6 functions as a classic signaling molecule that directly binds an effector protein in the mRNA export machinery.	bind
46652	1	7680	6	10	NULL	0	NULL	IP6			functions as		possibly			 classic signaling molecule					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_47_36575_s_319	10960485	3 Thus, it remains possible that IP6 functions as a classic signaling molecule that directly binds an effector protein in the mRNA export machinery.	bind
30890	1	7681	5	13	NULL	NULL	NULL	cTnC	GP		bind					cTnI	GP		1-80		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_24_16681_s_41	10358006	3 To confirm the assignments for cTnC bound to cTnI-(1-80) and cTnI-(1-80)DD, 1H-15N NOESY-HSQC experiments with mixing times of 85 and 200 ms were performed at 800 MHz.	bind
30891	2	7681	5	13	NULL	NULL	NULL	cTnC	GP		bind					cTnI	GP		(1-80)DD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_24_16681_s_41	10358006	3 To confirm the assignments for cTnC bound to cTnI-(1-80) and cTnI-(1-80)DD, 1H-15N NOESY-HSQC experiments with mixing times of 85 and 200 ms were performed at 800 MHz.	bind
23825	1	7681	6	NULL	NULL	0	NULL	cTnC	NULL		bind	NULL				cTnI	NULL		1-80		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_24_16681_s_41	10358006	3 To confirm the assignments for cTnC bound to cTnI-(1-80) and cTnI-(1-80)DD, 1H-15N NOESY-HSQC experiments with mixing times of 85 and 200 ms were performed at 800 MHz.	bind
23826	2	7681	6	NULL	NULL	0	NULL	cTnC	NULL		bind	NULL				cTnI	NULL		1-80 DD		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_24_16681_s_41	10358006	3 To confirm the assignments for cTnC bound to cTnI-(1-80) and cTnI-(1-80)DD, 1H-15N NOESY-HSQC experiments with mixing times of 85 and 200 ms were performed at 800 MHz.	bind
30892	1	7683	5	13	NULL	NULL	NULL	Ras	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39001_s_161	10967125	3 To rule out the possibility that the inhibition of apoptosis by hypoxic culture conditions, sodium butyrate treatment, or trichostatin A treatment were due to effects on Ras activity, Ras activity was analyzed by affinity binding to a Raf Ras-binding domain (RBD) peptide that only binds the activated (GTP-bound) form of Ras.	bind
30893	2	7683	5	13	NULL	NULL	NULL	Raf peptide	GP		bind			RBD		statement 1	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39001_s_161	10967125	3 To rule out the possibility that the inhibition of apoptosis by hypoxic culture conditions, sodium butyrate treatment, or trichostatin A treatment were due to effects on Ras activity, Ras activity was analyzed by affinity binding to a Raf Ras-binding domain (RBD) peptide that only binds the activated (GTP-bound) form of Ras.	bind
30894	3	7683	5	13	NULL	NULL	NULL	RBD	GP		is					Ras-binding domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39001_s_161	10967125	3 To rule out the possibility that the inhibition of apoptosis by hypoxic culture conditions, sodium butyrate treatment, or trichostatin A treatment were due to effects on Ras activity, Ras activity was analyzed by affinity binding to a Raf Ras-binding domain (RBD) peptide that only binds the activated (GTP-bound) form of Ras.	bind
23827	1	7683	6	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				Ras	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39001_s_161	10967125	3 To rule out the possibility that the inhibition of apoptosis by hypoxic culture conditions, sodium butyrate treatment, or trichostatin A treatment were due to effects on Ras activity, Ras activity was analyzed by affinity binding to a Raf Ras-binding domain (RBD) peptide that only binds the activated (GTP-bound) form of Ras.	bind
23828	2	7683	6	NULL	NULL	0	NULL	Raf	NULL		bind	NULL	only	RBD		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39001_s_161	10967125	3 To rule out the possibility that the inhibition of apoptosis by hypoxic culture conditions, sodium butyrate treatment, or trichostatin A treatment were due to effects on Ras activity, Ras activity was analyzed by affinity binding to a Raf Ras-binding domain (RBD) peptide that only binds the activated (GTP-bound) form of Ras.	bind
23829	3	7683	6	NULL	NULL	0	NULL	RBD	NULL		is	NULL				Ras-binding domain	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39001_s_161	10967125	3 To rule out the possibility that the inhibition of apoptosis by hypoxic culture conditions, sodium butyrate treatment, or trichostatin A treatment were due to effects on Ras activity, Ras activity was analyzed by affinity binding to a Raf Ras-binding domain (RBD) peptide that only binds the activated (GTP-bound) form of Ras.	bind
30895	1	7684	5	13	NULL	NULL	NULL	VEGF	GP		bind					KDR/Flk-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_8_796_s_19	16151023	3 VEGF binds to its receptors KDR/Flk-1 to mediate its effect on angiogenesis in physiological conditions and in human atherosclerosis.	bind
30896	2	7684	5	13	NULL	NULL	NULL	statement 1	Process		mediates					angiogenesis	Process	effect on			NULL	in physiological conditions	NULL	NULL	NULL	NULL	gw70_circulationres_97_8_796_s_19	16151023	3 VEGF binds to its receptors KDR/Flk-1 to mediate its effect on angiogenesis in physiological conditions and in human atherosclerosis.	bind
30897	3	7684	5	13	NULL	NULL	NULL	statement 1	Process		mediates					angiogenesis	Process	effect on			NULL	in human atherosclerosis	NULL	NULL	NULL	NULL	gw70_circulationres_97_8_796_s_19	16151023	3 VEGF binds to its receptors KDR/Flk-1 to mediate its effect on angiogenesis in physiological conditions and in human atherosclerosis.	bind
23830	1	7684	6	NULL	NULL	0	NULL	VEGF	NULL		bind	NULL				KDR/Flk-1 receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_8_796_s_19	16151023	3 VEGF binds to its receptors KDR/Flk-1 to mediate its effect on angiogenesis in physiological conditions and in human atherosclerosis.	bind
23831	2	7684	6	10	NULL	0	NULL	statement 1			mediates					angiogenesis		effect on			NULL	physiological conditions	NULL	NULL	NULL	NULL	gw70_circulationres_97_8_796_s_19	16151023	3 VEGF binds to its receptors KDR/Flk-1 to mediate its effect on angiogenesis in physiological conditions and in human atherosclerosis.	bind
23832	3	7684	6	10	NULL	0	NULL	statement 1			mediates					angiogenesis		effects on			NULL	human atherosclerosis	NULL	NULL	NULL	NULL	gw70_circulationres_97_8_796_s_19	16151023	3 VEGF binds to its receptors KDR/Flk-1 to mediate its effect on angiogenesis in physiological conditions and in human atherosclerosis.	bind
30898	1	7685	5	13	NULL	NULL	NULL	annexin V-FITC	GP		bind					platelets	Cell	PS-exposing			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_2_417_s_82	16339499	3 We determined platelet deposition and binding of annexin V-fluorescein isothiocyanate (FITC) to PS-exposing platelets after perfusion over a collagen-coated surface at a shear rate of 1000 s - 1.	bind
30899	2	7685	5	13	NULL	NULL	NULL	FITC	Chemical		is					fluorescein isothiocyanate	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_2_417_s_82	16339499	3 We determined platelet deposition and binding of annexin V-fluorescein isothiocyanate (FITC) to PS-exposing platelets after perfusion over a collagen-coated surface at a shear rate of 1000 s - 1.	bind
23834	1	7685	6	NULL	NULL	0	NULL	annexin V-fluorescein isothiocyanate	NULL		bind	NULL				platelets	NULL	PS-exposing			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_2_417_s_82	16339499	3 We determined platelet deposition and binding of annexin V-fluorescein isothiocyanate (FITC) to PS-exposing platelets after perfusion over a collagen-coated surface at a shear rate of 1000 s - 1.	bind
23835	2	7685	6	NULL	NULL	0	NULL	FITC	NULL		is	NULL				fluorescein isothiocyanate	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_2_417_s_82	16339499	3 We determined platelet deposition and binding of annexin V-fluorescein isothiocyanate (FITC) to PS-exposing platelets after perfusion over a collagen-coated surface at a shear rate of 1000 s - 1.	bind
30900	1	7686	5	13	NULL	NULL	NULL	LT	GP		is distinct from			GM1 binding site		LT	GP		LPS binding site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8070_s_182	14660669	3 We previously demonstrated that the GM1 and LPS binding sites on LT are distinct ( ), and we wondered if a LPS binding site could be elucidated from the solved crystal structures of LT and CT ( ,   -  ).	bind
46730	1	7686	6	NULL	NULL	0	NULL	LT	NULL		is distinct from	NULL		GM1 binding site		LT	NULL		LPS binding site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8070_s_182	14660669	3 We previously demonstrated that the GM1 and LPS binding sites on LT are distinct ( ), and we wondered if a LPS binding site could be elucidated from the solved crystal structures of LT and CT ( ,   -  ).	bind
30902	1	7687	5	13	NULL	NULL	NULL	COUP-TFII	GP		occupies					gAF1/PCK1	GP				NULL	in preadipocytes	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_32_30561_s_300	11399762	3 We propose that COUP-TFII occupies gAF1/PCK1 in preadipocytes and blocks activation of the PEPCK promoter via PPARgamma/RXR bound to PCK2.	bind
30903	2	7687	5	13	NULL	NULL	NULL	statement 1	Process		blocks					PEPCK	GP	activation of		promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_32_30561_s_300	11399762	3 We propose that COUP-TFII occupies gAF1/PCK1 in preadipocytes and blocks activation of the PEPCK promoter via PPARgamma/RXR bound to PCK2.	bind
30904	3	7687	5	13	NULL	NULL	NULL	PPARgamma/RXR	GP		bind					PCK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_32_30561_s_300	11399762	3 We propose that COUP-TFII occupies gAF1/PCK1 in preadipocytes and blocks activation of the PEPCK promoter via PPARgamma/RXR bound to PCK2.	bind
30905	4	7687	5	13	NULL	NULL	NULL	statement 2	Process		via					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_32_30561_s_300	11399762	3 We propose that COUP-TFII occupies gAF1/PCK1 in preadipocytes and blocks activation of the PEPCK promoter via PPARgamma/RXR bound to PCK2.	bind
23911	1	7687	6	NULL	NULL	0	NULL	PPARgamma/RXR	NULL		bind	NULL				PCK2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_32_30561_s_300	11399762	3 We propose that COUP-TFII occupies gAF1/PCK1 in preadipocytes and blocks activation of the PEPCK promoter via PPARgamma/RXR bound to PCK2.	bind
23912	2	7687	6	NULL	NULL	0	NULL	COUP-TFII	NULL		occupies	NULL				gAF1/PCK1	NULL				NULL	preadipocytes	0	NULL	NULL	NULL	gw60_jbiolchem_276_32_30561_s_300	11399762	3 We propose that COUP-TFII occupies gAF1/PCK1 in preadipocytes and blocks activation of the PEPCK promoter via PPARgamma/RXR bound to PCK2.	bind
23913	3	7687	6	NULL	NULL	0	NULL	COUP-TFII	NULL		blocks	NULL				PEPCK	NULL	activation of		promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_32_30561_s_300	11399762	3 We propose that COUP-TFII occupies gAF1/PCK1 in preadipocytes and blocks activation of the PEPCK promoter via PPARgamma/RXR bound to PCK2.	bind
23914	4	7687	6	NULL	NULL	0	NULL	statement 3	NULL		occurs via	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_32_30561_s_300	11399762	3 We propose that COUP-TFII occupies gAF1/PCK1 in preadipocytes and blocks activation of the PEPCK promoter via PPARgamma/RXR bound to PCK2.	bind
30907	1	7688	5	13	NULL	NULL	NULL	His6-Rvs167	GP	recombinant	bind					GST-Sla1	GP		1 - 420		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_16_16017_s_204	14761940	3 We were unable to test direct binding of Rvs167 to Sla1 720 - 1240 because GST-Sla1 720 - 1240 was not stably expressed in  E. coli; however, recombinant His6-Rvs167 bound to GST-Sla1 1 - 420 and weakly to GST-Sla1 420 - 720 ( Fig. 5 B), indicating that Rvs167 binds to Sla1 directly, perhaps via multiple sites.	bind
30908	2	7688	5	13	NULL	NULL	NULL	His6-Rvs167	GP	recombinant	bind		weakly			GST-Sla1	GP		420 - 720		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_16_16017_s_204	14761940	3 We were unable to test direct binding of Rvs167 to Sla1 720 - 1240 because GST-Sla1 720 - 1240 was not stably expressed in  E. coli; however, recombinant His6-Rvs167 bound to GST-Sla1 1 - 420 and weakly to GST-Sla1 420 - 720 ( Fig. 5 B), indicating that Rvs167 binds to Sla1 directly, perhaps via multiple sites.	bind
30909	3	7688	5	13	NULL	NULL	NULL	Rvs167	GP		bind		directly			Sla1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_16_16017_s_204	14761940	3 We were unable to test direct binding of Rvs167 to Sla1 720 - 1240 because GST-Sla1 720 - 1240 was not stably expressed in  E. coli; however, recombinant His6-Rvs167 bound to GST-Sla1 1 - 420 and weakly to GST-Sla1 420 - 720 ( Fig. 5 B), indicating that Rvs167 binds to Sla1 directly, perhaps via multiple sites.	bind
30910	4	7688	5	13	NULL	NULL	NULL	statement 3	Process		via					multiple sites	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_16_16017_s_204	14761940	3 We were unable to test direct binding of Rvs167 to Sla1 720 - 1240 because GST-Sla1 720 - 1240 was not stably expressed in  E. coli; however, recombinant His6-Rvs167 bound to GST-Sla1 1 - 420 and weakly to GST-Sla1 420 - 720 ( Fig. 5 B), indicating that Rvs167 binds to Sla1 directly, perhaps via multiple sites.	bind
23915	1	7688	6	NULL	NULL	0	NULL	His6-Rvs167	NULL	recombinant	bind	NULL				GST-Sla1	NULL		1-420		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_16017_s_204	14761940	3 We were unable to test direct binding of Rvs167 to Sla1 720 - 1240 because GST-Sla1 720 - 1240 was not stably expressed in  E. coli; however, recombinant His6-Rvs167 bound to GST-Sla1 1 - 420 and weakly to GST-Sla1 420 - 720 ( Fig. 5 B), indicating that Rvs167 binds to Sla1 directly, perhaps via multiple sites.	bind
23916	2	7688	6	NULL	NULL	0	NULL	His6-Rvs167	NULL	recombinant	bind	NULL	weakly			GST-Sla1	NULL		420-720		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_16017_s_204	14761940	3 We were unable to test direct binding of Rvs167 to Sla1 720 - 1240 because GST-Sla1 720 - 1240 was not stably expressed in  E. coli; however, recombinant His6-Rvs167 bound to GST-Sla1 1 - 420 and weakly to GST-Sla1 420 - 720 ( Fig. 5 B), indicating that Rvs167 binds to Sla1 directly, perhaps via multiple sites.	bind
46731	3	7688	6	10	NULL	0	NULL	Rvs167 	NULL		bind	NULL	directly			Sla1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_16017_s_204	14761940	3 We were unable to test direct binding of Rvs167 to Sla1 720 - 1240 because GST-Sla1 720 - 1240 was not stably expressed in  E. coli; however, recombinant His6-Rvs167 bound to GST-Sla1 1 - 420 and weakly to GST-Sla1 420 - 720 ( Fig. 5 B), indicating that Rvs167 binds to Sla1 directly, perhaps via multiple sites.	bind
46732	4	7688	6	10	NULL	0	NULL	statement 3	NULL		via	NULL				multiple sites	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_16017_s_204	14761940	3 We were unable to test direct binding of Rvs167 to Sla1 720 - 1240 because GST-Sla1 720 - 1240 was not stably expressed in  E. coli; however, recombinant His6-Rvs167 bound to GST-Sla1 1 - 420 and weakly to GST-Sla1 420 - 720 ( Fig. 5 B), indicating that Rvs167 binds to Sla1 directly, perhaps via multiple sites.	bind
30911	1	7689	5	13	NULL	NULL	NULL	IdceA unit	GP	2- O-sulfated	is a part of					3- O -sulfotransferase	GP		substrate recognition site 		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_30_18770_s_250	9668050	3 While this conclusion is probably correct, it is recalled that a 2- O-sulfated IdceA unit was identified as part of the substrate recognition site for the 3- O -sulfotransferaseinvolved in the biosynthesis of the antithrombin-binding region ( 52); a polysaccharide devoid of HexA 2- O-sulfate groups thus will probably lack GlcN 3- O-sulfate substituents.	bind
30912	2	7689	5	13	NULL	NULL	NULL	3- O -sulfotransferase	GP		is involved in							biosynthesis of	antithrombin-binding region		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_30_18770_s_250	9668050	3 While this conclusion is probably correct, it is recalled that a 2- O-sulfated IdceA unit was identified as part of the substrate recognition site for the 3- O -sulfotransferaseinvolved in the biosynthesis of the antithrombin-binding region ( 52); a polysaccharide devoid of HexA 2- O-sulfate groups thus will probably lack GlcN 3- O-sulfate substituents.	bind
30913	3	7689	5	13	NULL	NULL	NULL	polysaccharide	Chemical		devoid of					HexA 2- O-sulfate groups	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_30_18770_s_250	9668050	3 While this conclusion is probably correct, it is recalled that a 2- O-sulfated IdceA unit was identified as part of the substrate recognition site for the 3- O -sulfotransferaseinvolved in the biosynthesis of the antithrombin-binding region ( 52); a polysaccharide devoid of HexA 2- O-sulfate groups thus will probably lack GlcN 3- O-sulfate substituents.	bind
46733	4	7689	5	13	NULL	NULL	NULL	statement 3	Chemical		lack		probably			GlcN 3- O-sulfate substituents	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_30_18770_s_250	9668050	3 While this conclusion is probably correct, it is recalled that a 2- O-sulfated IdceA unit was identified as part of the substrate recognition site for the 3- O -sulfotransferaseinvolved in the biosynthesis of the antithrombin-binding region ( 52); a polysaccharide devoid of HexA 2- O-sulfate groups thus will probably lack GlcN 3- O-sulfate substituents.	bind
24473	1	7689	6	10	NULL	0	NULL	IdceA unit		2- O-sulfated	is part of the 					3- O -sulfotransferase			substrate recognition site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_30_18770_s_250	9668050	3 While this conclusion is probably correct, it is recalled that a 2- O-sulfated IdceA unit was identified as part of the substrate recognition site for the 3- O -sulfotransferaseinvolved in the biosynthesis of the antithrombin-binding region ( 52); a polysaccharide devoid of HexA 2- O-sulfate groups thus will probably lack GlcN 3- O-sulfate substituents.	bind
24474	2	7689	6	10	NULL	0	NULL	3-O-sulfotransferase	NULL		is involved in	NULL					NULL	biosynthesis of	antithrombin-binding region		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_30_18770_s_250	9668050	3 While this conclusion is probably correct, it is recalled that a 2- O-sulfated IdceA unit was identified as part of the substrate recognition site for the 3- O -sulfotransferaseinvolved in the biosynthesis of the antithrombin-binding region ( 52); a polysaccharide devoid of HexA 2- O-sulfate groups thus will probably lack GlcN 3- O-sulfate substituents.	bind
24475	3	7689	6	10	NULL	0	NULL	polysaccharide	NULL		devoid of	NULL				HexA 2- O-sulfate group	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_30_18770_s_250	9668050	3 While this conclusion is probably correct, it is recalled that a 2- O-sulfated IdceA unit was identified as part of the substrate recognition site for the 3- O -sulfotransferaseinvolved in the biosynthesis of the antithrombin-binding region ( 52); a polysaccharide devoid of HexA 2- O-sulfate groups thus will probably lack GlcN 3- O-sulfate substituents.	bind
46734	4	7689	6	10	NULL	0	NULL	statement 3	NULL		lack	NULL	probably			GlcN 3- O-sulfate substituents	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_30_18770_s_250	9668050	3 While this conclusion is probably correct, it is recalled that a 2- O-sulfated IdceA unit was identified as part of the substrate recognition site for the 3- O -sulfotransferaseinvolved in the biosynthesis of the antithrombin-binding region ( 52); a polysaccharide devoid of HexA 2- O-sulfate groups thus will probably lack GlcN 3- O-sulfate substituents.	bind
30914	1	7690	5	13	NULL	NULL	NULL	3' processing	Process		is dependent on					snoRNP protein	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5415_s_236	10891482	3' processing appears to be dependent on snoRNP protein binding, but assembly with the mature snoRNP proteins may be incompatible with assembly of a functional spliceosome.	bind
30916	2	7690	5	13	NULL	NULL	NULL	snoRNP proteins	GP	assembly with;;mature	incompatible with		may be			functional spliceosome	CellComponent	assembly of a 			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5415_s_236	10891482	3' processing appears to be dependent on snoRNP protein binding, but assembly with the mature snoRNP proteins may be incompatible with assembly of a functional spliceosome.	bind
24546	1	7690	6	10	NULL	0	NULL	3' processing			is dependent on					snoRNP protein 		binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5415_s_236	10891482	3' processing appears to be dependent on snoRNP protein binding, but assembly with the mature snoRNP proteins may be incompatible with assembly of a functional spliceosome.	bind
24547	2	7690	6	10	NULL	0	NULL	snoRNP proteins		assembly with;;mature 	is incompatible with		may			functional spliceosome		assembly of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5415_s_236	10891482	3' processing appears to be dependent on snoRNP protein binding, but assembly with the mature snoRNP proteins may be incompatible with assembly of a functional spliceosome.	bind
30921	1	7691	5	13	NULL	NULL	NULL	TCDD	GP		bind					AhR	GP	rat liver			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_55_4_716_s_172	10101030	3''-OMe-4''-NO2-flavone is a competitive inhibitor of TCDD binding to rat liver AhR.	bind
30923	2	7691	5	13	NULL	NULL	NULL	3''-OMe-4''-NO2-flavone	Chemical		inhibits		competitively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_55_4_716_s_172	10101030	3''-OMe-4''-NO2-flavone is a competitive inhibitor of TCDD binding to rat liver AhR.	bind
23917	1	7691	6	NULL	NULL	0	NULL	TCDD	NULL		bind	NULL				AhR	NULL	rat liver			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_55_4_716_s_172	10101030	3''-OMe-4''-NO2-flavone is a competitive inhibitor of TCDD binding to rat liver AhR.	bind
23918	2	7691	6	NULL	NULL	0	NULL	3''-OMe-4''-NO2-flavone	NULL		inhibits	NULL	competitively			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_55_4_716_s_172	10101030	3''-OMe-4''-NO2-flavone is a competitive inhibitor of TCDD binding to rat liver AhR.	bind
30931	1	7692	5	13	NULL	NULL	NULL	CDK2	GP		bind		stably			PCNA	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_faseb-j_20_7_16675840_s_7	16675840	3)  At DNA replication sites, PCNA function may be envisaged with a model  of "`dynamic hand-off"` of interacting partners that rapidly and transiently  exchange in a mutually exclusive manner, while cyclin-dependent kinase  (Cdk) 2 (CDK2) is stably bound to PCNA.	bind
30932	2	7692	5	13	NULL	NULL	NULL	CDK2	GP		is					cyclin-dependent kinase 2	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_faseb-j_20_7_16675840_s_7	16675840	3)  At DNA replication sites, PCNA function may be envisaged with a model  of "`dynamic hand-off"` of interacting partners that rapidly and transiently  exchange in a mutually exclusive manner, while cyclin-dependent kinase  (Cdk) 2 (CDK2) is stably bound to PCNA.	bind
23919	1	7692	6	NULL	NULL	0	NULL	cdk2	NULL		bind	NULL	stably			PCNA	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_faseb-j_20_7_16675840_s_7	16675840	3)  At DNA replication sites, PCNA function may be envisaged with a model  of "`dynamic hand-off"` of interacting partners that rapidly and transiently  exchange in a mutually exclusive manner, while cyclin-dependent kinase  (Cdk) 2 (CDK2) is stably bound to PCNA.	bind
23920	2	7692	6	NULL	NULL	0	NULL	cdk2	NULL		is	NULL				cyclin-dependent kinase	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_faseb-j_20_7_16675840_s_7	16675840	3)  At DNA replication sites, PCNA function may be envisaged with a model  of "`dynamic hand-off"` of interacting partners that rapidly and transiently  exchange in a mutually exclusive manner, while cyclin-dependent kinase  (Cdk) 2 (CDK2) is stably bound to PCNA.	bind
30933	1	7693	5	13	NULL	NULL	NULL	180 kDa protein	GP		bind					PCNA	GP			E2F-like site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_2_1218_s_252	8557653	3)  Results from a UV cross-linking experiment indicate that a protein of  180 kDa binds to the PCNA E2F-like site.	bind
23921	1	7693	6	NULL	NULL	0	NULL	protein 180kDa	NULL		bind	NULL				PCNA	NULL			E2F-like site	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_2_1218_s_252	8557653	3)  Results from a UV cross-linking experiment indicate that a protein of  180 kDa binds to the PCNA E2F-like site.	bind
30936	1	7694	5	13	NULL	NULL	NULL	troponin	GP		bind					tropomyosin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_187	7592713	3)  There is a direct relationship between the strength of troponin binding  to tropomyosin (as the amino-terminal region of TnT is progressively  deleted or included), and the ability of troponin to enhance  tropomyosin-actin binding.	bind
30938	2	7694	5	13	NULL	NULL	NULL	tropomyosin	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_187	7592713	3)  There is a direct relationship between the strength of troponin binding  to tropomyosin (as the amino-terminal region of TnT is progressively  deleted or included), and the ability of troponin to enhance  tropomyosin-actin binding.	bind
30939	3	7694	5	13	NULL	NULL	NULL	troponin	GP		enhance					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_187	7592713	3)  There is a direct relationship between the strength of troponin binding  to tropomyosin (as the amino-terminal region of TnT is progressively  deleted or included), and the ability of troponin to enhance  tropomyosin-actin binding.	bind
30940	4	7694	5	13	NULL	NULL	NULL	statement 1	Process	strength of	is related to		directly			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_187	7592713	3)  There is a direct relationship between the strength of troponin binding  to tropomyosin (as the amino-terminal region of TnT is progressively  deleted or included), and the ability of troponin to enhance  tropomyosin-actin binding.	bind
23922	1	7694	6	NULL	NULL	0	NULL	troponin	NULL		bind	NULL				tropomyosin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_187	7592713	3)  There is a direct relationship between the strength of troponin binding  to tropomyosin (as the amino-terminal region of TnT is progressively  deleted or included), and the ability of troponin to enhance  tropomyosin-actin binding.	bind
23923	2	7694	6	NULL	NULL	0	NULL	tropomyosin	NULL		bind	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_187	7592713	3)  There is a direct relationship between the strength of troponin binding  to tropomyosin (as the amino-terminal region of TnT is progressively  deleted or included), and the ability of troponin to enhance  tropomyosin-actin binding.	bind
23924	3	7694	6	NULL	NULL	0	NULL	troponin	NULL		enhance	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_187	7592713	3)  There is a direct relationship between the strength of troponin binding  to tropomyosin (as the amino-terminal region of TnT is progressively  deleted or included), and the ability of troponin to enhance  tropomyosin-actin binding.	bind
46735	4	7694	6	10	NULL	0	NULL	statement 1	NULL	strength of	related to	NULL	directly			statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_43_25455_s_187	7592713	3)  There is a direct relationship between the strength of troponin binding  to tropomyosin (as the amino-terminal region of TnT is progressively  deleted or included), and the ability of troponin to enhance  tropomyosin-actin binding.	bind
30942	1	7695	5	13	NULL	NULL	NULL	STAT6	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_38095_s_260	10982806	3) A mutation in the DNA-binding domain of STAT6 selectively influenced STAT6 DNA binding preference leading to a blockade in IL-4-driven transcription.	bind
30944	2	7695	5	13	NULL	NULL	NULL	STAT6 	GP	mutant	influence		selectively	DNA-binding domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_38095_s_260	10982806	3) A mutation in the DNA-binding domain of STAT6 selectively influenced STAT6 DNA binding preference leading to a blockade in IL-4-driven transcription.	bind
30945	4	7695	5	13	NULL	NULL	NULL	statement 2	Process		blocks					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_38095_s_260	10982806	3) A mutation in the DNA-binding domain of STAT6 selectively influenced STAT6 DNA binding preference leading to a blockade in IL-4-driven transcription.	bind
46736	3	7695	5	13	NULL	NULL	NULL	IL-4	GP		drives					transcription	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_38095_s_260	10982806	3) A mutation in the DNA-binding domain of STAT6 selectively influenced STAT6 DNA binding preference leading to a blockade in IL-4-driven transcription.	bind
23925	1	7695	6	NULL	NULL	0	NULL	STAT6	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_48_38095_s_260	10982806	3) A mutation in the DNA-binding domain of STAT6 selectively influenced STAT6 DNA binding preference leading to a blockade in IL-4-driven transcription.	bind
23926	2	7695	6	NULL	NULL	0	NULL	STAT6	NULL	mutant	influence 	NULL	selectively	DNA binding domain 		statement 1	NULL	preference of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_48_38095_s_260	10982806	3) A mutation in the DNA-binding domain of STAT6 selectively influenced STAT6 DNA binding preference leading to a blockade in IL-4-driven transcription.	bind
23927	3	7695	6	10	NULL	0	NULL	IL-4	NULL		drives	NULL				transcription	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_38095_s_260	10982806	3) A mutation in the DNA-binding domain of STAT6 selectively influenced STAT6 DNA binding preference leading to a blockade in IL-4-driven transcription.	bind
46737	4	7695	6	10	NULL	0	NULL	statement 2	NULL		blocks	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_48_38095_s_260	10982806	3) A mutation in the DNA-binding domain of STAT6 selectively influenced STAT6 DNA binding preference leading to a blockade in IL-4-driven transcription.	bind
30948	1	7696	5	13	NULL	NULL	NULL	AGGTCA	GP		is a type of					single core motif	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_16_10565_s_184	9099702	3) A single core motif, AGGTCA, preceded by TCA (defined as 1/2-RTRE) is sufficient for RTR binding; however, the apparent affinity of RTR for 1/2-RTRE is significantly lower than that for conRTRE.	bind
30949	2	7696	5	NULL	NULL	0	NULL		NULL		is preceded by	NULL			AGGTCA		NULL			TCA	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_16_10565_s_184	9099702	3) A single core motif, AGGTCA, preceded by TCA (defined as 1/2-RTRE) is sufficient for RTR binding; however, the apparent affinity of RTR for 1/2-RTRE is significantly lower than that for conRTRE.	bind
30950	3	7696	5	13	NULL	NULL	NULL	AGGTCA	GP		is defined as					1/2-RTRE	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_16_10565_s_184	9099702	3) A single core motif, AGGTCA, preceded by TCA (defined as 1/2-RTRE) is sufficient for RTR binding; however, the apparent affinity of RTR for 1/2-RTRE is significantly lower than that for conRTRE.	bind
30951	4	7696	5	13	NULL	NULL	NULL				is sufficient for				AGGTCA	RTR	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_16_10565_s_184	9099702	3) A single core motif, AGGTCA, preceded by TCA (defined as 1/2-RTRE) is sufficient for RTR binding; however, the apparent affinity of RTR for 1/2-RTRE is significantly lower than that for conRTRE.	bind
30952	5	7696	5	13	NULL	NULL	NULL	RTR	GP		has affinity for									1/2-RTRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_16_10565_s_184	9099702	3) A single core motif, AGGTCA, preceded by TCA (defined as 1/2-RTRE) is sufficient for RTR binding; however, the apparent affinity of RTR for 1/2-RTRE is significantly lower than that for conRTRE.	bind
30953	6	7696	5	13	NULL	NULL	NULL	RTR	GP		has affinity for									conRTRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_16_10565_s_184	9099702	3) A single core motif, AGGTCA, preceded by TCA (defined as 1/2-RTRE) is sufficient for RTR binding; however, the apparent affinity of RTR for 1/2-RTRE is significantly lower than that for conRTRE.	bind
30958	7	7696	5	13	NULL	NULL	NULL	statement 5	Process	affinity of	lower than		significantly			statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_16_10565_s_184	9099702	3) A single core motif, AGGTCA, preceded by TCA (defined as 1/2-RTRE) is sufficient for RTR binding; however, the apparent affinity of RTR for 1/2-RTRE is significantly lower than that for conRTRE.	bind
24548	1	7696	6	NULL	NULL	0	NULL	RTR	NULL		has affinity for	NULL					NULL			1/2-RTRE	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10565_s_184	9099702	3) A single core motif, AGGTCA, preceded by TCA (defined as 1/2-RTRE) is sufficient for RTR binding; however, the apparent affinity of RTR for 1/2-RTRE is significantly lower than that for conRTRE.	bind
24549	2	7696	6	NULL	NULL	0	NULL	RTR	NULL		has affinity for	NULL					NULL			conRTRE	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10565_s_184	9099702	3) A single core motif, AGGTCA, preceded by TCA (defined as 1/2-RTRE) is sufficient for RTR binding; however, the apparent affinity of RTR for 1/2-RTRE is significantly lower than that for conRTRE.	bind
24550	3	7696	6	NULL	NULL	0	NULL	statement 1	NULL		is lower than	NULL	significantly			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10565_s_184	9099702	3) A single core motif, AGGTCA, preceded by TCA (defined as 1/2-RTRE) is sufficient for RTR binding; however, the apparent affinity of RTR for 1/2-RTRE is significantly lower than that for conRTRE.	bind
24551	4	7696	6	10	NULL	0	NULL	AGGTCA			is a type of					single core motif					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_16_10565_s_184	9099702	3) A single core motif, AGGTCA, preceded by TCA (defined as 1/2-RTRE) is sufficient for RTR binding; however, the apparent affinity of RTR for 1/2-RTRE is significantly lower than that for conRTRE.	bind
46890	5	7696	6	NULL	NULL	0	NULL		NULL		is sufficient for	NULL			1/2-RTRE	RTR	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10565_s_184	9099702	3) A single core motif, AGGTCA, preceded by TCA (defined as 1/2-RTRE) is sufficient for RTR binding; however, the apparent affinity of RTR for 1/2-RTRE is significantly lower than that for conRTRE.	bind
55542	6	7696	6	10	NULL	0	NULL				is preceded by				AGGTCA					TCA	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10565_s_184	9099702	3) A single core motif, AGGTCA, preceded by TCA (defined as 1/2-RTRE) is sufficient for RTR binding; however, the apparent affinity of RTR for 1/2-RTRE is significantly lower than that for conRTRE.	bind
55543	7	7696	6	10	NULL	0	NULL	AGGTCA			is defined as					1/2-RTRE					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10565_s_184	9099702	3) A single core motif, AGGTCA, preceded by TCA (defined as 1/2-RTRE) is sufficient for RTR binding; however, the apparent affinity of RTR for 1/2-RTRE is significantly lower than that for conRTRE.	bind
30960	1	7697	5	13	NULL	NULL	NULL				is a type of			Pro424 - Gly440		synthetic peptide	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34395_s_229	12816955	3) a synthetic  peptide (Pro424 - Gly440) corresponding to sequences  within W4, but not its scrambled control, bound C3bi directly with a   Kd of 20 muM  ( Fig. 5 A).	bind
30961	2	7697	5	13	NULL	NULL	NULL				corresponds to			Pro424 - Gly440		W4	GP	sequences within			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34395_s_229	12816955	3) a synthetic  peptide (Pro424 - Gly440) corresponding to sequences  within W4, but not its scrambled control, bound C3bi directly with a   Kd of 20 muM  ( Fig. 5 A).	bind
30963	3	7697	5	13	NULL	NULL	NULL				bind		directly	Pro424 - Gly440		C3bi	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34395_s_229	12816955	3) a synthetic  peptide (Pro424 - Gly440) corresponding to sequences  within W4, but not its scrambled control, bound C3bi directly with a   Kd of 20 muM  ( Fig. 5 A).	bind
23928	1	7697	6	10	NULL	0	NULL		NULL		bind	NULL	directly	Pro424-Gly440		C3bi	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34395_s_229	12816955	3) a synthetic  peptide (Pro424 - Gly440) corresponding to sequences  within W4, but not its scrambled control, bound C3bi directly with a   Kd of 20 muM  ( Fig. 5 A).	bind
46738	2	7697	6	10	NULL	0	NULL		NULL		is a type of	NULL		Pro424 - Gly440		synthetic peptide	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34395_s_229	12816955	3) a synthetic  peptide (Pro424 - Gly440) corresponding to sequences  within W4, but not its scrambled control, bound C3bi directly with a   Kd of 20 muM  ( Fig. 5 A).	bind
46739	3	7697	6	10	NULL	0	NULL		NULL		corresponds to	NULL		Pro424 - Gly440		W4	NULL	sequences within			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34395_s_229	12816955	3) a synthetic  peptide (Pro424 - Gly440) corresponding to sequences  within W4, but not its scrambled control, bound C3bi directly with a   Kd of 20 muM  ( Fig. 5 A).	bind
30964	1	7698	5	13	NULL	NULL	NULL	alpha beta	GP		bind					iC3b	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25866_s_149	7592772	3) Alanine substitution of Asp ,  Tyr , or deletion of residues  Phe -Tyr   (delta246-252)  abolished the binding of alpha beta   to iC3b as  well as the recognition of the function blocking anti-alpha   antibody 3H5.	bind
30965	2	7698	5	13	NULL	NULL	NULL	statement 8	Process		abolishes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25866_s_149	7592772	3) Alanine substitution of Asp ,  Tyr , or deletion of residues  Phe -Tyr   (delta246-252)  abolished the binding of alpha beta   to iC3b as  well as the recognition of the function blocking anti-alpha   antibody 3H5.	bind
30966	3	7698	5	13	NULL	NULL	NULL	statement 9	Process		abolishes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25866_s_149	7592772	3) Alanine substitution of Asp ,  Tyr , or deletion of residues  Phe -Tyr   (delta246-252)  abolished the binding of alpha beta   to iC3b as  well as the recognition of the function blocking anti-alpha   antibody 3H5.	bind
30968	4	7698	5	13	NULL	NULL	NULL			deletion of	abolishes			Phe -Tyr (delta246-252)		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25866_s_149	7592772	3) Alanine substitution of Asp ,  Tyr , or deletion of residues  Phe -Tyr   (delta246-252)  abolished the binding of alpha beta   to iC3b as  well as the recognition of the function blocking anti-alpha   antibody 3H5.	bind
30971	5	7698	5	13	NULL	NULL	NULL	statement 8	Process		blocks					anti-alpha antibody 3H5	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25866_s_149	7592772	3) Alanine substitution of Asp ,  Tyr , or deletion of residues  Phe -Tyr   (delta246-252)  abolished the binding of alpha beta   to iC3b as  well as the recognition of the function blocking anti-alpha   antibody 3H5.	bind
30973	6	7698	5	13	NULL	NULL	NULL	statement 9	Process		block					anti-alpha antibody 3H5	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25866_s_149	7592772	3) Alanine substitution of Asp ,  Tyr , or deletion of residues  Phe -Tyr   (delta246-252)  abolished the binding of alpha beta   to iC3b as  well as the recognition of the function blocking anti-alpha   antibody 3H5.	bind
30974	7	7698	5	13	NULL	NULL	NULL			deletion of	block			Phe -Tyr (delta246-252)		anti-alpha antibody 3H5	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25866_s_149	7592772	3) Alanine substitution of Asp ,  Tyr , or deletion of residues  Phe -Tyr   (delta246-252)  abolished the binding of alpha beta   to iC3b as  well as the recognition of the function blocking anti-alpha   antibody 3H5.	bind
55535	8	7698	5	10	NULL	0	NULL				is substituted for			Asp					alanine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25866_s_149	7592772	3) Alanine substitution of Asp ,  Tyr , or deletion of residues  Phe -Tyr   (delta246-252)  abolished the binding of alpha beta   to iC3b as  well as the recognition of the function blocking anti-alpha   antibody 3H5.	bind
55536	9	7698	5	10	NULL	0	NULL				is substituted for			Tyr					alanine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_43_25866_s_149	7592772	3) Alanine substitution of Asp ,  Tyr , or deletion of residues  Phe -Tyr   (delta246-252)  abolished the binding of alpha beta   to iC3b as  well as the recognition of the function blocking anti-alpha   antibody 3H5.	bind
23929	1	7698	6	NULL	NULL	0	NULL	alpha beta	NULL		bind	NULL				iC3b	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_43_25866_s_149	7592772	3) Alanine substitution of Asp ,  Tyr , or deletion of residues  Phe -Tyr   (delta246-252)  abolished the binding of alpha beta   to iC3b as  well as the recognition of the function blocking anti-alpha   antibody 3H5.	bind
23930	2	7698	6	NULL	NULL	0	NULL		NULL	deletion of	abolishes	NULL		residues Phe -Tyr (delta246-252)		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_43_25866_s_149	7592772	3) Alanine substitution of Asp ,  Tyr , or deletion of residues  Phe -Tyr   (delta246-252)  abolished the binding of alpha beta   to iC3b as  well as the recognition of the function blocking anti-alpha   antibody 3H5.	bind
24947	3	7698	6	10	NULL	0	NULL	statement 5			abolishes					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25866_s_149	7592772	3) Alanine substitution of Asp ,  Tyr , or deletion of residues  Phe -Tyr   (delta246-252)  abolished the binding of alpha beta   to iC3b as  well as the recognition of the function blocking anti-alpha   antibody 3H5.	bind
24948	4	7698	6	10	NULL	0	NULL	statement 6			abolishes					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25866_s_149	7592772	3) Alanine substitution of Asp ,  Tyr , or deletion of residues  Phe -Tyr   (delta246-252)  abolished the binding of alpha beta   to iC3b as  well as the recognition of the function blocking anti-alpha   antibody 3H5.	bind
55537	5	7698	6	10	NULL	0	NULL				is substituted for			Asp					alanine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25866_s_149	7592772	3) Alanine substitution of Asp ,  Tyr , or deletion of residues  Phe -Tyr   (delta246-252)  abolished the binding of alpha beta   to iC3b as  well as the recognition of the function blocking anti-alpha   antibody 3H5.	bind
55538	6	7698	6	10	NULL	0	NULL				is substituted for			Tyr					alanine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_43_25866_s_149	7592772	3) Alanine substitution of Asp ,  Tyr , or deletion of residues  Phe -Tyr   (delta246-252)  abolished the binding of alpha beta   to iC3b as  well as the recognition of the function blocking anti-alpha   antibody 3H5.	bind
55539	7	7698	6	10	NULL	0	NULL	statement 5			block					anti-alpha antibody 3H5					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_43_25866_s_149	7592772	3) Alanine substitution of Asp ,  Tyr , or deletion of residues  Phe -Tyr   (delta246-252)  abolished the binding of alpha beta   to iC3b as  well as the recognition of the function blocking anti-alpha   antibody 3H5.	bind
55540	8	7698	6	10	NULL	0	NULL	statement 6			block					anti-alpha antibody 3H5					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_43_25866_s_149	7592772	3) Alanine substitution of Asp ,  Tyr , or deletion of residues  Phe -Tyr   (delta246-252)  abolished the binding of alpha beta   to iC3b as  well as the recognition of the function blocking anti-alpha   antibody 3H5.	bind
55541	9	7698	6	10	NULL	0	NULL			deletion of	block			\tresidues Phe -Tyr (delta246-252)		anti-alpha antibody 3H5					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_43_25866_s_149	7592772	3) Alanine substitution of Asp ,  Tyr , or deletion of residues  Phe -Tyr   (delta246-252)  abolished the binding of alpha beta   to iC3b as  well as the recognition of the function blocking anti-alpha   antibody 3H5.	bind
30983	1	7699	5	13	NULL	NULL	NULL	ANP	GP		inhibit					NF-kappaB	GP	binding activity of			NULL	LPS-activated murine macrophages	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_13444_s_226	9593677	3) ANP inhibited binding activity of NF-kappaB, the predominant transcription factor for iNOS induction in LPS-activated murine macrophages ( 36).	bind
30988	2	7699	5	13	NULL	NULL	NULL	NF-kappaB	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_13444_s_226	9593677	3) ANP inhibited binding activity of NF-kappaB, the predominant transcription factor for iNOS induction in LPS-activated murine macrophages ( 36).	bind
30989	3	7699	5	13	NULL	NULL	NULL	NF-kappaB	GP		induces					iNOS	GP				NULL	in LPS-activated murine macrophages	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_13444_s_226	9593677	3) ANP inhibited binding activity of NF-kappaB, the predominant transcription factor for iNOS induction in LPS-activated murine macrophages ( 36).	bind
23931	1	7699	6	10	NULL	0	NULL	ANP			inhibits					NF-kappaB		binding activity of 			NULL	LPS-activated murine macrophages	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_13444_s_226	9593677	3) ANP inhibited binding activity of NF-kappaB, the predominant transcription factor for iNOS induction in LPS-activated murine macrophages ( 36).	bind
23932	2	7699	6	NULL	NULL	0	NULL	NF-kappaB	NULL		induces	NULL				iNOS 	NULL				NULL	LPS-activated murine macrophages	0	NULL	NULL	NULL	gw60_jbiolchem_273_22_13444_s_226	9593677	3) ANP inhibited binding activity of NF-kappaB, the predominant transcription factor for iNOS induction in LPS-activated murine macrophages ( 36).	bind
46740	3	7699	6	10	NULL	0	NULL	NF-kappaB	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_22_13444_s_226	9593677	3) ANP inhibited binding activity of NF-kappaB, the predominant transcription factor for iNOS induction in LPS-activated murine macrophages ( 36).	bind
30991	1	7700	5	13	NULL	NULL	NULL	Skp	GP		bind					OmpA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_11_9092_s_40	12509434	3) At which stoichiometries and how strong does Skp (or LPS) bind to OmpA?	bind
30992	2	7700	5	13	NULL	NULL	NULL	LPS	Chemical		bind					OmpA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_11_9092_s_40	12509434	3) At which stoichiometries and how strong does Skp (or LPS) bind to OmpA?	bind
30994	3	7700	5	13	NULL	NULL	NULL	statement 1	Process		is alternative to 					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_11_9092_s_40	12509434	3) At which stoichiometries and how strong does Skp (or LPS) bind to OmpA?	bind
23933	1	7700	6	NULL	NULL	0	NULL	Skp	NULL		bind	NULL				OmpA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9092_s_40	12509434	3) At which stoichiometries and how strong does Skp (or LPS) bind to OmpA?	bind
23934	2	7700	6	NULL	NULL	0	NULL	LPS	NULL		bind	NULL				OmpA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9092_s_40	12509434	3) At which stoichiometries and how strong does Skp (or LPS) bind to OmpA?	bind
46741	3	7700	6	10	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9092_s_40	12509434	3) At which stoichiometries and how strong does Skp (or LPS) bind to OmpA?	bind
30996	1	7701	5	13	NULL	NULL	NULL	UTI	Chemical		bind					UTI-BP40	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_247	11278581	3) Because UTI can bind UTI-BP40 ( K d = ~250 nM) and UTI-BP45 ( K d = ~10 nM), we believe that UTI binds initially to UTI-BP45 and subsequently to UTI-BP40, and 4) although essential for binding, either the amino terminus alone or the C4S side chain alone is not sufficient for UTI-dependent suppression of PMA-activated up-regulation of uPA.	bind
30998	2	7701	5	13	NULL	NULL	NULL	UTI	Chemical		bind					UTI-BP45	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_247	11278581	3) Because UTI can bind UTI-BP40 ( K d = ~250 nM) and UTI-BP45 ( K d = ~10 nM), we believe that UTI binds initially to UTI-BP45 and subsequently to UTI-BP40, and 4) although essential for binding, either the amino terminus alone or the C4S side chain alone is not sufficient for UTI-dependent suppression of PMA-activated up-regulation of uPA.	bind
30999	3	7701	5	13	NULL	NULL	NULL	statement 2	Process		is followed by					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_247	11278581	3) Because UTI can bind UTI-BP40 ( K d = ~250 nM) and UTI-BP45 ( K d = ~10 nM), we believe that UTI binds initially to UTI-BP45 and subsequently to UTI-BP40, and 4) although essential for binding, either the amino terminus alone or the C4S side chain alone is not sufficient for UTI-dependent suppression of PMA-activated up-regulation of uPA.	bind
31001	4	7701	5	13	NULL	NULL	NULL	PMA	Chemical		activate					uPA	GP	up-regulation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_247	11278581	3) Because UTI can bind UTI-BP40 ( K d = ~250 nM) and UTI-BP45 ( K d = ~10 nM), we believe that UTI binds initially to UTI-BP45 and subsequently to UTI-BP40, and 4) although essential for binding, either the amino terminus alone or the C4S side chain alone is not sufficient for UTI-dependent suppression of PMA-activated up-regulation of uPA.	bind
31002	5	7701	5	13	NULL	NULL	NULL	statement 4	Process	suppression of	is dependent on					UTI	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_247	11278581	3) Because UTI can bind UTI-BP40 ( K d = ~250 nM) and UTI-BP45 ( K d = ~10 nM), we believe that UTI binds initially to UTI-BP45 and subsequently to UTI-BP40, and 4) although essential for binding, either the amino terminus alone or the C4S side chain alone is not sufficient for UTI-dependent suppression of PMA-activated up-regulation of uPA.	bind
31005	6	7701	5	13	NULL	NULL	NULL				is not sufficient for			amino terminus		statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_247	11278581	3) Because UTI can bind UTI-BP40 ( K d = ~250 nM) and UTI-BP45 ( K d = ~10 nM), we believe that UTI binds initially to UTI-BP45 and subsequently to UTI-BP40, and 4) although essential for binding, either the amino terminus alone or the C4S side chain alone is not sufficient for UTI-dependent suppression of PMA-activated up-regulation of uPA.	bind
31007	7	7701	5	13	NULL	NULL	NULL				is not sufficient for			C4S side chain		statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_247	11278581	3) Because UTI can bind UTI-BP40 ( K d = ~250 nM) and UTI-BP45 ( K d = ~10 nM), we believe that UTI binds initially to UTI-BP45 and subsequently to UTI-BP40, and 4) although essential for binding, either the amino terminus alone or the C4S side chain alone is not sufficient for UTI-dependent suppression of PMA-activated up-regulation of uPA.	bind
24021	1	7701	6	NULL	NULL	0	NULL	UTI	NULL		bind	NULL				UTI-BP40	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_247	11278581	3) Because UTI can bind UTI-BP40 ( K d = ~250 nM) and UTI-BP45 ( K d = ~10 nM), we believe that UTI binds initially to UTI-BP45 and subsequently to UTI-BP40, and 4) although essential for binding, either the amino terminus alone or the C4S side chain alone is not sufficient for UTI-dependent suppression of PMA-activated up-regulation of uPA.	bind
24022	2	7701	6	NULL	NULL	0	NULL	UTI	NULL		bind	NULL				UTI-BP45	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_247	11278581	3) Because UTI can bind UTI-BP40 ( K d = ~250 nM) and UTI-BP45 ( K d = ~10 nM), we believe that UTI binds initially to UTI-BP45 and subsequently to UTI-BP40, and 4) although essential for binding, either the amino terminus alone or the C4S side chain alone is not sufficient for UTI-dependent suppression of PMA-activated up-regulation of uPA.	bind
24023	3	7701	6	NULL	NULL	0	NULL	statement 2	NULL		occurs before	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_247	11278581	3) Because UTI can bind UTI-BP40 ( K d = ~250 nM) and UTI-BP45 ( K d = ~10 nM), we believe that UTI binds initially to UTI-BP45 and subsequently to UTI-BP40, and 4) although essential for binding, either the amino terminus alone or the C4S side chain alone is not sufficient for UTI-dependent suppression of PMA-activated up-regulation of uPA.	bind
24024	4	7701	6	NULL	NULL	0	NULL	PMA	NULL		activates	NULL				uPA	NULL	up-regulation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_247	11278581	3) Because UTI can bind UTI-BP40 ( K d = ~250 nM) and UTI-BP45 ( K d = ~10 nM), we believe that UTI binds initially to UTI-BP45 and subsequently to UTI-BP40, and 4) although essential for binding, either the amino terminus alone or the C4S side chain alone is not sufficient for UTI-dependent suppression of PMA-activated up-regulation of uPA.	bind
24025	5	7701	6	NULL	NULL	0	NULL	statement 4	NULL		is suppressed by	NULL				UTI	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_247	11278581	3) Because UTI can bind UTI-BP40 ( K d = ~250 nM) and UTI-BP45 ( K d = ~10 nM), we believe that UTI binds initially to UTI-BP45 and subsequently to UTI-BP40, and 4) although essential for binding, either the amino terminus alone or the C4S side chain alone is not sufficient for UTI-dependent suppression of PMA-activated up-regulation of uPA.	bind
24026	6	7701	6	NULL	NULL	0	NULL		NULL		is not sufficient for	NULL		amino terminus		statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_247	11278581	3) Because UTI can bind UTI-BP40 ( K d = ~250 nM) and UTI-BP45 ( K d = ~10 nM), we believe that UTI binds initially to UTI-BP45 and subsequently to UTI-BP40, and 4) although essential for binding, either the amino terminus alone or the C4S side chain alone is not sufficient for UTI-dependent suppression of PMA-activated up-regulation of uPA.	bind
24027	7	7701	6	NULL	NULL	0	NULL		NULL	alone	is not sufficient for	NULL		C4S side chain		statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_13650_s_247	11278581	3) Because UTI can bind UTI-BP40 ( K d = ~250 nM) and UTI-BP45 ( K d = ~10 nM), we believe that UTI binds initially to UTI-BP45 and subsequently to UTI-BP40, and 4) although essential for binding, either the amino terminus alone or the C4S side chain alone is not sufficient for UTI-dependent suppression of PMA-activated up-regulation of uPA.	bind
31008	1	7702	5	13	NULL	NULL	NULL	hsp70	GP	purified	bind					K8/18	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_915_s_207	7529764	3) Binding of purified hsp70 to K8/18 is  partially facilitated by ATP, and release of the hsp/c70-K8/18 complex  in detergent cell lysates or in isolated immunoprecipitates requires  Mg-ATP and ATP hydrolysis.	bind
31009	2	7702	5	13	NULL	NULL	NULL	ATP	Chemical		facilitate		partially			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_915_s_207	7529764	3) Binding of purified hsp70 to K8/18 is  partially facilitated by ATP, and release of the hsp/c70-K8/18 complex  in detergent cell lysates or in isolated immunoprecipitates requires  Mg-ATP and ATP hydrolysis.	bind
31010	3	7702	5	13	NULL	NULL	NULL	hsp/c70-K8/18 complex	GP	release of	requires					Mg-ATP	Chemical				NULL	in detergent cell lysates	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_915_s_207	7529764	3) Binding of purified hsp70 to K8/18 is  partially facilitated by ATP, and release of the hsp/c70-K8/18 complex  in detergent cell lysates or in isolated immunoprecipitates requires  Mg-ATP and ATP hydrolysis.	bind
31011	4	7702	5	13	NULL	NULL	NULL	hsp/c70-K8/18 complex	GP	release of	requires					ATP 	Chemical	hydrolysis of			NULL	in detergent cell lysates	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_915_s_207	7529764	3) Binding of purified hsp70 to K8/18 is  partially facilitated by ATP, and release of the hsp/c70-K8/18 complex  in detergent cell lysates or in isolated immunoprecipitates requires  Mg-ATP and ATP hydrolysis.	bind
31013	5	7702	5	13	NULL	NULL	NULL	hsp/c70-K8/18 complex	GP	release of	requires					Mg-ATP	Chemical				NULL	in isolated immunoprecipitates 	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_915_s_207	7529764	3) Binding of purified hsp70 to K8/18 is  partially facilitated by ATP, and release of the hsp/c70-K8/18 complex  in detergent cell lysates or in isolated immunoprecipitates requires  Mg-ATP and ATP hydrolysis.	bind
31015	6	7702	5	13	NULL	NULL	NULL	hsp/c70-K8/18 complex	GP	release of	requires					ATP	Chemical	hydrolysis of			NULL	in isolated immunoprecipitates 	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_915_s_207	7529764	3) Binding of purified hsp70 to K8/18 is  partially facilitated by ATP, and release of the hsp/c70-K8/18 complex  in detergent cell lysates or in isolated immunoprecipitates requires  Mg-ATP and ATP hydrolysis.	bind
24028	1	7702	6	NULL	NULL	0	NULL	hsp70	NULL	purified	bind	NULL				K8/18	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_2_915_s_207	7529764	3) Binding of purified hsp70 to K8/18 is  partially facilitated by ATP, and release of the hsp/c70-K8/18 complex  in detergent cell lysates or in isolated immunoprecipitates requires  Mg-ATP and ATP hydrolysis.	bind
24029	2	7702	6	NULL	NULL	0	NULL	statement 1	NULL		is facilitated by	NULL	partially			ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_2_915_s_207	7529764	3) Binding of purified hsp70 to K8/18 is  partially facilitated by ATP, and release of the hsp/c70-K8/18 complex  in detergent cell lysates or in isolated immunoprecipitates requires  Mg-ATP and ATP hydrolysis.	bind
24030	3	7702	6	10	NULL	0	NULL	hsp/c70-K8/18 complex	NULL	release of	requires	NULL				Mg-ATP	NULL	hydrolysis of			NULL	detergent cell lysates	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_915_s_207	7529764	3) Binding of purified hsp70 to K8/18 is  partially facilitated by ATP, and release of the hsp/c70-K8/18 complex  in detergent cell lysates or in isolated immunoprecipitates requires  Mg-ATP and ATP hydrolysis.	bind
24031	4	7702	6	10	NULL	0	NULL	hsp/c70-K8/18 complex	NULL	release of	requires	NULL				ATP	NULL	hydrolysis of			NULL	detergent cell lysates	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_915_s_207	7529764	3) Binding of purified hsp70 to K8/18 is  partially facilitated by ATP, and release of the hsp/c70-K8/18 complex  in detergent cell lysates or in isolated immunoprecipitates requires  Mg-ATP and ATP hydrolysis.	bind
46742	5	7702	6	10	NULL	0	NULL	hsp/c70-K8/18 complex	NULL	release of	requires	NULL				Mg-ATP	NULL	hydrolysis of			NULL	in isolated immunoprecipitates	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_915_s_207	7529764	3) Binding of purified hsp70 to K8/18 is  partially facilitated by ATP, and release of the hsp/c70-K8/18 complex  in detergent cell lysates or in isolated immunoprecipitates requires  Mg-ATP and ATP hydrolysis.	bind
46743	6	7702	6	10	NULL	0	NULL	hsp/c70-K8/18 complex 		release of	requires					ATP		hydrolysis of			NULL	in isolated immunoprecipitates	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_915_s_207	7529764	3) Binding of purified hsp70 to K8/18 is  partially facilitated by ATP, and release of the hsp/c70-K8/18 complex  in detergent cell lysates or in isolated immunoprecipitates requires  Mg-ATP and ATP hydrolysis.	bind
24032	1	7703	6	NULL	NULL	0	NULL	Stat3	NULL		bind	NULL		SH2 domain		pY XXQ-containing peptide	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18967_s_28	14966128	3) Binding of Stat3 SH2 to pY XXQ-containing peptides does not require the side chains of Glu-638, Tyr-640, and Tyr-657 or Tyr-657, Cys-687, Ser-691, and Glu-692 proposed to form pocket 2 in the Chakraborty  et al. ( ) and Hemmann  et al. ( ) models, respectively.	bind
24033	2	7703	6	10	NULL	0	NULL	statement 1	NULL		does not require	NULL					NULL	side chains of	 Glu-638		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18967_s_28	14966128	3) Binding of Stat3 SH2 to pY XXQ-containing peptides does not require the side chains of Glu-638, Tyr-640, and Tyr-657 or Tyr-657, Cys-687, Ser-691, and Glu-692 proposed to form pocket 2 in the Chakraborty  et al. ( ) and Hemmann  et al. ( ) models, respectively.	bind
24034	3	7703	6	10	NULL	0	NULL	statement 1	NULL		does not require	NULL					NULL	side chains of 	Tyr-640		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18967_s_28	14966128	3) Binding of Stat3 SH2 to pY XXQ-containing peptides does not require the side chains of Glu-638, Tyr-640, and Tyr-657 or Tyr-657, Cys-687, Ser-691, and Glu-692 proposed to form pocket 2 in the Chakraborty  et al. ( ) and Hemmann  et al. ( ) models, respectively.	bind
46748	4	7703	6	10	NULL	0	NULL	statement 1	NULL		does not require	NULL					NULL	side chains of	Tyr-657		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_18967_s_28	14966128	3) Binding of Stat3 SH2 to pY XXQ-containing peptides does not require the side chains of Glu-638, Tyr-640, and Tyr-657 or Tyr-657, Cys-687, Ser-691, and Glu-692 proposed to form pocket 2 in the Chakraborty  et al. ( ) and Hemmann  et al. ( ) models, respectively.	bind
46749	5	7703	6	10	NULL	0	NULL	statement 1	NULL		does not require	NULL					NULL	side chains of	Cys-687		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_18967_s_28	14966128	3) Binding of Stat3 SH2 to pY XXQ-containing peptides does not require the side chains of Glu-638, Tyr-640, and Tyr-657 or Tyr-657, Cys-687, Ser-691, and Glu-692 proposed to form pocket 2 in the Chakraborty  et al. ( ) and Hemmann  et al. ( ) models, respectively.	bind
46750	6	7703	6	10	NULL	0	NULL	statement 1	NULL		does not require	NULL					NULL	side chains of	Ser-691		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_18967_s_28	14966128	3) Binding of Stat3 SH2 to pY XXQ-containing peptides does not require the side chains of Glu-638, Tyr-640, and Tyr-657 or Tyr-657, Cys-687, Ser-691, and Glu-692 proposed to form pocket 2 in the Chakraborty  et al. ( ) and Hemmann  et al. ( ) models, respectively.	bind
46751	7	7703	6	10	NULL	0	NULL	statement 1	NULL		does not require	NULL					NULL	side chains of	Glu-692		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_18967_s_28	14966128	3) Binding of Stat3 SH2 to pY XXQ-containing peptides does not require the side chains of Glu-638, Tyr-640, and Tyr-657 or Tyr-657, Cys-687, Ser-691, and Glu-692 proposed to form pocket 2 in the Chakraborty  et al. ( ) and Hemmann  et al. ( ) models, respectively.	bind
31071	1	7704	5	13	NULL	NULL	NULL	p53	GP		bind					PKD1 gene	GP	endogenous		p53 consensus-like DNA sequences	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_42_31234_s_276	16931520	3) ChIP assays performed in p53-transfected cells reveals that p53 binds the endogenous  PKD1 gene in regions containing p53 consensus-like DNA sequences.	bind
24036	1	7704	6	10	NULL	0	NULL	p53	NULL		bind	NULL				PKD1 gene	NULL	endogenous		p53 consensus-like DNA sequences	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_42_31234_s_276	16931520	3) ChIP assays performed in p53-transfected cells reveals that p53 binds the endogenous  PKD1 gene in regions containing p53 consensus-like DNA sequences.	bind
31073	1	7705	5	13	NULL	NULL	NULL	lin-benzo-ADP	Chemical		bind					F1	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_267_3_1530942_s_6	1530942	3) Fluorescence  properties of lin-benzo-ADP bound to F1 differed widely, depending on  the residue present at position beta 331.	bind
24037	1	7705	6	NULL	NULL	0	NULL	lin-benzo-ADP	NULL		bind	NULL				F1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_267_3_1530942_s_6	1530942	3) Fluorescence  properties of lin-benzo-ADP bound to F1 differed widely, depending on  the residue present at position beta 331.	bind
31075	1	7706	5	13	NULL	NULL	NULL	GR	GP		bind							putative;;mitochondrial		GR elements	NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_steroids_61_4_8733006_s_9	8733006	3) Gel  shift analysis has demonstrated binding of GR to putative mitochondrial  GR elements.	bind
24038	1	7706	6	10	NULL	0	NULL	GR	NULL		bind	NULL					NULL	putative;;mitochondrial		GR elements	NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_steroids_61_4_8733006_s_9	8733006	3) Gel  shift analysis has demonstrated binding of GR to putative mitochondrial  GR elements.	bind
31076	1	7707	5	13	NULL	NULL	NULL	DAG	Chemical		bind		predominantly						C1a domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_26_17815_s_480	16613842	3) In concert, DAG binding with C1 domains (predominantly C1a), Thr588 phosphorylation, and the protein configuration within the PH domain create a conformation that allows expression of maximal kinase activity.	bind
24039	1	7707	6	NULL	NULL	0	NULL	DAG	NULL		bind	NULL					NULL		C1 domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_26_17815_s_480	16613842	3) In concert, DAG binding with C1 domains (predominantly C1a), Thr588 phosphorylation, and the protein configuration within the PH domain create a conformation that allows expression of maximal kinase activity.	bind
31079	1	7708	5	13	NULL	NULL	NULL	SOCS3	GP		does not bind					OSMR	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_13_8458_s_237	16459330	3) in contrast to the inhibitory mechanisms of SOCS3 described so far, no binding of SOCS3 to the OSMR was found, but a direct association with JAK1 was found.	bind
31082	2	7708	5	13	NULL	NULL	NULL	SOCS3	GP		associates with		directly			JAK1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_13_8458_s_237	16459330	3) in contrast to the inhibitory mechanisms of SOCS3 described so far, no binding of SOCS3 to the OSMR was found, but a direct association with JAK1 was found.	bind
24043	1	7708	6	NULL	NULL	0	NULL	SOCS3	NULL		does not bind	NULL				OSMR	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_13_8458_s_237	16459330	3) in contrast to the inhibitory mechanisms of SOCS3 described so far, no binding of SOCS3 to the OSMR was found, but a direct association with JAK1 was found.	bind
24044	2	7708	6	NULL	NULL	0	NULL	SOCS3	NULL		associates with	NULL	directly			JAK1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_13_8458_s_237	16459330	3) in contrast to the inhibitory mechanisms of SOCS3 described so far, no binding of SOCS3 to the OSMR was found, but a direct association with JAK1 was found.	bind
31083	1	7709	5	13	NULL	NULL	NULL	LPS	Chemical		bind					CD14	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_17_9904_s_7	7537270	3) In contrast, substoichiometric concentrations of dLPS (1  ng/ml) inhibited LPS-induced (3 ng/ml) interleukin-8 release without  blocking LPS binding to CD14.	bind
31084	2	7709	5	13	NULL	NULL	NULL	LPS	Chemical		induces					interleukin-8	GP	release of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_17_9904_s_7	7537270	3) In contrast, substoichiometric concentrations of dLPS (1  ng/ml) inhibited LPS-induced (3 ng/ml) interleukin-8 release without  blocking LPS binding to CD14.	bind
31085	3	7709	5	13	NULL	NULL	NULL	dLPS	Chemical		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_17_9904_s_7	7537270	3) In contrast, substoichiometric concentrations of dLPS (1  ng/ml) inhibited LPS-induced (3 ng/ml) interleukin-8 release without  blocking LPS binding to CD14.	bind
31086	4	7709	5	13	NULL	NULL	NULL	statement 3	Process		occurs without					statement 1	Process	blocking			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_17_9904_s_7	7537270	3) In contrast, substoichiometric concentrations of dLPS (1  ng/ml) inhibited LPS-induced (3 ng/ml) interleukin-8 release without  blocking LPS binding to CD14.	bind
24045	1	7709	6	NULL	NULL	0	NULL	LPS	NULL		bind	NULL				CD14	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_17_9904_s_7	7537270	3) In contrast, substoichiometric concentrations of dLPS (1  ng/ml) inhibited LPS-induced (3 ng/ml) interleukin-8 release without  blocking LPS binding to CD14.	bind
24046	2	7709	6	NULL	NULL	0	NULL	LPS	NULL		induces	NULL				interleukin-8	NULL	release of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_17_9904_s_7	7537270	3) In contrast, substoichiometric concentrations of dLPS (1  ng/ml) inhibited LPS-induced (3 ng/ml) interleukin-8 release without  blocking LPS binding to CD14.	bind
24047	3	7709	6	NULL	NULL	0	NULL	dLPS	NULL		inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_17_9904_s_7	7537270	3) In contrast, substoichiometric concentrations of dLPS (1  ng/ml) inhibited LPS-induced (3 ng/ml) interleukin-8 release without  blocking LPS binding to CD14.	bind
24048	4	7709	6	10	NULL	0	NULL	statement 3	NULL		occurs without 	NULL				statement 1	NULL	blocking			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_17_9904_s_7	7537270	3) In contrast, substoichiometric concentrations of dLPS (1  ng/ml) inhibited LPS-induced (3 ng/ml) interleukin-8 release without  blocking LPS binding to CD14.	bind
31087	1	7710	5	13	NULL	NULL	NULL	eptifibatide	Chemical		induce					GPIIb/IIa	GP	conformational change of			NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_308_3_1002_s_187	14617694	3) In the presence of fibrinogen, the eptifibatide-induced conformational change of GPIIb/IIa is only partially reversible upon dissociation of the GPIIb/IIa blocker, as detected by the binding of a mAb specific for a LIBS, the binding of the ligand-mimetic mAb Pac-1, and the binding of the GPIIb/IIIa ligand fibrinogen.	bind
31088	2	7710	5	13	NULL	NULL	NULL	statement 1	Process		in the presence of					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_308_3_1002_s_187	14617694	3) In the presence of fibrinogen, the eptifibatide-induced conformational change of GPIIb/IIa is only partially reversible upon dissociation of the GPIIb/IIa blocker, as detected by the binding of a mAb specific for a LIBS, the binding of the ligand-mimetic mAb Pac-1, and the binding of the GPIIb/IIIa ligand fibrinogen.	bind
31089	3	7710	5	13	NULL	NULL	NULL	GPIIb/IIa blocker	Chemical	dissociation of	reverse		partially			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_308_3_1002_s_187	14617694	3) In the presence of fibrinogen, the eptifibatide-induced conformational change of GPIIb/IIa is only partially reversible upon dissociation of the GPIIb/IIa blocker, as detected by the binding of a mAb specific for a LIBS, the binding of the ligand-mimetic mAb Pac-1, and the binding of the GPIIb/IIIa ligand fibrinogen.	bind
24049	1	7710	6	NULL	NULL	0	NULL	eptifibatide	NULL		induces	NULL				GPIIb/IIa	NULL	conformational change of			NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_308_3_1002_s_187	14617694	3) In the presence of fibrinogen, the eptifibatide-induced conformational change of GPIIb/IIa is only partially reversible upon dissociation of the GPIIb/IIa blocker, as detected by the binding of a mAb specific for a LIBS, the binding of the ligand-mimetic mAb Pac-1, and the binding of the GPIIb/IIIa ligand fibrinogen.	bind
24050	2	7710	6	10	NULL	0	NULL	GPIIb/IIa blocker	NULL	dissociation of	reverse	NULL	partially			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_308_3_1002_s_187	14617694	3) In the presence of fibrinogen, the eptifibatide-induced conformational change of GPIIb/IIa is only partially reversible upon dissociation of the GPIIb/IIa blocker, as detected by the binding of a mAb specific for a LIBS, the binding of the ligand-mimetic mAb Pac-1, and the binding of the GPIIb/IIIa ligand fibrinogen.	bind
24051	3	7710	6	10	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				fibrinogen	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_308_3_1002_s_187	14617694	3) In the presence of fibrinogen, the eptifibatide-induced conformational change of GPIIb/IIa is only partially reversible upon dissociation of the GPIIb/IIa blocker, as detected by the binding of a mAb specific for a LIBS, the binding of the ligand-mimetic mAb Pac-1, and the binding of the GPIIb/IIIa ligand fibrinogen.	bind
31090	1	7711	5	13	NULL	NULL	NULL	Src's	GP		interacts with			SH2 domain		tyrosine	AminoAcid	phosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_22_16788_s_223	10747984	3) Interaction of Src's SH2 domain with a phosphorylated tyrosine on another protein could outcompete the binding of the SH2 domain to the COOH-terminal tyrosine, and thus disrupt the closed conformation.	bind
31093	2	7711	5	13	NULL	NULL	NULL				bind			SH2 domain		tyrosine	AminoAcid		COOH-terminus		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_22_16788_s_223	10747984	3) Interaction of Src's SH2 domain with a phosphorylated tyrosine on another protein could outcompete the binding of the SH2 domain to the COOH-terminal tyrosine, and thus disrupt the closed conformation.	bind
31094	3	7711	5	13	NULL	NULL	NULL	statement 1	Process		outcompetes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_22_16788_s_223	10747984	3) Interaction of Src's SH2 domain with a phosphorylated tyrosine on another protein could outcompete the binding of the SH2 domain to the COOH-terminal tyrosine, and thus disrupt the closed conformation.	bind
31095	4	7711	5	13	NULL	NULL	NULL	statement 3	Process		disrupt					conformation	Process	closed			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_22_16788_s_223	10747984	3) Interaction of Src's SH2 domain with a phosphorylated tyrosine on another protein could outcompete the binding of the SH2 domain to the COOH-terminal tyrosine, and thus disrupt the closed conformation.	bind
24052	1	7711	6	NULL	NULL	0	NULL	Src	NULL		interacts with	NULL		SH2 domain		tyrosine	NULL	phosphorylated			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_22_16788_s_223	10747984	3) Interaction of Src's SH2 domain with a phosphorylated tyrosine on another protein could outcompete the binding of the SH2 domain to the COOH-terminal tyrosine, and thus disrupt the closed conformation.	bind
24053	2	7711	6	NULL	NULL	0	NULL		NULL		bind	NULL		SH2 domain			NULL		COOH terminal tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_22_16788_s_223	10747984	3) Interaction of Src's SH2 domain with a phosphorylated tyrosine on another protein could outcompete the binding of the SH2 domain to the COOH-terminal tyrosine, and thus disrupt the closed conformation.	bind
24054	3	7711	6	NULL	NULL	0	NULL	statement 1	NULL		out competes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_22_16788_s_223	10747984	3) Interaction of Src's SH2 domain with a phosphorylated tyrosine on another protein could outcompete the binding of the SH2 domain to the COOH-terminal tyrosine, and thus disrupt the closed conformation.	bind
31096	1	7712	5	13	NULL	NULL	NULL	prothrombin	GP		bind					FXI	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31954_s_226	10924522	3) PF1.2 inhibits the binding of prothrombin to FXI (with a IC50 of 5 x 10-7M), whereas PF1 has no effect (Fig.  1 B, Table  I).	bind
31097	2	7712	5	13	NULL	NULL	NULL	PF1.2	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31954_s_226	10924522	3) PF1.2 inhibits the binding of prothrombin to FXI (with a IC50 of 5 x 10-7M), whereas PF1 has no effect (Fig.  1 B, Table  I).	bind
31098	3	7712	5	13	NULL	NULL	NULL	PF1	GP		does not effect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31954_s_226	10924522	3) PF1.2 inhibits the binding of prothrombin to FXI (with a IC50 of 5 x 10-7M), whereas PF1 has no effect (Fig.  1 B, Table  I).	bind
24055	1	7712	6	NULL	NULL	0	NULL	prothrombin	NULL		bind	NULL				FXI	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_41_31954_s_226	10924522	3) PF1.2 inhibits the binding of prothrombin to FXI (with a IC50 of 5 x 10-7M), whereas PF1 has no effect (Fig.  1 B, Table  I).	bind
24056	2	7712	6	NULL	NULL	0	NULL	PF1.2	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_41_31954_s_226	10924522	3) PF1.2 inhibits the binding of prothrombin to FXI (with a IC50 of 5 x 10-7M), whereas PF1 has no effect (Fig.  1 B, Table  I).	bind
24057	3	7712	6	NULL	NULL	0	NULL	PF1	NULL		has no effect on	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_41_31954_s_226	10924522	3) PF1.2 inhibits the binding of prothrombin to FXI (with a IC50 of 5 x 10-7M), whereas PF1 has no effect (Fig.  1 B, Table  I).	bind
31099	1	7713	5	13	NULL	NULL	NULL	alphaMbeta2	GP	wild-type	bind					C3bi	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34395_s_8	12816955	3) Polyclonal antibodies recognizing sequences  within the W4 blade significantly blocked C3bi binding by wild-type  alphaMbeta2.	bind
31100	2	7713	5	13	NULL	NULL	NULL	polyclonal antibodies	GP		recognize								sequences within W4 blade		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34395_s_8	12816955	3) Polyclonal antibodies recognizing sequences  within the W4 blade significantly blocked C3bi binding by wild-type  alphaMbeta2.	bind
46752	3	7713	5	13	NULL	NULL	NULL	statement 2	Process		blocks		significantly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34395_s_8	12816955	3) Polyclonal antibodies recognizing sequences  within the W4 blade significantly blocked C3bi binding by wild-type  alphaMbeta2.	bind
24059	1	7713	6	NULL	NULL	0	NULL	C3bi	NULL		bind	NULL				alphaMbeta2	NULL	wild type			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34395_s_8	12816955	3) Polyclonal antibodies recognizing sequences  within the W4 blade significantly blocked C3bi binding by wild-type  alphaMbeta2.	bind
24060	2	7713	6	NULL	NULL	0	NULL	Polyclonal antibodies	NULL		recognize	NULL					NULL		sequences within W4 blade		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34395_s_8	12816955	3) Polyclonal antibodies recognizing sequences  within the W4 blade significantly blocked C3bi binding by wild-type  alphaMbeta2.	bind
24061	3	7713	6	NULL	NULL	0	NULL	statement 2	NULL		blocks	NULL	significantly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34395_s_8	12816955	3) Polyclonal antibodies recognizing sequences  within the W4 blade significantly blocked C3bi binding by wild-type  alphaMbeta2.	bind
31101	1	7714	5	13	NULL	NULL	NULL	PP2A	GP		bind					tau	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
31102	2	7714	5	13	NULL	NULL	NULL	PP2A	GP		bind					MTs	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
31103	3	7714	5	13	NULL	NULL	NULL	statement 1 	Process		occurs through					distinct sites	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
31104	4	7714	5	13	NULL	NULL	NULL	tau	GP		is anchored to					MTs	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
31105	5	7714	5	13	NULL	NULL	NULL	PP2A	GP		is required for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
31106	6	7714	5	13	NULL	NULL	NULL	MTs	CellComponent		bind					tau	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
31107	7	7714	5	13	NULL	NULL	NULL	statement 1	Process		competes with					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
31108	8	7714	5	13	NULL	NULL	NULL	statement 2	Process		inhibit					PP2A	GP	catalytic activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
31109	9	7714	5	13	NULL	NULL	NULL	PP2A	GP		dephosphorylate		efficiently			tau	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
31110	10	7714	5	13	NULL	NULL	NULL	statement 9	Process		occur under conditions of					PP2A	GP	unbound			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
31111	11	7714	5	13	NULL	NULL	NULL	statement 9	Process		occur under conditions of					tau	GP	unbound			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
31112	12	7714	5	13	NULL	NULL	NULL	MTs	CellComponent	depolymerization of	potentiates					PP2A	GP	phosphatase activity			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
31113	13	7714	5	13	NULL	NULL	NULL	PP2A	GP		dissociates from					MTs	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
31114	14	7714	5	13	NULL	NULL	NULL	statement 13	Process		potentiates					PP2A	GP	phosphatase activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
46762	15	7714	5	13	NULL	NULL	NULL	statement 2	Process		occur through					distinct sites	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
24062	1	7714	6	NULL	NULL	0	NULL	PP2A	NULL		bind	NULL				tau	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
24063	2	7714	6	NULL	NULL	0	NULL	PP2A	NULL		bind	NULL				MT	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
24066	3	7714	6	NULL	NULL	0	NULL	tau	NULL		anchored to	NULL				MT	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
24067	4	7714	6	NULL	NULL	0	NULL	Tau	NULL		bind	NULL				MT	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
24068	5	7714	6	NULL	NULL	0	NULL	statement 2	NULL		competes	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
24070	6	7714	6	10	NULL	0	NULL	statement 2			inhibits					PP2A		catalytic activity of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
24072	7	7714	6	NULL	NULL	0	NULL	PP2A	NULL		dephosphorylate	NULL	efficiently			tau	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
24075	8	7714	6	NULL	NULL	0	NULL	statement 7	NULL		occurs under conditions of	NULL				tau	NULL	unbound			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
24076	9	7714	6	NULL	NULL	0	NULL	PP2A	NULL		exhibits	NULL				phosphatase activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
24077	10	7714	6	NULL	NULL	0	NULL	MT	NULL	depolymerization of 	potentiates	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
24123	11	7714	6	NULL	NULL	0	NULL	PP2A	NULL		dissociates from	NULL				MT	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
24124	12	7714	6	NULL	NULL	0	NULL	statement 10	NULL		potentiates	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
46763	13	7714	6	10	NULL	0	NULL	statement 7	NULL		occur under conditions of	NULL				PP2A	NULL	unbound			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_250	10464280	3) PP2A binds to tau and MTs through distinct sites and therefore might be able to anchor tau to MTs. 4) Since MTs and PP2A compete for binding to the same region on tau and binding of PP2A to MTs inhibits its catalytic activity, PP2A can efficiently dephosphorylate tau only when neither protein is bound to MTs. Depolymerization of MTs or dissociation of PP2A from MTs thus potentiates the phosphatase activity of PP2A for soluble tau.	bind
31115	1	7715	5	13	NULL	NULL	NULL	NTAB  fragments	GP	soluble 	bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_35355_s_251	9857078	3) Soluble fragments of NTAB bind to heparin better than LDL does.	bind
31116	2	7715	5	13	NULL	NULL	NULL	LDL	GP		bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_35355_s_251	9857078	3) Soluble fragments of NTAB bind to heparin better than LDL does.	bind
31117	3	7715	5	13	NULL	NULL	NULL	statement 1	Process		better than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_35355_s_251	9857078	3) Soluble fragments of NTAB bind to heparin better than LDL does.	bind
24125	1	7715	6	10	NULL	0	NULL	NTAB fragments	NULL	soluble	bind	NULL				heparin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_35355_s_251	9857078	3) Soluble fragments of NTAB bind to heparin better than LDL does.	bind
24126	2	7715	6	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_35355_s_251	9857078	3) Soluble fragments of NTAB bind to heparin better than LDL does.	bind
24127	3	7715	6	NULL	NULL	0	NULL	statement 1	NULL		is better than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_35355_s_251	9857078	3) Soluble fragments of NTAB bind to heparin better than LDL does.	bind
31118	1	7716	5	13	NULL	NULL	NULL	PDI	GP		bind					TG	GP		Ser789-Met1178 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1920_s_346	10636893	3) Surface plasmon resonance analysis of TG/PDI interaction characteristics indicated: (i) that PDI binds TG, but only in acidic conditions, and that it preferentially recognizes immature molecules, and (ii) that the Ser789-Met1178 domain is involved in binding, even if the cysteine-rich module is deleted.	bind
31119	2	7716	5	13	NULL	NULL	NULL	statement 1	Process		occurs in		only			acidic conditions					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1920_s_346	10636893	3) Surface plasmon resonance analysis of TG/PDI interaction characteristics indicated: (i) that PDI binds TG, but only in acidic conditions, and that it preferentially recognizes immature molecules, and (ii) that the Ser789-Met1178 domain is involved in binding, even if the cysteine-rich module is deleted.	bind
31120	3	7716	5	13	NULL	NULL	NULL	PDI	GP		recognizes		preferentially			immature molecules	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1920_s_346	10636893	3) Surface plasmon resonance analysis of TG/PDI interaction characteristics indicated: (i) that PDI binds TG, but only in acidic conditions, and that it preferentially recognizes immature molecules, and (ii) that the Ser789-Met1178 domain is involved in binding, even if the cysteine-rich module is deleted.	bind
31122	4	7716	5	13	NULL	NULL	NULL	statement 1	Process		absence of					TG	GP		cysteine-rich module		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1920_s_346	10636893	3) Surface plasmon resonance analysis of TG/PDI interaction characteristics indicated: (i) that PDI binds TG, but only in acidic conditions, and that it preferentially recognizes immature molecules, and (ii) that the Ser789-Met1178 domain is involved in binding, even if the cysteine-rich module is deleted.	bind
24129	2	7716	6	NULL	NULL	0	NULL	statement 1	NULL		occurs in	NULL	only			acidic conditions	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_3_1920_s_346	10636893	3) Surface plasmon resonance analysis of TG/PDI interaction characteristics indicated: (i) that PDI binds TG, but only in acidic conditions, and that it preferentially recognizes immature molecules, and (ii) that the Ser789-Met1178 domain is involved in binding, even if the cysteine-rich module is deleted.	bind
24131	4	7716	6	NULL	NULL	0	NULL	statement 3	NULL		occurs even after	NULL					NULL	deletion of	cysteine-rich module		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_3_1920_s_346	10636893	3) Surface plasmon resonance analysis of TG/PDI interaction characteristics indicated: (i) that PDI binds TG, but only in acidic conditions, and that it preferentially recognizes immature molecules, and (ii) that the Ser789-Met1178 domain is involved in binding, even if the cysteine-rich module is deleted.	bind
46764	5	7716	6	10	NULL	0	NULL	PDI	NULL		recognizes	NULL	preferentially			immature molecules	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_3_1920_s_346	10636893	3) Surface plasmon resonance analysis of TG/PDI interaction characteristics indicated: (i) that PDI binds TG, but only in acidic conditions, and that it preferentially recognizes immature molecules, and (ii) that the Ser789-Met1178 domain is involved in binding, even if the cysteine-rich module is deleted.	bind
55544	1	7716	6	10	NULL	0	NULL	PDI			bind					TG			Ser789-Met1178 domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_3_1920_s_346	10636893	3) Surface plasmon resonance analysis of TG/PDI interaction characteristics indicated: (i) that PDI binds TG, but only in acidic conditions, and that it preferentially recognizes immature molecules, and (ii) that the Ser789-Met1178 domain is involved in binding, even if the cysteine-rich module is deleted.	bind
31130	1	7717	5	13	NULL	NULL	NULL	Synapsins	GP		bind					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1425_s_157	9430678	3) Synapsins bind ADP with a much lower affinity than ATP, indicating that after hydrolysis, ADP would be exchanged for ATP.	bind
31131	2	7717	5	13	NULL	NULL	NULL	Synapsins	GP		bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1425_s_157	9430678	3) Synapsins bind ADP with a much lower affinity than ATP, indicating that after hydrolysis, ADP would be exchanged for ATP.	bind
31133	3	7717	5	13	NULL	NULL	NULL	statement 1	Process		lower affinity than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1425_s_157	9430678	3) Synapsins bind ADP with a much lower affinity than ATP, indicating that after hydrolysis, ADP would be exchanged for ATP.	bind
31134	4	7717	5	13	NULL	NULL	NULL	ADP	Chemical		is exchanged for					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1425_s_157	9430678	3) Synapsins bind ADP with a much lower affinity than ATP, indicating that after hydrolysis, ADP would be exchanged for ATP.	bind
31136	5	7717	5	13	NULL	NULL	NULL	statement 4	Process		occurs after					hydrolysis	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1425_s_157	9430678	3) Synapsins bind ADP with a much lower affinity than ATP, indicating that after hydrolysis, ADP would be exchanged for ATP.	bind
24132	1	7717	6	NULL	NULL	0	NULL	Synapsins	NULL		bind	NULL				ADP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1425_s_157	9430678	3) Synapsins bind ADP with a much lower affinity than ATP, indicating that after hydrolysis, ADP would be exchanged for ATP.	bind
24133	2	7717	6	NULL	NULL	0	NULL	Synapsins	NULL		bind	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1425_s_157	9430678	3) Synapsins bind ADP with a much lower affinity than ATP, indicating that after hydrolysis, ADP would be exchanged for ATP.	bind
24134	3	7717	6	10	NULL	0	NULL	statement 2	NULL		 lower affinity than	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1425_s_157	9430678	3) Synapsins bind ADP with a much lower affinity than ATP, indicating that after hydrolysis, ADP would be exchanged for ATP.	bind
24135	4	7717	6	NULL	NULL	0	NULL	ADP	NULL		is exchanged for	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1425_s_157	9430678	3) Synapsins bind ADP with a much lower affinity than ATP, indicating that after hydrolysis, ADP would be exchanged for ATP.	bind
24136	5	7717	6	NULL	NULL	0	NULL	statement 4	NULL		occurs after	NULL				hydrolysis	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1425_s_157	9430678	3) Synapsins bind ADP with a much lower affinity than ATP, indicating that after hydrolysis, ADP would be exchanged for ATP.	bind
31137	1	7718	5	13	NULL	NULL	NULL	DnaK	GP		bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_158	8626401	3) The absence of K   inhibits  DnaK's ATPase activity and conformational change but not the  binding of ATP to DnaK (Palleros  et al., 1993).	bind
44705	2	7718	5	13	NULL	NULL	NULL	DnaK	GP		exhibit					ATPase activity 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_158	8626401	3) The absence of K   inhibits  DnaK's ATPase activity and conformational change but not the  binding of ATP to DnaK (Palleros  et al., 1993).	bind
44706	4	7718	5	13	NULL	NULL	NULL			absence of	inhibit			K		DnaK	GP	conformational change of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_158	8626401	3) The absence of K   inhibits  DnaK's ATPase activity and conformational change but not the  binding of ATP to DnaK (Palleros  et al., 1993).	bind
44707	5	7718	5	13	NULL	NULL	NULL			absence of	does not inhibit			K		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_158	8626401	3) The absence of K   inhibits  DnaK's ATPase activity and conformational change but not the  binding of ATP to DnaK (Palleros  et al., 1993).	bind
46765	3	7718	5	13	NULL	NULL	NULL			absence of	inhibit			K		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_158	8626401	3) The absence of K   inhibits  DnaK's ATPase activity and conformational change but not the  binding of ATP to DnaK (Palleros  et al., 1993).	bind
24137	1	7718	6	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				DnaK	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_158	8626401	3) The absence of K   inhibits  DnaK's ATPase activity and conformational change but not the  binding of ATP to DnaK (Palleros  et al., 1993).	bind
24138	2	7718	6	10	NULL	0	NULL	DnaK	NULL		exhibit	NULL				 ATPase activity	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_158	8626401	3) The absence of K   inhibits  DnaK's ATPase activity and conformational change but not the  binding of ATP to DnaK (Palleros  et al., 1993).	bind
24139	3	7718	6	NULL	NULL	0	NULL		NULL	absence of	inhibits	NULL		K		Dnak	NULL	conformational change of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_158	8626401	3) The absence of K   inhibits  DnaK's ATPase activity and conformational change but not the  binding of ATP to DnaK (Palleros  et al., 1993).	bind
24140	4	7718	6	NULL	NULL	0	NULL		NULL	absence of	does not inhibit	NULL		K		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_158	8626401	3) The absence of K   inhibits  DnaK's ATPase activity and conformational change but not the  binding of ATP to DnaK (Palleros  et al., 1993).	bind
46766	5	7718	6	10	NULL	0	NULL		NULL	absence of	inhibit	NULL		K		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_158	8626401	3) The absence of K   inhibits  DnaK's ATPase activity and conformational change but not the  binding of ATP to DnaK (Palleros  et al., 1993).	bind
31140	1	7719	5	13	NULL	NULL	NULL	TCF	GP		is required in					bromocomplex	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_7_5213_s_322	11083868	3) The DNA-dependent  in vitro interactions can be reconstituted on the Ets protein binding site E74, where Elk-1 binds in the absence of SRF, suggesting a sole requirement for TCF in bromocomplex formation.	bind
31354	2	7719	5	13	NULL	NULL	NULL	Elk-1	GP		bind									E74	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_7_5213_s_322	11083868	3) The DNA-dependent  in vitro interactions can be reconstituted on the Ets protein binding site E74, where Elk-1 binds in the absence of SRF, suggesting a sole requirement for TCF in bromocomplex formation.	bind
31355	3	7719	5	13	NULL	NULL	NULL	statement 2	Process		absence of					SRF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_7_5213_s_322	11083868	3) The DNA-dependent  in vitro interactions can be reconstituted on the Ets protein binding site E74, where Elk-1 binds in the absence of SRF, suggesting a sole requirement for TCF in bromocomplex formation.	bind
31356	4	7719	5	13	NULL	NULL	NULL	E74	GP		is					Ets protein binding site	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_7_5213_s_322	11083868	3) The DNA-dependent  in vitro interactions can be reconstituted on the Ets protein binding site E74, where Elk-1 binds in the absence of SRF, suggesting a sole requirement for TCF in bromocomplex formation.	bind
24552	1	7719	6	NULL	NULL	0	NULL	TCF	NULL		plays a role in	NULL				bromocomplex	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_7_5213_s_322	11083868	3) The DNA-dependent  in vitro interactions can be reconstituted on the Ets protein binding site E74, where Elk-1 binds in the absence of SRF, suggesting a sole requirement for TCF in bromocomplex formation.	bind
24553	2	7719	6	NULL	NULL	0	NULL	Elk1	NULL	binding of	occurs in absence of	NULL				SRF	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_7_5213_s_322	11083868	3) The DNA-dependent  in vitro interactions can be reconstituted on the Ets protein binding site E74, where Elk-1 binds in the absence of SRF, suggesting a sole requirement for TCF in bromocomplex formation.	bind
24949	3	7719	6	10	NULL	0	NULL	Elk1	NULL		bind	NULL					NULL			 E74	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_7_5213_s_322	11083868	3) The DNA-dependent  in vitro interactions can be reconstituted on the Ets protein binding site E74, where Elk-1 binds in the absence of SRF, suggesting a sole requirement for TCF in bromocomplex formation.	bind
46767	4	7719	6	10	NULL	0	NULL	E74	NULL		is	NULL				Ets protein binding site	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_7_5213_s_322	11083868	3) The DNA-dependent  in vitro interactions can be reconstituted on the Ets protein binding site E74, where Elk-1 binds in the absence of SRF, suggesting a sole requirement for TCF in bromocomplex formation.	bind
31357	1	7721	5	13	NULL	NULL	NULL	insulin receptor	GP		bind					Hsp90	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_11_3071_s_33	9802897	3) The insulin receptor binds Hsp90, and antibodies to Hsp90 interfere with insulin signaling (Takata  et al., 1997  ).	bind
31358	2	7721	5	13	NULL	NULL	NULL	Hsp90 antibodies	GP		interfere with					insulin signaling	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_11_3071_s_33	9802897	3) The insulin receptor binds Hsp90, and antibodies to Hsp90 interfere with insulin signaling (Takata  et al., 1997  ).	bind
24143	1	7721	6	NULL	NULL	0	NULL	insulin receptor	NULL		bind	NULL				Hsp90	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_11_3071_s_33	9802897	3) The insulin receptor binds Hsp90, and antibodies to Hsp90 interfere with insulin signaling (Takata  et al., 1997  ).	bind
24144	2	7721	6	10	NULL	0	NULL	Hsp90 antibodies	NULL		interfere with	NULL				insulin signaling	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_11_3071_s_33	9802897	3) The insulin receptor binds Hsp90, and antibodies to Hsp90 interfere with insulin signaling (Takata  et al., 1997  ).	bind
31369	1	7722	5	13	NULL	NULL	NULL				bind			SH3 domain		linker	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_33_23776_s_282	16790421	3) The SH3 domain binds to the linker, which results in Src inactivation.	bind
31370	2	7722	5	13	NULL	NULL	NULL	statement 1	Process		results in					Src	GP	inactivation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_33_23776_s_282	16790421	3) The SH3 domain binds to the linker, which results in Src inactivation.	bind
24145	1	7722	6	NULL	NULL	0	NULL		NULL		bind	NULL		SH3 domain		linker	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_33_23776_s_282	16790421	3) The SH3 domain binds to the linker, which results in Src inactivation.	bind
24146	2	7722	6	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				src 	NULL	inactivation of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_33_23776_s_282	16790421	3) The SH3 domain binds to the linker, which results in Src inactivation.	bind
31371	1	7723	5	13	NULL	NULL	NULL	Taq	Organism		bind		might							GC-rich sequences	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5694_s_216	12466277	3) The two polymerases might show significant differences in sequence specificity,  e.g. Taq might bind GC-rich sequences (more common in thermostable bacteria) tighter than mixed DNA sequences.	bind
31372	2	7723	5	13	NULL	NULL	NULL	statement 1	Process		occurs in		commonly			thermostable bacteria	Organism				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5694_s_216	12466277	3) The two polymerases might show significant differences in sequence specificity,  e.g. Taq might bind GC-rich sequences (more common in thermostable bacteria) tighter than mixed DNA sequences.	bind
31373	3	7723	5	13	NULL	NULL	NULL	Taq	Organism		bind					DNA sequences	NucleicAcid	mixed			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5694_s_216	12466277	3) The two polymerases might show significant differences in sequence specificity,  e.g. Taq might bind GC-rich sequences (more common in thermostable bacteria) tighter than mixed DNA sequences.	bind
31374	4	7723	5	13	NULL	NULL	NULL	statement 1	Process		tighter than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5694_s_216	12466277	3) The two polymerases might show significant differences in sequence specificity,  e.g. Taq might bind GC-rich sequences (more common in thermostable bacteria) tighter than mixed DNA sequences.	bind
24147	1	7723	6	NULL	NULL	0	NULL	Taq	NULL		bind	NULL	may				NULL			GC rich sequences	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_8_5694_s_216	12466277	3) The two polymerases might show significant differences in sequence specificity,  e.g. Taq might bind GC-rich sequences (more common in thermostable bacteria) tighter than mixed DNA sequences.	bind
24148	2	7723	6	10	NULL	0	NULL	Taq			bind		may			DNA sequences				mixed	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5694_s_216	12466277	3) The two polymerases might show significant differences in sequence specificity,  e.g. Taq might bind GC-rich sequences (more common in thermostable bacteria) tighter than mixed DNA sequences.	bind
24149	3	7723	6	NULL	NULL	0	NULL	statement 1	NULL		is tighter than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_8_5694_s_216	12466277	3) The two polymerases might show significant differences in sequence specificity,  e.g. Taq might bind GC-rich sequences (more common in thermostable bacteria) tighter than mixed DNA sequences.	bind
24150	4	7723	6	10	NULL	0	NULL	statement 1			occurs in		commonly			thermostable bacteria					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5694_s_216	12466277	3) The two polymerases might show significant differences in sequence specificity,  e.g. Taq might bind GC-rich sequences (more common in thermostable bacteria) tighter than mixed DNA sequences.	bind
31375	1	7724	5	13	NULL	NULL	NULL	gp43	GP		bind			C terminus		gp45	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_39340_s_288	11504721	3) The x-ray crystal structure of the C terminus of gp43 bound to gp45 yielded a stoichiometry of 1 peptide per gp45 trimer ( 22), whereas fluorescence measurements in solution yielded a stoichiometry of 1 peptide per gp45 monomer ( 32).	bind
24151	1	7724	6	NULL	NULL	0	NULL	gp43	NULL		bind	NULL		C terminus		gp45	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39340_s_288	11504721	3) The x-ray crystal structure of the C terminus of gp43 bound to gp45 yielded a stoichiometry of 1 peptide per gp45 trimer ( 22), whereas fluorescence measurements in solution yielded a stoichiometry of 1 peptide per gp45 monomer ( 32).	bind
31376	1	7725	5	13	NULL	NULL	NULL	pro-uPA	GP		bind					tumor cell receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_14899_s_8	14747469	3) Tumor cell receptor-bound pro-uPA could be efficiently cleaved by matriptase to generate enzymatically active two-chain uPA.	bind
31377	2	7725	5	13	NULL	NULL	NULL	matriptase	GP		cleaves		efficiently			statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_14899_s_8	14747469	3) Tumor cell receptor-bound pro-uPA could be efficiently cleaved by matriptase to generate enzymatically active two-chain uPA.	bind
31378	3	7725	5	13	NULL	NULL	NULL	statement 2	Process		generates					two-chain uPA	GP	enzymatically active			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_14899_s_8	14747469	3) Tumor cell receptor-bound pro-uPA could be efficiently cleaved by matriptase to generate enzymatically active two-chain uPA.	bind
24152	1	7725	6	NULL	NULL	0	NULL	Tumor cell receptor	NULL		bind	NULL				pro-uPA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_15_14899_s_8	14747469	3) Tumor cell receptor-bound pro-uPA could be efficiently cleaved by matriptase to generate enzymatically active two-chain uPA.	bind
24153	2	7725	6	10	NULL	0	NULL	statement 1			is cleaved by		efficiently			matriptase					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_14899_s_8	14747469	3) Tumor cell receptor-bound pro-uPA could be efficiently cleaved by matriptase to generate enzymatically active two-chain uPA.	bind
46770	3	7725	6	10	NULL	0	NULL	statement 2	NULL		generates	NULL				two-chain uPA	NULL	enzymatically active			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_15_14899_s_8	14747469	3) Tumor cell receptor-bound pro-uPA could be efficiently cleaved by matriptase to generate enzymatically active two-chain uPA.	bind
31379	1	7726	5	13	NULL	NULL	NULL	intersectin	GP		bind		specifically			SCAMP1	GP		N-terminal NPF repeats		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_17_12752_s_162	10777571	3) Two proteins with a known function in clathrin coats are specifically bound to the N-terminal NPF repeats of SCAMP1, namely intersectin and gamma-synergin.	bind
31380	2	7726	5	13	NULL	NULL	NULL	gamma-synergin	GP		bind		specifically			SCAMP1	GP		N-terminal NPF repeats		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_17_12752_s_162	10777571	3) Two proteins with a known function in clathrin coats are specifically bound to the N-terminal NPF repeats of SCAMP1, namely intersectin and gamma-synergin.	bind
46771	3	7726	5	13	NULL	NULL	NULL	intersectin 	GP		function in					clathrin coats	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_17_12752_s_162	10777571	3) Two proteins with a known function in clathrin coats are specifically bound to the N-terminal NPF repeats of SCAMP1, namely intersectin and gamma-synergin.	bind
46772	4	7726	5	13	NULL	NULL	NULL	gamma-synergin	GP		function in					clathrin coats	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_17_12752_s_162	10777571	3) Two proteins with a known function in clathrin coats are specifically bound to the N-terminal NPF repeats of SCAMP1, namely intersectin and gamma-synergin.	bind
24154	1	7726	6	10	NULL	0	NULL	intersectin			bind		specifically			SCAMP1			N-terminal NPF repeats		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_17_12752_s_162	10777571	3) Two proteins with a known function in clathrin coats are specifically bound to the N-terminal NPF repeats of SCAMP1, namely intersectin and gamma-synergin.	bind
24155	2	7726	6	10	NULL	0	NULL	gamma-synergin			bind		specifically			SCAMP1			N-terminal NPF repeats		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_17_12752_s_162	10777571	3) Two proteins with a known function in clathrin coats are specifically bound to the N-terminal NPF repeats of SCAMP1, namely intersectin and gamma-synergin.	bind
24156	3	7726	6	NULL	NULL	0	NULL	intersectin	NULL		function in	NULL				clathrin coats	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_17_12752_s_162	10777571	3) Two proteins with a known function in clathrin coats are specifically bound to the N-terminal NPF repeats of SCAMP1, namely intersectin and gamma-synergin.	bind
24157	4	7726	6	NULL	NULL	0	NULL	gamma-synergin	NULL		function in	NULL				clathrin coats	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_17_12752_s_162	10777571	3) Two proteins with a known function in clathrin coats are specifically bound to the N-terminal NPF repeats of SCAMP1, namely intersectin and gamma-synergin.	bind
31381	1	7727	5	13	NULL	NULL	NULL	Ras	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25157_s_248	11274179	3) Vincristine and paclitaxel have been shown to stimulate Ras binding to GTP, one of the avenues leading to activation of JNK/SAPK pathway ( 47), whereas our current data indicate that nocodazole activates Raf-1 through a Ras-independent mechanism.	bind
31382	2	7727	5	13	NULL	NULL	NULL	vincristine	Chemical		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25157_s_248	11274179	3) Vincristine and paclitaxel have been shown to stimulate Ras binding to GTP, one of the avenues leading to activation of JNK/SAPK pathway ( 47), whereas our current data indicate that nocodazole activates Raf-1 through a Ras-independent mechanism.	bind
31383	3	7727	5	13	NULL	NULL	NULL	paclitaxel	Chemical		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25157_s_248	11274179	3) Vincristine and paclitaxel have been shown to stimulate Ras binding to GTP, one of the avenues leading to activation of JNK/SAPK pathway ( 47), whereas our current data indicate that nocodazole activates Raf-1 through a Ras-independent mechanism.	bind
31384	4	7727	5	13	NULL	NULL	NULL	statement 1	Process		leads to					JNK/SAPK pathway	Process	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25157_s_248	11274179	3) Vincristine and paclitaxel have been shown to stimulate Ras binding to GTP, one of the avenues leading to activation of JNK/SAPK pathway ( 47), whereas our current data indicate that nocodazole activates Raf-1 through a Ras-independent mechanism.	bind
31385	5	7727	5	13	NULL	NULL	NULL	nocodazole	Chemical		activates					Raf-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25157_s_248	11274179	3) Vincristine and paclitaxel have been shown to stimulate Ras binding to GTP, one of the avenues leading to activation of JNK/SAPK pathway ( 47), whereas our current data indicate that nocodazole activates Raf-1 through a Ras-independent mechanism.	bind
31386	6	7727	5	13	NULL	NULL	NULL	statement 5	Process		is independent of					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25157_s_248	11274179	3) Vincristine and paclitaxel have been shown to stimulate Ras binding to GTP, one of the avenues leading to activation of JNK/SAPK pathway ( 47), whereas our current data indicate that nocodazole activates Raf-1 through a Ras-independent mechanism.	bind
24158	1	7727	6	NULL	NULL	0	NULL	Ras	NULL		bind	NULL				GTP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_27_25157_s_248	11274179	3) Vincristine and paclitaxel have been shown to stimulate Ras binding to GTP, one of the avenues leading to activation of JNK/SAPK pathway ( 47), whereas our current data indicate that nocodazole activates Raf-1 through a Ras-independent mechanism.	bind
24159	2	7727	6	NULL	NULL	0	NULL	Vincristine	NULL		stimulates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_27_25157_s_248	11274179	3) Vincristine and paclitaxel have been shown to stimulate Ras binding to GTP, one of the avenues leading to activation of JNK/SAPK pathway ( 47), whereas our current data indicate that nocodazole activates Raf-1 through a Ras-independent mechanism.	bind
24160	3	7727	6	NULL	NULL	0	NULL	paclitaxel	NULL		stimulates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_27_25157_s_248	11274179	3) Vincristine and paclitaxel have been shown to stimulate Ras binding to GTP, one of the avenues leading to activation of JNK/SAPK pathway ( 47), whereas our current data indicate that nocodazole activates Raf-1 through a Ras-independent mechanism.	bind
24161	4	7727	6	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				JNK/SAPK pathway	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_27_25157_s_248	11274179	3) Vincristine and paclitaxel have been shown to stimulate Ras binding to GTP, one of the avenues leading to activation of JNK/SAPK pathway ( 47), whereas our current data indicate that nocodazole activates Raf-1 through a Ras-independent mechanism.	bind
24162	5	7727	6	NULL	NULL	0	NULL	Nocodazole	NULL		activates	NULL				Raf-1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_27_25157_s_248	11274179	3) Vincristine and paclitaxel have been shown to stimulate Ras binding to GTP, one of the avenues leading to activation of JNK/SAPK pathway ( 47), whereas our current data indicate that nocodazole activates Raf-1 through a Ras-independent mechanism.	bind
24163	6	7727	6	NULL	NULL	0	NULL	statement 5	NULL		is independent of	NULL				ras	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_27_25157_s_248	11274179	3) Vincristine and paclitaxel have been shown to stimulate Ras binding to GTP, one of the avenues leading to activation of JNK/SAPK pathway ( 47), whereas our current data indicate that nocodazole activates Raf-1 through a Ras-independent mechanism.	bind
31387	2	7728	5	13	NULL	NULL	NULL	LDL-c	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_1_90_s_18	12524230	3, 4 LDL-c binds to the LDLR expressed on the surface of hepatocytes and is removed from the circulation by LDLR-mediated endocytosis.	bind
31388	4	7728	5	13	NULL	NULL	NULL	statement 3	Process		removes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_1_90_s_18	12524230	3, 4 LDL-c binds to the LDLR expressed on the surface of hepatocytes and is removed from the circulation by LDLR-mediated endocytosis.	bind
31389	3	7728	5	13	NULL	NULL	NULL	LDLR	GP		mediates					endocytosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_1_90_s_18	12524230	3, 4 LDL-c binds to the LDLR expressed on the surface of hepatocytes and is removed from the circulation by LDLR-mediated endocytosis.	bind
46773	1	7728	5	13	NULL	NULL	NULL	LDLR	GP		is expressed on					hepatocytes	Cell	surface of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_1_90_s_18	12524230	3, 4 LDL-c binds to the LDLR expressed on the surface of hepatocytes and is removed from the circulation by LDLR-mediated endocytosis.	bind
24164	2	7728	6	10	NULL	0	NULL	LDL-c 	NULL		bind	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_1_90_s_18	12524230	3, 4 LDL-c binds to the LDLR expressed on the surface of hepatocytes and is removed from the circulation by LDLR-mediated endocytosis.	bind
24166	1	7728	6	10	NULL	0	NULL	LDLR	NULL		is expressed on	NULL				hepatocytes	NULL	surface of 			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_1_90_s_18	12524230	3, 4 LDL-c binds to the LDLR expressed on the surface of hepatocytes and is removed from the circulation by LDLR-mediated endocytosis.	bind
24167	3	7728	6	10	NULL	0	NULL	LDLR	NULL		mediates	NULL				endocytosis	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_1_90_s_18	12524230	3, 4 LDL-c binds to the LDLR expressed on the surface of hepatocytes and is removed from the circulation by LDLR-mediated endocytosis.	bind
24168	4	7728	6	10	NULL	0	NULL	statement 2	NULL		is removed by	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_1_90_s_18	12524230	3, 4 LDL-c binds to the LDLR expressed on the surface of hepatocytes and is removed from the circulation by LDLR-mediated endocytosis.	bind
31390	1	7729	5	13	NULL	NULL	NULL	BAFF/BLyS receptor 3	GP		bind			surface loop		BAFF ligand 	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_431_7007_456_s_207	15361883	3, 958 965 (2002) |  Article |  PubMed |  ISI |  ChemPort |                    Kayagaki, N.  et al. BAFF/BLyS receptor 3 binds the B cell survival factor BAFF ligand through a discrete  surface loop and promotes processing of NF-kappaB2.	bind
31391	2	7729	5	13	NULL	NULL	NULL	statement 1	Process		promote					NF-kappaB2	GP	processing of			NULL		NULL	NULL	NULL	NULL	gw70_nature_431_7007_456_s_207	15361883	3, 958 965 (2002) |  Article |  PubMed |  ISI |  ChemPort |                    Kayagaki, N.  et al. BAFF/BLyS receptor 3 binds the B cell survival factor BAFF ligand through a discrete  surface loop and promotes processing of NF-kappaB2.	bind
46774	3	7729	5	13	NULL	NULL	NULL	BAFF ligand	GP		is a type of					B cell survival factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_431_7007_456_s_207	15361883	3, 958 965 (2002) |  Article |  PubMed |  ISI |  ChemPort |                    Kayagaki, N.  et al. BAFF/BLyS receptor 3 binds the B cell survival factor BAFF ligand through a discrete  surface loop and promotes processing of NF-kappaB2.	bind
24169	1	7729	6	13	NULL	NULL	NULL	BAFF/BLyS receptor 3	GP		bind					 BAFF ligand	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_431_7007_456_s_207	15361883	3, 958 965 (2002) |  Article |  PubMed |  ISI |  ChemPort |                    Kayagaki, N.  et al. BAFF/BLyS receptor 3 binds the B cell survival factor BAFF ligand through a discrete  surface loop and promotes processing of NF-kappaB2.	bind
24170	2	7729	6	NULL	NULL	0	NULL	statement 1	NULL		occurs through	NULL				surface loop	NULL	discrete			NULL		0	NULL	NULL	NULL	gw70_nature_431_7007_456_s_207	15361883	3, 958 965 (2002) |  Article |  PubMed |  ISI |  ChemPort |                    Kayagaki, N.  et al. BAFF/BLyS receptor 3 binds the B cell survival factor BAFF ligand through a discrete  surface loop and promotes processing of NF-kappaB2.	bind
24171	3	7729	6	NULL	NULL	0	NULL	statement 1	NULL		promotes	NULL				NF-kappaB2	NULL	processing of			NULL		0	NULL	NULL	NULL	gw70_nature_431_7007_456_s_207	15361883	3, 958 965 (2002) |  Article |  PubMed |  ISI |  ChemPort |                    Kayagaki, N.  et al. BAFF/BLyS receptor 3 binds the B cell survival factor BAFF ligand through a discrete  surface loop and promotes processing of NF-kappaB2.	bind
46775	4	7729	6	10	NULL	0	NULL	BAFF ligand	NULL		is a type of	NULL				B cell survival factor	NULL				NULL		0	NULL	NULL	NULL	gw70_nature_431_7007_456_s_207	15361883	3, 958 965 (2002) |  Article |  PubMed |  ISI |  ChemPort |                    Kayagaki, N.  et al. BAFF/BLyS receptor 3 binds the B cell survival factor BAFF ligand through a discrete  surface loop and promotes processing of NF-kappaB2.	bind
31392	1	7730	5	13	NULL	NULL	NULL	Hop	GP		bind					hsp90	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38294_s_380	12161444	3, Hop that is bound to hsp90 binds to hsp70-ADP.	bind
31393	2	7730	5	13	NULL	NULL	NULL	statement 1	GP		bind					hsp70-ADP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38294_s_380	12161444	3, Hop that is bound to hsp90 binds to hsp70-ADP.	bind
24211	1	7730	6	NULL	NULL	0	NULL	Hop	NULL		bind	NULL				hsp90	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_41_38294_s_380	12161444	3, Hop that is bound to hsp90 binds to hsp70-ADP.	bind
24212	2	7730	6	10	NULL	0	NULL	statement 1			bind					hsp70-ADP					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_41_38294_s_380	12161444	3, Hop that is bound to hsp90 binds to hsp70-ADP.	bind
31561	1	7731	5	13	NULL	NULL	NULL	T complex	GP		associates with					cellular factors	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_54_0_187_s_347	11018128	3, T complex associates with cellular factors; VirD2 binds to AtKAP  ( 3a) and cyclophilins ( 3b), VirE2 binds to VIP1 and/or VIP2 ( 3c), the VirD2 NLS region is phosphorylated ( 3d), and AtKAP  may interact with the putative AtKAPbeta ( 3e).	bind
31562	2	7731	5	13	NULL	NULL	NULL	VirD2	GP		bind					AtKAP	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_54_0_187_s_347	11018128	3, T complex associates with cellular factors; VirD2 binds to AtKAP  ( 3a) and cyclophilins ( 3b), VirE2 binds to VIP1 and/or VIP2 ( 3c), the VirD2 NLS region is phosphorylated ( 3d), and AtKAP  may interact with the putative AtKAPbeta ( 3e).	bind
31563	3	7731	5	13	NULL	NULL	NULL	VirD2	GP		bind					cyclophilins	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_54_0_187_s_347	11018128	3, T complex associates with cellular factors; VirD2 binds to AtKAP  ( 3a) and cyclophilins ( 3b), VirE2 binds to VIP1 and/or VIP2 ( 3c), the VirD2 NLS region is phosphorylated ( 3d), and AtKAP  may interact with the putative AtKAPbeta ( 3e).	bind
31564	4	7731	5	13	NULL	NULL	NULL	VirE2	GP		bind					VIP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_54_0_187_s_347	11018128	3, T complex associates with cellular factors; VirD2 binds to AtKAP  ( 3a) and cyclophilins ( 3b), VirE2 binds to VIP1 and/or VIP2 ( 3c), the VirD2 NLS region is phosphorylated ( 3d), and AtKAP  may interact with the putative AtKAPbeta ( 3e).	bind
31565	5	7731	5	13	NULL	NULL	NULL	VirE2	GP		bind					VIP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_54_0_187_s_347	11018128	3, T complex associates with cellular factors; VirD2 binds to AtKAP  ( 3a) and cyclophilins ( 3b), VirE2 binds to VIP1 and/or VIP2 ( 3c), the VirD2 NLS region is phosphorylated ( 3d), and AtKAP  may interact with the putative AtKAPbeta ( 3e).	bind
31566	6	7731	5	13	NULL	NULL	NULL	statement 4	Process		is alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_54_0_187_s_347	11018128	3, T complex associates with cellular factors; VirD2 binds to AtKAP  ( 3a) and cyclophilins ( 3b), VirE2 binds to VIP1 and/or VIP2 ( 3c), the VirD2 NLS region is phosphorylated ( 3d), and AtKAP  may interact with the putative AtKAPbeta ( 3e).	bind
31567	7	7731	5	13	NULL	NULL	NULL	VirD2	GP		undergoes			NLS		phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_54_0_187_s_347	11018128	3, T complex associates with cellular factors; VirD2 binds to AtKAP  ( 3a) and cyclophilins ( 3b), VirE2 binds to VIP1 and/or VIP2 ( 3c), the VirD2 NLS region is phosphorylated ( 3d), and AtKAP  may interact with the putative AtKAPbeta ( 3e).	bind
31568	8	7731	5	13	NULL	NULL	NULL	AtKAP	GP		interacts with		may			AtKAPbeta	GP	putative			NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_54_0_187_s_347	11018128	3, T complex associates with cellular factors; VirD2 binds to AtKAP  ( 3a) and cyclophilins ( 3b), VirE2 binds to VIP1 and/or VIP2 ( 3c), the VirD2 NLS region is phosphorylated ( 3d), and AtKAP  may interact with the putative AtKAPbeta ( 3e).	bind
24213	1	7731	6	NULL	NULL	0	NULL	VirE2	NULL		bind	NULL				VIP1	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_54_0_187_s_347	11018128	3, T complex associates with cellular factors; VirD2 binds to AtKAP  ( 3a) and cyclophilins ( 3b), VirE2 binds to VIP1 and/or VIP2 ( 3c), the VirD2 NLS region is phosphorylated ( 3d), and AtKAP  may interact with the putative AtKAPbeta ( 3e).	bind
24214	2	7731	6	NULL	NULL	0	NULL	VirE2	NULL		bind	NULL				VIP2	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_54_0_187_s_347	11018128	3, T complex associates with cellular factors; VirD2 binds to AtKAP  ( 3a) and cyclophilins ( 3b), VirE2 binds to VIP1 and/or VIP2 ( 3c), the VirD2 NLS region is phosphorylated ( 3d), and AtKAP  may interact with the putative AtKAPbeta ( 3e).	bind
24215	3	7731	6	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_54_0_187_s_347	11018128	3, T complex associates with cellular factors; VirD2 binds to AtKAP  ( 3a) and cyclophilins ( 3b), VirE2 binds to VIP1 and/or VIP2 ( 3c), the VirD2 NLS region is phosphorylated ( 3d), and AtKAP  may interact with the putative AtKAPbeta ( 3e).	bind
24216	4	7731	6	NULL	NULL	0	NULL	VirD2	NULL		bind	NULL				AtKAP	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_54_0_187_s_347	11018128	3, T complex associates with cellular factors; VirD2 binds to AtKAP  ( 3a) and cyclophilins ( 3b), VirE2 binds to VIP1 and/or VIP2 ( 3c), the VirD2 NLS region is phosphorylated ( 3d), and AtKAP  may interact with the putative AtKAPbeta ( 3e).	bind
24234	5	7731	6	10	NULL	0	NULL	VirD2	NULL		undergoes	NULL		NLS		phosphorylation	NULL				NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_54_0_187_s_347	11018128	3, T complex associates with cellular factors; VirD2 binds to AtKAP  ( 3a) and cyclophilins ( 3b), VirE2 binds to VIP1 and/or VIP2 ( 3c), the VirD2 NLS region is phosphorylated ( 3d), and AtKAP  may interact with the putative AtKAPbeta ( 3e).	bind
24235	6	7731	6	NULL	NULL	0	NULL	AtKAP	NULL		interact with	NULL	may			AtKAPbeta	NULL	putative			NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_54_0_187_s_347	11018128	3, T complex associates with cellular factors; VirD2 binds to AtKAP  ( 3a) and cyclophilins ( 3b), VirE2 binds to VIP1 and/or VIP2 ( 3c), the VirD2 NLS region is phosphorylated ( 3d), and AtKAP  may interact with the putative AtKAPbeta ( 3e).	bind
46776	7	7731	6	10	NULL	0	NULL	T complex	NULL		associate with	NULL				cellular factors	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_54_0_187_s_347	11018128	3, T complex associates with cellular factors; VirD2 binds to AtKAP  ( 3a) and cyclophilins ( 3b), VirE2 binds to VIP1 and/or VIP2 ( 3c), the VirD2 NLS region is phosphorylated ( 3d), and AtKAP  may interact with the putative AtKAPbeta ( 3e).	bind
46777	8	7731	6	10	NULL	0	NULL	VirD2	NULL		bind	NULL				cyclophilins	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_54_0_187_s_347	11018128	3, T complex associates with cellular factors; VirD2 binds to AtKAP  ( 3a) and cyclophilins ( 3b), VirE2 binds to VIP1 and/or VIP2 ( 3c), the VirD2 NLS region is phosphorylated ( 3d), and AtKAP  may interact with the putative AtKAPbeta ( 3e).	bind
31569	1	7733	5	13	NULL	NULL	NULL				bind			C domain		actin monomer	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_15_10589_s_277	16403731	3, the C domain then binds the actin monomer and, with the WH2 domain, positions it  on the Arp2/3 complex.	bind
24236	1	7733	6	NULL	NULL	0	NULL		NULL		bind	NULL		C domain		actin monomer	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_15_10589_s_277	16403731	3, the C domain then binds the actin monomer and, with the WH2 domain, positions it  on the Arp2/3 complex.	bind
31572	1	7735	5	13	NULL	NULL	NULL	s-FasL	GP		bind					Fas (APO-1/CD95) receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1947_s_17	9846984	3- 5  Both tm- and s-FasL bind to the Fas (APO-1/CD95) receptor and induce apoptosis.	bind
31573	2	7735	5	13	NULL	NULL	NULL	statement 1	Process		induces					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1947_s_17	9846984	3- 5  Both tm- and s-FasL bind to the Fas (APO-1/CD95) receptor and induce apoptosis.	bind
31575	3	7735	5	13	NULL	NULL	NULL	tm-FasL	GP		bind					Fas (APO-1/CD95) receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1947_s_17	9846984	3- 5  Both tm- and s-FasL bind to the Fas (APO-1/CD95) receptor and induce apoptosis.	bind
31577	4	7735	5	13	NULL	NULL	NULL	statement 3	Process		induces					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1947_s_17	9846984	3- 5  Both tm- and s-FasL bind to the Fas (APO-1/CD95) receptor and induce apoptosis.	bind
24237	1	7735	6	NULL	NULL	0	NULL	tm-FasL	NULL		bind	NULL				Fas (APO-1/CD95) receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1947_s_17	9846984	3- 5  Both tm- and s-FasL bind to the Fas (APO-1/CD95) receptor and induce apoptosis.	bind
24554	2	7735	6	NULL	NULL	0	NULL	s-FasL	NULL		bind	NULL				Fas (APO-1/CD95) receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_6_1947_s_17	9846984	3- 5  Both tm- and s-FasL bind to the Fas (APO-1/CD95) receptor and induce apoptosis.	bind
24555	3	7735	6	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL				apoptosis	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_6_1947_s_17	9846984	3- 5  Both tm- and s-FasL bind to the Fas (APO-1/CD95) receptor and induce apoptosis.	bind
24556	4	7735	6	NULL	NULL	0	NULL	statement 2	NULL		induce	NULL				apoptosis	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_6_1947_s_17	9846984	3- 5  Both tm- and s-FasL bind to the Fas (APO-1/CD95) receptor and induce apoptosis.	bind
31578	1	7737	5	13	NULL	NULL	NULL	3-Hydroxyphthaloyl lg	GP		bind					HSV-1 virus particles	Organism				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
31581	2	7737	5	13	NULL	NULL	NULL	3-Hydroxyphthaloyl lg	GP		bind					HSV-2 virus particles	Organism				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
31582	3	7737	5	13	NULL	NULL	NULL	3-Hydroxyphthaloyl lg	GP		bind					HCMV virus particles	Organism				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
31593	4	7737	5	13	NULL	NULL	NULL	HSV-1 virus particles	Organism		bind					anti-glycoprotein E	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
31594	5	7737	5	13	NULL	NULL	NULL	HSV-2 virus particles	Organism		bind					anti-glycoprotein E	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
31595	6	7737	5	13	NULL	NULL	NULL	HCMV virus particles	Organism		bind					anti-glycoprotein E	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
31598	7	7737	5	13	NULL	NULL	NULL	statement 1	Process		inhibits					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
31610	8	7737	5	13	NULL	NULL	NULL	statement 2	Process		inhibits					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
31611	9	7737	5	13	NULL	NULL	NULL	statement 3	Process		inhibits					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
31612	10	7737	5	13	NULL	NULL	NULL	HSV-1 virus particles	Organism		bind					anti-gC monoclonal antibodies	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
31613	11	7737	5	13	NULL	NULL	NULL	HSV-2 virus particles	Organism		bind					anti-gC monoclonal antibodies	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
31614	12	7737	5	13	NULL	NULL	NULL	HCMV virus particles	Organism		bind					anti-gC monoclonal antibodies	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
31615	13	7737	5	13	NULL	NULL	NULL	statement 1	Process		inhibits					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
31616	14	7737	5	13	NULL	NULL	NULL	statement 2	Process		inhibits					statement 11	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
31617	15	7737	5	13	NULL	NULL	NULL	statement 3	Process		inhibits					statement 12	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
24238	1	7737	6	NULL	NULL	0	NULL	Hydroxyphthaloyl lg	NULL		bind	NULL				HSV-1	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
24239	2	7737	6	NULL	NULL	0	NULL	Hydroxyphthaloyl lg	NULL		bind	NULL				HSV-2	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
24240	3	7737	6	NULL	NULL	0	NULL	Hydroxyphthaloyl lg	NULL		bind	NULL				HCMV virus particles	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
24557	4	7737	6	NULL	NULL	0	NULL	HSV-1	NULL		bind	NULL				anti-glycoprotein E monoclonal antibody	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
24558	5	7737	6	NULL	NULL	0	NULL	HSV-2	NULL		bind	NULL				anti-glycoprotein E monoclonal antibody	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
24559	6	7737	6	NULL	NULL	0	NULL	HCMV	NULL		bind	NULL				anti-glycoprotein E monoclonal antibody	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
24560	7	7737	6	NULL	NULL	0	NULL	HSV-1	NULL		bind	NULL				anti-gC monoclonal antibody	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
24561	8	7737	6	NULL	NULL	0	NULL	HSV-2	NULL		bind	NULL				anti-gC monoclonal antibody	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
24562	9	7737	6	NULL	NULL	0	NULL	HCMV	NULL		bind	NULL				anti-gC monoclonal antibody	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
24563	10	7737	6	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
24564	11	7737	6	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
24565	12	7737	6	NULL	NULL	0	NULL	statement 2	NULL		inhibits	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
24566	13	7737	6	NULL	NULL	0	NULL	statement 2	NULL		inhibits	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
24567	14	7737	6	NULL	NULL	0	NULL	statement 3	NULL		inhibits	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
24568	15	7737	6	NULL	NULL	0	NULL	statement 3	NULL		inhibits	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1482_1_327_s_136	11058773	3-Hydroxyphthaloyl  lg binds to HSV-1, HSV-2 and HCMV virus particles and inhibits their binding of anti-glycoprotein E and anti-gC monoclonal antibodies.	bind
31618	1	7738	5	13	NULL	NULL	NULL	p53	GP		bind					AhR	GP			mdr1 promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_7_4819_s_8	11096091	3-MC treatment of the cells increased the levels of p53 and induced p53 binding to the  mdr1 promoter in an AhR.	bind
31619	2	7738	5	13	NULL	NULL	NULL	MC	Chemical	treatment	increases					p53	GP	levels of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_7_4819_s_8	11096091	3-MC treatment of the cells increased the levels of p53 and induced p53 binding to the  mdr1 promoter in an AhR.	bind
31620	3	7738	5	13	NULL	NULL	NULL	statement 2	Process		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_7_4819_s_8	11096091	3-MC treatment of the cells increased the levels of p53 and induced p53 binding to the  mdr1 promoter in an AhR.	bind
24241	1	7738	6	10	NULL	0	NULL	p53	NULL		bind	NULL				AhR	NULL			mdr1 promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_7_4819_s_8	11096091	3-MC treatment of the cells increased the levels of p53 and induced p53 binding to the  mdr1 promoter in an AhR.	bind
24242	2	7738	6	NULL	NULL	0	NULL	MC	NULL	treatment with	increased	NULL				p53	NULL	levels of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_7_4819_s_8	11096091	3-MC treatment of the cells increased the levels of p53 and induced p53 binding to the  mdr1 promoter in an AhR.	bind
24348	3	7738	6	10	NULL	0	NULL	statement 2			induce					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_7_4819_s_8	11096091	3-MC treatment of the cells increased the levels of p53 and induced p53 binding to the  mdr1 promoter in an AhR.	bind
31621	1	7739	5	13	NULL	NULL	NULL	3-Methyl- cis,cis-muconate	Chemical		bind		high affinity			muconate cycloisomerase	GP	P. putida			NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_9_3290_s_229	9726873	3-Methyl- cis,cis-muconate binds to the  P. putida muconate cycloisomerase with a very high affinity and is converted with a moderate  kcat (Table  3), suggesting that steric problems should be of limited importance.	bind
24349	1	7739	6	NULL	NULL	0	NULL	3-Methyl- cis,cis-muconate	NULL		bind	NULL	high affinity			muconate cycloisomerase	NULL	P. putida			NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_9_3290_s_229	9726873	3-Methyl- cis,cis-muconate binds to the  P. putida muconate cycloisomerase with a very high affinity and is converted with a moderate  kcat (Table  3), suggesting that steric problems should be of limited importance.	bind
31629	1	7740	5	13	NULL	NULL	NULL	3-OxoC66HSL	Chemical		bind					LuxR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_6_1617_s_18	11872713	3-OxoC66HSL then binds to the transcriptional activator LuxR, and the resulting LuxR/3-oxo-C6-HSL complex triggers transcription of the luminescence ( lux) operon, resulting in the emission of light ( 39).	bind
31630	2	7740	5	13	NULL	NULL	NULL	statement 1	Process		forms					LuxR/3-oxo-C6-HSL complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_6_1617_s_18	11872713	3-OxoC66HSL then binds to the transcriptional activator LuxR, and the resulting LuxR/3-oxo-C6-HSL complex triggers transcription of the luminescence ( lux) operon, resulting in the emission of light ( 39).	bind
31631	3	7740	5	13	NULL	NULL	NULL	LuxR	GP		is a type of					transcriptional activator	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_6_1617_s_18	11872713	3-OxoC66HSL then binds to the transcriptional activator LuxR, and the resulting LuxR/3-oxo-C6-HSL complex triggers transcription of the luminescence ( lux) operon, resulting in the emission of light ( 39).	bind
31632	4	7740	5	13	NULL	NULL	NULL	LuxR/3-oxo-C6-HSL complex	GP		triggers							transcription of		 lux operon	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_6_1617_s_18	11872713	3-OxoC66HSL then binds to the transcriptional activator LuxR, and the resulting LuxR/3-oxo-C6-HSL complex triggers transcription of the luminescence ( lux) operon, resulting in the emission of light ( 39).	bind
31633	5	7740	5	13	NULL	NULL	NULL	statement 4	Process		results in					light		emission of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_6_1617_s_18	11872713	3-OxoC66HSL then binds to the transcriptional activator LuxR, and the resulting LuxR/3-oxo-C6-HSL complex triggers transcription of the luminescence ( lux) operon, resulting in the emission of light ( 39).	bind
46778	6	7740	5	13	NULL	NULL	NULL	lux operon	NucleicAcid		is 					luminescence operon	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_6_1617_s_18	11872713	3-OxoC66HSL then binds to the transcriptional activator LuxR, and the resulting LuxR/3-oxo-C6-HSL complex triggers transcription of the luminescence ( lux) operon, resulting in the emission of light ( 39).	bind
24350	1	7740	6	10	NULL	0	NULL	3-OxoC66HSL	NULL		bind	NULL				LuxR 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_6_1617_s_18	11872713	3-OxoC66HSL then binds to the transcriptional activator LuxR, and the resulting LuxR/3-oxo-C6-HSL complex triggers transcription of the luminescence ( lux) operon, resulting in the emission of light ( 39).	bind
24351	2	7740	6	NULL	NULL	0	NULL	statement 1	NULL		forms 	NULL				LuxR/3-oxo-C6-HSL complex 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_6_1617_s_18	11872713	3-OxoC66HSL then binds to the transcriptional activator LuxR, and the resulting LuxR/3-oxo-C6-HSL complex triggers transcription of the luminescence ( lux) operon, resulting in the emission of light ( 39).	bind
46779	3	7740	6	10	NULL	0	NULL	LuxR	NULL		is a type of	NULL				transcriptional activator	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_6_1617_s_18	11872713	3-OxoC66HSL then binds to the transcriptional activator LuxR, and the resulting LuxR/3-oxo-C6-HSL complex triggers transcription of the luminescence ( lux) operon, resulting in the emission of light ( 39).	bind
46780	4	7740	6	10	NULL	0	NULL	LuxR/3-oxo-C6-HSL complex	NULL		triggers	NULL					NULL	transcription of		lux operon	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_6_1617_s_18	11872713	3-OxoC66HSL then binds to the transcriptional activator LuxR, and the resulting LuxR/3-oxo-C6-HSL complex triggers transcription of the luminescence ( lux) operon, resulting in the emission of light ( 39).	bind
46781	5	7740	6	10	NULL	0	NULL	statement 4	NULL		results in	NULL				emission of light	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_6_1617_s_18	11872713	3-OxoC66HSL then binds to the transcriptional activator LuxR, and the resulting LuxR/3-oxo-C6-HSL complex triggers transcription of the luminescence ( lux) operon, resulting in the emission of light ( 39).	bind
46782	6	7740	6	10	NULL	0	NULL	lux operon	NULL		is	NULL				luminescence operon	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_6_1617_s_18	11872713	3-OxoC66HSL then binds to the transcriptional activator LuxR, and the resulting LuxR/3-oxo-C6-HSL complex triggers transcription of the luminescence ( lux) operon, resulting in the emission of light ( 39).	bind
31634	1	7741	5	13	NULL	NULL	NULL	3-oxoC88HSL	Chemical		bind		tightly			TraR	GP	active			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_19_5212_s_66	11013223	3-oxoC88HSL is bound very tightly to the active form of TraR; in previous studies prolonged dialysis was required to remove the ligand ( Zhu and Winans, 1999).	bind
24352	1	7741	6	NULL	NULL	0	NULL	3-oxoC88HSL	NULL		bind	NULL	very tightly			TraR	NULL	active form of			NULL		0	NULL	NULL	NULL	gw60_embo_19_19_5212_s_66	11013223	3-oxoC88HSL is bound very tightly to the active form of TraR; in previous studies prolonged dialysis was required to remove the ligand ( Zhu and Winans, 1999).	bind
31635	1	7742	5	13	NULL	NULL	NULL	PDK1	GP		is					3-Phosphoinositide-dependent protein kinase 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_253_s_5	11057898	3-Phosphoinositide-dependent protein kinase 1 (PDK1) phosphorylates and activates the p70 S6 kinase  in vivo and  in vitro.	bind
31636	2	7742	5	13	NULL	NULL	NULL	PDK1	GP		phosphorylates					p70 S6 kinase	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_cell_103_2_253_s_5	11057898	3-Phosphoinositide-dependent protein kinase 1 (PDK1) phosphorylates and activates the p70 S6 kinase  in vivo and  in vitro.	bind
31637	3	7742	5	13	NULL	NULL	NULL	statement 2	Process		activates					p70 S6 kinase	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_cell_103_2_253_s_5	11057898	3-Phosphoinositide-dependent protein kinase 1 (PDK1) phosphorylates and activates the p70 S6 kinase  in vivo and  in vitro.	bind
31638	4	7742	5	13	NULL	NULL	NULL	PDK1	GP		phosphorylates					p70 S6 kinase	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cell_103_2_253_s_5	11057898	3-Phosphoinositide-dependent protein kinase 1 (PDK1) phosphorylates and activates the p70 S6 kinase  in vivo and  in vitro.	bind
31639	5	7742	5	13	NULL	NULL	NULL	statement 4	Process		activates					p70 S6 kinase	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cell_103_2_253_s_5	11057898	3-Phosphoinositide-dependent protein kinase 1 (PDK1) phosphorylates and activates the p70 S6 kinase  in vivo and  in vitro.	bind
24353	1	7742	6	NULL	NULL	0	NULL	PDK1	NULL		is	NULL				Phosphoinositide-dependent protein kinase 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_103_2_253_s_5	11057898	3-Phosphoinositide-dependent protein kinase 1 (PDK1) phosphorylates and activates the p70 S6 kinase  in vivo and  in vitro.	bind
24354	2	7742	6	NULL	NULL	0	NULL	PDK1	NULL		phosphorylates	NULL				p70 S6 kinase	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_cell_103_2_253_s_5	11057898	3-Phosphoinositide-dependent protein kinase 1 (PDK1) phosphorylates and activates the p70 S6 kinase  in vivo and  in vitro.	bind
24355	3	7742	6	10	NULL	0	NULL	statement 2			activates					p70 S6 kinase					NULL	in vivo	NULL	NULL	NULL	NULL	gw60_cell_103_2_253_s_5	11057898	3-Phosphoinositide-dependent protein kinase 1 (PDK1) phosphorylates and activates the p70 S6 kinase  in vivo and  in vitro.	bind
46783	4	7742	6	10	NULL	0	NULL	PDK1	NULL		phosphorylates	NULL				p70 S6 kinase	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_cell_103_2_253_s_5	11057898	3-Phosphoinositide-dependent protein kinase 1 (PDK1) phosphorylates and activates the p70 S6 kinase  in vivo and  in vitro.	bind
46784	5	7742	6	10	NULL	0	NULL	statement 4			activates					p70 S6 kinase					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cell_103_2_253_s_5	11057898	3-Phosphoinositide-dependent protein kinase 1 (PDK1) phosphorylates and activates the p70 S6 kinase  in vivo and  in vitro.	bind
31640	1	7745	5	13	NULL	NULL	NULL	DNA ligase IV	GP		bind			motif located between BRCT domains		XRCC4	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1653_s_323	11292837	30       Grawunder,U., Zimmer,D. and Lieber,M.R. (1998) DNA ligase IV binds to XRCC4 via a motif located between rather than within its BRCT domains.	bind
24356	1	7745	6	NULL	NULL	0	NULL	DNA ligase IV	NULL		bind	NULL		motif located between BRCT domains		XRCC4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1653_s_323	11292837	30       Grawunder,U., Zimmer,D. and Lieber,M.R. (1998) DNA ligase IV binds to XRCC4 via a motif located between rather than within its BRCT domains.	bind
31641	1	7746	5	13	NULL	NULL	NULL	hnRNP L	GP		bind									cis-acting RNA sequence element	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_823_s_306	11809897	30       Liu,X. and Mertz,J.E. (1995) hnRNP L binds a  cis-acting RNA sequence element that enables intron-independent gene expression.	bind
31642	3	7746	5	13	NULL	NULL	NULL				enables				cis-acting RNA sequence element	statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_823_s_306	11809897	30       Liu,X. and Mertz,J.E. (1995) hnRNP L binds a  cis-acting RNA sequence element that enables intron-independent gene expression.	bind
46785	2	7746	5	13	NULL	NULL	NULL	gene expression	Process		is independent of					intron	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_823_s_306	11809897	30       Liu,X. and Mertz,J.E. (1995) hnRNP L binds a  cis-acting RNA sequence element that enables intron-independent gene expression.	bind
24357	1	7746	6	10	NULL	0	NULL	hnRNP L	NULL		bind	NULL					NULL			cis-acting RNA sequence element	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_823_s_306	11809897	30       Liu,X. and Mertz,J.E. (1995) hnRNP L binds a  cis-acting RNA sequence element that enables intron-independent gene expression.	bind
24358	3	7746	6	10	NULL	0	NULL		NULL		enables	NULL			cis-acting RNA sequence element	statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_823_s_306	11809897	30       Liu,X. and Mertz,J.E. (1995) hnRNP L binds a  cis-acting RNA sequence element that enables intron-independent gene expression.	bind
46786	2	7746	6	10	NULL	0	NULL	gene expression	NULL		is independent of	NULL				intron	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_823_s_306	11809897	30       Liu,X. and Mertz,J.E. (1995) hnRNP L binds a  cis-acting RNA sequence element that enables intron-independent gene expression.	bind
31643	1	7747	5	13	NULL	NULL	NULL	transcription factor	GP		bind					HER2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_23_4873_s_268	11726697	30       Noonberg,S.B., Scott,G.K., Hunt,C.A., Hogan,M.E. and Benz,C.C. (1994) Inhibition of transcription factor binding to the HER2 promoter by triplex-forming oligodeoxyribonucleotides.	bind
31644	3	7747	5	13	NULL	NULL	NULL	statement 2	Process		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_23_4873_s_268	11726697	30       Noonberg,S.B., Scott,G.K., Hunt,C.A., Hogan,M.E. and Benz,C.C. (1994) Inhibition of transcription factor binding to the HER2 promoter by triplex-forming oligodeoxyribonucleotides.	bind
46787	2	7747	5	13	NULL	NULL	NULL	oligodeoxyribonucleotides	NucleicAcid		forms					triplex	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_23_4873_s_268	11726697	30       Noonberg,S.B., Scott,G.K., Hunt,C.A., Hogan,M.E. and Benz,C.C. (1994) Inhibition of transcription factor binding to the HER2 promoter by triplex-forming oligodeoxyribonucleotides.	bind
24359	1	7747	6	NULL	NULL	0	NULL	transcription factor	NULL		bind	NULL				HER2	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_23_4873_s_268	11726697	30       Noonberg,S.B., Scott,G.K., Hunt,C.A., Hogan,M.E. and Benz,C.C. (1994) Inhibition of transcription factor binding to the HER2 promoter by triplex-forming oligodeoxyribonucleotides.	bind
24360	3	7747	6	10	NULL	0	NULL	statement 2	NULL		inhibits	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_23_4873_s_268	11726697	30       Noonberg,S.B., Scott,G.K., Hunt,C.A., Hogan,M.E. and Benz,C.C. (1994) Inhibition of transcription factor binding to the HER2 promoter by triplex-forming oligodeoxyribonucleotides.	bind
46788	2	7747	6	10	NULL	0	NULL	oligodeoxyribonucleotides	NULL		forms	NULL				triplex	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_23_4873_s_268	11726697	30       Noonberg,S.B., Scott,G.K., Hunt,C.A., Hogan,M.E. and Benz,C.C. (1994) Inhibition of transcription factor binding to the HER2 promoter by triplex-forming oligodeoxyribonucleotides.	bind
31645	1	7748	5	13	NULL	NULL	NULL	Vav	GP		bind					hnRNP	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1300_s_348	11238996	30       Romero,F., Germani,A., Puvion,E., Camonis,J., Varin-Blank,N., Gisselbrecht,S. and Fischer,S. (1998) Vav binding to heterogeneous nuclear ribonucleoprotein (hnRNP) C. Evidence for Vav-hnRNP interactions in an RNA-dependent manner.	bind
31654	2	7748	5	13	NULL	NULL	NULL	hnRNP	GP		is					heterogeneous nuclear ribonucleoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1300_s_348	11238996	30       Romero,F., Germani,A., Puvion,E., Camonis,J., Varin-Blank,N., Gisselbrecht,S. and Fischer,S. (1998) Vav binding to heterogeneous nuclear ribonucleoprotein (hnRNP) C. Evidence for Vav-hnRNP interactions in an RNA-dependent manner.	bind
31656	3	7748	5	13	NULL	NULL	NULL	statement 1	Process		is dependent on					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1300_s_348	11238996	30       Romero,F., Germani,A., Puvion,E., Camonis,J., Varin-Blank,N., Gisselbrecht,S. and Fischer,S. (1998) Vav binding to heterogeneous nuclear ribonucleoprotein (hnRNP) C. Evidence for Vav-hnRNP interactions in an RNA-dependent manner.	bind
24361	1	7748	6	NULL	NULL	0	NULL	Vav	NULL		bind	NULL				hnRNP	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1300_s_348	11238996	30       Romero,F., Germani,A., Puvion,E., Camonis,J., Varin-Blank,N., Gisselbrecht,S. and Fischer,S. (1998) Vav binding to heterogeneous nuclear ribonucleoprotein (hnRNP) C. Evidence for Vav-hnRNP interactions in an RNA-dependent manner.	bind
24362	2	7748	6	NULL	NULL	0	NULL	hnRNP	NULL		is	NULL				heterogeneous nuclear ribonucleoprotein	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1300_s_348	11238996	30       Romero,F., Germani,A., Puvion,E., Camonis,J., Varin-Blank,N., Gisselbrecht,S. and Fischer,S. (1998) Vav binding to heterogeneous nuclear ribonucleoprotein (hnRNP) C. Evidence for Vav-hnRNP interactions in an RNA-dependent manner.	bind
24363	3	7748	6	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_6_1300_s_348	11238996	30       Romero,F., Germani,A., Puvion,E., Camonis,J., Varin-Blank,N., Gisselbrecht,S. and Fischer,S. (1998) Vav binding to heterogeneous nuclear ribonucleoprotein (hnRNP) C. Evidence for Vav-hnRNP interactions in an RNA-dependent manner.	bind
31658	1	7749	5	13	NULL	NULL	NULL	nucleosomal DNA	NucleicAcid		regulates					hat1 acetyltransferase	GP	human	core-histone binding subunit		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_629_s_333	11160883	30       Verreault,A., Kaufman,P.D., Kobayashi,R. and Stillman,B. (1998) Nucleosomal DNA regulates the core-histone binding subunit of the human hat1 acetyltransferase.	bind
24364	1	7749	6	NULL	NULL	0	NULL	Nucleosomal DNA	NULL		regulates	NULL				Hat1 acetyltransferase	NULL	human	core-histone binding subunit		NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_629_s_333	11160883	30       Verreault,A., Kaufman,P.D., Kobayashi,R. and Stillman,B. (1998) Nucleosomal DNA regulates the core-histone binding subunit of the human hat1 acetyltransferase.	bind
31659	1	7750	5	13	NULL	NULL	NULL	FGF-1	GP		bind					FGFR-2 IIIb	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_3_207_s_218	10926871	30  Both FGF-1 and FGF-7 can bind to FGFR-2 IIIb. 31  It is tempting to speculate that different members of the FGF gene family exert similar biological functions, with regard to the regulation of the branching morphogenesis of different embryonic structures.	bind
31660	2	7750	5	13	NULL	NULL	NULL	FGF-7	GP		bind					FGFR-2 IIIb	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_3_207_s_218	10926871	30  Both FGF-1 and FGF-7 can bind to FGFR-2 IIIb. 31  It is tempting to speculate that different members of the FGF gene family exert similar biological functions, with regard to the regulation of the branching morphogenesis of different embryonic structures.	bind
46789	3	7750	5	13	NULL	NULL	NULL	FGF gene family members	GP		play a role in					branching morphogenesis of different embryonic structures	Process	regulation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_3_207_s_218	10926871	30  Both FGF-1 and FGF-7 can bind to FGFR-2 IIIb. 31  It is tempting to speculate that different members of the FGF gene family exert similar biological functions, with regard to the regulation of the branching morphogenesis of different embryonic structures.	bind
24365	1	7750	6	NULL	NULL	0	NULL	FGF-1	NULL		bind	NULL				FGFR-2 IIIb	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_3_207_s_218	10926871	30  Both FGF-1 and FGF-7 can bind to FGFR-2 IIIb. 31  It is tempting to speculate that different members of the FGF gene family exert similar biological functions, with regard to the regulation of the branching morphogenesis of different embryonic structures.	bind
24366	2	7750	6	NULL	NULL	0	NULL	FGF-7	NULL		bind	NULL				FGFR-2 IIIb	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_3_207_s_218	10926871	30  Both FGF-1 and FGF-7 can bind to FGFR-2 IIIb. 31  It is tempting to speculate that different members of the FGF gene family exert similar biological functions, with regard to the regulation of the branching morphogenesis of different embryonic structures.	bind
24367	3	7750	6	NULL	NULL	0	NULL	FGF gene family members	NULL		plays a role in	NULL				branching morphogenesis of embryonic structures	NULL	regulation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_3_207_s_218	10926871	30  Both FGF-1 and FGF-7 can bind to FGFR-2 IIIb. 31  It is tempting to speculate that different members of the FGF gene family exert similar biological functions, with regard to the regulation of the branching morphogenesis of different embryonic structures.	bind
31662	1	7751	5	13	NULL	NULL	NULL	substance P	GP		inhibits					endothelin-1	GP	 binding of			NULL	rat cardiac membranes in vitro	NULL	NULL	NULL	NULL	gw60_circulation_102_14_1617_s_136	11015337	30  In rat cardiac membranes in vitro, specific binding of endothelin-1 can be inhibited by substance P.	bind
24368	1	7751	6	NULL	NULL	0	NULL	substance P	NULL		inhibits	NULL				endothelin-1	NULL	binding of			NULL	rat cardiac membranes in vitro	0	NULL	NULL	NULL	gw60_circulation_102_14_1617_s_136	11015337	30  In rat cardiac membranes in vitro, specific binding of endothelin-1 can be inhibited by substance P.	bind
31666	1	7752	5	13	NULL	NULL	NULL	HK	GP		bind					glycoprotein Ib/IX complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2245_s_144	10479669	30  Recently, we 31  and others 32  have shown that HK binds to the glycoprotein Ib/IX complex.	bind
24369	1	7752	6	NULL	NULL	0	NULL	HK	NULL		bind	NULL				glycoprotein Ib/IX complex	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2245_s_144	10479669	30  Recently, we 31  and others 32  have shown that HK binds to the glycoprotein Ib/IX complex.	bind
31669	1	7753	5	13	NULL	NULL	NULL	WDR1 proteins	GP	yeast	bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_5_460_s_170	11249868	30  The highly homologous yeast and slime mold WDR1 proteins bind actin, which suggests that WDR1 protein may be an actin binding protein as well.	bind
31670	2	7753	5	13	NULL	NULL	NULL	WDR1 proteins	GP	slime mold	bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_5_460_s_170	11249868	30  The highly homologous yeast and slime mold WDR1 proteins bind actin, which suggests that WDR1 protein may be an actin binding protein as well.	bind
31672	3	7753	5	13	NULL	NULL	NULL	WDR1 proteins	GP	yeast	is homologus to		highly			WDR1 proteins	GP	slime mold			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_5_460_s_170	11249868	30  The highly homologous yeast and slime mold WDR1 proteins bind actin, which suggests that WDR1 protein may be an actin binding protein as well.	bind
24370	1	7753	6	NULL	NULL	0	NULL	WDR1 protein	NULL	yeast	bind	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_88_5_460_s_170	11249868	30  The highly homologous yeast and slime mold WDR1 proteins bind actin, which suggests that WDR1 protein may be an actin binding protein as well.	bind
24371	2	7753	6	NULL	NULL	0	NULL	WDR1 protein	NULL	slime mold	bind	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_88_5_460_s_170	11249868	30  The highly homologous yeast and slime mold WDR1 proteins bind actin, which suggests that WDR1 protein may be an actin binding protein as well.	bind
46823	3	7753	6	10	NULL	0	NULL	WDR1 proteins	NULL	yeast	is homologous to	NULL				WDR1 proteins	NULL	slime mold			NULL		0	NULL	NULL	NULL	gw60_circulationres_88_5_460_s_170	11249868	30  The highly homologous yeast and slime mold WDR1 proteins bind actin, which suggests that WDR1 protein may be an actin binding protein as well.	bind
31674	1	7754	5	13	NULL	NULL	NULL	Src	GP		does not undergo					palmitylation	Process				NULL	resting rat platelets	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3278_s_202	9409323	30 - 32 The fact that Src is not palmitylated, but a portion is still Triton-insoluble in resting rat platelets, suggests that Src in resting rat platelets is not bound to the same Triton-insoluble macromolecules as the other Src family members.	bind
31683	2	7754	5	13	NULL	NULL	NULL	Src	GP		does not bind					macromolecules	CellComponent	Triton-insoluble			NULL	resting rat platelets	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3278_s_202	9409323	30 - 32 The fact that Src is not palmitylated, but a portion is still Triton-insoluble in resting rat platelets, suggests that Src in resting rat platelets is not bound to the same Triton-insoluble macromolecules as the other Src family members.	bind
24372	1	7754	6	NULL	NULL	0	NULL	Src	NULL		does not bind	NULL				macromolecules	NULL	triton-insoluble			NULL	resting rat platelets	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3278_s_202	9409323	30 - 32 The fact that Src is not palmitylated, but a portion is still Triton-insoluble in resting rat platelets, suggests that Src in resting rat platelets is not bound to the same Triton-insoluble macromolecules as the other Src family members.	bind
24373	2	7754	6	10	NULL	0	NULL	src			does not undergo					palmitylation					NULL	resting rat platelets	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3278_s_202	9409323	30 - 32 The fact that Src is not palmitylated, but a portion is still Triton-insoluble in resting rat platelets, suggests that Src in resting rat platelets is not bound to the same Triton-insoluble macromolecules as the other Src family members.	bind
31684	1	7755	5	13	NULL	NULL	NULL	F1 	GP		bind					F0	GP	mutant			NULL	in membranes	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_23797_s_140	15849185	30 - 80% of the F1 ATPase activity was inhibited when F1 was bound to mutant F0 in membranes, as estimated from the increase in ATPase activity after detachment from the membranes.	bind
31685	2	7755	5	13	NULL	NULL	NULL	statement 1	Process		inhibits					F1 ATPase activity	GP				NULL	membranes	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_23797_s_140	15849185	30 - 80% of the F1 ATPase activity was inhibited when F1 was bound to mutant F0 in membranes, as estimated from the increase in ATPase activity after detachment from the membranes.	bind
24374	1	7755	6	NULL	NULL	0	NULL	F1	NULL		bind	NULL				F0	NULL	mutant			NULL	membranes	0	NULL	NULL	NULL	gw70_jbiolchem_280_25_23797_s_140	15849185	30 - 80% of the F1 ATPase activity was inhibited when F1 was bound to mutant F0 in membranes, as estimated from the increase in ATPase activity after detachment from the membranes.	bind
24375	2	7755	6	10	NULL	0	NULL	statement 1			inhibits					F1 ATPase activity					NULL	membranes	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_23797_s_140	15849185	30 - 80% of the F1 ATPase activity was inhibited when F1 was bound to mutant F0 in membranes, as estimated from the increase in ATPase activity after detachment from the membranes.	bind
31686	1	7757	5	13	NULL	NULL	NULL	NHE-1	GP		bind		strongly	cytoplasmic domain		calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_8_824_s_228	9776729	30 31 32  Binding experiments with calmodulin-Sepharose, as well as fluorescence measurements with dansylated calmodulin, revealed that the NHE-1 cytoplasmic domain strongly binds calmodulin in a Ca2+-dependent manner.	bind
31687	2	7757	5	13	NULL	NULL	NULL	statement 1	Process		is dependent on					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_8_824_s_228	9776729	30 31 32  Binding experiments with calmodulin-Sepharose, as well as fluorescence measurements with dansylated calmodulin, revealed that the NHE-1 cytoplasmic domain strongly binds calmodulin in a Ca2+-dependent manner.	bind
24376	1	7757	6	NULL	NULL	0	NULL	NHE-1	NULL		bind	NULL	strongly	cytoplasmic domain		calmodulin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_8_824_s_228	9776729	30 31 32  Binding experiments with calmodulin-Sepharose, as well as fluorescence measurements with dansylated calmodulin, revealed that the NHE-1 cytoplasmic domain strongly binds calmodulin in a Ca2+-dependent manner.	bind
24377	2	7757	6	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				Ca2+	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_8_824_s_228	9776729	30 31 32  Binding experiments with calmodulin-Sepharose, as well as fluorescence measurements with dansylated calmodulin, revealed that the NHE-1 cytoplasmic domain strongly binds calmodulin in a Ca2+-dependent manner.	bind
31690	1	7758	5	13	NULL	NULL	NULL	tie-2	GP		contains					tie-2	GP			GATA consensus sequences in promoter	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_7_749_s_197	12637368	30 Although no direct proof for a direct interaction between GATA-4 and Ets-1 or Ets-2 is available, the notion that several genes involved in vascular biology have both GATA and Ets consensus sequences in their promoters (eg, in the tie-2 31 and Flk-1 32 genes) and proven cooperative binding between Ets-1 and Ets-2 with GATA-3 33 may give further clues for the mode of action by which Ets transcription factors influence coronary development.	bind
31691	2	7758	5	13	NULL	NULL	NULL	tie-2	GP		contains					tie-2	GP			Ets consensus sequences in promoter	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_7_749_s_197	12637368	30 Although no direct proof for a direct interaction between GATA-4 and Ets-1 or Ets-2 is available, the notion that several genes involved in vascular biology have both GATA and Ets consensus sequences in their promoters (eg, in the tie-2 31 and Flk-1 32 genes) and proven cooperative binding between Ets-1 and Ets-2 with GATA-3 33 may give further clues for the mode of action by which Ets transcription factors influence coronary development.	bind
31692	3	7758	5	13	NULL	NULL	NULL	Flk-1	GP		contains					Flk-1	GP			GATA consensus sequences in promoter	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_7_749_s_197	12637368	30 Although no direct proof for a direct interaction between GATA-4 and Ets-1 or Ets-2 is available, the notion that several genes involved in vascular biology have both GATA and Ets consensus sequences in their promoters (eg, in the tie-2 31 and Flk-1 32 genes) and proven cooperative binding between Ets-1 and Ets-2 with GATA-3 33 may give further clues for the mode of action by which Ets transcription factors influence coronary development.	bind
31693	4	7758	5	13	NULL	NULL	NULL	Flk-1	GP		contains					Flk-1	GP			Ets consensus sequences in promoter	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_7_749_s_197	12637368	30 Although no direct proof for a direct interaction between GATA-4 and Ets-1 or Ets-2 is available, the notion that several genes involved in vascular biology have both GATA and Ets consensus sequences in their promoters (eg, in the tie-2 31 and Flk-1 32 genes) and proven cooperative binding between Ets-1 and Ets-2 with GATA-3 33 may give further clues for the mode of action by which Ets transcription factors influence coronary development.	bind
31694	5	7758	5	13	NULL	NULL	NULL	Ets-1	GP		bind					GATA-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_7_749_s_197	12637368	30 Although no direct proof for a direct interaction between GATA-4 and Ets-1 or Ets-2 is available, the notion that several genes involved in vascular biology have both GATA and Ets consensus sequences in their promoters (eg, in the tie-2 31 and Flk-1 32 genes) and proven cooperative binding between Ets-1 and Ets-2 with GATA-3 33 may give further clues for the mode of action by which Ets transcription factors influence coronary development.	bind
31695	6	7758	5	13	NULL	NULL	NULL	Ets-2	GP		bind					GATA-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_7_749_s_197	12637368	30 Although no direct proof for a direct interaction between GATA-4 and Ets-1 or Ets-2 is available, the notion that several genes involved in vascular biology have both GATA and Ets consensus sequences in their promoters (eg, in the tie-2 31 and Flk-1 32 genes) and proven cooperative binding between Ets-1 and Ets-2 with GATA-3 33 may give further clues for the mode of action by which Ets transcription factors influence coronary development.	bind
31696	7	7758	5	13	NULL	NULL	NULL	statement 5	Process		cooperative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_7_749_s_197	12637368	30 Although no direct proof for a direct interaction between GATA-4 and Ets-1 or Ets-2 is available, the notion that several genes involved in vascular biology have both GATA and Ets consensus sequences in their promoters (eg, in the tie-2 31 and Flk-1 32 genes) and proven cooperative binding between Ets-1 and Ets-2 with GATA-3 33 may give further clues for the mode of action by which Ets transcription factors influence coronary development.	bind
31697	8	7758	5	13	NULL	NULL	NULL	Ets transcription factors	GP		influence					coronary development	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_7_749_s_197	12637368	30 Although no direct proof for a direct interaction between GATA-4 and Ets-1 or Ets-2 is available, the notion that several genes involved in vascular biology have both GATA and Ets consensus sequences in their promoters (eg, in the tie-2 31 and Flk-1 32 genes) and proven cooperative binding between Ets-1 and Ets-2 with GATA-3 33 may give further clues for the mode of action by which Ets transcription factors influence coronary development.	bind
24378	1	7758	6	NULL	NULL	0	NULL	Ets-1	NULL		bind	NULL				GATA-3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_7_749_s_197	12637368	30 Although no direct proof for a direct interaction between GATA-4 and Ets-1 or Ets-2 is available, the notion that several genes involved in vascular biology have both GATA and Ets consensus sequences in their promoters (eg, in the tie-2 31 and Flk-1 32 genes) and proven cooperative binding between Ets-1 and Ets-2 with GATA-3 33 may give further clues for the mode of action by which Ets transcription factors influence coronary development.	bind
24379	2	7758	6	NULL	NULL	0	NULL	Ets-2	NULL		bind	NULL				GATA-3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_7_749_s_197	12637368	30 Although no direct proof for a direct interaction between GATA-4 and Ets-1 or Ets-2 is available, the notion that several genes involved in vascular biology have both GATA and Ets consensus sequences in their promoters (eg, in the tie-2 31 and Flk-1 32 genes) and proven cooperative binding between Ets-1 and Ets-2 with GATA-3 33 may give further clues for the mode of action by which Ets transcription factors influence coronary development.	bind
24380	3	7758	6	NULL	NULL	0	NULL	statement 1	NULL		acts in cooperation with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_7_749_s_197	12637368	30 Although no direct proof for a direct interaction between GATA-4 and Ets-1 or Ets-2 is available, the notion that several genes involved in vascular biology have both GATA and Ets consensus sequences in their promoters (eg, in the tie-2 31 and Flk-1 32 genes) and proven cooperative binding between Ets-1 and Ets-2 with GATA-3 33 may give further clues for the mode of action by which Ets transcription factors influence coronary development.	bind
24381	4	7758	6	NULL	NULL	0	NULL	Ets transcription factors	NULL		influence	NULL				coronary development	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_7_749_s_197	12637368	30 Although no direct proof for a direct interaction between GATA-4 and Ets-1 or Ets-2 is available, the notion that several genes involved in vascular biology have both GATA and Ets consensus sequences in their promoters (eg, in the tie-2 31 and Flk-1 32 genes) and proven cooperative binding between Ets-1 and Ets-2 with GATA-3 33 may give further clues for the mode of action by which Ets transcription factors influence coronary development.	bind
31698	1	7759	5	13	NULL	NULL	NULL	PTX3	GP		bind					fibroblast growth factor-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_16_2349_s_103	15477419	30 Finally, recent results indicate that PTX3 binds and inactivates fibroblast growth factor-2.	bind
31699	2	7759	5	13	NULL	NULL	NULL	statement 1	Process		inactivates					fibroblast growth factor-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_16_2349_s_103	15477419	30 Finally, recent results indicate that PTX3 binds and inactivates fibroblast growth factor-2.	bind
24382	1	7759	6	NULL	NULL	0	NULL	PTX3	NULL		bind	NULL				fibroblast growth factor-2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_110_16_2349_s_103	15477419	30 Finally, recent results indicate that PTX3 binds and inactivates fibroblast growth factor-2.	bind
24383	2	7759	6	10	NULL	0	NULL	statement 1			inactivates					fibroblast growth factor-2					NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_16_2349_s_103	15477419	30 Finally, recent results indicate that PTX3 binds and inactivates fibroblast growth factor-2.	bind
31700	1	7760	5	13	NULL	NULL	NULL	p65	GP		bind					DNA	NucleicAcid				NULL	LPS-treated cells	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_91	15718493	30 However, no p65-DNA binding was observed in the nuclear extracts of the cells treated with mmLDL, whereas the LPS-treated cells showed the expected p65-DNA binding ( Figure 1B).	bind
31701	2	7760	5	13	NULL	NULL	NULL	p65	GP		does not bind					DNA	NucleicAcid				NULL	nuclear extracts of cells treated with mmLDL	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_91	15718493	30 However, no p65-DNA binding was observed in the nuclear extracts of the cells treated with mmLDL, whereas the LPS-treated cells showed the expected p65-DNA binding ( Figure 1B).	bind
24384	1	7760	6	NULL	NULL	0	NULL	p65	NULL		does not bind	NULL				DNA	NULL				NULL	nuclear extracts of the cells treated with mmLDL	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_91	15718493	30 However, no p65-DNA binding was observed in the nuclear extracts of the cells treated with mmLDL, whereas the LPS-treated cells showed the expected p65-DNA binding ( Figure 1B).	bind
24385	2	7760	6	NULL	NULL	0	NULL	p65	NULL		bind	NULL				DNA	NULL				NULL	nuclear extracts of the cells treated with LPS	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1213_s_91	15718493	30 However, no p65-DNA binding was observed in the nuclear extracts of the cells treated with mmLDL, whereas the LPS-treated cells showed the expected p65-DNA binding ( Figure 1B).	bind
31702	1	7761	5	13	NULL	NULL	NULL	NO	Chemical		supress		may			PKG	GP	expression of			NULL	VSMCs	NULL	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_220	11884369	30 In VSMCs, NO may suppress PKG expression by directly inhibiting Sp1 transcription factor binding activity to the PKG promoter, an observation supported by the direct effect of NO on Sp1 binding in nuclear extracts of cells pretreated with NO donors.	bind
31703	2	7761	5	13	NULL	NULL	NULL	Sp1	GP		bind					PKG	GP			promoter	NULL	VSMCs	NULL	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_220	11884369	30 In VSMCs, NO may suppress PKG expression by directly inhibiting Sp1 transcription factor binding activity to the PKG promoter, an observation supported by the direct effect of NO on Sp1 binding in nuclear extracts of cells pretreated with NO donors.	bind
31704	3	7761	5	13	NULL	NULL	NULL	Sp1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_220	11884369	30 In VSMCs, NO may suppress PKG expression by directly inhibiting Sp1 transcription factor binding activity to the PKG promoter, an observation supported by the direct effect of NO on Sp1 binding in nuclear extracts of cells pretreated with NO donors.	bind
31705	4	7761	5	NULL	NULL	NULL	NULL	NO	Chemical		inhibits		directly			statement 1	Process				NULL	VSMCs	NULL	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_220	11884369	30 In VSMCs, NO may suppress PKG expression by directly inhibiting Sp1 transcription factor binding activity to the PKG promoter, an observation supported by the direct effect of NO on Sp1 binding in nuclear extracts of cells pretreated with NO donors.	bind
31706	5	7761	5	NULL	NULL	NULL	NULL	statement 4	Process		leads to					statement 1	Process				NULL	VSMCs	NULL	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_220	11884369	30 In VSMCs, NO may suppress PKG expression by directly inhibiting Sp1 transcription factor binding activity to the PKG promoter, an observation supported by the direct effect of NO on Sp1 binding in nuclear extracts of cells pretreated with NO donors.	bind
31707	6	7761	5	13	NULL	NULL	NULL	NO	Chemical		effects		directly			Sp1	GP	binding of			NULL	in nuclear extracts of cells pretreated with NO donors	NULL	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_220	11884369	30 In VSMCs, NO may suppress PKG expression by directly inhibiting Sp1 transcription factor binding activity to the PKG promoter, an observation supported by the direct effect of NO on Sp1 binding in nuclear extracts of cells pretreated with NO donors.	bind
68025	1	7761	5	11	NULL	0	NULL	 NO	Chemical		suppress		may			PKG	GP	expression			NULL	In VSMCs	0	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_220	11884369	30 In VSMCs, NO may suppress PKG expression by directly inhibiting Sp1 transcription factor binding activity to the PKG promoter, an observation supported by the direct effect of NO on Sp1 binding in nuclear extracts of cells pretreated with NO donors.	bind
68026	1	7761	5	11	NULL	0	NULL	Sp1	GP		is					 transcription factor	GP				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_220	11884369	30 In VSMCs, NO may suppress PKG expression by directly inhibiting Sp1 transcription factor binding activity to the PKG promoter, an observation supported by the direct effect of NO on Sp1 binding in nuclear extracts of cells pretreated with NO donors.	bind
68027	1	7761	5	11	NULL	0	NULL	Sp1	GP		binding					 PKG	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_220	11884369	30 In VSMCs, NO may suppress PKG expression by directly inhibiting Sp1 transcription factor binding activity to the PKG promoter, an observation supported by the direct effect of NO on Sp1 binding in nuclear extracts of cells pretreated with NO donors.	bind
24386	1	7761	6	10	NULL	0	NULL	Sp1			bind					PKG				promoter	NULL	VSMC	NULL	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_220	11884369	30 In VSMCs, NO may suppress PKG expression by directly inhibiting Sp1 transcription factor binding activity to the PKG promoter, an observation supported by the direct effect of NO on Sp1 binding in nuclear extracts of cells pretreated with NO donors.	bind
24387	2	7761	6	10	NULL	0	NULL	NO			effects		directly			Sp1		binding of			NULL	nuclear extracts of cells pretreated with NO donors	NULL	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_220	11884369	30 In VSMCs, NO may suppress PKG expression by directly inhibiting Sp1 transcription factor binding activity to the PKG promoter, an observation supported by the direct effect of NO on Sp1 binding in nuclear extracts of cells pretreated with NO donors.	bind
24388	3	7761	6	NULL	NULL	0	NULL	NO	NULL		inhibits	NULL				statement 1	NULL				NULL	VSMC	0	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_220	11884369	30 In VSMCs, NO may suppress PKG expression by directly inhibiting Sp1 transcription factor binding activity to the PKG promoter, an observation supported by the direct effect of NO on Sp1 binding in nuclear extracts of cells pretreated with NO donors.	bind
24389	4	7761	6	NULL	NULL	0	NULL	NO	NULL		suppress	NULL	may			PKG	NULL	expression of			NULL	VSMC	0	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_220	11884369	30 In VSMCs, NO may suppress PKG expression by directly inhibiting Sp1 transcription factor binding activity to the PKG promoter, an observation supported by the direct effect of NO on Sp1 binding in nuclear extracts of cells pretreated with NO donors.	bind
24390	5	7761	6	NULL	NULL	0	NULL	statement 4	NULL		occurs by	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_220	11884369	30 In VSMCs, NO may suppress PKG expression by directly inhibiting Sp1 transcription factor binding activity to the PKG promoter, an observation supported by the direct effect of NO on Sp1 binding in nuclear extracts of cells pretreated with NO donors.	bind
46824	6	7761	6	10	NULL	0	NULL	Sp1	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_220	11884369	30 In VSMCs, NO may suppress PKG expression by directly inhibiting Sp1 transcription factor binding activity to the PKG promoter, an observation supported by the direct effect of NO on Sp1 binding in nuclear extracts of cells pretreated with NO donors.	bind
31708	1	7762	5	13	NULL	NULL	NULL	JNK	GP		phosphorylates					c-Jun	GP		Ser-63		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_970_s_185	15718494	30 JNK phosphorylates c-Jun at Ser-63, resulting in the binding of c-Jun to the CREB-binding protein/p300 family of transcriptional coactivators.	bind
31709	2	7762	5	13	NULL	NULL	NULL	c-Jun	GP		bind					CREB-binding protein/p300	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_970_s_185	15718494	30 JNK phosphorylates c-Jun at Ser-63, resulting in the binding of c-Jun to the CREB-binding protein/p300 family of transcriptional coactivators.	bind
31710	3	7762	5	13	NULL	NULL	NULL	statement 1	Process		results in					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_970_s_185	15718494	30 JNK phosphorylates c-Jun at Ser-63, resulting in the binding of c-Jun to the CREB-binding protein/p300 family of transcriptional coactivators.	bind
31711	4	7762	5	13	NULL	NULL	NULL	CREB-binding protein/p300	GP		is a family of					transcriptional coactivators	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_970_s_185	15718494	30 JNK phosphorylates c-Jun at Ser-63, resulting in the binding of c-Jun to the CREB-binding protein/p300 family of transcriptional coactivators.	bind
24412	1	7762	6	NULL	NULL	0	NULL	JNK	NULL		phosphorylates	NULL				c-jun	NULL		Ser-63		NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_970_s_185	15718494	30 JNK phosphorylates c-Jun at Ser-63, resulting in the binding of c-Jun to the CREB-binding protein/p300 family of transcriptional coactivators.	bind
24417	2	7762	6	10	NULL	0	NULL	c-Jun	NULL		bind	NULL				CREB-binding protein/p300 	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_970_s_185	15718494	30 JNK phosphorylates c-Jun at Ser-63, resulting in the binding of c-Jun to the CREB-binding protein/p300 family of transcriptional coactivators.	bind
24418	3	7762	6	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_970_s_185	15718494	30 JNK phosphorylates c-Jun at Ser-63, resulting in the binding of c-Jun to the CREB-binding protein/p300 family of transcriptional coactivators.	bind
46825	4	7762	6	10	NULL	0	NULL	CREB-binding protein/p300	NULL		is a type of	NULL				transcriptional coactivators	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_5_970_s_185	15718494	30 JNK phosphorylates c-Jun at Ser-63, resulting in the binding of c-Jun to the CREB-binding protein/p300 family of transcriptional coactivators.	bind
31765	1	7764	5	13	NULL	NULL	NULL	GTP	Chemical		bind					p3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2553_s_102	9446556	30 mug of anti-p3 or anti-p5 antibodies reduced hydrolysis of GTP bound to p3 by only 26.5  plus-or-minus  2.3% and 32.3  plus-or-minus  1.9%, respectively, when added to p3 simultaneously with p5 (data not shown).	bind
31766	2	7764	5	13	NULL	NULL	NULL	anti-p3 antibodies	GP		reduces					statement 1	Process	hydrolysis of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2553_s_102	9446556	30 mug of anti-p3 or anti-p5 antibodies reduced hydrolysis of GTP bound to p3 by only 26.5  plus-or-minus  2.3% and 32.3  plus-or-minus  1.9%, respectively, when added to p3 simultaneously with p5 (data not shown).	bind
31767	3	7764	5	13	NULL	NULL	NULL	anti-p5 antibodies	GP		reduces					statement 1	Process	hydrolysis of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2553_s_102	9446556	30 mug of anti-p3 or anti-p5 antibodies reduced hydrolysis of GTP bound to p3 by only 26.5  plus-or-minus  2.3% and 32.3  plus-or-minus  1.9%, respectively, when added to p3 simultaneously with p5 (data not shown).	bind
24422	1	7764	6	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				p3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2553_s_102	9446556	30 mug of anti-p3 or anti-p5 antibodies reduced hydrolysis of GTP bound to p3 by only 26.5  plus-or-minus  2.3% and 32.3  plus-or-minus  1.9%, respectively, when added to p3 simultaneously with p5 (data not shown).	bind
24423	2	7764	6	10	NULL	0	NULL	anti-p3 antibodies	NULL		reduce	NULL				statement 1	NULL	hydrolysis of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2553_s_102	9446556	30 mug of anti-p3 or anti-p5 antibodies reduced hydrolysis of GTP bound to p3 by only 26.5  plus-or-minus  2.3% and 32.3  plus-or-minus  1.9%, respectively, when added to p3 simultaneously with p5 (data not shown).	bind
24424	3	7764	6	10	NULL	0	NULL	anti-p5 antibodies	NULL		reduce	NULL				statement 1	NULL	 hydrolysis of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2553_s_102	9446556	30 mug of anti-p3 or anti-p5 antibodies reduced hydrolysis of GTP bound to p3 by only 26.5  plus-or-minus  2.3% and 32.3  plus-or-minus  1.9%, respectively, when added to p3 simultaneously with p5 (data not shown).	bind
31712	1	7766	5	13	NULL	NULL	NULL	VBP	GP		bind									cis element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_44_34826_s_144	10942764	30 nm VBP was bound to its cis element and competed with 1, 10, or 100 molar eq of the indicated A-ZIP.	bind
31713	2	7766	5	13	NULL	NULL	NULL	A-ZIP	GP		bind									cis element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_44_34826_s_144	10942764	30 nm VBP was bound to its cis element and competed with 1, 10, or 100 molar eq of the indicated A-ZIP.	bind
31714	3	7766	5	13	NULL	NULL	NULL	statement 1	Process		competes with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_44_34826_s_144	10942764	30 nm VBP was bound to its cis element and competed with 1, 10, or 100 molar eq of the indicated A-ZIP.	bind
24425	1	7766	6	NULL	NULL	0	NULL	VBP	NULL		bind	NULL					NULL			cis-element	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34826_s_144	10942764	30 nm VBP was bound to its cis element and competed with 1, 10, or 100 molar eq of the indicated A-ZIP.	bind
24426	2	7766	6	NULL	NULL	0	NULL	A-ZIP	NULL		bind	NULL					NULL			cis-element	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34826_s_144	10942764	30 nm VBP was bound to its cis element and competed with 1, 10, or 100 molar eq of the indicated A-ZIP.	bind
24427	3	7766	6	NULL	NULL	0	NULL	statement 1	NULL		competes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34826_s_144	10942764	30 nm VBP was bound to its cis element and competed with 1, 10, or 100 molar eq of the indicated A-ZIP.	bind
31715	1	7767	5	13	NULL	NULL	NULL	IgM autoantibodies	GP		bind					MDA-LDL	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_108_9_1059_s_63	12912807	30 Plasma titers of IgM and IgG autoantibodies binding to MDA-LDL and Cu-OxLDL were determined by chemiluminescence ELISA as previously described.	bind
31716	2	7767	5	13	NULL	NULL	NULL	IgG autoantibodies	GP		bind					MDA-LDL	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_108_9_1059_s_63	12912807	30 Plasma titers of IgM and IgG autoantibodies binding to MDA-LDL and Cu-OxLDL were determined by chemiluminescence ELISA as previously described.	bind
31717	3	7767	5	13	NULL	NULL	NULL	IgM autoantibodies	GP		bind					Cu-OxLDL	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_108_9_1059_s_63	12912807	30 Plasma titers of IgM and IgG autoantibodies binding to MDA-LDL and Cu-OxLDL were determined by chemiluminescence ELISA as previously described.	bind
31718	4	7767	5	13	NULL	NULL	NULL	IgG autoantibodies	GP		bind					Cu-OxLDL	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_108_9_1059_s_63	12912807	30 Plasma titers of IgM and IgG autoantibodies binding to MDA-LDL and Cu-OxLDL were determined by chemiluminescence ELISA as previously described.	bind
24428	1	7767	6	NULL	NULL	0	NULL	IgM autoantibody	NULL		bind	NULL				MDA-LDL	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_108_9_1059_s_63	12912807	30 Plasma titers of IgM and IgG autoantibodies binding to MDA-LDL and Cu-OxLDL were determined by chemiluminescence ELISA as previously described.	bind
24429	2	7767	6	NULL	NULL	0	NULL	IgG autoantibody	NULL		bind	NULL				Cu-OxLDL	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_108_9_1059_s_63	12912807	30 Plasma titers of IgM and IgG autoantibodies binding to MDA-LDL and Cu-OxLDL were determined by chemiluminescence ELISA as previously described.	bind
31755	1	7768	5	13	NULL	NULL	NULL	TnI	GP		bind		cooperatively			actin-tropomyosin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_159	11739284	30 This conformational change weakens the cooperative binding of TnI to actin-tropomyosin 31 and reduces the affinity of TnI for TnC, especially in the presence of Ca2+.	bind
31756	2	7768	5	13	NULL	NULL	NULL	TnI	GP		has affinity for					TnC	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_159	11739284	30 This conformational change weakens the cooperative binding of TnI to actin-tropomyosin 31 and reduces the affinity of TnI for TnC, especially in the presence of Ca2+.	bind
24430	1	7768	6	NULL	NULL	0	NULL	TnI	NULL		bind	NULL	cooperatively			actin-tropomyosin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_159	11739284	30 This conformational change weakens the cooperative binding of TnI to actin-tropomyosin 31 and reduces the affinity of TnI for TnC, especially in the presence of Ca2+.	bind
24431	2	7768	6	NULL	NULL	0	NULL	TnI	NULL		has affinity for	NULL				TnC	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_159	11739284	30 This conformational change weakens the cooperative binding of TnI to actin-tropomyosin 31 and reduces the affinity of TnI for TnC, especially in the presence of Ca2+.	bind
31758	1	7769	5	13	NULL	NULL	NULL	CD4 co-receptor	GP		bind					gp120	GP				NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_54_2_333_s_37	15231762	30, 31 The binding of both CD4 and chemokine co-receptor by gp120 are the first two steps of viral entry, and the prevention of co-receptor binding, like the prevention of attachment, is an important therapeutic target.	bind
31759	2	7769	5	13	NULL	NULL	NULL	chemokine co-receptor	GP		bind					gp120	GP				NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_54_2_333_s_37	15231762	30, 31 The binding of both CD4 and chemokine co-receptor by gp120 are the first two steps of viral entry, and the prevention of co-receptor binding, like the prevention of attachment, is an important therapeutic target.	bind
31760	3	7769	5	13	NULL	NULL	NULL	viral entry	Process		leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_54_2_333_s_37	15231762	30, 31 The binding of both CD4 and chemokine co-receptor by gp120 are the first two steps of viral entry, and the prevention of co-receptor binding, like the prevention of attachment, is an important therapeutic target.	bind
31761	4	7769	5	13	NULL	NULL	NULL	viral entry	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_54_2_333_s_37	15231762	30, 31 The binding of both CD4 and chemokine co-receptor by gp120 are the first two steps of viral entry, and the prevention of co-receptor binding, like the prevention of attachment, is an important therapeutic target.	bind
24432	1	7769	6	NULL	NULL	0	NULL	CD4	NULL		bind	NULL				gp120	NULL				NULL		0	NULL	NULL	NULL	gw70_jantimicrobchemoth_54_2_333_s_37	15231762	30, 31 The binding of both CD4 and chemokine co-receptor by gp120 are the first two steps of viral entry, and the prevention of co-receptor binding, like the prevention of attachment, is an important therapeutic target.	bind
24433	2	7769	6	NULL	NULL	0	NULL	chemokine co-receptor	NULL		bind	NULL				gp120	NULL				NULL		0	NULL	NULL	NULL	gw70_jantimicrobchemoth_54_2_333_s_37	15231762	30, 31 The binding of both CD4 and chemokine co-receptor by gp120 are the first two steps of viral entry, and the prevention of co-receptor binding, like the prevention of attachment, is an important therapeutic target.	bind
24434	3	7769	6	NULL	NULL	0	NULL	statement 1	NULL		is the first step for	NULL				viral entry	NULL				NULL		0	NULL	NULL	NULL	gw70_jantimicrobchemoth_54_2_333_s_37	15231762	30, 31 The binding of both CD4 and chemokine co-receptor by gp120 are the first two steps of viral entry, and the prevention of co-receptor binding, like the prevention of attachment, is an important therapeutic target.	bind
24435	4	7769	6	NULL	NULL	0	NULL	statement 2	NULL		is the first step for	NULL				viral entry	NULL				NULL		0	NULL	NULL	NULL	gw70_jantimicrobchemoth_54_2_333_s_37	15231762	30, 31 The binding of both CD4 and chemokine co-receptor by gp120 are the first two steps of viral entry, and the prevention of co-receptor binding, like the prevention of attachment, is an important therapeutic target.	bind
24436	5	7769	6	10	NULL	0	NULL	co-receptor	NULL	prevention of binding of	is an important	NULL				therapeutic target	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_54_2_333_s_37	15231762	30, 31 The binding of both CD4 and chemokine co-receptor by gp120 are the first two steps of viral entry, and the prevention of co-receptor binding, like the prevention of attachment, is an important therapeutic target.	bind
24437	6	7769	6	NULL	NULL	0	NULL	attachment	NULL	prevention of	is an important	NULL				therapeutic target	NULL				NULL		0	NULL	NULL	NULL	gw70_jantimicrobchemoth_54_2_333_s_37	15231762	30, 31 The binding of both CD4 and chemokine co-receptor by gp120 are the first two steps of viral entry, and the prevention of co-receptor binding, like the prevention of attachment, is an important therapeutic target.	bind
31762	1	7770	5	13	NULL	NULL	NULL	cytokeratin-1	GP		bind					uPAR	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1227_s_169	15044324	30,31  It has been shown that cytokeratin-1 binds to both uPAR and gC1qR, but uPAR and gC1qR do not bind to each other.	bind
31763	2	7770	5	13	NULL	NULL	NULL	cytokeratin-1	GP		bind					gC1qR	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1227_s_169	15044324	30,31  It has been shown that cytokeratin-1 binds to both uPAR and gC1qR, but uPAR and gC1qR do not bind to each other.	bind
31764	3	7770	5	13	NULL	NULL	NULL	uPAR	GP		does not bind					gC1qR	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1227_s_169	15044324	30,31  It has been shown that cytokeratin-1 binds to both uPAR and gC1qR, but uPAR and gC1qR do not bind to each other.	bind
24438	1	7770	6	NULL	NULL	0	NULL	cytokeratin-1	NULL		bind	NULL				uPAR	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_9_1227_s_169	15044324	30,31  It has been shown that cytokeratin-1 binds to both uPAR and gC1qR, but uPAR and gC1qR do not bind to each other.	bind
24439	2	7770	6	NULL	NULL	0	NULL	cytokeratin-1	NULL		bind	NULL				gC1qR	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_9_1227_s_169	15044324	30,31  It has been shown that cytokeratin-1 binds to both uPAR and gC1qR, but uPAR and gC1qR do not bind to each other.	bind
24440	3	7770	6	NULL	NULL	0	NULL	uPAR	NULL		does not bind	NULL				gC1qR	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_9_1227_s_169	15044324	30,31  It has been shown that cytokeratin-1 binds to both uPAR and gC1qR, but uPAR and gC1qR do not bind to each other.	bind
46846	1	7773	5	13	NULL	NULL	NULL	cells	Cell		express					CCR8	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17251_s_84	9211859	300-19 cells expressing CCR8 bound radiolabeled I-309 with high affinity (Fig.  3).	bind
46847	2	7773	5	13	NULL	NULL	NULL	statement 1	GP		bind		high affinity			I-309	GP	radiolabeled			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17251_s_84	9211859	300-19 cells expressing CCR8 bound radiolabeled I-309 with high affinity (Fig.  3).	bind
24442	2	7773	6	10	NULL	0	NULL	statement 1	NULL		bind	NULL	high affinity			I-309	NULL	radiolabeled			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_28_17251_s_84	9211859	300-19 cells expressing CCR8 bound radiolabeled I-309 with high affinity (Fig.  3).	bind
46848	1	7773	6	10	NULL	0	NULL	cells	NULL		express	NULL				CCR8	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_28_17251_s_84	9211859	300-19 cells expressing CCR8 bound radiolabeled I-309 with high affinity (Fig.  3).	bind
31768	1	7774	5	13	NULL	NULL	NULL	CAND1	GP		bind					CUL1	GP	unneddylated			NULL		NULL	NULL	NULL	NULL	gw70_nature_435_7046_1257_s_232	15988528	301, 392 398 (2003) |  Article |  PubMed |  ISI |  ChemPort |                        Zheng, J.  et al. CAND1 binds to unneddylated CUL1 and regulates the formation of SCF ubiquitin E3  ligase complex.	bind
31769	2	7774	5	13	NULL	NULL	NULL	statement 1	Process		regulates					SCF ubiquitin E3 ligase complex	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw70_nature_435_7046_1257_s_232	15988528	301, 392 398 (2003) |  Article |  PubMed |  ISI |  ChemPort |                        Zheng, J.  et al. CAND1 binds to unneddylated CUL1 and regulates the formation of SCF ubiquitin E3  ligase complex.	bind
24443	1	7774	6	NULL	NULL	0	NULL	CAND1	NULL		bind	NULL				CUL1	NULL	unneddylated			NULL		0	NULL	NULL	NULL	gw70_nature_435_7046_1257_s_232	15988528	301, 392 398 (2003) |  Article |  PubMed |  ISI |  ChemPort |                        Zheng, J.  et al. CAND1 binds to unneddylated CUL1 and regulates the formation of SCF ubiquitin E3  ligase complex.	bind
24444	2	7774	6	10	NULL	0	NULL	statement 1			regulates					SCF ubiquitin E3 ligase complex		formation of			NULL		NULL	NULL	NULL	NULL	gw70_nature_435_7046_1257_s_232	15988528	301, 392 398 (2003) |  Article |  PubMed |  ISI |  ChemPort |                        Zheng, J.  et al. CAND1 binds to unneddylated CUL1 and regulates the formation of SCF ubiquitin E3  ligase complex.	bind
31770	1	7775	5	13	NULL	NULL	NULL	125I-Lac-LDL	GP		bind					Kupffer cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_6_1847_s_110	7882496	30125I-Lac-LDL binding to Kupffer cells could be inhibited up to 78% by excess unlabeled Lac-LDL at an  Ki of 1.15 plus-or-minus 0.30 nmol/L (Fig 2B  ).	bind
31771	2	7775	5	13	NULL	NULL	NULL	Lac-LDL	GP	excess unlabeled	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_6_1847_s_110	7882496	30125I-Lac-LDL binding to Kupffer cells could be inhibited up to 78% by excess unlabeled Lac-LDL at an  Ki of 1.15 plus-or-minus 0.30 nmol/L (Fig 2B  ).	bind
24445	1	7775	6	NULL	NULL	0	NULL	125I-Lac-LDL	NULL		bind	NULL				Kupffer cells	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_6_1847_s_110	7882496	30125I-Lac-LDL binding to Kupffer cells could be inhibited up to 78% by excess unlabeled Lac-LDL at an  Ki of 1.15 plus-or-minus 0.30 nmol/L (Fig 2B  ).	bind
24446	2	7775	6	NULL	NULL	0	NULL	Lac-LDL	NULL	unlabeled	inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_6_1847_s_110	7882496	30125I-Lac-LDL binding to Kupffer cells could be inhibited up to 78% by excess unlabeled Lac-LDL at an  Ki of 1.15 plus-or-minus 0.30 nmol/L (Fig 2B  ).	bind
55545	1	7776	5	13	NULL	NULL	NULL	30K	GP		bind					p94	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31158_s_19	8537379	30K is the  first candidate to bind to and regulate p94, since the calmodulin-like  Ca -binding domains of muCL and mCL (see  Fig. 2), which are the binding sites for 30K, are highly  homologous to p94( 5) .	bind
55546	2	7776	5	13	NULL	NULL	NULL	statement 1	Process		regulates					p94	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31158_s_19	8537379	30K is the  first candidate to bind to and regulate p94, since the calmodulin-like  Ca -binding domains of muCL and mCL (see  Fig. 2), which are the binding sites for 30K, are highly  homologous to p94( 5) .	bind
55547	3	7776	5	13	NULL	NULL	NULL	muCL	GP		is a binding site for			calmodulin-like Ca -binding domains		30K	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31158_s_19	8537379	30K is the  first candidate to bind to and regulate p94, since the calmodulin-like  Ca -binding domains of muCL and mCL (see  Fig. 2), which are the binding sites for 30K, are highly  homologous to p94( 5) .	bind
55548	4	7776	5	13	NULL	NULL	NULL	mCL	GP		is a binding site for			calmodulin-like Ca -binding domains		30K	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31158_s_19	8537379	30K is the  first candidate to bind to and regulate p94, since the calmodulin-like  Ca -binding domains of muCL and mCL (see  Fig. 2), which are the binding sites for 30K, are highly  homologous to p94( 5) .	bind
55549	5	7776	5	13	NULL	NULL	NULL	statement 3	GP		is homologous to		highly			p94	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31158_s_19	8537379	30K is the  first candidate to bind to and regulate p94, since the calmodulin-like  Ca -binding domains of muCL and mCL (see  Fig. 2), which are the binding sites for 30K, are highly  homologous to p94( 5) .	bind
55550	6	7776	5	13	NULL	NULL	NULL	statement 4	GP		is homologous to		highly			p94	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31158_s_19	8537379	30K is the  first candidate to bind to and regulate p94, since the calmodulin-like  Ca -binding domains of muCL and mCL (see  Fig. 2), which are the binding sites for 30K, are highly  homologous to p94( 5) .	bind
24447	1	7776	6	NULL	NULL	0	NULL	30K	NULL		bind	NULL				p94	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31158_s_19	8537379	30K is the  first candidate to bind to and regulate p94, since the calmodulin-like  Ca -binding domains of muCL and mCL (see  Fig. 2), which are the binding sites for 30K, are highly  homologous to p94( 5) .	bind
24448	2	7776	6	NULL	NULL	0	NULL	30K	NULL		regulate	NULL				p94	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31158_s_19	8537379	30K is the  first candidate to bind to and regulate p94, since the calmodulin-like  Ca -binding domains of muCL and mCL (see  Fig. 2), which are the binding sites for 30K, are highly  homologous to p94( 5) .	bind
24569	3	7776	6	NULL	NULL	0	NULL	muCL	NULL		are homologous to	NULL		calmodulin-like Ca -binding domains		p94	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31158_s_19	8537379	30K is the  first candidate to bind to and regulate p94, since the calmodulin-like  Ca -binding domains of muCL and mCL (see  Fig. 2), which are the binding sites for 30K, are highly  homologous to p94( 5) .	bind
24570	4	7776	6	NULL	NULL	0	NULL	mCL	NULL		are homologous to	NULL		calmodulin-like Ca -binding domains		p94	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31158_s_19	8537379	30K is the  first candidate to bind to and regulate p94, since the calmodulin-like  Ca -binding domains of muCL and mCL (see  Fig. 2), which are the binding sites for 30K, are highly  homologous to p94( 5) .	bind
24950	5	7776	6	NULL	NULL	0	NULL	statement 3	NULL		is binding site for	NULL				30K	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31158_s_19	8537379	30K is the  first candidate to bind to and regulate p94, since the calmodulin-like  Ca -binding domains of muCL and mCL (see  Fig. 2), which are the binding sites for 30K, are highly  homologous to p94( 5) .	bind
24951	6	7776	6	NULL	NULL	0	NULL	statement 4	NULL		is binding site for	NULL				30K	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31158_s_19	8537379	30K is the  first candidate to bind to and regulate p94, since the calmodulin-like  Ca -binding domains of muCL and mCL (see  Fig. 2), which are the binding sites for 30K, are highly  homologous to p94( 5) .	bind
31772	1	7777	5	13	NULL	NULL	NULL	Gar1p	GP		bind			RNA binding element		snR10	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2733_s_514	11433018	31       Bagni,C. and Lapeyre,B. (1998) Gar1p binds to the small nucleolar RNAs snR10 and snR30  in vitro through a nontypical RNA binding element.	bind
31773	2	7777	5	13	NULL	NULL	NULL	Gar1p	GP		bind			RNA binding element		snR30	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2733_s_514	11433018	31       Bagni,C. and Lapeyre,B. (1998) Gar1p binds to the small nucleolar RNAs snR10 and snR30  in vitro through a nontypical RNA binding element.	bind
31774	3	7777	5	13	NULL	NULL	NULL	snR10	NucleicAcid		is a type of					small nucleolar RNAs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2733_s_514	11433018	31       Bagni,C. and Lapeyre,B. (1998) Gar1p binds to the small nucleolar RNAs snR10 and snR30  in vitro through a nontypical RNA binding element.	bind
31775	4	7777	5	13	NULL	NULL	NULL	snR30	NucleicAcid		is a type of					small nucleolar RNAs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2733_s_514	11433018	31       Bagni,C. and Lapeyre,B. (1998) Gar1p binds to the small nucleolar RNAs snR10 and snR30  in vitro through a nontypical RNA binding element.	bind
24449	1	7777	6	10	NULL	0	NULL	Gar1p	NULL		bind	NULL		nontypical RNA binding element		 snR10	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2733_s_514	11433018	31       Bagni,C. and Lapeyre,B. (1998) Gar1p binds to the small nucleolar RNAs snR10 and snR30  in vitro through a nontypical RNA binding element.	bind
24450	2	7777	6	10	NULL	0	NULL	Gar1p	NULL		bind	NULL		nontypical RNA binding element		 snR30	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2733_s_514	11433018	31       Bagni,C. and Lapeyre,B. (1998) Gar1p binds to the small nucleolar RNAs snR10 and snR30  in vitro through a nontypical RNA binding element.	bind
46849	3	7777	6	10	NULL	0	NULL	snR10	NULL		is a type of	NULL				 small nucleolar RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2733_s_514	11433018	31       Bagni,C. and Lapeyre,B. (1998) Gar1p binds to the small nucleolar RNAs snR10 and snR30  in vitro through a nontypical RNA binding element.	bind
46850	4	7777	6	10	NULL	0	NULL	snR30	NULL		is a type of	NULL				small nucleolar RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2733_s_514	11433018	31       Bagni,C. and Lapeyre,B. (1998) Gar1p binds to the small nucleolar RNAs snR10 and snR30  in vitro through a nontypical RNA binding element.	bind
31776	1	7778	5	13	NULL	NULL	NULL	Ets1	GP		bind		specifically			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_20_4154_s_455	11600704	31       Bosselut,R., Levin,J., Adjadj,E. and Ghysdael,J. (1993) A single amino-acid substitution in the Ets domain alters core DNA binding specificity of Ets1 to that of the related transcription factors Elf1 and E74.	bind
31777	2	7778	5	13	NULL	NULL	NULL	Ets1	GP	single amino-acid substitution in	alters			Ets domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_20_4154_s_455	11600704	31       Bosselut,R., Levin,J., Adjadj,E. and Ghysdael,J. (1993) A single amino-acid substitution in the Ets domain alters core DNA binding specificity of Ets1 to that of the related transcription factors Elf1 and E74.	bind
31778	3	7778	5	13	NULL	NULL	NULL	Elf1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_20_4154_s_455	11600704	31       Bosselut,R., Levin,J., Adjadj,E. and Ghysdael,J. (1993) A single amino-acid substitution in the Ets domain alters core DNA binding specificity of Ets1 to that of the related transcription factors Elf1 and E74.	bind
31779	4	7778	5	13	NULL	NULL	NULL	E74	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_20_4154_s_455	11600704	31       Bosselut,R., Levin,J., Adjadj,E. and Ghysdael,J. (1993) A single amino-acid substitution in the Ets domain alters core DNA binding specificity of Ets1 to that of the related transcription factors Elf1 and E74.	bind
24451	1	7778	6	10	NULL	0	NULL	Ets1	NULL		bind	NULL	specifically			DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_20_4154_s_455	11600704	31       Bosselut,R., Levin,J., Adjadj,E. and Ghysdael,J. (1993) A single amino-acid substitution in the Ets domain alters core DNA binding specificity of Ets1 to that of the related transcription factors Elf1 and E74.	bind
24452	2	7778	6	10	NULL	0	NULL	Ets1	NULL	single amino-acid substitution	alters	NULL		ETS domain		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_20_4154_s_455	11600704	31       Bosselut,R., Levin,J., Adjadj,E. and Ghysdael,J. (1993) A single amino-acid substitution in the Ets domain alters core DNA binding specificity of Ets1 to that of the related transcription factors Elf1 and E74.	bind
47498	3	7778	6	10	NULL	0	NULL	Elf1	NULL		is a type of	NULL				transcription factor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_20_4154_s_455	11600704	31       Bosselut,R., Levin,J., Adjadj,E. and Ghysdael,J. (1993) A single amino-acid substitution in the Ets domain alters core DNA binding specificity of Ets1 to that of the related transcription factors Elf1 and E74.	bind
47500	4	7778	6	10	NULL	0	NULL	E74	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_20_4154_s_455	11600704	31       Bosselut,R., Levin,J., Adjadj,E. and Ghysdael,J. (1993) A single amino-acid substitution in the Ets domain alters core DNA binding specificity of Ets1 to that of the related transcription factors Elf1 and E74.	bind
31780	1	7779	5	13	NULL	NULL	NULL	ogg1 protein	GP	Saccharomyces cerevisiae	bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_23_4583_s_400	11095666	31       Guibourt,N., Castaing,B., Van Der Kemp,P.A. and Boiteux,S. (2000) Catalytic and DNA binding properties of the ogg1 protein of Saccharomyces cerevisiae: comparison between the wild type and the K241R and K241Q active-site mutant proteins.	bind
24455	1	7779	6	13	NULL	NULL	NULL	ogg1 protein	GP	Saccharomyces cerevisiae	exhibits					catalytic activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_23_4583_s_400	11095666	31       Guibourt,N., Castaing,B., Van Der Kemp,P.A. and Boiteux,S. (2000) Catalytic and DNA binding properties of the ogg1 protein of Saccharomyces cerevisiae: comparison between the wild type and the K241R and K241Q active-site mutant proteins.	bind
24456	2	7779	6	NULL	NULL	0	NULL	ogg1 protein	NULL	Saccharomyces cerevisiae	bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_23_4583_s_400	11095666	31       Guibourt,N., Castaing,B., Van Der Kemp,P.A. and Boiteux,S. (2000) Catalytic and DNA binding properties of the ogg1 protein of Saccharomyces cerevisiae: comparison between the wild type and the K241R and K241Q active-site mutant proteins.	bind
31781	1	7780	5	13	NULL	NULL	NULL	C/EBP	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3311_s_337	11504868	31       Koldin,B., Suckow,M., Seydel,A., von Wilcken-Bergmann,B. and Muller-Hill,B. (1995) A comparison of the different DNA-binding specificities of the bZIP proteins C/EBP and GCN4.	bind
31782	2	7780	5	13	NULL	NULL	NULL	GCN4	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3311_s_337	11504868	31       Koldin,B., Suckow,M., Seydel,A., von Wilcken-Bergmann,B. and Muller-Hill,B. (1995) A comparison of the different DNA-binding specificities of the bZIP proteins C/EBP and GCN4.	bind
31783	3	7780	5	13	NULL	NULL	NULL	C/EBP	GP		is a type of					bZIP proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3311_s_337	11504868	31       Koldin,B., Suckow,M., Seydel,A., von Wilcken-Bergmann,B. and Muller-Hill,B. (1995) A comparison of the different DNA-binding specificities of the bZIP proteins C/EBP and GCN4.	bind
31784	4	7780	5	13	NULL	NULL	NULL	GCN4	GP		is a type of					bZIP proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3311_s_337	11504868	31       Koldin,B., Suckow,M., Seydel,A., von Wilcken-Bergmann,B. and Muller-Hill,B. (1995) A comparison of the different DNA-binding specificities of the bZIP proteins C/EBP and GCN4.	bind
24457	1	7780	6	NULL	NULL	0	NULL	C/EBP protein	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3311_s_337	11504868	31       Koldin,B., Suckow,M., Seydel,A., von Wilcken-Bergmann,B. and Muller-Hill,B. (1995) A comparison of the different DNA-binding specificities of the bZIP proteins C/EBP and GCN4.	bind
24458	2	7780	6	NULL	NULL	0	NULL	GCN4 protein	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3311_s_337	11504868	31       Koldin,B., Suckow,M., Seydel,A., von Wilcken-Bergmann,B. and Muller-Hill,B. (1995) A comparison of the different DNA-binding specificities of the bZIP proteins C/EBP and GCN4.	bind
46851	3	7780	6	10	NULL	0	NULL	C/EBP	NULL		is a type of	NULL				bZIP proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3311_s_337	11504868	31       Koldin,B., Suckow,M., Seydel,A., von Wilcken-Bergmann,B. and Muller-Hill,B. (1995) A comparison of the different DNA-binding specificities of the bZIP proteins C/EBP and GCN4.	bind
46852	4	7780	6	10	NULL	0	NULL	GCN4	NULL		is a type of	NULL				bZIP proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3311_s_337	11504868	31       Koldin,B., Suckow,M., Seydel,A., von Wilcken-Bergmann,B. and Muller-Hill,B. (1995) A comparison of the different DNA-binding specificities of the bZIP proteins C/EBP and GCN4.	bind
31785	1	7781	5	13	NULL	NULL	NULL	U2 snRNA sequences	NucleicAcid		bind					U2-specific proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3841_s_318	11557816	31       Pan,Z.-Q. and Prives,C. (1989) U2 snRNA sequences that bind U2-specific proteins are dispensable for the function of U2 snRNP in splicing.	bind
31786	2	7781	5	13	NULL	NULL	NULL	U2 snRNP	NucleicAcid		function in					splicing	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3841_s_318	11557816	31       Pan,Z.-Q. and Prives,C. (1989) U2 snRNA sequences that bind U2-specific proteins are dispensable for the function of U2 snRNP in splicing.	bind
31787	3	7781	5	13	NULL	NULL	NULL	statement 1	Process		dispensable for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3841_s_318	11557816	31       Pan,Z.-Q. and Prives,C. (1989) U2 snRNA sequences that bind U2-specific proteins are dispensable for the function of U2 snRNP in splicing.	bind
24459	1	7781	6	NULL	NULL	0	NULL	U2 snRNA sequences	NULL		bind	NULL				U2-specific protein	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3841_s_318	11557816	31       Pan,Z.-Q. and Prives,C. (1989) U2 snRNA sequences that bind U2-specific proteins are dispensable for the function of U2 snRNP in splicing.	bind
24460	2	7781	6	NULL	NULL	0	NULL	U2 snRNP	NULL		plays a role in	NULL				splicing	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3841_s_318	11557816	31       Pan,Z.-Q. and Prives,C. (1989) U2 snRNA sequences that bind U2-specific proteins are dispensable for the function of U2 snRNP in splicing.	bind
24461	3	7781	6	NULL	NULL	0	NULL	statement 1	NULL		is dispensable for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3841_s_318	11557816	31       Pan,Z.-Q. and Prives,C. (1989) U2 snRNA sequences that bind U2-specific proteins are dispensable for the function of U2 snRNP in splicing.	bind
31788	1	7782	5	13	NULL	NULL	NULL	PG	GP		bind					C9 monomer	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_164_s_123	9012652	31  Because C9 has a carboxyl-terminal lysine and has lysines at amino acid positions 15 and 17 from the carboxyl terminus and since the greatest increase in PG binding occurred after the incorporation of C9 into the terminal attack complex, we hypothesized that PG bound to C9 monomer or polymer.	bind
31789	2	7782	5	13	NULL	NULL	NULL	PG	GP		bind					C9 polymer	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_164_s_123	9012652	31  Because C9 has a carboxyl-terminal lysine and has lysines at amino acid positions 15 and 17 from the carboxyl terminus and since the greatest increase in PG binding occurred after the incorporation of C9 into the terminal attack complex, we hypothesized that PG bound to C9 monomer or polymer.	bind
31790	3	7782	5	13	NULL	NULL	NULL	statement 1	Process		is alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_164_s_123	9012652	31  Because C9 has a carboxyl-terminal lysine and has lysines at amino acid positions 15 and 17 from the carboxyl terminus and since the greatest increase in PG binding occurred after the incorporation of C9 into the terminal attack complex, we hypothesized that PG bound to C9 monomer or polymer.	bind
31791	4	7782	5	13	NULL	NULL	NULL	C9	GP		contains					lysine	AminoAcid		carboxyl-terminus		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_164_s_123	9012652	31  Because C9 has a carboxyl-terminal lysine and has lysines at amino acid positions 15 and 17 from the carboxyl terminus and since the greatest increase in PG binding occurred after the incorporation of C9 into the terminal attack complex, we hypothesized that PG bound to C9 monomer or polymer.	bind
31792	5	7782	5	13	NULL	NULL	NULL	C9	GP		contains					lysine	AminoAcid		aa 15		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_164_s_123	9012652	31  Because C9 has a carboxyl-terminal lysine and has lysines at amino acid positions 15 and 17 from the carboxyl terminus and since the greatest increase in PG binding occurred after the incorporation of C9 into the terminal attack complex, we hypothesized that PG bound to C9 monomer or polymer.	bind
31793	6	7782	5	13	NULL	NULL	NULL	C9	GP		contains					lysine	AminoAcid		aa 17		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_164_s_123	9012652	31  Because C9 has a carboxyl-terminal lysine and has lysines at amino acid positions 15 and 17 from the carboxyl terminus and since the greatest increase in PG binding occurred after the incorporation of C9 into the terminal attack complex, we hypothesized that PG bound to C9 monomer or polymer.	bind
31794	7	7782	5	13	NULL	NULL	NULL	C9	GP		incorporated into					terminal attack complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_164_s_123	9012652	31  Because C9 has a carboxyl-terminal lysine and has lysines at amino acid positions 15 and 17 from the carboxyl terminus and since the greatest increase in PG binding occurred after the incorporation of C9 into the terminal attack complex, we hypothesized that PG bound to C9 monomer or polymer.	bind
31795	8	7782	5	13	NULL	NULL	NULL	statement 7	Process		increases					PG	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_164_s_123	9012652	31  Because C9 has a carboxyl-terminal lysine and has lysines at amino acid positions 15 and 17 from the carboxyl terminus and since the greatest increase in PG binding occurred after the incorporation of C9 into the terminal attack complex, we hypothesized that PG bound to C9 monomer or polymer.	bind
24462	1	7782	6	NULL	NULL	0	NULL	PG	NULL		bind	NULL				C9 monomer	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_164_s_123	9012652	31  Because C9 has a carboxyl-terminal lysine and has lysines at amino acid positions 15 and 17 from the carboxyl terminus and since the greatest increase in PG binding occurred after the incorporation of C9 into the terminal attack complex, we hypothesized that PG bound to C9 monomer or polymer.	bind
24463	2	7782	6	NULL	NULL	0	NULL	PG	NULL		bind	NULL				C9 polymer	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_164_s_123	9012652	31  Because C9 has a carboxyl-terminal lysine and has lysines at amino acid positions 15 and 17 from the carboxyl terminus and since the greatest increase in PG binding occurred after the incorporation of C9 into the terminal attack complex, we hypothesized that PG bound to C9 monomer or polymer.	bind
24464	3	7782	6	10	NULL	0	NULL	C9	NULL		contains	NULL					NULL		carboxyl-terminal lysine		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_164_s_123	9012652	31  Because C9 has a carboxyl-terminal lysine and has lysines at amino acid positions 15 and 17 from the carboxyl terminus and since the greatest increase in PG binding occurred after the incorporation of C9 into the terminal attack complex, we hypothesized that PG bound to C9 monomer or polymer.	bind
24571	4	7782	6	10	NULL	0	NULL	C9	NULL		contains	NULL					NULL		lysine at amino acid position 15 from the carboxyl terminus		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_164_s_123	9012652	31  Because C9 has a carboxyl-terminal lysine and has lysines at amino acid positions 15 and 17 from the carboxyl terminus and since the greatest increase in PG binding occurred after the incorporation of C9 into the terminal attack complex, we hypothesized that PG bound to C9 monomer or polymer.	bind
24572	5	7782	6	10	NULL	0	NULL	C9	NULL		contains	NULL					NULL		lysine at amino acid position 17 from the carboxyl terminus		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_164_s_123	9012652	31  Because C9 has a carboxyl-terminal lysine and has lysines at amino acid positions 15 and 17 from the carboxyl terminus and since the greatest increase in PG binding occurred after the incorporation of C9 into the terminal attack complex, we hypothesized that PG bound to C9 monomer or polymer.	bind
46853	6	7782	6	10	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_164_s_123	9012652	31  Because C9 has a carboxyl-terminal lysine and has lysines at amino acid positions 15 and 17 from the carboxyl terminus and since the greatest increase in PG binding occurred after the incorporation of C9 into the terminal attack complex, we hypothesized that PG bound to C9 monomer or polymer.	bind
46854	7	7782	6	10	NULL	0	NULL	C9	NULL		incorporated into	NULL				terminal attack complex	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_164_s_123	9012652	31  Because C9 has a carboxyl-terminal lysine and has lysines at amino acid positions 15 and 17 from the carboxyl terminus and since the greatest increase in PG binding occurred after the incorporation of C9 into the terminal attack complex, we hypothesized that PG bound to C9 monomer or polymer.	bind
46855	8	7782	6	10	NULL	0	NULL	statement 7	NULL		increase	NULL				PG	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_164_s_123	9012652	31  Because C9 has a carboxyl-terminal lysine and has lysines at amino acid positions 15 and 17 from the carboxyl terminus and since the greatest increase in PG binding occurred after the incorporation of C9 into the terminal attack complex, we hypothesized that PG bound to C9 monomer or polymer.	bind
31796	1	7783	5	13	NULL	NULL	NULL	HMG-1 protein	GP	recombinant	bind									KRE	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_201	10222341	31  Moreover, recombinant HMG-1 protein binds to KRE in the absence of poly(dI-dC).	bind
31797	2	7783	5	13	NULL	NULL	NULL	statement 1	Process		absence of					poly(dI-dC)	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_201	10222341	31  Moreover, recombinant HMG-1 protein binds to KRE in the absence of poly(dI-dC).	bind
24465	1	7783	6	NULL	NULL	0	NULL	HMG-1 protein	NULL	recombinant	bind	NULL					NULL			KRE	NULL		0	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_201	10222341	31  Moreover, recombinant HMG-1 protein binds to KRE in the absence of poly(dI-dC).	bind
24466	2	7783	6	NULL	NULL	0	NULL	statement 1	NULL		occurs in absence of	NULL				poly(dI-dC)	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_201	10222341	31  Moreover, recombinant HMG-1 protein binds to KRE in the absence of poly(dI-dC).	bind
31798	1	7784	5	13	NULL	NULL	NULL	PGE1 receptor subtype	GP		bind					PGI2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2066_s_156	9351373	31  One subtype of the PGE1 receptor binds PGI2, the other one binds PGE2.	bind
31799	2	7784	5	13	NULL	NULL	NULL	PGE1 receptor subtype	GP		bind					PGE2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2066_s_156	9351373	31  One subtype of the PGE1 receptor binds PGI2, the other one binds PGE2.	bind
24467	1	7784	6	10	NULL	0	NULL	PGE1 receptor subtype \t			bind					PGI2					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2066_s_156	9351373	31  One subtype of the PGE1 receptor binds PGI2, the other one binds PGE2.	bind
24468	2	7784	6	10	NULL	0	NULL	PGE1 receptor subtype			bind					PGE2					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2066_s_156	9351373	31  One subtype of the PGE1 receptor binds PGI2, the other one binds PGE2.	bind
31800	1	7785	5	13	NULL	NULL	NULL	fibroblast	Cell	human;;cardiac	bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_10_1130_s_175	10715259	31  Our data further suggest beta1 integrin is the major receptor involved in human cardiac fibroblast binding to collagen.	bind
31801	2	7785	5	13	NULL	NULL	NULL	beta1 integrin	GP		is a type of					receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_10_1130_s_175	10715259	31  Our data further suggest beta1 integrin is the major receptor involved in human cardiac fibroblast binding to collagen.	bind
31802	3	7785	5	13	NULL	NULL	NULL	beta1 integrin	GP		is involved in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_10_1130_s_175	10715259	31  Our data further suggest beta1 integrin is the major receptor involved in human cardiac fibroblast binding to collagen.	bind
24469	1	7785	6	10	NULL	0	NULL	fibroblast		human;;cardiac	bind					collagen					NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_10_1130_s_175	10715259	31  Our data further suggest beta1 integrin is the major receptor involved in human cardiac fibroblast binding to collagen.	bind
24470	2	7785	6	NULL	NULL	0	NULL	beta1 integrin receptor	NULL		is involved in	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_101_10_1130_s_175	10715259	31  Our data further suggest beta1 integrin is the major receptor involved in human cardiac fibroblast binding to collagen.	bind
31848	1	7786	5	13	NULL	NULL	NULL	platelets	Cell	resting	adhere to					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_8_1248_s_69	9714131	31  The adhesion of resting platelets to fibrinogen was reduced by 29.4 plus-or-minus 4.1% (n=5,  P<0.001) when the binding of fibrinogen to its platelet receptor was prevented by using the specific antibody PAC1.	bind
31849	2	7786	5	13	NULL	NULL	NULL	fibrinogen	GP		bind					platelet receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_8_1248_s_69	9714131	31  The adhesion of resting platelets to fibrinogen was reduced by 29.4 plus-or-minus 4.1% (n=5,  P<0.001) when the binding of fibrinogen to its platelet receptor was prevented by using the specific antibody PAC1.	bind
31850	3	7786	5	13	NULL	NULL	NULL	PAC1 antibody	GP		prevents					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_8_1248_s_69	9714131	31  The adhesion of resting platelets to fibrinogen was reduced by 29.4 plus-or-minus 4.1% (n=5,  P<0.001) when the binding of fibrinogen to its platelet receptor was prevented by using the specific antibody PAC1.	bind
46857	4	7786	5	13	NULL	NULL	NULL	statement 3	Process		reduces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_8_1248_s_69	9714131	31  The adhesion of resting platelets to fibrinogen was reduced by 29.4 plus-or-minus 4.1% (n=5,  P<0.001) when the binding of fibrinogen to its platelet receptor was prevented by using the specific antibody PAC1.	bind
24471	1	7786	6	NULL	NULL	0	NULL	platelets 	NULL	resting	adhere to	NULL				fibrinogen	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_8_1248_s_69	9714131	31  The adhesion of resting platelets to fibrinogen was reduced by 29.4 plus-or-minus 4.1% (n=5,  P<0.001) when the binding of fibrinogen to its platelet receptor was prevented by using the specific antibody PAC1.	bind
24472	3	7786	6	10	NULL	0	NULL	antibody PAC1	NULL	specific	prevents	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_8_1248_s_69	9714131	31  The adhesion of resting platelets to fibrinogen was reduced by 29.4 plus-or-minus 4.1% (n=5,  P<0.001) when the binding of fibrinogen to its platelet receptor was prevented by using the specific antibody PAC1.	bind
46856	2	7786	6	10	NULL	0	NULL	fibrinogen	NULL		bind	NULL				platelet receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_8_1248_s_69	9714131	31  The adhesion of resting platelets to fibrinogen was reduced by 29.4 plus-or-minus 4.1% (n=5,  P<0.001) when the binding of fibrinogen to its platelet receptor was prevented by using the specific antibody PAC1.	bind
46858	4	7786	6	10	NULL	0	NULL	statement 3	NULL		reduces	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_8_1248_s_69	9714131	31  The adhesion of resting platelets to fibrinogen was reduced by 29.4 plus-or-minus 4.1% (n=5,  P<0.001) when the binding of fibrinogen to its platelet receptor was prevented by using the specific antibody PAC1.	bind
31852	1	7787	5	13	NULL	NULL	NULL	anti-LIBS1	GP	binding of	indicates					fibrinogen	GP	receptor activity of			NULL	platelet surface	NULL	NULL	NULL	NULL	gw60_circulation_93_2_229_s_63	8548893	31  Thus, anti-LIBS1 binding indicates fibrinogen receptor activity on the platelet surface.	bind
24627	1	7787	6	10	NULL	0	NULL	anti-LIBS1	NULL	binding of	indicates	NULL				fibrinogen	NULL	receptor activity of			NULL	platelet surface	NULL	NULL	NULL	NULL	gw60_circulation_93_2_229_s_63	8548893	31  Thus, anti-LIBS1 binding indicates fibrinogen receptor activity on the platelet surface.	bind
31853	1	7789	5	13	NULL	NULL	NULL	Vitronectin	GP		bind					type 1 plasminogen activator inhibitor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_270_s_219	9710119	31  Vitronectin binds another proteinase inhibitor, type 1 plasminogen activator inhibitor.	bind
31854	2	7789	5	13	NULL	NULL	NULL	type 1 plasminogen activator inhibitor	GP		is a type of					proteinase inhibitor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_270_s_219	9710119	31  Vitronectin binds another proteinase inhibitor, type 1 plasminogen activator inhibitor.	bind
24631	1	7789	6	NULL	NULL	0	NULL	vitronectin	NULL		bind	NULL				type 1 plasminogen activator inhibitor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_3_270_s_219	9710119	31  Vitronectin binds another proteinase inhibitor, type 1 plasminogen activator inhibitor.	bind
38662	2	7789	6	NULL	NULL	0	NULL	type 1 plasminogen activator inhibitor	NULL		is a type of	NULL				proteinase inhibitor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_3_270_s_219	9710119	31  Vitronectin binds another proteinase inhibitor, type 1 plasminogen activator inhibitor.	bind
31855	1	7790	5	13	NULL	NULL	NULL	BiP	GP		bind					ER stress sensors	GP		ER luminal domain		NULL	in unstressed condition	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1439_s_78	16645155	31 - 33   In unstressed condition, ER chaperone BiP binds to the ER luminal domain of 3 ER stress sensors.	bind
31856	2	7790	5	13	NULL	NULL	NULL	BiP	GP		is a type of					ER chaperone	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1439_s_78	16645155	31 - 33   In unstressed condition, ER chaperone BiP binds to the ER luminal domain of 3 ER stress sensors.	bind
24632	1	7790	6	NULL	NULL	0	NULL	BiP	NULL		bind	NULL				ER	NULL		luminal domain		NULL	unstressed condition	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1439_s_78	16645155	31 - 33   In unstressed condition, ER chaperone BiP binds to the ER luminal domain of 3 ER stress sensors.	bind
38663	2	7790	6	NULL	NULL	0	NULL	BiP	NULL		is a type of	NULL				ER chaperone	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1439_s_78	16645155	31 - 33   In unstressed condition, ER chaperone BiP binds to the ER luminal domain of 3 ER stress sensors.	bind
31857	1	7791	5	13	NULL	NULL	NULL	mAb 8A2	GP		bind					integrin receptor	GP		beta1 subunit		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_4_596_s_92	8635217	31 32 33  We have shown that mAb 8A2 binds to the beta1 subunit of the integrin receptor and enhances beta1-integrin - dependent adherence of leukocytes to cellular and matrix ligands.	bind
31858	2	7791	5	13	NULL	NULL	NULL	leukocytes	Cell		adhere to					cellular ligands	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_4_596_s_92	8635217	31 32 33  We have shown that mAb 8A2 binds to the beta1 subunit of the integrin receptor and enhances beta1-integrin - dependent adherence of leukocytes to cellular and matrix ligands.	bind
31859	3	7791	5	13	NULL	NULL	NULL	statement 2	Process		is dependent on					beta1-integrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_4_596_s_92	8635217	31 32 33  We have shown that mAb 8A2 binds to the beta1 subunit of the integrin receptor and enhances beta1-integrin - dependent adherence of leukocytes to cellular and matrix ligands.	bind
31860	4	7791	5	13	NULL	NULL	NULL	statement 1	Process		enhances					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_4_596_s_92	8635217	31 32 33  We have shown that mAb 8A2 binds to the beta1 subunit of the integrin receptor and enhances beta1-integrin - dependent adherence of leukocytes to cellular and matrix ligands.	bind
31861	5	7791	5	13	NULL	NULL	NULL	leukocytes	Cell		adhere to					matrix ligands	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_4_596_s_92	8635217	31 32 33  We have shown that mAb 8A2 binds to the beta1 subunit of the integrin receptor and enhances beta1-integrin - dependent adherence of leukocytes to cellular and matrix ligands.	bind
31862	6	7791	5	13	NULL	NULL	NULL	statement 5	Process		is dependent on					beta1-integrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_4_596_s_92	8635217	31 32 33  We have shown that mAb 8A2 binds to the beta1 subunit of the integrin receptor and enhances beta1-integrin - dependent adherence of leukocytes to cellular and matrix ligands.	bind
31863	7	7791	5	13	NULL	NULL	NULL	statement 1	Process		enhances					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_4_596_s_92	8635217	31 32 33  We have shown that mAb 8A2 binds to the beta1 subunit of the integrin receptor and enhances beta1-integrin - dependent adherence of leukocytes to cellular and matrix ligands.	bind
24633	1	7791	6	NULL	NULL	0	NULL	mAb 8A2	NULL		bind	NULL				integrin receptor	NULL		beta1 subunit		NULL		0	NULL	NULL	NULL	gw60_circulationres_78_4_596_s_92	8635217	31 32 33  We have shown that mAb 8A2 binds to the beta1 subunit of the integrin receptor and enhances beta1-integrin - dependent adherence of leukocytes to cellular and matrix ligands.	bind
24634	2	7791	6	NULL	NULL	0	NULL	leukocytes	NULL		adhers to	NULL				cellular ligands	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_4_596_s_92	8635217	31 32 33  We have shown that mAb 8A2 binds to the beta1 subunit of the integrin receptor and enhances beta1-integrin - dependent adherence of leukocytes to cellular and matrix ligands.	bind
24635	3	7791	6	NULL	NULL	0	NULL	leukocytes	NULL		adhere to	NULL				matrix ligands	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_4_596_s_92	8635217	31 32 33  We have shown that mAb 8A2 binds to the beta1 subunit of the integrin receptor and enhances beta1-integrin - dependent adherence of leukocytes to cellular and matrix ligands.	bind
24636	4	7791	6	NULL	NULL	0	NULL	statement 2	NULL		is dependent on	NULL				beta1-integrin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_4_596_s_92	8635217	31 32 33  We have shown that mAb 8A2 binds to the beta1 subunit of the integrin receptor and enhances beta1-integrin - dependent adherence of leukocytes to cellular and matrix ligands.	bind
24637	5	7791	6	NULL	NULL	0	NULL	statement 3	NULL		is dependent on	NULL				beta1-integrin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_4_596_s_92	8635217	31 32 33  We have shown that mAb 8A2 binds to the beta1 subunit of the integrin receptor and enhances beta1-integrin - dependent adherence of leukocytes to cellular and matrix ligands.	bind
46859	6	7791	6	10	NULL	0	NULL	statement 1	NULL		enhance	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_4_596_s_92	8635217	31 32 33  We have shown that mAb 8A2 binds to the beta1 subunit of the integrin receptor and enhances beta1-integrin - dependent adherence of leukocytes to cellular and matrix ligands.	bind
46860	7	7791	6	10	NULL	0	NULL	statement 1	NULL		enhance	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_4_596_s_92	8635217	31 32 33  We have shown that mAb 8A2 binds to the beta1 subunit of the integrin receptor and enhances beta1-integrin - dependent adherence of leukocytes to cellular and matrix ligands.	bind
31864	1	7792	5	13	NULL	NULL	NULL	Va receptor	GP	occupancy of	is essential for					factor Xa	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_7_2339_s_289	9337209	31 32 33 34  The occupancy of Va receptor is essential for the subsequent binding of factor Xa, whereas binding of factor VIIIa, though not essential for factor IXa binding, enhances the binding affinity of IXa by fivefold.	bind
31865	2	7792	5	13	NULL	NULL	NULL	factor VIIIa	GP	binding of	is not essential for					factor IXa	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_7_2339_s_289	9337209	31 32 33 34  The occupancy of Va receptor is essential for the subsequent binding of factor Xa, whereas binding of factor VIIIa, though not essential for factor IXa binding, enhances the binding affinity of IXa by fivefold.	bind
31866	3	7792	5	13	NULL	NULL	NULL	factor VIIIa	GP	binding of	enhances					IXa	GP	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_7_2339_s_289	9337209	31 32 33 34  The occupancy of Va receptor is essential for the subsequent binding of factor Xa, whereas binding of factor VIIIa, though not essential for factor IXa binding, enhances the binding affinity of IXa by fivefold.	bind
24888	1	7792	6	NULL	NULL	0	NULL	Va receptor	NULL	occupancy of	is essential for	NULL				factor Xa	NULL	binding of 			NULL		0	NULL	NULL	NULL	gw60_circulation_96_7_2339_s_289	9337209	31 32 33 34  The occupancy of Va receptor is essential for the subsequent binding of factor Xa, whereas binding of factor VIIIa, though not essential for factor IXa binding, enhances the binding affinity of IXa by fivefold.	bind
24889	2	7792	6	NULL	NULL	0	NULL	factor VIIIa	NULL	binding of	is not essential for	NULL				factor IXa	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_circulation_96_7_2339_s_289	9337209	31 32 33 34  The occupancy of Va receptor is essential for the subsequent binding of factor Xa, whereas binding of factor VIIIa, though not essential for factor IXa binding, enhances the binding affinity of IXa by fivefold.	bind
24890	3	7792	6	NULL	NULL	0	NULL	factor VIIIa	NULL	binding of	enhances	NULL				factor IXa	NULL	binding affinity of			NULL		0	NULL	NULL	NULL	gw60_circulation_96_7_2339_s_289	9337209	31 32 33 34  The occupancy of Va receptor is essential for the subsequent binding of factor Xa, whereas binding of factor VIIIa, though not essential for factor IXa binding, enhances the binding affinity of IXa by fivefold.	bind
31867	1	7793	5	13	NULL	NULL	NULL	NHE-1	GP		bind		strongly	cytoplasmic domain		calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_6_962_s_223	8635246	31 50 51  Binding experiments with calmodulin-Sepharose, as well as fluorescence measurements with dansylated calmodulin, revealed that the NHE-1 cytoplasmic domain strongly binds calmodulin in a Ca2+-dependent manner.	bind
31868	2	7793	5	13	NULL	NULL	NULL	statement 1	Process		is dependent on					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_6_962_s_223	8635246	31 50 51  Binding experiments with calmodulin-Sepharose, as well as fluorescence measurements with dansylated calmodulin, revealed that the NHE-1 cytoplasmic domain strongly binds calmodulin in a Ca2+-dependent manner.	bind
24638	1	7793	6	NULL	NULL	0	NULL	NHE-1	NULL		bind	NULL	strongly	cytoplasmic domain		calmodulin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_6_962_s_223	8635246	31 50 51  Binding experiments with calmodulin-Sepharose, as well as fluorescence measurements with dansylated calmodulin, revealed that the NHE-1 cytoplasmic domain strongly binds calmodulin in a Ca2+-dependent manner.	bind
24639	2	7793	6	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				Ca2+	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_6_962_s_223	8635246	31 50 51  Binding experiments with calmodulin-Sepharose, as well as fluorescence measurements with dansylated calmodulin, revealed that the NHE-1 cytoplasmic domain strongly binds calmodulin in a Ca2+-dependent manner.	bind
31869	1	7794	5	13	NULL	NULL	NULL	fibrinogen	GP		is a type of					plasma ligand	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
31870	2	7794	5	13	NULL	NULL	NULL	VWF	GP		is a type of					plasma ligand	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
31871	3	7794	5	13	NULL	NULL	NULL	fibrinogen	GP		bind					GP IIb/IIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
31872	4	7794	5	13	NULL	NULL	NULL	VWF	GP		bind					GP IIb/IIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
31873	5	7794	5	13	NULL	NULL	NULL	Abciximab	Chemical		is a type of					anti - GP IIb/IIa agent	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
31874	6	7794	5	13	NULL	NULL	NULL	Abciximab	Chemical		blocks					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
31875	7	7794	5	13	NULL	NULL	NULL	Abciximab	Chemical		blocks					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
31876	8	7794	5	13	NULL	NULL	NULL	Abciximab	Chemical		prevents					acute thrombotic occlusion	MedicalFinding				NULL	coronary arteries	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
31877	9	7794	5	13	NULL	NULL	NULL	statement 8	Process		occurs after					interventional treatment	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
31878	10	7794	5	13	NULL	NULL	NULL	statement 8	Process		occurs after					stent implantation	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
24891	1	7794	6	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL				GP IIb/IIa	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
24893	2	7794	6	NULL	NULL	0	NULL	VWF	NULL		bind	NULL				GP IIb/IIa	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
24894	3	7794	6	NULL	NULL	0	NULL	Abciximab	NULL		blocks	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
24895	4	7794	6	NULL	NULL	0	NULL	Abciximab	NULL		blocks	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
24896	5	7794	6	10	NULL	0	NULL	Abciximab	NULL		prevents	NULL				acute thrombotic occlusion	NULL				NULL	coronary arteries	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
24897	6	7794	6	NULL	NULL	0	NULL	statement 5	NULL		occurs after	NULL				interventional treatment	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
24898	7	7794	6	NULL	NULL	0	NULL	statement 5	NULL		occurs after	NULL				stent implantation	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
38664	8	7794	6	NULL	NULL	0	NULL	fibrinogen	NULL		is a type of	NULL				plasma ligand	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
38665	9	7794	6	NULL	NULL	0	NULL	vWF	NULL		is a type of	NULL				plasma ligand	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
38666	10	7794	6	NULL	NULL	0	NULL	Abciximab	NULL		is a type of	NULL				anti - GP IIb/IIa agent	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_59	12171801	31 Abciximab was used as an anti - GP IIb/IIa agent, which blocks the binding of plasma ligands such as fibrinogen and VWF to GP IIb/IIa. 32, 33 Recent clinical investigations have revealed abciximab to be effective in preventing acute thrombotic occlusion of the coronary arteries after interventional treatment 34 and stent implantation.	bind
31879	1	7795	5	13	NULL	NULL	NULL	CBP/p300	GP		bind					PPARalpha/RXR heterodimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_15_1861_s_39	11956132	31 Co factors that bind to the PPARalpha/RXR heterodimer include CBP/p300, PBP/TRAP220, PGC-1, and SRC-1.	bind
31880	2	7795	5	13	NULL	NULL	NULL	PBP/TRAP220	GP		bind					PPARalpha/RXR heterodimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_15_1861_s_39	11956132	31 Co factors that bind to the PPARalpha/RXR heterodimer include CBP/p300, PBP/TRAP220, PGC-1, and SRC-1.	bind
31881	3	7795	5	13	NULL	NULL	NULL	PGC-1	GP		bind					PPARalpha/RXR heterodimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_15_1861_s_39	11956132	31 Co factors that bind to the PPARalpha/RXR heterodimer include CBP/p300, PBP/TRAP220, PGC-1, and SRC-1.	bind
31882	4	7795	5	13	NULL	NULL	NULL	SRC-1	GP		bind					PPARalpha/RXR heterodimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_15_1861_s_39	11956132	31 Co factors that bind to the PPARalpha/RXR heterodimer include CBP/p300, PBP/TRAP220, PGC-1, and SRC-1.	bind
31883	5	7795	5	13	NULL	NULL	NULL	CBP/p300	GP		is a type of					co factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_15_1861_s_39	11956132	31 Co factors that bind to the PPARalpha/RXR heterodimer include CBP/p300, PBP/TRAP220, PGC-1, and SRC-1.	bind
31884	6	7795	5	13	NULL	NULL	NULL	PBP/TRAP220	GP		is a type of					co factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_15_1861_s_39	11956132	31 Co factors that bind to the PPARalpha/RXR heterodimer include CBP/p300, PBP/TRAP220, PGC-1, and SRC-1.	bind
31885	7	7795	5	13	NULL	NULL	NULL	PGC-1	GP		is a type of					co factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_15_1861_s_39	11956132	31 Co factors that bind to the PPARalpha/RXR heterodimer include CBP/p300, PBP/TRAP220, PGC-1, and SRC-1.	bind
31886	8	7795	5	13	NULL	NULL	NULL	SRC-1	GP		is a type of					co factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_15_1861_s_39	11956132	31 Co factors that bind to the PPARalpha/RXR heterodimer include CBP/p300, PBP/TRAP220, PGC-1, and SRC-1.	bind
24640	1	7795	6	NULL	NULL	0	NULL	CBP/p300	NULL		bind	NULL				PPARalpha/RXR heterodimer	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_15_1861_s_39	11956132	31 Co factors that bind to the PPARalpha/RXR heterodimer include CBP/p300, PBP/TRAP220, PGC-1, and SRC-1.	bind
24641	2	7795	6	NULL	NULL	0	NULL	PBP/TRAP220	NULL		bind	NULL				PPARalpha/RXR heterodimer	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_15_1861_s_39	11956132	31 Co factors that bind to the PPARalpha/RXR heterodimer include CBP/p300, PBP/TRAP220, PGC-1, and SRC-1.	bind
24642	3	7795	6	NULL	NULL	0	NULL	PGC-1	NULL		bind	NULL				PPARalpha/RXR heterodimer	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_15_1861_s_39	11956132	31 Co factors that bind to the PPARalpha/RXR heterodimer include CBP/p300, PBP/TRAP220, PGC-1, and SRC-1.	bind
24643	4	7795	6	NULL	NULL	0	NULL	SRC-1	NULL		bind	NULL				PPARalpha/RXR heterodimer	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_15_1861_s_39	11956132	31 Co factors that bind to the PPARalpha/RXR heterodimer include CBP/p300, PBP/TRAP220, PGC-1, and SRC-1.	bind
38667	5	7795	6	NULL	NULL	0	NULL	CBP/p300	NULL		is a type of	NULL				cofactor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_15_1861_s_39	11956132	31 Co factors that bind to the PPARalpha/RXR heterodimer include CBP/p300, PBP/TRAP220, PGC-1, and SRC-1.	bind
38668	6	7795	6	NULL	NULL	0	NULL	PBP/TRAP220	NULL		is a type of	NULL				cofactor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_15_1861_s_39	11956132	31 Co factors that bind to the PPARalpha/RXR heterodimer include CBP/p300, PBP/TRAP220, PGC-1, and SRC-1.	bind
38669	7	7795	6	NULL	NULL	0	NULL	PGC-1	NULL		is a type of	NULL				cofactor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_15_1861_s_39	11956132	31 Co factors that bind to the PPARalpha/RXR heterodimer include CBP/p300, PBP/TRAP220, PGC-1, and SRC-1.	bind
38670	8	7795	6	NULL	NULL	0	NULL	SRC-1	NULL		is a type of	NULL				cofactor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_15_1861_s_39	11956132	31 Co factors that bind to the PPARalpha/RXR heterodimer include CBP/p300, PBP/TRAP220, PGC-1, and SRC-1.	bind
31887	1	7796	5	13	NULL	NULL	NULL	estrogen	Chemical		induces					IGF-1R mRNA	NucleicAcid	downregulation of			NULL	rat aortic VSMCs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_67	14604834	31 Estrogen-induced downregulation of IGF-1R mRNA and protein in rat aortic VSMCs was mediated by the inhibition of SP-1 binding to the IGF-1R promoter.	bind
31888	2	7796	5	13	NULL	NULL	NULL	estrogen	Chemical		induces					IGF-1R protein	GP	downregulation of			NULL	rat aortic VSMCs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_67	14604834	31 Estrogen-induced downregulation of IGF-1R mRNA and protein in rat aortic VSMCs was mediated by the inhibition of SP-1 binding to the IGF-1R promoter.	bind
31889	3	7796	5	13	NULL	NULL	NULL	SP-1	GP		bind					IGF-1R	GP			promoter	NULL	rat aortic VSMCs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_67	14604834	31 Estrogen-induced downregulation of IGF-1R mRNA and protein in rat aortic VSMCs was mediated by the inhibition of SP-1 binding to the IGF-1R promoter.	bind
31890	4	7796	5	13	NULL	NULL	NULL	statement 3	Process	inhibition of	mediates					statement 1	Process				NULL	rat aortic VSMCs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_67	14604834	31 Estrogen-induced downregulation of IGF-1R mRNA and protein in rat aortic VSMCs was mediated by the inhibition of SP-1 binding to the IGF-1R promoter.	bind
31891	5	7796	5	13	NULL	NULL	NULL	statement 3	Process	inhibition of	mediates					statement 2	Process				NULL	rat aortic VSMCs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_67	14604834	31 Estrogen-induced downregulation of IGF-1R mRNA and protein in rat aortic VSMCs was mediated by the inhibition of SP-1 binding to the IGF-1R promoter.	bind
24644	1	7796	6	10	NULL	0	NULL	SP-1			bind					IGF-1R				promoter	NULL	rat aortic VSMCs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_67	14604834	31 Estrogen-induced downregulation of IGF-1R mRNA and protein in rat aortic VSMCs was mediated by the inhibition of SP-1 binding to the IGF-1R promoter.	bind
24645	2	7796	6	NULL	NULL	0	NULL	estrogen	NULL		induces	NULL				IGF-1R mRNA	NULL	downregulation of			NULL	rat aortic VSMCs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_67	14604834	31 Estrogen-induced downregulation of IGF-1R mRNA and protein in rat aortic VSMCs was mediated by the inhibition of SP-1 binding to the IGF-1R promoter.	bind
24646	3	7796	6	NULL	NULL	0	NULL	estrogen	NULL		induces	NULL				IGF-1R protein	NULL	downregulation of			NULL	rat aortic VSMCs	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_67	14604834	31 Estrogen-induced downregulation of IGF-1R mRNA and protein in rat aortic VSMCs was mediated by the inhibition of SP-1 binding to the IGF-1R promoter.	bind
24647	4	7796	6	10	NULL	0	NULL	statement 2			is mediated by					statement 1		inhibiton of			NULL	rat aortic VSMCs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_67	14604834	31 Estrogen-induced downregulation of IGF-1R mRNA and protein in rat aortic VSMCs was mediated by the inhibition of SP-1 binding to the IGF-1R promoter.	bind
24648	5	7796	6	10	NULL	0	NULL	statement 3			is mediated by					statement 1		inhibiton of			NULL	rat aortic VSMCs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_67	14604834	31 Estrogen-induced downregulation of IGF-1R mRNA and protein in rat aortic VSMCs was mediated by the inhibition of SP-1 binding to the IGF-1R promoter.	bind
31892	1	7797	5	13	NULL	NULL	NULL	TNF-alpha	GP		stimulates					endothelial proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
31893	2	7797	5	13	NULL	NULL	NULL	IL-1beta 	GP		stimulates					endothelial proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
31894	5	7797	5	13	NULL	NULL	NULL	SP-1	GP		bind					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
31895	6	7797	5	13	NULL	NULL	NULL	SP-1	GP		bind					statement 4	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
31896	7	7797	5	13	NULL	NULL	NULL	NF-kappaB	GP		bind					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
31897	8	7797	5	13	NULL	NULL	NULL	NF-kappaB	GP		bind					statement 4	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
31898	9	7797	5	13	NULL	NULL	NULL	LA	Chemical		supress					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
31899	10	7797	5	13	NULL	NULL	NULL	LA	Chemical		supress					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
31900	11	7797	5	13	NULL	NULL	NULL	LA	Chemical		supress					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
31901	12	7797	5	13	NULL	NULL	NULL	LA	Chemical		supress					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
46861	3	7797	5	13	NULL	NULL	NULL	statement 1	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
46862	4	7797	5	13	NULL	NULL	NULL	statement 2	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
24649	1	7797	6	10	NULL	0	NULL	TNF-alpha	NULL		stimulate	NULL				endothelial protein	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
24650	2	7797	6	10	NULL	0	NULL	IL-1beta	NULL		stimulate	NULL				endothelial protein	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
24651	5	7797	6	10	NULL	0	NULL	NF-kappaB	NULL		bind	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
24652	6	7797	6	10	NULL	0	NULL	NF-kappaB	NULL		bind	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
24653	7	7797	6	10	NULL	0	NULL	Sp1	NULL		bind	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
24654	8	7797	6	10	NULL	0	NULL	Sp1	NULL		bind	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
38750	9	7797	6	10	NULL	0	NULL	LA	NULL		suppresses	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
38751	10	7797	6	10	NULL	0	NULL	LA	NULL		suppresses	NULL				statement 6	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
38752	11	7797	6	10	NULL	0	NULL	LA	NULL		suppresses	NULL				statement 7	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
38753	12	7797	6	10	NULL	0	NULL	LA	NULL		suppresses	NULL				statement 8	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
46863	3	7797	6	10	NULL	0	NULL	statement 1	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
46864	4	7797	6	10	NULL	0	NULL	statement 2	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_9_880_s_256	16166554	31 Our EMSA indicated that LA suppressed not only NF-kappaB binding but also SP-1 binding of TNF-alpha - or IL-1beta - stimulated endothelial proteins to the DNA.	bind
31902	1	7798	5	13	NULL	NULL	NULL	tetracycline repression system	Process		induces					FAK	GP	expression of			NULL	FAK-null fibroblasts	NULL	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_191	16397143	31 Surprisingly, induced expression of FAK using a tetracycline repression system in FAK-null fibroblasts led to a marked expression of LPP consistent with FAK regulating the expression of LPP, as it has been reported to induce expression of the homeodomain protein Prx1, 32 and Prx1 has been shown to increase SRF binding to CArG elements before the recruitment of myocardin in SMCs. 33 The role of FAK and LPP in nonmotile cells is less clear.	bind
31903	2	7798	5	13	NULL	NULL	NULL	statement 1	Process		leads to					LPP	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_191	16397143	31 Surprisingly, induced expression of FAK using a tetracycline repression system in FAK-null fibroblasts led to a marked expression of LPP consistent with FAK regulating the expression of LPP, as it has been reported to induce expression of the homeodomain protein Prx1, 32 and Prx1 has been shown to increase SRF binding to CArG elements before the recruitment of myocardin in SMCs. 33 The role of FAK and LPP in nonmotile cells is less clear.	bind
31904	3	7798	5	13	NULL	NULL	NULL	FAK	GP		regulates					LPP	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_191	16397143	31 Surprisingly, induced expression of FAK using a tetracycline repression system in FAK-null fibroblasts led to a marked expression of LPP consistent with FAK regulating the expression of LPP, as it has been reported to induce expression of the homeodomain protein Prx1, 32 and Prx1 has been shown to increase SRF binding to CArG elements before the recruitment of myocardin in SMCs. 33 The role of FAK and LPP in nonmotile cells is less clear.	bind
31905	4	7798	5	13	NULL	NULL	NULL	statement 2	Process		consistent with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_191	16397143	31 Surprisingly, induced expression of FAK using a tetracycline repression system in FAK-null fibroblasts led to a marked expression of LPP consistent with FAK regulating the expression of LPP, as it has been reported to induce expression of the homeodomain protein Prx1, 32 and Prx1 has been shown to increase SRF binding to CArG elements before the recruitment of myocardin in SMCs. 33 The role of FAK and LPP in nonmotile cells is less clear.	bind
31906	5	7798	5	13	NULL	NULL	NULL	FAK	GP		induces					Prx1	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_191	16397143	31 Surprisingly, induced expression of FAK using a tetracycline repression system in FAK-null fibroblasts led to a marked expression of LPP consistent with FAK regulating the expression of LPP, as it has been reported to induce expression of the homeodomain protein Prx1, 32 and Prx1 has been shown to increase SRF binding to CArG elements before the recruitment of myocardin in SMCs. 33 The role of FAK and LPP in nonmotile cells is less clear.	bind
31907	6	7798	5	13	NULL	NULL	NULL	Prx1	GP		is a type of					homeodomain protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_191	16397143	31 Surprisingly, induced expression of FAK using a tetracycline repression system in FAK-null fibroblasts led to a marked expression of LPP consistent with FAK regulating the expression of LPP, as it has been reported to induce expression of the homeodomain protein Prx1, 32 and Prx1 has been shown to increase SRF binding to CArG elements before the recruitment of myocardin in SMCs. 33 The role of FAK and LPP in nonmotile cells is less clear.	bind
31908	7	7798	5	13	NULL	NULL	NULL	SRF	GP		bind									CArG elements	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_191	16397143	31 Surprisingly, induced expression of FAK using a tetracycline repression system in FAK-null fibroblasts led to a marked expression of LPP consistent with FAK regulating the expression of LPP, as it has been reported to induce expression of the homeodomain protein Prx1, 32 and Prx1 has been shown to increase SRF binding to CArG elements before the recruitment of myocardin in SMCs. 33 The role of FAK and LPP in nonmotile cells is less clear.	bind
31909	8	7798	5	13	NULL	NULL	NULL	Prx1	GP		increases					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_191	16397143	31 Surprisingly, induced expression of FAK using a tetracycline repression system in FAK-null fibroblasts led to a marked expression of LPP consistent with FAK regulating the expression of LPP, as it has been reported to induce expression of the homeodomain protein Prx1, 32 and Prx1 has been shown to increase SRF binding to CArG elements before the recruitment of myocardin in SMCs. 33 The role of FAK and LPP in nonmotile cells is less clear.	bind
31910	9	7798	5	13	NULL	NULL	NULL	myocardin	GP		is recruited to					SMCs	Cell				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_191	16397143	31 Surprisingly, induced expression of FAK using a tetracycline repression system in FAK-null fibroblasts led to a marked expression of LPP consistent with FAK regulating the expression of LPP, as it has been reported to induce expression of the homeodomain protein Prx1, 32 and Prx1 has been shown to increase SRF binding to CArG elements before the recruitment of myocardin in SMCs. 33 The role of FAK and LPP in nonmotile cells is less clear.	bind
31911	10	7798	5	13	NULL	NULL	NULL	statement 8	Process		occurs before					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_191	16397143	31 Surprisingly, induced expression of FAK using a tetracycline repression system in FAK-null fibroblasts led to a marked expression of LPP consistent with FAK regulating the expression of LPP, as it has been reported to induce expression of the homeodomain protein Prx1, 32 and Prx1 has been shown to increase SRF binding to CArG elements before the recruitment of myocardin in SMCs. 33 The role of FAK and LPP in nonmotile cells is less clear.	bind
24899	1	7798	6	NULL	NULL	0	NULL	SRF	NULL		bind	NULL					NULL			CArG element	NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_191	16397143	31 Surprisingly, induced expression of FAK using a tetracycline repression system in FAK-null fibroblasts led to a marked expression of LPP consistent with FAK regulating the expression of LPP, as it has been reported to induce expression of the homeodomain protein Prx1, 32 and Prx1 has been shown to increase SRF binding to CArG elements before the recruitment of myocardin in SMCs. 33 The role of FAK and LPP in nonmotile cells is less clear.	bind
24900	2	7798	6	NULL	NULL	0	NULL	Prx1	NULL		increase	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_191	16397143	31 Surprisingly, induced expression of FAK using a tetracycline repression system in FAK-null fibroblasts led to a marked expression of LPP consistent with FAK regulating the expression of LPP, as it has been reported to induce expression of the homeodomain protein Prx1, 32 and Prx1 has been shown to increase SRF binding to CArG elements before the recruitment of myocardin in SMCs. 33 The role of FAK and LPP in nonmotile cells is less clear.	bind
24901	3	7798	6	NULL	NULL	0	NULL	myocardin	NULL		is recruited on	NULL				SMC	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_191	16397143	31 Surprisingly, induced expression of FAK using a tetracycline repression system in FAK-null fibroblasts led to a marked expression of LPP consistent with FAK regulating the expression of LPP, as it has been reported to induce expression of the homeodomain protein Prx1, 32 and Prx1 has been shown to increase SRF binding to CArG elements before the recruitment of myocardin in SMCs. 33 The role of FAK and LPP in nonmotile cells is less clear.	bind
24902	4	7798	6	NULL	NULL	0	NULL	statement 1	NULL		occurs before	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_191	16397143	31 Surprisingly, induced expression of FAK using a tetracycline repression system in FAK-null fibroblasts led to a marked expression of LPP consistent with FAK regulating the expression of LPP, as it has been reported to induce expression of the homeodomain protein Prx1, 32 and Prx1 has been shown to increase SRF binding to CArG elements before the recruitment of myocardin in SMCs. 33 The role of FAK and LPP in nonmotile cells is less clear.	bind
24903	5	7798	6	NULL	NULL	0	NULL	statement 8	NULL		leads to	NULL				LPP	NULL	expression of			NULL	FAK-null fibroblasts	NULL	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_191	16397143	31 Surprisingly, induced expression of FAK using a tetracycline repression system in FAK-null fibroblasts led to a marked expression of LPP consistent with FAK regulating the expression of LPP, as it has been reported to induce expression of the homeodomain protein Prx1, 32 and Prx1 has been shown to increase SRF binding to CArG elements before the recruitment of myocardin in SMCs. 33 The role of FAK and LPP in nonmotile cells is less clear.	bind
24904	6	7798	6	NULL	NULL	0	NULL	FAK	NULL		regulates	NULL				LPP	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_191	16397143	31 Surprisingly, induced expression of FAK using a tetracycline repression system in FAK-null fibroblasts led to a marked expression of LPP consistent with FAK regulating the expression of LPP, as it has been reported to induce expression of the homeodomain protein Prx1, 32 and Prx1 has been shown to increase SRF binding to CArG elements before the recruitment of myocardin in SMCs. 33 The role of FAK and LPP in nonmotile cells is less clear.	bind
24905	7	7798	6	NULL	NULL	0	NULL	FAK	NULL		induce	NULL				Prx1	NULL	expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_191	16397143	31 Surprisingly, induced expression of FAK using a tetracycline repression system in FAK-null fibroblasts led to a marked expression of LPP consistent with FAK regulating the expression of LPP, as it has been reported to induce expression of the homeodomain protein Prx1, 32 and Prx1 has been shown to increase SRF binding to CArG elements before the recruitment of myocardin in SMCs. 33 The role of FAK and LPP in nonmotile cells is less clear.	bind
38754	8	7798	6	NULL	NULL	0	NULL	tetracycline repression system	NULL		induces	NULL				FAK	NULL	expression of			NULL	FAK-null fibroblasts	0	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_191	16397143	31 Surprisingly, induced expression of FAK using a tetracycline repression system in FAK-null fibroblasts led to a marked expression of LPP consistent with FAK regulating the expression of LPP, as it has been reported to induce expression of the homeodomain protein Prx1, 32 and Prx1 has been shown to increase SRF binding to CArG elements before the recruitment of myocardin in SMCs. 33 The role of FAK and LPP in nonmotile cells is less clear.	bind
38755	9	7798	6	NULL	NULL	0	NULL	Prx1	NULL		is a type of	NULL				homeodomain protein	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_378_s_191	16397143	31 Surprisingly, induced expression of FAK using a tetracycline repression system in FAK-null fibroblasts led to a marked expression of LPP consistent with FAK regulating the expression of LPP, as it has been reported to induce expression of the homeodomain protein Prx1, 32 and Prx1 has been shown to increase SRF binding to CArG elements before the recruitment of myocardin in SMCs. 33 The role of FAK and LPP in nonmotile cells is less clear.	bind
31912	1	7799	5	13	NULL	NULL	NULL	decorin	GP		bind					hydroxyapatite	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2391_s_148	15472131	31 The binding of decorin to hydroxyapatite was demonstrated at concentrations >1 mg/mL.	bind
24655	1	7799	6	NULL	NULL	0	NULL	decorin	NULL		bind	NULL				hydroxyapatite	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2391_s_148	15472131	31 The binding of decorin to hydroxyapatite was demonstrated at concentrations >1 mg/mL.	bind
31913	1	7801	5	13	NULL	NULL	NULL	ATP	Chemical		bind					receptor	GP		TK domain		NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_3_423_s_198	16027270	31 TKI inhibition works via competitive inhibition of the binding of ATP to the TK domain of the receptor, which results in attenuated autophosphorylation.	bind
31914	2	7801	5	13	NULL	NULL	NULL	TKI	GP		inhibits		competitively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_3_423_s_198	16027270	31 TKI inhibition works via competitive inhibition of the binding of ATP to the TK domain of the receptor, which results in attenuated autophosphorylation.	bind
31915	3	7801	5	13	NULL	NULL	NULL	statement 2	Process		results in					autophosphorylation	Process	attenuated			NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_3_423_s_198	16027270	31 TKI inhibition works via competitive inhibition of the binding of ATP to the TK domain of the receptor, which results in attenuated autophosphorylation.	bind
24656	1	7801	6	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				receptor	NULL		TK domain		NULL		0	NULL	NULL	NULL	gw70_circulation_112_3_423_s_198	16027270	31 TKI inhibition works via competitive inhibition of the binding of ATP to the TK domain of the receptor, which results in attenuated autophosphorylation.	bind
24657	2	7801	6	NULL	NULL	0	NULL	TKI	NULL		inhibits	NULL	competitively			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_112_3_423_s_198	16027270	31 TKI inhibition works via competitive inhibition of the binding of ATP to the TK domain of the receptor, which results in attenuated autophosphorylation.	bind
24658	3	7801	6	NULL	NULL	0	NULL	statement 2	NULL		results in	NULL				autophosphorylation	NULL	attenuated			NULL		0	NULL	NULL	NULL	gw70_circulation_112_3_423_s_198	16027270	31 TKI inhibition works via competitive inhibition of the binding of ATP to the TK domain of the receptor, which results in attenuated autophosphorylation.	bind
47121	1	7802	5	13	NULL	NULL	NULL	HgCl2	Chemical		bind					humic acids	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5416_939_s_148	0010320369	31, 233 (1997)  [CrossRef] [ISI];   H. Biester and H. Zimmer,       ibid. 32, 2755 (1998)] have demonstrated that Hg degrees  is the only Hg species that has significant thermal desorption below 100 degrees C, whereas HgCl2 and Hg bound to humic acids have maximum Hg releases at much higher temperatures (200 degrees  to 300 degrees C).	bind
47122	1	7802	5	13	NULL	NULL	NULL	Hg	Chemical		bind					humic acids	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5416_939_s_148	0010320369	31, 233 (1997)  [CrossRef] [ISI];   H. Biester and H. Zimmer,       ibid. 32, 2755 (1998)] have demonstrated that Hg degrees  is the only Hg species that has significant thermal desorption below 100 degrees C, whereas HgCl2 and Hg bound to humic acids have maximum Hg releases at much higher temperatures (200 degrees  to 300 degrees C).	bind
24659	1	7802	6	NULL	NULL	0	NULL	HgCl2	NULL		bind	NULL				humic acids	NULL				NULL		0	NULL	NULL	NULL	gw60_science_284_5416_939_s_148	0010320369	31, 233 (1997)  [CrossRef] [ISI];   H. Biester and H. Zimmer,       ibid. 32, 2755 (1998)] have demonstrated that Hg degrees  is the only Hg species that has significant thermal desorption below 100 degrees C, whereas HgCl2 and Hg bound to humic acids have maximum Hg releases at much higher temperatures (200 degrees  to 300 degrees C).	bind
24660	2	7802	6	NULL	NULL	0	NULL	Hg	NULL		bind	NULL				humic acids	NULL				NULL		0	NULL	NULL	NULL	gw60_science_284_5416_939_s_148	0010320369	31, 233 (1997)  [CrossRef] [ISI];   H. Biester and H. Zimmer,       ibid. 32, 2755 (1998)] have demonstrated that Hg degrees  is the only Hg species that has significant thermal desorption below 100 degrees C, whereas HgCl2 and Hg bound to humic acids have maximum Hg releases at much higher temperatures (200 degrees  to 300 degrees C).	bind
31916	1	7803	5	13	NULL	NULL	NULL	serum	OrganismPart		induces					TF	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_163	12600889	31, 32 In contrast, the SRR mediates induction of TF expression by serum, lipoproteins, or shear stress 12, 13, 32 and contains three Sp1 and one Egr-1 binding sites.	bind
31917	2	7803	5	13	NULL	NULL	NULL	lipoproteins	GP		induces					TF	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_163	12600889	31, 32 In contrast, the SRR mediates induction of TF expression by serum, lipoproteins, or shear stress 12, 13, 32 and contains three Sp1 and one Egr-1 binding sites.	bind
31918	3	7803	5	13	NULL	NULL	NULL	shear stress			induces					TF	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_163	12600889	31, 32 In contrast, the SRR mediates induction of TF expression by serum, lipoproteins, or shear stress 12, 13, 32 and contains three Sp1 and one Egr-1 binding sites.	bind
31919	4	7803	5	13	NULL	NULL	NULL				mediates				SRR	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_163	12600889	31, 32 In contrast, the SRR mediates induction of TF expression by serum, lipoproteins, or shear stress 12, 13, 32 and contains three Sp1 and one Egr-1 binding sites.	bind
31920	5	7803	5	13	NULL	NULL	NULL				mediates				SRR	statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_163	12600889	31, 32 In contrast, the SRR mediates induction of TF expression by serum, lipoproteins, or shear stress 12, 13, 32 and contains three Sp1 and one Egr-1 binding sites.	bind
31921	6	7803	5	13	NULL	NULL	NULL				mediates				SRR	statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_163	12600889	31, 32 In contrast, the SRR mediates induction of TF expression by serum, lipoproteins, or shear stress 12, 13, 32 and contains three Sp1 and one Egr-1 binding sites.	bind
31922	7	7803	5	NULL	NULL	0	NULL		NULL		contains	NULL			SRR		NULL			Egr-1 binding sites	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_163	12600889	31, 32 In contrast, the SRR mediates induction of TF expression by serum, lipoproteins, or shear stress 12, 13, 32 and contains three Sp1 and one Egr-1 binding sites.	bind
31923	8	7803	5	NULL	NULL	0	NULL		NULL		contains	NULL			SRR		NULL			Sp1 binding sites	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_163	12600889	31, 32 In contrast, the SRR mediates induction of TF expression by serum, lipoproteins, or shear stress 12, 13, 32 and contains three Sp1 and one Egr-1 binding sites.	bind
24661	1	7803	6	NULL	NULL	0	NULL	serum	NULL		induces	NULL				TF	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_163	12600889	31, 32 In contrast, the SRR mediates induction of TF expression by serum, lipoproteins, or shear stress 12, 13, 32 and contains three Sp1 and one Egr-1 binding sites.	bind
24662	2	7803	6	NULL	NULL	0	NULL		NULL		mediates	NULL			SRR	statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_163	12600889	31, 32 In contrast, the SRR mediates induction of TF expression by serum, lipoproteins, or shear stress 12, 13, 32 and contains three Sp1 and one Egr-1 binding sites.	bind
24663	3	7803	6	NULL	NULL	0	NULL	lipoproteins	NULL		induce	NULL				TF	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_163	12600889	31, 32 In contrast, the SRR mediates induction of TF expression by serum, lipoproteins, or shear stress 12, 13, 32 and contains three Sp1 and one Egr-1 binding sites.	bind
24664	4	7803	6	NULL	NULL	0	NULL	shear stress	NULL		induces	NULL				TF	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_163	12600889	31, 32 In contrast, the SRR mediates induction of TF expression by serum, lipoproteins, or shear stress 12, 13, 32 and contains three Sp1 and one Egr-1 binding sites.	bind
24665	5	7803	6	NULL	NULL	0	NULL		NULL		mediates	NULL			SRR	statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_163	12600889	31, 32 In contrast, the SRR mediates induction of TF expression by serum, lipoproteins, or shear stress 12, 13, 32 and contains three Sp1 and one Egr-1 binding sites.	bind
24666	6	7803	6	NULL	NULL	0	NULL		NULL		mediates	NULL			SRR	statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_163	12600889	31, 32 In contrast, the SRR mediates induction of TF expression by serum, lipoproteins, or shear stress 12, 13, 32 and contains three Sp1 and one Egr-1 binding sites.	bind
24667	7	7803	6	NULL	NULL	0	NULL		NULL		contains	NULL			SRR		NULL			Sp1 binding site	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_163	12600889	31, 32 In contrast, the SRR mediates induction of TF expression by serum, lipoproteins, or shear stress 12, 13, 32 and contains three Sp1 and one Egr-1 binding sites.	bind
24668	8	7803	6	NULL	NULL	0	NULL		NULL		contains	NULL			SRR		NULL			Egr-1 binding site	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_4_394_s_163	12600889	31, 32 In contrast, the SRR mediates induction of TF expression by serum, lipoproteins, or shear stress 12, 13, 32 and contains three Sp1 and one Egr-1 binding sites.	bind
31924	1	7804	5	13	NULL	NULL	NULL	5''-AMP	Chemical		bind					glycogen phosphorylase	GP	bovine;;liver			NULL		NULL	NULL	NULL	NULL	gw70_nature_439_7074_340_s_264	16421573	31, 57-64 (1982) |  PubMed |  ISI |  ChemPort |    arcia-Fuentes, L. ,  Camara-Artigas, A. ,  Lopez-Mayorga, [[ O.  &  Baron ]], C.   Thermodynamic characterization of 5''-AMP binding to bovine liver glycogen phosphorylase  a.  J. Biol. Chem. 271, 27569-27574 (1996) |  PubMed |  ChemPort |    aasik, [[ K.  &  Lee ]], C. C.  Reciprocal regulation of haem biosynthesis and the  circadian clock in mammals.	bind
24669	1	7804	6	10	NULL	0	NULL	5''-AMP	NULL		bind	NULL				 glycogen phosphorylase	NULL	bovine;;liver			NULL		NULL	NULL	NULL	NULL	gw70_nature_439_7074_340_s_264	16421573	31, 57-64 (1982) |  PubMed |  ISI |  ChemPort |    arcia-Fuentes, L. ,  Camara-Artigas, A. ,  Lopez-Mayorga, [[ O.  &  Baron ]], C.   Thermodynamic characterization of 5''-AMP binding to bovine liver glycogen phosphorylase  a.  J. Biol. Chem. 271, 27569-27574 (1996) |  PubMed |  ChemPort |    aasik, [[ K.  &  Lee ]], C. C.  Reciprocal regulation of haem biosynthesis and the  circadian clock in mammals.	bind
31925	1	7805	5	13	NULL	NULL	NULL	E2A	GP		mediates					p21Waf1/Cip1 gene	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8333_s_124	14660614	31-kDa Represses E2A-mediated p21Waf1/Cip1 Gene Transcription by Inhibiting DNA Binding of E2A --	bind
31926	2	7805	5	13	NULL	NULL	NULL	E2A	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8333_s_124	14660614	31-kDa Represses E2A-mediated p21Waf1/Cip1 Gene Transcription by Inhibiting DNA Binding of E2A --	bind
31927	3	7805	5	13	NULL	NULL	NULL	31-kDa protein	GP		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8333_s_124	14660614	31-kDa Represses E2A-mediated p21Waf1/Cip1 Gene Transcription by Inhibiting DNA Binding of E2A --	bind
31928	4	7805	5	13	NULL	NULL	NULL	statement 3	Process		represses					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8333_s_124	14660614	31-kDa Represses E2A-mediated p21Waf1/Cip1 Gene Transcription by Inhibiting DNA Binding of E2A --	bind
38957	5	7805	5	13	NULL	NULL	NULL	statement 4	Process		causes					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8333_s_124	14660614	31-kDa Represses E2A-mediated p21Waf1/Cip1 Gene Transcription by Inhibiting DNA Binding of E2A --	bind
24670	1	7805	6	NULL	NULL	0	NULL	E2A	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8333_s_124	14660614	31-kDa Represses E2A-mediated p21Waf1/Cip1 Gene Transcription by Inhibiting DNA Binding of E2A --	bind
24671	2	7805	6	NULL	NULL	0	NULL	E2A	NULL		mediates	NULL				p21Waf1/Cip1 Gene	NULL	transcription of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8333_s_124	14660614	31-kDa Represses E2A-mediated p21Waf1/Cip1 Gene Transcription by Inhibiting DNA Binding of E2A --	bind
24672	3	7805	6	NULL	NULL	0	NULL	31-kDa protein	NULL		represses	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8333_s_124	14660614	31-kDa Represses E2A-mediated p21Waf1/Cip1 Gene Transcription by Inhibiting DNA Binding of E2A --	bind
24673	4	7805	6	10	NULL	0	NULL	statement 3			inhibits					statement 1					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8333_s_124	14660614	31-kDa Represses E2A-mediated p21Waf1/Cip1 Gene Transcription by Inhibiting DNA Binding of E2A --	bind
24674	5	7805	6	NULL	NULL	0	NULL	statement 3	NULL		occurs by	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8333_s_124	14660614	31-kDa Represses E2A-mediated p21Waf1/Cip1 Gene Transcription by Inhibiting DNA Binding of E2A --	bind
31929	1	7807	5	13	NULL	NULL	NULL	PGA trianion	Chemical		bind					TIM	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_11_9544_s_47	12522213	31P NMR studies indicate that PGA binds to TIM as a trianion ( ).	bind
24676	1	7807	6	NULL	NULL	0	NULL	PGA 	NULL		bind	NULL				TIM	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9544_s_47	12522213	31P NMR studies indicate that PGA binds to TIM as a trianion ( ).	bind
31930	1	7809	5	13	NULL	NULL	NULL	NADPH	Chemical		bind					dihydrofolate reductase	GP	 L. casei			NULL		NULL	NULL	NULL	NULL	gw60_structure_4_1_33_s_488	8805511	31P NMR studies of NADPH and NADP+ binding to  L. casei dihydrofolate reductase.	bind
31931	2	7809	5	13	NULL	NULL	NULL	NADP+	Chemical		bind					dihydrofolate reductase	GP	L. casei			NULL		NULL	NULL	NULL	NULL	gw60_structure_4_1_33_s_488	8805511	31P NMR studies of NADPH and NADP+ binding to  L. casei dihydrofolate reductase.	bind
24677	1	7809	6	NULL	NULL	0	NULL	NADPH	NULL		bind	NULL				dihydrofolate reductase	NULL	L.casei			NULL		0	NULL	NULL	NULL	gw60_structure_4_1_33_s_488	8805511	31P NMR studies of NADPH and NADP+ binding to  L. casei dihydrofolate reductase.	bind
24678	2	7809	6	NULL	NULL	0	NULL	NADP+	NULL		bind	NULL				dihydrofolate reductase	NULL	L.casei			NULL		0	NULL	NULL	NULL	gw60_structure_4_1_33_s_488	8805511	31P NMR studies of NADPH and NADP+ binding to  L. casei dihydrofolate reductase.	bind
31932	1	7810	5	13	NULL	NULL	NULL	d9	NucleicAcid		bind					XPA	GP		MBD		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2635_s_211	11410673	31P resonances in the interior of d9 broadened and/or shifted before 31P resonances at the termini, suggesting that when d9 is bound to XPA-MBD the motion of the DNA is more restricted in the interior of the sequence than at the termini.	bind
31933	2	7810	5	13	NULL	NULL	NULL	statement 1	Process		restrict					DNA	NucleicAcid	motion of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2635_s_211	11410673	31P resonances in the interior of d9 broadened and/or shifted before 31P resonances at the termini, suggesting that when d9 is bound to XPA-MBD the motion of the DNA is more restricted in the interior of the sequence than at the termini.	bind
47123	3	7810	5	13	NULL	NULL	NULL	statement 2	Process		occurs upon					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2635_s_211	11410673	31P resonances in the interior of d9 broadened and/or shifted before 31P resonances at the termini, suggesting that when d9 is bound to XPA-MBD the motion of the DNA is more restricted in the interior of the sequence than at the termini.	bind
24679	1	7810	6	NULL	NULL	0	NULL	d9	NULL		bind	NULL				XPA	NULL		MBD		NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2635_s_211	11410673	31P resonances in the interior of d9 broadened and/or shifted before 31P resonances at the termini, suggesting that when d9 is bound to XPA-MBD the motion of the DNA is more restricted in the interior of the sequence than at the termini.	bind
24680	2	7810	6	10	NULL	0	NULL	statement 1	NULL		restrict	NULL				DNA	NULL	motion of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2635_s_211	11410673	31P resonances in the interior of d9 broadened and/or shifted before 31P resonances at the termini, suggesting that when d9 is bound to XPA-MBD the motion of the DNA is more restricted in the interior of the sequence than at the termini.	bind
24681	3	7810	6	10	NULL	0	NULL	statement 2	NULL		occurs upon	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2635_s_211	11410673	31P resonances in the interior of d9 broadened and/or shifted before 31P resonances at the termini, suggesting that when d9 is bound to XPA-MBD the motion of the DNA is more restricted in the interior of the sequence than at the termini.	bind
31934	1	7813	5	13	NULL	NULL	NULL	HVTs-SM1 cells	Cell	rapid;;continuous proliferation of	is associated with					SV40 LT antigen	Chemical	expression of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_3_636_s_205	10712385	32  Our results indicate that the rapid and continuous proliferation of HVTs-SM1 cells under permissive temperature conditions is associated with the expression of SV40 LT antigen and with LT-antigen binding and inactivation of p53.	bind
31935	2	7813	5	13	NULL	NULL	NULL	LT-antigen	Chemical		bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_3_636_s_205	10712385	32  Our results indicate that the rapid and continuous proliferation of HVTs-SM1 cells under permissive temperature conditions is associated with the expression of SV40 LT antigen and with LT-antigen binding and inactivation of p53.	bind
31936	3	7813	5	13	NULL	NULL	NULL	statement 2	Process		inactivates					p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_3_636_s_205	10712385	32  Our results indicate that the rapid and continuous proliferation of HVTs-SM1 cells under permissive temperature conditions is associated with the expression of SV40 LT antigen and with LT-antigen binding and inactivation of p53.	bind
31937	4	7813	5	13	NULL	NULL	NULL	HVTs-SM1 cells	Cell	rapid;;continuous proliferation of	is associated with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_3_636_s_205	10712385	32  Our results indicate that the rapid and continuous proliferation of HVTs-SM1 cells under permissive temperature conditions is associated with the expression of SV40 LT antigen and with LT-antigen binding and inactivation of p53.	bind
31938	5	7813	5	13	NULL	NULL	NULL	HVTs-SM1 cells	Cell	rapid;;continuous proliferation of	is associated with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_3_636_s_205	10712385	32  Our results indicate that the rapid and continuous proliferation of HVTs-SM1 cells under permissive temperature conditions is associated with the expression of SV40 LT antigen and with LT-antigen binding and inactivation of p53.	bind
24907	1	7813	6	10	NULL	0	NULL	HVTs-SM1 cells	NULL	rapid;;continuous proliferation of	is associated with	NULL				SV40 LT antigen	NULL	expression of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_3_636_s_205	10712385	32  Our results indicate that the rapid and continuous proliferation of HVTs-SM1 cells under permissive temperature conditions is associated with the expression of SV40 LT antigen and with LT-antigen binding and inactivation of p53.	bind
24908	2	7813	6	NULL	NULL	0	NULL	LT-antigen	NULL		bind	NULL				p53	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_3_636_s_205	10712385	32  Our results indicate that the rapid and continuous proliferation of HVTs-SM1 cells under permissive temperature conditions is associated with the expression of SV40 LT antigen and with LT-antigen binding and inactivation of p53.	bind
24909	3	7813	6	10	NULL	0	NULL	statement 2			inactivates					p53					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_3_636_s_205	10712385	32  Our results indicate that the rapid and continuous proliferation of HVTs-SM1 cells under permissive temperature conditions is associated with the expression of SV40 LT antigen and with LT-antigen binding and inactivation of p53.	bind
24910	4	7813	6	10	NULL	0	NULL	HVTs-SM1 cells	NULL	rapid;;continuous proliferation of	is associated with	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_3_636_s_205	10712385	32  Our results indicate that the rapid and continuous proliferation of HVTs-SM1 cells under permissive temperature conditions is associated with the expression of SV40 LT antigen and with LT-antigen binding and inactivation of p53.	bind
24911	5	7813	6	10	NULL	0	NULL	HVTs-SM1 cells	NULL	rapid;;continuous proliferation of	is associated with	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_3_636_s_205	10712385	32  Our results indicate that the rapid and continuous proliferation of HVTs-SM1 cells under permissive temperature conditions is associated with the expression of SV40 LT antigen and with LT-antigen binding and inactivation of p53.	bind
31939	1	7815	5	13	NULL	NULL	NULL	IGTPase	GP		located in		predominantly			endoplasmic reticulum	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_6_704_s_243	10189358	32  Recent reports indicate that IGTPase is located predominantly in the endoplasmic reticulum of cells; however, GTP binding status of IGTPase is independent of its capacity to localize in the cellular compartment.	bind
31940	2	7815	5	13	NULL	NULL	NULL	IGTPase	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_6_704_s_243	10189358	32  Recent reports indicate that IGTPase is located predominantly in the endoplasmic reticulum of cells; however, GTP binding status of IGTPase is independent of its capacity to localize in the cellular compartment.	bind
31941	3	7815	5	13	NULL	NULL	NULL	statement 2	Process		is independent of					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_6_704_s_243	10189358	32  Recent reports indicate that IGTPase is located predominantly in the endoplasmic reticulum of cells; however, GTP binding status of IGTPase is independent of its capacity to localize in the cellular compartment.	bind
24682	1	7815	6	NULL	NULL	0	NULL	IGTPase	NULL		is located on	NULL	predominantly			endoplasmic reticulum	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_6_704_s_243	10189358	32  Recent reports indicate that IGTPase is located predominantly in the endoplasmic reticulum of cells; however, GTP binding status of IGTPase is independent of its capacity to localize in the cellular compartment.	bind
24683	2	7815	6	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				IGTPase	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_6_704_s_243	10189358	32  Recent reports indicate that IGTPase is located predominantly in the endoplasmic reticulum of cells; however, GTP binding status of IGTPase is independent of its capacity to localize in the cellular compartment.	bind
24684	3	7815	6	NULL	NULL	0	NULL	statement 2	NULL		is independent of	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_6_704_s_243	10189358	32  Recent reports indicate that IGTPase is located predominantly in the endoplasmic reticulum of cells; however, GTP binding status of IGTPase is independent of its capacity to localize in the cellular compartment.	bind
31942	1	7816	5	13	NULL	NULL	NULL	transcription factor	GP	nuclear	bind					AP-1/ets probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1872_s_269	10446065	32  This result is consistent with our current observation (Figure 11  ) that anti - c-Jun and Jun-B antibodies blocked the binding of a nuclear transcription factor to the AP-1/ets probe.	bind
31943	2	7816	5	13	NULL	NULL	NULL	anti - c-Jun antibodies	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1872_s_269	10446065	32  This result is consistent with our current observation (Figure 11  ) that anti - c-Jun and Jun-B antibodies blocked the binding of a nuclear transcription factor to the AP-1/ets probe.	bind
31944	3	7816	5	13	NULL	NULL	NULL	anti - Jun-B antibodies	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1872_s_269	10446065	32  This result is consistent with our current observation (Figure 11  ) that anti - c-Jun and Jun-B antibodies blocked the binding of a nuclear transcription factor to the AP-1/ets probe.	bind
24685	1	7816	6	NULL	NULL	0	NULL	transcription factor	NULL	nuclear	bind	NULL				AP-1/ets probe	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1872_s_269	10446065	32  This result is consistent with our current observation (Figure 11  ) that anti - c-Jun and Jun-B antibodies blocked the binding of a nuclear transcription factor to the AP-1/ets probe.	bind
24686	2	7816	6	NULL	NULL	0	NULL	anti - c-Jun antibody	NULL		blocks	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1872_s_269	10446065	32  This result is consistent with our current observation (Figure 11  ) that anti - c-Jun and Jun-B antibodies blocked the binding of a nuclear transcription factor to the AP-1/ets probe.	bind
24687	3	7816	6	NULL	NULL	0	NULL	Jun-B antibody	NULL		blocks	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1872_s_269	10446065	32  This result is consistent with our current observation (Figure 11  ) that anti - c-Jun and Jun-B antibodies blocked the binding of a nuclear transcription factor to the AP-1/ets probe.	bind
31945	1	7818	5	13	NULL	NULL	NULL	BTEB2	GP		bind									SE1	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_2_182_s_39	10417400	32  We demonstrate that basic transcriptional element (BTE) binding protein-2 (BTEB2) binds to the SE1 and regulates transcription of the SMemb gene.	bind
31946	2	7818	5	13	NULL	NULL	NULL	BTEB2	GP		is					basic transcriptional element binding protein-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_2_182_s_39	10417400	32  We demonstrate that basic transcriptional element (BTE) binding protein-2 (BTEB2) binds to the SE1 and regulates transcription of the SMemb gene.	bind
31947	3	7818	5	13	NULL	NULL	NULL	statement 1	Process		regulates					SMemb gene	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_2_182_s_39	10417400	32  We demonstrate that basic transcriptional element (BTE) binding protein-2 (BTEB2) binds to the SE1 and regulates transcription of the SMemb gene.	bind
24688	1	7818	6	NULL	NULL	0	NULL	BTEB2	NULL		bind	NULL				SE1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_2_182_s_39	10417400	32  We demonstrate that basic transcriptional element (BTE) binding protein-2 (BTEB2) binds to the SE1 and regulates transcription of the SMemb gene.	bind
24689	2	7818	6	NULL	NULL	0	NULL	BTEB-2	NULL		is	NULL				basic transcriptional element binding protein-2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_2_182_s_39	10417400	32  We demonstrate that basic transcriptional element (BTE) binding protein-2 (BTEB2) binds to the SE1 and regulates transcription of the SMemb gene.	bind
24691	3	7818	6	NULL	NULL	0	NULL	BTEB2	NULL		regulates	NULL				SMemb gene	NULL	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_2_182_s_39	10417400	32  We demonstrate that basic transcriptional element (BTE) binding protein-2 (BTEB2) binds to the SE1 and regulates transcription of the SMemb gene.	bind
31948	1	7819	5	13	NULL	NULL	NULL	Factor VII	GP		bind					TF	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_62	12231555	32 -  34 Factor VII binds to TF and is rapidly activated 35 by coagulation proteases 36 and by noncoagulation proteases, depending on the cellular location of the TF.	bind
31949	2	7819	5	13	NULL	NULL	NULL	coagulation proteases	GP		activates		rapidly			Factor VII	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_62	12231555	32 -  34 Factor VII binds to TF and is rapidly activated 35 by coagulation proteases 36 and by noncoagulation proteases, depending on the cellular location of the TF.	bind
31950	3	7819	5	13	NULL	NULL	NULL	noncoagulation proteases	GP		activates		rapidly			Factor VII	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_62	12231555	32 -  34 Factor VII binds to TF and is rapidly activated 35 by coagulation proteases 36 and by noncoagulation proteases, depending on the cellular location of the TF.	bind
31951	4	7819	5	13	NULL	NULL	NULL	statement 2	Process		is dependent on					TF	GP	cellular location of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_62	12231555	32 -  34 Factor VII binds to TF and is rapidly activated 35 by coagulation proteases 36 and by noncoagulation proteases, depending on the cellular location of the TF.	bind
31952	5	7819	5	13	NULL	NULL	NULL	statement 3	Process		is dependent on					TF	GP	cellular location of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_62	12231555	32 -  34 Factor VII binds to TF and is rapidly activated 35 by coagulation proteases 36 and by noncoagulation proteases, depending on the cellular location of the TF.	bind
24692	1	7819	6	NULL	NULL	0	NULL	factor VII	NULL		bind	NULL				TF	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_62	12231555	32 -  34 Factor VII binds to TF and is rapidly activated 35 by coagulation proteases 36 and by noncoagulation proteases, depending on the cellular location of the TF.	bind
24693	2	7819	6	10	NULL	0	NULL	coagulation proteases	NULL		activate	NULL	rapidly			factor VII	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_62	12231555	32 -  34 Factor VII binds to TF and is rapidly activated 35 by coagulation proteases 36 and by noncoagulation proteases, depending on the cellular location of the TF.	bind
24694	3	7819	6	10	NULL	0	NULL	noncoagulation proteases	NULL		activate	NULL	rapidly			factor VII	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_62	12231555	32 -  34 Factor VII binds to TF and is rapidly activated 35 by coagulation proteases 36 and by noncoagulation proteases, depending on the cellular location of the TF.	bind
38761	4	7819	6	NULL	NULL	0	NULL	statement 2	NULL		is dependent on	NULL				TF	NULL	cellular location of 			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_62	12231555	32 -  34 Factor VII binds to TF and is rapidly activated 35 by coagulation proteases 36 and by noncoagulation proteases, depending on the cellular location of the TF.	bind
38763	5	7819	6	NULL	NULL	0	NULL	statement 3	NULL		is dependent on	NULL				TF	NULL	cellular location of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_62	12231555	32 -  34 Factor VII binds to TF and is rapidly activated 35 by coagulation proteases 36 and by noncoagulation proteases, depending on the cellular location of the TF.	bind
31953	1	7820	5	13	NULL	NULL	NULL	uPAR	GP		colocalize with					cytokeratin-1	GP				NULL	endothelial cells	NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1227_s_170	15044324	32 A recent study revealed that uPAR and cytokeratin-1 colocalize on endothelial cells and may form a receptor complex that mediates HK binding and the subsequent release of bradykinin.	bind
31954	2	7820	5	13	NULL	NULL	NULL	statement 1	Process		forms		may			receptor complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1227_s_170	15044324	32 A recent study revealed that uPAR and cytokeratin-1 colocalize on endothelial cells and may form a receptor complex that mediates HK binding and the subsequent release of bradykinin.	bind
31955	3	7820	5	13	NULL	NULL	NULL	receptor complex	GP		mediates					HK	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1227_s_170	15044324	32 A recent study revealed that uPAR and cytokeratin-1 colocalize on endothelial cells and may form a receptor complex that mediates HK binding and the subsequent release of bradykinin.	bind
31956	4	7820	5	13	NULL	NULL	NULL	statement 3	Process		mediates					bradykinin	GP	release of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1227_s_170	15044324	32 A recent study revealed that uPAR and cytokeratin-1 colocalize on endothelial cells and may form a receptor complex that mediates HK binding and the subsequent release of bradykinin.	bind
24695	1	7820	6	NULL	NULL	0	NULL	uPAR	NULL		colocalize with	NULL				cytokeratin-1	NULL				NULL	endothelial cells	NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1227_s_170	15044324	32 A recent study revealed that uPAR and cytokeratin-1 colocalize on endothelial cells and may form a receptor complex that mediates HK binding and the subsequent release of bradykinin.	bind
24697	2	7820	6	10	NULL	0	NULL	statement 1	NULL		form	NULL	may			receptor complex	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1227_s_170	15044324	32 A recent study revealed that uPAR and cytokeratin-1 colocalize on endothelial cells and may form a receptor complex that mediates HK binding and the subsequent release of bradykinin.	bind
24698	3	7820	6	3	NULL	0	NULL	receptor complex	NULL		mediates	NULL				HK	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1227_s_170	15044324	32 A recent study revealed that uPAR and cytokeratin-1 colocalize on endothelial cells and may form a receptor complex that mediates HK binding and the subsequent release of bradykinin.	bind
24699	4	7820	6	NULL	NULL	0	NULL	statement 3	NULL		mediates	NULL				bradykinin	NULL	release of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1227_s_170	15044324	32 A recent study revealed that uPAR and cytokeratin-1 colocalize on endothelial cells and may form a receptor complex that mediates HK binding and the subsequent release of bradykinin.	bind
31957	1	7821	5	13	NULL	NULL	NULL	plasminogen	GP		bind					fibrin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1397_s_179	16574890	32 Because lysine residues in the fibrinogen molecule mediate the binding of plasminogen and tPA to fibrin, 38 lysine modification may impair plasminogen activation and fibrin cleavage by plasmin.	bind
31958	2	7821	5	13	NULL	NULL	NULL	tPA	GP		bind					fibrin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1397_s_179	16574890	32 Because lysine residues in the fibrinogen molecule mediate the binding of plasminogen and tPA to fibrin, 38 lysine modification may impair plasminogen activation and fibrin cleavage by plasmin.	bind
31959	3	7821	5	13	NULL	NULL	NULL	fibrinogen molecule	GP		mediates			lysine residues		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1397_s_179	16574890	32 Because lysine residues in the fibrinogen molecule mediate the binding of plasminogen and tPA to fibrin, 38 lysine modification may impair plasminogen activation and fibrin cleavage by plasmin.	bind
31960	4	7821	5	13	NULL	NULL	NULL	fibrinogen molecule	GP		mediates			lysine residues		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1397_s_179	16574890	32 Because lysine residues in the fibrinogen molecule mediate the binding of plasminogen and tPA to fibrin, 38 lysine modification may impair plasminogen activation and fibrin cleavage by plasmin.	bind
31961	5	7821	5	13	NULL	NULL	NULL	fibrinogen molecule	GP	modification of	impairs		may	lysine		plasminogen	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1397_s_179	16574890	32 Because lysine residues in the fibrinogen molecule mediate the binding of plasminogen and tPA to fibrin, 38 lysine modification may impair plasminogen activation and fibrin cleavage by plasmin.	bind
31962	6	7821	5	13	NULL	NULL	NULL	plasmin	GP		cleaves					fibrin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1397_s_179	16574890	32 Because lysine residues in the fibrinogen molecule mediate the binding of plasminogen and tPA to fibrin, 38 lysine modification may impair plasminogen activation and fibrin cleavage by plasmin.	bind
31963	7	7821	5	13	NULL	NULL	NULL	fibrinogen molecule	GP	modification of	impairs		may	lysine		statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1397_s_179	16574890	32 Because lysine residues in the fibrinogen molecule mediate the binding of plasminogen and tPA to fibrin, 38 lysine modification may impair plasminogen activation and fibrin cleavage by plasmin.	bind
24700	1	7821	6	NULL	NULL	0	NULL	plasminogen	NULL		bind	NULL				fibrin	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1397_s_179	16574890	32 Because lysine residues in the fibrinogen molecule mediate the binding of plasminogen and tPA to fibrin, 38 lysine modification may impair plasminogen activation and fibrin cleavage by plasmin.	bind
24701	2	7821	6	NULL	NULL	0	NULL	tPA	NULL		bind	NULL				fibrin	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1397_s_179	16574890	32 Because lysine residues in the fibrinogen molecule mediate the binding of plasminogen and tPA to fibrin, 38 lysine modification may impair plasminogen activation and fibrin cleavage by plasmin.	bind
24702	3	7821	6	NULL	NULL	0	NULL	fibrinogen molecule	NULL		mediate	NULL		lysine residues		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1397_s_179	16574890	32 Because lysine residues in the fibrinogen molecule mediate the binding of plasminogen and tPA to fibrin, 38 lysine modification may impair plasminogen activation and fibrin cleavage by plasmin.	bind
24703	4	7821	6	NULL	NULL	0	NULL	fibrinogen molecule	NULL		mediate	NULL		lysine residues		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1397_s_179	16574890	32 Because lysine residues in the fibrinogen molecule mediate the binding of plasminogen and tPA to fibrin, 38 lysine modification may impair plasminogen activation and fibrin cleavage by plasmin.	bind
24704	5	7821	6	NULL	NULL	0	NULL	fibrinogen molecule	NULL	modification of	impair	NULL	may	lysine		plasminogen	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1397_s_179	16574890	32 Because lysine residues in the fibrinogen molecule mediate the binding of plasminogen and tPA to fibrin, 38 lysine modification may impair plasminogen activation and fibrin cleavage by plasmin.	bind
24705	6	7821	6	NULL	NULL	0	NULL	plasmin	NULL		cleaves	NULL				fibrin	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1397_s_179	16574890	32 Because lysine residues in the fibrinogen molecule mediate the binding of plasminogen and tPA to fibrin, 38 lysine modification may impair plasminogen activation and fibrin cleavage by plasmin.	bind
24706	7	7821	6	NULL	NULL	0	NULL	fibrinogen molecule	NULL	modification of	impair	NULL	may	lysine residues		statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1397_s_179	16574890	32 Because lysine residues in the fibrinogen molecule mediate the binding of plasminogen and tPA to fibrin, 38 lysine modification may impair plasminogen activation and fibrin cleavage by plasmin.	bind
31964	1	7822	5	13	NULL	NULL	NULL	VEGF-B	GP		bind					neuropilin 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_2_114_s_256	12805240	32 Binding of VEGF-B to neuropilin 1 might also mediate biological responses of VEGF-B.	bind
31965	2	7822	5	13	NULL	NULL	NULL	statement 1	Process		mediates					VEGF-B	GP	biological responses of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_2_114_s_256	12805240	32 Binding of VEGF-B to neuropilin 1 might also mediate biological responses of VEGF-B.	bind
24707	1	7822	6	NULL	NULL	0	NULL	VEGF-B	NULL		bind	NULL				neuropilin 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_2_114_s_256	12805240	32 Binding of VEGF-B to neuropilin 1 might also mediate biological responses of VEGF-B.	bind
24708	2	7822	6	NULL	NULL	0	NULL	statement 1	NULL		mediates	NULL	may			VEGF-B	NULL	biological responses of 			NULL		0	NULL	NULL	NULL	gw60_circulationres_93_2_114_s_256	12805240	32 Binding of VEGF-B to neuropilin 1 might also mediate biological responses of VEGF-B.	bind
31966	1	7823	5	13	NULL	NULL	NULL	SRF	GP		bind									CArG boxes	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_737_s_74	12740224	32 In addition to regulating growth-responsive genes such as c-fos, SRF binding to CArG boxes has been shown to regulate numerous muscle-specific genes.	bind
31967	2	7823	5	13	NULL	NULL	NULL	statement 1	Process		regulates					c-fos	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_737_s_74	12740224	32 In addition to regulating growth-responsive genes such as c-fos, SRF binding to CArG boxes has been shown to regulate numerous muscle-specific genes.	bind
31968	3	7823	5	13	NULL	NULL	NULL	c-fos	GP		is a type of					growth-responsive genes	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_737_s_74	12740224	32 In addition to regulating growth-responsive genes such as c-fos, SRF binding to CArG boxes has been shown to regulate numerous muscle-specific genes.	bind
31969	4	7823	5	13	NULL	NULL	NULL	statement 1	Process		regulates					muscle-specific genes	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_737_s_74	12740224	32 In addition to regulating growth-responsive genes such as c-fos, SRF binding to CArG boxes has been shown to regulate numerous muscle-specific genes.	bind
38960	5	7823	5	13	NULL	NULL	NULL	statement 1	Process		regulates					growth response genes	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_737_s_74	12740224	32 In addition to regulating growth-responsive genes such as c-fos, SRF binding to CArG boxes has been shown to regulate numerous muscle-specific genes.	bind
24709	1	7823	6	NULL	NULL	0	NULL	SRF	NULL		bind	NULL					NULL			CArG box	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_737_s_74	12740224	32 In addition to regulating growth-responsive genes such as c-fos, SRF binding to CArG boxes has been shown to regulate numerous muscle-specific genes.	bind
24710	2	7823	6	NULL	NULL	0	NULL	statement 1	NULL		regulate	NULL				muscle specific genes	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_737_s_74	12740224	32 In addition to regulating growth-responsive genes such as c-fos, SRF binding to CArG boxes has been shown to regulate numerous muscle-specific genes.	bind
24711	3	7823	6	NULL	NULL	0	NULL	statement 1	NULL		regulates	NULL				growth responsive genes	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_737_s_74	12740224	32 In addition to regulating growth-responsive genes such as c-fos, SRF binding to CArG boxes has been shown to regulate numerous muscle-specific genes.	bind
38765	4	7823	6	NULL	NULL	0	NULL	c-fos	NULL		is a type of	NULL				growth responsive gene	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_737_s_74	12740224	32 In addition to regulating growth-responsive genes such as c-fos, SRF binding to CArG boxes has been shown to regulate numerous muscle-specific genes.	bind
38766	5	7823	6	NULL	NULL	0	NULL	statement 1	NULL		regulates	NULL				c-fos	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_737_s_74	12740224	32 In addition to regulating growth-responsive genes such as c-fos, SRF binding to CArG boxes has been shown to regulate numerous muscle-specific genes.	bind
31970	1	7824	5	13	NULL	NULL	NULL	p50-p65 heterodimer	GP		bind					I-kappaB	GP				NULL	cytosol of cells that have inducible NF-kappaB activity	NULL	NULL	NULL	NULL	gw60_circulation_98_21_2255_s_174	9826311	32 In cells that have inducible NF-kappaB activity, the factor comprises a p50-p65 heterodimer bound by an inhibitory subunit I-kappaB in the cytosol and can be activated by dissociation of I-kappaB.	bind
31971	2	7824	5	13	NULL	NULL	NULL	I-kappaB	GP	dissociation of	activates					p50-p65 heterodimer	GP				NULL	\tcytosol of cells that have inducible NF-kappaB activity	NULL	NULL	NULL	NULL	gw60_circulation_98_21_2255_s_174	9826311	32 In cells that have inducible NF-kappaB activity, the factor comprises a p50-p65 heterodimer bound by an inhibitory subunit I-kappaB in the cytosol and can be activated by dissociation of I-kappaB.	bind
31972	3	7824	5	13	NULL	NULL	NULL	I-kappaB	GP		is a type of					inhibitory subunit 	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_98_21_2255_s_174	9826311	32 In cells that have inducible NF-kappaB activity, the factor comprises a p50-p65 heterodimer bound by an inhibitory subunit I-kappaB in the cytosol and can be activated by dissociation of I-kappaB.	bind
24712	1	7824	6	10	NULL	0	NULL	p50-p65 heterodimer			bind					I-kappaB					NULL	\tcytosol of cells that have inducible NF-kappaB activity	NULL	NULL	NULL	NULL	gw60_circulation_98_21_2255_s_174	9826311	32 In cells that have inducible NF-kappaB activity, the factor comprises a p50-p65 heterodimer bound by an inhibitory subunit I-kappaB in the cytosol and can be activated by dissociation of I-kappaB.	bind
24713	2	7824	6	10	NULL	0	NULL	I-kappaB		dissociation of	activates					statement 1					NULL	\tcytosol of cells that have inducible NF-kappaB activity	NULL	NULL	NULL	NULL	gw60_circulation_98_21_2255_s_174	9826311	32 In cells that have inducible NF-kappaB activity, the factor comprises a p50-p65 heterodimer bound by an inhibitory subunit I-kappaB in the cytosol and can be activated by dissociation of I-kappaB.	bind
38767	3	7824	6	NULL	NULL	0	NULL	I-kappaB	NULL		is a type of	NULL				inhibitory subunit	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_98_21_2255_s_174	9826311	32 In cells that have inducible NF-kappaB activity, the factor comprises a p50-p65 heterodimer bound by an inhibitory subunit I-kappaB in the cytosol and can be activated by dissociation of I-kappaB.	bind
31973	1	7825	5	13	NULL	NULL	NULL	moesin	GP	phosphorylated;;human	bind			Thr558		ezrin	GP	phosphorylated	Thr567		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_181_s_70	14592842	32 Phosphorylation of the ezrin/radixin/moesin (ERM) substrates of Rho-kinase was measured, using a rabbit polyclonal antibody to phosphorylated human moesin (Thr558), which also binds to phosphorylated ezrin (Thr567) and radixin (Thr564).	bind
31974	2	7825	5	13	NULL	NULL	NULL	moesin	GP	phosphorylated;;human	bind			Thr558		radixin	GP	phosphorylated	Thr564		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_181_s_70	14592842	32 Phosphorylation of the ezrin/radixin/moesin (ERM) substrates of Rho-kinase was measured, using a rabbit polyclonal antibody to phosphorylated human moesin (Thr558), which also binds to phosphorylated ezrin (Thr567) and radixin (Thr564).	bind
38961	3	7825	5	13	NULL	NULL	NULL	ERM	GP		is					ezrin/radixin/moesin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_181_s_70	14592842	32 Phosphorylation of the ezrin/radixin/moesin (ERM) substrates of Rho-kinase was measured, using a rabbit polyclonal antibody to phosphorylated human moesin (Thr558), which also binds to phosphorylated ezrin (Thr567) and radixin (Thr564).	bind
24714	1	7825	6	NULL	NULL	0	NULL	ERM	NULL		is	NULL				ezrin/radixin/moesin	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_181_s_70	14592842	32 Phosphorylation of the ezrin/radixin/moesin (ERM) substrates of Rho-kinase was measured, using a rabbit polyclonal antibody to phosphorylated human moesin (Thr558), which also binds to phosphorylated ezrin (Thr567) and radixin (Thr564).	bind
24715	2	7825	6	10	NULL	0	NULL	moesin		human;;phosphorylated	bind			Thr558		ezrin		phosphorylated	Thr567		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_181_s_70	14592842	32 Phosphorylation of the ezrin/radixin/moesin (ERM) substrates of Rho-kinase was measured, using a rabbit polyclonal antibody to phosphorylated human moesin (Thr558), which also binds to phosphorylated ezrin (Thr567) and radixin (Thr564).	bind
24716	3	7825	6	10	NULL	0	NULL	moesin		phosphorylated;;human	bind					radixin		phosphorylated	Thr564		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_181_s_70	14592842	32 Phosphorylation of the ezrin/radixin/moesin (ERM) substrates of Rho-kinase was measured, using a rabbit polyclonal antibody to phosphorylated human moesin (Thr558), which also binds to phosphorylated ezrin (Thr567) and radixin (Thr564).	bind
31975	1	7826	5	13	NULL	NULL	NULL	LPS	Chemical		express					inflammatory mediators	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_3_236_s_236	16002747	32 Similarly, anti-CD14 antibodies inhibit the expression of inflammatory mediators by LPS. 25 In the current study, we found that L-4F prevented the binding of LPS to LBP in a concentration-dependent manner.	bind
31976	2	7826	5	13	NULL	NULL	NULL	anti-CD14 antibodies	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_3_236_s_236	16002747	32 Similarly, anti-CD14 antibodies inhibit the expression of inflammatory mediators by LPS. 25 In the current study, we found that L-4F prevented the binding of LPS to LBP in a concentration-dependent manner.	bind
31977	3	7826	5	13	NULL	NULL	NULL	LPS	Chemical		bind					LBP	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_3_236_s_236	16002747	32 Similarly, anti-CD14 antibodies inhibit the expression of inflammatory mediators by LPS. 25 In the current study, we found that L-4F prevented the binding of LPS to LBP in a concentration-dependent manner.	bind
31978	4	7826	5	13	NULL	NULL	NULL	L-4F	GP		prevents					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_3_236_s_236	16002747	32 Similarly, anti-CD14 antibodies inhibit the expression of inflammatory mediators by LPS. 25 In the current study, we found that L-4F prevented the binding of LPS to LBP in a concentration-dependent manner.	bind
31979	5	7826	5	13	NULL	NULL	NULL	statement 4	Process		is dependent on					concentration					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_3_236_s_236	16002747	32 Similarly, anti-CD14 antibodies inhibit the expression of inflammatory mediators by LPS. 25 In the current study, we found that L-4F prevented the binding of LPS to LBP in a concentration-dependent manner.	bind
24717	1	7826	6	NULL	NULL	0	NULL	LPS	NULL		bind	NULL				LBP	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_3_236_s_236	16002747	32 Similarly, anti-CD14 antibodies inhibit the expression of inflammatory mediators by LPS. 25 In the current study, we found that L-4F prevented the binding of LPS to LBP in a concentration-dependent manner.	bind
24718	2	7826	6	NULL	NULL	0	NULL	L-4F	NULL		prevents	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_3_236_s_236	16002747	32 Similarly, anti-CD14 antibodies inhibit the expression of inflammatory mediators by LPS. 25 In the current study, we found that L-4F prevented the binding of LPS to LBP in a concentration-dependent manner.	bind
24719	3	7826	6	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				concentration	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_3_236_s_236	16002747	32 Similarly, anti-CD14 antibodies inhibit the expression of inflammatory mediators by LPS. 25 In the current study, we found that L-4F prevented the binding of LPS to LBP in a concentration-dependent manner.	bind
24721	5	7826	6	10	NULL	0	NULL	anti-CD14 antibodies			inhibits					statement 4					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_3_236_s_236	16002747	32 Similarly, anti-CD14 antibodies inhibit the expression of inflammatory mediators by LPS. 25 In the current study, we found that L-4F prevented the binding of LPS to LBP in a concentration-dependent manner.	bind
24740	4	7826	6	10	NULL	0	NULL	LPS			express					\tinflammatory mediators					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_3_236_s_236	16002747	32 Similarly, anti-CD14 antibodies inhibit the expression of inflammatory mediators by LPS. 25 In the current study, we found that L-4F prevented the binding of LPS to LBP in a concentration-dependent manner.	bind
31980	1	7827	5	13	NULL	NULL	NULL	p27Kip1	GP		inhibits					cdk	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1129_s_150	10514396	32 The mechanism by which p27Kip1 inhibits cdk activity is not fully understood, but it appears that binding of p27Kip1 to the cyclin D2/cdk4 complex sequesters the inhibitor away from the cyclin E/cdk2 complex, causing inactivation of the latter.	bind
31981	2	7827	5	13	NULL	NULL	NULL	p27Kip1	GP		bind					cyclin D2/cdk4 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1129_s_150	10514396	32 The mechanism by which p27Kip1 inhibits cdk activity is not fully understood, but it appears that binding of p27Kip1 to the cyclin D2/cdk4 complex sequesters the inhibitor away from the cyclin E/cdk2 complex, causing inactivation of the latter.	bind
31982	3	7827	5	13	NULL	NULL	NULL	p27Kip1	GP		sequestered from					cyclin E/cdk2 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1129_s_150	10514396	32 The mechanism by which p27Kip1 inhibits cdk activity is not fully understood, but it appears that binding of p27Kip1 to the cyclin D2/cdk4 complex sequesters the inhibitor away from the cyclin E/cdk2 complex, causing inactivation of the latter.	bind
31983	4	7827	5	13	NULL	NULL	NULL	statement 2	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1129_s_150	10514396	32 The mechanism by which p27Kip1 inhibits cdk activity is not fully understood, but it appears that binding of p27Kip1 to the cyclin D2/cdk4 complex sequesters the inhibitor away from the cyclin E/cdk2 complex, causing inactivation of the latter.	bind
31984	5	7827	5	13	NULL	NULL	NULL	statement 3	Process		inactivates					cyclin E/cdk2 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1129_s_150	10514396	32 The mechanism by which p27Kip1 inhibits cdk activity is not fully understood, but it appears that binding of p27Kip1 to the cyclin D2/cdk4 complex sequesters the inhibitor away from the cyclin E/cdk2 complex, causing inactivation of the latter.	bind
24741	1	7827	6	NULL	NULL	0	NULL	p27Kip1	NULL		bind	NULL				cyclin D2/cdk4 complex	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_4_1129_s_150	10514396	32 The mechanism by which p27Kip1 inhibits cdk activity is not fully understood, but it appears that binding of p27Kip1 to the cyclin D2/cdk4 complex sequesters the inhibitor away from the cyclin E/cdk2 complex, causing inactivation of the latter.	bind
24912	2	7827	6	NULL	NULL	0	NULL	statement 1	NULL		sequesters	NULL				p27Kip1 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1129_s_150	10514396	32 The mechanism by which p27Kip1 inhibits cdk activity is not fully understood, but it appears that binding of p27Kip1 to the cyclin D2/cdk4 complex sequesters the inhibitor away from the cyclin E/cdk2 complex, causing inactivation of the latter.	bind
24913	3	7827	6	NULL	NULL	0	NULL	p27kip1	NULL		is sequestered from	NULL				cyclin E/cdk2 complex	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1129_s_150	10514396	32 The mechanism by which p27Kip1 inhibits cdk activity is not fully understood, but it appears that binding of p27Kip1 to the cyclin D2/cdk4 complex sequesters the inhibitor away from the cyclin E/cdk2 complex, causing inactivation of the latter.	bind
24914	4	7827	6	NULL	NULL	0	NULL	statement 2	NULL		inactivates	NULL				cyclin E/cdk2 complex	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_4_1129_s_150	10514396	32 The mechanism by which p27Kip1 inhibits cdk activity is not fully understood, but it appears that binding of p27Kip1 to the cyclin D2/cdk4 complex sequesters the inhibitor away from the cyclin E/cdk2 complex, causing inactivation of the latter.	bind
25133	5	7827	6	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_4_1129_s_150	10514396	32 The mechanism by which p27Kip1 inhibits cdk activity is not fully understood, but it appears that binding of p27Kip1 to the cyclin D2/cdk4 complex sequesters the inhibitor away from the cyclin E/cdk2 complex, causing inactivation of the latter.	bind
31985	1	7828	5	13	NULL	NULL	NULL	ephrin-B1	GP		bind					Grb4	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_2_190_s_224	12588758	32 The observation that the region of ephrin-B1 binding to Grb4 is conserved in ephrin-B2 cytoplasmic tail suggests that EphB4 reverse signaling through ephrin-B2 may be similar through EphB2 reverse signaling through ephrin-B1.	bind
31986	2	7828	5	13	NULL	NULL	NULL	statement 1	Process	region of	is conserved in					ephrin-B2	GP		cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_2_190_s_224	12588758	32 The observation that the region of ephrin-B1 binding to Grb4 is conserved in ephrin-B2 cytoplasmic tail suggests that EphB4 reverse signaling through ephrin-B2 may be similar through EphB2 reverse signaling through ephrin-B1.	bind
31987	3	7828	5	13	NULL	NULL	NULL	EphB4	GP		reverse signal through					ephrin-B2	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_2_190_s_224	12588758	32 The observation that the region of ephrin-B1 binding to Grb4 is conserved in ephrin-B2 cytoplasmic tail suggests that EphB4 reverse signaling through ephrin-B2 may be similar through EphB2 reverse signaling through ephrin-B1.	bind
31988	4	7828	5	13	NULL	NULL	NULL	EphB2	GP		reverse signal through					ephrin-B1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_2_190_s_224	12588758	32 The observation that the region of ephrin-B1 binding to Grb4 is conserved in ephrin-B2 cytoplasmic tail suggests that EphB4 reverse signaling through ephrin-B2 may be similar through EphB2 reverse signaling through ephrin-B1.	bind
31989	5	7828	5	13	NULL	NULL	NULL	statement 3	Process		similar to		may			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_2_190_s_224	12588758	32 The observation that the region of ephrin-B1 binding to Grb4 is conserved in ephrin-B2 cytoplasmic tail suggests that EphB4 reverse signaling through ephrin-B2 may be similar through EphB2 reverse signaling through ephrin-B1.	bind
24742	1	7828	6	NULL	NULL	0	NULL	ephrin-B1	NULL		bind	NULL				Grb4	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_2_190_s_224	12588758	32 The observation that the region of ephrin-B1 binding to Grb4 is conserved in ephrin-B2 cytoplasmic tail suggests that EphB4 reverse signaling through ephrin-B2 may be similar through EphB2 reverse signaling through ephrin-B1.	bind
24915	2	7828	6	NULL	NULL	0	NULL	EphB4	NULL		reverse signals through	NULL				ephrin-B2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_2_190_s_224	12588758	32 The observation that the region of ephrin-B1 binding to Grb4 is conserved in ephrin-B2 cytoplasmic tail suggests that EphB4 reverse signaling through ephrin-B2 may be similar through EphB2 reverse signaling through ephrin-B1.	bind
24916	3	7828	6	NULL	NULL	0	NULL	EphB2	NULL		reverse signals through	NULL				ephrin-B1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_2_190_s_224	12588758	32 The observation that the region of ephrin-B1 binding to Grb4 is conserved in ephrin-B2 cytoplasmic tail suggests that EphB4 reverse signaling through ephrin-B2 may be similar through EphB2 reverse signaling through ephrin-B1.	bind
24917	4	7828	6	10	NULL	0	NULL	statement 2	NULL		 similar to	NULL	may be			statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_2_190_s_224	12588758	32 The observation that the region of ephrin-B1 binding to Grb4 is conserved in ephrin-B2 cytoplasmic tail suggests that EphB4 reverse signaling through ephrin-B2 may be similar through EphB2 reverse signaling through ephrin-B1.	bind
38768	5	7828	6	NULL	NULL	0	NULL	statement 1	NULL	region of	is conserved in	NULL				ephrin-B2	NULL		cytoplasmic tail		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_2_190_s_224	12588758	32 The observation that the region of ephrin-B1 binding to Grb4 is conserved in ephrin-B2 cytoplasmic tail suggests that EphB4 reverse signaling through ephrin-B2 may be similar through EphB2 reverse signaling through ephrin-B1.	bind
31990	1	7829	5	13	NULL	NULL	NULL	TnI	GP		bind					TnC	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_160	11739284	32, 33 Because the interaction between TnI and TnC increases Ca2+ binding, reduced TnI/TnC binding lowers the affinity of TnC for Ca2+.	bind
31991	2	7829	5	13	NULL	NULL	NULL	statement 1	Process		increases					Ca2+	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_160	11739284	32, 33 Because the interaction between TnI and TnC increases Ca2+ binding, reduced TnI/TnC binding lowers the affinity of TnC for Ca2+.	bind
31992	3	7829	5	13	NULL	NULL	NULL	TnC	GP		bind					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_160	11739284	32, 33 Because the interaction between TnI and TnC increases Ca2+ binding, reduced TnI/TnC binding lowers the affinity of TnC for Ca2+.	bind
31993	4	7829	5	13	NULL	NULL	NULL	statement 1	Process	reduced	lowers					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_160	11739284	32, 33 Because the interaction between TnI and TnC increases Ca2+ binding, reduced TnI/TnC binding lowers the affinity of TnC for Ca2+.	bind
24743	1	7829	6	NULL	NULL	0	NULL	TnI	NULL		interacts with	NULL				TnC	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_160	11739284	32, 33 Because the interaction between TnI and TnC increases Ca2+ binding, reduced TnI/TnC binding lowers the affinity of TnC for Ca2+.	bind
24744	2	7829	6	NULL	NULL	0	NULL	statement 1	NULL		increases	NULL				Ca2+	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_160	11739284	32, 33 Because the interaction between TnI and TnC increases Ca2+ binding, reduced TnI/TnC binding lowers the affinity of TnC for Ca2+.	bind
24745	3	7829	6	NULL	NULL	0	NULL	TnC	NULL		has affinity for	NULL				Ca2+	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_160	11739284	32, 33 Because the interaction between TnI and TnC increases Ca2+ binding, reduced TnI/TnC binding lowers the affinity of TnC for Ca2+.	bind
24746	4	7829	6	NULL	NULL	0	NULL	statement 1	NULL	reduced	lowers	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_160	11739284	32, 33 Because the interaction between TnI and TnC increases Ca2+ binding, reduced TnI/TnC binding lowers the affinity of TnC for Ca2+.	bind
31994	1	7830	5	13	NULL	NULL	NULL	RANTES	GP		bind					CCR5	GP				NULL	T cells	NULL	NULL	NULL	NULL	gw60_amjpathol_162_5_1591_s_124	12707043	32,33 For function-blocking studies, the binding of RANTES to CCR5 on the T cells was neutralized by preincubating the T cells with an anti-CCR5 monoclonal antibody (20 mug/ml final concentration) for 15 minutes on ice.	bind
24747	1	7830	6	NULL	NULL	0	NULL	RANTES	NULL		bind	NULL				CCR5	NULL				NULL	T cells	0	NULL	NULL	NULL	gw60_amjpathol_162_5_1591_s_124	12707043	32,33 For function-blocking studies, the binding of RANTES to CCR5 on the T cells was neutralized by preincubating the T cells with an anti-CCR5 monoclonal antibody (20 mug/ml final concentration) for 15 minutes on ice.	bind
31995	1	7831	5	13	NULL	NULL	NULL	HDL core	GP		becomes rich in					triglyceride	Chemical				NULL	hypertriglyceridemia	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3021_s_224	9409289	32,52,54 In hypertriglyceridemia, the core of HDL may become rich in triglyceride whereby subsequent lipolysis of HDL core by hepatic lipase may loosen the binding of apoA-I to HDL particle and facilitate clearance of apoA-I by the kidneys.	bind
31996	2	7831	5	13	NULL	NULL	NULL	lipase	GP	hepatic	lipolyse					HDL core	GP				NULL	hypertriglyceridemia	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3021_s_224	9409289	32,52,54 In hypertriglyceridemia, the core of HDL may become rich in triglyceride whereby subsequent lipolysis of HDL core by hepatic lipase may loosen the binding of apoA-I to HDL particle and facilitate clearance of apoA-I by the kidneys.	bind
31997	3	7831	5	13	NULL	NULL	NULL	apoA-I	GP		bind					HDL particle	GP				NULL	hypertriglyceridemia	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3021_s_224	9409289	32,52,54 In hypertriglyceridemia, the core of HDL may become rich in triglyceride whereby subsequent lipolysis of HDL core by hepatic lipase may loosen the binding of apoA-I to HDL particle and facilitate clearance of apoA-I by the kidneys.	bind
31998	4	7831	5	13	NULL	NULL	NULL	statement 2	Process		loosen		may			statement 3	Process				NULL	hypertriglyceridemia	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3021_s_224	9409289	32,52,54 In hypertriglyceridemia, the core of HDL may become rich in triglyceride whereby subsequent lipolysis of HDL core by hepatic lipase may loosen the binding of apoA-I to HDL particle and facilitate clearance of apoA-I by the kidneys.	bind
31999	5	7831	5	13	NULL	NULL	NULL	apoA-I 	GP		cleared by					kidneys	OrganismPart				NULL	hypertriglyceridemia	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3021_s_224	9409289	32,52,54 In hypertriglyceridemia, the core of HDL may become rich in triglyceride whereby subsequent lipolysis of HDL core by hepatic lipase may loosen the binding of apoA-I to HDL particle and facilitate clearance of apoA-I by the kidneys.	bind
32000	6	7831	5	13	NULL	NULL	NULL	statement 2	Process		facilitate					statement 5	Process				NULL	hypertriglyceridemia	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3021_s_224	9409289	32,52,54 In hypertriglyceridemia, the core of HDL may become rich in triglyceride whereby subsequent lipolysis of HDL core by hepatic lipase may loosen the binding of apoA-I to HDL particle and facilitate clearance of apoA-I by the kidneys.	bind
24748	1	7831	6	NULL	NULL	0	NULL	apoA-I	NULL		bind	NULL				HDL particle	NULL				NULL	hypertriglyceridemia	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3021_s_224	9409289	32,52,54 In hypertriglyceridemia, the core of HDL may become rich in triglyceride whereby subsequent lipolysis of HDL core by hepatic lipase may loosen the binding of apoA-I to HDL particle and facilitate clearance of apoA-I by the kidneys.	bind
24918	2	7831	6	NULL	NULL	0	NULL	HDL core 	NULL		becomes rich in	NULL				triglyceride	NULL				NULL	hypertriglyceridemia	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3021_s_224	9409289	32,52,54 In hypertriglyceridemia, the core of HDL may become rich in triglyceride whereby subsequent lipolysis of HDL core by hepatic lipase may loosen the binding of apoA-I to HDL particle and facilitate clearance of apoA-I by the kidneys.	bind
24919	3	7831	6	10	NULL	0	NULL	apoA-I			cleared by					kidney					NULL	hypertriglyceridemia	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3021_s_224	9409289	32,52,54 In hypertriglyceridemia, the core of HDL may become rich in triglyceride whereby subsequent lipolysis of HDL core by hepatic lipase may loosen the binding of apoA-I to HDL particle and facilitate clearance of apoA-I by the kidneys.	bind
24920	4	7831	6	NULL	NULL	0	NULL	hepatic lipase	NULL		lipolyse	NULL				HDL core	NULL				NULL	hypertriglyceridemia	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3021_s_224	9409289	32,52,54 In hypertriglyceridemia, the core of HDL may become rich in triglyceride whereby subsequent lipolysis of HDL core by hepatic lipase may loosen the binding of apoA-I to HDL particle and facilitate clearance of apoA-I by the kidneys.	bind
24921	5	7831	6	NULL	NULL	0	NULL	statement 4	NULL		loosen	NULL	may			statement 1	NULL				NULL	hypertriglyceridemia	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3021_s_224	9409289	32,52,54 In hypertriglyceridemia, the core of HDL may become rich in triglyceride whereby subsequent lipolysis of HDL core by hepatic lipase may loosen the binding of apoA-I to HDL particle and facilitate clearance of apoA-I by the kidneys.	bind
24922	6	7831	6	10	NULL	0	NULL	statement 4			facilitate					statement 3					NULL	hypertriglyceridemia	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3021_s_224	9409289	32,52,54 In hypertriglyceridemia, the core of HDL may become rich in triglyceride whereby subsequent lipolysis of HDL core by hepatic lipase may loosen the binding of apoA-I to HDL particle and facilitate clearance of apoA-I by the kidneys.	bind
32001	1	7833	5	13	NULL	NULL	NULL	p47phox species	GP		bind					TRAF4	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_6_2320_s_154	15743827	32P labeling to assess the nature of the p47phox species bound to TRAF4.	bind
24749	1	7833	6	NULL	NULL	0	NULL	p47phox species	NULL		bind	NULL				TRAF4	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_6_2320_s_154	15743827	32P labeling to assess the nature of the p47phox species bound to TRAF4.	bind
32002	1	7834	5	13	NULL	NULL	NULL	Ku70/86	GP	purified;;native	bind					PARP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_29_20521_s_219	10400681	32P-End-labeled DNA fragments were circularized by blunt end ligation, and the binding of column purified native Ku70/86 and PARP was analyzed by EMSA as described under	bind
24751	1	7834	6	10	NULL	0	NULL	Ku70/86	NULL	purified;; native	bind	NULL				PARP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_29_20521_s_219	10400681	32P-End-labeled DNA fragments were circularized by blunt end ligation, and the binding of column purified native Ku70/86 and PARP was analyzed by EMSA as described under	bind
32003	1	7835	5	13	NULL	NULL	NULL	GST-Yra1p	GP		bind					Mex67p/Mtr2p	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_3_410_s_142	10722314	32P-labeled  SSA1 RNA (bp 818-1152) was incubated with GST, GST-Yra1p on beads, and GST-Yra1p bound to Mex67p/Mtr2p on beads.	bind
24764	1	7835	6	NULL	NULL	0	NULL	GST-Yra1p	NULL		bind	NULL				Mex67p/Mtr2p	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_19_3_410_s_142	10722314	32P-labeled  SSA1 RNA (bp 818-1152) was incubated with GST, GST-Yra1p on beads, and GST-Yra1p bound to Mex67p/Mtr2p on beads.	bind
32004	1	7836	5	13	NULL	NULL	NULL	5ABC	GP	32P-labeled	bind					GST-MSP142	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_9_5164_s_159	12692305	32P-labeled 5ABC (10, 20, 40, and 80 muM) and 5BC (21, 42, 84, and 168 muM) bound to GST-MSP142	bind
32005	2	7836	5	13	NULL	NULL	NULL	5BC	GP	32P-labeled	bind					GST-MSP142	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_9_5164_s_159	12692305	32P-labeled 5ABC (10, 20, 40, and 80 muM) and 5BC (21, 42, 84, and 168 muM) bound to GST-MSP142	bind
24779	1	7836	6	10	NULL	0	NULL	5ABC		32P-labeled 	bind					GST-MSP142					NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_9_5164_s_159	12692305	32P-labeled 5ABC (10, 20, 40, and 80 muM) and 5BC (21, 42, 84, and 168 muM) bound to GST-MSP142	bind
24780	2	7836	6	10	NULL	0	NULL	5BC		32P-labeled 	bind					GST-MSP142					NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_9_5164_s_159	12692305	32P-labeled 5ABC (10, 20, 40, and 80 muM) and 5BC (21, 42, 84, and 168 muM) bound to GST-MSP142	bind
32006	1	7837	5	13	NULL	NULL	NULL	guanidine nucleotides	Chemical	 labeled	bind					Rap1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_278_5335_124_s_96	9311917	32P-labeled anergic or control cells (2 x 107 cells per sample) were unstimulated ( ) or stimulated (+) ( 33) for 5 min. Labeled guanidine nucleotides bound to Rap1 or Ras were quantitated, and results were expressed as percent of GTP bound to Rap1 or Ras proteins relative to the total amount of guanidine nucleotides (GTP+GDP) complexed to these proteins.	bind
32007	2	7837	5	13	NULL	NULL	NULL	guanidine nucleotides	Chemical	labeled	bind					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_278_5335_124_s_96	9311917	32P-labeled anergic or control cells (2 x 107 cells per sample) were unstimulated ( ) or stimulated (+) ( 33) for 5 min. Labeled guanidine nucleotides bound to Rap1 or Ras were quantitated, and results were expressed as percent of GTP bound to Rap1 or Ras proteins relative to the total amount of guanidine nucleotides (GTP+GDP) complexed to these proteins.	bind
32008	3	7837	5	13	NULL	NULL	NULL	statement 1	Process		is alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_278_5335_124_s_96	9311917	32P-labeled anergic or control cells (2 x 107 cells per sample) were unstimulated ( ) or stimulated (+) ( 33) for 5 min. Labeled guanidine nucleotides bound to Rap1 or Ras were quantitated, and results were expressed as percent of GTP bound to Rap1 or Ras proteins relative to the total amount of guanidine nucleotides (GTP+GDP) complexed to these proteins.	bind
55551	4	7837	5	13	NULL	NULL	NULL	guanidine nucleotides	Chemical		is					GTP+GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_278_5335_124_s_96	9311917	32P-labeled anergic or control cells (2 x 107 cells per sample) were unstimulated ( ) or stimulated (+) ( 33) for 5 min. Labeled guanidine nucleotides bound to Rap1 or Ras were quantitated, and results were expressed as percent of GTP bound to Rap1 or Ras proteins relative to the total amount of guanidine nucleotides (GTP+GDP) complexed to these proteins.	bind
24923	1	7837	6	NULL	NULL	0	NULL	guanidine nucleotides	NULL	labeled	bind	NULL				Rap1	NULL				NULL		0	NULL	NULL	NULL	gw60_science_278_5335_124_s_96	9311917	32P-labeled anergic or control cells (2 x 107 cells per sample) were unstimulated ( ) or stimulated (+) ( 33) for 5 min. Labeled guanidine nucleotides bound to Rap1 or Ras were quantitated, and results were expressed as percent of GTP bound to Rap1 or Ras proteins relative to the total amount of guanidine nucleotides (GTP+GDP) complexed to these proteins.	bind
24924	2	7837	6	NULL	NULL	0	NULL	guanidine nucleotides	NULL	labeled	bind	NULL				Ras	NULL				NULL		0	NULL	NULL	NULL	gw60_science_278_5335_124_s_96	9311917	32P-labeled anergic or control cells (2 x 107 cells per sample) were unstimulated ( ) or stimulated (+) ( 33) for 5 min. Labeled guanidine nucleotides bound to Rap1 or Ras were quantitated, and results were expressed as percent of GTP bound to Rap1 or Ras proteins relative to the total amount of guanidine nucleotides (GTP+GDP) complexed to these proteins.	bind
25134	3	7837	6	10	NULL	0	NULL	guanidine nucleotides			is					GTP+GDP					NULL		NULL	NULL	NULL	NULL	gw60_science_278_5335_124_s_96	9311917	32P-labeled anergic or control cells (2 x 107 cells per sample) were unstimulated ( ) or stimulated (+) ( 33) for 5 min. Labeled guanidine nucleotides bound to Rap1 or Ras were quantitated, and results were expressed as percent of GTP bound to Rap1 or Ras proteins relative to the total amount of guanidine nucleotides (GTP+GDP) complexed to these proteins.	bind
47358	4	7837	6	10	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_science_278_5335_124_s_96	9311917	32P-labeled anergic or control cells (2 x 107 cells per sample) were unstimulated ( ) or stimulated (+) ( 33) for 5 min. Labeled guanidine nucleotides bound to Rap1 or Ras were quantitated, and results were expressed as percent of GTP bound to Rap1 or Ras proteins relative to the total amount of guanidine nucleotides (GTP+GDP) complexed to these proteins.	bind
32009	1	7838	5	13	NULL	NULL	NULL	GST-N-Shh	GP	32P-Labeled	bind					megalin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25660_s_148	11964399	32P-Labeled GST-N-Shh bound to megalin, and the binding was inhibited in a dose-dependent manner by the addition of unlabeled GST-N-Shh (Fig.  4 B).	bind
32010	2	7838	5	13	NULL	NULL	NULL	GST-N-Shh	GP	unlabeled	inhibits		dose dependent			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25660_s_148	11964399	32P-Labeled GST-N-Shh bound to megalin, and the binding was inhibited in a dose-dependent manner by the addition of unlabeled GST-N-Shh (Fig.  4 B).	bind
24783	1	7838	6	10	NULL	0	NULL	GST-N-Shh	NULL	32P-Labeled 	bind	NULL				megalin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_28_25660_s_148	11964399	32P-Labeled GST-N-Shh bound to megalin, and the binding was inhibited in a dose-dependent manner by the addition of unlabeled GST-N-Shh (Fig.  4 B).	bind
24785	2	7838	6	NULL	NULL	0	NULL	GST-N-Shh	NULL	unlabeled	inhibits	NULL	dose dependently			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_28_25660_s_148	11964399	32P-Labeled GST-N-Shh bound to megalin, and the binding was inhibited in a dose-dependent manner by the addition of unlabeled GST-N-Shh (Fig.  4 B).	bind
32011	1	7841	5	13	NULL	NULL	NULL	nicotinamide adenine dinucleotide	Chemical	folded conformation of	bind					flavin reductase	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4294_s_544	11691917	33       Tanner,J.J., Tu,S.C., Barbour,L.J., Barnes,C.L. and Krause,K.L. (1999) Unusual folded conformation of nicotinamide adenine dinucleotide bound to flavin reductase P.  Protein Sci.,  8, 1725 - 1732.	bind
24787	1	7841	6	NULL	NULL	0	NULL	nicotinamide adenine dinucleotide	NULL	folded conformation of 	bind	NULL				flavin reductase	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4294_s_544	11691917	33       Tanner,J.J., Tu,S.C., Barbour,L.J., Barnes,C.L. and Krause,K.L. (1999) Unusual folded conformation of nicotinamide adenine dinucleotide bound to flavin reductase P.  Protein Sci.,  8, 1725 - 1732.	bind
32012	1	7842	5	13	NULL	NULL	NULL	VEGF	GP		bind					KDR	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_8_832_s_255	9776730	33  Functional studies indicate that neuropilin enhanced the binding of VEGF to KDR resulting in VEGF-mediated chemotaxis.	bind
32013	2	7842	5	13	NULL	NULL	NULL	neuropilin	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_8_832_s_255	9776730	33  Functional studies indicate that neuropilin enhanced the binding of VEGF to KDR resulting in VEGF-mediated chemotaxis.	bind
32014	4	7842	5	13	NULL	NULL	NULL	statement 2	Process		results in					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_8_832_s_255	9776730	33  Functional studies indicate that neuropilin enhanced the binding of VEGF to KDR resulting in VEGF-mediated chemotaxis.	bind
47359	3	7842	5	13	NULL	NULL	NULL	VEGF	GP		mediates					chemotaxis	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_8_832_s_255	9776730	33  Functional studies indicate that neuropilin enhanced the binding of VEGF to KDR resulting in VEGF-mediated chemotaxis.	bind
24788	1	7842	6	NULL	NULL	0	NULL	VEGF	NULL		bind	NULL				KDR	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_8_832_s_255	9776730	33  Functional studies indicate that neuropilin enhanced the binding of VEGF to KDR resulting in VEGF-mediated chemotaxis.	bind
24789	2	7842	6	NULL	NULL	0	NULL	neuropilin	NULL		enhance	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_8_832_s_255	9776730	33  Functional studies indicate that neuropilin enhanced the binding of VEGF to KDR resulting in VEGF-mediated chemotaxis.	bind
24790	4	7842	6	10	NULL	0	NULL	statement 2	NULL		results in	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_8_832_s_255	9776730	33  Functional studies indicate that neuropilin enhanced the binding of VEGF to KDR resulting in VEGF-mediated chemotaxis.	bind
47360	3	7842	6	10	NULL	0	NULL	VEGF	NULL		mediates	NULL				chemotaxis	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_8_832_s_255	9776730	33  Functional studies indicate that neuropilin enhanced the binding of VEGF to KDR resulting in VEGF-mediated chemotaxis.	bind
32015	1	7843	5	13	NULL	NULL	NULL	c-Myc	GP	induction of	leads to					RB	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_47	10205150	33  Induction of c-Myc can lead to rapid phosphorylation of RB and activation of both cyclin D1- and cyclin E-associated kinases in the absence of significant changes in the absolute amounts of cyclin-cdk complexes.	bind
32016	2	7843	5	13	NULL	NULL	NULL	c-Myc	GP	induction of	activates					cyclin E-associated kinases	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_47	10205150	33  Induction of c-Myc can lead to rapid phosphorylation of RB and activation of both cyclin D1- and cyclin E-associated kinases in the absence of significant changes in the absolute amounts of cyclin-cdk complexes.	bind
32017	3	7843	5	13	NULL	NULL	NULL	c-Myc	GP	induction of	activates					cyclin D1-associated kinases	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_47	10205150	33  Induction of c-Myc can lead to rapid phosphorylation of RB and activation of both cyclin D1- and cyclin E-associated kinases in the absence of significant changes in the absolute amounts of cyclin-cdk complexes.	bind
32018	4	7843	5	13	NULL	NULL	NULL	statement 1	Process		absence of					cyclin-cdk complexes	GP	significant changes in			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_47	10205150	33  Induction of c-Myc can lead to rapid phosphorylation of RB and activation of both cyclin D1- and cyclin E-associated kinases in the absence of significant changes in the absolute amounts of cyclin-cdk complexes.	bind
32019	5	7843	5	13	NULL	NULL	NULL	statement 2	Process		absence of					cyclin-cdk complexes	GP	significant changes in			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_47	10205150	33  Induction of c-Myc can lead to rapid phosphorylation of RB and activation of both cyclin D1- and cyclin E-associated kinases in the absence of significant changes in the absolute amounts of cyclin-cdk complexes.	bind
32020	6	7843	5	13	NULL	NULL	NULL	statement 3	Process		absence of					cyclin-cdk complexes	GP	significant changes in			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_47	10205150	33  Induction of c-Myc can lead to rapid phosphorylation of RB and activation of both cyclin D1- and cyclin E-associated kinases in the absence of significant changes in the absolute amounts of cyclin-cdk complexes.	bind
24792	1	7843	6	NULL	NULL	0	NULL	c-Myc	NULL	induction of	lead to	NULL				RB	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_47	10205150	33  Induction of c-Myc can lead to rapid phosphorylation of RB and activation of both cyclin D1- and cyclin E-associated kinases in the absence of significant changes in the absolute amounts of cyclin-cdk complexes.	bind
24793	2	7843	6	NULL	NULL	0	NULL	c-Myc	NULL	induction of	results in	NULL				cyclin D1 associated kinases	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_47	10205150	33  Induction of c-Myc can lead to rapid phosphorylation of RB and activation of both cyclin D1- and cyclin E-associated kinases in the absence of significant changes in the absolute amounts of cyclin-cdk complexes.	bind
24794	3	7843	6	NULL	NULL	0	NULL	c-Myc	NULL	induction of	results in	NULL				cyclin E-associated kinases	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_47	10205150	33  Induction of c-Myc can lead to rapid phosphorylation of RB and activation of both cyclin D1- and cyclin E-associated kinases in the absence of significant changes in the absolute amounts of cyclin-cdk complexes.	bind
38773	4	7843	6	10	NULL	0	NULL	statement 1	NULL		occurs in absence of	NULL				cyclin-cdk complexes	NULL	significant changes in 			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_47	10205150	33  Induction of c-Myc can lead to rapid phosphorylation of RB and activation of both cyclin D1- and cyclin E-associated kinases in the absence of significant changes in the absolute amounts of cyclin-cdk complexes.	bind
38775	5	7843	6	10	NULL	0	NULL	statement 2	NULL		occurs in absence of	NULL				cyclin-cdk complexes	NULL	significant changes in 			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_47	10205150	33  Induction of c-Myc can lead to rapid phosphorylation of RB and activation of both cyclin D1- and cyclin E-associated kinases in the absence of significant changes in the absolute amounts of cyclin-cdk complexes.	bind
38776	6	7843	6	10	NULL	0	NULL	statement 3	NULL		occurs in absence of	NULL				cyclin-cdk complexes	NULL	significant changes in 			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_820_s_47	10205150	33  Induction of c-Myc can lead to rapid phosphorylation of RB and activation of both cyclin D1- and cyclin E-associated kinases in the absence of significant changes in the absolute amounts of cyclin-cdk complexes.	bind
32021	1	7844	5	13	NULL	NULL	NULL	PH1-IgG1 antibody	GP		bind		specifically			tumor	MedicalFinding				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1597_s_246	12000712	33  Summarized, the staining pattern of the PH1 epitope is only moderately different from staining patterns of other glycosylation-sensitive antibodies, it thus can be expected that the PH1-IgG1 antibody will specifically bind to tumor  in vivo.	bind
24795	1	7844	6	NULL	NULL	0	NULL	PH1-IgG1 antibody	NULL		bind	NULL	specifically			tumor	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_amjpathol_160_5_1597_s_246	12000712	33  Summarized, the staining pattern of the PH1 epitope is only moderately different from staining patterns of other glycosylation-sensitive antibodies, it thus can be expected that the PH1-IgG1 antibody will specifically bind to tumor  in vivo.	bind
33804	1	7846	5	13	NULL	NULL	NULL	matrix proteins	GP		are scaffold for					tissue formation	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_217_s_216	12107106	33  These matrix proteins are the scaffold for tissue formation and growth, initiate intercellular signaling events through binding to cell receptor (integrins), and bind to growth factors and thus supply sustained concentration of these factors for epithelial cell migration, proliferation, and differentiation.	bind
33805	2	7846	5	13	NULL	NULL	NULL	matrix proteins	GP		are scaffold for					growth	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_217_s_216	12107106	33  These matrix proteins are the scaffold for tissue formation and growth, initiate intercellular signaling events through binding to cell receptor (integrins), and bind to growth factors and thus supply sustained concentration of these factors for epithelial cell migration, proliferation, and differentiation.	bind
33806	3	7846	5	13	NULL	NULL	NULL	matrix proteins	GP		bind					integrins	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_217_s_216	12107106	33  These matrix proteins are the scaffold for tissue formation and growth, initiate intercellular signaling events through binding to cell receptor (integrins), and bind to growth factors and thus supply sustained concentration of these factors for epithelial cell migration, proliferation, and differentiation.	bind
33807	4	7846	5	13	NULL	NULL	NULL	matrix proteins	GP		initiates					signaling events	Process	intercellular			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_217_s_216	12107106	33  These matrix proteins are the scaffold for tissue formation and growth, initiate intercellular signaling events through binding to cell receptor (integrins), and bind to growth factors and thus supply sustained concentration of these factors for epithelial cell migration, proliferation, and differentiation.	bind
33808	5	7846	5	13	NULL	NULL	NULL	statement 4	Process		occurs through					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_217_s_216	12107106	33  These matrix proteins are the scaffold for tissue formation and growth, initiate intercellular signaling events through binding to cell receptor (integrins), and bind to growth factors and thus supply sustained concentration of these factors for epithelial cell migration, proliferation, and differentiation.	bind
33809	6	7846	5	13	NULL	NULL	NULL	matrix proteins	GP		bind					growth factors	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_217_s_216	12107106	33  These matrix proteins are the scaffold for tissue formation and growth, initiate intercellular signaling events through binding to cell receptor (integrins), and bind to growth factors and thus supply sustained concentration of these factors for epithelial cell migration, proliferation, and differentiation.	bind
33810	7	7846	5	13	NULL	NULL	NULL	statement 6	Process		plays a role in					epithelial cell	Cell	migration of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_217_s_216	12107106	33  These matrix proteins are the scaffold for tissue formation and growth, initiate intercellular signaling events through binding to cell receptor (integrins), and bind to growth factors and thus supply sustained concentration of these factors for epithelial cell migration, proliferation, and differentiation.	bind
33811	8	7846	5	13	NULL	NULL	NULL	statement 6	Process		plays a role in					epithelial cell	Chemical	proliferation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_217_s_216	12107106	33  These matrix proteins are the scaffold for tissue formation and growth, initiate intercellular signaling events through binding to cell receptor (integrins), and bind to growth factors and thus supply sustained concentration of these factors for epithelial cell migration, proliferation, and differentiation.	bind
33812	9	7846	5	13	NULL	NULL	NULL	statement 6	Process		plays a role in					epithelial cell	Cell	differentiation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_217_s_216	12107106	33  These matrix proteins are the scaffold for tissue formation and growth, initiate intercellular signaling events through binding to cell receptor (integrins), and bind to growth factors and thus supply sustained concentration of these factors for epithelial cell migration, proliferation, and differentiation.	bind
24925	1	7846	6	NULL	NULL	0	NULL	matrix proteins	NULL		are scaffold for	NULL				tissue formation	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_1_217_s_216	12107106	33  These matrix proteins are the scaffold for tissue formation and growth, initiate intercellular signaling events through binding to cell receptor (integrins), and bind to growth factors and thus supply sustained concentration of these factors for epithelial cell migration, proliferation, and differentiation.	bind
24926	2	7846	6	NULL	NULL	0	NULL	matrix proteins	NULL		are scaffold for	NULL				tissue growth	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_1_217_s_216	12107106	33  These matrix proteins are the scaffold for tissue formation and growth, initiate intercellular signaling events through binding to cell receptor (integrins), and bind to growth factors and thus supply sustained concentration of these factors for epithelial cell migration, proliferation, and differentiation.	bind
24927	3	7846	6	NULL	NULL	0	NULL	matrix proteins	NULL		bind	NULL				cell receptor (integrins)	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_1_217_s_216	12107106	33  These matrix proteins are the scaffold for tissue formation and growth, initiate intercellular signaling events through binding to cell receptor (integrins), and bind to growth factors and thus supply sustained concentration of these factors for epithelial cell migration, proliferation, and differentiation.	bind
24928	4	7846	6	NULL	NULL	0	NULL	matrix proteins	NULL		bind	NULL				growth factors	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_1_217_s_216	12107106	33  These matrix proteins are the scaffold for tissue formation and growth, initiate intercellular signaling events through binding to cell receptor (integrins), and bind to growth factors and thus supply sustained concentration of these factors for epithelial cell migration, proliferation, and differentiation.	bind
32201	1	7847	5	13	NULL	NULL	NULL	LDL ligand	GP		bind					CRP	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2372_s_190	15486314	33 (2) Does ligand (for example, LDL) binding to CRP increase its affinity to Fc receptors?	bind
24796	1	7847	6	10	NULL	0	NULL	LDL ligand			bind					CRP					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_12_2372_s_190	15486314	33 (2) Does ligand (for example, LDL) binding to CRP increase its affinity to Fc receptors?	bind
32202	1	7848	5	13	NULL	NULL	NULL	Hh	GP		bind					Ptc1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_113_20_2413_s_338	16702471	33 After Hh binds Ptc1, subsequent activation of Smo initiates signaling events that lead to the regulation of transcriptional factors belonging to the Gli family, which modify the expression of downstream target genes of the Hh pathway, including  Ptch and  Gli themselves.	bind
32203	2	7848	5	13	NULL	NULL	NULL	statement 1	Process		activates		subsequently			Smo	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_113_20_2413_s_338	16702471	33 After Hh binds Ptc1, subsequent activation of Smo initiates signaling events that lead to the regulation of transcriptional factors belonging to the Gli family, which modify the expression of downstream target genes of the Hh pathway, including  Ptch and  Gli themselves.	bind
32204	3	7848	5	13	NULL	NULL	NULL	statement 2	Process		initiates					signaling events	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_113_20_2413_s_338	16702471	33 After Hh binds Ptc1, subsequent activation of Smo initiates signaling events that lead to the regulation of transcriptional factors belonging to the Gli family, which modify the expression of downstream target genes of the Hh pathway, including  Ptch and  Gli themselves.	bind
32205	4	7848	5	13	NULL	NULL	NULL	statement 3	Process		leads to					Gli family transcriptional factors 	GP	regulation of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_113_20_2413_s_338	16702471	33 After Hh binds Ptc1, subsequent activation of Smo initiates signaling events that lead to the regulation of transcriptional factors belonging to the Gli family, which modify the expression of downstream target genes of the Hh pathway, including  Ptch and  Gli themselves.	bind
32206	5	7848	5	13	NULL	NULL	NULL	Gli family transcriptional factors 	GP		modify					Ptch	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_113_20_2413_s_338	16702471	33 After Hh binds Ptc1, subsequent activation of Smo initiates signaling events that lead to the regulation of transcriptional factors belonging to the Gli family, which modify the expression of downstream target genes of the Hh pathway, including  Ptch and  Gli themselves.	bind
32207	6	7848	5	13	NULL	NULL	NULL	Gli family transcriptional factors  	GP		modify					Gli	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_113_20_2413_s_338	16702471	33 After Hh binds Ptc1, subsequent activation of Smo initiates signaling events that lead to the regulation of transcriptional factors belonging to the Gli family, which modify the expression of downstream target genes of the Hh pathway, including  Ptch and  Gli themselves.	bind
32208	7	7848	5	13	NULL	NULL	NULL	Ptch	GP		is a type of					downstream target genes of Hh pathway	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_113_20_2413_s_338	16702471	33 After Hh binds Ptc1, subsequent activation of Smo initiates signaling events that lead to the regulation of transcriptional factors belonging to the Gli family, which modify the expression of downstream target genes of the Hh pathway, including  Ptch and  Gli themselves.	bind
32209	8	7848	5	13	NULL	NULL	NULL	Gli	GP		is a type of					downstream target genes of Hh pathway	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_113_20_2413_s_338	16702471	33 After Hh binds Ptc1, subsequent activation of Smo initiates signaling events that lead to the regulation of transcriptional factors belonging to the Gli family, which modify the expression of downstream target genes of the Hh pathway, including  Ptch and  Gli themselves.	bind
24881	1	7848	6	NULL	NULL	0	NULL	Hh	NULL		bind	NULL				Ptc1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_113_20_2413_s_338	16702471	33 After Hh binds Ptc1, subsequent activation of Smo initiates signaling events that lead to the regulation of transcriptional factors belonging to the Gli family, which modify the expression of downstream target genes of the Hh pathway, including  Ptch and  Gli themselves.	bind
24882	3	7848	6	10	NULL	0	NULL	statement 2	NULL		initiates	NULL				signaling events	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulation_113_20_2413_s_338	16702471	33 After Hh binds Ptc1, subsequent activation of Smo initiates signaling events that lead to the regulation of transcriptional factors belonging to the Gli family, which modify the expression of downstream target genes of the Hh pathway, including  Ptch and  Gli themselves.	bind
24883	2	7848	6	10	NULL	0	NULL	statement 1	NULL		activates	NULL	subsequently			Smo	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulation_113_20_2413_s_338	16702471	33 After Hh binds Ptc1, subsequent activation of Smo initiates signaling events that lead to the regulation of transcriptional factors belonging to the Gli family, which modify the expression of downstream target genes of the Hh pathway, including  Ptch and  Gli themselves.	bind
24884	5	7848	6	10	NULL	0	NULL	statement 4	NULL		modify the	NULL				Ptch	NULL	expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_113_20_2413_s_338	16702471	33 After Hh binds Ptc1, subsequent activation of Smo initiates signaling events that lead to the regulation of transcriptional factors belonging to the Gli family, which modify the expression of downstream target genes of the Hh pathway, including  Ptch and  Gli themselves.	bind
24885	6	7848	6	10	NULL	0	NULL	statement 4	NULL		modify the 	NULL				Gli	NULL	expression of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_113_20_2413_s_338	16702471	33 After Hh binds Ptc1, subsequent activation of Smo initiates signaling events that lead to the regulation of transcriptional factors belonging to the Gli family, which modify the expression of downstream target genes of the Hh pathway, including  Ptch and  Gli themselves.	bind
24886	7	7848	6	10	NULL	0	NULL	Ptch	NULL		is a type of	NULL				target gene of Hh pathway	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulation_113_20_2413_s_338	16702471	33 After Hh binds Ptc1, subsequent activation of Smo initiates signaling events that lead to the regulation of transcriptional factors belonging to the Gli family, which modify the expression of downstream target genes of the Hh pathway, including  Ptch and  Gli themselves.	bind
24887	8	7848	6	10	NULL	0	NULL	Gli	NULL		is a type of	NULL				target gene of Hh pathway	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulation_113_20_2413_s_338	16702471	33 After Hh binds Ptc1, subsequent activation of Smo initiates signaling events that lead to the regulation of transcriptional factors belonging to the Gli family, which modify the expression of downstream target genes of the Hh pathway, including  Ptch and  Gli themselves.	bind
47361	4	7848	6	10	NULL	0	NULL	statement 3	NULL		lead to	NULL				Gli family transcriptional factors 	NULL	regulation of			NULL		0	NULL	NULL	NULL	gw70_circulation_113_20_2413_s_338	16702471	33 After Hh binds Ptc1, subsequent activation of Smo initiates signaling events that lead to the regulation of transcriptional factors belonging to the Gli family, which modify the expression of downstream target genes of the Hh pathway, including  Ptch and  Gli themselves.	bind
32210	1	7849	5	13	NULL	NULL	NULL	CBP	GP		bind					AR	GP		LBD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_31853_s_175	9822653	33 and  34), we have found that CBP can bind to both the NTD and LBD of AR.	bind
38968	2	7849	5	13	NULL	NULL	NULL	CBP	GP		bind					AR	GP		LBD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_31853_s_175	9822653	33 and  34), we have found that CBP can bind to both the NTD and LBD of AR.	bind
24929	1	7849	6	NULL	NULL	0	NULL	CBP	NULL		bind	NULL				AR	NULL		NTD		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_48_31853_s_175	9822653	33 and  34), we have found that CBP can bind to both the NTD and LBD of AR.	bind
24930	2	7849	6	NULL	NULL	0	NULL	CBP	NULL		bind	NULL				AR	NULL		LBD		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_48_31853_s_175	9822653	33 and  34), we have found that CBP can bind to both the NTD and LBD of AR.	bind
32211	1	7850	5	13	NULL	NULL	NULL	adenosine	NucleicAcid		bind					A2A receptors	GP				NULL	neutrophils	NULL	NULL	NULL	NULL	gw70_circulationres_95_8_814_s_180	15358667	33 In neutrophils, adenosine binding to A2A receptors has been shown to counteract the stimulation of VLA-4 expression and binding to VCAM-1 by chemoattractants via a cAMP-mediated pathway.	bind
32212	2	7850	5	13	NULL	NULL	NULL	statement 1	Process		counteract					VLA-4 	GP	stimulation of;;expression of			NULL	neutrophils	NULL	NULL	NULL	NULL	gw70_circulationres_95_8_814_s_180	15358667	33 In neutrophils, adenosine binding to A2A receptors has been shown to counteract the stimulation of VLA-4 expression and binding to VCAM-1 by chemoattractants via a cAMP-mediated pathway.	bind
32213	3	7850	5	13	NULL	NULL	NULL	chemoattractants	GP		bind					VCAM-1	GP				NULL	neutrophils	NULL	NULL	NULL	NULL	gw70_circulationres_95_8_814_s_180	15358667	33 In neutrophils, adenosine binding to A2A receptors has been shown to counteract the stimulation of VLA-4 expression and binding to VCAM-1 by chemoattractants via a cAMP-mediated pathway.	bind
32214	4	7850	5	13	NULL	NULL	NULL	statement 3	Process		is mediated by					cAMP-pathway	Process				NULL	neutrophils	NULL	NULL	NULL	NULL	gw70_circulationres_95_8_814_s_180	15358667	33 In neutrophils, adenosine binding to A2A receptors has been shown to counteract the stimulation of VLA-4 expression and binding to VCAM-1 by chemoattractants via a cAMP-mediated pathway.	bind
24931	1	7850	6	NULL	NULL	0	NULL	adenosine	NULL		bind	NULL				A2A receptors	NULL				NULL	neutrophils	0	NULL	NULL	NULL	gw70_circulationres_95_8_814_s_180	15358667	33 In neutrophils, adenosine binding to A2A receptors has been shown to counteract the stimulation of VLA-4 expression and binding to VCAM-1 by chemoattractants via a cAMP-mediated pathway.	bind
24932	2	7850	6	10	NULL	0	NULL	chemoattractants	NULL		bind	NULL				VCAM-1	NULL				NULL	neutrophils	NULL	NULL	NULL	NULL	gw70_circulationres_95_8_814_s_180	15358667	33 In neutrophils, adenosine binding to A2A receptors has been shown to counteract the stimulation of VLA-4 expression and binding to VCAM-1 by chemoattractants via a cAMP-mediated pathway.	bind
24933	3	7850	6	10	NULL	0	NULL	statement 1	NULL		counteracts	NULL				VLA-4	NULL	stimulation of;; expression of			NULL	neutrophils	NULL	NULL	NULL	NULL	gw70_circulationres_95_8_814_s_180	15358667	33 In neutrophils, adenosine binding to A2A receptors has been shown to counteract the stimulation of VLA-4 expression and binding to VCAM-1 by chemoattractants via a cAMP-mediated pathway.	bind
24934	4	7850	6	NULL	NULL	0	NULL	statement 2	NULL		is mediated by	NULL				cAMP pathway	NULL				NULL	neutrophils	NULL	NULL	NULL	NULL	gw70_circulationres_95_8_814_s_180	15358667	33 In neutrophils, adenosine binding to A2A receptors has been shown to counteract the stimulation of VLA-4 expression and binding to VCAM-1 by chemoattractants via a cAMP-mediated pathway.	bind
32215	1	7851	5	13	NULL	NULL	NULL	LDLR	GP		bind				promoter	SREBP-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_164	15178557	33 It has been suggested that in LDLR promoter, the respective directional binding of SREBP-2 and Sp1 to their sites, which are head to head in repeats 2 and 3, allows the interaction of SREBP-2 with the N-terminal region of Sp1 and facilitates Sp1 recruitment 28 ( Figure 5).	bind
32216	2	7851	5	13	NULL	NULL	NULL	LDLR	GP		bind				promoter	Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_164	15178557	33 It has been suggested that in LDLR promoter, the respective directional binding of SREBP-2 and Sp1 to their sites, which are head to head in repeats 2 and 3, allows the interaction of SREBP-2 with the N-terminal region of Sp1 and facilitates Sp1 recruitment 28 ( Figure 5).	bind
32217	3	7851	5	13	NULL	NULL	NULL	SREBP-2	GP		interacts with					Sp1	GP		N-terminal region		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_164	15178557	33 It has been suggested that in LDLR promoter, the respective directional binding of SREBP-2 and Sp1 to their sites, which are head to head in repeats 2 and 3, allows the interaction of SREBP-2 with the N-terminal region of Sp1 and facilitates Sp1 recruitment 28 ( Figure 5).	bind
32218	4	7851	5	13	NULL	NULL	NULL	statement 1	Process		allows					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_164	15178557	33 It has been suggested that in LDLR promoter, the respective directional binding of SREBP-2 and Sp1 to their sites, which are head to head in repeats 2 and 3, allows the interaction of SREBP-2 with the N-terminal region of Sp1 and facilitates Sp1 recruitment 28 ( Figure 5).	bind
32219	5	7851	5	13	NULL	NULL	NULL	statement 2	Process		allows					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_164	15178557	33 It has been suggested that in LDLR promoter, the respective directional binding of SREBP-2 and Sp1 to their sites, which are head to head in repeats 2 and 3, allows the interaction of SREBP-2 with the N-terminal region of Sp1 and facilitates Sp1 recruitment 28 ( Figure 5).	bind
32220	6	7851	5	13	NULL	NULL	NULL	statement 1	Process		facilitate					Sp1	GP	recruitment of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_164	15178557	33 It has been suggested that in LDLR promoter, the respective directional binding of SREBP-2 and Sp1 to their sites, which are head to head in repeats 2 and 3, allows the interaction of SREBP-2 with the N-terminal region of Sp1 and facilitates Sp1 recruitment 28 ( Figure 5).	bind
32221	7	7851	5	13	NULL	NULL	NULL	statement 2	Process		facilitate					Sp1	GP	recruitment of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_164	15178557	33 It has been suggested that in LDLR promoter, the respective directional binding of SREBP-2 and Sp1 to their sites, which are head to head in repeats 2 and 3, allows the interaction of SREBP-2 with the N-terminal region of Sp1 and facilitates Sp1 recruitment 28 ( Figure 5).	bind
24936	1	7851	6	NULL	NULL	0	NULL	SREBP-2	NULL		bind	NULL				Sp1	NULL		N-terminal region		NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_164	15178557	33 It has been suggested that in LDLR promoter, the respective directional binding of SREBP-2 and Sp1 to their sites, which are head to head in repeats 2 and 3, allows the interaction of SREBP-2 with the N-terminal region of Sp1 and facilitates Sp1 recruitment 28 ( Figure 5).	bind
24937	2	7851	6	NULL	NULL	0	NULL	SREBP-2	NULL		bind	NULL				LDLR	NULL			site of promoter	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_164	15178557	33 It has been suggested that in LDLR promoter, the respective directional binding of SREBP-2 and Sp1 to their sites, which are head to head in repeats 2 and 3, allows the interaction of SREBP-2 with the N-terminal region of Sp1 and facilitates Sp1 recruitment 28 ( Figure 5).	bind
24938	3	7851	6	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				LDLR	NULL			site of promoter	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_164	15178557	33 It has been suggested that in LDLR promoter, the respective directional binding of SREBP-2 and Sp1 to their sites, which are head to head in repeats 2 and 3, allows the interaction of SREBP-2 with the N-terminal region of Sp1 and facilitates Sp1 recruitment 28 ( Figure 5).	bind
24941	4	7851	6	NULL	NULL	0	NULL	LDLR	NULL		is located on	NULL			SREBP-2 binding site		NULL			repeat 2	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_164	15178557	33 It has been suggested that in LDLR promoter, the respective directional binding of SREBP-2 and Sp1 to their sites, which are head to head in repeats 2 and 3, allows the interaction of SREBP-2 with the N-terminal region of Sp1 and facilitates Sp1 recruitment 28 ( Figure 5).	bind
24942	5	7851	6	NULL	NULL	0	NULL	LDLR	NULL		is located on	NULL			Sp1 binding site		NULL			repeat 3	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_164	15178557	33 It has been suggested that in LDLR promoter, the respective directional binding of SREBP-2 and Sp1 to their sites, which are head to head in repeats 2 and 3, allows the interaction of SREBP-2 with the N-terminal region of Sp1 and facilitates Sp1 recruitment 28 ( Figure 5).	bind
24943	6	7851	6	NULL	NULL	0	NULL	statement 2	NULL		allows	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_164	15178557	33 It has been suggested that in LDLR promoter, the respective directional binding of SREBP-2 and Sp1 to their sites, which are head to head in repeats 2 and 3, allows the interaction of SREBP-2 with the N-terminal region of Sp1 and facilitates Sp1 recruitment 28 ( Figure 5).	bind
24944	7	7851	6	NULL	NULL	0	NULL	statement 3	NULL		allows	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_164	15178557	33 It has been suggested that in LDLR promoter, the respective directional binding of SREBP-2 and Sp1 to their sites, which are head to head in repeats 2 and 3, allows the interaction of SREBP-2 with the N-terminal region of Sp1 and facilitates Sp1 recruitment 28 ( Figure 5).	bind
24945	8	7851	6	NULL	NULL	0	NULL	statement 2	NULL		facilitate	NULL				Sp1	NULL	recruitment of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_164	15178557	33 It has been suggested that in LDLR promoter, the respective directional binding of SREBP-2 and Sp1 to their sites, which are head to head in repeats 2 and 3, allows the interaction of SREBP-2 with the N-terminal region of Sp1 and facilitates Sp1 recruitment 28 ( Figure 5).	bind
24946	9	7851	6	NULL	NULL	0	NULL	statement 3	NULL		facilitate	NULL				Sp1	NULL	recruitment of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1454_s_164	15178557	33 It has been suggested that in LDLR promoter, the respective directional binding of SREBP-2 and Sp1 to their sites, which are head to head in repeats 2 and 3, allows the interaction of SREBP-2 with the N-terminal region of Sp1 and facilitates Sp1 recruitment 28 ( Figure 5).	bind
32222	1	7852	5	13	NULL	NULL	NULL	L-4F	GP		bind					LPS	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_3_236_s_240	16002747	33 Our data suggest that L-4F binds LPS and alters its aggregation state.	bind
32223	2	7852	5	13	NULL	NULL	NULL	statement 1	Process		alters					LPS	Chemical	aggregation state of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_3_236_s_240	16002747	33 Our data suggest that L-4F binds LPS and alters its aggregation state.	bind
24939	1	7852	6	NULL	NULL	0	NULL	L-4F	NULL		bind	NULL				LPS	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_3_236_s_240	16002747	33 Our data suggest that L-4F binds LPS and alters its aggregation state.	bind
24940	2	7852	6	NULL	NULL	0	NULL	statement 1	NULL		alters	NULL				LPS	NULL	aggregation state of 			NULL		0	NULL	NULL	NULL	gw70_circulationres_97_3_236_s_240	16002747	33 Our data suggest that L-4F binds LPS and alters its aggregation state.	bind
32224	1	7853	5	13	NULL	NULL	NULL	NRRE-1	GP		is a type of					complex response element	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_6_568_s_84	15375023	33 The complex response element (NRRE-1) conferring PPARalpha responsiveness binds several NRs and dictates the developmental and FA responsiveness of the MCAD gene.	bind
32225	2	7853	5	13	NULL	NULL	NULL				confers				NRRE-1	PPARalpha	GP	responsiveness of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_6_568_s_84	15375023	33 The complex response element (NRRE-1) conferring PPARalpha responsiveness binds several NRs and dictates the developmental and FA responsiveness of the MCAD gene.	bind
32226	3	7853	5	13	NULL	NULL	NULL				bind				NRRE-1	NRs	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_6_568_s_84	15375023	33 The complex response element (NRRE-1) conferring PPARalpha responsiveness binds several NRs and dictates the developmental and FA responsiveness of the MCAD gene.	bind
32227	4	7853	5	13	NULL	NULL	NULL	statement 3	Process		dictates					MCAD gene	GP	development of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_6_568_s_84	15375023	33 The complex response element (NRRE-1) conferring PPARalpha responsiveness binds several NRs and dictates the developmental and FA responsiveness of the MCAD gene.	bind
32228	5	7853	5	13	NULL	NULL	NULL	statement 3	Process		dictates					MCAD gene	GP	FA responsiveness of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_6_568_s_84	15375023	33 The complex response element (NRRE-1) conferring PPARalpha responsiveness binds several NRs and dictates the developmental and FA responsiveness of the MCAD gene.	bind
24958	1	7853	6	10	NULL	0	NULL	NRRE-1	NULL		is a type of	NULL				complex response element	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_6_568_s_84	15375023	33 The complex response element (NRRE-1) conferring PPARalpha responsiveness binds several NRs and dictates the developmental and FA responsiveness of the MCAD gene.	bind
24977	2	7853	6	NULL	NULL	0	NULL		NULL		confers	NULL			NRRE-1	PPARalpha	NULL	 responsiveness of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_6_568_s_84	15375023	33 The complex response element (NRRE-1) conferring PPARalpha responsiveness binds several NRs and dictates the developmental and FA responsiveness of the MCAD gene.	bind
24978	3	7853	6	NULL	NULL	0	NULL		NULL		bind	NULL			NRRE-1	NRs	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_6_568_s_84	15375023	33 The complex response element (NRRE-1) conferring PPARalpha responsiveness binds several NRs and dictates the developmental and FA responsiveness of the MCAD gene.	bind
24980	4	7853	6	NULL	NULL	0	NULL		NULL		dictates	NULL			NRRE-1	MCAD gene	NULL	developmental responsiveness of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_6_568_s_84	15375023	33 The complex response element (NRRE-1) conferring PPARalpha responsiveness binds several NRs and dictates the developmental and FA responsiveness of the MCAD gene.	bind
24981	5	7853	6	NULL	NULL	0	NULL		NULL		dictates	NULL			NRRE-1	MCAD gene	NULL	FA responsiveness of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_6_568_s_84	15375023	33 The complex response element (NRRE-1) conferring PPARalpha responsiveness binds several NRs and dictates the developmental and FA responsiveness of the MCAD gene.	bind
32229	1	7854	5	13	NULL	NULL	NULL	IGF-1	GP		bind					IGF-1 receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_20_2588_s_172	15883206	33 We have previously shown that IGF-1 binding to the IGF-1 receptors results in a Ca2+-dependent positive inotropic effect.	bind
32230	2	7854	5	13	NULL	NULL	NULL	statement 1	Process		results in					inotropic effect	Process	positive			NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_20_2588_s_172	15883206	33 We have previously shown that IGF-1 binding to the IGF-1 receptors results in a Ca2+-dependent positive inotropic effect.	bind
32231	3	7854	5	13	NULL	NULL	NULL	statement 2	Process		is dependent on					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_20_2588_s_172	15883206	33 We have previously shown that IGF-1 binding to the IGF-1 receptors results in a Ca2+-dependent positive inotropic effect.	bind
24983	1	7854	6	NULL	NULL	0	NULL	IGF-1	NULL		bind	NULL				IGF-1 receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_111_20_2588_s_172	15883206	33 We have previously shown that IGF-1 binding to the IGF-1 receptors results in a Ca2+-dependent positive inotropic effect.	bind
24984	2	7854	6	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				inotropic effect	NULL	positive			NULL		0	NULL	NULL	NULL	gw70_circulation_111_20_2588_s_172	15883206	33 We have previously shown that IGF-1 binding to the IGF-1 receptors results in a Ca2+-dependent positive inotropic effect.	bind
24985	3	7854	6	NULL	NULL	0	NULL	statement 2	NULL		is dependent on	NULL				Ca2+	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_111_20_2588_s_172	15883206	33 We have previously shown that IGF-1 binding to the IGF-1 receptors results in a Ca2+-dependent positive inotropic effect.	bind
32232	1	7855	5	13	NULL	NULL	NULL	Smad1	GP		does not bind									AGAC	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_10_992_s_110	16224060	33,34  However, Smad1 or Smad4 did not bind to the 3 AGAC and flanking &10 bp by EMSA (data not shown).	bind
32233	2	7855	5	13	NULL	NULL	NULL	Smad4	GP		does not bind									AGAC	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_10_992_s_110	16224060	33,34  However, Smad1 or Smad4 did not bind to the 3 AGAC and flanking &10 bp by EMSA (data not shown).	bind
24987	1	7855	6	10	NULL	0	NULL	Smad1	NULL		does not bind	NULL					NULL			AGAC	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_10_992_s_110	16224060	33,34  However, Smad1 or Smad4 did not bind to the 3 AGAC and flanking &10 bp by EMSA (data not shown).	bind
24988	2	7855	6	10	NULL	0	NULL	Smad4	NULL		does not bind	NULL					NULL			AGAC	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_10_992_s_110	16224060	33,34  However, Smad1 or Smad4 did not bind to the 3 AGAC and flanking &10 bp by EMSA (data not shown).	bind
32391	1	7856	5	13	NULL	NULL	NULL	nitric oxide	Chemical		inhibits					thrombus		formation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_454_s_168	15569820	33,34  Nitric oxide inhibits the formation of thrombus under high-shear flow 37 and attenuates agonist-induced upregulation of P-selectin and the binding of vWF to platelet GPIb complex by negatively regulating the cGMP in platelets.	bind
32392	2	7856	5	13	NULL	NULL	NULL	high-shear flow			is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_454_s_168	15569820	33,34  Nitric oxide inhibits the formation of thrombus under high-shear flow 37 and attenuates agonist-induced upregulation of P-selectin and the binding of vWF to platelet GPIb complex by negatively regulating the cGMP in platelets.	bind
32393	3	7856	5	13	NULL	NULL	NULL	agonist	Chemical		induces					P-selectin	GP	upregulation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_454_s_168	15569820	33,34  Nitric oxide inhibits the formation of thrombus under high-shear flow 37 and attenuates agonist-induced upregulation of P-selectin and the binding of vWF to platelet GPIb complex by negatively regulating the cGMP in platelets.	bind
32394	4	7856	5	13	NULL	NULL	NULL	nitric oxide	Chemical		attenuates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_454_s_168	15569820	33,34  Nitric oxide inhibits the formation of thrombus under high-shear flow 37 and attenuates agonist-induced upregulation of P-selectin and the binding of vWF to platelet GPIb complex by negatively regulating the cGMP in platelets.	bind
32395	5	7856	5	13	NULL	NULL	NULL	VWF	GP		bind					platelet GPIb complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_454_s_168	15569820	33,34  Nitric oxide inhibits the formation of thrombus under high-shear flow 37 and attenuates agonist-induced upregulation of P-selectin and the binding of vWF to platelet GPIb complex by negatively regulating the cGMP in platelets.	bind
32396	6	7856	5	13	NULL	NULL	NULL	nitric oxide	Chemical		regulates		negatively			cGMP	Chemical				NULL	in platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_454_s_168	15569820	33,34  Nitric oxide inhibits the formation of thrombus under high-shear flow 37 and attenuates agonist-induced upregulation of P-selectin and the binding of vWF to platelet GPIb complex by negatively regulating the cGMP in platelets.	bind
32397	7	7856	5	13	NULL	NULL	NULL	statement 6	Process		attenuates					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_454_s_168	15569820	33,34  Nitric oxide inhibits the formation of thrombus under high-shear flow 37 and attenuates agonist-induced upregulation of P-selectin and the binding of vWF to platelet GPIb complex by negatively regulating the cGMP in platelets.	bind
24989	1	7856	6	NULL	NULL	0	NULL	Nitric oxide	NULL		inhibits	NULL				thrombus	NULL	formation of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_454_s_168	15569820	33,34  Nitric oxide inhibits the formation of thrombus under high-shear flow 37 and attenuates agonist-induced upregulation of P-selectin and the binding of vWF to platelet GPIb complex by negatively regulating the cGMP in platelets.	bind
24990	2	7856	6	NULL	NULL	0	NULL	statement 1	NULL		occurs under	NULL				high shear flow	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_454_s_168	15569820	33,34  Nitric oxide inhibits the formation of thrombus under high-shear flow 37 and attenuates agonist-induced upregulation of P-selectin and the binding of vWF to platelet GPIb complex by negatively regulating the cGMP in platelets.	bind
24991	3	7856	6	NULL	NULL	0	NULL	vWF	NULL		bind	NULL				platelet GPIb complex	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_454_s_168	15569820	33,34  Nitric oxide inhibits the formation of thrombus under high-shear flow 37 and attenuates agonist-induced upregulation of P-selectin and the binding of vWF to platelet GPIb complex by negatively regulating the cGMP in platelets.	bind
24992	4	7856	6	NULL	NULL	0	NULL	agonist	NULL		induces	NULL				P-selectin	NULL	upregulation of 			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_454_s_168	15569820	33,34  Nitric oxide inhibits the formation of thrombus under high-shear flow 37 and attenuates agonist-induced upregulation of P-selectin and the binding of vWF to platelet GPIb complex by negatively regulating the cGMP in platelets.	bind
24994	5	7856	6	NULL	NULL	0	NULL	Nitric oxide	NULL		attenuates	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_454_s_168	15569820	33,34  Nitric oxide inhibits the formation of thrombus under high-shear flow 37 and attenuates agonist-induced upregulation of P-selectin and the binding of vWF to platelet GPIb complex by negatively regulating the cGMP in platelets.	bind
24997	6	7856	6	NULL	NULL	0	NULL	Nitric oxide	NULL		attenuates	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_454_s_168	15569820	33,34  Nitric oxide inhibits the formation of thrombus under high-shear flow 37 and attenuates agonist-induced upregulation of P-selectin and the binding of vWF to platelet GPIb complex by negatively regulating the cGMP in platelets.	bind
24999	7	7856	6	10	NULL	0	NULL	statement 6	NULL		regulates	NULL	negatively			cGMP 	NULL				NULL	in platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_454_s_168	15569820	33,34  Nitric oxide inhibits the formation of thrombus under high-shear flow 37 and attenuates agonist-induced upregulation of P-selectin and the binding of vWF to platelet GPIb complex by negatively regulating the cGMP in platelets.	bind
32398	1	7857	5	13	NULL	NULL	NULL	decorin	GP		bind					PDGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_3_869_s_288	12937128	33,35  Decorin-PDGF binding and inhibition of PDGFR phosphorylation by decorin reported in this study indicate an additional mechanism of ECM regulation by decorin.	bind
32399	2	7857	5	13	NULL	NULL	NULL	decorin	GP		inhibits					PDGFR	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_3_869_s_288	12937128	33,35  Decorin-PDGF binding and inhibition of PDGFR phosphorylation by decorin reported in this study indicate an additional mechanism of ECM regulation by decorin.	bind
32400	3	7857	5	13	NULL	NULL	NULL	decorin	GP		regulates					ECM	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_3_869_s_288	12937128	33,35  Decorin-PDGF binding and inhibition of PDGFR phosphorylation by decorin reported in this study indicate an additional mechanism of ECM regulation by decorin.	bind
25000	1	7857	6	NULL	NULL	0	NULL	decorin	NULL		bind	NULL				PDGF	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_163_3_869_s_288	12937128	33,35  Decorin-PDGF binding and inhibition of PDGFR phosphorylation by decorin reported in this study indicate an additional mechanism of ECM regulation by decorin.	bind
25001	2	7857	6	NULL	NULL	0	NULL	decorin	NULL		inhibits	NULL				PDGFR	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_163_3_869_s_288	12937128	33,35  Decorin-PDGF binding and inhibition of PDGFR phosphorylation by decorin reported in this study indicate an additional mechanism of ECM regulation by decorin.	bind
25002	3	7857	6	NULL	NULL	0	NULL	decorin	NULL		regulates	NULL				ECM	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_163_3_869_s_288	12937128	33,35  Decorin-PDGF binding and inhibition of PDGFR phosphorylation by decorin reported in this study indicate an additional mechanism of ECM regulation by decorin.	bind
32401	1	7859	5	13	NULL	NULL	NULL	zinc finger/homeodomain protein	GP		bind									T3-response elements	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4846_s_383	11121475	34       Cabanillas,A.M. and Darling,D.S. (1996) Alternative splicing gives rise to two isoforms of Zfhep, a zinc finger/homeodomain protein that binds  T3-response elements.	bind
38970	2	7859	5	13	NULL	NULL	NULL	Zfhep	GP		is a type of					zinc finger/homeodomain protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4846_s_383	11121475	34       Cabanillas,A.M. and Darling,D.S. (1996) Alternative splicing gives rise to two isoforms of Zfhep, a zinc finger/homeodomain protein that binds  T3-response elements.	bind
25004	1	7859	6	13	NULL	NULL	NULL	Zfhep	GP		is a type of					zinc finger/homeodomain protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4846_s_383	11121475	34       Cabanillas,A.M. and Darling,D.S. (1996) Alternative splicing gives rise to two isoforms of Zfhep, a zinc finger/homeodomain protein that binds  T3-response elements.	bind
25005	2	7859	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL					NULL			T3-response elements	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4846_s_383	11121475	34       Cabanillas,A.M. and Darling,D.S. (1996) Alternative splicing gives rise to two isoforms of Zfhep, a zinc finger/homeodomain protein that binds  T3-response elements.	bind
25007	3	7859	6	NULL	NULL	0	NULL	Alternative splicing	NULL		gives rise to	NULL				Zfhep	NULL	two isoforms of 			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4846_s_383	11121475	34       Cabanillas,A.M. and Darling,D.S. (1996) Alternative splicing gives rise to two isoforms of Zfhep, a zinc finger/homeodomain protein that binds  T3-response elements.	bind
32402	1	7860	5	13	NULL	NULL	NULL	Ni2+	Chemical		bind					polynucleotides	NucleicAcid	synthetic		regularly alternating purine - pyrimidine sequences	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2795_s_307	11433025	34       Kankia,B.I. (2000) Hydration effects of Ni2+ binding to synthetic polynucleotides with regularly alternating purine - pyrimidine sequences.	bind
25008	1	7860	6	NULL	NULL	0	NULL	Ni2+	NULL		bind	NULL				polynucleotides	NULL	synthetic		 regularly alternating purine - pyrimidine sequences	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2795_s_307	11433025	34       Kankia,B.I. (2000) Hydration effects of Ni2+ binding to synthetic polynucleotides with regularly alternating purine - pyrimidine sequences.	bind
32403	1	7861	5	13	NULL	NULL	NULL	U1A protein	GP	human	does not bind			C-terminal RNA binding domain		RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_550_s_360	11788718	34       Lu,J. and Hall,K.B. (1995) An RBD that does not bind RNA: NMR secondary structure determination and biochemical properties of the  C-terminal RNA binding domain from the human U1A protein.	bind
25010	1	7861	6	NULL	NULL	0	NULL	U1A protein	NULL	human	does not bind	NULL		C-terminal RNA binding domain		RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_550_s_360	11788718	34       Lu,J. and Hall,K.B. (1995) An RBD that does not bind RNA: NMR secondary structure determination and biochemical properties of the  C-terminal RNA binding domain from the human U1A protein.	bind
32404	1	7862	5	13	NULL	NULL	NULL	SR protein	GP		bind		sequence-specific			RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4822_s_354	11121472	34       Tacke,R., Chen,Y. and Manley,J.L. (1997) Sequence-specific RNA binding by an SR protein requires RS domain phosphorylation: creation of an SRp40-specific splicing enhancer.	bind
32405	2	7862	5	13	NULL	NULL	NULL			phosphorylation of	is required for			RS domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4822_s_354	11121472	34       Tacke,R., Chen,Y. and Manley,J.L. (1997) Sequence-specific RNA binding by an SR protein requires RS domain phosphorylation: creation of an SRp40-specific splicing enhancer.	bind
25011	1	7862	6	NULL	NULL	0	NULL	SR protein	NULL		bind	NULL	sequence specifically			RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4822_s_354	11121472	34       Tacke,R., Chen,Y. and Manley,J.L. (1997) Sequence-specific RNA binding by an SR protein requires RS domain phosphorylation: creation of an SRp40-specific splicing enhancer.	bind
25012	2	7862	6	NULL	NULL	0	NULL	statement 1	NULL		requires	NULL					NULL	phosphorylation of	RS domain		NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_24_4822_s_354	11121472	34       Tacke,R., Chen,Y. and Manley,J.L. (1997) Sequence-specific RNA binding by an SR protein requires RS domain phosphorylation: creation of an SRp40-specific splicing enhancer.	bind
32406	1	7863	5	13	NULL	NULL	NULL	RNAI	GP		bind					RNAII	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3145_s_368	11470871	34       Tomizawa,J. (1990) Control of ColE1 plasmid replication: intermediates in the binding of RNAI and RNAII.	bind
25013	1	7863	6	NULL	NULL	0	NULL	RNAI	NULL		bind	NULL				RNAII	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3145_s_368	11470871	34       Tomizawa,J. (1990) Control of ColE1 plasmid replication: intermediates in the binding of RNAI and RNAII.	bind
32407	1	7864	5	13	NULL	NULL	NULL	heparin	Chemical		bind					platelet factor 4	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_9_2877_s_179	9386152	34  In addition, heparin binds to platelet factor 4, another alpha-granule constituent.	bind
32408	2	7864	5	13	NULL	NULL	NULL	platelet factor 4	GP		is a type of					alpha-granule constituent	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_9_2877_s_179	9386152	34  In addition, heparin binds to platelet factor 4, another alpha-granule constituent.	bind
25014	1	7864	6	NULL	NULL	0	NULL	heparin	NULL		bind	NULL				platelet factor 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_96_9_2877_s_179	9386152	34  In addition, heparin binds to platelet factor 4, another alpha-granule constituent.	bind
25015	2	7864	6	10	NULL	0	NULL	platelet factor 4	NULL		is a type of	NULL				alpha-granule constituent	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_9_2877_s_179	9386152	34  In addition, heparin binds to platelet factor 4, another alpha-granule constituent.	bind
32409	1	7865	5	13	NULL	NULL	NULL	TNF-alpha	GP		bind					ECM	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_13	12000736	34  In addition, TNF-alpha bound to ECM exhibits biological activity, as demonstrated by findings that when bound to fibronectin, this cytokine modifies beta1-integrin-mediated adhesion of T lymphocytes, 31 provides a stop signal for migration of T cells, 32  and stimulates MMP-9 expression by monocytes.	bind
32410	2	7865	5	13	NULL	NULL	NULL	TNF-alpha	GP		bind					fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_13	12000736	34  In addition, TNF-alpha bound to ECM exhibits biological activity, as demonstrated by findings that when bound to fibronectin, this cytokine modifies beta1-integrin-mediated adhesion of T lymphocytes, 31 provides a stop signal for migration of T cells, 32  and stimulates MMP-9 expression by monocytes.	bind
32411	3	7865	5	13	NULL	NULL	NULL	beta1-integrin	GP		mediates					T lymphocytes	Cell	adhesion of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_13	12000736	34  In addition, TNF-alpha bound to ECM exhibits biological activity, as demonstrated by findings that when bound to fibronectin, this cytokine modifies beta1-integrin-mediated adhesion of T lymphocytes, 31 provides a stop signal for migration of T cells, 32  and stimulates MMP-9 expression by monocytes.	bind
32412	4	7865	5	13	NULL	NULL	NULL	statement 2	Process		modify					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_13	12000736	34  In addition, TNF-alpha bound to ECM exhibits biological activity, as demonstrated by findings that when bound to fibronectin, this cytokine modifies beta1-integrin-mediated adhesion of T lymphocytes, 31 provides a stop signal for migration of T cells, 32  and stimulates MMP-9 expression by monocytes.	bind
32413	5	7865	5	13	NULL	NULL	NULL	statement 2	Process		stops					T cells	Cell	 signal for migration of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_13	12000736	34  In addition, TNF-alpha bound to ECM exhibits biological activity, as demonstrated by findings that when bound to fibronectin, this cytokine modifies beta1-integrin-mediated adhesion of T lymphocytes, 31 provides a stop signal for migration of T cells, 32  and stimulates MMP-9 expression by monocytes.	bind
32414	6	7865	5	13	NULL	NULL	NULL	monocytes	Cell		express					MMP-9	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_13	12000736	34  In addition, TNF-alpha bound to ECM exhibits biological activity, as demonstrated by findings that when bound to fibronectin, this cytokine modifies beta1-integrin-mediated adhesion of T lymphocytes, 31 provides a stop signal for migration of T cells, 32  and stimulates MMP-9 expression by monocytes.	bind
32415	7	7865	5	13	NULL	NULL	NULL	statement 2	Process		stimulates					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_13	12000736	34  In addition, TNF-alpha bound to ECM exhibits biological activity, as demonstrated by findings that when bound to fibronectin, this cytokine modifies beta1-integrin-mediated adhesion of T lymphocytes, 31 provides a stop signal for migration of T cells, 32  and stimulates MMP-9 expression by monocytes.	bind
25016	1	7865	6	NULL	NULL	0	NULL	TNF-alpha	NULL		bind	NULL				ECM	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_13	12000736	34  In addition, TNF-alpha bound to ECM exhibits biological activity, as demonstrated by findings that when bound to fibronectin, this cytokine modifies beta1-integrin-mediated adhesion of T lymphocytes, 31 provides a stop signal for migration of T cells, 32  and stimulates MMP-9 expression by monocytes.	bind
25017	2	7865	6	NULL	NULL	0	NULL	statement 1	NULL		exhibits	NULL				biological activity	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_13	12000736	34  In addition, TNF-alpha bound to ECM exhibits biological activity, as demonstrated by findings that when bound to fibronectin, this cytokine modifies beta1-integrin-mediated adhesion of T lymphocytes, 31 provides a stop signal for migration of T cells, 32  and stimulates MMP-9 expression by monocytes.	bind
25018	3	7865	6	NULL	NULL	0	NULL	TNF-alpha	NULL		bind	NULL				fibronectin	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_13	12000736	34  In addition, TNF-alpha bound to ECM exhibits biological activity, as demonstrated by findings that when bound to fibronectin, this cytokine modifies beta1-integrin-mediated adhesion of T lymphocytes, 31 provides a stop signal for migration of T cells, 32  and stimulates MMP-9 expression by monocytes.	bind
25019	4	7865	6	NULL	NULL	0	NULL	beta1 integrin	NULL		mediates	NULL				T lymphocytes	NULL	adhesion of 			NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_13	12000736	34  In addition, TNF-alpha bound to ECM exhibits biological activity, as demonstrated by findings that when bound to fibronectin, this cytokine modifies beta1-integrin-mediated adhesion of T lymphocytes, 31 provides a stop signal for migration of T cells, 32  and stimulates MMP-9 expression by monocytes.	bind
25020	5	7865	6	NULL	NULL	0	NULL	statement 3	NULL		modifies	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_13	12000736	34  In addition, TNF-alpha bound to ECM exhibits biological activity, as demonstrated by findings that when bound to fibronectin, this cytokine modifies beta1-integrin-mediated adhesion of T lymphocytes, 31 provides a stop signal for migration of T cells, 32  and stimulates MMP-9 expression by monocytes.	bind
25851	6	7865	6	NULL	NULL	0	NULL	statement 3	NULL		stops	NULL				T cells	NULL	migration of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_13	12000736	34  In addition, TNF-alpha bound to ECM exhibits biological activity, as demonstrated by findings that when bound to fibronectin, this cytokine modifies beta1-integrin-mediated adhesion of T lymphocytes, 31 provides a stop signal for migration of T cells, 32  and stimulates MMP-9 expression by monocytes.	bind
25852	7	7865	6	NULL	NULL	0	NULL	monocytes	NULL		express	NULL				MMP-9	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_13	12000736	34  In addition, TNF-alpha bound to ECM exhibits biological activity, as demonstrated by findings that when bound to fibronectin, this cytokine modifies beta1-integrin-mediated adhesion of T lymphocytes, 31 provides a stop signal for migration of T cells, 32  and stimulates MMP-9 expression by monocytes.	bind
25853	8	7865	6	NULL	NULL	0	NULL	TNF-alpha	NULL		stimulates	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_13	12000736	34  In addition, TNF-alpha bound to ECM exhibits biological activity, as demonstrated by findings that when bound to fibronectin, this cytokine modifies beta1-integrin-mediated adhesion of T lymphocytes, 31 provides a stop signal for migration of T cells, 32  and stimulates MMP-9 expression by monocytes.	bind
32416	1	7866	5	13	NULL	NULL	NULL	PlGF homodimers	GP		bind					VEGFR-1	GP				NULL	HUVEC	NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_993_s_349	11549592	34  Moreover, the fact that PlGF homodimers that bind to VEGFR-1 and PlGF:VEGF heterodimers that bind to VEGFR-2 induced tyrosine phosphorylation of a 38-kd protein in HUVECs whereas VEGF homodimers did not 29  supports the view that PlGF and VEGF can exert different biological actions through the same receptor.	bind
32418	2	7866	5	13	NULL	NULL	NULL	PlGF:VEGF heterodimers	GP		bind					VEGFR-2	GP				NULL	HUVEC	NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_993_s_349	11549592	34  Moreover, the fact that PlGF homodimers that bind to VEGFR-1 and PlGF:VEGF heterodimers that bind to VEGFR-2 induced tyrosine phosphorylation of a 38-kd protein in HUVECs whereas VEGF homodimers did not 29  supports the view that PlGF and VEGF can exert different biological actions through the same receptor.	bind
32419	3	7866	5	13	NULL	NULL	NULL	statement 1	Process		induces					38-kd protein	GP	phosphorylation of	tyrosine		NULL	in HUVECs 	NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_993_s_349	11549592	34  Moreover, the fact that PlGF homodimers that bind to VEGFR-1 and PlGF:VEGF heterodimers that bind to VEGFR-2 induced tyrosine phosphorylation of a 38-kd protein in HUVECs whereas VEGF homodimers did not 29  supports the view that PlGF and VEGF can exert different biological actions through the same receptor.	bind
32420	4	7866	5	13	NULL	NULL	NULL	statement 3	Process		induces					38-kd protein	GP	phosphorylation of	tyrosine		NULL	in HUVECs	NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_993_s_349	11549592	34  Moreover, the fact that PlGF homodimers that bind to VEGFR-1 and PlGF:VEGF heterodimers that bind to VEGFR-2 induced tyrosine phosphorylation of a 38-kd protein in HUVECs whereas VEGF homodimers did not 29  supports the view that PlGF and VEGF can exert different biological actions through the same receptor.	bind
25021	1	7866	6	10	NULL	0	NULL	PlGF homodimers			bind					VEGFR-1					NULL	HUVEC	NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_993_s_349	11549592	34  Moreover, the fact that PlGF homodimers that bind to VEGFR-1 and PlGF:VEGF heterodimers that bind to VEGFR-2 induced tyrosine phosphorylation of a 38-kd protein in HUVECs whereas VEGF homodimers did not 29  supports the view that PlGF and VEGF can exert different biological actions through the same receptor.	bind
25022	2	7866	6	10	NULL	0	NULL	PlGF:VEGF heterodimers			bind					VEGFR-2					NULL	HUVEC	NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_993_s_349	11549592	34  Moreover, the fact that PlGF homodimers that bind to VEGFR-1 and PlGF:VEGF heterodimers that bind to VEGFR-2 induced tyrosine phosphorylation of a 38-kd protein in HUVECs whereas VEGF homodimers did not 29  supports the view that PlGF and VEGF can exert different biological actions through the same receptor.	bind
25024	3	7866	6	NULL	NULL	0	NULL	statement 1	NULL		induces	NULL				38-kd protein	NULL	phosphorylation of	tyrosine		NULL	HUVEC	0	NULL	NULL	NULL	gw60_amjpathol_159_3_993_s_349	11549592	34  Moreover, the fact that PlGF homodimers that bind to VEGFR-1 and PlGF:VEGF heterodimers that bind to VEGFR-2 induced tyrosine phosphorylation of a 38-kd protein in HUVECs whereas VEGF homodimers did not 29  supports the view that PlGF and VEGF can exert different biological actions through the same receptor.	bind
25025	4	7866	6	NULL	NULL	0	NULL	statement 2	NULL		induces	NULL				38-kd protein	NULL	phosphorylation of	tyrosine		NULL	HUVECs	0	NULL	NULL	NULL	gw60_amjpathol_159_3_993_s_349	11549592	34  Moreover, the fact that PlGF homodimers that bind to VEGFR-1 and PlGF:VEGF heterodimers that bind to VEGFR-2 induced tyrosine phosphorylation of a 38-kd protein in HUVECs whereas VEGF homodimers did not 29  supports the view that PlGF and VEGF can exert different biological actions through the same receptor.	bind
32422	1	7867	5	13	NULL	NULL	NULL	HSPGs	GP		modulate					FGF-2	GP	signaling of			NULL	human breast cancer	NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_31	11786412	34  The goal of this project was to investigate HSPGs as modulators of FGF-2 signaling in human breast cancer by addressing the following unresolved questions: 1) Do breast carcinoma HSPGs differ from normal breast epithelial cell HSPGs in their capacity to promote FGF-2 binding to FGFR-1?	bind
32423	2	7867	5	13	NULL	NULL	NULL	FGF-2	GP		bind					FGFR-1	GP				NULL	human breast cancer	NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_31	11786412	34  The goal of this project was to investigate HSPGs as modulators of FGF-2 signaling in human breast cancer by addressing the following unresolved questions: 1) Do breast carcinoma HSPGs differ from normal breast epithelial cell HSPGs in their capacity to promote FGF-2 binding to FGFR-1?	bind
39445	3	7867	5	13	NULL	NULL	NULL	HSPGs	GP		promotes					statement 2	Process				NULL	human breast cancer	NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_31	11786412	34  The goal of this project was to investigate HSPGs as modulators of FGF-2 signaling in human breast cancer by addressing the following unresolved questions: 1) Do breast carcinoma HSPGs differ from normal breast epithelial cell HSPGs in their capacity to promote FGF-2 binding to FGFR-1?	bind
25026	1	7867	6	NULL	NULL	0	NULL	FGF-2	NULL		bind	NULL				FGFR-1	NULL				NULL	human breast cancer 	NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_31	11786412	34  The goal of this project was to investigate HSPGs as modulators of FGF-2 signaling in human breast cancer by addressing the following unresolved questions: 1) Do breast carcinoma HSPGs differ from normal breast epithelial cell HSPGs in their capacity to promote FGF-2 binding to FGFR-1?	bind
25027	2	7867	6	NULL	NULL	0	NULL	HSPG	NULL		promote	NULL				statement 1	NULL				NULL	human breast cancer	NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_31	11786412	34  The goal of this project was to investigate HSPGs as modulators of FGF-2 signaling in human breast cancer by addressing the following unresolved questions: 1) Do breast carcinoma HSPGs differ from normal breast epithelial cell HSPGs in their capacity to promote FGF-2 binding to FGFR-1?	bind
25028	3	7867	6	NULL	NULL	0	NULL	HSPG	NULL		modulate	NULL				FGF-2	NULL	signaling of			NULL	human breast cancer	NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_31	11786412	34  The goal of this project was to investigate HSPGs as modulators of FGF-2 signaling in human breast cancer by addressing the following unresolved questions: 1) Do breast carcinoma HSPGs differ from normal breast epithelial cell HSPGs in their capacity to promote FGF-2 binding to FGFR-1?	bind
32425	1	7868	5	13	NULL	NULL	NULL	RAR alpha	GP		is a type of					RA receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
32426	2	7868	5	13	NULL	NULL	NULL	RAR beta	GP		is a type of					RA receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
32427	3	7868	5	13	NULL	NULL	NULL	RAR gamma	GP		is a type of					RA receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
32428	4	7868	5	13	NULL	NULL	NULL	RAR alpha	GP		bind					atRA	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
32429	5	7868	5	13	NULL	NULL	NULL	RAR alpha	GP		bind					9- cis RA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
32430	6	7868	5	13	NULL	NULL	NULL	RAR beta	GP		bind					atRA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
32431	7	7868	5	13	NULL	NULL	NULL	RAR beta	GP		bind					9- cis RA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
32432	8	7868	5	13	NULL	NULL	NULL	RAR gamma	GP		bind					atRA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
32433	9	7868	5	13	NULL	NULL	NULL	RAR gamma	GP		bind					9- cis RA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
32434	10	7868	5	13	NULL	NULL	NULL	RXR alpha	GP		is a type of					retinoid X receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
32435	11	7868	5	13	NULL	NULL	NULL	RXR beta	GP		is a type of					retinoid X receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
32436	12	7868	5	13	NULL	NULL	NULL	RXR gamma	GP		is a type of					retinoid X receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
32438	13	7868	5	13	NULL	NULL	NULL	RXR alpha	GP		bind					9- cis RA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
32439	14	7868	5	13	NULL	NULL	NULL	RXR beta	GP		bind					9- cis RA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
32440	15	7868	5	13	NULL	NULL	NULL	RXR gamma	GP		bind					9- cis RA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
55552	16	7868	5	13	NULL	NULL	NULL	RXR	GP		is					retinoid X receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
25029	1	7868	6	NULL	NULL	0	NULL	RAR alpha	NULL		bind	NULL				atRA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
25030	2	7868	6	NULL	NULL	0	NULL	RAR beta	NULL		bind	NULL				atRA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
25031	3	7868	6	NULL	NULL	0	NULL	RAR gamma	NULL		bind	NULL				atRA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
25032	4	7868	6	NULL	NULL	0	NULL	RAR alpha	NULL		bind	NULL				9- cis RA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
25033	5	7868	6	NULL	NULL	0	NULL	RAR beta	NULL		bind	NULL				9- cis RA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
25034	6	7868	6	NULL	NULL	0	NULL	RAR gamma	NULL		bind	NULL				9- cis RA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
25035	7	7868	6	NULL	NULL	0	NULL	RXR	NULL		is	NULL				retinoid X receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
25036	8	7868	6	NULL	NULL	0	NULL	RXR alpha	NULL		bind	NULL				9- cis RA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
25037	9	7868	6	NULL	NULL	0	NULL	RXR beta	NULL		bind	NULL				9- cis RA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
25038	10	7868	6	NULL	NULL	0	NULL	RXR gamma	NULL		bind	NULL				9- cis RA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
38833	11	7868	6	NULL	NULL	0	NULL	RAR alpha	NULL		is a type of	NULL				RA receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
38834	12	7868	6	NULL	NULL	0	NULL	RAR beta	NULL		is a type of	NULL				RA receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
38835	13	7868	6	NULL	NULL	0	NULL	RAR gamma	NULL		is a type of	NULL				RA receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
38836	14	7868	6	NULL	NULL	0	NULL	RXR alpha	NULL		is a type of	NULL				retinoid X receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
38837	15	7868	6	NULL	NULL	0	NULL	RXR beta	NULL		is a type of	NULL				retinoid X receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
38838	16	7868	6	NULL	NULL	0	NULL	RXR gamma	NULL		is a type of	NULL				retinoid X receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_5_355_s_50	10969032	34  The RA receptors (RARs alpha, beta, and gamma) bind both atRA and 9- cis RA, whereas the retinoid X receptors (RXRs alpha, beta, and gamma) bind 9- cis RA (Figure  ).	bind
32444	1	7869	5	13	NULL	NULL	NULL	apo A-I genes	GP	rabbit	is homologus to		highly			apo A-I genes	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1424_s_154	8977445	34  Therefore, despite a high sequence homology (>78%) of the 200 bp of the 5' upstream flanking region of the rabbit and human apo A-I genes, the nonparenchymal cell - secreted factor that attenuates rabbit hepatic apo A-I gene expression may not bind to this human apo A-I gene fragment.	bind
32526	2	7869	5	13	NULL	NULL	NULL	nonparenchymal cell - secreted factor	GP		attenuates					hepatic apo A-I gene	GP	expression of;; rabbit hepatic			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1424_s_154	8977445	34  Therefore, despite a high sequence homology (>78%) of the 200 bp of the 5' upstream flanking region of the rabbit and human apo A-I genes, the nonparenchymal cell - secreted factor that attenuates rabbit hepatic apo A-I gene expression may not bind to this human apo A-I gene fragment.	bind
32531	3	7869	5	13	NULL	NULL	NULL	nonparenchymal cell - secreted factor	GP		 not bind		may			apo A-I gene fragment	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1424_s_154	8977445	34  Therefore, despite a high sequence homology (>78%) of the 200 bp of the 5' upstream flanking region of the rabbit and human apo A-I genes, the nonparenchymal cell - secreted factor that attenuates rabbit hepatic apo A-I gene expression may not bind to this human apo A-I gene fragment.	bind
25854	1	7869	6	NULL	NULL	0	NULL	apo A-I gene	NULL	rabbit	has homology to	NULL	highly			apo A-I gene	NULL	human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1424_s_154	8977445	34  Therefore, despite a high sequence homology (>78%) of the 200 bp of the 5' upstream flanking region of the rabbit and human apo A-I genes, the nonparenchymal cell - secreted factor that attenuates rabbit hepatic apo A-I gene expression may not bind to this human apo A-I gene fragment.	bind
25855	2	7869	6	NULL	NULL	0	NULL	nonparenchymal cell - secreted factor	NULL		attenuates	NULL				apo A-I gene	NULL	rabbit;; hepatic;; expression of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1424_s_154	8977445	34  Therefore, despite a high sequence homology (>78%) of the 200 bp of the 5' upstream flanking region of the rabbit and human apo A-I genes, the nonparenchymal cell - secreted factor that attenuates rabbit hepatic apo A-I gene expression may not bind to this human apo A-I gene fragment.	bind
25856	3	7869	6	NULL	NULL	0	NULL	nonparenchymal cell - secreted factor	NULL		not bind	NULL	may			apo A-I gene fragment	NULL	human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1424_s_154	8977445	34  Therefore, despite a high sequence homology (>78%) of the 200 bp of the 5' upstream flanking region of the rabbit and human apo A-I genes, the nonparenchymal cell - secreted factor that attenuates rabbit hepatic apo A-I gene expression may not bind to this human apo A-I gene fragment.	bind
32441	1	7870	5	13	NULL	NULL	NULL	calcium/calmodulin	GP		bind					eNOS	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1161_s_82	12689915	34 - 36   Optimal eNOS activity occurs when the eNOS/caveolin-1 interaction is competitively disrupted by calcium/calmodulin binding to eNOS.	bind
32442	2	7870	5	13	NULL	NULL	NULL	statement 1	Process		disrupt		competitively			eNOS/caveolin-1	GP	interaction of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1161_s_82	12689915	34 - 36   Optimal eNOS activity occurs when the eNOS/caveolin-1 interaction is competitively disrupted by calcium/calmodulin binding to eNOS.	bind
32443	3	7870	5	13	NULL	NULL	NULL	statement 2	Process		results in					eNOS	GP	optimal activity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1161_s_82	12689915	34 - 36   Optimal eNOS activity occurs when the eNOS/caveolin-1 interaction is competitively disrupted by calcium/calmodulin binding to eNOS.	bind
25054	1	7870	6	NULL	NULL	0	NULL	calcium/calmodulin	NULL		bind	NULL				eNOS	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1161_s_82	12689915	34 - 36   Optimal eNOS activity occurs when the eNOS/caveolin-1 interaction is competitively disrupted by calcium/calmodulin binding to eNOS.	bind
25057	2	7870	6	NULL	NULL	0	NULL	eNOS/caveolin-1	NULL	interaction of	is disrupted by	NULL	competitively			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1161_s_82	12689915	34 - 36   Optimal eNOS activity occurs when the eNOS/caveolin-1 interaction is competitively disrupted by calcium/calmodulin binding to eNOS.	bind
25059	3	7870	6	10	NULL	0	NULL	statement 2			results in					eNOS		optimal activity of 			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1161_s_82	12689915	34 - 36   Optimal eNOS activity occurs when the eNOS/caveolin-1 interaction is competitively disrupted by calcium/calmodulin binding to eNOS.	bind
32561	1	7871	5	13	NULL	NULL	NULL	LDL	GP		bind					mast cell granules	CellComponent	exocytosed			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_6_801_s_32	7773737	34 35 36  For the present article, we studied whether SMCs, the other potential precursor of foam cells in the arterial intima, would also be capable of taking up LDL bound to exocytosed mast cell granules.	bind
38971	2	7871	5	13	NULL	NULL	NULL	SMC	Cell		precursor of		potentially			foam cells	Cell				NULL	arterial intima	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_6_801_s_32	7773737	34 35 36  For the present article, we studied whether SMCs, the other potential precursor of foam cells in the arterial intima, would also be capable of taking up LDL bound to exocytosed mast cell granules.	bind
25061	1	7871	6	NULL	NULL	0	NULL	SMC	NULL		are precursor of	NULL	potentially			foam cells	NULL				NULL	arterial intima	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_6_801_s_32	7773737	34 35 36  For the present article, we studied whether SMCs, the other potential precursor of foam cells in the arterial intima, would also be capable of taking up LDL bound to exocytosed mast cell granules.	bind
25064	2	7871	6	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				mast cell granules	NULL	exocytosed			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_6_801_s_32	7773737	34 35 36  For the present article, we studied whether SMCs, the other potential precursor of foam cells in the arterial intima, would also be capable of taking up LDL bound to exocytosed mast cell granules.	bind
32562	1	7872	5	13	NULL	NULL	NULL	CREB	GP		is					CRE binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
32563	2	7872	5	13	NULL	NULL	NULL	CREB	GP		is a type of					transactivator	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
32564	3	7872	5	13	NULL	NULL	NULL	ATF	GP		is a type of					transactivator	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
32565	4	7872	5	13	NULL	NULL	NULL	C/EBP	GP		is a type of					transactivator	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
32566	5	7872	5	13	NULL	NULL	NULL	C-Jun	GP		is a type of					transactivator	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
32567	6	7872	5	13	NULL	NULL	NULL	C-Fos	GP		is a type of					transactivator	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
32568	7	7872	5	13	NULL	NULL	NULL	USF	GP		is a type of					transactivator	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
32569	8	7872	5	NULL	NULL	0	NULL		NULL	overlapped	is located at	NULL			CRE;;AP-1 region		NULL			 - 60 to - 40 from transcription start site	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
32787	9	7872	5	13	NULL	NULL	NULL	CREB	GP		bind					statement 15	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
32788	10	7872	5	13	NULL	NULL	NULL	ATF	GP		bind					statement 15	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
32789	11	7872	5	13	NULL	NULL	NULL	C/EBP	GP		bind					statement 15	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
32791	12	7872	5	13	NULL	NULL	NULL	C-Jun	GP		bind					statement 15	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
32792	13	7872	5	13	NULL	NULL	NULL	C-Fos	GP		bind					statement 15	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
32793	14	7872	5	13	NULL	NULL	NULL	USF	GP		bind					statement 15	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
55553	15	7872	5	10	NULL	0	NULL				overlaps				CRE					AP-1 region	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
25074	1	7872	6	NULL	NULL	0	NULL	CREB	NULL		is	NULL				CRE binding protein	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
25076	2	7872	6	10	NULL	0	NULL				overlaps with				CRE	AP-1 region					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
25079	3	7872	6	NULL	NULL	0	NULL	statement 2	NULL		is located at	NULL					NULL			- 60 to - 40 from the transcription start site	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
25082	4	7872	6	NULL	NULL	0	NULL	CREB	NULL		bind	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
25083	5	7872	6	NULL	NULL	0	NULL	ATF	NULL		bind	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
25084	6	7872	6	NULL	NULL	0	NULL	C/EBP	NULL		bind	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
25085	7	7872	6	NULL	NULL	0	NULL	C-jun	NULL		bind	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
25086	8	7872	6	NULL	NULL	0	NULL	C-Fos	NULL		bind	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
25087	9	7872	6	NULL	NULL	0	NULL	USF	NULL		bind	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
38839	10	7872	6	NULL	NULL	0	NULL	CREB	NULL		is a type of	NULL				transactivator	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
38840	11	7872	6	NULL	NULL	0	NULL	ATF	NULL		is a type of	NULL				transactivator	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
38841	12	7872	6	NULL	NULL	0	NULL	C/EBP	NULL		is a type of	NULL				transactivator	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
38842	13	7872	6	NULL	NULL	0	NULL	C-jun	NULL		is a type of	NULL				transactivator	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
38843	14	7872	6	NULL	NULL	0	NULL	C-fos	NULL		is a type of	NULL				transactivator	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
38844	15	7872	6	NULL	NULL	0	NULL	USF	NULL		is a type of	NULL				transactivator	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_68	15681294	34 A large number of transactivators including CRE binding protein (CREB), ATF, C/EBP, C-Jun, C-Fos, and USF bind to an overlapped CRE and AP-1 region located at  - 60 to  - 40 from the transcription start site.	bind
32532	1	7873	5	13	NULL	NULL	NULL	FGF2	GP		bind					HSPG	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_226	14684627	34 Alternatively, the binding of FGF2 to HSPG could facilitate the interaction of the heparan sulfate chains with heparin receptors on the cell, which have been demonstrated to lead to ERK1/2 activation in VSMCs. 35	bind
32538	2	7873	5	13	NULL	NULL	NULL	heparan sulfate chains	Chemical		interacts with					heparin receptors	GP				NULL	on cell	NULL	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_226	14684627	34 Alternatively, the binding of FGF2 to HSPG could facilitate the interaction of the heparan sulfate chains with heparin receptors on the cell, which have been demonstrated to lead to ERK1/2 activation in VSMCs. 35	bind
32539	3	7873	5	13	NULL	NULL	NULL	statement 1	Process		facilitate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_226	14684627	34 Alternatively, the binding of FGF2 to HSPG could facilitate the interaction of the heparan sulfate chains with heparin receptors on the cell, which have been demonstrated to lead to ERK1/2 activation in VSMCs. 35	bind
32540	4	7873	5	13	NULL	NULL	NULL	statement 2	Process		leads to					ERK1/2	GP	activation of			NULL	VSMCs	NULL	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_226	14684627	34 Alternatively, the binding of FGF2 to HSPG could facilitate the interaction of the heparan sulfate chains with heparin receptors on the cell, which have been demonstrated to lead to ERK1/2 activation in VSMCs. 35	bind
25088	1	7873	6	NULL	NULL	0	NULL	FGF2	NULL		bind	NULL				HSPG	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_226	14684627	34 Alternatively, the binding of FGF2 to HSPG could facilitate the interaction of the heparan sulfate chains with heparin receptors on the cell, which have been demonstrated to lead to ERK1/2 activation in VSMCs. 35	bind
25089	2	7873	6	NULL	NULL	0	NULL	heparan sulfate chains	NULL		interacts with	NULL				heparin receptors	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_226	14684627	34 Alternatively, the binding of FGF2 to HSPG could facilitate the interaction of the heparan sulfate chains with heparin receptors on the cell, which have been demonstrated to lead to ERK1/2 activation in VSMCs. 35	bind
25090	3	7873	6	NULL	NULL	0	NULL	statement 1	NULL		facilitate	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_226	14684627	34 Alternatively, the binding of FGF2 to HSPG could facilitate the interaction of the heparan sulfate chains with heparin receptors on the cell, which have been demonstrated to lead to ERK1/2 activation in VSMCs. 35	bind
25091	4	7873	6	NULL	NULL	0	NULL	statement 3	NULL		lead to	NULL				ERK1/2	NULL	activation of			NULL	VSMCs	0	NULL	NULL	NULL	gw70_circulationres_94_3_316_s_226	14684627	34 Alternatively, the binding of FGF2 to HSPG could facilitate the interaction of the heparan sulfate chains with heparin receptors on the cell, which have been demonstrated to lead to ERK1/2 activation in VSMCs. 35	bind
32541	1	7874	5	13	NULL	NULL	NULL	CRP	GP		does not bind					ECs	Cell	healthy;; cultured			NULL	in vitro in cultured vascular cells	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1225_s_157	15802626	34 In the in vitro investigations using cultured vascular cells, the initiating step of CRP binding to healthy cultured ECs has simply not been met, which explains the absence of any effect of CRP in our in vitro studies.	bind
25138	1	7874	6	10	NULL	0	NULL	CRP	NULL		does not bind	NULL				EC	NULL	healthy;;cultured			NULL	in vitro in cultured vascular cells	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1225_s_157	15802626	34 In the in vitro investigations using cultured vascular cells, the initiating step of CRP binding to healthy cultured ECs has simply not been met, which explains the absence of any effect of CRP in our in vitro studies.	bind
32543	1	7875	5	13	NULL	NULL	NULL	ABCA1	GP		bind					apoA-I	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_58	12738681	34 Like scavenger receptor BI, ABCA1 binds not only apoA-I but also other apolipoproteins, including apoE. 35 Thus, the antiatherogenic effect of apoE in vivo could be partially explained by lipid efflux from macrophage foam cells coordinated with ABCA1.	bind
32544	2	7875	5	13	NULL	NULL	NULL	ABCA1	GP		bind					apoE	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_58	12738681	34 Like scavenger receptor BI, ABCA1 binds not only apoA-I but also other apolipoproteins, including apoE. 35 Thus, the antiatherogenic effect of apoE in vivo could be partially explained by lipid efflux from macrophage foam cells coordinated with ABCA1.	bind
32545	3	7875	5	13	NULL	NULL	NULL	apoE	GP		is a type of					apolipoproteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_58	12738681	34 Like scavenger receptor BI, ABCA1 binds not only apoA-I but also other apolipoproteins, including apoE. 35 Thus, the antiatherogenic effect of apoE in vivo could be partially explained by lipid efflux from macrophage foam cells coordinated with ABCA1.	bind
32547	4	7875	5	13	NULL	NULL	NULL	 BI	GP		bind					apoA-I	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_58	12738681	34 Like scavenger receptor BI, ABCA1 binds not only apoA-I but also other apolipoproteins, including apoE. 35 Thus, the antiatherogenic effect of apoE in vivo could be partially explained by lipid efflux from macrophage foam cells coordinated with ABCA1.	bind
32549	5	7875	5	13	NULL	NULL	NULL	 BI	GP		bind					apoE	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_58	12738681	34 Like scavenger receptor BI, ABCA1 binds not only apoA-I but also other apolipoproteins, including apoE. 35 Thus, the antiatherogenic effect of apoE in vivo could be partially explained by lipid efflux from macrophage foam cells coordinated with ABCA1.	bind
32554	6	7875	5	13	NULL	NULL	NULL	lipid efflux	Process	macrophage foam cells	coordinate with					ABCA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_58	12738681	34 Like scavenger receptor BI, ABCA1 binds not only apoA-I but also other apolipoproteins, including apoE. 35 Thus, the antiatherogenic effect of apoE in vivo could be partially explained by lipid efflux from macrophage foam cells coordinated with ABCA1.	bind
32555	7	7875	5	13	NULL	NULL	NULL	statement 6	Process		explains		partially			apoE	GP	antiatherogenic effect of 			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_58	12738681	34 Like scavenger receptor BI, ABCA1 binds not only apoA-I but also other apolipoproteins, including apoE. 35 Thus, the antiatherogenic effect of apoE in vivo could be partially explained by lipid efflux from macrophage foam cells coordinated with ABCA1.	bind
47547	8	7875	5	13	NULL	NULL	NULL	BI	GP		is a type of					scavenger receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_58	12738681	34 Like scavenger receptor BI, ABCA1 binds not only apoA-I but also other apolipoproteins, including apoE. 35 Thus, the antiatherogenic effect of apoE in vivo could be partially explained by lipid efflux from macrophage foam cells coordinated with ABCA1.	bind
25139	1	7875	6	NULL	NULL	0	NULL	ABCA1	NULL		bind	NULL				apoA-I	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_58	12738681	34 Like scavenger receptor BI, ABCA1 binds not only apoA-I but also other apolipoproteins, including apoE. 35 Thus, the antiatherogenic effect of apoE in vivo could be partially explained by lipid efflux from macrophage foam cells coordinated with ABCA1.	bind
25140	2	7875	6	NULL	NULL	0	NULL	ABCA1	NULL		bind	NULL				apoE	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_58	12738681	34 Like scavenger receptor BI, ABCA1 binds not only apoA-I but also other apolipoproteins, including apoE. 35 Thus, the antiatherogenic effect of apoE in vivo could be partially explained by lipid efflux from macrophage foam cells coordinated with ABCA1.	bind
25141	3	7875	6	NULL	NULL	0	NULL	scavenger receptor BI	NULL		bind	NULL				apoA-I	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_58	12738681	34 Like scavenger receptor BI, ABCA1 binds not only apoA-I but also other apolipoproteins, including apoE. 35 Thus, the antiatherogenic effect of apoE in vivo could be partially explained by lipid efflux from macrophage foam cells coordinated with ABCA1.	bind
25142	4	7875	6	NULL	NULL	0	NULL	scavenger receptor BI	NULL		bind	NULL				apoE	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_58	12738681	34 Like scavenger receptor BI, ABCA1 binds not only apoA-I but also other apolipoproteins, including apoE. 35 Thus, the antiatherogenic effect of apoE in vivo could be partially explained by lipid efflux from macrophage foam cells coordinated with ABCA1.	bind
25848	6	7875	6	NULL	NULL	0	NULL	macrophage foam cells	NULL		exhibits	NULL				lipid efflux	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_58	12738681	34 Like scavenger receptor BI, ABCA1 binds not only apoA-I but also other apolipoproteins, including apoE. 35 Thus, the antiatherogenic effect of apoE in vivo could be partially explained by lipid efflux from macrophage foam cells coordinated with ABCA1.	bind
25849	7	7875	6	NULL	NULL	0	NULL	statement 6	NULL		is coordinated with	NULL				ABCA1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_58	12738681	34 Like scavenger receptor BI, ABCA1 binds not only apoA-I but also other apolipoproteins, including apoE. 35 Thus, the antiatherogenic effect of apoE in vivo could be partially explained by lipid efflux from macrophage foam cells coordinated with ABCA1.	bind
25850	8	7875	6	10	NULL	0	NULL	statement 5			because of		may			apoE		antiatherogenic effect of 			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_58	12738681	34 Like scavenger receptor BI, ABCA1 binds not only apoA-I but also other apolipoproteins, including apoE. 35 Thus, the antiatherogenic effect of apoE in vivo could be partially explained by lipid efflux from macrophage foam cells coordinated with ABCA1.	bind
47548	9	7875	6	10	NULL	0	NULL	BI	NULL		is a type of	NULL				scavenger receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_58	12738681	34 Like scavenger receptor BI, ABCA1 binds not only apoA-I but also other apolipoproteins, including apoE. 35 Thus, the antiatherogenic effect of apoE in vivo could be partially explained by lipid efflux from macrophage foam cells coordinated with ABCA1.	bind
32556	1	7876	5	13	NULL	NULL	NULL	MyBP-C	GP		bind					myosin	GP		S2 portion		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_166	11739284	34 Phosphorylation of MyBP-C has been reported to relieve the binding of the MyBP-C to the S2 portion of myosin, 35 which may allow greater crossbridge extension from the thick filament and alter crossbridge orientation.	bind
32557	2	7876	5	13	NULL	NULL	NULL	MyBP-C	GP	phosphorylation of	relieve					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_166	11739284	34 Phosphorylation of MyBP-C has been reported to relieve the binding of the MyBP-C to the S2 portion of myosin, 35 which may allow greater crossbridge extension from the thick filament and alter crossbridge orientation.	bind
32558	3	7876	5	13	NULL	NULL	NULL	statement 2	Process		allows					crossbridge extension	Process	greater			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_166	11739284	34 Phosphorylation of MyBP-C has been reported to relieve the binding of the MyBP-C to the S2 portion of myosin, 35 which may allow greater crossbridge extension from the thick filament and alter crossbridge orientation.	bind
32560	4	7876	5	13	NULL	NULL	NULL	statement 2	Process		alters					crossbridge orientation	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_166	11739284	34 Phosphorylation of MyBP-C has been reported to relieve the binding of the MyBP-C to the S2 portion of myosin, 35 which may allow greater crossbridge extension from the thick filament and alter crossbridge orientation.	bind
25143	1	7876	6	NULL	NULL	0	NULL	MyBP-C	NULL		bind	NULL				myosin	NULL		S2 portion		NULL		0	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_166	11739284	34 Phosphorylation of MyBP-C has been reported to relieve the binding of the MyBP-C to the S2 portion of myosin, 35 which may allow greater crossbridge extension from the thick filament and alter crossbridge orientation.	bind
25144	2	7876	6	NULL	NULL	0	NULL	MyBP-C	NULL	phosphorylation of	relieves	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_166	11739284	34 Phosphorylation of MyBP-C has been reported to relieve the binding of the MyBP-C to the S2 portion of myosin, 35 which may allow greater crossbridge extension from the thick filament and alter crossbridge orientation.	bind
25258	3	7876	6	NULL	NULL	0	NULL	statement 2	NULL		allow	NULL	may			crossbridge extension	NULL	greater			NULL		0	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_166	11739284	34 Phosphorylation of MyBP-C has been reported to relieve the binding of the MyBP-C to the S2 portion of myosin, 35 which may allow greater crossbridge extension from the thick filament and alter crossbridge orientation.	bind
25259	4	7876	6	NULL	NULL	0	NULL	statement 2	NULL		alter	NULL				crossbridge orientation	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_89_12_1184_s_166	11739284	34 Phosphorylation of MyBP-C has been reported to relieve the binding of the MyBP-C to the S2 portion of myosin, 35 which may allow greater crossbridge extension from the thick filament and alter crossbridge orientation.	bind
32794	1	7877	5	13	NULL	NULL	NULL	Sp1	GP		bind					PKG-Ialpha	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_226	11884369	34, 35 Our data show that a decrease in Sp1 binding activity to the PKG-Ialpha promoter by cyclic nucleotide analogues are dependent on activation of PKA consistent with the role of phosphorylation in modifying Sp1 binding activity.	bind
32795	2	7877	5	13	NULL	NULL	NULL	cyclic nucleotide analogues	Chemical		decrease					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_226	11884369	34, 35 Our data show that a decrease in Sp1 binding activity to the PKG-Ialpha promoter by cyclic nucleotide analogues are dependent on activation of PKA consistent with the role of phosphorylation in modifying Sp1 binding activity.	bind
32796	3	7877	5	13	NULL	NULL	NULL	statement 2	Process		is dependent on					PKA	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_226	11884369	34, 35 Our data show that a decrease in Sp1 binding activity to the PKG-Ialpha promoter by cyclic nucleotide analogues are dependent on activation of PKA consistent with the role of phosphorylation in modifying Sp1 binding activity.	bind
32797	4	7877	5	13	NULL	NULL	NULL	phosphorylation	Process		modify					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_226	11884369	34, 35 Our data show that a decrease in Sp1 binding activity to the PKG-Ialpha promoter by cyclic nucleotide analogues are dependent on activation of PKA consistent with the role of phosphorylation in modifying Sp1 binding activity.	bind
32798	5	7877	5	13	NULL	NULL	NULL	statement 3	Process		consistent with					statement 4	Process	role of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_226	11884369	34, 35 Our data show that a decrease in Sp1 binding activity to the PKG-Ialpha promoter by cyclic nucleotide analogues are dependent on activation of PKA consistent with the role of phosphorylation in modifying Sp1 binding activity.	bind
25260	1	7877	6	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				PKG-Ialpha	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_226	11884369	34, 35 Our data show that a decrease in Sp1 binding activity to the PKG-Ialpha promoter by cyclic nucleotide analogues are dependent on activation of PKA consistent with the role of phosphorylation in modifying Sp1 binding activity.	bind
25261	2	7877	6	NULL	NULL	0	NULL	cyclic nucleotide analogues	NULL		decrease	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_226	11884369	34, 35 Our data show that a decrease in Sp1 binding activity to the PKG-Ialpha promoter by cyclic nucleotide analogues are dependent on activation of PKA consistent with the role of phosphorylation in modifying Sp1 binding activity.	bind
25262	3	7877	6	NULL	NULL	0	NULL	statement 2	NULL		is dependent on	NULL				PKA	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_226	11884369	34, 35 Our data show that a decrease in Sp1 binding activity to the PKG-Ialpha promoter by cyclic nucleotide analogues are dependent on activation of PKA consistent with the role of phosphorylation in modifying Sp1 binding activity.	bind
25263	4	7877	6	NULL	NULL	0	NULL	phosphorylation	NULL		modifies	NULL				statement 1	NULL	binding activity of 			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_226	11884369	34, 35 Our data show that a decrease in Sp1 binding activity to the PKG-Ialpha promoter by cyclic nucleotide analogues are dependent on activation of PKA consistent with the role of phosphorylation in modifying Sp1 binding activity.	bind
38845	5	7877	6	10	NULL	0	NULL	statement 3	NULL		consistent with 	NULL				statement 4	NULL	role of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_4_405_s_226	11884369	34, 35 Our data show that a decrease in Sp1 binding activity to the PKG-Ialpha promoter by cyclic nucleotide analogues are dependent on activation of PKA consistent with the role of phosphorylation in modifying Sp1 binding activity.	bind
32799	1	7878	5	13	NULL	NULL	NULL	TIMP-1	GP		bind					MMP-9	GP	inactive			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1837_s_211	9327785	34,50 Therefore, the expression of TIMP-1, which binds to the inactive form of MMP-9, was examined.	bind
25264	1	7878	6	NULL	NULL	0	NULL	TIMP-1	NULL		bind	NULL				MMP-9	NULL	inactive			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1837_s_211	9327785	34,50 Therefore, the expression of TIMP-1, which binds to the inactive form of MMP-9, was examined.	bind
32800	1	7879	5	13	NULL	NULL	NULL	YY1	GP		is a type of					ubiquitous nuclear transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4493_s_371	11691937	35       Becker,K.G., Swergold,G.D., Ozato,K. and Thayer,R.E. (1993) Binding of the ubiquitous nuclear transcription factor YY1 to a  cis regulatory sequence in the human LINE-1 transposable element.	bind
32801	3	7879	5	13	NULL	NULL	NULL	YY1	GP		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4493_s_371	11691937	35       Becker,K.G., Swergold,G.D., Ozato,K. and Thayer,R.E. (1993) Binding of the ubiquitous nuclear transcription factor YY1 to a  cis regulatory sequence in the human LINE-1 transposable element.	bind
55567	2	7879	5	10	NULL	0	NULL	resides in		human					cis regulatory sequence			human		LINE-1 transposable element	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4493_s_371	11691937	35       Becker,K.G., Swergold,G.D., Ozato,K. and Thayer,R.E. (1993) Binding of the ubiquitous nuclear transcription factor YY1 to a  cis regulatory sequence in the human LINE-1 transposable element.	bind
25265	2	7879	6	10	NULL	0	NULL	YY1			bind					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4493_s_371	11691937	35       Becker,K.G., Swergold,G.D., Ozato,K. and Thayer,R.E. (1993) Binding of the ubiquitous nuclear transcription factor YY1 to a  cis regulatory sequence in the human LINE-1 transposable element.	bind
38846	2	7879	6	NULL	NULL	0	NULL	YY1	NULL		is a type of	NULL				ubiquitous nuclear transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4493_s_371	11691937	35       Becker,K.G., Swergold,G.D., Ozato,K. and Thayer,R.E. (1993) Binding of the ubiquitous nuclear transcription factor YY1 to a  cis regulatory sequence in the human LINE-1 transposable element.	bind
55568	1	7879	6	10	NULL	0	NULL			human	resides in				cis regulatory sequence			human		LINE-1 transposable element	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4493_s_371	11691937	35       Becker,K.G., Swergold,G.D., Ozato,K. and Thayer,R.E. (1993) Binding of the ubiquitous nuclear transcription factor YY1 to a  cis regulatory sequence in the human LINE-1 transposable element.	bind
32802	1	7880	5	13	NULL	NULL	NULL	renin	GP	porcine	bind		high affinity			cardiac membranes	OrganismPart	porcine			NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_1_220_s_148	9236437	35  36  In the present study, we observed high-affinity binding of porcine renin to porcine cardiac membranes.	bind
25266	1	7880	6	NULL	NULL	0	NULL	renin	NULL	porcine	bind	NULL	high affinity			cardiac membranes	NULL	porcine			NULL		0	NULL	NULL	NULL	gw60_circulation_96_1_220_s_148	9236437	35  36  In the present study, we observed high-affinity binding of porcine renin to porcine cardiac membranes.	bind
32803	1	7881	5	13	NULL	NULL	NULL	apoB	GP		bind					MBP 200	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_140	9633939	35  Further, it suggests that the domain in apoB that binds to MBP 200, 235 is not in a heparin-binding domain of apoB.	bind
32804	2	7881	5	13	NULL	NULL	NULL	apoB	GP		bind					MBP 235	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_140	9633939	35  Further, it suggests that the domain in apoB that binds to MBP 200, 235 is not in a heparin-binding domain of apoB.	bind
32805	3	7881	5	13	NULL	NULL	NULL	apoB	GP		does not bind			heparin-binding domain		MBP 200	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_140	9633939	35  Further, it suggests that the domain in apoB that binds to MBP 200, 235 is not in a heparin-binding domain of apoB.	bind
32806	4	7881	5	13	NULL	NULL	NULL	apoB	GP		does not bind			heparin-binding domain		MBP 235	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_140	9633939	35  Further, it suggests that the domain in apoB that binds to MBP 200, 235 is not in a heparin-binding domain of apoB.	bind
25267	1	7881	6	NULL	NULL	0	NULL	apoB	NULL		bind	NULL				MBP 200	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_140	9633939	35  Further, it suggests that the domain in apoB that binds to MBP 200, 235 is not in a heparin-binding domain of apoB.	bind
25268	2	7881	6	10	NULL	0	NULL	apoB	NULL		bind	NULL				MBP 235	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_140	9633939	35  Further, it suggests that the domain in apoB that binds to MBP 200, 235 is not in a heparin-binding domain of apoB.	bind
38860	3	7881	6	NULL	NULL	0	NULL	apoB	NULL		does not bind	NULL		heparin binding domain		MBP 200	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_140	9633939	35  Further, it suggests that the domain in apoB that binds to MBP 200, 235 is not in a heparin-binding domain of apoB.	bind
38861	4	7881	6	NULL	NULL	0	NULL	apoB	NULL		does not bind	NULL		heparin binding domain		MBP 235	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_968_s_140	9633939	35  Further, it suggests that the domain in apoB that binds to MBP 200, 235 is not in a heparin-binding domain of apoB.	bind
32807	1	7882	5	13	NULL	NULL	NULL	Fos-Jun heterodimers	GP		bind					TF	GP			AP-1 sites in enhancer	NULL	in stimulated endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_5_612_s_234	7749875	35  Here, we showed that in stimulated endothelial cells, Fos-Jun heterodimers bound to the two AP-1 sites and c-Rel - p65 heterodimers bound to an adjacent kappaB-like site in the 56-bp TF enhancer.	bind
32808	2	7882	5	13	NULL	NULL	NULL	c-Rel - p65 heterodimers	GP		bind					TF	GP			adjacent kappaB-like site in enhancer	NULL	in stimulated endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_5_612_s_234	7749875	35  Here, we showed that in stimulated endothelial cells, Fos-Jun heterodimers bound to the two AP-1 sites and c-Rel - p65 heterodimers bound to an adjacent kappaB-like site in the 56-bp TF enhancer.	bind
25269	1	7882	6	NULL	NULL	0	NULL	Fos-Jun heterodimers	NULL		bind	NULL				TF	NULL			AP-1 site of enhancer	NULL	stimulated endothelial cells	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_5_612_s_234	7749875	35  Here, we showed that in stimulated endothelial cells, Fos-Jun heterodimers bound to the two AP-1 sites and c-Rel - p65 heterodimers bound to an adjacent kappaB-like site in the 56-bp TF enhancer.	bind
25270	2	7882	6	NULL	NULL	0	NULL	c-Rel - p65 heterodimers	NULL		bind	NULL				TF	NULL			kappaB-like site of enhancer	NULL	stimulated endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_5_612_s_234	7749875	35  Here, we showed that in stimulated endothelial cells, Fos-Jun heterodimers bound to the two AP-1 sites and c-Rel - p65 heterodimers bound to an adjacent kappaB-like site in the 56-bp TF enhancer.	bind
32809	1	7883	5	13	NULL	NULL	NULL	IGF-BP3	GP		bind					IGFs	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_5_1535_s_115	12414501	35  IGF-BP3 binds the IGFs and prevents the activation of the IGF-1 receptor, which normally mediates cell signals to promote myogenesis.	bind
32810	2	7883	5	13	NULL	NULL	NULL	statement 1	Process		prevents					IGF-1 receptor	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_5_1535_s_115	12414501	35  IGF-BP3 binds the IGFs and prevents the activation of the IGF-1 receptor, which normally mediates cell signals to promote myogenesis.	bind
32811	3	7883	5	13	NULL	NULL	NULL	IGF-1 receptor	GP		promote					myogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_5_1535_s_115	12414501	35  IGF-BP3 binds the IGFs and prevents the activation of the IGF-1 receptor, which normally mediates cell signals to promote myogenesis.	bind
32812	5	7883	5	13	NULL	NULL	NULL	statement 3	Process		via					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_5_1535_s_115	12414501	35  IGF-BP3 binds the IGFs and prevents the activation of the IGF-1 receptor, which normally mediates cell signals to promote myogenesis.	bind
38972	4	7883	5	13	NULL	NULL	NULL	IGF-1 receptor	GP		mediate					cell signals	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_5_1535_s_115	12414501	35  IGF-BP3 binds the IGFs and prevents the activation of the IGF-1 receptor, which normally mediates cell signals to promote myogenesis.	bind
25271	1	7883	6	NULL	NULL	0	NULL	IGF-BP3	NULL		bind	NULL				IGF	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_5_1535_s_115	12414501	35  IGF-BP3 binds the IGFs and prevents the activation of the IGF-1 receptor, which normally mediates cell signals to promote myogenesis.	bind
25272	2	7883	6	NULL	NULL	0	NULL	statement 1	NULL		prevent	NULL				IGF-1 receptor	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_5_1535_s_115	12414501	35  IGF-BP3 binds the IGFs and prevents the activation of the IGF-1 receptor, which normally mediates cell signals to promote myogenesis.	bind
25273	3	7883	6	NULL	NULL	0	NULL	IGF-1 receptor	NULL		promotes	NULL				myogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_5_1535_s_115	12414501	35  IGF-BP3 binds the IGFs and prevents the activation of the IGF-1 receptor, which normally mediates cell signals to promote myogenesis.	bind
25274	4	7883	6	NULL	NULL	0	NULL	IGF-1 receptor	NULL		mediates	NULL				cell signals	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_5_1535_s_115	12414501	35  IGF-BP3 binds the IGFs and prevents the activation of the IGF-1 receptor, which normally mediates cell signals to promote myogenesis.	bind
25275	5	7883	6	NULL	NULL	0	NULL	statement 3	NULL		occurs via	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_5_1535_s_115	12414501	35  IGF-BP3 binds the IGFs and prevents the activation of the IGF-1 receptor, which normally mediates cell signals to promote myogenesis.	bind
32813	1	7884	5	13	NULL	NULL	NULL	MEKK1	GP	dominant-interfering	inhibits					ERK	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_167_s_220	9686756	35  In order to establish that inhibition of ERK activation by dominant-interfering MEKK1 is not responsible for the inhibitory effect on genetic markers of hypertrophic growth, we performed parallel experiments using dominant-interfering Raf-1, which binds Ras and inhibits the MEK/ERK pathway.	bind
32816	2	7884	5	13	NULL	NULL	NULL	Raf-1	GP	dominant-interfering	bind					Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_167_s_220	9686756	35  In order to establish that inhibition of ERK activation by dominant-interfering MEKK1 is not responsible for the inhibitory effect on genetic markers of hypertrophic growth, we performed parallel experiments using dominant-interfering Raf-1, which binds Ras and inhibits the MEK/ERK pathway.	bind
32817	3	7884	5	13	NULL	NULL	NULL	statement 2	Process		inhibits					MEK/ERK pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_2_167_s_220	9686756	35  In order to establish that inhibition of ERK activation by dominant-interfering MEKK1 is not responsible for the inhibitory effect on genetic markers of hypertrophic growth, we performed parallel experiments using dominant-interfering Raf-1, which binds Ras and inhibits the MEK/ERK pathway.	bind
25844	1	7884	6	NULL	NULL	0	NULL	MEKK1	NULL	dominant-interfering	inhibits	NULL				ERK	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_167_s_220	9686756	35  In order to establish that inhibition of ERK activation by dominant-interfering MEKK1 is not responsible for the inhibitory effect on genetic markers of hypertrophic growth, we performed parallel experiments using dominant-interfering Raf-1, which binds Ras and inhibits the MEK/ERK pathway.	bind
25845	2	7884	6	NULL	NULL	0	NULL	Raf-1	NULL	dominant-interfering	bind	NULL				Ras	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_167_s_220	9686756	35  In order to establish that inhibition of ERK activation by dominant-interfering MEKK1 is not responsible for the inhibitory effect on genetic markers of hypertrophic growth, we performed parallel experiments using dominant-interfering Raf-1, which binds Ras and inhibits the MEK/ERK pathway.	bind
25846	3	7884	6	NULL	NULL	0	NULL	statement 2	NULL		inhibits	NULL				MEK/ERK pathway	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_2_167_s_220	9686756	35  In order to establish that inhibition of ERK activation by dominant-interfering MEKK1 is not responsible for the inhibitory effect on genetic markers of hypertrophic growth, we performed parallel experiments using dominant-interfering Raf-1, which binds Ras and inhibits the MEK/ERK pathway.	bind
32819	1	7885	5	13	NULL	NULL	NULL	TNF-alpha	GP		bind					ECM	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_14	12000736	35  On this basis, it is likely that TNF-alpha bound to ECM during processes of retinal fibrosis and neovascularization may affect Muller cell function, and hence influence the development of retinal proliferative disease.	bind
32820	2	7885	5	13	NULL	NULL	NULL	statement 1	Process		occurs during					retinal fibrosis	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_14	12000736	35  On this basis, it is likely that TNF-alpha bound to ECM during processes of retinal fibrosis and neovascularization may affect Muller cell function, and hence influence the development of retinal proliferative disease.	bind
32821	3	7885	5	13	NULL	NULL	NULL	statement 1	Process		occurs during					neovascularization	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_14	12000736	35  On this basis, it is likely that TNF-alpha bound to ECM during processes of retinal fibrosis and neovascularization may affect Muller cell function, and hence influence the development of retinal proliferative disease.	bind
32823	4	7885	5	13	NULL	NULL	NULL	statement 2	Process		affects		may			Muller cell 	Cell	function of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_14	12000736	35  On this basis, it is likely that TNF-alpha bound to ECM during processes of retinal fibrosis and neovascularization may affect Muller cell function, and hence influence the development of retinal proliferative disease.	bind
32825	5	7885	5	13	NULL	NULL	NULL	statement 3	Process		affects		may			Muller cell	Cell	function of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_14	12000736	35  On this basis, it is likely that TNF-alpha bound to ECM during processes of retinal fibrosis and neovascularization may affect Muller cell function, and hence influence the development of retinal proliferative disease.	bind
32826	6	7885	5	13	NULL	NULL	NULL	statement 4	Process		influence					retinal proliferative disease	MedicalFinding	development of 			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_14	12000736	35  On this basis, it is likely that TNF-alpha bound to ECM during processes of retinal fibrosis and neovascularization may affect Muller cell function, and hence influence the development of retinal proliferative disease.	bind
32827	7	7885	5	13	NULL	NULL	NULL	statement 5	Process		influence					retinal proliferative disease	MedicalFinding	development of 			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_14	12000736	35  On this basis, it is likely that TNF-alpha bound to ECM during processes of retinal fibrosis and neovascularization may affect Muller cell function, and hence influence the development of retinal proliferative disease.	bind
25276	1	7885	6	NULL	NULL	0	NULL	TNF-alpha	NULL		bind	NULL				ECM	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_14	12000736	35  On this basis, it is likely that TNF-alpha bound to ECM during processes of retinal fibrosis and neovascularization may affect Muller cell function, and hence influence the development of retinal proliferative disease.	bind
25277	2	7885	6	NULL	NULL	0	NULL	statement 1	NULL		occurs during	NULL				retinal fibrosis	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_14	12000736	35  On this basis, it is likely that TNF-alpha bound to ECM during processes of retinal fibrosis and neovascularization may affect Muller cell function, and hence influence the development of retinal proliferative disease.	bind
25278	3	7885	6	NULL	NULL	0	NULL	statement 1	NULL		occurs during	NULL				neovascularization	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_14	12000736	35  On this basis, it is likely that TNF-alpha bound to ECM during processes of retinal fibrosis and neovascularization may affect Muller cell function, and hence influence the development of retinal proliferative disease.	bind
25279	4	7885	6	10	NULL	0	NULL	statement 2			affect		may			Muller cell		function of 			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_14	12000736	35  On this basis, it is likely that TNF-alpha bound to ECM during processes of retinal fibrosis and neovascularization may affect Muller cell function, and hence influence the development of retinal proliferative disease.	bind
25280	5	7885	6	10	NULL	0	NULL	statement 3			affects		may			Muller cell		function of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_14	12000736	35  On this basis, it is likely that TNF-alpha bound to ECM during processes of retinal fibrosis and neovascularization may affect Muller cell function, and hence influence the development of retinal proliferative disease.	bind
55573	6	7885	6	10	NULL	0	NULL	statement 4			influences					retinal proliferative disease		development of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_14	12000736	35  On this basis, it is likely that TNF-alpha bound to ECM during processes of retinal fibrosis and neovascularization may affect Muller cell function, and hence influence the development of retinal proliferative disease.	bind
55574	7	7885	6	10	NULL	0	NULL	statement 5			influences					retinal proliferative disease		development of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_5_1847_s_14	12000736	35  On this basis, it is likely that TNF-alpha bound to ECM during processes of retinal fibrosis and neovascularization may affect Muller cell function, and hence influence the development of retinal proliferative disease.	bind
32828	1	7886	5	13	NULL	NULL	NULL	platelet glycoprotein IIb/IIa complex	GP		bind					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
32829	2	7886	5	13	NULL	NULL	NULL	platelet glycoprotein IIb/IIa complex	GP		bind					Fn	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
32830	3	7886	5	13	NULL	NULL	NULL	platelet glycoprotein IIb/IIa complex	GP		bind					vWF	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
32831	4	7886	5	13	NULL	NULL	NULL	platelet glycoprotein IIb/IIa complex	GP		bind					Vn	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
32832	5	7886	5	13	NULL	NULL	NULL	platelet	Cell	activation of	is dependent on					divalent cation	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
32833	6	7886	5	13	NULL	NULL	NULL	statement 5	Process		is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
32834	7	7886	5	13	NULL	NULL	NULL	statement 5	Process		is required for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
32835	8	7886	5	13	NULL	NULL	NULL	statement 5	Process		is required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
32836	9	7886	5	13	NULL	NULL	NULL	statement 5	Process		is required for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
32837	10	7886	5	13	NULL	NULL	NULL	peptides	GP		inhibits			containing Arg-Gly-Asp sequence		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
32838	11	7886	5	13	NULL	NULL	NULL	peptides	GP		inhibits			containing Arg-Gly-Asp sequence		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
32839	12	7886	5	13	NULL	NULL	NULL	peptides	GP		inhibits			containing Arg-Gly-Asp sequence		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
32840	13	7886	5	13	NULL	NULL	NULL	peptides	GP		inhibits			containing Arg-Gly-Asp sequence		statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
25747	1	7886	6	NULL	NULL	0	NULL	fibrinogen	NULL		react with	NULL				platelet glycoprotein IIb/IIa complex	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
25748	2	7886	6	NULL	NULL	0	NULL	Fn	NULL		react with	NULL				platelet glycoprotein IIb/IIa complex	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
25749	3	7886	6	NULL	NULL	0	NULL	vWF	NULL		react with	NULL				platelet glycoprotein IIb/IIa complex	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
25751	4	7886	6	NULL	NULL	0	NULL	Vn	NULL		react with	NULL				platelet glycoprotein IIb/IIa complex	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
25835	5	7886	6	NULL	NULL	0	NULL	statement 1	NULL		occurs after	NULL	only			platelet	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
25836	6	7886	6	NULL	NULL	0	NULL	platelet	NULL	activation of	is dependent on	NULL				divalent cation	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
25837	7	7886	6	NULL	NULL	0	NULL	statement 2	NULL		occurs after	NULL	only			platelet	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
25838	8	7886	6	NULL	NULL	0	NULL	statement 3	NULL		occurs after	NULL	only			platelets	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
25839	9	7886	6	NULL	NULL	0	NULL	statement 4	NULL		occurs after	NULL	only			platelets	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
25840	10	7886	6	NULL	NULL	0	NULL	statement 1	NULL		is inhibited by	NULL				peptides	NULL		Arg-Gly-Asp sequence		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
25841	11	7886	6	NULL	NULL	0	NULL	statement 2	NULL		is inhibited by	NULL				peptides	NULL		Arg-Gly-Asp sequence		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
25842	12	7886	6	NULL	NULL	0	NULL	statement 3	NULL		is inhibited by	NULL				peptides	NULL		Arg-Gly-Asp sequence		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
25843	13	7886	6	NULL	NULL	0	NULL	statement 4	NULL		is inhibited by	NULL				peptides	NULL		Arg-Gly-Asp sequence		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3461_s_203	9437193	35 36  Platelet glycoprotein IIb/IIa complex provides binding sites for fibrinogen, 37 38  Fn, 39  vWF, 40  and also for Vn. 41  All these ligands react with platelet glycoprotein IIb/IIa complex only after platelet activation in a divalent cation - dependent manner, and the binding is inhibited by peptides containing an Arg-Gly-Asp sequence.	bind
32841	1	7887	5	13	NULL	NULL	NULL	CD40L	GP		bind					CD40 	GP				NULL	on endothelium	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1321_s_100	15831808	35 CD40L binding to CD40 on endothelium induces inflammation, and this biological activity is also preserved in platelet CD40L.	bind
32842	2	7887	5	13	NULL	NULL	NULL	statement 1	Process		induces					inflammation	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1321_s_100	15831808	35 CD40L binding to CD40 on endothelium induces inflammation, and this biological activity is also preserved in platelet CD40L.	bind
32843	3	7887	5	13	NULL	NULL	NULL	CD40L	GP	platelet 	bind					CD40	GP				NULL	on endothelium	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1321_s_100	15831808	35 CD40L binding to CD40 on endothelium induces inflammation, and this biological activity is also preserved in platelet CD40L.	bind
32844	4	7887	5	13	NULL	NULL	NULL	statement 3	Process		induces					inflammation	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1321_s_100	15831808	35 CD40L binding to CD40 on endothelium induces inflammation, and this biological activity is also preserved in platelet CD40L.	bind
25281	1	7887	6	NULL	NULL	0	NULL	CD40L	NULL		bind	NULL				CD40	NULL				NULL	endothelium	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1321_s_100	15831808	35 CD40L binding to CD40 on endothelium induces inflammation, and this biological activity is also preserved in platelet CD40L.	bind
25282	2	7887	6	NULL	NULL	0	NULL	statement 1	NULL		induces	NULL				inflammation	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1321_s_100	15831808	35 CD40L binding to CD40 on endothelium induces inflammation, and this biological activity is also preserved in platelet CD40L.	bind
25283	3	7887	6	NULL	NULL	0	NULL	CD40L	NULL	platelet	bind	NULL				CD40	NULL				NULL	endothelium	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1321_s_100	15831808	35 CD40L binding to CD40 on endothelium induces inflammation, and this biological activity is also preserved in platelet CD40L.	bind
25284	4	7887	6	NULL	NULL	0	NULL	statement 3	NULL		induces	NULL				inflammation	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1321_s_100	15831808	35 CD40L binding to CD40 on endothelium induces inflammation, and this biological activity is also preserved in platelet CD40L.	bind
32846	1	7888	5	13	NULL	NULL	NULL	p300	GP		bind					p160 member	GP		AD1 domain		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_703_s_166	14764426	35 Concomitantly, p300 (or CBP) binds to the AD1 domain of the p160 member.	bind
32848	2	7888	5	13	NULL	NULL	NULL	CBP	GP		bind					p160 member	GP		AD1 domain		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_703_s_166	14764426	35 Concomitantly, p300 (or CBP) binds to the AD1 domain of the p160 member.	bind
32849	3	7888	5	13	NULL	NULL	NULL	statement 1	Process		is alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_703_s_166	14764426	35 Concomitantly, p300 (or CBP) binds to the AD1 domain of the p160 member.	bind
25285	1	7888	6	NULL	NULL	0	NULL	p300	NULL		bind	NULL	concomitantly			p160	NULL		AD1 domain		NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_703_s_166	14764426	35 Concomitantly, p300 (or CBP) binds to the AD1 domain of the p160 member.	bind
25286	2	7888	6	NULL	NULL	0	NULL	CBP	NULL		bind	NULL	concomitantly			p160	NULL		AD1 domain		NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_703_s_166	14764426	35 Concomitantly, p300 (or CBP) binds to the AD1 domain of the p160 member.	bind
47549	3	7888	6	10	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_4_703_s_166	14764426	35 Concomitantly, p300 (or CBP) binds to the AD1 domain of the p160 member.	bind
32851	1	7889	5	13	NULL	NULL	NULL	serum response factor	GP		bind									CArG element	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_2_158_s_207	11834708	35 Gel-mobility supershift analysis demonstrated that the serum response factor binds to the CArG element and that GATA-4 binds to the GATA element.	bind
32852	2	7889	5	13	NULL	NULL	NULL	GATA-4	GP		bind									GATA element	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_2_158_s_207	11834708	35 Gel-mobility supershift analysis demonstrated that the serum response factor binds to the CArG element and that GATA-4 binds to the GATA element.	bind
25287	1	7889	6	NULL	NULL	0	NULL	serum response factor	NULL		bind	NULL					NULL			CArG element	NULL		0	NULL	NULL	NULL	gw60_circulationres_90_2_158_s_207	11834708	35 Gel-mobility supershift analysis demonstrated that the serum response factor binds to the CArG element and that GATA-4 binds to the GATA element.	bind
25288	2	7889	6	NULL	NULL	0	NULL	GATA-4	NULL		bind	NULL					NULL			GATA element	NULL		0	NULL	NULL	NULL	gw60_circulationres_90_2_158_s_207	11834708	35 Gel-mobility supershift analysis demonstrated that the serum response factor binds to the CArG element and that GATA-4 binds to the GATA element.	bind
32854	1	7890	5	13	NULL	NULL	NULL	TNF-alpha	GP		induces					AP-1	GP	binding activity of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_334_s_183	15576639	35 In this study, SOD overexpression suppressed the increase in AP-1 and NF-kappaB binding activity induced by TNF-alpha.	bind
32855	2	7890	5	13	NULL	NULL	NULL	TNF-alpha	GP		induces					NF-kappaB	GP	binding activity of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_334_s_183	15576639	35 In this study, SOD overexpression suppressed the increase in AP-1 and NF-kappaB binding activity induced by TNF-alpha.	bind
32857	3	7890	5	13	NULL	NULL	NULL	SOD	GP	overexpression of	supress					statement 1	Process	increase in			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_334_s_183	15576639	35 In this study, SOD overexpression suppressed the increase in AP-1 and NF-kappaB binding activity induced by TNF-alpha.	bind
32858	4	7890	5	13	NULL	NULL	NULL	SOD	GP	overexpression of	supress					statement 2	Process	increase in			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_334_s_183	15576639	35 In this study, SOD overexpression suppressed the increase in AP-1 and NF-kappaB binding activity induced by TNF-alpha.	bind
25289	1	7890	6	NULL	NULL	0	NULL	TNF-alpha	NULL		induce	NULL				AP-1	NULL	binding activity of 			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_334_s_183	15576639	35 In this study, SOD overexpression suppressed the increase in AP-1 and NF-kappaB binding activity induced by TNF-alpha.	bind
25290	2	7890	6	NULL	NULL	0	NULL	TNF-alpha	NULL		induce	NULL				NF-kappaB	NULL	binding activity of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_334_s_183	15576639	35 In this study, SOD overexpression suppressed the increase in AP-1 and NF-kappaB binding activity induced by TNF-alpha.	bind
25291	3	7890	6	NULL	NULL	0	NULL	SOD	NULL	overexpression of	suppresses	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_334_s_183	15576639	35 In this study, SOD overexpression suppressed the increase in AP-1 and NF-kappaB binding activity induced by TNF-alpha.	bind
38870	4	7890	6	NULL	NULL	0	NULL	SOD	NULL	overexpression of	suppresses	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_2_334_s_183	15576639	35 In this study, SOD overexpression suppressed the increase in AP-1 and NF-kappaB binding activity induced by TNF-alpha.	bind
32870	2	7891	5	13	NULL	NULL	NULL	statement 1	GP		bind					target genes	GP			XRE	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1652_s_206	15271786	35 It is a ligand-activated transcription factor that binds to the XRE of target genes regulating expression of a number of xenobiotic-metabolizing enzymes.	bind
32871	3	7891	5	13	NULL	NULL	NULL	statement 2	Process		regulates					xenobiotic-metabolizing enzymes	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1652_s_206	15271786	35 It is a ligand-activated transcription factor that binds to the XRE of target genes regulating expression of a number of xenobiotic-metabolizing enzymes.	bind
47550	1	7891	5	13	NULL	NULL	NULL	ligand	GP		activates					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1652_s_206	15271786	35 It is a ligand-activated transcription factor that binds to the XRE of target genes regulating expression of a number of xenobiotic-metabolizing enzymes.	bind
25292	2	7891	6	10	NULL	0	NULL	statement 1	NULL		bind	NULL				target genes	NULL			XRE	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1652_s_206	15271786	35 It is a ligand-activated transcription factor that binds to the XRE of target genes regulating expression of a number of xenobiotic-metabolizing enzymes.	bind
25293	3	7891	6	10	NULL	0	NULL	statement 2	NULL		regulate	NULL				xenobiotic-metabolizing enzymes	NULL	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1652_s_206	15271786	35 It is a ligand-activated transcription factor that binds to the XRE of target genes regulating expression of a number of xenobiotic-metabolizing enzymes.	bind
47551	1	7891	6	10	NULL	0	NULL	ligand	NULL		activates	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1652_s_206	15271786	35 It is a ligand-activated transcription factor that binds to the XRE of target genes regulating expression of a number of xenobiotic-metabolizing enzymes.	bind
32872	1	7893	5	13	NULL	NULL	NULL	Pex5p	GP	35 S-Labeled	bind		dose dependent			Pex13p	GP		SH3 domain		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_6_4127_s_146	10660573	35 S-Labeled Pex5p binding to the Pex13p  SH3  domain  in vitro occurs in a dose-dependent manner and is inhibited by the addition of unlabeled Pex5p.	bind
32873	2	7893	5	13	NULL	NULL	NULL	Pex5p	GP	unlabeled	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_6_4127_s_146	10660573	35 S-Labeled Pex5p binding to the Pex13p  SH3  domain  in vitro occurs in a dose-dependent manner and is inhibited by the addition of unlabeled Pex5p.	bind
25294	1	7893	6	NULL	NULL	0	NULL	Pex5p	NULL	35 S-labeled	bind	NULL	dose dependently			Pex13p	NULL		SH3 domain		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_6_4127_s_146	10660573	35 S-Labeled Pex5p binding to the Pex13p  SH3  domain  in vitro occurs in a dose-dependent manner and is inhibited by the addition of unlabeled Pex5p.	bind
25295	2	7893	6	NULL	NULL	0	NULL	Pex5p	NULL	unlabeled	inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_6_4127_s_146	10660573	35 S-Labeled Pex5p binding to the Pex13p  SH3  domain  in vitro occurs in a dose-dependent manner and is inhibited by the addition of unlabeled Pex5p.	bind
32874	1	7895	5	13	NULL	NULL	NULL	AML1	GP	35S-labeled	bind					GST-MEF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3635_s_104	10207087	35S-labeled AML1, AML1B, AML1/ETO, and TEL/AML1 [the oncogenic product generated by the t(12;21) translocation in childhood acute lymphoblastic leukemia] bound to GST-MEF (lanes 2, 4, 6, and 8) but not to GST alone (lanes 1, 3, 5, and 7).	bind
32876	2	7895	5	13	NULL	NULL	NULL	AML1B	GP	35S-labeled	bind					GST-MEF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3635_s_104	10207087	35S-labeled AML1, AML1B, AML1/ETO, and TEL/AML1 [the oncogenic product generated by the t(12;21) translocation in childhood acute lymphoblastic leukemia] bound to GST-MEF (lanes 2, 4, 6, and 8) but not to GST alone (lanes 1, 3, 5, and 7).	bind
32878	3	7895	5	13	NULL	NULL	NULL	AML1/ETO	GP	35S-labeled	bind					GST-MEF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3635_s_104	10207087	35S-labeled AML1, AML1B, AML1/ETO, and TEL/AML1 [the oncogenic product generated by the t(12;21) translocation in childhood acute lymphoblastic leukemia] bound to GST-MEF (lanes 2, 4, 6, and 8) but not to GST alone (lanes 1, 3, 5, and 7).	bind
32880	4	7895	5	13	NULL	NULL	NULL	TEL/AML1	GP	35S-labeled	bind					GST-MEF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3635_s_104	10207087	35S-labeled AML1, AML1B, AML1/ETO, and TEL/AML1 [the oncogenic product generated by the t(12;21) translocation in childhood acute lymphoblastic leukemia] bound to GST-MEF (lanes 2, 4, 6, and 8) but not to GST alone (lanes 1, 3, 5, and 7).	bind
38973	5	7895	5	13	NULL	NULL	NULL	TEL/AML1	GP		is a type of					oncogenic product	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3635_s_104	10207087	35S-labeled AML1, AML1B, AML1/ETO, and TEL/AML1 [the oncogenic product generated by the t(12;21) translocation in childhood acute lymphoblastic leukemia] bound to GST-MEF (lanes 2, 4, 6, and 8) but not to GST alone (lanes 1, 3, 5, and 7).	bind
25296	1	7895	6	NULL	NULL	0	NULL	AML1	NULL	35S-labeled	bind	NULL				GST-MEF	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3635_s_104	10207087	35S-labeled AML1, AML1B, AML1/ETO, and TEL/AML1 [the oncogenic product generated by the t(12;21) translocation in childhood acute lymphoblastic leukemia] bound to GST-MEF (lanes 2, 4, 6, and 8) but not to GST alone (lanes 1, 3, 5, and 7).	bind
25297	2	7895	6	NULL	NULL	0	NULL	AML1B	NULL	35S-labeled	bind	NULL				GST-MEF	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3635_s_104	10207087	35S-labeled AML1, AML1B, AML1/ETO, and TEL/AML1 [the oncogenic product generated by the t(12;21) translocation in childhood acute lymphoblastic leukemia] bound to GST-MEF (lanes 2, 4, 6, and 8) but not to GST alone (lanes 1, 3, 5, and 7).	bind
25298	3	7895	6	NULL	NULL	0	NULL	AML1/ETO	NULL	35S-labeled	bind	NULL				GST-MEF	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3635_s_104	10207087	35S-labeled AML1, AML1B, AML1/ETO, and TEL/AML1 [the oncogenic product generated by the t(12;21) translocation in childhood acute lymphoblastic leukemia] bound to GST-MEF (lanes 2, 4, 6, and 8) but not to GST alone (lanes 1, 3, 5, and 7).	bind
25299	4	7895	6	NULL	NULL	0	NULL	TEL/AML1	NULL	35S-labeled	bind	NULL				GST-MEF	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3635_s_104	10207087	35S-labeled AML1, AML1B, AML1/ETO, and TEL/AML1 [the oncogenic product generated by the t(12;21) translocation in childhood acute lymphoblastic leukemia] bound to GST-MEF (lanes 2, 4, 6, and 8) but not to GST alone (lanes 1, 3, 5, and 7).	bind
25746	5	7895	6	NULL	NULL	0	NULL	TEL/AML1	NULL		is a type of	NULL				oncogenic product	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3635_s_104	10207087	35S-labeled AML1, AML1B, AML1/ETO, and TEL/AML1 [the oncogenic product generated by the t(12;21) translocation in childhood acute lymphoblastic leukemia] bound to GST-MEF (lanes 2, 4, 6, and 8) but not to GST alone (lanes 1, 3, 5, and 7).	bind
32882	1	7896	5	13	NULL	NULL	NULL	AP1	GP	35S-labeled	bind					SEU-GST	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_133_16_3159_s_116	16854969	35S-labeled AP1, SEP3 or AP3 was bound to SEU-GST resins.	bind
32883	2	7896	5	13	NULL	NULL	NULL	SEP3	GP	35S-labeled	bind					SEU-GST	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_133_16_3159_s_116	16854969	35S-labeled AP1, SEP3 or AP3 was bound to SEU-GST resins.	bind
32884	3	7896	5	13	NULL	NULL	NULL	AP3	GP	35S-labeled	bind					SEU-GST	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_133_16_3159_s_116	16854969	35S-labeled AP1, SEP3 or AP3 was bound to SEU-GST resins.	bind
25300	1	7896	6	NULL	NULL	0	NULL	AP1	NULL	35S-labeled	bind	NULL				SEU-GST resin	NULL				NULL		0	NULL	NULL	NULL	gw70_development_133_16_3159_s_116	16854969	35S-labeled AP1, SEP3 or AP3 was bound to SEU-GST resins.	bind
25301	2	7896	6	NULL	NULL	0	NULL	SEP3	NULL	35S-labeled	bind	NULL				SEU-GST resin	NULL				NULL		0	NULL	NULL	NULL	gw70_development_133_16_3159_s_116	16854969	35S-labeled AP1, SEP3 or AP3 was bound to SEU-GST resins.	bind
25302	3	7896	6	NULL	NULL	0	NULL	AP3	NULL	35S-labeled	bind	NULL				SEU-GST resin	NULL				NULL		0	NULL	NULL	NULL	gw70_development_133_16_3159_s_116	16854969	35S-labeled AP1, SEP3 or AP3 was bound to SEU-GST resins.	bind
32885	1	7897	5	13	NULL	NULL	NULL	Arp1	GP	35S-labeled	bind					DI constructs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36598_s_99	11461920	35S-Labeled Arp1 bound to both the DI and DIII constructs but did not bind significantly to the DII construct or to the GST control column (Fig.  2 a).	bind
32886	2	7897	5	13	NULL	NULL	NULL	Arp1	GP	35S-labeled	bind					DIII constructs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36598_s_99	11461920	35S-Labeled Arp1 bound to both the DI and DIII constructs but did not bind significantly to the DII construct or to the GST control column (Fig.  2 a).	bind
32887	3	7897	5	13	NULL	NULL	NULL	Arp1	GP	35S-labeled	does not bind		significantly			DII construct	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36598_s_99	11461920	35S-Labeled Arp1 bound to both the DI and DIII constructs but did not bind significantly to the DII construct or to the GST control column (Fig.  2 a).	bind
25303	1	7897	6	NULL	NULL	0	NULL	Arp1	NULL	35S-labeled	bind	NULL				DI construct	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_39_36598_s_99	11461920	35S-Labeled Arp1 bound to both the DI and DIII constructs but did not bind significantly to the DII construct or to the GST control column (Fig.  2 a).	bind
25304	2	7897	6	NULL	NULL	0	NULL	Arp1	NULL	35S-labeled	bind	NULL				DIII construct	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_39_36598_s_99	11461920	35S-Labeled Arp1 bound to both the DI and DIII constructs but did not bind significantly to the DII construct or to the GST control column (Fig.  2 a).	bind
25305	3	7897	6	NULL	NULL	0	NULL	Arp1	NULL	35S-labeled	did not bind	NULL	significantly			DII construct	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_39_36598_s_99	11461920	35S-Labeled Arp1 bound to both the DI and DIII constructs but did not bind significantly to the DII construct or to the GST control column (Fig.  2 a).	bind
32889	1	7898	5	13	NULL	NULL	NULL	Arr2	GP	35S-labeled	bind					PIP3	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_1_121_s_108	12848937	35S-labeled Arr2 bound to PIP3 beads but not to control beads   (Figure 2D).	bind
25306	1	7898	6	NULL	NULL	0	NULL	Arr2	NULL	35S-labeled	bind	NULL				PIP3	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_39_1_121_s_108	12848937	35S-labeled Arr2 bound to PIP3 beads but not to control beads   (Figure 2D).	bind
32890	1	7899	5	13	NULL	NULL	NULL	BAX	GP	35S-labeled	bind					GST-BCL-xL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_20_12415_s_120	9575197	35S-labeled BAX bound to GST-BCL-xL was analyzed by SDS-PAGE.	bind
25307	1	7899	6	NULL	NULL	0	NULL	BAX	NULL	35S-labeled	bind	NULL				GST-BCL-xL	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_20_12415_s_120	9575197	35S-labeled BAX bound to GST-BCL-xL was analyzed by SDS-PAGE.	bind
32891	1	7900	5	13	NULL	NULL	NULL	Cbfa2	GP	35S-labeled	bind					GST-Cbfbeta	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4197_s_258	9632804	35S-labeled Cbfa2 was bound by immobilized GST-Cbfbeta but not by GST alone (Fig.  7A, lanes 4 to 6).	bind
32892	2	7900	5	13	NULL	NULL	NULL	Cbfa2	GP	35S-labeled	does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4197_s_258	9632804	35S-labeled Cbfa2 was bound by immobilized GST-Cbfbeta but not by GST alone (Fig.  7A, lanes 4 to 6).	bind
25308	1	7900	6	NULL	NULL	0	NULL	Cbfa2	NULL	35S-labeled	bind	NULL				GST-Cbfbeta	NULL	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4197_s_258	9632804	35S-labeled Cbfa2 was bound by immobilized GST-Cbfbeta but not by GST alone (Fig.  7A, lanes 4 to 6).	bind
25309	2	7900	6	NULL	NULL	0	NULL	Cbfa2	NULL	35S-labeled	does not bind	NULL				GST	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_4197_s_258	9632804	35S-labeled Cbfa2 was bound by immobilized GST-Cbfbeta but not by GST alone (Fig.  7A, lanes 4 to 6).	bind
32893	1	7901	5	13	NULL	NULL	NULL	Cdc20p	GP	35S-labeled	bind					MBP-Hsl1p	GP		667-872		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_18_2381_s_162	11562348	35S-labeled Cdc20p bound to MBP-Hsl1p667-872 and MBP-Hsl1p667-872mkb, but not to MBP alone or to MBP-Hsl1p667-872mdb (Fig.  6, top, left panel, lanes 1-4).	bind
32894	2	7901	5	13	NULL	NULL	NULL	Cdc20p	GP	35S-labeled	bind					MBP-Hsl1p	GP		667-872mkb		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_18_2381_s_162	11562348	35S-labeled Cdc20p bound to MBP-Hsl1p667-872 and MBP-Hsl1p667-872mkb, but not to MBP alone or to MBP-Hsl1p667-872mdb (Fig.  6, top, left panel, lanes 1-4).	bind
32895	3	7901	5	13	NULL	NULL	NULL	Cdc20p	GP	35S-labeled	does not bind					MBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_18_2381_s_162	11562348	35S-labeled Cdc20p bound to MBP-Hsl1p667-872 and MBP-Hsl1p667-872mkb, but not to MBP alone or to MBP-Hsl1p667-872mdb (Fig.  6, top, left panel, lanes 1-4).	bind
32896	4	7901	5	13	NULL	NULL	NULL	Cdc20p	GP	35S-labeled	does not bind					MBP-Hsl1p	GP		667-872mdb		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_18_2381_s_162	11562348	35S-labeled Cdc20p bound to MBP-Hsl1p667-872 and MBP-Hsl1p667-872mkb, but not to MBP alone or to MBP-Hsl1p667-872mdb (Fig.  6, top, left panel, lanes 1-4).	bind
25310	1	7901	6	NULL	NULL	0	NULL	Cdc20p	NULL	35S-labeled	bind	NULL				MBP-Hsl1	NULL		p667-872		NULL		0	NULL	NULL	NULL	gw60_genesdev_15_18_2381_s_162	11562348	35S-labeled Cdc20p bound to MBP-Hsl1p667-872 and MBP-Hsl1p667-872mkb, but not to MBP alone or to MBP-Hsl1p667-872mdb (Fig.  6, top, left panel, lanes 1-4).	bind
25311	2	7901	6	NULL	NULL	0	NULL	Cdc20p	NULL	35S-labeled	bind	NULL				MBP-Hsl1	NULL		p667-872mkb		NULL		0	NULL	NULL	NULL	gw60_genesdev_15_18_2381_s_162	11562348	35S-labeled Cdc20p bound to MBP-Hsl1p667-872 and MBP-Hsl1p667-872mkb, but not to MBP alone or to MBP-Hsl1p667-872mdb (Fig.  6, top, left panel, lanes 1-4).	bind
25312	3	7901	6	NULL	NULL	0	NULL	Cdc20p	NULL	35S-labeled	does not bind	NULL				MBP-Hsl1	NULL		p667-872mdb		NULL		0	NULL	NULL	NULL	gw60_genesdev_15_18_2381_s_162	11562348	35S-labeled Cdc20p bound to MBP-Hsl1p667-872 and MBP-Hsl1p667-872mkb, but not to MBP alone or to MBP-Hsl1p667-872mdb (Fig.  6, top, left panel, lanes 1-4).	bind
25313	4	7901	6	NULL	NULL	0	NULL	Cdc20p	NULL	35S-labeled	does not bind	NULL				MBP alone	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_15_18_2381_s_162	11562348	35S-labeled Cdc20p bound to MBP-Hsl1p667-872 and MBP-Hsl1p667-872mkb, but not to MBP alone or to MBP-Hsl1p667-872mdb (Fig.  6, top, left panel, lanes 1-4).	bind
32898	1	7902	5	13	NULL	NULL	NULL	dTopors	GP	35S-labeled	bind					GST-Hairy	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17126_s_132	14871887	35S-Labeled dTopors (20% input;  lane 1) did not bind GST ( lane 2), but did bind GST-Hairy ( lane 3).	bind
25315	1	7902	6	NULL	NULL	0	NULL	dTopors	NULL	35S-labeled	bind	NULL				GST-Hairy	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17126_s_132	14871887	35S-Labeled dTopors (20% input;  lane 1) did not bind GST ( lane 2), but did bind GST-Hairy ( lane 3).	bind
32900	1	7903	5	13	NULL	NULL	NULL	E2F1	GP	35S-labeled	bind					GST-Phb	GP		CC		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_2_459_s_97	14637159	35S-labeled E2F1 does not bind to GST beads but binds to GST-Phb-CC beads.	bind
25317	1	7903	6	10	NULL	0	NULL	E2F1		35S-labeled	bind					GST-Phb			CC		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_2_459_s_97	14637159	35S-labeled E2F1 does not bind to GST beads but binds to GST-Phb-CC beads.	bind
32901	1	7904	5	13	NULL	NULL	NULL	EBNA3C	GP	35S-labeled	bind					GST-ProTalpha protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5722_s_202	10891508	35S-labeled EBNA3C bound to GST-ProTalpha protein in this experiment at levels approximately 20-fold over binding with GST beads alone as determined by arbitrary counts using the Molecular Dynamics software ImageQuant supplied with the PhosphorImager unit (Fig.  3B, compare lane 3 with lane 5).	bind
25745	1	7904	6	NULL	NULL	0	NULL	EBNA3C	NULL	35S-labeled	bind	NULL				GST-ProTalpha protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5722_s_202	10891508	35S-labeled EBNA3C bound to GST-ProTalpha protein in this experiment at levels approximately 20-fold over binding with GST beads alone as determined by arbitrary counts using the Molecular Dynamics software ImageQuant supplied with the PhosphorImager unit (Fig.  3B, compare lane 3 with lane 5).	bind
32902	1	7905	5	13	NULL	NULL	NULL	GSK3beta	GP	35S-labeled	bind					MEKK1	GP		N1 amino acids 1-401		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_16_13995_s_129	12584189	35S-Labeled GSK3beta bound to MEKK1-N1 (amino acids 1-401 of MEKK1) and MEKK1-N2 (amino acids 402-821) but not to MEKK1-deltaNC (amino acids 822-1172) or deltaMEKK1 (amino acids 1173-1493) (Fig.  5 A).	bind
32903	2	7905	5	13	NULL	NULL	NULL	GSK3beta	GP	35S-labeled	bind					MEKK1	GP		N2 amino acids 402-821		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_16_13995_s_129	12584189	35S-Labeled GSK3beta bound to MEKK1-N1 (amino acids 1-401 of MEKK1) and MEKK1-N2 (amino acids 402-821) but not to MEKK1-deltaNC (amino acids 822-1172) or deltaMEKK1 (amino acids 1173-1493) (Fig.  5 A).	bind
32904	3	7905	5	13	NULL	NULL	NULL	GSK3beta	GP	35S-labeled	does not bind					MEKK1	GP		deltaNC amino acids 822-1172		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_16_13995_s_129	12584189	35S-Labeled GSK3beta bound to MEKK1-N1 (amino acids 1-401 of MEKK1) and MEKK1-N2 (amino acids 402-821) but not to MEKK1-deltaNC (amino acids 822-1172) or deltaMEKK1 (amino acids 1173-1493) (Fig.  5 A).	bind
32905	4	7905	5	13	NULL	NULL	NULL	GSK3beta	GP	35S-labeled	does not bind					deltaMEKK1	GP		amino acids 1173-1493		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_16_13995_s_129	12584189	35S-Labeled GSK3beta bound to MEKK1-N1 (amino acids 1-401 of MEKK1) and MEKK1-N2 (amino acids 402-821) but not to MEKK1-deltaNC (amino acids 822-1172) or deltaMEKK1 (amino acids 1173-1493) (Fig.  5 A).	bind
25318	1	7905	6	NULL	NULL	0	NULL	GSK3beta	NULL	35S-labeled	bind	NULL				MEKK1-N1	NULL		amino acids 1-401		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_16_13995_s_129	12584189	35S-Labeled GSK3beta bound to MEKK1-N1 (amino acids 1-401 of MEKK1) and MEKK1-N2 (amino acids 402-821) but not to MEKK1-deltaNC (amino acids 822-1172) or deltaMEKK1 (amino acids 1173-1493) (Fig.  5 A).	bind
25319	2	7905	6	NULL	NULL	0	NULL	GSK3beta	NULL	35S-labeled	bind	NULL				MEKK1-N2	NULL		amino acids 402-821		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_16_13995_s_129	12584189	35S-Labeled GSK3beta bound to MEKK1-N1 (amino acids 1-401 of MEKK1) and MEKK1-N2 (amino acids 402-821) but not to MEKK1-deltaNC (amino acids 822-1172) or deltaMEKK1 (amino acids 1173-1493) (Fig.  5 A).	bind
25320	3	7905	6	NULL	NULL	0	NULL	GSK3beta	NULL	35S-labeled	does not bind	NULL				MEKK1-deltaNC	NULL		amino acids 822-1172		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_16_13995_s_129	12584189	35S-Labeled GSK3beta bound to MEKK1-N1 (amino acids 1-401 of MEKK1) and MEKK1-N2 (amino acids 402-821) but not to MEKK1-deltaNC (amino acids 822-1172) or deltaMEKK1 (amino acids 1173-1493) (Fig.  5 A).	bind
25339	4	7905	6	NULL	NULL	0	NULL	GSK3beta	NULL	35S-labeled	does not bind	NULL				deltaMEKK1	NULL		amino acids 1173-1493		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_16_13995_s_129	12584189	35S-Labeled GSK3beta bound to MEKK1-N1 (amino acids 1-401 of MEKK1) and MEKK1-N2 (amino acids 402-821) but not to MEKK1-deltaNC (amino acids 822-1172) or deltaMEKK1 (amino acids 1173-1493) (Fig.  5 A).	bind
32906	1	7906	5	13	NULL	NULL	NULL	Hairy protein	GP	35S-labeled	does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17126_s_130	14871887	35S-Labeled Hairy protein was used as a control for the integrity of purified GST-proteins,  as Hairy did not bind GST ( lane 8), but could homodimerize ( lane 9) and heterodimerize with GST-E(spl)m3 ( lane 10), GST-E(spl)m8 ( lane 11), and GST-Deadpan ( lane 12).	bind
32907	2	7906	5	13	NULL	NULL	NULL	Hairy protein	GP	35S-labeled	homodimerize with					Hairy protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17126_s_130	14871887	35S-Labeled Hairy protein was used as a control for the integrity of purified GST-proteins,  as Hairy did not bind GST ( lane 8), but could homodimerize ( lane 9) and heterodimerize with GST-E(spl)m3 ( lane 10), GST-E(spl)m8 ( lane 11), and GST-Deadpan ( lane 12).	bind
32908	3	7906	5	13	NULL	NULL	NULL	Hairy protein	GP	35S-labeled	heterodimerize with					GST-E(spl)m3	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17126_s_130	14871887	35S-Labeled Hairy protein was used as a control for the integrity of purified GST-proteins,  as Hairy did not bind GST ( lane 8), but could homodimerize ( lane 9) and heterodimerize with GST-E(spl)m3 ( lane 10), GST-E(spl)m8 ( lane 11), and GST-Deadpan ( lane 12).	bind
32909	4	7906	5	13	NULL	NULL	NULL	Hairy protein	GP	35S-labeled	heterodimerize with					GST-E(spl)m8	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17126_s_130	14871887	35S-Labeled Hairy protein was used as a control for the integrity of purified GST-proteins,  as Hairy did not bind GST ( lane 8), but could homodimerize ( lane 9) and heterodimerize with GST-E(spl)m3 ( lane 10), GST-E(spl)m8 ( lane 11), and GST-Deadpan ( lane 12).	bind
32910	5	7906	5	13	NULL	NULL	NULL	Hairy protein	GP	35S-labeled	heterodimerize with					GST-Deadpan	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17126_s_130	14871887	35S-Labeled Hairy protein was used as a control for the integrity of purified GST-proteins,  as Hairy did not bind GST ( lane 8), but could homodimerize ( lane 9) and heterodimerize with GST-E(spl)m3 ( lane 10), GST-E(spl)m8 ( lane 11), and GST-Deadpan ( lane 12).	bind
25340	1	7906	6	10	NULL	0	NULL	Hairy protein		35S-Labeled	does not bind					GST					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17126_s_130	14871887	35S-Labeled Hairy protein was used as a control for the integrity of purified GST-proteins,  as Hairy did not bind GST ( lane 8), but could homodimerize ( lane 9) and heterodimerize with GST-E(spl)m3 ( lane 10), GST-E(spl)m8 ( lane 11), and GST-Deadpan ( lane 12).	bind
25341	2	7906	6	10	NULL	0	NULL	Hairy protein		35S-Labeled	bind					Hairy protein					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17126_s_130	14871887	35S-Labeled Hairy protein was used as a control for the integrity of purified GST-proteins,  as Hairy did not bind GST ( lane 8), but could homodimerize ( lane 9) and heterodimerize with GST-E(spl)m3 ( lane 10), GST-E(spl)m8 ( lane 11), and GST-Deadpan ( lane 12).	bind
25342	3	7906	6	10	NULL	0	NULL	Hairy protein		35S-Labeled	bind					GST-E(spl)m3					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17126_s_130	14871887	35S-Labeled Hairy protein was used as a control for the integrity of purified GST-proteins,  as Hairy did not bind GST ( lane 8), but could homodimerize ( lane 9) and heterodimerize with GST-E(spl)m3 ( lane 10), GST-E(spl)m8 ( lane 11), and GST-Deadpan ( lane 12).	bind
25343	4	7906	6	10	NULL	0	NULL	Hairy protein		35S-Labeled	bind					GST-E(spl)m8					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17126_s_130	14871887	35S-Labeled Hairy protein was used as a control for the integrity of purified GST-proteins,  as Hairy did not bind GST ( lane 8), but could homodimerize ( lane 9) and heterodimerize with GST-E(spl)m3 ( lane 10), GST-E(spl)m8 ( lane 11), and GST-Deadpan ( lane 12).	bind
25344	5	7906	6	10	NULL	0	NULL	Hairy protein		35S-Labeled	bind					GST-Deadpan					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17126_s_130	14871887	35S-Labeled Hairy protein was used as a control for the integrity of purified GST-proteins,  as Hairy did not bind GST ( lane 8), but could homodimerize ( lane 9) and heterodimerize with GST-E(spl)m3 ( lane 10), GST-E(spl)m8 ( lane 11), and GST-Deadpan ( lane 12).	bind
32911	1	7907	5	13	NULL	NULL	NULL	HEF1	GP	35S-labeled	bind					GST-AIP4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_28_29681_s_136	15051726	35S-Labeled HEF1 and Smad3 bound to GST-AIP4 were eluted from the beads, separated onto  SDS-PAGE, and detected by autoradiography.	bind
32912	2	7907	5	13	NULL	NULL	NULL	Smad3	GP	35S-labeled	bind					GST-AIP4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_28_29681_s_136	15051726	35S-Labeled HEF1 and Smad3 bound to GST-AIP4 were eluted from the beads, separated onto  SDS-PAGE, and detected by autoradiography.	bind
25345	1	7907	6	NULL	NULL	0	NULL	HEF1	NULL	35S-labeled	bind	NULL				GST-AIP4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_28_29681_s_136	15051726	35S-Labeled HEF1 and Smad3 bound to GST-AIP4 were eluted from the beads, separated onto  SDS-PAGE, and detected by autoradiography.	bind
25346	2	7907	6	NULL	NULL	0	NULL	Smad3	NULL	35S-labeled	bind	NULL				GST-AIP4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_28_29681_s_136	15051726	35S-Labeled HEF1 and Smad3 bound to GST-AIP4 were eluted from the beads, separated onto  SDS-PAGE, and detected by autoradiography.	bind
32913	1	7908	5	13	NULL	NULL	NULL	INAD	GP	35S-labeled	bind					TRP GST fusion proteins	GP	wild-type	COOH-terminal 246 residues		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_6_1411_s_168	10995445	35S-labeled INAD bound to the GST fusion proteins consisting of the COOH-terminal 246 or 29 residues from wild-type TRP (referred to as long and short tails, respectively;   Fig 4A and   Fig B).	bind
32914	2	7908	5	13	NULL	NULL	NULL	INAD	GP	35S-labeled	bind					TRP GST fusion proteins	GP	wild-type	COOH-terminal 29 residues		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_6_1411_s_168	10995445	35S-labeled INAD bound to the GST fusion proteins consisting of the COOH-terminal 246 or 29 residues from wild-type TRP (referred to as long and short tails, respectively;   Fig 4A and   Fig B).	bind
32915	3	7908	5	13	NULL	NULL	NULL	statement 1	Process		is alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_6_1411_s_168	10995445	35S-labeled INAD bound to the GST fusion proteins consisting of the COOH-terminal 246 or 29 residues from wild-type TRP (referred to as long and short tails, respectively;   Fig 4A and   Fig B).	bind
25347	1	7908	6	NULL	NULL	0	NULL	INAD	NULL	35S-labeled	bind	NULL				TRP	NULL	wild type	COOH-terminal 246 residues		NULL		0	NULL	NULL	NULL	gw60_cellbiol_150_6_1411_s_168	10995445	35S-labeled INAD bound to the GST fusion proteins consisting of the COOH-terminal 246 or 29 residues from wild-type TRP (referred to as long and short tails, respectively;   Fig 4A and   Fig B).	bind
37306	2	7908	6	NULL	NULL	0	NULL	INAD	NULL	35S-labeled	bind	NULL				TRP	NULL	wild type	COOH-terminal 29 residues		NULL		0	NULL	NULL	NULL	gw60_cellbiol_150_6_1411_s_168	10995445	35S-labeled INAD bound to the GST fusion proteins consisting of the COOH-terminal 246 or 29 residues from wild-type TRP (referred to as long and short tails, respectively;   Fig 4A and   Fig B).	bind
47822	3	7908	6	10	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_150_6_1411_s_168	10995445	35S-labeled INAD bound to the GST fusion proteins consisting of the COOH-terminal 246 or 29 residues from wild-type TRP (referred to as long and short tails, respectively;   Fig 4A and   Fig B).	bind
32916	1	7909	5	13	NULL	NULL	NULL	Xsecurin	GP	35S-labeled;;IVT	bind					Cdc20	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_24_3278_s_113	11751633	35S-labeled IVT  Xsecurin was then added and the amount of securin bound to Cdc20 was analyzed as in  A and was quantitated on a PhosphorImager (graph).	bind
25348	1	7909	6	10	NULL	0	NULL	Xsecurin		35S-labeled;;IVT 	bind					Cdc20					NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_24_3278_s_113	11751633	35S-labeled IVT  Xsecurin was then added and the amount of securin bound to Cdc20 was analyzed as in  A and was quantitated on a PhosphorImager (graph).	bind
32917	1	7911	5	13	NULL	NULL	NULL	Mad2	GP	35S-labeled	bind					GST-Slp1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5353_1045_s_26	9461438	35S-labeled Mad2 bound to GST-Slp1, but not to GST (Fig.  1C).	bind
36181	2	7911	5	13	NULL	NULL	NULL	Mad2	GP	35S-labeled	does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5353_1045_s_26	9461438	35S-labeled Mad2 bound to GST-Slp1, but not to GST (Fig.  1C).	bind
25350	1	7911	6	NULL	NULL	0	NULL	Mad2	NULL	35S-labeled	bind	NULL				GST-Slp1	NULL				NULL		0	NULL	NULL	NULL	gw60_science_279_5353_1045_s_26	9461438	35S-labeled Mad2 bound to GST-Slp1, but not to GST (Fig.  1C).	bind
25351	2	7911	6	NULL	NULL	0	NULL	Mad2	NULL	35S-labeled	does not bind	NULL				GST	NULL				NULL		0	NULL	NULL	NULL	gw60_science_279_5353_1045_s_26	9461438	35S-labeled Mad2 bound to GST-Slp1, but not to GST (Fig.  1C).	bind
32918	1	7912	5	13	NULL	NULL	NULL	MAN1	GP	35S-labeled	does not bind			N-terminus		emerin 	GP	mutant	delta95		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_14_13863_s_103	15681850	35S-Labeled MAN1-N did not bind the emerin mutant delta95 but recognized both lamin tails, particularly the B1 tail ( Fig. 3 B), independently confirming that MAN1 binds directly to both A- and B-type lamins.	bind
32919	2	7912	5	13	NULL	NULL	NULL	MAN1	GP	35S-labeled	bind			N-terminus		lamin	GP		B1 tail		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_14_13863_s_103	15681850	35S-Labeled MAN1-N did not bind the emerin mutant delta95 but recognized both lamin tails, particularly the B1 tail ( Fig. 3 B), independently confirming that MAN1 binds directly to both A- and B-type lamins.	bind
32920	3	7912	5	13	NULL	NULL	NULL	MAN1	GP		bind		directly			A-type lamins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_14_13863_s_103	15681850	35S-Labeled MAN1-N did not bind the emerin mutant delta95 but recognized both lamin tails, particularly the B1 tail ( Fig. 3 B), independently confirming that MAN1 binds directly to both A- and B-type lamins.	bind
32921	4	7912	5	13	NULL	NULL	NULL	MAN1	GP		bind		directly			B-type lamins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_14_13863_s_103	15681850	35S-Labeled MAN1-N did not bind the emerin mutant delta95 but recognized both lamin tails, particularly the B1 tail ( Fig. 3 B), independently confirming that MAN1 binds directly to both A- and B-type lamins.	bind
25352	1	7912	6	NULL	NULL	0	NULL	MAN1	NULL	35S-labeled	does not bind	NULL		N-terminus		emerin	NULL	mutant	delta95		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_14_13863_s_103	15681850	35S-Labeled MAN1-N did not bind the emerin mutant delta95 but recognized both lamin tails, particularly the B1 tail ( Fig. 3 B), independently confirming that MAN1 binds directly to both A- and B-type lamins.	bind
25353	2	7912	6	10	NULL	0	NULL	MAN1			bind		directly			A-type lamins					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_14_13863_s_103	15681850	35S-Labeled MAN1-N did not bind the emerin mutant delta95 but recognized both lamin tails, particularly the B1 tail ( Fig. 3 B), independently confirming that MAN1 binds directly to both A- and B-type lamins.	bind
25354	3	7912	6	10	NULL	0	NULL	MAN1			bind		directly			B-type lamins					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_14_13863_s_103	15681850	35S-Labeled MAN1-N did not bind the emerin mutant delta95 but recognized both lamin tails, particularly the B1 tail ( Fig. 3 B), independently confirming that MAN1 binds directly to both A- and B-type lamins.	bind
47823	4	7912	6	10	NULL	0	NULL	MAN1		35S-labeled	bind			N-terminus		lamin			B1 tail		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_14_13863_s_103	15681850	35S-Labeled MAN1-N did not bind the emerin mutant delta95 but recognized both lamin tails, particularly the B1 tail ( Fig. 3 B), independently confirming that MAN1 binds directly to both A- and B-type lamins.	bind
32922	1	7914	5	13	NULL	NULL	NULL	p150Glued	GP	35S-labeled	does not bind					betaIII spectrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36598_s_94	11461920	35S-labeled p150Glued did not bind to either the betaIII spectrin column or the GST column.	bind
32923	2	7914	5	13	NULL	NULL	NULL	p150Glued	GP	35S-labeled	does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36598_s_94	11461920	35S-labeled p150Glued did not bind to either the betaIII spectrin column or the GST column.	bind
25357	1	7914	6	NULL	NULL	0	NULL	p150Glued	NULL	35S-labeled	does not bind	NULL				betaIII spectrin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_39_36598_s_94	11461920	35S-labeled p150Glued did not bind to either the betaIII spectrin column or the GST column.	bind
25358	2	7914	6	NULL	NULL	0	NULL	p150Glued	NULL	35S-labeled	does not bind	NULL				GST column	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_39_36598_s_94	11461920	35S-labeled p150Glued did not bind to either the betaIII spectrin column or the GST column.	bind
32924	1	7922	5	13	NULL	NULL	NULL	RpS21 protein	GP	35S-labeled	bind					GST-P40	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2308_s_331	10022917	35S-labeled RpS21 proteins bound to GST-P40 (lane 1) or GST proteins (lane 2) were analyzed by SDS-PAGE and detected by autoradiography.	bind
25359	1	7922	6	NULL	NULL	0	NULL	RpS21 protein	NULL	35S-labeled	bind	NULL				GST-P40	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2308_s_331	10022917	35S-labeled RpS21 proteins bound to GST-P40 (lane 1) or GST proteins (lane 2) were analyzed by SDS-PAGE and detected by autoradiography.	bind
32925	1	7923	5	13	NULL	NULL	NULL	SFV	GP	35S-labeled	bind					BHK cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_1_111_s_190	16216925	35S-labeled SFV was bound to BHK cells on ice and treated at pH 7.4 or 5.5 at 37 degrees  C for 1 min in the presence of the indicated domain III proteins.	bind
32926	2	7923	5	13	NULL	NULL	NULL	statement 1	Process		in presence of					domain III proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_1_111_s_190	16216925	35S-labeled SFV was bound to BHK cells on ice and treated at pH 7.4 or 5.5 at 37 degrees  C for 1 min in the presence of the indicated domain III proteins.	bind
25360	1	7923	6	NULL	NULL	0	NULL	SFV	NULL	35S-labeled	bind	NULL				BHK cells	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_171_1_111_s_190	16216925	35S-labeled SFV was bound to BHK cells on ice and treated at pH 7.4 or 5.5 at 37 degrees  C for 1 min in the presence of the indicated domain III proteins.	bind
47824	2	7923	6	10	NULL	0	NULL	statement 1	NULL		in presence of	NULL				domain III proteins	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_171_1_111_s_190	16216925	35S-labeled SFV was bound to BHK cells on ice and treated at pH 7.4 or 5.5 at 37 degrees  C for 1 min in the presence of the indicated domain III proteins.	bind
32927	1	7924	5	13	NULL	NULL	NULL	Smad3	GP	35S-labeled	bind					GST-AIP4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_28_29681_s_155	15051726	35S-Labeled Smad3 and HEF1 were found to bind GST-AIP4 ( Fig. 1 D,  lanes 3 and  4).	bind
32928	2	7924	5	13	NULL	NULL	NULL	HEF1	GP	35S-labeled	bind					GST-AIP4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_28_29681_s_155	15051726	35S-Labeled Smad3 and HEF1 were found to bind GST-AIP4 ( Fig. 1 D,  lanes 3 and  4).	bind
25361	1	7924	6	NULL	NULL	0	NULL	Smad3	NULL	35S-labeled	bind	NULL				GST-AIP4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_28_29681_s_155	15051726	35S-Labeled Smad3 and HEF1 were found to bind GST-AIP4 ( Fig. 1 D,  lanes 3 and  4).	bind
25362	2	7924	6	NULL	NULL	0	NULL	HEF1	NULL	35S-labeled	bind	NULL				GST-AIP4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_28_29681_s_155	15051726	35S-Labeled Smad3 and HEF1 were found to bind GST-AIP4 ( Fig. 1 D,  lanes 3 and  4).	bind
32929	1	7925	5	13	NULL	NULL	NULL	SR1-5	GP	35S-labeled	bind		specifically			GST-SR5-6	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_525_1_135_s_81	12163176	35S-labeled SR1-5 also bound specifically to GST-SR5-6 on GST-sepharose columns (data not shown).	bind
25363	1	7925	6	NULL	NULL	0	NULL	SR1-5	NULL	35 S-labeled	bind	NULL	specifically			GST-SR5-6	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_525_1_135_s_81	12163176	35S-labeled SR1-5 also bound specifically to GST-SR5-6 on GST-sepharose columns (data not shown).	bind
32930	1	7926	5	13	NULL	NULL	NULL	SR2-3	GP	35S-labeled	bind					GST-SR5-6	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_525_1_135_s_84	12163176	35S-labeled SR2-3 and SR3 each bound to GST-SR5-6 ( Fig. 2D,F), but SR2 did not (  Fig. 2E), suggesting that SR3 is sufficient to bind SR5-6.	bind
32931	2	7926	5	13	NULL	NULL	NULL	SR3	GP	35S-labeled	bind					GST-SR5-6	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_525_1_135_s_84	12163176	35S-labeled SR2-3 and SR3 each bound to GST-SR5-6 ( Fig. 2D,F), but SR2 did not (  Fig. 2E), suggesting that SR3 is sufficient to bind SR5-6.	bind
32932	3	7926	5	13	NULL	NULL	NULL	SR2	GP	35S-labeled	does not bind					GST-SR5-6	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_525_1_135_s_84	12163176	35S-labeled SR2-3 and SR3 each bound to GST-SR5-6 ( Fig. 2D,F), but SR2 did not (  Fig. 2E), suggesting that SR3 is sufficient to bind SR5-6.	bind
32933	4	7926	5	13	NULL	NULL	NULL	SR3	GP	35S-labeled	bind					SR5-6	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_525_1_135_s_84	12163176	35S-labeled SR2-3 and SR3 each bound to GST-SR5-6 ( Fig. 2D,F), but SR2 did not (  Fig. 2E), suggesting that SR3 is sufficient to bind SR5-6.	bind
36178	5	7926	5	13	NULL	NULL	NULL	statement 1	Process		suggest					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_525_1_135_s_84	12163176	35S-labeled SR2-3 and SR3 each bound to GST-SR5-6 ( Fig. 2D,F), but SR2 did not (  Fig. 2E), suggesting that SR3 is sufficient to bind SR5-6.	bind
36179	6	7926	5	13	NULL	NULL	NULL	statement 2	Process		suggest					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_525_1_135_s_84	12163176	35S-labeled SR2-3 and SR3 each bound to GST-SR5-6 ( Fig. 2D,F), but SR2 did not (  Fig. 2E), suggesting that SR3 is sufficient to bind SR5-6.	bind
36180	7	7926	5	13	NULL	NULL	NULL	statement 3	Process		suggest					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_525_1_135_s_84	12163176	35S-labeled SR2-3 and SR3 each bound to GST-SR5-6 ( Fig. 2D,F), but SR2 did not (  Fig. 2E), suggesting that SR3 is sufficient to bind SR5-6.	bind
25365	1	7926	6	10	NULL	0	NULL	SR2-3		35S-labeled	bind					GST-SR5-6					NULL		NULL	NULL	NULL	NULL	gw60_febslett_525_1_135_s_84	12163176	35S-labeled SR2-3 and SR3 each bound to GST-SR5-6 ( Fig. 2D,F), but SR2 did not (  Fig. 2E), suggesting that SR3 is sufficient to bind SR5-6.	bind
25366	2	7926	6	10	NULL	0	NULL	SR3		35S-labeled	bind					GST-SR5-6					NULL		NULL	NULL	NULL	NULL	gw60_febslett_525_1_135_s_84	12163176	35S-labeled SR2-3 and SR3 each bound to GST-SR5-6 ( Fig. 2D,F), but SR2 did not (  Fig. 2E), suggesting that SR3 is sufficient to bind SR5-6.	bind
25367	3	7926	6	10	NULL	0	NULL	SR2		35S-labeled	does not bind					GST-SR5-6					NULL		NULL	NULL	NULL	NULL	gw60_febslett_525_1_135_s_84	12163176	35S-labeled SR2-3 and SR3 each bound to GST-SR5-6 ( Fig. 2D,F), but SR2 did not (  Fig. 2E), suggesting that SR3 is sufficient to bind SR5-6.	bind
37307	4	7926	6	10	NULL	0	NULL	SR3		35S-labeled	bind					SR5-6					NULL		NULL	NULL	NULL	NULL	gw60_febslett_525_1_135_s_84	12163176	35S-labeled SR2-3 and SR3 each bound to GST-SR5-6 ( Fig. 2D,F), but SR2 did not (  Fig. 2E), suggesting that SR3 is sufficient to bind SR5-6.	bind
37308	5	7926	6	NULL	NULL	0	NULL	statement 1	NULL		suggests	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_525_1_135_s_84	12163176	35S-labeled SR2-3 and SR3 each bound to GST-SR5-6 ( Fig. 2D,F), but SR2 did not (  Fig. 2E), suggesting that SR3 is sufficient to bind SR5-6.	bind
37309	6	7926	6	NULL	NULL	0	NULL	statement 2	NULL		suggests	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_525_1_135_s_84	12163176	35S-labeled SR2-3 and SR3 each bound to GST-SR5-6 ( Fig. 2D,F), but SR2 did not (  Fig. 2E), suggesting that SR3 is sufficient to bind SR5-6.	bind
37310	7	7926	6	NULL	NULL	0	NULL	statement 3	NULL		suggests	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_525_1_135_s_84	12163176	35S-labeled SR2-3 and SR3 each bound to GST-SR5-6 ( Fig. 2D,F), but SR2 did not (  Fig. 2E), suggesting that SR3 is sufficient to bind SR5-6.	bind
32934	1	7931	5	13	NULL	NULL	NULL	HIRA	GP	35S-labeled	bind					GST-HIRIP5	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1517_3_376_s_66	11342215	35S-labelled HIRA (arrow) binds GST-HIRIP5 but not GST immobilized on glutathione beads.	bind
32935	2	7931	5	13	NULL	NULL	NULL	HIRA	GP	35S-labeled	does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1517_3_376_s_66	11342215	35S-labelled HIRA (arrow) binds GST-HIRIP5 but not GST immobilized on glutathione beads.	bind
25368	1	7931	6	NULL	NULL	0	NULL	HIRA	NULL	35S-labeled	bind	NULL				GST-HIRIP5	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1517_3_376_s_66	11342215	35S-labelled HIRA (arrow) binds GST-HIRIP5 but not GST immobilized on glutathione beads.	bind
25369	2	7931	6	NULL	NULL	0	NULL	HIRA	NULL	35S-labeled	does not bind	NULL				GST	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1517_3_376_s_66	11342215	35S-labelled HIRA (arrow) binds GST-HIRIP5 but not GST immobilized on glutathione beads.	bind
32936	1	7933	5	13	NULL	NULL	NULL	IB1	GP	35S-radiolabeled;;full-length	bind					IB1	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_50	16456539	35S-radiolabeled full-length IB1 was found to bind to the SH3 domains of IB1 and to  a weaker extent to that of IB2, but neither to GST alone nor to the GAP or Grb2 SH3  domains ( Figure 2A).	bind
32937	2	7933	5	13	NULL	NULL	NULL	IB1	GP	35S-radiolabeled;;full-length	bind		weakly			IB2	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_50	16456539	35S-radiolabeled full-length IB1 was found to bind to the SH3 domains of IB1 and to  a weaker extent to that of IB2, but neither to GST alone nor to the GAP or Grb2 SH3  domains ( Figure 2A).	bind
32938	3	7933	5	13	NULL	NULL	NULL	IB1	GP	35S-radiolabeled;;full-length	does not bind					GST	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_50	16456539	35S-radiolabeled full-length IB1 was found to bind to the SH3 domains of IB1 and to  a weaker extent to that of IB2, but neither to GST alone nor to the GAP or Grb2 SH3  domains ( Figure 2A).	bind
32939	4	7933	5	13	NULL	NULL	NULL	IB1	GP	35S-radiolabeled;;full-length	does not bind					GAP	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_50	16456539	35S-radiolabeled full-length IB1 was found to bind to the SH3 domains of IB1 and to  a weaker extent to that of IB2, but neither to GST alone nor to the GAP or Grb2 SH3  domains ( Figure 2A).	bind
32940	5	7933	5	13	NULL	NULL	NULL	IB1	GP	35S-radiolabeled;;full-length	does not bind					Grb2	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_50	16456539	35S-radiolabeled full-length IB1 was found to bind to the SH3 domains of IB1 and to  a weaker extent to that of IB2, but neither to GST alone nor to the GAP or Grb2 SH3  domains ( Figure 2A).	bind
25370	1	7933	6	10	NULL	0	NULL	IB1	NULL	35S-radiolabeled;;full-length 	bind	NULL				IB1	NULL		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_50	16456539	35S-radiolabeled full-length IB1 was found to bind to the SH3 domains of IB1 and to  a weaker extent to that of IB2, but neither to GST alone nor to the GAP or Grb2 SH3  domains ( Figure 2A).	bind
25371	2	7933	6	10	NULL	0	NULL	IB1	NULL	35S-radiolabeled;;full-length 	bind	NULL	weakly			IB2	NULL		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_50	16456539	35S-radiolabeled full-length IB1 was found to bind to the SH3 domains of IB1 and to  a weaker extent to that of IB2, but neither to GST alone nor to the GAP or Grb2 SH3  domains ( Figure 2A).	bind
25372	3	7933	6	10	NULL	0	NULL	IB1	NULL	35S-radiolabeled;;full-length 	does not bind	NULL				GAP	NULL		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_50	16456539	35S-radiolabeled full-length IB1 was found to bind to the SH3 domains of IB1 and to  a weaker extent to that of IB2, but neither to GST alone nor to the GAP or Grb2 SH3  domains ( Figure 2A).	bind
25373	4	7933	6	10	NULL	0	NULL	IB1	NULL	35S-radiolabeled;;full-length 	does not bind	NULL				Grb2	NULL		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_4_785_s_50	16456539	35S-radiolabeled full-length IB1 was found to bind to the SH3 domains of IB1 and to  a weaker extent to that of IB2, but neither to GST alone nor to the GAP or Grb2 SH3  domains ( Figure 2A).	bind
32941	2	7934	5	13	NULL	NULL	NULL	35S-Stbm	GP		defines			CtermdeltaC2					85 amino acids region		NULL		NULL	NULL	NULL	NULL	gw70_development_131_18_4467_s_247	15306567	35S-Stbm CtermdeltaN2 and 35S-Stbm CtermdeltaC2 define a region of 85 amino acids required for binding of Stbm to Dgo.	bind
32942	3	7934	5	13	NULL	NULL	NULL	Stbm	GP		bind					Dgo	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_131_18_4467_s_247	15306567	35S-Stbm CtermdeltaN2 and 35S-Stbm CtermdeltaC2 define a region of 85 amino acids required for binding of Stbm to Dgo.	bind
32943	4	7934	5	13	NULL	NULL	NULL	statement 1	Process		is required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_131_18_4467_s_247	15306567	35S-Stbm CtermdeltaN2 and 35S-Stbm CtermdeltaC2 define a region of 85 amino acids required for binding of Stbm to Dgo.	bind
32944	1	7934	5	13	NULL	NULL	NULL	35S-Stbm	GP		defines			CtermdeltaN2					85 amino acids region		NULL		NULL	NULL	NULL	NULL	gw70_development_131_18_4467_s_247	15306567	35S-Stbm CtermdeltaN2 and 35S-Stbm CtermdeltaC2 define a region of 85 amino acids required for binding of Stbm to Dgo.	bind
47825	5	7934	5	13	NULL	NULL	NULL	statement 2	Process		is required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_131_18_4467_s_247	15306567	35S-Stbm CtermdeltaN2 and 35S-Stbm CtermdeltaC2 define a region of 85 amino acids required for binding of Stbm to Dgo.	bind
25742	1	7934	6	NULL	NULL	0	NULL	Stbm	NULL		bind	NULL				Dgo	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_18_4467_s_247	15306567	35S-Stbm CtermdeltaN2 and 35S-Stbm CtermdeltaC2 define a region of 85 amino acids required for binding of Stbm to Dgo.	bind
25743	2	7934	6	NULL	NULL	0	NULL	Stbm	NULL		is required for	NULL		CtermdeltaN2		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_18_4467_s_247	15306567	35S-Stbm CtermdeltaN2 and 35S-Stbm CtermdeltaC2 define a region of 85 amino acids required for binding of Stbm to Dgo.	bind
25744	3	7934	6	NULL	NULL	0	NULL	Stbm	NULL		is required for	NULL		CtermdeltaC2		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_18_4467_s_247	15306567	35S-Stbm CtermdeltaN2 and 35S-Stbm CtermdeltaC2 define a region of 85 amino acids required for binding of Stbm to Dgo.	bind
47826	4	7934	6	10	NULL	0	NULL	35S-Stbm	NULL		defines	NULL		CtermdeltaC2		85 amino acid region	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_18_4467_s_247	15306567	35S-Stbm CtermdeltaN2 and 35S-Stbm CtermdeltaC2 define a region of 85 amino acids required for binding of Stbm to Dgo.	bind
47827	5	7934	6	10	NULL	0	NULL	35S-Stbm	NULL		defines	NULL		CtermdeltaN2		85 amino acid region	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_18_4467_s_247	15306567	35S-Stbm CtermdeltaN2 and 35S-Stbm CtermdeltaC2 define a region of 85 amino acids required for binding of Stbm to Dgo.	bind
32945	1	7936	5	13	NULL	NULL	NULL	Zinc(II) ions	Chemical		interacts with		selectively			5S-RNA gene	GP	Xenopus		DNA sequences at TFIIIA binding site	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2772_s_381	11433022	36       Martinez-Balbas,M.A., Jimenez-Garcia,E. and Azorin,F. (1995) Zinc(II) ions selectively interact with DNA sequences present at the TFIIIA binding site of the  Xenopus 5S-RNA gene.	bind
25494	1	7936	6	NULL	NULL	0	NULL	Zinc(II) ions	NULL		interact with	NULL	selectively			5S-RNA gene	NULL	Xenopus		TFIIIA binding site 	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2772_s_381	11433022	36       Martinez-Balbas,M.A., Jimenez-Garcia,E. and Azorin,F. (1995) Zinc(II) ions selectively interact with DNA sequences present at the TFIIIA binding site of the  Xenopus 5S-RNA gene.	bind
32946	1	7937	5	13	NULL	NULL	NULL	c-myb proto-oncogene product	GP		bind									simian virus 40 enhancer	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3546_s_453	11522824	36       Nakagoshi,H., Nagase,T., Kanei-Ishii,C., Ueno,Y. and Ishii,S. (1990) Binding of the c-myb proto-oncogene product to the simian virus 40 enhancer stimulates transcription.	bind
32947	2	7937	5	13	NULL	NULL	NULL	statement 1	Process		stimulates					transcription	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3546_s_453	11522824	36       Nakagoshi,H., Nagase,T., Kanei-Ishii,C., Ueno,Y. and Ishii,S. (1990) Binding of the c-myb proto-oncogene product to the simian virus 40 enhancer stimulates transcription.	bind
25495	1	7937	6	NULL	NULL	0	NULL	c-myb proto-oncogene	NULL		bind	NULL					NULL			simian virus 40 enhancer	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3546_s_453	11522824	36       Nakagoshi,H., Nagase,T., Kanei-Ishii,C., Ueno,Y. and Ishii,S. (1990) Binding of the c-myb proto-oncogene product to the simian virus 40 enhancer stimulates transcription.	bind
25497	2	7937	6	NULL	NULL	0	NULL	statement 1	NULL		stimulates	NULL				transcription	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3546_s_453	11522824	36       Nakagoshi,H., Nagase,T., Kanei-Ishii,C., Ueno,Y. and Ishii,S. (1990) Binding of the c-myb proto-oncogene product to the simian virus 40 enhancer stimulates transcription.	bind
32948	1	7938	5	13	NULL	NULL	NULL	Poly (rC) binding protein 2	GP		forms ternary complex with					poliovirus RNA	NucleicAcid			5''-terminal sequences	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2715_s_499	11433016	36       Parsley,T.B., Towner,J.S., Blyn,L.B., Ehrenfeld,E. and Semler,B.L. (1997) Poly (rC) binding protein 2 forms a ternary complex with the 5''-terminal sequences of poliovirus RNA and the viral 3CD proteinase.	bind
32949	2	7938	5	13	NULL	NULL	NULL	Poly (rC) binding protein 2	GP		forms ternary complex with					3CD proteinase	GP	viral			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2715_s_499	11433016	36       Parsley,T.B., Towner,J.S., Blyn,L.B., Ehrenfeld,E. and Semler,B.L. (1997) Poly (rC) binding protein 2 forms a ternary complex with the 5''-terminal sequences of poliovirus RNA and the viral 3CD proteinase.	bind
37891	3	7938	5	13	NULL	NULL	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2715_s_499	11433016	36       Parsley,T.B., Towner,J.S., Blyn,L.B., Ehrenfeld,E. and Semler,B.L. (1997) Poly (rC) binding protein 2 forms a ternary complex with the 5''-terminal sequences of poliovirus RNA and the viral 3CD proteinase.	bind
25740	1	7938	6	NULL	NULL	0	NULL	Poly (rC) binding protein 2	NULL		forms ternary complex with	NULL				poliovirus RNA	NULL			5''-terminal sequences	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2715_s_499	11433016	36       Parsley,T.B., Towner,J.S., Blyn,L.B., Ehrenfeld,E. and Semler,B.L. (1997) Poly (rC) binding protein 2 forms a ternary complex with the 5''-terminal sequences of poliovirus RNA and the viral 3CD proteinase.	bind
25741	2	7938	6	NULL	NULL	0	NULL	Poly (rC) binding protein 2	NULL		forms a ternary complex with	NULL				3CD proteinase	NULL	viral			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2715_s_499	11433016	36       Parsley,T.B., Towner,J.S., Blyn,L.B., Ehrenfeld,E. and Semler,B.L. (1997) Poly (rC) binding protein 2 forms a ternary complex with the 5''-terminal sequences of poliovirus RNA and the viral 3CD proteinase.	bind
37880	3	7938	6	NULL	NULL	0	NULL	statement 1	NULL		occurs simultaneously with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2715_s_499	11433016	36       Parsley,T.B., Towner,J.S., Blyn,L.B., Ehrenfeld,E. and Semler,B.L. (1997) Poly (rC) binding protein 2 forms a ternary complex with the 5''-terminal sequences of poliovirus RNA and the viral 3CD proteinase.	bind
32950	1	7939	5	13	NULL	NULL	NULL	Cu2+	Chemical		bind					LDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3338_s_54	9409331	36  37  To investigate the possible role of histidine residues in the binding of Cu2+ to LDL and the resulting peroxidation of LDL lipid, we used DEPC to modify this amino acid.	bind
32953	2	7939	5	13	NULL	NULL	NULL	histidine residues	AminoAcid		plays a role in		possibly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3338_s_54	9409331	36  37  To investigate the possible role of histidine residues in the binding of Cu2+ to LDL and the resulting peroxidation of LDL lipid, we used DEPC to modify this amino acid.	bind
32954	3	7939	5	13	NULL	NULL	NULL	statement 2	Process		results in					LDL lipid	Chemical	peroxidation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3338_s_54	9409331	36  37  To investigate the possible role of histidine residues in the binding of Cu2+ to LDL and the resulting peroxidation of LDL lipid, we used DEPC to modify this amino acid.	bind
25498	1	7939	6	NULL	NULL	0	NULL	Cu2+	NULL		bind	NULL				LDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3338_s_54	9409331	36  37  To investigate the possible role of histidine residues in the binding of Cu2+ to LDL and the resulting peroxidation of LDL lipid, we used DEPC to modify this amino acid.	bind
37311	2	7939	6	NULL	NULL	0	NULL	histidine residues	NULL		plays a role in	NULL	possibly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3338_s_54	9409331	36  37  To investigate the possible role of histidine residues in the binding of Cu2+ to LDL and the resulting peroxidation of LDL lipid, we used DEPC to modify this amino acid.	bind
37312	3	7939	6	NULL	NULL	0	NULL	statement 2	NULL		results in	NULL				LDL lipid	NULL	peroxidation of 			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_3338_s_54	9409331	36  37  To investigate the possible role of histidine residues in the binding of Cu2+ to LDL and the resulting peroxidation of LDL lipid, we used DEPC to modify this amino acid.	bind
32955	1	7940	5	13	NULL	NULL	NULL	bFGF	GP	active	bind					HS	Chemical				NULL	lumenal surface of blood vessels	NULL	NULL	NULL	NULL	gw60_circulation_95_7_1853_s_234	9107173	36  41 42  The present study raises the possibility that in spite of its antiproliferative effect, heparin may also exert an undesirable effect, ie, displacement of active bFGF that is normally bound to HS on the lumenal surface of blood vessels.	bind
32956	2	7940	5	13	NULL	NULL	NULL	heparin	Chemical		displace					bFGF	GP	active			NULL	lumenal surface of blood vessels	NULL	NULL	NULL	NULL	gw60_circulation_95_7_1853_s_234	9107173	36  41 42  The present study raises the possibility that in spite of its antiproliferative effect, heparin may also exert an undesirable effect, ie, displacement of active bFGF that is normally bound to HS on the lumenal surface of blood vessels.	bind
25510	1	7940	6	NULL	NULL	0	NULL	bFGF	NULL	active	bind	NULL	normally			HS	NULL				NULL	lumenal surface of blood vessels	NULL	NULL	NULL	NULL	gw60_circulation_95_7_1853_s_234	9107173	36  41 42  The present study raises the possibility that in spite of its antiproliferative effect, heparin may also exert an undesirable effect, ie, displacement of active bFGF that is normally bound to HS on the lumenal surface of blood vessels.	bind
25511	2	7940	6	NULL	NULL	0	NULL	heparin	NULL		displaces	NULL				bFGF	NULL	active			NULL	lumenal surface of blood vessels	NULL	NULL	NULL	NULL	gw60_circulation_95_7_1853_s_234	9107173	36  41 42  The present study raises the possibility that in spite of its antiproliferative effect, heparin may also exert an undesirable effect, ie, displacement of active bFGF that is normally bound to HS on the lumenal surface of blood vessels.	bind
32957	1	7941	5	13	NULL	NULL	NULL	SRF	GP		bind									A/T-rich DNA sequence	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_2_188_s_193	8575061	36  SRF binds an A/T-rich DNA sequence, referred to as the serum response element, or CArG box.	bind
32958	2	7941	5	13	NULL	NULL	NULL	A/T-rich DNA sequence	NucleicAcid		referred to as					serum response element	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_2_188_s_193	8575061	36  SRF binds an A/T-rich DNA sequence, referred to as the serum response element, or CArG box.	bind
32959	3	7941	5	13	NULL	NULL	NULL	A/T-rich DNA sequence	NucleicAcid		referred to as					CArG box	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_2_188_s_193	8575061	36  SRF binds an A/T-rich DNA sequence, referred to as the serum response element, or CArG box.	bind
32960	4	7941	5	13	NULL	NULL	NULL	statement 2	Process		is alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_2_188_s_193	8575061	36  SRF binds an A/T-rich DNA sequence, referred to as the serum response element, or CArG box.	bind
25512	1	7941	6	10	NULL	0	NULL	A/T-rich DNA sequence	NULL		referred as	NULL				serum response element	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_2_188_s_193	8575061	36  SRF binds an A/T-rich DNA sequence, referred to as the serum response element, or CArG box.	bind
25513	2	7941	6	NULL	NULL	0	NULL	SRF	NULL		bind	NULL					NULL			A/T-rich DNA sequence	NULL		0	NULL	NULL	NULL	gw60_circulationres_78_2_188_s_193	8575061	36  SRF binds an A/T-rich DNA sequence, referred to as the serum response element, or CArG box.	bind
47828	3	7941	6	10	NULL	0	NULL	A/T-rich DNA sequence	NULL		referred as	NULL				CArG box	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_2_188_s_193	8575061	36  SRF binds an A/T-rich DNA sequence, referred to as the serum response element, or CArG box.	bind
47830	4	7941	6	10	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_2_188_s_193	8575061	36  SRF binds an A/T-rich DNA sequence, referred to as the serum response element, or CArG box.	bind
32961	1	7942	5	13	NULL	NULL	NULL	platelet glycoprotein Ia/IIa	GP		bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
32962	2	7942	5	13	NULL	NULL	NULL	glycoprotein IIb/IIa	GP		bind					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
32963	3	7942	5	13	NULL	NULL	NULL	statement 1	Process		is dependent on					integrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
32964	4	7942	5	13	NULL	NULL	NULL	statement 2	Process		is dependent on					integrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
32965	5	7942	5	13	NULL	NULL	NULL	statement 1	Process		results in					shape	Process	change of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
32966	6	7942	5	13	NULL	NULL	NULL	statement 1	Process		results in					granule contents	Process	release of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
32967	7	7942	5	13	NULL	NULL	NULL	statement 1	Process		results in					aggregation	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
32968	8	7942	5	13	NULL	NULL	NULL	statement 5	Process		leads to					thrombus	Process	growth of			NULL	at the sites of arterial injury	NULL	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
32969	9	7942	5	13	NULL	NULL	NULL	statement 6	Process		leads to					thrombus	Process	growth of			NULL	at the sites of arterial injury	NULL	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
32970	10	7942	5	13	NULL	NULL	NULL	statement 7	Process		leads to					thrombus	Process	growth of			NULL	at the sites of arterial injury	NULL	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
32971	11	7942	5	13	NULL	NULL	NULL	statement 2	Process		results in					shape	Process	change of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
32972	12	7942	5	13	NULL	NULL	NULL	statement 2	Process		results in					granule contents	Process	release of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
32974	14	7942	5	13	NULL	NULL	NULL	statement 11	Process		leads to					thrombus	Process	growth of			NULL	at the sites of arterial injury	NULL	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
32975	15	7942	5	13	NULL	NULL	NULL	statement 12	Process		leads to					thrombus	Process	growth of			NULL	at the sites of arterial injury	NULL	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
32976	16	7942	5	13	NULL	NULL	NULL	statement 13	Process		leads to					thrombus	Process	growth of			NULL	at the sites of arterial injury	NULL	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
25728	1	7942	6	NULL	NULL	0	NULL	platelet glycoprotein Ia/IIa	NULL		bind	NULL				collagen	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
25729	2	7942	6	NULL	NULL	0	NULL	glycoprotein IIb/IIa	NULL		bind	NULL				fibrinogen	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
25730	3	7942	6	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				integrin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
25731	4	7942	6	NULL	NULL	0	NULL	statement 2	NULL		is dependent on	NULL				integrin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
25732	5	7942	6	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				shape change	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
25733	6	7942	6	NULL	NULL	0	NULL	statement 2	NULL		results in	NULL				shape change	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
25734	7	7942	6	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				granule contents	NULL	release of			NULL		0	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
25735	8	7942	6	NULL	NULL	0	NULL	statement 2	NULL		results in	NULL				granule contents	NULL	release of			NULL		0	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
25736	9	7942	6	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				platelet aggregation	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
25737	10	7942	6	NULL	NULL	0	NULL	statement 2	NULL		results in	NULL				platelet aggregation	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
25738	11	7942	6	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				thrombus	NULL	growth of			NULL	sites of arterial injury	0	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
25739	12	7942	6	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				thrombus	NULL	growth of			NULL	sites of arterial injury	0	NULL	NULL	NULL	gw60_circulation_103_8_1128_s_141	11222477	36  The reactions of platelets are mostly integrin-dependent, involving the binding of platelet glycoprotein Ia/IIa to collagen and glycoprotein IIb/IIa to fibrinogen, which results in shape change, release of granule contents, and aggregation, leading to thrombus growth at the sites of arterial injury.	bind
32977	1	7943	5	13	NULL	NULL	NULL	mAbs OB/04	GP		bind					oxLDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_5_704_s_144	7749884	36  We studied a possible cross-reactivity of the mAbs with acetylated LDL (REM, 3.3), comparing it with oxLDL (REM, 3.2; modified apoB, 40%) in preventing the binding of mAbs OB/04 and OB/09 to oxLDL in the wells at competitor concentrations from 0.01 mug/mL to 1 mg/mL.	bind
32978	2	7943	5	13	NULL	NULL	NULL	mAbs OB/09	GP		bind					oxLDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_5_704_s_144	7749884	36  We studied a possible cross-reactivity of the mAbs with acetylated LDL (REM, 3.3), comparing it with oxLDL (REM, 3.2; modified apoB, 40%) in preventing the binding of mAbs OB/04 and OB/09 to oxLDL in the wells at competitor concentrations from 0.01 mug/mL to 1 mg/mL.	bind
25514	1	7943	6	NULL	NULL	0	NULL	mAb OB/04	NULL		bind	NULL				OxLDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_5_704_s_144	7749884	36  We studied a possible cross-reactivity of the mAbs with acetylated LDL (REM, 3.3), comparing it with oxLDL (REM, 3.2; modified apoB, 40%) in preventing the binding of mAbs OB/04 and OB/09 to oxLDL in the wells at competitor concentrations from 0.01 mug/mL to 1 mg/mL.	bind
25515	2	7943	6	NULL	NULL	0	NULL	mAb OB/09	NULL		bind	NULL				oxLDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_5_704_s_144	7749884	36  We studied a possible cross-reactivity of the mAbs with acetylated LDL (REM, 3.3), comparing it with oxLDL (REM, 3.2; modified apoB, 40%) in preventing the binding of mAbs OB/04 and OB/09 to oxLDL in the wells at competitor concentrations from 0.01 mug/mL to 1 mg/mL.	bind
33048	1	7944	5	13	NULL	NULL	NULL	Sp1	GP		bind					LDL receptor gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_8_1248_s_214	7627719	36 37  Alternatively, we cannot rule out the possibility that cell cycle - specific cofactors are required for the enhancement of binding of Sp1 to the LDL receptor gene after PDGF stimulation.	bind
33049	2	7944	5	13	NULL	NULL	NULL	statement 1	Process		occurs after					PDGF	GP	stimulation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_8_1248_s_214	7627719	36 37  Alternatively, we cannot rule out the possibility that cell cycle - specific cofactors are required for the enhancement of binding of Sp1 to the LDL receptor gene after PDGF stimulation.	bind
33050	3	7944	5	13	NULL	NULL	NULL	cofactors	Chemical	cell cycle - specific 	is required for					statement 1	Process	enhancement of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_8_1248_s_214	7627719	36 37  Alternatively, we cannot rule out the possibility that cell cycle - specific cofactors are required for the enhancement of binding of Sp1 to the LDL receptor gene after PDGF stimulation.	bind
25524	2	7944	6	NULL	NULL	0	NULL	statement 1	NULL		occurs after	NULL				PDGF	NULL	stimulation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_8_1248_s_214	7627719	36 37  Alternatively, we cannot rule out the possibility that cell cycle - specific cofactors are required for the enhancement of binding of Sp1 to the LDL receptor gene after PDGF stimulation.	bind
25526	3	7944	6	NULL	NULL	0	NULL	cofactors	NULL	cell cycle specific	are required for	NULL				statement 1	NULL	enhancement of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_8_1248_s_214	7627719	36 37  Alternatively, we cannot rule out the possibility that cell cycle - specific cofactors are required for the enhancement of binding of Sp1 to the LDL receptor gene after PDGF stimulation.	bind
25535	1	7944	6	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				LDL receptor gene	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_8_1248_s_214	7627719	36 37  Alternatively, we cannot rule out the possibility that cell cycle - specific cofactors are required for the enhancement of binding of Sp1 to the LDL receptor gene after PDGF stimulation.	bind
33051	1	7945	5	13	NULL	NULL	NULL	LDL	GP		bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_134	7867176	36 37  In this respect, it is interesting that the binding of LDL to collagen may induce conformational changes in apo B that facilitate its binding to collagen-like domains of the scavenger receptor.	bind
33052	2	7945	5	13	NULL	NULL	NULL	statement 1	Process		induces		may			apo B	GP	conformational changes in			NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_134	7867176	36 37  In this respect, it is interesting that the binding of LDL to collagen may induce conformational changes in apo B that facilitate its binding to collagen-like domains of the scavenger receptor.	bind
33053	3	7945	5	13	NULL	NULL	NULL	apo B	GP		bind					scavenger receptor	GP		collagen-like domains		NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_134	7867176	36 37  In this respect, it is interesting that the binding of LDL to collagen may induce conformational changes in apo B that facilitate its binding to collagen-like domains of the scavenger receptor.	bind
36177	4	7945	5	13	NULL	NULL	NULL	statement 2	Process		facilitates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_134	7867176	36 37  In this respect, it is interesting that the binding of LDL to collagen may induce conformational changes in apo B that facilitate its binding to collagen-like domains of the scavenger receptor.	bind
25536	1	7945	6	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				collagen	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_134	7867176	36 37  In this respect, it is interesting that the binding of LDL to collagen may induce conformational changes in apo B that facilitate its binding to collagen-like domains of the scavenger receptor.	bind
25537	2	7945	6	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL	may			apo B	NULL	conformational change in			NULL		0	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_134	7867176	36 37  In this respect, it is interesting that the binding of LDL to collagen may induce conformational changes in apo B that facilitate its binding to collagen-like domains of the scavenger receptor.	bind
25538	3	7945	6	NULL	NULL	0	NULL	apo B	NULL		bind	NULL				scavenger receptor	NULL		collagen-like domain		NULL		0	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_134	7867176	36 37  In this respect, it is interesting that the binding of LDL to collagen may induce conformational changes in apo B that facilitate its binding to collagen-like domains of the scavenger receptor.	bind
25539	4	7945	6	NULL	NULL	0	NULL	statement 2	NULL		facilitates	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_134	7867176	36 37  In this respect, it is interesting that the binding of LDL to collagen may induce conformational changes in apo B that facilitate its binding to collagen-like domains of the scavenger receptor.	bind
33054	1	7946	5	13	NULL	NULL	NULL	oligonucleotides	NucleicAcid		bind		potentially		four sequential guanosines	bFGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
33055	2	7946	5	13	NULL	NULL	NULL	bFGF	GP		is a type of					growth factors	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
33056	3	7946	5	13	NULL	NULL	NULL	bFGF	GP		is a type of					serum protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
33057	4	7946	5	13	NULL	NULL	NULL	oligonucleotides	NucleicAcid		bind		potentially		four sequential guanosines	PDGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
33058	5	7946	5	13	NULL	NULL	NULL	PDGF	GP		is a type of					acidic fibroblast growth factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
33059	6	7946	5	13	NULL	NULL	NULL	PDGF	GP		is a type of					serum protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
33060	7	7946	5	13	NULL	NULL	NULL	oligonucleotides	NucleicAcid		bind		potentially		four sequential guanosines	vascular endothelial growth factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
33061	8	7946	5	13	NULL	NULL	NULL	bFGF	GP		interacts with					receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
33062	9	7946	5	13	NULL	NULL	NULL	statement 1	Process		reduces					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
33063	10	7946	5	13	NULL	NULL	NULL	PDGF	GP		interacts with					receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
33064	11	7946	5	13	NULL	NULL	NULL	statement 4	Process		reduces					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
33065	12	7946	5	13	NULL	NULL	NULL	vascular endothelial growth factor	GP		interacts with					receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
33066	13	7946	5	13	NULL	NULL	NULL	statement 7	Process		reduces					statement 12	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
33069	14	7946	5	13	NULL	NULL	NULL	c- myc	GP		is involved in					cell-cycle 	Process	progression of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
33070	15	7946	5	13	NULL	NULL	NULL	c- myb	GP		is involved in					cell-cycle	Process	progression of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
25723	1	7946	6	NULL	NULL	0	NULL	oligonucleotides with four sequential guanosines	NULL		bind	NULL	may			bFGF	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
25724	2	7946	6	NULL	NULL	0	NULL	oligonucleotides with four sequential guanosines	NULL		bind	NULL	may			acidic fibroblast growth factor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
25725	3	7946	6	NULL	NULL	0	NULL	oligonucleotides with four sequential guanosines	NULL		bind	NULL	may			vascular endothelial growth factor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
25726	4	7946	6	NULL	NULL	0	NULL	oligonucleotides with four sequential guanosines	NULL		bind	NULL	may			PDGF	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
25727	5	7946	6	NULL	NULL	0	NULL	bFGF	NULL		is a type of	NULL				growth factor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
26089	6	7946	6	NULL	NULL	0	NULL	PDGF	NULL		is a type of	NULL				growth factor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_95_3_669_s_176	9024156	36 37  It was hypothesized that oligonucleotides with four sequential guanosines might bind to serum proteins, including growth factors such as bFGF, acidic fibroblast growth factor, PDGF, and vascular endothelial growth factor, reducing the interaction of these growth factors with their receptors and the intracellular signal transduction leading to gene protein expression (such as c- myc and c- myb) involved in cell-cycle progression.	bind
33898	1	7947	5	13	NULL	NULL	NULL	apoE	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_244	9012650	36 37  Thus, eliminating only one of the positive charges in the LDL receptor - binding segment of apoE may reduce the affinity of apoE (dimer) in VLDL or a liposome to the level of affinity of apoB-100 in LDL for the LDL receptor.	bind
33902	3	7947	5	13	NULL	NULL	NULL	statement 2	Process		reduce		may			apoE (dimer)	GP	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_244	9012650	36 37  Thus, eliminating only one of the positive charges in the LDL receptor - binding segment of apoE may reduce the affinity of apoE (dimer) in VLDL or a liposome to the level of affinity of apoB-100 in LDL for the LDL receptor.	bind
33904	4	7947	5	13	NULL	NULL	NULL	apoB-100	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_244	9012650	36 37  Thus, eliminating only one of the positive charges in the LDL receptor - binding segment of apoE may reduce the affinity of apoE (dimer) in VLDL or a liposome to the level of affinity of apoB-100 in LDL for the LDL receptor.	bind
36176	2	7947	5	13	NULL	NULL	NULL	one positive charge	Chemical		is eliminated from					apoE	GP		LDL receptor - binding segment		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_244	9012650	36 37  Thus, eliminating only one of the positive charges in the LDL receptor - binding segment of apoE may reduce the affinity of apoE (dimer) in VLDL or a liposome to the level of affinity of apoB-100 in LDL for the LDL receptor.	bind
25718	1	7947	6	NULL	NULL	0	NULL	apoE (dimer)	NULL		bind	NULL				VLDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_244	9012650	36 37  Thus, eliminating only one of the positive charges in the LDL receptor - binding segment of apoE may reduce the affinity of apoE (dimer) in VLDL or a liposome to the level of affinity of apoB-100 in LDL for the LDL receptor.	bind
25722	2	7947	6	NULL	NULL	0	NULL	apoE	NULL	elimination of	reduces	NULL		LDL receptor - binding segment		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_244	9012650	36 37  Thus, eliminating only one of the positive charges in the LDL receptor - binding segment of apoE may reduce the affinity of apoE (dimer) in VLDL or a liposome to the level of affinity of apoB-100 in LDL for the LDL receptor.	bind
33077	1	7948	5	13	NULL	NULL	NULL	ROS	Chemical		is generated during					strain					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_44	10205148	36 37 38 39  We also illustrated that strain-induced MCP-1 expression was a result of increased activator protein-1 binding by ROS generated during strain.	bind
33078	2	7948	5	13	NULL	NULL	NULL	statement 1	Chemical		bind					activator protein-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_44	10205148	36 37 38 39  We also illustrated that strain-induced MCP-1 expression was a result of increased activator protein-1 binding by ROS generated during strain.	bind
33079	4	7948	5	13	NULL	NULL	NULL	statement 2	Process	increase in	results in					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_44	10205148	36 37 38 39  We also illustrated that strain-induced MCP-1 expression was a result of increased activator protein-1 binding by ROS generated during strain.	bind
33080	3	7948	5	13	NULL	NULL	NULL	strain			induces					MCP-1	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_44	10205148	36 37 38 39  We also illustrated that strain-induced MCP-1 expression was a result of increased activator protein-1 binding by ROS generated during strain.	bind
25540	1	7948	6	NULL	NULL	0	NULL	strain	NULL		induces	NULL				MCP-1	NULL	expression of			NULL		0	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_44	10205148	36 37 38 39  We also illustrated that strain-induced MCP-1 expression was a result of increased activator protein-1 binding by ROS generated during strain.	bind
25542	2	7948	6	NULL	NULL	0	NULL	activator protein-1 	NULL		bind	NULL				ROS	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_44	10205148	36 37 38 39  We also illustrated that strain-induced MCP-1 expression was a result of increased activator protein-1 binding by ROS generated during strain.	bind
25544	3	7948	6	NULL	NULL	0	NULL	ROS	NULL		is generated during	NULL				strain	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_44	10205148	36 37 38 39  We also illustrated that strain-induced MCP-1 expression was a result of increased activator protein-1 binding by ROS generated during strain.	bind
37313	4	7948	6	NULL	NULL	0	NULL	statement 2	NULL		occurs by	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_44	10205148	36 37 38 39  We also illustrated that strain-induced MCP-1 expression was a result of increased activator protein-1 binding by ROS generated during strain.	bind
33081	1	7949	5	13	NULL	NULL	NULL	importin	GP		bind								NLS		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_35_22134_s_123	9268357	36 and  42), that the initial events of nuclear transport, and NLS-binding by importin in particular, are critical in determining overall nuclear protein import kinetics.	bind
33082	2	7949	5	13	NULL	NULL	NULL	statement 1	Process		determines					nuclear protein import kinetics	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_35_22134_s_123	9268357	36 and  42), that the initial events of nuclear transport, and NLS-binding by importin in particular, are critical in determining overall nuclear protein import kinetics.	bind
33083	3	7949	5	13	NULL	NULL	NULL	statement 1	Process		is initial event of					nuclear transport	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_35_22134_s_123	9268357	36 and  42), that the initial events of nuclear transport, and NLS-binding by importin in particular, are critical in determining overall nuclear protein import kinetics.	bind
25545	1	7949	6	NULL	NULL	0	NULL	NLS	NULL		bind	NULL				importin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_35_22134_s_123	9268357	36 and  42), that the initial events of nuclear transport, and NLS-binding by importin in particular, are critical in determining overall nuclear protein import kinetics.	bind
33151	1	7950	5	13	NULL	NULL	NULL	36 peptide antibody	GP		is directed to					alpha3(IV)NC1	GP		last 36 residues containing COOH-terminal epitope		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_20027_s_100	10748075	36 peptide antibody directed to the last 36 residues containing the COOH-terminal epitope in the alpha3(IV)NC1 bound equally well to the NC1 hexamer and the control antibody, demonstrating that all epitopes were now exposed for binding.	bind
33162	2	7950	5	13	NULL	NULL	NULL	36 peptide antibody	GP		bind					NC1 hexamer	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_20027_s_100	10748075	36 peptide antibody directed to the last 36 residues containing the COOH-terminal epitope in the alpha3(IV)NC1 bound equally well to the NC1 hexamer and the control antibody, demonstrating that all epitopes were now exposed for binding.	bind
25695	2	7950	6	10	NULL	0	NULL	36 peptide antibody			bind					NC1 hexamer					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_20027_s_100	10748075	36 peptide antibody directed to the last 36 residues containing the COOH-terminal epitope in the alpha3(IV)NC1 bound equally well to the NC1 hexamer and the control antibody, demonstrating that all epitopes were now exposed for binding.	bind
25700	1	7950	6	10	NULL	0	NULL	36 peptide antibody			is directed to					alpha3(IV)NC1			last 36 residues containing COOH-terminal epitope		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_20027_s_100	10748075	36 peptide antibody directed to the last 36 residues containing the COOH-terminal epitope in the alpha3(IV)NC1 bound equally well to the NC1 hexamer and the control antibody, demonstrating that all epitopes were now exposed for binding.	bind
33084	1	7951	5	13	NULL	NULL	NULL	thrombin	GP		stimulates					VCAM-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_41_s_118	14551154	36 Similarly, thrombin stimulation of VCAM-1 involves the inducible binding of p65 NF-kappaB to a tandem NF-kappaB motif in the 5' flanking region.	bind
33085	2	7951	5	13	NULL	NULL	NULL	p65 NF-kappaB	GP		bind									tandem NF-kappaB motif in 5' flanking region	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_41_s_118	14551154	36 Similarly, thrombin stimulation of VCAM-1 involves the inducible binding of p65 NF-kappaB to a tandem NF-kappaB motif in the 5' flanking region.	bind
33086	3	7951	5	13	NULL	NULL	NULL	statement 1	Process		involves					statement 2	Process	inducible			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_41_s_118	14551154	36 Similarly, thrombin stimulation of VCAM-1 involves the inducible binding of p65 NF-kappaB to a tandem NF-kappaB motif in the 5' flanking region.	bind
25546	1	7951	6	NULL	NULL	0	NULL	p65 NF-kappaB	NULL		bind	NULL					NULL			tandem NF-kappaB motif in 5' flanking region	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_41_s_118	14551154	36 Similarly, thrombin stimulation of VCAM-1 involves the inducible binding of p65 NF-kappaB to a tandem NF-kappaB motif in the 5' flanking region.	bind
25547	2	7951	6	NULL	NULL	0	NULL	thrombin	NULL		stimulates	NULL				VCAM-1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_41_s_118	14551154	36 Similarly, thrombin stimulation of VCAM-1 involves the inducible binding of p65 NF-kappaB to a tandem NF-kappaB motif in the 5' flanking region.	bind
25548	3	7951	6	NULL	NULL	0	NULL	statement 2	NULL		induces	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_41_s_118	14551154	36 Similarly, thrombin stimulation of VCAM-1 involves the inducible binding of p65 NF-kappaB to a tandem NF-kappaB motif in the 5' flanking region.	bind
33169	1	7952	5	13	NULL	NULL	NULL	nuclear proteins	GP		bind									Egr-1 consensus DNA sequence	NULL	mouse macrophages	NULL	NULL	NULL	NULL	gw70_circulationres_94_3_333_s_170	14670837	36 When these concepts were probed in tissue culture, these investigators found that mouse macrophages displayed decreased lipopolysaccharide-induced binding of nuclear proteins to the Egr-1 consensus DNA sequence after pretreatment with simvastatin.	bind
33172	2	7952	5	13	NULL	NULL	NULL	lipopolysaccharide	Chemical		induces					statement 1	Process				NULL	mouse macrophages	NULL	NULL	NULL	NULL	gw70_circulationres_94_3_333_s_170	14670837	36 When these concepts were probed in tissue culture, these investigators found that mouse macrophages displayed decreased lipopolysaccharide-induced binding of nuclear proteins to the Egr-1 consensus DNA sequence after pretreatment with simvastatin.	bind
33174	3	7952	5	13	NULL	NULL	NULL	simvastatin	Chemical	pretreatment	decrease					statement 2	Process				NULL	mouse macrophages	NULL	NULL	NULL	NULL	gw70_circulationres_94_3_333_s_170	14670837	36 When these concepts were probed in tissue culture, these investigators found that mouse macrophages displayed decreased lipopolysaccharide-induced binding of nuclear proteins to the Egr-1 consensus DNA sequence after pretreatment with simvastatin.	bind
25549	1	7952	6	NULL	NULL	0	NULL	nuclear proteins	NULL		bind	NULL					NULL			Egr-1 consensus DNA sequence	NULL	mouse macrophages	NULL	NULL	NULL	NULL	gw70_circulationres_94_3_333_s_170	14670837	36 When these concepts were probed in tissue culture, these investigators found that mouse macrophages displayed decreased lipopolysaccharide-induced binding of nuclear proteins to the Egr-1 consensus DNA sequence after pretreatment with simvastatin.	bind
25550	2	7952	6	NULL	NULL	0	NULL	lipopolysaccharide	NULL		induces	NULL				statement 1	NULL				NULL	mouse macrophages	NULL	NULL	NULL	NULL	gw70_circulationres_94_3_333_s_170	14670837	36 When these concepts were probed in tissue culture, these investigators found that mouse macrophages displayed decreased lipopolysaccharide-induced binding of nuclear proteins to the Egr-1 consensus DNA sequence after pretreatment with simvastatin.	bind
25552	3	7952	6	NULL	NULL	0	NULL	simvastatin	NULL	pretreatment with	decreases	NULL				statement 2	NULL				NULL	mouse macrophages	NULL	NULL	NULL	NULL	gw70_circulationres_94_3_333_s_170	14670837	36 When these concepts were probed in tissue culture, these investigators found that mouse macrophages displayed decreased lipopolysaccharide-induced binding of nuclear proteins to the Egr-1 consensus DNA sequence after pretreatment with simvastatin.	bind
33175	1	7953	5	13	NULL	NULL	NULL	p47 phox	GP		bind			N-terminal SH3 domain		p22 phox	GP		proline-rich region		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_63	16514078	36,41,42   The p47 phox N-terminal SH3 domain then binds the proline-rich region in p22 phox 42,43  and the PX domain of p47 phox binds 3'phosphoinositides, the products of PI3K.	bind
33179	2	7953	5	13	NULL	NULL	NULL	p47 phox	GP		bind			PX domain		3'phosphoinositides	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_63	16514078	36,41,42   The p47 phox N-terminal SH3 domain then binds the proline-rich region in p22 phox 42,43  and the PX domain of p47 phox binds 3'phosphoinositides, the products of PI3K.	bind
33181	3	7953	5	13	NULL	NULL	NULL	3'phosphoinositides	Chemical		is a product of					PI3K	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_63	16514078	36,41,42   The p47 phox N-terminal SH3 domain then binds the proline-rich region in p22 phox 42,43  and the PX domain of p47 phox binds 3'phosphoinositides, the products of PI3K.	bind
25553	1	7953	6	NULL	NULL	0	NULL	p47 phox	NULL		bind	NULL		N-terminal SH3 domain		p22 phox	NULL		proline-rich region		NULL		0	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_63	16514078	36,41,42   The p47 phox N-terminal SH3 domain then binds the proline-rich region in p22 phox 42,43  and the PX domain of p47 phox binds 3'phosphoinositides, the products of PI3K.	bind
25554	2	7953	6	NULL	NULL	0	NULL	p47 phox	NULL		bind	NULL		PX domain		3' phosphoinositides	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_63	16514078	36,41,42   The p47 phox N-terminal SH3 domain then binds the proline-rich region in p22 phox 42,43  and the PX domain of p47 phox binds 3'phosphoinositides, the products of PI3K.	bind
25555	3	7953	6	NULL	NULL	0	NULL	3' phosphoinositides	NULL		are products of	NULL				PI3K	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_63	16514078	36,41,42   The p47 phox N-terminal SH3 domain then binds the proline-rich region in p22 phox 42,43  and the PX domain of p47 phox binds 3'phosphoinositides, the products of PI3K.	bind
33188	1	7954	5	13	NULL	NULL	NULL	unidentified protein	GP		bind							mice		Sp1 sites	NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_1129_s_166	11549606	36- [[ 38  This latter defect ]] is exemplified by the adenine phosphoribosyltransferase gene in mice, in which an unidentified protein that binds to the Sp1 sites seems to prevent methylation of the CpG island.	bind
33190	2	7954	5	13	NULL	NULL	NULL	statement 1	Process		prevents		may					methylation of		CpG island	NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_1129_s_166	11549606	36- [[ 38  This latter defect ]] is exemplified by the adenine phosphoribosyltransferase gene in mice, in which an unidentified protein that binds to the Sp1 sites seems to prevent methylation of the CpG island.	bind
25556	1	7954	6	NULL	NULL	0	NULL	unidentified protein	NULL		bind	NULL					NULL			Sp1 site	NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_1129_s_166	11549606	36- [[ 38  This latter defect ]] is exemplified by the adenine phosphoribosyltransferase gene in mice, in which an unidentified protein that binds to the Sp1 sites seems to prevent methylation of the CpG island.	bind
25557	2	7954	6	NULL	NULL	0	NULL	statement 1	NULL		prevent	NULL	may				NULL	methylation of 		CpG island	NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_1129_s_166	11549606	36- [[ 38  This latter defect ]] is exemplified by the adenine phosphoribosyltransferase gene in mice, in which an unidentified protein that binds to the Sp1 sites seems to prevent methylation of the CpG island.	bind
33191	1	7955	5	13	NULL	NULL	NULL	VLDL particle	GP		bind					CLA-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2341_s_169	9409200	37  According to this model, the large size of a given VLDL particle bound to CLA-1 may impede, by steric hindrance, the binding of other VLDL particles to nearby unoccupied receptors but not the binding of the much smaller particles such as HDL.	bind
33813	2	7955	5	13	NULL	NULL	NULL	VLDL particles	GP		bind					unoccupied receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2341_s_169	9409200	37  According to this model, the large size of a given VLDL particle bound to CLA-1 may impede, by steric hindrance, the binding of other VLDL particles to nearby unoccupied receptors but not the binding of the much smaller particles such as HDL.	bind
33815	4	7955	5	13	NULL	NULL	NULL	statement 1	Process		impede		may			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2341_s_169	9409200	37  According to this model, the large size of a given VLDL particle bound to CLA-1 may impede, by steric hindrance, the binding of other VLDL particles to nearby unoccupied receptors but not the binding of the much smaller particles such as HDL.	bind
33816	5	7955	5	13	NULL	NULL	NULL	statement 4	Process		occurs by					steric hindrance	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2341_s_169	9409200	37  According to this model, the large size of a given VLDL particle bound to CLA-1 may impede, by steric hindrance, the binding of other VLDL particles to nearby unoccupied receptors but not the binding of the much smaller particles such as HDL.	bind
33817	6	7955	5	13	NULL	NULL	NULL	statement 1	Process		does not impede					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2341_s_169	9409200	37  According to this model, the large size of a given VLDL particle bound to CLA-1 may impede, by steric hindrance, the binding of other VLDL particles to nearby unoccupied receptors but not the binding of the much smaller particles such as HDL.	bind
25558	1	7955	6	NULL	NULL	0	NULL	VLDL particle	NULL	large size of	bind	NULL				CLA-1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2341_s_169	9409200	37  According to this model, the large size of a given VLDL particle bound to CLA-1 may impede, by steric hindrance, the binding of other VLDL particles to nearby unoccupied receptors but not the binding of the much smaller particles such as HDL.	bind
25559	2	7955	6	NULL	NULL	0	NULL	VLDL particle	NULL		bind	NULL				unoccupied receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2341_s_169	9409200	37  According to this model, the large size of a given VLDL particle bound to CLA-1 may impede, by steric hindrance, the binding of other VLDL particles to nearby unoccupied receptors but not the binding of the much smaller particles such as HDL.	bind
25560	3	7955	6	NULL	NULL	0	NULL	statement 1	NULL		impede	NULL	may			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2341_s_169	9409200	37  According to this model, the large size of a given VLDL particle bound to CLA-1 may impede, by steric hindrance, the binding of other VLDL particles to nearby unoccupied receptors but not the binding of the much smaller particles such as HDL.	bind
25561	4	7955	6	NULL	NULL	0	NULL	HDL	NULL		bind	NULL				receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2341_s_169	9409200	37  According to this model, the large size of a given VLDL particle bound to CLA-1 may impede, by steric hindrance, the binding of other VLDL particles to nearby unoccupied receptors but not the binding of the much smaller particles such as HDL.	bind
25562	5	7955	6	NULL	NULL	0	NULL	statement 1	NULL		does not impede	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2341_s_169	9409200	37  According to this model, the large size of a given VLDL particle bound to CLA-1 may impede, by steric hindrance, the binding of other VLDL particles to nearby unoccupied receptors but not the binding of the much smaller particles such as HDL.	bind
33200	1	7956	5	13	NULL	NULL	NULL	laminin	GP		bind					apo(a)	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1162_s_177	10323765	37  Also laminin and fibrinogen bind recombinant apo(a).	bind
33202	2	7956	5	13	NULL	NULL	NULL	fibrinogen	GP		bind					apo(a)	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1162_s_177	10323765	37  Also laminin and fibrinogen bind recombinant apo(a).	bind
25563	1	7956	6	NULL	NULL	0	NULL	laminin	NULL		bind	NULL				apo(a)	NULL	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1162_s_177	10323765	37  Also laminin and fibrinogen bind recombinant apo(a).	bind
25564	2	7956	6	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL				apo(a)	NULL	recombinant			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1162_s_177	10323765	37  Also laminin and fibrinogen bind recombinant apo(a).	bind
33204	1	7957	5	13	NULL	NULL	NULL	c-Jun homodimers	GP		bind									TRE at -58 to -50	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3025_s_208	10591684	37  Binding of c-Jun homodimers to TRE at positions -58 to -50 is important in the basal activity and phorbol 12-myristate 13-acetate activation of the PAI-1 promoter in HepG2 cells.	bind
33206	2	7957	5	13	NULL	NULL	NULL	statement 1	Process		is important in					basal activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3025_s_208	10591684	37  Binding of c-Jun homodimers to TRE at positions -58 to -50 is important in the basal activity and phorbol 12-myristate 13-acetate activation of the PAI-1 promoter in HepG2 cells.	bind
33207	3	7957	5	13	NULL	NULL	NULL	phorbol 12-myristate 13-acetate	Chemical		activates					PAI-1	GP			promoter	NULL	in HepG2 cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3025_s_208	10591684	37  Binding of c-Jun homodimers to TRE at positions -58 to -50 is important in the basal activity and phorbol 12-myristate 13-acetate activation of the PAI-1 promoter in HepG2 cells.	bind
33208	4	7957	5	13	NULL	NULL	NULL	statement 1	Process		is important in					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3025_s_208	10591684	37  Binding of c-Jun homodimers to TRE at positions -58 to -50 is important in the basal activity and phorbol 12-myristate 13-acetate activation of the PAI-1 promoter in HepG2 cells.	bind
25565	1	7957	6	NULL	NULL	0	NULL		NULL		is located at	NULL			TRE		NULL			-58 to -50	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3025_s_208	10591684	37  Binding of c-Jun homodimers to TRE at positions -58 to -50 is important in the basal activity and phorbol 12-myristate 13-acetate activation of the PAI-1 promoter in HepG2 cells.	bind
25566	2	7957	6	NULL	NULL	0	NULL	c-jun homodimers	NULL		bind	NULL					NULL			TRE	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3025_s_208	10591684	37  Binding of c-Jun homodimers to TRE at positions -58 to -50 is important in the basal activity and phorbol 12-myristate 13-acetate activation of the PAI-1 promoter in HepG2 cells.	bind
25567	3	7957	6	NULL	NULL	0	NULL	statement 2	NULL		is important for	NULL				basal activity	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3025_s_208	10591684	37  Binding of c-Jun homodimers to TRE at positions -58 to -50 is important in the basal activity and phorbol 12-myristate 13-acetate activation of the PAI-1 promoter in HepG2 cells.	bind
25568	4	7957	6	NULL	NULL	0	NULL	phorbol 12-myristate 13-acetate	NULL		activates	NULL				PAI-1	NULL			promoter	NULL	HepG2 cells	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3025_s_208	10591684	37  Binding of c-Jun homodimers to TRE at positions -58 to -50 is important in the basal activity and phorbol 12-myristate 13-acetate activation of the PAI-1 promoter in HepG2 cells.	bind
25569	5	7957	6	NULL	NULL	0	NULL	statement 2	NULL		is important for	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3025_s_208	10591684	37  Binding of c-Jun homodimers to TRE at positions -58 to -50 is important in the basal activity and phorbol 12-myristate 13-acetate activation of the PAI-1 promoter in HepG2 cells.	bind
33210	3	7958	5	13	NULL	NULL	NULL	statement 2	Process		attenuates					ischemia reperfusion injury	MedicalFinding				NULL	in myocardium	NULL	NULL	NULL	NULL	gw60_circulationres_86_2_139_s_127	10666408	37  In addition, it has recently been reported that transfecting rat hearts with a  cis element decoy against NF-kappaB binding site attenuates ischemia reperfusion injury in the myocardium.	bind
47831	1	7958	5	10	NULL	0	NULL		NULL		target against	NULL			cis element decoy		NULL			NF-kappaB binding site 	NULL		0	NULL	NULL	NULL	gw60_circulationres_86_2_139_s_127	10666408	37  In addition, it has recently been reported that transfecting rat hearts with a  cis element decoy against NF-kappaB binding site attenuates ischemia reperfusion injury in the myocardium.	bind
47832	2	7958	5	13	NULL	NULL	NULL	heart	OrganismPart	rat	transfected with					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_139_s_127	10666408	37  In addition, it has recently been reported that transfecting rat hearts with a  cis element decoy against NF-kappaB binding site attenuates ischemia reperfusion injury in the myocardium.	bind
25687	1	7958	6	NULL	NULL	0	NULL		NULL		targets against	NULL			cis element decoy		NULL			NF-kappaB binding site	NULL		0	NULL	NULL	NULL	gw60_circulationres_86_2_139_s_127	10666408	37  In addition, it has recently been reported that transfecting rat hearts with a  cis element decoy against NF-kappaB binding site attenuates ischemia reperfusion injury in the myocardium.	bind
25689	2	7958	6	10	NULL	0	NULL	 heart	NULL	rat	transfected with	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_139_s_127	10666408	37  In addition, it has recently been reported that transfecting rat hearts with a  cis element decoy against NF-kappaB binding site attenuates ischemia reperfusion injury in the myocardium.	bind
25690	3	7958	6	NULL	NULL	0	NULL	statement 2	NULL		attenuates	NULL				ischemia reperfusion injury	NULL				NULL	myocardium	0	NULL	NULL	NULL	gw60_circulationres_86_2_139_s_127	10666408	37  In addition, it has recently been reported that transfecting rat hearts with a  cis element decoy against NF-kappaB binding site attenuates ischemia reperfusion injury in the myocardium.	bind
33211	1	7959	5	13	NULL	NULL	NULL	C4	GP		bind		aspecific			myocardium	OrganismPart	infarcted			NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_1_97_s_149	8994423	37  Therefore, positive immunostaining with these MAbs ruled out the possibility that the results were influenced by aspecific binding of C4 and C3 to the infarcted myocardium.	bind
33212	2	7959	5	13	NULL	NULL	NULL	C3	GP		bind		aspecific			myocardium	OrganismPart	infarcted			NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_1_97_s_149	8994423	37  Therefore, positive immunostaining with these MAbs ruled out the possibility that the results were influenced by aspecific binding of C4 and C3 to the infarcted myocardium.	bind
25570	1	7959	6	NULL	NULL	0	NULL	C4	NULL		bind	NULL	aspecifically			myocardium	NULL	infarcted			NULL		0	NULL	NULL	NULL	gw60_circulation_95_1_97_s_149	8994423	37  Therefore, positive immunostaining with these MAbs ruled out the possibility that the results were influenced by aspecific binding of C4 and C3 to the infarcted myocardium.	bind
25571	2	7959	6	NULL	NULL	0	NULL	C3	NULL		bind	NULL	aspecifically			myocardium	NULL	infarcted			NULL		0	NULL	NULL	NULL	gw60_circulation_95_1_97_s_149	8994423	37  Therefore, positive immunostaining with these MAbs ruled out the possibility that the results were influenced by aspecific binding of C4 and C3 to the infarcted myocardium.	bind
33221	1	7960	5	13	NULL	NULL	NULL	p27Kip1	GP		bind					cyclin D/CDK4 complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_1091_s_239	11238057	37  These changes will disrupt binding of p27Kip1 to cyclin D/CDK4 complexes leading to a redistribution and binding of p27Kip1 to cyclin E/CDK2 and cyclin A/CDK2 complexes with their inhibition.	bind
33223	2	7960	5	13	NULL	NULL	NULL	p27Kip1	GP		bind					cyclin E/cdk2 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_1091_s_239	11238057	37  These changes will disrupt binding of p27Kip1 to cyclin D/CDK4 complexes leading to a redistribution and binding of p27Kip1 to cyclin E/CDK2 and cyclin A/CDK2 complexes with their inhibition.	bind
33224	3	7960	5	13	NULL	NULL	NULL	p27Kip1	GP		bind					cyclin A/CDK2 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_1091_s_239	11238057	37  These changes will disrupt binding of p27Kip1 to cyclin D/CDK4 complexes leading to a redistribution and binding of p27Kip1 to cyclin E/CDK2 and cyclin A/CDK2 complexes with their inhibition.	bind
33226	4	7960	5	13	NULL	NULL	NULL	statement 1	Process	disruption of	leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_1091_s_239	11238057	37  These changes will disrupt binding of p27Kip1 to cyclin D/CDK4 complexes leading to a redistribution and binding of p27Kip1 to cyclin E/CDK2 and cyclin A/CDK2 complexes with their inhibition.	bind
33227	5	7960	5	13	NULL	NULL	NULL	statement 1	Process	disruption of	leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_1091_s_239	11238057	37  These changes will disrupt binding of p27Kip1 to cyclin D/CDK4 complexes leading to a redistribution and binding of p27Kip1 to cyclin E/CDK2 and cyclin A/CDK2 complexes with their inhibition.	bind
33228	6	7960	5	13	NULL	NULL	NULL	statement 1	Process	disruption of	leads to					statement 2	Process	redistribution of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_1091_s_239	11238057	37  These changes will disrupt binding of p27Kip1 to cyclin D/CDK4 complexes leading to a redistribution and binding of p27Kip1 to cyclin E/CDK2 and cyclin A/CDK2 complexes with their inhibition.	bind
33229	7	7960	5	13	NULL	NULL	NULL	statement 1	Process	disruption of	leads to					statement 3	Process	redistribution of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_1091_s_239	11238057	37  These changes will disrupt binding of p27Kip1 to cyclin D/CDK4 complexes leading to a redistribution and binding of p27Kip1 to cyclin E/CDK2 and cyclin A/CDK2 complexes with their inhibition.	bind
33230	8	7960	5	13	NULL	NULL	NULL	statement 2	Process		inhibits					cyclin E/cdk2 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_1091_s_239	11238057	37  These changes will disrupt binding of p27Kip1 to cyclin D/CDK4 complexes leading to a redistribution and binding of p27Kip1 to cyclin E/CDK2 and cyclin A/CDK2 complexes with their inhibition.	bind
33231	9	7960	5	13	NULL	NULL	NULL	statement 3	Process		inhibits					cyclin A/CDK2 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_3_1091_s_239	11238057	37  These changes will disrupt binding of p27Kip1 to cyclin D/CDK4 complexes leading to a redistribution and binding of p27Kip1 to cyclin E/CDK2 and cyclin A/CDK2 complexes with their inhibition.	bind
25572	1	7960	6	NULL	NULL	0	NULL	p27Kip1	NULL		bind	NULL				cyclin D/CDK4 complexes	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_1091_s_239	11238057	37  These changes will disrupt binding of p27Kip1 to cyclin D/CDK4 complexes leading to a redistribution and binding of p27Kip1 to cyclin E/CDK2 and cyclin A/CDK2 complexes with their inhibition.	bind
25573	2	7960	6	NULL	NULL	0	NULL	p27Kip1	NULL		bind	NULL				cyclin E/cdk2 complex	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_1091_s_239	11238057	37  These changes will disrupt binding of p27Kip1 to cyclin D/CDK4 complexes leading to a redistribution and binding of p27Kip1 to cyclin E/CDK2 and cyclin A/CDK2 complexes with their inhibition.	bind
25574	3	7960	6	NULL	NULL	0	NULL	p27Kip1	NULL		bind	NULL				cyclin A/CDK2 complex	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_1091_s_239	11238057	37  These changes will disrupt binding of p27Kip1 to cyclin D/CDK4 complexes leading to a redistribution and binding of p27Kip1 to cyclin E/CDK2 and cyclin A/CDK2 complexes with their inhibition.	bind
37375	4	7960	6	NULL	NULL	0	NULL	statement 1	NULL	disruption of	leads to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_1091_s_239	11238057	37  These changes will disrupt binding of p27Kip1 to cyclin D/CDK4 complexes leading to a redistribution and binding of p27Kip1 to cyclin E/CDK2 and cyclin A/CDK2 complexes with their inhibition.	bind
37377	5	7960	6	NULL	NULL	0	NULL	statement 1	NULL	disruption of	leads to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_1091_s_239	11238057	37  These changes will disrupt binding of p27Kip1 to cyclin D/CDK4 complexes leading to a redistribution and binding of p27Kip1 to cyclin E/CDK2 and cyclin A/CDK2 complexes with their inhibition.	bind
37379	6	7960	6	NULL	NULL	0	NULL	statement 1	NULL	disruption of	leads to	NULL				statement 2	NULL	redistribution of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_1091_s_239	11238057	37  These changes will disrupt binding of p27Kip1 to cyclin D/CDK4 complexes leading to a redistribution and binding of p27Kip1 to cyclin E/CDK2 and cyclin A/CDK2 complexes with their inhibition.	bind
37381	7	7960	6	NULL	NULL	0	NULL	statement 1	NULL	disruption of	leads to	NULL				statement 3	NULL	redistribution of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_1091_s_239	11238057	37  These changes will disrupt binding of p27Kip1 to cyclin D/CDK4 complexes leading to a redistribution and binding of p27Kip1 to cyclin E/CDK2 and cyclin A/CDK2 complexes with their inhibition.	bind
37382	8	7960	6	NULL	NULL	0	NULL	statement 2	NULL		inhibits	NULL				cyclin E/cdk2 complex	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_1091_s_239	11238057	37  These changes will disrupt binding of p27Kip1 to cyclin D/CDK4 complexes leading to a redistribution and binding of p27Kip1 to cyclin E/CDK2 and cyclin A/CDK2 complexes with their inhibition.	bind
37383	9	7960	6	NULL	NULL	0	NULL	statement 3	NULL		inhibits	NULL				cyclin A/CDK2 complex	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_3_1091_s_239	11238057	37  These changes will disrupt binding of p27Kip1 to cyclin D/CDK4 complexes leading to a redistribution and binding of p27Kip1 to cyclin E/CDK2 and cyclin A/CDK2 complexes with their inhibition.	bind
33234	1	7961	5	13	NULL	NULL	NULL	Lp(a)	GP		bind		weakly			LDL receptor	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1774_s_172	7583555	37 38  Lp(a) binds weakly to the LDL receptor in vitro, 39  and LDL receptors probably play a minor role in the in vivo catabolism of Lp(a).	bind
33236	2	7961	5	13	NULL	NULL	NULL	LDL receptors	GP		plays a role in		probably;;minor			Lp(a)	GP	catabolism of			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1774_s_172	7583555	37 38  Lp(a) binds weakly to the LDL receptor in vitro, 39  and LDL receptors probably play a minor role in the in vivo catabolism of Lp(a).	bind
25575	1	7961	6	NULL	NULL	0	NULL	Lp(a)	NULL		bind	NULL	weakly			LDL receptor	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1774_s_172	7583555	37 38  Lp(a) binds weakly to the LDL receptor in vitro, 39  and LDL receptors probably play a minor role in the in vivo catabolism of Lp(a).	bind
25576	2	7961	6	10	NULL	0	NULL	LDL receptor	NULL		plays a role in	NULL	probably;; minor			Lp(a)	NULL	catabolism of 			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1774_s_172	7583555	37 38  Lp(a) binds weakly to the LDL receptor in vitro, 39  and LDL receptors probably play a minor role in the in vivo catabolism of Lp(a).	bind
33237	1	7962	5	13	NULL	NULL	NULL	aspirin	Chemical		decreases					fibrinogen	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
33238	2	7962	5	13	NULL	NULL	NULL	aspirin	Chemical		decreases					platelet	Cell	aggregation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
49165	3	7962	5	13	NULL	NULL	NULL	ADP antagonist	Chemical		decreases					fibrinogen	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
49166	4	7962	5	13	NULL	NULL	NULL	ADP antagonist	Chemical		decreases					platelet	Cell	aggregation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
49167	5	7962	5	13	NULL	NULL	NULL	aspirin plus an ADP antagonist	Chemical		decreases					fibrinogen	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
49168	6	7962	5	13	NULL	NULL	NULL	aspirin plus an ADP antagonist	Chemical		decreases					platelet	Cell	aggregation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
49169	7	7962	5	13	NULL	NULL	NULL	statement 5	Process	efficiency of	is more than		significantly			statement 1	Process	efficiency of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
49170	8	7962	5	13	NULL	NULL	NULL	statement 5	Process	efficiency of	is more than		significantly			statement 3	Process	efficiency of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
49171	9	7962	5	13	NULL	NULL	NULL	statement 6	Process	efficiency of	is more than		significantly			statement 2	Process	efficiency of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
49172	10	7962	5	13	NULL	NULL	NULL	statement 6	Process	efficiency of	is more than		significantly			statement 4	Process	efficiency of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
25677	1	7962	6	NULL	NULL	0	NULL	aspirin	NULL		decreases	NULL				fibrinogen	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
25678	2	7962	6	NULL	NULL	0	NULL	aspirin	NULL		decreases	NULL				platelet	NULL	aggregation of			NULL		0	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
25679	3	7962	6	NULL	NULL	0	NULL	ADP antagonist	NULL		decreases	NULL				fibrinogen	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
25680	4	7962	6	NULL	NULL	0	NULL	ADP antagonist	NULL		decreases	NULL				platelet	NULL	aggregation of			NULL		0	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
25681	5	7962	6	NULL	NULL	0	NULL	aspirin plus an ADP antagonist	NULL		decreases	NULL				fibrinogen	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
25682	6	7962	6	NULL	NULL	0	NULL	aspirin plus an ADP antagonist	NULL		decreases	NULL				platelet	NULL	aggregation of			NULL		0	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
25683	7	7962	6	NULL	NULL	0	NULL	statement 5	NULL	efficiency of	is more	NULL	significantly			statement 1	NULL	efficiency of 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
25684	8	7962	6	NULL	NULL	0	NULL	statement 5	NULL	efficiency of	is more	NULL	significantly			statement 3	NULL	efficiency of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
25685	9	7962	6	NULL	NULL	0	NULL	statement 6	NULL	efficiency of	is more	NULL	significantly			statement 2	NULL	efficiency of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
25686	10	7962	6	NULL	NULL	0	NULL	statement 6	NULL	efficiency of	is more	NULL	significantly			statement 4	NULL	efficiency of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_3_363_s_112	11157686	37 38 39 40 41 42 43  The combination of aspirin plus an ADP antagonist decreases fibrinogen binding and platelet aggregation significantly more than either agent alone.	bind
33384	1	7963	5	13	NULL	NULL	NULL	FXR	GP		modulate					ET-1	GP	expression of			NULL	EC	NULL	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_235	16357303	37 FXR may similarly modulate ET-1 expression in EC via inhibition of AP-1 signaling as supported by the following observations: (1) pharmacological or genetic activation of FXR inhibited the activity of a heterologous promoter driven by AP-1 response elements ( Figure 7) and (2) FXR inhibited the binding of transcription factors to the AP-1 consensus site as shown in EMSA ( Figure 8A and 8B).	bind
33385	2	7963	5	13	NULL	NULL	NULL	statement 1	Process		via					AP-1 signaling	Process	inhibition of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_235	16357303	37 FXR may similarly modulate ET-1 expression in EC via inhibition of AP-1 signaling as supported by the following observations: (1) pharmacological or genetic activation of FXR inhibited the activity of a heterologous promoter driven by AP-1 response elements ( Figure 7) and (2) FXR inhibited the binding of transcription factors to the AP-1 consensus site as shown in EMSA ( Figure 8A and 8B).	bind
33386	3	7963	5	NULL	NULL	0	NULL		NULL		is driven by	NULL			heterologous promoter		NULL			AP-1 response elements	NULL		0	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_235	16357303	37 FXR may similarly modulate ET-1 expression in EC via inhibition of AP-1 signaling as supported by the following observations: (1) pharmacological or genetic activation of FXR inhibited the activity of a heterologous promoter driven by AP-1 response elements ( Figure 7) and (2) FXR inhibited the binding of transcription factors to the AP-1 consensus site as shown in EMSA ( Figure 8A and 8B).	bind
33387	4	7963	5	13	NULL	NULL	NULL	FXR	GP	pharmacological activation of	inhibits					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_235	16357303	37 FXR may similarly modulate ET-1 expression in EC via inhibition of AP-1 signaling as supported by the following observations: (1) pharmacological or genetic activation of FXR inhibited the activity of a heterologous promoter driven by AP-1 response elements ( Figure 7) and (2) FXR inhibited the binding of transcription factors to the AP-1 consensus site as shown in EMSA ( Figure 8A and 8B).	bind
33388	5	7963	5	13	NULL	NULL	NULL	FXR	GP	genetic activation of	inhibits					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_235	16357303	37 FXR may similarly modulate ET-1 expression in EC via inhibition of AP-1 signaling as supported by the following observations: (1) pharmacological or genetic activation of FXR inhibited the activity of a heterologous promoter driven by AP-1 response elements ( Figure 7) and (2) FXR inhibited the binding of transcription factors to the AP-1 consensus site as shown in EMSA ( Figure 8A and 8B).	bind
33389	6	7963	5	13	NULL	NULL	NULL	statement 4	Process		is alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_235	16357303	37 FXR may similarly modulate ET-1 expression in EC via inhibition of AP-1 signaling as supported by the following observations: (1) pharmacological or genetic activation of FXR inhibited the activity of a heterologous promoter driven by AP-1 response elements ( Figure 7) and (2) FXR inhibited the binding of transcription factors to the AP-1 consensus site as shown in EMSA ( Figure 8A and 8B).	bind
33390	7	7963	5	13	NULL	NULL	NULL	transcription factors	GP		bind									AP-1 consensus site	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_235	16357303	37 FXR may similarly modulate ET-1 expression in EC via inhibition of AP-1 signaling as supported by the following observations: (1) pharmacological or genetic activation of FXR inhibited the activity of a heterologous promoter driven by AP-1 response elements ( Figure 7) and (2) FXR inhibited the binding of transcription factors to the AP-1 consensus site as shown in EMSA ( Figure 8A and 8B).	bind
33391	8	7963	5	13	NULL	NULL	NULL	FXR	GP		inhibits					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_235	16357303	37 FXR may similarly modulate ET-1 expression in EC via inhibition of AP-1 signaling as supported by the following observations: (1) pharmacological or genetic activation of FXR inhibited the activity of a heterologous promoter driven by AP-1 response elements ( Figure 7) and (2) FXR inhibited the binding of transcription factors to the AP-1 consensus site as shown in EMSA ( Figure 8A and 8B).	bind
25671	1	7963	6	NULL	NULL	0	NULL	heterologous promoter 	NULL		is driven by	NULL					NULL			AP-1 response element	NULL		0	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_235	16357303	37 FXR may similarly modulate ET-1 expression in EC via inhibition of AP-1 signaling as supported by the following observations: (1) pharmacological or genetic activation of FXR inhibited the activity of a heterologous promoter driven by AP-1 response elements ( Figure 7) and (2) FXR inhibited the binding of transcription factors to the AP-1 consensus site as shown in EMSA ( Figure 8A and 8B).	bind
25672	2	7963	6	NULL	NULL	0	NULL	FXR	NULL	genetic activation of	inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_235	16357303	37 FXR may similarly modulate ET-1 expression in EC via inhibition of AP-1 signaling as supported by the following observations: (1) pharmacological or genetic activation of FXR inhibited the activity of a heterologous promoter driven by AP-1 response elements ( Figure 7) and (2) FXR inhibited the binding of transcription factors to the AP-1 consensus site as shown in EMSA ( Figure 8A and 8B).	bind
25673	3	7963	6	NULL	NULL	0	NULL	transcription factor	NULL		bind	NULL					NULL			AP-1 consensus site	NULL		0	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_235	16357303	37 FXR may similarly modulate ET-1 expression in EC via inhibition of AP-1 signaling as supported by the following observations: (1) pharmacological or genetic activation of FXR inhibited the activity of a heterologous promoter driven by AP-1 response elements ( Figure 7) and (2) FXR inhibited the binding of transcription factors to the AP-1 consensus site as shown in EMSA ( Figure 8A and 8B).	bind
25674	4	7963	6	NULL	NULL	0	NULL	FXR	NULL		inhibits	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_235	16357303	37 FXR may similarly modulate ET-1 expression in EC via inhibition of AP-1 signaling as supported by the following observations: (1) pharmacological or genetic activation of FXR inhibited the activity of a heterologous promoter driven by AP-1 response elements ( Figure 7) and (2) FXR inhibited the binding of transcription factors to the AP-1 consensus site as shown in EMSA ( Figure 8A and 8B).	bind
48135	5	7963	6	10	NULL	0	NULL	FXR	NULL		modulate	NULL	may			ET-1	NULL	expression of			NULL	EC	0	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_235	16357303	37 FXR may similarly modulate ET-1 expression in EC via inhibition of AP-1 signaling as supported by the following observations: (1) pharmacological or genetic activation of FXR inhibited the activity of a heterologous promoter driven by AP-1 response elements ( Figure 7) and (2) FXR inhibited the binding of transcription factors to the AP-1 consensus site as shown in EMSA ( Figure 8A and 8B).	bind
48136	6	7963	6	10	NULL	0	NULL	statement 5	NULL		occurs via	NULL				AP-1 signaling	NULL	inhibiton of			NULL		0	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_235	16357303	37 FXR may similarly modulate ET-1 expression in EC via inhibition of AP-1 signaling as supported by the following observations: (1) pharmacological or genetic activation of FXR inhibited the activity of a heterologous promoter driven by AP-1 response elements ( Figure 7) and (2) FXR inhibited the binding of transcription factors to the AP-1 consensus site as shown in EMSA ( Figure 8A and 8B).	bind
48137	7	7963	6	10	NULL	0	NULL	FXR	NULL	pharmacological activation of	inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_235	16357303	37 FXR may similarly modulate ET-1 expression in EC via inhibition of AP-1 signaling as supported by the following observations: (1) pharmacological or genetic activation of FXR inhibited the activity of a heterologous promoter driven by AP-1 response elements ( Figure 7) and (2) FXR inhibited the binding of transcription factors to the AP-1 consensus site as shown in EMSA ( Figure 8A and 8B).	bind
48138	8	7963	6	10	NULL	0	NULL	statement 2	NULL		is an alternative to	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_235	16357303	37 FXR may similarly modulate ET-1 expression in EC via inhibition of AP-1 signaling as supported by the following observations: (1) pharmacological or genetic activation of FXR inhibited the activity of a heterologous promoter driven by AP-1 response elements ( Figure 7) and (2) FXR inhibited the binding of transcription factors to the AP-1 consensus site as shown in EMSA ( Figure 8A and 8B).	bind
33241	1	7964	5	13	NULL	NULL	NULL	A20	GP		bind					IKKgamma/NEMO	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_6_630_s_203	12609966	37 Interestingly, binding of A20 alone to IKKgamma/NEMO is not sufficient to inhibit NF-kappaB, suggesting possible involvement of additional molecules.	bind
33242	2	7964	5	13	NULL	NULL	NULL	statement 1	Process		does not inhibit					NF-kappaB	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_6_630_s_203	12609966	37 Interestingly, binding of A20 alone to IKKgamma/NEMO is not sufficient to inhibit NF-kappaB, suggesting possible involvement of additional molecules.	bind
25577	1	7964	6	NULL	NULL	0	NULL	A20	NULL		bind	NULL				IKKgamma/NEMO	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_6_630_s_203	12609966	37 Interestingly, binding of A20 alone to IKKgamma/NEMO is not sufficient to inhibit NF-kappaB, suggesting possible involvement of additional molecules.	bind
25578	2	7964	6	NULL	NULL	0	NULL	statement 1	NULL		does not inhibit	NULL				NF-kappaB	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_6_630_s_203	12609966	37 Interestingly, binding of A20 alone to IKKgamma/NEMO is not sufficient to inhibit NF-kappaB, suggesting possible involvement of additional molecules.	bind
33239	1	7965	5	13	NULL	NULL	NULL	TSP1	GP		bind					TGF-beta1	GP	latent			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_3_831_s_248	12213711	37 Recent studies have shown that TSP1 binds and activates latent TGF-beta1.	bind
33240	2	7965	5	13	NULL	NULL	NULL	statement 1	Process		activates					TGF-beta1	GP	latent			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_3_831_s_248	12213711	37 Recent studies have shown that TSP1 binds and activates latent TGF-beta1.	bind
25579	1	7965	6	NULL	NULL	0	NULL	TSP1	NULL		bind	NULL				TGF-beta1	NULL	latent			NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_3_831_s_248	12213711	37 Recent studies have shown that TSP1 binds and activates latent TGF-beta1.	bind
25580	2	7965	6	NULL	NULL	0	NULL	TSP1	NULL		activates	NULL				TGF-beta1	NULL	latent			NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_3_831_s_248	12213711	37 Recent studies have shown that TSP1 binds and activates latent TGF-beta1.	bind
37881	3	7965	6	NULL	NULL	0	NULL	statement 1	NULL		occurs simultaneously with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_3_831_s_248	12213711	37 Recent studies have shown that TSP1 binds and activates latent TGF-beta1.	bind
33244	1	7966	5	13	NULL	NULL	NULL	gp120	GP		is a type of					HIV-1 envelope protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_5_1631_s_243	9811356	37, 39 In cultured human fetal neurons, CD4-independent binding of the HIV-1 envelope protein gp120 to CXCR4 was recently reported.	bind
33245	2	7966	5	13	NULL	NULL	NULL	gp120	GP		bind					CXCR4	GP				NULL	cultured human fetal neurons	NULL	NULL	NULL	NULL	gw60_amjpathol_153_5_1631_s_243	9811356	37, 39 In cultured human fetal neurons, CD4-independent binding of the HIV-1 envelope protein gp120 to CXCR4 was recently reported.	bind
33247	3	7966	5	13	NULL	NULL	NULL	statement 2	Process		is independent of					CD4	GP				NULL	cultured human fetal neurons	NULL	NULL	NULL	NULL	gw60_amjpathol_153_5_1631_s_243	9811356	37, 39 In cultured human fetal neurons, CD4-independent binding of the HIV-1 envelope protein gp120 to CXCR4 was recently reported.	bind
25581	1	7966	6	NULL	NULL	0	NULL	gp120	NULL		bind	NULL				CXCR4	NULL				NULL	cultured human fetal neurons	NULL	NULL	NULL	NULL	gw60_amjpathol_153_5_1631_s_243	9811356	37, 39 In cultured human fetal neurons, CD4-independent binding of the HIV-1 envelope protein gp120 to CXCR4 was recently reported.	bind
25582	2	7966	6	10	NULL	0	NULL	statement 1			is independent of					CD4					NULL	cultured human fetal neurons	NULL	NULL	NULL	NULL	gw60_amjpathol_153_5_1631_s_243	9811356	37, 39 In cultured human fetal neurons, CD4-independent binding of the HIV-1 envelope protein gp120 to CXCR4 was recently reported.	bind
37388	3	7966	6	NULL	NULL	0	NULL	gp120	NULL		is a type of	NULL				HIV-1 envelope protein	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_5_1631_s_243	9811356	37, 39 In cultured human fetal neurons, CD4-independent binding of the HIV-1 envelope protein gp120 to CXCR4 was recently reported.	bind
33350	1	7967	5	13	NULL	NULL	NULL	E-selectin gene	GP	endothelial	contain		may			NF-kappaB	GP			DNA-binding sequences	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2075_s_174	15374848	37,38  Furthermore, endothelial E-selectin gene may present DNA-binding sequences for both NF-kappaB and AP-1, 39 and multiple NF-kappaB binding sites in the human E-selectin gene are required for maximal TNF-alpha - induced expression.	bind
33354	2	7967	5	13	NULL	NULL	NULL	E-selectin gene	GP	endothelial	contain		may			AP-1	GP			DNA-binding sequences	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2075_s_174	15374848	37,38  Furthermore, endothelial E-selectin gene may present DNA-binding sequences for both NF-kappaB and AP-1, 39 and multiple NF-kappaB binding sites in the human E-selectin gene are required for maximal TNF-alpha - induced expression.	bind
33355	4	7967	5	13	NULL	NULL	NULL	E-selectin gene	GP	human	is required for				multiple NF-kappaB binding sites	statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2075_s_174	15374848	37,38  Furthermore, endothelial E-selectin gene may present DNA-binding sequences for both NF-kappaB and AP-1, 39 and multiple NF-kappaB binding sites in the human E-selectin gene are required for maximal TNF-alpha - induced expression.	bind
47833	3	7967	5	13	NULL	NULL	NULL	TNF-alpha	GP		induce					expression	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2075_s_174	15374848	37,38  Furthermore, endothelial E-selectin gene may present DNA-binding sequences for both NF-kappaB and AP-1, 39 and multiple NF-kappaB binding sites in the human E-selectin gene are required for maximal TNF-alpha - induced expression.	bind
25583	4	7967	6	10	NULL	0	NULL	E-selectin gene	NULL	human	is required for	NULL			NF-kappaB binding sites	statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2075_s_174	15374848	37,38  Furthermore, endothelial E-selectin gene may present DNA-binding sequences for both NF-kappaB and AP-1, 39 and multiple NF-kappaB binding sites in the human E-selectin gene are required for maximal TNF-alpha - induced expression.	bind
37389	2	7967	6	NULL	NULL	0	NULL	E-selectin gene	NULL	endothelial	contain	NULL	may			NF-kappaB	NULL			DNA binding sequences	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2075_s_174	15374848	37,38  Furthermore, endothelial E-selectin gene may present DNA-binding sequences for both NF-kappaB and AP-1, 39 and multiple NF-kappaB binding sites in the human E-selectin gene are required for maximal TNF-alpha - induced expression.	bind
37391	1	7967	6	10	NULL	0	NULL	E-selectin gene	NULL	endothelial	contain	NULL	may			AP-1	NULL			DNA binding sequences	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2075_s_174	15374848	37,38  Furthermore, endothelial E-selectin gene may present DNA-binding sequences for both NF-kappaB and AP-1, 39 and multiple NF-kappaB binding sites in the human E-selectin gene are required for maximal TNF-alpha - induced expression.	bind
47834	3	7967	6	10	NULL	0	NULL	TNF-alpha	NULL		induce	NULL				expression	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2075_s_174	15374848	37,38  Furthermore, endothelial E-selectin gene may present DNA-binding sequences for both NF-kappaB and AP-1, 39 and multiple NF-kappaB binding sites in the human E-selectin gene are required for maximal TNF-alpha - induced expression.	bind
33358	1	7968	5	13	NULL	NULL	NULL	estrogen	Chemical		bind					membrane receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_2_245_s_157	14670845	37,38  Previous studies demonstrated that after estrogen binds to membrane receptors, followed by the activation of G proteins, 34 multiple signaling pathways that have been linked to either the stimulation of gene transcription or posttranslational modification of proteins, 39 - 41   are rapidly activated.	bind
33360	2	7968	5	13	NULL	NULL	NULL	statement 1	Process		followed by					G proteins	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_2_245_s_157	14670845	37,38  Previous studies demonstrated that after estrogen binds to membrane receptors, followed by the activation of G proteins, 34 multiple signaling pathways that have been linked to either the stimulation of gene transcription or posttranslational modification of proteins, 39 - 41   are rapidly activated.	bind
33361	3	7968	5	13	NULL	NULL	NULL	signaling pathways	Process	multiple	stimulates					gene transcription	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_2_245_s_157	14670845	37,38  Previous studies demonstrated that after estrogen binds to membrane receptors, followed by the activation of G proteins, 34 multiple signaling pathways that have been linked to either the stimulation of gene transcription or posttranslational modification of proteins, 39 - 41   are rapidly activated.	bind
33362	4	7968	5	13	NULL	NULL	NULL	signaling pathways	Process	multiple	stimulates					proteins	GP	posttranslational modification of 			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_2_245_s_157	14670845	37,38  Previous studies demonstrated that after estrogen binds to membrane receptors, followed by the activation of G proteins, 34 multiple signaling pathways that have been linked to either the stimulation of gene transcription or posttranslational modification of proteins, 39 - 41   are rapidly activated.	bind
33363	5	7968	5	13	NULL	NULL	NULL	statement 2	Process		activates		rapidly			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_2_245_s_157	14670845	37,38  Previous studies demonstrated that after estrogen binds to membrane receptors, followed by the activation of G proteins, 34 multiple signaling pathways that have been linked to either the stimulation of gene transcription or posttranslational modification of proteins, 39 - 41   are rapidly activated.	bind
33364	6	7968	5	13	NULL	NULL	NULL	statement 2	Process		activates		rapidly			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_2_245_s_157	14670845	37,38  Previous studies demonstrated that after estrogen binds to membrane receptors, followed by the activation of G proteins, 34 multiple signaling pathways that have been linked to either the stimulation of gene transcription or posttranslational modification of proteins, 39 - 41   are rapidly activated.	bind
25589	1	7968	6	NULL	NULL	0	NULL	estrogen	NULL		bind	NULL				membrane receptors	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_2_245_s_157	14670845	37,38  Previous studies demonstrated that after estrogen binds to membrane receptors, followed by the activation of G proteins, 34 multiple signaling pathways that have been linked to either the stimulation of gene transcription or posttranslational modification of proteins, 39 - 41   are rapidly activated.	bind
25590	2	7968	6	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				G proteins	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_2_245_s_157	14670845	37,38  Previous studies demonstrated that after estrogen binds to membrane receptors, followed by the activation of G proteins, 34 multiple signaling pathways that have been linked to either the stimulation of gene transcription or posttranslational modification of proteins, 39 - 41   are rapidly activated.	bind
25591	3	7968	6	NULL	NULL	0	NULL	signaling pathways	NULL		linked to	NULL				gene transcription	NULL	stimulation of			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_2_245_s_157	14670845	37,38  Previous studies demonstrated that after estrogen binds to membrane receptors, followed by the activation of G proteins, 34 multiple signaling pathways that have been linked to either the stimulation of gene transcription or posttranslational modification of proteins, 39 - 41   are rapidly activated.	bind
25592	4	7968	6	NULL	NULL	0	NULL	signaling pathways	NULL		linked to	NULL				proteins	NULL	posttranslational modification of			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_2_245_s_157	14670845	37,38  Previous studies demonstrated that after estrogen binds to membrane receptors, followed by the activation of G proteins, 34 multiple signaling pathways that have been linked to either the stimulation of gene transcription or posttranslational modification of proteins, 39 - 41   are rapidly activated.	bind
25593	5	7968	6	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_2_245_s_157	14670845	37,38  Previous studies demonstrated that after estrogen binds to membrane receptors, followed by the activation of G proteins, 34 multiple signaling pathways that have been linked to either the stimulation of gene transcription or posttranslational modification of proteins, 39 - 41   are rapidly activated.	bind
25594	6	7968	6	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_2_245_s_157	14670845	37,38  Previous studies demonstrated that after estrogen binds to membrane receptors, followed by the activation of G proteins, 34 multiple signaling pathways that have been linked to either the stimulation of gene transcription or posttranslational modification of proteins, 39 - 41   are rapidly activated.	bind
33365	1	7969	5	13	NULL	NULL	NULL	PKC	GP		enhances					NF-kappaB	GP	activity of			NULL	C pneumoniae - infected HAECs	NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1130_s_200	12714566	37,41  Hence, in  C pneumoniae - infected HAECs, we demonstrate that PKC enhances NF-kappaB activity by direct phosphorylation of its cytoplasmic inhibitor, I-kappaBalpha, thus facilitating NF-kappaB binding to the NF-kappaB motif in the ICAM-1 promoter.	bind
33368	2	7969	5	13	NULL	NULL	NULL	PKC	GP		phosphorylates		directly			I-kappaBalpha	GP				NULL	C pneumoniae - infected HAECs	NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1130_s_200	12714566	37,41  Hence, in  C pneumoniae - infected HAECs, we demonstrate that PKC enhances NF-kappaB activity by direct phosphorylation of its cytoplasmic inhibitor, I-kappaBalpha, thus facilitating NF-kappaB binding to the NF-kappaB motif in the ICAM-1 promoter.	bind
33370	3	7969	5	13	NULL	NULL	NULL	I-kappaBalpha	GP		inhibit					NF-kappaB	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1130_s_200	12714566	37,41  Hence, in  C pneumoniae - infected HAECs, we demonstrate that PKC enhances NF-kappaB activity by direct phosphorylation of its cytoplasmic inhibitor, I-kappaBalpha, thus facilitating NF-kappaB binding to the NF-kappaB motif in the ICAM-1 promoter.	bind
33371	4	7969	5	13	NULL	NULL	NULL	NF-kappaB	GP		bind					ICAM-1	GP			NF-kappaB motif in promoter	NULL	C pneumoniae - infected HAECs	NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1130_s_200	12714566	37,41  Hence, in  C pneumoniae - infected HAECs, we demonstrate that PKC enhances NF-kappaB activity by direct phosphorylation of its cytoplasmic inhibitor, I-kappaBalpha, thus facilitating NF-kappaB binding to the NF-kappaB motif in the ICAM-1 promoter.	bind
33373	5	7969	5	13	NULL	NULL	NULL	statement 1	Process		facilitate					statement 4	Process				NULL	C pneumoniae - infected HAECs	NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1130_s_200	12714566	37,41  Hence, in  C pneumoniae - infected HAECs, we demonstrate that PKC enhances NF-kappaB activity by direct phosphorylation of its cytoplasmic inhibitor, I-kappaBalpha, thus facilitating NF-kappaB binding to the NF-kappaB motif in the ICAM-1 promoter.	bind
36175	6	7969	5	13	NULL	NULL	NULL	I-kappaBalpha	GP		is a type of					cytoplasmic inhibitor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1130_s_200	12714566	37,41  Hence, in  C pneumoniae - infected HAECs, we demonstrate that PKC enhances NF-kappaB activity by direct phosphorylation of its cytoplasmic inhibitor, I-kappaBalpha, thus facilitating NF-kappaB binding to the NF-kappaB motif in the ICAM-1 promoter.	bind
25584	1	7969	6	10	NULL	0	NULL	PKC	NULL		phosphorylates	NULL	directly			I-kappaBalpha	NULL				NULL	C pneumoniae - infected HAEC	NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1130_s_200	12714566	37,41  Hence, in  C pneumoniae - infected HAECs, we demonstrate that PKC enhances NF-kappaB activity by direct phosphorylation of its cytoplasmic inhibitor, I-kappaBalpha, thus facilitating NF-kappaB binding to the NF-kappaB motif in the ICAM-1 promoter.	bind
25585	2	7969	6	NULL	NULL	0	NULL	PKC	NULL		enhances	NULL				NF-kappaB	NULL	activity of			NULL	C pneumoniae - infected HAEC	NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1130_s_200	12714566	37,41  Hence, in  C pneumoniae - infected HAECs, we demonstrate that PKC enhances NF-kappaB activity by direct phosphorylation of its cytoplasmic inhibitor, I-kappaBalpha, thus facilitating NF-kappaB binding to the NF-kappaB motif in the ICAM-1 promoter.	bind
25586	3	7969	6	NULL	NULL	0	NULL	statement 2	NULL		occurs via	NULL				statement 1	NULL				NULL	C pneumoniae - infected HAEC	NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1130_s_200	12714566	37,41  Hence, in  C pneumoniae - infected HAECs, we demonstrate that PKC enhances NF-kappaB activity by direct phosphorylation of its cytoplasmic inhibitor, I-kappaBalpha, thus facilitating NF-kappaB binding to the NF-kappaB motif in the ICAM-1 promoter.	bind
25587	4	7969	6	NULL	NULL	0	NULL	NF-kappaB	NULL		bind	NULL				ICAM-1	NULL			NF-kappaB motif of the promoter	NULL	C pneumoniae - infected HAEC	NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1130_s_200	12714566	37,41  Hence, in  C pneumoniae - infected HAECs, we demonstrate that PKC enhances NF-kappaB activity by direct phosphorylation of its cytoplasmic inhibitor, I-kappaBalpha, thus facilitating NF-kappaB binding to the NF-kappaB motif in the ICAM-1 promoter.	bind
25588	5	7969	6	NULL	NULL	0	NULL	statement 2	NULL		facilitate	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1130_s_200	12714566	37,41  Hence, in  C pneumoniae - infected HAECs, we demonstrate that PKC enhances NF-kappaB activity by direct phosphorylation of its cytoplasmic inhibitor, I-kappaBalpha, thus facilitating NF-kappaB binding to the NF-kappaB motif in the ICAM-1 promoter.	bind
37393	6	7969	6	NULL	NULL	0	NULL	I-kappaBalpha	NULL		is a type of	NULL				cytoplasmic inhibitor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_10_1130_s_200	12714566	37,41  Hence, in  C pneumoniae - infected HAECs, we demonstrate that PKC enhances NF-kappaB activity by direct phosphorylation of its cytoplasmic inhibitor, I-kappaBalpha, thus facilitating NF-kappaB binding to the NF-kappaB motif in the ICAM-1 promoter.	bind
37394	7	7969	6	NULL	NULL	0	NULL	IkappaBalpha	NULL		inhibits	NULL				NF-kappaB	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_10_1130_s_200	12714566	37,41  Hence, in  C pneumoniae - infected HAECs, we demonstrate that PKC enhances NF-kappaB activity by direct phosphorylation of its cytoplasmic inhibitor, I-kappaBalpha, thus facilitating NF-kappaB binding to the NF-kappaB motif in the ICAM-1 promoter.	bind
33376	1	7970	5	13	NULL	NULL	NULL	GST fusion protein	GP	bait	contains					SHP-2	GP		tandem SH2 domains		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_63	12689916	37,41,45,46,48,50,54,57 - 59           Interestingly, in a completely unbiased approach, a bait GST fusion protein containing the tandem SH2 domains of SHP-2 exclusively bound a peptide comprised of PECAM-1 residues 617 to 711 (ie, containing its dual ITIM), when tyrosine-phosphorylated, out of an entire phage display cDNA library.	bind
33377	2	7970	5	13	NULL	NULL	NULL	statement 1	Process		bind					PECAM-1 peptide	GP		residues 617 to 711		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_63	12689916	37,41,45,46,48,50,54,57 - 59           Interestingly, in a completely unbiased approach, a bait GST fusion protein containing the tandem SH2 domains of SHP-2 exclusively bound a peptide comprised of PECAM-1 residues 617 to 711 (ie, containing its dual ITIM), when tyrosine-phosphorylated, out of an entire phage display cDNA library.	bind
33379	3	7970	5	13	NULL	NULL	NULL	PECAM-1 peptide	GP		contains			residues 617 to 711					dual ITIM		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_63	12689916	37,41,45,46,48,50,54,57 - 59           Interestingly, in a completely unbiased approach, a bait GST fusion protein containing the tandem SH2 domains of SHP-2 exclusively bound a peptide comprised of PECAM-1 residues 617 to 711 (ie, containing its dual ITIM), when tyrosine-phosphorylated, out of an entire phage display cDNA library.	bind
33380	4	7970	5	13	NULL	NULL	NULL	tyrosine	AminoAcid	phosphorylation of	is required for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_63	12689916	37,41,45,46,48,50,54,57 - 59           Interestingly, in a completely unbiased approach, a bait GST fusion protein containing the tandem SH2 domains of SHP-2 exclusively bound a peptide comprised of PECAM-1 residues 617 to 711 (ie, containing its dual ITIM), when tyrosine-phosphorylated, out of an entire phage display cDNA library.	bind
26257	1	7970	6	NULL	NULL	0	NULL	GST fusion protein	NULL		contains	NULL				SHP-2	NULL		tandem SH2 domains		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_63	12689916	37,41,45,46,48,50,54,57 - 59           Interestingly, in a completely unbiased approach, a bait GST fusion protein containing the tandem SH2 domains of SHP-2 exclusively bound a peptide comprised of PECAM-1 residues 617 to 711 (ie, containing its dual ITIM), when tyrosine-phosphorylated, out of an entire phage display cDNA library.	bind
26258	2	7970	6	NULL	NULL	0	NULL	peptide	NULL		comprises of	NULL				PECAM-1	NULL		residues 617-711		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_63	12689916	37,41,45,46,48,50,54,57 - 59           Interestingly, in a completely unbiased approach, a bait GST fusion protein containing the tandem SH2 domains of SHP-2 exclusively bound a peptide comprised of PECAM-1 residues 617 to 711 (ie, containing its dual ITIM), when tyrosine-phosphorylated, out of an entire phage display cDNA library.	bind
26259	3	7970	6	NULL	NULL	0	NULL	GST fusion protein	NULL	phosphorylated	bind	NULL		tyrosine		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_63	12689916	37,41,45,46,48,50,54,57 - 59           Interestingly, in a completely unbiased approach, a bait GST fusion protein containing the tandem SH2 domains of SHP-2 exclusively bound a peptide comprised of PECAM-1 residues 617 to 711 (ie, containing its dual ITIM), when tyrosine-phosphorylated, out of an entire phage display cDNA library.	bind
37396	4	7970	6	NULL	NULL	0	NULL	PECAM-1	NULL		contains	NULL		residues 617-711		dual ITIM	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_63	12689916	37,41,45,46,48,50,54,57 - 59           Interestingly, in a completely unbiased approach, a bait GST fusion protein containing the tandem SH2 domains of SHP-2 exclusively bound a peptide comprised of PECAM-1 residues 617 to 711 (ie, containing its dual ITIM), when tyrosine-phosphorylated, out of an entire phage display cDNA library.	bind
33393	1	7971	5	13	NULL	NULL	NULL				bind		directly	amphipathic helices		ABCA1	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_j-lipid-res_47_1_16210729_s_6	16210729	37pA was cross-linked  to ABCA1, confirming the direct binding of amphipathic helices to ABCA1.	bind
25863	1	7971	6	NULL	NULL	0	NULL		NULL		bind	NULL	directly	amphipathic helices		ABCA1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0570-0579_j-lipid-res_47_1_16210729_s_6	16210729	37pA was cross-linked  to ABCA1, confirming the direct binding of amphipathic helices to ABCA1.	bind
33395	1	7973	5	13	NULL	NULL	NULL	Tb(III)	GP		bind					hammerhead ribozyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_22_4428_s_347	11071929	38       Feig,A.L., Panek,M., Horrocks,W.D. and Uhlenbeck,O.C. (1999) Probing the binding of Tb(III) and Eu(III) to the hammerhead ribozyme using luminescence spectroscopy.	bind
33396	2	7973	5	13	NULL	NULL	NULL	Eu(III)	GP		bind					hammerhead ribozyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_22_4428_s_347	11071929	38       Feig,A.L., Panek,M., Horrocks,W.D. and Uhlenbeck,O.C. (1999) Probing the binding of Tb(III) and Eu(III) to the hammerhead ribozyme using luminescence spectroscopy.	bind
25864	1	7973	6	NULL	NULL	0	NULL	Tb(III)	NULL		bind	NULL				hammerhead ribozyme	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_22_4428_s_347	11071929	38       Feig,A.L., Panek,M., Horrocks,W.D. and Uhlenbeck,O.C. (1999) Probing the binding of Tb(III) and Eu(III) to the hammerhead ribozyme using luminescence spectroscopy.	bind
25865	2	7973	6	NULL	NULL	0	NULL	Eu(III)	NULL		bind	NULL				hammerhead ribozyme	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_22_4428_s_347	11071929	38       Feig,A.L., Panek,M., Horrocks,W.D. and Uhlenbeck,O.C. (1999) Probing the binding of Tb(III) and Eu(III) to the hammerhead ribozyme using luminescence spectroscopy.	bind
33397	1	7975	5	13	NULL	NULL	NULL	nuclear proteins	GP	rice	bind		sequence specifically;; independently					rice bacilliform virus		vascular bundle expression element	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_497_s_399	11788712	38       He,X., Futterer,J. and Hohn,T. (2001) Sequence specific, methylation dependent and independent binding of rice nuclear proteins to a rice bacilliform virus vascular bundle expression element  J. Biol.	bind
36174	2	7975	5	13	NULL	NULL	NULL	statement 1	Process		is dependent on					methylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_497_s_399	11788712	38       He,X., Futterer,J. and Hohn,T. (2001) Sequence specific, methylation dependent and independent binding of rice nuclear proteins to a rice bacilliform virus vascular bundle expression element  J. Biol.	bind
25866	1	7975	6	NULL	NULL	0	NULL	nuclear proteins	NULL	rice	bind	NULL	sequence specifically;; independently				NULL	rice bacilliform virus		vascular bundle expression element	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_497_s_399	11788712	38       He,X., Futterer,J. and Hohn,T. (2001) Sequence specific, methylation dependent and independent binding of rice nuclear proteins to a rice bacilliform virus vascular bundle expression element  J. Biol.	bind
25867	2	7975	6	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				methylation	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_497_s_399	11788712	38       He,X., Futterer,J. and Hohn,T. (2001) Sequence specific, methylation dependent and independent binding of rice nuclear proteins to a rice bacilliform virus vascular bundle expression element  J. Biol.	bind
33398	1	7976	5	13	NULL	NULL	NULL	U1A protein	GP		bind		high affinity			U1 hairpin II RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_550_s_375	11788718	38       Katsamba,P.S., Myszka,D.G. and Laird-Offringa,I.A. (2001) Two functionally distinct steps mediate high affinity binding of U1A protein to U1 hairpin II RNA.	bind
25868	1	7976	6	NULL	NULL	0	NULL	U1A protein	NULL		bind	NULL	high affinity			U1 hairpin II RNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_550_s_375	11788718	38       Katsamba,P.S., Myszka,D.G. and Laird-Offringa,I.A. (2001) Two functionally distinct steps mediate high affinity binding of U1A protein to U1 hairpin II RNA.	bind
33399	1	7977	5	13	NULL	NULL	NULL	nuclear protein	GP		bind					Ki-ras	GP	human		promoter	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_622_s_325	11160882	38       Mayfield,C., Squibb,M. and Miller,D. (1994) Inhibition of nuclear protein binding to the human Ki-ras promoter by triplex-forming oligonucleotides.	bind
33400	2	7977	5	13	NULL	NULL	NULL	oligonucleotides	NucleicAcid	triplex-forming	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_622_s_325	11160882	38       Mayfield,C., Squibb,M. and Miller,D. (1994) Inhibition of nuclear protein binding to the human Ki-ras promoter by triplex-forming oligonucleotides.	bind
25869	1	7977	6	NULL	NULL	0	NULL	nuclear protein	NULL		bind	NULL				Ki-ras	NULL	human		promoter	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_622_s_325	11160882	38       Mayfield,C., Squibb,M. and Miller,D. (1994) Inhibition of nuclear protein binding to the human Ki-ras promoter by triplex-forming oligonucleotides.	bind
25870	2	7977	6	NULL	NULL	0	NULL	oligonucleotides	NULL	triplex-forming	inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_622_s_325	11160882	38       Mayfield,C., Squibb,M. and Miller,D. (1994) Inhibition of nuclear protein binding to the human Ki-ras promoter by triplex-forming oligonucleotides.	bind
33401	1	7979	5	13	NULL	NULL	NULL	LDL	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_9_1287_s_72	7670940	38  Antibody B1B3 54  but not antibody D7.2 37  inhibits the binding of LDL to the LDL receptor.	bind
33402	2	7979	5	13	NULL	NULL	NULL	antibody B1B3 54	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_9_1287_s_72	7670940	38  Antibody B1B3 54  but not antibody D7.2 37  inhibits the binding of LDL to the LDL receptor.	bind
33403	3	7979	5	13	NULL	NULL	NULL	antibody D7.2 37	GP		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_9_1287_s_72	7670940	38  Antibody B1B3 54  but not antibody D7.2 37  inhibits the binding of LDL to the LDL receptor.	bind
25871	1	7979	6	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_9_1287_s_72	7670940	38  Antibody B1B3 54  but not antibody D7.2 37  inhibits the binding of LDL to the LDL receptor.	bind
25872	2	7979	6	NULL	NULL	0	NULL	Antibody B1B3	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_9_1287_s_72	7670940	38  Antibody B1B3 54  but not antibody D7.2 37  inhibits the binding of LDL to the LDL receptor.	bind
25873	3	7979	6	NULL	NULL	0	NULL	antibody D7.2	NULL		does not inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_9_1287_s_72	7670940	38  Antibody B1B3 54  but not antibody D7.2 37  inhibits the binding of LDL to the LDL receptor.	bind
33404	1	7980	5	13	NULL	NULL	NULL	LDL	GP	oxidation of	is a critical process in					atherogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
33405	2	7980	5	13	NULL	NULL	NULL	LDL	GP		bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
33406	3	7980	5	13	NULL	NULL	NULL	LDL	GP	oxidation of	increases					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
33407	4	7980	5	13	NULL	NULL	NULL	free radicals	Chemical		derived from					lipid hydroperoxides	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
33408	5	7980	5	13	NULL	NULL	NULL	free radicals	Chemical		derived from					intermediaries	Chemical	reactive			NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
33409	6	7980	5	13	NULL	NULL	NULL	statement 3	Process		damages		possibly			collagen fibers	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
33410	7	7980	5	13	NULL	NULL	NULL	statement 4	Process		mediates					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
33411	8	7980	5	13	NULL	NULL	NULL	statement 5	Process		mediates					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
33412	9	7980	5	13	NULL	NULL	NULL	statement 3	Process		damages		possibly			elastin fibers	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
33413	10	7980	5	13	NULL	NULL	NULL	statement 4	Process		mediates					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
33414	11	7980	5	13	NULL	NULL	NULL	statement 5	Process		mediates					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
25874	1	7980	6	NULL	NULL	0	NULL	LDL	NULL	oxidation of	is a critical process in	NULL				atherogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
25875	2	7980	6	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				collagen	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
26261	3	7980	6	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				collagen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
26262	4	7980	6	NULL	NULL	0	NULL	LDL	NULL	oxidation of	increases	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
26263	5	7980	6	NULL	NULL	0	NULL	free radicles	NULL		derived from	NULL				lipid hydroperoxides	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
26264	6	7980	6	NULL	NULL	0	NULL	free radicles	NULL		mediates	NULL				elastin fibres	NULL	damage to			NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
26265	7	7980	6	NULL	NULL	0	NULL	free radicles	NULL		mediates	NULL				collagen fibres	NULL	damage to			NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
26266	8	7980	6	NULL	NULL	0	NULL	LDL	NULL	oxidation of	increases	NULL				statement 6	NULL	possibility of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
26267	9	7980	6	NULL	NULL	0	NULL	LDL	NULL	oxidation of	increases	NULL				statement 7	NULL	possibility of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_5_1375_s_135	7867176	38  Furthermore, oxidation of LDL, now thought to be a critical process in atherogenesis, 39  increases binding of LDL to collagen, 40  raising the possibility of damage to collagen or elastin fibers mediated by free radicals derived from lipid hydroperoxides and other reactive intermediaries.	bind
33415	1	7981	5	13	NULL	NULL	NULL	LDL	GP		bind					LDLr	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_5_1301_s_40	10807746	38  Methods to determine the abilities of anti-apoB mAbs to block the binding of LDL to the LDLr and to bind to LDL in LDL-LDLr complexes have been described previously.	bind
33416	2	7981	5	13	NULL	NULL	NULL	anti-apoB mAbs	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_5_1301_s_40	10807746	38  Methods to determine the abilities of anti-apoB mAbs to block the binding of LDL to the LDLr and to bind to LDL in LDL-LDLr complexes have been described previously.	bind
33417	4	7981	5	13	NULL	NULL	NULL	anti-apoB mAbs	GP		bind					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_5_1301_s_40	10807746	38  Methods to determine the abilities of anti-apoB mAbs to block the binding of LDL to the LDLr and to bind to LDL in LDL-LDLr complexes have been described previously.	bind
47835	3	7981	5	13	NULL	NULL	NULL	LDL	GP		complex with					LDLr	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_5_1301_s_40	10807746	38  Methods to determine the abilities of anti-apoB mAbs to block the binding of LDL to the LDLr and to bind to LDL in LDL-LDLr complexes have been described previously.	bind
25876	1	7981	6	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				LDLr	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_5_1301_s_40	10807746	38  Methods to determine the abilities of anti-apoB mAbs to block the binding of LDL to the LDLr and to bind to LDL in LDL-LDLr complexes have been described previously.	bind
25877	2	7981	6	NULL	NULL	0	NULL	anti-apoB mAbs	NULL		block	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_5_1301_s_40	10807746	38  Methods to determine the abilities of anti-apoB mAbs to block the binding of LDL to the LDLr and to bind to LDL in LDL-LDLr complexes have been described previously.	bind
47836	3	7981	6	10	NULL	0	NULL	LDL	NULL		complex with	NULL				LDLr	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_5_1301_s_40	10807746	38  Methods to determine the abilities of anti-apoB mAbs to block the binding of LDL to the LDLr and to bind to LDL in LDL-LDLr complexes have been described previously.	bind
47837	4	7981	6	10	NULL	0	NULL	anti-apoB mAbs	NULL		bind	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_5_1301_s_40	10807746	38  Methods to determine the abilities of anti-apoB mAbs to block the binding of LDL to the LDLr and to bind to LDL in LDL-LDLr complexes have been described previously.	bind
33418	1	7982	5	13	NULL	NULL	NULL	EKLF	GP		is					erythroid-specific Kruppel factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_6_978_s_254	8635248	38  Miller and Bieker 39  have isolated an erythroid-specific Kruppel factor (EKLF), containing proline-rich domains and three zinc-finger structures that bear some similarities with those in the Kruppel family of transcription factors, as a protein binding to the CACC-box of beta-globin.	bind
33419	2	7982	5	13	NULL	NULL	NULL	EKLF	GP		similar to			proline-rich domains;;zinc-finger structures		Kruppel transcription factors family	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_6_978_s_254	8635248	38  Miller and Bieker 39  have isolated an erythroid-specific Kruppel factor (EKLF), containing proline-rich domains and three zinc-finger structures that bear some similarities with those in the Kruppel family of transcription factors, as a protein binding to the CACC-box of beta-globin.	bind
33420	3	7982	5	13	NULL	NULL	NULL	EKLF	GP		bind					beta-globin	GP			CACC-box	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_6_978_s_254	8635248	38  Miller and Bieker 39  have isolated an erythroid-specific Kruppel factor (EKLF), containing proline-rich domains and three zinc-finger structures that bear some similarities with those in the Kruppel family of transcription factors, as a protein binding to the CACC-box of beta-globin.	bind
26268	1	7982	6	NULL	NULL	0	NULL	EKLF	NULL		is	NULL				erythroid-specific Kruppel factor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_6_978_s_254	8635248	38  Miller and Bieker 39  have isolated an erythroid-specific Kruppel factor (EKLF), containing proline-rich domains and three zinc-finger structures that bear some similarities with those in the Kruppel family of transcription factors, as a protein binding to the CACC-box of beta-globin.	bind
26269	2	7982	6	NULL	NULL	0	NULL	EKLF	NULL		contains	NULL					NULL		proline-rich domains		NULL		0	NULL	NULL	NULL	gw60_circulationres_78_6_978_s_254	8635248	38  Miller and Bieker 39  have isolated an erythroid-specific Kruppel factor (EKLF), containing proline-rich domains and three zinc-finger structures that bear some similarities with those in the Kruppel family of transcription factors, as a protein binding to the CACC-box of beta-globin.	bind
26270	3	7982	6	NULL	NULL	0	NULL	EKLF	NULL		contains	NULL					NULL		zinc-finger structures		NULL		0	NULL	NULL	NULL	gw60_circulationres_78_6_978_s_254	8635248	38  Miller and Bieker 39  have isolated an erythroid-specific Kruppel factor (EKLF), containing proline-rich domains and three zinc-finger structures that bear some similarities with those in the Kruppel family of transcription factors, as a protein binding to the CACC-box of beta-globin.	bind
26271	4	7982	6	NULL	NULL	0	NULL	EKLF	NULL		bind	NULL				beta-globin	NULL			CACC box	NULL		0	NULL	NULL	NULL	gw60_circulationres_78_6_978_s_254	8635248	38  Miller and Bieker 39  have isolated an erythroid-specific Kruppel factor (EKLF), containing proline-rich domains and three zinc-finger structures that bear some similarities with those in the Kruppel family of transcription factors, as a protein binding to the CACC-box of beta-globin.	bind
26917	5	7982	6	NULL	NULL	0	NULL	statement 2	NULL		occurs simultaneously with	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_6_978_s_254	8635248	38  Miller and Bieker 39  have isolated an erythroid-specific Kruppel factor (EKLF), containing proline-rich domains and three zinc-finger structures that bear some similarities with those in the Kruppel family of transcription factors, as a protein binding to the CACC-box of beta-globin.	bind
47838	6	7982	6	10	NULL	0	NULL	EKLF	NULL		is similar to	NULL		proline-rich domains;;zinc-finger structures		Kruppel transcription factors family	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_6_978_s_254	8635248	38  Miller and Bieker 39  have isolated an erythroid-specific Kruppel factor (EKLF), containing proline-rich domains and three zinc-finger structures that bear some similarities with those in the Kruppel family of transcription factors, as a protein binding to the CACC-box of beta-globin.	bind
33421	1	7983	5	13	NULL	NULL	NULL	fibrinogen	GP		bind					GP IIb/IIa receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_15_1481_s_171	9576429	38  The results of the present study are comparable to these findings, because the binding of fibrinogen to the GP IIb/IIa receptor was inhibited in vitro and during NO inhalation in patients with ARDS.	bind
33422	2	7983	5	13	NULL	NULL	NULL	NO	Chemical	inhalation of	inhibits					statement 1	Process				NULL	in patients with ARDS	NULL	NULL	NULL	NULL	gw60_circulation_97_15_1481_s_171	9576429	38  The results of the present study are comparable to these findings, because the binding of fibrinogen to the GP IIb/IIa receptor was inhibited in vitro and during NO inhalation in patients with ARDS.	bind
33423	3	7983	5	13	NULL	NULL	NULL	statement 1	Process		undergoes					inhibition	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_97_15_1481_s_171	9576429	38  The results of the present study are comparable to these findings, because the binding of fibrinogen to the GP IIb/IIa receptor was inhibited in vitro and during NO inhalation in patients with ARDS.	bind
25878	1	7983	6	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL				GP IIb/IIa receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_97_15_1481_s_171	9576429	38  The results of the present study are comparable to these findings, because the binding of fibrinogen to the GP IIb/IIa receptor was inhibited in vitro and during NO inhalation in patients with ARDS.	bind
25879	2	7983	6	NULL	NULL	0	NULL	NO	NULL	inhalation of	inhibits	NULL				statement 1	NULL				NULL	patients with ARDS	NULL	NULL	NULL	NULL	gw60_circulation_97_15_1481_s_171	9576429	38  The results of the present study are comparable to these findings, because the binding of fibrinogen to the GP IIb/IIa receptor was inhibited in vitro and during NO inhalation in patients with ARDS.	bind
37882	3	7983	6	NULL	NULL	0	NULL	statement 1	NULL		undergoes 	NULL				inhibition	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_97_15_1481_s_171	9576429	38  The results of the present study are comparable to these findings, because the binding of fibrinogen to the GP IIb/IIa receptor was inhibited in vitro and during NO inhalation in patients with ARDS.	bind
33427	1	7985	5	13	NULL	NULL	NULL	insulin	GP		activates					p21ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1086_s_219	12117721	38 The mechanism leading to the activation of p21ras by insulin is thought to involve binding of the phosphotyrosine-binding domain of IRS-1 to tyrosine-phosphorylated IRbeta.	bind
33428	2	7985	5	13	NULL	NULL	NULL	IRS-1	GP		bind			phosphotyrosine-binding domain		IRbeta	GP	tyrosine-phosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1086_s_219	12117721	38 The mechanism leading to the activation of p21ras by insulin is thought to involve binding of the phosphotyrosine-binding domain of IRS-1 to tyrosine-phosphorylated IRbeta.	bind
33429	3	7985	5	13	NULL	NULL	NULL	statement 2	Process		leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1086_s_219	12117721	38 The mechanism leading to the activation of p21ras by insulin is thought to involve binding of the phosphotyrosine-binding domain of IRS-1 to tyrosine-phosphorylated IRbeta.	bind
25960	1	7985	6	NULL	NULL	0	NULL	insulin	NULL		activates	NULL				p21ras	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1086_s_219	12117721	38 The mechanism leading to the activation of p21ras by insulin is thought to involve binding of the phosphotyrosine-binding domain of IRS-1 to tyrosine-phosphorylated IRbeta.	bind
25961	2	7985	6	NULL	NULL	0	NULL	IRS-1	NULL		bind	NULL		phosphotyrosine-binding domain		IRbeta	NULL	phosphorylated	tyrosine		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1086_s_219	12117721	38 The mechanism leading to the activation of p21ras by insulin is thought to involve binding of the phosphotyrosine-binding domain of IRS-1 to tyrosine-phosphorylated IRbeta.	bind
25962	3	7985	6	NULL	NULL	0	NULL	statement 1	NULL		occurs via	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1086_s_219	12117721	38 The mechanism leading to the activation of p21ras by insulin is thought to involve binding of the phosphotyrosine-binding domain of IRS-1 to tyrosine-phosphorylated IRbeta.	bind
33430	1	7986	5	13	NULL	NULL	NULL	p16INK4a	GP		bind					Cdk4	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_661_s_195	11485924	38, 39 The second mutation detected (c.262G>A; E88K) maps to a site implicated in the binding of p16INK4a to Cdk4 and Cdk6 39  and thus likely results in a functional impairment of the protein.	bind
33431	2	7986	5	13	NULL	NULL	NULL	p16INK4a	GP		bind					Cdk6	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_661_s_195	11485924	38, 39 The second mutation detected (c.262G>A; E88K) maps to a site implicated in the binding of p16INK4a to Cdk4 and Cdk6 39  and thus likely results in a functional impairment of the protein.	bind
33432	3	7986	5	13	NULL	NULL	NULL	p16INK4a	GP	mutant	impairs			c.262G>A;;E88K		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_661_s_195	11485924	38, 39 The second mutation detected (c.262G>A; E88K) maps to a site implicated in the binding of p16INK4a to Cdk4 and Cdk6 39  and thus likely results in a functional impairment of the protein.	bind
33433	4	7986	5	13	NULL	NULL	NULL	p16INK4a	GP	mutant	impairs			c.262G>A;;E88K		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_661_s_195	11485924	38, 39 The second mutation detected (c.262G>A; E88K) maps to a site implicated in the binding of p16INK4a to Cdk4 and Cdk6 39  and thus likely results in a functional impairment of the protein.	bind
36173	5	7986	5	13	NULL	NULL	NULL	p16INK4a	GP	mutant	impairs			c.262G>A;;E88K		p16INK4a	GP	function of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_661_s_195	11485924	38, 39 The second mutation detected (c.262G>A; E88K) maps to a site implicated in the binding of p16INK4a to Cdk4 and Cdk6 39  and thus likely results in a functional impairment of the protein.	bind
25963	1	7986	6	NULL	NULL	0	NULL	p16INK4a	NULL		bind	NULL				Cdk4	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_2_661_s_195	11485924	38, 39 The second mutation detected (c.262G>A; E88K) maps to a site implicated in the binding of p16INK4a to Cdk4 and Cdk6 39  and thus likely results in a functional impairment of the protein.	bind
25964	2	7986	6	NULL	NULL	0	NULL	p16INK4a	NULL		bind	NULL				Cdk6	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_2_661_s_195	11485924	38, 39 The second mutation detected (c.262G>A; E88K) maps to a site implicated in the binding of p16INK4a to Cdk4 and Cdk6 39  and thus likely results in a functional impairment of the protein.	bind
25965	3	7986	6	NULL	NULL	0	NULL	p16INK4a	NULL	mutant	impairs	NULL		c.262G>A; E88K		p16INK4a	NULL	function of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_2_661_s_195	11485924	38, 39 The second mutation detected (c.262G>A; E88K) maps to a site implicated in the binding of p16INK4a to Cdk4 and Cdk6 39  and thus likely results in a functional impairment of the protein.	bind
25966	4	7986	6	NULL	NULL	0	NULL	p16INK4a	NULL	mutant	impairs	NULL		c.262G>A; E88K		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_2_661_s_195	11485924	38, 39 The second mutation detected (c.262G>A; E88K) maps to a site implicated in the binding of p16INK4a to Cdk4 and Cdk6 39  and thus likely results in a functional impairment of the protein.	bind
25967	5	7986	6	NULL	NULL	0	NULL	p16INK4a	NULL	mutant	impairs	NULL		c.262G>A; E88K		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_2_661_s_195	11485924	38, 39 The second mutation detected (c.262G>A; E88K) maps to a site implicated in the binding of p16INK4a to Cdk4 and Cdk6 39  and thus likely results in a functional impairment of the protein.	bind
33434	2	7988	5	13	NULL	NULL	NULL	statement 1	NucleicAcid		acts as					transcriptional repressor	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_783_s_363	11160902	39       Grigoriev,M., Praseuth,D., Robin,P., Hemar,A., Saison-Behmoaras,T., Dautry-Varsat,A., Thuong,N.T., Helene,C. and Harel-Bellan,A. (1992) A triple helix-forming oligonucleotide - intercalator conjugate acts as a transcriptional repressor via inhibition of NF kappa B binding to interleukin-2 receptor alpha-regulatory sequence.	bind
33435	3	7988	5	13	NULL	NULL	NULL	NF kappa B	GP		bind					interleukin-2 receptor	GP			alpha-regulatory sequence	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_783_s_363	11160902	39       Grigoriev,M., Praseuth,D., Robin,P., Hemar,A., Saison-Behmoaras,T., Dautry-Varsat,A., Thuong,N.T., Helene,C. and Harel-Bellan,A. (1992) A triple helix-forming oligonucleotide - intercalator conjugate acts as a transcriptional repressor via inhibition of NF kappa B binding to interleukin-2 receptor alpha-regulatory sequence.	bind
33436	4	7988	5	13	NULL	NULL	NULL	statement 1	Process		inhibit					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_783_s_363	11160902	39       Grigoriev,M., Praseuth,D., Robin,P., Hemar,A., Saison-Behmoaras,T., Dautry-Varsat,A., Thuong,N.T., Helene,C. and Harel-Bellan,A. (1992) A triple helix-forming oligonucleotide - intercalator conjugate acts as a transcriptional repressor via inhibition of NF kappa B binding to interleukin-2 receptor alpha-regulatory sequence.	bind
47839	1	7988	5	13	NULL	NULL	NULL	oligonucleotide-intercalator conjugate	NucleicAcid		forms					triple helix	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_783_s_363	11160902	39       Grigoriev,M., Praseuth,D., Robin,P., Hemar,A., Saison-Behmoaras,T., Dautry-Varsat,A., Thuong,N.T., Helene,C. and Harel-Bellan,A. (1992) A triple helix-forming oligonucleotide - intercalator conjugate acts as a transcriptional repressor via inhibition of NF kappa B binding to interleukin-2 receptor alpha-regulatory sequence.	bind
47841	5	7988	5	13	NULL	NULL	NULL	statement 2	Process		occur via					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_783_s_363	11160902	39       Grigoriev,M., Praseuth,D., Robin,P., Hemar,A., Saison-Behmoaras,T., Dautry-Varsat,A., Thuong,N.T., Helene,C. and Harel-Bellan,A. (1992) A triple helix-forming oligonucleotide - intercalator conjugate acts as a transcriptional repressor via inhibition of NF kappa B binding to interleukin-2 receptor alpha-regulatory sequence.	bind
25968	1	7988	6	NULL	NULL	0	NULL	NF kappa B	NULL		bind	NULL				interleukin-2 receptor	NULL			alpha-regulatory sequence	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_783_s_363	11160902	39       Grigoriev,M., Praseuth,D., Robin,P., Hemar,A., Saison-Behmoaras,T., Dautry-Varsat,A., Thuong,N.T., Helene,C. and Harel-Bellan,A. (1992) A triple helix-forming oligonucleotide - intercalator conjugate acts as a transcriptional repressor via inhibition of NF kappa B binding to interleukin-2 receptor alpha-regulatory sequence.	bind
25969	3	7988	6	10	NULL	0	NULL	statement 2	NULL		acts as a	NULL				transcriptional repressor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_783_s_363	11160902	39       Grigoriev,M., Praseuth,D., Robin,P., Hemar,A., Saison-Behmoaras,T., Dautry-Varsat,A., Thuong,N.T., Helene,C. and Harel-Bellan,A. (1992) A triple helix-forming oligonucleotide - intercalator conjugate acts as a transcriptional repressor via inhibition of NF kappa B binding to interleukin-2 receptor alpha-regulatory sequence.	bind
25970	4	7988	6	10	NULL	0	NULL	statement 2	NULL		inhibits	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_783_s_363	11160902	39       Grigoriev,M., Praseuth,D., Robin,P., Hemar,A., Saison-Behmoaras,T., Dautry-Varsat,A., Thuong,N.T., Helene,C. and Harel-Bellan,A. (1992) A triple helix-forming oligonucleotide - intercalator conjugate acts as a transcriptional repressor via inhibition of NF kappa B binding to interleukin-2 receptor alpha-regulatory sequence.	bind
37402	5	7988	6	10	NULL	0	NULL	statement 3	NULL		occurs via	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_783_s_363	11160902	39       Grigoriev,M., Praseuth,D., Robin,P., Hemar,A., Saison-Behmoaras,T., Dautry-Varsat,A., Thuong,N.T., Helene,C. and Harel-Bellan,A. (1992) A triple helix-forming oligonucleotide - intercalator conjugate acts as a transcriptional repressor via inhibition of NF kappa B binding to interleukin-2 receptor alpha-regulatory sequence.	bind
47840	2	7988	6	10	NULL	0	NULL	oligonucleotide-intercalator conjugate	NULL		forms	NULL				triple helix	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_783_s_363	11160902	39       Grigoriev,M., Praseuth,D., Robin,P., Hemar,A., Saison-Behmoaras,T., Dautry-Varsat,A., Thuong,N.T., Helene,C. and Harel-Bellan,A. (1992) A triple helix-forming oligonucleotide - intercalator conjugate acts as a transcriptional repressor via inhibition of NF kappa B binding to interleukin-2 receptor alpha-regulatory sequence.	bind
33437	1	7990	5	13	NULL	NULL	NULL	BBF-1	GP	binding activity of	is distinguishable from					MEF-2	GP	cardiac;;binding activity of			NULL	chicken embryos	NULL	NULL	NULL	NULL	gw60_circulationres_79_1_4_s_111	8925567	39  Analysis of chicken embryos revealed that binding activity of BBF-1 is distinguishable from cardiac MEF-2 and appears before that of MEF-2.	bind
33438	2	7990	5	13	NULL	NULL	NULL	BBF-1	GP	binding activity of	appears before					MEF-2	GP	binding activity of			NULL	chicken embryos	NULL	NULL	NULL	NULL	gw60_circulationres_79_1_4_s_111	8925567	39  Analysis of chicken embryos revealed that binding activity of BBF-1 is distinguishable from cardiac MEF-2 and appears before that of MEF-2.	bind
26272	1	7990	6	10	NULL	0	NULL	BBF-1	NULL	binding activity of	is distinguishable from	NULL				MEF-2	NULL	cardiac;; binding activity of			NULL	 chicken embryos	NULL	NULL	NULL	NULL	gw60_circulationres_79_1_4_s_111	8925567	39  Analysis of chicken embryos revealed that binding activity of BBF-1 is distinguishable from cardiac MEF-2 and appears before that of MEF-2.	bind
37403	2	7990	6	10	NULL	0	NULL	BBF-1		binding activity of	appears before					MEF-2		binding activity of			NULL	chicken embryos	NULL	NULL	NULL	NULL	gw60_circulationres_79_1_4_s_111	8925567	39  Analysis of chicken embryos revealed that binding activity of BBF-1 is distinguishable from cardiac MEF-2 and appears before that of MEF-2.	bind
33439	1	7991	5	13	NULL	NULL	NULL	tyrosine phosphatase beta	GP		is a type of					receptor protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_6_1857_s_22	12759243	39  In addition, the receptor protein tyrosine phosphatase beta present on glial tumor cells binds to FNIII A1, 2, and 4, suggesting it to be an adhesion receptor to ECM. 40  However, it is unclear whether the alternatively spliced region of Tn-C directly enhances progressive behavior of tumor cells.	bind
33440	2	7991	5	13	NULL	NULL	NULL	tyrosine phosphatase beta	GP		bind					FNIII A1	GP				NULL	glial tumor cells	NULL	NULL	NULL	NULL	gw60_amjpathol_162_6_1857_s_22	12759243	39  In addition, the receptor protein tyrosine phosphatase beta present on glial tumor cells binds to FNIII A1, 2, and 4, suggesting it to be an adhesion receptor to ECM. 40  However, it is unclear whether the alternatively spliced region of Tn-C directly enhances progressive behavior of tumor cells.	bind
33441	3	7991	5	13	NULL	NULL	NULL	tyrosine phosphatase beta	GP		bind					FNIII A2	GP				NULL	glial tumor cells	NULL	NULL	NULL	NULL	gw60_amjpathol_162_6_1857_s_22	12759243	39  In addition, the receptor protein tyrosine phosphatase beta present on glial tumor cells binds to FNIII A1, 2, and 4, suggesting it to be an adhesion receptor to ECM. 40  However, it is unclear whether the alternatively spliced region of Tn-C directly enhances progressive behavior of tumor cells.	bind
33442	4	7991	5	13	NULL	NULL	NULL	tyrosine phosphatase beta	GP		bind					FNIII A4	GP				NULL	glial tumor cells	NULL	NULL	NULL	NULL	gw60_amjpathol_162_6_1857_s_22	12759243	39  In addition, the receptor protein tyrosine phosphatase beta present on glial tumor cells binds to FNIII A1, 2, and 4, suggesting it to be an adhesion receptor to ECM. 40  However, it is unclear whether the alternatively spliced region of Tn-C directly enhances progressive behavior of tumor cells.	bind
33443	5	7991	5	13	NULL	NULL	NULL	tyrosine phosphatase beta	GP		adhere to					ECM	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_6_1857_s_22	12759243	39  In addition, the receptor protein tyrosine phosphatase beta present on glial tumor cells binds to FNIII A1, 2, and 4, suggesting it to be an adhesion receptor to ECM. 40  However, it is unclear whether the alternatively spliced region of Tn-C directly enhances progressive behavior of tumor cells.	bind
33444	6	7991	5	13	NULL	NULL	NULL	statement 2	Process		suggests					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_6_1857_s_22	12759243	39  In addition, the receptor protein tyrosine phosphatase beta present on glial tumor cells binds to FNIII A1, 2, and 4, suggesting it to be an adhesion receptor to ECM. 40  However, it is unclear whether the alternatively spliced region of Tn-C directly enhances progressive behavior of tumor cells.	bind
33445	7	7991	5	13	NULL	NULL	NULL	statement 3	Process		suggests					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_6_1857_s_22	12759243	39  In addition, the receptor protein tyrosine phosphatase beta present on glial tumor cells binds to FNIII A1, 2, and 4, suggesting it to be an adhesion receptor to ECM. 40  However, it is unclear whether the alternatively spliced region of Tn-C directly enhances progressive behavior of tumor cells.	bind
33446	8	7991	5	13	NULL	NULL	NULL	statement 4	Process		suggests					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_6_1857_s_22	12759243	39  In addition, the receptor protein tyrosine phosphatase beta present on glial tumor cells binds to FNIII A1, 2, and 4, suggesting it to be an adhesion receptor to ECM. 40  However, it is unclear whether the alternatively spliced region of Tn-C directly enhances progressive behavior of tumor cells.	bind
25971	1	7991	6	NULL	NULL	0	NULL	tyrosine phosphatase beta receptor protein	NULL		is present on	NULL				glial tumor cells	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_162_6_1857_s_22	12759243	39  In addition, the receptor protein tyrosine phosphatase beta present on glial tumor cells binds to FNIII A1, 2, and 4, suggesting it to be an adhesion receptor to ECM. 40  However, it is unclear whether the alternatively spliced region of Tn-C directly enhances progressive behavior of tumor cells.	bind
25982	2	7991	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				FNIII A1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_6_1857_s_22	12759243	39  In addition, the receptor protein tyrosine phosphatase beta present on glial tumor cells binds to FNIII A1, 2, and 4, suggesting it to be an adhesion receptor to ECM. 40  However, it is unclear whether the alternatively spliced region of Tn-C directly enhances progressive behavior of tumor cells.	bind
25984	3	7991	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				FNIII A2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_162_6_1857_s_22	12759243	39  In addition, the receptor protein tyrosine phosphatase beta present on glial tumor cells binds to FNIII A1, 2, and 4, suggesting it to be an adhesion receptor to ECM. 40  However, it is unclear whether the alternatively spliced region of Tn-C directly enhances progressive behavior of tumor cells.	bind
25986	4	7991	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				FNIII A4	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_162_6_1857_s_22	12759243	39  In addition, the receptor protein tyrosine phosphatase beta present on glial tumor cells binds to FNIII A1, 2, and 4, suggesting it to be an adhesion receptor to ECM. 40  However, it is unclear whether the alternatively spliced region of Tn-C directly enhances progressive behavior of tumor cells.	bind
25989	5	7991	6	NULL	NULL	0	NULL	tyrosine phosphatase beta	NULL		adhers to	NULL				ECM	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_6_1857_s_22	12759243	39  In addition, the receptor protein tyrosine phosphatase beta present on glial tumor cells binds to FNIII A1, 2, and 4, suggesting it to be an adhesion receptor to ECM. 40  However, it is unclear whether the alternatively spliced region of Tn-C directly enhances progressive behavior of tumor cells.	bind
47842	6	7991	6	10	NULL	0	NULL	statement 2	NULL		suggests	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_162_6_1857_s_22	12759243	39  In addition, the receptor protein tyrosine phosphatase beta present on glial tumor cells binds to FNIII A1, 2, and 4, suggesting it to be an adhesion receptor to ECM. 40  However, it is unclear whether the alternatively spliced region of Tn-C directly enhances progressive behavior of tumor cells.	bind
47844	7	7991	6	10	NULL	0	NULL	statement 3	NULL		suggests	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_162_6_1857_s_22	12759243	39  In addition, the receptor protein tyrosine phosphatase beta present on glial tumor cells binds to FNIII A1, 2, and 4, suggesting it to be an adhesion receptor to ECM. 40  However, it is unclear whether the alternatively spliced region of Tn-C directly enhances progressive behavior of tumor cells.	bind
47845	8	7991	6	10	NULL	0	NULL	statement 4	NULL		suggests	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_6_1857_s_22	12759243	39  In addition, the receptor protein tyrosine phosphatase beta present on glial tumor cells binds to FNIII A1, 2, and 4, suggesting it to be an adhesion receptor to ECM. 40  However, it is unclear whether the alternatively spliced region of Tn-C directly enhances progressive behavior of tumor cells.	bind
33448	1	7992	5	13	NULL	NULL	NULL	130 kDa protein	GP	mouse	bind		tightly			calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_1846_s_45	9351345	39  The cDNA encodes a protein of 130 kDa that in the mouse (and partially in humans) tightly binds calmodulin even when intracellular calcium levels are low.	bind
33449	2	7992	5	13	NULL	NULL	NULL	statement 1	Process		in presence of					intracellular calcium 	Chemical	low levels of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_1846_s_45	9351345	39  The cDNA encodes a protein of 130 kDa that in the mouse (and partially in humans) tightly binds calmodulin even when intracellular calcium levels are low.	bind
25991	1	7992	6	10	NULL	0	NULL	130 kDa protein	NULL	mouse	bind	NULL	tightly			calmodulin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_1846_s_45	9351345	39  The cDNA encodes a protein of 130 kDa that in the mouse (and partially in humans) tightly binds calmodulin even when intracellular calcium levels are low.	bind
25993	2	7992	6	NULL	NULL	0	NULL	statement 1	NULL		occurs in presence of	NULL				intracellular calcium 	NULL	low levels of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_1846_s_45	9351345	39  The cDNA encodes a protein of 130 kDa that in the mouse (and partially in humans) tightly binds calmodulin even when intracellular calcium levels are low.	bind
33450	1	7993	5	13	NULL	NULL	NULL	MMP-2	GP		bind					MT-MMP	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_1_82_s_207	null	39 42  MMP-2 binds MT-MMP and becomes activated possibly through its limited proteolysis by MT - MMP-1.	bind
33451	2	7993	5	13	NULL	NULL	NULL	MMP-2	GP		is proteolysed by					MT - MMP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_1_82_s_207	null	39 42  MMP-2 binds MT-MMP and becomes activated possibly through its limited proteolysis by MT - MMP-1.	bind
33452	3	7993	5	13	NULL	NULL	NULL	statement 2	Process		activates					MMP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_1_82_s_207	null	39 42  MMP-2 binds MT-MMP and becomes activated possibly through its limited proteolysis by MT - MMP-1.	bind
26004	1	7993	6	NULL	NULL	0	NULL	MMP-2	NULL		bind	NULL				MT-MMP	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_97_1_82_s_207	null	39 42  MMP-2 binds MT-MMP and becomes activated possibly through its limited proteolysis by MT - MMP-1.	bind
26005	3	7993	6	10	NULL	0	NULL	statement 2			activates					MMP-2					NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_1_82_s_207	null	39 42  MMP-2 binds MT-MMP and becomes activated possibly through its limited proteolysis by MT - MMP-1.	bind
26006	2	7993	6	10	NULL	0	NULL	MT-MMP-1			proteolyse					MMP-2					NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_1_82_s_207	null	39 42  MMP-2 binds MT-MMP and becomes activated possibly through its limited proteolysis by MT - MMP-1.	bind
33453	1	7994	5	13	NULL	NULL	NULL	IRS-1	GP		is dissociated from					PI3-K	GP		p85 subunit		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1142_s_171	15802620	39,40  In other cell types, phosphorylation of Ser612 and Ser302 are involved in dissociation of IRS-1 from the p85 subunit of PI3-K, whereas Ser307 phosphorylation inhibits the binding of IRS-1 to the insulin receptor and triggers IRS-1 degradation.	bind
33454	2	7994	5	13	NULL	NULL	NULL			phosphorylation of	is involved in			Ser612		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1142_s_171	15802620	39,40  In other cell types, phosphorylation of Ser612 and Ser302 are involved in dissociation of IRS-1 from the p85 subunit of PI3-K, whereas Ser307 phosphorylation inhibits the binding of IRS-1 to the insulin receptor and triggers IRS-1 degradation.	bind
33455	3	7994	5	13	NULL	NULL	NULL	IRS-1	GP		bind					insulin receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1142_s_171	15802620	39,40  In other cell types, phosphorylation of Ser612 and Ser302 are involved in dissociation of IRS-1 from the p85 subunit of PI3-K, whereas Ser307 phosphorylation inhibits the binding of IRS-1 to the insulin receptor and triggers IRS-1 degradation.	bind
33456	4	7994	5	13	NULL	NULL	NULL			phosphorylation of	inhibits			Ser307		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1142_s_171	15802620	39,40  In other cell types, phosphorylation of Ser612 and Ser302 are involved in dissociation of IRS-1 from the p85 subunit of PI3-K, whereas Ser307 phosphorylation inhibits the binding of IRS-1 to the insulin receptor and triggers IRS-1 degradation.	bind
33457	5	7994	5	13	NULL	NULL	NULL	statement 4	Process		triggers					IRS-1	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1142_s_171	15802620	39,40  In other cell types, phosphorylation of Ser612 and Ser302 are involved in dissociation of IRS-1 from the p85 subunit of PI3-K, whereas Ser307 phosphorylation inhibits the binding of IRS-1 to the insulin receptor and triggers IRS-1 degradation.	bind
55575	6	7994	5	13	NULL	NULL	NULL			phosphorylation of	is involved in			Ser302		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1142_s_171	15802620	39,40  In other cell types, phosphorylation of Ser612 and Ser302 are involved in dissociation of IRS-1 from the p85 subunit of PI3-K, whereas Ser307 phosphorylation inhibits the binding of IRS-1 to the insulin receptor and triggers IRS-1 degradation.	bind
26007	1	7994	6	NULL	NULL	0	NULL	IRS-1	NULL		bind	NULL				insulin receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1142_s_171	15802620	39,40  In other cell types, phosphorylation of Ser612 and Ser302 are involved in dissociation of IRS-1 from the p85 subunit of PI3-K, whereas Ser307 phosphorylation inhibits the binding of IRS-1 to the insulin receptor and triggers IRS-1 degradation.	bind
26273	2	7994	6	NULL	NULL	0	NULL		NULL	phosphorylation of	inhibits	NULL		Ser307		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1142_s_171	15802620	39,40  In other cell types, phosphorylation of Ser612 and Ser302 are involved in dissociation of IRS-1 from the p85 subunit of PI3-K, whereas Ser307 phosphorylation inhibits the binding of IRS-1 to the insulin receptor and triggers IRS-1 degradation.	bind
26274	3	7994	6	NULL	NULL	0	NULL		NULL	phosphorylation of	triggers	NULL		Ser307		IRS-1	NULL	degradation of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1142_s_171	15802620	39,40  In other cell types, phosphorylation of Ser612 and Ser302 are involved in dissociation of IRS-1 from the p85 subunit of PI3-K, whereas Ser307 phosphorylation inhibits the binding of IRS-1 to the insulin receptor and triggers IRS-1 degradation.	bind
26275	4	7994	6	10	NULL	0	NULL	IRS-1			dissociates from					PI3-K			p85 subunit		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1142_s_171	15802620	39,40  In other cell types, phosphorylation of Ser612 and Ser302 are involved in dissociation of IRS-1 from the p85 subunit of PI3-K, whereas Ser307 phosphorylation inhibits the binding of IRS-1 to the insulin receptor and triggers IRS-1 degradation.	bind
26276	5	7994	6	NULL	NULL	0	NULL		NULL	phosphorylation of	is involved in	NULL		Ser612		statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1142_s_171	15802620	39,40  In other cell types, phosphorylation of Ser612 and Ser302 are involved in dissociation of IRS-1 from the p85 subunit of PI3-K, whereas Ser307 phosphorylation inhibits the binding of IRS-1 to the insulin receptor and triggers IRS-1 degradation.	bind
26277	6	7994	6	NULL	NULL	0	NULL		NULL	phosphorylation of	is involved in	NULL		Ser302		statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1142_s_171	15802620	39,40  In other cell types, phosphorylation of Ser612 and Ser302 are involved in dissociation of IRS-1 from the p85 subunit of PI3-K, whereas Ser307 phosphorylation inhibits the binding of IRS-1 to the insulin receptor and triggers IRS-1 degradation.	bind
33458	1	7995	5	13	NULL	NULL	NULL	Rac1	GP		bind					p67 PHOX	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_730_s_84	16574914	39,40  The cardiovascular literature is, in contrast, replete with examinations of ROS-mediated effects that can be triggered, at least in part, by Rac1 binding to p67 PHOX, leading to activation of the NADPH oxidase system.	bind
33459	2	7995	5	13	NULL	NULL	NULL	ROS-mediated effects	Process		triggered by		partly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_730_s_84	16574914	39,40  The cardiovascular literature is, in contrast, replete with examinations of ROS-mediated effects that can be triggered, at least in part, by Rac1 binding to p67 PHOX, leading to activation of the NADPH oxidase system.	bind
33460	3	7995	5	13	NULL	NULL	NULL	statement 2	Process		leads to					NADPH oxidase system	Process	activation of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_730_s_84	16574914	39,40  The cardiovascular literature is, in contrast, replete with examinations of ROS-mediated effects that can be triggered, at least in part, by Rac1 binding to p67 PHOX, leading to activation of the NADPH oxidase system.	bind
26008	1	7995	6	NULL	NULL	0	NULL	Rac1	NULL		bind	NULL				p67 PHOX	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_6_730_s_84	16574914	39,40  The cardiovascular literature is, in contrast, replete with examinations of ROS-mediated effects that can be triggered, at least in part, by Rac1 binding to p67 PHOX, leading to activation of the NADPH oxidase system.	bind
26042	3	7995	6	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				NADPH oxidase system	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_730_s_84	16574914	39,40  The cardiovascular literature is, in contrast, replete with examinations of ROS-mediated effects that can be triggered, at least in part, by Rac1 binding to p67 PHOX, leading to activation of the NADPH oxidase system.	bind
37404	2	7995	6	NULL	NULL	0	NULL	ROS-mediated effects	NULL		are triggered by	NULL	partly			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_730_s_84	16574914	39,40  The cardiovascular literature is, in contrast, replete with examinations of ROS-mediated effects that can be triggered, at least in part, by Rac1 binding to p67 PHOX, leading to activation of the NADPH oxidase system.	bind
33514	1	7996	5	13	NULL	NULL	NULL	ZO-1	GP		bind					occludin	GP		COOH-terminal cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_62_s_162	16269664	39,43,45   Published evidence also indicates that binding of ZO-1 (and ZO-2/3) to the COOH-terminal cytoplasmic tail of occludin is important for targeting of the latter to the tight junction, as well as for its cytoskeletal tethering, 46 a process that is almost certainly sensitive to the phosphorylation state of the junctional and cytoskeletal components involved.	bind
33515	2	7996	5	13	NULL	NULL	NULL	ZO-2/3	GP		bind					occludin	GP		COOH-terminal cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_62_s_162	16269664	39,43,45   Published evidence also indicates that binding of ZO-1 (and ZO-2/3) to the COOH-terminal cytoplasmic tail of occludin is important for targeting of the latter to the tight junction, as well as for its cytoskeletal tethering, 46 a process that is almost certainly sensitive to the phosphorylation state of the junctional and cytoskeletal components involved.	bind
33516	3	7996	5	13	NULL	NULL	NULL	occludin	GP		is targeted to					tight junction	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_62_s_162	16269664	39,43,45   Published evidence also indicates that binding of ZO-1 (and ZO-2/3) to the COOH-terminal cytoplasmic tail of occludin is important for targeting of the latter to the tight junction, as well as for its cytoskeletal tethering, 46 a process that is almost certainly sensitive to the phosphorylation state of the junctional and cytoskeletal components involved.	bind
33517	4	7996	5	13	NULL	NULL	NULL	occludin	GP		is tethered to					cytoskeleton	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_62_s_162	16269664	39,43,45   Published evidence also indicates that binding of ZO-1 (and ZO-2/3) to the COOH-terminal cytoplasmic tail of occludin is important for targeting of the latter to the tight junction, as well as for its cytoskeletal tethering, 46 a process that is almost certainly sensitive to the phosphorylation state of the junctional and cytoskeletal components involved.	bind
33518	5	7996	5	13	NULL	NULL	NULL	statement 1	Process		is important for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_62_s_162	16269664	39,43,45   Published evidence also indicates that binding of ZO-1 (and ZO-2/3) to the COOH-terminal cytoplasmic tail of occludin is important for targeting of the latter to the tight junction, as well as for its cytoskeletal tethering, 46 a process that is almost certainly sensitive to the phosphorylation state of the junctional and cytoskeletal components involved.	bind
33519	6	7996	5	13	NULL	NULL	NULL	statement 1	Process		is important for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_62_s_162	16269664	39,43,45   Published evidence also indicates that binding of ZO-1 (and ZO-2/3) to the COOH-terminal cytoplasmic tail of occludin is important for targeting of the latter to the tight junction, as well as for its cytoskeletal tethering, 46 a process that is almost certainly sensitive to the phosphorylation state of the junctional and cytoskeletal components involved.	bind
33520	7	7996	5	13	NULL	NULL	NULL	statement 2	Process		is important for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_62_s_162	16269664	39,43,45   Published evidence also indicates that binding of ZO-1 (and ZO-2/3) to the COOH-terminal cytoplasmic tail of occludin is important for targeting of the latter to the tight junction, as well as for its cytoskeletal tethering, 46 a process that is almost certainly sensitive to the phosphorylation state of the junctional and cytoskeletal components involved.	bind
33521	8	7996	5	13	NULL	NULL	NULL	statement 2	Process		is important for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_62_s_162	16269664	39,43,45   Published evidence also indicates that binding of ZO-1 (and ZO-2/3) to the COOH-terminal cytoplasmic tail of occludin is important for targeting of the latter to the tight junction, as well as for its cytoskeletal tethering, 46 a process that is almost certainly sensitive to the phosphorylation state of the junctional and cytoskeletal components involved.	bind
33522	9	7996	5	13	NULL	NULL	NULL	cytoskeletal tethering	Process		is sensitive to					junctional components	CellComponent	phosphorylation state of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_62_s_162	16269664	39,43,45   Published evidence also indicates that binding of ZO-1 (and ZO-2/3) to the COOH-terminal cytoplasmic tail of occludin is important for targeting of the latter to the tight junction, as well as for its cytoskeletal tethering, 46 a process that is almost certainly sensitive to the phosphorylation state of the junctional and cytoskeletal components involved.	bind
33523	10	7996	5	13	NULL	NULL	NULL	cytoskeletal tethering	Process		is sensitive to					cytoskeletal components	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_62_s_162	16269664	39,43,45   Published evidence also indicates that binding of ZO-1 (and ZO-2/3) to the COOH-terminal cytoplasmic tail of occludin is important for targeting of the latter to the tight junction, as well as for its cytoskeletal tethering, 46 a process that is almost certainly sensitive to the phosphorylation state of the junctional and cytoskeletal components involved.	bind
26043	1	7996	6	NULL	NULL	0	NULL	ZO-1	NULL		bind	NULL				occludin	NULL		COOH-terminal cytoplasmic tail 		NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_62_s_162	16269664	39,43,45   Published evidence also indicates that binding of ZO-1 (and ZO-2/3) to the COOH-terminal cytoplasmic tail of occludin is important for targeting of the latter to the tight junction, as well as for its cytoskeletal tethering, 46 a process that is almost certainly sensitive to the phosphorylation state of the junctional and cytoskeletal components involved.	bind
26044	2	7996	6	NULL	NULL	0	NULL	occludin	NULL		is targeted to	NULL				tight junction	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_62_s_162	16269664	39,43,45   Published evidence also indicates that binding of ZO-1 (and ZO-2/3) to the COOH-terminal cytoplasmic tail of occludin is important for targeting of the latter to the tight junction, as well as for its cytoskeletal tethering, 46 a process that is almost certainly sensitive to the phosphorylation state of the junctional and cytoskeletal components involved.	bind
26045	3	7996	6	NULL	NULL	0	NULL	statement 1	NULL		is important for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_62_s_162	16269664	39,43,45   Published evidence also indicates that binding of ZO-1 (and ZO-2/3) to the COOH-terminal cytoplasmic tail of occludin is important for targeting of the latter to the tight junction, as well as for its cytoskeletal tethering, 46 a process that is almost certainly sensitive to the phosphorylation state of the junctional and cytoskeletal components involved.	bind
26046	4	7996	6	NULL	NULL	0	NULL	statement 1	NULL		is important for	NULL				occludin	NULL	cytoskeletal tethering of 			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_62_s_162	16269664	39,43,45   Published evidence also indicates that binding of ZO-1 (and ZO-2/3) to the COOH-terminal cytoplasmic tail of occludin is important for targeting of the latter to the tight junction, as well as for its cytoskeletal tethering, 46 a process that is almost certainly sensitive to the phosphorylation state of the junctional and cytoskeletal components involved.	bind
26047	5	7996	6	NULL	NULL	0	NULL	ZO-2/3	NULL		bind	NULL				occludin	NULL		COOH-terminal cytoplasmic tail		NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_62_s_162	16269664	39,43,45   Published evidence also indicates that binding of ZO-1 (and ZO-2/3) to the COOH-terminal cytoplasmic tail of occludin is important for targeting of the latter to the tight junction, as well as for its cytoskeletal tethering, 46 a process that is almost certainly sensitive to the phosphorylation state of the junctional and cytoskeletal components involved.	bind
26048	6	7996	6	NULL	NULL	0	NULL	statement 1	NULL		is sensitive to	NULL				junctional components	NULL	phosphorylation state of 			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_62_s_162	16269664	39,43,45   Published evidence also indicates that binding of ZO-1 (and ZO-2/3) to the COOH-terminal cytoplasmic tail of occludin is important for targeting of the latter to the tight junction, as well as for its cytoskeletal tethering, 46 a process that is almost certainly sensitive to the phosphorylation state of the junctional and cytoskeletal components involved.	bind
26050	7	7996	6	NULL	NULL	0	NULL	statement 1	NULL		is sensitive to	NULL				cytoskeletal components	NULL	phosphorylation state of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_62_s_162	16269664	39,43,45   Published evidence also indicates that binding of ZO-1 (and ZO-2/3) to the COOH-terminal cytoplasmic tail of occludin is important for targeting of the latter to the tight junction, as well as for its cytoskeletal tethering, 46 a process that is almost certainly sensitive to the phosphorylation state of the junctional and cytoskeletal components involved.	bind
33461	1	7997	5	13	NULL	NULL	NULL	Pten	GP		bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_cancercell_3_2_97_s_37	12620402	3: Pten binds to p53 resulting in increased p53 half-life.	bind
33462	2	7997	5	13	NULL	NULL	NULL	statement 1	Process		increase					p53	GP	half life of			NULL		NULL	NULL	NULL	NULL	gw60_cancercell_3_2_97_s_37	12620402	3: Pten binds to p53 resulting in increased p53 half-life.	bind
26052	1	7997	6	NULL	NULL	0	NULL	Pten	NULL		bind	NULL				p53	NULL				NULL		0	NULL	NULL	NULL	gw60_cancercell_3_2_97_s_37	12620402	3: Pten binds to p53 resulting in increased p53 half-life.	bind
26053	2	7997	6	NULL	NULL	0	NULL	statement 1	NULL		increases	NULL				p53	NULL	half life of			NULL		0	NULL	NULL	NULL	gw60_cancercell_3_2_97_s_37	12620402	3: Pten binds to p53 resulting in increased p53 half-life.	bind
33819	1	7998	5	13	NULL	NULL	NULL	3A9 cells	Cell		is specific for					 HEL	GP	epitope of	46-61		NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_3_1067_s_53	9448286	3A9 cells are specific for the epitope of residues 46-61 of hen egg lysozyme (46-61 HEL) ( 59), which associate in B cells with newly synthesized IAk molecules only when they are targeted to the loading compartment by Ii. 3B11 T cells recognize the epitope of residues 34-45 of HEL (34-45 HEL) that binds to recycling class II molecules ( 61).	bind
33820	2	7998	5	13	NULL	NULL	NULL	 46-61 HEL	GP		is					hen egg lysozyme	GP		residues 46-61 of		NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_3_1067_s_53	9448286	3A9 cells are specific for the epitope of residues 46-61 of hen egg lysozyme (46-61 HEL) ( 59), which associate in B cells with newly synthesized IAk molecules only when they are targeted to the loading compartment by Ii. 3B11 T cells recognize the epitope of residues 34-45 of HEL (34-45 HEL) that binds to recycling class II molecules ( 61).	bind
33822	3	7998	5	13	NULL	NULL	NULL	46-61 HEL	GP		associates with					IAk molecules	GP	newly synthesized			NULL	in B cells	NULL	NULL	NULL	NULL	gw60_pnas_95_3_1067_s_53	9448286	3A9 cells are specific for the epitope of residues 46-61 of hen egg lysozyme (46-61 HEL) ( 59), which associate in B cells with newly synthesized IAk molecules only when they are targeted to the loading compartment by Ii. 3B11 T cells recognize the epitope of residues 34-45 of HEL (34-45 HEL) that binds to recycling class II molecules ( 61).	bind
33823	4	7998	5	13	NULL	NULL	NULL	IAk molecules	GP	newly synthesized	is targeted to					loading compartment	CellComponent				NULL	in B cells	NULL	NULL	NULL	NULL	gw60_pnas_95_3_1067_s_53	9448286	3A9 cells are specific for the epitope of residues 46-61 of hen egg lysozyme (46-61 HEL) ( 59), which associate in B cells with newly synthesized IAk molecules only when they are targeted to the loading compartment by Ii. 3B11 T cells recognize the epitope of residues 34-45 of HEL (34-45 HEL) that binds to recycling class II molecules ( 61).	bind
33824	5	7998	5	13	NULL	NULL	NULL	Ii	GP		is required for					statement 4	Process				NULL	in B cells	NULL	NULL	NULL	NULL	gw60_pnas_95_3_1067_s_53	9448286	3A9 cells are specific for the epitope of residues 46-61 of hen egg lysozyme (46-61 HEL) ( 59), which associate in B cells with newly synthesized IAk molecules only when they are targeted to the loading compartment by Ii. 3B11 T cells recognize the epitope of residues 34-45 of HEL (34-45 HEL) that binds to recycling class II molecules ( 61).	bind
33825	6	7998	5	13	NULL	NULL	NULL	statement 3	Process		occurs following		only			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_3_1067_s_53	9448286	3A9 cells are specific for the epitope of residues 46-61 of hen egg lysozyme (46-61 HEL) ( 59), which associate in B cells with newly synthesized IAk molecules only when they are targeted to the loading compartment by Ii. 3B11 T cells recognize the epitope of residues 34-45 of HEL (34-45 HEL) that binds to recycling class II molecules ( 61).	bind
33826	7	7998	5	13	NULL	NULL	NULL	34-45 HEL	GP		is					residues 34-45 of HEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_3_1067_s_53	9448286	3A9 cells are specific for the epitope of residues 46-61 of hen egg lysozyme (46-61 HEL) ( 59), which associate in B cells with newly synthesized IAk molecules only when they are targeted to the loading compartment by Ii. 3B11 T cells recognize the epitope of residues 34-45 of HEL (34-45 HEL) that binds to recycling class II molecules ( 61).	bind
33827	8	7998	5	13	NULL	NULL	NULL	3B11 T cells	Cell		recognize					34-45 HEL	GP	epitope of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_3_1067_s_53	9448286	3A9 cells are specific for the epitope of residues 46-61 of hen egg lysozyme (46-61 HEL) ( 59), which associate in B cells with newly synthesized IAk molecules only when they are targeted to the loading compartment by Ii. 3B11 T cells recognize the epitope of residues 34-45 of HEL (34-45 HEL) that binds to recycling class II molecules ( 61).	bind
33828	9	7998	5	13	NULL	NULL	NULL	34-45 HEL	GP		bind					class II molecules	GP	recycling			NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_3_1067_s_53	9448286	3A9 cells are specific for the epitope of residues 46-61 of hen egg lysozyme (46-61 HEL) ( 59), which associate in B cells with newly synthesized IAk molecules only when they are targeted to the loading compartment by Ii. 3B11 T cells recognize the epitope of residues 34-45 of HEL (34-45 HEL) that binds to recycling class II molecules ( 61).	bind
26278	1	7998	6	13	NULL	NULL	NULL	HEL	GP		is					hen egg lysozyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_3_1067_s_53	9448286	3A9 cells are specific for the epitope of residues 46-61 of hen egg lysozyme (46-61 HEL) ( 59), which associate in B cells with newly synthesized IAk molecules only when they are targeted to the loading compartment by Ii. 3B11 T cells recognize the epitope of residues 34-45 of HEL (34-45 HEL) that binds to recycling class II molecules ( 61).	bind
26279	2	7998	6	NULL	NULL	0	NULL	HEL	NULL		bind	NULL		residues 34-45		recycling class II molecules	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_3_1067_s_53	9448286	3A9 cells are specific for the epitope of residues 46-61 of hen egg lysozyme (46-61 HEL) ( 59), which associate in B cells with newly synthesized IAk molecules only when they are targeted to the loading compartment by Ii. 3B11 T cells recognize the epitope of residues 34-45 of HEL (34-45 HEL) that binds to recycling class II molecules ( 61).	bind
26280	3	7998	6	NULL	NULL	0	NULL	3B11 T cells	NULL		recognize	NULL				HEL	NULL		epitope of residues 34-45		NULL		0	NULL	NULL	NULL	gw60_pnas_95_3_1067_s_53	9448286	3A9 cells are specific for the epitope of residues 46-61 of hen egg lysozyme (46-61 HEL) ( 59), which associate in B cells with newly synthesized IAk molecules only when they are targeted to the loading compartment by Ii. 3B11 T cells recognize the epitope of residues 34-45 of HEL (34-45 HEL) that binds to recycling class II molecules ( 61).	bind
26281	4	7998	6	NULL	NULL	0	NULL	3A9 cells	NULL		recognize	NULL				HEL	NULL		epitope of residues 46-61		NULL		0	NULL	NULL	NULL	gw60_pnas_95_3_1067_s_53	9448286	3A9 cells are specific for the epitope of residues 46-61 of hen egg lysozyme (46-61 HEL) ( 59), which associate in B cells with newly synthesized IAk molecules only when they are targeted to the loading compartment by Ii. 3B11 T cells recognize the epitope of residues 34-45 of HEL (34-45 HEL) that binds to recycling class II molecules ( 61).	bind
26282	5	7998	6	NULL	NULL	0	NULL	HEL	NULL		associate with	NULL		epitope of residues 46-61		IAk molecules	NULL	newly synthesized			NULL	B cells	NULL	NULL	NULL	NULL	gw60_pnas_95_3_1067_s_53	9448286	3A9 cells are specific for the epitope of residues 46-61 of hen egg lysozyme (46-61 HEL) ( 59), which associate in B cells with newly synthesized IAk molecules only when they are targeted to the loading compartment by Ii. 3B11 T cells recognize the epitope of residues 34-45 of HEL (34-45 HEL) that binds to recycling class II molecules ( 61).	bind
26283	6	7998	6	10	NULL	0	NULL	IAk molecules	NULL	newly synthesized	are targeted to	NULL				loading compartment	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_3_1067_s_53	9448286	3A9 cells are specific for the epitope of residues 46-61 of hen egg lysozyme (46-61 HEL) ( 59), which associate in B cells with newly synthesized IAk molecules only when they are targeted to the loading compartment by Ii. 3B11 T cells recognize the epitope of residues 34-45 of HEL (34-45 HEL) that binds to recycling class II molecules ( 61).	bind
26284	7	7998	6	NULL	NULL	0	NULL	statement 6	NULL		occurs by	NULL				Ii	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_3_1067_s_53	9448286	3A9 cells are specific for the epitope of residues 46-61 of hen egg lysozyme (46-61 HEL) ( 59), which associate in B cells with newly synthesized IAk molecules only when they are targeted to the loading compartment by Ii. 3B11 T cells recognize the epitope of residues 34-45 of HEL (34-45 HEL) that binds to recycling class II molecules ( 61).	bind
26285	8	7998	6	NULL	NULL	0	NULL	statement 5	NULL		occurs in presence of	NULL	only			statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_3_1067_s_53	9448286	3A9 cells are specific for the epitope of residues 46-61 of hen egg lysozyme (46-61 HEL) ( 59), which associate in B cells with newly synthesized IAk molecules only when they are targeted to the loading compartment by Ii. 3B11 T cells recognize the epitope of residues 34-45 of HEL (34-45 HEL) that binds to recycling class II molecules ( 61).	bind
33538	1	7999	5	13	NULL	NULL	NULL	3Ac/Sub1 G-actin	GP		exchange					epsilonATP	Chemical	bound			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_40_29916_s_8	16882670	3Ac/Sub1 G-actin exchanged bound epsilonATP more slowly than wild type actin, and the exchange rate for 3Ac/Sub12 was even slower, similar to that for muscle actin.	bind
33539	2	7999	5	13	NULL	NULL	NULL	3Ac/Sub1 G-actin	GP		exchange					actin	GP	muscle			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_40_29916_s_8	16882670	3Ac/Sub1 G-actin exchanged bound epsilonATP more slowly than wild type actin, and the exchange rate for 3Ac/Sub12 was even slower, similar to that for muscle actin.	bind
33540	3	7999	5	13	NULL	NULL	NULL	statement 1	Process		slower than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_40_29916_s_8	16882670	3Ac/Sub1 G-actin exchanged bound epsilonATP more slowly than wild type actin, and the exchange rate for 3Ac/Sub12 was even slower, similar to that for muscle actin.	bind
33542	4	7999	5	13	NULL	NULL	NULL	3Ac/Sub12	GP	exchange rate for	is similar to					actin	GP	muscle			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_40_29916_s_8	16882670	3Ac/Sub1 G-actin exchanged bound epsilonATP more slowly than wild type actin, and the exchange rate for 3Ac/Sub12 was even slower, similar to that for muscle actin.	bind
26092	1	7999	6	10	NULL	0	NULL	3Ac/Sub1 G-actin	NULL		exchange	NULL				epsilonATP	NULL	bound			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_40_29916_s_8	16882670	3Ac/Sub1 G-actin exchanged bound epsilonATP more slowly than wild type actin, and the exchange rate for 3Ac/Sub12 was even slower, similar to that for muscle actin.	bind
26093	2	7999	6	10	NULL	0	NULL	3Ac/Sub1 G-actin	NULL		exchange	NULL				actin	NULL	wild type			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_40_29916_s_8	16882670	3Ac/Sub1 G-actin exchanged bound epsilonATP more slowly than wild type actin, and the exchange rate for 3Ac/Sub12 was even slower, similar to that for muscle actin.	bind
26094	3	7999	6	NULL	NULL	0	NULL	statement 1	NULL		is slower than	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_40_29916_s_8	16882670	3Ac/Sub1 G-actin exchanged bound epsilonATP more slowly than wild type actin, and the exchange rate for 3Ac/Sub12 was even slower, similar to that for muscle actin.	bind
37405	4	7999	6	10	NULL	0	NULL	3Ac/Sub12		exchange rate of 	is similar to					actin		muscle			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_40_29916_s_8	16882670	3Ac/Sub1 G-actin exchanged bound epsilonATP more slowly than wild type actin, and the exchange rate for 3Ac/Sub12 was even slower, similar to that for muscle actin.	bind
33544	1	8000	5	13	NULL	NULL	NULL	TAG	Chemical		is					6-aminomethyl-3-methyl-4H-1,2,4-benzothiadiazine 1,1-dioxide	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
33546	2	8000	5	13	NULL	NULL	NULL	TAG	Chemical		displaces					[3H]taurine	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
33548	3	8000	5	13	NULL	NULL	NULL	AEA	Chemical		is					2-aminoethylarsonic	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
33551	4	8000	5	13	NULL	NULL	NULL	AEA	Chemical		displaces					[3H]taurine	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
33552	5	8000	5	13	NULL	NULL	NULL	ISE	Chemical		is					2-hydroxyethanesulfonic	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
33553	6	8000	5	13	NULL	NULL	NULL	ISE	Chemical		displaces					[3H]taurine	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
33555	7	8000	5	13	NULL	NULL	NULL	CAHS	Chemical		is					( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
33556	8	8000	5	13	NULL	NULL	NULL	CAHS	Chemical		displaces					[3H]taurine	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
33558	9	8000	5	13	NULL	NULL	NULL	TAG	Chemical		is a structural analogue of					taurine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
33559	10	8000	5	13	NULL	NULL	NULL	AEA	Chemical		is a structural analogue of					taurine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
33561	11	8000	5	13	NULL	NULL	NULL	ISE	Chemical		is a structural analogue of					taurine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
33562	12	8000	5	13	NULL	NULL	NULL	CAHS	Chemical		is structural analogue of					taurine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
26095	1	8000	6	NULL	NULL	0	NULL	TAG	NULL		is	NULL				taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide 	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
26098	2	8000	6	NULL	NULL	0	NULL	AEA	NULL		is	NULL				2-aminoethylarsonic	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
26099	3	8000	6	NULL	NULL	0	NULL	ISE	NULL		is	NULL				2-hydroxyethanesulfonic	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
26100	4	8000	6	NULL	NULL	0	NULL	CAHS	NULL		is	NULL				cis-2-aminocyclohexane sulfonic acids	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
26101	5	8000	6	NULL	NULL	0	NULL	TAG	NULL		displaces	NULL				taurine	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
26102	6	8000	6	NULL	NULL	0	NULL	AEA	NULL		displaces	NULL				taurine	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
26105	7	8000	6	NULL	NULL	0	NULL	ISE	NULL		displaces	NULL				taurine	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
26107	8	8000	6	NULL	NULL	0	NULL	CAHS	NULL		displaces	NULL				taurine	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
37314	9	8000	6	10	NULL	0	NULL	TAG	NULL		is structural analogue of	NULL				 taurine	NULL				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
37364	10	8000	6	10	NULL	0	NULL	AEA	NULL		is structural analogue of	NULL				 taurine	NULL				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
37371	11	8000	6	10	NULL	0	NULL	ISE	NULL		is structural analogue of 	NULL				taurine	NULL				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
37372	12	8000	6	10	NULL	0	NULL	CAHS	NULL		is structural analogue of	NULL				 taurine	NULL				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_6_1163_s_5	12684273	3Among the 19 structural analogues of taurine, 6-aminomethyl-3-methyl4HH1,2,4-benzothiadiazine 1,1-dioxide (TAG), 2-aminoethylarsonic (AEA), 2-hydroxyethanesulfonic (ISE) and ( plus-or-minus ) cis-2-aminocyclohexane sulfonic acids (CAHS) displaced [3]taurine binding ( Ki=0.13, 0.13, 13.5 and 4.0  muM, respectively).	bind
26108	1	8001	6	13	NULL	NULL	NULL	3beta,17betaAdiol	Chemical		is a type of					androgen metabolite	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_32086_s_68	12065592	3beta,17betaAdiol is a major androgen metabolite that binds human SHBG with high affinity ( 1).	bind
26109	2	8001	6	13	NULL	NULL	NULL	3beta,17betaAdiol	Chemical		bind		high affinity			SHBG	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_32086_s_68	12065592	3beta,17betaAdiol is a major androgen metabolite that binds human SHBG with high affinity ( 1).	bind
31329	1	8001	7	NULL	NULL	0	NULL	3beta,17betaAdiol	NULL		is a type of	NULL				androgen metabolite	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_35_32086_s_68	12065592	3beta,17betaAdiol is a major androgen metabolite that binds human SHBG with high affinity ( 1).	bind
31330	2	8001	7	NULL	NULL	0	NULL	3beta,17betaAdiol 	NULL		binds	NULL	high affinity			SHBG	NULL	human			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_35_32086_s_68	12065592	3beta,17betaAdiol is a major androgen metabolite that binds human SHBG with high affinity ( 1).	bind
26110	1	8002	6	13	NULL	NULL	NULL	3BP-1	GP		bind								SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_4_7_615_s_27	7953536	3BP-1 was found to bind to several different SH3 domains, but with significantly varying relative affinities.	bind
31331	1	8002	7	10	NULL	0	NULL	3BP-1 			bind								SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_4_7_615_s_27	7953536	3BP-1 was found to bind to several different SH3 domains, but with significantly varying relative affinities.	bind
26112	1	8003	6	13	NULL	NULL	NULL	3BP2	GP		bind					PTK c-Abl	GP		SH3 domain		NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7146_s_22	12501243	3BP2 has been originally described as an  in vitro binding partner of the SH3 domain of the PTK c-Abl ( ).	bind
31332	1	8003	7	10	NULL	0	NULL	3BP2			bind					PTK c-Abl			SH3 domain		NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7146_s_22	12501243	3BP2 has been originally described as an  in vitro binding partner of the SH3 domain of the PTK c-Abl ( ).	bind
26113	1	8007	6	13	NULL	NULL	NULL	MIB	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_1_155_s_118	9531555	3D map of MIB bound to actin.	bind
31333	1	8007	7	NULL	NULL	0	NULL	MIB	NULL		bind	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_141_1_155_s_118	9531555	3D map of MIB bound to actin.	bind
26114	1	8008	6	13	NULL	NULL	NULL	ATP	Chemical		bind					CCT	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_4_923_s_1976	10585970	3D reconstruction of the ATP-bound form of CCT reveals the asymetric folding conformation of a type II chaperonin.	bind
31334	1	8008	7	NULL	NULL	0	NULL	ATP	NULL		binds	NULL				CCT	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_4_923_s_1976	10585970	3D reconstruction of the ATP-bound form of CCT reveals the asymetric folding conformation of a type II chaperonin.	bind
26117	1	8012	6	13	NULL	NULL	NULL	hRI	GP		bind					ANG	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_1_53_s_86	14681553	3D structures of hRI variants were modeled from the crystal structures of free pRI, pRI in its complex with RNase A, and hRI bound to human ANG [Protein Data Bank ID codes 1BNH [PDB] ( ), 1DFJ [PDB] ( ), and 1A4Y [PDB] ( ), respectively at the SWISS-MODEL server [ http://swissmodel.	bind
26118	2	8012	6	13	NULL	NULL	NULL	pRI	GP		forms a complex with					RNase A	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_1_53_s_86	14681553	3D structures of hRI variants were modeled from the crystal structures of free pRI, pRI in its complex with RNase A, and hRI bound to human ANG [Protein Data Bank ID codes 1BNH [PDB] ( ), 1DFJ [PDB] ( ), and 1A4Y [PDB] ( ), respectively at the SWISS-MODEL server [ http://swissmodel.	bind
31459	1	8012	7	NULL	NULL	0	NULL	pRI	NULL		complex with	NULL				RNase A	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_1_53_s_86	14681553	3D structures of hRI variants were modeled from the crystal structures of free pRI, pRI in its complex with RNase A, and hRI bound to human ANG [Protein Data Bank ID codes 1BNH [PDB] ( ), 1DFJ [PDB] ( ), and 1A4Y [PDB] ( ), respectively at the SWISS-MODEL server [ http://swissmodel.	bind
31460	2	8012	7	NULL	NULL	0	NULL	 hRI	NULL		bind	NULL				ANG	NULL	human			NULL		0	NULL	NULL	NULL	gw70_pnas_101_1_53_s_86	14681553	3D structures of hRI variants were modeled from the crystal structures of free pRI, pRI in its complex with RNase A, and hRI bound to human ANG [Protein Data Bank ID codes 1BNH [PDB] ( ), 1DFJ [PDB] ( ), and 1A4Y [PDB] ( ), respectively at the SWISS-MODEL server [ http://swissmodel.	bind
26119	1	8013	6	13	NULL	NULL	NULL	SfbI	GP		bind								NTD		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_37_39017_s_132	15247227	3F1 Is Involved in Binding of SfbI to the NTD --	bind
26120	2	8013	6	13	NULL	NULL	NULL	F1	GP		is involved in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_37_39017_s_132	15247227	3F1 Is Involved in Binding of SfbI to the NTD --	bind
31461	1	8013	7	NULL	NULL	0	NULL	SfbI	NULL		bind	NULL					NULL		NTD		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_37_39017_s_132	15247227	3F1 Is Involved in Binding of SfbI to the NTD --	bind
31462	2	8013	7	NULL	NULL	0	NULL	F1	NULL		is involved in	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_37_39017_s_132	15247227	3F1 Is Involved in Binding of SfbI to the NTD --	bind
26122	1	8014	6	13	NULL	NULL	NULL	F10	GP		bind					SPN	GP	intracellular			NULL	rat pituitary cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_1_361_s_87	9417089	3F10 binding to intracellular SPN from rat pituitary cells is specifically blocked by preincubation of the mAb with pure native SPN ( 2).	bind
31463	1	8014	7	NULL	NULL	0	NULL	F10	NULL		bind	NULL				SPN	NULL	intracellular			NULL	rat pituitary cells	0	NULL	NULL	NULL	gw60_jbiolchem_273_1_361_s_87	9417089	3F10 binding to intracellular SPN from rat pituitary cells is specifically blocked by preincubation of the mAb with pure native SPN ( 2).	bind
26123	1	8016	6	13	NULL	NULL	NULL	3H Inhibitors	Chemical		does not bind					PDE5	GP	isolated	regulatory domain		NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_66_1_144_s_6	15213306	3H Inhibitors did not bind to isolated PDE5 regulatory domain.	bind
31465	1	8016	7	NULL	NULL	0	NULL	3H Inhibitors	NULL		does not bind	NULL				PDE5	NULL	isolated	regulatory domain		NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_66_1_144_s_6	15213306	3H Inhibitors did not bind to isolated PDE5 regulatory domain.	bind
46531	1	8018	6	13	NULL	NULL	NULL	3H-glutamate	Chemical		bind					NMDA receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_42_5_619_s_122	11985819	3H-glutamate binding to NMDA receptors	bind
31466	1	8018	7	NULL	NULL	0	NULL	3H-glutamate	NULL		bind	NULL				NMDA receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_42_5_619_s_122	11985819	3H-glutamate binding to NMDA receptors	bind
26124	1	8019	6	13	NULL	NULL	NULL	3H-heparin	Chemical		bind					whole Gc	Organism				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-exp-med_182_2_7629509_s_6	7629509	3H-heparin binding to whole Gc parallels  their adherence abilities (OpaA+ > OpaC+ > OpaH+ >> Opas B, D, E, F, G,  I = Opa- = 0).	bind
31467	1	8019	7	NULL	NULL	0	NULL	3H-heparin	NULL		bind	NULL				whole Gc	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_j-exp-med_182_2_7629509_s_6	7629509	3H-heparin binding to whole Gc parallels  their adherence abilities (OpaA+ > OpaC+ > OpaH+ >> Opas B, D, E, F, G,  I = Opa- = 0).	bind
26125	1	8020	6	13	NULL	NULL	NULL	3H-InsP3	Chemical		bind					InsP3R1	GP		NH2 terminus (aa 1-581)		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_2_312_s_299	14685260	3H-InsP3 binding to the NH2-terminal (aa 1 581) part of InsP3R1 (Lbs-1) was performed as described previously (  et al).	bind
46532	2	8020	6	13	NULL	NULL	NULL	InsP3R1	GP		is					Lbs-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_2_312_s_299	14685260	3H-InsP3 binding to the NH2-terminal (aa 1 581) part of InsP3R1 (Lbs-1) was performed as described previously (  et al).	bind
31469	1	8020	7	10	NULL	0	NULL	3H-InsP3			bind					 InsP3R1			NH2-terminal (aa-1581)		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_2_312_s_299	14685260	3H-InsP3 binding to the NH2-terminal (aa 1 581) part of InsP3R1 (Lbs-1) was performed as described previously (  et al).	bind
31470	2	8020	7	NULL	NULL	0	NULL	 InsP3R1	NULL		is	NULL				Lbs-1	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_23_2_312_s_299	14685260	3H-InsP3 binding to the NH2-terminal (aa 1 581) part of InsP3R1 (Lbs-1) was performed as described previously (  et al).	bind
26127	1	8021	6	13	NULL	NULL	NULL	kainate	Chemical		bind					hippocampus	OrganismPart				NULL	wild type mice	NULL	NULL	NULL	NULL	gw60_jneurosci_17_2_543_s_101	8987777	3H-kainate binding to the hippocampus in wild-type and  tPA /  mice	bind
26128	2	8021	6	13	NULL	NULL	NULL	kainate	Chemical		bind					hippocampus	OrganismPart				NULL	tPA mice	NULL	NULL	NULL	NULL	gw60_jneurosci_17_2_543_s_101	8987777	3H-kainate binding to the hippocampus in wild-type and  tPA /  mice	bind
31471	1	8021	7	NULL	NULL	0	NULL	3H-kainate	NULL		bind	NULL				hippocampus	NULL				NULL	wild-type mice	NULL	NULL	NULL	NULL	gw60_jneurosci_17_2_543_s_101	8987777	3H-kainate binding to the hippocampus in wild-type and  tPA /  mice	bind
31472	2	8021	7	NULL	NULL	0	NULL	3H-kainate	NULL		bind	NULL				hippocampus	NULL				NULL	tPA / mice	0	NULL	NULL	NULL	gw60_jneurosci_17_2_543_s_101	8987777	3H-kainate binding to the hippocampus in wild-type and  tPA /  mice	bind
26129	1	8024	6	13	NULL	NULL	NULL	GM1	Chemical	3H-labeled	bind					CD1b	GP	soluble			NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_2_255_s_156	10981968	3H-labeled GM1 bound to soluble CD1b was displaced by cold GM2 (  Figure 5C).	bind
26130	2	8024	6	13	NULL	NULL	NULL	GM2	Chemical	cold	bind					CD1b	GP	soluble			NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_2_255_s_156	10981968	3H-labeled GM1 bound to soluble CD1b was displaced by cold GM2 (  Figure 5C).	bind
55615	3	8024	6	13	NULL	NULL	NULL	statement 2	Process		displace					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_2_255_s_156	10981968	3H-labeled GM1 bound to soluble CD1b was displaced by cold GM2 (  Figure 5C).	bind
31473	1	8024	7	NULL	NULL	0	NULL	GM1	NULL	3H-labeled	bind	NULL				CD1b	NULL	soluble			NULL		0	NULL	NULL	NULL	gw60_immunity_13_2_255_s_156	10981968	3H-labeled GM1 bound to soluble CD1b was displaced by cold GM2 (  Figure 5C).	bind
31474	2	8024	7	10	NULL	0	NULL	GM2		cold	bind					CD1b		soluble			NULL		NULL	NULL	NULL	NULL	gw60_immunity_13_2_255_s_156	10981968	3H-labeled GM1 bound to soluble CD1b was displaced by cold GM2 (  Figure 5C).	bind
55804	3	8024	7	10	NULL	0	NULL	statement 2			displace					statement 1					NULL		0	NULL	NULL	NULL	gw60_immunity_13_2_255_s_156	10981968	3H-labeled GM1 bound to soluble CD1b was displaced by cold GM2 (  Figure 5C).	bind
26132	1	8026	6	13	NULL	NULL	NULL	prazosin	Chemical	3H-labeled	bind					cell membranes	CellComponent	fractionated			NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_286_2_984_s_87	9694959	3H-prazosin binding to fractionated cell membranes is the common method used to determine  alpha-1 adrenoceptor number and affinity (Kenny  et al., 1996  ).	bind
31475	1	8026	7	10	NULL	0	NULL	prazosin		3H labeled	bind					cell membranes		fractionated			NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_286_2_984_s_87	9694959	3H-prazosin binding to fractionated cell membranes is the common method used to determine  alpha-1 adrenoceptor number and affinity (Kenny  et al., 1996  ).	bind
26133	1	8027	6	13	NULL	NULL	NULL	reserpine	Chemical	3H-labeled	bind		irreversibly			transport protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevneurosci_20_0_125_s_152	9056710	3H-reserpine binds almost irreversibly to the transport protein, indicating that the  on-rate determines the affinity and providing a way to follow the protein during  purification ( Stern-Bach et al 1990).	bind
31477	1	8027	7	10	NULL	0	NULL	reserpine		3H-labeled	bind		irreversibly			transport protein					NULL		NULL	NULL	NULL	NULL	gw70_annurevneurosci_20_0_125_s_152	9056710	3H-reserpine binds almost irreversibly to the transport protein, indicating that the  on-rate determines the affinity and providing a way to follow the protein during  purification ( Stern-Bach et al 1990).	bind
26134	1	8028	6	13	NULL	NULL	NULL	RTX	Chemical	3H-labeled	bind							mutant	S512C		NULL		NULL	NULL	NULL	NULL	gw60_cell_108_3_421_s_162	11853675	3H-RTX bound to the S512C mutant with a KD of 310  plus-or-minus  20 pM (n = 2), only slightly higher than that of the wild-type receptor (200 pM).	bind
31478	1	8028	7	10	NULL	0	NULL	RTX 		3H-labeled \t	bind							mutant	S512C		NULL		NULL	NULL	NULL	NULL	gw60_cell_108_3_421_s_162	11853675	3H-RTX bound to the S512C mutant with a KD of 310  plus-or-minus  20 pM (n = 2), only slightly higher than that of the wild-type receptor (200 pM).	bind
26137	1	8029	6	13	NULL	NULL	NULL	SC52012B	Chemical	3H-labeled	bind					caspase-3	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_244	10681563	3H-SC52012B bound to human caspase-3 to a greater extent than to a control milk protein.	bind
26765	2	8029	6	13	NULL	NULL	NULL	SC52012B	Chemical	3H-labeled	bind					milk protein	GP	control			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_244	10681563	3H-SC52012B bound to human caspase-3 to a greater extent than to a control milk protein.	bind
26766	3	8029	6	13	NULL	NULL	NULL	statement 1	Process	affinity of	is greater than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_244	10681563	3H-SC52012B bound to human caspase-3 to a greater extent than to a control milk protein.	bind
31481	1	8029	7	10	NULL	0	NULL	SC52012B		3H-labeled	bind					caspase-3		human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_244	10681563	3H-SC52012B bound to human caspase-3 to a greater extent than to a control milk protein.	bind
31482	2	8029	7	10	NULL	0	NULL	SC52012B		3H-labeled	bind					milk protein		control			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_244	10681563	3H-SC52012B bound to human caspase-3 to a greater extent than to a control milk protein.	bind
31483	3	8029	7	NULL	NULL	0	NULL	statement 1	NULL	binding of	is greater than	NULL				statement 2	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_244	10681563	3H-SC52012B bound to human caspase-3 to a greater extent than to a control milk protein.	bind
26136	1	8030	6	13	NULL	NULL	NULL	SC52012B	Chemical	3H-labeled	does not bind		specifically			milk protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_188	10681563	3H-SC52012B showed no specific binding to 10% milk protein.	bind
31484	1	8030	7	10	NULL	0	NULL	SC52012B		3H-labeled	does not bind		specifically			milk protein					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_188	10681563	3H-SC52012B showed no specific binding to 10% milk protein.	bind
26139	1	8031	6	13	NULL	NULL	NULL	SC52021B	Chemical	3H-labeled	bind					caspase-3	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_178	10681563	3H-SC52021B binding to human caspase-3 (Fig.  5) was competed by unlabeled SC-52021B, orbofiban, xemilofiban, and by the monoclonal 7E3 antibody.	bind
26140	2	8031	6	13	NULL	NULL	NULL	SC-52021B	Chemical	unlabeled	bind					caspase-3	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_178	10681563	3H-SC52021B binding to human caspase-3 (Fig.  5) was competed by unlabeled SC-52021B, orbofiban, xemilofiban, and by the monoclonal 7E3 antibody.	bind
26141	3	8031	6	13	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_178	10681563	3H-SC52021B binding to human caspase-3 (Fig.  5) was competed by unlabeled SC-52021B, orbofiban, xemilofiban, and by the monoclonal 7E3 antibody.	bind
26142	4	8031	6	13	NULL	NULL	NULL	orbofiban	Chemical		bind					caspase-3	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_178	10681563	3H-SC52021B binding to human caspase-3 (Fig.  5) was competed by unlabeled SC-52021B, orbofiban, xemilofiban, and by the monoclonal 7E3 antibody.	bind
26143	5	8031	6	13	NULL	NULL	NULL	statement 1	Process		competes					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_178	10681563	3H-SC52021B binding to human caspase-3 (Fig.  5) was competed by unlabeled SC-52021B, orbofiban, xemilofiban, and by the monoclonal 7E3 antibody.	bind
26144	6	8031	6	13	NULL	NULL	NULL	xemilofiban	Chemical		bind					caspase-3	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_178	10681563	3H-SC52021B binding to human caspase-3 (Fig.  5) was competed by unlabeled SC-52021B, orbofiban, xemilofiban, and by the monoclonal 7E3 antibody.	bind
26145	7	8031	6	13	NULL	NULL	NULL	statement 1	Process		competes					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_178	10681563	3H-SC52021B binding to human caspase-3 (Fig.  5) was competed by unlabeled SC-52021B, orbofiban, xemilofiban, and by the monoclonal 7E3 antibody.	bind
26146	8	8031	6	13	NULL	NULL	NULL	monoclonal 7E3 antibody	GP		bind					caspase-3	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_178	10681563	3H-SC52021B binding to human caspase-3 (Fig.  5) was competed by unlabeled SC-52021B, orbofiban, xemilofiban, and by the monoclonal 7E3 antibody.	bind
26147	9	8031	6	13	NULL	NULL	NULL	statement 1	Process		competes					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_178	10681563	3H-SC52021B binding to human caspase-3 (Fig.  5) was competed by unlabeled SC-52021B, orbofiban, xemilofiban, and by the monoclonal 7E3 antibody.	bind
31493	1	8031	7	10	NULL	0	NULL	SC52021B		3H-labeled	bind					caspase-3		human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_178	10681563	3H-SC52021B binding to human caspase-3 (Fig.  5) was competed by unlabeled SC-52021B, orbofiban, xemilofiban, and by the monoclonal 7E3 antibody.	bind
31494	2	8031	7	NULL	NULL	0	NULL	SC-52021B	NULL	unlabeled	bind	NULL				caspase-3	NULL	human			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_178	10681563	3H-SC52021B binding to human caspase-3 (Fig.  5) was competed by unlabeled SC-52021B, orbofiban, xemilofiban, and by the monoclonal 7E3 antibody.	bind
31495	3	8031	7	NULL	NULL	0	NULL	orbofiban	NULL		bind	NULL				caspase-3	NULL	human			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_178	10681563	3H-SC52021B binding to human caspase-3 (Fig.  5) was competed by unlabeled SC-52021B, orbofiban, xemilofiban, and by the monoclonal 7E3 antibody.	bind
31498	4	8031	7	NULL	NULL	0	NULL	xemilofiban	NULL		bind	NULL				caspase-3	NULL	human			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_178	10681563	3H-SC52021B binding to human caspase-3 (Fig.  5) was competed by unlabeled SC-52021B, orbofiban, xemilofiban, and by the monoclonal 7E3 antibody.	bind
31500	5	8031	7	NULL	NULL	0	NULL	 monoclonal 7E3 antibody	NULL		bind	NULL				caspase-3	NULL	human			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_178	10681563	3H-SC52021B binding to human caspase-3 (Fig.  5) was competed by unlabeled SC-52021B, orbofiban, xemilofiban, and by the monoclonal 7E3 antibody.	bind
31502	6	8031	7	NULL	NULL	0	NULL	statement 2	NULL		compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_178	10681563	3H-SC52021B binding to human caspase-3 (Fig.  5) was competed by unlabeled SC-52021B, orbofiban, xemilofiban, and by the monoclonal 7E3 antibody.	bind
31503	7	8031	7	NULL	NULL	0	NULL	statement 3	NULL		compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_178	10681563	3H-SC52021B binding to human caspase-3 (Fig.  5) was competed by unlabeled SC-52021B, orbofiban, xemilofiban, and by the monoclonal 7E3 antibody.	bind
31504	8	8031	7	NULL	NULL	0	NULL	statement 4	NULL		compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_178	10681563	3H-SC52021B binding to human caspase-3 (Fig.  5) was competed by unlabeled SC-52021B, orbofiban, xemilofiban, and by the monoclonal 7E3 antibody.	bind
31505	9	8031	7	NULL	NULL	0	NULL	statement 5	NULL		compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_178	10681563	3H-SC52021B binding to human caspase-3 (Fig.  5) was competed by unlabeled SC-52021B, orbofiban, xemilofiban, and by the monoclonal 7E3 antibody.	bind
26148	1	8032	6	13	NULL	NULL	NULL	SC52021B	Chemical	3H-labeled	bind					caspase-3	GP	recombinant;;human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_177	10681563	3H-SC52021B Binding to Human Recombinant Caspase-3--3H-SC52021B bound to human recombinant caspase-3 with a  K d of 59  plus-or-minus  2 nM and a  Bmax of 324  plus-or-minus  32 fmol/mug of protein, ( n = 3).	bind
31511	1	8032	7	10	NULL	0	NULL	SC52021B		3H-labeled	bind					Caspase-3		human;;recombinant			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5760_s_177	10681563	3H-SC52021B Binding to Human Recombinant Caspase-3--3H-SC52021B bound to human recombinant caspase-3 with a  K d of 59  plus-or-minus  2 nM and a  Bmax of 324  plus-or-minus  32 fmol/mug of protein, ( n = 3).	bind
26149	1	8035	6	13	NULL	NULL	NULL	LuxR	GP	purified	bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_3_631_s_82	14729687	3OC6-HSL-dependent DNA binding of purified LuxR.	bind
26150	2	8035	6	13	NULL	NULL	NULL	statement 1	Process		is dependent on					3OC6-HSL	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_3_631_s_82	14729687	3OC6-HSL-dependent DNA binding of purified LuxR.	bind
31512	1	8035	7	NULL	NULL	0	NULL	LuxR	NULL	purified	bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_3_631_s_82	14729687	3OC6-HSL-dependent DNA binding of purified LuxR.	bind
31513	2	8035	7	NULL	NULL	0	NULL	statement 1	NULL		depends on	NULL				3OC6-HSL	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_3_631_s_82	14729687	3OC6-HSL-dependent DNA binding of purified LuxR.	bind
26151	1	8037	6	13	NULL	NULL	NULL	3pK	GP		bind					E47	GP				NULL	in vivo in Yeast	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20239_s_75	10781029	3pK Binds to E47 in Vivo in Yeast and Mammalian Cells-- To unravel the unknown physiological function of 3pK, we searched for binding partners in a yeast two-hybrid screen.	bind
46533	2	8037	6	13	NULL	NULL	NULL	3pK	GP		bind					E47	GP				NULL	in vivo in mammalian cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20239_s_75	10781029	3pK Binds to E47 in Vivo in Yeast and Mammalian Cells-- To unravel the unknown physiological function of 3pK, we searched for binding partners in a yeast two-hybrid screen.	bind
31535	1	8037	7	NULL	NULL	0	NULL	3pK	NULL		binds to	NULL				 E47	NULL				NULL	in Vivo in Yeast 	0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20239_s_75	10781029	3pK Binds to E47 in Vivo in Yeast and Mammalian Cells-- To unravel the unknown physiological function of 3pK, we searched for binding partners in a yeast two-hybrid screen.	bind
31536	2	8037	7	NULL	NULL	0	NULL	3pK	NULL		binds to	NULL				E47	NULL				NULL	in vivo in mammalian cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20239_s_75	10781029	3pK Binds to E47 in Vivo in Yeast and Mammalian Cells-- To unravel the unknown physiological function of 3pK, we searched for binding partners in a yeast two-hybrid screen.	bind
26152	1	8038	6	13	NULL	NULL	NULL	3R-tau	GP		bind					Fyn	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35119_s_87	16115884	3R-tau Binds to Fyn SH3 with a Higher Affinity than 4R-tau --	bind
26153	2	8038	6	13	NULL	NULL	NULL	4R-tau	GP		bind					Fyn	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35119_s_87	16115884	3R-tau Binds to Fyn SH3 with a Higher Affinity than 4R-tau --	bind
26154	3	8038	6	13	NULL	NULL	NULL	statement 1	Process	affinity of	is higher as compared to					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35119_s_87	16115884	3R-tau Binds to Fyn SH3 with a Higher Affinity than 4R-tau --	bind
31537	1	8038	7	10	NULL	0	NULL	3R-tau			binds					Fyn			SH3		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35119_s_87	16115884	3R-tau Binds to Fyn SH3 with a Higher Affinity than 4R-tau --	bind
31538	2	8038	7	NULL	NULL	0	NULL	4R-tau	NULL		binds	NULL				Fyn	NULL		SH3		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_42_35119_s_87	16115884	3R-tau Binds to Fyn SH3 with a Higher Affinity than 4R-tau --	bind
31539	3	8038	7	10	NULL	0	NULL	statement 1	NULL		higher affinity than	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35119_s_87	16115884	3R-tau Binds to Fyn SH3 with a Higher Affinity than 4R-tau --	bind
31540	1	8039	7	13	NULL	NULL	NULL	3R-tau	GP		binds					GST-Fyn	GP		SH3		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35119_s_109	16115884	3R-tau binds to GST-Fyn SH3 with a higher affinity than 4R-tau.	bind
31541	2	8039	7	13	NULL	NULL	NULL	4R-tau	GP		binds					GST-Fyn	GP		SH3		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35119_s_109	16115884	3R-tau binds to GST-Fyn SH3 with a higher affinity than 4R-tau.	bind
31542	3	8039	7	13	NULL	NULL	NULL	statement 1	Process		higher affinity than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35119_s_109	16115884	3R-tau binds to GST-Fyn SH3 with a higher affinity than 4R-tau.	bind
26155	1	8040	6	13	NULL	NULL	NULL	3T3 cells	Cell		express					ApoER2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_19_s_165	16354676	3T3 cells expressing ApoER2 or VLDLR bind Reelin.	bind
26156	2	8040	6	13	NULL	NULL	NULL	statement 1	GP		bind					Reelin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_19_s_165	16354676	3T3 cells expressing ApoER2 or VLDLR bind Reelin.	bind
26157	3	8040	6	13	NULL	NULL	NULL	3T3 cells	Cell		express					VLDLR	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_19_s_165	16354676	3T3 cells expressing ApoER2 or VLDLR bind Reelin.	bind
26158	4	8040	6	13	NULL	NULL	NULL	statement 3	GP		bind					Reelin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_19_s_165	16354676	3T3 cells expressing ApoER2 or VLDLR bind Reelin.	bind
26159	5	8040	6	13	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_19_s_165	16354676	3T3 cells expressing ApoER2 or VLDLR bind Reelin.	bind
31543	3	8040	7	10	NULL	0	NULL	statement 1	NULL		bind	NULL				Reelin	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_19_s_165	16354676	3T3 cells expressing ApoER2 or VLDLR bind Reelin.	bind
31544	4	8040	7	10	NULL	0	NULL	statement 3	NULL		bind	NULL				Reelin	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_1_19_s_165	16354676	3T3 cells expressing ApoER2 or VLDLR bind Reelin.	bind
46534	1	8040	7	10	NULL	0	NULL	3T3 cells	NULL		express	NULL				ApoER2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_1_19_s_165	16354676	3T3 cells expressing ApoER2 or VLDLR bind Reelin.	bind
46535	2	8040	7	10	NULL	0	NULL	3T3 cells	NULL		express	NULL				VLDLR	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_1_19_s_165	16354676	3T3 cells expressing ApoER2 or VLDLR bind Reelin.	bind
46536	5	8040	7	10	NULL	0	NULL	statement 3	NULL		is an alternative to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_1_19_s_165	16354676	3T3 cells expressing ApoER2 or VLDLR bind Reelin.	bind
26160	1	8042	6	13	NULL	NULL	NULL	M4 oligonucleotide	NucleicAcid		bind					NF1 proteins	GP				NULL	3T3-L1 adipocyte nuclear extract	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1712_s_191	11696544	3T3-L1 adipocyte nuclear extract was incubated with the  glut4-response element probe in the presence of increasing amounts of competitor M4 oligonucleotide which is bound by NF1 proteins but is not bound by O/E proteins.	bind
26161	2	8042	6	13	NULL	NULL	NULL	M4 oligonucleotide	NucleicAcid		does not bind					O/E proteins	GP				NULL	3T3-L1 adipocyte nuclear extract	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1712_s_191	11696544	3T3-L1 adipocyte nuclear extract was incubated with the  glut4-response element probe in the presence of increasing amounts of competitor M4 oligonucleotide which is bound by NF1 proteins but is not bound by O/E proteins.	bind
31570	1	8042	7	NULL	NULL	0	NULL	NF1 proteins 	NULL		bind	NULL				M4 oligonucleotide	NULL				NULL	3T3-L1 adipocyte nuclear extract 	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1712_s_191	11696544	3T3-L1 adipocyte nuclear extract was incubated with the  glut4-response element probe in the presence of increasing amounts of competitor M4 oligonucleotide which is bound by NF1 proteins but is not bound by O/E proteins.	bind
31571	2	8042	7	NULL	NULL	0	NULL	O/E proteins	NULL		does not bind	NULL				M4 oligonucleotide	NULL				NULL	3T3-L1 adipocyte nuclear extract 	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1712_s_191	11696544	3T3-L1 adipocyte nuclear extract was incubated with the  glut4-response element probe in the presence of increasing amounts of competitor M4 oligonucleotide which is bound by NF1 proteins but is not bound by O/E proteins.	bind
26162	1	8043	6	13	NULL	NULL	NULL	spectrin	GP		does not bind			SH3 domain		dynamin	GP				NULL	3T3-L1 adipocytes	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8169_s_176	9525921	3T3-L1 adipocytes were microinjected with fusion proteins containing the SH3 domains of spectrin and Crk (Fig.  5 A), which do not bind dynamin ( 23).	bind
26163	2	8043	6	13	NULL	NULL	NULL	Crk	GP		does not bind			SH3 domain		dynamin	GP				NULL	3T3-L1 adipocytes	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8169_s_176	9525921	3T3-L1 adipocytes were microinjected with fusion proteins containing the SH3 domains of spectrin and Crk (Fig.  5 A), which do not bind dynamin ( 23).	bind
31574	1	8043	7	NULL	NULL	0	NULL	 spectrin	NULL		does not bind	NULL		SH3 domain		dynamin	NULL				NULL	3T3-L1 adipocytes 	0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8169_s_176	9525921	3T3-L1 adipocytes were microinjected with fusion proteins containing the SH3 domains of spectrin and Crk (Fig.  5 A), which do not bind dynamin ( 23).	bind
31576	2	8043	7	NULL	NULL	0	NULL	Crk	NULL		does not bind	NULL		SH3 domain		dynamin	NULL				NULL	3T3-L1 adipocytes	0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8169_s_176	9525921	3T3-L1 adipocytes were microinjected with fusion proteins containing the SH3 domains of spectrin and Crk (Fig.  5 A), which do not bind dynamin ( 23).	bind
26164	1	8044	6	13	NULL	NULL	NULL	AFP	GP	unlabeled	bind					MDM	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_3_507_s_40	12176010	3x105 cpm) binding to MDM by unlabeled AFP or MIP-1  were analyzed by fitting to a logistic curve or according to Scatchard.	bind
26165	2	8044	6	13	NULL	NULL	NULL	MIP-1	GP	unlabeled	bind					MDM	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_3_507_s_40	12176010	3x105 cpm) binding to MDM by unlabeled AFP or MIP-1  were analyzed by fitting to a logistic curve or according to Scatchard.	bind
31579	1	8044	7	NULL	NULL	0	NULL	AFP	NULL	unlabeled	bind	NULL				MDM	NULL				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_3_507_s_40	12176010	3x105 cpm) binding to MDM by unlabeled AFP or MIP-1  were analyzed by fitting to a logistic curve or according to Scatchard.	bind
31580	2	8044	7	NULL	NULL	0	NULL	MIP-1	NULL	unlabeled	bind	NULL				MDM	NULL				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_3_507_s_40	12176010	3x105 cpm) binding to MDM by unlabeled AFP or MIP-1  were analyzed by fitting to a logistic curve or according to Scatchard.	bind
26166	1	8046	6	13	NULL	NULL	NULL	Y-box binding protein 1	GP		bind		preferentially			DNA	NucleicAcid	cisplatin-modified			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1200_s_259	11222770	4       Ise,T., Nagatani,G., Imamura,T., Kato,K., Takano,H., Nomoto,M., Izumi,H., Ohmori,H., Okamoto,T., Ohga,T., Uchiumi,T., Kuwano,M. and Kohno,K. (1999) Transcription factor Y-box binding protein 1 binds preferentially to cisplatin-modified DNA and interacts with proliferating cell nuclear antigen.	bind
26167	2	8046	6	13	NULL	NULL	NULL	Y-box binding protein 1	GP		interacts with					proliferating cell nuclear antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1200_s_259	11222770	4       Ise,T., Nagatani,G., Imamura,T., Kato,K., Takano,H., Nomoto,M., Izumi,H., Ohmori,H., Okamoto,T., Ohga,T., Uchiumi,T., Kuwano,M. and Kohno,K. (1999) Transcription factor Y-box binding protein 1 binds preferentially to cisplatin-modified DNA and interacts with proliferating cell nuclear antigen.	bind
46537	3	8046	6	13	NULL	NULL	NULL	\tY-box binding protein 1 	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1200_s_259	11222770	4       Ise,T., Nagatani,G., Imamura,T., Kato,K., Takano,H., Nomoto,M., Izumi,H., Ohmori,H., Okamoto,T., Ohga,T., Uchiumi,T., Kuwano,M. and Kohno,K. (1999) Transcription factor Y-box binding protein 1 binds preferentially to cisplatin-modified DNA and interacts with proliferating cell nuclear antigen.	bind
31583	1	8046	7	10	NULL	0	NULL	Y-box binding protein 1	NULL		binds	NULL	preferentially			DNA	NULL	 cisplatin-modified			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1200_s_259	11222770	4       Ise,T., Nagatani,G., Imamura,T., Kato,K., Takano,H., Nomoto,M., Izumi,H., Ohmori,H., Okamoto,T., Ohga,T., Uchiumi,T., Kuwano,M. and Kohno,K. (1999) Transcription factor Y-box binding protein 1 binds preferentially to cisplatin-modified DNA and interacts with proliferating cell nuclear antigen.	bind
31584	2	8046	7	10	NULL	0	NULL	Y-box binding protein 1	NULL		interacts with	NULL				proliferating cell nuclear antigen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1200_s_259	11222770	4       Ise,T., Nagatani,G., Imamura,T., Kato,K., Takano,H., Nomoto,M., Izumi,H., Ohmori,H., Okamoto,T., Ohga,T., Uchiumi,T., Kuwano,M. and Kohno,K. (1999) Transcription factor Y-box binding protein 1 binds preferentially to cisplatin-modified DNA and interacts with proliferating cell nuclear antigen.	bind
46538	3	8046	7	10	NULL	0	NULL	Y-box binding protein 1	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1200_s_259	11222770	4       Ise,T., Nagatani,G., Imamura,T., Kato,K., Takano,H., Nomoto,M., Izumi,H., Ohmori,H., Okamoto,T., Ohga,T., Uchiumi,T., Kuwano,M. and Kohno,K. (1999) Transcription factor Y-box binding protein 1 binds preferentially to cisplatin-modified DNA and interacts with proliferating cell nuclear antigen.	bind
26168	1	8047	6	13	NULL	NULL	NULL	uterine estrogen receptor	GP	purified;;calf	bind		high affinity			DNA	NucleicAcid			estrogen response element	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_219	11452016	4       Klinge,C.M., Brolly,C.L., Bambara,R.A. and Hilf,R. (1997) Hsp70 is not required for high affinity binding of purified calf uterine estrogen receptor to estrogen response element DNA  in vitro.	bind
26169	2	8047	6	13	NULL	NULL	NULL	Hsp70	GP		is not required for					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_219	11452016	4       Klinge,C.M., Brolly,C.L., Bambara,R.A. and Hilf,R. (1997) Hsp70 is not required for high affinity binding of purified calf uterine estrogen receptor to estrogen response element DNA  in vitro.	bind
31585	1	8047	7	10	NULL	0	NULL	uterine estrogen receptor	NULL	purified;;calf	bind	NULL	high affinity			DNA	NULL			estrogen response element	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_219	11452016	4       Klinge,C.M., Brolly,C.L., Bambara,R.A. and Hilf,R. (1997) Hsp70 is not required for high affinity binding of purified calf uterine estrogen receptor to estrogen response element DNA  in vitro.	bind
31586	2	8047	7	10	NULL	0	NULL	Hsp70			is not required for					statement 1					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_219	11452016	4       Klinge,C.M., Brolly,C.L., Bambara,R.A. and Hilf,R. (1997) Hsp70 is not required for high affinity binding of purified calf uterine estrogen receptor to estrogen response element DNA  in vitro.	bind
26170	1	8048	6	13	NULL	NULL	NULL	GCN4-bZIP	GP		bind					DNA	NucleicAcid			ATF CREB site 	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3311_s_240	11504868	4       Konig,P. and Richmond,T.J. (1993) The X-ray structure of the GCN4-bZIP bound to ATF CREB site DNA shows the complex depends on DNA flexibility.	bind
26171	2	8048	6	13	NULL	NULL	NULL	statement 1	Process		depends on					DNA	NucleicAcid	flexibility of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3311_s_240	11504868	4       Konig,P. and Richmond,T.J. (1993) The X-ray structure of the GCN4-bZIP bound to ATF CREB site DNA shows the complex depends on DNA flexibility.	bind
31587	1	8048	7	NULL	NULL	0	NULL	GCN4-bZIP	NULL		bind	NULL				DNA	NULL			ATF CREB site	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3311_s_240	11504868	4       Konig,P. and Richmond,T.J. (1993) The X-ray structure of the GCN4-bZIP bound to ATF CREB site DNA shows the complex depends on DNA flexibility.	bind
31588	2	8048	7	NULL	NULL	0	NULL	statement 1	NULL		depends on	NULL				DNA 	NULL	flexibility of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3311_s_240	11504868	4       Konig,P. and Richmond,T.J. (1993) The X-ray structure of the GCN4-bZIP bound to ATF CREB site DNA shows the complex depends on DNA flexibility.	bind
26172	1	8049	6	13	NULL	NULL	NULL	NF-kappaB	GP	nuclear	bind		directly			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_55_2_135_s_49	15650002	4   Electrophoretic mobility shift assays revealed that the drugs inhibit the TNF-alpha-induced DNA binding of nuclear NF-kappaB, but not the binding of NF-kappaB to DNA directly.	bind
26173	2	8049	6	13	NULL	NULL	NULL	TNF-alpha	GP		induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_55_2_135_s_49	15650002	4   Electrophoretic mobility shift assays revealed that the drugs inhibit the TNF-alpha-induced DNA binding of nuclear NF-kappaB, but not the binding of NF-kappaB to DNA directly.	bind
31589	1	8049	7	NULL	NULL	0	NULL	NF-kappaB	NULL	nuclear	bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_jantimicrobchemoth_55_2_135_s_49	15650002	4   Electrophoretic mobility shift assays revealed that the drugs inhibit the TNF-alpha-induced DNA binding of nuclear NF-kappaB, but not the binding of NF-kappaB to DNA directly.	bind
31590	2	8049	7	NULL	NULL	0	NULL	TNF-alpha	NULL		induce	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jantimicrobchemoth_55_2_135_s_49	15650002	4   Electrophoretic mobility shift assays revealed that the drugs inhibit the TNF-alpha-induced DNA binding of nuclear NF-kappaB, but not the binding of NF-kappaB to DNA directly.	bind
26174	1	8050	6	13	NULL	NULL	NULL	p67 phox	GP		bind		poorly			Rac143Rho	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18834_s_230	9228059	4   It is not clear from the Rac structure whether the poor binding of p67 phox by the Rac143Rho chimera reflects an additional binding surface for p67 phox within the 143-175 range.	bind
46539	2	8050	6	13	NULL	NULL	NULL	Rac143Rho	GP		is a type of					chimera	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18834_s_230	9228059	4   It is not clear from the Rac structure whether the poor binding of p67 phox by the Rac143Rho chimera reflects an additional binding surface for p67 phox within the 143-175 range.	bind
31596	1	8050	7	10	NULL	0	NULL	Rac143Rho	NULL		bind	NULL	poorly			p67 phox	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18834_s_230	9228059	4   It is not clear from the Rac structure whether the poor binding of p67 phox by the Rac143Rho chimera reflects an additional binding surface for p67 phox within the 143-175 range.	bind
46540	2	8050	7	10	NULL	0	NULL	Rac143Rho	NULL		is a type of	NULL				chimera	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_30_18834_s_230	9228059	4   It is not clear from the Rac structure whether the poor binding of p67 phox by the Rac143Rho chimera reflects an additional binding surface for p67 phox within the 143-175 range.	bind
26175	1	8051	6	13	NULL	NULL	NULL	apoE	GP		bind					Abeta-peptide	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_869_s_13	10487844	4  Although apoE binds Abeta-peptide and promotes beta-amyloid fibrillogenesis 5 in vitro, it is unclear whether the APOE4 genotype is associated with accelerated cognitive deterioration.	bind
26176	2	8051	6	13	NULL	NULL	NULL	statement 1	Process		promotes					beta-amyloid fibrillogenesis	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_869_s_13	10487844	4  Although apoE binds Abeta-peptide and promotes beta-amyloid fibrillogenesis 5 in vitro, it is unclear whether the APOE4 genotype is associated with accelerated cognitive deterioration.	bind
31599	1	8051	7	NULL	NULL	0	NULL	 apoE 	NULL		binds	NULL				Abeta-peptide	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_amjpathol_155_3_869_s_13	10487844	4  Although apoE binds Abeta-peptide and promotes beta-amyloid fibrillogenesis 5 in vitro, it is unclear whether the APOE4 genotype is associated with accelerated cognitive deterioration.	bind
31600	2	8051	7	NULL	NULL	0	NULL	statement 1	NULL		promotes	NULL				beta-amyloid fibrillogenesis	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_amjpathol_155_3_869_s_13	10487844	4  Although apoE binds Abeta-peptide and promotes beta-amyloid fibrillogenesis 5 in vitro, it is unclear whether the APOE4 genotype is associated with accelerated cognitive deterioration.	bind
26177	1	8052	6	13	NULL	NULL	NULL	MCP-1	GP		does not bind					CCR2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_6_1951_s_226	10854218	4  Another intriguing possibility is the binding of MCP-1 to receptors other than CCR2.	bind
55805	2	8052	6	13	NULL	NULL	NULL	CCR2	GP		is a type of					receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_6_1951_s_226	10854218	4  Another intriguing possibility is the binding of MCP-1 to receptors other than CCR2.	bind
31601	1	8052	7	NULL	NULL	0	NULL	MCP-1	NULL		does not bind	NULL				CCR2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_6_1951_s_226	10854218	4  Another intriguing possibility is the binding of MCP-1 to receptors other than CCR2.	bind
31602	2	8052	7	NULL	NULL	0	NULL	CCR2	NULL		is a type of	NULL				receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_6_1951_s_226	10854218	4  Another intriguing possibility is the binding of MCP-1 to receptors other than CCR2.	bind
26178	1	8053	6	13	NULL	NULL	NULL	VSMC	Cell		is					vascular smooth muscle cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_7_648_s_6	11304484	4  Both macrophages and vascular smooth muscle cells (VSMCs) bind oxidized LDL via specific scavenger receptors, 5 6  forming foam cells.	bind
26179	2	8053	6	13	NULL	NULL	NULL	macrophages	Cell		bind					LDL	GP	oxidized			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_7_648_s_6	11304484	4  Both macrophages and vascular smooth muscle cells (VSMCs) bind oxidized LDL via specific scavenger receptors, 5 6  forming foam cells.	bind
26180	3	8053	6	13	NULL	NULL	NULL	VSMC	Cell		bind					LDL	GP	oxidized			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_7_648_s_6	11304484	4  Both macrophages and vascular smooth muscle cells (VSMCs) bind oxidized LDL via specific scavenger receptors, 5 6  forming foam cells.	bind
26181	4	8053	6	13	NULL	NULL	NULL	statement 2	Process		occurs via					scavenger receptors	GP	specific			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_7_648_s_6	11304484	4  Both macrophages and vascular smooth muscle cells (VSMCs) bind oxidized LDL via specific scavenger receptors, 5 6  forming foam cells.	bind
26182	5	8053	6	13	NULL	NULL	NULL	statement 3	Process		occurs via					scavenger receptors	GP	specific			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_7_648_s_6	11304484	4  Both macrophages and vascular smooth muscle cells (VSMCs) bind oxidized LDL via specific scavenger receptors, 5 6  forming foam cells.	bind
31603	1	8053	7	10	NULL	0	NULL	macrophages	NULL		bind	NULL				LDL	NULL	oxidized			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_7_648_s_6	11304484	4  Both macrophages and vascular smooth muscle cells (VSMCs) bind oxidized LDL via specific scavenger receptors, 5 6  forming foam cells.	bind
31604	2	8053	7	10	NULL	0	NULL	VSMCs	NULL		bind	NULL				LDL	NULL	oxidized			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_7_648_s_6	11304484	4  Both macrophages and vascular smooth muscle cells (VSMCs) bind oxidized LDL via specific scavenger receptors, 5 6  forming foam cells.	bind
31605	3	8053	7	10	NULL	0	NULL	statement 1			via					scaveger receptor		specific			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_7_648_s_6	11304484	4  Both macrophages and vascular smooth muscle cells (VSMCs) bind oxidized LDL via specific scavenger receptors, 5 6  forming foam cells.	bind
31606	4	8053	7	10	NULL	0	NULL	statement 2			via					scaveger receptor		specific			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_7_648_s_6	11304484	4  Both macrophages and vascular smooth muscle cells (VSMCs) bind oxidized LDL via specific scavenger receptors, 5 6  forming foam cells.	bind
31607	5	8053	7	NULL	NULL	0	NULL	statement 3	NULL		forms	NULL				foam cells	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_88_7_648_s_6	11304484	4  Both macrophages and vascular smooth muscle cells (VSMCs) bind oxidized LDL via specific scavenger receptors, 5 6  forming foam cells.	bind
31608	6	8053	7	NULL	NULL	0	NULL	statement 4	NULL		forms	NULL				foam cells	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_88_7_648_s_6	11304484	4  Both macrophages and vascular smooth muscle cells (VSMCs) bind oxidized LDL via specific scavenger receptors, 5 6  forming foam cells.	bind
31609	7	8053	7	NULL	NULL	0	NULL	VSMCs	NULL		is	NULL				vascular smooth muscle cells	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_88_7_648_s_6	11304484	4  Both macrophages and vascular smooth muscle cells (VSMCs) bind oxidized LDL via specific scavenger receptors, 5 6  forming foam cells.	bind
26183	1	8054	6	13	NULL	NULL	NULL	HIT antibodies	GP		bind					PF4 complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_10_1479_s_16	11245656	4  HIT antibodies bind to heparin platelet factor 4 (PF4) complexes, 5  thereby activating platelets, 6 7 8  generating platelet microparticles, 9  and altering endothelial cells, 10  11 12  leading to enhanced thrombin generation and paradoxical development of new thrombi.	bind
26184	2	8054	6	13	NULL	NULL	NULL	PF4	GP		is					heparin platelet factor 4	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_10_1479_s_16	11245656	4  HIT antibodies bind to heparin platelet factor 4 (PF4) complexes, 5  thereby activating platelets, 6 7 8  generating platelet microparticles, 9  and altering endothelial cells, 10  11 12  leading to enhanced thrombin generation and paradoxical development of new thrombi.	bind
26185	3	8054	6	13	NULL	NULL	NULL	statement 1	Process		activates					platelets	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_10_1479_s_16	11245656	4  HIT antibodies bind to heparin platelet factor 4 (PF4) complexes, 5  thereby activating platelets, 6 7 8  generating platelet microparticles, 9  and altering endothelial cells, 10  11 12  leading to enhanced thrombin generation and paradoxical development of new thrombi.	bind
26186	4	8054	6	13	NULL	NULL	NULL	statement 3	Process		generates					platelet microparticles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_10_1479_s_16	11245656	4  HIT antibodies bind to heparin platelet factor 4 (PF4) complexes, 5  thereby activating platelets, 6 7 8  generating platelet microparticles, 9  and altering endothelial cells, 10  11 12  leading to enhanced thrombin generation and paradoxical development of new thrombi.	bind
26187	5	8054	6	13	NULL	NULL	NULL	statement 4	Process		leads to					thrombin	GP	generation of;; enhanced			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_10_1479_s_16	11245656	4  HIT antibodies bind to heparin platelet factor 4 (PF4) complexes, 5  thereby activating platelets, 6 7 8  generating platelet microparticles, 9  and altering endothelial cells, 10  11 12  leading to enhanced thrombin generation and paradoxical development of new thrombi.	bind
26188	6	8054	6	13	NULL	NULL	NULL	statement 4	Process		leads to					new thrombin	GP	paradoxical development of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_10_1479_s_16	11245656	4  HIT antibodies bind to heparin platelet factor 4 (PF4) complexes, 5  thereby activating platelets, 6 7 8  generating platelet microparticles, 9  and altering endothelial cells, 10  11 12  leading to enhanced thrombin generation and paradoxical development of new thrombi.	bind
26189	7	8054	6	13	NULL	NULL	NULL	statement 1	Process		alters					endothelial cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_10_1479_s_16	11245656	4  HIT antibodies bind to heparin platelet factor 4 (PF4) complexes, 5  thereby activating platelets, 6 7 8  generating platelet microparticles, 9  and altering endothelial cells, 10  11 12  leading to enhanced thrombin generation and paradoxical development of new thrombi.	bind
31622	1	8054	7	NULL	NULL	0	NULL	HIT antibody	NULL		bind	NULL				heparin PF4 complex	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_10_1479_s_16	11245656	4  HIT antibodies bind to heparin platelet factor 4 (PF4) complexes, 5  thereby activating platelets, 6 7 8  generating platelet microparticles, 9  and altering endothelial cells, 10  11 12  leading to enhanced thrombin generation and paradoxical development of new thrombi.	bind
31623	2	8054	7	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				platelets	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_10_1479_s_16	11245656	4  HIT antibodies bind to heparin platelet factor 4 (PF4) complexes, 5  thereby activating platelets, 6 7 8  generating platelet microparticles, 9  and altering endothelial cells, 10  11 12  leading to enhanced thrombin generation and paradoxical development of new thrombi.	bind
31624	3	8054	7	NULL	NULL	0	NULL	statement 2	NULL		generate	NULL				platelet microparticles	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_10_1479_s_16	11245656	4  HIT antibodies bind to heparin platelet factor 4 (PF4) complexes, 5  thereby activating platelets, 6 7 8  generating platelet microparticles, 9  and altering endothelial cells, 10  11 12  leading to enhanced thrombin generation and paradoxical development of new thrombi.	bind
31625	4	8054	7	NULL	NULL	0	NULL	statement 3	NULL		alters	NULL				endothelial cells	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_10_1479_s_16	11245656	4  HIT antibodies bind to heparin platelet factor 4 (PF4) complexes, 5  thereby activating platelets, 6 7 8  generating platelet microparticles, 9  and altering endothelial cells, 10  11 12  leading to enhanced thrombin generation and paradoxical development of new thrombi.	bind
31626	5	8054	7	10	NULL	0	NULL	statement 4	NULL		leads to	NULL				thrombin	NULL	enhanced;;generation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_10_1479_s_16	11245656	4  HIT antibodies bind to heparin platelet factor 4 (PF4) complexes, 5  thereby activating platelets, 6 7 8  generating platelet microparticles, 9  and altering endothelial cells, 10  11 12  leading to enhanced thrombin generation and paradoxical development of new thrombi.	bind
31627	6	8054	7	NULL	NULL	0	NULL	statement 4	NULL		leads to	NULL				new thrombin	NULL	development of			NULL		0	NULL	NULL	NULL	gw60_circulation_103_10_1479_s_16	11245656	4  HIT antibodies bind to heparin platelet factor 4 (PF4) complexes, 5  thereby activating platelets, 6 7 8  generating platelet microparticles, 9  and altering endothelial cells, 10  11 12  leading to enhanced thrombin generation and paradoxical development of new thrombi.	bind
31628	7	8054	7	NULL	NULL	0	NULL	PF4	NULL		is	NULL				platelet factor 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_10_1479_s_16	11245656	4  HIT antibodies bind to heparin platelet factor 4 (PF4) complexes, 5  thereby activating platelets, 6 7 8  generating platelet microparticles, 9  and altering endothelial cells, 10  11 12  leading to enhanced thrombin generation and paradoxical development of new thrombi.	bind
26190	1	8055	6	13	NULL	NULL	NULL	T3	Chemical		bind					T3 receptors 	GP	specific;; nuclear			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_3_260_s_8	11179190	4  In most tissues, the mechanism of TH biological action occurs by the entry of T3 into the cell by facilitated transport and the binding of T3 to specific nuclear T3 receptors (TRs), which regulate transcription of target genes.	bind
26191	2	8055	6	13	NULL	NULL	NULL	T3	Chemical		enters into					cell	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_3_260_s_8	11179190	4  In most tissues, the mechanism of TH biological action occurs by the entry of T3 into the cell by facilitated transport and the binding of T3 to specific nuclear T3 receptors (TRs), which regulate transcription of target genes.	bind
26192	3	8055	6	13	NULL	NULL	NULL	statement 2	Process		leads to					TH	Chemical	biological action of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_3_260_s_8	11179190	4  In most tissues, the mechanism of TH biological action occurs by the entry of T3 into the cell by facilitated transport and the binding of T3 to specific nuclear T3 receptors (TRs), which regulate transcription of target genes.	bind
55815	4	8055	6	13	NULL	NULL	NULL	statement 2	Process		via					facilitated transport	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_3_260_s_8	11179190	4  In most tissues, the mechanism of TH biological action occurs by the entry of T3 into the cell by facilitated transport and the binding of T3 to specific nuclear T3 receptors (TRs), which regulate transcription of target genes.	bind
55816	5	8055	6	13	NULL	NULL	NULL	TRs	GP		is					T3 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_3_260_s_8	11179190	4  In most tissues, the mechanism of TH biological action occurs by the entry of T3 into the cell by facilitated transport and the binding of T3 to specific nuclear T3 receptors (TRs), which regulate transcription of target genes.	bind
55817	6	8055	6	13	NULL	NULL	NULL	statement 1	Process		regulates					target genes	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_3_260_s_8	11179190	4  In most tissues, the mechanism of TH biological action occurs by the entry of T3 into the cell by facilitated transport and the binding of T3 to specific nuclear T3 receptors (TRs), which regulate transcription of target genes.	bind
31646	1	8055	7	NULL	NULL	0	NULL	T3	NULL		enters into the	NULL				Cell	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_3_260_s_8	11179190	4  In most tissues, the mechanism of TH biological action occurs by the entry of T3 into the cell by facilitated transport and the binding of T3 to specific nuclear T3 receptors (TRs), which regulate transcription of target genes.	bind
31647	2	8055	7	10	NULL	0	NULL	statement 1			via					facilitated transport					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_3_260_s_8	11179190	4  In most tissues, the mechanism of TH biological action occurs by the entry of T3 into the cell by facilitated transport and the binding of T3 to specific nuclear T3 receptors (TRs), which regulate transcription of target genes.	bind
31648	3	8055	7	10	NULL	0	NULL	T3	NULL		bind	NULL				T3 receptors	NULL	specific;;nuclear			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_3_260_s_8	11179190	4  In most tissues, the mechanism of TH biological action occurs by the entry of T3 into the cell by facilitated transport and the binding of T3 to specific nuclear T3 receptors (TRs), which regulate transcription of target genes.	bind
31649	4	8055	7	NULL	NULL	0	NULL	statement 3	NULL		regulate	NULL				target genes	NULL	transcription of			NULL		0	NULL	NULL	NULL	gw60_circulationres_88_3_260_s_8	11179190	4  In most tissues, the mechanism of TH biological action occurs by the entry of T3 into the cell by facilitated transport and the binding of T3 to specific nuclear T3 receptors (TRs), which regulate transcription of target genes.	bind
31650	5	8055	7	NULL	NULL	0	NULL	TRs	NULL		is	NULL				T3 receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_88_3_260_s_8	11179190	4  In most tissues, the mechanism of TH biological action occurs by the entry of T3 into the cell by facilitated transport and the binding of T3 to specific nuclear T3 receptors (TRs), which regulate transcription of target genes.	bind
55818	6	8055	7	10	NULL	0	NULL	statement 2			leads to					TH		action of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_3_260_s_8	11179190	4  In most tissues, the mechanism of TH biological action occurs by the entry of T3 into the cell by facilitated transport and the binding of T3 to specific nuclear T3 receptors (TRs), which regulate transcription of target genes.	bind
26286	1	8056	6	13	NULL	NULL	NULL	MHC	GP		repressed in					NB	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_291_s_236	12107114	4  In this study, we have demonstrated that the repression of MHC in NB is also caused by deficient CIITA expression and that neuroendocrine cell-specific bHLH factors competitively bind to the CIITA promoter and repress the promoter IV activity in both NB and SCLC.	bind
26287	2	8056	6	13	NULL	NULL	NULL	CIITA	GP	expression of	is deficient in					NB	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_291_s_236	12107114	4  In this study, we have demonstrated that the repression of MHC in NB is also caused by deficient CIITA expression and that neuroendocrine cell-specific bHLH factors competitively bind to the CIITA promoter and repress the promoter IV activity in both NB and SCLC.	bind
26288	3	8056	6	13	NULL	NULL	NULL	statement 8	GP		bind		competitively			CIITA	GP			promoter	NULL	NB	NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_291_s_236	12107114	4  In this study, we have demonstrated that the repression of MHC in NB is also caused by deficient CIITA expression and that neuroendocrine cell-specific bHLH factors competitively bind to the CIITA promoter and repress the promoter IV activity in both NB and SCLC.	bind
26289	4	8056	6	13	NULL	NULL	NULL	statement 3	Process		repress					CIITA	GP	activity of		promoter IV	NULL	NB	NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_291_s_236	12107114	4  In this study, we have demonstrated that the repression of MHC in NB is also caused by deficient CIITA expression and that neuroendocrine cell-specific bHLH factors competitively bind to the CIITA promoter and repress the promoter IV activity in both NB and SCLC.	bind
26290	5	8056	6	13	NULL	NULL	NULL	statement 8	GP		bind		competitively			CIITA	GP			promoter	NULL	SCLC	NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_291_s_236	12107114	4  In this study, we have demonstrated that the repression of MHC in NB is also caused by deficient CIITA expression and that neuroendocrine cell-specific bHLH factors competitively bind to the CIITA promoter and repress the promoter IV activity in both NB and SCLC.	bind
26291	6	8056	6	13	NULL	NULL	NULL	statement 5	Process		repress					CIITA	GP	activity of		promoter IV	NULL	SCLC	NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_291_s_236	12107114	4  In this study, we have demonstrated that the repression of MHC in NB is also caused by deficient CIITA expression and that neuroendocrine cell-specific bHLH factors competitively bind to the CIITA promoter and repress the promoter IV activity in both NB and SCLC.	bind
55819	7	8056	6	13	NULL	NULL	NULL	statement 2	Process		causes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_291_s_236	12107114	4  In this study, we have demonstrated that the repression of MHC in NB is also caused by deficient CIITA expression and that neuroendocrine cell-specific bHLH factors competitively bind to the CIITA promoter and repress the promoter IV activity in both NB and SCLC.	bind
55820	8	8056	6	13	NULL	NULL	NULL	bHLH factors	GP		specific to					neuroendocrine cell	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_291_s_236	12107114	4  In this study, we have demonstrated that the repression of MHC in NB is also caused by deficient CIITA expression and that neuroendocrine cell-specific bHLH factors competitively bind to the CIITA promoter and repress the promoter IV activity in both NB and SCLC.	bind
31651	1	8056	7	10	NULL	0	NULL	MHC			repressed in					NB					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_291_s_236	12107114	4  In this study, we have demonstrated that the repression of MHC in NB is also caused by deficient CIITA expression and that neuroendocrine cell-specific bHLH factors competitively bind to the CIITA promoter and repress the promoter IV activity in both NB and SCLC.	bind
31652	2	8056	7	10	NULL	0	NULL	statement 8			bind		competitively			CIITA				promoter	NULL	NB	NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_291_s_236	12107114	4  In this study, we have demonstrated that the repression of MHC in NB is also caused by deficient CIITA expression and that neuroendocrine cell-specific bHLH factors competitively bind to the CIITA promoter and repress the promoter IV activity in both NB and SCLC.	bind
31653	3	8056	7	10	NULL	0	NULL	statement 8			bind		competitively			CIITA				promoter	NULL	SCLC	NULL	NULL	NULL	NULL	gw60_amjpathol_161_1_291_s_236	12107114	4  In this study, we have demonstrated that the repression of MHC in NB is also caused by deficient CIITA expression and that neuroendocrine cell-specific bHLH factors competitively bind to the CIITA promoter and repress the promoter IV activity in both NB and SCLC.	bind
31655	4	8056	7	NULL	NULL	0	NULL	statement 2	NULL		repress	NULL					NULL	activity of		promoter IV	NULL	NB	0	NULL	NULL	NULL	gw60_amjpathol_161_1_291_s_236	12107114	4  In this study, we have demonstrated that the repression of MHC in NB is also caused by deficient CIITA expression and that neuroendocrine cell-specific bHLH factors competitively bind to the CIITA promoter and repress the promoter IV activity in both NB and SCLC.	bind
31657	5	8056	7	NULL	NULL	0	NULL	statement 3	NULL		repress	NULL					NULL	activity of		promoter IV	NULL	SCLC	0	NULL	NULL	NULL	gw60_amjpathol_161_1_291_s_236	12107114	4  In this study, we have demonstrated that the repression of MHC in NB is also caused by deficient CIITA expression and that neuroendocrine cell-specific bHLH factors competitively bind to the CIITA promoter and repress the promoter IV activity in both NB and SCLC.	bind
55821	6	8056	7	10	NULL	0	NULL	CIITA		expression of	is deficient in					NB					NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_1_291_s_236	12107114	4  In this study, we have demonstrated that the repression of MHC in NB is also caused by deficient CIITA expression and that neuroendocrine cell-specific bHLH factors competitively bind to the CIITA promoter and repress the promoter IV activity in both NB and SCLC.	bind
55822	7	8056	7	10	NULL	0	NULL	statement 6			causes					statement 1					NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_1_291_s_236	12107114	4  In this study, we have demonstrated that the repression of MHC in NB is also caused by deficient CIITA expression and that neuroendocrine cell-specific bHLH factors competitively bind to the CIITA promoter and repress the promoter IV activity in both NB and SCLC.	bind
55823	8	8056	7	10	NULL	0	NULL	bHLH factors			specific to					neuroendocrine cell					NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_1_291_s_236	12107114	4  In this study, we have demonstrated that the repression of MHC in NB is also caused by deficient CIITA expression and that neuroendocrine cell-specific bHLH factors competitively bind to the CIITA promoter and repress the promoter IV activity in both NB and SCLC.	bind
26193	1	8057	6	13	NULL	NULL	NULL	fibrinogen	GP		bind					platelet GP IIb/IIa receptor	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_2_149_s_21	10889124	4  Orbofiban is an oral ethyl-ester pro-drug that specifically blocks the binding of fibrinogen to the platelet GP IIb/IIa receptor (with a higher affinity for the activated versus unactivated receptor), thereby interfering with the platelet aggregation induced by various agonists.	bind
26194	2	8057	6	13	NULL	NULL	NULL	Orbofiban	Chemical		blocks 		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_2_149_s_21	10889124	4  Orbofiban is an oral ethyl-ester pro-drug that specifically blocks the binding of fibrinogen to the platelet GP IIb/IIa receptor (with a higher affinity for the activated versus unactivated receptor), thereby interfering with the platelet aggregation induced by various agonists.	bind
26195	3	8057	6	13	NULL	NULL	NULL	Orbofiban	Chemical		is a type of					oral ethyl-ester pro-drug	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_2_149_s_21	10889124	4  Orbofiban is an oral ethyl-ester pro-drug that specifically blocks the binding of fibrinogen to the platelet GP IIb/IIa receptor (with a higher affinity for the activated versus unactivated receptor), thereby interfering with the platelet aggregation induced by various agonists.	bind
26196	4	8057	6	13	NULL	NULL	NULL	fibrinogen	GP		bind					platelet glycoprotein IIb/IIa complex	GP	unactivated			NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_2_149_s_21	10889124	4  Orbofiban is an oral ethyl-ester pro-drug that specifically blocks the binding of fibrinogen to the platelet GP IIb/IIa receptor (with a higher affinity for the activated versus unactivated receptor), thereby interfering with the platelet aggregation induced by various agonists.	bind
26197	5	8057	6	13	NULL	NULL	NULL	statement 1	Process	affinity of	is higher than					statement 4	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_2_149_s_21	10889124	4  Orbofiban is an oral ethyl-ester pro-drug that specifically blocks the binding of fibrinogen to the platelet GP IIb/IIa receptor (with a higher affinity for the activated versus unactivated receptor), thereby interfering with the platelet aggregation induced by various agonists.	bind
26198	6	8057	6	13	NULL	NULL	NULL	statement 2	Process		interferes with					platelet aggregation	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_2_149_s_21	10889124	4  Orbofiban is an oral ethyl-ester pro-drug that specifically blocks the binding of fibrinogen to the platelet GP IIb/IIa receptor (with a higher affinity for the activated versus unactivated receptor), thereby interfering with the platelet aggregation induced by various agonists.	bind
31661	1	8057	7	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL	high affinity			GP IIb/IIa receptor	NULL	activated			NULL		0	NULL	NULL	NULL	gw60_circulation_102_2_149_s_21	10889124	4  Orbofiban is an oral ethyl-ester pro-drug that specifically blocks the binding of fibrinogen to the platelet GP IIb/IIa receptor (with a higher affinity for the activated versus unactivated receptor), thereby interfering with the platelet aggregation induced by various agonists.	bind
31664	2	8057	7	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL				platelet GP IIb/IIa receptor	NULL	unactivated			NULL		0	NULL	NULL	NULL	gw60_circulation_102_2_149_s_21	10889124	4  Orbofiban is an oral ethyl-ester pro-drug that specifically blocks the binding of fibrinogen to the platelet GP IIb/IIa receptor (with a higher affinity for the activated versus unactivated receptor), thereby interfering with the platelet aggregation induced by various agonists.	bind
31665	3	8057	7	10	NULL	0	NULL	statement 1	NULL		higher affinity than	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_2_149_s_21	10889124	4  Orbofiban is an oral ethyl-ester pro-drug that specifically blocks the binding of fibrinogen to the platelet GP IIb/IIa receptor (with a higher affinity for the activated versus unactivated receptor), thereby interfering with the platelet aggregation induced by various agonists.	bind
31667	4	8057	7	NULL	NULL	0	NULL	Orbofiban	NULL		blocks	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_2_149_s_21	10889124	4  Orbofiban is an oral ethyl-ester pro-drug that specifically blocks the binding of fibrinogen to the platelet GP IIb/IIa receptor (with a higher affinity for the activated versus unactivated receptor), thereby interfering with the platelet aggregation induced by various agonists.	bind
31668	5	8057	7	NULL	NULL	0	NULL	Orbofiban	NULL		blocks	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_2_149_s_21	10889124	4  Orbofiban is an oral ethyl-ester pro-drug that specifically blocks the binding of fibrinogen to the platelet GP IIb/IIa receptor (with a higher affinity for the activated versus unactivated receptor), thereby interfering with the platelet aggregation induced by various agonists.	bind
31671	6	8057	7	NULL	NULL	0	NULL	Orbofiban	NULL		is a type of	NULL				oral ethyl-ester pro-drug	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_2_149_s_21	10889124	4  Orbofiban is an oral ethyl-ester pro-drug that specifically blocks the binding of fibrinogen to the platelet GP IIb/IIa receptor (with a higher affinity for the activated versus unactivated receptor), thereby interfering with the platelet aggregation induced by various agonists.	bind
31673	7	8057	7	NULL	NULL	0	NULL	agonists	NULL		induce	NULL				platelet aggregation	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_2_149_s_21	10889124	4  Orbofiban is an oral ethyl-ester pro-drug that specifically blocks the binding of fibrinogen to the platelet GP IIb/IIa receptor (with a higher affinity for the activated versus unactivated receptor), thereby interfering with the platelet aggregation induced by various agonists.	bind
31675	8	8057	7	NULL	NULL	0	NULL	Orbofiban	NULL		interferes with	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_2_149_s_21	10889124	4  Orbofiban is an oral ethyl-ester pro-drug that specifically blocks the binding of fibrinogen to the platelet GP IIb/IIa receptor (with a higher affinity for the activated versus unactivated receptor), thereby interfering with the platelet aggregation induced by various agonists.	bind
26199	1	8058	6	13	NULL	NULL	NULL	Cdc24	GP		bind		directly			Ste5	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_13084_s_214	15657049	4  These data substantiate the evidence that Cdc24 binds directly to Ste5 and argue that Cdc24-Ste5 complexes are distinct from Cdc24-Far1 complexes.	bind
46541	2	8058	6	13	NULL	NULL	NULL	Cdc24-Ste5 complex	GP		is distinct from					Cdc24-Far1 complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_13084_s_214	15657049	4  These data substantiate the evidence that Cdc24 binds directly to Ste5 and argue that Cdc24-Ste5 complexes are distinct from Cdc24-Far1 complexes.	bind
31676	1	8058	7	NULL	NULL	0	NULL	Cdc24	NULL		binds	NULL	directly			 Ste5	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_13_13084_s_214	15657049	4  These data substantiate the evidence that Cdc24 binds directly to Ste5 and argue that Cdc24-Ste5 complexes are distinct from Cdc24-Far1 complexes.	bind
31677	2	8058	7	NULL	NULL	0	NULL	Cdc24-Ste5 complex	NULL		is distinct from	NULL				Cdc24-Far1 complex	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_13_13084_s_214	15657049	4  These data substantiate the evidence that Cdc24 binds directly to Ste5 and argue that Cdc24-Ste5 complexes are distinct from Cdc24-Far1 complexes.	bind
26200	1	8059	6	13	NULL	NULL	NULL	vWF	GP		bind					GP Ib	GP	platelet			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_19	7664419	4  vWf must bind to both platelet GP Ib and GP IIb/IIa to support full platelet aggregation at these elevated levels of shear stress.	bind
26201	2	8059	6	13	NULL	NULL	NULL	vWF	GP		bind					GP IIb/IIa	GP	platelet			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_19	7664419	4  vWf must bind to both platelet GP Ib and GP IIb/IIa to support full platelet aggregation at these elevated levels of shear stress.	bind
26202	3	8059	6	13	NULL	NULL	NULL	statement 1	Process		occurs along with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_19	7664419	4  vWf must bind to both platelet GP Ib and GP IIb/IIa to support full platelet aggregation at these elevated levels of shear stress.	bind
26203	4	8059	6	13	NULL	NULL	NULL	statement 3	Process		support					platelet	Cell	aggregation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_19	7664419	4  vWf must bind to both platelet GP Ib and GP IIb/IIa to support full platelet aggregation at these elevated levels of shear stress.	bind
31678	1	8059	7	10	NULL	0	NULL	vWf			bind					GP Ib 		platelet			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_19	7664419	4  vWf must bind to both platelet GP Ib and GP IIb/IIa to support full platelet aggregation at these elevated levels of shear stress.	bind
31679	2	8059	7	10	NULL	0	NULL	vWF			bind					GP IIb/IIa		platelet			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_19	7664419	4  vWf must bind to both platelet GP Ib and GP IIb/IIa to support full platelet aggregation at these elevated levels of shear stress.	bind
31680	3	8059	7	NULL	NULL	0	NULL	statement 1	NULL		occurs along with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_19	7664419	4  vWf must bind to both platelet GP Ib and GP IIb/IIa to support full platelet aggregation at these elevated levels of shear stress.	bind
31681	4	8059	7	10	NULL	0	NULL	statement 3			support					platelet		aggregation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_19	7664419	4  vWf must bind to both platelet GP Ib and GP IIb/IIa to support full platelet aggregation at these elevated levels of shear stress.	bind
31682	5	8059	7	NULL	NULL	0	NULL	statement 4	NULL		occurs at	NULL				shear stress	NULL	elevated levels of			NULL		0	NULL	NULL	NULL	gw60_circulation_92_6_1399_s_19	7664419	4  vWf must bind to both platelet GP Ib and GP IIb/IIa to support full platelet aggregation at these elevated levels of shear stress.	bind
26204	1	8060	6	13	NULL	NULL	NULL	apoE2	GP		bind					LDLR	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_91_s_22	12969990	4 - 6   Additionally, individuals homozygous for apoE2, which binds to the LDLR with much less affinity than either apoE3 or apoE4, have low plasma cholesterol and are generally protected from atherosclerosis, except for the 5% to 10% of apoE2 homozygotes who develop type III hyperlipoproteinemia.	bind
26205	2	8060	6	13	NULL	NULL	NULL	apoE3	GP		bind					LDLR	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_91_s_22	12969990	4 - 6   Additionally, individuals homozygous for apoE2, which binds to the LDLR with much less affinity than either apoE3 or apoE4, have low plasma cholesterol and are generally protected from atherosclerosis, except for the 5% to 10% of apoE2 homozygotes who develop type III hyperlipoproteinemia.	bind
26206	3	8060	6	13	NULL	NULL	NULL	apoE4	GP		bind					LDLR	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_91_s_22	12969990	4 - 6   Additionally, individuals homozygous for apoE2, which binds to the LDLR with much less affinity than either apoE3 or apoE4, have low plasma cholesterol and are generally protected from atherosclerosis, except for the 5% to 10% of apoE2 homozygotes who develop type III hyperlipoproteinemia.	bind
26207	4	8060	6	13	NULL	NULL	NULL	statement 1	Process	affinity of	is less than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_91_s_22	12969990	4 - 6   Additionally, individuals homozygous for apoE2, which binds to the LDLR with much less affinity than either apoE3 or apoE4, have low plasma cholesterol and are generally protected from atherosclerosis, except for the 5% to 10% of apoE2 homozygotes who develop type III hyperlipoproteinemia.	bind
26208	5	8060	6	13	NULL	NULL	NULL	statement 1	Process	affinity of	is less than					statement 3	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_91_s_22	12969990	4 - 6   Additionally, individuals homozygous for apoE2, which binds to the LDLR with much less affinity than either apoE3 or apoE4, have low plasma cholesterol and are generally protected from atherosclerosis, except for the 5% to 10% of apoE2 homozygotes who develop type III hyperlipoproteinemia.	bind
26209	6	8060	6	13	NULL	NULL	NULL	homozygous apoE2	Organism	human	correlates with					plasma cholesterol	Chemical	low levels of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_91_s_22	12969990	4 - 6   Additionally, individuals homozygous for apoE2, which binds to the LDLR with much less affinity than either apoE3 or apoE4, have low plasma cholesterol and are generally protected from atherosclerosis, except for the 5% to 10% of apoE2 homozygotes who develop type III hyperlipoproteinemia.	bind
26210	7	8060	6	13	NULL	NULL	NULL	homozygous apoE2	Organism	human	are protected from					atherosclerosis	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_91_s_22	12969990	4 - 6   Additionally, individuals homozygous for apoE2, which binds to the LDLR with much less affinity than either apoE3 or apoE4, have low plasma cholesterol and are generally protected from atherosclerosis, except for the 5% to 10% of apoE2 homozygotes who develop type III hyperlipoproteinemia.	bind
26211	8	8060	6	13	NULL	NULL	NULL	apoE2 homozygotes	Organism		develop					type III hyperlipoproteinemia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_91_s_22	12969990	4 - 6   Additionally, individuals homozygous for apoE2, which binds to the LDLR with much less affinity than either apoE3 or apoE4, have low plasma cholesterol and are generally protected from atherosclerosis, except for the 5% to 10% of apoE2 homozygotes who develop type III hyperlipoproteinemia.	bind
31719	1	8060	7	NULL	NULL	0	NULL	apoE2	NULL		binds	NULL	less affinity			LDLR	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_91_s_22	12969990	4 - 6   Additionally, individuals homozygous for apoE2, which binds to the LDLR with much less affinity than either apoE3 or apoE4, have low plasma cholesterol and are generally protected from atherosclerosis, except for the 5% to 10% of apoE2 homozygotes who develop type III hyperlipoproteinemia.	bind
31720	2	8060	7	NULL	NULL	0	NULL	apoE3	NULL		binds	NULL				LDLR	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_91_s_22	12969990	4 - 6   Additionally, individuals homozygous for apoE2, which binds to the LDLR with much less affinity than either apoE3 or apoE4, have low plasma cholesterol and are generally protected from atherosclerosis, except for the 5% to 10% of apoE2 homozygotes who develop type III hyperlipoproteinemia.	bind
31721	3	8060	7	NULL	NULL	0	NULL	apoE4	NULL		binds	NULL				LDLR	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_91_s_22	12969990	4 - 6   Additionally, individuals homozygous for apoE2, which binds to the LDLR with much less affinity than either apoE3 or apoE4, have low plasma cholesterol and are generally protected from atherosclerosis, except for the 5% to 10% of apoE2 homozygotes who develop type III hyperlipoproteinemia.	bind
31722	4	8060	7	10	NULL	0	NULL	statement 2	NULL		lower affinity than	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_91_s_22	12969990	4 - 6   Additionally, individuals homozygous for apoE2, which binds to the LDLR with much less affinity than either apoE3 or apoE4, have low plasma cholesterol and are generally protected from atherosclerosis, except for the 5% to 10% of apoE2 homozygotes who develop type III hyperlipoproteinemia.	bind
31723	5	8060	7	10	NULL	0	NULL	statement 3	NULL		lower affinity than	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_91_s_22	12969990	4 - 6   Additionally, individuals homozygous for apoE2, which binds to the LDLR with much less affinity than either apoE3 or apoE4, have low plasma cholesterol and are generally protected from atherosclerosis, except for the 5% to 10% of apoE2 homozygotes who develop type III hyperlipoproteinemia.	bind
31724	6	8060	7	NULL	NULL	0	NULL	plasma cholesterol	NULL		is less in	NULL				homozygous apoE2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_91_s_22	12969990	4 - 6   Additionally, individuals homozygous for apoE2, which binds to the LDLR with much less affinity than either apoE3 or apoE4, have low plasma cholesterol and are generally protected from atherosclerosis, except for the 5% to 10% of apoE2 homozygotes who develop type III hyperlipoproteinemia.	bind
31725	7	8060	7	NULL	NULL	0	NULL	statement 6	NULL		protects from	NULL				atherosclerosis	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_1_91_s_22	12969990	4 - 6   Additionally, individuals homozygous for apoE2, which binds to the LDLR with much less affinity than either apoE3 or apoE4, have low plasma cholesterol and are generally protected from atherosclerosis, except for the 5% to 10% of apoE2 homozygotes who develop type III hyperlipoproteinemia.	bind
26292	1	8061	6	13	NULL	NULL	NULL	LDL receptor	GP		mediates					LDL particles	GP	uptake of 			NULL	in liver	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2376_s_17	9409204	4 - 6 A deletion of four amino acids from the cysteine-rich ligand binding domain of the LDL receptor7,8 preventing the LDL receptor-mediated uptake of LDL particles in the liver results in a dramatic increase of LDL cholesterol that is associated with accelerated atherosclerosis.	bind
26293	2	8061	6	13	NULL	NULL	NULL	statement 5	AminoAcid		prevents					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2376_s_17	9409204	4 - 6 A deletion of four amino acids from the cysteine-rich ligand binding domain of the LDL receptor7,8 preventing the LDL receptor-mediated uptake of LDL particles in the liver results in a dramatic increase of LDL cholesterol that is associated with accelerated atherosclerosis.	bind
26294	3	8061	6	13	NULL	NULL	NULL	statement 2	Process		results in					LDL cholesterol	Chemical	increase in			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2376_s_17	9409204	4 - 6 A deletion of four amino acids from the cysteine-rich ligand binding domain of the LDL receptor7,8 preventing the LDL receptor-mediated uptake of LDL particles in the liver results in a dramatic increase of LDL cholesterol that is associated with accelerated atherosclerosis.	bind
26295	4	8061	6	13	NULL	NULL	NULL	statement 3	Process		is associated with					atherosclerosis	MedicalFinding	accelerated			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2376_s_17	9409204	4 - 6 A deletion of four amino acids from the cysteine-rich ligand binding domain of the LDL receptor7,8 preventing the LDL receptor-mediated uptake of LDL particles in the liver results in a dramatic increase of LDL cholesterol that is associated with accelerated atherosclerosis.	bind
55824	5	8061	6	13	NULL	NULL	NULL	four amino acids	AminoAcid		deleted from					LDL receptor	GP		cysteine-rich ligand binding domain		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2376_s_17	9409204	4 - 6 A deletion of four amino acids from the cysteine-rich ligand binding domain of the LDL receptor7,8 preventing the LDL receptor-mediated uptake of LDL particles in the liver results in a dramatic increase of LDL cholesterol that is associated with accelerated atherosclerosis.	bind
31726	1	8061	7	NULL	NULL	0	NULL	LDL receptor	NULL		mediates	NULL				LDL particles	NULL	uptake of			NULL	in the liver	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2376_s_17	9409204	4 - 6 A deletion of four amino acids from the cysteine-rich ligand binding domain of the LDL receptor7,8 preventing the LDL receptor-mediated uptake of LDL particles in the liver results in a dramatic increase of LDL cholesterol that is associated with accelerated atherosclerosis.	bind
31727	2	8061	7	10	NULL	0	NULL	statement 5			prevents					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2376_s_17	9409204	4 - 6 A deletion of four amino acids from the cysteine-rich ligand binding domain of the LDL receptor7,8 preventing the LDL receptor-mediated uptake of LDL particles in the liver results in a dramatic increase of LDL cholesterol that is associated with accelerated atherosclerosis.	bind
31728	3	8061	7	NULL	NULL	0	NULL	statement 2	NULL		increase	NULL				LDL cholesterol	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2376_s_17	9409204	4 - 6 A deletion of four amino acids from the cysteine-rich ligand binding domain of the LDL receptor7,8 preventing the LDL receptor-mediated uptake of LDL particles in the liver results in a dramatic increase of LDL cholesterol that is associated with accelerated atherosclerosis.	bind
31729	4	8061	7	NULL	NULL	0	NULL	statement 3	NULL		is associated with	NULL				atherosclerosis	NULL	accelerated			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2376_s_17	9409204	4 - 6 A deletion of four amino acids from the cysteine-rich ligand binding domain of the LDL receptor7,8 preventing the LDL receptor-mediated uptake of LDL particles in the liver results in a dramatic increase of LDL cholesterol that is associated with accelerated atherosclerosis.	bind
55825	5	8061	7	10	NULL	0	NULL	four amino acids			deleted from					LDL receptor			cysteine-rich ligand binding domain		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2376_s_17	9409204	4 - 6 A deletion of four amino acids from the cysteine-rich ligand binding domain of the LDL receptor7,8 preventing the LDL receptor-mediated uptake of LDL particles in the liver results in a dramatic increase of LDL cholesterol that is associated with accelerated atherosclerosis.	bind
26212	1	8062	6	13	NULL	NULL	NULL	CrkL	GP		bind					Cbl	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_4_934_s_40	12589802	4 1 Integrin cross-linking induces tyrosine phosphorylation of Cbl, Pyk2,  and Shc as well as binding of CrkL with Cbl. 32D/EpoR-Wt cells were starved overnight  from Epo and then stimulated by cross-linking with anti- 4 antibody for 15 min or  for the indicated times at 37  degrees C before solubilization.	bind
26213	2	8062	6	13	NULL	NULL	NULL	integrin	GP	crosslinking of	induces					Cbl	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_4_934_s_40	12589802	4 1 Integrin cross-linking induces tyrosine phosphorylation of Cbl, Pyk2,  and Shc as well as binding of CrkL with Cbl. 32D/EpoR-Wt cells were starved overnight  from Epo and then stimulated by cross-linking with anti- 4 antibody for 15 min or  for the indicated times at 37  degrees C before solubilization.	bind
26214	3	8062	6	13	NULL	NULL	NULL	integrin	GP	crosslinking of	induces					Pyk2	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_4_934_s_40	12589802	4 1 Integrin cross-linking induces tyrosine phosphorylation of Cbl, Pyk2,  and Shc as well as binding of CrkL with Cbl. 32D/EpoR-Wt cells were starved overnight  from Epo and then stimulated by cross-linking with anti- 4 antibody for 15 min or  for the indicated times at 37  degrees C before solubilization.	bind
26215	4	8062	6	13	NULL	NULL	NULL	integrin	GP	crosslinking of	induces					Shc	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_4_934_s_40	12589802	4 1 Integrin cross-linking induces tyrosine phosphorylation of Cbl, Pyk2,  and Shc as well as binding of CrkL with Cbl. 32D/EpoR-Wt cells were starved overnight  from Epo and then stimulated by cross-linking with anti- 4 antibody for 15 min or  for the indicated times at 37  degrees C before solubilization.	bind
26216	5	8062	6	13	NULL	NULL	NULL	integrin	GP	crosslinking of	induces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_4_934_s_40	12589802	4 1 Integrin cross-linking induces tyrosine phosphorylation of Cbl, Pyk2,  and Shc as well as binding of CrkL with Cbl. 32D/EpoR-Wt cells were starved overnight  from Epo and then stimulated by cross-linking with anti- 4 antibody for 15 min or  for the indicated times at 37  degrees C before solubilization.	bind
31730	1	8062	7	NULL	NULL	0	NULL	Integrin	NULL	 cross-linking of	induce	NULL				Cbl	NULL	phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_4_934_s_40	12589802	4 1 Integrin cross-linking induces tyrosine phosphorylation of Cbl, Pyk2,  and Shc as well as binding of CrkL with Cbl. 32D/EpoR-Wt cells were starved overnight  from Epo and then stimulated by cross-linking with anti- 4 antibody for 15 min or  for the indicated times at 37  degrees C before solubilization.	bind
31731	2	8062	7	NULL	NULL	0	NULL	Integrin	NULL	cross-linking of	induce	NULL				Pyk2	NULL	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_4_934_s_40	12589802	4 1 Integrin cross-linking induces tyrosine phosphorylation of Cbl, Pyk2,  and Shc as well as binding of CrkL with Cbl. 32D/EpoR-Wt cells were starved overnight  from Epo and then stimulated by cross-linking with anti- 4 antibody for 15 min or  for the indicated times at 37  degrees C before solubilization.	bind
31732	3	8062	7	NULL	NULL	0	NULL	Integrin	NULL	cross-linking of	induce	NULL				Shc	NULL	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_4_934_s_40	12589802	4 1 Integrin cross-linking induces tyrosine phosphorylation of Cbl, Pyk2,  and Shc as well as binding of CrkL with Cbl. 32D/EpoR-Wt cells were starved overnight  from Epo and then stimulated by cross-linking with anti- 4 antibody for 15 min or  for the indicated times at 37  degrees C before solubilization.	bind
31733	4	8062	7	NULL	NULL	0	NULL	CrkL	NULL		bind	NULL				Cbl	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_4_934_s_40	12589802	4 1 Integrin cross-linking induces tyrosine phosphorylation of Cbl, Pyk2,  and Shc as well as binding of CrkL with Cbl. 32D/EpoR-Wt cells were starved overnight  from Epo and then stimulated by cross-linking with anti- 4 antibody for 15 min or  for the indicated times at 37  degrees C before solubilization.	bind
26217	1	8064	6	13	NULL	NULL	NULL	CGP 12177	Chemical	3H-labeled	bind					beta2-adrenoceptors	GP				NULL	CHO-beta2 cells	NULL	NULL	NULL	NULL	gw60_brjpharmacol_137_3_400_s_7	12237261	4 3H-CGP 12177 binding to beta2-adrenoceptors in intact CHO-beta2 cells yielded a log  K D value of -9.84 plus-or-minus 0.06, but indicated that the ligand dissociates very slowly from the receptor (t  for dissociation=65 min).	bind
31734	1	8064	7	10	NULL	0	NULL	CGP 12177		3H-labeled	bind					beta2-adrenoceptors					NULL	intact CHO-beta2 cells	NULL	NULL	NULL	NULL	gw60_brjpharmacol_137_3_400_s_7	12237261	4 3H-CGP 12177 binding to beta2-adrenoceptors in intact CHO-beta2 cells yielded a log  K D value of -9.84 plus-or-minus 0.06, but indicated that the ligand dissociates very slowly from the receptor (t  for dissociation=65 min).	bind
26218	1	8065	6	13	NULL	NULL	NULL	ETA receptors	GP		bind					endothelin-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_3_316_s_124	8759071	4 5  8 11  ETA receptors bind endothelin-1 and, to a lesser degree, endothelin-3; ETB receptors bind endothelin-1 and endothelin-3 with similar affinity.	bind
26219	2	8065	6	13	NULL	NULL	NULL	ETA receptors	GP		bind					endothelin-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_3_316_s_124	8759071	4 5  8 11  ETA receptors bind endothelin-1 and, to a lesser degree, endothelin-3; ETB receptors bind endothelin-1 and endothelin-3 with similar affinity.	bind
26220	3	8065	6	13	NULL	NULL	NULL	statement 1	Process	affinity of	is higher than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_3_316_s_124	8759071	4 5  8 11  ETA receptors bind endothelin-1 and, to a lesser degree, endothelin-3; ETB receptors bind endothelin-1 and endothelin-3 with similar affinity.	bind
26221	4	8065	6	13	NULL	NULL	NULL	ETB receptor	GP		bind					endothelin-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_3_316_s_124	8759071	4 5  8 11  ETA receptors bind endothelin-1 and, to a lesser degree, endothelin-3; ETB receptors bind endothelin-1 and endothelin-3 with similar affinity.	bind
26222	5	8065	6	13	NULL	NULL	NULL	ETB receptor	GP		bind					endothelin-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_3_316_s_124	8759071	4 5  8 11  ETA receptors bind endothelin-1 and, to a lesser degree, endothelin-3; ETB receptors bind endothelin-1 and endothelin-3 with similar affinity.	bind
26223	6	8065	6	13	NULL	NULL	NULL	statement 4	Process	affinity of	is equal to					statement 5	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_94_3_316_s_124	8759071	4 5  8 11  ETA receptors bind endothelin-1 and, to a lesser degree, endothelin-3; ETB receptors bind endothelin-1 and endothelin-3 with similar affinity.	bind
31737	1	8065	7	NULL	NULL	0	NULL	ETA receptors	NULL		bind	NULL				endothelin-1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_94_3_316_s_124	8759071	4 5  8 11  ETA receptors bind endothelin-1 and, to a lesser degree, endothelin-3; ETB receptors bind endothelin-1 and endothelin-3 with similar affinity.	bind
31738	2	8065	7	NULL	NULL	0	NULL	ETA receptors	NULL		bind	NULL				endothelin-3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_94_3_316_s_124	8759071	4 5  8 11  ETA receptors bind endothelin-1 and, to a lesser degree, endothelin-3; ETB receptors bind endothelin-1 and endothelin-3 with similar affinity.	bind
31739	3	8065	7	NULL	NULL	0	NULL	statement 2	NULL	binding of	is less than	NULL				statement 1	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_circulation_94_3_316_s_124	8759071	4 5  8 11  ETA receptors bind endothelin-1 and, to a lesser degree, endothelin-3; ETB receptors bind endothelin-1 and endothelin-3 with similar affinity.	bind
31740	4	8065	7	NULL	NULL	0	NULL	ETB receptors 	NULL		bind	NULL				endothelin-1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_94_3_316_s_124	8759071	4 5  8 11  ETA receptors bind endothelin-1 and, to a lesser degree, endothelin-3; ETB receptors bind endothelin-1 and endothelin-3 with similar affinity.	bind
31741	5	8065	7	NULL	NULL	0	NULL	ETB receptors	NULL		bind	NULL				endothelin-3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_94_3_316_s_124	8759071	4 5  8 11  ETA receptors bind endothelin-1 and, to a lesser degree, endothelin-3; ETB receptors bind endothelin-1 and endothelin-3 with similar affinity.	bind
31742	6	8065	7	NULL	NULL	0	NULL	statement 4	NULL	affinity of	is similar to	NULL				statement 5	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_circulation_94_3_316_s_124	8759071	4 5  8 11  ETA receptors bind endothelin-1 and, to a lesser degree, endothelin-3; ETB receptors bind endothelin-1 and endothelin-3 with similar affinity.	bind
26224	1	8066	6	13	NULL	NULL	NULL	P1GF homodimer	GP		bind		only			Flt-1 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_8_1493_s_60	8608615	4 5  The PlGF homodimer binds only to the Flt-1 receptor.	bind
31743	1	8066	7	10	NULL	0	NULL	 PlGF homodimer			binds		only			Flt-1 receptor					NULL		NULL	NULL	NULL	NULL	gw60_circulation_93_8_1493_s_60	8608615	4 5  The PlGF homodimer binds only to the Flt-1 receptor.	bind
26225	1	8068	6	13	NULL	NULL	NULL	MyBP-C	GP		bind					myosin subfragment-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_9_841_s_20	10532952	4 5 6  MyBP-C binds with myosin subfragment-2 and light meromyosin 7  and also interacts with titin (or connectin).	bind
26226	2	8068	6	13	NULL	NULL	NULL	MyBP-C	GP		bind					light meromyosin 7	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_9_841_s_20	10532952	4 5 6  MyBP-C binds with myosin subfragment-2 and light meromyosin 7  and also interacts with titin (or connectin).	bind
26227	3	8068	6	13	NULL	NULL	NULL	MyBP-C	GP		interacts with					titin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_9_841_s_20	10532952	4 5 6  MyBP-C binds with myosin subfragment-2 and light meromyosin 7  and also interacts with titin (or connectin).	bind
26228	4	8068	6	13	NULL	NULL	NULL	MyBP-C	GP		interacts with					connectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_9_841_s_20	10532952	4 5 6  MyBP-C binds with myosin subfragment-2 and light meromyosin 7  and also interacts with titin (or connectin).	bind
26229	5	8068	6	13	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_9_841_s_20	10532952	4 5 6  MyBP-C binds with myosin subfragment-2 and light meromyosin 7  and also interacts with titin (or connectin).	bind
31746	1	8068	7	NULL	NULL	0	NULL	MyBP-C	NULL		binds	NULL				myosin subfragment-2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_9_841_s_20	10532952	4 5 6  MyBP-C binds with myosin subfragment-2 and light meromyosin 7  and also interacts with titin (or connectin).	bind
31747	2	8068	7	NULL	NULL	0	NULL	MyBP-C 	NULL		binds	NULL				light meromyosin 7	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_9_841_s_20	10532952	4 5 6  MyBP-C binds with myosin subfragment-2 and light meromyosin 7  and also interacts with titin (or connectin).	bind
31748	3	8068	7	NULL	NULL	0	NULL	MyBP-C	NULL		interacts with	NULL				titin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_9_841_s_20	10532952	4 5 6  MyBP-C binds with myosin subfragment-2 and light meromyosin 7  and also interacts with titin (or connectin).	bind
31749	4	8068	7	NULL	NULL	0	NULL	MyBP-C	NULL		interacts with	NULL				connectin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_9_841_s_20	10532952	4 5 6  MyBP-C binds with myosin subfragment-2 and light meromyosin 7  and also interacts with titin (or connectin).	bind
26230	1	8069	6	13	NULL	NULL	NULL	fibrinogen	GP		bind					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_156_s_35	9012651	4 5 6 7 8 9 10 11 12 13 14 15 16 17 18  Furthermore, instead of inducing inhibition, LDL particles increased the binding of fibrinogen to both ADP and proteolytic enzyme - activated platelets.	bind
26231	2	8069	6	13	NULL	NULL	NULL	fibrinogen	GP		bind					platelets	Cell	proteolytic enzyme - activated			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_156_s_35	9012651	4 5 6 7 8 9 10 11 12 13 14 15 16 17 18  Furthermore, instead of inducing inhibition, LDL particles increased the binding of fibrinogen to both ADP and proteolytic enzyme - activated platelets.	bind
26232	3	8069	6	13	NULL	NULL	NULL	LDL particles	GP		increased					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_156_s_35	9012651	4 5 6 7 8 9 10 11 12 13 14 15 16 17 18  Furthermore, instead of inducing inhibition, LDL particles increased the binding of fibrinogen to both ADP and proteolytic enzyme - activated platelets.	bind
26233	4	8069	6	13	NULL	NULL	NULL	LDL particles	GP		increased					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_156_s_35	9012651	4 5 6 7 8 9 10 11 12 13 14 15 16 17 18  Furthermore, instead of inducing inhibition, LDL particles increased the binding of fibrinogen to both ADP and proteolytic enzyme - activated platelets.	bind
31750	1	8069	7	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL				ADP	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_156_s_35	9012651	4 5 6 7 8 9 10 11 12 13 14 15 16 17 18  Furthermore, instead of inducing inhibition, LDL particles increased the binding of fibrinogen to both ADP and proteolytic enzyme - activated platelets.	bind
31751	2	8069	7	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL				 platelets	NULL	proteolytic enzyme - activated			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_156_s_35	9012651	4 5 6 7 8 9 10 11 12 13 14 15 16 17 18  Furthermore, instead of inducing inhibition, LDL particles increased the binding of fibrinogen to both ADP and proteolytic enzyme - activated platelets.	bind
31752	3	8069	7	NULL	NULL	0	NULL	LDL particles	NULL		increase	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_156_s_35	9012651	4 5 6 7 8 9 10 11 12 13 14 15 16 17 18  Furthermore, instead of inducing inhibition, LDL particles increased the binding of fibrinogen to both ADP and proteolytic enzyme - activated platelets.	bind
31753	4	8069	7	NULL	NULL	0	NULL	LDL particles	NULL		increase	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_156_s_35	9012651	4 5 6 7 8 9 10 11 12 13 14 15 16 17 18  Furthermore, instead of inducing inhibition, LDL particles increased the binding of fibrinogen to both ADP and proteolytic enzyme - activated platelets.	bind
26234	1	8070	6	13	NULL	NULL	NULL	Ab	GP		bind		less affinity			p185her2/neu form	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_10_5497_s_46	11320219	4 Ab also binds to the human p185her2/neu form with reduced affinity ( 14).	bind
31754	1	8070	7	NULL	NULL	0	NULL	Ab	NULL		binds	NULL	reduced affinity			p185her2/neu form	NULL	human			NULL		0	NULL	NULL	NULL	gw60_pnas_98_10_5497_s_46	11320219	4 Ab also binds to the human p185her2/neu form with reduced affinity ( 14).	bind
26235	1	8071	6	13	NULL	NULL	NULL	L-canavanine	AminoAcid		bind					eNOS	GP		oxygenase domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25218_s_254	10464242	4 Absence of the  N5 proton and H-bond has been independently described based on an x-ray crystallographic structure of L-canavanine bound to the eNOS oxygenase domain (C. S. Raman, H. Li, P. Martasek, V. Kral, B. S. S. Masters, and T. L. Poulos, submitted for publication).	bind
31757	1	8071	7	NULL	NULL	0	NULL	L-canavanine	NULL		bind	NULL				eNOS	NULL		oxygenase domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_36_25218_s_254	10464242	4 Absence of the  N5 proton and H-bond has been independently described based on an x-ray crystallographic structure of L-canavanine bound to the eNOS oxygenase domain (C. S. Raman, H. Li, P. Martasek, V. Kral, B. S. S. Masters, and T. L. Poulos, submitted for publication).	bind
26236	1	8072	6	13	NULL	NULL	NULL	clathrin	GP	cytosolic	bind		avidly			HIP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_46230_s_201	11577110	4 Although cytosolic clathrin binds avidly to the HIP1 GST fusions, we note that HIP1M1 reproducibly interacts more efficiently with soluble trimers than the HIP1M2 segment.	bind
26237	2	8072	6	13	NULL	NULL	NULL	HIP1M1	GP		interacts with					trimers	GP	soluble			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_46230_s_201	11577110	4 Although cytosolic clathrin binds avidly to the HIP1 GST fusions, we note that HIP1M1 reproducibly interacts more efficiently with soluble trimers than the HIP1M2 segment.	bind
26238	3	8072	6	13	NULL	NULL	NULL	HIP1M1	GP		interacts with					HIP1M2 segment	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_46230_s_201	11577110	4 Although cytosolic clathrin binds avidly to the HIP1 GST fusions, we note that HIP1M1 reproducibly interacts more efficiently with soluble trimers than the HIP1M2 segment.	bind
26239	4	8072	6	13	NULL	NULL	NULL	statement 2	Process		is more efficient than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_46230_s_201	11577110	4 Although cytosolic clathrin binds avidly to the HIP1 GST fusions, we note that HIP1M1 reproducibly interacts more efficiently with soluble trimers than the HIP1M2 segment.	bind
46542	5	8072	6	13	NULL	NULL	NULL	HIP1	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_46230_s_201	11577110	4 Although cytosolic clathrin binds avidly to the HIP1 GST fusions, we note that HIP1M1 reproducibly interacts more efficiently with soluble trimers than the HIP1M2 segment.	bind
32059	1	8072	7	10	NULL	0	NULL	clathrin	NULL	cytosolic	binds	NULL	avidly			HIP1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_46230_s_201	11577110	4 Although cytosolic clathrin binds avidly to the HIP1 GST fusions, we note that HIP1M1 reproducibly interacts more efficiently with soluble trimers than the HIP1M2 segment.	bind
32060	2	8072	7	NULL	NULL	0	NULL	HIP1M1	NULL		interacts with	NULL	reproducibly			 trimers	NULL	soluble			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_46230_s_201	11577110	4 Although cytosolic clathrin binds avidly to the HIP1 GST fusions, we note that HIP1M1 reproducibly interacts more efficiently with soluble trimers than the HIP1M2 segment.	bind
32061	3	8072	7	NULL	NULL	0	NULL	HIP1M1	NULL		interacts with	NULL				HIP1M2 segment	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_49_46230_s_201	11577110	4 Although cytosolic clathrin binds avidly to the HIP1 GST fusions, we note that HIP1M1 reproducibly interacts more efficiently with soluble trimers than the HIP1M2 segment.	bind
32062	4	8072	7	NULL	NULL	0	NULL	statement 2	NULL		is more efficient than	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_49_46230_s_201	11577110	4 Although cytosolic clathrin binds avidly to the HIP1 GST fusions, we note that HIP1M1 reproducibly interacts more efficiently with soluble trimers than the HIP1M2 segment.	bind
46543	5	8072	7	10	NULL	0	NULL	HIP1	NULL		is a type of	NULL				GST fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_49_46230_s_201	11577110	4 Although cytosolic clathrin binds avidly to the HIP1 GST fusions, we note that HIP1M1 reproducibly interacts more efficiently with soluble trimers than the HIP1M2 segment.	bind
26240	1	8073	6	13	NULL	NULL	NULL	CHD3	GP		does not bind							methylated	lysine residues		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41789_s_111	16263726	4 Based on the requirement of the KW xxW motif, it is unlikely that CHD3 or CHD4 bind to methylated lysine residues ( Fig. 3).	bind
26241	2	8073	6	13	NULL	NULL	NULL	CHD4	GP		does not bind							methylated	lysine residues		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41789_s_111	16263726	4 Based on the requirement of the KW xxW motif, it is unlikely that CHD3 or CHD4 bind to methylated lysine residues ( Fig. 3).	bind
26242	3	8073	6	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41789_s_111	16263726	4 Based on the requirement of the KW xxW motif, it is unlikely that CHD3 or CHD4 bind to methylated lysine residues ( Fig. 3).	bind
32063	1	8073	7	10	NULL	0	NULL	CHD3	NULL		does not bind	NULL					NULL	methylated	lysine residues		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41789_s_111	16263726	4 Based on the requirement of the KW xxW motif, it is unlikely that CHD3 or CHD4 bind to methylated lysine residues ( Fig. 3).	bind
32064	2	8073	7	10	NULL	0	NULL	CHD4	NULL		does not bind	NULL					NULL	methylated	lysine residues		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41789_s_111	16263726	4 Based on the requirement of the KW xxW motif, it is unlikely that CHD3 or CHD4 bind to methylated lysine residues ( Fig. 3).	bind
32065	3	8073	7	10	NULL	0	NULL	statement 1			is an alternative to					statement 2					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41789_s_111	16263726	4 Based on the requirement of the KW xxW motif, it is unlikely that CHD3 or CHD4 bind to methylated lysine residues ( Fig. 3).	bind
26243	1	8075	6	13	NULL	NULL	NULL	C7	NucleicAcid		bind					TBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_14623_s_156	11278275	4 C7 binding to TBP in buffer ( light solid line) differs profoundly from that of the consensus sequence, but successively approaches the AdMLP.	bind
32067	1	8075	7	NULL	NULL	0	NULL	 C7	NULL		bind	NULL				TBP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_18_14623_s_156	11278275	4 C7 binding to TBP in buffer ( light solid line) differs profoundly from that of the consensus sequence, but successively approaches the AdMLP.	bind
32072	1	8076	7	13	NULL	NULL	NULL	ERalphaKOCH	Organism	mice	bind		high-affinity			estradiol	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_10_1087_s_118	12039798	4 ERalphaKOCH mice have marked reproductive phenotypes, 4, 12 but also display a low level of residual, high-affinity estradiol binding, as well as expression of two ERalpha-derived transcripts, one of which encodes a truncated ERalpha with intact DNA- and hormone-binding domains.	bind
32079	2	8076	7	13	NULL	NULL	NULL	ERalphaKOCH	Organism	mice	express					ERalpha-derived transcripts	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_10_1087_s_118	12039798	4 ERalphaKOCH mice have marked reproductive phenotypes, 4, 12 but also display a low level of residual, high-affinity estradiol binding, as well as expression of two ERalpha-derived transcripts, one of which encodes a truncated ERalpha with intact DNA- and hormone-binding domains.	bind
32080	3	8076	7	13	NULL	NULL	NULL	ERalpha-derived transcripts	GP		encode					ERalpha	GP	truncated	DNA binding domain		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_10_1087_s_118	12039798	4 ERalphaKOCH mice have marked reproductive phenotypes, 4, 12 but also display a low level of residual, high-affinity estradiol binding, as well as expression of two ERalpha-derived transcripts, one of which encodes a truncated ERalpha with intact DNA- and hormone-binding domains.	bind
32081	4	8076	7	13	NULL	NULL	NULL	ERalpha-derived transcripts	GP		encode					ERalpha	GP		hormone-binding domain		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_10_1087_s_118	12039798	4 ERalphaKOCH mice have marked reproductive phenotypes, 4, 12 but also display a low level of residual, high-affinity estradiol binding, as well as expression of two ERalpha-derived transcripts, one of which encodes a truncated ERalpha with intact DNA- and hormone-binding domains.	bind
26296	1	8077	6	13	NULL	NULL	NULL	AR structures	GP		bind					DHT	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_10_6648_s_489	16365032	4 From our original report ( ), a recent report ( ), and as shown here, the absence of a C-19 methyl group in R1881 allows the Trp-741 and Met-745 side chains to adopt a conformation that differs from previously reported AR structures bound with DHT that has the C-19 methyl ( ,  ).	bind
55826	2	8077	6	13	NULL	NULL	NULL	DHT	Chemical		contains								C-19 methyl group		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_10_6648_s_489	16365032	4 From our original report ( ), a recent report ( ), and as shown here, the absence of a C-19 methyl group in R1881 allows the Trp-741 and Met-745 side chains to adopt a conformation that differs from previously reported AR structures bound with DHT that has the C-19 methyl ( ,  ).	bind
32084	1	8077	7	10	NULL	0	NULL	AR structure			bind					DHT					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_10_6648_s_489	16365032	4 From our original report ( ), a recent report ( ), and as shown here, the absence of a C-19 methyl group in R1881 allows the Trp-741 and Met-745 side chains to adopt a conformation that differs from previously reported AR structures bound with DHT that has the C-19 methyl ( ,  ).	bind
32085	2	8077	7	10	NULL	0	NULL	DHT			contains								C-19 methyl group		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_10_6648_s_489	16365032	4 From our original report ( ), a recent report ( ), and as shown here, the absence of a C-19 methyl group in R1881 allows the Trp-741 and Met-745 side chains to adopt a conformation that differs from previously reported AR structures bound with DHT that has the C-19 methyl ( ,  ).	bind
26244	1	8078	6	13	NULL	NULL	NULL	GST-M-RIP	GP		bind			545-878;; CC2 		MBS	GP	endogenous	leucine zipper domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_51484_s_250	14506264	4 GST-M-RIP-(545 - 878) bound both endogenous MBS and GFP-MBS, but failed to bind the GFP-MBSLZ mutant ( Fig. 4 E), supporting further that the M-RIP-MBS interaction is mediated by the CC2 of M-RIP and the leucine zipper domain of MBS.	bind
26245	2	8078	6	13	NULL	NULL	NULL	GST-M-RIP	GP		bind			545-878;; CC2		GFP-MBS	GP		leucine zipper domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_51484_s_250	14506264	4 GST-M-RIP-(545 - 878) bound both endogenous MBS and GFP-MBS, but failed to bind the GFP-MBSLZ mutant ( Fig. 4 E), supporting further that the M-RIP-MBS interaction is mediated by the CC2 of M-RIP and the leucine zipper domain of MBS.	bind
26246	3	8078	6	13	NULL	NULL	NULL	GST-M-RIP	GP		does not bind					GFP-MBS	GP	mutant	LZ		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_51484_s_250	14506264	4 GST-M-RIP-(545 - 878) bound both endogenous MBS and GFP-MBS, but failed to bind the GFP-MBSLZ mutant ( Fig. 4 E), supporting further that the M-RIP-MBS interaction is mediated by the CC2 of M-RIP and the leucine zipper domain of MBS.	bind
32086	1	8078	7	13	NULL	NULL	NULL	GST-M-RIP	GP		bind			545 - 878		MBS	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_51484_s_250	14506264	4 GST-M-RIP-(545 - 878) bound both endogenous MBS and GFP-MBS, but failed to bind the GFP-MBSLZ mutant ( Fig. 4 E), supporting further that the M-RIP-MBS interaction is mediated by the CC2 of M-RIP and the leucine zipper domain of MBS.	bind
32087	2	8078	7	NULL	NULL	0	NULL	GST-M-RIP	NULL		bind	NULL		545 - 878		GFP-MBS	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_51_51484_s_250	14506264	4 GST-M-RIP-(545 - 878) bound both endogenous MBS and GFP-MBS, but failed to bind the GFP-MBSLZ mutant ( Fig. 4 E), supporting further that the M-RIP-MBS interaction is mediated by the CC2 of M-RIP and the leucine zipper domain of MBS.	bind
32088	3	8078	7	NULL	NULL	0	NULL	GST-M-RIP	NULL		does not bind	NULL				GFP-MBSLZ	NULL	mutant			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_51_51484_s_250	14506264	4 GST-M-RIP-(545 - 878) bound both endogenous MBS and GFP-MBS, but failed to bind the GFP-MBSLZ mutant ( Fig. 4 E), supporting further that the M-RIP-MBS interaction is mediated by the CC2 of M-RIP and the leucine zipper domain of MBS.	bind
32089	4	8078	7	NULL	NULL	0	NULL	M-RIP 	NULL		mediates	NULL		CC2		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_51_51484_s_250	14506264	4 GST-M-RIP-(545 - 878) bound both endogenous MBS and GFP-MBS, but failed to bind the GFP-MBSLZ mutant ( Fig. 4 E), supporting further that the M-RIP-MBS interaction is mediated by the CC2 of M-RIP and the leucine zipper domain of MBS.	bind
32090	5	8078	7	NULL	NULL	0	NULL	M-RIP 	NULL		mediates	NULL		CC2		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_51_51484_s_250	14506264	4 GST-M-RIP-(545 - 878) bound both endogenous MBS and GFP-MBS, but failed to bind the GFP-MBSLZ mutant ( Fig. 4 E), supporting further that the M-RIP-MBS interaction is mediated by the CC2 of M-RIP and the leucine zipper domain of MBS.	bind
32091	6	8078	7	NULL	NULL	0	NULL	MBS	NULL		mediates	NULL		leucine zipper domain		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_51_51484_s_250	14506264	4 GST-M-RIP-(545 - 878) bound both endogenous MBS and GFP-MBS, but failed to bind the GFP-MBSLZ mutant ( Fig. 4 E), supporting further that the M-RIP-MBS interaction is mediated by the CC2 of M-RIP and the leucine zipper domain of MBS.	bind
32092	7	8078	7	NULL	NULL	0	NULL	MBS	NULL		mediates	NULL		leucine zipper domain		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_51_51484_s_250	14506264	4 GST-M-RIP-(545 - 878) bound both endogenous MBS and GFP-MBS, but failed to bind the GFP-MBSLZ mutant ( Fig. 4 E), supporting further that the M-RIP-MBS interaction is mediated by the CC2 of M-RIP and the leucine zipper domain of MBS.	bind
26247	1	8079	6	13	NULL	NULL	NULL	SecY	GP	mutant	bind					SecA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_10_9097_s_264	15618215	4 However, when tested with mutant SecY(prlA4), which binds SecA with higher affinity ( ), its efficiency reached 74%.	bind
46544	2	8079	6	13	NULL	NULL	NULL	SecY	GP	mutant	is					SecY	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_10_9097_s_264	15618215	4 However, when tested with mutant SecY(prlA4), which binds SecA with higher affinity ( ), its efficiency reached 74%.	bind
32093	1	8079	7	NULL	NULL	0	NULL	 SecY	NULL	mutant	binds	NULL	high affinity			SecA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_9097_s_264	15618215	4 However, when tested with mutant SecY(prlA4), which binds SecA with higher affinity ( ), its efficiency reached 74%.	bind
32094	2	8079	7	10	NULL	0	NULL	 SecY	NULL	mutant	is	NULL				prlA4	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_10_9097_s_264	15618215	4 However, when tested with mutant SecY(prlA4), which binds SecA with higher affinity ( ), its efficiency reached 74%.	bind
26248	1	8080	6	13	NULL	NULL	NULL	TIMP-4	GP	exogenous	bind					MT1-MMP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41415_s_167	10998420	4 Immunoblot analysis demonstrated the cell association of the exogenous TIMP-4 with ( / )  Timp2 mutant cells expressing MT1-MMP (Fig.  2 C,  lane 2) suggesting the binding of TIMP-4 to MT1-MMP.	bind
46550	2	8080	6	13	NULL	NULL	NULL	Timp2 mutant cells	Cell		express					MT1-MMP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41415_s_167	10998420	4 Immunoblot analysis demonstrated the cell association of the exogenous TIMP-4 with ( / )  Timp2 mutant cells expressing MT1-MMP (Fig.  2 C,  lane 2) suggesting the binding of TIMP-4 to MT1-MMP.	bind
46551	3	8080	6	13	NULL	NULL	NULL	statement 1	Process		occurs in					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41415_s_167	10998420	4 Immunoblot analysis demonstrated the cell association of the exogenous TIMP-4 with ( / )  Timp2 mutant cells expressing MT1-MMP (Fig.  2 C,  lane 2) suggesting the binding of TIMP-4 to MT1-MMP.	bind
32095	1	8080	7	10	NULL	0	NULL	TIMP-4	NULL	exogenous	bind	NULL				MT1-MMP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41415_s_167	10998420	4 Immunoblot analysis demonstrated the cell association of the exogenous TIMP-4 with ( / )  Timp2 mutant cells expressing MT1-MMP (Fig.  2 C,  lane 2) suggesting the binding of TIMP-4 to MT1-MMP.	bind
46552	2	8080	7	10	NULL	0	NULL	Timp2 mutant cells	NULL		express	NULL				MT1-MMP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41415_s_167	10998420	4 Immunoblot analysis demonstrated the cell association of the exogenous TIMP-4 with ( / )  Timp2 mutant cells expressing MT1-MMP (Fig.  2 C,  lane 2) suggesting the binding of TIMP-4 to MT1-MMP.	bind
46553	3	8080	7	10	NULL	0	NULL	statement 1	NULL		occurs in	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41415_s_167	10998420	4 Immunoblot analysis demonstrated the cell association of the exogenous TIMP-4 with ( / )  Timp2 mutant cells expressing MT1-MMP (Fig.  2 C,  lane 2) suggesting the binding of TIMP-4 to MT1-MMP.	bind
26249	1	8081	6	13	NULL	NULL	NULL				does not bind			NP XY motifs		AP-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_18_12751_s_283	16517607	4 In addition, a potential adaptor-binding NP XY motif (N19 PGY) is also present nearby; however, NP XY motifs do not bind to AP-1.	bind
55827	2	8081	6	13	NULL	NULL	NULL	N19 PGY	GP		is					NP XY motif	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_18_12751_s_283	16517607	4 In addition, a potential adaptor-binding NP XY motif (N19 PGY) is also present nearby; however, NP XY motifs do not bind to AP-1.	bind
55828	3	8081	6	13	NULL	NULL	NULL	NP XY motif	GP		is a type of					potential adaptor-binding motif	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_18_12751_s_283	16517607	4 In addition, a potential adaptor-binding NP XY motif (N19 PGY) is also present nearby; however, NP XY motifs do not bind to AP-1.	bind
32096	1	8081	7	NULL	NULL	0	NULL		NULL		does not bind	NULL		NP XY motifs		AP-1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_18_12751_s_283	16517607	4 In addition, a potential adaptor-binding NP XY motif (N19 PGY) is also present nearby; however, NP XY motifs do not bind to AP-1.	bind
32097	2	8081	7	10	NULL	0	NULL	N19 PGY			is					NP XY motif					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_18_12751_s_283	16517607	4 In addition, a potential adaptor-binding NP XY motif (N19 PGY) is also present nearby; however, NP XY motifs do not bind to AP-1.	bind
32098	3	8081	7	10	NULL	0	NULL	NP XY motif			is a type of					potential adaptor-binding motif					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_18_12751_s_283	16517607	4 In addition, a potential adaptor-binding NP XY motif (N19 PGY) is also present nearby; however, NP XY motifs do not bind to AP-1.	bind
26250	1	8082	6	13	NULL	NULL	NULL	Munc-18-1	GP		bind					syntaxins	GP				NULL	neurons	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_31633_s_145	9822620	4 In neurons, the X11alpha.mLin-2.mLin-7 protein complexes may bind to specific target membranes sites via Munc-18-1, a protein that can bind syntaxins and possibly modulate trafficking and secretion ( 29).	bind
26251	2	8082	6	13	NULL	NULL	NULL	X11alpha.mLin-2.mLin-7 protein complex	GP		bind		may			target membranes sites	CellComponent	specific			NULL	neurons	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_31633_s_145	9822620	4 In neurons, the X11alpha.mLin-2.mLin-7 protein complexes may bind to specific target membranes sites via Munc-18-1, a protein that can bind syntaxins and possibly modulate trafficking and secretion ( 29).	bind
26252	3	8082	6	13	NULL	NULL	NULL	statement 2	Process		occurs via					Munc-18-1	GP				NULL	neurons	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_31633_s_145	9822620	4 In neurons, the X11alpha.mLin-2.mLin-7 protein complexes may bind to specific target membranes sites via Munc-18-1, a protein that can bind syntaxins and possibly modulate trafficking and secretion ( 29).	bind
26253	4	8082	6	13	NULL	NULL	NULL	Munc-18-1	GP		modulate		possibly			trafficking	Process				NULL	neurons	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_31633_s_145	9822620	4 In neurons, the X11alpha.mLin-2.mLin-7 protein complexes may bind to specific target membranes sites via Munc-18-1, a protein that can bind syntaxins and possibly modulate trafficking and secretion ( 29).	bind
26254	5	8082	6	13	NULL	NULL	NULL	Munc-18-1	GP		modulate		possibly			secretion	Process				NULL	neurons	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_31633_s_145	9822620	4 In neurons, the X11alpha.mLin-2.mLin-7 protein complexes may bind to specific target membranes sites via Munc-18-1, a protein that can bind syntaxins and possibly modulate trafficking and secretion ( 29).	bind
32100	1	8082	7	10	NULL	0	NULL	X11alpha.mLin-2.mLin-7 protein complex	NULL		bind	NULL	may			target membranes sites	NULL	specific			NULL	neurons	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_31633_s_145	9822620	4 In neurons, the X11alpha.mLin-2.mLin-7 protein complexes may bind to specific target membranes sites via Munc-18-1, a protein that can bind syntaxins and possibly modulate trafficking and secretion ( 29).	bind
32104	2	8082	7	NULL	NULL	0	NULL	statement 1	NULL		occurs via	NULL				Munc-18-1	NULL				NULL	neurons	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_31633_s_145	9822620	4 In neurons, the X11alpha.mLin-2.mLin-7 protein complexes may bind to specific target membranes sites via Munc-18-1, a protein that can bind syntaxins and possibly modulate trafficking and secretion ( 29).	bind
32105	3	8082	7	NULL	NULL	0	NULL	Munc-18-1	NULL		bind	NULL				syntaxins	NULL				NULL	neurons	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_31633_s_145	9822620	4 In neurons, the X11alpha.mLin-2.mLin-7 protein complexes may bind to specific target membranes sites via Munc-18-1, a protein that can bind syntaxins and possibly modulate trafficking and secretion ( 29).	bind
32107	4	8082	7	10	NULL	0	NULL	statement 3	NULL		modulate	NULL	possibly			trafficking	NULL				NULL	neurons	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_31633_s_145	9822620	4 In neurons, the X11alpha.mLin-2.mLin-7 protein complexes may bind to specific target membranes sites via Munc-18-1, a protein that can bind syntaxins and possibly modulate trafficking and secretion ( 29).	bind
32108	5	8082	7	10	NULL	0	NULL	statement 3	NULL		modulate	NULL	possibly			secretion	NULL				NULL	neurons	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_31633_s_145	9822620	4 In neurons, the X11alpha.mLin-2.mLin-7 protein complexes may bind to specific target membranes sites via Munc-18-1, a protein that can bind syntaxins and possibly modulate trafficking and secretion ( 29).	bind
26255	1	8083	6	13	NULL	NULL	NULL	GA	Chemical		bind					hsp90	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_38_23843_s_257	9295332	4 Instead, we propose that GA binding to hsp90 locks the chaperone into its ADP-dependent configuration.	bind
26256	2	8083	6	13	NULL	NULL	NULL	hsp90	GP		is a type of					chaperone	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_38_23843_s_257	9295332	4 Instead, we propose that GA binding to hsp90 locks the chaperone into its ADP-dependent configuration.	bind
55829	3	8083	6	13	NULL	NULL	NULL	hsp90	GP		locked into					ADP-dependent configuration	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_38_23843_s_257	9295332	4 Instead, we propose that GA binding to hsp90 locks the chaperone into its ADP-dependent configuration.	bind
55830	4	8083	6	13	NULL	NULL	NULL	statement 1	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_38_23843_s_257	9295332	4 Instead, we propose that GA binding to hsp90 locks the chaperone into its ADP-dependent configuration.	bind
32113	1	8083	7	NULL	NULL	0	NULL	GA	NULL		bind	NULL				hsp90	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_38_23843_s_257	9295332	4 Instead, we propose that GA binding to hsp90 locks the chaperone into its ADP-dependent configuration.	bind
32114	2	8083	7	10	NULL	0	NULL	hsp90			is a type of					chaperone					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_38_23843_s_257	9295332	4 Instead, we propose that GA binding to hsp90 locks the chaperone into its ADP-dependent configuration.	bind
32115	3	8083	7	10	NULL	0	NULL	hsp90			locked into					ADP-dependent configuration					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_38_23843_s_257	9295332	4 Instead, we propose that GA binding to hsp90 locks the chaperone into its ADP-dependent configuration.	bind
55831	4	8083	7	10	NULL	0	NULL	statement 1			leads to					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_38_23843_s_257	9295332	4 Instead, we propose that GA binding to hsp90 locks the chaperone into its ADP-dependent configuration.	bind
26297	1	8084	6	13	NULL	NULL	NULL	ADP	Chemical		bind					Hsp70	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_35_22506_s_293	9712876	4 Interestingly, BAG-1 and Hip regulate Hsp70 activity in opposite manners: Hip stabilizes the ADP-bound form of Hsp70, promoting formation with target peptides ( 50), while BAG-1 stimulates the release of ADP and peptide substrates ( 21).	bind
26298	2	8084	6	13	NULL	NULL	NULL	Hip	GP		stabilizes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_35_22506_s_293	9712876	4 Interestingly, BAG-1 and Hip regulate Hsp70 activity in opposite manners: Hip stabilizes the ADP-bound form of Hsp70, promoting formation with target peptides ( 50), while BAG-1 stimulates the release of ADP and peptide substrates ( 21).	bind
26299	3	8084	6	13	NULL	NULL	NULL	BAG-1	GP		stimulates					ADP	Chemical	release of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_35_22506_s_293	9712876	4 Interestingly, BAG-1 and Hip regulate Hsp70 activity in opposite manners: Hip stabilizes the ADP-bound form of Hsp70, promoting formation with target peptides ( 50), while BAG-1 stimulates the release of ADP and peptide substrates ( 21).	bind
26300	4	8084	6	13	NULL	NULL	NULL	BAG-1	GP		stimulates					peptide substrates	GP	release of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_35_22506_s_293	9712876	4 Interestingly, BAG-1 and Hip regulate Hsp70 activity in opposite manners: Hip stabilizes the ADP-bound form of Hsp70, promoting formation with target peptides ( 50), while BAG-1 stimulates the release of ADP and peptide substrates ( 21).	bind
32116	1	8084	7	NULL	NULL	0	NULL	ADP	NULL		bind	NULL				Hsp70	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22506_s_293	9712876	4 Interestingly, BAG-1 and Hip regulate Hsp70 activity in opposite manners: Hip stabilizes the ADP-bound form of Hsp70, promoting formation with target peptides ( 50), while BAG-1 stimulates the release of ADP and peptide substrates ( 21).	bind
32117	2	8084	7	NULL	NULL	0	NULL	Hip	NULL		stabilizes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22506_s_293	9712876	4 Interestingly, BAG-1 and Hip regulate Hsp70 activity in opposite manners: Hip stabilizes the ADP-bound form of Hsp70, promoting formation with target peptides ( 50), while BAG-1 stimulates the release of ADP and peptide substrates ( 21).	bind
32118	3	8084	7	NULL	NULL	0	NULL	statement 2	NULL		promotes	NULL				target peptides	NULL	formation with			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22506_s_293	9712876	4 Interestingly, BAG-1 and Hip regulate Hsp70 activity in opposite manners: Hip stabilizes the ADP-bound form of Hsp70, promoting formation with target peptides ( 50), while BAG-1 stimulates the release of ADP and peptide substrates ( 21).	bind
32119	4	8084	7	NULL	NULL	0	NULL	BAG-1 	NULL		stimulate	NULL				ADP	NULL	release of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22506_s_293	9712876	4 Interestingly, BAG-1 and Hip regulate Hsp70 activity in opposite manners: Hip stabilizes the ADP-bound form of Hsp70, promoting formation with target peptides ( 50), while BAG-1 stimulates the release of ADP and peptide substrates ( 21).	bind
32120	5	8084	7	NULL	NULL	0	NULL	BAG-1 	NULL		stimulates	NULL				peptide substrates	NULL	release of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22506_s_293	9712876	4 Interestingly, BAG-1 and Hip regulate Hsp70 activity in opposite manners: Hip stabilizes the ADP-bound form of Hsp70, promoting formation with target peptides ( 50), while BAG-1 stimulates the release of ADP and peptide substrates ( 21).	bind
32121	6	8084	7	NULL	NULL	0	NULL	BAG-1 	NULL		regulate	NULL				Hsp70	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22506_s_293	9712876	4 Interestingly, BAG-1 and Hip regulate Hsp70 activity in opposite manners: Hip stabilizes the ADP-bound form of Hsp70, promoting formation with target peptides ( 50), while BAG-1 stimulates the release of ADP and peptide substrates ( 21).	bind
32122	7	8084	7	NULL	NULL	0	NULL	Hip	NULL		regulate	NULL				Hsp70	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22506_s_293	9712876	4 Interestingly, BAG-1 and Hip regulate Hsp70 activity in opposite manners: Hip stabilizes the ADP-bound form of Hsp70, promoting formation with target peptides ( 50), while BAG-1 stimulates the release of ADP and peptide substrates ( 21).	bind
32123	8	8084	7	NULL	NULL	0	NULL	statement 6 	NULL		is in opposite way to	NULL				statement 7	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_35_22506_s_293	9712876	4 Interestingly, BAG-1 and Hip regulate Hsp70 activity in opposite manners: Hip stabilizes the ADP-bound form of Hsp70, promoting formation with target peptides ( 50), while BAG-1 stimulates the release of ADP and peptide substrates ( 21).	bind
26301	1	8085	6	13	NULL	NULL	NULL				bind			E191A		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_14306_s_194	11827971	4 It is important to note that E191A, E233A, and K235A show largely unaltered DNA binding and cleavage activity.	bind
26302	2	8085	6	13	NULL	NULL	NULL				exhibits			E191A		clevage activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_14306_s_194	11827971	4 It is important to note that E191A, E233A, and K235A show largely unaltered DNA binding and cleavage activity.	bind
26303	3	8085	6	13	NULL	NULL	NULL				bind			E233A		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_14306_s_194	11827971	4 It is important to note that E191A, E233A, and K235A show largely unaltered DNA binding and cleavage activity.	bind
26304	4	8085	6	13	NULL	NULL	NULL				exhibits			E233A		clevage activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_14306_s_194	11827971	4 It is important to note that E191A, E233A, and K235A show largely unaltered DNA binding and cleavage activity.	bind
26305	5	8085	6	13	NULL	NULL	NULL				bind			K235A		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_14306_s_194	11827971	4 It is important to note that E191A, E233A, and K235A show largely unaltered DNA binding and cleavage activity.	bind
26306	6	8085	6	13	NULL	NULL	NULL				exhibits			K235A		clevage activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_14306_s_194	11827971	4 It is important to note that E191A, E233A, and K235A show largely unaltered DNA binding and cleavage activity.	bind
26307	1	8086	6	13	NULL	NULL	NULL	apo A-I	GP		is abundant on					HDL3-E	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_178	12089072	4 It may be that apo A-I, which is abundant on HDL3-E, interacts with non-proteoglycan ECM components, because previous studies have shown that apo A-I can bind fibronectin and collagen, for example.	bind
26308	2	8086	6	13	NULL	NULL	NULL	apo A-I	GP		interacts with					ECM components	CellComponent	non-proteoglycan			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_178	12089072	4 It may be that apo A-I, which is abundant on HDL3-E, interacts with non-proteoglycan ECM components, because previous studies have shown that apo A-I can bind fibronectin and collagen, for example.	bind
26309	3	8086	6	13	NULL	NULL	NULL	apo A-I	GP		bind					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_178	12089072	4 It may be that apo A-I, which is abundant on HDL3-E, interacts with non-proteoglycan ECM components, because previous studies have shown that apo A-I can bind fibronectin and collagen, for example.	bind
26310	4	8086	6	13	NULL	NULL	NULL	apo A-I	GP		bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_178	12089072	4 It may be that apo A-I, which is abundant on HDL3-E, interacts with non-proteoglycan ECM components, because previous studies have shown that apo A-I can bind fibronectin and collagen, for example.	bind
32130	1	8086	7	10	NULL	0	NULL	apo A-I			interacts with					ECM components		non-proteoglycan			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_178	12089072	4 It may be that apo A-I, which is abundant on HDL3-E, interacts with non-proteoglycan ECM components, because previous studies have shown that apo A-I can bind fibronectin and collagen, for example.	bind
32131	2	8086	7	NULL	NULL	0	NULL	apo A-I 	NULL		bind	NULL				fibronectin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_178	12089072	4 It may be that apo A-I, which is abundant on HDL3-E, interacts with non-proteoglycan ECM components, because previous studies have shown that apo A-I can bind fibronectin and collagen, for example.	bind
32132	3	8086	7	NULL	NULL	0	NULL	apo A-I	NULL		bind	NULL				collagen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_178	12089072	4 It may be that apo A-I, which is abundant on HDL3-E, interacts with non-proteoglycan ECM components, because previous studies have shown that apo A-I can bind fibronectin and collagen, for example.	bind
32133	4	8086	7	NULL	NULL	0	NULL	apo A-I	NULL		is abundant on	NULL				HDL3-E	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_178	12089072	4 It may be that apo A-I, which is abundant on HDL3-E, interacts with non-proteoglycan ECM components, because previous studies have shown that apo A-I can bind fibronectin and collagen, for example.	bind
26311	1	8087	6	13	NULL	NULL	NULL	CCR2	GP		is					CC chemokine receptor 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_2_244_s_26	12588766	4 MCP-1 specifically binds to CC chemokine receptor 2 (CCR2) and fulfills its function.	bind
26312	2	8087	6	13	NULL	NULL	NULL	MCP-1	GP		bind		specifically			CCR2	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_2_244_s_26	12588766	4 MCP-1 specifically binds to CC chemokine receptor 2 (CCR2) and fulfills its function.	bind
32135	1	8087	7	NULL	NULL	0	NULL	MCP-1	NULL		binds	NULL	specifically			CCR2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_2_244_s_26	12588766	4 MCP-1 specifically binds to CC chemokine receptor 2 (CCR2) and fulfills its function.	bind
32136	2	8087	7	10	NULL	0	NULL	CCR2			is					CC chemokine receptor 2					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_2_244_s_26	12588766	4 MCP-1 specifically binds to CC chemokine receptor 2 (CCR2) and fulfills its function.	bind
26313	1	8089	6	13	NULL	NULL	NULL	CCR2	GP		is					CC chemokine receptor 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_864_s_21	15016641	4 Monocytes express CC chemokine receptor 2 (CCR2), which binds monocyte chemoattractant protein-1 (MCP-1), leading to beta integrin-mediated firm adhesion and subsequent transmigration of adhered monocytes through the vascular endothelium.	bind
26314	2	8089	6	13	NULL	NULL	NULL	MCP-1	GP		is					monocyte chemoattractant protein-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_864_s_21	15016641	4 Monocytes express CC chemokine receptor 2 (CCR2), which binds monocyte chemoattractant protein-1 (MCP-1), leading to beta integrin-mediated firm adhesion and subsequent transmigration of adhered monocytes through the vascular endothelium.	bind
26315	3	8089	6	13	NULL	NULL	NULL	monocytes	Cell		express					CCR2 	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_864_s_21	15016641	4 Monocytes express CC chemokine receptor 2 (CCR2), which binds monocyte chemoattractant protein-1 (MCP-1), leading to beta integrin-mediated firm adhesion and subsequent transmigration of adhered monocytes through the vascular endothelium.	bind
26316	4	8089	6	13	NULL	NULL	NULL	statement 3	GP		bind					MCP-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_864_s_21	15016641	4 Monocytes express CC chemokine receptor 2 (CCR2), which binds monocyte chemoattractant protein-1 (MCP-1), leading to beta integrin-mediated firm adhesion and subsequent transmigration of adhered monocytes through the vascular endothelium.	bind
26317	5	8089	6	13	NULL	NULL	NULL	beta integrin	GP		mediates					firm adhesion	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_864_s_21	15016641	4 Monocytes express CC chemokine receptor 2 (CCR2), which binds monocyte chemoattractant protein-1 (MCP-1), leading to beta integrin-mediated firm adhesion and subsequent transmigration of adhered monocytes through the vascular endothelium.	bind
26318	6	8089	6	13	NULL	NULL	NULL	statement 4	Process		leads to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_864_s_21	15016641	4 Monocytes express CC chemokine receptor 2 (CCR2), which binds monocyte chemoattractant protein-1 (MCP-1), leading to beta integrin-mediated firm adhesion and subsequent transmigration of adhered monocytes through the vascular endothelium.	bind
26319	7	8089	6	13	NULL	NULL	NULL	monocytes	Cell	adhered	migrate through					vascular endothelium	Cell				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_864_s_21	15016641	4 Monocytes express CC chemokine receptor 2 (CCR2), which binds monocyte chemoattractant protein-1 (MCP-1), leading to beta integrin-mediated firm adhesion and subsequent transmigration of adhered monocytes through the vascular endothelium.	bind
26320	8	8089	6	13	NULL	NULL	NULL	statement 4	Process		leads to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_864_s_21	15016641	4 Monocytes express CC chemokine receptor 2 (CCR2), which binds monocyte chemoattractant protein-1 (MCP-1), leading to beta integrin-mediated firm adhesion and subsequent transmigration of adhered monocytes through the vascular endothelium.	bind
32137	1	8089	7	10	NULL	0	NULL	statement 8	NULL		binds	NULL				MCP-1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_864_s_21	15016641	4 Monocytes express CC chemokine receptor 2 (CCR2), which binds monocyte chemoattractant protein-1 (MCP-1), leading to beta integrin-mediated firm adhesion and subsequent transmigration of adhered monocytes through the vascular endothelium.	bind
32138	2	8089	7	10	NULL	0	NULL	beta integrin	NULL		mediates	NULL				firm adhesion	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_864_s_21	15016641	4 Monocytes express CC chemokine receptor 2 (CCR2), which binds monocyte chemoattractant protein-1 (MCP-1), leading to beta integrin-mediated firm adhesion and subsequent transmigration of adhered monocytes through the vascular endothelium.	bind
32139	3	8089	7	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_864_s_21	15016641	4 Monocytes express CC chemokine receptor 2 (CCR2), which binds monocyte chemoattractant protein-1 (MCP-1), leading to beta integrin-mediated firm adhesion and subsequent transmigration of adhered monocytes through the vascular endothelium.	bind
32140	4	8089	7	10	NULL	0	NULL	monocytes		adhered	migrates through					vascular endothelium					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_864_s_21	15016641	4 Monocytes express CC chemokine receptor 2 (CCR2), which binds monocyte chemoattractant protein-1 (MCP-1), leading to beta integrin-mediated firm adhesion and subsequent transmigration of adhered monocytes through the vascular endothelium.	bind
32141	5	8089	7	10	NULL	0	NULL	statement 1			leads to					statement 4					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_864_s_21	15016641	4 Monocytes express CC chemokine receptor 2 (CCR2), which binds monocyte chemoattractant protein-1 (MCP-1), leading to beta integrin-mediated firm adhesion and subsequent transmigration of adhered monocytes through the vascular endothelium.	bind
32142	6	8089	7	NULL	NULL	0	NULL	CCR2	NULL		is	NULL				CC chemokine receptor 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_864_s_21	15016641	4 Monocytes express CC chemokine receptor 2 (CCR2), which binds monocyte chemoattractant protein-1 (MCP-1), leading to beta integrin-mediated firm adhesion and subsequent transmigration of adhered monocytes through the vascular endothelium.	bind
32143	7	8089	7	NULL	NULL	0	NULL	MCP-1	NULL		is	NULL				monocyte chemoattractant protein-1 	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_864_s_21	15016641	4 Monocytes express CC chemokine receptor 2 (CCR2), which binds monocyte chemoattractant protein-1 (MCP-1), leading to beta integrin-mediated firm adhesion and subsequent transmigration of adhered monocytes through the vascular endothelium.	bind
46564	8	8089	7	10	NULL	0	NULL	monocytes	NULL		express	NULL				CCR2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_864_s_21	15016641	4 Monocytes express CC chemokine receptor 2 (CCR2), which binds monocyte chemoattractant protein-1 (MCP-1), leading to beta integrin-mediated firm adhesion and subsequent transmigration of adhered monocytes through the vascular endothelium.	bind
26767	1	8090	6	13	NULL	NULL	NULL	Tpr-Met protein	GP	wild type	bind					Grb2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_13116_s_154	8662733	4 Moreover, the Tpr-Met mutants that were unable to bind Shc or Grb2 were impaired in their ability to activate the  c-fos promoter compared with the wild-type or Y482F Tpr-Met proteins, which bind to both Grb2 and Shc.	bind
26768	2	8090	6	13	NULL	NULL	NULL	Tpr-Met protein	GP		bind			Y482F		Grb2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_13116_s_154	8662733	4 Moreover, the Tpr-Met mutants that were unable to bind Shc or Grb2 were impaired in their ability to activate the  c-fos promoter compared with the wild-type or Y482F Tpr-Met proteins, which bind to both Grb2 and Shc.	bind
26769	3	8090	6	13	NULL	NULL	NULL	Tpr-Met protein	GP	wild type	bind					Shc	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_13116_s_154	8662733	4 Moreover, the Tpr-Met mutants that were unable to bind Shc or Grb2 were impaired in their ability to activate the  c-fos promoter compared with the wild-type or Y482F Tpr-Met proteins, which bind to both Grb2 and Shc.	bind
26770	4	8090	6	13	NULL	NULL	NULL	Tpr-Met protein	GP		bind			Y482F		Shc	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_13116_s_154	8662733	4 Moreover, the Tpr-Met mutants that were unable to bind Shc or Grb2 were impaired in their ability to activate the  c-fos promoter compared with the wild-type or Y482F Tpr-Met proteins, which bind to both Grb2 and Shc.	bind
26771	5	8090	6	13	NULL	NULL	NULL	Tpr-Met protein	GP	mutant	does not bind					Grb2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_13116_s_154	8662733	4 Moreover, the Tpr-Met mutants that were unable to bind Shc or Grb2 were impaired in their ability to activate the  c-fos promoter compared with the wild-type or Y482F Tpr-Met proteins, which bind to both Grb2 and Shc.	bind
26772	6	8090	6	13	NULL	NULL	NULL	Tpr-Met protein	GP	mutant	does not bind					Shc	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_13116_s_154	8662733	4 Moreover, the Tpr-Met mutants that were unable to bind Shc or Grb2 were impaired in their ability to activate the  c-fos promoter compared with the wild-type or Y482F Tpr-Met proteins, which bind to both Grb2 and Shc.	bind
26773	7	8090	6	13	NULL	NULL	NULL	Tpr-Met protein	GP		activates					c-fos	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_13116_s_154	8662733	4 Moreover, the Tpr-Met mutants that were unable to bind Shc or Grb2 were impaired in their ability to activate the  c-fos promoter compared with the wild-type or Y482F Tpr-Met proteins, which bind to both Grb2 and Shc.	bind
26774	8	8090	6	13	NULL	NULL	NULL	Tpr-Met protein	GP	mutant	does not activate					c-fos	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_13116_s_154	8662733	4 Moreover, the Tpr-Met mutants that were unable to bind Shc or Grb2 were impaired in their ability to activate the  c-fos promoter compared with the wild-type or Y482F Tpr-Met proteins, which bind to both Grb2 and Shc.	bind
32144	1	8090	7	NULL	NULL	0	NULL	Tpr-Met	NULL	mutant	does not bind	NULL					NULL		Shc		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_13116_s_154	8662733	4 Moreover, the Tpr-Met mutants that were unable to bind Shc or Grb2 were impaired in their ability to activate the  c-fos promoter compared with the wild-type or Y482F Tpr-Met proteins, which bind to both Grb2 and Shc.	bind
32145	2	8090	7	NULL	NULL	0	NULL	Tpr-Met	NULL	mutant	does not bind	NULL					NULL		Grb2		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_13116_s_154	8662733	4 Moreover, the Tpr-Met mutants that were unable to bind Shc or Grb2 were impaired in their ability to activate the  c-fos promoter compared with the wild-type or Y482F Tpr-Met proteins, which bind to both Grb2 and Shc.	bind
32146	3	8090	7	NULL	NULL	0	NULL	statement 1	NULL		is impaired	NULL				c-fos	NULL	to activate		promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_13116_s_154	8662733	4 Moreover, the Tpr-Met mutants that were unable to bind Shc or Grb2 were impaired in their ability to activate the  c-fos promoter compared with the wild-type or Y482F Tpr-Met proteins, which bind to both Grb2 and Shc.	bind
32147	4	8090	7	NULL	NULL	0	NULL	Tpr-Met proteins	NULL	wild-type	bind	NULL					NULL		Shc		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_13116_s_154	8662733	4 Moreover, the Tpr-Met mutants that were unable to bind Shc or Grb2 were impaired in their ability to activate the  c-fos promoter compared with the wild-type or Y482F Tpr-Met proteins, which bind to both Grb2 and Shc.	bind
32148	5	8090	7	NULL	NULL	0	NULL	Tpr-Met proteins	NULL	wild-type	bind	NULL					NULL		Grb2		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_13116_s_154	8662733	4 Moreover, the Tpr-Met mutants that were unable to bind Shc or Grb2 were impaired in their ability to activate the  c-fos promoter compared with the wild-type or Y482F Tpr-Met proteins, which bind to both Grb2 and Shc.	bind
32149	6	8090	7	NULL	NULL	0	NULL	Tpr-Met proteins	NULL		bind	NULL		 Y482F 			NULL		Shc		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_13116_s_154	8662733	4 Moreover, the Tpr-Met mutants that were unable to bind Shc or Grb2 were impaired in their ability to activate the  c-fos promoter compared with the wild-type or Y482F Tpr-Met proteins, which bind to both Grb2 and Shc.	bind
32150	7	8090	7	NULL	NULL	0	NULL	Tpr-Met proteins	NULL		bind	NULL		Y482F			NULL		Grb2		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_13116_s_154	8662733	4 Moreover, the Tpr-Met mutants that were unable to bind Shc or Grb2 were impaired in their ability to activate the  c-fos promoter compared with the wild-type or Y482F Tpr-Met proteins, which bind to both Grb2 and Shc.	bind
32151	8	8090	7	NULL	NULL	0	NULL	statement 2	NULL		is impaired	NULL				c-fos	NULL	to activate		promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_13116_s_154	8662733	4 Moreover, the Tpr-Met mutants that were unable to bind Shc or Grb2 were impaired in their ability to activate the  c-fos promoter compared with the wild-type or Y482F Tpr-Met proteins, which bind to both Grb2 and Shc.	bind
26322	1	8091	6	13	NULL	NULL	NULL	GIPC	GP		bind					type III receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24627_s_268	11323414	4 Mutating the Class I PDZ binding motif of the type III receptor abolishes binding of GIPC to the type III receptor, but does not effect the interaction between the type III receptor and the type II receptor studied here, establishing that this protein is not an adaptor protein in this interaction.	bind
26323	2	8091	6	13	NULL	NULL	NULL	type III receptor	GP	mutant	abolishes			Class I PDZ binding motif		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24627_s_268	11323414	4 Mutating the Class I PDZ binding motif of the type III receptor abolishes binding of GIPC to the type III receptor, but does not effect the interaction between the type III receptor and the type II receptor studied here, establishing that this protein is not an adaptor protein in this interaction.	bind
26324	3	8091	6	13	NULL	NULL	NULL	type III receptor	GP		interacts with					type II receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24627_s_268	11323414	4 Mutating the Class I PDZ binding motif of the type III receptor abolishes binding of GIPC to the type III receptor, but does not effect the interaction between the type III receptor and the type II receptor studied here, establishing that this protein is not an adaptor protein in this interaction.	bind
26325	4	8091	6	13	NULL	NULL	NULL	type III receptor	GP	mutant	has no effect on			Class I PDZ binding motif		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24627_s_268	11323414	4 Mutating the Class I PDZ binding motif of the type III receptor abolishes binding of GIPC to the type III receptor, but does not effect the interaction between the type III receptor and the type II receptor studied here, establishing that this protein is not an adaptor protein in this interaction.	bind
32156	1	8091	7	NULL	NULL	0	NULL	GIPC	NULL		bind	NULL				type III receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_27_24627_s_268	11323414	4 Mutating the Class I PDZ binding motif of the type III receptor abolishes binding of GIPC to the type III receptor, but does not effect the interaction between the type III receptor and the type II receptor studied here, establishing that this protein is not an adaptor protein in this interaction.	bind
32157	2	8091	7	NULL	NULL	0	NULL	Type III receptor	NULL	mutant	abolishes	NULL		Class I PDZ binding motif		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24627_s_268	11323414	4 Mutating the Class I PDZ binding motif of the type III receptor abolishes binding of GIPC to the type III receptor, but does not effect the interaction between the type III receptor and the type II receptor studied here, establishing that this protein is not an adaptor protein in this interaction.	bind
32158	3	8091	7	NULL	NULL	0	NULL	type III receptor	NULL		interacts with	NULL				type II receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_27_24627_s_268	11323414	4 Mutating the Class I PDZ binding motif of the type III receptor abolishes binding of GIPC to the type III receptor, but does not effect the interaction between the type III receptor and the type II receptor studied here, establishing that this protein is not an adaptor protein in this interaction.	bind
32159	4	8091	7	NULL	NULL	0	NULL	Type III receptor	NULL	mutant	does not affect	NULL		Class I PDZ binding motif		statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_27_24627_s_268	11323414	4 Mutating the Class I PDZ binding motif of the type III receptor abolishes binding of GIPC to the type III receptor, but does not effect the interaction between the type III receptor and the type II receptor studied here, establishing that this protein is not an adaptor protein in this interaction.	bind
26775	1	8092	6	13	NULL	NULL	NULL	zonadhesin	GP		bind					ZP	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41502_s_287	11526117	4 Our detection of differences in ZP binding activity among the various zonadhesin forms suggests that the heterogeneous processing of this protein is functionally important, just as proteolytic activation and heterogeneous multimerization are important for the proper function of vWF ( 10).	bind
26776	2	8092	6	13	NULL	NULL	NULL	zonadhesin	GP	heterogeneous processing of	is important for					zonadhesin	GP	proper function of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41502_s_287	11526117	4 Our detection of differences in ZP binding activity among the various zonadhesin forms suggests that the heterogeneous processing of this protein is functionally important, just as proteolytic activation and heterogeneous multimerization are important for the proper function of vWF ( 10).	bind
26777	3	8092	6	13	NULL	NULL	NULL	vWF	GP	proteolytic activation of	is important for					vWF	GP	proper function of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41502_s_287	11526117	4 Our detection of differences in ZP binding activity among the various zonadhesin forms suggests that the heterogeneous processing of this protein is functionally important, just as proteolytic activation and heterogeneous multimerization are important for the proper function of vWF ( 10).	bind
26778	4	8092	6	13	NULL	NULL	NULL	vWF	GP	heterogeneous multimerization of	is important for					vWF	GP	proper function of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_41502_s_287	11526117	4 Our detection of differences in ZP binding activity among the various zonadhesin forms suggests that the heterogeneous processing of this protein is functionally important, just as proteolytic activation and heterogeneous multimerization are important for the proper function of vWF ( 10).	bind
32161	1	8092	7	NULL	NULL	0	NULL	ZP	NULL		binds	NULL				zonadhesin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_41502_s_287	11526117	4 Our detection of differences in ZP binding activity among the various zonadhesin forms suggests that the heterogeneous processing of this protein is functionally important, just as proteolytic activation and heterogeneous multimerization are important for the proper function of vWF ( 10).	bind
32162	2	8092	7	NULL	NULL	0	NULL	statement 1	NULL	different binding  activity of	suggests	NULL				zonadhesin	NULL	heterogeneous processing of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_41502_s_287	11526117	4 Our detection of differences in ZP binding activity among the various zonadhesin forms suggests that the heterogeneous processing of this protein is functionally important, just as proteolytic activation and heterogeneous multimerization are important for the proper function of vWF ( 10).	bind
32163	3	8092	7	NULL	NULL	0	NULL	vWF	NULL	proteolytic activation	is important for	NULL				vWF	NULL	function of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_41502_s_287	11526117	4 Our detection of differences in ZP binding activity among the various zonadhesin forms suggests that the heterogeneous processing of this protein is functionally important, just as proteolytic activation and heterogeneous multimerization are important for the proper function of vWF ( 10).	bind
32164	4	8092	7	NULL	NULL	0	NULL	vWF	NULL	heterogeneous multimerization of	is important for	NULL				vWF	NULL	function of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_41502_s_287	11526117	4 Our detection of differences in ZP binding activity among the various zonadhesin forms suggests that the heterogeneous processing of this protein is functionally important, just as proteolytic activation and heterogeneous multimerization are important for the proper function of vWF ( 10).	bind
26328	1	8094	6	13	NULL	NULL	NULL	Galectin-3	GP	purified;;rat	bind					bone acidic glycoprotein-75	GP	isolated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18840_s_306	11886849	4 Recent quantitative studies show that purified rat galectin-3 binds as well to isolated bone acidic glycoprotein-75 as to monoclonal anti-DNP IgE, the commonly used standard ligand for this receptor.	bind
26329	2	8094	6	13	NULL	NULL	NULL	Galectin-3	GP	purified;;rat	bind					anti-DNP IgE	GP	monoclonal			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18840_s_306	11886849	4 Recent quantitative studies show that purified rat galectin-3 binds as well to isolated bone acidic glycoprotein-75 as to monoclonal anti-DNP IgE, the commonly used standard ligand for this receptor.	bind
32172	1	8094	7	10	NULL	0	NULL	 galectin-3	NULL	purified;;rat	binds	NULL				bone acidic glycoprotein-75	NULL	 isolated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18840_s_306	11886849	4 Recent quantitative studies show that purified rat galectin-3 binds as well to isolated bone acidic glycoprotein-75 as to monoclonal anti-DNP IgE, the commonly used standard ligand for this receptor.	bind
32173	2	8094	7	10	NULL	0	NULL	galectin-3	NULL	purified;;rat	binds	NULL				anti-DNP IgE	NULL	monoclonal 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18840_s_306	11886849	4 Recent quantitative studies show that purified rat galectin-3 binds as well to isolated bone acidic glycoprotein-75 as to monoclonal anti-DNP IgE, the commonly used standard ligand for this receptor.	bind
26330	1	8095	6	13	NULL	NULL	NULL	GTP	Chemical		bind					ARF3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_18_13465_s_120	10788460	4 Sat1delta5 (8 muM) failed to promote enhanced GTP binding to ARF3 (data not shown) despite its ability to bind to mammalian ARFs.	bind
26331	2	8095	6	13	NULL	NULL	NULL	Sat1delta5	GP		failed to promote					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_18_13465_s_120	10788460	4 Sat1delta5 (8 muM) failed to promote enhanced GTP binding to ARF3 (data not shown) despite its ability to bind to mammalian ARFs.	bind
26332	3	8095	6	13	NULL	NULL	NULL	GTP	Chemical		bind					ARF	GP	mammalian			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_18_13465_s_120	10788460	4 Sat1delta5 (8 muM) failed to promote enhanced GTP binding to ARF3 (data not shown) despite its ability to bind to mammalian ARFs.	bind
32174	1	8095	7	NULL	NULL	0	NULL	GTP	NULL		bind	NULL	enhanced			ARF3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_18_13465_s_120	10788460	4 Sat1delta5 (8 muM) failed to promote enhanced GTP binding to ARF3 (data not shown) despite its ability to bind to mammalian ARFs.	bind
32175	2	8095	7	NULL	NULL	0	NULL	Sat1delta5	NULL		does not promote	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13465_s_120	10788460	4 Sat1delta5 (8 muM) failed to promote enhanced GTP binding to ARF3 (data not shown) despite its ability to bind to mammalian ARFs.	bind
32176	3	8095	7	NULL	NULL	0	NULL	GTP 	NULL		bind	NULL				ARFs	NULL	mammalian			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13465_s_120	10788460	4 Sat1delta5 (8 muM) failed to promote enhanced GTP binding to ARF3 (data not shown) despite its ability to bind to mammalian ARFs.	bind
26333	1	8096	6	13	NULL	NULL	NULL	cTnI	GP	phosphorylated	bind					cTnC	GP		COOH-terminal domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_24_16681_s_63	10358006	4 Taken together, these results allow us to propose that both nonphosphorylated and phosphorylated forms of cTnI bind to the COOH-terminal domain of cTnC with the nonphosphorylated form making limited contacts with the NH2-terminal domain of cTnC.	bind
26334	2	8096	6	13	NULL	NULL	NULL	cTnI	GP	nonphosphorylated	bind					cTnC	GP		COOH-terminal domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_24_16681_s_63	10358006	4 Taken together, these results allow us to propose that both nonphosphorylated and phosphorylated forms of cTnI bind to the COOH-terminal domain of cTnC with the nonphosphorylated form making limited contacts with the NH2-terminal domain of cTnC.	bind
26335	3	8096	6	13	NULL	NULL	NULL	cTnI	GP	nonphosphorylated	contacts with		limited			cTnC	GP		NH2 terminus		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_24_16681_s_63	10358006	4 Taken together, these results allow us to propose that both nonphosphorylated and phosphorylated forms of cTnI bind to the COOH-terminal domain of cTnC with the nonphosphorylated form making limited contacts with the NH2-terminal domain of cTnC.	bind
32177	1	8096	7	10	NULL	0	NULL	cTnI	NULL	nonphosphorylated	binds to	NULL				cTnC	NULL		COOH-terminal domain of		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_24_16681_s_63	10358006	4 Taken together, these results allow us to propose that both nonphosphorylated and phosphorylated forms of cTnI bind to the COOH-terminal domain of cTnC with the nonphosphorylated form making limited contacts with the NH2-terminal domain of cTnC.	bind
32178	2	8096	7	10	NULL	0	NULL	cTnI	NULL	phosphorylated	binds to	NULL				cTnC	NULL		COOH-terminal domain 		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_24_16681_s_63	10358006	4 Taken together, these results allow us to propose that both nonphosphorylated and phosphorylated forms of cTnI bind to the COOH-terminal domain of cTnC with the nonphosphorylated form making limited contacts with the NH2-terminal domain of cTnC.	bind
32179	3	8096	7	10	NULL	0	NULL	cTnI	NULL	nonphosphorylated	 contacts with	NULL	limited			cTnC	NULL		NH2-terminal domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_24_16681_s_63	10358006	4 Taken together, these results allow us to propose that both nonphosphorylated and phosphorylated forms of cTnI bind to the COOH-terminal domain of cTnC with the nonphosphorylated form making limited contacts with the NH2-terminal domain of cTnC.	bind
26336	1	8101	6	13	NULL	NULL	NULL	DNA polymerase	GP		is encoded by					SP01	Organism	Bacillus subtilis phage			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24207_s_175	8798663	4 The DNA polymerase encoded by SP01, a  Bacillus subtilis phage, contains a domain of approximately 45 residues that resemble the putative thioredoxin binding domain of T7 DNA polymerase ( 42).	bind
26337	2	8101	6	13	NULL	NULL	NULL	DNA polymerase	GP		resemble			45 residue domain		T7 DNA polymerase	GP	putative	thioredoxin binding domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24207_s_175	8798663	4 The DNA polymerase encoded by SP01, a  Bacillus subtilis phage, contains a domain of approximately 45 residues that resemble the putative thioredoxin binding domain of T7 DNA polymerase ( 42).	bind
32180	1	8101	7	NULL	NULL	0	NULL	SP01	NULL	Bacillus subtilis phage	encodes	NULL				DNA polymerase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_39_24207_s_175	8798663	4 The DNA polymerase encoded by SP01, a  Bacillus subtilis phage, contains a domain of approximately 45 residues that resemble the putative thioredoxin binding domain of T7 DNA polymerase ( 42).	bind
32181	2	8101	7	10	NULL	0	NULL	DNA polymerase			resemble			45 residues		T7 DNA polymerase		putative	thioredoxin binding domain of		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24207_s_175	8798663	4 The DNA polymerase encoded by SP01, a  Bacillus subtilis phage, contains a domain of approximately 45 residues that resemble the putative thioredoxin binding domain of T7 DNA polymerase ( 42).	bind
26338	1	8102	6	13	NULL	NULL	NULL	nNOS	GP		bind					L-canavanine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25218_s_187	10464242	4 The modestly decreased binding affinity of nNOS for L-canavanine is attributed to loss of this H-bond.	bind
26339	2	8102	6	13	NULL	NULL	NULL			loss of	decreases		modestly	H-bond		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25218_s_187	10464242	4 The modestly decreased binding affinity of nNOS for L-canavanine is attributed to loss of this H-bond.	bind
32182	1	8102	7	NULL	NULL	0	NULL	nNOS	NULL		bind	NULL				L-canavanine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_36_25218_s_187	10464242	4 The modestly decreased binding affinity of nNOS for L-canavanine is attributed to loss of this H-bond.	bind
32183	2	8102	7	NULL	NULL	0	NULL	statement 1	NULL	decreased affinity of	is attributed to	NULL				 H-bond	NULL	loss of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_36_25218_s_187	10464242	4 The modestly decreased binding affinity of nNOS for L-canavanine is attributed to loss of this H-bond.	bind
26781	1	8103	6	13	NULL	NULL	NULL	Ess1	GP		reconfigures							phosphorylated	CTD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_44_31583_s_151	10531363	4 The possibility that Ess1 reconfigures the phosphorylated CTD though processive isomerization of its proline residues certainly adds an unexpected twist to the investigation of eukaryotic pre-mRNA transcription and 3''-end formation.	bind
26782	2	8103	6	13	NULL	NULL	NULL	statement 1	Process		occurs through							processive isomerization of	proline residues		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_44_31583_s_151	10531363	4 The possibility that Ess1 reconfigures the phosphorylated CTD though processive isomerization of its proline residues certainly adds an unexpected twist to the investigation of eukaryotic pre-mRNA transcription and 3''-end formation.	bind
32184	1	8103	7	NULL	NULL	0	NULL	Ess1	NULL		reconfigures 	NULL					NULL	phosphorylated	CTD		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_44_31583_s_151	10531363	4 The possibility that Ess1 reconfigures the phosphorylated CTD though processive isomerization of its proline residues certainly adds an unexpected twist to the investigation of eukaryotic pre-mRNA transcription and 3''-end formation.	bind
32185	2	8103	7	NULL	NULL	0	NULL	statement 1	NULL		occurs through	NULL					NULL	 processive isomerization of 	 proline residues 		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_44_31583_s_151	10531363	4 The possibility that Ess1 reconfigures the phosphorylated CTD though processive isomerization of its proline residues certainly adds an unexpected twist to the investigation of eukaryotic pre-mRNA transcription and 3''-end formation.	bind
26340	1	8104	6	13	NULL	NULL	NULL	MxA	GP		bind					RNP structure	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_7_4370_s_224	9933640	4 The present data strongly suggest that MxA binds to the RNP structure by recognizing its major protein component, NP.	bind
26341	2	8104	6	13	NULL	NULL	NULL	MxA	GP		recognize					protein component NP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_7_4370_s_224	9933640	4 The present data strongly suggest that MxA binds to the RNP structure by recognizing its major protein component, NP.	bind
26342	3	8104	6	13	NULL	NULL	NULL	statement 1	Process		occurs via					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_7_4370_s_224	9933640	4 The present data strongly suggest that MxA binds to the RNP structure by recognizing its major protein component, NP.	bind
32186	1	8104	7	NULL	NULL	0	NULL	MxA	NULL		binds to	NULL				RNP structure	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_7_4370_s_224	9933640	4 The present data strongly suggest that MxA binds to the RNP structure by recognizing its major protein component, NP.	bind
32187	2	8104	7	10	NULL	0	NULL	MxA	NULL		recognizes	NULL				protein component NP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_7_4370_s_224	9933640	4 The present data strongly suggest that MxA binds to the RNP structure by recognizing its major protein component, NP.	bind
46565	3	8104	7	10	NULL	0	NULL	statement 1	NULL		occurs via	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_7_4370_s_224	9933640	4 The present data strongly suggest that MxA binds to the RNP structure by recognizing its major protein component, NP.	bind
26343	1	8105	6	13	NULL	NULL	NULL	EKLF	GP		bind					LCR gene	GP			promoter	NULL	yolk sac	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_23_16052_s_148	16606611	4 Therefore, EKLF binding to both LCR and globin gene promoter sequences in the yolk sac, fetal liver, and bone marrow appears to be critical for correct globin gene regulation during development.	bind
26344	2	8105	6	13	NULL	NULL	NULL	EKLF	GP		bind					LCR gene	GP			promoter	NULL	fetal liver	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_23_16052_s_148	16606611	4 Therefore, EKLF binding to both LCR and globin gene promoter sequences in the yolk sac, fetal liver, and bone marrow appears to be critical for correct globin gene regulation during development.	bind
26345	3	8105	6	13	NULL	NULL	NULL	EKLF	GP		bind					LCR gene	GP			promoter	NULL	bone marrow	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_23_16052_s_148	16606611	4 Therefore, EKLF binding to both LCR and globin gene promoter sequences in the yolk sac, fetal liver, and bone marrow appears to be critical for correct globin gene regulation during development.	bind
26346	4	8105	6	13	NULL	NULL	NULL	EKLF	GP		bind					globin gene	GP			promoter	NULL	yolk sac	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_23_16052_s_148	16606611	4 Therefore, EKLF binding to both LCR and globin gene promoter sequences in the yolk sac, fetal liver, and bone marrow appears to be critical for correct globin gene regulation during development.	bind
26347	5	8105	6	13	NULL	NULL	NULL	EKLF	GP		bind					globin gene	GP			promoter	NULL	fetal liver	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_23_16052_s_148	16606611	4 Therefore, EKLF binding to both LCR and globin gene promoter sequences in the yolk sac, fetal liver, and bone marrow appears to be critical for correct globin gene regulation during development.	bind
26348	6	8105	6	13	NULL	NULL	NULL	EKLF	GP		bind					globin gene	GP			promoter	NULL	bone marrow	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_23_16052_s_148	16606611	4 Therefore, EKLF binding to both LCR and globin gene promoter sequences in the yolk sac, fetal liver, and bone marrow appears to be critical for correct globin gene regulation during development.	bind
32189	1	8105	7	NULL	NULL	0	NULL	EKLF	NULL		bind	NULL				LCR gene	NULL			promoter	NULL	yolk sac	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_23_16052_s_148	16606611	4 Therefore, EKLF binding to both LCR and globin gene promoter sequences in the yolk sac, fetal liver, and bone marrow appears to be critical for correct globin gene regulation during development.	bind
32190	2	8105	7	NULL	NULL	0	NULL	EKLF	NULL		bind	NULL				globin gene	NULL			promoter	NULL	yolk sac	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_23_16052_s_148	16606611	4 Therefore, EKLF binding to both LCR and globin gene promoter sequences in the yolk sac, fetal liver, and bone marrow appears to be critical for correct globin gene regulation during development.	bind
32191	3	8105	7	NULL	NULL	0	NULL	EKLF	NULL		bind	NULL				LCR gene	NULL			promoter	NULL	fetal liver	0	NULL	NULL	NULL	gw70_jbiolchem_281_23_16052_s_148	16606611	4 Therefore, EKLF binding to both LCR and globin gene promoter sequences in the yolk sac, fetal liver, and bone marrow appears to be critical for correct globin gene regulation during development.	bind
32192	4	8105	7	NULL	NULL	0	NULL	EKLF	NULL		bind	NULL				globin gene	NULL			promoter	NULL	fetal liver	0	NULL	NULL	NULL	gw70_jbiolchem_281_23_16052_s_148	16606611	4 Therefore, EKLF binding to both LCR and globin gene promoter sequences in the yolk sac, fetal liver, and bone marrow appears to be critical for correct globin gene regulation during development.	bind
32193	5	8105	7	NULL	NULL	0	NULL	EKLF	NULL		bind	NULL				LCR gene	NULL			promoter	NULL	 bone marrow	0	NULL	NULL	NULL	gw70_jbiolchem_281_23_16052_s_148	16606611	4 Therefore, EKLF binding to both LCR and globin gene promoter sequences in the yolk sac, fetal liver, and bone marrow appears to be critical for correct globin gene regulation during development.	bind
32194	6	8105	7	NULL	NULL	0	NULL	EKLF	NULL		bind	NULL				globin gene	NULL			promoter	NULL	bone marrow	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_23_16052_s_148	16606611	4 Therefore, EKLF binding to both LCR and globin gene promoter sequences in the yolk sac, fetal liver, and bone marrow appears to be critical for correct globin gene regulation during development.	bind
32195	7	8105	7	NULL	NULL	0	NULL	statement 1	NULL		is critical for	NULL				globin gene	NULL	regulation of			NULL	during development	0	NULL	NULL	NULL	gw70_jbiolchem_281_23_16052_s_148	16606611	4 Therefore, EKLF binding to both LCR and globin gene promoter sequences in the yolk sac, fetal liver, and bone marrow appears to be critical for correct globin gene regulation during development.	bind
32196	8	8105	7	NULL	NULL	0	NULL	statement 2	NULL		is critical for	NULL				globin gene	NULL	regulation of			NULL	during development	0	NULL	NULL	NULL	gw70_jbiolchem_281_23_16052_s_148	16606611	4 Therefore, EKLF binding to both LCR and globin gene promoter sequences in the yolk sac, fetal liver, and bone marrow appears to be critical for correct globin gene regulation during development.	bind
32197	9	8105	7	NULL	NULL	0	NULL	statement 3	NULL		is critical for	NULL				globin gene	NULL	regulation of			NULL	during development	0	NULL	NULL	NULL	gw70_jbiolchem_281_23_16052_s_148	16606611	4 Therefore, EKLF binding to both LCR and globin gene promoter sequences in the yolk sac, fetal liver, and bone marrow appears to be critical for correct globin gene regulation during development.	bind
32198	10	8105	7	NULL	NULL	0	NULL	statement 4	NULL		is critical for	NULL				globin gene	NULL	regulation of			NULL	during development	0	NULL	NULL	NULL	gw70_jbiolchem_281_23_16052_s_148	16606611	4 Therefore, EKLF binding to both LCR and globin gene promoter sequences in the yolk sac, fetal liver, and bone marrow appears to be critical for correct globin gene regulation during development.	bind
32199	11	8105	7	NULL	NULL	0	NULL	statement 5	NULL		is critical for	NULL				globin gene	NULL	regulation of			NULL	during development	0	NULL	NULL	NULL	gw70_jbiolchem_281_23_16052_s_148	16606611	4 Therefore, EKLF binding to both LCR and globin gene promoter sequences in the yolk sac, fetal liver, and bone marrow appears to be critical for correct globin gene regulation during development.	bind
32200	12	8105	7	NULL	NULL	0	NULL	statement 6	NULL		is critical for	NULL				globin gene	NULL	regulation of			NULL	during development	0	NULL	NULL	NULL	gw70_jbiolchem_281_23_16052_s_148	16606611	4 Therefore, EKLF binding to both LCR and globin gene promoter sequences in the yolk sac, fetal liver, and bone marrow appears to be critical for correct globin gene regulation during development.	bind
26349	1	8106	6	13	NULL	NULL	NULL	synaptotagmin I	GP		bind					synaptotagmin I	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_49_32966_s_101	9830048	4 Therefore, the analysis of the C2B-effector recognition site, described below, is focused on the self-association of synaptotagmin I and the binding of synaptotagmin to AP-2.	bind
26350	2	8106	6	13	NULL	NULL	NULL	synaptotagmin	GP		bind					AP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_49_32966_s_101	9830048	4 Therefore, the analysis of the C2B-effector recognition site, described below, is focused on the self-association of synaptotagmin I and the binding of synaptotagmin to AP-2.	bind
32270	1	8106	7	NULL	NULL	0	NULL	synaptotagmin I 	NULL		self-associate with	NULL				synaptotagmin I 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32966_s_101	9830048	4 Therefore, the analysis of the C2B-effector recognition site, described below, is focused on the self-association of synaptotagmin I and the binding of synaptotagmin to AP-2.	bind
32271	2	8106	7	NULL	NULL	0	NULL	synaptotagmin 	NULL		bind	NULL				AP-2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32966_s_101	9830048	4 Therefore, the analysis of the C2B-effector recognition site, described below, is focused on the self-association of synaptotagmin I and the binding of synaptotagmin to AP-2.	bind
26353	1	8107	6	13	NULL	NULL	NULL	FX cluster	GP		is a prerequisite for					PsaC	GP	binding of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20355_s_288	11914374	4 These  in vitro studies, therefore, show that the FX cluster is a prerequisite for the binding of PsaC, which, in turn, is required for the binding of PsaD and PsaE.	bind
26354	2	8107	6	13	NULL	NULL	NULL	PsaD	GP		bind					PsaE	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20355_s_288	11914374	4 These  in vitro studies, therefore, show that the FX cluster is a prerequisite for the binding of PsaC, which, in turn, is required for the binding of PsaD and PsaE.	bind
26355	3	8107	6	13	NULL	NULL	NULL	statement 1	Process		is required for					statement 2	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20355_s_288	11914374	4 These  in vitro studies, therefore, show that the FX cluster is a prerequisite for the binding of PsaC, which, in turn, is required for the binding of PsaD and PsaE.	bind
32272	1	8107	7	NULL	NULL	0	NULL	FX cluster	NULL		is a prerequisite for	NULL				PsaC	NULL	binding of			NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_277_23_20355_s_288	11914374	4 These  in vitro studies, therefore, show that the FX cluster is a prerequisite for the binding of PsaC, which, in turn, is required for the binding of PsaD and PsaE.	bind
32273	2	8107	7	NULL	NULL	0	NULL	PsaD	NULL		bind	NULL				PsaE	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20355_s_288	11914374	4 These  in vitro studies, therefore, show that the FX cluster is a prerequisite for the binding of PsaC, which, in turn, is required for the binding of PsaD and PsaE.	bind
32274	3	8107	7	NULL	NULL	0	NULL	PsaC	NULL		is required for	NULL				statement 2	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20355_s_288	11914374	4 These  in vitro studies, therefore, show that the FX cluster is a prerequisite for the binding of PsaC, which, in turn, is required for the binding of PsaD and PsaE.	bind
26783	1	8108	6	13	NULL	NULL	NULL	Spo0B	GP		bind					Spo0F	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_23_20483_s_267	11923303	4 These observations prompted us to predict that Spo0E and Rap phosphatases may assume a structural conformation with strong similarity to the helical organization of the Spo0B binding interface to Spo0F.	bind
32275	1	8108	7	NULL	NULL	0	NULL	Spo0B	NULL		bind	NULL				Spo0F	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_23_20483_s_267	11923303	4 These observations prompted us to predict that Spo0E and Rap phosphatases may assume a structural conformation with strong similarity to the helical organization of the Spo0B binding interface to Spo0F.	bind
26784	1	8109	6	13	NULL	NULL	NULL	mAChR	GP		dissociates from			M1 		TRPC6 channesls	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_330	15994335	4 These observations, together with the results described above, imply that disassociation of M1 mAChRs from TRPC6 channels requires three sequential events as follows: 1) phosphorylation of TRPC6 channels on Ser768/714 by PKC; 2) binding of FKBP12 to a site immediately adjacent to Ser768/714; and 3) dephosphorylation of Ser768/714 by calcineurin targeted to the TRPC6/FKBP12 anchor.	bind
26785	2	8109	6	13	NULL	NULL	NULL	PKC	GP		phosphorylates					TRPC6	GP		Ser768/714		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_330	15994335	4 These observations, together with the results described above, imply that disassociation of M1 mAChRs from TRPC6 channels requires three sequential events as follows: 1) phosphorylation of TRPC6 channels on Ser768/714 by PKC; 2) binding of FKBP12 to a site immediately adjacent to Ser768/714; and 3) dephosphorylation of Ser768/714 by calcineurin targeted to the TRPC6/FKBP12 anchor.	bind
26877	3	8109	6	13	NULL	NULL	NULL	FKB12	GP		bind					TRPC6	GP	site immediately adjacent to	Ser768/714		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_330	15994335	4 These observations, together with the results described above, imply that disassociation of M1 mAChRs from TRPC6 channels requires three sequential events as follows: 1) phosphorylation of TRPC6 channels on Ser768/714 by PKC; 2) binding of FKBP12 to a site immediately adjacent to Ser768/714; and 3) dephosphorylation of Ser768/714 by calcineurin targeted to the TRPC6/FKBP12 anchor.	bind
26878	4	8109	6	13	NULL	NULL	NULL	calcineurin	GP		is targeted to					TRPC6/FKBP12 anchor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_330	15994335	4 These observations, together with the results described above, imply that disassociation of M1 mAChRs from TRPC6 channels requires three sequential events as follows: 1) phosphorylation of TRPC6 channels on Ser768/714 by PKC; 2) binding of FKBP12 to a site immediately adjacent to Ser768/714; and 3) dephosphorylation of Ser768/714 by calcineurin targeted to the TRPC6/FKBP12 anchor.	bind
26879	5	8109	6	13	NULL	NULL	NULL	statement 4	Process		dephosphorylates					TRPC6	GP		Ser768/714		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_330	15994335	4 These observations, together with the results described above, imply that disassociation of M1 mAChRs from TRPC6 channels requires three sequential events as follows: 1) phosphorylation of TRPC6 channels on Ser768/714 by PKC; 2) binding of FKBP12 to a site immediately adjacent to Ser768/714; and 3) dephosphorylation of Ser768/714 by calcineurin targeted to the TRPC6/FKBP12 anchor.	bind
26880	6	8109	6	13	NULL	NULL	NULL	statement 1	Process		occurs via					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_330	15994335	4 These observations, together with the results described above, imply that disassociation of M1 mAChRs from TRPC6 channels requires three sequential events as follows: 1) phosphorylation of TRPC6 channels on Ser768/714 by PKC; 2) binding of FKBP12 to a site immediately adjacent to Ser768/714; and 3) dephosphorylation of Ser768/714 by calcineurin targeted to the TRPC6/FKBP12 anchor.	bind
26881	7	8109	6	13	NULL	NULL	NULL	statement 1	Process		occurs via					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_330	15994335	4 These observations, together with the results described above, imply that disassociation of M1 mAChRs from TRPC6 channels requires three sequential events as follows: 1) phosphorylation of TRPC6 channels on Ser768/714 by PKC; 2) binding of FKBP12 to a site immediately adjacent to Ser768/714; and 3) dephosphorylation of Ser768/714 by calcineurin targeted to the TRPC6/FKBP12 anchor.	bind
26882	8	8109	6	13	NULL	NULL	NULL	statement 1	Process		occurs via					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_330	15994335	4 These observations, together with the results described above, imply that disassociation of M1 mAChRs from TRPC6 channels requires three sequential events as follows: 1) phosphorylation of TRPC6 channels on Ser768/714 by PKC; 2) binding of FKBP12 to a site immediately adjacent to Ser768/714; and 3) dephosphorylation of Ser768/714 by calcineurin targeted to the TRPC6/FKBP12 anchor.	bind
32280	1	8109	7	NULL	NULL	0	NULL	PKC	NULL		phosphorylates	NULL				TRPC6 channels	NULL		Ser768/714		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_330	15994335	4 These observations, together with the results described above, imply that disassociation of M1 mAChRs from TRPC6 channels requires three sequential events as follows: 1) phosphorylation of TRPC6 channels on Ser768/714 by PKC; 2) binding of FKBP12 to a site immediately adjacent to Ser768/714; and 3) dephosphorylation of Ser768/714 by calcineurin targeted to the TRPC6/FKBP12 anchor.	bind
32281	2	8109	7	10	NULL	0	NULL	FKBP12 	NULL		bind	NULL				TRPC6	NULL	site adjacent to	 Ser768/714		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_330	15994335	4 These observations, together with the results described above, imply that disassociation of M1 mAChRs from TRPC6 channels requires three sequential events as follows: 1) phosphorylation of TRPC6 channels on Ser768/714 by PKC; 2) binding of FKBP12 to a site immediately adjacent to Ser768/714; and 3) dephosphorylation of Ser768/714 by calcineurin targeted to the TRPC6/FKBP12 anchor.	bind
32282	3	8109	7	NULL	NULL	0	NULL	calcineurin 	NULL		dephosphorylates	NULL					NULL		Ser768/714		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_330	15994335	4 These observations, together with the results described above, imply that disassociation of M1 mAChRs from TRPC6 channels requires three sequential events as follows: 1) phosphorylation of TRPC6 channels on Ser768/714 by PKC; 2) binding of FKBP12 to a site immediately adjacent to Ser768/714; and 3) dephosphorylation of Ser768/714 by calcineurin targeted to the TRPC6/FKBP12 anchor.	bind
32283	4	8109	7	NULL	NULL	0	NULL	statement 3	NULL		is targeted to	NULL				TRPC6/FKBP12 anchor	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_330	15994335	4 These observations, together with the results described above, imply that disassociation of M1 mAChRs from TRPC6 channels requires three sequential events as follows: 1) phosphorylation of TRPC6 channels on Ser768/714 by PKC; 2) binding of FKBP12 to a site immediately adjacent to Ser768/714; and 3) dephosphorylation of Ser768/714 by calcineurin targeted to the TRPC6/FKBP12 anchor.	bind
32284	5	8109	7	NULL	NULL	0	NULL	M1 mAChRs	NULL		dissociates from	NULL				 TRPC6 channels 	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_330	15994335	4 These observations, together with the results described above, imply that disassociation of M1 mAChRs from TRPC6 channels requires three sequential events as follows: 1) phosphorylation of TRPC6 channels on Ser768/714 by PKC; 2) binding of FKBP12 to a site immediately adjacent to Ser768/714; and 3) dephosphorylation of Ser768/714 by calcineurin targeted to the TRPC6/FKBP12 anchor.	bind
32285	6	8109	7	NULL	NULL	0	NULL	statement 5	NULL		requires	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_330	15994335	4 These observations, together with the results described above, imply that disassociation of M1 mAChRs from TRPC6 channels requires three sequential events as follows: 1) phosphorylation of TRPC6 channels on Ser768/714 by PKC; 2) binding of FKBP12 to a site immediately adjacent to Ser768/714; and 3) dephosphorylation of Ser768/714 by calcineurin targeted to the TRPC6/FKBP12 anchor.	bind
32286	7	8109	7	NULL	NULL	0	NULL	statement 5	NULL		requires	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_330	15994335	4 These observations, together with the results described above, imply that disassociation of M1 mAChRs from TRPC6 channels requires three sequential events as follows: 1) phosphorylation of TRPC6 channels on Ser768/714 by PKC; 2) binding of FKBP12 to a site immediately adjacent to Ser768/714; and 3) dephosphorylation of Ser768/714 by calcineurin targeted to the TRPC6/FKBP12 anchor.	bind
32287	8	8109	7	NULL	NULL	0	NULL	statement 5	NULL		requires	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_330	15994335	4 These observations, together with the results described above, imply that disassociation of M1 mAChRs from TRPC6 channels requires three sequential events as follows: 1) phosphorylation of TRPC6 channels on Ser768/714 by PKC; 2) binding of FKBP12 to a site immediately adjacent to Ser768/714; and 3) dephosphorylation of Ser768/714 by calcineurin targeted to the TRPC6/FKBP12 anchor.	bind
26357	1	8110	6	13	NULL	NULL	NULL	VLA-4	GP		bind					VCAM-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_51203_s_140	14532283	4 These results were surprising in light of the fact that VLA-4 binds this mAb at an affinity orders of magnitude higherR than it binds VCAM-1 ( ).	bind
32289	1	8110	7	10	NULL	0	NULL	VLA-4	NULL		binds	NULL				VCAM-1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_51203_s_140	14532283	4 These results were surprising in light of the fact that VLA-4 binds this mAb at an affinity orders of magnitude higherR than it binds VCAM-1 ( ).	bind
26359	1	8111	6	13	NULL	NULL	NULL	DnaA protein	GP	B. subtilis	does not bind					DnaB	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34255_s_220	9852089	4 This interpretation is supported by the observation that  B. subtilis DnaA protein failed to bind to DnaB.	bind
32291	1	8111	7	NULL	NULL	0	NULL	DnaA protein	NULL	 B. subtilis	does not bind	NULL				DnaB	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_51_34255_s_220	9852089	4 This interpretation is supported by the observation that  B. subtilis DnaA protein failed to bind to DnaB.	bind
55832	1	8112	6	13	NULL	NULL	NULL	P25 peptide	GP		bind					uPAR	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_14_9450_s_329	16461772	4 This is not particularly surprising, because the P25 peptide binds uPAR in a site distinct from both the vitronectin and uPA binding sites ( ).	bind
32292	1	8112	7	NULL	NULL	0	NULL	P25 peptide	NULL		binds	NULL				uPAR	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_14_9450_s_329	16461772	4 This is not particularly surprising, because the P25 peptide binds uPAR in a site distinct from both the vitronectin and uPA binding sites ( ).	bind
32293	2	8112	7	NULL	NULL	0	NULL	P25 peptide	NULL	binding site of	is distinct from	NULL				uPAR	NULL		uPA binding site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_14_9450_s_329	16461772	4 This is not particularly surprising, because the P25 peptide binds uPAR in a site distinct from both the vitronectin and uPA binding sites ( ).	bind
32294	3	8112	7	NULL	NULL	0	NULL	P25 peptide	NULL	binding site of	is distinct from	NULL				uPAR	NULL		vitronectin binding site		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_14_9450_s_329	16461772	4 This is not particularly surprising, because the P25 peptide binds uPAR in a site distinct from both the vitronectin and uPA binding sites ( ).	bind
26364	1	8113	6	13	NULL	NULL	NULL	TGF-beta1	GP		bind					TbetaR-II	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_17_11506_s_250	16492675	4 This suggests that the formation of Complex I (with a high ratio of TGF-beta1 binding to TbetaR-II and TbetaR-I) is a default process and that the formation of Complex II ( e.g. induced by heparan sulfate) is a regulatory event.	bind
26883	2	8113	6	13	NULL	NULL	NULL	TGF-beta1	GP		bind					TbetaR-I	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_17_11506_s_250	16492675	4 This suggests that the formation of Complex I (with a high ratio of TGF-beta1 binding to TbetaR-II and TbetaR-I) is a default process and that the formation of Complex II ( e.g. induced by heparan sulfate) is a regulatory event.	bind
26884	3	8113	6	13	NULL	NULL	NULL	Complex I	GP		consists of					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_17_11506_s_250	16492675	4 This suggests that the formation of Complex I (with a high ratio of TGF-beta1 binding to TbetaR-II and TbetaR-I) is a default process and that the formation of Complex II ( e.g. induced by heparan sulfate) is a regulatory event.	bind
26885	4	8113	6	13	NULL	NULL	NULL	Complex I	GP		consists of					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_17_11506_s_250	16492675	4 This suggests that the formation of Complex I (with a high ratio of TGF-beta1 binding to TbetaR-II and TbetaR-I) is a default process and that the formation of Complex II ( e.g. induced by heparan sulfate) is a regulatory event.	bind
26886	5	8113	6	13	NULL	NULL	NULL	complex II	GP	formation of	is induced by					heparan sulfate	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_17_11506_s_250	16492675	4 This suggests that the formation of Complex I (with a high ratio of TGF-beta1 binding to TbetaR-II and TbetaR-I) is a default process and that the formation of Complex II ( e.g. induced by heparan sulfate) is a regulatory event.	bind
32295	1	8113	7	NULL	NULL	0	NULL	TGF-beta1 	NULL		bind	NULL				TbetaR-II	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_17_11506_s_250	16492675	4 This suggests that the formation of Complex I (with a high ratio of TGF-beta1 binding to TbetaR-II and TbetaR-I) is a default process and that the formation of Complex II ( e.g. induced by heparan sulfate) is a regulatory event.	bind
32296	2	8113	7	NULL	NULL	0	NULL	TGF-beta1	NULL		bind	NULL				 TbetaR-I	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_17_11506_s_250	16492675	4 This suggests that the formation of Complex I (with a high ratio of TGF-beta1 binding to TbetaR-II and TbetaR-I) is a default process and that the formation of Complex II ( e.g. induced by heparan sulfate) is a regulatory event.	bind
32297	3	8113	7	NULL	NULL	0	NULL	Complex I	NULL		consist of	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_17_11506_s_250	16492675	4 This suggests that the formation of Complex I (with a high ratio of TGF-beta1 binding to TbetaR-II and TbetaR-I) is a default process and that the formation of Complex II ( e.g. induced by heparan sulfate) is a regulatory event.	bind
32298	4	8113	7	NULL	NULL	0	NULL	Complex I	NULL		consist of	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_17_11506_s_250	16492675	4 This suggests that the formation of Complex I (with a high ratio of TGF-beta1 binding to TbetaR-II and TbetaR-I) is a default process and that the formation of Complex II ( e.g. induced by heparan sulfate) is a regulatory event.	bind
32300	5	8113	7	10	NULL	0	NULL	heparan sulfate	NULL		induce	NULL				Complex II	NULL	formation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_17_11506_s_250	16492675	4 This suggests that the formation of Complex I (with a high ratio of TGF-beta1 binding to TbetaR-II and TbetaR-I) is a default process and that the formation of Complex II ( e.g. induced by heparan sulfate) is a regulatory event.	bind
26365	1	8114	6	13	NULL	NULL	NULL	Stm1p	GP		bind					Pu triplexes	NucleicAcid				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_8_5573_s_286	10681538	4 This would suggest that Stm1p could bind Pu triplexes  in vivo, should they occur.	bind
32301	1	8114	7	NULL	NULL	0	NULL	Stm1p	NULL		bind	NULL				Pu triplexes	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_jbiolchem_275_8_5573_s_286	10681538	4 This would suggest that Stm1p could bind Pu triplexes  in vivo, should they occur.	bind
26887	1	8115	6	13	NULL	NULL	NULL	FAK	GP		bind			vinculin homologous sequences		paxillin	GP		FAK binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_51_36684_s_333	10593973	4 Thus one can imagine that vinculin homologous sequences in FAK bind to the first FAK-binding site in paxillin and a second, unrelated sequence in FAK binds to the second paxillin interaction site.	bind
26888	2	8115	6	13	NULL	NULL	NULL	FAK	GP	unrelated sequence	bind								paxillin interaction site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_51_36684_s_333	10593973	4 Thus one can imagine that vinculin homologous sequences in FAK bind to the first FAK-binding site in paxillin and a second, unrelated sequence in FAK binds to the second paxillin interaction site.	bind
32302	1	8115	7	10	NULL	0	NULL	FAK	NULL		bind	NULL		vinculin homologous sequence		paxillin	NULL		FAK-binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_51_36684_s_333	10593973	4 Thus one can imagine that vinculin homologous sequences in FAK bind to the first FAK-binding site in paxillin and a second, unrelated sequence in FAK binds to the second paxillin interaction site.	bind
32304	3	8115	7	10	NULL	0	NULL	FAK	NULL	unrelated sequence	bind	NULL				paxillin	NULL		second interaction site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_51_36684_s_333	10593973	4 Thus one can imagine that vinculin homologous sequences in FAK bind to the first FAK-binding site in paxillin and a second, unrelated sequence in FAK binds to the second paxillin interaction site.	bind
26384	1	8116	6	13	NULL	NULL	NULL	DP1	GP	DN binding form of 	bind					E2F	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_27_19011_s_152	10383401	4 To test our hypothesis, we expressed a DN binding form of DP1, an obligate binding partner to E2F, wild type, and deletion mutants of DP1, which do not display DN characteristics ( 23).	bind
32305	1	8116	7	NULL	NULL	0	NULL	DP1	NULL	DN binding form	binds	NULL				E2F	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_27_19011_s_152	10383401	4 To test our hypothesis, we expressed a DN binding form of DP1, an obligate binding partner to E2F, wild type, and deletion mutants of DP1, which do not display DN characteristics ( 23).	bind
26385	1	8117	6	13	NULL	NULL	NULL	Runx2	GP		bind					C/EBPbeta	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_32_22695_s_345	16772287	4 Together these results indicate that binding of Runx2 and C/EBPbeta is one of the early events during chromatin remodeling and transcriptional activation of the OC gene.	bind
26386	2	8117	6	13	NULL	NULL	NULL	statement 1	Process		occurs during					chromatin remodeling	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_32_22695_s_345	16772287	4 Together these results indicate that binding of Runx2 and C/EBPbeta is one of the early events during chromatin remodeling and transcriptional activation of the OC gene.	bind
26392	3	8117	6	13	NULL	NULL	NULL	statement 1	Process		occurs during					OC gene	GP	transcriptional activation of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_32_22695_s_345	16772287	4 Together these results indicate that binding of Runx2 and C/EBPbeta is one of the early events during chromatin remodeling and transcriptional activation of the OC gene.	bind
32308	1	8117	7	NULL	NULL	0	NULL	Runx2	NULL		binds	NULL				C/EBPbeta	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_22695_s_345	16772287	4 Together these results indicate that binding of Runx2 and C/EBPbeta is one of the early events during chromatin remodeling and transcriptional activation of the OC gene.	bind
32309	2	8117	7	NULL	NULL	0	NULL	statement 1	NULL		occurs during	NULL				chromatin remodeling	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_22695_s_345	16772287	4 Together these results indicate that binding of Runx2 and C/EBPbeta is one of the early events during chromatin remodeling and transcriptional activation of the OC gene.	bind
32310	3	8117	7	NULL	NULL	0	NULL	statement 1	NULL		occurs during	NULL				OC gene	NULL	transcriptional activation of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_22695_s_345	16772287	4 Together these results indicate that binding of Runx2 and C/EBPbeta is one of the early events during chromatin remodeling and transcriptional activation of the OC gene.	bind
26393	1	8118	6	13	NULL	NULL	NULL	Cx43	GP		dissociates from					ZO-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_2_215_s_182	14699011	4 Toyofuku et al 4 argued that dissociation of Cx43 from ZO-1 was secondary to tyrosine phosphorylation of Cx43CT by binding of the SH2 domain of c-Src.	bind
26394	2	8118	6	13	NULL	NULL	NULL	c-Src	GP		bind			SH2 domain		Cx43CT	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_2_215_s_182	14699011	4 Toyofuku et al 4 argued that dissociation of Cx43 from ZO-1 was secondary to tyrosine phosphorylation of Cx43CT by binding of the SH2 domain of c-Src.	bind
55833	3	8118	6	13	NULL	NULL	NULL	statement 2	Process		phosphorylates					Cx43CT	GP		tyrosine		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_2_215_s_182	14699011	4 Toyofuku et al 4 argued that dissociation of Cx43 from ZO-1 was secondary to tyrosine phosphorylation of Cx43CT by binding of the SH2 domain of c-Src.	bind
55834	4	8118	6	13	NULL	NULL	NULL	statement 1	Process		is secondary to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_2_215_s_182	14699011	4 Toyofuku et al 4 argued that dissociation of Cx43 from ZO-1 was secondary to tyrosine phosphorylation of Cx43CT by binding of the SH2 domain of c-Src.	bind
32311	1	8118	7	NULL	NULL	0	NULL	Cx43	NULL		dissociates from	NULL				 ZO-1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_2_215_s_182	14699011	4 Toyofuku et al 4 argued that dissociation of Cx43 from ZO-1 was secondary to tyrosine phosphorylation of Cx43CT by binding of the SH2 domain of c-Src.	bind
32312	2	8118	7	NULL	NULL	0	NULL	c-Src	NULL		bind	NULL		SH2 domain		Cx43CT	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_2_215_s_182	14699011	4 Toyofuku et al 4 argued that dissociation of Cx43 from ZO-1 was secondary to tyrosine phosphorylation of Cx43CT by binding of the SH2 domain of c-Src.	bind
32313	3	8118	7	NULL	NULL	0	NULL	statement 2	NULL		phosphorylates	NULL				Cx43CT	NULL		tyrosine		NULL		0	NULL	NULL	NULL	gw70_circulationres_94_2_215_s_182	14699011	4 Toyofuku et al 4 argued that dissociation of Cx43 from ZO-1 was secondary to tyrosine phosphorylation of Cx43CT by binding of the SH2 domain of c-Src.	bind
32314	4	8118	7	NULL	NULL	0	NULL	statement 1	NULL		is secondary to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_2_215_s_182	14699011	4 Toyofuku et al 4 argued that dissociation of Cx43 from ZO-1 was secondary to tyrosine phosphorylation of Cx43CT by binding of the SH2 domain of c-Src.	bind
26395	1	8119	6	13	NULL	NULL	NULL	transmembrane protein	GP		bind					factor VIIa	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1217_s_17	15976319	4 Upon exposure to blood, the transmembrane protein binds and allosterically activates factor VIIa (FVIIa).	bind
26396	2	8119	6	13	NULL	NULL	NULL	transmembrane protein	GP		activates		allosterically			factor VIIa	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1217_s_17	15976319	4 Upon exposure to blood, the transmembrane protein binds and allosterically activates factor VIIa (FVIIa).	bind
26397	3	8119	6	13	NULL	NULL	NULL	FVIIa	GP		is					factor VIIa	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1217_s_17	15976319	4 Upon exposure to blood, the transmembrane protein binds and allosterically activates factor VIIa (FVIIa).	bind
26398	4	8119	6	13	NULL	NULL	NULL	statement 1	Process		occurs upon exposure to					blood	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1217_s_17	15976319	4 Upon exposure to blood, the transmembrane protein binds and allosterically activates factor VIIa (FVIIa).	bind
26399	5	8119	6	13	NULL	NULL	NULL	statement 2	Process		occurs upon exposure to					blood	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_12_1217_s_17	15976319	4 Upon exposure to blood, the transmembrane protein binds and allosterically activates factor VIIa (FVIIa).	bind
32315	1	8119	7	NULL	NULL	0	NULL	transmembrane protein	NULL		bind	NULL				FVIIa	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_12_1217_s_17	15976319	4 Upon exposure to blood, the transmembrane protein binds and allosterically activates factor VIIa (FVIIa).	bind
32316	2	8119	7	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL	allosterically			FVIIa	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_12_1217_s_17	15976319	4 Upon exposure to blood, the transmembrane protein binds and allosterically activates factor VIIa (FVIIa).	bind
32317	3	8119	7	NULL	NULL	0	NULL	statement 1	NULL		occurs upon	NULL				blood	NULL	exposure to			NULL		0	NULL	NULL	NULL	gw70_circulationres_96_12_1217_s_17	15976319	4 Upon exposure to blood, the transmembrane protein binds and allosterically activates factor VIIa (FVIIa).	bind
32318	4	8119	7	NULL	NULL	0	NULL	statement 2	NULL		occurs upon	NULL				blood	NULL	exposure to			NULL		0	NULL	NULL	NULL	gw70_circulationres_96_12_1217_s_17	15976319	4 Upon exposure to blood, the transmembrane protein binds and allosterically activates factor VIIa (FVIIa).	bind
32319	5	8119	7	NULL	NULL	0	NULL	FVIIa	NULL		is	NULL				factor VIIa	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_12_1217_s_17	15976319	4 Upon exposure to blood, the transmembrane protein binds and allosterically activates factor VIIa (FVIIa).	bind
26400	1	8120	6	13	NULL	NULL	NULL	Vps9p	GP		bind					ubiquitin	GP	free			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_19826_s_274	12654912	4 Vps9p  binding to free ubiquitin has been demonstrated here; however, CUE domain  binding may be preferential toward protein-conjugated ubiquityl moieties and  thereby target Vps9p to ubiquitylated membrane proteins during endocytosis.	bind
26401	2	8120	6	13	NULL	NULL	NULL	Vps9p	GP		is targeted to					membrane proteins	GP	ubiquitylated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_19826_s_274	12654912	4 Vps9p  binding to free ubiquitin has been demonstrated here; however, CUE domain  binding may be preferential toward protein-conjugated ubiquityl moieties and  thereby target Vps9p to ubiquitylated membrane proteins during endocytosis.	bind
26402	3	8120	6	13	NULL	NULL	NULL	statement 2	Process		occurs during					endocytosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_19826_s_274	12654912	4 Vps9p  binding to free ubiquitin has been demonstrated here; however, CUE domain  binding may be preferential toward protein-conjugated ubiquityl moieties and  thereby target Vps9p to ubiquitylated membrane proteins during endocytosis.	bind
32320	1	8120	7	NULL	NULL	0	NULL	 Vps9p	NULL		binds	NULL				Ubiquitin	NULL	free			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_22_19826_s_274	12654912	4 Vps9p  binding to free ubiquitin has been demonstrated here; however, CUE domain  binding may be preferential toward protein-conjugated ubiquityl moieties and  thereby target Vps9p to ubiquitylated membrane proteins during endocytosis.	bind
32321	2	8120	7	NULL	NULL	0	NULL		NULL		be preferred for	NULL	may	CUE domain		protein-conjugated ubiquityl moieties	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_22_19826_s_274	12654912	4 Vps9p  binding to free ubiquitin has been demonstrated here; however, CUE domain  binding may be preferential toward protein-conjugated ubiquityl moieties and  thereby target Vps9p to ubiquitylated membrane proteins during endocytosis.	bind
32322	3	8120	7	10	NULL	0	NULL	Vps9p			targeted to					membrane proteins		ubiquitylated 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_19826_s_274	12654912	4 Vps9p  binding to free ubiquitin has been demonstrated here; however, CUE domain  binding may be preferential toward protein-conjugated ubiquityl moieties and  thereby target Vps9p to ubiquitylated membrane proteins during endocytosis.	bind
32323	4	8120	7	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_22_19826_s_274	12654912	4 Vps9p  binding to free ubiquitin has been demonstrated here; however, CUE domain  binding may be preferential toward protein-conjugated ubiquityl moieties and  thereby target Vps9p to ubiquitylated membrane proteins during endocytosis.	bind
46566	5	8120	7	10	NULL	0	NULL	statement 3	NULL		occurs during	NULL				endocytosis	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_22_19826_s_274	12654912	4 Vps9p  binding to free ubiquitin has been demonstrated here; however, CUE domain  binding may be preferential toward protein-conjugated ubiquityl moieties and  thereby target Vps9p to ubiquitylated membrane proteins during endocytosis.	bind
26403	1	8121	6	13	NULL	NULL	NULL	substrates	GP	linear	contain							mutant		lox site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_33_31092_s_277	11406627	4 We found that Cre efficiently binds, cleaves, and recombines linear substrates containing the same mutant  lox site as chi4 (L. Lee and P. D. Sadowski, unpublished data).	bind
26404	2	8121	6	13	NULL	NULL	NULL	Cre	GP		bind		efficiently			statement 1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_33_31092_s_277	11406627	4 We found that Cre efficiently binds, cleaves, and recombines linear substrates containing the same mutant  lox site as chi4 (L. Lee and P. D. Sadowski, unpublished data).	bind
26405	3	8121	6	13	NULL	NULL	NULL	Cre	GP		cleaves					statement 1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_33_31092_s_277	11406627	4 We found that Cre efficiently binds, cleaves, and recombines linear substrates containing the same mutant  lox site as chi4 (L. Lee and P. D. Sadowski, unpublished data).	bind
26406	4	8121	6	13	NULL	NULL	NULL	Cre	GP		recombines					statement 1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_33_31092_s_277	11406627	4 We found that Cre efficiently binds, cleaves, and recombines linear substrates containing the same mutant  lox site as chi4 (L. Lee and P. D. Sadowski, unpublished data).	bind
32348	1	8121	7	NULL	NULL	0	NULL	 Cre	NULL		binds	NULL	efficiently			linear substrate	NULL	mutant	lox site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_33_31092_s_277	11406627	4 We found that Cre efficiently binds, cleaves, and recombines linear substrates containing the same mutant  lox site as chi4 (L. Lee and P. D. Sadowski, unpublished data).	bind
32349	2	8121	7	NULL	NULL	0	NULL	Cre	NULL		cleaves	NULL	efficiently			linear substrate	NULL	mutant	lox site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_33_31092_s_277	11406627	4 We found that Cre efficiently binds, cleaves, and recombines linear substrates containing the same mutant  lox site as chi4 (L. Lee and P. D. Sadowski, unpublished data).	bind
32350	3	8121	7	NULL	NULL	0	NULL	Cre	NULL		recombines	NULL	efficiently			linear substrate	NULL	mutant	lox site		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_33_31092_s_277	11406627	4 We found that Cre efficiently binds, cleaves, and recombines linear substrates containing the same mutant  lox site as chi4 (L. Lee and P. D. Sadowski, unpublished data).	bind
32351	4	8121	7	NULL	NULL	0	NULL	Cre	NULL		binds	NULL	efficiently			chi4	NULL	mutant	lox site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_33_31092_s_277	11406627	4 We found that Cre efficiently binds, cleaves, and recombines linear substrates containing the same mutant  lox site as chi4 (L. Lee and P. D. Sadowski, unpublished data).	bind
32352	5	8121	7	NULL	NULL	0	NULL	Cre	NULL		cleaves	NULL	efficiently			chi4	NULL	mutant	lox site		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_33_31092_s_277	11406627	4 We found that Cre efficiently binds, cleaves, and recombines linear substrates containing the same mutant  lox site as chi4 (L. Lee and P. D. Sadowski, unpublished data).	bind
32353	6	8121	7	NULL	NULL	0	NULL	Cre	NULL		recombines	NULL	efficiently			chi4	NULL	mutant	lox site		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_33_31092_s_277	11406627	4 We found that Cre efficiently binds, cleaves, and recombines linear substrates containing the same mutant  lox site as chi4 (L. Lee and P. D. Sadowski, unpublished data).	bind
26889	1	8122	6	13	NULL	NULL	NULL	hypoxia/reoxygenation	Process		decreases					HSP60	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_21_2727_s_27	12438300	4 We hypothesized that HSP60 would decrease with hypoxia/reoxygenation, based on previous observations, 5 and that this would precipitate translocation of bax to the mitochondria and release of cytochrome c, based on our prior work showing that cytosolic HSP60 binds bax and that reduction in HSP60 precipitates apoptosis.	bind
26890	2	8122	6	13	NULL	NULL	NULL	bax	GP		translocate into					mitochondria	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_21_2727_s_27	12438300	4 We hypothesized that HSP60 would decrease with hypoxia/reoxygenation, based on previous observations, 5 and that this would precipitate translocation of bax to the mitochondria and release of cytochrome c, based on our prior work showing that cytosolic HSP60 binds bax and that reduction in HSP60 precipitates apoptosis.	bind
26891	3	8122	6	13	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_21_2727_s_27	12438300	4 We hypothesized that HSP60 would decrease with hypoxia/reoxygenation, based on previous observations, 5 and that this would precipitate translocation of bax to the mitochondria and release of cytochrome c, based on our prior work showing that cytosolic HSP60 binds bax and that reduction in HSP60 precipitates apoptosis.	bind
26892	4	8122	6	13	NULL	NULL	NULL	statement 1	Process		leads to					cytochrome c	GP	release of 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_21_2727_s_27	12438300	4 We hypothesized that HSP60 would decrease with hypoxia/reoxygenation, based on previous observations, 5 and that this would precipitate translocation of bax to the mitochondria and release of cytochrome c, based on our prior work showing that cytosolic HSP60 binds bax and that reduction in HSP60 precipitates apoptosis.	bind
26893	5	8122	6	13	NULL	NULL	NULL	HSP60	GP	cytosolic	bind					bax	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_21_2727_s_27	12438300	4 We hypothesized that HSP60 would decrease with hypoxia/reoxygenation, based on previous observations, 5 and that this would precipitate translocation of bax to the mitochondria and release of cytochrome c, based on our prior work showing that cytosolic HSP60 binds bax and that reduction in HSP60 precipitates apoptosis.	bind
26894	6	8122	6	13	NULL	NULL	NULL	HSP60	GP	reduction in	precipitates					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_21_2727_s_27	12438300	4 We hypothesized that HSP60 would decrease with hypoxia/reoxygenation, based on previous observations, 5 and that this would precipitate translocation of bax to the mitochondria and release of cytochrome c, based on our prior work showing that cytosolic HSP60 binds bax and that reduction in HSP60 precipitates apoptosis.	bind
32354	1	8122	7	NULL	NULL	0	NULL	HSP60 	NULL		decrease with	NULL				hypoxia/reoxygenation	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_21_2727_s_27	12438300	4 We hypothesized that HSP60 would decrease with hypoxia/reoxygenation, based on previous observations, 5 and that this would precipitate translocation of bax to the mitochondria and release of cytochrome c, based on our prior work showing that cytosolic HSP60 binds bax and that reduction in HSP60 precipitates apoptosis.	bind
32355	2	8122	7	10	NULL	0	NULL	bax			is translocated to					mitochondria					NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_21_2727_s_27	12438300	4 We hypothesized that HSP60 would decrease with hypoxia/reoxygenation, based on previous observations, 5 and that this would precipitate translocation of bax to the mitochondria and release of cytochrome c, based on our prior work showing that cytosolic HSP60 binds bax and that reduction in HSP60 precipitates apoptosis.	bind
32359	3	8122	7	NULL	NULL	0	NULL	statement 1	NULL		release	NULL				cytochrome c	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_21_2727_s_27	12438300	4 We hypothesized that HSP60 would decrease with hypoxia/reoxygenation, based on previous observations, 5 and that this would precipitate translocation of bax to the mitochondria and release of cytochrome c, based on our prior work showing that cytosolic HSP60 binds bax and that reduction in HSP60 precipitates apoptosis.	bind
32360	4	8122	7	NULL	NULL	0	NULL	HSP60	NULL	cytosolic	binds	NULL				bax	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_21_2727_s_27	12438300	4 We hypothesized that HSP60 would decrease with hypoxia/reoxygenation, based on previous observations, 5 and that this would precipitate translocation of bax to the mitochondria and release of cytochrome c, based on our prior work showing that cytosolic HSP60 binds bax and that reduction in HSP60 precipitates apoptosis.	bind
32361	5	8122	7	NULL	NULL	0	NULL	HSP60	NULL	reduction in	precipitates	NULL				apoptosis	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_21_2727_s_27	12438300	4 We hypothesized that HSP60 would decrease with hypoxia/reoxygenation, based on previous observations, 5 and that this would precipitate translocation of bax to the mitochondria and release of cytochrome c, based on our prior work showing that cytosolic HSP60 binds bax and that reduction in HSP60 precipitates apoptosis.	bind
55835	6	8122	7	10	NULL	0	NULL	statement 1			leads to					statement 2					NULL		0	NULL	NULL	NULL	gw60_circulation_106_21_2727_s_27	12438300	4 We hypothesized that HSP60 would decrease with hypoxia/reoxygenation, based on previous observations, 5 and that this would precipitate translocation of bax to the mitochondria and release of cytochrome c, based on our prior work showing that cytosolic HSP60 binds bax and that reduction in HSP60 precipitates apoptosis.	bind
26895	1	8124	6	13	NULL	NULL	NULL	4'F-DMA	Chemical		has affinity for					ERalpha	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_chem-res-toxicol_19_6_16780356_s_8	16780356	4'F-DMA shows ligand binding affinity to  estrogen receptor (ER)alpha and ERbeta with similarity to both raloxifene  and to DMA.	bind
26896	2	8124	6	13	NULL	NULL	NULL	ER	GP		is					estrogen receptor	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_chem-res-toxicol_19_6_16780356_s_8	16780356	4'F-DMA shows ligand binding affinity to  estrogen receptor (ER)alpha and ERbeta with similarity to both raloxifene  and to DMA.	bind
26897	3	8124	6	13	NULL	NULL	NULL	4'F-DMA	Chemical		has affinity for					ERbeta	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_chem-res-toxicol_19_6_16780356_s_8	16780356	4'F-DMA shows ligand binding affinity to  estrogen receptor (ER)alpha and ERbeta with similarity to both raloxifene  and to DMA.	bind
26898	4	8124	6	13	NULL	NULL	NULL	raloxifene	Chemical		has affinity for					ERalpha	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_chem-res-toxicol_19_6_16780356_s_8	16780356	4'F-DMA shows ligand binding affinity to  estrogen receptor (ER)alpha and ERbeta with similarity to both raloxifene  and to DMA.	bind
26899	5	8124	6	13	NULL	NULL	NULL	raloxifene	Chemical		has affinity for					ERbeta	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_chem-res-toxicol_19_6_16780356_s_8	16780356	4'F-DMA shows ligand binding affinity to  estrogen receptor (ER)alpha and ERbeta with similarity to both raloxifene  and to DMA.	bind
26900	6	8124	6	13	NULL	NULL	NULL	DMA	Chemical		has affinity for					ERalpha	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_chem-res-toxicol_19_6_16780356_s_8	16780356	4'F-DMA shows ligand binding affinity to  estrogen receptor (ER)alpha and ERbeta with similarity to both raloxifene  and to DMA.	bind
26901	7	8124	6	13	NULL	NULL	NULL	DMA	Chemical		has affinity for					ERbeta	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_chem-res-toxicol_19_6_16780356_s_8	16780356	4'F-DMA shows ligand binding affinity to  estrogen receptor (ER)alpha and ERbeta with similarity to both raloxifene  and to DMA.	bind
32366	1	8124	7	NULL	NULL	0	NULL	4'F-DMA	NULL		bind	NULL				ER alpha	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_chem-res-toxicol_19_6_16780356_s_8	16780356	4'F-DMA shows ligand binding affinity to  estrogen receptor (ER)alpha and ERbeta with similarity to both raloxifene  and to DMA.	bind
32367	2	8124	7	NULL	NULL	0	NULL	4'F-DMA	NULL		bind	NULL				ERbeta	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_chem-res-toxicol_19_6_16780356_s_8	16780356	4'F-DMA shows ligand binding affinity to  estrogen receptor (ER)alpha and ERbeta with similarity to both raloxifene  and to DMA.	bind
32368	3	8124	7	NULL	NULL	0	NULL	raloxifene	NULL		bind	NULL				ER alpha	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_chem-res-toxicol_19_6_16780356_s_8	16780356	4'F-DMA shows ligand binding affinity to  estrogen receptor (ER)alpha and ERbeta with similarity to both raloxifene  and to DMA.	bind
32369	4	8124	7	NULL	NULL	0	NULL	raloxifene	NULL		bind	NULL				ERbeta	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_chem-res-toxicol_19_6_16780356_s_8	16780356	4'F-DMA shows ligand binding affinity to  estrogen receptor (ER)alpha and ERbeta with similarity to both raloxifene  and to DMA.	bind
32370	5	8124	7	NULL	NULL	0	NULL	DMA	NULL		bind	NULL				ER alpha	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_chem-res-toxicol_19_6_16780356_s_8	16780356	4'F-DMA shows ligand binding affinity to  estrogen receptor (ER)alpha and ERbeta with similarity to both raloxifene  and to DMA.	bind
32371	6	8124	7	NULL	NULL	0	NULL	DMA	NULL		bind	NULL				ERbeta	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_chem-res-toxicol_19_6_16780356_s_8	16780356	4'F-DMA shows ligand binding affinity to  estrogen receptor (ER)alpha and ERbeta with similarity to both raloxifene  and to DMA.	bind
55836	7	8124	7	10	NULL	0	NULL	ER			is					estrogen receptor					NULL		0	NULL	NULL	NULL	abs-batch0700-0719_chem-res-toxicol_19_6_16780356_s_8	16780356	4'F-DMA shows ligand binding affinity to  estrogen receptor (ER)alpha and ERbeta with similarity to both raloxifene  and to DMA.	bind
26485	1	8125	6	13	NULL	NULL	NULL	EPOR	GP	soluble;; phosphorylated	bind			serine		JAK2	GP	genetically engineered			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32430_s_155	8943308	4)  In vitro binding experiments showed that the soluble, serine-phosphorylated 78-kDa EPOR bound to genetically engineered JAK2 better than other forms of EPOR; however, EPO-induced tyrosine phosphorylation greatly increased the ability of the soluble, 78-kDa EPOR molecule to interact with immobilized JAK2.	bind
26486	2	8125	6	13	NULL	NULL	NULL	EPOR molecule	GP	soluble	interact with					JAK2	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32430_s_155	8943308	4)  In vitro binding experiments showed that the soluble, serine-phosphorylated 78-kDa EPOR bound to genetically engineered JAK2 better than other forms of EPOR; however, EPO-induced tyrosine phosphorylation greatly increased the ability of the soluble, 78-kDa EPOR molecule to interact with immobilized JAK2.	bind
26487	3	8125	6	13	NULL	NULL	NULL	EPO 	GP		induces							phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32430_s_155	8943308	4)  In vitro binding experiments showed that the soluble, serine-phosphorylated 78-kDa EPOR bound to genetically engineered JAK2 better than other forms of EPOR; however, EPO-induced tyrosine phosphorylation greatly increased the ability of the soluble, 78-kDa EPOR molecule to interact with immobilized JAK2.	bind
26488	4	8125	6	13	NULL	NULL	NULL	statement 3	Process		increases					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32430_s_155	8943308	4)  In vitro binding experiments showed that the soluble, serine-phosphorylated 78-kDa EPOR bound to genetically engineered JAK2 better than other forms of EPOR; however, EPO-induced tyrosine phosphorylation greatly increased the ability of the soluble, 78-kDa EPOR molecule to interact with immobilized JAK2.	bind
32372	1	8125	7	10	NULL	0	NULL	EPOR	NULL	soluble;;phosphorylated	bind	NULL		serine		JAK2	NULL	genetically engineered			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32430_s_155	8943308	4)  In vitro binding experiments showed that the soluble, serine-phosphorylated 78-kDa EPOR bound to genetically engineered JAK2 better than other forms of EPOR; however, EPO-induced tyrosine phosphorylation greatly increased the ability of the soluble, 78-kDa EPOR molecule to interact with immobilized JAK2.	bind
32373	2	8125	7	NULL	NULL	0	NULL	EPOR	NULL		bind	NULL				JAK2	NULL	genetically engineered			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32430_s_155	8943308	4)  In vitro binding experiments showed that the soluble, serine-phosphorylated 78-kDa EPOR bound to genetically engineered JAK2 better than other forms of EPOR; however, EPO-induced tyrosine phosphorylation greatly increased the ability of the soluble, 78-kDa EPOR molecule to interact with immobilized JAK2.	bind
32374	3	8125	7	NULL	NULL	0	NULL	EPOR	NULL		is a type of	NULL				78-kDa protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_50_32430_s_155	8943308	4)  In vitro binding experiments showed that the soluble, serine-phosphorylated 78-kDa EPOR bound to genetically engineered JAK2 better than other forms of EPOR; however, EPO-induced tyrosine phosphorylation greatly increased the ability of the soluble, 78-kDa EPOR molecule to interact with immobilized JAK2.	bind
32375	4	8125	7	NULL	NULL	0	NULL	statement 1	NULL	binding of	is better than 	NULL				statement 2	NULL	binding of			NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_271_50_32430_s_155	8943308	4)  In vitro binding experiments showed that the soluble, serine-phosphorylated 78-kDa EPOR bound to genetically engineered JAK2 better than other forms of EPOR; however, EPO-induced tyrosine phosphorylation greatly increased the ability of the soluble, 78-kDa EPOR molecule to interact with immobilized JAK2.	bind
32376	5	8125	7	NULL	NULL	0	NULL	EPOR molecule	NULL	soluble	interacts with	NULL				JAK2	NULL	immobilized			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_50_32430_s_155	8943308	4)  In vitro binding experiments showed that the soluble, serine-phosphorylated 78-kDa EPOR bound to genetically engineered JAK2 better than other forms of EPOR; however, EPO-induced tyrosine phosphorylation greatly increased the ability of the soluble, 78-kDa EPOR molecule to interact with immobilized JAK2.	bind
32377	6	8125	7	NULL	NULL	0	NULL	EPO	NULL		induce	NULL					NULL	phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_50_32430_s_155	8943308	4)  In vitro binding experiments showed that the soluble, serine-phosphorylated 78-kDa EPOR bound to genetically engineered JAK2 better than other forms of EPOR; however, EPO-induced tyrosine phosphorylation greatly increased the ability of the soluble, 78-kDa EPOR molecule to interact with immobilized JAK2.	bind
32378	7	8125	7	NULL	NULL	0	NULL	statement 6	NULL		increase	NULL	greatly			statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32430_s_155	8943308	4)  In vitro binding experiments showed that the soluble, serine-phosphorylated 78-kDa EPOR bound to genetically engineered JAK2 better than other forms of EPOR; however, EPO-induced tyrosine phosphorylation greatly increased the ability of the soluble, 78-kDa EPOR molecule to interact with immobilized JAK2.	bind
26489	1	8126	6	13	NULL	NULL	NULL	Cas	GP	dominant-negative mutant	does not bind					Crk	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_16_11706_s_193	10766791	4) A dominant negative mutant of Cas which fails to bind Crk blocked H2O2-mediated activation of JNK but not ERK1/2 and p38.	bind
26490	2	8126	6	13	NULL	NULL	NULL	H2O2	Chemical		mediates					JNK	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_16_11706_s_193	10766791	4) A dominant negative mutant of Cas which fails to bind Crk blocked H2O2-mediated activation of JNK but not ERK1/2 and p38.	bind
26491	3	8126	6	13	NULL	NULL	NULL	Cas	GP	dominant-negative mutant	blocks					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_16_11706_s_193	10766791	4) A dominant negative mutant of Cas which fails to bind Crk blocked H2O2-mediated activation of JNK but not ERK1/2 and p38.	bind
26492	4	8126	6	13	NULL	NULL	NULL	H2O2	Chemical		mediates					Erk1/2	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_16_11706_s_193	10766791	4) A dominant negative mutant of Cas which fails to bind Crk blocked H2O2-mediated activation of JNK but not ERK1/2 and p38.	bind
26493	5	8126	6	13	NULL	NULL	NULL	H2O2	Chemical		mediates					p38	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_16_11706_s_193	10766791	4) A dominant negative mutant of Cas which fails to bind Crk blocked H2O2-mediated activation of JNK but not ERK1/2 and p38.	bind
26494	6	8126	6	13	NULL	NULL	NULL	Cas	GP	dominant-negative mutant	does not block					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_16_11706_s_193	10766791	4) A dominant negative mutant of Cas which fails to bind Crk blocked H2O2-mediated activation of JNK but not ERK1/2 and p38.	bind
26495	7	8126	6	13	NULL	NULL	NULL	Cas	GP	dominant-negative mutant	does not block					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_16_11706_s_193	10766791	4) A dominant negative mutant of Cas which fails to bind Crk blocked H2O2-mediated activation of JNK but not ERK1/2 and p38.	bind
32379	1	8126	7	NULL	NULL	0	NULL	Cas	NULL	dominant negative mutant	does not bind	NULL				Crk	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_16_11706_s_193	10766791	4) A dominant negative mutant of Cas which fails to bind Crk blocked H2O2-mediated activation of JNK but not ERK1/2 and p38.	bind
32380	2	8126	7	NULL	NULL	0	NULL	H2O2	NULL		mediates	NULL				JNK	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_16_11706_s_193	10766791	4) A dominant negative mutant of Cas which fails to bind Crk blocked H2O2-mediated activation of JNK but not ERK1/2 and p38.	bind
32381	3	8126	7	NULL	NULL	0	NULL	H2O2	NULL		mediates	NULL				ERK1/2	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_16_11706_s_193	10766791	4) A dominant negative mutant of Cas which fails to bind Crk blocked H2O2-mediated activation of JNK but not ERK1/2 and p38.	bind
32382	4	8126	7	NULL	NULL	0	NULL	H2O2	NULL		mediates	NULL				p38	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_16_11706_s_193	10766791	4) A dominant negative mutant of Cas which fails to bind Crk blocked H2O2-mediated activation of JNK but not ERK1/2 and p38.	bind
32383	5	8126	7	NULL	NULL	0	NULL	statement 1	NULL		blocks	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_16_11706_s_193	10766791	4) A dominant negative mutant of Cas which fails to bind Crk blocked H2O2-mediated activation of JNK but not ERK1/2 and p38.	bind
32384	6	8126	7	NULL	NULL	0	NULL	statement 1	NULL		does not block	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_16_11706_s_193	10766791	4) A dominant negative mutant of Cas which fails to bind Crk blocked H2O2-mediated activation of JNK but not ERK1/2 and p38.	bind
32385	7	8126	7	NULL	NULL	0	NULL	statement 1	NULL		does not block	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_16_11706_s_193	10766791	4) A dominant negative mutant of Cas which fails to bind Crk blocked H2O2-mediated activation of JNK but not ERK1/2 and p38.	bind
26496	1	8127	6	13	NULL	NULL	NULL	calcineurin/calmodulin	GP	activated	bind					FKBP12/TRPC6 anchor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_428	15994335	4) Activated calcineurin/calmodulin binds to the FKBP12/TRPC6 anchor, either before or after calcineurin dephosphorylates the channels.	bind
26497	2	8127	6	13	NULL	NULL	NULL	calcineurin	GP		dephosphorylates					channels	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_428	15994335	4) Activated calcineurin/calmodulin binds to the FKBP12/TRPC6 anchor, either before or after calcineurin dephosphorylates the channels.	bind
32386	1	8127	7	NULL	NULL	0	NULL	calcineurin/calmodulin	NULL	activated	binds to	NULL				FKBP12/TRPC6 anchor	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_428	15994335	4) Activated calcineurin/calmodulin binds to the FKBP12/TRPC6 anchor, either before or after calcineurin dephosphorylates the channels.	bind
32387	2	8127	7	NULL	NULL	0	NULL	calcineurin	NULL		dephosphorylates	NULL				channels	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_428	15994335	4) Activated calcineurin/calmodulin binds to the FKBP12/TRPC6 anchor, either before or after calcineurin dephosphorylates the channels.	bind
26902	1	8128	6	13	NULL	NULL	NULL	Gbeta	GP		associates with					CCT/TRiC	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_20221_s_336	16702223	4) Addition of Ggamma to previously synthesized Gbeta under conditions allowing dimer formation ( Fig. 1) reduces Gbeta association with CCT/TRiC ( Fig. 10), indicating that Gbeta bound to CCT/TRiC is capable of functionally interacting with Ggamma and that exposure of the complex to Ggamma results in release of Gbeta from CCT/TRiC.	bind
26903	2	8128	6	13	NULL	NULL	NULL	statement 1	GP		interacts with		functionaly			Ggamma	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_20221_s_336	16702223	4) Addition of Ggamma to previously synthesized Gbeta under conditions allowing dimer formation ( Fig. 1) reduces Gbeta association with CCT/TRiC ( Fig. 10), indicating that Gbeta bound to CCT/TRiC is capable of functionally interacting with Ggamma and that exposure of the complex to Ggamma results in release of Gbeta from CCT/TRiC.	bind
26904	4	8128	6	13	NULL	NULL	NULL	Ggamma	GP	addition of	leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_20221_s_336	16702223	4) Addition of Ggamma to previously synthesized Gbeta under conditions allowing dimer formation ( Fig. 1) reduces Gbeta association with CCT/TRiC ( Fig. 10), indicating that Gbeta bound to CCT/TRiC is capable of functionally interacting with Ggamma and that exposure of the complex to Ggamma results in release of Gbeta from CCT/TRiC.	bind
46567	3	8128	6	13	NULL	NULL	NULL	Gbeta	GP		is released from					CCT/TRiC	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_20221_s_336	16702223	4) Addition of Ggamma to previously synthesized Gbeta under conditions allowing dimer formation ( Fig. 1) reduces Gbeta association with CCT/TRiC ( Fig. 10), indicating that Gbeta bound to CCT/TRiC is capable of functionally interacting with Ggamma and that exposure of the complex to Ggamma results in release of Gbeta from CCT/TRiC.	bind
32459	1	8128	7	NULL	NULL	0	NULL	Gbeta	NULL		associate with	NULL				CCT/TRiC	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_29_20221_s_336	16702223	4) Addition of Ggamma to previously synthesized Gbeta under conditions allowing dimer formation ( Fig. 1) reduces Gbeta association with CCT/TRiC ( Fig. 10), indicating that Gbeta bound to CCT/TRiC is capable of functionally interacting with Ggamma and that exposure of the complex to Ggamma results in release of Gbeta from CCT/TRiC.	bind
32460	2	8128	7	NULL	NULL	0	NULL	Gbeta 	NULL		bind	NULL				CCT/TRiC	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_29_20221_s_336	16702223	4) Addition of Ggamma to previously synthesized Gbeta under conditions allowing dimer formation ( Fig. 1) reduces Gbeta association with CCT/TRiC ( Fig. 10), indicating that Gbeta bound to CCT/TRiC is capable of functionally interacting with Ggamma and that exposure of the complex to Ggamma results in release of Gbeta from CCT/TRiC.	bind
32461	3	8128	7	NULL	NULL	0	NULL	statement 2	NULL		interacts with	NULL				Ggamma	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_29_20221_s_336	16702223	4) Addition of Ggamma to previously synthesized Gbeta under conditions allowing dimer formation ( Fig. 1) reduces Gbeta association with CCT/TRiC ( Fig. 10), indicating that Gbeta bound to CCT/TRiC is capable of functionally interacting with Ggamma and that exposure of the complex to Ggamma results in release of Gbeta from CCT/TRiC.	bind
32462	4	8128	7	10	NULL	0	NULL	statement 3	NULL	exposure of	leads to	NULL				statement 7	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_20221_s_336	16702223	4) Addition of Ggamma to previously synthesized Gbeta under conditions allowing dimer formation ( Fig. 1) reduces Gbeta association with CCT/TRiC ( Fig. 10), indicating that Gbeta bound to CCT/TRiC is capable of functionally interacting with Ggamma and that exposure of the complex to Ggamma results in release of Gbeta from CCT/TRiC.	bind
32463	5	8128	7	NULL	NULL	0	NULL	Ggamma	NULL	addition of	allows	NULL				dimer	NULL	formation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_29_20221_s_336	16702223	4) Addition of Ggamma to previously synthesized Gbeta under conditions allowing dimer formation ( Fig. 1) reduces Gbeta association with CCT/TRiC ( Fig. 10), indicating that Gbeta bound to CCT/TRiC is capable of functionally interacting with Ggamma and that exposure of the complex to Ggamma results in release of Gbeta from CCT/TRiC.	bind
32464	6	8128	7	NULL	NULL	0	NULL	statement 5	NULL		reduces	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_29_20221_s_336	16702223	4) Addition of Ggamma to previously synthesized Gbeta under conditions allowing dimer formation ( Fig. 1) reduces Gbeta association with CCT/TRiC ( Fig. 10), indicating that Gbeta bound to CCT/TRiC is capable of functionally interacting with Ggamma and that exposure of the complex to Ggamma results in release of Gbeta from CCT/TRiC.	bind
46568	7	8128	7	10	NULL	0	NULL	Gbeta	NULL		is released from	NULL				CCT/TRiC	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_29_20221_s_336	16702223	4) Addition of Ggamma to previously synthesized Gbeta under conditions allowing dimer formation ( Fig. 1) reduces Gbeta association with CCT/TRiC ( Fig. 10), indicating that Gbeta bound to CCT/TRiC is capable of functionally interacting with Ggamma and that exposure of the complex to Ggamma results in release of Gbeta from CCT/TRiC.	bind
26498	1	8129	6	13	NULL	NULL	NULL	AKT	GP		phosphorylates					p21Cip1	GP				NULL	HER-2/ neu-overexpressing cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_9684_s_176	11779850	4) AKT directly phosphorylates p21Cip1 in HER-2/ neu-overexpressing ( 14) as well as in native human endothelial cells ( 9), and 5) AKT phosphorylation regulates p21Cip1 binding to PCNA ( 9).	bind
26499	2	8129	6	13	NULL	NULL	NULL	AKT	GP		phosphorylates		directly			p21Cip1	GP				NULL	native human endothelial cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_9684_s_176	11779850	4) AKT directly phosphorylates p21Cip1 in HER-2/ neu-overexpressing ( 14) as well as in native human endothelial cells ( 9), and 5) AKT phosphorylation regulates p21Cip1 binding to PCNA ( 9).	bind
26500	3	8129	6	13	NULL	NULL	NULL	p21Cip1	GP		bind					PCNA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_9684_s_176	11779850	4) AKT directly phosphorylates p21Cip1 in HER-2/ neu-overexpressing ( 14) as well as in native human endothelial cells ( 9), and 5) AKT phosphorylation regulates p21Cip1 binding to PCNA ( 9).	bind
26501	4	8129	6	13	NULL	NULL	NULL	AKT	GP	phosphorylation of	regulates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_9684_s_176	11779850	4) AKT directly phosphorylates p21Cip1 in HER-2/ neu-overexpressing ( 14) as well as in native human endothelial cells ( 9), and 5) AKT phosphorylation regulates p21Cip1 binding to PCNA ( 9).	bind
32465	1	8129	7	NULL	NULL	0	NULL	AKT	NULL		phosphorylates	NULL	directly			p21Cip1	NULL				NULL	HER-2/ neu-overexpressing cells	0	NULL	NULL	NULL	gw60_jbiolchem_277_12_9684_s_176	11779850	4) AKT directly phosphorylates p21Cip1 in HER-2/ neu-overexpressing ( 14) as well as in native human endothelial cells ( 9), and 5) AKT phosphorylation regulates p21Cip1 binding to PCNA ( 9).	bind
32466	2	8129	7	NULL	NULL	0	NULL	AKT	NULL		phosphorylates	NULL	directly			p21Cip1	NULL				NULL	native human endothelial cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_9684_s_176	11779850	4) AKT directly phosphorylates p21Cip1 in HER-2/ neu-overexpressing ( 14) as well as in native human endothelial cells ( 9), and 5) AKT phosphorylation regulates p21Cip1 binding to PCNA ( 9).	bind
32467	3	8129	7	NULL	NULL	0	NULL	 p21Cip1	NULL		bind	NULL				PCNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_9684_s_176	11779850	4) AKT directly phosphorylates p21Cip1 in HER-2/ neu-overexpressing ( 14) as well as in native human endothelial cells ( 9), and 5) AKT phosphorylation regulates p21Cip1 binding to PCNA ( 9).	bind
32468	4	8129	7	NULL	NULL	0	NULL	AKT	NULL	phosphorylation of	regulates	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_9684_s_176	11779850	4) AKT directly phosphorylates p21Cip1 in HER-2/ neu-overexpressing ( 14) as well as in native human endothelial cells ( 9), and 5) AKT phosphorylation regulates p21Cip1 binding to PCNA ( 9).	bind
26502	1	8130	6	13	NULL	NULL	NULL	actin	GP		bind								C domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_15_10589_s_311	16403731	4) Binding of actin and the Arp2/3 complex to the C domain is mutually exclusive.	bind
26503	2	8130	6	13	NULL	NULL	NULL	Arp2/3 complex	GP		bind								C domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_15_10589_s_311	16403731	4) Binding of actin and the Arp2/3 complex to the C domain is mutually exclusive.	bind
26504	3	8130	6	13	NULL	NULL	NULL	statement 1	Process		is independent of					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_15_10589_s_311	16403731	4) Binding of actin and the Arp2/3 complex to the C domain is mutually exclusive.	bind
32469	1	8130	7	NULL	NULL	0	NULL	actin	NULL		bind	NULL					NULL		C domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_15_10589_s_311	16403731	4) Binding of actin and the Arp2/3 complex to the C domain is mutually exclusive.	bind
32470	2	8130	7	NULL	NULL	0	NULL	Arp2/3 complex 	NULL		bind	NULL					NULL		C domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_15_10589_s_311	16403731	4) Binding of actin and the Arp2/3 complex to the C domain is mutually exclusive.	bind
32471	3	8130	7	NULL	NULL	0	NULL	statement 1	NULL		is mutually exclusive to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_15_10589_s_311	16403731	4) Binding of actin and the Arp2/3 complex to the C domain is mutually exclusive.	bind
26505	1	8131	6	13	NULL	NULL	NULL	Ggamma	GP		bind					Gbeta	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_31_22261_s_358	16717095	4) Ggamma binds Gbeta forming a PhLP.	bind
26506	2	8131	6	13	NULL	NULL	NULL	statement 1	GP		forms a					PhLP	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_31_22261_s_358	16717095	4) Ggamma binds Gbeta forming a PhLP.	bind
32472	1	8131	7	NULL	NULL	0	NULL	Ggamma	NULL		binds	NULL				Gbeta	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_22261_s_358	16717095	4) Ggamma binds Gbeta forming a PhLP.	bind
32473	2	8131	7	NULL	NULL	0	NULL	statement 1	NULL		forms	NULL				PhLP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_22261_s_358	16717095	4) Ggamma binds Gbeta forming a PhLP.	bind
26507	1	8132	6	13	NULL	NULL	NULL	Grb2	GP		bind					TrkA	GP				NULL	yeast	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18225_s_237	10748052	4) Grb2 binding to TrkA in yeast is independent of Tyr499/Tyr679/Tyr794 but requires the activation loop tyrosines Tyr683/Tyr684.	bind
26508	2	8132	6	13	NULL	NULL	NULL	statement 1	Process		is independent of								Tyr499/Tyr679/Tyr794		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18225_s_237	10748052	4) Grb2 binding to TrkA in yeast is independent of Tyr499/Tyr679/Tyr794 but requires the activation loop tyrosines Tyr683/Tyr684.	bind
26509	3	8132	6	13	NULL	NULL	NULL	statement 1	Process		requires					activation loop	GP		tyrosines Tyr683/Tyr684		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18225_s_237	10748052	4) Grb2 binding to TrkA in yeast is independent of Tyr499/Tyr679/Tyr794 but requires the activation loop tyrosines Tyr683/Tyr684.	bind
32474	1	8132	7	NULL	NULL	0	NULL	Grb2	NULL		bind	NULL				 TrkA	NULL				NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_275_24_18225_s_237	10748052	4) Grb2 binding to TrkA in yeast is independent of Tyr499/Tyr679/Tyr794 but requires the activation loop tyrosines Tyr683/Tyr684.	bind
32475	2	8132	7	10	NULL	0	NULL	statement 1			is independent of								Tyr499/Tyr679/Tyr794		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18225_s_237	10748052	4) Grb2 binding to TrkA in yeast is independent of Tyr499/Tyr679/Tyr794 but requires the activation loop tyrosines Tyr683/Tyr684.	bind
32476	3	8132	7	NULL	NULL	0	NULL	statement 2	NULL		requires	NULL				activation loop	NULL		tyrosines Tyr683/Tyr684		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_24_18225_s_237	10748052	4) Grb2 binding to TrkA in yeast is independent of Tyr499/Tyr679/Tyr794 but requires the activation loop tyrosines Tyr683/Tyr684.	bind
26510	1	8133	6	13	NULL	NULL	NULL	FKBP12	GP		bind					TRPC6A/B channels	GP	site immediately adjacent to	phosphoserine (768/714)		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_349	15994335	4) Immunophilin FKBP12 binds to the TRPC6A/B channels at a site immediately adjacent  to the phosphoserine (768/714), creating a site for the binding of calcineurin/calmodulin.	bind
26511	2	8133	6	13	NULL	NULL	NULL	statement 1	Process		creates					calcineurin/calmodulin	GP	binding site for			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_349	15994335	4) Immunophilin FKBP12 binds to the TRPC6A/B channels at a site immediately adjacent  to the phosphoserine (768/714), creating a site for the binding of calcineurin/calmodulin.	bind
46569	3	8133	6	13	NULL	NULL	NULL	FKBP12	GP		is a type of					immunophilin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_349	15994335	4) Immunophilin FKBP12 binds to the TRPC6A/B channels at a site immediately adjacent  to the phosphoserine (768/714), creating a site for the binding of calcineurin/calmodulin.	bind
32477	1	8133	7	10	NULL	0	NULL	FKBP12 	NULL		binds to	NULL				TRPC6A/B channels	NULL	site adjacent to	phosphoserine (768/714)		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_349	15994335	4) Immunophilin FKBP12 binds to the TRPC6A/B channels at a site immediately adjacent  to the phosphoserine (768/714), creating a site for the binding of calcineurin/calmodulin.	bind
32478	2	8133	7	10	NULL	0	NULL	statement 1	NULL		create	NULL				calcineurin/calmodulin	NULL	binding site for			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_349	15994335	4) Immunophilin FKBP12 binds to the TRPC6A/B channels at a site immediately adjacent  to the phosphoserine (768/714), creating a site for the binding of calcineurin/calmodulin.	bind
46570	3	8133	7	10	NULL	0	NULL	FKBP12	NULL		is a type of	NULL				immunophilin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_36_32035_s_349	15994335	4) Immunophilin FKBP12 binds to the TRPC6A/B channels at a site immediately adjacent  to the phosphoserine (768/714), creating a site for the binding of calcineurin/calmodulin.	bind
26512	1	8134	6	13	NULL	NULL	NULL	Phosphatases	GP		dephosphorylate					phospholamban	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_52_33561_s_138	8969222	4) Phosphatases that dephosphorylate phospholamban could be inhibited by a PKA-dependent mechanism.	bind
26513	2	8134	6	13	NULL	NULL	NULL	statement 1	Process		is inhibited by					PKA-dependent mechanism	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_52_33561_s_138	8969222	4) Phosphatases that dephosphorylate phospholamban could be inhibited by a PKA-dependent mechanism.	bind
32479	1	8134	7	NULL	NULL	0	NULL	Phosphatases	NULL		dephosphorylate	NULL				phospholamban	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_52_33561_s_138	8969222	4) Phosphatases that dephosphorylate phospholamban could be inhibited by a PKA-dependent mechanism.	bind
32480	2	8134	7	NULL	NULL	0	NULL	PKA-dependent mechanism	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_52_33561_s_138	8969222	4) Phosphatases that dephosphorylate phospholamban could be inhibited by a PKA-dependent mechanism.	bind
26514	1	8135	6	13	NULL	NULL	NULL	gp180	GP	purified	bind					T cells	Cell	peripheral blood			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12786_s_10	9139738	4) Purified gp180 can bind to peripheral blood T cells and activate p56 lck. 5) gp180 can activate p56 lck in 3G8 (a murine T cell hybridoma transfected with human CD8alpha cDNA) but not in 3G4 (CD4 transfectant), suggesting that gp180 binds to CD8.	bind
26515	2	8135	6	13	NULL	NULL	NULL	statement 1	Process		activate					p56 lck	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12786_s_10	9139738	4) Purified gp180 can bind to peripheral blood T cells and activate p56 lck. 5) gp180 can activate p56 lck in 3G8 (a murine T cell hybridoma transfected with human CD8alpha cDNA) but not in 3G4 (CD4 transfectant), suggesting that gp180 binds to CD8.	bind
26516	3	8135	6	13	NULL	NULL	NULL	gp180	GP		bind					CD8	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12786_s_10	9139738	4) Purified gp180 can bind to peripheral blood T cells and activate p56 lck. 5) gp180 can activate p56 lck in 3G8 (a murine T cell hybridoma transfected with human CD8alpha cDNA) but not in 3G4 (CD4 transfectant), suggesting that gp180 binds to CD8.	bind
26517	4	8135	6	13	NULL	NULL	NULL	gp180	GP		activate					p56 lck	GP				NULL	3G8	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12786_s_10	9139738	4) Purified gp180 can bind to peripheral blood T cells and activate p56 lck. 5) gp180 can activate p56 lck in 3G8 (a murine T cell hybridoma transfected with human CD8alpha cDNA) but not in 3G4 (CD4 transfectant), suggesting that gp180 binds to CD8.	bind
26518	5	8135	6	13	NULL	NULL	NULL	T cell hybridoma	Cell	murine	transfected with					CD8alpha cDNA	NucleicAcid	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12786_s_10	9139738	4) Purified gp180 can bind to peripheral blood T cells and activate p56 lck. 5) gp180 can activate p56 lck in 3G8 (a murine T cell hybridoma transfected with human CD8alpha cDNA) but not in 3G4 (CD4 transfectant), suggesting that gp180 binds to CD8.	bind
26519	6	8135	6	13	NULL	NULL	NULL	3G8	Cell		is					statement 5	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12786_s_10	9139738	4) Purified gp180 can bind to peripheral blood T cells and activate p56 lck. 5) gp180 can activate p56 lck in 3G8 (a murine T cell hybridoma transfected with human CD8alpha cDNA) but not in 3G4 (CD4 transfectant), suggesting that gp180 binds to CD8.	bind
26520	7	8135	6	13	NULL	NULL	NULL	3G4	Cell		is a type of					CD4 transfectant	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12786_s_10	9139738	4) Purified gp180 can bind to peripheral blood T cells and activate p56 lck. 5) gp180 can activate p56 lck in 3G8 (a murine T cell hybridoma transfected with human CD8alpha cDNA) but not in 3G4 (CD4 transfectant), suggesting that gp180 binds to CD8.	bind
26521	8	8135	6	13	NULL	NULL	NULL	gp180	GP		does not activate					p56 lck	GP				NULL	3G4	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12786_s_10	9139738	4) Purified gp180 can bind to peripheral blood T cells and activate p56 lck. 5) gp180 can activate p56 lck in 3G8 (a murine T cell hybridoma transfected with human CD8alpha cDNA) but not in 3G4 (CD4 transfectant), suggesting that gp180 binds to CD8.	bind
26522	9	8135	6	13	NULL	NULL	NULL	statement 2	Process		suggests					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12786_s_10	9139738	4) Purified gp180 can bind to peripheral blood T cells and activate p56 lck. 5) gp180 can activate p56 lck in 3G8 (a murine T cell hybridoma transfected with human CD8alpha cDNA) but not in 3G4 (CD4 transfectant), suggesting that gp180 binds to CD8.	bind
32481	1	8135	7	10	NULL	0	NULL	gp180		purified	bind					T cells		 peripheral blood			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12786_s_10	9139738	4) Purified gp180 can bind to peripheral blood T cells and activate p56 lck. 5) gp180 can activate p56 lck in 3G8 (a murine T cell hybridoma transfected with human CD8alpha cDNA) but not in 3G4 (CD4 transfectant), suggesting that gp180 binds to CD8.	bind
32482	2	8135	7	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				p56 lck	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_19_12786_s_10	9139738	4) Purified gp180 can bind to peripheral blood T cells and activate p56 lck. 5) gp180 can activate p56 lck in 3G8 (a murine T cell hybridoma transfected with human CD8alpha cDNA) but not in 3G4 (CD4 transfectant), suggesting that gp180 binds to CD8.	bind
32483	3	8135	7	NULL	NULL	0	NULL	gp180	NULL		activate	NULL				p56 lck	NULL				NULL	3G8 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12786_s_10	9139738	4) Purified gp180 can bind to peripheral blood T cells and activate p56 lck. 5) gp180 can activate p56 lck in 3G8 (a murine T cell hybridoma transfected with human CD8alpha cDNA) but not in 3G4 (CD4 transfectant), suggesting that gp180 binds to CD8.	bind
32484	4	8135	7	NULL	NULL	0	NULL	gp 180	NULL		does not activate	NULL				p56 lck	NULL				NULL	3G4 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12786_s_10	9139738	4) Purified gp180 can bind to peripheral blood T cells and activate p56 lck. 5) gp180 can activate p56 lck in 3G8 (a murine T cell hybridoma transfected with human CD8alpha cDNA) but not in 3G4 (CD4 transfectant), suggesting that gp180 binds to CD8.	bind
32485	5	8135	7	NULL	NULL	0	NULL	gp180	NULL		binds to	NULL				CD8	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_19_12786_s_10	9139738	4) Purified gp180 can bind to peripheral blood T cells and activate p56 lck. 5) gp180 can activate p56 lck in 3G8 (a murine T cell hybridoma transfected with human CD8alpha cDNA) but not in 3G4 (CD4 transfectant), suggesting that gp180 binds to CD8.	bind
32486	6	8135	7	10	NULL	0	NULL	 3G8			is					statement 8					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12786_s_10	9139738	4) Purified gp180 can bind to peripheral blood T cells and activate p56 lck. 5) gp180 can activate p56 lck in 3G8 (a murine T cell hybridoma transfected with human CD8alpha cDNA) but not in 3G4 (CD4 transfectant), suggesting that gp180 binds to CD8.	bind
32487	7	8135	7	NULL	NULL	0	NULL	3G4	NULL		is a type of	NULL				CD4 transfectant	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_19_12786_s_10	9139738	4) Purified gp180 can bind to peripheral blood T cells and activate p56 lck. 5) gp180 can activate p56 lck in 3G8 (a murine T cell hybridoma transfected with human CD8alpha cDNA) but not in 3G4 (CD4 transfectant), suggesting that gp180 binds to CD8.	bind
46571	8	8135	7	10	NULL	0	NULL	T cell hybridoma	NULL	murine	is transfected with	NULL				CD8alpha cDNA	NULL	human			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_19_12786_s_10	9139738	4) Purified gp180 can bind to peripheral blood T cells and activate p56 lck. 5) gp180 can activate p56 lck in 3G8 (a murine T cell hybridoma transfected with human CD8alpha cDNA) but not in 3G4 (CD4 transfectant), suggesting that gp180 binds to CD8.	bind
26523	1	8136	6	13	NULL	NULL	NULL	MyoD	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_31_19140_s_318	9235903	4) S5a greatly enhanced the DNA binding of MyoD and E12 homodimers while having a less pronounced effect on MyoD-E12 heterodimers.	bind
26524	2	8136	6	13	NULL	NULL	NULL	E12 homodimers	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_31_19140_s_318	9235903	4) S5a greatly enhanced the DNA binding of MyoD and E12 homodimers while having a less pronounced effect on MyoD-E12 heterodimers.	bind
26525	3	8136	6	13	NULL	NULL	NULL	S5a	GP		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_31_19140_s_318	9235903	4) S5a greatly enhanced the DNA binding of MyoD and E12 homodimers while having a less pronounced effect on MyoD-E12 heterodimers.	bind
26526	4	8136	6	13	NULL	NULL	NULL	S5a	GP		enhance					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_31_19140_s_318	9235903	4) S5a greatly enhanced the DNA binding of MyoD and E12 homodimers while having a less pronounced effect on MyoD-E12 heterodimers.	bind
26527	5	8136	6	13	NULL	NULL	NULL	S5a	GP		has less effect on					MyoD-E12 heterodimers	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_31_19140_s_318	9235903	4) S5a greatly enhanced the DNA binding of MyoD and E12 homodimers while having a less pronounced effect on MyoD-E12 heterodimers.	bind
32488	1	8136	7	NULL	NULL	0	NULL	MyoD	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_31_19140_s_318	9235903	4) S5a greatly enhanced the DNA binding of MyoD and E12 homodimers while having a less pronounced effect on MyoD-E12 heterodimers.	bind
32489	2	8136	7	NULL	NULL	0	NULL	E12 homodimers	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_31_19140_s_318	9235903	4) S5a greatly enhanced the DNA binding of MyoD and E12 homodimers while having a less pronounced effect on MyoD-E12 heterodimers.	bind
32490	3	8136	7	NULL	NULL	0	NULL	S5a	NULL		enhance	NULL	greatly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_31_19140_s_318	9235903	4) S5a greatly enhanced the DNA binding of MyoD and E12 homodimers while having a less pronounced effect on MyoD-E12 heterodimers.	bind
32491	4	8136	7	NULL	NULL	0	NULL	S5a	NULL		enhance	NULL	greatly			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_31_19140_s_318	9235903	4) S5a greatly enhanced the DNA binding of MyoD and E12 homodimers while having a less pronounced effect on MyoD-E12 heterodimers.	bind
32492	5	8136	7	NULL	NULL	0	NULL	S5a	NULL		less effect on	NULL				MyoD-E12 heterodimers	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_31_19140_s_318	9235903	4) S5a greatly enhanced the DNA binding of MyoD and E12 homodimers while having a less pronounced effect on MyoD-E12 heterodimers.	bind
26528	1	8137	6	13	NULL	NULL	NULL	HO-1	GP		bind			amino acids 0-117		HO-2	GP				NULL	brain homogenates	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_50999_s_215	14514669	4) The addition of a fragment necessary for HO-1 binding to HO-2 (amino acids 0-117 of HO-1) to the brain homogenates significantly reduced total HO activity of the complex (decreased to 0.23  plus-or-minus  0.03  versus 0.36  plus-or-minus  0.04 nmol CO/mg protein/h in samples incubated with 0-117 fragment  versus brain homogenates alone).	bind
32493	1	8137	7	10	NULL	0	NULL	 HO-1 			bind			amino acids 0-117		HO-2					NULL	brain homogenates	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_50999_s_215	14514669	4) The addition of a fragment necessary for HO-1 binding to HO-2 (amino acids 0-117 of HO-1) to the brain homogenates significantly reduced total HO activity of the complex (decreased to 0.23  plus-or-minus  0.03  versus 0.36  plus-or-minus  0.04 nmol CO/mg protein/h in samples incubated with 0-117 fragment  versus brain homogenates alone).	bind
26529	1	8138	6	13	NULL	NULL	NULL	p67 phox	GP		bind					p22 phox peptides	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_277_10_11733522_s_12	11733522	4) The binding affinity of p67(phox) for p22(phox) peptides is lower than  that of p47(phox).	bind
26530	2	8138	6	13	NULL	NULL	NULL	p47 phox	GP		bind					p22 phox peptides	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_277_10_11733522_s_12	11733522	4) The binding affinity of p67(phox) for p22(phox) peptides is lower than  that of p47(phox).	bind
26531	3	8138	6	13	NULL	NULL	NULL	statement 1	Process	affinity of	is lower than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_277_10_11733522_s_12	11733522	4) The binding affinity of p67(phox) for p22(phox) peptides is lower than  that of p47(phox).	bind
32496	1	8138	7	NULL	NULL	0	NULL	 p67(phox)	NULL		bind	NULL				p22(phox) peptides	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_277_10_11733522_s_12	11733522	4) The binding affinity of p67(phox) for p22(phox) peptides is lower than  that of p47(phox).	bind
32497	2	8138	7	NULL	NULL	0	NULL	 p67(phox)	NULL		bind	NULL				p47(phox)	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_277_10_11733522_s_12	11733522	4) The binding affinity of p67(phox) for p22(phox) peptides is lower than  that of p47(phox).	bind
32498	3	8138	7	10	NULL	0	NULL	statement 1	NULL	affinity of	is lower than	NULL				statement 2	NULL	affinity of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_277_10_11733522_s_12	11733522	4) The binding affinity of p67(phox) for p22(phox) peptides is lower than  that of p47(phox).	bind
26533	1	8139	6	13	NULL	NULL	NULL	InsP(3)R1 splice variant	GP		bind			SII(+) coupling domain		AKAP9	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_j-biol-chem_279_18_14982933_s_15	14982933	4) The InsP(3)R association with AKAP9 is specific for  type 1 InsP(3)R. 5) Both the SII(+) and the SII(-) coupling domain splice  variants of InsP(3)R1 bind to AKAP9.	bind
26534	2	8139	6	13	NULL	NULL	NULL	InsP(3)R1 splice variant	GP		bind			SII(-) coupling domain		AKAP9	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_j-biol-chem_279_18_14982933_s_15	14982933	4) The InsP(3)R association with AKAP9 is specific for  type 1 InsP(3)R. 5) Both the SII(+) and the SII(-) coupling domain splice  variants of InsP(3)R1 bind to AKAP9.	bind
55932	3	8139	6	13	NULL	NULL	NULL	InsP(3)R	GP		associate with					AKAP9	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_j-biol-chem_279_18_14982933_s_15	14982933	4) The InsP(3)R association with AKAP9 is specific for  type 1 InsP(3)R. 5) Both the SII(+) and the SII(-) coupling domain splice  variants of InsP(3)R1 bind to AKAP9.	bind
55933	4	8139	6	13	NULL	NULL	NULL	statement 3	Process		is specific for					type 1 InsP(3)R	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_j-biol-chem_279_18_14982933_s_15	14982933	4) The InsP(3)R association with AKAP9 is specific for  type 1 InsP(3)R. 5) Both the SII(+) and the SII(-) coupling domain splice  variants of InsP(3)R1 bind to AKAP9.	bind
32499	1	8139	7	NULL	NULL	0	NULL	 InsP(3)R	NULL		associate with	NULL				AKAP9	NULL				NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-biol-chem_279_18_14982933_s_15	14982933	4) The InsP(3)R association with AKAP9 is specific for  type 1 InsP(3)R. 5) Both the SII(+) and the SII(-) coupling domain splice  variants of InsP(3)R1 bind to AKAP9.	bind
32500	2	8139	7	NULL	NULL	0	NULL	statement 1	NULL		is specific for	NULL				type 1 InsP(3)R	NULL				NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-biol-chem_279_18_14982933_s_15	14982933	4) The InsP(3)R association with AKAP9 is specific for  type 1 InsP(3)R. 5) Both the SII(+) and the SII(-) coupling domain splice  variants of InsP(3)R1 bind to AKAP9.	bind
32501	3	8139	7	10	NULL	0	NULL	 InsP(3)R1 splice variant			binds to			 SII(+) coupling domain		AKAP9					NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_j-biol-chem_279_18_14982933_s_15	14982933	4) The InsP(3)R association with AKAP9 is specific for  type 1 InsP(3)R. 5) Both the SII(+) and the SII(-) coupling domain splice  variants of InsP(3)R1 bind to AKAP9.	bind
32502	4	8139	7	10	NULL	0	NULL	InsP(3)R1 splice variant			binds to			SII(-) coupling domain		AKAP9					NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_j-biol-chem_279_18_14982933_s_15	14982933	4) The InsP(3)R association with AKAP9 is specific for  type 1 InsP(3)R. 5) Both the SII(+) and the SII(-) coupling domain splice  variants of InsP(3)R1 bind to AKAP9.	bind
26535	1	8140	6	13	NULL	NULL	NULL	nNOS	GP		contains an			FMN-binding subdomain of the reductase domain		autoinhibitory loop	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_19_16888_s_215	11884406	4) There is an autoinhibitory loop in the FMN-binding subdomain of the reductase domain in nNOS and eNOS not present in iNOS ( 18,  27,  34-36).	bind
26536	2	8140	6	13	NULL	NULL	NULL	eNOS	GP		contains an			FMN-binding subdomain of the reductase domain		autoinhibitory loop	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_19_16888_s_215	11884406	4) There is an autoinhibitory loop in the FMN-binding subdomain of the reductase domain in nNOS and eNOS not present in iNOS ( 18,  27,  34-36).	bind
26537	3	8140	6	13	NULL	NULL	NULL	iNOS	GP		does not contain			FMN-binding subdomain of the reductase domain		autoinhibitory loop	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_19_16888_s_215	11884406	4) There is an autoinhibitory loop in the FMN-binding subdomain of the reductase domain in nNOS and eNOS not present in iNOS ( 18,  27,  34-36).	bind
32503	1	8140	7	10	NULL	0	NULL	autoinhibitory loop			is present in					nNOS			\tFMN-binding subdomain of the reductase domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_19_16888_s_215	11884406	4) There is an autoinhibitory loop in the FMN-binding subdomain of the reductase domain in nNOS and eNOS not present in iNOS ( 18,  27,  34-36).	bind
32504	2	8140	7	10	NULL	0	NULL	autoinhibitory loop			is present in					eNOS			\tFMN-binding subdomain of the reductase domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_19_16888_s_215	11884406	4) There is an autoinhibitory loop in the FMN-binding subdomain of the reductase domain in nNOS and eNOS not present in iNOS ( 18,  27,  34-36).	bind
32505	3	8140	7	10	NULL	0	NULL	autoinhibitory loop			is not present in					iNOS			\tFMN-binding subdomain of the reductase domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_19_16888_s_215	11884406	4) There is an autoinhibitory loop in the FMN-binding subdomain of the reductase domain in nNOS and eNOS not present in iNOS ( 18,  27,  34-36).	bind
26538	1	8141	6	13	NULL	NULL	NULL	Type 1 fimbriated E.coli	Organism		bind					THP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_13_9924_s_191	11134021	4) Type 1 fimbriated  E. coli binds equally well to THP and to bovine RNase B, the latter of which is known to possess a single high-mannose chain.	bind
26539	2	8141	6	13	NULL	NULL	NULL	Type 1 fimbriated E.coli	Organism		bind					RNase B	GP	bovine			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_13_9924_s_191	11134021	4) Type 1 fimbriated  E. coli binds equally well to THP and to bovine RNase B, the latter of which is known to possess a single high-mannose chain.	bind
26540	3	8141	6	13	NULL	NULL	NULL	statement 1	Process	affinity of	is equal to					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_13_9924_s_191	11134021	4) Type 1 fimbriated  E. coli binds equally well to THP and to bovine RNase B, the latter of which is known to possess a single high-mannose chain.	bind
26541	4	8141	6	13	NULL	NULL	NULL	RNase B	GP	bovine	possess								high-mannose chain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_13_9924_s_191	11134021	4) Type 1 fimbriated  E. coli binds equally well to THP and to bovine RNase B, the latter of which is known to possess a single high-mannose chain.	bind
32506	1	8141	7	NULL	NULL	0	NULL	Type 1 fimbriated E. coli 	NULL		binds	NULL				THP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_13_9924_s_191	11134021	4) Type 1 fimbriated  E. coli binds equally well to THP and to bovine RNase B, the latter of which is known to possess a single high-mannose chain.	bind
32507	2	8141	7	NULL	NULL	0	NULL	Type 1 fimbriated E. coli 	NULL		binds	NULL				RNase B	NULL	bovine			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_13_9924_s_191	11134021	4) Type 1 fimbriated  E. coli binds equally well to THP and to bovine RNase B, the latter of which is known to possess a single high-mannose chain.	bind
32508	3	8141	7	10	NULL	0	NULL	RNase B			possess								high-mannose chain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_13_9924_s_191	11134021	4) Type 1 fimbriated  E. coli binds equally well to THP and to bovine RNase B, the latter of which is known to possess a single high-mannose chain.	bind
55934	4	8141	7	10	NULL	0	NULL	statement 1		affinity of	is equal to					statement 2		affinity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_13_9924_s_191	11134021	4) Type 1 fimbriated  E. coli binds equally well to THP and to bovine RNase B, the latter of which is known to possess a single high-mannose chain.	bind
26542	1	8142	6	13	NULL	NULL	NULL	casein kinase II	GP		phosphorylates					IkappaBalpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29840_s_41	10882738	4) When compared with its unphosphorylated form, casein kinase II-phosphorylated IkappaBalpha binds the p50/p65 heterodimer and the p65 homodimer with 33- and 9-fold higher binding affinity, respectively.	bind
26543	2	8142	6	13	NULL	NULL	NULL	IkappaBalpha	GP	unphosphorylated	bind					p50/p65 heterodimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29840_s_41	10882738	4) When compared with its unphosphorylated form, casein kinase II-phosphorylated IkappaBalpha binds the p50/p65 heterodimer and the p65 homodimer with 33- and 9-fold higher binding affinity, respectively.	bind
26544	3	8142	6	13	NULL	NULL	NULL	IkappaBalpha	GP	unphosphorylated	bind					p65 homodimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29840_s_41	10882738	4) When compared with its unphosphorylated form, casein kinase II-phosphorylated IkappaBalpha binds the p50/p65 heterodimer and the p65 homodimer with 33- and 9-fold higher binding affinity, respectively.	bind
26608	4	8142	6	13	NULL	NULL	NULL	IkappaBalpha	GP	phosphorylated	bind					p50/p65 heterodimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29840_s_41	10882738	4) When compared with its unphosphorylated form, casein kinase II-phosphorylated IkappaBalpha binds the p50/p65 heterodimer and the p65 homodimer with 33- and 9-fold higher binding affinity, respectively.	bind
26609	5	8142	6	13	NULL	NULL	NULL	IkappaBalpha	GP	phosphorylated	bind					p65 homodimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29840_s_41	10882738	4) When compared with its unphosphorylated form, casein kinase II-phosphorylated IkappaBalpha binds the p50/p65 heterodimer and the p65 homodimer with 33- and 9-fold higher binding affinity, respectively.	bind
26610	6	8142	6	13	NULL	NULL	NULL	statement 4	Process	affinity of	is higher than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29840_s_41	10882738	4) When compared with its unphosphorylated form, casein kinase II-phosphorylated IkappaBalpha binds the p50/p65 heterodimer and the p65 homodimer with 33- and 9-fold higher binding affinity, respectively.	bind
26611	7	8142	6	13	NULL	NULL	NULL	statement 5	Process	affinity of	is higher than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29840_s_41	10882738	4) When compared with its unphosphorylated form, casein kinase II-phosphorylated IkappaBalpha binds the p50/p65 heterodimer and the p65 homodimer with 33- and 9-fold higher binding affinity, respectively.	bind
32509	1	8142	7	NULL	NULL	0	NULL	casein kinase II	NULL		phosphorylates	NULL				IkappaBalpha	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29840_s_41	10882738	4) When compared with its unphosphorylated form, casein kinase II-phosphorylated IkappaBalpha binds the p50/p65 heterodimer and the p65 homodimer with 33- and 9-fold higher binding affinity, respectively.	bind
32510	2	8142	7	NULL	NULL	0	NULL	statement 1	NULL		binds	NULL				p50/p65 heterodimer	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29840_s_41	10882738	4) When compared with its unphosphorylated form, casein kinase II-phosphorylated IkappaBalpha binds the p50/p65 heterodimer and the p65 homodimer with 33- and 9-fold higher binding affinity, respectively.	bind
32511	3	8142	7	NULL	NULL	0	NULL	statement 1	NULL		binds	NULL				p65 homodimer 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29840_s_41	10882738	4) When compared with its unphosphorylated form, casein kinase II-phosphorylated IkappaBalpha binds the p50/p65 heterodimer and the p65 homodimer with 33- and 9-fold higher binding affinity, respectively.	bind
32512	4	8142	7	NULL	NULL	0	NULL	IkappaBalpha	NULL	unphosphorylated	binds	NULL				p50/p65 heterodimer	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29840_s_41	10882738	4) When compared with its unphosphorylated form, casein kinase II-phosphorylated IkappaBalpha binds the p50/p65 heterodimer and the p65 homodimer with 33- and 9-fold higher binding affinity, respectively.	bind
32513	5	8142	7	NULL	NULL	0	NULL	IkappaBalpha	NULL	unphosphorylated	binds	NULL				p65 homodimer	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29840_s_41	10882738	4) When compared with its unphosphorylated form, casein kinase II-phosphorylated IkappaBalpha binds the p50/p65 heterodimer and the p65 homodimer with 33- and 9-fold higher binding affinity, respectively.	bind
32514	6	8142	7	10	NULL	0	NULL	statement 2	NULL	affinity of	is higher than	NULL				statement 4	NULL	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29840_s_41	10882738	4) When compared with its unphosphorylated form, casein kinase II-phosphorylated IkappaBalpha binds the p50/p65 heterodimer and the p65 homodimer with 33- and 9-fold higher binding affinity, respectively.	bind
32515	7	8142	7	10	NULL	0	NULL	statement 3	NULL	affinity of	is higher than	NULL				statement 5	NULL	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29840_s_41	10882738	4) When compared with its unphosphorylated form, casein kinase II-phosphorylated IkappaBalpha binds the p50/p65 heterodimer and the p65 homodimer with 33- and 9-fold higher binding affinity, respectively.	bind
26612	1	8143	6	13	NULL	NULL	NULL	SHP-2	GP		bind					IRS-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1081_s_104	12117720	4, 23 SHP2 also binds to IRS-1, 7 as do other adapter proteins.	bind
26613	2	8143	6	13	NULL	NULL	NULL	Adaptor proteins	GP		bind					IRS-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1081_s_104	12117720	4, 23 SHP2 also binds to IRS-1, 7 as do other adapter proteins.	bind
32516	1	8143	7	NULL	NULL	0	NULL	 SHP2	NULL		binds to	NULL				IRS-1, 7	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1081_s_104	12117720	4, 23 SHP2 also binds to IRS-1, 7 as do other adapter proteins.	bind
32517	2	8143	7	NULL	NULL	0	NULL	adapter proteins	NULL		binds to	NULL				IRS-1, 7	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1081_s_104	12117720	4, 23 SHP2 also binds to IRS-1, 7 as do other adapter proteins.	bind
26614	1	8144	6	13	NULL	NULL	NULL	ASK1	GP		bind			C-terminal domain					TRAF domain		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_21	12089063	4, 5, 9, 10 The C-terminal domain of ASK1 binds to the TRAF-domain and this association is required for ASK1 activation by cytokines.	bind
26615	2	8144	6	13	NULL	NULL	NULL	cytokines	GP		activate					ASK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_21	12089063	4, 5, 9, 10 The C-terminal domain of ASK1 binds to the TRAF-domain and this association is required for ASK1 activation by cytokines.	bind
26616	3	8144	6	13	NULL	NULL	NULL	statement 1	Process		is required for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_21	12089063	4, 5, 9, 10 The C-terminal domain of ASK1 binds to the TRAF-domain and this association is required for ASK1 activation by cytokines.	bind
32518	1	8144	7	NULL	NULL	0	NULL	ASK1	NULL		binds to	NULL		C-terminal domain 			NULL		TRAF-domain		NULL		0	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_21	12089063	4, 5, 9, 10 The C-terminal domain of ASK1 binds to the TRAF-domain and this association is required for ASK1 activation by cytokines.	bind
32519	2	8144	7	NULL	NULL	0	NULL	cytokines	NULL		activates	NULL				ASK1 	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_21	12089063	4, 5, 9, 10 The C-terminal domain of ASK1 binds to the TRAF-domain and this association is required for ASK1 activation by cytokines.	bind
32520	3	8144	7	NULL	NULL	0	NULL	statement 1	NULL		is required for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_12_1259_s_21	12089063	4, 5, 9, 10 The C-terminal domain of ASK1 binds to the TRAF-domain and this association is required for ASK1 activation by cytokines.	bind
26617	1	8145	6	13	NULL	NULL	NULL	HDL	GP		bind					ECM	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_170	12089072	4, 8 Therefore, this further supports the idea that apo E is the principal determinant of HDL binding to the ECM via its binding to matrix proteoglycans.	bind
26618	2	8145	6	13	NULL	NULL	NULL	apoE	GP		bind					matrix proteoglycans	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_170	12089072	4, 8 Therefore, this further supports the idea that apo E is the principal determinant of HDL binding to the ECM via its binding to matrix proteoglycans.	bind
26619	3	8145	6	13	NULL	NULL	NULL	statement 2	Process		is the determinant		principal			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_170	12089072	4, 8 Therefore, this further supports the idea that apo E is the principal determinant of HDL binding to the ECM via its binding to matrix proteoglycans.	bind
32521	1	8145	7	NULL	NULL	0	NULL	HDL	NULL		binds	NULL				ECM	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_170	12089072	4, 8 Therefore, this further supports the idea that apo E is the principal determinant of HDL binding to the ECM via its binding to matrix proteoglycans.	bind
32522	2	8145	7	NULL	NULL	0	NULL	apo E	NULL		binds	NULL				matrix proteoglycans	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_170	12089072	4, 8 Therefore, this further supports the idea that apo E is the principal determinant of HDL binding to the ECM via its binding to matrix proteoglycans.	bind
32523	3	8145	7	10	NULL	0	NULL	statement 2	NULL		is the determinant of	NULL	principal			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_12_1333_s_170	12089072	4, 8 Therefore, this further supports the idea that apo E is the principal determinant of HDL binding to the ECM via its binding to matrix proteoglycans.	bind
26620	1	8146	6	13	NULL	NULL	NULL	CCR3	GP		bind					CCL8	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
26621	2	8146	6	13	NULL	NULL	NULL	CCR3	GP		bind					CCL7	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
26622	3	8146	6	13	NULL	NULL	NULL	CCR3	GP		bind					CCL13	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
26623	4	8146	6	13	NULL	NULL	NULL	CCR3	GP		bind					CCL5	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
26624	5	8146	6	13	NULL	NULL	NULL	CCR3	GP		bind					CCL24	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
26625	6	8146	6	13	NULL	NULL	NULL	CCR3	GP		bind					CCL26	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
26626	7	8146	6	13	NULL	NULL	NULL	CCR3	GP		bind					CCL15	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
26627	8	8146	6	13	NULL	NULL	NULL	CCR3	GP		bind					CCL11	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
55935	9	8146	6	13	NULL	NULL	NULL	CCL8	GP		is					MCP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
55936	10	8146	6	13	NULL	NULL	NULL	CCL7	GP		is					MCP3	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
55937	11	8146	6	13	NULL	NULL	NULL	CCL13	GP		is					MCP4	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
55938	12	8146	6	13	NULL	NULL	NULL	CCL5	GP		is					RANTES	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
55939	13	8146	6	13	NULL	NULL	NULL	CCL24	GP		is					eotaxin-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
55940	14	8146	6	13	NULL	NULL	NULL	CCL26	GP		is					eotaxin-3	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
55941	15	8146	6	13	NULL	NULL	NULL	CCL15	GP		is					MIP5	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
32596	1	8146	7	NULL	NULL	0	NULL	CCR3 	NULL		binds	NULL				CCL11	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
32597	2	8146	7	NULL	NULL	0	NULL	CCR3	NULL		binds	NULL				CCL8	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
32598	3	8146	7	NULL	NULL	0	NULL	CCR3	NULL		binds	NULL				CCL7	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
32599	4	8146	7	NULL	NULL	0	NULL	CCR3 	NULL		binds	NULL				CCL13	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
32600	5	8146	7	NULL	NULL	0	NULL	CCR3	NULL		binds	NULL				 CCL5	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
32601	6	8146	7	NULL	NULL	0	NULL	CCR3	NULL		binds	NULL				CCL24	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
32602	7	8146	7	NULL	NULL	0	NULL	CCR3	NULL		binds	NULL				CCL26	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
32603	8	8146	7	NULL	NULL	0	NULL	CCR3	NULL		binds	NULL				CCL15	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
32604	9	8146	7	NULL	NULL	0	NULL	CCL8	NULL		is	NULL				MCP2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
32605	10	8146	7	NULL	NULL	0	NULL	CCL7	NULL		is	NULL				MCP3	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
32606	11	8146	7	NULL	NULL	0	NULL	CCL13 	NULL		is	NULL				MCP4	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
32607	12	8146	7	NULL	NULL	0	NULL	CCL5	NULL		is	NULL				RANTES	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
32608	13	8146	7	NULL	NULL	0	NULL	CCL24	NULL		is	NULL				eotaxin-2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
32609	14	8146	7	NULL	NULL	0	NULL	CCL26 	NULL		is	NULL				eotaxin-3	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
32610	15	8146	7	NULL	NULL	0	NULL	CCL15	NULL		is	NULL				MIP5	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1211_s_29	15130922	4,14 - 16    In addition to being the major receptor for CCL11, CCR3 also binds to CCL8 (MCP2), CCL7 (MCP3), CCL13 (MCP4), CCL5 (RANTES), CCL24 (eotaxin-2), CCL26 (eotaxin-3), and CCL15 (MIP5).	bind
26681	1	8147	6	13	NULL	NULL	NULL	AMP	Chemical		bind					AMPK	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_4_323_s_133	16051890	4,21  It has been proposed that the binding of AMP to the AMPK makes it a better substrate whereas the binding of ATP makes it a poor substrate for the upstream kinase.	bind
26682	2	8147	6	13	NULL	NULL	NULL	ATP	Chemical		bind					AMPK	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_4_323_s_133	16051890	4,21  It has been proposed that the binding of AMP to the AMPK makes it a better substrate whereas the binding of ATP makes it a poor substrate for the upstream kinase.	bind
26906	3	8147	6	13	NULL	NULL	NULL	AMPK	GP		substrate for					upstream kinase	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_4_323_s_133	16051890	4,21  It has been proposed that the binding of AMP to the AMPK makes it a better substrate whereas the binding of ATP makes it a poor substrate for the upstream kinase.	bind
26907	4	8147	6	13	NULL	NULL	NULL	statement 1	Process		increases					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_4_323_s_133	16051890	4,21  It has been proposed that the binding of AMP to the AMPK makes it a better substrate whereas the binding of ATP makes it a poor substrate for the upstream kinase.	bind
26908	5	8147	6	13	NULL	NULL	NULL	statement 2	Process		decreases					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_4_323_s_133	16051890	4,21  It has been proposed that the binding of AMP to the AMPK makes it a better substrate whereas the binding of ATP makes it a poor substrate for the upstream kinase.	bind
32611	1	8147	7	NULL	NULL	0	NULL	AMP	NULL		bind	NULL				AMPK	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_4_323_s_133	16051890	4,21  It has been proposed that the binding of AMP to the AMPK makes it a better substrate whereas the binding of ATP makes it a poor substrate for the upstream kinase.	bind
32612	2	8147	7	10	NULL	0	NULL	statement 1	NULL		 substrate for	NULL	better			upstream kinase	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_4_323_s_133	16051890	4,21  It has been proposed that the binding of AMP to the AMPK makes it a better substrate whereas the binding of ATP makes it a poor substrate for the upstream kinase.	bind
32613	3	8147	7	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				AMPK	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_4_323_s_133	16051890	4,21  It has been proposed that the binding of AMP to the AMPK makes it a better substrate whereas the binding of ATP makes it a poor substrate for the upstream kinase.	bind
32614	4	8147	7	10	NULL	0	NULL	statement 3	NULL		substrate for	NULL	poor			upstream kinase	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_4_323_s_133	16051890	4,21  It has been proposed that the binding of AMP to the AMPK makes it a better substrate whereas the binding of ATP makes it a poor substrate for the upstream kinase.	bind
26683	1	8148	6	13	NULL	NULL	NULL	lithium	Chemical		inhibits					GSK-3beta	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_863_s_7	16614310	4,5  GSK-3beta can be inhibited by lithium and SB415286, which interfere with the binding of ATP to GSK-3 6 rather than acting directly on GSK-3 phosphorylation.	bind
26684	2	8148	6	13	NULL	NULL	NULL	SB415286	Chemical		inhibits					GSK-3beta	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_863_s_7	16614310	4,5  GSK-3beta can be inhibited by lithium and SB415286, which interfere with the binding of ATP to GSK-3 6 rather than acting directly on GSK-3 phosphorylation.	bind
26685	3	8148	6	13	NULL	NULL	NULL	ATP	Chemical		bind					GSK-3	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_863_s_7	16614310	4,5  GSK-3beta can be inhibited by lithium and SB415286, which interfere with the binding of ATP to GSK-3 6 rather than acting directly on GSK-3 phosphorylation.	bind
26709	4	8148	6	13	NULL	NULL	NULL	lithium	Chemical		interferes with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_863_s_7	16614310	4,5  GSK-3beta can be inhibited by lithium and SB415286, which interfere with the binding of ATP to GSK-3 6 rather than acting directly on GSK-3 phosphorylation.	bind
26710	5	8148	6	13	NULL	NULL	NULL	SB415286	Chemical		interferes with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_863_s_7	16614310	4,5  GSK-3beta can be inhibited by lithium and SB415286, which interfere with the binding of ATP to GSK-3 6 rather than acting directly on GSK-3 phosphorylation.	bind
55942	6	8148	6	13	NULL	NULL	NULL	GSK-3	GP		undergoes					phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_863_s_7	16614310	4,5  GSK-3beta can be inhibited by lithium and SB415286, which interfere with the binding of ATP to GSK-3 6 rather than acting directly on GSK-3 phosphorylation.	bind
55943	7	8148	6	13	NULL	NULL	NULL	lithium	Chemical		does not act on		directly			statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_863_s_7	16614310	4,5  GSK-3beta can be inhibited by lithium and SB415286, which interfere with the binding of ATP to GSK-3 6 rather than acting directly on GSK-3 phosphorylation.	bind
55944	8	8148	6	13	NULL	NULL	NULL	SB415286	Chemical		does not act on		directly			statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_863_s_7	16614310	4,5  GSK-3beta can be inhibited by lithium and SB415286, which interfere with the binding of ATP to GSK-3 6 rather than acting directly on GSK-3 phosphorylation.	bind
32615	1	8148	7	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				GSK-3	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_7_863_s_7	16614310	4,5  GSK-3beta can be inhibited by lithium and SB415286, which interfere with the binding of ATP to GSK-3 6 rather than acting directly on GSK-3 phosphorylation.	bind
32616	2	8148	7	NULL	NULL	0	NULL	lithium	NULL		inhibits	NULL				GSK-3beta	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_7_863_s_7	16614310	4,5  GSK-3beta can be inhibited by lithium and SB415286, which interfere with the binding of ATP to GSK-3 6 rather than acting directly on GSK-3 phosphorylation.	bind
32617	3	8148	7	NULL	NULL	0	NULL	SB415286	NULL		inhibits	NULL				GSK-3beta	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_7_863_s_7	16614310	4,5  GSK-3beta can be inhibited by lithium and SB415286, which interfere with the binding of ATP to GSK-3 6 rather than acting directly on GSK-3 phosphorylation.	bind
32618	4	8148	7	10	NULL	0	NULL	lithium			interferes with					statement 1					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_863_s_7	16614310	4,5  GSK-3beta can be inhibited by lithium and SB415286, which interfere with the binding of ATP to GSK-3 6 rather than acting directly on GSK-3 phosphorylation.	bind
32619	5	8148	7	10	NULL	0	NULL	SB415286			interferes with					statement 1					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_863_s_7	16614310	4,5  GSK-3beta can be inhibited by lithium and SB415286, which interfere with the binding of ATP to GSK-3 6 rather than acting directly on GSK-3 phosphorylation.	bind
32620	6	8148	7	NULL	NULL	0	NULL	GSK-3	NULL		undergoes	NULL				phosphorylation	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_7_863_s_7	16614310	4,5  GSK-3beta can be inhibited by lithium and SB415286, which interfere with the binding of ATP to GSK-3 6 rather than acting directly on GSK-3 phosphorylation.	bind
32621	7	8148	7	10	NULL	0	NULL	lithium			does not act on		directly			statement 6					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_863_s_7	16614310	4,5  GSK-3beta can be inhibited by lithium and SB415286, which interfere with the binding of ATP to GSK-3 6 rather than acting directly on GSK-3 phosphorylation.	bind
32622	8	8148	7	10	NULL	0	NULL	SB415286			does not act on		directly			statement 6					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_863_s_7	16614310	4,5  GSK-3beta can be inhibited by lithium and SB415286, which interfere with the binding of ATP to GSK-3 6 rather than acting directly on GSK-3 phosphorylation.	bind
26909	1	8149	6	13	NULL	NULL	NULL	TFPI-alpha	GP		lacks			K3 domain		proteinase inhibitory activity	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_23_3567_s_21	15557366	4,5  The Kunitz-1 and 2 domains are responsible for TFPI binding and inhibition of TF-FVIIa complex and FXa, respectively, whereas the K3 domain in TFPI-alpha appears to lack proteinase inhibitory activity, and its physiological function is not known.	bind
26912	2	8149	6	13	NULL	NULL	NULL	TFPI	GP		is responsible for			Kunitz-1 domain		TFPI	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_23_3567_s_21	15557366	4,5  The Kunitz-1 and 2 domains are responsible for TFPI binding and inhibition of TF-FVIIa complex and FXa, respectively, whereas the K3 domain in TFPI-alpha appears to lack proteinase inhibitory activity, and its physiological function is not known.	bind
26913	3	8149	6	13	NULL	NULL	NULL	TFPI	GP		plays a role in			Kunitz-1 domain		TFPI	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_23_3567_s_21	15557366	4,5  The Kunitz-1 and 2 domains are responsible for TFPI binding and inhibition of TF-FVIIa complex and FXa, respectively, whereas the K3 domain in TFPI-alpha appears to lack proteinase inhibitory activity, and its physiological function is not known.	bind
26914	4	8149	6	13	NULL	NULL	NULL	TFPI	GP		inhibits			Kunitz-2 domain		TF-FVIIa complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_23_3567_s_21	15557366	4,5  The Kunitz-1 and 2 domains are responsible for TFPI binding and inhibition of TF-FVIIa complex and FXa, respectively, whereas the K3 domain in TFPI-alpha appears to lack proteinase inhibitory activity, and its physiological function is not known.	bind
26915	5	8149	6	13	NULL	NULL	NULL	TFPI	GP		inhibits			Kunitz-2 domain		FXa	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_110_23_3567_s_21	15557366	4,5  The Kunitz-1 and 2 domains are responsible for TFPI binding and inhibition of TF-FVIIa complex and FXa, respectively, whereas the K3 domain in TFPI-alpha appears to lack proteinase inhibitory activity, and its physiological function is not known.	bind
32623	1	8149	7	NULL	NULL	0	NULL		NULL		is responsible for	NULL		Kunitz-1 domain		TFPI	NULL	binding of			NULL		0	NULL	NULL	NULL	gw70_circulation_110_23_3567_s_21	15557366	4,5  The Kunitz-1 and 2 domains are responsible for TFPI binding and inhibition of TF-FVIIa complex and FXa, respectively, whereas the K3 domain in TFPI-alpha appears to lack proteinase inhibitory activity, and its physiological function is not known.	bind
32624	2	8149	7	NULL	NULL	0	NULL		NULL		is responsible for	NULL		Kunitz-2 domain		TFPI	NULL	binding of			NULL		0	NULL	NULL	NULL	gw70_circulation_110_23_3567_s_21	15557366	4,5  The Kunitz-1 and 2 domains are responsible for TFPI binding and inhibition of TF-FVIIa complex and FXa, respectively, whereas the K3 domain in TFPI-alpha appears to lack proteinase inhibitory activity, and its physiological function is not known.	bind
32625	3	8149	7	NULL	NULL	0	NULL		NULL		inhibits	NULL		Kunitz-1 domain		TF-FVIIa complex	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_110_23_3567_s_21	15557366	4,5  The Kunitz-1 and 2 domains are responsible for TFPI binding and inhibition of TF-FVIIa complex and FXa, respectively, whereas the K3 domain in TFPI-alpha appears to lack proteinase inhibitory activity, and its physiological function is not known.	bind
32626	4	8149	7	NULL	NULL	0	NULL		NULL		inhibits	NULL		Kunitz-2 domain		FXa	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_110_23_3567_s_21	15557366	4,5  The Kunitz-1 and 2 domains are responsible for TFPI binding and inhibition of TF-FVIIa complex and FXa, respectively, whereas the K3 domain in TFPI-alpha appears to lack proteinase inhibitory activity, and its physiological function is not known.	bind
32627	5	8149	7	NULL	NULL	0	NULL	TFPI-alpha	NULL		lack 	NULL		K3 domain		proteinase inhibitory activity	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_110_23_3567_s_21	15557366	4,5  The Kunitz-1 and 2 domains are responsible for TFPI binding and inhibition of TF-FVIIa complex and FXa, respectively, whereas the K3 domain in TFPI-alpha appears to lack proteinase inhibitory activity, and its physiological function is not known.	bind
26711	1	8150	6	13	NULL	NULL	NULL	c-Src	GP		bind					Cx43CT	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_2_215_s_141	14699011	4,5  To test this hypothesis, we used RMS to evaluate whether c-Src binding to Cx43CT interferes with binding of ZO-1 ( Figure 6).	bind
26712	2	8150	6	13	NULL	NULL	NULL	statement 1	Process		interfere with		may			ZO-1	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_2_215_s_141	14699011	4,5  To test this hypothesis, we used RMS to evaluate whether c-Src binding to Cx43CT interferes with binding of ZO-1 ( Figure 6).	bind
32630	1	8150	7	NULL	NULL	0	NULL	 c-Src	NULL		bind	NULL				Cx43CT	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_2_215_s_141	14699011	4,5  To test this hypothesis, we used RMS to evaluate whether c-Src binding to Cx43CT interferes with binding of ZO-1 ( Figure 6).	bind
32631	2	8150	7	10	NULL	0	NULL	statement 1			interfere with		may			ZO-1		binding of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_2_215_s_141	14699011	4,5  To test this hypothesis, we used RMS to evaluate whether c-Src binding to Cx43CT interferes with binding of ZO-1 ( Figure 6).	bind
26714	1	8152	6	13	NULL	NULL	NULL	GPCR	GP		transactivate					EGFR	GP				NULL	cardiomyocytes	NULL	NULL	NULL	NULL	gw70_circulationres_94_1_68_s_18	14656925	4,8 - 12      These GPCRs transactivate the EGF receptor (EGFR) in cardiomyocytes via a shared pathway, whereby ADAM 12 sheds membrane-anchored HB-EGF, which then binds to the EGFR either directly or via an interaction with the proteoglycan matrix or cell membrane molecules (such as CD44) to signal growth.	bind
26715	2	8152	6	13	NULL	NULL	NULL	EGFR	GP		is					EGF receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_1_68_s_18	14656925	4,8 - 12      These GPCRs transactivate the EGF receptor (EGFR) in cardiomyocytes via a shared pathway, whereby ADAM 12 sheds membrane-anchored HB-EGF, which then binds to the EGFR either directly or via an interaction with the proteoglycan matrix or cell membrane molecules (such as CD44) to signal growth.	bind
26717	3	8152	6	13	NULL	NULL	NULL	ADAM	GP		sheds					HB-EGF	GP	membrane-anchored			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_1_68_s_18	14656925	4,8 - 12      These GPCRs transactivate the EGF receptor (EGFR) in cardiomyocytes via a shared pathway, whereby ADAM 12 sheds membrane-anchored HB-EGF, which then binds to the EGFR either directly or via an interaction with the proteoglycan matrix or cell membrane molecules (such as CD44) to signal growth.	bind
26719	4	8152	6	13	NULL	NULL	NULL	HB-EGF	GP		bind		directly			EGFR	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_1_68_s_18	14656925	4,8 - 12      These GPCRs transactivate the EGF receptor (EGFR) in cardiomyocytes via a shared pathway, whereby ADAM 12 sheds membrane-anchored HB-EGF, which then binds to the EGFR either directly or via an interaction with the proteoglycan matrix or cell membrane molecules (such as CD44) to signal growth.	bind
26720	5	8152	6	13	NULL	NULL	NULL	HB-EGF	GP		interacts with					proteoglycan matrix 	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_1_68_s_18	14656925	4,8 - 12      These GPCRs transactivate the EGF receptor (EGFR) in cardiomyocytes via a shared pathway, whereby ADAM 12 sheds membrane-anchored HB-EGF, which then binds to the EGFR either directly or via an interaction with the proteoglycan matrix or cell membrane molecules (such as CD44) to signal growth.	bind
26724	6	8152	6	13	NULL	NULL	NULL	HB-EGF	GP		bind					CD44	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_1_68_s_18	14656925	4,8 - 12      These GPCRs transactivate the EGF receptor (EGFR) in cardiomyocytes via a shared pathway, whereby ADAM 12 sheds membrane-anchored HB-EGF, which then binds to the EGFR either directly or via an interaction with the proteoglycan matrix or cell membrane molecules (such as CD44) to signal growth.	bind
26726	7	8152	6	13	NULL	NULL	NULL	CD44	GP		is a type of					cell membrane molecule	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_1_68_s_18	14656925	4,8 - 12      These GPCRs transactivate the EGF receptor (EGFR) in cardiomyocytes via a shared pathway, whereby ADAM 12 sheds membrane-anchored HB-EGF, which then binds to the EGFR either directly or via an interaction with the proteoglycan matrix or cell membrane molecules (such as CD44) to signal growth.	bind
32634	1	8152	7	NULL	NULL	0	NULL	GPCRs 	NULL		transactivate	NULL				EGFR	NULL				NULL	 cardiomyocytes 	0	NULL	NULL	NULL	gw70_circulationres_94_1_68_s_18	14656925	4,8 - 12      These GPCRs transactivate the EGF receptor (EGFR) in cardiomyocytes via a shared pathway, whereby ADAM 12 sheds membrane-anchored HB-EGF, which then binds to the EGFR either directly or via an interaction with the proteoglycan matrix or cell membrane molecules (such as CD44) to signal growth.	bind
32635	2	8152	7	10	NULL	0	NULL	ADAM 12	NULL		sheds	NULL				HB-EGF	NULL	membrane-anchored			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_1_68_s_18	14656925	4,8 - 12      These GPCRs transactivate the EGF receptor (EGFR) in cardiomyocytes via a shared pathway, whereby ADAM 12 sheds membrane-anchored HB-EGF, which then binds to the EGFR either directly or via an interaction with the proteoglycan matrix or cell membrane molecules (such as CD44) to signal growth.	bind
32636	3	8152	7	NULL	NULL	0	NULL	statement 1	NULL		via	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_1_68_s_18	14656925	4,8 - 12      These GPCRs transactivate the EGF receptor (EGFR) in cardiomyocytes via a shared pathway, whereby ADAM 12 sheds membrane-anchored HB-EGF, which then binds to the EGFR either directly or via an interaction with the proteoglycan matrix or cell membrane molecules (such as CD44) to signal growth.	bind
32637	4	8152	7	NULL	NULL	0	NULL	HB-EGF	NULL		bind	NULL	directly			EGFR	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_1_68_s_18	14656925	4,8 - 12      These GPCRs transactivate the EGF receptor (EGFR) in cardiomyocytes via a shared pathway, whereby ADAM 12 sheds membrane-anchored HB-EGF, which then binds to the EGFR either directly or via an interaction with the proteoglycan matrix or cell membrane molecules (such as CD44) to signal growth.	bind
32640	5	8152	7	NULL	NULL	0	NULL	HB-EGF	NULL		interacts with	NULL				proteoglycan matrix	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_1_68_s_18	14656925	4,8 - 12      These GPCRs transactivate the EGF receptor (EGFR) in cardiomyocytes via a shared pathway, whereby ADAM 12 sheds membrane-anchored HB-EGF, which then binds to the EGFR either directly or via an interaction with the proteoglycan matrix or cell membrane molecules (such as CD44) to signal growth.	bind
32644	6	8152	7	NULL	NULL	0	NULL	HB-EGF	NULL		bind	NULL				CD44	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_1_68_s_18	14656925	4,8 - 12      These GPCRs transactivate the EGF receptor (EGFR) in cardiomyocytes via a shared pathway, whereby ADAM 12 sheds membrane-anchored HB-EGF, which then binds to the EGFR either directly or via an interaction with the proteoglycan matrix or cell membrane molecules (such as CD44) to signal growth.	bind
32645	7	8152	7	NULL	NULL	0	NULL	EGFR	NULL		is	NULL				EGF receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_1_68_s_18	14656925	4,8 - 12      These GPCRs transactivate the EGF receptor (EGFR) in cardiomyocytes via a shared pathway, whereby ADAM 12 sheds membrane-anchored HB-EGF, which then binds to the EGFR either directly or via an interaction with the proteoglycan matrix or cell membrane molecules (such as CD44) to signal growth.	bind
32648	8	8152	7	NULL	NULL	0	NULL	CD44	NULL		is a type of	NULL				cell membrane molecule	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_1_68_s_18	14656925	4,8 - 12      These GPCRs transactivate the EGF receptor (EGFR) in cardiomyocytes via a shared pathway, whereby ADAM 12 sheds membrane-anchored HB-EGF, which then binds to the EGFR either directly or via an interaction with the proteoglycan matrix or cell membrane molecules (such as CD44) to signal growth.	bind
32662	9	8152	7	NULL	NULL	0	NULL	statement 4	NULL		signal	NULL				growth	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_1_68_s_18	14656925	4,8 - 12      These GPCRs transactivate the EGF receptor (EGFR) in cardiomyocytes via a shared pathway, whereby ADAM 12 sheds membrane-anchored HB-EGF, which then binds to the EGFR either directly or via an interaction with the proteoglycan matrix or cell membrane molecules (such as CD44) to signal growth.	bind
32663	10	8152	7	NULL	NULL	0	NULL	statement 5	NULL		signal	NULL				growth	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_1_68_s_18	14656925	4,8 - 12      These GPCRs transactivate the EGF receptor (EGFR) in cardiomyocytes via a shared pathway, whereby ADAM 12 sheds membrane-anchored HB-EGF, which then binds to the EGFR either directly or via an interaction with the proteoglycan matrix or cell membrane molecules (such as CD44) to signal growth.	bind
32664	11	8152	7	NULL	NULL	0	NULL	statement 6	NULL		signal	NULL				growth	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_1_68_s_18	14656925	4,8 - 12      These GPCRs transactivate the EGF receptor (EGFR) in cardiomyocytes via a shared pathway, whereby ADAM 12 sheds membrane-anchored HB-EGF, which then binds to the EGFR either directly or via an interaction with the proteoglycan matrix or cell membrane molecules (such as CD44) to signal growth.	bind
26727	1	8153	6	13	NULL	NULL	NULL	FasL	GP		bind					Fas	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_1_153_s_14	11141488	4- 7  Binding of FasL to Fas results in apoptosis of susceptible cells.	bind
26728	2	8153	6	13	NULL	NULL	NULL	statement 1	Process		results in					susceptible cell	Cell	apoptosis of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_158_1_153_s_14	11141488	4- 7  Binding of FasL to Fas results in apoptosis of susceptible cells.	bind
32665	1	8153	7	NULL	NULL	0	NULL	 FasL 	NULL		bind	NULL				Fas	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_1_153_s_14	11141488	4- 7  Binding of FasL to Fas results in apoptosis of susceptible cells.	bind
32666	2	8153	7	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				susceptible cells	NULL	apoptosis of 			NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_1_153_s_14	11141488	4- 7  Binding of FasL to Fas results in apoptosis of susceptible cells.	bind
26730	1	8154	6	13	NULL	NULL	NULL	T cell antigen	Chemical		bind					B cells	Cell	mature			NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_23_0_23_s_1462	15771565	4-1BB T cell  antigen binds to mature B cells and macrophages, and costimulates anti- -primed splenic  B cells.	bind
26736	2	8154	6	13	NULL	NULL	NULL	T cell antigen	Chemical		bind					macrophages	Cell				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_23_0_23_s_1462	15771565	4-1BB T cell  antigen binds to mature B cells and macrophages, and costimulates anti- -primed splenic  B cells.	bind
26737	3	8154	6	13	NULL	NULL	NULL	T cell antigen	Chemical		costimulates					B cells	Cell	anti--primed;;splenic			NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_23_0_23_s_1462	15771565	4-1BB T cell  antigen binds to mature B cells and macrophages, and costimulates anti- -primed splenic  B cells.	bind
32667	1	8154	7	10	NULL	0	NULL	T cell antigen			binds to					B cells		mature			NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_23_0_23_s_1462	15771565	4-1BB T cell  antigen binds to mature B cells and macrophages, and costimulates anti- -primed splenic  B cells.	bind
32668	2	8154	7	10	NULL	0	NULL	T cell antigen			binds to					macrophages					NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_23_0_23_s_1462	15771565	4-1BB T cell  antigen binds to mature B cells and macrophages, and costimulates anti- -primed splenic  B cells.	bind
32669	3	8154	7	10	NULL	0	NULL	T cell antigen			costimulates					B cells		anti--primed;;splenic			NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_23_0_23_s_1462	15771565	4-1BB T cell  antigen binds to mature B cells and macrophages, and costimulates anti- -primed splenic  B cells.	bind
32670	1	8155	7	13	NULL	NULL	NULL	T-cell antigen	Chemical		binds to					B cells	Cell	mature			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_1_196_s_368	12496166	4-1BB T-cell antigen binds to mature B cells and macrophage, and costimulates anti-mu-primed splenic B cells.	bind
32671	2	8155	7	13	NULL	NULL	NULL	T-cell antigen	Chemical		binds to					macrophages	Cell				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_1_196_s_368	12496166	4-1BB T-cell antigen binds to mature B cells and macrophage, and costimulates anti-mu-primed splenic B cells.	bind
32672	3	8155	7	13	NULL	NULL	NULL	T-cell antigen	Chemical		costimulates					B cells	Cell	anti-mu-primed;;splenic			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_1_196_s_368	12496166	4-1BB T-cell antigen binds to mature B cells and macrophage, and costimulates anti-mu-primed splenic B cells.	bind
26738	1	8156	6	13	NULL	NULL	NULL	4-DAMP mustard	Chemical		bind					mACh receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_314_2_891_s_20	15857948	4-Diphenylacetoxy- N-(2-chloroethyl)piperidine (4-DAMP mustard) is known to bind to mACh receptors (Thomas et al., 1992 ; Eglen et al., 1994 ; Ehlert and Griffin, 1998 ; Sawyer and Ehlert, 1999 ; Ragheb et al., 2001 ; Umland et al., 2001 ) with moderate selectivity for M3-mACh receptors.	bind
26739	2	8156	6	13	NULL	NULL	NULL	4-DAMP mustard	Chemical		is					4-Diphenylacetoxy- N-(2-chloroethyl)piperidine	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_314_2_891_s_20	15857948	4-Diphenylacetoxy- N-(2-chloroethyl)piperidine (4-DAMP mustard) is known to bind to mACh receptors (Thomas et al., 1992 ; Eglen et al., 1994 ; Ehlert and Griffin, 1998 ; Sawyer and Ehlert, 1999 ; Ragheb et al., 2001 ; Umland et al., 2001 ) with moderate selectivity for M3-mACh receptors.	bind
32673	1	8156	7	NULL	NULL	0	NULL	4-DAMP mustard	NULL		bind	NULL				mACh receptors	NULL				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_314_2_891_s_20	15857948	4-Diphenylacetoxy- N-(2-chloroethyl)piperidine (4-DAMP mustard) is known to bind to mACh receptors (Thomas et al., 1992 ; Eglen et al., 1994 ; Ehlert and Griffin, 1998 ; Sawyer and Ehlert, 1999 ; Ragheb et al., 2001 ; Umland et al., 2001 ) with moderate selectivity for M3-mACh receptors.	bind
32675	3	8156	7	NULL	NULL	0	NULL	4-DAMP	NULL		is	NULL				4-Diphenylacetoxy- N-(2-chloroethyl)piperidine 	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_314_2_891_s_20	15857948	4-Diphenylacetoxy- N-(2-chloroethyl)piperidine (4-DAMP mustard) is known to bind to mACh receptors (Thomas et al., 1992 ; Eglen et al., 1994 ; Ehlert and Griffin, 1998 ; Sawyer and Ehlert, 1999 ; Ragheb et al., 2001 ; Umland et al., 2001 ) with moderate selectivity for M3-mACh receptors.	bind
32676	4	8156	7	10	NULL	0	NULL	4-DAMP mustard	NULL		selectivity for	NULL	moderate			M3-mACh receptors	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_314_2_891_s_20	15857948	4-Diphenylacetoxy- N-(2-chloroethyl)piperidine (4-DAMP mustard) is known to bind to mACh receptors (Thomas et al., 1992 ; Eglen et al., 1994 ; Ehlert and Griffin, 1998 ; Sawyer and Ehlert, 1999 ; Ragheb et al., 2001 ; Umland et al., 2001 ) with moderate selectivity for M3-mACh receptors.	bind
26740	1	8157	6	13	NULL	NULL	NULL	4-Hydroxybutyrate dehydrogenase	GP		requires					NAD(H)	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_65_9_3901_s_141	10473393	4-Hydroxybutyrate dehydrogenase requires NAD(H) as a cofactor, but the highly conserved NAD(H) binding fingerprint pattern G-X-G-X-X-G ( 15) was not present in the amino acid sequence.	bind
26741	2	8157	6	13	NULL	NULL	NULL	NAD(H)	Chemical		acts as a 					cofactor	Chemical				NULL	statement 1	NULL	NULL	NULL	NULL	gw60_applenvironmicrob_65_9_3901_s_141	10473393	4-Hydroxybutyrate dehydrogenase requires NAD(H) as a cofactor, but the highly conserved NAD(H) binding fingerprint pattern G-X-G-X-X-G ( 15) was not present in the amino acid sequence.	bind
26742	3	8157	6	13	NULL	NULL	NULL				is the fingerprint pattern for		highly conserved	G-X-G-X-X-G		NAD(H)	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_65_9_3901_s_141	10473393	4-Hydroxybutyrate dehydrogenase requires NAD(H) as a cofactor, but the highly conserved NAD(H) binding fingerprint pattern G-X-G-X-X-G ( 15) was not present in the amino acid sequence.	bind
32677	1	8157	7	NULL	NULL	0	NULL	4-Hydroxybutyrate dehydrogenase	NULL		requires	NULL				NAD(H) cofactor	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_9_3901_s_141	10473393	4-Hydroxybutyrate dehydrogenase requires NAD(H) as a cofactor, but the highly conserved NAD(H) binding fingerprint pattern G-X-G-X-X-G ( 15) was not present in the amino acid sequence.	bind
32678	2	8157	7	10	NULL	0	NULL		NULL		is not present in	NULL		G-X-G-X-X-G		4-Hydroxybutyrate dehydrogenase	NULL				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_65_9_3901_s_141	10473393	4-Hydroxybutyrate dehydrogenase requires NAD(H) as a cofactor, but the highly conserved NAD(H) binding fingerprint pattern G-X-G-X-X-G ( 15) was not present in the amino acid sequence.	bind
46579	3	8157	7	10	NULL	0	NULL	G-X-G-X-X-G	NULL		is the fingerprint pattern for	NULL	highly conserved			NAD(H)	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_65_9_3901_s_141	10473393	4-Hydroxybutyrate dehydrogenase requires NAD(H) as a cofactor, but the highly conserved NAD(H) binding fingerprint pattern G-X-G-X-X-G ( 15) was not present in the amino acid sequence.	bind
26743	1	8158	6	13	NULL	NULL	NULL	mTAb1	GP		bind					mTOR	GP				NULL	MER-Akt cells	NULL	NULL	NULL	NULL	gw60_pnas_95_13_7772_s_163	9636226	4-Hydroxytamoxifen rapidly decreased mTAb1 binding to mTOR in the MER-Akt cells, but not in the parental NIH 3T3 cells (Fig.  5 A).	bind
26744	2	8158	6	13	NULL	NULL	NULL	mTAb1	GP		bind					mTOR	GP				NULL	parental NIH 3T3 cells	NULL	NULL	NULL	NULL	gw60_pnas_95_13_7772_s_163	9636226	4-Hydroxytamoxifen rapidly decreased mTAb1 binding to mTOR in the MER-Akt cells, but not in the parental NIH 3T3 cells (Fig.  5 A).	bind
26745	3	8158	6	13	NULL	NULL	NULL	Hydroxytamoxifen	Chemical		decreases		rapidly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_13_7772_s_163	9636226	4-Hydroxytamoxifen rapidly decreased mTAb1 binding to mTOR in the MER-Akt cells, but not in the parental NIH 3T3 cells (Fig.  5 A).	bind
26746	4	8158	6	13	NULL	NULL	NULL	Hydroxytamoxifen	Chemical		does not decrease					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_13_7772_s_163	9636226	4-Hydroxytamoxifen rapidly decreased mTAb1 binding to mTOR in the MER-Akt cells, but not in the parental NIH 3T3 cells (Fig.  5 A).	bind
32679	1	8158	7	NULL	NULL	0	NULL	mTAb1	NULL		bind	NULL				mTOR	NULL				NULL	MER-Akt cells	0	NULL	NULL	NULL	gw60_pnas_95_13_7772_s_163	9636226	4-Hydroxytamoxifen rapidly decreased mTAb1 binding to mTOR in the MER-Akt cells, but not in the parental NIH 3T3 cells (Fig.  5 A).	bind
32680	2	8158	7	NULL	NULL	0	NULL	4-Hydroxytamoxifen	NULL		decrease	NULL	rapidly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_13_7772_s_163	9636226	4-Hydroxytamoxifen rapidly decreased mTAb1 binding to mTOR in the MER-Akt cells, but not in the parental NIH 3T3 cells (Fig.  5 A).	bind
32681	3	8158	7	NULL	NULL	0	NULL	 mTAb1	NULL		bind	NULL				mTOR	NULL				NULL	 parental NIH 3T3 cells 	0	NULL	NULL	NULL	gw60_pnas_95_13_7772_s_163	9636226	4-Hydroxytamoxifen rapidly decreased mTAb1 binding to mTOR in the MER-Akt cells, but not in the parental NIH 3T3 cells (Fig.  5 A).	bind
32682	4	8158	7	NULL	NULL	0	NULL	4-Hydroxytamoxifen	NULL		does not decrease	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_13_7772_s_163	9636226	4-Hydroxytamoxifen rapidly decreased mTAb1 binding to mTOR in the MER-Akt cells, but not in the parental NIH 3T3 cells (Fig.  5 A).	bind
26747	1	8159	6	13	NULL	NULL	NULL	4-oxo-RA	Chemical		bind					atRA binding proteins	GP	cellular			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_10_6908_s_218	10702251	4-oxo-RA can also bind to cellular atRA binding proteins ( 40).	bind
32683	1	8159	7	10	NULL	0	NULL	4-oxo-RA	NULL		bind	NULL				atRA binding protein	NULL	cellular			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_10_6908_s_218	10702251	4-oxo-RA can also bind to cellular atRA binding proteins ( 40).	bind
26748	1	8160	6	13	NULL	NULL	NULL	E2	Chemical		bind					ER	GP				NULL	MCF-7 cells	NULL	NULL	NULL	NULL	abs-batch0600-0619_j-toxicol-environ-health-a_65_5-6_11936222_s_8	11936222	4-t-Octylphenol and  4-nonylphenol inhibited the binding of E2 to the ER of MCF-7 cells in  a competitive ER binding assay.	bind
26749	2	8160	6	13	NULL	NULL	NULL	4-t-Octylphenol	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-toxicol-environ-health-a_65_5-6_11936222_s_8	11936222	4-t-Octylphenol and  4-nonylphenol inhibited the binding of E2 to the ER of MCF-7 cells in  a competitive ER binding assay.	bind
26750	3	8160	6	13	NULL	NULL	NULL	4-nonylphenol	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-toxicol-environ-health-a_65_5-6_11936222_s_8	11936222	4-t-Octylphenol and  4-nonylphenol inhibited the binding of E2 to the ER of MCF-7 cells in  a competitive ER binding assay.	bind
32684	1	8160	7	NULL	NULL	0	NULL	 E2 	NULL		bind	NULL				ER	NULL				NULL	MCF-7 cells	0	NULL	NULL	NULL	abs-batch0600-0619_j-toxicol-environ-health-a_65_5-6_11936222_s_8	11936222	4-t-Octylphenol and  4-nonylphenol inhibited the binding of E2 to the ER of MCF-7 cells in  a competitive ER binding assay.	bind
32685	2	8160	7	NULL	NULL	0	NULL	4-t-Octylphenol	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-toxicol-environ-health-a_65_5-6_11936222_s_8	11936222	4-t-Octylphenol and  4-nonylphenol inhibited the binding of E2 to the ER of MCF-7 cells in  a competitive ER binding assay.	bind
32686	3	8160	7	NULL	NULL	0	NULL	4-nonylphenol	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-toxicol-environ-health-a_65_5-6_11936222_s_8	11936222	4-t-Octylphenol and  4-nonylphenol inhibited the binding of E2 to the ER of MCF-7 cells in  a competitive ER binding assay.	bind
26751	1	8161	6	13	NULL	NULL	NULL	r30kDa	GP		bind					GPC-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24540_s_86	10831591	4.1 and r30kDa also bound GPC-3 with a  K( D)kin value on the order of 0.1 muM (Table  I), but no binding could be documented between r30kDa and either GPC-1 or GPC-2	bind
26752	2	8161	6	13	NULL	NULL	NULL	r30kDa	GP		does not bind					GPC-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24540_s_86	10831591	4.1 and r30kDa also bound GPC-3 with a  K( D)kin value on the order of 0.1 muM (Table  I), but no binding could be documented between r30kDa and either GPC-1 or GPC-2	bind
26753	3	8161	6	13	NULL	NULL	NULL	r30kDa	GP		does not bind					GPC-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24540_s_86	10831591	4.1 and r30kDa also bound GPC-3 with a  K( D)kin value on the order of 0.1 muM (Table  I), but no binding could be documented between r30kDa and either GPC-1 or GPC-2	bind
32687	1	8161	7	NULL	NULL	0	NULL	r30kDa	NULL		bind	NULL				GPC-3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24540_s_86	10831591	4.1 and r30kDa also bound GPC-3 with a  K( D)kin value on the order of 0.1 muM (Table  I), but no binding could be documented between r30kDa and either GPC-1 or GPC-2	bind
32688	2	8161	7	NULL	NULL	0	NULL	 r30kDa	NULL		does not bind	NULL				 GPC-1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24540_s_86	10831591	4.1 and r30kDa also bound GPC-3 with a  K( D)kin value on the order of 0.1 muM (Table  I), but no binding could be documented between r30kDa and either GPC-1 or GPC-2	bind
32689	3	8161	7	NULL	NULL	0	NULL	r30kDa	NULL		does not bind	NULL				 GPC-2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24540_s_86	10831591	4.1 and r30kDa also bound GPC-3 with a  K( D)kin value on the order of 0.1 muM (Table  I), but no binding could be documented between r30kDa and either GPC-1 or GPC-2	bind
26754	1	8162	6	13	NULL	NULL	NULL	SAP97	GP		bind					AMPAR	GP		GluR1 subunits		NULL	hippocampal synapses	NULL	NULL	NULL	NULL	gw60_neuron_31_2_191_s_139	11502252	4.1 and SAP97 are the major binding partners for the GluR1 subunits of AMPARs at hippocampal synapses     (Leonard et al., 1998  ; Shen et al., 2000b  ; Valtschanoff et al., 2000  ; Walensky et al., 1999  ) and form sites where AMPARs can anchor.	bind
32690	1	8162	7	NULL	NULL	0	NULL	 SAP97 	NULL		bind	NULL				AMPARs	NULL		GluR1 subunits 		NULL	hippocampal synapses	0	NULL	NULL	NULL	gw60_neuron_31_2_191_s_139	11502252	4.1 and SAP97 are the major binding partners for the GluR1 subunits of AMPARs at hippocampal synapses     (Leonard et al., 1998  ; Shen et al., 2000b  ; Valtschanoff et al., 2000  ; Walensky et al., 1999  ) and form sites where AMPARs can anchor.	bind
26755	1	8163	6	13	NULL	NULL	NULL	p55	GP		bind					GPC	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24540_s_134	10831591	4.1 Modulates p55 Binding to GPC, but p55 Does Not Affect 4.1 Binding to GPC-- To further define the interactions among the three protein components of the ternary complex, 4.1, p55, and GPC, we determined whether p55-GPC and 4.1-GPC binary interactions can be regulated by the third member of the complex, namely, 4.1 and p55, respectively.	bind
26756	2	8163	6	13	NULL	NULL	NULL	4.1	GP		modulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24540_s_134	10831591	4.1 Modulates p55 Binding to GPC, but p55 Does Not Affect 4.1 Binding to GPC-- To further define the interactions among the three protein components of the ternary complex, 4.1, p55, and GPC, we determined whether p55-GPC and 4.1-GPC binary interactions can be regulated by the third member of the complex, namely, 4.1 and p55, respectively.	bind
26757	3	8163	6	13	NULL	NULL	NULL	4.1	GP		bind					GPC	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24540_s_134	10831591	4.1 Modulates p55 Binding to GPC, but p55 Does Not Affect 4.1 Binding to GPC-- To further define the interactions among the three protein components of the ternary complex, 4.1, p55, and GPC, we determined whether p55-GPC and 4.1-GPC binary interactions can be regulated by the third member of the complex, namely, 4.1 and p55, respectively.	bind
26758	4	8163	6	13	NULL	NULL	NULL	p55	GP		does not affect					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24540_s_134	10831591	4.1 Modulates p55 Binding to GPC, but p55 Does Not Affect 4.1 Binding to GPC-- To further define the interactions among the three protein components of the ternary complex, 4.1, p55, and GPC, we determined whether p55-GPC and 4.1-GPC binary interactions can be regulated by the third member of the complex, namely, 4.1 and p55, respectively.	bind
32692	1	8163	7	NULL	NULL	0	NULL	p55	NULL		bind	NULL				GPC	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24540_s_134	10831591	4.1 Modulates p55 Binding to GPC, but p55 Does Not Affect 4.1 Binding to GPC-- To further define the interactions among the three protein components of the ternary complex, 4.1, p55, and GPC, we determined whether p55-GPC and 4.1-GPC binary interactions can be regulated by the third member of the complex, namely, 4.1 and p55, respectively.	bind
32693	2	8163	7	NULL	NULL	0	NULL	4.1	NULL		modulates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24540_s_134	10831591	4.1 Modulates p55 Binding to GPC, but p55 Does Not Affect 4.1 Binding to GPC-- To further define the interactions among the three protein components of the ternary complex, 4.1, p55, and GPC, we determined whether p55-GPC and 4.1-GPC binary interactions can be regulated by the third member of the complex, namely, 4.1 and p55, respectively.	bind
32694	3	8163	7	NULL	NULL	0	NULL	 4.1	NULL		bind	NULL				GPC	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24540_s_134	10831591	4.1 Modulates p55 Binding to GPC, but p55 Does Not Affect 4.1 Binding to GPC-- To further define the interactions among the three protein components of the ternary complex, 4.1, p55, and GPC, we determined whether p55-GPC and 4.1-GPC binary interactions can be regulated by the third member of the complex, namely, 4.1 and p55, respectively.	bind
32695	4	8163	7	NULL	NULL	0	NULL	p55 	NULL		does not affect	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24540_s_134	10831591	4.1 Modulates p55 Binding to GPC, but p55 Does Not Affect 4.1 Binding to GPC-- To further define the interactions among the three protein components of the ternary complex, 4.1, p55, and GPC, we determined whether p55-GPC and 4.1-GPC binary interactions can be regulated by the third member of the complex, namely, 4.1 and p55, respectively.	bind
26759	1	8164	6	13	NULL	NULL	NULL	4.1G	GP		contains			CTD		peptidyl-prolyl bonds	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_1_143_s_247	9531554	4.1G-CTD contains three peptidyl-prolyl bonds that  could potentially participate in FKBP13 binding, including  val-pro at aa 18-19, ser-pro at 32-33, and his-pro at 107-108.	bind
26760	2	8164	6	13	NULL	NULL	NULL	statement 1	GP		participate in		potentially			FKBP13	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_1_143_s_247	9531554	4.1G-CTD contains three peptidyl-prolyl bonds that  could potentially participate in FKBP13 binding, including  val-pro at aa 18-19, ser-pro at 32-33, and his-pro at 107-108.	bind
26761	3	8164	6	13	NULL	NULL	NULL	4.1G	GP		contains			CTD					val-pro at aa 18-19		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_1_143_s_247	9531554	4.1G-CTD contains three peptidyl-prolyl bonds that  could potentially participate in FKBP13 binding, including  val-pro at aa 18-19, ser-pro at 32-33, and his-pro at 107-108.	bind
26762	4	8164	6	13	NULL	NULL	NULL	4.1G	GP		contains			CTD					ser-pro at 32-33		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_1_143_s_247	9531554	4.1G-CTD contains three peptidyl-prolyl bonds that  could potentially participate in FKBP13 binding, including  val-pro at aa 18-19, ser-pro at 32-33, and his-pro at 107-108.	bind
26763	5	8164	6	13	NULL	NULL	NULL	4.1G	GP		contains			CTD					his-pro at 107-108		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_1_143_s_247	9531554	4.1G-CTD contains three peptidyl-prolyl bonds that  could potentially participate in FKBP13 binding, including  val-pro at aa 18-19, ser-pro at 32-33, and his-pro at 107-108.	bind
32696	1	8164	7	10	NULL	0	NULL	4.1G	NULL		contains	NULL		CTD		peptidyl-prolyl bonds	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_1_143_s_247	9531554	4.1G-CTD contains three peptidyl-prolyl bonds that  could potentially participate in FKBP13 binding, including  val-pro at aa 18-19, ser-pro at 32-33, and his-pro at 107-108.	bind
32697	2	8164	7	10	NULL	0	NULL	4.1G	NULL		participate in	NULL	potentially	CTD		FKBP13	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_1_143_s_247	9531554	4.1G-CTD contains three peptidyl-prolyl bonds that  could potentially participate in FKBP13 binding, including  val-pro at aa 18-19, ser-pro at 32-33, and his-pro at 107-108.	bind
46581	3	8164	7	10	NULL	0	NULL	4.1G	NULL		contains	NULL		CTD			NULL		val-pro at aa 18-19		NULL		0	NULL	NULL	NULL	gw60_cellbiol_141_1_143_s_247	9531554	4.1G-CTD contains three peptidyl-prolyl bonds that  could potentially participate in FKBP13 binding, including  val-pro at aa 18-19, ser-pro at 32-33, and his-pro at 107-108.	bind
46582	4	8164	7	10	NULL	0	NULL	4.1G	NULL		contains	NULL		CTD			NULL		ser-pro at 32-33		NULL		0	NULL	NULL	NULL	gw60_cellbiol_141_1_143_s_247	9531554	4.1G-CTD contains three peptidyl-prolyl bonds that  could potentially participate in FKBP13 binding, including  val-pro at aa 18-19, ser-pro at 32-33, and his-pro at 107-108.	bind
46583	5	8164	7	10	NULL	0	NULL	4.1G	NULL		contains	NULL		CTD			NULL		his-pro at 107-108		NULL		0	NULL	NULL	NULL	gw60_cellbiol_141_1_143_s_247	9531554	4.1G-CTD contains three peptidyl-prolyl bonds that  could potentially participate in FKBP13 binding, including  val-pro at aa 18-19, ser-pro at 32-33, and his-pro at 107-108.	bind
26764	1	8165	6	13	NULL	NULL	NULL	NF1	GP		bind					MMTV	GP			promoter	NULL	nucleosomes	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3448_s_375	11504883	40       Eisfeld,K., Candau,R., Truss,M. and Beato,M. (1997) Binding of NF1 to the MMTV promoter in nucleosomes: influence of rotational phasing, translational positioning and histone H1.	bind
32700	1	8165	7	NULL	NULL	0	NULL	NF1	NULL		bind	NULL				MMTV	NULL			promoter	NULL	nucleosomes	0	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3448_s_375	11504883	40       Eisfeld,K., Candau,R., Truss,M. and Beato,M. (1997) Binding of NF1 to the MMTV promoter in nucleosomes: influence of rotational phasing, translational positioning and histone H1.	bind
26949	1	8166	6	13	NULL	NULL	NULL	Sp1	GP		bind					dihydrofolate reductase	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_783_s_367	11160902	40       Gee,J.E., Blume,S., Snyder,R.C., Ray,R. and Miller,D.M. (1992) Triplex formation prevents Sp1 binding to the dihydrofolate reductase promoter.	bind
26950	2	8166	6	13	NULL	NULL	NULL	triplex formation	GP		prevents					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_783_s_367	11160902	40       Gee,J.E., Blume,S., Snyder,R.C., Ray,R. and Miller,D.M. (1992) Triplex formation prevents Sp1 binding to the dihydrofolate reductase promoter.	bind
32701	1	8166	7	NULL	NULL	0	NULL	 Sp1	NULL		bind	NULL				dihydrofolate reductase	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_783_s_367	11160902	40       Gee,J.E., Blume,S., Snyder,R.C., Ray,R. and Miller,D.M. (1992) Triplex formation prevents Sp1 binding to the dihydrofolate reductase promoter.	bind
32702	2	8166	7	NULL	NULL	0	NULL	Triplex formation 	NULL		prevents	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_783_s_367	11160902	40       Gee,J.E., Blume,S., Snyder,R.C., Ray,R. and Miller,D.M. (1992) Triplex formation prevents Sp1 binding to the dihydrofolate reductase promoter.	bind
26951	1	8167	6	13	NULL	NULL	NULL	p53	GP		bind		sequence specifically			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_5207_s_415	11812854	40       Gu,W. and Roeder,R.G. (1997) Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.	bind
26952	2	8167	6	13	NULL	NULL	NULL	p53	GP	acetylation of	activates			C-terminal domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_5207_s_415	11812854	40       Gu,W. and Roeder,R.G. (1997) Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.	bind
32703	1	8167	7	10	NULL	0	NULL	 p53	NULL		bind	NULL	sequence specifically			DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_5207_s_415	11812854	40       Gu,W. and Roeder,R.G. (1997) Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.	bind
32705	2	8167	7	10	NULL	0	NULL	p53	NULL		undergoes	NULL		C-terminal domain		acetylation	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_5207_s_415	11812854	40       Gu,W. and Roeder,R.G. (1997) Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.	bind
32706	3	8167	7	10	NULL	0	NULL	statement 2	NULL		activates	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_5207_s_415	11812854	40       Gu,W. and Roeder,R.G. (1997) Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.	bind
26953	1	8168	6	13	NULL	NULL	NULL	U2AF	GP		is required for					U2 snRNP	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1741_s_328	11292847	40       Ruskin,B., Zamore,P.D. and Green,M.R. (1988) A factor, U2AF, is required for U2 snRNP binding and splicing complex assembly.	bind
26954	2	8168	6	13	NULL	NULL	NULL	U2AF	GP		is required for					splicing complex	GP	assembly of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1741_s_328	11292847	40       Ruskin,B., Zamore,P.D. and Green,M.R. (1988) A factor, U2AF, is required for U2 snRNP binding and splicing complex assembly.	bind
32713	1	8168	7	NULL	NULL	0	NULL	U2	NULL		bind	NULL				SnRNP	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1741_s_328	11292847	40       Ruskin,B., Zamore,P.D. and Green,M.R. (1988) A factor, U2AF, is required for U2 snRNP binding and splicing complex assembly.	bind
32714	2	8168	7	NULL	NULL	0	NULL	U2AF	NULL		is required for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1741_s_328	11292847	40       Ruskin,B., Zamore,P.D. and Green,M.R. (1988) A factor, U2AF, is required for U2 snRNP binding and splicing complex assembly.	bind
32715	3	8168	7	NULL	NULL	0	NULL	U2AF	NULL		is required for	NULL				splicing complex	NULL	assembly of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1741_s_328	11292847	40       Ruskin,B., Zamore,P.D. and Green,M.R. (1988) A factor, U2AF, is required for U2 snRNP binding and splicing complex assembly.	bind
26955	1	8169	6	13	NULL	NULL	NULL	LDL	GP		bind		may			GPIIb	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_377_s_163	7749848	40  Although ligand blotting experiments reveal that LDL and HDL may bind to GPIIb and GPIIIa, respectively, 15  only LDL seems to increase exposure of fibrinogen binding sites on ADP-stimulated GFPs. 46  Van Willigen et al 46  have shown that exposure of the GPIIb-IIIa complex, the so-called fibrinogen receptor, is not mediated by formation of proaggregatory eicosanoids, ie, PGG2/H2 and TXA2.	bind
26956	2	8169	6	13	NULL	NULL	NULL	HDL	GP		bind		may			GPIIIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_377_s_163	7749848	40  Although ligand blotting experiments reveal that LDL and HDL may bind to GPIIb and GPIIIa, respectively, 15  only LDL seems to increase exposure of fibrinogen binding sites on ADP-stimulated GFPs. 46  Van Willigen et al 46  have shown that exposure of the GPIIb-IIIa complex, the so-called fibrinogen receptor, is not mediated by formation of proaggregatory eicosanoids, ie, PGG2/H2 and TXA2.	bind
27035	3	8169	6	13	NULL	NULL	NULL	LDL	GP		increase		may			GFP	GP	exposure of;; ADP stimulated	fibrinogen binding sites		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_377_s_163	7749848	40  Although ligand blotting experiments reveal that LDL and HDL may bind to GPIIb and GPIIIa, respectively, 15  only LDL seems to increase exposure of fibrinogen binding sites on ADP-stimulated GFPs. 46  Van Willigen et al 46  have shown that exposure of the GPIIb-IIIa complex, the so-called fibrinogen receptor, is not mediated by formation of proaggregatory eicosanoids, ie, PGG2/H2 and TXA2.	bind
27036	4	8169	6	13	NULL	NULL	NULL	GPIIb-IIIa complex	GP		is a type of					fibrinogen receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_377_s_163	7749848	40  Although ligand blotting experiments reveal that LDL and HDL may bind to GPIIb and GPIIIa, respectively, 15  only LDL seems to increase exposure of fibrinogen binding sites on ADP-stimulated GFPs. 46  Van Willigen et al 46  have shown that exposure of the GPIIb-IIIa complex, the so-called fibrinogen receptor, is not mediated by formation of proaggregatory eicosanoids, ie, PGG2/H2 and TXA2.	bind
27037	5	8169	6	13	NULL	NULL	NULL	GPIIb-IIIa complex	GP	exposure of	is not mediated by					eicosanoids	Chemical	formation of;; proaggregatory			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_377_s_163	7749848	40  Although ligand blotting experiments reveal that LDL and HDL may bind to GPIIb and GPIIIa, respectively, 15  only LDL seems to increase exposure of fibrinogen binding sites on ADP-stimulated GFPs. 46  Van Willigen et al 46  have shown that exposure of the GPIIb-IIIa complex, the so-called fibrinogen receptor, is not mediated by formation of proaggregatory eicosanoids, ie, PGG2/H2 and TXA2.	bind
27038	6	8169	6	13	NULL	NULL	NULL	PGG2/H2	Chemical		is a type of					proaggregatory eicosanoid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_377_s_163	7749848	40  Although ligand blotting experiments reveal that LDL and HDL may bind to GPIIb and GPIIIa, respectively, 15  only LDL seems to increase exposure of fibrinogen binding sites on ADP-stimulated GFPs. 46  Van Willigen et al 46  have shown that exposure of the GPIIb-IIIa complex, the so-called fibrinogen receptor, is not mediated by formation of proaggregatory eicosanoids, ie, PGG2/H2 and TXA2.	bind
27055	7	8169	6	13	NULL	NULL	NULL	TXA2	Chemical		is a type of					proaggregatory eicosanoid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_377_s_163	7749848	40  Although ligand blotting experiments reveal that LDL and HDL may bind to GPIIb and GPIIIa, respectively, 15  only LDL seems to increase exposure of fibrinogen binding sites on ADP-stimulated GFPs. 46  Van Willigen et al 46  have shown that exposure of the GPIIb-IIIa complex, the so-called fibrinogen receptor, is not mediated by formation of proaggregatory eicosanoids, ie, PGG2/H2 and TXA2.	bind
32716	1	8169	7	NULL	NULL	0	NULL	LDL 	NULL		bind	NULL	may			GPIIb	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_377_s_163	7749848	40  Although ligand blotting experiments reveal that LDL and HDL may bind to GPIIb and GPIIIa, respectively, 15  only LDL seems to increase exposure of fibrinogen binding sites on ADP-stimulated GFPs. 46  Van Willigen et al 46  have shown that exposure of the GPIIb-IIIa complex, the so-called fibrinogen receptor, is not mediated by formation of proaggregatory eicosanoids, ie, PGG2/H2 and TXA2.	bind
32717	2	8169	7	NULL	NULL	0	NULL	HDL	NULL		bind	NULL	may			GPIIIa	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_377_s_163	7749848	40  Although ligand blotting experiments reveal that LDL and HDL may bind to GPIIb and GPIIIa, respectively, 15  only LDL seems to increase exposure of fibrinogen binding sites on ADP-stimulated GFPs. 46  Van Willigen et al 46  have shown that exposure of the GPIIb-IIIa complex, the so-called fibrinogen receptor, is not mediated by formation of proaggregatory eicosanoids, ie, PGG2/H2 and TXA2.	bind
32718	3	8169	7	NULL	NULL	0	NULL	ADP	NULL		stimulate	NULL				GFPs	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_377_s_163	7749848	40  Although ligand blotting experiments reveal that LDL and HDL may bind to GPIIb and GPIIIa, respectively, 15  only LDL seems to increase exposure of fibrinogen binding sites on ADP-stimulated GFPs. 46  Van Willigen et al 46  have shown that exposure of the GPIIb-IIIa complex, the so-called fibrinogen receptor, is not mediated by formation of proaggregatory eicosanoids, ie, PGG2/H2 and TXA2.	bind
32719	4	8169	7	10	NULL	0	NULL	LDL	NULL		increase	NULL				GFPs	NULL	exposure of;;ADP-stimulated	fibrinogen binding sites		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_377_s_163	7749848	40  Although ligand blotting experiments reveal that LDL and HDL may bind to GPIIb and GPIIIa, respectively, 15  only LDL seems to increase exposure of fibrinogen binding sites on ADP-stimulated GFPs. 46  Van Willigen et al 46  have shown that exposure of the GPIIb-IIIa complex, the so-called fibrinogen receptor, is not mediated by formation of proaggregatory eicosanoids, ie, PGG2/H2 and TXA2.	bind
32720	5	8169	7	NULL	NULL	0	NULL	 GPIIb-IIIa complex	NULL		is a type of	NULL				fibrinogen receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_377_s_163	7749848	40  Although ligand blotting experiments reveal that LDL and HDL may bind to GPIIb and GPIIIa, respectively, 15  only LDL seems to increase exposure of fibrinogen binding sites on ADP-stimulated GFPs. 46  Van Willigen et al 46  have shown that exposure of the GPIIb-IIIa complex, the so-called fibrinogen receptor, is not mediated by formation of proaggregatory eicosanoids, ie, PGG2/H2 and TXA2.	bind
32721	6	8169	7	NULL	NULL	0	NULL	 GPIIb-IIIa complex	NULL	exposure of	is not mediated by	NULL				PGG2/H2	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_377_s_163	7749848	40  Although ligand blotting experiments reveal that LDL and HDL may bind to GPIIb and GPIIIa, respectively, 15  only LDL seems to increase exposure of fibrinogen binding sites on ADP-stimulated GFPs. 46  Van Willigen et al 46  have shown that exposure of the GPIIb-IIIa complex, the so-called fibrinogen receptor, is not mediated by formation of proaggregatory eicosanoids, ie, PGG2/H2 and TXA2.	bind
32722	7	8169	7	NULL	NULL	0	NULL	GPIIb-IIIa complex	NULL	exposure of	is not mediated by	NULL				TXA2	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_377_s_163	7749848	40  Although ligand blotting experiments reveal that LDL and HDL may bind to GPIIb and GPIIIa, respectively, 15  only LDL seems to increase exposure of fibrinogen binding sites on ADP-stimulated GFPs. 46  Van Willigen et al 46  have shown that exposure of the GPIIb-IIIa complex, the so-called fibrinogen receptor, is not mediated by formation of proaggregatory eicosanoids, ie, PGG2/H2 and TXA2.	bind
32723	8	8169	7	NULL	NULL	0	NULL	PGG2/H2	NULL		is a type of	NULL				proaggregatory eicosanoids	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_377_s_163	7749848	40  Although ligand blotting experiments reveal that LDL and HDL may bind to GPIIb and GPIIIa, respectively, 15  only LDL seems to increase exposure of fibrinogen binding sites on ADP-stimulated GFPs. 46  Van Willigen et al 46  have shown that exposure of the GPIIb-IIIa complex, the so-called fibrinogen receptor, is not mediated by formation of proaggregatory eicosanoids, ie, PGG2/H2 and TXA2.	bind
32724	9	8169	7	NULL	NULL	0	NULL	TXA2	NULL		is a type of	NULL				proaggregatory eicosanoids	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_377_s_163	7749848	40  Although ligand blotting experiments reveal that LDL and HDL may bind to GPIIb and GPIIIa, respectively, 15  only LDL seems to increase exposure of fibrinogen binding sites on ADP-stimulated GFPs. 46  Van Willigen et al 46  have shown that exposure of the GPIIb-IIIa complex, the so-called fibrinogen receptor, is not mediated by formation of proaggregatory eicosanoids, ie, PGG2/H2 and TXA2.	bind
27508	1	8170	6	13	NULL	NULL	NULL	Rel A	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_205_s_322	11786414	40  As the DNA binding of RelA and p50 may also be disturbed by their hypophosphorylation 39 and as different NF-kappaB-inducing stimuli may cause phosphorylation of NF-kappaB proteins at unique sites, 41, 42  which possibly differentially affects their DNA binding, selective inhibition of RelA or p50 phosphorylation could be the mechanism by which SS blocks NF-kappaB DNA binding in human testicular cells under the conditions induced in the present model.	bind
27509	2	8170	6	13	NULL	NULL	NULL	p50	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_205_s_322	11786414	40  As the DNA binding of RelA and p50 may also be disturbed by their hypophosphorylation 39 and as different NF-kappaB-inducing stimuli may cause phosphorylation of NF-kappaB proteins at unique sites, 41, 42  which possibly differentially affects their DNA binding, selective inhibition of RelA or p50 phosphorylation could be the mechanism by which SS blocks NF-kappaB DNA binding in human testicular cells under the conditions induced in the present model.	bind
27510	3	8170	6	13	NULL	NULL	NULL	Rel A	GP	hyperphosphorylation of	disturb		may			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_205_s_322	11786414	40  As the DNA binding of RelA and p50 may also be disturbed by their hypophosphorylation 39 and as different NF-kappaB-inducing stimuli may cause phosphorylation of NF-kappaB proteins at unique sites, 41, 42  which possibly differentially affects their DNA binding, selective inhibition of RelA or p50 phosphorylation could be the mechanism by which SS blocks NF-kappaB DNA binding in human testicular cells under the conditions induced in the present model.	bind
27511	4	8170	6	13	NULL	NULL	NULL	p50	GP	hyperphosphorylation of	disturb		may			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_205_s_322	11786414	40  As the DNA binding of RelA and p50 may also be disturbed by their hypophosphorylation 39 and as different NF-kappaB-inducing stimuli may cause phosphorylation of NF-kappaB proteins at unique sites, 41, 42  which possibly differentially affects their DNA binding, selective inhibition of RelA or p50 phosphorylation could be the mechanism by which SS blocks NF-kappaB DNA binding in human testicular cells under the conditions induced in the present model.	bind
27512	5	8170	6	13	NULL	NULL	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL	human testicular cells	NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_205_s_322	11786414	40  As the DNA binding of RelA and p50 may also be disturbed by their hypophosphorylation 39 and as different NF-kappaB-inducing stimuli may cause phosphorylation of NF-kappaB proteins at unique sites, 41, 42  which possibly differentially affects their DNA binding, selective inhibition of RelA or p50 phosphorylation could be the mechanism by which SS blocks NF-kappaB DNA binding in human testicular cells under the conditions induced in the present model.	bind
27513	6	8170	6	13	NULL	NULL	NULL	SS	Chemical		blocks					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_205_s_322	11786414	40  As the DNA binding of RelA and p50 may also be disturbed by their hypophosphorylation 39 and as different NF-kappaB-inducing stimuli may cause phosphorylation of NF-kappaB proteins at unique sites, 41, 42  which possibly differentially affects their DNA binding, selective inhibition of RelA or p50 phosphorylation could be the mechanism by which SS blocks NF-kappaB DNA binding in human testicular cells under the conditions induced in the present model.	bind
27514	7	8170	6	13	NULL	NULL	NULL	Rel A	GP	selective inhibition of;;phosphorylation	is mechanism for		could			statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_205_s_322	11786414	40  As the DNA binding of RelA and p50 may also be disturbed by their hypophosphorylation 39 and as different NF-kappaB-inducing stimuli may cause phosphorylation of NF-kappaB proteins at unique sites, 41, 42  which possibly differentially affects their DNA binding, selective inhibition of RelA or p50 phosphorylation could be the mechanism by which SS blocks NF-kappaB DNA binding in human testicular cells under the conditions induced in the present model.	bind
27515	8	8170	6	13	NULL	NULL	NULL	p50	GP	selective inhibition of;;phosphorylation	is mechanism for		could			statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_205_s_322	11786414	40  As the DNA binding of RelA and p50 may also be disturbed by their hypophosphorylation 39 and as different NF-kappaB-inducing stimuli may cause phosphorylation of NF-kappaB proteins at unique sites, 41, 42  which possibly differentially affects their DNA binding, selective inhibition of RelA or p50 phosphorylation could be the mechanism by which SS blocks NF-kappaB DNA binding in human testicular cells under the conditions induced in the present model.	bind
32725	1	8170	7	NULL	NULL	0	NULL	RelA 	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_1_205_s_322	11786414	40  As the DNA binding of RelA and p50 may also be disturbed by their hypophosphorylation 39 and as different NF-kappaB-inducing stimuli may cause phosphorylation of NF-kappaB proteins at unique sites, 41, 42  which possibly differentially affects their DNA binding, selective inhibition of RelA or p50 phosphorylation could be the mechanism by which SS blocks NF-kappaB DNA binding in human testicular cells under the conditions induced in the present model.	bind
32726	2	8170	7	NULL	NULL	0	NULL	p50	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_1_205_s_322	11786414	40  As the DNA binding of RelA and p50 may also be disturbed by their hypophosphorylation 39 and as different NF-kappaB-inducing stimuli may cause phosphorylation of NF-kappaB proteins at unique sites, 41, 42  which possibly differentially affects their DNA binding, selective inhibition of RelA or p50 phosphorylation could be the mechanism by which SS blocks NF-kappaB DNA binding in human testicular cells under the conditions induced in the present model.	bind
32727	3	8170	7	NULL	NULL	0	NULL	statement 1	NULL		be disturbed by	NULL	may			hypophosphorylation 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_205_s_322	11786414	40  As the DNA binding of RelA and p50 may also be disturbed by their hypophosphorylation 39 and as different NF-kappaB-inducing stimuli may cause phosphorylation of NF-kappaB proteins at unique sites, 41, 42  which possibly differentially affects their DNA binding, selective inhibition of RelA or p50 phosphorylation could be the mechanism by which SS blocks NF-kappaB DNA binding in human testicular cells under the conditions induced in the present model.	bind
32728	4	8170	7	NULL	NULL	0	NULL	statement 2	NULL		 be disturbed by	NULL	may			hypophosphorylation 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_205_s_322	11786414	40  As the DNA binding of RelA and p50 may also be disturbed by their hypophosphorylation 39 and as different NF-kappaB-inducing stimuli may cause phosphorylation of NF-kappaB proteins at unique sites, 41, 42  which possibly differentially affects their DNA binding, selective inhibition of RelA or p50 phosphorylation could be the mechanism by which SS blocks NF-kappaB DNA binding in human testicular cells under the conditions induced in the present model.	bind
32729	5	8170	7	NULL	NULL	0	NULL	stimuli	NULL		induce	NULL				NF-kappaB	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_1_205_s_322	11786414	40  As the DNA binding of RelA and p50 may also be disturbed by their hypophosphorylation 39 and as different NF-kappaB-inducing stimuli may cause phosphorylation of NF-kappaB proteins at unique sites, 41, 42  which possibly differentially affects their DNA binding, selective inhibition of RelA or p50 phosphorylation could be the mechanism by which SS blocks NF-kappaB DNA binding in human testicular cells under the conditions induced in the present model.	bind
32730	6	8170	7	NULL	NULL	0	NULL	statement 5	NULL		cause	NULL	may			NF-kappaB proteins	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_1_205_s_322	11786414	40  As the DNA binding of RelA and p50 may also be disturbed by their hypophosphorylation 39 and as different NF-kappaB-inducing stimuli may cause phosphorylation of NF-kappaB proteins at unique sites, 41, 42  which possibly differentially affects their DNA binding, selective inhibition of RelA or p50 phosphorylation could be the mechanism by which SS blocks NF-kappaB DNA binding in human testicular cells under the conditions induced in the present model.	bind
32731	7	8170	7	NULL	NULL	0	NULL	NF-kappaB	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_1_205_s_322	11786414	40  As the DNA binding of RelA and p50 may also be disturbed by their hypophosphorylation 39 and as different NF-kappaB-inducing stimuli may cause phosphorylation of NF-kappaB proteins at unique sites, 41, 42  which possibly differentially affects their DNA binding, selective inhibition of RelA or p50 phosphorylation could be the mechanism by which SS blocks NF-kappaB DNA binding in human testicular cells under the conditions induced in the present model.	bind
32732	8	8170	7	NULL	NULL	0	NULL	statement 6	NULL		affect	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_1_205_s_322	11786414	40  As the DNA binding of RelA and p50 may also be disturbed by their hypophosphorylation 39 and as different NF-kappaB-inducing stimuli may cause phosphorylation of NF-kappaB proteins at unique sites, 41, 42  which possibly differentially affects their DNA binding, selective inhibition of RelA or p50 phosphorylation could be the mechanism by which SS blocks NF-kappaB DNA binding in human testicular cells under the conditions induced in the present model.	bind
32733	9	8170	7	NULL	NULL	0	NULL	SS 	NULL		blocks	NULL				statement 7	NULL				NULL	human testicular cells	0	NULL	NULL	NULL	gw60_amjpathol_160_1_205_s_322	11786414	40  As the DNA binding of RelA and p50 may also be disturbed by their hypophosphorylation 39 and as different NF-kappaB-inducing stimuli may cause phosphorylation of NF-kappaB proteins at unique sites, 41, 42  which possibly differentially affects their DNA binding, selective inhibition of RelA or p50 phosphorylation could be the mechanism by which SS blocks NF-kappaB DNA binding in human testicular cells under the conditions induced in the present model.	bind
32734	10	8170	7	10	NULL	0	NULL	RelA	NULL	inhibition of;;phosphorylation of	is the mechanism for	NULL				statement 9	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_205_s_322	11786414	40  As the DNA binding of RelA and p50 may also be disturbed by their hypophosphorylation 39 and as different NF-kappaB-inducing stimuli may cause phosphorylation of NF-kappaB proteins at unique sites, 41, 42  which possibly differentially affects their DNA binding, selective inhibition of RelA or p50 phosphorylation could be the mechanism by which SS blocks NF-kappaB DNA binding in human testicular cells under the conditions induced in the present model.	bind
32735	11	8170	7	10	NULL	0	NULL	p50	NULL	inhibition of;;phosphorylation of	is the mechanism for	NULL				statement 9	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_205_s_322	11786414	40  As the DNA binding of RelA and p50 may also be disturbed by their hypophosphorylation 39 and as different NF-kappaB-inducing stimuli may cause phosphorylation of NF-kappaB proteins at unique sites, 41, 42  which possibly differentially affects their DNA binding, selective inhibition of RelA or p50 phosphorylation could be the mechanism by which SS blocks NF-kappaB DNA binding in human testicular cells under the conditions induced in the present model.	bind
27059	1	8171	6	13	NULL	NULL	NULL	DEGR-VIIa	GP		bind					tissue factor	GP				NULL	cell surface	NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_254	7586275	40  DEGR-VIIa binds tissue factor with fivefold to sevenfold more affinity than native factor VIIa in the cell surface chromogenic assay, rendering the DEGR-VIIa - tissue factor complex enzymatically inactive and thus inhibiting the conversion of factor IX to IXa and factor X to Xa.	bind
27060	2	8171	6	13	NULL	NULL	NULL	factor VIIa	GP	native	bind					tissue factor	GP				NULL	cell surface	NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_254	7586275	40  DEGR-VIIa binds tissue factor with fivefold to sevenfold more affinity than native factor VIIa in the cell surface chromogenic assay, rendering the DEGR-VIIa - tissue factor complex enzymatically inactive and thus inhibiting the conversion of factor IX to IXa and factor X to Xa.	bind
27061	3	8171	6	13	NULL	NULL	NULL	statement 1	Process	affinity of	is higher than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_254	7586275	40  DEGR-VIIa binds tissue factor with fivefold to sevenfold more affinity than native factor VIIa in the cell surface chromogenic assay, rendering the DEGR-VIIa - tissue factor complex enzymatically inactive and thus inhibiting the conversion of factor IX to IXa and factor X to Xa.	bind
27062	4	8171	6	13	NULL	NULL	NULL	factor IX	GP		is converted to					factor IXa	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_254	7586275	40  DEGR-VIIa binds tissue factor with fivefold to sevenfold more affinity than native factor VIIa in the cell surface chromogenic assay, rendering the DEGR-VIIa - tissue factor complex enzymatically inactive and thus inhibiting the conversion of factor IX to IXa and factor X to Xa.	bind
27063	5	8171	6	13	NULL	NULL	NULL	factor X	GP		is converted to					factor Xa	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_254	7586275	40  DEGR-VIIa binds tissue factor with fivefold to sevenfold more affinity than native factor VIIa in the cell surface chromogenic assay, rendering the DEGR-VIIa - tissue factor complex enzymatically inactive and thus inhibiting the conversion of factor IX to IXa and factor X to Xa.	bind
27064	6	8171	6	13	NULL	NULL	NULL	statement 1	Process		inactivates					DEGR-VIIa - tissue factor complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_254	7586275	40  DEGR-VIIa binds tissue factor with fivefold to sevenfold more affinity than native factor VIIa in the cell surface chromogenic assay, rendering the DEGR-VIIa - tissue factor complex enzymatically inactive and thus inhibiting the conversion of factor IX to IXa and factor X to Xa.	bind
27065	7	8171	6	13	NULL	NULL	NULL	statement 6	Process		inhibits					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_254	7586275	40  DEGR-VIIa binds tissue factor with fivefold to sevenfold more affinity than native factor VIIa in the cell surface chromogenic assay, rendering the DEGR-VIIa - tissue factor complex enzymatically inactive and thus inhibiting the conversion of factor IX to IXa and factor X to Xa.	bind
27066	8	8171	6	13	NULL	NULL	NULL	statement 6	Process		inhibits					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_254	7586275	40  DEGR-VIIa binds tissue factor with fivefold to sevenfold more affinity than native factor VIIa in the cell surface chromogenic assay, rendering the DEGR-VIIa - tissue factor complex enzymatically inactive and thus inhibiting the conversion of factor IX to IXa and factor X to Xa.	bind
32736	1	8171	7	NULL	NULL	0	NULL	DEGR-VIIa	NULL		binds	NULL				tissue factor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_254	7586275	40  DEGR-VIIa binds tissue factor with fivefold to sevenfold more affinity than native factor VIIa in the cell surface chromogenic assay, rendering the DEGR-VIIa - tissue factor complex enzymatically inactive and thus inhibiting the conversion of factor IX to IXa and factor X to Xa.	bind
32737	2	8171	7	NULL	NULL	0	NULL	 factor VIIa	NULL	native	binds	NULL				tissue factor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_254	7586275	40  DEGR-VIIa binds tissue factor with fivefold to sevenfold more affinity than native factor VIIa in the cell surface chromogenic assay, rendering the DEGR-VIIa - tissue factor complex enzymatically inactive and thus inhibiting the conversion of factor IX to IXa and factor X to Xa.	bind
32738	3	8171	7	NULL	NULL	0	NULL	statement 1	NULL	affinity of	is higher than	NULL				statement 2	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_254	7586275	40  DEGR-VIIa binds tissue factor with fivefold to sevenfold more affinity than native factor VIIa in the cell surface chromogenic assay, rendering the DEGR-VIIa - tissue factor complex enzymatically inactive and thus inhibiting the conversion of factor IX to IXa and factor X to Xa.	bind
32739	4	8171	7	NULL	NULL	0	NULL	DEGR-VIIa - tissue factor complex 	NULL		is inactive as	NULL				enzyme	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_254	7586275	40  DEGR-VIIa binds tissue factor with fivefold to sevenfold more affinity than native factor VIIa in the cell surface chromogenic assay, rendering the DEGR-VIIa - tissue factor complex enzymatically inactive and thus inhibiting the conversion of factor IX to IXa and factor X to Xa.	bind
32740	5	8171	7	NULL	NULL	0	NULL	factor IX	NULL		converts to	NULL				factor IXa	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_254	7586275	40  DEGR-VIIa binds tissue factor with fivefold to sevenfold more affinity than native factor VIIa in the cell surface chromogenic assay, rendering the DEGR-VIIa - tissue factor complex enzymatically inactive and thus inhibiting the conversion of factor IX to IXa and factor X to Xa.	bind
32741	6	8171	7	NULL	NULL	0	NULL	factor X	NULL		converts to	NULL				factor Xa	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_254	7586275	40  DEGR-VIIa binds tissue factor with fivefold to sevenfold more affinity than native factor VIIa in the cell surface chromogenic assay, rendering the DEGR-VIIa - tissue factor complex enzymatically inactive and thus inhibiting the conversion of factor IX to IXa and factor X to Xa.	bind
32742	7	8171	7	NULL	NULL	0	NULL	statement 4	NULL		inhibits	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_254	7586275	40  DEGR-VIIa binds tissue factor with fivefold to sevenfold more affinity than native factor VIIa in the cell surface chromogenic assay, rendering the DEGR-VIIa - tissue factor complex enzymatically inactive and thus inhibiting the conversion of factor IX to IXa and factor X to Xa.	bind
32743	8	8171	7	NULL	NULL	0	NULL	statement 4	NULL		inhibits	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_254	7586275	40  DEGR-VIIa binds tissue factor with fivefold to sevenfold more affinity than native factor VIIa in the cell surface chromogenic assay, rendering the DEGR-VIIa - tissue factor complex enzymatically inactive and thus inhibiting the conversion of factor IX to IXa and factor X to Xa.	bind
27068	1	8172	6	13	NULL	NULL	NULL	anti-membrane glycoprotein MAb	GP		bind					SMC	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_6_1515_s_130	9118520	40  However, this possibility was unlikely because anti-membrane glycoprotein MAb, which binds SMC surface antigen, did not affect IH.	bind
27069	2	8172	6	13	NULL	NULL	NULL	anti-membrane glycoprotein MAb	GP		did not affect					IH	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_6_1515_s_130	9118520	40  However, this possibility was unlikely because anti-membrane glycoprotein MAb, which binds SMC surface antigen, did not affect IH.	bind
46605	3	8172	6	10	NULL	0	NULL	SMC	NULL		is a type of	NULL				surface antigen	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_95_6_1515_s_130	9118520	40  However, this possibility was unlikely because anti-membrane glycoprotein MAb, which binds SMC surface antigen, did not affect IH.	bind
32744	1	8172	7	NULL	NULL	0	NULL	anti-membrane glycoprotein MAb	NULL		binds	NULL				SMC	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_95_6_1515_s_130	9118520	40  However, this possibility was unlikely because anti-membrane glycoprotein MAb, which binds SMC surface antigen, did not affect IH.	bind
32745	2	8172	7	NULL	NULL	0	NULL	anti-membrane glycoprotein MAb	NULL		does not affect	NULL				IH	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_95_6_1515_s_130	9118520	40  However, this possibility was unlikely because anti-membrane glycoprotein MAb, which binds SMC surface antigen, did not affect IH.	bind
32746	3	8172	7	NULL	NULL	0	NULL	SMC	NULL		is a type of	NULL				surface antigen	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_95_6_1515_s_130	9118520	40  However, this possibility was unlikely because anti-membrane glycoprotein MAb, which binds SMC surface antigen, did not affect IH.	bind
27071	1	8173	6	13	NULL	NULL	NULL	factor VIII	GP		bind					von Willebrand factor	GP				NULL	plasma	NULL	NULL	NULL	NULL	gw60_circulation_96_4_1102_s_141	9286936	40  In women, factor VIII was also positively associated with CHD incidence, which might be expected because factor VIII is bound to von Willebrand factor in plasma and there is a correlation of 0.71 between these two factors.	bind
27072	2	8173	6	13	NULL	NULL	NULL	factor VIII	GP		is associated with		positively			CHD	MedicalFinding	incidence of 			NULL	women	NULL	NULL	NULL	NULL	gw60_circulation_96_4_1102_s_141	9286936	40  In women, factor VIII was also positively associated with CHD incidence, which might be expected because factor VIII is bound to von Willebrand factor in plasma and there is a correlation of 0.71 between these two factors.	bind
32747	1	8173	7	10	NULL	0	NULL	factor VIII			associated with		positively			CHD		incidence of			NULL	women	NULL	NULL	NULL	NULL	gw60_circulation_96_4_1102_s_141	9286936	40  In women, factor VIII was also positively associated with CHD incidence, which might be expected because factor VIII is bound to von Willebrand factor in plasma and there is a correlation of 0.71 between these two factors.	bind
32748	2	8173	7	NULL	NULL	0	NULL	factor VIII	NULL		bind	NULL				von Willebrand factor	NULL				NULL	plasma	0	NULL	NULL	NULL	gw60_circulation_96_4_1102_s_141	9286936	40  In women, factor VIII was also positively associated with CHD incidence, which might be expected because factor VIII is bound to von Willebrand factor in plasma and there is a correlation of 0.71 between these two factors.	bind
27073	1	8174	6	13	NULL	NULL	NULL	UPA	GP	mouse	bind		specifically			UPAR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_52	9598826	40  Moreover, comparison of the species-specific binding of UPA to UPAR with the amino acid sequence of the presumed binding sites in mouse, pig, and human UPA reveals that this species specificity must be mediated by very minor differences in amino acid sequence, most likely at positions 22, 27, 29, and 30, which are structurally close to each other 39  and wherein human and murine UPA have different amino acid residues.	bind
27696	2	8174	6	13	NULL	NULL	NULL	UPA	GP	pig	bind					UPAR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_52	9598826	40  Moreover, comparison of the species-specific binding of UPA to UPAR with the amino acid sequence of the presumed binding sites in mouse, pig, and human UPA reveals that this species specificity must be mediated by very minor differences in amino acid sequence, most likely at positions 22, 27, 29, and 30, which are structurally close to each other 39  and wherein human and murine UPA have different amino acid residues.	bind
27697	3	8174	6	13	NULL	NULL	NULL	UPA	GP	human	bind					UPAR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_52	9598826	40  Moreover, comparison of the species-specific binding of UPA to UPAR with the amino acid sequence of the presumed binding sites in mouse, pig, and human UPA reveals that this species specificity must be mediated by very minor differences in amino acid sequence, most likely at positions 22, 27, 29, and 30, which are structurally close to each other 39  and wherein human and murine UPA have different amino acid residues.	bind
32749	1	8174	7	NULL	NULL	0	NULL	UPA	NULL	mouse	binds	NULL				UPAR	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_52	9598826	40  Moreover, comparison of the species-specific binding of UPA to UPAR with the amino acid sequence of the presumed binding sites in mouse, pig, and human UPA reveals that this species specificity must be mediated by very minor differences in amino acid sequence, most likely at positions 22, 27, 29, and 30, which are structurally close to each other 39  and wherein human and murine UPA have different amino acid residues.	bind
32750	2	8174	7	NULL	NULL	0	NULL	UPA	NULL	pig	binds	NULL				UPAR	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_52	9598826	40  Moreover, comparison of the species-specific binding of UPA to UPAR with the amino acid sequence of the presumed binding sites in mouse, pig, and human UPA reveals that this species specificity must be mediated by very minor differences in amino acid sequence, most likely at positions 22, 27, 29, and 30, which are structurally close to each other 39  and wherein human and murine UPA have different amino acid residues.	bind
32751	3	8174	7	NULL	NULL	0	NULL	UPA	NULL	human	binds	NULL				UPAR	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_52	9598826	40  Moreover, comparison of the species-specific binding of UPA to UPAR with the amino acid sequence of the presumed binding sites in mouse, pig, and human UPA reveals that this species specificity must be mediated by very minor differences in amino acid sequence, most likely at positions 22, 27, 29, and 30, which are structurally close to each other 39  and wherein human and murine UPA have different amino acid residues.	bind
32752	4	8174	7	NULL	NULL	0	NULL	species specificity	NULL		is mediated by	NULL				UPA	NULL		aminoacid 22		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_52	9598826	40  Moreover, comparison of the species-specific binding of UPA to UPAR with the amino acid sequence of the presumed binding sites in mouse, pig, and human UPA reveals that this species specificity must be mediated by very minor differences in amino acid sequence, most likely at positions 22, 27, 29, and 30, which are structurally close to each other 39  and wherein human and murine UPA have different amino acid residues.	bind
32753	5	8174	7	NULL	NULL	0	NULL	species specificity	NULL		is mediated by	NULL				UPA	NULL		amino acid 27		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_52	9598826	40  Moreover, comparison of the species-specific binding of UPA to UPAR with the amino acid sequence of the presumed binding sites in mouse, pig, and human UPA reveals that this species specificity must be mediated by very minor differences in amino acid sequence, most likely at positions 22, 27, 29, and 30, which are structurally close to each other 39  and wherein human and murine UPA have different amino acid residues.	bind
32754	6	8174	7	NULL	NULL	0	NULL	species specificity	NULL		is mediated by	NULL				UPA	NULL		amino acid 29		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_52	9598826	40  Moreover, comparison of the species-specific binding of UPA to UPAR with the amino acid sequence of the presumed binding sites in mouse, pig, and human UPA reveals that this species specificity must be mediated by very minor differences in amino acid sequence, most likely at positions 22, 27, 29, and 30, which are structurally close to each other 39  and wherein human and murine UPA have different amino acid residues.	bind
32755	7	8174	7	NULL	NULL	0	NULL	species specificity	NULL		is mediated by	NULL				UPA	NULL		amino acid 30		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_52	9598826	40  Moreover, comparison of the species-specific binding of UPA to UPAR with the amino acid sequence of the presumed binding sites in mouse, pig, and human UPA reveals that this species specificity must be mediated by very minor differences in amino acid sequence, most likely at positions 22, 27, 29, and 30, which are structurally close to each other 39  and wherein human and murine UPA have different amino acid residues.	bind
27074	1	8175	6	13	NULL	NULL	NULL	RACK1	GP		bind					Src	GP				NULL	cells treated with PMA	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20346_s_281	11279199	40 and  41), we detected little increase in binding of RACK1 and Src after treating cells with PMA for 15 min (Fig.  8,  A ( lane 6) and  B ( lanes 4 and  7)).	bind
32996	1	8175	7	NULL	NULL	0	NULL	 RACK1	NULL		bind	NULL				Src	NULL				NULL	cells treated with PMA	0	NULL	NULL	NULL	gw60_jbiolchem_276_23_20346_s_281	11279199	40 and  41), we detected little increase in binding of RACK1 and Src after treating cells with PMA for 15 min (Fig.  8,  A ( lane 6) and  B ( lanes 4 and  7)).	bind
27075	1	8176	6	13	NULL	NULL	NULL	CaN	GP		bind					AKAP	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_7_866_s_115	15087426	40 From their studies, the authors concluded not only that AKAP79, PKA, CaN, and membrane-associated guanylate kinase are assembled in a macromolecular complex in intact cells but also that, by FRET imaging, CaN and PKA bind to AKAP 79 within 5 nm of each other, thus extending our understanding of the level of molecular compartmentation of signaling proteins that is made possible by scaffolding proteins.	bind
27076	2	8176	6	13	NULL	NULL	NULL	PKA	GP		bind					AKAP	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_7_866_s_115	15087426	40 From their studies, the authors concluded not only that AKAP79, PKA, CaN, and membrane-associated guanylate kinase are assembled in a macromolecular complex in intact cells but also that, by FRET imaging, CaN and PKA bind to AKAP 79 within 5 nm of each other, thus extending our understanding of the level of molecular compartmentation of signaling proteins that is made possible by scaffolding proteins.	bind
27077	3	8176	6	13	NULL	NULL	NULL	AKAP79	GP		is assembled in					macromolecular complex	GP				NULL	intact cells	NULL	NULL	NULL	NULL	gw70_circulationres_94_7_866_s_115	15087426	40 From their studies, the authors concluded not only that AKAP79, PKA, CaN, and membrane-associated guanylate kinase are assembled in a macromolecular complex in intact cells but also that, by FRET imaging, CaN and PKA bind to AKAP 79 within 5 nm of each other, thus extending our understanding of the level of molecular compartmentation of signaling proteins that is made possible by scaffolding proteins.	bind
27078	4	8176	6	13	NULL	NULL	NULL	PKA	GP		is assembled in					macromolecular complex	GP				NULL	intact cells	NULL	NULL	NULL	NULL	gw70_circulationres_94_7_866_s_115	15087426	40 From their studies, the authors concluded not only that AKAP79, PKA, CaN, and membrane-associated guanylate kinase are assembled in a macromolecular complex in intact cells but also that, by FRET imaging, CaN and PKA bind to AKAP 79 within 5 nm of each other, thus extending our understanding of the level of molecular compartmentation of signaling proteins that is made possible by scaffolding proteins.	bind
27079	5	8176	6	13	NULL	NULL	NULL	CaN	GP		is assembled in					macromolecular complex	GP				NULL	intact cells	NULL	NULL	NULL	NULL	gw70_circulationres_94_7_866_s_115	15087426	40 From their studies, the authors concluded not only that AKAP79, PKA, CaN, and membrane-associated guanylate kinase are assembled in a macromolecular complex in intact cells but also that, by FRET imaging, CaN and PKA bind to AKAP 79 within 5 nm of each other, thus extending our understanding of the level of molecular compartmentation of signaling proteins that is made possible by scaffolding proteins.	bind
27080	6	8176	6	13	NULL	NULL	NULL	guanylate kinase	GP	membrane associated	is assembled in					macromolecular complex	GP				NULL	intact cells	NULL	NULL	NULL	NULL	gw70_circulationres_94_7_866_s_115	15087426	40 From their studies, the authors concluded not only that AKAP79, PKA, CaN, and membrane-associated guanylate kinase are assembled in a macromolecular complex in intact cells but also that, by FRET imaging, CaN and PKA bind to AKAP 79 within 5 nm of each other, thus extending our understanding of the level of molecular compartmentation of signaling proteins that is made possible by scaffolding proteins.	bind
32756	1	8176	7	NULL	NULL	0	NULL	AKAP79	NULL		assemble in	NULL				macromolecular complex	NULL				NULL	intact cells	0	NULL	NULL	NULL	gw70_circulationres_94_7_866_s_115	15087426	40 From their studies, the authors concluded not only that AKAP79, PKA, CaN, and membrane-associated guanylate kinase are assembled in a macromolecular complex in intact cells but also that, by FRET imaging, CaN and PKA bind to AKAP 79 within 5 nm of each other, thus extending our understanding of the level of molecular compartmentation of signaling proteins that is made possible by scaffolding proteins.	bind
32757	2	8176	7	NULL	NULL	0	NULL	PKA	NULL		assemble in	NULL				macromolecular complex	NULL				NULL	intact cells	NULL	NULL	NULL	NULL	gw70_circulationres_94_7_866_s_115	15087426	40 From their studies, the authors concluded not only that AKAP79, PKA, CaN, and membrane-associated guanylate kinase are assembled in a macromolecular complex in intact cells but also that, by FRET imaging, CaN and PKA bind to AKAP 79 within 5 nm of each other, thus extending our understanding of the level of molecular compartmentation of signaling proteins that is made possible by scaffolding proteins.	bind
32758	3	8176	7	NULL	NULL	0	NULL	CaN	NULL		assemble in	NULL				macromolecular complex	NULL				NULL	intact cells	0	NULL	NULL	NULL	gw70_circulationres_94_7_866_s_115	15087426	40 From their studies, the authors concluded not only that AKAP79, PKA, CaN, and membrane-associated guanylate kinase are assembled in a macromolecular complex in intact cells but also that, by FRET imaging, CaN and PKA bind to AKAP 79 within 5 nm of each other, thus extending our understanding of the level of molecular compartmentation of signaling proteins that is made possible by scaffolding proteins.	bind
32759	4	8176	7	10	NULL	0	NULL	guanylate kinase	NULL	membrane-associated	assemble in	NULL				macromolecular complex	NULL				NULL	intact cells	NULL	NULL	NULL	NULL	gw70_circulationres_94_7_866_s_115	15087426	40 From their studies, the authors concluded not only that AKAP79, PKA, CaN, and membrane-associated guanylate kinase are assembled in a macromolecular complex in intact cells but also that, by FRET imaging, CaN and PKA bind to AKAP 79 within 5 nm of each other, thus extending our understanding of the level of molecular compartmentation of signaling proteins that is made possible by scaffolding proteins.	bind
32760	5	8176	7	NULL	NULL	0	NULL	CaN	NULL		binds to	NULL				AKAP 79	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_7_866_s_115	15087426	40 From their studies, the authors concluded not only that AKAP79, PKA, CaN, and membrane-associated guanylate kinase are assembled in a macromolecular complex in intact cells but also that, by FRET imaging, CaN and PKA bind to AKAP 79 within 5 nm of each other, thus extending our understanding of the level of molecular compartmentation of signaling proteins that is made possible by scaffolding proteins.	bind
32761	6	8176	7	NULL	NULL	0	NULL	PKA	NULL		binds to	NULL				AKAP 79	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_7_866_s_115	15087426	40 From their studies, the authors concluded not only that AKAP79, PKA, CaN, and membrane-associated guanylate kinase are assembled in a macromolecular complex in intact cells but also that, by FRET imaging, CaN and PKA bind to AKAP 79 within 5 nm of each other, thus extending our understanding of the level of molecular compartmentation of signaling proteins that is made possible by scaffolding proteins.	bind
27081	1	8177	6	13	NULL	NULL	NULL	CaM	GP		bind					Ral	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1315_s_127	15130921	40 It has been described that binding of CaM to Ral in the presence of Ca2+ stimulates GTP binding to Ral.	bind
27082	2	8177	6	13	NULL	NULL	NULL	GTP	Chemical		bind					Ral	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1315_s_127	15130921	40 It has been described that binding of CaM to Ral in the presence of Ca2+ stimulates GTP binding to Ral.	bind
27084	3	8177	6	13	NULL	NULL	NULL	statement 1	Process		occurs in presence of					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1315_s_127	15130921	40 It has been described that binding of CaM to Ral in the presence of Ca2+ stimulates GTP binding to Ral.	bind
27085	4	8177	6	13	NULL	NULL	NULL	statement 3	Process		stimulates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1315_s_127	15130921	40 It has been described that binding of CaM to Ral in the presence of Ca2+ stimulates GTP binding to Ral.	bind
32762	1	8177	7	NULL	NULL	0	NULL	CaM	NULL		bind	NULL				Ral	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1315_s_127	15130921	40 It has been described that binding of CaM to Ral in the presence of Ca2+ stimulates GTP binding to Ral.	bind
32763	2	8177	7	NULL	NULL	0	NULL	statement 1	NULL		in presence of	NULL				Ca2+	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1315_s_127	15130921	40 It has been described that binding of CaM to Ral in the presence of Ca2+ stimulates GTP binding to Ral.	bind
32764	3	8177	7	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				Ral	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1315_s_127	15130921	40 It has been described that binding of CaM to Ral in the presence of Ca2+ stimulates GTP binding to Ral.	bind
32765	4	8177	7	NULL	NULL	0	NULL	statement 1	NULL		stimulates	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1315_s_127	15130921	40 It has been described that binding of CaM to Ral in the presence of Ca2+ stimulates GTP binding to Ral.	bind
27086	1	8181	6	13	NULL	NULL	NULL	p53	GP		bind		sequence specifically			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4462_s_420	11691934	41       Gu,W. and Roeder,R.G. (1997) Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.	bind
27087	2	8181	6	13	NULL	NULL	NULL	statement 1	Process	activation of	occurs by					p53	GP	acetylation of	p53 C-terminal domain		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4462_s_420	11691934	41       Gu,W. and Roeder,R.G. (1997) Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.	bind
27102	1	8182	6	13	NULL	NULL	NULL	vWF	GP		bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3578_s_249	9437208	41  However, HEP-PG enhanced, rather than inhibited, the binding of vWf to collagen (Fig 8  ), which is mediated also by other domains of the vWf molecule than the A1 domain, where the GP Ib- and heparin-binding areas are located.	bind
27103	2	8182	6	13	NULL	NULL	NULL	HEP-PG	GP		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3578_s_249	9437208	41  However, HEP-PG enhanced, rather than inhibited, the binding of vWf to collagen (Fig 8  ), which is mediated also by other domains of the vWf molecule than the A1 domain, where the GP Ib- and heparin-binding areas are located.	bind
32766	1	8182	7	NULL	NULL	0	NULL	vWf	NULL		bind	NULL				collagen	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3578_s_249	9437208	41  However, HEP-PG enhanced, rather than inhibited, the binding of vWf to collagen (Fig 8  ), which is mediated also by other domains of the vWf molecule than the A1 domain, where the GP Ib- and heparin-binding areas are located.	bind
32767	2	8182	7	NULL	NULL	0	NULL	HEP-PG	NULL		enhance	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3578_s_249	9437208	41  However, HEP-PG enhanced, rather than inhibited, the binding of vWf to collagen (Fig 8  ), which is mediated also by other domains of the vWf molecule than the A1 domain, where the GP Ib- and heparin-binding areas are located.	bind
32768	3	8182	7	NULL	NULL	0	NULL	GP Ib binding site	NULL		is located in	NULL				 vWf molecule	NULL		A1 domain		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3578_s_249	9437208	41  However, HEP-PG enhanced, rather than inhibited, the binding of vWf to collagen (Fig 8  ), which is mediated also by other domains of the vWf molecule than the A1 domain, where the GP Ib- and heparin-binding areas are located.	bind
32769	4	8182	7	NULL	NULL	0	NULL	heparin-binding site	NULL		is located in	NULL				vWf molecule	NULL		A1 domain		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3578_s_249	9437208	41  However, HEP-PG enhanced, rather than inhibited, the binding of vWf to collagen (Fig 8  ), which is mediated also by other domains of the vWf molecule than the A1 domain, where the GP Ib- and heparin-binding areas are located.	bind
27104	1	8183	6	13	NULL	NULL	NULL	TnI	GP		bind		tightly			actin-Tm	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_82_2_261_s_316	9468197	41  In diastole, the actin-myosin reaction is believed to be inhibited in part by tight binding of TnI to actin-Tm.	bind
27105	2	8183	6	13	NULL	NULL	NULL	actin	GP		bind					myosin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_82_2_261_s_316	9468197	41  In diastole, the actin-myosin reaction is believed to be inhibited in part by tight binding of TnI to actin-Tm.	bind
27106	3	8183	6	13	NULL	NULL	NULL	statement 1	Process		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_82_2_261_s_316	9468197	41  In diastole, the actin-myosin reaction is believed to be inhibited in part by tight binding of TnI to actin-Tm.	bind
32770	1	8183	7	NULL	NULL	0	NULL	TnI	NULL		bind	NULL	tightly			actin-Tm	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_82_2_261_s_316	9468197	41  In diastole, the actin-myosin reaction is believed to be inhibited in part by tight binding of TnI to actin-Tm.	bind
32771	2	8183	7	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				actin-myosin reaction	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_82_2_261_s_316	9468197	41  In diastole, the actin-myosin reaction is believed to be inhibited in part by tight binding of TnI to actin-Tm.	bind
27518	1	8185	6	13	NULL	NULL	NULL	serum response factors	GP		bind									CArG element of promoter	NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_3_871_s_327	10079265	41  To express alpha-SMA in response to TGF-beta1, smooth muscle cells require the binding of an undescribed factor to a TGF-beta1 control element along with the binding of serum response factors to two CArG elements in the promoter region.	bind
27519	2	8185	6	13	NULL	NULL	NULL	alpha-SMA	GP	expression of	is in response to					TGF-beta1	GP				NULL	smooth muscle cells	NULL	NULL	NULL	NULL	gw60_amjpathol_154_3_871_s_327	10079265	41  To express alpha-SMA in response to TGF-beta1, smooth muscle cells require the binding of an undescribed factor to a TGF-beta1 control element along with the binding of serum response factors to two CArG elements in the promoter region.	bind
27520	3	8185	6	13	NULL	NULL	NULL	statement 2	Process		requires					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_3_871_s_327	10079265	41  To express alpha-SMA in response to TGF-beta1, smooth muscle cells require the binding of an undescribed factor to a TGF-beta1 control element along with the binding of serum response factors to two CArG elements in the promoter region.	bind
32772	1	8185	7	NULL	NULL	0	NULL	serum response factors	NULL		bind	NULL					NULL			CArG elements	NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_3_871_s_327	10079265	41  To express alpha-SMA in response to TGF-beta1, smooth muscle cells require the binding of an undescribed factor to a TGF-beta1 control element along with the binding of serum response factors to two CArG elements in the promoter region.	bind
32773	2	8185	7	10	NULL	0	NULL	alpha-SMA 		expression of	in response to					TGF-beta1					NULL	smooth muscle cells	NULL	NULL	NULL	NULL	gw60_amjpathol_154_3_871_s_327	10079265	41  To express alpha-SMA in response to TGF-beta1, smooth muscle cells require the binding of an undescribed factor to a TGF-beta1 control element along with the binding of serum response factors to two CArG elements in the promoter region.	bind
55945	3	8185	7	10	NULL	0	NULL	statement 2			requires					statement 1					NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_3_871_s_327	10079265	41  To express alpha-SMA in response to TGF-beta1, smooth muscle cells require the binding of an undescribed factor to a TGF-beta1 control element along with the binding of serum response factors to two CArG elements in the promoter region.	bind
27107	1	8186	6	13	NULL	NULL	NULL	PG	GP		bind					EC	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_164_s_201	9012652	41  To our knowledge, we are the first to observe acute (within 15 minutes) modulation of PG binding to ECs.	bind
32774	1	8186	7	NULL	NULL	0	NULL	PG	NULL		bind	NULL				ECs	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_164_s_201	9012652	41  To our knowledge, we are the first to observe acute (within 15 minutes) modulation of PG binding to ECs.	bind
27108	1	8187	6	13	NULL	NULL	NULL	TFPI	GP		bind					factor Xa	GP		active site		NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_257	7586275	41 42  In the first step, TFPI binds to the active site of factor Xa, with formation of a TFPI - factor Xa complex with inhibited factor Xa activity.	bind
27109	2	8187	6	13	NULL	NULL	NULL	statement 1	GP		forms					TFPI - factor Xa complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_257	7586275	41 42  In the first step, TFPI binds to the active site of factor Xa, with formation of a TFPI - factor Xa complex with inhibited factor Xa activity.	bind
27110	3	8187	6	13	NULL	NULL	NULL	statement 2	Process		exhibits					factor Xa	GP	inhibited activity of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_257	7586275	41 42  In the first step, TFPI binds to the active site of factor Xa, with formation of a TFPI - factor Xa complex with inhibited factor Xa activity.	bind
32775	1	8187	7	NULL	NULL	0	NULL	TFPI	NULL		binds to	NULL				factor Xa	NULL		active site		NULL		0	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_257	7586275	41 42  In the first step, TFPI binds to the active site of factor Xa, with formation of a TFPI - factor Xa complex with inhibited factor Xa activity.	bind
32776	2	8187	7	10	NULL	0	NULL	statement 1	NULL		forms	NULL				TFPI - factor Xa complex 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_257	7586275	41 42  In the first step, TFPI binds to the active site of factor Xa, with formation of a TFPI - factor Xa complex with inhibited factor Xa activity.	bind
32777	3	8187	7	10	NULL	0	NULL	statement 2	NULL		exhibits	NULL				factor Xa	NULL	inhibited activity of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_257	7586275	41 42  In the first step, TFPI binds to the active site of factor Xa, with formation of a TFPI - factor Xa complex with inhibited factor Xa activity.	bind
27111	1	8188	6	13	NULL	NULL	NULL	importin-alpha	GP		bind			amino acid motif		importin-beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_18_1031_s_161	9740803	41 amino acid motif in importin-alpha confers binding to importin-beta and hence transit into the nucleus.	bind
27112	2	8188	6	13	NULL	NULL	NULL	importin-alpha	GP		transits into					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_18_1031_s_161	9740803	41 amino acid motif in importin-alpha confers binding to importin-beta and hence transit into the nucleus.	bind
27113	3	8188	6	13	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_18_1031_s_161	9740803	41 amino acid motif in importin-alpha confers binding to importin-beta and hence transit into the nucleus.	bind
32778	1	8188	7	NULL	NULL	0	NULL	 importin-alpha	NULL		binds to	NULL		amino acid motif		 importin-beta	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_8_18_1031_s_161	9740803	41 amino acid motif in importin-alpha confers binding to importin-beta and hence transit into the nucleus.	bind
32779	2	8188	7	NULL	NULL	0	NULL	statement 1	NULL		transit into	NULL				nucleus	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_8_18_1031_s_161	9740803	41 amino acid motif in importin-alpha confers binding to importin-beta and hence transit into the nucleus.	bind
27114	1	8189	6	13	NULL	NULL	NULL	aptamer	NucleicAcid		bind		poorly			bFGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_9_5028_s_116	12692304	41 aptamer and the control Scramble RNA bound equally poorly to bFGF ( Kd   100 nM).	bind
27115	2	8189	6	13	NULL	NULL	NULL	Scramble RNA	NucleicAcid	control	bind		poorly			bFGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_9_5028_s_116	12692304	41 aptamer and the control Scramble RNA bound equally poorly to bFGF ( Kd   100 nM).	bind
27116	3	8189	6	13	NULL	NULL	NULL	statement 1	Process	affinity of	is equal to					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_9_5028_s_116	12692304	41 aptamer and the control Scramble RNA bound equally poorly to bFGF ( Kd   100 nM).	bind
32780	1	8189	7	NULL	NULL	0	NULL	aptamer	NULL		bind	NULL	poorly			bFGF	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_100_9_5028_s_116	12692304	41 aptamer and the control Scramble RNA bound equally poorly to bFGF ( Kd   100 nM).	bind
32781	2	8189	7	10	NULL	0	NULL	Scramble RNA	NULL	control	bind	NULL	poorly			bFGF	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_9_5028_s_116	12692304	41 aptamer and the control Scramble RNA bound equally poorly to bFGF ( Kd   100 nM).	bind
55946	3	8189	7	10	NULL	0	NULL	statement 1		affinity of	is equal to					statement 2		affinity of			NULL		0	NULL	NULL	NULL	gw60_pnas_100_9_5028_s_116	12692304	41 aptamer and the control Scramble RNA bound equally poorly to bFGF ( Kd   100 nM).	bind
27117	1	8190	6	13	NULL	NULL	NULL	Grb2	GP		bind		directly			SHP-2	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_81	12689916	41 Because both Grb2 65,66  and Gab1 67 can bind directly to tyrosine-phosphorylated SHP-2, it is possible that PECAM-1/SHP-2/Gab1 and PECAM-1/SHP-2/Grb2 ternary signaling complexes may form in response to certain forms of cellular stimulation.	bind
27118	2	8190	6	13	NULL	NULL	NULL	Gab1	GP		bind		directly			SHP-2	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_81	12689916	41 Because both Grb2 65,66  and Gab1 67 can bind directly to tyrosine-phosphorylated SHP-2, it is possible that PECAM-1/SHP-2/Gab1 and PECAM-1/SHP-2/Grb2 ternary signaling complexes may form in response to certain forms of cellular stimulation.	bind
27521	3	8190	6	13	NULL	NULL	NULL	PECAM-1/SHP-2/Gab1 complex	GP	formation of	occurs in response to		may			cellular stimulation	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_81	12689916	41 Because both Grb2 65,66  and Gab1 67 can bind directly to tyrosine-phosphorylated SHP-2, it is possible that PECAM-1/SHP-2/Gab1 and PECAM-1/SHP-2/Grb2 ternary signaling complexes may form in response to certain forms of cellular stimulation.	bind
27522	4	8190	6	13	NULL	NULL	NULL	PECAM-1/SHP-2/Grb2 complex	GP	formation of	occurs in response to		may			cellular stimulation	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_81	12689916	41 Because both Grb2 65,66  and Gab1 67 can bind directly to tyrosine-phosphorylated SHP-2, it is possible that PECAM-1/SHP-2/Gab1 and PECAM-1/SHP-2/Grb2 ternary signaling complexes may form in response to certain forms of cellular stimulation.	bind
32782	1	8190	7	NULL	NULL	0	NULL	Grb2	NULL		bind	NULL	directly			SHP-2	NULL	phosphorylated	tyrosine		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_81	12689916	41 Because both Grb2 65,66  and Gab1 67 can bind directly to tyrosine-phosphorylated SHP-2, it is possible that PECAM-1/SHP-2/Gab1 and PECAM-1/SHP-2/Grb2 ternary signaling complexes may form in response to certain forms of cellular stimulation.	bind
32783	2	8190	7	NULL	NULL	0	NULL	Gab1	NULL		bind	NULL	directly			SHP-2	NULL	phosphorylated	tyrosine		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_81	12689916	41 Because both Grb2 65,66  and Gab1 67 can bind directly to tyrosine-phosphorylated SHP-2, it is possible that PECAM-1/SHP-2/Gab1 and PECAM-1/SHP-2/Grb2 ternary signaling complexes may form in response to certain forms of cellular stimulation.	bind
32784	3	8190	7	NULL	NULL	0	NULL	cell stimulation	NULL		form	NULL	may			PECAM-1/SHP-2/Gab1 ternary complexes	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_81	12689916	41 Because both Grb2 65,66  and Gab1 67 can bind directly to tyrosine-phosphorylated SHP-2, it is possible that PECAM-1/SHP-2/Gab1 and PECAM-1/SHP-2/Grb2 ternary signaling complexes may form in response to certain forms of cellular stimulation.	bind
32785	4	8190	7	NULL	NULL	0	NULL	cell stimulation	NULL		form	NULL	may			PECAM-1/SHP-2/Grb2 ternary signaling complexes	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_81	12689916	41 Because both Grb2 65,66  and Gab1 67 can bind directly to tyrosine-phosphorylated SHP-2, it is possible that PECAM-1/SHP-2/Gab1 and PECAM-1/SHP-2/Grb2 ternary signaling complexes may form in response to certain forms of cellular stimulation.	bind
27119	1	8191	6	13	NULL	NULL	NULL	Gab1	GP		does not bind		directly			PECAM-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_80	12689916	41 Immunoprecipitation experiments, however, were unable to demonstrate direct binding of Gab1 to PECAM-1.	bind
32997	1	8191	7	10	NULL	0	NULL	Gab1	NULL		does not bind	NULL	directly			PECAM-1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_80	12689916	41 Immunoprecipitation experiments, however, were unable to demonstrate direct binding of Gab1 to PECAM-1.	bind
27120	1	8192	6	13	NULL	NULL	NULL	IalphaI	GP		bind		weakly			serine proteinases	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1267_s_232	9777958	41 In addition, IalphaI and bikunin bind weakly with serine proteinases and consequently even at high enzyme/inhibitor ratios they have little effect on elastase and cathepsin G activity.	bind
27121	2	8192	6	13	NULL	NULL	NULL	bikunin	GP		bind		weakly			serine proteinases	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1267_s_232	9777958	41 In addition, IalphaI and bikunin bind weakly with serine proteinases and consequently even at high enzyme/inhibitor ratios they have little effect on elastase and cathepsin G activity.	bind
27122	3	8192	6	13	NULL	NULL	NULL	IalphaI	GP		has little effect on					elastase 	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1267_s_232	9777958	41 In addition, IalphaI and bikunin bind weakly with serine proteinases and consequently even at high enzyme/inhibitor ratios they have little effect on elastase and cathepsin G activity.	bind
27123	4	8192	6	13	NULL	NULL	NULL	IalphaI	GP		has little effect on					cathepsin G	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1267_s_232	9777958	41 In addition, IalphaI and bikunin bind weakly with serine proteinases and consequently even at high enzyme/inhibitor ratios they have little effect on elastase and cathepsin G activity.	bind
27124	5	8192	6	13	NULL	NULL	NULL	bikunin	GP		has little effect on					elastase	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1267_s_232	9777958	41 In addition, IalphaI and bikunin bind weakly with serine proteinases and consequently even at high enzyme/inhibitor ratios they have little effect on elastase and cathepsin G activity.	bind
27125	6	8192	6	13	NULL	NULL	NULL	bikunin	GP		has little effect on					cathepsin G	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1267_s_232	9777958	41 In addition, IalphaI and bikunin bind weakly with serine proteinases and consequently even at high enzyme/inhibitor ratios they have little effect on elastase and cathepsin G activity.	bind
32998	1	8192	7	NULL	NULL	0	NULL	IalphaI 	NULL		bind	NULL	weakly			serine proteinases	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_4_1267_s_232	9777958	41 In addition, IalphaI and bikunin bind weakly with serine proteinases and consequently even at high enzyme/inhibitor ratios they have little effect on elastase and cathepsin G activity.	bind
32999	2	8192	7	NULL	NULL	0	NULL	bikunin 	NULL		bind	NULL	weakly			serine proteinases	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_4_1267_s_232	9777958	41 In addition, IalphaI and bikunin bind weakly with serine proteinases and consequently even at high enzyme/inhibitor ratios they have little effect on elastase and cathepsin G activity.	bind
33000	3	8192	7	10	NULL	0	NULL	IalphaI	NULL		little effect on	NULL				elastase	NULL	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1267_s_232	9777958	41 In addition, IalphaI and bikunin bind weakly with serine proteinases and consequently even at high enzyme/inhibitor ratios they have little effect on elastase and cathepsin G activity.	bind
33001	4	8192	7	10	NULL	0	NULL	 IalphaI 	NULL		little effect on	NULL				cathepsin G	NULL	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1267_s_232	9777958	41 In addition, IalphaI and bikunin bind weakly with serine proteinases and consequently even at high enzyme/inhibitor ratios they have little effect on elastase and cathepsin G activity.	bind
33002	5	8192	7	10	NULL	0	NULL	bikunin	NULL		little effect on	NULL				elastase	NULL	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1267_s_232	9777958	41 In addition, IalphaI and bikunin bind weakly with serine proteinases and consequently even at high enzyme/inhibitor ratios they have little effect on elastase and cathepsin G activity.	bind
33003	6	8192	7	10	NULL	0	NULL	bikunin	NULL		little effect on	NULL				cathepsin G	NULL	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_4_1267_s_232	9777958	41 In addition, IalphaI and bikunin bind weakly with serine proteinases and consequently even at high enzyme/inhibitor ratios they have little effect on elastase and cathepsin G activity.	bind
27523	1	8193	6	13	NULL	NULL	NULL	repressor	GP	absence of;;bound	increase					PAI-1	GP	basal;; transcription of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_3_304_s_135	11804984	41 In the absence of the bound repressor, basal and stimulated PAI-1 transcription is increased.	bind
27524	2	8193	6	13	NULL	NULL	NULL	repressor	GP	absence of;;bound	increase					PAI-1	GP	stimulated;;transcription of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_3_304_s_135	11804984	41 In the absence of the bound repressor, basal and stimulated PAI-1 transcription is increased.	bind
33006	1	8193	7	10	NULL	0	NULL	repressor	NULL	absence of;;bound	increase	NULL				PAI-1	NULL	basal;; transcription of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_3_304_s_135	11804984	41 In the absence of the bound repressor, basal and stimulated PAI-1 transcription is increased.	bind
33009	2	8193	7	10	NULL	0	NULL	repressor	NULL	absence of;;bound	increase	NULL				PAI-1	NULL	stimulated;;transcription of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_3_304_s_135	11804984	41 In the absence of the bound repressor, basal and stimulated PAI-1 transcription is increased.	bind
27126	1	8194	6	13	NULL	NULL	NULL				bind			MyBP-C motif 		S2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_5_594_s_215	11909824	41, 42 Although data from the present study do not address direct or indirect effects of MyBP-C motif binding to S2, the cMyBP-C-/- knockout mice provide an ideal null background on which to test the different hypotheses because competitive effects of endogenous cMyBP-C can be excluded.	bind
33014	1	8194	7	10	NULL	0	NULL		NULL		bind	NULL		MyBP-C motif 		S2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_5_594_s_215	11909824	41, 42 Although data from the present study do not address direct or indirect effects of MyBP-C motif binding to S2, the cMyBP-C-/- knockout mice provide an ideal null background on which to test the different hypotheses because competitive effects of endogenous cMyBP-C can be excluded.	bind
27127	1	8195	6	13	NULL	NULL	NULL	PU.1	GP		bind			activation domain		RB protein	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_429	11504882	42       Hagemeier,C., Bannister,A.J., Cook,A. and Kouzarides,T. (1993) The activation domain of the transcription factor PU.1 binds the retinoblastoma (RB) protein and the transcription factor TFIID  in vitro: RB shows sequence similarity to TFIID and TFIIB.	bind
27128	2	8195	6	13	NULL	NULL	NULL	PU.1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_429	11504882	42       Hagemeier,C., Bannister,A.J., Cook,A. and Kouzarides,T. (1993) The activation domain of the transcription factor PU.1 binds the retinoblastoma (RB) protein and the transcription factor TFIID  in vitro: RB shows sequence similarity to TFIID and TFIIB.	bind
27129	3	8195	6	13	NULL	NULL	NULL	RB	GP		is					retinoblastoma	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_429	11504882	42       Hagemeier,C., Bannister,A.J., Cook,A. and Kouzarides,T. (1993) The activation domain of the transcription factor PU.1 binds the retinoblastoma (RB) protein and the transcription factor TFIID  in vitro: RB shows sequence similarity to TFIID and TFIIB.	bind
27130	4	8195	6	13	NULL	NULL	NULL	PU.1	GP		bind			activation domain		TFIID	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_429	11504882	42       Hagemeier,C., Bannister,A.J., Cook,A. and Kouzarides,T. (1993) The activation domain of the transcription factor PU.1 binds the retinoblastoma (RB) protein and the transcription factor TFIID  in vitro: RB shows sequence similarity to TFIID and TFIIB.	bind
27131	5	8195	6	13	NULL	NULL	NULL	TFIID	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_429	11504882	42       Hagemeier,C., Bannister,A.J., Cook,A. and Kouzarides,T. (1993) The activation domain of the transcription factor PU.1 binds the retinoblastoma (RB) protein and the transcription factor TFIID  in vitro: RB shows sequence similarity to TFIID and TFIIB.	bind
27132	6	8195	6	13	NULL	NULL	NULL	RB	GP	sequence of	is similar to					TFIID	GP	sequence of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_429	11504882	42       Hagemeier,C., Bannister,A.J., Cook,A. and Kouzarides,T. (1993) The activation domain of the transcription factor PU.1 binds the retinoblastoma (RB) protein and the transcription factor TFIID  in vitro: RB shows sequence similarity to TFIID and TFIIB.	bind
27133	7	8195	6	13	NULL	NULL	NULL	RB	GP	sequence of	is similar to					TFIIB	GP	sequence of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_429	11504882	42       Hagemeier,C., Bannister,A.J., Cook,A. and Kouzarides,T. (1993) The activation domain of the transcription factor PU.1 binds the retinoblastoma (RB) protein and the transcription factor TFIID  in vitro: RB shows sequence similarity to TFIID and TFIIB.	bind
33019	1	8195	7	NULL	NULL	0	NULL	PU.1	NULL		binds	NULL		activation domain		RB protein	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_429	11504882	42       Hagemeier,C., Bannister,A.J., Cook,A. and Kouzarides,T. (1993) The activation domain of the transcription factor PU.1 binds the retinoblastoma (RB) protein and the transcription factor TFIID  in vitro: RB shows sequence similarity to TFIID and TFIIB.	bind
33020	2	8195	7	NULL	NULL	0	NULL	PU.1	NULL		binds	NULL		activation domain		TFIID	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_429	11504882	42       Hagemeier,C., Bannister,A.J., Cook,A. and Kouzarides,T. (1993) The activation domain of the transcription factor PU.1 binds the retinoblastoma (RB) protein and the transcription factor TFIID  in vitro: RB shows sequence similarity to TFIID and TFIIB.	bind
33022	3	8195	7	NULL	NULL	0	NULL	PU.1	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_429	11504882	42       Hagemeier,C., Bannister,A.J., Cook,A. and Kouzarides,T. (1993) The activation domain of the transcription factor PU.1 binds the retinoblastoma (RB) protein and the transcription factor TFIID  in vitro: RB shows sequence similarity to TFIID and TFIIB.	bind
33023	4	8195	7	NULL	NULL	0	NULL	TFIID	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_429	11504882	42       Hagemeier,C., Bannister,A.J., Cook,A. and Kouzarides,T. (1993) The activation domain of the transcription factor PU.1 binds the retinoblastoma (RB) protein and the transcription factor TFIID  in vitro: RB shows sequence similarity to TFIID and TFIIB.	bind
33024	5	8195	7	NULL	NULL	0	NULL	RB	NULL	Sequence of	is similar to	NULL				TFIID	NULL	sequence of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_429	11504882	42       Hagemeier,C., Bannister,A.J., Cook,A. and Kouzarides,T. (1993) The activation domain of the transcription factor PU.1 binds the retinoblastoma (RB) protein and the transcription factor TFIID  in vitro: RB shows sequence similarity to TFIID and TFIIB.	bind
33025	6	8195	7	NULL	NULL	0	NULL	RB	NULL	sequence of	is similar to	NULL				TFIIB	NULL	sequence of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_429	11504882	42       Hagemeier,C., Bannister,A.J., Cook,A. and Kouzarides,T. (1993) The activation domain of the transcription factor PU.1 binds the retinoblastoma (RB) protein and the transcription factor TFIID  in vitro: RB shows sequence similarity to TFIID and TFIIB.	bind
46606	7	8195	7	10	NULL	0	NULL	RB	NULL		is	NULL				retinoblastoma	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_429	11504882	42       Hagemeier,C., Bannister,A.J., Cook,A. and Kouzarides,T. (1993) The activation domain of the transcription factor PU.1 binds the retinoblastoma (RB) protein and the transcription factor TFIID  in vitro: RB shows sequence similarity to TFIID and TFIIB.	bind
27525	1	8196	6	13	NULL	NULL	NULL	U1A	GP		is a type of					spliceosomal protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_550_s_390	11788718	42       Rimmele,M. and Belasco,J. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
27526	2	8196	6	13	NULL	NULL	NULL	U2B'''	GP		is a type of					splicosomal protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_550_s_390	11788718	42       Rimmele,M. and Belasco,J. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
27527	3	8196	6	13	NULL	NULL	NULL	U2A"	GP		is a type of					ancillary protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_550_s_390	11788718	42       Rimmele,M. and Belasco,J. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
27528	4	8196	6	13	NULL	NULL	NULL	U1A	GP		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_550_s_390	11788718	42       Rimmele,M. and Belasco,J. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
27529	5	8196	6	13	NULL	NULL	NULL	U2B"'	GP		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_550_s_390	11788718	42       Rimmele,M. and Belasco,J. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
33026	1	8196	7	NULL	NULL	0	NULL	U1A 	NULL		bind	NULL				RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_550_s_390	11788718	42       Rimmele,M. and Belasco,J. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
33027	2	8196	7	10	NULL	0	NULL	U2B"'	NULL		bind	NULL				RNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_550_s_390	11788718	42       Rimmele,M. and Belasco,J. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
33028	3	8196	7	NULL	NULL	0	NULL	U1A	NULL		is a type of	NULL				spliceosomal proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_550_s_390	11788718	42       Rimmele,M. and Belasco,J. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
33029	4	8196	7	10	NULL	0	NULL	U2B"'	NULL		is a type of	NULL				spliceosomal proteins	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_550_s_390	11788718	42       Rimmele,M. and Belasco,J. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
46607	5	8196	7	10	NULL	0	NULL	U2A''	NULL		is a type of	NULL				ancillary protein	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_550_s_390	11788718	42       Rimmele,M. and Belasco,J. (1998) Target discrimination by RNA-binding proteins: role of the ancillary protein U2A'' and a critical leucine residue in differentiating the RNA-binding specificity of spliceosomal proteins U1A and U2B'''.	bind
33030	1	8197	7	13	NULL	NULL	NULL	protein	GP	mutant	bind					HDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_1_210_s_176	10634820	42  Although replacement of various amino acids in the  C-terminus demonstrated that substitution of specifically charged residues between 195 and 238 did not affect the binding of mutant protein to HDL, 16  penetration of exchangeable apolipoproteins in the phospholipid layer involves both electrostatic and hydrophobic interactions.	bind
33031	2	8197	7	NULL	NULL	0	NULL		NULL		substituted with	NULL		C-terminus aminoacid			NULL		charged residues between 195 and 238		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_1_210_s_176	10634820	42  Although replacement of various amino acids in the  C-terminus demonstrated that substitution of specifically charged residues between 195 and 238 did not affect the binding of mutant protein to HDL, 16  penetration of exchangeable apolipoproteins in the phospholipid layer involves both electrostatic and hydrophobic interactions.	bind
33032	3	8197	7	13	NULL	NULL	NULL	statement 2	Process		does not affect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_1_210_s_176	10634820	42  Although replacement of various amino acids in the  C-terminus demonstrated that substitution of specifically charged residues between 195 and 238 did not affect the binding of mutant protein to HDL, 16  penetration of exchangeable apolipoproteins in the phospholipid layer involves both electrostatic and hydrophobic interactions.	bind
33033	4	8197	7	13	NULL	NULL	NULL	apolipoproteins	GP	penetration of	involves					electrostatic interactions	Process				NULL	phospholipid layer	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_1_210_s_176	10634820	42  Although replacement of various amino acids in the  C-terminus demonstrated that substitution of specifically charged residues between 195 and 238 did not affect the binding of mutant protein to HDL, 16  penetration of exchangeable apolipoproteins in the phospholipid layer involves both electrostatic and hydrophobic interactions.	bind
33034	5	8197	7	13	NULL	NULL	NULL	apolipoproteins	GP	penetration of	involves					hydrophobic interactions	Process				NULL	phospholipid layer	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_1_210_s_176	10634820	42  Although replacement of various amino acids in the  C-terminus demonstrated that substitution of specifically charged residues between 195 and 238 did not affect the binding of mutant protein to HDL, 16  penetration of exchangeable apolipoproteins in the phospholipid layer involves both electrostatic and hydrophobic interactions.	bind
27134	1	8198	6	13	NULL	NULL	NULL	FKBP12.6	GP		bind					FK506	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_6_990_s_31	8635249	42  FKBP12.6 binds FK506 and rapamycin and is a candidate for the form associated with the cardiac RyR.	bind
27135	2	8198	6	13	NULL	NULL	NULL	FKBP12.6	GP		bind					rapamycin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_6_990_s_31	8635249	42  FKBP12.6 binds FK506 and rapamycin and is a candidate for the form associated with the cardiac RyR.	bind
27136	3	8198	6	13	NULL	NULL	NULL	FKBP12.6	GP		is associated with					RyR 	GP	cardiac			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_6_990_s_31	8635249	42  FKBP12.6 binds FK506 and rapamycin and is a candidate for the form associated with the cardiac RyR.	bind
33035	1	8198	7	NULL	NULL	0	NULL	FKBP12.6	NULL		binds	NULL				FK506	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_6_990_s_31	8635249	42  FKBP12.6 binds FK506 and rapamycin and is a candidate for the form associated with the cardiac RyR.	bind
33036	2	8198	7	NULL	NULL	0	NULL	FKBP12.6	NULL		binds	NULL				rapamycin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_6_990_s_31	8635249	42  FKBP12.6 binds FK506 and rapamycin and is a candidate for the form associated with the cardiac RyR.	bind
33037	3	8198	7	10	NULL	0	NULL	FKBP12.6	NULL		is associated with	NULL				RyR	NULL	cardiac			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_6_990_s_31	8635249	42  FKBP12.6 binds FK506 and rapamycin and is a candidate for the form associated with the cardiac RyR.	bind
27137	2	8199	6	13	NULL	NULL	NULL	Egr-1	GP		bind					SRR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3406_s_244	9437186	42  Further studies are needed to show whether the suppression of Egr-1 binding to SRR-2 in cells treated with curcumin is the result of inhibition of de novo synthesis of Egr-1 or the diminished phosphorylation of Egr-1.	bind
27138	4	8199	6	13	NULL	NULL	NULL	statement 2	Process		suppressed in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3406_s_244	9437186	42  Further studies are needed to show whether the suppression of Egr-1 binding to SRR-2 in cells treated with curcumin is the result of inhibition of de novo synthesis of Egr-1 or the diminished phosphorylation of Egr-1.	bind
46608	1	8199	6	13	NULL	NULL	NULL	cells	Cell		is treated with					curcumin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3406_s_244	9437186	42  Further studies are needed to show whether the suppression of Egr-1 binding to SRR-2 in cells treated with curcumin is the result of inhibition of de novo synthesis of Egr-1 or the diminished phosphorylation of Egr-1.	bind
46609	3	8199	6	13	NULL	NULL	NULL	statement 2	Process		occurs in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3406_s_244	9437186	42  Further studies are needed to show whether the suppression of Egr-1 binding to SRR-2 in cells treated with curcumin is the result of inhibition of de novo synthesis of Egr-1 or the diminished phosphorylation of Egr-1.	bind
33038	2	8199	7	10	NULL	0	NULL	Egr-1	NULL		bind	NULL				SRR-2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3406_s_244	9437186	42  Further studies are needed to show whether the suppression of Egr-1 binding to SRR-2 in cells treated with curcumin is the result of inhibition of de novo synthesis of Egr-1 or the diminished phosphorylation of Egr-1.	bind
46610	1	8199	7	10	NULL	0	NULL	cells	NULL		is treated with	NULL				curcumin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3406_s_244	9437186	42  Further studies are needed to show whether the suppression of Egr-1 binding to SRR-2 in cells treated with curcumin is the result of inhibition of de novo synthesis of Egr-1 or the diminished phosphorylation of Egr-1.	bind
46611	3	8199	7	10	NULL	0	NULL	statement 2	NULL		occurs in	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3406_s_244	9437186	42  Further studies are needed to show whether the suppression of Egr-1 binding to SRR-2 in cells treated with curcumin is the result of inhibition of de novo synthesis of Egr-1 or the diminished phosphorylation of Egr-1.	bind
46612	4	8199	7	10	NULL	0	NULL	statement 2	NULL		suppressed in	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3406_s_244	9437186	42  Further studies are needed to show whether the suppression of Egr-1 binding to SRR-2 in cells treated with curcumin is the result of inhibition of de novo synthesis of Egr-1 or the diminished phosphorylation of Egr-1.	bind
27139	1	8200	6	13	NULL	NULL	NULL	TGF-betaR:Fc	GP		does not bind					TGF-beta2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_10_1212_s_232	10347096	42  Similarly, TGF-betaR:Fc used here did not bind TGF-beta2 in an ELISA (data not shown), which is consistent with the notion that this isoform requires presentation by betaglycan for binding to the TGF-betaRII.	bind
27154	2	8200	6	13	NULL	NULL	NULL	TGF-betaR:Fc	GP		bind					TGF-betaRII	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_10_1212_s_232	10347096	42  Similarly, TGF-betaR:Fc used here did not bind TGF-beta2 in an ELISA (data not shown), which is consistent with the notion that this isoform requires presentation by betaglycan for binding to the TGF-betaRII.	bind
27156	3	8200	6	13	NULL	NULL	NULL	statement 2	Process		requires					betaglycan	GP	presentation by 			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_10_1212_s_232	10347096	42  Similarly, TGF-betaR:Fc used here did not bind TGF-beta2 in an ELISA (data not shown), which is consistent with the notion that this isoform requires presentation by betaglycan for binding to the TGF-betaRII.	bind
33039	1	8200	7	NULL	NULL	0	NULL	TGF-betaR:Fc	NULL		does not bind	NULL				TGF-beta2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_10_1212_s_232	10347096	42  Similarly, TGF-betaR:Fc used here did not bind TGF-beta2 in an ELISA (data not shown), which is consistent with the notion that this isoform requires presentation by betaglycan for binding to the TGF-betaRII.	bind
33040	2	8200	7	NULL	NULL	0	NULL	TGF-betaR:Fc	NULL		bind	NULL				TGF-betaRII	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_10_1212_s_232	10347096	42  Similarly, TGF-betaR:Fc used here did not bind TGF-beta2 in an ELISA (data not shown), which is consistent with the notion that this isoform requires presentation by betaglycan for binding to the TGF-betaRII.	bind
33041	3	8200	7	NULL	NULL	0	NULL	statement 2	NULL		requires	NULL				betaglycan	NULL	presentation by 			NULL		0	NULL	NULL	NULL	gw60_circulationres_84_10_1212_s_232	10347096	42  Similarly, TGF-betaR:Fc used here did not bind TGF-beta2 in an ELISA (data not shown), which is consistent with the notion that this isoform requires presentation by betaglycan for binding to the TGF-betaRII.	bind
27158	1	8201	6	13	NULL	NULL	NULL	vWF	GP		bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3578_s_250	9437208	42  The enhanced binding of vWf to collagen may have sealed the platelet-activating domains of collagen.	bind
27162	2	8201	6	13	NULL	NULL	NULL	statement 1	Process		seal		may			collagen	GP		platelet-activating domain		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3578_s_250	9437208	42  The enhanced binding of vWf to collagen may have sealed the platelet-activating domains of collagen.	bind
33042	1	8201	7	NULL	NULL	0	NULL	vWf	NULL		bind	NULL				collagen	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3578_s_250	9437208	42  The enhanced binding of vWf to collagen may have sealed the platelet-activating domains of collagen.	bind
33043	2	8201	7	10	NULL	0	NULL	statement 1	NULL		seal	NULL	may			collagen	NULL		 platelet-activating domains		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3578_s_250	9437208	42  The enhanced binding of vWf to collagen may have sealed the platelet-activating domains of collagen.	bind
27163	1	8202	6	13	NULL	NULL	NULL	BKLF/TEF-2	GP		bind		strongly							CACC box	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_2_182_s_265	10417400	42 43  The BKLF/TEF-2, another member of Kruppel family of transcription factors, which binds strongly to CACC box, contains a unique basic region and its expression is less tissue restricted.	bind
27164	2	8202	6	13	NULL	NULL	NULL	BKLF/TEF-2	GP		is a member of					Kruppel family of transcription factors	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_2_182_s_265	10417400	42 43  The BKLF/TEF-2, another member of Kruppel family of transcription factors, which binds strongly to CACC box, contains a unique basic region and its expression is less tissue restricted.	bind
27165	3	8202	6	13	NULL	NULL	NULL	BKLF/TEF-2	GP		contains a							unique	basic region		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_2_182_s_265	10417400	42 43  The BKLF/TEF-2, another member of Kruppel family of transcription factors, which binds strongly to CACC box, contains a unique basic region and its expression is less tissue restricted.	bind
27166	4	8202	6	13	NULL	NULL	NULL	BKLF/TEF-2	GP	expression of	is					tissue restricted		less			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_2_182_s_265	10417400	42 43  The BKLF/TEF-2, another member of Kruppel family of transcription factors, which binds strongly to CACC box, contains a unique basic region and its expression is less tissue restricted.	bind
33044	1	8202	7	NULL	NULL	0	NULL	BKLF/TEF-2	NULL		binds	NULL	strongly				NULL			CACC box	NULL		0	NULL	NULL	NULL	gw60_circulationres_85_2_182_s_265	10417400	42 43  The BKLF/TEF-2, another member of Kruppel family of transcription factors, which binds strongly to CACC box, contains a unique basic region and its expression is less tissue restricted.	bind
33045	2	8202	7	10	NULL	0	NULL	BKLF/TEF-2	NULL		is a member of	NULL				Kruppel family of transcription factors	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_2_182_s_265	10417400	42 43  The BKLF/TEF-2, another member of Kruppel family of transcription factors, which binds strongly to CACC box, contains a unique basic region and its expression is less tissue restricted.	bind
33046	3	8202	7	10	NULL	0	NULL		NULL		contains	NULL			CACC box	basic region	NULL	unique			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_2_182_s_265	10417400	42 43  The BKLF/TEF-2, another member of Kruppel family of transcription factors, which binds strongly to CACC box, contains a unique basic region and its expression is less tissue restricted.	bind
33047	4	8202	7	NULL	NULL	0	NULL		NULL	expression of	is less 	NULL			CACC box	tissue restricted	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_2_182_s_265	10417400	42 43  The BKLF/TEF-2, another member of Kruppel family of transcription factors, which binds strongly to CACC box, contains a unique basic region and its expression is less tissue restricted.	bind
27167	1	8203	6	13	NULL	NULL	NULL	apoA-I	GP		bind		directly			ABCA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_74	12738681	42 Because apoA-I directly binds ABCA1, we speculated that apoA-I might regulate ABCA1 protein turnover.	bind
27168	2	8203	6	13	NULL	NULL	NULL	apo A-I	GP		regulate		might			ABCA1 protein	GP	turnover of 			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_74	12738681	42 Because apoA-I directly binds ABCA1, we speculated that apoA-I might regulate ABCA1 protein turnover.	bind
33090	1	8203	7	NULL	NULL	0	NULL	apoA-I	NULL		binds	NULL	directly			ABCA1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_74	12738681	42 Because apoA-I directly binds ABCA1, we speculated that apoA-I might regulate ABCA1 protein turnover.	bind
33091	2	8203	7	10	NULL	0	NULL	apoA-I	NULL		regulate	NULL	might			ABCA1 protein	NULL	turnover of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_74	12738681	42 Because apoA-I directly binds ABCA1, we speculated that apoA-I might regulate ABCA1 protein turnover.	bind
27169	1	8204	6	13	NULL	NULL	NULL	E7	GP		bind					p130/Rb	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1623_s_237	11073822	42 In contrast to Rb, however, binding of E7 to p130/Rb does not lead to increase proteolytic degradation.	bind
27170	2	8204	6	13	NULL	NULL	NULL	statement 1	Process		does not increase					proteolytic degradation	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1623_s_237	11073822	42 In contrast to Rb, however, binding of E7 to p130/Rb does not lead to increase proteolytic degradation.	bind
33092	1	8204	7	NULL	NULL	0	NULL	E7 	NULL		bind	NULL				p130/Rb	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_5_1623_s_237	11073822	42 In contrast to Rb, however, binding of E7 to p130/Rb does not lead to increase proteolytic degradation.	bind
33093	2	8204	7	NULL	NULL	0	NULL	statement 1	NULL		does not increase	NULL				proteolytic degradation	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_5_1623_s_237	11073822	42 In contrast to Rb, however, binding of E7 to p130/Rb does not lead to increase proteolytic degradation.	bind
33094	3	8204	7	NULL	NULL	0	NULL	E7	NULL		bind	NULL				Rb	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_5_1623_s_237	11073822	42 In contrast to Rb, however, binding of E7 to p130/Rb does not lead to increase proteolytic degradation.	bind
27171	1	8205	6	13	NULL	NULL	NULL	MMP gene	GP		bind				AP-1 element of promoter	members of the AP-1 transcription factor family	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1353_s_112	15860743	42 Interestingly, a single AP-1 element, which binds members of the AP-1 transcription factor family, is found in the promoter region of each inducible MMP gene.	bind
33095	1	8205	7	NULL	NULL	0	NULL		NULL		binds	NULL			AP-1 element	AP-1 transcription factor family	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1353_s_112	15860743	42 Interestingly, a single AP-1 element, which binds members of the AP-1 transcription factor family, is found in the promoter region of each inducible MMP gene.	bind
33096	2	8205	7	10	NULL	0	NULL				is found in				AP-1 element	MMP gene				promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_7_1353_s_112	15860743	42 Interestingly, a single AP-1 element, which binds members of the AP-1 transcription factor family, is found in the promoter region of each inducible MMP gene.	bind
27530	1	8206	6	13	NULL	NULL	NULL	Ral GEF	GP		is			PH domain;; SH3 binding motif		RalGPS	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1315_s_132	15130921	42 This RalGPS (Ral GEFs with  PH domain and  SH3 binding motif) or RalGEF2 was unable to bind to and induce nucleotide exchange of a C-terminally truncated Ral mutant, suggesting that the C-terminus of Ral is required for RalGEF2 binding.	bind
27531	2	8206	6	13	NULL	NULL	NULL	RalGEF2	GP		does not bind					Ral	GP	truncated;;mutant	C-terminus		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1315_s_132	15130921	42 This RalGPS (Ral GEFs with  PH domain and  SH3 binding motif) or RalGEF2 was unable to bind to and induce nucleotide exchange of a C-terminally truncated Ral mutant, suggesting that the C-terminus of Ral is required for RalGEF2 binding.	bind
27532	3	8206	6	13	NULL	NULL	NULL	RalGEF2	GP		does not induce					Ral	GP	nucleotide exchange of;; mutant;; truncated	C-terminal		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1315_s_132	15130921	42 This RalGPS (Ral GEFs with  PH domain and  SH3 binding motif) or RalGEF2 was unable to bind to and induce nucleotide exchange of a C-terminally truncated Ral mutant, suggesting that the C-terminus of Ral is required for RalGEF2 binding.	bind
27533	4	8206	6	13	NULL	NULL	NULL	Ral	GP		is required for			C-terminus		RalGEF2	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1315_s_132	15130921	42 This RalGPS (Ral GEFs with  PH domain and  SH3 binding motif) or RalGEF2 was unable to bind to and induce nucleotide exchange of a C-terminally truncated Ral mutant, suggesting that the C-terminus of Ral is required for RalGEF2 binding.	bind
33097	1	8206	7	10	NULL	0	NULL	Ral	NULL	truncated;;mutant	exchange	NULL		C-terminal		nucleotide	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1315_s_132	15130921	42 This RalGPS (Ral GEFs with  PH domain and  SH3 binding motif) or RalGEF2 was unable to bind to and induce nucleotide exchange of a C-terminally truncated Ral mutant, suggesting that the C-terminus of Ral is required for RalGEF2 binding.	bind
33098	2	8206	7	NULL	NULL	0	NULL	RalGEF2	NULL		does not bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1315_s_132	15130921	42 This RalGPS (Ral GEFs with  PH domain and  SH3 binding motif) or RalGEF2 was unable to bind to and induce nucleotide exchange of a C-terminally truncated Ral mutant, suggesting that the C-terminus of Ral is required for RalGEF2 binding.	bind
33099	3	8206	7	NULL	NULL	0	NULL	RalGEF2	NULL		does not induce	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1315_s_132	15130921	42 This RalGPS (Ral GEFs with  PH domain and  SH3 binding motif) or RalGEF2 was unable to bind to and induce nucleotide exchange of a C-terminally truncated Ral mutant, suggesting that the C-terminus of Ral is required for RalGEF2 binding.	bind
33100	4	8206	7	NULL	NULL	0	NULL	RalGPS	NULL		does not bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1315_s_132	15130921	42 This RalGPS (Ral GEFs with  PH domain and  SH3 binding motif) or RalGEF2 was unable to bind to and induce nucleotide exchange of a C-terminally truncated Ral mutant, suggesting that the C-terminus of Ral is required for RalGEF2 binding.	bind
33101	5	8206	7	NULL	NULL	0	NULL	RalGPS	NULL		does not induce	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1315_s_132	15130921	42 This RalGPS (Ral GEFs with  PH domain and  SH3 binding motif) or RalGEF2 was unable to bind to and induce nucleotide exchange of a C-terminally truncated Ral mutant, suggesting that the C-terminus of Ral is required for RalGEF2 binding.	bind
33102	6	8206	7	10	NULL	0	NULL	RalGPS	NULL		consist of	NULL				Ral GEFs	NULL		PH domain;;SH3 binding motif		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1315_s_132	15130921	42 This RalGPS (Ral GEFs with  PH domain and  SH3 binding motif) or RalGEF2 was unable to bind to and induce nucleotide exchange of a C-terminally truncated Ral mutant, suggesting that the C-terminus of Ral is required for RalGEF2 binding.	bind
33103	7	8206	7	NULL	NULL	0	NULL	Ral	NULL		is required for	NULL		C-terminus		RalGEF2	NULL	binding of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_7_1315_s_132	15130921	42 This RalGPS (Ral GEFs with  PH domain and  SH3 binding motif) or RalGEF2 was unable to bind to and induce nucleotide exchange of a C-terminally truncated Ral mutant, suggesting that the C-terminus of Ral is required for RalGEF2 binding.	bind
27181	1	8208	6	13	NULL	NULL	NULL	uPAR	GP		bind					CD11b/CD18	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_2_517_s_275	12875972	42-44  This receptor is involved in cellular movement by generating cell-surface Pm activity, via uPA binding, and by uPAR binding to beta2-integrins, particularly CD11b/CD18 (Mac-1).	bind
27182	2	8208	6	13	NULL	NULL	NULL	CD11b/CD18	GP		is a type of					beta2-integrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_2_517_s_275	12875972	42-44  This receptor is involved in cellular movement by generating cell-surface Pm activity, via uPA binding, and by uPAR binding to beta2-integrins, particularly CD11b/CD18 (Mac-1).	bind
55947	3	8208	6	13	NULL	NULL	NULL	CD11b/CD18	GP		is					Mac-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_2_517_s_275	12875972	42-44  This receptor is involved in cellular movement by generating cell-surface Pm activity, via uPA binding, and by uPAR binding to beta2-integrins, particularly CD11b/CD18 (Mac-1).	bind
33106	2	8208	7	NULL	NULL	0	NULL	uPAR	NULL		bind	NULL				CD11b/CD18	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_163_2_517_s_275	12875972	42-44  This receptor is involved in cellular movement by generating cell-surface Pm activity, via uPA binding, and by uPAR binding to beta2-integrins, particularly CD11b/CD18 (Mac-1).	bind
33107	3	8208	7	NULL	NULL	0	NULL	CD11b/CD18	NULL		is	NULL				Mac-1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_163_2_517_s_275	12875972	42-44  This receptor is involved in cellular movement by generating cell-surface Pm activity, via uPA binding, and by uPAR binding to beta2-integrins, particularly CD11b/CD18 (Mac-1).	bind
33108	4	8208	7	NULL	NULL	0	NULL	CD11b/CD18	NULL		is a type of	NULL				beta2-integrins	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_163_2_517_s_275	12875972	42-44  This receptor is involved in cellular movement by generating cell-surface Pm activity, via uPA binding, and by uPAR binding to beta2-integrins, particularly CD11b/CD18 (Mac-1).	bind
27183	1	8209	6	13	NULL	NULL	NULL	type II nuclear receptors	GP		bind									full site estrogen response element	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_366	11452016	43       Klinge,C.M., Bodenner,D.L., Desai,D., Niles,R.M. and Traish,A.M. (1997) Binding of type II nuclear receptors and estrogen receptor to full and half-site estrogen response elements  in vitro.	bind
27184	2	8209	6	13	NULL	NULL	NULL	type II nuclear receptors	GP		bind									half-site estrogen response element	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_366	11452016	43       Klinge,C.M., Bodenner,D.L., Desai,D., Niles,R.M. and Traish,A.M. (1997) Binding of type II nuclear receptors and estrogen receptor to full and half-site estrogen response elements  in vitro.	bind
27185	3	8209	6	13	NULL	NULL	NULL	estrogen receptor	GP		bind									full site estrogen response element	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_366	11452016	43       Klinge,C.M., Bodenner,D.L., Desai,D., Niles,R.M. and Traish,A.M. (1997) Binding of type II nuclear receptors and estrogen receptor to full and half-site estrogen response elements  in vitro.	bind
27186	4	8209	6	13	NULL	NULL	NULL	estrogen receptor	GP		bind									half-site estrogen response element	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_366	11452016	43       Klinge,C.M., Bodenner,D.L., Desai,D., Niles,R.M. and Traish,A.M. (1997) Binding of type II nuclear receptors and estrogen receptor to full and half-site estrogen response elements  in vitro.	bind
33109	1	8209	7	NULL	NULL	0	NULL	type II nuclear receptors 	NULL		binds to	NULL					NULL			full-site estrogen response element	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_366	11452016	43       Klinge,C.M., Bodenner,D.L., Desai,D., Niles,R.M. and Traish,A.M. (1997) Binding of type II nuclear receptors and estrogen receptor to full and half-site estrogen response elements  in vitro.	bind
33110	2	8209	7	NULL	NULL	0	NULL	estrogen receptor	NULL		binds to	NULL					NULL			full-site estrogen response element	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_366	11452016	43       Klinge,C.M., Bodenner,D.L., Desai,D., Niles,R.M. and Traish,A.M. (1997) Binding of type II nuclear receptors and estrogen receptor to full and half-site estrogen response elements  in vitro.	bind
47494	3	8209	7	NULL	NULL	0	NULL	type II nuclear receptors	NULL		bind	NULL					NULL			half-site estrogen response element	NULL	in vitro	0	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_366	11452016	43       Klinge,C.M., Bodenner,D.L., Desai,D., Niles,R.M. and Traish,A.M. (1997) Binding of type II nuclear receptors and estrogen receptor to full and half-site estrogen response elements  in vitro.	bind
47495	4	8209	7	NULL	NULL	0	NULL	estrogen receptor	NULL		bind	NULL					NULL			half-site estrogen response element	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_366	11452016	43       Klinge,C.M., Bodenner,D.L., Desai,D., Niles,R.M. and Traish,A.M. (1997) Binding of type II nuclear receptors and estrogen receptor to full and half-site estrogen response elements  in vitro.	bind
27187	1	8210	6	13	NULL	NULL	NULL	RNA	NucleicAcid		bind		sequence specifically			Nova	GP		KH domain		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_638_s_301	11160884	43       Lewis,H.A., Musunuru,K., Jensen,K.B., Edo,C., Chen,H., Darnell,R.B. and Burley,S.K. (2000) Sequence-specific RNA binding by a Nova KH domain: implications for paraneoplastic disease and the fragile X syndrome.	bind
27188	2	8210	6	13	NULL	NULL	NULL	statement 1	Process		implies for					paraneoplastic disease	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_638_s_301	11160884	43       Lewis,H.A., Musunuru,K., Jensen,K.B., Edo,C., Chen,H., Darnell,R.B. and Burley,S.K. (2000) Sequence-specific RNA binding by a Nova KH domain: implications for paraneoplastic disease and the fragile X syndrome.	bind
27189	3	8210	6	13	NULL	NULL	NULL	statement 1	Process		implies for					fragile X syndrome	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_638_s_301	11160884	43       Lewis,H.A., Musunuru,K., Jensen,K.B., Edo,C., Chen,H., Darnell,R.B. and Burley,S.K. (2000) Sequence-specific RNA binding by a Nova KH domain: implications for paraneoplastic disease and the fragile X syndrome.	bind
33111	1	8210	7	10	NULL	0	NULL	Nova	NULL		bind	NULL	sequence-specific	KH domain		RNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_638_s_301	11160884	43       Lewis,H.A., Musunuru,K., Jensen,K.B., Edo,C., Chen,H., Darnell,R.B. and Burley,S.K. (2000) Sequence-specific RNA binding by a Nova KH domain: implications for paraneoplastic disease and the fragile X syndrome.	bind
33112	2	8210	7	NULL	NULL	0	NULL	statement 1	NULL		implicates	NULL				paraneoplastic disease	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_638_s_301	11160884	43       Lewis,H.A., Musunuru,K., Jensen,K.B., Edo,C., Chen,H., Darnell,R.B. and Burley,S.K. (2000) Sequence-specific RNA binding by a Nova KH domain: implications for paraneoplastic disease and the fragile X syndrome.	bind
33114	3	8210	7	NULL	NULL	0	NULL	statement 1	NULL		implicates	NULL				fragile X syndrome	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_638_s_301	11160884	43       Lewis,H.A., Musunuru,K., Jensen,K.B., Edo,C., Chen,H., Darnell,R.B. and Burley,S.K. (2000) Sequence-specific RNA binding by a Nova KH domain: implications for paraneoplastic disease and the fragile X syndrome.	bind
27190	1	8211	6	13	NULL	NULL	NULL	2C4 monoclonal mouse-antirabbit antibody	GP		bind					class II MHC antigen	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2515_s_81	9409222	43  As a marker of inflammation with activation of the immune system, the 2C4 monoclonal mouse-antirabbit antibody (Serotec, Oxford, England), which binds to the rabbit homologue of the class II major histocompatibility complex (MHC) antigen, was used in cryostat sections of aortic allografts.	bind
27191	2	8211	6	13	NULL	NULL	NULL	MHC	GP		is					major histocompatibility complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2515_s_81	9409222	43  As a marker of inflammation with activation of the immune system, the 2C4 monoclonal mouse-antirabbit antibody (Serotec, Oxford, England), which binds to the rabbit homologue of the class II major histocompatibility complex (MHC) antigen, was used in cryostat sections of aortic allografts.	bind
55948	3	8211	6	13	NULL	NULL	NULL	class II MHC antigen	GP		is homologous to					class II MHC antigen	GP	rabbit			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2515_s_81	9409222	43  As a marker of inflammation with activation of the immune system, the 2C4 monoclonal mouse-antirabbit antibody (Serotec, Oxford, England), which binds to the rabbit homologue of the class II major histocompatibility complex (MHC) antigen, was used in cryostat sections of aortic allografts.	bind
33126	1	8211	7	NULL	NULL	0	NULL	2C4 monoclonal mouse-antirabbit antibody 	NULL		binds to	NULL				class II MHC antigen	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2515_s_81	9409222	43  As a marker of inflammation with activation of the immune system, the 2C4 monoclonal mouse-antirabbit antibody (Serotec, Oxford, England), which binds to the rabbit homologue of the class II major histocompatibility complex (MHC) antigen, was used in cryostat sections of aortic allografts.	bind
33129	2	8211	7	NULL	NULL	0	NULL	class II MHC antigen	NULL		is homologous to	NULL				class II MHC antigen	NULL	rabbit			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2515_s_81	9409222	43  As a marker of inflammation with activation of the immune system, the 2C4 monoclonal mouse-antirabbit antibody (Serotec, Oxford, England), which binds to the rabbit homologue of the class II major histocompatibility complex (MHC) antigen, was used in cryostat sections of aortic allografts.	bind
33130	3	8211	7	NULL	NULL	0	NULL	MHC	NULL		is 	NULL				major histocompatibility complex	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2515_s_81	9409222	43  As a marker of inflammation with activation of the immune system, the 2C4 monoclonal mouse-antirabbit antibody (Serotec, Oxford, England), which binds to the rabbit homologue of the class II major histocompatibility complex (MHC) antigen, was used in cryostat sections of aortic allografts.	bind
27192	1	8212	6	13	NULL	NULL	NULL	S-1	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_5_471_s_148	9734469	43  In studies of the role of fsTnT in the regulation of myofilament activation, Schaertl et al 45  showed that TnT1 (residues 1 to 159) did not affect the rate of S-1 binding to actin in preparations reconstituted from myosin S-1 and regulated thin filaments.	bind
27193	2	8212	6	13	NULL	NULL	NULL	TnT1	GP		did not affect			1-159		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_5_471_s_148	9734469	43  In studies of the role of fsTnT in the regulation of myofilament activation, Schaertl et al 45  showed that TnT1 (residues 1 to 159) did not affect the rate of S-1 binding to actin in preparations reconstituted from myosin S-1 and regulated thin filaments.	bind
27194	3	8212	6	13	NULL	NULL	NULL	statement 2	Process		occurs in					myosin S-1	GP	 preparations reconstitued from			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_5_471_s_148	9734469	43  In studies of the role of fsTnT in the regulation of myofilament activation, Schaertl et al 45  showed that TnT1 (residues 1 to 159) did not affect the rate of S-1 binding to actin in preparations reconstituted from myosin S-1 and regulated thin filaments.	bind
27262	4	8212	6	13	NULL	NULL	NULL	statement 2	Process		occurs in					thin filaments	CellComponent	 preparations reconstitued from;;regulated			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_5_471_s_148	9734469	43  In studies of the role of fsTnT in the regulation of myofilament activation, Schaertl et al 45  showed that TnT1 (residues 1 to 159) did not affect the rate of S-1 binding to actin in preparations reconstituted from myosin S-1 and regulated thin filaments.	bind
33132	1	8212	7	NULL	NULL	0	NULL	S-1	NULL		bind	NULL				actin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_5_471_s_148	9734469	43  In studies of the role of fsTnT in the regulation of myofilament activation, Schaertl et al 45  showed that TnT1 (residues 1 to 159) did not affect the rate of S-1 binding to actin in preparations reconstituted from myosin S-1 and regulated thin filaments.	bind
33133	2	8212	7	NULL	NULL	0	NULL	S1	NULL		reconstituted from	NULL				myosin S-1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_5_471_s_148	9734469	43  In studies of the role of fsTnT in the regulation of myofilament activation, Schaertl et al 45  showed that TnT1 (residues 1 to 159) did not affect the rate of S-1 binding to actin in preparations reconstituted from myosin S-1 and regulated thin filaments.	bind
33134	3	8212	7	NULL	NULL	0	NULL	actin	NULL		reconstituted from	NULL				regulated thin filaments	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_5_471_s_148	9734469	43  In studies of the role of fsTnT in the regulation of myofilament activation, Schaertl et al 45  showed that TnT1 (residues 1 to 159) did not affect the rate of S-1 binding to actin in preparations reconstituted from myosin S-1 and regulated thin filaments.	bind
33135	4	8212	7	NULL	NULL	0	NULL	fsTnT 	NULL		regulates	NULL				myofilament	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_circulationres_83_5_471_s_148	9734469	43  In studies of the role of fsTnT in the regulation of myofilament activation, Schaertl et al 45  showed that TnT1 (residues 1 to 159) did not affect the rate of S-1 binding to actin in preparations reconstituted from myosin S-1 and regulated thin filaments.	bind
33136	5	8212	7	NULL	NULL	0	NULL	TnT1	NULL		does not affect	NULL		residues 1 to 159		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_5_471_s_148	9734469	43  In studies of the role of fsTnT in the regulation of myofilament activation, Schaertl et al 45  showed that TnT1 (residues 1 to 159) did not affect the rate of S-1 binding to actin in preparations reconstituted from myosin S-1 and regulated thin filaments.	bind
27263	1	8213	6	13	NULL	NULL	NULL	platelet	Cell		bind					neutrophils	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
27264	2	8213	6	13	NULL	NULL	NULL	platelet GPIIb/IIa	GP		bridges					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
27265	3	8213	6	13	NULL	NULL	NULL	MAC-1	GP	neutrophil	bridges					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
27535	4	8213	6	13	NULL	NULL	NULL	GPIa/Ia	GP		bridges					thrombospondin	GP				NULL	platelets	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
27536	5	8213	6	13	NULL	NULL	NULL	GPIIb/IIa	GP		bridges					thrombospondin	GP				NULL	platelets	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
27537	6	8213	6	13	NULL	NULL	NULL	GPIV	GP		bridges					thrombospondin	GP				NULL	platelets	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
27538	7	8213	6	13	NULL	NULL	NULL	ICAM-1	GP	platelet	bind					LFA-1	GP	neutrophil			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
27539	8	8213	6	13	NULL	NULL	NULL	Fc RII 	GP		is					CD32	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
27540	9	8213	6	13	NULL	NULL	NULL	Fc RIIIb	GP		is					CD16	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
27541	10	8213	6	13	NULL	NULL	NULL	Fc RII	GP	platelet	bind					Fc RIIIb	GP	neutrophil			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
55949	11	8213	6	13	NULL	NULL	NULL	GPIIb/IIa	GP	platelet	bridges					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
33137	1	8213	7	NULL	NULL	0	NULL	platelet	NULL		bind	NULL				neutrophils	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
33138	2	8213	7	NULL	NULL	0	NULL	fibrinogen	NULL		bridging via	NULL				platelet GPIIb/IIa 	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
33139	3	8213	7	NULL	NULL	0	NULL	fibrinogen	NULL		bridging via	NULL				neutrophil MAC-1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
33140	4	8213	7	NULL	NULL	0	NULL	thrombospondin	NULL		bridging via	NULL				 GPIa/Ia	NULL				NULL	platelets	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
33141	5	8213	7	NULL	NULL	0	NULL	thrombospondin	NULL		bridging via	NULL				GPIIb/IIa	NULL				NULL	platelets	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
33142	6	8213	7	NULL	NULL	0	NULL	thrombospondin 	NULL		bridging via	NULL				 GPIV	NULL				NULL	platelets	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
33144	8	8213	7	10	NULL	0	NULL	platelet ICAM-1			bind					LFA-1		neutrophil			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
33145	9	8213	7	10	NULL	0	NULL	platelet Fc RII			interacts with					Fc RIIIb		neutrophil			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
33146	10	8213	7	NULL	NULL	0	NULL	statement 9	NULL		is a type of	NULL				immune complex interaction	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
33147	11	8213	7	10	NULL	0	NULL	Fc RII			is					CD32					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
33148	12	8213	7	10	NULL	0	NULL	Fc RIIIb			is					CD16					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_372_s_155	9974421	43  Many studies have reported that other mechanisms may be implicated in platelet binding to neutrophils, such as (1) fibrinogen bridging via platelet GPIIb/IIa and neutrophil MAC-1, 44 45  (2) thrombospondin bridging via GPIa/Ia, GPIIb/IIa, or GPIV on platelets and a specific receptor on neutrophils, 46 47  (3) platelet ICAM-1 binding to neutrophil LFA-1, 48  and (4) immune complex interactions between platelet Fc RII (CD32) and neutrophil Fc RIIIb (CD16).	bind
27542	1	8214	6	13	NULL	NULL	NULL	fibroblasts	Cell	human;; skin	unable to take					Ang II-LDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
27543	2	8214	6	13	NULL	NULL	NULL	fibroblasts	Cell	human;; skin	lack					scavenger receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
27544	3	8214	6	13	NULL	NULL	NULL	Ox-LDL	GP	nonlabeled	bind					scavenger receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
27545	4	8214	6	13	NULL	NULL	NULL	Ac-LDL	GP	nonlabeled	bind					scavenger receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
27546	5	8214	6	13	NULL	NULL	NULL	fucoidin	GP	nonlabeled	bind					scavenger receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
27547	6	8214	6	13	NULL	NULL	NULL	LDL	GP	native	bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
27548	7	8214	6	13	NULL	NULL	NULL	LDL	GP	Ang II-125I - labeled	is degraded by					macrophages	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
27549	8	8214	6	13	NULL	NULL	NULL	Ang II - LDL	GP		does not bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
27550	9	8214	6	13	NULL	NULL	NULL	Ac-LDL	GP		does not bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
27551	10	8214	6	13	NULL	NULL	NULL	Ox-LDL	GP		does not bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
27552	11	8214	6	13	NULL	NULL	NULL	LDL	GP	native	bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
33149	1	8214	7	NULL	NULL	0	NULL	Ang II - LDL	NULL		uptake by	NULL				macrophages	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
33150	2	8214	7	NULL	NULL	0	NULL	LDL receptor	NULL		is not involved in	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
33152	3	8214	7	NULL	NULL	0	NULL	scavenger receptor	NULL		is involved in	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
33153	4	8214	7	10	NULL	0	NULL	fibroblasts 		human;;skin	lacks					scavenger receptor					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
33154	5	8214	7	10	NULL	0	NULL	fibroblasts 		human;;skin	unable to takeup					AngII - LDL					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
33155	6	8214	7	NULL	NULL	0	NULL	Ox-LDL	NULL	nonlabeled	binds to	NULL				scavenger receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
33156	7	8214	7	NULL	NULL	0	NULL	Ac-LDL	NULL		binds to	NULL				scavenger receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
33157	8	8214	7	NULL	NULL	0	NULL	fucoidin	NULL		binds to	NULL				scavenger receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
33158	9	8214	7	NULL	NULL	0	NULL	LDL	NULL	native	does not bind	NULL				scavenger receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
33159	10	8214	7	NULL	NULL	0	NULL	LDL	NULL		binds to	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
33160	11	8214	7	NULL	NULL	0	NULL	macrophages	NULL		degrade	NULL				Ang II-125I - labeled LDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
33161	13	8214	7	NULL	NULL	0	NULL	statement 11	NULL		compete with	NULL				statement 12	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
33163	14	8214	7	NULL	NULL	0	NULL	Ang II - LDL	NULL		does not bind	NULL				heparin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
33164	15	8214	7	NULL	NULL	0	NULL	Ac-LDL	NULL		does not bind	NULL				heparin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
33165	16	8214	7	NULL	NULL	0	NULL	Ox-LDL	NULL		does not bind	NULL				heparin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
33168	17	8214	7	NULL	NULL	0	NULL	LDL	NULL	native	bind	NULL				heparin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
33170	12	8214	7	NULL	NULL	0	NULL	macrophages	NULL		degrade	NULL				LDL	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_1_97_s_202	8548433	43  The involvement of the scavenger receptor and not the LDL receptor in the uptake of Ang II - LDL by macrophages is supported by the following data: (1) Human skin fibroblasts (which lack the scavenger receptor) are unable to take up Ang II - LDL; (2) nonlabeled Ox-LDL, Ac-LDL, and fucoidin, which bind to the scavenger receptor but not native LDL, which binds to the LDL receptor, significantly compete with Ang II-125I - labeled LDL for its degradation by macrophages; and (3) Ang II - LDL, like Ac-LDL and Ox-LDL but unlike native LDL, does not bind to heparin.	bind
27266	1	8215	6	13	NULL	NULL	NULL	TM	GP		interacts with					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_1_47_s_276	10400910	43  Thus, the increase in the Ca2+ sensitivity of the FHC myofilaments could be due to the changes in the cooperative activation of thin filaments by altering the interaction of TM and actin, by affecting the TnT binding to TM, or through both mechanisms.	bind
27267	2	8215	6	13	NULL	NULL	NULL	TnT	GP		bind					TM	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_1_47_s_276	10400910	43  Thus, the increase in the Ca2+ sensitivity of the FHC myofilaments could be due to the changes in the cooperative activation of thin filaments by altering the interaction of TM and actin, by affecting the TnT binding to TM, or through both mechanisms.	bind
27268	3	8215	6	13	NULL	NULL	NULL	Ca+2 sensitivity	Process		increased in					FHC myofilaments	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_1_47_s_276	10400910	43  Thus, the increase in the Ca2+ sensitivity of the FHC myofilaments could be due to the changes in the cooperative activation of thin filaments by altering the interaction of TM and actin, by affecting the TnT binding to TM, or through both mechanisms.	bind
27269	4	8215	6	13	NULL	NULL	NULL	statement 3	Process		occur due to		may			statement 1	Process	alteration of 			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_1_47_s_276	10400910	43  Thus, the increase in the Ca2+ sensitivity of the FHC myofilaments could be due to the changes in the cooperative activation of thin filaments by altering the interaction of TM and actin, by affecting the TnT binding to TM, or through both mechanisms.	bind
27553	5	8215	6	13	NULL	NULL	NULL	statement 3	Process		occur due to		may			statement 2	Process	alteration of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_1_47_s_276	10400910	43  Thus, the increase in the Ca2+ sensitivity of the FHC myofilaments could be due to the changes in the cooperative activation of thin filaments by altering the interaction of TM and actin, by affecting the TnT binding to TM, or through both mechanisms.	bind
27554	6	8215	6	13	NULL	NULL	NULL	statement 4	Process		acts in cooperation with		may			statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_1_47_s_276	10400910	43  Thus, the increase in the Ca2+ sensitivity of the FHC myofilaments could be due to the changes in the cooperative activation of thin filaments by altering the interaction of TM and actin, by affecting the TnT binding to TM, or through both mechanisms.	bind
33176	1	8215	7	NULL	NULL	0	NULL	TM	NULL		interacts with	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_1_47_s_276	10400910	43  Thus, the increase in the Ca2+ sensitivity of the FHC myofilaments could be due to the changes in the cooperative activation of thin filaments by altering the interaction of TM and actin, by affecting the TnT binding to TM, or through both mechanisms.	bind
33177	2	8215	7	NULL	NULL	0	NULL	TnT	NULL		bind	NULL				TM	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_1_47_s_276	10400910	43  Thus, the increase in the Ca2+ sensitivity of the FHC myofilaments could be due to the changes in the cooperative activation of thin filaments by altering the interaction of TM and actin, by affecting the TnT binding to TM, or through both mechanisms.	bind
33178	3	8215	7	NULL	NULL	0	NULL	Ca2+ sensitivity	NULL		increase in	NULL				FHC myofilaments	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_1_47_s_276	10400910	43  Thus, the increase in the Ca2+ sensitivity of the FHC myofilaments could be due to the changes in the cooperative activation of thin filaments by altering the interaction of TM and actin, by affecting the TnT binding to TM, or through both mechanisms.	bind
33180	4	8215	7	NULL	NULL	0	NULL	statement 3	NULL		due to changes in	NULL				thin filaments	NULL	cooperative activation of			NULL		0	NULL	NULL	NULL	gw60_circulationres_85_1_47_s_276	10400910	43  Thus, the increase in the Ca2+ sensitivity of the FHC myofilaments could be due to the changes in the cooperative activation of thin filaments by altering the interaction of TM and actin, by affecting the TnT binding to TM, or through both mechanisms.	bind
33182	5	8215	7	NULL	NULL	0	NULL	statement 4	NULL		occur by altering	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_1_47_s_276	10400910	43  Thus, the increase in the Ca2+ sensitivity of the FHC myofilaments could be due to the changes in the cooperative activation of thin filaments by altering the interaction of TM and actin, by affecting the TnT binding to TM, or through both mechanisms.	bind
33183	6	8215	7	NULL	NULL	0	NULL	statement 4	NULL		occur by affecting	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_1_47_s_276	10400910	43  Thus, the increase in the Ca2+ sensitivity of the FHC myofilaments could be due to the changes in the cooperative activation of thin filaments by altering the interaction of TM and actin, by affecting the TnT binding to TM, or through both mechanisms.	bind
33185	7	8215	7	NULL	NULL	0	NULL	statement 5	NULL		in simultaneous with	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_1_47_s_276	10400910	43  Thus, the increase in the Ca2+ sensitivity of the FHC myofilaments could be due to the changes in the cooperative activation of thin filaments by altering the interaction of TM and actin, by affecting the TnT binding to TM, or through both mechanisms.	bind
33186	8	8215	7	NULL	NULL	0	NULL	statement 5	NULL		is an alternative to	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_1_47_s_276	10400910	43  Thus, the increase in the Ca2+ sensitivity of the FHC myofilaments could be due to the changes in the cooperative activation of thin filaments by altering the interaction of TM and actin, by affecting the TnT binding to TM, or through both mechanisms.	bind
33187	9	8215	7	NULL	NULL	0	NULL	statement 6	NULL		is an alternative to	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_1_47_s_276	10400910	43  Thus, the increase in the Ca2+ sensitivity of the FHC myofilaments could be due to the changes in the cooperative activation of thin filaments by altering the interaction of TM and actin, by affecting the TnT binding to TM, or through both mechanisms.	bind
27270	1	8216	6	13	NULL	NULL	NULL	HSP90	GP		bind					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_25_3473_s_213	15967841	43 Moreover, HSP90 function is sensitive to the cellular energy charge, as HSP90 readily binds ADP, and this event promotes client protein degradation.	bind
27271	2	8216	6	13	NULL	NULL	NULL	statement 1	Process		promotes					HSP90	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_25_3473_s_213	15967841	43 Moreover, HSP90 function is sensitive to the cellular energy charge, as HSP90 readily binds ADP, and this event promotes client protein degradation.	bind
27272	3	8216	6	13	NULL	NULL	NULL	HSP90	GP	function of	is sensitive to					energy charge		cellular			NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_25_3473_s_213	15967841	43 Moreover, HSP90 function is sensitive to the cellular energy charge, as HSP90 readily binds ADP, and this event promotes client protein degradation.	bind
33192	1	8216	7	10	NULL	0	NULL	HSP90		function of	is sensitive to					cellular energy charge					NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_25_3473_s_213	15967841	43 Moreover, HSP90 function is sensitive to the cellular energy charge, as HSP90 readily binds ADP, and this event promotes client protein degradation.	bind
33193	2	8216	7	NULL	NULL	0	NULL	HSP90	NULL		binds	NULL				ADP	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_111_25_3473_s_213	15967841	43 Moreover, HSP90 function is sensitive to the cellular energy charge, as HSP90 readily binds ADP, and this event promotes client protein degradation.	bind
33194	3	8216	7	NULL	NULL	0	NULL	statement 2	NULL		promotes	NULL				client protein	NULL	degradation of			NULL		0	NULL	NULL	NULL	gw70_circulation_111_25_3473_s_213	15967841	43 Moreover, HSP90 function is sensitive to the cellular energy charge, as HSP90 readily binds ADP, and this event promotes client protein degradation.	bind
27273	1	8217	6	13	NULL	NULL	NULL	angiotensin II	GP		induces					SMC marker gene	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_131	15718508	43,44  In addition, angiotensin II - induced activation of SMC marker gene expression has  also been shown to be dependent on Prx1, a homeodomain protein shown to dramatically  increase SRF binding to the highly conserved degenerate CArG elements found in the  promoter region of most SMC marker genes.	bind
27274	2	8217	6	13	NULL	NULL	NULL	statement 1	Process		is dependent on					Prx1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_131	15718508	43,44  In addition, angiotensin II - induced activation of SMC marker gene expression has  also been shown to be dependent on Prx1, a homeodomain protein shown to dramatically  increase SRF binding to the highly conserved degenerate CArG elements found in the  promoter region of most SMC marker genes.	bind
27275	3	8217	6	13	NULL	NULL	NULL	Prx1	GP		is a type of					homeodomain protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_131	15718508	43,44  In addition, angiotensin II - induced activation of SMC marker gene expression has  also been shown to be dependent on Prx1, a homeodomain protein shown to dramatically  increase SRF binding to the highly conserved degenerate CArG elements found in the  promoter region of most SMC marker genes.	bind
27276	4	8217	6	13	NULL	NULL	NULL	SRF	GP		bind					SMC marker gene	GP			CArG element of promoter	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_131	15718508	43,44  In addition, angiotensin II - induced activation of SMC marker gene expression has  also been shown to be dependent on Prx1, a homeodomain protein shown to dramatically  increase SRF binding to the highly conserved degenerate CArG elements found in the  promoter region of most SMC marker genes.	bind
27277	5	8217	6	13	NULL	NULL	NULL	Prx1	GP		increases					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_131	15718508	43,44  In addition, angiotensin II - induced activation of SMC marker gene expression has  also been shown to be dependent on Prx1, a homeodomain protein shown to dramatically  increase SRF binding to the highly conserved degenerate CArG elements found in the  promoter region of most SMC marker genes.	bind
33195	1	8217	7	NULL	NULL	0	NULL	angiotensin II	NULL		induce	NULL				SMC marker gene	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_131	15718508	43,44  In addition, angiotensin II - induced activation of SMC marker gene expression has  also been shown to be dependent on Prx1, a homeodomain protein shown to dramatically  increase SRF binding to the highly conserved degenerate CArG elements found in the  promoter region of most SMC marker genes.	bind
33196	2	8217	7	NULL	NULL	0	NULL	statement 1	NULL		depends on	NULL				Prx1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_131	15718508	43,44  In addition, angiotensin II - induced activation of SMC marker gene expression has  also been shown to be dependent on Prx1, a homeodomain protein shown to dramatically  increase SRF binding to the highly conserved degenerate CArG elements found in the  promoter region of most SMC marker genes.	bind
33197	3	8217	7	NULL	NULL	0	NULL	Prx1	NULL		is a type of	NULL				homeodomain protein	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_131	15718508	43,44  In addition, angiotensin II - induced activation of SMC marker gene expression has  also been shown to be dependent on Prx1, a homeodomain protein shown to dramatically  increase SRF binding to the highly conserved degenerate CArG elements found in the  promoter region of most SMC marker genes.	bind
33198	4	8217	7	NULL	NULL	0	NULL	SRF	NULL		bind	NULL				SMC marker gene	NULL			highly conserved degenerate CArG elements	NULL		0	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_131	15718508	43,44  In addition, angiotensin II - induced activation of SMC marker gene expression has  also been shown to be dependent on Prx1, a homeodomain protein shown to dramatically  increase SRF binding to the highly conserved degenerate CArG elements found in the  promoter region of most SMC marker genes.	bind
33199	5	8217	7	NULL	NULL	0	NULL	Prx1	NULL		increase	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_131	15718508	43,44  In addition, angiotensin II - induced activation of SMC marker gene expression has  also been shown to be dependent on Prx1, a homeodomain protein shown to dramatically  increase SRF binding to the highly conserved degenerate CArG elements found in the  promoter region of most SMC marker genes.	bind
27278	1	8218	6	13	NULL	NULL	NULL	VASP	GP		bind					c-Abl	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1403_s_149	15178555	43,44  VASP binding to c-Abl might be involved in regulation of c-Abl activity, which may then regulate cell growth.	bind
27279	2	8218	6	13	NULL	NULL	NULL	statement 1	Process		is involved in		may			c-Abl activity	GP	regulation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1403_s_149	15178555	43,44  VASP binding to c-Abl might be involved in regulation of c-Abl activity, which may then regulate cell growth.	bind
27280	3	8218	6	13	NULL	NULL	NULL	statement 2	Process		regulate		may			cell growth	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1403_s_149	15178555	43,44  VASP binding to c-Abl might be involved in regulation of c-Abl activity, which may then regulate cell growth.	bind
33201	1	8218	7	NULL	NULL	0	NULL	VASP	NULL		bind	NULL				 c-Abl	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1403_s_149	15178555	43,44  VASP binding to c-Abl might be involved in regulation of c-Abl activity, which may then regulate cell growth.	bind
33203	2	8218	7	10	NULL	0	NULL	statement 1			is involved in		might			c-Abl activity		regulation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1403_s_149	15178555	43,44  VASP binding to c-Abl might be involved in regulation of c-Abl activity, which may then regulate cell growth.	bind
33205	3	8218	7	10	NULL	0	NULL	statement 2			regulate 		may			cell growth					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_8_1403_s_149	15178555	43,44  VASP binding to c-Abl might be involved in regulation of c-Abl activity, which may then regulate cell growth.	bind
27281	1	8219	6	13	NULL	NULL	NULL	GST-HPV16 L2	GP		bind			1-128		GSTrap FF	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_14_12546_s_42	12560332	43-kDa Protein Purification and Identification-- GST-HPV16 L2-(1-128)-GFP was bound to a GSTrap FF column, and detergent extracts  of 109 SiHa cells in buffer A were passed over the column.	bind
33209	1	8219	7	10	NULL	0	NULL	GST-HPV16 L2			bind			1-128		GSTrap FF					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_14_12546_s_42	12560332	43-kDa Protein Purification and Identification-- GST-HPV16 L2-(1-128)-GFP was bound to a GSTrap FF column, and detergent extracts  of 109 SiHa cells in buffer A were passed over the column.	bind
27282	1	8221	6	13	NULL	NULL	NULL	Synaptotagmin	GP		bind			C2B domain		AP-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_434_7031_409_s_238	15772668	436, 4 16 (2001) |  Article |  PubMed |  ISI |  ChemPort |                         Chapman, E. R., Desai, R. C., Davis, A. F. & Tornehl, C. K. Delineation of the  oligomerization, AP-2 binding, and synprint binding region of the C2B domain of synaptotagmin.	bind
33214	1	8221	7	10	NULL	0	NULL	synaptotagmin			bind			C2B domain		AP-2					NULL		NULL	NULL	NULL	NULL	gw70_nature_434_7031_409_s_238	15772668	436, 4 16 (2001) |  Article |  PubMed |  ISI |  ChemPort |                         Chapman, E. R., Desai, R. C., Davis, A. F. & Tornehl, C. K. Delineation of the  oligomerization, AP-2 binding, and synprint binding region of the C2B domain of synaptotagmin.	bind
27284	1	8222	6	13	NULL	NULL	NULL	retinoblastoma protein	GP		bind					E2F residues	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_438	11504882	44       Hagemeier,C., Cook,A. and Kouzarides,T. (1993) The retinoblastoma protein binds E2F residues required for activation  in vivo and TBP binding  in vitro.	bind
27285	2	8222	6	13	NULL	NULL	NULL	statement 1	Process		is required for					activation	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_438	11504882	44       Hagemeier,C., Cook,A. and Kouzarides,T. (1993) The retinoblastoma protein binds E2F residues required for activation  in vivo and TBP binding  in vitro.	bind
27286	3	8222	6	13	NULL	NULL	NULL	statement 1	Process		bind					TBP	GP	binding of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_438	11504882	44       Hagemeier,C., Cook,A. and Kouzarides,T. (1993) The retinoblastoma protein binds E2F residues required for activation  in vivo and TBP binding  in vitro.	bind
33215	1	8222	7	NULL	NULL	0	NULL	 retinoblastoma protein	NULL		bind	NULL				E2F residues	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_438	11504882	44       Hagemeier,C., Cook,A. and Kouzarides,T. (1993) The retinoblastoma protein binds E2F residues required for activation  in vivo and TBP binding  in vitro.	bind
33216	2	8222	7	NULL	NULL	0	NULL	statement 1	NULL		is required for	NULL				activation	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_438	11504882	44       Hagemeier,C., Cook,A. and Kouzarides,T. (1993) The retinoblastoma protein binds E2F residues required for activation  in vivo and TBP binding  in vitro.	bind
33217	3	8222	7	NULL	NULL	0	NULL	statement 1	NULL		is required for	NULL				TBP	NULL	binding of			NULL	in vitro	0	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3439_s_438	11504882	44       Hagemeier,C., Cook,A. and Kouzarides,T. (1993) The retinoblastoma protein binds E2F residues required for activation  in vivo and TBP binding  in vitro.	bind
27287	1	8223	6	13	NULL	NULL	NULL	ribosomal protein S8	GP	Escherichia coli	bind					16S rRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_447_s_458	11788706	44       Mougel,M., Ehresmann,B. and Ehresmann C. (1986) Binding of  Escherichia coli ribosomal protein S8 to 16S rRNA: kinetic and thermodynamic characterization.	bind
33218	1	8223	7	NULL	NULL	0	NULL	ribosomal protein S8 	NULL	Escherichia coli	bind	NULL				16S rRNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_447_s_458	11788706	44       Mougel,M., Ehresmann,B. and Ehresmann C. (1986) Binding of  Escherichia coli ribosomal protein S8 to 16S rRNA: kinetic and thermodynamic characterization.	bind
27288	1	8224	6	13	NULL	NULL	NULL	RBP-Jkappa/CBF1	GP	thymic	bind									NF-kappaB-like element	NULL	thymus nuclear extracts	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2284_s_357	11376147	44       Shirakata,Y., Shuman,J.D. and Coligan,J.E. (1996) Purification of a novel MHC class I element binding activity from thymus nuclear extracts reveals that thymic RBP-Jkappa/CBF1 binds to NF-kappaB-like elements.	bind
33219	1	8224	7	NULL	NULL	0	NULL	 RBP-Jkappa/CBF1	NULL	thymic	binds	NULL					NULL			NF-kappaB-like elements	NULL	thymus nuclear extracts 	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2284_s_357	11376147	44       Shirakata,Y., Shuman,J.D. and Coligan,J.E. (1996) Purification of a novel MHC class I element binding activity from thymus nuclear extracts reveals that thymic RBP-Jkappa/CBF1 binds to NF-kappaB-like elements.	bind
27289	1	8225	6	13	NULL	NULL	NULL	CRP	GP	Aggregated	bind		selectively			LDL	GP				NULL	whole plasma	NULL	NULL	NULL	NULL	gw60_circulation_99_2_237_s_139	9892589	44  45  Aggregated but not soluble native CRP selectively binds LDL and VLDL from whole plasma and, as we have previously proposed, could thereby participate in their atherogenic accumulation.	bind
27290	2	8225	6	13	NULL	NULL	NULL	CRP	GP	Aggregated	bind		selectively			VLDL	GP				NULL	whole plasma	NULL	NULL	NULL	NULL	gw60_circulation_99_2_237_s_139	9892589	44  45  Aggregated but not soluble native CRP selectively binds LDL and VLDL from whole plasma and, as we have previously proposed, could thereby participate in their atherogenic accumulation.	bind
55950	3	8225	6	13	NULL	NULL	NULL	CRP	GP	soluble;;native	does not bind					LDL	GP				NULL	whole plasma	NULL	NULL	NULL	NULL	gw60_circulation_99_2_237_s_139	9892589	44  45  Aggregated but not soluble native CRP selectively binds LDL and VLDL from whole plasma and, as we have previously proposed, could thereby participate in their atherogenic accumulation.	bind
55951	4	8225	6	13	NULL	NULL	NULL	CRP	GP	soluble;;native	does not bind					VLDL	GP				NULL	whole plasma	NULL	NULL	NULL	NULL	gw60_circulation_99_2_237_s_139	9892589	44  45  Aggregated but not soluble native CRP selectively binds LDL and VLDL from whole plasma and, as we have previously proposed, could thereby participate in their atherogenic accumulation.	bind
33220	1	8225	7	NULL	NULL	0	NULL	CRP	NULL	Aggregated	binds	NULL	selectively			LDL	NULL				NULL	whole plasma	0	NULL	NULL	NULL	gw60_circulation_99_2_237_s_139	9892589	44  45  Aggregated but not soluble native CRP selectively binds LDL and VLDL from whole plasma and, as we have previously proposed, could thereby participate in their atherogenic accumulation.	bind
33222	2	8225	7	NULL	NULL	0	NULL	CRP	NULL	Aggregated	binds	NULL	selectively			VLDL	NULL				NULL	whole plasma	0	NULL	NULL	NULL	gw60_circulation_99_2_237_s_139	9892589	44  45  Aggregated but not soluble native CRP selectively binds LDL and VLDL from whole plasma and, as we have previously proposed, could thereby participate in their atherogenic accumulation.	bind
33225	3	8225	7	NULL	NULL	0	NULL	CRP	NULL	soluble native	does not bind	NULL				LDL	NULL				NULL	whole plasma	NULL	NULL	NULL	NULL	gw60_circulation_99_2_237_s_139	9892589	44  45  Aggregated but not soluble native CRP selectively binds LDL and VLDL from whole plasma and, as we have previously proposed, could thereby participate in their atherogenic accumulation.	bind
33232	4	8225	7	NULL	NULL	0	NULL	CRP	NULL	soluble native	does not bind	NULL				VLDL	NULL				NULL	whole plasma	0	NULL	NULL	NULL	gw60_circulation_99_2_237_s_139	9892589	44  45  Aggregated but not soluble native CRP selectively binds LDL and VLDL from whole plasma and, as we have previously proposed, could thereby participate in their atherogenic accumulation.	bind
27291	1	8226	6	13	NULL	NULL	NULL	Caveolin-1	GP		interact		selectively			H-Ras	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_41	8781470	44  45  Caveolin-1 has also been shown to interact selectively with wild-type H-Ras but not with a mutationally activated soluble H-Ras, suggesting that caveolins may facilitate the binding of specific G proteins depending on their activation state.	bind
27292	2	8226	6	13	NULL	NULL	NULL	Caveolin-1	GP		does not interact with					H-Ras	GP	mutationally activated;;soluble			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_41	8781470	44  45  Caveolin-1 has also been shown to interact selectively with wild-type H-Ras but not with a mutationally activated soluble H-Ras, suggesting that caveolins may facilitate the binding of specific G proteins depending on their activation state.	bind
27293	3	8226	6	13	NULL	NULL	NULL	caveolins	GP		facilitate		may			G proteins	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_41	8781470	44  45  Caveolin-1 has also been shown to interact selectively with wild-type H-Ras but not with a mutationally activated soluble H-Ras, suggesting that caveolins may facilitate the binding of specific G proteins depending on their activation state.	bind
55952	4	8226	6	13	NULL	NULL	NULL	statement 3	Process		depends on					G proteins	GP	activation state of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_41	8781470	44  45  Caveolin-1 has also been shown to interact selectively with wild-type H-Ras but not with a mutationally activated soluble H-Ras, suggesting that caveolins may facilitate the binding of specific G proteins depending on their activation state.	bind
33243	1	8226	7	NULL	NULL	0	NULL	caveolin-1 	NULL		interacts with	NULL	selectively			H-Ras	NULL	wild-type			NULL		0	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_41	8781470	44  45  Caveolin-1 has also been shown to interact selectively with wild-type H-Ras but not with a mutationally activated soluble H-Ras, suggesting that caveolins may facilitate the binding of specific G proteins depending on their activation state.	bind
33246	2	8226	7	10	NULL	0	NULL	caveolin-1			does not interact with					H-Ras		mutationally activated;;soluble			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_41	8781470	44  45  Caveolin-1 has also been shown to interact selectively with wild-type H-Ras but not with a mutationally activated soluble H-Ras, suggesting that caveolins may facilitate the binding of specific G proteins depending on their activation state.	bind
33248	3	8226	7	10	NULL	0	NULL	caveolins			facilitate		may			G proteins		binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_41	8781470	44  45  Caveolin-1 has also been shown to interact selectively with wild-type H-Ras but not with a mutationally activated soluble H-Ras, suggesting that caveolins may facilitate the binding of specific G proteins depending on their activation state.	bind
33249	4	8226	7	NULL	NULL	0	NULL	statement 3	NULL		depends on	NULL				G proteins	NULL	activation state of			NULL		0	NULL	NULL	NULL	gw60_circulationres_79_3_363_s_41	8781470	44  45  Caveolin-1 has also been shown to interact selectively with wild-type H-Ras but not with a mutationally activated soluble H-Ras, suggesting that caveolins may facilitate the binding of specific G proteins depending on their activation state.	bind
27294	1	8227	6	13	NULL	NULL	NULL	Neuropilin-1	GP		plays a role in					developing embryo	Organism				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_14_1887_s_159	11294808	44  Neuropilin-1 mutant mice were shown to exhibit various types of vascular defects, indicating a crucial role for this receptor in the developing embryo 45 ; still, the physiological consequences of VEGF binding to neuropilin receptors are yet to be fully explored.	bind
27295	2	8227	6	13	NULL	NULL	NULL	VEGF	GP		bind					neuropilin receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_14_1887_s_159	11294808	44  Neuropilin-1 mutant mice were shown to exhibit various types of vascular defects, indicating a crucial role for this receptor in the developing embryo 45 ; still, the physiological consequences of VEGF binding to neuropilin receptors are yet to be fully explored.	bind
27296	3	8227	6	13	NULL	NULL	NULL	Neuropilin-1	GP	mutant;;mice	exhibit					vascular defects	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_14_1887_s_159	11294808	44  Neuropilin-1 mutant mice were shown to exhibit various types of vascular defects, indicating a crucial role for this receptor in the developing embryo 45 ; still, the physiological consequences of VEGF binding to neuropilin receptors are yet to be fully explored.	bind
33250	1	8227	7	10	NULL	0	NULL	Neuropilin-1		mice;;mutant 	exhibit					vascular defects					NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_14_1887_s_159	11294808	44  Neuropilin-1 mutant mice were shown to exhibit various types of vascular defects, indicating a crucial role for this receptor in the developing embryo 45 ; still, the physiological consequences of VEGF binding to neuropilin receptors are yet to be fully explored.	bind
33251	2	8227	7	NULL	NULL	0	NULL	statement 1	NULL		indicate	NULL				Neuropilin receptor	NULL	crucial role of			NULL	developing embryo	NULL	NULL	NULL	NULL	gw60_circulation_103_14_1887_s_159	11294808	44  Neuropilin-1 mutant mice were shown to exhibit various types of vascular defects, indicating a crucial role for this receptor in the developing embryo 45 ; still, the physiological consequences of VEGF binding to neuropilin receptors are yet to be fully explored.	bind
33252	3	8227	7	NULL	NULL	0	NULL	VEGF	NULL		binds to	NULL				neuropilin receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_14_1887_s_159	11294808	44  Neuropilin-1 mutant mice were shown to exhibit various types of vascular defects, indicating a crucial role for this receptor in the developing embryo 45 ; still, the physiological consequences of VEGF binding to neuropilin receptors are yet to be fully explored.	bind
27297	1	8228	6	13	NULL	NULL	NULL	Sp1	GP		bind					TF	GP	human		GC box in promoter	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_214	9081693	44 45  In our studies, EMSAs identified binding of Sp1 to five distinct GC boxes in the human TF promoter.	bind
33253	1	8228	7	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				TF	NULL	human		GC boxes in the promoter	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_2_365_s_214	9081693	44 45  In our studies, EMSAs identified binding of Sp1 to five distinct GC boxes in the human TF promoter.	bind
27298	1	8229	6	13	NULL	NULL	NULL	ATIII	GP		bind					thrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_4_495_s_171	7749861	44 45 46 47 48  Conard et al 45  have indicated that plasma ATIII levels can be underestimated when obtained by the active-site titration technique with thrombin in the presence of heparin because heparin can interfere with the stoichiometry of thrombin binding by ATIII.	bind
27299	2	8229	6	13	NULL	NULL	NULL	heparin	Chemical		interfere with					statement 1	Process	stoichiometry of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_4_495_s_171	7749861	44 45 46 47 48  Conard et al 45  have indicated that plasma ATIII levels can be underestimated when obtained by the active-site titration technique with thrombin in the presence of heparin because heparin can interfere with the stoichiometry of thrombin binding by ATIII.	bind
33254	1	8229	7	NULL	NULL	0	NULL	ATIII	NULL		bind	NULL				thrombin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_4_495_s_171	7749861	44 45 46 47 48  Conard et al 45  have indicated that plasma ATIII levels can be underestimated when obtained by the active-site titration technique with thrombin in the presence of heparin because heparin can interfere with the stoichiometry of thrombin binding by ATIII.	bind
33255	2	8229	7	NULL	NULL	0	NULL	heparin	NULL		interferes with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_4_495_s_171	7749861	44 45 46 47 48  Conard et al 45  have indicated that plasma ATIII levels can be underestimated when obtained by the active-site titration technique with thrombin in the presence of heparin because heparin can interfere with the stoichiometry of thrombin binding by ATIII.	bind
27555	1	8230	6	13	NULL	NULL	NULL	HDL3 containing apoA-I	GP		exhibits					CETP activity	GP	plasma			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_213_s_210	8620335	44 54 The majority of the plasma CETP activity has been located in HDL3, 43  with lipoproteins containing apoA-I but no apoA-II, 45  or in HDL3, VHDL, and to a lesser extent HDL2, but not in VLDL or LDL. 53  Others, however, have detected binding of CETP to both Sepharose-bound VLDL and LDL, in addition to HDL. 44 54  CETP has been observed in rabbits to be associated with small HDL particles.	bind
27556	2	8230	6	13	NULL	NULL	NULL	HDL3 containing apoA-II	GP		does not exhibit					CETP activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_213_s_210	8620335	44 54 The majority of the plasma CETP activity has been located in HDL3, 43  with lipoproteins containing apoA-I but no apoA-II, 45  or in HDL3, VHDL, and to a lesser extent HDL2, but not in VLDL or LDL. 53  Others, however, have detected binding of CETP to both Sepharose-bound VLDL and LDL, in addition to HDL. 44 54  CETP has been observed in rabbits to be associated with small HDL particles.	bind
27557	3	8230	6	13	NULL	NULL	NULL	HDL2	GP		exhibits					CETP activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_213_s_210	8620335	44 54 The majority of the plasma CETP activity has been located in HDL3, 43  with lipoproteins containing apoA-I but no apoA-II, 45  or in HDL3, VHDL, and to a lesser extent HDL2, but not in VLDL or LDL. 53  Others, however, have detected binding of CETP to both Sepharose-bound VLDL and LDL, in addition to HDL. 44 54  CETP has been observed in rabbits to be associated with small HDL particles.	bind
27558	4	8230	6	13	NULL	NULL	NULL	VLDL	GP		does not exhibit					CETP activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_213_s_210	8620335	44 54 The majority of the plasma CETP activity has been located in HDL3, 43  with lipoproteins containing apoA-I but no apoA-II, 45  or in HDL3, VHDL, and to a lesser extent HDL2, but not in VLDL or LDL. 53  Others, however, have detected binding of CETP to both Sepharose-bound VLDL and LDL, in addition to HDL. 44 54  CETP has been observed in rabbits to be associated with small HDL particles.	bind
27559	5	8230	6	13	NULL	NULL	NULL	LDL	GP		does not exhibit					CETP activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_213_s_210	8620335	44 54 The majority of the plasma CETP activity has been located in HDL3, 43  with lipoproteins containing apoA-I but no apoA-II, 45  or in HDL3, VHDL, and to a lesser extent HDL2, but not in VLDL or LDL. 53  Others, however, have detected binding of CETP to both Sepharose-bound VLDL and LDL, in addition to HDL. 44 54  CETP has been observed in rabbits to be associated with small HDL particles.	bind
27560	6	8230	6	13	NULL	NULL	NULL	CETP	GP		associates with					HDL particles	GP	small			NULL	rabbits	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_213_s_210	8620335	44 54 The majority of the plasma CETP activity has been located in HDL3, 43  with lipoproteins containing apoA-I but no apoA-II, 45  or in HDL3, VHDL, and to a lesser extent HDL2, but not in VLDL or LDL. 53  Others, however, have detected binding of CETP to both Sepharose-bound VLDL and LDL, in addition to HDL. 44 54  CETP has been observed in rabbits to be associated with small HDL particles.	bind
33256	1	8230	7	NULL	NULL	0	NULL	CETP activity	NULL	plasma	is located in	NULL				HDL3	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_213_s_210	8620335	44 54 The majority of the plasma CETP activity has been located in HDL3, 43  with lipoproteins containing apoA-I but no apoA-II, 45  or in HDL3, VHDL, and to a lesser extent HDL2, but not in VLDL or LDL. 53  Others, however, have detected binding of CETP to both Sepharose-bound VLDL and LDL, in addition to HDL. 44 54  CETP has been observed in rabbits to be associated with small HDL particles.	bind
33257	2	8230	7	NULL	NULL	0	NULL	HDL3	NULL		contains	NULL				apoA-I	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_213_s_210	8620335	44 54 The majority of the plasma CETP activity has been located in HDL3, 43  with lipoproteins containing apoA-I but no apoA-II, 45  or in HDL3, VHDL, and to a lesser extent HDL2, but not in VLDL or LDL. 53  Others, however, have detected binding of CETP to both Sepharose-bound VLDL and LDL, in addition to HDL. 44 54  CETP has been observed in rabbits to be associated with small HDL particles.	bind
33260	3	8230	7	NULL	NULL	0	NULL	HDL3	NULL		does not contain	NULL				apoA-II	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_213_s_210	8620335	44 54 The majority of the plasma CETP activity has been located in HDL3, 43  with lipoproteins containing apoA-I but no apoA-II, 45  or in HDL3, VHDL, and to a lesser extent HDL2, but not in VLDL or LDL. 53  Others, however, have detected binding of CETP to both Sepharose-bound VLDL and LDL, in addition to HDL. 44 54  CETP has been observed in rabbits to be associated with small HDL particles.	bind
33262	4	8230	7	NULL	NULL	0	NULL	CETP activity	NULL	plasma	is located in	NULL				VHDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_213_s_210	8620335	44 54 The majority of the plasma CETP activity has been located in HDL3, 43  with lipoproteins containing apoA-I but no apoA-II, 45  or in HDL3, VHDL, and to a lesser extent HDL2, but not in VLDL or LDL. 53  Others, however, have detected binding of CETP to both Sepharose-bound VLDL and LDL, in addition to HDL. 44 54  CETP has been observed in rabbits to be associated with small HDL particles.	bind
33263	5	8230	7	NULL	NULL	0	NULL	CETP activity	NULL	plasma	is located in	NULL	less extent			HDL2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_213_s_210	8620335	44 54 The majority of the plasma CETP activity has been located in HDL3, 43  with lipoproteins containing apoA-I but no apoA-II, 45  or in HDL3, VHDL, and to a lesser extent HDL2, but not in VLDL or LDL. 53  Others, however, have detected binding of CETP to both Sepharose-bound VLDL and LDL, in addition to HDL. 44 54  CETP has been observed in rabbits to be associated with small HDL particles.	bind
33264	6	8230	7	NULL	NULL	0	NULL	CETP activity	NULL		is not present in	NULL				VLDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_213_s_210	8620335	44 54 The majority of the plasma CETP activity has been located in HDL3, 43  with lipoproteins containing apoA-I but no apoA-II, 45  or in HDL3, VHDL, and to a lesser extent HDL2, but not in VLDL or LDL. 53  Others, however, have detected binding of CETP to both Sepharose-bound VLDL and LDL, in addition to HDL. 44 54  CETP has been observed in rabbits to be associated with small HDL particles.	bind
33265	7	8230	7	NULL	NULL	0	NULL	CETP activity	NULL		is not present in	NULL				LDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_213_s_210	8620335	44 54 The majority of the plasma CETP activity has been located in HDL3, 43  with lipoproteins containing apoA-I but no apoA-II, 45  or in HDL3, VHDL, and to a lesser extent HDL2, but not in VLDL or LDL. 53  Others, however, have detected binding of CETP to both Sepharose-bound VLDL and LDL, in addition to HDL. 44 54  CETP has been observed in rabbits to be associated with small HDL particles.	bind
33266	8	8230	7	NULL	NULL	0	NULL	CETP	NULL		bind	NULL				Sepharose-bound VLDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_213_s_210	8620335	44 54 The majority of the plasma CETP activity has been located in HDL3, 43  with lipoproteins containing apoA-I but no apoA-II, 45  or in HDL3, VHDL, and to a lesser extent HDL2, but not in VLDL or LDL. 53  Others, however, have detected binding of CETP to both Sepharose-bound VLDL and LDL, in addition to HDL. 44 54  CETP has been observed in rabbits to be associated with small HDL particles.	bind
33267	9	8230	7	NULL	NULL	0	NULL	CETP	NULL		bind	NULL				LDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_213_s_210	8620335	44 54 The majority of the plasma CETP activity has been located in HDL3, 43  with lipoproteins containing apoA-I but no apoA-II, 45  or in HDL3, VHDL, and to a lesser extent HDL2, but not in VLDL or LDL. 53  Others, however, have detected binding of CETP to both Sepharose-bound VLDL and LDL, in addition to HDL. 44 54  CETP has been observed in rabbits to be associated with small HDL particles.	bind
33269	10	8230	7	NULL	NULL	0	NULL	CETP	NULL		bind	NULL				HDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_213_s_210	8620335	44 54 The majority of the plasma CETP activity has been located in HDL3, 43  with lipoproteins containing apoA-I but no apoA-II, 45  or in HDL3, VHDL, and to a lesser extent HDL2, but not in VLDL or LDL. 53  Others, however, have detected binding of CETP to both Sepharose-bound VLDL and LDL, in addition to HDL. 44 54  CETP has been observed in rabbits to be associated with small HDL particles.	bind
33270	11	8230	7	NULL	NULL	0	NULL	CETP	NULL		 associate with	NULL				small HDL particles	NULL				NULL	rabbits	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_213_s_210	8620335	44 54 The majority of the plasma CETP activity has been located in HDL3, 43  with lipoproteins containing apoA-I but no apoA-II, 45  or in HDL3, VHDL, and to a lesser extent HDL2, but not in VLDL or LDL. 53  Others, however, have detected binding of CETP to both Sepharose-bound VLDL and LDL, in addition to HDL. 44 54  CETP has been observed in rabbits to be associated with small HDL particles.	bind
27300	1	8231	6	13	NULL	NULL	NULL	Cu2+	Chemical		bind					PrP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_6795_s_50	12454014	44 and  46), and the number of Cu2+ ions binding to PrP is in dispute.	bind
33300	1	8231	7	NULL	NULL	0	NULL	Cu2+ ions	NULL		bind	NULL				PrP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_6795_s_50	12454014	44 and  46), and the number of Cu2+ ions binding to PrP is in dispute.	bind
27301	1	8232	6	13	NULL	NULL	NULL	MGP	GP		bind					BMP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1423_s_126	16601233	44 MGP is a calcium-binding matrix protein that binds and inhibits BMP2 induction of ALP. 45 In addition, carboxylated MGP produced by VSMCs binds matrix elastin and inhibits calcification.	bind
27302	2	8232	6	13	NULL	NULL	NULL	BMP2	GP		induces					ALP	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1423_s_126	16601233	44 MGP is a calcium-binding matrix protein that binds and inhibits BMP2 induction of ALP. 45 In addition, carboxylated MGP produced by VSMCs binds matrix elastin and inhibits calcification.	bind
27303	3	8232	6	13	NULL	NULL	NULL	MGP	GP		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1423_s_126	16601233	44 MGP is a calcium-binding matrix protein that binds and inhibits BMP2 induction of ALP. 45 In addition, carboxylated MGP produced by VSMCs binds matrix elastin and inhibits calcification.	bind
27304	4	8232	6	13	NULL	NULL	NULL	MGP	GP		is a type of					calcium-binding matrix protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1423_s_126	16601233	44 MGP is a calcium-binding matrix protein that binds and inhibits BMP2 induction of ALP. 45 In addition, carboxylated MGP produced by VSMCs binds matrix elastin and inhibits calcification.	bind
27305	5	8232	6	13	NULL	NULL	NULL	VSMC	Cell		produce					MGP	GP	carboxylated			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1423_s_126	16601233	44 MGP is a calcium-binding matrix protein that binds and inhibits BMP2 induction of ALP. 45 In addition, carboxylated MGP produced by VSMCs binds matrix elastin and inhibits calcification.	bind
27306	6	8232	6	13	NULL	NULL	NULL	MGP	GP	carboxylated	bind					matrix elastin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1423_s_126	16601233	44 MGP is a calcium-binding matrix protein that binds and inhibits BMP2 induction of ALP. 45 In addition, carboxylated MGP produced by VSMCs binds matrix elastin and inhibits calcification.	bind
27307	7	8232	6	13	NULL	NULL	NULL	statement 6	Process		inhibits					calcification	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1423_s_126	16601233	44 MGP is a calcium-binding matrix protein that binds and inhibits BMP2 induction of ALP. 45 In addition, carboxylated MGP produced by VSMCs binds matrix elastin and inhibits calcification.	bind
33301	1	8232	7	NULL	NULL	0	NULL	 MGP	NULL		is a type of	NULL				calcium-binding matrix protein	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1423_s_126	16601233	44 MGP is a calcium-binding matrix protein that binds and inhibits BMP2 induction of ALP. 45 In addition, carboxylated MGP produced by VSMCs binds matrix elastin and inhibits calcification.	bind
33302	2	8232	7	NULL	NULL	0	NULL	MGP	NULL		binds	NULL				BMP2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1423_s_126	16601233	44 MGP is a calcium-binding matrix protein that binds and inhibits BMP2 induction of ALP. 45 In addition, carboxylated MGP produced by VSMCs binds matrix elastin and inhibits calcification.	bind
33303	3	8232	7	NULL	NULL	0	NULL	BMP2	NULL		induce	NULL				ALP	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1423_s_126	16601233	44 MGP is a calcium-binding matrix protein that binds and inhibits BMP2 induction of ALP. 45 In addition, carboxylated MGP produced by VSMCs binds matrix elastin and inhibits calcification.	bind
33304	4	8232	7	NULL	NULL	0	NULL	statement 2	NULL		inhibits	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1423_s_126	16601233	44 MGP is a calcium-binding matrix protein that binds and inhibits BMP2 induction of ALP. 45 In addition, carboxylated MGP produced by VSMCs binds matrix elastin and inhibits calcification.	bind
33305	5	8232	7	10	NULL	0	NULL	VSMCs	NULL		produce	NULL				MGP	NULL	carboxylated			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1423_s_126	16601233	44 MGP is a calcium-binding matrix protein that binds and inhibits BMP2 induction of ALP. 45 In addition, carboxylated MGP produced by VSMCs binds matrix elastin and inhibits calcification.	bind
33306	6	8232	7	10	NULL	0	NULL	MGP	NULL	carboxylated	binds	NULL				matrix elastin	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1423_s_126	16601233	44 MGP is a calcium-binding matrix protein that binds and inhibits BMP2 induction of ALP. 45 In addition, carboxylated MGP produced by VSMCs binds matrix elastin and inhibits calcification.	bind
33307	7	8232	7	NULL	NULL	0	NULL	statement 6	NULL		inhibits	NULL				calcification	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1423_s_126	16601233	44 MGP is a calcium-binding matrix protein that binds and inhibits BMP2 induction of ALP. 45 In addition, carboxylated MGP produced by VSMCs binds matrix elastin and inhibits calcification.	bind
27308	1	8233	6	13	NULL	NULL	NULL	heparin	Chemical		bind					growth factors	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_937_s_220	16195480	44 Though heparin binding to growth factors may be involved in the inhibition of PASMC proliferation, this is not the only mechanism.	bind
27309	2	8233	6	13	NULL	NULL	NULL	statement 1	Process		is involved in					PASMC	Cell	inhibiton of;;proliferation of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_937_s_220	16195480	44 Though heparin binding to growth factors may be involved in the inhibition of PASMC proliferation, this is not the only mechanism.	bind
33308	1	8233	7	NULL	NULL	0	NULL	heparin	NULL		bind	NULL				growth factors	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_9_937_s_220	16195480	44 Though heparin binding to growth factors may be involved in the inhibition of PASMC proliferation, this is not the only mechanism.	bind
33309	2	8233	7	10	NULL	0	NULL	statement 1	NULL		be involved in	NULL	may			PASMC 	NULL	inhibition of;;proliferation of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_9_937_s_220	16195480	44 Though heparin binding to growth factors may be involved in the inhibition of PASMC proliferation, this is not the only mechanism.	bind
27310	1	8234	6	13	NULL	NULL	NULL	TIMP-2	GP		bind					proMMP-2	GP		hemopexin domain		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_8_827_s_118	12730128	44 TIMP-2 binds to the hemopexin domain of proMMP-2.	bind
33310	1	8234	7	NULL	NULL	0	NULL	TIMP-2 	NULL		binds to	NULL				proMMP-2	NULL		hemopexin domain		NULL		0	NULL	NULL	NULL	gw70_circulationres_92_8_827_s_118	12730128	44 TIMP-2 binds to the hemopexin domain of proMMP-2.	bind
27311	1	8235	6	13	NULL	NULL	NULL	VEGF	GP		bind					VEGF receptor 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1143_s_113	12676799	44 We also discovered that the weak arteriogenic effects of chronically infused VEGF A is caused by the monocyte attractant effect of VEGF that binds to the VEGF receptor 1, which is exclusively present on monocytes.	bind
27312	2	8235	6	13	NULL	NULL	NULL	VEGF receptor	GP		is present on		exclusively			monocytes	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1143_s_113	12676799	44 We also discovered that the weak arteriogenic effects of chronically infused VEGF A is caused by the monocyte attractant effect of VEGF that binds to the VEGF receptor 1, which is exclusively present on monocytes.	bind
27313	3	8235	6	13	NULL	NULL	NULL	VEGF 	GP		exhibits					monocyte attractant effect	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1143_s_113	12676799	44 We also discovered that the weak arteriogenic effects of chronically infused VEGF A is caused by the monocyte attractant effect of VEGF that binds to the VEGF receptor 1, which is exclusively present on monocytes.	bind
27314	4	8235	6	13	NULL	NULL	NULL	VEGF A	GP	weak arteriogenic effects of	is caused by					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1143_s_113	12676799	44 We also discovered that the weak arteriogenic effects of chronically infused VEGF A is caused by the monocyte attractant effect of VEGF that binds to the VEGF receptor 1, which is exclusively present on monocytes.	bind
33311	1	8235	7	NULL	NULL	0	NULL	VEGF 	NULL		binds to	NULL				VEGF receptor 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1143_s_113	12676799	44 We also discovered that the weak arteriogenic effects of chronically infused VEGF A is caused by the monocyte attractant effect of VEGF that binds to the VEGF receptor 1, which is exclusively present on monocytes.	bind
33312	2	8235	7	NULL	NULL	0	NULL	VEGF	NULL		attract	NULL				monocyte	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1143_s_113	12676799	44 We also discovered that the weak arteriogenic effects of chronically infused VEGF A is caused by the monocyte attractant effect of VEGF that binds to the VEGF receptor 1, which is exclusively present on monocytes.	bind
33313	3	8235	7	NULL	NULL	0	NULL	statement 2	NULL		cause	NULL				VEGF A	NULL	weak arteriogenic effects of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1143_s_113	12676799	44 We also discovered that the weak arteriogenic effects of chronically infused VEGF A is caused by the monocyte attractant effect of VEGF that binds to the VEGF receptor 1, which is exclusively present on monocytes.	bind
33314	4	8235	7	NULL	NULL	0	NULL	VEGF receptor 1	NULL		 present in	NULL	exclusively			monocytes	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1143_s_113	12676799	44 We also discovered that the weak arteriogenic effects of chronically infused VEGF A is caused by the monocyte attractant effect of VEGF that binds to the VEGF receptor 1, which is exclusively present on monocytes.	bind
27315	1	8236	6	13	NULL	NULL	NULL	fibronectin	GP		bind					collagen	GP	native			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_5_1489_s_153	10793060	44, 105  Although fibronectin does bind native collagens, it shows a markedly increased affinity for denatured collagen.	bind
27316	2	8236	6	13	NULL	NULL	NULL	fibronectin	GP		bind					collagen	GP	denatured			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_5_1489_s_153	10793060	44, 105  Although fibronectin does bind native collagens, it shows a markedly increased affinity for denatured collagen.	bind
46708	3	8236	6	13	NULL	NULL	NULL	statement 2	Process	affinity of	is higher than					statement 1	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_5_1489_s_153	10793060	44, 105  Although fibronectin does bind native collagens, it shows a markedly increased affinity for denatured collagen.	bind
33315	1	8236	7	NULL	NULL	0	NULL	fibronectin	NULL		bind	NULL				collagen	NULL	native			NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_5_1489_s_153	10793060	44, 105  Although fibronectin does bind native collagens, it shows a markedly increased affinity for denatured collagen.	bind
33316	2	8236	7	NULL	NULL	0	NULL	fibronectin	NULL		bind	NULL				collagen	NULL	denatured			NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_5_1489_s_153	10793060	44, 105  Although fibronectin does bind native collagens, it shows a markedly increased affinity for denatured collagen.	bind
33317	3	8236	7	NULL	NULL	0	NULL	statement 2	NULL	affinity of	is higher than	NULL				statement 1	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_5_1489_s_153	10793060	44, 105  Although fibronectin does bind native collagens, it shows a markedly increased affinity for denatured collagen.	bind
27317	1	8237	6	13	NULL	NULL	NULL	IGF-1	GP		bind					IGF-1R	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
27318	2	8237	6	13	NULL	NULL	NULL	IGF-1	GP		bind					IGFBP	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
27319	3	8237	6	13	NULL	NULL	NULL	IGFBP	GP		bind					extracellular matrix	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
27320	4	8237	6	13	NULL	NULL	NULL	IGFBP	GP	proteolysis of	results in					statement 2	Process	loss of 			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
27321	5	8237	6	13	NULL	NULL	NULL	IGFBP	GP	polymerization of 	results in					statement 2	Process	loss of 			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
27322	6	8237	6	13	NULL	NULL	NULL	IGFBP	GP	proteolysis of	increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
27323	7	8237	6	13	NULL	NULL	NULL	IGFBP	GP	polymerization of	increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
27324	8	8237	6	13	NULL	NULL	NULL	IGFBP	GP	proteolysis of	increases					IGF-1	GP	activity of 			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
27325	9	8237	6	13	NULL	NULL	NULL	IGFBP	GP	polymerization of	increases					IGF-1	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33318	1	8237	7	NULL	NULL	0	NULL	IGFBPs	NULL		undergoes	NULL				polymerization 	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33319	2	8237	7	NULL	NULL	0	NULL	IGFBPs	NULL		undergoes	NULL				proteolysis	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33320	3	8237	7	NULL	NULL	0	NULL	IGFBPs	NULL		bind	NULL				extracellular matrix	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33321	4	8237	7	NULL	NULL	0	NULL	IGF-1	NULL		bind	NULL				IGFBPs	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33322	5	8237	7	NULL	NULL	0	NULL	statement 1	NULL		reduce	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33323	6	8237	7	NULL	NULL	0	NULL	statement 2	NULL		reduce	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33324	7	8237	7	NULL	NULL	0	NULL	statement 3	NULL		reduce	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33325	8	8237	7	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				statement 4	NULL	loss of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33326	9	8237	7	NULL	NULL	0	NULL	statement 2	NULL		results in	NULL				statement 4	NULL	loss of 			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33327	10	8237	7	NULL	NULL	0	NULL	statement 3	NULL		results in	NULL				statement 4	NULL	loss of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33328	11	8237	7	NULL	NULL	0	NULL	statement 5	NULL		is an alternative to	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33329	12	8237	7	NULL	NULL	0	NULL	statement 6	NULL		is an alternative to	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33330	13	8237	7	NULL	NULL	0	NULL	statement 7	NULL		is an alternative to	NULL				statement 10	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33331	14	8237	7	NULL	NULL	0	NULL	IGF-1	NULL		bind	NULL				IGF-1R 	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33332	15	8237	7	NULL	NULL	0	NULL	statement 11	NULL		increase	NULL				statement 14	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33333	16	8237	7	NULL	NULL	0	NULL	statement 12	NULL		increase	NULL				statement 14	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33334	17	8237	7	NULL	NULL	0	NULL	statement 13	NULL		increase	NULL				statement 14	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33335	18	8237	7	NULL	NULL	0	NULL	statement 11	NULL		increase	NULL				IGF-1	NULL	activity of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33336	19	8237	7	NULL	NULL	0	NULL	statement 12	NULL		increase	NULL				IGF-1	NULL	activity of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
33337	20	8237	7	NULL	NULL	0	NULL	statement 13	NULL		increase	NULL				IGF-1	NULL	activity of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_3_435_s_94	14604834	44,45  However, proteolysis or polymerization of IGFBPs or binding to extracellular matrix results in reduction or loss of IGF-1 binding to IGFBPs, thus increasing the binding of IGF-1 to IGF-1R and the activity of IGF-1.	bind
27326	1	8238	6	13	NULL	NULL	NULL	collagenase gene	GP		contains				promoter					TPA responsive unit	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1661_s_467	11292838	45       Gutman,A. and Wasylyk,B. (1990) The collagenase gene promoter contains a TPA and oncogene-responsive unit encompassing the PEA3 and AP-1 binding sites.	bind
27327	2	8238	6	13	NULL	NULL	NULL	collagenase gene	GP		contains				promoter					oncogene-responsive unit	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1661_s_467	11292838	45       Gutman,A. and Wasylyk,B. (1990) The collagenase gene promoter contains a TPA and oncogene-responsive unit encompassing the PEA3 and AP-1 binding sites.	bind
46709	3	8238	6	10	NULL	0	NULL		NULL		encompass	NULL			oncogene-responsive unit		NULL			AP-1 binding site	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1661_s_467	11292838	45       Gutman,A. and Wasylyk,B. (1990) The collagenase gene promoter contains a TPA and oncogene-responsive unit encompassing the PEA3 and AP-1 binding sites.	bind
46710	4	8238	6	10	NULL	0	NULL		NULL		encompass	NULL			TPA responsive unit		NULL			PEA3 binding site	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1661_s_467	11292838	45       Gutman,A. and Wasylyk,B. (1990) The collagenase gene promoter contains a TPA and oncogene-responsive unit encompassing the PEA3 and AP-1 binding sites.	bind
33338	1	8238	7	NULL	NULL	0	NULL	collagenase gene	NULL		contains	NULL			promoter		NULL			TPA responsive unit	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1661_s_467	11292838	45       Gutman,A. and Wasylyk,B. (1990) The collagenase gene promoter contains a TPA and oncogene-responsive unit encompassing the PEA3 and AP-1 binding sites.	bind
33339	2	8238	7	NULL	NULL	0	NULL	collagenase gene	NULL		contains	NULL			promoter		NULL			oncogene-responsive unit	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1661_s_467	11292838	45       Gutman,A. and Wasylyk,B. (1990) The collagenase gene promoter contains a TPA and oncogene-responsive unit encompassing the PEA3 and AP-1 binding sites.	bind
33340	3	8238	7	NULL	NULL	0	NULL		NULL		encompass	NULL			 TPA responsive unit		NULL			PEA3 binding site	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1661_s_467	11292838	45       Gutman,A. and Wasylyk,B. (1990) The collagenase gene promoter contains a TPA and oncogene-responsive unit encompassing the PEA3 and AP-1 binding sites.	bind
33341	4	8238	7	NULL	NULL	0	NULL		NULL		encompass	NULL			oncogene-responsive unit		NULL			AP-1 binding site	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1661_s_467	11292838	45       Gutman,A. and Wasylyk,B. (1990) The collagenase gene promoter contains a TPA and oncogene-responsive unit encompassing the PEA3 and AP-1 binding sites.	bind
27328	1	8239	6	13	NULL	NULL	NULL	GAL4	GP		bind		facilitated			nucleosomal template	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3520_s_420	11522821	45       Taylor,I.C.A., Workman,J.L., Schuetz,T.J. and Kingston,R.E. (1991) Facilitated binding of GAL4 and heat shock factor to nucleosomal templates: differential function of DNA binding domains.	bind
27329	2	8239	6	13	NULL	NULL	NULL	heat shock factor	GP		bind		facilitated			nucleosomal template	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3520_s_420	11522821	45       Taylor,I.C.A., Workman,J.L., Schuetz,T.J. and Kingston,R.E. (1991) Facilitated binding of GAL4 and heat shock factor to nucleosomal templates: differential function of DNA binding domains.	bind
33342	1	8239	7	NULL	NULL	0	NULL	GAL4	NULL		bind	NULL	facilitated			nucleosomal templates	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3520_s_420	11522821	45       Taylor,I.C.A., Workman,J.L., Schuetz,T.J. and Kingston,R.E. (1991) Facilitated binding of GAL4 and heat shock factor to nucleosomal templates: differential function of DNA binding domains.	bind
33343	2	8239	7	NULL	NULL	0	NULL	heat shock factor	NULL		bind	NULL	facilitated			nucleosomal templates	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3520_s_420	11522821	45       Taylor,I.C.A., Workman,J.L., Schuetz,T.J. and Kingston,R.E. (1991) Facilitated binding of GAL4 and heat shock factor to nucleosomal templates: differential function of DNA binding domains.	bind
27330	1	8240	6	13	NULL	NULL	NULL	MSG1	GP		bind					p300/CBP coactivators	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_732_s_406	11160896	45       Yahata,T., de Caestecker,M.P., Lechleider,R.J., Andriole,S., Roberts,A.B., Isselbacher,K.J. and Shioda,T. (2000) The MSG1 non-DNA-binding transactivator binds to the p300/CBP coactivators, enhancing their functional link to the Smad transcription factors.	bind
27331	2	8240	6	13	NULL	NULL	NULL	MSG1	GP		is a type of					non-DNA-binding transactivator	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_732_s_406	11160896	45       Yahata,T., de Caestecker,M.P., Lechleider,R.J., Andriole,S., Roberts,A.B., Isselbacher,K.J. and Shioda,T. (2000) The MSG1 non-DNA-binding transactivator binds to the p300/CBP coactivators, enhancing their functional link to the Smad transcription factors.	bind
27332	3	8240	6	13	NULL	NULL	NULL	p300/CBP coactivators	GP		exhibit					Smad	GP	functional link to			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_732_s_406	11160896	45       Yahata,T., de Caestecker,M.P., Lechleider,R.J., Andriole,S., Roberts,A.B., Isselbacher,K.J. and Shioda,T. (2000) The MSG1 non-DNA-binding transactivator binds to the p300/CBP coactivators, enhancing their functional link to the Smad transcription factors.	bind
27333	4	8240	6	13	NULL	NULL	NULL	statement 1	Process		enhances					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_732_s_406	11160896	45       Yahata,T., de Caestecker,M.P., Lechleider,R.J., Andriole,S., Roberts,A.B., Isselbacher,K.J. and Shioda,T. (2000) The MSG1 non-DNA-binding transactivator binds to the p300/CBP coactivators, enhancing their functional link to the Smad transcription factors.	bind
46712	5	8240	6	13	NULL	NULL	NULL	Smad	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_732_s_406	11160896	45       Yahata,T., de Caestecker,M.P., Lechleider,R.J., Andriole,S., Roberts,A.B., Isselbacher,K.J. and Shioda,T. (2000) The MSG1 non-DNA-binding transactivator binds to the p300/CBP coactivators, enhancing their functional link to the Smad transcription factors.	bind
33344	1	8240	7	NULL	NULL	0	NULL	MSG1	NULL		binds	NULL				p300/CBP 	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_732_s_406	11160896	45       Yahata,T., de Caestecker,M.P., Lechleider,R.J., Andriole,S., Roberts,A.B., Isselbacher,K.J. and Shioda,T. (2000) The MSG1 non-DNA-binding transactivator binds to the p300/CBP coactivators, enhancing their functional link to the Smad transcription factors.	bind
33345	2	8240	7	NULL	NULL	0	NULL	MSG1	NULL		is a type of	NULL				non-DNA-binding transactivator	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_732_s_406	11160896	45       Yahata,T., de Caestecker,M.P., Lechleider,R.J., Andriole,S., Roberts,A.B., Isselbacher,K.J. and Shioda,T. (2000) The MSG1 non-DNA-binding transactivator binds to the p300/CBP coactivators, enhancing their functional link to the Smad transcription factors.	bind
33346	3	8240	7	NULL	NULL	0	NULL	p300/CBP 	NULL		is a type of	NULL				coactivator	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_732_s_406	11160896	45       Yahata,T., de Caestecker,M.P., Lechleider,R.J., Andriole,S., Roberts,A.B., Isselbacher,K.J. and Shioda,T. (2000) The MSG1 non-DNA-binding transactivator binds to the p300/CBP coactivators, enhancing their functional link to the Smad transcription factors.	bind
33347	4	8240	7	NULL	NULL	0	NULL	statement 1	NULL		enhance	NULL				Smad	NULL	functional link to			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_732_s_406	11160896	45       Yahata,T., de Caestecker,M.P., Lechleider,R.J., Andriole,S., Roberts,A.B., Isselbacher,K.J. and Shioda,T. (2000) The MSG1 non-DNA-binding transactivator binds to the p300/CBP coactivators, enhancing their functional link to the Smad transcription factors.	bind
33348	5	8240	7	NULL	NULL	0	NULL	Smad	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_732_s_406	11160896	45       Yahata,T., de Caestecker,M.P., Lechleider,R.J., Andriole,S., Roberts,A.B., Isselbacher,K.J. and Shioda,T. (2000) The MSG1 non-DNA-binding transactivator binds to the p300/CBP coactivators, enhancing their functional link to the Smad transcription factors.	bind
27334	1	8241	6	13	NULL	NULL	NULL	decorin	GP		bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_6_676_s_200	10747004	45  46  It also may be that the binding of decorin to collagen inhibits collagen degradation and stabilizes the collagen fibrillar network.	bind
27335	2	8241	6	13	NULL	NULL	NULL	statement 1	Process		inhibits		may			collagen 	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_6_676_s_200	10747004	45  46  It also may be that the binding of decorin to collagen inhibits collagen degradation and stabilizes the collagen fibrillar network.	bind
27337	3	8241	6	13	NULL	NULL	NULL	statement 1	Process		stabilizes					collagen fibrillar network	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_6_676_s_200	10747004	45  46  It also may be that the binding of decorin to collagen inhibits collagen degradation and stabilizes the collagen fibrillar network.	bind
33351	1	8241	7	NULL	NULL	0	NULL	 decorin 	NULL		bind	NULL				collagen	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_6_676_s_200	10747004	45  46  It also may be that the binding of decorin to collagen inhibits collagen degradation and stabilizes the collagen fibrillar network.	bind
33352	2	8241	7	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				collagen	NULL	degradation of			NULL		0	NULL	NULL	NULL	gw60_circulationres_86_6_676_s_200	10747004	45  46  It also may be that the binding of decorin to collagen inhibits collagen degradation and stabilizes the collagen fibrillar network.	bind
33353	3	8241	7	NULL	NULL	0	NULL	statement 1	NULL		stabilizes	NULL				collagen fibrillar network	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_6_676_s_200	10747004	45  46  It also may be that the binding of decorin to collagen inhibits collagen degradation and stabilizes the collagen fibrillar network.	bind
27339	1	8242	6	13	NULL	NULL	NULL	heparin	Chemical		bind					thrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1414_s_216	9261275	45  Although the amino acid sequences in heparin that bind to thrombin have not been identified, the oligosaccharide sequence in heparin that binds to antithrombin is quite different from that of LPL. 46  Thus, a specific set of monocyte surface HSPGs may bind to LPL and mediate monocyte adhesion.	bind
27340	2	8242	6	13	NULL	NULL	NULL	heparin	Chemical		bind			oligosaccharide sequence		antithrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1414_s_216	9261275	45  Although the amino acid sequences in heparin that bind to thrombin have not been identified, the oligosaccharide sequence in heparin that binds to antithrombin is quite different from that of LPL. 46  Thus, a specific set of monocyte surface HSPGs may bind to LPL and mediate monocyte adhesion.	bind
27342	3	8242	6	13	NULL	NULL	NULL	HSPG	GP	monocyte surface	bind		may			LPL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1414_s_216	9261275	45  Although the amino acid sequences in heparin that bind to thrombin have not been identified, the oligosaccharide sequence in heparin that binds to antithrombin is quite different from that of LPL. 46  Thus, a specific set of monocyte surface HSPGs may bind to LPL and mediate monocyte adhesion.	bind
27345	4	8242	6	13	NULL	NULL	NULL	statement 3	Process		mediate					monocyte	Cell	adhesion of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1414_s_216	9261275	45  Although the amino acid sequences in heparin that bind to thrombin have not been identified, the oligosaccharide sequence in heparin that binds to antithrombin is quite different from that of LPL. 46  Thus, a specific set of monocyte surface HSPGs may bind to LPL and mediate monocyte adhesion.	bind
46714	5	8242	6	13	NULL	NULL	NULL	heparin	Chemical		bind			oligosaccharide sequence		LPL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1414_s_216	9261275	45  Although the amino acid sequences in heparin that bind to thrombin have not been identified, the oligosaccharide sequence in heparin that binds to antithrombin is quite different from that of LPL. 46  Thus, a specific set of monocyte surface HSPGs may bind to LPL and mediate monocyte adhesion.	bind
46715	6	8242	6	13	NULL	NULL	NULL	statement 2	Process	 	is different from					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1414_s_216	9261275	45  Although the amino acid sequences in heparin that bind to thrombin have not been identified, the oligosaccharide sequence in heparin that binds to antithrombin is quite different from that of LPL. 46  Thus, a specific set of monocyte surface HSPGs may bind to LPL and mediate monocyte adhesion.	bind
33356	1	8242	7	NULL	NULL	0	NULL	heparin	NULL		binds to	NULL				thrombin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1414_s_216	9261275	45  Although the amino acid sequences in heparin that bind to thrombin have not been identified, the oligosaccharide sequence in heparin that binds to antithrombin is quite different from that of LPL. 46  Thus, a specific set of monocyte surface HSPGs may bind to LPL and mediate monocyte adhesion.	bind
33357	2	8242	7	10	NULL	0	NULL	heparin	NULL		binds to	NULL		oligosaccharide sequence		antithrombin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1414_s_216	9261275	45  Although the amino acid sequences in heparin that bind to thrombin have not been identified, the oligosaccharide sequence in heparin that binds to antithrombin is quite different from that of LPL. 46  Thus, a specific set of monocyte surface HSPGs may bind to LPL and mediate monocyte adhesion.	bind
33359	3	8242	7	10	NULL	0	NULL	heparin	NULL		binds to	NULL		oligosaccharide sequence		LPL	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1414_s_216	9261275	45  Although the amino acid sequences in heparin that bind to thrombin have not been identified, the oligosaccharide sequence in heparin that binds to antithrombin is quite different from that of LPL. 46  Thus, a specific set of monocyte surface HSPGs may bind to LPL and mediate monocyte adhesion.	bind
33366	4	8242	7	10	NULL	0	NULL	statement 2	NULL		is different from	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1414_s_216	9261275	45  Although the amino acid sequences in heparin that bind to thrombin have not been identified, the oligosaccharide sequence in heparin that binds to antithrombin is quite different from that of LPL. 46  Thus, a specific set of monocyte surface HSPGs may bind to LPL and mediate monocyte adhesion.	bind
33367	5	8242	7	NULL	NULL	0	NULL	HSPGs	NULL	monocyte surface	bind	NULL	may			LPL	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1414_s_216	9261275	45  Although the amino acid sequences in heparin that bind to thrombin have not been identified, the oligosaccharide sequence in heparin that binds to antithrombin is quite different from that of LPL. 46  Thus, a specific set of monocyte surface HSPGs may bind to LPL and mediate monocyte adhesion.	bind
33369	6	8242	7	10	NULL	0	NULL	statement 5	NULL		mediate	NULL				monocyte	NULL	adhesion of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1414_s_216	9261275	45  Although the amino acid sequences in heparin that bind to thrombin have not been identified, the oligosaccharide sequence in heparin that binds to antithrombin is quite different from that of LPL. 46  Thus, a specific set of monocyte surface HSPGs may bind to LPL and mediate monocyte adhesion.	bind
27347	1	8243	6	13	NULL	NULL	NULL	fibrinogen	GP		bind					GP IIb/IIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1532_s_297	8977459	45  Although we cannot totally exclude the possibility that a rapidly reversible fibrinogen binding to GP IIb/IIa was a factor in limiting aggregate size, our results with FITC-fibrinogen point more to a low degree of activation of GP IIb/IIa and to a level of fibrinogen binding insufficient to permit the formation of the macroaggregates.	bind
33372	1	8243	7	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL	reversibly			GP IIb/IIa	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1532_s_297	8977459	45  Although we cannot totally exclude the possibility that a rapidly reversible fibrinogen binding to GP IIb/IIa was a factor in limiting aggregate size, our results with FITC-fibrinogen point more to a low degree of activation of GP IIb/IIa and to a level of fibrinogen binding insufficient to permit the formation of the macroaggregates.	bind
33374	2	8243	7	NULL	NULL	0	NULL	statement 1	NULL		limits	NULL				aggregate size	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1532_s_297	8977459	45  Although we cannot totally exclude the possibility that a rapidly reversible fibrinogen binding to GP IIb/IIa was a factor in limiting aggregate size, our results with FITC-fibrinogen point more to a low degree of activation of GP IIb/IIa and to a level of fibrinogen binding insufficient to permit the formation of the macroaggregates.	bind
33375	3	8243	7	NULL	NULL	0	NULL	statement 1	NULL		insufficient to permit	NULL				macroaggregates	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1532_s_297	8977459	45  Although we cannot totally exclude the possibility that a rapidly reversible fibrinogen binding to GP IIb/IIa was a factor in limiting aggregate size, our results with FITC-fibrinogen point more to a low degree of activation of GP IIb/IIa and to a level of fibrinogen binding insufficient to permit the formation of the macroaggregates.	bind
27352	1	8244	6	13	NULL	NULL	NULL	fibrinogen	GP		bind					GP IIb/IIIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_4_437_s_123	10421606	45  LIBS epitope expression seems to be a normal function of GP IIb/IIa, as evidenced by observations showing that fibrinogen binding to GP IIb/IIIa also induces this effect.	bind
27353	2	8244	6	13	NULL	NULL	NULL	GP IIb/IIa	GP		expresses					LIBS epitope	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_4_437_s_123	10421606	45  LIBS epitope expression seems to be a normal function of GP IIb/IIa, as evidenced by observations showing that fibrinogen binding to GP IIb/IIIa also induces this effect.	bind
27354	3	8244	6	13	NULL	NULL	NULL	statement 1	Process		induces					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_4_437_s_123	10421606	45  LIBS epitope expression seems to be a normal function of GP IIb/IIa, as evidenced by observations showing that fibrinogen binding to GP IIb/IIIa also induces this effect.	bind
33378	1	8244	7	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL				GP IIb/IIIa	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_4_437_s_123	10421606	45  LIBS epitope expression seems to be a normal function of GP IIb/IIa, as evidenced by observations showing that fibrinogen binding to GP IIb/IIIa also induces this effect.	bind
46717	2	8244	7	10	NULL	0	NULL	GP IIb/IIa	NULL		express	NULL				LIBS epitope	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_4_437_s_123	10421606	45  LIBS epitope expression seems to be a normal function of GP IIb/IIa, as evidenced by observations showing that fibrinogen binding to GP IIb/IIIa also induces this effect.	bind
46718	3	8244	7	10	NULL	0	NULL	statement 1	NULL		induce	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_4_437_s_123	10421606	45  LIBS epitope expression seems to be a normal function of GP IIb/IIa, as evidenced by observations showing that fibrinogen binding to GP IIb/IIIa also induces this effect.	bind
27355	1	8245	6	13	NULL	NULL	NULL	PEA-3	GP		bind					ets	GP			consensus binding site	NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_6_1777_s_171	11106549	45  PEA-3, another transcription factor that binds to the ets consensus binding site, has been shown by Trimble et al to be overexpressed in the mammary carcinomas that result from expression of the MMTV-polyoma middle T transgene, making it an attractive candidate for involvement in the induction of MMP-9 promoter activity during tumor progression.	bind
27357	2	8245	6	13	NULL	NULL	NULL	PEA-3	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_6_1777_s_171	11106549	45  PEA-3, another transcription factor that binds to the ets consensus binding site, has been shown by Trimble et al to be overexpressed in the mammary carcinomas that result from expression of the MMTV-polyoma middle T transgene, making it an attractive candidate for involvement in the induction of MMP-9 promoter activity during tumor progression.	bind
27362	3	8245	6	13	NULL	NULL	NULL	PEA-3	GP		is overexpressed in					mammary carcinomas	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_6_1777_s_171	11106549	45  PEA-3, another transcription factor that binds to the ets consensus binding site, has been shown by Trimble et al to be overexpressed in the mammary carcinomas that result from expression of the MMTV-polyoma middle T transgene, making it an attractive candidate for involvement in the induction of MMP-9 promoter activity during tumor progression.	bind
27366	4	8245	6	13	NULL	NULL	NULL	PEA-3	GP		is involved in					MMP-9	GP	induction of;; activity of		promoter	NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_6_1777_s_171	11106549	45  PEA-3, another transcription factor that binds to the ets consensus binding site, has been shown by Trimble et al to be overexpressed in the mammary carcinomas that result from expression of the MMTV-polyoma middle T transgene, making it an attractive candidate for involvement in the induction of MMP-9 promoter activity during tumor progression.	bind
27368	5	8245	6	13	NULL	NULL	NULL	statement 4	Process		occurs during					tumor progression	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_6_1777_s_171	11106549	45  PEA-3, another transcription factor that binds to the ets consensus binding site, has been shown by Trimble et al to be overexpressed in the mammary carcinomas that result from expression of the MMTV-polyoma middle T transgene, making it an attractive candidate for involvement in the induction of MMP-9 promoter activity during tumor progression.	bind
55954	6	8245	6	13	NULL	NULL	NULL	statement 3	Process		results from					MMTV-polyoma middle T transgene	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_6_1777_s_171	11106549	45  PEA-3, another transcription factor that binds to the ets consensus binding site, has been shown by Trimble et al to be overexpressed in the mammary carcinomas that result from expression of the MMTV-polyoma middle T transgene, making it an attractive candidate for involvement in the induction of MMP-9 promoter activity during tumor progression.	bind
33381	1	8245	7	10	NULL	0	NULL	 PEA-3			binds to					ets				consensus binding site	NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_6_1777_s_171	11106549	45  PEA-3, another transcription factor that binds to the ets consensus binding site, has been shown by Trimble et al to be overexpressed in the mammary carcinomas that result from expression of the MMTV-polyoma middle T transgene, making it an attractive candidate for involvement in the induction of MMP-9 promoter activity during tumor progression.	bind
33382	2	8245	7	NULL	NULL	0	NULL	PEA-3	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_6_1777_s_171	11106549	45  PEA-3, another transcription factor that binds to the ets consensus binding site, has been shown by Trimble et al to be overexpressed in the mammary carcinomas that result from expression of the MMTV-polyoma middle T transgene, making it an attractive candidate for involvement in the induction of MMP-9 promoter activity during tumor progression.	bind
33383	3	8245	7	10	NULL	0	NULL	statement  6			result from					MMTV-polyoma middle T transgene		expression of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_6_1777_s_171	11106549	45  PEA-3, another transcription factor that binds to the ets consensus binding site, has been shown by Trimble et al to be overexpressed in the mammary carcinomas that result from expression of the MMTV-polyoma middle T transgene, making it an attractive candidate for involvement in the induction of MMP-9 promoter activity during tumor progression.	bind
33463	4	8245	7	10	NULL	0	NULL	 PEA-3			is involved in					MMP-9 		induction of;;activity of		promoter	NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_6_1777_s_171	11106549	45  PEA-3, another transcription factor that binds to the ets consensus binding site, has been shown by Trimble et al to be overexpressed in the mammary carcinomas that result from expression of the MMTV-polyoma middle T transgene, making it an attractive candidate for involvement in the induction of MMP-9 promoter activity during tumor progression.	bind
33464	5	8245	7	NULL	NULL	0	NULL	statement 4	NULL		occurs during	NULL				tumor progression	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_6_1777_s_171	11106549	45  PEA-3, another transcription factor that binds to the ets consensus binding site, has been shown by Trimble et al to be overexpressed in the mammary carcinomas that result from expression of the MMTV-polyoma middle T transgene, making it an attractive candidate for involvement in the induction of MMP-9 promoter activity during tumor progression.	bind
55953	6	8245	7	10	NULL	0	NULL	PEA-3			is overexpressed in					mammary carcinomas					NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_6_1777_s_171	11106549	45  PEA-3, another transcription factor that binds to the ets consensus binding site, has been shown by Trimble et al to be overexpressed in the mammary carcinomas that result from expression of the MMTV-polyoma middle T transgene, making it an attractive candidate for involvement in the induction of MMP-9 promoter activity during tumor progression.	bind
27370	1	8246	6	13	NULL	NULL	NULL	LDL	GP		bind					PG	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_1053_s_143	11397719	45  Surprisingly, as shown in this study, after prolonged incubation (36 hours), mere binding of LDL to PGs can induce aggregation of a fraction of the LDL particles.	bind
27371	2	8246	6	13	NULL	NULL	NULL	statement 1	Process		induce					LDL particles	GP	aggregation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_1053_s_143	11397719	45  Surprisingly, as shown in this study, after prolonged incubation (36 hours), mere binding of LDL to PGs can induce aggregation of a fraction of the LDL particles.	bind
33465	1	8246	7	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				PGs	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_1053_s_143	11397719	45  Surprisingly, as shown in this study, after prolonged incubation (36 hours), mere binding of LDL to PGs can induce aggregation of a fraction of the LDL particles.	bind
33466	2	8246	7	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL				LDL particles	NULL	aggregation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_6_1053_s_143	11397719	45  Surprisingly, as shown in this study, after prolonged incubation (36 hours), mere binding of LDL to PGs can induce aggregation of a fraction of the LDL particles.	bind
27372	1	8247	6	13	NULL	NULL	NULL	Mox1 protein	GP		bind		directly	 		Pax1 protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_6_2181_s_241	12057921	45  The Mox1 and Mox2 proteins bind directly to Pax1 and Pax3 proteins, respectively.	bind
27374	2	8247	6	13	NULL	NULL	NULL	Mox2 protein	GP		bind		directly			Pax3 protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_6_2181_s_241	12057921	45  The Mox1 and Mox2 proteins bind directly to Pax1 and Pax3 proteins, respectively.	bind
33467	1	8247	7	NULL	NULL	0	NULL	Mox1 protein	NULL		bind	NULL	directly			Pax1 protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_6_2181_s_241	12057921	45  The Mox1 and Mox2 proteins bind directly to Pax1 and Pax3 proteins, respectively.	bind
33468	2	8247	7	NULL	NULL	0	NULL	Mox2 protein	NULL		bind	NULL	directly			Pax3 protein	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_6_2181_s_241	12057921	45  The Mox1 and Mox2 proteins bind directly to Pax1 and Pax3 proteins, respectively.	bind
27378	1	8248	6	13	NULL	NULL	NULL	endothelial cells	Cell		produce					1MCP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
27381	2	8248	6	13	NULL	NULL	NULL	endothelial cells	Cell		produce					M-CSF	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
27382	3	8248	6	13	NULL	NULL	NULL	endothelial cells	Cell		produce					GRO	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
27383	4	8248	6	13	NULL	NULL	NULL	LDL	GP	mildly oxidized	induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
27384	5	8248	6	13	NULL	NULL	NULL	LDL	GP	mildly oxidized	induce					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
27385	6	8248	6	13	NULL	NULL	NULL	LDL	GP	mildly oxidized	induce					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
27387	7	8248	6	13	NULL	NULL	NULL	GRO	GP		bind					heparin-like molecules	GP				NULL	endothelial cell surface	NULL	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
27390	8	8248	6	13	NULL	NULL	NULL	1MCP-1	GP		is					monocyte chemoattractant protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
27392	9	8248	6	13	NULL	NULL	NULL	M-CSF	GP		is					monocyte colony stimulating factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
27393	10	8248	6	13	NULL	NULL	NULL	M-CSF	GP		is a type of					soluble molecule	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
27395	11	8248	6	13	NULL	NULL	NULL	1MCP-1	GP		is a type of					soluble molecule	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
46719	12	8248	6	13	NULL	NULL	NULL	1MCP-1	GP		is a type of					monocyte activator	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
46720	13	8248	6	13	NULL	NULL	NULL	M-CSF	GP		is a type of					monocyte activator	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
33469	1	8248	7	10	NULL	0	NULL	LDL		mildly oxidized	induce					endothelial cells					NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
33470	2	8248	7	NULL	NULL	0	NULL	statement 1	NULL		produce	NULL				1MCP-1	NULL	potent			NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
33471	3	8248	7	NULL	NULL	0	NULL	statement 1	NULL		produce	NULL				M-CSF	NULL	potent			NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
33472	4	8248	7	NULL	NULL	0	NULL	statement 1	NULL		produce	NULL				GRO	NULL	potent			NULL		0	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
33473	5	8248	7	NULL	NULL	0	NULL	1MCP-1	NULL		is a type of	NULL				monocyte activators	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
33474	6	8248	7	NULL	NULL	0	NULL	M-CSF	NULL		is a type of	NULL				 monocyte activators	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
33475	7	8248	7	NULL	NULL	0	NULL	1MCP-1	NULL		is	NULL				monocyte chemoattractant protein	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
33476	8	8248	7	NULL	NULL	0	NULL	M-CSF	NULL		is	NULL				monocyte colony stimulating factor 	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
33477	9	8248	7	NULL	NULL	0	NULL	GRO	NULL		bind	NULL				heparin-like molecules	NULL				NULL	endothelial cell surface	0	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
33478	10	8248	7	NULL	NULL	0	NULL	M-CSF	NULL		is a type of	NULL				soluble molecule	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
33479	11	8248	7	NULL	NULL	0	NULL	MCP-1	NULL		is a type of	NULL				soluble molecule	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_9_2488_s_50	7729036	45 47  Moreover, mildly oxidized LDL induced endothelial cells to produce the potent monocyte activators monocyte chemoattractant protein (1MCP-1), 48  monocyte colony stimulating factor (M-CSF), 49  and GRO. 50  While M-CSF and MCP-1 appear to be soluble molecules, GRO was found bound to heparin-like molecules on the endothelial cell surface.	bind
27399	1	8249	6	13	NULL	NULL	NULL	Keap1	GP		bind					actin cytoskeleton	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_10_967_s_145	16284189	45 Curiously, Keap1 is a cysteine-rich protein that can bind to the actin cytoskeleton in addition to binding to Nrf2.	bind
27403	2	8249	6	13	NULL	NULL	NULL	Keap1	GP		is a type of					cysteine-rich protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_10_967_s_145	16284189	45 Curiously, Keap1 is a cysteine-rich protein that can bind to the actin cytoskeleton in addition to binding to Nrf2.	bind
27404	3	8249	6	13	NULL	NULL	NULL	Keap1	GP		bind					Nrf2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_10_967_s_145	16284189	45 Curiously, Keap1 is a cysteine-rich protein that can bind to the actin cytoskeleton in addition to binding to Nrf2.	bind
33480	1	8249	7	NULL	NULL	0	NULL	Keap1	NULL		bind	NULL				actin cytoskeleton	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_10_967_s_145	16284189	45 Curiously, Keap1 is a cysteine-rich protein that can bind to the actin cytoskeleton in addition to binding to Nrf2.	bind
33481	2	8249	7	NULL	NULL	0	NULL	 Keap1	NULL		bind	NULL				Nrf2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_10_967_s_145	16284189	45 Curiously, Keap1 is a cysteine-rich protein that can bind to the actin cytoskeleton in addition to binding to Nrf2.	bind
33482	3	8249	7	NULL	NULL	0	NULL	Keap1	NULL		is a type of	NULL				cysteine-rich protein	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_10_967_s_145	16284189	45 Curiously, Keap1 is a cysteine-rich protein that can bind to the actin cytoskeleton in addition to binding to Nrf2.	bind
27406	1	8250	6	13	NULL	NULL	NULL	HIF-1	GP		bind					VEGF	GP			hypoxia-response element of promoter	NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_16_2477_s_205	16230500	45 Hypoxia upregulates  VEGF gene transcription by activating the hypoxia-inducible transcription factors HIF-1 and HIF-2, which bind the hypoxia-response element in the  VEGF promotor.	bind
27408	2	8250	6	13	NULL	NULL	NULL	HIF-2	GP		bind					VEGF	GP			hypoxia-response element of promoter	NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_16_2477_s_205	16230500	45 Hypoxia upregulates  VEGF gene transcription by activating the hypoxia-inducible transcription factors HIF-1 and HIF-2, which bind the hypoxia-response element in the  VEGF promotor.	bind
27450	3	8250	6	13	NULL	NULL	NULL	hypoxia	MedicalFinding		upregulates					VEGF gene	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_16_2477_s_205	16230500	45 Hypoxia upregulates  VEGF gene transcription by activating the hypoxia-inducible transcription factors HIF-1 and HIF-2, which bind the hypoxia-response element in the  VEGF promotor.	bind
46722	4	8250	6	13	NULL	NULL	NULL	statement 1	Process		occurs by					HIF-1	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_16_2477_s_205	16230500	45 Hypoxia upregulates  VEGF gene transcription by activating the hypoxia-inducible transcription factors HIF-1 and HIF-2, which bind the hypoxia-response element in the  VEGF promotor.	bind
46723	5	8250	6	13	NULL	NULL	NULL	statement 1	Process		occurs by					HIF-2	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_16_2477_s_205	16230500	45 Hypoxia upregulates  VEGF gene transcription by activating the hypoxia-inducible transcription factors HIF-1 and HIF-2, which bind the hypoxia-response element in the  VEGF promotor.	bind
33483	1	8250	7	10	NULL	0	NULL	Hypoxia	NULL		upregulates	NULL				VEGF gene	NULL	transcription of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_16_2477_s_205	16230500	45 Hypoxia upregulates  VEGF gene transcription by activating the hypoxia-inducible transcription factors HIF-1 and HIF-2, which bind the hypoxia-response element in the  VEGF promotor.	bind
33484	2	8250	7	NULL	NULL	0	NULL	HIF-1	NULL		bind	NULL				VEGF	NULL			hypoxia-response element in the promoter	NULL		0	NULL	NULL	NULL	gw70_circulation_112_16_2477_s_205	16230500	45 Hypoxia upregulates  VEGF gene transcription by activating the hypoxia-inducible transcription factors HIF-1 and HIF-2, which bind the hypoxia-response element in the  VEGF promotor.	bind
33485	3	8250	7	NULL	NULL	0	NULL	HIF-2	NULL		bind	NULL				VEGF	NULL			hypoxia-response element in the promoter	NULL		0	NULL	NULL	NULL	gw70_circulation_112_16_2477_s_205	16230500	45 Hypoxia upregulates  VEGF gene transcription by activating the hypoxia-inducible transcription factors HIF-1 and HIF-2, which bind the hypoxia-response element in the  VEGF promotor.	bind
33486	4	8250	7	10	NULL	0	NULL	statement 1	NULL		occurs by	NULL				HIF-1	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_16_2477_s_205	16230500	45 Hypoxia upregulates  VEGF gene transcription by activating the hypoxia-inducible transcription factors HIF-1 and HIF-2, which bind the hypoxia-response element in the  VEGF promotor.	bind
33487	5	8250	7	10	NULL	0	NULL	statement 1	NULL		occurs by	NULL				HIF-2	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_16_2477_s_205	16230500	45 Hypoxia upregulates  VEGF gene transcription by activating the hypoxia-inducible transcription factors HIF-1 and HIF-2, which bind the hypoxia-response element in the  VEGF promotor.	bind
27459	1	8251	6	13	NULL	NULL	NULL	FAK	GP		bind			amino terminus		RIP	GP		death domain		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_82	16543511	45,46,55   The FAK amino terminus binds to the death domain of RIP, and prevents RIP interaction with the Fas-containing death complex, 56 and the FAK N-terminus also binds to the transactivation domain of p53 to block activation of the Bax promoter.	bind
27462	2	8251	6	13	NULL	NULL	NULL	FAK	GP		bind			N terminus		p53	GP		transactivation domain		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_82	16543511	45,46,55   The FAK amino terminus binds to the death domain of RIP, and prevents RIP interaction with the Fas-containing death complex, 56 and the FAK N-terminus also binds to the transactivation domain of p53 to block activation of the Bax promoter.	bind
27465	3	8251	6	13	NULL	NULL	NULL	statement 2	Process		block					Bax promoter	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_82	16543511	45,46,55   The FAK amino terminus binds to the death domain of RIP, and prevents RIP interaction with the Fas-containing death complex, 56 and the FAK N-terminus also binds to the transactivation domain of p53 to block activation of the Bax promoter.	bind
27466	4	8251	6	13	NULL	NULL	NULL	RIP	GP		interacts with					Fas-containing death complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_82	16543511	45,46,55   The FAK amino terminus binds to the death domain of RIP, and prevents RIP interaction with the Fas-containing death complex, 56 and the FAK N-terminus also binds to the transactivation domain of p53 to block activation of the Bax promoter.	bind
27467	5	8251	6	13	NULL	NULL	NULL	statement 1	Process		prevents					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_82	16543511	45,46,55   The FAK amino terminus binds to the death domain of RIP, and prevents RIP interaction with the Fas-containing death complex, 56 and the FAK N-terminus also binds to the transactivation domain of p53 to block activation of the Bax promoter.	bind
33488	1	8251	7	NULL	NULL	0	NULL	FAK	NULL		binds to	NULL		amino terminus		RIP	NULL		death domain		NULL		0	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_82	16543511	45,46,55   The FAK amino terminus binds to the death domain of RIP, and prevents RIP interaction with the Fas-containing death complex, 56 and the FAK N-terminus also binds to the transactivation domain of p53 to block activation of the Bax promoter.	bind
33489	2	8251	7	NULL	NULL	0	NULL	RIP	NULL		interacts with	NULL				Fas-containing death complex	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_82	16543511	45,46,55   The FAK amino terminus binds to the death domain of RIP, and prevents RIP interaction with the Fas-containing death complex, 56 and the FAK N-terminus also binds to the transactivation domain of p53 to block activation of the Bax promoter.	bind
33490	3	8251	7	NULL	NULL	0	NULL	statement 1	NULL		prevents	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_82	16543511	45,46,55   The FAK amino terminus binds to the death domain of RIP, and prevents RIP interaction with the Fas-containing death complex, 56 and the FAK N-terminus also binds to the transactivation domain of p53 to block activation of the Bax promoter.	bind
33491	4	8251	7	NULL	NULL	0	NULL	FAK	NULL		binds to	NULL		N-terminus		p53	NULL		transactivation domain		NULL		0	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_82	16543511	45,46,55   The FAK amino terminus binds to the death domain of RIP, and prevents RIP interaction with the Fas-containing death complex, 56 and the FAK N-terminus also binds to the transactivation domain of p53 to block activation of the Bax promoter.	bind
33492	5	8251	7	NULL	NULL	0	NULL	statement 4	NULL		block	NULL				Bax	NULL	activation of		promoter	NULL		0	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_82	16543511	45,46,55   The FAK amino terminus binds to the death domain of RIP, and prevents RIP interaction with the Fas-containing death complex, 56 and the FAK N-terminus also binds to the transactivation domain of p53 to block activation of the Bax promoter.	bind
47079	1	8252	6	13	NULL	NULL	NULL	Ca2+	Chemical		bind					GST-PLDbeta proteins	GP	engineered			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_46_47833_s_70	15356005	45Ca2+ Binding Assay -- 45Ca2+ binding of the engineered GST-PLDbeta proteins and GST was evaluated using a described method with some modifications ( ,  ).	bind
33493	1	8252	7	10	NULL	0	NULL	Ca2+			bind					GST-PLDbeta proteins		engineered			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_46_47833_s_70	15356005	45Ca2+ Binding Assay -- 45Ca2+ binding of the engineered GST-PLDbeta proteins and GST was evaluated using a described method with some modifications ( ,  ).	bind
27468	1	8253	6	13	NULL	NULL	NULL	ORC	GP	drosophila	bind		specifically			ACE3	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_809_s_393	11160905	46       Austin,R.J., Orr-Weaver,T.L. and Bell,S.P. (1999) Drosophila ORC specifically binds to ACE3, an origin of DNA replication control element.	bind
27469	2	8253	6	13	NULL	NULL	NULL	ACE3	GP		is a type of					origin of DNA replication control element	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_809_s_393	11160905	46       Austin,R.J., Orr-Weaver,T.L. and Bell,S.P. (1999) Drosophila ORC specifically binds to ACE3, an origin of DNA replication control element.	bind
33494	1	8253	7	NULL	NULL	0	NULL	ORC	NULL	Drosophila	binds	NULL	specifically			ACE3	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_809_s_393	11160905	46       Austin,R.J., Orr-Weaver,T.L. and Bell,S.P. (1999) Drosophila ORC specifically binds to ACE3, an origin of DNA replication control element.	bind
33495	2	8253	7	10	NULL	0	NULL	ACE3	NULL		is a type of	NULL				origin of DNA replication control element	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_809_s_393	11160905	46       Austin,R.J., Orr-Weaver,T.L. and Bell,S.P. (1999) Drosophila ORC specifically binds to ACE3, an origin of DNA replication control element.	bind
27470	1	8254	6	13	NULL	NULL	NULL	high mobility group 1 protein	GP		bind					DNA	NucleicAcid	cisplatin-modified			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1200_s_407	11222770	46       Imamura,T., Izumi,H., Nagatani,G., Ise,T., Nomoto,M., Iwamoto,Y. and Kohno,K. (2001) Interaction with p53 enhances binding of cisplatin-modified DNA by high mobility group 1 protein.	bind
27471	2	8254	6	13	NULL	NULL	NULL	DNA	NucleicAcid	cisplatin modified	interacts with					p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1200_s_407	11222770	46       Imamura,T., Izumi,H., Nagatani,G., Ise,T., Nomoto,M., Iwamoto,Y. and Kohno,K. (2001) Interaction with p53 enhances binding of cisplatin-modified DNA by high mobility group 1 protein.	bind
27472	3	8254	6	13	NULL	NULL	NULL	statement 2	Process		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1200_s_407	11222770	46       Imamura,T., Izumi,H., Nagatani,G., Ise,T., Nomoto,M., Iwamoto,Y. and Kohno,K. (2001) Interaction with p53 enhances binding of cisplatin-modified DNA by high mobility group 1 protein.	bind
33496	1	8254	7	10	NULL	0	NULL	high mobility group 1 protein	NULL		bind	NULL				DNA	NULL	cisplatin-modified			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1200_s_407	11222770	46       Imamura,T., Izumi,H., Nagatani,G., Ise,T., Nomoto,M., Iwamoto,Y. and Kohno,K. (2001) Interaction with p53 enhances binding of cisplatin-modified DNA by high mobility group 1 protein.	bind
33497	2	8254	7	NULL	NULL	0	NULL	p53	NULL		enhances	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1200_s_407	11222770	46       Imamura,T., Izumi,H., Nagatani,G., Ise,T., Nomoto,M., Iwamoto,Y. and Kohno,K. (2001) Interaction with p53 enhances binding of cisplatin-modified DNA by high mobility group 1 protein.	bind
27473	1	8257	6	13	NULL	NULL	NULL	VEGF-D	GP	human	bind					VEGFR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_4_1405_s_373	11943725	46  Human VEGF-D binds and activates VEGFR-2 and VEGFR-3, suggesting roles in angiogenesis and lymphangiogenesis.	bind
27474	2	8257	6	13	NULL	NULL	NULL	VEGF-D	GP	human	bind					VEGFR-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_4_1405_s_373	11943725	46  Human VEGF-D binds and activates VEGFR-2 and VEGFR-3, suggesting roles in angiogenesis and lymphangiogenesis.	bind
27475	3	8257	6	13	NULL	NULL	NULL	statement 1	Process		activates					VEGFR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_4_1405_s_373	11943725	46  Human VEGF-D binds and activates VEGFR-2 and VEGFR-3, suggesting roles in angiogenesis and lymphangiogenesis.	bind
27476	4	8257	6	13	NULL	NULL	NULL	statement 2	Process		activates					VEGFR-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_4_1405_s_373	11943725	46  Human VEGF-D binds and activates VEGFR-2 and VEGFR-3, suggesting roles in angiogenesis and lymphangiogenesis.	bind
27477	5	8257	6	13	NULL	NULL	NULL	statement 1	Process		plays a role in					angiogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_4_1405_s_373	11943725	46  Human VEGF-D binds and activates VEGFR-2 and VEGFR-3, suggesting roles in angiogenesis and lymphangiogenesis.	bind
27478	6	8257	6	13	NULL	NULL	NULL	statement 2	Process		plays a role in					lymphangiogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_4_1405_s_373	11943725	46  Human VEGF-D binds and activates VEGFR-2 and VEGFR-3, suggesting roles in angiogenesis and lymphangiogenesis.	bind
33498	1	8257	7	NULL	NULL	0	NULL	VEGF-D	NULL	human	binds	NULL				VEGFR-2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_4_1405_s_373	11943725	46  Human VEGF-D binds and activates VEGFR-2 and VEGFR-3, suggesting roles in angiogenesis and lymphangiogenesis.	bind
33499	2	8257	7	10	NULL	0	NULL	VEGF-D	NULL	human	binds	NULL				VEGFR-3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_4_1405_s_373	11943725	46  Human VEGF-D binds and activates VEGFR-2 and VEGFR-3, suggesting roles in angiogenesis and lymphangiogenesis.	bind
33500	3	8257	7	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				VEGFR-2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_4_1405_s_373	11943725	46  Human VEGF-D binds and activates VEGFR-2 and VEGFR-3, suggesting roles in angiogenesis and lymphangiogenesis.	bind
33501	4	8257	7	NULL	NULL	0	NULL	statement 2	NULL		activates	NULL				VEGFR-3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_4_1405_s_373	11943725	46  Human VEGF-D binds and activates VEGFR-2 and VEGFR-3, suggesting roles in angiogenesis and lymphangiogenesis.	bind
33502	5	8257	7	10	NULL	0	NULL	statement 1			plays a role in					angiogenesis					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_4_1405_s_373	11943725	46  Human VEGF-D binds and activates VEGFR-2 and VEGFR-3, suggesting roles in angiogenesis and lymphangiogenesis.	bind
33503	6	8257	7	10	NULL	0	NULL	statement 2			plays a role in					lymphangiogenesis					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_4_1405_s_373	11943725	46  Human VEGF-D binds and activates VEGFR-2 and VEGFR-3, suggesting roles in angiogenesis and lymphangiogenesis.	bind
27479	1	8258	6	13	NULL	NULL	NULL	Lp(a)	GP		bind					THP-1 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2036_s_210	9351369	46  Therefore, binding of either Lp(a) or plasminogen to THP-1 cells will be the result of interactions governed by their relative affinities and concentrations.	bind
27480	2	8258	6	13	NULL	NULL	NULL	plasminogen	GP		bind					THP-1 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2036_s_210	9351369	46  Therefore, binding of either Lp(a) or plasminogen to THP-1 cells will be the result of interactions governed by their relative affinities and concentrations.	bind
27481	3	8258	6	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2036_s_210	9351369	46  Therefore, binding of either Lp(a) or plasminogen to THP-1 cells will be the result of interactions governed by their relative affinities and concentrations.	bind
33504	1	8258	7	NULL	NULL	0	NULL	Lp(a)	NULL		bind	NULL				THP-1 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2036_s_210	9351369	46  Therefore, binding of either Lp(a) or plasminogen to THP-1 cells will be the result of interactions governed by their relative affinities and concentrations.	bind
33505	2	8258	7	NULL	NULL	0	NULL	plasminogen	NULL		bind	NULL				THP-1 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2036_s_210	9351369	46  Therefore, binding of either Lp(a) or plasminogen to THP-1 cells will be the result of interactions governed by their relative affinities and concentrations.	bind
46801	3	8258	7	10	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2036_s_210	9351369	46  Therefore, binding of either Lp(a) or plasminogen to THP-1 cells will be the result of interactions governed by their relative affinities and concentrations.	bind
27482	1	8259	6	13	NULL	NULL	NULL	vWF	GP		bind					GPIb	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_6_793_s_194	7773736	46  This agglutination is ADP dependent and is the result of the binding of vWF to both the GPIb and GPIIb/IIIa complexes.	bind
27483	2	8259	6	13	NULL	NULL	NULL	vWF	GP		bind					GPIIb/IIIa complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_6_793_s_194	7773736	46  This agglutination is ADP dependent and is the result of the binding of vWF to both the GPIb and GPIIb/IIIa complexes.	bind
27484	3	8259	6	13	NULL	NULL	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_6_793_s_194	7773736	46  This agglutination is ADP dependent and is the result of the binding of vWF to both the GPIb and GPIIb/IIIa complexes.	bind
27485	4	8259	6	13	NULL	NULL	NULL	statement 3	Process		results in					agglutination	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_6_793_s_194	7773736	46  This agglutination is ADP dependent and is the result of the binding of vWF to both the GPIb and GPIIb/IIIa complexes.	bind
27486	5	8259	6	13	NULL	NULL	NULL	statement 4	Process		is dependent on					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_6_793_s_194	7773736	46  This agglutination is ADP dependent and is the result of the binding of vWF to both the GPIb and GPIIb/IIIa complexes.	bind
33506	1	8259	7	NULL	NULL	0	NULL	vWF	NULL		bind	NULL				GPIb 	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_6_793_s_194	7773736	46  This agglutination is ADP dependent and is the result of the binding of vWF to both the GPIb and GPIIb/IIIa complexes.	bind
33507	2	8259	7	NULL	NULL	0	NULL	vWF	NULL		bind	NULL				GPIIb/IIIa complex	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_6_793_s_194	7773736	46  This agglutination is ADP dependent and is the result of the binding of vWF to both the GPIb and GPIIb/IIIa complexes.	bind
33508	3	8259	7	10	NULL	0	NULL	statement 1	NULL		occurs simultaneously with	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_6_793_s_194	7773736	46  This agglutination is ADP dependent and is the result of the binding of vWF to both the GPIb and GPIIb/IIIa complexes.	bind
33509	4	8259	7	10	NULL	0	NULL	statement 3	NULL		results in	NULL				agglutination	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_6_793_s_194	7773736	46  This agglutination is ADP dependent and is the result of the binding of vWF to both the GPIb and GPIIb/IIIa complexes.	bind
33510	5	8259	7	10	NULL	0	NULL	statement 4	NULL		is dependent on	NULL				ADP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_6_793_s_194	7773736	46  This agglutination is ADP dependent and is the result of the binding of vWF to both the GPIb and GPIIb/IIIa complexes.	bind
27487	1	8260	6	13	NULL	NULL	NULL	VEGF121	GP		does not bind					neuropilins	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_14_1887_s_162	11294808	46  VEGF121 is a secreted isoform that lacks the heparin-binding domain; it does not bind to neuropilins.	bind
27488	2	8260	6	13	NULL	NULL	NULL	VEGF121	GP		lacks								heparin binding domain		NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_14_1887_s_162	11294808	46  VEGF121 is a secreted isoform that lacks the heparin-binding domain; it does not bind to neuropilins.	bind
46802	3	8260	6	13	NULL	NULL	NULL	VEGF121	GP		is a type of					secreted isoform	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_14_1887_s_162	11294808	46  VEGF121 is a secreted isoform that lacks the heparin-binding domain; it does not bind to neuropilins.	bind
33511	1	8260	7	NULL	NULL	0	NULL	VEGF121	NULL		is a type of	NULL				secreted isoform	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_14_1887_s_162	11294808	46  VEGF121 is a secreted isoform that lacks the heparin-binding domain; it does not bind to neuropilins.	bind
33512	2	8260	7	NULL	NULL	0	NULL	VEGF121	NULL		lacks	NULL					NULL		heparin-binding domain		NULL		0	NULL	NULL	NULL	gw60_circulation_103_14_1887_s_162	11294808	46  VEGF121 is a secreted isoform that lacks the heparin-binding domain; it does not bind to neuropilins.	bind
33513	3	8260	7	NULL	NULL	0	NULL	VEGF121	NULL		does not bind	NULL				neuropilins	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_14_1887_s_162	11294808	46  VEGF121 is a secreted isoform that lacks the heparin-binding domain; it does not bind to neuropilins.	bind
27489	1	8261	6	13	NULL	NULL	NULL	large LDL particles	GP	apo E-enriched	bind					chondroitin sulfate PGs	GP	arterial			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1216_s_181	9261249	46 47  Previously, we showed that large, apo E-enriched LDL particles preferentially bind to arterial chondroitin sulfate PGs in vitro compared with small, apo E-poor LDL particles, and part of the increased binding was related to the apo E content of the LDL. 16 17  In addition, we have shown that apo E is responsible for an increased binding affinity of large LDL particles from cynomolgus monkeys to fibroblasts in culture.	bind
27490	2	8261	6	13	NULL	NULL	NULL	small LDL particles	GP	apo E-poor	bind					chondroitin sulfate PGs	GP	arterial			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1216_s_181	9261249	46 47  Previously, we showed that large, apo E-enriched LDL particles preferentially bind to arterial chondroitin sulfate PGs in vitro compared with small, apo E-poor LDL particles, and part of the increased binding was related to the apo E content of the LDL. 16 17  In addition, we have shown that apo E is responsible for an increased binding affinity of large LDL particles from cynomolgus monkeys to fibroblasts in culture.	bind
27491	3	8261	6	13	NULL	NULL	NULL	statement 1	Process		is more preferential than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1216_s_181	9261249	46 47  Previously, we showed that large, apo E-enriched LDL particles preferentially bind to arterial chondroitin sulfate PGs in vitro compared with small, apo E-poor LDL particles, and part of the increased binding was related to the apo E content of the LDL. 16 17  In addition, we have shown that apo E is responsible for an increased binding affinity of large LDL particles from cynomolgus monkeys to fibroblasts in culture.	bind
27492	4	8261	6	13	NULL	NULL	NULL	large LDL particles	GP	cynomolgus monkeys	bind					fibroblasts	Cell				NULL	culture	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1216_s_181	9261249	46 47  Previously, we showed that large, apo E-enriched LDL particles preferentially bind to arterial chondroitin sulfate PGs in vitro compared with small, apo E-poor LDL particles, and part of the increased binding was related to the apo E content of the LDL. 16 17  In addition, we have shown that apo E is responsible for an increased binding affinity of large LDL particles from cynomolgus monkeys to fibroblasts in culture.	bind
27493	5	8261	6	13	NULL	NULL	NULL	apoE	GP		is responsible for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1216_s_181	9261249	46 47  Previously, we showed that large, apo E-enriched LDL particles preferentially bind to arterial chondroitin sulfate PGs in vitro compared with small, apo E-poor LDL particles, and part of the increased binding was related to the apo E content of the LDL. 16 17  In addition, we have shown that apo E is responsible for an increased binding affinity of large LDL particles from cynomolgus monkeys to fibroblasts in culture.	bind
33524	1	8261	7	10	NULL	0	NULL	large LDL particles 	NULL	apo E-enriched	binds	NULL	preferentially			chondroitin sulfate PGs	NULL	arterial			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1216_s_181	9261249	46 47  Previously, we showed that large, apo E-enriched LDL particles preferentially bind to arterial chondroitin sulfate PGs in vitro compared with small, apo E-poor LDL particles, and part of the increased binding was related to the apo E content of the LDL. 16 17  In addition, we have shown that apo E is responsible for an increased binding affinity of large LDL particles from cynomolgus monkeys to fibroblasts in culture.	bind
33525	2	8261	7	10	NULL	0	NULL	small LDL particles	NULL	apo E-poor	bind	NULL				chondroitin sulfate PGs	NULL	arterial			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1216_s_181	9261249	46 47  Previously, we showed that large, apo E-enriched LDL particles preferentially bind to arterial chondroitin sulfate PGs in vitro compared with small, apo E-poor LDL particles, and part of the increased binding was related to the apo E content of the LDL. 16 17  In addition, we have shown that apo E is responsible for an increased binding affinity of large LDL particles from cynomolgus monkeys to fibroblasts in culture.	bind
33526	3	8261	7	NULL	NULL	0	NULL	statement 1	NULL		is preferred over	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1216_s_181	9261249	46 47  Previously, we showed that large, apo E-enriched LDL particles preferentially bind to arterial chondroitin sulfate PGs in vitro compared with small, apo E-poor LDL particles, and part of the increased binding was related to the apo E content of the LDL. 16 17  In addition, we have shown that apo E is responsible for an increased binding affinity of large LDL particles from cynomolgus monkeys to fibroblasts in culture.	bind
33527	4	8261	7	10	NULL	0	NULL	statement 3	NULL		is related to	NULL				LDL	NULL	apo E content of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1216_s_181	9261249	46 47  Previously, we showed that large, apo E-enriched LDL particles preferentially bind to arterial chondroitin sulfate PGs in vitro compared with small, apo E-poor LDL particles, and part of the increased binding was related to the apo E content of the LDL. 16 17  In addition, we have shown that apo E is responsible for an increased binding affinity of large LDL particles from cynomolgus monkeys to fibroblasts in culture.	bind
33528	5	8261	7	NULL	NULL	0	NULL	large LDL particles	NULL	cynomolgus monkeys	bind	NULL				fibroblasts	NULL				NULL	in culture	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1216_s_181	9261249	46 47  Previously, we showed that large, apo E-enriched LDL particles preferentially bind to arterial chondroitin sulfate PGs in vitro compared with small, apo E-poor LDL particles, and part of the increased binding was related to the apo E content of the LDL. 16 17  In addition, we have shown that apo E is responsible for an increased binding affinity of large LDL particles from cynomolgus monkeys to fibroblasts in culture.	bind
33529	6	8261	7	NULL	NULL	0	NULL	apo E	NULL		increase	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1216_s_181	9261249	46 47  Previously, we showed that large, apo E-enriched LDL particles preferentially bind to arterial chondroitin sulfate PGs in vitro compared with small, apo E-poor LDL particles, and part of the increased binding was related to the apo E content of the LDL. 16 17  In addition, we have shown that apo E is responsible for an increased binding affinity of large LDL particles from cynomolgus monkeys to fibroblasts in culture.	bind
27494	1	8262	6	13	NULL	NULL	NULL	LXR/RXR heterodimer	GP	activated;; nuclear	bind									DR4 element of promoter	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_10_1535_s_82	12377728	46 Expression of this gene is regulated by activated liver X receptor (LXR)/retinoid X receptor (RXR) nuclear heterodimers that bind to the DR4 element in its promoter region.	bind
27495	2	8262	6	13	NULL	NULL	NULL	LXR	GP		is					liver X receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_10_1535_s_82	12377728	46 Expression of this gene is regulated by activated liver X receptor (LXR)/retinoid X receptor (RXR) nuclear heterodimers that bind to the DR4 element in its promoter region.	bind
27496	3	8262	6	13	NULL	NULL	NULL	RXR	GP		is					retinoid X receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_10_1535_s_82	12377728	46 Expression of this gene is regulated by activated liver X receptor (LXR)/retinoid X receptor (RXR) nuclear heterodimers that bind to the DR4 element in its promoter region.	bind
33530	1	8262	7	10	NULL	0	NULL	LXR/RXR heterodimer	NULL	activated;;nuclear	binds to	NULL					NULL			DR4 element in the promoter	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_10_1535_s_82	12377728	46 Expression of this gene is regulated by activated liver X receptor (LXR)/retinoid X receptor (RXR) nuclear heterodimers that bind to the DR4 element in its promoter region.	bind
33531	2	8262	7	NULL	NULL	0	NULL	LXR	NULL		is	NULL				liver X receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_10_1535_s_82	12377728	46 Expression of this gene is regulated by activated liver X receptor (LXR)/retinoid X receptor (RXR) nuclear heterodimers that bind to the DR4 element in its promoter region.	bind
33532	3	8262	7	NULL	NULL	0	NULL	RXR	NULL		is	NULL				retinoid X receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_10_1535_s_82	12377728	46 Expression of this gene is regulated by activated liver X receptor (LXR)/retinoid X receptor (RXR) nuclear heterodimers that bind to the DR4 element in its promoter region.	bind
27497	1	8263	6	13	NULL	NULL	NULL	SMemb gene	GP		bind				KLF5-binding element	Sp1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1135_s_100	15817882	46 We have also shown that the KLF5-binding element in the SMemb gene also binds Sp1 in vitro.	bind
33533	1	8263	7	NULL	NULL	0	NULL	SMemb gene	NULL		binds	NULL			KLF5-binding element	Sp1	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1135_s_100	15817882	46 We have also shown that the KLF5-binding element in the SMemb gene also binds Sp1 in vitro.	bind
27498	1	8264	6	13	NULL	NULL	NULL	MCs	Cell	cultured	bind					IL12	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_623_s_257	10027419	46, 47  erein, we demonstrate that cultured MCs bind IL-12 and express the human low-affinity IL-12 beta1 chain receptor under basal conditions.	bind
27499	2	8264	6	13	NULL	NULL	NULL	MCs	Cell	cultured	express					IL-12 beta1 chain receptor	GP	human;; low affinity			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_623_s_257	10027419	46, 47  erein, we demonstrate that cultured MCs bind IL-12 and express the human low-affinity IL-12 beta1 chain receptor under basal conditions.	bind
33534	1	8264	7	10	NULL	0	NULL	MCs	NULL	cultured	bind	NULL				IL-12	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_623_s_257	10027419	46, 47  erein, we demonstrate that cultured MCs bind IL-12 and express the human low-affinity IL-12 beta1 chain receptor under basal conditions.	bind
33535	2	8264	7	10	NULL	0	NULL	MCs	NULL	cultured	express	NULL				IL-12 beta1 chain receptor	NULL	human;;low-affinity			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_2_623_s_257	10027419	46, 47  erein, we demonstrate that cultured MCs bind IL-12 and express the human low-affinity IL-12 beta1 chain receptor under basal conditions.	bind
27500	1	8265	6	13	NULL	NULL	NULL	VEGF-E	GP		bind		exclusively			VEGFR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1143_s_116	12676799	46,47  Because infusion of VEGF-E, which binds exclusively to VEGFR-2, did not influence arteriogenesis, we concluded that the effects of VEGF-A on arteriogenesis are caused by monocyte activation.	bind
27501	2	8265	6	13	NULL	NULL	NULL	statement 1	Process		did not influence					arteriogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1143_s_116	12676799	46,47  Because infusion of VEGF-E, which binds exclusively to VEGFR-2, did not influence arteriogenesis, we concluded that the effects of VEGF-A on arteriogenesis are caused by monocyte activation.	bind
27502	4	8265	6	13	NULL	NULL	NULL	monocyte	Cell	activation of	causes					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1143_s_116	12676799	46,47  Because infusion of VEGF-E, which binds exclusively to VEGFR-2, did not influence arteriogenesis, we concluded that the effects of VEGF-A on arteriogenesis are caused by monocyte activation.	bind
46803	3	8265	6	13	NULL	NULL	NULL	VEGF-A 	GP		effects					arteriogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1143_s_116	12676799	46,47  Because infusion of VEGF-E, which binds exclusively to VEGFR-2, did not influence arteriogenesis, we concluded that the effects of VEGF-A on arteriogenesis are caused by monocyte activation.	bind
33536	1	8265	7	NULL	NULL	0	NULL	VEGF-E	NULL		binds	NULL	exclusively			VEGFR-2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1143_s_116	12676799	46,47  Because infusion of VEGF-E, which binds exclusively to VEGFR-2, did not influence arteriogenesis, we concluded that the effects of VEGF-A on arteriogenesis are caused by monocyte activation.	bind
33537	2	8265	7	NULL	NULL	0	NULL	statement 1	NULL		does not influence	NULL				arteriogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1143_s_116	12676799	46,47  Because infusion of VEGF-E, which binds exclusively to VEGFR-2, did not influence arteriogenesis, we concluded that the effects of VEGF-A on arteriogenesis are caused by monocyte activation.	bind
33541	3	8265	7	NULL	NULL	0	NULL	VEGF-A	NULL		effects	NULL				arteriogenesis	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1143_s_116	12676799	46,47  Because infusion of VEGF-E, which binds exclusively to VEGFR-2, did not influence arteriogenesis, we concluded that the effects of VEGF-A on arteriogenesis are caused by monocyte activation.	bind
33543	4	8265	7	10	NULL	0	NULL	monocyte	NULL	activation of	causes	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1143_s_116	12676799	46,47  Because infusion of VEGF-E, which binds exclusively to VEGFR-2, did not influence arteriogenesis, we concluded that the effects of VEGF-A on arteriogenesis are caused by monocyte activation.	bind
27561	1	8266	6	13	NULL	NULL	NULL	PECAM-1 	GP		is required for			ITIM		SHP-1	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_69	12689916	46,50,57 - 59      As with SHP-2, both PECAM-1 ITIMs seem to be required to support SHP-1 binding 50; however, unlike SHP-2, the affinity between SHP-1 and pY663 is identical to that of pY686, and the affinities of both interactions are significantly lower than those reported for SHP-2.	bind
27562	2	8266	6	13	NULL	NULL	NULL	PECAM-1	GP		is required for			ITIM		SHP-2	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_69	12689916	46,50,57 - 59      As with SHP-2, both PECAM-1 ITIMs seem to be required to support SHP-1 binding 50; however, unlike SHP-2, the affinity between SHP-1 and pY663 is identical to that of pY686, and the affinities of both interactions are significantly lower than those reported for SHP-2.	bind
27563	3	8266	6	13	NULL	NULL	NULL	SHP-1	GP		interacts with								pY663		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_69	12689916	46,50,57 - 59      As with SHP-2, both PECAM-1 ITIMs seem to be required to support SHP-1 binding 50; however, unlike SHP-2, the affinity between SHP-1 and pY663 is identical to that of pY686, and the affinities of both interactions are significantly lower than those reported for SHP-2.	bind
27564	4	8266	6	13	NULL	NULL	NULL	SHP-1	GP		interacts with								pY686		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_69	12689916	46,50,57 - 59      As with SHP-2, both PECAM-1 ITIMs seem to be required to support SHP-1 binding 50; however, unlike SHP-2, the affinity between SHP-1 and pY663 is identical to that of pY686, and the affinities of both interactions are significantly lower than those reported for SHP-2.	bind
27565	5	8266	6	13	NULL	NULL	NULL	statement 3	Process	affinity of	is equal to					statement 4	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_69	12689916	46,50,57 - 59      As with SHP-2, both PECAM-1 ITIMs seem to be required to support SHP-1 binding 50; however, unlike SHP-2, the affinity between SHP-1 and pY663 is identical to that of pY686, and the affinities of both interactions are significantly lower than those reported for SHP-2.	bind
27566	6	8266	6	13	NULL	NULL	NULL	SHP-2	GP		interacts with								pY663		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_69	12689916	46,50,57 - 59      As with SHP-2, both PECAM-1 ITIMs seem to be required to support SHP-1 binding 50; however, unlike SHP-2, the affinity between SHP-1 and pY663 is identical to that of pY686, and the affinities of both interactions are significantly lower than those reported for SHP-2.	bind
27567	7	8266	6	13	NULL	NULL	NULL	SHP-2	GP		interacts with								pY686		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_69	12689916	46,50,57 - 59      As with SHP-2, both PECAM-1 ITIMs seem to be required to support SHP-1 binding 50; however, unlike SHP-2, the affinity between SHP-1 and pY663 is identical to that of pY686, and the affinities of both interactions are significantly lower than those reported for SHP-2.	bind
27568	8	8266	6	13	NULL	NULL	NULL	statement 3	Process	affinity of	is lower than		significantly			statement 6	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_69	12689916	46,50,57 - 59      As with SHP-2, both PECAM-1 ITIMs seem to be required to support SHP-1 binding 50; however, unlike SHP-2, the affinity between SHP-1 and pY663 is identical to that of pY686, and the affinities of both interactions are significantly lower than those reported for SHP-2.	bind
27569	9	8266	6	13	NULL	NULL	NULL	statement 4	Process	affinity of	is lower than		significantly			statement 7	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_69	12689916	46,50,57 - 59      As with SHP-2, both PECAM-1 ITIMs seem to be required to support SHP-1 binding 50; however, unlike SHP-2, the affinity between SHP-1 and pY663 is identical to that of pY686, and the affinities of both interactions are significantly lower than those reported for SHP-2.	bind
33545	1	8266	7	10	NULL	0	NULL	PECAM-1	NULL		support	NULL		ITIMs		SHP-1	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_69	12689916	46,50,57 - 59      As with SHP-2, both PECAM-1 ITIMs seem to be required to support SHP-1 binding 50; however, unlike SHP-2, the affinity between SHP-1 and pY663 is identical to that of pY686, and the affinities of both interactions are significantly lower than those reported for SHP-2.	bind
33547	2	8266	7	10	NULL	0	NULL	PECAM-1	NULL		support	NULL		ITIMs		SHP-2	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_69	12689916	46,50,57 - 59      As with SHP-2, both PECAM-1 ITIMs seem to be required to support SHP-1 binding 50; however, unlike SHP-2, the affinity between SHP-1 and pY663 is identical to that of pY686, and the affinities of both interactions are significantly lower than those reported for SHP-2.	bind
33549	3	8266	7	NULL	NULL	0	NULL	SHP-1	NULL		bind	NULL					NULL		pY663		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_69	12689916	46,50,57 - 59      As with SHP-2, both PECAM-1 ITIMs seem to be required to support SHP-1 binding 50; however, unlike SHP-2, the affinity between SHP-1 and pY663 is identical to that of pY686, and the affinities of both interactions are significantly lower than those reported for SHP-2.	bind
33550	4	8266	7	NULL	NULL	0	NULL	SHP-1	NULL		bind	NULL					NULL		pY686		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_69	12689916	46,50,57 - 59      As with SHP-2, both PECAM-1 ITIMs seem to be required to support SHP-1 binding 50; however, unlike SHP-2, the affinity between SHP-1 and pY663 is identical to that of pY686, and the affinities of both interactions are significantly lower than those reported for SHP-2.	bind
33554	5	8266	7	NULL	NULL	0	NULL	statement 3	NULL	affinity of	is identical to	NULL				statement 4	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_69	12689916	46,50,57 - 59      As with SHP-2, both PECAM-1 ITIMs seem to be required to support SHP-1 binding 50; however, unlike SHP-2, the affinity between SHP-1 and pY663 is identical to that of pY686, and the affinities of both interactions are significantly lower than those reported for SHP-2.	bind
33557	6	8266	7	NULL	NULL	0	NULL	 SHP-2	NULL		bind	NULL					NULL		pY663		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_69	12689916	46,50,57 - 59      As with SHP-2, both PECAM-1 ITIMs seem to be required to support SHP-1 binding 50; however, unlike SHP-2, the affinity between SHP-1 and pY663 is identical to that of pY686, and the affinities of both interactions are significantly lower than those reported for SHP-2.	bind
33560	7	8266	7	NULL	NULL	0	NULL	SHP-2	NULL		bind	NULL					NULL		pY686		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_69	12689916	46,50,57 - 59      As with SHP-2, both PECAM-1 ITIMs seem to be required to support SHP-1 binding 50; however, unlike SHP-2, the affinity between SHP-1 and pY663 is identical to that of pY686, and the affinities of both interactions are significantly lower than those reported for SHP-2.	bind
46804	8	8266	7	10	NULL	0	NULL	statement 3	NULL	affinity of	is lower than	NULL	significantly			statement 6	NULL	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_69	12689916	46,50,57 - 59      As with SHP-2, both PECAM-1 ITIMs seem to be required to support SHP-1 binding 50; however, unlike SHP-2, the affinity between SHP-1 and pY663 is identical to that of pY686, and the affinities of both interactions are significantly lower than those reported for SHP-2.	bind
46806	9	8266	7	10	NULL	0	NULL	statement 4	NULL	affinity of	is lower than	NULL	significantly			statement 7	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_6_953_s_69	12689916	46,50,57 - 59      As with SHP-2, both PECAM-1 ITIMs seem to be required to support SHP-1 binding 50; however, unlike SHP-2, the affinity between SHP-1 and pY663 is identical to that of pY686, and the affinities of both interactions are significantly lower than those reported for SHP-2.	bind
27503	1	8267	6	13	NULL	NULL	NULL	hypoxia	MedicalFinding		decreases					TGF-beta1 receptor	GP	binding of			NULL	dermal fibroblasts	NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_301_s_193	9916944	46- 48  It was also reported that hypoxia decreases TGF-beta1 receptor binding and synthesis in dermal fibroblasts.	bind
27504	2	8267	6	13	NULL	NULL	NULL	hypoxia	MedicalFinding		decreases					TGF-beta1 receptor	GP	synthesis of			NULL	dermal fibroblasts	NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_301_s_193	9916944	46- 48  It was also reported that hypoxia decreases TGF-beta1 receptor binding and synthesis in dermal fibroblasts.	bind
33567	1	8267	7	10	NULL	0	NULL	hypoxia 			decrease					TGF-beta1 receptor		binding of			NULL	dermal fibroblasts	NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_301_s_193	9916944	46- 48  It was also reported that hypoxia decreases TGF-beta1 receptor binding and synthesis in dermal fibroblasts.	bind
33572	2	8267	7	NULL	NULL	0	NULL	hypoxia	NULL		decrease	NULL				TGF-beta1 receptor	NULL	synthesis of			NULL	dermal fibroblasts	NULL	NULL	NULL	NULL	gw60_amjpathol_154_1_301_s_193	9916944	46- 48  It was also reported that hypoxia decreases TGF-beta1 receptor binding and synthesis in dermal fibroblasts.	bind
27505	1	8268	6	13	NULL	NULL	NULL	LDL	GP		does not bind					GPIIb-IIIa complex	GP				NULL	intact resting platelets	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_156_s_188	9012651	47  In conclusion, we present ample evidence indicating that neither the GPIIb-IIIa complex nor GPIIb and GPIIIa individually are the ligand binding proteins for LDL on intact resting platelets.	bind
27506	2	8268	6	13	NULL	NULL	NULL	LDL	GP		does not bind					GPIIb	GP				NULL	intact resting platelets	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_156_s_188	9012651	47  In conclusion, we present ample evidence indicating that neither the GPIIb-IIIa complex nor GPIIb and GPIIIa individually are the ligand binding proteins for LDL on intact resting platelets.	bind
27507	3	8268	6	13	NULL	NULL	NULL	LDL	GP		does not bind					GPIIIa	GP				NULL	intact resting platelets	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_156_s_188	9012651	47  In conclusion, we present ample evidence indicating that neither the GPIIb-IIIa complex nor GPIIb and GPIIIa individually are the ligand binding proteins for LDL on intact resting platelets.	bind
33579	1	8268	7	NULL	NULL	0	NULL	GPIIb-IIIa complex 	NULL		does not bind	NULL				LDL	NULL				NULL	intact resting platelets	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_156_s_188	9012651	47  In conclusion, we present ample evidence indicating that neither the GPIIb-IIIa complex nor GPIIb and GPIIIa individually are the ligand binding proteins for LDL on intact resting platelets.	bind
33580	2	8268	7	NULL	NULL	0	NULL	GPIIb	NULL		does not bind	NULL				LDL	NULL				NULL	intact resting platelets	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_156_s_188	9012651	47  In conclusion, we present ample evidence indicating that neither the GPIIb-IIIa complex nor GPIIb and GPIIIa individually are the ligand binding proteins for LDL on intact resting platelets.	bind
33751	3	8268	7	NULL	NULL	0	NULL	GPIIIa	NULL		does not bind	NULL				LDL	NULL				NULL	intact resting platelets	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_156_s_188	9012651	47  In conclusion, we present ample evidence indicating that neither the GPIIb-IIIa complex nor GPIIb and GPIIIa individually are the ligand binding proteins for LDL on intact resting platelets.	bind
27570	1	8269	6	13	NULL	NULL	NULL	FGF-2	GP		bind					FGFR-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_302	11786412	47  Interestingly, 6-O sulfate on glucosamine is the main structural feature within HS GAGs required to promote binding of FGF-2 to FGFR-1 and to stimulate signaling.	bind
28330	2	8269	6	13	NULL	NULL	NULL	HS GAGs	GP		contains					6-O sulfate on glucosamine	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_302	11786412	47  Interestingly, 6-O sulfate on glucosamine is the main structural feature within HS GAGs required to promote binding of FGF-2 to FGFR-1 and to stimulate signaling.	bind
28331	3	8269	6	13	NULL	NULL	NULL	statement 2	Process		is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_302	11786412	47  Interestingly, 6-O sulfate on glucosamine is the main structural feature within HS GAGs required to promote binding of FGF-2 to FGFR-1 and to stimulate signaling.	bind
28332	4	8269	6	13	NULL	NULL	NULL	statement 2	Process		stimulates					signaling	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_302	11786412	47  Interestingly, 6-O sulfate on glucosamine is the main structural feature within HS GAGs required to promote binding of FGF-2 to FGFR-1 and to stimulate signaling.	bind
33752	1	8269	7	NULL	NULL	0	NULL	FGF-2	NULL		bind	NULL				 FGFR-1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_302	11786412	47  Interestingly, 6-O sulfate on glucosamine is the main structural feature within HS GAGs required to promote binding of FGF-2 to FGFR-1 and to stimulate signaling.	bind
33753	2	8269	7	NULL	NULL	0	NULL	6-O sulfate glucosamine	NULL		is present in	NULL				HS GAGs	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_302	11786412	47  Interestingly, 6-O sulfate on glucosamine is the main structural feature within HS GAGs required to promote binding of FGF-2 to FGFR-1 and to stimulate signaling.	bind
33754	3	8269	7	NULL	NULL	0	NULL	statement 2	NULL		promote	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_302	11786412	47  Interestingly, 6-O sulfate on glucosamine is the main structural feature within HS GAGs required to promote binding of FGF-2 to FGFR-1 and to stimulate signaling.	bind
33755	4	8269	7	NULL	NULL	0	NULL	statement 3	NULL		stimulate	NULL				signaling	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_302	11786412	47  Interestingly, 6-O sulfate on glucosamine is the main structural feature within HS GAGs required to promote binding of FGF-2 to FGFR-1 and to stimulate signaling.	bind
27571	1	8270	6	13	NULL	NULL	NULL	Lp(a)	GP		bind					fibrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_385_s_193	7749849	47  Much of the binding of Lp(a) by fibrin is lysine mediated, and as the present results show, the lysine-binding properties of Lp(a) are not affected by in vitro glycation as performed under these conditions.	bind
27572	2	8270	6	13	NULL	NULL	NULL	statement 1	Process		is mediated by					lysine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_385_s_193	7749849	47  Much of the binding of Lp(a) by fibrin is lysine mediated, and as the present results show, the lysine-binding properties of Lp(a) are not affected by in vitro glycation as performed under these conditions.	bind
27573	3	8270	6	13	NULL	NULL	NULL	Lp(a)	GP		bind					lysine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_385_s_193	7749849	47  Much of the binding of Lp(a) by fibrin is lysine mediated, and as the present results show, the lysine-binding properties of Lp(a) are not affected by in vitro glycation as performed under these conditions.	bind
27574	4	8270	6	13	NULL	NULL	NULL	statement 3	Process		is not affected by					glycation	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_385_s_193	7749849	47  Much of the binding of Lp(a) by fibrin is lysine mediated, and as the present results show, the lysine-binding properties of Lp(a) are not affected by in vitro glycation as performed under these conditions.	bind
33756	1	8270	7	NULL	NULL	0	NULL	fibrin 	NULL		bind	NULL				Lp(a)	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_385_s_193	7749849	47  Much of the binding of Lp(a) by fibrin is lysine mediated, and as the present results show, the lysine-binding properties of Lp(a) are not affected by in vitro glycation as performed under these conditions.	bind
33757	2	8270	7	NULL	NULL	0	NULL	lysine	NULL		mediates	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_385_s_193	7749849	47  Much of the binding of Lp(a) by fibrin is lysine mediated, and as the present results show, the lysine-binding properties of Lp(a) are not affected by in vitro glycation as performed under these conditions.	bind
33758	3	8270	7	10	NULL	0	NULL	Lp(a)	NULL		bind	NULL				lusine	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_385_s_193	7749849	47  Much of the binding of Lp(a) by fibrin is lysine mediated, and as the present results show, the lysine-binding properties of Lp(a) are not affected by in vitro glycation as performed under these conditions.	bind
46807	4	8270	7	10	NULL	0	NULL	statement 3	NULL		is not affected by	NULL				glycation	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_385_s_193	7749849	47  Much of the binding of Lp(a) by fibrin is lysine mediated, and as the present results show, the lysine-binding properties of Lp(a) are not affected by in vitro glycation as performed under these conditions.	bind
28333	1	8271	6	13	NULL	NULL	NULL	large VLDL	GP		contains					prothrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_138	9445253	48  Bradley and Gianturco 27  reported that the large VLDLs that were separated from hypertriglyceridemic patients contained prothrombin, but not those of normal subjects; they also demonstrated that prothrombin can bind to plasma VLDLs in vitro at physiological concentrations of VLDLs, prothrombin, and calcium, whereas binding to LDLs and HDLs was negligible.	bind
28334	2	8271	6	13	NULL	NULL	NULL	statement 1	Process		occurs in					hypertriglyceridemia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_138	9445253	48  Bradley and Gianturco 27  reported that the large VLDLs that were separated from hypertriglyceridemic patients contained prothrombin, but not those of normal subjects; they also demonstrated that prothrombin can bind to plasma VLDLs in vitro at physiological concentrations of VLDLs, prothrombin, and calcium, whereas binding to LDLs and HDLs was negligible.	bind
28336	3	8271	6	13	NULL	NULL	NULL	prothrombin	GP		bind					VLDL	GP	plasma			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_138	9445253	48  Bradley and Gianturco 27  reported that the large VLDLs that were separated from hypertriglyceridemic patients contained prothrombin, but not those of normal subjects; they also demonstrated that prothrombin can bind to plasma VLDLs in vitro at physiological concentrations of VLDLs, prothrombin, and calcium, whereas binding to LDLs and HDLs was negligible.	bind
28337	4	8271	6	13	NULL	NULL	NULL	prothrombin	GP		bind		negligibly			LDLs	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_138	9445253	48  Bradley and Gianturco 27  reported that the large VLDLs that were separated from hypertriglyceridemic patients contained prothrombin, but not those of normal subjects; they also demonstrated that prothrombin can bind to plasma VLDLs in vitro at physiological concentrations of VLDLs, prothrombin, and calcium, whereas binding to LDLs and HDLs was negligible.	bind
28338	5	8271	6	13	NULL	NULL	NULL	prothrombin	GP		bind		negligibly			HDLs	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_138	9445253	48  Bradley and Gianturco 27  reported that the large VLDLs that were separated from hypertriglyceridemic patients contained prothrombin, but not those of normal subjects; they also demonstrated that prothrombin can bind to plasma VLDLs in vitro at physiological concentrations of VLDLs, prothrombin, and calcium, whereas binding to LDLs and HDLs was negligible.	bind
34028	1	8271	7	10	NULL	0	NULL	 prothrombin			bind					VLDL		plasma			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_138	9445253	48  Bradley and Gianturco 27  reported that the large VLDLs that were separated from hypertriglyceridemic patients contained prothrombin, but not those of normal subjects; they also demonstrated that prothrombin can bind to plasma VLDLs in vitro at physiological concentrations of VLDLs, prothrombin, and calcium, whereas binding to LDLs and HDLs was negligible.	bind
34029	2	8271	7	NULL	NULL	0	NULL	prothrombin	NULL		bind	NULL	negligibly			LDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_138	9445253	48  Bradley and Gianturco 27  reported that the large VLDLs that were separated from hypertriglyceridemic patients contained prothrombin, but not those of normal subjects; they also demonstrated that prothrombin can bind to plasma VLDLs in vitro at physiological concentrations of VLDLs, prothrombin, and calcium, whereas binding to LDLs and HDLs was negligible.	bind
34030	3	8271	7	NULL	NULL	0	NULL	prothrombin	NULL		bind	NULL	negligibly			HDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_138	9445253	48  Bradley and Gianturco 27  reported that the large VLDLs that were separated from hypertriglyceridemic patients contained prothrombin, but not those of normal subjects; they also demonstrated that prothrombin can bind to plasma VLDLs in vitro at physiological concentrations of VLDLs, prothrombin, and calcium, whereas binding to LDLs and HDLs was negligible.	bind
47534	4	8271	7	10	NULL	0	NULL	large VLDL	NULL		contains	NULL				prothrombin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_138	9445253	48  Bradley and Gianturco 27  reported that the large VLDLs that were separated from hypertriglyceridemic patients contained prothrombin, but not those of normal subjects; they also demonstrated that prothrombin can bind to plasma VLDLs in vitro at physiological concentrations of VLDLs, prothrombin, and calcium, whereas binding to LDLs and HDLs was negligible.	bind
47535	5	8271	7	10	NULL	0	NULL	statement 4	NULL		occurs in	NULL				hypertriglyceridemia	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_33_s_138	9445253	48  Bradley and Gianturco 27  reported that the large VLDLs that were separated from hypertriglyceridemic patients contained prothrombin, but not those of normal subjects; they also demonstrated that prothrombin can bind to plasma VLDLs in vitro at physiological concentrations of VLDLs, prothrombin, and calcium, whereas binding to LDLs and HDLs was negligible.	bind
27575	1	8272	6	13	NULL	NULL	NULL	FXa	GP	free	does not bind		efficiently			TFPI	GP	cellular			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_241	10479670	48  For ECs, where free FXa is not efficiently bound by cellular TFPI, 23  downregulation of TF .	bind
34031	1	8272	7	10	NULL	0	NULL	TFPI	NULL	cellular	does not bind	NULL	efficiently			FXa	NULL	free			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_9_2251_s_241	10479670	48  For ECs, where free FXa is not efficiently bound by cellular TFPI, 23  downregulation of TF .	bind
34722	1	8273	6	13	NULL	NULL	NULL	PMA	Chemical		does not affect					Sp1	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_377_s_231	10669633	48 49  In the present study, the binding affinity of Sp1 and Sp3 to the probe is not reproducibly affected by PMA.	bind
34723	2	8273	6	13	NULL	NULL	NULL	PMA	Chemical		does not affect					Sp3	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_377_s_231	10669633	48 49  In the present study, the binding affinity of Sp1 and Sp3 to the probe is not reproducibly affected by PMA.	bind
34032	1	8273	7	10	NULL	0	NULL	PMA	NULL		does not affect	NULL				Sp1	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_377_s_231	10669633	48 49  In the present study, the binding affinity of Sp1 and Sp3 to the probe is not reproducibly affected by PMA.	bind
34033	2	8273	7	10	NULL	0	NULL	PMA	NULL		does not affect	NULL				Sp3	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_377_s_231	10669633	48 49  In the present study, the binding affinity of Sp1 and Sp3 to the probe is not reproducibly affected by PMA.	bind
28339	1	8274	6	13	NULL	NULL	NULL	statement 8	Chromosome		controls		may;;selectively			SRF	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
28340	2	8274	6	13	NULL	NULL	NULL	statement 8	Process		control		may;;selectively			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
28341	3	8274	6	13	NULL	NULL	NULL	myocardin	GP		is recruited to					SMC marker gene	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
28343	4	8274	6	13	NULL	NULL	NULL	myocardin	GP		is not recruited to					c-fos	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
28344	5	8274	6	13	NULL	NULL	NULL	c-fos	GP		is a type of					growth response gene	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
28346	6	8274	6	13	NULL	NULL	NULL	myocardin	GP		is not recruited to					multiple CArG-containing genes	GP	skeletal			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
47518	7	8274	6	13	NULL	NULL	NULL	myocardin	GP		is not recruited to					multiple CArG-containing genes	GP	cardiac			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
56109	8	8274	6	13	NULL	NULL	NULL	chromatin	Chromosome	patterning of;;structure of	specific to					SMC-lineage	Cell				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
56111	9	8274	6	13	NULL	NULL	NULL	statement 8	Chromosome		controls		may;;selectively			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
56112	10	8274	6	13	NULL	NULL	NULL	statement 8	Chromosome		controls		may;;selectively			statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
56113	11	8274	6	13	NULL	NULL	NULL	statement 8	Chromosome		controls		may;;selectively			statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
34038	1	8274	7	NULL	NULL	0	NULL	myocardin	NULL		is recruited to	NULL				SMC marker gene	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
34039	2	8274	7	NULL	NULL	0	NULL	myocardin	NULL		is not recruited to	NULL				c-fos	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
34040	3	8274	7	10	NULL	0	NULL	myocardin			is not recruited to					multiple CArG-containing genes		skeletal			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
34041	4	8274	7	10	NULL	0	NULL	myocardin			is not recruited to					multiple CArG-containing genes		cardiac			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
34059	5	8274	7	10	NULL	0	NULL	statement 10			controls		may;;selectively			statement 1					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
34060	6	8274	7	10	NULL	0	NULL	statement 10			controls		may;;selectively			statement 2					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
34061	7	8274	7	10	NULL	0	NULL	statement 10			controls		may;;selectively			statement 3					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
34062	8	8274	7	10	NULL	0	NULL	statement 10			controls		may;;selectively			statement 4					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
34063	9	8274	7	NULL	NULL	0	NULL	c- fos	NULL		is a type of	NULL				growth response genes	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
47533	11	8274	7	10	NULL	0	NULL	statement 10			controls		selectively			SRF		binding of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
56110	10	8274	7	10	NULL	0	NULL	chromatin		patterning of;;structure of	specific to					SMC-lineage					NULL		0	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_148	15718508	48 As such, it is interesting to speculate that there may be SMC-lineage specific patterning of chromatin structure that selectively controls SRF binding and subsequent recruitment of myocardin to a very select subset of SMC marker genes but not growth response genes like c- fos or skeletal and cardiac multiple CArG-containing genes.	bind
27577	1	8275	6	13	NULL	NULL	NULL	SRF	GP		bind					SM alpha-actin	GP			CArG element of promoter	NULL	A404 SMC progenitor line	NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_147	15718508	48 Briefly, we found selective enrichment of SRF binding to CArG-containing regions of SMC promoters, including the  SM alpha-actin and  SM-MHC genes, within intact chromatin after retinoic acid - induced expression of SMC marker genes in an A404 SMC progenitor line developed in our laboratory.	bind
27578	2	8275	6	13	NULL	NULL	NULL	SRF	GP		bind					SM-MHC gene	GP			CArG element of promoter	NULL	A404 SMC progenitor line	NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_147	15718508	48 Briefly, we found selective enrichment of SRF binding to CArG-containing regions of SMC promoters, including the  SM alpha-actin and  SM-MHC genes, within intact chromatin after retinoic acid - induced expression of SMC marker genes in an A404 SMC progenitor line developed in our laboratory.	bind
27580	3	8275	6	13	NULL	NULL	NULL	retinoic acid	Chemical		induces					SMC marker gene	GP	expression of			NULL	A404 SMC progenitor line	NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_147	15718508	48 Briefly, we found selective enrichment of SRF binding to CArG-containing regions of SMC promoters, including the  SM alpha-actin and  SM-MHC genes, within intact chromatin after retinoic acid - induced expression of SMC marker genes in an A404 SMC progenitor line developed in our laboratory.	bind
27582	4	8275	6	13	NULL	NULL	NULL	statement 1	Process		occurs after					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_147	15718508	48 Briefly, we found selective enrichment of SRF binding to CArG-containing regions of SMC promoters, including the  SM alpha-actin and  SM-MHC genes, within intact chromatin after retinoic acid - induced expression of SMC marker genes in an A404 SMC progenitor line developed in our laboratory.	bind
27583	5	8275	6	13	NULL	NULL	NULL	statement 2	Process		occurs after					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_147	15718508	48 Briefly, we found selective enrichment of SRF binding to CArG-containing regions of SMC promoters, including the  SM alpha-actin and  SM-MHC genes, within intact chromatin after retinoic acid - induced expression of SMC marker genes in an A404 SMC progenitor line developed in our laboratory.	bind
34073	1	8275	7	NULL	NULL	0	NULL	SRF	NULL		bind	NULL				 SM alpha-actin	NULL			CArG-containing regions of promoter	NULL	A404 SMC progenitor line	NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_147	15718508	48 Briefly, we found selective enrichment of SRF binding to CArG-containing regions of SMC promoters, including the  SM alpha-actin and  SM-MHC genes, within intact chromatin after retinoic acid - induced expression of SMC marker genes in an A404 SMC progenitor line developed in our laboratory.	bind
34076	2	8275	7	NULL	NULL	0	NULL	SRF	NULL		bind	NULL				SM-MHC genes	NULL			CArG-containing regions of promoter	NULL	A404 SMC progenitor line	NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_147	15718508	48 Briefly, we found selective enrichment of SRF binding to CArG-containing regions of SMC promoters, including the  SM alpha-actin and  SM-MHC genes, within intact chromatin after retinoic acid - induced expression of SMC marker genes in an A404 SMC progenitor line developed in our laboratory.	bind
34078	3	8275	7	NULL	NULL	0	NULL	retinoic acid	NULL		induce	NULL				SMC marker gene	NULL	expression of			NULL	A404 SMC progenitor line	NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_147	15718508	48 Briefly, we found selective enrichment of SRF binding to CArG-containing regions of SMC promoters, including the  SM alpha-actin and  SM-MHC genes, within intact chromatin after retinoic acid - induced expression of SMC marker genes in an A404 SMC progenitor line developed in our laboratory.	bind
34079	4	8275	7	NULL	NULL	0	NULL	statement 1	NULL		occurs after	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_147	15718508	48 Briefly, we found selective enrichment of SRF binding to CArG-containing regions of SMC promoters, including the  SM alpha-actin and  SM-MHC genes, within intact chromatin after retinoic acid - induced expression of SMC marker genes in an A404 SMC progenitor line developed in our laboratory.	bind
34081	5	8275	7	NULL	NULL	0	NULL	statement 2	NULL		occurs after	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_147	15718508	48 Briefly, we found selective enrichment of SRF binding to CArG-containing regions of SMC promoters, including the  SM alpha-actin and  SM-MHC genes, within intact chromatin after retinoic acid - induced expression of SMC marker genes in an A404 SMC progenitor line developed in our laboratory.	bind
27584	1	8276	6	13	NULL	NULL	NULL	collagen	GP		bind					fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_3_238_s_199	12855673	48 Thus, although the r/r mutation was designed to encode collagenase resistance, it also alters collagen binding to fibronectin.	bind
27585	2	8276	6	13	NULL	NULL	NULL	r/r mutation	Process		alters					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_3_238_s_199	12855673	48 Thus, although the r/r mutation was designed to encode collagenase resistance, it also alters collagen binding to fibronectin.	bind
27586	3	8276	6	13	NULL	NULL	NULL	r/r mutation	Process		encodes					collagenase resistance	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_3_238_s_199	12855673	48 Thus, although the r/r mutation was designed to encode collagenase resistance, it also alters collagen binding to fibronectin.	bind
34083	1	8276	7	NULL	NULL	0	NULL	collagen 	NULL		bind	NULL				fibronectin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_3_238_s_199	12855673	48 Thus, although the r/r mutation was designed to encode collagenase resistance, it also alters collagen binding to fibronectin.	bind
34085	2	8276	7	NULL	NULL	0	NULL	r/r mutation	NULL		encode	NULL				collagenase resistance	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_3_238_s_199	12855673	48 Thus, although the r/r mutation was designed to encode collagenase resistance, it also alters collagen binding to fibronectin.	bind
34087	3	8276	7	NULL	NULL	0	NULL	r/r mutation	NULL		alters	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_3_238_s_199	12855673	48 Thus, although the r/r mutation was designed to encode collagenase resistance, it also alters collagen binding to fibronectin.	bind
27589	1	8277	6	13	NULL	NULL	NULL	Vpr protein	GP	Human immunodeficiency virus type 1	bind					uracil DNA glycosylase	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_581_s_458	11788722	49       Bouhamdan,M., Benichou,S., Rey,F., Navarro,J.M., Agostini,I., Spire,B., Camonis,J., Slupphaug,G., Vigne,R., Benarous,R. and Sire,J. (1996) Human immunodeficiency virus type 1 Vpr protein binds to the uracil DNA glycosylase DNA repair enzyme.	bind
27590	2	8277	6	13	NULL	NULL	NULL	uracil DNA glycosylase	GP		is a type of					DNA repair enzyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_581_s_458	11788722	49       Bouhamdan,M., Benichou,S., Rey,F., Navarro,J.M., Agostini,I., Spire,B., Camonis,J., Slupphaug,G., Vigne,R., Benarous,R. and Sire,J. (1996) Human immunodeficiency virus type 1 Vpr protein binds to the uracil DNA glycosylase DNA repair enzyme.	bind
34092	1	8277	7	NULL	NULL	0	NULL	Vpr protein	NULL	Human immunodeficiency virus type 1	binds to	NULL				uracil DNA glycosylase DNA repair enzyme	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_581_s_458	11788722	49       Bouhamdan,M., Benichou,S., Rey,F., Navarro,J.M., Agostini,I., Spire,B., Camonis,J., Slupphaug,G., Vigne,R., Benarous,R. and Sire,J. (1996) Human immunodeficiency virus type 1 Vpr protein binds to the uracil DNA glycosylase DNA repair enzyme.	bind
46831	2	8277	7	10	NULL	0	NULL	uracil DNA glycosylase	NULL		is a type of	NULL				DNA repair enzyme	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_2_581_s_458	11788722	49       Bouhamdan,M., Benichou,S., Rey,F., Navarro,J.M., Agostini,I., Spire,B., Camonis,J., Slupphaug,G., Vigne,R., Benarous,R. and Sire,J. (1996) Human immunodeficiency virus type 1 Vpr protein binds to the uracil DNA glycosylase DNA repair enzyme.	bind
28349	1	8278	6	13	NULL	NULL	NULL	70kD protein	GP		bind		specifically			GM-CSF	GP	human		AU-rich region of 3' UTR	NULL	human embryonic lung fibroblasts	NULL	NULL	NULL	NULL	gw60_circulationres_82_7_794_s_230	9562439	49  Five distinct proteins, 70, 45, 40, 38, and 32.5 kD, which specifically bind to the AU-rich region of human GM-CSF 3' UTR, were found in human embryonic lung fibroblasts.	bind
28350	2	8278	6	13	NULL	NULL	NULL	45kD protein	GP		bind		specifically			GM-CSF	GP	human		AU-rich region of 3' UTR	NULL	human embryonic lung fibroblasts	NULL	NULL	NULL	NULL	gw60_circulationres_82_7_794_s_230	9562439	49  Five distinct proteins, 70, 45, 40, 38, and 32.5 kD, which specifically bind to the AU-rich region of human GM-CSF 3' UTR, were found in human embryonic lung fibroblasts.	bind
28351	3	8278	6	13	NULL	NULL	NULL	40 kD protein	GP		bind		specifically			GM-CSF 	GP	human		AU-rich region of 3' UTR	NULL	human embryonic lung fibroblasts	NULL	NULL	NULL	NULL	gw60_circulationres_82_7_794_s_230	9562439	49  Five distinct proteins, 70, 45, 40, 38, and 32.5 kD, which specifically bind to the AU-rich region of human GM-CSF 3' UTR, were found in human embryonic lung fibroblasts.	bind
28352	4	8278	6	13	NULL	NULL	NULL	38 kDa protein	GP		bind		specifically			GM-CSF	GP	human		AU-rich region of 3' UTR	NULL	human embryonic lung fibroblasts	NULL	NULL	NULL	NULL	gw60_circulationres_82_7_794_s_230	9562439	49  Five distinct proteins, 70, 45, 40, 38, and 32.5 kD, which specifically bind to the AU-rich region of human GM-CSF 3' UTR, were found in human embryonic lung fibroblasts.	bind
28353	5	8278	6	13	NULL	NULL	NULL	32.5 kD protein	GP		bind		specifically			GM-CSF	GP	human		AU-rich region of 3' UTR	NULL	human embryonic lung fibroblasts	NULL	NULL	NULL	NULL	gw60_circulationres_82_7_794_s_230	9562439	49  Five distinct proteins, 70, 45, 40, 38, and 32.5 kD, which specifically bind to the AU-rich region of human GM-CSF 3' UTR, were found in human embryonic lung fibroblasts.	bind
34093	1	8278	7	NULL	NULL	0	NULL	70 kD protein	NULL		binds to	NULL	specifically			GM-CSF	NULL	human		AU-rich region of 3' UTR	NULL	human embryonic lung fibroblasts	NULL	NULL	NULL	NULL	gw60_circulationres_82_7_794_s_230	9562439	49  Five distinct proteins, 70, 45, 40, 38, and 32.5 kD, which specifically bind to the AU-rich region of human GM-CSF 3' UTR, were found in human embryonic lung fibroblasts.	bind
34094	2	8278	7	NULL	NULL	0	NULL	45 kD protein	NULL		binds to	NULL	specifically			GM-CSF	NULL	human		AU-rich region of 3' UTR	NULL	human embryonic lung fibroblasts	0	NULL	NULL	NULL	gw60_circulationres_82_7_794_s_230	9562439	49  Five distinct proteins, 70, 45, 40, 38, and 32.5 kD, which specifically bind to the AU-rich region of human GM-CSF 3' UTR, were found in human embryonic lung fibroblasts.	bind
34095	3	8278	7	NULL	NULL	0	NULL	40 kD protein	NULL		binds to	NULL	specifically			GM-CSF	NULL	human		AU-rich region of 3' UTR	NULL	human embryonic lung fibroblasts	0	NULL	NULL	NULL	gw60_circulationres_82_7_794_s_230	9562439	49  Five distinct proteins, 70, 45, 40, 38, and 32.5 kD, which specifically bind to the AU-rich region of human GM-CSF 3' UTR, were found in human embryonic lung fibroblasts.	bind
34096	4	8278	7	NULL	NULL	0	NULL	38 kD protein	NULL		binds to	NULL	specifically			GM-CSF	NULL	human		AU-rich region of 3' UTR	NULL	human embryonic lung fibroblasts	0	NULL	NULL	NULL	gw60_circulationres_82_7_794_s_230	9562439	49  Five distinct proteins, 70, 45, 40, 38, and 32.5 kD, which specifically bind to the AU-rich region of human GM-CSF 3' UTR, were found in human embryonic lung fibroblasts.	bind
34097	5	8278	7	NULL	NULL	0	NULL	32.5 kD protein	NULL		binds to	NULL	specifically			GM-CSF	NULL	human		AU-rich region of 3' UTR	NULL	human embryonic lung fibroblasts	NULL	NULL	NULL	NULL	gw60_circulationres_82_7_794_s_230	9562439	49  Five distinct proteins, 70, 45, 40, 38, and 32.5 kD, which specifically bind to the AU-rich region of human GM-CSF 3' UTR, were found in human embryonic lung fibroblasts.	bind
27652	1	8279	6	13	NULL	NULL	NULL	fibroblast growth factor	GP		bind					fibroblast growth factor receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_9_2605_s_199	7586363	49  Heparan sulfate proteoglycans are obligate partners in the binding of basic fibroblast growth factors to their receptors; fibroblast growth factors do not bind to fibroblast growth factor receptors unless heparan sulfate, or its analog heparin, is present.	bind
27655	2	8279	6	13	NULL	NULL	NULL	statement 1	Process		occurs in presence of		only			heparan sulfate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_9_2605_s_199	7586363	49  Heparan sulfate proteoglycans are obligate partners in the binding of basic fibroblast growth factors to their receptors; fibroblast growth factors do not bind to fibroblast growth factor receptors unless heparan sulfate, or its analog heparin, is present.	bind
27657	3	8279	6	13	NULL	NULL	NULL	statement 1	Process		occurs in presence of		only			heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_9_2605_s_199	7586363	49  Heparan sulfate proteoglycans are obligate partners in the binding of basic fibroblast growth factors to their receptors; fibroblast growth factors do not bind to fibroblast growth factor receptors unless heparan sulfate, or its analog heparin, is present.	bind
34098	1	8279	7	10	NULL	0	NULL	fibroblast growth factors	NULL		does not bind	NULL				fibroblast growth factor receptors	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_9_2605_s_199	7586363	49  Heparan sulfate proteoglycans are obligate partners in the binding of basic fibroblast growth factors to their receptors; fibroblast growth factors do not bind to fibroblast growth factor receptors unless heparan sulfate, or its analog heparin, is present.	bind
34099	2	8279	7	NULL	NULL	0	NULL	statement 1	NULL		in absence of	NULL				heparan sulfate	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_9_2605_s_199	7586363	49  Heparan sulfate proteoglycans are obligate partners in the binding of basic fibroblast growth factors to their receptors; fibroblast growth factors do not bind to fibroblast growth factor receptors unless heparan sulfate, or its analog heparin, is present.	bind
34100	3	8279	7	NULL	NULL	0	NULL	statement 1	NULL		in absence of	NULL				heparin analog	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_9_2605_s_199	7586363	49  Heparan sulfate proteoglycans are obligate partners in the binding of basic fibroblast growth factors to their receptors; fibroblast growth factors do not bind to fibroblast growth factor receptors unless heparan sulfate, or its analog heparin, is present.	bind
34101	4	8279	7	NULL	NULL	0	NULL	fibroblast growth factors	NULL		bind	NULL				fibroblast growth factor receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_9_2605_s_199	7586363	49  Heparan sulfate proteoglycans are obligate partners in the binding of basic fibroblast growth factors to their receptors; fibroblast growth factors do not bind to fibroblast growth factor receptors unless heparan sulfate, or its analog heparin, is present.	bind
34102	5	8279	7	NULL	NULL	0	NULL	Heparan sulfate proteoglycans	NULL		are obligate partners of	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_9_2605_s_199	7586363	49  Heparan sulfate proteoglycans are obligate partners in the binding of basic fibroblast growth factors to their receptors; fibroblast growth factors do not bind to fibroblast growth factor receptors unless heparan sulfate, or its analog heparin, is present.	bind
27665	1	8280	6	13	NULL	NULL	NULL	AR	GP	intact	bind		functionaly			androgen	Chemical				NULL	hormone-dependent carcinoma	NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_79_s_451	11438457	49  Importantly, results from a past study 50  demonstrated the presence of structurally intact AR that functionally binds androgen in the majority of both hormone-dependent and -independent carcinomas.	bind
27667	2	8280	6	13	NULL	NULL	NULL	AR	GP	intact	bind		functionaly			androgen	Chemical				NULL	hormone independent carcinoma	NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_79_s_451	11438457	49  Importantly, results from a past study 50  demonstrated the presence of structurally intact AR that functionally binds androgen in the majority of both hormone-dependent and -independent carcinomas.	bind
34103	1	8280	7	10	NULL	0	NULL	AR	NULL	intact 	binds	NULL	functionally			androgen	NULL				NULL	hormone-dependent carcinomas	NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_79_s_451	11438457	49  Importantly, results from a past study 50  demonstrated the presence of structurally intact AR that functionally binds androgen in the majority of both hormone-dependent and -independent carcinomas.	bind
34104	2	8280	7	10	NULL	0	NULL	AR	NULL	intact	binds	NULL	functionally			androgen	NULL				NULL	hormone-independent carcinomas	NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_79_s_451	11438457	49  Importantly, results from a past study 50  demonstrated the presence of structurally intact AR that functionally binds androgen in the majority of both hormone-dependent and -independent carcinomas.	bind
27671	1	8281	6	13	NULL	NULL	NULL	apoA-I	GP		does not bind							mutant	W590S		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_108	12738681	49 However, an equally valid interpretation is that apoA-I fails to bind the W590S mutant in the correct orientation and therefore the appropriate conformational change of ABCA1 required to decrease calpain proteolysis does not occur.	bind
27673	2	8281	6	13	NULL	NULL	NULL	ABCA1	GP	conformational change of	decrease					calpain	GP	proteolysis of 			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_108	12738681	49 However, an equally valid interpretation is that apoA-I fails to bind the W590S mutant in the correct orientation and therefore the appropriate conformational change of ABCA1 required to decrease calpain proteolysis does not occur.	bind
34105	1	8281	7	10	NULL	0	NULL	apoA-I 	NULL		fails to bind	NULL					NULL	mutant	W590S		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_108	12738681	49 However, an equally valid interpretation is that apoA-I fails to bind the W590S mutant in the correct orientation and therefore the appropriate conformational change of ABCA1 required to decrease calpain proteolysis does not occur.	bind
34106	2	8281	7	NULL	NULL	0	NULL	ABCA1	NULL	conformational change of 	decrease	NULL				calpain	NULL	proteolysis of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_108	12738681	49 However, an equally valid interpretation is that apoA-I fails to bind the W590S mutant in the correct orientation and therefore the appropriate conformational change of ABCA1 required to decrease calpain proteolysis does not occur.	bind
34107	3	8281	7	NULL	NULL	0	NULL	statement 2	NULL		does not occur with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1178_s_108	12738681	49 However, an equally valid interpretation is that apoA-I fails to bind the W590S mutant in the correct orientation and therefore the appropriate conformational change of ABCA1 required to decrease calpain proteolysis does not occur.	bind
27674	1	8282	6	13	NULL	NULL	NULL	ICP8	GP		bind					UL9 protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_66_0_347_s_214	9242911	4: binding of ICP8 to   the UL9 protein and distorted DNA.  5: ATP-dependent DNA unwinding that generates ICP8-coated DNA strands.	bind
27675	2	8282	6	13	NULL	NULL	NULL	ICP8	GP		bind					DNA	NucleicAcid	distorted			NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_66_0_347_s_214	9242911	4: binding of ICP8 to   the UL9 protein and distorted DNA.  5: ATP-dependent DNA unwinding that generates ICP8-coated DNA strands.	bind
27798	3	8282	6	13	NULL	NULL	NULL	DNA	NucleicAcid	unwinding of	generates					DNA strands	NucleicAcid	ICP8-coated			NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_66_0_347_s_214	9242911	4: binding of ICP8 to   the UL9 protein and distorted DNA.  5: ATP-dependent DNA unwinding that generates ICP8-coated DNA strands.	bind
27799	4	8282	6	13	NULL	NULL	NULL	statement 3	Process		is dependent on					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_66_0_347_s_214	9242911	4: binding of ICP8 to   the UL9 protein and distorted DNA.  5: ATP-dependent DNA unwinding that generates ICP8-coated DNA strands.	bind
34108	1	8282	7	NULL	NULL	0	NULL	ICP8	NULL		binds to	NULL				UL9 protein	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_66_0_347_s_214	9242911	4: binding of ICP8 to   the UL9 protein and distorted DNA.  5: ATP-dependent DNA unwinding that generates ICP8-coated DNA strands.	bind
34109	2	8282	7	10	NULL	0	NULL	ICP8	NULL		bind	NULL				DNA	NULL	distorted			NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_66_0_347_s_214	9242911	4: binding of ICP8 to   the UL9 protein and distorted DNA.  5: ATP-dependent DNA unwinding that generates ICP8-coated DNA strands.	bind
34110	3	8282	7	NULL	NULL	0	NULL	DNA	NULL	unwinding of	depends on	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_66_0_347_s_214	9242911	4: binding of ICP8 to   the UL9 protein and distorted DNA.  5: ATP-dependent DNA unwinding that generates ICP8-coated DNA strands.	bind
34111	4	8282	7	10	NULL	0	NULL	statement 2	NULL		generates	NULL				DNA strands	NULL	ICP8-coated			NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_66_0_347_s_214	9242911	4: binding of ICP8 to   the UL9 protein and distorted DNA.  5: ATP-dependent DNA unwinding that generates ICP8-coated DNA strands.	bind
27801	1	8285	6	13	NULL	NULL	NULL	4E-BP	GP		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_20788_s_185	16720573	4E-BP Binding Suppresses eIF4E Ubiquitination and Degradation -- 4E-BP proteins bind eIF4E and negatively regulate cap-dependent translation initiation.	bind
27802	2	8285	6	13	NULL	NULL	NULL	statement 1	Process		suppresses					eIF4E	GP	ubiquitination of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_20788_s_185	16720573	4E-BP Binding Suppresses eIF4E Ubiquitination and Degradation -- 4E-BP proteins bind eIF4E and negatively regulate cap-dependent translation initiation.	bind
27803	3	8285	6	13	NULL	NULL	NULL	statement 1	Process		suppresses					eIF4E	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_20788_s_185	16720573	4E-BP Binding Suppresses eIF4E Ubiquitination and Degradation -- 4E-BP proteins bind eIF4E and negatively regulate cap-dependent translation initiation.	bind
27804	4	8285	6	13	NULL	NULL	NULL	translation	Process	initiation of	is dependent on					cap	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_20788_s_185	16720573	4E-BP Binding Suppresses eIF4E Ubiquitination and Degradation -- 4E-BP proteins bind eIF4E and negatively regulate cap-dependent translation initiation.	bind
27805	5	8285	6	13	NULL	NULL	NULL	statement 1	Process		regulates		negatively			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_20788_s_185	16720573	4E-BP Binding Suppresses eIF4E Ubiquitination and Degradation -- 4E-BP proteins bind eIF4E and negatively regulate cap-dependent translation initiation.	bind
34115	1	8285	7	NULL	NULL	0	NULL	4E-BP	NULL	binding of	suppress	NULL				eIF4E	NULL	ubiquitination of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_20788_s_185	16720573	4E-BP Binding Suppresses eIF4E Ubiquitination and Degradation -- 4E-BP proteins bind eIF4E and negatively regulate cap-dependent translation initiation.	bind
34116	2	8285	7	NULL	NULL	0	NULL	4E-BP	NULL	binding of	suppress	NULL				eIF4E	NULL	degradation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_20788_s_185	16720573	4E-BP Binding Suppresses eIF4E Ubiquitination and Degradation -- 4E-BP proteins bind eIF4E and negatively regulate cap-dependent translation initiation.	bind
34117	3	8285	7	NULL	NULL	0	NULL	 4E-BP proteins	NULL		bind	NULL				eIF4E	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_20788_s_185	16720573	4E-BP Binding Suppresses eIF4E Ubiquitination and Degradation -- 4E-BP proteins bind eIF4E and negatively regulate cap-dependent translation initiation.	bind
34118	4	8285	7	NULL	NULL	0	NULL	translation	NULL	initiation of	depends on	NULL				cap	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_20788_s_185	16720573	4E-BP Binding Suppresses eIF4E Ubiquitination and Degradation -- 4E-BP proteins bind eIF4E and negatively regulate cap-dependent translation initiation.	bind
34119	5	8285	7	NULL	NULL	0	NULL	statement 3	NULL		regulate	NULL	negatively			statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_20788_s_185	16720573	4E-BP Binding Suppresses eIF4E Ubiquitination and Degradation -- 4E-BP proteins bind eIF4E and negatively regulate cap-dependent translation initiation.	bind
27806	1	8286	6	13	NULL	NULL	NULL	4E-BP	GP		bind					heIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_14_4068_s_92	10406811	4E-BP binding to heIF4E enhances cap affinity.	bind
27807	2	8286	6	13	NULL	NULL	NULL	statement 1	Process		enhances					cap	NucleicAcid	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_14_4068_s_92	10406811	4E-BP binding to heIF4E enhances cap affinity.	bind
34120	1	8286	7	NULL	NULL	0	NULL	4E-BP	NULL		bind	NULL				heIF4E	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_18_14_4068_s_92	10406811	4E-BP binding to heIF4E enhances cap affinity.	bind
34121	2	8286	7	10	NULL	0	NULL	statement 1	NULL		enhances	NULL				cap	NULL	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_14_4068_s_92	10406811	4E-BP binding to heIF4E enhances cap affinity.	bind
27808	1	8287	6	13	NULL	NULL	NULL	4E-BP	GP		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_20788_s_269	16720573	4E-BP binds eIF4E under conditions of stress or reduced growth stimuli.	bind
27809	2	8287	6	13	NULL	NULL	NULL	statement 1	Process		occurs under conditions of					stress					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_20788_s_269	16720573	4E-BP binds eIF4E under conditions of stress or reduced growth stimuli.	bind
27810	3	8287	6	13	NULL	NULL	NULL	statement 1	Process		occurs under conditions of					growth stimuli	Process	reduced			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_20788_s_269	16720573	4E-BP binds eIF4E under conditions of stress or reduced growth stimuli.	bind
34122	1	8287	7	10	NULL	0	NULL	4E-BP	NULL		binds	NULL				 eIF4E	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_20788_s_269	16720573	4E-BP binds eIF4E under conditions of stress or reduced growth stimuli.	bind
34123	2	8287	7	10	NULL	0	NULL	statement 1	NULL		occurs under conditions of	NULL				stress	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_20788_s_269	16720573	4E-BP binds eIF4E under conditions of stress or reduced growth stimuli.	bind
46832	3	8287	7	10	NULL	0	NULL	statement 1	NULL		occurs under conditions of	NULL				growth stimuli	NULL	reduced			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_20788_s_269	16720573	4E-BP binds eIF4E under conditions of stress or reduced growth stimuli.	bind
27811	1	8288	6	13	NULL	NULL	NULL	4E-BP1	GP		is a synonym of					PHAS-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_24_21960_s_415	12668683	4E-BP1 (also known as PHAS-1) normally binds eIF4E, initiating  cap-dependent phosphorylation  ( ).	bind
27812	2	8288	6	13	NULL	NULL	NULL	4E-BP1	GP		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_24_21960_s_415	12668683	4E-BP1 (also known as PHAS-1) normally binds eIF4E, initiating  cap-dependent phosphorylation  ( ).	bind
27813	3	8288	6	13	NULL	NULL	NULL	eIF4E	GP	phosphorylation of	is dependent on					cap	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_24_21960_s_415	12668683	4E-BP1 (also known as PHAS-1) normally binds eIF4E, initiating  cap-dependent phosphorylation  ( ).	bind
27814	4	8288	6	13	NULL	NULL	NULL	statement 2	Process		initiates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_24_21960_s_415	12668683	4E-BP1 (also known as PHAS-1) normally binds eIF4E, initiating  cap-dependent phosphorylation  ( ).	bind
34124	1	8288	7	NULL	NULL	0	NULL	4E-BP1	NULL		binds	NULL	normally			eIF4E	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_24_21960_s_415	12668683	4E-BP1 (also known as PHAS-1) normally binds eIF4E, initiating  cap-dependent phosphorylation  ( ).	bind
34125	2	8288	7	NULL	NULL	0	NULL	phosphorylation	NULL		depends on	NULL				cap	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_24_21960_s_415	12668683	4E-BP1 (also known as PHAS-1) normally binds eIF4E, initiating  cap-dependent phosphorylation  ( ).	bind
34126	3	8288	7	NULL	NULL	0	NULL	statement 1	NULL		initiate	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_24_21960_s_415	12668683	4E-BP1 (also known as PHAS-1) normally binds eIF4E, initiating  cap-dependent phosphorylation  ( ).	bind
34127	4	8288	7	10	NULL	0	NULL	4E-BP1	NULL		is a synonym of	NULL				PHAS-1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_24_21960_s_415	12668683	4E-BP1 (also known as PHAS-1) normally binds eIF4E, initiating  cap-dependent phosphorylation  ( ).	bind
27815	1	8289	6	13	NULL	NULL	NULL	4E-BP1	GP		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_15_10779_s_27	10753870	4E-BP1 and 4E-BP2 bind to eIF4E by a mechanism dependent on their phosphorylation state ( 31-33).	bind
27816	2	8289	6	13	NULL	NULL	NULL	4E-BP2	GP		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_15_10779_s_27	10753870	4E-BP1 and 4E-BP2 bind to eIF4E by a mechanism dependent on their phosphorylation state ( 31-33).	bind
27817	3	8289	6	13	NULL	NULL	NULL	statement 1	Process		is dependent on					4E-BP1	GP	phosphorylation state of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_15_10779_s_27	10753870	4E-BP1 and 4E-BP2 bind to eIF4E by a mechanism dependent on their phosphorylation state ( 31-33).	bind
27818	4	8289	6	13	NULL	NULL	NULL	statement 2	Process		is dependent on					4E-BP2	GP	phosphorylation state of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_15_10779_s_27	10753870	4E-BP1 and 4E-BP2 bind to eIF4E by a mechanism dependent on their phosphorylation state ( 31-33).	bind
34128	1	8289	7	NULL	NULL	0	NULL	4E-BP1	NULL		binds to	NULL				eIF4E	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_15_10779_s_27	10753870	4E-BP1 and 4E-BP2 bind to eIF4E by a mechanism dependent on their phosphorylation state ( 31-33).	bind
34129	2	8289	7	NULL	NULL	0	NULL	4E-BP2	NULL		binds to	NULL				eIF4E 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_15_10779_s_27	10753870	4E-BP1 and 4E-BP2 bind to eIF4E by a mechanism dependent on their phosphorylation state ( 31-33).	bind
34130	3	8289	7	NULL	NULL	0	NULL	statement 1	NULL		depends on	NULL				4E-BP1	NULL	phosphorylation state of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_15_10779_s_27	10753870	4E-BP1 and 4E-BP2 bind to eIF4E by a mechanism dependent on their phosphorylation state ( 31-33).	bind
34131	4	8289	7	NULL	NULL	0	NULL	statement 2	NULL		depends on	NULL				4E-BP2	NULL	phosphorylation state of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_15_10779_s_27	10753870	4E-BP1 and 4E-BP2 bind to eIF4E by a mechanism dependent on their phosphorylation state ( 31-33).	bind
27819	1	8290	6	13	NULL	NULL	NULL	4E-BP1	GP	underphosphorylated	bind		high affinity			eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_20_11831_s_25	8662663	4E-BP1 and 4E-BP2 binding to eIF4E is  regulated by phosphorylation: the underphosphorylated species possess a  high affinity for eIF4E, whereas the hyperphosphorylated species do not  bind to eIF4E( 9,  10) .	bind
27820	2	8290	6	13	NULL	NULL	NULL	4E-BP2	GP	underphosphorylated	bind		high affinity			eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_20_11831_s_25	8662663	4E-BP1 and 4E-BP2 binding to eIF4E is  regulated by phosphorylation: the underphosphorylated species possess a  high affinity for eIF4E, whereas the hyperphosphorylated species do not  bind to eIF4E( 9,  10) .	bind
27821	3	8290	6	13	NULL	NULL	NULL	4E-BP1	GP	hyperphosphorylated	does not bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_20_11831_s_25	8662663	4E-BP1 and 4E-BP2 binding to eIF4E is  regulated by phosphorylation: the underphosphorylated species possess a  high affinity for eIF4E, whereas the hyperphosphorylated species do not  bind to eIF4E( 9,  10) .	bind
27822	4	8290	6	13	NULL	NULL	NULL	4E-BP2	GP	hyperphosphorylated	does not bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_20_11831_s_25	8662663	4E-BP1 and 4E-BP2 binding to eIF4E is  regulated by phosphorylation: the underphosphorylated species possess a  high affinity for eIF4E, whereas the hyperphosphorylated species do not  bind to eIF4E( 9,  10) .	bind
34136	1	8290	7	10	NULL	0	NULL	4E-BP1		underphosphorylated	bind		high affinity			eIF4E					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_20_11831_s_25	8662663	4E-BP1 and 4E-BP2 binding to eIF4E is  regulated by phosphorylation: the underphosphorylated species possess a  high affinity for eIF4E, whereas the hyperphosphorylated species do not  bind to eIF4E( 9,  10) .	bind
34137	2	8290	7	10	NULL	0	NULL	4E-BP2		underphosphorylated	bind		high affinity			eIF4E					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_20_11831_s_25	8662663	4E-BP1 and 4E-BP2 binding to eIF4E is  regulated by phosphorylation: the underphosphorylated species possess a  high affinity for eIF4E, whereas the hyperphosphorylated species do not  bind to eIF4E( 9,  10) .	bind
46833	3	8290	7	10	NULL	0	NULL	4E-BP1		hyperphosphorylated	does not bind					eIF4E					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_20_11831_s_25	8662663	4E-BP1 and 4E-BP2 binding to eIF4E is  regulated by phosphorylation: the underphosphorylated species possess a  high affinity for eIF4E, whereas the hyperphosphorylated species do not  bind to eIF4E( 9,  10) .	bind
46834	4	8290	7	10	NULL	0	NULL	4E-BP2		hyperphosphorylated	does not bind					eIF4E					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_20_11831_s_25	8662663	4E-BP1 and 4E-BP2 binding to eIF4E is  regulated by phosphorylation: the underphosphorylated species possess a  high affinity for eIF4E, whereas the hyperphosphorylated species do not  bind to eIF4E( 9,  10) .	bind
27823	1	8291	6	13	NULL	NULL	NULL	eIF-4E	GP		is a type of					eukaryotic initiation factor 4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_2_283_s_65	9728910	4E-BP1 binds to eukaryotic initiation factor 4E (eIF-4E), the mRNA 7-methylguanylate (M7-GppN) cap-binding protein, and inhibits formation of the initiation complex.	bind
27824	2	8291	6	13	NULL	NULL	NULL	7-methylguanylate 	NucleicAcid		is					M7-GppN	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_2_283_s_65	9728910	4E-BP1 binds to eukaryotic initiation factor 4E (eIF-4E), the mRNA 7-methylguanylate (M7-GppN) cap-binding protein, and inhibits formation of the initiation complex.	bind
27825	3	8291	6	13	NULL	NULL	NULL	4E-BP1	GP		bind					eIF-4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_2_283_s_65	9728910	4E-BP1 binds to eukaryotic initiation factor 4E (eIF-4E), the mRNA 7-methylguanylate (M7-GppN) cap-binding protein, and inhibits formation of the initiation complex.	bind
27826	4	8291	6	13	NULL	NULL	NULL	4E-BP1	GP		bind					M7-GppN cap binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_2_283_s_65	9728910	4E-BP1 binds to eukaryotic initiation factor 4E (eIF-4E), the mRNA 7-methylguanylate (M7-GppN) cap-binding protein, and inhibits formation of the initiation complex.	bind
27827	5	8291	6	13	NULL	NULL	NULL	statement 3	Process		inhibits					initiation complex	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_2_283_s_65	9728910	4E-BP1 binds to eukaryotic initiation factor 4E (eIF-4E), the mRNA 7-methylguanylate (M7-GppN) cap-binding protein, and inhibits formation of the initiation complex.	bind
27828	6	8291	6	13	NULL	NULL	NULL	statement 4	Process		inhibits					initiation complex	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_2_283_s_65	9728910	4E-BP1 binds to eukaryotic initiation factor 4E (eIF-4E), the mRNA 7-methylguanylate (M7-GppN) cap-binding protein, and inhibits formation of the initiation complex.	bind
34138	1	8291	7	NULL	NULL	0	NULL	4E-BP1	NULL		binds to	NULL				eIF-4E	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_21_2_283_s_65	9728910	4E-BP1 binds to eukaryotic initiation factor 4E (eIF-4E), the mRNA 7-methylguanylate (M7-GppN) cap-binding protein, and inhibits formation of the initiation complex.	bind
34139	2	8291	7	NULL	NULL	0	NULL	4E-BP1	NULL		binds to	NULL				M7-GppN cap-binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_21_2_283_s_65	9728910	4E-BP1 binds to eukaryotic initiation factor 4E (eIF-4E), the mRNA 7-methylguanylate (M7-GppN) cap-binding protein, and inhibits formation of the initiation complex.	bind
34140	3	8291	7	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				initiation complex	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_neuron_21_2_283_s_65	9728910	4E-BP1 binds to eukaryotic initiation factor 4E (eIF-4E), the mRNA 7-methylguanylate (M7-GppN) cap-binding protein, and inhibits formation of the initiation complex.	bind
34141	4	8291	7	NULL	NULL	0	NULL	statement 2	NULL		inhibits	NULL				initiation complex	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_neuron_21_2_283_s_65	9728910	4E-BP1 binds to eukaryotic initiation factor 4E (eIF-4E), the mRNA 7-methylguanylate (M7-GppN) cap-binding protein, and inhibits formation of the initiation complex.	bind
34142	5	8291	7	10	NULL	0	NULL	eIF-4E	NULL		is a type of	NULL				eukaryotic initiation factor 4E	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_2_283_s_65	9728910	4E-BP1 binds to eukaryotic initiation factor 4E (eIF-4E), the mRNA 7-methylguanylate (M7-GppN) cap-binding protein, and inhibits formation of the initiation complex.	bind
34143	6	8291	7	NULL	NULL	0	NULL	M7-GppN	NULL		is	NULL				mRNA 7-methylguanylate	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_21_2_283_s_65	9728910	4E-BP1 binds to eukaryotic initiation factor 4E (eIF-4E), the mRNA 7-methylguanylate (M7-GppN) cap-binding protein, and inhibits formation of the initiation complex.	bind
27829	1	8292	6	13	NULL	NULL	NULL	protein translation	Process		is dependent on					cap	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_23_6_2333_s_101	12657692	4E-BP1 normally binds to eIF4E, thereby inhibiting cap-dependent protein translation (Gingras et al., 1999  ).	bind
27830	2	8292	6	13	NULL	NULL	NULL	4E-BP1	GP		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_23_6_2333_s_101	12657692	4E-BP1 normally binds to eIF4E, thereby inhibiting cap-dependent protein translation (Gingras et al., 1999  ).	bind
27831	3	8292	6	13	NULL	NULL	NULL	statement 2	Process		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_23_6_2333_s_101	12657692	4E-BP1 normally binds to eIF4E, thereby inhibiting cap-dependent protein translation (Gingras et al., 1999  ).	bind
34144	1	8292	7	NULL	NULL	0	NULL	4E-BP1	NULL		binds	NULL	normally			eIF4E	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_23_6_2333_s_101	12657692	4E-BP1 normally binds to eIF4E, thereby inhibiting cap-dependent protein translation (Gingras et al., 1999  ).	bind
34145	2	8292	7	NULL	NULL	0	NULL	protein translation	NULL		depends on	NULL				cap	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_23_6_2333_s_101	12657692	4E-BP1 normally binds to eIF4E, thereby inhibiting cap-dependent protein translation (Gingras et al., 1999  ).	bind
34146	3	8292	7	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_23_6_2333_s_101	12657692	4E-BP1 normally binds to eIF4E, thereby inhibiting cap-dependent protein translation (Gingras et al., 1999  ).	bind
27832	1	8293	6	13	NULL	NULL	NULL	eIF4E	GP	phosphorylated	bind					capped mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3303_s_207	11723111	4E-BP1 Stabilizes the Binding of Phosphorylated eIF4E to Capped mRNA-- Since eIF4E interacts with other proteins  in vivo (eIF4G, 4E-BPs), it was important to examine whether they modified the effect of phosphorylation on the binding of eIF4E to capped RNA.	bind
27833	2	8293	6	13	NULL	NULL	NULL	4E-BP1	GP		stabilizes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3303_s_207	11723111	4E-BP1 Stabilizes the Binding of Phosphorylated eIF4E to Capped mRNA-- Since eIF4E interacts with other proteins  in vivo (eIF4G, 4E-BPs), it was important to examine whether they modified the effect of phosphorylation on the binding of eIF4E to capped RNA.	bind
27834	3	8293	6	13	NULL	NULL	NULL	eIF4E 	GP		interacts with					eIF4G	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3303_s_207	11723111	4E-BP1 Stabilizes the Binding of Phosphorylated eIF4E to Capped mRNA-- Since eIF4E interacts with other proteins  in vivo (eIF4G, 4E-BPs), it was important to examine whether they modified the effect of phosphorylation on the binding of eIF4E to capped RNA.	bind
27835	4	8293	6	13	NULL	NULL	NULL	eIF4E	GP		interacts with					4E-BPs	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3303_s_207	11723111	4E-BP1 Stabilizes the Binding of Phosphorylated eIF4E to Capped mRNA-- Since eIF4E interacts with other proteins  in vivo (eIF4G, 4E-BPs), it was important to examine whether they modified the effect of phosphorylation on the binding of eIF4E to capped RNA.	bind
27836	5	8293	6	13	NULL	NULL	NULL	eIF4E	GP		bind					capped RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3303_s_207	11723111	4E-BP1 Stabilizes the Binding of Phosphorylated eIF4E to Capped mRNA-- Since eIF4E interacts with other proteins  in vivo (eIF4G, 4E-BPs), it was important to examine whether they modified the effect of phosphorylation on the binding of eIF4E to capped RNA.	bind
34147	1	8293	7	NULL	NULL	0	NULL	eIF4E	NULL	phosphorylated	binds	NULL				Capped mRNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3303_s_207	11723111	4E-BP1 Stabilizes the Binding of Phosphorylated eIF4E to Capped mRNA-- Since eIF4E interacts with other proteins  in vivo (eIF4G, 4E-BPs), it was important to examine whether they modified the effect of phosphorylation on the binding of eIF4E to capped RNA.	bind
34148	2	8293	7	NULL	NULL	0	NULL	4E-BP1	NULL		stabilizes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_5_3303_s_207	11723111	4E-BP1 Stabilizes the Binding of Phosphorylated eIF4E to Capped mRNA-- Since eIF4E interacts with other proteins  in vivo (eIF4G, 4E-BPs), it was important to examine whether they modified the effect of phosphorylation on the binding of eIF4E to capped RNA.	bind
34149	3	8293	7	NULL	NULL	0	NULL	eIF4E	NULL		interacts with	NULL				eIF4G	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3303_s_207	11723111	4E-BP1 Stabilizes the Binding of Phosphorylated eIF4E to Capped mRNA-- Since eIF4E interacts with other proteins  in vivo (eIF4G, 4E-BPs), it was important to examine whether they modified the effect of phosphorylation on the binding of eIF4E to capped RNA.	bind
34150	4	8293	7	NULL	NULL	0	NULL	eIF4E	NULL		interacts with	NULL				4E-BPs	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_jbiolchem_277_5_3303_s_207	11723111	4E-BP1 Stabilizes the Binding of Phosphorylated eIF4E to Capped mRNA-- Since eIF4E interacts with other proteins  in vivo (eIF4G, 4E-BPs), it was important to examine whether they modified the effect of phosphorylation on the binding of eIF4E to capped RNA.	bind
27837	1	8294	6	13	NULL	NULL	NULL	4E-BP3	GP		bind					eIF4E	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_14002_s_8	9593750	4E-BP3 is a heat stable protein that binds to eIF4E  in vitro as well as  in vivo.	bind
27838	2	8294	6	13	NULL	NULL	NULL	4E-BP3	GP		bind					eIF4E	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_14002_s_8	9593750	4E-BP3 is a heat stable protein that binds to eIF4E  in vitro as well as  in vivo.	bind
27839	3	8294	6	13	NULL	NULL	NULL	4E-BP3	GP		is a type of					heat stable protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_14002_s_8	9593750	4E-BP3 is a heat stable protein that binds to eIF4E  in vitro as well as  in vivo.	bind
34151	1	8294	7	NULL	NULL	0	NULL	4E-BP3	NULL		binds to	NULL				eIF4E	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_273_22_14002_s_8	9593750	4E-BP3 is a heat stable protein that binds to eIF4E  in vitro as well as  in vivo.	bind
34152	2	8294	7	NULL	NULL	0	NULL	4E-BP3	NULL		binds to	NULL				eIF4E	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_jbiolchem_273_22_14002_s_8	9593750	4E-BP3 is a heat stable protein that binds to eIF4E  in vitro as well as  in vivo.	bind
34153	3	8294	7	NULL	NULL	0	NULL	4E-BP3 	NULL		is a type of	NULL				heat stable protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_22_14002_s_8	9593750	4E-BP3 is a heat stable protein that binds to eIF4E  in vitro as well as  in vivo.	bind
27840	1	8295	6	13	NULL	NULL	NULL	4E-T	GP		bind					eIF4E	GP		dorsal site		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_16_5692_s_358	12897141	4E-T binds to the dorsal site of eIF4E ( ), a region also involved in binding eIF4G and 4E-BP1.	bind
27841	2	8295	6	13	NULL	NULL	NULL	eIF4G	GP		bind					eIF4E	GP		dorsal site 		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_16_5692_s_358	12897141	4E-T binds to the dorsal site of eIF4E ( ), a region also involved in binding eIF4G and 4E-BP1.	bind
47519	3	8295	6	13	NULL	NULL	NULL	4E-BP1	GP		bind					eIF4E	GP		dorsal site 		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_16_5692_s_358	12897141	4E-T binds to the dorsal site of eIF4E ( ), a region also involved in binding eIF4G and 4E-BP1.	bind
34154	1	8295	7	NULL	NULL	0	NULL	4E-T	NULL		binds to	NULL				eIF4E	NULL		dorsal site of		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_16_5692_s_358	12897141	4E-T binds to the dorsal site of eIF4E ( ), a region also involved in binding eIF4G and 4E-BP1.	bind
34155	2	8295	7	NULL	NULL	0	NULL	eIF4G	NULL		binds to	NULL				eIF4E	NULL		dorsal site of		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_16_5692_s_358	12897141	4E-T binds to the dorsal site of eIF4E ( ), a region also involved in binding eIF4G and 4E-BP1.	bind
34156	3	8295	7	NULL	NULL	0	NULL	4E-BP1	NULL		binds to	NULL				eIF4E	NULL		dorsal site of		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_16_5692_s_358	12897141	4E-T binds to the dorsal site of eIF4E ( ), a region also involved in binding eIF4G and 4E-BP1.	bind
27842	1	8297	6	13	NULL	NULL	NULL	eIF4E	GP		bind					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24293_s_14	16798736	4EBP1 binds eIF4E, the mRNA cap-binding protein, and it represses cap-dependent translation by competitively blocking the binding of eIF4G to eIF4E ( ,  ).	bind
27843	2	8297	6	13	NULL	NULL	NULL	4EBP1	GP		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24293_s_14	16798736	4EBP1 binds eIF4E, the mRNA cap-binding protein, and it represses cap-dependent translation by competitively blocking the binding of eIF4G to eIF4E ( ,  ).	bind
27844	3	8297	6	13	NULL	NULL	NULL	4EBP1	GP		bind					mRNA cap-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24293_s_14	16798736	4EBP1 binds eIF4E, the mRNA cap-binding protein, and it represses cap-dependent translation by competitively blocking the binding of eIF4G to eIF4E ( ,  ).	bind
27845	4	8297	6	13	NULL	NULL	NULL	translation	Process		is dependent on					cap	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24293_s_14	16798736	4EBP1 binds eIF4E, the mRNA cap-binding protein, and it represses cap-dependent translation by competitively blocking the binding of eIF4G to eIF4E ( ,  ).	bind
27846	5	8297	6	13	NULL	NULL	NULL	4EBP1	GP		represses					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24293_s_14	16798736	4EBP1 binds eIF4E, the mRNA cap-binding protein, and it represses cap-dependent translation by competitively blocking the binding of eIF4G to eIF4E ( ,  ).	bind
27847	6	8297	6	13	NULL	NULL	NULL	4EBP1	GP		blocks		competitively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24293_s_14	16798736	4EBP1 binds eIF4E, the mRNA cap-binding protein, and it represses cap-dependent translation by competitively blocking the binding of eIF4G to eIF4E ( ,  ).	bind
27848	7	8297	6	13	NULL	NULL	NULL	statement 5	Process		occurs via					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24293_s_14	16798736	4EBP1 binds eIF4E, the mRNA cap-binding protein, and it represses cap-dependent translation by competitively blocking the binding of eIF4G to eIF4E ( ,  ).	bind
34177	1	8297	7	NULL	NULL	0	NULL	4EBP1	NULL		binds	NULL				eIF4E	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24293_s_14	16798736	4EBP1 binds eIF4E, the mRNA cap-binding protein, and it represses cap-dependent translation by competitively blocking the binding of eIF4G to eIF4E ( ,  ).	bind
34179	2	8297	7	NULL	NULL	0	NULL	4EBP1	NULL		binds	NULL				mRNA cap-binding protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24293_s_14	16798736	4EBP1 binds eIF4E, the mRNA cap-binding protein, and it represses cap-dependent translation by competitively blocking the binding of eIF4G to eIF4E ( ,  ).	bind
34181	3	8297	7	NULL	NULL	0	NULL	 eIF4G	NULL		bind	NULL				eIF4E	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24293_s_14	16798736	4EBP1 binds eIF4E, the mRNA cap-binding protein, and it represses cap-dependent translation by competitively blocking the binding of eIF4G to eIF4E ( ,  ).	bind
34182	4	8297	7	10	NULL	0	NULL	4EBP1	NULL		repress	NULL				statement 6	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24293_s_14	16798736	4EBP1 binds eIF4E, the mRNA cap-binding protein, and it represses cap-dependent translation by competitively blocking the binding of eIF4G to eIF4E ( ,  ).	bind
34183	5	8297	7	10	NULL	0	NULL	4EBP1	NULL		blocks	NULL	competitively			statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24293_s_14	16798736	4EBP1 binds eIF4E, the mRNA cap-binding protein, and it represses cap-dependent translation by competitively blocking the binding of eIF4G to eIF4E ( ,  ).	bind
46835	6	8297	7	10	NULL	0	NULL	translation	NULL		is dependent on	NULL				cap	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24293_s_14	16798736	4EBP1 binds eIF4E, the mRNA cap-binding protein, and it represses cap-dependent translation by competitively blocking the binding of eIF4G to eIF4E ( ,  ).	bind
46836	7	8297	7	10	NULL	0	NULL	statement 4	NULL		occurs via	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24293_s_14	16798736	4EBP1 binds eIF4E, the mRNA cap-binding protein, and it represses cap-dependent translation by competitively blocking the binding of eIF4G to eIF4E ( ,  ).	bind
27849	1	8298	6	13	NULL	NULL	NULL	eIF-4E	GP		is a type of					7-methyl-guanosine mRNA cap binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_2_177_s_19	12150926	4EBP1 binds to the eIF-4E (a 7-methyl-guanosine mRNA cap binding protein) and prevents eIF-4E from binding to a scaffold protein eIF-4G, thereby inhibiting the formation of the active translational complex, eIF-4F (Sonenberg, 1996   ).	bind
27850	2	8298	6	13	NULL	NULL	NULL	4EBP1	GP		bind					eIF-4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_2_177_s_19	12150926	4EBP1 binds to the eIF-4E (a 7-methyl-guanosine mRNA cap binding protein) and prevents eIF-4E from binding to a scaffold protein eIF-4G, thereby inhibiting the formation of the active translational complex, eIF-4F (Sonenberg, 1996   ).	bind
27851	3	8298	6	13	NULL	NULL	NULL	eIF-4G	GP		is a type of					scaffold protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_2_177_s_19	12150926	4EBP1 binds to the eIF-4E (a 7-methyl-guanosine mRNA cap binding protein) and prevents eIF-4E from binding to a scaffold protein eIF-4G, thereby inhibiting the formation of the active translational complex, eIF-4F (Sonenberg, 1996   ).	bind
28354	4	8298	6	13	NULL	NULL	NULL	eIF-4E	GP		bind					eIF-4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_2_177_s_19	12150926	4EBP1 binds to the eIF-4E (a 7-methyl-guanosine mRNA cap binding protein) and prevents eIF-4E from binding to a scaffold protein eIF-4G, thereby inhibiting the formation of the active translational complex, eIF-4F (Sonenberg, 1996   ).	bind
28355	5	8298	6	13	NULL	NULL	NULL	statement 2	Process		prevents					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_2_177_s_19	12150926	4EBP1 binds to the eIF-4E (a 7-methyl-guanosine mRNA cap binding protein) and prevents eIF-4E from binding to a scaffold protein eIF-4G, thereby inhibiting the formation of the active translational complex, eIF-4F (Sonenberg, 1996   ).	bind
28357	6	8298	6	13	NULL	NULL	NULL	statement 5	Process		inhibits					active translational complex	GP	formation of 			NULL		NULL	NULL	NULL	NULL	gw60_cell_110_2_177_s_19	12150926	4EBP1 binds to the eIF-4E (a 7-methyl-guanosine mRNA cap binding protein) and prevents eIF-4E from binding to a scaffold protein eIF-4G, thereby inhibiting the formation of the active translational complex, eIF-4F (Sonenberg, 1996   ).	bind
46837	7	8298	6	13	NULL	NULL	NULL	active translational complex	GP		is					eIF-4F	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_2_177_s_19	12150926	4EBP1 binds to the eIF-4E (a 7-methyl-guanosine mRNA cap binding protein) and prevents eIF-4E from binding to a scaffold protein eIF-4G, thereby inhibiting the formation of the active translational complex, eIF-4F (Sonenberg, 1996   ).	bind
34185	1	8298	7	NULL	NULL	0	NULL	4EBP1	NULL		binds to	NULL				eIF-4E	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_110_2_177_s_19	12150926	4EBP1 binds to the eIF-4E (a 7-methyl-guanosine mRNA cap binding protein) and prevents eIF-4E from binding to a scaffold protein eIF-4G, thereby inhibiting the formation of the active translational complex, eIF-4F (Sonenberg, 1996   ).	bind
34187	2	8298	7	NULL	NULL	0	NULL	eIF-4E	NULL		bind	NULL				eIF-4G	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_110_2_177_s_19	12150926	4EBP1 binds to the eIF-4E (a 7-methyl-guanosine mRNA cap binding protein) and prevents eIF-4E from binding to a scaffold protein eIF-4G, thereby inhibiting the formation of the active translational complex, eIF-4F (Sonenberg, 1996   ).	bind
34188	3	8298	7	NULL	NULL	0	NULL	statement 1	NULL		prevents	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_110_2_177_s_19	12150926	4EBP1 binds to the eIF-4E (a 7-methyl-guanosine mRNA cap binding protein) and prevents eIF-4E from binding to a scaffold protein eIF-4G, thereby inhibiting the formation of the active translational complex, eIF-4F (Sonenberg, 1996   ).	bind
34189	4	8298	7	10	NULL	0	NULL	eIF-4E	NULL		is a type of	NULL				7-methyl-guanosine mRNA cap binding protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_2_177_s_19	12150926	4EBP1 binds to the eIF-4E (a 7-methyl-guanosine mRNA cap binding protein) and prevents eIF-4E from binding to a scaffold protein eIF-4G, thereby inhibiting the formation of the active translational complex, eIF-4F (Sonenberg, 1996   ).	bind
34190	5	8298	7	NULL	NULL	0	NULL	eIF-4G	NULL		is a type of	NULL				scaffold protein	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_110_2_177_s_19	12150926	4EBP1 binds to the eIF-4E (a 7-methyl-guanosine mRNA cap binding protein) and prevents eIF-4E from binding to a scaffold protein eIF-4G, thereby inhibiting the formation of the active translational complex, eIF-4F (Sonenberg, 1996   ).	bind
34192	6	8298	7	NULL	NULL	0	NULL	statement 3	NULL		inhibits	NULL				eIF-4F	NULL	 formation of			NULL		0	NULL	NULL	NULL	gw60_cell_110_2_177_s_19	12150926	4EBP1 binds to the eIF-4E (a 7-methyl-guanosine mRNA cap binding protein) and prevents eIF-4E from binding to a scaffold protein eIF-4G, thereby inhibiting the formation of the active translational complex, eIF-4F (Sonenberg, 1996   ).	bind
34194	7	8298	7	NULL	NULL	0	NULL	eIF-4F	NULL		is	NULL				active translational complex	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_110_2_177_s_19	12150926	4EBP1 binds to the eIF-4E (a 7-methyl-guanosine mRNA cap binding protein) and prevents eIF-4E from binding to a scaffold protein eIF-4G, thereby inhibiting the formation of the active translational complex, eIF-4F (Sonenberg, 1996   ).	bind
27867	1	8299	6	13	NULL	NULL	NULL	eIF4E	GP		bind					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_1871_s_29	10022874	4EBPs prevent eIF4E binding to eIF4G without altering mRNA binding to eIF4E ( 23,  44,  52).	bind
27868	2	8299	6	13	NULL	NULL	NULL	4EBPs	GP		prevents					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_1871_s_29	10022874	4EBPs prevent eIF4E binding to eIF4G without altering mRNA binding to eIF4E ( 23,  44,  52).	bind
27869	3	8299	6	13	NULL	NULL	NULL	eIF4E	GP		bind					mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_1871_s_29	10022874	4EBPs prevent eIF4E binding to eIF4G without altering mRNA binding to eIF4E ( 23,  44,  52).	bind
27870	4	8299	6	13	NULL	NULL	NULL	4EBPs	GP		does not alter					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_1871_s_29	10022874	4EBPs prevent eIF4E binding to eIF4G without altering mRNA binding to eIF4E ( 23,  44,  52).	bind
34197	1	8299	7	NULL	NULL	0	NULL	eIF4E	NULL		bind	NULL				eIF4G	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_1871_s_29	10022874	4EBPs prevent eIF4E binding to eIF4G without altering mRNA binding to eIF4E ( 23,  44,  52).	bind
34198	2	8299	7	NULL	NULL	0	NULL	mRNA	NULL		bind	NULL				eIF4E	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_1871_s_29	10022874	4EBPs prevent eIF4E binding to eIF4G without altering mRNA binding to eIF4E ( 23,  44,  52).	bind
34199	3	8299	7	NULL	NULL	0	NULL	4EBPs	NULL		prevents	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_1871_s_29	10022874	4EBPs prevent eIF4E binding to eIF4G without altering mRNA binding to eIF4E ( 23,  44,  52).	bind
34201	4	8299	7	NULL	NULL	0	NULL	statement 3	NULL		does not alter	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_1871_s_29	10022874	4EBPs prevent eIF4E binding to eIF4G without altering mRNA binding to eIF4E ( 23,  44,  52).	bind
27871	1	8300	6	13	NULL	NULL	NULL	4P-PDOT	Chemical		bind					MT1	GP				NULL		NULL	NULL	NULL	NULL	gw70_brainres_970_1_169_s_184	12706258	4P-PDOT is highly selective for MT2, and will bind MT1 as well.	bind
27874	2	8300	6	13	NULL	NULL	NULL	4P-PDOT	Chemical		selective for		highly			MT2	GP				NULL		NULL	NULL	NULL	NULL	gw70_brainres_970_1_169_s_184	12706258	4P-PDOT is highly selective for MT2, and will bind MT1 as well.	bind
34205	1	8300	7	NULL	NULL	0	NULL	4P-PDOT	NULL		selective for	NULL	highly			MT2	NULL				NULL		0	NULL	NULL	NULL	gw70_brainres_970_1_169_s_184	12706258	4P-PDOT is highly selective for MT2, and will bind MT1 as well.	bind
34207	2	8300	7	NULL	NULL	0	NULL	4P-PDOT	NULL		bind	NULL				MT1	NULL				NULL		0	NULL	NULL	NULL	gw70_brainres_970_1_169_s_184	12706258	4P-PDOT is highly selective for MT2, and will bind MT1 as well.	bind
28360	1	8301	6	13	NULL	NULL	NULL	4PS	GP		interacts with					PI 3 kinase	GP				NULL	IRS-1-deficient Mice	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_42_24670_s_100	7559579	4PS Is the Dominant Phosphoprotein Interacting with PI  3-Kinase in IRS-1-deficient MiceTo determine if 4PS was the  only, or at least the major, alternative substrate of the insulin  receptor which binds to PI 3-kinase, we performed sequential  immunoprecipitation with anti-4PS antibodies followed by  phosphotyrosine blotting and PI 3-kinase assays.	bind
28361	2	8301	6	13	NULL	NULL	NULL	4PS	GP		is a type of					phosphoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_42_24670_s_100	7559579	4PS Is the Dominant Phosphoprotein Interacting with PI  3-Kinase in IRS-1-deficient MiceTo determine if 4PS was the  only, or at least the major, alternative substrate of the insulin  receptor which binds to PI 3-kinase, we performed sequential  immunoprecipitation with anti-4PS antibodies followed by  phosphotyrosine blotting and PI 3-kinase assays.	bind
34210	1	8301	7	NULL	NULL	0	NULL	4PS	NULL		interacts with	NULL				 PI 3-Kinase	NULL				NULL	IRS-1-deficient Mice	0	NULL	NULL	NULL	gw60_jbiolchem_270_42_24670_s_100	7559579	4PS Is the Dominant Phosphoprotein Interacting with PI  3-Kinase in IRS-1-deficient MiceTo determine if 4PS was the  only, or at least the major, alternative substrate of the insulin  receptor which binds to PI 3-kinase, we performed sequential  immunoprecipitation with anti-4PS antibodies followed by  phosphotyrosine blotting and PI 3-kinase assays.	bind
34212	2	8301	7	NULL	NULL	0	NULL	insulin receptor 	NULL		binds	NULL				PI 3-kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_42_24670_s_100	7559579	4PS Is the Dominant Phosphoprotein Interacting with PI  3-Kinase in IRS-1-deficient MiceTo determine if 4PS was the  only, or at least the major, alternative substrate of the insulin  receptor which binds to PI 3-kinase, we performed sequential  immunoprecipitation with anti-4PS antibodies followed by  phosphotyrosine blotting and PI 3-kinase assays.	bind
34216	3	8301	7	NULL	NULL	0	NULL	4PS	NULL		is a type of	NULL				 Dominant Phosphoprotein 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_42_24670_s_100	7559579	4PS Is the Dominant Phosphoprotein Interacting with PI  3-Kinase in IRS-1-deficient MiceTo determine if 4PS was the  only, or at least the major, alternative substrate of the insulin  receptor which binds to PI 3-kinase, we performed sequential  immunoprecipitation with anti-4PS antibodies followed by  phosphotyrosine blotting and PI 3-kinase assays.	bind
27877	1	8302	6	13	NULL	NULL	NULL	EBNA1	GP		is					Epstein-Barr virus nuclear antigen	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3520_s_270	11522821	5       Rawlins,D.R., Milman,G., Hayward,S.D. and Hayward,G.S. (1985) Sequence-specific DNA binding of the Epstein-Barr virus nuclear antigen (EBNA1) to clustered sites in the plasmid maintenance region.	bind
27878	2	8302	6	13	NULL	NULL	NULL	EBNA1	GP		bind		sequence specifically			DNA	NucleicAcid			clustered sites in the plasmid maintenance region	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3520_s_270	11522821	5       Rawlins,D.R., Milman,G., Hayward,S.D. and Hayward,G.S. (1985) Sequence-specific DNA binding of the Epstein-Barr virus nuclear antigen (EBNA1) to clustered sites in the plasmid maintenance region.	bind
34219	1	8302	7	10	NULL	0	NULL	EBNA1			bind		sequence-specific			DNA				clustered sites in the plasmid maintenance region	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3520_s_270	11522821	5       Rawlins,D.R., Milman,G., Hayward,S.D. and Hayward,G.S. (1985) Sequence-specific DNA binding of the Epstein-Barr virus nuclear antigen (EBNA1) to clustered sites in the plasmid maintenance region.	bind
34221	2	8302	7	NULL	NULL	0	NULL	EBNA1	NULL		is	NULL				Epstein-Barr virus nuclear antigen 	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3520_s_270	11522821	5       Rawlins,D.R., Milman,G., Hayward,S.D. and Hayward,G.S. (1985) Sequence-specific DNA binding of the Epstein-Barr virus nuclear antigen (EBNA1) to clustered sites in the plasmid maintenance region.	bind
27881	1	8303	6	13	NULL	NULL	NULL	RNA I	GP		bind					RNA II	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2401_s_195	11376159	5       Tomizawa,J. (1986) Control of ColE1 plasmid replication: binding of RNA I to RNA II and inhibition of primer formation.	bind
34279	1	8303	7	NULL	NULL	0	NULL	RNA I	NULL		bind	NULL				RNA II	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2401_s_195	11376159	5       Tomizawa,J. (1986) Control of ColE1 plasmid replication: binding of RNA I to RNA II and inhibition of primer formation.	bind
27884	1	8304	6	13	NULL	NULL	NULL	gp43	GP		bind					gp45	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31685_s_233	9395510	5   Berdis and Benkovic ( 30), in their measurement of the "`shutdown"` of the gp44/62 ATPase, have reported that the binding of gp43 to gp45 in the polymerase holoenzyme increases linearly with the addition of increasing numbers of equivalents of gp43.	bind
27885	2	8304	6	13	NULL	NULL	NULL	statement 1	Process		increases upon		linearly			gp43	GP	addition of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31685_s_233	9395510	5   Berdis and Benkovic ( 30), in their measurement of the "`shutdown"` of the gp44/62 ATPase, have reported that the binding of gp43 to gp45 in the polymerase holoenzyme increases linearly with the addition of increasing numbers of equivalents of gp43.	bind
46838	3	8304	6	13	NULL	NULL	NULL	statement 1	Process		occurs in					polymerase holoenzyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31685_s_233	9395510	5   Berdis and Benkovic ( 30), in their measurement of the "`shutdown"` of the gp44/62 ATPase, have reported that the binding of gp43 to gp45 in the polymerase holoenzyme increases linearly with the addition of increasing numbers of equivalents of gp43.	bind
34280	1	8304	7	NULL	NULL	0	NULL	 gp43	NULL		bind	NULL				gp45	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31685_s_233	9395510	5   Berdis and Benkovic ( 30), in their measurement of the "`shutdown"` of the gp44/62 ATPase, have reported that the binding of gp43 to gp45 in the polymerase holoenzyme increases linearly with the addition of increasing numbers of equivalents of gp43.	bind
34281	2	8304	7	NULL	NULL	0	NULL	statement 1	NULL		occurs in	NULL				 polymerase holoenzyme 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31685_s_233	9395510	5   Berdis and Benkovic ( 30), in their measurement of the "`shutdown"` of the gp44/62 ATPase, have reported that the binding of gp43 to gp45 in the polymerase holoenzyme increases linearly with the addition of increasing numbers of equivalents of gp43.	bind
34282	3	8304	7	NULL	NULL	0	NULL	gp43	NULL	increase of	increase	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31685_s_233	9395510	5   Berdis and Benkovic ( 30), in their measurement of the "`shutdown"` of the gp44/62 ATPase, have reported that the binding of gp43 to gp45 in the polymerase holoenzyme increases linearly with the addition of increasing numbers of equivalents of gp43.	bind
27886	1	8305	6	13	NULL	NULL	NULL	tropomodulin	GP		bind					actin	GP				NULL	cardiomyocytes	NULL	NULL	NULL	NULL	gw60_circulationres_82_1_94_s_27	null	5  6  Inhibition of tropomodulin binding to actin by microinjection of anti-tropomodulin antibody into cardiomyocytes results in actin filament elongation.	bind
27891	2	8305	6	13	NULL	NULL	NULL	anti-tropomodulin antibody	GP		inhibits					statement 1	Process				NULL	cardiomyocytes	NULL	NULL	NULL	NULL	gw60_circulationres_82_1_94_s_27	null	5  6  Inhibition of tropomodulin binding to actin by microinjection of anti-tropomodulin antibody into cardiomyocytes results in actin filament elongation.	bind
27894	3	8305	6	13	NULL	NULL	NULL	statement 2	Process		results in					actin filament	GP	elongation of 			NULL	cardiomyocytes	NULL	NULL	NULL	NULL	gw60_circulationres_82_1_94_s_27	null	5  6  Inhibition of tropomodulin binding to actin by microinjection of anti-tropomodulin antibody into cardiomyocytes results in actin filament elongation.	bind
34283	1	8305	7	NULL	NULL	0	NULL	tropomodulin	NULL		bind	NULL				actin	NULL				NULL	cardiomyocytes	0	NULL	NULL	NULL	gw60_circulationres_82_1_94_s_27	null	5  6  Inhibition of tropomodulin binding to actin by microinjection of anti-tropomodulin antibody into cardiomyocytes results in actin filament elongation.	bind
34284	3	8305	7	10	NULL	0	NULL	statement 2	NULL		results in	NULL				actin filament	NULL	elongation of			NULL	cardiomyocytes	NULL	NULL	NULL	NULL	gw60_circulationres_82_1_94_s_27	null	5  6  Inhibition of tropomodulin binding to actin by microinjection of anti-tropomodulin antibody into cardiomyocytes results in actin filament elongation.	bind
46839	2	8305	7	10	NULL	0	NULL	anti-tropomodulin antibody	NULL		inhibit	NULL				statement 1	NULL				NULL	cardiomyocytes	NULL	NULL	NULL	NULL	gw60_circulationres_82_1_94_s_27	null	5  6  Inhibition of tropomodulin binding to actin by microinjection of anti-tropomodulin antibody into cardiomyocytes results in actin filament elongation.	bind
27896	1	8306	6	13	NULL	NULL	NULL	Rho	GP		bind					Rho kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_10_1186_s_208	10347093	5  A recent report suggests that the binding of Rho to Rho kinase correlates with its ability to produce cell transformation.	bind
27899	2	8306	6	13	NULL	NULL	NULL	Rho	GP		produce					cell transformation	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_10_1186_s_208	10347093	5  A recent report suggests that the binding of Rho to Rho kinase correlates with its ability to produce cell transformation.	bind
27901	3	8306	6	13	NULL	NULL	NULL	statement 1	Process		correlates with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_10_1186_s_208	10347093	5  A recent report suggests that the binding of Rho to Rho kinase correlates with its ability to produce cell transformation.	bind
34285	1	8306	7	NULL	NULL	0	NULL	Rho	NULL		bind	NULL				Rho kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_10_1186_s_208	10347093	5  A recent report suggests that the binding of Rho to Rho kinase correlates with its ability to produce cell transformation.	bind
34286	2	8306	7	NULL	NULL	0	NULL	statement 1	NULL		produce	NULL				cell transformation	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_10_1186_s_208	10347093	5  A recent report suggests that the binding of Rho to Rho kinase correlates with its ability to produce cell transformation.	bind
56114	3	8306	7	10	NULL	0	NULL	statement 1			correlates with					statement 2					NULL		0	NULL	NULL	NULL	gw60_circulationres_84_10_1186_s_208	10347093	5  A recent report suggests that the binding of Rho to Rho kinase correlates with its ability to produce cell transformation.	bind
27902	1	8307	6	13	NULL	NULL	NULL	ANP	GP		bind		primarily			NPRA	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_25	10785505	5  ANP and BNP bind primarily to NPRA, which exerts its effect on the vasculature, causing vasodilation and inhibition of the proliferation of vascular smooth muscle cells.	bind
27903	2	8307	6	13	NULL	NULL	NULL	BNP	GP		bind		primarily			NPRA	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_25	10785505	5  ANP and BNP bind primarily to NPRA, which exerts its effect on the vasculature, causing vasodilation and inhibition of the proliferation of vascular smooth muscle cells.	bind
27906	3	8307	6	13	NULL	NULL	NULL	statement 1	Process		causes					vascular smooth muscle cells	Cell	vasodilation of 			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_25	10785505	5  ANP and BNP bind primarily to NPRA, which exerts its effect on the vasculature, causing vasodilation and inhibition of the proliferation of vascular smooth muscle cells.	bind
27907	4	8307	6	13	NULL	NULL	NULL	statement 2	Process		causes					vascular smooth muscle cells	Cell	vasodilation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_25	10785505	5  ANP and BNP bind primarily to NPRA, which exerts its effect on the vasculature, causing vasodilation and inhibition of the proliferation of vascular smooth muscle cells.	bind
27908	5	8307	6	13	NULL	NULL	NULL	statement 1	Process		inhibits					vascular smooth muscle cells	Cell	proliferation of 			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_25	10785505	5  ANP and BNP bind primarily to NPRA, which exerts its effect on the vasculature, causing vasodilation and inhibition of the proliferation of vascular smooth muscle cells.	bind
27909	6	8307	6	13	NULL	NULL	NULL	statement 2	Process		inhibits					vascular smooth muscle cells	Cell	proliferation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_25	10785505	5  ANP and BNP bind primarily to NPRA, which exerts its effect on the vasculature, causing vasodilation and inhibition of the proliferation of vascular smooth muscle cells.	bind
56115	7	8307	6	13	NULL	NULL	NULL	statement 1	Process		exerts effect on					vasculature	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_25	10785505	5  ANP and BNP bind primarily to NPRA, which exerts its effect on the vasculature, causing vasodilation and inhibition of the proliferation of vascular smooth muscle cells.	bind
56116	8	8307	6	13	NULL	NULL	NULL	statement 2	Process		exerts effect on					vasculature	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_25	10785505	5  ANP and BNP bind primarily to NPRA, which exerts its effect on the vasculature, causing vasodilation and inhibition of the proliferation of vascular smooth muscle cells.	bind
34293	1	8307	7	NULL	NULL	0	NULL	 ANP	NULL		bind	NULL	primarily			NPRA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_25	10785505	5  ANP and BNP bind primarily to NPRA, which exerts its effect on the vasculature, causing vasodilation and inhibition of the proliferation of vascular smooth muscle cells.	bind
34294	2	8307	7	NULL	NULL	0	NULL	BNP	NULL		bind	NULL	primarily			NPRA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_25	10785505	5  ANP and BNP bind primarily to NPRA, which exerts its effect on the vasculature, causing vasodilation and inhibition of the proliferation of vascular smooth muscle cells.	bind
34295	3	8307	7	NULL	NULL	0	NULL	statement 1	NULL		exerts effect on	NULL				vasculature	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_25	10785505	5  ANP and BNP bind primarily to NPRA, which exerts its effect on the vasculature, causing vasodilation and inhibition of the proliferation of vascular smooth muscle cells.	bind
34297	4	8307	7	NULL	NULL	0	NULL	statement 2	NULL		exerts effect on	NULL				vasculature	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_25	10785505	5  ANP and BNP bind primarily to NPRA, which exerts its effect on the vasculature, causing vasodilation and inhibition of the proliferation of vascular smooth muscle cells.	bind
34298	5	8307	7	10	NULL	0	NULL	statement 3	NULL		cause	NULL				vascular smooth muscle cells	NULL	vasodilation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_25	10785505	5  ANP and BNP bind primarily to NPRA, which exerts its effect on the vasculature, causing vasodilation and inhibition of the proliferation of vascular smooth muscle cells.	bind
34300	6	8307	7	10	NULL	0	NULL	statement 4	NULL		cause	NULL				vascular smooth muscle cells	NULL	vasodilation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_25	10785505	5  ANP and BNP bind primarily to NPRA, which exerts its effect on the vasculature, causing vasodilation and inhibition of the proliferation of vascular smooth muscle cells.	bind
34304	7	8307	7	NULL	NULL	0	NULL	statement 3	NULL		inhibits	NULL				vascular smooth muscle cells	NULL	 proliferation of 			NULL		0	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_25	10785505	5  ANP and BNP bind primarily to NPRA, which exerts its effect on the vasculature, causing vasodilation and inhibition of the proliferation of vascular smooth muscle cells.	bind
34306	8	8307	7	NULL	NULL	0	NULL	statement 4	NULL		inhibits	NULL				vascular smooth muscle cells	NULL	proliferation of			NULL		0	NULL	NULL	NULL	gw60_circulationres_86_8_841_s_25	10785505	5  ANP and BNP bind primarily to NPRA, which exerts its effect on the vasculature, causing vasodilation and inhibition of the proliferation of vascular smooth muscle cells.	bind
28363	1	8309	6	13	NULL	NULL	NULL	NFT	GP		are composed of					six tau isoforms	GP				NULL	AD	NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_14	11549586	5  Further, since NFTs in AD are composed of six tau isoforms in about equal proportions, 6- 10 but in other neurodegenerative diseases abnormal accumulations of tau proteins in neurons and/or glial cells are predominantly composed of either three or four microtubule (MT) binding repeat tau isoforms, we also asked if BSB binds all or a subset of tau inclusions.	bind
47520	3	8309	6	13	NULL	NULL	NULL	tau proteins	GP		are accumulated in		abnormally			neurons	Cell				NULL	neurodegenerative diseases	NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_14	11549586	5  Further, since NFTs in AD are composed of six tau isoforms in about equal proportions, 6- 10 but in other neurodegenerative diseases abnormal accumulations of tau proteins in neurons and/or glial cells are predominantly composed of either three or four microtubule (MT) binding repeat tau isoforms, we also asked if BSB binds all or a subset of tau inclusions.	bind
47521	4	8309	6	13	NULL	NULL	NULL	tau proteins	GP		are accumulated in		abnormally			glial cells	Cell				NULL	neurodegenerative diseases	NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_14	11549586	5  Further, since NFTs in AD are composed of six tau isoforms in about equal proportions, 6- 10 but in other neurodegenerative diseases abnormal accumulations of tau proteins in neurons and/or glial cells are predominantly composed of either three or four microtubule (MT) binding repeat tau isoforms, we also asked if BSB binds all or a subset of tau inclusions.	bind
47522	5	8309	6	13	NULL	NULL	NULL	tau proteins	GP		consists of					three or four microtubule (MT) binding repeat tau isoforms	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_14	11549586	5  Further, since NFTs in AD are composed of six tau isoforms in about equal proportions, 6- 10 but in other neurodegenerative diseases abnormal accumulations of tau proteins in neurons and/or glial cells are predominantly composed of either three or four microtubule (MT) binding repeat tau isoforms, we also asked if BSB binds all or a subset of tau inclusions.	bind
47523	6	8309	6	13	NULL	NULL	NULL	statement 5	GP		are occured in					statement 3	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_14	11549586	5  Further, since NFTs in AD are composed of six tau isoforms in about equal proportions, 6- 10 but in other neurodegenerative diseases abnormal accumulations of tau proteins in neurons and/or glial cells are predominantly composed of either three or four microtubule (MT) binding repeat tau isoforms, we also asked if BSB binds all or a subset of tau inclusions.	bind
47524	7	8309	6	13	NULL	NULL	NULL	statement 5	GP		are occured in					statement 4	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_14	11549586	5  Further, since NFTs in AD are composed of six tau isoforms in about equal proportions, 6- 10 but in other neurodegenerative diseases abnormal accumulations of tau proteins in neurons and/or glial cells are predominantly composed of either three or four microtubule (MT) binding repeat tau isoforms, we also asked if BSB binds all or a subset of tau inclusions.	bind
34307	1	8309	7	NULL	NULL	0	NULL	tau proteins	NULL		accumulates in	NULL	abnormally			neurons	NULL				NULL	neurodegenerative diseases 	NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_14	11549586	5  Further, since NFTs in AD are composed of six tau isoforms in about equal proportions, 6- 10 but in other neurodegenerative diseases abnormal accumulations of tau proteins in neurons and/or glial cells are predominantly composed of either three or four microtubule (MT) binding repeat tau isoforms, we also asked if BSB binds all or a subset of tau inclusions.	bind
34308	2	8309	7	NULL	NULL	0	NULL	tau proteins	NULL		accumulates in	NULL	abnormally			glial cells	NULL				NULL	neurodegenerative diseases 	NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_14	11549586	5  Further, since NFTs in AD are composed of six tau isoforms in about equal proportions, 6- 10 but in other neurodegenerative diseases abnormal accumulations of tau proteins in neurons and/or glial cells are predominantly composed of either three or four microtubule (MT) binding repeat tau isoforms, we also asked if BSB binds all or a subset of tau inclusions.	bind
34309	3	8309	7	NULL	NULL	0	NULL	statement 1	NULL		is composed of	NULL				MT binding repeat tau isoforms	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_14	11549586	5  Further, since NFTs in AD are composed of six tau isoforms in about equal proportions, 6- 10 but in other neurodegenerative diseases abnormal accumulations of tau proteins in neurons and/or glial cells are predominantly composed of either three or four microtubule (MT) binding repeat tau isoforms, we also asked if BSB binds all or a subset of tau inclusions.	bind
34310	4	8309	7	NULL	NULL	0	NULL	MT	NULL		is	NULL				microtubule	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_14	11549586	5  Further, since NFTs in AD are composed of six tau isoforms in about equal proportions, 6- 10 but in other neurodegenerative diseases abnormal accumulations of tau proteins in neurons and/or glial cells are predominantly composed of either three or four microtubule (MT) binding repeat tau isoforms, we also asked if BSB binds all or a subset of tau inclusions.	bind
47525	4	8309	7	NULL	NULL	0	NULL	statement 2	NULL		is composed of	NULL				MT binding repeat tau isoforms	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_14	11549586	5  Further, since NFTs in AD are composed of six tau isoforms in about equal proportions, 6- 10 but in other neurodegenerative diseases abnormal accumulations of tau proteins in neurons and/or glial cells are predominantly composed of either three or four microtubule (MT) binding repeat tau isoforms, we also asked if BSB binds all or a subset of tau inclusions.	bind
47527	5	8309	7	NULL	NULL	0	NULL	NFT	NULL		is composed of	NULL				six tau isoforms	NULL				NULL	AD	NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_937_s_14	11549586	5  Further, since NFTs in AD are composed of six tau isoforms in about equal proportions, 6- 10 but in other neurodegenerative diseases abnormal accumulations of tau proteins in neurons and/or glial cells are predominantly composed of either three or four microtubule (MT) binding repeat tau isoforms, we also asked if BSB binds all or a subset of tau inclusions.	bind
27910	1	8310	6	13	NULL	NULL	NULL	skeletal S1	GP		bind			alkali light chain 1		F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_81_5_688_s_21	9351442	5  Further, we have shown that the alkali light chain 1 of skeletal S1 can bind F-actin only when the molar ratio is low.	bind
34311	1	8310	7	10	NULL	0	NULL	skeletal S1	NULL		bind	NULL		alkali light chain 1		F-actin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_81_5_688_s_21	9351442	5  Further, we have shown that the alkali light chain 1 of skeletal S1 can bind F-actin only when the molar ratio is low.	bind
27912	1	8311	6	13	NULL	NULL	NULL	Lp(a)	GP		bind		competitively			plasminogen	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_575_s_226	10669658	5  Furthermore, the current in vitro experiments that used whole plasma failed to show any effect of plasma proteins, including high fibrinogen concentrations, on the competitive binding of Lp(a) and plasminogen.	bind
34316	1	8311	7	NULL	NULL	0	NULL	Lp(a)	NULL		binds	NULL	competitively			plasminogen	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_2_575_s_226	10669658	5  Furthermore, the current in vitro experiments that used whole plasma failed to show any effect of plasma proteins, including high fibrinogen concentrations, on the competitive binding of Lp(a) and plasminogen.	bind
27913	1	8312	6	13	NULL	NULL	NULL	SMC	Cell		adhere to					ECM substrates	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_80_5_627_s_250	9130443	5  Furthermore, using an anti - beta1 integrin antibody that augments the binding affinity of beta1 integrins, Seki et al 10  and Koyama et al 28  observed enhanced adhesion of SMCs to ECM substrates but decreased SMC migration to PDGF on Matrigel.	bind
28015	2	8312	6	13	NULL	NULL	NULL	SMC	Cell		migrate to					PDGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_80_5_627_s_250	9130443	5  Furthermore, using an anti - beta1 integrin antibody that augments the binding affinity of beta1 integrins, Seki et al 10  and Koyama et al 28  observed enhanced adhesion of SMCs to ECM substrates but decreased SMC migration to PDGF on Matrigel.	bind
28016	3	8312	6	13	NULL	NULL	NULL	anti - beta1 integrin antibody	GP		augments					beta1-integrins	GP	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_80_5_627_s_250	9130443	5  Furthermore, using an anti - beta1 integrin antibody that augments the binding affinity of beta1 integrins, Seki et al 10  and Koyama et al 28  observed enhanced adhesion of SMCs to ECM substrates but decreased SMC migration to PDGF on Matrigel.	bind
46840	4	8312	6	13	NULL	NULL	NULL	statement 3	Process		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_80_5_627_s_250	9130443	5  Furthermore, using an anti - beta1 integrin antibody that augments the binding affinity of beta1 integrins, Seki et al 10  and Koyama et al 28  observed enhanced adhesion of SMCs to ECM substrates but decreased SMC migration to PDGF on Matrigel.	bind
46841	5	8312	6	13	NULL	NULL	NULL	statement 3	Process		decrease					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_80_5_627_s_250	9130443	5  Furthermore, using an anti - beta1 integrin antibody that augments the binding affinity of beta1 integrins, Seki et al 10  and Koyama et al 28  observed enhanced adhesion of SMCs to ECM substrates but decreased SMC migration to PDGF on Matrigel.	bind
34317	1	8312	7	NULL	NULL	0	NULL	anti - beta1 integrin antibody 	NULL		augments	NULL				beta1 integrins	NULL	binding affinity of			NULL		0	NULL	NULL	NULL	gw60_circulationres_80_5_627_s_250	9130443	5  Furthermore, using an anti - beta1 integrin antibody that augments the binding affinity of beta1 integrins, Seki et al 10  and Koyama et al 28  observed enhanced adhesion of SMCs to ECM substrates but decreased SMC migration to PDGF on Matrigel.	bind
34318	2	8312	7	NULL	NULL	0	NULL	SMCs	NULL		adhere to	NULL				ECM substrates	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_80_5_627_s_250	9130443	5  Furthermore, using an anti - beta1 integrin antibody that augments the binding affinity of beta1 integrins, Seki et al 10  and Koyama et al 28  observed enhanced adhesion of SMCs to ECM substrates but decreased SMC migration to PDGF on Matrigel.	bind
34319	3	8312	7	NULL	NULL	0	NULL	statement 1	NULL		enhance	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_80_5_627_s_250	9130443	5  Furthermore, using an anti - beta1 integrin antibody that augments the binding affinity of beta1 integrins, Seki et al 10  and Koyama et al 28  observed enhanced adhesion of SMCs to ECM substrates but decreased SMC migration to PDGF on Matrigel.	bind
34320	4	8312	7	NULL	NULL	0	NULL	SMC	NULL		migrate to	NULL				PDGF	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_80_5_627_s_250	9130443	5  Furthermore, using an anti - beta1 integrin antibody that augments the binding affinity of beta1 integrins, Seki et al 10  and Koyama et al 28  observed enhanced adhesion of SMCs to ECM substrates but decreased SMC migration to PDGF on Matrigel.	bind
34321	5	8312	7	NULL	NULL	0	NULL	statement 1	NULL		decrease	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_80_5_627_s_250	9130443	5  Furthermore, using an anti - beta1 integrin antibody that augments the binding affinity of beta1 integrins, Seki et al 10  and Koyama et al 28  observed enhanced adhesion of SMCs to ECM substrates but decreased SMC migration to PDGF on Matrigel.	bind
28368	1	8314	6	13	NULL	NULL	NULL	calmodulin binding proteins 	GP		inhibits					NOSIII	GP	activity of 			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_82_6_686_s_18	9546377	5  Little physiological relevance was attributed to this phenomenon, and the identification of a calmodulin-binding domain in the primary structure of NOS III 6 7 8  together with the finding that calmodulin binding proteins inhibited enzyme activity 1  strengthened the hypothesis that the binding of a Ca2+/calmodulin complex is essential to activate the constitutive enzyme.	bind
28370	2	8314	6	13	NULL	NULL	NULL	Ca2+/calmodulin complex	GP	binding of	is essential for					constitutive enzyme	GP	activation of 			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_82_6_686_s_18	9546377	5  Little physiological relevance was attributed to this phenomenon, and the identification of a calmodulin-binding domain in the primary structure of NOS III 6 7 8  together with the finding that calmodulin binding proteins inhibited enzyme activity 1  strengthened the hypothesis that the binding of a Ca2+/calmodulin complex is essential to activate the constitutive enzyme.	bind
28874	3	8314	6	13	NULL	NULL	NULL	NOSIII	GP		possesses								calmodulin-binding domain		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_82_6_686_s_18	9546377	5  Little physiological relevance was attributed to this phenomenon, and the identification of a calmodulin-binding domain in the primary structure of NOS III 6 7 8  together with the finding that calmodulin binding proteins inhibited enzyme activity 1  strengthened the hypothesis that the binding of a Ca2+/calmodulin complex is essential to activate the constitutive enzyme.	bind
34325	1	8314	7	NULL	NULL	0	NULL		NULL		is present in	NULL		calmodulin-binding domain		NOS III	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_82_6_686_s_18	9546377	5  Little physiological relevance was attributed to this phenomenon, and the identification of a calmodulin-binding domain in the primary structure of NOS III 6 7 8  together with the finding that calmodulin binding proteins inhibited enzyme activity 1  strengthened the hypothesis that the binding of a Ca2+/calmodulin complex is essential to activate the constitutive enzyme.	bind
34326	2	8314	7	10	NULL	0	NULL	calmodulin binding proteins	NULL		inhibits	NULL				NOSIII	NULL	activity of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_82_6_686_s_18	9546377	5  Little physiological relevance was attributed to this phenomenon, and the identification of a calmodulin-binding domain in the primary structure of NOS III 6 7 8  together with the finding that calmodulin binding proteins inhibited enzyme activity 1  strengthened the hypothesis that the binding of a Ca2+/calmodulin complex is essential to activate the constitutive enzyme.	bind
34327	3	8314	7	NULL	NULL	0	NULL	 Ca2+/calmodulin complex	NULL	binding of	activates	NULL	essentially			constitutive enzyme	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_82_6_686_s_18	9546377	5  Little physiological relevance was attributed to this phenomenon, and the identification of a calmodulin-binding domain in the primary structure of NOS III 6 7 8  together with the finding that calmodulin binding proteins inhibited enzyme activity 1  strengthened the hypothesis that the binding of a Ca2+/calmodulin complex is essential to activate the constitutive enzyme.	bind
28018	1	8315	6	13	NULL	NULL	NULL	vWF	GP	native	bind					GPIb	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_30	9484984	5  Moreover, the GPIb-binding domain of vWF expressed in  Escherichia coli has been shown to inhibit the binding of native vWF to GPIb, 12  and unlike native vWF, this vWF domain binds to GPIb in the absence of any modulator.	bind
28019	2	8315	6	13	NULL	NULL	NULL	vWF	GP		is expressed in			GPIb-binding domain		Escherichia coli	Organism				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_30	9484984	5  Moreover, the GPIb-binding domain of vWF expressed in  Escherichia coli has been shown to inhibit the binding of native vWF to GPIb, 12  and unlike native vWF, this vWF domain binds to GPIb in the absence of any modulator.	bind
28020	3	8315	6	13	NULL	NULL	NULL	statement 2	Process		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_30	9484984	5  Moreover, the GPIb-binding domain of vWF expressed in  Escherichia coli has been shown to inhibit the binding of native vWF to GPIb, 12  and unlike native vWF, this vWF domain binds to GPIb in the absence of any modulator.	bind
28021	4	8315	6	13	NULL	NULL	NULL	vWF	GP		bind			GPIb-binding domain		GPIb	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_30	9484984	5  Moreover, the GPIb-binding domain of vWF expressed in  Escherichia coli has been shown to inhibit the binding of native vWF to GPIb, 12  and unlike native vWF, this vWF domain binds to GPIb in the absence of any modulator.	bind
28024	5	8315	6	13	NULL	NULL	NULL	statement 4	Process		occurs in absence of					modulator	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_30	9484984	5  Moreover, the GPIb-binding domain of vWF expressed in  Escherichia coli has been shown to inhibit the binding of native vWF to GPIb, 12  and unlike native vWF, this vWF domain binds to GPIb in the absence of any modulator.	bind
34328	1	8315	7	NULL	NULL	0	NULL	 vWF	NULL	native	bind	NULL				GPIb	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_30	9484984	5  Moreover, the GPIb-binding domain of vWF expressed in  Escherichia coli has been shown to inhibit the binding of native vWF to GPIb, 12  and unlike native vWF, this vWF domain binds to GPIb in the absence of any modulator.	bind
34329	2	8315	7	10	NULL	0	NULL	statement 5	NULL		inhibits	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_30	9484984	5  Moreover, the GPIb-binding domain of vWF expressed in  Escherichia coli has been shown to inhibit the binding of native vWF to GPIb, 12  and unlike native vWF, this vWF domain binds to GPIb in the absence of any modulator.	bind
34331	3	8315	7	NULL	NULL	0	NULL	vWF	NULL		binds to	NULL		GPIb-binding domain 		GPIb	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_30	9484984	5  Moreover, the GPIb-binding domain of vWF expressed in  Escherichia coli has been shown to inhibit the binding of native vWF to GPIb, 12  and unlike native vWF, this vWF domain binds to GPIb in the absence of any modulator.	bind
34332	4	8315	7	NULL	NULL	0	NULL	statement 3	NULL		in absence of	NULL				modulator	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_30	9484984	5  Moreover, the GPIb-binding domain of vWF expressed in  Escherichia coli has been shown to inhibit the binding of native vWF to GPIb, 12  and unlike native vWF, this vWF domain binds to GPIb in the absence of any modulator.	bind
46867	5	8315	7	10	NULL	0	NULL	vWF	NULL		is expressed in	NULL		GPIb-binding domain		Escherichia coli	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_30	9484984	5  Moreover, the GPIb-binding domain of vWF expressed in  Escherichia coli has been shown to inhibit the binding of native vWF to GPIb, 12  and unlike native vWF, this vWF domain binds to GPIb in the absence of any modulator.	bind
28026	1	8316	6	13	NULL	NULL	NULL	IRS-1	GP		is					insulin receptor substrate-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1081_s_19	12117720	5 -  10 The N- and C-terminal SH2 domains bind to tyrosine-phosphorylated insulin receptor substrate (IRS)-1, 11 suggesting that SHP2 is involved in positive signaling pathways serving multiple hormone receptors.	bind
28027	2	8316	6	13	NULL	NULL	NULL				bind			N-terminal SH2 domain		IRS-1	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1081_s_19	12117720	5 -  10 The N- and C-terminal SH2 domains bind to tyrosine-phosphorylated insulin receptor substrate (IRS)-1, 11 suggesting that SHP2 is involved in positive signaling pathways serving multiple hormone receptors.	bind
28028	3	8316	6	13	NULL	NULL	NULL				bind			C-terminal SH2 domain		IRS-1	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1081_s_19	12117720	5 -  10 The N- and C-terminal SH2 domains bind to tyrosine-phosphorylated insulin receptor substrate (IRS)-1, 11 suggesting that SHP2 is involved in positive signaling pathways serving multiple hormone receptors.	bind
28029	4	8316	6	13	NULL	NULL	NULL	SHP2	GP		is involved in					positive signaling pathways	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1081_s_19	12117720	5 -  10 The N- and C-terminal SH2 domains bind to tyrosine-phosphorylated insulin receptor substrate (IRS)-1, 11 suggesting that SHP2 is involved in positive signaling pathways serving multiple hormone receptors.	bind
34333	1	8316	7	NULL	NULL	0	NULL		NULL		binds to	NULL		N-terminal SH2 domain		IRS-1	NULL	phosphorylated	tyrosine		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1081_s_19	12117720	5 -  10 The N- and C-terminal SH2 domains bind to tyrosine-phosphorylated insulin receptor substrate (IRS)-1, 11 suggesting that SHP2 is involved in positive signaling pathways serving multiple hormone receptors.	bind
34335	2	8316	7	NULL	NULL	0	NULL		NULL		binds to	NULL		C-terminal SH2 domain		IRS-1	NULL	phophorylated	tyrosine		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1081_s_19	12117720	5 -  10 The N- and C-terminal SH2 domains bind to tyrosine-phosphorylated insulin receptor substrate (IRS)-1, 11 suggesting that SHP2 is involved in positive signaling pathways serving multiple hormone receptors.	bind
34336	3	8316	7	NULL	NULL	0	NULL	SHP2	NULL		is involved in	NULL				positive signaling pathways	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1081_s_19	12117720	5 -  10 The N- and C-terminal SH2 domains bind to tyrosine-phosphorylated insulin receptor substrate (IRS)-1, 11 suggesting that SHP2 is involved in positive signaling pathways serving multiple hormone receptors.	bind
34337	4	8316	7	NULL	NULL	0	NULL	statement 3	NULL		serves	NULL				multiple hormone receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1081_s_19	12117720	5 -  10 The N- and C-terminal SH2 domains bind to tyrosine-phosphorylated insulin receptor substrate (IRS)-1, 11 suggesting that SHP2 is involved in positive signaling pathways serving multiple hormone receptors.	bind
34338	5	8316	7	NULL	NULL	0	NULL	statement 1	NULL		suggests	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1081_s_19	12117720	5 -  10 The N- and C-terminal SH2 domains bind to tyrosine-phosphorylated insulin receptor substrate (IRS)-1, 11 suggesting that SHP2 is involved in positive signaling pathways serving multiple hormone receptors.	bind
34339	6	8316	7	NULL	NULL	0	NULL	statement 2	NULL		suggests	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1081_s_19	12117720	5 -  10 The N- and C-terminal SH2 domains bind to tyrosine-phosphorylated insulin receptor substrate (IRS)-1, 11 suggesting that SHP2 is involved in positive signaling pathways serving multiple hormone receptors.	bind
46868	7	8316	7	10	NULL	0	NULL	IRS-1	NULL		is	NULL				\tinsulin receptor substrate-1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_7_1081_s_19	12117720	5 -  10 The N- and C-terminal SH2 domains bind to tyrosine-phosphorylated insulin receptor substrate (IRS)-1, 11 suggesting that SHP2 is involved in positive signaling pathways serving multiple hormone receptors.	bind
28030	1	8317	6	13	NULL	NULL	NULL	125I - Ang II	GP		bind					chromatin fragments	Chromosome	solubilized;;rat liver			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_12_1138_s_20	11739278	5 -  7 Re and colleagues further demonstrated 125I - Ang II binding to solubilized rat liver chromatin fragments, the existence of a discrete Ang II - binding nucleoprotein particle by deoxynucleoprotein gel electrophoresis, and direct effects of nuclear angiotensin on transcription.	bind
56117	2	8317	6	13	NULL	NULL	NULL	angiotensin	GP	nuclear	effect		directly			transcription	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_12_1138_s_20	11739278	5 -  7 Re and colleagues further demonstrated 125I - Ang II binding to solubilized rat liver chromatin fragments, the existence of a discrete Ang II - binding nucleoprotein particle by deoxynucleoprotein gel electrophoresis, and direct effects of nuclear angiotensin on transcription.	bind
34340	1	8317	7	10	NULL	0	NULL	125I - Ang II 	NULL		bind	NULL				chromatin fragments	NULL	solubilized;;rat liver			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_89_12_1138_s_20	11739278	5 -  7 Re and colleagues further demonstrated 125I - Ang II binding to solubilized rat liver chromatin fragments, the existence of a discrete Ang II - binding nucleoprotein particle by deoxynucleoprotein gel electrophoresis, and direct effects of nuclear angiotensin on transcription.	bind
34341	2	8317	7	NULL	NULL	0	NULL	angiotensin	NULL	nuclear	effect	NULL	directly			transcription	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_89_12_1138_s_20	11739278	5 -  7 Re and colleagues further demonstrated 125I - Ang II binding to solubilized rat liver chromatin fragments, the existence of a discrete Ang II - binding nucleoprotein particle by deoxynucleoprotein gel electrophoresis, and direct effects of nuclear angiotensin on transcription.	bind
28031	1	8318	6	13	NULL	NULL	NULL	BTC	GP		bind					ErbB1/ErbB1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
28032	2	8318	6	13	NULL	NULL	NULL	BTC	GP		stimulates					ErbB1/ErbB1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
28190	3	8318	6	13	NULL	NULL	NULL	BTC	GP		bind					ErbB4/ErbB4	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
28191	4	8318	6	13	NULL	NULL	NULL	BTC	GP		stimulates					ErbB4/ErbB4	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
28192	5	8318	6	13	NULL	NULL	NULL	BTC	GP		bind					ErbB1/ErbB2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
28193	6	8318	6	13	NULL	NULL	NULL	BTC	GP		stimulates					ErbB1/ErbB2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
28194	7	8318	6	13	NULL	NULL	NULL	BTC	GP		bind					ErbB1/ErbB3	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
28195	8	8318	6	13	NULL	NULL	NULL	BTC	GP		stimulates					ErbB1/ErbB3	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
28196	9	8318	6	13	NULL	NULL	NULL	BTC	GP		bind					ErbB1/ErbB4	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
28197	10	8318	6	13	NULL	NULL	NULL	BTC	GP		stimulates					ErbB1/ErbB4	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
28198	11	8318	6	13	NULL	NULL	NULL	BTC	GP		bind					ErbB2/ErbB3	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
28199	12	8318	6	13	NULL	NULL	NULL	BTC	GP		stimulates					ErbB2/ErbB3	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
28200	13	8318	6	13	NULL	NULL	NULL	BTC	GP		bind					ErbB2/ErbB4	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
28201	14	8318	6	13	NULL	NULL	NULL	BTC	GP		stimulates					ErbB2/ErbB4	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
34344	1	8318	7	10	NULL	0	NULL	BTC	NULL		bind	NULL				ErbB1 homodimer	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
34345	2	8318	7	10	NULL	0	NULL	BTC 	NULL		bind	NULL				ErbB4 homodimer	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
34347	3	8318	7	10	NULL	0	NULL	statement 1	NULL		stimulate	NULL				ErbB1 homodimer	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
34348	4	8318	7	10	NULL	0	NULL	statement 2	NULL		stimulate	NULL				ErbB4 homodimer	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
34350	5	8318	7	NULL	NULL	0	NULL	BTC	NULL		bind	NULL				ErbB1/ErbB2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
34351	6	8318	7	NULL	NULL	0	NULL	BTC	NULL		bind	NULL				ErbB1/ErbB3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
34354	7	8318	7	NULL	NULL	0	NULL	BTC	NULL		bind	NULL				ErbB1/ErbB4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
34355	8	8318	7	NULL	NULL	0	NULL	BTC	NULL		bind	NULL				ErbB2/ErbB3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
34358	9	8318	7	NULL	NULL	0	NULL	BTC	NULL		bind	NULL				ErbB2/ErbB4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
34364	10	8318	7	NULL	NULL	0	NULL	statement 5	NULL		stimulate	NULL				ErbB1/ErbB2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
34365	11	8318	7	NULL	NULL	0	NULL	statement 6	NULL		stimulate	NULL				ErbB1/ErbB3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
34366	12	8318	7	NULL	NULL	0	NULL	statement 7	NULL		stimulate	NULL				ErbB1/ErbB4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
34367	13	8318	7	NULL	NULL	0	NULL	statement 8	NULL		stimulate	NULL				ErbB2/ErbB3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
34368	14	8318	7	NULL	NULL	0	NULL	statement 9	NULL		stimulate	NULL				ErbB2/ErbB4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_30	12869389	5 - 7   BTC is known to bind and stimulate homodimers of ErbB1 and ErbB4, and heterodimers of ErbB1/ErbB2, ErbB1/ErbB3, ErbB1/ErbB4, ErbB2/ErbB3, and, ErbB2/ErbB4.	bind
28213	1	8320	6	13	NULL	NULL	NULL	AR	GP		bind		preferentially			ErbB1 homodimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_31	12869389	5 - 8    AR is known to preferentially bind and stimulate homodimers of ErbB1.	bind
28214	2	8320	6	13	NULL	NULL	NULL	AR	GP		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_31	12869389	5 - 8    AR is known to preferentially bind and stimulate homodimers of ErbB1.	bind
34391	1	8320	7	10	NULL	0	NULL	AR	NULL		bind	NULL	preferentially			ErbB1 homodimer	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_31	12869389	5 - 8    AR is known to preferentially bind and stimulate homodimers of ErbB1.	bind
34392	2	8320	7	NULL	NULL	0	NULL	AR	NULL		stimulate	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_93_4_302_s_31	12869389	5 - 8    AR is known to preferentially bind and stimulate homodimers of ErbB1.	bind
28215	1	8321	6	13	NULL	NULL	NULL	AMP	Chemical		bind					phosphorylase a	GP	liver			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27569_s_186	8910343	5 -AMP binding to liver phosphorylase  a involves a large negative delta C p.	bind
28216	2	8321	6	13	NULL	NULL	NULL	delta C p	GP	negative	plays a role in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27569_s_186	8910343	5 -AMP binding to liver phosphorylase  a involves a large negative delta C p.	bind
34413	1	8321	7	10	NULL	0	NULL	AMP	NULL		bind	NULL				phosphorylase a	NULL	liver			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27569_s_186	8910343	5 -AMP binding to liver phosphorylase  a involves a large negative delta C p.	bind
34414	2	8321	7	10	NULL	0	NULL	statement 1			involves					delta Cp		negative			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27569_s_186	8910343	5 -AMP binding to liver phosphorylase  a involves a large negative delta C p.	bind
28217	1	8322	6	13	NULL	NULL	NULL	Fos-Jun	GP		bind					AP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_5_940_s_191	9157959	5 21  Blocking any one of the above steps, including  Fos-Jun binding to AP-1, could downregulate the induction of TF expression.	bind
28218	2	8322	6	13	NULL	NULL	NULL	statement 1	Process	blocking of	downregulates					TF	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_5_940_s_191	9157959	5 21  Blocking any one of the above steps, including  Fos-Jun binding to AP-1, could downregulate the induction of TF expression.	bind
34415	1	8322	7	NULL	NULL	0	NULL	Fos-Jun	NULL		bind	NULL				 AP-1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_5_940_s_191	9157959	5 21  Blocking any one of the above steps, including  Fos-Jun binding to AP-1, could downregulate the induction of TF expression.	bind
34416	2	8322	7	10	NULL	0	NULL	statement 1	NULL	blocking of	downregulate	NULL				TF	NULL	expression of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_5_940_s_191	9157959	5 21  Blocking any one of the above steps, including  Fos-Jun binding to AP-1, could downregulate the induction of TF expression.	bind
28219	1	8323	6	13	NULL	NULL	NULL	SAA	GP		is					serum amyloid A	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2355_s_19	10521364	5 6  Serum amyloid A (SAA), an apolipoprotein predominantly bound to HDL, is an acute-phase reactant that indicates systemic inflammatory activity with at least the sensitivity of CRP. 7  SAA levels were also reported to be increased in coronary atherosclerosis.	bind
28220	2	8323	6	13	NULL	NULL	NULL	SAA	GP		is a type of					apolipoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2355_s_19	10521364	5 6  Serum amyloid A (SAA), an apolipoprotein predominantly bound to HDL, is an acute-phase reactant that indicates systemic inflammatory activity with at least the sensitivity of CRP. 7  SAA levels were also reported to be increased in coronary atherosclerosis.	bind
28221	3	8323	6	13	NULL	NULL	NULL	SAA	GP		bind					HDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2355_s_19	10521364	5 6  Serum amyloid A (SAA), an apolipoprotein predominantly bound to HDL, is an acute-phase reactant that indicates systemic inflammatory activity with at least the sensitivity of CRP. 7  SAA levels were also reported to be increased in coronary atherosclerosis.	bind
28222	4	8323	6	13	NULL	NULL	NULL	SAA	GP	levels of	are increased in					coronary atherosclerosis	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2355_s_19	10521364	5 6  Serum amyloid A (SAA), an apolipoprotein predominantly bound to HDL, is an acute-phase reactant that indicates systemic inflammatory activity with at least the sensitivity of CRP. 7  SAA levels were also reported to be increased in coronary atherosclerosis.	bind
28262	5	8323	6	13	NULL	NULL	NULL	SAA	GP		is a type of					acute phase reactant	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2355_s_19	10521364	5 6  Serum amyloid A (SAA), an apolipoprotein predominantly bound to HDL, is an acute-phase reactant that indicates systemic inflammatory activity with at least the sensitivity of CRP. 7  SAA levels were also reported to be increased in coronary atherosclerosis.	bind
56118	6	8323	6	13	NULL	NULL	NULL	statement 3	Process		indicates					systemic inflammatory activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2355_s_19	10521364	5 6  Serum amyloid A (SAA), an apolipoprotein predominantly bound to HDL, is an acute-phase reactant that indicates systemic inflammatory activity with at least the sensitivity of CRP. 7  SAA levels were also reported to be increased in coronary atherosclerosis.	bind
34417	1	8323	7	NULL	NULL	0	NULL	SAA	NULL		bind	NULL				HDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2355_s_19	10521364	5 6  Serum amyloid A (SAA), an apolipoprotein predominantly bound to HDL, is an acute-phase reactant that indicates systemic inflammatory activity with at least the sensitivity of CRP. 7  SAA levels were also reported to be increased in coronary atherosclerosis.	bind
34418	2	8323	7	NULL	NULL	0	NULL	SAA	NULL		is a type of	NULL				apolipoprotein	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2355_s_19	10521364	5 6  Serum amyloid A (SAA), an apolipoprotein predominantly bound to HDL, is an acute-phase reactant that indicates systemic inflammatory activity with at least the sensitivity of CRP. 7  SAA levels were also reported to be increased in coronary atherosclerosis.	bind
34419	3	8323	7	NULL	NULL	0	NULL	SAA	NULL		is a type of	NULL				acute phase reactant	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2355_s_19	10521364	5 6  Serum amyloid A (SAA), an apolipoprotein predominantly bound to HDL, is an acute-phase reactant that indicates systemic inflammatory activity with at least the sensitivity of CRP. 7  SAA levels were also reported to be increased in coronary atherosclerosis.	bind
34420	4	8323	7	NULL	NULL	0	NULL	statement 1	NULL		indicates	NULL				systemic inflammatory activity	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2355_s_19	10521364	5 6  Serum amyloid A (SAA), an apolipoprotein predominantly bound to HDL, is an acute-phase reactant that indicates systemic inflammatory activity with at least the sensitivity of CRP. 7  SAA levels were also reported to be increased in coronary atherosclerosis.	bind
34421	5	8323	7	NULL	NULL	0	NULL	statement 1	NULL		indicate	NULL				CRP	NULL	sensitivity of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2355_s_19	10521364	5 6  Serum amyloid A (SAA), an apolipoprotein predominantly bound to HDL, is an acute-phase reactant that indicates systemic inflammatory activity with at least the sensitivity of CRP. 7  SAA levels were also reported to be increased in coronary atherosclerosis.	bind
34422	6	8323	7	NULL	NULL	0	NULL	SAA	NULL	levels of	increase in	NULL				coronary atherosclerosis	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2355_s_19	10521364	5 6  Serum amyloid A (SAA), an apolipoprotein predominantly bound to HDL, is an acute-phase reactant that indicates systemic inflammatory activity with at least the sensitivity of CRP. 7  SAA levels were also reported to be increased in coronary atherosclerosis.	bind
34423	7	8323	7	NULL	NULL	0	NULL	SAA	NULL		is	NULL				Serum amyloid A	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2355_s_19	10521364	5 6  Serum amyloid A (SAA), an apolipoprotein predominantly bound to HDL, is an acute-phase reactant that indicates systemic inflammatory activity with at least the sensitivity of CRP. 7  SAA levels were also reported to be increased in coronary atherosclerosis.	bind
28263	1	8324	6	13	NULL	NULL	NULL	AT1-R antagonists	Chemical	treatment	elevates					Ang II	GP	levels of;;plasma			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_12_1182_s_30	null	5 6  Treatment with AT1-R antagonists causes a marked elevation of levels of plasma Ang II, which selectively binds to AT2-R and exerts as yet undefined effects.	bind
28264	2	8324	6	13	NULL	NULL	NULL	Ang II	GP	plasma	bind		selectively			AT2-R	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_12_1182_s_30	null	5 6  Treatment with AT1-R antagonists causes a marked elevation of levels of plasma Ang II, which selectively binds to AT2-R and exerts as yet undefined effects.	bind
34424	1	8324	7	NULL	NULL	0	NULL	Ang II	NULL	plasma	binds to	NULL	selectively			 AT2-R 	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_12_1182_s_30	null	5 6  Treatment with AT1-R antagonists causes a marked elevation of levels of plasma Ang II, which selectively binds to AT2-R and exerts as yet undefined effects.	bind
34425	2	8324	7	10	NULL	0	NULL	AT1-R antagonists	NULL	treatment	elevates	NULL				Ang II	NULL	levels of;;plasma			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_12_1182_s_30	null	5 6  Treatment with AT1-R antagonists causes a marked elevation of levels of plasma Ang II, which selectively binds to AT2-R and exerts as yet undefined effects.	bind
28265	1	8325	6	13	NULL	NULL	NULL	vessel wall	OrganismPart		bind					vWF	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_28	9484984	5 6 7 8 9 10 11  Because the first event in thrombogenesis is the recognition of vessel wall - bound vWF by platelets through the GPIb receptor, it is apparent that the selective inhibition of binding of endogenous vWF to GPIb may be an appropriate early intervention likely to result in a beneficial antithrombotic effect.	bind
28266	2	8325	6	13	NULL	NULL	NULL	platelets	Cell		recognize					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_28	9484984	5 6 7 8 9 10 11  Because the first event in thrombogenesis is the recognition of vessel wall - bound vWF by platelets through the GPIb receptor, it is apparent that the selective inhibition of binding of endogenous vWF to GPIb may be an appropriate early intervention likely to result in a beneficial antithrombotic effect.	bind
28267	3	8325	6	13	NULL	NULL	NULL	statement 2	Process		is the first step for					thrombogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_28	9484984	5 6 7 8 9 10 11  Because the first event in thrombogenesis is the recognition of vessel wall - bound vWF by platelets through the GPIb receptor, it is apparent that the selective inhibition of binding of endogenous vWF to GPIb may be an appropriate early intervention likely to result in a beneficial antithrombotic effect.	bind
28268	4	8325	6	13	NULL	NULL	NULL	statement 2	Process		occurs through					GPIb receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_28	9484984	5 6 7 8 9 10 11  Because the first event in thrombogenesis is the recognition of vessel wall - bound vWF by platelets through the GPIb receptor, it is apparent that the selective inhibition of binding of endogenous vWF to GPIb may be an appropriate early intervention likely to result in a beneficial antithrombotic effect.	bind
28269	5	8325	6	13	NULL	NULL	NULL	vWF	GP	endogenous	bind					GPIb	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_28	9484984	5 6 7 8 9 10 11  Because the first event in thrombogenesis is the recognition of vessel wall - bound vWF by platelets through the GPIb receptor, it is apparent that the selective inhibition of binding of endogenous vWF to GPIb may be an appropriate early intervention likely to result in a beneficial antithrombotic effect.	bind
28270	6	8325	6	13	NULL	NULL	NULL	statement 5	Process	inhibition of	results in		may			antithrombotic effect	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_28	9484984	5 6 7 8 9 10 11  Because the first event in thrombogenesis is the recognition of vessel wall - bound vWF by platelets through the GPIb receptor, it is apparent that the selective inhibition of binding of endogenous vWF to GPIb may be an appropriate early intervention likely to result in a beneficial antithrombotic effect.	bind
34426	1	8325	7	10	NULL	0	NULL	platelets	NULL		recognize	NULL				statement 6	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_28	9484984	5 6 7 8 9 10 11  Because the first event in thrombogenesis is the recognition of vessel wall - bound vWF by platelets through the GPIb receptor, it is apparent that the selective inhibition of binding of endogenous vWF to GPIb may be an appropriate early intervention likely to result in a beneficial antithrombotic effect.	bind
34427	2	8325	7	NULL	NULL	0	NULL	statement 1	NULL		occurs through	NULL				GPIb receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_28	9484984	5 6 7 8 9 10 11  Because the first event in thrombogenesis is the recognition of vessel wall - bound vWF by platelets through the GPIb receptor, it is apparent that the selective inhibition of binding of endogenous vWF to GPIb may be an appropriate early intervention likely to result in a beneficial antithrombotic effect.	bind
34428	3	8325	7	NULL	NULL	0	NULL	vWF	NULL	endogenous	bind	NULL				GPIb	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_28	9484984	5 6 7 8 9 10 11  Because the first event in thrombogenesis is the recognition of vessel wall - bound vWF by platelets through the GPIb receptor, it is apparent that the selective inhibition of binding of endogenous vWF to GPIb may be an appropriate early intervention likely to result in a beneficial antithrombotic effect.	bind
34429	4	8325	7	NULL	NULL	0	NULL	statement 1	NULL		is the first event in	NULL				thrombogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_28	9484984	5 6 7 8 9 10 11  Because the first event in thrombogenesis is the recognition of vessel wall - bound vWF by platelets through the GPIb receptor, it is apparent that the selective inhibition of binding of endogenous vWF to GPIb may be an appropriate early intervention likely to result in a beneficial antithrombotic effect.	bind
34430	5	8325	7	NULL	NULL	0	NULL	statement 3	NULL	inhibition of	result in	NULL				antithrombotic effect	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_28	9484984	5 6 7 8 9 10 11  Because the first event in thrombogenesis is the recognition of vessel wall - bound vWF by platelets through the GPIb receptor, it is apparent that the selective inhibition of binding of endogenous vWF to GPIb may be an appropriate early intervention likely to result in a beneficial antithrombotic effect.	bind
46869	6	8325	7	10	NULL	0	NULL	vessel wall	NULL		bind	NULL				vWF	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_2_200_s_28	9484984	5 6 7 8 9 10 11  Because the first event in thrombogenesis is the recognition of vessel wall - bound vWF by platelets through the GPIb receptor, it is apparent that the selective inhibition of binding of endogenous vWF to GPIb may be an appropriate early intervention likely to result in a beneficial antithrombotic effect.	bind
28271	1	8326	6	13	NULL	NULL	NULL	PC	GP	activation of	occurs via					PC pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2765_s_22	9409254	5 6 7 8 9 10 11  PC activation in vivo occurs via the PC pathway, in which thrombin binds to the endothelial transmembrane protein TM, which acts as a cofactor in accelerating PC activation by thrombin.	bind
28272	2	8326	6	13	NULL	NULL	NULL	thrombin	GP		bind					TM	GP	endothelial			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2765_s_22	9409254	5 6 7 8 9 10 11  PC activation in vivo occurs via the PC pathway, in which thrombin binds to the endothelial transmembrane protein TM, which acts as a cofactor in accelerating PC activation by thrombin.	bind
28273	3	8326	6	13	NULL	NULL	NULL	TM	GP		is a type of					transmembrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2765_s_22	9409254	5 6 7 8 9 10 11  PC activation in vivo occurs via the PC pathway, in which thrombin binds to the endothelial transmembrane protein TM, which acts as a cofactor in accelerating PC activation by thrombin.	bind
28274	4	8326	6	13	NULL	NULL	NULL	thrombin	GP		activates					PC	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2765_s_22	9409254	5 6 7 8 9 10 11  PC activation in vivo occurs via the PC pathway, in which thrombin binds to the endothelial transmembrane protein TM, which acts as a cofactor in accelerating PC activation by thrombin.	bind
28275	5	8326	6	13	NULL	NULL	NULL	TM	GP	endothelial	acts as a cofactor for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2765_s_22	9409254	5 6 7 8 9 10 11  PC activation in vivo occurs via the PC pathway, in which thrombin binds to the endothelial transmembrane protein TM, which acts as a cofactor in accelerating PC activation by thrombin.	bind
34431	1	8326	7	NULL	NULL	0	NULL	PC	NULL	activation of	occurs via	NULL				PC pathway	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2765_s_22	9409254	5 6 7 8 9 10 11  PC activation in vivo occurs via the PC pathway, in which thrombin binds to the endothelial transmembrane protein TM, which acts as a cofactor in accelerating PC activation by thrombin.	bind
34432	2	8326	7	10	NULL	0	NULL	thrombin	NULL		binds	NULL				TM	NULL	endothelial			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2765_s_22	9409254	5 6 7 8 9 10 11  PC activation in vivo occurs via the PC pathway, in which thrombin binds to the endothelial transmembrane protein TM, which acts as a cofactor in accelerating PC activation by thrombin.	bind
34433	3	8326	7	NULL	NULL	0	NULL	TM	NULL		is a type of	NULL				transmembrane protein	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2765_s_22	9409254	5 6 7 8 9 10 11  PC activation in vivo occurs via the PC pathway, in which thrombin binds to the endothelial transmembrane protein TM, which acts as a cofactor in accelerating PC activation by thrombin.	bind
34434	4	8326	7	NULL	NULL	0	NULL	thrombin	NULL		activates	NULL				PC	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2765_s_22	9409254	5 6 7 8 9 10 11  PC activation in vivo occurs via the PC pathway, in which thrombin binds to the endothelial transmembrane protein TM, which acts as a cofactor in accelerating PC activation by thrombin.	bind
34435	5	8326	7	10	NULL	0	NULL	TM	NULL	endothelial	acts as a	NULL				cofactor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2765_s_22	9409254	5 6 7 8 9 10 11  PC activation in vivo occurs via the PC pathway, in which thrombin binds to the endothelial transmembrane protein TM, which acts as a cofactor in accelerating PC activation by thrombin.	bind
34436	6	8326	7	NULL	NULL	0	NULL	statement 5	NULL		accelerates	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2765_s_22	9409254	5 6 7 8 9 10 11  PC activation in vivo occurs via the PC pathway, in which thrombin binds to the endothelial transmembrane protein TM, which acts as a cofactor in accelerating PC activation by thrombin.	bind
28276	1	8327	6	13	NULL	NULL	NULL	colchicine	Chemical		bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_451_s_45	11266419	5 Also, two of the compounds used for the present study, compounds  1 and  3, inhibit competitively the binding of colchicine to tubulin and the polymerization of tubulin.	bind
46870	2	8327	6	13	NULL	NULL	NULL	tubulin	GP		undergoes					polymerization	Process				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_451_s_45	11266419	5 Also, two of the compounds used for the present study, compounds  1 and  3, inhibit competitively the binding of colchicine to tubulin and the polymerization of tubulin.	bind
34437	1	8327	7	NULL	NULL	0	NULL	colchicine	NULL		bind	NULL				tubulin	NULL				NULL		0	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_451_s_45	11266419	5 Also, two of the compounds used for the present study, compounds  1 and  3, inhibit competitively the binding of colchicine to tubulin and the polymerization of tubulin.	bind
34438	2	8327	7	NULL	NULL	0	NULL	tubulin 	NULL		undergoes	NULL				polymerization	NULL				NULL		0	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_451_s_45	11266419	5 Also, two of the compounds used for the present study, compounds  1 and  3, inhibit competitively the binding of colchicine to tubulin and the polymerization of tubulin.	bind
28277	1	8328	6	13	NULL	NULL	NULL	MP	GP		bind					myosin	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulationres_90_5_546_s_155	11909818	5 Although binding of MP to myosin has been demonstrated in fractionated cells 6 and in vitro, 7 imaging studies of intact cells have raised some questions on this issue.	bind
34439	1	8328	7	NULL	NULL	0	NULL	MP	NULL		bind	NULL				myosin	NULL				NULL	 fractionated cells in vitro	0	NULL	NULL	NULL	gw60_circulationres_90_5_546_s_155	11909818	5 Although binding of MP to myosin has been demonstrated in fractionated cells 6 and in vitro, 7 imaging studies of intact cells have raised some questions on this issue.	bind
28278	1	8330	6	13	NULL	NULL	NULL	ATP	Chemical		bind							isolated	epsilon subunit		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_48_40130_s_226	16203732	5 ATP binding to the isolated epsilon subunit was not affected by lauryldodecylamine oxide ( Kd = 1.4 muM at 35  degrees C).	bind
28279	2	8330	6	13	NULL	NULL	NULL	statement 1	Process		was not affected by					lauryldodecylamine oxide	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_48_40130_s_226	16203732	5 ATP binding to the isolated epsilon subunit was not affected by lauryldodecylamine oxide ( Kd = 1.4 muM at 35  degrees C).	bind
34442	1	8330	7	NULL	NULL	0	NULL	ATP	NULL		bind	NULL					NULL	isolated	epsilon subunit		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_48_40130_s_226	16203732	5 ATP binding to the isolated epsilon subunit was not affected by lauryldodecylamine oxide ( Kd = 1.4 muM at 35  degrees C).	bind
34443	2	8330	7	10	NULL	0	NULL	lauryldodecylamine oxide	NULL		does not affect	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_48_40130_s_226	16203732	5 ATP binding to the isolated epsilon subunit was not affected by lauryldodecylamine oxide ( Kd = 1.4 muM at 35  degrees C).	bind
28281	1	8332	6	13	NULL	NULL	NULL	beta-lactam	GP		bind					BlaR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_13	11266408	5 Binding of a beta-lactam to BlaR1, the signal transducer, is presumed to alter its conformation so that a signal is transmitted across the bacterial membrane and this signal renders BlaI unable to bind to operator DNA, thus allowing transcription of  blaZ, and hence production of beta-lactamase.	bind
28282	2	8332	6	13	NULL	NULL	NULL	BlaI	GP		does not bind					operator DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_13	11266408	5 Binding of a beta-lactam to BlaR1, the signal transducer, is presumed to alter its conformation so that a signal is transmitted across the bacterial membrane and this signal renders BlaI unable to bind to operator DNA, thus allowing transcription of  blaZ, and hence production of beta-lactamase.	bind
28283	3	8332	6	13	NULL	NULL	NULL	statement 1	Process		disrupts					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_13	11266408	5 Binding of a beta-lactam to BlaR1, the signal transducer, is presumed to alter its conformation so that a signal is transmitted across the bacterial membrane and this signal renders BlaI unable to bind to operator DNA, thus allowing transcription of  blaZ, and hence production of beta-lactamase.	bind
28284	4	8332	6	13	NULL	NULL	NULL	statement 3	Process		allows					blaZ	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_13	11266408	5 Binding of a beta-lactam to BlaR1, the signal transducer, is presumed to alter its conformation so that a signal is transmitted across the bacterial membrane and this signal renders BlaI unable to bind to operator DNA, thus allowing transcription of  blaZ, and hence production of beta-lactamase.	bind
28285	5	8332	6	13	NULL	NULL	NULL	statement 4	Process		leads to					beta-lactamase	GP	production of 			NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_13	11266408	5 Binding of a beta-lactam to BlaR1, the signal transducer, is presumed to alter its conformation so that a signal is transmitted across the bacterial membrane and this signal renders BlaI unable to bind to operator DNA, thus allowing transcription of  blaZ, and hence production of beta-lactamase.	bind
46871	6	8332	6	13	NULL	NULL	NULL	BlaR1	GP		is a type of					signal transducer	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_13	11266408	5 Binding of a beta-lactam to BlaR1, the signal transducer, is presumed to alter its conformation so that a signal is transmitted across the bacterial membrane and this signal renders BlaI unable to bind to operator DNA, thus allowing transcription of  blaZ, and hence production of beta-lactamase.	bind
47087	7	8332	6	13	NULL	NULL	NULL	signal	Process		is transmitted across					bacterial membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_13	11266408	5 Binding of a beta-lactam to BlaR1, the signal transducer, is presumed to alter its conformation so that a signal is transmitted across the bacterial membrane and this signal renders BlaI unable to bind to operator DNA, thus allowing transcription of  blaZ, and hence production of beta-lactamase.	bind
47088	8	8332	6	13	NULL	NULL	NULL	statement 7	Process		renders					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_13	11266408	5 Binding of a beta-lactam to BlaR1, the signal transducer, is presumed to alter its conformation so that a signal is transmitted across the bacterial membrane and this signal renders BlaI unable to bind to operator DNA, thus allowing transcription of  blaZ, and hence production of beta-lactamase.	bind
47089	9	8332	6	13	NULL	NULL	NULL	statement 1	Process		alter		may			BlaR1	GP	conformation of 			NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_13	11266408	5 Binding of a beta-lactam to BlaR1, the signal transducer, is presumed to alter its conformation so that a signal is transmitted across the bacterial membrane and this signal renders BlaI unable to bind to operator DNA, thus allowing transcription of  blaZ, and hence production of beta-lactamase.	bind
34445	1	8332	7	NULL	NULL	0	NULL	beta-lactam	NULL		bind	NULL				BlaR1	NULL				NULL		0	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_13	11266408	5 Binding of a beta-lactam to BlaR1, the signal transducer, is presumed to alter its conformation so that a signal is transmitted across the bacterial membrane and this signal renders BlaI unable to bind to operator DNA, thus allowing transcription of  blaZ, and hence production of beta-lactamase.	bind
34446	2	8332	7	NULL	NULL	0	NULL	BlaR1	NULL		is a type of	NULL				signal transducer	NULL				NULL		0	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_13	11266408	5 Binding of a beta-lactam to BlaR1, the signal transducer, is presumed to alter its conformation so that a signal is transmitted across the bacterial membrane and this signal renders BlaI unable to bind to operator DNA, thus allowing transcription of  blaZ, and hence production of beta-lactamase.	bind
34447	3	8332	7	10	NULL	0	NULL	statement 1	NULL		alters	NULL	may			BlaR1	NULL	conformation of			NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_13	11266408	5 Binding of a beta-lactam to BlaR1, the signal transducer, is presumed to alter its conformation so that a signal is transmitted across the bacterial membrane and this signal renders BlaI unable to bind to operator DNA, thus allowing transcription of  blaZ, and hence production of beta-lactamase.	bind
34448	4	8332	7	10	NULL	0	NULL	statement 3	NULL		leads to	NULL				statement 9	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_13	11266408	5 Binding of a beta-lactam to BlaR1, the signal transducer, is presumed to alter its conformation so that a signal is transmitted across the bacterial membrane and this signal renders BlaI unable to bind to operator DNA, thus allowing transcription of  blaZ, and hence production of beta-lactamase.	bind
34449	5	8332	7	NULL	NULL	0	NULL	BlaI 	NULL		does not bind	NULL				operator DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_13	11266408	5 Binding of a beta-lactam to BlaR1, the signal transducer, is presumed to alter its conformation so that a signal is transmitted across the bacterial membrane and this signal renders BlaI unable to bind to operator DNA, thus allowing transcription of  blaZ, and hence production of beta-lactamase.	bind
34450	6	8332	7	10	NULL	0	NULL	statement 9	NULL		renders	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_13	11266408	5 Binding of a beta-lactam to BlaR1, the signal transducer, is presumed to alter its conformation so that a signal is transmitted across the bacterial membrane and this signal renders BlaI unable to bind to operator DNA, thus allowing transcription of  blaZ, and hence production of beta-lactamase.	bind
34451	7	8332	7	NULL	NULL	0	NULL	statement 5	NULL		allows	NULL				blaZ	NULL	transcription of			NULL		0	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_13	11266408	5 Binding of a beta-lactam to BlaR1, the signal transducer, is presumed to alter its conformation so that a signal is transmitted across the bacterial membrane and this signal renders BlaI unable to bind to operator DNA, thus allowing transcription of  blaZ, and hence production of beta-lactamase.	bind
34452	8	8332	7	NULL	NULL	0	NULL	statement 5	NULL		allows	NULL				beta-lactamase	NULL	production of			NULL		0	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_13	11266408	5 Binding of a beta-lactam to BlaR1, the signal transducer, is presumed to alter its conformation so that a signal is transmitted across the bacterial membrane and this signal renders BlaI unable to bind to operator DNA, thus allowing transcription of  blaZ, and hence production of beta-lactamase.	bind
46872	9	8332	7	10	NULL	0	NULL	signal	NULL		is transmitted across	NULL				bacterial membrane	NULL				NULL		0	NULL	NULL	NULL	gw60_jantimicrobchemoth_47_4_377_s_13	11266408	5 Binding of a beta-lactam to BlaR1, the signal transducer, is presumed to alter its conformation so that a signal is transmitted across the bacterial membrane and this signal renders BlaI unable to bind to operator DNA, thus allowing transcription of  blaZ, and hence production of beta-lactamase.	bind
28286	1	8333	6	13	NULL	NULL	NULL	Bruno proteins	GP		bind									BRE element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_37_28583_s_280	10893231	5 Consistent with the Bruno proteins binding to BRE elements, the  Xenopus EDEN-BP (BrunoL-2) also has been shown to bind to an RNA element that is identical to the consensus BRE ( 26,  60).	bind
28287	2	8333	6	13	NULL	NULL	NULL	EDEN-BP	GP	Xenopus	is					BrunoL-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_37_28583_s_280	10893231	5 Consistent with the Bruno proteins binding to BRE elements, the  Xenopus EDEN-BP (BrunoL-2) also has been shown to bind to an RNA element that is identical to the consensus BRE ( 26,  60).	bind
28288	3	8333	6	13	NULL	NULL	NULL	BrunoL-2	GP	Xenopus	bind									RNA element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_37_28583_s_280	10893231	5 Consistent with the Bruno proteins binding to BRE elements, the  Xenopus EDEN-BP (BrunoL-2) also has been shown to bind to an RNA element that is identical to the consensus BRE ( 26,  60).	bind
28289	4	8333	6	NULL	NULL	0	NULL		NULL		is identical to	NULL			RNA element		NULL	consensus		BRE	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_37_28583_s_280	10893231	5 Consistent with the Bruno proteins binding to BRE elements, the  Xenopus EDEN-BP (BrunoL-2) also has been shown to bind to an RNA element that is identical to the consensus BRE ( 26,  60).	bind
34453	1	8333	7	NULL	NULL	0	NULL	Bruno proteins	NULL		bind	NULL					NULL			BRE elements	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_37_28583_s_280	10893231	5 Consistent with the Bruno proteins binding to BRE elements, the  Xenopus EDEN-BP (BrunoL-2) also has been shown to bind to an RNA element that is identical to the consensus BRE ( 26,  60).	bind
34454	2	8333	7	NULL	NULL	0	NULL	BrunoL-2	NULL	Xenopus 	bind	NULL					NULL			RNA element	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_37_28583_s_280	10893231	5 Consistent with the Bruno proteins binding to BRE elements, the  Xenopus EDEN-BP (BrunoL-2) also has been shown to bind to an RNA element that is identical to the consensus BRE ( 26,  60).	bind
34455	3	8333	7	10	NULL	0	NULL		NULL		is identical to	NULL			RNA element		NULL	consensus		BRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_37_28583_s_280	10893231	5 Consistent with the Bruno proteins binding to BRE elements, the  Xenopus EDEN-BP (BrunoL-2) also has been shown to bind to an RNA element that is identical to the consensus BRE ( 26,  60).	bind
34456	4	8333	7	NULL	NULL	0	NULL	BrunoL-2	NULL		is	NULL				EDEN-BP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_37_28583_s_280	10893231	5 Consistent with the Bruno proteins binding to BRE elements, the  Xenopus EDEN-BP (BrunoL-2) also has been shown to bind to an RNA element that is identical to the consensus BRE ( 26,  60).	bind
28290	1	8334	6	13	NULL	NULL	NULL	endothelial cells	Cell		secrete					uPA	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
28291	2	8334	6	13	NULL	NULL	NULL	endothelial cells	Cell		secrete					tPA	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
28292	3	8334	6	13	NULL	NULL	NULL	endothelial cells	Cell		secrete					MMP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
28293	4	8334	6	13	NULL	NULL	NULL	endothelial cells	Cell		secretes					MMP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
28294	5	8334	6	13	NULL	NULL	NULL	endothelial cells	Cell		secretes					MMP-9	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
28372	6	8334	6	13	NULL	NULL	NULL	uPAR	GP		is					urokinase receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
28373	7	8334	6	13	NULL	NULL	NULL	uPAR	GP		is a type of					membrane-anchored protease receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
28382	8	8334	6	13	NULL	NULL	NULL	proteolytic activity	Process		is restricted to the					cell surface	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
28384	9	8334	6	13	NULL	NULL	NULL	statement 8	Process		occurs via					uPAR	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
28385	10	8334	6	13	NULL	NULL	NULL	statement 8	Process		occurs via					MT1-MMP	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
28386	11	8334	6	13	NULL	NULL	NULL	statement 8	Process		occurs via					MMP-14	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
28387	12	8334	6	13	NULL	NULL	NULL	MT1-MMP	GP		is a type of					membrane type-1 MMP	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
28388	13	8334	6	13	NULL	NULL	NULL	MMP-14	GP		is a type of					membrane type-1 MMP	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
28389	14	8334	6	13	NULL	NULL	NULL	MT1-MMP	GP		bind					uPA	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
28390	15	8334	6	13	NULL	NULL	NULL	MT1-MMP	GP		activate					uPA	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
28392	16	8334	6	13	NULL	NULL	NULL	MMP-14	GP		bind					MMP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
28393	17	8334	6	13	NULL	NULL	NULL	MMP-14	GP		activate					MMP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34457	1	8334	7	NULL	NULL	0	NULL	Endothelial cells	NULL		secrete	NULL				uPA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34458	2	8334	7	NULL	NULL	0	NULL	Endothelial cells	NULL		secrete	NULL				tPA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34459	3	8334	7	NULL	NULL	0	NULL	Endothelial cells	NULL		secrete	NULL				MMP-1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34460	4	8334	7	NULL	NULL	0	NULL	Endothelial cells	NULL		secrete	NULL				MMP-2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34461	5	8334	7	NULL	NULL	0	NULL	Endothelial cells	NULL		secrete	NULL				MMP-9	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34462	6	8334	7	NULL	NULL	0	NULL	statement 1	NULL		occurs in an	NULL				activation-dependent manner	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34463	7	8334	7	NULL	NULL	0	NULL	statement 2	NULL		occurs in an	NULL				activation-dependent manner	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34464	8	8334	7	NULL	NULL	0	NULL	statement 3	NULL		occurs in an	NULL				activation-dependent manner	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34465	9	8334	7	NULL	NULL	0	NULL	statement 4	NULL		occurs in an	NULL				activation-dependent manner	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34466	10	8334	7	NULL	NULL	0	NULL	statement 5	NULL		occurs in an	NULL				activation-dependent manner	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34467	11	8334	7	NULL	NULL	0	NULL	statement 1	NULL		restrict	NULL				 cell surface proteolytic activity	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34468	12	8334	7	NULL	NULL	0	NULL	statement 2	NULL		restrict	NULL				 cell surface proteolytic activity	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34469	13	8334	7	NULL	NULL	0	NULL	statement 3	NULL		restrict	NULL				cell surface proteolytic activity	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34470	14	8334	7	NULL	NULL	0	NULL	statement 4	NULL		restrict	NULL				cell surface proteolytic activity	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34471	15	8334	7	NULL	NULL	0	NULL	statement 5	NULL		restrict	NULL				cell surface proteolytic activity	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34472	16	8334	7	NULL	NULL	0	NULL	statement 11	NULL		occurs via	NULL				uPAR	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34473	17	8334	7	NULL	NULL	0	NULL	statement 12	NULL		occurs via	NULL				uPAR	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34474	18	8334	7	NULL	NULL	0	NULL	statement 13	NULL		occurs via	NULL				uPAR	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34475	19	8334	7	NULL	NULL	0	NULL	statement 14	NULL		occurs via	NULL				uPAR	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34476	20	8334	7	NULL	NULL	0	NULL	statement 15	NULL		occurs via	NULL				uPAR	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34477	21	8334	7	NULL	NULL	0	NULL	statement 11	NULL		occurs via	NULL				MT1-MMP	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34478	22	8334	7	NULL	NULL	0	NULL	statement 12	NULL		occurs via	NULL				MT1-MMP	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34479	23	8334	7	NULL	NULL	0	NULL	statement 13	NULL		occurs via	NULL				MT1-MMP	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34480	24	8334	7	NULL	NULL	0	NULL	statement 14	NULL		occurs via	NULL				MT1-MMP	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34481	25	8334	7	NULL	NULL	0	NULL	statement 15	NULL		occurs via	NULL				MT1-MMP	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34482	26	8334	7	NULL	NULL	0	NULL	uPAR	NULL		bind	NULL				uPA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34483	27	8334	7	NULL	NULL	0	NULL	MT1-MMP	NULL		bind	NULL				MMP-2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34484	28	8334	7	NULL	NULL	0	NULL	statement 26	NULL		activate	NULL				uPA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34485	29	8334	7	NULL	NULL	0	NULL	statement 27	NULL		activate	NULL				MMP-2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34486	30	8334	7	NULL	NULL	0	NULL	uPAR	NULL		is	NULL				urokinase receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34487	31	8334	7	NULL	NULL	0	NULL	MT1-MMP	NULL		is	NULL				membrane type-1 MMP	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34488	32	8334	7	NULL	NULL	0	NULL	MMP-14	NULL		bind	NULL				MMP-2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34489	33	8334	7	NULL	NULL	0	NULL	statement 32	NULL		activate	NULL				MMP-2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34490	34	8334	7	NULL	NULL	0	NULL	uPAR	NULL		is a type of	NULL				membrane-anchored protease receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
34491	35	8334	7	NULL	NULL	0	NULL	MT1-MMP	NULL		is a type of	NULL				membrane-anchored protease receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_106_16_2111_s_21	12379582	5 Endothelial cells secrete uPA, tPA, MMP-1, MMP-2, and MMP-9 in an activation-dependent manner 1, 6 and restrict proteolytic activity to the cell surface via membrane-anchored protease receptors such as urokinase receptor (uPAR) and membrane type-1 MMP (MT1-MMP, MMP-14), which bind and activate uPA and MMP-2, respectively.	bind
28297	1	8336	6	13	NULL	NULL	NULL	flavocytochrome b	GP		bind					p47 phox	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_29_17013_s_118	8663333	5 h after activation of the assay containing p47 phox and p67 phox) almost completely blocked (~91% inhibition) flavocytochrome  b binding to p47 phox compared with controls, supporting the formation of a stable complex that renders the 323-332 binding region inaccessible as was indicated by our peptide studies.	bind
34507	1	8336	7	NULL	NULL	0	NULL	flavocytochrome b	NULL		bind	NULL				p47phox	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_29_17013_s_118	8663333	5 h after activation of the assay containing p47 phox and p67 phox) almost completely blocked (~91% inhibition) flavocytochrome  b binding to p47 phox compared with controls, supporting the formation of a stable complex that renders the 323-332 binding region inaccessible as was indicated by our peptide studies.	bind
28298	1	8337	6	13	NULL	NULL	NULL	VEGFR1	GP		is a type of					tyrosine kinase receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_18_2347_s_27	15867174	5 In ECs, VEGF binds to 2 tyrosine kinase receptors, VEGF receptor (VEGFR) 1 (Flt-1), and VEGFR2 (KDR/Flk1).	bind
28299	2	8337	6	13	NULL	NULL	NULL	VEGFR1	GP		is					VEGF receptor 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_18_2347_s_27	15867174	5 In ECs, VEGF binds to 2 tyrosine kinase receptors, VEGF receptor (VEGFR) 1 (Flt-1), and VEGFR2 (KDR/Flk1).	bind
28300	3	8337	6	13	NULL	NULL	NULL	Flt-1	GP		is a synonym of					VEGFR1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_18_2347_s_27	15867174	5 In ECs, VEGF binds to 2 tyrosine kinase receptors, VEGF receptor (VEGFR) 1 (Flt-1), and VEGFR2 (KDR/Flk1).	bind
28301	4	8337	6	13	NULL	NULL	NULL	KDR/Flk1	GP		is a synonym of					VEGFR2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_18_2347_s_27	15867174	5 In ECs, VEGF binds to 2 tyrosine kinase receptors, VEGF receptor (VEGFR) 1 (Flt-1), and VEGFR2 (KDR/Flk1).	bind
28302	5	8337	6	13	NULL	NULL	NULL	VEGF	GP		bind					VEGFR1	GP				NULL	ECs	NULL	NULL	NULL	NULL	gw70_circulation_111_18_2347_s_27	15867174	5 In ECs, VEGF binds to 2 tyrosine kinase receptors, VEGF receptor (VEGFR) 1 (Flt-1), and VEGFR2 (KDR/Flk1).	bind
28304	6	8337	6	13	NULL	NULL	NULL	VEGF	GP		bind					VEGFR2	GP				NULL	ECs	NULL	NULL	NULL	NULL	gw70_circulation_111_18_2347_s_27	15867174	5 In ECs, VEGF binds to 2 tyrosine kinase receptors, VEGF receptor (VEGFR) 1 (Flt-1), and VEGFR2 (KDR/Flk1).	bind
46873	7	8337	6	13	NULL	NULL	NULL	VEGFR2	GP		is a type of					tyrosine kinase receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_18_2347_s_27	15867174	5 In ECs, VEGF binds to 2 tyrosine kinase receptors, VEGF receptor (VEGFR) 1 (Flt-1), and VEGFR2 (KDR/Flk1).	bind
34512	1	8337	7	10	NULL	0	NULL	VEGFR1	NULL		is a type of	NULL				tyrosine kinase receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_18_2347_s_27	15867174	5 In ECs, VEGF binds to 2 tyrosine kinase receptors, VEGF receptor (VEGFR) 1 (Flt-1), and VEGFR2 (KDR/Flk1).	bind
34513	2	8337	7	10	NULL	0	NULL	VEGF	NULL		bind	NULL				VEGFR1	NULL				NULL	ECs	NULL	NULL	NULL	NULL	gw70_circulation_111_18_2347_s_27	15867174	5 In ECs, VEGF binds to 2 tyrosine kinase receptors, VEGF receptor (VEGFR) 1 (Flt-1), and VEGFR2 (KDR/Flk1).	bind
34514	3	8337	7	NULL	NULL	0	NULL	VEGF	NULL		bind	NULL				VEGFR2	NULL				NULL	ECs	NULL	NULL	NULL	NULL	gw70_circulation_111_18_2347_s_27	15867174	5 In ECs, VEGF binds to 2 tyrosine kinase receptors, VEGF receptor (VEGFR) 1 (Flt-1), and VEGFR2 (KDR/Flk1).	bind
34515	4	8337	7	10	NULL	0	NULL	Flt-1	NULL		is a synonym of	NULL				VEGFR1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_18_2347_s_27	15867174	5 In ECs, VEGF binds to 2 tyrosine kinase receptors, VEGF receptor (VEGFR) 1 (Flt-1), and VEGFR2 (KDR/Flk1).	bind
34516	5	8337	7	10	NULL	0	NULL	KDR/Flk1	NULL		is a synonym of	NULL				VEGFR2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_18_2347_s_27	15867174	5 In ECs, VEGF binds to 2 tyrosine kinase receptors, VEGF receptor (VEGFR) 1 (Flt-1), and VEGFR2 (KDR/Flk1).	bind
34517	6	8337	7	10	NULL	0	NULL	VEGFR1	NULL		is	NULL				VEGF receptor 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_18_2347_s_27	15867174	5 In ECs, VEGF binds to 2 tyrosine kinase receptors, VEGF receptor (VEGFR) 1 (Flt-1), and VEGFR2 (KDR/Flk1).	bind
46874	7	8337	7	10	NULL	0	NULL	VEGFR2	NULL		is a type of	NULL				tyrosine kinase receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_111_18_2347_s_27	15867174	5 In ECs, VEGF binds to 2 tyrosine kinase receptors, VEGF receptor (VEGFR) 1 (Flt-1), and VEGFR2 (KDR/Flk1).	bind
28305	1	8338	6	13	NULL	NULL	NULL	PAR3	GP		bind					thrombin	GP				NULL	mouse platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1640_s_26	16675723	5 In mouse platelets, PAR3 itself does not mediate transmembrane signaling on interaction with thrombin but instead functions as a cofactor that binds thrombin and promotes productive cleavage and activation of PAR4, which then induces intracellular signaling through G-proteins.	bind
28306	2	8338	6	13	NULL	NULL	NULL	PAR3	GP		acts as a cofactor for					statement 1	Process				NULL	mouse platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1640_s_26	16675723	5 In mouse platelets, PAR3 itself does not mediate transmembrane signaling on interaction with thrombin but instead functions as a cofactor that binds thrombin and promotes productive cleavage and activation of PAR4, which then induces intracellular signaling through G-proteins.	bind
28307	3	8338	6	13	NULL	NULL	NULL	statement 2	Process		promotes					PAR4	GP	productive clevage of 			NULL	mouse platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1640_s_26	16675723	5 In mouse platelets, PAR3 itself does not mediate transmembrane signaling on interaction with thrombin but instead functions as a cofactor that binds thrombin and promotes productive cleavage and activation of PAR4, which then induces intracellular signaling through G-proteins.	bind
28308	4	8338	6	13	NULL	NULL	NULL	statement 3	Process		activates					PAR4	GP				NULL	mouse platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1640_s_26	16675723	5 In mouse platelets, PAR3 itself does not mediate transmembrane signaling on interaction with thrombin but instead functions as a cofactor that binds thrombin and promotes productive cleavage and activation of PAR4, which then induces intracellular signaling through G-proteins.	bind
28309	5	8338	6	13	NULL	NULL	NULL	PAR4	GP		induces					intracellular signaling	Process				NULL	mouse platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1640_s_26	16675723	5 In mouse platelets, PAR3 itself does not mediate transmembrane signaling on interaction with thrombin but instead functions as a cofactor that binds thrombin and promotes productive cleavage and activation of PAR4, which then induces intracellular signaling through G-proteins.	bind
28310	6	8338	6	13	NULL	NULL	NULL	statement 5	Process		occurs through					G-proteins	GP				NULL	mouse platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1640_s_26	16675723	5 In mouse platelets, PAR3 itself does not mediate transmembrane signaling on interaction with thrombin but instead functions as a cofactor that binds thrombin and promotes productive cleavage and activation of PAR4, which then induces intracellular signaling through G-proteins.	bind
34521	1	8338	7	10	NULL	0	NULL	PAR3	NULL		bind	NULL				thrombin	NULL				NULL	mouse platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1640_s_26	16675723	5 In mouse platelets, PAR3 itself does not mediate transmembrane signaling on interaction with thrombin but instead functions as a cofactor that binds thrombin and promotes productive cleavage and activation of PAR4, which then induces intracellular signaling through G-proteins.	bind
34522	2	8338	7	NULL	NULL	0	NULL	 PAR3	NULL		does not mediate	NULL				transmembrane signaling	NULL				NULL	mouse platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1640_s_26	16675723	5 In mouse platelets, PAR3 itself does not mediate transmembrane signaling on interaction with thrombin but instead functions as a cofactor that binds thrombin and promotes productive cleavage and activation of PAR4, which then induces intracellular signaling through G-proteins.	bind
34523	3	8338	7	NULL	NULL	0	NULL	statement 2	NULL		occurs upon	NULL				statement 1	NULL				NULL	mouse platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1640_s_26	16675723	5 In mouse platelets, PAR3 itself does not mediate transmembrane signaling on interaction with thrombin but instead functions as a cofactor that binds thrombin and promotes productive cleavage and activation of PAR4, which then induces intracellular signaling through G-proteins.	bind
34524	4	8338	7	10	NULL	0	NULL	PAR3	NULL		acts as a cofactor for	NULL				statement 1	NULL				NULL	mouse platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1640_s_26	16675723	5 In mouse platelets, PAR3 itself does not mediate transmembrane signaling on interaction with thrombin but instead functions as a cofactor that binds thrombin and promotes productive cleavage and activation of PAR4, which then induces intracellular signaling through G-proteins.	bind
34526	5	8338	7	10	NULL	0	NULL	statement 4	NULL		promotes	NULL				PAR4	NULL	productive cleavage of			NULL	mouse platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1640_s_26	16675723	5 In mouse platelets, PAR3 itself does not mediate transmembrane signaling on interaction with thrombin but instead functions as a cofactor that binds thrombin and promotes productive cleavage and activation of PAR4, which then induces intracellular signaling through G-proteins.	bind
34527	6	8338	7	10	NULL	0	NULL	PAR3	NULL		activates	NULL				PAR4	NULL				NULL	mouse platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1640_s_26	16675723	5 In mouse platelets, PAR3 itself does not mediate transmembrane signaling on interaction with thrombin but instead functions as a cofactor that binds thrombin and promotes productive cleavage and activation of PAR4, which then induces intracellular signaling through G-proteins.	bind
34528	7	8338	7	10	NULL	0	NULL	PAR4	NULL		induces	NULL				intracellular signaling	NULL				NULL	mouse platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1640_s_26	16675723	5 In mouse platelets, PAR3 itself does not mediate transmembrane signaling on interaction with thrombin but instead functions as a cofactor that binds thrombin and promotes productive cleavage and activation of PAR4, which then induces intracellular signaling through G-proteins.	bind
34529	8	8338	7	10	NULL	0	NULL	statement 7	NULL		via	NULL				G-proteins	NULL				NULL	mouse platelets	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1640_s_26	16675723	5 In mouse platelets, PAR3 itself does not mediate transmembrane signaling on interaction with thrombin but instead functions as a cofactor that binds thrombin and promotes productive cleavage and activation of PAR4, which then induces intracellular signaling through G-proteins.	bind
28311	1	8339	6	13	NULL	NULL	NULL	HDL3	GP		bind					HSPG	GP	secreted			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_108_3_270_s_145	12835223	5 In the present study, PLTP did mediate a modest increase in HDL3 binding to secreted HSPGs in vitro.	bind
28312	2	8339	6	13	NULL	NULL	NULL	PLTP	GP		increases					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_108_3_270_s_145	12835223	5 In the present study, PLTP did mediate a modest increase in HDL3 binding to secreted HSPGs in vitro.	bind
34531	1	8339	7	10	NULL	0	NULL	HDL3	NULL		bind	NULL				HSPGs	NULL	secreted			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_108_3_270_s_145	12835223	5 In the present study, PLTP did mediate a modest increase in HDL3 binding to secreted HSPGs in vitro.	bind
34532	2	8339	7	NULL	NULL	0	NULL	PLTP	NULL		increase	NULL				statement 1	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulation_108_3_270_s_145	12835223	5 In the present study, PLTP did mediate a modest increase in HDL3 binding to secreted HSPGs in vitro.	bind
28313	1	8340	6	13	NULL	NULL	NULL	PST PIP	GP		bind					PTP HSCF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_2_989_s_208	9422760	5 Interestingly, the tryptophan located NH2-terminal to the critical tryptophan involved with binding of PST PIP to PTP HSCF does not seem to be required for ligand recognition, a result similar to that found for the NH2-terminal tryptophan of the WW domain in Yes kinase-associated protein ( 14).	bind
34534	1	8340	7	NULL	NULL	0	NULL	PST PIP	NULL		bind	NULL				PTP HSCF	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_2_989_s_208	9422760	5 Interestingly, the tryptophan located NH2-terminal to the critical tryptophan involved with binding of PST PIP to PTP HSCF does not seem to be required for ligand recognition, a result similar to that found for the NH2-terminal tryptophan of the WW domain in Yes kinase-associated protein ( 14).	bind
28405	1	8342	6	13	NULL	NULL	NULL	polyclonal anti-calcitonin antibody	GP	sheep	bind					calcitonin precursor molecules	GP		katacalcin sequence		NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_14_1707_s_42	15066945	5 Kryptor-PCT is based on a sheep polyclonal anti-calcitonin antibody and a monoclonal anti-katacalcin antibody, which bind either to the katacalcin or the calcitonin sequence of calcitonin precursor molecules.	bind
28406	2	8342	6	13	NULL	NULL	NULL	polyclonal anti-calcitonin antibody	GP	sheep	bind					calcitonin precursor molecules	GP		calcitonin sequence		NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_14_1707_s_42	15066945	5 Kryptor-PCT is based on a sheep polyclonal anti-calcitonin antibody and a monoclonal anti-katacalcin antibody, which bind either to the katacalcin or the calcitonin sequence of calcitonin precursor molecules.	bind
28408	3	8342	6	13	NULL	NULL	NULL	anti-katacalcin antibody	GP	monoclonal	bind					calcitonin precursor molecules	GP		katacalcin sequence		NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_14_1707_s_42	15066945	5 Kryptor-PCT is based on a sheep polyclonal anti-calcitonin antibody and a monoclonal anti-katacalcin antibody, which bind either to the katacalcin or the calcitonin sequence of calcitonin precursor molecules.	bind
28409	4	8342	6	13	NULL	NULL	NULL	anti-katacalcin antibody	GP	monoclonal	bind					calcitonin precursor molecules	GP		calcitonin sequence		NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_14_1707_s_42	15066945	5 Kryptor-PCT is based on a sheep polyclonal anti-calcitonin antibody and a monoclonal anti-katacalcin antibody, which bind either to the katacalcin or the calcitonin sequence of calcitonin precursor molecules.	bind
34574	1	8342	7	NULL	NULL	0	NULL	Kryptor-PCT	NULL		is based on	NULL				polyclonal anti-calcitonin antibody	NULL	sheep			NULL		0	NULL	NULL	NULL	gw70_circulation_109_14_1707_s_42	15066945	5 Kryptor-PCT is based on a sheep polyclonal anti-calcitonin antibody and a monoclonal anti-katacalcin antibody, which bind either to the katacalcin or the calcitonin sequence of calcitonin precursor molecules.	bind
34575	2	8342	7	NULL	NULL	0	NULL	Kryptor-PCT 	NULL		is based on	NULL				monoclonal anti-katacalcin antibody	NULL	sheep			NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_14_1707_s_42	15066945	5 Kryptor-PCT is based on a sheep polyclonal anti-calcitonin antibody and a monoclonal anti-katacalcin antibody, which bind either to the katacalcin or the calcitonin sequence of calcitonin precursor molecules.	bind
34576	3	8342	7	10	NULL	0	NULL	Kryptor-PCT	NULL		bind	NULL				katacalcin	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_14_1707_s_42	15066945	5 Kryptor-PCT is based on a sheep polyclonal anti-calcitonin antibody and a monoclonal anti-katacalcin antibody, which bind either to the katacalcin or the calcitonin sequence of calcitonin precursor molecules.	bind
34577	4	8342	7	NULL	NULL	0	NULL	Kryptor-PCT	NULL		bind	NULL				calcitonin precursor molecules	NULL		calcitonin sequence 		NULL		0	NULL	NULL	NULL	gw70_circulation_109_14_1707_s_42	15066945	5 Kryptor-PCT is based on a sheep polyclonal anti-calcitonin antibody and a monoclonal anti-katacalcin antibody, which bind either to the katacalcin or the calcitonin sequence of calcitonin precursor molecules.	bind
28314	1	8346	6	13	NULL	NULL	NULL	decorin	GP		bind					type VI collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_26110_s_137	8824254	5 mug of NG2 inhibits the binding of decorin (0.5 mug) to type VI collagen by only 15%.	bind
28315	2	8346	6	13	NULL	NULL	NULL	NG2	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_26110_s_137	8824254	5 mug of NG2 inhibits the binding of decorin (0.5 mug) to type VI collagen by only 15%.	bind
34578	1	8346	7	NULL	NULL	0	NULL	decorin	NULL		bind	NULL				type VI collagen	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_42_26110_s_137	8824254	5 mug of NG2 inhibits the binding of decorin (0.5 mug) to type VI collagen by only 15%.	bind
34579	2	8346	7	NULL	NULL	0	NULL	NG2	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_42_26110_s_137	8824254	5 mug of NG2 inhibits the binding of decorin (0.5 mug) to type VI collagen by only 15%.	bind
28318	1	8353	6	13	NULL	NULL	NULL	B-box proteins	GP	WT	bind					BLT DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_23_16536_s_89	10347218	5 muM amounts of either the correctly folded hybrid or the WT B-box proteins were bound to BLT DNA (0.1 ng) in the footprinting reactions.	bind
34580	1	8353	7	10	NULL	0	NULL	B-box protein	NULL	WT	bind	NULL				BLT DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_23_16536_s_89	10347218	5 muM amounts of either the correctly folded hybrid or the WT B-box proteins were bound to BLT DNA (0.1 ng) in the footprinting reactions.	bind
47093	1	8354	6	13	NULL	NULL	NULL	18A9	GP		bind					PDHc	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
47097	2	8354	6	13	NULL	NULL	NULL	21C3	GP		bind					PDHc	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
47098	3	8354	6	13	NULL	NULL	NULL	15A9	GP		bind					PDHc	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
47099	4	8354	6	13	NULL	NULL	NULL	1F2 	GP		bind					PDHc	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
47100	5	8354	6	13	NULL	NULL	NULL	3G1 	GP		bind					PDHc	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
47101	6	8354	6	13	NULL	NULL	NULL	18A9	GP		bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
47102	7	8354	6	13	NULL	NULL	NULL	21C3	GP		bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
47103	8	8354	6	13	NULL	NULL	NULL	15A9	GP		bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
47104	9	8354	6	13	NULL	NULL	NULL	1F2	GP		bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
47105	10	8354	6	13	NULL	NULL	NULL	3G1	GP		bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
47106	11	8354	6	13	NULL	NULL	NULL	8C9 	GP		does not bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
47107	12	8354	6	13	NULL	NULL	NULL	7C9	GP		does not bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
47108	13	8354	6	13	NULL	NULL	NULL	13A8	GP		does not bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
47109	14	8354	6	13	NULL	NULL	NULL	23H4	GP		does not bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
47110	15	8354	6	13	NULL	NULL	NULL	8G10	GP		does not bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34581	1	8354	7	NULL	NULL	0	NULL	18A9 MAb	NULL		bind	NULL				PDHc	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34582	2	8354	7	NULL	NULL	0	NULL	 21C3 MAb	NULL		bind	NULL				PDHc	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34583	3	8354	7	NULL	NULL	0	NULL	15A9 MAb	NULL		bind	NULL				PDHc	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34584	4	8354	7	NULL	NULL	0	NULL	1F2MAb	NULL		bind	NULL				PDHc	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34585	5	8354	7	NULL	NULL	0	NULL	3G1MAb	NULL		bind	NULL				PDHc	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34586	6	8354	7	NULL	NULL	0	NULL	18A9 MAb	NULL		bind	NULL				E1 antigen	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34587	7	8354	7	NULL	NULL	0	NULL	21C3 MAb	NULL		bind	NULL				E1 antigen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34588	8	8354	7	NULL	NULL	0	NULL	15A9 MAb	NULL		bind	NULL				E1 antigen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34589	9	8354	7	NULL	NULL	0	NULL	1F2MAb	NULL		bind	NULL				E1 antigen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34590	10	8354	7	NULL	NULL	0	NULL	3G1MAb	NULL		bind	NULL				E1 antigen	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34596	11	8354	7	10	NULL	0	NULL	8C9			does not bind					E1 antigen					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34597	12	8354	7	10	NULL	0	NULL	7C9			does not bind					E1 antigen					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34598	13	8354	7	10	NULL	0	NULL	13A8			does not bind					E1 antigen					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34599	14	8354	7	10	NULL	0	NULL	23H4			does not bind					E1 antigen					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34600	15	8354	7	10	NULL	0	NULL	8G10			does not bind					E1 antigen					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_196	7649984	5 of the 10 MAbs  that bound PDHc (18A9, 21C3, 15A9, 1F2, and 3G1) bound the E1 antigen,  and 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
28319	1	8355	6	13	NULL	NULL	NULL	18A9	GP		bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
28320	2	8355	6	13	NULL	NULL	NULL	21C3 MAb	GP		bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
28321	3	8355	6	13	NULL	NULL	NULL	15A9 MAb	GP		bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
28322	4	8355	6	13	NULL	NULL	NULL	1F2 MAb	GP		bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
28323	5	8355	6	13	NULL	NULL	NULL	3G1 MAb	GP		bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
28324	6	8355	6	13	NULL	NULL	NULL	8C9 MAb	GP		does not bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
28325	7	8355	6	13	NULL	NULL	NULL	7C9	GP		does not bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
28326	8	8355	6	13	NULL	NULL	NULL	13A8	GP		does not bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
28327	9	8355	6	13	NULL	NULL	NULL	23H4	GP		does not bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
28328	10	8355	6	13	NULL	NULL	NULL	8G10	GP		does not bind					E1 antigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34649	1	8355	7	NULL	NULL	0	NULL	18A9 MAb	NULL		bind	NULL				E1 antigen	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34650	2	8355	7	NULL	NULL	0	NULL	21C3 MAb	NULL		bind	NULL				E1 antigen	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34651	3	8355	7	NULL	NULL	0	NULL	15A9 MAb	NULL		bind	NULL				E1 antigen	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34652	4	8355	7	NULL	NULL	0	NULL	 1F2 MAb	NULL		bind	NULL				E1 antigen	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34653	5	8355	7	NULL	NULL	0	NULL	3G1MAb	NULL		bind	NULL				E1 antigen	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34654	6	8355	7	NULL	NULL	0	NULL	8C9 MAb	NULL		does not bind	NULL				E1 antigen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34655	7	8355	7	NULL	NULL	0	NULL	7C9 MAb	NULL		does not bind	NULL				E1 antigen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34656	8	8355	7	NULL	NULL	0	NULL	13A8MAb	NULL		does not bind	NULL				E1 antigen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34657	9	8355	7	NULL	NULL	0	NULL	23H4 MAb	NULL		does not bind	NULL				E1 antigen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
34658	10	8355	7	NULL	NULL	0	NULL	8G10 MAb	NULL		does not bind	NULL				E1 antigen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19744_s_152	7649984	5 of these 10 MAbs bound the E1 antigen (18A9, 21C3, 15A9,  1F2, and 3G1), while 5 did not (8C9, 7C9, 13A8, 23H4, and 8G10).	bind
28329	1	8356	6	13	NULL	NULL	NULL	L5 protein	GP	rat	bind					5S rRNA	NucleicAcid	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_16_12061_s_130	10766838	5 S rRNA Binding Characteristics of Wild-type and Mutant L5 Proteins-- The binding of rat L5 protein to human 5 S rRNA has been investigated previously ( 29).	bind
34659	1	8356	7	10	NULL	0	NULL	L5 protein	NULL	rat	bind	NULL				5 S rRNA	NULL	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_16_12061_s_130	10766838	5 S rRNA Binding Characteristics of Wild-type and Mutant L5 Proteins-- The binding of rat L5 protein to human 5 S rRNA has been investigated previously ( 29).	bind
28421	1	8358	6	13	NULL	NULL	NULL	5 S rRNA	NucleicAcid		bind					TFIIIA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_47_33198_s_15	10559190	5 S rRNA binds not only to TFIIIA but also to ribosomal protein L5.	bind
28423	2	8358	6	13	NULL	NULL	NULL	5 S rRNA	NucleicAcid		bind					L5 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_47_33198_s_15	10559190	5 S rRNA binds not only to TFIIIA but also to ribosomal protein L5.	bind
46875	3	8358	6	13	NULL	NULL	NULL	L5	GP		is a type of					ribosomal protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_47_33198_s_15	10559190	5 S rRNA binds not only to TFIIIA but also to ribosomal protein L5.	bind
34661	1	8358	7	NULL	NULL	0	NULL	TFIIIA	NULL		bind	NULL				5 S rRNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33198_s_15	10559190	5 S rRNA binds not only to TFIIIA but also to ribosomal protein L5.	bind
34662	2	8358	7	NULL	NULL	0	NULL	L5	NULL		bind	NULL				5 S rRNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33198_s_15	10559190	5 S rRNA binds not only to TFIIIA but also to ribosomal protein L5.	bind
34663	3	8358	7	NULL	NULL	0	NULL	L5	NULL		is a type of	NULL				ribosomal protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33198_s_15	10559190	5 S rRNA binds not only to TFIIIA but also to ribosomal protein L5.	bind
28426	1	8359	6	13	NULL	NULL	NULL	5 S rRNA gene	NucleicAcid		bind					TFIIIA	GP	partially proteolyzed			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_4_2539_s_150	9891026	5 S rRNA gene binding and transcriptional activation properties of partially proteolyzed TFIIIA.	bind
28427	2	8359	6	13	NULL	NULL	NULL	5 S rRNA gene	NucleicAcid		activates		transcriptionaly			TFIIIA	GP	partially proteolyzed			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_4_2539_s_150	9891026	5 S rRNA gene binding and transcriptional activation properties of partially proteolyzed TFIIIA.	bind
34664	1	8359	7	NULL	NULL	0	NULL	TFIIIA	NULL	partially proteolyzed	bind	NULL				5 S rRNA gene	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_4_2539_s_150	9891026	5 S rRNA gene binding and transcriptional activation properties of partially proteolyzed TFIIIA.	bind
34665	2	8359	7	10	NULL	0	NULL	5 S rRNA gene	NULL		activates	NULL	transcriptionaly 			TFIIIA	NULL	partially proteolyzed			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_4_2539_s_150	9891026	5 S rRNA gene binding and transcriptional activation properties of partially proteolyzed TFIIIA.	bind
28430	1	8360	6	13	NULL	NULL	NULL	rpL1 	GP		bind			carboxyl-terminal 47 amino acids		5S rRNA	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_50_30148_s_228	8530422	5 S rRNA-binding Domain in rpL1-HAPrevious  results indicated that a peptide fragment corresponding to the  carboxyl-terminal 47 amino acids of rpL1 can bind 5 S rRNA  in vitro  (Nazar  et al., 1979; Yaguchi  et al., 1984).	bind
34666	1	8360	7	NULL	NULL	0	NULL	rpL1	NULL		bind	NULL		carboxyl-terminal 47 amino acids		5 S rRNA	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_270_50_30148_s_228	8530422	5 S rRNA-binding Domain in rpL1-HAPrevious  results indicated that a peptide fragment corresponding to the  carboxyl-terminal 47 amino acids of rpL1 can bind 5 S rRNA  in vitro  (Nazar  et al., 1979; Yaguchi  et al., 1984).	bind
28432	1	8361	6	13	NULL	NULL	NULL	PN-1	GP	secreted	bind		tightly			ECM	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_1_142_s_19	12524238	5 Secreted PN-1 binds tightly to the extracellular matrix (ECM).	bind
28434	2	8361	6	13	NULL	NULL	NULL	ECM	CellComponent		is					extracellular matrix	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_1_142_s_19	12524238	5 Secreted PN-1 binds tightly to the extracellular matrix (ECM).	bind
34667	1	8361	7	10	NULL	0	NULL	PN-1	NULL	secreted	binds	NULL	tightly			ECM	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_1_142_s_19	12524238	5 Secreted PN-1 binds tightly to the extracellular matrix (ECM).	bind
34668	2	8361	7	NULL	NULL	0	NULL	ECM	NULL		is	NULL				extracellular matrix	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_1_142_s_19	12524238	5 Secreted PN-1 binds tightly to the extracellular matrix (ECM).	bind
28436	1	8362	6	13	NULL	NULL	NULL	Ox-PAPC	Chemical		activates					SREBP	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_768_s_27	16497987	5 SREBP activation by Ox-PAPC was maintained for at least 8 hours, and Ox-PAPC treatment also increased binding of SREBP to a novel SRE sequence in the IL-8 promoter.	bind
28437	2	8362	6	13	NULL	NULL	NULL	SREBP	GP		bind					IL-8	GP			SRE sequence of promoter	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_768_s_27	16497987	5 SREBP activation by Ox-PAPC was maintained for at least 8 hours, and Ox-PAPC treatment also increased binding of SREBP to a novel SRE sequence in the IL-8 promoter.	bind
28438	3	8362	6	13	NULL	NULL	NULL	Ox-PAPC	Chemical	treatment of	increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_768_s_27	16497987	5 SREBP activation by Ox-PAPC was maintained for at least 8 hours, and Ox-PAPC treatment also increased binding of SREBP to a novel SRE sequence in the IL-8 promoter.	bind
34669	1	8362	7	NULL	NULL	0	NULL	Ox-PAPC	NULL		activates	NULL				SREBP	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_6_768_s_27	16497987	5 SREBP activation by Ox-PAPC was maintained for at least 8 hours, and Ox-PAPC treatment also increased binding of SREBP to a novel SRE sequence in the IL-8 promoter.	bind
34670	2	8362	7	10	NULL	0	NULL	SREBP 	NULL		bind	NULL				IL-8	NULL			SRE sequence of promoter	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_768_s_27	16497987	5 SREBP activation by Ox-PAPC was maintained for at least 8 hours, and Ox-PAPC treatment also increased binding of SREBP to a novel SRE sequence in the IL-8 promoter.	bind
34671	3	8362	7	10	NULL	0	NULL	Ox-PAPC	NULL	treatment	increase	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_768_s_27	16497987	5 SREBP activation by Ox-PAPC was maintained for at least 8 hours, and Ox-PAPC treatment also increased binding of SREBP to a novel SRE sequence in the IL-8 promoter.	bind
28439	1	8363	6	13	NULL	NULL	NULL	heparin	Chemical		bind					antithrombin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_20_20824_s_393	14996843	5 The  Kd value for the binding of heparin to antithrombin was calculated from the quenching of tryptophan fluorescence emission ( closed circles in  Fig. 8).	bind
34672	1	8363	7	NULL	NULL	0	NULL	heparin	NULL		bind	NULL				antithrombin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_20_20824_s_393	14996843	5 The  Kd value for the binding of heparin to antithrombin was calculated from the quenching of tryptophan fluorescence emission ( closed circles in  Fig. 8).	bind
28440	1	8364	6	13	NULL	NULL	NULL	quinidine	Chemical		bind							mutant	E216Q		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_46_38617_s_244	16162505	5 The difference spectra reported here for quinidine binding to the E216Q and E216A mutants appear to be different from those reported by Guengerich  et al. ( ).	bind
28441	2	8364	6	13	NULL	NULL	NULL	quinidine	Chemical		bind							mutant	E216A		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_46_38617_s_244	16162505	5 The difference spectra reported here for quinidine binding to the E216Q and E216A mutants appear to be different from those reported by Guengerich  et al. ( ).	bind
34673	1	8364	7	NULL	NULL	0	NULL	quinidine	NULL		bind	NULL					NULL	mutant	E216Q		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_46_38617_s_244	16162505	5 The difference spectra reported here for quinidine binding to the E216Q and E216A mutants appear to be different from those reported by Guengerich  et al. ( ).	bind
34674	2	8364	7	NULL	NULL	0	NULL	quinidine	NULL		bind	NULL					NULL	mutant	 E216A 		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_46_38617_s_244	16162505	5 The difference spectra reported here for quinidine binding to the E216Q and E216A mutants appear to be different from those reported by Guengerich  et al. ( ).	bind
28442	1	8365	6	13	NULL	NULL	NULL	SRF	GP		is					serum response factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_8_858_s_21	11988486	5 The serum response factor (SRF) binds to the CArG box.	bind
28443	2	8365	6	13	NULL	NULL	NULL	SRF	GP		bind									CArG box	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_8_858_s_21	11988486	5 The serum response factor (SRF) binds to the CArG box.	bind
34675	1	8365	7	NULL	NULL	0	NULL	SRF	NULL		binds to	NULL					NULL			 CArG box	NULL		0	NULL	NULL	NULL	gw60_circulationres_90_8_858_s_21	11988486	5 The serum response factor (SRF) binds to the CArG box.	bind
34676	2	8365	7	NULL	NULL	0	NULL	SRF	NULL		is	NULL				serum response factor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_8_858_s_21	11988486	5 The serum response factor (SRF) binds to the CArG box.	bind
28446	1	8366	6	13	NULL	NULL	NULL	ETF	GP	oxidized	bind					TMADH	GP	oxidized			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_17_12546_s_253	10777543	5 The slight difference seen between the observed and calculated difference spectra is most likely a result of the minor spectral perturbation associated with binding of ETF to TMADH, which is known to occur when the oxidized form of the two proteins bind to each other.	bind
34677	1	8366	7	NULL	NULL	0	NULL	ETF	NULL	Oxidized	bind	NULL				TMADH	NULL	Oxidized			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_17_12546_s_253	10777543	5 The slight difference seen between the observed and calculated difference spectra is most likely a result of the minor spectral perturbation associated with binding of ETF to TMADH, which is known to occur when the oxidized form of the two proteins bind to each other.	bind
28448	1	8367	6	13	NULL	NULL	NULL	MHCI	GP		bind					LILRA5	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_28_19536_s_152	16675463	5 These changes would be likely to inhibit MHCI binding to LILRA5 ( Fig. 3).	bind
34678	1	8367	7	NULL	NULL	0	NULL	MHCI	NULL		bind	NULL				LILRA5	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_28_19536_s_152	16675463	5 These changes would be likely to inhibit MHCI binding to LILRA5 ( Fig. 3).	bind
28449	1	8368	6	13	NULL	NULL	NULL	C-Raf kinase	GP		bind		high affinity			phosphospecific antibody	GP		Ser-621		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_14074_s_188	14688280	5 These results reflect a high affinity binding between C-Raf kinase and Ser-621 phosphospecific antibody.	bind
34679	1	8368	7	NULL	NULL	0	NULL	C-Raf kinase	NULL		bind	NULL	high affinity			phosphospecific antibody	NULL		Ser-621		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_14_14074_s_188	14688280	5 These results reflect a high affinity binding between C-Raf kinase and Ser-621 phosphospecific antibody.	bind
28452	1	8369	6	13	NULL	NULL	NULL	Sp1	GP		induces					SMC genes	GP	repression of 			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_156	15486317	5 These results suggest that Sp1-induced repression of SMC genes may not be a simple function of binding of Sp1 to the G/C repressor and subsequent inhibition of cooperative interactions between CArG elements, as suggested previously by our laboratory.	bind
28454	2	8369	6	13	NULL	NULL	NULL	Sp1	GP		bind									G/C repressor	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_156	15486317	5 These results suggest that Sp1-induced repression of SMC genes may not be a simple function of binding of Sp1 to the G/C repressor and subsequent inhibition of cooperative interactions between CArG elements, as suggested previously by our laboratory.	bind
34680	1	8369	7	10	NULL	0	NULL	Sp1	NULL		bind	NULL					NULL			G/C repressor	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_156	15486317	5 These results suggest that Sp1-induced repression of SMC genes may not be a simple function of binding of Sp1 to the G/C repressor and subsequent inhibition of cooperative interactions between CArG elements, as suggested previously by our laboratory.	bind
34681	2	8369	7	NULL	NULL	0	NULL	Sp1	NULL		induce	NULL				SMC genes	NULL	repression of			NULL		0	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_156	15486317	5 These results suggest that Sp1-induced repression of SMC genes may not be a simple function of binding of Sp1 to the G/C repressor and subsequent inhibition of cooperative interactions between CArG elements, as suggested previously by our laboratory.	bind
28456	1	8370	6	13	NULL	NULL	NULL	SHP-1	GP		bind					TCR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35223_s_134	11435448	5 Unexpectedly, the pace of this SHP-1 binding to the TCR is inversely related to the potency of the TCR ligand used, fast for antagonists and slow for agonists, even though the latter would be expected to be better activators of Lck, enhancing SHP-1 phosphorylation and its recruitment to the TCR.	bind
29018	2	8370	6	13	NULL	NULL	NULL	SHP-1	GP		is recruited to					TCR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35223_s_134	11435448	5 Unexpectedly, the pace of this SHP-1 binding to the TCR is inversely related to the potency of the TCR ligand used, fast for antagonists and slow for agonists, even though the latter would be expected to be better activators of Lck, enhancing SHP-1 phosphorylation and its recruitment to the TCR.	bind
29019	3	8370	6	13	NULL	NULL	NULL	TCR ligand antagonist	Chemical		increases					statement 1	Process	pace of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35223_s_134	11435448	5 Unexpectedly, the pace of this SHP-1 binding to the TCR is inversely related to the potency of the TCR ligand used, fast for antagonists and slow for agonists, even though the latter would be expected to be better activators of Lck, enhancing SHP-1 phosphorylation and its recruitment to the TCR.	bind
29020	4	8370	6	13	NULL	NULL	NULL	TCR ligand agonist	Chemical		decreases					statement 1	Process	pace of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35223_s_134	11435448	5 Unexpectedly, the pace of this SHP-1 binding to the TCR is inversely related to the potency of the TCR ligand used, fast for antagonists and slow for agonists, even though the latter would be expected to be better activators of Lck, enhancing SHP-1 phosphorylation and its recruitment to the TCR.	bind
29021	5	8370	6	13	NULL	NULL	NULL	TCR ligand agonist	Chemical		activates		might			Lck	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35223_s_134	11435448	5 Unexpectedly, the pace of this SHP-1 binding to the TCR is inversely related to the potency of the TCR ligand used, fast for antagonists and slow for agonists, even though the latter would be expected to be better activators of Lck, enhancing SHP-1 phosphorylation and its recruitment to the TCR.	bind
29022	6	8370	6	13	NULL	NULL	NULL	statement 5	Process		enhances					SHP-1	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35223_s_134	11435448	5 Unexpectedly, the pace of this SHP-1 binding to the TCR is inversely related to the potency of the TCR ligand used, fast for antagonists and slow for agonists, even though the latter would be expected to be better activators of Lck, enhancing SHP-1 phosphorylation and its recruitment to the TCR.	bind
29023	7	8370	6	13	NULL	NULL	NULL	statement 6	Process		enhances					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35223_s_134	11435448	5 Unexpectedly, the pace of this SHP-1 binding to the TCR is inversely related to the potency of the TCR ligand used, fast for antagonists and slow for agonists, even though the latter would be expected to be better activators of Lck, enhancing SHP-1 phosphorylation and its recruitment to the TCR.	bind
34683	1	8370	7	NULL	NULL	0	NULL	SHP-1	NULL		bind	NULL				TCR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_38_35223_s_134	11435448	5 Unexpectedly, the pace of this SHP-1 binding to the TCR is inversely related to the potency of the TCR ligand used, fast for antagonists and slow for agonists, even though the latter would be expected to be better activators of Lck, enhancing SHP-1 phosphorylation and its recruitment to the TCR.	bind
34685	3	8370	7	10	NULL	0	NULL	TCR ligand agonists	NULL		activate	NULL				Lck	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35223_s_134	11435448	5 Unexpectedly, the pace of this SHP-1 binding to the TCR is inversely related to the potency of the TCR ligand used, fast for antagonists and slow for agonists, even though the latter would be expected to be better activators of Lck, enhancing SHP-1 phosphorylation and its recruitment to the TCR.	bind
34686	4	8370	7	NULL	NULL	0	NULL	statement 3	NULL		enhance	NULL				SHP-1	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_38_35223_s_134	11435448	5 Unexpectedly, the pace of this SHP-1 binding to the TCR is inversely related to the potency of the TCR ligand used, fast for antagonists and slow for agonists, even though the latter would be expected to be better activators of Lck, enhancing SHP-1 phosphorylation and its recruitment to the TCR.	bind
34687	5	8370	7	10	NULL	0	NULL	statement 3	NULL		enhance	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35223_s_134	11435448	5 Unexpectedly, the pace of this SHP-1 binding to the TCR is inversely related to the potency of the TCR ligand used, fast for antagonists and slow for agonists, even though the latter would be expected to be better activators of Lck, enhancing SHP-1 phosphorylation and its recruitment to the TCR.	bind
46876	2	8370	7	10	NULL	0	NULL	SHP-1	NULL		is recruited to	NULL				TCR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_38_35223_s_134	11435448	5 Unexpectedly, the pace of this SHP-1 binding to the TCR is inversely related to the potency of the TCR ligand used, fast for antagonists and slow for agonists, even though the latter would be expected to be better activators of Lck, enhancing SHP-1 phosphorylation and its recruitment to the TCR.	bind
46877	6	8370	7	10	NULL	0	NULL	TCR ligand antagonist	NULL		increases	NULL				statement 1	NULL	pace of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_38_35223_s_134	11435448	5 Unexpectedly, the pace of this SHP-1 binding to the TCR is inversely related to the potency of the TCR ligand used, fast for antagonists and slow for agonists, even though the latter would be expected to be better activators of Lck, enhancing SHP-1 phosphorylation and its recruitment to the TCR.	bind
46878	7	8370	7	10	NULL	0	NULL	TCR ligand agonist	NULL		decreases	NULL				statement 1	NULL	pace of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_38_35223_s_134	11435448	5 Unexpectedly, the pace of this SHP-1 binding to the TCR is inversely related to the potency of the TCR ligand used, fast for antagonists and slow for agonists, even though the latter would be expected to be better activators of Lck, enhancing SHP-1 phosphorylation and its recruitment to the TCR.	bind
28457	1	8371	6	13	NULL	NULL	NULL	actin capping protein	GP		bind					actin filaments	GP	barbed ends of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_26	14976140	5 Whereas both populations of actin capping protein bind the barbed ends of actin filaments with equal affinities and kinetics 6 the function of beta1-containing actin capping protein is to anchor sarcomeric actin to Z-disc.	bind
28458	2	8371	6	13	NULL	NULL	NULL	actin	GP	sarcomeric	is anchored to					Z-disc	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_26	14976140	5 Whereas both populations of actin capping protein bind the barbed ends of actin filaments with equal affinities and kinetics 6 the function of beta1-containing actin capping protein is to anchor sarcomeric actin to Z-disc.	bind
28459	4	8371	6	13	NULL	NULL	NULL	statement 3	Process		performs					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_26	14976140	5 Whereas both populations of actin capping protein bind the barbed ends of actin filaments with equal affinities and kinetics 6 the function of beta1-containing actin capping protein is to anchor sarcomeric actin to Z-disc.	bind
46883	3	8371	6	13	NULL	NULL	NULL	actin capping protein	GP		contains					beta1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_26	14976140	5 Whereas both populations of actin capping protein bind the barbed ends of actin filaments with equal affinities and kinetics 6 the function of beta1-containing actin capping protein is to anchor sarcomeric actin to Z-disc.	bind
34688	1	8371	7	10	NULL	0	NULL	actin capping protein	NULL		bind	NULL				actin filaments	NULL	barbed ends of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_26	14976140	5 Whereas both populations of actin capping protein bind the barbed ends of actin filaments with equal affinities and kinetics 6 the function of beta1-containing actin capping protein is to anchor sarcomeric actin to Z-disc.	bind
34689	2	8371	7	10	NULL	0	NULL	actin	NULL	sarcomeric	bind	NULL				Z-disc	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_26	14976140	5 Whereas both populations of actin capping protein bind the barbed ends of actin filaments with equal affinities and kinetics 6 the function of beta1-containing actin capping protein is to anchor sarcomeric actin to Z-disc.	bind
34692	4	8371	7	10	NULL	0	NULL	statement 3	NULL		anchor	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_26	14976140	5 Whereas both populations of actin capping protein bind the barbed ends of actin filaments with equal affinities and kinetics 6 the function of beta1-containing actin capping protein is to anchor sarcomeric actin to Z-disc.	bind
46884	3	8371	7	10	NULL	0	NULL	actin capping protein	NULL		contains	NULL				beta1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_3_296_s_26	14976140	5 Whereas both populations of actin capping protein bind the barbed ends of actin filaments with equal affinities and kinetics 6 the function of beta1-containing actin capping protein is to anchor sarcomeric actin to Z-disc.	bind
28460	1	8374	6	13	NULL	NULL	NULL	5' hox genes	GP		is expressed in					epididymis	OrganismPart	adult;; mouse			NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_68_2_644_s_1	12533430	5' hox genes and meis 1, a hox-DNA binding cofactor, are expressed in the adult mouse epididymis.	bind
28461	2	8374	6	13	NULL	NULL	NULL	meis 1	GP		is expressed in					epididymis	OrganismPart	adult;; mouse			NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_68_2_644_s_1	12533430	5' hox genes and meis 1, a hox-DNA binding cofactor, are expressed in the adult mouse epididymis.	bind
28462	3	8374	6	13	NULL	NULL	NULL	meis 1	GP		is a type of					hox-DNA binding cofactor	GP				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_68_2_644_s_1	12533430	5' hox genes and meis 1, a hox-DNA binding cofactor, are expressed in the adult mouse epididymis.	bind
46885	4	8374	6	13	NULL	NULL	NULL	5' hox genes	GP		is a type of					hox-DNA binding cofactor	GP				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_68_2_644_s_1	12533430	5' hox genes and meis 1, a hox-DNA binding cofactor, are expressed in the adult mouse epididymis.	bind
34694	1	8374	7	NULL	NULL	0	NULL	5' hox genes	NULL		is a type of	NULL				 hox-DNA binding cofactor	NULL				NULL		0	NULL	NULL	NULL	gw70_biolreprod_68_2_644_s_1	12533430	5' hox genes and meis 1, a hox-DNA binding cofactor, are expressed in the adult mouse epididymis.	bind
34695	2	8374	7	NULL	NULL	0	NULL	meis 1	NULL		is a type of	NULL				hox-DNA binding cofactor	NULL				NULL		0	NULL	NULL	NULL	gw70_biolreprod_68_2_644_s_1	12533430	5' hox genes and meis 1, a hox-DNA binding cofactor, are expressed in the adult mouse epididymis.	bind
34696	3	8374	7	10	NULL	0	NULL	5' hox genes	NULL		is expressed in	NULL				epididymis	NULL	adult;;mouse			NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_68_2_644_s_1	12533430	5' hox genes and meis 1, a hox-DNA binding cofactor, are expressed in the adult mouse epididymis.	bind
34697	4	8374	7	10	NULL	0	NULL	meis 1	NULL		is expressed in	NULL				epididymis	NULL	adult;;mouse			NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_68_2_644_s_1	12533430	5' hox genes and meis 1, a hox-DNA binding cofactor, are expressed in the adult mouse epididymis.	bind
29024	1	8377	6	13	NULL	NULL	NULL	ADP complex	GP		occupies			beta-phosphate					P1 subsite		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_15009_s_256	11154698	5''-ADP complex it is the beta-phosphate rather than the alpha-phosphate that occupies the P1 subsite while the adenosine binds close to the EDN pyrimidine binding subsite B1.	bind
29025	2	8377	6	13	NULL	NULL	NULL	ADP complex	GP		bind			adenosine		EDN 	GP		pyrimidine binding subsite B1		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_15009_s_256	11154698	5''-ADP complex it is the beta-phosphate rather than the alpha-phosphate that occupies the P1 subsite while the adenosine binds close to the EDN pyrimidine binding subsite B1.	bind
34871	1	8377	7	NULL	NULL	0	NULL	 adenosine	NULL		binds	NULL				 EDN	NULL		close to pyrimidine binding subsite B1		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_18_15009_s_256	11154698	5''-ADP complex it is the beta-phosphate rather than the alpha-phosphate that occupies the P1 subsite while the adenosine binds close to the EDN pyrimidine binding subsite B1.	bind
34872	2	8377	7	NULL	NULL	0	NULL	5''-ADP complex	NULL		occupies the	NULL		 beta-phosphate			NULL		P1 subsite		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_18_15009_s_256	11154698	5''-ADP complex it is the beta-phosphate rather than the alpha-phosphate that occupies the P1 subsite while the adenosine binds close to the EDN pyrimidine binding subsite B1.	bind
34873	3	8377	7	NULL	NULL	0	NULL	5''-ADP complex	NULL		does not occupy	NULL		alpha-phosphate			NULL		P1 subsite		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_15009_s_256	11154698	5''-ADP complex it is the beta-phosphate rather than the alpha-phosphate that occupies the P1 subsite while the adenosine binds close to the EDN pyrimidine binding subsite B1.	bind
28463	1	8378	6	13	NULL	NULL	NULL	transcription factor	GP	novel	bind					SR-BI	GP			myeloid zing finger protein-1-like element (-476 to -456) of promoter	NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_j-biol-chem_276_50_11585816_s_11	11585816	5''-Deletion analysis  and gel shift data suggest that LPS inhibits binding of a novel transcription  factor to a myeloid zing finger protein-1-like element (-476 to -456)  in the human SR-BI promoter.	bind
28464	2	8378	6	13	NULL	NULL	NULL	LPS	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_j-biol-chem_276_50_11585816_s_11	11585816	5''-Deletion analysis  and gel shift data suggest that LPS inhibits binding of a novel transcription  factor to a myeloid zing finger protein-1-like element (-476 to -456)  in the human SR-BI promoter.	bind
34874	1	8378	7	10	NULL	0	NULL	transcription factor	NULL	novel	bind	NULL				SR-BI 	NULL	human		 myeloid zing finger protein-1-like element -476 to -456 in the promoter	NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_j-biol-chem_276_50_11585816_s_11	11585816	5''-Deletion analysis  and gel shift data suggest that LPS inhibits binding of a novel transcription  factor to a myeloid zing finger protein-1-like element (-476 to -456)  in the human SR-BI promoter.	bind
34875	2	8378	7	NULL	NULL	0	NULL	LPS	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0550-0559_j-biol-chem_276_50_11585816_s_11	11585816	5''-Deletion analysis  and gel shift data suggest that LPS inhibits binding of a novel transcription  factor to a myeloid zing finger protein-1-like element (-476 to -456)  in the human SR-BI promoter.	bind
47526	1	8380	6	13	NULL	NULL	NULL	5''-GTP	Chemical		bind			purine N1 nitrogen		[4Fe - 4] cluster 	GP		Fe site of the C-terminal		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_18_6829_s_98	16632608	5''-GTP binds with its purine N1 nitrogen (2.8- Ang  distance) and its exocyclic amino group (2.4- Ang  distance) in an unprecedented manner to the unique Fe site of the C-terminal [4Fe - 4] cluster ( Fig. 3 A and  C).	bind
47528	2	8380	6	13	NULL	NULL	NULL	5''-GTP	Chemical		bind			exocyclic amino group		[4Fe - 4] cluster	GP		Fe site of the C-terminal		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_18_6829_s_98	16632608	5''-GTP binds with its purine N1 nitrogen (2.8- Ang  distance) and its exocyclic amino group (2.4- Ang  distance) in an unprecedented manner to the unique Fe site of the C-terminal [4Fe - 4] cluster ( Fig. 3 A and  C).	bind
34876	1	8380	7	NULL	NULL	0	NULL	5''-GTP	NULL		bind	NULL		purine N1 nitrogen		 [4Fe - 4] cluster	NULL		unique Fe site of the C-terminal		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_18_6829_s_98	16632608	5''-GTP binds with its purine N1 nitrogen (2.8- Ang  distance) and its exocyclic amino group (2.4- Ang  distance) in an unprecedented manner to the unique Fe site of the C-terminal [4Fe - 4] cluster ( Fig. 3 A and  C).	bind
34878	3	8380	7	NULL	NULL	0	NULL	5''-GTP 	NULL		bind	NULL		exocyclic amino group 		[4Fe - 4] cluster	NULL		unique Fe site of the C-terminal		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_18_6829_s_98	16632608	5''-GTP binds with its purine N1 nitrogen (2.8- Ang  distance) and its exocyclic amino group (2.4- Ang  distance) in an unprecedented manner to the unique Fe site of the C-terminal [4Fe - 4] cluster ( Fig. 3 A and  C).	bind
28545	1	8381	6	13	NULL	NULL	NULL	tau molecule	GP		bind					MTs	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_252	10464280	5) As long as the tau kinases and phosphatases remain in proper balance, the phosphorylation state of tau will remain within limits that favor binding of tau molecules to MTs, as opposed to other tau molecules.	bind
28550	2	8381	6	13	NULL	NULL	NULL	statement 1	Process		is dependent on					tau molecules	GP	phosphorylation state of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_252	10464280	5) As long as the tau kinases and phosphatases remain in proper balance, the phosphorylation state of tau will remain within limits that favor binding of tau molecules to MTs, as opposed to other tau molecules.	bind
34879	1	8381	7	NULL	NULL	0	NULL	 tau molecules	NULL		bind	NULL				MTs	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_252	10464280	5) As long as the tau kinases and phosphatases remain in proper balance, the phosphorylation state of tau will remain within limits that favor binding of tau molecules to MTs, as opposed to other tau molecules.	bind
34880	2	8381	7	NULL	NULL	0	NULL	tau	NULL	 phosphorylation of	favor	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_36_25490_s_252	10464280	5) As long as the tau kinases and phosphatases remain in proper balance, the phosphorylation state of tau will remain within limits that favor binding of tau molecules to MTs, as opposed to other tau molecules.	bind
28559	1	8382	6	13	NULL	NULL	NULL	p47 phox	GP		bind					p22 phox peptides	GP		proline rich		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_13	11733522	5) Binding of both p47 phox and p67 phox to proline-rich p22 phox peptides occurs in the absence of an anionic amphiphile.	bind
28560	2	8382	6	13	NULL	NULL	NULL	p67 phox	GP		bind					p22 phox peptides	GP		proline rich		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_13	11733522	5) Binding of both p47 phox and p67 phox to proline-rich p22 phox peptides occurs in the absence of an anionic amphiphile.	bind
28561	3	8382	6	13	NULL	NULL	NULL	statement 1	Process		occurs in absence of					anionic amphiphile	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_13	11733522	5) Binding of both p47 phox and p67 phox to proline-rich p22 phox peptides occurs in the absence of an anionic amphiphile.	bind
28562	4	8382	6	13	NULL	NULL	NULL	statement 2	Process		occurs in absence of					anionic amphiphile	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_13	11733522	5) Binding of both p47 phox and p67 phox to proline-rich p22 phox peptides occurs in the absence of an anionic amphiphile.	bind
34881	1	8382	7	NULL	NULL	0	NULL	p47 phox 	NULL		bind	NULL				p22 phox peptides	NULL		 proline-rich		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_13	11733522	5) Binding of both p47 phox and p67 phox to proline-rich p22 phox peptides occurs in the absence of an anionic amphiphile.	bind
34882	2	8382	7	NULL	NULL	0	NULL	p67 phox	NULL		bind	NULL				p22 phox peptides	NULL		proline-rich		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_13	11733522	5) Binding of both p47 phox and p67 phox to proline-rich p22 phox peptides occurs in the absence of an anionic amphiphile.	bind
34883	3	8382	7	NULL	NULL	0	NULL	statement 1	NULL		in absence of	NULL				anionic amphiphile	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_13	11733522	5) Binding of both p47 phox and p67 phox to proline-rich p22 phox peptides occurs in the absence of an anionic amphiphile.	bind
34884	4	8382	7	NULL	NULL	0	NULL	statement 2	NULL		in absence of	NULL				anionic amphiphile	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_13	11733522	5) Binding of both p47 phox and p67 phox to proline-rich p22 phox peptides occurs in the absence of an anionic amphiphile.	bind
28563	1	8384	6	13	NULL	NULL	NULL	hsp70	GP		bind					K8/18	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_915_s_209	7529764	5) Binding of hsp70 to K8/18 does not significantly  affect filament assembly  in vitro.	bind
28564	2	8384	6	13	NULL	NULL	NULL	statement 1	Process		does not affect		significantly			filament assembly	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_915_s_209	7529764	5) Binding of hsp70 to K8/18 does not significantly  affect filament assembly  in vitro.	bind
34885	1	8384	7	NULL	NULL	0	NULL	hsp70	NULL		bind	NULL				K8/18	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_270_2_915_s_209	7529764	5) Binding of hsp70 to K8/18 does not significantly  affect filament assembly  in vitro.	bind
34886	2	8384	7	NULL	NULL	0	NULL	statement 1	NULL		does not affect	NULL	significantly			filament assembly	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_270_2_915_s_209	7529764	5) Binding of hsp70 to K8/18 does not significantly  affect filament assembly  in vitro.	bind
28565	1	8385	6	13	NULL	NULL	NULL	InsP(3)R1	GP		bind			SII(+) coupling domain splice variant		AKAP9	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_19375_s_16	14982933	5) Both the SII(+) and the SII(-) coupling domain splice variants of InsP3R1 bind to AKAP9.	bind
28566	2	8385	6	13	NULL	NULL	NULL	InsP(3)R1	GP		bind			SII(-) coupling domain splice variant		AKAP9	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_19375_s_16	14982933	5) Both the SII(+) and the SII(-) coupling domain splice variants of InsP3R1 bind to AKAP9.	bind
34887	1	8385	7	NULL	NULL	0	NULL	InsP3R1	NULL		bind	NULL		SII(+) coupling domain		AKAP9	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_19375_s_16	14982933	5) Both the SII(+) and the SII(-) coupling domain splice variants of InsP3R1 bind to AKAP9.	bind
34888	2	8385	7	NULL	NULL	0	NULL	InsP3R1 	NULL		bind	NULL		SII(-) coupling domain		AKAP9	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_19375_s_16	14982933	5) Both the SII(+) and the SII(-) coupling domain splice variants of InsP3R1 bind to AKAP9.	bind
28567	1	8386	6	13	NULL	NULL	NULL	ANP	GP		induce		specifically			iNOS mRNA	NucleicAcid	acceleration of;;decay of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_13444_s_8	9593677	5) Importantly, two basic mechanisms seem to be responsible for this observation,  i.e. ANP specifically induced acceleration of iNOS mRNA decay and ANP reduced binding activity of NF-kappaB, the transcription factor predominantly responsible for LPS-induced iNOS expression in murine macrophages.	bind
28568	2	8386	6	13	NULL	NULL	NULL	ANP	GP		reduce					NF-kappaB	GP	binding activity of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_13444_s_8	9593677	5) Importantly, two basic mechanisms seem to be responsible for this observation,  i.e. ANP specifically induced acceleration of iNOS mRNA decay and ANP reduced binding activity of NF-kappaB, the transcription factor predominantly responsible for LPS-induced iNOS expression in murine macrophages.	bind
28569	3	8386	6	13	NULL	NULL	NULL	NF-kappaB	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_13444_s_8	9593677	5) Importantly, two basic mechanisms seem to be responsible for this observation,  i.e. ANP specifically induced acceleration of iNOS mRNA decay and ANP reduced binding activity of NF-kappaB, the transcription factor predominantly responsible for LPS-induced iNOS expression in murine macrophages.	bind
28570	4	8386	6	13	NULL	NULL	NULL	LPS	Chemical		induces					iNOS 	GP	expression of			NULL	murine macrophages	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_13444_s_8	9593677	5) Importantly, two basic mechanisms seem to be responsible for this observation,  i.e. ANP specifically induced acceleration of iNOS mRNA decay and ANP reduced binding activity of NF-kappaB, the transcription factor predominantly responsible for LPS-induced iNOS expression in murine macrophages.	bind
28571	5	8386	6	13	NULL	NULL	NULL	NF-kappaB	GP		is responsible for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_13444_s_8	9593677	5) Importantly, two basic mechanisms seem to be responsible for this observation,  i.e. ANP specifically induced acceleration of iNOS mRNA decay and ANP reduced binding activity of NF-kappaB, the transcription factor predominantly responsible for LPS-induced iNOS expression in murine macrophages.	bind
34889	1	8386	7	10	NULL	0	NULL	ANP	NULL		induce	NULL	specifically			iNOS mRNA	NULL	acceleration of;;decay of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_13444_s_8	9593677	5) Importantly, two basic mechanisms seem to be responsible for this observation,  i.e. ANP specifically induced acceleration of iNOS mRNA decay and ANP reduced binding activity of NF-kappaB, the transcription factor predominantly responsible for LPS-induced iNOS expression in murine macrophages.	bind
34890	2	8386	7	NULL	NULL	0	NULL	ANP	NULL		reduce	NULL				NF-kappaB	NULL	binding activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_22_13444_s_8	9593677	5) Importantly, two basic mechanisms seem to be responsible for this observation,  i.e. ANP specifically induced acceleration of iNOS mRNA decay and ANP reduced binding activity of NF-kappaB, the transcription factor predominantly responsible for LPS-induced iNOS expression in murine macrophages.	bind
34891	3	8386	7	NULL	NULL	0	NULL	LPS	NULL		induce	NULL				iNOS	NULL	expression of			NULL	murine macrophages	0	NULL	NULL	NULL	gw60_jbiolchem_273_22_13444_s_8	9593677	5) Importantly, two basic mechanisms seem to be responsible for this observation,  i.e. ANP specifically induced acceleration of iNOS mRNA decay and ANP reduced binding activity of NF-kappaB, the transcription factor predominantly responsible for LPS-induced iNOS expression in murine macrophages.	bind
34892	4	8386	7	NULL	NULL	0	NULL	NF-kappaB	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_22_13444_s_8	9593677	5) Importantly, two basic mechanisms seem to be responsible for this observation,  i.e. ANP specifically induced acceleration of iNOS mRNA decay and ANP reduced binding activity of NF-kappaB, the transcription factor predominantly responsible for LPS-induced iNOS expression in murine macrophages.	bind
46891	5	8386	7	10	NULL	0	NULL	NF-kappaB	NULL		is responsible for	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_22_13444_s_8	9593677	5) Importantly, two basic mechanisms seem to be responsible for this observation,  i.e. ANP specifically induced acceleration of iNOS mRNA decay and ANP reduced binding activity of NF-kappaB, the transcription factor predominantly responsible for LPS-induced iNOS expression in murine macrophages.	bind
28572	1	8387	6	13	NULL	NULL	NULL	mannitol	Chemical		bind								C domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_16_12756_s_27	11278734	5) Isothermal titration calorimetry experiments indicated that a significant part of the structural changes upon the binding of mannitol to the C domain reside in the B domain.	bind
34893	1	8387	7	10	NULL	0	NULL	mannitol	NULL		bind	NULL					NULL		C domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_16_12756_s_27	11278734	5) Isothermal titration calorimetry experiments indicated that a significant part of the structural changes upon the binding of mannitol to the C domain reside in the B domain.	bind
28580	1	8388	6	13	NULL	NULL	NULL	FOXO1	GP		bind		directly			PPARgamma2	GP			promoter	NULL	nucleus	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_19881_s_286	16670091	5) Once in the nucleus, FOXO1 binds directly to  the PPARgamma2 promoter via at least one specific DNA sequence encompassing bp 270 - 310.	bind
28581	2	8388	6	13	NULL	NULL	NULL	DNA sequence	NucleicAcid		encompass									bp 270 - 310	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_19881_s_286	16670091	5) Once in the nucleus, FOXO1 binds directly to  the PPARgamma2 promoter via at least one specific DNA sequence encompassing bp 270 - 310.	bind
56149	3	8388	6	13	NULL	NULL	NULL	statement 1	Process		via					statement 2	Process				NULL	nucleus	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_19881_s_286	16670091	5) Once in the nucleus, FOXO1 binds directly to  the PPARgamma2 promoter via at least one specific DNA sequence encompassing bp 270 - 310.	bind
34894	1	8388	7	10	NULL	0	NULL	FOXO1			bind		directly			PPARgamma2				promoter	NULL	nucleus	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_19881_s_286	16670091	5) Once in the nucleus, FOXO1 binds directly to  the PPARgamma2 promoter via at least one specific DNA sequence encompassing bp 270 - 310.	bind
56150	2	8388	7	10	NULL	0	NULL	DNA sequence			encompass									bp 270 - 310	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_29_19881_s_286	16670091	5) Once in the nucleus, FOXO1 binds directly to  the PPARgamma2 promoter via at least one specific DNA sequence encompassing bp 270 - 310.	bind
56151	3	8388	7	10	NULL	0	NULL	statement 1			via					statement 2					NULL	nucleus	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_19881_s_286	16670091	5) Once in the nucleus, FOXO1 binds directly to  the PPARgamma2 promoter via at least one specific DNA sequence encompassing bp 270 - 310.	bind
28582	1	8389	6	13	NULL	NULL	NULL	p66	GP		bind					apoB RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27700_s_203	9346911	5) p66 and p44, previously characterized as simultaneously binding to apoB RNA, are shown here to have independent RNA cross-linking capabilities.	bind
28583	2	8389	6	13	NULL	NULL	NULL	p44	GP		bind					apoB RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27700_s_203	9346911	5) p66 and p44, previously characterized as simultaneously binding to apoB RNA, are shown here to have independent RNA cross-linking capabilities.	bind
28584	3	8389	6	13	NULL	NULL	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27700_s_203	9346911	5) p66 and p44, previously characterized as simultaneously binding to apoB RNA, are shown here to have independent RNA cross-linking capabilities.	bind
46892	4	8389	6	13	NULL	NULL	NULL	p66	GP		is capable of					RNA cross-linking	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27700_s_203	9346911	5) p66 and p44, previously characterized as simultaneously binding to apoB RNA, are shown here to have independent RNA cross-linking capabilities.	bind
46893	5	8389	6	13	NULL	NULL	NULL	p44	GP		is capable of					RNA cross-linking	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27700_s_203	9346911	5) p66 and p44, previously characterized as simultaneously binding to apoB RNA, are shown here to have independent RNA cross-linking capabilities.	bind
46894	6	8389	6	13	NULL	NULL	NULL	statement 4	Process		is independent of					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27700_s_203	9346911	5) p66 and p44, previously characterized as simultaneously binding to apoB RNA, are shown here to have independent RNA cross-linking capabilities.	bind
34895	1	8389	7	NULL	NULL	0	NULL	p66	NULL		bind	NULL				apoB RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27700_s_203	9346911	5) p66 and p44, previously characterized as simultaneously binding to apoB RNA, are shown here to have independent RNA cross-linking capabilities.	bind
34896	2	8389	7	NULL	NULL	0	NULL	p44	NULL		bind	NULL				apoB RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27700_s_203	9346911	5) p66 and p44, previously characterized as simultaneously binding to apoB RNA, are shown here to have independent RNA cross-linking capabilities.	bind
34897	3	8389	7	NULL	NULL	0	NULL	 p66	NULL		capable of	NULL				RNA cross-linking 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27700_s_203	9346911	5) p66 and p44, previously characterized as simultaneously binding to apoB RNA, are shown here to have independent RNA cross-linking capabilities.	bind
34898	4	8389	7	NULL	NULL	0	NULL	p44	NULL		capable of	NULL				RNA cross-linking 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27700_s_203	9346911	5) p66 and p44, previously characterized as simultaneously binding to apoB RNA, are shown here to have independent RNA cross-linking capabilities.	bind
46895	5	8389	7	10	NULL	0	NULL	statement 1	NULL		occurs simultaneously with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27700_s_203	9346911	5) p66 and p44, previously characterized as simultaneously binding to apoB RNA, are shown here to have independent RNA cross-linking capabilities.	bind
46896	6	8389	7	10	NULL	0	NULL	statement 3	NULL		is independent of	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27700_s_203	9346911	5) p66 and p44, previously characterized as simultaneously binding to apoB RNA, are shown here to have independent RNA cross-linking capabilities.	bind
28617	1	8390	6	13	NULL	NULL	NULL	Nek6	GP	recombinant	bind		specifically			Nercc1	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_37_34897_s_267	12840024	5) Recombinant Nek6 binds to endogenous Nercc1  specifically and in a detergent-resistant manner.	bind
28618	2	8390	6	13	NULL	NULL	NULL	statement 1	Process		is resistant to					detergent	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_37_34897_s_267	12840024	5) Recombinant Nek6 binds to endogenous Nercc1  specifically and in a detergent-resistant manner.	bind
34899	1	8390	7	NULL	NULL	0	NULL	Nek6	NULL	recombinant	binds to	NULL	specifically			Nercc1 	NULL	endogenous			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_34897_s_267	12840024	5) Recombinant Nek6 binds to endogenous Nercc1  specifically and in a detergent-resistant manner.	bind
34900	2	8390	7	NULL	NULL	0	NULL	statement 1	NULL		is resistant to	NULL				detergent	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_34897_s_267	12840024	5) Recombinant Nek6 binds to endogenous Nercc1  specifically and in a detergent-resistant manner.	bind
28620	2	8391	6	13	NULL	NULL	NULL	statement 1	Process		occurs via									DNA sequence that encompasses bp 270 - 310	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_19881_s_212	16670091	5) When in the nucleus, FOXO1 binds directly to the PPARgamma2 promoter via a specific DNA sequence that encompasses bp 270 - 310, but probably extends beyond this region (as shown by ChIP).	bind
34901	1	8391	7	NULL	NULL	0	NULL	FOXO1	NULL		binds	NULL	directly			PPARgamma2	NULL			specific DNA sequence that encompasses bp 270 - 310 promoter	NULL	nucleus	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_19881_s_212	16670091	5) When in the nucleus, FOXO1 binds directly to the PPARgamma2 promoter via a specific DNA sequence that encompasses bp 270 - 310, but probably extends beyond this region (as shown by ChIP).	bind
28622	1	8394	6	13	NULL	NULL	NULL	rPC	GP		associates with		physically			37-kd laminin receptor precursor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_94	11073804	5, 6  rPC is reported to physically associate with 37-kd laminin receptor precursor, which binds to the matrix protein laminin and mediates attachment, differentiation, movement, and growth of the cells.	bind
28623	2	8394	6	13	NULL	NULL	NULL	37-kd laminin receptor precursor	GP		bind					laminin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_94	11073804	5, 6  rPC is reported to physically associate with 37-kd laminin receptor precursor, which binds to the matrix protein laminin and mediates attachment, differentiation, movement, and growth of the cells.	bind
28624	3	8394	6	13	NULL	NULL	NULL	laminin	GP		is a type of					matrix protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_94	11073804	5, 6  rPC is reported to physically associate with 37-kd laminin receptor precursor, which binds to the matrix protein laminin and mediates attachment, differentiation, movement, and growth of the cells.	bind
28625	4	8394	6	13	NULL	NULL	NULL	statement 2	Process		mediates					cells	Cell	attachment of 			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_94	11073804	5, 6  rPC is reported to physically associate with 37-kd laminin receptor precursor, which binds to the matrix protein laminin and mediates attachment, differentiation, movement, and growth of the cells.	bind
28626	5	8394	6	13	NULL	NULL	NULL	statement 2	Process		mediates					cells	Cell	differentiation of 			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_94	11073804	5, 6  rPC is reported to physically associate with 37-kd laminin receptor precursor, which binds to the matrix protein laminin and mediates attachment, differentiation, movement, and growth of the cells.	bind
28627	6	8394	6	13	NULL	NULL	NULL	statement 2	Process		mediates					cells	Cell	movement of 			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_94	11073804	5, 6  rPC is reported to physically associate with 37-kd laminin receptor precursor, which binds to the matrix protein laminin and mediates attachment, differentiation, movement, and growth of the cells.	bind
28628	7	8394	6	13	NULL	NULL	NULL	statement 2	Process		mediates					cells	Cell	growth of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_94	11073804	5, 6  rPC is reported to physically associate with 37-kd laminin receptor precursor, which binds to the matrix protein laminin and mediates attachment, differentiation, movement, and growth of the cells.	bind
34907	1	8394	7	NULL	NULL	0	NULL	rPC	NULL		associate with	NULL	physically			37-kd laminin receptor precursor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_94	11073804	5, 6  rPC is reported to physically associate with 37-kd laminin receptor precursor, which binds to the matrix protein laminin and mediates attachment, differentiation, movement, and growth of the cells.	bind
34908	2	8394	7	NULL	NULL	0	NULL	37-kd laminin receptor precursor	NULL		binds to	NULL				laminin	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_94	11073804	5, 6  rPC is reported to physically associate with 37-kd laminin receptor precursor, which binds to the matrix protein laminin and mediates attachment, differentiation, movement, and growth of the cells.	bind
34909	3	8394	7	NULL	NULL	0	NULL	laminin	NULL		is a type of	NULL				matrix protein	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_94	11073804	5, 6  rPC is reported to physically associate with 37-kd laminin receptor precursor, which binds to the matrix protein laminin and mediates attachment, differentiation, movement, and growth of the cells.	bind
34910	4	8394	7	10	NULL	0	NULL	statement 2	NULL		mediates	NULL				cells	NULL	attachment of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_94	11073804	5, 6  rPC is reported to physically associate with 37-kd laminin receptor precursor, which binds to the matrix protein laminin and mediates attachment, differentiation, movement, and growth of the cells.	bind
34911	5	8394	7	10	NULL	0	NULL	statement 2	NULL		mediates	NULL				cells	NULL	differentiation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_94	11073804	5, 6  rPC is reported to physically associate with 37-kd laminin receptor precursor, which binds to the matrix protein laminin and mediates attachment, differentiation, movement, and growth of the cells.	bind
34912	6	8394	7	10	NULL	0	NULL	statement 2	NULL		mediates	NULL				cells	NULL	movement of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_94	11073804	5, 6  rPC is reported to physically associate with 37-kd laminin receptor precursor, which binds to the matrix protein laminin and mediates attachment, differentiation, movement, and growth of the cells.	bind
34913	7	8394	7	10	NULL	0	NULL	statement 2	NULL		mediates	NULL				cells	NULL	growth of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_5_1447_s_94	11073804	5, 6  rPC is reported to physically associate with 37-kd laminin receptor precursor, which binds to the matrix protein laminin and mediates attachment, differentiation, movement, and growth of the cells.	bind
28629	1	8395	6	13	NULL	NULL	NULL	IGF-1	GP		bind					cell-surface receptor	GP	specific			NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_17_2088_s_22	11673351	5, 6 Binding of IGF-I to its specific cell-surface receptor results in activation of an intracytoplasmatic tyrosin kinase, which phosphorylates insulin receptor substrate-1.	bind
28630	2	8395	6	13	NULL	NULL	NULL	statement 1	Process		results in					tyrosin kinase	GP	activation of;;intracytoplasmatic			NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_17_2088_s_22	11673351	5, 6 Binding of IGF-I to its specific cell-surface receptor results in activation of an intracytoplasmatic tyrosin kinase, which phosphorylates insulin receptor substrate-1.	bind
28631	3	8395	6	13	NULL	NULL	NULL	tyrosin kinase	GP	intracytoplasmatic	phosphorylates					insulin receptor substrate-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_17_2088_s_22	11673351	5, 6 Binding of IGF-I to its specific cell-surface receptor results in activation of an intracytoplasmatic tyrosin kinase, which phosphorylates insulin receptor substrate-1.	bind
34914	1	8395	7	10	NULL	0	NULL	IGF-I	NULL		bind	NULL				cell-surface receptor	NULL	specific			NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_17_2088_s_22	11673351	5, 6 Binding of IGF-I to its specific cell-surface receptor results in activation of an intracytoplasmatic tyrosin kinase, which phosphorylates insulin receptor substrate-1.	bind
34915	2	8395	7	10	NULL	0	NULL	statement 1	NULL		results in	NULL				tyrosine kinase	NULL	activation of;;intracytoplasmatic			NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_17_2088_s_22	11673351	5, 6 Binding of IGF-I to its specific cell-surface receptor results in activation of an intracytoplasmatic tyrosin kinase, which phosphorylates insulin receptor substrate-1.	bind
34916	3	8395	7	NULL	NULL	0	NULL	tyrosin kinase	NULL	intracytoplasmatic	phosphorylates	NULL				 insulin receptor substrate-1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_104_17_2088_s_22	11673351	5, 6 Binding of IGF-I to its specific cell-surface receptor results in activation of an intracytoplasmatic tyrosin kinase, which phosphorylates insulin receptor substrate-1.	bind
28632	1	8396	6	13	NULL	NULL	NULL	IGF-1	GP		prevents					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_10_1220_s_24	11889017	5, 6 Furthermore, IGF-1 prevents apoptosis, 7 and its activity is modulated by IGF-1 binding proteins (IGFBPs), including IGFBP-3.	bind
28633	2	8396	6	13	NULL	NULL	NULL	IGFBP-3	GP		modulate					IGF-1	GP	activity of 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_10_1220_s_24	11889017	5, 6 Furthermore, IGF-1 prevents apoptosis, 7 and its activity is modulated by IGF-1 binding proteins (IGFBPs), including IGFBP-3.	bind
28634	3	8396	6	13	NULL	NULL	NULL	IGFBP-3	GP		is a type of					IGF-1 binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_10_1220_s_24	11889017	5, 6 Furthermore, IGF-1 prevents apoptosis, 7 and its activity is modulated by IGF-1 binding proteins (IGFBPs), including IGFBP-3.	bind
46897	4	8396	6	13	NULL	NULL	NULL	IGFBPs	GP		is					IGF-1 binding proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_10_1220_s_24	11889017	5, 6 Furthermore, IGF-1 prevents apoptosis, 7 and its activity is modulated by IGF-1 binding proteins (IGFBPs), including IGFBP-3.	bind
34917	1	8396	7	NULL	NULL	0	NULL	IGF-1	NULL		prevents	NULL				apoptosis	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_10_1220_s_24	11889017	5, 6 Furthermore, IGF-1 prevents apoptosis, 7 and its activity is modulated by IGF-1 binding proteins (IGFBPs), including IGFBP-3.	bind
34918	2	8396	7	10	NULL	0	NULL	IGFBP-3			modulates					IGF-1		activity of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_105_10_1220_s_24	11889017	5, 6 Furthermore, IGF-1 prevents apoptosis, 7 and its activity is modulated by IGF-1 binding proteins (IGFBPs), including IGFBP-3.	bind
34919	3	8396	7	NULL	NULL	0	NULL	IGFBP-3	NULL		is a type of	NULL				IGFBPs	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_10_1220_s_24	11889017	5, 6 Furthermore, IGF-1 prevents apoptosis, 7 and its activity is modulated by IGF-1 binding proteins (IGFBPs), including IGFBP-3.	bind
34920	4	8396	7	NULL	NULL	0	NULL	IGFBPs	NULL		is	NULL				IGF-1 binding proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_105_10_1220_s_24	11889017	5, 6 Furthermore, IGF-1 prevents apoptosis, 7 and its activity is modulated by IGF-1 binding proteins (IGFBPs), including IGFBP-3.	bind
28635	1	8397	6	13	NULL	NULL	NULL	VEGF-D	GP		bind					VEGFR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_2_395_s_16	9708800	5, 6, 10- 15  The recently identified specific receptor for VEGF-B is VEGFR-1 (B. Olofsson et al, manuscript in preparation), whereas VEGF-D binds both VEGFR-2 and VEGFR-3.	bind
28636	2	8397	6	13	NULL	NULL	NULL	VEGF-D	GP		bind					VEGFR-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_2_395_s_16	9708800	5, 6, 10- 15  The recently identified specific receptor for VEGF-B is VEGFR-1 (B. Olofsson et al, manuscript in preparation), whereas VEGF-D binds both VEGFR-2 and VEGFR-3.	bind
28637	3	8397	6	13	NULL	NULL	NULL	VEGFR-1	GP		is the receptor for					VEGF-B	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_2_395_s_16	9708800	5, 6, 10- 15  The recently identified specific receptor for VEGF-B is VEGFR-1 (B. Olofsson et al, manuscript in preparation), whereas VEGF-D binds both VEGFR-2 and VEGFR-3.	bind
34921	1	8397	7	NULL	NULL	0	NULL	VEGF-B	NULL		bind	NULL	specifically			VEGFR-1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_2_395_s_16	9708800	5, 6, 10- 15  The recently identified specific receptor for VEGF-B is VEGFR-1 (B. Olofsson et al, manuscript in preparation), whereas VEGF-D binds both VEGFR-2 and VEGFR-3.	bind
34922	2	8397	7	NULL	NULL	0	NULL	VEGF-D	NULL		bind	NULL				VEGFR-2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_2_395_s_16	9708800	5, 6, 10- 15  The recently identified specific receptor for VEGF-B is VEGFR-1 (B. Olofsson et al, manuscript in preparation), whereas VEGF-D binds both VEGFR-2 and VEGFR-3.	bind
34923	3	8397	7	NULL	NULL	0	NULL	VEGF-D 	NULL		bind	NULL				VEGFR-3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_2_395_s_16	9708800	5, 6, 10- 15  The recently identified specific receptor for VEGF-B is VEGFR-1 (B. Olofsson et al, manuscript in preparation), whereas VEGF-D binds both VEGFR-2 and VEGFR-3.	bind
28638	1	8398	6	13	NULL	NULL	NULL	SOCS1	GP		is recruited to			SH2 domain		Cbp	GP	phosphorylated	Tyr314		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_42_31920_s_266	16920712	5, the SH2 domain of SOCS1 is recruited to phosphorylated Tyr314 of Cbp.  6, SOCS1 mediates polyubiquitination and proteasomal degradation of Lyn.	bind
28639	2	8398	6	13	NULL	NULL	NULL	SOCS1	GP		mediates					Lyn	GP	polyubiquitination of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_42_31920_s_266	16920712	5, the SH2 domain of SOCS1 is recruited to phosphorylated Tyr314 of Cbp.  6, SOCS1 mediates polyubiquitination and proteasomal degradation of Lyn.	bind
28640	3	8398	6	13	NULL	NULL	NULL	SOCS1	GP		mediates					Lyn	GP	proteasomal degradation of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_42_31920_s_266	16920712	5, the SH2 domain of SOCS1 is recruited to phosphorylated Tyr314 of Cbp.  6, SOCS1 mediates polyubiquitination and proteasomal degradation of Lyn.	bind
34924	1	8398	7	NULL	NULL	0	NULL	SOCS1	NULL		is recruited to	NULL		SH2 domain		Cbp	NULL	 phosphorylated	Tyr314		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_42_31920_s_266	16920712	5, the SH2 domain of SOCS1 is recruited to phosphorylated Tyr314 of Cbp.  6, SOCS1 mediates polyubiquitination and proteasomal degradation of Lyn.	bind
34925	2	8398	7	10	NULL	0	NULL	SOCS1	NULL		mediates	NULL				Lyn	NULL	polyubiquitination of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_42_31920_s_266	16920712	5, the SH2 domain of SOCS1 is recruited to phosphorylated Tyr314 of Cbp.  6, SOCS1 mediates polyubiquitination and proteasomal degradation of Lyn.	bind
34926	3	8398	7	NULL	NULL	0	NULL	 SOCS1	NULL		mediates	NULL				Lyn	NULL	proteasomal degradation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_42_31920_s_266	16920712	5, the SH2 domain of SOCS1 is recruited to phosphorylated Tyr314 of Cbp.  6, SOCS1 mediates polyubiquitination and proteasomal degradation of Lyn.	bind
28641	1	8399	6	13	NULL	NULL	NULL	Fe3+	Chemical		bind					adenine N7	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_43_42495_s_181	12913009	5, whereas binding of Fe3+ to the adenine N7 is favored at neutral pH ( ).	bind
34927	1	8399	7	NULL	NULL	0	NULL	Fe3+	NULL		bind	NULL				adenine N7	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_43_42495_s_181	12913009	5, whereas binding of Fe3+ to the adenine N7 is favored at neutral pH ( ).	bind
28642	1	8400	6	13	NULL	NULL	NULL	Bcl-2	GP		is localized to					outer mitochondrial membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_21	15345651	5,10,11   Bcl-2 is localized to the outer mitochondrial membrane and Bcl-2 family proteins have been reported to interact with VDAC. 5,7  There is controversy as to whether Bcl-2 binding to VDAC promotes the opening or closing of VDAC. 10,13  Thompson and coworkers 8,10  report that Bcl-2 maintains VDAC in an open state, whereas Shimizu et al 5,11,13   report that Bcl-2 promotes VDAC closure.	bind
28643	2	8400	6	13	NULL	NULL	NULL	Bcl-2 family proteins	GP		interact with					VDAC	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_21	15345651	5,10,11   Bcl-2 is localized to the outer mitochondrial membrane and Bcl-2 family proteins have been reported to interact with VDAC. 5,7  There is controversy as to whether Bcl-2 binding to VDAC promotes the opening or closing of VDAC. 10,13  Thompson and coworkers 8,10  report that Bcl-2 maintains VDAC in an open state, whereas Shimizu et al 5,11,13   report that Bcl-2 promotes VDAC closure.	bind
46900	3	8400	6	13	NULL	NULL	NULL	Bcl-2	GP		maintains					VDAC	GP	open state of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_21	15345651	5,10,11   Bcl-2 is localized to the outer mitochondrial membrane and Bcl-2 family proteins have been reported to interact with VDAC. 5,7  There is controversy as to whether Bcl-2 binding to VDAC promotes the opening or closing of VDAC. 10,13  Thompson and coworkers 8,10  report that Bcl-2 maintains VDAC in an open state, whereas Shimizu et al 5,11,13   report that Bcl-2 promotes VDAC closure.	bind
46901	4	8400	6	13	NULL	NULL	NULL	Bcl-2	GP		promotes					VDAC	GP	closure of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_21	15345651	5,10,11   Bcl-2 is localized to the outer mitochondrial membrane and Bcl-2 family proteins have been reported to interact with VDAC. 5,7  There is controversy as to whether Bcl-2 binding to VDAC promotes the opening or closing of VDAC. 10,13  Thompson and coworkers 8,10  report that Bcl-2 maintains VDAC in an open state, whereas Shimizu et al 5,11,13   report that Bcl-2 promotes VDAC closure.	bind
34929	1	8400	7	NULL	NULL	0	NULL	Bcl-2	NULL		is localized to	NULL				outer mitochondrial membrane	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_21	15345651	5,10,11   Bcl-2 is localized to the outer mitochondrial membrane and Bcl-2 family proteins have been reported to interact with VDAC. 5,7  There is controversy as to whether Bcl-2 binding to VDAC promotes the opening or closing of VDAC. 10,13  Thompson and coworkers 8,10  report that Bcl-2 maintains VDAC in an open state, whereas Shimizu et al 5,11,13   report that Bcl-2 promotes VDAC closure.	bind
34930	2	8400	7	NULL	NULL	0	NULL	Bcl-2 family proteins	NULL		interacts with	NULL				VDAC	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_21	15345651	5,10,11   Bcl-2 is localized to the outer mitochondrial membrane and Bcl-2 family proteins have been reported to interact with VDAC. 5,7  There is controversy as to whether Bcl-2 binding to VDAC promotes the opening or closing of VDAC. 10,13  Thompson and coworkers 8,10  report that Bcl-2 maintains VDAC in an open state, whereas Shimizu et al 5,11,13   report that Bcl-2 promotes VDAC closure.	bind
34931	3	8400	7	10	NULL	0	NULL	Bcl-2	NULL		maintains	NULL				VDAC	NULL	open state of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_21	15345651	5,10,11   Bcl-2 is localized to the outer mitochondrial membrane and Bcl-2 family proteins have been reported to interact with VDAC. 5,7  There is controversy as to whether Bcl-2 binding to VDAC promotes the opening or closing of VDAC. 10,13  Thompson and coworkers 8,10  report that Bcl-2 maintains VDAC in an open state, whereas Shimizu et al 5,11,13   report that Bcl-2 promotes VDAC closure.	bind
46899	4	8400	7	10	NULL	0	NULL	Bcl-2	NULL		promotes	NULL				VDAC	NULL	closure of			NULL		0	NULL	NULL	NULL	gw70_circulationres_95_7_734_s_21	15345651	5,10,11   Bcl-2 is localized to the outer mitochondrial membrane and Bcl-2 family proteins have been reported to interact with VDAC. 5,7  There is controversy as to whether Bcl-2 binding to VDAC promotes the opening or closing of VDAC. 10,13  Thompson and coworkers 8,10  report that Bcl-2 maintains VDAC in an open state, whereas Shimizu et al 5,11,13   report that Bcl-2 promotes VDAC closure.	bind
34802	1	8401	5	13	NULL	NULL	NULL	actin	GP		bind					eNOS	GP			3'UTR	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_5_488_s_214	15256481	5,10,39   Shear stress did not significantly affect actin binding to the eNOS 3'UTR, but treatment with H2O2 resulted in a dramatic decrease in binding activity (online Figure II).	bind
34803	2	8401	5	13	NULL	NULL	NULL	shear stress			does not affect		significantly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_5_488_s_214	15256481	5,10,39   Shear stress did not significantly affect actin binding to the eNOS 3'UTR, but treatment with H2O2 resulted in a dramatic decrease in binding activity (online Figure II).	bind
34804	3	8401	5	13	NULL	NULL	NULL	H2O2	Chemical	treatment	decrease		dramatically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_5_488_s_214	15256481	5,10,39   Shear stress did not significantly affect actin binding to the eNOS 3'UTR, but treatment with H2O2 resulted in a dramatic decrease in binding activity (online Figure II).	bind
28644	1	8401	6	NULL	NULL	0	NULL	actin	NULL		bind	NULL				eNOS	NULL			3'UTR	NULL		0	NULL	NULL	NULL	gw70_circulationres_95_5_488_s_214	15256481	5,10,39   Shear stress did not significantly affect actin binding to the eNOS 3'UTR, but treatment with H2O2 resulted in a dramatic decrease in binding activity (online Figure II).	bind
28645	2	8401	6	10	NULL	0	NULL	H2O2		treatment	decrease		dramatically			statement 1					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_5_488_s_214	15256481	5,10,39   Shear stress did not significantly affect actin binding to the eNOS 3'UTR, but treatment with H2O2 resulted in a dramatic decrease in binding activity (online Figure II).	bind
28646	3	8401	6	NULL	NULL	0	NULL	shear stress	NULL		did not affect	NULL	significantly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_5_488_s_214	15256481	5,10,39   Shear stress did not significantly affect actin binding to the eNOS 3'UTR, but treatment with H2O2 resulted in a dramatic decrease in binding activity (online Figure II).	bind
34805	1	8402	5	13	NULL	NULL	NULL	Sp1	GP		bind					SMMHC	GP			G/C repressor	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_128	15486317	5,14,15   However, we further demonstrated that Sp1 binding to the SMMHC G/C repressor did not prevent SRF binding to the adjacent CArG2, which is separated from the G/C repressor by 6 nucleotides 14 ( Figure 6a).	bind
34807	2	8402	5	13	NULL	NULL	NULL	SMMHC	GP		is separated from				CArG2	SMMHC	GP			G/C repressor	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_128	15486317	5,14,15   However, we further demonstrated that Sp1 binding to the SMMHC G/C repressor did not prevent SRF binding to the adjacent CArG2, which is separated from the G/C repressor by 6 nucleotides 14 ( Figure 6a).	bind
34808	3	8402	5	13	NULL	NULL	NULL	nucleotides	NucleicAcid		separate					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_128	15486317	5,14,15   However, we further demonstrated that Sp1 binding to the SMMHC G/C repressor did not prevent SRF binding to the adjacent CArG2, which is separated from the G/C repressor by 6 nucleotides 14 ( Figure 6a).	bind
34809	4	8402	5	13	NULL	NULL	NULL	SRF	GP		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_128	15486317	5,14,15   However, we further demonstrated that Sp1 binding to the SMMHC G/C repressor did not prevent SRF binding to the adjacent CArG2, which is separated from the G/C repressor by 6 nucleotides 14 ( Figure 6a).	bind
34810	5	8402	5	13	NULL	NULL	NULL	statement 1	Process		does not prevent					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_128	15486317	5,14,15   However, we further demonstrated that Sp1 binding to the SMMHC G/C repressor did not prevent SRF binding to the adjacent CArG2, which is separated from the G/C repressor by 6 nucleotides 14 ( Figure 6a).	bind
28647	1	8402	6	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				SMMHC	NULL			G/C repressor	NULL		0	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_128	15486317	5,14,15   However, we further demonstrated that Sp1 binding to the SMMHC G/C repressor did not prevent SRF binding to the adjacent CArG2, which is separated from the G/C repressor by 6 nucleotides 14 ( Figure 6a).	bind
28648	2	8402	6	10	NULL	0	NULL	SRF			bind					SMMHC				CArG2	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_128	15486317	5,14,15   However, we further demonstrated that Sp1 binding to the SMMHC G/C repressor did not prevent SRF binding to the adjacent CArG2, which is separated from the G/C repressor by 6 nucleotides 14 ( Figure 6a).	bind
28649	3	8402	6	NULL	NULL	0	NULL	statement 1	NULL		did not prevent	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_128	15486317	5,14,15   However, we further demonstrated that Sp1 binding to the SMMHC G/C repressor did not prevent SRF binding to the adjacent CArG2, which is separated from the G/C repressor by 6 nucleotides 14 ( Figure 6a).	bind
28650	4	8402	6	10	NULL	0	NULL	SMMHC			is separated from				CArG2	SMMHC				G/C repressor	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_128	15486317	5,14,15   However, we further demonstrated that Sp1 binding to the SMMHC G/C repressor did not prevent SRF binding to the adjacent CArG2, which is separated from the G/C repressor by 6 nucleotides 14 ( Figure 6a).	bind
34811	1	8403	5	13	NULL	NULL	NULL	Fos protein	GP		bind					Jun protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2808_s_23	9409259	5,6 In vitro studies have demonstrated that Fos and Jun proteins combine to form stable AP-1 heterodimers, which bind to AP-1 consensus sequences present in numerous genes associated with cell proliferative response and extracellular matrix production.	bind
34812	2	8403	5	13	NULL	NULL	NULL	statement 1	GP		forms					AP-1 heterodimers	GP	stable			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2808_s_23	9409259	5,6 In vitro studies have demonstrated that Fos and Jun proteins combine to form stable AP-1 heterodimers, which bind to AP-1 consensus sequences present in numerous genes associated with cell proliferative response and extracellular matrix production.	bind
35852	3	8403	5	13	NULL	NULL	NULL	AP-1 heterodimers	GP		bind					genes associated with cell proliferative response	GP			AP-1 consensus sequences	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2808_s_23	9409259	5,6 In vitro studies have demonstrated that Fos and Jun proteins combine to form stable AP-1 heterodimers, which bind to AP-1 consensus sequences present in numerous genes associated with cell proliferative response and extracellular matrix production.	bind
35854	4	8403	5	13	NULL	NULL	NULL	AP-1 heterodimers	GP		bind					genes associated with extracellular matrix production	GP			AP-1 consensus sequences	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2808_s_23	9409259	5,6 In vitro studies have demonstrated that Fos and Jun proteins combine to form stable AP-1 heterodimers, which bind to AP-1 consensus sequences present in numerous genes associated with cell proliferative response and extracellular matrix production.	bind
28651	1	8403	6	NULL	NULL	0	NULL	Fox protein	NULL		combine with	NULL				Jun protein	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2808_s_23	9409259	5,6 In vitro studies have demonstrated that Fos and Jun proteins combine to form stable AP-1 heterodimers, which bind to AP-1 consensus sequences present in numerous genes associated with cell proliferative response and extracellular matrix production.	bind
28652	2	8403	6	NULL	NULL	0	NULL	statement 1	NULL		form stable complex with	NULL				AP-1 heterodimers	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2808_s_23	9409259	5,6 In vitro studies have demonstrated that Fos and Jun proteins combine to form stable AP-1 heterodimers, which bind to AP-1 consensus sequences present in numerous genes associated with cell proliferative response and extracellular matrix production.	bind
29027	3	8403	6	NULL	NULL	0	NULL	AP-1 heterodimers	NULL		bind	NULL				gene associated with cell proliferative response	NULL			AP-1 consensus site	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2808_s_23	9409259	5,6 In vitro studies have demonstrated that Fos and Jun proteins combine to form stable AP-1 heterodimers, which bind to AP-1 consensus sequences present in numerous genes associated with cell proliferative response and extracellular matrix production.	bind
29028	4	8403	6	NULL	NULL	0	NULL	AP-1 heterodimers	NULL		bind	NULL				genes associated with extracellular matrix production	NULL			AP-1 consensus site	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2808_s_23	9409259	5,6 In vitro studies have demonstrated that Fos and Jun proteins combine to form stable AP-1 heterodimers, which bind to AP-1 consensus sequences present in numerous genes associated with cell proliferative response and extracellular matrix production.	bind
35858	1	8404	5	13	NULL	NULL	NULL	angiopoietins	GP		bind					Tie2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_6_2179_s_13	10854238	5- 7  All known angiopoietins bind to Tie2, but it is still unclear as to whether they use the closely related receptor Tie1.	bind
28653	1	8404	6	NULL	NULL	0	NULL	angiopoietins	NULL		bind	NULL				Tie2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_6_2179_s_13	10854238	5- 7  All known angiopoietins bind to Tie2, but it is still unclear as to whether they use the closely related receptor Tie1.	bind
35860	1	8407	5	13	NULL	NULL	NULL	5-Br-nosc	Chemical		bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_63_4_799_s_111	12644580	5-Br-nosc and Rd 5-Br-nosc Have Higher Tubulin Binding Activity than Noscapine.	bind
35861	2	8407	5	13	NULL	NULL	NULL	Rd 5-Br-nosc	Chemical		bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_63_4_799_s_111	12644580	5-Br-nosc and Rd 5-Br-nosc Have Higher Tubulin Binding Activity than Noscapine.	bind
35862	3	8407	5	13	NULL	NULL	NULL	noscapine	Chemical		bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_63_4_799_s_111	12644580	5-Br-nosc and Rd 5-Br-nosc Have Higher Tubulin Binding Activity than Noscapine.	bind
35863	4	8407	5	13	NULL	NULL	NULL	statement 1	Process		higher affinity than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_63_4_799_s_111	12644580	5-Br-nosc and Rd 5-Br-nosc Have Higher Tubulin Binding Activity than Noscapine.	bind
35864	5	8407	5	13	NULL	NULL	NULL	statement 2	Process		higher affinity than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_63_4_799_s_111	12644580	5-Br-nosc and Rd 5-Br-nosc Have Higher Tubulin Binding Activity than Noscapine.	bind
28654	1	8407	6	NULL	NULL	0	NULL	5-Br-nosc	NULL		bind	NULL				tubulin	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_63_4_799_s_111	12644580	5-Br-nosc and Rd 5-Br-nosc Have Higher Tubulin Binding Activity than Noscapine.	bind
28655	2	8407	6	NULL	NULL	0	NULL	Rd 5-Br-nosc	NULL		bind	NULL				tubulin	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_63_4_799_s_111	12644580	5-Br-nosc and Rd 5-Br-nosc Have Higher Tubulin Binding Activity than Noscapine.	bind
28656	3	8407	6	NULL	NULL	0	NULL	noscapine	NULL		bind	NULL				tubulin	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_63_4_799_s_111	12644580	5-Br-nosc and Rd 5-Br-nosc Have Higher Tubulin Binding Activity than Noscapine.	bind
28669	4	8407	6	10	NULL	0	NULL	statement 1	NULL	affinity of	is higher than	NULL				statement 3	NULL	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_63_4_799_s_111	12644580	5-Br-nosc and Rd 5-Br-nosc Have Higher Tubulin Binding Activity than Noscapine.	bind
28670	5	8407	6	NULL	NULL	0	NULL	statement 2	NULL	affinity of	is higher than	NULL				statement 3	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_63_4_799_s_111	12644580	5-Br-nosc and Rd 5-Br-nosc Have Higher Tubulin Binding Activity than Noscapine.	bind
36736	1	8408	5	13	NULL	NULL	NULL	ephrin B1	GP		does not increase					JNK	GP	activity of			NULL	cells transfected with kinase defective (K652R) mutant receptors	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1303_s_148	9430661	5-fold increases in JNK activity in cells transfected with either vector control (pSRalpha) or wild type EphB1 (pSRalpha-EphB1/HA). In contrast, ephrin B1 failed to increase JNK activity in cells transfected with either kinase defective (K652R) or Nck binding defective (Y594F) mutant receptors.	bind
36737	2	8408	5	13	NULL	NULL	NULL	ephrin B1	GP		does not increase					JNK	GP	activity of			NULL	cells transfected with Nck binding defective (Y594F) mutant receptors	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1303_s_148	9430661	5-fold increases in JNK activity in cells transfected with either vector control (pSRalpha) or wild type EphB1 (pSRalpha-EphB1/HA). In contrast, ephrin B1 failed to increase JNK activity in cells transfected with either kinase defective (K652R) or Nck binding defective (Y594F) mutant receptors.	bind
28828	1	8408	6	10	NULL	0	NULL	ephrin B1	NULL		failed to increase	NULL				JNK	NULL	activity of			NULL	cells transfected with kinase defective (K652R) mutant receptors	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1303_s_148	9430661	5-fold increases in JNK activity in cells transfected with either vector control (pSRalpha) or wild type EphB1 (pSRalpha-EphB1/HA). In contrast, ephrin B1 failed to increase JNK activity in cells transfected with either kinase defective (K652R) or Nck binding defective (Y594F) mutant receptors.	bind
28829	2	8408	6	10	NULL	0	NULL	ephrin B1	NULL		failed to increase	NULL				JNK	NULL	activity of			NULL	cells transfected with Nck binding defective (Y594F) mutant receptors	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1303_s_148	9430661	5-fold increases in JNK activity in cells transfected with either vector control (pSRalpha) or wild type EphB1 (pSRalpha-EphB1/HA). In contrast, ephrin B1 failed to increase JNK activity in cells transfected with either kinase defective (K652R) or Nck binding defective (Y594F) mutant receptors.	bind
35865	1	8409	5	13	NULL	NULL	NULL	DnaA protein	GP		bind					oriC fragment	NucleicAcid	radiolabeled			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23017_s_168	9287298	5-fold molar excess of unlabeled  oriC was required as a competitor to reduce to about 50% the binding of either DnaA protein or T435M to the radiolabeled  oriC fragment.	bind
35866	2	8409	5	13	NULL	NULL	NULL	T435M	GP		bind					oriC fragment	NucleicAcid	radiolabeled			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23017_s_168	9287298	5-fold molar excess of unlabeled  oriC was required as a competitor to reduce to about 50% the binding of either DnaA protein or T435M to the radiolabeled  oriC fragment.	bind
35867	3	8409	5	13	NULL	NULL	NULL	oriC	NucleicAcid	unlabeled	bind					 oriC fragment	NucleicAcid	radiolabeled			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23017_s_168	9287298	5-fold molar excess of unlabeled  oriC was required as a competitor to reduce to about 50% the binding of either DnaA protein or T435M to the radiolabeled  oriC fragment.	bind
35869	4	8409	5	13	NULL	NULL	NULL	statement 1	Process		competes with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23017_s_168	9287298	5-fold molar excess of unlabeled  oriC was required as a competitor to reduce to about 50% the binding of either DnaA protein or T435M to the radiolabeled  oriC fragment.	bind
35870	6	8409	5	13	NULL	NULL	NULL	statement 3	Process		reduces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23017_s_168	9287298	5-fold molar excess of unlabeled  oriC was required as a competitor to reduce to about 50% the binding of either DnaA protein or T435M to the radiolabeled  oriC fragment.	bind
35871	5	8409	5	13	NULL	NULL	NULL	statement 2	Process		competes with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23017_s_168	9287298	5-fold molar excess of unlabeled  oriC was required as a competitor to reduce to about 50% the binding of either DnaA protein or T435M to the radiolabeled  oriC fragment.	bind
35872	7	8409	5	13	NULL	NULL	NULL	statement 3	Process		reduces					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23017_s_168	9287298	5-fold molar excess of unlabeled  oriC was required as a competitor to reduce to about 50% the binding of either DnaA protein or T435M to the radiolabeled  oriC fragment.	bind
28830	1	8409	6	NULL	NULL	0	NULL	DnaA protein	NULL		bind	NULL				oriC fragment	NULL	radiolabeled			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_37_23017_s_168	9287298	5-fold molar excess of unlabeled  oriC was required as a competitor to reduce to about 50% the binding of either DnaA protein or T435M to the radiolabeled  oriC fragment.	bind
28831	2	8409	6	NULL	NULL	0	NULL		NULL		bind	NULL		T435M		oriC fragment	NULL	radiolabeled			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_37_23017_s_168	9287298	5-fold molar excess of unlabeled  oriC was required as a competitor to reduce to about 50% the binding of either DnaA protein or T435M to the radiolabeled  oriC fragment.	bind
28832	3	8409	6	NULL	NULL	0	NULL	oriC	NULL	unlabeled	bind	NULL				oriC fragment	NULL	radiolabeled			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_37_23017_s_168	9287298	5-fold molar excess of unlabeled  oriC was required as a competitor to reduce to about 50% the binding of either DnaA protein or T435M to the radiolabeled  oriC fragment.	bind
28833	4	8409	6	NULL	NULL	0	NULL	statement 1	NULL		competes	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23017_s_168	9287298	5-fold molar excess of unlabeled  oriC was required as a competitor to reduce to about 50% the binding of either DnaA protein or T435M to the radiolabeled  oriC fragment.	bind
28834	5	8409	6	NULL	NULL	0	NULL	statement 2	NULL		competes	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_37_23017_s_168	9287298	5-fold molar excess of unlabeled  oriC was required as a competitor to reduce to about 50% the binding of either DnaA protein or T435M to the radiolabeled  oriC fragment.	bind
35873	1	8410	5	13	NULL	NULL	NULL	1,25(OH)2D3-receptor complex	GP	intestinal;;cytosolic	bind					DNA	NucleicAcid	heterologous			NULL		NULL	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_106_12_2850038_s_3	2850038	5-fold)  increase of intestinal cytosolic 1,25(OH)2D3-receptor complex binding  with heterologous DNA, whereas maximum binding capacity and equilibrium  dissociation constant of cytosolic 1,25 (OH)2D3 receptors did not change.	bind
28835	1	8410	6	10	NULL	0	NULL	1,25(OH)2D3-receptor complex		intestinal;; cytosolic	bind					DNA		heterologous			NULL		NULL	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_106_12_2850038_s_3	2850038	5-fold)  increase of intestinal cytosolic 1,25(OH)2D3-receptor complex binding  with heterologous DNA, whereas maximum binding capacity and equilibrium  dissociation constant of cytosolic 1,25 (OH)2D3 receptors did not change.	bind
35876	1	8411	5	13	NULL	NULL	NULL	5-HT1A receptor	GP		bind					G proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_135_5_1115_s_6	11877317	5-HT1A receptor binding and coupling to G proteins were assessed using [3]-8-OH-DPAT and [35]-GTPgammaS autoradiography, respectively.	bind
35878	2	8411	5	13	NULL	NULL	NULL	5-HT1A receptor	GP		couple to					G proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_135_5_1115_s_6	11877317	5-HT1A receptor binding and coupling to G proteins were assessed using [3]-8-OH-DPAT and [35]-GTPgammaS autoradiography, respectively.	bind
28836	1	8411	6	NULL	NULL	0	NULL	HT1A receptor	NULL		bind	NULL				G proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_5_1115_s_6	11877317	5-HT1A receptor binding and coupling to G proteins were assessed using [3]-8-OH-DPAT and [35]-GTPgammaS autoradiography, respectively.	bind
28837	2	8411	6	NULL	NULL	0	NULL	HT1A receptor	NULL		couples to	NULL				G proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_5_1115_s_6	11877317	5-HT1A receptor binding and coupling to G proteins were assessed using [3]-8-OH-DPAT and [35]-GTPgammaS autoradiography, respectively.	bind
35880	1	8412	5	13	NULL	NULL	NULL	5-HT2A receptor	GP		bind					VMAT2	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_835_2_104_s_62	10415365	5-HT2A receptor and vesicular monoamine transporter (VMAT2) binding ( Kd and  Bmax) were measured by [3]ketanserin (DuPont, specific activity 85.1 Ci/mmol) and [125]TBZ (synthesized by Dr. M.-P. Kung, specific activity 2200 Ci/mmol) using saturation assays.	bind
35882	2	8412	5	13	NULL	NULL	NULL	VMAT2	GP		is					vesicular monoamine transporter	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_835_2_104_s_62	10415365	5-HT2A receptor and vesicular monoamine transporter (VMAT2) binding ( Kd and  Bmax) were measured by [3]ketanserin (DuPont, specific activity 85.1 Ci/mmol) and [125]TBZ (synthesized by Dr. M.-P. Kung, specific activity 2200 Ci/mmol) using saturation assays.	bind
28838	1	8412	6	NULL	NULL	0	NULL	VMAT	NULL		is	NULL				vesicular monoamine transporter	NULL				NULL		0	NULL	NULL	NULL	gw60_brainres_835_2_104_s_62	10415365	5-HT2A receptor and vesicular monoamine transporter (VMAT2) binding ( Kd and  Bmax) were measured by [3]ketanserin (DuPont, specific activity 85.1 Ci/mmol) and [125]TBZ (synthesized by Dr. M.-P. Kung, specific activity 2200 Ci/mmol) using saturation assays.	bind
28839	2	8412	6	NULL	NULL	0	NULL	HT2A receptor	NULL		bind	NULL				VMAT2	NULL				NULL		0	NULL	NULL	NULL	gw60_brainres_835_2_104_s_62	10415365	5-HT2A receptor and vesicular monoamine transporter (VMAT2) binding ( Kd and  Bmax) were measured by [3]ketanserin (DuPont, specific activity 85.1 Ci/mmol) and [125]TBZ (synthesized by Dr. M.-P. Kung, specific activity 2200 Ci/mmol) using saturation assays.	bind
35883	1	8413	5	13	NULL	NULL	NULL	Rho GTPase	GP	stimulation of	activates					SRF	GP				NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_25_34_7821_s_309	16120784	5-HT7R/12 signaling and regulation of gene transcription   One of the physiological consequences of Rho GTPase stimulation is the activation of a transcription factor, SRF, which binds to the SRE.	bind
35884	2	8413	5	13	NULL	NULL	NULL	SRF	GP		bind									SRE	NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_25_34_7821_s_309	16120784	5-HT7R/12 signaling and regulation of gene transcription   One of the physiological consequences of Rho GTPase stimulation is the activation of a transcription factor, SRF, which binds to the SRE.	bind
35885	3	8413	5	13	NULL	NULL	NULL	SRF	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_25_34_7821_s_309	16120784	5-HT7R/12 signaling and regulation of gene transcription   One of the physiological consequences of Rho GTPase stimulation is the activation of a transcription factor, SRF, which binds to the SRE.	bind
28840	1	8413	6	NULL	NULL	0	NULL	SRF	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_25_34_7821_s_309	16120784	5-HT7R/12 signaling and regulation of gene transcription   One of the physiological consequences of Rho GTPase stimulation is the activation of a transcription factor, SRF, which binds to the SRE.	bind
28841	2	8413	6	NULL	NULL	0	NULL	rho GTPase	NULL	stimulation of	leads to	NULL				SRF	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_jneurosci_25_34_7821_s_309	16120784	5-HT7R/12 signaling and regulation of gene transcription   One of the physiological consequences of Rho GTPase stimulation is the activation of a transcription factor, SRF, which binds to the SRE.	bind
28842	3	8413	6	NULL	NULL	0	NULL	SRF	NULL		bind	NULL					NULL			SRE	NULL		0	NULL	NULL	NULL	gw70_jneurosci_25_34_7821_s_309	16120784	5-HT7R/12 signaling and regulation of gene transcription   One of the physiological consequences of Rho GTPase stimulation is the activation of a transcription factor, SRF, which binds to the SRE.	bind
35886	1	8414	5	13	NULL	NULL	NULL	5-Lipoxygenase	GP		does not bind					GTPase-activating protein	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_269_39_7929073_s_7	7929073	5-Lipoxygenase did not bind to the SH3 domains of other  signaling proteins, such as GTPase-activating protein and phospholipase  C gamma; however, it bound to certain cytoskeletal proteins including  alpha-actinin and actin.	bind
35888	2	8414	5	13	NULL	NULL	NULL	5-Lipoxygenase	GP		does not bind					phospholipase C gamma	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_269_39_7929073_s_7	7929073	5-Lipoxygenase did not bind to the SH3 domains of other  signaling proteins, such as GTPase-activating protein and phospholipase  C gamma; however, it bound to certain cytoskeletal proteins including  alpha-actinin and actin.	bind
35890	3	8414	5	13	NULL	NULL	NULL	5-Lipoxygenase	GP		bind					alpha-actinin	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_269_39_7929073_s_7	7929073	5-Lipoxygenase did not bind to the SH3 domains of other  signaling proteins, such as GTPase-activating protein and phospholipase  C gamma; however, it bound to certain cytoskeletal proteins including  alpha-actinin and actin.	bind
35892	4	8414	5	13	NULL	NULL	NULL	5-Lipoxygenase	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_269_39_7929073_s_7	7929073	5-Lipoxygenase did not bind to the SH3 domains of other  signaling proteins, such as GTPase-activating protein and phospholipase  C gamma; however, it bound to certain cytoskeletal proteins including  alpha-actinin and actin.	bind
35893	5	8414	5	13	NULL	NULL	NULL	alpha-actinin	GP		is a type of					cytoskeletal proteins	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_269_39_7929073_s_7	7929073	5-Lipoxygenase did not bind to the SH3 domains of other  signaling proteins, such as GTPase-activating protein and phospholipase  C gamma; however, it bound to certain cytoskeletal proteins including  alpha-actinin and actin.	bind
35894	6	8414	5	13	NULL	NULL	NULL	actin	GP		is a type of					cytoskeletal proteins	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_269_39_7929073_s_7	7929073	5-Lipoxygenase did not bind to the SH3 domains of other  signaling proteins, such as GTPase-activating protein and phospholipase  C gamma; however, it bound to certain cytoskeletal proteins including  alpha-actinin and actin.	bind
35897	7	8414	5	13	NULL	NULL	NULL	GTPase-activating protein	GP		is a type of					signaling proteins	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_269_39_7929073_s_7	7929073	5-Lipoxygenase did not bind to the SH3 domains of other  signaling proteins, such as GTPase-activating protein and phospholipase  C gamma; however, it bound to certain cytoskeletal proteins including  alpha-actinin and actin.	bind
35898	8	8414	5	13	NULL	NULL	NULL	phospholipase C gamma	GP		is a type of					signaling proteins	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_269_39_7929073_s_7	7929073	5-Lipoxygenase did not bind to the SH3 domains of other  signaling proteins, such as GTPase-activating protein and phospholipase  C gamma; however, it bound to certain cytoskeletal proteins including  alpha-actinin and actin.	bind
28843	1	8414	6	NULL	NULL	0	NULL	GTPase-activating protein	NULL		is a type of	NULL				signaling protein	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_269_39_7929073_s_7	7929073	5-Lipoxygenase did not bind to the SH3 domains of other  signaling proteins, such as GTPase-activating protein and phospholipase  C gamma; however, it bound to certain cytoskeletal proteins including  alpha-actinin and actin.	bind
28844	2	8414	6	NULL	NULL	0	NULL	phospholipase C gamma	NULL		is a type of	NULL				signaling protein	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_269_39_7929073_s_7	7929073	5-Lipoxygenase did not bind to the SH3 domains of other  signaling proteins, such as GTPase-activating protein and phospholipase  C gamma; however, it bound to certain cytoskeletal proteins including  alpha-actinin and actin.	bind
28846	3	8414	6	NULL	NULL	0	NULL	alpha-actinin	NULL		is a type of	NULL				cytoskeletal protein	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_269_39_7929073_s_7	7929073	5-Lipoxygenase did not bind to the SH3 domains of other  signaling proteins, such as GTPase-activating protein and phospholipase  C gamma; however, it bound to certain cytoskeletal proteins including  alpha-actinin and actin.	bind
28847	4	8414	6	NULL	NULL	0	NULL	actin	NULL		is a type of	NULL				cytoskeletal protein	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_269_39_7929073_s_7	7929073	5-Lipoxygenase did not bind to the SH3 domains of other  signaling proteins, such as GTPase-activating protein and phospholipase  C gamma; however, it bound to certain cytoskeletal proteins including  alpha-actinin and actin.	bind
28848	5	8414	6	NULL	NULL	0	NULL	5-Lipoxygenase	NULL		does not bind	NULL				GTPase-activating protein	NULL		SH3 domain		NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_269_39_7929073_s_7	7929073	5-Lipoxygenase did not bind to the SH3 domains of other  signaling proteins, such as GTPase-activating protein and phospholipase  C gamma; however, it bound to certain cytoskeletal proteins including  alpha-actinin and actin.	bind
28849	6	8414	6	NULL	NULL	0	NULL	5-Lipoxygenase	NULL		does not bind	NULL				phospholipase C gamma	NULL		SH3 domain		NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_269_39_7929073_s_7	7929073	5-Lipoxygenase did not bind to the SH3 domains of other  signaling proteins, such as GTPase-activating protein and phospholipase  C gamma; however, it bound to certain cytoskeletal proteins including  alpha-actinin and actin.	bind
28850	7	8414	6	NULL	NULL	0	NULL	5-Lipoxygenase	NULL		bind	NULL				alpha-actinin	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_269_39_7929073_s_7	7929073	5-Lipoxygenase did not bind to the SH3 domains of other  signaling proteins, such as GTPase-activating protein and phospholipase  C gamma; however, it bound to certain cytoskeletal proteins including  alpha-actinin and actin.	bind
28851	8	8414	6	NULL	NULL	0	NULL	5-Lipoxygenase	NULL		bind	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_269_39_7929073_s_7	7929073	5-Lipoxygenase did not bind to the SH3 domains of other  signaling proteins, such as GTPase-activating protein and phospholipase  C gamma; however, it bound to certain cytoskeletal proteins including  alpha-actinin and actin.	bind
35900	1	8415	5	13	NULL	NULL	NULL	Histone H1	GP		bind		preferentially			superhelical DNA molecules	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_19_4043_s_480	11574687	50       Ivanchenko,M., Zlatanova,J. and van Holde,K. (1997) Histone H1 preferentially binds to superhelical DNA molecules of higher compaction.	bind
28852	1	8415	6	NULL	NULL	0	NULL	Histone H1	NULL		bind	NULL	preferentially			superhelical DNA molecules	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_19_4043_s_480	11574687	50       Ivanchenko,M., Zlatanova,J. and van Holde,K. (1997) Histone H1 preferentially binds to superhelical DNA molecules of higher compaction.	bind
35902	2	8419	5	13	NULL	NULL	NULL	statement 1	GP		bind					GST-p38alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_6905_s_103	11238443	50 mug of thrombin-digested GST-ERK1 was added to GST-p38alpha beads, and ERK1 that bound to p38 was detected by Western blotting with anti-ERK1-CT antibody.	bind
47874	1	8419	5	13	NULL	NULL	NULL	GST-ERK1 	GP		digested with					thrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_6905_s_103	11238443	50 mug of thrombin-digested GST-ERK1 was added to GST-p38alpha beads, and ERK1 that bound to p38 was detected by Western blotting with anti-ERK1-CT antibody.	bind
28853	2	8419	6	10	NULL	0	NULL	statement 1	NULL		bind	NULL				p38	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_6905_s_103	11238443	50 mug of thrombin-digested GST-ERK1 was added to GST-p38alpha beads, and ERK1 that bound to p38 was detected by Western blotting with anti-ERK1-CT antibody.	bind
47875	1	8419	6	10	NULL	0	NULL	GST-ERK1 	NULL		digested with	NULL				thrombin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_10_6905_s_103	11238443	50 mug of thrombin-digested GST-ERK1 was added to GST-p38alpha beads, and ERK1 that bound to p38 was detected by Western blotting with anti-ERK1-CT antibody.	bind
35903	1	8424	5	13	NULL	NULL	NULL	OKA	Chemical		induce					NF-kappaB	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_28_25804_s_193	11320078	50 nM OKA was able to both induce NF-kappaB binding (Fig.  4 A, lane 18) and block the effects of TPA (Fig.  4 A, lane 12) on the mobility of the pets complex.	bind
35904	2	8424	5	13	NULL	NULL	NULL	TPA	Chemical		effect					pets complex	GP	mobility of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_28_25804_s_193	11320078	50 nM OKA was able to both induce NF-kappaB binding (Fig.  4 A, lane 18) and block the effects of TPA (Fig.  4 A, lane 12) on the mobility of the pets complex.	bind
35905	3	8424	5	13	NULL	NULL	NULL	OKA	Chemical		block					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_28_25804_s_193	11320078	50 nM OKA was able to both induce NF-kappaB binding (Fig.  4 A, lane 18) and block the effects of TPA (Fig.  4 A, lane 12) on the mobility of the pets complex.	bind
28854	1	8424	6	NULL	NULL	0	NULL	OKA	NULL		induce	NULL				NF-kappaB	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_28_25804_s_193	11320078	50 nM OKA was able to both induce NF-kappaB binding (Fig.  4 A, lane 18) and block the effects of TPA (Fig.  4 A, lane 12) on the mobility of the pets complex.	bind
28855	2	8424	6	NULL	NULL	0	NULL	TPA	NULL		effects	NULL				pets complex	NULL	mobility of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_28_25804_s_193	11320078	50 nM OKA was able to both induce NF-kappaB binding (Fig.  4 A, lane 18) and block the effects of TPA (Fig.  4 A, lane 12) on the mobility of the pets complex.	bind
28856	3	8424	6	NULL	NULL	0	NULL	OKA	NULL		block	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_28_25804_s_193	11320078	50 nM OKA was able to both induce NF-kappaB binding (Fig.  4 A, lane 18) and block the effects of TPA (Fig.  4 A, lane 12) on the mobility of the pets complex.	bind
35906	1	8425	5	13	NULL	NULL	NULL	VEGF	GP		bind					KDR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_20556_s_341	9685413	50% inhibition of VEGF binding to KDR required about 2 or 3 x 10 12M for aptamers t22-OMe and t44-OMe, respectively, 6 x 10 11M for t2-OMe, and 5 x 10 8M for scr-t44-OMe.	bind
35907	2	8425	5	13	NULL	NULL	NULL	t22-OMe	NucleicAcid		is a type of					aptamer	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_20556_s_341	9685413	50% inhibition of VEGF binding to KDR required about 2 or 3 x 10 12M for aptamers t22-OMe and t44-OMe, respectively, 6 x 10 11M for t2-OMe, and 5 x 10 8M for scr-t44-OMe.	bind
35908	3	8425	5	13	NULL	NULL	NULL	t44-OMe	NucleicAcid		is a type of					aptamer	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_20556_s_341	9685413	50% inhibition of VEGF binding to KDR required about 2 or 3 x 10 12M for aptamers t22-OMe and t44-OMe, respectively, 6 x 10 11M for t2-OMe, and 5 x 10 8M for scr-t44-OMe.	bind
35909	4	8425	5	13	NULL	NULL	NULL	t22-OMe	NucleicAcid		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_20556_s_341	9685413	50% inhibition of VEGF binding to KDR required about 2 or 3 x 10 12M for aptamers t22-OMe and t44-OMe, respectively, 6 x 10 11M for t2-OMe, and 5 x 10 8M for scr-t44-OMe.	bind
35910	5	8425	5	13	NULL	NULL	NULL	t44-OMe	NucleicAcid		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_20556_s_341	9685413	50% inhibition of VEGF binding to KDR required about 2 or 3 x 10 12M for aptamers t22-OMe and t44-OMe, respectively, 6 x 10 11M for t2-OMe, and 5 x 10 8M for scr-t44-OMe.	bind
28857	1	8425	6	NULL	NULL	0	NULL	VEGF	NULL		bind	NULL				KDR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_20556_s_341	9685413	50% inhibition of VEGF binding to KDR required about 2 or 3 x 10 12M for aptamers t22-OMe and t44-OMe, respectively, 6 x 10 11M for t2-OMe, and 5 x 10 8M for scr-t44-OMe.	bind
48139	2	8425	6	10	NULL	0	NULL	t22-OMe	NULL		is a type of	NULL				aptamer	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_20556_s_341	9685413	50% inhibition of VEGF binding to KDR required about 2 or 3 x 10 12M for aptamers t22-OMe and t44-OMe, respectively, 6 x 10 11M for t2-OMe, and 5 x 10 8M for scr-t44-OMe.	bind
48140	3	8425	6	10	NULL	0	NULL	t44-OMe	NULL		is a type of	NULL				aptamer	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_20556_s_341	9685413	50% inhibition of VEGF binding to KDR required about 2 or 3 x 10 12M for aptamers t22-OMe and t44-OMe, respectively, 6 x 10 11M for t2-OMe, and 5 x 10 8M for scr-t44-OMe.	bind
48141	4	8425	6	10	NULL	0	NULL	t22-OMe	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_20556_s_341	9685413	50% inhibition of VEGF binding to KDR required about 2 or 3 x 10 12M for aptamers t22-OMe and t44-OMe, respectively, 6 x 10 11M for t2-OMe, and 5 x 10 8M for scr-t44-OMe.	bind
48142	5	8425	6	10	NULL	0	NULL	t44-OMe	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_20556_s_341	9685413	50% inhibition of VEGF binding to KDR required about 2 or 3 x 10 12M for aptamers t22-OMe and t44-OMe, respectively, 6 x 10 11M for t2-OMe, and 5 x 10 8M for scr-t44-OMe.	bind
35911	1	8426	5	13	NULL	NULL	NULL	pRB	GP		associate with		specifically			E2F-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_3_919_s_275	10980131	50, 55- 61 pRB seems to associate specifically with E2F-1, E2F-2, and E2F-3, 59 whereas p107 binds E2F-4 56, 61  and p130 binds E2F-4 and E2F-5.	bind
35913	2	8426	5	13	NULL	NULL	NULL	pRB	GP		associate with		specifically			E2F-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_3_919_s_275	10980131	50, 55- 61 pRB seems to associate specifically with E2F-1, E2F-2, and E2F-3, 59 whereas p107 binds E2F-4 56, 61  and p130 binds E2F-4 and E2F-5.	bind
35914	3	8426	5	13	NULL	NULL	NULL	pRB	GP		associate with		specifically			E2F-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_3_919_s_275	10980131	50, 55- 61 pRB seems to associate specifically with E2F-1, E2F-2, and E2F-3, 59 whereas p107 binds E2F-4 56, 61  and p130 binds E2F-4 and E2F-5.	bind
35915	4	8426	5	13	NULL	NULL	NULL	p107	GP		bind					E2F-4	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_3_919_s_275	10980131	50, 55- 61 pRB seems to associate specifically with E2F-1, E2F-2, and E2F-3, 59 whereas p107 binds E2F-4 56, 61  and p130 binds E2F-4 and E2F-5.	bind
35916	5	8426	5	13	NULL	NULL	NULL	p130	GP		bind					E2F-4	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_3_919_s_275	10980131	50, 55- 61 pRB seems to associate specifically with E2F-1, E2F-2, and E2F-3, 59 whereas p107 binds E2F-4 56, 61  and p130 binds E2F-4 and E2F-5.	bind
35917	6	8426	5	13	NULL	NULL	NULL	p130	GP		bind					E2F-5	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_3_919_s_275	10980131	50, 55- 61 pRB seems to associate specifically with E2F-1, E2F-2, and E2F-3, 59 whereas p107 binds E2F-4 56, 61  and p130 binds E2F-4 and E2F-5.	bind
28858	1	8426	6	NULL	NULL	0	NULL	pRB	NULL		associate	NULL	specifically			E2F-1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_3_919_s_275	10980131	50, 55- 61 pRB seems to associate specifically with E2F-1, E2F-2, and E2F-3, 59 whereas p107 binds E2F-4 56, 61  and p130 binds E2F-4 and E2F-5.	bind
28859	2	8426	6	NULL	NULL	0	NULL	pRB	NULL		associate	NULL	specifically			E2F-2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_3_919_s_275	10980131	50, 55- 61 pRB seems to associate specifically with E2F-1, E2F-2, and E2F-3, 59 whereas p107 binds E2F-4 56, 61  and p130 binds E2F-4 and E2F-5.	bind
28860	3	8426	6	NULL	NULL	0	NULL	pRB	NULL		associate	NULL	specifically			E2F-3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_3_919_s_275	10980131	50, 55- 61 pRB seems to associate specifically with E2F-1, E2F-2, and E2F-3, 59 whereas p107 binds E2F-4 56, 61  and p130 binds E2F-4 and E2F-5.	bind
28861	4	8426	6	NULL	NULL	0	NULL	p107	NULL		bind	NULL				E2F-4	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_3_919_s_275	10980131	50, 55- 61 pRB seems to associate specifically with E2F-1, E2F-2, and E2F-3, 59 whereas p107 binds E2F-4 56, 61  and p130 binds E2F-4 and E2F-5.	bind
28862	5	8426	6	NULL	NULL	0	NULL	p130	NULL		bind	NULL				E2F-4	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_3_919_s_275	10980131	50, 55- 61 pRB seems to associate specifically with E2F-1, E2F-2, and E2F-3, 59 whereas p107 binds E2F-4 56, 61  and p130 binds E2F-4 and E2F-5.	bind
28863	6	8426	6	NULL	NULL	0	NULL	p130	NULL		bind	NULL				E2F-5	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_3_919_s_275	10980131	50, 55- 61 pRB seems to associate specifically with E2F-1, E2F-2, and E2F-3, 59 whereas p107 binds E2F-4 56, 61  and p130 binds E2F-4 and E2F-5.	bind
36086	1	8427	5	13	NULL	NULL	NULL	Pit-1	GP		enhance					Pitx2 bound complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_20066_s_195	9685346	50-fold molar excess of unlabeled  bicoid competitor DNA competed for the Pit-1-enhanced Pitx2 bound complex.	bind
36104	2	8427	5	13	NULL	NULL	NULL	bicoid DNA	NucleicAcid	unlabeled	bind					Pitx2 bound complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_20066_s_195	9685346	50-fold molar excess of unlabeled  bicoid competitor DNA competed for the Pit-1-enhanced Pitx2 bound complex.	bind
36105	3	8427	5	13	NULL	NULL	NULL	statement 2	Process		competes with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_20066_s_195	9685346	50-fold molar excess of unlabeled  bicoid competitor DNA competed for the Pit-1-enhanced Pitx2 bound complex.	bind
28864	1	8427	6	NULL	NULL	0	NULL	Pit-1	NULL		enhances	NULL				Pitx2 bound complex	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_20066_s_195	9685346	50-fold molar excess of unlabeled  bicoid competitor DNA competed for the Pit-1-enhanced Pitx2 bound complex.	bind
29029	2	8427	6	NULL	NULL	0	NULL	bicoid competitor DNA	NULL	unlabeled	competes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_20066_s_195	9685346	50-fold molar excess of unlabeled  bicoid competitor DNA competed for the Pit-1-enhanced Pitx2 bound complex.	bind
47876	3	8427	6	10	NULL	0	NULL	statement 2	NULL		compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_20066_s_195	9685346	50-fold molar excess of unlabeled  bicoid competitor DNA competed for the Pit-1-enhanced Pitx2 bound complex.	bind
36106	1	8435	5	13	NULL	NULL	NULL	PDGF-AA	GP		does not supress					SMC	Cell	migration of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_305_s_239	9710123	51  Our data that PDGF-AA failed to suppress SMC migration on a Vitrogen-coated filter are consistent with the report that HSPG binds to intact fibrillar type I collagen but not to pepsin-digested type I collagen, such as Vitrogen.	bind
36107	2	8435	5	13	NULL	NULL	NULL	HSPG	GP		bind					fibrillar type I collagen	GP	intact			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_305_s_239	9710123	51  Our data that PDGF-AA failed to suppress SMC migration on a Vitrogen-coated filter are consistent with the report that HSPG binds to intact fibrillar type I collagen but not to pepsin-digested type I collagen, such as Vitrogen.	bind
36108	3	8435	5	13	NULL	NULL	NULL	HSPG	GP		does not bind					Vitrogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_305_s_239	9710123	51  Our data that PDGF-AA failed to suppress SMC migration on a Vitrogen-coated filter are consistent with the report that HSPG binds to intact fibrillar type I collagen but not to pepsin-digested type I collagen, such as Vitrogen.	bind
36109	4	8435	5	13	NULL	NULL	NULL	Vitrogen	GP		is a type of					pepsin-digested type I collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_305_s_239	9710123	51  Our data that PDGF-AA failed to suppress SMC migration on a Vitrogen-coated filter are consistent with the report that HSPG binds to intact fibrillar type I collagen but not to pepsin-digested type I collagen, such as Vitrogen.	bind
28865	1	8435	6	10	NULL	0	NULL	vitrogen			is a type of					pepsin-digested type I collagen					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_305_s_239	9710123	51  Our data that PDGF-AA failed to suppress SMC migration on a Vitrogen-coated filter are consistent with the report that HSPG binds to intact fibrillar type I collagen but not to pepsin-digested type I collagen, such as Vitrogen.	bind
28866	2	8435	6	NULL	NULL	0	NULL	HSPG	NULL		bind	NULL				fibrillar type I collagen	NULL	intact			NULL		0	NULL	NULL	NULL	gw60_circulationres_83_3_305_s_239	9710123	51  Our data that PDGF-AA failed to suppress SMC migration on a Vitrogen-coated filter are consistent with the report that HSPG binds to intact fibrillar type I collagen but not to pepsin-digested type I collagen, such as Vitrogen.	bind
28867	3	8435	6	NULL	NULL	0	NULL	HSPG	NULL		does not bind	NULL				vitrogen	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_3_305_s_239	9710123	51  Our data that PDGF-AA failed to suppress SMC migration on a Vitrogen-coated filter are consistent with the report that HSPG binds to intact fibrillar type I collagen but not to pepsin-digested type I collagen, such as Vitrogen.	bind
28868	4	8435	6	NULL	NULL	0	NULL	PDGF-AA	NULL		failed to suppress	NULL				SMC	NULL	migration of			NULL		0	NULL	NULL	NULL	gw60_circulationres_83_3_305_s_239	9710123	51  Our data that PDGF-AA failed to suppress SMC migration on a Vitrogen-coated filter are consistent with the report that HSPG binds to intact fibrillar type I collagen but not to pepsin-digested type I collagen, such as Vitrogen.	bind
36110	1	8436	5	13	NULL	NULL	NULL	serum response factors	GP		bind									SRE	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_284	10205148	51  SRE is regulated by the binding of serum response factors and TCF, the transcriptional activities of which are enhanced by their phosphorylation.	bind
36111	2	8436	5	13	NULL	NULL	NULL	statement 1	Process		regulates									SRE	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_284	10205148	51  SRE is regulated by the binding of serum response factors and TCF, the transcriptional activities of which are enhanced by their phosphorylation.	bind
36112	3	8436	5	13	NULL	NULL	NULL	TCF	GP		bind									SRE	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_284	10205148	51  SRE is regulated by the binding of serum response factors and TCF, the transcriptional activities of which are enhanced by their phosphorylation.	bind
36113	4	8436	5	13	NULL	NULL	NULL	statement 3	Process		regulates									SRE	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_284	10205148	51  SRE is regulated by the binding of serum response factors and TCF, the transcriptional activities of which are enhanced by their phosphorylation.	bind
36114	5	8436	5	13	NULL	NULL	NULL	TCF	GP	phosphorylation of	enhance					TCF	GP	transcriptional activities of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_284	10205148	51  SRE is regulated by the binding of serum response factors and TCF, the transcriptional activities of which are enhanced by their phosphorylation.	bind
36115	6	8436	5	13	NULL	NULL	NULL	serum response factors	GP	phosphorylation of	enhance					serum response factors	GP	transcriptional activities of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_284	10205148	51  SRE is regulated by the binding of serum response factors and TCF, the transcriptional activities of which are enhanced by their phosphorylation.	bind
28869	1	8436	6	10	NULL	0	NULL	serum response factors	NULL		bind	NULL					NULL			SRE	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_284	10205148	51  SRE is regulated by the binding of serum response factors and TCF, the transcriptional activities of which are enhanced by their phosphorylation.	bind
28870	2	8436	6	NULL	NULL	0	NULL	statement 1	NULL		regulates	NULL					NULL			SRE	NULL		0	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_284	10205148	51  SRE is regulated by the binding of serum response factors and TCF, the transcriptional activities of which are enhanced by their phosphorylation.	bind
28871	3	8436	6	NULL	NULL	0	NULL	serum response factors	NULL	phosphorylation of	enhances	NULL				serum response factor	NULL	transcriptional activity of			NULL		0	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_284	10205148	51  SRE is regulated by the binding of serum response factors and TCF, the transcriptional activities of which are enhanced by their phosphorylation.	bind
28872	4	8436	6	NULL	NULL	0	NULL	TCF	NULL	phosphorylation of	enhances	NULL				TCF	NULL	transcriptional activity of			NULL		0	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_284	10205148	51  SRE is regulated by the binding of serum response factors and TCF, the transcriptional activities of which are enhanced by their phosphorylation.	bind
48143	5	8436	6	10	NULL	0	NULL	TCF	NULL		bind	NULL					NULL			SRE	NULL		0	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_284	10205148	51  SRE is regulated by the binding of serum response factors and TCF, the transcriptional activities of which are enhanced by their phosphorylation.	bind
48144	6	8436	6	10	NULL	0	NULL	statement 5	NULL		regulates	NULL					NULL			SRE	NULL		0	NULL	NULL	NULL	gw60_circulationres_84_7_804_s_284	10205148	51  SRE is regulated by the binding of serum response factors and TCF, the transcriptional activities of which are enhanced by their phosphorylation.	bind
36116	1	8437	5	13	NULL	NULL	NULL	cdk4	GP		complex with		stably			p16Ink4a	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_2_405_s_177	12163365	51, 52  Moreover, stable complexes between cdk4 and p16Ink4a were detected in several cell types and induction of these binary complexes caused marked inhibition of cdk2 activity by redistribution of cyclin and CKI subunits, particularly those involving p27Kip1 that bind and inhibit cdk2 activity.	bind
36117	2	8437	5	13	NULL	NULL	NULL	cdk4-p16Ink4a cpmplex	GP	induction of	inhibit					cdk2	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_2_405_s_177	12163365	51, 52  Moreover, stable complexes between cdk4 and p16Ink4a were detected in several cell types and induction of these binary complexes caused marked inhibition of cdk2 activity by redistribution of cyclin and CKI subunits, particularly those involving p27Kip1 that bind and inhibit cdk2 activity.	bind
36118	3	8437	5	13	NULL	NULL	NULL	cyclin subunits	GP	redistribution of 	leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_2_405_s_177	12163365	51, 52  Moreover, stable complexes between cdk4 and p16Ink4a were detected in several cell types and induction of these binary complexes caused marked inhibition of cdk2 activity by redistribution of cyclin and CKI subunits, particularly those involving p27Kip1 that bind and inhibit cdk2 activity.	bind
36119	4	8437	5	13	NULL	NULL	NULL	CKI subunits	GP	redistribution of	leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_2_405_s_177	12163365	51, 52  Moreover, stable complexes between cdk4 and p16Ink4a were detected in several cell types and induction of these binary complexes caused marked inhibition of cdk2 activity by redistribution of cyclin and CKI subunits, particularly those involving p27Kip1 that bind and inhibit cdk2 activity.	bind
36120	5	8437	5	13	NULL	NULL	NULL	p27Kip1	GP		bind					cdk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_2_405_s_177	12163365	51, 52  Moreover, stable complexes between cdk4 and p16Ink4a were detected in several cell types and induction of these binary complexes caused marked inhibition of cdk2 activity by redistribution of cyclin and CKI subunits, particularly those involving p27Kip1 that bind and inhibit cdk2 activity.	bind
36121	6	8437	5	13	NULL	NULL	NULL	statement 5	Process		inhibit					cdk2	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_2_405_s_177	12163365	51, 52  Moreover, stable complexes between cdk4 and p16Ink4a were detected in several cell types and induction of these binary complexes caused marked inhibition of cdk2 activity by redistribution of cyclin and CKI subunits, particularly those involving p27Kip1 that bind and inhibit cdk2 activity.	bind
28873	1	8437	6	NULL	NULL	0	NULL	cdk4	NULL		forms a complex with	NULL				p16INK4a	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_2_405_s_177	12163365	51, 52  Moreover, stable complexes between cdk4 and p16Ink4a were detected in several cell types and induction of these binary complexes caused marked inhibition of cdk2 activity by redistribution of cyclin and CKI subunits, particularly those involving p27Kip1 that bind and inhibit cdk2 activity.	bind
28875	2	8437	6	NULL	NULL	0	NULL	p27Kip1	NULL		bind	NULL				cdk2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_2_405_s_177	12163365	51, 52  Moreover, stable complexes between cdk4 and p16Ink4a were detected in several cell types and induction of these binary complexes caused marked inhibition of cdk2 activity by redistribution of cyclin and CKI subunits, particularly those involving p27Kip1 that bind and inhibit cdk2 activity.	bind
28876	3	8437	6	NULL	NULL	0	NULL	p27Kip1	NULL		inhibit	NULL				cdk2	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_2_405_s_177	12163365	51, 52  Moreover, stable complexes between cdk4 and p16Ink4a were detected in several cell types and induction of these binary complexes caused marked inhibition of cdk2 activity by redistribution of cyclin and CKI subunits, particularly those involving p27Kip1 that bind and inhibit cdk2 activity.	bind
28877	4	8437	6	NULL	NULL	0	NULL	statement 1	NULL	induction of	causes	NULL				cdk2 	NULL	inhibiton of;; activity of 			NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_2_405_s_177	12163365	51, 52  Moreover, stable complexes between cdk4 and p16Ink4a were detected in several cell types and induction of these binary complexes caused marked inhibition of cdk2 activity by redistribution of cyclin and CKI subunits, particularly those involving p27Kip1 that bind and inhibit cdk2 activity.	bind
28878	5	8437	6	NULL	NULL	0	NULL	statement 4	NULL		occurs via	NULL				cyclin subunit	NULL	redistribution of 			NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_2_405_s_177	12163365	51, 52  Moreover, stable complexes between cdk4 and p16Ink4a were detected in several cell types and induction of these binary complexes caused marked inhibition of cdk2 activity by redistribution of cyclin and CKI subunits, particularly those involving p27Kip1 that bind and inhibit cdk2 activity.	bind
28879	6	8437	6	NULL	NULL	0	NULL	statement 4	NULL		occurs via	NULL				CKI subunit	NULL	redistribution of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_2_405_s_177	12163365	51, 52  Moreover, stable complexes between cdk4 and p16Ink4a were detected in several cell types and induction of these binary complexes caused marked inhibition of cdk2 activity by redistribution of cyclin and CKI subunits, particularly those involving p27Kip1 that bind and inhibit cdk2 activity.	bind
36122	1	8439	5	13	NULL	NULL	NULL	C/EBP decoy oligonucleotide	NucleicAcid		reduces					intimal hyperplasia	MedicalFinding				NULL	balloon-injured carotid artery of a rabbit atherosclerosis model	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_112	15681294	51,52  The results of a recent study have shown that administration of a C/EBP decoy oligonucleotide into a balloon-injured carotid artery of a rabbit atherosclerosis model reduced intimal hyperplasia and attenuated vascular inflammation accompanied by a complete inhibition of C/EBP protein binding to a consensus C/EBP sequence.	bind
36123	2	8439	5	13	NULL	NULL	NULL	C/EBP decoy oligonucleotide	NucleicAcid		attenuates					vascular inflammation	MedicalFinding				NULL	balloon-injured carotid artery of a rabbit atherosclerosis model	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_112	15681294	51,52  The results of a recent study have shown that administration of a C/EBP decoy oligonucleotide into a balloon-injured carotid artery of a rabbit atherosclerosis model reduced intimal hyperplasia and attenuated vascular inflammation accompanied by a complete inhibition of C/EBP protein binding to a consensus C/EBP sequence.	bind
36124	3	8439	5	13	NULL	NULL	NULL	C/EBP protein	GP		bind							consensus		C/EBP sequence	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_112	15681294	51,52  The results of a recent study have shown that administration of a C/EBP decoy oligonucleotide into a balloon-injured carotid artery of a rabbit atherosclerosis model reduced intimal hyperplasia and attenuated vascular inflammation accompanied by a complete inhibition of C/EBP protein binding to a consensus C/EBP sequence.	bind
36125	4	8439	5	13	NULL	NULL	NULL	statement 1	Process		is followed by					statement 3	Process	inhibition of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_112	15681294	51,52  The results of a recent study have shown that administration of a C/EBP decoy oligonucleotide into a balloon-injured carotid artery of a rabbit atherosclerosis model reduced intimal hyperplasia and attenuated vascular inflammation accompanied by a complete inhibition of C/EBP protein binding to a consensus C/EBP sequence.	bind
36126	5	8439	5	13	NULL	NULL	NULL	statement 2	Process		is followed by					statement 3	Process	inhibition of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_112	15681294	51,52  The results of a recent study have shown that administration of a C/EBP decoy oligonucleotide into a balloon-injured carotid artery of a rabbit atherosclerosis model reduced intimal hyperplasia and attenuated vascular inflammation accompanied by a complete inhibition of C/EBP protein binding to a consensus C/EBP sequence.	bind
28880	1	8439	6	NULL	NULL	0	NULL	C/EBP decoy oligonucleotide	NULL		reduces	NULL				intimal hyperplasia	NULL				NULL	rabbit atherosclerosis model	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_112	15681294	51,52  The results of a recent study have shown that administration of a C/EBP decoy oligonucleotide into a balloon-injured carotid artery of a rabbit atherosclerosis model reduced intimal hyperplasia and attenuated vascular inflammation accompanied by a complete inhibition of C/EBP protein binding to a consensus C/EBP sequence.	bind
28881	2	8439	6	NULL	NULL	0	NULL	C/EBP decoy oligonucleotide	NULL		attenuates	NULL				vascular inflammation	NULL				NULL	rabbit atherosclerosis model	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_112	15681294	51,52  The results of a recent study have shown that administration of a C/EBP decoy oligonucleotide into a balloon-injured carotid artery of a rabbit atherosclerosis model reduced intimal hyperplasia and attenuated vascular inflammation accompanied by a complete inhibition of C/EBP protein binding to a consensus C/EBP sequence.	bind
28882	3	8439	6	NULL	NULL	0	NULL	C/EBP protein	NULL		bind	NULL					NULL	consensus		C/EBP sequence	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_112	15681294	51,52  The results of a recent study have shown that administration of a C/EBP decoy oligonucleotide into a balloon-injured carotid artery of a rabbit atherosclerosis model reduced intimal hyperplasia and attenuated vascular inflammation accompanied by a complete inhibition of C/EBP protein binding to a consensus C/EBP sequence.	bind
28883	4	8439	6	NULL	NULL	0	NULL	C/EBP decoy oligonucleotide	NULL		inhibits	NULL	completely			statement 3	NULL				NULL	rabbit atherosclerosis model	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_112	15681294	51,52  The results of a recent study have shown that administration of a C/EBP decoy oligonucleotide into a balloon-injured carotid artery of a rabbit atherosclerosis model reduced intimal hyperplasia and attenuated vascular inflammation accompanied by a complete inhibition of C/EBP protein binding to a consensus C/EBP sequence.	bind
36127	1	8440	5	13	NULL	NULL	NULL	EBNA1 protein	GP		bind		constitutively					Epstein-Barr virus		oriP	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3520_s_443	11522821	52       Hsieh,D.-J., Camiolo,S.M. and Yates,J.L. (1993) Constitutive binding of EBNA1 protein to the Epstein-Barr virus replication origin, oriP, with distortion of DNA structure during latent infection.	bind
36128	2	8440	5	13	NULL	NULL	NULL	oriP	NucleicAcid		is					replication origin	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3520_s_443	11522821	52       Hsieh,D.-J., Camiolo,S.M. and Yates,J.L. (1993) Constitutive binding of EBNA1 protein to the Epstein-Barr virus replication origin, oriP, with distortion of DNA structure during latent infection.	bind
36129	3	8440	5	13	NULL	NULL	NULL	statement 1	Process		distorts					DNA	NucleicAcid	structure of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3520_s_443	11522821	52       Hsieh,D.-J., Camiolo,S.M. and Yates,J.L. (1993) Constitutive binding of EBNA1 protein to the Epstein-Barr virus replication origin, oriP, with distortion of DNA structure during latent infection.	bind
28884	1	8440	6	NULL	NULL	0	NULL	EBNA1 protein	NULL		bind	NULL				oriP	NULL	epstein-Barr virus			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3520_s_443	11522821	52       Hsieh,D.-J., Camiolo,S.M. and Yates,J.L. (1993) Constitutive binding of EBNA1 protein to the Epstein-Barr virus replication origin, oriP, with distortion of DNA structure during latent infection.	bind
28885	2	8440	6	NULL	NULL	0	NULL	oriP	NULL		is	NULL				replication origin	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3520_s_443	11522821	52       Hsieh,D.-J., Camiolo,S.M. and Yates,J.L. (1993) Constitutive binding of EBNA1 protein to the Epstein-Barr virus replication origin, oriP, with distortion of DNA structure during latent infection.	bind
36131	1	8441	5	13	NULL	NULL	NULL	estrogen receptor	GP		bind		cooperative					imperfect		estrogen-responsive DNA elements	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_399	11452016	52       Martinez,E., Givel,F. and Wahli,W. (1989) Cooperative binding of estrogen receptor to imperfect estrogen-responsive DNA elements correlates with their synergistic hormone-dependent enhancer activity.	bind
36132	2	8441	5	13	NULL	NULL	NULL	statement 1	Process		coorelates with					estrogen receptor	GP	synergistic;;enhancer activity of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_399	11452016	52       Martinez,E., Givel,F. and Wahli,W. (1989) Cooperative binding of estrogen receptor to imperfect estrogen-responsive DNA elements correlates with their synergistic hormone-dependent enhancer activity.	bind
36133	3	8441	5	13	NULL	NULL	NULL	estrogen receptor	GP	enhancer activity of	dependent on					hormone	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_399	11452016	52       Martinez,E., Givel,F. and Wahli,W. (1989) Cooperative binding of estrogen receptor to imperfect estrogen-responsive DNA elements correlates with their synergistic hormone-dependent enhancer activity.	bind
28886	1	8441	6	NULL	NULL	0	NULL	estrogen receptor	NULL		bind	NULL	cooperatively				NULL	imperfect		estrogen-responsive DNA element	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_399	11452016	52       Martinez,E., Givel,F. and Wahli,W. (1989) Cooperative binding of estrogen receptor to imperfect estrogen-responsive DNA elements correlates with their synergistic hormone-dependent enhancer activity.	bind
28888	2	8441	6	10	NULL	0	NULL	estrogen receptor		enhancer activity of	is dependent on					hormone					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_399	11452016	52       Martinez,E., Givel,F. and Wahli,W. (1989) Cooperative binding of estrogen receptor to imperfect estrogen-responsive DNA elements correlates with their synergistic hormone-dependent enhancer activity.	bind
28889	3	8441	6	10	NULL	0	NULL	statement 1			correlates with					estrogen receptor		synergistic;;enhancer activity of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_399	11452016	52       Martinez,E., Givel,F. and Wahli,W. (1989) Cooperative binding of estrogen receptor to imperfect estrogen-responsive DNA elements correlates with their synergistic hormone-dependent enhancer activity.	bind
36134	1	8442	5	13	NULL	NULL	NULL	SCF protein	GP		bind					mast cells	Cell	skin			NULL	lesions of patients with urticaria pigmentosa	NULL	NULL	NULL	NULL	gw60_circulation_97_10_971_s_210	9529265	52  Moreover, SCF protein has been detected bound to skin mast cells in lesions of patients with urticaria pigmentosa.	bind
28890	1	8442	6	NULL	NULL	0	NULL	SCF protein	NULL		bind	NULL				mast cells	NULL	skin			NULL	lesions of patients with urticaria pigmentosa	0	NULL	NULL	NULL	gw60_circulation_97_10_971_s_210	9529265	52  Moreover, SCF protein has been detected bound to skin mast cells in lesions of patients with urticaria pigmentosa.	bind
36136	1	8443	5	13	NULL	NULL	NULL	membrane receptor	GP		bind					E2	Chemical				NULL	in endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
36137	2	8443	5	13	NULL	NULL	NULL	membrane receptor	GP		bind					E2-BSA	Chemical				NULL	in endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
36138	3	8443	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
36139	4	8443	5	13	NULL	NULL	NULL	statement 1	Process		activate		selectively			p38beta MAPK	GP	antiapoptotic			NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
36140	5	8443	5	13	NULL	NULL	NULL	statement 1	Process		inhibit		selectively			p38alpha	GP	proapoptotic			NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
36141	6	8443	5	13	NULL	NULL	NULL	statement 2	Process		activates		selectively			p38beta MAPK	GP	antiapoptotic			NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
36142	7	8443	5	13	NULL	NULL	NULL	statement 2	Process		inhibit		selectively			p38alpha	GP	proapoptotic			NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
36143	8	8443	5	13	NULL	NULL	NULL	statement 4	Process		leads to					MAPK-activated protein kinase-2 kinase	GP	upregulation of			NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
36144	9	8443	5	13	NULL	NULL	NULL	statement 5	Process		leads to					MAPK-activated protein kinase-2 kinase	GP	upregulation of			NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
36145	10	8443	5	13	NULL	NULL	NULL	statement 6	Process		leads to					MAPK-activated protein kinase-2 kinase	GP	upregulation of			NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
36146	11	8443	5	13	NULL	NULL	NULL	statement 7	Process		leads to					MAPK-activated protein kinase-2 kinase	GP	upregulation of			NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
36147	12	8443	5	13	NULL	NULL	NULL	statement 4	Process		leads to					hsp27	GP	phosphorylation of			NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
36148	13	8443	5	13	NULL	NULL	NULL	statement 5	Process		leads to					hsp27	GP	phosphorylation of			NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
36149	14	8443	5	13	NULL	NULL	NULL	statement 6	Process		leads to					hsp27	GP	phosphorylation of			NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
36150	15	8443	5	13	NULL	NULL	NULL	statement 7	Process		leads to					hsp27	GP	phosphorylation of			NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
36151	16	8443	5	13	NULL	NULL	NULL	hsp27	GP		is a type of					heat shock protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
56156	17	8443	5	13	NULL	NULL	NULL	EC	Cell		is					endothelial cell	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
28891	1	8443	6	10	NULL	0	NULL	membrane receptor			bind					E2					NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
28892	2	8443	6	10	NULL	0	NULL	membrane receptor			bind					E2-BSA					NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
28893	3	8443	6	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
28894	4	8443	6	NULL	NULL	0	NULL	endothelial cell membrane receptor	NULL		activates	NULL	selectively			p38beta MAPK	NULL	antiapoptotic			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
28895	5	8443	6	NULL	NULL	0	NULL	endothelial cell membrane receptor	NULL		inhibits	NULL				p38alpha	NULL	proapoptotic			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
28896	6	8443	6	NULL	NULL	0	NULL	statement 4	NULL		leads to	NULL				MAPK-activated protein kinase-2 kinase	NULL	upregulation of 			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
28897	7	8443	6	NULL	NULL	0	NULL	statement 5	NULL		leads to	NULL				MAPK-activated protein kinase-2 kinase	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
28898	8	8443	6	NULL	NULL	0	NULL	statement 4	NULL		leads to	NULL				hsp27	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
28899	9	8443	6	NULL	NULL	0	NULL	statement 5	NULL		leads to	NULL				hsp27	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
28900	10	8443	6	NULL	NULL	0	NULL	hsp27	NULL		is a type of	NULL				heat shock protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
28901	11	8443	6	NULL	NULL	0	NULL	EC	NULL		is	NULL				endothelial cells	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1952_s_67	12482819	52 Of particular relevance to the vascular system is the observation of a membrane receptor in endothelial cells (ECs) that binds either E2 or E2-BSA rapidly and selectively activates antiapoptotic p38beta MAPK and inhibits proapoptotic p38alpha, leading to upregulation of MAPK-activated protein kinase-2 kinase and phosphorylation of heat shock protein hsp27.	bind
36152	1	8444	5	13	NULL	NULL	NULL	apoA-I	GP		bind					ABCA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_720_s_139	12615680	52 These studies imply that binding of apoA-I to ABCA1 may be necessary but not sufficient for stimulating cholesterol efflux.	bind
36153	2	8444	5	13	NULL	NULL	NULL	statement 1	Process		stimulate					cholesterol efflux	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_720_s_139	12615680	52 These studies imply that binding of apoA-I to ABCA1 may be necessary but not sufficient for stimulating cholesterol efflux.	bind
36154	3	8444	5	13	NULL	NULL	NULL	statement 1	Process		is necessary for		may be			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_720_s_139	12615680	52 These studies imply that binding of apoA-I to ABCA1 may be necessary but not sufficient for stimulating cholesterol efflux.	bind
36155	4	8444	5	13	NULL	NULL	NULL	statement 1	Process		not sufficient for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_720_s_139	12615680	52 These studies imply that binding of apoA-I to ABCA1 may be necessary but not sufficient for stimulating cholesterol efflux.	bind
28902	1	8444	6	NULL	NULL	0	NULL	apoA-I	NULL		bind	NULL				ABCA1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_720_s_139	12615680	52 These studies imply that binding of apoA-I to ABCA1 may be necessary but not sufficient for stimulating cholesterol efflux.	bind
28903	2	8444	6	NULL	NULL	0	NULL	statement 1	NULL		is necessary for	NULL	may			cholesterol efflux	NULL	stimulation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_720_s_139	12615680	52 These studies imply that binding of apoA-I to ABCA1 may be necessary but not sufficient for stimulating cholesterol efflux.	bind
28904	3	8444	6	NULL	NULL	0	NULL	statement 1	NULL		is not sufficient for	NULL				cholesterol efflux	NULL	stimulation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_720_s_139	12615680	52 These studies imply that binding of apoA-I to ABCA1 may be necessary but not sufficient for stimulating cholesterol efflux.	bind
36156	1	8445	5	13	NULL	NULL	NULL	lipocalins	GP	tear	bind					lipid ligands	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1514_s_495	11266553	53       Glasgow,B.J., Abduragimov,A.R., Farabakhsh,Z.T., Faull,K.F. and Hubbell,W.L. (1995) Tear lipocalins bind a broad array of lipid ligands.	bind
28905	1	8445	6	10	NULL	0	NULL	lipocalins		tear	bind					lipid ligands					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1514_s_495	11266553	53       Glasgow,B.J., Abduragimov,A.R., Farabakhsh,Z.T., Faull,K.F. and Hubbell,W.L. (1995) Tear lipocalins bind a broad array of lipid ligands.	bind
36157	1	8446	5	13	NULL	NULL	NULL	53BP1	GP		bind					BRCA1	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_8_6993_s_209	15569676	53BP1 also binds to BRCA1  in vivo; however, it does not bind after ionizing radiation and therefore is unlikely to directly anchor BRCA1 at focal assemblies ( ).	bind
36158	2	8446	5	13	NULL	NULL	NULL	statement 1	Process		does not occur after					ionizing radiation					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_8_6993_s_209	15569676	53BP1 also binds to BRCA1  in vivo; however, it does not bind after ionizing radiation and therefore is unlikely to directly anchor BRCA1 at focal assemblies ( ).	bind
36159	4	8446	5	13	NULL	NULL	NULL	statement 3	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_8_6993_s_209	15569676	53BP1 also binds to BRCA1  in vivo; however, it does not bind after ionizing radiation and therefore is unlikely to directly anchor BRCA1 at focal assemblies ( ).	bind
36160	3	8446	5	13	NULL	NULL	NULL	BRCA1	GP		cannot be anchored at		directly			focal assemblies	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_8_6993_s_209	15569676	53BP1 also binds to BRCA1  in vivo; however, it does not bind after ionizing radiation and therefore is unlikely to directly anchor BRCA1 at focal assemblies ( ).	bind
28906	1	8446	6	NULL	NULL	0	NULL	53BP1	NULL		bind	NULL				BRCA1	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw70_jbiolchem_280_8_6993_s_209	15569676	53BP1 also binds to BRCA1  in vivo; however, it does not bind after ionizing radiation and therefore is unlikely to directly anchor BRCA1 at focal assemblies ( ).	bind
28907	2	8446	6	NULL	NULL	0	NULL	statement 1	NULL		does not occur after	NULL				ionizing radiation	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_6993_s_209	15569676	53BP1 also binds to BRCA1  in vivo; however, it does not bind after ionizing radiation and therefore is unlikely to directly anchor BRCA1 at focal assemblies ( ).	bind
28908	3	8446	6	NULL	NULL	0	NULL	BRCA1	NULL		cannot be anchored at	NULL	directly			focal assemblies	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_6993_s_209	15569676	53BP1 also binds to BRCA1  in vivo; however, it does not bind after ionizing radiation and therefore is unlikely to directly anchor BRCA1 at focal assemblies ( ).	bind
28909	4	8446	6	NULL	NULL	0	NULL	statement 3	NULL		is due to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_6993_s_209	15569676	53BP1 also binds to BRCA1  in vivo; however, it does not bind after ionizing radiation and therefore is unlikely to directly anchor BRCA1 at focal assemblies ( ).	bind
36161	1	8447	5	13	NULL	NULL	NULL	53BP1	GP		bind			BRCT domain		p53	GP		CD		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_9_8051_s_277	15611070	53BP1 binds p53CD via its BRCT domain, which is another general protein recognition motif ( ,  ).	bind
28910	1	8447	6	10	NULL	0	NULL	53BP1	NULL		bind	NULL		BRCT domain		p53	NULL		CD		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_9_8051_s_277	15611070	53BP1 binds p53CD via its BRCT domain, which is another general protein recognition motif ( ,  ).	bind
36162	1	8448	5	13	NULL	NULL	NULL	53BP1	GP		bind			carboxyl terminus		p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_24_3387_s_360	9407031	53BP1 binds to a tumor suppressor protein p53 by the two-hybrid method, and the carboxyl terminus of 53BP1 is the site for binding to p53 (Iwabuchi et al. 1994  ).	bind
36163	2	8448	5	13	NULL	NULL	NULL	p53	GP		is a type of					tumor suppressor protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_24_3387_s_360	9407031	53BP1 binds to a tumor suppressor protein p53 by the two-hybrid method, and the carboxyl terminus of 53BP1 is the site for binding to p53 (Iwabuchi et al. 1994  ).	bind
28911	1	8448	6	NULL	NULL	0	NULL	53BP1	NULL		bind	NULL		carboxyl-terminal region		p53	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_11_24_3387_s_360	9407031	53BP1 binds to a tumor suppressor protein p53 by the two-hybrid method, and the carboxyl terminus of 53BP1 is the site for binding to p53 (Iwabuchi et al. 1994  ).	bind
28912	2	8448	6	NULL	NULL	0	NULL	p53	NULL		is a type of	NULL				tumor suppressor protein	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_11_24_3387_s_360	9407031	53BP1 binds to a tumor suppressor protein p53 by the two-hybrid method, and the carboxyl terminus of 53BP1 is the site for binding to p53 (Iwabuchi et al. 1994  ).	bind
36164	1	8449	5	13	NULL	NULL	NULL	53BP1	GP		bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_298_5597_1435_s_7	12364621	53BP1 binds to the tumor suppressor protein p53 and has a potential role in DNA damage responses.	bind
36165	2	8449	5	13	NULL	NULL	NULL	p53	GP		is a type of					tumor suppressor protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_298_5597_1435_s_7	12364621	53BP1 binds to the tumor suppressor protein p53 and has a potential role in DNA damage responses.	bind
36166	3	8449	5	13	NULL	NULL	NULL	53BP1	GP		plays a role in		potentially			DNA damage responses	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_298_5597_1435_s_7	12364621	53BP1 binds to the tumor suppressor protein p53 and has a potential role in DNA damage responses.	bind
28913	1	8449	6	NULL	NULL	0	NULL	53BP1	NULL		bind	NULL				p53	NULL				NULL		0	NULL	NULL	NULL	gw60_science_298_5597_1435_s_7	12364621	53BP1 binds to the tumor suppressor protein p53 and has a potential role in DNA damage responses.	bind
28914	2	8449	6	NULL	NULL	0	NULL	p53	NULL		is a type of	NULL				tumor suppressor protein	NULL				NULL		0	NULL	NULL	NULL	gw60_science_298_5597_1435_s_7	12364621	53BP1 binds to the tumor suppressor protein p53 and has a potential role in DNA damage responses.	bind
28915	3	8449	6	NULL	NULL	0	NULL	53BP1	NULL		has a role in	NULL	potential			DNA damage response	NULL				NULL		0	NULL	NULL	NULL	gw60_science_298_5597_1435_s_7	12364621	53BP1 binds to the tumor suppressor protein p53 and has a potential role in DNA damage responses.	bind
36167	1	8450	5	13	NULL	NULL	NULL	53BP1	GP		bind					p53	GP		central DNA-binding domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_7_2556_s_2	12640136	53BP1 is a p53 binding protein of unknown function that binds to the central DNA-binding domain of p53.	bind
47883	2	8450	5	13	NULL	NULL	NULL	53BP1 	GP		is a type of					p53 binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_7_2556_s_2	12640136	53BP1 is a p53 binding protein of unknown function that binds to the central DNA-binding domain of p53.	bind
28916	1	8450	6	NULL	NULL	0	NULL	53BP1	NULL		bind	NULL				p53	NULL		central DNA-binding domain		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_7_2556_s_2	12640136	53BP1 is a p53 binding protein of unknown function that binds to the central DNA-binding domain of p53.	bind
47884	2	8450	6	10	NULL	0	NULL	53BP1	NULL		is a type of	NULL				p53 binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_7_2556_s_2	12640136	53BP1 is a p53 binding protein of unknown function that binds to the central DNA-binding domain of p53.	bind
36168	1	8451	5	13	NULL	NULL	NULL	53BP2	GP		bind					p53C	GP		DNA binding site		NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_2_937_s_87	11782540	53BP2 binds p53C in its DNA binding site, with three loops making the contacts with p53 (ref.  10; Fig.  1).	bind
28917	1	8451	6	NULL	NULL	0	NULL	53BP2	NULL		bind	NULL		three loops		p53C	NULL		DNA binding site		NULL		0	NULL	NULL	NULL	gw60_pnas_99_2_937_s_87	11782540	53BP2 binds p53C in its DNA binding site, with three loops making the contacts with p53 (ref.  10; Fig.  1).	bind
36169	1	8452	5	13	NULL	NULL	NULL	53BP2	GP		bind		tightly			p53C	GP		R273H		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_43_32526_s_112	16887812	53BP2 bound tightly to p53C-R273H, although it is a contact mutant with substantially reduced DNA binding ( ).	bind
47885	2	8452	5	13	NULL	NULL	NULL	 p53C	GP	mutant	bind		reduced	R273H		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_43_32526_s_112	16887812	53BP2 bound tightly to p53C-R273H, although it is a contact mutant with substantially reduced DNA binding ( ).	bind
28918	1	8452	6	NULL	NULL	0	NULL	53BP2	NULL		bind	NULL	tightly			p53C	NULL	mutant	R273H		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32526_s_112	16887812	53BP2 bound tightly to p53C-R273H, although it is a contact mutant with substantially reduced DNA binding ( ).	bind
28919	2	8452	6	NULL	NULL	0	NULL	p53C	NULL	mutant	has reduced	NULL		R273H		DNA	NULL	binding of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32526_s_112	16887812	53BP2 bound tightly to p53C-R273H, although it is a contact mutant with substantially reduced DNA binding ( ).	bind
36170	1	8453	5	13	NULL	NULL	NULL	estrogen receptor	GP		bind									estrogen-responsive elements	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_405	11452016	54       Ludwig,L.B., Peale,F.V.,Jr, Klinge,C.M., Bambara,R.A., Zain,S. and Hilf,R. (1990) A microtiter well assay for quantitative measurement of estrogen receptor binding to estrogen-responsive elements.	bind
28920	1	8453	6	NULL	NULL	0	NULL	estrogen receptor	NULL		bind	NULL					NULL			estrogen-responsive element	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_405	11452016	54       Ludwig,L.B., Peale,F.V.,Jr, Klinge,C.M., Bambara,R.A., Zain,S. and Hilf,R. (1990) A microtiter well assay for quantitative measurement of estrogen receptor binding to estrogen-responsive elements.	bind
36171	1	8454	5	13	NULL	NULL	NULL	p53	GP		bind					bax	GP			promoter	NULL	myocytes of transgenic mice	NULL	NULL	NULL	NULL	gw60_circulationres_84_7_752_s_311	10205143	54  The quantity of Bax decreased in myocytes of transgenic mice, thus reflecting the attenuation in p53 binding to the bax promoter in these cells.	bind
36172	2	8454	5	13	NULL	NULL	NULL	statement 1	Process	attenuation of	decrease					Bax	GP	quantity of			NULL	myocytes of transgenic mice	NULL	NULL	NULL	NULL	gw60_circulationres_84_7_752_s_311	10205143	54  The quantity of Bax decreased in myocytes of transgenic mice, thus reflecting the attenuation in p53 binding to the bax promoter in these cells.	bind
28921	1	8454	6	NULL	NULL	0	NULL	p53	NULL		bind	NULL				bax	NULL			promoter	NULL	myocytes of transgenic mice	0	NULL	NULL	NULL	gw60_circulationres_84_7_752_s_311	10205143	54  The quantity of Bax decreased in myocytes of transgenic mice, thus reflecting the attenuation in p53 binding to the bax promoter in these cells.	bind
28922	2	8454	6	NULL	NULL	0	NULL	statement 1	NULL	attenuation of	decreases	NULL				Bax	NULL	quantity of			NULL	myocytes of transgenic mice	0	NULL	NULL	NULL	gw60_circulationres_84_7_752_s_311	10205143	54  The quantity of Bax decreased in myocytes of transgenic mice, thus reflecting the attenuation in p53 binding to the bax promoter in these cells.	bind
36733	1	8455	5	13	NULL	NULL	NULL	preheparin LPL	GP		does not bind					endothelium	Cell				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1236_s_117	16574898	54,57  Not bound to the endothelium, it is likely that this preheparin LPL concerns primarily catalytically inactive monomers, probably representing turnover of active dimeric LPL bound to HS-containing proteoglycans as indicated by the group of Olivecrona in 1993.	bind
36735	2	8455	5	13	NULL	NULL	NULL	LPL dimer	GP	active	bind					proteoglycans	GP	HS-containing			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1236_s_117	16574898	54,57  Not bound to the endothelium, it is likely that this preheparin LPL concerns primarily catalytically inactive monomers, probably representing turnover of active dimeric LPL bound to HS-containing proteoglycans as indicated by the group of Olivecrona in 1993.	bind
28923	1	8455	6	10	NULL	0	NULL	LPL dimer		active 	bind					proteoglycans		HS-containing			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1236_s_117	16574898	54,57  Not bound to the endothelium, it is likely that this preheparin LPL concerns primarily catalytically inactive monomers, probably representing turnover of active dimeric LPL bound to HS-containing proteoglycans as indicated by the group of Olivecrona in 1993.	bind
47886	2	8455	6	10	NULL	0	NULL	preheparin LPL	NULL		does not bind	NULL				endothelium	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_6_1236_s_117	16574898	54,57  Not bound to the endothelium, it is likely that this preheparin LPL concerns primarily catalytically inactive monomers, probably representing turnover of active dimeric LPL bound to HS-containing proteoglycans as indicated by the group of Olivecrona in 1993.	bind
36189	1	8456	5	13	NULL	NULL	NULL	54CP	GP		bind					LHCP	GP		third transmembrane domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_17_11622_s_123	9111079	54CP Binds to the Third Transmembrane Domain of LHCP	bind
28924	1	8456	6	NULL	NULL	0	NULL	54CP	NULL		bind	NULL				LHCP	NULL		Third Transmembrane Domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_17_11622_s_123	9111079	54CP Binds to the Third Transmembrane Domain of LHCP	bind
36190	1	8457	5	13	NULL	NULL	NULL	CKIs	GP		inhibit					CDK2	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_369_s_263	11438484	55  ikewise, transforming growth factor-beta growth arrest depends on the inhibition of CDK4 synthesis and further inhibition of CDK2 activity by CKIs. 56 Also, CDK4 disruption was associated with increased binding of p27Kip1 to cyclin E/CDK2 and diminished activation of CDK2 was accompanied by impaired pRb phosphorylation.	bind
36191	2	8457	5	13	NULL	NULL	NULL	CKIs	GP		inhibit					CDK4	GP	synthesis of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_369_s_263	11438484	55  ikewise, transforming growth factor-beta growth arrest depends on the inhibition of CDK4 synthesis and further inhibition of CDK2 activity by CKIs. 56 Also, CDK4 disruption was associated with increased binding of p27Kip1 to cyclin E/CDK2 and diminished activation of CDK2 was accompanied by impaired pRb phosphorylation.	bind
36192	3	8457	5	13	NULL	NULL	NULL	transforming growth factor-beta	GP	growth arrest of	depends on					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_369_s_263	11438484	55  ikewise, transforming growth factor-beta growth arrest depends on the inhibition of CDK4 synthesis and further inhibition of CDK2 activity by CKIs. 56 Also, CDK4 disruption was associated with increased binding of p27Kip1 to cyclin E/CDK2 and diminished activation of CDK2 was accompanied by impaired pRb phosphorylation.	bind
36193	4	8457	5	13	NULL	NULL	NULL	transforming growth factor-beta	GP	growth arrest of	depends on					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_369_s_263	11438484	55  ikewise, transforming growth factor-beta growth arrest depends on the inhibition of CDK4 synthesis and further inhibition of CDK2 activity by CKIs. 56 Also, CDK4 disruption was associated with increased binding of p27Kip1 to cyclin E/CDK2 and diminished activation of CDK2 was accompanied by impaired pRb phosphorylation.	bind
36194	5	8457	5	13	NULL	NULL	NULL	p27Kip1	GP		bind					cyclin E/CDK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_369_s_263	11438484	55  ikewise, transforming growth factor-beta growth arrest depends on the inhibition of CDK4 synthesis and further inhibition of CDK2 activity by CKIs. 56 Also, CDK4 disruption was associated with increased binding of p27Kip1 to cyclin E/CDK2 and diminished activation of CDK2 was accompanied by impaired pRb phosphorylation.	bind
36195	6	8457	5	13	NULL	NULL	NULL	CDK4	GP	disruption of	is associated with					statement 5	Process	increased			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_369_s_263	11438484	55  ikewise, transforming growth factor-beta growth arrest depends on the inhibition of CDK4 synthesis and further inhibition of CDK2 activity by CKIs. 56 Also, CDK4 disruption was associated with increased binding of p27Kip1 to cyclin E/CDK2 and diminished activation of CDK2 was accompanied by impaired pRb phosphorylation.	bind
36196	7	8457	5	13	NULL	NULL	NULL	CDK2	GP	diminished activation of	is accompanied by					pRb	GP	impaired phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_369_s_263	11438484	55  ikewise, transforming growth factor-beta growth arrest depends on the inhibition of CDK4 synthesis and further inhibition of CDK2 activity by CKIs. 56 Also, CDK4 disruption was associated with increased binding of p27Kip1 to cyclin E/CDK2 and diminished activation of CDK2 was accompanied by impaired pRb phosphorylation.	bind
29030	3	8457	6	10	NULL	0	NULL	transforming growth factor-beta	NULL	growth arrest of	depends on	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_369_s_263	11438484	55  ikewise, transforming growth factor-beta growth arrest depends on the inhibition of CDK4 synthesis and further inhibition of CDK2 activity by CKIs. 56 Also, CDK4 disruption was associated with increased binding of p27Kip1 to cyclin E/CDK2 and diminished activation of CDK2 was accompanied by impaired pRb phosphorylation.	bind
29031	2	8457	6	10	NULL	0	NULL	CKI	NULL		inhibits	NULL				CDK2 	NULL	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_369_s_263	11438484	55  ikewise, transforming growth factor-beta growth arrest depends on the inhibition of CDK4 synthesis and further inhibition of CDK2 activity by CKIs. 56 Also, CDK4 disruption was associated with increased binding of p27Kip1 to cyclin E/CDK2 and diminished activation of CDK2 was accompanied by impaired pRb phosphorylation.	bind
29032	4	8457	6	10	NULL	0	NULL	transforming growth factor-beta	NULL	growth arrest of	depends on	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_369_s_263	11438484	55  ikewise, transforming growth factor-beta growth arrest depends on the inhibition of CDK4 synthesis and further inhibition of CDK2 activity by CKIs. 56 Also, CDK4 disruption was associated with increased binding of p27Kip1 to cyclin E/CDK2 and diminished activation of CDK2 was accompanied by impaired pRb phosphorylation.	bind
29033	5	8457	6	10	NULL	0	NULL	p27Kip1	NULL		bind	NULL				cyclin E/cdk2 complex	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_369_s_263	11438484	55  ikewise, transforming growth factor-beta growth arrest depends on the inhibition of CDK4 synthesis and further inhibition of CDK2 activity by CKIs. 56 Also, CDK4 disruption was associated with increased binding of p27Kip1 to cyclin E/CDK2 and diminished activation of CDK2 was accompanied by impaired pRb phosphorylation.	bind
29034	6	8457	6	10	NULL	0	NULL	CDK4	NULL	disruption of	is associated with	NULL				statement 5	NULL	increased			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_369_s_263	11438484	55  ikewise, transforming growth factor-beta growth arrest depends on the inhibition of CDK4 synthesis and further inhibition of CDK2 activity by CKIs. 56 Also, CDK4 disruption was associated with increased binding of p27Kip1 to cyclin E/CDK2 and diminished activation of CDK2 was accompanied by impaired pRb phosphorylation.	bind
29035	7	8457	6	10	NULL	0	NULL	CDK2	NULL	diminished activation of	is accompanied by	NULL				pRb	NULL	impaired phosphorylation of 			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_1_369_s_263	11438484	55  ikewise, transforming growth factor-beta growth arrest depends on the inhibition of CDK4 synthesis and further inhibition of CDK2 activity by CKIs. 56 Also, CDK4 disruption was associated with increased binding of p27Kip1 to cyclin E/CDK2 and diminished activation of CDK2 was accompanied by impaired pRb phosphorylation.	bind
47887	1	8457	6	10	NULL	0	NULL	CKI	NULL		inhibit	NULL				CDK4	NULL	synthesis of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_1_369_s_263	11438484	55  ikewise, transforming growth factor-beta growth arrest depends on the inhibition of CDK4 synthesis and further inhibition of CDK2 activity by CKIs. 56 Also, CDK4 disruption was associated with increased binding of p27Kip1 to cyclin E/CDK2 and diminished activation of CDK2 was accompanied by impaired pRb phosphorylation.	bind
36182	1	8458	5	13	NULL	NULL	NULL	GDP	Chemical		bind					Rac1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_74	16514078	55 GDP-bound Rac1 or Rac2 does not bind NOXA1, nor does active or inactive Cdc42.	bind
36183	2	8458	5	13	NULL	NULL	NULL	statement 1	GP		does not bind					NOXA1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_74	16514078	55 GDP-bound Rac1 or Rac2 does not bind NOXA1, nor does active or inactive Cdc42.	bind
36184	3	8458	5	13	NULL	NULL	NULL	GDP	Chemical		bind					Rac2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_74	16514078	55 GDP-bound Rac1 or Rac2 does not bind NOXA1, nor does active or inactive Cdc42.	bind
36185	4	8458	5	13	NULL	NULL	NULL	statement 3	GP		does not bind					NOXA1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_74	16514078	55 GDP-bound Rac1 or Rac2 does not bind NOXA1, nor does active or inactive Cdc42.	bind
36186	5	8458	5	13	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_74	16514078	55 GDP-bound Rac1 or Rac2 does not bind NOXA1, nor does active or inactive Cdc42.	bind
36187	6	8458	5	13	NULL	NULL	NULL	Cdc42	GP	active	does not bind					NOXA1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_74	16514078	55 GDP-bound Rac1 or Rac2 does not bind NOXA1, nor does active or inactive Cdc42.	bind
36188	7	8458	5	13	NULL	NULL	NULL	Cdc42	GP	inactive	does not bind					NOXA1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_74	16514078	55 GDP-bound Rac1 or Rac2 does not bind NOXA1, nor does active or inactive Cdc42.	bind
28925	1	8458	6	NULL	NULL	0	NULL	GDP	NULL		bind	NULL				Rac1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_74	16514078	55 GDP-bound Rac1 or Rac2 does not bind NOXA1, nor does active or inactive Cdc42.	bind
28926	2	8458	6	NULL	NULL	0	NULL	GDP	NULL		bind	NULL				Rac2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_74	16514078	55 GDP-bound Rac1 or Rac2 does not bind NOXA1, nor does active or inactive Cdc42.	bind
28927	3	8458	6	NULL	NULL	0	NULL	statement 1	NULL		does not bind	NULL				NOXA1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_74	16514078	55 GDP-bound Rac1 or Rac2 does not bind NOXA1, nor does active or inactive Cdc42.	bind
28928	4	8458	6	NULL	NULL	0	NULL	statement 2	NULL		does not bind	NULL				NOXA1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_74	16514078	55 GDP-bound Rac1 or Rac2 does not bind NOXA1, nor does active or inactive Cdc42.	bind
28929	5	8458	6	NULL	NULL	0	NULL	cdc42	NULL	active	does not bind	NULL				NOXA1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_74	16514078	55 GDP-bound Rac1 or Rac2 does not bind NOXA1, nor does active or inactive Cdc42.	bind
28930	6	8458	6	NULL	NULL	0	NULL	cdc42	NULL	inactive	does not bind	NULL				NOXA1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_74	16514078	55 GDP-bound Rac1 or Rac2 does not bind NOXA1, nor does active or inactive Cdc42.	bind
36303	1	8459	5	13	NULL	NULL	NULL	TNF	GP		bind					TNF-R1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_12_1543_s_116	15217919	55 In this phase, the binding of TNF to TNF-R1 leads to the release of sphingolipid metabolite (stress-induced second messenger) via sphingomyelin degeneration.	bind
36304	2	8459	5	13	NULL	NULL	NULL	statement 1	Process		leads to					sphingolipid metabolite	Chemical	release of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_12_1543_s_116	15217919	55 In this phase, the binding of TNF to TNF-R1 leads to the release of sphingolipid metabolite (stress-induced second messenger) via sphingomyelin degeneration.	bind
36305	5	8459	5	13	NULL	NULL	NULL	sphingolipid metabolite	Chemical		is a type of					statement 3	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_12_1543_s_116	15217919	55 In this phase, the binding of TNF to TNF-R1 leads to the release of sphingolipid metabolite (stress-induced second messenger) via sphingomyelin degeneration.	bind
36306	4	8459	5	13	NULL	NULL	NULL	statement 2	Process		via					sphingomyelin	Chemical	degeneration of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_12_1543_s_116	15217919	55 In this phase, the binding of TNF to TNF-R1 leads to the release of sphingolipid metabolite (stress-induced second messenger) via sphingomyelin degeneration.	bind
47888	3	8459	5	13	NULL	NULL	NULL	stress			induce					secondary messenger	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_12_1543_s_116	15217919	55 In this phase, the binding of TNF to TNF-R1 leads to the release of sphingolipid metabolite (stress-induced second messenger) via sphingomyelin degeneration.	bind
28931	1	8459	6	NULL	NULL	0	NULL	TNF	NULL		bind	NULL				TNF-R1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_12_1543_s_116	15217919	55 In this phase, the binding of TNF to TNF-R1 leads to the release of sphingolipid metabolite (stress-induced second messenger) via sphingomyelin degeneration.	bind
28932	2	8459	6	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				sphingolipid metabolite	NULL	release of			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_12_1543_s_116	15217919	55 In this phase, the binding of TNF to TNF-R1 leads to the release of sphingolipid metabolite (stress-induced second messenger) via sphingomyelin degeneration.	bind
28933	3	8459	6	10	NULL	0	NULL	statement 2	NULL		occurs via	NULL				sphingomyelin 	NULL	degeneration of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_12_1543_s_116	15217919	55 In this phase, the binding of TNF to TNF-R1 leads to the release of sphingolipid metabolite (stress-induced second messenger) via sphingomyelin degeneration.	bind
28934	5	8459	6	10	NULL	0	NULL	sphingolipid metabolite 	NULL		is a type of	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_12_1543_s_116	15217919	55 In this phase, the binding of TNF to TNF-R1 leads to the release of sphingolipid metabolite (stress-induced second messenger) via sphingomyelin degeneration.	bind
47889	4	8459	6	10	NULL	0	NULL	stress	NULL		induce	NULL				secondary messenger	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_12_1543_s_116	15217919	55 In this phase, the binding of TNF to TNF-R1 leads to the release of sphingolipid metabolite (stress-induced second messenger) via sphingomyelin degeneration.	bind
36307	1	8460	5	13	NULL	NULL	NULL	versican	GP		isolated from					ASMCs	Cell	cultured			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1158_s_90	15142969	55 In vitro studies of versican isolated from cultured ASMCs demonstrate that this proteoglycan binds to LDL with saturable kinetics and with a binding affinity for versican of 2.3x10 - 8 mol/L. 56,57  The composition of the CS chains of versican may effect LDL interaction as well.	bind
36308	2	8460	5	13	NULL	NULL	NULL	statement 1	GP		bind					LDL	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1158_s_90	15142969	55 In vitro studies of versican isolated from cultured ASMCs demonstrate that this proteoglycan binds to LDL with saturable kinetics and with a binding affinity for versican of 2.3x10 - 8 mol/L. 56,57  The composition of the CS chains of versican may effect LDL interaction as well.	bind
36309	3	8460	5	13	NULL	NULL	NULL	versican	GP		is a type of					proteoglycan	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1158_s_90	15142969	55 In vitro studies of versican isolated from cultured ASMCs demonstrate that this proteoglycan binds to LDL with saturable kinetics and with a binding affinity for versican of 2.3x10 - 8 mol/L. 56,57  The composition of the CS chains of versican may effect LDL interaction as well.	bind
36310	4	8460	5	13	NULL	NULL	NULL	versican	GP	composition of	effect		may	CS chains		LDL	GP	interaction of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_9_1158_s_90	15142969	55 In vitro studies of versican isolated from cultured ASMCs demonstrate that this proteoglycan binds to LDL with saturable kinetics and with a binding affinity for versican of 2.3x10 - 8 mol/L. 56,57  The composition of the CS chains of versican may effect LDL interaction as well.	bind
29036	1	8460	6	NULL	NULL	0	NULL	versican	NULL		is a type of	NULL				proteoglycan	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_9_1158_s_90	15142969	55 In vitro studies of versican isolated from cultured ASMCs demonstrate that this proteoglycan binds to LDL with saturable kinetics and with a binding affinity for versican of 2.3x10 - 8 mol/L. 56,57  The composition of the CS chains of versican may effect LDL interaction as well.	bind
29037	2	8460	6	NULL	NULL	0	NULL	versican	NULL		bind	NULL				LDL	NULL				NULL	cultured ASMCs	0	NULL	NULL	NULL	gw70_circulationres_94_9_1158_s_90	15142969	55 In vitro studies of versican isolated from cultured ASMCs demonstrate that this proteoglycan binds to LDL with saturable kinetics and with a binding affinity for versican of 2.3x10 - 8 mol/L. 56,57  The composition of the CS chains of versican may effect LDL interaction as well.	bind
36311	1	8461	5	13	NULL	NULL	NULL	Gh	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_5_737_s_144	8620593	56  Interestingly, binding of GTP by Gh inhibits its transglutaminase activity, whereas binding of Ca2+, which is required for transglutaminase activity, prevents GTP binding.	bind
36312	2	8461	5	13	NULL	NULL	NULL	statement 1	Process		inhibit					Gh	GP	transglutaminase activity of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_5_737_s_144	8620593	56  Interestingly, binding of GTP by Gh inhibits its transglutaminase activity, whereas binding of Ca2+, which is required for transglutaminase activity, prevents GTP binding.	bind
36313	3	8461	5	13	NULL	NULL	NULL	Ca2+	Chemical		bind					Gh	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_5_737_s_144	8620593	56  Interestingly, binding of GTP by Gh inhibits its transglutaminase activity, whereas binding of Ca2+, which is required for transglutaminase activity, prevents GTP binding.	bind
36314	4	8461	5	13	NULL	NULL	NULL	statement 3	Process		is required for					Gh	GP	transglutaminase activity of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_5_737_s_144	8620593	56  Interestingly, binding of GTP by Gh inhibits its transglutaminase activity, whereas binding of Ca2+, which is required for transglutaminase activity, prevents GTP binding.	bind
36315	5	8461	5	13	NULL	NULL	NULL	statement 3	Process		prevents					GTP	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_5_737_s_144	8620593	56  Interestingly, binding of GTP by Gh inhibits its transglutaminase activity, whereas binding of Ca2+, which is required for transglutaminase activity, prevents GTP binding.	bind
28935	1	8461	6	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				Gh	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_5_737_s_144	8620593	56  Interestingly, binding of GTP by Gh inhibits its transglutaminase activity, whereas binding of Ca2+, which is required for transglutaminase activity, prevents GTP binding.	bind
28937	3	8461	6	10	NULL	0	NULL	statement 1			inhibits					Gh		transglutaminase activity of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_5_737_s_144	8620593	56  Interestingly, binding of GTP by Gh inhibits its transglutaminase activity, whereas binding of Ca2+, which is required for transglutaminase activity, prevents GTP binding.	bind
28938	4	8461	6	NULL	NULL	0	NULL	Ca2+	NULL		bind	NULL				Gh	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_5_737_s_144	8620593	56  Interestingly, binding of GTP by Gh inhibits its transglutaminase activity, whereas binding of Ca2+, which is required for transglutaminase activity, prevents GTP binding.	bind
28939	5	8461	6	NULL	NULL	0	NULL	statement 4	NULL		is required for	NULL				transglutaminase activity	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_5_737_s_144	8620593	56  Interestingly, binding of GTP by Gh inhibits its transglutaminase activity, whereas binding of Ca2+, which is required for transglutaminase activity, prevents GTP binding.	bind
28940	6	8461	6	NULL	NULL	0	NULL	statement 4	NULL		prevents	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_78_5_737_s_144	8620593	56  Interestingly, binding of GTP by Gh inhibits its transglutaminase activity, whereas binding of Ca2+, which is required for transglutaminase activity, prevents GTP binding.	bind
36316	1	8462	5	13	NULL	NULL	NULL	Egr-1	GP	phosphorylated	bind		less avidly			Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_3_665_s_146	10079243	56  Phosphorylated Egr-1 binds less avidly to Sp1, resulting in higher levels of free transcription factor and the ability to interact with promoters.	bind
28941	1	8462	6	NULL	NULL	0	NULL	Egr-1	NULL	phosphorylated	bind	NULL	less avidly			Sp1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_3_665_s_146	10079243	56  Phosphorylated Egr-1 binds less avidly to Sp1, resulting in higher levels of free transcription factor and the ability to interact with promoters.	bind
36320	1	8463	5	13	NULL	NULL	NULL	factor VIIa	GP		bind					tissue factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_265	7586275	56  Therefore, binding of increased factor VIIa and tissue factor could potentially activate the coagulation cascade and generate thrombin continuously, 57  suggesting a significant role of factor VIIa and tissue factor in this animal model.	bind
36321	2	8463	5	13	NULL	NULL	NULL	statement 1	Process	increased	activates		potentially			coagulation cascade	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_265	7586275	56  Therefore, binding of increased factor VIIa and tissue factor could potentially activate the coagulation cascade and generate thrombin continuously, 57  suggesting a significant role of factor VIIa and tissue factor in this animal model.	bind
36322	3	8463	5	13	NULL	NULL	NULL	statement 2	Process		generates		continuously			thrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_265	7586275	56  Therefore, binding of increased factor VIIa and tissue factor could potentially activate the coagulation cascade and generate thrombin continuously, 57  suggesting a significant role of factor VIIa and tissue factor in this animal model.	bind
28944	1	8463	6	NULL	NULL	0	NULL	factor VIIa	NULL		bind	NULL				tissue factor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_265	7586275	56  Therefore, binding of increased factor VIIa and tissue factor could potentially activate the coagulation cascade and generate thrombin continuously, 57  suggesting a significant role of factor VIIa and tissue factor in this animal model.	bind
28945	2	8463	6	10	NULL	0	NULL	statement 1		increased	activate		potentially			coagulation cascade					NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_265	7586275	56  Therefore, binding of increased factor VIIa and tissue factor could potentially activate the coagulation cascade and generate thrombin continuously, 57  suggesting a significant role of factor VIIa and tissue factor in this animal model.	bind
28946	3	8463	6	10	NULL	0	NULL	statement 2			generate		continuously			thrombin					NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_10_3041_s_265	7586275	56  Therefore, binding of increased factor VIIa and tissue factor could potentially activate the coagulation cascade and generate thrombin continuously, 57  suggesting a significant role of factor VIIa and tissue factor in this animal model.	bind
36323	1	8464	5	13	NULL	NULL	NULL	LDL	GP	oxidized	activates					MAP kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_141_s_218	9012649	56  These reports suggest that activation of MAP kinase by oxidized LDL may be mediated directly by oxidized LDL binding to a cell-surface receptor that recognizes components of oxidized LDL and then initiates signal transduction.	bind
36324	2	8464	5	13	NULL	NULL	NULL	LDL	GP	oxidized	bind					cell-surface receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_141_s_218	9012649	56  These reports suggest that activation of MAP kinase by oxidized LDL may be mediated directly by oxidized LDL binding to a cell-surface receptor that recognizes components of oxidized LDL and then initiates signal transduction.	bind
36325	3	8464	5	13	NULL	NULL	NULL	statement 2	Process		mediate		directly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_141_s_218	9012649	56  These reports suggest that activation of MAP kinase by oxidized LDL may be mediated directly by oxidized LDL binding to a cell-surface receptor that recognizes components of oxidized LDL and then initiates signal transduction.	bind
36326	4	8464	5	13	NULL	NULL	NULL	cell-surface receptor	GP		recognizes					LDL	GP	components of;;oxidized			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_141_s_218	9012649	56  These reports suggest that activation of MAP kinase by oxidized LDL may be mediated directly by oxidized LDL binding to a cell-surface receptor that recognizes components of oxidized LDL and then initiates signal transduction.	bind
36327	5	8464	5	13	NULL	NULL	NULL	statement 4	Process		initiate					signal transduction	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_141_s_218	9012649	56  These reports suggest that activation of MAP kinase by oxidized LDL may be mediated directly by oxidized LDL binding to a cell-surface receptor that recognizes components of oxidized LDL and then initiates signal transduction.	bind
28947	1	8464	6	NULL	NULL	0	NULL	LDL	NULL	oxidized	activates	NULL				MAP kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_141_s_218	9012649	56  These reports suggest that activation of MAP kinase by oxidized LDL may be mediated directly by oxidized LDL binding to a cell-surface receptor that recognizes components of oxidized LDL and then initiates signal transduction.	bind
28948	2	8464	6	NULL	NULL	0	NULL	LDL	NULL	oxidized	bind	NULL				cell-surface receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_141_s_218	9012649	56  These reports suggest that activation of MAP kinase by oxidized LDL may be mediated directly by oxidized LDL binding to a cell-surface receptor that recognizes components of oxidized LDL and then initiates signal transduction.	bind
28949	3	8464	6	10	NULL	0	NULL	statement 2			mediates		directly			statement 1					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_141_s_218	9012649	56  These reports suggest that activation of MAP kinase by oxidized LDL may be mediated directly by oxidized LDL binding to a cell-surface receptor that recognizes components of oxidized LDL and then initiates signal transduction.	bind
28950	4	8464	6	10	NULL	0	NULL	cell-surface receptors			recognize					LDL		components of;;oxidized			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_141_s_218	9012649	56  These reports suggest that activation of MAP kinase by oxidized LDL may be mediated directly by oxidized LDL binding to a cell-surface receptor that recognizes components of oxidized LDL and then initiates signal transduction.	bind
47891	5	8464	6	10	NULL	0	NULL	statement 4	NULL		initiate	NULL				signal transduction	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_141_s_218	9012649	56  These reports suggest that activation of MAP kinase by oxidized LDL may be mediated directly by oxidized LDL binding to a cell-surface receptor that recognizes components of oxidized LDL and then initiates signal transduction.	bind
36328	1	8465	5	13	NULL	NULL	NULL	SMCs	Cell		uptake					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
36329	2	8465	5	13	NULL	NULL	NULL	statement 1	Process		is essential for					heparin	Chemical	inhibitory action of			NULL	heparin-sensitive SMCs	NULL	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
36722	4	8465	5	13	NULL	NULL	NULL	heparin	Chemical		bind					SMCs	Cell				NULL	heparin-sensitive SMCs	NULL	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
36723	6	8465	5	13	NULL	NULL	NULL	statement 4	Process	upregulation of	is linked to 		strongly			heparin	Chemical	internalization of			NULL	heparin-sensitive SMCs	NULL	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
36724	3	8465	5	13	NULL	NULL	NULL	statement 1	Process		is essential for					heparin	Chemical	inhibitory action of			NULL	heparin-resistant SMCs	NULL	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
36725	5	8465	5	13	NULL	NULL	NULL	heparin	Chemical		bind					SMCs	Cell				NULL	heparin-resistant SMCs	NULL	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
36726	7	8465	5	13	NULL	NULL	NULL	statement 5	Process	upregulation of	is linked to		strongly			heparin	Chemical	internalization of			NULL	heparin-resistant SMCs	NULL	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
36727	8	8465	5	13	NULL	NULL	NULL	statement 4	Process	upregulation of	is linked to		strongly			heparin	Chemical	degradation of			NULL	heparin-sensitive SMCs	NULL	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
36728	9	8465	5	13	NULL	NULL	NULL	statement 5	Process	upregulation of	is linked to		strongly			heparin	Chemical	degradation of			NULL	heparin-resistant SMCs	NULL	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
36729	10	8465	5	13	NULL	NULL	NULL	statement 4	Process	upregulation of	is required for					heparin	Chemical	antiproliferative effect of 			NULL	heparin-sensitive SMCs	NULL	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
36730	11	8465	5	13	NULL	NULL	NULL	statement 4	Process	upregulation of	is required for					heparin	Chemical	antiproliferative effect of			NULL	heparin-resistant SMCs	NULL	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
36731	12	8465	5	13	NULL	NULL	NULL	statement 5	Process	upregulation of	is required for					heparin	Chemical	antiproliferative effect of			NULL	heparin-sensitive SMCs	NULL	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
36732	13	8465	5	13	NULL	NULL	NULL	statement 5	Process	upregulation of	is required for					heparin	Chemical	antiproliferative effect of			NULL	heparin-resistant SMCs	NULL	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
28951	1	8465	6	NULL	NULL	0	NULL	SMC	NULL		plays a role in	NULL				heparin	NULL	uptake of			NULL		0	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
28952	2	8465	6	NULL	NULL	0	NULL	heparin	NULL		exhibits	NULL				inhibitory activity	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
28953	3	8465	6	NULL	NULL	0	NULL	statement 1	NULL		is essential for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
28954	4	8465	6	NULL	NULL	0	NULL	heparin	NULL		bind	NULL				SMCs	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
28955	5	8465	6	NULL	NULL	0	NULL	statement 4	NULL	upregulation of	is linked to	NULL	strongly			heparin	NULL	internalization of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
28956	6	8465	6	NULL	NULL	0	NULL	statement 4	NULL	upregulation of	is linked to	NULL	strongly			heparin	NULL	degradation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
28957	7	8465	6	NULL	NULL	0	NULL	heparin	NULL		exhibits	NULL				antiproliferative effect	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
28958	8	8465	6	NULL	NULL	0	NULL	statement 4	NULL	upregulation of	is required for	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_1_74_s_232	null	56 57  The conclusion that heparin uptake by SMCs is essential for the inhibitory action of heparin was also reached in a study with heparin-sensitive and heparin-resistant SMCs, in which it was found that upregulation of heparin binding to the SMCs was strongly linked to subsequent internalization and degradation of heparin and was required for the antiproliferative effect of heparin.	bind
36335	1	8466	5	13	NULL	NULL	NULL	calmodulin	GP		stimulate					type I adenylyl cyclase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_80_3_297_s_134	9048648	57  Another study showed that the mutation, F503 to R503, in type I adenylyl cyclase within the region corresponding to this peptide abolished calmodulin stimulation of type I adenylyl cyclase, 58  suggesting that this is the calmodulin binding domain of the type I isoform.	bind
36336	2	8466	5	13	NULL	NULL	NULL	type I adenylyl cyclase	GP		is mutated to			F503		type I adenylyl cyclase	GP		R503		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_80_3_297_s_134	9048648	57  Another study showed that the mutation, F503 to R503, in type I adenylyl cyclase within the region corresponding to this peptide abolished calmodulin stimulation of type I adenylyl cyclase, 58  suggesting that this is the calmodulin binding domain of the type I isoform.	bind
36337	3	8466	5	13	NULL	NULL	NULL	statement 2	Process		abolishes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_80_3_297_s_134	9048648	57  Another study showed that the mutation, F503 to R503, in type I adenylyl cyclase within the region corresponding to this peptide abolished calmodulin stimulation of type I adenylyl cyclase, 58  suggesting that this is the calmodulin binding domain of the type I isoform.	bind
36338	4	8466	5	13	NULL	NULL	NULL	type I adenylyl cyclase	GP		is			F503					calmodulin binding domain		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_80_3_297_s_134	9048648	57  Another study showed that the mutation, F503 to R503, in type I adenylyl cyclase within the region corresponding to this peptide abolished calmodulin stimulation of type I adenylyl cyclase, 58  suggesting that this is the calmodulin binding domain of the type I isoform.	bind
29038	1	8466	6	NULL	NULL	0	NULL	type I adenylyl cyclase	NULL		is mutated to	NULL		F503		type I adenylyl cyclase	NULL		R503		NULL		0	NULL	NULL	NULL	gw60_circulationres_80_3_297_s_134	9048648	57  Another study showed that the mutation, F503 to R503, in type I adenylyl cyclase within the region corresponding to this peptide abolished calmodulin stimulation of type I adenylyl cyclase, 58  suggesting that this is the calmodulin binding domain of the type I isoform.	bind
29039	2	8466	6	NULL	NULL	0	NULL	calmodulin	NULL		stimulates	NULL				type I adenylyl cyclase	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_80_3_297_s_134	9048648	57  Another study showed that the mutation, F503 to R503, in type I adenylyl cyclase within the region corresponding to this peptide abolished calmodulin stimulation of type I adenylyl cyclase, 58  suggesting that this is the calmodulin binding domain of the type I isoform.	bind
29040	3	8466	6	NULL	NULL	0	NULL	statement 1	NULL		abolishes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_80_3_297_s_134	9048648	57  Another study showed that the mutation, F503 to R503, in type I adenylyl cyclase within the region corresponding to this peptide abolished calmodulin stimulation of type I adenylyl cyclase, 58  suggesting that this is the calmodulin binding domain of the type I isoform.	bind
29041	4	8466	6	NULL	NULL	0	NULL	type I adenylyl cyclase	NULL		is	NULL		F503			NULL		calmodulin binding domain		NULL		0	NULL	NULL	NULL	gw60_circulationres_80_3_297_s_134	9048648	57  Another study showed that the mutation, F503 to R503, in type I adenylyl cyclase within the region corresponding to this peptide abolished calmodulin stimulation of type I adenylyl cyclase, 58  suggesting that this is the calmodulin binding domain of the type I isoform.	bind
36339	1	8467	5	13	NULL	NULL	NULL	ARVCF	GP		is					Armadillo-repeat gene deleted in Velo-cardio-facial syndrome	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1431_s_141	16556854	57 In this context, it should be mentioned that also the product of the Armadillo-repeat gene deleted in Velo-cardio-facial syndrome (ARVCF) was demonstrated to be a binding partner of ZO-1 and ZO-2, which in turn differentially regulated ARCF localization to the membrane and the nucleus, respectively.	bind
36340	2	8467	5	13	NULL	NULL	NULL	ARVCF	GP	product of	bind					ZO-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1431_s_141	16556854	57 In this context, it should be mentioned that also the product of the Armadillo-repeat gene deleted in Velo-cardio-facial syndrome (ARVCF) was demonstrated to be a binding partner of ZO-1 and ZO-2, which in turn differentially regulated ARCF localization to the membrane and the nucleus, respectively.	bind
36341	3	8467	5	13	NULL	NULL	NULL	ARVCF	GP	product of	bind					ZO-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1431_s_141	16556854	57 In this context, it should be mentioned that also the product of the Armadillo-repeat gene deleted in Velo-cardio-facial syndrome (ARVCF) was demonstrated to be a binding partner of ZO-1 and ZO-2, which in turn differentially regulated ARCF localization to the membrane and the nucleus, respectively.	bind
36342	4	8467	5	13	NULL	NULL	NULL	ARCF	GP		is localized to					membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1431_s_141	16556854	57 In this context, it should be mentioned that also the product of the Armadillo-repeat gene deleted in Velo-cardio-facial syndrome (ARVCF) was demonstrated to be a binding partner of ZO-1 and ZO-2, which in turn differentially regulated ARCF localization to the membrane and the nucleus, respectively.	bind
36343	5	8467	5	13	NULL	NULL	NULL	ARCF	GP		is localized to					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1431_s_141	16556854	57 In this context, it should be mentioned that also the product of the Armadillo-repeat gene deleted in Velo-cardio-facial syndrome (ARVCF) was demonstrated to be a binding partner of ZO-1 and ZO-2, which in turn differentially regulated ARCF localization to the membrane and the nucleus, respectively.	bind
36344	6	8467	5	13	NULL	NULL	NULL	ZO-1	GP		regulates		differentially			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1431_s_141	16556854	57 In this context, it should be mentioned that also the product of the Armadillo-repeat gene deleted in Velo-cardio-facial syndrome (ARVCF) was demonstrated to be a binding partner of ZO-1 and ZO-2, which in turn differentially regulated ARCF localization to the membrane and the nucleus, respectively.	bind
36345	7	8467	5	13	NULL	NULL	NULL	ZO-2	GP		regulates		differentially			statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1431_s_141	16556854	57 In this context, it should be mentioned that also the product of the Armadillo-repeat gene deleted in Velo-cardio-facial syndrome (ARVCF) was demonstrated to be a binding partner of ZO-1 and ZO-2, which in turn differentially regulated ARCF localization to the membrane and the nucleus, respectively.	bind
28959	1	8467	6	NULL	NULL	0	NULL	Armadillo-repeat gene	NULL		is deleted in	NULL				Velo-cardio-facial syndrome	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1431_s_141	16556854	57 In this context, it should be mentioned that also the product of the Armadillo-repeat gene deleted in Velo-cardio-facial syndrome (ARVCF) was demonstrated to be a binding partner of ZO-1 and ZO-2, which in turn differentially regulated ARCF localization to the membrane and the nucleus, respectively.	bind
28960	2	8467	6	10	NULL	0	NULL	ARVCF	NULL		is	NULL				Armadillo-repeat gene deleted in Velo-cardio-facial syndrome	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1431_s_141	16556854	57 In this context, it should be mentioned that also the product of the Armadillo-repeat gene deleted in Velo-cardio-facial syndrome (ARVCF) was demonstrated to be a binding partner of ZO-1 and ZO-2, which in turn differentially regulated ARCF localization to the membrane and the nucleus, respectively.	bind
28961	3	8467	6	NULL	NULL	0	NULL	Armadillo-repeat gene product	NULL		bind	NULL				ZO-1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1431_s_141	16556854	57 In this context, it should be mentioned that also the product of the Armadillo-repeat gene deleted in Velo-cardio-facial syndrome (ARVCF) was demonstrated to be a binding partner of ZO-1 and ZO-2, which in turn differentially regulated ARCF localization to the membrane and the nucleus, respectively.	bind
28962	4	8467	6	NULL	NULL	0	NULL	Armadillo-repeat gene product	NULL		bind	NULL				ZO-2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1431_s_141	16556854	57 In this context, it should be mentioned that also the product of the Armadillo-repeat gene deleted in Velo-cardio-facial syndrome (ARVCF) was demonstrated to be a binding partner of ZO-1 and ZO-2, which in turn differentially regulated ARCF localization to the membrane and the nucleus, respectively.	bind
28963	5	8467	6	NULL	NULL	0	NULL	ARCF	NULL		localizes to	NULL				membrane	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1431_s_141	16556854	57 In this context, it should be mentioned that also the product of the Armadillo-repeat gene deleted in Velo-cardio-facial syndrome (ARVCF) was demonstrated to be a binding partner of ZO-1 and ZO-2, which in turn differentially regulated ARCF localization to the membrane and the nucleus, respectively.	bind
28964	6	8467	6	NULL	NULL	0	NULL	ARCF	NULL		localizes to	NULL				nucleus	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1431_s_141	16556854	57 In this context, it should be mentioned that also the product of the Armadillo-repeat gene deleted in Velo-cardio-facial syndrome (ARVCF) was demonstrated to be a binding partner of ZO-1 and ZO-2, which in turn differentially regulated ARCF localization to the membrane and the nucleus, respectively.	bind
28965	7	8467	6	10	NULL	0	NULL	statement 3	NULL		regulates	NULL	differentially			statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1431_s_141	16556854	57 In this context, it should be mentioned that also the product of the Armadillo-repeat gene deleted in Velo-cardio-facial syndrome (ARVCF) was demonstrated to be a binding partner of ZO-1 and ZO-2, which in turn differentially regulated ARCF localization to the membrane and the nucleus, respectively.	bind
28966	8	8467	6	10	NULL	0	NULL	statement 3	NULL		regulates	NULL	differentially			statement 6	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1431_s_141	16556854	57 In this context, it should be mentioned that also the product of the Armadillo-repeat gene deleted in Velo-cardio-facial syndrome (ARVCF) was demonstrated to be a binding partner of ZO-1 and ZO-2, which in turn differentially regulated ARCF localization to the membrane and the nucleus, respectively.	bind
28967	9	8467	6	10	NULL	0	NULL	statement 4	NULL		regulates	NULL	differentially			statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1431_s_141	16556854	57 In this context, it should be mentioned that also the product of the Armadillo-repeat gene deleted in Velo-cardio-facial syndrome (ARVCF) was demonstrated to be a binding partner of ZO-1 and ZO-2, which in turn differentially regulated ARCF localization to the membrane and the nucleus, respectively.	bind
28968	10	8467	6	10	NULL	0	NULL	statement 4	NULL		regulates	NULL	differentially			statement 6	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1431_s_141	16556854	57 In this context, it should be mentioned that also the product of the Armadillo-repeat gene deleted in Velo-cardio-facial syndrome (ARVCF) was demonstrated to be a binding partner of ZO-1 and ZO-2, which in turn differentially regulated ARCF localization to the membrane and the nucleus, respectively.	bind
36346	1	8468	5	13	NULL	NULL	NULL	E2F	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2810_s_566	11433027	58       Pagano,M., Durst,M., Joswig,S., Draetta,G. and Jansen-Durr,P. (1992) Binding of the human E2F transcription factor to the retinoblastoma protein but not to cyclin A is abolished in HPV-16-immortalized cells.	bind
36347	2	8468	5	13	NULL	NULL	NULL	E2F	GP	human	bind					retinoblastoma protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2810_s_566	11433027	58       Pagano,M., Durst,M., Joswig,S., Draetta,G. and Jansen-Durr,P. (1992) Binding of the human E2F transcription factor to the retinoblastoma protein but not to cyclin A is abolished in HPV-16-immortalized cells.	bind
36348	3	8468	5	13	NULL	NULL	NULL	E2F	GP	human	does not bind					cyclin A	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2810_s_566	11433027	58       Pagano,M., Durst,M., Joswig,S., Draetta,G. and Jansen-Durr,P. (1992) Binding of the human E2F transcription factor to the retinoblastoma protein but not to cyclin A is abolished in HPV-16-immortalized cells.	bind
36349	4	8468	5	13	NULL	NULL	NULL	statement 2	Process		is abolished in					HPV-16-immortalized cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2810_s_566	11433027	58       Pagano,M., Durst,M., Joswig,S., Draetta,G. and Jansen-Durr,P. (1992) Binding of the human E2F transcription factor to the retinoblastoma protein but not to cyclin A is abolished in HPV-16-immortalized cells.	bind
47892	5	8468	5	13	NULL	NULL	NULL	statement 3	Process		is abolished in					HPV-16-immortalized cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2810_s_566	11433027	58       Pagano,M., Durst,M., Joswig,S., Draetta,G. and Jansen-Durr,P. (1992) Binding of the human E2F transcription factor to the retinoblastoma protein but not to cyclin A is abolished in HPV-16-immortalized cells.	bind
28969	1	8468	6	NULL	NULL	0	NULL	E2F 	NULL	human	bind	NULL				retinoblastoma protein	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2810_s_566	11433027	58       Pagano,M., Durst,M., Joswig,S., Draetta,G. and Jansen-Durr,P. (1992) Binding of the human E2F transcription factor to the retinoblastoma protein but not to cyclin A is abolished in HPV-16-immortalized cells.	bind
28970	2	8468	6	NULL	NULL	0	NULL	E2F	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2810_s_566	11433027	58       Pagano,M., Durst,M., Joswig,S., Draetta,G. and Jansen-Durr,P. (1992) Binding of the human E2F transcription factor to the retinoblastoma protein but not to cyclin A is abolished in HPV-16-immortalized cells.	bind
28971	3	8468	6	NULL	NULL	0	NULL	E2F	NULL	human	does not bind	NULL				cyclin A	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2810_s_566	11433027	58       Pagano,M., Durst,M., Joswig,S., Draetta,G. and Jansen-Durr,P. (1992) Binding of the human E2F transcription factor to the retinoblastoma protein but not to cyclin A is abolished in HPV-16-immortalized cells.	bind
28972	4	8468	6	NULL	NULL	0	NULL	statement 1	NULL		is abolished in	NULL				HPV-16-immortalized cells	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2810_s_566	11433027	58       Pagano,M., Durst,M., Joswig,S., Draetta,G. and Jansen-Durr,P. (1992) Binding of the human E2F transcription factor to the retinoblastoma protein but not to cyclin A is abolished in HPV-16-immortalized cells.	bind
28973	5	8468	6	NULL	NULL	0	NULL	statement 3	NULL		is abolished in	NULL				HPV-16-immortalized cells	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_13_2810_s_566	11433027	58       Pagano,M., Durst,M., Joswig,S., Draetta,G. and Jansen-Durr,P. (1992) Binding of the human E2F transcription factor to the retinoblastoma protein but not to cyclin A is abolished in HPV-16-immortalized cells.	bind
36331	1	8470	5	13	NULL	NULL	NULL	Trx	GP		is					thioredoxin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1439_s_158	16645155	58,72  In unstressed condition, thioredoxin (Trx) directly binds to ASK1, and inhibits kinase activity.	bind
36332	2	8470	5	13	NULL	NULL	NULL	Trx	GP		bind		directly			ASK1	GP				NULL	unstressed condition	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1439_s_158	16645155	58,72  In unstressed condition, thioredoxin (Trx) directly binds to ASK1, and inhibits kinase activity.	bind
36334	3	8470	5	13	NULL	NULL	NULL	statement 2	Process		inhibit					ASK1	GP	kinase activity of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1439_s_158	16645155	58,72  In unstressed condition, thioredoxin (Trx) directly binds to ASK1, and inhibits kinase activity.	bind
28974	1	8470	6	NULL	NULL	0	NULL	Trx	NULL		bind	NULL	directly			ASK1	NULL				NULL	unstressed condition	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1439_s_158	16645155	58,72  In unstressed condition, thioredoxin (Trx) directly binds to ASK1, and inhibits kinase activity.	bind
28975	2	8470	6	NULL	NULL	0	NULL	Trx	NULL		is	NULL				thioredoxin	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1439_s_158	16645155	58,72  In unstressed condition, thioredoxin (Trx) directly binds to ASK1, and inhibits kinase activity.	bind
28976	3	8470	6	10	NULL	0	NULL	Trx			inhibits					ASK1		kinase activity of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1439_s_158	16645155	58,72  In unstressed condition, thioredoxin (Trx) directly binds to ASK1, and inhibits kinase activity.	bind
36351	2	8471	5	13	NULL	NULL	NULL	decorin	GP		bind		potentially	chondroitin/dermatan sulfate GAG chains		LDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_4_519_s_142	9555856	59  Furthermore, decorin and biglycan have chondroitin/dermatan sulfate GAG chains that can potentially bind both LDL and snpPLA2.	bind
36352	1	8471	5	13	NULL	NULL	NULL	decorin	GP		bind		potentially	chondroitin/dermatan sulfate GAG chains		snpPLA2	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_4_519_s_142	9555856	59  Furthermore, decorin and biglycan have chondroitin/dermatan sulfate GAG chains that can potentially bind both LDL and snpPLA2.	bind
36354	4	8471	5	13	NULL	NULL	NULL	biglycan	GP		bind		potentially	chondroitin/dermatan sulfate GAG chains		LDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_4_519_s_142	9555856	59  Furthermore, decorin and biglycan have chondroitin/dermatan sulfate GAG chains that can potentially bind both LDL and snpPLA2.	bind
36355	3	8471	5	13	NULL	NULL	NULL	biglycan	GP		bind		potentially	chondroitin/dermatan sulfate GAG chains		snpPLA2	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_4_519_s_142	9555856	59  Furthermore, decorin and biglycan have chondroitin/dermatan sulfate GAG chains that can potentially bind both LDL and snpPLA2.	bind
28977	1	8471	6	NULL	NULL	0	NULL	decorin	NULL		bind	NULL	potentially	chondroitin/dermatan sulfate GAG chains		LDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_4_519_s_142	9555856	59  Furthermore, decorin and biglycan have chondroitin/dermatan sulfate GAG chains that can potentially bind both LDL and snpPLA2.	bind
28978	2	8471	6	10	NULL	0	NULL	decorin			bind		potentially	chondroitin/dermatan sulfate GAG chains		snpPLA2					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_4_519_s_142	9555856	59  Furthermore, decorin and biglycan have chondroitin/dermatan sulfate GAG chains that can potentially bind both LDL and snpPLA2.	bind
28979	3	8471	6	10	NULL	0	NULL	biglycan			bind		potentially	chondroitin/dermatan sulfate GAG chains		LDL					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_4_519_s_142	9555856	59  Furthermore, decorin and biglycan have chondroitin/dermatan sulfate GAG chains that can potentially bind both LDL and snpPLA2.	bind
28980	4	8471	6	10	NULL	0	NULL	biglycan			bind		potentially	chondroitin/dermatan sulfate GAG chains		snpPLA2					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_4_519_s_142	9555856	59  Furthermore, decorin and biglycan have chondroitin/dermatan sulfate GAG chains that can potentially bind both LDL and snpPLA2.	bind
36356	1	8472	5	13	NULL	NULL	NULL	helicase	GP		exhibits					ATPase activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_35_27145_s_18	10871615	59 protein binds to the helicase, even in the absence of DNA, and stimulates the DNA-dependent and -independent ATPase and DNA unwinding activities of the helicase.	bind
36357	2	8472	5	13	NULL	NULL	NULL	helicase	GP		exhibits					DNA unwinding activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_35_27145_s_18	10871615	59 protein binds to the helicase, even in the absence of DNA, and stimulates the DNA-dependent and -independent ATPase and DNA unwinding activities of the helicase.	bind
49157	3	8472	5	13	NULL	NULL	NULL	59 protein	GP		bind					helicase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_35_27145_s_18	10871615	59 protein binds to the helicase, even in the absence of DNA, and stimulates the DNA-dependent and -independent ATPase and DNA unwinding activities of the helicase.	bind
49158	4	8472	5	13	NULL	NULL	NULL	statement 3	Process		in the absence of					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_35_27145_s_18	10871615	59 protein binds to the helicase, even in the absence of DNA, and stimulates the DNA-dependent and -independent ATPase and DNA unwinding activities of the helicase.	bind
49159	5	8472	5	13	NULL	NULL	NULL	59 protein	GP		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_35_27145_s_18	10871615	59 protein binds to the helicase, even in the absence of DNA, and stimulates the DNA-dependent and -independent ATPase and DNA unwinding activities of the helicase.	bind
49160	6	8472	5	13	NULL	NULL	NULL	59 protein	GP		stimulates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_35_27145_s_18	10871615	59 protein binds to the helicase, even in the absence of DNA, and stimulates the DNA-dependent and -independent ATPase and DNA unwinding activities of the helicase.	bind
28981	1	8472	6	NULL	NULL	0	NULL	59 protein	NULL		bind	NULL				helicase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_27145_s_18	10871615	59 protein binds to the helicase, even in the absence of DNA, and stimulates the DNA-dependent and -independent ATPase and DNA unwinding activities of the helicase.	bind
28982	2	8472	6	NULL	NULL	0	NULL	statement 1	NULL		occurs in absence of	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_27145_s_18	10871615	59 protein binds to the helicase, even in the absence of DNA, and stimulates the DNA-dependent and -independent ATPase and DNA unwinding activities of the helicase.	bind
28983	3	8472	6	NULL	NULL	0	NULL	helicase	NULL		exhibits	NULL				DNA unwinding activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_27145_s_18	10871615	59 protein binds to the helicase, even in the absence of DNA, and stimulates the DNA-dependent and -independent ATPase and DNA unwinding activities of the helicase.	bind
28984	4	8472	6	NULL	NULL	0	NULL	59 protein	NULL		stimulates	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_27145_s_18	10871615	59 protein binds to the helicase, even in the absence of DNA, and stimulates the DNA-dependent and -independent ATPase and DNA unwinding activities of the helicase.	bind
28985	5	8472	6	NULL	NULL	0	NULL	helicase	NULL		exhibits	NULL				ATPase activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_27145_s_18	10871615	59 protein binds to the helicase, even in the absence of DNA, and stimulates the DNA-dependent and -independent ATPase and DNA unwinding activities of the helicase.	bind
28986	6	8472	6	NULL	NULL	0	NULL	59 protein	NULL		stimulates	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_27145_s_18	10871615	59 protein binds to the helicase, even in the absence of DNA, and stimulates the DNA-dependent and -independent ATPase and DNA unwinding activities of the helicase.	bind
36358	1	8473	5	13	NULL	NULL	NULL	Troponin T	GP		bind					tropomyosin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_5_1336_s_103	7648684	59 Troponin T binds to tropomyosin and is responsible for positioning of the troponin complex on the thin filaments.	bind
36359	2	8473	5	13	NULL	NULL	NULL	troponin complex	GP		is positioned on					thin filaments	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_5_1336_s_103	7648684	59 Troponin T binds to tropomyosin and is responsible for positioning of the troponin complex on the thin filaments.	bind
36360	3	8473	5	13	NULL	NULL	NULL	Troponin T	GP		is responsible for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_5_1336_s_103	7648684	59 Troponin T binds to tropomyosin and is responsible for positioning of the troponin complex on the thin filaments.	bind
28987	1	8473	6	NULL	NULL	0	NULL	Troponin T	NULL		bind	NULL				tropomyosin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_5_1336_s_103	7648684	59 Troponin T binds to tropomyosin and is responsible for positioning of the troponin complex on the thin filaments.	bind
29007	2	8473	6	NULL	NULL	0	NULL	troponin complex	NULL		is positioned on	NULL				thin filaments	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_5_1336_s_103	7648684	59 Troponin T binds to tropomyosin and is responsible for positioning of the troponin complex on the thin filaments.	bind
29008	3	8473	6	NULL	NULL	0	NULL	statement 1	NULL		is responsible for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_5_1336_s_103	7648684	59 Troponin T binds to tropomyosin and is responsible for positioning of the troponin complex on the thin filaments.	bind
36527	1	8474	5	13	NULL	NULL	NULL	RepA	GP		bind					RS sequences	NucleicAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-bacteriol_175_13_8320230_s_17	8320230	5:631-640, 1991), confirm that the binding of RepA  to RS sequences plays a crucial role in the regulation of plasmid replication  and that its binding to IR sequences plays a role in the autoregulation  of RepA expression.	bind
36528	2	8474	5	13	NULL	NULL	NULL	statement 1	Process		plays a role in		crucial			plasmid replication	Process	regulation of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-bacteriol_175_13_8320230_s_17	8320230	5:631-640, 1991), confirm that the binding of RepA  to RS sequences plays a crucial role in the regulation of plasmid replication  and that its binding to IR sequences plays a role in the autoregulation  of RepA expression.	bind
36529	3	8474	5	13	NULL	NULL	NULL	RepA	GP		bind									IR sequences	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-bacteriol_175_13_8320230_s_17	8320230	5:631-640, 1991), confirm that the binding of RepA  to RS sequences plays a crucial role in the regulation of plasmid replication  and that its binding to IR sequences plays a role in the autoregulation  of RepA expression.	bind
36530	4	8474	5	13	NULL	NULL	NULL	statement 3	Process		plays a role in		crucial			RepA 	GP	autoregulation of;;expression of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-bacteriol_175_13_8320230_s_17	8320230	5:631-640, 1991), confirm that the binding of RepA  to RS sequences plays a crucial role in the regulation of plasmid replication  and that its binding to IR sequences plays a role in the autoregulation  of RepA expression.	bind
29134	1	8474	6	NULL	NULL	0	NULL	RepA	NULL		bind	NULL				RS sequences	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-bacteriol_175_13_8320230_s_17	8320230	5:631-640, 1991), confirm that the binding of RepA  to RS sequences plays a crucial role in the regulation of plasmid replication  and that its binding to IR sequences plays a role in the autoregulation  of RepA expression.	bind
29135	2	8474	6	NULL	NULL	0	NULL	statement 1	NULL		plays a role in	NULL				plasmid replication	NULL	regulation of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-bacteriol_175_13_8320230_s_17	8320230	5:631-640, 1991), confirm that the binding of RepA  to RS sequences plays a crucial role in the regulation of plasmid replication  and that its binding to IR sequences plays a role in the autoregulation  of RepA expression.	bind
29139	3	8474	6	NULL	NULL	0	NULL	RepA	NULL		bind	NULL					NULL			IR sequences	NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-bacteriol_175_13_8320230_s_17	8320230	5:631-640, 1991), confirm that the binding of RepA  to RS sequences plays a crucial role in the regulation of plasmid replication  and that its binding to IR sequences plays a role in the autoregulation  of RepA expression.	bind
29140	4	8474	6	NULL	NULL	0	NULL	statement 3	NULL		plays a role in	NULL				RepA	NULL	autoregulation of;; expression of 			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-bacteriol_175_13_8320230_s_17	8320230	5:631-640, 1991), confirm that the binding of RepA  to RS sequences plays a crucial role in the regulation of plasmid replication  and that its binding to IR sequences plays a role in the autoregulation  of RepA expression.	bind
36531	1	8476	5	13	NULL	NULL	NULL	5alpha-DHT	Chemical		is a type of					androgen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42091_s_15	11514561	5alpha-DHT is a more potent androgen than testosterone in stimulating prostate cancer growth ( 4,  5) and preferentially binds to the androgen receptor (dissociation constant ( K d) for the androgen receptor of 10 11M) ( 6).	bind
36532	2	8476	5	13	NULL	NULL	NULL	testosterone	Chemical		is a type of					androgen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42091_s_15	11514561	5alpha-DHT is a more potent androgen than testosterone in stimulating prostate cancer growth ( 4,  5) and preferentially binds to the androgen receptor (dissociation constant ( K d) for the androgen receptor of 10 11M) ( 6).	bind
36533	3	8476	5	13	NULL	NULL	NULL	statement 1	Chemical		more potent than					statement 2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42091_s_15	11514561	5alpha-DHT is a more potent androgen than testosterone in stimulating prostate cancer growth ( 4,  5) and preferentially binds to the androgen receptor (dissociation constant ( K d) for the androgen receptor of 10 11M) ( 6).	bind
36534	4	8476	5	13	NULL	NULL	NULL	5alpha-DHT	Chemical		stimulate					prostate cancer	MedicalFinding	growth of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42091_s_15	11514561	5alpha-DHT is a more potent androgen than testosterone in stimulating prostate cancer growth ( 4,  5) and preferentially binds to the androgen receptor (dissociation constant ( K d) for the androgen receptor of 10 11M) ( 6).	bind
36535	5	8476	5	13	NULL	NULL	NULL	testosterone	Chemical		stimulate					prostate cancer	MedicalFinding	growth of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42091_s_15	11514561	5alpha-DHT is a more potent androgen than testosterone in stimulating prostate cancer growth ( 4,  5) and preferentially binds to the androgen receptor (dissociation constant ( K d) for the androgen receptor of 10 11M) ( 6).	bind
36536	6	8476	5	13	NULL	NULL	NULL	5alpha-DHT	Chemical		bind		preferentially			androgen receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_42091_s_15	11514561	5alpha-DHT is a more potent androgen than testosterone in stimulating prostate cancer growth ( 4,  5) and preferentially binds to the androgen receptor (dissociation constant ( K d) for the androgen receptor of 10 11M) ( 6).	bind
29142	1	8476	6	NULL	NULL	0	NULL	5alpha-DHT	NULL		is a type of	NULL				androgen	NULL	potent			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_42091_s_15	11514561	5alpha-DHT is a more potent androgen than testosterone in stimulating prostate cancer growth ( 4,  5) and preferentially binds to the androgen receptor (dissociation constant ( K d) for the androgen receptor of 10 11M) ( 6).	bind
29143	2	8476	6	NULL	NULL	0	NULL	testosterone	NULL		is a type of	NULL				androgen	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_42091_s_15	11514561	5alpha-DHT is a more potent androgen than testosterone in stimulating prostate cancer growth ( 4,  5) and preferentially binds to the androgen receptor (dissociation constant ( K d) for the androgen receptor of 10 11M) ( 6).	bind
29144	3	8476	6	NULL	NULL	0	NULL	5alpha-DHT	NULL		stimulates	NULL				prostate cancer	NULL	growth of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_42091_s_15	11514561	5alpha-DHT is a more potent androgen than testosterone in stimulating prostate cancer growth ( 4,  5) and preferentially binds to the androgen receptor (dissociation constant ( K d) for the androgen receptor of 10 11M) ( 6).	bind
29145	4	8476	6	NULL	NULL	0	NULL	5alpha-DHT	NULL		bind	NULL	preferentially			androgen receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_42091_s_15	11514561	5alpha-DHT is a more potent androgen than testosterone in stimulating prostate cancer growth ( 4,  5) and preferentially binds to the androgen receptor (dissociation constant ( K d) for the androgen receptor of 10 11M) ( 6).	bind
29148	5	8476	6	NULL	NULL	0	NULL	testosterone	NULL		stimulates	NULL				prostate cancer	NULL	growth of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_42091_s_15	11514561	5alpha-DHT is a more potent androgen than testosterone in stimulating prostate cancer growth ( 4,  5) and preferentially binds to the androgen receptor (dissociation constant ( K d) for the androgen receptor of 10 11M) ( 6).	bind
29149	6	8476	6	NULL	NULL	0	NULL	statement 3	NULL		is more potent than	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_42091_s_15	11514561	5alpha-DHT is a more potent androgen than testosterone in stimulating prostate cancer growth ( 4,  5) and preferentially binds to the androgen receptor (dissociation constant ( K d) for the androgen receptor of 10 11M) ( 6).	bind
36537	1	8477	5	13	NULL	NULL	NULL	 scFv	GP		bind			5B-12B7		NS5B	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_1_593_s_238	11641406	5B-12B7 scFv Binds to NS5B Both in Vitro and in Transfected Cells-- The mAb heavy and light chain variable domains were cloned, and a scFv was assembled to assess the potential of mAb 5B-12B7 to bind to NS5B intracellularly.	bind
36538	2	8477	5	13	NULL	NULL	NULL	 scFv	GP		bind			5B-12B7		NS5B	GP				NULL	transfected cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_1_593_s_238	11641406	5B-12B7 scFv Binds to NS5B Both in Vitro and in Transfected Cells-- The mAb heavy and light chain variable domains were cloned, and a scFv was assembled to assess the potential of mAb 5B-12B7 to bind to NS5B intracellularly.	bind
29152	1	8477	6	NULL	NULL	0	NULL	scFv	NULL		bind	NULL		5B-12B7		NS5B	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_277_1_593_s_238	11641406	5B-12B7 scFv Binds to NS5B Both in Vitro and in Transfected Cells-- The mAb heavy and light chain variable domains were cloned, and a scFv was assembled to assess the potential of mAb 5B-12B7 to bind to NS5B intracellularly.	bind
29154	2	8477	6	NULL	NULL	0	NULL	scFv	NULL		bind	NULL		5B-12B7		NS5B	NULL				NULL	transfected cells	0	NULL	NULL	NULL	gw60_jbiolchem_277_1_593_s_238	11641406	5B-12B7 scFv Binds to NS5B Both in Vitro and in Transfected Cells-- The mAb heavy and light chain variable domains were cloned, and a scFv was assembled to assess the potential of mAb 5B-12B7 to bind to NS5B intracellularly.	bind
36539	1	8478	5	13	NULL	NULL	NULL	5c8 mAb	GP		bind					CD154	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_47_33545_s_78	10559240	5c8 mAb binds to CD154 and blocks the interaction of CD154 with its receptor, CD40 ( 23).	bind
36540	2	8478	5	13	NULL	NULL	NULL	CD154	GP		interact with					CD40	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_47_33545_s_78	10559240	5c8 mAb binds to CD154 and blocks the interaction of CD154 with its receptor, CD40 ( 23).	bind
36541	3	8478	5	13	NULL	NULL	NULL	CD40	GP		is a type of					receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_47_33545_s_78	10559240	5c8 mAb binds to CD154 and blocks the interaction of CD154 with its receptor, CD40 ( 23).	bind
36542	4	8478	5	13	NULL	NULL	NULL	statement 1	Process		block					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_47_33545_s_78	10559240	5c8 mAb binds to CD154 and blocks the interaction of CD154 with its receptor, CD40 ( 23).	bind
29167	1	8478	6	NULL	NULL	0	NULL	5c8 mAb	NULL		bind	NULL				CD154	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33545_s_78	10559240	5c8 mAb binds to CD154 and blocks the interaction of CD154 with its receptor, CD40 ( 23).	bind
29168	2	8478	6	NULL	NULL	0	NULL	CD154	NULL		interacts with	NULL				CD40	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33545_s_78	10559240	5c8 mAb binds to CD154 and blocks the interaction of CD154 with its receptor, CD40 ( 23).	bind
29170	3	8478	6	NULL	NULL	0	NULL	statement 1	NULL		blocks	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33545_s_78	10559240	5c8 mAb binds to CD154 and blocks the interaction of CD154 with its receptor, CD40 ( 23).	bind
36543	1	8479	5	13	NULL	NULL	NULL	5D2 Mabs	GP		bind					LPL	GP				NULL	membrane	NULL	NULL	NULL	NULL	gw70_jlipidres_45_5_859_s_74	14967813	5D2 Mabs bound to LPL on the membrane were then detected using a horseradish peroxidase-linked secondary antibody against mouse and with the ECL-Western blotting analysis system (Amersham).	bind
29171	1	8479	6	NULL	NULL	0	NULL	5D2 Mabs	NULL		bind	NULL				LPL	NULL				NULL	membranes	0	NULL	NULL	NULL	gw70_jlipidres_45_5_859_s_74	14967813	5D2 Mabs bound to LPL on the membrane were then detected using a horseradish peroxidase-linked secondary antibody against mouse and with the ECL-Western blotting analysis system (Amersham).	bind
36544	1	8480	5	13	NULL	NULL	NULL	Shh	GP		bind					Ptc1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_108_4_479_s_62	12860919	5E1 blocks the binding of Shh to Ptc1; it was obtained from Curis Inc and Dr Thomas Jessell (Columbia University) and prepared as purified IgG1 in PBS. 18 Seven days after induction of ischemia, mice were killed.	bind
36545	2	8480	5	13	NULL	NULL	NULL	5E1	GP		block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_108_4_479_s_62	12860919	5E1 blocks the binding of Shh to Ptc1; it was obtained from Curis Inc and Dr Thomas Jessell (Columbia University) and prepared as purified IgG1 in PBS. 18 Seven days after induction of ischemia, mice were killed.	bind
29172	1	8480	6	NULL	NULL	0	NULL	Shh	NULL		bind	NULL				Ptc1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_108_4_479_s_62	12860919	5E1 blocks the binding of Shh to Ptc1; it was obtained from Curis Inc and Dr Thomas Jessell (Columbia University) and prepared as purified IgG1 in PBS. 18 Seven days after induction of ischemia, mice were killed.	bind
29174	2	8480	6	NULL	NULL	0	NULL	5E1	NULL		blocks	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_108_4_479_s_62	12860919	5E1 blocks the binding of Shh to Ptc1; it was obtained from Curis Inc and Dr Thomas Jessell (Columbia University) and prepared as purified IgG1 in PBS. 18 Seven days after induction of ischemia, mice were killed.	bind
36548	1	8482	5	13	NULL	NULL	NULL	5GG	Chemical		inhibit					AR protein	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_7_1109_s_149	14963012	5GG and TF3 inhibit the expression of AR protein   fter T is transformed into DHT by the enzyme 5alpha-reductases, DHT will bind to AR and result in a series of androgen actions.	bind
36549	2	8482	5	13	NULL	NULL	NULL	TF3	Chemical		inhibit					AR protein	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_7_1109_s_149	14963012	5GG and TF3 inhibit the expression of AR protein   fter T is transformed into DHT by the enzyme 5alpha-reductases, DHT will bind to AR and result in a series of androgen actions.	bind
36550	3	8482	5	13	NULL	NULL	NULL	T	Chemical		is transformed into					DHT	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_7_1109_s_149	14963012	5GG and TF3 inhibit the expression of AR protein   fter T is transformed into DHT by the enzyme 5alpha-reductases, DHT will bind to AR and result in a series of androgen actions.	bind
36551	4	8482	5	13	NULL	NULL	NULL	enzyme 5alpha-reductases	GP		is required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_7_1109_s_149	14963012	5GG and TF3 inhibit the expression of AR protein   fter T is transformed into DHT by the enzyme 5alpha-reductases, DHT will bind to AR and result in a series of androgen actions.	bind
36552	5	8482	5	13	NULL	NULL	NULL	DHT	Chemical		bind					AR	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_7_1109_s_149	14963012	5GG and TF3 inhibit the expression of AR protein   fter T is transformed into DHT by the enzyme 5alpha-reductases, DHT will bind to AR and result in a series of androgen actions.	bind
36553	6	8482	5	13	NULL	NULL	NULL	statement 3	Process		leads to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_7_1109_s_149	14963012	5GG and TF3 inhibit the expression of AR protein   fter T is transformed into DHT by the enzyme 5alpha-reductases, DHT will bind to AR and result in a series of androgen actions.	bind
36554	7	8482	5	13	NULL	NULL	NULL	statement 5	Process		results in					androgen actions	Process	series of			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_7_1109_s_149	14963012	5GG and TF3 inhibit the expression of AR protein   fter T is transformed into DHT by the enzyme 5alpha-reductases, DHT will bind to AR and result in a series of androgen actions.	bind
29592	1	8482	6	10	NULL	0	NULL	DHT			bind					AR					NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_7_1109_s_149	14963012	5GG and TF3 inhibit the expression of AR protein   fter T is transformed into DHT by the enzyme 5alpha-reductases, DHT will bind to AR and result in a series of androgen actions.	bind
29593	2	8482	6	NULL	NULL	0	NULL	5GG	NULL		inhibit	NULL				AR protein	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_25_7_1109_s_149	14963012	5GG and TF3 inhibit the expression of AR protein   fter T is transformed into DHT by the enzyme 5alpha-reductases, DHT will bind to AR and result in a series of androgen actions.	bind
29594	3	8482	6	NULL	NULL	0	NULL	TF3	NULL		inhibit	NULL				AR protein	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_25_7_1109_s_149	14963012	5GG and TF3 inhibit the expression of AR protein   fter T is transformed into DHT by the enzyme 5alpha-reductases, DHT will bind to AR and result in a series of androgen actions.	bind
29595	4	8482	6	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				androgen actions	NULL				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_25_7_1109_s_149	14963012	5GG and TF3 inhibit the expression of AR protein   fter T is transformed into DHT by the enzyme 5alpha-reductases, DHT will bind to AR and result in a series of androgen actions.	bind
29596	5	8482	6	NULL	NULL	0	NULL	T	NULL		is transformed into	NULL				DHT	NULL				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_25_7_1109_s_149	14963012	5GG and TF3 inhibit the expression of AR protein   fter T is transformed into DHT by the enzyme 5alpha-reductases, DHT will bind to AR and result in a series of androgen actions.	bind
29597	6	8482	6	NULL	NULL	0	NULL	5alpha-reductases	NULL		carries out	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_25_7_1109_s_149	14963012	5GG and TF3 inhibit the expression of AR protein   fter T is transformed into DHT by the enzyme 5alpha-reductases, DHT will bind to AR and result in a series of androgen actions.	bind
36555	1	8483	5	13	NULL	NULL	NULL	5H2	GP		is a type of					mouse monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_4_844_s_94	9710454	5H2 is a mouse monoclonal antibody which binds to the  COOH-terminal 80-kD segment of the human but not mouse laminin  alpha2.	bind
36556	2	8483	5	13	NULL	NULL	NULL	5H2	GP		bind					laminin alpha2	GP	human	COOH-terminal		NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_4_844_s_94	9710454	5H2 is a mouse monoclonal antibody which binds to the  COOH-terminal 80-kD segment of the human but not mouse laminin  alpha2.	bind
36557	3	8483	5	13	NULL	NULL	NULL	5H2	GP		does not bind					laminin alpha2	GP	mouse	COOH-terminal		NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_4_844_s_94	9710454	5H2 is a mouse monoclonal antibody which binds to the  COOH-terminal 80-kD segment of the human but not mouse laminin  alpha2.	bind
29176	1	8483	6	10	NULL	0	NULL	5H2			bind					laminin alpha2		human	COOH-terminal		NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_4_844_s_94	9710454	5H2 is a mouse monoclonal antibody which binds to the  COOH-terminal 80-kD segment of the human but not mouse laminin  alpha2.	bind
29177	2	8483	6	10	NULL	0	NULL	5H2			does not bind					laminin alpha2		mouse	COOH-terminal		NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_4_844_s_94	9710454	5H2 is a mouse monoclonal antibody which binds to the  COOH-terminal 80-kD segment of the human but not mouse laminin  alpha2.	bind
56157	3	8483	6	10	NULL	0	NULL	5H2			is a type of					mouse monoclonal antibody					NULL		0	NULL	NULL	NULL	gw60_jclininvest_102_4_844_s_94	9710454	5H2 is a mouse monoclonal antibody which binds to the  COOH-terminal 80-kD segment of the human but not mouse laminin  alpha2.	bind
36558	1	8485	5	13	NULL	NULL	NULL	5HT	Chemical		bind					SERTs	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_12_4705_s_298	10366604	5HT can bind to SERTs in the absence of Na+ and Cl  (Humphreys et al., 1994  ), but the amine does not translocate.	bind
36559	2	8485	5	13	NULL	NULL	NULL	statement 1	Process		in the absence of					Na+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_12_4705_s_298	10366604	5HT can bind to SERTs in the absence of Na+ and Cl  (Humphreys et al., 1994  ), but the amine does not translocate.	bind
36560	3	8485	5	13	NULL	NULL	NULL	statement 1	Process		in the absence of					Cl	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_12_4705_s_298	10366604	5HT can bind to SERTs in the absence of Na+ and Cl  (Humphreys et al., 1994  ), but the amine does not translocate.	bind
29179	1	8485	6	NULL	NULL	0	NULL	5HT	NULL		bind	NULL				SERT	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_12_4705_s_298	10366604	5HT can bind to SERTs in the absence of Na+ and Cl  (Humphreys et al., 1994  ), but the amine does not translocate.	bind
29180	2	8485	6	NULL	NULL	0	NULL	statement 1	NULL		occurs in absence of	NULL				Na+	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_12_4705_s_298	10366604	5HT can bind to SERTs in the absence of Na+ and Cl  (Humphreys et al., 1994  ), but the amine does not translocate.	bind
29181	3	8485	6	NULL	NULL	0	NULL	statement 1	NULL		occurs in absence of	NULL				Cl	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_12_4705_s_298	10366604	5HT can bind to SERTs in the absence of Na+ and Cl  (Humphreys et al., 1994  ), but the amine does not translocate.	bind
36561	1	8486	5	13	NULL	NULL	NULL	TFIIIA	GP		bind					5S rDNA	NucleicAcid	naked			NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12169_s_135	9770458	5S DNA ternary complexes could be detected at TFIIIA concentrations only slightly higher than needed for TFIIIA to bind to naked 5S rDNA, and occurred before TFIIIA had bound to all available naked 5S rDNA binding sites (Fig.  4 A).	bind
36562	2	8486	5	13	NULL	NULL	NULL	TFIIIA	GP		bind					5S DNA ternary complexes	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12169_s_135	9770458	5S DNA ternary complexes could be detected at TFIIIA concentrations only slightly higher than needed for TFIIIA to bind to naked 5S rDNA, and occurred before TFIIIA had bound to all available naked 5S rDNA binding sites (Fig.  4 A).	bind
36563	3	8486	5	13	NULL	NULL	NULL	statement 2	Process		occurs before					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12169_s_135	9770458	5S DNA ternary complexes could be detected at TFIIIA concentrations only slightly higher than needed for TFIIIA to bind to naked 5S rDNA, and occurred before TFIIIA had bound to all available naked 5S rDNA binding sites (Fig.  4 A).	bind
29274	1	8486	6	NULL	NULL	0	NULL	TFIIIA	NULL		bind	NULL				5S rDNA	NULL	naked			NULL		0	NULL	NULL	NULL	gw60_pnas_95_21_12169_s_135	9770458	5S DNA ternary complexes could be detected at TFIIIA concentrations only slightly higher than needed for TFIIIA to bind to naked 5S rDNA, and occurred before TFIIIA had bound to all available naked 5S rDNA binding sites (Fig.  4 A).	bind
47894	2	8486	6	10	NULL	0	NULL	TFIIIA	NULL		bind	NULL				5S DNA ternary complexes 	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_21_12169_s_135	9770458	5S DNA ternary complexes could be detected at TFIIIA concentrations only slightly higher than needed for TFIIIA to bind to naked 5S rDNA, and occurred before TFIIIA had bound to all available naked 5S rDNA binding sites (Fig.  4 A).	bind
56158	3	8486	6	10	NULL	0	NULL	statement 2			occurs before					statement 1					NULL		0	NULL	NULL	NULL	gw60_pnas_95_21_12169_s_135	9770458	5S DNA ternary complexes could be detected at TFIIIA concentrations only slightly higher than needed for TFIIIA to bind to naked 5S rDNA, and occurred before TFIIIA had bound to all available naked 5S rDNA binding sites (Fig.  4 A).	bind
36564	1	8487	5	13	NULL	NULL	NULL	5S	GP		is a type of					mouse monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_biotechnol-appl-biochem_43_pt-2_16253117_s_4	16253117	5S is  a mouse monoclonal antibody that binds to HBsAg with very high affinity.	bind
36565	2	8487	5	13	NULL	NULL	NULL	5S	GP		bind		high affinity			HBsAg	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_biotechnol-appl-biochem_43_pt-2_16253117_s_4	16253117	5S is  a mouse monoclonal antibody that binds to HBsAg with very high affinity.	bind
29275	1	8487	6	10	NULL	0	NULL	5S 			bind		high affinity			HbsAg					NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_biotechnol-appl-biochem_43_pt-2_16253117_s_4	16253117	5S is  a mouse monoclonal antibody that binds to HBsAg with very high affinity.	bind
47895	2	8487	6	10	NULL	0	NULL	5S	NULL		is a type of	NULL				 mouse monoclonal antibody	NULL				NULL		0	NULL	NULL	NULL	abs-batch0580-0599_biotechnol-appl-biochem_43_pt-2_16253117_s_4	16253117	5S is  a mouse monoclonal antibody that binds to HBsAg with very high affinity.	bind
36566	1	8488	5	13	NULL	NULL	NULL	5S rDNA	NucleicAcid		complex with					histone octamers	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12169_s_153	9770458	5S rDNA ternary complexes, no TFIIIA binding to 5S rDNA complexed with histone octamers could be detected (Fig.  4 B).	bind
36567	2	8488	5	13	NULL	NULL	NULL	TFIIIA	GP		does not bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12169_s_153	9770458	5S rDNA ternary complexes, no TFIIIA binding to 5S rDNA complexed with histone octamers could be detected (Fig.  4 B).	bind
29277	1	8488	6	NULL	NULL	0	NULL	5S rDNA	NULL		complexes with	NULL				histone octamers	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_21_12169_s_153	9770458	5S rDNA ternary complexes, no TFIIIA binding to 5S rDNA complexed with histone octamers could be detected (Fig.  4 B).	bind
29278	2	8488	6	NULL	NULL	0	NULL	TFIIIA	NULL		does not bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_21_12169_s_153	9770458	5S rDNA ternary complexes, no TFIIIA binding to 5S rDNA complexed with histone octamers could be detected (Fig.  4 B).	bind
36711	1	8490	5	13	NULL	NULL	NULL	5S rRNA	NucleicAcid		bind					viral protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_1_166_s_37	10592212	5S rRNA binds the viral protein ( 32) and enhances the methionyl- and isoleucyl-tRNA synthetase activities by direct interactions with MetRS and tRNAMet in the macromolecular aminoacyl-tRNA synthetase complex ( 33).	bind
36712	2	8490	5	13	NULL	NULL	NULL	statement 1	GP		interact with		directly			MetRS	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_1_166_s_37	10592212	5S rRNA binds the viral protein ( 32) and enhances the methionyl- and isoleucyl-tRNA synthetase activities by direct interactions with MetRS and tRNAMet in the macromolecular aminoacyl-tRNA synthetase complex ( 33).	bind
36713	3	8490	5	13	NULL	NULL	NULL	statement 1	GP		interact with		directly			tRNAMet	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_1_166_s_37	10592212	5S rRNA binds the viral protein ( 32) and enhances the methionyl- and isoleucyl-tRNA synthetase activities by direct interactions with MetRS and tRNAMet in the macromolecular aminoacyl-tRNA synthetase complex ( 33).	bind
36714	4	8490	5	13	NULL	NULL	NULL	statement 2	Process		occurs in					aminoacyl-tRNA synthetase complex	GP	macromolecular			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_1_166_s_37	10592212	5S rRNA binds the viral protein ( 32) and enhances the methionyl- and isoleucyl-tRNA synthetase activities by direct interactions with MetRS and tRNAMet in the macromolecular aminoacyl-tRNA synthetase complex ( 33).	bind
36715	5	8490	5	13	NULL	NULL	NULL	statement 3	Process		occurs in					aminoacyl-tRNA synthetase complex	GP	macromolecular			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_1_166_s_37	10592212	5S rRNA binds the viral protein ( 32) and enhances the methionyl- and isoleucyl-tRNA synthetase activities by direct interactions with MetRS and tRNAMet in the macromolecular aminoacyl-tRNA synthetase complex ( 33).	bind
36716	6	8490	5	13	NULL	NULL	NULL	statement 1	Process		enhance					methionyl-tRNA synthetase	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_1_166_s_37	10592212	5S rRNA binds the viral protein ( 32) and enhances the methionyl- and isoleucyl-tRNA synthetase activities by direct interactions with MetRS and tRNAMet in the macromolecular aminoacyl-tRNA synthetase complex ( 33).	bind
36717	7	8490	5	13	NULL	NULL	NULL	statement 1	Process		enhance					isoleucyl-tRNA synthetase	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_1_166_s_37	10592212	5S rRNA binds the viral protein ( 32) and enhances the methionyl- and isoleucyl-tRNA synthetase activities by direct interactions with MetRS and tRNAMet in the macromolecular aminoacyl-tRNA synthetase complex ( 33).	bind
36718	8	8490	5	13	NULL	NULL	NULL	statement 2	Process		leads to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_1_166_s_37	10592212	5S rRNA binds the viral protein ( 32) and enhances the methionyl- and isoleucyl-tRNA synthetase activities by direct interactions with MetRS and tRNAMet in the macromolecular aminoacyl-tRNA synthetase complex ( 33).	bind
36719	9	8490	5	13	NULL	NULL	NULL	statement 2	Process		leads to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_1_166_s_37	10592212	5S rRNA binds the viral protein ( 32) and enhances the methionyl- and isoleucyl-tRNA synthetase activities by direct interactions with MetRS and tRNAMet in the macromolecular aminoacyl-tRNA synthetase complex ( 33).	bind
36720	10	8490	5	13	NULL	NULL	NULL	statement 3	Process		leads to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_1_166_s_37	10592212	5S rRNA binds the viral protein ( 32) and enhances the methionyl- and isoleucyl-tRNA synthetase activities by direct interactions with MetRS and tRNAMet in the macromolecular aminoacyl-tRNA synthetase complex ( 33).	bind
36721	11	8490	5	13	NULL	NULL	NULL	statement 3	Process		leads to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_1_166_s_37	10592212	5S rRNA binds the viral protein ( 32) and enhances the methionyl- and isoleucyl-tRNA synthetase activities by direct interactions with MetRS and tRNAMet in the macromolecular aminoacyl-tRNA synthetase complex ( 33).	bind
29281	1	8490	6	NULL	NULL	0	NULL	5S rRNA	NULL		bind	NULL				viral protein	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_1_166_s_37	10592212	5S rRNA binds the viral protein ( 32) and enhances the methionyl- and isoleucyl-tRNA synthetase activities by direct interactions with MetRS and tRNAMet in the macromolecular aminoacyl-tRNA synthetase complex ( 33).	bind
29282	2	8490	6	NULL	NULL	0	NULL	5S rRNA	NULL		interacts with	NULL	directly			MetRS	NULL				NULL	macromolecular aminoacyl-tRNA synthetase complex	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_1_166_s_37	10592212	5S rRNA binds the viral protein ( 32) and enhances the methionyl- and isoleucyl-tRNA synthetase activities by direct interactions with MetRS and tRNAMet in the macromolecular aminoacyl-tRNA synthetase complex ( 33).	bind
29283	3	8490	6	NULL	NULL	0	NULL	5S rRNA	NULL		interacts with	NULL	directly			tRNAMet	NULL				NULL	macromolecular aminoacyl-tRNA synthetase complex	0	NULL	NULL	NULL	gw60_nucleicacidsres_28_1_166_s_37	10592212	5S rRNA binds the viral protein ( 32) and enhances the methionyl- and isoleucyl-tRNA synthetase activities by direct interactions with MetRS and tRNAMet in the macromolecular aminoacyl-tRNA synthetase complex ( 33).	bind
29286	4	8490	6	NULL	NULL	0	NULL	statement 2	NULL		enhances	NULL				methionyl tRNA synthetase	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_1_166_s_37	10592212	5S rRNA binds the viral protein ( 32) and enhances the methionyl- and isoleucyl-tRNA synthetase activities by direct interactions with MetRS and tRNAMet in the macromolecular aminoacyl-tRNA synthetase complex ( 33).	bind
29288	5	8490	6	NULL	NULL	0	NULL	statement 3	NULL		enhances	NULL				isoleucyl-tRNA synthetase	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_1_166_s_37	10592212	5S rRNA binds the viral protein ( 32) and enhances the methionyl- and isoleucyl-tRNA synthetase activities by direct interactions with MetRS and tRNAMet in the macromolecular aminoacyl-tRNA synthetase complex ( 33).	bind
36568	1	8491	5	13	NULL	NULL	NULL	tmRNA	NucleicAcid		bind					alanyl-tRNA synthetase	GP	Escherichia coli			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1602_s_156	11266563	6       Barends,S., Wower,J. and Kraal,B. (2000) Kinetic parameters for tmRNA binding to alanyl-tRNA synthetase and elongation factor Tu from  Escherichia coli.	bind
36569	2	8491	5	13	NULL	NULL	NULL	tmRNA	NucleicAcid		bind					Tu	GP	Escherichia coli			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1602_s_156	11266563	6       Barends,S., Wower,J. and Kraal,B. (2000) Kinetic parameters for tmRNA binding to alanyl-tRNA synthetase and elongation factor Tu from  Escherichia coli.	bind
47896	3	8491	5	13	NULL	NULL	NULL	Tu	GP		is a type of					elongation factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1602_s_156	11266563	6       Barends,S., Wower,J. and Kraal,B. (2000) Kinetic parameters for tmRNA binding to alanyl-tRNA synthetase and elongation factor Tu from  Escherichia coli.	bind
29289	1	8491	6	10	NULL	0	NULL	tmRNA			bind					alanyl-tRNA synthetase		Escherichia coli			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1602_s_156	11266563	6       Barends,S., Wower,J. and Kraal,B. (2000) Kinetic parameters for tmRNA binding to alanyl-tRNA synthetase and elongation factor Tu from  Escherichia coli.	bind
29290	2	8491	6	10	NULL	0	NULL	tmRNA			bind					Tu		Escherichia coli			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1602_s_156	11266563	6       Barends,S., Wower,J. and Kraal,B. (2000) Kinetic parameters for tmRNA binding to alanyl-tRNA synthetase and elongation factor Tu from  Escherichia coli.	bind
29291	3	8491	6	NULL	NULL	0	NULL	Tu	NULL		is a type of	NULL				elongation factor	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1602_s_156	11266563	6       Barends,S., Wower,J. and Kraal,B. (2000) Kinetic parameters for tmRNA binding to alanyl-tRNA synthetase and elongation factor Tu from  Escherichia coli.	bind
36570	1	8494	5	13	NULL	NULL	NULL	fibrin(ogen)	GP		bind					ECs	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1544_s_180	8977460	6  32 42 43 45 46 47 48  The lack of association between FBG and ECs contradicts these other studies, in which specific binding of FBG to ECs was demonstrated; however, the lack of FBG binding to ECs in our study most likely reflects differences in the methods used to study the heparin-dependent binding of fibrin(ogen) to ECs.	bind
36571	2	8494	5	13	NULL	NULL	NULL	statement 1	Process		is dependent on					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1544_s_180	8977460	6  32 42 43 45 46 47 48  The lack of association between FBG and ECs contradicts these other studies, in which specific binding of FBG to ECs was demonstrated; however, the lack of FBG binding to ECs in our study most likely reflects differences in the methods used to study the heparin-dependent binding of fibrin(ogen) to ECs.	bind
29292	1	8494	6	NULL	NULL	0	NULL	fibrinogen	NULL		bind	NULL				EC	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1544_s_180	8977460	6  32 42 43 45 46 47 48  The lack of association between FBG and ECs contradicts these other studies, in which specific binding of FBG to ECs was demonstrated; however, the lack of FBG binding to ECs in our study most likely reflects differences in the methods used to study the heparin-dependent binding of fibrin(ogen) to ECs.	bind
29293	2	8494	6	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1544_s_180	8977460	6  32 42 43 45 46 47 48  The lack of association between FBG and ECs contradicts these other studies, in which specific binding of FBG to ECs was demonstrated; however, the lack of FBG binding to ECs in our study most likely reflects differences in the methods used to study the heparin-dependent binding of fibrin(ogen) to ECs.	bind
36572	1	8495	5	13	NULL	NULL	NULL	zymogen factor X	GP		bind					Mac-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_27	10510057	6  7  Binding of the zymogen factor X to Mac-1 results in the acceleration of its conversion to activated factor Xa and thus constitutes an alternative pathway for the initiation of the coagulation serine protease cascade.	bind
36573	2	8495	5	13	NULL	NULL	NULL	zymogen factor X	GP		is converted to					factor Xa	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_27	10510057	6  7  Binding of the zymogen factor X to Mac-1 results in the acceleration of its conversion to activated factor Xa and thus constitutes an alternative pathway for the initiation of the coagulation serine protease cascade.	bind
36574	3	8495	5	13	NULL	NULL	NULL	statement 1	Process		accelerate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_27	10510057	6  7  Binding of the zymogen factor X to Mac-1 results in the acceleration of its conversion to activated factor Xa and thus constitutes an alternative pathway for the initiation of the coagulation serine protease cascade.	bind
36575	4	8495	5	13	NULL	NULL	NULL	statement 3	Process		initiates					coagulation serine protease cascade	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_27	10510057	6  7  Binding of the zymogen factor X to Mac-1 results in the acceleration of its conversion to activated factor Xa and thus constitutes an alternative pathway for the initiation of the coagulation serine protease cascade.	bind
29294	1	8495	6	NULL	NULL	0	NULL	zymogen factor X	NULL		bind	NULL				Mac-1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_27	10510057	6  7  Binding of the zymogen factor X to Mac-1 results in the acceleration of its conversion to activated factor Xa and thus constitutes an alternative pathway for the initiation of the coagulation serine protease cascade.	bind
29295	2	8495	6	NULL	NULL	0	NULL	zymogen factor X	NULL		is converted to	NULL				factor Xa	NULL	activated			NULL		0	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_27	10510057	6  7  Binding of the zymogen factor X to Mac-1 results in the acceleration of its conversion to activated factor Xa and thus constitutes an alternative pathway for the initiation of the coagulation serine protease cascade.	bind
29296	3	8495	6	NULL	NULL	0	NULL	statement 1	NULL		accelerates 	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_27	10510057	6  7  Binding of the zymogen factor X to Mac-1 results in the acceleration of its conversion to activated factor Xa and thus constitutes an alternative pathway for the initiation of the coagulation serine protease cascade.	bind
29297	4	8495	6	NULL	NULL	0	NULL	statement 3	NULL		initiates	NULL				coagulation serine protease cascade	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_27	10510057	6  7  Binding of the zymogen factor X to Mac-1 results in the acceleration of its conversion to activated factor Xa and thus constitutes an alternative pathway for the initiation of the coagulation serine protease cascade.	bind
36576	1	8496	5	13	NULL	NULL	NULL	p53	GP		bind					bax	GP			promoter	NULL	myocytes	NULL	NULL	NULL	NULL	gw60_circulationres_88_3_298_s_214	11179197	6  7  p53 binding to the bax promoter is enhanced, and the amount of Bax protein in myocytes increases several fold.	bind
36577	2	8496	5	13	NULL	NULL	NULL	statement 1	Process	enhanced	results in					Bax protein	GP	increased			NULL	myocytes	NULL	NULL	NULL	NULL	gw60_circulationres_88_3_298_s_214	11179197	6  7  p53 binding to the bax promoter is enhanced, and the amount of Bax protein in myocytes increases several fold.	bind
29298	1	8496	6	10	NULL	0	NULL	p53			bind					bax				promoter	NULL	myocytes	NULL	NULL	NULL	NULL	gw60_circulationres_88_3_298_s_214	11179197	6  7  p53 binding to the bax promoter is enhanced, and the amount of Bax protein in myocytes increases several fold.	bind
47897	2	8496	6	10	NULL	0	NULL	statement 1	NULL		results in	NULL				Bax protein	NULL	increased			NULL	myocytes	0	NULL	NULL	NULL	gw60_circulationres_88_3_298_s_214	11179197	6  7  p53 binding to the bax promoter is enhanced, and the amount of Bax protein in myocytes increases several fold.	bind
36691	1	8497	5	13	NULL	NULL	NULL	Aogen	GP		is a limiting factor in					Ang II	GP	synthesis of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_3_298_s_35	11179197	6  7 26 27 28  Aogen is the limiting factor in the synthesis of Ang II, 28  and binding to AT1 conditions myocyte growth and death.	bind
36692	2	8497	5	13	NULL	NULL	NULL	Aogen	GP		bind					AT1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_3_298_s_35	11179197	6  7 26 27 28  Aogen is the limiting factor in the synthesis of Ang II, 28  and binding to AT1 conditions myocyte growth and death.	bind
36693	3	8497	5	13	NULL	NULL	NULL	statement 2	Process		conditions					myocyte	Cell	growth of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_3_298_s_35	11179197	6  7 26 27 28  Aogen is the limiting factor in the synthesis of Ang II, 28  and binding to AT1 conditions myocyte growth and death.	bind
36694	4	8497	5	13	NULL	NULL	NULL	statement 2	Process		conditions					myocyte	Cell	death of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_3_298_s_35	11179197	6  7 26 27 28  Aogen is the limiting factor in the synthesis of Ang II, 28  and binding to AT1 conditions myocyte growth and death.	bind
29299	1	8497	6	NULL	NULL	0	NULL	Aogen	NULL		is the limiting factor for	NULL				Ang II	NULL	synthesis of			NULL		0	NULL	NULL	NULL	gw60_circulationres_88_3_298_s_35	11179197	6  7 26 27 28  Aogen is the limiting factor in the synthesis of Ang II, 28  and binding to AT1 conditions myocyte growth and death.	bind
29300	2	8497	6	NULL	NULL	0	NULL	Aogen	NULL		bind	NULL				AT1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_88_3_298_s_35	11179197	6  7 26 27 28  Aogen is the limiting factor in the synthesis of Ang II, 28  and binding to AT1 conditions myocyte growth and death.	bind
29301	3	8497	6	NULL	NULL	0	NULL	statement 2	NULL		conditions	NULL				myocyte	NULL	growth of 			NULL		0	NULL	NULL	NULL	gw60_circulationres_88_3_298_s_35	11179197	6  7 26 27 28  Aogen is the limiting factor in the synthesis of Ang II, 28  and binding to AT1 conditions myocyte growth and death.	bind
29302	4	8497	6	NULL	NULL	0	NULL	statement 2	NULL		conditions	NULL				myocyte	NULL	death of 			NULL		0	NULL	NULL	NULL	gw60_circulationres_88_3_298_s_35	11179197	6  7 26 27 28  Aogen is the limiting factor in the synthesis of Ang II, 28  and binding to AT1 conditions myocyte growth and death.	bind
36695	1	8498	5	13	NULL	NULL	NULL	THM	GP		bind					thrombin	GP				NULL	normal arteries	NULL	NULL	NULL	NULL	gw60_circulation_102_3_332_s_110	10899098	6  7 8  In normal arteries, THM binds thrombin and prevents PAR activation while also catalytically activating protein C, which adds additional antithrombotic and anti-inflammatory effects.	bind
36696	2	8498	5	13	NULL	NULL	NULL	statement 1	Process		prevents					PAR	GP	activation of			NULL	normal arteries	NULL	NULL	NULL	NULL	gw60_circulation_102_3_332_s_110	10899098	6  7 8  In normal arteries, THM binds thrombin and prevents PAR activation while also catalytically activating protein C, which adds additional antithrombotic and anti-inflammatory effects.	bind
36697	3	8498	5	13	NULL	NULL	NULL	statement 1	Process		activates		catalytically			protein C	GP				NULL	normal arteries	NULL	NULL	NULL	NULL	gw60_circulation_102_3_332_s_110	10899098	6  7 8  In normal arteries, THM binds thrombin and prevents PAR activation while also catalytically activating protein C, which adds additional antithrombotic and anti-inflammatory effects.	bind
36698	4	8498	5	13	NULL	NULL	NULL	statement 3	Process		results in					antithrombotic effect	Process				NULL	normal arteries	NULL	NULL	NULL	NULL	gw60_circulation_102_3_332_s_110	10899098	6  7 8  In normal arteries, THM binds thrombin and prevents PAR activation while also catalytically activating protein C, which adds additional antithrombotic and anti-inflammatory effects.	bind
36699	5	8498	5	13	NULL	NULL	NULL	statement 3	Process		results in					anti-inflammatory effect	Process				NULL	normal arteries	NULL	NULL	NULL	NULL	gw60_circulation_102_3_332_s_110	10899098	6  7 8  In normal arteries, THM binds thrombin and prevents PAR activation while also catalytically activating protein C, which adds additional antithrombotic and anti-inflammatory effects.	bind
29303	1	8498	6	10	NULL	0	NULL	THM	NULL		bind	NULL				thrombin	NULL				NULL	 normal arteries	NULL	NULL	NULL	NULL	gw60_circulation_102_3_332_s_110	10899098	6  7 8  In normal arteries, THM binds thrombin and prevents PAR activation while also catalytically activating protein C, which adds additional antithrombotic and anti-inflammatory effects.	bind
29304	2	8498	6	10	NULL	0	NULL	statement 1	NULL		prevents	NULL				PAR	NULL	activation of			NULL	 normal arteries	NULL	NULL	NULL	NULL	gw60_circulation_102_3_332_s_110	10899098	6  7 8  In normal arteries, THM binds thrombin and prevents PAR activation while also catalytically activating protein C, which adds additional antithrombotic and anti-inflammatory effects.	bind
29305	3	8498	6	10	NULL	0	NULL	THM	NULL		activates	NULL	catalytically			protein C	NULL				NULL	 normal arteries	NULL	NULL	NULL	NULL	gw60_circulation_102_3_332_s_110	10899098	6  7 8  In normal arteries, THM binds thrombin and prevents PAR activation while also catalytically activating protein C, which adds additional antithrombotic and anti-inflammatory effects.	bind
29306	4	8498	6	10	NULL	0	NULL	statement 3	NULL		provides	NULL				antithrombotic effect	NULL				NULL	 normal arteries	NULL	NULL	NULL	NULL	gw60_circulation_102_3_332_s_110	10899098	6  7 8  In normal arteries, THM binds thrombin and prevents PAR activation while also catalytically activating protein C, which adds additional antithrombotic and anti-inflammatory effects.	bind
29307	5	8498	6	10	NULL	0	NULL	statement 3	NULL		provides	NULL				anti-inflammatory effects	NULL				NULL	 normal arteries	NULL	NULL	NULL	NULL	gw60_circulation_102_3_332_s_110	10899098	6  7 8  In normal arteries, THM binds thrombin and prevents PAR activation while also catalytically activating protein C, which adds additional antithrombotic and anti-inflammatory effects.	bind
36700	1	8499	5	13	NULL	NULL	NULL	apoB-100	GP	single copies of	bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_1013_s_30	9633945	6  Even though single copies of apoB-100 and apoE bind to the LDL receptor with similar affinities, lipoproteins with multiple copies of apoE bind to multiple LDL receptors, increasing the affinity of the lipoprotein-receptor interaction.	bind
36701	2	8499	5	13	NULL	NULL	NULL	apoE	GP	single copies of	bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_1013_s_30	9633945	6  Even though single copies of apoB-100 and apoE bind to the LDL receptor with similar affinities, lipoproteins with multiple copies of apoE bind to multiple LDL receptors, increasing the affinity of the lipoprotein-receptor interaction.	bind
36702	3	8499	5	13	NULL	NULL	NULL	statement 1	Process		similar affinity to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_1013_s_30	9633945	6  Even though single copies of apoB-100 and apoE bind to the LDL receptor with similar affinities, lipoproteins with multiple copies of apoE bind to multiple LDL receptors, increasing the affinity of the lipoprotein-receptor interaction.	bind
36703	4	8499	5	13	NULL	NULL	NULL	lipoproteins	GP		contains					apoE	GP	multiple copies of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_1013_s_30	9633945	6  Even though single copies of apoB-100 and apoE bind to the LDL receptor with similar affinities, lipoproteins with multiple copies of apoE bind to multiple LDL receptors, increasing the affinity of the lipoprotein-receptor interaction.	bind
36704	5	8499	5	13	NULL	NULL	NULL	statement 4	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_1013_s_30	9633945	6  Even though single copies of apoB-100 and apoE bind to the LDL receptor with similar affinities, lipoproteins with multiple copies of apoE bind to multiple LDL receptors, increasing the affinity of the lipoprotein-receptor interaction.	bind
36705	6	8499	5	13	NULL	NULL	NULL	statement 5	Process		increase					lipoprotein-receptor 	GP	affinity of;;interaction of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_1013_s_30	9633945	6  Even though single copies of apoB-100 and apoE bind to the LDL receptor with similar affinities, lipoproteins with multiple copies of apoE bind to multiple LDL receptors, increasing the affinity of the lipoprotein-receptor interaction.	bind
29308	1	8499	6	NULL	NULL	0	NULL	apoB-100	NULL		bind	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_1013_s_30	9633945	6  Even though single copies of apoB-100 and apoE bind to the LDL receptor with similar affinities, lipoproteins with multiple copies of apoE bind to multiple LDL receptors, increasing the affinity of the lipoprotein-receptor interaction.	bind
29309	2	8499	6	NULL	NULL	0	NULL	apoE	NULL		bind	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_1013_s_30	9633945	6  Even though single copies of apoB-100 and apoE bind to the LDL receptor with similar affinities, lipoproteins with multiple copies of apoE bind to multiple LDL receptors, increasing the affinity of the lipoprotein-receptor interaction.	bind
47898	3	8499	6	10	NULL	0	NULL	statement 1	NULL	affinity of	similar to	NULL				statement 2	NULL	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_1013_s_30	9633945	6  Even though single copies of apoB-100 and apoE bind to the LDL receptor with similar affinities, lipoproteins with multiple copies of apoE bind to multiple LDL receptors, increasing the affinity of the lipoprotein-receptor interaction.	bind
47899	4	8499	6	10	NULL	0	NULL	lipoproteins	NULL		contains	NULL				apoE	NULL	multiple copies of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_1013_s_30	9633945	6  Even though single copies of apoB-100 and apoE bind to the LDL receptor with similar affinities, lipoproteins with multiple copies of apoE bind to multiple LDL receptors, increasing the affinity of the lipoprotein-receptor interaction.	bind
47900	5	8499	6	10	NULL	0	NULL	statement 4	NULL		bind	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_1013_s_30	9633945	6  Even though single copies of apoB-100 and apoE bind to the LDL receptor with similar affinities, lipoproteins with multiple copies of apoE bind to multiple LDL receptors, increasing the affinity of the lipoprotein-receptor interaction.	bind
47901	6	8499	6	10	NULL	0	NULL	statement 5	NULL		increase	NULL				 lipoprotein-receptor	NULL	affinity of;;interaction of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_6_1013_s_30	9633945	6  Even though single copies of apoB-100 and apoE bind to the LDL receptor with similar affinities, lipoproteins with multiple copies of apoE bind to multiple LDL receptors, increasing the affinity of the lipoprotein-receptor interaction.	bind
36706	1	8500	5	13	NULL	NULL	NULL	heparin	Chemical	soluble	bind					Mac-1	GP				NULL	patients treated with heparin	NULL	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_168	10510057	6  Furthermore, binding of soluble heparin to Mac-1 in patients treated with heparin may inhibit leukocyte adhesion, which was recently described to be partially mediated by binding of Mac-1 to heparin-like structures bound on endothelial cells.	bind
36707	2	8500	5	13	NULL	NULL	NULL	statement 1	Process		inhibit		may			leukocyte 	Cell	adhesion of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_168	10510057	6  Furthermore, binding of soluble heparin to Mac-1 in patients treated with heparin may inhibit leukocyte adhesion, which was recently described to be partially mediated by binding of Mac-1 to heparin-like structures bound on endothelial cells.	bind
36708	3	8500	5	13	NULL	NULL	NULL	heparin-like structures	Chemical		bind					endothelial cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_168	10510057	6  Furthermore, binding of soluble heparin to Mac-1 in patients treated with heparin may inhibit leukocyte adhesion, which was recently described to be partially mediated by binding of Mac-1 to heparin-like structures bound on endothelial cells.	bind
36709	4	8500	5	13	NULL	NULL	NULL	Mac-1	GP		bind					statement 3	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_168	10510057	6  Furthermore, binding of soluble heparin to Mac-1 in patients treated with heparin may inhibit leukocyte adhesion, which was recently described to be partially mediated by binding of Mac-1 to heparin-like structures bound on endothelial cells.	bind
36710	5	8500	5	13	NULL	NULL	NULL	statement 2	Process		mediated by		partially			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_168	10510057	6  Furthermore, binding of soluble heparin to Mac-1 in patients treated with heparin may inhibit leukocyte adhesion, which was recently described to be partially mediated by binding of Mac-1 to heparin-like structures bound on endothelial cells.	bind
29310	1	8500	6	NULL	NULL	0	NULL	heparin	NULL	soluble	bind	NULL				Mac-1	NULL				NULL	patients treated with heparin	0	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_168	10510057	6  Furthermore, binding of soluble heparin to Mac-1 in patients treated with heparin may inhibit leukocyte adhesion, which was recently described to be partially mediated by binding of Mac-1 to heparin-like structures bound on endothelial cells.	bind
29311	2	8500	6	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL	may			leukocyte	NULL	adhesion of 			NULL		0	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_168	10510057	6  Furthermore, binding of soluble heparin to Mac-1 in patients treated with heparin may inhibit leukocyte adhesion, which was recently described to be partially mediated by binding of Mac-1 to heparin-like structures bound on endothelial cells.	bind
29312	3	8500	6	NULL	NULL	0	NULL	heparin-like structures	NULL		bind	NULL				endothelial cells	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_168	10510057	6  Furthermore, binding of soluble heparin to Mac-1 in patients treated with heparin may inhibit leukocyte adhesion, which was recently described to be partially mediated by binding of Mac-1 to heparin-like structures bound on endothelial cells.	bind
29313	4	8500	6	NULL	NULL	0	NULL	Mac-1	NULL		bind	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_168	10510057	6  Furthermore, binding of soluble heparin to Mac-1 in patients treated with heparin may inhibit leukocyte adhesion, which was recently described to be partially mediated by binding of Mac-1 to heparin-like structures bound on endothelial cells.	bind
29314	5	8500	6	NULL	NULL	0	NULL	statement 2	NULL		is mediated by	NULL	partially			statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_168	10510057	6  Furthermore, binding of soluble heparin to Mac-1 in patients treated with heparin may inhibit leukocyte adhesion, which was recently described to be partially mediated by binding of Mac-1 to heparin-like structures bound on endothelial cells.	bind
33563	1	8501	5	13	NULL	NULL	NULL	KY3	Chemical		bind					VDR	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_23_2867_s_24	11104746	6  KY3 has  20 times higher affinity for VDR than 1,25(OH)2D3 and does not bind to the transport protein vitamin D - binding protein.	bind
33564	2	8501	5	13	NULL	NULL	NULL	KY3	Chemical		bind					1,25(OH)2D3	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_23_2867_s_24	11104746	6  KY3 has  20 times higher affinity for VDR than 1,25(OH)2D3 and does not bind to the transport protein vitamin D - binding protein.	bind
33565	3	8501	5	13	NULL	NULL	NULL	statement 1	Chemical		high affinity than					statement 2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_23_2867_s_24	11104746	6  KY3 has  20 times higher affinity for VDR than 1,25(OH)2D3 and does not bind to the transport protein vitamin D - binding protein.	bind
33566	4	8501	5	13	NULL	NULL	NULL	KY3	Chemical		does not bind					vitamin D - binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_23_2867_s_24	11104746	6  KY3 has  20 times higher affinity for VDR than 1,25(OH)2D3 and does not bind to the transport protein vitamin D - binding protein.	bind
55723	5	8501	5	13	NULL	NULL	NULL	vitamin D - binding protein	GP		is a type of 					transport protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_23_2867_s_24	11104746	6  KY3 has  20 times higher affinity for VDR than 1,25(OH)2D3 and does not bind to the transport protein vitamin D - binding protein.	bind
35123	1	8501	7	NULL	NULL	0	NULL	 KY3	NULL		bind	NULL	high affinity			VDR	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_23_2867_s_24	11104746	6  KY3 has  20 times higher affinity for VDR than 1,25(OH)2D3 and does not bind to the transport protein vitamin D - binding protein.	bind
35124	2	8501	7	NULL	NULL	0	NULL	 1,25(OH)2D3	NULL		bind	NULL				VDR	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_23_2867_s_24	11104746	6  KY3 has  20 times higher affinity for VDR than 1,25(OH)2D3 and does not bind to the transport protein vitamin D - binding protein.	bind
35125	3	8501	7	NULL	NULL	0	NULL	statement 1	NULL	affinity of	is higher than	NULL				statement 2	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_circulation_102_23_2867_s_24	11104746	6  KY3 has  20 times higher affinity for VDR than 1,25(OH)2D3 and does not bind to the transport protein vitamin D - binding protein.	bind
35126	4	8501	7	NULL	NULL	0	NULL	KY3 	NULL		does not bind	NULL				vitamin D - binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_23_2867_s_24	11104746	6  KY3 has  20 times higher affinity for VDR than 1,25(OH)2D3 and does not bind to the transport protein vitamin D - binding protein.	bind
35127	5	8501	7	NULL	NULL	0	NULL	vitamin D - binding protein	NULL		is a type of	NULL				transport protein	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_23_2867_s_24	11104746	6  KY3 has  20 times higher affinity for VDR than 1,25(OH)2D3 and does not bind to the transport protein vitamin D - binding protein.	bind
33568	1	8502	5	13	NULL	NULL	NULL	PlGF	GP		is					placenta growth factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_993_s_22	11549592	6  lacenta growth factor (PlGF) that binds to VEGFR-1 and not VEGFR-2 also stimulates monocyte migration.	bind
33569	2	8502	5	13	NULL	NULL	NULL	PlGF	GP		bind					VEGFR-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_993_s_22	11549592	6  lacenta growth factor (PlGF) that binds to VEGFR-1 and not VEGFR-2 also stimulates monocyte migration.	bind
33570	3	8502	5	13	NULL	NULL	NULL	PlGF	GP		bind					VEGFR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_993_s_22	11549592	6  lacenta growth factor (PlGF) that binds to VEGFR-1 and not VEGFR-2 also stimulates monocyte migration.	bind
33571	4	8502	5	13	NULL	NULL	NULL	PlGF	GP		stimulates					monocyte	Cell	migration of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_993_s_22	11549592	6  lacenta growth factor (PlGF) that binds to VEGFR-1 and not VEGFR-2 also stimulates monocyte migration.	bind
35128	1	8502	7	NULL	NULL	0	NULL	PlGF	NULL		binds to	NULL				VEGFR-1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_993_s_22	11549592	6  lacenta growth factor (PlGF) that binds to VEGFR-1 and not VEGFR-2 also stimulates monocyte migration.	bind
35129	2	8502	7	NULL	NULL	0	NULL	PlGF	NULL		does not bind	NULL				VEGFR-2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_993_s_22	11549592	6  lacenta growth factor (PlGF) that binds to VEGFR-1 and not VEGFR-2 also stimulates monocyte migration.	bind
35130	3	8502	7	NULL	NULL	0	NULL	PIGF	NULL		stimulates	NULL				monocyte	NULL	migration of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_993_s_22	11549592	6  lacenta growth factor (PlGF) that binds to VEGFR-1 and not VEGFR-2 also stimulates monocyte migration.	bind
35131	4	8502	7	NULL	NULL	0	NULL	PlGF	NULL		is	NULL				placenta growth factor 	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_993_s_22	11549592	6  lacenta growth factor (PlGF) that binds to VEGFR-1 and not VEGFR-2 also stimulates monocyte migration.	bind
33573	1	8503	5	13	NULL	NULL	NULL	lectin	GP		bind					galactose residues	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_1055_s_170	10702421	6  Microglia could not be visualized with the GS lectin in mice given an intracarotid injection of arabinose, because arabinose interferes with the binding of the lectin to the galactose residues.	bind
33574	2	8503	5	13	NULL	NULL	NULL	arabinose	Chemical		interfere with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_1055_s_170	10702421	6  Microglia could not be visualized with the GS lectin in mice given an intracarotid injection of arabinose, because arabinose interferes with the binding of the lectin to the galactose residues.	bind
35132	1	8503	7	NULL	NULL	0	NULL	lectin	NULL		bind	NULL				galactose residues	NULL				NULL	mice	NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_1055_s_170	10702421	6  Microglia could not be visualized with the GS lectin in mice given an intracarotid injection of arabinose, because arabinose interferes with the binding of the lectin to the galactose residues.	bind
35133	2	8503	7	NULL	NULL	0	NULL	 arabinose	NULL		interferes with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_3_1055_s_170	10702421	6  Microglia could not be visualized with the GS lectin in mice given an intracarotid injection of arabinose, because arabinose interferes with the binding of the lectin to the galactose residues.	bind
33575	1	8504	5	13	NULL	NULL	NULL	mdm2	GP		regulates					p53	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_977_s_27	10702413	6  p53 activity is regulated by mdm2, which binds to p53, inhibits its transcriptional activity, and targets its degradation.	bind
33576	2	8504	5	13	NULL	NULL	NULL	mdm2	GP		bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_977_s_27	10702413	6  p53 activity is regulated by mdm2, which binds to p53, inhibits its transcriptional activity, and targets its degradation.	bind
33577	3	8504	5	13	NULL	NULL	NULL	statement 2	Process		inhibits					p53	GP	transcriptional activity of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_977_s_27	10702413	6  p53 activity is regulated by mdm2, which binds to p53, inhibits its transcriptional activity, and targets its degradation.	bind
33578	4	8504	5	13	NULL	NULL	NULL	statement 2	Process		targets					p53	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_3_977_s_27	10702413	6  p53 activity is regulated by mdm2, which binds to p53, inhibits its transcriptional activity, and targets its degradation.	bind
35134	1	8504	7	NULL	NULL	0	NULL	mdm2	NULL		regulates	NULL				p53 	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_3_977_s_27	10702413	6  p53 activity is regulated by mdm2, which binds to p53, inhibits its transcriptional activity, and targets its degradation.	bind
35135	2	8504	7	NULL	NULL	0	NULL	mdm2	NULL		binds to	NULL				p53	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_3_977_s_27	10702413	6  p53 activity is regulated by mdm2, which binds to p53, inhibits its transcriptional activity, and targets its degradation.	bind
35136	3	8504	7	NULL	NULL	0	NULL	mdm2	NULL		inhibits	NULL				p53	NULL	transcriptional activity of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_3_977_s_27	10702413	6  p53 activity is regulated by mdm2, which binds to p53, inhibits its transcriptional activity, and targets its degradation.	bind
35137	4	8504	7	NULL	NULL	0	NULL	mdm2	NULL		target	NULL				p53	NULL	degradation of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_3_977_s_27	10702413	6  p53 activity is regulated by mdm2, which binds to p53, inhibits its transcriptional activity, and targets its degradation.	bind
33581	1	8505	5	13	NULL	NULL	NULL	apoB	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_154	7583549	6  Since the radius of the LDL particle may vary considerably and, according to this model, also that of the apoB, 25  the stabilization of the two amino acid clusters may be of importance to maintain the binding affinity of the apoB to the LDL receptor.	bind
35146	1	8505	7	NULL	NULL	0	NULL	apoB 	NULL		bind	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_154	7583549	6  Since the radius of the LDL particle may vary considerably and, according to this model, also that of the apoB, 25  the stabilization of the two amino acid clusters may be of importance to maintain the binding affinity of the apoB to the LDL receptor.	bind
33586	1	8506	5	13	NULL	NULL	NULL	SMCs	Cell		bind					fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_25	9848876	6  SMCs bind to fibronectin, laminin, collagen I, and collagen IV primarily by means of beta1 integrins.	bind
33587	2	8506	5	13	NULL	NULL	NULL	statement 1	Process		occurs via					beta1 integrins	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_25	9848876	6  SMCs bind to fibronectin, laminin, collagen I, and collagen IV primarily by means of beta1 integrins.	bind
33588	3	8506	5	13	NULL	NULL	NULL	SMCs	Cell		bind					laminin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_25	9848876	6  SMCs bind to fibronectin, laminin, collagen I, and collagen IV primarily by means of beta1 integrins.	bind
33589	4	8506	5	13	NULL	NULL	NULL	statement 3	Process		occurs via					beta1 integrins	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_25	9848876	6  SMCs bind to fibronectin, laminin, collagen I, and collagen IV primarily by means of beta1 integrins.	bind
33590	5	8506	5	13	NULL	NULL	NULL	SMCs	Cell		bind					collagen I	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_25	9848876	6  SMCs bind to fibronectin, laminin, collagen I, and collagen IV primarily by means of beta1 integrins.	bind
33591	6	8506	5	13	NULL	NULL	NULL	statement 5	Process		occurs via					beta1 integrins	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_25	9848876	6  SMCs bind to fibronectin, laminin, collagen I, and collagen IV primarily by means of beta1 integrins.	bind
33592	7	8506	5	13	NULL	NULL	NULL	SMCs	Cell		bind					collagen IV	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_25	9848876	6  SMCs bind to fibronectin, laminin, collagen I, and collagen IV primarily by means of beta1 integrins.	bind
33593	8	8506	5	13	NULL	NULL	NULL	statement 7	Process		occurs via					beta1 integrins	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_25	9848876	6  SMCs bind to fibronectin, laminin, collagen I, and collagen IV primarily by means of beta1 integrins.	bind
35148	1	8506	7	NULL	NULL	0	NULL	SMCs	NULL		bind	NULL				fibronectin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_25	9848876	6  SMCs bind to fibronectin, laminin, collagen I, and collagen IV primarily by means of beta1 integrins.	bind
35149	2	8506	7	NULL	NULL	0	NULL	SMCs	NULL		bind	NULL				laminin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_25	9848876	6  SMCs bind to fibronectin, laminin, collagen I, and collagen IV primarily by means of beta1 integrins.	bind
35150	3	8506	7	NULL	NULL	0	NULL	SMCs	NULL		bind	NULL				collagen I	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_25	9848876	6  SMCs bind to fibronectin, laminin, collagen I, and collagen IV primarily by means of beta1 integrins.	bind
35151	4	8506	7	NULL	NULL	0	NULL	SMCs	NULL		bind	NULL				collagen IV	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_25	9848876	6  SMCs bind to fibronectin, laminin, collagen I, and collagen IV primarily by means of beta1 integrins.	bind
35178	5	8506	7	NULL	NULL	0	NULL	statement 1	NULL		occurs via	NULL				beta1 integrins	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_25	9848876	6  SMCs bind to fibronectin, laminin, collagen I, and collagen IV primarily by means of beta1 integrins.	bind
35179	6	8506	7	NULL	NULL	0	NULL	statement 2	NULL		occurs via	NULL				beta1 integrins	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_25	9848876	6  SMCs bind to fibronectin, laminin, collagen I, and collagen IV primarily by means of beta1 integrins.	bind
35180	7	8506	7	NULL	NULL	0	NULL	statement 3	NULL		occurs via	NULL				beta1 integrins	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_25	9848876	6  SMCs bind to fibronectin, laminin, collagen I, and collagen IV primarily by means of beta1 integrins.	bind
35181	8	8506	7	NULL	NULL	0	NULL	statement 4	NULL		occurs via	NULL				beta1 integrins	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_12_1855_s_25	9848876	6  SMCs bind to fibronectin, laminin, collagen I, and collagen IV primarily by means of beta1 integrins.	bind
33594	1	8507	5	13	NULL	NULL	NULL	cell wall	CellComponent	changes in;; thickness of 	results in					vancomycin	Chemical	resistance of			NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_2_255_s_19	11815565	6 -  8 It is believed that the reason such changes in cell wall thickness and cross-linking result in vancomycin resistance is that the modified cell wall binds more vancomycin, due to the increased amount of terminal d-alanyl-d-alanine dipeptide.	bind
33595	2	8507	5	13	NULL	NULL	NULL	cell wall	CellComponent	changes in;; thickness of	results in					vancomycin	Chemical	resistance of			NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_2_255_s_19	11815565	6 -  8 It is believed that the reason such changes in cell wall thickness and cross-linking result in vancomycin resistance is that the modified cell wall binds more vancomycin, due to the increased amount of terminal d-alanyl-d-alanine dipeptide.	bind
33596	3	8507	5	13	NULL	NULL	NULL	cell wall	CellComponent	modified	bind					vancomycin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_2_255_s_19	11815565	6 -  8 It is believed that the reason such changes in cell wall thickness and cross-linking result in vancomycin resistance is that the modified cell wall binds more vancomycin, due to the increased amount of terminal d-alanyl-d-alanine dipeptide.	bind
33597	4	8507	5	13	NULL	NULL	NULL	d-alanyl-d-alanine dipeptide	AminoAcid	increased amount of terminal	results in					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_2_255_s_19	11815565	6 -  8 It is believed that the reason such changes in cell wall thickness and cross-linking result in vancomycin resistance is that the modified cell wall binds more vancomycin, due to the increased amount of terminal d-alanyl-d-alanine dipeptide.	bind
33598	5	8507	5	13	NULL	NULL	NULL	statement 3	Process		leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_2_255_s_19	11815565	6 -  8 It is believed that the reason such changes in cell wall thickness and cross-linking result in vancomycin resistance is that the modified cell wall binds more vancomycin, due to the increased amount of terminal d-alanyl-d-alanine dipeptide.	bind
33599	6	8507	5	13	NULL	NULL	NULL	statement 3	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_2_255_s_19	11815565	6 -  8 It is believed that the reason such changes in cell wall thickness and cross-linking result in vancomycin resistance is that the modified cell wall binds more vancomycin, due to the increased amount of terminal d-alanyl-d-alanine dipeptide.	bind
35182	1	8507	7	NULL	NULL	0	NULL	cell wall	NULL	modified	binds	NULL				vancomycin	NULL				NULL		0	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_2_255_s_19	11815565	6 -  8 It is believed that the reason such changes in cell wall thickness and cross-linking result in vancomycin resistance is that the modified cell wall binds more vancomycin, due to the increased amount of terminal d-alanyl-d-alanine dipeptide.	bind
35185	2	8507	7	NULL	NULL	0	NULL	statement 1	NULL		occurs due to	NULL				 d-alanyl-d-alanine dipeptide	NULL		terminal		NULL		0	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_2_255_s_19	11815565	6 -  8 It is believed that the reason such changes in cell wall thickness and cross-linking result in vancomycin resistance is that the modified cell wall binds more vancomycin, due to the increased amount of terminal d-alanyl-d-alanine dipeptide.	bind
46725	3	8507	7	NULL	NULL	0	NULL	cell wall 	NULL	changes in thickness of	result in	NULL				vancomycin	NULL	resistance of			NULL		0	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_2_255_s_19	11815565	6 -  8 It is believed that the reason such changes in cell wall thickness and cross-linking result in vancomycin resistance is that the modified cell wall binds more vancomycin, due to the increased amount of terminal d-alanyl-d-alanine dipeptide.	bind
46726	4	8507	7	NULL	NULL	0	NULL	cross-linking	NULL	changes in	result in	NULL				vancomycin	NULL	resistance of			NULL		0	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_2_255_s_19	11815565	6 -  8 It is believed that the reason such changes in cell wall thickness and cross-linking result in vancomycin resistance is that the modified cell wall binds more vancomycin, due to the increased amount of terminal d-alanyl-d-alanine dipeptide.	bind
46727	5	8507	7	10	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_2_255_s_19	11815565	6 -  8 It is believed that the reason such changes in cell wall thickness and cross-linking result in vancomycin resistance is that the modified cell wall binds more vancomycin, due to the increased amount of terminal d-alanyl-d-alanine dipeptide.	bind
46728	6	8507	7	10	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_2_255_s_19	11815565	6 -  8 It is believed that the reason such changes in cell wall thickness and cross-linking result in vancomycin resistance is that the modified cell wall binds more vancomycin, due to the increased amount of terminal d-alanyl-d-alanine dipeptide.	bind
33600	1	8509	5	13	NULL	NULL	NULL	RGD	AminoAcid		is					tripeptide arginine-glycine aspartate	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_4_705_s_23	7641347	6 10 11  Many of the biological effects of OPN appear to be mediated by binding of a tripeptide arginine-glycine aspartate (RGD) sequence to cell-surface integrin receptors.	bind
33601	2	8509	5	13	NULL	NULL	NULL	RGD sequence	AminoAcid		bind					integrin receptors	GP	cell-surface			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_4_705_s_23	7641347	6 10 11  Many of the biological effects of OPN appear to be mediated by binding of a tripeptide arginine-glycine aspartate (RGD) sequence to cell-surface integrin receptors.	bind
33602	3	8509	5	13	NULL	NULL	NULL	OPN	GP	biological effects of	is mediated by					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_4_705_s_23	7641347	6 10 11  Many of the biological effects of OPN appear to be mediated by binding of a tripeptide arginine-glycine aspartate (RGD) sequence to cell-surface integrin receptors.	bind
35187	1	8509	7	10	NULL	0	NULL	RGD tripeptide			bind					integrin receptors		cell-surface			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_4_705_s_23	7641347	6 10 11  Many of the biological effects of OPN appear to be mediated by binding of a tripeptide arginine-glycine aspartate (RGD) sequence to cell-surface integrin receptors.	bind
35188	2	8509	7	NULL	NULL	0	NULL	statement 1	NULL		mediates	NULL				OPN	NULL	biological effects of			NULL		0	NULL	NULL	NULL	gw60_circulation_92_4_705_s_23	7641347	6 10 11  Many of the biological effects of OPN appear to be mediated by binding of a tripeptide arginine-glycine aspartate (RGD) sequence to cell-surface integrin receptors.	bind
35189	3	8509	7	NULL	NULL	0	NULL	RGD	NULL		is	NULL				arginine-glycine aspartate	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_4_705_s_23	7641347	6 10 11  Many of the biological effects of OPN appear to be mediated by binding of a tripeptide arginine-glycine aspartate (RGD) sequence to cell-surface integrin receptors.	bind
33603	1	8510	5	13	NULL	NULL	NULL	Wg protein	GP	soluble	bind					fz proteins	GP	Drosophila			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1433_s_30	10381896	6 11 12  The importance of the fz-Wnt interaction was highlighted by the fact that cells transfected with soluble Wg protein bind both  Drosophila and mammalian fz proteins and initiate signal.	bind
33604	2	8510	5	13	NULL	NULL	NULL	statement 1	Process		initiates					signal	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1433_s_30	10381896	6 11 12  The importance of the fz-Wnt interaction was highlighted by the fact that cells transfected with soluble Wg protein bind both  Drosophila and mammalian fz proteins and initiate signal.	bind
33605	3	8510	5	13	NULL	NULL	NULL	Wg protein	GP	soluble	bind					fz proteins	GP	mammalian			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1433_s_30	10381896	6 11 12  The importance of the fz-Wnt interaction was highlighted by the fact that cells transfected with soluble Wg protein bind both  Drosophila and mammalian fz proteins and initiate signal.	bind
33606	4	8510	5	13	NULL	NULL	NULL	statement 3	Process		initiates					signal	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1433_s_30	10381896	6 11 12  The importance of the fz-Wnt interaction was highlighted by the fact that cells transfected with soluble Wg protein bind both  Drosophila and mammalian fz proteins and initiate signal.	bind
35192	1	8510	7	NULL	NULL	0	NULL	 Wg protein	NULL	soluble	bind	NULL				 fz proteins	NULL	Drosophila 			NULL		0	NULL	NULL	NULL	gw60_circulationres_84_12_1433_s_30	10381896	6 11 12  The importance of the fz-Wnt interaction was highlighted by the fact that cells transfected with soluble Wg protein bind both  Drosophila and mammalian fz proteins and initiate signal.	bind
35193	2	8510	7	NULL	NULL	0	NULL	Wg protein	NULL	soluble	bind	NULL				fz proteins	NULL	mammalian			NULL		0	NULL	NULL	NULL	gw60_circulationres_84_12_1433_s_30	10381896	6 11 12  The importance of the fz-Wnt interaction was highlighted by the fact that cells transfected with soluble Wg protein bind both  Drosophila and mammalian fz proteins and initiate signal.	bind
35196	3	8510	7	NULL	NULL	0	NULL	statement 1	NULL		initiate	NULL				signal	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_12_1433_s_30	10381896	6 11 12  The importance of the fz-Wnt interaction was highlighted by the fact that cells transfected with soluble Wg protein bind both  Drosophila and mammalian fz proteins and initiate signal.	bind
35197	4	8510	7	NULL	NULL	0	NULL	statement 2	NULL		initiate	NULL				signal	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_12_1433_s_30	10381896	6 11 12  The importance of the fz-Wnt interaction was highlighted by the fact that cells transfected with soluble Wg protein bind both  Drosophila and mammalian fz proteins and initiate signal.	bind
33607	1	8511	5	13	NULL	NULL	NULL	apoB	GP	defective	bind					LDLR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_210	7583549	6 25 26  Since the size of the LDL particles has been demonstrated to be of importance for the binding of the defective apoB to the LDLR, 6  dietary changes may therefore cause a change in the binding affinity of the apoB.	bind
33609	2	8511	5	13	NULL	NULL	NULL	dietary changes			change		may			apoB	GP	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_210	7583549	6 25 26  Since the size of the LDL particles has been demonstrated to be of importance for the binding of the defective apoB to the LDLR, 6  dietary changes may therefore cause a change in the binding affinity of the apoB.	bind
35200	1	8511	7	10	NULL	0	NULL	apoB		defective 	bind					LDLR					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_210	7583549	6 25 26  Since the size of the LDL particles has been demonstrated to be of importance for the binding of the defective apoB to the LDLR, 6  dietary changes may therefore cause a change in the binding affinity of the apoB.	bind
35201	2	8511	7	NULL	NULL	0	NULL	dietary changes	NULL		change	NULL	may			apoB	NULL	binding affinity of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_210	7583549	6 25 26  Since the size of the LDL particles has been demonstrated to be of importance for the binding of the defective apoB to the LDLR, 6  dietary changes may therefore cause a change in the binding affinity of the apoB.	bind
33615	1	8512	5	13	NULL	NULL	NULL	VLDLR	GP		bind					beta-VLDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_407_s_23	8630667	6 7  LRP, like the VLDLR, also binds beta-VLDL; however, unlike the VLDLR, LRP binds beta-VLDL only when the latter particle has been supplemented with exogenous apoE. 1 8	bind
33616	2	8512	5	13	NULL	NULL	NULL	LRP	GP		bind					beta-VLDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_407_s_23	8630667	6 7  LRP, like the VLDLR, also binds beta-VLDL; however, unlike the VLDLR, LRP binds beta-VLDL only when the latter particle has been supplemented with exogenous apoE. 1 8	bind
33617	3	8512	5	13	NULL	NULL	NULL	beta-VLDL	GP		is supplemented with					apoE	GP	exogenous			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_407_s_23	8630667	6 7  LRP, like the VLDLR, also binds beta-VLDL; however, unlike the VLDLR, LRP binds beta-VLDL only when the latter particle has been supplemented with exogenous apoE. 1 8	bind
33618	4	8512	5	13	NULL	NULL	NULL	statement 2	Process		occurs following		only			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_407_s_23	8630667	6 7  LRP, like the VLDLR, also binds beta-VLDL; however, unlike the VLDLR, LRP binds beta-VLDL only when the latter particle has been supplemented with exogenous apoE. 1 8	bind
35202	1	8512	7	NULL	NULL	0	NULL	LRP	NULL		binds	NULL				beta-VLDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_407_s_23	8630667	6 7  LRP, like the VLDLR, also binds beta-VLDL; however, unlike the VLDLR, LRP binds beta-VLDL only when the latter particle has been supplemented with exogenous apoE. 1 8	bind
35203	2	8512	7	NULL	NULL	0	NULL	VLDLR	NULL		binds	NULL				beta-VLDL	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_407_s_23	8630667	6 7  LRP, like the VLDLR, also binds beta-VLDL; however, unlike the VLDLR, LRP binds beta-VLDL only when the latter particle has been supplemented with exogenous apoE. 1 8	bind
35204	3	8512	7	10	NULL	0	NULL	beta-VLDL			is supplemented with					apoE		exogenous 			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_407_s_23	8630667	6 7  LRP, like the VLDLR, also binds beta-VLDL; however, unlike the VLDLR, LRP binds beta-VLDL only when the latter particle has been supplemented with exogenous apoE. 1 8	bind
55799	4	8512	7	10	NULL	0	NULL	statement 2			occurs following		only			statement 3					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_3_407_s_23	8630667	6 7  LRP, like the VLDLR, also binds beta-VLDL; however, unlike the VLDLR, LRP binds beta-VLDL only when the latter particle has been supplemented with exogenous apoE. 1 8	bind
33610	1	8513	5	13	NULL	NULL	NULL	LDL particles	GP		bind					LDL B receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1573_s_159	8977464	6 7  Oxidation of LDL particles impairs their binding to LDL B,E receptors and thus confines their uptake mainly by macrophages via the scavenger receptor pathway.	bind
33611	2	8513	5	13	NULL	NULL	NULL	LDL particles	GP	oxidation of	impairs					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1573_s_159	8977464	6 7  Oxidation of LDL particles impairs their binding to LDL B,E receptors and thus confines their uptake mainly by macrophages via the scavenger receptor pathway.	bind
33613	4	8513	5	13	NULL	NULL	NULL	statement 2	Process		confines					macrophages	Cell	uptake by			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1573_s_159	8977464	6 7  Oxidation of LDL particles impairs their binding to LDL B,E receptors and thus confines their uptake mainly by macrophages via the scavenger receptor pathway.	bind
33614	5	8513	5	13	NULL	NULL	NULL	statement 4	Process		via					scavenger receptor pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1573_s_159	8977464	6 7  Oxidation of LDL particles impairs their binding to LDL B,E receptors and thus confines their uptake mainly by macrophages via the scavenger receptor pathway.	bind
56464	3	8513	5	13	NULL	NULL	NULL	LDL particles	GP		bind					LDL E receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1573_s_159	8977464	6 7  Oxidation of LDL particles impairs their binding to LDL B,E receptors and thus confines their uptake mainly by macrophages via the scavenger receptor pathway.	bind
56465	6	8513	5	13	NULL	NULL	NULL	statement 3	Process		confines					macrophages	Cell	uptake by			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1573_s_159	8977464	6 7  Oxidation of LDL particles impairs their binding to LDL B,E receptors and thus confines their uptake mainly by macrophages via the scavenger receptor pathway.	bind
56466	7	8513	5	13	NULL	NULL	NULL	statement 6	Process		via					scavenger receptor pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1573_s_159	8977464	6 7  Oxidation of LDL particles impairs their binding to LDL B,E receptors and thus confines their uptake mainly by macrophages via the scavenger receptor pathway.	bind
56467	8	8513	5	13	NULL	NULL	NULL	LDL particles	GP	oxidation of	impairs					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1573_s_159	8977464	6 7  Oxidation of LDL particles impairs their binding to LDL B,E receptors and thus confines their uptake mainly by macrophages via the scavenger receptor pathway.	bind
35206	1	8513	7	NULL	NULL	0	NULL	 LDL particles	NULL		bind	NULL				LDL B receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1573_s_159	8977464	6 7  Oxidation of LDL particles impairs their binding to LDL B,E receptors and thus confines their uptake mainly by macrophages via the scavenger receptor pathway.	bind
35207	2	8513	7	NULL	NULL	0	NULL	LDL particles	NULL		bind	NULL				LDL E receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1573_s_159	8977464	6 7  Oxidation of LDL particles impairs their binding to LDL B,E receptors and thus confines their uptake mainly by macrophages via the scavenger receptor pathway.	bind
35208	3	8513	7	NULL	NULL	0	NULL	LDL particles	NULL	oxidation of	impair	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1573_s_159	8977464	6 7  Oxidation of LDL particles impairs their binding to LDL B,E receptors and thus confines their uptake mainly by macrophages via the scavenger receptor pathway.	bind
35209	4	8513	7	NULL	NULL	0	NULL	LDL particles	NULL	oxidation of	impair	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1573_s_159	8977464	6 7  Oxidation of LDL particles impairs their binding to LDL B,E receptors and thus confines their uptake mainly by macrophages via the scavenger receptor pathway.	bind
35210	5	8513	7	NULL	NULL	0	NULL	statement 1	NULL		confines	NULL				macrophages	NULL	uptake by			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1573_s_159	8977464	6 7  Oxidation of LDL particles impairs their binding to LDL B,E receptors and thus confines their uptake mainly by macrophages via the scavenger receptor pathway.	bind
35211	6	8513	7	NULL	NULL	0	NULL	statement 2	NULL		confines	NULL				macrophages	NULL	uptake by			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1573_s_159	8977464	6 7  Oxidation of LDL particles impairs their binding to LDL B,E receptors and thus confines their uptake mainly by macrophages via the scavenger receptor pathway.	bind
35219	7	8513	7	NULL	NULL	0	NULL	statement 5	NULL		occurs via	NULL				scavenger receptor pathway	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1573_s_159	8977464	6 7  Oxidation of LDL particles impairs their binding to LDL B,E receptors and thus confines their uptake mainly by macrophages via the scavenger receptor pathway.	bind
35220	8	8513	7	NULL	NULL	0	NULL	statement 6	NULL		occurs via	NULL				scavenger receptor pathway	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_12_1573_s_159	8977464	6 7  Oxidation of LDL particles impairs their binding to LDL B,E receptors and thus confines their uptake mainly by macrophages via the scavenger receptor pathway.	bind
46667	1	8514	5	13	NULL	NULL	NULL	[3]SCH58261	Chemical		bind		specifically			crude membranes	CellComponent				NULL	porcine striatum	NULL	NULL	NULL	NULL	gw60_circulationres_79_6_1153_s_194	8943953	6 7  The specific binding of [3]SCH58261 to crude membranes prepared from porcine striatum and PC12 cells was 85% and 90% of total binding at the  Kd value, respectively, whereas the specific binding of [3]KF 178375 and [125]ZM 241385 to membranes prepared from rat and bovine striatum was 60% to 70% of total binding.	bind
46668	2	8514	5	13	NULL	NULL	NULL	[3]SCH58261	Chemical		bind		specifically			crude membranes	CellComponent				NULL	PC12 cells	NULL	NULL	NULL	NULL	gw60_circulationres_79_6_1153_s_194	8943953	6 7  The specific binding of [3]SCH58261 to crude membranes prepared from porcine striatum and PC12 cells was 85% and 90% of total binding at the  Kd value, respectively, whereas the specific binding of [3]KF 178375 and [125]ZM 241385 to membranes prepared from rat and bovine striatum was 60% to 70% of total binding.	bind
46669	3	8514	5	13	NULL	NULL	NULL	[3]KF 178375	Chemical		bind		specifically			membranes	CellComponent				NULL	rat striatum	NULL	NULL	NULL	NULL	gw60_circulationres_79_6_1153_s_194	8943953	6 7  The specific binding of [3]SCH58261 to crude membranes prepared from porcine striatum and PC12 cells was 85% and 90% of total binding at the  Kd value, respectively, whereas the specific binding of [3]KF 178375 and [125]ZM 241385 to membranes prepared from rat and bovine striatum was 60% to 70% of total binding.	bind
46672	4	8514	5	13	NULL	NULL	NULL	[125]ZM 241385	Chemical		bind		specifically			membrane	CellComponent				NULL	bovine striatum	NULL	NULL	NULL	NULL	gw60_circulationres_79_6_1153_s_194	8943953	6 7  The specific binding of [3]SCH58261 to crude membranes prepared from porcine striatum and PC12 cells was 85% and 90% of total binding at the  Kd value, respectively, whereas the specific binding of [3]KF 178375 and [125]ZM 241385 to membranes prepared from rat and bovine striatum was 60% to 70% of total binding.	bind
35221	1	8514	7	NULL	NULL	0	NULL	[3]SCH58261	NULL		bind	NULL	specifically			crude membranes	NULL				NULL	porcine striatum	0	NULL	NULL	NULL	gw60_circulationres_79_6_1153_s_194	8943953	6 7  The specific binding of [3]SCH58261 to crude membranes prepared from porcine striatum and PC12 cells was 85% and 90% of total binding at the  Kd value, respectively, whereas the specific binding of [3]KF 178375 and [125]ZM 241385 to membranes prepared from rat and bovine striatum was 60% to 70% of total binding.	bind
35222	2	8514	7	NULL	NULL	0	NULL	[3]SCH58261	NULL		bind	NULL	specifically			crude membranes	NULL				NULL	PC12 cells	NULL	NULL	NULL	NULL	gw60_circulationres_79_6_1153_s_194	8943953	6 7  The specific binding of [3]SCH58261 to crude membranes prepared from porcine striatum and PC12 cells was 85% and 90% of total binding at the  Kd value, respectively, whereas the specific binding of [3]KF 178375 and [125]ZM 241385 to membranes prepared from rat and bovine striatum was 60% to 70% of total binding.	bind
35223	3	8514	7	NULL	NULL	0	NULL	[3]KF 178375	NULL		bind	NULL	specifically			membranes	NULL				NULL	rat striatum	0	NULL	NULL	NULL	gw60_circulationres_79_6_1153_s_194	8943953	6 7  The specific binding of [3]SCH58261 to crude membranes prepared from porcine striatum and PC12 cells was 85% and 90% of total binding at the  Kd value, respectively, whereas the specific binding of [3]KF 178375 and [125]ZM 241385 to membranes prepared from rat and bovine striatum was 60% to 70% of total binding.	bind
35224	4	8514	7	NULL	NULL	0	NULL	 [125]ZM 241385	NULL		bind	NULL	specifically			membranes	NULL				NULL	bovine striatum	NULL	NULL	NULL	NULL	gw60_circulationres_79_6_1153_s_194	8943953	6 7  The specific binding of [3]SCH58261 to crude membranes prepared from porcine striatum and PC12 cells was 85% and 90% of total binding at the  Kd value, respectively, whereas the specific binding of [3]KF 178375 and [125]ZM 241385 to membranes prepared from rat and bovine striatum was 60% to 70% of total binding.	bind
33625	1	8515	5	13	NULL	NULL	NULL	plasminogen	GP		bind					lysine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_656_s_24	8963723	6 7  This activity is responsible for the binding of plasminogen to lysine-Sepharose and, more importantly, for the interaction of plasminogen and plasmin with substrates, 8 9  inhibitors, 10  and cellular receptors.	bind
35229	1	8515	7	10	NULL	0	NULL	plasminogen			bind					lysine					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_5_656_s_24	8963723	6 7  This activity is responsible for the binding of plasminogen to lysine-Sepharose and, more importantly, for the interaction of plasminogen and plasmin with substrates, 8 9  inhibitors, 10  and cellular receptors.	bind
33639	1	8516	5	13	NULL	NULL	NULL	FKBP12	GP		bind					RyR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_2_188_s_29	11157671	6 7 8 9  Although FKBP12 can bind to both RyR1 and RyR2, FKBP12.6 specifically associates with RyR2.	bind
33640	2	8516	5	13	NULL	NULL	NULL	FKBP12	GP		bind					RyR2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_2_188_s_29	11157671	6 7 8 9  Although FKBP12 can bind to both RyR1 and RyR2, FKBP12.6 specifically associates with RyR2.	bind
33641	3	8516	5	13	NULL	NULL	NULL	FKBP12.6	GP		associates with		specifically			RyR2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_2_188_s_29	11157671	6 7 8 9  Although FKBP12 can bind to both RyR1 and RyR2, FKBP12.6 specifically associates with RyR2.	bind
35237	1	8516	7	NULL	NULL	0	NULL	FKBP12	NULL		bind	NULL				RyR1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_88_2_188_s_29	11157671	6 7 8 9  Although FKBP12 can bind to both RyR1 and RyR2, FKBP12.6 specifically associates with RyR2.	bind
35238	2	8516	7	NULL	NULL	0	NULL	FKBP12	NULL		bind	NULL				RyR2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_88_2_188_s_29	11157671	6 7 8 9  Although FKBP12 can bind to both RyR1 and RyR2, FKBP12.6 specifically associates with RyR2.	bind
35239	3	8516	7	NULL	NULL	0	NULL	FKBP12.6	NULL		associate with	NULL	specifically			RyR2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_88_2_188_s_29	11157671	6 7 8 9  Although FKBP12 can bind to both RyR1 and RyR2, FKBP12.6 specifically associates with RyR2.	bind
33642	1	8517	5	13	NULL	NULL	NULL	myosin	GP		interacts with					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_11_1310_s_177	10364569	6 7 8 9  In addition, as there appear to be differences in this reciprocal coupling process dependent on whether the myosin interaction with actin is noncycling (rigor) or cycling, 8  it seems possible that crossbridges with different inherent rates of cycling may also differentially affect the activation of the thin filament.	bind
33643	2	8517	5	13	NULL	NULL	NULL	statement 1	Process		is					noncycling	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_11_1310_s_177	10364569	6 7 8 9  In addition, as there appear to be differences in this reciprocal coupling process dependent on whether the myosin interaction with actin is noncycling (rigor) or cycling, 8  it seems possible that crossbridges with different inherent rates of cycling may also differentially affect the activation of the thin filament.	bind
46661	3	8517	5	13	NULL	NULL	NULL	statement 1	Process		is					cycling	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_11_1310_s_177	10364569	6 7 8 9  In addition, as there appear to be differences in this reciprocal coupling process dependent on whether the myosin interaction with actin is noncycling (rigor) or cycling, 8  it seems possible that crossbridges with different inherent rates of cycling may also differentially affect the activation of the thin filament.	bind
46662	4	8517	5	13	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_11_1310_s_177	10364569	6 7 8 9  In addition, as there appear to be differences in this reciprocal coupling process dependent on whether the myosin interaction with actin is noncycling (rigor) or cycling, 8  it seems possible that crossbridges with different inherent rates of cycling may also differentially affect the activation of the thin filament.	bind
46663	5	8517	5	13	NULL	NULL	NULL	statement 2	Process		affects					thin filament	CellComponent	activation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_11_1310_s_177	10364569	6 7 8 9  In addition, as there appear to be differences in this reciprocal coupling process dependent on whether the myosin interaction with actin is noncycling (rigor) or cycling, 8  it seems possible that crossbridges with different inherent rates of cycling may also differentially affect the activation of the thin filament.	bind
46664	6	8517	5	13	NULL	NULL	NULL	statement 3	Process		affects					thin filament	CellComponent	activation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_11_1310_s_177	10364569	6 7 8 9  In addition, as there appear to be differences in this reciprocal coupling process dependent on whether the myosin interaction with actin is noncycling (rigor) or cycling, 8  it seems possible that crossbridges with different inherent rates of cycling may also differentially affect the activation of the thin filament.	bind
35240	1	8517	7	NULL	NULL	0	NULL	myosin	NULL		interacts with	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_11_1310_s_177	10364569	6 7 8 9  In addition, as there appear to be differences in this reciprocal coupling process dependent on whether the myosin interaction with actin is noncycling (rigor) or cycling, 8  it seems possible that crossbridges with different inherent rates of cycling may also differentially affect the activation of the thin filament.	bind
35241	2	8517	7	NULL	NULL	0	NULL	statement 1	NULL		is	NULL				noncycling	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_11_1310_s_177	10364569	6 7 8 9  In addition, as there appear to be differences in this reciprocal coupling process dependent on whether the myosin interaction with actin is noncycling (rigor) or cycling, 8  it seems possible that crossbridges with different inherent rates of cycling may also differentially affect the activation of the thin filament.	bind
35242	3	8517	7	NULL	NULL	0	NULL	statement 1	NULL		is	NULL				cycling	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_11_1310_s_177	10364569	6 7 8 9  In addition, as there appear to be differences in this reciprocal coupling process dependent on whether the myosin interaction with actin is noncycling (rigor) or cycling, 8  it seems possible that crossbridges with different inherent rates of cycling may also differentially affect the activation of the thin filament.	bind
35243	4	8517	7	NULL	NULL	0	NULL	statement 2	NULL		is an alternative to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_11_1310_s_177	10364569	6 7 8 9  In addition, as there appear to be differences in this reciprocal coupling process dependent on whether the myosin interaction with actin is noncycling (rigor) or cycling, 8  it seems possible that crossbridges with different inherent rates of cycling may also differentially affect the activation of the thin filament.	bind
35244	5	8517	7	NULL	NULL	0	NULL	statement 2	NULL		affect	NULL				thin filament	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_11_1310_s_177	10364569	6 7 8 9  In addition, as there appear to be differences in this reciprocal coupling process dependent on whether the myosin interaction with actin is noncycling (rigor) or cycling, 8  it seems possible that crossbridges with different inherent rates of cycling may also differentially affect the activation of the thin filament.	bind
35245	6	8517	7	NULL	NULL	0	NULL	statement 3	NULL		affect	NULL				thin filament	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_circulationres_84_11_1310_s_177	10364569	6 7 8 9  In addition, as there appear to be differences in this reciprocal coupling process dependent on whether the myosin interaction with actin is noncycling (rigor) or cycling, 8  it seems possible that crossbridges with different inherent rates of cycling may also differentially affect the activation of the thin filament.	bind
33644	1	8518	5	13	NULL	NULL	NULL	VEGF-A isoforms	GP		bind					VEGFR-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1578_s_52	15231518	6 All VEGF-A isoforms bind to VEGFR-1 and VEGFR-2.	bind
33645	2	8518	5	13	NULL	NULL	NULL	VEGF-A isoforms	GP		bind					VEGFR-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1578_s_52	15231518	6 All VEGF-A isoforms bind to VEGFR-1 and VEGFR-2.	bind
35246	1	8518	7	NULL	NULL	0	NULL	VEGF-A isoform	NULL		bind	NULL				VEGFR-1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1578_s_52	15231518	6 All VEGF-A isoforms bind to VEGFR-1 and VEGFR-2.	bind
35247	2	8518	7	NULL	NULL	0	NULL	VEGF-A isoforms	NULL		bind	NULL				VEGFR-2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1578_s_52	15231518	6 All VEGF-A isoforms bind to VEGFR-1 and VEGFR-2.	bind
33829	1	8519	5	13	NULL	NULL	NULL	Ang1	GP		bind					Tie2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_8_1014_s_45	16645151	6 Ang1 and Ang2 bind to Tie2 with similar affinities; however, whereas Ang1 is an agonist, the ability of Ang2 to activate Tie2 appears to depend on the cell type and context.	bind
33830	2	8519	5	13	NULL	NULL	NULL	Ang2	GP		bind					Tie2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_8_1014_s_45	16645151	6 Ang1 and Ang2 bind to Tie2 with similar affinities; however, whereas Ang1 is an agonist, the ability of Ang2 to activate Tie2 appears to depend on the cell type and context.	bind
33831	3	8519	5	13	NULL	NULL	NULL	statement 1	Process		similar affinity to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_8_1014_s_45	16645151	6 Ang1 and Ang2 bind to Tie2 with similar affinities; however, whereas Ang1 is an agonist, the ability of Ang2 to activate Tie2 appears to depend on the cell type and context.	bind
33832	4	8519	5	13	NULL	NULL	NULL	Ang1	GP		is agonist of					Tie2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_8_1014_s_45	16645151	6 Ang1 and Ang2 bind to Tie2 with similar affinities; however, whereas Ang1 is an agonist, the ability of Ang2 to activate Tie2 appears to depend on the cell type and context.	bind
33833	5	8519	5	13	NULL	NULL	NULL	Ang2	GP		activates					Tie2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_8_1014_s_45	16645151	6 Ang1 and Ang2 bind to Tie2 with similar affinities; however, whereas Ang1 is an agonist, the ability of Ang2 to activate Tie2 appears to depend on the cell type and context.	bind
33834	6	8519	5	13	NULL	NULL	NULL	statement 5	Process		depends on		may			cell type	Cell				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_8_1014_s_45	16645151	6 Ang1 and Ang2 bind to Tie2 with similar affinities; however, whereas Ang1 is an agonist, the ability of Ang2 to activate Tie2 appears to depend on the cell type and context.	bind
33835	7	8519	5	13	NULL	NULL	NULL	statement 5	Process		depends on		may			context					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_8_1014_s_45	16645151	6 Ang1 and Ang2 bind to Tie2 with similar affinities; however, whereas Ang1 is an agonist, the ability of Ang2 to activate Tie2 appears to depend on the cell type and context.	bind
35248	1	8519	7	NULL	NULL	0	NULL	Ang1	NULL		binds to	NULL				Tie2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_8_1014_s_45	16645151	6 Ang1 and Ang2 bind to Tie2 with similar affinities; however, whereas Ang1 is an agonist, the ability of Ang2 to activate Tie2 appears to depend on the cell type and context.	bind
35249	2	8519	7	NULL	NULL	0	NULL	Ang2	NULL		binds to	NULL				Tie2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_8_1014_s_45	16645151	6 Ang1 and Ang2 bind to Tie2 with similar affinities; however, whereas Ang1 is an agonist, the ability of Ang2 to activate Tie2 appears to depend on the cell type and context.	bind
35250	3	8519	7	NULL	NULL	0	NULL	statement 1	NULL	affinity of	is similar to	NULL				statement 2	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw70_circulationres_98_8_1014_s_45	16645151	6 Ang1 and Ang2 bind to Tie2 with similar affinities; however, whereas Ang1 is an agonist, the ability of Ang2 to activate Tie2 appears to depend on the cell type and context.	bind
35251	4	8519	7	NULL	NULL	0	NULL	Ang1	NULL		is a type of	NULL				agonist	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_8_1014_s_45	16645151	6 Ang1 and Ang2 bind to Tie2 with similar affinities; however, whereas Ang1 is an agonist, the ability of Ang2 to activate Tie2 appears to depend on the cell type and context.	bind
35252	5	8519	7	NULL	NULL	0	NULL	Ang2	NULL		activate	NULL				Tie2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_8_1014_s_45	16645151	6 Ang1 and Ang2 bind to Tie2 with similar affinities; however, whereas Ang1 is an agonist, the ability of Ang2 to activate Tie2 appears to depend on the cell type and context.	bind
35253	6	8519	7	10	NULL	0	NULL	statement 5			depend on		may			cell type					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_8_1014_s_45	16645151	6 Ang1 and Ang2 bind to Tie2 with similar affinities; however, whereas Ang1 is an agonist, the ability of Ang2 to activate Tie2 appears to depend on the cell type and context.	bind
35254	7	8519	7	10	NULL	0	NULL	statement 5			depend on		may			cell context					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_8_1014_s_45	16645151	6 Ang1 and Ang2 bind to Tie2 with similar affinities; however, whereas Ang1 is an agonist, the ability of Ang2 to activate Tie2 appears to depend on the cell type and context.	bind
33646	1	8520	5	13	NULL	NULL	NULL	VLDL	GP	apoE-rich	bind					LDL receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
33647	2	8520	5	13	NULL	NULL	NULL	ApoC-III	GP		reduces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
33648	3	8520	5	13	NULL	NULL	NULL	VLDL	GP	apoE-rich	bind					LDL receptor - related protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
33649	4	8520	5	13	NULL	NULL	NULL	ApoC-III	GP		reduces					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
33650	5	8520	5	13	NULL	NULL	NULL	VLDL	GP	apoE-rich	bind					proteoglycan	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
33651	6	8520	5	13	NULL	NULL	NULL	ApoC-III	GP		reduces					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
33652	7	8520	5	13	NULL	NULL	NULL	VLDL	GP		uptake by					liver	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
33653	8	8520	5	13	NULL	NULL	NULL	apoE 	GP		accelerates					particle clearance	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
33654	9	8520	5	13	NULL	NULL	NULL	statement 7	Process		antagonize					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
55800	10	8520	5	13	NULL	NULL	NULL	ApoC-III	GP		inhibits					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
35255	1	8520	7	10	NULL	0	NULL	VLDL	NULL	 apoE-rich 	bind	NULL				LDL receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
35256	2	8520	7	10	NULL	0	NULL	VLDL	NULL	apoE-rich	bind	NULL				LDL receptor - related protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
35257	3	8520	7	10	NULL	0	NULL	VLDL	NULL	apoE-rich 	bind	NULL				proteoglycan	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
35258	4	8520	7	NULL	NULL	0	NULL	ApoC-III 	NULL		reduce	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
35260	5	8520	7	NULL	NULL	0	NULL	ApoC-III 	NULL		reduce	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
35262	6	8520	7	NULL	NULL	0	NULL	ApoC-III 	NULL		reduce	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
35264	7	8520	7	NULL	NULL	0	NULL	VLDL	NULL		uptake by	NULL				liver	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
35265	8	8520	7	NULL	NULL	0	NULL	ApoC-III 	NULL		inhibits	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
35266	9	8520	7	NULL	NULL	0	NULL	apoE	NULL		accelerates	NULL				particle clearance	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
35267	10	8520	7	NULL	NULL	0	NULL	ApoC-III 	NULL		antagonize	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_9_1494_s_146	11557678	6 ApoC-III reduces the binding of apoE-rich VLDL to LDL receptors, 26 the LDL receptor - related protein, 8 and proteoglycan 11, 27 and inhibits VLDL uptake by the liver, 28 antagonizing the accelerating effect of apoE on particle clearance.	bind
33655	1	8521	5	13	NULL	NULL	NULL	E1A	GP		bind					CBP/p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_31629_s_127	9822619	6 Because E1A binding to CBP/p300 is well characterized as a major mechanism by which adenovirus controls host cell function, it is likely that CBP/p300 is also a critical factor in the transcriptional response of PEPCK to hormones (see Fig.  2).	bind
35268	1	8521	7	NULL	NULL	0	NULL	E1A 	NULL		bind	NULL				CBP/p300	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_48_31629_s_127	9822619	6 Because E1A binding to CBP/p300 is well characterized as a major mechanism by which adenovirus controls host cell function, it is likely that CBP/p300 is also a critical factor in the transcriptional response of PEPCK to hormones (see Fig.  2).	bind
33658	1	8522	5	13	NULL	NULL	NULL	HSP90	GP		bind					eNOS	GP				NULL	cardiac myocytes	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
33659	2	8522	5	13	NULL	NULL	NULL	HSP90	GP		bind					eNOS	GP				NULL	vascular endothelial cells	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
33660	3	8522	5	13	NULL	NULL	NULL	estrogen	Chemical		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
33661	4	8522	5	13	NULL	NULL	NULL	estrogen	Chemical		stimulates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
33662	5	8522	5	13	NULL	NULL	NULL	hypoxia	MedicalFinding		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
33663	6	8522	5	13	NULL	NULL	NULL	hypoxia	MedicalFinding		stimulates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
33664	7	8522	5	13	NULL	NULL	NULL	estrogen	Chemical		regulates					NO	Chemical	release of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
33665	8	8522	5	13	NULL	NULL	NULL	hypoxia	MedicalFinding		regulates					NO	Chemical	release of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
33666	9	8522	5	13	NULL	NULL	NULL	estrogen	Chemical		regulates					PI3-Akt	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
33667	10	8522	5	13	NULL	NULL	NULL	hypoxia	MedicalFinding		regulates					PI3-Akt	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
33668	11	8522	5	13	NULL	NULL	NULL	estrogen	Chemical		regulates					calcium sensitivity	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
33669	12	8522	5	13	NULL	NULL	NULL	hypoxia	MedicalFinding		regulates					calcium sensitivity	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
35279	1	8522	7	NULL	NULL	0	NULL	HSP90	NULL		bind	NULL				eNOS	NULL				NULL	cardiac myocytes	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
35283	2	8522	7	NULL	NULL	0	NULL	HSP90	NULL		bind	NULL				eNOS	NULL				NULL	vascular endothelial cells	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
35284	3	8522	7	NULL	NULL	0	NULL	estrogen	NULL		stimulates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
35285	4	8522	7	NULL	NULL	0	NULL	estrogen	NULL		stimulates	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
35286	5	8522	7	NULL	NULL	0	NULL	hypoxia	NULL		stimulates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
35287	6	8522	7	NULL	NULL	0	NULL	hypoxia	NULL		stimulates	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
35288	7	8522	7	10	NULL	0	NULL	estrogen			regulates					NO 		release of 			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
35289	8	8522	7	10	NULL	0	NULL	hypoxia			regulates					NO 		release of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
35290	9	8522	7	NULL	NULL	0	NULL	estrogen	NULL		activates	NULL				PI3-Akt	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
35291	10	8522	7	NULL	NULL	0	NULL	hypoxia	NULL		activates	NULL				PI3-Akt	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
35292	11	8522	7	NULL	NULL	0	NULL	estrogen	NULL		effect	NULL				calcium sensitivity	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
35293	12	8522	7	NULL	NULL	0	NULL	hypoxia	NULL		effect	NULL				calcium sensitivity	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_42	15231513	6 Estrogen, as well as hypoxia, stimulates HSP90 binding to eNOS in cardiac myocytes and vascular endothelial cells, 9 with subsequent regulation of NO release, PI3-Akt activation, and calcium sensitivity.	bind
33670	1	8523	5	13	NULL	NULL	NULL	FGFRs	GP		bind					FGFs	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1465_s_20	10329600	6 FGFRs bind to fibroblast growth factors (FGFs), which are known to regulate proliferation, survival, differentiation, and migration of a wide variety of cells.	bind
33671	2	8523	5	13	NULL	NULL	NULL	FGFs	GP		is					fibroblast growth factors	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1465_s_20	10329600	6 FGFRs bind to fibroblast growth factors (FGFs), which are known to regulate proliferation, survival, differentiation, and migration of a wide variety of cells.	bind
33672	3	8523	5	13	NULL	NULL	NULL	FGFs	GP		regulates					cell proliferation	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1465_s_20	10329600	6 FGFRs bind to fibroblast growth factors (FGFs), which are known to regulate proliferation, survival, differentiation, and migration of a wide variety of cells.	bind
33673	4	8523	5	13	NULL	NULL	NULL	FGFs	GP		regulates					cell survival	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1465_s_20	10329600	6 FGFRs bind to fibroblast growth factors (FGFs), which are known to regulate proliferation, survival, differentiation, and migration of a wide variety of cells.	bind
33674	5	8523	5	13	NULL	NULL	NULL	FGFs	GP		regulates					cell differentiation	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1465_s_20	10329600	6 FGFRs bind to fibroblast growth factors (FGFs), which are known to regulate proliferation, survival, differentiation, and migration of a wide variety of cells.	bind
33675	6	8523	5	13	NULL	NULL	NULL	FGFs	GP		regulates					cell migration	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1465_s_20	10329600	6 FGFRs bind to fibroblast growth factors (FGFs), which are known to regulate proliferation, survival, differentiation, and migration of a wide variety of cells.	bind
35294	1	8523	7	NULL	NULL	0	NULL	FGFRs	NULL		bind to	NULL				FGFs	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_5_1465_s_20	10329600	6 FGFRs bind to fibroblast growth factors (FGFs), which are known to regulate proliferation, survival, differentiation, and migration of a wide variety of cells.	bind
35295	2	8523	7	10	NULL	0	NULL	FGFs			regulate					cell proliferation					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1465_s_20	10329600	6 FGFRs bind to fibroblast growth factors (FGFs), which are known to regulate proliferation, survival, differentiation, and migration of a wide variety of cells.	bind
35296	3	8523	7	10	NULL	0	NULL	FGFs			regulate					cell survival					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1465_s_20	10329600	6 FGFRs bind to fibroblast growth factors (FGFs), which are known to regulate proliferation, survival, differentiation, and migration of a wide variety of cells.	bind
35297	4	8523	7	NULL	NULL	0	NULL	FGFs	NULL		regulate	NULL				cell differentiation	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_5_1465_s_20	10329600	6 FGFRs bind to fibroblast growth factors (FGFs), which are known to regulate proliferation, survival, differentiation, and migration of a wide variety of cells.	bind
35298	5	8523	7	NULL	NULL	0	NULL	FGFs	NULL		regulate	NULL				cell migration	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_5_1465_s_20	10329600	6 FGFRs bind to fibroblast growth factors (FGFs), which are known to regulate proliferation, survival, differentiation, and migration of a wide variety of cells.	bind
35299	6	8523	7	NULL	NULL	0	NULL	FGFs	NULL		is	NULL				fibroblast growth factors	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_5_1465_s_20	10329600	6 FGFRs bind to fibroblast growth factors (FGFs), which are known to regulate proliferation, survival, differentiation, and migration of a wide variety of cells.	bind
33676	1	8524	5	13	NULL	NULL	NULL	nuclear protein	GP		bind					TH	GP			CRE	NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_70_2_219_s_176	10407170	6 in PC12 cells results in a decrease in the nuclear protein binding to the TH CRE.	bind
35300	1	8524	7	10	NULL	0	NULL	nuclear protein			bind					TH				CRE	NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_70_2_219_s_176	10407170	6 in PC12 cells results in a decrease in the nuclear protein binding to the TH CRE.	bind
33677	1	8525	5	13	NULL	NULL	NULL	protein C	GP		bind					phospholipid vesicles	CellComponent				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_275_8_10681521_s_8	10681521	6 mM MgCl(2),  sEPCR inhibited the binding of protein C and APC to phospholipid vesicles  (K(i) = 40 +/- 7 and 33 +/- 4 nM, respectively).	bind
33678	2	8525	5	13	NULL	NULL	NULL	APC	GP		bind					phospholipid vesicles	CellComponent				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_275_8_10681521_s_8	10681521	6 mM MgCl(2),  sEPCR inhibited the binding of protein C and APC to phospholipid vesicles  (K(i) = 40 +/- 7 and 33 +/- 4 nM, respectively).	bind
33679	3	8525	5	13	NULL	NULL	NULL	sEPCR	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_275_8_10681521_s_8	10681521	6 mM MgCl(2),  sEPCR inhibited the binding of protein C and APC to phospholipid vesicles  (K(i) = 40 +/- 7 and 33 +/- 4 nM, respectively).	bind
33680	4	8525	5	13	NULL	NULL	NULL	sEPCR	GP		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_275_8_10681521_s_8	10681521	6 mM MgCl(2),  sEPCR inhibited the binding of protein C and APC to phospholipid vesicles  (K(i) = 40 +/- 7 and 33 +/- 4 nM, respectively).	bind
35302	1	8525	7	NULL	NULL	0	NULL	protein C	NULL		bind	NULL				 phospholipid vesicles	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_275_8_10681521_s_8	10681521	6 mM MgCl(2),  sEPCR inhibited the binding of protein C and APC to phospholipid vesicles  (K(i) = 40 +/- 7 and 33 +/- 4 nM, respectively).	bind
35303	2	8525	7	NULL	NULL	0	NULL	APC	NULL		bind	NULL				phospholipid vesicles	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_275_8_10681521_s_8	10681521	6 mM MgCl(2),  sEPCR inhibited the binding of protein C and APC to phospholipid vesicles  (K(i) = 40 +/- 7 and 33 +/- 4 nM, respectively).	bind
35304	3	8525	7	NULL	NULL	0	NULL	sEPCR	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_275_8_10681521_s_8	10681521	6 mM MgCl(2),  sEPCR inhibited the binding of protein C and APC to phospholipid vesicles  (K(i) = 40 +/- 7 and 33 +/- 4 nM, respectively).	bind
35305	4	8525	7	NULL	NULL	0	NULL	sEPCR	NULL		inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_275_8_10681521_s_8	10681521	6 mM MgCl(2),  sEPCR inhibited the binding of protein C and APC to phospholipid vesicles  (K(i) = 40 +/- 7 and 33 +/- 4 nM, respectively).	bind
33707	1	8526	5	13	NULL	NULL	NULL	Grb-IRbeta/Grb10	GP		interacts with					insulin-like growth factor-1 receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_5_2659_s_314	9006901	6 O'NeillP  et al. ( 47) demonstrated interactions of Grb-IRbeta/Grb10 with insulin-like growth factor-1 receptors, whereas we showed binding to activated PDGF and EGF receptors.	bind
33708	2	8526	5	13	NULL	NULL	NULL	Grb-IRbeta/Grb10	GP		bind					PDGF receptor	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_5_2659_s_314	9006901	6 O'NeillP  et al. ( 47) demonstrated interactions of Grb-IRbeta/Grb10 with insulin-like growth factor-1 receptors, whereas we showed binding to activated PDGF and EGF receptors.	bind
33709	3	8526	5	13	NULL	NULL	NULL	Grb-IRbeta/Grb10	GP		bind					EGF receptor	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_5_2659_s_314	9006901	6 O'NeillP  et al. ( 47) demonstrated interactions of Grb-IRbeta/Grb10 with insulin-like growth factor-1 receptors, whereas we showed binding to activated PDGF and EGF receptors.	bind
35306	1	8526	7	NULL	NULL	0	NULL	Grb-IRbeta/Grb10	NULL		interacts with	NULL				insulin-like growth factor-1 receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_5_2659_s_314	9006901	6 O'NeillP  et al. ( 47) demonstrated interactions of Grb-IRbeta/Grb10 with insulin-like growth factor-1 receptors, whereas we showed binding to activated PDGF and EGF receptors.	bind
35307	2	8526	7	NULL	NULL	0	NULL	Grb-IRbeta/Grb10	NULL		bind	NULL				PDGF	NULL	activated			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_5_2659_s_314	9006901	6 O'NeillP  et al. ( 47) demonstrated interactions of Grb-IRbeta/Grb10 with insulin-like growth factor-1 receptors, whereas we showed binding to activated PDGF and EGF receptors.	bind
35308	3	8526	7	NULL	NULL	0	NULL	Grb-IRbeta/Grb10	NULL		bind	NULL				EGF receptors	NULL	activated			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_5_2659_s_314	9006901	6 O'NeillP  et al. ( 47) demonstrated interactions of Grb-IRbeta/Grb10 with insulin-like growth factor-1 receptors, whereas we showed binding to activated PDGF and EGF receptors.	bind
33710	1	8528	5	13	NULL	NULL	NULL				bind			StAR domain		cholesterol	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_7_682_s_25	16141411	6 The StAR domain binds cholesterol and stimulates its movement from donor vesicles to the acceptor membrane.	bind
33711	2	8528	5	13	NULL	NULL	NULL	cholesterol	Chemical		moves from					donor vesicles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_7_682_s_25	16141411	6 The StAR domain binds cholesterol and stimulates its movement from donor vesicles to the acceptor membrane.	bind
33712	5	8528	5	13	NULL	NULL	NULL	statement 1	Process		stimulates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_7_682_s_25	16141411	6 The StAR domain binds cholesterol and stimulates its movement from donor vesicles to the acceptor membrane.	bind
33799	3	8528	5	13	NULL	NULL	NULL	cholesterol	Chemical		moves to					acceptor membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_7_682_s_25	16141411	6 The StAR domain binds cholesterol and stimulates its movement from donor vesicles to the acceptor membrane.	bind
33800	4	8528	5	13	NULL	NULL	NULL	statement 2	Process		occurs after					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_7_682_s_25	16141411	6 The StAR domain binds cholesterol and stimulates its movement from donor vesicles to the acceptor membrane.	bind
33801	6	8528	5	13	NULL	NULL	NULL	statement 1	Process		stimulates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_7_682_s_25	16141411	6 The StAR domain binds cholesterol and stimulates its movement from donor vesicles to the acceptor membrane.	bind
35309	1	8528	7	NULL	NULL	0	NULL		NULL		binds	NULL		StAR domain		cholesterol	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_7_682_s_25	16141411	6 The StAR domain binds cholesterol and stimulates its movement from donor vesicles to the acceptor membrane.	bind
35310	2	8528	7	NULL	NULL	0	NULL	cholesterol	NULL		move from	NULL				donor vesicles	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_7_682_s_25	16141411	6 The StAR domain binds cholesterol and stimulates its movement from donor vesicles to the acceptor membrane.	bind
35311	3	8528	7	NULL	NULL	0	NULL	cholesterol	NULL		move to	NULL				acceptor membrane	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_7_682_s_25	16141411	6 The StAR domain binds cholesterol and stimulates its movement from donor vesicles to the acceptor membrane.	bind
35312	4	8528	7	NULL	NULL	0	NULL	statement 2	NULL		occurs after	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_7_682_s_25	16141411	6 The StAR domain binds cholesterol and stimulates its movement from donor vesicles to the acceptor membrane.	bind
35313	5	8528	7	NULL	NULL	0	NULL	statement 1	NULL		stimulates	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_7_682_s_25	16141411	6 The StAR domain binds cholesterol and stimulates its movement from donor vesicles to the acceptor membrane.	bind
33713	1	8529	5	13	NULL	NULL	NULL	ATP	Chemical		bind					F1	GP		epsilon subunit		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_48_40130_s_193	16203732	6 Therefore, we assume that ATP binding to the epsilon subunit may stabilize the folded-hairpin form of the epsilon subunit in F1 to shift the equilibrium from the extended form.	bind
33714	2	8529	5	13	NULL	NULL	NULL	statement 1	Process		stabilize		may			F1	GP	folded hairpin form of	epsilon subunit		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_48_40130_s_193	16203732	6 Therefore, we assume that ATP binding to the epsilon subunit may stabilize the folded-hairpin form of the epsilon subunit in F1 to shift the equilibrium from the extended form.	bind
35314	1	8529	7	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				F1	NULL		epsilon subunit 		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_48_40130_s_193	16203732	6 Therefore, we assume that ATP binding to the epsilon subunit may stabilize the folded-hairpin form of the epsilon subunit in F1 to shift the equilibrium from the extended form.	bind
35315	2	8529	7	10	NULL	0	NULL	statement 1	NULL		stabilize	NULL	may			F1	NULL	folded-hairpin form of	epsilon subunit 		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_48_40130_s_193	16203732	6 Therefore, we assume that ATP binding to the epsilon subunit may stabilize the folded-hairpin form of the epsilon subunit in F1 to shift the equilibrium from the extended form.	bind
33716	1	8530	5	13	NULL	NULL	NULL	SATB1	GP		is required for					mature CD8-positive T lymphocytes	Cell	production of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_29_18440_s_338	9218488	6 These results suggest that SATB1 is required for production of mature CD8-positive T lymphocytes and are consistent with our suggestion that binding of SATB1 to the L2a element plays a role in regulating expression of the  CD8a gene.	bind
33717	2	8530	5	13	NULL	NULL	NULL	SATB1	GP		bind									L2a element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_29_18440_s_338	9218488	6 These results suggest that SATB1 is required for production of mature CD8-positive T lymphocytes and are consistent with our suggestion that binding of SATB1 to the L2a element plays a role in regulating expression of the  CD8a gene.	bind
33718	3	8530	5	13	NULL	NULL	NULL	statement 2	Process		regulates					CD8a gene	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_29_18440_s_338	9218488	6 These results suggest that SATB1 is required for production of mature CD8-positive T lymphocytes and are consistent with our suggestion that binding of SATB1 to the L2a element plays a role in regulating expression of the  CD8a gene.	bind
35317	1	8530	7	NULL	NULL	0	NULL	SATB1	NULL		is required for	NULL				mature CD8-positive T lymphocytes 	NULL	production of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_29_18440_s_338	9218488	6 These results suggest that SATB1 is required for production of mature CD8-positive T lymphocytes and are consistent with our suggestion that binding of SATB1 to the L2a element plays a role in regulating expression of the  CD8a gene.	bind
35318	2	8530	7	NULL	NULL	0	NULL	SATB1	NULL		bind	NULL					NULL			L2a element	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_29_18440_s_338	9218488	6 These results suggest that SATB1 is required for production of mature CD8-positive T lymphocytes and are consistent with our suggestion that binding of SATB1 to the L2a element plays a role in regulating expression of the  CD8a gene.	bind
35319	3	8530	7	NULL	NULL	0	NULL	statement 2	NULL		regulates	NULL				CD8a gene	NULL	expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_29_18440_s_338	9218488	6 These results suggest that SATB1 is required for production of mature CD8-positive T lymphocytes and are consistent with our suggestion that binding of SATB1 to the L2a element plays a role in regulating expression of the  CD8a gene.	bind
33719	1	8531	5	13	NULL	NULL	NULL	Sp1	GP		induces					SMC genes	GP	repression of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_135	15486317	6 These results suggest that Sp1-induced repression of SMC genes may involve more complex mechanisms than simple binding of Sp1 to the G/C repressor and subsequent inhibition of cooperative interactions between CArG elements (see Discussion for a detailed consideration of this issue).	bind
33720	2	8531	5	13	NULL	NULL	NULL	Sp1	GP		bind					G/C repressor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_135	15486317	6 These results suggest that Sp1-induced repression of SMC genes may involve more complex mechanisms than simple binding of Sp1 to the G/C repressor and subsequent inhibition of cooperative interactions between CArG elements (see Discussion for a detailed consideration of this issue).	bind
33721	3	8531	5	10	NULL	0	NULL				interacts with		cooperatively		CArG element					CArG element	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_135	15486317	6 These results suggest that Sp1-induced repression of SMC genes may involve more complex mechanisms than simple binding of Sp1 to the G/C repressor and subsequent inhibition of cooperative interactions between CArG elements (see Discussion for a detailed consideration of this issue).	bind
55801	4	8531	5	13	NULL	NULL	NULL	statement 1	Process		involve					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_135	15486317	6 These results suggest that Sp1-induced repression of SMC genes may involve more complex mechanisms than simple binding of Sp1 to the G/C repressor and subsequent inhibition of cooperative interactions between CArG elements (see Discussion for a detailed consideration of this issue).	bind
55802	5	8531	5	13	NULL	NULL	NULL	statement 1	Process		involve					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_135	15486317	6 These results suggest that Sp1-induced repression of SMC genes may involve more complex mechanisms than simple binding of Sp1 to the G/C repressor and subsequent inhibition of cooperative interactions between CArG elements (see Discussion for a detailed consideration of this issue).	bind
35320	1	8531	7	NULL	NULL	0	NULL	Sp1	NULL		induce	NULL				SMC genes	NULL	repression of			NULL		0	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_135	15486317	6 These results suggest that Sp1-induced repression of SMC genes may involve more complex mechanisms than simple binding of Sp1 to the G/C repressor and subsequent inhibition of cooperative interactions between CArG elements (see Discussion for a detailed consideration of this issue).	bind
35321	2	8531	7	10	NULL	0	NULL	Sp1	NULL		bind	NULL				G/C repressor	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_135	15486317	6 These results suggest that Sp1-induced repression of SMC genes may involve more complex mechanisms than simple binding of Sp1 to the G/C repressor and subsequent inhibition of cooperative interactions between CArG elements (see Discussion for a detailed consideration of this issue).	bind
35322	3	8531	7	NULL	NULL	0	NULL		NULL		interacts	NULL	cooperatively		CArG elements		NULL			CArG elements	NULL		0	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_135	15486317	6 These results suggest that Sp1-induced repression of SMC genes may involve more complex mechanisms than simple binding of Sp1 to the G/C repressor and subsequent inhibition of cooperative interactions between CArG elements (see Discussion for a detailed consideration of this issue).	bind
35323	4	8531	7	NULL	NULL	0	NULL	statement 1	NULL		involve	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_135	15486317	6 These results suggest that Sp1-induced repression of SMC genes may involve more complex mechanisms than simple binding of Sp1 to the G/C repressor and subsequent inhibition of cooperative interactions between CArG elements (see Discussion for a detailed consideration of this issue).	bind
35324	5	8531	7	NULL	NULL	0	NULL	statement 1	NULL		involve	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_10_981_s_135	15486317	6 These results suggest that Sp1-induced repression of SMC genes may involve more complex mechanisms than simple binding of Sp1 to the G/C repressor and subsequent inhibition of cooperative interactions between CArG elements (see Discussion for a detailed consideration of this issue).	bind
33722	1	8532	5	13	NULL	NULL	NULL	rA1	GP		bind					prothrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31954_s_229	10924522	6) Based on a molecular model of the Al domain, conformationally constrained peptides were synthesized, which act synergistically to inhibit rA1 binding to prothrombin (Fig.  4,  A and  B) or PF2 binding to FXI (Fig.  6 ( A and  B), Table  I).	bind
33723	2	8532	5	13	NULL	NULL	NULL	PF2	GP		bind					FXI	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31954_s_229	10924522	6) Based on a molecular model of the Al domain, conformationally constrained peptides were synthesized, which act synergistically to inhibit rA1 binding to prothrombin (Fig.  4,  A and  B) or PF2 binding to FXI (Fig.  6 ( A and  B), Table  I).	bind
33725	4	8532	5	13	NULL	NULL	NULL	peptides	GP	conformationally;; constrained	inhibits		synergistically			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31954_s_229	10924522	6) Based on a molecular model of the Al domain, conformationally constrained peptides were synthesized, which act synergistically to inhibit rA1 binding to prothrombin (Fig.  4,  A and  B) or PF2 binding to FXI (Fig.  6 ( A and  B), Table  I).	bind
55803	3	8532	5	13	NULL	NULL	NULL	peptides	GP	conformationally constrained	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31954_s_229	10924522	6) Based on a molecular model of the Al domain, conformationally constrained peptides were synthesized, which act synergistically to inhibit rA1 binding to prothrombin (Fig.  4,  A and  B) or PF2 binding to FXI (Fig.  6 ( A and  B), Table  I).	bind
35325	1	8532	7	NULL	NULL	0	NULL	 rA1	NULL		bind	NULL				prothrombin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_41_31954_s_229	10924522	6) Based on a molecular model of the Al domain, conformationally constrained peptides were synthesized, which act synergistically to inhibit rA1 binding to prothrombin (Fig.  4,  A and  B) or PF2 binding to FXI (Fig.  6 ( A and  B), Table  I).	bind
35326	2	8532	7	NULL	NULL	0	NULL	PF2	NULL		bind	NULL				FXI	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_41_31954_s_229	10924522	6) Based on a molecular model of the Al domain, conformationally constrained peptides were synthesized, which act synergistically to inhibit rA1 binding to prothrombin (Fig.  4,  A and  B) or PF2 binding to FXI (Fig.  6 ( A and  B), Table  I).	bind
35327	3	8532	7	10	NULL	0	NULL	peptides		conformationally;; constrained	inhibit					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31954_s_229	10924522	6) Based on a molecular model of the Al domain, conformationally constrained peptides were synthesized, which act synergistically to inhibit rA1 binding to prothrombin (Fig.  4,  A and  B) or PF2 binding to FXI (Fig.  6 ( A and  B), Table  I).	bind
35328	4	8532	7	10	NULL	0	NULL	peptides		conformationally;; constrained	inhibit					statement 2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31954_s_229	10924522	6) Based on a molecular model of the Al domain, conformationally constrained peptides were synthesized, which act synergistically to inhibit rA1 binding to prothrombin (Fig.  4,  A and  B) or PF2 binding to FXI (Fig.  6 ( A and  B), Table  I).	bind
34274	1	8533	5	13	NULL	NULL	NULL	p47 phox	GP		bind								target domains in cytosolic loop		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
34275	2	8533	5	13	NULL	NULL	NULL	p67 phox	GP		bind								target domains in cytosolic loop		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
34276	3	8533	5	13	NULL	NULL	NULL	p47 phox	GP		bind								root of the cytosolic tail		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
34277	4	8533	5	13	NULL	NULL	NULL	p67 phox	GP		bind								root of the cytosolic tail		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
34278	5	8533	5	13	NULL	NULL	NULL	statement 1	Process		is not mediated by								SH3 domains;;proline-rich regions		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
34287	6	8533	5	13	NULL	NULL	NULL	statement 2	Process		is not mediated by								SH3 domains;;proline-rich regions		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
34288	7	8533	5	13	NULL	NULL	NULL	statement 3	Process		is not mediated by								SH3 domains;;proline-rich regions		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
34289	8	8533	5	13	NULL	NULL	NULL	statement 4	Process		is not mediated by								SH3 domains;;proline-rich regions		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
35329	1	8533	7	NULL	NULL	0	NULL	p47	NULL		bind	NULL					NULL		domains in the cytosolic loop		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
35330	2	8533	7	NULL	NULL	0	NULL	p67 phox 	NULL		bind	NULL					NULL		domains in the cytosolic loop		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
35331	3	8533	7	NULL	NULL	0	NULL	p47 phox	NULL		bind	NULL					NULL		cytosolic tail		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
35332	4	8533	7	NULL	NULL	0	NULL	p67 phox	NULL		bind	NULL					NULL		cytosolic tail		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
35333	5	8533	7	NULL	NULL	0	NULL		NULL		does not mediate	NULL		SH3 domain		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
35334	6	8533	7	NULL	NULL	0	NULL		NULL		does not mediate	NULL		SH3 domain		statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
35335	7	8533	7	NULL	NULL	0	NULL		NULL		does not mediate	NULL		SH3 domain		statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
35336	8	8533	7	NULL	NULL	0	NULL		NULL		does not mediate	NULL		SH3 domain		statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
35337	9	8533	7	NULL	NULL	0	NULL		NULL		does not mediate	NULL		proline-rich region		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
35338	10	8533	7	NULL	NULL	0	NULL		NULL		does not mediate	NULL		proline-rich region		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
35339	11	8533	7	NULL	NULL	0	NULL		NULL		does not mediate	NULL		proline-rich region		statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
35340	12	8533	7	NULL	NULL	0	NULL		NULL		does not mediate	NULL		proline-rich region		statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_316	11733522	6) Binding of p47 phox and p67 phox to their target domains in the cytosolic loop and at the root of the cytosolic tail is mediated by interactions other than those involving SH3 domains and proline-rich regions, the nature of which remains to be established.	bind
33726	1	8534	5	13	NULL	NULL	NULL	GM1	Chemical		bind					Trk protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_26001_s_192	9748278	6) D-PDMP treatment causes down-regulation of endogenous gangliosides as well as binding of GM1 to the Trk protein.	bind
33727	2	8534	5	13	NULL	NULL	NULL	D-PDMP	Chemical		down regulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_26001_s_192	9748278	6) D-PDMP treatment causes down-regulation of endogenous gangliosides as well as binding of GM1 to the Trk protein.	bind
33728	3	8534	5	13	NULL	NULL	NULL	D-PDMP	Chemical		down regulates					gangliosides	Chemical	endogenous			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_26001_s_192	9748278	6) D-PDMP treatment causes down-regulation of endogenous gangliosides as well as binding of GM1 to the Trk protein.	bind
35341	1	8534	7	NULL	NULL	0	NULL	GM1	NULL		bind	NULL				Trk protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_40_26001_s_192	9748278	6) D-PDMP treatment causes down-regulation of endogenous gangliosides as well as binding of GM1 to the Trk protein.	bind
35342	2	8534	7	10	NULL	0	NULL	 D-PDMP			downregulates					gangliosides		endogenous			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_26001_s_192	9748278	6) D-PDMP treatment causes down-regulation of endogenous gangliosides as well as binding of GM1 to the Trk protein.	bind
35343	3	8534	7	10	NULL	0	NULL	D-PDMP			downregulates					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_26001_s_192	9748278	6) D-PDMP treatment causes down-regulation of endogenous gangliosides as well as binding of GM1 to the Trk protein.	bind
33729	1	8536	5	13	NULL	NULL	NULL	gammadelta T cells	Cell	proliferation of 	is induced by					CMV extracts	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_103_10_1437_s_217	10330426	6), CD1c (L161), and CD1d (51.1) did not block the proliferation of gammadelta T cells induced by CMV extracts (data not shown).	bind
33730	2	8536	5	13	NULL	NULL	NULL	CD1c	GP		does not block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_103_10_1437_s_217	10330426	6), CD1c (L161), and CD1d (51.1) did not block the proliferation of gammadelta T cells induced by CMV extracts (data not shown).	bind
33731	3	8536	5	13	NULL	NULL	NULL	CD1d	GP		does not block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_103_10_1437_s_217	10330426	6), CD1c (L161), and CD1d (51.1) did not block the proliferation of gammadelta T cells induced by CMV extracts (data not shown).	bind
35404	1	8536	7	NULL	NULL	0	NULL	CMV extracts	NULL		induce	NULL				gammadelta T cells	NULL	proliferation of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_103_10_1437_s_217	10330426	6), CD1c (L161), and CD1d (51.1) did not block the proliferation of gammadelta T cells induced by CMV extracts (data not shown).	bind
35405	2	8536	7	10	NULL	0	NULL	CD1c			does not block					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_103_10_1437_s_217	10330426	6), CD1c (L161), and CD1d (51.1) did not block the proliferation of gammadelta T cells induced by CMV extracts (data not shown).	bind
35406	3	8536	7	NULL	NULL	0	NULL	CD1d	NULL		does not block	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_103_10_1437_s_217	10330426	6), CD1c (L161), and CD1d (51.1) did not block the proliferation of gammadelta T cells induced by CMV extracts (data not shown).	bind
33733	1	8537	5	13	NULL	NULL	NULL	trkA	GP		bind					NGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1661_s_17	10550322	6, 7  The tyrosine kinase receptors selectively bind to their cognate ligands: trkA for nerve growth factor (NGF) and NT-3; trkB for BDNF, NT-4/5, and NT-3; and trkC for NT-3.	bind
33734	2	8537	5	13	NULL	NULL	NULL	NGF	GP		is					nerve growth factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1661_s_17	10550322	6, 7  The tyrosine kinase receptors selectively bind to their cognate ligands: trkA for nerve growth factor (NGF) and NT-3; trkB for BDNF, NT-4/5, and NT-3; and trkC for NT-3.	bind
33735	3	8537	5	13	NULL	NULL	NULL	trkA	GP		bind					NT-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1661_s_17	10550322	6, 7  The tyrosine kinase receptors selectively bind to their cognate ligands: trkA for nerve growth factor (NGF) and NT-3; trkB for BDNF, NT-4/5, and NT-3; and trkC for NT-3.	bind
33736	4	8537	5	13	NULL	NULL	NULL	trkB	GP		bind					BDNF	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1661_s_17	10550322	6, 7  The tyrosine kinase receptors selectively bind to their cognate ligands: trkA for nerve growth factor (NGF) and NT-3; trkB for BDNF, NT-4/5, and NT-3; and trkC for NT-3.	bind
33737	5	8537	5	13	NULL	NULL	NULL	trkB	GP		bind					NT-4/5	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1661_s_17	10550322	6, 7  The tyrosine kinase receptors selectively bind to their cognate ligands: trkA for nerve growth factor (NGF) and NT-3; trkB for BDNF, NT-4/5, and NT-3; and trkC for NT-3.	bind
33738	6	8537	5	13	NULL	NULL	NULL	trkB	GP		bind					NT-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1661_s_17	10550322	6, 7  The tyrosine kinase receptors selectively bind to their cognate ligands: trkA for nerve growth factor (NGF) and NT-3; trkB for BDNF, NT-4/5, and NT-3; and trkC for NT-3.	bind
33739	7	8537	5	13	NULL	NULL	NULL	trkC	GP		bind					NT-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1661_s_17	10550322	6, 7  The tyrosine kinase receptors selectively bind to their cognate ligands: trkA for nerve growth factor (NGF) and NT-3; trkB for BDNF, NT-4/5, and NT-3; and trkC for NT-3.	bind
35407	1	8537	7	NULL	NULL	0	NULL	 trkA	NULL		bind	NULL				NGF	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_5_1661_s_17	10550322	6, 7  The tyrosine kinase receptors selectively bind to their cognate ligands: trkA for nerve growth factor (NGF) and NT-3; trkB for BDNF, NT-4/5, and NT-3; and trkC for NT-3.	bind
35408	2	8537	7	NULL	NULL	0	NULL	trkA	NULL		bind	NULL				NT-3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_5_1661_s_17	10550322	6, 7  The tyrosine kinase receptors selectively bind to their cognate ligands: trkA for nerve growth factor (NGF) and NT-3; trkB for BDNF, NT-4/5, and NT-3; and trkC for NT-3.	bind
35409	3	8537	7	NULL	NULL	0	NULL	trkB	NULL		bind	NULL				BDNF	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_5_1661_s_17	10550322	6, 7  The tyrosine kinase receptors selectively bind to their cognate ligands: trkA for nerve growth factor (NGF) and NT-3; trkB for BDNF, NT-4/5, and NT-3; and trkC for NT-3.	bind
35410	4	8537	7	NULL	NULL	0	NULL	trkB	NULL		bind	NULL				NT-4/5	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_5_1661_s_17	10550322	6, 7  The tyrosine kinase receptors selectively bind to their cognate ligands: trkA for nerve growth factor (NGF) and NT-3; trkB for BDNF, NT-4/5, and NT-3; and trkC for NT-3.	bind
35411	5	8537	7	NULL	NULL	0	NULL	trkB	NULL		bind	NULL				NT-3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_5_1661_s_17	10550322	6, 7  The tyrosine kinase receptors selectively bind to their cognate ligands: trkA for nerve growth factor (NGF) and NT-3; trkB for BDNF, NT-4/5, and NT-3; and trkC for NT-3.	bind
35412	6	8537	7	NULL	NULL	0	NULL	trkC	NULL		bind	NULL				NT-3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_5_1661_s_17	10550322	6, 7  The tyrosine kinase receptors selectively bind to their cognate ligands: trkA for nerve growth factor (NGF) and NT-3; trkB for BDNF, NT-4/5, and NT-3; and trkC for NT-3.	bind
35413	7	8537	7	NULL	NULL	0	NULL	NGF	NULL		is	NULL				nerve growth factor 	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_5_1661_s_17	10550322	6, 7  The tyrosine kinase receptors selectively bind to their cognate ligands: trkA for nerve growth factor (NGF) and NT-3; trkB for BDNF, NT-4/5, and NT-3; and trkC for NT-3.	bind
33740	1	8538	5	13	NULL	NULL	NULL	VEGF	GP		bind					type III tyrosine kinase receptors	GP				NULL	on vascular endothelial cells	NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_159_s_12	10623663	6, 7  VEGF binds to two type III tyrosine kinase receptors on vascular endothelial cells, Flt-1 and KDR/Flk-1.	bind
33741	2	8538	5	13	NULL	NULL	NULL	VEGF	GP		bind					Flt-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_159_s_12	10623663	6, 7  VEGF binds to two type III tyrosine kinase receptors on vascular endothelial cells, Flt-1 and KDR/Flk-1.	bind
33742	3	8538	5	13	NULL	NULL	NULL	VEGF	GP		bind					KDR/Flk-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_1_159_s_12	10623663	6, 7  VEGF binds to two type III tyrosine kinase receptors on vascular endothelial cells, Flt-1 and KDR/Flk-1.	bind
35414	1	8538	7	NULL	NULL	0	NULL	VEGF	NULL		binds	NULL				type III tyrosine kinase receptors 	NULL				NULL	 vascular endothelial cells	0	NULL	NULL	NULL	gw60_amjpathol_156_1_159_s_12	10623663	6, 7  VEGF binds to two type III tyrosine kinase receptors on vascular endothelial cells, Flt-1 and KDR/Flk-1.	bind
35415	2	8538	7	NULL	NULL	0	NULL	VEGF	NULL		binds	NULL				Flt-1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_1_159_s_12	10623663	6, 7  VEGF binds to two type III tyrosine kinase receptors on vascular endothelial cells, Flt-1 and KDR/Flk-1.	bind
35416	3	8538	7	NULL	NULL	0	NULL	VEGF	NULL		binds	NULL				KDR/Flk-1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_1_159_s_12	10623663	6, 7  VEGF binds to two type III tyrosine kinase receptors on vascular endothelial cells, Flt-1 and KDR/Flk-1.	bind
33743	1	8539	5	13	NULL	NULL	NULL	LDL	GP		bind					versican	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_387_s_16	11884279	6, 7 The binding between LDL and versican or biglycan seems to be enhanced in the presence of lipoprotein lipase 8 or phospholipase A2.	bind
33744	2	8539	5	13	NULL	NULL	NULL	LDL	GP		bind					biglycan	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_387_s_16	11884279	6, 7 The binding between LDL and versican or biglycan seems to be enhanced in the presence of lipoprotein lipase 8 or phospholipase A2.	bind
33745	3	8539	5	13	NULL	NULL	NULL	statement 1	Process		is alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_387_s_16	11884279	6, 7 The binding between LDL and versican or biglycan seems to be enhanced in the presence of lipoprotein lipase 8 or phospholipase A2.	bind
33746	4	8539	5	13	NULL	NULL	NULL	lipoprotein lipase 8	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_387_s_16	11884279	6, 7 The binding between LDL and versican or biglycan seems to be enhanced in the presence of lipoprotein lipase 8 or phospholipase A2.	bind
33747	5	8539	5	13	NULL	NULL	NULL	lipoprotein lipase 8	GP		enhances					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_387_s_16	11884279	6, 7 The binding between LDL and versican or biglycan seems to be enhanced in the presence of lipoprotein lipase 8 or phospholipase A2.	bind
33748	6	8539	5	13	NULL	NULL	NULL	phospholipase A2	GP		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_387_s_16	11884279	6, 7 The binding between LDL and versican or biglycan seems to be enhanced in the presence of lipoprotein lipase 8 or phospholipase A2.	bind
33749	7	8539	5	13	NULL	NULL	NULL	phospholipase A2	GP		enhances					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_387_s_16	11884279	6, 7 The binding between LDL and versican or biglycan seems to be enhanced in the presence of lipoprotein lipase 8 or phospholipase A2.	bind
35417	1	8539	7	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				versican	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_387_s_16	11884279	6, 7 The binding between LDL and versican or biglycan seems to be enhanced in the presence of lipoprotein lipase 8 or phospholipase A2.	bind
35418	2	8539	7	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				biglycan	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_387_s_16	11884279	6, 7 The binding between LDL and versican or biglycan seems to be enhanced in the presence of lipoprotein lipase 8 or phospholipase A2.	bind
35419	3	8539	7	NULL	NULL	0	NULL	lipoprotein lipase 8	NULL		enhance	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_387_s_16	11884279	6, 7 The binding between LDL and versican or biglycan seems to be enhanced in the presence of lipoprotein lipase 8 or phospholipase A2.	bind
35420	4	8539	7	NULL	NULL	0	NULL	lipoprotein lipase 8	NULL		enhance	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_387_s_16	11884279	6, 7 The binding between LDL and versican or biglycan seems to be enhanced in the presence of lipoprotein lipase 8 or phospholipase A2.	bind
35421	5	8539	7	NULL	NULL	0	NULL	phospholipase A2	NULL		enhance	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_387_s_16	11884279	6, 7 The binding between LDL and versican or biglycan seems to be enhanced in the presence of lipoprotein lipase 8 or phospholipase A2.	bind
35422	6	8539	7	NULL	NULL	0	NULL	phospholipase A2	NULL		enhance	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_3_387_s_16	11884279	6, 7 The binding between LDL and versican or biglycan seems to be enhanced in the presence of lipoprotein lipase 8 or phospholipase A2.	bind
33750	1	8540	5	13	NULL	NULL	NULL	PROb cells	Cell		bind					TGF-beta1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1867_s_262	10362813	6, 8, 25, 31 Based on radioimmunoassay data, PROb cells bind TGF-beta1.	bind
35423	1	8540	7	NULL	NULL	0	NULL	PROb cells	NULL		bind	NULL				TGF-beta1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_6_1867_s_262	10362813	6, 8, 25, 31 Based on radioimmunoassay data, PROb cells bind TGF-beta1.	bind
33917	1	8541	5	13	NULL	NULL	NULL	PDGF-BB	GP		induces					SMCs	Cell	phenotypic switching of vascular			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_132	15718508	6,11  B, PDGF-BB - induced phenotypic switching of vascular SMCs has been shown to be mediated  by multiple mechanisms, including activation of Elk-1, 45 KLF4-dependent downregulation of myocardin expression (Y. Liu and G.K. Owens, unpublished  data, 2004), and possible disruption of SRF binding to degenerate CArG elements.	bind
33926	2	8541	5	13	NULL	NULL	NULL	Elk-1	GP	activation of	mediates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_132	15718508	6,11  B, PDGF-BB - induced phenotypic switching of vascular SMCs has been shown to be mediated  by multiple mechanisms, including activation of Elk-1, 45 KLF4-dependent downregulation of myocardin expression (Y. Liu and G.K. Owens, unpublished  data, 2004), and possible disruption of SRF binding to degenerate CArG elements.	bind
33928	3	8541	5	13	NULL	NULL	NULL	myocardin	GP	downregulation of expression of	is dependent on					KLF4	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_132	15718508	6,11  B, PDGF-BB - induced phenotypic switching of vascular SMCs has been shown to be mediated  by multiple mechanisms, including activation of Elk-1, 45 KLF4-dependent downregulation of myocardin expression (Y. Liu and G.K. Owens, unpublished  data, 2004), and possible disruption of SRF binding to degenerate CArG elements.	bind
33929	4	8541	5	13	NULL	NULL	NULL	statement 3	Process		mediates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_132	15718508	6,11  B, PDGF-BB - induced phenotypic switching of vascular SMCs has been shown to be mediated  by multiple mechanisms, including activation of Elk-1, 45 KLF4-dependent downregulation of myocardin expression (Y. Liu and G.K. Owens, unpublished  data, 2004), and possible disruption of SRF binding to degenerate CArG elements.	bind
33931	5	8541	5	13	NULL	NULL	NULL	SRF	GP		bind							degenerate		CArG elements	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_132	15718508	6,11  B, PDGF-BB - induced phenotypic switching of vascular SMCs has been shown to be mediated  by multiple mechanisms, including activation of Elk-1, 45 KLF4-dependent downregulation of myocardin expression (Y. Liu and G.K. Owens, unpublished  data, 2004), and possible disruption of SRF binding to degenerate CArG elements.	bind
33933	6	8541	5	13	NULL	NULL	NULL	statement 5	Process	disruption of	mediates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_132	15718508	6,11  B, PDGF-BB - induced phenotypic switching of vascular SMCs has been shown to be mediated  by multiple mechanisms, including activation of Elk-1, 45 KLF4-dependent downregulation of myocardin expression (Y. Liu and G.K. Owens, unpublished  data, 2004), and possible disruption of SRF binding to degenerate CArG elements.	bind
35424	1	8541	7	NULL	NULL	0	NULL	PDGF-BB	NULL		induce	NULL				vascular SMCs 	NULL	phenotypic switching of			NULL		0	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_132	15718508	6,11  B, PDGF-BB - induced phenotypic switching of vascular SMCs has been shown to be mediated  by multiple mechanisms, including activation of Elk-1, 45 KLF4-dependent downregulation of myocardin expression (Y. Liu and G.K. Owens, unpublished  data, 2004), and possible disruption of SRF binding to degenerate CArG elements.	bind
35425	2	8541	7	NULL	NULL	0	NULL	Elk-1	NULL	activation of	mediates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_132	15718508	6,11  B, PDGF-BB - induced phenotypic switching of vascular SMCs has been shown to be mediated  by multiple mechanisms, including activation of Elk-1, 45 KLF4-dependent downregulation of myocardin expression (Y. Liu and G.K. Owens, unpublished  data, 2004), and possible disruption of SRF binding to degenerate CArG elements.	bind
35426	3	8541	7	NULL	NULL	0	NULL	 KLF4	NULL		downregulates	NULL				myocardin	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_132	15718508	6,11  B, PDGF-BB - induced phenotypic switching of vascular SMCs has been shown to be mediated  by multiple mechanisms, including activation of Elk-1, 45 KLF4-dependent downregulation of myocardin expression (Y. Liu and G.K. Owens, unpublished  data, 2004), and possible disruption of SRF binding to degenerate CArG elements.	bind
35427	4	8541	7	NULL	NULL	0	NULL	statement 3	NULL		mediates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_132	15718508	6,11  B, PDGF-BB - induced phenotypic switching of vascular SMCs has been shown to be mediated  by multiple mechanisms, including activation of Elk-1, 45 KLF4-dependent downregulation of myocardin expression (Y. Liu and G.K. Owens, unpublished  data, 2004), and possible disruption of SRF binding to degenerate CArG elements.	bind
35428	5	8541	7	NULL	NULL	0	NULL	SRF	NULL	binding of	degenerate	NULL					NULL			CArG elements	NULL		0	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_132	15718508	6,11  B, PDGF-BB - induced phenotypic switching of vascular SMCs has been shown to be mediated  by multiple mechanisms, including activation of Elk-1, 45 KLF4-dependent downregulation of myocardin expression (Y. Liu and G.K. Owens, unpublished  data, 2004), and possible disruption of SRF binding to degenerate CArG elements.	bind
35429	6	8541	7	NULL	NULL	0	NULL	statement 5	NULL	disruption of	mediates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_132	15718508	6,11  B, PDGF-BB - induced phenotypic switching of vascular SMCs has been shown to be mediated  by multiple mechanisms, including activation of Elk-1, 45 KLF4-dependent downregulation of myocardin expression (Y. Liu and G.K. Owens, unpublished  data, 2004), and possible disruption of SRF binding to degenerate CArG elements.	bind
33935	1	8542	5	13	NULL	NULL	NULL	VEGF	GP	mutant	bind			C156S		VEGFR-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1098_s_26	12714562	6,13,16   In addition to the naturally occurring forms, Joukov et al 18 have generated a mutant factor (VEGF-C156S) that binds to VEGFR-3 but not to VEGFR-2.	bind
33936	2	8542	5	13	NULL	NULL	NULL	VEGF	GP	mutant	does not bind			C156S		VEGFR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_10_1098_s_26	12714562	6,13,16   In addition to the naturally occurring forms, Joukov et al 18 have generated a mutant factor (VEGF-C156S) that binds to VEGFR-3 but not to VEGFR-2.	bind
35430	1	8542	7	NULL	NULL	0	NULL	VEGF	NULL		bind	NULL		C156S		 VEGFR-3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_10_1098_s_26	12714562	6,13,16   In addition to the naturally occurring forms, Joukov et al 18 have generated a mutant factor (VEGF-C156S) that binds to VEGFR-3 but not to VEGFR-2.	bind
35431	2	8542	7	NULL	NULL	0	NULL	VEGF	NULL		does not bind	NULL		C156S		VEGFR-2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_10_1098_s_26	12714562	6,13,16   In addition to the naturally occurring forms, Joukov et al 18 have generated a mutant factor (VEGF-C156S) that binds to VEGFR-3 but not to VEGFR-2.	bind
33938	1	8543	5	13	NULL	NULL	NULL	MCP-1	GP		bind					CCR2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_9_1177_s_183	16574901	6,7  The signaling events initiated by MCP-1 binding to CCR2 probably leads to transcriptional activation of genes for which products could lead to pathophysiological changes.	bind
33939	2	8543	5	13	NULL	NULL	NULL	statement 1	Process		initiates					signaling events	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_9_1177_s_183	16574901	6,7  The signaling events initiated by MCP-1 binding to CCR2 probably leads to transcriptional activation of genes for which products could lead to pathophysiological changes.	bind
33940	3	8543	5	13	NULL	NULL	NULL	statement 2	Process		leads to		probably			genes	GP	transcriptional activation of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_9_1177_s_183	16574901	6,7  The signaling events initiated by MCP-1 binding to CCR2 probably leads to transcriptional activation of genes for which products could lead to pathophysiological changes.	bind
35432	1	8543	7	NULL	NULL	0	NULL	MCP-1	NULL		bind	NULL				CCR2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_9_1177_s_183	16574901	6,7  The signaling events initiated by MCP-1 binding to CCR2 probably leads to transcriptional activation of genes for which products could lead to pathophysiological changes.	bind
35433	2	8543	7	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				genes	NULL	transcriptional activation of			NULL		0	NULL	NULL	NULL	gw70_circulationres_98_9_1177_s_183	16574901	6,7  The signaling events initiated by MCP-1 binding to CCR2 probably leads to transcriptional activation of genes for which products could lead to pathophysiological changes.	bind
35434	3	8543	7	NULL	NULL	0	NULL	statement 1	NULL		initiates	NULL				signaling events	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_9_1177_s_183	16574901	6,7  The signaling events initiated by MCP-1 binding to CCR2 probably leads to transcriptional activation of genes for which products could lead to pathophysiological changes.	bind
33947	1	8545	5	13	NULL	NULL	NULL	growth factors	GP		activates					Akt	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_431_s_13	11485901	6- 9 Activation of Akt by growth factors depends on the integrity of the PH domain, which binds to the PI 3-kinase product, PI(3,4,5)P3, and phosphorylation of Thr-308 and Ser-473 by PDK1 and PDK2/ILK, respectively.	bind
33948	2	8545	5	13	NULL	NULL	NULL	statement 1	Process		depends on					Akt	GP	 integrity of	PH domain		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_431_s_13	11485901	6- 9 Activation of Akt by growth factors depends on the integrity of the PH domain, which binds to the PI 3-kinase product, PI(3,4,5)P3, and phosphorylation of Thr-308 and Ser-473 by PDK1 and PDK2/ILK, respectively.	bind
33949	3	8545	5	13	NULL	NULL	NULL	Akt	GP		bind			PH domain		PI(3,4,5)P3	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_431_s_13	11485901	6- 9 Activation of Akt by growth factors depends on the integrity of the PH domain, which binds to the PI 3-kinase product, PI(3,4,5)P3, and phosphorylation of Thr-308 and Ser-473 by PDK1 and PDK2/ILK, respectively.	bind
33950	4	8545	5	13	NULL	NULL	NULL	PI(3,4,5)P3	Chemical		is a product of					PI 3-kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_431_s_13	11485901	6- 9 Activation of Akt by growth factors depends on the integrity of the PH domain, which binds to the PI 3-kinase product, PI(3,4,5)P3, and phosphorylation of Thr-308 and Ser-473 by PDK1 and PDK2/ILK, respectively.	bind
33951	5	8545	5	13	NULL	NULL	NULL	Akt	GP		is phosphorylated by			Thr-308		PDK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_431_s_13	11485901	6- 9 Activation of Akt by growth factors depends on the integrity of the PH domain, which binds to the PI 3-kinase product, PI(3,4,5)P3, and phosphorylation of Thr-308 and Ser-473 by PDK1 and PDK2/ILK, respectively.	bind
33952	6	8545	5	13	NULL	NULL	NULL	Akt	GP		is phosphorylated by			Ser-473		PDK2/ILK	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_431_s_13	11485901	6- 9 Activation of Akt by growth factors depends on the integrity of the PH domain, which binds to the PI 3-kinase product, PI(3,4,5)P3, and phosphorylation of Thr-308 and Ser-473 by PDK1 and PDK2/ILK, respectively.	bind
33953	7	8545	5	13	NULL	NULL	NULL	statement 1	Process		depends on					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_431_s_13	11485901	6- 9 Activation of Akt by growth factors depends on the integrity of the PH domain, which binds to the PI 3-kinase product, PI(3,4,5)P3, and phosphorylation of Thr-308 and Ser-473 by PDK1 and PDK2/ILK, respectively.	bind
33954	8	8545	5	13	NULL	NULL	NULL	statement 1	Process		depends on					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_2_431_s_13	11485901	6- 9 Activation of Akt by growth factors depends on the integrity of the PH domain, which binds to the PI 3-kinase product, PI(3,4,5)P3, and phosphorylation of Thr-308 and Ser-473 by PDK1 and PDK2/ILK, respectively.	bind
35436	1	8545	7	NULL	NULL	0	NULL	 growth factors	NULL		activates	NULL				Akt	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_2_431_s_13	11485901	6- 9 Activation of Akt by growth factors depends on the integrity of the PH domain, which binds to the PI 3-kinase product, PI(3,4,5)P3, and phosphorylation of Thr-308 and Ser-473 by PDK1 and PDK2/ILK, respectively.	bind
35439	2	8545	7	NULL	NULL	0	NULL	statement 1	NULL		depends on	NULL					NULL	integrity of	PH domain		NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_2_431_s_13	11485901	6- 9 Activation of Akt by growth factors depends on the integrity of the PH domain, which binds to the PI 3-kinase product, PI(3,4,5)P3, and phosphorylation of Thr-308 and Ser-473 by PDK1 and PDK2/ILK, respectively.	bind
35443	3	8545	7	NULL	NULL	0	NULL		NULL		binds to	NULL		PH domain		 PI 3-kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_2_431_s_13	11485901	6- 9 Activation of Akt by growth factors depends on the integrity of the PH domain, which binds to the PI 3-kinase product, PI(3,4,5)P3, and phosphorylation of Thr-308 and Ser-473 by PDK1 and PDK2/ILK, respectively.	bind
35446	4	8545	7	NULL	NULL	0	NULL		NULL		binds to	NULL		PH domain		PI(3,4,5)P3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_2_431_s_13	11485901	6- 9 Activation of Akt by growth factors depends on the integrity of the PH domain, which binds to the PI 3-kinase product, PI(3,4,5)P3, and phosphorylation of Thr-308 and Ser-473 by PDK1 and PDK2/ILK, respectively.	bind
35450	5	8545	7	NULL	NULL	0	NULL	PDK1	NULL		phosphorylates	NULL					NULL		Thr-308		NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_2_431_s_13	11485901	6- 9 Activation of Akt by growth factors depends on the integrity of the PH domain, which binds to the PI 3-kinase product, PI(3,4,5)P3, and phosphorylation of Thr-308 and Ser-473 by PDK1 and PDK2/ILK, respectively.	bind
35452	6	8545	7	NULL	NULL	0	NULL	PDK2/ILK	NULL		phosphorylates	NULL					NULL		Ser-473		NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_2_431_s_13	11485901	6- 9 Activation of Akt by growth factors depends on the integrity of the PH domain, which binds to the PI 3-kinase product, PI(3,4,5)P3, and phosphorylation of Thr-308 and Ser-473 by PDK1 and PDK2/ILK, respectively.	bind
35562	7	8545	7	NULL	NULL	0	NULL	statement 1	NULL		depends on	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_2_431_s_13	11485901	6- 9 Activation of Akt by growth factors depends on the integrity of the PH domain, which binds to the PI 3-kinase product, PI(3,4,5)P3, and phosphorylation of Thr-308 and Ser-473 by PDK1 and PDK2/ILK, respectively.	bind
35563	8	8545	7	NULL	NULL	0	NULL	statement 1	NULL		depends on	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_2_431_s_13	11485901	6- 9 Activation of Akt by growth factors depends on the integrity of the PH domain, which binds to the PI 3-kinase product, PI(3,4,5)P3, and phosphorylation of Thr-308 and Ser-473 by PDK1 and PDK2/ILK, respectively.	bind
33955	1	8546	5	13	NULL	NULL	NULL	6- 9alpha-DG	GP		linked to		noncovalently			beta-DG	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_5_1749_s_16	10793086	6- 9alpha-DG remains noncovalently linked to beta-DG, which through its cytoplasmic tail, binds directly to the C-terminal portion of dystrophin 10, 11  whereas the N-terminal domain of dystrophin binds to the subsarcolemmal actin cytoskeleton.	bind
33956	2	8546	5	13	NULL	NULL	NULL	beta-DG	GP		bind		directly	cytoplasmic tail		dystrophin	GP		C-terminal portion		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_5_1749_s_16	10793086	6- 9alpha-DG remains noncovalently linked to beta-DG, which through its cytoplasmic tail, binds directly to the C-terminal portion of dystrophin 10, 11  whereas the N-terminal domain of dystrophin binds to the subsarcolemmal actin cytoskeleton.	bind
33957	3	8546	5	13	NULL	NULL	NULL	dystrophin	GP		bind			N-terminal domain		subsarcolemmal actin cytoskeleton	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_5_1749_s_16	10793086	6- 9alpha-DG remains noncovalently linked to beta-DG, which through its cytoplasmic tail, binds directly to the C-terminal portion of dystrophin 10, 11  whereas the N-terminal domain of dystrophin binds to the subsarcolemmal actin cytoskeleton.	bind
35460	1	8546	7	NULL	NULL	0	NULL	9alpha-DG	NULL		linked to	NULL	noncovalently			beta-DG	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_5_1749_s_16	10793086	6- 9alpha-DG remains noncovalently linked to beta-DG, which through its cytoplasmic tail, binds directly to the C-terminal portion of dystrophin 10, 11  whereas the N-terminal domain of dystrophin binds to the subsarcolemmal actin cytoskeleton.	bind
35462	2	8546	7	NULL	NULL	0	NULL	beta-DG	NULL		binds	NULL	directly	cytoplasmic tail		dystrophin	NULL		C-terminal		NULL		0	NULL	NULL	NULL	gw60_amjpathol_156_5_1749_s_16	10793086	6- 9alpha-DG remains noncovalently linked to beta-DG, which through its cytoplasmic tail, binds directly to the C-terminal portion of dystrophin 10, 11  whereas the N-terminal domain of dystrophin binds to the subsarcolemmal actin cytoskeleton.	bind
35463	3	8546	7	10	NULL	0	NULL	dystrophin	NULL		binds to	NULL		N-terminal domain 		actin cytoskeleton	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_156_5_1749_s_16	10793086	6- 9alpha-DG remains noncovalently linked to beta-DG, which through its cytoplasmic tail, binds directly to the C-terminal portion of dystrophin 10, 11  whereas the N-terminal domain of dystrophin binds to the subsarcolemmal actin cytoskeleton.	bind
33958	1	8547	5	13	NULL	NULL	NULL	L-selectin	GP		bind		high affinity			HEV-associated ligands	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40226_s_18	10956661	6- O-Sulfation on galactose and  N-acetylglucosamine ( i.e. GlcNAc-6-SO4 and Gal-6-SO4) which is found in the context of sialyl Lewis X, is necessary for high affinity binding between L-selectin and these HEV-associated ligands ( 9).	bind
33959	2	8547	5	13	NULL	NULL	NULL	GlcNAc-6-SO4	Chemical		is					6- O-Sulfation on N-acetylglucosamine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40226_s_18	10956661	6- O-Sulfation on galactose and  N-acetylglucosamine ( i.e. GlcNAc-6-SO4 and Gal-6-SO4) which is found in the context of sialyl Lewis X, is necessary for high affinity binding between L-selectin and these HEV-associated ligands ( 9).	bind
33960	3	8547	5	13	NULL	NULL	NULL	Gal-6-SO4	Chemical		is					6- O-Sulfation on galactose	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40226_s_18	10956661	6- O-Sulfation on galactose and  N-acetylglucosamine ( i.e. GlcNAc-6-SO4 and Gal-6-SO4) which is found in the context of sialyl Lewis X, is necessary for high affinity binding between L-selectin and these HEV-associated ligands ( 9).	bind
35465	1	8547	7	NULL	NULL	0	NULL	L-selectin	NULL		bind	NULL	high affinity			HEV-associated ligands	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40226_s_18	10956661	6- O-Sulfation on galactose and  N-acetylglucosamine ( i.e. GlcNAc-6-SO4 and Gal-6-SO4) which is found in the context of sialyl Lewis X, is necessary for high affinity binding between L-selectin and these HEV-associated ligands ( 9).	bind
35467	2	8547	7	10	NULL	0	NULL	GlcNAc-6-SO4			is 					6- O-Sulfation on N-acetylglucosamine					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40226_s_18	10956661	6- O-Sulfation on galactose and  N-acetylglucosamine ( i.e. GlcNAc-6-SO4 and Gal-6-SO4) which is found in the context of sialyl Lewis X, is necessary for high affinity binding between L-selectin and these HEV-associated ligands ( 9).	bind
35468	3	8547	7	10	NULL	0	NULL	Gal-6-SO4			is					6- O-Sulfation on galactose					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40226_s_18	10956661	6- O-Sulfation on galactose and  N-acetylglucosamine ( i.e. GlcNAc-6-SO4 and Gal-6-SO4) which is found in the context of sialyl Lewis X, is necessary for high affinity binding between L-selectin and these HEV-associated ligands ( 9).	bind
33965	1	8549	5	13	NULL	NULL	NULL	Ins(1,4,5)P3	Chemical		bind					receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_4_1262_s_174	15249226	6-Deoxy-Ins(1,3,4,5)P4, however, inhibits the binding of [3]Ins(1,4,5)P3 to its receptor only slightly less effectively than Ins(1,3,4,5)P4.	bind
33966	2	8549	5	13	NULL	NULL	NULL	6-Deoxy-Ins(1,3,4,5)P4	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_4_1262_s_174	15249226	6-Deoxy-Ins(1,3,4,5)P4, however, inhibits the binding of [3]Ins(1,4,5)P3 to its receptor only slightly less effectively than Ins(1,3,4,5)P4.	bind
33967	3	8549	5	13	NULL	NULL	NULL	Ins(1,3,4,5)P4	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_4_1262_s_174	15249226	6-Deoxy-Ins(1,3,4,5)P4, however, inhibits the binding of [3]Ins(1,4,5)P3 to its receptor only slightly less effectively than Ins(1,3,4,5)P4.	bind
33968	4	8549	5	13	NULL	NULL	NULL	statement 2	Process		less effective than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_4_1262_s_174	15249226	6-Deoxy-Ins(1,3,4,5)P4, however, inhibits the binding of [3]Ins(1,4,5)P3 to its receptor only slightly less effectively than Ins(1,3,4,5)P4.	bind
35470	1	8549	7	NULL	NULL	0	NULL	[3]Ins(1,4,5)P3	NULL		binds	NULL				 receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_4_1262_s_174	15249226	6-Deoxy-Ins(1,3,4,5)P4, however, inhibits the binding of [3]Ins(1,4,5)P3 to its receptor only slightly less effectively than Ins(1,3,4,5)P4.	bind
35472	3	8549	7	NULL	NULL	0	NULL	6-Deoxy-Ins(1,3,4,5)P4	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_4_1262_s_174	15249226	6-Deoxy-Ins(1,3,4,5)P4, however, inhibits the binding of [3]Ins(1,4,5)P3 to its receptor only slightly less effectively than Ins(1,3,4,5)P4.	bind
35473	2	8549	7	NULL	NULL	0	NULL	Ins(1,3,4,5)P4	NULL		inhibits	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_4_1262_s_174	15249226	6-Deoxy-Ins(1,3,4,5)P4, however, inhibits the binding of [3]Ins(1,4,5)P3 to its receptor only slightly less effectively than Ins(1,3,4,5)P4.	bind
35474	5	8549	7	NULL	NULL	0	NULL	statement 3	NULL		is less effictive than	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_320_4_1262_s_174	15249226	6-Deoxy-Ins(1,3,4,5)P4, however, inhibits the binding of [3]Ins(1,4,5)P3 to its receptor only slightly less effectively than Ins(1,3,4,5)P4.	bind
33969	1	8550	5	13	NULL	NULL	NULL	6-Hydroxy-D-nicotine oxidase	GP		is a type of					monomeric protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_51307_s_24	14534317	6-Hydroxy-D-nicotine oxidase is a monomeric protein with FAD covalently bound to a histidine  residue.	bind
33970	2	8550	5	13	NULL	NULL	NULL	FAD	NucleicAcid		bind		covalently						histidine residue		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_51307_s_24	14534317	6-Hydroxy-D-nicotine oxidase is a monomeric protein with FAD covalently bound to a histidine  residue.	bind
33971	3	8550	5	13	NULL	NULL	NULL	6-Hydroxy-D-nicotine oxidase	GP		contains					statement 2	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_51307_s_24	14534317	6-Hydroxy-D-nicotine oxidase is a monomeric protein with FAD covalently bound to a histidine  residue.	bind
35475	1	8550	7	NULL	NULL	0	NULL	6-Hydroxy-D-nicotine oxidase	NULL		contains	NULL				FAD	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_51_51307_s_24	14534317	6-Hydroxy-D-nicotine oxidase is a monomeric protein with FAD covalently bound to a histidine  residue.	bind
35476	2	8550	7	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL	covalently				NULL		histidine residue		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_51_51307_s_24	14534317	6-Hydroxy-D-nicotine oxidase is a monomeric protein with FAD covalently bound to a histidine  residue.	bind
35477	3	8550	7	NULL	NULL	0	NULL	6-Hydroxy-D-nicotine oxidase	NULL		is a type of	NULL				monomeric protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_51_51307_s_24	14534317	6-Hydroxy-D-nicotine oxidase is a monomeric protein with FAD covalently bound to a histidine  residue.	bind
33972	1	8551	5	13	NULL	NULL	NULL	6-Mer heparin	Chemical		bind					GST-Tat	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_40_28198_s_8	10497173	6-Mer heparin binds GST-Tat with a dissociation constant ( K d) equal to 0.7  plus-or-minus  0.4 muM and a molar oligosaccharide:GST-Tat ratio of about 1:1.	bind
35478	1	8551	7	NULL	NULL	0	NULL	6-Mer heparin	NULL		binds	NULL				GST-Tat	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_40_28198_s_8	10497173	6-Mer heparin binds GST-Tat with a dissociation constant ( K d) equal to 0.7  plus-or-minus  0.4 muM and a molar oligosaccharide:GST-Tat ratio of about 1:1.	bind
33973	1	8553	5	13	NULL	NULL	NULL	FGF-2	GP		induces					FGFR-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
33974	2	8553	5	13	NULL	NULL	NULL	Heparin	Chemical		amplify					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
33975	3	8553	5	13	NULL	NULL	NULL	6- O-desulfated heparin	Chemical		inhibits		potentially			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
33976	4	8553	5	13	NULL	NULL	NULL	FGF-2	GP		induces					Erk2	GP	kinase activities of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
33977	5	8553	5	13	NULL	NULL	NULL	Heparin	Chemical		amplify					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
33978	6	8553	5	13	NULL	NULL	NULL	6- O-desulfated heparin	Chemical		inhibits		potentially			statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
33979	7	8553	5	13	NULL	NULL	NULL	6-O-Desulfated Heparin	Chemical		inhibits					mitogenicity	Process	subsequent			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
33980	8	8553	5	13	NULL	NULL	NULL	6- O-desulfated heparin	Chemical		bind					FGF-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
33981	9	8553	5	13	NULL	NULL	NULL	6- O-desulfated heparin	Chemical		bind		weakly			receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
33982	10	8553	5	13	NULL	NULL	NULL	6- O-desulfated heparin	Chemical		blocks					ternary FGF-2-heparin-FGFR-1 complex	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
35479	1	8553	7	NULL	NULL	0	NULL	Heparin	NULL		amplify	NULL				FGFR- 1 activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
35480	2	8553	7	NULL	NULL	0	NULL	Heparin	NULL		amplify	NULL				Erk2 Kinase Activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
35482	3	8553	7	NULL	NULL	0	NULL	FGF-2	NULL		induce	NULL				FGFR-1 activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
35483	4	8553	7	NULL	NULL	0	NULL	FGF-2	NULL		induce	NULL				Erk2 Kinase Activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
35484	5	8553	7	NULL	NULL	0	NULL	6-O-Desulfated Heparin	NULL		inhibits	NULL	potently			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
35485	6	8553	7	NULL	NULL	0	NULL	6-O-Desulfated Heparin	NULL		inhibits	NULL	potently			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
35486	7	8553	7	NULL	NULL	0	NULL	6-O-Desulfated Heparin	NULL		inhibits	NULL	potently			statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
35487	8	8553	7	NULL	NULL	0	NULL	6-O-Desulfated Heparin	NULL		inhibits	NULL	potently			statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
35488	9	8553	7	NULL	NULL	0	NULL	6- O-desulfated heparin 	NULL		binds to	NULL				FGF-2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
35489	10	8553	7	NULL	NULL	0	NULL	Heparin	NULL		amplify	NULL				mitogenicity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
35490	11	8553	7	NULL	NULL	0	NULL	FGF-2	NULL		induce	NULL				mitogenicity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
35491	12	8553	7	NULL	NULL	0	NULL	6- O-desulfated heparin	NULL		binds 	NULL	weakly			receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
35492	13	8553	7	NULL	NULL	0	NULL	statement 9	NULL		blocks	NULL				ternary FGF-2-heparin-FGFR-1 complex	NULL	 formation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
35493	14	8553	7	NULL	NULL	0	NULL	statement 12	NULL		blocks	NULL				ternary FGF-2-heparin-FGFR-1 complex	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_180	10816596	6-O-Desulfated Heparin Is a Potent Inhibitor of Heparin-amplified, FGF-2-induced FGFR-1 and Erk2 Kinase Activities and Subsequent Mitogenicity-- Because 6- O-desulfated heparin binds to FGF-2 but only weakly to the receptor (see Fig.  4,  A and  C), it may block formation of the ternary FGF-2-heparin-FGFR-1 complex.	bind
33983	1	8554	5	13	NULL	NULL	NULL	6-Thiocyanato-FAD	Chemical		bind					DT-diaphorase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_6_2512_s_124	7531691	6-Thiocyanato-FAD binds  to DT-diaphorase with an absorption maximum at 441 nm.	bind
35494	1	8554	7	NULL	NULL	0	NULL	6-Thiocyanato-FAD	NULL		binds to	NULL				DT-diaphorase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_6_2512_s_124	7531691	6-Thiocyanato-FAD binds  to DT-diaphorase with an absorption maximum at 441 nm.	bind
33984	1	8555	5	13	NULL	NULL	NULL	apobec-1	GP		bind					apo B RNA	NucleicAcid	mammalian			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1772_s_475	11292850	60       Anant,S., MacGinnitie,A.J. and Davidson,N.O. (1995) The binding of apobec-1 to mammalian apo B RNA is stabilized by the presence of complementation factors which are required for post-transcriptional editing.	bind
33985	2	8555	5	13	NULL	NULL	NULL	statement 1	Process		stabilized by					complementation factors	GP	presence of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1772_s_475	11292850	60       Anant,S., MacGinnitie,A.J. and Davidson,N.O. (1995) The binding of apobec-1 to mammalian apo B RNA is stabilized by the presence of complementation factors which are required for post-transcriptional editing.	bind
33986	3	8555	5	13	NULL	NULL	NULL	complementation factors	GP		is required for					post-transcriptional editing	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1772_s_475	11292850	60       Anant,S., MacGinnitie,A.J. and Davidson,N.O. (1995) The binding of apobec-1 to mammalian apo B RNA is stabilized by the presence of complementation factors which are required for post-transcriptional editing.	bind
35495	1	8555	7	NULL	NULL	0	NULL	apobec-1	NULL		binds	NULL				apo B RNA	NULL	mammalian			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1772_s_475	11292850	60       Anant,S., MacGinnitie,A.J. and Davidson,N.O. (1995) The binding of apobec-1 to mammalian apo B RNA is stabilized by the presence of complementation factors which are required for post-transcriptional editing.	bind
35496	2	8555	7	NULL	NULL	0	NULL	complementation factors	NULL		stabilize	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1772_s_475	11292850	60       Anant,S., MacGinnitie,A.J. and Davidson,N.O. (1995) The binding of apobec-1 to mammalian apo B RNA is stabilized by the presence of complementation factors which are required for post-transcriptional editing.	bind
35497	3	8555	7	NULL	NULL	0	NULL	complementation factors	NULL		is required for	NULL				post-transcriptional editing	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1772_s_475	11292850	60       Anant,S., MacGinnitie,A.J. and Davidson,N.O. (1995) The binding of apobec-1 to mammalian apo B RNA is stabilized by the presence of complementation factors which are required for post-transcriptional editing.	bind
33987	1	8556	5	13	NULL	NULL	NULL	[1,2-13C]acetyl-CoA	Chemical		bind					HMG-CoA synthase	GP	wild-type			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_17946_s_256	10748155	600-MHz 1H,13C (omega2) half-filtered spectra of [1,2-13C]acetyl-CoA binding to wild type  HMG-CoA  synthase.	bind
35499	1	8556	7	NULL	NULL	0	NULL	[1,2-13C]acetyl-CoA	NULL		bind	NULL				HMG-CoA synthase	NULL	wild type			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_24_17946_s_256	10748155	600-MHz 1H,13C (omega2) half-filtered spectra of [1,2-13C]acetyl-CoA binding to wild type  HMG-CoA  synthase.	bind
33988	1	8557	5	13	NULL	NULL	NULL	60bca	GP		is					murine monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_186	9784544	60bca is a murine monoclonal antibody that binds to CD14 and blocks LPS-CD14 interaction.	bind
33989	2	8557	5	13	NULL	NULL	NULL	60bca	GP		bind					CD14	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_186	9784544	60bca is a murine monoclonal antibody that binds to CD14 and blocks LPS-CD14 interaction.	bind
33990	3	8557	5	13	NULL	NULL	NULL	LPS	Chemical		interacts with					CD14	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_186	9784544	60bca is a murine monoclonal antibody that binds to CD14 and blocks LPS-CD14 interaction.	bind
33991	4	8557	5	13	NULL	NULL	NULL	statement 2	Process		blocks					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_186	9784544	60bca is a murine monoclonal antibody that binds to CD14 and blocks LPS-CD14 interaction.	bind
35500	1	8557	7	NULL	NULL	0	NULL	60bca	NULL		is a type of	NULL				murine monoclonal antibody	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_186	9784544	60bca is a murine monoclonal antibody that binds to CD14 and blocks LPS-CD14 interaction.	bind
35501	2	8557	7	NULL	NULL	0	NULL	60bca	NULL		binds to	NULL				CD14	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_186	9784544	60bca is a murine monoclonal antibody that binds to CD14 and blocks LPS-CD14 interaction.	bind
35502	3	8557	7	NULL	NULL	0	NULL	LPS	NULL		interacts with	NULL				CD14	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_186	9784544	60bca is a murine monoclonal antibody that binds to CD14 and blocks LPS-CD14 interaction.	bind
35503	4	8557	7	NULL	NULL	0	NULL	60bca	NULL		blocks	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_186	9784544	60bca is a murine monoclonal antibody that binds to CD14 and blocks LPS-CD14 interaction.	bind
33992	1	8558	5	13	NULL	NULL	NULL	XPG	GP		is a type of					DNA repair endonuclease	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_3123_s_478	11452038	61       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
33993	2	8558	5	13	NULL	NULL	NULL	PCNA	GP		is					proliferating cell nuclear antigen	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_3123_s_478	11452038	61       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
33994	3	8558	5	13	NULL	NULL	NULL	XPG	GP		bind					PCNA	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_3123_s_478	11452038	61       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
33995	4	8558	5	13	NULL	NULL	NULL	XPG	GP		shares					FEN-1	GP	sequence elements with	PCNA-binding regions		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_3123_s_478	11452038	61       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
33996	5	8558	5	13	NULL	NULL	NULL	XPG	GP		shares					p21	GP	sequence elements with			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_3123_s_478	11452038	61       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
33997	6	8558	5	13	NULL	NULL	NULL	p21	GP		is a type of					cyclin-dependent kinase inhibitor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_3123_s_478	11452038	61       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
35504	1	8558	7	NULL	NULL	0	NULL	XPG	NULL		binds to	NULL				PCNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_3123_s_478	11452038	61       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
35505	2	8558	7	NULL	NULL	0	NULL	XPG	NULL		is a type of	NULL				DNA repair endonuclease	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_3123_s_478	11452038	61       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
35506	3	8558	7	NULL	NULL	0	NULL	PCNA	NULL		is	NULL				proliferating cell nuclear antigen	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_3123_s_478	11452038	61       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
35507	4	8558	7	NULL	NULL	0	NULL	XPG	NULL		shares	NULL				FEN-1	NULL	sequence elements with	PCNA-binding regions of 		NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_3123_s_478	11452038	61       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
35508	5	8558	7	NULL	NULL	0	NULL	p21	NULL		is a type of	NULL				cyclin-dependent kinase inhibitor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_3123_s_478	11452038	61       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
35509	6	8558	7	NULL	NULL	0	NULL	XPG	NULL		shares	NULL				p21	NULL	sequence elements with	PCNA-binding regions of		NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_3123_s_478	11452038	61       Gary,R., Ludwig,D.L., Cornelius,H.L., MacInnes,M.A. and Park,M.S. (1997) The DNA repair endonuclease XPG binds to proliferating cell nuclear antigen (PCNA) and shares sequence elements with the PCNA-binding regions of FEN-1 and cyclin-dependent kinase inhibitor p21.	bind
35510	1	8559	7	NULL	NULL	0	NULL	U2 snRNP	NULL		bind	NULL				pre-mRNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1741_s_406	11292847	61       Ruby,S.W., Chang,T.-H. and Abelson,J. (1993) Four yeast spliceosomal proteins (PRP5, PRP9, PRP11, and PRP21) interact to promote U2 snRNP binding to pre-mRNA.	bind
35511	2	8559	7	NULL	NULL	0	NULL	PRP5	NULL		promote	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1741_s_406	11292847	61       Ruby,S.W., Chang,T.-H. and Abelson,J. (1993) Four yeast spliceosomal proteins (PRP5, PRP9, PRP11, and PRP21) interact to promote U2 snRNP binding to pre-mRNA.	bind
35512	3	8559	7	NULL	NULL	0	NULL	PRP9	NULL		promote	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1741_s_406	11292847	61       Ruby,S.W., Chang,T.-H. and Abelson,J. (1993) Four yeast spliceosomal proteins (PRP5, PRP9, PRP11, and PRP21) interact to promote U2 snRNP binding to pre-mRNA.	bind
35513	4	8559	7	NULL	NULL	0	NULL	PRP11	NULL		promote	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1741_s_406	11292847	61       Ruby,S.W., Chang,T.-H. and Abelson,J. (1993) Four yeast spliceosomal proteins (PRP5, PRP9, PRP11, and PRP21) interact to promote U2 snRNP binding to pre-mRNA.	bind
35514	5	8559	7	NULL	NULL	0	NULL	PRP21	NULL		promote	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1741_s_406	11292847	61       Ruby,S.W., Chang,T.-H. and Abelson,J. (1993) Four yeast spliceosomal proteins (PRP5, PRP9, PRP11, and PRP21) interact to promote U2 snRNP binding to pre-mRNA.	bind
35515	6	8559	7	NULL	NULL	0	NULL	PRP5	NULL		is a type of	NULL				yeast spliceosomal protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1741_s_406	11292847	61       Ruby,S.W., Chang,T.-H. and Abelson,J. (1993) Four yeast spliceosomal proteins (PRP5, PRP9, PRP11, and PRP21) interact to promote U2 snRNP binding to pre-mRNA.	bind
35516	7	8559	7	NULL	NULL	0	NULL	PRP9	NULL		is a type of	NULL				yeast spliceosomal protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1741_s_406	11292847	61       Ruby,S.W., Chang,T.-H. and Abelson,J. (1993) Four yeast spliceosomal proteins (PRP5, PRP9, PRP11, and PRP21) interact to promote U2 snRNP binding to pre-mRNA.	bind
35517	8	8559	7	NULL	NULL	0	NULL	PRP11	NULL		is a type of	NULL				yeast spliceosomal protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1741_s_406	11292847	61       Ruby,S.W., Chang,T.-H. and Abelson,J. (1993) Four yeast spliceosomal proteins (PRP5, PRP9, PRP11, and PRP21) interact to promote U2 snRNP binding to pre-mRNA.	bind
35518	9	8559	7	NULL	NULL	0	NULL	 PRP21	NULL		is a type of	NULL				yeast spliceosomal protein	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1741_s_406	11292847	61       Ruby,S.W., Chang,T.-H. and Abelson,J. (1993) Four yeast spliceosomal proteins (PRP5, PRP9, PRP11, and PRP21) interact to promote U2 snRNP binding to pre-mRNA.	bind
34296	1	8560	5	13	NULL	NULL	NULL	angiotensin II	GP		upregulates					SM alpha-actin	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_221_s_248	10666419	61  Interestingly, in previous studies, we found that when the "`weak"' SM alpha-actin CArGs were replaced with the much stronger SRE CArG, promoter activity increased dramatically and was no longer limited to SMCs. 48  In addition, we presented evidence indicating that angiotensin II - induced upregulation of SM alpha-actin expression was mediated by increased expression of the homeodomain protein, Mhox, which increased SRF binding to CArG B. 61  Importantly, Mhox itself was not found within the SRF-containing gel-shift complexes and could not account for the SMC SRF-containing higher order complex.	bind
34299	2	8560	5	13	NULL	NULL	NULL	Mhox	GP	increased expression of	increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_221_s_248	10666419	61  Interestingly, in previous studies, we found that when the "`weak"' SM alpha-actin CArGs were replaced with the much stronger SRE CArG, promoter activity increased dramatically and was no longer limited to SMCs. 48  In addition, we presented evidence indicating that angiotensin II - induced upregulation of SM alpha-actin expression was mediated by increased expression of the homeodomain protein, Mhox, which increased SRF binding to CArG B. 61  Importantly, Mhox itself was not found within the SRF-containing gel-shift complexes and could not account for the SMC SRF-containing higher order complex.	bind
34301	3	8560	5	13	NULL	NULL	NULL	Mhox	GP		is a type of					homeodomain protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_221_s_248	10666419	61  Interestingly, in previous studies, we found that when the "`weak"' SM alpha-actin CArGs were replaced with the much stronger SRE CArG, promoter activity increased dramatically and was no longer limited to SMCs. 48  In addition, we presented evidence indicating that angiotensin II - induced upregulation of SM alpha-actin expression was mediated by increased expression of the homeodomain protein, Mhox, which increased SRF binding to CArG B. 61  Importantly, Mhox itself was not found within the SRF-containing gel-shift complexes and could not account for the SMC SRF-containing higher order complex.	bind
34302	4	8560	5	13	NULL	NULL	NULL	SRF	GP		bind									CArG B	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_221_s_248	10666419	61  Interestingly, in previous studies, we found that when the "`weak"' SM alpha-actin CArGs were replaced with the much stronger SRE CArG, promoter activity increased dramatically and was no longer limited to SMCs. 48  In addition, we presented evidence indicating that angiotensin II - induced upregulation of SM alpha-actin expression was mediated by increased expression of the homeodomain protein, Mhox, which increased SRF binding to CArG B. 61  Importantly, Mhox itself was not found within the SRF-containing gel-shift complexes and could not account for the SMC SRF-containing higher order complex.	bind
34303	5	8560	5	13	NULL	NULL	NULL	Mhox	GP		increases					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_221_s_248	10666419	61  Interestingly, in previous studies, we found that when the "`weak"' SM alpha-actin CArGs were replaced with the much stronger SRE CArG, promoter activity increased dramatically and was no longer limited to SMCs. 48  In addition, we presented evidence indicating that angiotensin II - induced upregulation of SM alpha-actin expression was mediated by increased expression of the homeodomain protein, Mhox, which increased SRF binding to CArG B. 61  Importantly, Mhox itself was not found within the SRF-containing gel-shift complexes and could not account for the SMC SRF-containing higher order complex.	bind
35528	1	8560	7	10	NULL	0	NULL	angiotensin II			upregulates					SM alpha-actin expression		expression of 			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_2_221_s_248	10666419	61  Interestingly, in previous studies, we found that when the "`weak"' SM alpha-actin CArGs were replaced with the much stronger SRE CArG, promoter activity increased dramatically and was no longer limited to SMCs. 48  In addition, we presented evidence indicating that angiotensin II - induced upregulation of SM alpha-actin expression was mediated by increased expression of the homeodomain protein, Mhox, which increased SRF binding to CArG B. 61  Importantly, Mhox itself was not found within the SRF-containing gel-shift complexes and could not account for the SMC SRF-containing higher order complex.	bind
35533	2	8560	7	NULL	NULL	0	NULL	Mhox	NULL	expression of	increase	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_2_221_s_248	10666419	61  Interestingly, in previous studies, we found that when the "`weak"' SM alpha-actin CArGs were replaced with the much stronger SRE CArG, promoter activity increased dramatically and was no longer limited to SMCs. 48  In addition, we presented evidence indicating that angiotensin II - induced upregulation of SM alpha-actin expression was mediated by increased expression of the homeodomain protein, Mhox, which increased SRF binding to CArG B. 61  Importantly, Mhox itself was not found within the SRF-containing gel-shift complexes and could not account for the SMC SRF-containing higher order complex.	bind
35540	3	8560	7	NULL	NULL	0	NULL	Mhox	NULL		is a type of	NULL				homeodomain protein	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_2_221_s_248	10666419	61  Interestingly, in previous studies, we found that when the "`weak"' SM alpha-actin CArGs were replaced with the much stronger SRE CArG, promoter activity increased dramatically and was no longer limited to SMCs. 48  In addition, we presented evidence indicating that angiotensin II - induced upregulation of SM alpha-actin expression was mediated by increased expression of the homeodomain protein, Mhox, which increased SRF binding to CArG B. 61  Importantly, Mhox itself was not found within the SRF-containing gel-shift complexes and could not account for the SMC SRF-containing higher order complex.	bind
35541	4	8560	7	NULL	NULL	0	NULL	SRF	NULL		bind	NULL					NULL			CArG B	NULL		0	NULL	NULL	NULL	gw60_circulationres_86_2_221_s_248	10666419	61  Interestingly, in previous studies, we found that when the "`weak"' SM alpha-actin CArGs were replaced with the much stronger SRE CArG, promoter activity increased dramatically and was no longer limited to SMCs. 48  In addition, we presented evidence indicating that angiotensin II - induced upregulation of SM alpha-actin expression was mediated by increased expression of the homeodomain protein, Mhox, which increased SRF binding to CArG B. 61  Importantly, Mhox itself was not found within the SRF-containing gel-shift complexes and could not account for the SMC SRF-containing higher order complex.	bind
35542	5	8560	7	NULL	NULL	0	NULL	Mhox	NULL		increase	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_2_221_s_248	10666419	61  Interestingly, in previous studies, we found that when the "`weak"' SM alpha-actin CArGs were replaced with the much stronger SRE CArG, promoter activity increased dramatically and was no longer limited to SMCs. 48  In addition, we presented evidence indicating that angiotensin II - induced upregulation of SM alpha-actin expression was mediated by increased expression of the homeodomain protein, Mhox, which increased SRF binding to CArG B. 61  Importantly, Mhox itself was not found within the SRF-containing gel-shift complexes and could not account for the SMC SRF-containing higher order complex.	bind
33999	1	8561	5	13	NULL	NULL	NULL	collagen	GP		bind					GPVI	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_144	11788455	61 -  63 Collagen binding to GPVI induces platelet activation through a pathway that involves phosphorylation of the FcRgamma chain followed by the binding of Syk and the phosphorylation-dependent activation of PLCgamma2.	bind
34000	2	8561	5	13	NULL	NULL	NULL	statement 1	Process		induces					platelet	Cell	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_144	11788455	61 -  63 Collagen binding to GPVI induces platelet activation through a pathway that involves phosphorylation of the FcRgamma chain followed by the binding of Syk and the phosphorylation-dependent activation of PLCgamma2.	bind
34001	3	8561	5	13	NULL	NULL	NULL	statement 2	Process		occurs through					pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_144	11788455	61 -  63 Collagen binding to GPVI induces platelet activation through a pathway that involves phosphorylation of the FcRgamma chain followed by the binding of Syk and the phosphorylation-dependent activation of PLCgamma2.	bind
34002	4	8561	5	13	NULL	NULL	NULL	FcRgamma chain	GP	phosphorylation of	is followed by					Syk	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_144	11788455	61 -  63 Collagen binding to GPVI induces platelet activation through a pathway that involves phosphorylation of the FcRgamma chain followed by the binding of Syk and the phosphorylation-dependent activation of PLCgamma2.	bind
34003	5	8561	5	13	NULL	NULL	NULL	statement 3	Process		involves					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_144	11788455	61 -  63 Collagen binding to GPVI induces platelet activation through a pathway that involves phosphorylation of the FcRgamma chain followed by the binding of Syk and the phosphorylation-dependent activation of PLCgamma2.	bind
34004	6	8561	5	13	NULL	NULL	NULL	PLCgamma2	GP	activation of	is dependent on					phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_144	11788455	61 -  63 Collagen binding to GPVI induces platelet activation through a pathway that involves phosphorylation of the FcRgamma chain followed by the binding of Syk and the phosphorylation-dependent activation of PLCgamma2.	bind
34005	7	8561	5	13	NULL	NULL	NULL	statement 3	Process		involves					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_144	11788455	61 -  63 Collagen binding to GPVI induces platelet activation through a pathway that involves phosphorylation of the FcRgamma chain followed by the binding of Syk and the phosphorylation-dependent activation of PLCgamma2.	bind
35544	1	8561	7	NULL	NULL	0	NULL	Collagen	NULL		bind	NULL				GPVI	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_144	11788455	61 -  63 Collagen binding to GPVI induces platelet activation through a pathway that involves phosphorylation of the FcRgamma chain followed by the binding of Syk and the phosphorylation-dependent activation of PLCgamma2.	bind
35545	2	8561	7	NULL	NULL	0	NULL	statement 1	NULL		induces	NULL				platelet	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_144	11788455	61 -  63 Collagen binding to GPVI induces platelet activation through a pathway that involves phosphorylation of the FcRgamma chain followed by the binding of Syk and the phosphorylation-dependent activation of PLCgamma2.	bind
35546	3	8561	7	NULL	NULL	0	NULL	statement 2	NULL		occurs through	NULL				FcRgamma chain	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_144	11788455	61 -  63 Collagen binding to GPVI induces platelet activation through a pathway that involves phosphorylation of the FcRgamma chain followed by the binding of Syk and the phosphorylation-dependent activation of PLCgamma2.	bind
35547	4	8561	7	NULL	NULL	0	NULL	statement 3	NULL		is followed by	NULL				Syk	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_144	11788455	61 -  63 Collagen binding to GPVI induces platelet activation through a pathway that involves phosphorylation of the FcRgamma chain followed by the binding of Syk and the phosphorylation-dependent activation of PLCgamma2.	bind
35548	5	8561	7	NULL	NULL	0	NULL	PLCgamma2	NULL	activation of	depends on	NULL				phosphorylation	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_144	11788455	61 -  63 Collagen binding to GPVI induces platelet activation through a pathway that involves phosphorylation of the FcRgamma chain followed by the binding of Syk and the phosphorylation-dependent activation of PLCgamma2.	bind
35549	6	8561	7	NULL	NULL	0	NULL	statement 3	NULL		is followed by	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_144	11788455	61 -  63 Collagen binding to GPVI induces platelet activation through a pathway that involves phosphorylation of the FcRgamma chain followed by the binding of Syk and the phosphorylation-dependent activation of PLCgamma2.	bind
34006	1	8562	5	13	NULL	NULL	NULL	Fas ligand	GP		induces					Fas	GP	conformational change in			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_80	15539639	61 - 63   Using the Fas death receptor as an example, the binding of Fas ligand is presumed to induce a conformational change in Fas.	bind
35550	1	8562	7	NULL	NULL	0	NULL	Fas ligand	NULL		induce	NULL				Fas	NULL	conformational change in			NULL		0	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_80	15539639	61 - 63   Using the Fas death receptor as an example, the binding of Fas ligand is presumed to induce a conformational change in Fas.	bind
34007	1	8563	5	13	NULL	NULL	NULL	C/EBPbeta	GP		bind					COX-2	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_127	15681294	61 Aspirin and sodium salicylate at 10 - 5 M selectively inhibited C/EBPbeta binding to COX-2 promoter without an effect on p50/RelA NF-kappaB binding.	bind
34008	2	8563	5	13	NULL	NULL	NULL	aspirin	Chemical		inhibits		selectively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_127	15681294	61 Aspirin and sodium salicylate at 10 - 5 M selectively inhibited C/EBPbeta binding to COX-2 promoter without an effect on p50/RelA NF-kappaB binding.	bind
34009	3	8563	5	13	NULL	NULL	NULL	sodium salicylate	Chemical		inhibits		selectively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_127	15681294	61 Aspirin and sodium salicylate at 10 - 5 M selectively inhibited C/EBPbeta binding to COX-2 promoter without an effect on p50/RelA NF-kappaB binding.	bind
34010	4	8563	5	13	NULL	NULL	NULL	p50/RelA	GP		bind					NF-kappaB	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_127	15681294	61 Aspirin and sodium salicylate at 10 - 5 M selectively inhibited C/EBPbeta binding to COX-2 promoter without an effect on p50/RelA NF-kappaB binding.	bind
34011	5	8563	5	13	NULL	NULL	NULL	aspirin	Chemical		does not effect					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_127	15681294	61 Aspirin and sodium salicylate at 10 - 5 M selectively inhibited C/EBPbeta binding to COX-2 promoter without an effect on p50/RelA NF-kappaB binding.	bind
34012	6	8563	5	13	NULL	NULL	NULL	sodium salicylate	Chemical		does not effect					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_127	15681294	61 Aspirin and sodium salicylate at 10 - 5 M selectively inhibited C/EBPbeta binding to COX-2 promoter without an effect on p50/RelA NF-kappaB binding.	bind
35551	1	8563	7	NULL	NULL	0	NULL	C/EBPbeta	NULL		bind	NULL				COX-2	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_127	15681294	61 Aspirin and sodium salicylate at 10 - 5 M selectively inhibited C/EBPbeta binding to COX-2 promoter without an effect on p50/RelA NF-kappaB binding.	bind
35552	2	8563	7	NULL	NULL	0	NULL	p50/RelA	NULL		bind	NULL				NF-kappaB	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_127	15681294	61 Aspirin and sodium salicylate at 10 - 5 M selectively inhibited C/EBPbeta binding to COX-2 promoter without an effect on p50/RelA NF-kappaB binding.	bind
35553	3	8563	7	NULL	NULL	0	NULL	 Aspirin	NULL		inhibits	NULL	selectively			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_127	15681294	61 Aspirin and sodium salicylate at 10 - 5 M selectively inhibited C/EBPbeta binding to COX-2 promoter without an effect on p50/RelA NF-kappaB binding.	bind
35554	4	8563	7	NULL	NULL	0	NULL	sodium salicylate	NULL		inhibits	NULL	selectively			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_127	15681294	61 Aspirin and sodium salicylate at 10 - 5 M selectively inhibited C/EBPbeta binding to COX-2 promoter without an effect on p50/RelA NF-kappaB binding.	bind
35555	5	8563	7	NULL	NULL	0	NULL	Aspirin	NULL		does not effect	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_127	15681294	61 Aspirin and sodium salicylate at 10 - 5 M selectively inhibited C/EBPbeta binding to COX-2 promoter without an effect on p50/RelA NF-kappaB binding.	bind
35556	6	8563	7	NULL	NULL	0	NULL	sodium salicylate	NULL		does not effect	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_679_s_127	15681294	61 Aspirin and sodium salicylate at 10 - 5 M selectively inhibited C/EBPbeta binding to COX-2 promoter without an effect on p50/RelA NF-kappaB binding.	bind
34013	1	8564	5	13	NULL	NULL	NULL	erythropoietin ligand	GP		bind					homodimeric erythropoietin receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_113_20_2454_s_92	16717164	61 Ligand binding of erythropoietin to the homodimeric erythropoietin receptor activates antiapoptotic signal transduction pathways.	bind
34014	2	8564	5	13	NULL	NULL	NULL	statement 1	Process		activates					antiapoptotic signal transduction pathways	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_113_20_2454_s_92	16717164	61 Ligand binding of erythropoietin to the homodimeric erythropoietin receptor activates antiapoptotic signal transduction pathways.	bind
35557	1	8564	7	NULL	NULL	0	NULL	erythropoietin	NULL		bind	NULL				homodimeric erythropoietin receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulation_113_20_2454_s_92	16717164	61 Ligand binding of erythropoietin to the homodimeric erythropoietin receptor activates antiapoptotic signal transduction pathways.	bind
35558	2	8564	7	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				antiapoptotic signal transduction pathways	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_113_20_2454_s_92	16717164	61 Ligand binding of erythropoietin to the homodimeric erythropoietin receptor activates antiapoptotic signal transduction pathways.	bind
34015	1	8565	5	13	NULL	NULL	NULL	CD4+ cells	Cell		bind					ECM proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_157_4_1207_s_234	11021825	61- 64  Indeed, it has been reported that binding of CD4+ cells to ECM proteins, most likely through conformational changes resulting in better presentation to their receptor, may in turn enhance cytokine activity.	bind
35559	1	8565	7	NULL	NULL	0	NULL	CD4+ cells 	NULL		bind	NULL				ECM proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_157_4_1207_s_234	11021825	61- 64  Indeed, it has been reported that binding of CD4+ cells to ECM proteins, most likely through conformational changes resulting in better presentation to their receptor, may in turn enhance cytokine activity.	bind
34019	1	8566	5	13	NULL	NULL	NULL	heparin	Chemical		bind					Tat	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_5_3254_s_143	11024024	61-63), thus suggesting that heparin could compete with cell surface HS proteoglycans for binding to Tat, as observed for other heparin binding growth factors.	bind
34020	2	8566	5	13	NULL	NULL	NULL	HS proteoglycans	GP	cell surface	bind					Tat	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_5_3254_s_143	11024024	61-63), thus suggesting that heparin could compete with cell surface HS proteoglycans for binding to Tat, as observed for other heparin binding growth factors.	bind
34021	3	8566	5	13	NULL	NULL	NULL	statement 1	Process		competes with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_5_3254_s_143	11024024	61-63), thus suggesting that heparin could compete with cell surface HS proteoglycans for binding to Tat, as observed for other heparin binding growth factors.	bind
35564	1	8566	7	10	NULL	0	NULL	HS proteoglycans		cell surface	bind					Tat					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_5_3254_s_143	11024024	61-63), thus suggesting that heparin could compete with cell surface HS proteoglycans for binding to Tat, as observed for other heparin binding growth factors.	bind
35565	2	8566	7	NULL	NULL	0	NULL	heparin	NULL		bind	NULL				Tat	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_5_3254_s_143	11024024	61-63), thus suggesting that heparin could compete with cell surface HS proteoglycans for binding to Tat, as observed for other heparin binding growth factors.	bind
35566	3	8566	7	NULL	NULL	0	NULL	statement 2	NULL		compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_5_3254_s_143	11024024	61-63), thus suggesting that heparin could compete with cell surface HS proteoglycans for binding to Tat, as observed for other heparin binding growth factors.	bind
34022	1	8567	5	13	NULL	NULL	NULL	EBNA-1	GP		bind		sequence-specific			plasmid DNA	NucleicAcid			clustered sites in maintenance region	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_23_4881_s_495	11726698	62       Rawlins,D.R., Milman,G., Hayward,S.D. and Hayward,G.S. (1985) Sequence-specific DNA binding of the Epstein-Barr virus nuclear antigen (EBNA-1) to clustered sites in the plasmid maintenance region.	bind
34023	2	8567	5	13	NULL	NULL	NULL	EBNA-1	GP		is					Epstein-Barr virus nuclear antigen	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_23_4881_s_495	11726698	62       Rawlins,D.R., Milman,G., Hayward,S.D. and Hayward,G.S. (1985) Sequence-specific DNA binding of the Epstein-Barr virus nuclear antigen (EBNA-1) to clustered sites in the plasmid maintenance region.	bind
35568	1	8567	7	NULL	NULL	0	NULL	EBNA-1	NULL		bind	NULL	sequence-specific			plasmid DNA	NULL			clustered sites in the maintenance region	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_23_4881_s_495	11726698	62       Rawlins,D.R., Milman,G., Hayward,S.D. and Hayward,G.S. (1985) Sequence-specific DNA binding of the Epstein-Barr virus nuclear antigen (EBNA-1) to clustered sites in the plasmid maintenance region.	bind
35569	2	8567	7	NULL	NULL	0	NULL	EBNA-1	NULL		is	NULL				Epstein-Barr virus nuclear antigen	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_23_4881_s_495	11726698	62       Rawlins,D.R., Milman,G., Hayward,S.D. and Hayward,G.S. (1985) Sequence-specific DNA binding of the Epstein-Barr virus nuclear antigen (EBNA-1) to clustered sites in the plasmid maintenance region.	bind
34024	1	8568	5	13	NULL	NULL	NULL	FGF-2	GP		interacts with					FGFR	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_3_977_s_295	12598330	62  Thus the location of the HS sequences that bind to the FGFR, together with steric constraints may strongly influence the FGF-2 to FGFR interaction.	bind
34025	2	8568	5	13	NULL	NULL	NULL	HS sequences	GP		bind					FGFR	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_3_977_s_295	12598330	62  Thus the location of the HS sequences that bind to the FGFR, together with steric constraints may strongly influence the FGF-2 to FGFR interaction.	bind
34026	3	8568	5	13	NULL	NULL	NULL	statement 2	Process	location of	influence		strongly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_3_977_s_295	12598330	62  Thus the location of the HS sequences that bind to the FGFR, together with steric constraints may strongly influence the FGF-2 to FGFR interaction.	bind
34027	4	8568	5	13	NULL	NULL	NULL	steric constraints			influence		strongly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_3_977_s_295	12598330	62  Thus the location of the HS sequences that bind to the FGFR, together with steric constraints may strongly influence the FGF-2 to FGFR interaction.	bind
35570	1	8568	7	10	NULL	0	NULL	HS sequences	NULL		bind	NULL				FGFR	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_162_3_977_s_295	12598330	62  Thus the location of the HS sequences that bind to the FGFR, together with steric constraints may strongly influence the FGF-2 to FGFR interaction.	bind
35571	2	8568	7	NULL	NULL	0	NULL	FGF-2 	NULL		interacts with	NULL				FGFR	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_162_3_977_s_295	12598330	62  Thus the location of the HS sequences that bind to the FGFR, together with steric constraints may strongly influence the FGF-2 to FGFR interaction.	bind
35572	3	8568	7	NULL	NULL	0	NULL	steric constraints	NULL		influence	NULL	may strongly			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_162_3_977_s_295	12598330	62  Thus the location of the HS sequences that bind to the FGFR, together with steric constraints may strongly influence the FGF-2 to FGFR interaction.	bind
35573	4	8568	7	NULL	NULL	0	NULL	statement 1	NULL		influence	NULL	strongly			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_162_3_977_s_295	12598330	62  Thus the location of the HS sequences that bind to the FGFR, together with steric constraints may strongly influence the FGF-2 to FGFR interaction.	bind
34044	1	8569	5	13	NULL	NULL	NULL	EBNA1 protein	GP		bind		constitutively			Epstein-Barr virus	Organism			oriP	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_23_4881_s_498	11726698	63       Hsieh,D.J., Camiolo,S.M. and Yates,J.L. (1993) Constitutive binding of EBNA1 protein to the Epstein-Barr virus replication origin, oriP, with distortion of DNA structure during latent infection.	bind
34045	2	8569	5	13	NULL	NULL	NULL	oriP	NucleicAcid		is					replication origin	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_23_4881_s_498	11726698	63       Hsieh,D.J., Camiolo,S.M. and Yates,J.L. (1993) Constitutive binding of EBNA1 protein to the Epstein-Barr virus replication origin, oriP, with distortion of DNA structure during latent infection.	bind
35575	1	8569	7	10	NULL	0	NULL	EBNA1 protein 			binds		constitutively			Epstein-Barr virus				oriP	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_23_4881_s_498	11726698	63       Hsieh,D.J., Camiolo,S.M. and Yates,J.L. (1993) Constitutive binding of EBNA1 protein to the Epstein-Barr virus replication origin, oriP, with distortion of DNA structure during latent infection.	bind
35576	2	8569	7	NULL	NULL	0	NULL	oriP	NULL		is 	NULL				Epstein-Barr virus replication origin	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_23_4881_s_498	11726698	63       Hsieh,D.J., Camiolo,S.M. and Yates,J.L. (1993) Constitutive binding of EBNA1 protein to the Epstein-Barr virus replication origin, oriP, with distortion of DNA structure during latent infection.	bind
34047	1	8570	5	13	NULL	NULL	NULL	CCR3	GP		bind					eotaxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1861_s_251	9846976	63  CCR3 was originally described as the receptor for eotaxin, but in the mouse CCR3 will bind MIP-1alpha.	bind
34048	2	8570	5	13	NULL	NULL	NULL	CCR3	GP		bind					MIP-1alpha	GP	mouse			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_6_1861_s_251	9846976	63  CCR3 was originally described as the receptor for eotaxin, but in the mouse CCR3 will bind MIP-1alpha.	bind
35577	1	8570	7	NULL	NULL	0	NULL	eotaxin	NULL		bind	NULL				CCR3 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_6_1861_s_251	9846976	63  CCR3 was originally described as the receptor for eotaxin, but in the mouse CCR3 will bind MIP-1alpha.	bind
35578	2	8570	7	NULL	NULL	0	NULL	MIP-1alpha	NULL		bind	NULL				CCR3	NULL	mouse			NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_6_1861_s_251	9846976	63  CCR3 was originally described as the receptor for eotaxin, but in the mouse CCR3 will bind MIP-1alpha.	bind
34049	1	8571	5	13	NULL	NULL	NULL	cytochrome c	GP		bind					Apaf-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_6_2229_s_244	12466137	63  The cytochrome c is known to bind with the adaptor molecule Apaf-1 and form the apoptosome that activates caspase-9, a caspase that cleaves and activates caspase-3.	bind
34050	2	8571	5	13	NULL	NULL	NULL	Apaf-1	GP		is a type of					adaptor molecule	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_6_2229_s_244	12466137	63  The cytochrome c is known to bind with the adaptor molecule Apaf-1 and form the apoptosome that activates caspase-9, a caspase that cleaves and activates caspase-3.	bind
34051	3	8571	5	13	NULL	NULL	NULL	statement 1	Process		forms					apoptosome	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_6_2229_s_244	12466137	63  The cytochrome c is known to bind with the adaptor molecule Apaf-1 and form the apoptosome that activates caspase-9, a caspase that cleaves and activates caspase-3.	bind
34052	4	8571	5	13	NULL	NULL	NULL	apoptosome	GP		activates					caspase-9	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_6_2229_s_244	12466137	63  The cytochrome c is known to bind with the adaptor molecule Apaf-1 and form the apoptosome that activates caspase-9, a caspase that cleaves and activates caspase-3.	bind
34053	5	8571	5	13	NULL	NULL	NULL	caspase-9	GP		cleaves					caspase-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_6_2229_s_244	12466137	63  The cytochrome c is known to bind with the adaptor molecule Apaf-1 and form the apoptosome that activates caspase-9, a caspase that cleaves and activates caspase-3.	bind
34054	6	8571	5	13	NULL	NULL	NULL	statement 5	Process		activates					caspase-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_6_2229_s_244	12466137	63  The cytochrome c is known to bind with the adaptor molecule Apaf-1 and form the apoptosome that activates caspase-9, a caspase that cleaves and activates caspase-3.	bind
35579	1	8571	7	NULL	NULL	0	NULL	 cytochrome c	NULL		bind	NULL				Apaf-1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_6_2229_s_244	12466137	63  The cytochrome c is known to bind with the adaptor molecule Apaf-1 and form the apoptosome that activates caspase-9, a caspase that cleaves and activates caspase-3.	bind
35580	2	8571	7	NULL	NULL	0	NULL	Apaf-1	NULL		is a type of	NULL				adaptor molecule	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_6_2229_s_244	12466137	63  The cytochrome c is known to bind with the adaptor molecule Apaf-1 and form the apoptosome that activates caspase-9, a caspase that cleaves and activates caspase-3.	bind
35581	3	8571	7	NULL	NULL	0	NULL	statement 1	NULL		forms	NULL				apoptosome	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_6_2229_s_244	12466137	63  The cytochrome c is known to bind with the adaptor molecule Apaf-1 and form the apoptosome that activates caspase-9, a caspase that cleaves and activates caspase-3.	bind
35582	4	8571	7	NULL	NULL	0	NULL	apoptosome	NULL		activates	NULL				caspase-9	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_6_2229_s_244	12466137	63  The cytochrome c is known to bind with the adaptor molecule Apaf-1 and form the apoptosome that activates caspase-9, a caspase that cleaves and activates caspase-3.	bind
35583	5	8571	7	NULL	NULL	0	NULL	 caspase-9	NULL		cleaves	NULL				caspase-3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_6_2229_s_244	12466137	63  The cytochrome c is known to bind with the adaptor molecule Apaf-1 and form the apoptosome that activates caspase-9, a caspase that cleaves and activates caspase-3.	bind
35584	6	8571	7	NULL	NULL	0	NULL	caspase-9	NULL		activates	NULL				caspase-3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_6_2229_s_244	12466137	63  The cytochrome c is known to bind with the adaptor molecule Apaf-1 and form the apoptosome that activates caspase-9, a caspase that cleaves and activates caspase-3.	bind
34191	1	8572	5	13	NULL	NULL	NULL	gp120	GP		is a type of					viral proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1599_s_327	10550317	63 Binding of viral proteins (gp120) and SDF-1 to CXCR4 expressed on neurons could be a pathway for the neuronal apoptosis, suggesting an additional mechanism for neurodegeneration developed in HAD and HIVE.	bind
34193	2	8572	5	13	NULL	NULL	NULL	CXCR4	GP		is expressed on					neurons	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1599_s_327	10550317	63 Binding of viral proteins (gp120) and SDF-1 to CXCR4 expressed on neurons could be a pathway for the neuronal apoptosis, suggesting an additional mechanism for neurodegeneration developed in HAD and HIVE.	bind
34195	3	8572	5	13	NULL	NULL	NULL	gp120	GP		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1599_s_327	10550317	63 Binding of viral proteins (gp120) and SDF-1 to CXCR4 expressed on neurons could be a pathway for the neuronal apoptosis, suggesting an additional mechanism for neurodegeneration developed in HAD and HIVE.	bind
34196	4	8572	5	13	NULL	NULL	NULL	SDF-1	GP		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1599_s_327	10550317	63 Binding of viral proteins (gp120) and SDF-1 to CXCR4 expressed on neurons could be a pathway for the neuronal apoptosis, suggesting an additional mechanism for neurodegeneration developed in HAD and HIVE.	bind
34200	5	8572	5	13	NULL	NULL	NULL	statement 3	Process		pathway for		could be			neuronal apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1599_s_327	10550317	63 Binding of viral proteins (gp120) and SDF-1 to CXCR4 expressed on neurons could be a pathway for the neuronal apoptosis, suggesting an additional mechanism for neurodegeneration developed in HAD and HIVE.	bind
34202	6	8572	5	13	NULL	NULL	NULL	statement 4	Process		pathway for		could be			neuronal apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1599_s_327	10550317	63 Binding of viral proteins (gp120) and SDF-1 to CXCR4 expressed on neurons could be a pathway for the neuronal apoptosis, suggesting an additional mechanism for neurodegeneration developed in HAD and HIVE.	bind
35585	6	8572	7	10	NULL	0	NULL	gp120			bind					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1599_s_327	10550317	63 Binding of viral proteins (gp120) and SDF-1 to CXCR4 expressed on neurons could be a pathway for the neuronal apoptosis, suggesting an additional mechanism for neurodegeneration developed in HAD and HIVE.	bind
35586	2	8572	7	NULL	NULL	0	NULL	gp 120	NULL		is a type of	NULL				viral protein	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_5_1599_s_327	10550317	63 Binding of viral proteins (gp120) and SDF-1 to CXCR4 expressed on neurons could be a pathway for the neuronal apoptosis, suggesting an additional mechanism for neurodegeneration developed in HAD and HIVE.	bind
35587	3	8572	7	10	NULL	0	NULL	SDF-1			bind					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_5_1599_s_327	10550317	63 Binding of viral proteins (gp120) and SDF-1 to CXCR4 expressed on neurons could be a pathway for the neuronal apoptosis, suggesting an additional mechanism for neurodegeneration developed in HAD and HIVE.	bind
35588	4	8572	7	NULL	NULL	0	NULL	statement 1	NULL		pathway for	NULL				neuronal apoptosis	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_5_1599_s_327	10550317	63 Binding of viral proteins (gp120) and SDF-1 to CXCR4 expressed on neurons could be a pathway for the neuronal apoptosis, suggesting an additional mechanism for neurodegeneration developed in HAD and HIVE.	bind
35589	5	8572	7	NULL	NULL	0	NULL	statement 2	NULL		pathway for	NULL				neuronal apoptosis	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_5_1599_s_327	10550317	63 Binding of viral proteins (gp120) and SDF-1 to CXCR4 expressed on neurons could be a pathway for the neuronal apoptosis, suggesting an additional mechanism for neurodegeneration developed in HAD and HIVE.	bind
55813	1	8572	7	10	NULL	0	NULL	CXCR4			is expressed in					neurons					NULL		0	NULL	NULL	NULL	gw60_amjpathol_155_5_1599_s_327	10550317	63 Binding of viral proteins (gp120) and SDF-1 to CXCR4 expressed on neurons could be a pathway for the neuronal apoptosis, suggesting an additional mechanism for neurodegeneration developed in HAD and HIVE.	bind
34178	1	8573	5	13	NULL	NULL	NULL	cGKIalpha	GP		bind					MLC phosphatase	GP		myosin-binding subunit		NULL		NULL	NULL	NULL	NULL	gw70_circulation_108_18_2172_s_78	14597579	63 cGKIalpha binds to and phosphorylates the myosin-binding subunit of MLC phosphatase, which could be important for localization of cGKI near the enzyme it regulates.	bind
34180	2	8573	5	13	NULL	NULL	NULL	statement 1	Process		phosphorylates					MLC phosphatase	GP		myosin-binding subunit		NULL		NULL	NULL	NULL	NULL	gw70_circulation_108_18_2172_s_78	14597579	63 cGKIalpha binds to and phosphorylates the myosin-binding subunit of MLC phosphatase, which could be important for localization of cGKI near the enzyme it regulates.	bind
34214	3	8573	5	13	NULL	NULL	NULL	statement 1	Process		is important for					cGKI	GP	localization of 			NULL		NULL	NULL	NULL	NULL	gw70_circulation_108_18_2172_s_78	14597579	63 cGKIalpha binds to and phosphorylates the myosin-binding subunit of MLC phosphatase, which could be important for localization of cGKI near the enzyme it regulates.	bind
34215	4	8573	5	13	NULL	NULL	NULL	statement 1	Process		is important for					cGKI	GP	localization of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_108_18_2172_s_78	14597579	63 cGKIalpha binds to and phosphorylates the myosin-binding subunit of MLC phosphatase, which could be important for localization of cGKI near the enzyme it regulates.	bind
35652	1	8573	7	NULL	NULL	0	NULL	cGKIalpha	NULL		binds to	NULL				MLC phosphatase	NULL		myosin-binding subunit		NULL		0	NULL	NULL	NULL	gw70_circulation_108_18_2172_s_78	14597579	63 cGKIalpha binds to and phosphorylates the myosin-binding subunit of MLC phosphatase, which could be important for localization of cGKI near the enzyme it regulates.	bind
35653	2	8573	7	NULL	NULL	0	NULL	cGKIalpha	NULL		phosphorylates	NULL				MLC phosphatase	NULL		 myosin-binding subunit		NULL		0	NULL	NULL	NULL	gw70_circulation_108_18_2172_s_78	14597579	63 cGKIalpha binds to and phosphorylates the myosin-binding subunit of MLC phosphatase, which could be important for localization of cGKI near the enzyme it regulates.	bind
35654	3	8573	7	NULL	NULL	0	NULL	statement 1	NULL		is important for	NULL				cGKI	NULL	localization of			NULL		0	NULL	NULL	NULL	gw70_circulation_108_18_2172_s_78	14597579	63 cGKIalpha binds to and phosphorylates the myosin-binding subunit of MLC phosphatase, which could be important for localization of cGKI near the enzyme it regulates.	bind
35655	4	8573	7	NULL	NULL	0	NULL	statement 2	NULL		is important for	NULL				cGKI	NULL	localization of			NULL		0	NULL	NULL	NULL	gw70_circulation_108_18_2172_s_78	14597579	63 cGKIalpha binds to and phosphorylates the myosin-binding subunit of MLC phosphatase, which could be important for localization of cGKI near the enzyme it regulates.	bind
34222	1	8574	5	13	NULL	NULL	NULL	p300	GP		bind					myocardin	GP		TAD region		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_219	16614312	64 Myocardin HAT activity was dependent on p300 binding to the TAD region (transcriptional activating domain) of myocardin.	bind
34223	2	8574	5	13	NULL	NULL	NULL	TAD region	GP		is					transcriptional activating domain	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_219	16614312	64 Myocardin HAT activity was dependent on p300 binding to the TAD region (transcriptional activating domain) of myocardin.	bind
46682	3	8574	5	13	NULL	NULL	NULL	Myocardin HAT activity	Process		is dependent on					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_219	16614312	64 Myocardin HAT activity was dependent on p300 binding to the TAD region (transcriptional activating domain) of myocardin.	bind
35656	1	8574	7	NULL	NULL	0	NULL	p300	NULL		bind	NULL				myocardin	NULL		TAD region		NULL		0	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_219	16614312	64 Myocardin HAT activity was dependent on p300 binding to the TAD region (transcriptional activating domain) of myocardin.	bind
35657	2	8574	7	NULL	NULL	0	NULL	TAD	NULL		is	NULL				transcriptional activating domain	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_219	16614312	64 Myocardin HAT activity was dependent on p300 binding to the TAD region (transcriptional activating domain) of myocardin.	bind
35658	3	8574	7	NULL	NULL	0	NULL	Myocardin HAT activity	NULL		depends on	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_7_868_s_219	16614312	64 Myocardin HAT activity was dependent on p300 binding to the TAD region (transcriptional activating domain) of myocardin.	bind
34226	1	8575	5	13	NULL	NULL	NULL	Cu	Chemical		bind					SOD1	GP		Cu binding site		NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_24_36_7945_s_164	15356208	64Cu binding to lower-affinity Cu binding sites on SOD1 would not have survived this procedure, and therefore no conclusion about the total stoichiometry of Cu binding to SOD1 can be made from these results.	bind
35659	1	8575	7	10	NULL	0	NULL	Cu			bind					SOD1			Cu binding site		NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_24_36_7945_s_164	15356208	64Cu binding to lower-affinity Cu binding sites on SOD1 would not have survived this procedure, and therefore no conclusion about the total stoichiometry of Cu binding to SOD1 can be made from these results.	bind
34227	1	8576	5	13	NULL	NULL	NULL	FAK	GP		bind					paxillin	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_86	16543511	65 FAK also binds the adapter protein paxillin and tyrosine phosphorylates it at Y31 and Y118, thereby altering paxillin interactions with the alpha4beta1 integrin and the PKL-PIX-PAK complex at the leading edges of spreading lamellipodia.	bind
34228	2	8576	5	13	NULL	NULL	NULL	paxillin	GP		is a type of					adapter protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_86	16543511	65 FAK also binds the adapter protein paxillin and tyrosine phosphorylates it at Y31 and Y118, thereby altering paxillin interactions with the alpha4beta1 integrin and the PKL-PIX-PAK complex at the leading edges of spreading lamellipodia.	bind
34230	3	8576	5	13	NULL	NULL	NULL	statement 1	Process		phosphorylates					paxillin	GP		Y31;;Y118		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_86	16543511	65 FAK also binds the adapter protein paxillin and tyrosine phosphorylates it at Y31 and Y118, thereby altering paxillin interactions with the alpha4beta1 integrin and the PKL-PIX-PAK complex at the leading edges of spreading lamellipodia.	bind
34231	4	8576	5	13	NULL	NULL	NULL	paxillin	GP		interacts with					alpha4beta1 integrin	GP				NULL	at the leading edges of spreading lamellipodia	NULL	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_86	16543511	65 FAK also binds the adapter protein paxillin and tyrosine phosphorylates it at Y31 and Y118, thereby altering paxillin interactions with the alpha4beta1 integrin and the PKL-PIX-PAK complex at the leading edges of spreading lamellipodia.	bind
34232	5	8576	5	13	NULL	NULL	NULL	paxillin	GP		interacts with					PKL-PIX-PAK complex	GP				NULL	at the leading edges of spreading lamellipodia	NULL	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_86	16543511	65 FAK also binds the adapter protein paxillin and tyrosine phosphorylates it at Y31 and Y118, thereby altering paxillin interactions with the alpha4beta1 integrin and the PKL-PIX-PAK complex at the leading edges of spreading lamellipodia.	bind
34233	6	8576	5	13	NULL	NULL	NULL	statement 3	Process		alters					statement 4	Process				NULL	at the leading edges of spreading lamellipodia	NULL	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_86	16543511	65 FAK also binds the adapter protein paxillin and tyrosine phosphorylates it at Y31 and Y118, thereby altering paxillin interactions with the alpha4beta1 integrin and the PKL-PIX-PAK complex at the leading edges of spreading lamellipodia.	bind
34234	7	8576	5	13	NULL	NULL	NULL	statement 3	Process		alters					statement 5	Process				NULL	at the leading edges of spreading lamellipodia	NULL	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_86	16543511	65 FAK also binds the adapter protein paxillin and tyrosine phosphorylates it at Y31 and Y118, thereby altering paxillin interactions with the alpha4beta1 integrin and the PKL-PIX-PAK complex at the leading edges of spreading lamellipodia.	bind
35660	1	8576	7	NULL	NULL	0	NULL	FAK 	NULL		binds	NULL				paxillin	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_86	16543511	65 FAK also binds the adapter protein paxillin and tyrosine phosphorylates it at Y31 and Y118, thereby altering paxillin interactions with the alpha4beta1 integrin and the PKL-PIX-PAK complex at the leading edges of spreading lamellipodia.	bind
35661	2	8576	7	NULL	NULL	0	NULL	Paxillin	NULL		is a type of	NULL				adapter protein	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_86	16543511	65 FAK also binds the adapter protein paxillin and tyrosine phosphorylates it at Y31 and Y118, thereby altering paxillin interactions with the alpha4beta1 integrin and the PKL-PIX-PAK complex at the leading edges of spreading lamellipodia.	bind
35662	3	8576	7	NULL	NULL	0	NULL	FAK	NULL		phosphorylates	NULL				paxillin	NULL		Y31		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_86	16543511	65 FAK also binds the adapter protein paxillin and tyrosine phosphorylates it at Y31 and Y118, thereby altering paxillin interactions with the alpha4beta1 integrin and the PKL-PIX-PAK complex at the leading edges of spreading lamellipodia.	bind
35663	4	8576	7	NULL	NULL	0	NULL	FAK	NULL		phosphorylates	NULL				paxillin	NULL		Y118		NULL		0	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_86	16543511	65 FAK also binds the adapter protein paxillin and tyrosine phosphorylates it at Y31 and Y118, thereby altering paxillin interactions with the alpha4beta1 integrin and the PKL-PIX-PAK complex at the leading edges of spreading lamellipodia.	bind
35664	5	8576	7	10	NULL	0	NULL	paxillin			interacts with					alpha4beta1 integrin					NULL	at the leading edges of spreading lamellipodia	NULL	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_86	16543511	65 FAK also binds the adapter protein paxillin and tyrosine phosphorylates it at Y31 and Y118, thereby altering paxillin interactions with the alpha4beta1 integrin and the PKL-PIX-PAK complex at the leading edges of spreading lamellipodia.	bind
35665	6	8576	7	10	NULL	0	NULL	statement 3			alters					statement 5					NULL	at the leading edges of spreading lamellipodia	NULL	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_86	16543511	65 FAK also binds the adapter protein paxillin and tyrosine phosphorylates it at Y31 and Y118, thereby altering paxillin interactions with the alpha4beta1 integrin and the PKL-PIX-PAK complex at the leading edges of spreading lamellipodia.	bind
35666	7	8576	7	10	NULL	0	NULL	statement 4			alters					statement 5					NULL	at the leading edges of spreading lamellipodia	NULL	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_86	16543511	65 FAK also binds the adapter protein paxillin and tyrosine phosphorylates it at Y31 and Y118, thereby altering paxillin interactions with the alpha4beta1 integrin and the PKL-PIX-PAK complex at the leading edges of spreading lamellipodia.	bind
35667	9	8576	7	10	NULL	0	NULL	statement 3			alters					statement 8					NULL	at the leading edges of spreading lamellipodia	NULL	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_86	16543511	65 FAK also binds the adapter protein paxillin and tyrosine phosphorylates it at Y31 and Y118, thereby altering paxillin interactions with the alpha4beta1 integrin and the PKL-PIX-PAK complex at the leading edges of spreading lamellipodia.	bind
35668	10	8576	7	10	NULL	0	NULL	statement 4			alters					statement 8					NULL	at the leading edges of spreading lamellipodia	NULL	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_86	16543511	65 FAK also binds the adapter protein paxillin and tyrosine phosphorylates it at Y31 and Y118, thereby altering paxillin interactions with the alpha4beta1 integrin and the PKL-PIX-PAK complex at the leading edges of spreading lamellipodia.	bind
35669	8	8576	7	10	NULL	0	NULL	paxillin			interacts with					PKL-PIX-PAK complex					NULL	at the leading edges of spreading lamellipodia	NULL	NULL	NULL	NULL	gw70_circulationres_98_5_606_s_86	16543511	65 FAK also binds the adapter protein paxillin and tyrosine phosphorylates it at Y31 and Y118, thereby altering paxillin interactions with the alpha4beta1 integrin and the PKL-PIX-PAK complex at the leading edges of spreading lamellipodia.	bind
34235	1	8578	5	13	NULL	NULL	NULL	Caveolin	GP		bind		directly			nNOS	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_8_1023_s_165	15117830	66 Caveolin binds directly to nNOS.	bind
35671	1	8578	7	NULL	NULL	0	NULL	Caveolin	NULL		binds	NULL	directly			nNOS	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_8_1023_s_165	15117830	66 Caveolin binds directly to nNOS.	bind
34236	1	8579	5	13	NULL	NULL	NULL	CIB	GP		is					calcium- and integrin-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_1971_s_111	12947018	66,67  Several proteins are known to interact with the cytoplasmic domains of alphaIIb and beta3, and both the calcium- and integrin-binding protein CIB (which binds alphaIIb) and talin (which binds beta3) have been reported to activate alphaIIbbeta3 in vitro.	bind
34237	2	8579	5	13	NULL	NULL	NULL	CIB	GP		bind					alphaIIb	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_1971_s_111	12947018	66,67  Several proteins are known to interact with the cytoplasmic domains of alphaIIb and beta3, and both the calcium- and integrin-binding protein CIB (which binds alphaIIb) and talin (which binds beta3) have been reported to activate alphaIIbbeta3 in vitro.	bind
34238	3	8579	5	13	NULL	NULL	NULL	talin	GP		bind					beta3	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_1971_s_111	12947018	66,67  Several proteins are known to interact with the cytoplasmic domains of alphaIIb and beta3, and both the calcium- and integrin-binding protein CIB (which binds alphaIIb) and talin (which binds beta3) have been reported to activate alphaIIbbeta3 in vitro.	bind
34239	4	8579	5	13	NULL	NULL	NULL	statement 2	Process		activates					alphaIIbbeta3	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_1971_s_111	12947018	66,67  Several proteins are known to interact with the cytoplasmic domains of alphaIIb and beta3, and both the calcium- and integrin-binding protein CIB (which binds alphaIIb) and talin (which binds beta3) have been reported to activate alphaIIbbeta3 in vitro.	bind
34240	5	8579	5	13	NULL	NULL	NULL	statement 3	Process		activates					alphaIIbbeta3	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_1971_s_111	12947018	66,67  Several proteins are known to interact with the cytoplasmic domains of alphaIIb and beta3, and both the calcium- and integrin-binding protein CIB (which binds alphaIIb) and talin (which binds beta3) have been reported to activate alphaIIbbeta3 in vitro.	bind
35672	1	8579	7	NULL	NULL	0	NULL	CIB	NULL		binds	NULL				alphaIIb	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_1971_s_111	12947018	66,67  Several proteins are known to interact with the cytoplasmic domains of alphaIIb and beta3, and both the calcium- and integrin-binding protein CIB (which binds alphaIIb) and talin (which binds beta3) have been reported to activate alphaIIbbeta3 in vitro.	bind
35673	2	8579	7	10	NULL	0	NULL	CIB			is					calcium- and integrin-binding protein					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_1971_s_111	12947018	66,67  Several proteins are known to interact with the cytoplasmic domains of alphaIIb and beta3, and both the calcium- and integrin-binding protein CIB (which binds alphaIIb) and talin (which binds beta3) have been reported to activate alphaIIbbeta3 in vitro.	bind
35674	3	8579	7	NULL	NULL	0	NULL	talin	NULL		binds	NULL				beta3	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_1971_s_111	12947018	66,67  Several proteins are known to interact with the cytoplasmic domains of alphaIIb and beta3, and both the calcium- and integrin-binding protein CIB (which binds alphaIIb) and talin (which binds beta3) have been reported to activate alphaIIbbeta3 in vitro.	bind
35677	4	8579	7	NULL	NULL	0	NULL	CIB 	NULL		activate	NULL				alphaIIbbeta3	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_1971_s_111	12947018	66,67  Several proteins are known to interact with the cytoplasmic domains of alphaIIb and beta3, and both the calcium- and integrin-binding protein CIB (which binds alphaIIb) and talin (which binds beta3) have been reported to activate alphaIIbbeta3 in vitro.	bind
35678	5	8579	7	NULL	NULL	0	NULL	talin 	NULL		activate	NULL				alphaIIbbeta3	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_1971_s_111	12947018	66,67  Several proteins are known to interact with the cytoplasmic domains of alphaIIb and beta3, and both the calcium- and integrin-binding protein CIB (which binds alphaIIb) and talin (which binds beta3) have been reported to activate alphaIIbbeta3 in vitro.	bind
34246	1	8580	5	13	NULL	NULL	NULL	Poly(ADP-ribose) polymerase	GP		bind					transcription factor 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_841_s_411	11160908	67       Butler,A. and Ordahl,C. (1999) Poly(ADP-ribose) polymerase binds with transcription factor 1 to MCAT1 elements to regulate muscle-specific transcription.	bind
34247	2	8580	5	13	NULL	NULL	NULL	statement 1	GP		bind									MCAT1 elements	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_841_s_411	11160908	67       Butler,A. and Ordahl,C. (1999) Poly(ADP-ribose) polymerase binds with transcription factor 1 to MCAT1 elements to regulate muscle-specific transcription.	bind
34248	3	8580	5	13	NULL	NULL	NULL	statement 2	GP		regulates					muscle-specific transcription	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_841_s_411	11160908	67       Butler,A. and Ordahl,C. (1999) Poly(ADP-ribose) polymerase binds with transcription factor 1 to MCAT1 elements to regulate muscle-specific transcription.	bind
35680	1	8580	7	NULL	NULL	0	NULL	Poly(ADP-ribose) polymerase	NULL		bind	NULL				transcription factor 1 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_841_s_411	11160908	67       Butler,A. and Ordahl,C. (1999) Poly(ADP-ribose) polymerase binds with transcription factor 1 to MCAT1 elements to regulate muscle-specific transcription.	bind
35681	2	8580	7	NULL	NULL	0	NULL	Poly(ADP-ribose) polymerase	NULL		bind	NULL					NULL			MCAT1 elements	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_841_s_411	11160908	67       Butler,A. and Ordahl,C. (1999) Poly(ADP-ribose) polymerase binds with transcription factor 1 to MCAT1 elements to regulate muscle-specific transcription.	bind
35682	3	8580	7	NULL	NULL	0	NULL	statement 2	NULL		regulate	NULL				muscle-specific transcription	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_841_s_411	11160908	67       Butler,A. and Ordahl,C. (1999) Poly(ADP-ribose) polymerase binds with transcription factor 1 to MCAT1 elements to regulate muscle-specific transcription.	bind
34249	1	8581	5	13	NULL	NULL	NULL	Retinyl esters	Chemical		stored in					liver	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1765_s_205	9327775	67  Retinyl esters are either stored in the liver or resecreted as unesterified retinol bound to retinol-binding protein.	bind
34250	2	8581	5	13	NULL	NULL	NULL	retinol	Chemical	unesterified	bind					retinol-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1765_s_205	9327775	67  Retinyl esters are either stored in the liver or resecreted as unesterified retinol bound to retinol-binding protein.	bind
34251	3	8581	5	13	NULL	NULL	NULL	Retinyl esters	Chemical		resecreted as					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1765_s_205	9327775	67  Retinyl esters are either stored in the liver or resecreted as unesterified retinol bound to retinol-binding protein.	bind
35683	1	8581	7	NULL	NULL	0	NULL	Retinyl esters	NULL		are stored in the	NULL				liver	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1765_s_205	9327775	67  Retinyl esters are either stored in the liver or resecreted as unesterified retinol bound to retinol-binding protein.	bind
35684	2	8581	7	10	NULL	0	NULL	Retinyl esters	NULL		resecreted as	NULL				retinol 	NULL	unesterified 			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1765_s_205	9327775	67  Retinyl esters are either stored in the liver or resecreted as unesterified retinol bound to retinol-binding protein.	bind
35685	3	8581	7	NULL	NULL	0	NULL	statement 2	NULL		binds	NULL				 retinol-binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_9_1765_s_205	9327775	67  Retinyl esters are either stored in the liver or resecreted as unesterified retinol bound to retinol-binding protein.	bind
36363	1	8582	5	13	NULL	NULL	NULL	SV40 T antigen	GP		bind					pocket protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_4_319_s_228	10455060	67 68 69 70  Consistent with the interpretation that a second region of E1A may be required in addition, it is noteworthy that pocket protein binding by SV40 T antigen did not induce S phase in the presence of dominant-negative Cdk2.	bind
36364	2	8582	5	13	NULL	NULL	NULL	statement 1	Process		does not induce					S phase	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_4_319_s_228	10455060	67 68 69 70  Consistent with the interpretation that a second region of E1A may be required in addition, it is noteworthy that pocket protein binding by SV40 T antigen did not induce S phase in the presence of dominant-negative Cdk2.	bind
36365	3	8582	5	13	NULL	NULL	NULL	statement 2	Process		in the presence of					dominant-negative Cdk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_4_319_s_228	10455060	67 68 69 70  Consistent with the interpretation that a second region of E1A may be required in addition, it is noteworthy that pocket protein binding by SV40 T antigen did not induce S phase in the presence of dominant-negative Cdk2.	bind
35686	1	8582	7	NULL	NULL	0	NULL	SV40 T antigen	NULL		bind	NULL				pocket protein	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_4_319_s_228	10455060	67 68 69 70  Consistent with the interpretation that a second region of E1A may be required in addition, it is noteworthy that pocket protein binding by SV40 T antigen did not induce S phase in the presence of dominant-negative Cdk2.	bind
35687	2	8582	7	NULL	NULL	0	NULL	statement 1	NULL		does not induce	NULL				S phase	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_4_319_s_228	10455060	67 68 69 70  Consistent with the interpretation that a second region of E1A may be required in addition, it is noteworthy that pocket protein binding by SV40 T antigen did not induce S phase in the presence of dominant-negative Cdk2.	bind
35688	3	8582	7	NULL	NULL	0	NULL	statement 2	NULL		in the presence of 	NULL				dominant-negative Cdk2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_4_319_s_228	10455060	67 68 69 70  Consistent with the interpretation that a second region of E1A may be required in addition, it is noteworthy that pocket protein binding by SV40 T antigen did not induce S phase in the presence of dominant-negative Cdk2.	bind
36366	1	8583	5	13	NULL	NULL	NULL	TFPI	GP		bind					smooth muscle cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_4_539_s_158	11950688	67, 68 A synthetic peptide with C-terminal Lys254-Met276 inhibited the binding of TFPI with human smooth muscle cells.	bind
36367	2	8583	5	13	NULL	NULL	NULL	synthetic peptide	GP		inhibit			C-terminal Lys254-Met276		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_4_539_s_158	11950688	67, 68 A synthetic peptide with C-terminal Lys254-Met276 inhibited the binding of TFPI with human smooth muscle cells.	bind
35689	1	8583	7	NULL	NULL	0	NULL	TFPI	NULL		bind	NULL				smooth muscle cells	NULL	human			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_4_539_s_158	11950688	67, 68 A synthetic peptide with C-terminal Lys254-Met276 inhibited the binding of TFPI with human smooth muscle cells.	bind
35690	2	8583	7	NULL	NULL	0	NULL	synthetic peptide	NULL		inhibits	NULL		C-terminal Lys254-Met276		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_4_539_s_158	11950688	67, 68 A synthetic peptide with C-terminal Lys254-Met276 inhibited the binding of TFPI with human smooth muscle cells.	bind
36368	1	8585	5	13	NULL	NULL	NULL	6Ckine	GP		bind					CXCR3	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_14_8205_s_113	9653165	6Ckine Binds to CXCR3.	bind
35691	1	8585	7	NULL	NULL	0	NULL	6Ckine	NULL		binds to	NULL				CXCR3	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_14_8205_s_113	9653165	6Ckine Binds to CXCR3.	bind
36369	1	8587	5	13	NULL	NULL	NULL	6HisC-r GRP	GP		bind		dose dependently			LPS	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_insectbiochemmolbiol_33_6_579_s_285	12770576	6HisC-r GRP bound to LPS and LTA in a dose dependent manner that reached  saturation at approximately 10  g/mL ( Fig. 6B).	bind
36370	2	8587	5	13	NULL	NULL	NULL	6HisC-r GRP	GP		bind		dose dependently			LTA	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_insectbiochemmolbiol_33_6_579_s_285	12770576	6HisC-r GRP bound to LPS and LTA in a dose dependent manner that reached  saturation at approximately 10  g/mL ( Fig. 6B).	bind
35695	1	8587	7	NULL	NULL	0	NULL	6HisC-r GRP	NULL		bind	NULL	dose-dependently			LPS	NULL				NULL		0	NULL	NULL	NULL	gw70_insectbiochemmolbiol_33_6_579_s_285	12770576	6HisC-r GRP bound to LPS and LTA in a dose dependent manner that reached  saturation at approximately 10  g/mL ( Fig. 6B).	bind
35696	2	8587	7	NULL	NULL	0	NULL	6HisC-r GRP	NULL		bind	NULL	dose-dependently			LTA	NULL				NULL		0	NULL	NULL	NULL	gw70_insectbiochemmolbiol_33_6_579_s_285	12770576	6HisC-r GRP bound to LPS and LTA in a dose dependent manner that reached  saturation at approximately 10  g/mL ( Fig. 6B).	bind
36371	1	8588	5	13	NULL	NULL	NULL	RNA	NucleicAcid		bind					RNAP	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_101_6_613_s_262	10892648	6S RNA may bind RNAP  in a manner analogous to DNA promoter binding to RNAP.	bind
36372	2	8588	5	13	NULL	NULL	NULL	DNA	NucleicAcid		bind				promoter	RNAP	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_101_6_613_s_262	10892648	6S RNA may bind RNAP  in a manner analogous to DNA promoter binding to RNAP.	bind
36373	3	8588	5	13	NULL	NULL	NULL	statement 1	Process		analogous to		may be			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_101_6_613_s_262	10892648	6S RNA may bind RNAP  in a manner analogous to DNA promoter binding to RNAP.	bind
35697	1	8588	7	NULL	NULL	0	NULL	6S RNA	NULL		bind	NULL	may			RNAP	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_101_6_613_s_262	10892648	6S RNA may bind RNAP  in a manner analogous to DNA promoter binding to RNAP.	bind
35698	2	8588	7	NULL	NULL	0	NULL	RNAP	NULL		bind	NULL				DNA	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_cell_101_6_613_s_262	10892648	6S RNA may bind RNAP  in a manner analogous to DNA promoter binding to RNAP.	bind
35699	3	8588	7	NULL	NULL	0	NULL	statement 1	NULL		is similar to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_101_6_613_s_262	10892648	6S RNA may bind RNAP  in a manner analogous to DNA promoter binding to RNAP.	bind
36374	1	8591	5	13	NULL	NULL	NULL	Vsr	GP		bind					DNA	NucleicAcid	heteroduplex 			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3775_s_265	11557809	7       Drotschmann,K., Aronshtam,A., Fritz,H.J. and Marinus,M.G. (1998) The  Escherichia coli MutL protein stimulates binding of Vsr and MutS to heteroduplex DNA.	bind
36375	2	8591	5	13	NULL	NULL	NULL	MutS	GP		bind					DNA	NucleicAcid	heteroduplex			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3775_s_265	11557809	7       Drotschmann,K., Aronshtam,A., Fritz,H.J. and Marinus,M.G. (1998) The  Escherichia coli MutL protein stimulates binding of Vsr and MutS to heteroduplex DNA.	bind
36376	3	8591	5	13	NULL	NULL	NULL	MutL protein	GP	Escherichia coli	stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3775_s_265	11557809	7       Drotschmann,K., Aronshtam,A., Fritz,H.J. and Marinus,M.G. (1998) The  Escherichia coli MutL protein stimulates binding of Vsr and MutS to heteroduplex DNA.	bind
36377	4	8591	5	13	NULL	NULL	NULL	MutL protein	GP	Escherichia coli	stimulate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3775_s_265	11557809	7       Drotschmann,K., Aronshtam,A., Fritz,H.J. and Marinus,M.G. (1998) The  Escherichia coli MutL protein stimulates binding of Vsr and MutS to heteroduplex DNA.	bind
35700	1	8591	7	10	NULL	0	NULL	Vsr 			bind					DNA		heteroduplex			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3775_s_265	11557809	7       Drotschmann,K., Aronshtam,A., Fritz,H.J. and Marinus,M.G. (1998) The  Escherichia coli MutL protein stimulates binding of Vsr and MutS to heteroduplex DNA.	bind
35701	2	8591	7	10	NULL	0	NULL	MutS			bind					DNA		heteroduplex 			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3775_s_265	11557809	7       Drotschmann,K., Aronshtam,A., Fritz,H.J. and Marinus,M.G. (1998) The  Escherichia coli MutL protein stimulates binding of Vsr and MutS to heteroduplex DNA.	bind
35702	3	8591	7	NULL	NULL	0	NULL	MutL protein	NULL	Escherichia coli	stimulates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3775_s_265	11557809	7       Drotschmann,K., Aronshtam,A., Fritz,H.J. and Marinus,M.G. (1998) The  Escherichia coli MutL protein stimulates binding of Vsr and MutS to heteroduplex DNA.	bind
35703	4	8591	7	NULL	NULL	0	NULL	MutL protein	NULL	Escherichia coli	stimulates	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_18_3775_s_265	11557809	7       Drotschmann,K., Aronshtam,A., Fritz,H.J. and Marinus,M.G. (1998) The  Escherichia coli MutL protein stimulates binding of Vsr and MutS to heteroduplex DNA.	bind
36378	1	8592	5	13	NULL	NULL	NULL	Arc	GP		is a type of					repressor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2471_s_232	11410653	7       Knight,K.L. and Sauer,R.T. (1989) DNA binding specificity of the Arc and Mnt repressors is determined by a short region of N-terminal residues.	bind
36379	2	8592	5	13	NULL	NULL	NULL	Mnt	GP		is a type of					repressor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2471_s_232	11410653	7       Knight,K.L. and Sauer,R.T. (1989) DNA binding specificity of the Arc and Mnt repressors is determined by a short region of N-terminal residues.	bind
36380	3	8592	5	13	NULL	NULL	NULL	Arc	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2471_s_232	11410653	7       Knight,K.L. and Sauer,R.T. (1989) DNA binding specificity of the Arc and Mnt repressors is determined by a short region of N-terminal residues.	bind
36381	4	8592	5	13	NULL	NULL	NULL	Mnt	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2471_s_232	11410653	7       Knight,K.L. and Sauer,R.T. (1989) DNA binding specificity of the Arc and Mnt repressors is determined by a short region of N-terminal residues.	bind
35704	1	8592	7	10	NULL	0	NULL	Arc	NULL		bind	NULL				DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2471_s_232	11410653	7       Knight,K.L. and Sauer,R.T. (1989) DNA binding specificity of the Arc and Mnt repressors is determined by a short region of N-terminal residues.	bind
35705	4	8592	7	10	NULL	0	NULL	Mnt			bind					DNA					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2471_s_232	11410653	7       Knight,K.L. and Sauer,R.T. (1989) DNA binding specificity of the Arc and Mnt repressors is determined by a short region of N-terminal residues.	bind
46683	3	8592	7	10	NULL	0	NULL	Arc	NULL		is a type of 	NULL				repressor	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2471_s_232	11410653	7       Knight,K.L. and Sauer,R.T. (1989) DNA binding specificity of the Arc and Mnt repressors is determined by a short region of N-terminal residues.	bind
46684	2	8592	7	10	NULL	0	NULL	Mnt	NULL		is a type of 	NULL				repressor	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2471_s_232	11410653	7       Knight,K.L. and Sauer,R.T. (1989) DNA binding specificity of the Arc and Mnt repressors is determined by a short region of N-terminal residues.	bind
36382	1	8593	5	13	NULL	NULL	NULL	TFB homolog	GP	S.shibatae	bind		sequence specific			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_701_s_312	11809882	7       Qureshi,S.A. and Jackson,S.P. (1998) Sequence-specific DNA binding by the  S.shibatae TFB homolog, TFB, and its effect on promoter strength.	bind
36383	2	8593	5	13	NULL	NULL	NULL	TFB	GP		bind		sequence specifically			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_701_s_312	11809882	7       Qureshi,S.A. and Jackson,S.P. (1998) Sequence-specific DNA binding by the  S.shibatae TFB homolog, TFB, and its effect on promoter strength.	bind
35708	1	8593	7	NULL	NULL	0	NULL	TFB homolog	NULL	S.shibatae	bind	NULL	sequence-specific			DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_701_s_312	11809882	7       Qureshi,S.A. and Jackson,S.P. (1998) Sequence-specific DNA binding by the  S.shibatae TFB homolog, TFB, and its effect on promoter strength.	bind
35709	2	8593	7	NULL	NULL	0	NULL	TFB	NULL		bind	NULL	sequence-specific			DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_3_701_s_312	11809882	7       Qureshi,S.A. and Jackson,S.P. (1998) Sequence-specific DNA binding by the  S.shibatae TFB homolog, TFB, and its effect on promoter strength.	bind
36384	1	8594	5	13	NULL	NULL	NULL	Hrp1p	GP		bind									efficiency element	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3377_s_224	11504875	7       Valentini,S.R., Weiss,V.H. and Silver,P.A. (1999) Arginine methylation and binding of Hrp1p to the efficiency element for mRNA 3''-end formation.	bind
36385	2	8594	5	13	NULL	NULL	NULL	statement 1	Process		is required for					mRNA 3''-end	NucleicAcid	formation of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3377_s_224	11504875	7       Valentini,S.R., Weiss,V.H. and Silver,P.A. (1999) Arginine methylation and binding of Hrp1p to the efficiency element for mRNA 3''-end formation.	bind
36386	3	8594	5	13	NULL	NULL	NULL	arginine	AminoAcid	methylation	is required for					mRNA 3''-end	NucleicAcid	formation of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3377_s_224	11504875	7       Valentini,S.R., Weiss,V.H. and Silver,P.A. (1999) Arginine methylation and binding of Hrp1p to the efficiency element for mRNA 3''-end formation.	bind
35710	1	8594	7	10	NULL	0	NULL	Arginine		methylation of	is required for					3'' mRNA		formation of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3377_s_224	11504875	7       Valentini,S.R., Weiss,V.H. and Silver,P.A. (1999) Arginine methylation and binding of Hrp1p to the efficiency element for mRNA 3''-end formation.	bind
35711	2	8594	7	NULL	NULL	0	NULL	 Hrp1p	NULL		bind	NULL					NULL			efficiency element	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3377_s_224	11504875	7       Valentini,S.R., Weiss,V.H. and Silver,P.A. (1999) Arginine methylation and binding of Hrp1p to the efficiency element for mRNA 3''-end formation.	bind
35712	3	8594	7	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				3'' mRNA	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_16_3377_s_224	11504875	7       Valentini,S.R., Weiss,V.H. and Silver,P.A. (1999) Arginine methylation and binding of Hrp1p to the efficiency element for mRNA 3''-end formation.	bind
37635	1	8595	5	13	NULL	NULL	NULL	Pg/Pm	GP		interact with			lysine binding sites of kringle domains		ligand	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_2_517_s_18	12875972	7  Binding of Pg and Pm to a variety of cell types occurs, and principally involves interactions of the lysine binding sites of kringle domains of Pg/Pm with appropriate ligands.	bind
35715	1	8595	7	10	NULL	0	NULL	Pg/Pm	NULL		bind	NULL		 lysine binding sites of kringle domain		ligand	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_2_517_s_18	12875972	7  Binding of Pg and Pm to a variety of cell types occurs, and principally involves interactions of the lysine binding sites of kringle domains of Pg/Pm with appropriate ligands.	bind
36741	1	8596	5	13	NULL	NULL	NULL	tRA	Chemical		upregulates					CRBP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_7_1118_s_168	11451739	7  CRBP-1 upregulation is a direct transcriptional effect of tRA, mediated through the binding of retinoic acid receptor (RAR)-alpha to the CRBP-1 promoter.	bind
36742	2	8596	5	13	NULL	NULL	NULL	RAR	GP		is					retinoic acid receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_7_1118_s_168	11451739	7  CRBP-1 upregulation is a direct transcriptional effect of tRA, mediated through the binding of retinoic acid receptor (RAR)-alpha to the CRBP-1 promoter.	bind
36743	3	8596	5	13	NULL	NULL	NULL	(RAR)-alpha	GP		bind					CRBP-1 promoter	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_7_1118_s_168	11451739	7  CRBP-1 upregulation is a direct transcriptional effect of tRA, mediated through the binding of retinoic acid receptor (RAR)-alpha to the CRBP-1 promoter.	bind
36744	4	8596	5	13	NULL	NULL	NULL	statement 3	Process		mediate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_7_1118_s_168	11451739	7  CRBP-1 upregulation is a direct transcriptional effect of tRA, mediated through the binding of retinoic acid receptor (RAR)-alpha to the CRBP-1 promoter.	bind
35717	1	8596	7	NULL	NULL	0	NULL	RAR-alpha	NULL		bind	NULL				CRBP-1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_7_1118_s_168	11451739	7  CRBP-1 upregulation is a direct transcriptional effect of tRA, mediated through the binding of retinoic acid receptor (RAR)-alpha to the CRBP-1 promoter.	bind
35718	2	8596	7	NULL	NULL	0	NULL	tRA	NULL		upregulates	NULL				CRBP-1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_7_1118_s_168	11451739	7  CRBP-1 upregulation is a direct transcriptional effect of tRA, mediated through the binding of retinoic acid receptor (RAR)-alpha to the CRBP-1 promoter.	bind
35719	3	8596	7	NULL	NULL	0	NULL	statement 2	NULL		transcriptional effect	NULL	direct			tRA	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_7_1118_s_168	11451739	7  CRBP-1 upregulation is a direct transcriptional effect of tRA, mediated through the binding of retinoic acid receptor (RAR)-alpha to the CRBP-1 promoter.	bind
35720	4	8596	7	NULL	NULL	0	NULL	statement 1	NULL		mediates	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_7_1118_s_168	11451739	7  CRBP-1 upregulation is a direct transcriptional effect of tRA, mediated through the binding of retinoic acid receptor (RAR)-alpha to the CRBP-1 promoter.	bind
36738	1	8598	5	13	NULL	NULL	NULL	mucin-like proteins	GP	glycosylated	is expressed by					high endothelial venules	Cell				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_amjpathol_161_5_1607_s_16	12414509	7  In vitro, L-selectin binds to several glycosylated mucin-like proteins expressed by high endothelial venules.	bind
36739	2	8598	5	13	NULL	NULL	NULL	L-selectin	GP		bind					statement 1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_amjpathol_161_5_1607_s_16	12414509	7  In vitro, L-selectin binds to several glycosylated mucin-like proteins expressed by high endothelial venules.	bind
35721	2	8598	7	10	NULL	0	NULL	L-selectin			binds					statement 1					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_amjpathol_161_5_1607_s_16	12414509	7  In vitro, L-selectin binds to several glycosylated mucin-like proteins expressed by high endothelial venules.	bind
35722	1	8598	7	10	NULL	0	NULL	mucin-like proteins		glycosylated	is expressed by					high endothelial venules					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_amjpathol_161_5_1607_s_16	12414509	7  In vitro, L-selectin binds to several glycosylated mucin-like proteins expressed by high endothelial venules.	bind
36745	1	8599	5	13	NULL	NULL	NULL	erbB1	GP		bind		specifically			EGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
36746	2	8599	5	13	NULL	NULL	NULL	erbB1	GP		bind		specifically			EGF-like gene products	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
36749	5	8599	5	13	NULL	NULL	NULL	EGF	GP		does not interact		directly			erbB2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
36750	6	8599	5	13	NULL	NULL	NULL	EGF	GP		does not interact		directly			erbB3	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
36751	7	8599	5	13	NULL	NULL	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
36752	8	8599	5	13	NULL	NULL	NULL	EGF-like gene products	GP		does not interact		directly			erbB2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
36753	9	8599	5	13	NULL	NULL	NULL	EGF-like gene products	GP		does not interact		directly			erbB3	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
36754	10	8599	5	13	NULL	NULL	NULL	statement 8	Process		is an alternative to					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
36755	11	8599	5	13	NULL	NULL	NULL	EGF	GP		bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
36756	12	8599	5	NULL	NULL	0	NULL	statement 11	NULL		bind	NULL				erbB4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
36757	3	8599	5	13	NULL	NULL	NULL	betacellulin	GP		bind					erbB4	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
36758	4	8599	5	13	NULL	NULL	NULL	epiregulin	GP		bind					erbB4	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
35723	1	8599	7	NULL	NULL	0	NULL	EGF	NULL		bind	NULL	specifically			erbB1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
35724	2	8599	7	NULL	NULL	0	NULL	EGF-like gene products	NULL		bind	NULL	specifically			erbB1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
35725	3	8599	7	NULL	NULL	0	NULL	EGF	NULL		does not interact with	NULL	directly			erbB2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
35726	4	8599	7	NULL	NULL	0	NULL	EGF	NULL		does not interact with	NULL	directly			erbB3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
35727	5	8599	7	NULL	NULL	0	NULL	EGF-like gene products	NULL		does not interact with	NULL	directly			erbB2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
35728	6	8599	7	NULL	NULL	0	NULL	EGF-like gene products	NULL		does not interact with	NULL	directly			erbB3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
35729	7	8599	7	NULL	NULL	0	NULL	heparin	NULL		bind	NULL				EGF	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
35730	8	8599	7	10	NULL	0	NULL	betacellulin			bind					erbB4					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
35731	9	8599	7	NULL	NULL	0	NULL	epiregulin	NULL		bind	NULL				erbB4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
56474	10	8599	7	10	NULL	0	NULL	statement 3			is an alternative to					statement 4					NULL		0	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
56475	11	8599	7	10	NULL	0	NULL	statement 5			is an alternative to					statement 6					NULL		0	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
56476	12	8599	7	10	NULL	0	NULL	statement 7			bind					erbB4					NULL		0	NULL	NULL	NULL	gw60_circulationres_84_12_1380_s_18	10381889	7  Ligands that specifically bind to the erbB1, including EGF and several EGF-like gene products, do not directly interact with erbB2 or erbB3, although several recent reports have documented binding of heparin-binding EGF, betacellulin, and epiregulin to erbB4.	bind
36759	1	8600	5	13	NULL	NULL	NULL	thrombin	GP		bind					TM	GP				NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_circulationres_88_7_681_s_32	11304490	7  On endothelial cells, the inhibition of thrombin binding to TM by a monoclonal antibody 3E2, directed against the fourth EGF-like domain, 8  resulted in an increase of thrombin mitogenic effect.	bind
36760	2	8600	5	13	NULL	NULL	NULL	3E2	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_7_681_s_32	11304490	7  On endothelial cells, the inhibition of thrombin binding to TM by a monoclonal antibody 3E2, directed against the fourth EGF-like domain, 8  resulted in an increase of thrombin mitogenic effect.	bind
36761	3	8600	5	13	NULL	NULL	NULL	3E2	GP		inhibit					statement 1	Process				NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_circulationres_88_7_681_s_32	11304490	7  On endothelial cells, the inhibition of thrombin binding to TM by a monoclonal antibody 3E2, directed against the fourth EGF-like domain, 8  resulted in an increase of thrombin mitogenic effect.	bind
36762	4	8600	5	13	NULL	NULL	NULL	3E2	GP		is directed against								fourth EGF-like domain		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_7_681_s_32	11304490	7  On endothelial cells, the inhibition of thrombin binding to TM by a monoclonal antibody 3E2, directed against the fourth EGF-like domain, 8  resulted in an increase of thrombin mitogenic effect.	bind
36763	5	8600	5	13	NULL	NULL	NULL	statement 3	Process		increase					thrombin	GP	mitogenic effect of			NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_circulationres_88_7_681_s_32	11304490	7  On endothelial cells, the inhibition of thrombin binding to TM by a monoclonal antibody 3E2, directed against the fourth EGF-like domain, 8  resulted in an increase of thrombin mitogenic effect.	bind
35732	1	8600	7	NULL	NULL	0	NULL	thrombin	NULL		bind	NULL				TM	NULL				NULL	endothelial cells	0	NULL	NULL	NULL	gw60_circulationres_88_7_681_s_32	11304490	7  On endothelial cells, the inhibition of thrombin binding to TM by a monoclonal antibody 3E2, directed against the fourth EGF-like domain, 8  resulted in an increase of thrombin mitogenic effect.	bind
35733	2	8600	7	10	NULL	0	NULL	3E2			inhibits					statement 1					NULL	endothelial cells	NULL	NULL	NULL	NULL	gw60_circulationres_88_7_681_s_32	11304490	7  On endothelial cells, the inhibition of thrombin binding to TM by a monoclonal antibody 3E2, directed against the fourth EGF-like domain, 8  resulted in an increase of thrombin mitogenic effect.	bind
35734	3	8600	7	10	NULL	0	NULL	3E2			is directed against								 EGF-like domain		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_7_681_s_32	11304490	7  On endothelial cells, the inhibition of thrombin binding to TM by a monoclonal antibody 3E2, directed against the fourth EGF-like domain, 8  resulted in an increase of thrombin mitogenic effect.	bind
35735	4	8600	7	NULL	NULL	0	NULL	statement 2	NULL		increase	NULL				thrombin	NULL	mitogenic effect			NULL		0	NULL	NULL	NULL	gw60_circulationres_88_7_681_s_32	11304490	7  On endothelial cells, the inhibition of thrombin binding to TM by a monoclonal antibody 3E2, directed against the fourth EGF-like domain, 8  resulted in an increase of thrombin mitogenic effect.	bind
55814	5	8600	7	10	NULL	0	NULL	3E2			is a type of					monoclonal antibody					NULL		0	NULL	NULL	NULL	gw60_circulationres_88_7_681_s_32	11304490	7  On endothelial cells, the inhibition of thrombin binding to TM by a monoclonal antibody 3E2, directed against the fourth EGF-like domain, 8  resulted in an increase of thrombin mitogenic effect.	bind
36764	1	8601	5	13	NULL	NULL	NULL	TSP-1	GP		bind					CD36	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_13_1423_s_218	10500044	7  Our data are consistent with the observations of Dawson et al 7  but do not correlate with evidence that the CSVTCG sequence alone, responsible for binding of TSP-1 to CD36, has an effect.	bind
35736	1	8601	7	NULL	NULL	0	NULL	 TSP-1	NULL		bind	NULL				CD36	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_13_1423_s_218	10500044	7  Our data are consistent with the observations of Dawson et al 7  but do not correlate with evidence that the CSVTCG sequence alone, responsible for binding of TSP-1 to CD36, has an effect.	bind
37636	1	8602	5	13	NULL	NULL	NULL	shear stress			express					signal transduction regulating gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_334_s_23	9710127	7  The signal transduction regulating gene expression by shear stress is not exactly defined but appears to include the activation of mitogen-activated protein kinases, 8  9 10  the c-Jun NH2-terminal kinase, 11 12  and modulation of DNA-binding activities of transcription factor activator protein-1 and nuclear factor-kappaB.	bind
37637	2	8602	5	13	NULL	NULL	NULL	statement 1	GP		include		may			mitogen-activated protein kinases	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_334_s_23	9710127	7  The signal transduction regulating gene expression by shear stress is not exactly defined but appears to include the activation of mitogen-activated protein kinases, 8  9 10  the c-Jun NH2-terminal kinase, 11 12  and modulation of DNA-binding activities of transcription factor activator protein-1 and nuclear factor-kappaB.	bind
37638	3	8602	5	13	NULL	NULL	NULL	statement 1	GP		include		may			c-Jun NH2-terminal kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_334_s_23	9710127	7  The signal transduction regulating gene expression by shear stress is not exactly defined but appears to include the activation of mitogen-activated protein kinases, 8  9 10  the c-Jun NH2-terminal kinase, 11 12  and modulation of DNA-binding activities of transcription factor activator protein-1 and nuclear factor-kappaB.	bind
37639	4	8602	5	13	NULL	NULL	NULL	activator protein-1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_334_s_23	9710127	7  The signal transduction regulating gene expression by shear stress is not exactly defined but appears to include the activation of mitogen-activated protein kinases, 8  9 10  the c-Jun NH2-terminal kinase, 11 12  and modulation of DNA-binding activities of transcription factor activator protein-1 and nuclear factor-kappaB.	bind
37640	5	8602	5	13	NULL	NULL	NULL	nuclear factor-kappaB	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_334_s_23	9710127	7  The signal transduction regulating gene expression by shear stress is not exactly defined but appears to include the activation of mitogen-activated protein kinases, 8  9 10  the c-Jun NH2-terminal kinase, 11 12  and modulation of DNA-binding activities of transcription factor activator protein-1 and nuclear factor-kappaB.	bind
37641	6	8602	5	13	NULL	NULL	NULL	nuclear factor-kappaB	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_334_s_23	9710127	7  The signal transduction regulating gene expression by shear stress is not exactly defined but appears to include the activation of mitogen-activated protein kinases, 8  9 10  the c-Jun NH2-terminal kinase, 11 12  and modulation of DNA-binding activities of transcription factor activator protein-1 and nuclear factor-kappaB.	bind
37642	7	8602	5	13	NULL	NULL	NULL	activator protein-1	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_334_s_23	9710127	7  The signal transduction regulating gene expression by shear stress is not exactly defined but appears to include the activation of mitogen-activated protein kinases, 8  9 10  the c-Jun NH2-terminal kinase, 11 12  and modulation of DNA-binding activities of transcription factor activator protein-1 and nuclear factor-kappaB.	bind
37643	8	8602	5	13	NULL	NULL	NULL	statement 1	Process		include		may			statement 6	Process	modulation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_334_s_23	9710127	7  The signal transduction regulating gene expression by shear stress is not exactly defined but appears to include the activation of mitogen-activated protein kinases, 8  9 10  the c-Jun NH2-terminal kinase, 11 12  and modulation of DNA-binding activities of transcription factor activator protein-1 and nuclear factor-kappaB.	bind
37644	9	8602	5	13	NULL	NULL	NULL	statement 1	Process		include		may			statement 7	Process	modulation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_3_334_s_23	9710127	7  The signal transduction regulating gene expression by shear stress is not exactly defined but appears to include the activation of mitogen-activated protein kinases, 8  9 10  the c-Jun NH2-terminal kinase, 11 12  and modulation of DNA-binding activities of transcription factor activator protein-1 and nuclear factor-kappaB.	bind
35769	1	8602	7	NULL	NULL	0	NULL	mitogen-activated protein kinases	NULL	activation of	regulates	NULL				gene expression	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_3_334_s_23	9710127	7  The signal transduction regulating gene expression by shear stress is not exactly defined but appears to include the activation of mitogen-activated protein kinases, 8  9 10  the c-Jun NH2-terminal kinase, 11 12  and modulation of DNA-binding activities of transcription factor activator protein-1 and nuclear factor-kappaB.	bind
35770	2	8602	7	NULL	NULL	0	NULL	c-Jun NH2-terminal kinase	NULL		regulates	NULL				gene expression	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_3_334_s_23	9710127	7  The signal transduction regulating gene expression by shear stress is not exactly defined but appears to include the activation of mitogen-activated protein kinases, 8  9 10  the c-Jun NH2-terminal kinase, 11 12  and modulation of DNA-binding activities of transcription factor activator protein-1 and nuclear factor-kappaB.	bind
35771	3	8602	7	NULL	NULL	0	NULL	transcription factor activator protein-1	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_3_334_s_23	9710127	7  The signal transduction regulating gene expression by shear stress is not exactly defined but appears to include the activation of mitogen-activated protein kinases, 8  9 10  the c-Jun NH2-terminal kinase, 11 12  and modulation of DNA-binding activities of transcription factor activator protein-1 and nuclear factor-kappaB.	bind
35772	4	8602	7	NULL	NULL	0	NULL	nuclear factor-kappaB	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_3_334_s_23	9710127	7  The signal transduction regulating gene expression by shear stress is not exactly defined but appears to include the activation of mitogen-activated protein kinases, 8  9 10  the c-Jun NH2-terminal kinase, 11 12  and modulation of DNA-binding activities of transcription factor activator protein-1 and nuclear factor-kappaB.	bind
35773	5	8602	7	NULL	NULL	0	NULL	statement 3	NULL	modulation of	regulates	NULL				gene expression	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_3_334_s_23	9710127	7  The signal transduction regulating gene expression by shear stress is not exactly defined but appears to include the activation of mitogen-activated protein kinases, 8  9 10  the c-Jun NH2-terminal kinase, 11 12  and modulation of DNA-binding activities of transcription factor activator protein-1 and nuclear factor-kappaB.	bind
35774	6	8602	7	NULL	NULL	0	NULL	statement 4	NULL	modulation of	regulates	NULL				gene expression	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_3_334_s_23	9710127	7  The signal transduction regulating gene expression by shear stress is not exactly defined but appears to include the activation of mitogen-activated protein kinases, 8  9 10  the c-Jun NH2-terminal kinase, 11 12  and modulation of DNA-binding activities of transcription factor activator protein-1 and nuclear factor-kappaB.	bind
36765	1	8603	5	13	NULL	NULL	NULL	macrophage	Cell		uptake					CRP - LDL complexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_29	15692104	7 - 11     However, macrophage uptake of CRP - LDL complexes might be increased by subsequent binding of CRP to Fcgamma receptors.	bind
36766	2	8603	5	13	NULL	NULL	NULL	CRP	GP		bind					Fcgamma receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_29	15692104	7 - 11     However, macrophage uptake of CRP - LDL complexes might be increased by subsequent binding of CRP to Fcgamma receptors.	bind
36767	3	8603	5	13	NULL	NULL	NULL	statement 2	Process		increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_29	15692104	7 - 11     However, macrophage uptake of CRP - LDL complexes might be increased by subsequent binding of CRP to Fcgamma receptors.	bind
35737	1	8603	7	NULL	NULL	0	NULL	CRP	NULL		bind	NULL				Fcgamma receptors	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_29	15692104	7 - 11     However, macrophage uptake of CRP - LDL complexes might be increased by subsequent binding of CRP to Fcgamma receptors.	bind
35738	2	8603	7	10	NULL	0	NULL	macrophage			uptake					 CRP - LDL complexes					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_29	15692104	7 - 11     However, macrophage uptake of CRP - LDL complexes might be increased by subsequent binding of CRP to Fcgamma receptors.	bind
56152	3	8603	7	10	NULL	0	NULL	statement 1			increase					statement 2					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_4_717_s_29	15692104	7 - 11     However, macrophage uptake of CRP - LDL complexes might be increased by subsequent binding of CRP to Fcgamma receptors.	bind
36768	1	8604	5	13	NULL	NULL	NULL	immunoglobulin	GP		neutralize					microbial toxin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1604_s_226	7664447	7 13 14  This rapid effect in such children may be due to the neutralization of a microbial toxin by immunoglobulin, which acts as a superantigen that binds nonspecifically to major histocompatibility class II molecules or to certain viable regions of the T-cell - antigen receptor.	bind
36769	2	8604	5	13	NULL	NULL	NULL	immunoglobulin	GP		act as					superantigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1604_s_226	7664447	7 13 14  This rapid effect in such children may be due to the neutralization of a microbial toxin by immunoglobulin, which acts as a superantigen that binds nonspecifically to major histocompatibility class II molecules or to certain viable regions of the T-cell - antigen receptor.	bind
36770	3	8604	5	13	NULL	NULL	NULL	immunoglobulin	GP		bind		nonspecifically			major histocompatibility class II molecules	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1604_s_226	7664447	7 13 14  This rapid effect in such children may be due to the neutralization of a microbial toxin by immunoglobulin, which acts as a superantigen that binds nonspecifically to major histocompatibility class II molecules or to certain viable regions of the T-cell - antigen receptor.	bind
36771	4	8604	5	13	NULL	NULL	NULL	immunoglobulin	GP		bind		nonspecifically			T-cell - antigen receptor	GP	viable regions of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1604_s_226	7664447	7 13 14  This rapid effect in such children may be due to the neutralization of a microbial toxin by immunoglobulin, which acts as a superantigen that binds nonspecifically to major histocompatibility class II molecules or to certain viable regions of the T-cell - antigen receptor.	bind
35739	1	8604	7	NULL	NULL	0	NULL	immunoglobulin	NULL		neutralizes	NULL				microbial toxin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_6_1604_s_226	7664447	7 13 14  This rapid effect in such children may be due to the neutralization of a microbial toxin by immunoglobulin, which acts as a superantigen that binds nonspecifically to major histocompatibility class II molecules or to certain viable regions of the T-cell - antigen receptor.	bind
35740	2	8604	7	NULL	NULL	0	NULL	immunoglobulin	NULL		acts as a 	NULL				superantigen	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_92_6_1604_s_226	7664447	7 13 14  This rapid effect in such children may be due to the neutralization of a microbial toxin by immunoglobulin, which acts as a superantigen that binds nonspecifically to major histocompatibility class II molecules or to certain viable regions of the T-cell - antigen receptor.	bind
35741	3	8604	7	NULL	NULL	0	NULL	immunoglobulin	NULL		binds	NULL	nonspecifically			 major histocompatibility class II molecules	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1604_s_226	7664447	7 13 14  This rapid effect in such children may be due to the neutralization of a microbial toxin by immunoglobulin, which acts as a superantigen that binds nonspecifically to major histocompatibility class II molecules or to certain viable regions of the T-cell - antigen receptor.	bind
35742	4	8604	7	10	NULL	0	NULL	immunoglobulin			binds		nonspecifically			T-cell - antigen receptor		viable regions of 			NULL		NULL	NULL	NULL	NULL	gw60_circulation_92_6_1604_s_226	7664447	7 13 14  This rapid effect in such children may be due to the neutralization of a microbial toxin by immunoglobulin, which acts as a superantigen that binds nonspecifically to major histocompatibility class II molecules or to certain viable regions of the T-cell - antigen receptor.	bind
36772	1	8605	5	13	NULL	NULL	NULL	GP IIb/IIa	GP		bind					vWF	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_5_925_s_27	9157957	7 8  GP IIb/IIa binds to vWF after activation, leading to platelet spreading and aggregation at sites of injury.	bind
36773	2	8605	5	13	NULL	NULL	NULL	statement 1	Process		occurs after					activation	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_5_925_s_27	9157957	7 8  GP IIb/IIa binds to vWF after activation, leading to platelet spreading and aggregation at sites of injury.	bind
36774	3	8605	5	13	NULL	NULL	NULL	statement 1	Process		leads to					platelet spreading	Process				NULL	sites of injury	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_5_925_s_27	9157957	7 8  GP IIb/IIa binds to vWF after activation, leading to platelet spreading and aggregation at sites of injury.	bind
36775	4	8605	5	13	NULL	NULL	NULL	statement 1	Process		leads to					platelet aggregation	Process				NULL	sites of injury	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_5_925_s_27	9157957	7 8  GP IIb/IIa binds to vWF after activation, leading to platelet spreading and aggregation at sites of injury.	bind
35743	1	8605	7	NULL	NULL	0	NULL	GP IIb/IIa	NULL		binds to	NULL				vWF	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_5_925_s_27	9157957	7 8  GP IIb/IIa binds to vWF after activation, leading to platelet spreading and aggregation at sites of injury.	bind
35744	2	8605	7	NULL	NULL	0	NULL	statement 1	NULL		occurs after	NULL				activation	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_5_925_s_27	9157957	7 8  GP IIb/IIa binds to vWF after activation, leading to platelet spreading and aggregation at sites of injury.	bind
35745	3	8605	7	10	NULL	0	NULL	statement 1	NULL		leads to	NULL				platelet spreading	NULL				NULL	sites of injury	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_5_925_s_27	9157957	7 8  GP IIb/IIa binds to vWF after activation, leading to platelet spreading and aggregation at sites of injury.	bind
35746	4	8605	7	10	NULL	0	NULL	statement 1	NULL		leads to	NULL				aggregation	NULL				NULL	sites of injury	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_5_925_s_27	9157957	7 8  GP IIb/IIa binds to vWF after activation, leading to platelet spreading and aggregation at sites of injury.	bind
36776	1	8606	5	13	NULL	NULL	NULL	ERs	GP		bind					17beta-estradiol	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_15_1792_s_24	10769279	7 8  The 2 ERs have a similar affinity for 17beta-estradiol, and they bind to the same estrogen response elements (EREs).	bind
36777	2	8606	5	13	NULL	NULL	NULL	ERs	GP		bind									EREs	NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_15_1792_s_24	10769279	7 8  The 2 ERs have a similar affinity for 17beta-estradiol, and they bind to the same estrogen response elements (EREs).	bind
36778	3	8606	5	13	NULL	NULL	NULL	EREs	GP		is					estrogen response elements	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_15_1792_s_24	10769279	7 8  The 2 ERs have a similar affinity for 17beta-estradiol, and they bind to the same estrogen response elements (EREs).	bind
35749	1	8606	7	10	NULL	0	NULL	ER	NULL		bind	NULL				17beta-estradiol	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_15_1792_s_24	10769279	7 8  The 2 ERs have a similar affinity for 17beta-estradiol, and they bind to the same estrogen response elements (EREs).	bind
35750	2	8606	7	NULL	NULL	0	NULL	ERs	NULL		bind	NULL					NULL			EREs	NULL		0	NULL	NULL	NULL	gw60_circulation_101_15_1792_s_24	10769279	7 8  The 2 ERs have a similar affinity for 17beta-estradiol, and they bind to the same estrogen response elements (EREs).	bind
35751	3	8606	7	NULL	NULL	0	NULL	EREs	NULL		is	NULL				estrogen response elements	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_101_15_1792_s_24	10769279	7 8  The 2 ERs have a similar affinity for 17beta-estradiol, and they bind to the same estrogen response elements (EREs).	bind
36779	1	8607	5	13	NULL	NULL	NULL	PDGF	GP		is secreted as					PDGF-AA	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
36780	2	8607	5	13	NULL	NULL	NULL	PDGF	GP		is secreted as					PDGF-BB	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
36781	3	8607	5	13	NULL	NULL	NULL	PDGF	GP		is secreted as					PDGF-AB	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
36782	4	8607	5	13	NULL	NULL	NULL	PDGF-AA	GP		bind					PDGFR-alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
36783	5	8607	5	13	NULL	NULL	NULL	PDGF-AA	GP		bind					PDGFR-beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
36784	6	8607	5	13	NULL	NULL	NULL	PDGF-AB	GP		bind					PDGFR-alpha 	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
56468	7	8607	5	13	NULL	NULL	NULL	PDGF-AB	GP		bind					PDGFR-beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
56469	8	8607	5	13	NULL	NULL	NULL	PDGF-BB	GP		bind					PDGFR-alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
56470	9	8607	5	13	NULL	NULL	NULL	PDGF-BB	GP		bind					PDGFR-beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
56471	10	8607	5	13	NULL	NULL	NULL	PDGFR-alpha	GP		homodimerize with					PDGFR-alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
56472	11	8607	5	13	NULL	NULL	NULL	PDGFR-beta	GP		homodimerize with					PDGFR-beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
56473	12	8607	5	13	NULL	NULL	NULL	PDGFR-alpha	GP		heterodimerize with					PDGFR-beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
35752	1	8607	7	NULL	NULL	0	NULL	PDGF-AA	NULL		binds to	NULL				PDGFR-alpha	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
35753	2	8607	7	NULL	NULL	0	NULL	PDGF-AA	NULL		binds to	NULL				PDGFR-beta	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
35754	3	8607	7	NULL	NULL	0	NULL	PDGF-AB	NULL		binds to	NULL				 PDGFR-alpha	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
35755	4	8607	7	NULL	NULL	0	NULL	PDGF-AB	NULL		binds to	NULL				PDGFR-beta	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
35756	5	8607	7	NULL	NULL	0	NULL	PDGF-BB	NULL		binds to	NULL				PDGFR-alpha	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
35757	6	8607	7	NULL	NULL	0	NULL	PDGF-BB	NULL		binds to	NULL				PDGFR-beta	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
35758	7	8607	7	10	NULL	0	NULL	PDGFR-alpha			 homodimerize with					PDGFR-alpha					NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
35759	8	8607	7	10	NULL	0	NULL	PDGFR-beta			homodimerize with					PDGFR-beta					NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
35760	9	8607	7	10	NULL	0	NULL	PDGFR-alpha			heterodimerize with					PDGFR-beta					NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_11_1330_s_19	10982551	7 8 9 10  PDGF is secreted as 3 different isoforms: PDGF-AA, -AB, and -BB, and binds to 2 distinct subtype receptors, PDGFR-alpha and -beta, which can form homodimers and heterodimers.	bind
36785	1	8608	5	13	NULL	NULL	NULL	calcineurin	GP	activated	bind					NFAT	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1531_s_28	16675727	7 Activated calcineurin binds and dephosphorylates NFAT, which then translocates to the nucleus to activate cells and induce cytokine expression.	bind
36786	2	8608	5	13	NULL	NULL	NULL	statement 1	GP		dephosphorylates					NFAT	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1531_s_28	16675727	7 Activated calcineurin binds and dephosphorylates NFAT, which then translocates to the nucleus to activate cells and induce cytokine expression.	bind
36787	3	8608	5	13	NULL	NULL	NULL	statement 1	GP		is translocated to					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1531_s_28	16675727	7 Activated calcineurin binds and dephosphorylates NFAT, which then translocates to the nucleus to activate cells and induce cytokine expression.	bind
36788	4	8608	5	13	NULL	NULL	NULL	statement 3	GP		activates					cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1531_s_28	16675727	7 Activated calcineurin binds and dephosphorylates NFAT, which then translocates to the nucleus to activate cells and induce cytokine expression.	bind
36789	5	8608	5	13	NULL	NULL	NULL	statement 4	Process		induce					cytokine	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1531_s_28	16675727	7 Activated calcineurin binds and dephosphorylates NFAT, which then translocates to the nucleus to activate cells and induce cytokine expression.	bind
35761	1	8608	7	NULL	NULL	0	NULL	calcineurin	NULL	activated	binds	NULL				NFAT	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1531_s_28	16675727	7 Activated calcineurin binds and dephosphorylates NFAT, which then translocates to the nucleus to activate cells and induce cytokine expression.	bind
35762	2	8608	7	NULL	NULL	0	NULL	statement 1	NULL		dephosphorylates	NULL				NFAT	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1531_s_28	16675727	7 Activated calcineurin binds and dephosphorylates NFAT, which then translocates to the nucleus to activate cells and induce cytokine expression.	bind
35763	3	8608	7	NULL	NULL	0	NULL	NFAT	NULL		translocate to	NULL				nucleus	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1531_s_28	16675727	7 Activated calcineurin binds and dephosphorylates NFAT, which then translocates to the nucleus to activate cells and induce cytokine expression.	bind
35764	4	8608	7	NULL	NULL	0	NULL	statement 3	NULL		activates	NULL				cells	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1531_s_28	16675727	7 Activated calcineurin binds and dephosphorylates NFAT, which then translocates to the nucleus to activate cells and induce cytokine expression.	bind
35765	5	8608	7	NULL	NULL	0	NULL	statement 4	NULL		induce	NULL				cytokine expression	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_7_1531_s_28	16675727	7 Activated calcineurin binds and dephosphorylates NFAT, which then translocates to the nucleus to activate cells and induce cytokine expression.	bind
37645	1	8609	5	13	NULL	NULL	NULL	vancomycin	Chemical		bind					cell wall	CellComponent	pre-existing;; modified			NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_43_6_846_s_23	10404328	7 All of these alterations produce a so-called ``trapping effect'' , whereby increased amounts of vancomycin are bound to the pre-existing modified cell wall, thus reducing the amount of drug that reaches its vital targets --  the lipid II precursors of new cell-wall synthesis which are found in the outer leaflet of the cytoplasmic membrane beneath the pre-existing cell wall.	bind
37646	2	8609	5	13	NULL	NULL	NULL	vancomycin	Chemical		reaches					lipid II precursors	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_43_6_846_s_23	10404328	7 All of these alterations produce a so-called ``trapping effect'' , whereby increased amounts of vancomycin are bound to the pre-existing modified cell wall, thus reducing the amount of drug that reaches its vital targets --  the lipid II precursors of new cell-wall synthesis which are found in the outer leaflet of the cytoplasmic membrane beneath the pre-existing cell wall.	bind
37647	3	8609	5	13	NULL	NULL	NULL	lipid II precursors	Chemical		is a type of					vital drug targets	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_43_6_846_s_23	10404328	7 All of these alterations produce a so-called ``trapping effect'' , whereby increased amounts of vancomycin are bound to the pre-existing modified cell wall, thus reducing the amount of drug that reaches its vital targets --  the lipid II precursors of new cell-wall synthesis which are found in the outer leaflet of the cytoplasmic membrane beneath the pre-existing cell wall.	bind
37648	4	8609	5	13	NULL	NULL	NULL	lipid II precursors	Chemical		is present in					cytoplasmic membrane	CellComponent	outer leaflet of			NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_43_6_846_s_23	10404328	7 All of these alterations produce a so-called ``trapping effect'' , whereby increased amounts of vancomycin are bound to the pre-existing modified cell wall, thus reducing the amount of drug that reaches its vital targets --  the lipid II precursors of new cell-wall synthesis which are found in the outer leaflet of the cytoplasmic membrane beneath the pre-existing cell wall.	bind
37649	5	8609	5	13	NULL	NULL	NULL	statement 1	Process	increased amounts of	reduces					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_43_6_846_s_23	10404328	7 All of these alterations produce a so-called ``trapping effect'' , whereby increased amounts of vancomycin are bound to the pre-existing modified cell wall, thus reducing the amount of drug that reaches its vital targets --  the lipid II precursors of new cell-wall synthesis which are found in the outer leaflet of the cytoplasmic membrane beneath the pre-existing cell wall.	bind
35766	1	8609	7	10	NULL	0	NULL	vancomycin			bind					 cell wall		pre-existing;; modified			NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_43_6_846_s_23	10404328	7 All of these alterations produce a so-called ``trapping effect'' , whereby increased amounts of vancomycin are bound to the pre-existing modified cell wall, thus reducing the amount of drug that reaches its vital targets --  the lipid II precursors of new cell-wall synthesis which are found in the outer leaflet of the cytoplasmic membrane beneath the pre-existing cell wall.	bind
35767	2	8609	7	NULL	NULL	0	NULL	lipid II precursors	NULL		is found in the	NULL				cytoplasmic membrane	NULL	outer leaflet of 			NULL		0	NULL	NULL	NULL	gw60_jantimicrobchemoth_43_6_846_s_23	10404328	7 All of these alterations produce a so-called ``trapping effect'' , whereby increased amounts of vancomycin are bound to the pre-existing modified cell wall, thus reducing the amount of drug that reaches its vital targets --  the lipid II precursors of new cell-wall synthesis which are found in the outer leaflet of the cytoplasmic membrane beneath the pre-existing cell wall.	bind
35768	3	8609	7	10	NULL	0	NULL	vancomycin			reaches					lipid II precursors					NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_43_6_846_s_23	10404328	7 All of these alterations produce a so-called ``trapping effect'' , whereby increased amounts of vancomycin are bound to the pre-existing modified cell wall, thus reducing the amount of drug that reaches its vital targets --  the lipid II precursors of new cell-wall synthesis which are found in the outer leaflet of the cytoplasmic membrane beneath the pre-existing cell wall.	bind
56153	4	8609	7	10	NULL	0	NULL	statement 1		increased amounts of	reduces					statement 2					NULL		0	NULL	NULL	NULL	gw60_jantimicrobchemoth_43_6_846_s_23	10404328	7 All of these alterations produce a so-called ``trapping effect'' , whereby increased amounts of vancomycin are bound to the pre-existing modified cell wall, thus reducing the amount of drug that reaches its vital targets --  the lipid II precursors of new cell-wall synthesis which are found in the outer leaflet of the cytoplasmic membrane beneath the pre-existing cell wall.	bind
56155	5	8609	7	10	NULL	0	NULL	lipid II precursors			is a type of					vital drug targets					NULL		0	NULL	NULL	NULL	gw60_jantimicrobchemoth_43_6_846_s_23	10404328	7 All of these alterations produce a so-called ``trapping effect'' , whereby increased amounts of vancomycin are bound to the pre-existing modified cell wall, thus reducing the amount of drug that reaches its vital targets --  the lipid II precursors of new cell-wall synthesis which are found in the outer leaflet of the cytoplasmic membrane beneath the pre-existing cell wall.	bind
36790	1	8611	5	13	NULL	NULL	NULL	BNP	GP		bind					NPR-A	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
36791	2	8611	5	13	NULL	NULL	NULL	NPR-A	GP		is					natriuretic peptide receptor-A	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
36792	3	8611	5	13	NULL	NULL	NULL	NPR-A	GP		is a type of					membrane-bound receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
36793	4	8611	5	13	NULL	NULL	NULL	NPR-A	GP		is located on					cardiomyocytes	Cell				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
36795	9	8611	5	13	NULL	NULL	NULL	cGMP	Chemical		is a type of					second messenger	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
36796	5	8611	5	13	NULL	NULL	NULL	NPR-A	GP		is located on					vascular endothelium	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
36798	6	8611	5	13	NULL	NULL	NULL	NPR-A	GP		is located on					smooth muscle	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
36800	7	8611	5	13	NULL	NULL	NULL	NPR-A	GP		is located on					kidneys	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
36801	10	8611	5	13	NULL	NULL	NULL	statement 1	Process		activates					cGMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
36802	8	8611	5	13	NULL	NULL	NULL	NPR-A	GP		is located on					lungs	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
35918	1	8611	7	NULL	NULL	0	NULL	BNP	NULL		binds to	NULL				NPR-A	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
35919	2	8611	7	NULL	NULL	0	NULL	NPR-A	NULL		is	NULL				natriuretic peptide receptor-A	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
35920	3	8611	7	NULL	NULL	0	NULL	NPR-A	NULL		is a type of	NULL				membrane-bound receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
35921	4	8611	7	NULL	NULL	0	NULL	NPR-A	NULL		is located on 	NULL				cardiomyocytes	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
35922	5	8611	7	NULL	NULL	0	NULL	NPR-A	NULL		is located on	NULL				vascular endothelium	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
35923	6	8611	7	NULL	NULL	0	NULL	NPR-A	NULL		is located on	NULL				smooth muscle	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
35924	7	8611	7	NULL	NULL	0	NULL	NPR-A	NULL		is located on	NULL				kidneys	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
35925	8	8611	7	NULL	NULL	0	NULL	NPR-A	NULL		is located on	NULL				lungs	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
35926	9	8611	7	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				cGMP	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
35927	10	8611	7	NULL	NULL	0	NULL	cGMP	NULL		is a type of	NULL				second messenger	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_112_6_836_s_26	16061734	7 BNP binds to the natriuretic peptide receptor-A (NPR-A), which is a membrane-bound receptor located on cardiomyocytes, vascular endothelium, smooth muscle, kidneys, and lungs, resulting in activation of its second messenger, cGMP.	bind
36803	1	8612	5	13	NULL	NULL	NULL	ES	Chemical		bind					KDR	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
36804	2	8612	5	13	NULL	NULL	NULL	KDR	GP		is					kinase - inserted domain-containing receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
36805	3	8612	5	13	NULL	NULL	NULL	KDR	GP		is a type of					VEGF receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
36806	4	8612	5	13	NULL	NULL	NULL	statement 1	Process		block					MAPK	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
36807	5	8612	5	13	NULL	NULL	NULL	statement 1	Process		block					MAPK	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
36808	6	8612	5	13	NULL	NULL	NULL	MAPK	GP		is					mitogen-activated protein kinase	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
36809	7	8612	5	13	NULL	NULL	NULL	VEGF	GP		induce					migration	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
36810	8	8612	5	13	NULL	NULL	NULL	VEGF	GP		induce					proliferation	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
36811	9	8612	5	13	NULL	NULL	NULL	MAPK	GP	activation of	inhibit					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
36812	10	8612	5	13	NULL	NULL	NULL	MAPK	GP	activation of	inhibit					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
35928	1	8612	7	NULL	NULL	0	NULL	ES	NULL		bind	NULL				KDR	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
35929	2	8612	7	10	NULL	0	NULL	statement 1			blocks					MAPK		phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
35930	3	8612	7	NULL	NULL	0	NULL	statement 1	NULL		blocks	NULL				MAPK	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
35931	4	8612	7	NULL	NULL	0	NULL	VEGF	NULL		induce	NULL				migration	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
35932	5	8612	7	NULL	NULL	0	NULL	VEGF	NULL		induce	NULL				proliferation	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
35933	6	8612	7	10	NULL	0	NULL	MAPK		activation of	inhibits					statement 4					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
35934	7	8612	7	10	NULL	0	NULL	MAPK		activation of	inhibits					statement 5					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
35935	8	8612	7	NULL	NULL	0	NULL	KDR	NULL		is	NULL				VEGF receptor kinase - inserted domain-containing receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
56477	9	8612	7	10	NULL	0	NULL	MAPK			is 					mitogen-activated protein kinase					NULL		0	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
56478	10	8612	7	10	NULL	0	NULL	KDR			is a type of					VEGF receptor					NULL		0	NULL	NULL	NULL	gw70_circulationres_98_9_1203_s_25	16574906	7 ES was found to bind to the VEGF receptor kinase - inserted domain-containing receptor (KDR), thereby blocking tyrosine phosphorylation and the activation of mitogen-activated protein kinase (MAPK), which leads to an inhibition of VEGF-induced migration and proliferation.	bind
36813	1	8613	5	13	NULL	NULL	NULL	Trx1	GP	reduced form of	bind					ASK1	GP		N-terminal		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1483_s_39	15117824	7 Interestingly, only the reduced form of Trx1 binds to the N-terminal part of ASK1 and blocks activation of ASK1 by TNF. 7,9  Neither the oxidized form (intramolecular disulfide between C32 and C35) nor the redox-inactive form (the double-mutation at catalytic sites C32 and C35) of Trx1 binds to ASK1.	bind
36814	2	8613	5	13	NULL	NULL	NULL	ASK1	GP		is activated by					TNF	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1483_s_39	15117824	7 Interestingly, only the reduced form of Trx1 binds to the N-terminal part of ASK1 and blocks activation of ASK1 by TNF. 7,9  Neither the oxidized form (intramolecular disulfide between C32 and C35) nor the redox-inactive form (the double-mutation at catalytic sites C32 and C35) of Trx1 binds to ASK1.	bind
36815	3	8613	5	13	NULL	NULL	NULL	statement 1	Process		block					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1483_s_39	15117824	7 Interestingly, only the reduced form of Trx1 binds to the N-terminal part of ASK1 and blocks activation of ASK1 by TNF. 7,9  Neither the oxidized form (intramolecular disulfide between C32 and C35) nor the redox-inactive form (the double-mutation at catalytic sites C32 and C35) of Trx1 binds to ASK1.	bind
36816	4	8613	5	13	NULL	NULL	NULL	Trx1	GP	oxidized form	does not bind					ASK1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1483_s_39	15117824	7 Interestingly, only the reduced form of Trx1 binds to the N-terminal part of ASK1 and blocks activation of ASK1 by TNF. 7,9  Neither the oxidized form (intramolecular disulfide between C32 and C35) nor the redox-inactive form (the double-mutation at catalytic sites C32 and C35) of Trx1 binds to ASK1.	bind
36817	5	8613	5	13	NULL	NULL	NULL	Trx1	GP	redox-inactive form	does not bind					ASK1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1483_s_39	15117824	7 Interestingly, only the reduced form of Trx1 binds to the N-terminal part of ASK1 and blocks activation of ASK1 by TNF. 7,9  Neither the oxidized form (intramolecular disulfide between C32 and C35) nor the redox-inactive form (the double-mutation at catalytic sites C32 and C35) of Trx1 binds to ASK1.	bind
36818	6	8613	5	13	NULL	NULL	NULL	Trx1	GP	oxidized form	contains							intramolecular disulfide between	C32 and C35		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1483_s_39	15117824	7 Interestingly, only the reduced form of Trx1 binds to the N-terminal part of ASK1 and blocks activation of ASK1 by TNF. 7,9  Neither the oxidized form (intramolecular disulfide between C32 and C35) nor the redox-inactive form (the double-mutation at catalytic sites C32 and C35) of Trx1 binds to ASK1.	bind
36819	7	8613	5	13	NULL	NULL	NULL	Trx1	GP	redox-inactive form	contains							double-mutation at	catalytic sites C32;;C35		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1483_s_39	15117824	7 Interestingly, only the reduced form of Trx1 binds to the N-terminal part of ASK1 and blocks activation of ASK1 by TNF. 7,9  Neither the oxidized form (intramolecular disulfide between C32 and C35) nor the redox-inactive form (the double-mutation at catalytic sites C32 and C35) of Trx1 binds to ASK1.	bind
35936	1	8613	7	NULL	NULL	0	NULL	Trx1	NULL	reduced	binds to	NULL				ASK1	NULL		 N-terminal part		NULL		0	NULL	NULL	NULL	gw70_circulationres_94_11_1483_s_39	15117824	7 Interestingly, only the reduced form of Trx1 binds to the N-terminal part of ASK1 and blocks activation of ASK1 by TNF. 7,9  Neither the oxidized form (intramolecular disulfide between C32 and C35) nor the redox-inactive form (the double-mutation at catalytic sites C32 and C35) of Trx1 binds to ASK1.	bind
35937	2	8613	7	NULL	NULL	0	NULL	TNF	NULL		activates	NULL				ASK1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_11_1483_s_39	15117824	7 Interestingly, only the reduced form of Trx1 binds to the N-terminal part of ASK1 and blocks activation of ASK1 by TNF. 7,9  Neither the oxidized form (intramolecular disulfide between C32 and C35) nor the redox-inactive form (the double-mutation at catalytic sites C32 and C35) of Trx1 binds to ASK1.	bind
35938	3	8613	7	NULL	NULL	0	NULL	statement 1	NULL		blocks	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_11_1483_s_39	15117824	7 Interestingly, only the reduced form of Trx1 binds to the N-terminal part of ASK1 and blocks activation of ASK1 by TNF. 7,9  Neither the oxidized form (intramolecular disulfide between C32 and C35) nor the redox-inactive form (the double-mutation at catalytic sites C32 and C35) of Trx1 binds to ASK1.	bind
35939	4	8613	7	NULL	NULL	0	NULL	Trx1	NULL	Oxidized form	does not bind	NULL				ASK1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_11_1483_s_39	15117824	7 Interestingly, only the reduced form of Trx1 binds to the N-terminal part of ASK1 and blocks activation of ASK1 by TNF. 7,9  Neither the oxidized form (intramolecular disulfide between C32 and C35) nor the redox-inactive form (the double-mutation at catalytic sites C32 and C35) of Trx1 binds to ASK1.	bind
35940	5	8613	7	NULL	NULL	0	NULL	Trx1	NULL	 redox-inactive form	does not bind	NULL				ASK1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_11_1483_s_39	15117824	7 Interestingly, only the reduced form of Trx1 binds to the N-terminal part of ASK1 and blocks activation of ASK1 by TNF. 7,9  Neither the oxidized form (intramolecular disulfide between C32 and C35) nor the redox-inactive form (the double-mutation at catalytic sites C32 and C35) of Trx1 binds to ASK1.	bind
35941	6	8613	7	10	NULL	0	NULL	Trx1	NULL	oxidized form	contains	NULL				C32 and C35	NULL	intramolecular disulfide between			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1483_s_39	15117824	7 Interestingly, only the reduced form of Trx1 binds to the N-terminal part of ASK1 and blocks activation of ASK1 by TNF. 7,9  Neither the oxidized form (intramolecular disulfide between C32 and C35) nor the redox-inactive form (the double-mutation at catalytic sites C32 and C35) of Trx1 binds to ASK1.	bind
35942	7	8613	7	10	NULL	0	NULL	Trx1	NULL	oxidized form	contains	NULL				C32 and C35	NULL	double-mutation at catalytic sites			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_11_1483_s_39	15117824	7 Interestingly, only the reduced form of Trx1 binds to the N-terminal part of ASK1 and blocks activation of ASK1 by TNF. 7,9  Neither the oxidized form (intramolecular disulfide between C32 and C35) nor the redox-inactive form (the double-mutation at catalytic sites C32 and C35) of Trx1 binds to ASK1.	bind
36820	1	8614	5	13	NULL	NULL	NULL	Msx-1	GP		contains				promoter	Msx-1	GP			consensus binding sites	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_36_22667_s_260	9278425	7 Msx-1 promoter itself contains two  Msx-1 consensus binding sites and the binding of  Msx-1 homeodomain polypeptide to the predicted  Msx-1 motif was previously demonstrated ( 43).	bind
36821	2	8614	5	13	NULL	NULL	NULL	Msx-1 homeodomain polypeptide	GP		bind					Msx-1 motif	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_36_22667_s_260	9278425	7 Msx-1 promoter itself contains two  Msx-1 consensus binding sites and the binding of  Msx-1 homeodomain polypeptide to the predicted  Msx-1 motif was previously demonstrated ( 43).	bind
35943	1	8614	7	NULL	NULL	0	NULL	Msx-1	NULL		contains	NULL			promoter	Msx-1	NULL		consensus binding sites		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_36_22667_s_260	9278425	7 Msx-1 promoter itself contains two  Msx-1 consensus binding sites and the binding of  Msx-1 homeodomain polypeptide to the predicted  Msx-1 motif was previously demonstrated ( 43).	bind
35944	2	8614	7	NULL	NULL	0	NULL	Msx-1 homeodomain polypeptide	NULL		binds to	NULL				predicted Msx-1	NULL		motif		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_36_22667_s_260	9278425	7 Msx-1 promoter itself contains two  Msx-1 consensus binding sites and the binding of  Msx-1 homeodomain polypeptide to the predicted  Msx-1 motif was previously demonstrated ( 43).	bind
36822	1	8615	5	13	NULL	NULL	NULL	Pepf gene	GP		is expressed in					ZCs	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36823	2	8615	5	13	NULL	NULL	NULL	Pepf	GP		is					pepsinogen F	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36824	3	8615	5	13	NULL	NULL	NULL	Cckar gene	GP		is expressed in					ZCs	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36825	4	8615	5	13	NULL	NULL	NULL	Cckar	GP		is					cholecystokinin receptor A	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36826	5	8615	5	13	NULL	NULL	NULL	Cckar	GP		bind					cholecystokinin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36827	6	8615	5	13	NULL	NULL	NULL	Cckar	GP		regulates					pepsinogen	GP	secretion of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36828	7	8615	5	13	NULL	NULL	NULL	Amy2 gene	GP		is expressed in					ZCs	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36829	8	8615	5	13	NULL	NULL	NULL	Amy2	GP		is					alpha-amylase	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36830	9	8615	5	13	NULL	NULL	NULL	Try2/4 gene	GP		is expressed in					ZCs	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36831	10	8615	5	13	NULL	NULL	NULL	Try2/4	GP		is					trypsin 2/4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36832	11	8615	5	13	NULL	NULL	NULL	Gif gene	GP		is expressed in					ZCs	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36833	12	8615	5	13	NULL	NULL	NULL	Gif	GP		is					gastric intrinsic factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36834	13	8615	5	13	NULL	NULL	NULL	Anpep gene	GP		is expressed in					ZCs	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36835	14	8615	5	13	NULL	NULL	NULL	Anpep	GP		is					alanyl aminopeptidase N	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36836	15	8615	5	13	NULL	NULL	NULL	Anpep	GP		also known as					CD13	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36837	16	8615	5	13	NULL	NULL	NULL	Anpep	GP		is a type of					metalloproteinase	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36838	17	8615	5	13	NULL	NULL	NULL	Anpep	GP		is present in					ZC vesicles	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36839	18	8615	5	13	NULL	NULL	NULL	Spp1 gene	GP		is expressed in					ZCs	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36840	19	8615	5	13	NULL	NULL	NULL	Spp1	GP		is					secreted phosphoprotein 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36841	20	8615	5	13	NULL	NULL	NULL	Spp1	GP		also known as					osteopontin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36842	21	8615	5	13	NULL	NULL	NULL	Spp1	GP		is a type of					adhesive glycoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36843	22	8615	5	13	NULL	NULL	NULL	Spp1	GP		is implicated in					mucosal barrier function	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35945	1	8615	7	NULL	NULL	0	NULL	Pepf 	NULL		is	NULL				pepsinogen F	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35946	3	8615	7	NULL	NULL	0	NULL	cholecystokinin	NULL		bind	NULL				cholecystokinin receptor A	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35947	4	8615	7	NULL	NULL	0	NULL	statement 2	NULL		regulates	NULL				pepsinogen 	NULL	secretion of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35949	2	8615	7	NULL	NULL	0	NULL	Pepf	NULL		is expressed in	NULL				ZCs	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35950	5	8615	7	NULL	NULL	0	NULL	Cckar	NULL		is	NULL				cholecystokinin receptor A	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35951	6	8615	7	NULL	NULL	0	NULL	Cckar	NULL		is expressed in	NULL				ZCs	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35952	7	8615	7	NULL	NULL	0	NULL	Amy2	NULL		is	NULL				alpha-amylase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35953	8	8615	7	NULL	NULL	0	NULL	Amy2	NULL		is expressed in	NULL				ZCs	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35954	9	8615	7	NULL	NULL	0	NULL	Try2/4 	NULL		is	NULL				trypsin 2/4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35955	10	8615	7	NULL	NULL	0	NULL	Try2/4 	NULL		is expressed in	NULL				ZCs	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35956	11	8615	7	NULL	NULL	0	NULL	Gif	NULL		is	NULL				gastric intrinsic factor	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35957	12	8615	7	NULL	NULL	0	NULL	Gif	NULL		is involved in	NULL				cobalamin	NULL	intestinal absorption of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35958	13	8615	7	NULL	NULL	0	NULL	Gif	NULL		is expressed in	NULL				ZCs	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35959	14	8615	7	NULL	NULL	0	NULL	Anpep 	NULL		is	NULL				alanyl aminopeptidase N	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35960	15	8615	7	NULL	NULL	0	NULL	Anpep	NULL		is known as	NULL				CD13	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35961	16	8615	7	NULL	NULL	0	NULL	Anpep	NULL		is a type of	NULL				metalloproteinase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35962	17	8615	7	NULL	NULL	0	NULL	Anpep	NULL		is found in	NULL				ZC vesicles	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35963	18	8615	7	NULL	NULL	0	NULL	Spp1 	NULL		is	NULL				secreted phosphoprotein 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35964	19	8615	7	NULL	NULL	0	NULL	Spp1 	NULL		is also known as	NULL				osteopontin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35974	20	8615	7	NULL	NULL	0	NULL	Spp1	NULL		is a type of	NULL				adhesive glycoprotein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35976	21	8615	7	NULL	NULL	0	NULL	Spp1	NULL		is implicated in	NULL				mucosal barrier function	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
35978	22	8615	7	NULL	NULL	0	NULL	Spp1	NULL		is expressed in	NULL				ZCs	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46138_s_135	12963718	7 of the 12 genes were known to be expressed in ZCs:  Pepf (pepsinogen F, see Ref.  );  Cckar (cholecystokinin receptor A, binds cholecystokinin and is involved in regulating pepsinogen secretion) ( );  Amy2 (alpha-amylase);  Try2/4 (trypsin 2/4);  Gif (gastric intrinsic factor, intestinal absorption of cobalamin);  Anpep (alanyl aminopeptidase N, also known as CD13, a metalloproteinase found in ZC vesicles, see Ref.  ); and  Spp1 (secreted phosphoprotein 1 or osteopontin, an adhesive glycoprotein implicated in mucosal barrier function, Ref.  ).	bind
36844	1	8616	5	13	NULL	NULL	NULL	Rab3A	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_3_889_s_15	12937130	7 Rabphilin-3A binds to Rab3A only in its GTP-bound state, and the complex is required for the correct docking of synaptic vesicles to their target membrane.	bind
36845	2	8616	5	13	NULL	NULL	NULL	Rabphilin-3A	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_3_889_s_15	12937130	7 Rabphilin-3A binds to Rab3A only in its GTP-bound state, and the complex is required for the correct docking of synaptic vesicles to their target membrane.	bind
36846	3	8616	5	13	NULL	NULL	NULL	synaptic vesicles	OrganismPart		is docked to					target membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_3_889_s_15	12937130	7 Rabphilin-3A binds to Rab3A only in its GTP-bound state, and the complex is required for the correct docking of synaptic vesicles to their target membrane.	bind
36847	4	8616	5	13	NULL	NULL	NULL	statement 2	Process		is required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_3_889_s_15	12937130	7 Rabphilin-3A binds to Rab3A only in its GTP-bound state, and the complex is required for the correct docking of synaptic vesicles to their target membrane.	bind
35986	1	8616	7	10	NULL	0	NULL	Rab3A			bind					GTP					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_3_889_s_15	12937130	7 Rabphilin-3A binds to Rab3A only in its GTP-bound state, and the complex is required for the correct docking of synaptic vesicles to their target membrane.	bind
35987	2	8616	7	10	NULL	0	NULL	Rabphilin-3A			bind					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_3_889_s_15	12937130	7 Rabphilin-3A binds to Rab3A only in its GTP-bound state, and the complex is required for the correct docking of synaptic vesicles to their target membrane.	bind
35988	3	8616	7	NULL	NULL	0	NULL	synaptic vesicles	NULL		docked to	NULL				target membrane	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_163_3_889_s_15	12937130	7 Rabphilin-3A binds to Rab3A only in its GTP-bound state, and the complex is required for the correct docking of synaptic vesicles to their target membrane.	bind
35991	4	8616	7	NULL	NULL	0	NULL	statement 1	NULL		is required for	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_163_3_889_s_15	12937130	7 Rabphilin-3A binds to Rab3A only in its GTP-bound state, and the complex is required for the correct docking of synaptic vesicles to their target membrane.	bind
36848	1	8617	5	13	NULL	NULL	NULL	RWJ-54428	Chemical		is a type of					parenteral cephalosporin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_5_845_s_48	12003982	7 RWJ-54428 is a parenteral cephalosporin that binds PBP2'' in staphylococci 5 and shows  in vitro activity against other Gram-positive bacteria, as well as  Haemophilus influenzae and  Moraxella catarrhalis.	bind
36849	2	8617	5	13	NULL	NULL	NULL	RWJ-54428	Chemical		bind					PBP2''	GP	staphylococci			NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_5_845_s_48	12003982	7 RWJ-54428 is a parenteral cephalosporin that binds PBP2'' in staphylococci 5 and shows  in vitro activity against other Gram-positive bacteria, as well as  Haemophilus influenzae and  Moraxella catarrhalis.	bind
36850	3	8617	5	13	NULL	NULL	NULL	RWJ-54428	Chemical		is active against					Gram-positive bacteria	Organism				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_5_845_s_48	12003982	7 RWJ-54428 is a parenteral cephalosporin that binds PBP2'' in staphylococci 5 and shows  in vitro activity against other Gram-positive bacteria, as well as  Haemophilus influenzae and  Moraxella catarrhalis.	bind
36851	4	8617	5	13	NULL	NULL	NULL	RWJ-54428	Chemical		is active against					Haemophilus influenzae	Organism				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_5_845_s_48	12003982	7 RWJ-54428 is a parenteral cephalosporin that binds PBP2'' in staphylococci 5 and shows  in vitro activity against other Gram-positive bacteria, as well as  Haemophilus influenzae and  Moraxella catarrhalis.	bind
36852	5	8617	5	13	NULL	NULL	NULL	RWJ-54428	Chemical		is active against					Moraxella catarrhalis	Organism				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_5_845_s_48	12003982	7 RWJ-54428 is a parenteral cephalosporin that binds PBP2'' in staphylococci 5 and shows  in vitro activity against other Gram-positive bacteria, as well as  Haemophilus influenzae and  Moraxella catarrhalis.	bind
35996	1	8617	7	NULL	NULL	0	NULL	RWJ-54428	NULL		is a type of	NULL				parenteral cephalosporin	NULL				NULL		0	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_5_845_s_48	12003982	7 RWJ-54428 is a parenteral cephalosporin that binds PBP2'' in staphylococci 5 and shows  in vitro activity against other Gram-positive bacteria, as well as  Haemophilus influenzae and  Moraxella catarrhalis.	bind
35998	2	8617	7	10	NULL	0	NULL	RWJ-54428	NULL		binds	NULL				PBP2	NULL	staphylococci			NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_5_845_s_48	12003982	7 RWJ-54428 is a parenteral cephalosporin that binds PBP2'' in staphylococci 5 and shows  in vitro activity against other Gram-positive bacteria, as well as  Haemophilus influenzae and  Moraxella catarrhalis.	bind
36000	3	8617	7	10	NULL	0	NULL	RWJ-54428			is active against					Gram-positive bacteria					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_5_845_s_48	12003982	7 RWJ-54428 is a parenteral cephalosporin that binds PBP2'' in staphylococci 5 and shows  in vitro activity against other Gram-positive bacteria, as well as  Haemophilus influenzae and  Moraxella catarrhalis.	bind
36001	4	8617	7	10	NULL	0	NULL	RWJ-54428			is active against					Haemophilus influenzae					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_5_845_s_48	12003982	7 RWJ-54428 is a parenteral cephalosporin that binds PBP2'' in staphylococci 5 and shows  in vitro activity against other Gram-positive bacteria, as well as  Haemophilus influenzae and  Moraxella catarrhalis.	bind
36002	5	8617	7	10	NULL	0	NULL	RWJ-54428			is active against					Moraxella catarrhalis					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_49_5_845_s_48	12003982	7 RWJ-54428 is a parenteral cephalosporin that binds PBP2'' in staphylococci 5 and shows  in vitro activity against other Gram-positive bacteria, as well as  Haemophilus influenzae and  Moraxella catarrhalis.	bind
36853	1	8618	5	13	NULL	NULL	NULL	WGA	GP		bind					alveolar epithelium	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_54_4_761_s_122	15329364	7 Sustained release of drugs upon administration of nebulized WGA-coated PLG-NPs indicates the binding of WGA on the alveolar epithelium.	bind
36003	1	8618	7	NULL	NULL	0	NULL	WGA	NULL		bind	NULL				alveolar epithelium	NULL				NULL		0	NULL	NULL	NULL	gw70_jantimicrobchemoth_54_4_761_s_122	15329364	7 Sustained release of drugs upon administration of nebulized WGA-coated PLG-NPs indicates the binding of WGA on the alveolar epithelium.	bind
37060	1	8619	5	13	NULL	NULL	NULL				bind		high affinity	extracellular domain of alpha subunit		PDGF-A chain	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2395_s_27	9409207	7 The extracellular domain of the alpha subunit binds both PDGF-A and -B chains with high affinity, whereas the beta subunit binds only the B-chain specifically.	bind
37061	2	8619	5	13	NULL	NULL	NULL				bind		high affinity	extracellular domain of alpha subunit		PDGF-B chain	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2395_s_27	9409207	7 The extracellular domain of the alpha subunit binds both PDGF-A and -B chains with high affinity, whereas the beta subunit binds only the B-chain specifically.	bind
37062	3	8619	5	13	NULL	NULL	NULL				bind		specifically	beta subunit		PDGF-B chain	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2395_s_27	9409207	7 The extracellular domain of the alpha subunit binds both PDGF-A and -B chains with high affinity, whereas the beta subunit binds only the B-chain specifically.	bind
36004	1	8619	7	NULL	NULL	0	NULL		NULL		bind	NULL	high affinity	extracellular domain of the alpha subunit 		PDGF	NULL		A chain		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2395_s_27	9409207	7 The extracellular domain of the alpha subunit binds both PDGF-A and -B chains with high affinity, whereas the beta subunit binds only the B-chain specifically.	bind
36005	2	8619	7	NULL	NULL	0	NULL		NULL		bind	NULL	high affinity	extracellular domain of the alpha subunit		PDGF	NULL		B chain		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2395_s_27	9409207	7 The extracellular domain of the alpha subunit binds both PDGF-A and -B chains with high affinity, whereas the beta subunit binds only the B-chain specifically.	bind
36006	3	8619	7	NULL	NULL	0	NULL		NULL		bind	NULL	specifically	beta subunit		B-chain	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2395_s_27	9409207	7 The extracellular domain of the alpha subunit binds both PDGF-A and -B chains with high affinity, whereas the beta subunit binds only the B-chain specifically.	bind
37063	1	8621	5	13	NULL	NULL	NULL	Chk1	GP	exogenous	bind					chromatin	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_27_25207_s_209	12676962	7 Therefore,  the amount of exogenous Chk1 bound to the chromatin argues against a  Chk1-EYFP-Chk1 dimer mechanism.	bind
36007	1	8621	7	NULL	NULL	0	NULL	Chk1	NULL	exogenous	bind	NULL				chromatin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_27_25207_s_209	12676962	7 Therefore,  the amount of exogenous Chk1 bound to the chromatin argues against a  Chk1-EYFP-Chk1 dimer mechanism.	bind
37705	1	8622	5	13	NULL	NULL	NULL	negatively charged groove	GP		attracts					positively charged surface	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18849_s_130	9228061	7 This negatively charged groove could attract the positively charged surface formed by the putative adenylyl cyclase binding region of Gsalpha (alpha2/beta4 (switch 2), alpha3/beta5, and alpha4/beta6) ( 13,  14,  17) (Fig.  6,  B and  C).	bind
37706	2	8622	5	13	NULL	NULL	NULL	positively charged surface	GP		is formed by					Gsalpha	GP	putative 	adenylyl cyclase binding region		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18849_s_130	9228061	7 This negatively charged groove could attract the positively charged surface formed by the putative adenylyl cyclase binding region of Gsalpha (alpha2/beta4 (switch 2), alpha3/beta5, and alpha4/beta6) ( 13,  14,  17) (Fig.  6,  B and  C).	bind
36008	1	8622	7	10	NULL	0	NULL	positively charged surface			is formed by					Gsalpha		putative	adenylyl cyclase binding region		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18849_s_130	9228061	7 This negatively charged groove could attract the positively charged surface formed by the putative adenylyl cyclase binding region of Gsalpha (alpha2/beta4 (switch 2), alpha3/beta5, and alpha4/beta6) ( 13,  14,  17) (Fig.  6,  B and  C).	bind
46812	2	8622	7	10	NULL	0	NULL	 negatively charged groove 			attracts					positively charged surface					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18849_s_130	9228061	7 This negatively charged groove could attract the positively charged surface formed by the putative adenylyl cyclase binding region of Gsalpha (alpha2/beta4 (switch 2), alpha3/beta5, and alpha4/beta6) ( 13,  14,  17) (Fig.  6,  B and  C).	bind
37065	1	8623	5	13	NULL	NULL	NULL	TIMPs	GP		bind					MMPs	GP	activated			NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_9_1166_s_266	15723986	7 TIMPs bind with activated MMPs in a 1:1 stoichiometric ratio and inhibit proteolytic activity.	bind
37066	2	8623	5	13	NULL	NULL	NULL	statement 1	GP		inhibit					proteolytic activity	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_111_9_1166_s_266	15723986	7 TIMPs bind with activated MMPs in a 1:1 stoichiometric ratio and inhibit proteolytic activity.	bind
36011	1	8623	7	NULL	NULL	0	NULL	TIMPs	NULL		bind	NULL				MMPs	NULL	activated			NULL		0	NULL	NULL	NULL	gw70_circulation_111_9_1166_s_266	15723986	7 TIMPs bind with activated MMPs in a 1:1 stoichiometric ratio and inhibit proteolytic activity.	bind
36012	2	8623	7	NULL	NULL	0	NULL	statement 1	NULL		inhibit	NULL				proteolytic activity	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_111_9_1166_s_266	15723986	7 TIMPs bind with activated MMPs in a 1:1 stoichiometric ratio and inhibit proteolytic activity.	bind
37067	1	8624	5	13	NULL	NULL	NULL	VWF	GP		is					von Willebrand factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_26	12171801	7 We also tested the effects of the agent known to block von Willebrand factor (VWF) binding to platelet GP Ibalpha, which was reported to play crucial roles in platelet thrombus formation at sites exposed to high shear stress, 18 -  22 on platelet accumulation around stents.	bind
37068	2	8624	5	13	NULL	NULL	NULL	VWF	GP		bind					GP Ibalpha	GP	platelet			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_26	12171801	7 We also tested the effects of the agent known to block von Willebrand factor (VWF) binding to platelet GP Ibalpha, which was reported to play crucial roles in platelet thrombus formation at sites exposed to high shear stress, 18 -  22 on platelet accumulation around stents.	bind
36013	1	8624	7	10	NULL	0	NULL	VWF			bind					GP Ibalpha		platelet			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_26	12171801	7 We also tested the effects of the agent known to block von Willebrand factor (VWF) binding to platelet GP Ibalpha, which was reported to play crucial roles in platelet thrombus formation at sites exposed to high shear stress, 18 -  22 on platelet accumulation around stents.	bind
36014	2	8624	7	10	NULL	0	NULL	VWF			is					von Willebrand factor					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_8_1360_s_26	12171801	7 We also tested the effects of the agent known to block von Willebrand factor (VWF) binding to platelet GP Ibalpha, which was reported to play crucial roles in platelet thrombus formation at sites exposed to high shear stress, 18 -  22 on platelet accumulation around stents.	bind
37069	1	8625	5	13	NULL	NULL	NULL	dynamin	GP		bind		specifically			EHSH1	GP		C-terminal SH3 domains		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_26_18446_s_299	10373452	7) Binding of dynamin to EHSH1 was specific for three of the five C-terminal SH3 domains.	bind
36019	1	8625	7	10	NULL	0	NULL	dynamin 			bind		specifically			EHSH1			C-terminal SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_26_18446_s_299	10373452	7) Binding of dynamin to EHSH1 was specific for three of the five C-terminal SH3 domains.	bind
37070	1	8626	5	13	NULL	NULL	NULL	caveolin-1	GP		bind					eNOS	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_8_866_s_22	11988487	7, 12 -  16 With this in mind, a reasonable working model is that caveolin-1 binding to eNOS renders it less active.	bind
37071	2	8626	5	13	NULL	NULL	NULL	caveolin-1	GP		is rendered					less active	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_8_866_s_22	11988487	7, 12 -  16 With this in mind, a reasonable working model is that caveolin-1 binding to eNOS renders it less active.	bind
37072	3	8626	5	13	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_8_866_s_22	11988487	7, 12 -  16 With this in mind, a reasonable working model is that caveolin-1 binding to eNOS renders it less active.	bind
36029	1	8626	7	NULL	NULL	0	NULL	caveolin-1	NULL		bind	NULL				eNOS	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_8_866_s_22	11988487	7, 12 -  16 With this in mind, a reasonable working model is that caveolin-1 binding to eNOS renders it less active.	bind
36035	2	8626	7	NULL	NULL	0	NULL	eNOS	NULL		become	NULL				less active	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_8_866_s_22	11988487	7, 12 -  16 With this in mind, a reasonable working model is that caveolin-1 binding to eNOS renders it less active.	bind
36037	3	8626	7	NULL	NULL	0	NULL	statement 2	NULL		occurs upon	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_8_866_s_22	11988487	7, 12 -  16 With this in mind, a reasonable working model is that caveolin-1 binding to eNOS renders it less active.	bind
37073	1	8627	5	13	NULL	NULL	NULL	VEGF-C	GP		bind					VEGFR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_893_s_17	11549582	7, 14  However, VEGF-C also binds VEGFR-2 (KDR), that is mainly expressed by activated endothelium of blood vessels, suggesting a potential function of VEGF-C in the induction of angiogenesis.	bind
37074	2	8627	5	13	NULL	NULL	NULL	VEGFR-2	GP		also known as					KDR	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_893_s_17	11549582	7, 14  However, VEGF-C also binds VEGFR-2 (KDR), that is mainly expressed by activated endothelium of blood vessels, suggesting a potential function of VEGF-C in the induction of angiogenesis.	bind
37075	3	8627	5	13	NULL	NULL	NULL	VEGFR-2	GP		is expressed by					endothelium of blood vessels	Cell	activated			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_893_s_17	11549582	7, 14  However, VEGF-C also binds VEGFR-2 (KDR), that is mainly expressed by activated endothelium of blood vessels, suggesting a potential function of VEGF-C in the induction of angiogenesis.	bind
37076	4	8627	5	13	NULL	NULL	NULL	VEGF-C	GP		induce		potentially			angiogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_893_s_17	11549582	7, 14  However, VEGF-C also binds VEGFR-2 (KDR), that is mainly expressed by activated endothelium of blood vessels, suggesting a potential function of VEGF-C in the induction of angiogenesis.	bind
37077	5	8627	5	13	NULL	NULL	NULL	statement 1	Process		suggest					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_3_893_s_17	11549582	7, 14  However, VEGF-C also binds VEGFR-2 (KDR), that is mainly expressed by activated endothelium of blood vessels, suggesting a potential function of VEGF-C in the induction of angiogenesis.	bind
36042	1	8627	7	NULL	NULL	0	NULL	VEGF-C	NULL		binds	NULL				KDR	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_893_s_17	11549582	7, 14  However, VEGF-C also binds VEGFR-2 (KDR), that is mainly expressed by activated endothelium of blood vessels, suggesting a potential function of VEGF-C in the induction of angiogenesis.	bind
36045	2	8627	7	NULL	NULL	0	NULL	KDR	NULL		is expressed in	NULL				endothelium of blood vessels	NULL	activated			NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_893_s_17	11549582	7, 14  However, VEGF-C also binds VEGFR-2 (KDR), that is mainly expressed by activated endothelium of blood vessels, suggesting a potential function of VEGF-C in the induction of angiogenesis.	bind
36047	3	8627	7	NULL	NULL	0	NULL	VEGF-C	NULL		induce	NULL				angiogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_893_s_17	11549582	7, 14  However, VEGF-C also binds VEGFR-2 (KDR), that is mainly expressed by activated endothelium of blood vessels, suggesting a potential function of VEGF-C in the induction of angiogenesis.	bind
36048	4	8627	7	NULL	NULL	0	NULL	statement 1	NULL		suggests	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_893_s_17	11549582	7, 14  However, VEGF-C also binds VEGFR-2 (KDR), that is mainly expressed by activated endothelium of blood vessels, suggesting a potential function of VEGF-C in the induction of angiogenesis.	bind
36049	5	8627	7	NULL	NULL	0	NULL	KDR	NULL		is	NULL				VEGFR-2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_3_893_s_17	11549582	7, 14  However, VEGF-C also binds VEGFR-2 (KDR), that is mainly expressed by activated endothelium of blood vessels, suggesting a potential function of VEGF-C in the induction of angiogenesis.	bind
37078	1	8629	5	13	NULL	NULL	NULL	CRP	GP		bind					E-LDL	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_15_1870_s_162	15037531	7,8  CRP bound to E-LDL probably tempers terminal complement activation via the same mechanisms that have previously been delineated in other systems.	bind
37079	2	8629	5	13	NULL	NULL	NULL	statement 1	Process		temper					terminal complement	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_circulation_109_15_1870_s_162	15037531	7,8  CRP bound to E-LDL probably tempers terminal complement activation via the same mechanisms that have previously been delineated in other systems.	bind
36052	1	8629	7	NULL	NULL	0	NULL	CRP 	NULL		bind	NULL				E-LDL	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_109_15_1870_s_162	15037531	7,8  CRP bound to E-LDL probably tempers terminal complement activation via the same mechanisms that have previously been delineated in other systems.	bind
36053	2	8629	7	NULL	NULL	0	NULL	statement 1	NULL		tempers	NULL				complement	NULL	activation of	terminal		NULL		0	NULL	NULL	NULL	gw70_circulation_109_15_1870_s_162	15037531	7,8  CRP bound to E-LDL probably tempers terminal complement activation via the same mechanisms that have previously been delineated in other systems.	bind
37080	1	8630	5	13	NULL	NULL	NULL	cdk	GP		bind					cyclin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_5_501_s_21	12600884	7,8 Binding of the cdk to its specific cyclin leads to partial kinase activity, but full activity occurs only after phosphorylation by the cdk activating kinase (CAK).	bind
37081	2	8630	5	13	NULL	NULL	NULL	cdk	GP		exhibits					kinase activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_5_501_s_21	12600884	7,8 Binding of the cdk to its specific cyclin leads to partial kinase activity, but full activity occurs only after phosphorylation by the cdk activating kinase (CAK).	bind
37082	3	8630	5	13	NULL	NULL	NULL	CAK	GP		is					cdk activating kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_5_501_s_21	12600884	7,8 Binding of the cdk to its specific cyclin leads to partial kinase activity, but full activity occurs only after phosphorylation by the cdk activating kinase (CAK).	bind
37218	4	8630	5	13	NULL	NULL	NULL	CAK	GP		phosphorylate					cdk	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_5_501_s_21	12600884	7,8 Binding of the cdk to its specific cyclin leads to partial kinase activity, but full activity occurs only after phosphorylation by the cdk activating kinase (CAK).	bind
37219	5	8630	5	13	NULL	NULL	NULL	statement 4	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_5_501_s_21	12600884	7,8 Binding of the cdk to its specific cyclin leads to partial kinase activity, but full activity occurs only after phosphorylation by the cdk activating kinase (CAK).	bind
46711	6	8630	5	13	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process	partial			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_5_501_s_21	12600884	7,8 Binding of the cdk to its specific cyclin leads to partial kinase activity, but full activity occurs only after phosphorylation by the cdk activating kinase (CAK).	bind
36054	1	8630	7	NULL	NULL	0	NULL	 cdk	NULL		bind	NULL				cyclin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_5_501_s_21	12600884	7,8 Binding of the cdk to its specific cyclin leads to partial kinase activity, but full activity occurs only after phosphorylation by the cdk activating kinase (CAK).	bind
36055	2	8630	7	10	NULL	0	NULL	cdk	NULL		exhibits	NULL				kinase activity	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_5_501_s_21	12600884	7,8 Binding of the cdk to its specific cyclin leads to partial kinase activity, but full activity occurs only after phosphorylation by the cdk activating kinase (CAK).	bind
36056	3	8630	7	10	NULL	0	NULL	CAK	NULL		phosphorylate	NULL				Cdk	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_5_501_s_21	12600884	7,8 Binding of the cdk to its specific cyclin leads to partial kinase activity, but full activity occurs only after phosphorylation by the cdk activating kinase (CAK).	bind
36057	4	8630	7	10	NULL	0	NULL	statement 3	NULL		leads to	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_92_5_501_s_21	12600884	7,8 Binding of the cdk to its specific cyclin leads to partial kinase activity, but full activity occurs only after phosphorylation by the cdk activating kinase (CAK).	bind
36058	5	8630	7	NULL	NULL	0	NULL	CAK	NULL		is	NULL				cdk activating kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_92_5_501_s_21	12600884	7,8 Binding of the cdk to its specific cyclin leads to partial kinase activity, but full activity occurs only after phosphorylation by the cdk activating kinase (CAK).	bind
46713	6	8630	7	10	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 2	NULL	partial			NULL		0	NULL	NULL	NULL	gw60_circulationres_92_5_501_s_21	12600884	7,8 Binding of the cdk to its specific cyclin leads to partial kinase activity, but full activity occurs only after phosphorylation by the cdk activating kinase (CAK).	bind
37220	1	8631	5	13	NULL	NULL	NULL	BPDE-I	Chemical		is					7,8-Dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_21_4_629_s_4	10753196	7,8-Dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[ apyrene(BPDE-I), an ultimate carcinogenic form of B[ aP, was covalently bound to triglyceride (TG).	bind
37221	2	8631	5	13	NULL	NULL	NULL	BPDE-I	Chemical		is a type of					ultimate carcinogenic form of B[a]P	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_21_4_629_s_4	10753196	7,8-Dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[ apyrene(BPDE-I), an ultimate carcinogenic form of B[ aP, was covalently bound to triglyceride (TG).	bind
37222	3	8631	5	13	NULL	NULL	NULL	BPDE-I	GP		bind		covalently			TG	GP				NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_21_4_629_s_4	10753196	7,8-Dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[ apyrene(BPDE-I), an ultimate carcinogenic form of B[ aP, was covalently bound to triglyceride (TG).	bind
37223	4	8631	5	13	NULL	NULL	NULL	TG	Chemical		is					triglyceride	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_21_4_629_s_4	10753196	7,8-Dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[ apyrene(BPDE-I), an ultimate carcinogenic form of B[ aP, was covalently bound to triglyceride (TG).	bind
36059	1	8631	7	NULL	NULL	0	NULL	BPDE-I	NULL		bind	NULL	covalently			TG	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_21_4_629_s_4	10753196	7,8-Dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[ apyrene(BPDE-I), an ultimate carcinogenic form of B[ aP, was covalently bound to triglyceride (TG).	bind
36060	2	8631	7	NULL	NULL	0	NULL	BPDE-I	NULL		is	NULL				7,8-Dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[ apyrene	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_21_4_629_s_4	10753196	7,8-Dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[ apyrene(BPDE-I), an ultimate carcinogenic form of B[ aP, was covalently bound to triglyceride (TG).	bind
36061	3	8631	7	NULL	NULL	0	NULL	TG	NULL		is	NULL				triglyceride 	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_21_4_629_s_4	10753196	7,8-Dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[ apyrene(BPDE-I), an ultimate carcinogenic form of B[ aP, was covalently bound to triglyceride (TG).	bind
36062	4	8631	7	NULL	NULL	0	NULL	BPDE-I	NULL		is a type of	NULL				 carcinogenic form of B[ aP	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_21_4_629_s_4	10753196	7,8-Dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[ apyrene(BPDE-I), an ultimate carcinogenic form of B[ aP, was covalently bound to triglyceride (TG).	bind
37224	1	8632	5	13	NULL	NULL	NULL	7,8-S-OctaF7	Chemical		complex with					FGFR2IIIb	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21052_s_94	16728399	7,8-S-OctaF7 forms complexes with FGFR2IIIb that bind FGF7 to form FGF7-(7,8-S-OctaF7)-FGFR2IIIb complexes with high specificity and specific activity relative to octasaccharides with lower affinity for FGF7 ( ).	bind
37225	2	8632	5	13	NULL	NULL	NULL	statement 1	GP		bind					FGF7	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21052_s_94	16728399	7,8-S-OctaF7 forms complexes with FGFR2IIIb that bind FGF7 to form FGF7-(7,8-S-OctaF7)-FGFR2IIIb complexes with high specificity and specific activity relative to octasaccharides with lower affinity for FGF7 ( ).	bind
37226	3	8632	5	13	NULL	NULL	NULL	statement 2	GP		forms		high specificity			FGF7-(7,8-S-OctaF7)-FGFR2IIIb complexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21052_s_94	16728399	7,8-S-OctaF7 forms complexes with FGFR2IIIb that bind FGF7 to form FGF7-(7,8-S-OctaF7)-FGFR2IIIb complexes with high specificity and specific activity relative to octasaccharides with lower affinity for FGF7 ( ).	bind
37227	4	8632	5	13	NULL	NULL	NULL	FGF7-(7,8-S-OctaF7)-FGFR2IIIb complexes	GP	specific activity of	is relative to					octasaccharides	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21052_s_94	16728399	7,8-S-OctaF7 forms complexes with FGFR2IIIb that bind FGF7 to form FGF7-(7,8-S-OctaF7)-FGFR2IIIb complexes with high specificity and specific activity relative to octasaccharides with lower affinity for FGF7 ( ).	bind
37228	5	8632	5	13	NULL	NULL	NULL	octasaccharides	Chemical		affinity for		less			FGF7	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21052_s_94	16728399	7,8-S-OctaF7 forms complexes with FGFR2IIIb that bind FGF7 to form FGF7-(7,8-S-OctaF7)-FGFR2IIIb complexes with high specificity and specific activity relative to octasaccharides with lower affinity for FGF7 ( ).	bind
36063	1	8632	7	NULL	NULL	0	NULL	7,8-S-OctaF7	NULL		complex with	NULL				FGFR2IIIb	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21052_s_94	16728399	7,8-S-OctaF7 forms complexes with FGFR2IIIb that bind FGF7 to form FGF7-(7,8-S-OctaF7)-FGFR2IIIb complexes with high specificity and specific activity relative to octasaccharides with lower affinity for FGF7 ( ).	bind
36064	2	8632	7	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				FGF7	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21052_s_94	16728399	7,8-S-OctaF7 forms complexes with FGFR2IIIb that bind FGF7 to form FGF7-(7,8-S-OctaF7)-FGFR2IIIb complexes with high specificity and specific activity relative to octasaccharides with lower affinity for FGF7 ( ).	bind
36065	3	8632	7	NULL	NULL	0	NULL	statement 2	NULL		forms	NULL	high specificity			FGF7-(7,8-S-OctaF7)-FGFR2IIIb complexes 	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21052_s_94	16728399	7,8-S-OctaF7 forms complexes with FGFR2IIIb that bind FGF7 to form FGF7-(7,8-S-OctaF7)-FGFR2IIIb complexes with high specificity and specific activity relative to octasaccharides with lower affinity for FGF7 ( ).	bind
36066	4	8632	7	NULL	NULL	0	NULL	octasaccharides 	NULL		affinity for	NULL	less			FGF7	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21052_s_94	16728399	7,8-S-OctaF7 forms complexes with FGFR2IIIb that bind FGF7 to form FGF7-(7,8-S-OctaF7)-FGFR2IIIb complexes with high specificity and specific activity relative to octasaccharides with lower affinity for FGF7 ( ).	bind
36067	5	8632	7	NULL	NULL	0	NULL	statement 3	NULL		occurs with	NULL				specific activity	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21052_s_94	16728399	7,8-S-OctaF7 forms complexes with FGFR2IIIb that bind FGF7 to form FGF7-(7,8-S-OctaF7)-FGFR2IIIb complexes with high specificity and specific activity relative to octasaccharides with lower affinity for FGF7 ( ).	bind
37229	1	8633	5	13	NULL	NULL	NULL	ATP	Chemical		bind					P2Y receptors	GP				NULL	endothelium	NULL	NULL	NULL	NULL	gw70_circulationres_96_2_189_s_25	15604418	7,9  The released ATP then binds to P2Y receptors on the endothelium and stimulates vasodilatation by the release of nitric oxide (NO), prostaglandins, 2 and endothelium-derived hyperpolarizing factor (EDHF).	bind
37230	2	8633	5	13	NULL	NULL	NULL	statement 1	Process		stimulate					vasodilatation	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_189_s_25	15604418	7,9  The released ATP then binds to P2Y receptors on the endothelium and stimulates vasodilatation by the release of nitric oxide (NO), prostaglandins, 2 and endothelium-derived hyperpolarizing factor (EDHF).	bind
37231	3	8633	5	13	NULL	NULL	NULL	statement 2	Process		occurs by					NO	Chemical	release of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_189_s_25	15604418	7,9  The released ATP then binds to P2Y receptors on the endothelium and stimulates vasodilatation by the release of nitric oxide (NO), prostaglandins, 2 and endothelium-derived hyperpolarizing factor (EDHF).	bind
37232	4	8633	5	13	NULL	NULL	NULL	NO	Chemical		is					nitric oxide	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_189_s_25	15604418	7,9  The released ATP then binds to P2Y receptors on the endothelium and stimulates vasodilatation by the release of nitric oxide (NO), prostaglandins, 2 and endothelium-derived hyperpolarizing factor (EDHF).	bind
37233	5	8633	5	13	NULL	NULL	NULL	statement 2	Process		occurs by					prostaglandins	Chemical	release of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_189_s_25	15604418	7,9  The released ATP then binds to P2Y receptors on the endothelium and stimulates vasodilatation by the release of nitric oxide (NO), prostaglandins, 2 and endothelium-derived hyperpolarizing factor (EDHF).	bind
37234	6	8633	5	13	NULL	NULL	NULL	statement 2	Process		occurs by					EDHF	GP	release of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_189_s_25	15604418	7,9  The released ATP then binds to P2Y receptors on the endothelium and stimulates vasodilatation by the release of nitric oxide (NO), prostaglandins, 2 and endothelium-derived hyperpolarizing factor (EDHF).	bind
37235	7	8633	5	13	NULL	NULL	NULL	EDHF	GP		is					endothelium-derived hyperpolarizing factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_189_s_25	15604418	7,9  The released ATP then binds to P2Y receptors on the endothelium and stimulates vasodilatation by the release of nitric oxide (NO), prostaglandins, 2 and endothelium-derived hyperpolarizing factor (EDHF).	bind
36069	1	8633	7	NULL	NULL	0	NULL	ATP	NULL		binds	NULL				P2Y receptors	NULL				NULL	endothelium	0	NULL	NULL	NULL	gw70_circulationres_96_2_189_s_25	15604418	7,9  The released ATP then binds to P2Y receptors on the endothelium and stimulates vasodilatation by the release of nitric oxide (NO), prostaglandins, 2 and endothelium-derived hyperpolarizing factor (EDHF).	bind
36070	2	8633	7	NULL	NULL	0	NULL	statement 1	NULL		stimulates	NULL				vasodilatation	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_2_189_s_25	15604418	7,9  The released ATP then binds to P2Y receptors on the endothelium and stimulates vasodilatation by the release of nitric oxide (NO), prostaglandins, 2 and endothelium-derived hyperpolarizing factor (EDHF).	bind
36071	3	8633	7	NULL	NULL	0	NULL	statement 2	NULL		occurs by	NULL				NO	NULL	release of			NULL		0	NULL	NULL	NULL	gw70_circulationres_96_2_189_s_25	15604418	7,9  The released ATP then binds to P2Y receptors on the endothelium and stimulates vasodilatation by the release of nitric oxide (NO), prostaglandins, 2 and endothelium-derived hyperpolarizing factor (EDHF).	bind
36072	4	8633	7	NULL	NULL	0	NULL	statement 2	NULL		occurs by	NULL				prostaglandins	NULL	release of			NULL		0	NULL	NULL	NULL	gw70_circulationres_96_2_189_s_25	15604418	7,9  The released ATP then binds to P2Y receptors on the endothelium and stimulates vasodilatation by the release of nitric oxide (NO), prostaglandins, 2 and endothelium-derived hyperpolarizing factor (EDHF).	bind
36073	5	8633	7	NULL	NULL	0	NULL	statement 2	NULL		occurs by	NULL				EDHF	NULL	release of			NULL		0	NULL	NULL	NULL	gw70_circulationres_96_2_189_s_25	15604418	7,9  The released ATP then binds to P2Y receptors on the endothelium and stimulates vasodilatation by the release of nitric oxide (NO), prostaglandins, 2 and endothelium-derived hyperpolarizing factor (EDHF).	bind
36074	6	8633	7	NULL	NULL	0	NULL	NO	NULL		is	NULL				nitric oxide	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_2_189_s_25	15604418	7,9  The released ATP then binds to P2Y receptors on the endothelium and stimulates vasodilatation by the release of nitric oxide (NO), prostaglandins, 2 and endothelium-derived hyperpolarizing factor (EDHF).	bind
36075	7	8633	7	NULL	NULL	0	NULL	EDHF	NULL		is	NULL				endothelium-derived hyperpolarizing factor	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_2_189_s_25	15604418	7,9  The released ATP then binds to P2Y receptors on the endothelium and stimulates vasodilatation by the release of nitric oxide (NO), prostaglandins, 2 and endothelium-derived hyperpolarizing factor (EDHF).	bind
37236	1	8634	5	13	NULL	NULL	NULL	thrombin	GP		induce					SMCs	Cell	migration of;;rat			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
37237	2	8634	5	13	NULL	NULL	NULL	thrombin	GP		induce					SMCs	Cell	proliferation of;;rat			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
37238	3	8634	5	13	NULL	NULL	NULL	heparin	Chemical		inhibit		may;;partly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
37239	4	8634	5	13	NULL	NULL	NULL	heparin	Chemical		inhibit		may;;partly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
37240	5	8634	5	13	NULL	NULL	NULL	HB-EGF	GP		bind					HSPGs	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
37241	6	8634	5	13	NULL	NULL	NULL	HSPGs	GP		is					heparan sulfate proteoglycans	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
37242	7	8634	5	13	NULL	NULL	NULL	heparin	Chemical		prevents					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
37243	8	8634	5	13	NULL	NULL	NULL	statement 7	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
37244	9	8634	5	13	NULL	NULL	NULL	statement 7	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
37245	10	8634	5	13	NULL	NULL	NULL	HB-EGF	GP		is a type of					heparin binding growth factors	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
37246	11	8634	5	13	NULL	NULL	NULL	bFGF	GP		is					basic fibroblast growth factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
37247	12	8634	5	13	NULL	NULL	NULL	bFGF	GP		is a type of					heparin binding growth factors	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
37248	13	8634	5	13	NULL	NULL	NULL	HSPGs	GP		acts as					coreceptors for biological activity	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
37249	14	8634	5	13	NULL	NULL	NULL	HB-EGF	GP		require					statement 13	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
37250	15	8634	5	13	NULL	NULL	NULL	bFGF	GP		requires					statement 13	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
36076	1	8634	7	10	NULL	0	NULL	thrombin			induce					SMCs		migration of;; rat			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
36077	2	8634	7	10	NULL	0	NULL	thrombin			induce					SMCs		proliferation of;; rat			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
36078	3	8634	7	NULL	NULL	0	NULL	heparin	NULL		inhibit	NULL	may			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
36079	4	8634	7	NULL	NULL	0	NULL	heparin	NULL		inhibit	NULL	may			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
36080	5	8634	7	NULL	NULL	0	NULL	HB-EGF	NULL		bind	NULL				HSPGs	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
36081	6	8634	7	NULL	NULL	0	NULL	HSPG	NULL		acts as	NULL				coreceptors	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
36082	7	8634	7	NULL	NULL	0	NULL	HB-EGF	NULL		requires	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
36083	8	8634	7	NULL	NULL	0	NULL	bFGF	NULL		requires	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
36084	9	8634	7	NULL	NULL	0	NULL	statement 3	NULL		occurs by	NULL				statement 5	NULL	prevention of			NULL		0	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
36085	10	8634	7	NULL	NULL	0	NULL	statement 4	NULL		occurs by	NULL				statement 5	NULL	prevention of			NULL		0	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
36087	11	8634	7	NULL	NULL	0	NULL	statement 9	NULL		because of	NULL				statement 7	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
36088	12	8634	7	NULL	NULL	0	NULL	statement 10	NULL		because of	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
36089	13	8634	7	NULL	NULL	0	NULL	HSPGs	NULL		is	NULL				heparan sulfate proteoglycans 	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
36090	14	8634	7	NULL	NULL	0	NULL	HB-EGF	NULL		is a type of	NULL				heparin binding growth factors	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
36091	15	8634	7	NULL	NULL	0	NULL	bFGF	NULL		is a type of	NULL				heparin binding growth factors	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
36092	16	8634	7	NULL	NULL	0	NULL	bFGF	NULL		is	NULL				basic fibroblast growth factor	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_2_172_s_20	15625285	7,9,10   Heparin may inhibit thrombin-induced migration and proliferation of rat SMCs, in part, by preventing the binding of HB-EGF to heparan sulfate proteoglycans (HSPGs), 7,11  because heparin binding growth factors (eg, HB-EGF, basic fibroblast growth factor [bFGF]) require HSPGs as coreceptors for biological activity.	bind
37888	1	8635	5	13	NULL	NULL	NULL	PDGF dimers	GP		bind					specific receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1763_s_16	10362801	7- 9  PDGF dimers bind to specific receptors that themselves are dimers formed from two types of subunits, alpha and beta, that differentially bind PDGF isoforms.	bind
37889	2	8635	5	13	NULL	NULL	NULL	PDGF receptors	GP		are					dimers	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1763_s_16	10362801	7- 9  PDGF dimers bind to specific receptors that themselves are dimers formed from two types of subunits, alpha and beta, that differentially bind PDGF isoforms.	bind
37890	3	8635	5	13	NULL	NULL	NULL	PDGF receptors	GP		are formed by								alpha and beta subunits		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1763_s_16	10362801	7- 9  PDGF dimers bind to specific receptors that themselves are dimers formed from two types of subunits, alpha and beta, that differentially bind PDGF isoforms.	bind
46716	4	8635	5	13	NULL	NULL	NULL	PDGF receptor	GP		bind		differentially			PDGF isoforms	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1763_s_16	10362801	7- 9  PDGF dimers bind to specific receptors that themselves are dimers formed from two types of subunits, alpha and beta, that differentially bind PDGF isoforms.	bind
36093	1	8635	7	NULL	NULL	0	NULL	PDGF dimers	NULL		bind	NULL				specific receptors	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1763_s_16	10362801	7- 9  PDGF dimers bind to specific receptors that themselves are dimers formed from two types of subunits, alpha and beta, that differentially bind PDGF isoforms.	bind
36094	4	8635	7	10	NULL	0	NULL	PDGF receptor	NULL		bind	NULL	differentially			PDGF isoforms	NULL				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_154_6_1763_s_16	10362801	7- 9  PDGF dimers bind to specific receptors that themselves are dimers formed from two types of subunits, alpha and beta, that differentially bind PDGF isoforms.	bind
37912	2	8635	7	NULL	NULL	0	NULL	PDGF receptors	NULL		are	NULL				dimers	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_6_1763_s_16	10362801	7- 9  PDGF dimers bind to specific receptors that themselves are dimers formed from two types of subunits, alpha and beta, that differentially bind PDGF isoforms.	bind
37913	3	8635	7	NULL	NULL	0	NULL	PDGF receptors	NULL		are formed by	NULL					NULL		alpha and beta subunit		NULL		0	NULL	NULL	NULL	gw60_amjpathol_154_6_1763_s_16	10362801	7- 9  PDGF dimers bind to specific receptors that themselves are dimers formed from two types of subunits, alpha and beta, that differentially bind PDGF isoforms.	bind
37252	1	8636	5	13	NULL	NULL	NULL	7-Deaza-cAMP	Chemical		bind					CRP	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1547_1_1_s_278	11343786	7-Deaza-cAMP binds to CRP, mediates a CRP conformation change, and promotes CRP-mediated  lacP activity in vivo and  catP activity in vitro to levels comparable to those attained with cAMP.	bind
37253	2	8636	5	13	NULL	NULL	NULL	statement 1	Process		mediate					CRP	GP	conformational changes in			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1547_1_1_s_278	11343786	7-Deaza-cAMP binds to CRP, mediates a CRP conformation change, and promotes CRP-mediated  lacP activity in vivo and  catP activity in vitro to levels comparable to those attained with cAMP.	bind
37254	3	8636	5	13	NULL	NULL	NULL	CRP	GP		mediate					lacP	GP	activity of			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1547_1_1_s_278	11343786	7-Deaza-cAMP binds to CRP, mediates a CRP conformation change, and promotes CRP-mediated  lacP activity in vivo and  catP activity in vitro to levels comparable to those attained with cAMP.	bind
37255	4	8636	5	13	NULL	NULL	NULL	statement 2	Process		promotes					statement 3	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1547_1_1_s_278	11343786	7-Deaza-cAMP binds to CRP, mediates a CRP conformation change, and promotes CRP-mediated  lacP activity in vivo and  catP activity in vitro to levels comparable to those attained with cAMP.	bind
37256	5	8636	5	13	NULL	NULL	NULL	CRP	GP		mediate					catP	GP	activity of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1547_1_1_s_278	11343786	7-Deaza-cAMP binds to CRP, mediates a CRP conformation change, and promotes CRP-mediated  lacP activity in vivo and  catP activity in vitro to levels comparable to those attained with cAMP.	bind
37257	6	8636	5	13	NULL	NULL	NULL	statement 2	Process		promotes					statement 5	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1547_1_1_s_278	11343786	7-Deaza-cAMP binds to CRP, mediates a CRP conformation change, and promotes CRP-mediated  lacP activity in vivo and  catP activity in vitro to levels comparable to those attained with cAMP.	bind
36095	1	8636	7	NULL	NULL	0	NULL	7-Deaza-cAMP 	NULL		binds to	NULL				CRP	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1547_1_1_s_278	11343786	7-Deaza-cAMP binds to CRP, mediates a CRP conformation change, and promotes CRP-mediated  lacP activity in vivo and  catP activity in vitro to levels comparable to those attained with cAMP.	bind
36096	2	8636	7	NULL	NULL	0	NULL	statement 1	NULL		mediates	NULL				CRP	NULL	conformation change of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1547_1_1_s_278	11343786	7-Deaza-cAMP binds to CRP, mediates a CRP conformation change, and promotes CRP-mediated  lacP activity in vivo and  catP activity in vitro to levels comparable to those attained with cAMP.	bind
36097	3	8636	7	NULL	NULL	0	NULL	CRP	NULL		mediates	NULL				lacP activity	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1547_1_1_s_278	11343786	7-Deaza-cAMP binds to CRP, mediates a CRP conformation change, and promotes CRP-mediated  lacP activity in vivo and  catP activity in vitro to levels comparable to those attained with cAMP.	bind
36098	4	8636	7	NULL	NULL	0	NULL	statement 1	NULL		promotes	NULL				statement 3	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1547_1_1_s_278	11343786	7-Deaza-cAMP binds to CRP, mediates a CRP conformation change, and promotes CRP-mediated  lacP activity in vivo and  catP activity in vitro to levels comparable to those attained with cAMP.	bind
36099	5	8636	7	NULL	NULL	0	NULL	CRP	NULL		mediates	NULL				catP activity	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1547_1_1_s_278	11343786	7-Deaza-cAMP binds to CRP, mediates a CRP conformation change, and promotes CRP-mediated  lacP activity in vivo and  catP activity in vitro to levels comparable to those attained with cAMP.	bind
37908	6	8636	7	NULL	NULL	0	NULL	statement 1	NULL		promotes	NULL				statement 5	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1547_1_1_s_278	11343786	7-Deaza-cAMP binds to CRP, mediates a CRP conformation change, and promotes CRP-mediated  lacP activity in vivo and  catP activity in vitro to levels comparable to those attained with cAMP.	bind
37258	1	8637	5	13	NULL	NULL	NULL	RF	GP		bind					IgG	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_mol-immunol_32_1_7532785_s_8	7532785	7-mer  peptides representing RF-reactive sites on CH3 preincubated with polyclonal  IgM RF showed strong inhibition (55-66%) of RF binding to whole IgG on  the ELISA plate.	bind
37259	2	8637	5	13	NULL	NULL	NULL	7-mer peptides	GP		represents					CH3	GP		RF-reactive sites on		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_mol-immunol_32_1_7532785_s_8	7532785	7-mer  peptides representing RF-reactive sites on CH3 preincubated with polyclonal  IgM RF showed strong inhibition (55-66%) of RF binding to whole IgG on  the ELISA plate.	bind
37260	3	8637	5	13	NULL	NULL	NULL	statement 2	Process		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_mol-immunol_32_1_7532785_s_8	7532785	7-mer  peptides representing RF-reactive sites on CH3 preincubated with polyclonal  IgM RF showed strong inhibition (55-66%) of RF binding to whole IgG on  the ELISA plate.	bind
36197	1	8637	7	NULL	NULL	0	NULL	RF	NULL		bind	NULL				IgG	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_mol-immunol_32_1_7532785_s_8	7532785	7-mer  peptides representing RF-reactive sites on CH3 preincubated with polyclonal  IgM RF showed strong inhibition (55-66%) of RF binding to whole IgG on  the ELISA plate.	bind
36198	2	8637	7	NULL	NULL	0	NULL	7-mer peptides	NULL		represent	NULL				CH3	NULL		RF-reactive sites		NULL		0	NULL	NULL	NULL	abs-batch0720-0739_mol-immunol_32_1_7532785_s_8	7532785	7-mer  peptides representing RF-reactive sites on CH3 preincubated with polyclonal  IgM RF showed strong inhibition (55-66%) of RF binding to whole IgG on  the ELISA plate.	bind
36199	3	8637	7	10	NULL	0	NULL	statement  2	NULL		inhibits	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_mol-immunol_32_1_7532785_s_8	7532785	7-mer  peptides representing RF-reactive sites on CH3 preincubated with polyclonal  IgM RF showed strong inhibition (55-66%) of RF binding to whole IgG on  the ELISA plate.	bind
37261	1	8638	5	13	NULL	NULL	NULL	7-methyl-GDP	Chemical		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_6_951_s_123	9200613	7-methyl-GDP  binding to eIF4E Selected ligand atoms are labeled using lower case and italics  to distinguish them from protein components.	bind
36200	1	8638	7	NULL	NULL	0	NULL	7-methyl-GDP	NULL		bind	NULL				eIF4E	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_89_6_951_s_123	9200613	7-methyl-GDP  binding to eIF4E Selected ligand atoms are labeled using lower case and italics  to distinguish them from protein components.	bind
37262	1	8639	5	13	NULL	NULL	NULL	LD78	GP	receptor binding of	higher affinity than					MIP-1	GP	receptor binding of			NULL		NULL	NULL	NULL	NULL	gw60_febslett_457_2_219_s_69	10471782	70 ng/ml of MIP-1  was required for 50% inhibition of radiolabeled MIP-1  binding, while 20 ng/ml of LD78  was sufficient for 50% inhibition, indicating that LD78  has higher receptor binding affinity than MIP-1 .	bind
36201	1	8639	7	10	NULL	0	NULL	LD78	NULL	receptor binding of	higher affinity than	NULL				MIP-1	NULL	receptor binding of			NULL		NULL	NULL	NULL	NULL	gw60_febslett_457_2_219_s_69	10471782	70 ng/ml of MIP-1  was required for 50% inhibition of radiolabeled MIP-1  binding, while 20 ng/ml of LD78  was sufficient for 50% inhibition, indicating that LD78  has higher receptor binding affinity than MIP-1 .	bind
37263	1	8642	5	13	NULL	NULL	NULL	p53	GP		bind		sequence specifically			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_5207_s_531	11812854	71       Hupp,T.R., Sparks,A. and Lane,D.P. (1995) Small peptides activate the latent sequence-specific DNA binding function of p53.	bind
37264	2	8642	5	13	NULL	NULL	NULL	peptides	GP	small	activates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_5207_s_531	11812854	71       Hupp,T.R., Sparks,A. and Lane,D.P. (1995) Small peptides activate the latent sequence-specific DNA binding function of p53.	bind
36207	1	8642	7	NULL	NULL	0	NULL	p53	NULL		bind	NULL	latent sequence-specific			DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_5207_s_531	11812854	71       Hupp,T.R., Sparks,A. and Lane,D.P. (1995) Small peptides activate the latent sequence-specific DNA binding function of p53.	bind
36208	2	8642	7	NULL	NULL	0	NULL	Small peptides	NULL		activate	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_5207_s_531	11812854	71       Hupp,T.R., Sparks,A. and Lane,D.P. (1995) Small peptides activate the latent sequence-specific DNA binding function of p53.	bind
37707	1	8643	5	13	NULL	NULL	NULL	vitamin B12	Chemical		is a type of					Cbl III	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
37708	2	8643	5	13	NULL	NULL	NULL	CN-Cbl	Chemical		is a type of					Cbl III	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
37709	3	8643	5	13	NULL	NULL	NULL	Cbl III	Chemical		undergoes					beta-axial ligand exchange	Process				NULL	intracellularly	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
37710	4	8643	5	13	NULL	NULL	NULL	Cbl III	Chemical		undergoes					cobalt reduction reactions	Process				NULL	intracellularly	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
37711	5	8643	5	13	NULL	NULL	NULL	statement 3	Process		is catalyzed by					beta-axial ligand transferase/Cbl reductase complex	GP				NULL	intracellularly	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
37712	6	8643	5	13	NULL	NULL	NULL	statement 4	Process		is catalyzed by					beta-axial ligand transferase/Cbl reductase complex	Process				NULL	intracellularly	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
37713	7	8643	5	13	NULL	NULL	NULL	Cbl III	Chemical		forms					Cbl II	Chemical				NULL	intracellularly	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
37714	8	8643	5	13	NULL	NULL	NULL	statement 3	Process		leads to					statement 7	Process				NULL	intracellularly	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
37715	9	8643	5	13	NULL	NULL	NULL	statement 4	Process		leads to					statement 7	Process				NULL	intracellularly	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
37716	10	8643	5	13	NULL	NULL	NULL	Cbl II	Chemical		bind		initially			apo-methionine synthase	GP				NULL	intracellularly	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
36209	4	8643	7	NULL	NULL	0	NULL	Cbl III	NULL		forms	NULL				Cbl II	NULL				NULL	Intracellular	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
36211	1	8643	7	NULL	NULL	0	NULL	Cbl II	NULL		bind	NULL				apo-methionine synthase	NULL				NULL	Intracellular	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
36212	2	8643	7	NULL	NULL	0	NULL	Cbl III	NULL		undergoes	NULL				 beta-axial ligand exchange	NULL				NULL	Intracellular	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
36213	3	8643	7	NULL	NULL	0	NULL	Cbl III	NULL		undergoes	NULL				cobalt reduction reactions	NULL				NULL	Intracellular	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
36214	5	8643	7	NULL	NULL	0	NULL	beta-axial ligand transferase/Cbl reductase complex 	NULL		catalyse	NULL				statement 2	NULL				NULL	Intracellular	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
36215	6	8643	7	NULL	NULL	0	NULL	beta-axial ligand transferase/Cbl reductase complex 	NULL		catalyse	NULL				statement 3	NULL				NULL	Intracellular	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
36216	7	8643	7	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
36217	8	8643	7	NULL	NULL	0	NULL	statement 3	NULL		leads to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
36218	9	8643	7	NULL	NULL	0	NULL	vitamin B12	NULL		is a type of	NULL				Cbl III	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
36219	10	8643	7	NULL	NULL	0	NULL	CN-Cbl	NULL		is a type of	NULL				Cbl III	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_10_2074_s_30	9351374	71  Intracellularly, Cbl III (eg, vitamin B12, CN-Cbl) undergoes a beta-axial ligand exchange and cobalt reduction reactions catalyzed by the beta-axial ligand transferase/Cbl reductase complex to form Cbl II, which is initially bound to apo-methionine synthase.	bind
37265	1	8644	5	13	NULL	NULL	NULL	estrogen receptor	GP		bind			DNA binding domain						estrogen response element	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_479	11452016	72       Romine,L.E., Wood,J.R., Lamia,L.A., Prendergast,P., Edwards,D.P. and Nardulli,A.M. (1998) The high mobility group protein 1 enhances binding of the estrogen receptor DNA binding domain to the estrogen response element.	bind
37266	2	8644	5	13	NULL	NULL	NULL	high mobility group protein 1	GP		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_479	11452016	72       Romine,L.E., Wood,J.R., Lamia,L.A., Prendergast,P., Edwards,D.P. and Nardulli,A.M. (1998) The high mobility group protein 1 enhances binding of the estrogen receptor DNA binding domain to the estrogen response element.	bind
36220	1	8644	7	10	NULL	0	NULL	estrogen receptor			bind			DNA binding domain						estrogen response element	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_479	11452016	72       Romine,L.E., Wood,J.R., Lamia,L.A., Prendergast,P., Edwards,D.P. and Nardulli,A.M. (1998) The high mobility group protein 1 enhances binding of the estrogen receptor DNA binding domain to the estrogen response element.	bind
36221	2	8644	7	NULL	NULL	0	NULL	high mobility group protein 1	NULL		enhances	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_479	11452016	72       Romine,L.E., Wood,J.R., Lamia,L.A., Prendergast,P., Edwards,D.P. and Nardulli,A.M. (1998) The high mobility group protein 1 enhances binding of the estrogen receptor DNA binding domain to the estrogen response element.	bind
37267	1	8645	5	13	NULL	NULL	NULL	thrombin	GP		bind					GP Ib-IX-V complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_138	12231555	72 The binding of thrombin to the GP Ib-IX-V complex significantly enhances the ability of thrombin to cleave PAR1 and catalyze platelet activation.	bind
37268	2	8645	5	13	NULL	NULL	NULL	thrombin	GP		cleave					PAR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_138	12231555	72 The binding of thrombin to the GP Ib-IX-V complex significantly enhances the ability of thrombin to cleave PAR1 and catalyze platelet activation.	bind
37269	3	8645	5	13	NULL	NULL	NULL	statement 2	Process		catalyze					platelet	Cell	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_138	12231555	72 The binding of thrombin to the GP Ib-IX-V complex significantly enhances the ability of thrombin to cleave PAR1 and catalyze platelet activation.	bind
37270	4	8645	5	13	NULL	NULL	NULL	statement 1	Process		enhance		significantly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_138	12231555	72 The binding of thrombin to the GP Ib-IX-V complex significantly enhances the ability of thrombin to cleave PAR1 and catalyze platelet activation.	bind
37271	5	8645	5	13	NULL	NULL	NULL	statement 1	Process		enhance		significantly			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_138	12231555	72 The binding of thrombin to the GP Ib-IX-V complex significantly enhances the ability of thrombin to cleave PAR1 and catalyze platelet activation.	bind
36222	1	8645	7	NULL	NULL	0	NULL	thrombin	NULL		bind	NULL				GP Ib-IX-V complex	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_138	12231555	72 The binding of thrombin to the GP Ib-IX-V complex significantly enhances the ability of thrombin to cleave PAR1 and catalyze platelet activation.	bind
36223	2	8645	7	NULL	NULL	0	NULL	thrombin	NULL		cleave	NULL				PAR1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_138	12231555	72 The binding of thrombin to the GP Ib-IX-V complex significantly enhances the ability of thrombin to cleave PAR1 and catalyze platelet activation.	bind
36224	3	8645	7	NULL	NULL	0	NULL	thrombin	NULL		catalyze	NULL				platelet	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_138	12231555	72 The binding of thrombin to the GP Ib-IX-V complex significantly enhances the ability of thrombin to cleave PAR1 and catalyze platelet activation.	bind
36225	4	8645	7	NULL	NULL	0	NULL	statement 1	NULL		enhance	NULL	significantly			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_138	12231555	72 The binding of thrombin to the GP Ib-IX-V complex significantly enhances the ability of thrombin to cleave PAR1 and catalyze platelet activation.	bind
36226	5	8645	7	NULL	NULL	0	NULL	statement 1	NULL		enhance	NULL	significantly			statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_138	12231555	72 The binding of thrombin to the GP Ib-IX-V complex significantly enhances the ability of thrombin to cleave PAR1 and catalyze platelet activation.	bind
37272	1	8646	5	13	NULL	NULL	NULL	p53	GP		is a type of					T antigen binding proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_10_1044_s_132	12039793	72, 73 These studies revealed that 2 of T antigen binding proteins (namely p53 and p193) encode proapoptotic activity and suggested that minimally these 2 pathways must be circumvented to promote sustained cardiomyocyte proliferation.	bind
37273	2	8646	5	13	NULL	NULL	NULL	p193	GP		is a type of					T antigen binding proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_10_1044_s_132	12039793	72, 73 These studies revealed that 2 of T antigen binding proteins (namely p53 and p193) encode proapoptotic activity and suggested that minimally these 2 pathways must be circumvented to promote sustained cardiomyocyte proliferation.	bind
37274	3	8646	5	13	NULL	NULL	NULL	p53	GP		encode					proapoptotic activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_10_1044_s_132	12039793	72, 73 These studies revealed that 2 of T antigen binding proteins (namely p53 and p193) encode proapoptotic activity and suggested that minimally these 2 pathways must be circumvented to promote sustained cardiomyocyte proliferation.	bind
37275	4	8646	5	13	NULL	NULL	NULL	p193	GP		encode					proapoptotic activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_10_1044_s_132	12039793	72, 73 These studies revealed that 2 of T antigen binding proteins (namely p53 and p193) encode proapoptotic activity and suggested that minimally these 2 pathways must be circumvented to promote sustained cardiomyocyte proliferation.	bind
37276	5	8646	5	13	NULL	NULL	NULL	statement 3	Process		promotes					cardiomyocyte	Cell	proliferation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_10_1044_s_132	12039793	72, 73 These studies revealed that 2 of T antigen binding proteins (namely p53 and p193) encode proapoptotic activity and suggested that minimally these 2 pathways must be circumvented to promote sustained cardiomyocyte proliferation.	bind
37277	6	8646	5	13	NULL	NULL	NULL	statement 4	Process		promotes					cardiomyocyte	Cell	proliferation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_10_1044_s_132	12039793	72, 73 These studies revealed that 2 of T antigen binding proteins (namely p53 and p193) encode proapoptotic activity and suggested that minimally these 2 pathways must be circumvented to promote sustained cardiomyocyte proliferation.	bind
36227	1	8646	7	NULL	NULL	0	NULL	p53 	NULL		encode	NULL				proapoptotic activity	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_10_1044_s_132	12039793	72, 73 These studies revealed that 2 of T antigen binding proteins (namely p53 and p193) encode proapoptotic activity and suggested that minimally these 2 pathways must be circumvented to promote sustained cardiomyocyte proliferation.	bind
36228	2	8646	7	NULL	NULL	0	NULL	p193	NULL		encode	NULL				proapoptotic activity	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_10_1044_s_132	12039793	72, 73 These studies revealed that 2 of T antigen binding proteins (namely p53 and p193) encode proapoptotic activity and suggested that minimally these 2 pathways must be circumvented to promote sustained cardiomyocyte proliferation.	bind
36229	3	8646	7	NULL	NULL	0	NULL	statement 1	NULL		promote	NULL				cardiomyocytes	NULL	proliferation of 			NULL		0	NULL	NULL	NULL	gw60_circulationres_90_10_1044_s_132	12039793	72, 73 These studies revealed that 2 of T antigen binding proteins (namely p53 and p193) encode proapoptotic activity and suggested that minimally these 2 pathways must be circumvented to promote sustained cardiomyocyte proliferation.	bind
36230	4	8646	7	NULL	NULL	0	NULL	p53	NULL		is a type of	NULL				T antigen binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_10_1044_s_132	12039793	72, 73 These studies revealed that 2 of T antigen binding proteins (namely p53 and p193) encode proapoptotic activity and suggested that minimally these 2 pathways must be circumvented to promote sustained cardiomyocyte proliferation.	bind
36231	5	8646	7	NULL	NULL	0	NULL	p193	NULL		is a type of	NULL				T antigen binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_10_1044_s_132	12039793	72, 73 These studies revealed that 2 of T antigen binding proteins (namely p53 and p193) encode proapoptotic activity and suggested that minimally these 2 pathways must be circumvented to promote sustained cardiomyocyte proliferation.	bind
36232	6	8646	7	NULL	NULL	0	NULL	statement 2	NULL		promote	NULL				cardiomyocytes	NULL	proliferation of			NULL		0	NULL	NULL	NULL	gw60_circulationres_90_10_1044_s_132	12039793	72, 73 These studies revealed that 2 of T antigen binding proteins (namely p53 and p193) encode proapoptotic activity and suggested that minimally these 2 pathways must be circumvented to promote sustained cardiomyocyte proliferation.	bind
37278	1	8647	5	13	NULL	NULL	NULL	IgE	GP		bind		strongly			nLol p 5	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_462_3_435_s_130	10622741	72.7% of the patient sera showed strong IgE binding to nLol p 5 and rLol p 5C.	bind
37279	2	8647	5	13	NULL	NULL	NULL	IgE	GP		bind		strongly			rLol p 5C	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_462_3_435_s_130	10622741	72.7% of the patient sera showed strong IgE binding to nLol p 5 and rLol p 5C.	bind
36233	1	8647	7	NULL	NULL	0	NULL	 IgE	NULL		bind	NULL	strongly			nLol p 5 	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_462_3_435_s_130	10622741	72.7% of the patient sera showed strong IgE binding to nLol p 5 and rLol p 5C.	bind
36234	2	8647	7	NULL	NULL	0	NULL	IgE	NULL		bind	NULL	strongly			rLol p 5C	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_462_3_435_s_130	10622741	72.7% of the patient sera showed strong IgE binding to nLol p 5 and rLol p 5C.	bind
37280	1	8648	5	13	NULL	NULL	NULL	thrombin	GP		bind					GP Ib-IX-V complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_139	12231555	73 The binding of thrombin to the GP Ib-IX-V complex may also signal platelet activation through a fibrin-dependent mechanism.	bind
37281	2	8648	5	13	NULL	NULL	NULL	statement 1	Process		signal					platelet	Cell	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_139	12231555	73 The binding of thrombin to the GP Ib-IX-V complex may also signal platelet activation through a fibrin-dependent mechanism.	bind
37282	3	8648	5	13	NULL	NULL	NULL	statement 2	Process		through					fibrin-dependent mechanism	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_139	12231555	73 The binding of thrombin to the GP Ib-IX-V complex may also signal platelet activation through a fibrin-dependent mechanism.	bind
36235	1	8648	7	NULL	NULL	0	NULL	thrombin	NULL		bind	NULL				GP Ib-IX-V complex	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_139	12231555	73 The binding of thrombin to the GP Ib-IX-V complex may also signal platelet activation through a fibrin-dependent mechanism.	bind
36236	2	8648	7	NULL	NULL	0	NULL	statement 1	NULL		signal	NULL				platelet	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_139	12231555	73 The binding of thrombin to the GP Ib-IX-V complex may also signal platelet activation through a fibrin-dependent mechanism.	bind
36237	3	8648	7	NULL	NULL	0	NULL	statement 2	NULL		occurs through	NULL				fibrin-dependent mechanism	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_9_1381_s_139	12231555	73 The binding of thrombin to the GP Ib-IX-V complex may also signal platelet activation through a fibrin-dependent mechanism.	bind
37283	1	8649	5	13	NULL	NULL	NULL	HDL	GP		isolated from					atheroma	MedicalFinding	human			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1102_s_100	15790935	73,74  Moreover, HDL isolated from human atheroma contains MPO, consistent with the recent finding that MPO selectively binds to apolipoprotein A-I within plasma via a specific region on helix 8 of the lipoprotein.	bind
37284	2	8649	5	13	NULL	NULL	NULL	statement 1	GP		contains					MPO	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1102_s_100	15790935	73,74  Moreover, HDL isolated from human atheroma contains MPO, consistent with the recent finding that MPO selectively binds to apolipoprotein A-I within plasma via a specific region on helix 8 of the lipoprotein.	bind
37285	3	8649	5	13	NULL	NULL	NULL	MPO	GP		bind		selectively			apolipoprotein A-I	GP		helix 8		NULL	plasma	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1102_s_100	15790935	73,74  Moreover, HDL isolated from human atheroma contains MPO, consistent with the recent finding that MPO selectively binds to apolipoprotein A-I within plasma via a specific region on helix 8 of the lipoprotein.	bind
36238	1	8649	7	NULL	NULL	0	NULL	MPO	NULL		binds	NULL	selectively			apolipoprotein A-I 	NULL		helix 8		NULL	within plasma	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1102_s_100	15790935	73,74  Moreover, HDL isolated from human atheroma contains MPO, consistent with the recent finding that MPO selectively binds to apolipoprotein A-I within plasma via a specific region on helix 8 of the lipoprotein.	bind
36239	2	8649	7	NULL	NULL	0	NULL	HDL	NULL		contains	NULL				MPO	NULL				NULL	human atheroma	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_6_1102_s_100	15790935	73,74  Moreover, HDL isolated from human atheroma contains MPO, consistent with the recent finding that MPO selectively binds to apolipoprotein A-I within plasma via a specific region on helix 8 of the lipoprotein.	bind
37286	1	8650	5	13	NULL	NULL	NULL	estrogen receptor	GP		bind									estrogen response element	NULL	stably transfected HeLa cells	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_485	11452016	74       Zhang,C.C., Krieg,S. and Shapiro,D.J. (1999) HMG-1 stimulates estrogen response element binding by estrogen receptor from stably transfected HeLa cells.	bind
37287	2	8650	5	13	NULL	NULL	NULL	HMG-1	GP		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_485	11452016	74       Zhang,C.C., Krieg,S. and Shapiro,D.J. (1999) HMG-1 stimulates estrogen response element binding by estrogen receptor from stably transfected HeLa cells.	bind
36240	1	8650	7	10	NULL	0	NULL	estrogen receptor	NULL		bind	NULL					NULL			estrogen response element	NULL	transfected HeLa cells	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_485	11452016	74       Zhang,C.C., Krieg,S. and Shapiro,D.J. (1999) HMG-1 stimulates estrogen response element binding by estrogen receptor from stably transfected HeLa cells.	bind
36241	2	8650	7	NULL	NULL	0	NULL	HMG-1	NULL		stimulates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_485	11452016	74       Zhang,C.C., Krieg,S. and Shapiro,D.J. (1999) HMG-1 stimulates estrogen response element binding by estrogen receptor from stably transfected HeLa cells.	bind
37288	1	8651	5	13	NULL	NULL	NULL	74-5H7	GP		bind					L1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_7_1223_s_157	12082080	74-5H7 binding to L1 is dynamically regulated by cell - cell contact, L1 - L1 homophilic interactions, and L1 cross-linking   The results of immunocytochemical studies reported in  Fig. 1 suggested that 74-5H7-IR might be induced by cell - cell contact.	bind
37289	2	8651	5	13	NULL	NULL	NULL	statement 1	Process		regulated by		dynamically			cell - cell contact	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_7_1223_s_157	12082080	74-5H7 binding to L1 is dynamically regulated by cell - cell contact, L1 - L1 homophilic interactions, and L1 cross-linking   The results of immunocytochemical studies reported in  Fig. 1 suggested that 74-5H7-IR might be induced by cell - cell contact.	bind
37290	3	8651	5	13	NULL	NULL	NULL	L1	GP		interacts with		homophilically			L1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_7_1223_s_157	12082080	74-5H7 binding to L1 is dynamically regulated by cell - cell contact, L1 - L1 homophilic interactions, and L1 cross-linking   The results of immunocytochemical studies reported in  Fig. 1 suggested that 74-5H7-IR might be induced by cell - cell contact.	bind
37291	4	8651	5	13	NULL	NULL	NULL	statement 1	Process		regulated by		dynamically			L1 	GP	cross-linking of 			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_7_1223_s_157	12082080	74-5H7 binding to L1 is dynamically regulated by cell - cell contact, L1 - L1 homophilic interactions, and L1 cross-linking   The results of immunocytochemical studies reported in  Fig. 1 suggested that 74-5H7-IR might be induced by cell - cell contact.	bind
37292	5	8651	5	13	NULL	NULL	NULL	74-5H7-IR	GP		induced by		might be			cell - cell contact	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_7_1223_s_157	12082080	74-5H7 binding to L1 is dynamically regulated by cell - cell contact, L1 - L1 homophilic interactions, and L1 cross-linking   The results of immunocytochemical studies reported in  Fig. 1 suggested that 74-5H7-IR might be induced by cell - cell contact.	bind
56233	6	8651	5	13	NULL	NULL	NULL	statement 1	Process		is regulated by		dynamically			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_7_1223_s_157	12082080	74-5H7 binding to L1 is dynamically regulated by cell - cell contact, L1 - L1 homophilic interactions, and L1 cross-linking   The results of immunocytochemical studies reported in  Fig. 1 suggested that 74-5H7-IR might be induced by cell - cell contact.	bind
36242	1	8651	7	NULL	NULL	0	NULL	74-5H7	NULL		bind	NULL				L1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_7_1223_s_157	12082080	74-5H7 binding to L1 is dynamically regulated by cell - cell contact, L1 - L1 homophilic interactions, and L1 cross-linking   The results of immunocytochemical studies reported in  Fig. 1 suggested that 74-5H7-IR might be induced by cell - cell contact.	bind
36243	2	8651	7	NULL	NULL	0	NULL	cell - cell contact	NULL		regulates	NULL	dynamically			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_157_7_1223_s_157	12082080	74-5H7 binding to L1 is dynamically regulated by cell - cell contact, L1 - L1 homophilic interactions, and L1 cross-linking   The results of immunocytochemical studies reported in  Fig. 1 suggested that 74-5H7-IR might be induced by cell - cell contact.	bind
36244	3	8651	7	NULL	NULL	0	NULL	L1	NULL		interacts with	NULL	homophilic			L1	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_157_7_1223_s_157	12082080	74-5H7 binding to L1 is dynamically regulated by cell - cell contact, L1 - L1 homophilic interactions, and L1 cross-linking   The results of immunocytochemical studies reported in  Fig. 1 suggested that 74-5H7-IR might be induced by cell - cell contact.	bind
36245	4	8651	7	NULL	NULL	0	NULL	statement 3	NULL		regulates	NULL	dynamically			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_157_7_1223_s_157	12082080	74-5H7 binding to L1 is dynamically regulated by cell - cell contact, L1 - L1 homophilic interactions, and L1 cross-linking   The results of immunocytochemical studies reported in  Fig. 1 suggested that 74-5H7-IR might be induced by cell - cell contact.	bind
36246	5	8651	7	NULL	NULL	0	NULL	L1	NULL	crosslinking of	regulates	NULL	dynamically			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_157_7_1223_s_157	12082080	74-5H7 binding to L1 is dynamically regulated by cell - cell contact, L1 - L1 homophilic interactions, and L1 cross-linking   The results of immunocytochemical studies reported in  Fig. 1 suggested that 74-5H7-IR might be induced by cell - cell contact.	bind
36247	6	8651	7	NULL	NULL	0	NULL	cell - cell contact	NULL		induce	NULL	may			74-5H7-IR	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_157_7_1223_s_157	12082080	74-5H7 binding to L1 is dynamically regulated by cell - cell contact, L1 - L1 homophilic interactions, and L1 cross-linking   The results of immunocytochemical studies reported in  Fig. 1 suggested that 74-5H7-IR might be induced by cell - cell contact.	bind
37293	1	8652	5	13	NULL	NULL	NULL	74-5H7	GP		bind		strongly			L1	GP				NULL	extract lacking inhibitors	NULL	NULL	NULL	NULL	gw60_cellbiol_157_7_1223_s_143	12082080	74-5H7 binds much more strongly to L1 in the extract lacking the inhibitors.	bind
36248	1	8652	7	10	NULL	0	NULL	74-5H7	NULL		bind	NULL	strongly			L1	NULL				NULL	extract lacking the inhibitors	NULL	NULL	NULL	NULL	gw60_cellbiol_157_7_1223_s_143	12082080	74-5H7 binds much more strongly to L1 in the extract lacking the inhibitors.	bind
37294	1	8653	5	13	NULL	NULL	NULL	HMG-I	GP		is a type of					DNA-bending protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_489	11452016	75       Onate,S., Prendergast,P., Wagner,J.P., Nissen,M., Reeves,R., Pettijohn,D.E. and Edwards,D.P. (1994) The DNA-bending protein HMG-I enhances progesterone receptor binding to its target DNA sequences.	bind
37295	2	8653	5	13	NULL	NULL	NULL	progesterone receptor	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_489	11452016	75       Onate,S., Prendergast,P., Wagner,J.P., Nissen,M., Reeves,R., Pettijohn,D.E. and Edwards,D.P. (1994) The DNA-bending protein HMG-I enhances progesterone receptor binding to its target DNA sequences.	bind
37296	3	8653	5	13	NULL	NULL	NULL	HMG-1	GP		enhance					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_489	11452016	75       Onate,S., Prendergast,P., Wagner,J.P., Nissen,M., Reeves,R., Pettijohn,D.E. and Edwards,D.P. (1994) The DNA-bending protein HMG-I enhances progesterone receptor binding to its target DNA sequences.	bind
36250	1	8653	7	NULL	NULL	0	NULL	progesterone receptor	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_489	11452016	75       Onate,S., Prendergast,P., Wagner,J.P., Nissen,M., Reeves,R., Pettijohn,D.E. and Edwards,D.P. (1994) The DNA-bending protein HMG-I enhances progesterone receptor binding to its target DNA sequences.	bind
36251	2	8653	7	NULL	NULL	0	NULL	HMG-I	NULL		enhance	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_489	11452016	75       Onate,S., Prendergast,P., Wagner,J.P., Nissen,M., Reeves,R., Pettijohn,D.E. and Edwards,D.P. (1994) The DNA-bending protein HMG-I enhances progesterone receptor binding to its target DNA sequences.	bind
36252	3	8653	7	NULL	NULL	0	NULL	HMG-1	NULL		is a type of	NULL				DNA-bending protein	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_489	11452016	75       Onate,S., Prendergast,P., Wagner,J.P., Nissen,M., Reeves,R., Pettijohn,D.E. and Edwards,D.P. (1994) The DNA-bending protein HMG-I enhances progesterone receptor binding to its target DNA sequences.	bind
37297	1	8654	5	13	NULL	NULL	NULL	talin	GP		does not bind					beta3	GP	phosphorylated;; cytoplasmic	 tyrosine		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_1971_s_129	12947018	75 - 77   Neither talin nor Syk binds to beta3 when both cytoplasmic tyrosine residues are phosphorylated, 70,78  whereas nonmuscle myosin A only binds to beta3 when both cytoplasmic tyrosine residues are phosphorylated.	bind
37298	2	8654	5	13	NULL	NULL	NULL	Syk	GP		does not bind					beta3	GP	phosphorylated;; cytoplasmic	tyrosine		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_1971_s_129	12947018	75 - 77   Neither talin nor Syk binds to beta3 when both cytoplasmic tyrosine residues are phosphorylated, 70,78  whereas nonmuscle myosin A only binds to beta3 when both cytoplasmic tyrosine residues are phosphorylated.	bind
37299	3	8654	5	13	NULL	NULL	NULL	myosin A	GP	nonmuscle	bind					beta3	GP	phosphorylated;; cytoplasmic	tyrosine		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_1971_s_129	12947018	75 - 77   Neither talin nor Syk binds to beta3 when both cytoplasmic tyrosine residues are phosphorylated, 70,78  whereas nonmuscle myosin A only binds to beta3 when both cytoplasmic tyrosine residues are phosphorylated.	bind
36253	1	8654	7	10	NULL	0	NULL	talin	NULL		does not bind	NULL				beta3	NULL	phosphorylated;; cytoplasmic	tyrosine		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_1971_s_129	12947018	75 - 77   Neither talin nor Syk binds to beta3 when both cytoplasmic tyrosine residues are phosphorylated, 70,78  whereas nonmuscle myosin A only binds to beta3 when both cytoplasmic tyrosine residues are phosphorylated.	bind
36254	2	8654	7	10	NULL	0	NULL	Syk	NULL		does not bind	NULL				beta3	NULL	phosphorylated;; cytoplasmic	tyrosine		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_1971_s_129	12947018	75 - 77   Neither talin nor Syk binds to beta3 when both cytoplasmic tyrosine residues are phosphorylated, 70,78  whereas nonmuscle myosin A only binds to beta3 when both cytoplasmic tyrosine residues are phosphorylated.	bind
36256	5	8654	7	10	NULL	0	NULL	myosin A		nonmuscle 	binds					beta3		phosphorylated;; cytoplasmic	tyrosine		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_1971_s_129	12947018	75 - 77   Neither talin nor Syk binds to beta3 when both cytoplasmic tyrosine residues are phosphorylated, 70,78  whereas nonmuscle myosin A only binds to beta3 when both cytoplasmic tyrosine residues are phosphorylated.	bind
37300	1	8655	5	13	NULL	NULL	NULL	tropomyosin	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_6_580_s_170	9742053	75 89 90 91  Two of them, A63V and K70T, are located in exon 2b within the consensus pattern of sequence repeats of alpha-TM and could alter tropomyosin binding to actin.	bind
37301	2	8655	5	13	NULL	NULL	NULL	alpha-TM	GP		located in			A63V;;K70T		alpha-TM	GP			exon 2b	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_6_580_s_170	9742053	75 89 90 91  Two of them, A63V and K70T, are located in exon 2b within the consensus pattern of sequence repeats of alpha-TM and could alter tropomyosin binding to actin.	bind
37302	3	8655	5	13	NULL	NULL	NULL	statement 2	Process		alters					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_83_6_580_s_170	9742053	75 89 90 91  Two of them, A63V and K70T, are located in exon 2b within the consensus pattern of sequence repeats of alpha-TM and could alter tropomyosin binding to actin.	bind
36259	1	8655	7	NULL	NULL	0	NULL	tropomyosin 	NULL		bind	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_6_580_s_170	9742053	75 89 90 91  Two of them, A63V and K70T, are located in exon 2b within the consensus pattern of sequence repeats of alpha-TM and could alter tropomyosin binding to actin.	bind
36260	2	8655	7	NULL	NULL	0	NULL		NULL		is located in	NULL		 A63V		alpha-TM	NULL			exon 2b	NULL		0	NULL	NULL	NULL	gw60_circulationres_83_6_580_s_170	9742053	75 89 90 91  Two of them, A63V and K70T, are located in exon 2b within the consensus pattern of sequence repeats of alpha-TM and could alter tropomyosin binding to actin.	bind
36261	3	8655	7	NULL	NULL	0	NULL		NULL		is located in	NULL		 K70T		alpha-TM	NULL			exon 2b	NULL		0	NULL	NULL	NULL	gw60_circulationres_83_6_580_s_170	9742053	75 89 90 91  Two of them, A63V and K70T, are located in exon 2b within the consensus pattern of sequence repeats of alpha-TM and could alter tropomyosin binding to actin.	bind
36262	4	8655	7	NULL	NULL	0	NULL		NULL		alters	NULL		A63V		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_6_580_s_170	9742053	75 89 90 91  Two of them, A63V and K70T, are located in exon 2b within the consensus pattern of sequence repeats of alpha-TM and could alter tropomyosin binding to actin.	bind
36263	5	8655	7	NULL	NULL	0	NULL		NULL		alters	NULL		K70T		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_6_580_s_170	9742053	75 89 90 91  Two of them, A63V and K70T, are located in exon 2b within the consensus pattern of sequence repeats of alpha-TM and could alter tropomyosin binding to actin.	bind
37717	1	8656	5	13	NULL	NULL	NULL	alpha2beta1	GP		bind					collagens	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_196	10617582	75 mug/ml or 7 muM;  Mr 11,112 (Fig.  8 A), and of alpha2beta1 and alpha2 A-domain binding to these collagens (IC50 ~30 mug/ml or 3 muM; Fig.  8,  B-D), confirming the identity of GFOGER as an alpha2beta1 integrin recognition site and establishing the crucial importance of this sequence as a platelet alpha2beta1-binding locus in collagens I and IV.	bind
37718	2	8656	5	13	NULL	NULL	NULL	alpha2	GP		bind			A domain		collagens	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_196	10617582	75 mug/ml or 7 muM;  Mr 11,112 (Fig.  8 A), and of alpha2beta1 and alpha2 A-domain binding to these collagens (IC50 ~30 mug/ml or 3 muM; Fig.  8,  B-D), confirming the identity of GFOGER as an alpha2beta1 integrin recognition site and establishing the crucial importance of this sequence as a platelet alpha2beta1-binding locus in collagens I and IV.	bind
37719	3	8656	5	13	NULL	NULL	NULL	GFOGER	GP		recognizes					alpha2beta1 integrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_196	10617582	75 mug/ml or 7 muM;  Mr 11,112 (Fig.  8 A), and of alpha2beta1 and alpha2 A-domain binding to these collagens (IC50 ~30 mug/ml or 3 muM; Fig.  8,  B-D), confirming the identity of GFOGER as an alpha2beta1 integrin recognition site and establishing the crucial importance of this sequence as a platelet alpha2beta1-binding locus in collagens I and IV.	bind
37720	4	8656	5	13	NULL	NULL	NULL				acts as			GFOGER		collagen I	GP	platelet 	alpha2beta1-binding locus		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_196	10617582	75 mug/ml or 7 muM;  Mr 11,112 (Fig.  8 A), and of alpha2beta1 and alpha2 A-domain binding to these collagens (IC50 ~30 mug/ml or 3 muM; Fig.  8,  B-D), confirming the identity of GFOGER as an alpha2beta1 integrin recognition site and establishing the crucial importance of this sequence as a platelet alpha2beta1-binding locus in collagens I and IV.	bind
37721	5	8656	5	13	NULL	NULL	NULL				acts as			GFOGER		collagen IV	GP	platelet	alpha2beta1-binding locus		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_196	10617582	75 mug/ml or 7 muM;  Mr 11,112 (Fig.  8 A), and of alpha2beta1 and alpha2 A-domain binding to these collagens (IC50 ~30 mug/ml or 3 muM; Fig.  8,  B-D), confirming the identity of GFOGER as an alpha2beta1 integrin recognition site and establishing the crucial importance of this sequence as a platelet alpha2beta1-binding locus in collagens I and IV.	bind
36264	1	8656	7	10	NULL	0	NULL	alpha2beta1			bind					collagen					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_196	10617582	75 mug/ml or 7 muM;  Mr 11,112 (Fig.  8 A), and of alpha2beta1 and alpha2 A-domain binding to these collagens (IC50 ~30 mug/ml or 3 muM; Fig.  8,  B-D), confirming the identity of GFOGER as an alpha2beta1 integrin recognition site and establishing the crucial importance of this sequence as a platelet alpha2beta1-binding locus in collagens I and IV.	bind
36265	2	8656	7	NULL	NULL	0	NULL	alpha2	NULL		bind	NULL		A-domain		collagen	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_196	10617582	75 mug/ml or 7 muM;  Mr 11,112 (Fig.  8 A), and of alpha2beta1 and alpha2 A-domain binding to these collagens (IC50 ~30 mug/ml or 3 muM; Fig.  8,  B-D), confirming the identity of GFOGER as an alpha2beta1 integrin recognition site and establishing the crucial importance of this sequence as a platelet alpha2beta1-binding locus in collagens I and IV.	bind
36266	3	8656	7	NULL	NULL	0	NULL		NULL		recognizes	NULL		GFOGER 		alpha2beta1 integrin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_196	10617582	75 mug/ml or 7 muM;  Mr 11,112 (Fig.  8 A), and of alpha2beta1 and alpha2 A-domain binding to these collagens (IC50 ~30 mug/ml or 3 muM; Fig.  8,  B-D), confirming the identity of GFOGER as an alpha2beta1 integrin recognition site and establishing the crucial importance of this sequence as a platelet alpha2beta1-binding locus in collagens I and IV.	bind
36267	4	8656	7	10	NULL	0	NULL	GFOGER			acts as					collagen I		platelet	alpha2beta1 binding locus		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_196	10617582	75 mug/ml or 7 muM;  Mr 11,112 (Fig.  8 A), and of alpha2beta1 and alpha2 A-domain binding to these collagens (IC50 ~30 mug/ml or 3 muM; Fig.  8,  B-D), confirming the identity of GFOGER as an alpha2beta1 integrin recognition site and establishing the crucial importance of this sequence as a platelet alpha2beta1-binding locus in collagens I and IV.	bind
36268	5	8656	7	10	NULL	0	NULL	GFOGER			acts as					collagen IV		platelet	alpha2beta1 binding locus		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_1_35_s_196	10617582	75 mug/ml or 7 muM;  Mr 11,112 (Fig.  8 A), and of alpha2beta1 and alpha2 A-domain binding to these collagens (IC50 ~30 mug/ml or 3 muM; Fig.  8,  B-D), confirming the identity of GFOGER as an alpha2beta1 integrin recognition site and establishing the crucial importance of this sequence as a platelet alpha2beta1-binding locus in collagens I and IV.	bind
37303	1	8657	5	13	NULL	NULL	NULL	p53	GP		bind		sequence specifically			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_20_4114_s_620	11600700	77       Gu,W. and Roeder,R.G. (1997) Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.	bind
37304	2	8657	5	13	NULL	NULL	NULL	p53	GP	acetylation of	activates			C-terminal domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_20_4114_s_620	11600700	77       Gu,W. and Roeder,R.G. (1997) Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.	bind
36271	1	8657	7	NULL	NULL	0	NULL	 p53	NULL		bind	NULL	sequence-specific			DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_20_4114_s_620	11600700	77       Gu,W. and Roeder,R.G. (1997) Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.	bind
36272	2	8657	7	NULL	NULL	0	NULL	p53	NULL	acetylation of	activates	NULL		C-terminal domain		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_20_4114_s_620	11600700	77       Gu,W. and Roeder,R.G. (1997) Activation of p53 sequence-specific DNA binding by acetylation of the p53 C-terminal domain.	bind
37315	1	8658	5	13	NULL	NULL	NULL	LDL	GP	131 I-cyclohexanedione treated	does not bind					receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3542_s_302	9437204	77  111 113  We also found that tracer  131 I-cyclohexanedione treated LDL that does not bind to receptors gave a relatively constant low daily U/P ratio 111 (Fig 5B  ), evidence that the early rapid clearance of LDL from plasma was due to the action of LDL receptors.	bind
37316	2	8658	5	13	NULL	NULL	NULL	LDL	GP		is cleared from		early;;rapidly			plasma	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3542_s_302	9437204	77  111 113  We also found that tracer  131 I-cyclohexanedione treated LDL that does not bind to receptors gave a relatively constant low daily U/P ratio 111 (Fig 5B  ), evidence that the early rapid clearance of LDL from plasma was due to the action of LDL receptors.	bind
36273	1	8658	7	NULL	NULL	0	NULL	LDL receptor	NULL		clears	NULL				LDL	NULL				NULL	plasma	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3542_s_302	9437204	77  111 113  We also found that tracer  131 I-cyclohexanedione treated LDL that does not bind to receptors gave a relatively constant low daily U/P ratio 111 (Fig 5B  ), evidence that the early rapid clearance of LDL from plasma was due to the action of LDL receptors.	bind
36274	2	8658	7	NULL	NULL	0	NULL	 LDL	NULL	131 I-cyclohexanedione treated	does not bind	NULL				receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3542_s_302	9437204	77  111 113  We also found that tracer  131 I-cyclohexanedione treated LDL that does not bind to receptors gave a relatively constant low daily U/P ratio 111 (Fig 5B  ), evidence that the early rapid clearance of LDL from plasma was due to the action of LDL receptors.	bind
37318	1	8659	5	13	NULL	NULL	NULL	transcription factors	GP		bind					DNA	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulationres_85_8_753_s_195	10521248	78 111  112 113  Many of the reported studies demonstrate changes in the in vitro DNA binding activity of transcription factors in response to oxidants or reductants.	bind
37319	2	8659	5	13	NULL	NULL	NULL	oxidants	Chemical		changes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_8_753_s_195	10521248	78 111  112 113  Many of the reported studies demonstrate changes in the in vitro DNA binding activity of transcription factors in response to oxidants or reductants.	bind
37320	3	8659	5	13	NULL	NULL	NULL	reductants	Chemical		changes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_8_753_s_195	10521248	78 111  112 113  Many of the reported studies demonstrate changes in the in vitro DNA binding activity of transcription factors in response to oxidants or reductants.	bind
36275	1	8659	7	NULL	NULL	0	NULL	transcription factor	NULL		bind	NULL				DNA	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulationres_85_8_753_s_195	10521248	78 111  112 113  Many of the reported studies demonstrate changes in the in vitro DNA binding activity of transcription factors in response to oxidants or reductants.	bind
36276	2	8659	7	NULL	NULL	0	NULL	oxidants	NULL		change	NULL				statement 1	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulationres_85_8_753_s_195	10521248	78 111  112 113  Many of the reported studies demonstrate changes in the in vitro DNA binding activity of transcription factors in response to oxidants or reductants.	bind
36277	3	8659	7	NULL	NULL	0	NULL	reductants	NULL		change	NULL				statement 2	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_circulationres_85_8_753_s_195	10521248	78 111  112 113  Many of the reported studies demonstrate changes in the in vitro DNA binding activity of transcription factors in response to oxidants or reductants.	bind
37321	1	8660	5	13	NULL	NULL	NULL	7E cell line	Cell		is a type of					IgG2b isotype	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_10_2251_s_47	8636404	7E cell line is of the IgG2b isotype, and binds both PC and dsDNA by ELISA.	bind
37322	2	8660	5	13	NULL	NULL	NULL	7E cell line	Cell		bind					PC	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_10_2251_s_47	8636404	7E cell line is of the IgG2b isotype, and binds both PC and dsDNA by ELISA.	bind
37323	3	8660	5	13	NULL	NULL	NULL	7E cell line	Cell		bind					dsDNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_10_2251_s_47	8636404	7E cell line is of the IgG2b isotype, and binds both PC and dsDNA by ELISA.	bind
36278	1	8660	7	NULL	NULL	0	NULL	PC	NULL		bind	NULL				7E cell line	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_10_2251_s_47	8636404	7E cell line is of the IgG2b isotype, and binds both PC and dsDNA by ELISA.	bind
36279	2	8660	7	NULL	NULL	0	NULL	dsDNA	NULL		bind	NULL				7E cell line	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_10_2251_s_47	8636404	7E cell line is of the IgG2b isotype, and binds both PC and dsDNA by ELISA.	bind
36280	3	8660	7	NULL	NULL	0	NULL	7E cell line	NULL		is a type of	NULL				IgG2b isotype	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_10_2251_s_47	8636404	7E cell line is of the IgG2b isotype, and binds both PC and dsDNA by ELISA.	bind
37324	1	8661	5	13	NULL	NULL	NULL	transducin	GP		bind					rhodopsin membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51203_s_67	15351781	7PP and arrestin inhibit light- and GTP-dependent binding of transducin to rhodopsin  membranes.	bind
37325	2	8661	5	13	NULL	NULL	NULL	statement 1	Process		is dependent on					light					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51203_s_67	15351781	7PP and arrestin inhibit light- and GTP-dependent binding of transducin to rhodopsin  membranes.	bind
37326	3	8661	5	13	NULL	NULL	NULL	statement 1	Process		is dependent on					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51203_s_67	15351781	7PP and arrestin inhibit light- and GTP-dependent binding of transducin to rhodopsin  membranes.	bind
37327	4	8661	5	13	NULL	NULL	NULL	7PP	GP		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51203_s_67	15351781	7PP and arrestin inhibit light- and GTP-dependent binding of transducin to rhodopsin  membranes.	bind
37328	5	8661	5	13	NULL	NULL	NULL	7PP	GP		inhibit					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51203_s_67	15351781	7PP and arrestin inhibit light- and GTP-dependent binding of transducin to rhodopsin  membranes.	bind
37329	6	8661	5	13	NULL	NULL	NULL	arrestin	GP		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51203_s_67	15351781	7PP and arrestin inhibit light- and GTP-dependent binding of transducin to rhodopsin  membranes.	bind
37330	7	8661	5	13	NULL	NULL	NULL	arrestin	GP		inhibit					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51203_s_67	15351781	7PP and arrestin inhibit light- and GTP-dependent binding of transducin to rhodopsin  membranes.	bind
36281	1	8661	7	NULL	NULL	0	NULL	transducin	NULL		bind	NULL				rhodopsin membrane	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_49_51203_s_67	15351781	7PP and arrestin inhibit light- and GTP-dependent binding of transducin to rhodopsin  membranes.	bind
36282	2	8661	7	NULL	NULL	0	NULL	statement 1	NULL		depends on	NULL				GTP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_49_51203_s_67	15351781	7PP and arrestin inhibit light- and GTP-dependent binding of transducin to rhodopsin  membranes.	bind
36283	3	8661	7	NULL	NULL	0	NULL	statement 1	NULL		depends on	NULL				light	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_49_51203_s_67	15351781	7PP and arrestin inhibit light- and GTP-dependent binding of transducin to rhodopsin  membranes.	bind
36284	4	8661	7	NULL	NULL	0	NULL	7PP	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_49_51203_s_67	15351781	7PP and arrestin inhibit light- and GTP-dependent binding of transducin to rhodopsin  membranes.	bind
36285	5	8661	7	NULL	NULL	0	NULL	7PP	NULL		inhibits	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51203_s_67	15351781	7PP and arrestin inhibit light- and GTP-dependent binding of transducin to rhodopsin  membranes.	bind
36286	6	8661	7	NULL	NULL	0	NULL	arrestin	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_49_51203_s_67	15351781	7PP and arrestin inhibit light- and GTP-dependent binding of transducin to rhodopsin  membranes.	bind
36287	7	8661	7	NULL	NULL	0	NULL	arrestin	NULL		inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_49_51203_s_67	15351781	7PP and arrestin inhibit light- and GTP-dependent binding of transducin to rhodopsin  membranes.	bind
37331	1	8662	5	13	NULL	NULL	NULL	nod factor	GP		bind					lectin	GP				NULL	legume roots	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3459_s_256	11522814	8       Etzler,M.E., Kalsi,G., Ewing,N.N., Roberts,N.J., Day,R.B. and Murphy,J.B. (1999) A nod factor binding lectin with apyrase activity from legume roots.	bind
37332	2	8662	5	13	NULL	NULL	NULL	lectin	GP		contains					apyrase activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3459_s_256	11522814	8       Etzler,M.E., Kalsi,G., Ewing,N.N., Roberts,N.J., Day,R.B. and Murphy,J.B. (1999) A nod factor binding lectin with apyrase activity from legume roots.	bind
36288	1	8662	7	NULL	NULL	0	NULL	nod factor	NULL		bind	NULL				lectin	NULL				NULL	legume roots	0	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3459_s_256	11522814	8       Etzler,M.E., Kalsi,G., Ewing,N.N., Roberts,N.J., Day,R.B. and Murphy,J.B. (1999) A nod factor binding lectin with apyrase activity from legume roots.	bind
36289	2	8662	7	NULL	NULL	0	NULL	lectin	NULL		contains	NULL				apyrase activity	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_17_3459_s_256	11522814	8       Etzler,M.E., Kalsi,G., Ewing,N.N., Roberts,N.J., Day,R.B. and Murphy,J.B. (1999) A nod factor binding lectin with apyrase activity from legume roots.	bind
37333	1	8663	5	13	NULL	NULL	NULL	nuclear cap binding complex	GP	yeast	interact with					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1080_s_254	11222757	8       Fortes,P., Inada,T., Preiss,T., Hentze,M.W., Mattaj,I.W. and Sachs,A.B. (2000) The yeast nuclear cap binding complex can interact with translation factor eIF4G and mediate translation initiation.	bind
37334	2	8663	5	13	NULL	NULL	NULL	eIF4G	GP		is a type of					translation factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1080_s_254	11222757	8       Fortes,P., Inada,T., Preiss,T., Hentze,M.W., Mattaj,I.W. and Sachs,A.B. (2000) The yeast nuclear cap binding complex can interact with translation factor eIF4G and mediate translation initiation.	bind
37335	3	8663	5	13	NULL	NULL	NULL	statement 1	Process		mediate					translation	Process	initiation of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1080_s_254	11222757	8       Fortes,P., Inada,T., Preiss,T., Hentze,M.W., Mattaj,I.W. and Sachs,A.B. (2000) The yeast nuclear cap binding complex can interact with translation factor eIF4G and mediate translation initiation.	bind
36290	1	8663	7	NULL	NULL	0	NULL	nuclear cap binding complex	NULL	yeast	interacts with	NULL				eIF4G	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1080_s_254	11222757	8       Fortes,P., Inada,T., Preiss,T., Hentze,M.W., Mattaj,I.W. and Sachs,A.B. (2000) The yeast nuclear cap binding complex can interact with translation factor eIF4G and mediate translation initiation.	bind
36291	2	8663	7	NULL	NULL	0	NULL	statement 1	NULL		mediate	NULL				translation	NULL	initiation of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1080_s_254	11222757	8       Fortes,P., Inada,T., Preiss,T., Hentze,M.W., Mattaj,I.W. and Sachs,A.B. (2000) The yeast nuclear cap binding complex can interact with translation factor eIF4G and mediate translation initiation.	bind
36292	3	8663	7	NULL	NULL	0	NULL	eIF4G	NULL		is a type of	NULL				translation factor	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_5_1080_s_254	11222757	8       Fortes,P., Inada,T., Preiss,T., Hentze,M.W., Mattaj,I.W. and Sachs,A.B. (2000) The yeast nuclear cap binding complex can interact with translation factor eIF4G and mediate translation initiation.	bind
37336	1	8664	5	13	NULL	NULL	NULL	retinoblastoma protein	GP		bind					E2F residues	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3131_s_207	11470869	8       Hagemeier,C., Cook,A. and Kouzarides,T. (1993) The retinoblastoma protein binds E2F residues required for activation  in vivo and TBP binding  in vitro.	bind
37337	2	8664	5	13	NULL	NULL	NULL	E2F residues	GP		is required for					TBP	GP	binding of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3131_s_207	11470869	8       Hagemeier,C., Cook,A. and Kouzarides,T. (1993) The retinoblastoma protein binds E2F residues required for activation  in vivo and TBP binding  in vitro.	bind
36293	1	8664	7	NULL	NULL	0	NULL	 retinoblastoma protein	NULL		binds	NULL				E2F residues	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3131_s_207	11470869	8       Hagemeier,C., Cook,A. and Kouzarides,T. (1993) The retinoblastoma protein binds E2F residues required for activation  in vivo and TBP binding  in vitro.	bind
36295	2	8664	7	10	NULL	0	NULL	statement 1			is required for					TBP		binding of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3131_s_207	11470869	8       Hagemeier,C., Cook,A. and Kouzarides,T. (1993) The retinoblastoma protein binds E2F residues required for activation  in vivo and TBP binding  in vitro.	bind
37338	1	8665	5	13	NULL	NULL	NULL	XPA	GP		bind					RPA	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4948_s_197	11812824	8       Matsuda,T., Saijo,M., Kuraoka,I., Kobayashi,T., Nakatsu,Y., Nagai,A., Enjoji,T., Masutani,C., Sugasawa,K., Hanaoka,F., Yasui,A. and Tanaka,K. (1995) DNA repair protein XPA binds replication protein A (RPA).	bind
37339	2	8665	5	13	NULL	NULL	NULL	XPA	GP		is a type of					DNA repair protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4948_s_197	11812824	8       Matsuda,T., Saijo,M., Kuraoka,I., Kobayashi,T., Nakatsu,Y., Nagai,A., Enjoji,T., Masutani,C., Sugasawa,K., Hanaoka,F., Yasui,A. and Tanaka,K. (1995) DNA repair protein XPA binds replication protein A (RPA).	bind
37340	3	8665	5	13	NULL	NULL	NULL	RPA	GP		is					replication protein A	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4948_s_197	11812824	8       Matsuda,T., Saijo,M., Kuraoka,I., Kobayashi,T., Nakatsu,Y., Nagai,A., Enjoji,T., Masutani,C., Sugasawa,K., Hanaoka,F., Yasui,A. and Tanaka,K. (1995) DNA repair protein XPA binds replication protein A (RPA).	bind
36296	1	8665	7	NULL	NULL	0	NULL	XPA	NULL		binds	NULL				RPA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4948_s_197	11812824	8       Matsuda,T., Saijo,M., Kuraoka,I., Kobayashi,T., Nakatsu,Y., Nagai,A., Enjoji,T., Masutani,C., Sugasawa,K., Hanaoka,F., Yasui,A. and Tanaka,K. (1995) DNA repair protein XPA binds replication protein A (RPA).	bind
36297	2	8665	7	NULL	NULL	0	NULL	XPA	NULL		is a type of	NULL				DNA repair protein	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4948_s_197	11812824	8       Matsuda,T., Saijo,M., Kuraoka,I., Kobayashi,T., Nakatsu,Y., Nagai,A., Enjoji,T., Masutani,C., Sugasawa,K., Hanaoka,F., Yasui,A. and Tanaka,K. (1995) DNA repair protein XPA binds replication protein A (RPA).	bind
36298	3	8665	7	10	NULL	0	NULL	RPA			is					replication protein A					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_24_4948_s_197	11812824	8       Matsuda,T., Saijo,M., Kuraoka,I., Kobayashi,T., Nakatsu,Y., Nagai,A., Enjoji,T., Masutani,C., Sugasawa,K., Hanaoka,F., Yasui,A. and Tanaka,K. (1995) DNA repair protein XPA binds replication protein A (RPA).	bind
37341	1	8667	5	13	NULL	NULL	NULL	heparin	Chemical		associate with					antithrombin III	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_163	10510057	8  9 10 11  Besides the anticoagulative effects of heparin mediated by its association with antithrombin III, the described blockade of factor X binding to Mac-1 may participate in the anticoagulative properties of heparin.	bind
37342	2	8667	5	13	NULL	NULL	NULL	heparin	Chemical	anticoagulative effects of	is mediated by					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_163	10510057	8  9 10 11  Besides the anticoagulative effects of heparin mediated by its association with antithrombin III, the described blockade of factor X binding to Mac-1 may participate in the anticoagulative properties of heparin.	bind
37343	3	8667	5	13	NULL	NULL	NULL	factor X	GP		bind					Mac-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_163	10510057	8  9 10 11  Besides the anticoagulative effects of heparin mediated by its association with antithrombin III, the described blockade of factor X binding to Mac-1 may participate in the anticoagulative properties of heparin.	bind
37344	4	8667	5	13	NULL	NULL	NULL	statement 3	Process	blockade of	participate in					heparin	Chemical	anticoagulative properties of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_163	10510057	8  9 10 11  Besides the anticoagulative effects of heparin mediated by its association with antithrombin III, the described blockade of factor X binding to Mac-1 may participate in the anticoagulative properties of heparin.	bind
36610	1	8667	7	NULL	NULL	0	NULL	heparin	NULL		associate with	NULL				antithrombin III	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_163	10510057	8  9 10 11  Besides the anticoagulative effects of heparin mediated by its association with antithrombin III, the described blockade of factor X binding to Mac-1 may participate in the anticoagulative properties of heparin.	bind
36612	2	8667	7	NULL	NULL	0	NULL	factor X	NULL		bind	NULL				Mac-1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_163	10510057	8  9 10 11  Besides the anticoagulative effects of heparin mediated by its association with antithrombin III, the described blockade of factor X binding to Mac-1 may participate in the anticoagulative properties of heparin.	bind
36614	4	8667	7	NULL	NULL	0	NULL	statement 1	NULL		mediates	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_163	10510057	8  9 10 11  Besides the anticoagulative effects of heparin mediated by its association with antithrombin III, the described blockade of factor X binding to Mac-1 may participate in the anticoagulative properties of heparin.	bind
36615	4	8667	7	NULL	NULL	0	NULL	statement 2	NULL	blocking of	participate in	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_163	10510057	8  9 10 11  Besides the anticoagulative effects of heparin mediated by its association with antithrombin III, the described blockade of factor X binding to Mac-1 may participate in the anticoagulative properties of heparin.	bind
46729	3	8667	7	NULL	NULL	0	NULL	heparin	NULL		exhibit	NULL				 anticoagulative properties	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_14_1533_s_163	10510057	8  9 10 11  Besides the anticoagulative effects of heparin mediated by its association with antithrombin III, the described blockade of factor X binding to Mac-1 may participate in the anticoagulative properties of heparin.	bind
37345	1	8668	5	13	NULL	NULL	NULL	GSK-3beta	GP		phosphorylate					glycogen synthase	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_5_1597_s_12	11696419	8  Among them are the serine/threonine protein kinase glycogen synthase kinase-3beta (GSK-3beta) 9 and a novel presenilin binding protein named PBP. 10  GSK-3beta was initially purified as an enzyme that phosphorylates and inactivates glycogen synthase, but it was later shown that it has the ability to phosphorylate [[ the neurofibrillary protein tau. 11  PBP ]] was identified by its ability to bind to the large cytoplasmic loop of PS1 in the yeast two-hybrid system.	bind
37346	2	8668	5	13	NULL	NULL	NULL	statement 1	Process		inactivate					glycogen synthase	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_5_1597_s_12	11696419	8  Among them are the serine/threonine protein kinase glycogen synthase kinase-3beta (GSK-3beta) 9 and a novel presenilin binding protein named PBP. 10  GSK-3beta was initially purified as an enzyme that phosphorylates and inactivates glycogen synthase, but it was later shown that it has the ability to phosphorylate [[ the neurofibrillary protein tau. 11  PBP ]] was identified by its ability to bind to the large cytoplasmic loop of PS1 in the yeast two-hybrid system.	bind
37347	3	8668	5	13	NULL	NULL	NULL	GSK-3beta	GP		is					glycogen synthase kinase-3beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_5_1597_s_12	11696419	8  Among them are the serine/threonine protein kinase glycogen synthase kinase-3beta (GSK-3beta) 9 and a novel presenilin binding protein named PBP. 10  GSK-3beta was initially purified as an enzyme that phosphorylates and inactivates glycogen synthase, but it was later shown that it has the ability to phosphorylate [[ the neurofibrillary protein tau. 11  PBP ]] was identified by its ability to bind to the large cytoplasmic loop of PS1 in the yeast two-hybrid system.	bind
37348	4	8668	5	13	NULL	NULL	NULL	GSK-3beta	GP		is a type of					serine/threonine protein kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_5_1597_s_12	11696419	8  Among them are the serine/threonine protein kinase glycogen synthase kinase-3beta (GSK-3beta) 9 and a novel presenilin binding protein named PBP. 10  GSK-3beta was initially purified as an enzyme that phosphorylates and inactivates glycogen synthase, but it was later shown that it has the ability to phosphorylate [[ the neurofibrillary protein tau. 11  PBP ]] was identified by its ability to bind to the large cytoplasmic loop of PS1 in the yeast two-hybrid system.	bind
37350	6	8668	5	13	NULL	NULL	NULL	tau	GP		is a type of					neurofibrillary protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_5_1597_s_12	11696419	8  Among them are the serine/threonine protein kinase glycogen synthase kinase-3beta (GSK-3beta) 9 and a novel presenilin binding protein named PBP. 10  GSK-3beta was initially purified as an enzyme that phosphorylates and inactivates glycogen synthase, but it was later shown that it has the ability to phosphorylate [[ the neurofibrillary protein tau. 11  PBP ]] was identified by its ability to bind to the large cytoplasmic loop of PS1 in the yeast two-hybrid system.	bind
37351	7	8668	5	13	NULL	NULL	NULL	PBP	GP		is					presenilin binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_5_1597_s_12	11696419	8  Among them are the serine/threonine protein kinase glycogen synthase kinase-3beta (GSK-3beta) 9 and a novel presenilin binding protein named PBP. 10  GSK-3beta was initially purified as an enzyme that phosphorylates and inactivates glycogen synthase, but it was later shown that it has the ability to phosphorylate [[ the neurofibrillary protein tau. 11  PBP ]] was identified by its ability to bind to the large cytoplasmic loop of PS1 in the yeast two-hybrid system.	bind
37352	8	8668	5	13	NULL	NULL	NULL	PBP	GP		bind					PS1	GP		cytoplasmic loop		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_159_5_1597_s_12	11696419	8  Among them are the serine/threonine protein kinase glycogen synthase kinase-3beta (GSK-3beta) 9 and a novel presenilin binding protein named PBP. 10  GSK-3beta was initially purified as an enzyme that phosphorylates and inactivates glycogen synthase, but it was later shown that it has the ability to phosphorylate [[ the neurofibrillary protein tau. 11  PBP ]] was identified by its ability to bind to the large cytoplasmic loop of PS1 in the yeast two-hybrid system.	bind
36617	1	8668	7	NULL	NULL	0	NULL	GSK-3beta	NULL		phosphorylates	NULL				glycogen synthase	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_5_1597_s_12	11696419	8  Among them are the serine/threonine protein kinase glycogen synthase kinase-3beta (GSK-3beta) 9 and a novel presenilin binding protein named PBP. 10  GSK-3beta was initially purified as an enzyme that phosphorylates and inactivates glycogen synthase, but it was later shown that it has the ability to phosphorylate [[ the neurofibrillary protein tau. 11  PBP ]] was identified by its ability to bind to the large cytoplasmic loop of PS1 in the yeast two-hybrid system.	bind
36619	2	8668	7	NULL	NULL	0	NULL	statement 1	NULL		inactivates	NULL				glycogen synthase	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_5_1597_s_12	11696419	8  Among them are the serine/threonine protein kinase glycogen synthase kinase-3beta (GSK-3beta) 9 and a novel presenilin binding protein named PBP. 10  GSK-3beta was initially purified as an enzyme that phosphorylates and inactivates glycogen synthase, but it was later shown that it has the ability to phosphorylate [[ the neurofibrillary protein tau. 11  PBP ]] was identified by its ability to bind to the large cytoplasmic loop of PS1 in the yeast two-hybrid system.	bind
36621	3	8668	7	NULL	NULL	0	NULL	GSK-3beta	NULL		phosphorylate	NULL				tau	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_5_1597_s_12	11696419	8  Among them are the serine/threonine protein kinase glycogen synthase kinase-3beta (GSK-3beta) 9 and a novel presenilin binding protein named PBP. 10  GSK-3beta was initially purified as an enzyme that phosphorylates and inactivates glycogen synthase, but it was later shown that it has the ability to phosphorylate [[ the neurofibrillary protein tau. 11  PBP ]] was identified by its ability to bind to the large cytoplasmic loop of PS1 in the yeast two-hybrid system.	bind
36624	4	8668	7	NULL	NULL	0	NULL	tau	NULL		is a type of	NULL				neurofibrillary protein	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_5_1597_s_12	11696419	8  Among them are the serine/threonine protein kinase glycogen synthase kinase-3beta (GSK-3beta) 9 and a novel presenilin binding protein named PBP. 10  GSK-3beta was initially purified as an enzyme that phosphorylates and inactivates glycogen synthase, but it was later shown that it has the ability to phosphorylate [[ the neurofibrillary protein tau. 11  PBP ]] was identified by its ability to bind to the large cytoplasmic loop of PS1 in the yeast two-hybrid system.	bind
36626	5	8668	7	NULL	NULL	0	NULL	PBP	NULL		bind	NULL				PS1	NULL		large cytoplasmic loop of 		NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_5_1597_s_12	11696419	8  Among them are the serine/threonine protein kinase glycogen synthase kinase-3beta (GSK-3beta) 9 and a novel presenilin binding protein named PBP. 10  GSK-3beta was initially purified as an enzyme that phosphorylates and inactivates glycogen synthase, but it was later shown that it has the ability to phosphorylate [[ the neurofibrillary protein tau. 11  PBP ]] was identified by its ability to bind to the large cytoplasmic loop of PS1 in the yeast two-hybrid system.	bind
36627	6	8668	7	NULL	NULL	0	NULL	PBP	NULL		is	NULL				presenilin binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_5_1597_s_12	11696419	8  Among them are the serine/threonine protein kinase glycogen synthase kinase-3beta (GSK-3beta) 9 and a novel presenilin binding protein named PBP. 10  GSK-3beta was initially purified as an enzyme that phosphorylates and inactivates glycogen synthase, but it was later shown that it has the ability to phosphorylate [[ the neurofibrillary protein tau. 11  PBP ]] was identified by its ability to bind to the large cytoplasmic loop of PS1 in the yeast two-hybrid system.	bind
36628	7	8668	7	NULL	NULL	0	NULL	GSK-3beta	NULL		is	NULL				serine/threonine protein kinase glycogen synthase kinase-3beta 	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_159_5_1597_s_12	11696419	8  Among them are the serine/threonine protein kinase glycogen synthase kinase-3beta (GSK-3beta) 9 and a novel presenilin binding protein named PBP. 10  GSK-3beta was initially purified as an enzyme that phosphorylates and inactivates glycogen synthase, but it was later shown that it has the ability to phosphorylate [[ the neurofibrillary protein tau. 11  PBP ]] was identified by its ability to bind to the large cytoplasmic loop of PS1 in the yeast two-hybrid system.	bind
37496	1	8669	5	13	NULL	NULL	NULL	factor VII	GP		inhibit					thrombin	GP	generation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_21_2555_s_124	11382723	8  An alternative explanation might be provided by the hypothesis that factor VIIa is able to overcome the inhibitory effect of factor VII on thrombin generation, thereby displacing factor VII bound to tissue factor, resulting in additional thrombin generation.	bind
37497	2	8669	5	13	NULL	NULL	NULL	factor VIIa	GP		overcomes		potentially			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_21_2555_s_124	11382723	8  An alternative explanation might be provided by the hypothesis that factor VIIa is able to overcome the inhibitory effect of factor VII on thrombin generation, thereby displacing factor VII bound to tissue factor, resulting in additional thrombin generation.	bind
37498	3	8669	5	13	NULL	NULL	NULL	factor VII	GP		bind					tissue factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_21_2555_s_124	11382723	8  An alternative explanation might be provided by the hypothesis that factor VIIa is able to overcome the inhibitory effect of factor VII on thrombin generation, thereby displacing factor VII bound to tissue factor, resulting in additional thrombin generation.	bind
37499	4	8669	5	13	NULL	NULL	NULL	factor VIIa	GP		displaces		potentially			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_21_2555_s_124	11382723	8  An alternative explanation might be provided by the hypothesis that factor VIIa is able to overcome the inhibitory effect of factor VII on thrombin generation, thereby displacing factor VII bound to tissue factor, resulting in additional thrombin generation.	bind
37500	5	8669	5	13	NULL	NULL	NULL	statement 4	Process		results in		potentially			thrombin	GP	generation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_21_2555_s_124	11382723	8  An alternative explanation might be provided by the hypothesis that factor VIIa is able to overcome the inhibitory effect of factor VII on thrombin generation, thereby displacing factor VII bound to tissue factor, resulting in additional thrombin generation.	bind
36629	1	8669	7	NULL	NULL	0	NULL	 factor VII 	NULL		bind	NULL				tissue factor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_21_2555_s_124	11382723	8  An alternative explanation might be provided by the hypothesis that factor VIIa is able to overcome the inhibitory effect of factor VII on thrombin generation, thereby displacing factor VII bound to tissue factor, resulting in additional thrombin generation.	bind
36630	2	8669	7	NULL	NULL	0	NULL	factor VII	NULL		inhibits	NULL				thrombin	NULL	generation of			NULL		0	NULL	NULL	NULL	gw60_circulation_103_21_2555_s_124	11382723	8  An alternative explanation might be provided by the hypothesis that factor VIIa is able to overcome the inhibitory effect of factor VII on thrombin generation, thereby displacing factor VII bound to tissue factor, resulting in additional thrombin generation.	bind
36631	3	8669	7	NULL	NULL	0	NULL	factor VIIa	NULL		displace	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_21_2555_s_124	11382723	8  An alternative explanation might be provided by the hypothesis that factor VIIa is able to overcome the inhibitory effect of factor VII on thrombin generation, thereby displacing factor VII bound to tissue factor, resulting in additional thrombin generation.	bind
36632	4	8669	7	NULL	NULL	0	NULL	factor VIIa	NULL		overcome	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_21_2555_s_124	11382723	8  An alternative explanation might be provided by the hypothesis that factor VIIa is able to overcome the inhibitory effect of factor VII on thrombin generation, thereby displacing factor VII bound to tissue factor, resulting in additional thrombin generation.	bind
36633	5	8669	7	NULL	NULL	0	NULL	statement 4	NULL		results in	NULL				thrombin	NULL	generation of			NULL		0	NULL	NULL	NULL	gw60_circulation_103_21_2555_s_124	11382723	8  An alternative explanation might be provided by the hypothesis that factor VIIa is able to overcome the inhibitory effect of factor VII on thrombin generation, thereby displacing factor VII bound to tissue factor, resulting in additional thrombin generation.	bind
37503	1	8671	5	13	NULL	NULL	NULL	beta2GPI	GP		bind			lysine-rich locus in fifth domain		PLs	Chemical	negatively charged			NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_9_900_s_27	9521339	8  beta2GPI binds negatively charged PLs through a lysine-rich locus in the fifth domain 9  10  and possesses several in vitro properties that define it as an anticoagulant (ie, inhibition of prothrombinase activity, ADP-induced platelet aggregation, or platelet factor IX production).	bind
37504	2	8671	5	13	NULL	NULL	NULL	beta2GPI	GP		is a type of					anticoagulant	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_9_900_s_27	9521339	8  beta2GPI binds negatively charged PLs through a lysine-rich locus in the fifth domain 9  10  and possesses several in vitro properties that define it as an anticoagulant (ie, inhibition of prothrombinase activity, ADP-induced platelet aggregation, or platelet factor IX production).	bind
37505	3	8671	5	13	NULL	NULL	NULL	beta2GPI	GP		inhibit					prothrombinase activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_9_900_s_27	9521339	8  beta2GPI binds negatively charged PLs through a lysine-rich locus in the fifth domain 9  10  and possesses several in vitro properties that define it as an anticoagulant (ie, inhibition of prothrombinase activity, ADP-induced platelet aggregation, or platelet factor IX production).	bind
37506	4	8671	5	13	NULL	NULL	NULL	ADP	Chemical		induce					platelet	Cell	aggregation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_9_900_s_27	9521339	8  beta2GPI binds negatively charged PLs through a lysine-rich locus in the fifth domain 9  10  and possesses several in vitro properties that define it as an anticoagulant (ie, inhibition of prothrombinase activity, ADP-induced platelet aggregation, or platelet factor IX production).	bind
37507	5	8671	5	13	NULL	NULL	NULL	beta2GPI	GP		inhibit					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_9_900_s_27	9521339	8  beta2GPI binds negatively charged PLs through a lysine-rich locus in the fifth domain 9  10  and possesses several in vitro properties that define it as an anticoagulant (ie, inhibition of prothrombinase activity, ADP-induced platelet aggregation, or platelet factor IX production).	bind
37508	6	8671	5	13	NULL	NULL	NULL	beta2GPI	GP		inhibit					platelet factor IX	GP	production of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_9_900_s_27	9521339	8  beta2GPI binds negatively charged PLs through a lysine-rich locus in the fifth domain 9  10  and possesses several in vitro properties that define it as an anticoagulant (ie, inhibition of prothrombinase activity, ADP-induced platelet aggregation, or platelet factor IX production).	bind
36635	1	8671	7	10	NULL	0	NULL	beta2GPI 			binds			lysine-rich locus in the fifth domain		PLs		negatively charged			NULL		NULL	NULL	NULL	NULL	gw60_circulation_97_9_900_s_27	9521339	8  beta2GPI binds negatively charged PLs through a lysine-rich locus in the fifth domain 9  10  and possesses several in vitro properties that define it as an anticoagulant (ie, inhibition of prothrombinase activity, ADP-induced platelet aggregation, or platelet factor IX production).	bind
36636	2	8671	7	NULL	NULL	0	NULL	statement 1	NULL		possess	NULL				in vitro properties	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_97_9_900_s_27	9521339	8  beta2GPI binds negatively charged PLs through a lysine-rich locus in the fifth domain 9  10  and possesses several in vitro properties that define it as an anticoagulant (ie, inhibition of prothrombinase activity, ADP-induced platelet aggregation, or platelet factor IX production).	bind
36637	3	8671	7	NULL	NULL	0	NULL	statement 1	NULL		act as an	NULL				anticoagulant	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_97_9_900_s_27	9521339	8  beta2GPI binds negatively charged PLs through a lysine-rich locus in the fifth domain 9  10  and possesses several in vitro properties that define it as an anticoagulant (ie, inhibition of prothrombinase activity, ADP-induced platelet aggregation, or platelet factor IX production).	bind
36638	4	8671	7	NULL	NULL	0	NULL	ADP	NULL		induce	NULL				platelet 	NULL	aggregation of			NULL		0	NULL	NULL	NULL	gw60_circulation_97_9_900_s_27	9521339	8  beta2GPI binds negatively charged PLs through a lysine-rich locus in the fifth domain 9  10  and possesses several in vitro properties that define it as an anticoagulant (ie, inhibition of prothrombinase activity, ADP-induced platelet aggregation, or platelet factor IX production).	bind
36639	5	8671	7	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				prothrombinase activity	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_97_9_900_s_27	9521339	8  beta2GPI binds negatively charged PLs through a lysine-rich locus in the fifth domain 9  10  and possesses several in vitro properties that define it as an anticoagulant (ie, inhibition of prothrombinase activity, ADP-induced platelet aggregation, or platelet factor IX production).	bind
36640	6	8671	7	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_97_9_900_s_27	9521339	8  beta2GPI binds negatively charged PLs through a lysine-rich locus in the fifth domain 9  10  and possesses several in vitro properties that define it as an anticoagulant (ie, inhibition of prothrombinase activity, ADP-induced platelet aggregation, or platelet factor IX production).	bind
36641	7	8671	7	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				platelet factor IX	NULL	production of			NULL		0	NULL	NULL	NULL	gw60_circulation_97_9_900_s_27	9521339	8  beta2GPI binds negatively charged PLs through a lysine-rich locus in the fifth domain 9  10  and possesses several in vitro properties that define it as an anticoagulant (ie, inhibition of prothrombinase activity, ADP-induced platelet aggregation, or platelet factor IX production).	bind
37509	1	8672	5	13	NULL	NULL	NULL	rabphilin-3A	GP		bind			amino (NH2)-terminal half		Rab3A	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_3_889_s_16	12937130	8  Binding of rabphilin-3A to Rab3A occurs via the amino (NH2)-terminal half of rabphilin-3A.	bind
36642	1	8672	7	NULL	NULL	0	NULL	rabphilin-3A	NULL		bind	NULL		amino (NH2)-terminal half of		Rab3A	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_163_3_889_s_16	12937130	8  Binding of rabphilin-3A to Rab3A occurs via the amino (NH2)-terminal half of rabphilin-3A.	bind
37510	1	8673	5	13	NULL	NULL	NULL	apoB-100	GP		bind					LDLR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_5_826_s_24	9157944	8  Defective apoB-100 has been shown to reduce significantly the binding of apoB-100 to the LDLR, 2 9 10  which results in elevated LDL cholesterol levels in carriers of this mutation.	bind
37511	2	8673	5	13	NULL	NULL	NULL	apoB-100	GP	mutant	reduce		significantly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_5_826_s_24	9157944	8  Defective apoB-100 has been shown to reduce significantly the binding of apoB-100 to the LDLR, 2 9 10  which results in elevated LDL cholesterol levels in carriers of this mutation.	bind
37512	3	8673	5	13	NULL	NULL	NULL	statement 2	Process		results in					LDL cholesterol	Chemical	elevated levels of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_5_826_s_24	9157944	8  Defective apoB-100 has been shown to reduce significantly the binding of apoB-100 to the LDLR, 2 9 10  which results in elevated LDL cholesterol levels in carriers of this mutation.	bind
36643	1	8673	7	NULL	NULL	0	NULL	apoB-100	NULL		bind	NULL				LDLR	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_5_826_s_24	9157944	8  Defective apoB-100 has been shown to reduce significantly the binding of apoB-100 to the LDLR, 2 9 10  which results in elevated LDL cholesterol levels in carriers of this mutation.	bind
36644	2	8673	7	10	NULL	0	NULL	apoB-100		mutant	reduce		significantly			statement 1					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_5_826_s_24	9157944	8  Defective apoB-100 has been shown to reduce significantly the binding of apoB-100 to the LDLR, 2 9 10  which results in elevated LDL cholesterol levels in carriers of this mutation.	bind
36645	3	8673	7	NULL	NULL	0	NULL	statement 2	NULL		results in	NULL				LDL cholesterol	NULL	elevated levels of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_5_826_s_24	9157944	8  Defective apoB-100 has been shown to reduce significantly the binding of apoB-100 to the LDLR, 2 9 10  which results in elevated LDL cholesterol levels in carriers of this mutation.	bind
37513	1	8674	5	13	NULL	NULL	NULL	VLDL	GP		bind					macrophages	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_392_s_205	7538426	8  LPL increases the binding of VLDL and LDL to macrophages, thus enhancing their uptake of triglyceride-rich lipoproteins.	bind
37514	2	8674	5	13	NULL	NULL	NULL	LDL	GP		bind					macrophages	Cell				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_392_s_205	7538426	8  LPL increases the binding of VLDL and LDL to macrophages, thus enhancing their uptake of triglyceride-rich lipoproteins.	bind
37515	3	8674	5	13	NULL	NULL	NULL	LPL	GP		increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_392_s_205	7538426	8  LPL increases the binding of VLDL and LDL to macrophages, thus enhancing their uptake of triglyceride-rich lipoproteins.	bind
37516	5	8674	5	13	NULL	NULL	NULL	VLDL	GP		uptake					lipoproteins	GP	triglyceride-rich			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_392_s_205	7538426	8  LPL increases the binding of VLDL and LDL to macrophages, thus enhancing their uptake of triglyceride-rich lipoproteins.	bind
37517	6	8674	5	13	NULL	NULL	NULL	LDL	GP		uptake					lipoproteins	GP	triglyceride-rich			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_392_s_205	7538426	8  LPL increases the binding of VLDL and LDL to macrophages, thus enhancing their uptake of triglyceride-rich lipoproteins.	bind
37518	4	8674	5	13	NULL	NULL	NULL	LPL	GP		increase					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_392_s_205	7538426	8  LPL increases the binding of VLDL and LDL to macrophages, thus enhancing their uptake of triglyceride-rich lipoproteins.	bind
37519	7	8674	5	13	NULL	NULL	NULL	LPL	GP		enhance					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_392_s_205	7538426	8  LPL increases the binding of VLDL and LDL to macrophages, thus enhancing their uptake of triglyceride-rich lipoproteins.	bind
37520	8	8674	5	13	NULL	NULL	NULL	LPL	GP		enhance					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_392_s_205	7538426	8  LPL increases the binding of VLDL and LDL to macrophages, thus enhancing their uptake of triglyceride-rich lipoproteins.	bind
36646	1	8674	7	NULL	NULL	0	NULL	VLDL	NULL		bind	NULL				macrophages	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_392_s_205	7538426	8  LPL increases the binding of VLDL and LDL to macrophages, thus enhancing their uptake of triglyceride-rich lipoproteins.	bind
36647	2	8674	7	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				macrophages	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_392_s_205	7538426	8  LPL increases the binding of VLDL and LDL to macrophages, thus enhancing their uptake of triglyceride-rich lipoproteins.	bind
36648	3	8674	7	NULL	NULL	0	NULL	LPL	NULL		increase	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_392_s_205	7538426	8  LPL increases the binding of VLDL and LDL to macrophages, thus enhancing their uptake of triglyceride-rich lipoproteins.	bind
36649	4	8674	7	NULL	NULL	0	NULL	LPL	NULL		increase	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_392_s_205	7538426	8  LPL increases the binding of VLDL and LDL to macrophages, thus enhancing their uptake of triglyceride-rich lipoproteins.	bind
36650	5	8674	7	10	NULL	0	NULL	VLDL	NULL		uptake of	NULL				lipoproteins	NULL	triglyceride-rich			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_392_s_205	7538426	8  LPL increases the binding of VLDL and LDL to macrophages, thus enhancing their uptake of triglyceride-rich lipoproteins.	bind
36651	6	8674	7	10	NULL	0	NULL	LDL	NULL		uptake of	NULL				lipoproteins	NULL	triglyceride-rich 			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_392_s_205	7538426	8  LPL increases the binding of VLDL and LDL to macrophages, thus enhancing their uptake of triglyceride-rich lipoproteins.	bind
36652	7	8674	7	NULL	NULL	0	NULL	LPL	NULL		enhance	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_392_s_205	7538426	8  LPL increases the binding of VLDL and LDL to macrophages, thus enhancing their uptake of triglyceride-rich lipoproteins.	bind
36653	8	8674	7	NULL	NULL	0	NULL	LPL	NULL		enhance	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_3_392_s_205	7538426	8  LPL increases the binding of VLDL and LDL to macrophages, thus enhancing their uptake of triglyceride-rich lipoproteins.	bind
37521	1	8675	5	13	NULL	NULL	NULL	LDL	GP		activates					p44mapk isoform	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2412_s_22	10521371	8  Recently we demonstrated that LDL activates the 44 kDa and the 42 kDa mitogen-activated protein (MAP) kinase (p44mapk/p42mapk) isoforms as well as elevates [Ca2+]i via a pertussis-toxin (PTX)-sensitive guanosine triphosphate binding protein (Gi protein)-coupled receptor that is independent from its classical receptor.	bind
37522	2	8675	5	13	NULL	NULL	NULL	LDL	GP		activates					p42mapk isoform	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2412_s_22	10521371	8  Recently we demonstrated that LDL activates the 44 kDa and the 42 kDa mitogen-activated protein (MAP) kinase (p44mapk/p42mapk) isoforms as well as elevates [Ca2+]i via a pertussis-toxin (PTX)-sensitive guanosine triphosphate binding protein (Gi protein)-coupled receptor that is independent from its classical receptor.	bind
37523	3	8675	5	13	NULL	NULL	NULL	p44mapk	GP		is					44 kDa mitogen-activated protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2412_s_22	10521371	8  Recently we demonstrated that LDL activates the 44 kDa and the 42 kDa mitogen-activated protein (MAP) kinase (p44mapk/p42mapk) isoforms as well as elevates [Ca2+]i via a pertussis-toxin (PTX)-sensitive guanosine triphosphate binding protein (Gi protein)-coupled receptor that is independent from its classical receptor.	bind
37524	4	8675	5	13	NULL	NULL	NULL	p42mapk	GP		is					42 kDa mitogen-activated protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2412_s_22	10521371	8  Recently we demonstrated that LDL activates the 44 kDa and the 42 kDa mitogen-activated protein (MAP) kinase (p44mapk/p42mapk) isoforms as well as elevates [Ca2+]i via a pertussis-toxin (PTX)-sensitive guanosine triphosphate binding protein (Gi protein)-coupled receptor that is independent from its classical receptor.	bind
37525	5	8675	5	13	NULL	NULL	NULL	LDL	GP		elevate					[Ca2+]i	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2412_s_22	10521371	8  Recently we demonstrated that LDL activates the 44 kDa and the 42 kDa mitogen-activated protein (MAP) kinase (p44mapk/p42mapk) isoforms as well as elevates [Ca2+]i via a pertussis-toxin (PTX)-sensitive guanosine triphosphate binding protein (Gi protein)-coupled receptor that is independent from its classical receptor.	bind
37526	6	8675	5	13	NULL	NULL	NULL	statement 5	Process		via					Gi protein-coupled receptor	GP	PTX-sensitive			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2412_s_22	10521371	8  Recently we demonstrated that LDL activates the 44 kDa and the 42 kDa mitogen-activated protein (MAP) kinase (p44mapk/p42mapk) isoforms as well as elevates [Ca2+]i via a pertussis-toxin (PTX)-sensitive guanosine triphosphate binding protein (Gi protein)-coupled receptor that is independent from its classical receptor.	bind
37527	7	8675	5	13	NULL	NULL	NULL	Gi protein-coupled receptor	GP	PTX-sensitive	is independent from					classical receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2412_s_22	10521371	8  Recently we demonstrated that LDL activates the 44 kDa and the 42 kDa mitogen-activated protein (MAP) kinase (p44mapk/p42mapk) isoforms as well as elevates [Ca2+]i via a pertussis-toxin (PTX)-sensitive guanosine triphosphate binding protein (Gi protein)-coupled receptor that is independent from its classical receptor.	bind
37528	8	8675	5	13	NULL	NULL	NULL	PTX	Chemical		is					pertussis-toxin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2412_s_22	10521371	8  Recently we demonstrated that LDL activates the 44 kDa and the 42 kDa mitogen-activated protein (MAP) kinase (p44mapk/p42mapk) isoforms as well as elevates [Ca2+]i via a pertussis-toxin (PTX)-sensitive guanosine triphosphate binding protein (Gi protein)-coupled receptor that is independent from its classical receptor.	bind
37529	9	8675	5	13	NULL	NULL	NULL	Gi protein	GP		is					guanosine triphosphate binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2412_s_22	10521371	8  Recently we demonstrated that LDL activates the 44 kDa and the 42 kDa mitogen-activated protein (MAP) kinase (p44mapk/p42mapk) isoforms as well as elevates [Ca2+]i via a pertussis-toxin (PTX)-sensitive guanosine triphosphate binding protein (Gi protein)-coupled receptor that is independent from its classical receptor.	bind
36654	1	8675	7	10	NULL	0	NULL	 LDL			activates					p44mapk isoform					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2412_s_22	10521371	8  Recently we demonstrated that LDL activates the 44 kDa and the 42 kDa mitogen-activated protein (MAP) kinase (p44mapk/p42mapk) isoforms as well as elevates [Ca2+]i via a pertussis-toxin (PTX)-sensitive guanosine triphosphate binding protein (Gi protein)-coupled receptor that is independent from its classical receptor.	bind
36655	2	8675	7	10	NULL	0	NULL	p44mapk isoform			is a type of					MAP kinase					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2412_s_22	10521371	8  Recently we demonstrated that LDL activates the 44 kDa and the 42 kDa mitogen-activated protein (MAP) kinase (p44mapk/p42mapk) isoforms as well as elevates [Ca2+]i via a pertussis-toxin (PTX)-sensitive guanosine triphosphate binding protein (Gi protein)-coupled receptor that is independent from its classical receptor.	bind
36656	3	8675	7	NULL	NULL	0	NULL	LDL	NULL		elevates	NULL				[Ca2+]i 	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2412_s_22	10521371	8  Recently we demonstrated that LDL activates the 44 kDa and the 42 kDa mitogen-activated protein (MAP) kinase (p44mapk/p42mapk) isoforms as well as elevates [Ca2+]i via a pertussis-toxin (PTX)-sensitive guanosine triphosphate binding protein (Gi protein)-coupled receptor that is independent from its classical receptor.	bind
36657	4	8675	7	10	NULL	0	NULL	statement 3	NULL		occurs via	NULL				Gi protein coupled receptor	NULL	PTX-sensitive			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2412_s_22	10521371	8  Recently we demonstrated that LDL activates the 44 kDa and the 42 kDa mitogen-activated protein (MAP) kinase (p44mapk/p42mapk) isoforms as well as elevates [Ca2+]i via a pertussis-toxin (PTX)-sensitive guanosine triphosphate binding protein (Gi protein)-coupled receptor that is independent from its classical receptor.	bind
36658	5	8675	7	NULL	NULL	0	NULL	MAP	NULL		is 	NULL				mitogen-activated protein	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2412_s_22	10521371	8  Recently we demonstrated that LDL activates the 44 kDa and the 42 kDa mitogen-activated protein (MAP) kinase (p44mapk/p42mapk) isoforms as well as elevates [Ca2+]i via a pertussis-toxin (PTX)-sensitive guanosine triphosphate binding protein (Gi protein)-coupled receptor that is independent from its classical receptor.	bind
36659	6	8675	7	NULL	NULL	0	NULL	PTX	NULL		is	NULL				pertussis-toxin 	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2412_s_22	10521371	8  Recently we demonstrated that LDL activates the 44 kDa and the 42 kDa mitogen-activated protein (MAP) kinase (p44mapk/p42mapk) isoforms as well as elevates [Ca2+]i via a pertussis-toxin (PTX)-sensitive guanosine triphosphate binding protein (Gi protein)-coupled receptor that is independent from its classical receptor.	bind
36660	7	8675	7	NULL	NULL	0	NULL	Gi protein	NULL		is	NULL				guanosine triphosphate binding protein 	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2412_s_22	10521371	8  Recently we demonstrated that LDL activates the 44 kDa and the 42 kDa mitogen-activated protein (MAP) kinase (p44mapk/p42mapk) isoforms as well as elevates [Ca2+]i via a pertussis-toxin (PTX)-sensitive guanosine triphosphate binding protein (Gi protein)-coupled receptor that is independent from its classical receptor.	bind
56305	8	8675	7	10	NULL	0	NULL	LDL			activates					p42mapk					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2412_s_22	10521371	8  Recently we demonstrated that LDL activates the 44 kDa and the 42 kDa mitogen-activated protein (MAP) kinase (p44mapk/p42mapk) isoforms as well as elevates [Ca2+]i via a pertussis-toxin (PTX)-sensitive guanosine triphosphate binding protein (Gi protein)-coupled receptor that is independent from its classical receptor.	bind
56306	9	8675	7	10	NULL	0	NULL	p42mapk isoform			is a type of					MAP kinase					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2412_s_22	10521371	8  Recently we demonstrated that LDL activates the 44 kDa and the 42 kDa mitogen-activated protein (MAP) kinase (p44mapk/p42mapk) isoforms as well as elevates [Ca2+]i via a pertussis-toxin (PTX)-sensitive guanosine triphosphate binding protein (Gi protein)-coupled receptor that is independent from its classical receptor.	bind
37531	1	8676	5	13	NULL	NULL	NULL	polycystin-1	GP		bind		may	cytoplasmic tail		heterotrimeric G proteins	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_973_s_19	11891195	8  The cytoplasmic tail of polycystin-1 may bind heterotrimeric G proteins  in vitro, 9  activate the transcription factor AP-1, 10  and have a role in modulating Wnt signaling.	bind
37532	2	8676	5	13	NULL	NULL	NULL	polycystin-1	GP		activates		may	cytoplasmic tail		AP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_973_s_19	11891195	8  The cytoplasmic tail of polycystin-1 may bind heterotrimeric G proteins  in vitro, 9  activate the transcription factor AP-1, 10  and have a role in modulating Wnt signaling.	bind
37533	3	8676	5	13	NULL	NULL	NULL	AP-1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_973_s_19	11891195	8  The cytoplasmic tail of polycystin-1 may bind heterotrimeric G proteins  in vitro, 9  activate the transcription factor AP-1, 10  and have a role in modulating Wnt signaling.	bind
37534	4	8676	5	13	NULL	NULL	NULL	polycystin-1	GP		modulates		may	cytoplasmic tail		Wnt signaling	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_973_s_19	11891195	8  The cytoplasmic tail of polycystin-1 may bind heterotrimeric G proteins  in vitro, 9  activate the transcription factor AP-1, 10  and have a role in modulating Wnt signaling.	bind
36661	1	8676	7	NULL	NULL	0	NULL	polycystin-1	NULL		bind	NULL	may	cytoplasmic tail of 		 heterotrimeric G proteins	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_amjpathol_160_3_973_s_19	11891195	8  The cytoplasmic tail of polycystin-1 may bind heterotrimeric G proteins  in vitro, 9  activate the transcription factor AP-1, 10  and have a role in modulating Wnt signaling.	bind
36662	2	8676	7	NULL	NULL	0	NULL	statement 1	NULL		activate	NULL				AP-1	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_3_973_s_19	11891195	8  The cytoplasmic tail of polycystin-1 may bind heterotrimeric G proteins  in vitro, 9  activate the transcription factor AP-1, 10  and have a role in modulating Wnt signaling.	bind
36663	3	8676	7	NULL	NULL	0	NULL	AP-1	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_3_973_s_19	11891195	8  The cytoplasmic tail of polycystin-1 may bind heterotrimeric G proteins  in vitro, 9  activate the transcription factor AP-1, 10  and have a role in modulating Wnt signaling.	bind
36664	4	8676	7	NULL	NULL	0	NULL	statement 2	NULL		modulates	NULL				Wnt signaling	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_3_973_s_19	11891195	8  The cytoplasmic tail of polycystin-1 may bind heterotrimeric G proteins  in vitro, 9  activate the transcription factor AP-1, 10  and have a role in modulating Wnt signaling.	bind
37536	1	8678	5	13	NULL	NULL	NULL	UPA	GP		bind					pro-UPA	GP	inactive			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_29	9598826	8  UPA can bind to the UPAR in either its inactive proenzyme form (pro-UPA) or active two-chain form without affecting its proteolytic activity.	bind
37537	2	8678	5	13	NULL	NULL	NULL	pro-UPA	GP		is					proenzyme form of UPAR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_29	9598826	8  UPA can bind to the UPAR in either its inactive proenzyme form (pro-UPA) or active two-chain form without affecting its proteolytic activity.	bind
37538	3	8678	5	13	NULL	NULL	NULL	UPA	GP		bind					UPAR	GP	active two-chain form of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_29	9598826	8  UPA can bind to the UPAR in either its inactive proenzyme form (pro-UPA) or active two-chain form without affecting its proteolytic activity.	bind
37539	4	8678	5	13	NULL	NULL	NULL	statement 1	Process		does not effect					UPAR	GP	proteolytic activity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_29	9598826	8  UPA can bind to the UPAR in either its inactive proenzyme form (pro-UPA) or active two-chain form without affecting its proteolytic activity.	bind
37540	5	8678	5	13	NULL	NULL	NULL	statement 3	Process		does not effect					UPAR	GP	proteolytic activity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_29	9598826	8  UPA can bind to the UPAR in either its inactive proenzyme form (pro-UPA) or active two-chain form without affecting its proteolytic activity.	bind
36665	1	8678	7	NULL	NULL	0	NULL	UPA 	NULL		bind	NULL				UPAR	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_29	9598826	8  UPA can bind to the UPAR in either its inactive proenzyme form (pro-UPA) or active two-chain form without affecting its proteolytic activity.	bind
36666	2	8678	7	NULL	NULL	0	NULL	pro-UPA	NULL		bind	NULL				UPAR	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_29	9598826	8  UPA can bind to the UPAR in either its inactive proenzyme form (pro-UPA) or active two-chain form without affecting its proteolytic activity.	bind
36667	3	8678	7	NULL	NULL	0	NULL	pro-UPA	NULL		is	NULL				inactive proenzyme form	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_29	9598826	8  UPA can bind to the UPAR in either its inactive proenzyme form (pro-UPA) or active two-chain form without affecting its proteolytic activity.	bind
36669	4	8678	7	10	NULL	0	NULL	statement 1			does not affect					UPAR		proteolytic activity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_29	9598826	8  UPA can bind to the UPAR in either its inactive proenzyme form (pro-UPA) or active two-chain form without affecting its proteolytic activity.	bind
36670	5	8678	7	10	NULL	0	NULL	statement 2			does not affect					UPAR		proteolytic activity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_29	9598826	8  UPA can bind to the UPAR in either its inactive proenzyme form (pro-UPA) or active two-chain form without affecting its proteolytic activity.	bind
37541	1	8679	5	13	NULL	NULL	NULL	sera	OrganismPart		bind		progressively			CL	Chemical	oxidized			NULL	APS patients	NULL	NULL	NULL	NULL	gw60_circulation_103_7_941_s_21	11181467	8  We also showed that a few selected reference sera and affinity-purified aCL-IgG from APS patients progressively bound to CL as it was oxidized but not to a "`reduced"' CL (CLred) analogue that was unable to undergo lipid peroxidation (all 4 unsaturated fatty acids in CLred are hydrogenated to saturated fatty acids).	bind
37542	2	8679	5	13	NULL	NULL	NULL	aCL-IgG	GP		bind		progressively			CL	Chemical	oxidized			NULL	APS patients	NULL	NULL	NULL	NULL	gw60_circulation_103_7_941_s_21	11181467	8  We also showed that a few selected reference sera and affinity-purified aCL-IgG from APS patients progressively bound to CL as it was oxidized but not to a "`reduced"' CL (CLred) analogue that was unable to undergo lipid peroxidation (all 4 unsaturated fatty acids in CLred are hydrogenated to saturated fatty acids).	bind
37543	3	8679	5	13	NULL	NULL	NULL	sera	OrganismPart		does not bind		progressively			CLred	Chemical				NULL	APS patients	NULL	NULL	NULL	NULL	gw60_circulation_103_7_941_s_21	11181467	8  We also showed that a few selected reference sera and affinity-purified aCL-IgG from APS patients progressively bound to CL as it was oxidized but not to a "`reduced"' CL (CLred) analogue that was unable to undergo lipid peroxidation (all 4 unsaturated fatty acids in CLred are hydrogenated to saturated fatty acids).	bind
37544	4	8679	5	13	NULL	NULL	NULL	aCL-IgG	GP		does not bind					CLred	Chemical				NULL	APS patients	NULL	NULL	NULL	NULL	gw60_circulation_103_7_941_s_21	11181467	8  We also showed that a few selected reference sera and affinity-purified aCL-IgG from APS patients progressively bound to CL as it was oxidized but not to a "`reduced"' CL (CLred) analogue that was unable to undergo lipid peroxidation (all 4 unsaturated fatty acids in CLred are hydrogenated to saturated fatty acids).	bind
37545	5	8679	5	13	NULL	NULL	NULL	CLred	Chemical		is					reduced CL	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_7_941_s_21	11181467	8  We also showed that a few selected reference sera and affinity-purified aCL-IgG from APS patients progressively bound to CL as it was oxidized but not to a "`reduced"' CL (CLred) analogue that was unable to undergo lipid peroxidation (all 4 unsaturated fatty acids in CLred are hydrogenated to saturated fatty acids).	bind
37546	6	8679	5	13	NULL	NULL	NULL	CLred	Chemical		does not undergo					lipid peroxidation	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_7_941_s_21	11181467	8  We also showed that a few selected reference sera and affinity-purified aCL-IgG from APS patients progressively bound to CL as it was oxidized but not to a "`reduced"' CL (CLred) analogue that was unable to undergo lipid peroxidation (all 4 unsaturated fatty acids in CLred are hydrogenated to saturated fatty acids).	bind
37547	7	8679	5	13	NULL	NULL	NULL	CLred	Chemical	unsaturated fatty acids in	is hydrogenated to					CLred	Chemical	saturated fatty acids in			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_7_941_s_21	11181467	8  We also showed that a few selected reference sera and affinity-purified aCL-IgG from APS patients progressively bound to CL as it was oxidized but not to a "`reduced"' CL (CLred) analogue that was unable to undergo lipid peroxidation (all 4 unsaturated fatty acids in CLred are hydrogenated to saturated fatty acids).	bind
36671	1	8679	7	10	NULL	0	NULL	 aCL-IgG			binds		progressively			CL		oxidized 			NULL	APS patients	NULL	NULL	NULL	NULL	gw60_circulation_103_7_941_s_21	11181467	8  We also showed that a few selected reference sera and affinity-purified aCL-IgG from APS patients progressively bound to CL as it was oxidized but not to a "`reduced"' CL (CLred) analogue that was unable to undergo lipid peroxidation (all 4 unsaturated fatty acids in CLred are hydrogenated to saturated fatty acids).	bind
36672	2	8679	7	NULL	NULL	0	NULL	aCL-IgG	NULL		does not bind	NULL				CLred analogue	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_7_941_s_21	11181467	8  We also showed that a few selected reference sera and affinity-purified aCL-IgG from APS patients progressively bound to CL as it was oxidized but not to a "`reduced"' CL (CLred) analogue that was unable to undergo lipid peroxidation (all 4 unsaturated fatty acids in CLred are hydrogenated to saturated fatty acids).	bind
36673	3	8679	7	NULL	NULL	0	NULL	CLred	NULL		is	NULL				reduced CL	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_7_941_s_21	11181467	8  We also showed that a few selected reference sera and affinity-purified aCL-IgG from APS patients progressively bound to CL as it was oxidized but not to a "`reduced"' CL (CLred) analogue that was unable to undergo lipid peroxidation (all 4 unsaturated fatty acids in CLred are hydrogenated to saturated fatty acids).	bind
36674	4	8679	7	10	NULL	0	NULL	CLred			does not undergo					lipid peroxidation					NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_7_941_s_21	11181467	8  We also showed that a few selected reference sera and affinity-purified aCL-IgG from APS patients progressively bound to CL as it was oxidized but not to a "`reduced"' CL (CLred) analogue that was unable to undergo lipid peroxidation (all 4 unsaturated fatty acids in CLred are hydrogenated to saturated fatty acids).	bind
36675	5	8679	7	10	NULL	0	NULL	CLred	NULL	unsaturated fatty acids in	hydrogenated to	NULL				saturated fatty acids	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_7_941_s_21	11181467	8  We also showed that a few selected reference sera and affinity-purified aCL-IgG from APS patients progressively bound to CL as it was oxidized but not to a "`reduced"' CL (CLred) analogue that was unable to undergo lipid peroxidation (all 4 unsaturated fatty acids in CLred are hydrogenated to saturated fatty acids).	bind
56307	6	8679	7	10	NULL	0	NULL	sera			bind		progressively			CL		oxidized			NULL	APS patients	0	NULL	NULL	NULL	gw60_circulation_103_7_941_s_21	11181467	8  We also showed that a few selected reference sera and affinity-purified aCL-IgG from APS patients progressively bound to CL as it was oxidized but not to a "`reduced"' CL (CLred) analogue that was unable to undergo lipid peroxidation (all 4 unsaturated fatty acids in CLred are hydrogenated to saturated fatty acids).	bind
56310	7	8679	7	10	NULL	0	NULL	sera			does not bind		progressively			CLred					NULL	APS patients	0	NULL	NULL	NULL	gw60_circulation_103_7_941_s_21	11181467	8  We also showed that a few selected reference sera and affinity-purified aCL-IgG from APS patients progressively bound to CL as it was oxidized but not to a "`reduced"' CL (CLred) analogue that was unable to undergo lipid peroxidation (all 4 unsaturated fatty acids in CLred are hydrogenated to saturated fatty acids).	bind
37722	1	8680	5	13	NULL	NULL	NULL	alphavbeta8	GP		bind					latent TGF-beta	GP		RGD sequence of LAP		NULL	lung cancer cell lines	NULL	NULL	NULL	NULL	gw60_amjpathol_163_2_533_s_19	12875973	8  We have recently shown in lung cancer cell lines that alphavbeta8 binds to the RGD sequence of the LAP of latent TGF-beta and mediates activation of the latent TGF-beta complex through a mechanism that is dependent on the transmembrane protease, MT1-MMP.	bind
37723	2	8680	5	13	NULL	NULL	NULL	statement 1	GP		mediate					latent TGF-beta complex 	GP	activation of			NULL	lung cancer cell lines	NULL	NULL	NULL	NULL	gw60_amjpathol_163_2_533_s_19	12875973	8  We have recently shown in lung cancer cell lines that alphavbeta8 binds to the RGD sequence of the LAP of latent TGF-beta and mediates activation of the latent TGF-beta complex through a mechanism that is dependent on the transmembrane protease, MT1-MMP.	bind
37724	3	8680	5	13	NULL	NULL	NULL	statement 2	Process		is dependent on					MT1-MMP	GP				NULL	lung cancer cell lines	NULL	NULL	NULL	NULL	gw60_amjpathol_163_2_533_s_19	12875973	8  We have recently shown in lung cancer cell lines that alphavbeta8 binds to the RGD sequence of the LAP of latent TGF-beta and mediates activation of the latent TGF-beta complex through a mechanism that is dependent on the transmembrane protease, MT1-MMP.	bind
37725	4	8680	5	13	NULL	NULL	NULL	MT1-MMP	GP		is a type of					transmembrane protease	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_2_533_s_19	12875973	8  We have recently shown in lung cancer cell lines that alphavbeta8 binds to the RGD sequence of the LAP of latent TGF-beta and mediates activation of the latent TGF-beta complex through a mechanism that is dependent on the transmembrane protease, MT1-MMP.	bind
36676	1	8680	7	NULL	NULL	0	NULL	alphavbeta8	NULL		binds to	NULL				latent TGF-beta	NULL		RGD sequence of the LAP		NULL	lung cancer cell lines	0	NULL	NULL	NULL	gw60_amjpathol_163_2_533_s_19	12875973	8  We have recently shown in lung cancer cell lines that alphavbeta8 binds to the RGD sequence of the LAP of latent TGF-beta and mediates activation of the latent TGF-beta complex through a mechanism that is dependent on the transmembrane protease, MT1-MMP.	bind
36677	2	8680	7	NULL	NULL	0	NULL	statement 1	NULL		mediates	NULL				latent TGF-beta complex	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_2_533_s_19	12875973	8  We have recently shown in lung cancer cell lines that alphavbeta8 binds to the RGD sequence of the LAP of latent TGF-beta and mediates activation of the latent TGF-beta complex through a mechanism that is dependent on the transmembrane protease, MT1-MMP.	bind
36678	3	8680	7	NULL	NULL	0	NULL	statement 2	NULL		depends on	NULL				MT1-MMP	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_163_2_533_s_19	12875973	8  We have recently shown in lung cancer cell lines that alphavbeta8 binds to the RGD sequence of the LAP of latent TGF-beta and mediates activation of the latent TGF-beta complex through a mechanism that is dependent on the transmembrane protease, MT1-MMP.	bind
36679	4	8680	7	NULL	NULL	0	NULL	MT1-MMP	NULL		is a type of	NULL				transmembrane protease	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_163_2_533_s_19	12875973	8  We have recently shown in lung cancer cell lines that alphavbeta8 binds to the RGD sequence of the LAP of latent TGF-beta and mediates activation of the latent TGF-beta complex through a mechanism that is dependent on the transmembrane protease, MT1-MMP.	bind
37726	1	8682	5	13	NULL	NULL	NULL	NP-1	GP		is					neuropilin-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_3_358_s_25	11457758	8 -  10 Specific isoforms of VEGF and PlGF and both isoforms of VEGF-B bind to neuropilin-1 (NP-1).	bind
37727	2	8682	5	13	NULL	NULL	NULL	VEGF isoform	GP		bind					NP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_3_358_s_25	11457758	8 -  10 Specific isoforms of VEGF and PlGF and both isoforms of VEGF-B bind to neuropilin-1 (NP-1).	bind
37728	3	8682	5	13	NULL	NULL	NULL	PIGF isoform	GP		bind					NP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_3_358_s_25	11457758	8 -  10 Specific isoforms of VEGF and PlGF and both isoforms of VEGF-B bind to neuropilin-1 (NP-1).	bind
37729	4	8682	5	13	NULL	NULL	NULL	isoforms of VEGF-B	GP		bind					NP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_3_358_s_25	11457758	8 -  10 Specific isoforms of VEGF and PlGF and both isoforms of VEGF-B bind to neuropilin-1 (NP-1).	bind
36683	1	8682	7	NULL	NULL	0	NULL	VEGF isoform	NULL		bind	NULL				NP-1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_3_358_s_25	11457758	8 -  10 Specific isoforms of VEGF and PlGF and both isoforms of VEGF-B bind to neuropilin-1 (NP-1).	bind
36684	2	8682	7	NULL	NULL	0	NULL	PIGF isoform	NULL		bind	NULL				NP-1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_104_3_358_s_25	11457758	8 -  10 Specific isoforms of VEGF and PlGF and both isoforms of VEGF-B bind to neuropilin-1 (NP-1).	bind
36685	3	8682	7	NULL	NULL	0	NULL	VEGF-B	NULL		bind	NULL				NP-1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_104_3_358_s_25	11457758	8 -  10 Specific isoforms of VEGF and PlGF and both isoforms of VEGF-B bind to neuropilin-1 (NP-1).	bind
36686	4	8682	7	NULL	NULL	0	NULL	NP-1	NULL		is	NULL				neuropilin-1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_104_3_358_s_25	11457758	8 -  10 Specific isoforms of VEGF and PlGF and both isoforms of VEGF-B bind to neuropilin-1 (NP-1).	bind
37730	1	8683	5	13	NULL	NULL	NULL	paraoxonase	GP		bind					HDL	GP	large			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_10_1243_s_170	8857920	8 14  While the relation between paraoxonase and HDL may reflect enzyme binding to large HDL (with apoA-I), 14  this would not account for the reported associations with plasma TG or apoB levels that others have reported.	bind
46798	2	8683	5	13	NULL	NULL	NULL	HDL	GP	large	contains					apoA-I	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_10_1243_s_170	8857920	8 14  While the relation between paraoxonase and HDL may reflect enzyme binding to large HDL (with apoA-I), 14  this would not account for the reported associations with plasma TG or apoB levels that others have reported.	bind
36687	1	8683	7	10	NULL	0	NULL	paraoxonase			bind					HDL		large			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_10_1243_s_170	8857920	8 14  While the relation between paraoxonase and HDL may reflect enzyme binding to large HDL (with apoA-I), 14  this would not account for the reported associations with plasma TG or apoB levels that others have reported.	bind
36688	2	8683	7	10	NULL	0	NULL	HDL		large	contains					apoA-I					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_10_1243_s_170	8857920	8 14  While the relation between paraoxonase and HDL may reflect enzyme binding to large HDL (with apoA-I), 14  this would not account for the reported associations with plasma TG or apoB levels that others have reported.	bind
37731	1	8685	5	13	NULL	NULL	NULL	UPA	GP		bind					UPAR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_51	9598826	8 38  The binding of UPA to its receptor is rather species specific, since human UPA cannot bind to mouse UPAR and vice versa.	bind
37732	2	8685	5	13	NULL	NULL	NULL	UPA	GP	human	does not bind					UPAR	GP	mouse			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_51	9598826	8 38  The binding of UPA to its receptor is rather species specific, since human UPA cannot bind to mouse UPAR and vice versa.	bind
37733	3	8685	5	13	NULL	NULL	NULL	UPA	GP	mouse	does not bind					UPAR	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_51	9598826	8 38  The binding of UPA to its receptor is rather species specific, since human UPA cannot bind to mouse UPAR and vice versa.	bind
36877	1	8685	7	NULL	NULL	0	NULL	UPA	NULL		bind	NULL				UPA receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_51	9598826	8 38  The binding of UPA to its receptor is rather species specific, since human UPA cannot bind to mouse UPAR and vice versa.	bind
36879	2	8685	7	10	NULL	0	NULL	UPA		human	does not bind					UPAR		mouse			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_51	9598826	8 38  The binding of UPA to its receptor is rather species specific, since human UPA cannot bind to mouse UPAR and vice versa.	bind
36880	3	8685	7	10	NULL	0	NULL	UPA		mouse	does not bind					UPAR		human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_5_693_s_51	9598826	8 38  The binding of UPA to its receptor is rather species specific, since human UPA cannot bind to mouse UPAR and vice versa.	bind
37734	1	8686	5	13	NULL	NULL	NULL	IGF-1	GP		bind					smooth muscle cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_6_1689_s_29	7882475	8 9  In addition, [[ fibroblast growth factor ]] increases the binding of IGF-1 to smooth muscle cells, promoting the growth stimulation of IGF-1.	bind
37735	2	8686	5	13	NULL	NULL	NULL	fibroblast growth factor	GP		increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_6_1689_s_29	7882475	8 9  In addition, [[ fibroblast growth factor ]] increases the binding of IGF-1 to smooth muscle cells, promoting the growth stimulation of IGF-1.	bind
37736	3	8686	5	13	NULL	NULL	NULL	statement 2	Process		promotes					IGF-1	GP	growth stimulation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_91_6_1689_s_29	7882475	8 9  In addition, [[ fibroblast growth factor ]] increases the binding of IGF-1 to smooth muscle cells, promoting the growth stimulation of IGF-1.	bind
36881	1	8686	7	NULL	NULL	0	NULL	IGF-1	NULL		bind	NULL				smooth muscle cells	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_6_1689_s_29	7882475	8 9  In addition, [[ fibroblast growth factor ]] increases the binding of IGF-1 to smooth muscle cells, promoting the growth stimulation of IGF-1.	bind
36882	2	8686	7	NULL	NULL	0	NULL	 fibroblast growth factor	NULL		increase	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_91_6_1689_s_29	7882475	8 9  In addition, [[ fibroblast growth factor ]] increases the binding of IGF-1 to smooth muscle cells, promoting the growth stimulation of IGF-1.	bind
36883	3	8686	7	NULL	NULL	0	NULL	fibroblast growth factor	NULL		promote	NULL				IGF-1	NULL	growth stimulation of			NULL		0	NULL	NULL	NULL	gw60_circulation_91_6_1689_s_29	7882475	8 9  In addition, [[ fibroblast growth factor ]] increases the binding of IGF-1 to smooth muscle cells, promoting the growth stimulation of IGF-1.	bind
37737	1	8687	5	13	NULL	NULL	NULL	NIF	GP		bind					CD11b integrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_3_254_s_19	10926878	8 9 10 11  We showed that NIF can bind to both CD11b and CD11a integrins and thereby prevent PMN adhesion to endothelial cells to a degree equivalent to anti-CD18 monoclonal antibodies.	bind
37738	2	8687	5	13	NULL	NULL	NULL	NIF	GP		bind					CD11a integrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_3_254_s_19	10926878	8 9 10 11  We showed that NIF can bind to both CD11b and CD11a integrins and thereby prevent PMN adhesion to endothelial cells to a degree equivalent to anti-CD18 monoclonal antibodies.	bind
37739	3	8687	5	13	NULL	NULL	NULL	PMN	Cell		adhere to					endothelial cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_3_254_s_19	10926878	8 9 10 11  We showed that NIF can bind to both CD11b and CD11a integrins and thereby prevent PMN adhesion to endothelial cells to a degree equivalent to anti-CD18 monoclonal antibodies.	bind
37740	4	8687	5	13	NULL	NULL	NULL	PMN	Cell		adhere to					anti-CD18 monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_3_254_s_19	10926878	8 9 10 11  We showed that NIF can bind to both CD11b and CD11a integrins and thereby prevent PMN adhesion to endothelial cells to a degree equivalent to anti-CD18 monoclonal antibodies.	bind
37741	5	8687	5	13	NULL	NULL	NULL	statement 1	Process		prevents					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_3_254_s_19	10926878	8 9 10 11  We showed that NIF can bind to both CD11b and CD11a integrins and thereby prevent PMN adhesion to endothelial cells to a degree equivalent to anti-CD18 monoclonal antibodies.	bind
37742	6	8687	5	13	NULL	NULL	NULL	statement 2	Process		prevents					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_3_254_s_19	10926878	8 9 10 11  We showed that NIF can bind to both CD11b and CD11a integrins and thereby prevent PMN adhesion to endothelial cells to a degree equivalent to anti-CD18 monoclonal antibodies.	bind
37743	7	8687	5	13	NULL	NULL	NULL	statement 1	Process		prevents					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_3_254_s_19	10926878	8 9 10 11  We showed that NIF can bind to both CD11b and CD11a integrins and thereby prevent PMN adhesion to endothelial cells to a degree equivalent to anti-CD18 monoclonal antibodies.	bind
37744	8	8687	5	13	NULL	NULL	NULL	statement 2	Process		prevents					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_3_254_s_19	10926878	8 9 10 11  We showed that NIF can bind to both CD11b and CD11a integrins and thereby prevent PMN adhesion to endothelial cells to a degree equivalent to anti-CD18 monoclonal antibodies.	bind
36884	1	8687	7	NULL	NULL	0	NULL	 NIF	NULL		bind	NULL				CD11b integrin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_3_254_s_19	10926878	8 9 10 11  We showed that NIF can bind to both CD11b and CD11a integrins and thereby prevent PMN adhesion to endothelial cells to a degree equivalent to anti-CD18 monoclonal antibodies.	bind
36885	2	8687	7	NULL	NULL	0	NULL	NIF	NULL		bind	NULL				CD11a integrin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_3_254_s_19	10926878	8 9 10 11  We showed that NIF can bind to both CD11b and CD11a integrins and thereby prevent PMN adhesion to endothelial cells to a degree equivalent to anti-CD18 monoclonal antibodies.	bind
36886	3	8687	7	NULL	NULL	0	NULL	PMN	NULL		adhere to	NULL				endothelial cells	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_3_254_s_19	10926878	8 9 10 11  We showed that NIF can bind to both CD11b and CD11a integrins and thereby prevent PMN adhesion to endothelial cells to a degree equivalent to anti-CD18 monoclonal antibodies.	bind
36887	4	8687	7	NULL	NULL	0	NULL	PMN	NULL		adhere to	NULL				anti-CD18 monoclonal antibodies	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_3_254_s_19	10926878	8 9 10 11  We showed that NIF can bind to both CD11b and CD11a integrins and thereby prevent PMN adhesion to endothelial cells to a degree equivalent to anti-CD18 monoclonal antibodies.	bind
36888	5	8687	7	NULL	NULL	0	NULL	statement 1	NULL		prevent	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_3_254_s_19	10926878	8 9 10 11  We showed that NIF can bind to both CD11b and CD11a integrins and thereby prevent PMN adhesion to endothelial cells to a degree equivalent to anti-CD18 monoclonal antibodies.	bind
36889	6	8687	7	NULL	NULL	0	NULL	statement 2	NULL		prevent	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_3_254_s_19	10926878	8 9 10 11  We showed that NIF can bind to both CD11b and CD11a integrins and thereby prevent PMN adhesion to endothelial cells to a degree equivalent to anti-CD18 monoclonal antibodies.	bind
36890	7	8687	7	NULL	NULL	0	NULL	statement 1	NULL		prevent	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_3_254_s_19	10926878	8 9 10 11  We showed that NIF can bind to both CD11b and CD11a integrins and thereby prevent PMN adhesion to endothelial cells to a degree equivalent to anti-CD18 monoclonal antibodies.	bind
36891	8	8687	7	NULL	NULL	0	NULL	statement 2	NULL		prevent	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_3_254_s_19	10926878	8 9 10 11  We showed that NIF can bind to both CD11b and CD11a integrins and thereby prevent PMN adhesion to endothelial cells to a degree equivalent to anti-CD18 monoclonal antibodies.	bind
37745	1	8688	5	13	NULL	NULL	NULL	VEGF-E	GP		bind		selectively			VEGFR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_85_11_992_s_26	10571529	8 9 10 11 18  VEGF-E binds selectively to VEGFR-2.	bind
36892	1	8688	7	NULL	NULL	0	NULL	VEGF-E 	NULL		binds	NULL	selectively			VEGFR-2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_85_11_992_s_26	10571529	8 9 10 11 18  VEGF-E binds selectively to VEGFR-2.	bind
37746	1	8689	5	13	NULL	NULL	NULL	HB-EGF	GP		bind					EGF receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
37747	2	8689	5	13	NULL	NULL	NULL	HB-EGF	GP		stimulate					cell migration	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
37748	3	8689	5	13	NULL	NULL	NULL	heparitinase	GP	treatment	inhibit					statement 1	Process				NULL	bovine SMCs	NULL	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
37749	4	8689	5	13	NULL	NULL	NULL	heparitinase	GP	treatment	inhibit					statement 2	Process				NULL	bovine SMCs	NULL	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
37750	5	8689	5	13	NULL	NULL	NULL	heparitinase	GP		degrade					heparan sulfate chains	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
37751	6	8689	5	13	NULL	NULL	NULL	chlorate	Chemical	treatment	inhibit					statement 1	Process				NULL	bovine SMCs	NULL	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
37752	7	8689	5	13	NULL	NULL	NULL	chlorate	Chemical	treatment	inhibit					statement 2	Process				NULL	bovine SMCs	NULL	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
37753	8	8689	5	13	NULL	NULL	NULL	chlorate	Chemical		inhibit					glycosaminoglycans	GP	sulfation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
37754	9	8689	5	13	NULL	NULL	NULL	synthetic peptide	GP		corresponds to					HB-EGF	GP		heparin-binding domain		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
37755	10	8689	5	13	NULL	NULL	NULL	statement 9	Process	treatment	inhibit					statement 1	Process				NULL	bovine SMCs	NULL	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
37756	11	8689	5	13	NULL	NULL	NULL	statement 9	Process	treatment	inhibit					statement 2	Process				NULL	bovine SMCs	NULL	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
36893	1	8689	7	NULL	NULL	0	NULL	HB-EGF	NULL		bind	NULL				EGF receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
36894	2	8689	7	NULL	NULL	0	NULL	HB-EGF	NULL		stimulate	NULL				cell migration	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
36895	3	8689	7	NULL	NULL	0	NULL	heparitinase 	NULL		degrades	NULL				heparan sulfate chains	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
36896	4	8689	7	NULL	NULL	0	NULL	heparitinase	NULL		inhibits	NULL				statement 1	NULL				NULL	bovine SMCs	0	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
36897	5	8689	7	NULL	NULL	0	NULL	chlorate	NULL		inhibits	NULL				 glycosaminoglycans	NULL	sulfation of			NULL		0	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
36898	6	8689	7	NULL	NULL	0	NULL	cholrate	NULL		inhibits	NULL				statement 1	NULL				NULL	bovine SMCs	0	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
36899	7	8689	7	NULL	NULL	0	NULL	heparitinase	NULL		inhibits	NULL				statement 2	NULL				NULL	bovine SMCs	0	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
36900	8	8689	7	NULL	NULL	0	NULL	chlorate	NULL		inhibits	NULL				statement 2	NULL				NULL	bovine SMCs	0	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
36901	9	8689	7	NULL	NULL	0	NULL	synthetic peptide 	NULL		corresponds to	NULL				HB-EGF	NULL		heparin-binding domain of		NULL		0	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
36902	10	8689	7	NULL	NULL	0	NULL	Synthetic peptide	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_79_2_263_s_153	8756003	8 9 12 13 14  For example, treatment of bovine SMCs with either heparitinase (which degrades heparan sulfate chains), chlorate (which inhibits sulfation of glycosaminoglycans), or a synthetic peptide corresponding to the heparin-binding domain of HB-EGF inhibits HB-EGF binding to the EGF receptor as well as HB-EGF - stimulated cell migration.	bind
37757	1	8690	5	13	NULL	NULL	NULL	FasL	GP	membrane-bound	bind					Fas-bearing cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_5_1783_s_21	12414525	8 Apoptosis is induced when membrane-bound or soluble FasL binds to Fas-bearing cells.	bind
37758	2	8690	5	13	NULL	NULL	NULL	statement 1	Process		induce					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_5_1783_s_21	12414525	8 Apoptosis is induced when membrane-bound or soluble FasL binds to Fas-bearing cells.	bind
37759	3	8690	5	13	NULL	NULL	NULL	FasL	GP	soluble	bind					Fas-bearing cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_5_1783_s_21	12414525	8 Apoptosis is induced when membrane-bound or soluble FasL binds to Fas-bearing cells.	bind
37760	4	8690	5	13	NULL	NULL	NULL	statement 3	Process		induce					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_5_1783_s_21	12414525	8 Apoptosis is induced when membrane-bound or soluble FasL binds to Fas-bearing cells.	bind
37761	5	8690	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_5_1783_s_21	12414525	8 Apoptosis is induced when membrane-bound or soluble FasL binds to Fas-bearing cells.	bind
36903	1	8690	7	NULL	NULL	0	NULL	FasL	NULL	 membrane-bound	binds to	NULL				Fas-bearing cells	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_5_1783_s_21	12414525	8 Apoptosis is induced when membrane-bound or soluble FasL binds to Fas-bearing cells.	bind
36904	2	8690	7	NULL	NULL	0	NULL	FasL	NULL	soluble	binds to	NULL				Fas-bearing cells	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_5_1783_s_21	12414525	8 Apoptosis is induced when membrane-bound or soluble FasL binds to Fas-bearing cells.	bind
36905	3	8690	7	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL				apoptosis	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_5_1783_s_21	12414525	8 Apoptosis is induced when membrane-bound or soluble FasL binds to Fas-bearing cells.	bind
36906	4	8690	7	NULL	NULL	0	NULL	statement 2	NULL		induce	NULL				apoptosis	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_5_1783_s_21	12414525	8 Apoptosis is induced when membrane-bound or soluble FasL binds to Fas-bearing cells.	bind
37762	1	8691	5	13	NULL	NULL	NULL	VWF	GP		bind					GPIb complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_30	11788455	8 Because the binding of VWF to the GPIb complex is known to activate another platelet integrin, alphaIIbbeta3, it is conceivable that it may also activate alpha2beta1.	bind
37763	2	8691	5	13	NULL	NULL	NULL	statement 1	Process		activate					alphaIIbbeta3	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_30	11788455	8 Because the binding of VWF to the GPIb complex is known to activate another platelet integrin, alphaIIbbeta3, it is conceivable that it may also activate alpha2beta1.	bind
37764	3	8691	5	13	NULL	NULL	NULL	alphaIIbbeta3	GP		is a type of					platelet integrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_30	11788455	8 Because the binding of VWF to the GPIb complex is known to activate another platelet integrin, alphaIIbbeta3, it is conceivable that it may also activate alpha2beta1.	bind
37765	4	8691	5	13	NULL	NULL	NULL	statement 1	Process		activate					alpha2beta1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_30	11788455	8 Because the binding of VWF to the GPIb complex is known to activate another platelet integrin, alphaIIbbeta3, it is conceivable that it may also activate alpha2beta1.	bind
36907	1	8691	7	NULL	NULL	0	NULL	VWF	NULL		bind	NULL				GPIb complex 	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_30	11788455	8 Because the binding of VWF to the GPIb complex is known to activate another platelet integrin, alphaIIbbeta3, it is conceivable that it may also activate alpha2beta1.	bind
36908	2	8691	7	NULL	NULL	0	NULL	statement 1	NULL		activate	NULL				alphaIIbbeta3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_30	11788455	8 Because the binding of VWF to the GPIb complex is known to activate another platelet integrin, alphaIIbbeta3, it is conceivable that it may also activate alpha2beta1.	bind
36909	3	8691	7	NULL	NULL	0	NULL	statement 1	NULL		activate	NULL				alpha2beta1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_30	11788455	8 Because the binding of VWF to the GPIb complex is known to activate another platelet integrin, alphaIIbbeta3, it is conceivable that it may also activate alpha2beta1.	bind
36910	4	8691	7	NULL	NULL	0	NULL	alphaIIbbeta3	NULL		is a type of	NULL				platelet integrin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_1_14_s_30	11788455	8 Because the binding of VWF to the GPIb complex is known to activate another platelet integrin, alphaIIbbeta3, it is conceivable that it may also activate alpha2beta1.	bind
37766	1	8692	5	13	NULL	NULL	NULL	thrombin	GP		bind					thrombomodulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2273_s_66	16123318	8 Binding of thrombin to thrombomodulin changes its substrate specificity from fibrinogen to protein C, whereas binding of protein C to EPCR facilitates its cleavage by the thrombomodulin-thrombin complex.	bind
37767	2	8692	5	13	NULL	NULL	NULL	fibrinogen	GP		is substrate for					thrombomodulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2273_s_66	16123318	8 Binding of thrombin to thrombomodulin changes its substrate specificity from fibrinogen to protein C, whereas binding of protein C to EPCR facilitates its cleavage by the thrombomodulin-thrombin complex.	bind
37768	3	8692	5	13	NULL	NULL	NULL	protein C	GP		is substrate for					thrombomodulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2273_s_66	16123318	8 Binding of thrombin to thrombomodulin changes its substrate specificity from fibrinogen to protein C, whereas binding of protein C to EPCR facilitates its cleavage by the thrombomodulin-thrombin complex.	bind
37769	4	8692	5	13	NULL	NULL	NULL	statement 2	Process		change to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2273_s_66	16123318	8 Binding of thrombin to thrombomodulin changes its substrate specificity from fibrinogen to protein C, whereas binding of protein C to EPCR facilitates its cleavage by the thrombomodulin-thrombin complex.	bind
37770	5	8692	5	13	NULL	NULL	NULL	statement 1	Process		cause					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2273_s_66	16123318	8 Binding of thrombin to thrombomodulin changes its substrate specificity from fibrinogen to protein C, whereas binding of protein C to EPCR facilitates its cleavage by the thrombomodulin-thrombin complex.	bind
37771	6	8692	5	13	NULL	NULL	NULL	protein C	GP		bind					EPCR	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2273_s_66	16123318	8 Binding of thrombin to thrombomodulin changes its substrate specificity from fibrinogen to protein C, whereas binding of protein C to EPCR facilitates its cleavage by the thrombomodulin-thrombin complex.	bind
37772	7	8692	5	13	NULL	NULL	NULL	thrombomodulin-thrombin complex	GP		cleave					protein C	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2273_s_66	16123318	8 Binding of thrombin to thrombomodulin changes its substrate specificity from fibrinogen to protein C, whereas binding of protein C to EPCR facilitates its cleavage by the thrombomodulin-thrombin complex.	bind
37773	8	8692	5	13	NULL	NULL	NULL	statement 6	Process		facilitates					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2273_s_66	16123318	8 Binding of thrombin to thrombomodulin changes its substrate specificity from fibrinogen to protein C, whereas binding of protein C to EPCR facilitates its cleavage by the thrombomodulin-thrombin complex.	bind
36911	1	8692	7	NULL	NULL	0	NULL	thrombin	NULL		bind	NULL				thrombomodulin	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2273_s_66	16123318	8 Binding of thrombin to thrombomodulin changes its substrate specificity from fibrinogen to protein C, whereas binding of protein C to EPCR facilitates its cleavage by the thrombomodulin-thrombin complex.	bind
36912	2	8692	7	NULL	NULL	0	NULL	fibrinogen	NULL		substrate for	NULL				thrombomodulin	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2273_s_66	16123318	8 Binding of thrombin to thrombomodulin changes its substrate specificity from fibrinogen to protein C, whereas binding of protein C to EPCR facilitates its cleavage by the thrombomodulin-thrombin complex.	bind
36913	3	8692	7	NULL	NULL	0	NULL	protein C	NULL		substrate for	NULL				thrombomodulin	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2273_s_66	16123318	8 Binding of thrombin to thrombomodulin changes its substrate specificity from fibrinogen to protein C, whereas binding of protein C to EPCR facilitates its cleavage by the thrombomodulin-thrombin complex.	bind
36914	4	8692	7	NULL	NULL	0	NULL	statement 2	NULL		change to	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2273_s_66	16123318	8 Binding of thrombin to thrombomodulin changes its substrate specificity from fibrinogen to protein C, whereas binding of protein C to EPCR facilitates its cleavage by the thrombomodulin-thrombin complex.	bind
36915	5	8692	7	NULL	NULL	0	NULL	statement 1	NULL		cause	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2273_s_66	16123318	8 Binding of thrombin to thrombomodulin changes its substrate specificity from fibrinogen to protein C, whereas binding of protein C to EPCR facilitates its cleavage by the thrombomodulin-thrombin complex.	bind
36916	6	8692	7	NULL	NULL	0	NULL	protein C	NULL		bind	NULL				EPCR	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2273_s_66	16123318	8 Binding of thrombin to thrombomodulin changes its substrate specificity from fibrinogen to protein C, whereas binding of protein C to EPCR facilitates its cleavage by the thrombomodulin-thrombin complex.	bind
36917	7	8692	7	NULL	NULL	0	NULL	thrombomodulin-thrombin complex	NULL		cleaves	NULL				EPCR	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2273_s_66	16123318	8 Binding of thrombin to thrombomodulin changes its substrate specificity from fibrinogen to protein C, whereas binding of protein C to EPCR facilitates its cleavage by the thrombomodulin-thrombin complex.	bind
36918	8	8692	7	NULL	NULL	0	NULL	statement 6	NULL		facilitates	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_11_2273_s_66	16123318	8 Binding of thrombin to thrombomodulin changes its substrate specificity from fibrinogen to protein C, whereas binding of protein C to EPCR facilitates its cleavage by the thrombomodulin-thrombin complex.	bind
37774	1	8693	5	13	NULL	NULL	NULL	Cbfa1	GP		bind		sequence specifically					proximal		OSE2 element	NULL	Cbfa1-transfected COS1 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_33_25163_s_274	10833509	8 cells and Cbfa1-transfected COS1 cells, showed that Cbfa1 binds to the proximal OSE2 element in a sequence-specific manner.	bind
36919	1	8693	7	NULL	NULL	0	NULL	 Cbfa1	NULL		binds to	NULL	sequence-specific				NULL	proximal		OSE2 element	NULL	Cbfa1-transfected COS1 cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_33_25163_s_274	10833509	8 cells and Cbfa1-transfected COS1 cells, showed that Cbfa1 binds to the proximal OSE2 element in a sequence-specific manner.	bind
37775	1	8694	5	13	NULL	NULL	NULL	BMP-7	GP		bind					HS	Chemical	endogenous			NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_4_858_s_170	12927798	8 cells and that exogenous heparin competitively inhibits BMP-7 binding to endogenous HS.	bind
37776	2	8694	5	13	NULL	NULL	NULL	heparin	Chemical	exogenous	inhibit		competitively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_4_858_s_170	12927798	8 cells and that exogenous heparin competitively inhibits BMP-7 binding to endogenous HS.	bind
36920	1	8694	7	10	NULL	0	NULL	BMP-7	NULL		bind	NULL				HS	NULL	endogenous 			NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_4_858_s_170	12927798	8 cells and that exogenous heparin competitively inhibits BMP-7 binding to endogenous HS.	bind
36921	2	8694	7	10	NULL	0	NULL	heparin	NULL	exogenous 	inhibits	NULL	competitively			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_4_858_s_170	12927798	8 cells and that exogenous heparin competitively inhibits BMP-7 binding to endogenous HS.	bind
37777	1	8696	5	13	NULL	NULL	NULL	Sp1	GP		is a type of					nuclear protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_22	12067897	8 DNase I footprinting analysis and electrophoretic mobility shift assay (EMSA) have demonstrated that Sp1 is the major nuclear protein binding to the Flk-1/KDR core promoter region.	bind
37778	2	8696	5	13	NULL	NULL	NULL	Sp1	GP		bind					Flk-1/KDR	GP			core promoter region	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_22	12067897	8 DNase I footprinting analysis and electrophoretic mobility shift assay (EMSA) have demonstrated that Sp1 is the major nuclear protein binding to the Flk-1/KDR core promoter region.	bind
36922	1	8696	7	NULL	NULL	0	NULL	 Sp1	NULL		bind	NULL				Flk-1/KDR	NULL			core promoter	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_22	12067897	8 DNase I footprinting analysis and electrophoretic mobility shift assay (EMSA) have demonstrated that Sp1 is the major nuclear protein binding to the Flk-1/KDR core promoter region.	bind
36923	2	8696	7	NULL	NULL	0	NULL	Sp1	NULL		is a type of	NULL				nuclear binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_22	12067897	8 DNase I footprinting analysis and electrophoretic mobility shift assay (EMSA) have demonstrated that Sp1 is the major nuclear protein binding to the Flk-1/KDR core promoter region.	bind
37779	1	8697	5	13	NULL	NULL	NULL	FKBP12.6	GP		bind					RyR2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_25	14715536	8 Furthermore, a single mutation of serine-2808 to aspartate (S2808D) abolished FKBP12.6 binding to RyR2.	bind
37780	2	8697	5	13	NULL	NULL	NULL	FKBP12.6	GP	mutant	abolishes			S2808D		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_25	14715536	8 Furthermore, a single mutation of serine-2808 to aspartate (S2808D) abolished FKBP12.6 binding to RyR2.	bind
46721	3	8697	5	13	NULL	NULL	NULL	S2808D	AminoAcid		is					 serine-2808 to aspartate	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_25	14715536	8 Furthermore, a single mutation of serine-2808 to aspartate (S2808D) abolished FKBP12.6 binding to RyR2.	bind
36924	1	8697	7	NULL	NULL	0	NULL	FKBP12.6 	NULL		bind	NULL				RyR2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_25	14715536	8 Furthermore, a single mutation of serine-2808 to aspartate (S2808D) abolished FKBP12.6 binding to RyR2.	bind
36925	2	8697	7	NULL	NULL	0	NULL		NULL	mutant	abolish	NULL		S2808D		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_25	14715536	8 Furthermore, a single mutation of serine-2808 to aspartate (S2808D) abolished FKBP12.6 binding to RyR2.	bind
36926	3	8697	7	10	NULL	0	NULL	S2808D	NULL		is	NULL				serine-2808 to aspartate	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_4_487_s_25	14715536	8 Furthermore, a single mutation of serine-2808 to aspartate (S2808D) abolished FKBP12.6 binding to RyR2.	bind
37781	1	8698	5	13	NULL	NULL	NULL	PBEF	GP		bind					insulin receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_97_1_25_s_205	15947248	8 However, the physiological relevance of PBEF binding to the insulin receptor binding has been questioned.	bind
36927	1	8698	7	NULL	NULL	0	NULL	 PBEF	NULL		bind	NULL				insulin receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_97_1_25_s_205	15947248	8 However, the physiological relevance of PBEF binding to the insulin receptor binding has been questioned.	bind
37782	1	8699	5	13	NULL	NULL	NULL	HSP90	GP		bind					hormone receptors	GP	intracellular			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_40	15231513	8 HSP90 binds intracellular hormone receptors.	bind
36928	1	8699	7	NULL	NULL	0	NULL	HSP90	NULL		binds	NULL				 hormone receptors	NULL	intracellular			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_9_1628_s_40	15231513	8 HSP90 binds intracellular hormone receptors.	bind
37783	1	8700	5	13	NULL	NULL	NULL	LPS	Chemical		associate with					lipoprotein classes	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2174_s_30	15388525	8 In the circulation, LPS associates with all lipoprotein classes, but it may promote atherogenesis when it invades the arterial wall complexed with LDL. 9,10  An LDL - LPS complex is recognized as minimally modified LDL, which readily binds to macrophage LPS receptors.	bind
37784	2	8700	5	13	NULL	NULL	NULL	arterial wall	OrganismPart		complex with					LDL	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2174_s_30	15388525	8 In the circulation, LPS associates with all lipoprotein classes, but it may promote atherogenesis when it invades the arterial wall complexed with LDL. 9,10  An LDL - LPS complex is recognized as minimally modified LDL, which readily binds to macrophage LPS receptors.	bind
37785	3	8700	5	13	NULL	NULL	NULL	statement 1	Process		occurs during					circulation	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2174_s_30	15388525	8 In the circulation, LPS associates with all lipoprotein classes, but it may promote atherogenesis when it invades the arterial wall complexed with LDL. 9,10  An LDL - LPS complex is recognized as minimally modified LDL, which readily binds to macrophage LPS receptors.	bind
37786	4	8700	5	13	NULL	NULL	NULL	LPS	Chemical		promotes					atherogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2174_s_30	15388525	8 In the circulation, LPS associates with all lipoprotein classes, but it may promote atherogenesis when it invades the arterial wall complexed with LDL. 9,10  An LDL - LPS complex is recognized as minimally modified LDL, which readily binds to macrophage LPS receptors.	bind
37787	5	8700	5	13	NULL	NULL	NULL	LPS	Chemical		invades					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2174_s_30	15388525	8 In the circulation, LPS associates with all lipoprotein classes, but it may promote atherogenesis when it invades the arterial wall complexed with LDL. 9,10  An LDL - LPS complex is recognized as minimally modified LDL, which readily binds to macrophage LPS receptors.	bind
37788	6	8700	5	13	NULL	NULL	NULL	statement 5	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2174_s_30	15388525	8 In the circulation, LPS associates with all lipoprotein classes, but it may promote atherogenesis when it invades the arterial wall complexed with LDL. 9,10  An LDL - LPS complex is recognized as minimally modified LDL, which readily binds to macrophage LPS receptors.	bind
37789	7	8700	5	13	NULL	NULL	NULL	LDL - LPS complex	GP		is recognized as					LDL	GP	minimally modified			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2174_s_30	15388525	8 In the circulation, LPS associates with all lipoprotein classes, but it may promote atherogenesis when it invades the arterial wall complexed with LDL. 9,10  An LDL - LPS complex is recognized as minimally modified LDL, which readily binds to macrophage LPS receptors.	bind
37790	8	8700	5	13	NULL	NULL	NULL	statement 7	Process		bind		readily			LPS receptors	GP	macrophage			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2174_s_30	15388525	8 In the circulation, LPS associates with all lipoprotein classes, but it may promote atherogenesis when it invades the arterial wall complexed with LDL. 9,10  An LDL - LPS complex is recognized as minimally modified LDL, which readily binds to macrophage LPS receptors.	bind
37791	9	8700	5	13	NULL	NULL	NULL	statement 4	Process		occurs during					circulation	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2174_s_30	15388525	8 In the circulation, LPS associates with all lipoprotein classes, but it may promote atherogenesis when it invades the arterial wall complexed with LDL. 9,10  An LDL - LPS complex is recognized as minimally modified LDL, which readily binds to macrophage LPS receptors.	bind
36929	1	8700	7	NULL	NULL	0	NULL	LPS	NULL		associate with	NULL				lipoproteins	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2174_s_30	15388525	8 In the circulation, LPS associates with all lipoprotein classes, but it may promote atherogenesis when it invades the arterial wall complexed with LDL. 9,10  An LDL - LPS complex is recognized as minimally modified LDL, which readily binds to macrophage LPS receptors.	bind
36930	2	8700	7	NULL	NULL	0	NULL	LPS	NULL		complex with	NULL				LDL	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2174_s_30	15388525	8 In the circulation, LPS associates with all lipoprotein classes, but it may promote atherogenesis when it invades the arterial wall complexed with LDL. 9,10  An LDL - LPS complex is recognized as minimally modified LDL, which readily binds to macrophage LPS receptors.	bind
36931	3	8700	7	NULL	NULL	0	NULL	statement 2	NULL		promote	NULL	may			atherogenesis	NULL				NULL	arterial wall	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2174_s_30	15388525	8 In the circulation, LPS associates with all lipoprotein classes, but it may promote atherogenesis when it invades the arterial wall complexed with LDL. 9,10  An LDL - LPS complex is recognized as minimally modified LDL, which readily binds to macrophage LPS receptors.	bind
36932	4	8700	7	NULL	NULL	0	NULL	LDL-LPS	NULL		binds to	NULL				LPS receptors	NULL	macrophage			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2174_s_30	15388525	8 In the circulation, LPS associates with all lipoprotein classes, but it may promote atherogenesis when it invades the arterial wall complexed with LDL. 9,10  An LDL - LPS complex is recognized as minimally modified LDL, which readily binds to macrophage LPS receptors.	bind
36933	5	8700	7	NULL	NULL	0	NULL	LDL-LPS complex	NULL		is recognized as	NULL				LDL	NULL	minimally modified			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2174_s_30	15388525	8 In the circulation, LPS associates with all lipoprotein classes, but it may promote atherogenesis when it invades the arterial wall complexed with LDL. 9,10  An LDL - LPS complex is recognized as minimally modified LDL, which readily binds to macrophage LPS receptors.	bind
37792	1	8701	5	13	NULL	NULL	NULL	SR	CellComponent		bind					FKBP12.6	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_107_3_477_s_104	12551874	8 Note that the MCA fluorescence (net value, in arbitrary units: labeled SR minus unlabeled  SR) increased as SR became FKBP12.6-deficient but decreased as SR bound FKBP12.6  again.	bind
36934	1	8701	7	NULL	NULL	0	NULL	SR	NULL		bind	NULL				FKBP12.6	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_107_3_477_s_104	12551874	8 Note that the MCA fluorescence (net value, in arbitrary units: labeled SR minus unlabeled  SR) increased as SR became FKBP12.6-deficient but decreased as SR bound FKBP12.6  again.	bind
37793	1	8703	5	13	NULL	NULL	NULL	VDR	GP		bind					RXR(s)	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_269_4_8300629_s_11	8300629	8 nuclear extracts suggest  that the VDR binds to the mouse osteopontin VDRE predominantly as a heterodimer  with retinoid X receptor(s) (RXR(s)).	bind
37794	2	8703	5	13	NULL	NULL	NULL	RXR(s)	GP		is					retinoid X receptor(s)	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_269_4_8300629_s_11	8300629	8 nuclear extracts suggest  that the VDR binds to the mouse osteopontin VDRE predominantly as a heterodimer  with retinoid X receptor(s) (RXR(s)).	bind
37795	3	8703	5	13	NULL	NULL	NULL	statement 1	GP		forms					VDR-RXR(s) heterodimer	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_269_4_8300629_s_11	8300629	8 nuclear extracts suggest  that the VDR binds to the mouse osteopontin VDRE predominantly as a heterodimer  with retinoid X receptor(s) (RXR(s)).	bind
37796	4	8703	5	13	NULL	NULL	NULL	VDR-RXR(s) heterodimer	GP		bind					osteopontin	GP	mouse		VDRE	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_269_4_8300629_s_11	8300629	8 nuclear extracts suggest  that the VDR binds to the mouse osteopontin VDRE predominantly as a heterodimer  with retinoid X receptor(s) (RXR(s)).	bind
36938	1	8703	7	NULL	NULL	0	NULL	VDR	NULL		heterodimerizes with	NULL				RXR	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_269_4_8300629_s_11	8300629	8 nuclear extracts suggest  that the VDR binds to the mouse osteopontin VDRE predominantly as a heterodimer  with retinoid X receptor(s) (RXR(s)).	bind
36939	2	8703	7	10	NULL	0	NULL	statement 1			binds to					osteopontin		mouse		VDRE	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_269_4_8300629_s_11	8300629	8 nuclear extracts suggest  that the VDR binds to the mouse osteopontin VDRE predominantly as a heterodimer  with retinoid X receptor(s) (RXR(s)).	bind
36940	3	8703	7	NULL	NULL	0	NULL	RXR	NULL		is	NULL				retinoid X receptor	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_269_4_8300629_s_11	8300629	8 nuclear extracts suggest  that the VDR binds to the mouse osteopontin VDRE predominantly as a heterodimer  with retinoid X receptor(s) (RXR(s)).	bind
37798	1	8704	5	13	NULL	NULL	NULL	PDGF-A	GP		bind					PDGFR-alpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_5_479_s_22	15297375	8 Of the 2 high-affinity PDGF receptors (PDGFRs), PDGF-A binds to PDGFR-alpha but not receptor-beta.	bind
37799	2	8704	5	13	NULL	NULL	NULL	PDGF-A	GP		does not bind					PDGFR-beta	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_5_479_s_22	15297375	8 Of the 2 high-affinity PDGF receptors (PDGFRs), PDGF-A binds to PDGFR-alpha but not receptor-beta.	bind
37800	3	8704	5	13	NULL	NULL	NULL	PDGFR-alpha	GP		is a type of					PDGF receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_5_479_s_22	15297375	8 Of the 2 high-affinity PDGF receptors (PDGFRs), PDGF-A binds to PDGFR-alpha but not receptor-beta.	bind
37801	4	8704	5	13	NULL	NULL	NULL	PDGFR-beta	GP		is a type of					PDGF receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_5_479_s_22	15297375	8 Of the 2 high-affinity PDGF receptors (PDGFRs), PDGF-A binds to PDGFR-alpha but not receptor-beta.	bind
36941	1	8704	7	NULL	NULL	0	NULL	PDGF-A	NULL		bind	NULL				PDGFR-alpha	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_5_479_s_22	15297375	8 Of the 2 high-affinity PDGF receptors (PDGFRs), PDGF-A binds to PDGFR-alpha but not receptor-beta.	bind
36943	2	8704	7	NULL	NULL	0	NULL	PDGF-A 	NULL		does not bind	NULL				PDGFR-beta	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_5_479_s_22	15297375	8 Of the 2 high-affinity PDGF receptors (PDGFRs), PDGF-A binds to PDGFR-alpha but not receptor-beta.	bind
36944	3	8704	7	10	NULL	0	NULL	PDGFR	NULL		is a type of 	NULL				PDGF receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_5_479_s_22	15297375	8 Of the 2 high-affinity PDGF receptors (PDGFRs), PDGF-A binds to PDGFR-alpha but not receptor-beta.	bind
37802	1	8705	5	13	NULL	NULL	NULL	cytochrome c	GP		bind					CcP	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1597_2_193_s_1550	12044899	8 The reaction of CcP and hydrogen peroxide is not inhibited by binding of cytochrome  c to CcP [  159].	bind
37803	2	8705	5	13	NULL	NULL	NULL	CcP	GP	reaction of	is not inhibited by					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1597_2_193_s_1550	12044899	8 The reaction of CcP and hydrogen peroxide is not inhibited by binding of cytochrome  c to CcP [  159].	bind
37804	3	8705	5	13	NULL	NULL	NULL	hydrogen peroxide	Chemical	reaction of	is not inhibited by					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1597_2_193_s_1550	12044899	8 The reaction of CcP and hydrogen peroxide is not inhibited by binding of cytochrome  c to CcP [  159].	bind
36945	1	8705	7	NULL	NULL	0	NULL	cytochrome c 	NULL		bind	NULL				CcP	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1597_2_193_s_1550	12044899	8 The reaction of CcP and hydrogen peroxide is not inhibited by binding of cytochrome  c to CcP [  159].	bind
36946	2	8705	7	NULL	NULL	0	NULL	statement 1	NULL		does not inhibit	NULL				CcP	NULL	reaction of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1597_2_193_s_1550	12044899	8 The reaction of CcP and hydrogen peroxide is not inhibited by binding of cytochrome  c to CcP [  159].	bind
36947	3	8705	7	NULL	NULL	0	NULL	statement 1	NULL		does not inhibit	NULL				hydrogen peroxide	NULL	reaction of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1597_2_193_s_1550	12044899	8 The reaction of CcP and hydrogen peroxide is not inhibited by binding of cytochrome  c to CcP [  159].	bind
37805	1	8706	5	13	NULL	NULL	NULL	KLF5	GP		bind					PDGF-A	GP	endogenous		promoter	NULL	SMCs	NULL	NULL	NULL	NULL	gw70_circulationres_97_11_1132_s_147	16224062	8 The results showed that KLF5, RARalpha, and RXRalpha all bound to the endogenous  PDGF-A promoter in SMCs and that Am80 markedly reduced the abundance of the  PDGF-A promoter sequence in the immunoprecipitates pulled down with anti-KLF5, anti-RARalpha, or anti-RXRalpha antibody.	bind
37806	2	8706	5	13	NULL	NULL	NULL	RARalpha	GP		bind					PDGF-A	GP	endogenous		promoter	NULL	SMCs	NULL	NULL	NULL	NULL	gw70_circulationres_97_11_1132_s_147	16224062	8 The results showed that KLF5, RARalpha, and RXRalpha all bound to the endogenous  PDGF-A promoter in SMCs and that Am80 markedly reduced the abundance of the  PDGF-A promoter sequence in the immunoprecipitates pulled down with anti-KLF5, anti-RARalpha, or anti-RXRalpha antibody.	bind
37807	3	8706	5	13	NULL	NULL	NULL	RXRalpha	GP		bind					PDGF-A	GP	endogenous		promoter	NULL	SMCs	NULL	NULL	NULL	NULL	gw70_circulationres_97_11_1132_s_147	16224062	8 The results showed that KLF5, RARalpha, and RXRalpha all bound to the endogenous  PDGF-A promoter in SMCs and that Am80 markedly reduced the abundance of the  PDGF-A promoter sequence in the immunoprecipitates pulled down with anti-KLF5, anti-RARalpha, or anti-RXRalpha antibody.	bind
36951	1	8706	7	NULL	NULL	0	NULL	 KLF5	NULL		bind	NULL				PDGF-A	NULL	endogenous		promoter	NULL	SMCs	0	NULL	NULL	NULL	gw70_circulationres_97_11_1132_s_147	16224062	8 The results showed that KLF5, RARalpha, and RXRalpha all bound to the endogenous  PDGF-A promoter in SMCs and that Am80 markedly reduced the abundance of the  PDGF-A promoter sequence in the immunoprecipitates pulled down with anti-KLF5, anti-RARalpha, or anti-RXRalpha antibody.	bind
36952	2	8706	7	NULL	NULL	0	NULL	RARalpha	NULL		bind	NULL				PDGF-A	NULL	endogenous		promoter	NULL	SMCs	NULL	NULL	NULL	NULL	gw70_circulationres_97_11_1132_s_147	16224062	8 The results showed that KLF5, RARalpha, and RXRalpha all bound to the endogenous  PDGF-A promoter in SMCs and that Am80 markedly reduced the abundance of the  PDGF-A promoter sequence in the immunoprecipitates pulled down with anti-KLF5, anti-RARalpha, or anti-RXRalpha antibody.	bind
36953	3	8706	7	NULL	NULL	0	NULL	 RXRalpha	NULL		bind	NULL				PDGF-A	NULL	endogenous		promoter	NULL	SMcs	0	NULL	NULL	NULL	gw70_circulationres_97_11_1132_s_147	16224062	8 The results showed that KLF5, RARalpha, and RXRalpha all bound to the endogenous  PDGF-A promoter in SMCs and that Am80 markedly reduced the abundance of the  PDGF-A promoter sequence in the immunoprecipitates pulled down with anti-KLF5, anti-RARalpha, or anti-RXRalpha antibody.	bind
37811	1	8707	5	13	NULL	NULL	NULL	ATP	Chemical		bind					ArsA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_23_16153_s_336	10347168	8 The second-order association rate constant ( k1) for the binding of ATP to ArsA was calculated from the measured  Kd and the apparent rate of dissociation.	bind
36954	1	8707	7	NULL	NULL	0	NULL	 ATP	NULL		bind	NULL				ArsA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_23_16153_s_336	10347168	8 The second-order association rate constant ( k1) for the binding of ATP to ArsA was calculated from the measured  Kd and the apparent rate of dissociation.	bind
38745	1	8708	5	13	NULL	NULL	NULL	NOS3	GP	stimulated	does not bind					calmodulin	GP				NULL	oxLDL-treated cells	NULL	NULL	NULL	NULL	gw70_circulationres_98_6_717_s_63	16574911	8 These authors found that NOS3 from the oxLDL-treated cells no longer bound calmodulin when stimulated, and that NOS3 was less prominently associated with the Golgi and plasma membranes resulting in cytosolic NOS3 distribution.	bind
38746	2	8708	5	13	NULL	NULL	NULL	NOS3	GP		associate with		less prominently			Golgi	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_717_s_63	16574911	8 These authors found that NOS3 from the oxLDL-treated cells no longer bound calmodulin when stimulated, and that NOS3 was less prominently associated with the Golgi and plasma membranes resulting in cytosolic NOS3 distribution.	bind
38747	3	8708	5	13	NULL	NULL	NULL	NOS3	GP		associate with		less prominently			plasma membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_717_s_63	16574911	8 These authors found that NOS3 from the oxLDL-treated cells no longer bound calmodulin when stimulated, and that NOS3 was less prominently associated with the Golgi and plasma membranes resulting in cytosolic NOS3 distribution.	bind
38748	4	8708	5	13	NULL	NULL	NULL	statement 2	Process		results in					NOS3	GP	distribution of;;cytosolic			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_717_s_63	16574911	8 These authors found that NOS3 from the oxLDL-treated cells no longer bound calmodulin when stimulated, and that NOS3 was less prominently associated with the Golgi and plasma membranes resulting in cytosolic NOS3 distribution.	bind
38749	5	8708	5	13	NULL	NULL	NULL	statement 3	Process		results in					NOS3	GP	distribution of;;cytosolic			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_717_s_63	16574911	8 These authors found that NOS3 from the oxLDL-treated cells no longer bound calmodulin when stimulated, and that NOS3 was less prominently associated with the Golgi and plasma membranes resulting in cytosolic NOS3 distribution.	bind
36955	1	8708	7	10	NULL	0	NULL	NOS3 		stimulated	does not bind					calmodulin 					NULL	oxLDL-treated cells	NULL	NULL	NULL	NULL	gw70_circulationres_98_6_717_s_63	16574911	8 These authors found that NOS3 from the oxLDL-treated cells no longer bound calmodulin when stimulated, and that NOS3 was less prominently associated with the Golgi and plasma membranes resulting in cytosolic NOS3 distribution.	bind
36956	2	8708	7	NULL	NULL	0	NULL	NOS3	NULL		associate with	NULL				golgi membrane	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_6_717_s_63	16574911	8 These authors found that NOS3 from the oxLDL-treated cells no longer bound calmodulin when stimulated, and that NOS3 was less prominently associated with the Golgi and plasma membranes resulting in cytosolic NOS3 distribution.	bind
36957	3	8708	7	NULL	NULL	0	NULL	NOS3	NULL		associate with	NULL				plasma membrane	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_6_717_s_63	16574911	8 These authors found that NOS3 from the oxLDL-treated cells no longer bound calmodulin when stimulated, and that NOS3 was less prominently associated with the Golgi and plasma membranes resulting in cytosolic NOS3 distribution.	bind
36958	4	8708	7	10	NULL	0	NULL	statement 2	NULL		result in	NULL				NOS3	NULL	cytosolic;; distribution of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_717_s_63	16574911	8 These authors found that NOS3 from the oxLDL-treated cells no longer bound calmodulin when stimulated, and that NOS3 was less prominently associated with the Golgi and plasma membranes resulting in cytosolic NOS3 distribution.	bind
36959	5	8708	7	10	NULL	0	NULL	statement 3	NULL		result in	NULL				NOS3	NULL	cytosolic;; distribution of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_6_717_s_63	16574911	8 These authors found that NOS3 from the oxLDL-treated cells no longer bound calmodulin when stimulated, and that NOS3 was less prominently associated with the Golgi and plasma membranes resulting in cytosolic NOS3 distribution.	bind
37812	1	8709	5	13	NULL	NULL	NULL	CCR2	GP		is					CC type chemokine receptor 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_12_1436_s_163	11560862	8, 24 The CC type chemokine receptor 2 (CCR2), which binds to MCP-1, is necessary for the development of Ang II-induced macrophage infiltration and vascular hypertrophy.	bind
37813	2	8709	5	13	NULL	NULL	NULL	CCR2	GP		bind					MCP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_12_1436_s_163	11560862	8, 24 The CC type chemokine receptor 2 (CCR2), which binds to MCP-1, is necessary for the development of Ang II-induced macrophage infiltration and vascular hypertrophy.	bind
37814	3	8709	5	13	NULL	NULL	NULL	Ang II	GP		induce					macrophage infiltration	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_12_1436_s_163	11560862	8, 24 The CC type chemokine receptor 2 (CCR2), which binds to MCP-1, is necessary for the development of Ang II-induced macrophage infiltration and vascular hypertrophy.	bind
37815	4	8709	5	13	NULL	NULL	NULL	Ang II	GP		induce					vascular hypertrophy	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_12_1436_s_163	11560862	8, 24 The CC type chemokine receptor 2 (CCR2), which binds to MCP-1, is necessary for the development of Ang II-induced macrophage infiltration and vascular hypertrophy.	bind
37816	5	8709	5	13	NULL	NULL	NULL	statement 2	Process		is necessary for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_12_1436_s_163	11560862	8, 24 The CC type chemokine receptor 2 (CCR2), which binds to MCP-1, is necessary for the development of Ang II-induced macrophage infiltration and vascular hypertrophy.	bind
37817	6	8709	5	13	NULL	NULL	NULL	statement 3	Process		is necessary for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_104_12_1436_s_163	11560862	8, 24 The CC type chemokine receptor 2 (CCR2), which binds to MCP-1, is necessary for the development of Ang II-induced macrophage infiltration and vascular hypertrophy.	bind
36961	1	8709	7	NULL	NULL	0	NULL	CCR2	NULL		binds to	NULL				MCP-1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_104_12_1436_s_163	11560862	8, 24 The CC type chemokine receptor 2 (CCR2), which binds to MCP-1, is necessary for the development of Ang II-induced macrophage infiltration and vascular hypertrophy.	bind
36962	2	8709	7	NULL	NULL	0	NULL	CCR2	NULL		is	NULL				CC type chemokine receptor 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_104_12_1436_s_163	11560862	8, 24 The CC type chemokine receptor 2 (CCR2), which binds to MCP-1, is necessary for the development of Ang II-induced macrophage infiltration and vascular hypertrophy.	bind
36963	3	8709	7	NULL	NULL	0	NULL	Ang II 	NULL		induce	NULL				macrophage infiltration	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_104_12_1436_s_163	11560862	8, 24 The CC type chemokine receptor 2 (CCR2), which binds to MCP-1, is necessary for the development of Ang II-induced macrophage infiltration and vascular hypertrophy.	bind
36964	4	8709	7	NULL	NULL	0	NULL	Ang II 	NULL		induce	NULL				vascular hypertrophy	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_104_12_1436_s_163	11560862	8, 24 The CC type chemokine receptor 2 (CCR2), which binds to MCP-1, is necessary for the development of Ang II-induced macrophage infiltration and vascular hypertrophy.	bind
36965	5	8709	7	NULL	NULL	0	NULL	statement 1	NULL		is necessary for	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_104_12_1436_s_163	11560862	8, 24 The CC type chemokine receptor 2 (CCR2), which binds to MCP-1, is necessary for the development of Ang II-induced macrophage infiltration and vascular hypertrophy.	bind
36966	6	8709	7	NULL	NULL	0	NULL	statement 1	NULL		is necessary for	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_104_12_1436_s_163	11560862	8, 24 The CC type chemokine receptor 2 (CCR2), which binds to MCP-1, is necessary for the development of Ang II-induced macrophage infiltration and vascular hypertrophy.	bind
37937	1	8710	5	13	NULL	NULL	NULL				bind		noncovalently	carboxy-terminal	4-kDa carboxy-terminal fragment of 36 residues (C-36)	complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_11_1801_s_22	11701469	8, 9 The resulting 4-kDa carboxy-terminal fragment of 36 residues (C-36) still binds the complex noncovalently, but under denaturing conditions in vitro, the C-36 fragment dissociates from the complex.	bind
37938	2	8710	5	13	NULL	NULL	NULL				dissociates from			C-36 fragment		complex	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_11_1801_s_22	11701469	8, 9 The resulting 4-kDa carboxy-terminal fragment of 36 residues (C-36) still binds the complex noncovalently, but under denaturing conditions in vitro, the C-36 fragment dissociates from the complex.	bind
37939	3	8710	5	13	NULL	NULL	NULL	statement 2	Process		occurs under					denaturing conditions					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_11_1801_s_22	11701469	8, 9 The resulting 4-kDa carboxy-terminal fragment of 36 residues (C-36) still binds the complex noncovalently, but under denaturing conditions in vitro, the C-36 fragment dissociates from the complex.	bind
37909	1	8710	7	NULL	NULL	0	NULL		NULL		binds	NULL	noncovalently	4-kDa carboxy-terminal fragment of 36 residues (C-36)		complex	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_11_1801_s_22	11701469	8, 9 The resulting 4-kDa carboxy-terminal fragment of 36 residues (C-36) still binds the complex noncovalently, but under denaturing conditions in vitro, the C-36 fragment dissociates from the complex.	bind
37910	2	8710	7	NULL	NULL	0	NULL		NULL		dissociates from	NULL		C-36 fragment		complex	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_11_1801_s_22	11701469	8, 9 The resulting 4-kDa carboxy-terminal fragment of 36 residues (C-36) still binds the complex noncovalently, but under denaturing conditions in vitro, the C-36 fragment dissociates from the complex.	bind
37911	3	8710	7	NULL	NULL	0	NULL	statement 2	NULL		occurs under	NULL				denaturing condition	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_11_1801_s_22	11701469	8, 9 The resulting 4-kDa carboxy-terminal fragment of 36 residues (C-36) still binds the complex noncovalently, but under denaturing conditions in vitro, the C-36 fragment dissociates from the complex.	bind
37818	1	8711	5	13	NULL	NULL	NULL	MPO	GP		bind					vessel wall	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_circulation_113_15_1871_s_84	16606792	8,10  To test whether heparins also reverse MPO binding to the vessel wall, isolated extracellular matrix proteins, cultured endothelial cells, and saphenous vein graft specimens from patients undergoing aortocoronary bypass surgery were analyzed for MPO before and after treatment with heparin.	bind
36967	1	8711	7	NULL	NULL	0	NULL	MPO	NULL		bind	NULL				vessel wall	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_113_15_1871_s_84	16606792	8,10  To test whether heparins also reverse MPO binding to the vessel wall, isolated extracellular matrix proteins, cultured endothelial cells, and saphenous vein graft specimens from patients undergoing aortocoronary bypass surgery were analyzed for MPO before and after treatment with heparin.	bind
37819	1	8712	5	13	NULL	NULL	NULL	Ang2	GP		bind					Tie2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_31	16690881	8,26  Ang2 binds to Tie2 and acts as a competing Ang1 antagonist but can also phosphorylate Tie2.	bind
37822	2	8712	5	13	NULL	NULL	NULL	Ang2	GP		acts as a					Ang1 antagonist	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_31	16690881	8,26  Ang2 binds to Tie2 and acts as a competing Ang1 antagonist but can also phosphorylate Tie2.	bind
37823	3	8712	5	13	NULL	NULL	NULL	Ang2	GP		phosphorylate					Tie2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_31	16690881	8,26  Ang2 binds to Tie2 and acts as a competing Ang1 antagonist but can also phosphorylate Tie2.	bind
36975	1	8712	7	NULL	NULL	0	NULL	Ang2	NULL		binds to	NULL				Tie2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_31	16690881	8,26  Ang2 binds to Tie2 and acts as a competing Ang1 antagonist but can also phosphorylate Tie2.	bind
36976	2	8712	7	NULL	NULL	0	NULL	Ang2	NULL		acts as a	NULL				Ang1 antagonist	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_31	16690881	8,26  Ang2 binds to Tie2 and acts as a competing Ang1 antagonist but can also phosphorylate Tie2.	bind
36977	3	8712	7	NULL	NULL	0	NULL	Ang2	NULL		phosphorylate	NULL				Tie2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_11_1373_s_31	16690881	8,26  Ang2 binds to Tie2 and acts as a competing Ang1 antagonist but can also phosphorylate Tie2.	bind
56311	1	8713	5	13	NULL	NULL	NULL	cAMP	Chemical		bind					52 kDa protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_37_8_1081_s_92	9833637	8- N3-[32]cAMP binding to the 52 kDa protein band (indicated by arrow) in microtubules	bind
36978	1	8713	7	10	NULL	0	NULL	cAMP			bind					52 kDa protein 					NULL	microtubules	NULL	NULL	NULL	NULL	gw60_neuropharmacology_37_8_1081_s_92	9833637	8- N3-[32]cAMP binding to the 52 kDa protein band (indicated by arrow) in microtubules	bind
37824	1	8714	5	13	NULL	NULL	NULL	ANS	Chemical		bind					N-PLA2	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_453_3_395_s_36	10405184	8-Anilino-1-naphthalene sulfonate (ANS) was included in the N-PLA2 containing solution to monitor the possible heparin-induced fluorescence changes of the ANS bound to N-PLA2.	bind
46753	2	8714	5	13	NULL	NULL	NULL	ANS	Chemical		is					8-Anilino-1-naphthalene sulfonate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_453_3_395_s_36	10405184	8-Anilino-1-naphthalene sulfonate (ANS) was included in the N-PLA2 containing solution to monitor the possible heparin-induced fluorescence changes of the ANS bound to N-PLA2.	bind
36979	1	8714	7	NULL	NULL	0	NULL	ANS 	NULL		bind	NULL				N-PLA2	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_453_3_395_s_36	10405184	8-Anilino-1-naphthalene sulfonate (ANS) was included in the N-PLA2 containing solution to monitor the possible heparin-induced fluorescence changes of the ANS bound to N-PLA2.	bind
36980	2	8714	7	NULL	NULL	0	NULL	ANS	NULL		is	NULL				8-Anilino-1-naphthalene sulfonate	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_453_3_395_s_36	10405184	8-Anilino-1-naphthalene sulfonate (ANS) was included in the N-PLA2 containing solution to monitor the possible heparin-induced fluorescence changes of the ANS bound to N-PLA2.	bind
37825	1	8716	5	13	NULL	NULL	NULL	8-Azido-ATP	Chemical		bind					ABCG1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_47_8_1791_s_173	16702602	8-Azido-ATP binding of ABCG1.	bind
36984	1	8716	7	NULL	NULL	0	NULL	8-Azido-ATP	NULL		bind	NULL				ABCG1	NULL				NULL		0	NULL	NULL	NULL	gw70_jlipidres_47_8_1791_s_173	16702602	8-Azido-ATP binding of ABCG1.	bind
37826	1	8717	5	13	NULL	NULL	NULL	8-Azido-ATP	Chemical		bind							mutant	C431A		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1461_2_305_s_157	10581363	8-Azido-ATP binding of the C431A mutant form appeared not to be affected by treatment with 100  M NEM.	bind
36985	1	8717	7	NULL	NULL	0	NULL	8-Azido-ATP	NULL		bind	NULL					NULL	mutant	C431A		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1461_2_305_s_157	10581363	8-Azido-ATP binding of the C431A mutant form appeared not to be affected by treatment with 100  M NEM.	bind
37828	1	8718	5	13	NULL	NULL	NULL	8-Azido-ATP	Chemical		bind					SURx	GP		NBF1		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_37_28757_s_84	10893240	8-Azido-ATP Binding to NBF1 and NBF2 of SURx-- To investigate the ATP-binding properties of NBFs of SURx, SURx was photoaffinity-labeled with 50 muM 8-azido-[alpha-32]ATP under various conditions and mildly digested with trypsin (Fig.  3).	bind
37829	2	8718	5	13	NULL	NULL	NULL	8-Azido-ATP	Chemical		bind					SURx	GP		NBF2		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_37_28757_s_84	10893240	8-Azido-ATP Binding to NBF1 and NBF2 of SURx-- To investigate the ATP-binding properties of NBFs of SURx, SURx was photoaffinity-labeled with 50 muM 8-azido-[alpha-32]ATP under various conditions and mildly digested with trypsin (Fig.  3).	bind
36986	1	8718	7	10	NULL	0	NULL	8-azido-[alpha-32]ATP	NULL		bind	NULL				SURx	NULL		NBF1		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_37_28757_s_84	10893240	8-Azido-ATP Binding to NBF1 and NBF2 of SURx-- To investigate the ATP-binding properties of NBFs of SURx, SURx was photoaffinity-labeled with 50 muM 8-azido-[alpha-32]ATP under various conditions and mildly digested with trypsin (Fig.  3).	bind
36987	2	8718	7	10	NULL	0	NULL	 8-azido-[alpha-32]ATP	NULL		bind	NULL				SURx	NULL		NBF2		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_37_28757_s_84	10893240	8-Azido-ATP Binding to NBF1 and NBF2 of SURx-- To investigate the ATP-binding properties of NBFs of SURx, SURx was photoaffinity-labeled with 50 muM 8-azido-[alpha-32]ATP under various conditions and mildly digested with trypsin (Fig.  3).	bind
37830	1	8719	5	13	NULL	NULL	NULL	8-Azido-ATP	Chemical		bind					TAP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_129	12777379	8-Azido-ATP Binding to TAP1 and TAP2 Is Magnesium- and  Temperature-dependent -- Magnesium is well known to be required for  ATP hydrolysis by most ATPases.	bind
37831	2	8719	5	13	NULL	NULL	NULL	statement 1	Process		is dependent on					magnesium	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_129	12777379	8-Azido-ATP Binding to TAP1 and TAP2 Is Magnesium- and  Temperature-dependent -- Magnesium is well known to be required for  ATP hydrolysis by most ATPases.	bind
37832	3	8719	5	13	NULL	NULL	NULL	statement 1	Process		is dependent on					temperature					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_129	12777379	8-Azido-ATP Binding to TAP1 and TAP2 Is Magnesium- and  Temperature-dependent -- Magnesium is well known to be required for  ATP hydrolysis by most ATPases.	bind
37833	4	8719	5	13	NULL	NULL	NULL	8-Azido-ATP	Chemical		bind					TAP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_129	12777379	8-Azido-ATP Binding to TAP1 and TAP2 Is Magnesium- and  Temperature-dependent -- Magnesium is well known to be required for  ATP hydrolysis by most ATPases.	bind
37834	5	8719	5	13	NULL	NULL	NULL	statement 4	Process		is dependent on					magnesium	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_129	12777379	8-Azido-ATP Binding to TAP1 and TAP2 Is Magnesium- and  Temperature-dependent -- Magnesium is well known to be required for  ATP hydrolysis by most ATPases.	bind
37835	6	8719	5	13	NULL	NULL	NULL	statement 4	Process		is dependent on					temperature					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_129	12777379	8-Azido-ATP Binding to TAP1 and TAP2 Is Magnesium- and  Temperature-dependent -- Magnesium is well known to be required for  ATP hydrolysis by most ATPases.	bind
56312	7	8719	5	13	NULL	NULL	NULL	ATPase	GP		hydrolyse					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_129	12777379	8-Azido-ATP Binding to TAP1 and TAP2 Is Magnesium- and  Temperature-dependent -- Magnesium is well known to be required for  ATP hydrolysis by most ATPases.	bind
56313	8	8719	5	13	NULL	NULL	NULL	magnesium	Chemical		ia required for					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_129	12777379	8-Azido-ATP Binding to TAP1 and TAP2 Is Magnesium- and  Temperature-dependent -- Magnesium is well known to be required for  ATP hydrolysis by most ATPases.	bind
36988	1	8719	7	NULL	NULL	0	NULL	8-Azido-ATP	NULL		bind	NULL				TAP1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_129	12777379	8-Azido-ATP Binding to TAP1 and TAP2 Is Magnesium- and  Temperature-dependent -- Magnesium is well known to be required for  ATP hydrolysis by most ATPases.	bind
36989	2	8719	7	NULL	NULL	0	NULL	8-Azido-ATP	NULL		bind	NULL				TAP2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_129	12777379	8-Azido-ATP Binding to TAP1 and TAP2 Is Magnesium- and  Temperature-dependent -- Magnesium is well known to be required for  ATP hydrolysis by most ATPases.	bind
36990	3	8719	7	NULL	NULL	0	NULL	statement 1	NULL		depends on	NULL				Magnesium	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_129	12777379	8-Azido-ATP Binding to TAP1 and TAP2 Is Magnesium- and  Temperature-dependent -- Magnesium is well known to be required for  ATP hydrolysis by most ATPases.	bind
36991	4	8719	7	NULL	NULL	0	NULL	statement 2	NULL		depends on	NULL				Magnesium	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_129	12777379	8-Azido-ATP Binding to TAP1 and TAP2 Is Magnesium- and  Temperature-dependent -- Magnesium is well known to be required for  ATP hydrolysis by most ATPases.	bind
36992	5	8719	7	NULL	NULL	0	NULL	statement 1	NULL		depends on	NULL				temperature	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_129	12777379	8-Azido-ATP Binding to TAP1 and TAP2 Is Magnesium- and  Temperature-dependent -- Magnesium is well known to be required for  ATP hydrolysis by most ATPases.	bind
36993	6	8719	7	NULL	NULL	0	NULL	statement 2	NULL		depends on	NULL				temperature	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_129	12777379	8-Azido-ATP Binding to TAP1 and TAP2 Is Magnesium- and  Temperature-dependent -- Magnesium is well known to be required for  ATP hydrolysis by most ATPases.	bind
36994	7	8719	7	NULL	NULL	0	NULL	ATPases	NULL		hydrolyse	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_129	12777379	8-Azido-ATP Binding to TAP1 and TAP2 Is Magnesium- and  Temperature-dependent -- Magnesium is well known to be required for  ATP hydrolysis by most ATPases.	bind
36995	8	8719	7	NULL	NULL	0	NULL	Magnesium	NULL		is required for	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_129	12777379	8-Azido-ATP Binding to TAP1 and TAP2 Is Magnesium- and  Temperature-dependent -- Magnesium is well known to be required for  ATP hydrolysis by most ATPases.	bind
37836	1	8720	5	13	NULL	NULL	NULL	8-Azido-ATP	Chemical		bind					MDR1	GP	wild-type			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1461_2_305_s_156	10581363	8-Azido-ATP binding with the wild-type MDR1 was inhibited by 100  M NEM, while 8-azido-ATP binding with the C431A/C1074A mutant form was not, suggesting that the cysteines of Walker A motifs in both NBFs are responsible for the effects of NEM on ATP binding.	bind
37837	2	8720	5	13	NULL	NULL	NULL	NEM	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1461_2_305_s_156	10581363	8-Azido-ATP binding with the wild-type MDR1 was inhibited by 100  M NEM, while 8-azido-ATP binding with the C431A/C1074A mutant form was not, suggesting that the cysteines of Walker A motifs in both NBFs are responsible for the effects of NEM on ATP binding.	bind
37838	3	8720	5	13	NULL	NULL	NULL	8-azido-ATP	Chemical		bind					MDR1	GP	mutant	C431A;;C1074A		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1461_2_305_s_156	10581363	8-Azido-ATP binding with the wild-type MDR1 was inhibited by 100  M NEM, while 8-azido-ATP binding with the C431A/C1074A mutant form was not, suggesting that the cysteines of Walker A motifs in both NBFs are responsible for the effects of NEM on ATP binding.	bind
37839	4	8720	5	13	NULL	NULL	NULL	NEM	Chemical		does not inhibit					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1461_2_305_s_156	10581363	8-Azido-ATP binding with the wild-type MDR1 was inhibited by 100  M NEM, while 8-azido-ATP binding with the C431A/C1074A mutant form was not, suggesting that the cysteines of Walker A motifs in both NBFs are responsible for the effects of NEM on ATP binding.	bind
37840	5	8720	5	13	NULL	NULL	NULL	MDR1	GP		contains			NBFs					cysteines in Walker A motifs		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1461_2_305_s_156	10581363	8-Azido-ATP binding with the wild-type MDR1 was inhibited by 100  M NEM, while 8-azido-ATP binding with the C431A/C1074A mutant form was not, suggesting that the cysteines of Walker A motifs in both NBFs are responsible for the effects of NEM on ATP binding.	bind
37841	6	8720	5	13	NULL	NULL	NULL	statement 5	Process		is responsible for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1461_2_305_s_156	10581363	8-Azido-ATP binding with the wild-type MDR1 was inhibited by 100  M NEM, while 8-azido-ATP binding with the C431A/C1074A mutant form was not, suggesting that the cysteines of Walker A motifs in both NBFs are responsible for the effects of NEM on ATP binding.	bind
36996	1	8720	7	NULL	NULL	0	NULL	8-Azido-ATP	NULL		bind	NULL				MDR1	NULL	wild-type			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1461_2_305_s_156	10581363	8-Azido-ATP binding with the wild-type MDR1 was inhibited by 100  M NEM, while 8-azido-ATP binding with the C431A/C1074A mutant form was not, suggesting that the cysteines of Walker A motifs in both NBFs are responsible for the effects of NEM on ATP binding.	bind
36997	2	8720	7	NULL	NULL	0	NULL	NEM	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1461_2_305_s_156	10581363	8-Azido-ATP binding with the wild-type MDR1 was inhibited by 100  M NEM, while 8-azido-ATP binding with the C431A/C1074A mutant form was not, suggesting that the cysteines of Walker A motifs in both NBFs are responsible for the effects of NEM on ATP binding.	bind
36998	3	8720	7	NULL	NULL	0	NULL	8-Azido-ATP	NULL		bind	NULL				MDR1	NULL	mutant	C431A/C1074A		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1461_2_305_s_156	10581363	8-Azido-ATP binding with the wild-type MDR1 was inhibited by 100  M NEM, while 8-azido-ATP binding with the C431A/C1074A mutant form was not, suggesting that the cysteines of Walker A motifs in both NBFs are responsible for the effects of NEM on ATP binding.	bind
36999	4	8720	7	NULL	NULL	0	NULL	NEM	NULL		does not inhibit	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1461_2_305_s_156	10581363	8-Azido-ATP binding with the wild-type MDR1 was inhibited by 100  M NEM, while 8-azido-ATP binding with the C431A/C1074A mutant form was not, suggesting that the cysteines of Walker A motifs in both NBFs are responsible for the effects of NEM on ATP binding.	bind
37000	5	8720	7	NULL	NULL	0	NULL	NBF	NULL		is responsible for	NULL		cysteines of Walker A motifs 		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1461_2_305_s_156	10581363	8-Azido-ATP binding with the wild-type MDR1 was inhibited by 100  M NEM, while 8-azido-ATP binding with the C431A/C1074A mutant form was not, suggesting that the cysteines of Walker A motifs in both NBFs are responsible for the effects of NEM on ATP binding.	bind
37001	6	8720	7	NULL	NULL	0	NULL	NBF	NULL		is responsible for	NULL		cysteines of Walker A motifs 		statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1461_2_305_s_156	10581363	8-Azido-ATP binding with the wild-type MDR1 was inhibited by 100  M NEM, while 8-azido-ATP binding with the C431A/C1074A mutant form was not, suggesting that the cysteines of Walker A motifs in both NBFs are responsible for the effects of NEM on ATP binding.	bind
37842	1	8721	5	13	NULL	NULL	NULL	8-Azido-ATP	Chemical		bind		specifically			TAP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_115	12777379	8-Azido-ATP Binds Specifically to TAP1 and TAP2 --	bind
37843	2	8721	5	13	NULL	NULL	NULL	8-Azido-ATP	Chemical		bind		specifically			TAP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_115	12777379	8-Azido-ATP Binds Specifically to TAP1 and TAP2 --	bind
37002	1	8721	7	NULL	NULL	0	NULL	8-Azido-ATP	NULL		binds	NULL	specifically			TAP1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_115	12777379	8-Azido-ATP Binds Specifically to TAP1 and TAP2 --	bind
37003	2	8721	7	NULL	NULL	0	NULL	8-Azido-ATP	NULL		binds	NULL	specifically			TAP2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_32_29686_s_115	12777379	8-Azido-ATP Binds Specifically to TAP1 and TAP2 --	bind
37844	1	8722	5	13	NULL	NULL	NULL	8-Azido-[alpha-32]ATP	Chemical		bind					SURx	GP		NBFs		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_37_28757_s_90	10893240	8-Azido-[alpha-32]ATP binding of NBFs of SURx.	bind
37004	1	8722	7	NULL	NULL	0	NULL	8-Azido-[alpha-32]ATP	NULL		bind	NULL				SURx	NULL		NBFs		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_37_28757_s_90	10893240	8-Azido-[alpha-32]ATP binding of NBFs of SURx.	bind
37845	1	8723	5	13	NULL	NULL	NULL	8-Azido[alpha -32]ATP	Chemical		bind					G5	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_7_4507_s_99	16352607	8-Azido[alpha -32]ATP Binding to G5 and G8 Does Not Require G5G8 Dimerization --	bind
37846	2	8723	5	13	NULL	NULL	NULL	8-Azido[alpha -32]ATP	Chemical		bind					G8	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_7_4507_s_99	16352607	8-Azido[alpha -32]ATP Binding to G5 and G8 Does Not Require G5G8 Dimerization --	bind
37847	3	8723	5	13	NULL	NULL	NULL	statement 1	Process		does not require					G5G8	GP	dimerization of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_7_4507_s_99	16352607	8-Azido[alpha -32]ATP Binding to G5 and G8 Does Not Require G5G8 Dimerization --	bind
37848	4	8723	5	13	NULL	NULL	NULL	statement 2	Process		does not require					G5G8	GP	dimerization of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_7_4507_s_99	16352607	8-Azido[alpha -32]ATP Binding to G5 and G8 Does Not Require G5G8 Dimerization --	bind
37005	1	8723	7	NULL	NULL	0	NULL	8-Azido[alpha -32]ATP	NULL		bind	NULL				G5	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_7_4507_s_99	16352607	8-Azido[alpha -32]ATP Binding to G5 and G8 Does Not Require G5G8 Dimerization --	bind
37006	2	8723	7	NULL	NULL	0	NULL	8-Azido[alpha -32]ATP	NULL		bind	NULL				G8	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_7_4507_s_99	16352607	8-Azido[alpha -32]ATP Binding to G5 and G8 Does Not Require G5G8 Dimerization --	bind
37007	3	8723	7	10	NULL	0	NULL	statement 1			does not require					G5G8 		dimerization of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_7_4507_s_99	16352607	8-Azido[alpha -32]ATP Binding to G5 and G8 Does Not Require G5G8 Dimerization --	bind
37008	4	8723	7	10	NULL	0	NULL	statement 2			does not require					G5G8 		dimerization of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_7_4507_s_99	16352607	8-Azido[alpha -32]ATP Binding to G5 and G8 Does Not Require G5G8 Dimerization --	bind
37849	1	8724	5	13	NULL	NULL	NULL	8-Azido[alpha -32]ATP	Chemical		bind					MRP4	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_47_48855_s_92	15364914	8-Azido[alpha -32]ATP Binds to Human MRP4  --	bind
37009	1	8724	7	NULL	NULL	0	NULL	8-Azido[alpha -32]ATP	NULL		binds to	NULL				MRP4	NULL	human			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_48855_s_92	15364914	8-Azido[alpha -32]ATP Binds to Human MRP4  --	bind
37850	1	8725	5	13	NULL	NULL	NULL	8-Azido[alpha-32]ATP	Chemical		bind					MRP4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_47_48855_s_6	15364914	8-Azido[alpha-32]ATP binds to MRP4 (concentration for half-maximal binding  3 muM) and is displaced by ATP or by its non-hydrolyzable analog AMPPNP (concentrations for half-maximal inhibition of 13.3 and 308 muM).	bind
37851	2	8725	5	13	NULL	NULL	NULL	ATP	Chemical		bind					MRP4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_47_48855_s_6	15364914	8-Azido[alpha-32]ATP binds to MRP4 (concentration for half-maximal binding  3 muM) and is displaced by ATP or by its non-hydrolyzable analog AMPPNP (concentrations for half-maximal inhibition of 13.3 and 308 muM).	bind
37852	3	8725	5	13	NULL	NULL	NULL	statement 2	Process		displaces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_47_48855_s_6	15364914	8-Azido[alpha-32]ATP binds to MRP4 (concentration for half-maximal binding  3 muM) and is displaced by ATP or by its non-hydrolyzable analog AMPPNP (concentrations for half-maximal inhibition of 13.3 and 308 muM).	bind
37853	4	8725	5	13	NULL	NULL	NULL	AMPPNP	Chemical		is an analog of		non-hydrolyzable			8-Azido[alpha-32]ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_47_48855_s_6	15364914	8-Azido[alpha-32]ATP binds to MRP4 (concentration for half-maximal binding  3 muM) and is displaced by ATP or by its non-hydrolyzable analog AMPPNP (concentrations for half-maximal inhibition of 13.3 and 308 muM).	bind
37854	5	8725	5	13	NULL	NULL	NULL	AMPPNP	Chemical		bind					MRP4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_47_48855_s_6	15364914	8-Azido[alpha-32]ATP binds to MRP4 (concentration for half-maximal binding  3 muM) and is displaced by ATP or by its non-hydrolyzable analog AMPPNP (concentrations for half-maximal inhibition of 13.3 and 308 muM).	bind
37855	6	8725	5	13	NULL	NULL	NULL	statement 5	Process		displaces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_47_48855_s_6	15364914	8-Azido[alpha-32]ATP binds to MRP4 (concentration for half-maximal binding  3 muM) and is displaced by ATP or by its non-hydrolyzable analog AMPPNP (concentrations for half-maximal inhibition of 13.3 and 308 muM).	bind
37856	7	8725	5	13	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_47_48855_s_6	15364914	8-Azido[alpha-32]ATP binds to MRP4 (concentration for half-maximal binding  3 muM) and is displaced by ATP or by its non-hydrolyzable analog AMPPNP (concentrations for half-maximal inhibition of 13.3 and 308 muM).	bind
37010	1	8725	7	NULL	NULL	0	NULL	8-Azido[alpha-32]ATP	NULL		binds to	NULL				MRP4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_48855_s_6	15364914	8-Azido[alpha-32]ATP binds to MRP4 (concentration for half-maximal binding  3 muM) and is displaced by ATP or by its non-hydrolyzable analog AMPPNP (concentrations for half-maximal inhibition of 13.3 and 308 muM).	bind
37011	2	8725	7	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				MRP4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_48855_s_6	15364914	8-Azido[alpha-32]ATP binds to MRP4 (concentration for half-maximal binding  3 muM) and is displaced by ATP or by its non-hydrolyzable analog AMPPNP (concentrations for half-maximal inhibition of 13.3 and 308 muM).	bind
37012	3	8725	7	NULL	NULL	0	NULL	statement 2	NULL		displace	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_48855_s_6	15364914	8-Azido[alpha-32]ATP binds to MRP4 (concentration for half-maximal binding  3 muM) and is displaced by ATP or by its non-hydrolyzable analog AMPPNP (concentrations for half-maximal inhibition of 13.3 and 308 muM).	bind
37013	4	8725	7	NULL	NULL	0	NULL	AMPPNP	NULL		bind	NULL				MRP4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_48855_s_6	15364914	8-Azido[alpha-32]ATP binds to MRP4 (concentration for half-maximal binding  3 muM) and is displaced by ATP or by its non-hydrolyzable analog AMPPNP (concentrations for half-maximal inhibition of 13.3 and 308 muM).	bind
37014	5	8725	7	NULL	NULL	0	NULL	statement 4	NULL		displace	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_48855_s_6	15364914	8-Azido[alpha-32]ATP binds to MRP4 (concentration for half-maximal binding  3 muM) and is displaced by ATP or by its non-hydrolyzable analog AMPPNP (concentrations for half-maximal inhibition of 13.3 and 308 muM).	bind
37015	6	8725	7	NULL	NULL	0	NULL	AMPPNP	NULL		is a type of	NULL				non-hydrolyzable analog	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_48855_s_6	15364914	8-Azido[alpha-32]ATP binds to MRP4 (concentration for half-maximal binding  3 muM) and is displaced by ATP or by its non-hydrolyzable analog AMPPNP (concentrations for half-maximal inhibition of 13.3 and 308 muM).	bind
38741	1	8726	5	13	NULL	NULL	NULL	8-Cl-cAMP	Chemical		targets		specifically			PKA	GP		cAMP binding sites in regulatory R-I subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_34_21137_s_78	9261118	8-Cl-cAMP specifically targets the high affinity cAMP binding sites in the regulatory R-I subunit of PKA ( 35), which results in the sustained activation and proteolysis of type I PKA and the down-regulation of cAMP-dependent transcription factors ( 26,  28).	bind
38742	2	8726	5	13	NULL	NULL	NULL	statement 1	Process		results in					type I PKA	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_34_21137_s_78	9261118	8-Cl-cAMP specifically targets the high affinity cAMP binding sites in the regulatory R-I subunit of PKA ( 35), which results in the sustained activation and proteolysis of type I PKA and the down-regulation of cAMP-dependent transcription factors ( 26,  28).	bind
38743	3	8726	5	13	NULL	NULL	NULL	statement 1	Process		results in					type I PKA	GP	proteolysis of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_34_21137_s_78	9261118	8-Cl-cAMP specifically targets the high affinity cAMP binding sites in the regulatory R-I subunit of PKA ( 35), which results in the sustained activation and proteolysis of type I PKA and the down-regulation of cAMP-dependent transcription factors ( 26,  28).	bind
38744	4	8726	5	13	NULL	NULL	NULL	statement 1	Process		results in					cAMP-dependent transcription factors	GP	down-regulation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_34_21137_s_78	9261118	8-Cl-cAMP specifically targets the high affinity cAMP binding sites in the regulatory R-I subunit of PKA ( 35), which results in the sustained activation and proteolysis of type I PKA and the down-regulation of cAMP-dependent transcription factors ( 26,  28).	bind
37083	1	8726	7	NULL	NULL	0	NULL	8-Cl-cAMP	NULL		targets	NULL	specifically			pKA	NULL		cAMP binding sites in the regulatory R-I subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_34_21137_s_78	9261118	8-Cl-cAMP specifically targets the high affinity cAMP binding sites in the regulatory R-I subunit of PKA ( 35), which results in the sustained activation and proteolysis of type I PKA and the down-regulation of cAMP-dependent transcription factors ( 26,  28).	bind
37084	2	8726	7	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				type I PKA	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_34_21137_s_78	9261118	8-Cl-cAMP specifically targets the high affinity cAMP binding sites in the regulatory R-I subunit of PKA ( 35), which results in the sustained activation and proteolysis of type I PKA and the down-regulation of cAMP-dependent transcription factors ( 26,  28).	bind
37085	3	8726	7	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				type I PKA	NULL	proteolysis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_34_21137_s_78	9261118	8-Cl-cAMP specifically targets the high affinity cAMP binding sites in the regulatory R-I subunit of PKA ( 35), which results in the sustained activation and proteolysis of type I PKA and the down-regulation of cAMP-dependent transcription factors ( 26,  28).	bind
37086	4	8726	7	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				cAMP-dependent transcription factors 	NULL	down-regulation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_34_21137_s_78	9261118	8-Cl-cAMP specifically targets the high affinity cAMP binding sites in the regulatory R-I subunit of PKA ( 35), which results in the sustained activation and proteolysis of type I PKA and the down-regulation of cAMP-dependent transcription factors ( 26,  28).	bind
37947	1	8727	5	13	NULL	NULL	NULL	8-N3-[32]cAMP	Chemical		bind					52 kDa protein	GP				NULL	microtubule fraction from total cortex of rats treated with vehicle	NULL	NULL	NULL	NULL	gw60_neuropharmacology_40_3_448_s_97	11166338	8-N3-[32]cAMP binding to the 52 kDa protein band (indicated by arrow) in microtubule fraction from total cortex of rats treated with vehicle (1, 2) or reboxetine (3, 4).	bind
37948	2	8727	5	13	NULL	NULL	NULL	8-N3-[32]cAMP	Chemical		bind					52 kDa protein	GP				NULL	microtubule fraction from total cortex of rats treated with reboxetine	NULL	NULL	NULL	NULL	gw60_neuropharmacology_40_3_448_s_97	11166338	8-N3-[32]cAMP binding to the 52 kDa protein band (indicated by arrow) in microtubule fraction from total cortex of rats treated with vehicle (1, 2) or reboxetine (3, 4).	bind
37956	3	8727	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_40_3_448_s_97	11166338	8-N3-[32]cAMP binding to the 52 kDa protein band (indicated by arrow) in microtubule fraction from total cortex of rats treated with vehicle (1, 2) or reboxetine (3, 4).	bind
37087	1	8727	7	NULL	NULL	0	NULL	8-N3-[32]cAMP	NULL		bind	NULL				52 kDa protein 	NULL				NULL	vehicle treated microtubule fraction from total cortex of rats	0	NULL	NULL	NULL	gw60_neuropharmacology_40_3_448_s_97	11166338	8-N3-[32]cAMP binding to the 52 kDa protein band (indicated by arrow) in microtubule fraction from total cortex of rats treated with vehicle (1, 2) or reboxetine (3, 4).	bind
37088	2	8727	7	NULL	NULL	0	NULL	8-N3-[32]cAMP	NULL		bind	NULL				52 kDa protein 	NULL				NULL	reboxetine treated microtubule fraction from total cortex of rats	0	NULL	NULL	NULL	gw60_neuropharmacology_40_3_448_s_97	11166338	8-N3-[32]cAMP binding to the 52 kDa protein band (indicated by arrow) in microtubule fraction from total cortex of rats treated with vehicle (1, 2) or reboxetine (3, 4).	bind
46754	3	8727	7	10	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_40_3_448_s_97	11166338	8-N3-[32]cAMP binding to the 52 kDa protein band (indicated by arrow) in microtubule fraction from total cortex of rats treated with vehicle (1, 2) or reboxetine (3, 4).	bind
37957	1	8728	5	13	NULL	NULL	NULL	8-N3-[32]cAMP	Chemical		bind					52 kDa protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_40_3_448_s_104	11166338	8-N3-[32]cAMP binding to the 52 kDa protein band (indicated by arrows) in	bind
37089	1	8728	7	NULL	NULL	0	NULL	8-N3-[32]cAMP	NULL		bind	NULL				52 kDa protein 	NULL				NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_40_3_448_s_104	11166338	8-N3-[32]cAMP binding to the 52 kDa protein band (indicated by arrows) in	bind
37959	1	8729	5	13	NULL	NULL	NULL	FdUMP	Chemical		bind					enzyme	GP	wild-type			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_31_28901_s_260	12754260	80% of *FdUMP remains bound  to the  wild-type enzyme in the presence of excess CH2H4folate  and dUMP, whereas only 33% remains bound to the K282E/R283E mutant.	bind
37961	2	8729	5	13	NULL	NULL	NULL	statement 1	Process		in the presence of					CH2H4folate	Chemical	excess			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_31_28901_s_260	12754260	80% of *FdUMP remains bound  to the  wild-type enzyme in the presence of excess CH2H4folate  and dUMP, whereas only 33% remains bound to the K282E/R283E mutant.	bind
37962	3	8729	5	13	NULL	NULL	NULL	statement 1	Process		in the presence of					dUMP	Chemical	excess			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_31_28901_s_260	12754260	80% of *FdUMP remains bound  to the  wild-type enzyme in the presence of excess CH2H4folate  and dUMP, whereas only 33% remains bound to the K282E/R283E mutant.	bind
37963	4	8729	5	13	NULL	NULL	NULL	FdUMP	Chemical		bind					enzyme	GP	mutant	K282E/R283E		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_31_28901_s_260	12754260	80% of *FdUMP remains bound  to the  wild-type enzyme in the presence of excess CH2H4folate  and dUMP, whereas only 33% remains bound to the K282E/R283E mutant.	bind
37090	1	8729	7	NULL	NULL	0	NULL	FdUMP 	NULL		bind	NULL				enzyme	NULL	wild-type			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_31_28901_s_260	12754260	80% of *FdUMP remains bound  to the  wild-type enzyme in the presence of excess CH2H4folate  and dUMP, whereas only 33% remains bound to the K282E/R283E mutant.	bind
37091	2	8729	7	10	NULL	0	NULL	statement 1			in presence of					CH2H4folate		excess			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_31_28901_s_260	12754260	80% of *FdUMP remains bound  to the  wild-type enzyme in the presence of excess CH2H4folate  and dUMP, whereas only 33% remains bound to the K282E/R283E mutant.	bind
37092	3	8729	7	10	NULL	0	NULL	statement 1			in presence of					dUMP		excess			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_31_28901_s_260	12754260	80% of *FdUMP remains bound  to the  wild-type enzyme in the presence of excess CH2H4folate  and dUMP, whereas only 33% remains bound to the K282E/R283E mutant.	bind
37093	4	8729	7	NULL	NULL	0	NULL	FdUMP 	NULL		bind	NULL				enzyme	NULL	mutant	K282E/R283E		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_31_28901_s_260	12754260	80% of *FdUMP remains bound  to the  wild-type enzyme in the presence of excess CH2H4folate  and dUMP, whereas only 33% remains bound to the K282E/R283E mutant.	bind
37964	1	8730	5	13	NULL	NULL	NULL	80K-H protein	GP		bind		specifically			TRPV5	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_25_26351_s_99	15100231	80K-H protein bound specifically to TRPV5 in both conditions because no interaction was observed with GST alone ( Fig. 2 C).	bind
37094	1	8730	7	NULL	NULL	0	NULL	80K-H protein	NULL		bind	NULL	specifically			TRPV5	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_25_26351_s_99	15100231	80K-H protein bound specifically to TRPV5 in both conditions because no interaction was observed with GST alone ( Fig. 2 C).	bind
37857	1	8731	5	13	NULL	NULL	NULL	S1	GP		bind					ACE2 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_8_2536_s_136	14983044	80R scFv inhibiting the binding of S1 to ACE2 receptor.	bind
37858	2	8731	5	13	NULL	NULL	NULL	80R scFv	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_8_2536_s_136	14983044	80R scFv inhibiting the binding of S1 to ACE2 receptor.	bind
37095	1	8731	7	NULL	NULL	0	NULL	S1	NULL		bind	NULL				ACE2 receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_8_2536_s_136	14983044	80R scFv inhibiting the binding of S1 to ACE2 receptor.	bind
37096	2	8731	7	NULL	NULL	0	NULL	80R scFv	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_8_2536_s_136	14983044	80R scFv inhibiting the binding of S1 to ACE2 receptor.	bind
37859	1	8732	5	13	NULL	NULL	NULL	Rac1	GP		bind					p67 phox	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_162	16514078	86 This region is not required for Rac1 binding to p67 phox, implicating another protein, binding to this domain, in the activation of the oxidase.	bind
37097	1	8732	7	NULL	NULL	0	NULL	Rac1	NULL		bind	NULL				p67 phox	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_4_453_s_162	16514078	86 This region is not required for Rac1 binding to p67 phox, implicating another protein, binding to this domain, in the activation of the oxidase.	bind
37860	1	8733	5	13	NULL	NULL	NULL	synectin	GP		bind					syndecan-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_5_488_s_172	15774861	87 However, synectin also binds syndecan-2.	bind
37098	1	8733	7	NULL	NULL	0	NULL	synectin	NULL		bind	NULL				 syndecan-2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_5_488_s_172	15774861	87 However, synectin also binds syndecan-2.	bind
37861	1	8734	5	13	NULL	NULL	NULL	ezrin	GP		links					syndecan-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_824_s_141	14976004	87,88  Moreover, it appears that ezrin links the proteoglycan syndecan-2, which might possibly bind SDF-1, to the actin cytoskeleton.	bind
37862	2	8734	5	13	NULL	NULL	NULL	syndecan-2	GP		is a type of					proteoglycan	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_824_s_141	14976004	87,88  Moreover, it appears that ezrin links the proteoglycan syndecan-2, which might possibly bind SDF-1, to the actin cytoskeleton.	bind
37863	3	8734	5	13	NULL	NULL	NULL	SDF-1	GP		bind					actin cytoskeleton	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_824_s_141	14976004	87,88  Moreover, it appears that ezrin links the proteoglycan syndecan-2, which might possibly bind SDF-1, to the actin cytoskeleton.	bind
37864	4	8734	5	13	NULL	NULL	NULL	syndecan-2	GP		is required for		possibly			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_824_s_141	14976004	87,88  Moreover, it appears that ezrin links the proteoglycan syndecan-2, which might possibly bind SDF-1, to the actin cytoskeleton.	bind
37099	1	8734	7	NULL	NULL	0	NULL	ezrin	NULL		links	NULL				syndecan-2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_824_s_141	14976004	87,88  Moreover, it appears that ezrin links the proteoglycan syndecan-2, which might possibly bind SDF-1, to the actin cytoskeleton.	bind
37100	2	8734	7	NULL	NULL	0	NULL	SDF-1	NULL		bind	NULL				actin cytoskeleton	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_824_s_141	14976004	87,88  Moreover, it appears that ezrin links the proteoglycan syndecan-2, which might possibly bind SDF-1, to the actin cytoskeleton.	bind
37101	3	8734	7	NULL	NULL	0	NULL	syndecan-2	NULL		is a type of	NULL				proteoglycan	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_824_s_141	14976004	87,88  Moreover, it appears that ezrin links the proteoglycan syndecan-2, which might possibly bind SDF-1, to the actin cytoskeleton.	bind
46756	4	8734	7	10	NULL	0	NULL	syndecan-2	NULL		is involved in	NULL	possibly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_824_s_141	14976004	87,88  Moreover, it appears that ezrin links the proteoglycan syndecan-2, which might possibly bind SDF-1, to the actin cytoskeleton.	bind
37865	1	8735	5	13	NULL	NULL	NULL	Mcl-1	GP		bind					Bak	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
37866	2	8735	5	13	NULL	NULL	NULL	p53	GP		disrupt					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
37867	3	8735	5	13	NULL	NULL	NULL	statement 2	Process		occurs during					apoptosis	Process	initiation of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
37868	4	8735	5	13	NULL	NULL	NULL	VDAC2	GP		bind					Bak	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
37869	5	8735	5	13	NULL	NULL	NULL	Bid	GP	activated;;truncated	bind					Bak	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
37870	6	8735	5	13	NULL	NULL	NULL	statement 5	Process		displaces					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
37871	7	8735	5	13	NULL	NULL	NULL	statement 6	Process		occurs during					apoptosis	Process	initiation of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
38756	8	8735	5	13	NULL	NULL	NULL	Bim	GP	activated;;truncated	bind					Bak	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
38757	9	8735	5	13	NULL	NULL	NULL	statement 8	Process		displaces					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
38758	10	8735	5	13	NULL	NULL	NULL	statement 9	Process		occurs during					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
38759	11	8735	5	13	NULL	NULL	NULL	Bad	GP	activated;;truncated	bind					Bak	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
38760	12	8735	5	13	NULL	NULL	NULL	statement 11	Process		displaces					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
38762	13	8735	5	13	NULL	NULL	NULL	statement 12	Process		occurs during					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
37102	4	8735	7	10	NULL	0	NULL	VDAC2			bind					Bak					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
37103	3	8735	7	10	NULL	0	NULL	statement 2			occurs upon					apoptosis		initiation of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
37104	5	8735	7	10	NULL	0	NULL	Bid		acitvated;;truncated	bind					Bak					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
37105	6	8735	7	10	NULL	0	NULL	statement 5			displaces					statement 4					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
37106	7	8735	7	10	NULL	0	NULL	statement 6			occurs during					apoptosis		initiation of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
37107	1	8735	7	10	NULL	0	NULL	Mcl-1			bind					Bak					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
37108	2	8735	7	10	NULL	0	NULL	p53			disrupts					statement 1					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
56479	8	8735	7	10	NULL	0	NULL	Bim		activated;;truncated	bind					Bak					NULL		0	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
56480	9	8735	7	10	NULL	0	NULL	statement 8			displaces					statement 4					NULL		0	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
56481	10	8735	7	10	NULL	0	NULL	statement 9			occur during					apoptosis		initiation of			NULL		0	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
56482	11	8735	7	10	NULL	0	NULL	Bad		activated;;truncated	bind					Bak					NULL		0	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
56483	12	8735	7	10	NULL	0	NULL	statement 11			displaces					statement 4					NULL		0	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
56484	13	8735	7	10	NULL	0	NULL	statement 12			occur during					apoptosis		initiation of			NULL		0	NULL	NULL	NULL	gw70_circulationres_95_10_957_s_118	15539639	88 On initiation of apoptosis, VDAC2 is displaced from Bak by activated (truncated) Bid, Bim, and Bad, whereas Mcl-1 binding to Bak is disrupted by p53.	bind
37872	1	8736	5	13	NULL	NULL	NULL	amphotericin B	Chemical		is a type of					antibiotic	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_11_1182_s_209	12805236	88,89  Treatment with amphotericin B, an antibiotic that binds cholesterol, causes the disruption of t-tubules in C2C12 myotubes.	bind
37873	2	8736	5	13	NULL	NULL	NULL	amphotericin B	Chemical		bind					cholesterol	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_11_1182_s_209	12805236	88,89  Treatment with amphotericin B, an antibiotic that binds cholesterol, causes the disruption of t-tubules in C2C12 myotubes.	bind
37874	3	8736	5	13	NULL	NULL	NULL	statement 2	Process		disrupt					t-tubules	OrganismPart				NULL	C2C12 myotubes	NULL	NULL	NULL	NULL	gw70_circulationres_92_11_1182_s_209	12805236	88,89  Treatment with amphotericin B, an antibiotic that binds cholesterol, causes the disruption of t-tubules in C2C12 myotubes.	bind
37109	1	8736	7	NULL	NULL	0	NULL	amphotericin B	NULL		binds	NULL				cholesterol	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_92_11_1182_s_209	12805236	88,89  Treatment with amphotericin B, an antibiotic that binds cholesterol, causes the disruption of t-tubules in C2C12 myotubes.	bind
37110	2	8736	7	NULL	NULL	0	NULL	amphotericin B	NULL		is a type of	NULL				antibiotic	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_92_11_1182_s_209	12805236	88,89  Treatment with amphotericin B, an antibiotic that binds cholesterol, causes the disruption of t-tubules in C2C12 myotubes.	bind
37111	3	8736	7	10	NULL	0	NULL	statement 1	NULL		disrupts	NULL				t-tubules	NULL				NULL	C2C12 myotubes	NULL	NULL	NULL	NULL	gw70_circulationres_92_11_1182_s_209	12805236	88,89  Treatment with amphotericin B, an antibiotic that binds cholesterol, causes the disruption of t-tubules in C2C12 myotubes.	bind
37892	1	8737	5	13	NULL	NULL	NULL	EGF	GP		stimulate					MAPK	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_3_1671_s_120	11805301	8Br-cAMP did not inhibit EGF stimulation of MAPK (Fig.  2 A).	bind
37893	2	8737	5	13	NULL	NULL	NULL	8Br-cAMP	Chemical		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_3_1671_s_120	11805301	8Br-cAMP did not inhibit EGF stimulation of MAPK (Fig.  2 A).	bind
37138	1	8737	7	NULL	NULL	0	NULL	EGF	NULL		stimulates	NULL				MAPK	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_3_1671_s_120	11805301	8Br-cAMP did not inhibit EGF stimulation of MAPK (Fig.  2 A).	bind
37139	2	8737	7	NULL	NULL	0	NULL	8Br-cAMP	NULL		does not inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_3_1671_s_120	11805301	8Br-cAMP did not inhibit EGF stimulation of MAPK (Fig.  2 A).	bind
37894	1	8738	5	13	NULL	NULL	NULL	Pax6	GP		controls					radial glia	OrganismPart	differentiation of			NULL	cerebral cortex	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_19_4070_s_251	11574690	9       Gotz,M., Stoykova,A. and Gruss,P. (1998) Pax6 controls radial glia differentiation in the cerebral cortex.	bind
37140	1	8738	7	10	NULL	0	NULL	Pax6 	NULL		controls	NULL				 radial glia 	NULL	differentiation 			NULL	cerebral cortex	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_19_4070_s_251	11574690	9       Gotz,M., Stoykova,A. and Gruss,P. (1998) Pax6 controls radial glia differentiation in the cerebral cortex.	bind
37895	1	8740	5	13	NULL	NULL	NULL	VP16	GP		bind			acidic transcriptional activation domains		replication protein A	GP	cellular			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3270_s_216	11470885	9       Li,R. and Botchan,M.R. (1993) The acidic transcriptional activation domains of VP16 and p53 bind the cellular replication protein A and stimulate  in vitro BPV-1 DNA replication.	bind
37896	2	8740	5	13	NULL	NULL	NULL	statement 1	Process		stimulate					BPV-1 DNA	NucleicAcid	replication of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3270_s_216	11470885	9       Li,R. and Botchan,M.R. (1993) The acidic transcriptional activation domains of VP16 and p53 bind the cellular replication protein A and stimulate  in vitro BPV-1 DNA replication.	bind
37897	3	8740	5	13	NULL	NULL	NULL	p53	GP		bind			acidic transcriptional activation domains		replication protein A	GP	cellular			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3270_s_216	11470885	9       Li,R. and Botchan,M.R. (1993) The acidic transcriptional activation domains of VP16 and p53 bind the cellular replication protein A and stimulate  in vitro BPV-1 DNA replication.	bind
37898	4	8740	5	13	NULL	NULL	NULL	statement 3	Process		stimulate					BPV-1 DNA	NucleicAcid	replication of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3270_s_216	11470885	9       Li,R. and Botchan,M.R. (1993) The acidic transcriptional activation domains of VP16 and p53 bind the cellular replication protein A and stimulate  in vitro BPV-1 DNA replication.	bind
37141	1	8740	7	NULL	NULL	0	NULL	VP16	NULL		bind	NULL		acidic transcriptional activation domains of		cellular replication protein A	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3270_s_216	11470885	9       Li,R. and Botchan,M.R. (1993) The acidic transcriptional activation domains of VP16 and p53 bind the cellular replication protein A and stimulate  in vitro BPV-1 DNA replication.	bind
37142	2	8740	7	10	NULL	0	NULL	p53	NULL		bind	NULL		acidic transcriptional activation domain		cellular replication protein A	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3270_s_216	11470885	9       Li,R. and Botchan,M.R. (1993) The acidic transcriptional activation domains of VP16 and p53 bind the cellular replication protein A and stimulate  in vitro BPV-1 DNA replication.	bind
37143	3	8740	7	NULL	NULL	0	NULL	statement 1	NULL		stimulate	NULL				BPV-1 DNA	NULL	replication of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3270_s_216	11470885	9       Li,R. and Botchan,M.R. (1993) The acidic transcriptional activation domains of VP16 and p53 bind the cellular replication protein A and stimulate  in vitro BPV-1 DNA replication.	bind
37144	4	8740	7	NULL	NULL	0	NULL	statement 2	NULL		stimulate	NULL				BPV-1 DNA	NULL	replication of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3270_s_216	11470885	9       Li,R. and Botchan,M.R. (1993) The acidic transcriptional activation domains of VP16 and p53 bind the cellular replication protein A and stimulate  in vitro BPV-1 DNA replication.	bind
37899	1	8741	5	13	NULL	NULL	NULL	CRP	GP		bind					LDL	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2094_s_181	10978254	9  10 11  (2) CRP displays in vitro binding to LDL and, thus, may be entrapped in the intima by deposited lipids.	bind
37900	2	8741	5	13	NULL	NULL	NULL	lipids	Chemical	deposited	entrap					statement 1	Process				NULL	intima	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2094_s_181	10978254	9  10 11  (2) CRP displays in vitro binding to LDL and, thus, may be entrapped in the intima by deposited lipids.	bind
37145	1	8741	7	NULL	NULL	0	NULL	CRP 	NULL		bind	NULL				LDL	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2094_s_181	10978254	9  10 11  (2) CRP displays in vitro binding to LDL and, thus, may be entrapped in the intima by deposited lipids.	bind
37146	2	8741	7	NULL	NULL	0	NULL	CRP	NULL		is entrapped in	NULL				intima 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2094_s_181	10978254	9  10 11  (2) CRP displays in vitro binding to LDL and, thus, may be entrapped in the intima by deposited lipids.	bind
37147	3	8741	7	NULL	NULL	0	NULL	statement 2	NULL		occurs by	NULL				deposited lipids	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2094_s_181	10978254	9  10 11  (2) CRP displays in vitro binding to LDL and, thus, may be entrapped in the intima by deposited lipids.	bind
38734	1	8742	5	13	NULL	NULL	NULL	selectins	GP		bind		high affinity			SLex	Chemical	sialylated;;fucosylated			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_93_s_361	null	9  14  All 3 selectins demonstrate a high affinity for sialylated, fucosylated saccharide structures such as SLex, and although there are several leukocyte-bound structures that present SLex, it appears as though P-selectin must bind with PSGL-1 in order for leukocytes to efficiently roll along the endothelium under physiological flow conditions.	bind
38735	2	8742	5	13	NULL	NULL	NULL	SLex	Chemical		is a type of					saccharide	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_93_s_361	null	9  14  All 3 selectins demonstrate a high affinity for sialylated, fucosylated saccharide structures such as SLex, and although there are several leukocyte-bound structures that present SLex, it appears as though P-selectin must bind with PSGL-1 in order for leukocytes to efficiently roll along the endothelium under physiological flow conditions.	bind
38736	3	8742	5	13	NULL	NULL	NULL	leukocyte-bound structures	Chemical		present					SLex	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_93_s_361	null	9  14  All 3 selectins demonstrate a high affinity for sialylated, fucosylated saccharide structures such as SLex, and although there are several leukocyte-bound structures that present SLex, it appears as though P-selectin must bind with PSGL-1 in order for leukocytes to efficiently roll along the endothelium under physiological flow conditions.	bind
38737	4	8742	5	13	NULL	NULL	NULL	P-selectin	GP		bind		possibly			PSGL-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_93_s_361	null	9  14  All 3 selectins demonstrate a high affinity for sialylated, fucosylated saccharide structures such as SLex, and although there are several leukocyte-bound structures that present SLex, it appears as though P-selectin must bind with PSGL-1 in order for leukocytes to efficiently roll along the endothelium under physiological flow conditions.	bind
38738	5	8742	5	13	NULL	NULL	NULL	leukocytes	Cell		roll along		efficiently			endothelium	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_93_s_361	null	9  14  All 3 selectins demonstrate a high affinity for sialylated, fucosylated saccharide structures such as SLex, and although there are several leukocyte-bound structures that present SLex, it appears as though P-selectin must bind with PSGL-1 in order for leukocytes to efficiently roll along the endothelium under physiological flow conditions.	bind
38740	7	8742	5	13	NULL	NULL	NULL	statement 5	Process		requires					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_93_s_361	null	9  14  All 3 selectins demonstrate a high affinity for sialylated, fucosylated saccharide structures such as SLex, and although there are several leukocyte-bound structures that present SLex, it appears as though P-selectin must bind with PSGL-1 in order for leukocytes to efficiently roll along the endothelium under physiological flow conditions.	bind
56357	6	8742	5	13	NULL	NULL	NULL	statement 2	Process		occurs under					physiological flow conditions					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_93_s_361	null	9  14  All 3 selectins demonstrate a high affinity for sialylated, fucosylated saccharide structures such as SLex, and although there are several leukocyte-bound structures that present SLex, it appears as though P-selectin must bind with PSGL-1 in order for leukocytes to efficiently roll along the endothelium under physiological flow conditions.	bind
37148	1	8742	7	NULL	NULL	0	NULL	P-selectin 	NULL		bind	NULL				PSGL-1 	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_1_93_s_361	null	9  14  All 3 selectins demonstrate a high affinity for sialylated, fucosylated saccharide structures such as SLex, and although there are several leukocyte-bound structures that present SLex, it appears as though P-selectin must bind with PSGL-1 in order for leukocytes to efficiently roll along the endothelium under physiological flow conditions.	bind
37149	2	8742	7	10	NULL	0	NULL	leukocytes			roll along		efficiently			endothelium					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_93_s_361	null	9  14  All 3 selectins demonstrate a high affinity for sialylated, fucosylated saccharide structures such as SLex, and although there are several leukocyte-bound structures that present SLex, it appears as though P-selectin must bind with PSGL-1 in order for leukocytes to efficiently roll along the endothelium under physiological flow conditions.	bind
37150	4	8742	7	NULL	NULL	0	NULL	 selectins 	NULL		demonstrate	NULL	high affinity			SLex	NULL	sialylated			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_1_93_s_361	null	9  14  All 3 selectins demonstrate a high affinity for sialylated, fucosylated saccharide structures such as SLex, and although there are several leukocyte-bound structures that present SLex, it appears as though P-selectin must bind with PSGL-1 in order for leukocytes to efficiently roll along the endothelium under physiological flow conditions.	bind
37151	3	8742	7	NULL	NULL	0	NULL	statement 1	NULL		is required for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_1_93_s_361	null	9  14  All 3 selectins demonstrate a high affinity for sialylated, fucosylated saccharide structures such as SLex, and although there are several leukocyte-bound structures that present SLex, it appears as though P-selectin must bind with PSGL-1 in order for leukocytes to efficiently roll along the endothelium under physiological flow conditions.	bind
37152	5	8742	7	NULL	NULL	0	NULL	selectins	NULL		demonstrate	NULL	high affinity			SLex	NULL	fucosylated			NULL		0	NULL	NULL	NULL	gw60_circulationres_84_1_93_s_361	null	9  14  All 3 selectins demonstrate a high affinity for sialylated, fucosylated saccharide structures such as SLex, and although there are several leukocyte-bound structures that present SLex, it appears as though P-selectin must bind with PSGL-1 in order for leukocytes to efficiently roll along the endothelium under physiological flow conditions.	bind
56358	6	8742	7	10	NULL	0	NULL	statement 2			occurs under					physiological flow conditions					NULL		0	NULL	NULL	NULL	gw60_circulationres_84_1_93_s_361	null	9  14  All 3 selectins demonstrate a high affinity for sialylated, fucosylated saccharide structures such as SLex, and although there are several leukocyte-bound structures that present SLex, it appears as though P-selectin must bind with PSGL-1 in order for leukocytes to efficiently roll along the endothelium under physiological flow conditions.	bind
37901	1	8743	5	13	NULL	NULL	NULL	AP-1	GP		bind					MMP-12	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_9_998_s_97	10807873	9  17 18  Both PMA and insulin increased the binding of AP-1 to the MMP-12 promoter, with higher affinity for the A allele (mean plus-or-minus SE, 57 plus-or-minus 37% [n=4] and 47 plus-or-minus 13% [n=3 higher binding affinity for the A probe than the G probe when stimulated with PMA or insulin, respectively) (Figures 3A   and 3B  ).	bind
37902	2	8743	5	13	NULL	NULL	NULL	PMA	Chemical		increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_9_998_s_97	10807873	9  17 18  Both PMA and insulin increased the binding of AP-1 to the MMP-12 promoter, with higher affinity for the A allele (mean plus-or-minus SE, 57 plus-or-minus 37% [n=4] and 47 plus-or-minus 13% [n=3 higher binding affinity for the A probe than the G probe when stimulated with PMA or insulin, respectively) (Figures 3A   and 3B  ).	bind
37903	3	8743	5	13	NULL	NULL	NULL	insulin	GP		increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_9_998_s_97	10807873	9  17 18  Both PMA and insulin increased the binding of AP-1 to the MMP-12 promoter, with higher affinity for the A allele (mean plus-or-minus SE, 57 plus-or-minus 37% [n=4] and 47 plus-or-minus 13% [n=3 higher binding affinity for the A probe than the G probe when stimulated with PMA or insulin, respectively) (Figures 3A   and 3B  ).	bind
37153	1	8743	7	NULL	NULL	0	NULL	AP-1	NULL		bind	NULL				MMP-12	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_circulationres_86_9_998_s_97	10807873	9  17 18  Both PMA and insulin increased the binding of AP-1 to the MMP-12 promoter, with higher affinity for the A allele (mean plus-or-minus SE, 57 plus-or-minus 37% [n=4] and 47 plus-or-minus 13% [n=3 higher binding affinity for the A probe than the G probe when stimulated with PMA or insulin, respectively) (Figures 3A   and 3B  ).	bind
37154	2	8743	7	NULL	NULL	0	NULL	PMA	NULL		increase	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_86_9_998_s_97	10807873	9  17 18  Both PMA and insulin increased the binding of AP-1 to the MMP-12 promoter, with higher affinity for the A allele (mean plus-or-minus SE, 57 plus-or-minus 37% [n=4] and 47 plus-or-minus 13% [n=3 higher binding affinity for the A probe than the G probe when stimulated with PMA or insulin, respectively) (Figures 3A   and 3B  ).	bind
37155	3	8743	7	NULL	NULL	0	NULL	insulin	NULL		increase	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_86_9_998_s_97	10807873	9  17 18  Both PMA and insulin increased the binding of AP-1 to the MMP-12 promoter, with higher affinity for the A allele (mean plus-or-minus SE, 57 plus-or-minus 37% [n=4] and 47 plus-or-minus 13% [n=3 higher binding affinity for the A probe than the G probe when stimulated with PMA or insulin, respectively) (Figures 3A   and 3B  ).	bind
37904	1	8744	5	13	NULL	NULL	NULL	Rab3A	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_3_889_s_170	12937130	9  Because the binding is inhibited by the GTP-bound form of Rab3A, the authors have hypothesized that, through switching the GTPase on and off and alternatively binding of rabphilin to Rab3A and alpha-actinin, these molecules behave like a timer that prepares vesicles for docking/fusion events by cytoskeletal reorganization.	bind
37905	2	8744	5	13	NULL	NULL	NULL	GTPase	GP	switching on	occurs simultaneously with					GTPase	GP	switching off			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_3_889_s_170	12937130	9  Because the binding is inhibited by the GTP-bound form of Rab3A, the authors have hypothesized that, through switching the GTPase on and off and alternatively binding of rabphilin to Rab3A and alpha-actinin, these molecules behave like a timer that prepares vesicles for docking/fusion events by cytoskeletal reorganization.	bind
37906	3	8744	5	13	NULL	NULL	NULL	rabphilin	GP		bind					Rab3A	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_3_889_s_170	12937130	9  Because the binding is inhibited by the GTP-bound form of Rab3A, the authors have hypothesized that, through switching the GTPase on and off and alternatively binding of rabphilin to Rab3A and alpha-actinin, these molecules behave like a timer that prepares vesicles for docking/fusion events by cytoskeletal reorganization.	bind
37907	4	8744	5	13	NULL	NULL	NULL	rabphilin	GP		bind					alpha-actinin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_3_889_s_170	12937130	9  Because the binding is inhibited by the GTP-bound form of Rab3A, the authors have hypothesized that, through switching the GTPase on and off and alternatively binding of rabphilin to Rab3A and alpha-actinin, these molecules behave like a timer that prepares vesicles for docking/fusion events by cytoskeletal reorganization.	bind
37156	1	8744	7	NULL	NULL	0	NULL	 rabphilin	NULL		bind	NULL				Rab3A	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_163_3_889_s_170	12937130	9  Because the binding is inhibited by the GTP-bound form of Rab3A, the authors have hypothesized that, through switching the GTPase on and off and alternatively binding of rabphilin to Rab3A and alpha-actinin, these molecules behave like a timer that prepares vesicles for docking/fusion events by cytoskeletal reorganization.	bind
37157	2	8744	7	NULL	NULL	0	NULL	rabphilin	NULL		bind	NULL				alpha-actinin	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_163_3_889_s_170	12937130	9  Because the binding is inhibited by the GTP-bound form of Rab3A, the authors have hypothesized that, through switching the GTPase on and off and alternatively binding of rabphilin to Rab3A and alpha-actinin, these molecules behave like a timer that prepares vesicles for docking/fusion events by cytoskeletal reorganization.	bind
37160	4	8744	7	10	NULL	0	NULL	GTPase	NULL	switching on	occurs simultaneous with	NULL				GTPase	NULL	switching off			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_163_3_889_s_170	12937130	9  Because the binding is inhibited by the GTP-bound form of Rab3A, the authors have hypothesized that, through switching the GTPase on and off and alternatively binding of rabphilin to Rab3A and alpha-actinin, these molecules behave like a timer that prepares vesicles for docking/fusion events by cytoskeletal reorganization.	bind
46813	3	8744	7	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				Rab3A	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_163_3_889_s_170	12937130	9  Because the binding is inhibited by the GTP-bound form of Rab3A, the authors have hypothesized that, through switching the GTPase on and off and alternatively binding of rabphilin to Rab3A and alpha-actinin, these molecules behave like a timer that prepares vesicles for docking/fusion events by cytoskeletal reorganization.	bind
37923	1	8745	5	13	NULL	NULL	NULL	Fibronectin	GP		is a type of					ECM protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1162_s_175	10323765	9  Fibronectin is another ECM protein that binds Lp(a).	bind
37924	2	8745	5	13	NULL	NULL	NULL	Fibronectin	GP		bind					Lp(a)	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1162_s_175	10323765	9  Fibronectin is another ECM protein that binds Lp(a).	bind
37161	1	8745	7	NULL	NULL	0	NULL	Fibronectin	NULL		binds	NULL				Lp(a)	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1162_s_175	10323765	9  Fibronectin is another ECM protein that binds Lp(a).	bind
37162	2	8745	7	NULL	NULL	0	NULL	fibronectin	NULL		is a type of	NULL				ECM protein	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_5_1162_s_175	10323765	9  Fibronectin is another ECM protein that binds Lp(a).	bind
37927	1	8746	5	10	NULL	0	NULL		NULL		associate with	NULL			KRE		NULL			KRE	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
37928	2	8746	5	13	NULL	NULL	NULL	KBF	GP		interfere with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
37929	3	8746	5	13	NULL	NULL	NULL	statement 2	Process		abolishes		may			silencer effect	Process				NULL	GH3 cells	NULL	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
37930	4	8746	5	13	NULL	NULL	NULL	statement 2	Process		abolishes		may			silencer effect	Process				NULL	heart	NULL	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
37931	5	8746	5	13	NULL	NULL	NULL	KBF	GP		interfere with					HMG-1	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
37932	6	8746	5	13	NULL	NULL	NULL	KBF	GP		interfere with					HMG-2	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
37933	7	8746	5	13	NULL	NULL	NULL	statement 5	Process		abolishes		may			silencer effect	Process				NULL	GH3 cells	NULL	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
37934	8	8746	5	13	NULL	NULL	NULL	statement 5	Process		abolishes		may			silencer effect	Process				NULL	heart	NULL	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
37935	9	8746	5	13	NULL	NULL	NULL	statement 6	Process		abolishes		may			silencer effect	Process				NULL	GH3 cells	NULL	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
37936	10	8746	5	13	NULL	NULL	NULL	statement 6	Process		abolishes		may			silencer effect	Process				NULL	heart	NULL	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
37163	1	8746	7	10	NULL	0	NULL	KRE			associates with					KRE					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
37164	2	8746	7	10	NULL	0	NULL	KBF			interfers with					HMG-1		binding of 			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
37165	3	8746	7	10	NULL	0	NULL	KBF			interfers with					HMG-2		binding of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
37166	4	8746	7	10	NULL	0	NULL	statement 2			abolish		may			silencer effect					NULL	Heart	NULL	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
37167	5	8746	7	NULL	NULL	0	NULL	statement 2	NULL		abolish	NULL	may			silencer effect	NULL				NULL	GH3 cells	0	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
37168	6	8746	7	NULL	NULL	0	NULL	statement 3	NULL		abolish	NULL	may			silencer effect	NULL				NULL	GH3 cells	0	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
56359	7	8746	7	10	NULL	0	NULL	KBF			interfers with					statement 1					NULL		0	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
56360	8	8746	7	10	NULL	0	NULL	statement 3			abolish		may			silencer effect					NULL	Heart	0	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
56361	9	8746	7	10	NULL	0	NULL	statement 7			abolish		may			silencer effect					NULL	Heart	0	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
56362	8	8746	7	10	NULL	0	NULL	statement 7			abolish		may			silencer effect					NULL	GH3 cells	0	NULL	NULL	NULL	gw60_circulationres_84_8_937_s_202	10222341	9  KBF, by interfering with the self-association of KRE and/or the binding of HMG-1 and HMG-2, may abolish the silencer effect in GH3 cells (or heart).	bind
38000	1	8747	5	13	NULL	NULL	NULL	IgE antibodies	GP		bind					mast cells	Cell				NULL	lamina propria	NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_681_s_28	11159205	9  Once in the lamina propria, antigen cross-links IgE antibodies bound to mast cells releasing mediators that act on epithelial receptors to induce ion secretion and enhance permeability of the paracellular pathway (both of which contribute to diarrhea).	bind
38001	2	8747	5	13	NULL	NULL	NULL	antigen	Chemical		cross-links					statement 1	Process				NULL	lamina propria	NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_681_s_28	11159205	9  Once in the lamina propria, antigen cross-links IgE antibodies bound to mast cells releasing mediators that act on epithelial receptors to induce ion secretion and enhance permeability of the paracellular pathway (both of which contribute to diarrhea).	bind
38004	3	8747	5	13	NULL	NULL	NULL	statement 2	Process		release					mediators	GP				NULL	lamina propria	NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_681_s_28	11159205	9  Once in the lamina propria, antigen cross-links IgE antibodies bound to mast cells releasing mediators that act on epithelial receptors to induce ion secretion and enhance permeability of the paracellular pathway (both of which contribute to diarrhea).	bind
38005	4	8747	5	13	NULL	NULL	NULL	mediators	GP		act on					epithelial receptors	GP				NULL	lamina propria	NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_681_s_28	11159205	9  Once in the lamina propria, antigen cross-links IgE antibodies bound to mast cells releasing mediators that act on epithelial receptors to induce ion secretion and enhance permeability of the paracellular pathway (both of which contribute to diarrhea).	bind
38007	5	8747	5	13	NULL	NULL	NULL	statement 4	Process		induce					ion	Chemical	secretion of			NULL	lamina propria	NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_681_s_28	11159205	9  Once in the lamina propria, antigen cross-links IgE antibodies bound to mast cells releasing mediators that act on epithelial receptors to induce ion secretion and enhance permeability of the paracellular pathway (both of which contribute to diarrhea).	bind
38008	6	8747	5	13	NULL	NULL	NULL	statement 4	Process		enhance					paracellular pathway	Process	permeability of			NULL	lamina propria	NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_681_s_28	11159205	9  Once in the lamina propria, antigen cross-links IgE antibodies bound to mast cells releasing mediators that act on epithelial receptors to induce ion secretion and enhance permeability of the paracellular pathway (both of which contribute to diarrhea).	bind
38009	9	8747	5	13	NULL	NULL	NULL	statement 5	Process		contribute to					diarrhea	MedicalFinding				NULL	lamina propria	NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_681_s_28	11159205	9  Once in the lamina propria, antigen cross-links IgE antibodies bound to mast cells releasing mediators that act on epithelial receptors to induce ion secretion and enhance permeability of the paracellular pathway (both of which contribute to diarrhea).	bind
38010	10	8747	5	13	NULL	NULL	NULL	statement 6	Process		contribute to					diarrhea	MedicalFinding				NULL	lamina propria	NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_681_s_28	11159205	9  Once in the lamina propria, antigen cross-links IgE antibodies bound to mast cells releasing mediators that act on epithelial receptors to induce ion secretion and enhance permeability of the paracellular pathway (both of which contribute to diarrhea).	bind
37169	1	8747	7	NULL	NULL	0	NULL	IgE antibodies	NULL		bind	NULL				mast cells	NULL				NULL	lamina propria	0	NULL	NULL	NULL	gw60_amjpathol_158_2_681_s_28	11159205	9  Once in the lamina propria, antigen cross-links IgE antibodies bound to mast cells releasing mediators that act on epithelial receptors to induce ion secretion and enhance permeability of the paracellular pathway (both of which contribute to diarrhea).	bind
37170	2	8747	7	NULL	NULL	0	NULL	antigen	NULL		cross-links	NULL				statement 1	NULL				NULL	lamina propria	NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_681_s_28	11159205	9  Once in the lamina propria, antigen cross-links IgE antibodies bound to mast cells releasing mediators that act on epithelial receptors to induce ion secretion and enhance permeability of the paracellular pathway (both of which contribute to diarrhea).	bind
37171	3	8747	7	NULL	NULL	0	NULL	statement 1	NULL		release	NULL				mediators	NULL				NULL	lamina propria	NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_681_s_28	11159205	9  Once in the lamina propria, antigen cross-links IgE antibodies bound to mast cells releasing mediators that act on epithelial receptors to induce ion secretion and enhance permeability of the paracellular pathway (both of which contribute to diarrhea).	bind
37172	4	8747	7	NULL	NULL	0	NULL	mediators	NULL		act on	NULL				epithelial receptors	NULL				NULL	lamina propria	NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_681_s_28	11159205	9  Once in the lamina propria, antigen cross-links IgE antibodies bound to mast cells releasing mediators that act on epithelial receptors to induce ion secretion and enhance permeability of the paracellular pathway (both of which contribute to diarrhea).	bind
37173	5	8747	7	10	NULL	0	NULL	statement 4			induce					ion		secretion of 			NULL	lamina propria	NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_681_s_28	11159205	9  Once in the lamina propria, antigen cross-links IgE antibodies bound to mast cells releasing mediators that act on epithelial receptors to induce ion secretion and enhance permeability of the paracellular pathway (both of which contribute to diarrhea).	bind
37174	6	8747	7	10	NULL	0	NULL	statement 4			enhance					paracellular pathway		permeabilty of 			NULL	lamina propria	NULL	NULL	NULL	NULL	gw60_amjpathol_158_2_681_s_28	11159205	9  Once in the lamina propria, antigen cross-links IgE antibodies bound to mast cells releasing mediators that act on epithelial receptors to induce ion secretion and enhance permeability of the paracellular pathway (both of which contribute to diarrhea).	bind
37175	7	8747	7	NULL	NULL	0	NULL	statement 5	NULL		contribute to	NULL				diarrhea	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_2_681_s_28	11159205	9  Once in the lamina propria, antigen cross-links IgE antibodies bound to mast cells releasing mediators that act on epithelial receptors to induce ion secretion and enhance permeability of the paracellular pathway (both of which contribute to diarrhea).	bind
37176	8	8747	7	NULL	NULL	0	NULL	statement 6	NULL		contribute to	NULL				diarrhea	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_158_2_681_s_28	11159205	9  Once in the lamina propria, antigen cross-links IgE antibodies bound to mast cells releasing mediators that act on epithelial receptors to induce ion secretion and enhance permeability of the paracellular pathway (both of which contribute to diarrhea).	bind
38020	1	8748	5	13	NULL	NULL	NULL	Raf	GP	activation of	mediated by					H-Ras	GP				NULL	hamster kidney cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_11_2465_s_209	11073854	9  Recently, Roy et al 26  reported that in hamster kidney cells, dominant-negative caveolin-3 completely blocked Raf activation mediated by H-Ras, and the inhibitory effect was reversed by replenishing cell membranes with cholesterol.	bind
38021	2	8748	5	13	NULL	NULL	NULL	caveolin-3	GP	dominant-negative	block		completely			statement 1	Process				NULL	hamster kidney cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_11_2465_s_209	11073854	9  Recently, Roy et al 26  reported that in hamster kidney cells, dominant-negative caveolin-3 completely blocked Raf activation mediated by H-Ras, and the inhibitory effect was reversed by replenishing cell membranes with cholesterol.	bind
38023	3	8748	5	13	NULL	NULL	NULL	cell membranes	CellComponent		is replenished with					cholesterol	Chemical				NULL	hamster kidney cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_11_2465_s_209	11073854	9  Recently, Roy et al 26  reported that in hamster kidney cells, dominant-negative caveolin-3 completely blocked Raf activation mediated by H-Ras, and the inhibitory effect was reversed by replenishing cell membranes with cholesterol.	bind
38024	4	8748	5	13	NULL	NULL	NULL	statement 2	Process	inhibitory effect of	is reversed by					statement 3	Process				NULL	hamster kidney cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_11_2465_s_209	11073854	9  Recently, Roy et al 26  reported that in hamster kidney cells, dominant-negative caveolin-3 completely blocked Raf activation mediated by H-Ras, and the inhibitory effect was reversed by replenishing cell membranes with cholesterol.	bind
37177	1	8748	7	NULL	NULL	0	NULL	H-Ras	NULL		mediate	NULL				Raf	NULL	activation of			NULL	hamster kidney cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_11_2465_s_209	11073854	9  Recently, Roy et al 26  reported that in hamster kidney cells, dominant-negative caveolin-3 completely blocked Raf activation mediated by H-Ras, and the inhibitory effect was reversed by replenishing cell membranes with cholesterol.	bind
37178	2	8748	7	10	NULL	0	NULL	caveolin-3	NULL	dominant-negative 	blocks	NULL	completely			statement 1	NULL				NULL	hamster kidney cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_11_2465_s_209	11073854	9  Recently, Roy et al 26  reported that in hamster kidney cells, dominant-negative caveolin-3 completely blocked Raf activation mediated by H-Ras, and the inhibitory effect was reversed by replenishing cell membranes with cholesterol.	bind
37179	3	8748	7	NULL	NULL	0	NULL	cell membranes	NULL		replenished with	NULL				cholesterol	NULL				NULL	hamster kidney cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_11_2465_s_209	11073854	9  Recently, Roy et al 26  reported that in hamster kidney cells, dominant-negative caveolin-3 completely blocked Raf activation mediated by H-Ras, and the inhibitory effect was reversed by replenishing cell membranes with cholesterol.	bind
37180	4	8748	7	10	NULL	0	NULL	statement 2	NULL	inhibitory effect of 	reversed by	NULL				statement 3	NULL				NULL	hamster kidney cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_11_2465_s_209	11073854	9  Recently, Roy et al 26  reported that in hamster kidney cells, dominant-negative caveolin-3 completely blocked Raf activation mediated by H-Ras, and the inhibitory effect was reversed by replenishing cell membranes with cholesterol.	bind
38068	1	8749	5	13	NULL	NULL	NULL	CREB	GP		is					cAMP-responsive element - binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_7_805_s_23	10683356	9  The cyclin A promoter contains activating transcription factor (ATF) or cAMP-responsive element (CRE), which are bound by cAMP-responsive element - binding protein (CREB) and ATF-1 by heterodimer formation.	bind
38069	2	8749	5	13	NULL	NULL	NULL	CREB	GP		bind					ATF-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_7_805_s_23	10683356	9  The cyclin A promoter contains activating transcription factor (ATF) or cAMP-responsive element (CRE), which are bound by cAMP-responsive element - binding protein (CREB) and ATF-1 by heterodimer formation.	bind
38070	4	8749	5	13	NULL	NULL	NULL	statement 3	GP		bind					cyclin A	GP			ATF site in promoter	NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_7_805_s_23	10683356	9  The cyclin A promoter contains activating transcription factor (ATF) or cAMP-responsive element (CRE), which are bound by cAMP-responsive element - binding protein (CREB) and ATF-1 by heterodimer formation.	bind
38071	5	8749	5	13	NULL	NULL	NULL	statement 3	GP		bind					cyclin A	GP			CRE in promoter	NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_7_805_s_23	10683356	9  The cyclin A promoter contains activating transcription factor (ATF) or cAMP-responsive element (CRE), which are bound by cAMP-responsive element - binding protein (CREB) and ATF-1 by heterodimer formation.	bind
38072	6	8749	5	13	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_7_805_s_23	10683356	9  The cyclin A promoter contains activating transcription factor (ATF) or cAMP-responsive element (CRE), which are bound by cAMP-responsive element - binding protein (CREB) and ATF-1 by heterodimer formation.	bind
38073	7	8749	5	13	NULL	NULL	NULL	CRE	GP		is					cAMP-responsive element	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_7_805_s_23	10683356	9  The cyclin A promoter contains activating transcription factor (ATF) or cAMP-responsive element (CRE), which are bound by cAMP-responsive element - binding protein (CREB) and ATF-1 by heterodimer formation.	bind
38074	8	8749	5	13	NULL	NULL	NULL	ATF	GP		is					activating transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_7_805_s_23	10683356	9  The cyclin A promoter contains activating transcription factor (ATF) or cAMP-responsive element (CRE), which are bound by cAMP-responsive element - binding protein (CREB) and ATF-1 by heterodimer formation.	bind
38075	3	8749	5	13	NULL	NULL	NULL	statement 2	GP		forms					CREB/ATF-1 heterodimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_7_805_s_23	10683356	9  The cyclin A promoter contains activating transcription factor (ATF) or cAMP-responsive element (CRE), which are bound by cAMP-responsive element - binding protein (CREB) and ATF-1 by heterodimer formation.	bind
37181	1	8749	7	10	NULL	0	NULL	cyclin A 			contains					ATF					NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_7_805_s_23	10683356	9  The cyclin A promoter contains activating transcription factor (ATF) or cAMP-responsive element (CRE), which are bound by cAMP-responsive element - binding protein (CREB) and ATF-1 by heterodimer formation.	bind
37182	2	8749	7	10	NULL	0	NULL	cyclin A			contains					CRE					NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_7_805_s_23	10683356	9  The cyclin A promoter contains activating transcription factor (ATF) or cAMP-responsive element (CRE), which are bound by cAMP-responsive element - binding protein (CREB) and ATF-1 by heterodimer formation.	bind
37183	3	8749	7	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_7_805_s_23	10683356	9  The cyclin A promoter contains activating transcription factor (ATF) or cAMP-responsive element (CRE), which are bound by cAMP-responsive element - binding protein (CREB) and ATF-1 by heterodimer formation.	bind
37184	4	8749	7	NULL	NULL	0	NULL	CREB	NULL		heterodimerizes with	NULL				ATF1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_101_7_805_s_23	10683356	9  The cyclin A promoter contains activating transcription factor (ATF) or cAMP-responsive element (CRE), which are bound by cAMP-responsive element - binding protein (CREB) and ATF-1 by heterodimer formation.	bind
37185	5	8749	7	NULL	NULL	0	NULL	statement 4	NULL		bind	NULL				cyclin A	NULL			ATF	NULL		0	NULL	NULL	NULL	gw60_circulation_101_7_805_s_23	10683356	9  The cyclin A promoter contains activating transcription factor (ATF) or cAMP-responsive element (CRE), which are bound by cAMP-responsive element - binding protein (CREB) and ATF-1 by heterodimer formation.	bind
37186	6	8749	7	NULL	NULL	0	NULL	statement 4	NULL		bind	NULL				cyclin A	NULL			CRE	NULL		0	NULL	NULL	NULL	gw60_circulation_101_7_805_s_23	10683356	9  The cyclin A promoter contains activating transcription factor (ATF) or cAMP-responsive element (CRE), which are bound by cAMP-responsive element - binding protein (CREB) and ATF-1 by heterodimer formation.	bind
37187	7	8749	7	NULL	NULL	0	NULL	ATF	NULL		is	NULL				activating transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_101_7_805_s_23	10683356	9  The cyclin A promoter contains activating transcription factor (ATF) or cAMP-responsive element (CRE), which are bound by cAMP-responsive element - binding protein (CREB) and ATF-1 by heterodimer formation.	bind
37188	8	8749	7	NULL	NULL	0	NULL	CRE	NULL		is	NULL				cAMP-responsive element 	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_101_7_805_s_23	10683356	9  The cyclin A promoter contains activating transcription factor (ATF) or cAMP-responsive element (CRE), which are bound by cAMP-responsive element - binding protein (CREB) and ATF-1 by heterodimer formation.	bind
37189	9	8749	7	NULL	NULL	0	NULL	CREB	NULL		is	NULL				cAMP-responsive element - binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_101_7_805_s_23	10683356	9  The cyclin A promoter contains activating transcription factor (ATF) or cAMP-responsive element (CRE), which are bound by cAMP-responsive element - binding protein (CREB) and ATF-1 by heterodimer formation.	bind
38076	1	8750	5	13	NULL	NULL	NULL	VASP	GP		bind			tandem repeat of 3 GP5 motifs		profilin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_28	10978248	9  VASP binds profilin, zyxin, vinculin, and the bacterial coat protein ActA. 10 11 12  13  Binding of the G-actin binding protein profilin is likely to be mediated by the tandem repeat of 3 GP5 motifs within VASP. 11  14 15 16  The amino-terminal EVH-1 domain of VASP is responsible for binding ActA as well as the adhesion proteins zyxin and vinculin.	bind
38077	2	8750	5	13	NULL	NULL	NULL	VASP	GP		bind			amino-terminal EVH-1 domain		zyxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_28	10978248	9  VASP binds profilin, zyxin, vinculin, and the bacterial coat protein ActA. 10 11 12  13  Binding of the G-actin binding protein profilin is likely to be mediated by the tandem repeat of 3 GP5 motifs within VASP. 11  14 15 16  The amino-terminal EVH-1 domain of VASP is responsible for binding ActA as well as the adhesion proteins zyxin and vinculin.	bind
38078	3	8750	5	13	NULL	NULL	NULL	VASP	GP		bind			amino-terminal EVH-1 domain		vinculin	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_28	10978248	9  VASP binds profilin, zyxin, vinculin, and the bacterial coat protein ActA. 10 11 12  13  Binding of the G-actin binding protein profilin is likely to be mediated by the tandem repeat of 3 GP5 motifs within VASP. 11  14 15 16  The amino-terminal EVH-1 domain of VASP is responsible for binding ActA as well as the adhesion proteins zyxin and vinculin.	bind
38079	4	8750	5	13	NULL	NULL	NULL	VASP	GP		bind			amino-terminal EVH-1 domain		ActA	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_28	10978248	9  VASP binds profilin, zyxin, vinculin, and the bacterial coat protein ActA. 10 11 12  13  Binding of the G-actin binding protein profilin is likely to be mediated by the tandem repeat of 3 GP5 motifs within VASP. 11  14 15 16  The amino-terminal EVH-1 domain of VASP is responsible for binding ActA as well as the adhesion proteins zyxin and vinculin.	bind
38080	5	8750	5	13	NULL	NULL	NULL	ActA	GP		is a type of					bacterial coat protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_28	10978248	9  VASP binds profilin, zyxin, vinculin, and the bacterial coat protein ActA. 10 11 12  13  Binding of the G-actin binding protein profilin is likely to be mediated by the tandem repeat of 3 GP5 motifs within VASP. 11  14 15 16  The amino-terminal EVH-1 domain of VASP is responsible for binding ActA as well as the adhesion proteins zyxin and vinculin.	bind
38081	6	8750	5	13	NULL	NULL	NULL	profilin	GP		is a type of					G-actin binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_28	10978248	9  VASP binds profilin, zyxin, vinculin, and the bacterial coat protein ActA. 10 11 12  13  Binding of the G-actin binding protein profilin is likely to be mediated by the tandem repeat of 3 GP5 motifs within VASP. 11  14 15 16  The amino-terminal EVH-1 domain of VASP is responsible for binding ActA as well as the adhesion proteins zyxin and vinculin.	bind
38082	7	8750	5	13	NULL	NULL	NULL	zyxin	GP		is a type of					adhesion proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_28	10978248	9  VASP binds profilin, zyxin, vinculin, and the bacterial coat protein ActA. 10 11 12  13  Binding of the G-actin binding protein profilin is likely to be mediated by the tandem repeat of 3 GP5 motifs within VASP. 11  14 15 16  The amino-terminal EVH-1 domain of VASP is responsible for binding ActA as well as the adhesion proteins zyxin and vinculin.	bind
38083	8	8750	5	13	NULL	NULL	NULL	vinculin	GP		is a type of					adhesion proteins					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_28	10978248	9  VASP binds profilin, zyxin, vinculin, and the bacterial coat protein ActA. 10 11 12  13  Binding of the G-actin binding protein profilin is likely to be mediated by the tandem repeat of 3 GP5 motifs within VASP. 11  14 15 16  The amino-terminal EVH-1 domain of VASP is responsible for binding ActA as well as the adhesion proteins zyxin and vinculin.	bind
37190	1	8750	7	NULL	NULL	0	NULL	VASP	NULL		binds	NULL				profilin	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_28	10978248	9  VASP binds profilin, zyxin, vinculin, and the bacterial coat protein ActA. 10 11 12  13  Binding of the G-actin binding protein profilin is likely to be mediated by the tandem repeat of 3 GP5 motifs within VASP. 11  14 15 16  The amino-terminal EVH-1 domain of VASP is responsible for binding ActA as well as the adhesion proteins zyxin and vinculin.	bind
37191	2	8750	7	NULL	NULL	0	NULL	VASP	NULL		binds	NULL		amino-terminal EVH-1 domain		zyxin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_28	10978248	9  VASP binds profilin, zyxin, vinculin, and the bacterial coat protein ActA. 10 11 12  13  Binding of the G-actin binding protein profilin is likely to be mediated by the tandem repeat of 3 GP5 motifs within VASP. 11  14 15 16  The amino-terminal EVH-1 domain of VASP is responsible for binding ActA as well as the adhesion proteins zyxin and vinculin.	bind
37192	3	8750	7	NULL	NULL	0	NULL	VASP	NULL		binds	NULL		amino-terminal EVH-1 domain		vinculin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_28	10978248	9  VASP binds profilin, zyxin, vinculin, and the bacterial coat protein ActA. 10 11 12  13  Binding of the G-actin binding protein profilin is likely to be mediated by the tandem repeat of 3 GP5 motifs within VASP. 11  14 15 16  The amino-terminal EVH-1 domain of VASP is responsible for binding ActA as well as the adhesion proteins zyxin and vinculin.	bind
37193	4	8750	7	NULL	NULL	0	NULL	VASP	NULL		binds	NULL		amino-terminal EVH-1 domain		ActA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_28	10978248	9  VASP binds profilin, zyxin, vinculin, and the bacterial coat protein ActA. 10 11 12  13  Binding of the G-actin binding protein profilin is likely to be mediated by the tandem repeat of 3 GP5 motifs within VASP. 11  14 15 16  The amino-terminal EVH-1 domain of VASP is responsible for binding ActA as well as the adhesion proteins zyxin and vinculin.	bind
37194	5	8750	7	NULL	NULL	0	NULL	VASP	NULL		mediates	NULL		tandem repeat of 3 GP5 motifs		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_28	10978248	9  VASP binds profilin, zyxin, vinculin, and the bacterial coat protein ActA. 10 11 12  13  Binding of the G-actin binding protein profilin is likely to be mediated by the tandem repeat of 3 GP5 motifs within VASP. 11  14 15 16  The amino-terminal EVH-1 domain of VASP is responsible for binding ActA as well as the adhesion proteins zyxin and vinculin.	bind
37195	6	8750	7	NULL	NULL	0	NULL	ActA	NULL		is a type of	NULL				bacterial coat protein	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_28	10978248	9  VASP binds profilin, zyxin, vinculin, and the bacterial coat protein ActA. 10 11 12  13  Binding of the G-actin binding protein profilin is likely to be mediated by the tandem repeat of 3 GP5 motifs within VASP. 11  14 15 16  The amino-terminal EVH-1 domain of VASP is responsible for binding ActA as well as the adhesion proteins zyxin and vinculin.	bind
37196	7	8750	7	NULL	NULL	0	NULL	profilin	NULL		is a type of	NULL				G-actin binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_28	10978248	9  VASP binds profilin, zyxin, vinculin, and the bacterial coat protein ActA. 10 11 12  13  Binding of the G-actin binding protein profilin is likely to be mediated by the tandem repeat of 3 GP5 motifs within VASP. 11  14 15 16  The amino-terminal EVH-1 domain of VASP is responsible for binding ActA as well as the adhesion proteins zyxin and vinculin.	bind
37197	8	8750	7	NULL	NULL	0	NULL	zyxin	NULL		is a type of	NULL				adhesion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_28	10978248	9  VASP binds profilin, zyxin, vinculin, and the bacterial coat protein ActA. 10 11 12  13  Binding of the G-actin binding protein profilin is likely to be mediated by the tandem repeat of 3 GP5 motifs within VASP. 11  14 15 16  The amino-terminal EVH-1 domain of VASP is responsible for binding ActA as well as the adhesion proteins zyxin and vinculin.	bind
37198	9	8750	7	NULL	NULL	0	NULL	vinculin	NULL		is a type of	NULL				adhesion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_9_2051_s_28	10978248	9  VASP binds profilin, zyxin, vinculin, and the bacterial coat protein ActA. 10 11 12  13  Binding of the G-actin binding protein profilin is likely to be mediated by the tandem repeat of 3 GP5 motifs within VASP. 11  14 15 16  The amino-terminal EVH-1 domain of VASP is responsible for binding ActA as well as the adhesion proteins zyxin and vinculin.	bind
38084	1	8751	5	13	NULL	NULL	NULL	LDL	GP		bind					GAGs	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1902_s_15	11742862	9 -  11 Most important, Boren et al 12 have shown that despite hypercholesterolemia, the development of atherosclerotic lesions is delayed in mice expressing proteoglycan-binding-deficient LDL, suggesting that binding of LDL to GAGs has a causal role in the development of atherosclerosis.	bind
38085	2	8751	5	13	NULL	NULL	NULL	statement 1	Process		plays a role in					atherosclerosis	MedicalFinding	development of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1902_s_15	11742862	9 -  11 Most important, Boren et al 12 have shown that despite hypercholesterolemia, the development of atherosclerotic lesions is delayed in mice expressing proteoglycan-binding-deficient LDL, suggesting that binding of LDL to GAGs has a causal role in the development of atherosclerosis.	bind
37199	1	8751	7	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				GAGs	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1902_s_15	11742862	9 -  11 Most important, Boren et al 12 have shown that despite hypercholesterolemia, the development of atherosclerotic lesions is delayed in mice expressing proteoglycan-binding-deficient LDL, suggesting that binding of LDL to GAGs has a causal role in the development of atherosclerosis.	bind
37200	2	8751	7	10	NULL	0	NULL	statement 1	NULL		plays a role in	NULL				atherosclerosis	NULL	development of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_21_12_1902_s_15	11742862	9 -  11 Most important, Boren et al 12 have shown that despite hypercholesterolemia, the development of atherosclerotic lesions is delayed in mice expressing proteoglycan-binding-deficient LDL, suggesting that binding of LDL to GAGs has a causal role in the development of atherosclerosis.	bind
38089	1	8752	5	13	NULL	NULL	NULL	Gab1	GP	mutant	does not bind					SHP2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_26	12855672	9 - 12    The functional significance of Gab1-SHP2 interaction has been extensively studied using mutants of Gab1 unable to bind SHP2 in vitro and in vivo.	bind
38090	2	8752	5	13	NULL	NULL	NULL	Gab1	GP	mutant	does not bind					SHP2	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_26	12855672	9 - 12    The functional significance of Gab1-SHP2 interaction has been extensively studied using mutants of Gab1 unable to bind SHP2 in vitro and in vivo.	bind
37202	1	8752	7	10	NULL	0	NULL	Gab1		mutant	does not bind					SHP2					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_26	12855672	9 - 12    The functional significance of Gab1-SHP2 interaction has been extensively studied using mutants of Gab1 unable to bind SHP2 in vitro and in vivo.	bind
56363	2	8752	7	10	NULL	0	NULL	Gab1		mutant	does not bind					SHP2					NULL	in vivo	0	NULL	NULL	NULL	gw60_circulationres_93_3_221_s_26	12855672	9 - 12    The functional significance of Gab1-SHP2 interaction has been extensively studied using mutants of Gab1 unable to bind SHP2 in vitro and in vivo.	bind
38091	1	8753	5	13	NULL	NULL	NULL	vWF	GP		bind					GP Ib/IX	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3281_s_24	9396417	9 - 14 It is now believed that binding of vWF to GP Ib/IX initiates intracellular signals resulting in activation of another platelet receptor, GP IIb/IIa complex, to form platelet clumps.	bind
38092	2	8753	5	13	NULL	NULL	NULL	statement 1	Process		initiate					intracellular signals	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3281_s_24	9396417	9 - 14 It is now believed that binding of vWF to GP Ib/IX initiates intracellular signals resulting in activation of another platelet receptor, GP IIb/IIa complex, to form platelet clumps.	bind
38093	3	8753	5	13	NULL	NULL	NULL	statement 2	Process		activates					GP IIb/IIa complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3281_s_24	9396417	9 - 14 It is now believed that binding of vWF to GP Ib/IX initiates intracellular signals resulting in activation of another platelet receptor, GP IIb/IIa complex, to form platelet clumps.	bind
38094	4	8753	5	13	NULL	NULL	NULL	GP IIb/IIa complex	GP		is a type of					platelet receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3281_s_24	9396417	9 - 14 It is now believed that binding of vWF to GP Ib/IX initiates intracellular signals resulting in activation of another platelet receptor, GP IIb/IIa complex, to form platelet clumps.	bind
38095	5	8753	5	13	NULL	NULL	NULL	statement 3	Process		forms					platelet clumps	Cell				NULL		NULL	NULL	NULL	NULL	gw60_circulation_96_10_3281_s_24	9396417	9 - 14 It is now believed that binding of vWF to GP Ib/IX initiates intracellular signals resulting in activation of another platelet receptor, GP IIb/IIa complex, to form platelet clumps.	bind
37204	1	8753	7	NULL	NULL	0	NULL	vWF	NULL		bind	NULL				GP Ib/IX	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_96_10_3281_s_24	9396417	9 - 14 It is now believed that binding of vWF to GP Ib/IX initiates intracellular signals resulting in activation of another platelet receptor, GP IIb/IIa complex, to form platelet clumps.	bind
37205	2	8753	7	NULL	NULL	0	NULL	statement 1	NULL		initiates	NULL				intracellular signals	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_96_10_3281_s_24	9396417	9 - 14 It is now believed that binding of vWF to GP Ib/IX initiates intracellular signals resulting in activation of another platelet receptor, GP IIb/IIa complex, to form platelet clumps.	bind
37206	3	8753	7	NULL	NULL	0	NULL	statement 2	NULL		results in	NULL				GP IIb/IIa complex	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_circulation_96_10_3281_s_24	9396417	9 - 14 It is now believed that binding of vWF to GP Ib/IX initiates intracellular signals resulting in activation of another platelet receptor, GP IIb/IIa complex, to form platelet clumps.	bind
37207	4	8753	7	NULL	NULL	0	NULL	statement 3	NULL		form	NULL				platelet clumps	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_96_10_3281_s_24	9396417	9 - 14 It is now believed that binding of vWF to GP Ib/IX initiates intracellular signals resulting in activation of another platelet receptor, GP IIb/IIa complex, to form platelet clumps.	bind
37208	5	8753	7	NULL	NULL	0	NULL	GP IIb/IIa complex	NULL		is a type of	NULL				platelet receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_96_10_3281_s_24	9396417	9 - 14 It is now believed that binding of vWF to GP Ib/IX initiates intracellular signals resulting in activation of another platelet receptor, GP IIb/IIa complex, to form platelet clumps.	bind
38096	1	8754	5	13	NULL	NULL	NULL	VEGF-B	GP		bind					VEGFR-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2262_s_34	11056103	9 10  Other members of the VEGF family have also been characterized: VEGF-B 11  binds to VEGFR-1, and VEGF-D 12  binds to VEGFR-2 and VEGFR-3.	bind
38097	2	8754	5	13	NULL	NULL	NULL	VEGF-D	GP		bind					VEGFR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2262_s_34	11056103	9 10  Other members of the VEGF family have also been characterized: VEGF-B 11  binds to VEGFR-1, and VEGF-D 12  binds to VEGFR-2 and VEGFR-3.	bind
38098	3	8754	5	13	NULL	NULL	NULL	VEGF-D	GP		bind					VEGFR-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2262_s_34	11056103	9 10  Other members of the VEGF family have also been characterized: VEGF-B 11  binds to VEGFR-1, and VEGF-D 12  binds to VEGFR-2 and VEGFR-3.	bind
37209	1	8754	7	10	NULL	0	NULL	VEGF-B	NULL		binds to	NULL				VEGFR-1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2262_s_34	11056103	9 10  Other members of the VEGF family have also been characterized: VEGF-B 11  binds to VEGFR-1, and VEGF-D 12  binds to VEGFR-2 and VEGFR-3.	bind
37210	2	8754	7	10	NULL	0	NULL	 VEGF-D	NULL		binds to	NULL				VEGFR-2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2262_s_34	11056103	9 10  Other members of the VEGF family have also been characterized: VEGF-B 11  binds to VEGFR-1, and VEGF-D 12  binds to VEGFR-2 and VEGFR-3.	bind
37211	3	8754	7	10	NULL	0	NULL	 VEGF-D	NULL		binds to	NULL				VEGFR-3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2262_s_34	11056103	9 10  Other members of the VEGF family have also been characterized: VEGF-B 11  binds to VEGFR-1, and VEGF-D 12  binds to VEGFR-2 and VEGFR-3.	bind
38113	1	8755	5	13	NULL	NULL	NULL	p47 phox	GP		bind			second SH3 domain		p67 phox	GP		proline-rich region		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_12_1195_s_202	11110778	9 10  The second SH3 domain of p47 phox binds to the proline-rich region of p67 phox, and the N-terminal half of p67 phox contains a binding region for Rac.	bind
38114	2	8755	5	13	NULL	NULL	NULL	p67 phox	GP		contains			N-terminal half					binding region for Rac		NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_12_1195_s_202	11110778	9 10  The second SH3 domain of p47 phox binds to the proline-rich region of p67 phox, and the N-terminal half of p67 phox contains a binding region for Rac.	bind
37212	1	8755	7	NULL	NULL	0	NULL	p47 phox 	NULL		binds to	NULL		second SH3 domain		 p67 phox	NULL		proline-rich region		NULL		0	NULL	NULL	NULL	gw60_circulationres_87_12_1195_s_202	11110778	9 10  The second SH3 domain of p47 phox binds to the proline-rich region of p67 phox, and the N-terminal half of p67 phox contains a binding region for Rac.	bind
37213	2	8755	7	NULL	NULL	0	NULL	p67 phox	NULL		contains	NULL		 N-terminal half of		Rac	NULL		binding region 		NULL		0	NULL	NULL	NULL	gw60_circulationres_87_12_1195_s_202	11110778	9 10  The second SH3 domain of p47 phox binds to the proline-rich region of p67 phox, and the N-terminal half of p67 phox contains a binding region for Rac.	bind
38107	1	8756	5	13	NULL	NULL	NULL	VEGF-C	GP		bind					VEGFR-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2262_s_33	11056103	9 10  VEGF-C binds to VEGFR-2 and VEGFR-3 and has been shown to stimulate both angiogenesis and formation of lymphatic vessels.	bind
38108	2	8756	5	13	NULL	NULL	NULL	VEGF-C	GP		bind					VEGFR-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2262_s_33	11056103	9 10  VEGF-C binds to VEGFR-2 and VEGFR-3 and has been shown to stimulate both angiogenesis and formation of lymphatic vessels.	bind
38109	3	8756	5	13	NULL	NULL	NULL	statement 1	Process		stimulate					angiogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2262_s_33	11056103	9 10  VEGF-C binds to VEGFR-2 and VEGFR-3 and has been shown to stimulate both angiogenesis and formation of lymphatic vessels.	bind
38110	4	8756	5	13	NULL	NULL	NULL	statement 2	Process		stimulate					angiogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2262_s_33	11056103	9 10  VEGF-C binds to VEGFR-2 and VEGFR-3 and has been shown to stimulate both angiogenesis and formation of lymphatic vessels.	bind
38111	5	8756	5	13	NULL	NULL	NULL	statement 1	Process		stimulate					lymphatic vessels	OrganismPart	formation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2262_s_33	11056103	9 10  VEGF-C binds to VEGFR-2 and VEGFR-3 and has been shown to stimulate both angiogenesis and formation of lymphatic vessels.	bind
38112	6	8756	5	13	NULL	NULL	NULL	statement 2	Process		stimulate					lymphatic vessels	OrganismPart	formation of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_18_2262_s_33	11056103	9 10  VEGF-C binds to VEGFR-2 and VEGFR-3 and has been shown to stimulate both angiogenesis and formation of lymphatic vessels.	bind
37353	1	8756	7	NULL	NULL	0	NULL	VEGF-C	NULL		binds to	NULL				VEGFR-2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_18_2262_s_33	11056103	9 10  VEGF-C binds to VEGFR-2 and VEGFR-3 and has been shown to stimulate both angiogenesis and formation of lymphatic vessels.	bind
37354	2	8756	7	NULL	NULL	0	NULL	VEGF-C	NULL		binds to	NULL				VEGFR-3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_18_2262_s_33	11056103	9 10  VEGF-C binds to VEGFR-2 and VEGFR-3 and has been shown to stimulate both angiogenesis and formation of lymphatic vessels.	bind
37355	3	8756	7	NULL	NULL	0	NULL	statement 1	NULL		stimulate	NULL				angiogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_18_2262_s_33	11056103	9 10  VEGF-C binds to VEGFR-2 and VEGFR-3 and has been shown to stimulate both angiogenesis and formation of lymphatic vessels.	bind
37356	4	8756	7	NULL	NULL	0	NULL	statement 2	NULL		stimulate	NULL				angiogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_18_2262_s_33	11056103	9 10  VEGF-C binds to VEGFR-2 and VEGFR-3 and has been shown to stimulate both angiogenesis and formation of lymphatic vessels.	bind
37357	5	8756	7	NULL	NULL	0	NULL	statement 1	NULL		stimulate	NULL				lymphatic vessels	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_circulation_102_18_2262_s_33	11056103	9 10  VEGF-C binds to VEGFR-2 and VEGFR-3 and has been shown to stimulate both angiogenesis and formation of lymphatic vessels.	bind
37358	6	8756	7	NULL	NULL	0	NULL	statement 2	NULL		stimulate	NULL				lymphatic vessels	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_circulation_102_18_2262_s_33	11056103	9 10  VEGF-C binds to VEGFR-2 and VEGFR-3 and has been shown to stimulate both angiogenesis and formation of lymphatic vessels.	bind
38104	1	8757	5	13	NULL	NULL	NULL	SMCs	Cell		express					IAP	GP				NULL	cell surface	NULL	NULL	NULL	NULL	gw70_circulationres_93_10_925_s_62	14563713	9 Because we have also determined that SMCs express both IAP 12 and alphaVbeta3 2 on their cell surface, we wished to specifically determine whether TS-1 binding to IAP contributes to this enhancement effect.	bind
38105	2	8757	5	13	NULL	NULL	NULL	SMCs	Cell		express					alphaVbeta3	GP				NULL	cell surface	NULL	NULL	NULL	NULL	gw70_circulationres_93_10_925_s_62	14563713	9 Because we have also determined that SMCs express both IAP 12 and alphaVbeta3 2 on their cell surface, we wished to specifically determine whether TS-1 binding to IAP contributes to this enhancement effect.	bind
38106	3	8757	5	13	NULL	NULL	NULL	TS-1	GP		bind					IAP	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_93_10_925_s_62	14563713	9 Because we have also determined that SMCs express both IAP 12 and alphaVbeta3 2 on their cell surface, we wished to specifically determine whether TS-1 binding to IAP contributes to this enhancement effect.	bind
37359	1	8757	7	NULL	NULL	0	NULL	 TS-1 	NULL		bind	NULL				 IAP	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_93_10_925_s_62	14563713	9 Because we have also determined that SMCs express both IAP 12 and alphaVbeta3 2 on their cell surface, we wished to specifically determine whether TS-1 binding to IAP contributes to this enhancement effect.	bind
37360	2	8757	7	NULL	NULL	0	NULL	SMCs	NULL		express	NULL				IAP 12	NULL				NULL	cell surface	0	NULL	NULL	NULL	gw70_circulationres_93_10_925_s_62	14563713	9 Because we have also determined that SMCs express both IAP 12 and alphaVbeta3 2 on their cell surface, we wished to specifically determine whether TS-1 binding to IAP contributes to this enhancement effect.	bind
37361	3	8757	7	NULL	NULL	0	NULL	SMCs	NULL		express	NULL				alphaVbeta3 2	NULL				NULL	cell surface	0	NULL	NULL	NULL	gw70_circulationres_93_10_925_s_62	14563713	9 Because we have also determined that SMCs express both IAP 12 and alphaVbeta3 2 on their cell surface, we wished to specifically determine whether TS-1 binding to IAP contributes to this enhancement effect.	bind
38102	1	8758	5	13	NULL	NULL	NULL	Sp1	GP		bind					Flk-1/KDR	GP			CT-rich recognition sequence within -79 to -68 region of promoter	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_23	12067897	9 EMSA has demonstrated that expression of human Flk-1/KDR is mediated by Sp1 binding to a CT-rich recognition sequence within the -79 to -68 region of the Flk-1/KDR promoter.	bind
38103	2	8758	5	13	NULL	NULL	NULL	statement 1	Process		mediate					Flk-1/KDR	GP	expression of;;human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_23	12067897	9 EMSA has demonstrated that expression of human Flk-1/KDR is mediated by Sp1 binding to a CT-rich recognition sequence within the -79 to -68 region of the Flk-1/KDR promoter.	bind
37362	1	8758	7	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				Flk-1/KDR	NULL			CT-rich recognition sequence within the -79 to -68 region of  promoter	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_23	12067897	9 EMSA has demonstrated that expression of human Flk-1/KDR is mediated by Sp1 binding to a CT-rich recognition sequence within the -79 to -68 region of the Flk-1/KDR promoter.	bind
37363	2	8758	7	10	NULL	0	NULL	statement 1	NULL		mediates	NULL				Flk-1/KDR 	NULL	expression of;; human			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_907_s_23	12067897	9 EMSA has demonstrated that expression of human Flk-1/KDR is mediated by Sp1 binding to a CT-rich recognition sequence within the -79 to -68 region of the Flk-1/KDR promoter.	bind
38099	1	8760	5	13	NULL	NULL	NULL	microbicides	Chemical		interact with					virus	Organism				NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_52_6_890_s_67	14613946	9 However, most microbicides intended to interact with the virus bind to the viral envelope glycoproteins (Env).	bind
38100	2	8760	5	13	NULL	NULL	NULL	statement 1	Chemical		bind					Env	GP				NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_52_6_890_s_67	14613946	9 However, most microbicides intended to interact with the virus bind to the viral envelope glycoproteins (Env).	bind
38101	3	8760	5	13	NULL	NULL	NULL	Env	GP		is					viral envelope glycoproteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jantimicrobchemoth_52_6_890_s_67	14613946	9 However, most microbicides intended to interact with the virus bind to the viral envelope glycoproteins (Env).	bind
37365	1	8760	7	NULL	NULL	0	NULL	virus	NULL		binds to	NULL				viral Env	NULL				NULL		0	NULL	NULL	NULL	gw70_jantimicrobchemoth_52_6_890_s_67	14613946	9 However, most microbicides intended to interact with the virus bind to the viral envelope glycoproteins (Env).	bind
37366	2	8760	7	NULL	NULL	0	NULL	microbicides	NULL		interacts with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jantimicrobchemoth_52_6_890_s_67	14613946	9 However, most microbicides intended to interact with the virus bind to the viral envelope glycoproteins (Env).	bind
37367	3	8760	7	NULL	NULL	0	NULL	Env	NULL		is	NULL				envelope glycoproteins	NULL				NULL		0	NULL	NULL	NULL	gw70_jantimicrobchemoth_52_6_890_s_67	14613946	9 However, most microbicides intended to interact with the virus bind to the viral envelope glycoproteins (Env).	bind
38115	1	8761	5	13	NULL	NULL	NULL	MCP-1	GP		bind					CCR2 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_969_s_155	12067906	9 However, this drug inhibits neither the activity of MCP-1 nor the binding of MCP-1 to its receptor CCR2.	bind
37368	1	8761	7	NULL	NULL	0	NULL	 MCP-1	NULL		binds to	NULL				CCR2 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_969_s_155	12067906	9 However, this drug inhibits neither the activity of MCP-1 nor the binding of MCP-1 to its receptor CCR2.	bind
38117	1	8762	5	13	NULL	NULL	NULL	Sp1	GP		bind					PON1	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_2083_s_169	14500290	9 In recent studies, we have demonstrated that the polymorphism modulates binding of Sp1 to the  PON1 promoter.	bind
38118	2	8762	5	13	NULL	NULL	NULL	polymorphism	Process		modulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_2083_s_169	14500290	9 In recent studies, we have demonstrated that the polymorphism modulates binding of Sp1 to the  PON1 promoter.	bind
37369	1	8762	7	NULL	NULL	0	NULL	Sp1 	NULL		bind	NULL				PON1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_2083_s_169	14500290	9 In recent studies, we have demonstrated that the polymorphism modulates binding of Sp1 to the  PON1 promoter.	bind
37370	2	8762	7	NULL	NULL	0	NULL	polymorphism	NULL		modulates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_11_2083_s_169	14500290	9 In recent studies, we have demonstrated that the polymorphism modulates binding of Sp1 to the  PON1 promoter.	bind
38712	1	8763	5	13	NULL	NULL	NULL	c-fos	GP		respond to					Ca2+	Chemical				NULL	neurons	NULL	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
38713	2	8763	5	13	NULL	NULL	NULL	SRF	GP		is phosphorylated by					CaMK	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
38714	3	8763	5	13	NULL	NULL	NULL	statement 2	Process		regulates		partially			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
38715	4	8763	5	13	NULL	NULL	NULL	SRF	GP		bind					c-fos	GP			CArG	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
38716	5	8763	5	13	NULL	NULL	NULL	statement 4	Process	increased	regulates		partially			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
38717	6	8763	5	13	NULL	NULL	NULL	VGCC	GP	activation of	stimulate					signaling pathways	Process	multiple distinct			NULL	SMCs	NULL	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
38718	7	8763	5	13	NULL	NULL	NULL	statement 6	Process		regulates					SM alpha-actin gene	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
38719	8	8763	5	13	NULL	NULL	NULL	statement 6	Process		regulates					SMMHC gene	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
38720	9	8763	5	13	NULL	NULL	NULL	statement 6	Process		regulates					c-fos gene	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
38721	10	8763	5	13	NULL	NULL	NULL	c-fos gene	GP		mediate					cell growth	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
38722	11	8763	5	13	NULL	NULL	NULL	SM alpha-actin gene	GP		defines					"`contractile"' SMC	Cell				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
38723	12	8763	5	13	NULL	NULL	NULL	SMMHC gene	GP		defines					"`contractile"' SMC	Cell				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
37373	1	8763	7	NULL	NULL	0	NULL	 c-fos	NULL		respond to	NULL				Ca2+	NULL				NULL	neurons	0	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
37374	2	8763	7	NULL	NULL	0	NULL	CaMK	NULL		phosphorylates	NULL				SRF	NULL				NULL	neurons	NULL	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
37376	3	8763	7	NULL	NULL	0	NULL	statement 2	NULL		regulates	NULL	partially			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
37378	4	8763	7	NULL	NULL	0	NULL	SRF	NULL		bind	NULL				c-fos	NULL			CArG	NULL		0	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
37380	5	8763	7	NULL	NULL	0	NULL	statement 4	NULL	increase of	regulates	NULL	partially			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
37384	6	8763	7	NULL	NULL	0	NULL	VGCC	NULL	activation of	stimulates	NULL				multiple distinct signaling pathways	NULL				NULL	SMCs	0	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
37385	7	8763	7	NULL	NULL	0	NULL	statement 6	NULL		regulate	NULL				SM alpha-actin	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
37386	8	8763	7	NULL	NULL	0	NULL	SM alpha-actin	NULL		define	NULL				contractile SMC	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
37387	9	8763	7	NULL	NULL	0	NULL	statement 6	NULL		regulate	NULL				SMMHC	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
37390	10	8763	7	NULL	NULL	0	NULL	SMMHC	NULL		define	NULL				contractile SMC	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
37392	11	8763	7	10	NULL	0	NULL	c-fos	NULL		mediates	NULL				cell growth	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
37395	12	8763	7	NULL	NULL	0	NULL	statement 6	NULL		regulate	NULL				statement 11	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_4_406_s_177	15256479	9 Interestingly, the c-fos response to Ca2+ in neurons is partially regulated by SRF phosphorylation by CaMK and increased SRF binding to the c-fos CArG. 25 Therefore, it is plausible that VGCC activation stimulates multiple distinct signaling pathways in SMCs that regulate distinct subsets of genes, such as genes that define the "`contractile"' SMC, eg, SM alpha-actin and SMMHC, versus genes involved in mediating cell growth, eg, c-fos.	bind
38119	1	8764	5	13	NULL	NULL	NULL	RI	GP		associate with								RI-subunits		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_8_993_s_32	16645149	9 RI associates with other RI-subunits, whereas RII binds only other RII-subunits.	bind
38120	2	8764	5	13	NULL	NULL	NULL	RII	GP		bind		only						RII-subunits		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_8_993_s_32	16645149	9 RI associates with other RI-subunits, whereas RII binds only other RII-subunits.	bind
37397	1	8764	7	10	NULL	0	NULL	RI	NULL		associate with	NULL					NULL		RI-subunits		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_8_993_s_32	16645149	9 RI associates with other RI-subunits, whereas RII binds only other RII-subunits.	bind
37398	2	8764	7	10	NULL	0	NULL	RII	NULL		binds	NULL	only				NULL		RII-subunit		NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_8_993_s_32	16645149	9 RI associates with other RI-subunits, whereas RII binds only other RII-subunits.	bind
38121	1	8765	5	13	NULL	NULL	NULL	FXa	GP		bind					TF FVIIa	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2964_s_21	9409283	9 Then TFPI uses the tandem Kunitz-type domains in its structure to form a quaternary complex with FXa bound to TF FVIIa.	bind
38122	2	8765	5	13	NULL	NULL	NULL	TFPI	GP		bind			tandem Kunitz-type domains		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2964_s_21	9409283	9 Then TFPI uses the tandem Kunitz-type domains in its structure to form a quaternary complex with FXa bound to TF FVIIa.	bind
38123	3	8765	5	13	NULL	NULL	NULL	statement 2	GP		forms					quaternary complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2964_s_21	9409283	9 Then TFPI uses the tandem Kunitz-type domains in its structure to form a quaternary complex with FXa bound to TF FVIIa.	bind
37399	1	8765	7	NULL	NULL	0	NULL	FXa	NULL		bind	NULL				TF FVIIa	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2964_s_21	9409283	9 Then TFPI uses the tandem Kunitz-type domains in its structure to form a quaternary complex with FXa bound to TF FVIIa.	bind
37400	2	8765	7	10	NULL	0	NULL	TFPI	NULL		bind	NULL		tandem Kunitz-type domains		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2964_s_21	9409283	9 Then TFPI uses the tandem Kunitz-type domains in its structure to form a quaternary complex with FXa bound to TF FVIIa.	bind
46757	3	8765	7	10	NULL	0	NULL	statement 2	NULL		forms	NULL				quaternary complex	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2964_s_21	9409283	9 Then TFPI uses the tandem Kunitz-type domains in its structure to form a quaternary complex with FXa bound to TF FVIIa.	bind
38124	1	8766	5	13	NULL	NULL	NULL	yeasts	Organism		bind					BSA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jantimicrobchemoth_43_4_583_s_90	10350392	9 These agents do not significantly affect the binding of yeasts to BSA.	bind
37401	1	8766	7	NULL	NULL	0	NULL	 yeasts 	NULL		bind	NULL				BSA	NULL				NULL		0	NULL	NULL	NULL	gw60_jantimicrobchemoth_43_4_583_s_90	10350392	9 These agents do not significantly affect the binding of yeasts to BSA.	bind
38125	1	8767	5	13	NULL	NULL	NULL	Smad3	GP		bind					SM22alpha	GP			SBE region of promoter	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_circulationres_97_10_983_s_80	16224064	9 To determine whether Smad3 binds to the SBE region of the SM22alpha promoter in vivo, we performed ChIP assays on cultured cells.	bind
37412	1	8767	7	NULL	NULL	0	NULL	 Smad3	NULL		binds to	NULL				SM22alpha	NULL			SBE region of promoter	NULL	in vivo	0	NULL	NULL	NULL	gw70_circulationres_97_10_983_s_80	16224064	9 To determine whether Smad3 binds to the SBE region of the SM22alpha promoter in vivo, we performed ChIP assays on cultured cells.	bind
38126	1	8768	5	13	NULL	NULL	NULL	VEGF-B	GP		bind					VEGFR-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_5_664_s_31	14739162	9 VEGF-B and PlGF bind to VEGFR-1 and modulate the effects of VEGF-A, but their roles in stimulation of angiogenesis remain controversial.	bind
38127	2	8768	5	13	NULL	NULL	NULL	statement 1	Process		modulates					VEGF-A	GP	effects of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_5_664_s_31	14739162	9 VEGF-B and PlGF bind to VEGFR-1 and modulate the effects of VEGF-A, but their roles in stimulation of angiogenesis remain controversial.	bind
38128	3	8768	5	13	NULL	NULL	NULL	PlGF	GP		bind					VEGFR-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_94_5_664_s_31	14739162	9 VEGF-B and PlGF bind to VEGFR-1 and modulate the effects of VEGF-A, but their roles in stimulation of angiogenesis remain controversial.	bind
38129	4	8768	5	NULL	NULL	0	NULL	statement 3	NULL		modulates	NULL				VEGF-A	NULL	effects of			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_5_664_s_31	14739162	9 VEGF-B and PlGF bind to VEGFR-1 and modulate the effects of VEGF-A, but their roles in stimulation of angiogenesis remain controversial.	bind
37413	1	8768	7	NULL	NULL	0	NULL	VEGF-B 	NULL		bind	NULL				VEGFR-1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_5_664_s_31	14739162	9 VEGF-B and PlGF bind to VEGFR-1 and modulate the effects of VEGF-A, but their roles in stimulation of angiogenesis remain controversial.	bind
37414	2	8768	7	NULL	NULL	0	NULL	PlGF	NULL		bind	NULL				VEGFR-1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_94_5_664_s_31	14739162	9 VEGF-B and PlGF bind to VEGFR-1 and modulate the effects of VEGF-A, but their roles in stimulation of angiogenesis remain controversial.	bind
37415	3	8768	7	NULL	NULL	0	NULL	statement 1	NULL		modulate	NULL				VEGF-A	NULL	effects of			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_5_664_s_31	14739162	9 VEGF-B and PlGF bind to VEGFR-1 and modulate the effects of VEGF-A, but their roles in stimulation of angiogenesis remain controversial.	bind
37416	4	8768	7	NULL	NULL	0	NULL	statement 2	NULL		modulate	NULL				VEGF-A	NULL	effects of			NULL		0	NULL	NULL	NULL	gw70_circulationres_94_5_664_s_31	14739162	9 VEGF-B and PlGF bind to VEGFR-1 and modulate the effects of VEGF-A, but their roles in stimulation of angiogenesis remain controversial.	bind
38256	1	8769	5	13	NULL	NULL	NULL	Cdc37	GP		bind		potentially			eNOS	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
38257	2	8769	5	13	NULL	NULL	NULL	statement 1	Process		in the absence of		potentially			regulatory proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
38258	3	8769	5	13	NULL	NULL	NULL	statement 2	Process		serves		potentially			protective function	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
38259	4	8769	5	13	NULL	NULL	NULL	statement 3	Process		inhibit		potentially			eNOS	GP	uncoupled;;activity of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
38260	5	8769	5	13	NULL	NULL	NULL	statement 3	Process		inhibit		potentially			eNOS	GP	unregulated;;activity of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
38261	6	8769	5	13	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
38262	7	8769	5	13	NULL	NULL	NULL	eNOS	GP		interact with					Hsp90 	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
38263	8	8769	5	13	NULL	NULL	NULL	eNOS	GP		interact with					Akt	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
38264	9	8769	5	13	NULL	NULL	NULL	statement 7	Process		activates		subsequently			Hsp90	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
38265	10	8769	5	13	NULL	NULL	NULL	statement 8	Process		activates		subsequently			Akt	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
38266	11	8769	5	13	NULL	NULL	NULL	Cdc37	GP	overexpression of	interfere with		potentially			statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
38267	12	8769	5	13	NULL	NULL	NULL	Cdc37	GP	overexpression of	interfere with		potentially			statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
38268	13	8769	5	13	NULL	NULL	NULL	Cdc37	GP	overexpression of	interfere with		potentially			statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
38269	14	8769	5	13	NULL	NULL	NULL	Cdc37	GP	overexpression of	interfere with		potentially			statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
37419	1	8769	7	NULL	NULL	0	NULL	Cdc37 	NULL		bind	NULL				eNOS	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
37420	2	8769	7	NULL	NULL	0	NULL	statement 1	NULL		in the absence of	NULL				regulatory proteins	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
37422	3	8769	7	10	NULL	0	NULL	statement 2	NULL		inhibit	NULL				eNOS	NULL	uncoupled;; activity of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
37423	4	8769	7	10	NULL	0	NULL	statement 2	NULL		inhibit	NULL				eNOS	NULL	unregulated;; activity of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
37435	5	8769	7	NULL	NULL	0	NULL	statement 2	NULL		serves a	NULL				protective funtion	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
37436	6	8769	7	NULL	NULL	0	NULL	statement 5	NULL		occurs by	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
37437	7	8769	7	NULL	NULL	0	NULL	statement 5	NULL		occurs by	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
37438	8	8769	7	NULL	NULL	0	NULL	eNOS	NULL		interacts with	NULL				Hsp90	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
37439	9	8769	7	NULL	NULL	0	NULL	eNOS	NULL		interacts with	NULL				Akt	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
37440	10	8769	7	NULL	NULL	0	NULL	Cdc37	NULL	overexpression of	interferes with	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
37441	11	8769	7	NULL	NULL	0	NULL	Cdc37	NULL	overexpression of	interferes with	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_3_335_s_204	16410463	9 With this in mind, we hypothesize that Cdc37 bound to the eNOS in the absence of other regulatory proteins serves a protective function inhibiting uncoupled or unregulated eNOS activity and that overexpression of Cdc37 interferes with the proper interactions of eNOS with Hsp90 and Akt and subsequent activation.	bind
38270	1	8770	5	13	NULL	NULL	NULL	67LR	GP		bind					laminin beta1	GP		cysteine-rich domain of short arm of		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_307_s_15	11786424	9, 10  his receptor (designated 67LR) binds to a cysteine-rich domain of the short arm of laminin beta1.	bind
56426	2	8770	5	13	NULL	NULL	NULL	67LR	GP		is 					his receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_307_s_15	11786424	9, 10  his receptor (designated 67LR) binds to a cysteine-rich domain of the short arm of laminin beta1.	bind
37442	1	8770	7	NULL	NULL	0	NULL	his receptor	NULL		binds to	NULL				laminin beta1	NULL		cysteine-rich domain of the short arm of 		NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_1_307_s_15	11786424	9, 10  his receptor (designated 67LR) binds to a cysteine-rich domain of the short arm of laminin beta1.	bind
37443	2	8770	7	NULL	NULL	0	NULL	his receptor	NULL		is	NULL				67LR	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_1_307_s_15	11786424	9, 10  his receptor (designated 67LR) binds to a cysteine-rich domain of the short arm of laminin beta1.	bind
38271	1	8771	5	13	NULL	NULL	NULL	Ang-1	GP		bind					Tie-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_773_s_13	11891175	9, 13- 15  Ang-1 binds and induces autophosphorylation of Tie-2, 10  promoting endothelial cell migration, 16  sprouting, 17, 18  and survival 19, 20  in vitro; and increases new vessel growth, branching, maturation, and integrity  in vivo.	bind
38272	2	8771	5	13	NULL	NULL	NULL	statement 1	Process		induce					Tie-2	GP	autophosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_773_s_13	11891175	9, 13- 15  Ang-1 binds and induces autophosphorylation of Tie-2, 10  promoting endothelial cell migration, 16  sprouting, 17, 18  and survival 19, 20  in vitro; and increases new vessel growth, branching, maturation, and integrity  in vivo.	bind
38273	3	8771	5	13	NULL	NULL	NULL	statement 2	Process		promotes					endothelial cell	Cell	migration of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_773_s_13	11891175	9, 13- 15  Ang-1 binds and induces autophosphorylation of Tie-2, 10  promoting endothelial cell migration, 16  sprouting, 17, 18  and survival 19, 20  in vitro; and increases new vessel growth, branching, maturation, and integrity  in vivo.	bind
38275	4	8771	5	13	NULL	NULL	NULL	statement 2	Process		promotes					endothelial cell	Cell	sprouting of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_773_s_13	11891175	9, 13- 15  Ang-1 binds and induces autophosphorylation of Tie-2, 10  promoting endothelial cell migration, 16  sprouting, 17, 18  and survival 19, 20  in vitro; and increases new vessel growth, branching, maturation, and integrity  in vivo.	bind
38276	5	8771	5	13	NULL	NULL	NULL	statement 2	Process		promotes					endothelial cell	Cell	survival of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_773_s_13	11891175	9, 13- 15  Ang-1 binds and induces autophosphorylation of Tie-2, 10  promoting endothelial cell migration, 16  sprouting, 17, 18  and survival 19, 20  in vitro; and increases new vessel growth, branching, maturation, and integrity  in vivo.	bind
38283	6	8771	5	13	NULL	NULL	NULL	statement 2	Process		increase					new vessel	OrganismPart	growth of			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_773_s_13	11891175	9, 13- 15  Ang-1 binds and induces autophosphorylation of Tie-2, 10  promoting endothelial cell migration, 16  sprouting, 17, 18  and survival 19, 20  in vitro; and increases new vessel growth, branching, maturation, and integrity  in vivo.	bind
38284	7	8771	5	13	NULL	NULL	NULL	statement 2	Process		increase					new vessel	OrganismPart	branching of			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_773_s_13	11891175	9, 13- 15  Ang-1 binds and induces autophosphorylation of Tie-2, 10  promoting endothelial cell migration, 16  sprouting, 17, 18  and survival 19, 20  in vitro; and increases new vessel growth, branching, maturation, and integrity  in vivo.	bind
38285	8	8771	5	13	NULL	NULL	NULL	statement 2	Process		increase					new vessel	OrganismPart	maturation of			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_773_s_13	11891175	9, 13- 15  Ang-1 binds and induces autophosphorylation of Tie-2, 10  promoting endothelial cell migration, 16  sprouting, 17, 18  and survival 19, 20  in vitro; and increases new vessel growth, branching, maturation, and integrity  in vivo.	bind
38286	9	8771	5	13	NULL	NULL	NULL	statement 2	Process		increase					new vessel	OrganismPart	integrity of			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_773_s_13	11891175	9, 13- 15  Ang-1 binds and induces autophosphorylation of Tie-2, 10  promoting endothelial cell migration, 16  sprouting, 17, 18  and survival 19, 20  in vitro; and increases new vessel growth, branching, maturation, and integrity  in vivo.	bind
37444	1	8771	7	NULL	NULL	0	NULL	Ang-1	NULL		binds	NULL				Tie-2	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_3_773_s_13	11891175	9, 13- 15  Ang-1 binds and induces autophosphorylation of Tie-2, 10  promoting endothelial cell migration, 16  sprouting, 17, 18  and survival 19, 20  in vitro; and increases new vessel growth, branching, maturation, and integrity  in vivo.	bind
37445	2	8771	7	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL				Tie-2	NULL	autophosphorylation of			NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_3_773_s_13	11891175	9, 13- 15  Ang-1 binds and induces autophosphorylation of Tie-2, 10  promoting endothelial cell migration, 16  sprouting, 17, 18  and survival 19, 20  in vitro; and increases new vessel growth, branching, maturation, and integrity  in vivo.	bind
37446	3	8771	7	10	NULL	0	NULL	statement 2	NULL		promote	NULL				endothelial cell 	NULL	migration of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_773_s_13	11891175	9, 13- 15  Ang-1 binds and induces autophosphorylation of Tie-2, 10  promoting endothelial cell migration, 16  sprouting, 17, 18  and survival 19, 20  in vitro; and increases new vessel growth, branching, maturation, and integrity  in vivo.	bind
37447	4	8771	7	NULL	NULL	0	NULL	statement 2	NULL		promote	NULL				endothelial cell	NULL	sprouting of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_773_s_13	11891175	9, 13- 15  Ang-1 binds and induces autophosphorylation of Tie-2, 10  promoting endothelial cell migration, 16  sprouting, 17, 18  and survival 19, 20  in vitro; and increases new vessel growth, branching, maturation, and integrity  in vivo.	bind
37448	5	8771	7	NULL	NULL	0	NULL	statement 2	NULL		promote	NULL				endothelial cell	NULL	survival of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_773_s_13	11891175	9, 13- 15  Ang-1 binds and induces autophosphorylation of Tie-2, 10  promoting endothelial cell migration, 16  sprouting, 17, 18  and survival 19, 20  in vitro; and increases new vessel growth, branching, maturation, and integrity  in vivo.	bind
37449	6	8771	7	NULL	NULL	0	NULL	statement 2	NULL		increase	NULL				new vessel 	NULL	growth of			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_773_s_13	11891175	9, 13- 15  Ang-1 binds and induces autophosphorylation of Tie-2, 10  promoting endothelial cell migration, 16  sprouting, 17, 18  and survival 19, 20  in vitro; and increases new vessel growth, branching, maturation, and integrity  in vivo.	bind
37450	7	8771	7	NULL	NULL	0	NULL	statement 2	NULL		increase	NULL				new vessel	NULL	branching of			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_773_s_13	11891175	9, 13- 15  Ang-1 binds and induces autophosphorylation of Tie-2, 10  promoting endothelial cell migration, 16  sprouting, 17, 18  and survival 19, 20  in vitro; and increases new vessel growth, branching, maturation, and integrity  in vivo.	bind
37451	8	8771	7	NULL	NULL	0	NULL	statement 2	NULL		increase	NULL				new vessel	NULL	maturation of			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_773_s_13	11891175	9, 13- 15  Ang-1 binds and induces autophosphorylation of Tie-2, 10  promoting endothelial cell migration, 16  sprouting, 17, 18  and survival 19, 20  in vitro; and increases new vessel growth, branching, maturation, and integrity  in vivo.	bind
37452	9	8771	7	NULL	NULL	0	NULL	statement 2	NULL		increase	NULL				new vessel	NULL	integrity of			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_amjpathol_160_3_773_s_13	11891175	9, 13- 15  Ang-1 binds and induces autophosphorylation of Tie-2, 10  promoting endothelial cell migration, 16  sprouting, 17, 18  and survival 19, 20  in vitro; and increases new vessel growth, branching, maturation, and integrity  in vivo.	bind
38287	1	8772	5	13	NULL	NULL	NULL	alphavbeta3	GP		is expressed by					melanoma cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_5_1435_s_164	9811334	9, 53 alphavbeta3 expressed by melanoma cells can bind to L1, another member of the Ig gene superfamily found on melanoma cells.	bind
38288	2	8772	5	13	NULL	NULL	NULL	statement 1	GP		bind					L1	GP				NULL	melanoma cells	NULL	NULL	NULL	NULL	gw60_amjpathol_153_5_1435_s_164	9811334	9, 53 alphavbeta3 expressed by melanoma cells can bind to L1, another member of the Ig gene superfamily found on melanoma cells.	bind
38290	3	8772	5	13	NULL	NULL	NULL	L1	GP		is a type of					Ig gene superfamily	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_153_5_1435_s_164	9811334	9, 53 alphavbeta3 expressed by melanoma cells can bind to L1, another member of the Ig gene superfamily found on melanoma cells.	bind
37453	1	8772	7	NULL	NULL	0	NULL	 alphavbeta3 	NULL		bind	NULL				L1	NULL				NULL	melanoma cells	NULL	NULL	NULL	NULL	gw60_amjpathol_153_5_1435_s_164	9811334	9, 53 alphavbeta3 expressed by melanoma cells can bind to L1, another member of the Ig gene superfamily found on melanoma cells.	bind
37454	2	8772	7	NULL	NULL	0	NULL	 alphavbeta3 	NULL		is expressed by	NULL				melanoma cells	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_5_1435_s_164	9811334	9, 53 alphavbeta3 expressed by melanoma cells can bind to L1, another member of the Ig gene superfamily found on melanoma cells.	bind
37455	3	8772	7	NULL	NULL	0	NULL	L1	NULL		is a type of	NULL				Ig gene superfamily	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_153_5_1435_s_164	9811334	9, 53 alphavbeta3 expressed by melanoma cells can bind to L1, another member of the Ig gene superfamily found on melanoma cells.	bind
38291	1	8773	5	13	NULL	NULL	NULL	fVIII	GP		bind					vWf	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_29_18007_s_118	9218428	9, which does not interfere with fVIII binding to vWf ( 19).	bind
37456	1	8773	7	NULL	NULL	0	NULL	fVIII	NULL		bind	NULL				vWf	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_29_18007_s_118	9218428	9, which does not interfere with fVIII binding to vWf ( 19).	bind
38442	1	8774	5	13	NULL	NULL	NULL	cholesterol efflux	Process		is mediated to					apoAI	GP				NULL	macrophages 	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2155_s_29	15358601	9,10  In contrast, unsaturated fatty acids markedly inhibit ABCA1-mediated cholesterol efflux to apoAI in macrophages by increasing ABCA1 turnover and subsequently decreasing cell-surface ABCA1 and apoAI binding to cells.	bind
38443	2	8774	5	13	NULL	NULL	NULL	ABCA1	GP		mediate					statement 1	Process				NULL	macrophages	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2155_s_29	15358601	9,10  In contrast, unsaturated fatty acids markedly inhibit ABCA1-mediated cholesterol efflux to apoAI in macrophages by increasing ABCA1 turnover and subsequently decreasing cell-surface ABCA1 and apoAI binding to cells.	bind
38444	3	8774	5	13	NULL	NULL	NULL	unsaturated fatty acids	Chemical		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2155_s_29	15358601	9,10  In contrast, unsaturated fatty acids markedly inhibit ABCA1-mediated cholesterol efflux to apoAI in macrophages by increasing ABCA1 turnover and subsequently decreasing cell-surface ABCA1 and apoAI binding to cells.	bind
38445	4	8774	5	13	NULL	NULL	NULL	unsaturated fatty acids	Chemical		increase					ABCA1 turnover 	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2155_s_29	15358601	9,10  In contrast, unsaturated fatty acids markedly inhibit ABCA1-mediated cholesterol efflux to apoAI in macrophages by increasing ABCA1 turnover and subsequently decreasing cell-surface ABCA1 and apoAI binding to cells.	bind
38446	5	8774	5	13	NULL	NULL	NULL	ABCA1	GP	cell-surface	bind					cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2155_s_29	15358601	9,10  In contrast, unsaturated fatty acids markedly inhibit ABCA1-mediated cholesterol efflux to apoAI in macrophages by increasing ABCA1 turnover and subsequently decreasing cell-surface ABCA1 and apoAI binding to cells.	bind
38447	6	8774	5	13	NULL	NULL	NULL	apoAI	GP	cell-surface	bind					cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2155_s_29	15358601	9,10  In contrast, unsaturated fatty acids markedly inhibit ABCA1-mediated cholesterol efflux to apoAI in macrophages by increasing ABCA1 turnover and subsequently decreasing cell-surface ABCA1 and apoAI binding to cells.	bind
38448	7	8774	5	13	NULL	NULL	NULL	statement 4	Process		decrease		subsequently			statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2155_s_29	15358601	9,10  In contrast, unsaturated fatty acids markedly inhibit ABCA1-mediated cholesterol efflux to apoAI in macrophages by increasing ABCA1 turnover and subsequently decreasing cell-surface ABCA1 and apoAI binding to cells.	bind
38449	8	8774	5	13	NULL	NULL	NULL	statement 4	Process		decrease		subsequently			statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2155_s_29	15358601	9,10  In contrast, unsaturated fatty acids markedly inhibit ABCA1-mediated cholesterol efflux to apoAI in macrophages by increasing ABCA1 turnover and subsequently decreasing cell-surface ABCA1 and apoAI binding to cells.	bind
37457	1	8774	7	NULL	NULL	0	NULL	cholesterol	NULL		efflux to	NULL				apoAI	NULL				NULL	macrophages	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2155_s_29	15358601	9,10  In contrast, unsaturated fatty acids markedly inhibit ABCA1-mediated cholesterol efflux to apoAI in macrophages by increasing ABCA1 turnover and subsequently decreasing cell-surface ABCA1 and apoAI binding to cells.	bind
37458	2	8774	7	NULL	NULL	0	NULL	ABCA1	NULL		mediates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2155_s_29	15358601	9,10  In contrast, unsaturated fatty acids markedly inhibit ABCA1-mediated cholesterol efflux to apoAI in macrophages by increasing ABCA1 turnover and subsequently decreasing cell-surface ABCA1 and apoAI binding to cells.	bind
37459	3	8774	7	NULL	NULL	0	NULL	unsaturated fatty acids	NULL		inhibit	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2155_s_29	15358601	9,10  In contrast, unsaturated fatty acids markedly inhibit ABCA1-mediated cholesterol efflux to apoAI in macrophages by increasing ABCA1 turnover and subsequently decreasing cell-surface ABCA1 and apoAI binding to cells.	bind
37460	4	8774	7	NULL	NULL	0	NULL	statement 1	NULL		occurs by	NULL				ABCA1	NULL	increase of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2155_s_29	15358601	9,10  In contrast, unsaturated fatty acids markedly inhibit ABCA1-mediated cholesterol efflux to apoAI in macrophages by increasing ABCA1 turnover and subsequently decreasing cell-surface ABCA1 and apoAI binding to cells.	bind
37461	5	8774	7	NULL	NULL	0	NULL	statement 1	NULL		occurs by	NULL				cell surface ABCA1	NULL	decrease of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2155_s_29	15358601	9,10  In contrast, unsaturated fatty acids markedly inhibit ABCA1-mediated cholesterol efflux to apoAI in macrophages by increasing ABCA1 turnover and subsequently decreasing cell-surface ABCA1 and apoAI binding to cells.	bind
37462	6	8774	7	NULL	NULL	0	NULL	apoAI	NULL		bind	NULL				cells	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2155_s_29	15358601	9,10  In contrast, unsaturated fatty acids markedly inhibit ABCA1-mediated cholesterol efflux to apoAI in macrophages by increasing ABCA1 turnover and subsequently decreasing cell-surface ABCA1 and apoAI binding to cells.	bind
37463	7	8774	7	NULL	NULL	0	NULL	statement 1	NULL		occurs by	NULL				statement 6	NULL	decrease of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2155_s_29	15358601	9,10  In contrast, unsaturated fatty acids markedly inhibit ABCA1-mediated cholesterol efflux to apoAI in macrophages by increasing ABCA1 turnover and subsequently decreasing cell-surface ABCA1 and apoAI binding to cells.	bind
56430	8	8774	7	10	NULL	0	NULL	unsaturated fatty acids			increase					ABCA1 turnover					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_11_2155_s_29	15358601	9,10  In contrast, unsaturated fatty acids markedly inhibit ABCA1-mediated cholesterol efflux to apoAI in macrophages by increasing ABCA1 turnover and subsequently decreasing cell-surface ABCA1 and apoAI binding to cells.	bind
38454	1	8775	5	13	NULL	NULL	NULL	Rho-kinase	GP		is a target protein of		major			small Rho GTPase	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2209_s_24	14592852	9,11 - 15      Rho-kinase, one of the major target proteins of small Rho GTPase, 16,17  was upregulated in spastic coronary segment, leading to an increased phosphorylation of myosin-binding subunit of myosin phosphatase (MLCPh) and the resultant suppression of MLCPh. 11 - 15     Indeed, we recently demonstrated that Rho-kinase is substantially involved in hypercontractions of isolated arteriosclerotic human arteries in vitro 18 as well as in coronary artery spasm of patients with vasospastic angina in vivo.	bind
38455	2	8775	5	13	NULL	NULL	NULL	Rho-kinase	GP		is upregulated in					spastic coronary segment	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2209_s_24	14592852	9,11 - 15      Rho-kinase, one of the major target proteins of small Rho GTPase, 16,17  was upregulated in spastic coronary segment, leading to an increased phosphorylation of myosin-binding subunit of myosin phosphatase (MLCPh) and the resultant suppression of MLCPh. 11 - 15     Indeed, we recently demonstrated that Rho-kinase is substantially involved in hypercontractions of isolated arteriosclerotic human arteries in vitro 18 as well as in coronary artery spasm of patients with vasospastic angina in vivo.	bind
38460	3	8775	5	13	NULL	NULL	NULL	statement 2	Process		increase					MLCPh	GP	phosphorylation of	myosin-binding subunit		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2209_s_24	14592852	9,11 - 15      Rho-kinase, one of the major target proteins of small Rho GTPase, 16,17  was upregulated in spastic coronary segment, leading to an increased phosphorylation of myosin-binding subunit of myosin phosphatase (MLCPh) and the resultant suppression of MLCPh. 11 - 15     Indeed, we recently demonstrated that Rho-kinase is substantially involved in hypercontractions of isolated arteriosclerotic human arteries in vitro 18 as well as in coronary artery spasm of patients with vasospastic angina in vivo.	bind
38462	4	8775	5	13	NULL	NULL	NULL	MLCPh	GP		is					myosin phosphatase	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2209_s_24	14592852	9,11 - 15      Rho-kinase, one of the major target proteins of small Rho GTPase, 16,17  was upregulated in spastic coronary segment, leading to an increased phosphorylation of myosin-binding subunit of myosin phosphatase (MLCPh) and the resultant suppression of MLCPh. 11 - 15     Indeed, we recently demonstrated that Rho-kinase is substantially involved in hypercontractions of isolated arteriosclerotic human arteries in vitro 18 as well as in coronary artery spasm of patients with vasospastic angina in vivo.	bind
38463	5	8775	5	13	NULL	NULL	NULL	statement 3	Process		supress					MLCPh	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2209_s_24	14592852	9,11 - 15      Rho-kinase, one of the major target proteins of small Rho GTPase, 16,17  was upregulated in spastic coronary segment, leading to an increased phosphorylation of myosin-binding subunit of myosin phosphatase (MLCPh) and the resultant suppression of MLCPh. 11 - 15     Indeed, we recently demonstrated that Rho-kinase is substantially involved in hypercontractions of isolated arteriosclerotic human arteries in vitro 18 as well as in coronary artery spasm of patients with vasospastic angina in vivo.	bind
38464	6	8775	5	13	NULL	NULL	NULL	Rho-kinase	GP		is involved in					arteriosclerotic arteries	OrganismPart	hypercontractions of;;isolated;;human			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2209_s_24	14592852	9,11 - 15      Rho-kinase, one of the major target proteins of small Rho GTPase, 16,17  was upregulated in spastic coronary segment, leading to an increased phosphorylation of myosin-binding subunit of myosin phosphatase (MLCPh) and the resultant suppression of MLCPh. 11 - 15     Indeed, we recently demonstrated that Rho-kinase is substantially involved in hypercontractions of isolated arteriosclerotic human arteries in vitro 18 as well as in coronary artery spasm of patients with vasospastic angina in vivo.	bind
38468	7	8775	5	13	NULL	NULL	NULL	Rho-kinase	GP		is involved in					coronary artery spasm	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2209_s_24	14592852	9,11 - 15      Rho-kinase, one of the major target proteins of small Rho GTPase, 16,17  was upregulated in spastic coronary segment, leading to an increased phosphorylation of myosin-binding subunit of myosin phosphatase (MLCPh) and the resultant suppression of MLCPh. 11 - 15     Indeed, we recently demonstrated that Rho-kinase is substantially involved in hypercontractions of isolated arteriosclerotic human arteries in vitro 18 as well as in coronary artery spasm of patients with vasospastic angina in vivo.	bind
46758	8	8775	5	13	NULL	NULL	NULL	statement 7	MedicalFinding		occurs with					vasospastic angina	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2209_s_24	14592852	9,11 - 15      Rho-kinase, one of the major target proteins of small Rho GTPase, 16,17  was upregulated in spastic coronary segment, leading to an increased phosphorylation of myosin-binding subunit of myosin phosphatase (MLCPh) and the resultant suppression of MLCPh. 11 - 15     Indeed, we recently demonstrated that Rho-kinase is substantially involved in hypercontractions of isolated arteriosclerotic human arteries in vitro 18 as well as in coronary artery spasm of patients with vasospastic angina in vivo.	bind
37464	1	8775	7	NULL	NULL	0	NULL	small Rho GTPase	NULL		target	NULL				Rho-kinase	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2209_s_24	14592852	9,11 - 15      Rho-kinase, one of the major target proteins of small Rho GTPase, 16,17  was upregulated in spastic coronary segment, leading to an increased phosphorylation of myosin-binding subunit of myosin phosphatase (MLCPh) and the resultant suppression of MLCPh. 11 - 15     Indeed, we recently demonstrated that Rho-kinase is substantially involved in hypercontractions of isolated arteriosclerotic human arteries in vitro 18 as well as in coronary artery spasm of patients with vasospastic angina in vivo.	bind
37465	2	8775	7	NULL	NULL	0	NULL	Rho-kinase	NULL		is upregulated in	NULL				spastic coronary segment	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2209_s_24	14592852	9,11 - 15      Rho-kinase, one of the major target proteins of small Rho GTPase, 16,17  was upregulated in spastic coronary segment, leading to an increased phosphorylation of myosin-binding subunit of myosin phosphatase (MLCPh) and the resultant suppression of MLCPh. 11 - 15     Indeed, we recently demonstrated that Rho-kinase is substantially involved in hypercontractions of isolated arteriosclerotic human arteries in vitro 18 as well as in coronary artery spasm of patients with vasospastic angina in vivo.	bind
37466	3	8775	7	NULL	NULL	0	NULL	MLCPh	NULL		undergoes	NULL					NULL	phosphorylation of	myosin-binding subunit		NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2209_s_24	14592852	9,11 - 15      Rho-kinase, one of the major target proteins of small Rho GTPase, 16,17  was upregulated in spastic coronary segment, leading to an increased phosphorylation of myosin-binding subunit of myosin phosphatase (MLCPh) and the resultant suppression of MLCPh. 11 - 15     Indeed, we recently demonstrated that Rho-kinase is substantially involved in hypercontractions of isolated arteriosclerotic human arteries in vitro 18 as well as in coronary artery spasm of patients with vasospastic angina in vivo.	bind
37467	4	8775	7	NULL	NULL	0	NULL	statement 2	NULL		increase	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2209_s_24	14592852	9,11 - 15      Rho-kinase, one of the major target proteins of small Rho GTPase, 16,17  was upregulated in spastic coronary segment, leading to an increased phosphorylation of myosin-binding subunit of myosin phosphatase (MLCPh) and the resultant suppression of MLCPh. 11 - 15     Indeed, we recently demonstrated that Rho-kinase is substantially involved in hypercontractions of isolated arteriosclerotic human arteries in vitro 18 as well as in coronary artery spasm of patients with vasospastic angina in vivo.	bind
37468	5	8775	7	NULL	NULL	0	NULL	statement 4	NULL		suppress	NULL				MLCPh	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2209_s_24	14592852	9,11 - 15      Rho-kinase, one of the major target proteins of small Rho GTPase, 16,17  was upregulated in spastic coronary segment, leading to an increased phosphorylation of myosin-binding subunit of myosin phosphatase (MLCPh) and the resultant suppression of MLCPh. 11 - 15     Indeed, we recently demonstrated that Rho-kinase is substantially involved in hypercontractions of isolated arteriosclerotic human arteries in vitro 18 as well as in coronary artery spasm of patients with vasospastic angina in vivo.	bind
37469	6	8775	7	10	NULL	0	NULL	Rho-kinase	NULL		is involved in	NULL	substantially			arteriosclerotic arteries	NULL	hypercontractions of ;; isolated;; human			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2209_s_24	14592852	9,11 - 15      Rho-kinase, one of the major target proteins of small Rho GTPase, 16,17  was upregulated in spastic coronary segment, leading to an increased phosphorylation of myosin-binding subunit of myosin phosphatase (MLCPh) and the resultant suppression of MLCPh. 11 - 15     Indeed, we recently demonstrated that Rho-kinase is substantially involved in hypercontractions of isolated arteriosclerotic human arteries in vitro 18 as well as in coronary artery spasm of patients with vasospastic angina in vivo.	bind
37470	7	8775	7	NULL	NULL	0	NULL	Rho-kinase	NULL		is involved in	NULL				coronary artery spasm	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2209_s_24	14592852	9,11 - 15      Rho-kinase, one of the major target proteins of small Rho GTPase, 16,17  was upregulated in spastic coronary segment, leading to an increased phosphorylation of myosin-binding subunit of myosin phosphatase (MLCPh) and the resultant suppression of MLCPh. 11 - 15     Indeed, we recently demonstrated that Rho-kinase is substantially involved in hypercontractions of isolated arteriosclerotic human arteries in vitro 18 as well as in coronary artery spasm of patients with vasospastic angina in vivo.	bind
37471	8	8775	7	NULL	NULL	0	NULL	statement 7	NULL		occurs with	NULL				vasospastic angina	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2209_s_24	14592852	9,11 - 15      Rho-kinase, one of the major target proteins of small Rho GTPase, 16,17  was upregulated in spastic coronary segment, leading to an increased phosphorylation of myosin-binding subunit of myosin phosphatase (MLCPh) and the resultant suppression of MLCPh. 11 - 15     Indeed, we recently demonstrated that Rho-kinase is substantially involved in hypercontractions of isolated arteriosclerotic human arteries in vitro 18 as well as in coronary artery spasm of patients with vasospastic angina in vivo.	bind
37472	9	8775	7	NULL	NULL	0	NULL	MLCPh	NULL		is	NULL				 phosphorylated myosin-binding subunit of myosin phosphatase	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2209_s_24	14592852	9,11 - 15      Rho-kinase, one of the major target proteins of small Rho GTPase, 16,17  was upregulated in spastic coronary segment, leading to an increased phosphorylation of myosin-binding subunit of myosin phosphatase (MLCPh) and the resultant suppression of MLCPh. 11 - 15     Indeed, we recently demonstrated that Rho-kinase is substantially involved in hypercontractions of isolated arteriosclerotic human arteries in vitro 18 as well as in coronary artery spasm of patients with vasospastic angina in vivo.	bind
38470	1	8776	5	13	NULL	NULL	NULL	FAK	GP	activation of	generates					Src family tyrosine kinases	GP	high-affinity binding site to	SH2 domain		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_12_2548_s_39	16195476	9,18,24 - 29        FAK activation generates a high-affinity binding site to the SH2 domain of Src family tyrosine kinases and causes recruitment and activation of Src. 18,19,30   FAK activation also leads to activation of PI3K, which binds to SH2 domain of FAK.	bind
38473	2	8776	5	13	NULL	NULL	NULL	statement 1	GP		recruits					Src	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_12_2548_s_39	16195476	9,18,24 - 29        FAK activation generates a high-affinity binding site to the SH2 domain of Src family tyrosine kinases and causes recruitment and activation of Src. 18,19,30   FAK activation also leads to activation of PI3K, which binds to SH2 domain of FAK.	bind
38476	3	8776	5	13	NULL	NULL	NULL	statement 1	GP		causes					Src	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_12_2548_s_39	16195476	9,18,24 - 29        FAK activation generates a high-affinity binding site to the SH2 domain of Src family tyrosine kinases and causes recruitment and activation of Src. 18,19,30   FAK activation also leads to activation of PI3K, which binds to SH2 domain of FAK.	bind
38479	4	8776	5	13	NULL	NULL	NULL	FAK	GP	activation of	leads to					PI3K	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_12_2548_s_39	16195476	9,18,24 - 29        FAK activation generates a high-affinity binding site to the SH2 domain of Src family tyrosine kinases and causes recruitment and activation of Src. 18,19,30   FAK activation also leads to activation of PI3K, which binds to SH2 domain of FAK.	bind
38480	5	8776	5	13	NULL	NULL	NULL	PI3K	GP		bind					FAK	GP		SH2 domain		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_12_2548_s_39	16195476	9,18,24 - 29        FAK activation generates a high-affinity binding site to the SH2 domain of Src family tyrosine kinases and causes recruitment and activation of Src. 18,19,30   FAK activation also leads to activation of PI3K, which binds to SH2 domain of FAK.	bind
37473	1	8776	7	10	NULL	0	NULL	FAK	NULL	activation of	generates	NULL				Src family tyrosine kinases	NULL	high-affinity binding site to	SH2 domain		NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_12_2548_s_39	16195476	9,18,24 - 29        FAK activation generates a high-affinity binding site to the SH2 domain of Src family tyrosine kinases and causes recruitment and activation of Src. 18,19,30   FAK activation also leads to activation of PI3K, which binds to SH2 domain of FAK.	bind
37474	2	8776	7	NULL	NULL	0	NULL	FAK	NULL	activation of	recruits	NULL				Src	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_12_2548_s_39	16195476	9,18,24 - 29        FAK activation generates a high-affinity binding site to the SH2 domain of Src family tyrosine kinases and causes recruitment and activation of Src. 18,19,30   FAK activation also leads to activation of PI3K, which binds to SH2 domain of FAK.	bind
37475	3	8776	7	NULL	NULL	0	NULL	statement 2	NULL		activates	NULL				Src	NULL				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_12_2548_s_39	16195476	9,18,24 - 29        FAK activation generates a high-affinity binding site to the SH2 domain of Src family tyrosine kinases and causes recruitment and activation of Src. 18,19,30   FAK activation also leads to activation of PI3K, which binds to SH2 domain of FAK.	bind
37476	4	8776	7	NULL	NULL	0	NULL	FAK	NULL	activation of	leads to	NULL				PI3K	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_12_2548_s_39	16195476	9,18,24 - 29        FAK activation generates a high-affinity binding site to the SH2 domain of Src family tyrosine kinases and causes recruitment and activation of Src. 18,19,30   FAK activation also leads to activation of PI3K, which binds to SH2 domain of FAK.	bind
37477	5	8776	7	NULL	NULL	0	NULL	PI3K 	NULL		binds to	NULL				FAK	NULL		SH2 domain		NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_25_12_2548_s_39	16195476	9,18,24 - 29        FAK activation generates a high-affinity binding site to the SH2 domain of Src family tyrosine kinases and causes recruitment and activation of Src. 18,19,30   FAK activation also leads to activation of PI3K, which binds to SH2 domain of FAK.	bind
38484	1	8777	5	13	NULL	NULL	NULL	9- cis retinoic acid stereoisomer	Chemical		bind					RXR alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_33_s_615	11719067	9- cis retinoic acid stereoisomer binds and activates the nuclear receptor RXR alpha.	bind
38485	2	8777	5	13	NULL	NULL	NULL	statement 1	Process		activates					RXR alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_33_s_615	11719067	9- cis retinoic acid stereoisomer binds and activates the nuclear receptor RXR alpha.	bind
38486	3	8777	5	13	NULL	NULL	NULL	RXR alpha	GP		is a type of					nuclear receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_33_s_615	11719067	9- cis retinoic acid stereoisomer binds and activates the nuclear receptor RXR alpha.	bind
37478	1	8777	7	NULL	NULL	0	NULL	9- cis retinoic acid stereoisomer	NULL		binds	NULL				RXR alpha	NULL				NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_33_s_615	11719067	9- cis retinoic acid stereoisomer binds and activates the nuclear receptor RXR alpha.	bind
37479	2	8777	7	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				RXR alpha	NULL				NULL		0	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_33_s_615	11719067	9- cis retinoic acid stereoisomer binds and activates the nuclear receptor RXR alpha.	bind
37480	3	8777	7	NULL	NULL	0	NULL	RXR alpha	NULL		is a type of	NULL				nuclear receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_33_s_615	11719067	9- cis retinoic acid stereoisomer binds and activates the nuclear receptor RXR alpha.	bind
38488	1	8778	5	13	NULL	NULL	NULL	9- Cis-4-oxo-RA	Chemical		bind					RARs	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_95_26_15424_s_94	9860984	9- Cis-4-oxo-RA binds RARs and RXRs  in vitro	bind
38489	2	8778	5	13	NULL	NULL	NULL	9- Cis-4-oxo-RA	Chemical		bind					RXRs	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_95_26_15424_s_94	9860984	9- Cis-4-oxo-RA binds RARs and RXRs  in vitro	bind
37481	1	8778	7	NULL	NULL	0	NULL	9- Cis-4-oxo-RA	NULL		binds	NULL				RARs	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_pnas_95_26_15424_s_94	9860984	9- Cis-4-oxo-RA binds RARs and RXRs  in vitro	bind
37482	2	8778	7	NULL	NULL	0	NULL	9- Cis-4-oxo-RA	NULL		binds	NULL				RXRs	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_pnas_95_26_15424_s_94	9860984	9- Cis-4-oxo-RA binds RARs and RXRs  in vitro	bind
38490	1	8779	5	13	NULL	NULL	NULL	9- cis-RA	Chemical		bind					RARs	GP				NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_20_2_255_s_161	10069462	9- cis-RA binds both RARs and RXRs, while 4-HPR and probably 2-CPR appear not to bind these receptors ( 40, 41).	bind
38491	2	8779	5	13	NULL	NULL	NULL	9- cis-RA	Chemical		bind					RXRs	GP				NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_20_2_255_s_161	10069462	9- cis-RA binds both RARs and RXRs, while 4-HPR and probably 2-CPR appear not to bind these receptors ( 40, 41).	bind
38492	3	8779	5	13	NULL	NULL	NULL	4-HPR	Chemical		does not bind					RARs	GP				NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_20_2_255_s_161	10069462	9- cis-RA binds both RARs and RXRs, while 4-HPR and probably 2-CPR appear not to bind these receptors ( 40, 41).	bind
38493	4	8779	5	13	NULL	NULL	NULL	4-HPR	Chemical		does not bind					RXRs	GP				NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_20_2_255_s_161	10069462	9- cis-RA binds both RARs and RXRs, while 4-HPR and probably 2-CPR appear not to bind these receptors ( 40, 41).	bind
38494	5	8779	5	13	NULL	NULL	NULL	2-CPR	Chemical		does not bind		probably			RARs	GP				NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_20_2_255_s_161	10069462	9- cis-RA binds both RARs and RXRs, while 4-HPR and probably 2-CPR appear not to bind these receptors ( 40, 41).	bind
38495	6	8779	5	13	NULL	NULL	NULL	2-CPR	Chemical		does not bind		probably			RXRs	GP				NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_20_2_255_s_161	10069462	9- cis-RA binds both RARs and RXRs, while 4-HPR and probably 2-CPR appear not to bind these receptors ( 40, 41).	bind
37483	1	8779	7	NULL	NULL	0	NULL	9- cis-RA	NULL		binds	NULL				RARs	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_2_255_s_161	10069462	9- cis-RA binds both RARs and RXRs, while 4-HPR and probably 2-CPR appear not to bind these receptors ( 40, 41).	bind
37484	2	8779	7	NULL	NULL	0	NULL	9- cis-RA	NULL		binds	NULL				RXRs	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_2_255_s_161	10069462	9- cis-RA binds both RARs and RXRs, while 4-HPR and probably 2-CPR appear not to bind these receptors ( 40, 41).	bind
37485	3	8779	7	NULL	NULL	0	NULL	4-HPR 	NULL		does not bind	NULL				RARs	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_2_255_s_161	10069462	9- cis-RA binds both RARs and RXRs, while 4-HPR and probably 2-CPR appear not to bind these receptors ( 40, 41).	bind
37486	4	8779	7	NULL	NULL	0	NULL	4-HPR	NULL		does not bind	NULL				RXRs	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_2_255_s_161	10069462	9- cis-RA binds both RARs and RXRs, while 4-HPR and probably 2-CPR appear not to bind these receptors ( 40, 41).	bind
37487	5	8779	7	10	NULL	0	NULL	 2-CPR	NULL		does not bind	NULL	probably			RARs	NULL				NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_20_2_255_s_161	10069462	9- cis-RA binds both RARs and RXRs, while 4-HPR and probably 2-CPR appear not to bind these receptors ( 40, 41).	bind
37488	6	8779	7	10	NULL	0	NULL	2-CPR	NULL		does not bind	NULL	probably			RXRs	NULL				NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_20_2_255_s_161	10069462	9- cis-RA binds both RARs and RXRs, while 4-HPR and probably 2-CPR appear not to bind these receptors ( 40, 41).	bind
38496	1	8780	5	13	NULL	NULL	NULL	RXR	GP		bind									RXRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8483_s_160	9525962	9- cis-RA increases binding of RXR to an RXRE.	bind
38497	2	8780	5	13	NULL	NULL	NULL	9- cis-RA	Chemical		increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8483_s_160	9525962	9- cis-RA increases binding of RXR to an RXRE.	bind
37489	1	8780	7	NULL	NULL	0	NULL	 RXR	NULL		bind	NULL					NULL			RXRE	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8483_s_160	9525962	9- cis-RA increases binding of RXR to an RXRE.	bind
37490	2	8780	7	NULL	NULL	0	NULL	9- cis-RA	NULL		increase	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8483_s_160	9525962	9- cis-RA increases binding of RXR to an RXRE.	bind
38499	1	8781	5	13	NULL	NULL	NULL	9- cis-Retinoic acid stereoisomer	Chemical		bind					RXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_7_11_885_s_338	11094341	9- cis-Retinoic acid stereoisomer binds and activates the nuclear receptor RXR .	bind
38500	2	8781	5	13	NULL	NULL	NULL	statement 1	Process		activates					RXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_7_11_885_s_338	11094341	9- cis-Retinoic acid stereoisomer binds and activates the nuclear receptor RXR .	bind
38501	3	8781	5	13	NULL	NULL	NULL	RXR	GP		is a type of					nuclear receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_7_11_885_s_338	11094341	9- cis-Retinoic acid stereoisomer binds and activates the nuclear receptor RXR .	bind
37589	1	8781	7	NULL	NULL	0	NULL	9- cis-Retinoic acid stereoisomer	NULL		binds	NULL				RXR	NULL				NULL		0	NULL	NULL	NULL	gw60_chembiol_7_11_885_s_338	11094341	9- cis-Retinoic acid stereoisomer binds and activates the nuclear receptor RXR .	bind
37590	2	8781	7	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				RXR	NULL				NULL		0	NULL	NULL	NULL	gw60_chembiol_7_11_885_s_338	11094341	9- cis-Retinoic acid stereoisomer binds and activates the nuclear receptor RXR .	bind
37591	3	8781	7	NULL	NULL	0	NULL	RXR	NULL		is a type of	NULL				nuclear receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_chembiol_7_11_885_s_338	11094341	9- cis-Retinoic acid stereoisomer binds and activates the nuclear receptor RXR .	bind
38502	1	8782	5	13	NULL	NULL	NULL	DNA Ligase I	GP		bind					nicked substrates	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_20865_s_139	16731526	9-1-1 Promotes DNA Ligase I Binding to Nicked Substrates --	bind
38503	2	8782	5	13	NULL	NULL	NULL	9-1-1	GP		promotes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_20865_s_139	16731526	9-1-1 Promotes DNA Ligase I Binding to Nicked Substrates --	bind
37592	1	8782	7	NULL	NULL	0	NULL	DNA Ligase I 	NULL		bind	NULL				nicked substrates	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_20865_s_139	16731526	9-1-1 Promotes DNA Ligase I Binding to Nicked Substrates --	bind
46759	2	8782	7	10	NULL	0	NULL	9-1-1	NULL		promotes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_20865_s_139	16731526	9-1-1 Promotes DNA Ligase I Binding to Nicked Substrates --	bind
38507	1	8784	5	13	NULL	NULL	NULL	9-cis retinoic acid stereoisomer	Chemical		bind					RXR	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_68_0_159_s_487	16460270	9-cis retinoic acid stereoisomer binds and activates the nuclear receptor RXR  .	bind
38509	2	8784	5	13	NULL	NULL	NULL	statement 1	Process		activates					RXR	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_68_0_159_s_487	16460270	9-cis retinoic acid stereoisomer binds and activates the nuclear receptor RXR  .	bind
38510	3	8784	5	13	NULL	NULL	NULL	RXR	GP		is a type of					nuclear receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_68_0_159_s_487	16460270	9-cis retinoic acid stereoisomer binds and activates the nuclear receptor RXR  .	bind
38519	1	8788	5	13	NULL	NULL	NULL	estrogen	Chemical		induce					Ov gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_33890_s_140	12107170	900 (Fig.  4), which contains all the sequences necessary for proper induction of the  Ov gene by estrogen and corticosterone ( 9).	bind
38520	2	8788	5	13	NULL	NULL	NULL	corticosterone	Chemical		induce					Ov gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_33890_s_140	12107170	900 (Fig.  4), which contains all the sequences necessary for proper induction of the  Ov gene by estrogen and corticosterone ( 9).	bind
37593	1	8788	7	NULL	NULL	0	NULL	estrogen	NULL		induce	NULL				Ov gene	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_37_33890_s_140	12107170	900 (Fig.  4), which contains all the sequences necessary for proper induction of the  Ov gene by estrogen and corticosterone ( 9).	bind
37594	2	8788	7	NULL	NULL	0	NULL	corticosterone	NULL		induce	NULL				Ov gene	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_37_33890_s_140	12107170	900 (Fig.  4), which contains all the sequences necessary for proper induction of the  Ov gene by estrogen and corticosterone ( 9).	bind
38521	1	8789	5	13	NULL	NULL	NULL	tPA	GP		bind					annexin 2	GP	endothelial			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2146_s_153	14551156	91 Concomitant binding of tPA and plasminogen on endothelial annexin 2 results in a 60-fold increase in catalytic efficiency of plasmin generation.	bind
38522	2	8789	5	13	NULL	NULL	NULL	plasminogen	GP		bind					annexin 2	GP	endothelial			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2146_s_153	14551156	91 Concomitant binding of tPA and plasminogen on endothelial annexin 2 results in a 60-fold increase in catalytic efficiency of plasmin generation.	bind
38524	3	8789	5	13	NULL	NULL	NULL	statement 1	Process		increase					plasmin	GP	catalytic efficiency of;; generation of 			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2146_s_153	14551156	91 Concomitant binding of tPA and plasminogen on endothelial annexin 2 results in a 60-fold increase in catalytic efficiency of plasmin generation.	bind
38526	4	8789	5	13	NULL	NULL	NULL	statement 3	Process		increase					plasmin	GP	catalytic efficiency of;;  generation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2146_s_153	14551156	91 Concomitant binding of tPA and plasminogen on endothelial annexin 2 results in a 60-fold increase in catalytic efficiency of plasmin generation.	bind
37595	1	8789	7	10	NULL	0	NULL	 tPA			bind					annexin 2		endothelial 			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2146_s_153	14551156	91 Concomitant binding of tPA and plasminogen on endothelial annexin 2 results in a 60-fold increase in catalytic efficiency of plasmin generation.	bind
37596	2	8789	7	10	NULL	0	NULL	plasminogen			bind					annexin 2		endothelial 			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2146_s_153	14551156	91 Concomitant binding of tPA and plasminogen on endothelial annexin 2 results in a 60-fold increase in catalytic efficiency of plasmin generation.	bind
37597	3	8789	7	10	NULL	0	NULL	statement 1	NULL		increase	NULL				plasmin	NULL	catalytic efficiency of;;  generation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2146_s_153	14551156	91 Concomitant binding of tPA and plasminogen on endothelial annexin 2 results in a 60-fold increase in catalytic efficiency of plasmin generation.	bind
37598	4	8789	7	10	NULL	0	NULL	statement 2	NULL		increase	NULL				plasmin	NULL	catalytic efficiency of;; generation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_12_2146_s_153	14551156	91 Concomitant binding of tPA and plasminogen on endothelial annexin 2 results in a 60-fold increase in catalytic efficiency of plasmin generation.	bind
38529	1	8790	5	13	NULL	NULL	NULL	5''-S DNA	NucleicAcid		bind		covalently						R130K/K167A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_8_5711_s_81	11756402	91% of the input 5''-S DNA was bound covalently by R130K/K167A, and the apparent  kcl of 4.3 x 10 3 s 1 was within a factor of 3 of that of the single K167A mutant on the 5''-S substrate.	bind
37599	1	8790	7	NULL	NULL	0	NULL		NULL		bind	NULL	covalently	 R130K/K167A		5''-S DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_8_5711_s_81	11756402	91% of the input 5''-S DNA was bound covalently by R130K/K167A, and the apparent  kcl of 4.3 x 10 3 s 1 was within a factor of 3 of that of the single K167A mutant on the 5''-S substrate.	bind
38531	1	8791	5	13	NULL	NULL	NULL	c- fos	GP		bind					c- jun	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_8_1882_s_84	10938007	92  AP-1 is a heterodimer of c- fos and c- jun that binds to AP-1 consensus sequences and activates genes related to cell proliferation, migration, apoptosis, and ECM production.	bind
38532	2	8791	5	13	NULL	NULL	NULL	AP-1	GP		is a heterodimer of					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_8_1882_s_84	10938007	92  AP-1 is a heterodimer of c- fos and c- jun that binds to AP-1 consensus sequences and activates genes related to cell proliferation, migration, apoptosis, and ECM production.	bind
38533	3	8791	5	13	NULL	NULL	NULL	AP-1	GP		bind									AP-1 consensus sequences	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_8_1882_s_84	10938007	92  AP-1 is a heterodimer of c- fos and c- jun that binds to AP-1 consensus sequences and activates genes related to cell proliferation, migration, apoptosis, and ECM production.	bind
38535	4	8791	5	13	NULL	NULL	NULL	statement 3	GP		activates					\tcell proliferation genes	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_8_1882_s_84	10938007	92  AP-1 is a heterodimer of c- fos and c- jun that binds to AP-1 consensus sequences and activates genes related to cell proliferation, migration, apoptosis, and ECM production.	bind
38536	5	8791	5	13	NULL	NULL	NULL	statement 3	GP		activates					cell migration genes	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_8_1882_s_84	10938007	92  AP-1 is a heterodimer of c- fos and c- jun that binds to AP-1 consensus sequences and activates genes related to cell proliferation, migration, apoptosis, and ECM production.	bind
38537	6	8791	5	13	NULL	NULL	NULL	statement 3	GP		activates					cell apoptosis genes	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_8_1882_s_84	10938007	92  AP-1 is a heterodimer of c- fos and c- jun that binds to AP-1 consensus sequences and activates genes related to cell proliferation, migration, apoptosis, and ECM production.	bind
38538	7	8791	5	13	NULL	NULL	NULL	statement 3	GP		activates					ECM	GP	production of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_8_1882_s_84	10938007	92  AP-1 is a heterodimer of c- fos and c- jun that binds to AP-1 consensus sequences and activates genes related to cell proliferation, migration, apoptosis, and ECM production.	bind
37650	1	8791	7	10	NULL	0	NULL	c-fos			bind					c-jun					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_8_1882_s_84	10938007	92  AP-1 is a heterodimer of c- fos and c- jun that binds to AP-1 consensus sequences and activates genes related to cell proliferation, migration, apoptosis, and ECM production.	bind
37651	3	8791	7	10	NULL	0	NULL	AP-1			bind									AP-1 consensus sequences	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_8_1882_s_84	10938007	92  AP-1 is a heterodimer of c- fos and c- jun that binds to AP-1 consensus sequences and activates genes related to cell proliferation, migration, apoptosis, and ECM production.	bind
37652	4	8791	7	10	NULL	0	NULL	statement 2			activates					cell proliferation genes					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_8_1882_s_84	10938007	92  AP-1 is a heterodimer of c- fos and c- jun that binds to AP-1 consensus sequences and activates genes related to cell proliferation, migration, apoptosis, and ECM production.	bind
37653	7	8791	7	10	NULL	0	NULL	statement 2			activates					cell migration genes					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_8_1882_s_84	10938007	92  AP-1 is a heterodimer of c- fos and c- jun that binds to AP-1 consensus sequences and activates genes related to cell proliferation, migration, apoptosis, and ECM production.	bind
37654	5	8791	7	NULL	NULL	0	NULL	statement 2	NULL		activates	NULL				cell apoptosis genes	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_8_1882_s_84	10938007	92  AP-1 is a heterodimer of c- fos and c- jun that binds to AP-1 consensus sequences and activates genes related to cell proliferation, migration, apoptosis, and ECM production.	bind
37655	6	8791	7	NULL	NULL	0	NULL	statement 2	NULL		activates	NULL				ECM	NULL	production of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_8_1882_s_84	10938007	92  AP-1 is a heterodimer of c- fos and c- jun that binds to AP-1 consensus sequences and activates genes related to cell proliferation, migration, apoptosis, and ECM production.	bind
56463	2	8791	7	10	NULL	0	NULL	AP-1			is a heterodimer of					statement 1					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_8_1882_s_84	10938007	92  AP-1 is a heterodimer of c- fos and c- jun that binds to AP-1 consensus sequences and activates genes related to cell proliferation, migration, apoptosis, and ECM production.	bind
38547	1	8792	5	13	NULL	NULL	NULL	TSP-1	GP		bind					CD36 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_887_s_148	12067894	92 Binding of TSP-1 to CD36 receptor leads to the recruitment of the Src-related kinase, p59-fyn, and to activation of p38 MAPK.	bind
38549	2	8792	5	13	NULL	NULL	NULL	statement 1	Process		leads to					p59-fyn	GP	recruitment of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_887_s_148	12067894	92 Binding of TSP-1 to CD36 receptor leads to the recruitment of the Src-related kinase, p59-fyn, and to activation of p38 MAPK.	bind
38551	3	8792	5	13	NULL	NULL	NULL	p59-fyn	GP		is a type of					Src-related kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_887_s_148	12067894	92 Binding of TSP-1 to CD36 receptor leads to the recruitment of the Src-related kinase, p59-fyn, and to activation of p38 MAPK.	bind
38552	4	8792	5	13	NULL	NULL	NULL	statement 1	Process		leads to					p38 MAPK	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_887_s_148	12067894	92 Binding of TSP-1 to CD36 receptor leads to the recruitment of the Src-related kinase, p59-fyn, and to activation of p38 MAPK.	bind
37656	1	8792	7	NULL	NULL	0	NULL	TSP-1	NULL		bind	NULL				CD36 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_887_s_148	12067894	92 Binding of TSP-1 to CD36 receptor leads to the recruitment of the Src-related kinase, p59-fyn, and to activation of p38 MAPK.	bind
37657	2	8792	7	10	NULL	0	NULL	p59-fyn			is a type of					Src-related kinase					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_887_s_148	12067894	92 Binding of TSP-1 to CD36 receptor leads to the recruitment of the Src-related kinase, p59-fyn, and to activation of p38 MAPK.	bind
37658	3	8792	7	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				p59-fyn	NULL	recruitment of 			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_887_s_148	12067894	92 Binding of TSP-1 to CD36 receptor leads to the recruitment of the Src-related kinase, p59-fyn, and to activation of p38 MAPK.	bind
37659	4	8792	7	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				p38 MAPK	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_6_887_s_148	12067894	92 Binding of TSP-1 to CD36 receptor leads to the recruitment of the Src-related kinase, p59-fyn, and to activation of p38 MAPK.	bind
38554	1	8793	5	13	NULL	NULL	NULL	5''-S DNA	NucleicAcid		bind		covalently						R130K		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_8_5711_s_69	11756402	93% of the input 5''-S DNA was bound covalently by R130K, and the apparent  kcl was 3.7 x 10 2 s 1.	bind
37660	1	8793	7	NULL	NULL	0	NULL		NULL		bind	NULL	covalently	R130K		5''-S DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_8_5711_s_69	11756402	93% of the input 5''-S DNA was bound covalently by R130K, and the apparent  kcl was 3.7 x 10 2 s 1.	bind
38555	1	8794	5	13	NULL	NULL	NULL	Wnt molecules	GP		bind					Fz receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_10_1055_s_150	12039794	94, 95 Binding of the Wnt molecules to Fz receptors activates Dvl, which inhibits the activity of GSK-3beta,  96 thereby stabilizing beta-catenin.	bind
38556	2	8794	5	13	NULL	NULL	NULL	statement 1	Process		activates					Dvl	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_10_1055_s_150	12039794	94, 95 Binding of the Wnt molecules to Fz receptors activates Dvl, which inhibits the activity of GSK-3beta,  96 thereby stabilizing beta-catenin.	bind
38557	3	8794	5	13	NULL	NULL	NULL	statement 2	Process		inhibit					GSK-3beta	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_10_1055_s_150	12039794	94, 95 Binding of the Wnt molecules to Fz receptors activates Dvl, which inhibits the activity of GSK-3beta,  96 thereby stabilizing beta-catenin.	bind
38558	4	8794	5	13	NULL	NULL	NULL	statement 3	Process		stabilize					beta-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_10_1055_s_150	12039794	94, 95 Binding of the Wnt molecules to Fz receptors activates Dvl, which inhibits the activity of GSK-3beta,  96 thereby stabilizing beta-catenin.	bind
37661	1	8794	7	NULL	NULL	0	NULL	Wnt molecules	NULL		bind	NULL				Fz receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_10_1055_s_150	12039794	94, 95 Binding of the Wnt molecules to Fz receptors activates Dvl, which inhibits the activity of GSK-3beta,  96 thereby stabilizing beta-catenin.	bind
37662	2	8794	7	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				Dvl	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_10_1055_s_150	12039794	94, 95 Binding of the Wnt molecules to Fz receptors activates Dvl, which inhibits the activity of GSK-3beta,  96 thereby stabilizing beta-catenin.	bind
37663	3	8794	7	NULL	NULL	0	NULL	statement 2	NULL		inhibits	NULL				GSK-3beta	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_circulationres_90_10_1055_s_150	12039794	94, 95 Binding of the Wnt molecules to Fz receptors activates Dvl, which inhibits the activity of GSK-3beta,  96 thereby stabilizing beta-catenin.	bind
37664	4	8794	7	NULL	NULL	0	NULL	statement 3	NULL		stabilize	NULL				beta-catenin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_10_1055_s_150	12039794	94, 95 Binding of the Wnt molecules to Fz receptors activates Dvl, which inhibits the activity of GSK-3beta,  96 thereby stabilizing beta-catenin.	bind
38559	1	8795	5	13	NULL	NULL	NULL	95 kd sperm proteins	GP		bind					ZP3	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_85_5_629_s_136	8646772	95 kd sperm proteins bind ZP3 and serve as tyrosine kinase substrates in response to zona binding.	bind
38561	2	8795	5	13	NULL	NULL	NULL	statement 1	GP		serve as					tyrosine kinase substrates	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_85_5_629_s_136	8646772	95 kd sperm proteins bind ZP3 and serve as tyrosine kinase substrates in response to zona binding.	bind
38563	3	8795	5	13	NULL	NULL	NULL	statement 2	GP		in response to					zona	CellComponent	binding of			NULL		NULL	NULL	NULL	NULL	gw60_cell_85_5_629_s_136	8646772	95 kd sperm proteins bind ZP3 and serve as tyrosine kinase substrates in response to zona binding.	bind
37665	1	8795	7	NULL	NULL	0	NULL	sperm proteins	NULL		bind	NULL				ZP3	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_85_5_629_s_136	8646772	95 kd sperm proteins bind ZP3 and serve as tyrosine kinase substrates in response to zona binding.	bind
37666	2	8795	7	NULL	NULL	0	NULL	statement 1	NULL		serve as	NULL				tyrosine kinase substrates	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_85_5_629_s_136	8646772	95 kd sperm proteins bind ZP3 and serve as tyrosine kinase substrates in response to zona binding.	bind
37667	3	8795	7	NULL	NULL	0	NULL	statement 2	NULL		in response to	NULL				zona	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_cell_85_5_629_s_136	8646772	95 kd sperm proteins bind ZP3 and serve as tyrosine kinase substrates in response to zona binding.	bind
38565	1	8796	5	13	NULL	NULL	NULL	NGF	GP		bind					p75	GP		NTR		NULL	cell lines	NULL	NULL	NULL	NULL	gw60_neuroscience_81_3_861_s_68	9316034	9651 effectively reduces NGF binding to p75NTR on cell lines and on primary rat sympathetic neurons.	bind
38566	2	8796	5	13	NULL	NULL	NULL	NGF	GP		bind					p75	GP		NTR		NULL	primary rat sympathetic neurons	NULL	NULL	NULL	NULL	gw60_neuroscience_81_3_861_s_68	9316034	9651 effectively reduces NGF binding to p75NTR on cell lines and on primary rat sympathetic neurons.	bind
37668	1	8796	7	NULL	NULL	0	NULL	NGF	NULL		bind	NULL				p75	NULL		NTR		NULL	cell lines	0	NULL	NULL	NULL	gw60_neuroscience_81_3_861_s_68	9316034	9651 effectively reduces NGF binding to p75NTR on cell lines and on primary rat sympathetic neurons.	bind
37669	2	8796	7	NULL	NULL	0	NULL	NGF	NULL		bind	NULL				p75	NULL		NTR		NULL	primary rat sympathetic neurons	0	NULL	NULL	NULL	gw60_neuroscience_81_3_861_s_68	9316034	9651 effectively reduces NGF binding to p75NTR on cell lines and on primary rat sympathetic neurons.	bind
38572	1	8797	5	13	NULL	NULL	NULL	nerve growth factor	GP		bind					p75 neurotrophin receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_81_3_861_s_54	9316034	9651 serum and purified 9651 IgG effectively reduce nerve growth factor binding to p75 neurotrophin receptor	bind
38573	2	8797	5	13	NULL	NULL	NULL	9651 serum	OrganismPart		reduces		effectively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_81_3_861_s_54	9316034	9651 serum and purified 9651 IgG effectively reduce nerve growth factor binding to p75 neurotrophin receptor	bind
38574	3	8797	5	13	NULL	NULL	NULL	9651 IgG	GP	purified	reduces		effectively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_81_3_861_s_54	9316034	9651 serum and purified 9651 IgG effectively reduce nerve growth factor binding to p75 neurotrophin receptor	bind
37670	1	8797	7	NULL	NULL	0	NULL	 nerve growth factor	NULL		bind	NULL				p75 neurotrophin receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_neuroscience_81_3_861_s_54	9316034	9651 serum and purified 9651 IgG effectively reduce nerve growth factor binding to p75 neurotrophin receptor	bind
37671	2	8797	7	NULL	NULL	0	NULL	 9651 serum	NULL		reduce	NULL	effectively			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_neuroscience_81_3_861_s_54	9316034	9651 serum and purified 9651 IgG effectively reduce nerve growth factor binding to p75 neurotrophin receptor	bind
37672	3	8797	7	NULL	NULL	0	NULL	9651 IgG	NULL	purified	reduce	NULL	effectively			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_neuroscience_81_3_861_s_54	9316034	9651 serum and purified 9651 IgG effectively reduce nerve growth factor binding to p75 neurotrophin receptor	bind
38575	1	8798	5	13	NULL	NULL	NULL	E-cadherin	GP		bind					cell	Cell				NULL		NULL	NULL	NULL	NULL	gw70_nature_428_6986_950_s_262	15057245	98, 25A (1991)                               Nagafuchi, A. & Takeichi, M. Cell binding function of E-cadherin is regulated  by the cytoplasmic domain.	bind
46760	1	8798	5	13	NULL	NULL	NULL	E-cadherin	GP		regulates			cytoplasmic domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_nature_428_6986_950_s_262	15057245	98, 25A (1991)                               Nagafuchi, A. & Takeichi, M. Cell binding function of E-cadherin is regulated  by the cytoplasmic domain.	bind
37673	1	8798	7	NULL	NULL	0	NULL	E-cadherin	NULL		bind	NULL				Cell	NULL				NULL		0	NULL	NULL	NULL	gw70_nature_428_6986_950_s_262	15057245	98, 25A (1991)                               Nagafuchi, A. & Takeichi, M. Cell binding function of E-cadherin is regulated  by the cytoplasmic domain.	bind
37674	2	8798	7	10	NULL	0	NULL	E-cadherin	NULL		regulates	NULL		cytoplasmic domain		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_nature_428_6986_950_s_262	15057245	98, 25A (1991)                               Nagafuchi, A. & Takeichi, M. Cell binding function of E-cadherin is regulated  by the cytoplasmic domain.	bind
38576	1	8799	5	13	NULL	NULL	NULL	thrombin	GP		bind					subendothelial matrix proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_24_2994_s_171	11413093	99 100  Thrombin also binds to subendothelial matrix proteins, where it is protected from inhibition by heparin.	bind
38577	2	8799	5	13	NULL	NULL	NULL	heparin	Chemical		inhibits					thrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_24_2994_s_171	11413093	99 100  Thrombin also binds to subendothelial matrix proteins, where it is protected from inhibition by heparin.	bind
46761	3	8799	5	13	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process	protection of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_24_2994_s_171	11413093	99 100  Thrombin also binds to subendothelial matrix proteins, where it is protected from inhibition by heparin.	bind
37675	1	8799	7	NULL	NULL	0	NULL	Thrombin	NULL		binds to	NULL				subendothelial matrix proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_24_2994_s_171	11413093	99 100  Thrombin also binds to subendothelial matrix proteins, where it is protected from inhibition by heparin.	bind
37676	2	8799	7	NULL	NULL	0	NULL	heparin	NULL		inhibits	NULL				thrombin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_103_24_2994_s_171	11413093	99 100  Thrombin also binds to subendothelial matrix proteins, where it is protected from inhibition by heparin.	bind
37677	3	8799	7	10	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 2	NULL	protection of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_103_24_2994_s_171	11413093	99 100  Thrombin also binds to subendothelial matrix proteins, where it is protected from inhibition by heparin.	bind
38578	1	8800	5	13	NULL	NULL	NULL	GPVI	GP		bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_134	15466473	9E18 reduced the binding of GPVI to collagen by 45%, reduced the binding of GPVI to CRP by 85%, but had little effect on binding to convulxin (25% inhibition).	bind
38579	2	8800	5	13	NULL	NULL	NULL	9E18	GP		reduce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_134	15466473	9E18 reduced the binding of GPVI to collagen by 45%, reduced the binding of GPVI to CRP by 85%, but had little effect on binding to convulxin (25% inhibition).	bind
38580	3	8800	5	13	NULL	NULL	NULL	GPVI	GP		bind					CRP	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_134	15466473	9E18 reduced the binding of GPVI to collagen by 45%, reduced the binding of GPVI to CRP by 85%, but had little effect on binding to convulxin (25% inhibition).	bind
38581	4	8800	5	13	NULL	NULL	NULL	9E18	GP		reduce					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_134	15466473	9E18 reduced the binding of GPVI to collagen by 45%, reduced the binding of GPVI to CRP by 85%, but had little effect on binding to convulxin (25% inhibition).	bind
38582	5	8800	5	13	NULL	NULL	NULL	GPVI	GP		bind					convulxin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_134	15466473	9E18 reduced the binding of GPVI to collagen by 45%, reduced the binding of GPVI to CRP by 85%, but had little effect on binding to convulxin (25% inhibition).	bind
38583	6	8800	5	13	NULL	NULL	NULL	9E18	GP		has effect on		little			statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_134	15466473	9E18 reduced the binding of GPVI to collagen by 45%, reduced the binding of GPVI to CRP by 85%, but had little effect on binding to convulxin (25% inhibition).	bind
37678	1	8800	7	NULL	NULL	0	NULL	GPVI	NULL		bind	NULL				collagen	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_134	15466473	9E18 reduced the binding of GPVI to collagen by 45%, reduced the binding of GPVI to CRP by 85%, but had little effect on binding to convulxin (25% inhibition).	bind
37679	2	8800	7	NULL	NULL	0	NULL	9E18	NULL		reduce	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_134	15466473	9E18 reduced the binding of GPVI to collagen by 45%, reduced the binding of GPVI to CRP by 85%, but had little effect on binding to convulxin (25% inhibition).	bind
37680	3	8800	7	NULL	NULL	0	NULL	GPVI	NULL		bind	NULL				CRP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_134	15466473	9E18 reduced the binding of GPVI to collagen by 45%, reduced the binding of GPVI to CRP by 85%, but had little effect on binding to convulxin (25% inhibition).	bind
37681	4	8800	7	NULL	NULL	0	NULL	9E18	NULL		reduce	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_134	15466473	9E18 reduced the binding of GPVI to collagen by 45%, reduced the binding of GPVI to CRP by 85%, but had little effect on binding to convulxin (25% inhibition).	bind
37682	5	8800	7	NULL	NULL	0	NULL	GPVI	NULL		bind	NULL				convulxin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_134	15466473	9E18 reduced the binding of GPVI to collagen by 45%, reduced the binding of GPVI to CRP by 85%, but had little effect on binding to convulxin (25% inhibition).	bind
37683	6	8800	7	10	NULL	0	NULL	9E18	NULL		effect on	NULL	little			statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_50_52293_s_134	15466473	9E18 reduced the binding of GPVI to collagen by 45%, reduced the binding of GPVI to CRP by 85%, but had little effect on binding to convulxin (25% inhibition).	bind
29315	1	8801	6	13	NULL	NULL	NULL	9G8	GP		bind					BSE	GP		Pu1 motif		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7347_s_230	10523623	9G8 binds to the first part of the BSE (Pu1 motif) and stabilizes the binding of the U1 snRNP at the 5' splice site, either directly by interaction with one component of the U1 snRNP or indirectly.	bind
29316	2	8801	6	13	NULL	NULL	NULL	U1 snRNP	GP		bind									5' splice site	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7347_s_230	10523623	9G8 binds to the first part of the BSE (Pu1 motif) and stabilizes the binding of the U1 snRNP at the 5' splice site, either directly by interaction with one component of the U1 snRNP or indirectly.	bind
47529	3	8801	6	13	NULL	NULL	NULL	statement 1	GP		stabilizes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7347_s_230	10523623	9G8 binds to the first part of the BSE (Pu1 motif) and stabilizes the binding of the U1 snRNP at the 5' splice site, either directly by interaction with one component of the U1 snRNP or indirectly.	bind
56160	4	8801	6	13	NULL	NULL	NULL	statement 1	GP		interacts with					U1 snRNP	GP	component of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7347_s_230	10523623	9G8 binds to the first part of the BSE (Pu1 motif) and stabilizes the binding of the U1 snRNP at the 5' splice site, either directly by interaction with one component of the U1 snRNP or indirectly.	bind
56161	5	8801	6	13	NULL	NULL	NULL	statement 1	GP		via		directly			statement 4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7347_s_230	10523623	9G8 binds to the first part of the BSE (Pu1 motif) and stabilizes the binding of the U1 snRNP at the 5' splice site, either directly by interaction with one component of the U1 snRNP or indirectly.	bind
56162	6	8801	6	13	NULL	NULL	NULL	statement 1	GP		via		indirectly			statement 4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7347_s_230	10523623	9G8 binds to the first part of the BSE (Pu1 motif) and stabilizes the binding of the U1 snRNP at the 5' splice site, either directly by interaction with one component of the U1 snRNP or indirectly.	bind
56163	7	8801	6	13	NULL	NULL	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7347_s_230	10523623	9G8 binds to the first part of the BSE (Pu1 motif) and stabilizes the binding of the U1 snRNP at the 5' splice site, either directly by interaction with one component of the U1 snRNP or indirectly.	bind
37684	1	8801	7	NULL	NULL	0	NULL	9G8	NULL		binds to	NULL				BSE	NULL		Pu1 motif		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_11_7347_s_230	10523623	9G8 binds to the first part of the BSE (Pu1 motif) and stabilizes the binding of the U1 snRNP at the 5' splice site, either directly by interaction with one component of the U1 snRNP or indirectly.	bind
37685	3	8801	7	NULL	NULL	0	NULL	statement 1	NULL		interacts with	NULL				U1 snRNP	NULL	component of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7347_s_230	10523623	9G8 binds to the first part of the BSE (Pu1 motif) and stabilizes the binding of the U1 snRNP at the 5' splice site, either directly by interaction with one component of the U1 snRNP or indirectly.	bind
37686	2	8801	7	10	NULL	0	NULL	statement 1			stabilizes					statement 7					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7347_s_230	10523623	9G8 binds to the first part of the BSE (Pu1 motif) and stabilizes the binding of the U1 snRNP at the 5' splice site, either directly by interaction with one component of the U1 snRNP or indirectly.	bind
37689	4	8801	7	NULL	NULL	0	NULL	statement 1	NULL		occur via	NULL	directly			statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7347_s_230	10523623	9G8 binds to the first part of the BSE (Pu1 motif) and stabilizes the binding of the U1 snRNP at the 5' splice site, either directly by interaction with one component of the U1 snRNP or indirectly.	bind
47531	5	8801	7	NULL	NULL	0	NULL	statement 1	NULL		occur via	NULL	indirectly			statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_11_7347_s_230	10523623	9G8 binds to the first part of the BSE (Pu1 motif) and stabilizes the binding of the U1 snRNP at the 5' splice site, either directly by interaction with one component of the U1 snRNP or indirectly.	bind
47532	6	8801	7	NULL	NULL	0	NULL	statement 4	NULL		is an alternative to	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_11_7347_s_230	10523623	9G8 binds to the first part of the BSE (Pu1 motif) and stabilizes the binding of the U1 snRNP at the 5' splice site, either directly by interaction with one component of the U1 snRNP or indirectly.	bind
56159	7	8801	7	10	NULL	0	NULL	U1 snRNP			bind									5' splice site	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_11_7347_s_230	10523623	9G8 binds to the first part of the BSE (Pu1 motif) and stabilizes the binding of the U1 snRNP at the 5' splice site, either directly by interaction with one component of the U1 snRNP or indirectly.	bind
29317	1	8802	6	13	NULL	NULL	NULL	9G8	GP		bind					E34	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_1_401_s_172	16249178	9G8 bound to E34 and E3D RNA probes in the presence of the S100 extract and/or Tra2alpha.	bind
29318	2	8802	6	13	NULL	NULL	NULL	9G8	GP		bind					E3D RNA probes	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_1_401_s_172	16249178	9G8 bound to E34 and E3D RNA probes in the presence of the S100 extract and/or Tra2alpha.	bind
29319	3	8802	6	13	NULL	NULL	NULL	statement 1	Process		occurs in presence of					S100 extract	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_1_401_s_172	16249178	9G8 bound to E34 and E3D RNA probes in the presence of the S100 extract and/or Tra2alpha.	bind
29320	4	8802	6	13	NULL	NULL	NULL	statement 1	Process		occurs in presence of					Tra2alpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_1_401_s_172	16249178	9G8 bound to E34 and E3D RNA probes in the presence of the S100 extract and/or Tra2alpha.	bind
29321	5	8802	6	13	NULL	NULL	NULL	statement 2	Process		occurs in presence of					S100 extract	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_1_401_s_172	16249178	9G8 bound to E34 and E3D RNA probes in the presence of the S100 extract and/or Tra2alpha.	bind
29322	6	8802	6	13	NULL	NULL	NULL	statement 2	Process		occurs in presence of					Tra2alpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_1_401_s_172	16249178	9G8 bound to E34 and E3D RNA probes in the presence of the S100 extract and/or Tra2alpha.	bind
37690	1	8802	7	NULL	NULL	0	NULL	9G8	NULL		bind	NULL				E34 RNA probe	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_401_s_172	16249178	9G8 bound to E34 and E3D RNA probes in the presence of the S100 extract and/or Tra2alpha.	bind
37691	2	8802	7	NULL	NULL	0	NULL	9G8	NULL		bind	NULL				E3D RNA probe	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_401_s_172	16249178	9G8 bound to E34 and E3D RNA probes in the presence of the S100 extract and/or Tra2alpha.	bind
37692	3	8802	7	NULL	NULL	0	NULL	statement 1	NULL		in presence of	NULL				S100 extract	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_401_s_172	16249178	9G8 bound to E34 and E3D RNA probes in the presence of the S100 extract and/or Tra2alpha.	bind
37693	4	8802	7	NULL	NULL	0	NULL	statement 2	NULL		in presence of	NULL				S100 extract	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_401_s_172	16249178	9G8 bound to E34 and E3D RNA probes in the presence of the S100 extract and/or Tra2alpha.	bind
37694	5	8802	7	NULL	NULL	0	NULL	statement 1	NULL		in presence of	NULL				Tra2alpha	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_401_s_172	16249178	9G8 bound to E34 and E3D RNA probes in the presence of the S100 extract and/or Tra2alpha.	bind
37695	6	8802	7	NULL	NULL	0	NULL	statement 2	NULL		in presence of	NULL				Tra2alpha	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_401_s_172	16249178	9G8 bound to E34 and E3D RNA probes in the presence of the S100 extract and/or Tra2alpha.	bind
29323	1	8803	6	13	NULL	NULL	NULL	9G8	GP		bind					E3 RNA probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_1_401_s_158	16249178	9G8 bound to the E3 RNA probe only in the presence of S100 extract ( Fig. 3 B).	bind
29324	2	8803	6	13	NULL	NULL	NULL	statement 1	Process		occurs in presence of					S100 extract	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_1_401_s_158	16249178	9G8 bound to the E3 RNA probe only in the presence of S100 extract ( Fig. 3 B).	bind
37696	1	8803	7	NULL	NULL	0	NULL	9G8	NULL		bind	NULL				E3 RNA probe	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_401_s_158	16249178	9G8 bound to the E3 RNA probe only in the presence of S100 extract ( Fig. 3 B).	bind
37697	2	8803	7	NULL	NULL	0	NULL	statement 1	NULL		in presence of	NULL				S100 extract	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_401_s_158	16249178	9G8 bound to the E3 RNA probe only in the presence of S100 extract ( Fig. 3 B).	bind
29598	1	8804	6	13	NULL	NULL	NULL	9G8	GP		activates 					exon carrying v9b6-5-4 -- 9G8	NucleicAcid	splicing of;; heterologus			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_264	12826680	9G8, ASF/SF2, and SRp20 Activate Splicing in Vitro of a Heterologous  Exon Carrying v9b6-5-4  -- 9G8, ASF/SF2, and SRp20 bind to v9 exon  sequences, but will this binding activate splicing?	bind
29599	2	8804	6	13	NULL	NULL	NULL	ASF/SF2	GP		activates 					exon carrying ASF/SF2	NucleicAcid	splicing of;; heterologous			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_264	12826680	9G8, ASF/SF2, and SRp20 Activate Splicing in Vitro of a Heterologous  Exon Carrying v9b6-5-4  -- 9G8, ASF/SF2, and SRp20 bind to v9 exon  sequences, but will this binding activate splicing?	bind
29600	3	8804	6	13	NULL	NULL	NULL	SRp20	GP		activates					exon carrying SRp20	NucleicAcid	splicing of;; heterologous			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_264	12826680	9G8, ASF/SF2, and SRp20 Activate Splicing in Vitro of a Heterologous  Exon Carrying v9b6-5-4  -- 9G8, ASF/SF2, and SRp20 bind to v9 exon  sequences, but will this binding activate splicing?	bind
47094	4	8804	6	13	NULL	NULL	NULL	9G8	GP		bind					v9 exon sequences	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_264	12826680	9G8, ASF/SF2, and SRp20 Activate Splicing in Vitro of a Heterologous  Exon Carrying v9b6-5-4  -- 9G8, ASF/SF2, and SRp20 bind to v9 exon  sequences, but will this binding activate splicing?	bind
47095	5	8804	6	13	NULL	NULL	NULL	ASF/SF2	GP		bind					v9 exon sequences	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_264	12826680	9G8, ASF/SF2, and SRp20 Activate Splicing in Vitro of a Heterologous  Exon Carrying v9b6-5-4  -- 9G8, ASF/SF2, and SRp20 bind to v9 exon  sequences, but will this binding activate splicing?	bind
47096	6	8804	6	13	NULL	NULL	NULL	SRp20	GP		bind					v9 exon sequences	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_264	12826680	9G8, ASF/SF2, and SRp20 Activate Splicing in Vitro of a Heterologous  Exon Carrying v9b6-5-4  -- 9G8, ASF/SF2, and SRp20 bind to v9 exon  sequences, but will this binding activate splicing?	bind
37698	1	8804	7	10	NULL	0	NULL	9G8	NULL		activate	NULL				 Exon Carrying v9b6-5-4 -- 9G8	NULL	splicing of;;Heterologous			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_264	12826680	9G8, ASF/SF2, and SRp20 Activate Splicing in Vitro of a Heterologous  Exon Carrying v9b6-5-4  -- 9G8, ASF/SF2, and SRp20 bind to v9 exon  sequences, but will this binding activate splicing?	bind
37699	2	8804	7	10	NULL	0	NULL	ASF/SF2	NULL		activate	NULL				Exon Carrying v9b6-5-4 -- 9G8	NULL	splicing of;;Heterologous			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_264	12826680	9G8, ASF/SF2, and SRp20 Activate Splicing in Vitro of a Heterologous  Exon Carrying v9b6-5-4  -- 9G8, ASF/SF2, and SRp20 bind to v9 exon  sequences, but will this binding activate splicing?	bind
37700	3	8804	7	10	NULL	0	NULL	SRp20	NULL		activate	NULL				 Exon Carrying v9b6-5-4 -- 9G8	NULL	splicing of;;Heterologous			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_264	12826680	9G8, ASF/SF2, and SRp20 Activate Splicing in Vitro of a Heterologous  Exon Carrying v9b6-5-4  -- 9G8, ASF/SF2, and SRp20 bind to v9 exon  sequences, but will this binding activate splicing?	bind
37701	4	8804	7	NULL	NULL	0	NULL	9G8	NULL		bind	NULL					NULL			v9 exon sequence	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_264	12826680	9G8, ASF/SF2, and SRp20 Activate Splicing in Vitro of a Heterologous  Exon Carrying v9b6-5-4  -- 9G8, ASF/SF2, and SRp20 bind to v9 exon  sequences, but will this binding activate splicing?	bind
37702	5	8804	7	NULL	NULL	0	NULL	ASF/SF2	NULL		bind	NULL					NULL			v9 exon sequence	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_264	12826680	9G8, ASF/SF2, and SRp20 Activate Splicing in Vitro of a Heterologous  Exon Carrying v9b6-5-4  -- 9G8, ASF/SF2, and SRp20 bind to v9 exon  sequences, but will this binding activate splicing?	bind
37703	6	8804	7	NULL	NULL	0	NULL	SRp20	NULL		bind	NULL					NULL			v9 exon sequence	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_264	12826680	9G8, ASF/SF2, and SRp20 Activate Splicing in Vitro of a Heterologous  Exon Carrying v9b6-5-4  -- 9G8, ASF/SF2, and SRp20 bind to v9 exon  sequences, but will this binding activate splicing?	bind
47538	7	8804	7	NULL	NULL	0	NULL	9G8	NULL		activate	NULL				exon carrying ASF/SF2	NULL	splicing of;;Heterologous			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_264	12826680	9G8, ASF/SF2, and SRp20 Activate Splicing in Vitro of a Heterologous  Exon Carrying v9b6-5-4  -- 9G8, ASF/SF2, and SRp20 bind to v9 exon  sequences, but will this binding activate splicing?	bind
47539	8	8804	7	NULL	NULL	0	NULL	ASF/SF2	NULL		activate	NULL				exon carrying ASF/SF2	NULL	splicing of;;Heterologous			NULL	in vitro	0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_264	12826680	9G8, ASF/SF2, and SRp20 Activate Splicing in Vitro of a Heterologous  Exon Carrying v9b6-5-4  -- 9G8, ASF/SF2, and SRp20 bind to v9 exon  sequences, but will this binding activate splicing?	bind
47540	9	8804	7	NULL	NULL	0	NULL	SRp20	NULL		activate	NULL				exon carrying ASF/SF2	NULL	splicing of;;Heterologous			NULL	in vitro	0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_264	12826680	9G8, ASF/SF2, and SRp20 Activate Splicing in Vitro of a Heterologous  Exon Carrying v9b6-5-4  -- 9G8, ASF/SF2, and SRp20 bind to v9 exon  sequences, but will this binding activate splicing?	bind
47541	10	8804	7	NULL	NULL	0	NULL	9G8	NULL		activate	NULL				exon carrying SRp20	NULL	splicing of;;Heterologous			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_264	12826680	9G8, ASF/SF2, and SRp20 Activate Splicing in Vitro of a Heterologous  Exon Carrying v9b6-5-4  -- 9G8, ASF/SF2, and SRp20 bind to v9 exon  sequences, but will this binding activate splicing?	bind
47542	11	8804	7	NULL	NULL	0	NULL	ASF/SF2	NULL		activate	NULL				exon carrying SRp20	NULL	splicing of;;Heterologous			NULL	in vitro	0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_264	12826680	9G8, ASF/SF2, and SRp20 Activate Splicing in Vitro of a Heterologous  Exon Carrying v9b6-5-4  -- 9G8, ASF/SF2, and SRp20 bind to v9 exon  sequences, but will this binding activate splicing?	bind
47543	12	8804	7	NULL	NULL	0	NULL	 SRp20	NULL		activate	NULL				exon carrying SRp20	NULL	splicing of;;Heterologous			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_264	12826680	9G8, ASF/SF2, and SRp20 Activate Splicing in Vitro of a Heterologous  Exon Carrying v9b6-5-4  -- 9G8, ASF/SF2, and SRp20 bind to v9 exon  sequences, but will this binding activate splicing?	bind
29325	1	8805	6	13	NULL	NULL	NULL	Tdp-ICL	NucleicAcid		bind					XPC-hHR23B	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_9_2993_s_157	15914671	: RPA-Tdp-ICL super-shifted complex also migrated at the same position as when Tdp-ICL  was bound by XPC-hHR23B.	bind
37704	1	8805	7	NULL	NULL	0	NULL	XPC-hHR23B	NULL		bind	NULL				Tdp-ICL	NULL				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_9_2993_s_157	15914671	: RPA-Tdp-ICL super-shifted complex also migrated at the same position as when Tdp-ICL  was bound by XPC-hHR23B.	bind
29326	1	8806	6	13	NULL	NULL	NULL	Cl-	Chemical		bind					cyt bo3 plus NO2	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_5_1272_s_107	12207912	; and cyt  bo3 (~7  M) plus NO2- (10 mM) (- - -), and Cl- bound cyt  bo3 plus NO2- (-.	bind
37914	1	8806	7	NULL	NULL	0	NULL	 Cl-	NULL		bind	NULL				cyt bo3 plus NO2	NULL				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_5_1272_s_107	12207912	; and cyt  bo3 (~7  M) plus NO2- (10 mM) (- - -), and Cl- bound cyt  bo3 plus NO2- (-.	bind
29327	1	8807	6	13	NULL	NULL	NULL	XylR protein	GP		bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_51_0_341_s_294	9343354	A   ascade of Events Leading to Coordinate Expression of Upper and  Meta   Pathways    After binding an effector, the XylR protein binds ATP and oligomerizes   and undergoes a series of conformational changes that lead to a state   with enhanced ATPase activity that is active, from a transcriptional   point of view ( 104,  105).	bind
29328	3	8807	6	13	NULL	NULL	NULL	statement 2	Process		leads to					ATPase activity	Process	enhanced			NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_51_0_341_s_294	9343354	A   ascade of Events Leading to Coordinate Expression of Upper and  Meta   Pathways    After binding an effector, the XylR protein binds ATP and oligomerizes   and undergoes a series of conformational changes that lead to a state   with enhanced ATPase activity that is active, from a transcriptional   point of view ( 104,  105).	bind
46904	4	8807	6	13	NULL	NULL	NULL	effector	GP	binding of	leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_51_0_341_s_294	9343354	A   ascade of Events Leading to Coordinate Expression of Upper and  Meta   Pathways    After binding an effector, the XylR protein binds ATP and oligomerizes   and undergoes a series of conformational changes that lead to a state   with enhanced ATPase activity that is active, from a transcriptional   point of view ( 104,  105).	bind
56164	2	8807	6	13	NULL	NULL	NULL	statement 1	GP		oligomerize					XylR protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_51_0_341_s_294	9343354	A   ascade of Events Leading to Coordinate Expression of Upper and  Meta   Pathways    After binding an effector, the XylR protein binds ATP and oligomerizes   and undergoes a series of conformational changes that lead to a state   with enhanced ATPase activity that is active, from a transcriptional   point of view ( 104,  105).	bind
37915	1	8807	7	NULL	NULL	0	NULL	XylR protein 	NULL		binds	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_annurevmicrobiol_51_0_341_s_294	9343354	A   ascade of Events Leading to Coordinate Expression of Upper and  Meta   Pathways    After binding an effector, the XylR protein binds ATP and oligomerizes   and undergoes a series of conformational changes that lead to a state   with enhanced ATPase activity that is active, from a transcriptional   point of view ( 104,  105).	bind
37916	2	8807	7	NULL	NULL	0	NULL	statement 1	NULL		oligomerize	NULL				XylR protein 	NULL				NULL		0	NULL	NULL	NULL	gw60_annurevmicrobiol_51_0_341_s_294	9343354	A   ascade of Events Leading to Coordinate Expression of Upper and  Meta   Pathways    After binding an effector, the XylR protein binds ATP and oligomerizes   and undergoes a series of conformational changes that lead to a state   with enhanced ATPase activity that is active, from a transcriptional   point of view ( 104,  105).	bind
37919	3	8807	7	10	NULL	0	NULL	statement 2			enhance					ATPase activity					NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_51_0_341_s_294	9343354	A   ascade of Events Leading to Coordinate Expression of Upper and  Meta   Pathways    After binding an effector, the XylR protein binds ATP and oligomerizes   and undergoes a series of conformational changes that lead to a state   with enhanced ATPase activity that is active, from a transcriptional   point of view ( 104,  105).	bind
37921	4	8807	7	10	NULL	0	NULL	statement 1			occurs after					effector		binding of			NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_51_0_341_s_294	9343354	A   ascade of Events Leading to Coordinate Expression of Upper and  Meta   Pathways    After binding an effector, the XylR protein binds ATP and oligomerizes   and undergoes a series of conformational changes that lead to a state   with enhanced ATPase activity that is active, from a transcriptional   point of view ( 104,  105).	bind
29329	1	8808	6	13	NULL	NULL	NULL	neurotractin	GP		bind					CEPU-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_865_s_264	10330412	A   KD of 3 x 10 8 M was measured for the binding of neurotractin to the GPI-linked molecule CEPU-1 (Fig.  7), an  affinity that is lower than that usually reported for soluble  polypeptide ligands that bind to cell surface receptors, for  instance the neurotrophins (Dechant et al., 1994  ).	bind
29330	2	8808	6	13	NULL	NULL	NULL	CEPU-1	GP		is a type of					GPI-linked molecule	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_865_s_264	10330412	A   KD of 3 x 10 8 M was measured for the binding of neurotractin to the GPI-linked molecule CEPU-1 (Fig.  7), an  affinity that is lower than that usually reported for soluble  polypeptide ligands that bind to cell surface receptors, for  instance the neurotrophins (Dechant et al., 1994  ).	bind
29331	3	8808	6	13	NULL	NULL	NULL	polypeptide ligands	GP	soluble	bind					neurotrophins	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_865_s_264	10330412	A   KD of 3 x 10 8 M was measured for the binding of neurotractin to the GPI-linked molecule CEPU-1 (Fig.  7), an  affinity that is lower than that usually reported for soluble  polypeptide ligands that bind to cell surface receptors, for  instance the neurotrophins (Dechant et al., 1994  ).	bind
29332	4	8808	6	13	NULL	NULL	NULL	neurotrophins	GP		is a type of					cell-surface receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_865_s_264	10330412	A   KD of 3 x 10 8 M was measured for the binding of neurotractin to the GPI-linked molecule CEPU-1 (Fig.  7), an  affinity that is lower than that usually reported for soluble  polypeptide ligands that bind to cell surface receptors, for  instance the neurotrophins (Dechant et al., 1994  ).	bind
29333	5	8808	6	13	NULL	NULL	NULL	statement 1	Process	affinity of	is lower than					statement 3	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_865_s_264	10330412	A   KD of 3 x 10 8 M was measured for the binding of neurotractin to the GPI-linked molecule CEPU-1 (Fig.  7), an  affinity that is lower than that usually reported for soluble  polypeptide ligands that bind to cell surface receptors, for  instance the neurotrophins (Dechant et al., 1994  ).	bind
37922	1	8808	7	NULL	NULL	0	NULL	neurotractin	NULL		bind	NULL				CEPU-1	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_4_865_s_264	10330412	A   KD of 3 x 10 8 M was measured for the binding of neurotractin to the GPI-linked molecule CEPU-1 (Fig.  7), an  affinity that is lower than that usually reported for soluble  polypeptide ligands that bind to cell surface receptors, for  instance the neurotrophins (Dechant et al., 1994  ).	bind
37925	2	8808	7	NULL	NULL	0	NULL	polypeptide ligands 	NULL	soluble	binds to	NULL				neurotrophins	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_4_865_s_264	10330412	A   KD of 3 x 10 8 M was measured for the binding of neurotractin to the GPI-linked molecule CEPU-1 (Fig.  7), an  affinity that is lower than that usually reported for soluble  polypeptide ligands that bind to cell surface receptors, for  instance the neurotrophins (Dechant et al., 1994  ).	bind
37926	3	8808	7	NULL	NULL	0	NULL	CEPU-1	NULL		is a type of	NULL				GPI-linked molecule	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_4_865_s_264	10330412	A   KD of 3 x 10 8 M was measured for the binding of neurotractin to the GPI-linked molecule CEPU-1 (Fig.  7), an  affinity that is lower than that usually reported for soluble  polypeptide ligands that bind to cell surface receptors, for  instance the neurotrophins (Dechant et al., 1994  ).	bind
37949	4	8808	7	NULL	NULL	0	NULL	 neurotrophins	NULL		is a type of	NULL				cell surface receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_4_865_s_264	10330412	A   KD of 3 x 10 8 M was measured for the binding of neurotractin to the GPI-linked molecule CEPU-1 (Fig.  7), an  affinity that is lower than that usually reported for soluble  polypeptide ligands that bind to cell surface receptors, for  instance the neurotrophins (Dechant et al., 1994  ).	bind
37950	5	8808	7	NULL	NULL	0	NULL	statement 1	NULL	affinity of	is lower than	NULL				statement 2	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_4_865_s_264	10330412	A   KD of 3 x 10 8 M was measured for the binding of neurotractin to the GPI-linked molecule CEPU-1 (Fig.  7), an  affinity that is lower than that usually reported for soluble  polypeptide ligands that bind to cell surface receptors, for  instance the neurotrophins (Dechant et al., 1994  ).	bind
29335	1	8809	6	13	NULL	NULL	NULL	EGF ligand	GP		bind					EGFR	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1673_3_186_s_227	15279890	A   trans mechanism explains the activation of ErbB-2 in the cells by EGF, a ligand that binds  EGFR, but not ErbB-2.	bind
29336	2	8809	6	13	NULL	NULL	NULL	EGF ligand	GP		does not bind					ErbB-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1673_3_186_s_227	15279890	A   trans mechanism explains the activation of ErbB-2 in the cells by EGF, a ligand that binds  EGFR, but not ErbB-2.	bind
46943	3	8809	6	13	NULL	NULL	NULL	EGF ligand	GP		activates					ErbB-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1673_3_186_s_227	15279890	A   trans mechanism explains the activation of ErbB-2 in the cells by EGF, a ligand that binds  EGFR, but not ErbB-2.	bind
46944	4	8809	6	13	NULL	NULL	NULL	statement 3	Process		via					trans mechanism	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1673_3_186_s_227	15279890	A   trans mechanism explains the activation of ErbB-2 in the cells by EGF, a ligand that binds  EGFR, but not ErbB-2.	bind
37951	1	8809	7	10	NULL	0	NULL	EGF ligand	NULL		activates	NULL				ErbB-2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1673_3_186_s_227	15279890	A   trans mechanism explains the activation of ErbB-2 in the cells by EGF, a ligand that binds  EGFR, but not ErbB-2.	bind
37952	2	8809	7	10	NULL	0	NULL	EGF ligand	NULL		binds	NULL				EGFR	NULL				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1673_3_186_s_227	15279890	A   trans mechanism explains the activation of ErbB-2 in the cells by EGF, a ligand that binds  EGFR, but not ErbB-2.	bind
37953	3	8809	7	10	NULL	0	NULL	EGF ligand	NULL		does not bind	NULL				ErbB-2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1673_3_186_s_227	15279890	A   trans mechanism explains the activation of ErbB-2 in the cells by EGF, a ligand that binds  EGFR, but not ErbB-2.	bind
42308	4	8809	7	NULL	NULL	0	NULL	statement 1	NULL		via	NULL				trans mechanism	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1673_3_186_s_227	15279890	A   trans mechanism explains the activation of ErbB-2 in the cells by EGF, a ligand that binds  EGFR, but not ErbB-2.	bind
29337	1	8810	6	13	NULL	NULL	NULL	interferon-induced factor	GP		bind					H-2Kb gene	GP			interferon response sequence	NULL		NULL	NULL	NULL	NULL	gw60_immunity_5_4_365_s_384	8885869	A  -interferon-induced factor that binds the interferon response sequence of the MHC class I gene, H-2Kb.	bind
29338	2	8810	6	13	NULL	NULL	NULL	H-2Kb	GP		is a type of					MHC class I gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_5_4_365_s_384	8885869	A  -interferon-induced factor that binds the interferon response sequence of the MHC class I gene, H-2Kb.	bind
37954	1	8810	7	NULL	NULL	0	NULL	interferon-induced factor	NULL		binds to	NULL				H-2Kb	NULL			interferon response sequence	NULL		0	NULL	NULL	NULL	gw60_immunity_5_4_365_s_384	8885869	A  -interferon-induced factor that binds the interferon response sequence of the MHC class I gene, H-2Kb.	bind
37955	2	8810	7	NULL	NULL	0	NULL	H-2Kb	NULL		is a type of	NULL				MHC class I  gene	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_5_4_365_s_384	8885869	A  -interferon-induced factor that binds the interferon response sequence of the MHC class I gene, H-2Kb.	bind
29339	1	8811	6	13	NULL	NULL	NULL	Cbl	GP		bind		high affinity			Crk	GP		SH2 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8435_s_71	8626543	A  20-fold shorter exposure of this blot emphasizes the markedly higher  binding of Cbl to Crk SH2 ( Fig. 1  A,  middle  panel).	bind
37958	1	8811	7	NULL	NULL	0	NULL	 Cbl	NULL		bind	NULL				Crk	NULL		SH2		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8435_s_71	8626543	A  20-fold shorter exposure of this blot emphasizes the markedly higher  binding of Cbl to Crk SH2 ( Fig. 1  A,  middle  panel).	bind
29340	1	8812	6	13	NULL	NULL	NULL	DnaJ	GP		bind					DnaK	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_84	8626401	A  4-fold decrease in DnaJ concentration decreased in half the  DnaJ-dependent effect on DnaK's fluorescence (result not shown),  suggesting that binding of DnaJ to DnaK is the rate-limiting step.	bind
37960	1	8812	7	NULL	NULL	0	NULL	DnaJ 	NULL		bind	NULL				DnaK	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_11_6137_s_84	8626401	A  4-fold decrease in DnaJ concentration decreased in half the  DnaJ-dependent effect on DnaK's fluorescence (result not shown),  suggesting that binding of DnaJ to DnaK is the rate-limiting step.	bind
47111	1	8813	6	13	NULL	NULL	NULL	MCF-7	Cell		bind					nuclear protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_23_20490_s_116	12657623	A  50-molar excess of cold  - 1575G oligonucleotide strongly competed for  MCF-7 nuclear protein binding, resulting in the disappearance of the major  shifted complex ( Fig. 3,  lane 3), whereas a 50-molar excess of cold  - 1575A  oligonucleotide revealed only partial competition  ( Fig. 3,  lane 4).	bind
47112	2	8813	6	13	NULL	NULL	NULL	oligonucleotide	NucleicAcid		bind				1575G	nuclear protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_23_20490_s_116	12657623	A  50-molar excess of cold  - 1575G oligonucleotide strongly competed for  MCF-7 nuclear protein binding, resulting in the disappearance of the major  shifted complex ( Fig. 3,  lane 3), whereas a 50-molar excess of cold  - 1575A  oligonucleotide revealed only partial competition  ( Fig. 3,  lane 4).	bind
47113	3	8813	6	13	NULL	NULL	NULL	oligonucleotide	NucleicAcid		bind				1575A	nuclear protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_23_20490_s_116	12657623	A  50-molar excess of cold  - 1575G oligonucleotide strongly competed for  MCF-7 nuclear protein binding, resulting in the disappearance of the major  shifted complex ( Fig. 3,  lane 3), whereas a 50-molar excess of cold  - 1575A  oligonucleotide revealed only partial competition  ( Fig. 3,  lane 4).	bind
47114	4	8813	6	13	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_23_20490_s_116	12657623	A  50-molar excess of cold  - 1575G oligonucleotide strongly competed for  MCF-7 nuclear protein binding, resulting in the disappearance of the major  shifted complex ( Fig. 3,  lane 3), whereas a 50-molar excess of cold  - 1575A  oligonucleotide revealed only partial competition  ( Fig. 3,  lane 4).	bind
47115	5	8813	6	13	NULL	NULL	NULL	statement 1	Process		competes		partially			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_23_20490_s_116	12657623	A  50-molar excess of cold  - 1575G oligonucleotide strongly competed for  MCF-7 nuclear protein binding, resulting in the disappearance of the major  shifted complex ( Fig. 3,  lane 3), whereas a 50-molar excess of cold  - 1575A  oligonucleotide revealed only partial competition  ( Fig. 3,  lane 4).	bind
37966	1	8813	7	NULL	NULL	0	NULL	MCF-7	NULL		bind	NULL				nuclear protein	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_23_20490_s_116	12657623	A  50-molar excess of cold  - 1575G oligonucleotide strongly competed for  MCF-7 nuclear protein binding, resulting in the disappearance of the major  shifted complex ( Fig. 3,  lane 3), whereas a 50-molar excess of cold  - 1575A  oligonucleotide revealed only partial competition  ( Fig. 3,  lane 4).	bind
37967	2	8813	7	NULL	NULL	0	NULL	oligonucleotide	NULL		bind	NULL			1575G	nuclear protein	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_23_20490_s_116	12657623	A  50-molar excess of cold  - 1575G oligonucleotide strongly competed for  MCF-7 nuclear protein binding, resulting in the disappearance of the major  shifted complex ( Fig. 3,  lane 3), whereas a 50-molar excess of cold  - 1575A  oligonucleotide revealed only partial competition  ( Fig. 3,  lane 4).	bind
37968	3	8813	7	NULL	NULL	0	NULL	oligonucleotide	NULL		bind	NULL			1575A	nuclear protein	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_23_20490_s_116	12657623	A  50-molar excess of cold  - 1575G oligonucleotide strongly competed for  MCF-7 nuclear protein binding, resulting in the disappearance of the major  shifted complex ( Fig. 3,  lane 3), whereas a 50-molar excess of cold  - 1575A  oligonucleotide revealed only partial competition  ( Fig. 3,  lane 4).	bind
42309	4	8813	7	NULL	NULL	0	NULL	statement 2 	NULL		compete with	NULL	strongly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_23_20490_s_116	12657623	A  50-molar excess of cold  - 1575G oligonucleotide strongly competed for  MCF-7 nuclear protein binding, resulting in the disappearance of the major  shifted complex ( Fig. 3,  lane 3), whereas a 50-molar excess of cold  - 1575A  oligonucleotide revealed only partial competition  ( Fig. 3,  lane 4).	bind
42310	5	8813	7	NULL	NULL	0	NULL	statement 3	NULL		compete with	NULL	partially			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_23_20490_s_116	12657623	A  50-molar excess of cold  - 1575G oligonucleotide strongly competed for  MCF-7 nuclear protein binding, resulting in the disappearance of the major  shifted complex ( Fig. 3,  lane 3), whereas a 50-molar excess of cold  - 1575A  oligonucleotide revealed only partial competition  ( Fig. 3,  lane 4).	bind
29382	1	8814	6	13	NULL	NULL	NULL	Gbeta	GP		bind					CIR	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_49_29059_s_81	7493925	A  and  B  demonstrate the specificity  of Gbeta   binding to recombinant CIR ( rCIR) or to  recombinant GIRK1 ( rGIRK1).	bind
29383	2	8814	6	13	NULL	NULL	NULL	Gbeta	GP		bind					GIRK1	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_49_29059_s_81	7493925	A  and  B  demonstrate the specificity  of Gbeta   binding to recombinant CIR ( rCIR) or to  recombinant GIRK1 ( rGIRK1).	bind
29384	3	8814	6	13	NULL	NULL	NULL	recombinant CIR	GP		is					rCIR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_49_29059_s_81	7493925	A  and  B  demonstrate the specificity  of Gbeta   binding to recombinant CIR ( rCIR) or to  recombinant GIRK1 ( rGIRK1).	bind
29385	4	8814	6	13	NULL	NULL	NULL	recombinant GIRK1	GP		is					rGIRK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_49_29059_s_81	7493925	A  and  B  demonstrate the specificity  of Gbeta   binding to recombinant CIR ( rCIR) or to  recombinant GIRK1 ( rGIRK1).	bind
37969	1	8814	7	NULL	NULL	0	NULL	Gbeta	NULL		bind	NULL				rCIR	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_49_29059_s_81	7493925	A  and  B  demonstrate the specificity  of Gbeta   binding to recombinant CIR ( rCIR) or to  recombinant GIRK1 ( rGIRK1).	bind
37970	2	8814	7	NULL	NULL	0	NULL	Gbeta	NULL		bind	NULL				 rGIRK1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_49_29059_s_81	7493925	A  and  B  demonstrate the specificity  of Gbeta   binding to recombinant CIR ( rCIR) or to  recombinant GIRK1 ( rGIRK1).	bind
37971	3	8814	7	NULL	NULL	0	NULL	rCIR	NULL		is	NULL				recombinant CIR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_49_29059_s_81	7493925	A  and  B  demonstrate the specificity  of Gbeta   binding to recombinant CIR ( rCIR) or to  recombinant GIRK1 ( rGIRK1).	bind
37972	4	8814	7	NULL	NULL	0	NULL	 rGIRK1	NULL		is	NULL				recombinant  GIRK1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_49_29059_s_81	7493925	A  and  B  demonstrate the specificity  of Gbeta   binding to recombinant CIR ( rCIR) or to  recombinant GIRK1 ( rGIRK1).	bind
29392	1	8815	6	13	NULL	NULL	NULL	tropomyosin	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_14_7836_s_64	7713874	A  and  B  show that tropomyosin was bound to the actin    in both  the undiluted (100 nM  actin +  100 nM  tropomyosin) and the 10-fold diluted samples, respectively.	bind
37973	1	8815	7	NULL	NULL	0	NULL	tropomyosin	NULL		bind	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_14_7836_s_64	7713874	A  and  B  show that tropomyosin was bound to the actin    in both  the undiluted (100 nM  actin +  100 nM  tropomyosin) and the 10-fold diluted samples, respectively.	bind
29393	1	8816	6	13	NULL	NULL	NULL	Arg molecule	AminoAcid		bind					substrate binding helix	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_24100_s_58	10446182	A  blue Arg molecule is also shown bound to the substrate-binding helix and positioned  above the  red heme group contained in this subunit of the dimer.	bind
37974	1	8816	7	NULL	NULL	0	NULL	Arg molecule	NULL		bind	NULL				substrate-binding helix	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_34_24100_s_58	10446182	A  blue Arg molecule is also shown bound to the substrate-binding helix and positioned  above the  red heme group contained in this subunit of the dimer.	bind
29395	1	8817	6	13	NULL	NULL	NULL	cdc24	GP		bind					Rsr1/Bud1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_13084_s_298	15657049	A  bud1 null mutant is able to respond to mating pheromone and to form shmoos ( ,  ), suggesting that the defect in Ste5 recruitment is not linked to a defect in Cdc24 binding to Rsr1/Bud1.	bind
29396	2	8817	6	13	NULL	NULL	NULL	bud1	GP	null mutant	respond to					mating pheromone	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_13084_s_298	15657049	A  bud1 null mutant is able to respond to mating pheromone and to form shmoos ( ,  ), suggesting that the defect in Ste5 recruitment is not linked to a defect in Cdc24 binding to Rsr1/Bud1.	bind
46945	3	8817	6	13	NULL	NULL	NULL	statement 2	Process		forms					shmoos	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_13084_s_298	15657049	A  bud1 null mutant is able to respond to mating pheromone and to form shmoos ( ,  ), suggesting that the defect in Ste5 recruitment is not linked to a defect in Cdc24 binding to Rsr1/Bud1.	bind
46946	4	8817	6	13	NULL	NULL	NULL	Ste5	GP	\tdefect in recruitment of	is not linked to					statement 1	Process	defect in			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_13084_s_298	15657049	A  bud1 null mutant is able to respond to mating pheromone and to form shmoos ( ,  ), suggesting that the defect in Ste5 recruitment is not linked to a defect in Cdc24 binding to Rsr1/Bud1.	bind
37975	1	8817	7	NULL	NULL	0	NULL	 bud1	NULL	null mutant	respond to	NULL				mating pheromone	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_13_13084_s_298	15657049	A  bud1 null mutant is able to respond to mating pheromone and to form shmoos ( ,  ), suggesting that the defect in Ste5 recruitment is not linked to a defect in Cdc24 binding to Rsr1/Bud1.	bind
37976	2	8817	7	NULL	NULL	0	NULL	statement 1	NULL		form	NULL				shmoos	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_13_13084_s_298	15657049	A  bud1 null mutant is able to respond to mating pheromone and to form shmoos ( ,  ), suggesting that the defect in Ste5 recruitment is not linked to a defect in Cdc24 binding to Rsr1/Bud1.	bind
37977	3	8817	7	NULL	NULL	0	NULL	 Cdc24	NULL		bind	NULL				Rsr1/Bud1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_13_13084_s_298	15657049	A  bud1 null mutant is able to respond to mating pheromone and to form shmoos ( ,  ), suggesting that the defect in Ste5 recruitment is not linked to a defect in Cdc24 binding to Rsr1/Bud1.	bind
37978	4	8817	7	10	NULL	0	NULL	Ste5	NULL	defect in recruitment of	is not linked to	NULL				statement 3	NULL	defect in			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_13084_s_298	15657049	A  bud1 null mutant is able to respond to mating pheromone and to form shmoos ( ,  ), suggesting that the defect in Ste5 recruitment is not linked to a defect in Cdc24 binding to Rsr1/Bud1.	bind
29397	1	8818	6	13	NULL	NULL	NULL	lipoprotein lipase	GP		bind			carboxyl-terminal fragment		low density lipoprotein receptor-related protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_19_0_141_s_1074	10448520	A  carboxyl-terminal fragment of lipoprotein lipase binds to the low density lipoprotein  receptor-related protein and inhibits lipase-mediated uptake of lipoprotein in cells.	bind
29399	2	8818	6	13	NULL	NULL	NULL	lipoprotein	GP	uptake of	is mediated by					lipase	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_19_0_141_s_1074	10448520	A  carboxyl-terminal fragment of lipoprotein lipase binds to the low density lipoprotein  receptor-related protein and inhibits lipase-mediated uptake of lipoprotein in cells.	bind
29400	3	8818	6	13	NULL	NULL	NULL	statement 1	Process		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_19_0_141_s_1074	10448520	A  carboxyl-terminal fragment of lipoprotein lipase binds to the low density lipoprotein  receptor-related protein and inhibits lipase-mediated uptake of lipoprotein in cells.	bind
37979	1	8818	7	NULL	NULL	0	NULL	lipoprotein lipase	NULL		binds to	NULL		carboxyl-terminal fragment		low density lipoprotein receptor-related protein	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevnutr_19_0_141_s_1074	10448520	A  carboxyl-terminal fragment of lipoprotein lipase binds to the low density lipoprotein  receptor-related protein and inhibits lipase-mediated uptake of lipoprotein in cells.	bind
37980	2	8818	7	NULL	NULL	0	NULL	lipase	NULL		mediates	NULL				lipoprotein	NULL	uptake of			NULL	cells	0	NULL	NULL	NULL	gw70_annurevnutr_19_0_141_s_1074	10448520	A  carboxyl-terminal fragment of lipoprotein lipase binds to the low density lipoprotein  receptor-related protein and inhibits lipase-mediated uptake of lipoprotein in cells.	bind
37981	3	8818	7	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevnutr_19_0_141_s_1074	10448520	A  carboxyl-terminal fragment of lipoprotein lipase binds to the low density lipoprotein  receptor-related protein and inhibits lipase-mediated uptake of lipoprotein in cells.	bind
47116	1	8819	6	13	NULL	NULL	NULL	MC2	GP		delay					allograft rejection	Process				NULL	animal model	NULL	NULL	NULL	NULL	abs-batch0517-0529_int-immunopharmacol_5_11_16039552_s_5	16039552	A  cationic peptide (MC2) derived from the heparin-binding sequence of mouse  IFN-gamma was previously shown by our laboratory to delay allograft rejection  in an animal model.	bind
47117	2	8819	6	13	NULL	NULL	NULL	MC2	GP		is a type of					cationic peptide	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_int-immunopharmacol_5_11_16039552_s_5	16039552	A  cationic peptide (MC2) derived from the heparin-binding sequence of mouse  IFN-gamma was previously shown by our laboratory to delay allograft rejection  in an animal model.	bind
47118	3	8819	6	13	NULL	NULL	NULL	MC2	GP		is derived from					IFN-gamma	GP	mouse	heparin binding sequence		NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_int-immunopharmacol_5_11_16039552_s_5	16039552	A  cationic peptide (MC2) derived from the heparin-binding sequence of mouse  IFN-gamma was previously shown by our laboratory to delay allograft rejection  in an animal model.	bind
37982	1	8819	7	NULL	NULL	0	NULL	MC2	NULL		delay	NULL				allograft rejection	NULL				NULL	animal model	0	NULL	NULL	NULL	abs-batch0517-0529_int-immunopharmacol_5_11_16039552_s_5	16039552	A  cationic peptide (MC2) derived from the heparin-binding sequence of mouse  IFN-gamma was previously shown by our laboratory to delay allograft rejection  in an animal model.	bind
37983	2	8819	7	NULL	NULL	0	NULL	MC2	NULL		is a type of	NULL				cationic peptide	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_int-immunopharmacol_5_11_16039552_s_5	16039552	A  cationic peptide (MC2) derived from the heparin-binding sequence of mouse  IFN-gamma was previously shown by our laboratory to delay allograft rejection  in an animal model.	bind
37984	3	8819	7	NULL	NULL	0	NULL	MC2	NULL		is derived from	NULL				IFN-gamma	NULL	mouse	heparin-binding sequence		NULL		0	NULL	NULL	NULL	abs-batch0517-0529_int-immunopharmacol_5_11_16039552_s_5	16039552	A  cationic peptide (MC2) derived from the heparin-binding sequence of mouse  IFN-gamma was previously shown by our laboratory to delay allograft rejection  in an animal model.	bind
29601	1	8823	6	13	NULL	NULL	NULL			rat	restricts				OC box -76 to -99	OC	GP	expression of			NULL	osteoblasts	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_9248_s_42	15456894	A  cis regulatory sequence conserved in the segment of the proximal promoter of all species, known as the OC box ( - 76 to  - 99 in rat), encompasses a core HD protein binding site (CAATTAGT) that restricts OC expression to osteoblasts ( ,  ).	bind
29602	2	8823	6	13	NULL	NULL	NULL				is a binding site for				CAATTAGT	core HD protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_9248_s_42	15456894	A  cis regulatory sequence conserved in the segment of the proximal promoter of all species, known as the OC box ( - 76 to  - 99 in rat), encompasses a core HD protein binding site (CAATTAGT) that restricts OC expression to osteoblasts ( ,  ).	bind
29603	3	8823	6	13	NULL	NULL	NULL			rat	encompasses				OC box -76 to -99	statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_9248_s_42	15456894	A  cis regulatory sequence conserved in the segment of the proximal promoter of all species, known as the OC box ( - 76 to  - 99 in rat), encompasses a core HD protein binding site (CAATTAGT) that restricts OC expression to osteoblasts ( ,  ).	bind
37986	1	8823	7	NULL	NULL	0	NULL		NULL	rat	restricts	NULL			OC box - 76 to - 99	OC	NULL	expression of			NULL	osteoblasts	NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_9248_s_42	15456894	A  cis regulatory sequence conserved in the segment of the proximal promoter of all species, known as the OC box ( - 76 to  - 99 in rat), encompasses a core HD protein binding site (CAATTAGT) that restricts OC expression to osteoblasts ( ,  ).	bind
37987	2	8823	7	10	NULL	0	NULL		NULL		is a binding site for	NULL			CAATTAGT	core HD protein	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_9248_s_42	15456894	A  cis regulatory sequence conserved in the segment of the proximal promoter of all species, known as the OC box ( - 76 to  - 99 in rat), encompasses a core HD protein binding site (CAATTAGT) that restricts OC expression to osteoblasts ( ,  ).	bind
37988	3	8823	7	NULL	NULL	0	NULL		NULL		is conserved in	NULL			cis regulatory sequence		NULL			proximal promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_20_9248_s_42	15456894	A  cis regulatory sequence conserved in the segment of the proximal promoter of all species, known as the OC box ( - 76 to  - 99 in rat), encompasses a core HD protein binding site (CAATTAGT) that restricts OC expression to osteoblasts ( ,  ).	bind
46948	4	8823	7	10	NULL	0	NULL		NULL	rat	encompass	NULL			OC box -76 to -99	statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_20_9248_s_42	15456894	A  cis regulatory sequence conserved in the segment of the proximal promoter of all species, known as the OC box ( - 76 to  - 99 in rat), encompasses a core HD protein binding site (CAATTAGT) that restricts OC expression to osteoblasts ( ,  ).	bind
29402	1	8824	6	13	NULL	NULL	NULL	stat6	GP		bind					IL-4 gene	GP	downstream of 			NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_18_0_451_s_413	10837066	A  cis-element capable of Stat6 binding downstream of the IL-4 structural gene was proposed  to act as a subset-specific silencing element in Th1 cells ( 214).	bind
29403	2	8824	6	13	NULL	NULL	NULL	statement 1	Process		acts as a 									silencing element	NULL	Th1 cells	NULL	NULL	NULL	NULL	gw70_annurevimmunol_18_0_451_s_413	10837066	A  cis-element capable of Stat6 binding downstream of the IL-4 structural gene was proposed  to act as a subset-specific silencing element in Th1 cells ( 214).	bind
37989	1	8824	7	10	NULL	0	NULL	Stat6	NULL		bind	NULL				IL-4 gene	NULL	downstream of			NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_18_0_451_s_413	10837066	A  cis-element capable of Stat6 binding downstream of the IL-4 structural gene was proposed  to act as a subset-specific silencing element in Th1 cells ( 214).	bind
37990	2	8824	7	10	NULL	0	NULL	statement 1	NULL		acts as a	NULL					NULL	subset-specific		silencing element	NULL	Th1 cells	NULL	NULL	NULL	NULL	gw70_annurevimmunol_18_0_451_s_413	10837066	A  cis-element capable of Stat6 binding downstream of the IL-4 structural gene was proposed  to act as a subset-specific silencing element in Th1 cells ( 214).	bind
29405	1	8826	6	13	NULL	NULL	NULL	Replication Inhibitor	GP		bind					PCNA	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_99_2_155_s_188	10535734	A  Comparison of Replication Inhibitor Binding to PCNA and RB69 Sliding Clamp Interactions  with DNA Polymerase A comparison of pol-CT with a peptide derived from the  eukaryotic DNA replication inhibitor protein p21CIP1 (Gulbis et al., 1996   ).	bind
29406	2	8826	6	13	NULL	NULL	NULL	RB69 sliding clamp	GP		interacts with					DNA Polymerase	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_99_2_155_s_188	10535734	A  Comparison of Replication Inhibitor Binding to PCNA and RB69 Sliding Clamp Interactions  with DNA Polymerase A comparison of pol-CT with a peptide derived from the  eukaryotic DNA replication inhibitor protein p21CIP1 (Gulbis et al., 1996   ).	bind
46949	3	8826	6	13	NULL	NULL	NULL	p21CIP1	GP		is a type of					eukaryotic DNA replication inhibitor protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_99_2_155_s_188	10535734	A  Comparison of Replication Inhibitor Binding to PCNA and RB69 Sliding Clamp Interactions  with DNA Polymerase A comparison of pol-CT with a peptide derived from the  eukaryotic DNA replication inhibitor protein p21CIP1 (Gulbis et al., 1996   ).	bind
37994	1	8826	7	NULL	NULL	0	NULL	Replication Inhibitor	NULL		binds to	NULL				PCNA	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_99_2_155_s_188	10535734	A  Comparison of Replication Inhibitor Binding to PCNA and RB69 Sliding Clamp Interactions  with DNA Polymerase A comparison of pol-CT with a peptide derived from the  eukaryotic DNA replication inhibitor protein p21CIP1 (Gulbis et al., 1996   ).	bind
37995	2	8826	7	10	NULL	0	NULL	RB69 Sliding Clamp			interacts with					DNA polymerase					NULL		NULL	NULL	NULL	NULL	gw60_cell_99_2_155_s_188	10535734	A  Comparison of Replication Inhibitor Binding to PCNA and RB69 Sliding Clamp Interactions  with DNA Polymerase A comparison of pol-CT with a peptide derived from the  eukaryotic DNA replication inhibitor protein p21CIP1 (Gulbis et al., 1996   ).	bind
37996	3	8826	7	NULL	NULL	0	NULL	p21CIP1	NULL		is a type of	NULL				eukaryotic DNA replication inhibitor protein	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_99_2_155_s_188	10535734	A  Comparison of Replication Inhibitor Binding to PCNA and RB69 Sliding Clamp Interactions  with DNA Polymerase A comparison of pol-CT with a peptide derived from the  eukaryotic DNA replication inhibitor protein p21CIP1 (Gulbis et al., 1996   ).	bind
29407	1	8827	6	13	NULL	NULL	NULL	CD28	GP		bind					B7	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-exp-med_181_4_7535334_s_8	7535334	A  comparison of the effects of mutations on the binding of CD28 and CTLA4  reveals that CD28 and CTLA4 binds to the same site on B7.	bind
29408	2	8827	6	13	NULL	NULL	NULL	CTLA4	GP		bind					B7	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-exp-med_181_4_7535334_s_8	7535334	A  comparison of the effects of mutations on the binding of CD28 and CTLA4  reveals that CD28 and CTLA4 binds to the same site on B7.	bind
37997	1	8827	7	NULL	NULL	0	NULL	 CD28	NULL		binds to	NULL				B7	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_j-exp-med_181_4_7535334_s_8	7535334	A  comparison of the effects of mutations on the binding of CD28 and CTLA4  reveals that CD28 and CTLA4 binds to the same site on B7.	bind
37998	2	8827	7	NULL	NULL	0	NULL	CTLA4 	NULL		binds to	NULL				B7	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_j-exp-med_181_4_7535334_s_8	7535334	A  comparison of the effects of mutations on the binding of CD28 and CTLA4  reveals that CD28 and CTLA4 binds to the same site on B7.	bind
37999	3	8827	7	NULL	NULL	0	NULL	statement 1	NULL	binding site of	is same as	NULL				statement 2	NULL	binding site of			NULL		0	NULL	NULL	NULL	abs-batch0680-0699_j-exp-med_181_4_7535334_s_8	7535334	A  comparison of the effects of mutations on the binding of CD28 and CTLA4  reveals that CD28 and CTLA4 binds to the same site on B7.	bind
29409	1	8831	6	13	NULL	NULL	NULL	t cell clone	Cell		does not bind					PIM/CD1d tetramers	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_29_10685_s_174	15243159	A  conventional T cell clone did not bind the PIM/CD1d tetramers ( Left).	bind
38015	1	8831	7	NULL	NULL	0	NULL	T cell clone	NULL		does not bind	NULL				PIM/CD1d tetramers	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_29_10685_s_174	15243159	A  conventional T cell clone did not bind the PIM/CD1d tetramers ( Left).	bind
29462	1	8832	6	13	NULL	NULL	NULL				bind				cre element	CcpA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_1_7_s_126	12486034	A  cre element, which could bind the CcpA carbon catabolite protein A, is located upstream of this multipromoter region.	bind
29463	2	8832	6	13	NULL	NULL	NULL	CcpA	GP		is					carbon catabolite protein A	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_1_7_s_126	12486034	A  cre element, which could bind the CcpA carbon catabolite protein A, is located upstream of this multipromoter region.	bind
46950	3	8832	6	13	NULL	NULL	NULL				is located				cre element	CcpA	GP	upstream of		multipromoter region	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_1_7_s_126	12486034	A  cre element, which could bind the CcpA carbon catabolite protein A, is located upstream of this multipromoter region.	bind
38016	1	8832	7	NULL	NULL	0	NULL		NULL		bind	NULL			cre element	CcpA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_185_1_7_s_126	12486034	A  cre element, which could bind the CcpA carbon catabolite protein A, is located upstream of this multipromoter region.	bind
38017	2	8832	7	NULL	NULL	0	NULL	CcpA	NULL		is	NULL				carbon catabolite protein A	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_185_1_7_s_126	12486034	A  cre element, which could bind the CcpA carbon catabolite protein A, is located upstream of this multipromoter region.	bind
38018	3	8832	7	10	NULL	0	NULL		NULL		is located	NULL			cre element	CcpA	NULL	upstream of		multipromoter region	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_1_7_s_126	12486034	A  cre element, which could bind the CcpA carbon catabolite protein A, is located upstream of this multipromoter region.	bind
29473	1	8838	6	13	NULL	NULL	NULL	C3bot	GP		bind					RalA-GTP	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_20_3670_s_261	16177825	A  direct consequence would be that C3bot binding to the RalA-GTP state is impaired  or at least largely reduced.	bind
38027	1	8838	7	NULL	NULL	0	NULL	C3bot	NULL		bind	NULL				RalA-GTP	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_20_3670_s_261	16177825	A  direct consequence would be that C3bot binding to the RalA-GTP state is impaired  or at least largely reduced.	bind
29474	1	8839	6	13	NULL	NULL	NULL	I-hs-APP	GP		bind					CBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1613_s_134	8576160	A  dose-dependent inhibition of the binding of  I-hs-APP to  CBP by recombinant APP was observed in nanomolar concentrations ( B).	bind
29475	2	8839	6	13	NULL	NULL	NULL	APP	GP	recombinant	inhibits		dose dependently			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1613_s_134	8576160	A  dose-dependent inhibition of the binding of  I-hs-APP to  CBP by recombinant APP was observed in nanomolar concentrations ( B).	bind
38028	1	8839	7	NULL	NULL	0	NULL	I-hs-APP	NULL		bind	NULL				CBP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_3_1613_s_134	8576160	A  dose-dependent inhibition of the binding of  I-hs-APP to  CBP by recombinant APP was observed in nanomolar concentrations ( B).	bind
38029	2	8839	7	10	NULL	0	NULL	APP	NULL	recombinant	inhibit	NULL	dose dependently			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1613_s_134	8576160	A  dose-dependent inhibition of the binding of  I-hs-APP to  CBP by recombinant APP was observed in nanomolar concentrations ( B).	bind
29476	1	8841	6	13	NULL	NULL	NULL	rn-APP	GP	I-labeled	bind		saturably;;specifically			fibrillar collagen type I	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1613_s_91	8576160	A  dot blot assay revealed that  I-labeled rn-APP binding to  fibrillar collagen type I and basement membrane collagen type IV ( 38) was saturable and specific.	bind
29477	2	8841	6	13	NULL	NULL	NULL	rn-APP	GP	I-labeled	bind		saturably;;specifically			basement membrane collagen type IV	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1613_s_91	8576160	A  dot blot assay revealed that  I-labeled rn-APP binding to  fibrillar collagen type I and basement membrane collagen type IV ( 38) was saturable and specific.	bind
38031	1	8841	7	NULL	NULL	0	NULL	 rn-APP	NULL	I-labeled	bind	NULL	saturably;;specific			fibrillar collagen type I 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_3_1613_s_91	8576160	A  dot blot assay revealed that  I-labeled rn-APP binding to  fibrillar collagen type I and basement membrane collagen type IV ( 38) was saturable and specific.	bind
38032	2	8841	7	NULL	NULL	0	NULL	 rn-APP	NULL	I-labeled 	bind	NULL	saturably;;specific			basement membrane collagen type IV	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_3_1613_s_91	8576160	A  dot blot assay revealed that  I-labeled rn-APP binding to  fibrillar collagen type I and basement membrane collagen type IV ( 38) was saturable and specific.	bind
46951	1	8842	6	13	NULL	NULL	NULL	BLMA	GP		bind					Bm molecules	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2311_s_231	11706014	A  dotted curve is drawn by assuming that the binding affinities of BLMA for two Bm molecules to the pockets are identical ( K d1 = 137.5 nM and  K d2 = 550 nM).	bind
38033	1	8842	7	NULL	NULL	0	NULL	BLMA	NULL		bind	NULL				Bm molecules	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2311_s_231	11706014	A  dotted curve is drawn by assuming that the binding affinities of BLMA for two Bm molecules to the pockets are identical ( K d1 = 137.5 nM and  K d2 = 550 nM).	bind
29519	1	8843	6	13	NULL	NULL	NULL	GATA family member	GP	Drosophila	bind					Adh 	GP			regulatory sequences	NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_31_6_679_s_228	11267906	A  Drosophila GATA family member that binds  Adh regulatory sequences is expressed in the developing fat body.	bind
29520	2	8843	6	13	NULL	NULL	NULL	GATA family member	GP	Drosophila	is expressed in					developing fat body	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_31_6_679_s_228	11267906	A  Drosophila GATA family member that binds  Adh regulatory sequences is expressed in the developing fat body.	bind
38034	1	8843	7	10	NULL	0	NULL	 GATA family member	NULL	Drosophila	binds	NULL				Adh	NULL			regulatory sequences	NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_31_6_679_s_228	11267906	A  Drosophila GATA family member that binds  Adh regulatory sequences is expressed in the developing fat body.	bind
38035	2	8843	7	NULL	NULL	0	NULL	GATA family member	NULL	Drosophila	is expressed in	NULL				developing fat body	NULL				NULL		0	NULL	NULL	NULL	gw60_insectbiochemmolbiol_31_6_679_s_228	11267906	A  Drosophila GATA family member that binds  Adh regulatory sequences is expressed in the developing fat body.	bind
29521	1	8847	6	13	NULL	NULL	NULL	par-1	GP	Drosophila melanogaster 	plays a role in					embryonic-axis 	OrganismPart	formation of			NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4201_s_697	12874138	A  Drosophila melanogaster homologue of  Caenorhabditis elegans par-1 acts at an early step in embryonic-axis formation.	bind
29522	2	8847	6	13	NULL	NULL	NULL	par-1	GP	Drosophila melanogaster	is homologous to					par-1	GP	Caenorhabditis elegans			NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4201_s_697	12874138	A  Drosophila melanogaster homologue of  Caenorhabditis elegans par-1 acts at an early step in embryonic-axis formation.	bind
38176	1	8847	7	10	NULL	0	NULL	par-1	NULL	Drosophila melanogaster	plays a role in	NULL				embryonic axis	NULL	formation of			NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4201_s_697	12874138	A  Drosophila melanogaster homologue of  Caenorhabditis elegans par-1 acts at an early step in embryonic-axis formation.	bind
38177	2	8847	7	NULL	NULL	0	NULL	par-1	NULL	Caenorhabditis elegans	is homologous to	NULL				par-1	NULL	Drosophila melanogaster			NULL		0	NULL	NULL	NULL	gw60_development_130_17_4201_s_697	12874138	A  Drosophila melanogaster homologue of  Caenorhabditis elegans par-1 acts at an early step in embryonic-axis formation.	bind
29523	1	8848	6	13	NULL	NULL	NULL	TRAF	GP		is					TNF-receptor-associated factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_149_2_471_s_709	10769037	A  Drosophila TNF-receptor-associated factor (TRAF) binds the ste20 kinase Misshapen and activates Jun kinase.	bind
29524	2	8848	6	13	NULL	NULL	NULL	Misshapen	GP		is a type of					ste20 kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_149_2_471_s_709	10769037	A  Drosophila TNF-receptor-associated factor (TRAF) binds the ste20 kinase Misshapen and activates Jun kinase.	bind
29525	3	8848	6	13	NULL	NULL	NULL	TRAF	GP	drosophila	bind					misshapen	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_149_2_471_s_709	10769037	A  Drosophila TNF-receptor-associated factor (TRAF) binds the ste20 kinase Misshapen and activates Jun kinase.	bind
29526	4	8848	6	13	NULL	NULL	NULL	statement 1	GP		activates					jun kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_149_2_471_s_709	10769037	A  Drosophila TNF-receptor-associated factor (TRAF) binds the ste20 kinase Misshapen and activates Jun kinase.	bind
38178	1	8848	7	10	NULL	0	NULL	TRAF	NULL	Drosophila	binds 	NULL				Misshapen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_149_2_471_s_709	10769037	A  Drosophila TNF-receptor-associated factor (TRAF) binds the ste20 kinase Misshapen and activates Jun kinase.	bind
38179	2	8848	7	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				Jun kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_149_2_471_s_709	10769037	A  Drosophila TNF-receptor-associated factor (TRAF) binds the ste20 kinase Misshapen and activates Jun kinase.	bind
38180	3	8848	7	NULL	NULL	0	NULL	TRAF	NULL		is	NULL				TNF-receptor-associated factor	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_149_2_471_s_709	10769037	A  Drosophila TNF-receptor-associated factor (TRAF) binds the ste20 kinase Misshapen and activates Jun kinase.	bind
46952	4	8848	7	10	NULL	0	NULL	Misshapen	NULL		is a type of	NULL				ste20 kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_149_2_471_s_709	10769037	A  Drosophila TNF-receptor-associated factor (TRAF) binds the ste20 kinase Misshapen and activates Jun kinase.	bind
29527	1	8849	6	13	NULL	NULL	NULL	dSlo clone	GP		bind		high affinity			CTX	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_1_11_s_249	10665815	A  dSlo clone that binds CTX with high affinity would be a valuable tool in future studies of these channels.	bind
38181	1	8849	7	NULL	NULL	0	NULL	dSlo clone	NULL		binds	NULL	high affinity			CTX	NULL				NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_1_11_s_249	10665815	A  dSlo clone that binds CTX with high affinity would be a valuable tool in future studies of these channels.	bind
29528	1	8850	6	13	NULL	NULL	NULL	VDR/RXR heterodimer	GP		bind					TRPV6 gene	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_mol-endocrinol_20_6_16574738_s_11	16574738	A  final ChIP assay revealed that VDR/RXR heterodimer binding to the TRPV6  gene was accompanied by both the recruitment of steroid receptor coactivator  1 as well as a broad change in histone 4 acetylation.	bind
29529	2	8850	6	13	NULL	NULL	NULL	statement 1	Process		is accompanied by					steroid receptor coactivator 1	GP	recruitment of			NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_mol-endocrinol_20_6_16574738_s_11	16574738	A  final ChIP assay revealed that VDR/RXR heterodimer binding to the TRPV6  gene was accompanied by both the recruitment of steroid receptor coactivator  1 as well as a broad change in histone 4 acetylation.	bind
29530	3	8850	6	13	NULL	NULL	NULL	statement 1	Process		is accompanied by					histone 4	GP	change in acetylation of 			NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_mol-endocrinol_20_6_16574738_s_11	16574738	A  final ChIP assay revealed that VDR/RXR heterodimer binding to the TRPV6  gene was accompanied by both the recruitment of steroid receptor coactivator  1 as well as a broad change in histone 4 acetylation.	bind
38182	1	8850	7	NULL	NULL	0	NULL	VDR/RXR heterodimer	NULL		bind	NULL				TRPV6 gene	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_mol-endocrinol_20_6_16574738_s_11	16574738	A  final ChIP assay revealed that VDR/RXR heterodimer binding to the TRPV6  gene was accompanied by both the recruitment of steroid receptor coactivator  1 as well as a broad change in histone 4 acetylation.	bind
38183	2	8850	7	10	NULL	0	NULL	statement 1	NULL		is accompanied by	NULL				steroid receptor coactivator 1	NULL	recruitment of			NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_mol-endocrinol_20_6_16574738_s_11	16574738	A  final ChIP assay revealed that VDR/RXR heterodimer binding to the TRPV6  gene was accompanied by both the recruitment of steroid receptor coactivator  1 as well as a broad change in histone 4 acetylation.	bind
38184	3	8850	7	10	NULL	0	NULL	statement 1	NULL		is accompanied by	NULL				histone 4	NULL	change in acetylation of			NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_mol-endocrinol_20_6_16574738_s_11	16574738	A  final ChIP assay revealed that VDR/RXR heterodimer binding to the TRPV6  gene was accompanied by both the recruitment of steroid receptor coactivator  1 as well as a broad change in histone 4 acetylation.	bind
29531	1	8851	6	13	NULL	NULL	NULL	agrin	GP		bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_85_4_513_s_28	8653787	A  four amino acid insertion at the Y position causes a modest additional  increase in the activity of agrins having an insertion at the Z  position, and the Y insertion also seems to be involved in the binding  of agrin to heparin and proteoglycans (Ferns et al., 1993   ;  Hoch  et al., 1994   ).	bind
29532	2	8851	6	13	NULL	NULL	NULL	agrin	GP		bind					proteoglycans	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_85_4_513_s_28	8653787	A  four amino acid insertion at the Y position causes a modest additional  increase in the activity of agrins having an insertion at the Z  position, and the Y insertion also seems to be involved in the binding  of agrin to heparin and proteoglycans (Ferns et al., 1993   ;  Hoch  et al., 1994   ).	bind
29533	3	8851	6	13	NULL	NULL	NULL	four amino acid	AminoAcid		inserted at					Y position	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_85_4_513_s_28	8653787	A  four amino acid insertion at the Y position causes a modest additional  increase in the activity of agrins having an insertion at the Z  position, and the Y insertion also seems to be involved in the binding  of agrin to heparin and proteoglycans (Ferns et al., 1993   ;  Hoch  et al., 1994   ).	bind
29534	4	8851	6	13	NULL	NULL	NULL	statement 3	Process		is involved in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_85_4_513_s_28	8653787	A  four amino acid insertion at the Y position causes a modest additional  increase in the activity of agrins having an insertion at the Z  position, and the Y insertion also seems to be involved in the binding  of agrin to heparin and proteoglycans (Ferns et al., 1993   ;  Hoch  et al., 1994   ).	bind
29535	5	8851	6	13	NULL	NULL	NULL	statement 3	Process		is involved in					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_85_4_513_s_28	8653787	A  four amino acid insertion at the Y position causes a modest additional  increase in the activity of agrins having an insertion at the Z  position, and the Y insertion also seems to be involved in the binding  of agrin to heparin and proteoglycans (Ferns et al., 1993   ;  Hoch  et al., 1994   ).	bind
29536	6	8851	6	13	NULL	NULL	NULL	agrins	GP		have insertion at					Z postition	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_85_4_513_s_28	8653787	A  four amino acid insertion at the Y position causes a modest additional  increase in the activity of agrins having an insertion at the Z  position, and the Y insertion also seems to be involved in the binding  of agrin to heparin and proteoglycans (Ferns et al., 1993   ;  Hoch  et al., 1994   ).	bind
29537	7	8851	6	13	NULL	NULL	NULL	statement 3	Process		increases		modestly			statement 6	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_cell_85_4_513_s_28	8653787	A  four amino acid insertion at the Y position causes a modest additional  increase in the activity of agrins having an insertion at the Z  position, and the Y insertion also seems to be involved in the binding  of agrin to heparin and proteoglycans (Ferns et al., 1993   ;  Hoch  et al., 1994   ).	bind
38185	1	8851	7	NULL	NULL	0	NULL	agrin	NULL		bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_85_4_513_s_28	8653787	A  four amino acid insertion at the Y position causes a modest additional  increase in the activity of agrins having an insertion at the Z  position, and the Y insertion also seems to be involved in the binding  of agrin to heparin and proteoglycans (Ferns et al., 1993   ;  Hoch  et al., 1994   ).	bind
38186	2	8851	7	NULL	NULL	0	NULL	agrin	NULL		bind	NULL				proteoglycans	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_85_4_513_s_28	8653787	A  four amino acid insertion at the Y position causes a modest additional  increase in the activity of agrins having an insertion at the Z  position, and the Y insertion also seems to be involved in the binding  of agrin to heparin and proteoglycans (Ferns et al., 1993   ;  Hoch  et al., 1994   ).	bind
29538	1	8852	6	13	NULL	NULL	NULL	lectin	GP	Gal-specific	bind					asialyl-tetraantennary N-linked oligosaccharide	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_24024_s_23	7592600	A  Gal-specific lectin that binds asialyl-tetraantennary  N-linked  oligosaccharides and a Fuc/GlcNAc binding lectin have been found on rat  alveolar macrophages and Kupffer cells( 17,  18) .	bind
29539	2	8852	6	13	NULL	NULL	NULL	lectin	GP	Gal-specific	is found on					alveolar macrophages	Cell	rat			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_24024_s_23	7592600	A  Gal-specific lectin that binds asialyl-tetraantennary  N-linked  oligosaccharides and a Fuc/GlcNAc binding lectin have been found on rat  alveolar macrophages and Kupffer cells( 17,  18) .	bind
29540	3	8852	6	13	NULL	NULL	NULL	lectin	GP	Gal-specific	is found on					Kupffer cells	Cell	rat			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_24024_s_23	7592600	A  Gal-specific lectin that binds asialyl-tetraantennary  N-linked  oligosaccharides and a Fuc/GlcNAc binding lectin have been found on rat  alveolar macrophages and Kupffer cells( 17,  18) .	bind
29541	4	8852	6	13	NULL	NULL	NULL	lectin	GP		bind					Fuc/GlcNAc	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_24024_s_23	7592600	A  Gal-specific lectin that binds asialyl-tetraantennary  N-linked  oligosaccharides and a Fuc/GlcNAc binding lectin have been found on rat  alveolar macrophages and Kupffer cells( 17,  18) .	bind
29542	5	8852	6	13	NULL	NULL	NULL	lectin	GP		is found on					alveolar macrophages	Cell	rat			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_24024_s_23	7592600	A  Gal-specific lectin that binds asialyl-tetraantennary  N-linked  oligosaccharides and a Fuc/GlcNAc binding lectin have been found on rat  alveolar macrophages and Kupffer cells( 17,  18) .	bind
29543	6	8852	6	13	NULL	NULL	NULL	lectin	GP		is found on					Kupffer cells	Cell	rat			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_24024_s_23	7592600	A  Gal-specific lectin that binds asialyl-tetraantennary  N-linked  oligosaccharides and a Fuc/GlcNAc binding lectin have been found on rat  alveolar macrophages and Kupffer cells( 17,  18) .	bind
38190	1	8852	7	10	NULL	0	NULL	lectin	NULL	Gal-specific	bind	NULL				asialyl-tetraantennary N-linked oligosaccharides	NULL				NULL	rat alveolar macrophages	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_24024_s_23	7592600	A  Gal-specific lectin that binds asialyl-tetraantennary  N-linked  oligosaccharides and a Fuc/GlcNAc binding lectin have been found on rat  alveolar macrophages and Kupffer cells( 17,  18) .	bind
38191	2	8852	7	10	NULL	0	NULL	lectin	NULL	Gal-specific	bind	NULL				asialyl-tetraantennary N-linked oligosaccharides	NULL				NULL	rat Kupffer cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_24024_s_23	7592600	A  Gal-specific lectin that binds asialyl-tetraantennary  N-linked  oligosaccharides and a Fuc/GlcNAc binding lectin have been found on rat  alveolar macrophages and Kupffer cells( 17,  18) .	bind
38192	3	8852	7	NULL	NULL	0	NULL	Fuc/GlcNAc	NULL		bind	NULL				lectin	NULL				NULL	rat alveolar macrophages	0	NULL	NULL	NULL	gw60_jbiolchem_270_41_24024_s_23	7592600	A  Gal-specific lectin that binds asialyl-tetraantennary  N-linked  oligosaccharides and a Fuc/GlcNAc binding lectin have been found on rat  alveolar macrophages and Kupffer cells( 17,  18) .	bind
38194	4	8852	7	NULL	NULL	0	NULL	Fuc/GlcNAc	NULL		bind	NULL				lectin	NULL				NULL	rat Kupffer cells	0	NULL	NULL	NULL	gw60_jbiolchem_270_41_24024_s_23	7592600	A  Gal-specific lectin that binds asialyl-tetraantennary  N-linked  oligosaccharides and a Fuc/GlcNAc binding lectin have been found on rat  alveolar macrophages and Kupffer cells( 17,  18) .	bind
29544	2	8853	6	13	NULL	NULL	NULL	statement 1	GP		bind			amino terminal half		F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_32331_s_146	10915794	A  GST  fusion protein containing the amino-terminal half of B1 binds  F-actin.	bind
56165	1	8853	6	13	NULL	NULL	NULL	GST fusion protein	GP		contains					B1	GP		amino-terminal half		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_32331_s_146	10915794	A  GST  fusion protein containing the amino-terminal half of B1 binds  F-actin.	bind
38201	2	8853	7	NULL	NULL	0	NULL	statement 1	NULL		binds	NULL				F-actin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_32331_s_146	10915794	A  GST  fusion protein containing the amino-terminal half of B1 binds  F-actin.	bind
38203	1	8853	7	10	NULL	0	NULL	GST fusion protein			contains					B1			amino-terminal half		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_32331_s_146	10915794	A  GST  fusion protein containing the amino-terminal half of B1 binds  F-actin.	bind
29547	1	8855	6	13	NULL	NULL	NULL	JNK antisense oligonucleotide	NucleicAcid		downregulates					AP-1	GP	binding activity of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21618_s_274	11290748	A  JNK  antisense oligonucleotide down-regulates the binding activity of AP-1 and NF-kappaB.	bind
29548	2	8855	6	13	NULL	NULL	NULL	JNK antisense oligonucleotide	NucleicAcid		downregulates					NF-kappaB	GP	binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21618_s_274	11290748	A  JNK  antisense oligonucleotide down-regulates the binding activity of AP-1 and NF-kappaB.	bind
38211	1	8855	7	NULL	NULL	0	NULL	JNK antisense oligonucleotide	NULL		downregulates	NULL				AP-1	NULL	binding activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_24_21618_s_274	11290748	A  JNK  antisense oligonucleotide down-regulates the binding activity of AP-1 and NF-kappaB.	bind
38212	2	8855	7	NULL	NULL	0	NULL	JNK antisense oligonucleotide	NULL		downregulates	NULL				NF-kappaB	NULL	binding activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_24_21618_s_274	11290748	A  JNK  antisense oligonucleotide down-regulates the binding activity of AP-1 and NF-kappaB.	bind
47530	1	8856	6	13	NULL	NULL	NULL	FAD	Chemical		bind		specifically			apo-PchF	GP		flavin binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31202_s_212	8537385	A  K   value of 15 muM  at 25  degrees C and pH  7.0 was determined by fluorescence quenching of bound FAD; however, the  maximum fluorescence quenching was about 4 times greaterR than expected  if specific binding of FAD to the flavin binding site apo-PchF   had caused complete quenching of the FAD fluorescence.	bind
38215	1	8856	7	NULL	NULL	0	NULL	FAD 	NULL		bind	NULL	specifically			apo-PchF	NULL		flavin binding site 		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31202_s_212	8537385	A  K   value of 15 muM  at 25  degrees C and pH  7.0 was determined by fluorescence quenching of bound FAD; however, the  maximum fluorescence quenching was about 4 times greaterR than expected  if specific binding of FAD to the flavin binding site apo-PchF   had caused complete quenching of the FAD fluorescence.	bind
29549	1	8857	6	13	NULL	NULL	NULL	receptor	GP	mutant 	does not bind			N250A		[125]I-AB-MECA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_19056_s_127	11891221	A  K i value could not be determined (ND) for the N250A (6.55) mutant receptor, as this mutant receptor did bind to the agonist radioligand [125]I-AB-MECA or the antagonist radioligand [3]PSB-11.	bind
29550	2	8857	6	13	NULL	NULL	NULL	[125]I-AB-MECA	Chemical		is a type of					agonist radioligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_19056_s_127	11891221	A  K i value could not be determined (ND) for the N250A (6.55) mutant receptor, as this mutant receptor did bind to the agonist radioligand [125]I-AB-MECA or the antagonist radioligand [3]PSB-11.	bind
29551	3	8857	6	13	NULL	NULL	NULL	receptor	GP	mutant	does not bind			N250A		PSB-11	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_19056_s_127	11891221	A  K i value could not be determined (ND) for the N250A (6.55) mutant receptor, as this mutant receptor did bind to the agonist radioligand [125]I-AB-MECA or the antagonist radioligand [3]PSB-11.	bind
29552	4	8857	6	13	NULL	NULL	NULL	PSB-11	Chemical		is a type of					antagonist radioligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_19056_s_127	11891221	A  K i value could not be determined (ND) for the N250A (6.55) mutant receptor, as this mutant receptor did bind to the agonist radioligand [125]I-AB-MECA or the antagonist radioligand [3]PSB-11.	bind
38222	1	8857	7	10	NULL	0	NULL	receptor	NULL	mutant	does not bind	NULL		 N250A		[125]I-AB-MECA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_19056_s_127	11891221	A  K i value could not be determined (ND) for the N250A (6.55) mutant receptor, as this mutant receptor did bind to the agonist radioligand [125]I-AB-MECA or the antagonist radioligand [3]PSB-11.	bind
38223	2	8857	7	10	NULL	0	NULL	receptor	NULL	mutant	does not bind	NULL		N250A		[3]PSB-11	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_19056_s_127	11891221	A  K i value could not be determined (ND) for the N250A (6.55) mutant receptor, as this mutant receptor did bind to the agonist radioligand [125]I-AB-MECA or the antagonist radioligand [3]PSB-11.	bind
46953	3	8857	7	10	NULL	0	NULL	[125]I-AB-MECA	NULL		is a type of	NULL				agonist radioligand	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_19056_s_127	11891221	A  K i value could not be determined (ND) for the N250A (6.55) mutant receptor, as this mutant receptor did bind to the agonist radioligand [125]I-AB-MECA or the antagonist radioligand [3]PSB-11.	bind
46955	4	8857	7	10	NULL	0	NULL	[3]PSB-11	NULL		is a type of	NULL				antagonist radioligand 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_19056_s_127	11891221	A  K i value could not be determined (ND) for the N250A (6.55) mutant receptor, as this mutant receptor did bind to the agonist radioligand [125]I-AB-MECA or the antagonist radioligand [3]PSB-11.	bind
29553	1	8858	6	13	NULL	NULL	NULL	CcpA	GP		bind					phoPR	GP			cre site	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_4_1266_s_278	16452408	A  Kd of  0.5 nM was calculated for CcpA binding to the  phoPR cre site from the footprint data (data not shown) using the procedure described by Kim et. al ( ).	bind
38224	1	8858	7	NULL	NULL	0	NULL	 CcpA	NULL		bind	NULL				 phoPR	NULL			cre site	NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_4_1266_s_278	16452408	A  Kd of  0.5 nM was calculated for CcpA binding to the  phoPR cre site from the footprint data (data not shown) using the procedure described by Kim et. al ( ).	bind
29554	1	8860	6	13	NULL	NULL	NULL	dibucaine	Chemical		bind					spectrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_532_3_396_s_82	12482599	A  Kd of 35  M was estimated for dibucaine binding to spectrin and was independent of ionic strength of the buffer, in the presence of both low and high concentrations of NaCl ( Table 1).	bind
38225	1	8860	7	NULL	NULL	0	NULL	dibucaine	NULL		bind	NULL				spectrin	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_532_3_396_s_82	12482599	A  Kd of 35  M was estimated for dibucaine binding to spectrin and was independent of ionic strength of the buffer, in the presence of both low and high concentrations of NaCl ( Table 1).	bind
29555	1	8861	6	13	NULL	NULL	NULL	ferrocyanide	Chemical		bind					SOR	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_40_14750_s_51	17001016	A  Kd value of 0.80  plus-or-minus  0.07 muM was determined for the binding of ferrocyanide to SOR (Fig. 6, which is published as  supporting information on the PNAS web site).	bind
38228	1	8861	7	NULL	NULL	0	NULL	ferrocyanide	NULL		bind	NULL				SOR	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_40_14750_s_51	17001016	A  Kd value of 0.80  plus-or-minus  0.07 muM was determined for the binding of ferrocyanide to SOR (Fig. 6, which is published as  supporting information on the PNAS web site).	bind
29556	1	8862	6	13	NULL	NULL	NULL	CPX	GP		bind					CHO-hA1AdoR membrane	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_298_1_209_s_145	11408544	A  Kd value of 1 nM for [3]CPX binding to CHO-hA1AdoR membrane was used in calculation of  Ki values.	bind
38229	1	8862	7	NULL	NULL	0	NULL	[3]CPX	NULL		bind	NULL				CHO-hA1AdoR membrane	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_298_1_209_s_145	11408544	A  Kd value of 1 nM for [3]CPX binding to CHO-hA1AdoR membrane was used in calculation of  Ki values.	bind
29557	1	8863	6	13	NULL	NULL	NULL	MPT	GP		bind					XdhC	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_23_15701_s_149	16597619	A  KD value of 3.6  plus-or-minus  0.1 muM was obtained for Moco binding, and a  KD value of 3.5  plus-or-minus  0.3 muM was obtained for MPT binding to XdhC at 4  degrees C, showing that XdhC is able to bind both molecules with the same efficiency in stoichiometric amounts.	bind
46956	2	8863	6	13	NULL	NULL	NULL	Moco	GP		bind					XdhC	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_23_15701_s_149	16597619	A  KD value of 3.6  plus-or-minus  0.1 muM was obtained for Moco binding, and a  KD value of 3.5  plus-or-minus  0.3 muM was obtained for MPT binding to XdhC at 4  degrees C, showing that XdhC is able to bind both molecules with the same efficiency in stoichiometric amounts.	bind
46957	3	8863	6	13	NULL	NULL	NULL	statement 1	Process		same efficiency as					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_23_15701_s_149	16597619	A  KD value of 3.6  plus-or-minus  0.1 muM was obtained for Moco binding, and a  KD value of 3.5  plus-or-minus  0.3 muM was obtained for MPT binding to XdhC at 4  degrees C, showing that XdhC is able to bind both molecules with the same efficiency in stoichiometric amounts.	bind
38230	1	8863	7	NULL	NULL	0	NULL	Moco	NULL		bind	NULL				XdhC	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_23_15701_s_149	16597619	A  KD value of 3.6  plus-or-minus  0.1 muM was obtained for Moco binding, and a  KD value of 3.5  plus-or-minus  0.3 muM was obtained for MPT binding to XdhC at 4  degrees C, showing that XdhC is able to bind both molecules with the same efficiency in stoichiometric amounts.	bind
38231	2	8863	7	NULL	NULL	0	NULL	MPT	NULL		bind	NULL				XdhC	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_23_15701_s_149	16597619	A  KD value of 3.6  plus-or-minus  0.1 muM was obtained for Moco binding, and a  KD value of 3.5  plus-or-minus  0.3 muM was obtained for MPT binding to XdhC at 4  degrees C, showing that XdhC is able to bind both molecules with the same efficiency in stoichiometric amounts.	bind
38232	3	8863	7	NULL	NULL	0	NULL	statement 1	NULL		has same efficiency as	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_23_15701_s_149	16597619	A  KD value of 3.6  plus-or-minus  0.1 muM was obtained for Moco binding, and a  KD value of 3.5  plus-or-minus  0.3 muM was obtained for MPT binding to XdhC at 4  degrees C, showing that XdhC is able to bind both molecules with the same efficiency in stoichiometric amounts.	bind
29558	1	8864	6	13	NULL	NULL	NULL	pregnenolone 	Chemical		bind					sigma 1	GP				NULL	SH-SY5Y cells	NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_306_3_934_s_157	12750428	A  Ki value at sigma receptors in brain tissue has  not been reported, but we found that pregnenolone competed for  sigma1 binding with a  Ki value of 980   plus-or-minus  340 nM in SH-SY5Y cells (Werling,  2002  ).	bind
38233	1	8864	7	NULL	NULL	0	NULL	pregnenolone	NULL		bind	NULL				sigma1	NULL				NULL	SH-SY5Y cells	0	NULL	NULL	NULL	gw60_jpharmacolexpther_306_3_934_s_157	12750428	A  Ki value at sigma receptors in brain tissue has  not been reported, but we found that pregnenolone competed for  sigma1 binding with a  Ki value of 980   plus-or-minus  340 nM in SH-SY5Y cells (Werling,  2002  ).	bind
29559	1	8867	6	13	NULL	NULL	NULL	RA	Chemical		bind					RAR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
50886	2	8867	6	13	NULL	NULL	NULL	statement 1	Process		folds around			ligand binding domain		ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
50887	3	8867	6	13	NULL	NULL	NULL	RAR	GP		interacts with			lysine 220		RAR	GP		carboxylate tail		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
50888	4	8867	6	13	NULL	NULL	NULL	RAR	GP		interacts with			arginine 269		RAR	GP		carboxylate tail		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
50889	5	8867	6	13	NULL	NULL	NULL	RAR	GP		interacts with			lysine 220		RAR	GP		methionine 406		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
50890	6	8867	6	13	NULL	NULL	NULL	RAR	GP		interacts with			arginine 269		RAR	GP		methionine 406		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
50891	7	8867	6	13	NULL	NULL	NULL	RAR	GP		interacts with			isoleucine 410		9-cis RA	Chemical		methyl group located at the 9 position		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
50892	8	8867	6	13	NULL	NULL	NULL	statement 2	Process		allows					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
50893	9	8867	6	13	NULL	NULL	NULL	statement 2	Process		allows					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
50894	10	8867	6	13	NULL	NULL	NULL	statement 2	Process		allows					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
50895	11	8867	6	13	NULL	NULL	NULL	statement 2	Process		allows					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
50896	12	8867	6	13	NULL	NULL	NULL	statement 2	Process		allows					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
38244	1	8867	7	NULL	NULL	0	NULL	RA	NULL		bind	NULL				RAR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
38247	2	8867	7	NULL	NULL	0	NULL	statement 1	NULL		folds around	NULL		ligand binding domain		ligand	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
38250	3	8867	7	NULL	NULL	0	NULL	RAR	NULL		interacts with	NULL		lysine 220 		RAR	NULL		carboxylate tail		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
38251	4	8867	7	NULL	NULL	0	NULL	RAR	NULL		interacts with	NULL		arginine 269		RAR	NULL		carboxylate tail		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
38252	5	8867	7	NULL	NULL	0	NULL	RAR	NULL		interacts with	NULL		lysine 220 		RAR	NULL		 methionine 406		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
38253	6	8867	7	NULL	NULL	0	NULL	RAR	NULL		interacts with	NULL		arginine 269		RAR	NULL		 methionine 406		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
38254	7	8867	7	NULL	NULL	0	NULL	RAR	NULL		interacts with	NULL		isoleucine 410		 9- cis-RA	NULL		methyl group  at  9th position		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
38255	8	8867	7	NULL	NULL	0	NULL	statement 2	NULL		allows	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
50851	9	8867	7	NULL	NULL	0	NULL	statement 2	NULL		allows	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
50852	10	8867	7	NULL	NULL	0	NULL	statement 2	NULL		allows	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
50853	11	8867	7	NULL	NULL	0	NULL	statement 2	NULL		allows	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
50854	12	8867	7	NULL	NULL	0	NULL	statement 2	NULL		allows	NULL	possibly			statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20258_s_166	7657595	A  ligand-induced three-dimensional conformation may occur upon binding of  RA to an RAR such that the ligand binding domain ```folds'''   around the ligand leaving lysine 220 and arginine 269 to interact with  the carboxylate tail and methionine 406 and, possibly, isoleucine 410,  to interact with the methyl group located at the 9 position on  9- cis-RA.	bind
29560	1	8868	6	13	NULL	NULL	NULL	zinc finger protein	GP	maize	bind					zein gene	GP			prolamine box of promoter	NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_2_201_s_694	9922448	A  maize zinc-finger protein binds the prolamine box in zein gene promotors  and interacts with the basic leucine zipper transcriptional activator opaque2.	bind
29561	2	8868	6	13	NULL	NULL	NULL	statement 1	GP		interacts with					opaque 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_2_201_s_694	9922448	A  maize zinc-finger protein binds the prolamine box in zein gene promotors  and interacts with the basic leucine zipper transcriptional activator opaque2.	bind
29562	3	8868	6	13	NULL	NULL	NULL	opaque 2	GP		is a type of					basic leucine zipper transcriptional activator	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_2_201_s_694	9922448	A  maize zinc-finger protein binds the prolamine box in zein gene promotors  and interacts with the basic leucine zipper transcriptional activator opaque2.	bind
38274	1	8868	7	10	NULL	0	NULL	zinc-finger protein	NULL	maize	binds	NULL				zein gene	NULL			prolamine box of promoter	NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_2_201_s_694	9922448	A  maize zinc-finger protein binds the prolamine box in zein gene promotors  and interacts with the basic leucine zipper transcriptional activator opaque2.	bind
38277	2	8868	7	10	NULL	0	NULL	statement 1	NULL		interacts with	NULL				opaque2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_2_201_s_694	9922448	A  maize zinc-finger protein binds the prolamine box in zein gene promotors  and interacts with the basic leucine zipper transcriptional activator opaque2.	bind
38278	3	8868	7	10	NULL	0	NULL	opaque2	NULL		is a type of	NULL				basic leucine zipper transcriptional activator	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_2_201_s_694	9922448	A  maize zinc-finger protein binds the prolamine box in zein gene promotors  and interacts with the basic leucine zipper transcriptional activator opaque2.	bind
29563	1	8869	6	13	NULL	NULL	NULL	c-Mycax	GP		bind					promoter	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_135	12808131	A  majority (603 of 1,157) of the promoters occupied by TFIID is also bound by  c-Mycax, whereas almost all the c-Myc/Max-bound promoters also harbor TFIID  in Daudi cells.	bind
29564	2	8869	6	13	NULL	NULL	NULL	c-Myc/Max	GP		bind					promoter	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_135	12808131	A  majority (603 of 1,157) of the promoters occupied by TFIID is also bound by  c-Mycax, whereas almost all the c-Myc/Max-bound promoters also harbor TFIID  in Daudi cells.	bind
29565	3	8869	6	13	NULL	NULL	NULL	statement 2	Process		harbour					TFIID	GP				NULL	daudi cells	NULL	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_135	12808131	A  majority (603 of 1,157) of the promoters occupied by TFIID is also bound by  c-Mycax, whereas almost all the c-Myc/Max-bound promoters also harbor TFIID  in Daudi cells.	bind
30300	4	8869	6	13	NULL	NULL	NULL	TFIID	GP		bind					promoter	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_135	12808131	A  majority (603 of 1,157) of the promoters occupied by TFIID is also bound by  c-Mycax, whereas almost all the c-Myc/Max-bound promoters also harbor TFIID  in Daudi cells.	bind
30301	5	8869	6	13	NULL	NULL	NULL	statement 1	Process		occurs simultaneously with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_135	12808131	A  majority (603 of 1,157) of the promoters occupied by TFIID is also bound by  c-Mycax, whereas almost all the c-Myc/Max-bound promoters also harbor TFIID  in Daudi cells.	bind
38279	1	8869	7	10	NULL	0	NULL	c-Mycax	NULL		bind	NULL					NULL			promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_135	12808131	A  majority (603 of 1,157) of the promoters occupied by TFIID is also bound by  c-Mycax, whereas almost all the c-Myc/Max-bound promoters also harbor TFIID  in Daudi cells.	bind
38280	2	8869	7	10	NULL	0	NULL	 c-Myc/Max	NULL		bind	NULL					NULL			promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_135	12808131	A  majority (603 of 1,157) of the promoters occupied by TFIID is also bound by  c-Mycax, whereas almost all the c-Myc/Max-bound promoters also harbor TFIID  in Daudi cells.	bind
47544	3	8869	7	10	NULL	0	NULL	TFIID	NULL		bind	NULL					NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_135	12808131	A  majority (603 of 1,157) of the promoters occupied by TFIID is also bound by  c-Mycax, whereas almost all the c-Myc/Max-bound promoters also harbor TFIID  in Daudi cells.	bind
47545	4	8869	7	10	NULL	0	NULL	statement 1	NULL		occur simultaneously with	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_135	12808131	A  majority (603 of 1,157) of the promoters occupied by TFIID is also bound by  c-Mycax, whereas almost all the c-Myc/Max-bound promoters also harbor TFIID  in Daudi cells.	bind
47546	5	8869	7	10	NULL	0	NULL	statement 2	NULL		harbor	NULL				TFIID	NULL				NULL	Daudi cells	0	NULL	NULL	NULL	gw70_pnas_100_14_8164_s_135	12808131	A  majority (603 of 1,157) of the promoters occupied by TFIID is also bound by  c-Mycax, whereas almost all the c-Myc/Max-bound promoters also harbor TFIID  in Daudi cells.	bind
29566	1	8870	6	13	NULL	NULL	NULL	inscuteable	GP	mammalian partner of	bind					NuMA	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3144_s_380	12925752	A  mammalian partner of inscuteable binds NuMA and regulates mitotic spindle  organization.	bind
29567	2	8870	6	13	NULL	NULL	NULL	statement 1	Process		regulates					mitotic spindle	Chromosome	organization of			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3144_s_380	12925752	A  mammalian partner of inscuteable binds NuMA and regulates mitotic spindle  organization.	bind
38281	1	8870	7	NULL	NULL	0	NULL	inscuteable	NULL	mammalian partner of	binds	NULL				NuMA	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_8_3144_s_380	12925752	A  mammalian partner of inscuteable binds NuMA and regulates mitotic spindle  organization.	bind
38282	2	8870	7	NULL	NULL	0	NULL	statement 1	NULL		regulates	NULL				mitotic spindle	NULL	organization of			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_8_3144_s_380	12925752	A  mammalian partner of inscuteable binds NuMA and regulates mitotic spindle  organization.	bind
29568	1	8872	6	13	NULL	NULL	NULL	cT3Ralpha	GP		bind									K14RE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1416_s_93	8576132	A  mutated TREpal that does not bind cT3Ralpha  ( 28) does not  compete for the binding of cT3Ralpha  to K14RE ( Fig. 3).	bind
29569	2	8872	6	13	NULL	NULL	NULL	TREpal	GP	mutant	does not bind					cT3Ralpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1416_s_93	8576132	A  mutated TREpal that does not bind cT3Ralpha  ( 28) does not  compete for the binding of cT3Ralpha  to K14RE ( Fig. 3).	bind
29570	3	8872	6	13	NULL	NULL	NULL	statement 1	Process		does not compete					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1416_s_93	8576132	A  mutated TREpal that does not bind cT3Ralpha  ( 28) does not  compete for the binding of cT3Ralpha  to K14RE ( Fig. 3).	bind
38292	1	8872	7	NULL	NULL	0	NULL	TREpal	NULL	mutated	does not bind	NULL				cT3Ralpha	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_3_1416_s_93	8576132	A  mutated TREpal that does not bind cT3Ralpha  ( 28) does not  compete for the binding of cT3Ralpha  to K14RE ( Fig. 3).	bind
38293	2	8872	7	10	NULL	0	NULL	cT3Ralpha 	NULL		bind	NULL					NULL			K14RE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1416_s_93	8576132	A  mutated TREpal that does not bind cT3Ralpha  ( 28) does not  compete for the binding of cT3Ralpha  to K14RE ( Fig. 3).	bind
38294	3	8872	7	10	NULL	0	NULL	statement 1			does not compete with					statement 2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1416_s_93	8576132	A  mutated TREpal that does not bind cT3Ralpha  ( 28) does not  compete for the binding of cT3Ralpha  to K14RE ( Fig. 3).	bind
29571	1	8873	6	13	NULL	NULL	NULL	PRMT5 construct	GP	mutant;; myc tagged	leads to			S-adenosyl-l-methionine-binding motif I		enzymatic activity	Process	complete loss of			NULL	COS-1 cells	NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_276_35_11413150_s_9	11413150	A  mutation introduced into the S-adenosyl-l-methionine-binding motif I of  a myc-tagged PRMT5 construct in COS-1 cells led to a near complete loss  of observed enzymatic activity.	bind
38295	1	8873	7	10	NULL	0	NULL	PRMT5 construct	NULL	myc-tagged;;mutant	leads to	NULL		S-adenosyl-l-methionine-binding motif I 		enzymatic activity	NULL	near complete loss of			NULL	COS-1 cells 	NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_276_35_11413150_s_9	11413150	A  mutation introduced into the S-adenosyl-l-methionine-binding motif I of  a myc-tagged PRMT5 construct in COS-1 cells led to a near complete loss  of observed enzymatic activity.	bind
29572	1	8879	6	13	NULL	NULL	NULL	CIS gene	GP		is induced by					cytokine	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_22_0_503_s_373	15032587	A  novel cytokine-inducible gene CIS encodes an SH2-containing protein that binds to  tyrosine-phosphorylated interleukin 3 and erythropoietin receptors.	bind
29573	2	8879	6	13	NULL	NULL	NULL	CIS gene	GP		encodes					SH2-containing protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_22_0_503_s_373	15032587	A  novel cytokine-inducible gene CIS encodes an SH2-containing protein that binds to  tyrosine-phosphorylated interleukin 3 and erythropoietin receptors.	bind
29574	3	8879	6	13	NULL	NULL	NULL	statement 2	GP		bind					interleukin 3	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_22_0_503_s_373	15032587	A  novel cytokine-inducible gene CIS encodes an SH2-containing protein that binds to  tyrosine-phosphorylated interleukin 3 and erythropoietin receptors.	bind
29575	4	8879	6	13	NULL	NULL	NULL	statement 2	GP		bind					erythropoietin receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_22_0_503_s_373	15032587	A  novel cytokine-inducible gene CIS encodes an SH2-containing protein that binds to  tyrosine-phosphorylated interleukin 3 and erythropoietin receptors.	bind
38297	1	8879	7	NULL	NULL	0	NULL	CIS	NULL		encode	NULL				SH2-containing protein	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_22_0_503_s_373	15032587	A  novel cytokine-inducible gene CIS encodes an SH2-containing protein that binds to  tyrosine-phosphorylated interleukin 3 and erythropoietin receptors.	bind
38298	2	8879	7	NULL	NULL	0	NULL	CIS	NULL		is	NULL				cytokine-inducible gene	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_22_0_503_s_373	15032587	A  novel cytokine-inducible gene CIS encodes an SH2-containing protein that binds to  tyrosine-phosphorylated interleukin 3 and erythropoietin receptors.	bind
38299	3	8879	7	NULL	NULL	0	NULL	SH2-containing protein	NULL		binds to	NULL				interleukin 3 	NULL	phosphorylated	tyrosine		NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_22_0_503_s_373	15032587	A  novel cytokine-inducible gene CIS encodes an SH2-containing protein that binds to  tyrosine-phosphorylated interleukin 3 and erythropoietin receptors.	bind
38300	4	8879	7	NULL	NULL	0	NULL	SH2-containing protein	NULL		binds to	NULL				erythropoietin receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_22_0_503_s_373	15032587	A  novel cytokine-inducible gene CIS encodes an SH2-containing protein that binds to  tyrosine-phosphorylated interleukin 3 and erythropoietin receptors.	bind
29576	1	8880	6	13	NULL	NULL	NULL	PAR3	GP		bind		directly			PAR6	GP		PDZ domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_106_4_489_s_230	11525734	A  number of other PAR gene products have  been shown to be essential in establishing  polarity in the  C. elegans embryo, including a PDZ-containing  protein, PAR3, that binds directly to the PDZ domain  of PAR6.	bind
29577	2	8880	6	13	NULL	NULL	NULL	PAR gene products 	GP		establish					embryo	Organism	 polarity of;;C. elegans			NULL		NULL	NULL	NULL	NULL	gw60_cell_106_4_489_s_230	11525734	A  number of other PAR gene products have  been shown to be essential in establishing  polarity in the  C. elegans embryo, including a PDZ-containing  protein, PAR3, that binds directly to the PDZ domain  of PAR6.	bind
46958	3	8880	6	13	NULL	NULL	NULL	PAR3	GP		is a type of					PDZ-containing protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_106_4_489_s_230	11525734	A  number of other PAR gene products have  been shown to be essential in establishing  polarity in the  C. elegans embryo, including a PDZ-containing  protein, PAR3, that binds directly to the PDZ domain  of PAR6.	bind
38301	1	8880	7	NULL	NULL	0	NULL	 PAR3	NULL		binds	NULL	directly			PAR6	NULL		PDZ domain		NULL		0	NULL	NULL	NULL	gw60_cell_106_4_489_s_230	11525734	A  number of other PAR gene products have  been shown to be essential in establishing  polarity in the  C. elegans embryo, including a PDZ-containing  protein, PAR3, that binds directly to the PDZ domain  of PAR6.	bind
38302	2	8880	7	10	NULL	0	NULL	PAR gene products 	NULL		establishes	NULL				embryo	NULL	polarity of;;C. elegans			NULL		NULL	NULL	NULL	NULL	gw60_cell_106_4_489_s_230	11525734	A  number of other PAR gene products have  been shown to be essential in establishing  polarity in the  C. elegans embryo, including a PDZ-containing  protein, PAR3, that binds directly to the PDZ domain  of PAR6.	bind
38303	3	8880	7	NULL	NULL	0	NULL	PAR3	NULL		is a type of	NULL				PDZ-containing protein	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_106_4_489_s_230	11525734	A  number of other PAR gene products have  been shown to be essential in establishing  polarity in the  C. elegans embryo, including a PDZ-containing  protein, PAR3, that binds directly to the PDZ domain  of PAR6.	bind
29578	1	8881	6	13	NULL	NULL	NULL	virus	Organism		bind					CD4	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_23883_s_63	7592573	A  number of studies determined that antibodies to V3 were capable of  neutralizing virus infectivity(103-109) without affecting virus  binding to CD4( 108,  109) .	bind
29579	2	8881	6	13	NULL	NULL	NULL	antibodies to V3	GP		neutralize					virus	Organism	infectivity of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_23883_s_63	7592573	A  number of studies determined that antibodies to V3 were capable of  neutralizing virus infectivity(103-109) without affecting virus  binding to CD4( 108,  109) .	bind
29580	3	8881	6	13	NULL	NULL	NULL	statement 2	Process		does not affect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_23883_s_63	7592573	A  number of studies determined that antibodies to V3 were capable of  neutralizing virus infectivity(103-109) without affecting virus  binding to CD4( 108,  109) .	bind
38304	1	8881	7	10	NULL	0	NULL	V3 antibodies	NULL		neutralize	NULL				virus	NULL	infectivity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_23883_s_63	7592573	A  number of studies determined that antibodies to V3 were capable of  neutralizing virus infectivity(103-109) without affecting virus  binding to CD4( 108,  109) .	bind
38305	2	8881	7	NULL	NULL	0	NULL	virus	NULL		bind	NULL				CD4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_41_23883_s_63	7592573	A  number of studies determined that antibodies to V3 were capable of  neutralizing virus infectivity(103-109) without affecting virus  binding to CD4( 108,  109) .	bind
38306	3	8881	7	NULL	NULL	0	NULL	statement 1	NULL		does not affect	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_41_23883_s_63	7592573	A  number of studies determined that antibodies to V3 were capable of  neutralizing virus infectivity(103-109) without affecting virus  binding to CD4( 108,  109) .	bind
29581	1	8882	6	13	NULL	NULL	NULL	pde2delta	GP	mutant	lacks					cAMP-phosphodiesterase	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7064_s_153	9819393	A  pde2delta mutant strain lacks the cAMP-phosphodiesterase responsible for conversion of the majority of cytosolic cAMP to AMP, and as a consequence, addition of exogenous cAMP to the mutant cells increases the cytosolic cAMP concentration ( 64,  71,  72).	bind
29582	2	8882	6	13	NULL	NULL	NULL	cAMP	Chemical	cytosolic	is converted to					AMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7064_s_153	9819393	A  pde2delta mutant strain lacks the cAMP-phosphodiesterase responsible for conversion of the majority of cytosolic cAMP to AMP, and as a consequence, addition of exogenous cAMP to the mutant cells increases the cytosolic cAMP concentration ( 64,  71,  72).	bind
29583	3	8882	6	13	NULL	NULL	NULL	pde2delta	GP	mutant	is responsible for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7064_s_153	9819393	A  pde2delta mutant strain lacks the cAMP-phosphodiesterase responsible for conversion of the majority of cytosolic cAMP to AMP, and as a consequence, addition of exogenous cAMP to the mutant cells increases the cytosolic cAMP concentration ( 64,  71,  72).	bind
29584	4	8882	6	13	NULL	NULL	NULL	exogenous AMP	Chemical	addition of	increases					cAMP	Chemical	concentration of;; cytosolic			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7064_s_153	9819393	A  pde2delta mutant strain lacks the cAMP-phosphodiesterase responsible for conversion of the majority of cytosolic cAMP to AMP, and as a consequence, addition of exogenous cAMP to the mutant cells increases the cytosolic cAMP concentration ( 64,  71,  72).	bind
38307	1	8882	7	NULL	NULL	0	NULL	pde2delta	NULL	mutant	lacks	NULL				cAMP-phosphodiesterase	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_7064_s_153	9819393	A  pde2delta mutant strain lacks the cAMP-phosphodiesterase responsible for conversion of the majority of cytosolic cAMP to AMP, and as a consequence, addition of exogenous cAMP to the mutant cells increases the cytosolic cAMP concentration ( 64,  71,  72).	bind
38308	2	8882	7	NULL	NULL	0	NULL	cAMP	NULL	cytosolic	converts to	NULL				AMP	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_7064_s_153	9819393	A  pde2delta mutant strain lacks the cAMP-phosphodiesterase responsible for conversion of the majority of cytosolic cAMP to AMP, and as a consequence, addition of exogenous cAMP to the mutant cells increases the cytosolic cAMP concentration ( 64,  71,  72).	bind
38309	3	8882	7	NULL	NULL	0	NULL	statement 1	NULL		responsible for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_7064_s_153	9819393	A  pde2delta mutant strain lacks the cAMP-phosphodiesterase responsible for conversion of the majority of cytosolic cAMP to AMP, and as a consequence, addition of exogenous cAMP to the mutant cells increases the cytosolic cAMP concentration ( 64,  71,  72).	bind
38310	4	8882	7	10	NULL	0	NULL	exogenous cAMP	NULL	addition of	increase	NULL				cAMP	NULL	concentration of;;cytosolic			NULL	mutant cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7064_s_153	9819393	A  pde2delta mutant strain lacks the cAMP-phosphodiesterase responsible for conversion of the majority of cytosolic cAMP to AMP, and as a consequence, addition of exogenous cAMP to the mutant cells increases the cytosolic cAMP concentration ( 64,  71,  72).	bind
38311	5	8882	7	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_7064_s_153	9819393	A  pde2delta mutant strain lacks the cAMP-phosphodiesterase responsible for conversion of the majority of cytosolic cAMP to AMP, and as a consequence, addition of exogenous cAMP to the mutant cells increases the cytosolic cAMP concentration ( 64,  71,  72).	bind
29585	1	8883	6	13	NULL	NULL	NULL	peptide	GP		bind			Rev activation domain		CRM1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_2_255_s_200	10209022	A  peptide comprising the Rev activation domain plus a few  flanking residues bound CRM1 700 times weakerR ( Kd   7 muM), and the minimum Rev activation domain itself even  5,000-fold weaker ( Kd   50 muM) than snurportin 1.	bind
29586	2	8883	6	13	NULL	NULL	NULL	snurportin 1	GP		bind					CRM1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_2_255_s_200	10209022	A  peptide comprising the Rev activation domain plus a few  flanking residues bound CRM1 700 times weakerR ( Kd   7 muM), and the minimum Rev activation domain itself even  5,000-fold weaker ( Kd   50 muM) than snurportin 1.	bind
29587	3	8883	6	13	NULL	NULL	NULL	statement 1	Process	affinity of	is less than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_2_255_s_200	10209022	A  peptide comprising the Rev activation domain plus a few  flanking residues bound CRM1 700 times weakerR ( Kd   7 muM), and the minimum Rev activation domain itself even  5,000-fold weaker ( Kd   50 muM) than snurportin 1.	bind
38312	1	8883	7	NULL	NULL	0	NULL	peptide	NULL		bind	NULL		Rev activation domain plus a few flanking residues		CRM1	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_2_255_s_200	10209022	A  peptide comprising the Rev activation domain plus a few  flanking residues bound CRM1 700 times weakerR ( Kd   7 muM), and the minimum Rev activation domain itself even  5,000-fold weaker ( Kd   50 muM) than snurportin 1.	bind
38313	2	8883	7	NULL	NULL	0	NULL	peptide	NULL		bind	NULL		Rev activation domain		CRM1	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_2_255_s_200	10209022	A  peptide comprising the Rev activation domain plus a few  flanking residues bound CRM1 700 times weakerR ( Kd   7 muM), and the minimum Rev activation domain itself even  5,000-fold weaker ( Kd   50 muM) than snurportin 1.	bind
38314	3	8883	7	NULL	NULL	0	NULL	snurportin 1	NULL		bind	NULL				CRM1	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_2_255_s_200	10209022	A  peptide comprising the Rev activation domain plus a few  flanking residues bound CRM1 700 times weakerR ( Kd   7 muM), and the minimum Rev activation domain itself even  5,000-fold weaker ( Kd   50 muM) than snurportin 1.	bind
38315	4	8883	7	NULL	NULL	0	NULL	statement 1	NULL	binding of	is weaker than	NULL				statement 3	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_2_255_s_200	10209022	A  peptide comprising the Rev activation domain plus a few  flanking residues bound CRM1 700 times weakerR ( Kd   7 muM), and the minimum Rev activation domain itself even  5,000-fold weaker ( Kd   50 muM) than snurportin 1.	bind
38316	5	8883	7	NULL	NULL	0	NULL	statement 2	NULL	binding of	is weaker than	NULL				statement 3	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_2_255_s_200	10209022	A  peptide comprising the Rev activation domain plus a few  flanking residues bound CRM1 700 times weakerR ( Kd   7 muM), and the minimum Rev activation domain itself even  5,000-fold weaker ( Kd   50 muM) than snurportin 1.	bind
29588	1	8884	6	13	NULL	NULL	NULL	PhoP	GP		bind					PV	GP			core binding region of promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_15_5166_s_195	16030210	A  phoB promoter fragment containing only the PS promoter (from pPS2 [Fig.  1]) was used as a template for in vitro transcription to determine if reduction of the PS transcript from the  phoB-PS+V promoter in the presence of phosphorylated PhoP was exclusively the result of PhoP binding to the PV promoter core binding region, which blocked RNAP passage (Fig.  5A, top panel).	bind
29589	2	8884	6	13	NULL	NULL	NULL	statement 1	Process		blocks					RNAP	GP	passage of 			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_15_5166_s_195	16030210	A  phoB promoter fragment containing only the PS promoter (from pPS2 [Fig.  1]) was used as a template for in vitro transcription to determine if reduction of the PS transcript from the  phoB-PS+V promoter in the presence of phosphorylated PhoP was exclusively the result of PhoP binding to the PV promoter core binding region, which blocked RNAP passage (Fig.  5A, top panel).	bind
38317	1	8884	7	NULL	NULL	0	NULL	PhoP	NULL		bind	NULL				PV	NULL			promoter core binding region	NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_15_5166_s_195	16030210	A  phoB promoter fragment containing only the PS promoter (from pPS2 [Fig.  1]) was used as a template for in vitro transcription to determine if reduction of the PS transcript from the  phoB-PS+V promoter in the presence of phosphorylated PhoP was exclusively the result of PhoP binding to the PV promoter core binding region, which blocked RNAP passage (Fig.  5A, top panel).	bind
38318	2	8884	7	10	NULL	0	NULL	statement 1	NULL		blocks	NULL				RNAP	NULL	passage of			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_15_5166_s_195	16030210	A  phoB promoter fragment containing only the PS promoter (from pPS2 [Fig.  1]) was used as a template for in vitro transcription to determine if reduction of the PS transcript from the  phoB-PS+V promoter in the presence of phosphorylated PhoP was exclusively the result of PhoP binding to the PV promoter core binding region, which blocked RNAP passage (Fig.  5A, top panel).	bind
29612	1	8885	6	13	NULL	NULL	NULL	Cbl	GP		bind					Crk	GP		SH2 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8435_s_7	8626543	A  phosphopeptide corresponding to a potential Crk SH2 domain-binding  motif in Cbl (pYDVP) specifically inhibited binding between Cbl and Crk  SH2 domain.	bind
29693	2	8885	6	13	NULL	NULL	NULL	phosphopeptide	GP		corresponds to					Cbl	GP	potential	Crk SH2 domain-binding motif		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8435_s_7	8626543	A  phosphopeptide corresponding to a potential Crk SH2 domain-binding  motif in Cbl (pYDVP) specifically inhibited binding between Cbl and Crk  SH2 domain.	bind
29695	3	8885	6	13	NULL	NULL	NULL	statement 2	Process		inhibits					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8435_s_7	8626543	A  phosphopeptide corresponding to a potential Crk SH2 domain-binding  motif in Cbl (pYDVP) specifically inhibited binding between Cbl and Crk  SH2 domain.	bind
38319	1	8885	7	NULL	NULL	0	NULL	Cbl	NULL		bind	NULL				Crk	NULL		SH2 domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8435_s_7	8626543	A  phosphopeptide corresponding to a potential Crk SH2 domain-binding  motif in Cbl (pYDVP) specifically inhibited binding between Cbl and Crk  SH2 domain.	bind
38320	2	8885	7	NULL	NULL	0	NULL	phosphopeptide	NULL		corresponds to	NULL				Cbl	NULL		pYDVP Crk SH2 domain-binding motif		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8435_s_7	8626543	A  phosphopeptide corresponding to a potential Crk SH2 domain-binding  motif in Cbl (pYDVP) specifically inhibited binding between Cbl and Crk  SH2 domain.	bind
38321	3	8885	7	NULL	NULL	0	NULL	statement 2	NULL		inhibits	NULL	specifically			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8435_s_7	8626543	A  phosphopeptide corresponding to a potential Crk SH2 domain-binding  motif in Cbl (pYDVP) specifically inhibited binding between Cbl and Crk  SH2 domain.	bind
29696	1	8886	6	13	NULL	NULL	NULL	v-Crk	GP		bind					paxillin	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31219_s_7	8537387	A  phosphotyrosine peptide, which can inhibit v-Crk binding to paxillin,  did not inhibit Csk binding to paxillin, suggesting that v-Crk and Csk  bind to different tyrosine-phosphorylated sites in paxillin.	bind
29697	2	8886	6	13	NULL	NULL	NULL	Csk	GP		bind					paxillin	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31219_s_7	8537387	A  phosphotyrosine peptide, which can inhibit v-Crk binding to paxillin,  did not inhibit Csk binding to paxillin, suggesting that v-Crk and Csk  bind to different tyrosine-phosphorylated sites in paxillin.	bind
29698	3	8886	6	13	NULL	NULL	NULL	phosphotyrosine peptide	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31219_s_7	8537387	A  phosphotyrosine peptide, which can inhibit v-Crk binding to paxillin,  did not inhibit Csk binding to paxillin, suggesting that v-Crk and Csk  bind to different tyrosine-phosphorylated sites in paxillin.	bind
29699	4	8886	6	13	NULL	NULL	NULL	phosphotyrosine peptide	GP		does not inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31219_s_7	8537387	A  phosphotyrosine peptide, which can inhibit v-Crk binding to paxillin,  did not inhibit Csk binding to paxillin, suggesting that v-Crk and Csk  bind to different tyrosine-phosphorylated sites in paxillin.	bind
38402	1	8886	7	10	NULL	0	NULL	v-Crk	NULL		bind	NULL				paxillin	NULL	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31219_s_7	8537387	A  phosphotyrosine peptide, which can inhibit v-Crk binding to paxillin,  did not inhibit Csk binding to paxillin, suggesting that v-Crk and Csk  bind to different tyrosine-phosphorylated sites in paxillin.	bind
38403	2	8886	7	10	NULL	0	NULL	Csk	NULL		bind	NULL				paxillin	NULL	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31219_s_7	8537387	A  phosphotyrosine peptide, which can inhibit v-Crk binding to paxillin,  did not inhibit Csk binding to paxillin, suggesting that v-Crk and Csk  bind to different tyrosine-phosphorylated sites in paxillin.	bind
38404	3	8886	7	NULL	NULL	0	NULL	phosphotyrosine peptide	NULL		inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31219_s_7	8537387	A  phosphotyrosine peptide, which can inhibit v-Crk binding to paxillin,  did not inhibit Csk binding to paxillin, suggesting that v-Crk and Csk  bind to different tyrosine-phosphorylated sites in paxillin.	bind
38405	4	8886	7	NULL	NULL	0	NULL	phosphotyrosine peptide	NULL		does not inhibit	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31219_s_7	8537387	A  phosphotyrosine peptide, which can inhibit v-Crk binding to paxillin,  did not inhibit Csk binding to paxillin, suggesting that v-Crk and Csk  bind to different tyrosine-phosphorylated sites in paxillin.	bind
38406	5	8886	7	NULL	NULL	0	NULL	statement 1	NULL	binding site of	is different from	NULL				statement 2	NULL	binding site of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31219_s_7	8537387	A  phosphotyrosine peptide, which can inhibit v-Crk binding to paxillin,  did not inhibit Csk binding to paxillin, suggesting that v-Crk and Csk  bind to different tyrosine-phosphorylated sites in paxillin.	bind
29700	1	8887	6	13	NULL	NULL	NULL	Pex6p	GP		bind					Pex15p	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_6_2226_s_7	12808025	A  point mutation in the Walker A motif of D1 (K489A) decreased the binding of  Pex6p to Pex15p indicating that the interaction of Pex6p with Pex15p required  binding of ATP.	bind
29701	2	8887	6	13	NULL	NULL	NULL	D1	GP	point mutant	decreases			Walker A motif (K489A)		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_6_2226_s_7	12808025	A  point mutation in the Walker A motif of D1 (K489A) decreased the binding of  Pex6p to Pex15p indicating that the interaction of Pex6p with Pex15p required  binding of ATP.	bind
29702	3	8887	6	13	NULL	NULL	NULL	statement 1	Process		requires					ATP	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_6_2226_s_7	12808025	A  point mutation in the Walker A motif of D1 (K489A) decreased the binding of  Pex6p to Pex15p indicating that the interaction of Pex6p with Pex15p required  binding of ATP.	bind
38407	1	8887	7	NULL	NULL	0	NULL	Pex6p	NULL		bind	NULL				 Pex15p	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_6_2226_s_7	12808025	A  point mutation in the Walker A motif of D1 (K489A) decreased the binding of  Pex6p to Pex15p indicating that the interaction of Pex6p with Pex15p required  binding of ATP.	bind
38408	2	8887	7	NULL	NULL	0	NULL	D1	NULL	point mutant	decrease	NULL		Walker A motif K489A		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_6_2226_s_7	12808025	A  point mutation in the Walker A motif of D1 (K489A) decreased the binding of  Pex6p to Pex15p indicating that the interaction of Pex6p with Pex15p required  binding of ATP.	bind
38409	3	8887	7	NULL	NULL	0	NULL	statement 1	NULL		requires	NULL				ATP	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_6_2226_s_7	12808025	A  point mutation in the Walker A motif of D1 (K489A) decreased the binding of  Pex6p to Pex15p indicating that the interaction of Pex6p with Pex15p required  binding of ATP.	bind
29703	1	8888	6	13	NULL	NULL	NULL	Oct-1	GP		bind					TNF	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_annurevgenomicshum_2_0_373_s_643	null	A  polymorphism that affects OCT-1 binding to the TNF promoter region is associated  with severe malaria.	bind
29837	2	8888	6	13	NULL	NULL	NULL	gene polymorphism	Process		is associated with					severe malaria	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenomicshum_2_0_373_s_643	null	A  polymorphism that affects OCT-1 binding to the TNF promoter region is associated  with severe malaria.	bind
29838	3	8888	6	13	NULL	NULL	NULL	statement 2	Process		affects					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenomicshum_2_0_373_s_643	null	A  polymorphism that affects OCT-1 binding to the TNF promoter region is associated  with severe malaria.	bind
38410	1	8888	7	NULL	NULL	0	NULL	OCT-1	NULL		bind	NULL				TNF	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_annurevgenomicshum_2_0_373_s_643	null	A  polymorphism that affects OCT-1 binding to the TNF promoter region is associated  with severe malaria.	bind
38411	2	8888	7	NULL	NULL	0	NULL	polymorphism	NULL		affects	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevgenomicshum_2_0_373_s_643	null	A  polymorphism that affects OCT-1 binding to the TNF promoter region is associated  with severe malaria.	bind
38412	3	8888	7	NULL	NULL	0	NULL	statement 2	NULL		is associated with	NULL				malaria	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevgenomicshum_2_0_373_s_643	null	A  polymorphism that affects OCT-1 binding to the TNF promoter region is associated  with severe malaria.	bind
29704	1	8889	6	13	NULL	NULL	NULL	FK506	Chemical		bind					FKBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_6_875_s_118	9200606	A  portion of FK506 bound to FKBP, and the AlaPro dipeptides bound to Pin1  and CyPA are shown.	bind
29705	2	8889	6	13	NULL	NULL	NULL	AlaPro dipeptide	AminoAcid		bind					Pin1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_6_875_s_118	9200606	A  portion of FK506 bound to FKBP, and the AlaPro dipeptides bound to Pin1  and CyPA are shown.	bind
29708	3	8889	6	13	NULL	NULL	NULL	AlaPro dipeptide	AminoAcid		bind					CyPA	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_6_875_s_118	9200606	A  portion of FK506 bound to FKBP, and the AlaPro dipeptides bound to Pin1  and CyPA are shown.	bind
38413	1	8889	7	10	NULL	0	NULL	FK506	NULL		bind	NULL				FKBP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_6_875_s_118	9200606	A  portion of FK506 bound to FKBP, and the AlaPro dipeptides bound to Pin1  and CyPA are shown.	bind
38414	2	8889	7	NULL	NULL	0	NULL	AlaPro dipeptides	NULL		bind	NULL				Pin1	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_89_6_875_s_118	9200606	A  portion of FK506 bound to FKBP, and the AlaPro dipeptides bound to Pin1  and CyPA are shown.	bind
38415	3	8889	7	NULL	NULL	0	NULL	AlaPro dipeptides	NULL		bind	NULL				CyPA	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_89_6_875_s_118	9200606	A  portion of FK506 bound to FKBP, and the AlaPro dipeptides bound to Pin1  and CyPA are shown.	bind
29709	1	8890	6	13	NULL	NULL	NULL	fMLP	GP		bind					fMLP receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_305_3_846_s_130	12626661	A  previous study (Raiden et al.,  1997  ) reported that losartan blocked the binding of  [3]fMLP to the fMLP receptor, which was found to have 25 to 30%  structural homology with the AT1 receptor.	bind
29711	2	8890	6	13	NULL	NULL	NULL	losartan	Chemical		blocked					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_305_3_846_s_130	12626661	A  previous study (Raiden et al.,  1997  ) reported that losartan blocked the binding of  [3]fMLP to the fMLP receptor, which was found to have 25 to 30%  structural homology with the AT1 receptor.	bind
29714	3	8890	6	13	NULL	NULL	NULL	fMLP receptor	GP		is homologous to		structurally			AT1 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_305_3_846_s_130	12626661	A  previous study (Raiden et al.,  1997  ) reported that losartan blocked the binding of  [3]fMLP to the fMLP receptor, which was found to have 25 to 30%  structural homology with the AT1 receptor.	bind
38416	1	8890	7	10	NULL	0	NULL	fMLP 			bind					fMLP receptor					NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_305_3_846_s_130	12626661	A  previous study (Raiden et al.,  1997  ) reported that losartan blocked the binding of  [3]fMLP to the fMLP receptor, which was found to have 25 to 30%  structural homology with the AT1 receptor.	bind
38417	2	8890	7	NULL	NULL	0	NULL	losartan 	NULL		block	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_305_3_846_s_130	12626661	A  previous study (Raiden et al.,  1997  ) reported that losartan blocked the binding of  [3]fMLP to the fMLP receptor, which was found to have 25 to 30%  structural homology with the AT1 receptor.	bind
38418	3	8890	7	10	NULL	0	NULL	losartan 			is homologous to		structurally			AT1 receptor					NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_305_3_846_s_130	12626661	A  previous study (Raiden et al.,  1997  ) reported that losartan blocked the binding of  [3]fMLP to the fMLP receptor, which was found to have 25 to 30%  structural homology with the AT1 receptor.	bind
29717	1	8891	6	13	NULL	NULL	NULL	calponin	GP		bind			CH domain		actin	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-mol-biol_359_2_16626733_s_5	16626733	A  previous three-dimensional reconstruction of the calponin-F-actin complex  has led to the conclusion that the visualized portion of calponin bound  to actin belongs to its amino-terminal homology (CH) domain.	bind
29718	2	8891	6	13	NULL	NULL	NULL	CH domain	GP		is					amino-terminal homology domain	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-mol-biol_359_2_16626733_s_5	16626733	A  previous three-dimensional reconstruction of the calponin-F-actin complex  has led to the conclusion that the visualized portion of calponin bound  to actin belongs to its amino-terminal homology (CH) domain.	bind
38419	1	8891	7	10	NULL	0	NULL	calponin			bind			CH domain		actin					NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-mol-biol_359_2_16626733_s_5	16626733	A  previous three-dimensional reconstruction of the calponin-F-actin complex  has led to the conclusion that the visualized portion of calponin bound  to actin belongs to its amino-terminal homology (CH) domain.	bind
56166	2	8891	7	10	NULL	0	NULL	CH domain			is					amino-terminal homology domain					NULL		0	NULL	NULL	NULL	abs-batch0680-0699_j-mol-biol_359_2_16626733_s_5	16626733	A  previous three-dimensional reconstruction of the calponin-F-actin complex  has led to the conclusion that the visualized portion of calponin bound  to actin belongs to its amino-terminal homology (CH) domain.	bind
29719	1	8892	6	13	NULL	NULL	NULL	VWF	GP	proteolytic fragment of	bind		directly	Leu-480/Val-481 to Gly-718		GPIb	GP	platelet			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_22_13406_s_25	7539426	A  proteolytic fragment of VWF that contains residues Leu-480/Val-481 to  Gly-718  ( 7) binds directly to platelet GPIb.	bind
38420	1	8892	7	10	NULL	0	NULL	VWF	NULL	proteolytic fragment of	bind	NULL	directly	Leu-480/Val-481 to Gly-718		GPIb	NULL	platelet			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_22_13406_s_25	7539426	A  proteolytic fragment of VWF that contains residues Leu-480/Val-481 to  Gly-718  ( 7) binds directly to platelet GPIb.	bind
29839	1	8893	6	13	NULL	NULL	NULL	fusion protein	GP	purified	bind			 A subunit residues 328-390		CaN	GP		B subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_456_s_5	7814411	A  purified fusion protein containing residues 328-390 of the A  subunit 1) binds CaN B subunit, and 2) inhibits (IC   =  0.1 muM) the  in vitro  stimulation  of CaN A phosphatase activity by purified CaN B subunit.	bind
29841	2	8893	6	13	NULL	NULL	NULL	CaN	GP	purified	stimulates			B subunit		CaN A	GP	phosphatase activity of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_456_s_5	7814411	A  purified fusion protein containing residues 328-390 of the A  subunit 1) binds CaN B subunit, and 2) inhibits (IC   =  0.1 muM) the  in vitro  stimulation  of CaN A phosphatase activity by purified CaN B subunit.	bind
29842	3	8893	6	13	NULL	NULL	NULL	statement 1	Process		inhibits					statement 3	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_456_s_5	7814411	A  purified fusion protein containing residues 328-390 of the A  subunit 1) binds CaN B subunit, and 2) inhibits (IC   =  0.1 muM) the  in vitro  stimulation  of CaN A phosphatase activity by purified CaN B subunit.	bind
38422	1	8893	7	10	NULL	0	NULL	fusion protein		purified	binds			A subunit residues 328-390		CaN			B subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_456_s_5	7814411	A  purified fusion protein containing residues 328-390 of the A  subunit 1) binds CaN B subunit, and 2) inhibits (IC   =  0.1 muM) the  in vitro  stimulation  of CaN A phosphatase activity by purified CaN B subunit.	bind
38423	2	8893	7	10	NULL	0	NULL	CaN	NULL	purified	stimulates	NULL		B subunit		CaN A 	NULL	phosphatase activity of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_456_s_5	7814411	A  purified fusion protein containing residues 328-390 of the A  subunit 1) binds CaN B subunit, and 2) inhibits (IC   =  0.1 muM) the  in vitro  stimulation  of CaN A phosphatase activity by purified CaN B subunit.	bind
38424	3	8893	7	10	NULL	0	NULL	statement 1			inhibits					statement 2					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_456_s_5	7814411	A  purified fusion protein containing residues 328-390 of the A  subunit 1) binds CaN B subunit, and 2) inhibits (IC   =  0.1 muM) the  in vitro  stimulation  of CaN A phosphatase activity by purified CaN B subunit.	bind
29720	1	8894	6	13	NULL	NULL	NULL	SOM230	Chemical		is a type of					cyclohexapeptide somatostatin analog	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-endocrinol-invest_28_11-suppl_16625840_s_3	16625840	A  rational medicinal chemistry approach capitalising on structure activity  relationships has led to the discovery of SOM230, a novel, stable cyclohexapeptide  somatostatin analog which exhibits multi-receptor binding to human somatostatin  receptor (SSTR) subtypes (SSTR 1-5).	bind
29721	2	8894	6	13	NULL	NULL	NULL	SSTR 1-5	GP		is a type of					somatostatin receptor subtype	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-endocrinol-invest_28_11-suppl_16625840_s_3	16625840	A  rational medicinal chemistry approach capitalising on structure activity  relationships has led to the discovery of SOM230, a novel, stable cyclohexapeptide  somatostatin analog which exhibits multi-receptor binding to human somatostatin  receptor (SSTR) subtypes (SSTR 1-5).	bind
29722	3	8894	6	13	NULL	NULL	NULL	SOM230	Chemical		bind					SSTR 1-5	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-endocrinol-invest_28_11-suppl_16625840_s_3	16625840	A  rational medicinal chemistry approach capitalising on structure activity  relationships has led to the discovery of SOM230, a novel, stable cyclohexapeptide  somatostatin analog which exhibits multi-receptor binding to human somatostatin  receptor (SSTR) subtypes (SSTR 1-5).	bind
38425	1	8894	7	NULL	NULL	0	NULL	SOM230	NULL		exhibits	NULL				 multi-receptor binding	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-endocrinol-invest_28_11-suppl_16625840_s_3	16625840	A  rational medicinal chemistry approach capitalising on structure activity  relationships has led to the discovery of SOM230, a novel, stable cyclohexapeptide  somatostatin analog which exhibits multi-receptor binding to human somatostatin  receptor (SSTR) subtypes (SSTR 1-5).	bind
38426	2	8894	7	NULL	NULL	0	NULL	SOM230	NULL		bind	NULL				SSTR1	NULL	human			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-endocrinol-invest_28_11-suppl_16625840_s_3	16625840	A  rational medicinal chemistry approach capitalising on structure activity  relationships has led to the discovery of SOM230, a novel, stable cyclohexapeptide  somatostatin analog which exhibits multi-receptor binding to human somatostatin  receptor (SSTR) subtypes (SSTR 1-5).	bind
38427	3	8894	7	NULL	NULL	0	NULL	SOM230	NULL		bind	NULL				SSTR2	NULL	human			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-endocrinol-invest_28_11-suppl_16625840_s_3	16625840	A  rational medicinal chemistry approach capitalising on structure activity  relationships has led to the discovery of SOM230, a novel, stable cyclohexapeptide  somatostatin analog which exhibits multi-receptor binding to human somatostatin  receptor (SSTR) subtypes (SSTR 1-5).	bind
38428	4	8894	7	NULL	NULL	0	NULL	SOM230	NULL		bind	NULL				SSTR3	NULL	human			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-endocrinol-invest_28_11-suppl_16625840_s_3	16625840	A  rational medicinal chemistry approach capitalising on structure activity  relationships has led to the discovery of SOM230, a novel, stable cyclohexapeptide  somatostatin analog which exhibits multi-receptor binding to human somatostatin  receptor (SSTR) subtypes (SSTR 1-5).	bind
38429	5	8894	7	NULL	NULL	0	NULL	SOM230	NULL		bind	NULL				SSTR4	NULL	human			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-endocrinol-invest_28_11-suppl_16625840_s_3	16625840	A  rational medicinal chemistry approach capitalising on structure activity  relationships has led to the discovery of SOM230, a novel, stable cyclohexapeptide  somatostatin analog which exhibits multi-receptor binding to human somatostatin  receptor (SSTR) subtypes (SSTR 1-5).	bind
38430	6	8894	7	NULL	NULL	0	NULL	SOM230	NULL		bind	NULL				SSTR5	NULL	human			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-endocrinol-invest_28_11-suppl_16625840_s_3	16625840	A  rational medicinal chemistry approach capitalising on structure activity  relationships has led to the discovery of SOM230, a novel, stable cyclohexapeptide  somatostatin analog which exhibits multi-receptor binding to human somatostatin  receptor (SSTR) subtypes (SSTR 1-5).	bind
38431	7	8894	7	NULL	NULL	0	NULL	SSTR	NULL		is	NULL				somatostatin receptor	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-endocrinol-invest_28_11-suppl_16625840_s_3	16625840	A  rational medicinal chemistry approach capitalising on structure activity  relationships has led to the discovery of SOM230, a novel, stable cyclohexapeptide  somatostatin analog which exhibits multi-receptor binding to human somatostatin  receptor (SSTR) subtypes (SSTR 1-5).	bind
38432	8	8894	7	10	NULL	0	NULL	SOM230			is an analog of		stable			cyclohexapeptide somatostatin					NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-endocrinol-invest_28_11-suppl_16625840_s_3	16625840	A  rational medicinal chemistry approach capitalising on structure activity  relationships has led to the discovery of SOM230, a novel, stable cyclohexapeptide  somatostatin analog which exhibits multi-receptor binding to human somatostatin  receptor (SSTR) subtypes (SSTR 1-5).	bind
47902	9	8894	7	NULL	NULL	0	NULL	SSTR1	NULL		is a type of	NULL				somatostatin receptor subtype	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-endocrinol-invest_28_11-suppl_16625840_s_3	16625840	A  rational medicinal chemistry approach capitalising on structure activity  relationships has led to the discovery of SOM230, a novel, stable cyclohexapeptide  somatostatin analog which exhibits multi-receptor binding to human somatostatin  receptor (SSTR) subtypes (SSTR 1-5).	bind
47903	10	8894	7	NULL	NULL	0	NULL	SSTR2	NULL		is a type of	NULL				somatostatin receptor subtype	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-endocrinol-invest_28_11-suppl_16625840_s_3	16625840	A  rational medicinal chemistry approach capitalising on structure activity  relationships has led to the discovery of SOM230, a novel, stable cyclohexapeptide  somatostatin analog which exhibits multi-receptor binding to human somatostatin  receptor (SSTR) subtypes (SSTR 1-5).	bind
47904	11	8894	7	NULL	NULL	0	NULL	SSTR3	NULL		is a type of	NULL				somatostatin receptor subtype	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-endocrinol-invest_28_11-suppl_16625840_s_3	16625840	A  rational medicinal chemistry approach capitalising on structure activity  relationships has led to the discovery of SOM230, a novel, stable cyclohexapeptide  somatostatin analog which exhibits multi-receptor binding to human somatostatin  receptor (SSTR) subtypes (SSTR 1-5).	bind
47905	12	8894	7	NULL	NULL	0	NULL	SSTR4	NULL		is a type of	NULL				somatostatin receptor subtype	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-endocrinol-invest_28_11-suppl_16625840_s_3	16625840	A  rational medicinal chemistry approach capitalising on structure activity  relationships has led to the discovery of SOM230, a novel, stable cyclohexapeptide  somatostatin analog which exhibits multi-receptor binding to human somatostatin  receptor (SSTR) subtypes (SSTR 1-5).	bind
47906	13	8894	7	NULL	NULL	0	NULL	SSTR5	NULL		is a type of	NULL				somatostatin receptor subtype	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-endocrinol-invest_28_11-suppl_16625840_s_3	16625840	A  rational medicinal chemistry approach capitalising on structure activity  relationships has led to the discovery of SOM230, a novel, stable cyclohexapeptide  somatostatin analog which exhibits multi-receptor binding to human somatostatin  receptor (SSTR) subtypes (SSTR 1-5).	bind
29843	1	8895	6	13	NULL	NULL	NULL	Raf	GP	mutant	lacks								cysteine-rich domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_17_9809_s_77	7730360	A  recent investigation has demonstrated partially reduced coprecipitation  and   in vitro binding between Ras and a Raf mutant lacking the  cysteine-rich domain  ( 28) , supporting our finding of two Ras  binding sites in Raf.	bind
30302	2	8895	6	13	NULL	NULL	NULL	Ras	GP		bind					statement 1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_17_9809_s_77	7730360	A  recent investigation has demonstrated partially reduced coprecipitation  and   in vitro binding between Ras and a Raf mutant lacking the  cysteine-rich domain  ( 28) , supporting our finding of two Ras  binding sites in Raf.	bind
30304	3	8895	6	13	NULL	NULL	NULL	Raf	GP		possesses								Ras binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_17_9809_s_77	7730360	A  recent investigation has demonstrated partially reduced coprecipitation  and   in vitro binding between Ras and a Raf mutant lacking the  cysteine-rich domain  ( 28) , supporting our finding of two Ras  binding sites in Raf.	bind
38433	2	8895	7	10	NULL	0	NULL	Ras	NULL		bind	NULL				statement 1	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_17_9809_s_77	7730360	A  recent investigation has demonstrated partially reduced coprecipitation  and   in vitro binding between Ras and a Raf mutant lacking the  cysteine-rich domain  ( 28) , supporting our finding of two Ras  binding sites in Raf.	bind
38434	3	8895	7	10	NULL	0	NULL	Raf	NULL		contains	NULL					NULL		Ras binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_17_9809_s_77	7730360	A  recent investigation has demonstrated partially reduced coprecipitation  and   in vitro binding between Ras and a Raf mutant lacking the  cysteine-rich domain  ( 28) , supporting our finding of two Ras  binding sites in Raf.	bind
46999	1	8895	7	10	NULL	0	NULL	Raf	NULL	mutant	lacks	NULL					NULL		cysteine-rich domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_17_9809_s_77	7730360	A  recent investigation has demonstrated partially reduced coprecipitation  and   in vitro binding between Ras and a Raf mutant lacking the  cysteine-rich domain  ( 28) , supporting our finding of two Ras  binding sites in Raf.	bind
29723	1	8896	6	13	NULL	NULL	NULL	Nedd4-2	GP		bind		strongly	WW3		ENaC	GP		PY motif		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_22_20019_s_294	12654927	A  recent report, published after submission of our manuscript  ( ), supports the trend we  find here, in that WW3* of Nedd4-2 binds most strongly to the ENaC PY motifs,  followed by WW4.	bind
29724	2	8896	6	13	NULL	NULL	NULL	Nedd4-2	GP		bind			WW4		ENaC	GP		PY motif		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_22_20019_s_294	12654927	A  recent report, published after submission of our manuscript  ( ), supports the trend we  find here, in that WW3* of Nedd4-2 binds most strongly to the ENaC PY motifs,  followed by WW4.	bind
38435	1	8896	7	NULL	NULL	0	NULL	 Nedd4-2	NULL		binds	NULL	strongly	WW3		 ENaC	NULL		PY motifs		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_22_20019_s_294	12654927	A  recent report, published after submission of our manuscript  ( ), supports the trend we  find here, in that WW3* of Nedd4-2 binds most strongly to the ENaC PY motifs,  followed by WW4.	bind
38436	2	8896	7	NULL	NULL	0	NULL	Nedd4-2	NULL		bind	NULL		WW4		ENaC	NULL		PY motifs		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_22_20019_s_294	12654927	A  recent report, published after submission of our manuscript  ( ), supports the trend we  find here, in that WW3* of Nedd4-2 binds most strongly to the ENaC PY motifs,  followed by WW4.	bind
29725	1	8898	6	13	NULL	NULL	NULL	rgpA kgp hagA	GP	triple mutant	does not exhibit					hemagglutination	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17955_s_11	10364243	A  rgpA kgp hagA triple mutant constructed in this study exhibited no hemagglutination using sheep erythrocytes or hemoglobin binding activity, as determined by a solid-phase binding assay with horseradish peroxidase-conjugated human hemoglobin, indicating that the adhesin domains seem to be particularly important for  P. gingivalis cells to agglutinate erythrocytes and bind hemoglobin, leading to heme acquisition.	bind
29726	2	8898	6	13	NULL	NULL	NULL	P. gingivalis cells	Cell		agglutinate					erythrocytes	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17955_s_11	10364243	A  rgpA kgp hagA triple mutant constructed in this study exhibited no hemagglutination using sheep erythrocytes or hemoglobin binding activity, as determined by a solid-phase binding assay with horseradish peroxidase-conjugated human hemoglobin, indicating that the adhesin domains seem to be particularly important for  P. gingivalis cells to agglutinate erythrocytes and bind hemoglobin, leading to heme acquisition.	bind
29727	3	8898	6	13	NULL	NULL	NULL	P. gingivalis cells	Cell		bind					hemoglobin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17955_s_11	10364243	A  rgpA kgp hagA triple mutant constructed in this study exhibited no hemagglutination using sheep erythrocytes or hemoglobin binding activity, as determined by a solid-phase binding assay with horseradish peroxidase-conjugated human hemoglobin, indicating that the adhesin domains seem to be particularly important for  P. gingivalis cells to agglutinate erythrocytes and bind hemoglobin, leading to heme acquisition.	bind
29728	4	8898	6	13	NULL	NULL	NULL	statement 2	Process		leads to					heme acquisition	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17955_s_11	10364243	A  rgpA kgp hagA triple mutant constructed in this study exhibited no hemagglutination using sheep erythrocytes or hemoglobin binding activity, as determined by a solid-phase binding assay with horseradish peroxidase-conjugated human hemoglobin, indicating that the adhesin domains seem to be particularly important for  P. gingivalis cells to agglutinate erythrocytes and bind hemoglobin, leading to heme acquisition.	bind
29729	5	8898	6	13	NULL	NULL	NULL	statement 3	Process		leads to					heme acquisition	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17955_s_11	10364243	A  rgpA kgp hagA triple mutant constructed in this study exhibited no hemagglutination using sheep erythrocytes or hemoglobin binding activity, as determined by a solid-phase binding assay with horseradish peroxidase-conjugated human hemoglobin, indicating that the adhesin domains seem to be particularly important for  P. gingivalis cells to agglutinate erythrocytes and bind hemoglobin, leading to heme acquisition.	bind
29730	6	8898	6	13	NULL	NULL	NULL				are important for			adhesion domain		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17955_s_11	10364243	A  rgpA kgp hagA triple mutant constructed in this study exhibited no hemagglutination using sheep erythrocytes or hemoglobin binding activity, as determined by a solid-phase binding assay with horseradish peroxidase-conjugated human hemoglobin, indicating that the adhesin domains seem to be particularly important for  P. gingivalis cells to agglutinate erythrocytes and bind hemoglobin, leading to heme acquisition.	bind
29731	7	8898	6	13	NULL	NULL	NULL				are important for			adhesion domain		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17955_s_11	10364243	A  rgpA kgp hagA triple mutant constructed in this study exhibited no hemagglutination using sheep erythrocytes or hemoglobin binding activity, as determined by a solid-phase binding assay with horseradish peroxidase-conjugated human hemoglobin, indicating that the adhesin domains seem to be particularly important for  P. gingivalis cells to agglutinate erythrocytes and bind hemoglobin, leading to heme acquisition.	bind
47000	8	8898	6	13	NULL	NULL	NULL	rgpA kgp hagA	GP	triple mutant	does not exhibit					hemoglobin	GP	binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17955_s_11	10364243	A  rgpA kgp hagA triple mutant constructed in this study exhibited no hemagglutination using sheep erythrocytes or hemoglobin binding activity, as determined by a solid-phase binding assay with horseradish peroxidase-conjugated human hemoglobin, indicating that the adhesin domains seem to be particularly important for  P. gingivalis cells to agglutinate erythrocytes and bind hemoglobin, leading to heme acquisition.	bind
38437	1	8898	7	NULL	NULL	0	NULL	P. gingivalis cells	NULL		agglutinate	NULL				erythrocytes	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_17955_s_11	10364243	A  rgpA kgp hagA triple mutant constructed in this study exhibited no hemagglutination using sheep erythrocytes or hemoglobin binding activity, as determined by a solid-phase binding assay with horseradish peroxidase-conjugated human hemoglobin, indicating that the adhesin domains seem to be particularly important for  P. gingivalis cells to agglutinate erythrocytes and bind hemoglobin, leading to heme acquisition.	bind
38438	2	8898	7	NULL	NULL	0	NULL	P. gingivalis cells	NULL		bind	NULL				hemoglobin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_17955_s_11	10364243	A  rgpA kgp hagA triple mutant constructed in this study exhibited no hemagglutination using sheep erythrocytes or hemoglobin binding activity, as determined by a solid-phase binding assay with horseradish peroxidase-conjugated human hemoglobin, indicating that the adhesin domains seem to be particularly important for  P. gingivalis cells to agglutinate erythrocytes and bind hemoglobin, leading to heme acquisition.	bind
38439	3	8898	7	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				heme acquisition	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_17955_s_11	10364243	A  rgpA kgp hagA triple mutant constructed in this study exhibited no hemagglutination using sheep erythrocytes or hemoglobin binding activity, as determined by a solid-phase binding assay with horseradish peroxidase-conjugated human hemoglobin, indicating that the adhesin domains seem to be particularly important for  P. gingivalis cells to agglutinate erythrocytes and bind hemoglobin, leading to heme acquisition.	bind
38440	4	8898	7	NULL	NULL	0	NULL		NULL		is important for	NULL		adhesin domains		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_17955_s_11	10364243	A  rgpA kgp hagA triple mutant constructed in this study exhibited no hemagglutination using sheep erythrocytes or hemoglobin binding activity, as determined by a solid-phase binding assay with horseradish peroxidase-conjugated human hemoglobin, indicating that the adhesin domains seem to be particularly important for  P. gingivalis cells to agglutinate erythrocytes and bind hemoglobin, leading to heme acquisition.	bind
38441	5	8898	7	NULL	NULL	0	NULL		NULL		is important for	NULL		adhesin domains		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_17955_s_11	10364243	A  rgpA kgp hagA triple mutant constructed in this study exhibited no hemagglutination using sheep erythrocytes or hemoglobin binding activity, as determined by a solid-phase binding assay with horseradish peroxidase-conjugated human hemoglobin, indicating that the adhesin domains seem to be particularly important for  P. gingivalis cells to agglutinate erythrocytes and bind hemoglobin, leading to heme acquisition.	bind
38504	6	8898	7	NULL	NULL	0	NULL	rgpA kgp hagA	NULL	triple mutant	does not exhibit	NULL				hemagglutination	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_17955_s_11	10364243	A  rgpA kgp hagA triple mutant constructed in this study exhibited no hemagglutination using sheep erythrocytes or hemoglobin binding activity, as determined by a solid-phase binding assay with horseradish peroxidase-conjugated human hemoglobin, indicating that the adhesin domains seem to be particularly important for  P. gingivalis cells to agglutinate erythrocytes and bind hemoglobin, leading to heme acquisition.	bind
38508	7	8898	7	10	NULL	0	NULL	rgpA kgp hagA	NULL	triple mutant	does not exhibit	NULL				hemoglobin	NULL	binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17955_s_11	10364243	A  rgpA kgp hagA triple mutant constructed in this study exhibited no hemagglutination using sheep erythrocytes or hemoglobin binding activity, as determined by a solid-phase binding assay with horseradish peroxidase-conjugated human hemoglobin, indicating that the adhesin domains seem to be particularly important for  P. gingivalis cells to agglutinate erythrocytes and bind hemoglobin, leading to heme acquisition.	bind
47001	8	8898	7	10	NULL	0	NULL	statement 1	NULL		leads to	NULL				heme acquisition 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_17955_s_11	10364243	A  rgpA kgp hagA triple mutant constructed in this study exhibited no hemagglutination using sheep erythrocytes or hemoglobin binding activity, as determined by a solid-phase binding assay with horseradish peroxidase-conjugated human hemoglobin, indicating that the adhesin domains seem to be particularly important for  P. gingivalis cells to agglutinate erythrocytes and bind hemoglobin, leading to heme acquisition.	bind
29732	1	8900	6	13	NULL	NULL	NULL	tegument protein	GP		bind					VP1/2	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_j-virol_80_1_16352544_s_5	16352544	A  second tegument protein that binds to VP1/2, UL37, was necessary for wild-type  transport but was not essential for this process.	bind
29733	2	8900	6	13	NULL	NULL	NULL	tegument protein	GP		bind					UL37	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_j-virol_80_1_16352544_s_5	16352544	A  second tegument protein that binds to VP1/2, UL37, was necessary for wild-type  transport but was not essential for this process.	bind
29734	3	8900	6	13	NULL	NULL	NULL	statement 1	Process		is necessary for					transport	Process	wild type			NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_j-virol_80_1_16352544_s_5	16352544	A  second tegument protein that binds to VP1/2, UL37, was necessary for wild-type  transport but was not essential for this process.	bind
29735	4	8900	6	13	NULL	NULL	NULL	statement 2	Process		is necessary for					transport	Process	wild type			NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_j-virol_80_1_16352544_s_5	16352544	A  second tegument protein that binds to VP1/2, UL37, was necessary for wild-type  transport but was not essential for this process.	bind
38513	1	8900	7	NULL	NULL	0	NULL	tegument protein	NULL		binds to	NULL				VP1/2	NULL				NULL		0	NULL	NULL	NULL	abs-batch0550-0559_j-virol_80_1_16352544_s_5	16352544	A  second tegument protein that binds to VP1/2, UL37, was necessary for wild-type  transport but was not essential for this process.	bind
38514	2	8900	7	NULL	NULL	0	NULL	tegument protein	NULL		binds to	NULL				UL37	NULL				NULL		0	NULL	NULL	NULL	abs-batch0550-0559_j-virol_80_1_16352544_s_5	16352544	A  second tegument protein that binds to VP1/2, UL37, was necessary for wild-type  transport but was not essential for this process.	bind
38515	3	8900	7	10	NULL	0	NULL	statement 1	NULL		is necessary for	NULL				transport	NULL	wild-type			NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_j-virol_80_1_16352544_s_5	16352544	A  second tegument protein that binds to VP1/2, UL37, was necessary for wild-type  transport but was not essential for this process.	bind
38518	4	8900	7	10	NULL	0	NULL	statement 2	NULL		is necessary for	NULL				transport	NULL	wild-type			NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_j-virol_80_1_16352544_s_5	16352544	A  second tegument protein that binds to VP1/2, UL37, was necessary for wild-type  transport but was not essential for this process.	bind
29736	1	8901	6	13	NULL	NULL	NULL	synaptotagmin protein	GP		bind					trimeric SNARE complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_12_6567_s_96	8636067	A  second vesicle protein synaptotagmin can bind to the trimeric SNARE  complex, and there is compelling evidence that synaptotagmin acts as a  calcium-dependent regulator of transmitter release (reviewed by  Littleton and Bellen(1995)).	bind
29737	2	8901	6	13	NULL	NULL	NULL	synaptotagmin	GP		is a type of					second vesicle protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_12_6567_s_96	8636067	A  second vesicle protein synaptotagmin can bind to the trimeric SNARE  complex, and there is compelling evidence that synaptotagmin acts as a  calcium-dependent regulator of transmitter release (reviewed by  Littleton and Bellen(1995)).	bind
29738	3	8901	6	13	NULL	NULL	NULL	synaptotagmin	Process		acts as a 					transmitter release	GP	regulator of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_12_6567_s_96	8636067	A  second vesicle protein synaptotagmin can bind to the trimeric SNARE  complex, and there is compelling evidence that synaptotagmin acts as a  calcium-dependent regulator of transmitter release (reviewed by  Littleton and Bellen(1995)).	bind
29739	4	8901	6	13	NULL	NULL	NULL	statement 3	Process		is dependent on					calcium	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_12_6567_s_96	8636067	A  second vesicle protein synaptotagmin can bind to the trimeric SNARE  complex, and there is compelling evidence that synaptotagmin acts as a  calcium-dependent regulator of transmitter release (reviewed by  Littleton and Bellen(1995)).	bind
38528	1	8901	7	NULL	NULL	0	NULL	synaptotagmin	NULL		bind	NULL				trimeric SNARE complex	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_12_6567_s_96	8636067	A  second vesicle protein synaptotagmin can bind to the trimeric SNARE  complex, and there is compelling evidence that synaptotagmin acts as a  calcium-dependent regulator of transmitter release (reviewed by  Littleton and Bellen(1995)).	bind
38534	2	8901	7	10	NULL	0	NULL	synaptotagmin	NULL		acts as a	NULL				regulator release	NULL	regulator of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_12_6567_s_96	8636067	A  second vesicle protein synaptotagmin can bind to the trimeric SNARE  complex, and there is compelling evidence that synaptotagmin acts as a  calcium-dependent regulator of transmitter release (reviewed by  Littleton and Bellen(1995)).	bind
38544	3	8901	7	10	NULL	0	NULL	statement 2	NULL		is dependent on	NULL				calcium	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_12_6567_s_96	8636067	A  second vesicle protein synaptotagmin can bind to the trimeric SNARE  complex, and there is compelling evidence that synaptotagmin acts as a  calcium-dependent regulator of transmitter release (reviewed by  Littleton and Bellen(1995)).	bind
38550	4	8901	7	NULL	NULL	0	NULL	synaptotagmin	NULL		is a type of	NULL				second vesicle protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_12_6567_s_96	8636067	A  second vesicle protein synaptotagmin can bind to the trimeric SNARE  complex, and there is compelling evidence that synaptotagmin acts as a  calcium-dependent regulator of transmitter release (reviewed by  Littleton and Bellen(1995)).	bind
29740	1	8902	6	13	NULL	NULL	NULL	Ubiquitin	GP	binders of	is associated with					clathrin coat	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_j-biol-chem_281_31_16735510_s_6	16735510	A  set of clathrin coat-associated binders of ubiquitin also bind Nedd8,  but they undergo ubiquitylation, not neddylation.	bind
29741	2	8902	6	13	NULL	NULL	NULL	statement 1	GP		bind					Nedd8	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_j-biol-chem_281_31_16735510_s_6	16735510	A  set of clathrin coat-associated binders of ubiquitin also bind Nedd8,  but they undergo ubiquitylation, not neddylation.	bind
29742	3	8902	6	13	NULL	NULL	NULL	statement 1	GP		undergo					ubiquitylation	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_j-biol-chem_281_31_16735510_s_6	16735510	A  set of clathrin coat-associated binders of ubiquitin also bind Nedd8,  but they undergo ubiquitylation, not neddylation.	bind
29743	4	8902	6	13	NULL	NULL	NULL	statement 1	GP		does not undergo					neddylation	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_j-biol-chem_281_31_16735510_s_6	16735510	A  set of clathrin coat-associated binders of ubiquitin also bind Nedd8,  but they undergo ubiquitylation, not neddylation.	bind
38560	1	8902	7	10	NULL	0	NULL	Ubiquitin		binders of	is associated with					clathrin coat					NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_j-biol-chem_281_31_16735510_s_6	16735510	A  set of clathrin coat-associated binders of ubiquitin also bind Nedd8,  but they undergo ubiquitylation, not neddylation.	bind
38562	2	8902	7	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				Nedd8	NULL				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_j-biol-chem_281_31_16735510_s_6	16735510	A  set of clathrin coat-associated binders of ubiquitin also bind Nedd8,  but they undergo ubiquitylation, not neddylation.	bind
38564	3	8902	7	10	NULL	0	NULL	statement 1			undergo					ubiquitylation					NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_j-biol-chem_281_31_16735510_s_6	16735510	A  set of clathrin coat-associated binders of ubiquitin also bind Nedd8,  but they undergo ubiquitylation, not neddylation.	bind
38567	4	8902	7	10	NULL	0	NULL	statement 1			does not undergo					neddylation					NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_j-biol-chem_281_31_16735510_s_6	16735510	A  set of clathrin coat-associated binders of ubiquitin also bind Nedd8,  but they undergo ubiquitylation, not neddylation.	bind
29744	1	8903	6	13	NULL	NULL	NULL	I-CRS peptide	GP		bind					SK-Hep cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_4_1807_s_132	7829517	A  shows the concentration  dependence of the binding of  I-CRS peptide ( sis)  to SK-Hep cells at pH 7.4.	bind
38568	1	8903	7	NULL	NULL	0	NULL	I-CRS peptide( sis)	NULL		bind	NULL				SK-Hep cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_4_1807_s_132	7829517	A  shows the concentration  dependence of the binding of  I-CRS peptide ( sis)  to SK-Hep cells at pH 7.4.	bind
29844	1	8904	6	13	NULL	NULL	NULL	C4b	GP		bind					LOS	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_51_50853_s_156	14525973	A  siaD galE mutant of strain MC58 (unencapsulated; Glc   HepI and 3-PEA on HepII ( LOS PEA+)) and its isogenic  lpt-3 mutant (lacking PEA on HepII ( LOS PEA-)) were incubated with NHS (the 500-mul reaction mixture contained 3 x 108 bacteria and NHS at a final concentration of 30%), and C4b binding to LOS was analyzed  as described in the legend to  Fig. 1.	bind
38597	1	8904	7	NULL	NULL	0	NULL	C4b 	NULL		bind	NULL				LOS	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_51_50853_s_156	14525973	A  siaD galE mutant of strain MC58 (unencapsulated; Glc   HepI and 3-PEA on HepII ( LOS PEA+)) and its isogenic  lpt-3 mutant (lacking PEA on HepII ( LOS PEA-)) were incubated with NHS (the 500-mul reaction mixture contained 3 x 108 bacteria and NHS at a final concentration of 30%), and C4b binding to LOS was analyzed  as described in the legend to  Fig. 1.	bind
29745	1	8905	6	13	NULL	NULL	NULL	BARD1	GP		bind					GST-BARD1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_104_5_743_s_193	11257228	A  significant amount of the input BARD1 and  BRCA1 bound to GST-BARD1 but not to  GST.	bind
29746	2	8905	6	13	NULL	NULL	NULL	BRCA1	GP		bind					GST-BARD1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_104_5_743_s_193	11257228	A  significant amount of the input BARD1 and  BRCA1 bound to GST-BARD1 but not to  GST.	bind
29747	3	8905	6	13	NULL	NULL	NULL	BARD1	GP		does not bind					GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_104_5_743_s_193	11257228	A  significant amount of the input BARD1 and  BRCA1 bound to GST-BARD1 but not to  GST.	bind
29748	4	8905	6	13	NULL	NULL	NULL	BRCA1	GP		does not bind					GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_104_5_743_s_193	11257228	A  significant amount of the input BARD1 and  BRCA1 bound to GST-BARD1 but not to  GST.	bind
38598	1	8905	7	NULL	NULL	0	NULL	BARD1	NULL		bind	NULL				GST-BARD1	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_104_5_743_s_193	11257228	A  significant amount of the input BARD1 and  BRCA1 bound to GST-BARD1 but not to  GST.	bind
38599	2	8905	7	NULL	NULL	0	NULL	BRCA1	NULL		bind	NULL				GST-BARD1	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_104_5_743_s_193	11257228	A  significant amount of the input BARD1 and  BRCA1 bound to GST-BARD1 but not to  GST.	bind
38600	3	8905	7	NULL	NULL	0	NULL	BARD1	NULL		does not bind	NULL				GST	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_104_5_743_s_193	11257228	A  significant amount of the input BARD1 and  BRCA1 bound to GST-BARD1 but not to  GST.	bind
38601	4	8905	7	NULL	NULL	0	NULL	 BRCA1	NULL		does not bind	NULL				GST	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_104_5_743_s_193	11257228	A  significant amount of the input BARD1 and  BRCA1 bound to GST-BARD1 but not to  GST.	bind
29749	1	8906	6	13	NULL	NULL	NULL	BDNF	GP		bind					trkB	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19669_s_89	7649974	A  similar  K   has also been determined for  BDNF binding to  trkB( 64) .	bind
38602	1	8906	7	NULL	NULL	0	NULL	BDNF 	NULL		bind	NULL				trkB	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_34_19669_s_89	7649974	A  similar  K   has also been determined for  BDNF binding to  trkB( 64) .	bind
29750	1	8907	6	13	NULL	NULL	NULL	IgG3	GP		bind					carbohydrate antigen	Chemical	multivalent			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1527_s_146	8576148	A  similar finding was reported for IgG3 binding to a multivalent  carbohydrate antigen, and the effect was attributed to the tendency of  IgG3 to aggregate( 24) .	bind
29751	2	8907	6	13	NULL	NULL	NULL	statement 1	Process		contribute to					IgG3 	GP	aggregation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1527_s_146	8576148	A  similar finding was reported for IgG3 binding to a multivalent  carbohydrate antigen, and the effect was attributed to the tendency of  IgG3 to aggregate( 24) .	bind
38603	1	8907	7	10	NULL	0	NULL	IgG3			bind					carbohydrate antigen		multivalent			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1527_s_146	8576148	A  similar finding was reported for IgG3 binding to a multivalent  carbohydrate antigen, and the effect was attributed to the tendency of  IgG3 to aggregate( 24) .	bind
38604	2	8907	7	NULL	NULL	0	NULL	IgG3	NULL		tendency to	NULL				aggregate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_3_1527_s_146	8576148	A  similar finding was reported for IgG3 binding to a multivalent  carbohydrate antigen, and the effect was attributed to the tendency of  IgG3 to aggregate( 24) .	bind
38605	3	8907	7	10	NULL	0	NULL	statement 1	NULL		is attributed to	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1527_s_146	8576148	A  similar finding was reported for IgG3 binding to a multivalent  carbohydrate antigen, and the effect was attributed to the tendency of  IgG3 to aggregate( 24) .	bind
29845	1	8908	6	13	NULL	NULL	NULL	HP1	GP		functions in					heterochromatin	Chromosome	assembly of			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_15_1823_s_146	12897052	A  similar function for HP1 in the assembly of heterochromatin has been proposed,  although dimerization of HP1 via the C-terminal chromo shadow domain makes the  binding of two histone tails from the same nucleosome, as well as separate  ones, possible.	bind
29846	2	8908	6	13	NULL	NULL	NULL	HP1	GP		bind			C-terminal chromo shadow domain		HP1	GP		C-terminal chromo shadow domain		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_15_1823_s_146	12897052	A  similar function for HP1 in the assembly of heterochromatin has been proposed,  although dimerization of HP1 via the C-terminal chromo shadow domain makes the  binding of two histone tails from the same nucleosome, as well as separate  ones, possible.	bind
29847	3	8908	6	13	NULL	NULL	NULL	histone tails	GP		bind					histone tails	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_15_1823_s_146	12897052	A  similar function for HP1 in the assembly of heterochromatin has been proposed,  although dimerization of HP1 via the C-terminal chromo shadow domain makes the  binding of two histone tails from the same nucleosome, as well as separate  ones, possible.	bind
29848	4	8908	6	13	NULL	NULL	NULL	statement 2	Process		allows					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_15_1823_s_146	12897052	A  similar function for HP1 in the assembly of heterochromatin has been proposed,  although dimerization of HP1 via the C-terminal chromo shadow domain makes the  binding of two histone tails from the same nucleosome, as well as separate  ones, possible.	bind
38606	1	8908	7	NULL	NULL	0	NULL	HP1	NULL		assembles	NULL				heterochromatin	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_17_15_1823_s_146	12897052	A  similar function for HP1 in the assembly of heterochromatin has been proposed,  although dimerization of HP1 via the C-terminal chromo shadow domain makes the  binding of two histone tails from the same nucleosome, as well as separate  ones, possible.	bind
38607	2	8908	7	10	NULL	0	NULL	HP1		dimerization of	occurs via					HP1			C-terminal chromo shadow domain		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_15_1823_s_146	12897052	A  similar function for HP1 in the assembly of heterochromatin has been proposed,  although dimerization of HP1 via the C-terminal chromo shadow domain makes the  binding of two histone tails from the same nucleosome, as well as separate  ones, possible.	bind
38608	3	8908	7	NULL	NULL	0	NULL	histone tails	NULL		bind	NULL				histone tails	NULL				NULL	nucleosome	0	NULL	NULL	NULL	gw60_genesdev_17_15_1823_s_146	12897052	A  similar function for HP1 in the assembly of heterochromatin has been proposed,  although dimerization of HP1 via the C-terminal chromo shadow domain makes the  binding of two histone tails from the same nucleosome, as well as separate  ones, possible.	bind
38609	4	8908	7	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_17_15_1823_s_146	12897052	A  similar function for HP1 in the assembly of heterochromatin has been proposed,  although dimerization of HP1 via the C-terminal chromo shadow domain makes the  binding of two histone tails from the same nucleosome, as well as separate  ones, possible.	bind
29752	1	8910	6	13	NULL	NULL	NULL	sin3	GP	mutations of	allows					HO	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_124	16705163	A  sin3 mutation also allows  HO to be expressed despite a  gcn5 mutation ( ) and raises the question of whether SWI/SNF binds to the  HO promoter in the  gcn5 sin3 strain.	bind
38614	1	8910	7	10	NULL	0	NULL	sin3	NULL	mutation of	allows	NULL				HO	NULL	expression of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_124	16705163	A  sin3 mutation also allows  HO to be expressed despite a  gcn5 mutation ( ) and raises the question of whether SWI/SNF binds to the  HO promoter in the  gcn5 sin3 strain.	bind
38615	2	8910	7	10	NULL	0	NULL	statement 2	NULL		occurs despite	NULL				gcn5	NULL	mutation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_124	16705163	A  sin3 mutation also allows  HO to be expressed despite a  gcn5 mutation ( ) and raises the question of whether SWI/SNF binds to the  HO promoter in the  gcn5 sin3 strain.	bind
29753	1	8911	6	13	NULL	NULL	NULL	Aprataxin	GP		bind					DNA molecule	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_20_13939_s_129	16547001	A  single asterisk indicates unbound DNA,  two asterisks indicate the Aprataxin-DNA complex, and  three asterisks indicate more than one molecule of Aprataxin binding to one DNA molecule.	bind
38616	1	8911	7	NULL	NULL	0	NULL	Aprataxin	NULL		bind	NULL				DNA molecule	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_20_13939_s_129	16547001	A  single asterisk indicates unbound DNA,  two asterisks indicate the Aprataxin-DNA complex, and  three asterisks indicate more than one molecule of Aprataxin binding to one DNA molecule.	bind
29754	1	8912	6	13	NULL	NULL	NULL	p65	GP		bind					PPR	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_26_23570_s_174	12684509	A  small increase in p65 binding to the PPR was also detected.	bind
38617	1	8912	7	NULL	NULL	0	NULL	p65	NULL		bind	NULL				PPR	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_26_23570_s_174	12684509	A  small increase in p65 binding to the PPR was also detected.	bind
29755	1	8913	6	13	NULL	NULL	NULL	MAP4	GP		bind		directly	proline-rich region in the C-terminal half		Sept 2:6:7 heterotrimer	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_mol-biol-cell_16_10_16093351_s_6	16093351	A  small, proline-rich region in the C-terminal half of MAP4 bound directly  to a Sept 2:6:7 heterotrimer, and to the Sept2 monomer.	bind
29756	2	8913	6	13	NULL	NULL	NULL	MAP4	GP		bind		directly	proline-rich region in the C-terminal half		Sept2 monomer	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_mol-biol-cell_16_10_16093351_s_6	16093351	A  small, proline-rich region in the C-terminal half of MAP4 bound directly  to a Sept 2:6:7 heterotrimer, and to the Sept2 monomer.	bind
38618	1	8913	7	NULL	NULL	0	NULL	MAP4	NULL		bind	NULL	directly	proline-rich region in the C-terminal half		Sept 2:6:7 heterotrimer	NULL				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_mol-biol-cell_16_10_16093351_s_6	16093351	A  small, proline-rich region in the C-terminal half of MAP4 bound directly  to a Sept 2:6:7 heterotrimer, and to the Sept2 monomer.	bind
38619	2	8913	7	NULL	NULL	0	NULL	MAP4	NULL		bind	NULL	directly	proline-rich region in the C-terminal half		Sept2 monomer	NULL				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_mol-biol-cell_16_10_16093351_s_6	16093351	A  small, proline-rich region in the C-terminal half of MAP4 bound directly  to a Sept 2:6:7 heterotrimer, and to the Sept2 monomer.	bind
29757	1	8914	6	13	NULL	NULL	NULL	cholecystokinin-releasing peptide	GP		bind		specifically			small-intestinal cells	Cell	rat;;isolated			NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_59_0_221_s_857	9074762	A  specific binding of the cholecystokinin-releasing peptide (monitor peptide) to isolated  rat small-intestinal cells.	bind
29758	2	8914	6	13	NULL	NULL	NULL	cholecystokinin-releasing peptide	GP		is					monitor peptide	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_59_0_221_s_857	9074762	A  specific binding of the cholecystokinin-releasing peptide (monitor peptide) to isolated  rat small-intestinal cells.	bind
38620	1	8914	7	10	NULL	0	NULL	cholecystokinin-releasing peptide			bind		specifically			small-intestinal cells		isolated;;rat			NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_59_0_221_s_857	9074762	A  specific binding of the cholecystokinin-releasing peptide (monitor peptide) to isolated  rat small-intestinal cells.	bind
38621	2	8914	7	NULL	NULL	0	NULL	cholecystokinin-releasing peptide	NULL		is	NULL				monitor peptide	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevphysiol_59_0_221_s_857	9074762	A  specific binding of the cholecystokinin-releasing peptide (monitor peptide) to isolated  rat small-intestinal cells.	bind
29759	1	8916	6	13	NULL	NULL	NULL	influenza C virus	Organism		bind		preferentially			single cell surface glycoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_30_17815_s_294	7629082	A  surprising finding of our work was that influenza C virus  preferentially binds to a single cell surface glycoprotein.	bind
38622	1	8916	7	NULL	NULL	0	NULL	influenza C virus 	NULL		binds	NULL	preferentially			single cell surface glycoprotein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_30_17815_s_294	7629082	A  surprising finding of our work was that influenza C virus  preferentially binds to a single cell surface glycoprotein.	bind
29760	1	8917	6	13	NULL	NULL	NULL	oppA	GP	T. denticola;; mutant	bind					plasminogen	GP	reduced amount of;;soluble			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_4_1884_s_11	10722578	A  T. denticola oppA mutant bound reduced amounts of soluble plasminogen, and plasminogen binding to the parent strain was inhibited by the lysine analog  -aminocaproic acid.	bind
29761	2	8917	6	13	NULL	NULL	NULL	plasminogen	GP		bind					oppA	GP	T. denticola			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_4_1884_s_11	10722578	A  T. denticola oppA mutant bound reduced amounts of soluble plasminogen, and plasminogen binding to the parent strain was inhibited by the lysine analog  -aminocaproic acid.	bind
29762	3	8917	6	13	NULL	NULL	NULL	statement 2	Process		is inhibited by					aminocaproic acid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_4_1884_s_11	10722578	A  T. denticola oppA mutant bound reduced amounts of soluble plasminogen, and plasminogen binding to the parent strain was inhibited by the lysine analog  -aminocaproic acid.	bind
47008	4	8917	6	13	NULL	NULL	NULL	aminocaproic acid	Chemical		is a type of					lysine analog	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_4_1884_s_11	10722578	A  T. denticola oppA mutant bound reduced amounts of soluble plasminogen, and plasminogen binding to the parent strain was inhibited by the lysine analog  -aminocaproic acid.	bind
38623	1	8917	7	10	NULL	0	NULL	oppA	NULL	T. denticola;;mutant	bind	NULL				plasminogen	NULL	reduced amount of;;soluble			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_4_1884_s_11	10722578	A  T. denticola oppA mutant bound reduced amounts of soluble plasminogen, and plasminogen binding to the parent strain was inhibited by the lysine analog  -aminocaproic acid.	bind
38624	2	8917	7	10	NULL	0	NULL	plasminogen	NULL		bind	NULL				oppA	NULL	T. denticola			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_4_1884_s_11	10722578	A  T. denticola oppA mutant bound reduced amounts of soluble plasminogen, and plasminogen binding to the parent strain was inhibited by the lysine analog  -aminocaproic acid.	bind
38625	3	8917	7	NULL	NULL	0	NULL	aminocaproic acid	NULL		inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_4_1884_s_11	10722578	A  T. denticola oppA mutant bound reduced amounts of soluble plasminogen, and plasminogen binding to the parent strain was inhibited by the lysine analog  -aminocaproic acid.	bind
38626	4	8917	7	NULL	NULL	0	NULL	aminocaproic acid	NULL		is a type of	NULL				lysine analog	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_4_1884_s_11	10722578	A  T. denticola oppA mutant bound reduced amounts of soluble plasminogen, and plasminogen binding to the parent strain was inhibited by the lysine analog  -aminocaproic acid.	bind
29763	1	8918	6	13	NULL	NULL	NULL	secretion substrate	GP		bind			amino acid region		secretion chaperone 	GP	putative			NULL		NULL	NULL	NULL	NULL	gw60_cell_102_4_487_s_272	10966110	A  third would be the amino acid region of the secretion substrate bound  by its cognate putative secretion chaperone (translational regulator) and held at the base  of the secretion apparatus until secretion can occur.	bind
29764	2	8918	6	13	NULL	NULL	NULL	secretion chaperone	GP		is a type of					translational regulator	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_102_4_487_s_272	10966110	A  third would be the amino acid region of the secretion substrate bound  by its cognate putative secretion chaperone (translational regulator) and held at the base  of the secretion apparatus until secretion can occur.	bind
38627	1	8918	7	10	NULL	0	NULL	secretion chaperone	NULL	cognate putative	bind	NULL				secretion substrate	NULL		amino acid region of		NULL		NULL	NULL	NULL	NULL	gw60_cell_102_4_487_s_272	10966110	A  third would be the amino acid region of the secretion substrate bound  by its cognate putative secretion chaperone (translational regulator) and held at the base  of the secretion apparatus until secretion can occur.	bind
38628	2	8918	7	10	NULL	0	NULL	secretion chaperone	NULL		is a type of	NULL				translational regulator	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_102_4_487_s_272	10966110	A  third would be the amino acid region of the secretion substrate bound  by its cognate putative secretion chaperone (translational regulator) and held at the base  of the secretion apparatus until secretion can occur.	bind
29765	1	8919	6	13	NULL	NULL	NULL	v-Crk	GP		bind					paxillin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31219_s_101	8537387	A  titration experiment showed that half maximal binding was observed at  around 10-20 nM  of the GST-Csk SH3/2 protein ( Fig. 4 A), an affinity that is severalfold weaker than that  of v-Crk binding to paxillin.	bind
47011	2	8919	6	13	NULL	NULL	NULL	GST-Csk SH3/2 protein	GP		bind					paxillin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31219_s_101	8537387	A  titration experiment showed that half maximal binding was observed at  around 10-20 nM  of the GST-Csk SH3/2 protein ( Fig. 4 A), an affinity that is severalfold weaker than that  of v-Crk binding to paxillin.	bind
47012	3	8919	6	13	NULL	NULL	NULL	statement 2	Process	affinity of	is weaker than					statement 1	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31219_s_101	8537387	A  titration experiment showed that half maximal binding was observed at  around 10-20 nM  of the GST-Csk SH3/2 protein ( Fig. 4 A), an affinity that is severalfold weaker than that  of v-Crk binding to paxillin.	bind
38629	1	8919	7	NULL	NULL	0	NULL	v-Crk 	NULL		bind	NULL				paxillin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31219_s_101	8537387	A  titration experiment showed that half maximal binding was observed at  around 10-20 nM  of the GST-Csk SH3/2 protein ( Fig. 4 A), an affinity that is severalfold weaker than that  of v-Crk binding to paxillin.	bind
38630	2	8919	7	NULL	NULL	0	NULL	GST-Csk SH3/2 protein	NULL		bind	NULL				paxillin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31219_s_101	8537387	A  titration experiment showed that half maximal binding was observed at  around 10-20 nM  of the GST-Csk SH3/2 protein ( Fig. 4 A), an affinity that is severalfold weaker than that  of v-Crk binding to paxillin.	bind
38631	3	8919	7	NULL	NULL	0	NULL	statement 2	NULL	affinity of	is weaker than	NULL				statement 1	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31219_s_101	8537387	A  titration experiment showed that half maximal binding was observed at  around 10-20 nM  of the GST-Csk SH3/2 protein ( Fig. 4 A), an affinity that is severalfold weaker than that  of v-Crk binding to paxillin.	bind
29766	1	8920	6	13	NULL	NULL	NULL	Tax	GP		is a type of					transactivator	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4450_s_680	12052856	A  trans-activator Tax of human T-cell leukemia virus type 1 binds to NF-kappa B p50 and serum response factor (SRF) and associates with enhancer DNAs of the NF-kappa B site and CArG box.	bind
29767	2	8920	6	13	NULL	NULL	NULL	Tax	GP	human T-cell leukemia virus type 1	bind					NF-kappaB p50	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4450_s_680	12052856	A  trans-activator Tax of human T-cell leukemia virus type 1 binds to NF-kappa B p50 and serum response factor (SRF) and associates with enhancer DNAs of the NF-kappa B site and CArG box.	bind
29768	3	8920	6	13	NULL	NULL	NULL	Tax	GP	human T-cell leukemia virus type 1	bind					SRF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4450_s_680	12052856	A  trans-activator Tax of human T-cell leukemia virus type 1 binds to NF-kappa B p50 and serum response factor (SRF) and associates with enhancer DNAs of the NF-kappa B site and CArG box.	bind
29769	4	8920	6	13	NULL	NULL	NULL	SRF	GP		is 					serum response factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4450_s_680	12052856	A  trans-activator Tax of human T-cell leukemia virus type 1 binds to NF-kappa B p50 and serum response factor (SRF) and associates with enhancer DNAs of the NF-kappa B site and CArG box.	bind
29770	5	8920	6	13	NULL	NULL	NULL	Tax	GP	human T-cell leukemia virus type 1	associates with					DNA	NucleicAcid			NF-kappaB binding site of enhancer	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4450_s_680	12052856	A  trans-activator Tax of human T-cell leukemia virus type 1 binds to NF-kappa B p50 and serum response factor (SRF) and associates with enhancer DNAs of the NF-kappa B site and CArG box.	bind
29771	6	8920	6	13	NULL	NULL	NULL	Tax	GP	human T-cell leukemia virus type 1	bind					DNA	NucleicAcid			CArG box of enhancer	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4450_s_680	12052856	A  trans-activator Tax of human T-cell leukemia virus type 1 binds to NF-kappa B p50 and serum response factor (SRF) and associates with enhancer DNAs of the NF-kappa B site and CArG box.	bind
38632	1	8920	7	NULL	NULL	0	NULL	Tax 	NULL	human T-cell leukemia virus type 1	binds to	NULL				NF-kappa B p50	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_13_4450_s_680	12052856	A  trans-activator Tax of human T-cell leukemia virus type 1 binds to NF-kappa B p50 and serum response factor (SRF) and associates with enhancer DNAs of the NF-kappa B site and CArG box.	bind
38633	2	8920	7	NULL	NULL	0	NULL	Tax	NULL	human T-cell leukemia virus type 1 	binds to	NULL				SRF	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_13_4450_s_680	12052856	A  trans-activator Tax of human T-cell leukemia virus type 1 binds to NF-kappa B p50 and serum response factor (SRF) and associates with enhancer DNAs of the NF-kappa B site and CArG box.	bind
38634	3	8920	7	10	NULL	0	NULL	Tax	NULL	human T-cell leukemia virus type 1	associate with	NULL				DNA	NULL			NF-kappa B site of enhancer	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4450_s_680	12052856	A  trans-activator Tax of human T-cell leukemia virus type 1 binds to NF-kappa B p50 and serum response factor (SRF) and associates with enhancer DNAs of the NF-kappa B site and CArG box.	bind
38635	4	8920	7	10	NULL	0	NULL	Tax	NULL	human T-cell leukemia virus type 1	associate with	NULL				DNA	NULL			CArG box of enhancer	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4450_s_680	12052856	A  trans-activator Tax of human T-cell leukemia virus type 1 binds to NF-kappa B p50 and serum response factor (SRF) and associates with enhancer DNAs of the NF-kappa B site and CArG box.	bind
38636	5	8920	7	NULL	NULL	0	NULL	SRF	NULL		is	NULL				serum response factor	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_13_4450_s_680	12052856	A  trans-activator Tax of human T-cell leukemia virus type 1 binds to NF-kappa B p50 and serum response factor (SRF) and associates with enhancer DNAs of the NF-kappa B site and CArG box.	bind
38637	6	8920	7	NULL	NULL	0	NULL	Tax	NULL		is a type of	NULL				trans-activator	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_13_4450_s_680	12052856	A  trans-activator Tax of human T-cell leukemia virus type 1 binds to NF-kappa B p50 and serum response factor (SRF) and associates with enhancer DNAs of the NF-kappa B site and CArG box.	bind
29772	1	8921	6	13	NULL	NULL	NULL	GST-p65 -beta-delta3	GP	truncated	bind		strongly			Cdc42	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_49_29071_s_66	7493928	A  truncated p65 -beta  construct,  GST-p65 -beta-delta3, continued to show strong Cdc42  binding, although binding to Rac was reduced ( Fig. 1).	bind
29773	2	8921	6	13	NULL	NULL	NULL	GST-p65 -beta-delta3	GP		bind		redduced			Rac	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_49_29071_s_66	7493928	A  truncated p65 -beta  construct,  GST-p65 -beta-delta3, continued to show strong Cdc42  binding, although binding to Rac was reduced ( Fig. 1).	bind
38671	1	8921	7	NULL	NULL	0	NULL	GST-p65 -beta-delta3	NULL		bind	NULL	strongly			Cdc42	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_49_29071_s_66	7493928	A  truncated p65 -beta  construct,  GST-p65 -beta-delta3, continued to show strong Cdc42  binding, although binding to Rac was reduced ( Fig. 1).	bind
38672	2	8921	7	NULL	NULL	0	NULL	GST-p65 -beta-delta3	NULL		bind	NULL	reduced			Rac	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_49_29071_s_66	7493928	A  truncated p65 -beta  construct,  GST-p65 -beta-delta3, continued to show strong Cdc42  binding, although binding to Rac was reduced ( Fig. 1).	bind
38673	3	8921	7	NULL	NULL	0	NULL	GST-p65 -beta-delta3	NULL		is a type of	NULL				truncated p65 -beta construct	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_49_29071_s_66	7493928	A  truncated p65 -beta  construct,  GST-p65 -beta-delta3, continued to show strong Cdc42  binding, although binding to Rac was reduced ( Fig. 1).	bind
29774	1	8922	6	13	NULL	NULL	NULL	UspA1 protein	GP		bind					MAb 17C7	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_4_2400_s_207	15784586	A  uspA1 mutant of MC317 (MC317.1) was constructed for use in this assay to eliminate expression of the UspA1 protein which also binds MAb 17C7.	bind
29775	2	8922	6	13	NULL	NULL	NULL	MC317.1	GP		is					uspA1 mutant of MC317	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_4_2400_s_207	15784586	A  uspA1 mutant of MC317 (MC317.1) was constructed for use in this assay to eliminate expression of the UspA1 protein which also binds MAb 17C7.	bind
29776	3	8922	6	13	NULL	NULL	NULL	statement 2	GP		eliminates					UspA1 protein	GP	expression of 			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_4_2400_s_207	15784586	A  uspA1 mutant of MC317 (MC317.1) was constructed for use in this assay to eliminate expression of the UspA1 protein which also binds MAb 17C7.	bind
38674	1	8922	7	NULL	NULL	0	NULL	UspA1 protein	NULL		binds to	NULL				MAb 17C7	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_4_2400_s_207	15784586	A  uspA1 mutant of MC317 (MC317.1) was constructed for use in this assay to eliminate expression of the UspA1 protein which also binds MAb 17C7.	bind
47018	2	8922	7	10	NULL	0	NULL	MC317.1	NULL		is	NULL				uspA1 mutant of MC317	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_4_2400_s_207	15784586	A  uspA1 mutant of MC317 (MC317.1) was constructed for use in this assay to eliminate expression of the UspA1 protein which also binds MAb 17C7.	bind
47019	3	8922	7	10	NULL	0	NULL	statement 2	NULL		eliminates	NULL				UspA1 protein	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_4_2400_s_207	15784586	A  uspA1 mutant of MC317 (MC317.1) was constructed for use in this assay to eliminate expression of the UspA1 protein which also binds MAb 17C7.	bind
29777	1	8923	6	13	NULL	NULL	NULL	PA26	GP	Xenopus	is homologous to					p53-activated gene	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4161_s_502	12874135	A  Xenopus homolog of a human p53-activated gene,  PA26, is specifically expressed in the notochord.	bind
29778	2	8923	6	13	NULL	NULL	NULL	PA26	GP		is expressed in		specifically			notochord	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4161_s_502	12874135	A  Xenopus homolog of a human p53-activated gene,  PA26, is specifically expressed in the notochord.	bind
38675	1	8923	7	10	NULL	0	NULL	PA26	NULL	Xenopus	is homologous to	NULL				 p53-activated gene	NULL	 human			NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4161_s_502	12874135	A  Xenopus homolog of a human p53-activated gene,  PA26, is specifically expressed in the notochord.	bind
38676	2	8923	7	NULL	NULL	0	NULL	PA26	NULL		is expressed in	NULL	specifically			notochord	NULL				NULL		0	NULL	NULL	NULL	gw60_development_130_17_4161_s_502	12874135	A  Xenopus homolog of a human p53-activated gene,  PA26, is specifically expressed in the notochord.	bind
29779	1	8924	6	13	NULL	NULL	NULL	MP90	GP		is a type of					mitotic phosphoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3257_s_3	9920862	A  Xenopus mitotic phosphoprotein, MP90, is very similar to an abundant mammalian nerve terminal protein, epsin, which binds the Eps15 homology (EH) domain of Eps15 and the alpha-adaptin subunit of the clathrin adaptor AP-2.	bind
29780	2	8924	6	13	NULL	NULL	NULL	MP90	GP	Xenopus	is similar to					epsin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3257_s_3	9920862	A  Xenopus mitotic phosphoprotein, MP90, is very similar to an abundant mammalian nerve terminal protein, epsin, which binds the Eps15 homology (EH) domain of Eps15 and the alpha-adaptin subunit of the clathrin adaptor AP-2.	bind
29781	3	8924	6	13	NULL	NULL	NULL	epsin	GP		is a type of					mammalian nerve terminal protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3257_s_3	9920862	A  Xenopus mitotic phosphoprotein, MP90, is very similar to an abundant mammalian nerve terminal protein, epsin, which binds the Eps15 homology (EH) domain of Eps15 and the alpha-adaptin subunit of the clathrin adaptor AP-2.	bind
29782	4	8924	6	13	NULL	NULL	NULL	epsin	GP		bind					Eps15	GP		EH domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3257_s_3	9920862	A  Xenopus mitotic phosphoprotein, MP90, is very similar to an abundant mammalian nerve terminal protein, epsin, which binds the Eps15 homology (EH) domain of Eps15 and the alpha-adaptin subunit of the clathrin adaptor AP-2.	bind
29783	5	8924	6	13	NULL	NULL	NULL	Eps15 homology domain 	GP		is					EH domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3257_s_3	9920862	A  Xenopus mitotic phosphoprotein, MP90, is very similar to an abundant mammalian nerve terminal protein, epsin, which binds the Eps15 homology (EH) domain of Eps15 and the alpha-adaptin subunit of the clathrin adaptor AP-2.	bind
29784	6	8924	6	13	NULL	NULL	NULL	epsin	GP		bind					AP-2	GP		alpha-adaptin subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3257_s_3	9920862	A  Xenopus mitotic phosphoprotein, MP90, is very similar to an abundant mammalian nerve terminal protein, epsin, which binds the Eps15 homology (EH) domain of Eps15 and the alpha-adaptin subunit of the clathrin adaptor AP-2.	bind
29785	7	8924	6	13	NULL	NULL	NULL	AP-2	GP		is a type of					clathrin adaptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3257_s_3	9920862	A  Xenopus mitotic phosphoprotein, MP90, is very similar to an abundant mammalian nerve terminal protein, epsin, which binds the Eps15 homology (EH) domain of Eps15 and the alpha-adaptin subunit of the clathrin adaptor AP-2.	bind
38677	1	8924	7	10	NULL	0	NULL	MP90	NULL	Xenopus	is similar to	NULL				epsin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3257_s_3	9920862	A  Xenopus mitotic phosphoprotein, MP90, is very similar to an abundant mammalian nerve terminal protein, epsin, which binds the Eps15 homology (EH) domain of Eps15 and the alpha-adaptin subunit of the clathrin adaptor AP-2.	bind
38678	2	8924	7	NULL	NULL	0	NULL	epsin	NULL		bind	NULL				Eps15	NULL		EH domain 		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3257_s_3	9920862	A  Xenopus mitotic phosphoprotein, MP90, is very similar to an abundant mammalian nerve terminal protein, epsin, which binds the Eps15 homology (EH) domain of Eps15 and the alpha-adaptin subunit of the clathrin adaptor AP-2.	bind
38679	3	8924	7	NULL	NULL	0	NULL	epsin	NULL		bind	NULL				 AP-2	NULL		alpha-adaptin subunit 		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3257_s_3	9920862	A  Xenopus mitotic phosphoprotein, MP90, is very similar to an abundant mammalian nerve terminal protein, epsin, which binds the Eps15 homology (EH) domain of Eps15 and the alpha-adaptin subunit of the clathrin adaptor AP-2.	bind
38680	4	8924	7	10	NULL	0	NULL	MP90	NULL		is a type of	NULL				mitotic phosphoprotein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3257_s_3	9920862	A  Xenopus mitotic phosphoprotein, MP90, is very similar to an abundant mammalian nerve terminal protein, epsin, which binds the Eps15 homology (EH) domain of Eps15 and the alpha-adaptin subunit of the clathrin adaptor AP-2.	bind
38681	5	8924	7	10	NULL	0	NULL	epsin	NULL		is a type of	NULL				mammalian nerve terminal protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3257_s_3	9920862	A  Xenopus mitotic phosphoprotein, MP90, is very similar to an abundant mammalian nerve terminal protein, epsin, which binds the Eps15 homology (EH) domain of Eps15 and the alpha-adaptin subunit of the clathrin adaptor AP-2.	bind
38682	6	8924	7	NULL	NULL	0	NULL	EH domain	NULL		is	NULL				Eps15 homology domain	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3257_s_3	9920862	A  Xenopus mitotic phosphoprotein, MP90, is very similar to an abundant mammalian nerve terminal protein, epsin, which binds the Eps15 homology (EH) domain of Eps15 and the alpha-adaptin subunit of the clathrin adaptor AP-2.	bind
38683	7	8924	7	NULL	NULL	0	NULL	AP-2	NULL		is a type of	NULL				clathrin adaptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3257_s_3	9920862	A  Xenopus mitotic phosphoprotein, MP90, is very similar to an abundant mammalian nerve terminal protein, epsin, which binds the Eps15 homology (EH) domain of Eps15 and the alpha-adaptin subunit of the clathrin adaptor AP-2.	bind
29786	1	8926	6	13	NULL	NULL	NULL	HBV	Organism		bind					HDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
29787	2	8926	6	13	NULL	NULL	NULL	HBV	Organism		is					hepatitis B virus	Organism				NULL		NULL	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
29788	3	8926	6	13	NULL	NULL	NULL	HBV	Organism		bind					chylomicrons	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
29789	4	8926	6	13	NULL	NULL	NULL	statement 3	Process		is mediated by					apolipoprotein H	GP				NULL		NULL	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
29790	5	8926	6	13	NULL	NULL	NULL	HBV-LP complex	Organism		bind					hepatocytes	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
29791	6	8926	6	13	NULL	NULL	NULL	statement 5	Process		occurs via					LDLR	GP				NULL		NULL	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
29792	7	8926	6	13	NULL	NULL	NULL	LRP	GP		is					LDLR-related protein/ 2-macroglogulin receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
29793	8	8926	6	13	NULL	NULL	NULL	statement 5	Process		occurs via					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
47028	9	8926	6	13	NULL	NULL	NULL	LDLR	GP		is					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
47029	10	8926	6	13	NULL	NULL	NULL	statement 6	Process		is an alternative to					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
47030	11	8926	6	13	NULL	NULL	NULL	2-macroglogulin receptor	GP		is a synonym of					LRP	GP				NULL		NULL	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
47032	12	8926	6	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
38686	1	8926	7	NULL	NULL	0	NULL	HBV	NULL		bind	NULL				HDL	NULL				NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
38687	2	8926	7	NULL	NULL	0	NULL	HBV	NULL		bind	NULL				chylomicrons	NULL				NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
38688	3	8926	7	NULL	NULL	0	NULL	apolipoprotein H	NULL		mediates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
38689	4	8926	7	NULL	NULL	0	NULL	apolipoprotein H	NULL		mediates	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
38690	5	8926	7	NULL	NULL	0	NULL	HBV-LP complex 	NULL		bind	NULL				hepatocytes	NULL				NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
38691	6	8926	7	NULL	NULL	0	NULL	statement 5	NULL		via	NULL				LDLR	NULL				NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
38692	7	8926	7	NULL	NULL	0	NULL	statement 5	NULL		via	NULL				LRP	NULL				NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
38693	8	8926	7	NULL	NULL	0	NULL	HBV	NULL		is	NULL				hepatitis B virus	NULL				NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
38694	9	8926	7	NULL	NULL	0	NULL	LDLR	NULL		is	NULL				LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
38695	10	8926	7	NULL	NULL	0	NULL	LRP	NULL		is	NULL				LDLR-related protein	NULL				NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
38696	11	8926	7	10	NULL	0	NULL	2-macroglogulin receptor	NULL		is a synonym of	NULL				LRP 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
38697	12	8926	7	NULL	NULL	0	NULL	statement 6	NULL		is an alternative to	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
47033	13	8926	7	10	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_20_4_457_s_139	10604441	A "`hitchhiker"` method of cell entry has been suggested also for hepatitis B virus (HBV) bound to HDL or chylomicrons (this binding being mediated by apolipoprotein H), with the HBV-LP complex binding to hepatocytes via the LDL receptor (LDLR) or the LDLR-related protein/ 2-macroglogulin receptor (LRP) [  60].	bind
29794	1	8928	6	13	NULL	NULL	NULL	glycogen synthase	GP		bind		may			PP1C	GP				NULL	lysates of COS7 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_34_26074_s_81	10856301	A "`pull-down"` assay was used to test for binding of glycogen synthase and PP1C from lysates of COS7 cells.	bind
38698	1	8928	7	10	NULL	0	NULL	glycogen synthase	NULL		bind	NULL	may			PP1C	NULL				NULL	lysates of COS7 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_34_26074_s_81	10856301	A "`pull-down"` assay was used to test for binding of glycogen synthase and PP1C from lysates of COS7 cells.	bind
29795	1	8929	6	13	NULL	NULL	NULL	CNA	GP	Staphylococcus aureus	bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0560-0569_embo-j_24_24_16362049_s_1	16362049	A 'Collagen Hug' model for Staphylococcus aureus CNA binding to collagen..	bind
38699	1	8929	7	NULL	NULL	0	NULL	CNA	NULL	Staphylococcus aureus	bind	NULL				collagen	NULL				NULL		0	NULL	NULL	NULL	abs-batch0560-0569_embo-j_24_24_16362049_s_1	16362049	A 'Collagen Hug' model for Staphylococcus aureus CNA binding to collagen..	bind
29796	1	8931	6	13	NULL	NULL	NULL	CIS family protein	GP		bind					EPOR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29338_s_282	10882725	A , binding of the CIS family proteins with the EPOR.	bind
38703	1	8931	7	NULL	NULL	0	NULL	 CIS family protein	NULL		bind	NULL				EPOR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29338_s_282	10882725	A , binding of the CIS family proteins with the EPOR.	bind
29797	1	8932	6	13	NULL	NULL	NULL	cyclophilin A	GP	triple mutant	bind			ATM		cyclosporin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_13_761_s_57	9651680	A , the ATM triple mutant of cyclophilin A that binds cyclosporin and some cyclosporin derivatives  [70]  ;	bind
29798	2	8932	6	13	NULL	NULL	NULL	cyclophilin A	GP	triple mutant	bind			ATM		cyclosporin derivatives	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_13_761_s_57	9651680	A , the ATM triple mutant of cyclophilin A that binds cyclosporin and some cyclosporin derivatives  [70]  ;	bind
38704	1	8932	7	10	NULL	0	NULL	cyclophilin A	NULL	triple mutant	bind	NULL		ATM		cyclosporin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_13_761_s_57	9651680	A , the ATM triple mutant of cyclophilin A that binds cyclosporin and some cyclosporin derivatives  [70]  ;	bind
38705	2	8932	7	10	NULL	0	NULL	cyclophilin A	NULL	triple mutant	bind	NULL		ATM		 cyclosporin derivative	NULL				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_13_761_s_57	9651680	A , the ATM triple mutant of cyclophilin A that binds cyclosporin and some cyclosporin derivatives  [70]  ;	bind
29799	1	8935	6	13	NULL	NULL	NULL	FXR/RXR protein	GP		bind					BACS gene	GP	radiolabeled		IR-1 sequences	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_30_27703_s_138	12754200	A -  C, FXR/RXR proteins bind to radiolabeled IR-1  sequences from the BACS and BAT genes  with similar affinities as binding to an  IR-1 from the mouse IBABP gene.	bind
29800	2	8935	6	13	NULL	NULL	NULL	FXR/RXR protein	GP		bind					BAT gene	GP	radiolabeled		IR-1 sequences	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_30_27703_s_138	12754200	A -  C, FXR/RXR proteins bind to radiolabeled IR-1  sequences from the BACS and BAT genes  with similar affinities as binding to an  IR-1 from the mouse IBABP gene.	bind
29801	3	8935	6	13	NULL	NULL	NULL	FXR/RXR protein	GP		bind					IBABP gene	GP	mouse		IR-1 sequences	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_30_27703_s_138	12754200	A -  C, FXR/RXR proteins bind to radiolabeled IR-1  sequences from the BACS and BAT genes  with similar affinities as binding to an  IR-1 from the mouse IBABP gene.	bind
29802	4	8935	6	13	NULL	NULL	NULL	statement 1	Process	affinity of	is similar to					statement 3	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_30_27703_s_138	12754200	A -  C, FXR/RXR proteins bind to radiolabeled IR-1  sequences from the BACS and BAT genes  with similar affinities as binding to an  IR-1 from the mouse IBABP gene.	bind
29803	5	8935	6	13	NULL	NULL	NULL	statement 2	Process	affinity of	is similar to					statement 3	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_30_27703_s_138	12754200	A -  C, FXR/RXR proteins bind to radiolabeled IR-1  sequences from the BACS and BAT genes  with similar affinities as binding to an  IR-1 from the mouse IBABP gene.	bind
38706	1	8935	7	NULL	NULL	0	NULL	FXR/RXR proteins	NULL		bind	NULL				BACS gene	NULL	radiolabeled		IR-1 sequence	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_30_27703_s_138	12754200	A -  C, FXR/RXR proteins bind to radiolabeled IR-1  sequences from the BACS and BAT genes  with similar affinities as binding to an  IR-1 from the mouse IBABP gene.	bind
38707	2	8935	7	NULL	NULL	0	NULL	FXR/RXR proteins	NULL		bind	NULL				BAT genes	NULL	radiolabeled		IR-1 sequence	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_30_27703_s_138	12754200	A -  C, FXR/RXR proteins bind to radiolabeled IR-1  sequences from the BACS and BAT genes  with similar affinities as binding to an  IR-1 from the mouse IBABP gene.	bind
38708	3	8935	7	NULL	NULL	0	NULL	FXR/RXR proteins	NULL		bind	NULL				IBABP gene	NULL	mouse		IR-1 sequence	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_30_27703_s_138	12754200	A -  C, FXR/RXR proteins bind to radiolabeled IR-1  sequences from the BACS and BAT genes  with similar affinities as binding to an  IR-1 from the mouse IBABP gene.	bind
38709	4	8935	7	NULL	NULL	0	NULL	statement 1	NULL	affinity of	is similar to	NULL				statement 3	NULL	affinity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_30_27703_s_138	12754200	A -  C, FXR/RXR proteins bind to radiolabeled IR-1  sequences from the BACS and BAT genes  with similar affinities as binding to an  IR-1 from the mouse IBABP gene.	bind
38710	5	8935	7	NULL	NULL	0	NULL	statement 2	NULL	affinity of	is similar to	NULL				statement 3	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_30_27703_s_138	12754200	A -  C, FXR/RXR proteins bind to radiolabeled IR-1  sequences from the BACS and BAT genes  with similar affinities as binding to an  IR-1 from the mouse IBABP gene.	bind
29806	2	8937	6	13	NULL	NULL	NULL	LPC	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_13_s_71	9445250	A 0.5-mL portion of this solution was put on a NAP 5 column (Pharmacia) and eluted in water to separate [14]LPC bound to apoA-I - containing phospholipid particles from free [14]LPC.	bind
47077	1	8937	6	13	NULL	NULL	NULL	apoA-I	GP		contains					phospholipid particles	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_13_s_71	9445250	A 0.5-mL portion of this solution was put on a NAP 5 column (Pharmacia) and eluted in water to separate [14]LPC bound to apoA-I - containing phospholipid particles from free [14]LPC.	bind
38728	2	8937	7	10	NULL	0	NULL	LPC 			bind					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_13_s_71	9445250	A 0.5-mL portion of this solution was put on a NAP 5 column (Pharmacia) and eluted in water to separate [14]LPC bound to apoA-I - containing phospholipid particles from free [14]LPC.	bind
38729	1	8937	7	NULL	NULL	0	NULL	apoA-I	NULL		contain	NULL				phospholipid particles	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_18_1_13_s_71	9445250	A 0.5-mL portion of this solution was put on a NAP 5 column (Pharmacia) and eluted in water to separate [14]LPC bound to apoA-I - containing phospholipid particles from free [14]LPC.	bind
29807	1	8938	6	13	NULL	NULL	NULL	RII	GP		bind					ERM protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_1_35_s_57	9009265	A 1 muM concentration of the HT-31 peptide inhibited binding of [32]RII to all three ERM proteins (Figure  2).	bind
29808	2	8938	6	13	NULL	NULL	NULL	HT-31 peptide 	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_1_35_s_57	9009265	A 1 muM concentration of the HT-31 peptide inhibited binding of [32]RII to all three ERM proteins (Figure  2).	bind
38730	1	8938	7	10	NULL	0	NULL	RII			bind					ERM proteins					NULL		NULL	NULL	NULL	NULL	gw60_embo_16_1_35_s_57	9009265	A 1 muM concentration of the HT-31 peptide inhibited binding of [32]RII to all three ERM proteins (Figure  2).	bind
38731	2	8938	7	NULL	NULL	0	NULL	HT-31 peptide	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_1_35_s_57	9009265	A 1 muM concentration of the HT-31 peptide inhibited binding of [32]RII to all three ERM proteins (Figure  2).	bind
29849	1	8939	6	13	NULL	NULL	NULL	blr1 gene	GP		confers				360-bp 5'' flanking region	RA 	Chemical	response to			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_6_2423_s_266	14993281	A 1,360-bp 5''-flanking region of the  blr1 gene confers RA response and contains a distal 205-bp sequence necessary for response  A 5''-flanking region extending from -1096 to the 5' end of the first exon at +266 of the  blr1 gene confers response to RA.	bind
38732	1	8939	7	13	NULL	NULL	NULL	blr1 gene 	GP		confers				360-bp 5''-flanking region of	RA	Chemical	response to			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_6_2423_s_266	14993281	A 1,360-bp 5''-flanking region of the  blr1 gene confers RA response and contains a distal 205-bp sequence necessary for response  A 5''-flanking region extending from -1096 to the 5' end of the first exon at +266 of the  blr1 gene confers response to RA.	bind
38778	2	8939	7	13	NULL	NULL	NULL	blr1 gene	GP	distal	is necessary for				205-bp sequence	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_6_2423_s_266	14993281	A 1,360-bp 5''-flanking region of the  blr1 gene confers RA response and contains a distal 205-bp sequence necessary for response  A 5''-flanking region extending from -1096 to the 5' end of the first exon at +266 of the  blr1 gene confers response to RA.	bind
38783	3	8939	7	13	NULL	NULL	NULL				extend from				5''-flanking region	blr1 gene	GP			-1096	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_6_2423_s_266	14993281	A 1,360-bp 5''-flanking region of the  blr1 gene confers RA response and contains a distal 205-bp sequence necessary for response  A 5''-flanking region extending from -1096 to the 5' end of the first exon at +266 of the  blr1 gene confers response to RA.	bind
38784	4	8939	7	13	NULL	NULL	NULL				extend to				5''-flanking region	blr1 gene	GP			5' end of the first exon at +266	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_6_2423_s_266	14993281	A 1,360-bp 5''-flanking region of the  blr1 gene confers RA response and contains a distal 205-bp sequence necessary for response  A 5''-flanking region extending from -1096 to the 5' end of the first exon at +266 of the  blr1 gene confers response to RA.	bind
38786	5	8939	7	13	NULL	NULL	NULL	statement 3	Process		is necessary for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_6_2423_s_266	14993281	A 1,360-bp 5''-flanking region of the  blr1 gene confers RA response and contains a distal 205-bp sequence necessary for response  A 5''-flanking region extending from -1096 to the 5' end of the first exon at +266 of the  blr1 gene confers response to RA.	bind
38788	6	8939	7	13	NULL	NULL	NULL	statement 4	Process		is necessary for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_6_2423_s_266	14993281	A 1,360-bp 5''-flanking region of the  blr1 gene confers RA response and contains a distal 205-bp sequence necessary for response  A 5''-flanking region extending from -1096 to the 5' end of the first exon at +266 of the  blr1 gene confers response to RA.	bind
29809	1	8942	6	13	NULL	NULL	NULL	GTP S	Chemical		bind					G protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_38_3_403_s_186	10219978	A 1-week treatment regimen with the LiCl-containing diet did not influence [35]GTP  S binding to the G   proteins.	bind
29810	2	8942	6	13	NULL	NULL	NULL	LiCl	Chemical		does not influence					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_38_3_403_s_186	10219978	A 1-week treatment regimen with the LiCl-containing diet did not influence [35]GTP  S binding to the G   proteins.	bind
38797	1	8942	7	10	NULL	0	NULL	GTP S			bind					G proteins					NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_38_3_403_s_186	10219978	A 1-week treatment regimen with the LiCl-containing diet did not influence [35]GTP  S binding to the G   proteins.	bind
38798	2	8942	7	10	NULL	0	NULL	LiCl	NULL		does not influence	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_38_3_403_s_186	10219978	A 1-week treatment regimen with the LiCl-containing diet did not influence [35]GTP  S binding to the G   proteins.	bind
29811	1	8948	6	13	NULL	NULL	NULL	GLUT1 cDNA probe	NucleicAcid	human	bind					GLUT1 DNA	NucleicAcid	genomic			NULL		NULL	NULL	NULL	NULL	gw70_amjpathol_163_5_1873_s_44	14578187	A 1.66-kb human GLUT1 cDNA probe that binds to genomic  GLUT1 DNA immediately 3' to the point of insertion of the targeting construct was used as an adjacent probe to confirm insertion of the targeting construct inside the endogenous  GLUT1 gene of ES cells after homologous recombination.	bind
38805	1	8948	7	10	NULL	0	NULL	GLUT1 cDNA probe	NULL	human	bind	NULL				GLUT1 DNA	NULL	genomic			NULL		NULL	NULL	NULL	NULL	gw70_amjpathol_163_5_1873_s_44	14578187	A 1.66-kb human GLUT1 cDNA probe that binds to genomic  GLUT1 DNA immediately 3' to the point of insertion of the targeting construct was used as an adjacent probe to confirm insertion of the targeting construct inside the endogenous  GLUT1 gene of ES cells after homologous recombination.	bind
29812	1	8949	6	13	NULL	NULL	NULL	scFv2A-AP/S	GP	exogenous	bind					MBP-NIb	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_1_167_s_160	12535657	A 1/8  dilution of the agroinfiltrated plant extract inhibited binding of exogenous scFv2A-AP/S  to MBP-NIb by up to 32% ( Fig. 6).	bind
29813	2	8949	6	13	NULL	NULL	NULL	plant extract	Cell	agroinfiltrated	inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_1_167_s_160	12535657	A 1/8  dilution of the agroinfiltrated plant extract inhibited binding of exogenous scFv2A-AP/S  to MBP-NIb by up to 32% ( Fig. 6).	bind
38810	1	8949	7	10	NULL	0	NULL	scFv2A-AP/S	NULL	exogenous	bind	NULL				MBP-NIb	NULL				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_1_167_s_160	12535657	A 1/8  dilution of the agroinfiltrated plant extract inhibited binding of exogenous scFv2A-AP/S  to MBP-NIb by up to 32% ( Fig. 6).	bind
38811	2	8949	7	10	NULL	0	NULL	plant extract		agroinfiltrated	inhibits					statement 1					NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_1_167_s_160	12535657	A 1/8  dilution of the agroinfiltrated plant extract inhibited binding of exogenous scFv2A-AP/S  to MBP-NIb by up to 32% ( Fig. 6).	bind
29814	1	8951	6	13	NULL	NULL	NULL	EBNA2	GP		bind					CBF1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_13_4625_s_28	15070768	A 10-aa peptide was identified that was an effective competitor for EBNA2 binding to CBF1.	bind
38816	1	8951	7	NULL	NULL	0	NULL	EBNA2	NULL		bind	NULL				CBF1	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_13_4625_s_28	15070768	A 10-aa peptide was identified that was an effective competitor for EBNA2 binding to CBF1.	bind
29815	1	8952	6	13	NULL	NULL	NULL	HOAP	GP		bind			carboxyl terminal domain		HP1a	GP		hinge domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34491_s_156	12826664	A 10-fold  molar excess of the HP1a-specific peptide was able to compete with binding of  the HOAP carboxyl terminal domain to the HP1a hinge domain, whereas the HP1b  and HP1c peptides were unable to compete even at a 100-fold molar excess.	bind
29816	2	8952	6	13	NULL	NULL	NULL	HP1a-specific peptide	GP		bind					HP1a	GP		hinge domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34491_s_156	12826664	A 10-fold  molar excess of the HP1a-specific peptide was able to compete with binding of  the HOAP carboxyl terminal domain to the HP1a hinge domain, whereas the HP1b  and HP1c peptides were unable to compete even at a 100-fold molar excess.	bind
29817	3	8952	6	13	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34491_s_156	12826664	A 10-fold  molar excess of the HP1a-specific peptide was able to compete with binding of  the HOAP carboxyl terminal domain to the HP1a hinge domain, whereas the HP1b  and HP1c peptides were unable to compete even at a 100-fold molar excess.	bind
29818	4	8952	6	13	NULL	NULL	NULL	HP1b peptide	GP		does not bind					Hp1a	GP		hinge domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34491_s_156	12826664	A 10-fold  molar excess of the HP1a-specific peptide was able to compete with binding of  the HOAP carboxyl terminal domain to the HP1a hinge domain, whereas the HP1b  and HP1c peptides were unable to compete even at a 100-fold molar excess.	bind
29819	5	8952	6	13	NULL	NULL	NULL	HP1c peptide	GP		does not bind					HP1a	GP		hinge domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34491_s_156	12826664	A 10-fold  molar excess of the HP1a-specific peptide was able to compete with binding of  the HOAP carboxyl terminal domain to the HP1a hinge domain, whereas the HP1b  and HP1c peptides were unable to compete even at a 100-fold molar excess.	bind
38818	1	8952	7	NULL	NULL	0	NULL	HOAP	NULL		bind	NULL		carboxyl terminal domain		HP1a	NULL		hinge domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34491_s_156	12826664	A 10-fold  molar excess of the HP1a-specific peptide was able to compete with binding of  the HOAP carboxyl terminal domain to the HP1a hinge domain, whereas the HP1b  and HP1c peptides were unable to compete even at a 100-fold molar excess.	bind
38819	2	8952	7	10	NULL	0	NULL	statement 5	NULL		competes with	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34491_s_156	12826664	A 10-fold  molar excess of the HP1a-specific peptide was able to compete with binding of  the HOAP carboxyl terminal domain to the HP1a hinge domain, whereas the HP1b  and HP1c peptides were unable to compete even at a 100-fold molar excess.	bind
38820	3	8952	7	NULL	NULL	0	NULL	HP1b peptide	NULL		unable to compete with	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34491_s_156	12826664	A 10-fold  molar excess of the HP1a-specific peptide was able to compete with binding of  the HOAP carboxyl terminal domain to the HP1a hinge domain, whereas the HP1b  and HP1c peptides were unable to compete even at a 100-fold molar excess.	bind
38821	4	8952	7	NULL	NULL	0	NULL	HP1c peptide	NULL		unable to compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34491_s_156	12826664	A 10-fold  molar excess of the HP1a-specific peptide was able to compete with binding of  the HOAP carboxyl terminal domain to the HP1a hinge domain, whereas the HP1b  and HP1c peptides were unable to compete even at a 100-fold molar excess.	bind
47078	5	8952	7	10	NULL	0	NULL	\tHP1a-specific peptide	NULL		bind	NULL				HP1a	NULL		hinge domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34491_s_156	12826664	A 10-fold  molar excess of the HP1a-specific peptide was able to compete with binding of  the HOAP carboxyl terminal domain to the HP1a hinge domain, whereas the HP1b  and HP1c peptides were unable to compete even at a 100-fold molar excess.	bind
29820	1	8953	6	13	NULL	NULL	NULL	apoE protein	GP	full length	lowers					3H-LDL	GP	bound			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13333_s_262	16540478	A 10-fold dose of full-length apoE protein only lowered 34% of the bound 3H-LDL, whereas the same dose of apoE-DMPC lowered 58-59% of the bound 3H-LDL. The LDL-R binding ability of apoE-DMPC was higher than that of LDL at the same dose (20-fold), although apoE with or without DMPC did not show isoform specificity.	bind
29821	2	8953	6	13	NULL	NULL	NULL	apoE-DMPC	GP		lowers					3H-LDL	GP	bound			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13333_s_262	16540478	A 10-fold dose of full-length apoE protein only lowered 34% of the bound 3H-LDL, whereas the same dose of apoE-DMPC lowered 58-59% of the bound 3H-LDL. The LDL-R binding ability of apoE-DMPC was higher than that of LDL at the same dose (20-fold), although apoE with or without DMPC did not show isoform specificity.	bind
29822	3	8953	6	13	NULL	NULL	NULL	apoE-DMPC	GP		bind					LDL-R	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13333_s_262	16540478	A 10-fold dose of full-length apoE protein only lowered 34% of the bound 3H-LDL, whereas the same dose of apoE-DMPC lowered 58-59% of the bound 3H-LDL. The LDL-R binding ability of apoE-DMPC was higher than that of LDL at the same dose (20-fold), although apoE with or without DMPC did not show isoform specificity.	bind
29823	4	8953	6	13	NULL	NULL	NULL	LDL	GP		bind					apoE-DMPC	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13333_s_262	16540478	A 10-fold dose of full-length apoE protein only lowered 34% of the bound 3H-LDL, whereas the same dose of apoE-DMPC lowered 58-59% of the bound 3H-LDL. The LDL-R binding ability of apoE-DMPC was higher than that of LDL at the same dose (20-fold), although apoE with or without DMPC did not show isoform specificity.	bind
38822	1	8953	7	NULL	NULL	0	NULL	apoE protein	NULL	full-length	lowers	NULL				3H-LDL	NULL	bound			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13333_s_262	16540478	A 10-fold dose of full-length apoE protein only lowered 34% of the bound 3H-LDL, whereas the same dose of apoE-DMPC lowered 58-59% of the bound 3H-LDL. The LDL-R binding ability of apoE-DMPC was higher than that of LDL at the same dose (20-fold), although apoE with or without DMPC did not show isoform specificity.	bind
38823	2	8953	7	NULL	NULL	0	NULL	apoE-DMPC	NULL		lowers	NULL				 3H-LDL	NULL	bound			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13333_s_262	16540478	A 10-fold dose of full-length apoE protein only lowered 34% of the bound 3H-LDL, whereas the same dose of apoE-DMPC lowered 58-59% of the bound 3H-LDL. The LDL-R binding ability of apoE-DMPC was higher than that of LDL at the same dose (20-fold), although apoE with or without DMPC did not show isoform specificity.	bind
38824	3	8953	7	NULL	NULL	0	NULL	LDL-R	NULL		bind	NULL				apoE-DMPC	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13333_s_262	16540478	A 10-fold dose of full-length apoE protein only lowered 34% of the bound 3H-LDL, whereas the same dose of apoE-DMPC lowered 58-59% of the bound 3H-LDL. The LDL-R binding ability of apoE-DMPC was higher than that of LDL at the same dose (20-fold), although apoE with or without DMPC did not show isoform specificity.	bind
38825	4	8953	7	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				apoE-DMPC	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13333_s_262	16540478	A 10-fold dose of full-length apoE protein only lowered 34% of the bound 3H-LDL, whereas the same dose of apoE-DMPC lowered 58-59% of the bound 3H-LDL. The LDL-R binding ability of apoE-DMPC was higher than that of LDL at the same dose (20-fold), although apoE with or without DMPC did not show isoform specificity.	bind
38826	5	8953	7	NULL	NULL	0	NULL	statement 3	NULL	binding of	is higher than	NULL				statement 4	NULL	binding of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13333_s_262	16540478	A 10-fold dose of full-length apoE protein only lowered 34% of the bound 3H-LDL, whereas the same dose of apoE-DMPC lowered 58-59% of the bound 3H-LDL. The LDL-R binding ability of apoE-DMPC was higher than that of LDL at the same dose (20-fold), although apoE with or without DMPC did not show isoform specificity.	bind
29824	1	8954	6	13	NULL	NULL	NULL	GR	GP	phosphorylation of	is dependent on					Dex	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_29_26573_s_143	12000743	A 10-fold excess of ZK299 was not as effective at blocking the Dex-dependent phosphorylation of GR, presumably because of its lower affinity for the receptor.	bind
29825	2	8954	6	13	NULL	NULL	NULL	ZK299	Chemical		does not block		effectively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_29_26573_s_143	12000743	A 10-fold excess of ZK299 was not as effective at blocking the Dex-dependent phosphorylation of GR, presumably because of its lower affinity for the receptor.	bind
38827	1	8954	7	NULL	NULL	0	NULL	GR	NULL	 phosphorylation of	depends on	NULL				Dex	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26573_s_143	12000743	A 10-fold excess of ZK299 was not as effective at blocking the Dex-dependent phosphorylation of GR, presumably because of its lower affinity for the receptor.	bind
38828	2	8954	7	NULL	NULL	0	NULL	ZK299 	NULL		does not block	NULL	effectively			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26573_s_143	12000743	A 10-fold excess of ZK299 was not as effective at blocking the Dex-dependent phosphorylation of GR, presumably because of its lower affinity for the receptor.	bind
29826	1	8956	6	13	NULL	NULL	NULL	Tf-R	GP		bind		weakly			Tf	GP	bovine			NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_52_0_745_s_562	9891812	A 10-fold higher value was reported by Salmon et al ( 112), but this value is a priori implausible (as this high number of receptors could  occupy half the flagellar pocket wall), and it was based on inaccurate Tf binding  curves obtained with a Tf-R that binds bovine Tf weakly (cf  21,  125).	bind
38830	1	8956	7	NULL	NULL	0	NULL	 Tf-R	NULL		binds	NULL	weakly			Tf	NULL	bovine			NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_52_0_745_s_562	9891812	A 10-fold higher value was reported by Salmon et al ( 112), but this value is a priori implausible (as this high number of receptors could  occupy half the flagellar pocket wall), and it was based on inaccurate Tf binding  curves obtained with a Tf-R that binds bovine Tf weakly (cf  21,  125).	bind
29827	1	8957	6	13	NULL	NULL	NULL	MRP	GP		bind					PC/PS vesicles	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_34_19879_s_233	7650001	A 10-fold increase in Triton X-100,  e.g.  0.01%,  does not change the apparent partition coefficient for the binding of  MRP to PC/PS vesicles (4:1) (not shown).	bind
38831	1	8957	7	NULL	NULL	0	NULL	MRP	NULL		bind	NULL				PC/PS vesicles	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_34_19879_s_233	7650001	A 10-fold increase in Triton X-100,  e.g.  0.01%,  does not change the apparent partition coefficient for the binding of  MRP to PC/PS vesicles (4:1) (not shown).	bind
29828	1	8958	6	13	NULL	NULL	NULL	rpr	GP		bind				EcRE	EcR/USP heterodimer	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_445_s_186	10882130	A 10-fold molar excess of this mutated EcRE had no effect on formation of EcR/USP/ hsp27 EcRE complex, indicating that these conserved nucleotides are required for binding of the  rpr EcRE by the EcR/USP heterodimer (  Figure 6B, lane 9).	bind
29829	2	8958	6	13	NULL	NULL	NULL	statement 1	Process		forms a					EcR/USP/ hsp27 EcRE complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_445_s_186	10882130	A 10-fold molar excess of this mutated EcRE had no effect on formation of EcR/USP/ hsp27 EcRE complex, indicating that these conserved nucleotides are required for binding of the  rpr EcRE by the EcR/USP heterodimer (  Figure 6B, lane 9).	bind
29830	3	8958	6	13	NULL	NULL	NULL	EcRE	GP	mutant	has no effect on					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_445_s_186	10882130	A 10-fold molar excess of this mutated EcRE had no effect on formation of EcR/USP/ hsp27 EcRE complex, indicating that these conserved nucleotides are required for binding of the  rpr EcRE by the EcR/USP heterodimer (  Figure 6B, lane 9).	bind
38922	1	8958	7	10	NULL	0	NULL	EcR/USP heterodimer	NULL		bind	NULL				rpr	NULL			EcRE	NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_445_s_186	10882130	A 10-fold molar excess of this mutated EcRE had no effect on formation of EcR/USP/ hsp27 EcRE complex, indicating that these conserved nucleotides are required for binding of the  rpr EcRE by the EcR/USP heterodimer (  Figure 6B, lane 9).	bind
38923	2	8958	7	10	NULL	0	NULL	EcRE	NULL	mutant	does not affect	NULL				EcR/USP/ hsp27 EcRE complex	NULL	formation of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_3_445_s_186	10882130	A 10-fold molar excess of this mutated EcRE had no effect on formation of EcR/USP/ hsp27 EcRE complex, indicating that these conserved nucleotides are required for binding of the  rpr EcRE by the EcR/USP heterodimer (  Figure 6B, lane 9).	bind
38924	3	8958	7	NULL	NULL	0	NULL		NULL		is required for	NULL			conserved nucleotides	statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_5_3_445_s_186	10882130	A 10-fold molar excess of this mutated EcRE had no effect on formation of EcR/USP/ hsp27 EcRE complex, indicating that these conserved nucleotides are required for binding of the  rpr EcRE by the EcR/USP heterodimer (  Figure 6B, lane 9).	bind
29831	1	8960	6	13	NULL	NULL	NULL	AO	Chemical		bind					chromatin	Chromosome	sperm cell			NULL		NULL	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_95_4_6831026_s_6	6831026	A 10-time decrease in the fluorescence of AO bound with sperm  cell chromatin as compared to F530 AO bound with lymphocyte chromatin  structure of the same individual supports the data on the over condensation  of sperm cell nuclear chromatin as compared to that in lymphocytes.	bind
29832	2	8960	6	13	NULL	NULL	NULL	AO	Chemical		bind					lymphocyte chromatin structure	Chromosome				NULL		NULL	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_95_4_6831026_s_6	6831026	A 10-time decrease in the fluorescence of AO bound with sperm  cell chromatin as compared to F530 AO bound with lymphocyte chromatin  structure of the same individual supports the data on the over condensation  of sperm cell nuclear chromatin as compared to that in lymphocytes.	bind
38925	1	8960	7	10	NULL	0	NULL	chromatin 		sperm cell	bind					AO					NULL		NULL	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_95_4_6831026_s_6	6831026	A 10-time decrease in the fluorescence of AO bound with sperm  cell chromatin as compared to F530 AO bound with lymphocyte chromatin  structure of the same individual supports the data on the over condensation  of sperm cell nuclear chromatin as compared to that in lymphocytes.	bind
38926	2	8960	7	NULL	NULL	0	NULL	lymphocyte chromatin structure	NULL		bind	NULL				AO	NULL			F530	NULL		0	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_95_4_6831026_s_6	6831026	A 10-time decrease in the fluorescence of AO bound with sperm  cell chromatin as compared to F530 AO bound with lymphocyte chromatin  structure of the same individual supports the data on the over condensation  of sperm cell nuclear chromatin as compared to that in lymphocytes.	bind
29850	1	8963	6	13	NULL	NULL	NULL	LHR A	GP		bind					C4b	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_44_31160_s_112	10531307	A 100% value was assigned to the fraction of LHR A that bound to C4b- or iC3-Sepharose.	bind
29851	2	8963	6	13	NULL	NULL	NULL	LHR A	GP		bind					iC3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_44_31160_s_112	10531307	A 100% value was assigned to the fraction of LHR A that bound to C4b- or iC3-Sepharose.	bind
39339	1	8963	7	10	NULL	0	NULL	LHR A	NULL		bind	NULL				C4b	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_44_31160_s_112	10531307	A 100% value was assigned to the fraction of LHR A that bound to C4b- or iC3-Sepharose.	bind
39340	2	8963	7	10	NULL	0	NULL	LHR A	NULL		bind	NULL				iC3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_44_31160_s_112	10531307	A 100% value was assigned to the fraction of LHR A that bound to C4b- or iC3-Sepharose.	bind
29852	1	8964	6	13	NULL	NULL	NULL	oriR replication origin	NucleicAcid		bind				100 bp region	RepA protein plasmid	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_2_434_s_337	9618448	A 100-bp region in the  oriR replication origin is continuously bound by the plasmid RepA protein to form the initiation complex.	bind
29853	2	8964	6	13	NULL	NULL	NULL	statement 1	Process		forms					initiation complex	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_2_434_s_337	9618448	A 100-bp region in the  oriR replication origin is continuously bound by the plasmid RepA protein to form the initiation complex.	bind
39341	1	8964	7	NULL	NULL	0	NULL	oriR replication origin	NULL		bind	NULL				plasmid RepA protein	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_2_434_s_337	9618448	A 100-bp region in the  oriR replication origin is continuously bound by the plasmid RepA protein to form the initiation complex.	bind
39342	2	8964	7	NULL	NULL	0	NULL	statement 1	NULL		form	NULL				initiation complex	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_2_434_s_337	9618448	A 100-bp region in the  oriR replication origin is continuously bound by the plasmid RepA protein to form the initiation complex.	bind
31152	1	8967	6	13	NULL	NULL	NULL	TEC1	GP		competes with				FRE	Ty1	GP			FRE	NULL		NULL	NULL	NULL	NULL	gw60_science_275_5304_1314_s_99	9036858	A 100-fold excess of the unlabeled  TEC1 FRE also eliminated binding to the  Ty1 FRE (Fig.  4A, lane 9), whereas  TEC1 FREs containing point mutations in either the PRE or TCS did not compete.	bind
31154	2	8967	6	13	NULL	NULL	NULL	TEC1 	GP	mutant	does not compete				FRE	Ty1	GP			FRE	NULL		NULL	NULL	NULL	NULL	gw60_science_275_5304_1314_s_99	9036858	A 100-fold excess of the unlabeled  TEC1 FRE also eliminated binding to the  Ty1 FRE (Fig.  4A, lane 9), whereas  TEC1 FREs containing point mutations in either the PRE or TCS did not compete.	bind
39345	1	8967	7	NULL	NULL	0	NULL	TEC1	NULL	unlabeled 	bind	NULL			FRE	Ty1	NULL			FRE	NULL		0	NULL	NULL	NULL	gw60_science_275_5304_1314_s_99	9036858	A 100-fold excess of the unlabeled  TEC1 FRE also eliminated binding to the  Ty1 FRE (Fig.  4A, lane 9), whereas  TEC1 FREs containing point mutations in either the PRE or TCS did not compete.	bind
39346	2	8967	7	NULL	NULL	0	NULL	TEC1	NULL	point mutant	does not compete with	NULL			FREs containing PRE	statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_275_5304_1314_s_99	9036858	A 100-fold excess of the unlabeled  TEC1 FRE also eliminated binding to the  Ty1 FRE (Fig.  4A, lane 9), whereas  TEC1 FREs containing point mutations in either the PRE or TCS did not compete.	bind
39347	3	8967	7	NULL	NULL	0	NULL	TEC1	NULL	point mutant	does not compete with	NULL			FREs containing TCS	statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_science_275_5304_1314_s_99	9036858	A 100-fold excess of the unlabeled  TEC1 FRE also eliminated binding to the  Ty1 FRE (Fig.  4A, lane 9), whereas  TEC1 FREs containing point mutations in either the PRE or TCS did not compete.	bind
39348	4	8967	7	10	NULL	0	NULL	TEC1	NULL	excess of;;unlabeled	eliminate	NULL			FRE	statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_275_5304_1314_s_99	9036858	A 100-fold excess of the unlabeled  TEC1 FRE also eliminated binding to the  Ty1 FRE (Fig.  4A, lane 9), whereas  TEC1 FREs containing point mutations in either the PRE or TCS did not compete.	bind
30321	1	8968	6	13	NULL	NULL	NULL	Pab1p	GP		bind					MFA2	NucleicAcid	capped		3'' UTR	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9753_s_109	16260593	A 100-fold excess of unlabeled uncapped MFA2 or excess unlabeled capped pGEM4 polylinker (Cap A0) or 100 ng of poly(C) failed to compete Pab1p bound to capped MFA2 3''-UTR (Fig.  2A, lanes 3 to 6 compared to lanes 2 and 6).	bind
30322	2	8968	6	13	NULL	NULL	NULL	MFA2	NucleicAcid	unlabeled;;uncapped	failed to compete					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9753_s_109	16260593	A 100-fold excess of unlabeled uncapped MFA2 or excess unlabeled capped pGEM4 polylinker (Cap A0) or 100 ng of poly(C) failed to compete Pab1p bound to capped MFA2 3''-UTR (Fig.  2A, lanes 3 to 6 compared to lanes 2 and 6).	bind
30323	3	8968	6	13	NULL	NULL	NULL	MFA2	NucleicAcid	unlabeled;;uncapped	failed to compete					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9753_s_109	16260593	A 100-fold excess of unlabeled uncapped MFA2 or excess unlabeled capped pGEM4 polylinker (Cap A0) or 100 ng of poly(C) failed to compete Pab1p bound to capped MFA2 3''-UTR (Fig.  2A, lanes 3 to 6 compared to lanes 2 and 6).	bind
56167	4	8968	6	13	NULL	NULL	NULL	poly(C)	Chemical		failed to compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9753_s_109	16260593	A 100-fold excess of unlabeled uncapped MFA2 or excess unlabeled capped pGEM4 polylinker (Cap A0) or 100 ng of poly(C) failed to compete Pab1p bound to capped MFA2 3''-UTR (Fig.  2A, lanes 3 to 6 compared to lanes 2 and 6).	bind
39349	1	8968	7	10	NULL	0	NULL	Pab1p	NULL		bind	NULL				MFA2	NULL	capped	3''-UTR		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9753_s_109	16260593	A 100-fold excess of unlabeled uncapped MFA2 or excess unlabeled capped pGEM4 polylinker (Cap A0) or 100 ng of poly(C) failed to compete Pab1p bound to capped MFA2 3''-UTR (Fig.  2A, lanes 3 to 6 compared to lanes 2 and 6).	bind
39350	2	8968	7	10	NULL	0	NULL	MFA2		unlabeled;;uncapped	fail to compete with					statement 1					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9753_s_109	16260593	A 100-fold excess of unlabeled uncapped MFA2 or excess unlabeled capped pGEM4 polylinker (Cap A0) or 100 ng of poly(C) failed to compete Pab1p bound to capped MFA2 3''-UTR (Fig.  2A, lanes 3 to 6 compared to lanes 2 and 6).	bind
39351	3	8968	7	10	NULL	0	NULL	pGEM4 polylinker		unlabeled;;uncapped	fail to compete with					statement 1					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_22_9753_s_109	16260593	A 100-fold excess of unlabeled uncapped MFA2 or excess unlabeled capped pGEM4 polylinker (Cap A0) or 100 ng of poly(C) failed to compete Pab1p bound to capped MFA2 3''-UTR (Fig.  2A, lanes 3 to 6 compared to lanes 2 and 6).	bind
39372	4	8968	7	NULL	NULL	0	NULL	poly(C)	NULL		fail to compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_22_9753_s_109	16260593	A 100-fold excess of unlabeled uncapped MFA2 or excess unlabeled capped pGEM4 polylinker (Cap A0) or 100 ng of poly(C) failed to compete Pab1p bound to capped MFA2 3''-UTR (Fig.  2A, lanes 3 to 6 compared to lanes 2 and 6).	bind
30325	1	8969	6	13	NULL	NULL	NULL			radiolabelled;;Drosophila	bind				IRE	IRP1	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_febslett_436_3_476_s_167	9801172	A 100-fold molar excess of both cold human ferritin H like IRE (I-12.CAT, lane 4 in  Fig. 1B) and cold human ferritin H IRE (pSPT-fer, lane 5 in  Fig. 1B) significantly reduced the binding of the radiolabelled  Drosophila IRE to the human IRP1, whereas a 100-fold molar excess of the human mutated IRE was without any affect (lane 3 in  Fig. 1B).	bind
30326	2	8969	6	13	NULL	NULL	NULL	ferritin H like	GP	cold;;human	reduces		significantly		IRE	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_436_3_476_s_167	9801172	A 100-fold molar excess of both cold human ferritin H like IRE (I-12.CAT, lane 4 in  Fig. 1B) and cold human ferritin H IRE (pSPT-fer, lane 5 in  Fig. 1B) significantly reduced the binding of the radiolabelled  Drosophila IRE to the human IRP1, whereas a 100-fold molar excess of the human mutated IRE was without any affect (lane 3 in  Fig. 1B).	bind
30327	3	8969	6	13	NULL	NULL	NULL	ferritin H 	GP	cold;;human	reduces		significantly		IRE	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_436_3_476_s_167	9801172	A 100-fold molar excess of both cold human ferritin H like IRE (I-12.CAT, lane 4 in  Fig. 1B) and cold human ferritin H IRE (pSPT-fer, lane 5 in  Fig. 1B) significantly reduced the binding of the radiolabelled  Drosophila IRE to the human IRP1, whereas a 100-fold molar excess of the human mutated IRE was without any affect (lane 3 in  Fig. 1B).	bind
30328	4	8969	6	13	NULL	NULL	NULL	IRE	GP	human;;mutant	does not affect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_436_3_476_s_167	9801172	A 100-fold molar excess of both cold human ferritin H like IRE (I-12.CAT, lane 4 in  Fig. 1B) and cold human ferritin H IRE (pSPT-fer, lane 5 in  Fig. 1B) significantly reduced the binding of the radiolabelled  Drosophila IRE to the human IRP1, whereas a 100-fold molar excess of the human mutated IRE was without any affect (lane 3 in  Fig. 1B).	bind
39373	1	8969	7	10	NULL	0	NULL		NULL	radiolabelled;;Drosophila	bind	NULL			IRE	IRP1	NULL	human			NULL		NULL	NULL	NULL	NULL	gw60_febslett_436_3_476_s_167	9801172	A 100-fold molar excess of both cold human ferritin H like IRE (I-12.CAT, lane 4 in  Fig. 1B) and cold human ferritin H IRE (pSPT-fer, lane 5 in  Fig. 1B) significantly reduced the binding of the radiolabelled  Drosophila IRE to the human IRP1, whereas a 100-fold molar excess of the human mutated IRE was without any affect (lane 3 in  Fig. 1B).	bind
39374	2	8969	7	10	NULL	0	NULL	ferritin H like	NULL	cold;;human	reduce	NULL	significantly		IRE	statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_436_3_476_s_167	9801172	A 100-fold molar excess of both cold human ferritin H like IRE (I-12.CAT, lane 4 in  Fig. 1B) and cold human ferritin H IRE (pSPT-fer, lane 5 in  Fig. 1B) significantly reduced the binding of the radiolabelled  Drosophila IRE to the human IRP1, whereas a 100-fold molar excess of the human mutated IRE was without any affect (lane 3 in  Fig. 1B).	bind
39375	3	8969	7	10	NULL	0	NULL	ferritin H	NULL	cold;;human	reduce	NULL	significantly		 IRE	statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_436_3_476_s_167	9801172	A 100-fold molar excess of both cold human ferritin H like IRE (I-12.CAT, lane 4 in  Fig. 1B) and cold human ferritin H IRE (pSPT-fer, lane 5 in  Fig. 1B) significantly reduced the binding of the radiolabelled  Drosophila IRE to the human IRP1, whereas a 100-fold molar excess of the human mutated IRE was without any affect (lane 3 in  Fig. 1B).	bind
39376	4	8969	7	10	NULL	0	NULL		NULL	human;;mutant	does not affect	NULL			IRE	statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_436_3_476_s_167	9801172	A 100-fold molar excess of both cold human ferritin H like IRE (I-12.CAT, lane 4 in  Fig. 1B) and cold human ferritin H IRE (pSPT-fer, lane 5 in  Fig. 1B) significantly reduced the binding of the radiolabelled  Drosophila IRE to the human IRP1, whereas a 100-fold molar excess of the human mutated IRE was without any affect (lane 3 in  Fig. 1B).	bind
30329	1	8970	6	13	NULL	NULL	NULL	KKLF	GP		does not bind									SpI site (GGCGGG)	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7319_s_120	10982849	A 100-fold molar excess of cold SpI oligonucleotide (lane 3) did not compete with the GA element, suggesting that KKLF could not bind to the SpI site (GGCGGG).	bind
30330	2	8970	6	13	NULL	NULL	NULL	SpI oligonucleotide	NucleicAcid	cold	does not compete with									GA element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7319_s_120	10982849	A 100-fold molar excess of cold SpI oligonucleotide (lane 3) did not compete with the GA element, suggesting that KKLF could not bind to the SpI site (GGCGGG).	bind
39377	1	8970	7	10	NULL	0	NULL	KKLF	NULL		does not bind	NULL					NULL			SpI site (GGCGGG)	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7319_s_120	10982849	A 100-fold molar excess of cold SpI oligonucleotide (lane 3) did not compete with the GA element, suggesting that KKLF could not bind to the SpI site (GGCGGG).	bind
39378	2	8970	7	10	NULL	0	NULL	SpI oligonucleotide	NULL	cold	does not compete with	NULL					NULL			GA element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7319_s_120	10982849	A 100-fold molar excess of cold SpI oligonucleotide (lane 3) did not compete with the GA element, suggesting that KKLF could not bind to the SpI site (GGCGGG).	bind
30331	1	8971	6	13	NULL	NULL	NULL	TFPI	GP		bind					VLDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_15_12241_s_209	11278667	A 100-fold molar excess of RAP blocked more than 95% of TFPI binding to VLDL receptor.	bind
30332	2	8971	6	13	NULL	NULL	NULL	RAP	GP	excess of	block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_15_12241_s_209	11278667	A 100-fold molar excess of RAP blocked more than 95% of TFPI binding to VLDL receptor.	bind
39379	1	8971	7	NULL	NULL	0	NULL	TFPI	NULL		bind	NULL				VLDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_15_12241_s_209	11278667	A 100-fold molar excess of RAP blocked more than 95% of TFPI binding to VLDL receptor.	bind
39380	2	8971	7	10	NULL	0	NULL	RAP		excess	blocks					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_15_12241_s_209	11278667	A 100-fold molar excess of RAP blocked more than 95% of TFPI binding to VLDL receptor.	bind
30333	1	8972	6	13	NULL	NULL	NULL	TFPI	GP	125I	bind					TSP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31715_s_180	10922378	A 100-fold molar excess of TFPI-160 had no effect on the binding of 125I-TFPI to TSP-1, whereas a 100-fold molar excess of K1K2C decreased binding to 15% (Fig.  6 B), demonstrating that the C-terminal region of TFPI has a critical role in the binding of TFPI to TSP-1.	bind
30334	2	8972	6	13	NULL	NULL	NULL	K1K2C	GP	excess of	decreases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31715_s_180	10922378	A 100-fold molar excess of TFPI-160 had no effect on the binding of 125I-TFPI to TSP-1, whereas a 100-fold molar excess of K1K2C decreased binding to 15% (Fig.  6 B), demonstrating that the C-terminal region of TFPI has a critical role in the binding of TFPI to TSP-1.	bind
30335	3	8972	6	13	NULL	NULL	NULL	TFPI	GP		plays a role in			C-terminal region		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31715_s_180	10922378	A 100-fold molar excess of TFPI-160 had no effect on the binding of 125I-TFPI to TSP-1, whereas a 100-fold molar excess of K1K2C decreased binding to 15% (Fig.  6 B), demonstrating that the C-terminal region of TFPI has a critical role in the binding of TFPI to TSP-1.	bind
30336	4	8972	6	13	NULL	NULL	NULL	TFPI-160	GP	excess of	had no effect on					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31715_s_180	10922378	A 100-fold molar excess of TFPI-160 had no effect on the binding of 125I-TFPI to TSP-1, whereas a 100-fold molar excess of K1K2C decreased binding to 15% (Fig.  6 B), demonstrating that the C-terminal region of TFPI has a critical role in the binding of TFPI to TSP-1.	bind
39381	1	8972	7	10	NULL	0	NULL	TFPI	NULL	125I	bind	NULL				TSP-1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31715_s_180	10922378	A 100-fold molar excess of TFPI-160 had no effect on the binding of 125I-TFPI to TSP-1, whereas a 100-fold molar excess of K1K2C decreased binding to 15% (Fig.  6 B), demonstrating that the C-terminal region of TFPI has a critical role in the binding of TFPI to TSP-1.	bind
39382	2	8972	7	10	NULL	0	NULL	TFPI-160		excess	does not affect					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31715_s_180	10922378	A 100-fold molar excess of TFPI-160 had no effect on the binding of 125I-TFPI to TSP-1, whereas a 100-fold molar excess of K1K2C decreased binding to 15% (Fig.  6 B), demonstrating that the C-terminal region of TFPI has a critical role in the binding of TFPI to TSP-1.	bind
39383	3	8972	7	10	NULL	0	NULL	K1K2C		excess	decrease					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31715_s_180	10922378	A 100-fold molar excess of TFPI-160 had no effect on the binding of 125I-TFPI to TSP-1, whereas a 100-fold molar excess of K1K2C decreased binding to 15% (Fig.  6 B), demonstrating that the C-terminal region of TFPI has a critical role in the binding of TFPI to TSP-1.	bind
39384	4	8972	7	NULL	NULL	0	NULL	TFPI	NULL		is critical for	NULL		C-terminal region of		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_41_31715_s_180	10922378	A 100-fold molar excess of TFPI-160 had no effect on the binding of 125I-TFPI to TSP-1, whereas a 100-fold molar excess of K1K2C decreased binding to 15% (Fig.  6 B), demonstrating that the C-terminal region of TFPI has a critical role in the binding of TFPI to TSP-1.	bind
30337	1	8973	6	13	NULL	NULL	NULL	OBP	GP		is					octamer binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_21_7712_s_492	12370317	A 100-kD HeLa cell octamer binding protein (OBP 100) interacts differently with two separate octamer-related sequences within the SV40 enhancer.	bind
30338	2	8973	6	13	NULL	NULL	NULL	OBP 100	GP		interacts		differently			SV40	GP			octamer-related sequences of enhancer	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_21_7712_s_492	12370317	A 100-kD HeLa cell octamer binding protein (OBP 100) interacts differently with two separate octamer-related sequences within the SV40 enhancer.	bind
39385	1	8973	7	10	NULL	0	NULL	OBP 100			interacts with		differently			SV40				octamer-related sequences within enhancer	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_21_7712_s_492	12370317	A 100-kD HeLa cell octamer binding protein (OBP 100) interacts differently with two separate octamer-related sequences within the SV40 enhancer.	bind
39386	2	8973	7	NULL	NULL	0	NULL	OBP 100	NULL		is	NULL				100-kD HeLa cell octamer binding protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_21_7712_s_492	12370317	A 100-kD HeLa cell octamer binding protein (OBP 100) interacts differently with two separate octamer-related sequences within the SV40 enhancer.	bind
30340	1	8978	6	13	NULL	NULL	NULL	Kes1p	GP		defines			205-314		Kes1p	GP	putative	PH domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_1_63_s_106	11916983	A 110 amino acid region of Kes1p (residues 205 - 314) that defines the putative Kes1p PH domain ( Fig. 2 B) also binds IP3 photo-probe (unpublished data).	bind
30341	2	8978	6	13	NULL	NULL	NULL	statement 1	GP		bind					IP3 photo-probe	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_1_63_s_106	11916983	A 110 amino acid region of Kes1p (residues 205 - 314) that defines the putative Kes1p PH domain ( Fig. 2 B) also binds IP3 photo-probe (unpublished data).	bind
39396	1	8978	7	10	NULL	0	NULL	Kes1p			defines			110 amino acid region 205 - 314		Kes1p		putative	 PH domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_157_1_63_s_106	11916983	A 110 amino acid region of Kes1p (residues 205 - 314) that defines the putative Kes1p PH domain ( Fig. 2 B) also binds IP3 photo-probe (unpublished data).	bind
39398	2	8978	7	NULL	NULL	0	NULL	statement 1	NULL		binds	NULL				IP3 photo-probe 	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_157_1_63_s_106	11916983	A 110 amino acid region of Kes1p (residues 205 - 314) that defines the putative Kes1p PH domain ( Fig. 2 B) also binds IP3 photo-probe (unpublished data).	bind
30373	1	8979	6	13	NULL	NULL	NULL	Pce1	GP		is a type of					guanylyltransferase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_8	11893740	A 116-amino acid fragment of the guanylyltransferase Pce1 suffices for binding to the Spt5 C-terminal domain (CTD) but not for binding to the Pol-II CTD. Pct1 and Pce1 can bind simultaneously to the Spt5 CTD  in vitro.	bind
30374	2	8979	6	13	NULL	NULL	NULL	CTD	GP		is					C-terminal domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_8	11893740	A 116-amino acid fragment of the guanylyltransferase Pce1 suffices for binding to the Spt5 C-terminal domain (CTD) but not for binding to the Pol-II CTD. Pct1 and Pce1 can bind simultaneously to the Spt5 CTD  in vitro.	bind
30375	3	8979	6	13	NULL	NULL	NULL	Pct1	GP		bind					Spt5	GP		CTD		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_8	11893740	A 116-amino acid fragment of the guanylyltransferase Pce1 suffices for binding to the Spt5 C-terminal domain (CTD) but not for binding to the Pol-II CTD. Pct1 and Pce1 can bind simultaneously to the Spt5 CTD  in vitro.	bind
30376	4	8979	6	13	NULL	NULL	NULL	Pce1	GP		bind					Spt5	GP		CTD		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_8	11893740	A 116-amino acid fragment of the guanylyltransferase Pce1 suffices for binding to the Spt5 C-terminal domain (CTD) but not for binding to the Pol-II CTD. Pct1 and Pce1 can bind simultaneously to the Spt5 CTD  in vitro.	bind
30377	5	8979	6	13	NULL	NULL	NULL	statement 3	Process		occurs simultaneously with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_8	11893740	A 116-amino acid fragment of the guanylyltransferase Pce1 suffices for binding to the Spt5 C-terminal domain (CTD) but not for binding to the Pol-II CTD. Pct1 and Pce1 can bind simultaneously to the Spt5 CTD  in vitro.	bind
31156	6	8979	6	13	NULL	NULL	NULL	Pce1	GP		bind			116-amino acid fragment		Spt5	GP		CTD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_8	11893740	A 116-amino acid fragment of the guanylyltransferase Pce1 suffices for binding to the Spt5 C-terminal domain (CTD) but not for binding to the Pol-II CTD. Pct1 and Pce1 can bind simultaneously to the Spt5 CTD  in vitro.	bind
31157	7	8979	6	13	NULL	NULL	NULL	Pce1	GP		does not bind			116-amino acid fragment		Pol-II	GP		CTD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_8	11893740	A 116-amino acid fragment of the guanylyltransferase Pce1 suffices for binding to the Spt5 C-terminal domain (CTD) but not for binding to the Pol-II CTD. Pct1 and Pce1 can bind simultaneously to the Spt5 CTD  in vitro.	bind
39411	1	8979	7	10	NULL	0	NULL	Pce1	NULL		bind	NULL		116-amino acid fragment of		Spt5 	NULL		CTD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_8	11893740	A 116-amino acid fragment of the guanylyltransferase Pce1 suffices for binding to the Spt5 C-terminal domain (CTD) but not for binding to the Pol-II CTD. Pct1 and Pce1 can bind simultaneously to the Spt5 CTD  in vitro.	bind
39413	2	8979	7	10	NULL	0	NULL	Pce1	NULL		does not bind	NULL		116-amino acid fragment of		Pol-II 	NULL		CTD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_8	11893740	A 116-amino acid fragment of the guanylyltransferase Pce1 suffices for binding to the Spt5 C-terminal domain (CTD) but not for binding to the Pol-II CTD. Pct1 and Pce1 can bind simultaneously to the Spt5 CTD  in vitro.	bind
39414	3	8979	7	NULL	NULL	0	NULL	Pct1	NULL		bind	NULL				Spt5 	NULL		CTD		NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_8	11893740	A 116-amino acid fragment of the guanylyltransferase Pce1 suffices for binding to the Spt5 C-terminal domain (CTD) but not for binding to the Pol-II CTD. Pct1 and Pce1 can bind simultaneously to the Spt5 CTD  in vitro.	bind
39417	4	8979	7	NULL	NULL	0	NULL	Pce1 	NULL		bind	NULL				Spt5 	NULL		CTD		NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_8	11893740	A 116-amino acid fragment of the guanylyltransferase Pce1 suffices for binding to the Spt5 C-terminal domain (CTD) but not for binding to the Pol-II CTD. Pct1 and Pce1 can bind simultaneously to the Spt5 CTD  in vitro.	bind
39420	5	8979	7	NULL	NULL	0	NULL	statement 3	NULL		occur simultaneously with	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_8	11893740	A 116-amino acid fragment of the guanylyltransferase Pce1 suffices for binding to the Spt5 C-terminal domain (CTD) but not for binding to the Pol-II CTD. Pct1 and Pce1 can bind simultaneously to the Spt5 CTD  in vitro.	bind
39421	6	8979	7	NULL	NULL	0	NULL	CTD	NULL		is	NULL					NULL		C-terminal domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_8	11893740	A 116-amino acid fragment of the guanylyltransferase Pce1 suffices for binding to the Spt5 C-terminal domain (CTD) but not for binding to the Pol-II CTD. Pct1 and Pce1 can bind simultaneously to the Spt5 CTD  in vitro.	bind
47080	7	8979	7	10	NULL	0	NULL	Pce1	NULL		is a type of	NULL				guanylyltransferase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_22_19639_s_8	11893740	A 116-amino acid fragment of the guanylyltransferase Pce1 suffices for binding to the Spt5 C-terminal domain (CTD) but not for binding to the Pol-II CTD. Pct1 and Pce1 can bind simultaneously to the Spt5 CTD  in vitro.	bind
30378	1	8980	6	13	NULL	NULL	NULL	VEGF	GP	radiolabeled	bind					KDR receptor	GP				NULL	HUVEC	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_4_793_s_70	12646239	A 12 amino acid peptide corresponding to residueS 125-136 of the VEGF189 sequence is an effective inhibitor of radiolabelled VEGF binding to KDR and neuropilin-1  receptors in HUVECs and VEGF-dependent angiogenesis in an in vitro assay [ 22].	bind
30379	2	8980	6	13	NULL	NULL	NULL	VEGF	GP	radiolabeled	bind					neuropilin-1 receptor	GP				NULL	HUVEC	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_4_793_s_70	12646239	A 12 amino acid peptide corresponding to residueS 125-136 of the VEGF189 sequence is an effective inhibitor of radiolabelled VEGF binding to KDR and neuropilin-1  receptors in HUVECs and VEGF-dependent angiogenesis in an in vitro assay [ 22].	bind
30380	3	8980	6	13	NULL	NULL	NULL	VEGF189 peptide	GP		inhibits		effectively	residues 125-136		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_4_793_s_70	12646239	A 12 amino acid peptide corresponding to residueS 125-136 of the VEGF189 sequence is an effective inhibitor of radiolabelled VEGF binding to KDR and neuropilin-1  receptors in HUVECs and VEGF-dependent angiogenesis in an in vitro assay [ 22].	bind
30381	4	8980	6	13	NULL	NULL	NULL	VEGF189 peptide	GP		inhibits		effectively	residues 125-136		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_4_793_s_70	12646239	A 12 amino acid peptide corresponding to residueS 125-136 of the VEGF189 sequence is an effective inhibitor of radiolabelled VEGF binding to KDR and neuropilin-1  receptors in HUVECs and VEGF-dependent angiogenesis in an in vitro assay [ 22].	bind
30382	5	8980	6	13	NULL	NULL	NULL	angiogenesis	Process		is dependent on					VEGF	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_4_793_s_70	12646239	A 12 amino acid peptide corresponding to residueS 125-136 of the VEGF189 sequence is an effective inhibitor of radiolabelled VEGF binding to KDR and neuropilin-1  receptors in HUVECs and VEGF-dependent angiogenesis in an in vitro assay [ 22].	bind
30383	6	8980	6	13	NULL	NULL	NULL	VEGF189 peptide	GP		inhibits		effectively	residues 125-136		statement 5	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_4_793_s_70	12646239	A 12 amino acid peptide corresponding to residueS 125-136 of the VEGF189 sequence is an effective inhibitor of radiolabelled VEGF binding to KDR and neuropilin-1  receptors in HUVECs and VEGF-dependent angiogenesis in an in vitro assay [ 22].	bind
39425	1	8980	7	NULL	NULL	0	NULL	VEGF	NULL	radiolabelled 	bind	NULL				KDR	NULL				NULL	HUVECs	0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_4_793_s_70	12646239	A 12 amino acid peptide corresponding to residueS 125-136 of the VEGF189 sequence is an effective inhibitor of radiolabelled VEGF binding to KDR and neuropilin-1  receptors in HUVECs and VEGF-dependent angiogenesis in an in vitro assay [ 22].	bind
39427	2	8980	7	NULL	NULL	0	NULL	VEGF	NULL	radiolabelled	bind	NULL				neuropilin-1 receptors	NULL				NULL	HUVECs	0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_4_793_s_70	12646239	A 12 amino acid peptide corresponding to residueS 125-136 of the VEGF189 sequence is an effective inhibitor of radiolabelled VEGF binding to KDR and neuropilin-1  receptors in HUVECs and VEGF-dependent angiogenesis in an in vitro assay [ 22].	bind
39429	3	8980	7	10	NULL	0	NULL	VEGF189 	NULL		inhibits	NULL	effectively	residues 125-136 		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_4_793_s_70	12646239	A 12 amino acid peptide corresponding to residueS 125-136 of the VEGF189 sequence is an effective inhibitor of radiolabelled VEGF binding to KDR and neuropilin-1  receptors in HUVECs and VEGF-dependent angiogenesis in an in vitro assay [ 22].	bind
39431	4	8980	7	10	NULL	0	NULL	VEGF189	NULL		inhibits	NULL	effectively	residues 125-136 		statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_4_793_s_70	12646239	A 12 amino acid peptide corresponding to residueS 125-136 of the VEGF189 sequence is an effective inhibitor of radiolabelled VEGF binding to KDR and neuropilin-1  receptors in HUVECs and VEGF-dependent angiogenesis in an in vitro assay [ 22].	bind
39433	5	8980	7	NULL	NULL	0	NULL	angiogenesis	NULL		depends on	NULL				VEGF	NULL				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_4_793_s_70	12646239	A 12 amino acid peptide corresponding to residueS 125-136 of the VEGF189 sequence is an effective inhibitor of radiolabelled VEGF binding to KDR and neuropilin-1  receptors in HUVECs and VEGF-dependent angiogenesis in an in vitro assay [ 22].	bind
39435	6	8980	7	10	NULL	0	NULL	VEGF189	NULL		inhibits	NULL	effectively	residues 125-136 		statement 5	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_302_4_793_s_70	12646239	A 12 amino acid peptide corresponding to residueS 125-136 of the VEGF189 sequence is an effective inhibitor of radiolabelled VEGF binding to KDR and neuropilin-1  receptors in HUVECs and VEGF-dependent angiogenesis in an in vitro assay [ 22].	bind
30384	1	8984	6	13	NULL	NULL	NULL	Cbl protooncogene	GP		is a					120 kDa protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_5_3_197_s_123	8808675	A 120 kDa protein that binds to Grb2 has been shown to be the proto-oncogene Cbl (   Donovan et al. 1994  ; Fukazawa et al. 1995  ; Meisner et al. 1995  ).	bind
30385	2	8984	6	13	NULL	NULL	NULL	Cbl protooncogene	GP		bind					Grb2	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_5_3_197_s_123	8808675	A 120 kDa protein that binds to Grb2 has been shown to be the proto-oncogene Cbl (   Donovan et al. 1994  ; Fukazawa et al. 1995  ; Meisner et al. 1995  ).	bind
39437	1	8984	7	NULL	NULL	0	NULL	120 kDa protein	NULL		binds to	NULL				Grb2	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_5_3_197_s_123	8808675	A 120 kDa protein that binds to Grb2 has been shown to be the proto-oncogene Cbl (   Donovan et al. 1994  ; Fukazawa et al. 1995  ; Meisner et al. 1995  ).	bind
39438	2	8984	7	NULL	NULL	0	NULL	120 kDa protein	NULL		is 	NULL				 proto-oncogene Cbl	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_5_3_197_s_123	8808675	A 120 kDa protein that binds to Grb2 has been shown to be the proto-oncogene Cbl (   Donovan et al. 1994  ; Fukazawa et al. 1995  ; Meisner et al. 1995  ).	bind
30386	1	8986	6	13	NULL	NULL	NULL	UV-DDB	GP		is a 					127-kDa protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_30853_s_213	8537337	A 127-kDa Protein (UV-DDB) Binds to the Cytoplasmic Domain of the Alzheimer's Amyloid Precursor Protein.	bind
30387	2	8986	6	13	NULL	NULL	NULL	UV-DDB	GP		bind					Alzheimer's Amyloid Precursor Protein	GP		cytoplasmic domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_30853_s_213	8537337	A 127-kDa Protein (UV-DDB) Binds to the Cytoplasmic Domain of the Alzheimer's Amyloid Precursor Protein.	bind
39439	1	8986	7	10	NULL	0	NULL	UV-DDB	NULL		binds to	NULL				Alzheimer's Amyloid Precursor Protein	NULL		Cytoplasmic Domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_30853_s_213	8537337	A 127-kDa Protein (UV-DDB) Binds to the Cytoplasmic Domain of the Alzheimer's Amyloid Precursor Protein.	bind
47081	2	8986	7	10	NULL	0	NULL	UV-DDB	NULL		is	NULL				127-kDa Protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_30853_s_213	8537337	A 127-kDa Protein (UV-DDB) Binds to the Cytoplasmic Domain of the Alzheimer's Amyloid Precursor Protein.	bind
30388	1	8989	6	13	NULL	NULL	NULL	BAP-135	GP		is					135-kDa Btk-associated protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11526_s_226	9326643	A 135-kDa Btk-associated protein (BAP-135) binds to the Btk PH domain ( 53).	bind
30389	2	8989	6	13	NULL	NULL	NULL	BAP-135	GP		bind					Btk	GP		PH domain		NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_21_11526_s_226	9326643	A 135-kDa Btk-associated protein (BAP-135) binds to the Btk PH domain ( 53).	bind
39441	1	8989	7	NULL	NULL	0	NULL	BAP-135	NULL		binds to	NULL				Btk	NULL		PH domain		NULL		0	NULL	NULL	NULL	gw60_pnas_94_21_11526_s_226	9326643	A 135-kDa Btk-associated protein (BAP-135) binds to the Btk PH domain ( 53).	bind
39442	2	8989	7	NULL	NULL	0	NULL	BAP-135	NULL		is	NULL				135-kDa Btk-associated protein	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_94_21_11526_s_226	9326643	A 135-kDa Btk-associated protein (BAP-135) binds to the Btk PH domain ( 53).	bind
30390	1	8990	6	13	NULL	NULL	NULL				bind			A238L		calcineurin	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_4_1117_s_118	14623298	A 14-amino-acid region containing the core sequence PKIIIT is both necessary and  sufficient for binding of A238L to calcineurin [ 34].	bind
47084	2	8990	6	13	NULL	NULL	NULL	14-amino-acid region	AminoAcid		contains					core sequence PKIIIT	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_4_1117_s_118	14623298	A 14-amino-acid region containing the core sequence PKIIIT is both necessary and  sufficient for binding of A238L to calcineurin [ 34].	bind
47085	3	8990	6	13	NULL	NULL	NULL	statement 2	Process		is necessary for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_4_1117_s_118	14623298	A 14-amino-acid region containing the core sequence PKIIIT is both necessary and  sufficient for binding of A238L to calcineurin [ 34].	bind
47086	4	8990	6	13	NULL	NULL	NULL	statement 2	Process		is sufficient for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_4_1117_s_118	14623298	A 14-amino-acid region containing the core sequence PKIIIT is both necessary and  sufficient for binding of A238L to calcineurin [ 34].	bind
39443	1	8990	7	NULL	NULL	0	NULL		NULL		bind	NULL		A238L		calcineurin	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_4_1117_s_118	14623298	A 14-amino-acid region containing the core sequence PKIIIT is both necessary and  sufficient for binding of A238L to calcineurin [ 34].	bind
39444	2	8990	7	10	NULL	0	NULL	14-amino-acid region	NULL		contains	NULL				core sequence PKIIIT	NULL				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_4_1117_s_118	14623298	A 14-amino-acid region containing the core sequence PKIIIT is both necessary and  sufficient for binding of A238L to calcineurin [ 34].	bind
47082	3	8990	7	10	NULL	0	NULL	statement 2	NULL		is necessary for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_4_1117_s_118	14623298	A 14-amino-acid region containing the core sequence PKIIIT is both necessary and  sufficient for binding of A238L to calcineurin [ 34].	bind
47083	4	8990	7	10	NULL	0	NULL	statement 2	NULL		is sufficient for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_4_1117_s_118	14623298	A 14-amino-acid region containing the core sequence PKIIIT is both necessary and  sufficient for binding of A238L to calcineurin [ 34].	bind
30391	1	8991	6	13	NULL	NULL	NULL	MeCP2	GP		bind					RELN	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_35_12578_s_93	16113080	A 15-day MET treatment increases MeCP2 binding to  RELN and  GAD67 promoters to an extent similar to that measured after a 6-day treatment with MET ( Fig. 3).	bind
30392	2	8991	6	13	NULL	NULL	NULL	MeCP2	GP		bind					GAD67	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_35_12578_s_93	16113080	A 15-day MET treatment increases MeCP2 binding to  RELN and  GAD67 promoters to an extent similar to that measured after a 6-day treatment with MET ( Fig. 3).	bind
30393	3	8991	6	13	NULL	NULL	NULL	MET	AminoAcid	treatment	increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_35_12578_s_93	16113080	A 15-day MET treatment increases MeCP2 binding to  RELN and  GAD67 promoters to an extent similar to that measured after a 6-day treatment with MET ( Fig. 3).	bind
30394	4	8991	6	13	NULL	NULL	NULL	MET	AminoAcid	treatment	increases					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_35_12578_s_93	16113080	A 15-day MET treatment increases MeCP2 binding to  RELN and  GAD67 promoters to an extent similar to that measured after a 6-day treatment with MET ( Fig. 3).	bind
39479	1	8991	7	NULL	NULL	0	NULL	 MeCP2 	NULL		bind	NULL				RELN	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_pnas_102_35_12578_s_93	16113080	A 15-day MET treatment increases MeCP2 binding to  RELN and  GAD67 promoters to an extent similar to that measured after a 6-day treatment with MET ( Fig. 3).	bind
39480	2	8991	7	NULL	NULL	0	NULL	 MeCP2 	NULL		bind	NULL				GAD67	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_pnas_102_35_12578_s_93	16113080	A 15-day MET treatment increases MeCP2 binding to  RELN and  GAD67 promoters to an extent similar to that measured after a 6-day treatment with MET ( Fig. 3).	bind
39481	3	8991	7	10	NULL	0	NULL	MET	NULL	treatment	increase	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_35_12578_s_93	16113080	A 15-day MET treatment increases MeCP2 binding to  RELN and  GAD67 promoters to an extent similar to that measured after a 6-day treatment with MET ( Fig. 3).	bind
39482	4	8991	7	10	NULL	0	NULL	MET	NULL	treatment	increase	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_35_12578_s_93	16113080	A 15-day MET treatment increases MeCP2 binding to  RELN and  GAD67 promoters to an extent similar to that measured after a 6-day treatment with MET ( Fig. 3).	bind
30395	1	8992	6	13	NULL	NULL	NULL	hnRNP	GP		bind				E1 region	alpha-globin RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_49680_s_249	15364910	A 15-lipoxygenase differentiation control element sequence also serves as the minimal binding element for binding of hnRNPs E1 and E2 to alpha-globin RNA ( ).	bind
30396	2	8992	6	13	NULL	NULL	NULL	hnRNP 	GP		bind				E2 region	alpha-globin RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_49680_s_249	15364910	A 15-lipoxygenase differentiation control element sequence also serves as the minimal binding element for binding of hnRNPs E1 and E2 to alpha-globin RNA ( ).	bind
31158	3	8992	6	13	NULL	NULL	NULL	15-lipoxygenase	GP	sequence of	serves as				differentiation control element					minimal binding element	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_49680_s_249	15364910	A 15-lipoxygenase differentiation control element sequence also serves as the minimal binding element for binding of hnRNPs E1 and E2 to alpha-globin RNA ( ).	bind
31159	4	8992	6	13	NULL	NULL	NULL	statement 3	GP		occurs for					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_49680_s_249	15364910	A 15-lipoxygenase differentiation control element sequence also serves as the minimal binding element for binding of hnRNPs E1 and E2 to alpha-globin RNA ( ).	bind
31160	5	8992	6	13	NULL	NULL	NULL	statement 3	GP		occurs for					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_49680_s_249	15364910	A 15-lipoxygenase differentiation control element sequence also serves as the minimal binding element for binding of hnRNPs E1 and E2 to alpha-globin RNA ( ).	bind
39483	1	8992	7	NULL	NULL	0	NULL	hnRNPs E1	NULL		bind	NULL				alpha-globin RNA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_49680_s_249	15364910	A 15-lipoxygenase differentiation control element sequence also serves as the minimal binding element for binding of hnRNPs E1 and E2 to alpha-globin RNA ( ).	bind
39484	2	8992	7	NULL	NULL	0	NULL	hnRNPs E2	NULL		bind	NULL				alpha-globin RNA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_49680_s_249	15364910	A 15-lipoxygenase differentiation control element sequence also serves as the minimal binding element for binding of hnRNPs E1 and E2 to alpha-globin RNA ( ).	bind
39485	3	8992	7	NULL	NULL	0	NULL	15-lipoxygenase	NULL		serve as	NULL			differentiation control element sequence	minimal binding element	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_49680_s_249	15364910	A 15-lipoxygenase differentiation control element sequence also serves as the minimal binding element for binding of hnRNPs E1 and E2 to alpha-globin RNA ( ).	bind
39486	4	8992	7	NULL	NULL	0	NULL	statement 3	NULL		is required for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_49680_s_249	15364910	A 15-lipoxygenase differentiation control element sequence also serves as the minimal binding element for binding of hnRNPs E1 and E2 to alpha-globin RNA ( ).	bind
39487	5	8992	7	NULL	NULL	0	NULL	statement 3	NULL		is required for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_49680_s_249	15364910	A 15-lipoxygenase differentiation control element sequence also serves as the minimal binding element for binding of hnRNPs E1 and E2 to alpha-globin RNA ( ).	bind
40393	1	8995	6	13	NULL	NULL	NULL	Arg1	GP		contains				promoter					STAT6 binding site	NULL		NULL	NULL	NULL	NULL	gw70_gene_353_1_98_s_29	15922518	A 150-bp region containing  the STAT6 and CEBP binding site was created by PCR amplification of the  2850 to   2999 region of the Arg1 promoter and cloned into the  HindIII/ XhoI sites just upstream of the 81-bp thymidine kinase promoter in the pT81-luc reporter  plasmid (  Nordeen, 1988) to create IL4RE-pT81-luc.	bind
40394	2	8995	6	13	NULL	NULL	NULL	Arg1	GP		contains				promoter					CEBP binding site	NULL		NULL	NULL	NULL	NULL	gw70_gene_353_1_98_s_29	15922518	A 150-bp region containing  the STAT6 and CEBP binding site was created by PCR amplification of the  2850 to   2999 region of the Arg1 promoter and cloned into the  HindIII/ XhoI sites just upstream of the 81-bp thymidine kinase promoter in the pT81-luc reporter  plasmid (  Nordeen, 1988) to create IL4RE-pT81-luc.	bind
40401	1	8995	7	10	NULL	0	NULL	Arg1	NULL		contains	NULL			 promoter		NULL			STAT6 binding site	NULL		NULL	NULL	NULL	NULL	gw70_gene_353_1_98_s_29	15922518	A 150-bp region containing  the STAT6 and CEBP binding site was created by PCR amplification of the  2850 to   2999 region of the Arg1 promoter and cloned into the  HindIII/ XhoI sites just upstream of the 81-bp thymidine kinase promoter in the pT81-luc reporter  plasmid (  Nordeen, 1988) to create IL4RE-pT81-luc.	bind
40402	2	8995	7	10	NULL	0	NULL	Arg1	NULL		contains	NULL			promoter		NULL			CEBP binding site	NULL		NULL	NULL	NULL	NULL	gw70_gene_353_1_98_s_29	15922518	A 150-bp region containing  the STAT6 and CEBP binding site was created by PCR amplification of the  2850 to   2999 region of the Arg1 promoter and cloned into the  HindIII/ XhoI sites just upstream of the 81-bp thymidine kinase promoter in the pT81-luc reporter  plasmid (  Nordeen, 1988) to create IL4RE-pT81-luc.	bind
30398	1	8996	6	13	NULL	NULL	NULL	adhesin	GP	Porphyromonas (Bacteroides) gingivalis	bind					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_9_5218_s_226	10948147	A 150-kDa fibrinogen binding adhesin of  Porphyromonas (Bacteroides) gingivalis also recognized fibronectin ( 9,  10).	bind
30399	2	8996	6	13	NULL	NULL	NULL	adhesin	GP	Porphyromonas (Bacteroides) gingivalis	is					150-kDa protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_9_5218_s_226	10948147	A 150-kDa fibrinogen binding adhesin of  Porphyromonas (Bacteroides) gingivalis also recognized fibronectin ( 9,  10).	bind
30400	3	8996	6	13	NULL	NULL	NULL	adhesion	GP	Porphyromonas (Bacteroides) gingivalis	recognize					fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_9_5218_s_226	10948147	A 150-kDa fibrinogen binding adhesin of  Porphyromonas (Bacteroides) gingivalis also recognized fibronectin ( 9,  10).	bind
39488	1	8996	7	10	NULL	0	NULL	adhesin	NULL	Porphyromonas  gingivalis 	recognize	NULL		 		fibronectin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_9_5218_s_226	10948147	A 150-kDa fibrinogen binding adhesin of  Porphyromonas (Bacteroides) gingivalis also recognized fibronectin ( 9,  10).	bind
39489	2	8996	7	NULL	NULL	0	NULL	Porphyromonas gingivalis 	NULL		is a type of	NULL				Bacteroides	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_9_5218_s_226	10948147	A 150-kDa fibrinogen binding adhesin of  Porphyromonas (Bacteroides) gingivalis also recognized fibronectin ( 9,  10).	bind
47091	3	8996	7	10	NULL	0	NULL	adhesin	NULL	Porphyromonas gingivalis 	bind	NULL				fibrinogen	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_9_5218_s_226	10948147	A 150-kDa fibrinogen binding adhesin of  Porphyromonas (Bacteroides) gingivalis also recognized fibronectin ( 9,  10).	bind
47092	4	8996	7	10	NULL	0	NULL	adhesin	NULL	\tPorphyromonas gingivalis 	is	NULL				150-kDa protein	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_9_5218_s_226	10948147	A 150-kDa fibrinogen binding adhesin of  Porphyromonas (Bacteroides) gingivalis also recognized fibronectin ( 9,  10).	bind
30401	1	8997	6	13	NULL	NULL	NULL	150-kDa surface component	GP	P. gingivalis	bind					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_50_0_513_s_346	8905090	A 150-kDa surface component of  P. gingivalis binds to  fibrinogen ( 131).	bind
39490	1	8997	7	10	NULL	0	NULL	150-kDa surface component 	NULL	P. gingivalis	binds to	NULL				fibrinogen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_50_0_513_s_346	8905090	A 150-kDa surface component of  P. gingivalis binds to  fibrinogen ( 131).	bind
30402	1	8998	6	13	NULL	NULL	NULL	155-kDa protein	GP		is a subunit of		largest			pol III	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_14_7795_s_90	11416169	A 155-kDa protein, which was identified subsequently as the largest subunit of pol III by immunoblot analysis using RPC155-specific antibodies (lane 3), binds plakophilin 2 selectively.	bind
30403	2	8998	6	13	NULL	NULL	NULL	statement 1	GP		bind		selectively			plakophilin 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_14_7795_s_90	11416169	A 155-kDa protein, which was identified subsequently as the largest subunit of pol III by immunoblot analysis using RPC155-specific antibodies (lane 3), binds plakophilin 2 selectively.	bind
39491	1	8998	7	NULL	NULL	0	NULL	pol III	NULL		binds	NULL	selectively	155-kDa protein subunit		plakophilin 2 	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_98_14_7795_s_90	11416169	A 155-kDa protein, which was identified subsequently as the largest subunit of pol III by immunoblot analysis using RPC155-specific antibodies (lane 3), binds plakophilin 2 selectively.	bind
30404	1	8999	6	13	NULL	NULL	NULL	16-mer peptide	GP		represents					BAD	GP	bona fide	BH3 domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_25_17321_s_400	16603546	A 16-mer peptide representing the  bona fide BH3 domain of BAD bound Bcl-XL only poorly.	bind
30405	2	8999	6	13	NULL	NULL	NULL	BAD	GP		bind		poorly	BH3 domain		BCL-XL	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_25_17321_s_400	16603546	A 16-mer peptide representing the  bona fide BH3 domain of BAD bound Bcl-XL only poorly.	bind
39492	1	8999	7	10	NULL	0	NULL	BAD	NULL		binds	NULL	poorly	BH3 domain 		Bcl-XL	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_25_17321_s_400	16603546	A 16-mer peptide representing the  bona fide BH3 domain of BAD bound Bcl-XL only poorly.	bind
47090	2	8999	7	10	NULL	0	NULL	16-mer peptide	NULL		represents	NULL				BAD	NULL	bona fide	BH3 domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_17321_s_400	16603546	A 16-mer peptide representing the  bona fide BH3 domain of BAD bound Bcl-XL only poorly.	bind
38584	1	9001	5	11	NULL	NULL	NULL	160-kDa protein	GP		bind					Shc	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_23097_s_202	11312266	A 160-kDa protein that co-immunoprecipitated with Shc also showed increased tyrosine phosphorylation in response to p75NTR overexpression; this protein is likely SHIP, a 160-kDa lipid phosphatase that binds activated Shc with high affinity ( 53).	bind
38585	3	9001	5	11	NULL	NULL	NULL	p75NTR	GP	overexpression of	increase					SHIP	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_23097_s_202	11312266	A 160-kDa protein that co-immunoprecipitated with Shc also showed increased tyrosine phosphorylation in response to p75NTR overexpression; this protein is likely SHIP, a 160-kDa lipid phosphatase that binds activated Shc with high affinity ( 53).	bind
38711	4	9001	5	11	NULL	NULL	NULL	SHIP	GP		bind		high affinity			Shc	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_23097_s_202	11312266	A 160-kDa protein that co-immunoprecipitated with Shc also showed increased tyrosine phosphorylation in response to p75NTR overexpression; this protein is likely SHIP, a 160-kDa lipid phosphatase that binds activated Shc with high affinity ( 53).	bind
39020	2	9001	5	11	NULL	NULL	NULL	160-kDa protein	GP		is					SHIP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_23097_s_202	11312266	A 160-kDa protein that co-immunoprecipitated with Shc also showed increased tyrosine phosphorylation in response to p75NTR overexpression; this protein is likely SHIP, a 160-kDa lipid phosphatase that binds activated Shc with high affinity ( 53).	bind
39021	5	9001	5	11	NULL	NULL	NULL	SHIP	GP		is a type of					lipid phosphatase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_23097_s_202	11312266	A 160-kDa protein that co-immunoprecipitated with Shc also showed increased tyrosine phosphorylation in response to p75NTR overexpression; this protein is likely SHIP, a 160-kDa lipid phosphatase that binds activated Shc with high affinity ( 53).	bind
31161	1	9001	6	11	NULL	NULL	NULL	160-kDa protein	GP		bind					Shc	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_23097_s_202	11312266	A 160-kDa protein that co-immunoprecipitated with Shc also showed increased tyrosine phosphorylation in response to p75NTR overexpression; this protein is likely SHIP, a 160-kDa lipid phosphatase that binds activated Shc with high affinity ( 53).	bind
31162	2	9001	6	11	NULL	NULL	NULL	160-kDa protein	GP		is phosphorylated on								tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_23097_s_202	11312266	A 160-kDa protein that co-immunoprecipitated with Shc also showed increased tyrosine phosphorylation in response to p75NTR overexpression; this protein is likely SHIP, a 160-kDa lipid phosphatase that binds activated Shc with high affinity ( 53).	bind
31163	3	9001	6	11	NULL	NULL	NULL	statement 2	Process		occurs in response to					p75NTR	GP	overexpression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_23097_s_202	11312266	A 160-kDa protein that co-immunoprecipitated with Shc also showed increased tyrosine phosphorylation in response to p75NTR overexpression; this protein is likely SHIP, a 160-kDa lipid phosphatase that binds activated Shc with high affinity ( 53).	bind
31164	4	9001	6	11	NULL	NULL	NULL	160-kDa protein	GP		is 		probably			SHIP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_23097_s_202	11312266	A 160-kDa protein that co-immunoprecipitated with Shc also showed increased tyrosine phosphorylation in response to p75NTR overexpression; this protein is likely SHIP, a 160-kDa lipid phosphatase that binds activated Shc with high affinity ( 53).	bind
31165	5	9001	6	11	NULL	NULL	NULL	SHIP	GP		is a type of					lipid phosphatase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_23097_s_202	11312266	A 160-kDa protein that co-immunoprecipitated with Shc also showed increased tyrosine phosphorylation in response to p75NTR overexpression; this protein is likely SHIP, a 160-kDa lipid phosphatase that binds activated Shc with high affinity ( 53).	bind
31166	6	9001	6	11	NULL	NULL	NULL	SHIP	GP		bind		high affinity			Shc	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_23097_s_202	11312266	A 160-kDa protein that co-immunoprecipitated with Shc also showed increased tyrosine phosphorylation in response to p75NTR overexpression; this protein is likely SHIP, a 160-kDa lipid phosphatase that binds activated Shc with high affinity ( 53).	bind
49154	1	9002	5	11	NULL	NULL	NULL	p HP0294 probe	NucleicAcid		does not bind					HP0166-His6 protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_5_1750_s_125	16484186	A 161-bp probe for p HP0294 ( amiE) that did not bind to HP0166-His6 protein under the same experimental condition is shown in Fig.  2B to serve as a negative (nonspecific) control.	bind
30406	1	9002	6	11	NULL	NULL	NULL	p HP0294 probe	NucleicAcid		does not bind					HP0166-His6 protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_5_1750_s_125	16484186	A 161-bp probe for p HP0294 ( amiE) that did not bind to HP0166-His6 protein under the same experimental condition is shown in Fig.  2B to serve as a negative (nonspecific) control.	bind
38591	2	9005	5	11	NULL	NULL	NULL	statement1	AminoAcid		does not bind					RNAs	NucleicAcid	capped			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30551_s_122	10887196	A 17-amino acid peptide comprising the minimal eIF4E binding motif of eIF4G failed to produce any shift with capped RNAs.	bind
47907	1	9005	5	11	NULL	NULL	NULL	17-amino acid peptide 	AminoAcid		comprise					eIF4G	GP		minimal eIF4E binding motif   		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30551_s_122	10887196	A 17-amino acid peptide comprising the minimal eIF4E binding motif of eIF4G failed to produce any shift with capped RNAs.	bind
31167	2	9005	6	11	NULL	NULL	NULL	statement 1	AminoAcid		does not bind					 RNA	NucleicAcid	capped			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30551_s_122	10887196	A 17-amino acid peptide comprising the minimal eIF4E binding motif of eIF4G failed to produce any shift with capped RNAs.	bind
47908	1	9005	6	11	NULL	NULL	NULL	17-amino acid peptide 	AminoAcid		comprise					eIF4G	GP		minimal eIF4E binding motif 		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30551_s_122	10887196	A 17-amino acid peptide comprising the minimal eIF4E binding motif of eIF4G failed to produce any shift with capped RNAs.	bind
38592	1	9006	5	11	NULL	NULL	NULL	170-kD APN	GP		bind		high affinity			Cry1A toxins	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_857_s_43	11486086	A 170-kD APN (Receptor A) binds Cry1A toxins with high affinity and mediates Bt toxin-induced pore formation when reconstituted into phospholipid vesicles in vitro ( 7).	bind
38593	2	9006	5	11	NULL	NULL	NULL	Bt toxin	Chemical		induce					pore	CellComponent	formation of			NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_857_s_43	11486086	A 170-kD APN (Receptor A) binds Cry1A toxins with high affinity and mediates Bt toxin-induced pore formation when reconstituted into phospholipid vesicles in vitro ( 7).	bind
38594	3	9006	5	11	NULL	NULL	NULL	statement 1	Process		mediate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_857_s_43	11486086	A 170-kD APN (Receptor A) binds Cry1A toxins with high affinity and mediates Bt toxin-induced pore formation when reconstituted into phospholipid vesicles in vitro ( 7).	bind
38595	4	9006	5	11	NULL	NULL	NULL	170-kD APN	GP		is reconstituted into					phospholipid vesicles	CellComponent				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_science_293_5531_857_s_43	11486086	A 170-kD APN (Receptor A) binds Cry1A toxins with high affinity and mediates Bt toxin-induced pore formation when reconstituted into phospholipid vesicles in vitro ( 7).	bind
38596	5	9006	5	11	NULL	NULL	NULL	statement 4	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_857_s_43	11486086	A 170-kD APN (Receptor A) binds Cry1A toxins with high affinity and mediates Bt toxin-induced pore formation when reconstituted into phospholipid vesicles in vitro ( 7).	bind
57752	6	9006	5	11	NULL	NULL	NULL	APN	GP		is a type of					Receptor A	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_857_s_43	11486086	A 170-kD APN (Receptor A) binds Cry1A toxins with high affinity and mediates Bt toxin-induced pore formation when reconstituted into phospholipid vesicles in vitro ( 7).	bind
30407	1	9006	6	11	NULL	NULL	NULL	170-kD APN	GP		bind		high affinity			Cry1A toxins	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_857_s_43	11486086	A 170-kD APN (Receptor A) binds Cry1A toxins with high affinity and mediates Bt toxin-induced pore formation when reconstituted into phospholipid vesicles in vitro ( 7).	bind
30408	2	9006	6	11	NULL	NULL	NULL	Bt toxin	Chemical		induces					pore	CellComponent	formation of 			NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_857_s_43	11486086	A 170-kD APN (Receptor A) binds Cry1A toxins with high affinity and mediates Bt toxin-induced pore formation when reconstituted into phospholipid vesicles in vitro ( 7).	bind
30409	3	9006	6	11	NULL	NULL	NULL	APN	GP		is a type of					receptor A	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_857_s_43	11486086	A 170-kD APN (Receptor A) binds Cry1A toxins with high affinity and mediates Bt toxin-induced pore formation when reconstituted into phospholipid vesicles in vitro ( 7).	bind
30410	4	9006	6	11	NULL	NULL	NULL	statement 1	Process		mediates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_857_s_43	11486086	A 170-kD APN (Receptor A) binds Cry1A toxins with high affinity and mediates Bt toxin-induced pore formation when reconstituted into phospholipid vesicles in vitro ( 7).	bind
30411	5	9006	6	11	NULL	NULL	NULL	170-kD APN	GP		is reconstituted into					phospholipid vesicles	CellComponent				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_science_293_5531_857_s_43	11486086	A 170-kD APN (Receptor A) binds Cry1A toxins with high affinity and mediates Bt toxin-induced pore formation when reconstituted into phospholipid vesicles in vitro ( 7).	bind
30412	6	9006	6	11	NULL	NULL	NULL	statement 4	Process		occurs via					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5531_857_s_43	11486086	A 170-kD APN (Receptor A) binds Cry1A toxins with high affinity and mediates Bt toxin-induced pore formation when reconstituted into phospholipid vesicles in vitro ( 7).	bind
38769	1	9009	5	11	NULL	NULL	NULL	SARS coronavirus S protein 	GP		bind		efficiently	193-amino acid fragment		angiotensin-converting enzyme 2	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-biol-chem_279_5_14670965_s_1	14670965	A 193-amino acid fragment of the SARS coronavirus S protein efficiently binds angiotensin-converting enzyme 2..	bind
30413	1	9009	6	11	NULL	NULL	NULL	SARS coronavirus S protein	GP		bind		efficiently	193-amino acid fragment		angiotensin-converting enzyme 2	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-biol-chem_279_5_14670965_s_1	14670965	A 193-amino acid fragment of the SARS coronavirus S protein efficiently binds angiotensin-converting enzyme 2..	bind
38770	1	9011	5	11	NULL	NULL	NULL	fimbrin	GP		interact with					vimentin subunit	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_146_4_831_s_11	10459017	A 1:4 stoichiometry of fimbrin binding to vimentin and a low percentage (1%) of the extracted vimentin suggest that fimbrin interacts with a vimentin subunit.	bind
38771	2	9011	5	11	NULL	NULL	NULL	fimbrin	GP		bind					vimentin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_146_4_831_s_11	10459017	A 1:4 stoichiometry of fimbrin binding to vimentin and a low percentage (1%) of the extracted vimentin suggest that fimbrin interacts with a vimentin subunit.	bind
31168	1	9011	6	11	NULL	NULL	NULL	fimbrin	GP		interacts with					vimentin subunit	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_146_4_831_s_11	10459017	A 1:4 stoichiometry of fimbrin binding to vimentin and a low percentage (1%) of the extracted vimentin suggest that fimbrin interacts with a vimentin subunit.	bind
47909	2	9011	6	11	NULL	NULL	NULL	fimbrin	GP		bind					vimentin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_146_4_831_s_11	10459017	A 1:4 stoichiometry of fimbrin binding to vimentin and a low percentage (1%) of the extracted vimentin suggest that fimbrin interacts with a vimentin subunit.	bind
38772	1	9012	5	11	NULL	NULL	NULL	RNA aptamer	NucleicAcid		bind					hnps-PLA2	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_56_0_555_s_231	15660527	A 2''-fluoropyrimidine-modified RNA selection against hnps-PLA2 ( 65) isolated an RNA aptamer that binds to hnps-PLA2 with a Kd of 1.7 nM and inhibits hnps-PLA2 activity with an IC50 of 4 nM.	bind
38774	2	9012	5	11	NULL	NULL	NULL	statement 1	GP		inhibit					hnps-PLA2	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_56_0_555_s_231	15660527	A 2''-fluoropyrimidine-modified RNA selection against hnps-PLA2 ( 65) isolated an RNA aptamer that binds to hnps-PLA2 with a Kd of 1.7 nM and inhibits hnps-PLA2 activity with an IC50 of 4 nM.	bind
30445	1	9012	6	11	NULL	NULL	NULL	RNA aptamer 	NucleicAcid		bind					hnps-PLA2	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_56_0_555_s_231	15660527	A 2''-fluoropyrimidine-modified RNA selection against hnps-PLA2 ( 65) isolated an RNA aptamer that binds to hnps-PLA2 with a Kd of 1.7 nM and inhibits hnps-PLA2 activity with an IC50 of 4 nM.	bind
30446	2	9012	6	11	NULL	NULL	NULL	RNA aptamer	NucleicAcid		inhibits					hnps-PLA2	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_56_0_555_s_231	15660527	A 2''-fluoropyrimidine-modified RNA selection against hnps-PLA2 ( 65) isolated an RNA aptamer that binds to hnps-PLA2 with a Kd of 1.7 nM and inhibits hnps-PLA2 activity with an IC50 of 4 nM.	bind
38777	1	9013	5	11	NULL	NULL	NULL	DRIP205	GP		bind					VDR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2718_s_142	10733574	A 2- to 20-fold molar excess of NR2 peptide over DRIP205 was able to efficiently compete DRIP205 binding to VDR, but the same ratio of NR1 peptide or an unrelated nonspecific peptide was unable to compete for this interaction (Fig.  4B, compare lanes 5 to 7 to lanes 2 to 4 or 8 to 10).	bind
38779	2	9013	5	11	NULL	NULL	NULL	NR2 peptide	GP		bind					VDR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2718_s_142	10733574	A 2- to 20-fold molar excess of NR2 peptide over DRIP205 was able to efficiently compete DRIP205 binding to VDR, but the same ratio of NR1 peptide or an unrelated nonspecific peptide was unable to compete for this interaction (Fig.  4B, compare lanes 5 to 7 to lanes 2 to 4 or 8 to 10).	bind
38780	3	9013	5	11	NULL	NULL	NULL	statement 2	Process		competes with		efficiently			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2718_s_142	10733574	A 2- to 20-fold molar excess of NR2 peptide over DRIP205 was able to efficiently compete DRIP205 binding to VDR, but the same ratio of NR1 peptide or an unrelated nonspecific peptide was unable to compete for this interaction (Fig.  4B, compare lanes 5 to 7 to lanes 2 to 4 or 8 to 10).	bind
38781	4	9013	5	11	NULL	NULL	NULL	NR1 peptide	GP		does not compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2718_s_142	10733574	A 2- to 20-fold molar excess of NR2 peptide over DRIP205 was able to efficiently compete DRIP205 binding to VDR, but the same ratio of NR1 peptide or an unrelated nonspecific peptide was unable to compete for this interaction (Fig.  4B, compare lanes 5 to 7 to lanes 2 to 4 or 8 to 10).	bind
30448	1	9013	6	11	NULL	NULL	NULL	DRIP205	GP		bind					VDR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2718_s_142	10733574	A 2- to 20-fold molar excess of NR2 peptide over DRIP205 was able to efficiently compete DRIP205 binding to VDR, but the same ratio of NR1 peptide or an unrelated nonspecific peptide was unable to compete for this interaction (Fig.  4B, compare lanes 5 to 7 to lanes 2 to 4 or 8 to 10).	bind
30449	2	9013	6	11	NULL	NULL	NULL	NR2 peptide	GP	excess of	bind					VDR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2718_s_142	10733574	A 2- to 20-fold molar excess of NR2 peptide over DRIP205 was able to efficiently compete DRIP205 binding to VDR, but the same ratio of NR1 peptide or an unrelated nonspecific peptide was unable to compete for this interaction (Fig.  4B, compare lanes 5 to 7 to lanes 2 to 4 or 8 to 10).	bind
30450	3	9013	6	11	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2718_s_142	10733574	A 2- to 20-fold molar excess of NR2 peptide over DRIP205 was able to efficiently compete DRIP205 binding to VDR, but the same ratio of NR1 peptide or an unrelated nonspecific peptide was unable to compete for this interaction (Fig.  4B, compare lanes 5 to 7 to lanes 2 to 4 or 8 to 10).	bind
30451	4	9013	6	11	NULL	NULL	NULL	NR1 peptide	GP	excess of	does not bind					VDR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2718_s_142	10733574	A 2- to 20-fold molar excess of NR2 peptide over DRIP205 was able to efficiently compete DRIP205 binding to VDR, but the same ratio of NR1 peptide or an unrelated nonspecific peptide was unable to compete for this interaction (Fig.  4B, compare lanes 5 to 7 to lanes 2 to 4 or 8 to 10).	bind
38785	1	9014	5	11	NULL	NULL	NULL	alpha-Gal-(1,3)-beta-Gal-(1,4)-beta-GlcNAcO(CH(2))(8)CO(2)CH(3)	Chemical	extended conformation	bind					TcdA	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_nat-struct-mol-biol_13_5_16622409_s_3	16622409	A 2-A resolution cocrystal structure reveals  two molecules of alpha-Gal-(1,3)-beta-Gal-(1,4)-beta-GlcNAcO(CH(2))(8)CO(2)CH(3)  binding in an extended conformation to TcdA.	bind
30452	1	9014	6	11	NULL	NULL	NULL	alpha-Gal-(1,3)-beta-Gal-(1,4)-beta-GlcNAcO(CH(2))(8)CO(2)CH(3)	Chemical	extended conformation of	bind					TcdA	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_nat-struct-mol-biol_13_5_16622409_s_3	16622409	A 2-A resolution cocrystal structure reveals  two molecules of alpha-Gal-(1,3)-beta-Gal-(1,4)-beta-GlcNAcO(CH(2))(8)CO(2)CH(3)  binding in an extended conformation to TcdA.	bind
38787	1	9015	5	11	NULL	NULL	NULL	BF-1	GP		bind					double-stranded DNA	NucleicAcid			high-affinity site	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6201_s_310	10938097	A 2-amino-acid mutation (NH-AA) within the third alpha-helix of the WH domain abolishes the ability of BF-1 to bind to a high-affinity site on double-stranded DNA.	bind
38789	2	9015	5	11	NULL	NULL	NULL	BF-1	GP	mutant	abolishes			(NH-AA) within the third alpha-helix of WH domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6201_s_310	10938097	A 2-amino-acid mutation (NH-AA) within the third alpha-helix of the WH domain abolishes the ability of BF-1 to bind to a high-affinity site on double-stranded DNA.	bind
38790	3	9015	5	11	NULL	NULL	NULL	NH-AA	Chemical		is					2-amino-acid mutation	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6201_s_310	10938097	A 2-amino-acid mutation (NH-AA) within the third alpha-helix of the WH domain abolishes the ability of BF-1 to bind to a high-affinity site on double-stranded DNA.	bind
30453	1	9015	6	11	NULL	NULL	NULL	BF-1	GP		bind					double-stranded DNA	NucleicAcid			high-affinity site	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6201_s_310	10938097	A 2-amino-acid mutation (NH-AA) within the third alpha-helix of the WH domain abolishes the ability of BF-1 to bind to a high-affinity site on double-stranded DNA.	bind
30454	2	9015	6	11	NULL	NULL	NULL	BF-1	GP	mutant	abolishes			NH-AA within third alpha-helix of the WH domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6201_s_310	10938097	A 2-amino-acid mutation (NH-AA) within the third alpha-helix of the WH domain abolishes the ability of BF-1 to bind to a high-affinity site on double-stranded DNA.	bind
47910	3	9015	6	11	NULL	NULL	NULL	NH-AA	Chemical		is					2-amino-acid mutation 	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6201_s_310	10938097	A 2-amino-acid mutation (NH-AA) within the third alpha-helix of the WH domain abolishes the ability of BF-1 to bind to a high-affinity site on double-stranded DNA.	bind
38791	1	9016	5	13	NULL	NULL	NULL	CRP	GP	induced	bind					RBC(Mal)	Cell				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_glycoconj-j_23_3-4_16691506_s_8	16691506	A 2.3-fold increased binding of induced CRP to RBC(Mal) as  compared to normal erythrocytes (RBC(N)) confirmed disease-specificity.	bind
38795	3	9016	5	13	NULL	NULL	NULL	statement 1	Process	increased	confirms					disease-specificity	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_glycoconj-j_23_3-4_16691506_s_8	16691506	A 2.3-fold increased binding of induced CRP to RBC(Mal) as  compared to normal erythrocytes (RBC(N)) confirmed disease-specificity.	bind
47911	2	9016	5	13	NULL	NULL	NULL	CRP	GP	induced	bind					erythrocytes 	Cell	normal			NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_glycoconj-j_23_3-4_16691506_s_8	16691506	A 2.3-fold increased binding of induced CRP to RBC(Mal) as  compared to normal erythrocytes (RBC(N)) confirmed disease-specificity.	bind
47912	4	9016	5	13	NULL	NULL	NULL	RBC(N)	Cell		is					normal erythrocytes	Cell				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_glycoconj-j_23_3-4_16691506_s_8	16691506	A 2.3-fold increased binding of induced CRP to RBC(Mal) as  compared to normal erythrocytes (RBC(N)) confirmed disease-specificity.	bind
30455	1	9016	6	NULL	NULL	0	NULL	CRP	NULL	induced	bind	NULL				RBC(Mal)	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_glycoconj-j_23_3-4_16691506_s_8	16691506	A 2.3-fold increased binding of induced CRP to RBC(Mal) as  compared to normal erythrocytes (RBC(N)) confirmed disease-specificity.	bind
30456	2	9016	6	NULL	NULL	0	NULL	CRP	NULL	induced	bind	NULL				erythrocytes	NULL	normal			NULL		0	NULL	NULL	NULL	abs-batch0680-0699_glycoconj-j_23_3-4_16691506_s_8	16691506	A 2.3-fold increased binding of induced CRP to RBC(Mal) as  compared to normal erythrocytes (RBC(N)) confirmed disease-specificity.	bind
30457	3	9016	6	NULL	NULL	0	NULL	RBC(N)	NULL		is	NULL				normal erythrocytes	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_glycoconj-j_23_3-4_16691506_s_8	16691506	A 2.3-fold increased binding of induced CRP to RBC(Mal) as  compared to normal erythrocytes (RBC(N)) confirmed disease-specificity.	bind
47913	4	9016	6	10	NULL	0	NULL	statement 1	NULL	increased	confirms	NULL				disease-specificity	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_glycoconj-j_23_3-4_16691506_s_8	16691506	A 2.3-fold increased binding of induced CRP to RBC(Mal) as  compared to normal erythrocytes (RBC(N)) confirmed disease-specificity.	bind
38800	2	9017	5	13	NULL	NULL	NULL	HMG-1	GP		complex with			box A		statement 1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_33	10825199	A 2.5- Ang  crystal structure of the HMG-1 box A complexed to cisplatin-modified DNA reveals that DNA binding by HMG-1 shares many features with that of LEF-1 ( 40).	bind
47914	1	9017	5	13	NULL	NULL	NULL	cisplatin	Chemical		modifies					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_33	10825199	A 2.5- Ang  crystal structure of the HMG-1 box A complexed to cisplatin-modified DNA reveals that DNA binding by HMG-1 shares many features with that of LEF-1 ( 40).	bind
47915	3	9017	5	13	NULL	NULL	NULL	statement 1	Process		shares features with					LEF-1	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_33	10825199	A 2.5- Ang  crystal structure of the HMG-1 box A complexed to cisplatin-modified DNA reveals that DNA binding by HMG-1 shares many features with that of LEF-1 ( 40).	bind
30559	2	9017	6	10	NULL	0	NULL	HMG-1	NULL		complex with	NULL		box A		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_33	10825199	A 2.5- Ang  crystal structure of the HMG-1 box A complexed to cisplatin-modified DNA reveals that DNA binding by HMG-1 shares many features with that of LEF-1 ( 40).	bind
30563	3	9017	6	10	NULL	0	NULL	statement 1	NULL		shares features with	NULL				LEF-1	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_33	10825199	A 2.5- Ang  crystal structure of the HMG-1 box A complexed to cisplatin-modified DNA reveals that DNA binding by HMG-1 shares many features with that of LEF-1 ( 40).	bind
47916	1	9017	6	10	NULL	0	NULL	cisplatin	NULL		modifies	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_12_4359_s_33	10825199	A 2.5- Ang  crystal structure of the HMG-1 box A complexed to cisplatin-modified DNA reveals that DNA binding by HMG-1 shares many features with that of LEF-1 ( 40).	bind
38815	1	9018	5	13	NULL	NULL	NULL	importin beta	GP		bind					AhR complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_4_2677_s_210	12431985	A 2.5-fold increase in binding of importin beta to the AhR complex was detected relative to background binding.	bind
30566	1	9018	6	NULL	NULL	0	NULL	importin beta	NULL		bind	NULL				AhR complex	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_4_2677_s_210	12431985	A 2.5-fold increase in binding of importin beta to the AhR complex was detected relative to background binding.	bind
38812	1	9019	5	13	NULL	NULL	NULL	p53	GP		bind					PIG3	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3375_s_232	11313463	A 2.5-fold increase in p53 binding to the PIG3 promoter was observed by 4 h after ADR treatment (Fig.  2C); and although this increase in binding was accompanied by an increase in PIG3 mRNA, it was modest at 1.5-fold of the control level (Fig.  5A and B).	bind
38813	2	9019	5	13	NULL	NULL	NULL	ADR	Chemical	treatment	increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3375_s_232	11313463	A 2.5-fold increase in p53 binding to the PIG3 promoter was observed by 4 h after ADR treatment (Fig.  2C); and although this increase in binding was accompanied by an increase in PIG3 mRNA, it was modest at 1.5-fold of the control level (Fig.  5A and B).	bind
38814	3	9019	5	13	NULL	NULL	NULL	statement 2	Process		is accompanied by					PIG3 mRNA	NucleicAcid	increase in			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_10_3375_s_232	11313463	A 2.5-fold increase in p53 binding to the PIG3 promoter was observed by 4 h after ADR treatment (Fig.  2C); and although this increase in binding was accompanied by an increase in PIG3 mRNA, it was modest at 1.5-fold of the control level (Fig.  5A and B).	bind
30567	1	9019	6	NULL	NULL	0	NULL	p53	NULL		bind	NULL				PIG3	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_10_3375_s_232	11313463	A 2.5-fold increase in p53 binding to the PIG3 promoter was observed by 4 h after ADR treatment (Fig.  2C); and although this increase in binding was accompanied by an increase in PIG3 mRNA, it was modest at 1.5-fold of the control level (Fig.  5A and B).	bind
30568	2	9019	6	NULL	NULL	0	NULL	ADR	NULL	treatment with	increases	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_10_3375_s_232	11313463	A 2.5-fold increase in p53 binding to the PIG3 promoter was observed by 4 h after ADR treatment (Fig.  2C); and although this increase in binding was accompanied by an increase in PIG3 mRNA, it was modest at 1.5-fold of the control level (Fig.  5A and B).	bind
30569	3	9019	6	NULL	NULL	0	NULL	statement 2	NULL		is accompanied by	NULL				PIG3 mRNA	NULL	increase in			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_10_3375_s_232	11313463	A 2.5-fold increase in p53 binding to the PIG3 promoter was observed by 4 h after ADR treatment (Fig.  2C); and although this increase in binding was accompanied by an increase in PIG3 mRNA, it was modest at 1.5-fold of the control level (Fig.  5A and B).	bind
38806	1	9020	5	13	NULL	NULL	NULL	p97(N-D1) hexamer	GP		bind					p47	GP		UBX domain 		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_1967_s_25	16601695	A 2.9  Ang  crystal structure of p97(N-D1) hexamer bound to p47(UBX) domain revealed  that p47 interacts with the p97(N) domain via a conserved loop within the UBX domain  (S3/S4) that inserts into a hydrophobic pocket between the two p97(N) subdomains  (  et al).	bind
38807	2	9020	5	13	NULL	NULL	NULL	p47	GP		interact with					p97	GP		N domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_1967_s_25	16601695	A 2.9  Ang  crystal structure of p97(N-D1) hexamer bound to p47(UBX) domain revealed  that p47 interacts with the p97(N) domain via a conserved loop within the UBX domain  (S3/S4) that inserts into a hydrophobic pocket between the two p97(N) subdomains  (  et al).	bind
38808	3	9020	5	13	NULL	NULL	NULL			conserved loop within	inserts into			UBX domain (S3/S4)		p97	GP		hydrophobic pocket between the two (N) subdomains		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_1967_s_25	16601695	A 2.9  Ang  crystal structure of p97(N-D1) hexamer bound to p47(UBX) domain revealed  that p47 interacts with the p97(N) domain via a conserved loop within the UBX domain  (S3/S4) that inserts into a hydrophobic pocket between the two p97(N) subdomains  (  et al).	bind
38809	4	9020	5	13	NULL	NULL	NULL	statement 2	Process		via					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_1967_s_25	16601695	A 2.9  Ang  crystal structure of p97(N-D1) hexamer bound to p47(UBX) domain revealed  that p47 interacts with the p97(N) domain via a conserved loop within the UBX domain  (S3/S4) that inserts into a hydrophobic pocket between the two p97(N) subdomains  (  et al).	bind
31169	1	9020	6	10	NULL	0	NULL	p97 (N-D1)hexamer	NULL		bind	NULL				p47	NULL		UBX domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_1967_s_25	16601695	A 2.9  Ang  crystal structure of p97(N-D1) hexamer bound to p47(UBX) domain revealed  that p47 interacts with the p97(N) domain via a conserved loop within the UBX domain  (S3/S4) that inserts into a hydrophobic pocket between the two p97(N) subdomains  (  et al).	bind
31170	2	9020	6	NULL	NULL	0	NULL		NULL		comprises of	NULL		UBX domain		conserved loop	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_25_9_1967_s_25	16601695	A 2.9  Ang  crystal structure of p97(N-D1) hexamer bound to p47(UBX) domain revealed  that p47 interacts with the p97(N) domain via a conserved loop within the UBX domain  (S3/S4) that inserts into a hydrophobic pocket between the two p97(N) subdomains  (  et al).	bind
31171	3	9020	6	NULL	NULL	0	NULL	statement 2	NULL		insert into	NULL				p97	NULL		hydrophobic pocket between N subdomain		NULL		0	NULL	NULL	NULL	gw70_embo_25_9_1967_s_25	16601695	A 2.9  Ang  crystal structure of p97(N-D1) hexamer bound to p47(UBX) domain revealed  that p47 interacts with the p97(N) domain via a conserved loop within the UBX domain  (S3/S4) that inserts into a hydrophobic pocket between the two p97(N) subdomains  (  et al).	bind
31172	4	9020	6	10	NULL	0	NULL	p47	NULL		interacts with	NULL				p97	NULL		N domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_1967_s_25	16601695	A 2.9  Ang  crystal structure of p97(N-D1) hexamer bound to p47(UBX) domain revealed  that p47 interacts with the p97(N) domain via a conserved loop within the UBX domain  (S3/S4) that inserts into a hydrophobic pocket between the two p97(N) subdomains  (  et al).	bind
47917	5	9020	6	10	NULL	0	NULL	statement 4	NULL		via	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_25_9_1967_s_25	16601695	A 2.9  Ang  crystal structure of p97(N-D1) hexamer bound to p47(UBX) domain revealed  that p47 interacts with the p97(N) domain via a conserved loop within the UBX domain  (S3/S4) that inserts into a hydrophobic pocket between the two p97(N) subdomains  (  et al).	bind
38803	2	9022	5	13	NULL	NULL	NULL	statement 1	AminoAcid		is designated as					peptide G	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_49_31179_s_18	8940117	A 20-amino acid synthetic peptide derived from the 37LRP sequence, designated peptide G, was found to bind to laminin ( 9).	bind
38804	3	9022	5	13	NULL	NULL	NULL	peptide G	AminoAcid		bind					laminin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_49_31179_s_18	8940117	A 20-amino acid synthetic peptide derived from the 37LRP sequence, designated peptide G, was found to bind to laminin ( 9).	bind
47918	1	9022	5	13	NULL	NULL	NULL	20-amino acid synthetic peptide 	AminoAcid		is derived from					37LRP sequence	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_49_31179_s_18	8940117	A 20-amino acid synthetic peptide derived from the 37LRP sequence, designated peptide G, was found to bind to laminin ( 9).	bind
30572	1	9022	6	NULL	NULL	0	NULL	peptide G	NULL		is derived from	NULL				37LRP sequence	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_49_31179_s_18	8940117	A 20-amino acid synthetic peptide derived from the 37LRP sequence, designated peptide G, was found to bind to laminin ( 9).	bind
30576	2	9022	6	NULL	NULL	0	NULL	peptide G	NULL		comprises of	NULL					NULL		20 amino acids		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_49_31179_s_18	8940117	A 20-amino acid synthetic peptide derived from the 37LRP sequence, designated peptide G, was found to bind to laminin ( 9).	bind
30577	3	9022	6	NULL	NULL	0	NULL	peptide G	NULL		bind	NULL				laminin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_49_31179_s_18	8940117	A 20-amino acid synthetic peptide derived from the 37LRP sequence, designated peptide G, was found to bind to laminin ( 9).	bind
38847	1	9024	5	13	NULL	NULL	NULL				overlaps		partially	20-bp lux box-like sequence		cepI	GP			35 region of putative promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_7_2212_s_29	11244059	A 20-bp  lux box-like sequence that partially overlaps the  35 region of the putative  cepI promoter was identified, suggesting that CepR binds to the  cepI promoter to activate  cepI expression ( 17).	bind
38848	2	9024	5	13	NULL	NULL	NULL	CepR	GP		bind					cepI	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_7_2212_s_29	11244059	A 20-bp  lux box-like sequence that partially overlaps the  35 region of the putative  cepI promoter was identified, suggesting that CepR binds to the  cepI promoter to activate  cepI expression ( 17).	bind
38849	3	9024	5	13	NULL	NULL	NULL	statement 2	Process		activates					cepI	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_7_2212_s_29	11244059	A 20-bp  lux box-like sequence that partially overlaps the  35 region of the putative  cepI promoter was identified, suggesting that CepR binds to the  cepI promoter to activate  cepI expression ( 17).	bind
38850	4	9024	5	13	NULL	NULL	NULL	statement 1	Process		suggest					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_7_2212_s_29	11244059	A 20-bp  lux box-like sequence that partially overlaps the  35 region of the putative  cepI promoter was identified, suggesting that CepR binds to the  cepI promoter to activate  cepI expression ( 17).	bind
30588	1	9024	6	NULL	NULL	0	NULL		NULL		overlaps with	NULL	partially		20-bp lux box-like sequence	CepI	NULL	putative		35 region of the promoter	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_7_2212_s_29	11244059	A 20-bp  lux box-like sequence that partially overlaps the  35 region of the putative  cepI promoter was identified, suggesting that CepR binds to the  cepI promoter to activate  cepI expression ( 17).	bind
30589	2	9024	6	NULL	NULL	0	NULL	CepR	NULL		bind	NULL				cepI	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_7_2212_s_29	11244059	A 20-bp  lux box-like sequence that partially overlaps the  35 region of the putative  cepI promoter was identified, suggesting that CepR binds to the  cepI promoter to activate  cepI expression ( 17).	bind
30590	3	9024	6	NULL	NULL	0	NULL	statement 1	NULL		suggests	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_7_2212_s_29	11244059	A 20-bp  lux box-like sequence that partially overlaps the  35 region of the putative  cepI promoter was identified, suggesting that CepR binds to the  cepI promoter to activate  cepI expression ( 17).	bind
30591	4	9024	6	NULL	NULL	0	NULL	statement 2	NULL		activates	NULL				cepI	NULL	expression of			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_7_2212_s_29	11244059	A 20-bp  lux box-like sequence that partially overlaps the  35 region of the putative  cepI promoter was identified, suggesting that CepR binds to the  cepI promoter to activate  cepI expression ( 17).	bind
38851	1	9026	5	13	NULL	NULL	NULL	Ab C-597	GP		bind					PROT proteins	GP	native			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_26_15755_s_90	7797577	A 20-fold excess of peptide  efficiently blocked binding of Ab C-597 to native PROT proteins.	bind
30596	1	9026	6	NULL	NULL	0	NULL	Ab C-597	NULL		bind	NULL				PROT proteins	NULL	native			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_26_15755_s_90	7797577	A 20-fold excess of peptide  efficiently blocked binding of Ab C-597 to native PROT proteins.	bind
38852	1	9027	5	13	NULL	NULL	NULL	20-residue peptide	AminoAcid		encode					Cav ce	GP		predicted G protein binding region		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2437_s_15	8999956	A 20-residue peptide encoding the predicted G protein binding region of Cav ce possesses "`GDP dissociation inhibitor-like activity"` with the same potency as described earlier for mammalian caveolin-1.	bind
38853	2	9027	5	13	NULL	NULL	NULL	statement 1	AminoAcid		possesses					GDP dissociation inhibitor-like activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2437_s_15	8999956	A 20-residue peptide encoding the predicted G protein binding region of Cav ce possesses "`GDP dissociation inhibitor-like activity"` with the same potency as described earlier for mammalian caveolin-1.	bind
38854	3	9027	5	13	NULL	NULL	NULL	caveolin-1	GP	mammalian	possess					GDP dissociation inhibitor-like activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2437_s_15	8999956	A 20-residue peptide encoding the predicted G protein binding region of Cav ce possesses "`GDP dissociation inhibitor-like activity"` with the same potency as described earlier for mammalian caveolin-1.	bind
57756	4	9027	5	13	NULL	NULL	NULL	statement 2	Process		same potency as					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2437_s_15	8999956	A 20-residue peptide encoding the predicted G protein binding region of Cav ce possesses "`GDP dissociation inhibitor-like activity"` with the same potency as described earlier for mammalian caveolin-1.	bind
31173	2	9027	6	10	NULL	0	NULL	statement 1			possesses					GDP dissociation inhibitor-like activity					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2437_s_15	8999956	A 20-residue peptide encoding the predicted G protein binding region of Cav ce possesses "`GDP dissociation inhibitor-like activity"` with the same potency as described earlier for mammalian caveolin-1.	bind
31174	3	9027	6	10	NULL	0	NULL	Caveolin-1		mammalian	possesses					GDP dissociation inhibitor-like activity					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2437_s_15	8999956	A 20-residue peptide encoding the predicted G protein binding region of Cav ce possesses "`GDP dissociation inhibitor-like activity"` with the same potency as described earlier for mammalian caveolin-1.	bind
31175	4	9027	6	10	NULL	0	NULL	statement 2			same potency as					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2437_s_15	8999956	A 20-residue peptide encoding the predicted G protein binding region of Cav ce possesses "`GDP dissociation inhibitor-like activity"` with the same potency as described earlier for mammalian caveolin-1.	bind
57757	1	9027	6	10	NULL	0	NULL	20-residue peptide			encode					Cav ce			 predicted G protein binding region		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_4_2437_s_15	8999956	A 20-residue peptide encoding the predicted G protein binding region of Cav ce possesses "`GDP dissociation inhibitor-like activity"` with the same potency as described earlier for mammalian caveolin-1.	bind
38855	1	9028	5	13	NULL	NULL	NULL	CPD	GP		bind			20-residue region within the cytoplasmic tail		PP2A	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-cell-sci_114_pt-2_11148133_s_3	11148133	A 20-residue region within the cytoplasmic  tail of CPD binds protein phosphatase 2A (PP2A).	bind
38856	2	9028	5	13	NULL	NULL	NULL	PP2A	GP		is					protein phosphatase 2A	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-cell-sci_114_pt-2_11148133_s_3	11148133	A 20-residue region within the cytoplasmic  tail of CPD binds protein phosphatase 2A (PP2A).	bind
30601	1	9028	6	NULL	NULL	0	NULL	CPD	NULL		bind	NULL		20-residue region within the cytoplasmic tail		PP2A	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-cell-sci_114_pt-2_11148133_s_3	11148133	A 20-residue region within the cytoplasmic  tail of CPD binds protein phosphatase 2A (PP2A).	bind
30602	2	9028	6	NULL	NULL	0	NULL	PP2A	NULL		is	NULL				protein phosphatase 2A	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-cell-sci_114_pt-2_11148133_s_3	11148133	A 20-residue region within the cytoplasmic  tail of CPD binds protein phosphatase 2A (PP2A).	bind
38857	1	9029	5	13	NULL	NULL	NULL	RBD-Ig of TOR2 variants	GP	purified	bind					Sigma I-2136	GP	immobilized			NULL		NULL	NULL	NULL	NULL	gw70_embo_24_8_1634_s_252	15791205	A 200 nM portion of purified RBD-Ig of TOR2 variants was bound to an anti-human  antibody (Sigma I-2136) immobilized on a CM5 sensor chip.	bind
38858	2	9029	5	13	NULL	NULL	NULL	Sigma I-2136	GP		is a type of					anti-human antibody	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_8_1634_s_252	15791205	A 200 nM portion of purified RBD-Ig of TOR2 variants was bound to an anti-human  antibody (Sigma I-2136) immobilized on a CM5 sensor chip.	bind
30603	1	9029	6	10	NULL	0	NULL	Sigma I-2136	NULL		is a type of	NULL				anti-human antibody	NULL				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_8_1634_s_252	15791205	A 200 nM portion of purified RBD-Ig of TOR2 variants was bound to an anti-human  antibody (Sigma I-2136) immobilized on a CM5 sensor chip.	bind
30605	2	9029	6	10	NULL	0	NULL	RBD-Ig of TOR2 variants	NULL	purified	bind	NULL				Sigma I-2136	NULL				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_8_1634_s_252	15791205	A 200 nM portion of purified RBD-Ig of TOR2 variants was bound to an anti-human  antibody (Sigma I-2136) immobilized on a CM5 sensor chip.	bind
38859	1	9030	5	13	NULL	NULL	NULL	osk	GP		bind					Hrb27C	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_131_9_1949_s_155	15056611	A 200-fold excess  grk or  osk is able to compete binding of Hrb27C (arrow) from  osk, while excess  nos is not.	bind
38862	2	9030	5	13	NULL	NULL	NULL	grk	GP	excess	bind					Hrb27C	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_131_9_1949_s_155	15056611	A 200-fold excess  grk or  osk is able to compete binding of Hrb27C (arrow) from  osk, while excess  nos is not.	bind
38863	3	9030	5	13	NULL	NULL	NULL	statement 2	Process		competes with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_131_9_1949_s_155	15056611	A 200-fold excess  grk or  osk is able to compete binding of Hrb27C (arrow) from  osk, while excess  nos is not.	bind
57758	4	9030	5	13	NULL	NULL	NULL	nos	GP	excess of	does not compete with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_131_9_1949_s_155	15056611	A 200-fold excess  grk or  osk is able to compete binding of Hrb27C (arrow) from  osk, while excess  nos is not.	bind
57759	5	9030	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_131_9_1949_s_155	15056611	A 200-fold excess  grk or  osk is able to compete binding of Hrb27C (arrow) from  osk, while excess  nos is not.	bind
30607	1	9030	6	NULL	NULL	0	NULL	Hrb27C	NULL		bind	NULL				osk	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_9_1949_s_155	15056611	A 200-fold excess  grk or  osk is able to compete binding of Hrb27C (arrow) from  osk, while excess  nos is not.	bind
30608	2	9030	6	NULL	NULL	0	NULL	grk	NULL	excess of	bind	NULL				osk	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_9_1949_s_155	15056611	A 200-fold excess  grk or  osk is able to compete binding of Hrb27C (arrow) from  osk, while excess  nos is not.	bind
30609	3	9030	6	NULL	NULL	0	NULL	statement 1	NULL		competes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_9_1949_s_155	15056611	A 200-fold excess  grk or  osk is able to compete binding of Hrb27C (arrow) from  osk, while excess  nos is not.	bind
30612	5	9030	6	10	NULL	0	NULL	statement 1			is an alternative to					statement 2					NULL		NULL	NULL	NULL	NULL	gw70_development_131_9_1949_s_155	15056611	A 200-fold excess  grk or  osk is able to compete binding of Hrb27C (arrow) from  osk, while excess  nos is not.	bind
30613	4	9030	6	10	NULL	0	NULL	nos		excess of	does not compete with					statement 1					NULL		NULL	NULL	NULL	NULL	gw70_development_131_9_1949_s_155	15056611	A 200-fold excess  grk or  osk is able to compete binding of Hrb27C (arrow) from  osk, while excess  nos is not.	bind
42524	1	9031	5	13	NULL	NULL	NULL	HNF-3beta complex	GP		bind					HNF-3 consensus probe	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_34_26637_s_181	10859308	A 200-fold excess of nonradioactive site 1 oligonucleotide competes well for binding of the HNF-3 consensus probe for the upper HNF-3beta complex ( lane 3).	bind
30614	1	9031	6	NULL	NULL	0	NULL	HNF-3beta complex	NULL		bind	NULL				HNF-3 consensus probe	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_34_26637_s_181	10859308	A 200-fold excess of nonradioactive site 1 oligonucleotide competes well for binding of the HNF-3 consensus probe for the upper HNF-3beta complex ( lane 3).	bind
38864	1	9032	5	13	NULL	NULL	NULL	consensus Sp1 oligonucleotide probe	NucleicAcid		bind					Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_47_43713_s_173	11559712	A 200-fold molar excess of a consensus Sp1 oligonucleotide probe (which binds Sp1 and Sp3) competed for the binding of NF-1 and NF-3 but not the other complexes.	bind
38865	2	9032	5	13	NULL	NULL	NULL	consensus Sp1 oligonucleotide probe	NucleicAcid		bind					Sp3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_47_43713_s_173	11559712	A 200-fold molar excess of a consensus Sp1 oligonucleotide probe (which binds Sp1 and Sp3) competed for the binding of NF-1 and NF-3 but not the other complexes.	bind
38866	3	9032	5	13	NULL	NULL	NULL	consensus Sp1 oligonucleotide probe	NucleicAcid		bind					NF-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_47_43713_s_173	11559712	A 200-fold molar excess of a consensus Sp1 oligonucleotide probe (which binds Sp1 and Sp3) competed for the binding of NF-1 and NF-3 but not the other complexes.	bind
38867	4	9032	5	13	NULL	NULL	NULL	consensus Sp1 oligonucleotide probe	NucleicAcid		bind					NF-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_47_43713_s_173	11559712	A 200-fold molar excess of a consensus Sp1 oligonucleotide probe (which binds Sp1 and Sp3) competed for the binding of NF-1 and NF-3 but not the other complexes.	bind
38868	5	9032	5	13	NULL	NULL	NULL	statement 3	Process		competes with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_47_43713_s_173	11559712	A 200-fold molar excess of a consensus Sp1 oligonucleotide probe (which binds Sp1 and Sp3) competed for the binding of NF-1 and NF-3 but not the other complexes.	bind
30617	1	9032	6	NULL	NULL	0	NULL	Sp1 oligonucleotide probe	NULL		bind	NULL				Sp1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_47_43713_s_173	11559712	A 200-fold molar excess of a consensus Sp1 oligonucleotide probe (which binds Sp1 and Sp3) competed for the binding of NF-1 and NF-3 but not the other complexes.	bind
30618	2	9032	6	NULL	NULL	0	NULL	Sp1 oligonucleotide probe	NULL		bind	NULL				Sp3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_47_43713_s_173	11559712	A 200-fold molar excess of a consensus Sp1 oligonucleotide probe (which binds Sp1 and Sp3) competed for the binding of NF-1 and NF-3 but not the other complexes.	bind
30619	3	9032	6	10	NULL	0	NULL	 Sp1 oligonucleotide probe	NULL		bind	NULL				NF-1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_47_43713_s_173	11559712	A 200-fold molar excess of a consensus Sp1 oligonucleotide probe (which binds Sp1 and Sp3) competed for the binding of NF-1 and NF-3 but not the other complexes.	bind
30621	4	9032	6	NULL	NULL	0	NULL	Sp1 oligonucleotide probe	NULL	excess of	bind	NULL				NF-3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_47_43713_s_173	11559712	A 200-fold molar excess of a consensus Sp1 oligonucleotide probe (which binds Sp1 and Sp3) competed for the binding of NF-1 and NF-3 but not the other complexes.	bind
30622	5	9032	6	NULL	NULL	0	NULL	statement 4	NULL		competes	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_47_43713_s_173	11559712	A 200-fold molar excess of a consensus Sp1 oligonucleotide probe (which binds Sp1 and Sp3) competed for the binding of NF-1 and NF-3 but not the other complexes.	bind
38869	1	9033	5	13	NULL	NULL	NULL	isl-1	GP		bind					Ga probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_21_12646_s_62	7759514	A 200-fold molar excess of unlabeled Ga markedly  diminished the binding of  isl-1  to the Ga probe  ( Fig. 1).	bind
38871	2	9033	5	13	NULL	NULL	NULL	Ga	GP	excess;;unlabeled	diminished		markedly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_21_12646_s_62	7759514	A 200-fold molar excess of unlabeled Ga markedly  diminished the binding of  isl-1  to the Ga probe  ( Fig. 1).	bind
30623	1	9033	6	NULL	NULL	0	NULL	isl-1	NULL		bind	NULL				Ga probe	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_21_12646_s_62	7759514	A 200-fold molar excess of unlabeled Ga markedly  diminished the binding of  isl-1  to the Ga probe  ( Fig. 1).	bind
30624	2	9033	6	NULL	NULL	0	NULL	Ga	NULL	excess of;; unlabeled	diminishes	NULL	markedly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_21_12646_s_62	7759514	A 200-fold molar excess of unlabeled Ga markedly  diminished the binding of  isl-1  to the Ga probe  ( Fig. 1).	bind
38872	1	9034	5	13	NULL	NULL	NULL	21 kDa surface protein	GP	Mycobacterium leprae	bind					peripheral nerve laminin-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_511_s_521	11081637	A 21 kDa surface protein of  Mycobacterium leprae binds peripheral nerve laminin-2 and mediates Schwann cell invasion.	bind
38873	2	9034	5	13	NULL	NULL	NULL	statement 1	Process		mediate					Schwann cell 	Cell	invasion of			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_3_511_s_521	11081637	A 21 kDa surface protein of  Mycobacterium leprae binds peripheral nerve laminin-2 and mediates Schwann cell invasion.	bind
30627	1	9034	6	NULL	NULL	0	NULL	21 kDa surface protein	NULL	Mycobacterium leprae	bind	NULL				peripheral nerve laminin-2	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_103_3_511_s_521	11081637	A 21 kDa surface protein of  Mycobacterium leprae binds peripheral nerve laminin-2 and mediates Schwann cell invasion.	bind
30629	2	9034	6	NULL	NULL	0	NULL	statement 1	NULL		mediates	NULL				Schwann cell 	NULL	invasion of 			NULL		0	NULL	NULL	NULL	gw60_cell_103_3_511_s_521	11081637	A 21 kDa surface protein of  Mycobacterium leprae binds peripheral nerve laminin-2 and mediates Schwann cell invasion.	bind
38875	1	9038	5	13	NULL	NULL	NULL	Ht31	GP	full-length	bind					RII	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_38_23637_s_31	9295304	A 22-residue peptide mimicking the RII binding site of Ht31 has been synthesized which inhibits the binding of full-length Ht31 binding to RII ( 17).	bind
38876	2	9038	5	13	NULL	NULL	NULL	22-residue peptide	GP		mimick					Ht31	GP		RII binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_38_23637_s_31	9295304	A 22-residue peptide mimicking the RII binding site of Ht31 has been synthesized which inhibits the binding of full-length Ht31 binding to RII ( 17).	bind
38877	3	9038	5	13	NULL	NULL	NULL	statement 2	Process	synthesized	inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_38_23637_s_31	9295304	A 22-residue peptide mimicking the RII binding site of Ht31 has been synthesized which inhibits the binding of full-length Ht31 binding to RII ( 17).	bind
30654	1	9038	6	NULL	NULL	0	NULL	Ht31	NULL		bind	NULL				RII	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_38_23637_s_31	9295304	A 22-residue peptide mimicking the RII binding site of Ht31 has been synthesized which inhibits the binding of full-length Ht31 binding to RII ( 17).	bind
30655	3	9038	6	10	NULL	0	NULL	statement 2		synthesized	inhibits					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_38_23637_s_31	9295304	A 22-residue peptide mimicking the RII binding site of Ht31 has been synthesized which inhibits the binding of full-length Ht31 binding to RII ( 17).	bind
57760	2	9038	6	10	NULL	0	NULL	22-residue peptide			mimicks					Ht31			RII binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_38_23637_s_31	9295304	A 22-residue peptide mimicking the RII binding site of Ht31 has been synthesized which inhibits the binding of full-length Ht31 binding to RII ( 17).	bind
38878	1	9039	5	13	NULL	NULL	NULL	s-Sec1	GP		bind					s-syntaxin	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jneurosci_18_8_2923_s_6	9526009	A 24 amino acid peptide fragment of s-Sec1, which inhibited the binding of s-Sec1 to s-syntaxin   in vitro, completely blocked release, suggesting an essential function of the s-Sec1/s-syntaxin interaction in transmitter release.	bind
38879	2	9039	5	13	NULL	NULL	NULL	s-Sec1	GP		inhibit			24 amino acid peptide fragment of 		statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jneurosci_18_8_2923_s_6	9526009	A 24 amino acid peptide fragment of s-Sec1, which inhibited the binding of s-Sec1 to s-syntaxin   in vitro, completely blocked release, suggesting an essential function of the s-Sec1/s-syntaxin interaction in transmitter release.	bind
38880	4	9039	5	13	NULL	NULL	NULL	statement 2	Process		block		completely			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_8_2923_s_6	9526009	A 24 amino acid peptide fragment of s-Sec1, which inhibited the binding of s-Sec1 to s-syntaxin   in vitro, completely blocked release, suggesting an essential function of the s-Sec1/s-syntaxin interaction in transmitter release.	bind
38881	3	9039	5	13	NULL	NULL	NULL	statement 1	Process		function in					transmitter 	Chemical	release of			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_8_2923_s_6	9526009	A 24 amino acid peptide fragment of s-Sec1, which inhibited the binding of s-Sec1 to s-syntaxin   in vitro, completely blocked release, suggesting an essential function of the s-Sec1/s-syntaxin interaction in transmitter release.	bind
30656	1	9039	6	NULL	NULL	0	NULL	s-Sec1	NULL		bind	NULL				s-syntaxin	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_jneurosci_18_8_2923_s_6	9526009	A 24 amino acid peptide fragment of s-Sec1, which inhibited the binding of s-Sec1 to s-syntaxin   in vitro, completely blocked release, suggesting an essential function of the s-Sec1/s-syntaxin interaction in transmitter release.	bind
30657	2	9039	6	10	NULL	0	NULL	s-Sec1			inhibits			24 amino acid peptide fragment of 		statement 1					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jneurosci_18_8_2923_s_6	9526009	A 24 amino acid peptide fragment of s-Sec1, which inhibited the binding of s-Sec1 to s-syntaxin   in vitro, completely blocked release, suggesting an essential function of the s-Sec1/s-syntaxin interaction in transmitter release.	bind
30658	3	9039	6	NULL	NULL	0	NULL	statement 1	NULL		plays a role in	NULL				transmitter	NULL	release of 			NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_8_2923_s_6	9526009	A 24 amino acid peptide fragment of s-Sec1, which inhibited the binding of s-Sec1 to s-syntaxin   in vitro, completely blocked release, suggesting an essential function of the s-Sec1/s-syntaxin interaction in transmitter release.	bind
47976	4	9039	6	10	NULL	0	NULL	statement 2	NULL		block	NULL	completely			statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_8_2923_s_6	9526009	A 24 amino acid peptide fragment of s-Sec1, which inhibited the binding of s-Sec1 to s-syntaxin   in vitro, completely blocked release, suggesting an essential function of the s-Sec1/s-syntaxin interaction in transmitter release.	bind
38883	1	9040	5	13	NULL	NULL	NULL	 Tat-p21 fusion peptide	GP		encompass					nuclear localization signal	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3364_s_317	15798220	A 24-amino-acid Tat-p21 fusion peptide encompassing the nuclear localization signal  and the PCNA-binding region of p21 blocks p21 phosphorylation and results in cell  death.	bind
38884	4	9040	5	13	NULL	NULL	NULL	statement 3	Process		results in					cell death	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3364_s_317	15798220	A 24-amino-acid Tat-p21 fusion peptide encompassing the nuclear localization signal  and the PCNA-binding region of p21 blocks p21 phosphorylation and results in cell  death.	bind
47977	2	9040	5	13	NULL	NULL	NULL	Tat-p21 fusion peptide	GP		encompass					p21	GP		PCNA-binding region 		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3364_s_317	15798220	A 24-amino-acid Tat-p21 fusion peptide encompassing the nuclear localization signal  and the PCNA-binding region of p21 blocks p21 phosphorylation and results in cell  death.	bind
47978	3	9040	5	13	NULL	NULL	NULL	Tat-p21 fusion peptide	GP		blocks					p21	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3364_s_317	15798220	A 24-amino-acid Tat-p21 fusion peptide encompassing the nuclear localization signal  and the PCNA-binding region of p21 blocks p21 phosphorylation and results in cell  death.	bind
47979	5	9040	5	13	NULL	NULL	NULL	Tat-p21 fusion peptide	GP		contains					24-amino-acid	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_3364_s_317	15798220	A 24-amino-acid Tat-p21 fusion peptide encompassing the nuclear localization signal  and the PCNA-binding region of p21 blocks p21 phosphorylation and results in cell  death.	bind
31176	1	9040	6	NULL	NULL	0	NULL	Tat-p21 fusion peptide	NULL		encompasses	NULL				nuclear localization signal	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3364_s_317	15798220	A 24-amino-acid Tat-p21 fusion peptide encompassing the nuclear localization signal  and the PCNA-binding region of p21 blocks p21 phosphorylation and results in cell  death.	bind
31177	2	9040	6	NULL	NULL	0	NULL	Tat-p21 fusion peptide	NULL		comprises	NULL				p21	NULL		PCNA binding region		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3364_s_317	15798220	A 24-amino-acid Tat-p21 fusion peptide encompassing the nuclear localization signal  and the PCNA-binding region of p21 blocks p21 phosphorylation and results in cell  death.	bind
31178	3	9040	6	NULL	NULL	0	NULL	Tat-p21 fusion peptide	NULL		blocks	NULL				p21	NULL	phosphorylation of 			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3364_s_317	15798220	A 24-amino-acid Tat-p21 fusion peptide encompassing the nuclear localization signal  and the PCNA-binding region of p21 blocks p21 phosphorylation and results in cell  death.	bind
31179	4	9040	6	NULL	NULL	0	NULL	statement 3	NULL		leads to	NULL				cell death	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3364_s_317	15798220	A 24-amino-acid Tat-p21 fusion peptide encompassing the nuclear localization signal  and the PCNA-binding region of p21 blocks p21 phosphorylation and results in cell  death.	bind
47980	5	9040	6	10	NULL	0	NULL	Tat-p21 fusion peptide	NULL		contains	NULL				24-amino-acid	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3364_s_317	15798220	A 24-amino-acid Tat-p21 fusion peptide encompassing the nuclear localization signal  and the PCNA-binding region of p21 blocks p21 phosphorylation and results in cell  death.	bind
38885	1	9042	5	13	NULL	NULL	NULL	ORF3 protein	GP		bind			25-amino acid region		ORF2 protein	GP	full length			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_25_22759_s_158	11934888	A 25-Amino Acid Region of the ORF3 Protein Binds to the Full-length ORF2 Protein-- To characterize the domains involved in the ORF2-ORF3 interaction, an array of deletion mutations were constructed for both ORF2 and ORF3 and were cloned into the yeast two-hybrid AD and BD vectors as described in Table  I. Combinations of full-length fusion constructs and deletion mutants of each fusion construct were tested for  in vivo protein-protein interactions as shown in Fig.  5.	bind
30660	1	9042	6	NULL	NULL	0	NULL	ORF3 protein	NULL		bind	NULL		25-Amino Acid Region		ORF2 protein	NULL	full length			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_25_22759_s_158	11934888	A 25-Amino Acid Region of the ORF3 Protein Binds to the Full-length ORF2 Protein-- To characterize the domains involved in the ORF2-ORF3 interaction, an array of deletion mutations were constructed for both ORF2 and ORF3 and were cloned into the yeast two-hybrid AD and BD vectors as described in Table  I. Combinations of full-length fusion constructs and deletion mutants of each fusion construct were tested for  in vivo protein-protein interactions as shown in Fig.  5.	bind
38886	1	9043	5	13	NULL	NULL	NULL	Cyp2b10 gene	GP		bind				25-bp DNA fragment	nuclear protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_16_9746_s_232	8621653	A 25-bp DNA fragment at -1.2 kilobase pairs of  Cyp2b10  gene is 80%  similar to a portion of the 163-bp  sequence, and an overlapping segment (-1228/-1195 bp) can  bind nuclear protein(s).	bind
47981	1	9043	6	10	NULL	0	NULL	Cyp2b10 gene	NULL		bind	NULL			25-bp DNA fragment	nuclear proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_16_9746_s_232	8621653	A 25-bp DNA fragment at -1.2 kilobase pairs of  Cyp2b10  gene is 80%  similar to a portion of the 163-bp  sequence, and an overlapping segment (-1228/-1195 bp) can  bind nuclear protein(s).	bind
38888	1	9045	5	13	NULL	NULL	NULL				bind			26 S protease subunit		ubiquitin conjugates	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_140_3_499_s_377	9456312	A 26 S protease  subunit that binds ubiquitin conjugates.	bind
30661	1	9045	6	10	NULL	0	NULL				bind			26 S protease subunit		ubiquitin conjugates					NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_140_3_499_s_377	9456312	A 26 S protease  subunit that binds ubiquitin conjugates.	bind
38889	1	9048	5	13	NULL	NULL	NULL	S5a	GP		is a type of					26 S proteasome subunit	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_51_32538_s_231	8955078	A 26 S proteasome subunit (S5a) that binds Ub-conjugate substrates has already been identified and its cDNA has been cloned and expressed ( 61,  62).	bind
38890	2	9048	5	13	NULL	NULL	NULL	S5a	GP		bind					Ub-conjugate substrates	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_51_32538_s_231	8955078	A 26 S proteasome subunit (S5a) that binds Ub-conjugate substrates has already been identified and its cDNA has been cloned and expressed ( 61,  62).	bind
30662	1	9048	6	10	NULL	0	NULL	S5a	NULL		bind	NULL				Ub-conjugate substrate	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_51_32538_s_231	8955078	A 26 S proteasome subunit (S5a) that binds Ub-conjugate substrates has already been identified and its cDNA has been cloned and expressed ( 61,  62).	bind
30663	2	9048	6	10	NULL	0	NULL	S5a	NULL		is a type of	NULL				 26 S proteasome subunit	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_51_32538_s_231	8955078	A 26 S proteasome subunit (S5a) that binds Ub-conjugate substrates has already been identified and its cDNA has been cloned and expressed ( 61,  62).	bind
38891	1	9050	5	13	NULL	NULL	NULL	UBA molecules	GP		bind					Ub2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_7055_s_111	14645257	A 2:1 model, in addition, allows up to two UBA molecules bound to Ub2, one per Ub unit.	bind
30664	1	9050	6	NULL	NULL	0	NULL	UBA molecule	NULL		bind	NULL				Ub2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_7055_s_111	14645257	A 2:1 model, in addition, allows up to two UBA molecules bound to Ub2, one per Ub unit.	bind
38892	1	9051	5	13	NULL	NULL	NULL	zipper protein	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_15_9075_s_239	8621557	A 2:1 molar ratio of zipper  protein to actin appears to be maximally effective and is sufficient to  saturate binding of zipper protein to actin.	bind
30665	1	9051	6	NULL	NULL	0	NULL	zipper protein	NULL		bind	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_15_9075_s_239	8621557	A 2:1 molar ratio of zipper  protein to actin appears to be maximally effective and is sufficient to  saturate binding of zipper protein to actin.	bind
38893	1	9053	5	13	NULL	NULL	NULL	GTP	Chemical		bind					eIF-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_18_2396_s_320	9308967	A 3-bp codon/anticodon interaction occurs, which signals the eIF-5-dependent hydrolysis of GTP bound to eIF-2.	bind
38894	2	9053	5	13	NULL	NULL	NULL	statement 1	Process	hydrolysis of	is dependent on					eIF-5	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_18_2396_s_320	9308967	A 3-bp codon/anticodon interaction occurs, which signals the eIF-5-dependent hydrolysis of GTP bound to eIF-2.	bind
38895	4	9053	5	13	NULL	NULL	NULL	statement 3	Process		signals					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_18_2396_s_320	9308967	A 3-bp codon/anticodon interaction occurs, which signals the eIF-5-dependent hydrolysis of GTP bound to eIF-2.	bind
47982	3	9053	5	13	NULL	NULL	NULL	3-bp codon	NucleicAcid		interacts with					anticodon	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_18_2396_s_320	9308967	A 3-bp codon/anticodon interaction occurs, which signals the eIF-5-dependent hydrolysis of GTP bound to eIF-2.	bind
30848	1	9053	6	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				eIF-2	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_11_18_2396_s_320	9308967	A 3-bp codon/anticodon interaction occurs, which signals the eIF-5-dependent hydrolysis of GTP bound to eIF-2.	bind
30849	2	9053	6	NULL	NULL	0	NULL	statement 1	NULL	hydrolysis of	is dependent on	NULL				eIF-5	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_11_18_2396_s_320	9308967	A 3-bp codon/anticodon interaction occurs, which signals the eIF-5-dependent hydrolysis of GTP bound to eIF-2.	bind
30850	3	9053	6	NULL	NULL	0	NULL	3-bp codon	NULL		interacts with	NULL				anticodon	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_11_18_2396_s_320	9308967	A 3-bp codon/anticodon interaction occurs, which signals the eIF-5-dependent hydrolysis of GTP bound to eIF-2.	bind
30851	4	9053	6	NULL	NULL	0	NULL	statement 3	NULL		signals	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_11_18_2396_s_320	9308967	A 3-bp codon/anticodon interaction occurs, which signals the eIF-5-dependent hydrolysis of GTP bound to eIF-2.	bind
38896	1	9054	5	13	NULL	NULL	NULL	HisP	GP		is a type of					nucleotide-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_5_554_s_5	11909819	A 3-D structure model of the region containing the second nucleotide-binding domain (NBD2) of SUR and C42 was developed based on the structure of HisP, a nucleotide-binding protein forming the bacterial Histidine transporter complex.	bind
38898	2	9054	5	13	NULL	NULL	NULL	HisP	GP		forms					Histidine transporter complex	GP	bacterial			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_5_554_s_5	11909819	A 3-D structure model of the region containing the second nucleotide-binding domain (NBD2) of SUR and C42 was developed based on the structure of HisP, a nucleotide-binding protein forming the bacterial Histidine transporter complex.	bind
47983	3	9054	5	13	NULL	NULL	NULL	NBD2	GP		is					nucleotide-binding domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_5_554_s_5	11909819	A 3-D structure model of the region containing the second nucleotide-binding domain (NBD2) of SUR and C42 was developed based on the structure of HisP, a nucleotide-binding protein forming the bacterial Histidine transporter complex.	bind
30852	1	9054	6	NULL	NULL	0	NULL	HisP	NULL		is a type of	NULL				nucleotide-binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_90_5_554_s_5	11909819	A 3-D structure model of the region containing the second nucleotide-binding domain (NBD2) of SUR and C42 was developed based on the structure of HisP, a nucleotide-binding protein forming the bacterial Histidine transporter complex.	bind
30853	2	9054	6	10	NULL	0	NULL	HisP			forms					 Histidine transporter complex		bacterial			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_5_554_s_5	11909819	A 3-D structure model of the region containing the second nucleotide-binding domain (NBD2) of SUR and C42 was developed based on the structure of HisP, a nucleotide-binding protein forming the bacterial Histidine transporter complex.	bind
30854	3	9054	6	10	NULL	0	NULL	NBD2	NULL		is	NULL				nucleotide-binding domain	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_5_554_s_5	11909819	A 3-D structure model of the region containing the second nucleotide-binding domain (NBD2) of SUR and C42 was developed based on the structure of HisP, a nucleotide-binding protein forming the bacterial Histidine transporter complex.	bind
38900	1	9056	5	13	NULL	NULL	NULL	MTSEA	Chemical		inhibit		strongly					binding properties of ;;mutant	A104C		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51415_s_102	15452107	A 3-min treatment with 0.5 mM MTSEA ( Fig. 3 A) strongly inhibited the binding properties of mutants A104C(3.28) and L112C(3.36), whereas it had only a minor effect on the binding properties of the other mutant receptors.	bind
38901	2	9056	5	13	NULL	NULL	NULL	MTSEA	Chemical		inhibit		strongly					binding properties of;;mutant	L112C		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51415_s_102	15452107	A 3-min treatment with 0.5 mM MTSEA ( Fig. 3 A) strongly inhibited the binding properties of mutants A104C(3.28) and L112C(3.36), whereas it had only a minor effect on the binding properties of the other mutant receptors.	bind
30855	1	9056	6	NULL	NULL	0	NULL	MTSEA	NULL		inhibits	NULL	strongly				NULL	binding properties of;; mutant	A104C		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51415_s_102	15452107	A 3-min treatment with 0.5 mM MTSEA ( Fig. 3 A) strongly inhibited the binding properties of mutants A104C(3.28) and L112C(3.36), whereas it had only a minor effect on the binding properties of the other mutant receptors.	bind
30856	2	9056	6	NULL	NULL	0	NULL	MTSEA	NULL		inhibits	NULL	strongly				NULL	binding properties of;; mutant	L112C		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_51415_s_102	15452107	A 3-min treatment with 0.5 mM MTSEA ( Fig. 3 A) strongly inhibited the binding properties of mutants A104C(3.28) and L112C(3.36), whereas it had only a minor effect on the binding properties of the other mutant receptors.	bind
38902	1	9058	5	13	NULL	NULL	NULL	alpha1(V) chain	GP		bind			heparin-binding fragment 		heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29377_s_15	10862775	A 30-kDa heparin-binding fragment of the alpha1(V) chain has been isolated and was shown to bind heparin with the same affinity as the complete parental chain ( 12).	bind
38903	2	9058	5	13	NULL	NULL	NULL	alpha1(V) chain	GP	complete parental chain	bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29377_s_15	10862775	A 30-kDa heparin-binding fragment of the alpha1(V) chain has been isolated and was shown to bind heparin with the same affinity as the complete parental chain ( 12).	bind
38904	3	9058	5	13	NULL	NULL	NULL	statement 1	Process		same affinity as					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29377_s_15	10862775	A 30-kDa heparin-binding fragment of the alpha1(V) chain has been isolated and was shown to bind heparin with the same affinity as the complete parental chain ( 12).	bind
30858	1	9058	6	NULL	NULL	0	NULL	alpha1(V) chain	NULL		bind	NULL		heparin binding fragment		heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29377_s_15	10862775	A 30-kDa heparin-binding fragment of the alpha1(V) chain has been isolated and was shown to bind heparin with the same affinity as the complete parental chain ( 12).	bind
30859	2	9058	6	10	NULL	0	NULL	alpha1(V) chain	NULL	complete	bind	NULL				heparin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29377_s_15	10862775	A 30-kDa heparin-binding fragment of the alpha1(V) chain has been isolated and was shown to bind heparin with the same affinity as the complete parental chain ( 12).	bind
30860	3	9058	6	NULL	NULL	0	NULL	statement 1	NULL	affinity of	is same as	NULL				statement 2	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29377_s_15	10862775	A 30-kDa heparin-binding fragment of the alpha1(V) chain has been isolated and was shown to bind heparin with the same affinity as the complete parental chain ( 12).	bind
38905	1	9059	5	13	NULL	NULL	NULL	CBP/p300	GP		bind					CREB	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_8_3697_s_32	9108040	A 300-kDa protein (CBP/p300) which binds to the cAMP response element-binding protein (CREB) functions as a coactivator of CREB-mediated signaling pathways.	bind
38906	2	9059	5	13	NULL	NULL	NULL	CREB	GP		is					cAMP response element-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_8_3697_s_32	9108040	A 300-kDa protein (CBP/p300) which binds to the cAMP response element-binding protein (CREB) functions as a coactivator of CREB-mediated signaling pathways.	bind
38907	3	9059	5	13	NULL	NULL	NULL	CREB	GP		function as					coactivator	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_8_3697_s_32	9108040	A 300-kDa protein (CBP/p300) which binds to the cAMP response element-binding protein (CREB) functions as a coactivator of CREB-mediated signaling pathways.	bind
47984	4	9059	5	13	NULL	NULL	NULL	CREB	GP		mediates					signaling pathways	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_8_3697_s_32	9108040	A 300-kDa protein (CBP/p300) which binds to the cAMP response element-binding protein (CREB) functions as a coactivator of CREB-mediated signaling pathways.	bind
47985	5	9059	5	13	NULL	NULL	NULL	statement 3	Process		occurs in					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_8_3697_s_32	9108040	A 300-kDa protein (CBP/p300) which binds to the cAMP response element-binding protein (CREB) functions as a coactivator of CREB-mediated signaling pathways.	bind
47986	6	9059	5	13	NULL	NULL	NULL	CBP/p300	GP		is a type of					300-kDa protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_8_3697_s_32	9108040	A 300-kDa protein (CBP/p300) which binds to the cAMP response element-binding protein (CREB) functions as a coactivator of CREB-mediated signaling pathways.	bind
30861	1	9059	6	NULL	NULL	0	NULL	CREB	NULL		is	NULL				cAMP response element-binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_94_8_3697_s_32	9108040	A 300-kDa protein (CBP/p300) which binds to the cAMP response element-binding protein (CREB) functions as a coactivator of CREB-mediated signaling pathways.	bind
30862	2	9059	6	10	NULL	0	NULL	CBP/p300	NULL		is a type of	NULL				300-kDa protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_8_3697_s_32	9108040	A 300-kDa protein (CBP/p300) which binds to the cAMP response element-binding protein (CREB) functions as a coactivator of CREB-mediated signaling pathways.	bind
30863	3	9059	6	NULL	NULL	0	NULL	CBP/p300	NULL		bind	NULL				CREB	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_94_8_3697_s_32	9108040	A 300-kDa protein (CBP/p300) which binds to the cAMP response element-binding protein (CREB) functions as a coactivator of CREB-mediated signaling pathways.	bind
30864	4	9059	6	NULL	NULL	0	NULL	CBP/p300	NULL		functions as a	NULL				coactivator	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_94_8_3697_s_32	9108040	A 300-kDa protein (CBP/p300) which binds to the cAMP response element-binding protein (CREB) functions as a coactivator of CREB-mediated signaling pathways.	bind
30865	5	9059	6	NULL	NULL	0	NULL	CREB	NULL		mediates	NULL				signaling pathways	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_94_8_3697_s_32	9108040	A 300-kDa protein (CBP/p300) which binds to the cAMP response element-binding protein (CREB) functions as a coactivator of CREB-mediated signaling pathways.	bind
30866	6	9059	6	NULL	NULL	0	NULL	statement 4	NULL		occurs in	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_94_8_3697_s_32	9108040	A 300-kDa protein (CBP/p300) which binds to the cAMP response element-binding protein (CREB) functions as a coactivator of CREB-mediated signaling pathways.	bind
38908	1	9060	5	13	NULL	NULL	NULL	F3 peptide	GP		corresponds to					HMGN2	GP		nucleosomal binding domain		NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_11_7444_s_96	12032302	A 31-aa fragment encoded by exons 3 and 4 (F3 peptide) showed substantial tumor cell binding (Fig.  2); F3 corresponds to the nucleosomal binding domain of HMGN2.	bind
38909	2	9060	5	13	NULL	NULL	NULL	F3 peptide	GP		bind		substantially			tumor cell	Cell				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_11_7444_s_96	12032302	A 31-aa fragment encoded by exons 3 and 4 (F3 peptide) showed substantial tumor cell binding (Fig.  2); F3 corresponds to the nucleosomal binding domain of HMGN2.	bind
47987	3	9060	5	13	NULL	NULL	NULL	F3 peptide	GP		is					31-aa fragment 	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_11_7444_s_96	12032302	A 31-aa fragment encoded by exons 3 and 4 (F3 peptide) showed substantial tumor cell binding (Fig.  2); F3 corresponds to the nucleosomal binding domain of HMGN2.	bind
47988	4	9060	5	13	NULL	NULL	NULL				encodes				exon 3	F3 peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_11_7444_s_96	12032302	A 31-aa fragment encoded by exons 3 and 4 (F3 peptide) showed substantial tumor cell binding (Fig.  2); F3 corresponds to the nucleosomal binding domain of HMGN2.	bind
47989	5	9060	5	13	NULL	NULL	NULL				encodes				exon 4	F3 peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_11_7444_s_96	12032302	A 31-aa fragment encoded by exons 3 and 4 (F3 peptide) showed substantial tumor cell binding (Fig.  2); F3 corresponds to the nucleosomal binding domain of HMGN2.	bind
47990	6	9060	5	13	NULL	NULL	NULL	statement 4	Process		occur along with					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_11_7444_s_96	12032302	A 31-aa fragment encoded by exons 3 and 4 (F3 peptide) showed substantial tumor cell binding (Fig.  2); F3 corresponds to the nucleosomal binding domain of HMGN2.	bind
30868	1	9060	6	NULL	NULL	0	NULL	F3 peptide	NULL		corresponds to	NULL				HMGN2	NULL		nucleosomal binding domain		NULL		0	NULL	NULL	NULL	gw60_pnas_99_11_7444_s_96	12032302	A 31-aa fragment encoded by exons 3 and 4 (F3 peptide) showed substantial tumor cell binding (Fig.  2); F3 corresponds to the nucleosomal binding domain of HMGN2.	bind
30870	2	9060	6	NULL	NULL	0	NULL	F3 peptide	NULL		bind	NULL	substantially			tumor cell	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_11_7444_s_96	12032302	A 31-aa fragment encoded by exons 3 and 4 (F3 peptide) showed substantial tumor cell binding (Fig.  2); F3 corresponds to the nucleosomal binding domain of HMGN2.	bind
30871	4	9060	6	10	NULL	0	NULL		NULL		encode	NULL			exon 3	F3 peptide	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_11_7444_s_96	12032302	A 31-aa fragment encoded by exons 3 and 4 (F3 peptide) showed substantial tumor cell binding (Fig.  2); F3 corresponds to the nucleosomal binding domain of HMGN2.	bind
30874	3	9060	6	10	NULL	0	NULL	F3 peptide	NULL		is	NULL				31-aa fragment	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_11_7444_s_96	12032302	A 31-aa fragment encoded by exons 3 and 4 (F3 peptide) showed substantial tumor cell binding (Fig.  2); F3 corresponds to the nucleosomal binding domain of HMGN2.	bind
47991	5	9060	6	10	NULL	0	NULL		NULL		encode	NULL			exon 4	F3 peptide	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_11_7444_s_96	12032302	A 31-aa fragment encoded by exons 3 and 4 (F3 peptide) showed substantial tumor cell binding (Fig.  2); F3 corresponds to the nucleosomal binding domain of HMGN2.	bind
47992	6	9060	6	10	NULL	0	NULL	statement 4	NULL		occur along with	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_11_7444_s_96	12032302	A 31-aa fragment encoded by exons 3 and 4 (F3 peptide) showed substantial tumor cell binding (Fig.  2); F3 corresponds to the nucleosomal binding domain of HMGN2.	bind
38910	1	9061	5	13	NULL	NULL	NULL	double-stranded oligonucleotide probe	NucleicAcid	32P-labeled	contains					ApoJ/lusterin	GP	human;;putative		Myb binding site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_28_21055_s_114	10770937	A 32P-labeled double-stranded oligonucleotide probe containing the putative Myb binding site of the human ApoJ/lusterin promoter bound to GST/B- MYB, but not to GST alone (Fig.  6,  lanes 1 and  2).	bind
38911	2	9061	5	13	NULL	NULL	NULL	statement 1	NucleicAcid		bind					GST/B- MYB	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_28_21055_s_114	10770937	A 32P-labeled double-stranded oligonucleotide probe containing the putative Myb binding site of the human ApoJ/lusterin promoter bound to GST/B- MYB, but not to GST alone (Fig.  6,  lanes 1 and  2).	bind
38912	3	9061	5	13	NULL	NULL	NULL	statement 1	NucleicAcid		does not bind					GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_28_21055_s_114	10770937	A 32P-labeled double-stranded oligonucleotide probe containing the putative Myb binding site of the human ApoJ/lusterin promoter bound to GST/B- MYB, but not to GST alone (Fig.  6,  lanes 1 and  2).	bind
30875	1	9061	6	NULL	NULL	0	NULL	ApoJ/lusterin	NULL	32P-labeled;; human;; putative	bind	NULL			Myb binding site of promoter	GST/B- MYB	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_28_21055_s_114	10770937	A 32P-labeled double-stranded oligonucleotide probe containing the putative Myb binding site of the human ApoJ/lusterin promoter bound to GST/B- MYB, but not to GST alone (Fig.  6,  lanes 1 and  2).	bind
30876	2	9061	6	NULL	NULL	0	NULL	ApoJ/lusterin	NULL	32P-labeled;; human;; putative	does not bind	NULL			Myb binding site of promoter	GST	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_28_21055_s_114	10770937	A 32P-labeled double-stranded oligonucleotide probe containing the putative Myb binding site of the human ApoJ/lusterin promoter bound to GST/B- MYB, but not to GST alone (Fig.  6,  lanes 1 and  2).	bind
38986	2	9063	5	13	NULL	NULL	NULL	statement 1	GP		bind					CAM kinase II	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_20_0_253_s_636	11861604	A 33 amino acid  fragment containing residues of the juxta-membrane portion of the cytoplasmic region  of CD5 bound to CAM kinase II .	bind
47993	1	9063	5	13	NULL	NULL	NULL	33 amino acid fragment	GP		contains					CD5	GP		residues of  juxta-membrane portion of the cytoplasmic region 		NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_20_0_253_s_636	11861604	A 33 amino acid  fragment containing residues of the juxta-membrane portion of the cytoplasmic region  of CD5 bound to CAM kinase II .	bind
30877	2	9063	6	10	NULL	0	NULL	statement 1	NULL		bind	NULL				CAM kinase II	NULL				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_20_0_253_s_636	11861604	A 33 amino acid  fragment containing residues of the juxta-membrane portion of the cytoplasmic region  of CD5 bound to CAM kinase II .	bind
47994	1	9063	6	10	NULL	0	NULL	33 amino acid fragment	NULL		contains	NULL				CD5	NULL		residues of the juxta-membrane portion of the cytoplasmic region		NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_20_0_253_s_636	11861604	A 33 amino acid  fragment containing residues of the juxta-membrane portion of the cytoplasmic region  of CD5 bound to CAM kinase II .	bind
38987	1	9064	5	13	NULL	NULL	NULL				encode				exon 1	35-amino-acid-long presequence	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1592_1_63_s_263	12191769	A 35-amino-acid-long presequence is encoded by exon 1, and the entire metal-binding domain by exon 13.	bind
38988	2	9064	5	10	NULL	0	NULL				encode				exon 13				entire metal-binding domain		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1592_1_63_s_263	12191769	A 35-amino-acid-long presequence is encoded by exon 1, and the entire metal-binding domain by exon 13.	bind
31091	1	9064	6	10	NULL	0	NULL	exon 13			encodes								metal-binding domain		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1592_1_63_s_263	12191769	A 35-amino-acid-long presequence is encoded by exon 1, and the entire metal-binding domain by exon 13.	bind
31092	2	9064	6	NULL	NULL	0	NULL	exon 1	NULL		encodes	NULL				35-amino-acid-long presequence	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1592_1_63_s_263	12191769	A 35-amino-acid-long presequence is encoded by exon 1, and the entire metal-binding domain by exon 13.	bind
38989	1	9065	5	13	NULL	NULL	NULL	CIITA	GP		inhibit		effectively	36-amino-acid region of 		CBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_42_26562_s_307	9334236	A 36-Amino-Acid Region of CIITA Is an Effective Inhibitor of CBP: Novel Mechanism of Gamma Interferon-Mediated Suppression of Collagen {alpha}2	bind
38990	2	9065	5	13	NULL	NULL	NULL	Gamma Interferon	GP		mediate					Collagen {alpha}2	GP	suppression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_42_26562_s_307	9334236	A 36-Amino-Acid Region of CIITA Is an Effective Inhibitor of CBP: Novel Mechanism of Gamma Interferon-Mediated Suppression of Collagen {alpha}2	bind
30879	1	9065	6	NULL	NULL	0	NULL	Gamma Interferon	NULL		mediates	NULL				Collagen (alpha)2	NULL	suppression of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_42_26562_s_307	9334236	A 36-Amino-Acid Region of CIITA Is an Effective Inhibitor of CBP: Novel Mechanism of Gamma Interferon-Mediated Suppression of Collagen {alpha}2	bind
30880	2	9065	6	10	NULL	0	NULL	CIITA			inhibits		effectively	36 amino-acid region		CBP					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_42_26562_s_307	9334236	A 36-Amino-Acid Region of CIITA Is an Effective Inhibitor of CBP: Novel Mechanism of Gamma Interferon-Mediated Suppression of Collagen {alpha}2	bind
38991	1	9066	5	13	NULL	NULL	NULL				is purified from			36-kDa N-terminal fragment		liver nuclei	CellComponent	rabbit			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_49_31191_s_31	8940119	A 36-kDa N-terminal fragment was purified from rabbit liver nuclei that could bind GTP, suggesting that the N terminus of tTG plays an important role in nucleotide binding ( 17).	bind
38992	2	9066	5	13	NULL	NULL	NULL	tTG	GP		plays a role in			N terminus		nucleotide	NucleicAcid	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_49_31191_s_31	8940119	A 36-kDa N-terminal fragment was purified from rabbit liver nuclei that could bind GTP, suggesting that the N terminus of tTG plays an important role in nucleotide binding ( 17).	bind
38993	3	9066	5	13	NULL	NULL	NULL	statement 1	Process		suggest					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_49_31191_s_31	8940119	A 36-kDa N-terminal fragment was purified from rabbit liver nuclei that could bind GTP, suggesting that the N terminus of tTG plays an important role in nucleotide binding ( 17).	bind
47995	4	9066	5	13	NULL	NULL	NULL	statement 1	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_49_31191_s_31	8940119	A 36-kDa N-terminal fragment was purified from rabbit liver nuclei that could bind GTP, suggesting that the N terminus of tTG plays an important role in nucleotide binding ( 17).	bind
30881	1	9066	6	NULL	NULL	0	NULL	tTG	NULL		plays an important role in	NULL		N terminus		nucleotide	NULL	binding of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_49_31191_s_31	8940119	A 36-kDa N-terminal fragment was purified from rabbit liver nuclei that could bind GTP, suggesting that the N terminus of tTG plays an important role in nucleotide binding ( 17).	bind
30882	2	9066	6	NULL	NULL	0	NULL	36-kDa	NULL		is purified from	NULL		N-terminal fragment		liver nuclei	NULL	rabbit			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_49_31191_s_31	8940119	A 36-kDa N-terminal fragment was purified from rabbit liver nuclei that could bind GTP, suggesting that the N terminus of tTG plays an important role in nucleotide binding ( 17).	bind
30883	3	9066	6	NULL	NULL	0	NULL	statement 2	NULL		bind	NULL				GTP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_49_31191_s_31	8940119	A 36-kDa N-terminal fragment was purified from rabbit liver nuclei that could bind GTP, suggesting that the N terminus of tTG plays an important role in nucleotide binding ( 17).	bind
30884	4	9066	6	NULL	NULL	0	NULL	statement 3	NULL		suggests	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_49_31191_s_31	8940119	A 36-kDa N-terminal fragment was purified from rabbit liver nuclei that could bind GTP, suggesting that the N terminus of tTG plays an important role in nucleotide binding ( 17).	bind
39527	1	9067	5	13	NULL	NULL	NULL	Mrb-sat23 oligonucleotide	NucleicAcid		contains				38-bp segment			M. rufogriseus		17-bp CENP-B box 	NULL		NULL	NULL	NULL	NULL	gw70_genetics_172_2_1129_s_119	16387881	A 38-bp segment of the Mrb-sat23 oligonucleotide containing the 17-bp  M. rufogriseus CENP-B box ( Figure 1) bound selectively to  M. rufogriseus nuclear protein and shifted upon the addition of human anti-CENP-B (rabbit) antibody ( Figure 4A).	bind
39528	2	9067	5	13	NULL	NULL	NULL	statement 1	NucleicAcid		bind		selectively			nuclear protein	GP	M. rufogriseus			NULL		NULL	NULL	NULL	NULL	gw70_genetics_172_2_1129_s_119	16387881	A 38-bp segment of the Mrb-sat23 oligonucleotide containing the 17-bp  M. rufogriseus CENP-B box ( Figure 1) bound selectively to  M. rufogriseus nuclear protein and shifted upon the addition of human anti-CENP-B (rabbit) antibody ( Figure 4A).	bind
30956	2	9067	6	10	NULL	0	NULL	statement 1	NULL		bind	NULL	selectively			nuclear protein	NULL	M. rufogriseus			NULL		NULL	NULL	NULL	NULL	gw70_genetics_172_2_1129_s_119	16387881	A 38-bp segment of the Mrb-sat23 oligonucleotide containing the 17-bp  M. rufogriseus CENP-B box ( Figure 1) bound selectively to  M. rufogriseus nuclear protein and shifted upon the addition of human anti-CENP-B (rabbit) antibody ( Figure 4A).	bind
31012	1	9067	6	10	NULL	0	NULL	Mrb-sat23 oligonucleotide	NULL		contains	NULL			38-bp segment		NULL	M. rufogriseus		17-bp CENP-B box	NULL		NULL	NULL	NULL	NULL	gw70_genetics_172_2_1129_s_119	16387881	A 38-bp segment of the Mrb-sat23 oligonucleotide containing the 17-bp  M. rufogriseus CENP-B box ( Figure 1) bound selectively to  M. rufogriseus nuclear protein and shifted upon the addition of human anti-CENP-B (rabbit) antibody ( Figure 4A).	bind
38994	2	9068	5	13	NULL	NULL	NULL	statement 1	GP		bind					CD40	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_105_3_301_s_372	10675356	A 39 kDa protein on activated helper T cells binds CD40 and transduces signals to cognate activation of B cells.	bind
38995	3	9068	5	13	NULL	NULL	NULL	statement 2	Process		transduce signal to					B cells	Cell	cognate activation of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_105_3_301_s_372	10675356	A 39 kDa protein on activated helper T cells binds CD40 and transduces signals to cognate activation of B cells.	bind
47996	1	9068	5	13	NULL	NULL	NULL	39 kDa protein	GP		localized on					helper T cells	Cell	activated			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_105_3_301_s_372	10675356	A 39 kDa protein on activated helper T cells binds CD40 and transduces signals to cognate activation of B cells.	bind
31016	1	9068	6	NULL	NULL	0	NULL	39 kDa protein	NULL		is localized on	NULL				helper T cells	NULL	activated			NULL		0	NULL	NULL	NULL	gw60_jclininvest_105_3_301_s_372	10675356	A 39 kDa protein on activated helper T cells binds CD40 and transduces signals to cognate activation of B cells.	bind
31017	2	9068	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				CD40	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_105_3_301_s_372	10675356	A 39 kDa protein on activated helper T cells binds CD40 and transduces signals to cognate activation of B cells.	bind
31018	3	9068	6	10	NULL	0	NULL	statement 2	NULL		 transduce signals to	NULL				B cells 	NULL	 cognate activation of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_105_3_301_s_372	10675356	A 39 kDa protein on activated helper T cells binds CD40 and transduces signals to cognate activation of B cells.	bind
38996	1	9072	5	13	NULL	NULL	NULL	RAP	GP		is					receptor-associated protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_16_9543_s_20	7721883	A 39-kDa protein, termed the  receptor-associated protein (RAP) binds to LRP  ( 21) , gp330  ( 22) , and the VLDL receptor   ( 23) with high affinity,  and to the LDL receptor with weaker affinity  ( 24) .	bind
38997	2	9072	5	13	NULL	NULL	NULL	RAP	GP		is a type of					39-kDa protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_16_9543_s_20	7721883	A 39-kDa protein, termed the  receptor-associated protein (RAP) binds to LRP  ( 21) , gp330  ( 22) , and the VLDL receptor   ( 23) with high affinity,  and to the LDL receptor with weaker affinity  ( 24) .	bind
38998	3	9072	5	13	NULL	NULL	NULL	RAP	GP		bind		high affinity			LRP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_16_9543_s_20	7721883	A 39-kDa protein, termed the  receptor-associated protein (RAP) binds to LRP  ( 21) , gp330  ( 22) , and the VLDL receptor   ( 23) with high affinity,  and to the LDL receptor with weaker affinity  ( 24) .	bind
38999	4	9072	5	13	NULL	NULL	NULL	RAP	GP		bind		high affinity			gp330	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_16_9543_s_20	7721883	A 39-kDa protein, termed the  receptor-associated protein (RAP) binds to LRP  ( 21) , gp330  ( 22) , and the VLDL receptor   ( 23) with high affinity,  and to the LDL receptor with weaker affinity  ( 24) .	bind
39000	5	9072	5	13	NULL	NULL	NULL	RAP	GP		bind		high affinity			VLDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_16_9543_s_20	7721883	A 39-kDa protein, termed the  receptor-associated protein (RAP) binds to LRP  ( 21) , gp330  ( 22) , and the VLDL receptor   ( 23) with high affinity,  and to the LDL receptor with weaker affinity  ( 24) .	bind
39001	6	9072	5	13	NULL	NULL	NULL	RAP	GP		bind		weak affinity			LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_16_9543_s_20	7721883	A 39-kDa protein, termed the  receptor-associated protein (RAP) binds to LRP  ( 21) , gp330  ( 22) , and the VLDL receptor   ( 23) with high affinity,  and to the LDL receptor with weaker affinity  ( 24) .	bind
31019	1	9072	6	NULL	NULL	0	NULL	RAP	NULL		bind	NULL	high affinity			LRP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_16_9543_s_20	7721883	A 39-kDa protein, termed the  receptor-associated protein (RAP) binds to LRP  ( 21) , gp330  ( 22) , and the VLDL receptor   ( 23) with high affinity,  and to the LDL receptor with weaker affinity  ( 24) .	bind
31020	2	9072	6	NULL	NULL	0	NULL	RAP	NULL		is	NULL				receptor-associated protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_16_9543_s_20	7721883	A 39-kDa protein, termed the  receptor-associated protein (RAP) binds to LRP  ( 21) , gp330  ( 22) , and the VLDL receptor   ( 23) with high affinity,  and to the LDL receptor with weaker affinity  ( 24) .	bind
31021	3	9072	6	10	NULL	0	NULL	RAP	NULL		is a type of	NULL				39-kDa protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_16_9543_s_20	7721883	A 39-kDa protein, termed the  receptor-associated protein (RAP) binds to LRP  ( 21) , gp330  ( 22) , and the VLDL receptor   ( 23) with high affinity,  and to the LDL receptor with weaker affinity  ( 24) .	bind
31022	4	9072	6	NULL	NULL	0	NULL	RAP	NULL		bind	NULL	high affinity			gp330	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_16_9543_s_20	7721883	A 39-kDa protein, termed the  receptor-associated protein (RAP) binds to LRP  ( 21) , gp330  ( 22) , and the VLDL receptor   ( 23) with high affinity,  and to the LDL receptor with weaker affinity  ( 24) .	bind
31023	5	9072	6	NULL	NULL	0	NULL	RAP	NULL		bind	NULL	high affinity			VLDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_16_9543_s_20	7721883	A 39-kDa protein, termed the  receptor-associated protein (RAP) binds to LRP  ( 21) , gp330  ( 22) , and the VLDL receptor   ( 23) with high affinity,  and to the LDL receptor with weaker affinity  ( 24) .	bind
31024	6	9072	6	NULL	NULL	0	NULL	RAP	NULL		bind	NULL	weak affinity			LDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_16_9543_s_20	7721883	A 39-kDa protein, termed the  receptor-associated protein (RAP) binds to LRP  ( 21) , gp330  ( 22) , and the VLDL receptor   ( 23) with high affinity,  and to the LDL receptor with weaker affinity  ( 24) .	bind
39002	1	9073	5	13	NULL	NULL	NULL	RAP	GP		is a type of					39-kDa receptor-associated protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_44	10608826	A 39-kDa receptor-associated protein (RAP) binds to LRP with high affinity ( K d = 4 nM ( 27)) and inhibits binding and LRP-mediated internalization and degradation of all ligands ( 30,  33), therefore serving as a useful tool for testing whether LRP is involved in endocytosis of a given ligand.	bind
39003	2	9073	5	13	NULL	NULL	NULL	RAP	GP		bind		high affinity			LRP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_44	10608826	A 39-kDa receptor-associated protein (RAP) binds to LRP with high affinity ( K d = 4 nM ( 27)) and inhibits binding and LRP-mediated internalization and degradation of all ligands ( 30,  33), therefore serving as a useful tool for testing whether LRP is involved in endocytosis of a given ligand.	bind
39004	3	9073	5	13	NULL	NULL	NULL	statement 2	Process		inhibit					ligand	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_44	10608826	A 39-kDa receptor-associated protein (RAP) binds to LRP with high affinity ( K d = 4 nM ( 27)) and inhibits binding and LRP-mediated internalization and degradation of all ligands ( 30,  33), therefore serving as a useful tool for testing whether LRP is involved in endocytosis of a given ligand.	bind
39005	4	9073	5	13	NULL	NULL	NULL	LRP	GP		mediate					ligand	GP	internalization of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_44	10608826	A 39-kDa receptor-associated protein (RAP) binds to LRP with high affinity ( K d = 4 nM ( 27)) and inhibits binding and LRP-mediated internalization and degradation of all ligands ( 30,  33), therefore serving as a useful tool for testing whether LRP is involved in endocytosis of a given ligand.	bind
39006	5	9073	5	13	NULL	NULL	NULL	LRP	GP		mediate					ligand	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_44	10608826	A 39-kDa receptor-associated protein (RAP) binds to LRP with high affinity ( K d = 4 nM ( 27)) and inhibits binding and LRP-mediated internalization and degradation of all ligands ( 30,  33), therefore serving as a useful tool for testing whether LRP is involved in endocytosis of a given ligand.	bind
39007	6	9073	5	13	NULL	NULL	NULL	statement 2	Process		inhibit					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_44	10608826	A 39-kDa receptor-associated protein (RAP) binds to LRP with high affinity ( K d = 4 nM ( 27)) and inhibits binding and LRP-mediated internalization and degradation of all ligands ( 30,  33), therefore serving as a useful tool for testing whether LRP is involved in endocytosis of a given ligand.	bind
39008	7	9073	5	13	NULL	NULL	NULL	statement 2	Process		inhibit					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_44	10608826	A 39-kDa receptor-associated protein (RAP) binds to LRP with high affinity ( K d = 4 nM ( 27)) and inhibits binding and LRP-mediated internalization and degradation of all ligands ( 30,  33), therefore serving as a useful tool for testing whether LRP is involved in endocytosis of a given ligand.	bind
47997	8	9073	5	13	NULL	NULL	NULL	RAP	GP		is					receptor-associated protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_44	10608826	A 39-kDa receptor-associated protein (RAP) binds to LRP with high affinity ( K d = 4 nM ( 27)) and inhibits binding and LRP-mediated internalization and degradation of all ligands ( 30,  33), therefore serving as a useful tool for testing whether LRP is involved in endocytosis of a given ligand.	bind
31025	1	9073	6	NULL	NULL	0	NULL	RAP	NULL		bind	NULL	high affinity			LRP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_44	10608826	A 39-kDa receptor-associated protein (RAP) binds to LRP with high affinity ( K d = 4 nM ( 27)) and inhibits binding and LRP-mediated internalization and degradation of all ligands ( 30,  33), therefore serving as a useful tool for testing whether LRP is involved in endocytosis of a given ligand.	bind
31026	2	9073	6	NULL	NULL	0	NULL	RAP	NULL		is	NULL				receptor-associated protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_44	10608826	A 39-kDa receptor-associated protein (RAP) binds to LRP with high affinity ( K d = 4 nM ( 27)) and inhibits binding and LRP-mediated internalization and degradation of all ligands ( 30,  33), therefore serving as a useful tool for testing whether LRP is involved in endocytosis of a given ligand.	bind
31027	3	9073	6	10	NULL	0	NULL	RAP	NULL		is a type of	NULL				39-kDa protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_44	10608826	A 39-kDa receptor-associated protein (RAP) binds to LRP with high affinity ( K d = 4 nM ( 27)) and inhibits binding and LRP-mediated internalization and degradation of all ligands ( 30,  33), therefore serving as a useful tool for testing whether LRP is involved in endocytosis of a given ligand.	bind
31028	4	9073	6	NULL	NULL	0	NULL	LRP	NULL		mediates	NULL				ligands	NULL	internalization of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_44	10608826	A 39-kDa receptor-associated protein (RAP) binds to LRP with high affinity ( K d = 4 nM ( 27)) and inhibits binding and LRP-mediated internalization and degradation of all ligands ( 30,  33), therefore serving as a useful tool for testing whether LRP is involved in endocytosis of a given ligand.	bind
31029	5	9073	6	NULL	NULL	0	NULL	LRP	NULL		mediates	NULL				ligands	NULL	degradation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_44	10608826	A 39-kDa receptor-associated protein (RAP) binds to LRP with high affinity ( K d = 4 nM ( 27)) and inhibits binding and LRP-mediated internalization and degradation of all ligands ( 30,  33), therefore serving as a useful tool for testing whether LRP is involved in endocytosis of a given ligand.	bind
31030	6	9073	6	NULL	NULL	0	NULL	RAP	NULL		inhibits	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_44	10608826	A 39-kDa receptor-associated protein (RAP) binds to LRP with high affinity ( K d = 4 nM ( 27)) and inhibits binding and LRP-mediated internalization and degradation of all ligands ( 30,  33), therefore serving as a useful tool for testing whether LRP is involved in endocytosis of a given ligand.	bind
31031	7	9073	6	NULL	NULL	0	NULL	RAP	NULL		inhibits	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_44	10608826	A 39-kDa receptor-associated protein (RAP) binds to LRP with high affinity ( K d = 4 nM ( 27)) and inhibits binding and LRP-mediated internalization and degradation of all ligands ( 30,  33), therefore serving as a useful tool for testing whether LRP is involved in endocytosis of a given ligand.	bind
31032	8	9073	6	NULL	NULL	0	NULL	RAP	NULL		inhibits	NULL				ligands	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_53_37685_s_44	10608826	A 39-kDa receptor-associated protein (RAP) binds to LRP with high affinity ( K d = 4 nM ( 27)) and inhibits binding and LRP-mediated internalization and degradation of all ligands ( 30,  33), therefore serving as a useful tool for testing whether LRP is involved in endocytosis of a given ligand.	bind
39010	1	9076	5	13	NULL	NULL	NULL	LPL	GP		bind					ECM	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1329_s_100	8576120	A 4-fold excess of Cu-OxLDL was also able to  abolish the interaction of  I-LDL (12.5 mug/ml) with  LPL bound to the ECM ( Fig. 5).	bind
39011	2	9076	5	13	NULL	NULL	NULL	I-LDL	GP		interact with					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1329_s_100	8576120	A 4-fold excess of Cu-OxLDL was also able to  abolish the interaction of  I-LDL (12.5 mug/ml) with  LPL bound to the ECM ( Fig. 5).	bind
39012	3	9076	5	13	NULL	NULL	NULL	Cu-OxLDL	GP	excess	abolishes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1329_s_100	8576120	A 4-fold excess of Cu-OxLDL was also able to  abolish the interaction of  I-LDL (12.5 mug/ml) with  LPL bound to the ECM ( Fig. 5).	bind
31033	1	9076	6	NULL	NULL	0	NULL	LPL	NULL		bind	NULL				ECM	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_3_1329_s_100	8576120	A 4-fold excess of Cu-OxLDL was also able to  abolish the interaction of  I-LDL (12.5 mug/ml) with  LPL bound to the ECM ( Fig. 5).	bind
31034	2	9076	6	NULL	NULL	0	NULL	I-LDL	NULL		interacts with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_3_1329_s_100	8576120	A 4-fold excess of Cu-OxLDL was also able to  abolish the interaction of  I-LDL (12.5 mug/ml) with  LPL bound to the ECM ( Fig. 5).	bind
31035	3	9076	6	NULL	NULL	0	NULL	Cu-OxLDL	NULL	excess of	abolish	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_3_1329_s_100	8576120	A 4-fold excess of Cu-OxLDL was also able to  abolish the interaction of  I-LDL (12.5 mug/ml) with  LPL bound to the ECM ( Fig. 5).	bind
39013	1	9077	5	13	NULL	NULL	NULL	T cells	Cell	activated	bind					CHO-B7h cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_immunity_11_4_423_s_135	10549624	A 4-fold greater number of activated T cells bound to CHO-B7h cells over CHO-GFP cells (  Figure 4C).	bind
39014	2	9077	5	13	NULL	NULL	NULL	T cells	Cell	activated	bind					CHO-GFP cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_immunity_11_4_423_s_135	10549624	A 4-fold greater number of activated T cells bound to CHO-B7h cells over CHO-GFP cells (  Figure 4C).	bind
39015	3	9077	5	13	NULL	NULL	NULL	statement 1	Process		greater than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_11_4_423_s_135	10549624	A 4-fold greater number of activated T cells bound to CHO-B7h cells over CHO-GFP cells (  Figure 4C).	bind
31036	1	9077	6	NULL	NULL	0	NULL	T cells	NULL	activated	bind	NULL				CHO-B7h cells	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_11_4_423_s_135	10549624	A 4-fold greater number of activated T cells bound to CHO-B7h cells over CHO-GFP cells (  Figure 4C).	bind
31039	2	9077	6	NULL	NULL	0	NULL	T cells	NULL	activated	bind	NULL				CHO-GFP cells	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_11_4_423_s_135	10549624	A 4-fold greater number of activated T cells bound to CHO-B7h cells over CHO-GFP cells (  Figure 4C).	bind
31041	3	9077	6	10	NULL	0	NULL	statement 1	NULL	affinity of	is more than	NULL				statement 2	NULL	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_11_4_423_s_135	10549624	A 4-fold greater number of activated T cells bound to CHO-B7h cells over CHO-GFP cells (  Figure 4C).	bind
39016	1	9078	5	13	NULL	NULL	NULL	AP2	GP		bind					VEGF	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24602_s_200	16790435	A 4-fold induction of AP2 binding to the VEGF promoter region was observed following PGE2 treatment, whereas PGE2 doubled the binding of Sp1 to the VEGF promoter.	bind
39017	2	9078	5	13	NULL	NULL	NULL	PGE2	Chemical		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24602_s_200	16790435	A 4-fold induction of AP2 binding to the VEGF promoter region was observed following PGE2 treatment, whereas PGE2 doubled the binding of Sp1 to the VEGF promoter.	bind
39018	3	9078	5	13	NULL	NULL	NULL	Sp1	GP		bind					VEGF	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24602_s_200	16790435	A 4-fold induction of AP2 binding to the VEGF promoter region was observed following PGE2 treatment, whereas PGE2 doubled the binding of Sp1 to the VEGF promoter.	bind
39019	4	9078	5	13	NULL	NULL	NULL	PGE2	Chemical		increase					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24602_s_200	16790435	A 4-fold induction of AP2 binding to the VEGF promoter region was observed following PGE2 treatment, whereas PGE2 doubled the binding of Sp1 to the VEGF promoter.	bind
57761	5	9078	5	13	NULL	NULL	NULL	statement 2	Process	induction of	is higher than					statement 4	Process	induction of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24602_s_200	16790435	A 4-fold induction of AP2 binding to the VEGF promoter region was observed following PGE2 treatment, whereas PGE2 doubled the binding of Sp1 to the VEGF promoter.	bind
31042	1	9078	6	NULL	NULL	0	NULL	AP2	NULL		bind	NULL				VEGF	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24602_s_200	16790435	A 4-fold induction of AP2 binding to the VEGF promoter region was observed following PGE2 treatment, whereas PGE2 doubled the binding of Sp1 to the VEGF promoter.	bind
31043	2	9078	6	NULL	NULL	0	NULL	PGE2	NULL		induces	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24602_s_200	16790435	A 4-fold induction of AP2 binding to the VEGF promoter region was observed following PGE2 treatment, whereas PGE2 doubled the binding of Sp1 to the VEGF promoter.	bind
31045	3	9078	6	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				VEGF	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24602_s_200	16790435	A 4-fold induction of AP2 binding to the VEGF promoter region was observed following PGE2 treatment, whereas PGE2 doubled the binding of Sp1 to the VEGF promoter.	bind
31046	4	9078	6	NULL	NULL	0	NULL	PGE2	NULL		induces	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24602_s_200	16790435	A 4-fold induction of AP2 binding to the VEGF promoter region was observed following PGE2 treatment, whereas PGE2 doubled the binding of Sp1 to the VEGF promoter.	bind
31151	5	9078	6	10	NULL	0	NULL	statement 2		induction of	is higher than					statement 4		induction of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24602_s_200	16790435	A 4-fold induction of AP2 binding to the VEGF promoter region was observed following PGE2 treatment, whereas PGE2 doubled the binding of Sp1 to the VEGF promoter.	bind
39167	1	9080	5	13	NULL	NULL	NULL	NE proteins	GP		bind				A3 Enhancer	A3 RNA	NucleicAcid	biotinylated			NULL		NULL	NULL	NULL	NULL	gw60_cell_93_1_139_s_50	9546399	A 40 kDa SR Protein  Binds Specifically to the A3 Enhancer NE proteins bound to biotinylated A3 (lane  1) or S3 (lane 2) RNA were resolved by 9% SDS/PAGE and analyzed by Western  blot with mAb104.	bind
47998	5	9080	5	13	NULL	NULL	NULL	SR protein	GP		bind		specifically			statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_93_1_139_s_50	9546399	A 40 kDa SR Protein  Binds Specifically to the A3 Enhancer NE proteins bound to biotinylated A3 (lane  1) or S3 (lane 2) RNA were resolved by 9% SDS/PAGE and analyzed by Western  blot with mAb104.	bind
47999	2	9080	5	13	NULL	NULL	NULL	NE proteins	GP		bind				A3 Enhancer	S3 RNA	NucleicAcid	biotinylated			NULL		NULL	NULL	NULL	NULL	gw60_cell_93_1_139_s_50	9546399	A 40 kDa SR Protein  Binds Specifically to the A3 Enhancer NE proteins bound to biotinylated A3 (lane  1) or S3 (lane 2) RNA were resolved by 9% SDS/PAGE and analyzed by Western  blot with mAb104.	bind
48000	3	9080	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_93_1_139_s_50	9546399	A 40 kDa SR Protein  Binds Specifically to the A3 Enhancer NE proteins bound to biotinylated A3 (lane  1) or S3 (lane 2) RNA were resolved by 9% SDS/PAGE and analyzed by Western  blot with mAb104.	bind
48001	4	9080	5	13	NULL	NULL	NULL	SR protein	GP		is a type of					40 kDa protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_93_1_139_s_50	9546399	A 40 kDa SR Protein  Binds Specifically to the A3 Enhancer NE proteins bound to biotinylated A3 (lane  1) or S3 (lane 2) RNA were resolved by 9% SDS/PAGE and analyzed by Western  blot with mAb104.	bind
48002	6	9080	5	13	NULL	NULL	NULL	SR protein	GP		bind		specifically			statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_93_1_139_s_50	9546399	A 40 kDa SR Protein  Binds Specifically to the A3 Enhancer NE proteins bound to biotinylated A3 (lane  1) or S3 (lane 2) RNA were resolved by 9% SDS/PAGE and analyzed by Western  blot with mAb104.	bind
31072	1	9080	6	10	NULL	0	NULL	SR protein	NULL		is a type of	NULL				40 kDa protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_93_1_139_s_50	9546399	A 40 kDa SR Protein  Binds Specifically to the A3 Enhancer NE proteins bound to biotinylated A3 (lane  1) or S3 (lane 2) RNA were resolved by 9% SDS/PAGE and analyzed by Western  blot with mAb104.	bind
31074	2	9080	6	NULL	NULL	0	NULL	A3 NE proteins	NULL		bind	NULL			enhancer	A3 RNA	NULL	biotinylated			NULL		NULL	NULL	NULL	NULL	gw60_cell_93_1_139_s_50	9546399	A 40 kDa SR Protein  Binds Specifically to the A3 Enhancer NE proteins bound to biotinylated A3 (lane  1) or S3 (lane 2) RNA were resolved by 9% SDS/PAGE and analyzed by Western  blot with mAb104.	bind
31077	3	9080	6	NULL	NULL	0	NULL	A3 NE proteins	NULL		bind	NULL			enhancer	S3 RNA	NULL	biotinylated			NULL		0	NULL	NULL	NULL	gw60_cell_93_1_139_s_50	9546399	A 40 kDa SR Protein  Binds Specifically to the A3 Enhancer NE proteins bound to biotinylated A3 (lane  1) or S3 (lane 2) RNA were resolved by 9% SDS/PAGE and analyzed by Western  blot with mAb104.	bind
31078	4	9080	6	NULL	NULL	0	NULL	statement 2	NULL		is an alternative to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_93_1_139_s_50	9546399	A 40 kDa SR Protein  Binds Specifically to the A3 Enhancer NE proteins bound to biotinylated A3 (lane  1) or S3 (lane 2) RNA were resolved by 9% SDS/PAGE and analyzed by Western  blot with mAb104.	bind
31080	5	9080	6	NULL	NULL	0	NULL	SR protein	NULL		bind	NULL	specifically			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_93_1_139_s_50	9546399	A 40 kDa SR Protein  Binds Specifically to the A3 Enhancer NE proteins bound to biotinylated A3 (lane  1) or S3 (lane 2) RNA were resolved by 9% SDS/PAGE and analyzed by Western  blot with mAb104.	bind
31081	6	9080	6	NULL	NULL	0	NULL	SR protein	NULL		bind	NULL	specifically			statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_93_1_139_s_50	9546399	A 40 kDa SR Protein  Binds Specifically to the A3 Enhancer NE proteins bound to biotinylated A3 (lane  1) or S3 (lane 2) RNA were resolved by 9% SDS/PAGE and analyzed by Western  blot with mAb104.	bind
39166	1	9081	5	13	NULL	NULL	NULL	cytochrome aa3	GP		bind					40-kDa carbon monoxide	Chemical				NULL	Halobacterium halobium membranes	NULL	NULL	NULL	NULL	gw60_jbacteriol_184_3_840_s_151	11790755	A 40-kDa carbon monoxide binding cytochrome  aa3 was previously purified from  Halobacterium halobium membranes.	bind
31183	1	9081	6	10	NULL	0	NULL	cytochrome aa3	NULL		bind	NULL				40-kDa carbon monoxide	NULL				NULL	Halobacterium halobium membranes	NULL	NULL	NULL	NULL	gw60_jbacteriol_184_3_840_s_151	11790755	A 40-kDa carbon monoxide binding cytochrome  aa3 was previously purified from  Halobacterium halobium membranes.	bind
39171	1	9083	5	13	NULL	NULL	NULL	GABA	GP		saturate								GABA binding sites		NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_23_9083_s_167	11717341	A 400 msec pulse of 1 mM GABA presumably saturated all of the GABA binding sites.	bind
31184	1	9083	6	10	NULL	0	NULL	GABA	NULL		saturate	NULL					NULL		GABA binding sites		NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_23_9083_s_167	11717341	A 400 msec pulse of 1 mM GABA presumably saturated all of the GABA binding sites.	bind
39172	1	9084	5	13	NULL	NULL	NULL	importin alpha	GP		bind			41 amino acid motif		importin beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_2_255_s_469	10209022	A 41 amino  acid motif in importin alpha confers binding to importin beta and hence  transit into the nucleus.	bind
39173	2	9084	5	13	NULL	NULL	NULL	statement 1	Process		transit into					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_2_255_s_469	10209022	A 41 amino  acid motif in importin alpha confers binding to importin beta and hence  transit into the nucleus.	bind
57762	3	9084	5	13	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_2_255_s_469	10209022	A 41 amino  acid motif in importin alpha confers binding to importin beta and hence  transit into the nucleus.	bind
31185	1	9084	6	NULL	NULL	0	NULL	importin alpha	NULL		bind	NULL		41 amino acid		importin beta	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_2_255_s_469	10209022	A 41 amino  acid motif in importin alpha confers binding to importin beta and hence  transit into the nucleus.	bind
31186	2	9084	6	NULL	NULL	0	NULL	importin alpha	NULL		transits into	NULL				nucleus	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_2_255_s_469	10209022	A 41 amino  acid motif in importin alpha confers binding to importin beta and hence  transit into the nucleus.	bind
31187	3	9084	6	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_2_255_s_469	10209022	A 41 amino  acid motif in importin alpha confers binding to importin beta and hence  transit into the nucleus.	bind
39174	1	9089	5	13	NULL	NULL	NULL	importin	GP		bind			41 amino acid motif		importin beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_86_6_985_s_346	8808633	A 41 amino acid motif in importin   confers binding to importin beta and hence transit into the nucleus.	bind
39175	2	9089	5	13	NULL	NULL	NULL	statement 1	Process		transit into					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_86_6_985_s_346	8808633	A 41 amino acid motif in importin   confers binding to importin beta and hence transit into the nucleus.	bind
57763	3	9089	5	13	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_86_6_985_s_346	8808633	A 41 amino acid motif in importin   confers binding to importin beta and hence transit into the nucleus.	bind
31188	1	9089	6	NULL	NULL	0	NULL	importin	NULL		bind	NULL		41 amino acid motif		importin beta	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_86_6_985_s_346	8808633	A 41 amino acid motif in importin   confers binding to importin beta and hence transit into the nucleus.	bind
31189	2	9089	6	NULL	NULL	0	NULL	importin	NULL		transits into	NULL				nucleus	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_86_6_985_s_346	8808633	A 41 amino acid motif in importin   confers binding to importin beta and hence transit into the nucleus.	bind
31190	3	9089	6	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_86_6_985_s_346	8808633	A 41 amino acid motif in importin   confers binding to importin beta and hence transit into the nucleus.	bind
39176	1	9097	5	13	NULL	NULL	NULL	45-kDa protein	GP	yeast	is a homolog of			N-terminal		CyP-40	GP	mammalian			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20479_s_28	7657624	A 45-kDa yeast protein with N-terminal  homology to mammalian CyP-40 has been isolated in a multiprotein  complex with the yeast homolog of hsp90 ( 27) , and incubation  of a variety of tissue homogenates with a CyP-40/GST-fusion protein  bound to glutathione-agarose resulted in retention of hsp90,   suggesting that CyP-40 also binds directly to hsp90.	bind
39177	2	9097	5	13	NULL	NULL	NULL	statement 1	GP		is in complex with					 hsp90	GP	yeast homolog of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20479_s_28	7657624	A 45-kDa yeast protein with N-terminal  homology to mammalian CyP-40 has been isolated in a multiprotein  complex with the yeast homolog of hsp90 ( 27) , and incubation  of a variety of tissue homogenates with a CyP-40/GST-fusion protein  bound to glutathione-agarose resulted in retention of hsp90,   suggesting that CyP-40 also binds directly to hsp90.	bind
39178	3	9097	5	13	NULL	NULL	NULL	CyP-40	GP		bind		directly			hsp90	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20479_s_28	7657624	A 45-kDa yeast protein with N-terminal  homology to mammalian CyP-40 has been isolated in a multiprotein  complex with the yeast homolog of hsp90 ( 27) , and incubation  of a variety of tissue homogenates with a CyP-40/GST-fusion protein  bound to glutathione-agarose resulted in retention of hsp90,   suggesting that CyP-40 also binds directly to hsp90.	bind
32022	1	9097	6	NULL	NULL	0	NULL	CyP-40	NULL		bind	NULL	directly			hsp90	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20479_s_28	7657624	A 45-kDa yeast protein with N-terminal  homology to mammalian CyP-40 has been isolated in a multiprotein  complex with the yeast homolog of hsp90 ( 27) , and incubation  of a variety of tissue homogenates with a CyP-40/GST-fusion protein  bound to glutathione-agarose resulted in retention of hsp90,   suggesting that CyP-40 also binds directly to hsp90.	bind
48003	2	9097	6	10	NULL	0	NULL	 45-kDa protein	NULL	yeast	is a homolog of	NULL		N-terminal		CyP-40	NULL	mammalian			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20479_s_28	7657624	A 45-kDa yeast protein with N-terminal  homology to mammalian CyP-40 has been isolated in a multiprotein  complex with the yeast homolog of hsp90 ( 27) , and incubation  of a variety of tissue homogenates with a CyP-40/GST-fusion protein  bound to glutathione-agarose resulted in retention of hsp90,   suggesting that CyP-40 also binds directly to hsp90.	bind
57764	3	9097	6	10	NULL	0	NULL	statement 2			is in complex with					hsp90		yeast homolog of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20479_s_28	7657624	A 45-kDa yeast protein with N-terminal  homology to mammalian CyP-40 has been isolated in a multiprotein  complex with the yeast homolog of hsp90 ( 27) , and incubation  of a variety of tissue homogenates with a CyP-40/GST-fusion protein  bound to glutathione-agarose resulted in retention of hsp90,   suggesting that CyP-40 also binds directly to hsp90.	bind
39179	1	9099	5	13	NULL	NULL	NULL	 Nox	GP	Escherichia coli	bind		noncovalently			FAD	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_24_7007_s_38	11717257	A 47-kDa Nox from  Escherichia coli has a noncovalently bound flavin adenine dinucleotide (FAD) that catalyzes the reduction of a quinone, probably ubiquinone-8, in vivo ( 27).	bind
39180	2	9099	5	13	NULL	NULL	NULL	FAD	NucleicAcid		is					flavin adenine dinucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_24_7007_s_38	11717257	A 47-kDa Nox from  Escherichia coli has a noncovalently bound flavin adenine dinucleotide (FAD) that catalyzes the reduction of a quinone, probably ubiquinone-8, in vivo ( 27).	bind
39181	3	9099	5	13	NULL	NULL	NULL	FAD	NucleicAcid		catalyze					ubiquinone-8	Chemical	reduction of			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbacteriol_183_24_7007_s_38	11717257	A 47-kDa Nox from  Escherichia coli has a noncovalently bound flavin adenine dinucleotide (FAD) that catalyzes the reduction of a quinone, probably ubiquinone-8, in vivo ( 27).	bind
39182	4	9099	5	13	NULL	NULL	NULL	ubiquinone-8	Chemical		is a type of					quinone	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_24_7007_s_38	11717257	A 47-kDa Nox from  Escherichia coli has a noncovalently bound flavin adenine dinucleotide (FAD) that catalyzes the reduction of a quinone, probably ubiquinone-8, in vivo ( 27).	bind
39183	5	9099	5	13	NULL	NULL	NULL	Nox	GP		is a type of					 47-kDa protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_24_7007_s_38	11717257	A 47-kDa Nox from  Escherichia coli has a noncovalently bound flavin adenine dinucleotide (FAD) that catalyzes the reduction of a quinone, probably ubiquinone-8, in vivo ( 27).	bind
31191	1	9099	6	10	NULL	0	NULL	Nox	NULL	Escherichia coli	bind	NULL	noncovalently			FAD	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_24_7007_s_38	11717257	A 47-kDa Nox from  Escherichia coli has a noncovalently bound flavin adenine dinucleotide (FAD) that catalyzes the reduction of a quinone, probably ubiquinone-8, in vivo ( 27).	bind
31192	2	9099	6	NULL	NULL	0	NULL	FAD	NULL		is	NULL				flavin adenine dinucleotide 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_24_7007_s_38	11717257	A 47-kDa Nox from  Escherichia coli has a noncovalently bound flavin adenine dinucleotide (FAD) that catalyzes the reduction of a quinone, probably ubiquinone-8, in vivo ( 27).	bind
31193	3	9099	6	NULL	NULL	0	NULL	ubiquinone-8	NULL		is a type of	NULL				quinone	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_24_7007_s_38	11717257	A 47-kDa Nox from  Escherichia coli has a noncovalently bound flavin adenine dinucleotide (FAD) that catalyzes the reduction of a quinone, probably ubiquinone-8, in vivo ( 27).	bind
31194	4	9099	6	NULL	NULL	0	NULL	FAD	NULL		catalyzes	NULL				ubiquinone-8	NULL	reduction of 			NULL	in vivo	0	NULL	NULL	NULL	gw60_jbacteriol_183_24_7007_s_38	11717257	A 47-kDa Nox from  Escherichia coli has a noncovalently bound flavin adenine dinucleotide (FAD) that catalyzes the reduction of a quinone, probably ubiquinone-8, in vivo ( 27).	bind
31271	5	9099	6	10	NULL	0	NULL	Nox	NULL		is a type of	NULL				47-kDa protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_24_7007_s_38	11717257	A 47-kDa Nox from  Escherichia coli has a noncovalently bound flavin adenine dinucleotide (FAD) that catalyzes the reduction of a quinone, probably ubiquinone-8, in vivo ( 27).	bind
39184	1	9101	5	13	NULL	NULL	NULL	PAK-1	GP		bind		specifically			cdc42	GP	active			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_14_2821_s_273	15241473	A 5 mug portion of PAK-1 agarose beads, which specifically bound to active cdc42, was added  to the cell lysates and incubated for 1 h at 4 degrees C.	bind
31272	1	9101	6	NULL	NULL	0	NULL	PAK-1	NULL		bind	NULL	specifically			cdc42	NULL	active			NULL		0	NULL	NULL	NULL	gw70_embo_23_14_2821_s_273	15241473	A 5 mug portion of PAK-1 agarose beads, which specifically bound to active cdc42, was added  to the cell lysates and incubated for 1 h at 4 degrees C.	bind
39186	1	9102	5	13	NULL	NULL	NULL	Nanog	GP		regulates				Oct-4 binding sites in promoter	Nanog gene	GP	transcriptional activity of			NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_cell-res_16_3_16541131_s_3	16541131	A 5' flank sequence of the Nanog gene has been  reported to be regulated differentially, and two regulatory elements within  the Nanog promoter, namely Oct-4 and Sox-2 binding sites, have been identified  to regulate the transcriptional activity of Nanog gene.	bind
39187	2	9102	5	13	NULL	NULL	NULL	Nanog	GP		regulates				Sox-2 binding sites in promoter	Nanog gene	GP	transcriptional activity of			NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_cell-res_16_3_16541131_s_3	16541131	A 5' flank sequence of the Nanog gene has been  reported to be regulated differentially, and two regulatory elements within  the Nanog promoter, namely Oct-4 and Sox-2 binding sites, have been identified  to regulate the transcriptional activity of Nanog gene.	bind
39188	3	9102	5	13	NULL	NULL	NULL	Oct-4 binding sites	GP		is a type of					Nanog	GP			regulatory elements within  promoter	NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_cell-res_16_3_16541131_s_3	16541131	A 5' flank sequence of the Nanog gene has been  reported to be regulated differentially, and two regulatory elements within  the Nanog promoter, namely Oct-4 and Sox-2 binding sites, have been identified  to regulate the transcriptional activity of Nanog gene.	bind
39189	4	9102	5	13	NULL	NULL	NULL	Sox-2 binding sites	GP		is a type of					Nanog	GP			regulatory elements within  promoter	NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_cell-res_16_3_16541131_s_3	16541131	A 5' flank sequence of the Nanog gene has been  reported to be regulated differentially, and two regulatory elements within  the Nanog promoter, namely Oct-4 and Sox-2 binding sites, have been identified  to regulate the transcriptional activity of Nanog gene.	bind
31273	1	9102	6	NULL	NULL	0	NULL	Nanog	NULL		regulate	NULL			Oct-4 binding site of promoter	Nanog gene	NULL	transcriptional activity of 			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_cell-res_16_3_16541131_s_3	16541131	A 5' flank sequence of the Nanog gene has been  reported to be regulated differentially, and two regulatory elements within  the Nanog promoter, namely Oct-4 and Sox-2 binding sites, have been identified  to regulate the transcriptional activity of Nanog gene.	bind
31274	2	9102	6	NULL	NULL	0	NULL	Nanog	NULL		regulate	NULL			Sox-2 binding site of promoter	Nanog gene	NULL	transcriptional activity of			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_cell-res_16_3_16541131_s_3	16541131	A 5' flank sequence of the Nanog gene has been  reported to be regulated differentially, and two regulatory elements within  the Nanog promoter, namely Oct-4 and Sox-2 binding sites, have been identified  to regulate the transcriptional activity of Nanog gene.	bind
48004	3	9102	6	10	NULL	0	NULL		NULL		is a type of	NULL			Oct-4 binding site	Nanog	NULL			 regulatory elements within  promoter	NULL		0	NULL	NULL	NULL	abs-batch0620-0649_cell-res_16_3_16541131_s_3	16541131	A 5' flank sequence of the Nanog gene has been  reported to be regulated differentially, and two regulatory elements within  the Nanog promoter, namely Oct-4 and Sox-2 binding sites, have been identified  to regulate the transcriptional activity of Nanog gene.	bind
48005	4	9102	6	10	NULL	0	NULL		NULL		is a type of	NULL			Sox-2 binding site	Nanog	NULL			regulatory elements within  promoter	NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_cell-res_16_3_16541131_s_3	16541131	A 5' flank sequence of the Nanog gene has been  reported to be regulated differentially, and two regulatory elements within  the Nanog promoter, namely Oct-4 and Sox-2 binding sites, have been identified  to regulate the transcriptional activity of Nanog gene.	bind
49161	1	9104	5	13	NULL	NULL	NULL	PDGF-A gene	GP		is activated in				5''-distal enhanceosome	choriocarcinoma cells	Cell				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_oncogene_24_16_15829977_s_1	15829977	A 5''-distal enhanceosome in the PDGF-A gene is activated in choriocarcinoma cells via ligand-independent binding of vitamin D receptor and constitutive jun kinase signaling..	bind
49162	2	9104	5	13	NULL	NULL	NULL	statement 1	Process		occurs via					jun kinase signaling	Process	constitutive \t			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_oncogene_24_16_15829977_s_1	15829977	A 5''-distal enhanceosome in the PDGF-A gene is activated in choriocarcinoma cells via ligand-independent binding of vitamin D receptor and constitutive jun kinase signaling..	bind
49163	3	9104	5	13	NULL	NULL	NULL	vitamin D receptor	GP	binding of	is independent of					ligand	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_oncogene_24_16_15829977_s_1	15829977	A 5''-distal enhanceosome in the PDGF-A gene is activated in choriocarcinoma cells via ligand-independent binding of vitamin D receptor and constitutive jun kinase signaling..	bind
49164	4	9104	5	13	NULL	NULL	NULL	statement 1	Process		occurs via					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_oncogene_24_16_15829977_s_1	15829977	A 5''-distal enhanceosome in the PDGF-A gene is activated in choriocarcinoma cells via ligand-independent binding of vitamin D receptor and constitutive jun kinase signaling..	bind
31275	1	9104	6	NULL	NULL	0	NULL	PDGF-A gene	NULL		is activated in	NULL			distal enhanceosome	choriocarcinoma cells	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_oncogene_24_16_15829977_s_1	15829977	A 5''-distal enhanceosome in the PDGF-A gene is activated in choriocarcinoma cells via ligand-independent binding of vitamin D receptor and constitutive jun kinase signaling..	bind
31276	2	9104	6	NULL	NULL	0	NULL	statement 1	NULL		occurs via	NULL				jun kinase signaling	NULL	constitutive			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_oncogene_24_16_15829977_s_1	15829977	A 5''-distal enhanceosome in the PDGF-A gene is activated in choriocarcinoma cells via ligand-independent binding of vitamin D receptor and constitutive jun kinase signaling..	bind
31277	3	9104	6	NULL	NULL	0	NULL	vitamin D receptor	NULL	binding of	is independent of	NULL				ligand	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_oncogene_24_16_15829977_s_1	15829977	A 5''-distal enhanceosome in the PDGF-A gene is activated in choriocarcinoma cells via ligand-independent binding of vitamin D receptor and constitutive jun kinase signaling..	bind
31278	4	9104	6	NULL	NULL	0	NULL	statement 1	NULL		occurs via	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_oncogene_24_16_15829977_s_1	15829977	A 5''-distal enhanceosome in the PDGF-A gene is activated in choriocarcinoma cells via ligand-independent binding of vitamin D receptor and constitutive jun kinase signaling..	bind
39194	1	9105	5	13	NULL	NULL	NULL	GST-PSD fusion protein	GP	recombinant	bind					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_38_27201_s_278	10480937	A 5-fold molar excess of Ca2+-calmodulin effectively inhibited binding of recombinant GST-PSD fusion protein to F-actin (~85% decrease) (Fig.  6 A).	bind
39195	2	9105	5	13	NULL	NULL	NULL	Ca2+-calmodulin	GP	excess	inhibit		effectively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_38_27201_s_278	10480937	A 5-fold molar excess of Ca2+-calmodulin effectively inhibited binding of recombinant GST-PSD fusion protein to F-actin (~85% decrease) (Fig.  6 A).	bind
31279	1	9105	6	NULL	NULL	0	NULL	GST-PSD fusion protein	NULL	recombinant	bind	NULL				F-actin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_38_27201_s_278	10480937	A 5-fold molar excess of Ca2+-calmodulin effectively inhibited binding of recombinant GST-PSD fusion protein to F-actin (~85% decrease) (Fig.  6 A).	bind
31280	2	9105	6	NULL	NULL	0	NULL	Ca2+-calmodulin	NULL	excess of	inhibits	NULL	effectively			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_38_27201_s_278	10480937	A 5-fold molar excess of Ca2+-calmodulin effectively inhibited binding of recombinant GST-PSD fusion protein to F-actin (~85% decrease) (Fig.  6 A).	bind
39196	1	9108	5	13	NULL	NULL	NULL	PDPs CB1	GP		bind					CD4	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_508_1_67_s_172	11707270	A 50% inhibition of binding of PDPs CB1 and CB8 to CD4 was obtained for 13B8.	bind
39197	2	9108	5	13	NULL	NULL	NULL	PDPs CB8	GP		bind					CD4	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_508_1_67_s_172	11707270	A 50% inhibition of binding of PDPs CB1 and CB8 to CD4 was obtained for 13B8.	bind
48007	3	9108	5	13	NULL	NULL	NULL	13B8	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_508_1_67_s_172	11707270	A 50% inhibition of binding of PDPs CB1 and CB8 to CD4 was obtained for 13B8.	bind
48008	4	9108	5	13	NULL	NULL	NULL	13B8	GP		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_508_1_67_s_172	11707270	A 50% inhibition of binding of PDPs CB1 and CB8 to CD4 was obtained for 13B8.	bind
31282	1	9108	6	NULL	NULL	0	NULL	CB1 PDP	NULL		bind	NULL				CD4	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_508_1_67_s_172	11707270	A 50% inhibition of binding of PDPs CB1 and CB8 to CD4 was obtained for 13B8.	bind
31283	2	9108	6	NULL	NULL	0	NULL	CB8 PDP	NULL		bind	NULL				CD4	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_508_1_67_s_172	11707270	A 50% inhibition of binding of PDPs CB1 and CB8 to CD4 was obtained for 13B8.	bind
31284	3	9108	6	NULL	NULL	0	NULL	13B8	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_508_1_67_s_172	11707270	A 50% inhibition of binding of PDPs CB1 and CB8 to CD4 was obtained for 13B8.	bind
31285	4	9108	6	NULL	NULL	0	NULL	13B8	NULL		inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_508_1_67_s_172	11707270	A 50% inhibition of binding of PDPs CB1 and CB8 to CD4 was obtained for 13B8.	bind
39198	1	9109	5	13	NULL	NULL	NULL	toxaphene	Chemical		inhibit					ouabain	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_toxicol-lett_18_3_6141653_s_9	6141653	A 50% inhibition of ouabain and dopamine binding was obtained  at 150 and 200 microM of toxaphene.	bind
39199	2	9109	5	13	NULL	NULL	NULL	toxaphene	Chemical		inhibit					dopamine	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_toxicol-lett_18_3_6141653_s_9	6141653	A 50% inhibition of ouabain and dopamine binding was obtained  at 150 and 200 microM of toxaphene.	bind
31286	1	9109	6	10	NULL	0	NULL	toxaphene	NULL		inhibits	NULL				dopamine	NULL	binding of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_toxicol-lett_18_3_6141653_s_9	6141653	A 50% inhibition of ouabain and dopamine binding was obtained  at 150 and 200 microM of toxaphene.	bind
31287	2	9109	6	10	NULL	0	NULL	toxaphene	NULL		inhibits	NULL				ouabain	NULL	binding of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_toxicol-lett_18_3_6141653_s_9	6141653	A 50% inhibition of ouabain and dopamine binding was obtained  at 150 and 200 microM of toxaphene.	bind
39200	1	9110	5	13	NULL	NULL	NULL	PNUTS	GP		mediate			50-amino acid domain		PP1	GP	high affinity binding of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_16_12574161_s_6	12574161	A 50-amino acid domain  in the center of PNUTS mediated both high affinity PP1 binding and inhibition  of PP1 activity.	bind
39201	2	9110	5	13	NULL	NULL	NULL	PNUTS	GP		mediate			50-amino acid domain		PP1 activity	Process	inhibition of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_16_12574161_s_6	12574161	A 50-amino acid domain  in the center of PNUTS mediated both high affinity PP1 binding and inhibition  of PP1 activity.	bind
31288	1	9110	6	NULL	NULL	0	NULL	PNUTS	NULL		mediates	NULL		50-amino acid domain		PP1	NULL	high affinity binding of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_16_12574161_s_6	12574161	A 50-amino acid domain  in the center of PNUTS mediated both high affinity PP1 binding and inhibition  of PP1 activity.	bind
31289	2	9110	6	NULL	NULL	0	NULL	PNUTS	NULL		mediates	NULL		50-amino acid domain		PP1 activity	NULL	inhibiton of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_16_12574161_s_6	12574161	A 50-amino acid domain  in the center of PNUTS mediated both high affinity PP1 binding and inhibition  of PP1 activity.	bind
39202	1	9112	5	13	NULL	NULL	NULL	BPS domain	GP		is					50-amino acid region between the PH and SH2 domains	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_20_17172_s_21	11278563	A 50-amino acid region between the PH and SH2 domains (BPS domain) contributes to binding of Grb10 and Grb14 to the IR ( 11,  12).	bind
39203	2	9112	5	13	NULL	NULL	NULL	Grb10	GP		bind					IR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_20_17172_s_21	11278563	A 50-amino acid region between the PH and SH2 domains (BPS domain) contributes to binding of Grb10 and Grb14 to the IR ( 11,  12).	bind
39204	3	9112	5	13	NULL	NULL	NULL	Grb14	GP		bind					IR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_20_17172_s_21	11278563	A 50-amino acid region between the PH and SH2 domains (BPS domain) contributes to binding of Grb10 and Grb14 to the IR ( 11,  12).	bind
57765	4	9112	5	13	NULL	NULL	NULL				contributes to			BPS domain		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_20_17172_s_21	11278563	A 50-amino acid region between the PH and SH2 domains (BPS domain) contributes to binding of Grb10 and Grb14 to the IR ( 11,  12).	bind
57766	5	9112	5	13	NULL	NULL	NULL				contribute to			BPS domain		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_20_17172_s_21	11278563	A 50-amino acid region between the PH and SH2 domains (BPS domain) contributes to binding of Grb10 and Grb14 to the IR ( 11,  12).	bind
31290	1	9112	6	NULL	NULL	0	NULL	Grb10	NULL		bind	NULL				IR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_20_17172_s_21	11278563	A 50-amino acid region between the PH and SH2 domains (BPS domain) contributes to binding of Grb10 and Grb14 to the IR ( 11,  12).	bind
31291	2	9112	6	NULL	NULL	0	NULL	Grb14	NULL		bind	NULL				IR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_20_17172_s_21	11278563	A 50-amino acid region between the PH and SH2 domains (BPS domain) contributes to binding of Grb10 and Grb14 to the IR ( 11,  12).	bind
31292	3	9112	6	NULL	NULL	0	NULL	BPS domain	NULL		is	NULL				50-amino acid region between the PH and SH2 domains	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_20_17172_s_21	11278563	A 50-amino acid region between the PH and SH2 domains (BPS domain) contributes to binding of Grb10 and Grb14 to the IR ( 11,  12).	bind
31293	4	9112	6	NULL	NULL	0	NULL		NULL		contributes to	NULL		BPS domain		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_20_17172_s_21	11278563	A 50-amino acid region between the PH and SH2 domains (BPS domain) contributes to binding of Grb10 and Grb14 to the IR ( 11,  12).	bind
31294	5	9112	6	NULL	NULL	0	NULL		NULL		contributes to	NULL		BPS domain		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_20_17172_s_21	11278563	A 50-amino acid region between the PH and SH2 domains (BPS domain) contributes to binding of Grb10 and Grb14 to the IR ( 11,  12).	bind
39205	1	9113	5	13	NULL	NULL	NULL	NS1	NucleicAcid		bind					hnRNP A3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_20_18010_s_245	11886857	A 50-fold excess of either A2RE11 or NS1 11-mer eliminated binding of NS1 to hnRNP A3.	bind
39206	2	9113	5	13	NULL	NULL	NULL	A2RE11	NucleicAcid	excess	eliminate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_20_18010_s_245	11886857	A 50-fold excess of either A2RE11 or NS1 11-mer eliminated binding of NS1 to hnRNP A3.	bind
39207	3	9113	5	13	NULL	NULL	NULL	NS1 11-mer	NucleicAcid	excess	eliminate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_20_18010_s_245	11886857	A 50-fold excess of either A2RE11 or NS1 11-mer eliminated binding of NS1 to hnRNP A3.	bind
31295	1	9113	6	NULL	NULL	0	NULL	NS1	NULL		bind	NULL				hnRNP A3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_20_18010_s_245	11886857	A 50-fold excess of either A2RE11 or NS1 11-mer eliminated binding of NS1 to hnRNP A3.	bind
31296	2	9113	6	NULL	NULL	0	NULL	A2RE11	NULL	excess of	eliminates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_20_18010_s_245	11886857	A 50-fold excess of either A2RE11 or NS1 11-mer eliminated binding of NS1 to hnRNP A3.	bind
31297	3	9113	6	10	NULL	0	NULL	NS1 11-mer		excess of	eliminates					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_20_18010_s_245	11886857	A 50-fold excess of either A2RE11 or NS1 11-mer eliminated binding of NS1 to hnRNP A3.	bind
39208	1	9114	5	13	NULL	NULL	NULL	SREBP	GP		bind					DNA	NucleicAcid	labeled			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_19938_s_96	9685328	A 50-fold excess of unlabeled homologous competitor fragment displaced SREBP binding to the labeled DNA.	bind
39209	2	9114	5	13	NULL	NULL	NULL	homologous competitor fragment	GP	excess;;unlabeled	bind					DNA	NucleicAcid	labeled			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_19938_s_96	9685328	A 50-fold excess of unlabeled homologous competitor fragment displaced SREBP binding to the labeled DNA.	bind
39210	3	9114	5	13	NULL	NULL	NULL	statement 2	Process		displaces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_19938_s_96	9685328	A 50-fold excess of unlabeled homologous competitor fragment displaced SREBP binding to the labeled DNA.	bind
31298	1	9114	6	NULL	NULL	0	NULL	SREBP	NULL		bind	NULL				DNA	NULL	labeled			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_19938_s_96	9685328	A 50-fold excess of unlabeled homologous competitor fragment displaced SREBP binding to the labeled DNA.	bind
31299	2	9114	6	10	NULL	0	NULL	homologous competitor fragment		unlabeled;; excess of	bind					 DNA		labeled			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_19938_s_96	9685328	A 50-fold excess of unlabeled homologous competitor fragment displaced SREBP binding to the labeled DNA.	bind
57767	3	9114	6	10	NULL	0	NULL	statement 2			displaces					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_19938_s_96	9685328	A 50-fold excess of unlabeled homologous competitor fragment displaced SREBP binding to the labeled DNA.	bind
42534	1	9118	5	13	NULL	NULL	NULL	516-bp fragment	GP		encompass									DNase I-hypersensitive site	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_32_33398_s_4	15159395	A 516-bp fragment, encompassing a DNase I-hypersensitive site associated with P2 activity that is still retained in adult liver, contains functional HNF1 and HNF6 binding sites and confers full promoter activity in transient transfections.	bind
42535	2	9118	5	13	NULL	NULL	NULL	statement 1	GP		is associated with					P2	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_32_33398_s_4	15159395	A 516-bp fragment, encompassing a DNase I-hypersensitive site associated with P2 activity that is still retained in adult liver, contains functional HNF1 and HNF6 binding sites and confers full promoter activity in transient transfections.	bind
42536	3	9118	5	13	NULL	NULL	NULL	statement 2	Process		is retained in					liver	OrganismPart	adult			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_32_33398_s_4	15159395	A 516-bp fragment, encompassing a DNase I-hypersensitive site associated with P2 activity that is still retained in adult liver, contains functional HNF1 and HNF6 binding sites and confers full promoter activity in transient transfections.	bind
42537	4	9118	5	13	NULL	NULL	NULL	statement 1	GP		contains							functional		HNF1 binding sites	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_32_33398_s_4	15159395	A 516-bp fragment, encompassing a DNase I-hypersensitive site associated with P2 activity that is still retained in adult liver, contains functional HNF1 and HNF6 binding sites and confers full promoter activity in transient transfections.	bind
42538	5	9118	5	13	NULL	NULL	NULL	statement 1	GP		contains							functional		HNF6 binding sites	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_32_33398_s_4	15159395	A 516-bp fragment, encompassing a DNase I-hypersensitive site associated with P2 activity that is still retained in adult liver, contains functional HNF1 and HNF6 binding sites and confers full promoter activity in transient transfections.	bind
42539	6	9118	5	13	NULL	NULL	NULL	statement 1	GP		confer							full activity of		promoter	NULL	transient transfections	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_32_33398_s_4	15159395	A 516-bp fragment, encompassing a DNase I-hypersensitive site associated with P2 activity that is still retained in adult liver, contains functional HNF1 and HNF6 binding sites and confers full promoter activity in transient transfections.	bind
32023	2	9118	6	10	NULL	0	NULL	statement 1			is associated with					P2 		activity of			NULL	adult liver	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_32_33398_s_4	15159395	A 516-bp fragment, encompassing a DNase I-hypersensitive site associated with P2 activity that is still retained in adult liver, contains functional HNF1 and HNF6 binding sites and confers full promoter activity in transient transfections.	bind
32814	4	9118	6	10	NULL	0	NULL	statement 1	NULL		contains	NULL					NULL	functional		HNF-1 binding site	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_32_33398_s_4	15159395	A 516-bp fragment, encompassing a DNase I-hypersensitive site associated with P2 activity that is still retained in adult liver, contains functional HNF1 and HNF6 binding sites and confers full promoter activity in transient transfections.	bind
32815	5	9118	6	10	NULL	0	NULL	statement 1	NULL		contains	NULL					NULL	functional		HNF6 binding site	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_32_33398_s_4	15159395	A 516-bp fragment, encompassing a DNase I-hypersensitive site associated with P2 activity that is still retained in adult liver, contains functional HNF1 and HNF6 binding sites and confers full promoter activity in transient transfections.	bind
48009	1	9118	6	10	NULL	0	NULL	516-bp fragment			encompass									DNase I-hypersensitive site	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_32_33398_s_4	15159395	A 516-bp fragment, encompassing a DNase I-hypersensitive site associated with P2 activity that is still retained in adult liver, contains functional HNF1 and HNF6 binding sites and confers full promoter activity in transient transfections.	bind
48010	3	9118	6	10	NULL	0	NULL	statement 2			is retained in					 liver		adult			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_32_33398_s_4	15159395	A 516-bp fragment, encompassing a DNase I-hypersensitive site associated with P2 activity that is still retained in adult liver, contains functional HNF1 and HNF6 binding sites and confers full promoter activity in transient transfections.	bind
39211	1	9119	5	13	NULL	NULL	NULL	55 kDa protein	GP		bind					U3 snoRNA	NucleicAcid				NULL	CHO cells	NULL	NULL	NULL	NULL	gw60_gene_313_0_17_s_143	12957375	A 55 kDa protein that bound to U3 snoRNA was isolated for the first time by [  Lubben et al., 1993] in CHO cells.	bind
31352	1	9119	6	10	NULL	0	NULL	55 kDa protein 	NULL		bind	NULL				U3 snoRNA	NULL				NULL	CHO cells	NULL	NULL	NULL	NULL	gw60_gene_313_0_17_s_143	12957375	A 55 kDa protein that bound to U3 snoRNA was isolated for the first time by [  Lubben et al., 1993] in CHO cells.	bind
39213	1	9120	5	13	NULL	NULL	NULL	55-60-kDa protein	GP		bind					Ins	GP			PRS	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_2_1099_s_138	11696543	A 55-60-kDa Protein Binds to the Ins-PRS-- The findings that glucose-induced changes in insulin mRNA stability control insulin mRNA contents prompted us to next investigate the mechanisms that regulate insulin mRNA stability.	bind
39214	2	9120	5	13	NULL	NULL	NULL	glucose	NucleicAcid		induce					insulin mRNA	NucleicAcid	changes in stability of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_2_1099_s_138	11696543	A 55-60-kDa Protein Binds to the Ins-PRS-- The findings that glucose-induced changes in insulin mRNA stability control insulin mRNA contents prompted us to next investigate the mechanisms that regulate insulin mRNA stability.	bind
39215	3	9120	5	13	NULL	NULL	NULL	statement 2	Process		controls					insulin mRNA	NucleicAcid	contents of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_2_1099_s_138	11696543	A 55-60-kDa Protein Binds to the Ins-PRS-- The findings that glucose-induced changes in insulin mRNA stability control insulin mRNA contents prompted us to next investigate the mechanisms that regulate insulin mRNA stability.	bind
31353	1	9120	6	10	NULL	0	NULL	55-60-kDa Protein			bind					Ins				PRS	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_2_1099_s_138	11696543	A 55-60-kDa Protein Binds to the Ins-PRS-- The findings that glucose-induced changes in insulin mRNA stability control insulin mRNA contents prompted us to next investigate the mechanisms that regulate insulin mRNA stability.	bind
48011	2	9120	6	10	NULL	0	NULL	glucose	NULL		induce	NULL				insulin mRNA	NULL	changes in stability of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_2_1099_s_138	11696543	A 55-60-kDa Protein Binds to the Ins-PRS-- The findings that glucose-induced changes in insulin mRNA stability control insulin mRNA contents prompted us to next investigate the mechanisms that regulate insulin mRNA stability.	bind
48012	3	9120	6	10	NULL	0	NULL	statement 2	NULL		controls	NULL				insulin mRNA	NULL	contents of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_2_1099_s_138	11696543	A 55-60-kDa Protein Binds to the Ins-PRS-- The findings that glucose-induced changes in insulin mRNA stability control insulin mRNA contents prompted us to next investigate the mechanisms that regulate insulin mRNA stability.	bind
39216	1	9122	5	13	NULL	NULL	NULL	phage A1-10	Organism		bind					OppA-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_1_51_s_145	14679224	A 6 muM concentration of peptide A1-10P inhibited the binding of phage A1-10 to OppA-1 by 91%; the same concentration of the negative control peptide NB-21P did not inhibit the binding of phage A1-10 to OppA-1.	bind
39217	2	9122	5	13	NULL	NULL	NULL	A1-10P peptide	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_1_51_s_145	14679224	A 6 muM concentration of peptide A1-10P inhibited the binding of phage A1-10 to OppA-1 by 91%; the same concentration of the negative control peptide NB-21P did not inhibit the binding of phage A1-10 to OppA-1.	bind
39218	3	9122	5	13	NULL	NULL	NULL	NB-21P peptide	GP		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_1_51_s_145	14679224	A 6 muM concentration of peptide A1-10P inhibited the binding of phage A1-10 to OppA-1 by 91%; the same concentration of the negative control peptide NB-21P did not inhibit the binding of phage A1-10 to OppA-1.	bind
31359	1	9122	6	NULL	NULL	0	NULL	phage A1-10	NULL		bind	NULL				OppA-1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_1_51_s_145	14679224	A 6 muM concentration of peptide A1-10P inhibited the binding of phage A1-10 to OppA-1 by 91%; the same concentration of the negative control peptide NB-21P did not inhibit the binding of phage A1-10 to OppA-1.	bind
31360	2	9122	6	NULL	NULL	0	NULL	A1-10P peptide	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_1_51_s_145	14679224	A 6 muM concentration of peptide A1-10P inhibited the binding of phage A1-10 to OppA-1 by 91%; the same concentration of the negative control peptide NB-21P did not inhibit the binding of phage A1-10 to OppA-1.	bind
31361	3	9122	6	NULL	NULL	0	NULL	NB-21P peptide	NULL		does not inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_1_51_s_145	14679224	A 6 muM concentration of peptide A1-10P inhibited the binding of phage A1-10 to OppA-1 by 91%; the same concentration of the negative control peptide NB-21P did not inhibit the binding of phage A1-10 to OppA-1.	bind
39219	1	9123	5	13	NULL	NULL	NULL	6-mer heparin oligosaccharide	Chemical		bind					PRELP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_40695_s_9	11007795	A 6-mer heparin oligosaccharide was the smallest size showing binding to PRELP.	bind
31362	1	9123	6	10	NULL	0	NULL	6-mer heparin oligosaccharide	NULL		bind	NULL				PRELP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_40695_s_9	11007795	A 6-mer heparin oligosaccharide was the smallest size showing binding to PRELP.	bind
39220	1	9124	5	13	NULL	NULL	NULL	VSLAFS	GP		is a type of					6-mer peptide	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_37_27398_s_86	16844690	A 6-mer peptide (VSLAFS, the herein identified C9 consensus sequence that binds to CD59) and 8-mer peptide (DVSLAFSE, synthetic peptide shown to bind CD59) were created as objects in ICM ( ) and docked to both the closed and the open refined conformations of CD59, defined by the set of residues within 3  Ang  of the open structure pocket.	bind
39221	2	9124	5	13	NULL	NULL	NULL	VSLAFS	GP		is a type of					C9 consensus sequence	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_37_27398_s_86	16844690	A 6-mer peptide (VSLAFS, the herein identified C9 consensus sequence that binds to CD59) and 8-mer peptide (DVSLAFSE, synthetic peptide shown to bind CD59) were created as objects in ICM ( ) and docked to both the closed and the open refined conformations of CD59, defined by the set of residues within 3  Ang  of the open structure pocket.	bind
39222	3	9124	5	13	NULL	NULL	NULL	VSLAFS	GP		bind					CD59	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_37_27398_s_86	16844690	A 6-mer peptide (VSLAFS, the herein identified C9 consensus sequence that binds to CD59) and 8-mer peptide (DVSLAFSE, synthetic peptide shown to bind CD59) were created as objects in ICM ( ) and docked to both the closed and the open refined conformations of CD59, defined by the set of residues within 3  Ang  of the open structure pocket.	bind
39223	4	9124	5	13	NULL	NULL	NULL	DVSLAFSE	GP		is a type of					8-mer peptide	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_37_27398_s_86	16844690	A 6-mer peptide (VSLAFS, the herein identified C9 consensus sequence that binds to CD59) and 8-mer peptide (DVSLAFSE, synthetic peptide shown to bind CD59) were created as objects in ICM ( ) and docked to both the closed and the open refined conformations of CD59, defined by the set of residues within 3  Ang  of the open structure pocket.	bind
39224	5	9124	5	13	NULL	NULL	NULL	DVSLAFSE	GP		bind					CD59	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_37_27398_s_86	16844690	A 6-mer peptide (VSLAFS, the herein identified C9 consensus sequence that binds to CD59) and 8-mer peptide (DVSLAFSE, synthetic peptide shown to bind CD59) were created as objects in ICM ( ) and docked to both the closed and the open refined conformations of CD59, defined by the set of residues within 3  Ang  of the open structure pocket.	bind
39225	6	9124	5	13	NULL	NULL	NULL	VSLAFS	GP		is docked to					CD59	GP	closed refined conformations of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_37_27398_s_86	16844690	A 6-mer peptide (VSLAFS, the herein identified C9 consensus sequence that binds to CD59) and 8-mer peptide (DVSLAFSE, synthetic peptide shown to bind CD59) were created as objects in ICM ( ) and docked to both the closed and the open refined conformations of CD59, defined by the set of residues within 3  Ang  of the open structure pocket.	bind
39226	7	9124	5	13	NULL	NULL	NULL	DVSLAFSE	GP		is docked to					CD59	GP	open refined conformations of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_37_27398_s_86	16844690	A 6-mer peptide (VSLAFS, the herein identified C9 consensus sequence that binds to CD59) and 8-mer peptide (DVSLAFSE, synthetic peptide shown to bind CD59) were created as objects in ICM ( ) and docked to both the closed and the open refined conformations of CD59, defined by the set of residues within 3  Ang  of the open structure pocket.	bind
48017	8	9124	5	13	NULL	NULL	NULL	DVSLAFSE	GP		is a type of					synthetic peptide	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_37_27398_s_86	16844690	A 6-mer peptide (VSLAFS, the herein identified C9 consensus sequence that binds to CD59) and 8-mer peptide (DVSLAFSE, synthetic peptide shown to bind CD59) were created as objects in ICM ( ) and docked to both the closed and the open refined conformations of CD59, defined by the set of residues within 3  Ang  of the open structure pocket.	bind
32024	2	9124	6	10	NULL	0	NULL	VSLAFS	NULL		is a type of	NULL				C9 consensus sequence	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_37_27398_s_86	16844690	A 6-mer peptide (VSLAFS, the herein identified C9 consensus sequence that binds to CD59) and 8-mer peptide (DVSLAFSE, synthetic peptide shown to bind CD59) were created as objects in ICM ( ) and docked to both the closed and the open refined conformations of CD59, defined by the set of residues within 3  Ang  of the open structure pocket.	bind
32025	3	9124	6	10	NULL	0	NULL	VSLAFS	NULL		bind	NULL				CD59	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_37_27398_s_86	16844690	A 6-mer peptide (VSLAFS, the herein identified C9 consensus sequence that binds to CD59) and 8-mer peptide (DVSLAFSE, synthetic peptide shown to bind CD59) were created as objects in ICM ( ) and docked to both the closed and the open refined conformations of CD59, defined by the set of residues within 3  Ang  of the open structure pocket.	bind
32026	4	9124	6	10	NULL	0	NULL	DVSLAFSE peptide	NULL		bind	NULL				CD59	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_37_27398_s_86	16844690	A 6-mer peptide (VSLAFS, the herein identified C9 consensus sequence that binds to CD59) and 8-mer peptide (DVSLAFSE, synthetic peptide shown to bind CD59) were created as objects in ICM ( ) and docked to both the closed and the open refined conformations of CD59, defined by the set of residues within 3  Ang  of the open structure pocket.	bind
48013	1	9124	6	10	NULL	0	NULL	VSLAFS	NULL		is a type of	NULL				6-mer peptide	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_37_27398_s_86	16844690	A 6-mer peptide (VSLAFS, the herein identified C9 consensus sequence that binds to CD59) and 8-mer peptide (DVSLAFSE, synthetic peptide shown to bind CD59) were created as objects in ICM ( ) and docked to both the closed and the open refined conformations of CD59, defined by the set of residues within 3  Ang  of the open structure pocket.	bind
48014	5	9124	6	10	NULL	0	NULL	DVSLAFSE peptide	NULL		is a type of	NULL				8-mer peptide	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_37_27398_s_86	16844690	A 6-mer peptide (VSLAFS, the herein identified C9 consensus sequence that binds to CD59) and 8-mer peptide (DVSLAFSE, synthetic peptide shown to bind CD59) were created as objects in ICM ( ) and docked to both the closed and the open refined conformations of CD59, defined by the set of residues within 3  Ang  of the open structure pocket.	bind
48015	6	9124	6	10	NULL	0	NULL	VSLAFS	NULL		docked to	NULL				CD59	NULL	closed refined conformations of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_37_27398_s_86	16844690	A 6-mer peptide (VSLAFS, the herein identified C9 consensus sequence that binds to CD59) and 8-mer peptide (DVSLAFSE, synthetic peptide shown to bind CD59) were created as objects in ICM ( ) and docked to both the closed and the open refined conformations of CD59, defined by the set of residues within 3  Ang  of the open structure pocket.	bind
48016	7	9124	6	10	NULL	0	NULL	DVSLAFSE peptide	NULL		docked to	NULL				CD59	NULL	open refined conformations of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_37_27398_s_86	16844690	A 6-mer peptide (VSLAFS, the herein identified C9 consensus sequence that binds to CD59) and 8-mer peptide (DVSLAFSE, synthetic peptide shown to bind CD59) were created as objects in ICM ( ) and docked to both the closed and the open refined conformations of CD59, defined by the set of residues within 3  Ang  of the open structure pocket.	bind
48018	8	9124	6	10	NULL	0	NULL	DVSLAFSE	NULL		is a type of	NULL				synthetic peptide	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_37_27398_s_86	16844690	A 6-mer peptide (VSLAFS, the herein identified C9 consensus sequence that binds to CD59) and 8-mer peptide (DVSLAFSE, synthetic peptide shown to bind CD59) were created as objects in ICM ( ) and docked to both the closed and the open refined conformations of CD59, defined by the set of residues within 3  Ang  of the open structure pocket.	bind
39227	1	9125	5	13	NULL	NULL	NULL	60-kDa protein	GP		is designated as					FIR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_2_331_s_31	10882074	A 60 kDa Protein Designated FIR Binds the Central Domain of FBP	bind
39228	2	9125	5	13	NULL	NULL	NULL	FIR	GP		bind					FBP	GP		central domain		NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_2_331_s_31	10882074	A 60 kDa Protein Designated FIR Binds the Central Domain of FBP	bind
31363	1	9125	6	10	NULL	0	NULL	FIR	NULL		is a type of	NULL				60 kDa protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcell_5_2_331_s_31	10882074	A 60 kDa Protein Designated FIR Binds the Central Domain of FBP	bind
31364	2	9125	6	NULL	NULL	0	NULL	FIR	NULL		bind	NULL				FBP	NULL		central domain		NULL		0	NULL	NULL	NULL	gw60_molcell_5_2_331_s_31	10882074	A 60 kDa Protein Designated FIR Binds the Central Domain of FBP	bind
39229	1	9126	5	13	NULL	NULL	NULL	GDP molecule	Chemical		bind					EF-Tu	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_17_5899_s_66	15317795	A 60-mul prereaction mixture containing 50 mM Tris-HCl (pH 7.5), 10 mM magnesium acetate, 150 mM NH4Cl, 50 mM beta-mercaptoethanol, 60 muM GTP, 0.8 mM phosphoenolpyruvate (Sigma), 2 U of pyruvate kinase (Sigma), and EF-Tu at the concentrations indicated below was incubated on ice for 25 min in order to replace the GDP molecule bound to EF-Tu by GTP.	bind
48022	2	9126	5	13	NULL	NULL	NULL	GTP	Chemical		bind					EF-Tu	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_17_5899_s_66	15317795	A 60-mul prereaction mixture containing 50 mM Tris-HCl (pH 7.5), 10 mM magnesium acetate, 150 mM NH4Cl, 50 mM beta-mercaptoethanol, 60 muM GTP, 0.8 mM phosphoenolpyruvate (Sigma), 2 U of pyruvate kinase (Sigma), and EF-Tu at the concentrations indicated below was incubated on ice for 25 min in order to replace the GDP molecule bound to EF-Tu by GTP.	bind
48023	3	9126	5	13	NULL	NULL	NULL	statement 2	Process		replace					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_17_5899_s_66	15317795	A 60-mul prereaction mixture containing 50 mM Tris-HCl (pH 7.5), 10 mM magnesium acetate, 150 mM NH4Cl, 50 mM beta-mercaptoethanol, 60 muM GTP, 0.8 mM phosphoenolpyruvate (Sigma), 2 U of pyruvate kinase (Sigma), and EF-Tu at the concentrations indicated below was incubated on ice for 25 min in order to replace the GDP molecule bound to EF-Tu by GTP.	bind
32027	1	9126	6	NULL	NULL	0	NULL	GDP	NULL		bind	NULL				EF-Tu	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_17_5899_s_66	15317795	A 60-mul prereaction mixture containing 50 mM Tris-HCl (pH 7.5), 10 mM magnesium acetate, 150 mM NH4Cl, 50 mM beta-mercaptoethanol, 60 muM GTP, 0.8 mM phosphoenolpyruvate (Sigma), 2 U of pyruvate kinase (Sigma), and EF-Tu at the concentrations indicated below was incubated on ice for 25 min in order to replace the GDP molecule bound to EF-Tu by GTP.	bind
32028	2	9126	6	10	NULL	0	NULL	GTP			bind					EF-Tu					NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_17_5899_s_66	15317795	A 60-mul prereaction mixture containing 50 mM Tris-HCl (pH 7.5), 10 mM magnesium acetate, 150 mM NH4Cl, 50 mM beta-mercaptoethanol, 60 muM GTP, 0.8 mM phosphoenolpyruvate (Sigma), 2 U of pyruvate kinase (Sigma), and EF-Tu at the concentrations indicated below was incubated on ice for 25 min in order to replace the GDP molecule bound to EF-Tu by GTP.	bind
32029	3	9126	6	10	NULL	0	NULL	statement 2			replace					statement 1					NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_17_5899_s_66	15317795	A 60-mul prereaction mixture containing 50 mM Tris-HCl (pH 7.5), 10 mM magnesium acetate, 150 mM NH4Cl, 50 mM beta-mercaptoethanol, 60 muM GTP, 0.8 mM phosphoenolpyruvate (Sigma), 2 U of pyruvate kinase (Sigma), and EF-Tu at the concentrations indicated below was incubated on ice for 25 min in order to replace the GDP molecule bound to EF-Tu by GTP.	bind
39230	1	9127	5	13	NULL	NULL	NULL	61 kDa luciferase polypeptide	GP		does not bind					homopolymers	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_20_8091_s_201	11588182	A 61 kDa luciferase polypeptide showed no binding to any of the homopolymers, confirming the RNA-binding activity of the Msi2 and Msi1 proteins.	bind
39231	2	9127	5	13	NULL	NULL	NULL	Msi2 protein	GP		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_20_8091_s_201	11588182	A 61 kDa luciferase polypeptide showed no binding to any of the homopolymers, confirming the RNA-binding activity of the Msi2 and Msi1 proteins.	bind
39232	3	9127	5	13	NULL	NULL	NULL	Msi1 protein	GP		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_20_8091_s_201	11588182	A 61 kDa luciferase polypeptide showed no binding to any of the homopolymers, confirming the RNA-binding activity of the Msi2 and Msi1 proteins.	bind
48024	4	9127	5	13	NULL	NULL	NULL	statement 1	Process		confirms					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_20_8091_s_201	11588182	A 61 kDa luciferase polypeptide showed no binding to any of the homopolymers, confirming the RNA-binding activity of the Msi2 and Msi1 proteins.	bind
48025	5	9127	5	13	NULL	NULL	NULL	statement 1	Process		confirms					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_20_8091_s_201	11588182	A 61 kDa luciferase polypeptide showed no binding to any of the homopolymers, confirming the RNA-binding activity of the Msi2 and Msi1 proteins.	bind
31365	1	9127	6	NULL	NULL	0	NULL	Msi2 protein	NULL		bind	NULL				RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_20_8091_s_201	11588182	A 61 kDa luciferase polypeptide showed no binding to any of the homopolymers, confirming the RNA-binding activity of the Msi2 and Msi1 proteins.	bind
31366	2	9127	6	NULL	NULL	0	NULL	Msi1 protein	NULL		bind	NULL				RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_20_8091_s_201	11588182	A 61 kDa luciferase polypeptide showed no binding to any of the homopolymers, confirming the RNA-binding activity of the Msi2 and Msi1 proteins.	bind
31367	3	9127	6	NULL	NULL	0	NULL	61 kDa luciferase polypeptide	NULL		does not bind	NULL				homopolymers	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_20_8091_s_201	11588182	A 61 kDa luciferase polypeptide showed no binding to any of the homopolymers, confirming the RNA-binding activity of the Msi2 and Msi1 proteins.	bind
48026	4	9127	6	10	NULL	0	NULL	statement 3	NULL		confirms	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_20_8091_s_201	11588182	A 61 kDa luciferase polypeptide showed no binding to any of the homopolymers, confirming the RNA-binding activity of the Msi2 and Msi1 proteins.	bind
48027	5	9127	6	10	NULL	0	NULL	statement 3	NULL		confirms	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_20_8091_s_201	11588182	A 61 kDa luciferase polypeptide showed no binding to any of the homopolymers, confirming the RNA-binding activity of the Msi2 and Msi1 proteins.	bind
39233	1	9129	5	13	NULL	NULL	NULL	65-kDa cellular protein	GP		bind					 Riboprobe	NucleicAcid			NRE	NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_1_163_s_93	8990179	A 65-kDa Cellular Protein Binds to an NRE Riboprobe.	bind
31368	1	9129	6	NULL	NULL	0	NULL	65-kDa Cellular Protein	NULL		bind	NULL				riboprobe	NULL			NRE	NULL		0	NULL	NULL	NULL	gw60_pnas_94_1_163_s_93	8990179	A 65-kDa Cellular Protein Binds to an NRE Riboprobe.	bind
42525	1	9131	5	13	NULL	NULL	NULL	Tpardl	GP		contains				predicted promoter					E boxes	NULL		NULL	NULL	NULL	NULL	gw60_genomeres_10_12_1928_s_171	11116088	A 7-kb region comprising both predicted promoters of  Tpardl includes four E boxes (three subtypes of the 5''-CANNGT-3'' consensus), two fork-head transcription factor sites, a cyclic AMP response element binding (CREB) site, and four Sp1 sites near the P4 promoter.	bind
42526	2	9131	5	13	NULL	NULL	NULL	Tpardl	GP		contains				predicted promoter					fork-head transcription factor sites	NULL		NULL	NULL	NULL	NULL	gw60_genomeres_10_12_1928_s_171	11116088	A 7-kb region comprising both predicted promoters of  Tpardl includes four E boxes (three subtypes of the 5''-CANNGT-3'' consensus), two fork-head transcription factor sites, a cyclic AMP response element binding (CREB) site, and four Sp1 sites near the P4 promoter.	bind
42527	3	9131	5	13	NULL	NULL	NULL	Tpardl	GP		contains				predicted promoter					CREB site	NULL		NULL	NULL	NULL	NULL	gw60_genomeres_10_12_1928_s_171	11116088	A 7-kb region comprising both predicted promoters of  Tpardl includes four E boxes (three subtypes of the 5''-CANNGT-3'' consensus), two fork-head transcription factor sites, a cyclic AMP response element binding (CREB) site, and four Sp1 sites near the P4 promoter.	bind
42528	4	9131	5	13	NULL	NULL	NULL	CREB site	GP		is					cyclic AMP response element binding site	GP				NULL		NULL	NULL	NULL	NULL	gw60_genomeres_10_12_1928_s_171	11116088	A 7-kb region comprising both predicted promoters of  Tpardl includes four E boxes (three subtypes of the 5''-CANNGT-3'' consensus), two fork-head transcription factor sites, a cyclic AMP response element binding (CREB) site, and four Sp1 sites near the P4 promoter.	bind
42529	5	9131	5	13	NULL	NULL	NULL	Tpardl	GP		contains				predicted promoter					Sp1 sites	NULL		NULL	NULL	NULL	NULL	gw60_genomeres_10_12_1928_s_171	11116088	A 7-kb region comprising both predicted promoters of  Tpardl includes four E boxes (three subtypes of the 5''-CANNGT-3'' consensus), two fork-head transcription factor sites, a cyclic AMP response element binding (CREB) site, and four Sp1 sites near the P4 promoter.	bind
42533	6	9131	5	10	NULL	0	NULL		NULL		is located near	NULL			Sp1 sites		NULL			P4 promoter	NULL		NULL	NULL	NULL	NULL	gw60_genomeres_10_12_1928_s_171	11116088	A 7-kb region comprising both predicted promoters of  Tpardl includes four E boxes (three subtypes of the 5''-CANNGT-3'' consensus), two fork-head transcription factor sites, a cyclic AMP response element binding (CREB) site, and four Sp1 sites near the P4 promoter.	bind
40388	1	9131	6	NULL	NULL	0	NULL	Tpardl	NULL		contains	NULL			predicted promoter		NULL			E-boxes	NULL		0	NULL	NULL	NULL	gw60_genomeres_10_12_1928_s_171	11116088	A 7-kb region comprising both predicted promoters of  Tpardl includes four E boxes (three subtypes of the 5''-CANNGT-3'' consensus), two fork-head transcription factor sites, a cyclic AMP response element binding (CREB) site, and four Sp1 sites near the P4 promoter.	bind
40389	2	9131	6	NULL	NULL	0	NULL	Tpardl	NULL		includes	NULL			predicted promoter		NULL			fork-head transcription factor sites	NULL		0	NULL	NULL	NULL	gw60_genomeres_10_12_1928_s_171	11116088	A 7-kb region comprising both predicted promoters of  Tpardl includes four E boxes (three subtypes of the 5''-CANNGT-3'' consensus), two fork-head transcription factor sites, a cyclic AMP response element binding (CREB) site, and four Sp1 sites near the P4 promoter.	bind
40390	3	9131	6	NULL	NULL	0	NULL	Tpardl	NULL		contains	NULL			predicted promoter		NULL			CREB site	NULL		0	NULL	NULL	NULL	gw60_genomeres_10_12_1928_s_171	11116088	A 7-kb region comprising both predicted promoters of  Tpardl includes four E boxes (three subtypes of the 5''-CANNGT-3'' consensus), two fork-head transcription factor sites, a cyclic AMP response element binding (CREB) site, and four Sp1 sites near the P4 promoter.	bind
40391	4	9131	6	NULL	NULL	0	NULL	CREB	NULL		is	NULL				cyclic AMP response element binding	NULL				NULL		0	NULL	NULL	NULL	gw60_genomeres_10_12_1928_s_171	11116088	A 7-kb region comprising both predicted promoters of  Tpardl includes four E boxes (three subtypes of the 5''-CANNGT-3'' consensus), two fork-head transcription factor sites, a cyclic AMP response element binding (CREB) site, and four Sp1 sites near the P4 promoter.	bind
40392	5	9131	6	10	NULL	0	NULL		NULL		is present near	NULL			Sp1 site		NULL			P4 promoter	NULL		NULL	NULL	NULL	NULL	gw60_genomeres_10_12_1928_s_171	11116088	A 7-kb region comprising both predicted promoters of  Tpardl includes four E boxes (three subtypes of the 5''-CANNGT-3'' consensus), two fork-head transcription factor sites, a cyclic AMP response element binding (CREB) site, and four Sp1 sites near the P4 promoter.	bind
48101	6	9131	6	10	NULL	0	NULL	Tpardl	NULL		contains	NULL			predicted promoter	statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_genomeres_10_12_1928_s_171	11116088	A 7-kb region comprising both predicted promoters of  Tpardl includes four E boxes (three subtypes of the 5''-CANNGT-3'' consensus), two fork-head transcription factor sites, a cyclic AMP response element binding (CREB) site, and four Sp1 sites near the P4 promoter.	bind
39234	1	9132	5	13	NULL	NULL	NULL	p72fyn-R	GP		bind					TcR/CD3	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_149_1_181_s_423	10747096	A 72-kilodalton fyn related polypeptide (p72fyn-R) binds to the antigen receptor/CD3 (TcR/CD3) complex.	bind
39235	2	9132	5	13	NULL	NULL	NULL	p72fyn-R	GP		is					72-kilodalton fyn related polypeptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_149_1_181_s_423	10747096	A 72-kilodalton fyn related polypeptide (p72fyn-R) binds to the antigen receptor/CD3 (TcR/CD3) complex.	bind
39236	3	9132	5	13	NULL	NULL	NULL	TcR/CD3	GP		is					antigen receptor/CD3 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_149_1_181_s_423	10747096	A 72-kilodalton fyn related polypeptide (p72fyn-R) binds to the antigen receptor/CD3 (TcR/CD3) complex.	bind
31395	1	9132	6	NULL	NULL	0	NULL	p72fyn-R	NULL		is	NULL				72-kilodalton fyn related polypeptide	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_149_1_181_s_423	10747096	A 72-kilodalton fyn related polypeptide (p72fyn-R) binds to the antigen receptor/CD3 (TcR/CD3) complex.	bind
31396	2	9132	6	NULL	NULL	0	NULL	TcR/CD3 complex	NULL		is	NULL				antigen receptor/CD3 complex	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_149_1_181_s_423	10747096	A 72-kilodalton fyn related polypeptide (p72fyn-R) binds to the antigen receptor/CD3 (TcR/CD3) complex.	bind
31397	3	9132	6	NULL	NULL	0	NULL	p72fyn-R	NULL		bind	NULL				TcR/CD3 complex	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_149_1_181_s_423	10747096	A 72-kilodalton fyn related polypeptide (p72fyn-R) binds to the antigen receptor/CD3 (TcR/CD3) complex.	bind
39237	1	9133	5	13	NULL	NULL	NULL	75 kDa protein	GP		bind									41 nt region	NULL		NULL	NULL	NULL	NULL	gw60_cell_108_4_533_s_179	11909524	A 75 kDa protein has been shown to bind to a 41 nt region, and binding of this protein may be important for localization (see section on structure of elements below).	bind
39238	2	9133	5	13	NULL	NULL	NULL	statement 1	Process		important for		may be			localization	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_108_4_533_s_179	11909524	A 75 kDa protein has been shown to bind to a 41 nt region, and binding of this protein may be important for localization (see section on structure of elements below).	bind
31398	1	9133	6	NULL	NULL	0	NULL	75 kDa protein	NULL		bind	NULL					NULL			41 nt region	NULL		0	NULL	NULL	NULL	gw60_cell_108_4_533_s_179	11909524	A 75 kDa protein has been shown to bind to a 41 nt region, and binding of this protein may be important for localization (see section on structure of elements below).	bind
57768	2	9133	6	10	NULL	0	NULL	statement 1			important for		may be			localization					NULL		0	NULL	NULL	NULL	gw60_cell_108_4_533_s_179	11909524	A 75 kDa protein has been shown to bind to a 41 nt region, and binding of this protein may be important for localization (see section on structure of elements below).	bind
39239	1	9134	5	13	NULL	NULL	NULL	75-kDa brush border protein	GP		bind		directly			horseradish peroxidase-streptavidin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_6_3509_s_197	10816505	A 75-kDa brush border protein bound the horseradish peroxidase-streptavidin directly ( 9) and was stained prominently regardless of membrane treatment.	bind
31409	1	9134	6	NULL	NULL	0	NULL	75-kDa brush border protein	NULL		bind	NULL	directly			horseradish peroxidase-streptavidin	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3509_s_197	10816505	A 75-kDa brush border protein bound the horseradish peroxidase-streptavidin directly ( 9) and was stained prominently regardless of membrane treatment.	bind
48028	1	9135	5	13	NULL	NULL	NULL	anti-mouse Cdc21 antibody	GP		recognize					 86-kDa protein	GP				NULL	whole cell extracts	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24115_s_105	8798650	A 86-kDa protein in whole cell extracts that was recognized with the anti-mouse Cdc21 antibody did not bind with the histone column.	bind
31410	1	9135	6	NULL	NULL	0	NULL	Cdc21 antibody	NULL		recognizes	NULL				86-kDa protein	NULL				NULL	whole-cell extracts	0	NULL	NULL	NULL	gw60_jbiolchem_271_39_24115_s_105	8798650	A 86-kDa protein in whole cell extracts that was recognized with the anti-mouse Cdc21 antibody did not bind with the histone column.	bind
39240	1	9136	5	13	NULL	NULL	NULL	95-kDa protein	GP		corresponds to					STAT5	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_6850_s_86	9054369	A 95-kDa band corresponding to STAT5 was tyrosine-phosphorylated in response to EPO (Fig.  2 B,  lane 2) but not SCF (Fig.  2 B,  lane 3), and DNA binding to a STAT5 DNA element was observed only in EPO-treated cells (Fig.  2 C,  lane 2).	bind
39241	2	9136	5	13	NULL	NULL	NULL	EPO	GP		leads to					STAT5	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_6850_s_86	9054369	A 95-kDa band corresponding to STAT5 was tyrosine-phosphorylated in response to EPO (Fig.  2 B,  lane 2) but not SCF (Fig.  2 B,  lane 3), and DNA binding to a STAT5 DNA element was observed only in EPO-treated cells (Fig.  2 C,  lane 2).	bind
39242	3	9136	5	13	NULL	NULL	NULL	SCF	GP		does not lead to					STAT5	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_6850_s_86	9054369	A 95-kDa band corresponding to STAT5 was tyrosine-phosphorylated in response to EPO (Fig.  2 B,  lane 2) but not SCF (Fig.  2 B,  lane 3), and DNA binding to a STAT5 DNA element was observed only in EPO-treated cells (Fig.  2 C,  lane 2).	bind
39243	4	9136	5	13	NULL	NULL	NULL	DNA	NucleicAcid		bind					STAT5	GP			DNA element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_6850_s_86	9054369	A 95-kDa band corresponding to STAT5 was tyrosine-phosphorylated in response to EPO (Fig.  2 B,  lane 2) but not SCF (Fig.  2 B,  lane 3), and DNA binding to a STAT5 DNA element was observed only in EPO-treated cells (Fig.  2 C,  lane 2).	bind
39244	5	9136	5	13	NULL	NULL	NULL	statement 4	Process		occurs in		only			EPO-treated cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_6850_s_86	9054369	A 95-kDa band corresponding to STAT5 was tyrosine-phosphorylated in response to EPO (Fig.  2 B,  lane 2) but not SCF (Fig.  2 B,  lane 3), and DNA binding to a STAT5 DNA element was observed only in EPO-treated cells (Fig.  2 C,  lane 2).	bind
49193	1	9136	6	NULL	NULL	0	NULL	95-kDa protein	NULL		corresponds to	NULL				STAT5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_11_6850_s_86	9054369	A 95-kDa band corresponding to STAT5 was tyrosine-phosphorylated in response to EPO (Fig.  2 B,  lane 2) but not SCF (Fig.  2 B,  lane 3), and DNA binding to a STAT5 DNA element was observed only in EPO-treated cells (Fig.  2 C,  lane 2).	bind
49194	2	9136	6	NULL	NULL	0	NULL	STAT5	NULL	phosphorylation of	occurs in response to	NULL		tyrosine		EPO	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_11_6850_s_86	9054369	A 95-kDa band corresponding to STAT5 was tyrosine-phosphorylated in response to EPO (Fig.  2 B,  lane 2) but not SCF (Fig.  2 B,  lane 3), and DNA binding to a STAT5 DNA element was observed only in EPO-treated cells (Fig.  2 C,  lane 2).	bind
49214	3	9136	6	NULL	NULL	0	NULL	STAT5	NULL	phosphorylation of	does not occur in response to	NULL		tyrosine		SCF	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_11_6850_s_86	9054369	A 95-kDa band corresponding to STAT5 was tyrosine-phosphorylated in response to EPO (Fig.  2 B,  lane 2) but not SCF (Fig.  2 B,  lane 3), and DNA binding to a STAT5 DNA element was observed only in EPO-treated cells (Fig.  2 C,  lane 2).	bind
49215	4	9136	6	NULL	NULL	0	NULL	DNA	NULL		bind	NULL				STAT5 	NULL			DNA element	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_11_6850_s_86	9054369	A 95-kDa band corresponding to STAT5 was tyrosine-phosphorylated in response to EPO (Fig.  2 B,  lane 2) but not SCF (Fig.  2 B,  lane 3), and DNA binding to a STAT5 DNA element was observed only in EPO-treated cells (Fig.  2 C,  lane 2).	bind
49216	5	9136	6	NULL	NULL	0	NULL	statement 4	NULL		occurs in presence of	NULL	only			EPO-treated cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_11_6850_s_86	9054369	A 95-kDa band corresponding to STAT5 was tyrosine-phosphorylated in response to EPO (Fig.  2 B,  lane 2) but not SCF (Fig.  2 B,  lane 3), and DNA binding to a STAT5 DNA element was observed only in EPO-treated cells (Fig.  2 C,  lane 2).	bind
39245	1	9137	5	13	NULL	NULL	NULL	95-kDa protein	GP	phosphorylated	bind					Grb2	GP		C-terminal SH3 domain		NULL	CDMer cell lysate	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1171_s_179	9891051	A 95-kDa phosphorylated protein was immunoprecipitated by the C-terminal SH3 domain of Grb2 in the CDMer cell lysate (Fig.  4B), and it is likely that it corresponds to the p95 protein binding to the PI 3-kinase (Fig.  4C and D).	bind
39246	2	9137	5	13	NULL	NULL	NULL	p95 protein	GP		bind					PI 3-kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1171_s_179	9891051	A 95-kDa phosphorylated protein was immunoprecipitated by the C-terminal SH3 domain of Grb2 in the CDMer cell lysate (Fig.  4B), and it is likely that it corresponds to the p95 protein binding to the PI 3-kinase (Fig.  4C and D).	bind
57769	3	9137	5	13	NULL	NULL	NULL	95-kDa protein	GP	phosphorylated	corresponds to		may			p95 protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1171_s_179	9891051	A 95-kDa phosphorylated protein was immunoprecipitated by the C-terminal SH3 domain of Grb2 in the CDMer cell lysate (Fig.  4B), and it is likely that it corresponds to the p95 protein binding to the PI 3-kinase (Fig.  4C and D).	bind
31411	1	9137	6	NULL	NULL	0	NULL	95-kDa protein	NULL	phosphorylated	bind	NULL				Grb2	NULL		C-terminal SH3 domain		NULL	CDMer cell lysate	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1171_s_179	9891051	A 95-kDa phosphorylated protein was immunoprecipitated by the C-terminal SH3 domain of Grb2 in the CDMer cell lysate (Fig.  4B), and it is likely that it corresponds to the p95 protein binding to the PI 3-kinase (Fig.  4C and D).	bind
31412	2	9137	6	NULL	NULL	0	NULL	p95 protein	NULL		bind	NULL				PI 3-kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1171_s_179	9891051	A 95-kDa phosphorylated protein was immunoprecipitated by the C-terminal SH3 domain of Grb2 in the CDMer cell lysate (Fig.  4B), and it is likely that it corresponds to the p95 protein binding to the PI 3-kinase (Fig.  4C and D).	bind
57770	3	9137	6	10	NULL	0	NULL	95-kDa protein		phosphorylated	corresponds to		may			p95 protein					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1171_s_179	9891051	A 95-kDa phosphorylated protein was immunoprecipitated by the C-terminal SH3 domain of Grb2 in the CDMer cell lysate (Fig.  4B), and it is likely that it corresponds to the p95 protein binding to the PI 3-kinase (Fig.  4C and D).	bind
39248	1	9138	5	13	NULL	NULL	NULL	insulin receptor	GP		is			beta subunit		95-kDa protein	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_21_12595_s_115	8647870	A 95-kDa tyrosine-phosphorylated protein  (a beta  subunit of insulin receptor) more efficiently bound to  GST-full-length SHPTP2 rather than to GST-SH2 in response to insulin,  although its association with both GST proteins was weaker when  compared with two other major tyrosine-phosphorylated proteins.	bind
39249	2	9138	5	13	NULL	NULL	NULL	insulin receptor	GP		bind			beta subunit		GST-SHPTP2	GP	full-length			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_21_12595_s_115	8647870	A 95-kDa tyrosine-phosphorylated protein  (a beta  subunit of insulin receptor) more efficiently bound to  GST-full-length SHPTP2 rather than to GST-SH2 in response to insulin,  although its association with both GST proteins was weaker when  compared with two other major tyrosine-phosphorylated proteins.	bind
39250	3	9138	5	13	NULL	NULL	NULL	insulin receptor	GP		bind			beta subunit		GST-SH2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_21_12595_s_115	8647870	A 95-kDa tyrosine-phosphorylated protein  (a beta  subunit of insulin receptor) more efficiently bound to  GST-full-length SHPTP2 rather than to GST-SH2 in response to insulin,  although its association with both GST proteins was weaker when  compared with two other major tyrosine-phosphorylated proteins.	bind
39251	4	9138	5	13	NULL	NULL	NULL	statement 2	Process	affinity of	more efficient than					statement 3	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_21_12595_s_115	8647870	A 95-kDa tyrosine-phosphorylated protein  (a beta  subunit of insulin receptor) more efficiently bound to  GST-full-length SHPTP2 rather than to GST-SH2 in response to insulin,  although its association with both GST proteins was weaker when  compared with two other major tyrosine-phosphorylated proteins.	bind
39252	5	9138	5	13	NULL	NULL	NULL	statement 2	Process		in response to					insulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_21_12595_s_115	8647870	A 95-kDa tyrosine-phosphorylated protein  (a beta  subunit of insulin receptor) more efficiently bound to  GST-full-length SHPTP2 rather than to GST-SH2 in response to insulin,  although its association with both GST proteins was weaker when  compared with two other major tyrosine-phosphorylated proteins.	bind
39253	6	9138	5	13	NULL	NULL	NULL	statement 3	Process		in response to					insulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_21_12595_s_115	8647870	A 95-kDa tyrosine-phosphorylated protein  (a beta  subunit of insulin receptor) more efficiently bound to  GST-full-length SHPTP2 rather than to GST-SH2 in response to insulin,  although its association with both GST proteins was weaker when  compared with two other major tyrosine-phosphorylated proteins.	bind
31413	1	9138	6	10	NULL	0	NULL	 insulin receptor	NULL		is 	NULL		beta subunit of		95-kDa protein	NULL	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_21_12595_s_115	8647870	A 95-kDa tyrosine-phosphorylated protein  (a beta  subunit of insulin receptor) more efficiently bound to  GST-full-length SHPTP2 rather than to GST-SH2 in response to insulin,  although its association with both GST proteins was weaker when  compared with two other major tyrosine-phosphorylated proteins.	bind
31414	2	9138	6	10	NULL	0	NULL	 insulin receptor	NULL		bind	NULL		beta subunit of		GST- SHPTP2	NULL	full-length			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_21_12595_s_115	8647870	A 95-kDa tyrosine-phosphorylated protein  (a beta  subunit of insulin receptor) more efficiently bound to  GST-full-length SHPTP2 rather than to GST-SH2 in response to insulin,  although its association with both GST proteins was weaker when  compared with two other major tyrosine-phosphorylated proteins.	bind
31415	3	9138	6	10	NULL	0	NULL	insulin receptor	NULL		bind	NULL		beta subunit of 		GST-SH2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_21_12595_s_115	8647870	A 95-kDa tyrosine-phosphorylated protein  (a beta  subunit of insulin receptor) more efficiently bound to  GST-full-length SHPTP2 rather than to GST-SH2 in response to insulin,  although its association with both GST proteins was weaker when  compared with two other major tyrosine-phosphorylated proteins.	bind
31416	4	9138	6	NULL	NULL	0	NULL	statement 2	NULL		occurs in response to	NULL				insulin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_21_12595_s_115	8647870	A 95-kDa tyrosine-phosphorylated protein  (a beta  subunit of insulin receptor) more efficiently bound to  GST-full-length SHPTP2 rather than to GST-SH2 in response to insulin,  although its association with both GST proteins was weaker when  compared with two other major tyrosine-phosphorylated proteins.	bind
31417	5	9138	6	NULL	NULL	0	NULL	statement 3	NULL		occurs in response to	NULL				insulin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_21_12595_s_115	8647870	A 95-kDa tyrosine-phosphorylated protein  (a beta  subunit of insulin receptor) more efficiently bound to  GST-full-length SHPTP2 rather than to GST-SH2 in response to insulin,  although its association with both GST proteins was weaker when  compared with two other major tyrosine-phosphorylated proteins.	bind
31418	6	9138	6	NULL	NULL	0	NULL	statement 2	NULL	affinity of	is more than	NULL				statement 3	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_21_12595_s_115	8647870	A 95-kDa tyrosine-phosphorylated protein  (a beta  subunit of insulin receptor) more efficiently bound to  GST-full-length SHPTP2 rather than to GST-SH2 in response to insulin,  although its association with both GST proteins was weaker when  compared with two other major tyrosine-phosphorylated proteins.	bind
39254	1	9141	5	13	NULL	NULL	NULL	CRIM1	GP		does not bind					BMP4	GP				NULL	solution	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34181_s_157	12805376	A and   B, CRIM1 does not bind to BMP4 or BMP7 when incubated in solution.	bind
39255	2	9141	5	13	NULL	NULL	NULL	CRIM1	GP		does not bind					BMP7	GP				NULL	solution	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34181_s_157	12805376	A and   B, CRIM1 does not bind to BMP4 or BMP7 when incubated in solution.	bind
39256	3	9141	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34181_s_157	12805376	A and   B, CRIM1 does not bind to BMP4 or BMP7 when incubated in solution.	bind
31419	1	9141	6	NULL	NULL	0	NULL	CRIM1	NULL		does not bind	NULL				BMP4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34181_s_157	12805376	A and   B, CRIM1 does not bind to BMP4 or BMP7 when incubated in solution.	bind
31420	2	9141	6	NULL	NULL	0	NULL	CRIM1	NULL		does not bind	NULL				BMP7	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34181_s_157	12805376	A and   B, CRIM1 does not bind to BMP4 or BMP7 when incubated in solution.	bind
48029	3	9141	6	10	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34181_s_157	12805376	A and   B, CRIM1 does not bind to BMP4 or BMP7 when incubated in solution.	bind
39257	1	9146	5	13	NULL	NULL	NULL	Ub	GP		bind					UBA(1)	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_12_11926_s_151	14707125	a and  b, 1H,15N HSQC of free Ub and Ub bound to UBA(1) and UBA(2).	bind
39258	2	9146	5	13	NULL	NULL	NULL	Ub	GP		bind					UBA(2)	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_12_11926_s_151	14707125	a and  b, 1H,15N HSQC of free Ub and Ub bound to UBA(1) and UBA(2).	bind
31421	1	9146	6	NULL	NULL	0	NULL	Ub	NULL		bind	NULL				UBA(1)	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11926_s_151	14707125	a and  b, 1H,15N HSQC of free Ub and Ub bound to UBA(1) and UBA(2).	bind
31422	2	9146	6	NULL	NULL	0	NULL	Ub	NULL		bind	NULL				UBA(2)	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11926_s_151	14707125	a and  b, 1H,15N HSQC of free Ub and Ub bound to UBA(1) and UBA(2).	bind
39259	1	9147	5	13	NULL	NULL	NULL	UBA(1)	GP		bind					Ub	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_12_11926_s_95	14707125	a and  b, 500 MHz 1H-15N two-dimensional HSQC spectra of UBA(1) and UBA(2) free and bound to Ub.	bind
39260	2	9147	5	13	NULL	NULL	NULL	UBA(2)	GP		bind					Ub	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_12_11926_s_95	14707125	a and  b, 500 MHz 1H-15N two-dimensional HSQC spectra of UBA(1) and UBA(2) free and bound to Ub.	bind
48030	1	9147	6	10	NULL	0	NULL	UBA(1)	NULL		bind	NULL				Ub	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11926_s_95	14707125	a and  b, 500 MHz 1H-15N two-dimensional HSQC spectra of UBA(1) and UBA(2) free and bound to Ub.	bind
48031	2	9147	6	10	NULL	0	NULL	UBA(2)	NULL		bind	NULL				Ub	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11926_s_95	14707125	a and  b, 500 MHz 1H-15N two-dimensional HSQC spectra of UBA(1) and UBA(2) free and bound to Ub.	bind
39261	1	9148	5	13	NULL	NULL	NULL	BAF	GP		bind					H3	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_42252_s_215	16203725	A and  B, BAF binds core histone H3 with nanomolar affinity in microtiter assays.	bind
39262	2	9148	5	13	NULL	NULL	NULL	H3	GP		is a type of					core histone	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_42252_s_215	16203725	A and  B, BAF binds core histone H3 with nanomolar affinity in microtiter assays.	bind
31424	1	9148	6	10	NULL	0	NULL	BAF			bind					 H3					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_42252_s_215	16203725	A and  B, BAF binds core histone H3 with nanomolar affinity in microtiter assays.	bind
57848	2	9148	6	10	NULL	0	NULL	H3			is a type of					core histone					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_42252_s_215	16203725	A and  B, BAF binds core histone H3 with nanomolar affinity in microtiter assays.	bind
39263	1	9149	5	13	NULL	NULL	NULL	Dkk1-AP	GP		bind					LRP6	GP	full-length			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_19883_s_72	15778503	A and  B, binding of Dkk1-AP and sclerostin-AP to full-length LRP6, LRP5, or LacZ.	bind
39264	2	9149	5	13	NULL	NULL	NULL	Dkk1-AP	GP		bind					LRP5	GP	full-length			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_19883_s_72	15778503	A and  B, binding of Dkk1-AP and sclerostin-AP to full-length LRP6, LRP5, or LacZ.	bind
39265	3	9149	5	13	NULL	NULL	NULL	Dkk1-AP	GP		bind					LacZ	GP	full-length			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_19883_s_72	15778503	A and  B, binding of Dkk1-AP and sclerostin-AP to full-length LRP6, LRP5, or LacZ.	bind
39266	4	9149	5	13	NULL	NULL	NULL	sclerostin-AP	GP		bind					LRP6	GP	full-length			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_19883_s_72	15778503	A and  B, binding of Dkk1-AP and sclerostin-AP to full-length LRP6, LRP5, or LacZ.	bind
39267	5	9149	5	13	NULL	NULL	NULL	sclerostin-AP	GP		bind					LRP5	GP	full-length			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_19883_s_72	15778503	A and  B, binding of Dkk1-AP and sclerostin-AP to full-length LRP6, LRP5, or LacZ.	bind
39268	6	9149	5	13	NULL	NULL	NULL	sclerostin-AP	GP		bind					LacZ	GP	full-length			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_19883_s_72	15778503	A and  B, binding of Dkk1-AP and sclerostin-AP to full-length LRP6, LRP5, or LacZ.	bind
31425	1	9149	6	NULL	NULL	0	NULL	Dkk1-AP	NULL		bind	NULL				LRP6	NULL	full length			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19883_s_72	15778503	A and  B, binding of Dkk1-AP and sclerostin-AP to full-length LRP6, LRP5, or LacZ.	bind
31426	2	9149	6	NULL	NULL	0	NULL	Dkk1-AP	NULL		bind	NULL				LRP5	NULL	full length			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19883_s_72	15778503	A and  B, binding of Dkk1-AP and sclerostin-AP to full-length LRP6, LRP5, or LacZ.	bind
31427	3	9149	6	NULL	NULL	0	NULL	sclerostin-AP	NULL		bind	NULL				LRP6	NULL	full length			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19883_s_72	15778503	A and  B, binding of Dkk1-AP and sclerostin-AP to full-length LRP6, LRP5, or LacZ.	bind
31428	4	9149	6	NULL	NULL	0	NULL	sclerostin-AP	NULL		bind	NULL				LRP5	NULL	full length			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19883_s_72	15778503	A and  B, binding of Dkk1-AP and sclerostin-AP to full-length LRP6, LRP5, or LacZ.	bind
31429	5	9149	6	10	NULL	0	NULL	Dkk1-AP	NULL		bind	NULL				LacZ	NULL	full-length			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_19883_s_72	15778503	A and  B, binding of Dkk1-AP and sclerostin-AP to full-length LRP6, LRP5, or LacZ.	bind
31430	6	9149	6	10	NULL	0	NULL	sclerostin-AP	NULL		bind	NULL				LacZ	NULL	full-length			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_19883_s_72	15778503	A and  B, binding of Dkk1-AP and sclerostin-AP to full-length LRP6, LRP5, or LacZ.	bind
39269	1	9150	5	13	NULL	NULL	NULL	E2	GP		bind					HSC	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_12_11329_s_199	15611113	A and  B, binding of E2 to HSC was evaluated by a competition assay.	bind
31431	1	9150	6	NULL	NULL	0	NULL	E2	NULL		bind	NULL				HSC	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_12_11329_s_199	15611113	A and  B, binding of E2 to HSC was evaluated by a competition assay.	bind
39270	1	9151	5	13	NULL	NULL	NULL	JIP1b	GP		bind					APP constructs	GP		cytoplasmic domain		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_30_27567_s_85	12023290	A and  B, binding of JIP1b to the APP cytoplasmic domain (APPcyt) constructs  in vitro.	bind
39271	2	9151	5	13	NULL	NULL	NULL	APPcyt	GP		is					APP cytoplasmic domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_30_27567_s_85	12023290	A and  B, binding of JIP1b to the APP cytoplasmic domain (APPcyt) constructs  in vitro.	bind
31432	1	9151	6	10	NULL	0	NULL	JIP1b			bind					APP constructs			cytoplasmic domain		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_30_27567_s_85	12023290	A and  B, binding of JIP1b to the APP cytoplasmic domain (APPcyt) constructs  in vitro.	bind
31433	2	9151	6	10	NULL	0	NULL	APPcyt			is					APP cytoplasmic domain					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_30_27567_s_85	12023290	A and  B, binding of JIP1b to the APP cytoplasmic domain (APPcyt) constructs  in vitro.	bind
57849	1	9152	5	13	NULL	NULL	NULL	E-cadherin	GP	mutant	does not bind			E/761		PS1	GP		A431D-E/761		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_43_36007_s_71	16126725	a and  b, cadherin-negative A431D cell lines stably transfected with vector (A431D,  lanes 1 - 3), WT E-cadherin (A431D-E,  lanes 4 - 6), or E-cadherin mutant E/761 unable to bind PS1 (A431D-E/761,  lanes 7 - 9) were transiently transfected with the beta-catenin mutant S33Y.	bind
57850	1	9152	6	10	NULL	0	NULL	E-cadherin 		mutant	does not bind			E/761		PS1			A431D-E/761		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_43_36007_s_71	16126725	a and  b, cadherin-negative A431D cell lines stably transfected with vector (A431D,  lanes 1 - 3), WT E-cadherin (A431D-E,  lanes 4 - 6), or E-cadherin mutant E/761 unable to bind PS1 (A431D-E/761,  lanes 7 - 9) were transiently transfected with the beta-catenin mutant S33Y.	bind
39272	1	9153	5	13	NULL	NULL	NULL	brevican PLD chimera	GP		bind					B28	Cell				NULL	cell surface	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_16_11431_s_93	10196237	A and  B, cell surface binding of brevican PLD chimera to B28	bind
31434	1	9153	6	10	NULL	0	NULL	brevican PLD chimera	NULL		bind	NULL				B28	NULL				NULL	cell surface	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_16_11431_s_93	10196237	A and  B, cell surface binding of brevican PLD chimera to B28	bind
39273	1	9154	5	13	NULL	NULL	NULL	THP-1	GP		bind					Jurkat cells	Cell	necrotic			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35733_s_216	16107330	A and  B, confocal images of simultaneous  red and  green channels, showing binding between THP-1 and necrotic Jurkat cells that precedes ingestion.	bind
39274	2	9154	5	13	NULL	NULL	NULL	statement 1	Process		precedes					ingestion	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35733_s_216	16107330	A and  B, confocal images of simultaneous  red and  green channels, showing binding between THP-1 and necrotic Jurkat cells that precedes ingestion.	bind
31435	1	9154	6	NULL	NULL	0	NULL	THP-1	NULL		bind	NULL				jurkat cells	NULL	necrotic			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_42_35733_s_216	16107330	A and  B, confocal images of simultaneous  red and  green channels, showing binding between THP-1 and necrotic Jurkat cells that precedes ingestion.	bind
31436	2	9154	6	NULL	NULL	0	NULL	statement 1	NULL		precedes	NULL				ingestion	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_42_35733_s_216	16107330	A and  B, confocal images of simultaneous  red and  green channels, showing binding between THP-1 and necrotic Jurkat cells that precedes ingestion.	bind
39275	2	9155	5	13	NULL	NULL	NULL	COPII proteins	GP		bind					statement 1	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_9_7758_s_177	15623526	A and  B, COPII proteins bound to CHO-K1 derived microsomes were sedimented from unbound proteins  through a 0.3 M sucrose cushion and resolved by SDS-PAGE, then transferred to a polyvinylidene difluoride  membrane.	bind
48032	1	9155	5	13	NULL	NULL	NULL	microsomes	CellComponent		derived from					CHO-K1	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_9_7758_s_177	15623526	A and  B, COPII proteins bound to CHO-K1 derived microsomes were sedimented from unbound proteins  through a 0.3 M sucrose cushion and resolved by SDS-PAGE, then transferred to a polyvinylidene difluoride  membrane.	bind
31437	2	9155	6	10	NULL	0	NULL	COPII proteins	NULL		bind	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_9_7758_s_177	15623526	A and  B, COPII proteins bound to CHO-K1 derived microsomes were sedimented from unbound proteins  through a 0.3 M sucrose cushion and resolved by SDS-PAGE, then transferred to a polyvinylidene difluoride  membrane.	bind
48033	1	9155	6	10	NULL	0	NULL	microsomes	NULL		derived from	NULL				CHO-K1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_9_7758_s_177	15623526	A and  B, COPII proteins bound to CHO-K1 derived microsomes were sedimented from unbound proteins  through a 0.3 M sucrose cushion and resolved by SDS-PAGE, then transferred to a polyvinylidene difluoride  membrane.	bind
49155	1	9157	5	13	NULL	NULL	NULL	Stat1	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_867_s_109	10625620	A and  B, DNA binding activities of Stat1 and Stat3 in response to IFN-gamma and IL-3.	bind
49156	2	9157	5	13	NULL	NULL	NULL	Stat3	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_867_s_109	10625620	A and  B, DNA binding activities of Stat1 and Stat3 in response to IFN-gamma and IL-3.	bind
49541	3	9157	5	13	NULL	NULL	NULL	statement 1	Process		in response to					IFN-gamma	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_867_s_109	10625620	A and  B, DNA binding activities of Stat1 and Stat3 in response to IFN-gamma and IL-3.	bind
49542	4	9157	5	13	NULL	NULL	NULL	statement 2	Process		in response to					IFN-gamma	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_867_s_109	10625620	A and  B, DNA binding activities of Stat1 and Stat3 in response to IFN-gamma and IL-3.	bind
49543	5	9157	5	13	NULL	NULL	NULL	statement 1	Process		in response to					IL-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_867_s_109	10625620	A and  B, DNA binding activities of Stat1 and Stat3 in response to IFN-gamma and IL-3.	bind
49544	6	9157	5	13	NULL	NULL	NULL	statement 2	Process		in response to					IL-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_2_867_s_109	10625620	A and  B, DNA binding activities of Stat1 and Stat3 in response to IFN-gamma and IL-3.	bind
31438	1	9157	6	NULL	NULL	0	NULL	Stat1	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_2_867_s_109	10625620	A and  B, DNA binding activities of Stat1 and Stat3 in response to IFN-gamma and IL-3.	bind
31439	2	9157	6	NULL	NULL	0	NULL	Stat3	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_2_867_s_109	10625620	A and  B, DNA binding activities of Stat1 and Stat3 in response to IFN-gamma and IL-3.	bind
48034	3	9157	6	10	NULL	0	NULL	statement 1	NULL		in response to	NULL				IFN-gamma	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_2_867_s_109	10625620	A and  B, DNA binding activities of Stat1 and Stat3 in response to IFN-gamma and IL-3.	bind
48035	4	9157	6	10	NULL	0	NULL	statement 2	NULL		in response to	NULL				 IL-3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_2_867_s_109	10625620	A and  B, DNA binding activities of Stat1 and Stat3 in response to IFN-gamma and IL-3.	bind
49554	5	9157	6	10	NULL	0	NULL	statement 1	NULL		in response to	NULL				IL-3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_2_867_s_109	10625620	A and  B, DNA binding activities of Stat1 and Stat3 in response to IFN-gamma and IL-3.	bind
49555	6	9157	6	10	NULL	0	NULL	statement 2	NULL		in response to	NULL				IFN-gamma	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_2_867_s_109	10625620	A and  B, DNA binding activities of Stat1 and Stat3 in response to IFN-gamma and IL-3.	bind
39529	1	9159	5	13	NULL	NULL	NULL	GlnR	GP		bind					glnR	GP			(P glnR-1) promoter region	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_35_25097_s_260	16787930	A and  B, EMSA of binding of GlnR to the  glnR (P glnR-1) and  glnP (P glnP-1) promoter regions and to truncated  glnR (P glnR-2) and  glnP (P glnP-2) promoters, lacking their respective GlnR operators.	bind
39530	2	9159	5	13	NULL	NULL	NULL	GlnR	GP		bind					glnP	GP			(P glnP-1) promoter region	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_35_25097_s_260	16787930	A and  B, EMSA of binding of GlnR to the  glnR (P glnR-1) and  glnP (P glnP-1) promoter regions and to truncated  glnR (P glnR-2) and  glnP (P glnP-2) promoters, lacking their respective GlnR operators.	bind
39531	3	9159	5	13	NULL	NULL	NULL	glnR	GP	truncated	lacks				(P glnR-2) promoter	GlnR	GP	respective		operators	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_35_25097_s_260	16787930	A and  B, EMSA of binding of GlnR to the  glnR (P glnR-1) and  glnP (P glnP-1) promoter regions and to truncated  glnR (P glnR-2) and  glnP (P glnP-2) promoters, lacking their respective GlnR operators.	bind
39532	4	9159	5	13	NULL	NULL	NULL	glnP	GP	truncated	lacks				(P glnP-2) promoter	GlnR	GP	respective		operators	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_35_25097_s_260	16787930	A and  B, EMSA of binding of GlnR to the  glnR (P glnR-1) and  glnP (P glnP-1) promoter regions and to truncated  glnR (P glnR-2) and  glnP (P glnP-2) promoters, lacking their respective GlnR operators.	bind
39533	5	9159	5	13	NULL	NULL	NULL	GlnR	GP		bind					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_35_25097_s_260	16787930	A and  B, EMSA of binding of GlnR to the  glnR (P glnR-1) and  glnP (P glnP-1) promoter regions and to truncated  glnR (P glnR-2) and  glnP (P glnP-2) promoters, lacking their respective GlnR operators.	bind
39534	6	9159	5	13	NULL	NULL	NULL	GlnR	GP		bind					statement 4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_35_25097_s_260	16787930	A and  B, EMSA of binding of GlnR to the  glnR (P glnR-1) and  glnP (P glnP-1) promoter regions and to truncated  glnR (P glnR-2) and  glnP (P glnP-2) promoters, lacking their respective GlnR operators.	bind
31440	1	9159	6	NULL	NULL	0	NULL	GlnR	NULL		bind	NULL				glnR	NULL			P glnR-1 site on promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_35_25097_s_260	16787930	A and  B, EMSA of binding of GlnR to the  glnR (P glnR-1) and  glnP (P glnP-1) promoter regions and to truncated  glnR (P glnR-2) and  glnP (P glnP-2) promoters, lacking their respective GlnR operators.	bind
31444	2	9159	6	NULL	NULL	0	NULL	GlnR	NULL		bind	NULL				glnP	NULL			P glnP-1 site on promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_35_25097_s_260	16787930	A and  B, EMSA of binding of GlnR to the  glnR (P glnR-1) and  glnP (P glnP-1) promoter regions and to truncated  glnR (P glnR-2) and  glnP (P glnP-2) promoters, lacking their respective GlnR operators.	bind
31445	3	9159	6	NULL	NULL	0	NULL	GlnR	NULL		bind	NULL				glnR	NULL	truncated		P glnR-2 site on promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_35_25097_s_260	16787930	A and  B, EMSA of binding of GlnR to the  glnR (P glnR-1) and  glnP (P glnP-1) promoter regions and to truncated  glnR (P glnR-2) and  glnP (P glnP-2) promoters, lacking their respective GlnR operators.	bind
31446	4	9159	6	NULL	NULL	0	NULL	GlnR	NULL		bind	NULL				glnP	NULL	truncated		P glnP-2 site on promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_35_25097_s_260	16787930	A and  B, EMSA of binding of GlnR to the  glnR (P glnR-1) and  glnP (P glnP-1) promoter regions and to truncated  glnR (P glnR-2) and  glnP (P glnP-2) promoters, lacking their respective GlnR operators.	bind
48036	5	9159	6	10	NULL	0	NULL	glnR	NULL	truncated	lack	NULL			P glnR-2 site in promoter	glnR	NULL			operator	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_35_25097_s_260	16787930	A and  B, EMSA of binding of GlnR to the  glnR (P glnR-1) and  glnP (P glnP-1) promoter regions and to truncated  glnR (P glnR-2) and  glnP (P glnP-2) promoters, lacking their respective GlnR operators.	bind
48037	6	9159	6	10	NULL	0	NULL	glnP	NULL	truncated	lack	NULL			P glnP-2 site in promoter	glnP	NULL			operator	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_35_25097_s_260	16787930	A and  B, EMSA of binding of GlnR to the  glnR (P glnR-1) and  glnP (P glnP-1) promoter regions and to truncated  glnR (P glnR-2) and  glnP (P glnP-2) promoters, lacking their respective GlnR operators.	bind
39276	1	9160	5	13	NULL	NULL	NULL	FBP30	GP		bind			WW-A domain		PPR-based peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_14_10359_s_234	10744724	A and  B, fluorescence polarization anisotropy measurements demonstrate that the FBP30 WW-A domain binds a PPR-based peptide, but not a PP XY peptide, in contrast to YAP which binds a PP XY peptide, but not a PPR-based peptide.	bind
39277	2	9160	5	13	NULL	NULL	NULL	FBP30	GP		does not bind			WW-A domain		PP XY peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_14_10359_s_234	10744724	A and  B, fluorescence polarization anisotropy measurements demonstrate that the FBP30 WW-A domain binds a PPR-based peptide, but not a PP XY peptide, in contrast to YAP which binds a PP XY peptide, but not a PPR-based peptide.	bind
39278	3	9160	5	13	NULL	NULL	NULL	YAP	GP		bind					PP XY peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_14_10359_s_234	10744724	A and  B, fluorescence polarization anisotropy measurements demonstrate that the FBP30 WW-A domain binds a PPR-based peptide, but not a PP XY peptide, in contrast to YAP which binds a PP XY peptide, but not a PPR-based peptide.	bind
39279	4	9160	5	13	NULL	NULL	NULL	YAP	GP		does not bind					PPR-based peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_14_10359_s_234	10744724	A and  B, fluorescence polarization anisotropy measurements demonstrate that the FBP30 WW-A domain binds a PPR-based peptide, but not a PP XY peptide, in contrast to YAP which binds a PP XY peptide, but not a PPR-based peptide.	bind
31447	1	9160	6	NULL	NULL	0	NULL	FBP30	NULL		bind	NULL		WW-A domain		PPR-based peptide	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10359_s_234	10744724	A and  B, fluorescence polarization anisotropy measurements demonstrate that the FBP30 WW-A domain binds a PPR-based peptide, but not a PP XY peptide, in contrast to YAP which binds a PP XY peptide, but not a PPR-based peptide.	bind
31448	2	9160	6	NULL	NULL	0	NULL	FBP30	NULL		does not bind	NULL		WW-A domain		PP XY peptide	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10359_s_234	10744724	A and  B, fluorescence polarization anisotropy measurements demonstrate that the FBP30 WW-A domain binds a PPR-based peptide, but not a PP XY peptide, in contrast to YAP which binds a PP XY peptide, but not a PPR-based peptide.	bind
31449	3	9160	6	NULL	NULL	0	NULL	YAP	NULL		bind	NULL				PP XY peptide	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10359_s_234	10744724	A and  B, fluorescence polarization anisotropy measurements demonstrate that the FBP30 WW-A domain binds a PPR-based peptide, but not a PP XY peptide, in contrast to YAP which binds a PP XY peptide, but not a PPR-based peptide.	bind
31450	4	9160	6	NULL	NULL	0	NULL	YAP	NULL		does not bind	NULL				PPR-based peptide	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10359_s_234	10744724	A and  B, fluorescence polarization anisotropy measurements demonstrate that the FBP30 WW-A domain binds a PPR-based peptide, but not a PP XY peptide, in contrast to YAP which binds a PP XY peptide, but not a PPR-based peptide.	bind
39280	1	9161	5	13	NULL	NULL	NULL	SMAD3	GP		does not bind					apoCIII	GP	proximal		HRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41405_s_148	10995777	A and  B, gel electrophoretic mobility shift assays showing that SMAD3 cannot bind to the proximal apoCIII  HRE.	bind
31451	1	9161	6	NULL	NULL	0	NULL	SMAD3	NULL		does not bind	NULL				apoCIII	NULL	proximal		HRE 	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41405_s_148	10995777	A and  B, gel electrophoretic mobility shift assays showing that SMAD3 cannot bind to the proximal apoCIII  HRE.	bind
39281	1	9162	5	13	NULL	NULL	NULL	rSp1	GP		bind					Sp1-A oligos	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_39_40451_s_262	15265862	A and  B, gel shift assay of rSp1 binding to Sp1-A and Sp1-B oligos.	bind
39282	2	9162	5	13	NULL	NULL	NULL	rSp1	GP		bind					Sp1-B oligos	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_39_40451_s_262	15265862	A and  B, gel shift assay of rSp1 binding to Sp1-A and Sp1-B oligos.	bind
31452	1	9162	6	10	NULL	0	NULL	rSp1			bind					Sp1-A oligos					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_39_40451_s_262	15265862	A and  B, gel shift assay of rSp1 binding to Sp1-A and Sp1-B oligos.	bind
31453	2	9162	6	10	NULL	0	NULL	rSp1			bind					Sp1-B oligos					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_39_40451_s_262	15265862	A and  B, gel shift assay of rSp1 binding to Sp1-A and Sp1-B oligos.	bind
39283	1	9165	5	13	NULL	NULL	NULL	GAR	GP		bind					histones	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_50930_s_185	15456770	A and  B, in vitro binding of GAR and histones.	bind
31454	1	9165	6	10	NULL	0	NULL	GAR			bind					histones					NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_50930_s_185	15456770	A and  B, in vitro binding of GAR and histones.	bind
39284	1	9166	5	13	NULL	NULL	NULL	ERK1/2	GP		bind					MEK1	GP		KIM-SL		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37885_s_251	16148006	A and  B, increased binding of ERK1/2 to (KIM-SL)MEK1.	bind
31455	1	9166	6	NULL	NULL	0	NULL	ERK1/2	NULL		bind	NULL				MEK1	NULL		KIM-SL		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_45_37885_s_251	16148006	A and  B, increased binding of ERK1/2 to (KIM-SL)MEK1.	bind
39285	1	9168	5	13	NULL	NULL	NULL	MEKK2	GP		bind					PRK2	GP		residues 479-670		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24421_s_104	10818102	A and  B, MEKK2 binds PRK2 (residues 479-670) in the yeast two-hybrid system.	bind
31456	1	9168	6	NULL	NULL	0	NULL	MEKK2	NULL		bind	NULL				PRK2	NULL		479-670		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24421_s_104	10818102	A and  B, MEKK2 binds PRK2 (residues 479-670) in the yeast two-hybrid system.	bind
39286	1	9169	5	13	NULL	NULL	NULL	MyD88	GP		is required for					TLR8 	GP	signaling of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21013_s_137	16737960	a and  b, MyD88 and IRAK are required for TLR8 signaling.	bind
39287	2	9169	5	13	NULL	NULL	NULL	IRAK	GP		is required for					TLR8 	GP	signaling of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21013_s_137	16737960	a and  b, MyD88 and IRAK are required for TLR8 signaling.	bind
31457	1	9169	6	NULL	NULL	0	NULL	MyD88	NULL		is required for	NULL				TLR8	NULL	signaling of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21013_s_137	16737960	a and  b, MyD88 and IRAK are required for TLR8 signaling.	bind
31458	2	9169	6	NULL	NULL	0	NULL	IRAK	NULL		is required for	NULL				TLR8	NULL	signaling of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21013_s_137	16737960	a and  b, MyD88 and IRAK are required for TLR8 signaling.	bind
39535	1	9171	5	13	NULL	NULL	NULL	Rab11a	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_32_33430_s_133	15173169	A and  B, Rip11-F1 titration with the GDP- and Gpp(NH)p-bound forms of Rab11a, respectively;   C and  D, Rip11-F1 titration with the GDP- and Gpp(NH)p-bound forms of Rab11b, respectively;   E and  F, buffer titration with the GDP- and Gpp(NH)p-bound forms of Rab11a, respectively.	bind
39536	2	9171	5	13	NULL	NULL	NULL	Rab11a	GP		bind					Gpp(NH)p	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_32_33430_s_133	15173169	A and  B, Rip11-F1 titration with the GDP- and Gpp(NH)p-bound forms of Rab11a, respectively;   C and  D, Rip11-F1 titration with the GDP- and Gpp(NH)p-bound forms of Rab11b, respectively;   E and  F, buffer titration with the GDP- and Gpp(NH)p-bound forms of Rab11a, respectively.	bind
39537	3	9171	5	13	NULL	NULL	NULL	Rab11b	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_32_33430_s_133	15173169	A and  B, Rip11-F1 titration with the GDP- and Gpp(NH)p-bound forms of Rab11a, respectively;   C and  D, Rip11-F1 titration with the GDP- and Gpp(NH)p-bound forms of Rab11b, respectively;   E and  F, buffer titration with the GDP- and Gpp(NH)p-bound forms of Rab11a, respectively.	bind
39538	4	9171	5	13	NULL	NULL	NULL	Rab11b	GP		bind					Gpp(NH)p	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_32_33430_s_133	15173169	A and  B, Rip11-F1 titration with the GDP- and Gpp(NH)p-bound forms of Rab11a, respectively;   C and  D, Rip11-F1 titration with the GDP- and Gpp(NH)p-bound forms of Rab11b, respectively;   E and  F, buffer titration with the GDP- and Gpp(NH)p-bound forms of Rab11a, respectively.	bind
31545	1	9171	6	NULL	NULL	0	NULL	GDP	NULL		bind	NULL				Rab11a	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_32_33430_s_133	15173169	A and  B, Rip11-F1 titration with the GDP- and Gpp(NH)p-bound forms of Rab11a, respectively;   C and  D, Rip11-F1 titration with the GDP- and Gpp(NH)p-bound forms of Rab11b, respectively;   E and  F, buffer titration with the GDP- and Gpp(NH)p-bound forms of Rab11a, respectively.	bind
31546	2	9171	6	NULL	NULL	0	NULL	Gpp(NH)p	NULL		bind	NULL				Rab11a	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_32_33430_s_133	15173169	A and  B, Rip11-F1 titration with the GDP- and Gpp(NH)p-bound forms of Rab11a, respectively;   C and  D, Rip11-F1 titration with the GDP- and Gpp(NH)p-bound forms of Rab11b, respectively;   E and  F, buffer titration with the GDP- and Gpp(NH)p-bound forms of Rab11a, respectively.	bind
31547	3	9171	6	NULL	NULL	0	NULL	GDP	NULL		bind	NULL				Rab11b	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_32_33430_s_133	15173169	A and  B, Rip11-F1 titration with the GDP- and Gpp(NH)p-bound forms of Rab11a, respectively;   C and  D, Rip11-F1 titration with the GDP- and Gpp(NH)p-bound forms of Rab11b, respectively;   E and  F, buffer titration with the GDP- and Gpp(NH)p-bound forms of Rab11a, respectively.	bind
31548	4	9171	6	NULL	NULL	0	NULL	Gpp(NH)p	NULL		bind	NULL				Rab11b	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_32_33430_s_133	15173169	A and  B, Rip11-F1 titration with the GDP- and Gpp(NH)p-bound forms of Rab11a, respectively;   C and  D, Rip11-F1 titration with the GDP- and Gpp(NH)p-bound forms of Rab11b, respectively;   E and  F, buffer titration with the GDP- and Gpp(NH)p-bound forms of Rab11a, respectively.	bind
39288	1	9172	5	13	NULL	NULL	NULL	C2AB	GP		bind					PS/PtdIns(4, 5)P2-containing vesicles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10240_s_205	9553075	A and  B, Rp(676-695) specifically inhibits binding of C2AB to PS/PtdIns(4, 5)P2-containing vesicles,  C, a related peptide directly binds lipid vesicles.	bind
39289	2	9172	5	13	NULL	NULL	NULL	Rp	GP		inhibit		specifically	676-695		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10240_s_205	9553075	A and  B, Rp(676-695) specifically inhibits binding of C2AB to PS/PtdIns(4, 5)P2-containing vesicles,  C, a related peptide directly binds lipid vesicles.	bind
39290	3	9172	5	13	NULL	NULL	NULL	peptide related to Rp	GP		bind		directly	676-695		lipid vesicles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10240_s_205	9553075	A and  B, Rp(676-695) specifically inhibits binding of C2AB to PS/PtdIns(4, 5)P2-containing vesicles,  C, a related peptide directly binds lipid vesicles.	bind
31803	1	9172	6	NULL	NULL	0	NULL	C2AB	NULL		bind	NULL				PS/PtdIns(4, 5)P2-containing vesicles	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_17_10240_s_205	9553075	A and  B, Rp(676-695) specifically inhibits binding of C2AB to PS/PtdIns(4, 5)P2-containing vesicles,  C, a related peptide directly binds lipid vesicles.	bind
31804	2	9172	6	NULL	NULL	0	NULL	Rp	NULL		inhibits	NULL	specifically	676-695		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_17_10240_s_205	9553075	A and  B, Rp(676-695) specifically inhibits binding of C2AB to PS/PtdIns(4, 5)P2-containing vesicles,  C, a related peptide directly binds lipid vesicles.	bind
31805	3	9172	6	10	NULL	0	NULL	peptide related to Rp	NULL		bind	NULL	directly	676-695		lipid vesicles	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10240_s_205	9553075	A and  B, Rp(676-695) specifically inhibits binding of C2AB to PS/PtdIns(4, 5)P2-containing vesicles,  C, a related peptide directly binds lipid vesicles.	bind
48038	1	9173	5	13	NULL	NULL	NULL	tau	GP		does not bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_9_7614_s_168	15611092	A and  B, SDS-PAGE of free (tau not bound to heparin) and bound (tau bound to heparin) tau  following incubation with heparin-Sepharose in the absence ( Con.) or the presence of inhibitory compounds (exifone, methylene blue, and hematin).	bind
48039	2	9173	5	13	NULL	NULL	NULL	tau	GP		bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_9_7614_s_168	15611092	A and  B, SDS-PAGE of free (tau not bound to heparin) and bound (tau bound to heparin) tau  following incubation with heparin-Sepharose in the absence ( Con.) or the presence of inhibitory compounds (exifone, methylene blue, and hematin).	bind
31806	1	9173	6	NULL	NULL	0	NULL	tau	NULL		does not bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_9_7614_s_168	15611092	A and  B, SDS-PAGE of free (tau not bound to heparin) and bound (tau bound to heparin) tau  following incubation with heparin-Sepharose in the absence ( Con.) or the presence of inhibitory compounds (exifone, methylene blue, and hematin).	bind
31807	2	9173	6	NULL	NULL	0	NULL	tau	NULL		bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_9_7614_s_168	15611092	A and  B, SDS-PAGE of free (tau not bound to heparin) and bound (tau bound to heparin) tau  following incubation with heparin-Sepharose in the absence ( Con.) or the presence of inhibitory compounds (exifone, methylene blue, and hematin).	bind
39291	1	9174	5	13	NULL	NULL	NULL	CLOCK-BMAL1 heterodimer	GP		bind									E-box	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_42036_s_288	16249183	A and  B, shown are the transcription mechanisms of binding of the CLOCK-BMAL1 heterodimer  to the E-box for the rhythmic expression of  Per1 and of binding of CREB to the CRE for transient expression of  Per1, respectively.	bind
39292	2	9174	5	13	NULL	NULL	NULL	statement 1	Process		is required for					Per1	GP	rhythmic expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_42036_s_288	16249183	A and  B, shown are the transcription mechanisms of binding of the CLOCK-BMAL1 heterodimer  to the E-box for the rhythmic expression of  Per1 and of binding of CREB to the CRE for transient expression of  Per1, respectively.	bind
39293	3	9174	5	13	NULL	NULL	NULL	CREB	GP		bind									CRE	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_42036_s_288	16249183	A and  B, shown are the transcription mechanisms of binding of the CLOCK-BMAL1 heterodimer  to the E-box for the rhythmic expression of  Per1 and of binding of CREB to the CRE for transient expression of  Per1, respectively.	bind
39294	4	9174	5	13	NULL	NULL	NULL	statement 3	Process		is required for					Per1	GP	transient expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_42036_s_288	16249183	A and  B, shown are the transcription mechanisms of binding of the CLOCK-BMAL1 heterodimer  to the E-box for the rhythmic expression of  Per1 and of binding of CREB to the CRE for transient expression of  Per1, respectively.	bind
31808	1	9174	6	NULL	NULL	0	NULL	CLOCK-BMAL1 heterodimer	NULL		bind	NULL					NULL			E box	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_42036_s_288	16249183	A and  B, shown are the transcription mechanisms of binding of the CLOCK-BMAL1 heterodimer  to the E-box for the rhythmic expression of  Per1 and of binding of CREB to the CRE for transient expression of  Per1, respectively.	bind
31809	2	9174	6	NULL	NULL	0	NULL	statement 1	NULL		is required for	NULL				Per1	NULL	rhythmic expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_42036_s_288	16249183	A and  B, shown are the transcription mechanisms of binding of the CLOCK-BMAL1 heterodimer  to the E-box for the rhythmic expression of  Per1 and of binding of CREB to the CRE for transient expression of  Per1, respectively.	bind
31810	3	9174	6	NULL	NULL	0	NULL	CREB	NULL		bind	NULL					NULL			CRE	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_42036_s_288	16249183	A and  B, shown are the transcription mechanisms of binding of the CLOCK-BMAL1 heterodimer  to the E-box for the rhythmic expression of  Per1 and of binding of CREB to the CRE for transient expression of  Per1, respectively.	bind
31811	4	9174	6	NULL	NULL	0	NULL	statement 3	NULL		is required for	NULL				Per1	NULL	transient expression of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_42036_s_288	16249183	A and  B, shown are the transcription mechanisms of binding of the CLOCK-BMAL1 heterodimer  to the E-box for the rhythmic expression of  Per1 and of binding of CREB to the CRE for transient expression of  Per1, respectively.	bind
39295	1	9175	5	13	NULL	NULL	NULL	Sp1	GP		bind			ZFDBD		SMRT	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
39296	2	9175	5	13	NULL	NULL	NULL	Sp1	GP		bind			ZFDBD		NCoR	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
39297	3	9175	5	13	NULL	NULL	NULL	NCoR	GP		is a type of					corepressor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
39298	4	9175	5	13	NULL	NULL	NULL	SMRT	GP		is a type of					corepressor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
39299	7	9175	5	13	NULL	NULL	NULL	statement 1	GP		does not have access to					statement 5	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
39300	8	9175	5	13	NULL	NULL	NULL	statement 1	GP		does not have access to					statement 6	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
39302	9	9175	5	13	NULL	NULL	NULL	statement 2	GP		does not have access to					statement 5	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
39303	10	9175	5	13	NULL	NULL	NULL	statement 2	GP		does not have access to					statement 6	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
39304	11	9175	5	13	NULL	NULL	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
48040	5	9175	5	13	NULL	NULL	NULL	Sp-1	GP		bind									GC boxes in promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
48041	6	9175	5	13	NULL	NULL	NULL	Sp-1	GP		bind									GC boxes in enhancer	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
31812	1	9175	6	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL		ZFDBD		SMRT	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
31813	2	9175	6	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL		ZFDBD		NcoR	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
31814	3	9175	6	NULL	NULL	0	NULL	SMRT	NULL		is a type of	NULL				corepressor	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
31815	4	9175	6	NULL	NULL	0	NULL	NcoR	NULL		is a type of	NULL				corepressor	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
31816	6	9175	6	10	NULL	0	NULL	Sp1	NULL		bind	NULL					NULL			 GC boxes in the enhancer	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
31817	7	9175	6	10	NULL	0	NULL	statement 1	NULL		has no access to	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
31818	8	9175	6	10	NULL	0	NULL	statement 1	NULL		has no access to	NULL				statement 6	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
31819	9	9175	6	10	NULL	0	NULL	statement 2	NULL		has no access to	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
31820	10	9175	6	10	NULL	0	NULL	statement 2	NULL		has no access to	NULL				statement 6	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
31821	11	9175	6	10	NULL	0	NULL	statement 5	NULL		is an alternative to	NULL				statement 6	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
48042	5	9175	6	10	NULL	0	NULL	Sp1	NULL		bind	NULL					NULL			GC box in promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_30_28061_s_305	15878880	A and  B, Sp1ZFDBD is bound by the corepressors SMRT and NCoR, and has no access to the target  Sp1-binding GC boxes in the promoters or the enhancers.	bind
39305	1	9176	5	13	NULL	NULL	NULL	FGF	GP		forms binary complex with					FGFR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_31_21511_s_72	10419453	A and  B, specificity of the AT-binding fraction of heparin for formation of an FGF-binding binary complex with FGFR.	bind
39306	2	9176	5	13	NULL	NULL	NULL	heparin	Chemical		is required for		specifically	AT-binding fraction of		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_31_21511_s_72	10419453	A and  B, specificity of the AT-binding fraction of heparin for formation of an FGF-binding binary complex with FGFR.	bind
31822	1	9176	6	10	NULL	0	NULL	FGF 	NULL		forms binary complex with	NULL				FGFR	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_31_21511_s_72	10419453	A and  B, specificity of the AT-binding fraction of heparin for formation of an FGF-binding binary complex with FGFR.	bind
48043	2	9176	6	10	NULL	0	NULL	heparin	NULL		is required for	NULL	specifically	AT-binding fraction of 		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_31_21511_s_72	10419453	A and  B, specificity of the AT-binding fraction of heparin for formation of an FGF-binding binary complex with FGFR.	bind
39446	1	9179	5	13	NULL	NULL	NULL	p53	GP	wild type	bind					p21WAF1/CIP1	NucleicAcid			consensus DNA binding sites in promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_35_32990_s_243	11395510	A and  B, wild type p53 binds the consensus DNA binding sites in the p21WAF1/CIP1 and Bax promoters.	bind
39447	2	9179	5	13	NULL	NULL	NULL	p53	GP	wild type	bind					Bax	NucleicAcid			consensus DNA binding sites in promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_35_32990_s_243	11395510	A and  B, wild type p53 binds the consensus DNA binding sites in the p21WAF1/CIP1 and Bax promoters.	bind
31823	1	9179	6	NULL	NULL	0	NULL	p53	NULL	wild type	bind	NULL				p21WAF1/CIP1	NULL			DNA binding site of promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32990_s_243	11395510	A and  B, wild type p53 binds the consensus DNA binding sites in the p21WAF1/CIP1 and Bax promoters.	bind
31824	2	9179	6	NULL	NULL	0	NULL	p53	NULL	wild type	bind	NULL				Bax	NULL			DNA binding site of promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32990_s_243	11395510	A and  B, wild type p53 binds the consensus DNA binding sites in the p21WAF1/CIP1 and Bax promoters.	bind
39448	1	9180	5	13	NULL	NULL	NULL	spermine	Chemical		bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_47_30939_s_114	9812989	A and  C, binding constants of spermine for ATP without and with 1 mM Mg2+, respectively.	bind
31825	1	9180	6	NULL	NULL	0	NULL	spermine	NULL		bind	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_47_30939_s_114	9812989	A and  C, binding constants of spermine for ATP without and with 1 mM Mg2+, respectively.	bind
39449	1	9181	5	13	NULL	NULL	NULL	MM6.15 mAb	GP	Cy5 labeled	bind		specifically			Pgp molecules	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_4_942_s_85	14985103	A and B are internal controls  demonstrating that the Cy5 labeled MM6.15 mAb binds specifically to the Pgp molecules.	bind
31826	1	9181	6	NULL	NULL	0	NULL	MM6.15 mAb	NULL	Cy5 labeled	bind	NULL	specifically			Pgp molecules	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_4_942_s_85	14985103	A and B are internal controls  demonstrating that the Cy5 labeled MM6.15 mAb binds specifically to the Pgp molecules.	bind
39450	1	9182	5	13	NULL	NULL	NULL	RyhB	NucleicAcid		mediates					sodB mRNA	NucleicAcid	degradation of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_19_2374_s_69	12975324	A and B), indicating that RNase III is not required for RyhB-mediated  sodB mRNA degradation.	bind
39451	2	9182	5	13	NULL	NULL	NULL	RNase III	GP		is not required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_19_2374_s_69	12975324	A and B), indicating that RNase III is not required for RyhB-mediated  sodB mRNA degradation.	bind
31827	1	9182	6	NULL	NULL	0	NULL	RyhB	NULL		mediates	NULL				sodB mRNA	NULL	degradation of			NULL		0	NULL	NULL	NULL	gw70_genesdev_17_19_2374_s_69	12975324	A and B), indicating that RNase III is not required for RyhB-mediated  sodB mRNA degradation.	bind
31828	2	9182	6	NULL	NULL	0	NULL	RNase III	NULL		is not required for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_19_2374_s_69	12975324	A and B), indicating that RNase III is not required for RyhB-mediated  sodB mRNA degradation.	bind
39452	1	9184	5	13	NULL	NULL	NULL	TCDD-inducible protein	GP		bind					HES-1	GP			XRE element present in flanking region	NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_65_1_165_s_116	14722248	A and B, a TCDD-inducible protein binds the XRE element present in the HES-1 flanking  region.	bind
31829	1	9184	6	10	NULL	0	NULL	TCDD-inducible protein	NULL		bind	NULL				HES-1	NULL			XRE element in the  flanking region	NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_65_1_165_s_116	14722248	A and B, a TCDD-inducible protein binds the XRE element present in the HES-1 flanking  region.	bind
39453	1	9185	5	13	NULL	NULL	NULL	EB	Chemical		bind					splenocytes	Cell	mice			NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_66_6_1712_s_118	15383622	A and B, ligand-binding isotherms and Scatchard plots (insets) of [3]EB and 125I-alpha-BGT binding to mice splenocytes ( n = 3).	bind
39454	2	9185	5	13	NULL	NULL	NULL	alpha-BGT	Chemical	125I	bind					splenocytes	Cell	mice			NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_66_6_1712_s_118	15383622	A and B, ligand-binding isotherms and Scatchard plots (insets) of [3]EB and 125I-alpha-BGT binding to mice splenocytes ( n = 3).	bind
31830	1	9185	6	NULL	NULL	0	NULL	EB	NULL		bind	NULL				splenocytes	NULL	mice			NULL		0	NULL	NULL	NULL	gw70_molpharmacol_66_6_1712_s_118	15383622	A and B, ligand-binding isotherms and Scatchard plots (insets) of [3]EB and 125I-alpha-BGT binding to mice splenocytes ( n = 3).	bind
31831	2	9185	6	10	NULL	0	NULL	alpha-BGT		125I	bind					splenocytes		mice			NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_66_6_1712_s_118	15383622	A and B, ligand-binding isotherms and Scatchard plots (insets) of [3]EB and 125I-alpha-BGT binding to mice splenocytes ( n = 3).	bind
39455	1	9186	5	13	NULL	NULL	NULL	TRAX	GP		bind					A2A-R	GP	striatal			NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_70_2_454_s_181	16617164	A and B, TRAX bound the striatal  A2A-R in GST pull-down assays.	bind
31832	1	9186	6	NULL	NULL	0	NULL	TRAX	NULL		bind	NULL				A2A-R	NULL	striatal			NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_2_454_s_181	16617164	A and B, TRAX bound the striatal  A2A-R in GST pull-down assays.	bind
39456	1	9187	5	13	NULL	NULL	NULL	NGF	GP		is relocated inside					cytoplasm	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_neurobioldis_15_1_106_s_167	14751775	A and C. NGF was relocated inside the cytoplasm, presumably bound to TrkA receptors.	bind
39457	2	9187	5	13	NULL	NULL	NULL	statement 1	GP		bind		presumably			TrkA receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_neurobioldis_15_1_106_s_167	14751775	A and C. NGF was relocated inside the cytoplasm, presumably bound to TrkA receptors.	bind
31833	1	9187	6	NULL	NULL	0	NULL	NGF	NULL		bind	NULL	presumably			TrkA receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_neurobioldis_15_1_106_s_167	14751775	A and C. NGF was relocated inside the cytoplasm, presumably bound to TrkA receptors.	bind
31834	2	9187	6	NULL	NULL	0	NULL	statement 1	NULL		relocates inside	NULL				cytoplasm	NULL				NULL		0	NULL	NULL	NULL	gw70_neurobioldis_15_1_106_s_167	14751775	A and C. NGF was relocated inside the cytoplasm, presumably bound to TrkA receptors.	bind
39458	1	9188	5	13	NULL	NULL	NULL	ATP	Chemical		bind					A2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_46_29255_s_50	9361005	A and CPS.B. Chemical modification of CAD ( 41) and mammalian CPSase I ( 40,  42-45) as well as site-directed mutagenesis of  E. coli CPSase ( 23,  46,  47) showed that ATP binds to A2 and B2.	bind
39459	2	9188	5	13	NULL	NULL	NULL	ATP	Chemical		bind					B2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_46_29255_s_50	9361005	A and CPS.B. Chemical modification of CAD ( 41) and mammalian CPSase I ( 40,  42-45) as well as site-directed mutagenesis of  E. coli CPSase ( 23,  46,  47) showed that ATP binds to A2 and B2.	bind
31835	1	9188	6	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				A2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_46_29255_s_50	9361005	A and CPS.B. Chemical modification of CAD ( 41) and mammalian CPSase I ( 40,  42-45) as well as site-directed mutagenesis of  E. coli CPSase ( 23,  46,  47) showed that ATP binds to A2 and B2.	bind
31836	2	9188	6	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				B2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_46_29255_s_50	9361005	A and CPS.B. Chemical modification of CAD ( 41) and mammalian CPSase I ( 40,  42-45) as well as site-directed mutagenesis of  E. coli CPSase ( 23,  46,  47) showed that ATP binds to A2 and B2.	bind
39466	1	9189	5	13	NULL	NULL	NULL	ATP	Chemical		bind					F-6-P	Chemical				NULL	E. coli ATP-PFK enzyme	NULL	NULL	NULL	NULL	gw60_jbacteriol_183_24_7231_s_217	11717283	A and F indicate residues (solid boxes) involved in binding of ATP and F-6-P, respectively, in the  E. coli ATP-PFK enzyme ( 34).	bind
31837	1	9189	6	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				F-6-P	NULL				NULL	E. coli ATP-PFK enzyme	0	NULL	NULL	NULL	gw60_jbacteriol_183_24_7231_s_217	11717283	A and F indicate residues (solid boxes) involved in binding of ATP and F-6-P, respectively, in the  E. coli ATP-PFK enzyme ( 34).	bind
39468	1	9190	5	13	NULL	NULL	NULL	B cell	Cell		bind					autoantigen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_5_2_103_s_67	7743168	A B cell that has bound an autoantigen is very unlikely to find a specific helper T cell, for autoreactive T cells are normally eliminated by a rigorous selection process  [10]  .	bind
39469	2	9190	5	13	NULL	NULL	NULL	statement 1	Chemical		does not find					helper T cell	Cell	specific			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_5_2_103_s_67	7743168	A B cell that has bound an autoantigen is very unlikely to find a specific helper T cell, for autoreactive T cells are normally eliminated by a rigorous selection process  [10]  .	bind
39476	3	9190	5	13	NULL	NULL	NULL	T cells	Cell	autoreactive	eliminated by		normally			selection process	Process	rigorous			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_5_2_103_s_67	7743168	A B cell that has bound an autoantigen is very unlikely to find a specific helper T cell, for autoreactive T cells are normally eliminated by a rigorous selection process  [10]  .	bind
31838	1	9190	6	NULL	NULL	0	NULL	B cell 	NULL		bind	NULL				autoantigen	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_5_2_103_s_67	7743168	A B cell that has bound an autoantigen is very unlikely to find a specific helper T cell, for autoreactive T cells are normally eliminated by a rigorous selection process  [10]  .	bind
31839	2	9190	6	10	NULL	0	NULL	T cells		autoreactive	are eliminated		normally			 selection process		rigorous			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_5_2_103_s_67	7743168	A B cell that has bound an autoantigen is very unlikely to find a specific helper T cell, for autoreactive T cells are normally eliminated by a rigorous selection process  [10]  .	bind
31840	3	9190	6	NULL	NULL	0	NULL	statement 1	NULL		does not find	NULL				helper T cell	NULL	specific			NULL		0	NULL	NULL	NULL	gw60_currbiol_5_2_103_s_67	7743168	A B cell that has bound an autoantigen is very unlikely to find a specific helper T cell, for autoreactive T cells are normally eliminated by a rigorous selection process  [10]  .	bind
39478	1	9191	5	13	NULL	NULL	NULL	nuclear factor	GP	B-cell-specific	bind					RAG-2	NucleicAcid			core promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_2601_s_243	10082526	A B-cell-specific nuclear factor binds to the core  RAG-2 promoter.	bind
31841	1	9191	6	10	NULL	0	NULL	nuclear factor	NULL	B-cell specific	bind	NULL				RAG-2 	NULL			core promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_2601_s_243	10082526	A B-cell-specific nuclear factor binds to the core  RAG-2 promoter.	bind
39539	1	9192	5	13	NULL	NULL	NULL	mAb 6B2	GP		bind					CD45	GP	glycosylation variant of			NULL		NULL	NULL	NULL	NULL	gw70_microbesinfect_5_3_205_s_179	12681409	A B220- memory fraction (mAb 6B2 binding of a glycosylation variant of CD45) (B220- CD19- CD11b+ CD43+) divides again based on IgG or IgE expression [  47 and   48].	bind
31842	1	9192	6	NULL	NULL	0	NULL	CD45	NULL	glycosylation variant of	bind	NULL				6B2 mAb	NULL				NULL		0	NULL	NULL	NULL	gw70_microbesinfect_5_3_205_s_179	12681409	A B220- memory fraction (mAb 6B2 binding of a glycosylation variant of CD45) (B220- CD19- CD11b+ CD43+) divides again based on IgG or IgE expression [  47 and   48].	bind
39540	2	9193	5	13	NULL	NULL	NULL	B7x-Ig	GP		bind					statement 1	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_18_10388_s_25	12920180	A B7x-Ig fusion protein binds to  Th1 cells derived from WT mice, but not mice with induced null mutation for  the newly identified CD28 homolog BTLA (B and T lymphocyte attenuator)  ( ).	bind
39541	1	9193	5	13	NULL	NULL	NULL	Th1 cells	Cell		is derived from					mice	Organism	WT			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_18_10388_s_25	12920180	A B7x-Ig fusion protein binds to  Th1 cells derived from WT mice, but not mice with induced null mutation for  the newly identified CD28 homolog BTLA (B and T lymphocyte attenuator)  ( ).	bind
48044	3	9193	5	13	NULL	NULL	NULL	Th1 cells	Cell		derived from					mice	Organism	null mutant			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_18_10388_s_25	12920180	A B7x-Ig fusion protein binds to  Th1 cells derived from WT mice, but not mice with induced null mutation for  the newly identified CD28 homolog BTLA (B and T lymphocyte attenuator)  ( ).	bind
48045	4	9193	5	13	NULL	NULL	NULL	B7x-Ig 	GP		does not bind					statement 3	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_18_10388_s_25	12920180	A B7x-Ig fusion protein binds to  Th1 cells derived from WT mice, but not mice with induced null mutation for  the newly identified CD28 homolog BTLA (B and T lymphocyte attenuator)  ( ).	bind
48046	5	9193	5	13	NULL	NULL	NULL	 B7x-Ig	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_18_10388_s_25	12920180	A B7x-Ig fusion protein binds to  Th1 cells derived from WT mice, but not mice with induced null mutation for  the newly identified CD28 homolog BTLA (B and T lymphocyte attenuator)  ( ).	bind
48047	6	9193	5	13	NULL	NULL	NULL	BTLA	GP		is					B and T lymphocyte attenuator	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_18_10388_s_25	12920180	A B7x-Ig fusion protein binds to  Th1 cells derived from WT mice, but not mice with induced null mutation for  the newly identified CD28 homolog BTLA (B and T lymphocyte attenuator)  ( ).	bind
31843	1	9193	6	NULL	NULL	0	NULL	Th1 cells	NULL		are derived from	NULL				mice	NULL	WT			NULL		0	NULL	NULL	NULL	gw70_pnas_100_18_10388_s_25	12920180	A B7x-Ig fusion protein binds to  Th1 cells derived from WT mice, but not mice with induced null mutation for  the newly identified CD28 homolog BTLA (B and T lymphocyte attenuator)  ( ).	bind
31844	2	9193	6	10	NULL	0	NULL	B7x-Ig	NULL		bind	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_18_10388_s_25	12920180	A B7x-Ig fusion protein binds to  Th1 cells derived from WT mice, but not mice with induced null mutation for  the newly identified CD28 homolog BTLA (B and T lymphocyte attenuator)  ( ).	bind
31845	3	9193	6	NULL	NULL	0	NULL	Th1	NULL		derived from	NULL				mice	NULL	null mutant			NULL		0	NULL	NULL	NULL	gw70_pnas_100_18_10388_s_25	12920180	A B7x-Ig fusion protein binds to  Th1 cells derived from WT mice, but not mice with induced null mutation for  the newly identified CD28 homolog BTLA (B and T lymphocyte attenuator)  ( ).	bind
31846	4	9193	6	10	NULL	0	NULL	B7x-Ig 	NULL		does not bind	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_18_10388_s_25	12920180	A B7x-Ig fusion protein binds to  Th1 cells derived from WT mice, but not mice with induced null mutation for  the newly identified CD28 homolog BTLA (B and T lymphocyte attenuator)  ( ).	bind
31847	5	9193	6	NULL	NULL	0	NULL	BTLA	NULL		is	NULL				B and T lymphocyte attenuator	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_100_18_10388_s_25	12920180	A B7x-Ig fusion protein binds to  Th1 cells derived from WT mice, but not mice with induced null mutation for  the newly identified CD28 homolog BTLA (B and T lymphocyte attenuator)  ( ).	bind
48048	6	9193	6	10	NULL	0	NULL	B7x-Ig	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_100_18_10388_s_25	12920180	A B7x-Ig fusion protein binds to  Th1 cells derived from WT mice, but not mice with induced null mutation for  the newly identified CD28 homolog BTLA (B and T lymphocyte attenuator)  ( ).	bind
39542	1	9194	5	13	NULL	NULL	NULL	IgA-Fc-binding protein	GP	bacterial	is unrelated to					Sir22	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14521_s_148	10329638	A bacterial IgA-Fc-binding protein unrelated to Sir22 has been described in group B streptococcus ( 5,  23,  24), and a fusion protein including a 73-residue sequence from this protein was found to bind IgA ( 25).	bind
39543	2	9194	5	13	NULL	NULL	NULL	statement 1	GP		is described in					group B streptococcus	Organism				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14521_s_148	10329638	A bacterial IgA-Fc-binding protein unrelated to Sir22 has been described in group B streptococcus ( 5,  23,  24), and a fusion protein including a 73-residue sequence from this protein was found to bind IgA ( 25).	bind
39544	3	9194	5	13	NULL	NULL	NULL	fusion protein	GP		include					IgA-Fc-binding protein	GP	73-residue sequence from			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14521_s_148	10329638	A bacterial IgA-Fc-binding protein unrelated to Sir22 has been described in group B streptococcus ( 5,  23,  24), and a fusion protein including a 73-residue sequence from this protein was found to bind IgA ( 25).	bind
39545	4	9194	5	13	NULL	NULL	NULL	statement 3	GP		bind					IgA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14521_s_148	10329638	A bacterial IgA-Fc-binding protein unrelated to Sir22 has been described in group B streptococcus ( 5,  23,  24), and a fusion protein including a 73-residue sequence from this protein was found to bind IgA ( 25).	bind
32030	1	9194	6	NULL	NULL	0	NULL	IgA-Fc-binding protein	NULL	bacterial	bind	NULL		73 residue sequence		IgA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_14521_s_148	10329638	A bacterial IgA-Fc-binding protein unrelated to Sir22 has been described in group B streptococcus ( 5,  23,  24), and a fusion protein including a 73-residue sequence from this protein was found to bind IgA ( 25).	bind
32824	2	9194	6	NULL	NULL	0	NULL	IgA-Fc-binding protein	NULL		is unrelated to	NULL				Sir22	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_14521_s_148	10329638	A bacterial IgA-Fc-binding protein unrelated to Sir22 has been described in group B streptococcus ( 5,  23,  24), and a fusion protein including a 73-residue sequence from this protein was found to bind IgA ( 25).	bind
57851	3	9194	6	10	NULL	0	NULL	statement 2			is described in					group B streptococcus					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14521_s_148	10329638	A bacterial IgA-Fc-binding protein unrelated to Sir22 has been described in group B streptococcus ( 5,  23,  24), and a fusion protein including a 73-residue sequence from this protein was found to bind IgA ( 25).	bind
39546	1	9198	5	13	NULL	NULL	NULL	POP-1 fragment	GP	bacterially expressed	bind		specifically	HMG domain				optimal		 Tcf target site	NULL		NULL	NULL	NULL	NULL	gw60_nature_406_6795_527_s_32	10952315	A bacterially expressed POP-1 fragment containing the HMG domain specifically binds the optimal Tcf target site, but not a sequence that lacks the core Tcf target motif ( Fig. 1a).	bind
39547	3	9198	5	13	NULL	NULL	NULL	POP-1 fragment	GP	bacterially expressed	does not bind			HMG domain		statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_nature_406_6795_527_s_32	10952315	A bacterially expressed POP-1 fragment containing the HMG domain specifically binds the optimal Tcf target site, but not a sequence that lacks the core Tcf target motif ( Fig. 1a).	bind
48049	2	9198	5	13	NULL	NULL	NULL	sequence	GP		lacks								 core Tcf target motif		NULL		NULL	NULL	NULL	NULL	gw60_nature_406_6795_527_s_32	10952315	A bacterially expressed POP-1 fragment containing the HMG domain specifically binds the optimal Tcf target site, but not a sequence that lacks the core Tcf target motif ( Fig. 1a).	bind
32031	1	9198	6	NULL	NULL	0	NULL	POP-1 fragment	NULL	bacterially expressed	bind	NULL	specifically	HMG domain			NULL	optimal		Tcf target site	NULL		0	NULL	NULL	NULL	gw60_nature_406_6795_527_s_32	10952315	A bacterially expressed POP-1 fragment containing the HMG domain specifically binds the optimal Tcf target site, but not a sequence that lacks the core Tcf target motif ( Fig. 1a).	bind
48050	2	9198	6	10	NULL	0	NULL	sequence	NULL		lacks	NULL					NULL		 core Tcf target motif		NULL		0	NULL	NULL	NULL	gw60_nature_406_6795_527_s_32	10952315	A bacterially expressed POP-1 fragment containing the HMG domain specifically binds the optimal Tcf target site, but not a sequence that lacks the core Tcf target motif ( Fig. 1a).	bind
48051	3	9198	6	10	NULL	0	NULL	POP-1 fragment	NULL	bacterially expressed	does not bind	NULL		HMG domain		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_nature_406_6795_527_s_32	10952315	A bacterially expressed POP-1 fragment containing the HMG domain specifically binds the optimal Tcf target site, but not a sequence that lacks the core Tcf target motif ( Fig. 1a).	bind
39548	1	9201	5	13	NULL	NULL	NULL	Bak BH3 peptide	GP		antagonize					Bcl-xL	GP	protective effects of 			NULL	alpha-Fas-treated HeLa cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13298_s_17	10224090	A Bak BH3 peptide was found to antagonize the protective effects of microinjected Bcl-xL in alpha-Fas-treated HeLa cells, whereas a mutant Bak BH3 peptide that no longerR binds Bcl-xL was inactive.	bind
39549	2	9201	5	13	NULL	NULL	NULL	Bak BH3 peptide	GP	mutant	does not bind					Bcl-xL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13298_s_17	10224090	A Bak BH3 peptide was found to antagonize the protective effects of microinjected Bcl-xL in alpha-Fas-treated HeLa cells, whereas a mutant Bak BH3 peptide that no longerR binds Bcl-xL was inactive.	bind
49531	3	9201	5	13	NULL	NULL	NULL	Bak BH3 peptide	GP		bind					Bcl-xL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13298_s_17	10224090	A Bak BH3 peptide was found to antagonize the protective effects of microinjected Bcl-xL in alpha-Fas-treated HeLa cells, whereas a mutant Bak BH3 peptide that no longerR binds Bcl-xL was inactive.	bind
32032	1	9201	6	NULL	NULL	0	NULL	Bak BH3 peptide	NULL		bind	NULL				Bcl-xL	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_19_13298_s_17	10224090	A Bak BH3 peptide was found to antagonize the protective effects of microinjected Bcl-xL in alpha-Fas-treated HeLa cells, whereas a mutant Bak BH3 peptide that no longerR binds Bcl-xL was inactive.	bind
32034	2	9201	6	10	NULL	0	NULL	Bak BH3 peptide	NULL		antagonizes	NULL				Bcl-xL	NULL	protective effects of 			NULL	alpha-Fas-treated HeLa cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13298_s_17	10224090	A Bak BH3 peptide was found to antagonize the protective effects of microinjected Bcl-xL in alpha-Fas-treated HeLa cells, whereas a mutant Bak BH3 peptide that no longerR binds Bcl-xL was inactive.	bind
32035	3	9201	6	10	NULL	0	NULL	Bak BH3 peptide	NULL	mutant	does not bind	NULL				Bcl-xL	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13298_s_17	10224090	A Bak BH3 peptide was found to antagonize the protective effects of microinjected Bcl-xL in alpha-Fas-treated HeLa cells, whereas a mutant Bak BH3 peptide that no longerR binds Bcl-xL was inactive.	bind
39551	1	9202	5	13	NULL	NULL	NULL	180 kDa protein	GP		bind		specifically			NR2A	GP				NULL	WT tissue	NULL	NULL	NULL	NULL	gw70_jneurosci_24_49_11098_s_85	15590926	A band corresponding  to 180 kDa was detected in the lane containing WT but not NR2AKO tissue (arrowhead)  demonstrating specific binding to NR2A and no cross-reactivity with NR2B.	bind
39552	2	9202	5	13	NULL	NULL	NULL	statement 1	GP		does not cross react with					NR2B	GP				NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_24_49_11098_s_85	15590926	A band corresponding  to 180 kDa was detected in the lane containing WT but not NR2AKO tissue (arrowhead)  demonstrating specific binding to NR2A and no cross-reactivity with NR2B.	bind
32037	1	9202	6	NULL	NULL	0	NULL	protein 180kDa	NULL		bind	NULL	specifically			NR2A	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_24_49_11098_s_85	15590926	A band corresponding  to 180 kDa was detected in the lane containing WT but not NR2AKO tissue (arrowhead)  demonstrating specific binding to NR2A and no cross-reactivity with NR2B.	bind
32038	2	9202	6	10	NULL	0	NULL	 180kDa protein	NULL		does not cross react with	NULL				NR2B	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_24_49_11098_s_85	15590926	A band corresponding  to 180 kDa was detected in the lane containing WT but not NR2AKO tissue (arrowhead)  demonstrating specific binding to NR2A and no cross-reactivity with NR2B.	bind
39553	1	9203	5	13	NULL	NULL	NULL	20 kDa protein	GP		bind					calmodulin	GP	high concentrations of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_27_24500_s_168	12716903	A band of  unknown nature migrating at the front of the gel (<20 kDa) bound calmodulin  when the latter was present in high concentrations, but the binding persisted,  albeit weakly, in the presence of EGTA.	bind
39554	2	9203	5	13	NULL	NULL	NULL	statement 1	Process		persists		weakly			EGTA	Chemical	in presence of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_27_24500_s_168	12716903	A band of  unknown nature migrating at the front of the gel (<20 kDa) bound calmodulin  when the latter was present in high concentrations, but the binding persisted,  albeit weakly, in the presence of EGTA.	bind
39555	1	9204	5	13	NULL	NULL	NULL	30 kDa band	GP		corresponds to							size of	B subunit		NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_7623_s_114	10075648	A band of about 30 kDa, corresponding to the size of the B subunit  in vivo (Fig.  3,  lane NE), binds p300, which confirms the data obtained  in vitro (compare Figs.  2 and  3).	bind
39556	2	9204	5	13	NULL	NULL	NULL	statement 1	GP		bind					p300	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_7623_s_114	10075648	A band of about 30 kDa, corresponding to the size of the B subunit  in vivo (Fig.  3,  lane NE), binds p300, which confirms the data obtained  in vitro (compare Figs.  2 and  3).	bind
32039	1	9204	6	10	NULL	0	NULL	30kDa	NULL		bind	NULL				p300	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_7623_s_114	10075648	A band of about 30 kDa, corresponding to the size of the B subunit  in vivo (Fig.  3,  lane NE), binds p300, which confirms the data obtained  in vitro (compare Figs.  2 and  3).	bind
48052	2	9204	6	10	NULL	0	NULL	30 kDa	NULL		corresponds to	NULL					NULL	size of	B subunit		NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_12_7623_s_114	10075648	A band of about 30 kDa, corresponding to the size of the B subunit  in vivo (Fig.  3,  lane NE), binds p300, which confirms the data obtained  in vitro (compare Figs.  2 and  3).	bind
39630	1	9205	5	13	NULL	NULL	NULL	 Tenascin-C	GP		bind			 C terminus		Heparin	Chemical		C terminus of fibrinogen-like domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_7_3378_s_188	7531705	A Basic Peptide from the Extreme C Terminus of Tenascin-C  Binds to Heparin At the C terminus of the fibrinogen-like  domain, and hence at extreme end of the coding sequence of tenascin-C,  a conspicuous stretch of basic amino acids is found which is conserved  among species (but which is not found in fibrinogen itself).	bind
39631	2	9205	5	13	NULL	NULL	NULL	tenascin-C	GP		contains			extreme end of coding sequence of		basic amino acids	AminoAcid	conspicuous stretch of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_7_3378_s_188	7531705	A Basic Peptide from the Extreme C Terminus of Tenascin-C  Binds to Heparin At the C terminus of the fibrinogen-like  domain, and hence at extreme end of the coding sequence of tenascin-C,  a conspicuous stretch of basic amino acids is found which is conserved  among species (but which is not found in fibrinogen itself).	bind
39633	3	9205	5	13	NULL	NULL	NULL	statement 2	AminoAcid		is conserved among					species	Organism				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_7_3378_s_188	7531705	A Basic Peptide from the Extreme C Terminus of Tenascin-C  Binds to Heparin At the C terminus of the fibrinogen-like  domain, and hence at extreme end of the coding sequence of tenascin-C,  a conspicuous stretch of basic amino acids is found which is conserved  among species (but which is not found in fibrinogen itself).	bind
39634	4	9205	5	13	NULL	NULL	NULL	statement 2	AminoAcid		is not found in					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_7_3378_s_188	7531705	A Basic Peptide from the Extreme C Terminus of Tenascin-C  Binds to Heparin At the C terminus of the fibrinogen-like  domain, and hence at extreme end of the coding sequence of tenascin-C,  a conspicuous stretch of basic amino acids is found which is conserved  among species (but which is not found in fibrinogen itself).	bind
32559	1	9205	6	10	NULL	0	NULL	Tenascin-C	NULL		bind	NULL		C-terminus		heparin	NULL		C terminus of the fibrinogen-like domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_7_3378_s_188	7531705	A Basic Peptide from the Extreme C Terminus of Tenascin-C  Binds to Heparin At the C terminus of the fibrinogen-like  domain, and hence at extreme end of the coding sequence of tenascin-C,  a conspicuous stretch of basic amino acids is found which is conserved  among species (but which is not found in fibrinogen itself).	bind
57852	2	9205	6	10	NULL	0	NULL	tenascin-C			contains			extreme end of the coding sequence of 		basic amino acids		conspicuous stretch of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_7_3378_s_188	7531705	A Basic Peptide from the Extreme C Terminus of Tenascin-C  Binds to Heparin At the C terminus of the fibrinogen-like  domain, and hence at extreme end of the coding sequence of tenascin-C,  a conspicuous stretch of basic amino acids is found which is conserved  among species (but which is not found in fibrinogen itself).	bind
57853	3	9205	6	10	NULL	0	NULL	statement 2			is conserved among					species					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_7_3378_s_188	7531705	A Basic Peptide from the Extreme C Terminus of Tenascin-C  Binds to Heparin At the C terminus of the fibrinogen-like  domain, and hence at extreme end of the coding sequence of tenascin-C,  a conspicuous stretch of basic amino acids is found which is conserved  among species (but which is not found in fibrinogen itself).	bind
57854	4	9205	6	10	NULL	0	NULL	statement 2			is not found in					fibrinogen					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_7_3378_s_188	7531705	A Basic Peptide from the Extreme C Terminus of Tenascin-C  Binds to Heparin At the C terminus of the fibrinogen-like  domain, and hence at extreme end of the coding sequence of tenascin-C,  a conspicuous stretch of basic amino acids is found which is conserved  among species (but which is not found in fibrinogen itself).	bind
39635	1	9206	5	13	NULL	NULL	NULL				bind		differentially	SHP motif		LRH-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_27_9505_s_208	15976031	A basis for the differential binding of the SHP motif to LRH-1 and SF-1 becomes evident by comparing the surface topology of their coactivator-binding sites ( Fig. 5).	bind
39636	2	9206	5	13	NULL	NULL	NULL				bind		differentially	SHP motif		SF-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_27_9505_s_208	15976031	A basis for the differential binding of the SHP motif to LRH-1 and SF-1 becomes evident by comparing the surface topology of their coactivator-binding sites ( Fig. 5).	bind
32040	1	9206	6	NULL	NULL	0	NULL		NULL		bind	NULL	differentially	SHP motif		LRH-1	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_27_9505_s_208	15976031	A basis for the differential binding of the SHP motif to LRH-1 and SF-1 becomes evident by comparing the surface topology of their coactivator-binding sites ( Fig. 5).	bind
32041	2	9206	6	NULL	NULL	0	NULL		NULL		bind	NULL	differentially	SHP motif		SF-1	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_27_9505_s_208	15976031	A basis for the differential binding of the SHP motif to LRH-1 and SF-1 becomes evident by comparing the surface topology of their coactivator-binding sites ( Fig. 5).	bind
39637	1	9207	5	13	NULL	NULL	NULL	BCR pY177 peptide	GP		is					Lys-Pro-Phe- Tyr(P)-Val-Asn-Val-Glu-Phe	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_2_894_s_166	8995379	A BCR pY177 peptide (Lys-Pro-Phe- Tyr(P)-Val-Asn-Val-Glu-Phe) binds Grb2 and Grap SH2 domains with equivalent high affinity (ID50 = 2.1  plus-or-minus  0.4 muM and 0.8  plus-or-minus  0.3 muM, respectively).	bind
39638	2	9207	5	13	NULL	NULL	NULL	BCR pY177 peptide	GP		bind		high affinity			Grb2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_2_894_s_166	8995379	A BCR pY177 peptide (Lys-Pro-Phe- Tyr(P)-Val-Asn-Val-Glu-Phe) binds Grb2 and Grap SH2 domains with equivalent high affinity (ID50 = 2.1  plus-or-minus  0.4 muM and 0.8  plus-or-minus  0.3 muM, respectively).	bind
39639	3	9207	5	13	NULL	NULL	NULL	BCR pY177 peptide	GP		bind		high affinity			Grap	GP		SH2 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_2_894_s_166	8995379	A BCR pY177 peptide (Lys-Pro-Phe- Tyr(P)-Val-Asn-Val-Glu-Phe) binds Grb2 and Grap SH2 domains with equivalent high affinity (ID50 = 2.1  plus-or-minus  0.4 muM and 0.8  plus-or-minus  0.3 muM, respectively).	bind
39640	4	9207	5	13	NULL	NULL	NULL	statement 2	Process	affinity of	is equal to					statement 3	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_2_894_s_166	8995379	A BCR pY177 peptide (Lys-Pro-Phe- Tyr(P)-Val-Asn-Val-Glu-Phe) binds Grb2 and Grap SH2 domains with equivalent high affinity (ID50 = 2.1  plus-or-minus  0.4 muM and 0.8  plus-or-minus  0.3 muM, respectively).	bind
32042	1	9207	6	10	NULL	0	NULL	BCR pY177 peptide			bind		high affinity			Grb2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_2_894_s_166	8995379	A BCR pY177 peptide (Lys-Pro-Phe- Tyr(P)-Val-Asn-Val-Glu-Phe) binds Grb2 and Grap SH2 domains with equivalent high affinity (ID50 = 2.1  plus-or-minus  0.4 muM and 0.8  plus-or-minus  0.3 muM, respectively).	bind
32043	2	9207	6	10	NULL	0	NULL	BCR pY177 peptide			bind		high affinity			Grap			SH2 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_2_894_s_166	8995379	A BCR pY177 peptide (Lys-Pro-Phe- Tyr(P)-Val-Asn-Val-Glu-Phe) binds Grb2 and Grap SH2 domains with equivalent high affinity (ID50 = 2.1  plus-or-minus  0.4 muM and 0.8  plus-or-minus  0.3 muM, respectively).	bind
32044	3	9207	6	NULL	NULL	0	NULL	statement 1	NULL	affinity of	is equal to	NULL				statement 2	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_2_894_s_166	8995379	A BCR pY177 peptide (Lys-Pro-Phe- Tyr(P)-Val-Asn-Val-Glu-Phe) binds Grb2 and Grap SH2 domains with equivalent high affinity (ID50 = 2.1  plus-or-minus  0.4 muM and 0.8  plus-or-minus  0.3 muM, respectively).	bind
32045	4	9207	6	NULL	NULL	0	NULL	BCR pY177 peptide	NULL		is	NULL				Lys-Pro-Phe- Tyr(P)-Val-Asn-Val-Glu-Phe	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_2_894_s_166	8995379	A BCR pY177 peptide (Lys-Pro-Phe- Tyr(P)-Val-Asn-Val-Glu-Phe) binds Grb2 and Grap SH2 domains with equivalent high affinity (ID50 = 2.1  plus-or-minus  0.4 muM and 0.8  plus-or-minus  0.3 muM, respectively).	bind
39641	1	9208	5	13	NULL	NULL	NULL	Bem1p	GP		bind		directly			Cla4p	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7176_s_310	11113154	A Bem1p-dependent Complex Containing Cdc24p, Cdc42p, and Cla4p--  We report that Bem1p binds directly to Cla4p and to GTP-Cdc42p as well as to Cdc24p and can mediate the assembly of complexes containing each of these proteins  in vitro.	bind
39642	2	9208	5	13	NULL	NULL	NULL	Bem1p	GP		bind		directly			GTP-Cdc42p	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7176_s_310	11113154	A Bem1p-dependent Complex Containing Cdc24p, Cdc42p, and Cla4p--  We report that Bem1p binds directly to Cla4p and to GTP-Cdc42p as well as to Cdc24p and can mediate the assembly of complexes containing each of these proteins  in vitro.	bind
39643	3	9208	5	13	NULL	NULL	NULL	Bem1p	GP		bind		directly			Cdc24p	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7176_s_310	11113154	A Bem1p-dependent Complex Containing Cdc24p, Cdc42p, and Cla4p--  We report that Bem1p binds directly to Cla4p and to GTP-Cdc42p as well as to Cdc24p and can mediate the assembly of complexes containing each of these proteins  in vitro.	bind
39644	4	9208	5	13	NULL	NULL	NULL	Bem1p	GP		mediate					Cdc24p	GP	assembly of complexes containing			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7176_s_310	11113154	A Bem1p-dependent Complex Containing Cdc24p, Cdc42p, and Cla4p--  We report that Bem1p binds directly to Cla4p and to GTP-Cdc42p as well as to Cdc24p and can mediate the assembly of complexes containing each of these proteins  in vitro.	bind
39645	5	9208	5	13	NULL	NULL	NULL	Bem1p	GP		mediate					GTP-Cdc42p	GP	assembly of complexes containing			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7176_s_310	11113154	A Bem1p-dependent Complex Containing Cdc24p, Cdc42p, and Cla4p--  We report that Bem1p binds directly to Cla4p and to GTP-Cdc42p as well as to Cdc24p and can mediate the assembly of complexes containing each of these proteins  in vitro.	bind
39646	6	9208	5	13	NULL	NULL	NULL	Bem1p	GP		mediate					Cla4p	GP	assembly of complexes containing			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7176_s_310	11113154	A Bem1p-dependent Complex Containing Cdc24p, Cdc42p, and Cla4p--  We report that Bem1p binds directly to Cla4p and to GTP-Cdc42p as well as to Cdc24p and can mediate the assembly of complexes containing each of these proteins  in vitro.	bind
32046	1	9208	6	10	NULL	0	NULL	Bem1p	NULL		bind	NULL	directly			Cla4p	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7176_s_310	11113154	A Bem1p-dependent Complex Containing Cdc24p, Cdc42p, and Cla4p--  We report that Bem1p binds directly to Cla4p and to GTP-Cdc42p as well as to Cdc24p and can mediate the assembly of complexes containing each of these proteins  in vitro.	bind
32047	2	9208	6	10	NULL	0	NULL	Bem1p	NULL		bind	NULL	directly			GTP-Cdc42p	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7176_s_310	11113154	A Bem1p-dependent Complex Containing Cdc24p, Cdc42p, and Cla4p--  We report that Bem1p binds directly to Cla4p and to GTP-Cdc42p as well as to Cdc24p and can mediate the assembly of complexes containing each of these proteins  in vitro.	bind
32048	3	9208	6	10	NULL	0	NULL	Bem1p	NULL		bind	NULL	directly			Cdc24p	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7176_s_310	11113154	A Bem1p-dependent Complex Containing Cdc24p, Cdc42p, and Cla4p--  We report that Bem1p binds directly to Cla4p and to GTP-Cdc42p as well as to Cdc24p and can mediate the assembly of complexes containing each of these proteins  in vitro.	bind
32050	5	9208	6	10	NULL	0	NULL	Bem1p	NULL		mediate	NULL				Cla4p	NULL	assembly of complexes containing			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7176_s_310	11113154	A Bem1p-dependent Complex Containing Cdc24p, Cdc42p, and Cla4p--  We report that Bem1p binds directly to Cla4p and to GTP-Cdc42p as well as to Cdc24p and can mediate the assembly of complexes containing each of these proteins  in vitro.	bind
32051	6	9208	6	10	NULL	0	NULL	Bem1p	NULL		mediate	NULL				GTP-Cdc42p	NULL	assembly of complexes containing			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7176_s_310	11113154	A Bem1p-dependent Complex Containing Cdc24p, Cdc42p, and Cla4p--  We report that Bem1p binds directly to Cla4p and to GTP-Cdc42p as well as to Cdc24p and can mediate the assembly of complexes containing each of these proteins  in vitro.	bind
48053	4	9208	6	10	NULL	0	NULL	Bem1p			mediate					Cdc24p		assembly of complexes containing			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7176_s_310	11113154	A Bem1p-dependent Complex Containing Cdc24p, Cdc42p, and Cla4p--  We report that Bem1p binds directly to Cla4p and to GTP-Cdc42p as well as to Cdc24p and can mediate the assembly of complexes containing each of these proteins  in vitro.	bind
39647	1	9209	5	13	NULL	NULL	NULL	Bald	GP		is					benzaldehyde-activated transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_13_3926_s_7	12813087	A benzaldehyde-activated transcription factor (Bald) that specifically binds to the PAL  cis-acting element was also identified.	bind
39648	2	9209	5	13	NULL	NULL	NULL	Bald	GP		bind		specifically			PAL	GP			cis-acting element	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_13_3926_s_7	12813087	A benzaldehyde-activated transcription factor (Bald) that specifically binds to the PAL  cis-acting element was also identified.	bind
32052	1	9209	6	NULL	NULL	0	NULL	Bald	NULL		is	NULL				benzaldehyde-activated transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_185_13_3926_s_7	12813087	A benzaldehyde-activated transcription factor (Bald) that specifically binds to the PAL  cis-acting element was also identified.	bind
32053	2	9209	6	NULL	NULL	0	NULL	Bald	NULL		bind	NULL	specifically			PAL	NULL			cis-acting element	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_185_13_3926_s_7	12813087	A benzaldehyde-activated transcription factor (Bald) that specifically binds to the PAL  cis-acting element was also identified.	bind
39649	1	9210	5	13	NULL	NULL	NULL	beta-cell-specific protein	GP		bind					B8	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4702_s_177	12052878	A beta-cell-specific protein binds to B8.	bind
32054	1	9210	6	NULL	NULL	0	NULL	beta-cell-specific protein	NULL		bind	NULL				B8	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_13_4702_s_177	12052878	A beta-cell-specific protein binds to B8.	bind
39650	1	9211	5	13	NULL	NULL	NULL	U1 RNA	NucleicAcid		bind					U1A protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_45_32265_s_24	10542265	A beta-sheet also plays a critical role in the binding of U1 RNA to the small nuclear ribonucleoprotein U1A protein ( 12).	bind
39651	2	9211	5	13	NULL	NULL	NULL	U1A protein	GP		is a type of					small nuclear ribonucleoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_45_32265_s_24	10542265	A beta-sheet also plays a critical role in the binding of U1 RNA to the small nuclear ribonucleoprotein U1A protein ( 12).	bind
39652	3	9211	5	13	NULL	NULL	NULL	beta-sheet	GP		plays a role in		critical			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_45_32265_s_24	10542265	A beta-sheet also plays a critical role in the binding of U1 RNA to the small nuclear ribonucleoprotein U1A protein ( 12).	bind
32055	1	9211	6	10	NULL	0	NULL	U1 RNA	NULL		bind	NULL				 U1A protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_45_32265_s_24	10542265	A beta-sheet also plays a critical role in the binding of U1 RNA to the small nuclear ribonucleoprotein U1A protein ( 12).	bind
32056	2	9211	6	10	NULL	0	NULL	beta-sheet	NULL		plays a role in	NULL	critical			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_45_32265_s_24	10542265	A beta-sheet also plays a critical role in the binding of U1 RNA to the small nuclear ribonucleoprotein U1A protein ( 12).	bind
48054	3	9211	6	10	NULL	0	NULL	U1A protein	NULL		is a type of	NULL				small nuclear ribonucleoprotein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_45_32265_s_24	10542265	A beta-sheet also plays a critical role in the binding of U1 RNA to the small nuclear ribonucleoprotein U1A protein ( 12).	bind
40365	2	9214	5	13	NULL	NULL	NULL	beta4R1281W	GP		is					statement 1	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_3_1211_s_163	14668477	A beta4 subunit in which the binding site for the plectin-ABD is mutated (beta4R1281W) bound to plec1 - 606, plec284 - 1154, and plec1 - 1154.	bind
40366	3	9214	5	13	NULL	NULL	NULL				bind			beta4R1281W		plec	GP		1 - 606		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_3_1211_s_163	14668477	A beta4 subunit in which the binding site for the plectin-ABD is mutated (beta4R1281W) bound to plec1 - 606, plec284 - 1154, and plec1 - 1154.	bind
40367	5	9214	5	13	NULL	NULL	NULL				bind			beta4R1281W		plec	GP		284 - 1154		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_3_1211_s_163	14668477	A beta4 subunit in which the binding site for the plectin-ABD is mutated (beta4R1281W) bound to plec1 - 606, plec284 - 1154, and plec1 - 1154.	bind
40368	4	9214	5	13	NULL	NULL	NULL				bind			beta4R1281W		plec	GP		1 - 1154		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_3_1211_s_163	14668477	A beta4 subunit in which the binding site for the plectin-ABD is mutated (beta4R1281W) bound to plec1 - 606, plec284 - 1154, and plec1 - 1154.	bind
48055	1	9214	5	13	NULL	NULL	NULL	beta4 subunit	GP		contains								plectin-ABD binding site		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_3_1211_s_163	14668477	A beta4 subunit in which the binding site for the plectin-ABD is mutated (beta4R1281W) bound to plec1 - 606, plec284 - 1154, and plec1 - 1154.	bind
32069	1	9214	6	NULL	NULL	0	NULL	beta4 subunit	NULL	mutant	bind	NULL		plectin-ABD binding site		plec	NULL		1-606		NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_3_1211_s_163	14668477	A beta4 subunit in which the binding site for the plectin-ABD is mutated (beta4R1281W) bound to plec1 - 606, plec284 - 1154, and plec1 - 1154.	bind
32070	2	9214	6	NULL	NULL	0	NULL	beta4 subunit	NULL	mutant	bind	NULL		plectin-ABD binding site		plec	NULL		284-1154		NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_3_1211_s_163	14668477	A beta4 subunit in which the binding site for the plectin-ABD is mutated (beta4R1281W) bound to plec1 - 606, plec284 - 1154, and plec1 - 1154.	bind
32071	3	9214	6	NULL	NULL	0	NULL	beta4 subunit	NULL	mutant	bind	NULL		plectin-ABD binding site		plec	NULL		1-1154		NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_3_1211_s_163	14668477	A beta4 subunit in which the binding site for the plectin-ABD is mutated (beta4R1281W) bound to plec1 - 606, plec284 - 1154, and plec1 - 1154.	bind
48056	4	9214	6	10	NULL	0	NULL	beta4R1281W	NULL		is	NULL				beta4 subunit	NULL	mutant	 plectin-ABD binding site		NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_3_1211_s_163	14668477	A beta4 subunit in which the binding site for the plectin-ABD is mutated (beta4R1281W) bound to plec1 - 606, plec284 - 1154, and plec1 - 1154.	bind
39654	1	9215	5	13	NULL	NULL	NULL	SDF-1	GP		bind					CXCR4	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-clin-invest_115_1_15630439_s_3	15630439	A better understanding at a molecular level of how the binding of SDF-1  to its cell surface receptor, CXCR4, elicits specific biological responses  in these cells has now been achieved through the identification of PKC-zeta  activation as a common downstream signal.	bind
39655	2	9215	5	13	NULL	NULL	NULL	CXCR4	GP		is a type of					cell surface receptor	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-clin-invest_115_1_15630439_s_3	15630439	A better understanding at a molecular level of how the binding of SDF-1  to its cell surface receptor, CXCR4, elicits specific biological responses  in these cells has now been achieved through the identification of PKC-zeta  activation as a common downstream signal.	bind
39656	3	9215	5	13	NULL	NULL	NULL	statement 1	Process		elicits					biological responses	Process	specific			NULL	CXCR4	NULL	NULL	NULL	NULL	abs-batch0650-0679_j-clin-invest_115_1_15630439_s_3	15630439	A better understanding at a molecular level of how the binding of SDF-1  to its cell surface receptor, CXCR4, elicits specific biological responses  in these cells has now been achieved through the identification of PKC-zeta  activation as a common downstream signal.	bind
39657	4	9215	5	13	NULL	NULL	NULL	PKC-zeta	GP	activation of	acts as					downstream signal	Process	common			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-clin-invest_115_1_15630439_s_3	15630439	A better understanding at a molecular level of how the binding of SDF-1  to its cell surface receptor, CXCR4, elicits specific biological responses  in these cells has now been achieved through the identification of PKC-zeta  activation as a common downstream signal.	bind
39658	5	9215	5	13	NULL	NULL	NULL	statement 4	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-clin-invest_115_1_15630439_s_3	15630439	A better understanding at a molecular level of how the binding of SDF-1  to its cell surface receptor, CXCR4, elicits specific biological responses  in these cells has now been achieved through the identification of PKC-zeta  activation as a common downstream signal.	bind
32073	1	9215	6	NULL	NULL	0	NULL	SDF-1	NULL		bind	NULL				CXCR4	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-clin-invest_115_1_15630439_s_3	15630439	A better understanding at a molecular level of how the binding of SDF-1  to its cell surface receptor, CXCR4, elicits specific biological responses  in these cells has now been achieved through the identification of PKC-zeta  activation as a common downstream signal.	bind
32074	2	9215	6	NULL	NULL	0	NULL	CXCR4	NULL		is a type of	NULL				cell surface receptor	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-clin-invest_115_1_15630439_s_3	15630439	A better understanding at a molecular level of how the binding of SDF-1  to its cell surface receptor, CXCR4, elicits specific biological responses  in these cells has now been achieved through the identification of PKC-zeta  activation as a common downstream signal.	bind
32075	3	9215	6	10	NULL	0	NULL	statement 1			elicits					biological responses		specific			NULL	CXCR4	NULL	NULL	NULL	NULL	abs-batch0650-0679_j-clin-invest_115_1_15630439_s_3	15630439	A better understanding at a molecular level of how the binding of SDF-1  to its cell surface receptor, CXCR4, elicits specific biological responses  in these cells has now been achieved through the identification of PKC-zeta  activation as a common downstream signal.	bind
57855	4	9215	6	10	NULL	0	NULL	PKC-zeta		activation of	acts as					downstream signal		common			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-clin-invest_115_1_15630439_s_3	15630439	A better understanding at a molecular level of how the binding of SDF-1  to its cell surface receptor, CXCR4, elicits specific biological responses  in these cells has now been achieved through the identification of PKC-zeta  activation as a common downstream signal.	bind
57856	5	9215	6	10	NULL	0	NULL	statement 4			leads to					statement 3					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-clin-invest_115_1_15630439_s_3	15630439	A better understanding at a molecular level of how the binding of SDF-1  to its cell surface receptor, CXCR4, elicits specific biological responses  in these cells has now been achieved through the identification of PKC-zeta  activation as a common downstream signal.	bind
39659	1	9216	5	13	NULL	NULL	NULL	GTF3	GP		bind			R4		DNA sequence	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31722_s_296	15987678	A better understanding of the involvement of this area in DNA-protein interaction will require knowledge of the crystal structure of GTF3-R4 bound to its target DNA sequence.	bind
32076	1	9216	6	NULL	NULL	0	NULL	GTF3	NULL		bind	NULL		R4		DNA sequence	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_36_31722_s_296	15987678	A better understanding of the involvement of this area in DNA-protein interaction will require knowledge of the crystal structure of GTF3-R4 bound to its target DNA sequence.	bind
39660	1	9217	5	13	NULL	NULL	NULL	PAM2	GP		bind					HYD	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_20_14376_s_48	16554297	A better understanding of the PAM2 binding properties of HYD should help elucidate its function through identification of novel physiological partners and provide useful insight into the potential competition between HYD and PABP for shared binding partners.	bind
32077	1	9217	6	NULL	NULL	0	NULL	HYD	NULL		bind	NULL				PAM2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_20_14376_s_48	16554297	A better understanding of the PAM2 binding properties of HYD should help elucidate its function through identification of novel physiological partners and provide useful insight into the potential competition between HYD and PABP for shared binding partners.	bind
39661	1	9218	5	13	NULL	NULL	NULL	CD46	GP		bind					MVH	GP	soluble			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_32294_s_137	12065582	A BIAcore 2000 instrument was used to monitor CD46 binding to soluble MVH.	bind
32078	1	9218	6	NULL	NULL	0	NULL	CD46	NULL		bind	NULL				MVH	NULL	soluble			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_35_32294_s_137	12065582	A BIAcore 2000 instrument was used to monitor CD46 binding to soluble MVH.	bind
39662	1	9219	5	13	NULL	NULL	NULL	IL-1 ligands	GP		bind					T1/ST2 Fc	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_10_5784_s_29	8621446	A BIAcore biosensor  (Pharmacia Biosensor) was used to examine binding of IL-1 ligands to  the human T1/ST2 Fc fusion protein, essentially as described in detail  in Arend  et al.( 14 ) .	bind
48057	2	9219	5	13	NULL	NULL	NULL	T1/ST2 Fc	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_10_5784_s_29	8621446	A BIAcore biosensor  (Pharmacia Biosensor) was used to examine binding of IL-1 ligands to  the human T1/ST2 Fc fusion protein, essentially as described in detail  in Arend  et al.( 14 ) .	bind
32099	1	9219	6	10	NULL	0	NULL	IL-1 ligands	NULL		bind	NULL				T1/ST2 Fc 	NULL	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_10_5784_s_29	8621446	A BIAcore biosensor  (Pharmacia Biosensor) was used to examine binding of IL-1 ligands to  the human T1/ST2 Fc fusion protein, essentially as described in detail  in Arend  et al.( 14 ) .	bind
48058	2	9219	6	10	NULL	0	NULL	T1/ST2 Fc	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_10_5784_s_29	8621446	A BIAcore biosensor  (Pharmacia Biosensor) was used to examine binding of IL-1 ligands to  the human T1/ST2 Fc fusion protein, essentially as described in detail  in Arend  et al.( 14 ) .	bind
39663	1	9220	5	13	NULL	NULL	NULL	BirA	GP		is a type of					bifunctional protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_360	16533810	A bifunctional protein (BirA) acts as a protein-biotin ligase or as a sensor-like transcriptional regulator ( ), and after complexation of BirA with biotin-5''-AMP ( ) or with biotin ( ), BirA monomers bind cooperatively to the biotin operator.	bind
39664	2	9220	5	13	NULL	NULL	NULL	BirA	GP		acts as					protein-biotin ligase	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_360	16533810	A bifunctional protein (BirA) acts as a protein-biotin ligase or as a sensor-like transcriptional regulator ( ), and after complexation of BirA with biotin-5''-AMP ( ) or with biotin ( ), BirA monomers bind cooperatively to the biotin operator.	bind
39665	3	9220	5	13	NULL	NULL	NULL	BirA	GP		acts as					sensor-like transcriptional regulator	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_360	16533810	A bifunctional protein (BirA) acts as a protein-biotin ligase or as a sensor-like transcriptional regulator ( ), and after complexation of BirA with biotin-5''-AMP ( ) or with biotin ( ), BirA monomers bind cooperatively to the biotin operator.	bind
39666	4	9220	5	13	NULL	NULL	NULL	BirA	GP		complex with					biotin-5''-AMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_360	16533810	A bifunctional protein (BirA) acts as a protein-biotin ligase or as a sensor-like transcriptional regulator ( ), and after complexation of BirA with biotin-5''-AMP ( ) or with biotin ( ), BirA monomers bind cooperatively to the biotin operator.	bind
39667	5	9220	5	13	NULL	NULL	NULL	BirA	GP		complex with					biotin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_360	16533810	A bifunctional protein (BirA) acts as a protein-biotin ligase or as a sensor-like transcriptional regulator ( ), and after complexation of BirA with biotin-5''-AMP ( ) or with biotin ( ), BirA monomers bind cooperatively to the biotin operator.	bind
39668	6	9220	5	13	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_360	16533810	A bifunctional protein (BirA) acts as a protein-biotin ligase or as a sensor-like transcriptional regulator ( ), and after complexation of BirA with biotin-5''-AMP ( ) or with biotin ( ), BirA monomers bind cooperatively to the biotin operator.	bind
39669	7	9220	5	13	NULL	NULL	NULL	BirA monomers	GP		bind		cooperatively			biotin	Chemical			operator	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_360	16533810	A bifunctional protein (BirA) acts as a protein-biotin ligase or as a sensor-like transcriptional regulator ( ), and after complexation of BirA with biotin-5''-AMP ( ) or with biotin ( ), BirA monomers bind cooperatively to the biotin operator.	bind
39670	8	9220	5	13	NULL	NULL	NULL	statement 7	Process		occurs after					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_360	16533810	A bifunctional protein (BirA) acts as a protein-biotin ligase or as a sensor-like transcriptional regulator ( ), and after complexation of BirA with biotin-5''-AMP ( ) or with biotin ( ), BirA monomers bind cooperatively to the biotin operator.	bind
39671	9	9220	5	13	NULL	NULL	NULL	statement 7	Process		occurs after					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_360	16533810	A bifunctional protein (BirA) acts as a protein-biotin ligase or as a sensor-like transcriptional regulator ( ), and after complexation of BirA with biotin-5''-AMP ( ) or with biotin ( ), BirA monomers bind cooperatively to the biotin operator.	bind
32101	1	9220	6	NULL	NULL	0	NULL	BirA	NULL		is a type of	NULL				bifunctional protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_360	16533810	A bifunctional protein (BirA) acts as a protein-biotin ligase or as a sensor-like transcriptional regulator ( ), and after complexation of BirA with biotin-5''-AMP ( ) or with biotin ( ), BirA monomers bind cooperatively to the biotin operator.	bind
32102	2	9220	6	NULL	NULL	0	NULL	BirA	NULL		functions as a	NULL				protein-biotin ligase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_360	16533810	A bifunctional protein (BirA) acts as a protein-biotin ligase or as a sensor-like transcriptional regulator ( ), and after complexation of BirA with biotin-5''-AMP ( ) or with biotin ( ), BirA monomers bind cooperatively to the biotin operator.	bind
32103	3	9220	6	10	NULL	0	NULL	BirA			functions as a					sensor like transcriptional regulator					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_360	16533810	A bifunctional protein (BirA) acts as a protein-biotin ligase or as a sensor-like transcriptional regulator ( ), and after complexation of BirA with biotin-5''-AMP ( ) or with biotin ( ), BirA monomers bind cooperatively to the biotin operator.	bind
32106	4	9220	6	NULL	NULL	0	NULL	BirA	NULL		complexes with	NULL				biotin-5''-AMP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_360	16533810	A bifunctional protein (BirA) acts as a protein-biotin ligase or as a sensor-like transcriptional regulator ( ), and after complexation of BirA with biotin-5''-AMP ( ) or with biotin ( ), BirA monomers bind cooperatively to the biotin operator.	bind
32109	5	9220	6	NULL	NULL	0	NULL	BirA	NULL		complexes with	NULL				biotin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_360	16533810	A bifunctional protein (BirA) acts as a protein-biotin ligase or as a sensor-like transcriptional regulator ( ), and after complexation of BirA with biotin-5''-AMP ( ) or with biotin ( ), BirA monomers bind cooperatively to the biotin operator.	bind
32110	6	9220	6	NULL	NULL	0	NULL	BirA monomers	NULL		bind	NULL	cooperatively			biotin	NULL			operator	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_360	16533810	A bifunctional protein (BirA) acts as a protein-biotin ligase or as a sensor-like transcriptional regulator ( ), and after complexation of BirA with biotin-5''-AMP ( ) or with biotin ( ), BirA monomers bind cooperatively to the biotin operator.	bind
32111	7	9220	6	NULL	NULL	0	NULL	statement 6	NULL		occurs after	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_360	16533810	A bifunctional protein (BirA) acts as a protein-biotin ligase or as a sensor-like transcriptional regulator ( ), and after complexation of BirA with biotin-5''-AMP ( ) or with biotin ( ), BirA monomers bind cooperatively to the biotin operator.	bind
32112	8	9220	6	NULL	NULL	0	NULL	statement 6	NULL		occurs after	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_360	16533810	A bifunctional protein (BirA) acts as a protein-biotin ligase or as a sensor-like transcriptional regulator ( ), and after complexation of BirA with biotin-5''-AMP ( ) or with biotin ( ), BirA monomers bind cooperatively to the biotin operator.	bind
57857	9	9220	6	10	NULL	0	NULL	statement 4			is an alternative to					statement 5					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_360	16533810	A bifunctional protein (BirA) acts as a protein-biotin ligase or as a sensor-like transcriptional regulator ( ), and after complexation of BirA with biotin-5''-AMP ( ) or with biotin ( ), BirA monomers bind cooperatively to the biotin operator.	bind
39672	1	9221	5	13	NULL	NULL	NULL	Bim BH3 peptide	GP		interact with		potentially			anti-apoptotic proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_9_5750_s_286	16380381	A Bim BH3 peptide appears capable of interacting with most anti-apoptotic proteins including Mcl-1 with high affinity, whereas the Bid BH3 peptide does not bind Mcl-1.	bind
39673	2	9221	5	13	NULL	NULL	NULL	Mcl-1	GP		is a type of					anti-apoptotic proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_9_5750_s_286	16380381	A Bim BH3 peptide appears capable of interacting with most anti-apoptotic proteins including Mcl-1 with high affinity, whereas the Bid BH3 peptide does not bind Mcl-1.	bind
39674	3	9221	5	13	NULL	NULL	NULL	Bim BH3 peptide	GP		interact with		high affinity			Mcl-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_9_5750_s_286	16380381	A Bim BH3 peptide appears capable of interacting with most anti-apoptotic proteins including Mcl-1 with high affinity, whereas the Bid BH3 peptide does not bind Mcl-1.	bind
39675	4	9221	5	13	NULL	NULL	NULL	Bid BH3 peptide	GP		does not bind					Mcl-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_9_5750_s_286	16380381	A Bim BH3 peptide appears capable of interacting with most anti-apoptotic proteins including Mcl-1 with high affinity, whereas the Bid BH3 peptide does not bind Mcl-1.	bind
32238	1	9221	6	10	NULL	0	NULL	Bim BH3 peptide			interacts with		high affinity			Mcl-1					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_9_5750_s_286	16380381	A Bim BH3 peptide appears capable of interacting with most anti-apoptotic proteins including Mcl-1 with high affinity, whereas the Bid BH3 peptide does not bind Mcl-1.	bind
32239	2	9221	6	NULL	NULL	0	NULL	Mcl-1	NULL		is a type of	NULL				anti-apoptotic protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_9_5750_s_286	16380381	A Bim BH3 peptide appears capable of interacting with most anti-apoptotic proteins including Mcl-1 with high affinity, whereas the Bid BH3 peptide does not bind Mcl-1.	bind
32240	3	9221	6	NULL	NULL	0	NULL	Bid BH3 peptide	NULL		does not bind	NULL				Mcl-1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_9_5750_s_286	16380381	A Bim BH3 peptide appears capable of interacting with most anti-apoptotic proteins including Mcl-1 with high affinity, whereas the Bid BH3 peptide does not bind Mcl-1.	bind
39676	1	9222	5	13	NULL	NULL	NULL	Fos kinase	GP		bind					BIM	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3385_s_145	9920881	A BIM-insensitive Fos peptide kinase eluting at 70 mM NaCl (fraction 18) was used as a negative control to test the specific nature of Fos kinase binding to the BIM-Sepharose.	bind
48059	1	9222	6	10	NULL	0	NULL	Fos kinase	NULL		bind	NULL				BIM	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3385_s_145	9920881	A BIM-insensitive Fos peptide kinase eluting at 70 mM NaCl (fraction 18) was used as a negative control to test the specific nature of Fos kinase binding to the BIM-Sepharose.	bind
39677	1	9223	5	13	NULL	NULL	NULL	BRG1	GP	purified;;E.coli-expressed;;histidine-tagged	bind		directly	295 - 634		HP1alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
39678	2	9223	5	13	NULL	NULL	NULL	BRG1	GP	purified;;E.coli-expressed;;histidine-tagged	does not bind			295 - 634		HP1beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
39679	3	9223	5	13	NULL	NULL	NULL	BRG1	GP	purified;;E.coli-expressed;;histidine-tagged	does not bind			295 - 634		HP1gamma	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
39680	4	9223	5	13	NULL	NULL	NULL	H3	GP		is a type of					histone	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
39681	5	9223	5	13	NULL	NULL	NULL	H3	GP	purified;;calf thymus	bind					GST - HP1alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
39682	6	9223	5	13	NULL	NULL	NULL	H3	GP	purified;;calf thymus	bind					GST - HP1beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
39683	7	9223	5	13	NULL	NULL	NULL	H3	GP	purified;;calf thymus	bind					GST - HP1gamma	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
39684	8	9223	5	13	NULL	NULL	NULL	TIF1beta	GP	recombinant	bind					GST - HP1alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
39685	9	9223	5	13	NULL	NULL	NULL	TIF1beta	GP	recombinant	bind					GST - HP1beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
39686	10	9223	5	13	NULL	NULL	NULL	TIF1beta	GP	recombinant	bind					GST - HP1gamma	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
32548	1	9223	6	NULL	NULL	0	NULL	His-BRG1	NULL		bind	NULL	directly	295-634		Hp1alpha	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
32550	2	9223	6	10	NULL	0	NULL	His-BRG1	NULL		is	NULL				BRG1 fragment	NULL	purified;; E.coli-expressed;; histidine tagged			NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
32551	3	9223	6	NULL	NULL	0	NULL	His-BRG1	NULL		does not bind	NULL		295-634		HP1gamma	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
32552	4	9223	6	10	NULL	0	NULL	 H3		purified;; calf thymus	bind					GST-HP1alpha					NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
32553	5	9223	6	10	NULL	0	NULL	TIF1beta	NULL	recombinant	bind	NULL				GST-HP1alpha	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
48060	6	9223	6	10	NULL	0	NULL	His-BRG1	NULL		does not bind	NULL		295 - 634		HP1beta	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
48061	7	9223	6	10	NULL	0	NULL	 H3		purified;; calf thymus	bind					GST-HP1beta					NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
48062	8	9223	6	10	NULL	0	NULL	 H3		purified;; calf thymus	bind					GST-HP1gamma					NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
48063	9	9223	6	10	NULL	0	NULL	TIF1beta 	NULL	recombinant	bind	NULL				GST-HP1beta	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
48064	10	9223	6	10	NULL	0	NULL	TIF1beta 	NULL	recombinant	bind	NULL				GST-HP1gamma	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
57858	11	9223	6	10	NULL	0	NULL	H3			is a type of					histone					NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5797_s_81	12411497	A binding assay carried out with a purified  E.coli-expressed histidine-tagged BRG1 fragment bearing residues 295 - 634 [referred to here as His-BRG1(295 - 634) in Figure  4] demonstrated direct binding to HP1alpha (lane 3), but not to HP1beta (lane 5) and HP1gamma (lane 7), whereas, under similar conditions, purified calf thymus histone H3 and recombinant TIF1beta bound to all three GST - HP1s (Figure  4F and data not shown).	bind
39687	1	9224	5	13	NULL	NULL	NULL	GBR 12935	Chemical		bind					striatal membranes	CellComponent	rat			NULL		NULL	NULL	NULL	NULL	gw60_brainres_981_1_85_s_43	12885429	A binding assay for the DA uptake complex using [3]GBR 12935 binding to rat striatal membranes was conducted as per Anderson [  1.	bind
32241	1	9224	6	NULL	NULL	0	NULL	GBR 12935	NULL		bind	NULL				striatal membranes	NULL	rat			NULL		0	NULL	NULL	NULL	gw60_brainres_981_1_85_s_43	12885429	A binding assay for the DA uptake complex using [3]GBR 12935 binding to rat striatal membranes was conducted as per Anderson [  1.	bind
39688	1	9225	5	13	NULL	NULL	NULL	A1B	NucleicAcid	recombinant	bind		specifically			CE1d	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_29745_s_203	12060656	A binding assay performed with recombinant A1B also indicated specific binding to CE1d (Fig.  5 D,  top right panel) and stronger binding to M7* relative to M6* RNA ( bottom right panel).	bind
39689	2	9225	5	13	NULL	NULL	NULL	A1B	NucleicAcid	recombinant	bind					M7* RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_29745_s_203	12060656	A binding assay performed with recombinant A1B also indicated specific binding to CE1d (Fig.  5 D,  top right panel) and stronger binding to M7* relative to M6* RNA ( bottom right panel).	bind
39690	3	9225	5	13	NULL	NULL	NULL	A1B	NucleicAcid	recombinant	bind					M6* RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_29745_s_203	12060656	A binding assay performed with recombinant A1B also indicated specific binding to CE1d (Fig.  5 D,  top right panel) and stronger binding to M7* relative to M6* RNA ( bottom right panel).	bind
39691	4	9225	5	13	NULL	NULL	NULL	statement 2	Process		is stronger than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_29745_s_203	12060656	A binding assay performed with recombinant A1B also indicated specific binding to CE1d (Fig.  5 D,  top right panel) and stronger binding to M7* relative to M6* RNA ( bottom right panel).	bind
32242	1	9225	6	NULL	NULL	0	NULL	A1B	NULL	recombinant	bind	NULL	specifically			CE1d	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_33_29745_s_203	12060656	A binding assay performed with recombinant A1B also indicated specific binding to CE1d (Fig.  5 D,  top right panel) and stronger binding to M7* relative to M6* RNA ( bottom right panel).	bind
32243	2	9225	6	10	NULL	0	NULL	A1B		recombinant	bind					M7* RNA					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_29745_s_203	12060656	A binding assay performed with recombinant A1B also indicated specific binding to CE1d (Fig.  5 D,  top right panel) and stronger binding to M7* relative to M6* RNA ( bottom right panel).	bind
32244	3	9225	6	10	NULL	0	NULL	A1B		recombinant	bind					M6* RNA					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_33_29745_s_203	12060656	A binding assay performed with recombinant A1B also indicated specific binding to CE1d (Fig.  5 D,  top right panel) and stronger binding to M7* relative to M6* RNA ( bottom right panel).	bind
32245	4	9225	6	NULL	NULL	0	NULL	statement 2	NULL	affinity of	is greater than	NULL				statement 3	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_33_29745_s_203	12060656	A binding assay performed with recombinant A1B also indicated specific binding to CE1d (Fig.  5 D,  top right panel) and stronger binding to M7* relative to M6* RNA ( bottom right panel).	bind
39692	1	9226	5	13	NULL	NULL	NULL	vimentin	GP		bind			tail		F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_41_30393_s_173	16901892	A binding assay showed that the vimentin tail binds F-actin with a  Kd of  14 muM.	bind
32246	1	9226	6	10	NULL	0	NULL	vimentin 	NULL		bind	NULL		tail		F-actin	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_41_30393_s_173	16901892	A binding assay showed that the vimentin tail binds F-actin with a  Kd of  14 muM.	bind
39693	1	9227	5	13	NULL	NULL	NULL	CCL3	GP		bind					CCR1	GP				NULL	CCR1-transfected HEK 293 cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_42_40473_s_96	12909630	A binding assay using CCR1-transfected HEK 293 cells was used to screen our compound library for small molecular weight compounds that inhibit CCL3 binding to CCR1.	bind
39694	2	9227	5	13	NULL	NULL	NULL	small molecular weight compounds	Chemical		inhibit					statement 1	Process				NULL	CCR1-transfected HEK 293 cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_42_40473_s_96	12909630	A binding assay using CCR1-transfected HEK 293 cells was used to screen our compound library for small molecular weight compounds that inhibit CCL3 binding to CCR1.	bind
32247	1	9227	6	10	NULL	0	NULL	CCL3	NULL		bind	NULL				CCR1	NULL				NULL	CCR1-transfected HEK 293 cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_42_40473_s_96	12909630	A binding assay using CCR1-transfected HEK 293 cells was used to screen our compound library for small molecular weight compounds that inhibit CCL3 binding to CCR1.	bind
48065	2	9227	6	10	NULL	0	NULL	small molecular weight compounds	NULL		inhibit	NULL				statement 1	NULL				NULL	CCR1-transfected HEK 293 cells	0	NULL	NULL	NULL	gw70_jbiolchem_278_42_40473_s_96	12909630	A binding assay using CCR1-transfected HEK 293 cells was used to screen our compound library for small molecular weight compounds that inhibit CCL3 binding to CCR1.	bind
39695	1	9228	5	13	NULL	NULL	NULL	SecE	GP		bind		may	C2		SecY	GP		C4		NULL		NULL	NULL	NULL	NULL	gw60_febslett_408_1_11_s_17	9180258	A binding between C2 of SecE and C4 of SecY may thus be suggested.	bind
32248	1	9228	6	NULL	NULL	0	NULL	SecE	NULL		bind	NULL	may	C2		SecY	NULL		C4		NULL		0	NULL	NULL	NULL	gw60_febslett_408_1_11_s_17	9180258	A binding between C2 of SecE and C4 of SecY may thus be suggested.	bind
40369	1	9229	5	13	NULL	NULL	NULL			wild-type;;human	does not complex with				betaA/-rich element	UL	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_15_5143_s_241	12861002	A binding complex did not form when the wild-type human betaA/-rich element was reacted with UL, whereas a specific binding complex formed when in vitro-synthesized RTEF-1b was added to binding reaction mixtures (Fig.  3B, lane 16 versus 17).	bind
32249	1	9229	6	NULL	NULL	0	NULL		NULL	wild type;; human	does not form a complex with	NULL			betaA/-rich element	UL	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_15_5143_s_241	12861002	A binding complex did not form when the wild-type human betaA/-rich element was reacted with UL, whereas a specific binding complex formed when in vitro-synthesized RTEF-1b was added to binding reaction mixtures (Fig.  3B, lane 16 versus 17).	bind
40373	3	9230	5	13	NULL	NULL	NULL	statement 1	GP		bind					B8 binding complex	GP	beta-cell-enriched			NULL	unfractionated betaTC-3 nuclear extract	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4702_s_183	12052878	A binding complex was detected in fractions 6 (44-kDa lower limit) and 7 (58-kDa upper limit) that comigrated with the beta-cell-enriched B8 binding complex in unfractionated betaTC-3 nuclear extract.	bind
40374	1	9230	5	13	NULL	NULL	NULL	binding complex	GP		is present in					44-kDa fraction	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4702_s_183	12052878	A binding complex was detected in fractions 6 (44-kDa lower limit) and 7 (58-kDa upper limit) that comigrated with the beta-cell-enriched B8 binding complex in unfractionated betaTC-3 nuclear extract.	bind
40375	2	9230	5	13	NULL	NULL	NULL	binding complex	GP		is present in					58-kDa fraction	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4702_s_183	12052878	A binding complex was detected in fractions 6 (44-kDa lower limit) and 7 (58-kDa upper limit) that comigrated with the beta-cell-enriched B8 binding complex in unfractionated betaTC-3 nuclear extract.	bind
40376	4	9230	5	13	NULL	NULL	NULL	statement 2	GP		bind					B8 binding complex	GP	beta-cell-enriched			NULL	unfractionated betaTC-3 nuclear extract	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4702_s_183	12052878	A binding complex was detected in fractions 6 (44-kDa lower limit) and 7 (58-kDa upper limit) that comigrated with the beta-cell-enriched B8 binding complex in unfractionated betaTC-3 nuclear extract.	bind
48066	1	9230	6	10	NULL	0	NULL	44-kDa protein	NULL		bind	NULL				 B8 binding complex	NULL	beta-cell-enriched			NULL	unfractionated betaTC-3 nuclear extract	0	NULL	NULL	NULL	gw60_molcellbiol_22_13_4702_s_183	12052878	A binding complex was detected in fractions 6 (44-kDa lower limit) and 7 (58-kDa upper limit) that comigrated with the beta-cell-enriched B8 binding complex in unfractionated betaTC-3 nuclear extract.	bind
48067	2	9230	6	10	NULL	0	NULL	58-kDa protein	NULL		bind	NULL				B8 binding complex	NULL	beta-cell-enriched			NULL	unfractionated betaTC-3 nuclear extract	0	NULL	NULL	NULL	gw60_molcellbiol_22_13_4702_s_183	12052878	A binding complex was detected in fractions 6 (44-kDa lower limit) and 7 (58-kDa upper limit) that comigrated with the beta-cell-enriched B8 binding complex in unfractionated betaTC-3 nuclear extract.	bind
40371	1	9231	5	13	NULL	NULL	NULL	Stn	GP		bind			1-13		Ten1	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0760-0779_embo-j_20_5_11230140_s_5	11230140	A binding defect between Stn1-13 and Ten1 was  responsible for the long telomere phenotype of stn1-13 mutant cells.	bind
40372	2	9231	5	13	NULL	NULL	NULL	statement 1	Process	defect in	is responsible for					long telomere phenotype	Chromosome				NULL	stn1-13 mutant cells	NULL	NULL	NULL	NULL	abs-batch0760-0779_embo-j_20_5_11230140_s_5	11230140	A binding defect between Stn1-13 and Ten1 was  responsible for the long telomere phenotype of stn1-13 mutant cells.	bind
32250	1	9231	6	10	NULL	0	NULL	Stn	NULL		bind	NULL		1-13		Ten1	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0760-0779_embo-j_20_5_11230140_s_5	11230140	A binding defect between Stn1-13 and Ten1 was  responsible for the long telomere phenotype of stn1-13 mutant cells.	bind
32251	2	9231	6	10	NULL	0	NULL	statement 1	NULL	defect in	is responsible for	NULL				long telomere phenotype	NULL				NULL	stn1-13 mutant cells	NULL	NULL	NULL	NULL	abs-batch0760-0779_embo-j_20_5_11230140_s_5	11230140	A binding defect between Stn1-13 and Ten1 was  responsible for the long telomere phenotype of stn1-13 mutant cells.	bind
39696	1	9232	5	13	NULL	NULL	NULL	MANT-ATP	GP		bind					DnaA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_18_12526_s_122	16517983	A binding experiment fitted with a corresponding saturation function ( Fig. 2 A) showed that the fluorescence intensity of MANT-ATP bound to DnaA increases 1.4-fold.	bind
32252	1	9232	6	NULL	NULL	0	NULL	MANT-ATP	NULL		bind	NULL				DnaA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_18_12526_s_122	16517983	A binding experiment fitted with a corresponding saturation function ( Fig. 2 A) showed that the fluorescence intensity of MANT-ATP bound to DnaA increases 1.4-fold.	bind
39697	1	9233	5	13	NULL	NULL	NULL	camptothecin	Chemical		bind					DNA-topoisomerase I complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_clinmicrobiolrev_12_4_583_s_40	10515904	A binding model of  the three-dimensional structure of camptothecin (shown in green and labelled CPT)  bound to the DNA-topoisomerase I complex is shown.	bind
32253	1	9233	6	NULL	NULL	0	NULL	camptothecin	NULL		bind	NULL				DNA-topoisomerase I complex	NULL				NULL		0	NULL	NULL	NULL	gw70_clinmicrobiolrev_12_4_583_s_40	10515904	A binding model of  the three-dimensional structure of camptothecin (shown in green and labelled CPT)  bound to the DNA-topoisomerase I complex is shown.	bind
39698	1	9235	5	13	NULL	NULL	NULL	ceramide	Chemical		bind								cysteine-rich C1 domain		NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1634_1_30_s_197	14563411	A binding of ceramide  to a cysteine-rich C1 domain was also suggested for c-Raf [ 8,  10 and   31].	bind
32254	1	9235	6	10	NULL	0	NULL	ceramide	NULL		bind	NULL					NULL		cysteine-rich C1 domain		NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1634_1_30_s_197	14563411	A binding of ceramide  to a cysteine-rich C1 domain was also suggested for c-Raf [ 8,  10 and   31].	bind
39699	1	9236	5	13	NULL	NULL	NULL	FHL2	GP		bind					actin molecules	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
39700	2	9236	5	13	NULL	NULL	NULL	FHL3	GP		bind					actin molecules	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
39701	3	9236	5	13	NULL	NULL	NULL	cytoskeleton	CellComponent		is linked to		directly			ECM	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
39702	4	9236	5	13	NULL	NULL	NULL	LIM-only proteins	GP		is required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
39703	5	9236	5	13	NULL	NULL	NULL	LIM-only proteins	GP		bind					integrins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
39704	6	9236	5	13	NULL	NULL	NULL	LIM-only proteins	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
39705	7	9236	5	13	NULL	NULL	NULL	statement 4	Process		via					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
39706	8	9236	5	13	NULL	NULL	NULL	statement 4	Process		via					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
49545	9	9236	5	13	NULL	NULL	NULL	FHL2	GP		is a type of					LIM-only proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
49546	10	9236	5	13	NULL	NULL	NULL	FHL3	GP		is a type of					LIM-only proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
32257	1	9236	6	NULL	NULL	0	NULL	FHL2	NULL		bind	NULL				actin molecules	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
32258	2	9236	6	NULL	NULL	0	NULL	FHL3	NULL		bind	NULL				actin molecules	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
32259	3	9236	6	NULL	NULL	0	NULL	FHL2	NULL		is a type of	NULL				LIM-only protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
32260	4	9236	6	NULL	NULL	0	NULL	FHL3	NULL		is a type of	NULL				LIM-only protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
32261	5	9236	6	NULL	NULL	0	NULL	cytoskeleton	NULL		is linked to	NULL				ECM	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
32262	8	9236	6	10	NULL	0	NULL	LIM-only proteins	NULL		is required for	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
32263	10	9236	6	10	NULL	0	NULL	statement 5	NULL		occurs via	NULL				statement 7	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
33275	6	9236	6	10	NULL	0	NULL	LIM-only proteins	NULL		bind	NULL				actin	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
33276	9	9236	6	10	NULL	0	NULL	statement 5	NULL		occurs via	NULL				statement 6	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
48068	7	9236	6	10	NULL	0	NULL	LIM-only proteins	NULL		bind	NULL				integrins	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_359	15117962	A binding of FHL2 and FHL3 to actin molecules has recently been published ( ), which would suggest that the LIM-only proteins directly link the cytoskeleton to the ECM via binding to integrins and actin.	bind
39786	1	9237	5	13	NULL	NULL	NULL	MTK1	GP		interact with			N terminus		MTK1	GP		C terminus		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4544_s_341	12052864	A binding of the GADD45 protein to the GADD45-binding site near the autoinhibitory domain will interfere in the autoinhibitory interaction between the MTK1 N and C termini, leading to MKK6 binding and its activation by phosphorylation (Fig.  10B).	bind
39787	2	9237	5	13	NULL	NULL	NULL	statement 1	Process		is					autoinhibitory interaction	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4544_s_341	12052864	A binding of the GADD45 protein to the GADD45-binding site near the autoinhibitory domain will interfere in the autoinhibitory interaction between the MTK1 N and C termini, leading to MKK6 binding and its activation by phosphorylation (Fig.  10B).	bind
39788	3	9237	5	13	NULL	NULL	NULL	GADD45 protein	GP		bind					MTK1	GP		GADD45-binding site near autoinhibitory domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4544_s_341	12052864	A binding of the GADD45 protein to the GADD45-binding site near the autoinhibitory domain will interfere in the autoinhibitory interaction between the MTK1 N and C termini, leading to MKK6 binding and its activation by phosphorylation (Fig.  10B).	bind
39789	4	9237	5	13	NULL	NULL	NULL	statement 3	Process		interfere with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4544_s_341	12052864	A binding of the GADD45 protein to the GADD45-binding site near the autoinhibitory domain will interfere in the autoinhibitory interaction between the MTK1 N and C termini, leading to MKK6 binding and its activation by phosphorylation (Fig.  10B).	bind
39790	5	9237	5	13	NULL	NULL	NULL	statement 4	Process		leads to					MKK6	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4544_s_341	12052864	A binding of the GADD45 protein to the GADD45-binding site near the autoinhibitory domain will interfere in the autoinhibitory interaction between the MTK1 N and C termini, leading to MKK6 binding and its activation by phosphorylation (Fig.  10B).	bind
39791	6	9237	5	13	NULL	NULL	NULL	MKK6	GP		undergoes					phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4544_s_341	12052864	A binding of the GADD45 protein to the GADD45-binding site near the autoinhibitory domain will interfere in the autoinhibitory interaction between the MTK1 N and C termini, leading to MKK6 binding and its activation by phosphorylation (Fig.  10B).	bind
39792	7	9237	5	13	NULL	NULL	NULL	statement 6	Process		leads to					MKK6	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4544_s_341	12052864	A binding of the GADD45 protein to the GADD45-binding site near the autoinhibitory domain will interfere in the autoinhibitory interaction between the MTK1 N and C termini, leading to MKK6 binding and its activation by phosphorylation (Fig.  10B).	bind
39793	8	9237	5	13	NULL	NULL	NULL	statement 5	Process		leads to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4544_s_341	12052864	A binding of the GADD45 protein to the GADD45-binding site near the autoinhibitory domain will interfere in the autoinhibitory interaction between the MTK1 N and C termini, leading to MKK6 binding and its activation by phosphorylation (Fig.  10B).	bind
32533	1	9237	6	10	NULL	0	NULL	GADD45 protein			bind					MTK1			GADD45-binding site		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4544_s_341	12052864	A binding of the GADD45 protein to the GADD45-binding site near the autoinhibitory domain will interfere in the autoinhibitory interaction between the MTK1 N and C termini, leading to MKK6 binding and its activation by phosphorylation (Fig.  10B).	bind
32534	2	9237	6	NULL	NULL	0	NULL		NULL		is located near the	NULL		GADD45-binding site			NULL		autoinhibitory domain		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_13_4544_s_341	12052864	A binding of the GADD45 protein to the GADD45-binding site near the autoinhibitory domain will interfere in the autoinhibitory interaction between the MTK1 N and C termini, leading to MKK6 binding and its activation by phosphorylation (Fig.  10B).	bind
32535	3	9237	6	10	NULL	0	NULL	MTK1			autoinhibits			N terminus		MTK1			C terminus		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_13_4544_s_341	12052864	A binding of the GADD45 protein to the GADD45-binding site near the autoinhibitory domain will interfere in the autoinhibitory interaction between the MTK1 N and C termini, leading to MKK6 binding and its activation by phosphorylation (Fig.  10B).	bind
32536	4	9237	6	NULL	NULL	0	NULL	statement 1	NULL		interferes with	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_13_4544_s_341	12052864	A binding of the GADD45 protein to the GADD45-binding site near the autoinhibitory domain will interfere in the autoinhibitory interaction between the MTK1 N and C termini, leading to MKK6 binding and its activation by phosphorylation (Fig.  10B).	bind
32537	5	9237	6	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				MKK6	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_13_4544_s_341	12052864	A binding of the GADD45 protein to the GADD45-binding site near the autoinhibitory domain will interfere in the autoinhibitory interaction between the MTK1 N and C termini, leading to MKK6 binding and its activation by phosphorylation (Fig.  10B).	bind
32542	6	9237	6	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				MKK6	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_13_4544_s_341	12052864	A binding of the GADD45 protein to the GADD45-binding site near the autoinhibitory domain will interfere in the autoinhibitory interaction between the MTK1 N and C termini, leading to MKK6 binding and its activation by phosphorylation (Fig.  10B).	bind
32546	7	9237	6	NULL	NULL	0	NULL	MKK6	NULL	activation of	occurs by	NULL				phosphorylation	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_13_4544_s_341	12052864	A binding of the GADD45 protein to the GADD45-binding site near the autoinhibitory domain will interfere in the autoinhibitory interaction between the MTK1 N and C termini, leading to MKK6 binding and its activation by phosphorylation (Fig.  10B).	bind
39794	1	9238	5	13	NULL	NULL	NULL	TRs	GP		bind					target genes	GP	Xenopus laevis		TRE	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_8_3204_s_280	16581794	A binding of TRE by TRs has already been reported for  Xenopus laevis target genes ( ).	bind
32264	1	9238	6	NULL	NULL	0	NULL	TR	NULL		bind	NULL				target gene	NULL	Xenopus laevis		TRE	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_8_3204_s_280	16581794	A binding of TRE by TRs has already been reported for  Xenopus laevis target genes ( ).	bind
39795	1	9240	5	13	NULL	NULL	NULL	Pl	GP		bind					fibrin	GP	partially degraded			NULL	purified system with fibrin clots	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27912_s_47	8910391	A binding study in solution and experiments performed in a purified system with fibrin clots demonstrated that STA binds to Pl and to Pg, which is bound to partially degraded fibrin, but does not bind appreciably to Glu-Pg in solution.	bind
39796	2	9240	5	13	NULL	NULL	NULL	STA	GP		bind					statement 1	GP				NULL	purified system with fibrin clots	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27912_s_47	8910391	A binding study in solution and experiments performed in a purified system with fibrin clots demonstrated that STA binds to Pl and to Pg, which is bound to partially degraded fibrin, but does not bind appreciably to Glu-Pg in solution.	bind
39797	3	9240	5	13	NULL	NULL	NULL	Pg	GP		bind					fibrin	GP	partially degraded			NULL	purified system with fibrin clots	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27912_s_47	8910391	A binding study in solution and experiments performed in a purified system with fibrin clots demonstrated that STA binds to Pl and to Pg, which is bound to partially degraded fibrin, but does not bind appreciably to Glu-Pg in solution.	bind
39798	4	9240	5	13	NULL	NULL	NULL	STA	GP		bind					statement 3	GP				NULL	purified system with fibrin clots	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27912_s_47	8910391	A binding study in solution and experiments performed in a purified system with fibrin clots demonstrated that STA binds to Pl and to Pg, which is bound to partially degraded fibrin, but does not bind appreciably to Glu-Pg in solution.	bind
39799	5	9240	5	13	NULL	NULL	NULL	STA	GP		does not bind		appreciably			Glu-Pg	GP				NULL	solution	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27912_s_47	8910391	A binding study in solution and experiments performed in a purified system with fibrin clots demonstrated that STA binds to Pl and to Pg, which is bound to partially degraded fibrin, but does not bind appreciably to Glu-Pg in solution.	bind
32265	1	9240	6	10	NULL	0	NULL	P1			bind					fibrin		partially degraded			NULL	purified system with fibrin clots	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27912_s_47	8910391	A binding study in solution and experiments performed in a purified system with fibrin clots demonstrated that STA binds to Pl and to Pg, which is bound to partially degraded fibrin, but does not bind appreciably to Glu-Pg in solution.	bind
32528	2	9240	6	10	NULL	0	NULL	Pg			bind					fibrin		partially degraded			NULL	purified system with fibrin clots	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27912_s_47	8910391	A binding study in solution and experiments performed in a purified system with fibrin clots demonstrated that STA binds to Pl and to Pg, which is bound to partially degraded fibrin, but does not bind appreciably to Glu-Pg in solution.	bind
32529	3	9240	6	10	NULL	0	NULL	STA			bind					statement 2					NULL	purified system with fibrin clots	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27912_s_47	8910391	A binding study in solution and experiments performed in a purified system with fibrin clots demonstrated that STA binds to Pl and to Pg, which is bound to partially degraded fibrin, but does not bind appreciably to Glu-Pg in solution.	bind
32530	4	9240	6	NULL	NULL	0	NULL	STA	NULL		does not bind	NULL	appreciably			Glu-Pg	NULL				NULL	in solution	0	NULL	NULL	NULL	gw60_jbiolchem_271_44_27912_s_47	8910391	A binding study in solution and experiments performed in a purified system with fibrin clots demonstrated that STA binds to Pl and to Pg, which is bound to partially degraded fibrin, but does not bind appreciably to Glu-Pg in solution.	bind
48069	5	9240	6	10	NULL	0	NULL	STA			bind					statement 1					NULL	purified system with fibrin clots	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27912_s_47	8910391	A binding study in solution and experiments performed in a purified system with fibrin clots demonstrated that STA binds to Pl and to Pg, which is bound to partially degraded fibrin, but does not bind appreciably to Glu-Pg in solution.	bind
39800	1	9241	5	13	NULL	NULL	NULL	RyR3	GP		bind					FKBP12	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_24_17297_s_449	10358090	A binding study with GST-FKBP12 fusion protein revealed that RyR3 can bind FKBP12, as is true of RyR1 (Fig.  3).	bind
39801	2	9241	5	13	NULL	NULL	NULL	RyR1	GP		bind					FKBP12	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_24_17297_s_449	10358090	A binding study with GST-FKBP12 fusion protein revealed that RyR3 can bind FKBP12, as is true of RyR1 (Fig.  3).	bind
32266	1	9241	6	NULL	NULL	0	NULL	RyR3	NULL		bind	NULL				FKBP12	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_24_17297_s_449	10358090	A binding study with GST-FKBP12 fusion protein revealed that RyR3 can bind FKBP12, as is true of RyR1 (Fig.  3).	bind
32267	2	9241	6	NULL	NULL	0	NULL	RyR1	NULL		bind	NULL				FKBP12	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_24_17297_s_449	10358090	A binding study with GST-FKBP12 fusion protein revealed that RyR3 can bind FKBP12, as is true of RyR1 (Fig.  3).	bind
39802	1	9242	5	13	NULL	NULL	NULL	Ca2+	Chemical		bind					CnB	GP				NULL		NULL	NULL	NULL	NULL	gw70_febslett_573_1_121_s_9	15327986	A biochemical approach suggested that the Ca2+-binding to CnB caused to release the CaM-binding domain of CnA from its catalytic  domain to open the active site partially [  11 and   12].	bind
39803	2	9242	5	13	NULL	NULL	NULL	CnA	GP		released from			CaM-binding domain		CnA	GP		catalytic domain		NULL		NULL	NULL	NULL	NULL	gw70_febslett_573_1_121_s_9	15327986	A biochemical approach suggested that the Ca2+-binding to CnB caused to release the CaM-binding domain of CnA from its catalytic  domain to open the active site partially [  11 and   12].	bind
39804	3	9242	5	13	NULL	NULL	NULL	statement 2	Process		open		partially			CnA	GP		active site		NULL		NULL	NULL	NULL	NULL	gw70_febslett_573_1_121_s_9	15327986	A biochemical approach suggested that the Ca2+-binding to CnB caused to release the CaM-binding domain of CnA from its catalytic  domain to open the active site partially [  11 and   12].	bind
39805	4	9242	5	13	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_febslett_573_1_121_s_9	15327986	A biochemical approach suggested that the Ca2+-binding to CnB caused to release the CaM-binding domain of CnA from its catalytic  domain to open the active site partially [  11 and   12].	bind
32268	1	9242	6	NULL	NULL	0	NULL	Ca2+	NULL		bind	NULL				CnB	NULL				NULL		0	NULL	NULL	NULL	gw70_febslett_573_1_121_s_9	15327986	A biochemical approach suggested that the Ca2+-binding to CnB caused to release the CaM-binding domain of CnA from its catalytic  domain to open the active site partially [  11 and   12].	bind
32269	2	9242	6	10	NULL	0	NULL	CnA	NULL		release from 	NULL		CaM-binding domain		CnA	NULL		catalytic domain		NULL		NULL	NULL	NULL	NULL	gw70_febslett_573_1_121_s_9	15327986	A biochemical approach suggested that the Ca2+-binding to CnB caused to release the CaM-binding domain of CnA from its catalytic  domain to open the active site partially [  11 and   12].	bind
32324	3	9242	6	NULL	NULL	0	NULL	statement 2	NULL		opens	NULL	partially			active site	NULL				NULL		0	NULL	NULL	NULL	gw70_febslett_573_1_121_s_9	15327986	A biochemical approach suggested that the Ca2+-binding to CnB caused to release the CaM-binding domain of CnA from its catalytic  domain to open the active site partially [  11 and   12].	bind
48070	4	9242	6	10	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_febslett_573_1_121_s_9	15327986	A biochemical approach suggested that the Ca2+-binding to CnB caused to release the CaM-binding domain of CnA from its catalytic  domain to open the active site partially [  11 and   12].	bind
39806	1	9243	5	13	NULL	NULL	NULL	osteopontin	GP		bind					alpha v beta 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2734_s_367	10733576	A biochemical characterization of the binding of osteopontin to integrins alpha v beta 1 and alpha v beta 5.	bind
39807	2	9243	5	13	NULL	NULL	NULL	alpha v beta 1	GP		is a type of					integrins	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2734_s_367	10733576	A biochemical characterization of the binding of osteopontin to integrins alpha v beta 1 and alpha v beta 5.	bind
39808	3	9243	5	13	NULL	NULL	NULL	osteopontin	GP		bind					alpha v beta 5	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2734_s_367	10733576	A biochemical characterization of the binding of osteopontin to integrins alpha v beta 1 and alpha v beta 5.	bind
39809	4	9243	5	13	NULL	NULL	NULL	alpha v beta 5	GP		is a type of					integrins	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_8_2734_s_367	10733576	A biochemical characterization of the binding of osteopontin to integrins alpha v beta 1 and alpha v beta 5.	bind
32325	1	9243	6	NULL	NULL	0	NULL	osteopontin	NULL		bind	NULL				alpha v beta 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_8_2734_s_367	10733576	A biochemical characterization of the binding of osteopontin to integrins alpha v beta 1 and alpha v beta 5.	bind
32326	2	9243	6	NULL	NULL	0	NULL	osteopontin	NULL		bind	NULL				alpha v beta 5	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_8_2734_s_367	10733576	A biochemical characterization of the binding of osteopontin to integrins alpha v beta 1 and alpha v beta 5.	bind
32327	3	9243	6	NULL	NULL	0	NULL	alpha v beta 5	NULL		is a type of	NULL				integrin	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_8_2734_s_367	10733576	A biochemical characterization of the binding of osteopontin to integrins alpha v beta 1 and alpha v beta 5.	bind
32328	4	9243	6	NULL	NULL	0	NULL	alpha v beta 1	NULL		is a type of	NULL				integrin	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_8_2734_s_367	10733576	A biochemical characterization of the binding of osteopontin to integrins alpha v beta 1 and alpha v beta 5.	bind
39810	1	9245	5	13	NULL	NULL	NULL	ApoE	GP		bind					Abeta	GP	synthetic			NULL	CSF	NULL	NULL	NULL	NULL	gw70_annurevgenomicshum_3_0_67_s_327	null	A biochemical screen for proteins in CSF that bound synthetic Abeta led to  the identification of ApoE as such a protein and to the subsequent recognition that  its gene was in a region of chromosome 19q previously linked to AD in some late-onset  families ( 120).	bind
39811	2	9245	5	13	NULL	NULL	NULL	ApoE gene	GP		is located on					chromosome 19q	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenomicshum_3_0_67_s_327	null	A biochemical screen for proteins in CSF that bound synthetic Abeta led to  the identification of ApoE as such a protein and to the subsequent recognition that  its gene was in a region of chromosome 19q previously linked to AD in some late-onset  families ( 120).	bind
39812	3	9245	5	13	NULL	NULL	NULL	chromosome 19q	Chromosome		is linked to					AD	MedicalFinding				NULL	late-onset families	NULL	NULL	NULL	NULL	gw70_annurevgenomicshum_3_0_67_s_327	null	A biochemical screen for proteins in CSF that bound synthetic Abeta led to  the identification of ApoE as such a protein and to the subsequent recognition that  its gene was in a region of chromosome 19q previously linked to AD in some late-onset  families ( 120).	bind
32524	1	9245	6	10	NULL	0	NULL	ApoE			bind					Abeta		synthetic			NULL	CSF	NULL	NULL	NULL	NULL	gw70_annurevgenomicshum_3_0_67_s_327	null	A biochemical screen for proteins in CSF that bound synthetic Abeta led to  the identification of ApoE as such a protein and to the subsequent recognition that  its gene was in a region of chromosome 19q previously linked to AD in some late-onset  families ( 120).	bind
32525	2	9245	6	10	NULL	0	NULL	ApoE gene			is located on					chromosome 19q					NULL		NULL	NULL	NULL	NULL	gw70_annurevgenomicshum_3_0_67_s_327	null	A biochemical screen for proteins in CSF that bound synthetic Abeta led to  the identification of ApoE as such a protein and to the subsequent recognition that  its gene was in a region of chromosome 19q previously linked to AD in some late-onset  families ( 120).	bind
32527	3	9245	6	10	NULL	0	NULL	statement 2			is linked to					AD 					NULL	late onset families	NULL	NULL	NULL	NULL	gw70_annurevgenomicshum_3_0_67_s_327	null	A biochemical screen for proteins in CSF that bound synthetic Abeta led to  the identification of ApoE as such a protein and to the subsequent recognition that  its gene was in a region of chromosome 19q previously linked to AD in some late-onset  families ( 120).	bind
39813	2	9246	5	13	NULL	NULL	NULL	statement 1	GP		bind					HLA-E	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_23_0_225_s_299	15771571	A biological consequence of this is suggested by the studies of Michaelsson and  colleagues ( 212), who have shown that peptides derived from heat shock protein 60 (hsp60) bind to  HLA-E; however, these HLA-E molecules containing hsp60 peptides are not able to bind  the inhibitory CD94/NKG2A receptor.	bind
39814	3	9246	5	13	NULL	NULL	NULL	statement 2	GP		does not bind					CD94/NKG2A	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_23_0_225_s_299	15771571	A biological consequence of this is suggested by the studies of Michaelsson and  colleagues ( 212), who have shown that peptides derived from heat shock protein 60 (hsp60) bind to  HLA-E; however, these HLA-E molecules containing hsp60 peptides are not able to bind  the inhibitory CD94/NKG2A receptor.	bind
48071	1	9246	5	13	NULL	NULL	NULL	peptide	GP		derived from					hsp60	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_23_0_225_s_299	15771571	A biological consequence of this is suggested by the studies of Michaelsson and  colleagues ( 212), who have shown that peptides derived from heat shock protein 60 (hsp60) bind to  HLA-E; however, these HLA-E molecules containing hsp60 peptides are not able to bind  the inhibitory CD94/NKG2A receptor.	bind
48072	4	9246	5	13	NULL	NULL	NULL	CD94/NKG2A	GP		is a type of					inhibitory receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_23_0_225_s_299	15771571	A biological consequence of this is suggested by the studies of Michaelsson and  colleagues ( 212), who have shown that peptides derived from heat shock protein 60 (hsp60) bind to  HLA-E; however, these HLA-E molecules containing hsp60 peptides are not able to bind  the inhibitory CD94/NKG2A receptor.	bind
48073	5	9246	5	13	NULL	NULL	NULL	hsp60	GP		is					heat shock protein 60	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_23_0_225_s_299	15771571	A biological consequence of this is suggested by the studies of Michaelsson and  colleagues ( 212), who have shown that peptides derived from heat shock protein 60 (hsp60) bind to  HLA-E; however, these HLA-E molecules containing hsp60 peptides are not able to bind  the inhibitory CD94/NKG2A receptor.	bind
32329	1	9246	6	10	NULL	0	NULL	peptides	NULL		derived from	NULL				hsp60	NULL				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_23_0_225_s_299	15771571	A biological consequence of this is suggested by the studies of Michaelsson and  colleagues ( 212), who have shown that peptides derived from heat shock protein 60 (hsp60) bind to  HLA-E; however, these HLA-E molecules containing hsp60 peptides are not able to bind  the inhibitory CD94/NKG2A receptor.	bind
32330	2	9246	6	10	NULL	0	NULL	statement 1	NULL		bind	NULL				HLA-E	NULL				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_23_0_225_s_299	15771571	A biological consequence of this is suggested by the studies of Michaelsson and  colleagues ( 212), who have shown that peptides derived from heat shock protein 60 (hsp60) bind to  HLA-E; however, these HLA-E molecules containing hsp60 peptides are not able to bind  the inhibitory CD94/NKG2A receptor.	bind
32331	3	9246	6	NULL	NULL	0	NULL	statement 2	NULL		does not bind	NULL				CD94/NKG2A 	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_23_0_225_s_299	15771571	A biological consequence of this is suggested by the studies of Michaelsson and  colleagues ( 212), who have shown that peptides derived from heat shock protein 60 (hsp60) bind to  HLA-E; however, these HLA-E molecules containing hsp60 peptides are not able to bind  the inhibitory CD94/NKG2A receptor.	bind
32332	4	9246	6	NULL	NULL	0	NULL	CD94/NKG2A	NULL		is a type of	NULL				inhibitory receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_23_0_225_s_299	15771571	A biological consequence of this is suggested by the studies of Michaelsson and  colleagues ( 212), who have shown that peptides derived from heat shock protein 60 (hsp60) bind to  HLA-E; however, these HLA-E molecules containing hsp60 peptides are not able to bind  the inhibitory CD94/NKG2A receptor.	bind
48074	5	9246	6	10	NULL	0	NULL	hsp60	NULL		is	NULL				heat shock protein 60	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_23_0_225_s_299	15771571	A biological consequence of this is suggested by the studies of Michaelsson and  colleagues ( 212), who have shown that peptides derived from heat shock protein 60 (hsp60) bind to  HLA-E; however, these HLA-E molecules containing hsp60 peptides are not able to bind  the inhibitory CD94/NKG2A receptor.	bind
39815	1	9247	5	13	NULL	NULL	NULL	p85alpha	GP		bind			SH2 domains		Tyr(P) peptide	AminoAcid	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_22_15678_s_143	10336465	A biosensor-based competition assay was used to measure the binding of p85alpha SH2 domains to an immobilized Tyr(P) peptide with the sequence DMSKDESVDY(P)VPMLDMK (Y(P) is phosphotyrosine).	bind
39816	2	9247	5	13	NULL	NULL	NULL	Y(P)	AminoAcid		is					phosphotyrosine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_22_15678_s_143	10336465	A biosensor-based competition assay was used to measure the binding of p85alpha SH2 domains to an immobilized Tyr(P) peptide with the sequence DMSKDESVDY(P)VPMLDMK (Y(P) is phosphotyrosine).	bind
48075	3	9247	5	13	NULL	NULL	NULL	Tyr(P) peptide	AminoAcid		is					DMSKDESVDY(P)VPMLDMK	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_22_15678_s_143	10336465	A biosensor-based competition assay was used to measure the binding of p85alpha SH2 domains to an immobilized Tyr(P) peptide with the sequence DMSKDESVDY(P)VPMLDMK (Y(P) is phosphotyrosine).	bind
32333	1	9247	6	NULL	NULL	0	NULL	p85alpha	NULL		bind	NULL		SH2 domain		Tyr(P) peptide	NULL	immobilized			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_22_15678_s_143	10336465	A biosensor-based competition assay was used to measure the binding of p85alpha SH2 domains to an immobilized Tyr(P) peptide with the sequence DMSKDESVDY(P)VPMLDMK (Y(P) is phosphotyrosine).	bind
32334	2	9247	6	NULL	NULL	0	NULL	Tyr(P) peptide	NULL		is	NULL				DMSKDESVDY(P)VPMLDMK	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_22_15678_s_143	10336465	A biosensor-based competition assay was used to measure the binding of p85alpha SH2 domains to an immobilized Tyr(P) peptide with the sequence DMSKDESVDY(P)VPMLDMK (Y(P) is phosphotyrosine).	bind
32335	3	9247	6	NULL	NULL	0	NULL	Y(P)	NULL		is	NULL				phosphotyrosine	NULL				NULL	statement 2	0	NULL	NULL	NULL	gw60_jbiolchem_274_22_15678_s_143	10336465	A biosensor-based competition assay was used to measure the binding of p85alpha SH2 domains to an immobilized Tyr(P) peptide with the sequence DMSKDESVDY(P)VPMLDMK (Y(P) is phosphotyrosine).	bind
39817	1	9248	5	13	NULL	NULL	NULL	ParB	GP		bind					 DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_2_427_s_117	12191487	A biotinylated 26 bp double-stranded oligonucleotide containing sequence of the ParB binding site within the  gidABparAB operon promoter region was immobilized on a streptavidin sensor chip and used to investigate the effects of ParA on ParB DNA binding activity by SPR.	bind
32336	1	9248	6	NULL	NULL	0	NULL	ParB	NULL		bind	NULL				DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcell_10_2_427_s_117	12191487	A biotinylated 26 bp double-stranded oligonucleotide containing sequence of the ParB binding site within the  gidABparAB operon promoter region was immobilized on a streptavidin sensor chip and used to investigate the effects of ParA on ParB DNA binding activity by SPR.	bind
39818	1	9250	5	13	NULL	NULL	NULL	ATr	GP	biotinylated;;mutant	does not bind					MEF-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7575_s_309	11096067	A biotinylated mutant ATr did not bind to either MEF-2 or p300 (data not shown).	bind
39819	2	9250	5	13	NULL	NULL	NULL	ATr	GP	biotinylated;;mutant	does not bind					p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7575_s_309	11096067	A biotinylated mutant ATr did not bind to either MEF-2 or p300 (data not shown).	bind
39820	3	9250	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7575_s_309	11096067	A biotinylated mutant ATr did not bind to either MEF-2 or p300 (data not shown).	bind
32339	1	9250	6	NULL	NULL	0	NULL	ATr	NULL	biotinylated;; mutant	does not bind	NULL				MEF-2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_10_7575_s_309	11096067	A biotinylated mutant ATr did not bind to either MEF-2 or p300 (data not shown).	bind
32340	2	9250	6	NULL	NULL	0	NULL	ATr	NULL	biotinylated;; mutant	does not bind	NULL				p300	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_10_7575_s_309	11096067	A biotinylated mutant ATr did not bind to either MEF-2 or p300 (data not shown).	bind
48076	3	9250	6	10	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_10_7575_s_309	11096067	A biotinylated mutant ATr did not bind to either MEF-2 or p300 (data not shown).	bind
39821	1	9251	5	13	NULL	NULL	NULL	21 aa peptide	GP	biotinylated;;Plasmodium falciparum	bind					glycophorin A	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_9_4203_s_2	9712768	A biotinylated peptide covering a sequence of 21 amino acids (aa) from the erythrocyte binding antigen (EBA-175) of  Plasmodium falciparum bound to human glycophorin A, an erythrocyte receptor for merozoites, as demonstrated by enzyme-linked immunosorbent assay (ELISA) and to erythrocytes as demonstrated by flow cytometry analysis.	bind
39822	2	9251	5	13	NULL	NULL	NULL	glycophorin A	GP		is a type of					erythrocyte receptor for merozoites	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_9_4203_s_2	9712768	A biotinylated peptide covering a sequence of 21 amino acids (aa) from the erythrocyte binding antigen (EBA-175) of  Plasmodium falciparum bound to human glycophorin A, an erythrocyte receptor for merozoites, as demonstrated by enzyme-linked immunosorbent assay (ELISA) and to erythrocytes as demonstrated by flow cytometry analysis.	bind
39823	3	9251	5	13	NULL	NULL	NULL	21 aa peptide 	GP	biotinylated;;Plasmodium falciparum	bind					erythrocytes	Cell				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_9_4203_s_2	9712768	A biotinylated peptide covering a sequence of 21 amino acids (aa) from the erythrocyte binding antigen (EBA-175) of  Plasmodium falciparum bound to human glycophorin A, an erythrocyte receptor for merozoites, as demonstrated by enzyme-linked immunosorbent assay (ELISA) and to erythrocytes as demonstrated by flow cytometry analysis.	bind
48077	4	9251	5	13	NULL	NULL	NULL	21 aa peptide	GP		is derived from					EBA-175	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_9_4203_s_2	9712768	A biotinylated peptide covering a sequence of 21 amino acids (aa) from the erythrocyte binding antigen (EBA-175) of  Plasmodium falciparum bound to human glycophorin A, an erythrocyte receptor for merozoites, as demonstrated by enzyme-linked immunosorbent assay (ELISA) and to erythrocytes as demonstrated by flow cytometry analysis.	bind
48078	5	9251	5	13	NULL	NULL	NULL	EBA	GP		is					erythrocyte binding antigen	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_9_4203_s_2	9712768	A biotinylated peptide covering a sequence of 21 amino acids (aa) from the erythrocyte binding antigen (EBA-175) of  Plasmodium falciparum bound to human glycophorin A, an erythrocyte receptor for merozoites, as demonstrated by enzyme-linked immunosorbent assay (ELISA) and to erythrocytes as demonstrated by flow cytometry analysis.	bind
32456	1	9251	6	NULL	NULL	0	NULL	EBA	NULL		is	NULL				erythrocyte binding antigen	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_9_4203_s_2	9712768	A biotinylated peptide covering a sequence of 21 amino acids (aa) from the erythrocyte binding antigen (EBA-175) of  Plasmodium falciparum bound to human glycophorin A, an erythrocyte receptor for merozoites, as demonstrated by enzyme-linked immunosorbent assay (ELISA) and to erythrocytes as demonstrated by flow cytometry analysis.	bind
32457	2	9251	6	10	NULL	0	NULL	 21 aa peptide 	NULL	biotinylated;; Plasmodium falciparum	bind	NULL				glycophorin A	NULL	human			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_9_4203_s_2	9712768	A biotinylated peptide covering a sequence of 21 amino acids (aa) from the erythrocyte binding antigen (EBA-175) of  Plasmodium falciparum bound to human glycophorin A, an erythrocyte receptor for merozoites, as demonstrated by enzyme-linked immunosorbent assay (ELISA) and to erythrocytes as demonstrated by flow cytometry analysis.	bind
32458	3	9251	6	NULL	NULL	0	NULL	glycophorin A	NULL		is a type of	NULL				erythrocyte receptor for merozoites	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_9_4203_s_2	9712768	A biotinylated peptide covering a sequence of 21 amino acids (aa) from the erythrocyte binding antigen (EBA-175) of  Plasmodium falciparum bound to human glycophorin A, an erythrocyte receptor for merozoites, as demonstrated by enzyme-linked immunosorbent assay (ELISA) and to erythrocytes as demonstrated by flow cytometry analysis.	bind
48079	4	9251	6	10	NULL	0	NULL	21 aa peptide	NULL		bind	NULL				erythrocytes	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_9_4203_s_2	9712768	A biotinylated peptide covering a sequence of 21 amino acids (aa) from the erythrocyte binding antigen (EBA-175) of  Plasmodium falciparum bound to human glycophorin A, an erythrocyte receptor for merozoites, as demonstrated by enzyme-linked immunosorbent assay (ELISA) and to erythrocytes as demonstrated by flow cytometry analysis.	bind
48080	5	9251	6	10	NULL	0	NULL	21 aa peptide	NULL		is derived from	NULL				EBA-175	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_9_4203_s_2	9712768	A biotinylated peptide covering a sequence of 21 amino acids (aa) from the erythrocyte binding antigen (EBA-175) of  Plasmodium falciparum bound to human glycophorin A, an erythrocyte receptor for merozoites, as demonstrated by enzyme-linked immunosorbent assay (ELISA) and to erythrocytes as demonstrated by flow cytometry analysis.	bind
39824	1	9254	5	13	NULL	NULL	NULL	citron protein	GP	mouse	bind					GTP-Rho	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_1_96_s_123	9870942	A BLAST search of the GenBank database revealed that the remaining four peptide sequences (Table  1) are present in a protein named citron previously identified in mouse by the yeast two-hybrid method as a GTP-Rho binding partner and proposed to be a Rho/ac effector (Madaule et al., 1995  ).	bind
39825	2	9254	5	13	NULL	NULL	NULL	citron protein	GP		is a type of					Rho/ac effector	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_1_96_s_123	9870942	A BLAST search of the GenBank database revealed that the remaining four peptide sequences (Table  1) are present in a protein named citron previously identified in mouse by the yeast two-hybrid method as a GTP-Rho binding partner and proposed to be a Rho/ac effector (Madaule et al., 1995  ).	bind
32343	1	9254	6	10	NULL	0	NULL	citron	NULL		is a type of	NULL				Rho/ac effector	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_1_96_s_123	9870942	A BLAST search of the GenBank database revealed that the remaining four peptide sequences (Table  1) are present in a protein named citron previously identified in mouse by the yeast two-hybrid method as a GTP-Rho binding partner and proposed to be a Rho/ac effector (Madaule et al., 1995  ).	bind
32344	2	9254	6	NULL	NULL	0	NULL	citron	NULL	mouse	bind	NULL				GTP-Rho	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_1_96_s_123	9870942	A BLAST search of the GenBank database revealed that the remaining four peptide sequences (Table  1) are present in a protein named citron previously identified in mouse by the yeast two-hybrid method as a GTP-Rho binding partner and proposed to be a Rho/ac effector (Madaule et al., 1995  ).	bind
39827	1	9256	5	13	NULL	NULL	NULL	Mpeg1	GP	mouse	expressed in		predominantly			macrophage	Cell	mammalian			NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_468_s_7	15020241	A BLAST search [  17] of the sequences identified a homolog of mouse and human macrophage expressed gene  1 (Mpeg1), a protein thought at that time to be expressed predominantly in mammalian  macrophage [  18].	bind
39828	2	9256	5	13	NULL	NULL	NULL	Mpeg1	GP	human	expressed in		predominantly			macrophage	Cell	mammalian			NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_468_s_7	15020241	A BLAST search [  17] of the sequences identified a homolog of mouse and human macrophage expressed gene  1 (Mpeg1), a protein thought at that time to be expressed predominantly in mammalian  macrophage [  18].	bind
39829	3	9256	5	13	NULL	NULL	NULL	Mpeg1	GP		is					macrophage expressed gene 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_468_s_7	15020241	A BLAST search [  17] of the sequences identified a homolog of mouse and human macrophage expressed gene  1 (Mpeg1), a protein thought at that time to be expressed predominantly in mammalian  macrophage [  18].	bind
32345	1	9256	6	NULL	NULL	0	NULL	Mpeg1	NULL		is	NULL				macrophage expressed gene 1	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_468_s_7	15020241	A BLAST search [  17] of the sequences identified a homolog of mouse and human macrophage expressed gene  1 (Mpeg1), a protein thought at that time to be expressed predominantly in mammalian  macrophage [  18].	bind
32346	2	9256	6	10	NULL	0	NULL	Mpeg1		mouse	is expressed in		predominantly			macrophage		mammalian			NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_468_s_7	15020241	A BLAST search [  17] of the sequences identified a homolog of mouse and human macrophage expressed gene  1 (Mpeg1), a protein thought at that time to be expressed predominantly in mammalian  macrophage [  18].	bind
57861	3	9256	6	10	NULL	0	NULL	Mpeg1		human	expressed in		predominantly			macrophage		mammalian			NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_468_s_7	15020241	A BLAST search [  17] of the sequences identified a homolog of mouse and human macrophage expressed gene  1 (Mpeg1), a protein thought at that time to be expressed predominantly in mammalian  macrophage [  18].	bind
39830	1	9257	5	13	NULL	NULL	NULL	MSG1	GP		bind		specifically			p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_8825_s_99	10722728	A blocking peptide that disrupted binding of p300 to the anti-p300 antibody abolished the coprecipitation of MSG1 with p300 (Fig.  2 A), demonstrating that the MSG1 coprecipitation was specific.	bind
48081	2	9257	5	13	NULL	NULL	NULL	p300	GP		bind					anti-p300 antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_8825_s_99	10722728	A blocking peptide that disrupted binding of p300 to the anti-p300 antibody abolished the coprecipitation of MSG1 with p300 (Fig.  2 A), demonstrating that the MSG1 coprecipitation was specific.	bind
48082	3	9257	5	13	NULL	NULL	NULL	blocking peptide	GP		disrupts					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_8825_s_99	10722728	A blocking peptide that disrupted binding of p300 to the anti-p300 antibody abolished the coprecipitation of MSG1 with p300 (Fig.  2 A), demonstrating that the MSG1 coprecipitation was specific.	bind
48083	4	9257	5	13	NULL	NULL	NULL	blocking peptide	GP		abolish					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_8825_s_99	10722728	A blocking peptide that disrupted binding of p300 to the anti-p300 antibody abolished the coprecipitation of MSG1 with p300 (Fig.  2 A), demonstrating that the MSG1 coprecipitation was specific.	bind
32347	1	9257	6	10	NULL	0	NULL	MSG1	NULL		bind	NULL	specifically			p300	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_8825_s_99	10722728	A blocking peptide that disrupted binding of p300 to the anti-p300 antibody abolished the coprecipitation of MSG1 with p300 (Fig.  2 A), demonstrating that the MSG1 coprecipitation was specific.	bind
32363	2	9257	6	NULL	NULL	0	NULL	p300	NULL		bind	NULL				anti-p300 antibody	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_12_8825_s_99	10722728	A blocking peptide that disrupted binding of p300 to the anti-p300 antibody abolished the coprecipitation of MSG1 with p300 (Fig.  2 A), demonstrating that the MSG1 coprecipitation was specific.	bind
32364	3	9257	6	NULL	NULL	0	NULL	blocking peptide	NULL		disrupts	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_12_8825_s_99	10722728	A blocking peptide that disrupted binding of p300 to the anti-p300 antibody abolished the coprecipitation of MSG1 with p300 (Fig.  2 A), demonstrating that the MSG1 coprecipitation was specific.	bind
32365	4	9257	6	NULL	NULL	0	NULL	blocking peptide	NULL		abolishes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_12_8825_s_99	10722728	A blocking peptide that disrupted binding of p300 to the anti-p300 antibody abolished the coprecipitation of MSG1 with p300 (Fig.  2 A), demonstrating that the MSG1 coprecipitation was specific.	bind
39904	1	9258	5	13	NULL	NULL	NULL	dopamine	Chemical		bind		directly			NMDA receptor-channel macromolecule	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_126_8_1847_s_158	10372829	A blocking rate of the order of tens of milliseconds was not to be expected if the effect were mediated by a metabotropic pathway, and in turn suggests that dopamine was binding directly to the NMDA receptor-channel macromolecule.	bind
32421	1	9258	6	NULL	NULL	0	NULL	dopamine	NULL		bind	NULL	directly			NMDA receptor-channel macromolecule	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_8_1847_s_158	10372829	A blocking rate of the order of tens of milliseconds was not to be expected if the effect were mediated by a metabotropic pathway, and in turn suggests that dopamine was binding directly to the NMDA receptor-channel macromolecule.	bind
39905	1	9259	5	13	NULL	NULL	NULL	BMPR-II	GP	mutant	contains								COOH-terminal truncation		NULL	PPH	NULL	NULL	NULL	NULL	abs-batch0560-0569_j-cell-biol_162_6_12963706_s_8	12963706	A BMPR-II mutant containing  the smallest COOH-terminal truncation described in PPH failed to bind  or inhibit LIMK1.	bind
39906	2	9259	5	13	NULL	NULL	NULL	statement 1	GP		does not bind					LIMK1	GP				NULL	PPH	NULL	NULL	NULL	NULL	abs-batch0560-0569_j-cell-biol_162_6_12963706_s_8	12963706	A BMPR-II mutant containing  the smallest COOH-terminal truncation described in PPH failed to bind  or inhibit LIMK1.	bind
39907	3	9259	5	13	NULL	NULL	NULL	statement 1	GP		does not inhibit					LIMK1	GP				NULL	PPH	NULL	NULL	NULL	NULL	abs-batch0560-0569_j-cell-biol_162_6_12963706_s_8	12963706	A BMPR-II mutant containing  the smallest COOH-terminal truncation described in PPH failed to bind  or inhibit LIMK1.	bind
32424	1	9259	6	10	NULL	0	NULL	BMPR-II		mutant;; truncated	does not bind			COOH terminus		LIMK1					NULL	PPH	NULL	NULL	NULL	NULL	abs-batch0560-0569_j-cell-biol_162_6_12963706_s_8	12963706	A BMPR-II mutant containing  the smallest COOH-terminal truncation described in PPH failed to bind  or inhibit LIMK1.	bind
32437	2	9259	6	10	NULL	0	NULL	BMPR-II		mutant;; truncated	does not inhibit			COOH terminus		LIMK1					NULL	PPH	NULL	NULL	NULL	NULL	abs-batch0560-0569_j-cell-biol_162_6_12963706_s_8	12963706	A BMPR-II mutant containing  the smallest COOH-terminal truncation described in PPH failed to bind  or inhibit LIMK1.	bind
39908	1	9261	5	13	NULL	NULL	NULL	BmrR dimer	GP		bind					bmr DNA	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_299	12456787	A BmrR dimer concurrently bound to both  bmr promoter DNA and drugs (D) can correctly orient the -10 and -35 hexamers of this  promoter to facilitate the binding of RNA polymerase.	bind
39909	2	9261	5	13	NULL	NULL	NULL	BmrR dimer	GP		bind					drug	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_299	12456787	A BmrR dimer concurrently bound to both  bmr promoter DNA and drugs (D) can correctly orient the -10 and -35 hexamers of this  promoter to facilitate the binding of RNA polymerase.	bind
39910	3	9261	5	13	NULL	NULL	NULL	statement 1	Process		concurrent to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_299	12456787	A BmrR dimer concurrently bound to both  bmr promoter DNA and drugs (D) can correctly orient the -10 and -35 hexamers of this  promoter to facilitate the binding of RNA polymerase.	bind
39911	4	9261	5	13	NULL	NULL	NULL	BmrR dimer	GP		orient		correctly			bmr DNA	NucleicAcid			-10 and -35 hexamers of promoter	NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_299	12456787	A BmrR dimer concurrently bound to both  bmr promoter DNA and drugs (D) can correctly orient the -10 and -35 hexamers of this  promoter to facilitate the binding of RNA polymerase.	bind
39912	5	9261	5	13	NULL	NULL	NULL	statement 4	Process		facilitates					RNA polymerase	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_299	12456787	A BmrR dimer concurrently bound to both  bmr promoter DNA and drugs (D) can correctly orient the -10 and -35 hexamers of this  promoter to facilitate the binding of RNA polymerase.	bind
57863	6	9261	5	13	NULL	NULL	NULL	D	Chemical		is					drugs	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_299	12456787	A BmrR dimer concurrently bound to both  bmr promoter DNA and drugs (D) can correctly orient the -10 and -35 hexamers of this  promoter to facilitate the binding of RNA polymerase.	bind
32445	1	9261	6	10	NULL	0	NULL	BmrR dimer			bind					bmr DNA				promoter	NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_299	12456787	A BmrR dimer concurrently bound to both  bmr promoter DNA and drugs (D) can correctly orient the -10 and -35 hexamers of this  promoter to facilitate the binding of RNA polymerase.	bind
32446	2	9261	6	10	NULL	0	NULL	BmrR dimer	NULL		orient	NULL				bmr 	NULL			-10 and -35 hexamers of promoter	NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_299	12456787	A BmrR dimer concurrently bound to both  bmr promoter DNA and drugs (D) can correctly orient the -10 and -35 hexamers of this  promoter to facilitate the binding of RNA polymerase.	bind
32453	3	9261	6	10	NULL	0	NULL	BmrR dimer	NULL		bind	NULL				drug	NULL				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_299	12456787	A BmrR dimer concurrently bound to both  bmr promoter DNA and drugs (D) can correctly orient the -10 and -35 hexamers of this  promoter to facilitate the binding of RNA polymerase.	bind
32454	4	9261	6	10	NULL	0	NULL	statement 2	NULL		facilitates	NULL				RNA polymerase	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_299	12456787	A BmrR dimer concurrently bound to both  bmr promoter DNA and drugs (D) can correctly orient the -10 and -35 hexamers of this  promoter to facilitate the binding of RNA polymerase.	bind
32455	5	9261	6	NULL	NULL	0	NULL	D	NULL		is	NULL				drugs	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_299	12456787	A BmrR dimer concurrently bound to both  bmr promoter DNA and drugs (D) can correctly orient the -10 and -35 hexamers of this  promoter to facilitate the binding of RNA polymerase.	bind
57862	6	9261	6	10	NULL	0	NULL	statement 1			concurrent to					statement 3					NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_299	12456787	A BmrR dimer concurrently bound to both  bmr promoter DNA and drugs (D) can correctly orient the -10 and -35 hexamers of this  promoter to facilitate the binding of RNA polymerase.	bind
39913	1	9263	5	13	NULL	NULL	NULL	MD-2	GP		bind					TLR4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_17_11955_s_258	16467306	A body of evidence points to structural differences of MD-2 bound to TLR4 and soluble MD-2.	bind
48084	2	9263	5	13	NULL	NULL	NULL	MD-2	GP		bind					MD-2	GP	soluble			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_17_11955_s_258	16467306	A body of evidence points to structural differences of MD-2 bound to TLR4 and soluble MD-2.	bind
32447	1	9263	6	NULL	NULL	0	NULL	MD-2	NULL		bind	NULL				TLR4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_17_11955_s_258	16467306	A body of evidence points to structural differences of MD-2 bound to TLR4 and soluble MD-2.	bind
32448	2	9263	6	NULL	NULL	0	NULL	MD-2	NULL		bind	NULL				MD-2	NULL	soluble			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_17_11955_s_258	16467306	A body of evidence points to structural differences of MD-2 bound to TLR4 and soluble MD-2.	bind
39915	1	9264	5	13	NULL	NULL	NULL	MPD molecule	Chemical	bound	identifies							putative	GlcNAc binding pocket		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_12_3008_s_175	11406577	A bound MPD molecule identifies a putative GlcNAc binding pocket, located near the active site, and enables a hypothesis explaining the enzyme s dependency on the single GlcNAc substitution of the GlcNAcMan5GlcNAc2 substrate for binding.	bind
39916	2	9264	5	10	NULL	0	NULL			putative	is located near			GlcNAc binding pocket					active site		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_12_3008_s_175	11406577	A bound MPD molecule identifies a putative GlcNAc binding pocket, located near the active site, and enables a hypothesis explaining the enzyme s dependency on the single GlcNAc substitution of the GlcNAcMan5GlcNAc2 substrate for binding.	bind
39919	3	9264	5	13	NULL	NULL	NULL	GlcNAc	Chemical	single	is substituted in					GlcNAcMan5GlcNAc2 substrate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_12_3008_s_175	11406577	A bound MPD molecule identifies a putative GlcNAc binding pocket, located near the active site, and enables a hypothesis explaining the enzyme s dependency on the single GlcNAc substitution of the GlcNAcMan5GlcNAc2 substrate for binding.	bind
39920	4	9264	5	13	NULL	NULL	NULL	enzyme	GP	binding of	depends on		potentially			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_12_3008_s_175	11406577	A bound MPD molecule identifies a putative GlcNAc binding pocket, located near the active site, and enables a hypothesis explaining the enzyme s dependency on the single GlcNAc substitution of the GlcNAcMan5GlcNAc2 substrate for binding.	bind
32450	1	9264	6	NULL	NULL	0	NULL	MPD molecule	NULL	bound	identifies	NULL					NULL	putative	GlcNAc binding pocket		NULL		0	NULL	NULL	NULL	gw60_embo_20_12_3008_s_175	11406577	A bound MPD molecule identifies a putative GlcNAc binding pocket, located near the active site, and enables a hypothesis explaining the enzyme s dependency on the single GlcNAc substitution of the GlcNAcMan5GlcNAc2 substrate for binding.	bind
32451	2	9264	6	NULL	NULL	0	NULL	GlcNAcMan5GlcNAc2 substrate	NULL	binding of	is dependent on	NULL				GlcNAc	NULL	substitution of 			NULL		0	NULL	NULL	NULL	gw60_embo_20_12_3008_s_175	11406577	A bound MPD molecule identifies a putative GlcNAc binding pocket, located near the active site, and enables a hypothesis explaining the enzyme s dependency on the single GlcNAc substitution of the GlcNAcMan5GlcNAc2 substrate for binding.	bind
32452	3	9264	6	NULL	NULL	0	NULL	statement 2	NULL		enables	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_12_3008_s_175	11406577	A bound MPD molecule identifies a putative GlcNAc binding pocket, located near the active site, and enables a hypothesis explaining the enzyme s dependency on the single GlcNAc substitution of the GlcNAcMan5GlcNAc2 substrate for binding.	bind
57864	4	9264	6	10	NULL	0	NULL			putative	is located near			GlcNAc binding pocket					active site		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_12_3008_s_175	11406577	A bound MPD molecule identifies a putative GlcNAc binding pocket, located near the active site, and enables a hypothesis explaining the enzyme s dependency on the single GlcNAc substitution of the GlcNAcMan5GlcNAc2 substrate for binding.	bind
39921	1	9265	5	13	NULL	NULL	NULL	papillomavirus E1-related protein	GP	bovine	bind		specifically			papillomavirus DNA	NucleicAcid	bovine			NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_1_149_s_527	10949036	A bovine papillomavirus E1-related protein binds specifically to bovine papillomavirus DNA.	bind
32449	1	9265	6	NULL	NULL	0	NULL	papillomavirus E1-related protein	NULL	bovine	bind	NULL	specifically			papillomavirus DNA	NULL	bovine			NULL		0	NULL	NULL	NULL	gw60_molcell_6_1_149_s_527	10949036	A bovine papillomavirus E1-related protein binds specifically to bovine papillomavirus DNA.	bind
39931	1	9267	5	13	NULL	NULL	NULL	Cdc42	GP		activate					serine/threonine protein kinase	GP	brain			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6354_s_491	10938112	A brain serine/threonine protein kinase activated by Cdc42 and Rac1.	bind
39932	2	9267	5	13	NULL	NULL	NULL	Rac1	GP		activates					serine/threonine protein kinase	GP	brain			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6354_s_491	10938112	A brain serine/threonine protein kinase activated by Cdc42 and Rac1.	bind
32570	1	9267	6	10	NULL	0	NULL	serine/threonine protein kinase		brain 	is activated by					Cdc42					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6354_s_491	10938112	A brain serine/threonine protein kinase activated by Cdc42 and Rac1.	bind
32571	2	9267	6	10	NULL	0	NULL	 serine/threonine protein kinase		brain	is activated by					Rac1					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6354_s_491	10938112	A brain serine/threonine protein kinase activated by Cdc42 and Rac1.	bind
39933	1	9268	5	13	NULL	NULL	NULL	chondroitin sulfate proteoglycan	GP	brain-derived	is related to					phosphacan	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_11_4245_s_45	10341229	A brain-derived chondroitin sulfate proteoglycan related to phosphacan has been isolated by affinity to a recombinant amino-terminal EGF domain of TN-R (Xiao et al., 1997  ), and phosphacan binds with high affinity ( Kd ~2 nM) to native TN-R (Milev et al., 1998  ).	bind
39934	2	9268	5	13	NULL	NULL	NULL	statement 1	GP		bind					TN-R	GP	recombinant	amino-terminal EGF domain		NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_11_4245_s_45	10341229	A brain-derived chondroitin sulfate proteoglycan related to phosphacan has been isolated by affinity to a recombinant amino-terminal EGF domain of TN-R (Xiao et al., 1997  ), and phosphacan binds with high affinity ( Kd ~2 nM) to native TN-R (Milev et al., 1998  ).	bind
39935	3	9268	5	13	NULL	NULL	NULL	phosphacan	GP		bind		high affinity			TN-R	GP	native			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_11_4245_s_45	10341229	A brain-derived chondroitin sulfate proteoglycan related to phosphacan has been isolated by affinity to a recombinant amino-terminal EGF domain of TN-R (Xiao et al., 1997  ), and phosphacan binds with high affinity ( Kd ~2 nM) to native TN-R (Milev et al., 1998  ).	bind
32572	1	9268	6	NULL	NULL	0	NULL	phosphacan	NULL		bind	NULL	high affinity			TN-R	NULL	native			NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_11_4245_s_45	10341229	A brain-derived chondroitin sulfate proteoglycan related to phosphacan has been isolated by affinity to a recombinant amino-terminal EGF domain of TN-R (Xiao et al., 1997  ), and phosphacan binds with high affinity ( Kd ~2 nM) to native TN-R (Milev et al., 1998  ).	bind
32573	2	9268	6	NULL	NULL	0	NULL	chondroitin sulfate proteoglycan	NULL	brain-derived	is related to	NULL				phosphacan	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_11_4245_s_45	10341229	A brain-derived chondroitin sulfate proteoglycan related to phosphacan has been isolated by affinity to a recombinant amino-terminal EGF domain of TN-R (Xiao et al., 1997  ), and phosphacan binds with high affinity ( Kd ~2 nM) to native TN-R (Milev et al., 1998  ).	bind
32574	3	9268	6	NULL	NULL	0	NULL	chondroitin sulfate proteoglycan	NULL	brain-derived	has affinity for	NULL				TN-R	NULL	recombinant	amino-terminal EGF domain		NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_11_4245_s_45	10341229	A brain-derived chondroitin sulfate proteoglycan related to phosphacan has been isolated by affinity to a recombinant amino-terminal EGF domain of TN-R (Xiao et al., 1997  ), and phosphacan binds with high affinity ( Kd ~2 nM) to native TN-R (Milev et al., 1998  ).	bind
39936	1	9269	5	13	NULL	NULL	NULL	small glutamine-rich tetratricopeptide repeat-containing protein	GP	brain-specific isoform	bind					Hsc70	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_38376_s_1	12878599	A brain-specific isoform of small glutamine-rich tetratricopeptide repeat-containing protein binds to Hsc70 and the cysteine string protein.	bind
39937	2	9269	5	13	NULL	NULL	NULL	small glutamine-rich tetratricopeptide repeat-containing protein	GP	brain-specific isoform	bind					cysteine string protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_38376_s_1	12878599	A brain-specific isoform of small glutamine-rich tetratricopeptide repeat-containing protein binds to Hsc70 and the cysteine string protein.	bind
32575	1	9269	6	NULL	NULL	0	NULL	small glutamine-rich tetratricopeptide repeat-containing protein	NULL	brain-specific isoform	bind	NULL				Hsc70	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_40_38376_s_1	12878599	A brain-specific isoform of small glutamine-rich tetratricopeptide repeat-containing protein binds to Hsc70 and the cysteine string protein.	bind
32576	2	9269	6	NULL	NULL	0	NULL	small glutamine-rich tetratricopeptide repeat-containing protein	NULL	brain-specific isoform	bind	NULL				cysteine string protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_40_38376_s_1	12878599	A brain-specific isoform of small glutamine-rich tetratricopeptide repeat-containing protein binds to Hsc70 and the cysteine string protein.	bind
39938	1	9270	5	13	NULL	NULL	NULL	guanine nucleotides	NucleicAcid		bind					RF3	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_22_2_175_s_124	12514123	A breakthrough in our understanding of RF3 function occurred when   et al remeasured the binding of guanine nucleotides to this G protein.	bind
39939	2	9270	5	13	NULL	NULL	NULL	RF3	GP		is a type of					G protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_22_2_175_s_124	12514123	A breakthrough in our understanding of RF3 function occurred when   et al remeasured the binding of guanine nucleotides to this G protein.	bind
32577	1	9270	6	10	NULL	0	NULL	guanine nucleotides	NULL		bind	NULL				RF3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_embo_22_2_175_s_124	12514123	A breakthrough in our understanding of RF3 function occurred when   et al remeasured the binding of guanine nucleotides to this G protein.	bind
48085	2	9270	6	10	NULL	0	NULL	RF3	NULL		is a type of	NULL				G protein	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_22_2_175_s_124	12514123	A breakthrough in our understanding of RF3 function occurred when   et al remeasured the binding of guanine nucleotides to this G protein.	bind
40676	1	9272	5	13	NULL	NULL	NULL	BR	Chemical		bind					HSA	GP	native			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1523_2_147_s_121	11042378	A brief (1 min) irradiation of BR bound to native HSA under white fluorescent light, produced only little change in the magnitude of both positive and negative CDCEs (  Fig. 3A).	bind
57865	2	9272	5	13	NULL	NULL	NULL	CDCE	ResearchActivity		change					magnitude	QuantityOrMeasure				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1523_2_147_s_121	11042378	A brief (1 min) irradiation of BR bound to native HSA under white fluorescent light, produced only little change in the magnitude of both positive and negative CDCEs (  Fig. 3A).	bind
57866	3	9272	5	13	NULL	NULL	NULL	statement 1	Process		produced					statement 2	Process	little change in			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1523_2_147_s_121	11042378	A brief (1 min) irradiation of BR bound to native HSA under white fluorescent light, produced only little change in the magnitude of both positive and negative CDCEs (  Fig. 3A).	bind
32578	1	9272	6	NULL	NULL	0	NULL	BR	NULL		bind	NULL				HSA	NULL	native			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1523_2_147_s_121	11042378	A brief (1 min) irradiation of BR bound to native HSA under white fluorescent light, produced only little change in the magnitude of both positive and negative CDCEs (  Fig. 3A).	bind
32579	2	9272	6	NULL	NULL	0	NULL	CDCE	NULL		change	NULL				magnitude	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1523_2_147_s_121	11042378	A brief (1 min) irradiation of BR bound to native HSA under white fluorescent light, produced only little change in the magnitude of both positive and negative CDCEs (  Fig. 3A).	bind
40523	3	9272	6	NULL	NULL	0	NULL	statement 1	NULL		produced	NULL				statement 2	NULL	little change in			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1523_2_147_s_121	11042378	A brief (1 min) irradiation of BR bound to native HSA under white fluorescent light, produced only little change in the magnitude of both positive and negative CDCEs (  Fig. 3A).	bind
40052	3	9273	5	13	NULL	NULL	NULL	PCA	Chemical		disrupt		strongly			statement 1	Process	formation of			NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_67_8_3530_s_274	11472929	A brief survey of the effects of other aromatic compounds on CbaR binding identified PCA as a strong disrupter of the CbaR-P cbaA complex (Fig.  4F), suggesting that CbaR evolved so that it responds to both 3CBA, the substrate of the  cba pathway, and at least one downstream metabolite.	bind
40054	2	9273	5	13	NULL	NULL	NULL	PCA	Chemical		is a type of					aromatic compound	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_67_8_3530_s_274	11472929	A brief survey of the effects of other aromatic compounds on CbaR binding identified PCA as a strong disrupter of the CbaR-P cbaA complex (Fig.  4F), suggesting that CbaR evolved so that it responds to both 3CBA, the substrate of the  cba pathway, and at least one downstream metabolite.	bind
40057	4	9273	5	13	NULL	NULL	NULL	3CBA	Chemical		substrate of					cba pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_67_8_3530_s_274	11472929	A brief survey of the effects of other aromatic compounds on CbaR binding identified PCA as a strong disrupter of the CbaR-P cbaA complex (Fig.  4F), suggesting that CbaR evolved so that it responds to both 3CBA, the substrate of the  cba pathway, and at least one downstream metabolite.	bind
40058	5	9273	5	13	NULL	NULL	NULL	CbaR	GP		respond to					3CBA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_67_8_3530_s_274	11472929	A brief survey of the effects of other aromatic compounds on CbaR binding identified PCA as a strong disrupter of the CbaR-P cbaA complex (Fig.  4F), suggesting that CbaR evolved so that it responds to both 3CBA, the substrate of the  cba pathway, and at least one downstream metabolite.	bind
48086	1	9273	5	13	NULL	NULL	NULL	CbaR	GP		complex with					P cbaA	GP				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_67_8_3530_s_274	11472929	A brief survey of the effects of other aromatic compounds on CbaR binding identified PCA as a strong disrupter of the CbaR-P cbaA complex (Fig.  4F), suggesting that CbaR evolved so that it responds to both 3CBA, the substrate of the  cba pathway, and at least one downstream metabolite.	bind
32845	4	9273	6	10	NULL	0	NULL	PCA			disrupts		strongly			statement 1		formation of			NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_67_8_3530_s_274	11472929	A brief survey of the effects of other aromatic compounds on CbaR binding identified PCA as a strong disrupter of the CbaR-P cbaA complex (Fig.  4F), suggesting that CbaR evolved so that it responds to both 3CBA, the substrate of the  cba pathway, and at least one downstream metabolite.	bind
32847	2	9273	6	NULL	NULL	0	NULL	CbaR	NULL		responds to	NULL				3CBA	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_8_3530_s_274	11472929	A brief survey of the effects of other aromatic compounds on CbaR binding identified PCA as a strong disrupter of the CbaR-P cbaA complex (Fig.  4F), suggesting that CbaR evolved so that it responds to both 3CBA, the substrate of the  cba pathway, and at least one downstream metabolite.	bind
32850	3	9273	6	10	NULL	0	NULL	3CBA	NULL		substrate of	NULL				 cba pathway	NULL				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_67_8_3530_s_274	11472929	A brief survey of the effects of other aromatic compounds on CbaR binding identified PCA as a strong disrupter of the CbaR-P cbaA complex (Fig.  4F), suggesting that CbaR evolved so that it responds to both 3CBA, the substrate of the  cba pathway, and at least one downstream metabolite.	bind
48087	1	9273	6	10	NULL	0	NULL	CbaR	NULL		complex with	NULL				P cbaA	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_8_3530_s_274	11472929	A brief survey of the effects of other aromatic compounds on CbaR binding identified PCA as a strong disrupter of the CbaR-P cbaA complex (Fig.  4F), suggesting that CbaR evolved so that it responds to both 3CBA, the substrate of the  cba pathway, and at least one downstream metabolite.	bind
48088	5	9273	6	10	NULL	0	NULL	PCA	NULL		is a type of	NULL				aromatic compound	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_8_3530_s_274	11472929	A brief survey of the effects of other aromatic compounds on CbaR binding identified PCA as a strong disrupter of the CbaR-P cbaA complex (Fig.  4F), suggesting that CbaR evolved so that it responds to both 3CBA, the substrate of the  cba pathway, and at least one downstream metabolite.	bind
39944	1	9274	5	13	NULL	NULL	NULL	BrlA-like protein	GP		bind					ech42	NucleicAcid			promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_218_2_259_s_66	12586401	A BrlA-like protein binds to the  ech42 promoter under carbon starvation in vitro	bind
39945	2	9274	5	13	NULL	NULL	NULL	statement 1	Process		occurs under					carbon 	Chemical	starvation of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_218_2_259_s_66	12586401	A BrlA-like protein binds to the  ech42 promoter under carbon starvation in vitro	bind
32580	1	9274	6	NULL	NULL	0	NULL	BrlA-like protein	NULL		bind	NULL				ech42	NULL			promoter	NULL	in vitro	0	NULL	NULL	NULL	gw60_femsmicrobiollett_218_2_259_s_66	12586401	A BrlA-like protein binds to the  ech42 promoter under carbon starvation in vitro	bind
32581	2	9274	6	10	NULL	0	NULL	statement 1			occurs under					carbon 		starvation of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_218_2_259_s_66	12586401	A BrlA-like protein binds to the  ech42 promoter under carbon starvation in vitro	bind
40059	1	9278	5	13	NULL	NULL	NULL	C-C chemokine receptor	GP		bind					C-C chemokine family	GP	multiple members of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_18_10439_s_24	7737978	A C-C chemokine receptor, which  binds multiple members of the C-C chemokine family and two monocyte  chemotactic protein-1 receptors have also been cloned  ( 9,  10) .	bind
40060	2	9278	5	13	NULL	NULL	NULL	C-C chemokine receptor	GP		bind					monocyte chemotactic protein-1 receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_18_10439_s_24	7737978	A C-C chemokine receptor, which  binds multiple members of the C-C chemokine family and two monocyte  chemotactic protein-1 receptors have also been cloned  ( 9,  10) .	bind
32583	1	9278	6	NULL	NULL	0	NULL	C-C chemokine receptor	NULL		bind	NULL				C-C chemokine family	NULL	multiple members of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_18_10439_s_24	7737978	A C-C chemokine receptor, which  binds multiple members of the C-C chemokine family and two monocyte  chemotactic protein-1 receptors have also been cloned  ( 9,  10) .	bind
32584	2	9278	6	10	NULL	0	NULL	C-C chemokine receptor			bind					monocyte chemotactic protein-1 receptor					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_18_10439_s_24	7737978	A C-C chemokine receptor, which  binds multiple members of the C-C chemokine family and two monocyte  chemotactic protein-1 receptors have also been cloned  ( 9,  10) .	bind
40064	1	9279	5	13	NULL	NULL	NULL	c-FosJunD heterodimer	GP		bind					GST-BAF60a	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_4_2852_s_91	11053448	A c-FosunD heterodimer bound with GST-BAF60a, but the binding was less than that observed with c-Fos alone (Fig.  2 B), suggesting that dimerization of c-Fos and JunD did not appreciably contribute to BAF60a binding.	bind
40066	2	9279	5	13	NULL	NULL	NULL	c-Fos	GP		bind					GST-BAF60a	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_4_2852_s_91	11053448	A c-FosunD heterodimer bound with GST-BAF60a, but the binding was less than that observed with c-Fos alone (Fig.  2 B), suggesting that dimerization of c-Fos and JunD did not appreciably contribute to BAF60a binding.	bind
40068	3	9279	5	13	NULL	NULL	NULL	statement 1	Process	affinity of	less than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_4_2852_s_91	11053448	A c-FosunD heterodimer bound with GST-BAF60a, but the binding was less than that observed with c-Fos alone (Fig.  2 B), suggesting that dimerization of c-Fos and JunD did not appreciably contribute to BAF60a binding.	bind
40074	4	9279	5	13	NULL	NULL	NULL	c-Fos	GP		dimerize with					JunD	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_4_2852_s_91	11053448	A c-FosunD heterodimer bound with GST-BAF60a, but the binding was less than that observed with c-Fos alone (Fig.  2 B), suggesting that dimerization of c-Fos and JunD did not appreciably contribute to BAF60a binding.	bind
40075	5	9279	5	13	NULL	NULL	NULL	statement 4	Process		does not contribute to		appreciably			BAF60a	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_4_2852_s_91	11053448	A c-FosunD heterodimer bound with GST-BAF60a, but the binding was less than that observed with c-Fos alone (Fig.  2 B), suggesting that dimerization of c-Fos and JunD did not appreciably contribute to BAF60a binding.	bind
32585	1	9279	6	NULL	NULL	0	NULL	c-FosunD heterodimer	NULL		bind	NULL				GST-BAF60a	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_4_2852_s_91	11053448	A c-FosunD heterodimer bound with GST-BAF60a, but the binding was less than that observed with c-Fos alone (Fig.  2 B), suggesting that dimerization of c-Fos and JunD did not appreciably contribute to BAF60a binding.	bind
32586	2	9279	6	NULL	NULL	0	NULL	c-Fos	NULL		bind	NULL				GST-BAF60a	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_4_2852_s_91	11053448	A c-FosunD heterodimer bound with GST-BAF60a, but the binding was less than that observed with c-Fos alone (Fig.  2 B), suggesting that dimerization of c-Fos and JunD did not appreciably contribute to BAF60a binding.	bind
32587	3	9279	6	NULL	NULL	0	NULL	statement 1	NULL	affinity of	is less than	NULL				statement 2	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_4_2852_s_91	11053448	A c-FosunD heterodimer bound with GST-BAF60a, but the binding was less than that observed with c-Fos alone (Fig.  2 B), suggesting that dimerization of c-Fos and JunD did not appreciably contribute to BAF60a binding.	bind
32588	4	9279	6	NULL	NULL	0	NULL	c-Fos	NULL		dimerizes with	NULL				JunD	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_4_2852_s_91	11053448	A c-FosunD heterodimer bound with GST-BAF60a, but the binding was less than that observed with c-Fos alone (Fig.  2 B), suggesting that dimerization of c-Fos and JunD did not appreciably contribute to BAF60a binding.	bind
32589	5	9279	6	NULL	NULL	0	NULL	statement 4	NULL		did not contribute to	NULL				BAF60a	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_4_2852_s_91	11053448	A c-FosunD heterodimer bound with GST-BAF60a, but the binding was less than that observed with c-Fos alone (Fig.  2 B), suggesting that dimerization of c-Fos and JunD did not appreciably contribute to BAF60a binding.	bind
40079	1	9280	5	13	NULL	NULL	NULL	MarR	GP	deletion mutant	reduce			C-terminal 18 amino acid 		MarR	GP	binding properties of			NULL	clinical isolate of Escherichia coli 	NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_4_671_s_1443	12456787	A C-terminal 18 amino acid deletion in MarR in a clinical isolate of  Escherichia coli reduces MarR binding properties and increases the MIC of ciprofloxacin.	bind
40083	2	9280	5	13	NULL	NULL	NULL	statement 1	Process		increase					ciprofloxacin	Chemical	MIC of			NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_4_671_s_1443	12456787	A C-terminal 18 amino acid deletion in MarR in a clinical isolate of  Escherichia coli reduces MarR binding properties and increases the MIC of ciprofloxacin.	bind
32853	1	9280	6	NULL	NULL	0	NULL	MarR	NULL	deletion of	reduces	NULL		C-terminal 18 amino acid		MarR	NULL	binding properties of			NULL	clinical isolate of Escherichia coli 	NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_4_671_s_1443	12456787	A C-terminal 18 amino acid deletion in MarR in a clinical isolate of  Escherichia coli reduces MarR binding properties and increases the MIC of ciprofloxacin.	bind
32856	2	9280	6	NULL	NULL	0	NULL	MarR	NULL	deletion of	increases	NULL		C-terminal 18 amino acid		ciprofloxacin	NULL	MIC of 			NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_4_671_s_1443	12456787	A C-terminal 18 amino acid deletion in MarR in a clinical isolate of  Escherichia coli reduces MarR binding properties and increases the MIC of ciprofloxacin.	bind
40380	2	9282	5	13	NULL	NULL	NULL	ELL sequences	GP		is implicated in					leukemogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_17_7803_s_119	16107725	A C-terminal deletion removed the last 300 amino acids of dELL, which contain homology to the ELL sequences implicated in leukemogenesis ( ,  ), to the minimal p53 binding sequence of ELL ( ), and to the ZO-1 binding domain of occludin.	bind
40382	1	9282	5	13	NULL	NULL	NULL	dELL	GP		is homologous to			last 300 amino acids		ELL sequences	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_17_7803_s_119	16107725	A C-terminal deletion removed the last 300 amino acids of dELL, which contain homology to the ELL sequences implicated in leukemogenesis ( ,  ), to the minimal p53 binding sequence of ELL ( ), and to the ZO-1 binding domain of occludin.	bind
40383	3	9282	5	13	NULL	NULL	NULL	dELL	GP		is homologous to			last 300 amino acids		ELL	GP		p53 binding sequence		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_17_7803_s_119	16107725	A C-terminal deletion removed the last 300 amino acids of dELL, which contain homology to the ELL sequences implicated in leukemogenesis ( ,  ), to the minimal p53 binding sequence of ELL ( ), and to the ZO-1 binding domain of occludin.	bind
40384	4	9282	5	13	NULL	NULL	NULL	dELL	GP		is homologous to			last 300 amino acids		occludin	GP		ZO-1 binding domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_17_7803_s_119	16107725	A C-terminal deletion removed the last 300 amino acids of dELL, which contain homology to the ELL sequences implicated in leukemogenesis ( ,  ), to the minimal p53 binding sequence of ELL ( ), and to the ZO-1 binding domain of occludin.	bind
32859	1	9282	6	NULL	NULL	0	NULL	ELL sequences	NULL		are implicated in	NULL				leukemogenesis	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_17_7803_s_119	16107725	A C-terminal deletion removed the last 300 amino acids of dELL, which contain homology to the ELL sequences implicated in leukemogenesis ( ,  ), to the minimal p53 binding sequence of ELL ( ), and to the ZO-1 binding domain of occludin.	bind
32860	2	9282	6	10	NULL	0	NULL	dELL			is homologous to			last 300 amino acids		ELL sequences					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_17_7803_s_119	16107725	A C-terminal deletion removed the last 300 amino acids of dELL, which contain homology to the ELL sequences implicated in leukemogenesis ( ,  ), to the minimal p53 binding sequence of ELL ( ), and to the ZO-1 binding domain of occludin.	bind
48089	3	9282	6	10	NULL	0	NULL	dELL	NULL		is homologous to	NULL		last 300 amino acids		ELL	NULL		 p53 binding sequence		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_17_7803_s_119	16107725	A C-terminal deletion removed the last 300 amino acids of dELL, which contain homology to the ELL sequences implicated in leukemogenesis ( ,  ), to the minimal p53 binding sequence of ELL ( ), and to the ZO-1 binding domain of occludin.	bind
48090	4	9282	6	10	NULL	0	NULL	dELL	NULL		is homologous to	NULL		last 300 amino acids		occludin	NULL		ZO-1 binding domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_17_7803_s_119	16107725	A C-terminal deletion removed the last 300 amino acids of dELL, which contain homology to the ELL sequences implicated in leukemogenesis ( ,  ), to the minimal p53 binding sequence of ELL ( ), and to the ZO-1 binding domain of occludin.	bind
40087	1	9283	5	13	NULL	NULL	NULL	K cyclin-cdk6	GP		phosphorylate					p27Kip1	GP		C-terminal fragment		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_3_654_s_107	9927425	A C-terminal fragment of p27Kip1 synthesized as a GST fusion protein in bacteria was bound to glutathione-Sepharose beads and phosphorylated by either K cyclin-cdk6	bind
48091	2	9283	5	13	NULL	NULL	NULL	p27Kip1	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_3_654_s_107	9927425	A C-terminal fragment of p27Kip1 synthesized as a GST fusion protein in bacteria was bound to glutathione-Sepharose beads and phosphorylated by either K cyclin-cdk6	bind
32590	1	9283	6	10	NULL	0	NULL	K cyclin-cdk6	NULL		phosphorylates	NULL				p27Kip1	NULL		C-terminal fragment		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_3_654_s_107	9927425	A C-terminal fragment of p27Kip1 synthesized as a GST fusion protein in bacteria was bound to glutathione-Sepharose beads and phosphorylated by either K cyclin-cdk6	bind
48092	2	9283	6	10	NULL	0	NULL	p27Kip1	NULL		is a type of	NULL				GST fusion protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_3_654_s_107	9927425	A C-terminal fragment of p27Kip1 synthesized as a GST fusion protein in bacteria was bound to glutathione-Sepharose beads and phosphorylated by either K cyclin-cdk6	bind
40088	1	9284	5	13	NULL	NULL	NULL	 papillomavirus E1 protein	GP	human	bind			C-terminal helicase domain		E2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_1_149_s_427	10949036	A C-terminal helicase domain of the human papillomavirus E1 protein binds E2 and the DNA polymerase  -primase p68 subunit.	bind
40089	2	9284	5	13	NULL	NULL	NULL	 papillomavirus E1 protein	GP	human	bind			C-terminal helicase domain		DNA polymerase -primase	GP		p68 subunit		NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_1_149_s_427	10949036	A C-terminal helicase domain of the human papillomavirus E1 protein binds E2 and the DNA polymerase  -primase p68 subunit.	bind
32591	1	9284	6	NULL	NULL	0	NULL	papillomavirus E1 protein	NULL	human	bind	NULL		C-terminal helicase domain		E2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_6_1_149_s_427	10949036	A C-terminal helicase domain of the human papillomavirus E1 protein binds E2 and the DNA polymerase  -primase p68 subunit.	bind
32592	2	9284	6	10	NULL	0	NULL	papillomavirus E1 protein	NULL	human	bind	NULL		C-terminal helicase domain		DNA polymerase -primase 	NULL		p68 subunit		NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_1_149_s_427	10949036	A C-terminal helicase domain of the human papillomavirus E1 protein binds E2 and the DNA polymerase  -primase p68 subunit.	bind
40090	1	9286	5	13	NULL	NULL	NULL				bind			C-terminal IQ domain		calmodulin	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_blood_108_2_16569770_s_4	16569770	A C-terminal IQ domain binds calmodulin in the absence of calcium, and  conserved PKC phosphorylation motifs are targets of concanavalin A (ConA)-  or PMA/ionomycin-induced PKC activation.	bind
40091	2	9286	5	13	NULL	NULL	NULL	statement 1	Process		in the absence of					calcium	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_blood_108_2_16569770_s_4	16569770	A C-terminal IQ domain binds calmodulin in the absence of calcium, and  conserved PKC phosphorylation motifs are targets of concanavalin A (ConA)-  or PMA/ionomycin-induced PKC activation.	bind
40092	3	9286	5	13	NULL	NULL	NULL	ConA	GP		induce					PKC	GP	activation of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_blood_108_2_16569770_s_4	16569770	A C-terminal IQ domain binds calmodulin in the absence of calcium, and  conserved PKC phosphorylation motifs are targets of concanavalin A (ConA)-  or PMA/ionomycin-induced PKC activation.	bind
40093	4	9286	5	13	NULL	NULL	NULL	PMA/ionomycin	Chemical		induce					PKC	GP	activation of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_blood_108_2_16569770_s_4	16569770	A C-terminal IQ domain binds calmodulin in the absence of calcium, and  conserved PKC phosphorylation motifs are targets of concanavalin A (ConA)-  or PMA/ionomycin-induced PKC activation.	bind
40094	5	9286	5	13	NULL	NULL	NULL	PKC	GP		are targets of			conserved phosphorylation motifs		statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_blood_108_2_16569770_s_4	16569770	A C-terminal IQ domain binds calmodulin in the absence of calcium, and  conserved PKC phosphorylation motifs are targets of concanavalin A (ConA)-  or PMA/ionomycin-induced PKC activation.	bind
48093	6	9286	5	13	NULL	NULL	NULL	ConA	GP		is					concanavalin A	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_blood_108_2_16569770_s_4	16569770	A C-terminal IQ domain binds calmodulin in the absence of calcium, and  conserved PKC phosphorylation motifs are targets of concanavalin A (ConA)-  or PMA/ionomycin-induced PKC activation.	bind
57919	7	9286	5	13	NULL	NULL	NULL	PKC	GP		are targets of			conserved phosphorylation motifs		statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_blood_108_2_16569770_s_4	16569770	A C-terminal IQ domain binds calmodulin in the absence of calcium, and  conserved PKC phosphorylation motifs are targets of concanavalin A (ConA)-  or PMA/ionomycin-induced PKC activation.	bind
32593	1	9286	6	NULL	NULL	0	NULL		NULL		bind	NULL		C-terminal IQ domain		calmodulin	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_blood_108_2_16569770_s_4	16569770	A C-terminal IQ domain binds calmodulin in the absence of calcium, and  conserved PKC phosphorylation motifs are targets of concanavalin A (ConA)-  or PMA/ionomycin-induced PKC activation.	bind
32594	2	9286	6	NULL	NULL	0	NULL	statement 1	NULL		occurs in absence of	NULL				calcium	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_blood_108_2_16569770_s_4	16569770	A C-terminal IQ domain binds calmodulin in the absence of calcium, and  conserved PKC phosphorylation motifs are targets of concanavalin A (ConA)-  or PMA/ionomycin-induced PKC activation.	bind
32861	3	9286	6	NULL	NULL	0	NULL	ConA	NULL		is	NULL				concanavalin A	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_blood_108_2_16569770_s_4	16569770	A C-terminal IQ domain binds calmodulin in the absence of calcium, and  conserved PKC phosphorylation motifs are targets of concanavalin A (ConA)-  or PMA/ionomycin-induced PKC activation.	bind
32862	4	9286	6	NULL	NULL	0	NULL	ConA	NULL		induces	NULL				PKC	NULL	activation of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_blood_108_2_16569770_s_4	16569770	A C-terminal IQ domain binds calmodulin in the absence of calcium, and  conserved PKC phosphorylation motifs are targets of concanavalin A (ConA)-  or PMA/ionomycin-induced PKC activation.	bind
32863	5	9286	6	NULL	NULL	0	NULL	PMA/ionomycin	NULL		induces	NULL				PKC	NULL	activation of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_blood_108_2_16569770_s_4	16569770	A C-terminal IQ domain binds calmodulin in the absence of calcium, and  conserved PKC phosphorylation motifs are targets of concanavalin A (ConA)-  or PMA/ionomycin-induced PKC activation.	bind
32864	6	9286	6	NULL	NULL	0	NULL		NULL	conserved	are targets of	NULL		PKC phosphorylation motif		statement 4	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_blood_108_2_16569770_s_4	16569770	A C-terminal IQ domain binds calmodulin in the absence of calcium, and  conserved PKC phosphorylation motifs are targets of concanavalin A (ConA)-  or PMA/ionomycin-induced PKC activation.	bind
32865	7	9286	6	NULL	NULL	0	NULL		NULL	conserved	are targets of	NULL		PKC phosphorylation motif		statement 5	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_blood_108_2_16569770_s_4	16569770	A C-terminal IQ domain binds calmodulin in the absence of calcium, and  conserved PKC phosphorylation motifs are targets of concanavalin A (ConA)-  or PMA/ionomycin-induced PKC activation.	bind
40095	1	9287	5	13	NULL	NULL	NULL	Mst27p	GP		bind		directly	C-terminal KKXX motif		COPI complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3097_s_6	12925749	A C-terminal KKXX motif of Mst27p that allows direct  binding to the COPI complex is crucial for its suppression ability.	bind
40096	2	9287	5	13	NULL	NULL	NULL	Mst27p	GP		is required for		crucial	C-terminal KKXX motif		Mst27p	GP	suppression ability of			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3097_s_6	12925749	A C-terminal KKXX motif of Mst27p that allows direct  binding to the COPI complex is crucial for its suppression ability.	bind
32595	1	9287	6	NULL	NULL	0	NULL	Mst27p	NULL		bind	NULL	direct	C-terminal KKXX motif		COPI complex	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_8_3097_s_6	12925749	A C-terminal KKXX motif of Mst27p that allows direct  binding to the COPI complex is crucial for its suppression ability.	bind
32629	2	9287	6	10	NULL	0	NULL	Mst27p			is crucial for			C-terminal KKXX motif		Mst27p		 suppression ability of			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_8_3097_s_6	12925749	A C-terminal KKXX motif of Mst27p that allows direct  binding to the COPI complex is crucial for its suppression ability.	bind
40097	2	9290	5	13	NULL	NULL	NULL	PDK3	GP	truncated	abolishes			C-terminal delta392 406		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_10_1763_s_223	15861126	A C-terminal truncation (delta392 406) of PDK3 abolishes L2 binding to PDK3 as determined by ITC ( Figure 3).	bind
40098	1	9290	5	13	NULL	NULL	NULL	L2	GP		bind					PDK3	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_10_1763_s_223	15861126	A C-terminal truncation (delta392 406) of PDK3 abolishes L2 binding to PDK3 as determined by ITC ( Figure 3).	bind
32632	1	9290	6	NULL	NULL	0	NULL	L2	NULL		bind	NULL				PDK3	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_10_1763_s_223	15861126	A C-terminal truncation (delta392 406) of PDK3 abolishes L2 binding to PDK3 as determined by ITC ( Figure 3).	bind
32633	2	9290	6	10	NULL	0	NULL	PDK3		truncated	abolishes			C-terminal delta392 406		statement 1					NULL		NULL	NULL	NULL	NULL	gw70_embo_24_10_1763_s_223	15861126	A C-terminal truncation (delta392 406) of PDK3 abolishes L2 binding to PDK3 as determined by ITC ( Figure 3).	bind
40102	1	9292	5	13	NULL	NULL	NULL	IKKgamma	GP	 truncated	lacks			C-terminal					LZ		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4547_s_43	10373503	A C-terminally truncated version of IKKgamma lacking the LZ can still bind IKKalpha-IKKbeta heterodimers, but once expressed, it prevents IKK activation by a number of stimuli, including TNF and IL-1 ( 33).	bind
40103	2	9292	5	13	NULL	NULL	NULL	statement 1	GP		bind					IKKalpha-IKKbeta heterodimers	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4547_s_43	10373503	A C-terminally truncated version of IKKgamma lacking the LZ can still bind IKKalpha-IKKbeta heterodimers, but once expressed, it prevents IKK activation by a number of stimuli, including TNF and IL-1 ( 33).	bind
40104	3	9292	5	13	NULL	NULL	NULL	TNF	GP		stimulates					IKK	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4547_s_43	10373503	A C-terminally truncated version of IKKgamma lacking the LZ can still bind IKKalpha-IKKbeta heterodimers, but once expressed, it prevents IKK activation by a number of stimuli, including TNF and IL-1 ( 33).	bind
40105	4	9292	5	13	NULL	NULL	NULL	IL-1	GP		stimulates					IKK	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4547_s_43	10373503	A C-terminally truncated version of IKKgamma lacking the LZ can still bind IKKalpha-IKKbeta heterodimers, but once expressed, it prevents IKK activation by a number of stimuli, including TNF and IL-1 ( 33).	bind
40106	5	9292	5	13	NULL	NULL	NULL	IKKgamma	GP	expression of;;truncated	prevents			C-terminal		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4547_s_43	10373503	A C-terminally truncated version of IKKgamma lacking the LZ can still bind IKKalpha-IKKbeta heterodimers, but once expressed, it prevents IKK activation by a number of stimuli, including TNF and IL-1 ( 33).	bind
40107	6	9292	5	13	NULL	NULL	NULL	IKKgamma	GP	expression of;;truncated	prevents			C-terminal		statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4547_s_43	10373503	A C-terminally truncated version of IKKgamma lacking the LZ can still bind IKKalpha-IKKbeta heterodimers, but once expressed, it prevents IKK activation by a number of stimuli, including TNF and IL-1 ( 33).	bind
32638	1	9292	6	NULL	NULL	0	NULL	IKKgamma	NULL	truncated	bind	NULL		C-terminal		IKKalpha-IKKbeta heterodimers	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4547_s_43	10373503	A C-terminally truncated version of IKKgamma lacking the LZ can still bind IKKalpha-IKKbeta heterodimers, but once expressed, it prevents IKK activation by a number of stimuli, including TNF and IL-1 ( 33).	bind
32866	2	9292	6	NULL	NULL	0	NULL	TNF	NULL		stimulates	NULL				IKK	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4547_s_43	10373503	A C-terminally truncated version of IKKgamma lacking the LZ can still bind IKKalpha-IKKbeta heterodimers, but once expressed, it prevents IKK activation by a number of stimuli, including TNF and IL-1 ( 33).	bind
32867	3	9292	6	NULL	NULL	0	NULL	IL-1	NULL		stimulates	NULL				IKK	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4547_s_43	10373503	A C-terminally truncated version of IKKgamma lacking the LZ can still bind IKKalpha-IKKbeta heterodimers, but once expressed, it prevents IKK activation by a number of stimuli, including TNF and IL-1 ( 33).	bind
32868	4	9292	6	NULL	NULL	0	NULL	IKKgamma	NULL	expression of;; truncated	prevents	NULL		C-terminal		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4547_s_43	10373503	A C-terminally truncated version of IKKgamma lacking the LZ can still bind IKKalpha-IKKbeta heterodimers, but once expressed, it prevents IKK activation by a number of stimuli, including TNF and IL-1 ( 33).	bind
32869	5	9292	6	NULL	NULL	0	NULL	IKKgamma	NULL	expression of;; truncated	prevents	NULL		C-terminal		statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4547_s_43	10373503	A C-terminally truncated version of IKKgamma lacking the LZ can still bind IKKalpha-IKKbeta heterodimers, but once expressed, it prevents IKK activation by a number of stimuli, including TNF and IL-1 ( 33).	bind
48094	6	9292	6	10	NULL	0	NULL	IKKgamma	NULL	truncated	lacks	NULL		C-terminal			NULL		LZ		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4547_s_43	10373503	A C-terminally truncated version of IKKgamma lacking the LZ can still bind IKKalpha-IKKbeta heterodimers, but once expressed, it prevents IKK activation by a number of stimuli, including TNF and IL-1 ( 33).	bind
40111	1	9293	5	13	NULL	NULL	NULL	C/EBP-like transcription factor	GP		bind									X2 region of early promoters	NULL		NULL	NULL	NULL	NULL	gw70_insectbiochemmolbiol_33_5_525_s_211	12706632	A C/EBP-like transcription factor binds to the X2 region of early promoters	bind
32639	1	9293	6	NULL	NULL	0	NULL	C/EBP-like transcription factor	NULL		bind	NULL					NULL			X2 region of promoter	NULL		0	NULL	NULL	NULL	gw70_insectbiochemmolbiol_33_5_525_s_211	12706632	A C/EBP-like transcription factor binds to the X2 region of early promoters	bind
40112	1	9294	5	13	NULL	NULL	NULL	metalloid	Chemical		bind		high affinity			ArsA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_15_9925_s_26	16467301	A C113A/C422A mutation introduced into ArsA was found to eliminate high affinity metalloid binding to ArsA.	bind
40113	2	9294	5	13	NULL	NULL	NULL	ArsA	GP	mutant	prevents			C113A/C422A		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_15_9925_s_26	16467301	A C113A/C422A mutation introduced into ArsA was found to eliminate high affinity metalloid binding to ArsA.	bind
32641	1	9294	6	NULL	NULL	0	NULL	metalloid	NULL		bind	NULL	high affinity			ArsA	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_15_9925_s_26	16467301	A C113A/C422A mutation introduced into ArsA was found to eliminate high affinity metalloid binding to ArsA.	bind
32642	2	9294	6	NULL	NULL	0	NULL	ArsA	NULL	mutant	eliminates	NULL		C113A/C422A		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_15_9925_s_26	16467301	A C113A/C422A mutation introduced into ArsA was found to eliminate high affinity metalloid binding to ArsA.	bind
40114	1	9295	5	13	NULL	NULL	NULL	C3	GP		bind					HbhA	GP				NULL	cell lysates of M. tuberculosis	NULL	NULL	NULL	NULL	gw60_infectimmun_70_12_6751_s_254	12438350	A C3 ligand affinity blotting protocol was previously used by our group to demonstrate binding of C3 to HbhA present in cell lysates of  M. tuberculosis ( 20).	bind
32643	1	9295	6	NULL	NULL	0	NULL	C3	NULL		bind	NULL				HbhA	NULL				NULL	cell lysates of M. tuberculosis	0	NULL	NULL	NULL	gw60_infectimmun_70_12_6751_s_254	12438350	A C3 ligand affinity blotting protocol was previously used by our group to demonstrate binding of C3 to HbhA present in cell lysates of  M. tuberculosis ( 20).	bind
40115	1	9296	5	13	NULL	NULL	NULL	Ca-dependent receptor	GP		resemble					neurexin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_16_6113_s_16	9698306	A Ca-dependent receptor that resembles neurexin binds synaptotagmin, a putative Ca sensor (Petrenko et al., 1991  ; Ushkaryov et al., 1992  ); a Ca-independent receptor (CIRL/latrophilin) (Davletov et al., 1996  ; Krasnoperov et al., 1996  ) that resembles members of a family of G-protein-coupled membrane receptors binds to syntaxin, a putative component of the vesicle-docking complex (Bennett and Scheller, 1994  ).	bind
40116	2	9296	5	13	NULL	NULL	NULL	statement 1	GP		bind					synaptotagmin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_16_6113_s_16	9698306	A Ca-dependent receptor that resembles neurexin binds synaptotagmin, a putative Ca sensor (Petrenko et al., 1991  ; Ushkaryov et al., 1992  ); a Ca-independent receptor (CIRL/latrophilin) (Davletov et al., 1996  ; Krasnoperov et al., 1996  ) that resembles members of a family of G-protein-coupled membrane receptors binds to syntaxin, a putative component of the vesicle-docking complex (Bennett and Scheller, 1994  ).	bind
40117	3	9296	5	13	NULL	NULL	NULL	synaptotagmin	GP		is a type of					Ca sensor	GP	putative			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_16_6113_s_16	9698306	A Ca-dependent receptor that resembles neurexin binds synaptotagmin, a putative Ca sensor (Petrenko et al., 1991  ; Ushkaryov et al., 1992  ); a Ca-independent receptor (CIRL/latrophilin) (Davletov et al., 1996  ; Krasnoperov et al., 1996  ) that resembles members of a family of G-protein-coupled membrane receptors binds to syntaxin, a putative component of the vesicle-docking complex (Bennett and Scheller, 1994  ).	bind
40118	4	9296	5	13	NULL	NULL	NULL	CIRL/latrophilin	GP		resemble					 G-protein-coupled membrane receptors	GP	members of;;family of			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_16_6113_s_16	9698306	A Ca-dependent receptor that resembles neurexin binds synaptotagmin, a putative Ca sensor (Petrenko et al., 1991  ; Ushkaryov et al., 1992  ); a Ca-independent receptor (CIRL/latrophilin) (Davletov et al., 1996  ; Krasnoperov et al., 1996  ) that resembles members of a family of G-protein-coupled membrane receptors binds to syntaxin, a putative component of the vesicle-docking complex (Bennett and Scheller, 1994  ).	bind
40119	5	9296	5	13	NULL	NULL	NULL	CIRL/latrophilin	GP		is a type of					Ca-independent receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_16_6113_s_16	9698306	A Ca-dependent receptor that resembles neurexin binds synaptotagmin, a putative Ca sensor (Petrenko et al., 1991  ; Ushkaryov et al., 1992  ); a Ca-independent receptor (CIRL/latrophilin) (Davletov et al., 1996  ; Krasnoperov et al., 1996  ) that resembles members of a family of G-protein-coupled membrane receptors binds to syntaxin, a putative component of the vesicle-docking complex (Bennett and Scheller, 1994  ).	bind
40120	6	9296	5	13	NULL	NULL	NULL	CIRL/latrophilin	GP		bind					syntaxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_16_6113_s_16	9698306	A Ca-dependent receptor that resembles neurexin binds synaptotagmin, a putative Ca sensor (Petrenko et al., 1991  ; Ushkaryov et al., 1992  ); a Ca-independent receptor (CIRL/latrophilin) (Davletov et al., 1996  ; Krasnoperov et al., 1996  ) that resembles members of a family of G-protein-coupled membrane receptors binds to syntaxin, a putative component of the vesicle-docking complex (Bennett and Scheller, 1994  ).	bind
40121	7	9296	5	13	NULL	NULL	NULL	syntaxin	GP		is a component of		putative			vesicle-docking complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_16_6113_s_16	9698306	A Ca-dependent receptor that resembles neurexin binds synaptotagmin, a putative Ca sensor (Petrenko et al., 1991  ; Ushkaryov et al., 1992  ); a Ca-independent receptor (CIRL/latrophilin) (Davletov et al., 1996  ; Krasnoperov et al., 1996  ) that resembles members of a family of G-protein-coupled membrane receptors binds to syntaxin, a putative component of the vesicle-docking complex (Bennett and Scheller, 1994  ).	bind
32646	1	9296	6	NULL	NULL	0	NULL	Ca-dependent receptor	NULL		resembles	NULL				neurexin	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_16_6113_s_16	9698306	A Ca-dependent receptor that resembles neurexin binds synaptotagmin, a putative Ca sensor (Petrenko et al., 1991  ; Ushkaryov et al., 1992  ); a Ca-independent receptor (CIRL/latrophilin) (Davletov et al., 1996  ; Krasnoperov et al., 1996  ) that resembles members of a family of G-protein-coupled membrane receptors binds to syntaxin, a putative component of the vesicle-docking complex (Bennett and Scheller, 1994  ).	bind
32647	2	9296	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				synaptotagmin	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_16_6113_s_16	9698306	A Ca-dependent receptor that resembles neurexin binds synaptotagmin, a putative Ca sensor (Petrenko et al., 1991  ; Ushkaryov et al., 1992  ); a Ca-independent receptor (CIRL/latrophilin) (Davletov et al., 1996  ; Krasnoperov et al., 1996  ) that resembles members of a family of G-protein-coupled membrane receptors binds to syntaxin, a putative component of the vesicle-docking complex (Bennett and Scheller, 1994  ).	bind
32649	3	9296	6	NULL	NULL	0	NULL	synaptotagmin	NULL		is a type of	NULL				Ca sensor	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_16_6113_s_16	9698306	A Ca-dependent receptor that resembles neurexin binds synaptotagmin, a putative Ca sensor (Petrenko et al., 1991  ; Ushkaryov et al., 1992  ); a Ca-independent receptor (CIRL/latrophilin) (Davletov et al., 1996  ; Krasnoperov et al., 1996  ) that resembles members of a family of G-protein-coupled membrane receptors binds to syntaxin, a putative component of the vesicle-docking complex (Bennett and Scheller, 1994  ).	bind
32650	4	9296	6	NULL	NULL	0	NULL	CIRL/latrophilin	NULL		bind	NULL				syntaxin	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_16_6113_s_16	9698306	A Ca-dependent receptor that resembles neurexin binds synaptotagmin, a putative Ca sensor (Petrenko et al., 1991  ; Ushkaryov et al., 1992  ); a Ca-independent receptor (CIRL/latrophilin) (Davletov et al., 1996  ; Krasnoperov et al., 1996  ) that resembles members of a family of G-protein-coupled membrane receptors binds to syntaxin, a putative component of the vesicle-docking complex (Bennett and Scheller, 1994  ).	bind
32651	5	9296	6	NULL	NULL	0	NULL	CIRL/latrophilin	NULL		is a type of	NULL				Ca-independent receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_16_6113_s_16	9698306	A Ca-dependent receptor that resembles neurexin binds synaptotagmin, a putative Ca sensor (Petrenko et al., 1991  ; Ushkaryov et al., 1992  ); a Ca-independent receptor (CIRL/latrophilin) (Davletov et al., 1996  ; Krasnoperov et al., 1996  ) that resembles members of a family of G-protein-coupled membrane receptors binds to syntaxin, a putative component of the vesicle-docking complex (Bennett and Scheller, 1994  ).	bind
32652	6	9296	6	10	NULL	0	NULL	CIRL/latrophilin	NULL		resembles	NULL				 G-protein-coupled membrane receptors	NULL	members of ;;family of			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_16_6113_s_16	9698306	A Ca-dependent receptor that resembles neurexin binds synaptotagmin, a putative Ca sensor (Petrenko et al., 1991  ; Ushkaryov et al., 1992  ); a Ca-independent receptor (CIRL/latrophilin) (Davletov et al., 1996  ; Krasnoperov et al., 1996  ) that resembles members of a family of G-protein-coupled membrane receptors binds to syntaxin, a putative component of the vesicle-docking complex (Bennett and Scheller, 1994  ).	bind
32653	7	9296	6	NULL	NULL	0	NULL	Syntaxin	NULL		is a component of	NULL	putative			vesicle-docking complex	NULL	 			NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_16_6113_s_16	9698306	A Ca-dependent receptor that resembles neurexin binds synaptotagmin, a putative Ca sensor (Petrenko et al., 1991  ; Ushkaryov et al., 1992  ); a Ca-independent receptor (CIRL/latrophilin) (Davletov et al., 1996  ; Krasnoperov et al., 1996  ) that resembles members of a family of G-protein-coupled membrane receptors binds to syntaxin, a putative component of the vesicle-docking complex (Bennett and Scheller, 1994  ).	bind
40122	1	9297	5	13	NULL	NULL	NULL	EGFC	GP		is a part of		probably	Ca2+-requiring Site in catalytic domain					substrate recognition site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1855_s_323	11707438	A Ca2+-requiring Site in the EGFC-catalytic Domain Is Probably Part of the Substrate Recognition Site-- Direct measurement of stoichiometry by equilibrium dialysis measurements showed two C6PS binding sites in GDFXa in the presence of Ca2+ and none in the absence of Ca2+	bind
40123	2	9297	5	13	NULL	NULL	NULL	GDFXa	GP		contains								C6PS binding sites		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1855_s_323	11707438	A Ca2+-requiring Site in the EGFC-catalytic Domain Is Probably Part of the Substrate Recognition Site-- Direct measurement of stoichiometry by equilibrium dialysis measurements showed two C6PS binding sites in GDFXa in the presence of Ca2+ and none in the absence of Ca2+	bind
40124	3	9297	5	13	NULL	NULL	NULL	statement 2	Process		in the presence of					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1855_s_323	11707438	A Ca2+-requiring Site in the EGFC-catalytic Domain Is Probably Part of the Substrate Recognition Site-- Direct measurement of stoichiometry by equilibrium dialysis measurements showed two C6PS binding sites in GDFXa in the presence of Ca2+ and none in the absence of Ca2+	bind
40125	4	9297	5	13	NULL	NULL	NULL	GDFXa	GP		does not contain								C6PS binding sites		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1855_s_323	11707438	A Ca2+-requiring Site in the EGFC-catalytic Domain Is Probably Part of the Substrate Recognition Site-- Direct measurement of stoichiometry by equilibrium dialysis measurements showed two C6PS binding sites in GDFXa in the presence of Ca2+ and none in the absence of Ca2+	bind
40126	5	9297	5	13	NULL	NULL	NULL	statement 4	Process		in the absence of					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1855_s_323	11707438	A Ca2+-requiring Site in the EGFC-catalytic Domain Is Probably Part of the Substrate Recognition Site-- Direct measurement of stoichiometry by equilibrium dialysis measurements showed two C6PS binding sites in GDFXa in the presence of Ca2+ and none in the absence of Ca2+	bind
48095	1	9299	5	13	NULL	NULL	NULL	calcium ion	Chemical		bind					 ADAM33	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2388_s_67	16688218	A calcium ion and a water molecule bound to ADAM33 are represented as green and red  spheres, respectively.	bind
48096	2	9299	5	13	NULL	NULL	NULL	water molecule	Chemical		bind					ADAM33	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2388_s_67	16688218	A calcium ion and a water molecule bound to ADAM33 are represented as green and red  spheres, respectively.	bind
32654	1	9299	6	NULL	NULL	0	NULL	calcium ion	NULL		bind	NULL				ADAM33	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_25_11_2388_s_67	16688218	A calcium ion and a water molecule bound to ADAM33 are represented as green and red  spheres, respectively.	bind
32655	2	9299	6	NULL	NULL	0	NULL	water molecule	NULL		bind	NULL				ADAM33	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_25_11_2388_s_67	16688218	A calcium ion and a water molecule bound to ADAM33 are represented as green and red  spheres, respectively.	bind
40127	2	9300	5	13	NULL	NULL	NULL	statement 1	Process		activates					calcineurin phosphatase	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_3_907_s_28	15657420	A calcium-mediated signaling pathway is involved to activate the calcineurin phosphatase, which binds to the conserved NH2-terminal NFAT homology domain and dephosphorylates NFAT.	bind
40128	4	9300	5	13	NULL	NULL	NULL	calcineurin phosphatase	GP		bind							conserved	NH2-terminal NFAT homology domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_3_907_s_28	15657420	A calcium-mediated signaling pathway is involved to activate the calcineurin phosphatase, which binds to the conserved NH2-terminal NFAT homology domain and dephosphorylates NFAT.	bind
40129	3	9300	5	13	NULL	NULL	NULL	statement 2	Process		dephosphorylates					NFAT	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_3_907_s_28	15657420	A calcium-mediated signaling pathway is involved to activate the calcineurin phosphatase, which binds to the conserved NH2-terminal NFAT homology domain and dephosphorylates NFAT.	bind
48102	1	9300	5	13	NULL	NULL	NULL	calcium	Chemical		mediates					signaling pathway	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_3_907_s_28	15657420	A calcium-mediated signaling pathway is involved to activate the calcineurin phosphatase, which binds to the conserved NH2-terminal NFAT homology domain and dephosphorylates NFAT.	bind
32656	1	9300	6	NULL	NULL	0	NULL	calcineurin phosphatase	NULL		bind	NULL					NULL	conserved	NH2-terminal NFAT homology domain		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_3_907_s_28	15657420	A calcium-mediated signaling pathway is involved to activate the calcineurin phosphatase, which binds to the conserved NH2-terminal NFAT homology domain and dephosphorylates NFAT.	bind
32657	2	9300	6	NULL	NULL	0	NULL	calcineurin phosphatase	NULL		dephosphorylates	NULL				NFAT	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_3_907_s_28	15657420	A calcium-mediated signaling pathway is involved to activate the calcineurin phosphatase, which binds to the conserved NH2-terminal NFAT homology domain and dephosphorylates NFAT.	bind
32658	4	9300	6	10	NULL	0	NULL	statement 3	NULL		is involved in	NULL				calcineurin phosphatase	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_3_907_s_28	15657420	A calcium-mediated signaling pathway is involved to activate the calcineurin phosphatase, which binds to the conserved NH2-terminal NFAT homology domain and dephosphorylates NFAT.	bind
48103	3	9300	6	10	NULL	0	NULL	calcium	NULL		mediates	NULL				signaling pathway	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_3_907_s_28	15657420	A calcium-mediated signaling pathway is involved to activate the calcineurin phosphatase, which binds to the conserved NH2-terminal NFAT homology domain and dephosphorylates NFAT.	bind
40130	1	9301	5	13	NULL	NULL	NULL	RyR	GP		increase			calmodulin binding domain		spontaneous Ca2+ sparks	Process	activation of			NULL	frog skeletal muscle	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_12_11713_s_1	15640144	A calmodulin binding domain of RyR increases activation of spontaneous Ca2+ sparks in frog skeletal muscle.	bind
32659	1	9301	6	NULL	NULL	0	NULL	RyR	NULL		increases	NULL		calmodulin binding domain		Ca2+ sparks	NULL	activation of 			NULL	frog skeletal muscle	0	NULL	NULL	NULL	gw70_jbiolchem_280_12_11713_s_1	15640144	A calmodulin binding domain of RyR increases activation of spontaneous Ca2+ sparks in frog skeletal muscle.	bind
40131	2	9302	5	13	NULL	NULL	NULL	statement 1	GP		is important for					Ca2+-dependent inactivation	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_477_3_161_s_11	10908714	A calmodulin binding IQ region (1624-1635) within the K-motif has been shown to be important for Ca2+-dependent inactivation [  14,   15 and   16].	bind
48104	1	9302	5	10	NULL	0	NULL		NULL		is located within	NULL		calmodulin binding IQ region (1624-1635)			NULL		K-motif		NULL		0	NULL	NULL	NULL	gw60_febslett_477_3_161_s_11	10908714	A calmodulin binding IQ region (1624-1635) within the K-motif has been shown to be important for Ca2+-dependent inactivation [  14,   15 and   16].	bind
32660	1	9302	6	NULL	NULL	0	NULL		NULL		is located within	NULL		calmodulin binding IQ region (1624-1635)			NULL		K-motif		NULL		0	NULL	NULL	NULL	gw60_febslett_477_3_161_s_11	10908714	A calmodulin binding IQ region (1624-1635) within the K-motif has been shown to be important for Ca2+-dependent inactivation [  14,   15 and   16].	bind
32661	2	9302	6	10	NULL	0	NULL	statement 1			is important for					Ca2+-dependent inactivation					NULL		NULL	NULL	NULL	NULL	gw60_febslett_477_3_161_s_11	10908714	A calmodulin binding IQ region (1624-1635) within the K-motif has been shown to be important for Ca2+-dependent inactivation [  14,   15 and   16].	bind
40132	1	9304	5	13	NULL	NULL	NULL	NE-dlg/SAP102	GP		forms			calmodulin-binding region					basic amphiphilic alpha-helix		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_9_5782_s_35	10026200	A calmodulin-binding region of NE-dlg/SAP102 is predicted to form a basic amphiphilic alpha-helix, which was reported as a calmodulin-binding structure.	bind
40133	2	9304	5	13	NULL	NULL	NULL	basic amphiphilic alpha-helix	GP		is a type of					calmodulin-binding structure	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_9_5782_s_35	10026200	A calmodulin-binding region of NE-dlg/SAP102 is predicted to form a basic amphiphilic alpha-helix, which was reported as a calmodulin-binding structure.	bind
48105	1	9304	6	10	NULL	0	NULL	NE-dlg/SAP102	NULL		forms	NULL		calmodulin-binding region			NULL		basic amphiphilic alpha-helix		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5782_s_35	10026200	A calmodulin-binding region of NE-dlg/SAP102 is predicted to form a basic amphiphilic alpha-helix, which was reported as a calmodulin-binding structure.	bind
48106	2	9304	6	10	NULL	0	NULL	basic amphiphilic alpha-helix	NULL		is a type of	NULL				calmodulin-binding structure	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5782_s_35	10026200	A calmodulin-binding region of NE-dlg/SAP102 is predicted to form a basic amphiphilic alpha-helix, which was reported as a calmodulin-binding structure.	bind
40134	1	9305	5	13	NULL	NULL	NULL	calponin	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20400_s_7	7657614	A calponin peptide (calponin  Phe  -Arg  ), which inhibits the binding of  calponin to actin, blocks the action of calponin and enhances the  contraction induced by submaximal Ca  in permeabilized  vascular smooth muscle.	bind
40135	2	9305	5	13	NULL	NULL	NULL	calponin peptide	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20400_s_7	7657614	A calponin peptide (calponin  Phe  -Arg  ), which inhibits the binding of  calponin to actin, blocks the action of calponin and enhances the  contraction induced by submaximal Ca  in permeabilized  vascular smooth muscle.	bind
40136	3	9305	5	13	NULL	NULL	NULL	calponin peptide	GP		is					calponin Phe -Arg	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20400_s_7	7657614	A calponin peptide (calponin  Phe  -Arg  ), which inhibits the binding of  calponin to actin, blocks the action of calponin and enhances the  contraction induced by submaximal Ca  in permeabilized  vascular smooth muscle.	bind
40137	4	9305	5	13	NULL	NULL	NULL	calponin peptide	GP		block					calponin	GP	action of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20400_s_7	7657614	A calponin peptide (calponin  Phe  -Arg  ), which inhibits the binding of  calponin to actin, blocks the action of calponin and enhances the  contraction induced by submaximal Ca  in permeabilized  vascular smooth muscle.	bind
40138	5	9305	5	13	NULL	NULL	NULL	Ca	Chemical	submaximal	induce					contraction	Process				NULL	permeabilized vascular smooth muscle	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20400_s_7	7657614	A calponin peptide (calponin  Phe  -Arg  ), which inhibits the binding of  calponin to actin, blocks the action of calponin and enhances the  contraction induced by submaximal Ca  in permeabilized  vascular smooth muscle.	bind
40139	6	9305	5	13	NULL	NULL	NULL	calponin peptide	GP		enhance					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20400_s_7	7657614	A calponin peptide (calponin  Phe  -Arg  ), which inhibits the binding of  calponin to actin, blocks the action of calponin and enhances the  contraction induced by submaximal Ca  in permeabilized  vascular smooth muscle.	bind
32707	1	9305	6	NULL	NULL	0	NULL	calponin	NULL		bind	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20400_s_7	7657614	A calponin peptide (calponin  Phe  -Arg  ), which inhibits the binding of  calponin to actin, blocks the action of calponin and enhances the  contraction induced by submaximal Ca  in permeabilized  vascular smooth muscle.	bind
32708	2	9305	6	NULL	NULL	0	NULL	calponin peptide	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20400_s_7	7657614	A calponin peptide (calponin  Phe  -Arg  ), which inhibits the binding of  calponin to actin, blocks the action of calponin and enhances the  contraction induced by submaximal Ca  in permeabilized  vascular smooth muscle.	bind
32709	3	9305	6	NULL	NULL	0	NULL	calponin peptide	NULL		is	NULL				calponin Phe -Arg	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20400_s_7	7657614	A calponin peptide (calponin  Phe  -Arg  ), which inhibits the binding of  calponin to actin, blocks the action of calponin and enhances the  contraction induced by submaximal Ca  in permeabilized  vascular smooth muscle.	bind
32710	4	9305	6	NULL	NULL	0	NULL	calponin peptide	NULL		blocks 	NULL				calponin	NULL	action of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20400_s_7	7657614	A calponin peptide (calponin  Phe  -Arg  ), which inhibits the binding of  calponin to actin, blocks the action of calponin and enhances the  contraction induced by submaximal Ca  in permeabilized  vascular smooth muscle.	bind
32711	5	9305	6	NULL	NULL	0	NULL	Ca	NULL	submaximal	induces	NULL				contraction	NULL				NULL	permeabilized vascular smooth muscle	0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20400_s_7	7657614	A calponin peptide (calponin  Phe  -Arg  ), which inhibits the binding of  calponin to actin, blocks the action of calponin and enhances the  contraction induced by submaximal Ca  in permeabilized  vascular smooth muscle.	bind
32712	6	9305	6	NULL	NULL	0	NULL	calponin peptide	NULL		enhances	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20400_s_7	7657614	A calponin peptide (calponin  Phe  -Arg  ), which inhibits the binding of  calponin to actin, blocks the action of calponin and enhances the  contraction induced by submaximal Ca  in permeabilized  vascular smooth muscle.	bind
40140	1	9306	5	13	NULL	NULL	NULL	CaMKK	GP	pig brain	phosphorylate					AMPK	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_32_29060_s_87	15980064	A CaMKK preparation from pig brain (isolated prior to the recognition that there were two isoforms of the enzyme) has previously been shown to phosphorylate and activate AMPK  in vitro; this phosphorylation is enhanced by the binding of AMP to the AMPK heterotrimer ( ).	bind
40141	2	9306	5	13	NULL	NULL	NULL	statement 1	Process		activates					AMPK	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_32_29060_s_87	15980064	A CaMKK preparation from pig brain (isolated prior to the recognition that there were two isoforms of the enzyme) has previously been shown to phosphorylate and activate AMPK  in vitro; this phosphorylation is enhanced by the binding of AMP to the AMPK heterotrimer ( ).	bind
40142	3	9306	5	13	NULL	NULL	NULL	AMP	Chemical		bind					AMPK heterotrimer	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_32_29060_s_87	15980064	A CaMKK preparation from pig brain (isolated prior to the recognition that there were two isoforms of the enzyme) has previously been shown to phosphorylate and activate AMPK  in vitro; this phosphorylation is enhanced by the binding of AMP to the AMPK heterotrimer ( ).	bind
40143	4	9306	5	13	NULL	NULL	NULL	statement 3	Process		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_32_29060_s_87	15980064	A CaMKK preparation from pig brain (isolated prior to the recognition that there were two isoforms of the enzyme) has previously been shown to phosphorylate and activate AMPK  in vitro; this phosphorylation is enhanced by the binding of AMP to the AMPK heterotrimer ( ).	bind
32979	1	9306	6	NULL	NULL	0	NULL	AMP	NULL		bind	NULL				AMPK heterotrimer	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_32_29060_s_87	15980064	A CaMKK preparation from pig brain (isolated prior to the recognition that there were two isoforms of the enzyme) has previously been shown to phosphorylate and activate AMPK  in vitro; this phosphorylation is enhanced by the binding of AMP to the AMPK heterotrimer ( ).	bind
32980	2	9306	6	NULL	NULL	0	NULL	CaMKK	NULL	pig brain	phosphorylate	NULL				AMPK	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw70_jbiolchem_280_32_29060_s_87	15980064	A CaMKK preparation from pig brain (isolated prior to the recognition that there were two isoforms of the enzyme) has previously been shown to phosphorylate and activate AMPK  in vitro; this phosphorylation is enhanced by the binding of AMP to the AMPK heterotrimer ( ).	bind
32981	3	9306	6	NULL	NULL	0	NULL	CaMKK	NULL	pig brain	activate	NULL				AMPK	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw70_jbiolchem_280_32_29060_s_87	15980064	A CaMKK preparation from pig brain (isolated prior to the recognition that there were two isoforms of the enzyme) has previously been shown to phosphorylate and activate AMPK  in vitro; this phosphorylation is enhanced by the binding of AMP to the AMPK heterotrimer ( ).	bind
32982	4	9306	6	NULL	NULL	0	NULL	statement 1	NULL		enhances	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_32_29060_s_87	15980064	A CaMKK preparation from pig brain (isolated prior to the recognition that there were two isoforms of the enzyme) has previously been shown to phosphorylate and activate AMPK  in vitro; this phosphorylation is enhanced by the binding of AMP to the AMPK heterotrimer ( ).	bind
40144	1	9307	5	13	NULL	NULL	NULL				is present 				cAMP response element	immediate early genes	GP	upstream of 			NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_111_1_1_s_112	12654499	A cAMP response element can  be found upstream of the immediate early genes [  21], and this DNA region is bound by the phosphorylated form of CREB [ 6.	bind
40145	2	9307	5	13	NULL	NULL	NULL	CREB	GP	phosphorylated	bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_111_1_1_s_112	12654499	A cAMP response element can  be found upstream of the immediate early genes [  21], and this DNA region is bound by the phosphorylated form of CREB [ 6.	bind
32983	2	9307	6	10	NULL	0	NULL	statement 1	NULL		bind	NULL				CREB	NULL	phosphorylated form of			NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_111_1_1_s_112	12654499	A cAMP response element can  be found upstream of the immediate early genes [  21], and this DNA region is bound by the phosphorylated form of CREB [ 6.	bind
48107	1	9307	6	10	NULL	0	NULL		NULL		is present	NULL			cAMP response element	immediate early genes	NULL	upstream of			NULL		NULL	NULL	NULL	NULL	gw70_brainresmolbrainres_111_1_1_s_112	12654499	A cAMP response element can  be found upstream of the immediate early genes [  21], and this DNA region is bound by the phosphorylated form of CREB [ 6.	bind
40146	1	9309	5	13	NULL	NULL	NULL				undergoes			subunit IV		phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_466_1_130_s_74	10648827	A cAMP-independent phosphorylation of subunit IV, to which ATP binds and induces the allosteric ATP-inhibition [ 4, has been described by Steenaart and Shore [ 11].	bind
40147	2	9309	5	13	NULL	NULL	NULL	statement 1	Process		is independent of					cAMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_466_1_130_s_74	10648827	A cAMP-independent phosphorylation of subunit IV, to which ATP binds and induces the allosteric ATP-inhibition [ 4, has been described by Steenaart and Shore [ 11].	bind
40148	3	9309	5	13	NULL	NULL	NULL	ATP	Chemical		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_466_1_130_s_74	10648827	A cAMP-independent phosphorylation of subunit IV, to which ATP binds and induces the allosteric ATP-inhibition [ 4, has been described by Steenaart and Shore [ 11].	bind
40149	4	9309	5	13	NULL	NULL	NULL	statement 3	Process		induce					ATP	Chemical	allosteric inhibition of			NULL		NULL	NULL	NULL	NULL	gw60_febslett_466_1_130_s_74	10648827	A cAMP-independent phosphorylation of subunit IV, to which ATP binds and induces the allosteric ATP-inhibition [ 4, has been described by Steenaart and Shore [ 11].	bind
32984	1	9309	6	10	NULL	0	NULL			phosphorylated	bind			subunit IV		ATP					NULL		NULL	NULL	NULL	NULL	gw60_febslett_466_1_130_s_74	10648827	A cAMP-independent phosphorylation of subunit IV, to which ATP binds and induces the allosteric ATP-inhibition [ 4, has been described by Steenaart and Shore [ 11].	bind
32985	2	9309	6	10	NULL	0	NULL				induces			subunit IV		ATP		allosteric;; inhibition of 			NULL		NULL	NULL	NULL	NULL	gw60_febslett_466_1_130_s_74	10648827	A cAMP-independent phosphorylation of subunit IV, to which ATP binds and induces the allosteric ATP-inhibition [ 4, has been described by Steenaart and Shore [ 11].	bind
32986	3	9309	6	10	NULL	0	NULL			phosphorylation of	is independent of			subunit IV		cAMP					NULL		NULL	NULL	NULL	NULL	gw60_febslett_466_1_130_s_74	10648827	A cAMP-independent phosphorylation of subunit IV, to which ATP binds and induces the allosteric ATP-inhibition [ 4, has been described by Steenaart and Shore [ 11].	bind
40150	1	9310	5	13	NULL	NULL	NULL	ABL kinase inhibitor	GP		bind								SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_32_19585_s_19	8702653	A candidate ABL kinase inhibitor that binds to the SH3 domain has been purified, and this protein exhibits GTPase-activating protein homology, implying that ABL may interact with the ras related proteins ( 19).	bind
40151	2	9310	5	13	NULL	NULL	NULL	ABL kinase inhibitor	GP		is homologous to					GTPase-activating protein 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_32_19585_s_19	8702653	A candidate ABL kinase inhibitor that binds to the SH3 domain has been purified, and this protein exhibits GTPase-activating protein homology, implying that ABL may interact with the ras related proteins ( 19).	bind
40152	3	9310	5	13	NULL	NULL	NULL	ABL	GP		interact with		may			ras related proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_32_19585_s_19	8702653	A candidate ABL kinase inhibitor that binds to the SH3 domain has been purified, and this protein exhibits GTPase-activating protein homology, implying that ABL may interact with the ras related proteins ( 19).	bind
40153	4	9310	5	13	NULL	NULL	NULL	statement 2	Process		implies					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_32_19585_s_19	8702653	A candidate ABL kinase inhibitor that binds to the SH3 domain has been purified, and this protein exhibits GTPase-activating protein homology, implying that ABL may interact with the ras related proteins ( 19).	bind
32987	1	9310	6	NULL	NULL	0	NULL	ABL kinase inhibitor	NULL		bind	NULL					NULL		SH3 domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_32_19585_s_19	8702653	A candidate ABL kinase inhibitor that binds to the SH3 domain has been purified, and this protein exhibits GTPase-activating protein homology, implying that ABL may interact with the ras related proteins ( 19).	bind
32988	2	9310	6	10	NULL	0	NULL	ABL kinase inhibitor	NULL		is homologous to	NULL				GTPase-activating protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_32_19585_s_19	8702653	A candidate ABL kinase inhibitor that binds to the SH3 domain has been purified, and this protein exhibits GTPase-activating protein homology, implying that ABL may interact with the ras related proteins ( 19).	bind
32989	3	9310	6	NULL	NULL	0	NULL	ABL	NULL		interacts with	NULL	may			ras related proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_32_19585_s_19	8702653	A candidate ABL kinase inhibitor that binds to the SH3 domain has been purified, and this protein exhibits GTPase-activating protein homology, implying that ABL may interact with the ras related proteins ( 19).	bind
32990	4	9310	6	NULL	NULL	0	NULL	statement 2	NULL		implies	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_32_19585_s_19	8702653	A candidate ABL kinase inhibitor that binds to the SH3 domain has been purified, and this protein exhibits GTPase-activating protein homology, implying that ABL may interact with the ras related proteins ( 19).	bind
40154	1	9311	5	13	NULL	NULL	NULL	 anchoring/targeting protein	GP		bind					PKC3	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_2_1130_s_15	9422779	A candidate anchoring/targeting protein, which binds PKC3  in vitro, has been identified.	bind
32991	1	9311	6	NULL	NULL	0	NULL	anchoring/targeting protein	NULL		bind	NULL				PKC3	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_273_2_1130_s_15	9422779	A candidate anchoring/targeting protein, which binds PKC3  in vitro, has been identified.	bind
40385	1	9312	5	13	NULL	NULL	NULL	mammalian homolog to Upf1p	GP	S. cerevisiae	is involved in					decay	Process	nonsense-mediated			NULL	S. cerevisiae	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5272_s_288	9710612	A candidate for such a factor could be the mammalian homolog to  S. cerevisiae Upf1p, a factor involved in nonsense-mediated decay in  S. cerevisiae that is characterized by RNA binding and helicase activities ( 44).	bind
40386	2	9312	5	13	NULL	NULL	NULL	mammalian homolog to Upf1p	GP	S. cerevisiae	bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5272_s_288	9710612	A candidate for such a factor could be the mammalian homolog to  S. cerevisiae Upf1p, a factor involved in nonsense-mediated decay in  S. cerevisiae that is characterized by RNA binding and helicase activities ( 44).	bind
40387	3	9312	5	13	NULL	NULL	NULL	statement 1	Process		is characterized by					helicase	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5272_s_288	9710612	A candidate for such a factor could be the mammalian homolog to  S. cerevisiae Upf1p, a factor involved in nonsense-mediated decay in  S. cerevisiae that is characterized by RNA binding and helicase activities ( 44).	bind
48108	4	9312	5	13	NULL	NULL	NULL	statement 1	Process		is characterized by					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5272_s_288	9710612	A candidate for such a factor could be the mammalian homolog to  S. cerevisiae Upf1p, a factor involved in nonsense-mediated decay in  S. cerevisiae that is characterized by RNA binding and helicase activities ( 44).	bind
33882	1	9312	6	10	NULL	0	NULL	mammalian homolog to Upf1p		 S. cerevisiae	is involved in					 decay		nonsense-mediated			NULL	S.cerevisiae	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5272_s_288	9710612	A candidate for such a factor could be the mammalian homolog to  S. cerevisiae Upf1p, a factor involved in nonsense-mediated decay in  S. cerevisiae that is characterized by RNA binding and helicase activities ( 44).	bind
33883	2	9312	6	10	NULL	0	NULL	mammalian homolog to Upf1p	NULL	 S. cerevisiae	bind	NULL				RNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5272_s_288	9710612	A candidate for such a factor could be the mammalian homolog to  S. cerevisiae Upf1p, a factor involved in nonsense-mediated decay in  S. cerevisiae that is characterized by RNA binding and helicase activities ( 44).	bind
33885	4	9312	6	NULL	NULL	0	NULL	statement 1	NULL		is characterized by	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_9_5272_s_288	9710612	A candidate for such a factor could be the mammalian homolog to  S. cerevisiae Upf1p, a factor involved in nonsense-mediated decay in  S. cerevisiae that is characterized by RNA binding and helicase activities ( 44).	bind
33886	3	9312	6	10	NULL	0	NULL	statement 1			is characterized by					helicase		activity of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5272_s_288	9710612	A candidate for such a factor could be the mammalian homolog to  S. cerevisiae Upf1p, a factor involved in nonsense-mediated decay in  S. cerevisiae that is characterized by RNA binding and helicase activities ( 44).	bind
40155	1	9313	5	13	NULL	NULL	NULL	heparin	Chemical		bind					P4n	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18421_s_341	11882649	A candidate for such a site is P4n-(110-128), and preliminary observations in our laboratory, not presented here, indicate that heparin binding of P4n is abrogated by Cu(II).	bind
40156	2	9313	5	13	NULL	NULL	NULL	Cu(II)	Chemical		abrogates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18421_s_341	11882649	A candidate for such a site is P4n-(110-128), and preliminary observations in our laboratory, not presented here, indicate that heparin binding of P4n is abrogated by Cu(II).	bind
32992	1	9313	6	NULL	NULL	0	NULL	heparin	NULL		bind	NULL				P4n	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18421_s_341	11882649	A candidate for such a site is P4n-(110-128), and preliminary observations in our laboratory, not presented here, indicate that heparin binding of P4n is abrogated by Cu(II).	bind
32993	2	9313	6	NULL	NULL	0	NULL	Cu(II)	NULL		abrogates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18421_s_341	11882649	A candidate for such a site is P4n-(110-128), and preliminary observations in our laboratory, not presented here, indicate that heparin binding of P4n is abrogated by Cu(II).	bind
40157	1	9314	5	13	NULL	NULL	NULL	beta3-endonexin	GP		contains								Tyr residue		NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_6_1651_s_234	10845885	A candidate is beta3-endonexin, which contains a Tyr residue and in Chinese hamster ovary cells binds to the beta3 cytoplasmic tail, thereby increasing ligand binding to alphaIIbbeta3.	bind
40158	2	9314	5	13	NULL	NULL	NULL	statement 1	GP		bind					beta3	GP		cytoplasmic tail		NULL	Chinese hamster ovary cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_6_1651_s_234	10845885	A candidate is beta3-endonexin, which contains a Tyr residue and in Chinese hamster ovary cells binds to the beta3 cytoplasmic tail, thereby increasing ligand binding to alphaIIbbeta3.	bind
40159	3	9314	5	13	NULL	NULL	NULL	ligand	GP		bind					alphaIIbbeta3	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_6_1651_s_234	10845885	A candidate is beta3-endonexin, which contains a Tyr residue and in Chinese hamster ovary cells binds to the beta3 cytoplasmic tail, thereby increasing ligand binding to alphaIIbbeta3.	bind
40160	4	9314	5	13	NULL	NULL	NULL	statement 2	Process		increase					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_6_1651_s_234	10845885	A candidate is beta3-endonexin, which contains a Tyr residue and in Chinese hamster ovary cells binds to the beta3 cytoplasmic tail, thereby increasing ligand binding to alphaIIbbeta3.	bind
32994	1	9314	6	10	NULL	0	NULL	beta3-endonexin	NULL		contains 	NULL				Tyr residue	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_6_1651_s_234	10845885	A candidate is beta3-endonexin, which contains a Tyr residue and in Chinese hamster ovary cells binds to the beta3 cytoplasmic tail, thereby increasing ligand binding to alphaIIbbeta3.	bind
32995	2	9314	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				beta3	NULL		cytoplasmic tail		NULL	Chinese hamster ovary cells	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_6_1651_s_234	10845885	A candidate is beta3-endonexin, which contains a Tyr residue and in Chinese hamster ovary cells binds to the beta3 cytoplasmic tail, thereby increasing ligand binding to alphaIIbbeta3.	bind
33004	3	9314	6	NULL	NULL	0	NULL	alphaIIbbeta3	NULL		bind	NULL				ligand	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_6_1651_s_234	10845885	A candidate is beta3-endonexin, which contains a Tyr residue and in Chinese hamster ovary cells binds to the beta3 cytoplasmic tail, thereby increasing ligand binding to alphaIIbbeta3.	bind
33005	4	9314	6	NULL	NULL	0	NULL	statement 2	NULL		increases	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_6_1651_s_234	10845885	A candidate is beta3-endonexin, which contains a Tyr residue and in Chinese hamster ovary cells binds to the beta3 cytoplasmic tail, thereby increasing ligand binding to alphaIIbbeta3.	bind
40161	1	9315	5	13	NULL	NULL	NULL	KIF-4	GP		is a type of					kinesin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_3_393_s_43	12427864	A candidate motor for this transport is KIF-4, a kinesin that can bind to the matrix protein of HIV and SIV ( Tang et al., 1999).	bind
40162	2	9315	5	13	NULL	NULL	NULL	KIF-4	GP		bind					matrix protein	GP	HIV			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_3_393_s_43	12427864	A candidate motor for this transport is KIF-4, a kinesin that can bind to the matrix protein of HIV and SIV ( Tang et al., 1999).	bind
40163	3	9315	5	13	NULL	NULL	NULL	KIF-4	GP		bind					matrix protein	GP	SIV			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_159_3_393_s_43	12427864	A candidate motor for this transport is KIF-4, a kinesin that can bind to the matrix protein of HIV and SIV ( Tang et al., 1999).	bind
33007	1	9315	6	NULL	NULL	0	NULL	KIF-4	NULL		is a type of	NULL				kinesin	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_159_3_393_s_43	12427864	A candidate motor for this transport is KIF-4, a kinesin that can bind to the matrix protein of HIV and SIV ( Tang et al., 1999).	bind
33008	2	9315	6	NULL	NULL	0	NULL	KIF-4	NULL		bind	NULL				matrix protein	NULL	HIV			NULL		0	NULL	NULL	NULL	gw60_cellbiol_159_3_393_s_43	12427864	A candidate motor for this transport is KIF-4, a kinesin that can bind to the matrix protein of HIV and SIV ( Tang et al., 1999).	bind
33010	3	9315	6	NULL	NULL	0	NULL	KIF-4	NULL		bind	NULL				matrix protein	NULL	SIV			NULL		0	NULL	NULL	NULL	gw60_cellbiol_159_3_393_s_43	12427864	A candidate motor for this transport is KIF-4, a kinesin that can bind to the matrix protein of HIV and SIV ( Tang et al., 1999).	bind
40164	2	9316	5	13	NULL	NULL	NULL	AP-2	GP		is a candidate of					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1635_2_104_s_353	14729073	A candidate of the PMA-responsive transcription factor that binds AP-2 site is, of  course, AP-2 [  42 and   43].	bind
40165	3	9316	5	13	NULL	NULL	NULL	AP-2	GP		bind									AP-2 site	NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1635_2_104_s_353	14729073	A candidate of the PMA-responsive transcription factor that binds AP-2 site is, of  course, AP-2 [  42 and   43].	bind
48109	1	9316	5	13	NULL	NULL	NULL	transcription factor	GP		respond to					PMA	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1635_2_104_s_353	14729073	A candidate of the PMA-responsive transcription factor that binds AP-2 site is, of  course, AP-2 [  42 and   43].	bind
33011	2	9316	6	10	NULL	0	NULL	AP-2			is a candidate of					statement 1					NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1635_2_104_s_353	14729073	A candidate of the PMA-responsive transcription factor that binds AP-2 site is, of  course, AP-2 [  42 and   43].	bind
33012	3	9316	6	10	NULL	0	NULL	AP-2	NULL		bind	NULL					NULL			AP-2 site	NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1635_2_104_s_353	14729073	A candidate of the PMA-responsive transcription factor that binds AP-2 site is, of  course, AP-2 [  42 and   43].	bind
48110	1	9316	6	10	NULL	0	NULL	transcription factor	NULL		respond to	NULL				PMA	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1635_2_104_s_353	14729073	A candidate of the PMA-responsive transcription factor that binds AP-2 site is, of  course, AP-2 [  42 and   43].	bind
40166	1	9317	5	13	NULL	NULL	NULL	 calmodulin	GP		activates					PI3K	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_7591_s_235	12488453	A candidate target protein for activation of PI3K by calmodulin is Ras because it has been reported that calmodulin can bind directly to Ras and modulate its downstream signaling ( 52).	bind
40167	2	9317	5	13	NULL	NULL	NULL	calmodulin	GP		bind		directly			Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_7591_s_235	12488453	A candidate target protein for activation of PI3K by calmodulin is Ras because it has been reported that calmodulin can bind directly to Ras and modulate its downstream signaling ( 52).	bind
40168	3	9317	5	13	NULL	NULL	NULL	statement 2	Process		modulates					Ras	GP	downstream signaling of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_7591_s_235	12488453	A candidate target protein for activation of PI3K by calmodulin is Ras because it has been reported that calmodulin can bind directly to Ras and modulate its downstream signaling ( 52).	bind
33013	1	9317	6	NULL	NULL	0	NULL	Calmodulin	NULL		bind	NULL	directly			Ras	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_7591_s_235	12488453	A candidate target protein for activation of PI3K by calmodulin is Ras because it has been reported that calmodulin can bind directly to Ras and modulate its downstream signaling ( 52).	bind
33015	2	9317	6	NULL	NULL	0	NULL	Calmodulin	NULL		activates	NULL				PI3K	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_7591_s_235	12488453	A candidate target protein for activation of PI3K by calmodulin is Ras because it has been reported that calmodulin can bind directly to Ras and modulate its downstream signaling ( 52).	bind
33016	3	9317	6	NULL	NULL	0	NULL	Calmodulin	NULL		modulates	NULL				Ras	NULL	downstream signaling of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_7591_s_235	12488453	A candidate target protein for activation of PI3K by calmodulin is Ras because it has been reported that calmodulin can bind directly to Ras and modulate its downstream signaling ( 52).	bind
40169	1	9318	5	13	NULL	NULL	NULL	Crb	GP		is a type of					 transmembrane protein	GP	epithelium			NULL		NULL	NULL	NULL	NULL	gw70_mechdev_120_11_1297_s_45	14623439	A candidate transmembrane protein in the epithelium is Crb, which  binds directly to the MAGUK protein Sdt ([ Bachmann et al., 2001,  Hong et al., 2001 and   Roh et al., 2002]).	bind
40170	2	9318	5	13	NULL	NULL	NULL	Crb	GP		bind		directly			Sdt	GP				NULL		NULL	NULL	NULL	NULL	gw70_mechdev_120_11_1297_s_45	14623439	A candidate transmembrane protein in the epithelium is Crb, which  binds directly to the MAGUK protein Sdt ([ Bachmann et al., 2001,  Hong et al., 2001 and   Roh et al., 2002]).	bind
40171	3	9318	5	13	NULL	NULL	NULL	Sdt	GP		is a type of					MAGUK	GP				NULL		NULL	NULL	NULL	NULL	gw70_mechdev_120_11_1297_s_45	14623439	A candidate transmembrane protein in the epithelium is Crb, which  binds directly to the MAGUK protein Sdt ([ Bachmann et al., 2001,  Hong et al., 2001 and   Roh et al., 2002]).	bind
33017	1	9318	6	NULL	NULL	0	NULL	Crb	NULL		bind	NULL	directly			Sdt	NULL				NULL		NULL	NULL	NULL	NULL	gw70_mechdev_120_11_1297_s_45	14623439	A candidate transmembrane protein in the epithelium is Crb, which  binds directly to the MAGUK protein Sdt ([ Bachmann et al., 2001,  Hong et al., 2001 and   Roh et al., 2002]).	bind
33018	2	9318	6	10	NULL	0	NULL	Crb	NULL		is a type of	NULL				transmembrane protein	NULL	epithelium			NULL		NULL	NULL	NULL	NULL	gw70_mechdev_120_11_1297_s_45	14623439	A candidate transmembrane protein in the epithelium is Crb, which  binds directly to the MAGUK protein Sdt ([ Bachmann et al., 2001,  Hong et al., 2001 and   Roh et al., 2002]).	bind
33021	3	9318	6	NULL	NULL	0	NULL	Sdt	NULL		is a type of	NULL				MAGUK protein	NULL				NULL		0	NULL	NULL	NULL	gw70_mechdev_120_11_1297_s_45	14623439	A candidate transmembrane protein in the epithelium is Crb, which  binds directly to the MAGUK protein Sdt ([ Bachmann et al., 2001,  Hong et al., 2001 and   Roh et al., 2002]).	bind
40186	1	9319	5	13	NULL	NULL	NULL				bind				Meg1 repeat	CTCF	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_120	12595547	A canonical CTCF-binding sequence from chicken beta- globin (FII) specifically competed CTCF binding to the  Meg1 repeat (lane indicated by competitor F), although the recognition sequences for the SP1 and AP1 transcription factors did not interfere with CTCF binding (lanes indicated by competitors S and A).	bind
40187	2	9319	5	13	NULL	NULL	NULL	beta- globin (FII)	GP	chicken	bind				canonical CTCF-binding sequence					Meg1 repeat	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_120	12595547	A canonical CTCF-binding sequence from chicken beta- globin (FII) specifically competed CTCF binding to the  Meg1 repeat (lane indicated by competitor F), although the recognition sequences for the SP1 and AP1 transcription factors did not interfere with CTCF binding (lanes indicated by competitors S and A).	bind
40188	3	9319	5	13	NULL	NULL	NULL	statement 2	Process		competes with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_120	12595547	A canonical CTCF-binding sequence from chicken beta- globin (FII) specifically competed CTCF binding to the  Meg1 repeat (lane indicated by competitor F), although the recognition sequences for the SP1 and AP1 transcription factors did not interfere with CTCF binding (lanes indicated by competitors S and A).	bind
40189	4	9319	5	13	NULL	NULL	NULL	SP1	GP		does not interfere with				recognition sequences	CTCF	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_120	12595547	A canonical CTCF-binding sequence from chicken beta- globin (FII) specifically competed CTCF binding to the  Meg1 repeat (lane indicated by competitor F), although the recognition sequences for the SP1 and AP1 transcription factors did not interfere with CTCF binding (lanes indicated by competitors S and A).	bind
40190	5	9319	5	13	NULL	NULL	NULL	AP1	GP		does not interfere with				recognition sequences	CTCF	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_120	12595547	A canonical CTCF-binding sequence from chicken beta- globin (FII) specifically competed CTCF binding to the  Meg1 repeat (lane indicated by competitor F), although the recognition sequences for the SP1 and AP1 transcription factors did not interfere with CTCF binding (lanes indicated by competitors S and A).	bind
40191	6	9319	5	13	NULL	NULL	NULL	AP1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_120	12595547	A canonical CTCF-binding sequence from chicken beta- globin (FII) specifically competed CTCF binding to the  Meg1 repeat (lane indicated by competitor F), although the recognition sequences for the SP1 and AP1 transcription factors did not interfere with CTCF binding (lanes indicated by competitors S and A).	bind
40192	7	9319	5	13	NULL	NULL	NULL	SP1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_120	12595547	A canonical CTCF-binding sequence from chicken beta- globin (FII) specifically competed CTCF binding to the  Meg1 repeat (lane indicated by competitor F), although the recognition sequences for the SP1 and AP1 transcription factors did not interfere with CTCF binding (lanes indicated by competitors S and A).	bind
33087	1	9319	6	NULL	NULL	0	NULL	CTCF	NULL		bind	NULL					NULL			Meg1 repeat	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_120	12595547	A canonical CTCF-binding sequence from chicken beta- globin (FII) specifically competed CTCF binding to the  Meg1 repeat (lane indicated by competitor F), although the recognition sequences for the SP1 and AP1 transcription factors did not interfere with CTCF binding (lanes indicated by competitors S and A).	bind
33887	2	9319	6	NULL	NULL	0	NULL	beta- globin (FII)	NULL	chicken	bind	NULL			CTCF-binding sequence		NULL			Meg1 repeat	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_120	12595547	A canonical CTCF-binding sequence from chicken beta- globin (FII) specifically competed CTCF binding to the  Meg1 repeat (lane indicated by competitor F), although the recognition sequences for the SP1 and AP1 transcription factors did not interfere with CTCF binding (lanes indicated by competitors S and A).	bind
33888	3	9319	6	NULL	NULL	0	NULL	statement 1	NULL		competes	NULL	specifically			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_120	12595547	A canonical CTCF-binding sequence from chicken beta- globin (FII) specifically competed CTCF binding to the  Meg1 repeat (lane indicated by competitor F), although the recognition sequences for the SP1 and AP1 transcription factors did not interfere with CTCF binding (lanes indicated by competitors S and A).	bind
48111	4	9319	6	10	NULL	0	NULL	SP1	NULL		does not interfere with	NULL			recognition sequences	CTCF	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_120	12595547	A canonical CTCF-binding sequence from chicken beta- globin (FII) specifically competed CTCF binding to the  Meg1 repeat (lane indicated by competitor F), although the recognition sequences for the SP1 and AP1 transcription factors did not interfere with CTCF binding (lanes indicated by competitors S and A).	bind
48112	5	9319	6	10	NULL	0	NULL	AP1	NULL		does not interfere with	NULL			recognition sequences	CTCF	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_120	12595547	A canonical CTCF-binding sequence from chicken beta- globin (FII) specifically competed CTCF binding to the  Meg1 repeat (lane indicated by competitor F), although the recognition sequences for the SP1 and AP1 transcription factors did not interfere with CTCF binding (lanes indicated by competitors S and A).	bind
48113	6	9319	6	10	NULL	0	NULL	AP1	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_120	12595547	A canonical CTCF-binding sequence from chicken beta- globin (FII) specifically competed CTCF binding to the  Meg1 repeat (lane indicated by competitor F), although the recognition sequences for the SP1 and AP1 transcription factors did not interfere with CTCF binding (lanes indicated by competitors S and A).	bind
48114	7	9319	6	10	NULL	0	NULL	SP1	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_5_1398_s_120	12595547	A canonical CTCF-binding sequence from chicken beta- globin (FII) specifically competed CTCF binding to the  Meg1 repeat (lane indicated by competitor F), although the recognition sequences for the SP1 and AP1 transcription factors did not interfere with CTCF binding (lanes indicated by competitors S and A).	bind
40180	1	9320	5	13	NULL	NULL	NULL	Jun	GP		is activated by					EGF	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_10_9634_s_152	14676207	A canonical DEF domain rescues Jun activation by EGF.	bind
40181	2	9320	5	13	NULL	NULL	NULL			canonical	rescues			 DEF domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_10_9634_s_152	14676207	A canonical DEF domain rescues Jun activation by EGF.	bind
33088	1	9320	6	NULL	NULL	0	NULL	EGF	NULL		activates	NULL				Jun	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_10_9634_s_152	14676207	A canonical DEF domain rescues Jun activation by EGF.	bind
33089	2	9320	6	NULL	NULL	0	NULL		NULL	canonical	rescues	NULL		DEF domain		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_10_9634_s_152	14676207	A canonical DEF domain rescues Jun activation by EGF.	bind
40183	1	9321	5	13	NULL	NULL	NULL	Wnt proteins	GP	secreted	bind					Frizzled receptors	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_17_6027_s_248	15837931	A canonical pathway activated by the secreted Wnt proteins binding to the Frizzled receptors has been well characterized ( ,  ).	bind
40184	2	9321	5	13	NULL	NULL	NULL	statement 1	Process		activates					canonical pathway	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_17_6027_s_248	15837931	A canonical pathway activated by the secreted Wnt proteins binding to the Frizzled receptors has been well characterized ( ,  ).	bind
33113	1	9321	6	NULL	NULL	0	NULL	Wnt proteins	NULL	secreted	bind	NULL				Frizzled receptors	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_17_6027_s_248	15837931	A canonical pathway activated by the secreted Wnt proteins binding to the Frizzled receptors has been well characterized ( ,  ).	bind
58461	2	9321	6	10	NULL	0	NULL	statement 1			activates					canonical pathway					NULL		0	NULL	NULL	NULL	gw70_pnas_102_17_6027_s_248	15837931	A canonical pathway activated by the secreted Wnt proteins binding to the Frizzled receptors has been well characterized ( ,  ).	bind
40185	1	9322	5	13	NULL	NULL	NULL	I-GST	GP		does not bind		directly			ICAM-1 mAb	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_6_3358_s_110	9452454	A capture ELISA assay showed that there is no direct binding of I-GST to any ICAM-1 mAb tested (data not shown).	bind
33115	1	9322	6	NULL	NULL	0	NULL	I-GST	NULL		does not bind	NULL	directly			ICAM-1 mAb	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3358_s_110	9452454	A capture ELISA assay showed that there is no direct binding of I-GST to any ICAM-1 mAb tested (data not shown).	bind
40207	1	9324	5	NULL	NULL	0	NULL		NULL	deletion of	include	NULL		carboxy-terminal (aa 1 to 138)			NULL		putative TPR motifs		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_20_8938_s_107	15456868	A carboxy-terminal deletion (amino acids 1 to 138) that only includes the three putative TPR motifs bound to Ctf13p but failed to bind to Skp1p.	bind
40209	2	9324	5	13	NULL	NULL	NULL	statement 1	GP		bind					Ctf13p	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8938_s_107	15456868	A carboxy-terminal deletion (amino acids 1 to 138) that only includes the three putative TPR motifs bound to Ctf13p but failed to bind to Skp1p.	bind
40210	3	9324	5	13	NULL	NULL	NULL	statement 1	GP		does not bind					Skp1p	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_20_8938_s_107	15456868	A carboxy-terminal deletion (amino acids 1 to 138) that only includes the three putative TPR motifs bound to Ctf13p but failed to bind to Skp1p.	bind
33116	1	9324	6	NULL	NULL	0	NULL		NULL	deletion of	includes	NULL		carboxy-terminal (amino acids 1 to 138)			NULL	putative	TPR motifs		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_20_8938_s_107	15456868	A carboxy-terminal deletion (amino acids 1 to 138) that only includes the three putative TPR motifs bound to Ctf13p but failed to bind to Skp1p.	bind
33117	2	9324	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				Ctf13p	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_20_8938_s_107	15456868	A carboxy-terminal deletion (amino acids 1 to 138) that only includes the three putative TPR motifs bound to Ctf13p but failed to bind to Skp1p.	bind
33118	3	9324	6	NULL	NULL	0	NULL	statement 1	NULL		does not bind	NULL				Skp1p	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_20_8938_s_107	15456868	A carboxy-terminal deletion (amino acids 1 to 138) that only includes the three putative TPR motifs bound to Ctf13p but failed to bind to Skp1p.	bind
40202	1	9325	5	13	NULL	NULL	NULL	p53	GP		bind			carboxy-terminal region		XPB	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_9_1057_s_42	8805363	A carboxy-terminal region of p53 binds to XPB and XPD and this region of p53 inhibits their DNA helicase activities    [7,8,10]  .	bind
40203	2	9325	5	13	NULL	NULL	NULL	p53	GP		bind			carboxy-terminal region		XPD	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_9_1057_s_42	8805363	A carboxy-terminal region of p53 binds to XPB and XPD and this region of p53 inhibits their DNA helicase activities    [7,8,10]  .	bind
40204	5	9325	5	13	NULL	NULL	NULL	p53	GP		inhibit			carboxy-terminal region		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_9_1057_s_42	8805363	A carboxy-terminal region of p53 binds to XPB and XPD and this region of p53 inhibits their DNA helicase activities    [7,8,10]  .	bind
40205	6	9325	5	13	NULL	NULL	NULL	p53	GP		inhibit			carboxy-terminal region		statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_9_1057_s_42	8805363	A carboxy-terminal region of p53 binds to XPB and XPD and this region of p53 inhibits their DNA helicase activities    [7,8,10]  .	bind
58462	3	9325	5	13	NULL	NULL	NULL	XPB	GP		activates					DNA helicase	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_9_1057_s_42	8805363	A carboxy-terminal region of p53 binds to XPB and XPD and this region of p53 inhibits their DNA helicase activities    [7,8,10]  .	bind
58463	4	9325	5	13	NULL	NULL	NULL	XPD	GP		activates					DNA helicase	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_9_1057_s_42	8805363	A carboxy-terminal region of p53 binds to XPB and XPD and this region of p53 inhibits their DNA helicase activities    [7,8,10]  .	bind
33119	1	9325	6	NULL	NULL	0	NULL	p53	NULL		bind	NULL		carboxy-terminal region		XPB	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_6_9_1057_s_42	8805363	A carboxy-terminal region of p53 binds to XPB and XPD and this region of p53 inhibits their DNA helicase activities    [7,8,10]  .	bind
33120	2	9325	6	NULL	NULL	0	NULL	p53	NULL		bind	NULL		carboxy-terminal region		XPD	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_6_9_1057_s_42	8805363	A carboxy-terminal region of p53 binds to XPB and XPD and this region of p53 inhibits their DNA helicase activities    [7,8,10]  .	bind
33121	3	9325	6	10	NULL	0	NULL	XPB			activates					DNA helicase					NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_9_1057_s_42	8805363	A carboxy-terminal region of p53 binds to XPB and XPD and this region of p53 inhibits their DNA helicase activities    [7,8,10]  .	bind
33122	4	9325	6	10	NULL	0	NULL	XPD			activates					DNA helicase					NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_9_1057_s_42	8805363	A carboxy-terminal region of p53 binds to XPB and XPD and this region of p53 inhibits their DNA helicase activities    [7,8,10]  .	bind
33123	5	9325	6	NULL	NULL	0	NULL	p53	NULL		inhibits	NULL		carboxy-terminal region		statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_6_9_1057_s_42	8805363	A carboxy-terminal region of p53 binds to XPB and XPD and this region of p53 inhibits their DNA helicase activities    [7,8,10]  .	bind
33124	6	9325	6	NULL	NULL	0	NULL	p53	NULL		inhibits	NULL		carboxy-terminal region		statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_6_9_1057_s_42	8805363	A carboxy-terminal region of p53 binds to XPB and XPD and this region of p53 inhibits their DNA helicase activities    [7,8,10]  .	bind
40201	1	9326	5	13	NULL	NULL	NULL	NusA	GP	 truncated	bind		specifically	carboxy-terminal		RNA	NucleicAcid		nut -site		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_20_2664_s_161	11040219	A carboxy-terminally truncated NusA also binds specifically to nut -site RNA	bind
33125	1	9326	6	10	NULL	0	NULL	NusA	NULL	truncated	bind	NULL	specifically	carboxy terminal		 RNA	NULL		nut -site		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_20_2664_s_161	11040219	A carboxy-terminally truncated NusA also binds specifically to nut -site RNA	bind
40215	1	9327	5	13	NULL	NULL	NULL	lipoprotein lipase	GP		bind			carboxyl-terminal fragment		low density lipoprotein receptor-related protein	GP				NULL	cells	NULL	NULL	NULL	NULL	gw60_jlipidres_39_3_633_s_552	9548595	A carboxyl-terminal fragment of lipoprotein lipase binds to the low density lipoprotein receptor-related protein and inhibits lipase-mediated uptake of lipoprotein in cells.	bind
40216	2	9327	5	13	NULL	NULL	NULL	lipase	GP		mediate					lipoprotein	GP	uptake of			NULL	cells	NULL	NULL	NULL	NULL	gw60_jlipidres_39_3_633_s_552	9548595	A carboxyl-terminal fragment of lipoprotein lipase binds to the low density lipoprotein receptor-related protein and inhibits lipase-mediated uptake of lipoprotein in cells.	bind
40217	3	9327	5	13	NULL	NULL	NULL	statement 1	Process		inhibit					statement 2	Process				NULL	cells	NULL	NULL	NULL	NULL	gw60_jlipidres_39_3_633_s_552	9548595	A carboxyl-terminal fragment of lipoprotein lipase binds to the low density lipoprotein receptor-related protein and inhibits lipase-mediated uptake of lipoprotein in cells.	bind
33127	1	9327	6	10	NULL	0	NULL	lipoprotein lipase			bind			carboxy terminal fragment		low density lipoprotein receptor-related protein					NULL	cells	NULL	NULL	NULL	NULL	gw60_jlipidres_39_3_633_s_552	9548595	A carboxyl-terminal fragment of lipoprotein lipase binds to the low density lipoprotein receptor-related protein and inhibits lipase-mediated uptake of lipoprotein in cells.	bind
33128	2	9327	6	NULL	NULL	0	NULL	lipase	NULL		mediates	NULL				lipoprotein	NULL	uptake of			NULL	cells	0	NULL	NULL	NULL	gw60_jlipidres_39_3_633_s_552	9548595	A carboxyl-terminal fragment of lipoprotein lipase binds to the low density lipoprotein receptor-related protein and inhibits lipase-mediated uptake of lipoprotein in cells.	bind
33131	3	9327	6	10	NULL	0	NULL	statement 1			inhibits					statement 2					NULL	cells	NULL	NULL	NULL	NULL	gw60_jlipidres_39_3_633_s_552	9548595	A carboxyl-terminal fragment of lipoprotein lipase binds to the low density lipoprotein receptor-related protein and inhibits lipase-mediated uptake of lipoprotein in cells.	bind
40219	1	9329	5	13	NULL	NULL	NULL	IKKgamma	GP	 truncated	bind			carboxyl-terminal		IKKalpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29779_s_38	10893415	A carboxyl-terminal truncated IKKgamma, which still binds to IKKalpha and -beta, acts as an inhibitor of cytokine-induced, but not of basal IKK kinase activity, when overexpressed ( 27).	bind
40220	2	9329	5	13	NULL	NULL	NULL	IKKgamma	GP	 truncated	bind			carboxyl-terminal		IKKbeta	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29779_s_38	10893415	A carboxyl-terminal truncated IKKgamma, which still binds to IKKalpha and -beta, acts as an inhibitor of cytokine-induced, but not of basal IKK kinase activity, when overexpressed ( 27).	bind
40222	3	9329	5	13	NULL	NULL	NULL	cytokine	GP		induce					IKK kinase	GP	 activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29779_s_38	10893415	A carboxyl-terminal truncated IKKgamma, which still binds to IKKalpha and -beta, acts as an inhibitor of cytokine-induced, but not of basal IKK kinase activity, when overexpressed ( 27).	bind
40224	4	9329	5	13	NULL	NULL	NULL	IKKgamma	GP	 truncated;;overexpressed	inhibit			carboxyl-terminal		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29779_s_38	10893415	A carboxyl-terminal truncated IKKgamma, which still binds to IKKalpha and -beta, acts as an inhibitor of cytokine-induced, but not of basal IKK kinase activity, when overexpressed ( 27).	bind
40225	5	9329	5	13	NULL	NULL	NULL	IKKgamma	GP	truncated;;overexpressed	does not inhibit			carboxyl-terminal 		IKK kinase	GP	basal activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29779_s_38	10893415	A carboxyl-terminal truncated IKKgamma, which still binds to IKKalpha and -beta, acts as an inhibitor of cytokine-induced, but not of basal IKK kinase activity, when overexpressed ( 27).	bind
33171	1	9329	6	NULL	NULL	0	NULL	IKKgamma	NULL	truncated	bind	NULL		carboxy terminal		IKKalpha	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29779_s_38	10893415	A carboxyl-terminal truncated IKKgamma, which still binds to IKKalpha and -beta, acts as an inhibitor of cytokine-induced, but not of basal IKK kinase activity, when overexpressed ( 27).	bind
33173	2	9329	6	NULL	NULL	0	NULL	IKKgamma	NULL	truncated	bind	NULL		carboxy terminal		IKKbeta	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29779_s_38	10893415	A carboxyl-terminal truncated IKKgamma, which still binds to IKKalpha and -beta, acts as an inhibitor of cytokine-induced, but not of basal IKK kinase activity, when overexpressed ( 27).	bind
33889	3	9329	6	NULL	NULL	0	NULL	cytokine	NULL		induces	NULL				IKK kinase	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29779_s_38	10893415	A carboxyl-terminal truncated IKKgamma, which still binds to IKKalpha and -beta, acts as an inhibitor of cytokine-induced, but not of basal IKK kinase activity, when overexpressed ( 27).	bind
33890	4	9329	6	NULL	NULL	0	NULL	IKKgamma	NULL	truncated	inhibits	NULL		carboxyl-terminal		statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29779_s_38	10893415	A carboxyl-terminal truncated IKKgamma, which still binds to IKKalpha and -beta, acts as an inhibitor of cytokine-induced, but not of basal IKK kinase activity, when overexpressed ( 27).	bind
33891	5	9329	6	10	NULL	0	NULL	IKKgamma	NULL	truncated	does not inhibit	NULL		carboxyl-terminal		IKK kinase	NULL	basal activity of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29779_s_38	10893415	A carboxyl-terminal truncated IKKgamma, which still binds to IKKalpha and -beta, acts as an inhibitor of cytokine-induced, but not of basal IKK kinase activity, when overexpressed ( 27).	bind
40227	1	9330	5	13	NULL	NULL	NULL	CD40	GP	truncation mutant	lacks			carboxyl					last 32 amino acids		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_32_22414_s_7	10428814	A carboxyl-truncation mutant of CD40 lacking the last 32 amino acids required for TRAF2 and TRAF3 binding, CD40(delta32), mediated NF-kappaB induction through a mechanism that was suppressible by co-expression of TRAF6(deltaN), a dominant-negative version of TRAF6, but not by TRAF2(deltaN), implying that while TRAF6 does not directly bind CD40, it can participate in CD40 signaling.	bind
40524	3	9330	5	13	NULL	NULL	NULL	statement 1	GP		is required for					TRAF2	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_32_22414_s_7	10428814	A carboxyl-truncation mutant of CD40 lacking the last 32 amino acids required for TRAF2 and TRAF3 binding, CD40(delta32), mediated NF-kappaB induction through a mechanism that was suppressible by co-expression of TRAF6(deltaN), a dominant-negative version of TRAF6, but not by TRAF2(deltaN), implying that while TRAF6 does not directly bind CD40, it can participate in CD40 signaling.	bind
40525	4	9330	5	13	NULL	NULL	NULL	statement 1	GP		is required for					TRAF3	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_32_22414_s_7	10428814	A carboxyl-truncation mutant of CD40 lacking the last 32 amino acids required for TRAF2 and TRAF3 binding, CD40(delta32), mediated NF-kappaB induction through a mechanism that was suppressible by co-expression of TRAF6(deltaN), a dominant-negative version of TRAF6, but not by TRAF2(deltaN), implying that while TRAF6 does not directly bind CD40, it can participate in CD40 signaling.	bind
40535	2	9330	5	13	NULL	NULL	NULL	CD40(delta32)	GP		is					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_32_22414_s_7	10428814	A carboxyl-truncation mutant of CD40 lacking the last 32 amino acids required for TRAF2 and TRAF3 binding, CD40(delta32), mediated NF-kappaB induction through a mechanism that was suppressible by co-expression of TRAF6(deltaN), a dominant-negative version of TRAF6, but not by TRAF2(deltaN), implying that while TRAF6 does not directly bind CD40, it can participate in CD40 signaling.	bind
40536	5	9330	5	13	NULL	NULL	NULL	CD40(delta32)	GP		mediate					NF-kappaB	GP	induction of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_32_22414_s_7	10428814	A carboxyl-truncation mutant of CD40 lacking the last 32 amino acids required for TRAF2 and TRAF3 binding, CD40(delta32), mediated NF-kappaB induction through a mechanism that was suppressible by co-expression of TRAF6(deltaN), a dominant-negative version of TRAF6, but not by TRAF2(deltaN), implying that while TRAF6 does not directly bind CD40, it can participate in CD40 signaling.	bind
40538	6	9330	5	13	NULL	NULL	NULL	TRAF6(deltaN)	GP		is					dominant-negative version of TRAF6	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_32_22414_s_7	10428814	A carboxyl-truncation mutant of CD40 lacking the last 32 amino acids required for TRAF2 and TRAF3 binding, CD40(delta32), mediated NF-kappaB induction through a mechanism that was suppressible by co-expression of TRAF6(deltaN), a dominant-negative version of TRAF6, but not by TRAF2(deltaN), implying that while TRAF6 does not directly bind CD40, it can participate in CD40 signaling.	bind
40540	7	9330	5	13	NULL	NULL	NULL	TRAF6	GP		does not bind		directly			CD40	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_32_22414_s_7	10428814	A carboxyl-truncation mutant of CD40 lacking the last 32 amino acids required for TRAF2 and TRAF3 binding, CD40(delta32), mediated NF-kappaB induction through a mechanism that was suppressible by co-expression of TRAF6(deltaN), a dominant-negative version of TRAF6, but not by TRAF2(deltaN), implying that while TRAF6 does not directly bind CD40, it can participate in CD40 signaling.	bind
40541	8	9330	5	13	NULL	NULL	NULL	TRAF6	GP		participate in					CD40	GP	signaling of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_32_22414_s_7	10428814	A carboxyl-truncation mutant of CD40 lacking the last 32 amino acids required for TRAF2 and TRAF3 binding, CD40(delta32), mediated NF-kappaB induction through a mechanism that was suppressible by co-expression of TRAF6(deltaN), a dominant-negative version of TRAF6, but not by TRAF2(deltaN), implying that while TRAF6 does not directly bind CD40, it can participate in CD40 signaling.	bind
33892	1	9330	6	NULL	NULL	0	NULL	TRAF6	NULL		does not bind	NULL	directly			CD40	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_32_22414_s_7	10428814	A carboxyl-truncation mutant of CD40 lacking the last 32 amino acids required for TRAF2 and TRAF3 binding, CD40(delta32), mediated NF-kappaB induction through a mechanism that was suppressible by co-expression of TRAF6(deltaN), a dominant-negative version of TRAF6, but not by TRAF2(deltaN), implying that while TRAF6 does not directly bind CD40, it can participate in CD40 signaling.	bind
33893	2	9330	6	NULL	NULL	0	NULL	TRAF6	NULL		can participate	NULL				CD40	NULL	signaling of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_32_22414_s_7	10428814	A carboxyl-truncation mutant of CD40 lacking the last 32 amino acids required for TRAF2 and TRAF3 binding, CD40(delta32), mediated NF-kappaB induction through a mechanism that was suppressible by co-expression of TRAF6(deltaN), a dominant-negative version of TRAF6, but not by TRAF2(deltaN), implying that while TRAF6 does not directly bind CD40, it can participate in CD40 signaling.	bind
33894	3	9330	6	10	NULL	0	NULL	CD40(delta32)			is required for					TRAF2		binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_32_22414_s_7	10428814	A carboxyl-truncation mutant of CD40 lacking the last 32 amino acids required for TRAF2 and TRAF3 binding, CD40(delta32), mediated NF-kappaB induction through a mechanism that was suppressible by co-expression of TRAF6(deltaN), a dominant-negative version of TRAF6, but not by TRAF2(deltaN), implying that while TRAF6 does not directly bind CD40, it can participate in CD40 signaling.	bind
33895	4	9330	6	10	NULL	0	NULL	CD40(delta32)			is required for					TRAF3		binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_32_22414_s_7	10428814	A carboxyl-truncation mutant of CD40 lacking the last 32 amino acids required for TRAF2 and TRAF3 binding, CD40(delta32), mediated NF-kappaB induction through a mechanism that was suppressible by co-expression of TRAF6(deltaN), a dominant-negative version of TRAF6, but not by TRAF2(deltaN), implying that while TRAF6 does not directly bind CD40, it can participate in CD40 signaling.	bind
33896	5	9330	6	10	NULL	0	NULL	CD40(delta32)			mediates					NF-kappaB		induction of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_32_22414_s_7	10428814	A carboxyl-truncation mutant of CD40 lacking the last 32 amino acids required for TRAF2 and TRAF3 binding, CD40(delta32), mediated NF-kappaB induction through a mechanism that was suppressible by co-expression of TRAF6(deltaN), a dominant-negative version of TRAF6, but not by TRAF2(deltaN), implying that while TRAF6 does not directly bind CD40, it can participate in CD40 signaling.	bind
40526	6	9330	6	NULL	NULL	0	NULL	TRAF6(deltaN)	NULL		is	NULL				dominant-negative version of TRAF6	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_32_22414_s_7	10428814	A carboxyl-truncation mutant of CD40 lacking the last 32 amino acids required for TRAF2 and TRAF3 binding, CD40(delta32), mediated NF-kappaB induction through a mechanism that was suppressible by co-expression of TRAF6(deltaN), a dominant-negative version of TRAF6, but not by TRAF2(deltaN), implying that while TRAF6 does not directly bind CD40, it can participate in CD40 signaling.	bind
40527	7	9330	6	NULL	NULL	0	NULL	CD40(delta32)	NULL		is	NULL				carboxyl-truncation mutant of CD40 lacking the last 32 amino acids	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_32_22414_s_7	10428814	A carboxyl-truncation mutant of CD40 lacking the last 32 amino acids required for TRAF2 and TRAF3 binding, CD40(delta32), mediated NF-kappaB induction through a mechanism that was suppressible by co-expression of TRAF6(deltaN), a dominant-negative version of TRAF6, but not by TRAF2(deltaN), implying that while TRAF6 does not directly bind CD40, it can participate in CD40 signaling.	bind
40229	1	9331	5	13	NULL	NULL	NULL				similar to				CArG sequence	c- fos	GP			SRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_410_s_216	7814403	A CArG Box Is Required for Expression of the SkACT  Promoter, but Not the beta-MHC Promoter The CArG sequence is  similar to the c- fos  serum response element (SRE), and both  bind the SRF ( 46 ,  47 ) .	bind
40230	2	9331	5	13	NULL	NULL	NULL	SRE	GP		is					serum response element	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_410_s_216	7814403	A CArG Box Is Required for Expression of the SkACT  Promoter, but Not the beta-MHC Promoter The CArG sequence is  similar to the c- fos  serum response element (SRE), and both  bind the SRF ( 46 ,  47 ) .	bind
40232	3	9331	5	13	NULL	NULL	NULL				bind				CArG sequence	SRF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_410_s_216	7814403	A CArG Box Is Required for Expression of the SkACT  Promoter, but Not the beta-MHC Promoter The CArG sequence is  similar to the c- fos  serum response element (SRE), and both  bind the SRF ( 46 ,  47 ) .	bind
40233	4	9331	5	13	NULL	NULL	NULL	c- fos	GP		bind				SRE	SRF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_410_s_216	7814403	A CArG Box Is Required for Expression of the SkACT  Promoter, but Not the beta-MHC Promoter The CArG sequence is  similar to the c- fos  serum response element (SRE), and both  bind the SRF ( 46 ,  47 ) .	bind
40234	5	9331	5	13	NULL	NULL	NULL				is required for				CArG Box	SkACT	NucleicAcid	expression of		promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_410_s_216	7814403	A CArG Box Is Required for Expression of the SkACT  Promoter, but Not the beta-MHC Promoter The CArG sequence is  similar to the c- fos  serum response element (SRE), and both  bind the SRF ( 46 ,  47 ) .	bind
40235	6	9331	5	13	NULL	NULL	NULL				is not required for				CArG Box	beta-MHC	NucleicAcid	expression of		promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_410_s_216	7814403	A CArG Box Is Required for Expression of the SkACT  Promoter, but Not the beta-MHC Promoter The CArG sequence is  similar to the c- fos  serum response element (SRE), and both  bind the SRF ( 46 ,  47 ) .	bind
33184	1	9331	6	NULL	NULL	0	NULL		NULL		is required for	NULL			CArG Box	SkACT	NULL	expression of		promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_410_s_216	7814403	A CArG Box Is Required for Expression of the SkACT  Promoter, but Not the beta-MHC Promoter The CArG sequence is  similar to the c- fos  serum response element (SRE), and both  bind the SRF ( 46 ,  47 ) .	bind
33189	2	9331	6	NULL	NULL	0	NULL	CArG sequence	NULL		is similar to	NULL				c-fos	NULL			SRE	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_410_s_216	7814403	A CArG Box Is Required for Expression of the SkACT  Promoter, but Not the beta-MHC Promoter The CArG sequence is  similar to the c- fos  serum response element (SRE), and both  bind the SRF ( 46 ,  47 ) .	bind
33258	3	9331	6	NULL	NULL	0	NULL		NULL		is not required for	NULL			CArG box	beta-MHC	NULL	expression of		promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_410_s_216	7814403	A CArG Box Is Required for Expression of the SkACT  Promoter, but Not the beta-MHC Promoter The CArG sequence is  similar to the c- fos  serum response element (SRE), and both  bind the SRF ( 46 ,  47 ) .	bind
33259	4	9331	6	NULL	NULL	0	NULL	SRE	NULL		is	NULL				serum response element	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_410_s_216	7814403	A CArG Box Is Required for Expression of the SkACT  Promoter, but Not the beta-MHC Promoter The CArG sequence is  similar to the c- fos  serum response element (SRE), and both  bind the SRF ( 46 ,  47 ) .	bind
33261	5	9331	6	NULL	NULL	0	NULL	c-fos	NULL		bind	NULL			SRE	SRF	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_410_s_216	7814403	A CArG Box Is Required for Expression of the SkACT  Promoter, but Not the beta-MHC Promoter The CArG sequence is  similar to the c- fos  serum response element (SRE), and both  bind the SRF ( 46 ,  47 ) .	bind
33268	6	9331	6	NULL	NULL	0	NULL		NULL		bind	NULL			CArG box	SRF	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_410_s_216	7814403	A CArG Box Is Required for Expression of the SkACT  Promoter, but Not the beta-MHC Promoter The CArG sequence is  similar to the c- fos  serum response element (SRE), and both  bind the SRF ( 46 ,  47 ) .	bind
40238	1	9332	5	13	NULL	NULL	NULL	NES	GP		is					nuclear export signal	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_291_s_42	10611964	A cargo bearing a nuclear  export signal (NES) binds a soluble export receptor, known as exportin, in the nucleus.	bind
40239	2	9332	5	13	NULL	NULL	NULL	cargo	GP		bind			NES		exportin	GP				NULL	nucleus	NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_291_s_42	10611964	A cargo bearing a nuclear  export signal (NES) binds a soluble export receptor, known as exportin, in the nucleus.	bind
40241	3	9332	5	13	NULL	NULL	NULL	exportin	GP		is a type of					soluble export receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_291_s_42	10611964	A cargo bearing a nuclear  export signal (NES) binds a soluble export receptor, known as exportin, in the nucleus.	bind
33271	1	9332	6	NULL	NULL	0	NULL	NES	NULL		is	NULL				nuclear export signal	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_291_s_42	10611964	A cargo bearing a nuclear  export signal (NES) binds a soluble export receptor, known as exportin, in the nucleus.	bind
33272	2	9332	6	10	NULL	0	NULL	exportin	NULL		is a type of	NULL				soluble export receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_291_s_42	10611964	A cargo bearing a nuclear  export signal (NES) binds a soluble export receptor, known as exportin, in the nucleus.	bind
33274	3	9332	6	10	NULL	0	NULL	NES cargo			bind					exportin					NULL	nucleus	NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_291_s_42	10611964	A cargo bearing a nuclear  export signal (NES) binds a soluble export receptor, known as exportin, in the nucleus.	bind
40242	1	9334	5	13	NULL	NULL	NULL	carrier precursor	GP		exits					TOM channel	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5349_369_s_130	9430585	A carrier precursor exiting the TOM channel is captured by Tim10p in the intermembrane space and delivered to Tim12p, which is bound to Tim22p at the outer face of the inner membrane.	bind
40243	2	9334	5	13	NULL	NULL	NULL	statement 1	GP		is captured by					Tim10p	GP				NULL	intermembrane space	NULL	NULL	NULL	NULL	gw60_science_279_5349_369_s_130	9430585	A carrier precursor exiting the TOM channel is captured by Tim10p in the intermembrane space and delivered to Tim12p, which is bound to Tim22p at the outer face of the inner membrane.	bind
40244	4	9334	5	13	NULL	NULL	NULL	statement 2	GP		is delivered to					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5349_369_s_130	9430585	A carrier precursor exiting the TOM channel is captured by Tim10p in the intermembrane space and delivered to Tim12p, which is bound to Tim22p at the outer face of the inner membrane.	bind
40245	3	9334	5	13	NULL	NULL	NULL	Tim12p	GP		bind					Tim22p	GP				NULL	outer face of the inner membrane	NULL	NULL	NULL	NULL	gw60_science_279_5349_369_s_130	9430585	A carrier precursor exiting the TOM channel is captured by Tim10p in the intermembrane space and delivered to Tim12p, which is bound to Tim22p at the outer face of the inner membrane.	bind
33277	1	9334	6	NULL	NULL	0	NULL	carrier precursor	NULL		exit 	NULL				TOM channel	NULL				NULL	intermembrane space	NULL	NULL	NULL	NULL	gw60_science_279_5349_369_s_130	9430585	A carrier precursor exiting the TOM channel is captured by Tim10p in the intermembrane space and delivered to Tim12p, which is bound to Tim22p at the outer face of the inner membrane.	bind
33278	2	9334	6	10	NULL	0	NULL	statement 1			is captured by					Tim10p					NULL	intermembrane space	NULL	NULL	NULL	NULL	gw60_science_279_5349_369_s_130	9430585	A carrier precursor exiting the TOM channel is captured by Tim10p in the intermembrane space and delivered to Tim12p, which is bound to Tim22p at the outer face of the inner membrane.	bind
33280	3	9334	6	10	NULL	0	NULL	Tim12p			bind					Tim22p					NULL	outer face of the inner membrane	NULL	NULL	NULL	NULL	gw60_science_279_5349_369_s_130	9430585	A carrier precursor exiting the TOM channel is captured by Tim10p in the intermembrane space and delivered to Tim12p, which is bound to Tim22p at the outer face of the inner membrane.	bind
33281	4	9334	6	10	NULL	0	NULL	statement 2			is delivered to					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_science_279_5349_369_s_130	9430585	A carrier precursor exiting the TOM channel is captured by Tim10p in the intermembrane space and delivered to Tim12p, which is bound to Tim22p at the outer face of the inner membrane.	bind
40246	1	9335	5	13	NULL	NULL	NULL	NGF	GP		bind					TrkA receptors	GP				NULL	medulloblastoma tumor cells	NULL	NULL	NULL	NULL	gw60_jneurosci_18_9_3273_s_296	9547236	A case in point is the demonstration of apoptosis in medulloblastoma tumor cells by NGF binding to TrkA receptors (Muragaki et al., 1997  ).	bind
40247	2	9335	5	13	NULL	NULL	NULL	statement 1	Process		leads to					apoptosis	Process				NULL	medulloblastoma tumor cells	NULL	NULL	NULL	NULL	gw60_jneurosci_18_9_3273_s_296	9547236	A case in point is the demonstration of apoptosis in medulloblastoma tumor cells by NGF binding to TrkA receptors (Muragaki et al., 1997  ).	bind
33282	1	9335	6	10	NULL	0	NULL	NGF	NULL		bind	NULL				TrkA receptors	NULL				NULL	medulloblastoma tumor cells	NULL	NULL	NULL	NULL	gw60_jneurosci_18_9_3273_s_296	9547236	A case in point is the demonstration of apoptosis in medulloblastoma tumor cells by NGF binding to TrkA receptors (Muragaki et al., 1997  ).	bind
33283	2	9335	6	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				apoptosis	NULL				NULL	medulloblastoma tumor cells	0	NULL	NULL	NULL	gw60_jneurosci_18_9_3273_s_296	9547236	A case in point is the demonstration of apoptosis in medulloblastoma tumor cells by NGF binding to TrkA receptors (Muragaki et al., 1997  ).	bind
40248	1	9336	5	13	NULL	NULL	NULL	CARD	GP		is					caspase activation and recruitment domain	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_430_6996_213_s_32	15190255	A caspase activation and recruitment  domain (CARD) within ASC binds to the caspase-1 prodomain, and overexpression studies  have reported that ASC both promotes and inhibits activation of caspase-1 (refs  4,  7 9).	bind
40249	2	9336	5	13	NULL	NULL	NULL	ASC	GP		bind			CARD		caspase-1	GP		prodomain		NULL		NULL	NULL	NULL	NULL	gw70_nature_430_6996_213_s_32	15190255	A caspase activation and recruitment  domain (CARD) within ASC binds to the caspase-1 prodomain, and overexpression studies  have reported that ASC both promotes and inhibits activation of caspase-1 (refs  4,  7 9).	bind
40250	3	9336	5	13	NULL	NULL	NULL	ASC	GP		promotes					caspase-1	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_nature_430_6996_213_s_32	15190255	A caspase activation and recruitment  domain (CARD) within ASC binds to the caspase-1 prodomain, and overexpression studies  have reported that ASC both promotes and inhibits activation of caspase-1 (refs  4,  7 9).	bind
40251	4	9336	5	13	NULL	NULL	NULL	ASC	GP		inhibit					caspase-1	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_nature_430_6996_213_s_32	15190255	A caspase activation and recruitment  domain (CARD) within ASC binds to the caspase-1 prodomain, and overexpression studies  have reported that ASC both promotes and inhibits activation of caspase-1 (refs  4,  7 9).	bind
33284	1	9336	6	NULL	NULL	0	NULL	ASC	NULL		bind	NULL		CARD		caspase-1	NULL		prodomain		NULL		0	NULL	NULL	NULL	gw70_nature_430_6996_213_s_32	15190255	A caspase activation and recruitment  domain (CARD) within ASC binds to the caspase-1 prodomain, and overexpression studies  have reported that ASC both promotes and inhibits activation of caspase-1 (refs  4,  7 9).	bind
33285	2	9336	6	NULL	NULL	0	NULL	CARD	NULL		is	NULL				caspase activation and recruitment domain	NULL				NULL		0	NULL	NULL	NULL	gw70_nature_430_6996_213_s_32	15190255	A caspase activation and recruitment  domain (CARD) within ASC binds to the caspase-1 prodomain, and overexpression studies  have reported that ASC both promotes and inhibits activation of caspase-1 (refs  4,  7 9).	bind
33286	3	9336	6	NULL	NULL	0	NULL	ASC	NULL		promotes	NULL				caspase-1	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_nature_430_6996_213_s_32	15190255	A caspase activation and recruitment  domain (CARD) within ASC binds to the caspase-1 prodomain, and overexpression studies  have reported that ASC both promotes and inhibits activation of caspase-1 (refs  4,  7 9).	bind
33287	4	9336	6	NULL	NULL	0	NULL	ASC	NULL		inhibits	NULL				caspase-1	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_nature_430_6996_213_s_32	15190255	A caspase activation and recruitment  domain (CARD) within ASC binds to the caspase-1 prodomain, and overexpression studies  have reported that ASC both promotes and inhibits activation of caspase-1 (refs  4,  7 9).	bind
40312	1	9339	5	13	NULL	NULL	NULL	Ubc4	GP		is			C86A		Ubc4	GP	catalytically inactive derivative of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4691_s_213	10848595	A catalytically inactive derivative of Ubc4 (Ubc4C86A) can bind the proteasome.	bind
40313	2	9339	5	13	NULL	NULL	NULL	statement 1	GP		bind					proteasome	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4691_s_213	10848595	A catalytically inactive derivative of Ubc4 (Ubc4C86A) can bind the proteasome.	bind
33288	1	9339	6	NULL	NULL	0	NULL	Ubc4	NULL		bind	NULL		C86A		proteasome	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_13_4691_s_213	10848595	A catalytically inactive derivative of Ubc4 (Ubc4C86A) can bind the proteasome.	bind
33289	2	9339	6	NULL	NULL	0	NULL	Ubc4C86A	NULL		is	NULL				catalytically inactive derivative of Ubc4	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_13_4691_s_213	10848595	A catalytically inactive derivative of Ubc4 (Ubc4C86A) can bind the proteasome.	bind
40314	1	9340	5	13	NULL	NULL	NULL	MKP7 C/S	GP		is					catalytically inactive mutant of MKP7	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_12_10731_s_173	12524447	A catalytically inactive mutant of MKP7 (MKP7 C/S) that still binds JIP-1 did not block the JIP-1-mediated enhancement of JNK activation (Fig.  4 A,  lane 10).	bind
40315	2	9340	5	13	NULL	NULL	NULL	MKP7 C/S	GP		bind					JIP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_12_10731_s_173	12524447	A catalytically inactive mutant of MKP7 (MKP7 C/S) that still binds JIP-1 did not block the JIP-1-mediated enhancement of JNK activation (Fig.  4 A,  lane 10).	bind
40316	3	9340	5	13	NULL	NULL	NULL	JIP-1	GP		mediate					JNK	GP	enhancement of;;activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_12_10731_s_173	12524447	A catalytically inactive mutant of MKP7 (MKP7 C/S) that still binds JIP-1 did not block the JIP-1-mediated enhancement of JNK activation (Fig.  4 A,  lane 10).	bind
40317	4	9340	5	13	NULL	NULL	NULL	statement 2	Process		does not block					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_12_10731_s_173	12524447	A catalytically inactive mutant of MKP7 (MKP7 C/S) that still binds JIP-1 did not block the JIP-1-mediated enhancement of JNK activation (Fig.  4 A,  lane 10).	bind
33290	1	9340	6	NULL	NULL	0	NULL	MKP7 C/S	NULL		bind	NULL				JIP-1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_12_10731_s_173	12524447	A catalytically inactive mutant of MKP7 (MKP7 C/S) that still binds JIP-1 did not block the JIP-1-mediated enhancement of JNK activation (Fig.  4 A,  lane 10).	bind
33291	2	9340	6	NULL	NULL	0	NULL	MKP7 C/S	NULL		is	NULL				catalytically inactive mutant of MKP7	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_12_10731_s_173	12524447	A catalytically inactive mutant of MKP7 (MKP7 C/S) that still binds JIP-1 did not block the JIP-1-mediated enhancement of JNK activation (Fig.  4 A,  lane 10).	bind
33292	3	9340	6	NULL	NULL	0	NULL	JNK	NULL	activation of	is mediated by	NULL				JIP-1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_12_10731_s_173	12524447	A catalytically inactive mutant of MKP7 (MKP7 C/S) that still binds JIP-1 did not block the JIP-1-mediated enhancement of JNK activation (Fig.  4 A,  lane 10).	bind
33293	4	9340	6	NULL	NULL	0	NULL	MKP7 C/S	NULL		did not block	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_12_10731_s_173	12524447	A catalytically inactive mutant of MKP7 (MKP7 C/S) that still binds JIP-1 did not block the JIP-1-mediated enhancement of JNK activation (Fig.  4 A,  lane 10).	bind
40688	1	9341	5	13	NULL	NULL	NULL	Nedd4 construct	GP	catalytically inactive	does not bind					ER	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_4_1978_s_215	16314411	A catalytically inactive Nedd4 construct also failed to bind ER ( Fig. 5 D).	bind
33294	1	9341	6	NULL	NULL	0	NULL	Nedd4 construct	NULL	catalytically inactive	does not bind	NULL				ER	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_4_1978_s_215	16314411	A catalytically inactive Nedd4 construct also failed to bind ER ( Fig. 5 D).	bind
40689	1	9342	5	13	NULL	NULL	NULL	stathmin derivatives	GP	overexpression of truncated	bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_25_22718_s_242	11956188	A catastrophe-promoting activity of stathmin has also been postulated ( 40) to explain that overexpression of truncated stathmin derivatives, which bind tubulin less tightly than wild-type stathmin, still results in microtubule destabilization.	bind
40690	2	9342	5	13	NULL	NULL	NULL	stathmin	GP	wild type	bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_25_22718_s_242	11956188	A catastrophe-promoting activity of stathmin has also been postulated ( 40) to explain that overexpression of truncated stathmin derivatives, which bind tubulin less tightly than wild-type stathmin, still results in microtubule destabilization.	bind
40691	3	9342	5	13	NULL	NULL	NULL	statement 1	Process	affinity of	is more than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_25_22718_s_242	11956188	A catastrophe-promoting activity of stathmin has also been postulated ( 40) to explain that overexpression of truncated stathmin derivatives, which bind tubulin less tightly than wild-type stathmin, still results in microtubule destabilization.	bind
40692	4	9342	5	13	NULL	NULL	NULL	statement 1	Process		results in					microtubule	CellComponent	destabilization of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_25_22718_s_242	11956188	A catastrophe-promoting activity of stathmin has also been postulated ( 40) to explain that overexpression of truncated stathmin derivatives, which bind tubulin less tightly than wild-type stathmin, still results in microtubule destabilization.	bind
40693	5	9342	5	13	NULL	NULL	NULL	stathmin	GP		promote					catastrophe activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_25_22718_s_242	11956188	A catastrophe-promoting activity of stathmin has also been postulated ( 40) to explain that overexpression of truncated stathmin derivatives, which bind tubulin less tightly than wild-type stathmin, still results in microtubule destabilization.	bind
33897	1	9342	6	NULL	NULL	0	NULL	stathmin	NULL	wild type	bind	NULL				tubulin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_25_22718_s_242	11956188	A catastrophe-promoting activity of stathmin has also been postulated ( 40) to explain that overexpression of truncated stathmin derivatives, which bind tubulin less tightly than wild-type stathmin, still results in microtubule destabilization.	bind
33899	2	9342	6	NULL	NULL	0	NULL	stathmin derivatives	NULL	truncated	bind	NULL				tubulin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_25_22718_s_242	11956188	A catastrophe-promoting activity of stathmin has also been postulated ( 40) to explain that overexpression of truncated stathmin derivatives, which bind tubulin less tightly than wild-type stathmin, still results in microtubule destabilization.	bind
33900	3	9342	6	NULL	NULL	0	NULL	statement 1	NULL	affinity of	is more than	NULL				statement 2	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_25_22718_s_242	11956188	A catastrophe-promoting activity of stathmin has also been postulated ( 40) to explain that overexpression of truncated stathmin derivatives, which bind tubulin less tightly than wild-type stathmin, still results in microtubule destabilization.	bind
33901	4	9342	6	10	NULL	0	NULL	stathmin derivatives	NULL	overexpression of;; truncated	results in	NULL				microtubule 	NULL	destabilization of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_25_22718_s_242	11956188	A catastrophe-promoting activity of stathmin has also been postulated ( 40) to explain that overexpression of truncated stathmin derivatives, which bind tubulin less tightly than wild-type stathmin, still results in microtubule destabilization.	bind
58464	5	9342	6	10	NULL	0	NULL	stathmin			promote					catastrophe activity					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_25_22718_s_242	11956188	A catastrophe-promoting activity of stathmin has also been postulated ( 40) to explain that overexpression of truncated stathmin derivatives, which bind tubulin less tightly than wild-type stathmin, still results in microtubule destabilization.	bind
40694	1	9343	5	13	NULL	NULL	NULL	lanthanide complex	Chemical	cationic	bind		selectively			insulin receptor peptide fragment	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_org-biomol-chem_4_16_16886086_s_1	16886086	A cationic lanthanide complex binds selectively to phosphorylated tyrosine sites, aiding NMR analysis of the phosphorylated insulin receptor peptide fragment..	bind
33295	1	9343	6	10	NULL	0	NULL	lanthanide complex	NULL	cationic	bind	NULL	selectively			 insulin receptor peptide fragment	NULL	phosphorylated	tyrosine sites		NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_org-biomol-chem_4_16_16886086_s_1	16886086	A cationic lanthanide complex binds selectively to phosphorylated tyrosine sites, aiding NMR analysis of the phosphorylated insulin receptor peptide fragment..	bind
40695	1	9344	5	13	NULL	NULL	NULL	Ste5	GP	mutant	does not bind					Ste7	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1793_s_295	15713635	A caveat to this interpretation is that it is based upon analysis of a mutant of Ste5 that cannot bind Ste7; perhaps Ste7 binding to Ste5 reduces Ste11 dissociation from Ste5.	bind
40696	2	9344	5	13	NULL	NULL	NULL	Ste7	GP		bind					Ste5	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1793_s_295	15713635	A caveat to this interpretation is that it is based upon analysis of a mutant of Ste5 that cannot bind Ste7; perhaps Ste7 binding to Ste5 reduces Ste11 dissociation from Ste5.	bind
40697	3	9344	5	13	NULL	NULL	NULL	Ste11	GP		dissociates from					Ste5	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1793_s_295	15713635	A caveat to this interpretation is that it is based upon analysis of a mutant of Ste5 that cannot bind Ste7; perhaps Ste7 binding to Ste5 reduces Ste11 dissociation from Ste5.	bind
40698	4	9344	5	13	NULL	NULL	NULL	statement 2	Process		reduces					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_1793_s_295	15713635	A caveat to this interpretation is that it is based upon analysis of a mutant of Ste5 that cannot bind Ste7; perhaps Ste7 binding to Ste5 reduces Ste11 dissociation from Ste5.	bind
33296	1	9344	6	NULL	NULL	0	NULL	Ste5	NULL	mutant	does not bind	NULL				Ste7	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_5_1793_s_295	15713635	A caveat to this interpretation is that it is based upon analysis of a mutant of Ste5 that cannot bind Ste7; perhaps Ste7 binding to Ste5 reduces Ste11 dissociation from Ste5.	bind
33297	2	9344	6	NULL	NULL	0	NULL	Ste7	NULL		bind	NULL				Ste5	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_5_1793_s_295	15713635	A caveat to this interpretation is that it is based upon analysis of a mutant of Ste5 that cannot bind Ste7; perhaps Ste7 binding to Ste5 reduces Ste11 dissociation from Ste5.	bind
33298	3	9344	6	NULL	NULL	0	NULL	ste11	NULL		dissociates from	NULL				Ste5	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_5_1793_s_295	15713635	A caveat to this interpretation is that it is based upon analysis of a mutant of Ste5 that cannot bind Ste7; perhaps Ste7 binding to Ste5 reduces Ste11 dissociation from Ste5.	bind
33299	4	9344	6	NULL	NULL	0	NULL	statement 2	NULL		reduces	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_5_1793_s_295	15713635	A caveat to this interpretation is that it is based upon analysis of a mutant of Ste5 that cannot bind Ste7; perhaps Ste7 binding to Ste5 reduces Ste11 dissociation from Ste5.	bind
40699	1	9345	5	13	NULL	NULL	NULL	Galphaq/11	GP	activated	bind					caveolin-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30211_s_290	10862762	A caveolin-binding Galphaq/11 fragment that selectively blocked the binding of activated Galphaq/11 to caveolin-3 elicited by ACh prevented desensitization of responses mediated by other Gq/11-coupled receptors but not by Gi3-coupled receptors.	bind
40700	2	9345	5	13	NULL	NULL	NULL	Galphaq/11	GP		block		selectively	caveolin-binding fragment		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30211_s_290	10862762	A caveolin-binding Galphaq/11 fragment that selectively blocked the binding of activated Galphaq/11 to caveolin-3 elicited by ACh prevented desensitization of responses mediated by other Gq/11-coupled receptors but not by Gi3-coupled receptors.	bind
40701	3	9345	5	13	NULL	NULL	NULL	ACh	Chemical		elicits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30211_s_290	10862762	A caveolin-binding Galphaq/11 fragment that selectively blocked the binding of activated Galphaq/11 to caveolin-3 elicited by ACh prevented desensitization of responses mediated by other Gq/11-coupled receptors but not by Gi3-coupled receptors.	bind
40702	4	9345	5	13	NULL	NULL	NULL	Gq/11-coupled receptors	GP		mediate					responses	Process	desensitization of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30211_s_290	10862762	A caveolin-binding Galphaq/11 fragment that selectively blocked the binding of activated Galphaq/11 to caveolin-3 elicited by ACh prevented desensitization of responses mediated by other Gq/11-coupled receptors but not by Gi3-coupled receptors.	bind
40703	5	9345	5	13	NULL	NULL	NULL	Gi3-coupled receptors	GP		mediate					responses	Process	desensitization of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30211_s_290	10862762	A caveolin-binding Galphaq/11 fragment that selectively blocked the binding of activated Galphaq/11 to caveolin-3 elicited by ACh prevented desensitization of responses mediated by other Gq/11-coupled receptors but not by Gi3-coupled receptors.	bind
40704	6	9345	5	13	NULL	NULL	NULL	statement 2	Process		prevents					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30211_s_290	10862762	A caveolin-binding Galphaq/11 fragment that selectively blocked the binding of activated Galphaq/11 to caveolin-3 elicited by ACh prevented desensitization of responses mediated by other Gq/11-coupled receptors but not by Gi3-coupled receptors.	bind
40705	7	9345	5	13	NULL	NULL	NULL	statement 2	Process		does not prevent					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30211_s_290	10862762	A caveolin-binding Galphaq/11 fragment that selectively blocked the binding of activated Galphaq/11 to caveolin-3 elicited by ACh prevented desensitization of responses mediated by other Gq/11-coupled receptors but not by Gi3-coupled receptors.	bind
33903	1	9345	6	NULL	NULL	0	NULL	Galphaq/11	NULL	activated	bind	NULL				caveolin-3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_39_30211_s_290	10862762	A caveolin-binding Galphaq/11 fragment that selectively blocked the binding of activated Galphaq/11 to caveolin-3 elicited by ACh prevented desensitization of responses mediated by other Gq/11-coupled receptors but not by Gi3-coupled receptors.	bind
33905	2	9345	6	NULL	NULL	0	NULL	Galphaq/11 fragment	NULL		bind	NULL				caveolin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_39_30211_s_290	10862762	A caveolin-binding Galphaq/11 fragment that selectively blocked the binding of activated Galphaq/11 to caveolin-3 elicited by ACh prevented desensitization of responses mediated by other Gq/11-coupled receptors but not by Gi3-coupled receptors.	bind
33906	3	9345	6	NULL	NULL	0	NULL	ACh	NULL		elicits	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30211_s_290	10862762	A caveolin-binding Galphaq/11 fragment that selectively blocked the binding of activated Galphaq/11 to caveolin-3 elicited by ACh prevented desensitization of responses mediated by other Gq/11-coupled receptors but not by Gi3-coupled receptors.	bind
33907	4	9345	6	NULL	NULL	0	NULL	statement 2	NULL		blocks	NULL	selectively			statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_39_30211_s_290	10862762	A caveolin-binding Galphaq/11 fragment that selectively blocked the binding of activated Galphaq/11 to caveolin-3 elicited by ACh prevented desensitization of responses mediated by other Gq/11-coupled receptors but not by Gi3-coupled receptors.	bind
58465	5	9345	6	10	NULL	0	NULL	Gq/11-coupled receptors			mediate					responses		desensitization of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_39_30211_s_290	10862762	A caveolin-binding Galphaq/11 fragment that selectively blocked the binding of activated Galphaq/11 to caveolin-3 elicited by ACh prevented desensitization of responses mediated by other Gq/11-coupled receptors but not by Gi3-coupled receptors.	bind
58467	6	9345	6	10	NULL	0	NULL	Gi3-coupled receptors			mediate					responses		desensitization of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_39_30211_s_290	10862762	A caveolin-binding Galphaq/11 fragment that selectively blocked the binding of activated Galphaq/11 to caveolin-3 elicited by ACh prevented desensitization of responses mediated by other Gq/11-coupled receptors but not by Gi3-coupled receptors.	bind
58468	7	9345	6	10	NULL	0	NULL	statement 4			prevents					statement 5					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_39_30211_s_290	10862762	A caveolin-binding Galphaq/11 fragment that selectively blocked the binding of activated Galphaq/11 to caveolin-3 elicited by ACh prevented desensitization of responses mediated by other Gq/11-coupled receptors but not by Gi3-coupled receptors.	bind
58469	8	9345	6	10	NULL	0	NULL	statement 4			does not prevent					statement 6					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_39_30211_s_290	10862762	A caveolin-binding Galphaq/11 fragment that selectively blocked the binding of activated Galphaq/11 to caveolin-3 elicited by ACh prevented desensitization of responses mediated by other Gq/11-coupled receptors but not by Gi3-coupled receptors.	bind
40706	1	9346	5	13	NULL	NULL	NULL	PfEMP1	GP		bind			CD36 binding domain		CD36	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_4_1766_s_205	10677532	A CD36 binding domain has previously been shown to reside in the CIDR domain of PfEMP1 that bind CD36 ( 20,  21).	bind
40707	2	9346	5	13	NULL	NULL	NULL	PfEMP1	GP		reside in			CD36 binding domain		PfEMP1	GP		CIDR domain		NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_4_1766_s_205	10677532	A CD36 binding domain has previously been shown to reside in the CIDR domain of PfEMP1 that bind CD36 ( 20,  21).	bind
33582	1	9346	6	NULL	NULL	0	NULL	PfEMP1	NULL		bind	NULL		CIDR domain		CD36	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_4_1766_s_205	10677532	A CD36 binding domain has previously been shown to reside in the CIDR domain of PfEMP1 that bind CD36 ( 20,  21).	bind
33583	2	9346	6	NULL	NULL	0	NULL	PfEMP1	NULL		contains	NULL		CIDR domain			NULL		CD36 binding domain		NULL		0	NULL	NULL	NULL	gw60_pnas_97_4_1766_s_205	10677532	A CD36 binding domain has previously been shown to reside in the CIDR domain of PfEMP1 that bind CD36 ( 20,  21).	bind
40708	1	9347	5	13	NULL	NULL	NULL	AC-25	Cell		is a type of					CD4+ T cell clone	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_36_13279_s_63	15331779	A CD4+ T cell clone (AC-25) isolated from an individual acutely infected with HIV-1 recognizes an antigen derived from the HIV Gag (p24) protein bound to the human class II MHC protein HLA-DR1.	bind
40709	2	9347	5	13	NULL	NULL	NULL	AC-25	Cell		isolated from					individual infected with HIV-1	Organism	acutely 			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_36_13279_s_63	15331779	A CD4+ T cell clone (AC-25) isolated from an individual acutely infected with HIV-1 recognizes an antigen derived from the HIV Gag (p24) protein bound to the human class II MHC protein HLA-DR1.	bind
40710	3	9347	5	13	NULL	NULL	NULL	Gag  protein	GP	HIV	bind					HLA-DR1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_36_13279_s_63	15331779	A CD4+ T cell clone (AC-25) isolated from an individual acutely infected with HIV-1 recognizes an antigen derived from the HIV Gag (p24) protein bound to the human class II MHC protein HLA-DR1.	bind
40711	4	9347	5	13	NULL	NULL	NULL	HLA-DR1	GP		is a type of					human class II MHC protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_36_13279_s_63	15331779	A CD4+ T cell clone (AC-25) isolated from an individual acutely infected with HIV-1 recognizes an antigen derived from the HIV Gag (p24) protein bound to the human class II MHC protein HLA-DR1.	bind
40712	6	9347	5	13	NULL	NULL	NULL	antigen	GP		derived from					HIV Gag protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_36_13279_s_63	15331779	A CD4+ T cell clone (AC-25) isolated from an individual acutely infected with HIV-1 recognizes an antigen derived from the HIV Gag (p24) protein bound to the human class II MHC protein HLA-DR1.	bind
48115	5	9347	5	13	NULL	NULL	NULL	Gag protein	GP		is					p24	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_36_13279_s_63	15331779	A CD4+ T cell clone (AC-25) isolated from an individual acutely infected with HIV-1 recognizes an antigen derived from the HIV Gag (p24) protein bound to the human class II MHC protein HLA-DR1.	bind
48117	7	9347	5	13	NULL	NULL	NULL	statement 2	Cell		recognize					statement 6	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_36_13279_s_63	15331779	A CD4+ T cell clone (AC-25) isolated from an individual acutely infected with HIV-1 recognizes an antigen derived from the HIV Gag (p24) protein bound to the human class II MHC protein HLA-DR1.	bind
33584	1	9347	6	NULL	NULL	0	NULL	Gag	NULL	HIV	bind	NULL				HLA-DR1	NULL	human			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_36_13279_s_63	15331779	A CD4+ T cell clone (AC-25) isolated from an individual acutely infected with HIV-1 recognizes an antigen derived from the HIV Gag (p24) protein bound to the human class II MHC protein HLA-DR1.	bind
33585	2	9347	6	NULL	NULL	0	NULL	HLA-DR1	NULL	human	is a type of	NULL				class II MHC protein	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_36_13279_s_63	15331779	A CD4+ T cell clone (AC-25) isolated from an individual acutely infected with HIV-1 recognizes an antigen derived from the HIV Gag (p24) protein bound to the human class II MHC protein HLA-DR1.	bind
33681	3	9347	6	NULL	NULL	0	NULL	Gag	NULL		is	NULL				p24 	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_36_13279_s_63	15331779	A CD4+ T cell clone (AC-25) isolated from an individual acutely infected with HIV-1 recognizes an antigen derived from the HIV Gag (p24) protein bound to the human class II MHC protein HLA-DR1.	bind
48116	4	9347	6	10	NULL	0	NULL	AC-25	NULL		is a type of	NULL				CD4+ T cell clone	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_36_13279_s_63	15331779	A CD4+ T cell clone (AC-25) isolated from an individual acutely infected with HIV-1 recognizes an antigen derived from the HIV Gag (p24) protein bound to the human class II MHC protein HLA-DR1.	bind
40713	1	9348	5	13	NULL	NULL	NULL	CD44	GP		interact with		indirect;;may			alpha2beta1integrin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_42_43503_s_312	15292257	A CD44/alpha2beta1 integrin interaction may be indirect, because the CD44 cytoplasmic domain binds to ankyrin, which in turn is linked to actin by fodrin/spectrin ( ,  ).	bind
40714	2	9348	5	13	NULL	NULL	NULL	CD44	GP		bind			cytoplasmic domain		ankyrin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_42_43503_s_312	15292257	A CD44/alpha2beta1 integrin interaction may be indirect, because the CD44 cytoplasmic domain binds to ankyrin, which in turn is linked to actin by fodrin/spectrin ( ,  ).	bind
40715	3	9348	5	13	NULL	NULL	NULL	ankyrin	GP		is linked to			cytoplasmic domain		actin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_42_43503_s_312	15292257	A CD44/alpha2beta1 integrin interaction may be indirect, because the CD44 cytoplasmic domain binds to ankyrin, which in turn is linked to actin by fodrin/spectrin ( ,  ).	bind
40716	4	9348	5	13	NULL	NULL	NULL	statement 3	Process		via					fodrin/spectrin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_42_43503_s_312	15292257	A CD44/alpha2beta1 integrin interaction may be indirect, because the CD44 cytoplasmic domain binds to ankyrin, which in turn is linked to actin by fodrin/spectrin ( ,  ).	bind
48118	5	9348	5	13	NULL	NULL	NULL	statement 1	Process		because of					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_42_43503_s_312	15292257	A CD44/alpha2beta1 integrin interaction may be indirect, because the CD44 cytoplasmic domain binds to ankyrin, which in turn is linked to actin by fodrin/spectrin ( ,  ).	bind
33682	1	9348	6	NULL	NULL	0	NULL	CD44	NULL		bind	NULL		cytoplasmic domain		ankyrin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_42_43503_s_312	15292257	A CD44/alpha2beta1 integrin interaction may be indirect, because the CD44 cytoplasmic domain binds to ankyrin, which in turn is linked to actin by fodrin/spectrin ( ,  ).	bind
33683	2	9348	6	NULL	NULL	0	NULL	CD44	NULL		is linked to	NULL		cytoplasmic domain		actin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_42_43503_s_312	15292257	A CD44/alpha2beta1 integrin interaction may be indirect, because the CD44 cytoplasmic domain binds to ankyrin, which in turn is linked to actin by fodrin/spectrin ( ,  ).	bind
33684	3	9348	6	NULL	NULL	0	NULL	statement 2	NULL		occurs by	NULL				fodrin/spectrin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_42_43503_s_312	15292257	A CD44/alpha2beta1 integrin interaction may be indirect, because the CD44 cytoplasmic domain binds to ankyrin, which in turn is linked to actin by fodrin/spectrin ( ,  ).	bind
33685	4	9348	6	NULL	NULL	0	NULL	CD44	NULL		interacts with	NULL	may;; indirectly			alpha2beta1 integrin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_42_43503_s_312	15292257	A CD44/alpha2beta1 integrin interaction may be indirect, because the CD44 cytoplasmic domain binds to ankyrin, which in turn is linked to actin by fodrin/spectrin ( ,  ).	bind
33686	5	9348	6	NULL	NULL	0	NULL	statement 4	NULL		is because of	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_42_43503_s_312	15292257	A CD44/alpha2beta1 integrin interaction may be indirect, because the CD44 cytoplasmic domain binds to ankyrin, which in turn is linked to actin by fodrin/spectrin ( ,  ).	bind
40717	1	9349	5	13	NULL	NULL	NULL	CD8 variant	GP		contains					CDR-2-like loop	GP	mutations in	Q54E/N55D		NULL		NULL	NULL	NULL	NULL	gw60_immunity_10_2_219_s_18	10072074	A CD8   variant with mutations in the CDR-2-like loop (Q54E/N55D), which contacts the  3 domain of HLA-A2 (  Giblin et al. 1994  ; Gao et al. 1997  ), did not bind HLA-A2 (  Figure 1B), confirming the specificity of this interaction.	bind
40718	2	9349	5	13	NULL	NULL	NULL	statement 1	GP		contacts					HLA-A2	GP		3 domain		NULL		NULL	NULL	NULL	NULL	gw60_immunity_10_2_219_s_18	10072074	A CD8   variant with mutations in the CDR-2-like loop (Q54E/N55D), which contacts the  3 domain of HLA-A2 (  Giblin et al. 1994  ; Gao et al. 1997  ), did not bind HLA-A2 (  Figure 1B), confirming the specificity of this interaction.	bind
40719	3	9349	5	13	NULL	NULL	NULL	statement 1	GP		does not bind					HLA-A2	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_10_2_219_s_18	10072074	A CD8   variant with mutations in the CDR-2-like loop (Q54E/N55D), which contacts the  3 domain of HLA-A2 (  Giblin et al. 1994  ; Gao et al. 1997  ), did not bind HLA-A2 (  Figure 1B), confirming the specificity of this interaction.	bind
33908	1	9349	6	10	NULL	0	NULL	CD8 variant			contains							mutation in	 CDR-2-like loop (Q54E/N55D)		NULL		NULL	NULL	NULL	NULL	gw60_immunity_10_2_219_s_18	10072074	A CD8   variant with mutations in the CDR-2-like loop (Q54E/N55D), which contacts the  3 domain of HLA-A2 (  Giblin et al. 1994  ; Gao et al. 1997  ), did not bind HLA-A2 (  Figure 1B), confirming the specificity of this interaction.	bind
33909	2	9349	6	10	NULL	0	NULL	statement 1			contacts					HLA-A2			3 domain		NULL		NULL	NULL	NULL	NULL	gw60_immunity_10_2_219_s_18	10072074	A CD8   variant with mutations in the CDR-2-like loop (Q54E/N55D), which contacts the  3 domain of HLA-A2 (  Giblin et al. 1994  ; Gao et al. 1997  ), did not bind HLA-A2 (  Figure 1B), confirming the specificity of this interaction.	bind
58470	3	9349	6	10	NULL	0	NULL	statement 1			does not bind					HLA-A2					NULL		0	NULL	NULL	NULL	gw60_immunity_10_2_219_s_18	10072074	A CD8   variant with mutations in the CDR-2-like loop (Q54E/N55D), which contacts the  3 domain of HLA-A2 (  Giblin et al. 1994  ; Gao et al. 1997  ), did not bind HLA-A2 (  Figure 1B), confirming the specificity of this interaction.	bind
40722	1	9350	5	13	NULL	NULL	NULL	CD95-IgG antibody	GP		bind					CD95 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_613_s_118	9918566	A CD95-IgG antibody, which binds to the CD95 receptor without inducing apoptosis, could not prevent the effect of AKBA when the cells were preincubated with this antibody (data not shown).	bind
40723	2	9350	5	13	NULL	NULL	NULL	statement 1	Process		does not induce					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_613_s_118	9918566	A CD95-IgG antibody, which binds to the CD95 receptor without inducing apoptosis, could not prevent the effect of AKBA when the cells were preincubated with this antibody (data not shown).	bind
40724	3	9350	5	13	NULL	NULL	NULL	statement 1	Process		does not prevent					AKBA	Chemical	effect of			NULL	cells preincubated with CD95-IgG antibody	NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_613_s_118	9918566	A CD95-IgG antibody, which binds to the CD95 receptor without inducing apoptosis, could not prevent the effect of AKBA when the cells were preincubated with this antibody (data not shown).	bind
33687	1	9350	6	NULL	NULL	0	NULL	CD95-IgG antibody	NULL		bind	NULL				CD95 receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_613_s_118	9918566	A CD95-IgG antibody, which binds to the CD95 receptor without inducing apoptosis, could not prevent the effect of AKBA when the cells were preincubated with this antibody (data not shown).	bind
33688	2	9350	6	10	NULL	0	NULL	statement 1	NULL		does not induce	NULL				apoptosis	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_613_s_118	9918566	A CD95-IgG antibody, which binds to the CD95 receptor without inducing apoptosis, could not prevent the effect of AKBA when the cells were preincubated with this antibody (data not shown).	bind
48119	3	9350	6	10	NULL	0	NULL	statement 1	NULL		does not prevent 	NULL				AKBA	NULL	effect of			NULL	cells preincubated with CD95-IgG antibody	0	NULL	NULL	NULL	gw60_jpharmacolexpther_288_2_613_s_118	9918566	A CD95-IgG antibody, which binds to the CD95 receptor without inducing apoptosis, could not prevent the effect of AKBA when the cells were preincubated with this antibody (data not shown).	bind
40725	1	9351	5	13	NULL	NULL	NULL	Cdc20P1	GP		is					Cdc20 peptide	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_15_3133_s_187	15257285	A Cdc20 peptide (Cdc20P1) containing the Mad2-binding motif of Cdc20 bound to N2-Mad2R133A with a dissociation constant ( Kd) of 0.65 muM ( Figure 6C and D).	bind
40726	2	9351	5	13	NULL	NULL	NULL	Cdc20P1	GP		bind			Mad2-binding motif		N2-Mad2	GP		R133A		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_15_3133_s_187	15257285	A Cdc20 peptide (Cdc20P1) containing the Mad2-binding motif of Cdc20 bound to N2-Mad2R133A with a dissociation constant ( Kd) of 0.65 muM ( Figure 6C and D).	bind
33689	1	9351	6	NULL	NULL	0	NULL	Cdc20P1	NULL		is	NULL				Cdc20 peptide	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_23_15_3133_s_187	15257285	A Cdc20 peptide (Cdc20P1) containing the Mad2-binding motif of Cdc20 bound to N2-Mad2R133A with a dissociation constant ( Kd) of 0.65 muM ( Figure 6C and D).	bind
33690	2	9351	6	10	NULL	0	NULL	Cdc20P1			bind			Mad2-binding motif		N2-Mad2			R133A		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_15_3133_s_187	15257285	A Cdc20 peptide (Cdc20P1) containing the Mad2-binding motif of Cdc20 bound to N2-Mad2R133A with a dissociation constant ( Kd) of 0.65 muM ( Figure 6C and D).	bind
40727	1	9352	5	13	NULL	NULL	NULL	SPF1 cDNA	NucleicAcid	sweet potato petiole	bind									SP8 motif	NULL		NULL	NULL	NULL	NULL	gw70_annurevplantbiol_51_0_49_s_350	null	A cDNA clone encoding a new type of DNA-binding protein, SPF1, that binds the SP8  motif was isolated from a sweet potato petiole cDNA library ( 71).	bind
40728	2	9352	5	13	NULL	NULL	NULL	SPF1	GP		is a type of					DNA-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevplantbiol_51_0_49_s_350	null	A cDNA clone encoding a new type of DNA-binding protein, SPF1, that binds the SP8  motif was isolated from a sweet potato petiole cDNA library ( 71).	bind
33691	1	9352	6	10	NULL	0	NULL	SPF1		sweet potato petiole	bind									SP8 motif	NULL		NULL	NULL	NULL	NULL	gw70_annurevplantbiol_51_0_49_s_350	null	A cDNA clone encoding a new type of DNA-binding protein, SPF1, that binds the SP8  motif was isolated from a sweet potato petiole cDNA library ( 71).	bind
48120	2	9352	6	10	NULL	0	NULL	SPF1	NULL		is a type of	NULL				DNA-binding protein	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevplantbiol_51_0_49_s_350	null	A cDNA clone encoding a new type of DNA-binding protein, SPF1, that binds the SP8  motif was isolated from a sweet potato petiole cDNA library ( 71).	bind
40729	1	9354	5	13	NULL	NULL	NULL	RA	Chemical		induce					RACK1 gene	GP				NULL	chick wing bud	NULL	NULL	NULL	NULL	gw60_development_128_13_2451_s_4	11493562	A cDNA encoding RACK1, a protein that binds and stabilizes activated protein kinase C (PKC), was isolated in a screen for genes induced by retinoic acid (RA) in the chick wing bud.	bind
40730	2	9354	5	13	NULL	NULL	NULL	RACK1 protein	GP		bind					PKC	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_development_128_13_2451_s_4	11493562	A cDNA encoding RACK1, a protein that binds and stabilizes activated protein kinase C (PKC), was isolated in a screen for genes induced by retinoic acid (RA) in the chick wing bud.	bind
40731	3	9354	5	13	NULL	NULL	NULL	statement 2	Process		stabilize					PKC	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_development_128_13_2451_s_4	11493562	A cDNA encoding RACK1, a protein that binds and stabilizes activated protein kinase C (PKC), was isolated in a screen for genes induced by retinoic acid (RA) in the chick wing bud.	bind
40732	4	9354	5	13	NULL	NULL	NULL	PKC	GP		is					protein kinase C	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_128_13_2451_s_4	11493562	A cDNA encoding RACK1, a protein that binds and stabilizes activated protein kinase C (PKC), was isolated in a screen for genes induced by retinoic acid (RA) in the chick wing bud.	bind
40733	5	9354	5	13	NULL	NULL	NULL	RA	Chemical		is					retinoic acid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_development_128_13_2451_s_4	11493562	A cDNA encoding RACK1, a protein that binds and stabilizes activated protein kinase C (PKC), was isolated in a screen for genes induced by retinoic acid (RA) in the chick wing bud.	bind
33692	1	9354	6	NULL	NULL	0	NULL	RACK1	NULL		bind	NULL				PKC	NULL				NULL		0	NULL	NULL	NULL	gw60_development_128_13_2451_s_4	11493562	A cDNA encoding RACK1, a protein that binds and stabilizes activated protein kinase C (PKC), was isolated in a screen for genes induced by retinoic acid (RA) in the chick wing bud.	bind
33693	2	9354	6	NULL	NULL	0	NULL	RACK1	NULL		stabilizes	NULL				PKC	NULL				NULL		0	NULL	NULL	NULL	gw60_development_128_13_2451_s_4	11493562	A cDNA encoding RACK1, a protein that binds and stabilizes activated protein kinase C (PKC), was isolated in a screen for genes induced by retinoic acid (RA) in the chick wing bud.	bind
33694	3	9354	6	NULL	NULL	0	NULL	PKC	NULL		is	NULL				protein kinase C	NULL				NULL		0	NULL	NULL	NULL	gw60_development_128_13_2451_s_4	11493562	A cDNA encoding RACK1, a protein that binds and stabilizes activated protein kinase C (PKC), was isolated in a screen for genes induced by retinoic acid (RA) in the chick wing bud.	bind
48121	4	9354	6	10	NULL	0	NULL	RA	NULL		is	NULL				retinoic acid	NULL				NULL		0	NULL	NULL	NULL	gw60_development_128_13_2451_s_4	11493562	A cDNA encoding RACK1, a protein that binds and stabilizes activated protein kinase C (PKC), was isolated in a screen for genes induced by retinoic acid (RA) in the chick wing bud.	bind
58471	5	9354	6	10	NULL	0	NULL	RA			induce					RACK1 genes					NULL	chick wing bud	0	NULL	NULL	NULL	gw60_development_128_13_2451_s_4	11493562	A cDNA encoding RACK1, a protein that binds and stabilizes activated protein kinase C (PKC), was isolated in a screen for genes induced by retinoic acid (RA) in the chick wing bud.	bind
41257	1	9358	5	13	NULL	NULL	NULL	PBP10	GP		is a type of					cell permeable peptide	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-pharmacol_71_10_16549058_s_9	16549058	A cell permeable peptide (PBP10) corresponding to the phosphatidyl-inositol-bisphosphate  binding region of gelsolin, inhibited the FPRL1-, but not the FPR-induced  cellular response and induced the same type of receptor switch.	bind
41258	2	9358	5	13	NULL	NULL	NULL	PBP10	GP		corresponds to					gelsolin	GP		phosphatidyl-inositol-bisphosphate binding region		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-pharmacol_71_10_16549058_s_9	16549058	A cell permeable peptide (PBP10) corresponding to the phosphatidyl-inositol-bisphosphate  binding region of gelsolin, inhibited the FPRL1-, but not the FPR-induced  cellular response and induced the same type of receptor switch.	bind
41259	3	9358	5	13	NULL	NULL	NULL	FPRL1	GP		induce					cellular response	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-pharmacol_71_10_16549058_s_9	16549058	A cell permeable peptide (PBP10) corresponding to the phosphatidyl-inositol-bisphosphate  binding region of gelsolin, inhibited the FPRL1-, but not the FPR-induced  cellular response and induced the same type of receptor switch.	bind
41260	4	9358	5	13	NULL	NULL	NULL	PBP10	GP		inhibit					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-pharmacol_71_10_16549058_s_9	16549058	A cell permeable peptide (PBP10) corresponding to the phosphatidyl-inositol-bisphosphate  binding region of gelsolin, inhibited the FPRL1-, but not the FPR-induced  cellular response and induced the same type of receptor switch.	bind
41261	5	9358	5	13	NULL	NULL	NULL	FPR	GP		induce					cellular response	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-pharmacol_71_10_16549058_s_9	16549058	A cell permeable peptide (PBP10) corresponding to the phosphatidyl-inositol-bisphosphate  binding region of gelsolin, inhibited the FPRL1-, but not the FPR-induced  cellular response and induced the same type of receptor switch.	bind
41262	6	9358	5	13	NULL	NULL	NULL	PBP10	GP		does not inhibit					statement 5	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-pharmacol_71_10_16549058_s_9	16549058	A cell permeable peptide (PBP10) corresponding to the phosphatidyl-inositol-bisphosphate  binding region of gelsolin, inhibited the FPRL1-, but not the FPR-induced  cellular response and induced the same type of receptor switch.	bind
41263	7	9358	5	13	NULL	NULL	NULL	PBP10	GP		induce					receptor switch	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-pharmacol_71_10_16549058_s_9	16549058	A cell permeable peptide (PBP10) corresponding to the phosphatidyl-inositol-bisphosphate  binding region of gelsolin, inhibited the FPRL1-, but not the FPR-induced  cellular response and induced the same type of receptor switch.	bind
33695	1	9358	6	10	NULL	0	NULL	PBP10	NULL		is a type of	NULL				cell permeable peptide	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-pharmacol_71_10_16549058_s_9	16549058	A cell permeable peptide (PBP10) corresponding to the phosphatidyl-inositol-bisphosphate  binding region of gelsolin, inhibited the FPRL1-, but not the FPR-induced  cellular response and induced the same type of receptor switch.	bind
33910	2	9358	6	NULL	NULL	0	NULL	FPRL1	NULL		induces	NULL				cellular response	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biochem-pharmacol_71_10_16549058_s_9	16549058	A cell permeable peptide (PBP10) corresponding to the phosphatidyl-inositol-bisphosphate  binding region of gelsolin, inhibited the FPRL1-, but not the FPR-induced  cellular response and induced the same type of receptor switch.	bind
33911	3	9358	6	NULL	NULL	0	NULL	FPR	NULL		induces	NULL				cellular response	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biochem-pharmacol_71_10_16549058_s_9	16549058	A cell permeable peptide (PBP10) corresponding to the phosphatidyl-inositol-bisphosphate  binding region of gelsolin, inhibited the FPRL1-, but not the FPR-induced  cellular response and induced the same type of receptor switch.	bind
33912	4	9358	6	NULL	NULL	0	NULL	PBP10	NULL		corresponds to	NULL				gelsolin	NULL		phosphatidyl-inositol-bisphosphate binding region		NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biochem-pharmacol_71_10_16549058_s_9	16549058	A cell permeable peptide (PBP10) corresponding to the phosphatidyl-inositol-bisphosphate  binding region of gelsolin, inhibited the FPRL1-, but not the FPR-induced  cellular response and induced the same type of receptor switch.	bind
33913	5	9358	6	NULL	NULL	0	NULL	PBP10	NULL		inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biochem-pharmacol_71_10_16549058_s_9	16549058	A cell permeable peptide (PBP10) corresponding to the phosphatidyl-inositol-bisphosphate  binding region of gelsolin, inhibited the FPRL1-, but not the FPR-induced  cellular response and induced the same type of receptor switch.	bind
33914	6	9358	6	NULL	NULL	0	NULL	PBP10	NULL		does not inhibit	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biochem-pharmacol_71_10_16549058_s_9	16549058	A cell permeable peptide (PBP10) corresponding to the phosphatidyl-inositol-bisphosphate  binding region of gelsolin, inhibited the FPRL1-, but not the FPR-induced  cellular response and induced the same type of receptor switch.	bind
48122	7	9358	6	10	NULL	0	NULL	PBP10	NULL		induce	NULL				receptor switch	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biochem-pharmacol_71_10_16549058_s_9	16549058	A cell permeable peptide (PBP10) corresponding to the phosphatidyl-inositol-bisphosphate  binding region of gelsolin, inhibited the FPRL1-, but not the FPR-induced  cellular response and induced the same type of receptor switch.	bind
41255	1	9360	5	13	NULL	NULL	NULL	hsp70	GP		effect		cell type-specific			growth	Process	inhibition of			NULL	transgenic mice expressing hsp70	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7146_s_485	10982831	A cell type-specific effect of hsp70 on growth inhibition was observed in transgenic mice expressing hsp70 under the control of the mouse H-2K promoter ( 28).	bind
41256	2	9360	5	13	NULL	NULL	NULL	statement 1	Process		occurs under 					H-2K	NucleicAcid	control of;;mouse		promoter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7146_s_485	10982831	A cell type-specific effect of hsp70 on growth inhibition was observed in transgenic mice expressing hsp70 under the control of the mouse H-2K promoter ( 28).	bind
33696	1	9360	6	10	NULL	0	NULL	hsp70			effects		cell type-specific			growth 		inhibition of			NULL	transgenic mice	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7146_s_485	10982831	A cell type-specific effect of hsp70 on growth inhibition was observed in transgenic mice expressing hsp70 under the control of the mouse H-2K promoter ( 28).	bind
48123	2	9360	6	10	NULL	0	NULL	statement 1	NULL		occurs under	NULL				H-2K	NULL	control of;;mouse		promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7146_s_485	10982831	A cell type-specific effect of hsp70 on growth inhibition was observed in transgenic mice expressing hsp70 under the control of the mouse H-2K promoter ( 28).	bind
40734	1	9361	5	13	NULL	NULL	NULL	mAb 12G5	GP		bind					CXCR4-expressing cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1723_1_270_s_62	15823507	A cell-based ELISA was used for measuring the inhibitory activity of compounds on  the binding of mAb 12G5 to CXCR4-expressing cells   [26].	bind
33697	1	9361	6	NULL	NULL	0	NULL	mAb 12G5	NULL		bind	NULL				CXCR4-expressing cells	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1723_1_270_s_62	15823507	A cell-based ELISA was used for measuring the inhibitory activity of compounds on  the binding of mAb 12G5 to CXCR4-expressing cells   [26].	bind
40735	1	9362	5	13	NULL	NULL	NULL	AR	GP		bind					E2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_10_5527_s_94	9576916	A cell-free  in vitro transcription/translation system was used to test whether ARA70 can either bind to E2 or increase the AR binding to E2.	bind
33698	1	9362	6	NULL	NULL	0	NULL	AR	NULL		bind	NULL				E2	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_10_5527_s_94	9576916	A cell-free  in vitro transcription/translation system was used to test whether ARA70 can either bind to E2 or increase the AR binding to E2.	bind
40736	1	9363	5	13	NULL	NULL	NULL	RBP	GP		bind					Notch-1	GP		IC		NULL		NULL	NULL	NULL	NULL	gw60_embo_21_20_5417_s_76	12374742	A cell-free synthesized SHARP fragment lacking the RBP-binding site did not reduce RBP binding to Notch-1-IC (lane 12).	bind
40737	2	9363	5	13	NULL	NULL	NULL	SHARP fragment	GP	cell-free synthesized	lacks								RBP-binding site		NULL		NULL	NULL	NULL	NULL	gw60_embo_21_20_5417_s_76	12374742	A cell-free synthesized SHARP fragment lacking the RBP-binding site did not reduce RBP binding to Notch-1-IC (lane 12).	bind
40738	3	9363	5	13	NULL	NULL	NULL	statement 2	Process		does not reduce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_20_5417_s_76	12374742	A cell-free synthesized SHARP fragment lacking the RBP-binding site did not reduce RBP binding to Notch-1-IC (lane 12).	bind
33699	1	9363	6	10	NULL	0	NULL	RBP	NULL		bind	NULL				Notch-1	NULL		IC		NULL		NULL	NULL	NULL	NULL	gw60_embo_21_20_5417_s_76	12374742	A cell-free synthesized SHARP fragment lacking the RBP-binding site did not reduce RBP binding to Notch-1-IC (lane 12).	bind
33700	2	9363	6	10	NULL	0	NULL	SHARP fragment	cell-free synthesized		lacks 								RBP binding site		NULL		NULL	NULL	NULL	NULL	gw60_embo_21_20_5417_s_76	12374742	A cell-free synthesized SHARP fragment lacking the RBP-binding site did not reduce RBP binding to Notch-1-IC (lane 12).	bind
33701	3	9363	6	NULL	NULL	0	NULL	statement 2	NULL		did not reduce	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_21_20_5417_s_76	12374742	A cell-free synthesized SHARP fragment lacking the RBP-binding site did not reduce RBP binding to Notch-1-IC (lane 12).	bind
40739	1	9364	5	13	NULL	NULL	NULL	cell-permeable peptide	GP		is derived from					epidermal growth factor receptor	GP		Grb2-binding sequence		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_18081_s_207	10364261	A cell-permeable peptide derived from the Grb2-binding sequence of epidermal growth factor receptor was shown to inhibit MAP kinase activation in cells stimulated with epidermal growth factor or with platelet-derived growth factor, but not in cells stimulated with bFGF.	bind
40740	2	9364	5	13	NULL	NULL	NULL	statement 1	GP		inhibit					MAP kinase	GP	activation of			NULL	cells stimulated with epidermal growth factor	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_18081_s_207	10364261	A cell-permeable peptide derived from the Grb2-binding sequence of epidermal growth factor receptor was shown to inhibit MAP kinase activation in cells stimulated with epidermal growth factor or with platelet-derived growth factor, but not in cells stimulated with bFGF.	bind
40741	3	9364	5	13	NULL	NULL	NULL	statement 1	GP		inhibit					MAP kinase	GP	activation of			NULL	cells stimulated with platelet-derived growth factor	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_18081_s_207	10364261	A cell-permeable peptide derived from the Grb2-binding sequence of epidermal growth factor receptor was shown to inhibit MAP kinase activation in cells stimulated with epidermal growth factor or with platelet-derived growth factor, but not in cells stimulated with bFGF.	bind
40742	4	9364	5	13	NULL	NULL	NULL	statement 1	GP		does not inhibit					MAP kinase	GP	activation of			NULL	cells stimulated with bFGF	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_18081_s_207	10364261	A cell-permeable peptide derived from the Grb2-binding sequence of epidermal growth factor receptor was shown to inhibit MAP kinase activation in cells stimulated with epidermal growth factor or with platelet-derived growth factor, but not in cells stimulated with bFGF.	bind
40755	5	9364	5	13	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_18081_s_207	10364261	A cell-permeable peptide derived from the Grb2-binding sequence of epidermal growth factor receptor was shown to inhibit MAP kinase activation in cells stimulated with epidermal growth factor or with platelet-derived growth factor, but not in cells stimulated with bFGF.	bind
33915	1	9364	6	10	NULL	0	NULL	cell-permeable peptide			is derived from					epidermal growth factor receptor			Grb2-binding sequence		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_18081_s_207	10364261	A cell-permeable peptide derived from the Grb2-binding sequence of epidermal growth factor receptor was shown to inhibit MAP kinase activation in cells stimulated with epidermal growth factor or with platelet-derived growth factor, but not in cells stimulated with bFGF.	bind
33916	2	9364	6	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				MAP kinase	NULL	activation of			NULL	cells stimulated with epidermal growth factor	0	NULL	NULL	NULL	gw60_jbiolchem_274_25_18081_s_207	10364261	A cell-permeable peptide derived from the Grb2-binding sequence of epidermal growth factor receptor was shown to inhibit MAP kinase activation in cells stimulated with epidermal growth factor or with platelet-derived growth factor, but not in cells stimulated with bFGF.	bind
33918	3	9364	6	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				MAP kinase	NULL	activation of			NULL	cells stimulated with platelet-derived growth factor	0	NULL	NULL	NULL	gw60_jbiolchem_274_25_18081_s_207	10364261	A cell-permeable peptide derived from the Grb2-binding sequence of epidermal growth factor receptor was shown to inhibit MAP kinase activation in cells stimulated with epidermal growth factor or with platelet-derived growth factor, but not in cells stimulated with bFGF.	bind
33919	4	9364	6	NULL	NULL	0	NULL	statement 1	NULL		does not inhibit	NULL				MAP kinase	NULL				NULL	cells stimulated with bFGF	0	NULL	NULL	NULL	gw60_jbiolchem_274_25_18081_s_207	10364261	A cell-permeable peptide derived from the Grb2-binding sequence of epidermal growth factor receptor was shown to inhibit MAP kinase activation in cells stimulated with epidermal growth factor or with platelet-derived growth factor, but not in cells stimulated with bFGF.	bind
58472	5	9364	6	10	NULL	0	NULL	statement 2			is an alternative to					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_18081_s_207	10364261	A cell-permeable peptide derived from the Grb2-binding sequence of epidermal growth factor receptor was shown to inhibit MAP kinase activation in cells stimulated with epidermal growth factor or with platelet-derived growth factor, but not in cells stimulated with bFGF.	bind
40743	1	9365	5	13	NULL	NULL	NULL	Shc	GP		associate with					SHP-2	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_mol-biol-cell_16_7_15888547_s_11	15888547	A cell-permeable peptide that contained a polyproline sequence  from Shc selectively inhibited Shc/SHP-2 association and impaired Shc  but not SHP-2 binding to SHPS-1.	bind
40744	2	9365	5	13	NULL	NULL	NULL	cell-permeable peptide	GP		contains					Shc	GP		polyproline sequence		NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_mol-biol-cell_16_7_15888547_s_11	15888547	A cell-permeable peptide that contained a polyproline sequence  from Shc selectively inhibited Shc/SHP-2 association and impaired Shc  but not SHP-2 binding to SHPS-1.	bind
40745	3	9365	5	13	NULL	NULL	NULL	statement 2	Process		inhibit		selectively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_mol-biol-cell_16_7_15888547_s_11	15888547	A cell-permeable peptide that contained a polyproline sequence  from Shc selectively inhibited Shc/SHP-2 association and impaired Shc  but not SHP-2 binding to SHPS-1.	bind
40746	4	9365	5	13	NULL	NULL	NULL	SHP-2	GP		bind					SHPS-1	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_mol-biol-cell_16_7_15888547_s_11	15888547	A cell-permeable peptide that contained a polyproline sequence  from Shc selectively inhibited Shc/SHP-2 association and impaired Shc  but not SHP-2 binding to SHPS-1.	bind
40747	5	9365	5	13	NULL	NULL	NULL	Shc	GP		bind					SHPS-1	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_mol-biol-cell_16_7_15888547_s_11	15888547	A cell-permeable peptide that contained a polyproline sequence  from Shc selectively inhibited Shc/SHP-2 association and impaired Shc  but not SHP-2 binding to SHPS-1.	bind
40748	6	9365	5	13	NULL	NULL	NULL	statement 2	Process		impairs					statement 5	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_mol-biol-cell_16_7_15888547_s_11	15888547	A cell-permeable peptide that contained a polyproline sequence  from Shc selectively inhibited Shc/SHP-2 association and impaired Shc  but not SHP-2 binding to SHPS-1.	bind
40749	7	9365	5	13	NULL	NULL	NULL	statement 2	Process		does not impair					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_mol-biol-cell_16_7_15888547_s_11	15888547	A cell-permeable peptide that contained a polyproline sequence  from Shc selectively inhibited Shc/SHP-2 association and impaired Shc  but not SHP-2 binding to SHPS-1.	bind
33702	1	9365	6	NULL	NULL	0	NULL	Shc	NULL		associates with	NULL				SHP-2	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_mol-biol-cell_16_7_15888547_s_11	15888547	A cell-permeable peptide that contained a polyproline sequence  from Shc selectively inhibited Shc/SHP-2 association and impaired Shc  but not SHP-2 binding to SHPS-1.	bind
33703	2	9365	6	NULL	NULL	0	NULL	SHP-2	NULL		bind	NULL				SHPS-1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_mol-biol-cell_16_7_15888547_s_11	15888547	A cell-permeable peptide that contained a polyproline sequence  from Shc selectively inhibited Shc/SHP-2 association and impaired Shc  but not SHP-2 binding to SHPS-1.	bind
33704	3	9365	6	NULL	NULL	0	NULL	Shc	NULL		bind	NULL				SHPS-1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_mol-biol-cell_16_7_15888547_s_11	15888547	A cell-permeable peptide that contained a polyproline sequence  from Shc selectively inhibited Shc/SHP-2 association and impaired Shc  but not SHP-2 binding to SHPS-1.	bind
33705	4	9365	6	NULL	NULL	0	NULL	cell-permeable peptide	NULL		contains	NULL				Shc	NULL		polyproline sequence		NULL		0	NULL	NULL	NULL	abs-batch0517-0529_mol-biol-cell_16_7_15888547_s_11	15888547	A cell-permeable peptide that contained a polyproline sequence  from Shc selectively inhibited Shc/SHP-2 association and impaired Shc  but not SHP-2 binding to SHPS-1.	bind
33706	5	9365	6	10	NULL	0	NULL	statement 4			inhibits		selectively			statement 1					NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_mol-biol-cell_16_7_15888547_s_11	15888547	A cell-permeable peptide that contained a polyproline sequence  from Shc selectively inhibited Shc/SHP-2 association and impaired Shc  but not SHP-2 binding to SHPS-1.	bind
33759	6	9365	6	NULL	NULL	0	NULL	statement 4	NULL		inhibits	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_mol-biol-cell_16_7_15888547_s_11	15888547	A cell-permeable peptide that contained a polyproline sequence  from Shc selectively inhibited Shc/SHP-2 association and impaired Shc  but not SHP-2 binding to SHPS-1.	bind
33760	7	9365	6	NULL	NULL	0	NULL	statement 4	NULL		does not inhibit	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_mol-biol-cell_16_7_15888547_s_11	15888547	A cell-permeable peptide that contained a polyproline sequence  from Shc selectively inhibited Shc/SHP-2 association and impaired Shc  but not SHP-2 binding to SHPS-1.	bind
40750	1	9367	5	13	NULL	NULL	NULL	S-Ht31	GP		is					Ht31 counterpart	GP	cell-permeable stearated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_4747_s_99	9030527	A cell-permeable stearated Ht31 counterpart, S-Ht31, also inhibited  in vitro binding of RII to AKAP 110, albeit at a reduced potency (85% inhibition compared with 100% by the non-stearated Ht31).	bind
40751	2	9367	5	13	NULL	NULL	NULL	RII	GP		bind					AKAP 110	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_4747_s_99	9030527	A cell-permeable stearated Ht31 counterpart, S-Ht31, also inhibited  in vitro binding of RII to AKAP 110, albeit at a reduced potency (85% inhibition compared with 100% by the non-stearated Ht31).	bind
40752	3	9367	5	13	NULL	NULL	NULL	statement 1	Process		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_4747_s_99	9030527	A cell-permeable stearated Ht31 counterpart, S-Ht31, also inhibited  in vitro binding of RII to AKAP 110, albeit at a reduced potency (85% inhibition compared with 100% by the non-stearated Ht31).	bind
40753	4	9367	5	13	NULL	NULL	NULL	Ht31	GP	non-stearated	inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_4747_s_99	9030527	A cell-permeable stearated Ht31 counterpart, S-Ht31, also inhibited  in vitro binding of RII to AKAP 110, albeit at a reduced potency (85% inhibition compared with 100% by the non-stearated Ht31).	bind
40754	5	9367	5	13	NULL	NULL	NULL	statement 3	Process	affinity of	is less than					statement 4	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_4747_s_99	9030527	A cell-permeable stearated Ht31 counterpart, S-Ht31, also inhibited  in vitro binding of RII to AKAP 110, albeit at a reduced potency (85% inhibition compared with 100% by the non-stearated Ht31).	bind
33761	1	9367	6	NULL	NULL	0	NULL	RII	NULL		bind	NULL				AKAP 110	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4747_s_99	9030527	A cell-permeable stearated Ht31 counterpart, S-Ht31, also inhibited  in vitro binding of RII to AKAP 110, albeit at a reduced potency (85% inhibition compared with 100% by the non-stearated Ht31).	bind
33762	2	9367	6	NULL	NULL	0	NULL	S-Ht31	NULL	cell-permeable	inhibits	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_4747_s_99	9030527	A cell-permeable stearated Ht31 counterpart, S-Ht31, also inhibited  in vitro binding of RII to AKAP 110, albeit at a reduced potency (85% inhibition compared with 100% by the non-stearated Ht31).	bind
33763	3	9367	6	NULL	NULL	0	NULL	Ht31	NULL	non-stearated	inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4747_s_99	9030527	A cell-permeable stearated Ht31 counterpart, S-Ht31, also inhibited  in vitro binding of RII to AKAP 110, albeit at a reduced potency (85% inhibition compared with 100% by the non-stearated Ht31).	bind
33764	4	9367	6	NULL	NULL	0	NULL	statement 2	NULL	affinity of	is less than	NULL				statement 3	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4747_s_99	9030527	A cell-permeable stearated Ht31 counterpart, S-Ht31, also inhibited  in vitro binding of RII to AKAP 110, albeit at a reduced potency (85% inhibition compared with 100% by the non-stearated Ht31).	bind
33765	5	9367	6	10	NULL	0	NULL	S-Ht31			is					Ht31 counterpart		cell-permeable stearated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_4747_s_99	9030527	A cell-permeable stearated Ht31 counterpart, S-Ht31, also inhibited  in vitro binding of RII to AKAP 110, albeit at a reduced potency (85% inhibition compared with 100% by the non-stearated Ht31).	bind
40756	1	9368	5	13	NULL	NULL	NULL	cell-permeant peptide	GP	TAT-tagged 	encompass					PAK1	GP		second proline-rich SH3 binding domain		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
40803	2	9368	5	13	NULL	NULL	NULL	Grb2	GP		associate with					PAK1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
40804	3	9368	5	13	NULL	NULL	NULL	Grb2	GP		associate with					PAK1	GP				NULL	in vivo	NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
40805	4	9368	5	13	NULL	NULL	NULL	EGFR	GP	activated	associate with					PAK1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
40806	5	9368	5	13	NULL	NULL	NULL	EGFR	Process	activated	associate with					PAK1	Process				NULL	in vivo	NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
40807	6	9368	5	13	NULL	NULL	NULL	statement 1	Process		block					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
40808	7	9368	5	13	NULL	NULL	NULL	statement 1	Process		block					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
40809	8	9368	5	13	NULL	NULL	NULL	statement 1	Process		block					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
40810	9	9368	5	13	NULL	NULL	NULL	statement 1	Process		block					statement 5	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
40811	10	9368	5	13	NULL	NULL	NULL	statement 6	Process		occurs simultaneously with					statement 8	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
40812	11	9368	5	13	NULL	NULL	NULL	statement 7	Process		occurs simultaneously with					statement 9	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
40813	12	9368	5	13	NULL	NULL	NULL	PAK1	GP		interact with					EGFR	GP	activated			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
40814	13	9368	5	13	NULL	NULL	NULL	Grb2	GP		mediate					statement 12	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
40815	14	9368	5	13	NULL	NULL	NULL	statement 10	Process		indicate					statement 13	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
40816	15	9368	5	13	NULL	NULL	NULL	statement 11	Process		indicate					statement 13	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
33920	1	9368	6	NULL	NULL	0	NULL	Grb2	NULL		associates with	NULL				PAK1	NULL				NULL	in vitro	0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
33921	2	9368	6	NULL	NULL	0	NULL	EGFR	NULL	activated	associates with	NULL				PAK1	NULL				NULL	in vivo	0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
33922	5	9368	6	10	NULL	0	NULL	Grb2	NULL		mediates	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
33923	7	9368	6	10	NULL	0	NULL	TAT-tagged peptide	NULL		encompasses	NULL				PAK1	NULL		second proline-rich SH3 binding domain		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
49183	3	9368	6	10	NULL	0	NULL	Grb2	NULL		associates with	NULL				PAK1	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
49184	4	9368	6	10	NULL	0	NULL	EGFR	NULL	activated	associates with	NULL				PAK1	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
49185	6	9368	6	10	NULL	0	NULL	Grb2	NULL		mediates	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
49187	8	9368	6	10	NULL	0	NULL	statement 7	NULL		blocks	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
49188	9	9368	6	10	NULL	0	NULL	statement 7	NULL		blocks	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
49189	10	9368	6	10	NULL	0	NULL	statement 7	NULL		blocks	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
49190	11	9368	6	10	NULL	0	NULL	statement 7	NULL		blocks	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
49191	12	9368	6	10	NULL	0	NULL	statement 8	NULL		occurs simultaneously with	NULL				statement 10	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
49192	13	9368	6	10	NULL	0	NULL	statement 9	NULL		occurs simultaneously with	NULL				statement 11	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
58473	14	9368	6	10	NULL	0	NULL	statement 12			indicate					statement 5					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
58474	15	9368	6	10	NULL	0	NULL	statement 12			indicate					statement 6					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
58475	16	9368	6	10	NULL	0	NULL	statement 13			indicate					statement 5					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
58476	17	9368	6	10	NULL	0	NULL	statement 13			indicate					statement 6					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_11_12522133_s_7	12522133	A cell-permeant TAT-tagged peptide encompassing the  second proline-rich SH3 binding domain of PAK1 simultaneously blocked  Grb2 and activated EGFR association with PAK1, in vitro and in vivo, indicating  that Grb2 mediates the interaction of PAK1 with the activated EGFR.	bind
41249	1	9370	5	13	NULL	NULL	NULL	heparan sulfate proteoglycan	GP	cell-surface	mediate					neural cell	Cell	adhesion of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_1_43_s_457	7788881	A cell-surface heparan sulfate proteoglycan mediates neural cell adhesion and spreading on a defined sequence from the c-terminal cell and heparin binding domain of fibronectin, FN-C/-II.	bind
41251	2	9370	5	13	NULL	NULL	NULL	heparan sulfate proteoglycan	GP	cell-surface	mediate					neural cell	Cell	spreading of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_1_43_s_457	7788881	A cell-surface heparan sulfate proteoglycan mediates neural cell adhesion and spreading on a defined sequence from the c-terminal cell and heparin binding domain of fibronectin, FN-C/-II.	bind
33925	1	9370	6	10	NULL	0	NULL	heparan sulfate proteoglycan		cell-surface	mediates					neural cell 		adhesion of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_1_43_s_457	7788881	A cell-surface heparan sulfate proteoglycan mediates neural cell adhesion and spreading on a defined sequence from the c-terminal cell and heparin binding domain of fibronectin, FN-C/-II.	bind
33927	2	9370	6	10	NULL	0	NULL	heparan sulfate proteoglycan		cell-surface	mediates					neural cell 		spreading of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_1_43_s_457	7788881	A cell-surface heparan sulfate proteoglycan mediates neural cell adhesion and spreading on a defined sequence from the c-terminal cell and heparin binding domain of fibronectin, FN-C/-II.	bind
40817	1	9373	5	13	NULL	NULL	NULL	Zhangfei	GP		is a type of					cellular transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_clinmicrobiolrev_16_1_79_s_107	12525426	A cellular transcription factor, Zhangfei, binds to HCF and prevents activation of the ICP0 promoter ( ).	bind
40818	2	9373	5	13	NULL	NULL	NULL	Zhangfei	GP		bind					HCF	GP				NULL		NULL	NULL	NULL	NULL	gw70_clinmicrobiolrev_16_1_79_s_107	12525426	A cellular transcription factor, Zhangfei, binds to HCF and prevents activation of the ICP0 promoter ( ).	bind
40819	3	9373	5	13	NULL	NULL	NULL	statement 2	Process		prevents					ICP0	NucleicAcid	activation of		promoter	NULL		NULL	NULL	NULL	NULL	gw70_clinmicrobiolrev_16_1_79_s_107	12525426	A cellular transcription factor, Zhangfei, binds to HCF and prevents activation of the ICP0 promoter ( ).	bind
33766	1	9373	6	NULL	NULL	0	NULL	Zhangfei	NULL		is a type of	NULL				transcription factor	NULL	cellular			NULL		0	NULL	NULL	NULL	gw70_clinmicrobiolrev_16_1_79_s_107	12525426	A cellular transcription factor, Zhangfei, binds to HCF and prevents activation of the ICP0 promoter ( ).	bind
33767	2	9373	6	NULL	NULL	0	NULL	Zhangfei	NULL		bind	NULL				HCF	NULL				NULL		0	NULL	NULL	NULL	gw70_clinmicrobiolrev_16_1_79_s_107	12525426	A cellular transcription factor, Zhangfei, binds to HCF and prevents activation of the ICP0 promoter ( ).	bind
33768	3	9373	6	NULL	NULL	0	NULL	Zhangfei	NULL		prevents	NULL				ICP0	NULL	activation of		promoter	NULL		0	NULL	NULL	NULL	gw70_clinmicrobiolrev_16_1_79_s_107	12525426	A cellular transcription factor, Zhangfei, binds to HCF and prevents activation of the ICP0 promoter ( ).	bind
40820	1	9374	5	13	NULL	NULL	NULL	caveolin-1	GP		associate with								raft domains		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_4_673_s_17	12771123	A central dogma of the caveolae/glycolipid raft field, therefore, has been that the invaginated flask-shaped morphology of caveolae is a specific consequence of the association of caveolin-1 with select raft domains.	bind
40823	2	9374	5	13	NULL	NULL	NULL	caveolae	CellComponent		contains					flask-shaped morphology	CellComponent	invaginated			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_4_673_s_17	12771123	A central dogma of the caveolae/glycolipid raft field, therefore, has been that the invaginated flask-shaped morphology of caveolae is a specific consequence of the association of caveolin-1 with select raft domains.	bind
40824	3	9374	5	13	NULL	NULL	NULL	statement 2	Process		is a consequence of 					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_4_673_s_17	12771123	A central dogma of the caveolae/glycolipid raft field, therefore, has been that the invaginated flask-shaped morphology of caveolae is a specific consequence of the association of caveolin-1 with select raft domains.	bind
33769	1	9374	6	NULL	NULL	0	NULL	Caveolin-1	NULL		associates with	NULL					NULL		raft domains		NULL		0	NULL	NULL	NULL	gw70_cellbiol_161_4_673_s_17	12771123	A central dogma of the caveolae/glycolipid raft field, therefore, has been that the invaginated flask-shaped morphology of caveolae is a specific consequence of the association of caveolin-1 with select raft domains.	bind
33770	2	9374	6	10	NULL	0	NULL	caveolae			contains					flask-shaped morphology 		invaginated 			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_161_4_673_s_17	12771123	A central dogma of the caveolae/glycolipid raft field, therefore, has been that the invaginated flask-shaped morphology of caveolae is a specific consequence of the association of caveolin-1 with select raft domains.	bind
33771	3	9374	6	NULL	NULL	0	NULL	statement 2	NULL		is a consequence of 	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_161_4_673_s_17	12771123	A central dogma of the caveolae/glycolipid raft field, therefore, has been that the invaginated flask-shaped morphology of caveolae is a specific consequence of the association of caveolin-1 with select raft domains.	bind
40837	1	9376	5	13	NULL	NULL	NULL	Rb family	GP		regulates		negatively			E2F	GP	activities of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7455_s_12	9819431	A central function of the Rb family is to negatively regulate the activity of E2F transcription factors that control the transcription of many cell cycle-regulated genes ( 41).	bind
40838	2	9376	5	13	NULL	NULL	NULL	E2F	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7455_s_12	9819431	A central function of the Rb family is to negatively regulate the activity of E2F transcription factors that control the transcription of many cell cycle-regulated genes ( 41).	bind
40839	3	9376	5	13	NULL	NULL	NULL	E2F	GP		regulates					cell cycle-regulated genes	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7455_s_12	9819431	A central function of the Rb family is to negatively regulate the activity of E2F transcription factors that control the transcription of many cell cycle-regulated genes ( 41).	bind
33772	1	9376	6	10	NULL	0	NULL	Rb family	NULL		 regulates	NULL	negatively			E2F 	NULL	activity of 			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7455_s_12	9819431	A central function of the Rb family is to negatively regulate the activity of E2F transcription factors that control the transcription of many cell cycle-regulated genes ( 41).	bind
33773	2	9376	6	10	NULL	0	NULL	E2F 	NULL		regulate	NULL				cell cycle-regulated genes	NULL	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7455_s_12	9819431	A central function of the Rb family is to negatively regulate the activity of E2F transcription factors that control the transcription of many cell cycle-regulated genes ( 41).	bind
48124	3	9376	6	10	NULL	0	NULL	E2F	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_7455_s_12	9819431	A central function of the Rb family is to negatively regulate the activity of E2F transcription factors that control the transcription of many cell cycle-regulated genes ( 41).	bind
40886	1	9377	5	13	NULL	NULL	NULL	RasGAP	GP		is					Ras GTPase activating protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_17_0_701_s_436	10358772	A central protein involved in the regulation of small GTPases is the 120 kDa Ras GTPase  activating protein (RasGAP) that binds to the active, GTP-bound form of Ras and activates  its GTPase activity, catalyzing the formation of inactive Ras-GDP ( 177,  178).	bind
40887	2	9377	5	13	NULL	NULL	NULL	RasGAP	GP		is a type of					central protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_17_0_701_s_436	10358772	A central protein involved in the regulation of small GTPases is the 120 kDa Ras GTPase  activating protein (RasGAP) that binds to the active, GTP-bound form of Ras and activates  its GTPase activity, catalyzing the formation of inactive Ras-GDP ( 177,  178).	bind
40888	3	9377	5	13	NULL	NULL	NULL	RasGAP	GP		is involved in					small GTPases	GP	regulation of			NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_17_0_701_s_436	10358772	A central protein involved in the regulation of small GTPases is the 120 kDa Ras GTPase  activating protein (RasGAP) that binds to the active, GTP-bound form of Ras and activates  its GTPase activity, catalyzing the formation of inactive Ras-GDP ( 177,  178).	bind
40889	4	9377	5	13	NULL	NULL	NULL	Ras	GP		bind					GTP	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_17_0_701_s_436	10358772	A central protein involved in the regulation of small GTPases is the 120 kDa Ras GTPase  activating protein (RasGAP) that binds to the active, GTP-bound form of Ras and activates  its GTPase activity, catalyzing the formation of inactive Ras-GDP ( 177,  178).	bind
40890	5	9377	5	13	NULL	NULL	NULL	RasGAP	GP		bind					statement 4	GP	active			NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_17_0_701_s_436	10358772	A central protein involved in the regulation of small GTPases is the 120 kDa Ras GTPase  activating protein (RasGAP) that binds to the active, GTP-bound form of Ras and activates  its GTPase activity, catalyzing the formation of inactive Ras-GDP ( 177,  178).	bind
40892	7	9377	5	13	NULL	NULL	NULL	Ras-GTP	GP	active	is converted to					Ras-GDP	GP	inactive			NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_17_0_701_s_436	10358772	A central protein involved in the regulation of small GTPases is the 120 kDa Ras GTPase  activating protein (RasGAP) that binds to the active, GTP-bound form of Ras and activates  its GTPase activity, catalyzing the formation of inactive Ras-GDP ( 177,  178).	bind
40893	8	9377	5	13	NULL	NULL	NULL	statement 6	Process		catalyze					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_17_0_701_s_436	10358772	A central protein involved in the regulation of small GTPases is the 120 kDa Ras GTPase  activating protein (RasGAP) that binds to the active, GTP-bound form of Ras and activates  its GTPase activity, catalyzing the formation of inactive Ras-GDP ( 177,  178).	bind
48125	6	9377	5	13	NULL	NULL	NULL	statement 5	Process		activates					Ras	GP	GTPase activity of			NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_17_0_701_s_436	10358772	A central protein involved in the regulation of small GTPases is the 120 kDa Ras GTPase  activating protein (RasGAP) that binds to the active, GTP-bound form of Ras and activates  its GTPase activity, catalyzing the formation of inactive Ras-GDP ( 177,  178).	bind
33774	1	9377	6	NULL	NULL	0	NULL	RasGAP	NULL		is	NULL				Ras GTPase activating protein	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_701_s_436	10358772	A central protein involved in the regulation of small GTPases is the 120 kDa Ras GTPase  activating protein (RasGAP) that binds to the active, GTP-bound form of Ras and activates  its GTPase activity, catalyzing the formation of inactive Ras-GDP ( 177,  178).	bind
33775	2	9377	6	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				Ras	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_701_s_436	10358772	A central protein involved in the regulation of small GTPases is the 120 kDa Ras GTPase  activating protein (RasGAP) that binds to the active, GTP-bound form of Ras and activates  its GTPase activity, catalyzing the formation of inactive Ras-GDP ( 177,  178).	bind
33776	3	9377	6	NULL	NULL	0	NULL	RasGAP	NULL		bind	NULL				statement 2	NULL	active			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_701_s_436	10358772	A central protein involved in the regulation of small GTPases is the 120 kDa Ras GTPase  activating protein (RasGAP) that binds to the active, GTP-bound form of Ras and activates  its GTPase activity, catalyzing the formation of inactive Ras-GDP ( 177,  178).	bind
33777	4	9377	6	10	NULL	0	NULL	statement 2			activates					Ras		GTPase activity of			NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_17_0_701_s_436	10358772	A central protein involved in the regulation of small GTPases is the 120 kDa Ras GTPase  activating protein (RasGAP) that binds to the active, GTP-bound form of Ras and activates  its GTPase activity, catalyzing the formation of inactive Ras-GDP ( 177,  178).	bind
33779	7	9377	6	10	NULL	0	NULL	statement 4	NULL		catalyzes	NULL				statement 6	NULL				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_17_0_701_s_436	10358772	A central protein involved in the regulation of small GTPases is the 120 kDa Ras GTPase  activating protein (RasGAP) that binds to the active, GTP-bound form of Ras and activates  its GTPase activity, catalyzing the formation of inactive Ras-GDP ( 177,  178).	bind
48126	6	9377	6	10	NULL	0	NULL	RAS-GTP	NULL	active	is converted to	NULL				RAS-GDP	NULL	inactive			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_701_s_436	10358772	A central protein involved in the regulation of small GTPases is the 120 kDa Ras GTPase  activating protein (RasGAP) that binds to the active, GTP-bound form of Ras and activates  its GTPase activity, catalyzing the formation of inactive Ras-GDP ( 177,  178).	bind
58477	5	9377	6	10	NULL	0	NULL	RasGAP			is involved in					small GTPases		regulation of			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_701_s_436	10358772	A central protein involved in the regulation of small GTPases is the 120 kDa Ras GTPase  activating protein (RasGAP) that binds to the active, GTP-bound form of Ras and activates  its GTPase activity, catalyzing the formation of inactive Ras-GDP ( 177,  178).	bind
40894	1	9378	5	13	NULL	NULL	NULL	PSGL-1	GP		bind					E-selectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_45_28786_s_161	9353350	A central question arising from the current study is how the E-selectin and the P-selectin binding activities of PSGL-1 could be differentially regulated and what the structural differences between both recognition motifs are.	bind
40895	2	9378	5	13	NULL	NULL	NULL	PSGL-1	GP		bind					P-selectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_45_28786_s_161	9353350	A central question arising from the current study is how the E-selectin and the P-selectin binding activities of PSGL-1 could be differentially regulated and what the structural differences between both recognition motifs are.	bind
33780	1	9378	6	NULL	NULL	0	NULL	PSGL-1	NULL		bind	NULL				E-selectin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_45_28786_s_161	9353350	A central question arising from the current study is how the E-selectin and the P-selectin binding activities of PSGL-1 could be differentially regulated and what the structural differences between both recognition motifs are.	bind
33781	2	9378	6	NULL	NULL	0	NULL	PSGL-1	NULL		bind	NULL				P-selectin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_45_28786_s_161	9353350	A central question arising from the current study is how the E-selectin and the P-selectin binding activities of PSGL-1 could be differentially regulated and what the structural differences between both recognition motifs are.	bind
40896	1	9379	5	13	NULL	NULL	NULL	rhodopsin	GP	MII form of 	bind					transducin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_3_1683_s_17	9880548	A central question remains as to why only the MII form of rhodopsin can bind and activate transducin.	bind
40897	2	9379	5	13	NULL	NULL	NULL	statement 1	Process		activates					transducin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_3_1683_s_17	9880548	A central question remains as to why only the MII form of rhodopsin can bind and activate transducin.	bind
33782	1	9379	6	NULL	NULL	0	NULL	rhodopsin	NULL	MII form	bind	NULL				transducin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_3_1683_s_17	9880548	A central question remains as to why only the MII form of rhodopsin can bind and activate transducin.	bind
33783	2	9379	6	NULL	NULL	0	NULL	rhodopsin	NULL	MII form	activates	NULL				transducin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_3_1683_s_17	9880548	A central question remains as to why only the MII form of rhodopsin can bind and activate transducin.	bind
41234	1	9380	5	13	NULL	NULL	NULL	mTERF	GP		is					mitochondrial transcription termination factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15670_s_18	14744862	A central role in the attenuation phenomenon taking place at this site is played by the mitochondrial transcription termination factor (mTERF),  1 a 39-kDa DNA-binding protein that binds to a 28-base pair region (nucleotides 3229 to 3256) within the  tRNALeu(UUR) gene, at a position immediately adjacent to the  16 S rRNA gene.	bind
41237	2	9380	5	13	NULL	NULL	NULL	mTERF	GP		is a type of					DNA-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15670_s_18	14744862	A central role in the attenuation phenomenon taking place at this site is played by the mitochondrial transcription termination factor (mTERF),  1 a 39-kDa DNA-binding protein that binds to a 28-base pair region (nucleotides 3229 to 3256) within the  tRNALeu(UUR) gene, at a position immediately adjacent to the  16 S rRNA gene.	bind
41238	3	9380	5	13	NULL	NULL	NULL	mTERF	GP		bind					tRNALeu(UUR) gene	GP			28-base pair region (nucleotides 3229 to 3256)	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15670_s_18	14744862	A central role in the attenuation phenomenon taking place at this site is played by the mitochondrial transcription termination factor (mTERF),  1 a 39-kDa DNA-binding protein that binds to a 28-base pair region (nucleotides 3229 to 3256) within the  tRNALeu(UUR) gene, at a position immediately adjacent to the  16 S rRNA gene.	bind
41242	4	9380	5	13	NULL	NULL	NULL	statement 3	Process		occurs					16 S rRNA gene	GP	adjacent to			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15670_s_18	14744862	A central role in the attenuation phenomenon taking place at this site is played by the mitochondrial transcription termination factor (mTERF),  1 a 39-kDa DNA-binding protein that binds to a 28-base pair region (nucleotides 3229 to 3256) within the  tRNALeu(UUR) gene, at a position immediately adjacent to the  16 S rRNA gene.	bind
33784	1	9380	6	NULL	NULL	0	NULL	mTERF	NULL		is	NULL				mitochondrial transcription termination factor	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_15_15670_s_18	14744862	A central role in the attenuation phenomenon taking place at this site is played by the mitochondrial transcription termination factor (mTERF),  1 a 39-kDa DNA-binding protein that binds to a 28-base pair region (nucleotides 3229 to 3256) within the  tRNALeu(UUR) gene, at a position immediately adjacent to the  16 S rRNA gene.	bind
33930	2	9380	6	10	NULL	0	NULL	mTERF			bind					tRNALeu(UUR) gene				28-base pair region nucleotides 3229 to 3256	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15670_s_18	14744862	A central role in the attenuation phenomenon taking place at this site is played by the mitochondrial transcription termination factor (mTERF),  1 a 39-kDa DNA-binding protein that binds to a 28-base pair region (nucleotides 3229 to 3256) within the  tRNALeu(UUR) gene, at a position immediately adjacent to the  16 S rRNA gene.	bind
33932	3	9380	6	10	NULL	0	NULL	mTERF	NULL		is a type of	NULL				DNA-binding protein	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15670_s_18	14744862	A central role in the attenuation phenomenon taking place at this site is played by the mitochondrial transcription termination factor (mTERF),  1 a 39-kDa DNA-binding protein that binds to a 28-base pair region (nucleotides 3229 to 3256) within the  tRNALeu(UUR) gene, at a position immediately adjacent to the  16 S rRNA gene.	bind
48127	4	9380	6	10	NULL	0	NULL	statement 2	NULL		occurs	NULL				16 S rRNA gene	NULL	adjacent to			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_15_15670_s_18	14744862	A central role in the attenuation phenomenon taking place at this site is played by the mitochondrial transcription termination factor (mTERF),  1 a 39-kDa DNA-binding protein that binds to a 28-base pair region (nucleotides 3229 to 3256) within the  tRNALeu(UUR) gene, at a position immediately adjacent to the  16 S rRNA gene.	bind
40898	1	9381	5	13	NULL	NULL	NULL	CREB	GP		bind		constitutively							CRE	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_37_13572_s_6	15342915	A central tenet of the CREB - CBP model is that CREB binds constitutively to the CRE and that regulation occurs through the phosphorylation-dependent recruitment of CBP.	bind
40899	2	9381	5	13	NULL	NULL	NULL	CBP	GP	recruitment of	is dependent on					phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_37_13572_s_6	15342915	A central tenet of the CREB - CBP model is that CREB binds constitutively to the CRE and that regulation occurs through the phosphorylation-dependent recruitment of CBP.	bind
40900	3	9381	5	13	NULL	NULL	NULL	statement 1	Process	regulation of	occurs through					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_37_13572_s_6	15342915	A central tenet of the CREB - CBP model is that CREB binds constitutively to the CRE and that regulation occurs through the phosphorylation-dependent recruitment of CBP.	bind
33785	1	9381	6	10	NULL	0	NULL	CREB			bind 		constitutively							CRE	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_37_13572_s_6	15342915	A central tenet of the CREB - CBP model is that CREB binds constitutively to the CRE and that regulation occurs through the phosphorylation-dependent recruitment of CBP.	bind
33786	2	9381	6	NULL	NULL	0	NULL	CBP	NULL	recruitment of	is dependent on	NULL				phosphorylation	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_37_13572_s_6	15342915	A central tenet of the CREB - CBP model is that CREB binds constitutively to the CRE and that regulation occurs through the phosphorylation-dependent recruitment of CBP.	bind
33787	3	9381	6	10	NULL	0	NULL	statement 1	NULL	regulation of	occurs through	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_37_13572_s_6	15342915	A central tenet of the CREB - CBP model is that CREB binds constitutively to the CRE and that regulation occurs through the phosphorylation-dependent recruitment of CBP.	bind
40901	1	9382	5	13	NULL	NULL	NULL	cortactin	GP		constitutes					series of repeats	GP	centrally positioned			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_1_99_s_40	12835311	A centrally positioned series of repeats in cortactin bind and cross-link actin filaments in a tyrosine phosphorylation - dependent manner ( ;  ).	bind
40902	2	9382	5	13	NULL	NULL	NULL	statement 1	GP		bind					actin filaments	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_1_99_s_40	12835311	A centrally positioned series of repeats in cortactin bind and cross-link actin filaments in a tyrosine phosphorylation - dependent manner ( ;  ).	bind
40903	3	9382	5	13	NULL	NULL	NULL	statement 1	GP		cross-links					actin filaments	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_1_99_s_40	12835311	A centrally positioned series of repeats in cortactin bind and cross-link actin filaments in a tyrosine phosphorylation - dependent manner ( ;  ).	bind
40904	4	9382	5	13	NULL	NULL	NULL	statement 2	Process		is dependent on					phosphorylation	Process		tyrosine		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_1_99_s_40	12835311	A centrally positioned series of repeats in cortactin bind and cross-link actin filaments in a tyrosine phosphorylation - dependent manner ( ;  ).	bind
40905	5	9382	5	13	NULL	NULL	NULL	statement 3	Process		is dependent on					phosphorylation	Process		tyrosine		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_162_1_99_s_40	12835311	A centrally positioned series of repeats in cortactin bind and cross-link actin filaments in a tyrosine phosphorylation - dependent manner ( ;  ).	bind
33788	1	9382	6	NULL	NULL	0	NULL	cortactin	NULL		bind	NULL		centrally positioned series of repeats		actin filaments	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_162_1_99_s_40	12835311	A centrally positioned series of repeats in cortactin bind and cross-link actin filaments in a tyrosine phosphorylation - dependent manner ( ;  ).	bind
33789	2	9382	6	NULL	NULL	0	NULL	cortactin	NULL		cross link	NULL		centrally positioned series of repeats		actin filaments	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_162_1_99_s_40	12835311	A centrally positioned series of repeats in cortactin bind and cross-link actin filaments in a tyrosine phosphorylation - dependent manner ( ;  ).	bind
33790	3	9382	6	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				tyrosine	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw70_cellbiol_162_1_99_s_40	12835311	A centrally positioned series of repeats in cortactin bind and cross-link actin filaments in a tyrosine phosphorylation - dependent manner ( ;  ).	bind
33791	4	9382	6	NULL	NULL	0	NULL	statement 2	NULL		is dependent on	NULL				tyrosine	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw70_cellbiol_162_1_99_s_40	12835311	A centrally positioned series of repeats in cortactin bind and cross-link actin filaments in a tyrosine phosphorylation - dependent manner ( ;  ).	bind
40906	1	9383	5	13	NULL	NULL	NULL	TIMP-2	GP		bind					MT1-MMP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_38_24360_s_266	9733724	A certain amount of TIMP-2 bound to MT1-MMP appears to be required for efficient activation of pro-MMP-2.	bind
40907	2	9383	5	13	NULL	NULL	NULL	statement 1	Process		is required for					pro-MMP-2	GP	efficient activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_38_24360_s_266	9733724	A certain amount of TIMP-2 bound to MT1-MMP appears to be required for efficient activation of pro-MMP-2.	bind
33792	1	9383	6	NULL	NULL	0	NULL	TIMP-2	NULL		bind	NULL				MT1-MMP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_38_24360_s_266	9733724	A certain amount of TIMP-2 bound to MT1-MMP appears to be required for efficient activation of pro-MMP-2.	bind
33793	2	9383	6	NULL	NULL	0	NULL	statement 1	NULL		is required for	NULL				pro-MMP-2	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_38_24360_s_266	9733724	A certain amount of TIMP-2 bound to MT1-MMP appears to be required for efficient activation of pro-MMP-2.	bind
40908	1	9384	5	13	NULL	NULL	NULL	p85	GP		bind					Grb2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_26_16670_s_224	9195983	A certain conclusion is that binding of p85 and p120 to Grb2 occurs independently: while the binding of p85 is lost if only the C-SH3 domain is intact, this alteration does not affect the association of p120.	bind
40909	2	9384	5	13	NULL	NULL	NULL	p120	GP		bind					Grb2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_26_16670_s_224	9195983	A certain conclusion is that binding of p85 and p120 to Grb2 occurs independently: while the binding of p85 is lost if only the C-SH3 domain is intact, this alteration does not affect the association of p120.	bind
40910	3	9384	5	13	NULL	NULL	NULL	statement 1	Process		is independent of					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_26_16670_s_224	9195983	A certain conclusion is that binding of p85 and p120 to Grb2 occurs independently: while the binding of p85 is lost if only the C-SH3 domain is intact, this alteration does not affect the association of p120.	bind
40927	4	9384	5	13	NULL	NULL	NULL				disrupt			intact C-SH3 domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_26_16670_s_224	9195983	A certain conclusion is that binding of p85 and p120 to Grb2 occurs independently: while the binding of p85 is lost if only the C-SH3 domain is intact, this alteration does not affect the association of p120.	bind
40928	5	9384	5	13	NULL	NULL	NULL				does not affect			intact C-SH3 domain		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_26_16670_s_224	9195983	A certain conclusion is that binding of p85 and p120 to Grb2 occurs independently: while the binding of p85 is lost if only the C-SH3 domain is intact, this alteration does not affect the association of p120.	bind
33794	1	9384	6	NULL	NULL	0	NULL	p85	NULL		bind	NULL				Grb2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_26_16670_s_224	9195983	A certain conclusion is that binding of p85 and p120 to Grb2 occurs independently: while the binding of p85 is lost if only the C-SH3 domain is intact, this alteration does not affect the association of p120.	bind
33795	2	9384	6	NULL	NULL	0	NULL	p120	NULL		bind	NULL				Grb2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_26_16670_s_224	9195983	A certain conclusion is that binding of p85 and p120 to Grb2 occurs independently: while the binding of p85 is lost if only the C-SH3 domain is intact, this alteration does not affect the association of p120.	bind
33796	3	9384	6	NULL	NULL	0	NULL	statement 1	NULL		is independent of	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_26_16670_s_224	9195983	A certain conclusion is that binding of p85 and p120 to Grb2 occurs independently: while the binding of p85 is lost if only the C-SH3 domain is intact, this alteration does not affect the association of p120.	bind
33797	4	9384	6	10	NULL	0	NULL	p85	NULL	binding of	is lost 	NULL					NULL	in presence of;;intact	C-SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_26_16670_s_224	9195983	A certain conclusion is that binding of p85 and p120 to Grb2 occurs independently: while the binding of p85 is lost if only the C-SH3 domain is intact, this alteration does not affect the association of p120.	bind
33798	5	9384	6	10	NULL	0	NULL	p120	NULL	binding of	has no effect of	NULL					NULL	in presence of	C-SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_26_16670_s_224	9195983	A certain conclusion is that binding of p85 and p120 to Grb2 occurs independently: while the binding of p85 is lost if only the C-SH3 domain is intact, this alteration does not affect the association of p120.	bind
40931	2	9385	5	13	NULL	NULL	NULL	statement 1	GP		bind					AP-2 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3655_s_89	10652362	A CFTR-derived Fusion Protein Binds to the AP-2 Complex but Not the AP-1 Complex-- The role of the carboxyl terminus of CFTR as a site for AP-2 interaction was evaluated further by generating a GST fusion protein corresponding to amino acids 1404-1480.	bind
40932	3	9385	5	13	NULL	NULL	NULL	statement 1	GP		does not bind					AP-1 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3655_s_89	10652362	A CFTR-derived Fusion Protein Binds to the AP-2 Complex but Not the AP-1 Complex-- The role of the carboxyl terminus of CFTR as a site for AP-2 interaction was evaluated further by generating a GST fusion protein corresponding to amino acids 1404-1480.	bind
48128	1	9385	5	13	NULL	NULL	NULL	Fusion Protein	GP		derived from					CFTR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3655_s_89	10652362	A CFTR-derived Fusion Protein Binds to the AP-2 Complex but Not the AP-1 Complex-- The role of the carboxyl terminus of CFTR as a site for AP-2 interaction was evaluated further by generating a GST fusion protein corresponding to amino acids 1404-1480.	bind
33837	2	9385	6	10	NULL	0	NULL	statement 1	NULL		bind	NULL				AP-2 complex	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3655_s_89	10652362	A CFTR-derived Fusion Protein Binds to the AP-2 Complex but Not the AP-1 Complex-- The role of the carboxyl terminus of CFTR as a site for AP-2 interaction was evaluated further by generating a GST fusion protein corresponding to amino acids 1404-1480.	bind
33838	3	9385	6	10	NULL	0	NULL	statement 1	NULL		does not bind	NULL				AP-1 complex	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3655_s_89	10652362	A CFTR-derived Fusion Protein Binds to the AP-2 Complex but Not the AP-1 Complex-- The role of the carboxyl terminus of CFTR as a site for AP-2 interaction was evaluated further by generating a GST fusion protein corresponding to amino acids 1404-1480.	bind
48129	1	9385	6	10	NULL	0	NULL	fusion protein	NULL		derived from	NULL				CFTR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3655_s_89	10652362	A CFTR-derived Fusion Protein Binds to the AP-2 Complex but Not the AP-1 Complex-- The role of the carboxyl terminus of CFTR as a site for AP-2 interaction was evaluated further by generating a GST fusion protein corresponding to amino acids 1404-1480.	bind
40937	1	9388	5	13	NULL	NULL	NULL				bind			polyproline type II helix		Hck	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_32129_s_194	9822689	A change in accessibility of the SH3 domain is not surprising, given the proximity of Trp260 to the polyproline type II helix that is bound by the SH3 domain of Hck.	bind
33839	1	9388	6	NULL	NULL	0	NULL	Hck	NULL		bind	NULL		SH3 domain			NULL		polyproline type II helix		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_48_32129_s_194	9822689	A change in accessibility of the SH3 domain is not surprising, given the proximity of Trp260 to the polyproline type II helix that is bound by the SH3 domain of Hck.	bind
40938	1	9389	5	13	NULL	NULL	NULL	apolipoprotein E	GP		bind					very low density lipoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3542_s_628	9437204	A change in apolipoprotein B expression is required for the binding of apolipoprotein E to very low density lipoprotein.	bind
40939	2	9389	5	13	NULL	NULL	NULL	apolipoprotein B	GP	change in expression of	is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3542_s_628	9437204	A change in apolipoprotein B expression is required for the binding of apolipoprotein E to very low density lipoprotein.	bind
33840	1	9389	6	NULL	NULL	0	NULL	apolipoprotein E	NULL		bind	NULL				very low density lipoprotein	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3542_s_628	9437204	A change in apolipoprotein B expression is required for the binding of apolipoprotein E to very low density lipoprotein.	bind
33841	2	9389	6	10	NULL	0	NULL	statement 1	NULL		is required for 	NULL				apolipoprotein B 	NULL	change in expression of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_12_3542_s_628	9437204	A change in apolipoprotein B expression is required for the binding of apolipoprotein E to very low density lipoprotein.	bind
41027	1	9390	5	13	NULL	NULL	NULL	PO4 group	Chemical	negatively charged	is a constituent of					CPP ligand	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainres_891_1_266_s_151	11164831	A change in charge of the receptor may allow for increased binding of the negatively charged PO4 group of the CPP ligand, the critical structural component for CPP binding [  12].	bind
41028	2	9390	5	13	NULL	NULL	NULL	receptor	GP	change in charge of	increase		may			statement 1	Process	 binding of			NULL		NULL	NULL	NULL	NULL	gw60_brainres_891_1_266_s_151	11164831	A change in charge of the receptor may allow for increased binding of the negatively charged PO4 group of the CPP ligand, the critical structural component for CPP binding [  12].	bind
41029	3	9390	5	13	NULL	NULL	NULL	CPP ligand	GP	negatively charged	is critical for			PO4 group		CPP	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_brainres_891_1_266_s_151	11164831	A change in charge of the receptor may allow for increased binding of the negatively charged PO4 group of the CPP ligand, the critical structural component for CPP binding [  12].	bind
33842	1	9390	6	10	NULL	0	NULL	PO4 group	NULL	negatively charged	is a constituent of	NULL				CPP ligand	NULL				NULL		NULL	NULL	NULL	NULL	gw60_brainres_891_1_266_s_151	11164831	A change in charge of the receptor may allow for increased binding of the negatively charged PO4 group of the CPP ligand, the critical structural component for CPP binding [  12].	bind
34055	2	9390	6	10	NULL	0	NULL	CPP ligand	NULL	 negatively charged	is critical for	NULL		PO4 group		CPP	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_brainres_891_1_266_s_151	11164831	A change in charge of the receptor may allow for increased binding of the negatively charged PO4 group of the CPP ligand, the critical structural component for CPP binding [  12].	bind
34056	3	9390	6	10	NULL	0	NULL	receptor	NULL	change in charge of	increase	NULL	may			statement 1	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_brainres_891_1_266_s_151	11164831	A change in charge of the receptor may allow for increased binding of the negatively charged PO4 group of the CPP ligand, the critical structural component for CPP binding [  12].	bind
40950	1	9391	5	13	NULL	NULL	NULL	Cu2+	Chemical		bind					Abeta	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_2977_s_170	12435742	A change in the coordination mode of the Cu2+ bound to Abeta at higher pH that also reduces the oligomerization of the peptides would explain the observed reduction of copper-induced MLRC by Abeta40 at these pH values.	bind
40951	3	9391	5	13	NULL	NULL	NULL	statement 1	Process		occurs at					high pH	QuantityOrMeasure				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_2977_s_170	12435742	A change in the coordination mode of the Cu2+ bound to Abeta at higher pH that also reduces the oligomerization of the peptides would explain the observed reduction of copper-induced MLRC by Abeta40 at these pH values.	bind
40952	2	9391	5	13	NULL	NULL	NULL	statement 1	Process		reduce					peptides	GP	oligomerization of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_2977_s_170	12435742	A change in the coordination mode of the Cu2+ bound to Abeta at higher pH that also reduces the oligomerization of the peptides would explain the observed reduction of copper-induced MLRC by Abeta40 at these pH values.	bind
41013	4	9391	5	13	NULL	NULL	NULL	copper	Chemical		induce					MLRC	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_2977_s_170	12435742	A change in the coordination mode of the Cu2+ bound to Abeta at higher pH that also reduces the oligomerization of the peptides would explain the observed reduction of copper-induced MLRC by Abeta40 at these pH values.	bind
41014	5	9391	5	13	NULL	NULL	NULL	Abeta40	GP		reduce					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_2977_s_170	12435742	A change in the coordination mode of the Cu2+ bound to Abeta at higher pH that also reduces the oligomerization of the peptides would explain the observed reduction of copper-induced MLRC by Abeta40 at these pH values.	bind
41016	6	9391	5	13	NULL	NULL	NULL	statement 2	Process		explains					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_2977_s_170	12435742	A change in the coordination mode of the Cu2+ bound to Abeta at higher pH that also reduces the oligomerization of the peptides would explain the observed reduction of copper-induced MLRC by Abeta40 at these pH values.	bind
33843	1	9391	6	NULL	NULL	0	NULL	Cu2+	NULL		bind	NULL				Abeta	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_5_2977_s_170	12435742	A change in the coordination mode of the Cu2+ bound to Abeta at higher pH that also reduces the oligomerization of the peptides would explain the observed reduction of copper-induced MLRC by Abeta40 at these pH values.	bind
33934	3	9391	6	10	NULL	0	NULL	Abeta40	NULL		reduces	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_2977_s_170	12435742	A change in the coordination mode of the Cu2+ bound to Abeta at higher pH that also reduces the oligomerization of the peptides would explain the observed reduction of copper-induced MLRC by Abeta40 at these pH values.	bind
48130	2	9391	6	10	NULL	0	NULL	copper	NULL		induce	NULL				MLRC	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_5_2977_s_170	12435742	A change in the coordination mode of the Cu2+ bound to Abeta at higher pH that also reduces the oligomerization of the peptides would explain the observed reduction of copper-induced MLRC by Abeta40 at these pH values.	bind
48131	4	9391	6	10	NULL	0	NULL	statement 1	NULL		reduce	NULL				peptides	NULL	oligomerization of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_5_2977_s_170	12435742	A change in the coordination mode of the Cu2+ bound to Abeta at higher pH that also reduces the oligomerization of the peptides would explain the observed reduction of copper-induced MLRC by Abeta40 at these pH values.	bind
48132	5	9391	6	10	NULL	0	NULL	statement 1	NULL		occurs at	NULL				high pH	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_5_2977_s_170	12435742	A change in the coordination mode of the Cu2+ bound to Abeta at higher pH that also reduces the oligomerization of the peptides would explain the observed reduction of copper-induced MLRC by Abeta40 at these pH values.	bind
58478	6	9391	6	10	NULL	0	NULL	statement 4			explains					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_5_2977_s_170	12435742	A change in the coordination mode of the Cu2+ bound to Abeta at higher pH that also reduces the oligomerization of the peptides would explain the observed reduction of copper-induced MLRC by Abeta40 at these pH values.	bind
41017	1	9392	5	13	NULL	NULL	NULL	HIV-1 capsid	CellComponent	change in	decrease			cyclophilin A-binding loop		TRIM5alpha	GP	binding of;;human	R332P		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-virol_80_14_16809279_s_6	16809279	A change in the cyclophilin A-binding loop of the HIV-1 capsid  decreased TRIM5alpha(hu) R332P binding and allowed escape from restriction.	bind
41018	2	9392	5	13	NULL	NULL	NULL	statement 1	Process		allows					restriction	Process	escape from			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-virol_80_14_16809279_s_6	16809279	A change in the cyclophilin A-binding loop of the HIV-1 capsid  decreased TRIM5alpha(hu) R332P binding and allowed escape from restriction.	bind
33937	1	9392	6	10	NULL	0	NULL	HIV-1 capsid		change in	decreases			cyclophilin A-binding loop		TRIM5alpha(hu) 		binding of	R332P		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-virol_80_14_16809279_s_6	16809279	A change in the cyclophilin A-binding loop of the HIV-1 capsid  decreased TRIM5alpha(hu) R332P binding and allowed escape from restriction.	bind
58479	2	9392	6	10	NULL	0	NULL	statement 1			allows					restriction		escape from			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-virol_80_14_16809279_s_6	16809279	A change in the cyclophilin A-binding loop of the HIV-1 capsid  decreased TRIM5alpha(hu) R332P binding and allowed escape from restriction.	bind
41019	1	9393	5	13	NULL	NULL	NULL	FLP	GP		is changed to			arginine at position 191		FLP	GP		lysine		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-mol-biol_225_2_1593623_s_6	1593623	A change of arginine at position  191 to lysine resulted in a protein (FLP-R191K) that could bind to the  FRT site but could not catalyze recombination.	bind
41020	2	9393	5	13	NULL	NULL	NULL	statement 1	Process		results in					FLP	GP		R191K		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-mol-biol_225_2_1593623_s_6	1593623	A change of arginine at position  191 to lysine resulted in a protein (FLP-R191K) that could bind to the  FRT site but could not catalyze recombination.	bind
41021	3	9393	5	13	NULL	NULL	NULL	FLP	GP		bind			R191K						FRT site	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-mol-biol_225_2_1593623_s_6	1593623	A change of arginine at position  191 to lysine resulted in a protein (FLP-R191K) that could bind to the  FRT site but could not catalyze recombination.	bind
41022	4	9393	5	13	NULL	NULL	NULL	FLP	GP		does not catalyze			R191K		recombination					NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-mol-biol_225_2_1593623_s_6	1593623	A change of arginine at position  191 to lysine resulted in a protein (FLP-R191K) that could bind to the  FRT site but could not catalyze recombination.	bind
33844	1	9393	6	10	NULL	0	NULL	FLP			is changed to			arginine at position 191		FLP			Lysine at position 191		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-mol-biol_225_2_1593623_s_6	1593623	A change of arginine at position  191 to lysine resulted in a protein (FLP-R191K) that could bind to the  FRT site but could not catalyze recombination.	bind
33845	2	9393	6	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				FLP	NULL		R191K		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-mol-biol_225_2_1593623_s_6	1593623	A change of arginine at position  191 to lysine resulted in a protein (FLP-R191K) that could bind to the  FRT site but could not catalyze recombination.	bind
33846	3	9393	6	NULL	NULL	0	NULL	FLP	NULL		bind	NULL		R191K			NULL			FRT site	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-mol-biol_225_2_1593623_s_6	1593623	A change of arginine at position  191 to lysine resulted in a protein (FLP-R191K) that could bind to the  FRT site but could not catalyze recombination.	bind
33847	4	9393	6	10	NULL	0	NULL	FLP	NULL		does not catalyze	NULL		R191K		recombination	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-mol-biol_225_2_1593623_s_6	1593623	A change of arginine at position  191 to lysine resulted in a protein (FLP-R191K) that could bind to the  FRT site but could not catalyze recombination.	bind
41023	1	9394	5	13	NULL	NULL	NULL	channel/pore-like protein	GP		allows					plus-or-minus 107 molecules s 1	GP	transport of			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1613_1_57_s_330	12832087	A channel/pore-like protein should allow transport of  plus-or-minus 107 molecules s 1, while permeases allowing equilibrating facilitated diffusion characterised so far,  allow transport with  Vmax 105 molecules s 1 [  44] and active transporters generally present lower  Vmax, 10-103 molecules s 1 [ 44].	bind
41024	2	9394	5	13	NULL	NULL	NULL	permeases	GP		allows					facilitated diffusion	Process	equilibrating 			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1613_1_57_s_330	12832087	A channel/pore-like protein should allow transport of  plus-or-minus 107 molecules s 1, while permeases allowing equilibrating facilitated diffusion characterised so far,  allow transport with  Vmax 105 molecules s 1 [  44] and active transporters generally present lower  Vmax, 10-103 molecules s 1 [ 44].	bind
33942	1	9394	6	NULL	NULL	0	NULL	channel/pore-like protein	NULL		allows	NULL				plus-or-minus 107 molecules	NULL	transport of 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1613_1_57_s_330	12832087	A channel/pore-like protein should allow transport of  plus-or-minus 107 molecules s 1, while permeases allowing equilibrating facilitated diffusion characterised so far,  allow transport with  Vmax 105 molecules s 1 [  44] and active transporters generally present lower  Vmax, 10-103 molecules s 1 [ 44].	bind
33943	2	9394	6	NULL	NULL	0	NULL	permeases	NULL		equilibrate	NULL				facilitated diffusion	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1613_1_57_s_330	12832087	A channel/pore-like protein should allow transport of  plus-or-minus 107 molecules s 1, while permeases allowing equilibrating facilitated diffusion characterised so far,  allow transport with  Vmax 105 molecules s 1 [  44] and active transporters generally present lower  Vmax, 10-103 molecules s 1 [ 44].	bind
41030	1	9395	5	13	NULL	NULL	NULL	ETS domain	GP		is a type of					85-amino-acid-long DNA-binding motif	GP	highly conserved			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7300_s_13	10982847	A characteristic feature of this class of proteins is a highly conserved, 85-amino-acid-long DNA-binding motif termed the ETS domain, which specifically binds to GGA(A/T)-containing DNA target sequences.	bind
41031	2	9395	5	13	NULL	NULL	NULL				bind		specifically	ETS domain		DNA target sequences	NucleicAcid			GGA(A/T)	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7300_s_13	10982847	A characteristic feature of this class of proteins is a highly conserved, 85-amino-acid-long DNA-binding motif termed the ETS domain, which specifically binds to GGA(A/T)-containing DNA target sequences.	bind
33848	1	9395	6	10	NULL	0	NULL		NULL		bind	NULL	specifically	ETS domain		DNA target sequences	NULL			GGA(A/T)-containing 	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7300_s_13	10982847	A characteristic feature of this class of proteins is a highly conserved, 85-amino-acid-long DNA-binding motif termed the ETS domain, which specifically binds to GGA(A/T)-containing DNA target sequences.	bind
48133	2	9395	6	10	NULL	0	NULL	ETS domain	NULL		is a type of	NULL				85-amino-acid-long DNA-binding motif 	NULL	highly conserved			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7300_s_13	10982847	A characteristic feature of this class of proteins is a highly conserved, 85-amino-acid-long DNA-binding motif termed the ETS domain, which specifically binds to GGA(A/T)-containing DNA target sequences.	bind
41032	1	9396	5	13	NULL	NULL	NULL	adhesins	GP	bacterial	bind					extracellular matrix proteins	GP	eukaryotic			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_17_5842_s_290	15317790	A characteristic of bacterial adhesins that bind to eukaryotic extracellular matrix proteins is the presence of amino acid repeats ( ).	bind
41033	2	9396	5	13	NULL	NULL	NULL			presence of	is a characteristic of			amino acid repeats		adhesins	GP	bacterial			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_17_5842_s_290	15317790	A characteristic of bacterial adhesins that bind to eukaryotic extracellular matrix proteins is the presence of amino acid repeats ( ).	bind
33849	1	9396	6	NULL	NULL	0	NULL	adhesins	NULL	bacterial	bind	NULL				extracellular matrix proteins	NULL	eukaryotic			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_17_5842_s_290	15317790	A characteristic of bacterial adhesins that bind to eukaryotic extracellular matrix proteins is the presence of amino acid repeats ( ).	bind
48134	2	9396	6	10	NULL	0	NULL		NULL	presence of	is characteristic of	NULL		aminoacid repeats		adhesins	NULL	bacterial			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_17_5842_s_290	15317790	A characteristic of bacterial adhesins that bind to eukaryotic extracellular matrix proteins is the presence of amino acid repeats ( ).	bind
41034	1	9397	5	13	NULL	NULL	NULL	motor	GP		released from					F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31701_s_133	10882730	A characteristic of myosin V is the ability to release the motor from F-actin by activating the Ca2+-dependent Mg-ATPase found in the actin binding head of myosin V ( 14,  22).	bind
41035	2	9397	5	13	NULL	NULL	NULL	statement 1	Process		is a characteristic of					myosin V	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31701_s_133	10882730	A characteristic of myosin V is the ability to release the motor from F-actin by activating the Ca2+-dependent Mg-ATPase found in the actin binding head of myosin V ( 14,  22).	bind
41036	3	9397	5	13	NULL	NULL	NULL	myosin V	GP		activates					Mg-ATPase	GP	Ca2+-dependent			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31701_s_133	10882730	A characteristic of myosin V is the ability to release the motor from F-actin by activating the Ca2+-dependent Mg-ATPase found in the actin binding head of myosin V ( 14,  22).	bind
41037	4	9397	5	13	NULL	NULL	NULL	Mg-ATPase	GP	Ca2+-dependent	is present in					myosin V	GP		actin binding head		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31701_s_133	10882730	A characteristic of myosin V is the ability to release the motor from F-actin by activating the Ca2+-dependent Mg-ATPase found in the actin binding head of myosin V ( 14,  22).	bind
41038	5	9397	5	13	NULL	NULL	NULL	statement 3	Process		leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31701_s_133	10882730	A characteristic of myosin V is the ability to release the motor from F-actin by activating the Ca2+-dependent Mg-ATPase found in the actin binding head of myosin V ( 14,  22).	bind
33850	1	9397	6	NULL	NULL	0	NULL	F-actin	NULL		releases	NULL				motor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_41_31701_s_133	10882730	A characteristic of myosin V is the ability to release the motor from F-actin by activating the Ca2+-dependent Mg-ATPase found in the actin binding head of myosin V ( 14,  22).	bind
33851	2	9397	6	NULL	NULL	0	NULL	myosin V	NULL		performs	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_41_31701_s_133	10882730	A characteristic of myosin V is the ability to release the motor from F-actin by activating the Ca2+-dependent Mg-ATPase found in the actin binding head of myosin V ( 14,  22).	bind
33852	3	9397	6	NULL	NULL	0	NULL	Myosin V	NULL		contains	NULL		actin binding head		Mg-ATPase	NULL	Ca2+-dependent 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_41_31701_s_133	10882730	A characteristic of myosin V is the ability to release the motor from F-actin by activating the Ca2+-dependent Mg-ATPase found in the actin binding head of myosin V ( 14,  22).	bind
33853	4	9397	6	NULL	NULL	0	NULL	statement 2	NULL		occurs by 	NULL				Mg-ATPase	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_41_31701_s_133	10882730	A characteristic of myosin V is the ability to release the motor from F-actin by activating the Ca2+-dependent Mg-ATPase found in the actin binding head of myosin V ( 14,  22).	bind
41039	1	9398	5	13	NULL	NULL	NULL	gamma-carboxylate	Chemical		 interacts with			 Glu-361		arginine	AminoAcid		guanidinium of 		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6114_s_172	9045621	A charge interaction between gamma-carboxylate of Glu-361 and the guanidinium of arginine provides the major stabilization energy for the enzyme-substrate complex, as replacement of Glu-361 by a glutamine also removed L-arginine binding activity.	bind
41040	2	9398	5	13	NULL	NULL	NULL	statement 1	Process		provide					enzyme-substrate complex	GP	major stabilization energy of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6114_s_172	9045621	A charge interaction between gamma-carboxylate of Glu-361 and the guanidinium of arginine provides the major stabilization energy for the enzyme-substrate complex, as replacement of Glu-361 by a glutamine also removed L-arginine binding activity.	bind
41041	3	9398	5	NULL	NULL	0	NULL		NULL		is replaced by	NULL		Glu-361			NULL		glutamine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_10_6114_s_172	9045621	A charge interaction between gamma-carboxylate of Glu-361 and the guanidinium of arginine provides the major stabilization energy for the enzyme-substrate complex, as replacement of Glu-361 by a glutamine also removed L-arginine binding activity.	bind
41042	4	9398	5	13	NULL	NULL	NULL	statement 3	Process		removed							binding activity of	L-arginine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6114_s_172	9045621	A charge interaction between gamma-carboxylate of Glu-361 and the guanidinium of arginine provides the major stabilization energy for the enzyme-substrate complex, as replacement of Glu-361 by a glutamine also removed L-arginine binding activity.	bind
33944	1	9398	6	NULL	NULL	0	NULL	gamma-carboxylate	NULL		interacts with	NULL		Glu-361		arginine	NULL		guanidinium		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_10_6114_s_172	9045621	A charge interaction between gamma-carboxylate of Glu-361 and the guanidinium of arginine provides the major stabilization energy for the enzyme-substrate complex, as replacement of Glu-361 by a glutamine also removed L-arginine binding activity.	bind
58480	2	9398	6	10	NULL	0	NULL	statement 1			provide					enzyme-substrate complex		major stabilization energy for			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_10_6114_s_172	9045621	A charge interaction between gamma-carboxylate of Glu-361 and the guanidinium of arginine provides the major stabilization energy for the enzyme-substrate complex, as replacement of Glu-361 by a glutamine also removed L-arginine binding activity.	bind
58481	3	9398	6	10	NULL	0	NULL				replaced by			Glu-361					glutamine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_10_6114_s_172	9045621	A charge interaction between gamma-carboxylate of Glu-361 and the guanidinium of arginine provides the major stabilization energy for the enzyme-substrate complex, as replacement of Glu-361 by a glutamine also removed L-arginine binding activity.	bind
58482	4	9398	6	10	NULL	0	NULL	statement 3			removes					L-arginine		binding activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_10_6114_s_172	9045621	A charge interaction between gamma-carboxylate of Glu-361 and the guanidinium of arginine provides the major stabilization energy for the enzyme-substrate complex, as replacement of Glu-361 by a glutamine also removed L-arginine binding activity.	bind
41043	1	9399	5	13	NULL	NULL	NULL	Cc	GP		is					positively charged	Chemical	highly			NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_22_11928_s_108	11035811	A charged species may disrupt the binding of Cc and Apaf-1 through ionic interactions, because Cc and Apaf-1 are highly positively and negatively charged, respectively.	bind
41044	2	9399	5	13	NULL	NULL	NULL	Apaf-1	GP		is					negatively charged	Chemical	highly			NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_22_11928_s_108	11035811	A charged species may disrupt the binding of Cc and Apaf-1 through ionic interactions, because Cc and Apaf-1 are highly positively and negatively charged, respectively.	bind
41045	3	9399	5	13	NULL	NULL	NULL	Cc	GP		bind					Apaf-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_22_11928_s_108	11035811	A charged species may disrupt the binding of Cc and Apaf-1 through ionic interactions, because Cc and Apaf-1 are highly positively and negatively charged, respectively.	bind
41046	4	9399	5	13	NULL	NULL	NULL	charged species	Chemical		disrupt		may			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_22_11928_s_108	11035811	A charged species may disrupt the binding of Cc and Apaf-1 through ionic interactions, because Cc and Apaf-1 are highly positively and negatively charged, respectively.	bind
41047	5	9399	5	13	NULL	NULL	NULL	statement 4	Process		occurs through					ionic interactions	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_22_11928_s_108	11035811	A charged species may disrupt the binding of Cc and Apaf-1 through ionic interactions, because Cc and Apaf-1 are highly positively and negatively charged, respectively.	bind
33854	1	9399	6	NULL	NULL	0	NULL	Cc	NULL	highly positively charged	bind	NULL				Apaf-1	NULL	highly negatively charged			NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_22_11928_s_108	11035811	A charged species may disrupt the binding of Cc and Apaf-1 through ionic interactions, because Cc and Apaf-1 are highly positively and negatively charged, respectively.	bind
33855	2	9399	6	NULL	NULL	0	NULL	charged species	NULL		disrupts	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_11928_s_108	11035811	A charged species may disrupt the binding of Cc and Apaf-1 through ionic interactions, because Cc and Apaf-1 are highly positively and negatively charged, respectively.	bind
33856	3	9399	6	NULL	NULL	0	NULL	statement 2	NULL		occurs through	NULL				ionic interactions	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_11928_s_108	11035811	A charged species may disrupt the binding of Cc and Apaf-1 through ionic interactions, because Cc and Apaf-1 are highly positively and negatively charged, respectively.	bind
41048	1	9402	5	13	NULL	NULL	NULL	CD80	GP		is a type of					co-stimulating molecule	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_6_333_s_112	10744980	A chicken homologue of the co-stimulating molecule CD80 which binds to mammalian CTLA-4.	bind
41049	2	9402	5	13	NULL	NULL	NULL	CD80	GP	chicken homologue	bind					CTLA-4	GP	mammalian			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_6_333_s_112	10744980	A chicken homologue of the co-stimulating molecule CD80 which binds to mammalian CTLA-4.	bind
39493	1	9402	7	10	NULL	0	NULL	CD80	NULL	chicken homologue	bind	NULL				CTLA-4	NULL	mammalian			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_6_333_s_112	10744980	A chicken homologue of the co-stimulating molecule CD80 which binds to mammalian CTLA-4.	bind
39494	2	9402	7	NULL	NULL	0	NULL	CD80	NULL		is a type of	NULL				co-stimulating molecule	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_6_333_s_112	10744980	A chicken homologue of the co-stimulating molecule CD80 which binds to mammalian CTLA-4.	bind
42995	1	9403	5	13	NULL	NULL	NULL	chimera	GP		consists of					nNOS	GP		heme domain		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
42996	2	9403	5	13	NULL	NULL	NULL	chimera	GP		consists of								FMN binding subdomain		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
42997	3	9403	5	13	NULL	NULL	NULL	chimera	GP		consists of					CYPOR	GP		FAD binding subdomain		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
43009	4	9403	5	13	NULL	NULL	NULL	cytochrome c	GP		undergoes					reduction	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
43010	5	9403	5	13	NULL	NULL	NULL	statement 4	Process		in the absence of					CaM	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
43011	6	9403	5	13	NULL	NULL	NULL	statement 1	Process		catalyze		significantly			statement 4	Process	increased rates of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
43012	7	9403	5	13	NULL	NULL	NULL	statement 2	Process		catalyze		significantly			statement 4	Process	increased rates of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
43013	8	9403	5	13	NULL	NULL	NULL	statement 3	Process		catalyze		significantly			statement 4	Process	increased rates of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
43014	9	9403	5	13	NULL	NULL	NULL	statement 1	Process		catalyze					NO	Chemical	synthesis of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
43015	10	9403	5	13	NULL	NULL	NULL	statement 9	Process		in the presence of					CaM	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
43016	11	9403	5	13	NULL	NULL	NULL	statement 2	Process		catalyze					NO	Chemical	synthesis of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
43017	12	9403	5	13	NULL	NULL	NULL	statement 11	Process		in the presence of					CaM	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
43018	13	9403	5	13	NULL	NULL	NULL	statement 3	Process		catalyze					NO	Chemical	synthesis of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
43019	14	9403	5	13	NULL	NULL	NULL	statement 13	Process		in the presence of					CaM	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
39495	1	9403	7	NULL	NULL	0	NULL	 chimera	NULL		consist of	NULL					NULL		nNOS heme domain		NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
39496	2	9403	7	NULL	NULL	0	NULL	chimera	NULL		consist of	NULL					NULL		FMN binding subdomain		NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
39497	3	9403	7	10	NULL	0	NULL	chimera			consist of					CYPOR			FAD binding subdomain		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
39498	4	9403	7	NULL	NULL	0	NULL	statement 1	NULL		occur simultaneously with	NULL				statement 2 	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
39499	6	9403	7	NULL	NULL	0	NULL	chimera	NULL		increase	NULL				cytochrome c	NULL	reduction of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
39500	7	9403	7	NULL	NULL	0	NULL	statement 6	NULL		in absence of	NULL				CaM	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
39501	8	9403	7	NULL	NULL	0	NULL	chimera	NULL		increase	NULL				NO	NULL	synthesis of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
39502	9	9403	7	NULL	NULL	0	NULL	statement 8	NULL		in presence of	NULL				CaM	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
40403	5	9403	7	NULL	NULL	0	NULL	statement 1	NULL		occur simultaneously with	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_28_12730215_s_6	12730215	A chimera consisting  of the nNOS heme domain and FMN binding subdomain and the CYPOR FAD binding  subdomain catalyzed significantly increased rates of cytochrome c reduction  in the absence of CaM and of NO synthesis in its presence.	bind
43025	1	9404	5	13	NULL	NULL	NULL	chimera	GP		consists of					MKP-3	GP		N-terminal half		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_9323_s_6	9535927	A chimera consisting of the N-terminal half of MKP-3 with the C-terminal catalytic core of M3-6 also bound tightly to ERK1 but not to JNK3/SAPKbeta.	bind
43026	2	9404	5	13	NULL	NULL	NULL	chimera	GP		consists of					M3-6	GP		C-terminal catalytic core		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_9323_s_6	9535927	A chimera consisting of the N-terminal half of MKP-3 with the C-terminal catalytic core of M3-6 also bound tightly to ERK1 but not to JNK3/SAPKbeta.	bind
43041	3	9404	5	13	NULL	NULL	NULL	statement 1	GP		bind		tightly			ERK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_9323_s_6	9535927	A chimera consisting of the N-terminal half of MKP-3 with the C-terminal catalytic core of M3-6 also bound tightly to ERK1 but not to JNK3/SAPKbeta.	bind
43042	4	9404	5	13	NULL	NULL	NULL	statement 2	GP		bind		tightly			ERK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_9323_s_6	9535927	A chimera consisting of the N-terminal half of MKP-3 with the C-terminal catalytic core of M3-6 also bound tightly to ERK1 but not to JNK3/SAPKbeta.	bind
43043	5	9404	5	13	NULL	NULL	NULL	statement 1	GP		does not bind					JNK3/SAPKbeta	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_9323_s_6	9535927	A chimera consisting of the N-terminal half of MKP-3 with the C-terminal catalytic core of M3-6 also bound tightly to ERK1 but not to JNK3/SAPKbeta.	bind
43044	6	9404	5	13	NULL	NULL	NULL	statement 2	GP		does not bind					JNK3/SAPKbeta	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_9323_s_6	9535927	A chimera consisting of the N-terminal half of MKP-3 with the C-terminal catalytic core of M3-6 also bound tightly to ERK1 but not to JNK3/SAPKbeta.	bind
39503	1	9404	7	NULL	NULL	0	NULL	 chimera	NULL		consist of	NULL				MKP-3	NULL		N-terminal half of		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_15_9323_s_6	9535927	A chimera consisting of the N-terminal half of MKP-3 with the C-terminal catalytic core of M3-6 also bound tightly to ERK1 but not to JNK3/SAPKbeta.	bind
39504	2	9404	7	NULL	NULL	0	NULL	chimera	NULL		consist of	NULL				M3-6	NULL		C-terminal catalytic core 		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_15_9323_s_6	9535927	A chimera consisting of the N-terminal half of MKP-3 with the C-terminal catalytic core of M3-6 also bound tightly to ERK1 but not to JNK3/SAPKbeta.	bind
39505	3	9404	7	NULL	NULL	0	NULL	statement 1	NULL		is composed of	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_15_9323_s_6	9535927	A chimera consisting of the N-terminal half of MKP-3 with the C-terminal catalytic core of M3-6 also bound tightly to ERK1 but not to JNK3/SAPKbeta.	bind
39506	4	9404	7	NULL	NULL	0	NULL	statement 3	NULL		binds	NULL	tightly			ERK1 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_15_9323_s_6	9535927	A chimera consisting of the N-terminal half of MKP-3 with the C-terminal catalytic core of M3-6 also bound tightly to ERK1 but not to JNK3/SAPKbeta.	bind
39507	5	9404	7	NULL	NULL	0	NULL	statement 3	NULL		does not bind	NULL				JNK3/SAPKbeta	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_15_9323_s_6	9535927	A chimera consisting of the N-terminal half of MKP-3 with the C-terminal catalytic core of M3-6 also bound tightly to ERK1 but not to JNK3/SAPKbeta.	bind
43020	1	9406	5	13	NULL	NULL	NULL	ChiAVD	GP		is a type of					chimeric avidin protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10228_s_9	15649900	A chimeric avidin protein, ChiAVD, containing a 21-amino acid segment of AVR4 was found to be significantly more stable ( Tm = 96.5  degrees C) than native avidin ( Tm = 83.5  degrees C), and its biotin-binding properties resembled those of AVR4.	bind
43021	2	9406	5	13	NULL	NULL	NULL	ChiAVD	GP		contains					AVR4	GP	21-amino acid segment of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10228_s_9	15649900	A chimeric avidin protein, ChiAVD, containing a 21-amino acid segment of AVR4 was found to be significantly more stable ( Tm = 96.5  degrees C) than native avidin ( Tm = 83.5  degrees C), and its biotin-binding properties resembled those of AVR4.	bind
43022	3	9406	5	13	NULL	NULL	NULL	statement 2	GP		more stable than		significantly			avidin	GP	native			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10228_s_9	15649900	A chimeric avidin protein, ChiAVD, containing a 21-amino acid segment of AVR4 was found to be significantly more stable ( Tm = 96.5  degrees C) than native avidin ( Tm = 83.5  degrees C), and its biotin-binding properties resembled those of AVR4.	bind
43023	4	9406	5	13	NULL	NULL	NULL	ChiAVD	GP		bind					biotin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10228_s_9	15649900	A chimeric avidin protein, ChiAVD, containing a 21-amino acid segment of AVR4 was found to be significantly more stable ( Tm = 96.5  degrees C) than native avidin ( Tm = 83.5  degrees C), and its biotin-binding properties resembled those of AVR4.	bind
46826	5	9406	5	13	NULL	NULL	NULL	AVR4	GP		bind					biotin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10228_s_9	15649900	A chimeric avidin protein, ChiAVD, containing a 21-amino acid segment of AVR4 was found to be significantly more stable ( Tm = 96.5  degrees C) than native avidin ( Tm = 83.5  degrees C), and its biotin-binding properties resembled those of AVR4.	bind
46827	6	9406	5	13	NULL	NULL	NULL	statement 4	Process		is similar to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10228_s_9	15649900	A chimeric avidin protein, ChiAVD, containing a 21-amino acid segment of AVR4 was found to be significantly more stable ( Tm = 96.5  degrees C) than native avidin ( Tm = 83.5  degrees C), and its biotin-binding properties resembled those of AVR4.	bind
39508	1	9406	7	NULL	NULL	0	NULL	ChiAVD	NULL		is	NULL				chimeric avidin protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_11_10228_s_9	15649900	A chimeric avidin protein, ChiAVD, containing a 21-amino acid segment of AVR4 was found to be significantly more stable ( Tm = 96.5  degrees C) than native avidin ( Tm = 83.5  degrees C), and its biotin-binding properties resembled those of AVR4.	bind
39509	2	9406	7	NULL	NULL	0	NULL	ChiAVD	NULL		contains	NULL				AVR4	NULL		 21-amino acid segment		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_11_10228_s_9	15649900	A chimeric avidin protein, ChiAVD, containing a 21-amino acid segment of AVR4 was found to be significantly more stable ( Tm = 96.5  degrees C) than native avidin ( Tm = 83.5  degrees C), and its biotin-binding properties resembled those of AVR4.	bind
39510	3	9406	7	10	NULL	0	NULL	ChiAVD			is more stable than		significantly			avidin		native			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10228_s_9	15649900	A chimeric avidin protein, ChiAVD, containing a 21-amino acid segment of AVR4 was found to be significantly more stable ( Tm = 96.5  degrees C) than native avidin ( Tm = 83.5  degrees C), and its biotin-binding properties resembled those of AVR4.	bind
39511	4	9406	7	NULL	NULL	0	NULL	ChiAVD	NULL		bind	NULL				biotin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_11_10228_s_9	15649900	A chimeric avidin protein, ChiAVD, containing a 21-amino acid segment of AVR4 was found to be significantly more stable ( Tm = 96.5  degrees C) than native avidin ( Tm = 83.5  degrees C), and its biotin-binding properties resembled those of AVR4.	bind
39512	5	9406	7	10	NULL	0	NULL	AVR4	NULL		bind	NULL				biotin	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10228_s_9	15649900	A chimeric avidin protein, ChiAVD, containing a 21-amino acid segment of AVR4 was found to be significantly more stable ( Tm = 96.5  degrees C) than native avidin ( Tm = 83.5  degrees C), and its biotin-binding properties resembled those of AVR4.	bind
46828	6	9406	7	10	NULL	0	NULL	statement 4	NULL		resembles	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_11_10228_s_9	15649900	A chimeric avidin protein, ChiAVD, containing a 21-amino acid segment of AVR4 was found to be significantly more stable ( Tm = 96.5  degrees C) than native avidin ( Tm = 83.5  degrees C), and its biotin-binding properties resembled those of AVR4.	bind
43054	2	9407	5	13	NULL	NULL	NULL	chimeric beta4 integrin	GP		is replaced with			SDL sequence		beta1 integrin	GP	corresponding	SDL sequence		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49406_s_12	14512419	A chimeric beta4 integrin in which the indicated SDL sequence had been replaced with the corresponding sequence from the beta1 integrin failed to bind hCLCA2.	bind
43055	3	9407	5	13	NULL	NULL	NULL	statement 2	GP		does not bind					hCLCA2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49406_s_12	14512419	A chimeric beta4 integrin in which the indicated SDL sequence had been replaced with the corresponding sequence from the beta1 integrin failed to bind hCLCA2.	bind
39513	1	9407	7	10	NULL	0	NULL	chimeric beta4 integrin			is replaced with			SDL sequence		beta1 integrin		corresponding	SDL sequence		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49406_s_12	14512419	A chimeric beta4 integrin in which the indicated SDL sequence had been replaced with the corresponding sequence from the beta1 integrin failed to bind hCLCA2.	bind
39514	2	9407	7	NULL	NULL	0	NULL	chimeric beta4 integrin	NULL		fails to bind	NULL				hCLCA2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49406_s_12	14512419	A chimeric beta4 integrin in which the indicated SDL sequence had been replaced with the corresponding sequence from the beta1 integrin failed to bind hCLCA2.	bind
43056	1	9408	5	13	NULL	NULL	NULL	VEGF	GP	chimeric ligand of	fused to					alkaline phosphatase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_16_19_6089_s_172	8815891	A chimeric ligand of VEGF fused to alkaline phosphatase binds to [[ retinal progenitor cells           ]]Flk-1 receptor has been reported to bind VEGF with high affinity.	bind
43057	2	9408	5	13	NULL	NULL	NULL	statement 1	GP		bind					progenitor cells	Cell	retinal			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_16_19_6089_s_172	8815891	A chimeric ligand of VEGF fused to alkaline phosphatase binds to [[ retinal progenitor cells           ]]Flk-1 receptor has been reported to bind VEGF with high affinity.	bind
43058	3	9408	5	13	NULL	NULL	NULL	Flk-1 receptor	GP		bind		high affinity			VEGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_16_19_6089_s_172	8815891	A chimeric ligand of VEGF fused to alkaline phosphatase binds to [[ retinal progenitor cells           ]]Flk-1 receptor has been reported to bind VEGF with high affinity.	bind
39619	1	9408	7	10	NULL	0	NULL	VEGF 	NULL	chimeric ligand of 	fused to	NULL				alkaline phosphatase	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_16_19_6089_s_172	8815891	A chimeric ligand of VEGF fused to alkaline phosphatase binds to [[ retinal progenitor cells           ]]Flk-1 receptor has been reported to bind VEGF with high affinity.	bind
39620	2	9408	7	10	NULL	0	NULL	statement 1			binds to					progenitor cells		retinal 			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_16_19_6089_s_172	8815891	A chimeric ligand of VEGF fused to alkaline phosphatase binds to [[ retinal progenitor cells           ]]Flk-1 receptor has been reported to bind VEGF with high affinity.	bind
39621	3	9408	7	NULL	NULL	0	NULL	Flk-1 receptor	NULL		bind	NULL	high affinity			VEGF	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_16_19_6089_s_172	8815891	A chimeric ligand of VEGF fused to alkaline phosphatase binds to [[ retinal progenitor cells           ]]Flk-1 receptor has been reported to bind VEGF with high affinity.	bind
43059	1	9409	5	13	NULL	NULL	NULL	TTR	GP	crocodile	is replaced by			N-terminal end		TTR	GP	frog			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_25_26411_s_91	15082720	A chimeric molecule generated from crocodile TTR, in which the N-terminal end was replaced by that from frog, was shown to differ in both the specificity and affinity of T4 and T3 binding.	bind
43060	2	9409	5	13	NULL	NULL	NULL	chimeric molecule	GP		is generated from					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_25_26411_s_91	15082720	A chimeric molecule generated from crocodile TTR, in which the N-terminal end was replaced by that from frog, was shown to differ in both the specificity and affinity of T4 and T3 binding.	bind
43071	3	9409	5	13	NULL	NULL	NULL	statement 2	GP		bind					T4	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_25_26411_s_91	15082720	A chimeric molecule generated from crocodile TTR, in which the N-terminal end was replaced by that from frog, was shown to differ in both the specificity and affinity of T4 and T3 binding.	bind
43072	4	9409	5	13	NULL	NULL	NULL	statement 2	GP		bind					T3	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_25_26411_s_91	15082720	A chimeric molecule generated from crocodile TTR, in which the N-terminal end was replaced by that from frog, was shown to differ in both the specificity and affinity of T4 and T3 binding.	bind
43073	5	9409	5	13	NULL	NULL	NULL	statement 3	Process		differ in					statement 4	Process	specificity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_25_26411_s_91	15082720	A chimeric molecule generated from crocodile TTR, in which the N-terminal end was replaced by that from frog, was shown to differ in both the specificity and affinity of T4 and T3 binding.	bind
43074	6	9409	5	13	NULL	NULL	NULL	statement 3	Process		differ in					statement 4	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_25_26411_s_91	15082720	A chimeric molecule generated from crocodile TTR, in which the N-terminal end was replaced by that from frog, was shown to differ in both the specificity and affinity of T4 and T3 binding.	bind
39622	1	9409	7	10	NULL	0	NULL	TTR		crocodile	is replaced by			N-terminal end		TTR		frog			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_25_26411_s_91	15082720	A chimeric molecule generated from crocodile TTR, in which the N-terminal end was replaced by that from frog, was shown to differ in both the specificity and affinity of T4 and T3 binding.	bind
39623	2	9409	7	10	NULL	0	NULL	chimeric molecule			is generated from					statement 1					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_25_26411_s_91	15082720	A chimeric molecule generated from crocodile TTR, in which the N-terminal end was replaced by that from frog, was shown to differ in both the specificity and affinity of T4 and T3 binding.	bind
39624	3	9409	7	10	NULL	0	NULL	statement 2			bind					T4					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_25_26411_s_91	15082720	A chimeric molecule generated from crocodile TTR, in which the N-terminal end was replaced by that from frog, was shown to differ in both the specificity and affinity of T4 and T3 binding.	bind
39625	4	9409	7	10	NULL	0	NULL	statement 2			bind					T3					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_25_26411_s_91	15082720	A chimeric molecule generated from crocodile TTR, in which the N-terminal end was replaced by that from frog, was shown to differ in both the specificity and affinity of T4 and T3 binding.	bind
40405	5	9409	7	10	NULL	0	NULL	statement 3			differ in					statement 4		specificity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_25_26411_s_91	15082720	A chimeric molecule generated from crocodile TTR, in which the N-terminal end was replaced by that from frog, was shown to differ in both the specificity and affinity of T4 and T3 binding.	bind
46829	6	9409	7	10	NULL	0	NULL	statement 3			differ in					statement 4		affinity of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_25_26411_s_91	15082720	A chimeric molecule generated from crocodile TTR, in which the N-terminal end was replaced by that from frog, was shown to differ in both the specificity and affinity of T4 and T3 binding.	bind
43045	1	9410	5	13	NULL	NULL	NULL	Sec9p	GP		bind			helix		Sso1/2p	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_genetics_166_1_15020409_s_5	15020409	A chimeric molecule, in which the helices of Sec9p  that bind to Sso1/2p and Snc1/2p are replaced with the homologous regions  of Spo20p, will not support vesicle fusion in vegetative cells.	bind
43046	2	9410	5	13	NULL	NULL	NULL	Sec9p	GP		bind			helix		Snc1/2p	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_genetics_166_1_15020409_s_5	15020409	A chimeric molecule, in which the helices of Sec9p  that bind to Sso1/2p and Snc1/2p are replaced with the homologous regions  of Spo20p, will not support vesicle fusion in vegetative cells.	bind
43047	3	9410	5	13	NULL	NULL	NULL	statement 1	GP		is replaced with					Spo20p	GP	homologous regions of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_genetics_166_1_15020409_s_5	15020409	A chimeric molecule, in which the helices of Sec9p  that bind to Sso1/2p and Snc1/2p are replaced with the homologous regions  of Spo20p, will not support vesicle fusion in vegetative cells.	bind
43048	4	9410	5	13	NULL	NULL	NULL	statement 2	GP		is replaced with					Spo20p	GP	homologous regions of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_genetics_166_1_15020409_s_5	15020409	A chimeric molecule, in which the helices of Sec9p  that bind to Sso1/2p and Snc1/2p are replaced with the homologous regions  of Spo20p, will not support vesicle fusion in vegetative cells.	bind
43049	5	9410	5	13	NULL	NULL	NULL	chimera	GP		consists of					statement 3	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_genetics_166_1_15020409_s_5	15020409	A chimeric molecule, in which the helices of Sec9p  that bind to Sso1/2p and Snc1/2p are replaced with the homologous regions  of Spo20p, will not support vesicle fusion in vegetative cells.	bind
43050	6	9410	5	13	NULL	NULL	NULL	chimera	GP		consists of					statement 4	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_genetics_166_1_15020409_s_5	15020409	A chimeric molecule, in which the helices of Sec9p  that bind to Sso1/2p and Snc1/2p are replaced with the homologous regions  of Spo20p, will not support vesicle fusion in vegetative cells.	bind
43051	7	9410	5	13	NULL	NULL	NULL	statement 5	Process		does not support					vesicle	CellComponent	fusion of			NULL	in vegetative cells	NULL	NULL	NULL	NULL	abs-batch0650-0679_genetics_166_1_15020409_s_5	15020409	A chimeric molecule, in which the helices of Sec9p  that bind to Sso1/2p and Snc1/2p are replaced with the homologous regions  of Spo20p, will not support vesicle fusion in vegetative cells.	bind
43052	8	9410	5	13	NULL	NULL	NULL	statement 6	Process		does not support					vesicle	CellComponent	fusion of			NULL	in vegetative cells	NULL	NULL	NULL	NULL	abs-batch0650-0679_genetics_166_1_15020409_s_5	15020409	A chimeric molecule, in which the helices of Sec9p  that bind to Sso1/2p and Snc1/2p are replaced with the homologous regions  of Spo20p, will not support vesicle fusion in vegetative cells.	bind
39626	1	9410	7	NULL	NULL	0	NULL	Sec9p	NULL		bind	NULL		helix		Sso1/2p	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_genetics_166_1_15020409_s_5	15020409	A chimeric molecule, in which the helices of Sec9p  that bind to Sso1/2p and Snc1/2p are replaced with the homologous regions  of Spo20p, will not support vesicle fusion in vegetative cells.	bind
39627	2	9410	7	NULL	NULL	0	NULL	Sec9p	NULL		bind	NULL		helix		Snc1/2p	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_genetics_166_1_15020409_s_5	15020409	A chimeric molecule, in which the helices of Sec9p  that bind to Sso1/2p and Snc1/2p are replaced with the homologous regions  of Spo20p, will not support vesicle fusion in vegetative cells.	bind
39628	3	9410	7	NULL	NULL	0	NULL	statement 1	NULL		is replaced with	NULL				Spo20p	NULL	homologous regions of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_genetics_166_1_15020409_s_5	15020409	A chimeric molecule, in which the helices of Sec9p  that bind to Sso1/2p and Snc1/2p are replaced with the homologous regions  of Spo20p, will not support vesicle fusion in vegetative cells.	bind
39629	5	9410	7	NULL	NULL	0	NULL	chimeric molecule	NULL		consist of	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_genetics_166_1_15020409_s_5	15020409	A chimeric molecule, in which the helices of Sec9p  that bind to Sso1/2p and Snc1/2p are replaced with the homologous regions  of Spo20p, will not support vesicle fusion in vegetative cells.	bind
48773	4	9410	7	NULL	NULL	0	NULL	statement 2	NULL		is replaced with	NULL				Spo20p	NULL	homologous regions of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_genetics_166_1_15020409_s_5	15020409	A chimeric molecule, in which the helices of Sec9p  that bind to Sso1/2p and Snc1/2p are replaced with the homologous regions  of Spo20p, will not support vesicle fusion in vegetative cells.	bind
48774	6	9410	7	NULL	NULL	0	NULL	chimeric molecule	NULL		consist of	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_genetics_166_1_15020409_s_5	15020409	A chimeric molecule, in which the helices of Sec9p  that bind to Sso1/2p and Snc1/2p are replaced with the homologous regions  of Spo20p, will not support vesicle fusion in vegetative cells.	bind
48775	7	9410	7	NULL	NULL	0	NULL	statement 5	NULL		does not support	NULL				vesicle	NULL	fusion of			NULL	vegetative cells	0	NULL	NULL	NULL	abs-batch0650-0679_genetics_166_1_15020409_s_5	15020409	A chimeric molecule, in which the helices of Sec9p  that bind to Sso1/2p and Snc1/2p are replaced with the homologous regions  of Spo20p, will not support vesicle fusion in vegetative cells.	bind
48776	8	9410	7	NULL	NULL	0	NULL	statement 6	NULL		does not support	NULL				vesicle	NULL	fusion of			NULL	vegetative cells	0	NULL	NULL	NULL	abs-batch0650-0679_genetics_166_1_15020409_s_5	15020409	A chimeric molecule, in which the helices of Sec9p  that bind to Sso1/2p and Snc1/2p are replaced with the homologous regions  of Spo20p, will not support vesicle fusion in vegetative cells.	bind
43212	1	9412	5	13	NULL	NULL	NULL	chimeric receptor	GP		contains					GABAB	GP		ATD of R1a subunit		NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_180_s_248	10719229	A chimeric receptor containing the ATD of the GABAB R1a subunit encompassing all of the ATD except the last 40 amino acids immediately upstream of the first TMD (termed aN550) bound a GABAB receptor photoaffinity ligand, while a construct fused 60 amino acids upstream of the first TMD (termed aN530) did not bind the photoaffinity label [ 23].	bind
43213	2	9412	5	13	NULL	NULL	NULL	GABAB	GP		encompass			ATD of R1a subunit					ATD		NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_180_s_248	10719229	A chimeric receptor containing the ATD of the GABAB R1a subunit encompassing all of the ATD except the last 40 amino acids immediately upstream of the first TMD (termed aN550) bound a GABAB receptor photoaffinity ligand, while a construct fused 60 amino acids upstream of the first TMD (termed aN530) did not bind the photoaffinity label [ 23].	bind
43214	3	9412	5	13	NULL	NULL	NULL	40 amino acids	GP		upstream of		immediately						first TMD		NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_180_s_248	10719229	A chimeric receptor containing the ATD of the GABAB R1a subunit encompassing all of the ATD except the last 40 amino acids immediately upstream of the first TMD (termed aN550) bound a GABAB receptor photoaffinity ligand, while a construct fused 60 amino acids upstream of the first TMD (termed aN530) did not bind the photoaffinity label [ 23].	bind
43215	4	9412	5	13	NULL	NULL	NULL	statement 3	Process		is an exception for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_180_s_248	10719229	A chimeric receptor containing the ATD of the GABAB R1a subunit encompassing all of the ATD except the last 40 amino acids immediately upstream of the first TMD (termed aN550) bound a GABAB receptor photoaffinity ligand, while a construct fused 60 amino acids upstream of the first TMD (termed aN530) did not bind the photoaffinity label [ 23].	bind
43216	5	9412	5	13	NULL	NULL	NULL	statement 1	GP		bind					GABAB receptor photoaffinity ligand	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_180_s_248	10719229	A chimeric receptor containing the ATD of the GABAB R1a subunit encompassing all of the ATD except the last 40 amino acids immediately upstream of the first TMD (termed aN550) bound a GABAB receptor photoaffinity ligand, while a construct fused 60 amino acids upstream of the first TMD (termed aN530) did not bind the photoaffinity label [ 23].	bind
43217	6	9412	5	13	NULL	NULL	NULL	60 amino acids	GP		fused to							upstream of	first TMD		NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_180_s_248	10719229	A chimeric receptor containing the ATD of the GABAB R1a subunit encompassing all of the ATD except the last 40 amino acids immediately upstream of the first TMD (termed aN550) bound a GABAB receptor photoaffinity ligand, while a construct fused 60 amino acids upstream of the first TMD (termed aN530) did not bind the photoaffinity label [ 23].	bind
43218	7	9412	5	13	NULL	NULL	NULL	construct	GP		contains					statement 6	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_180_s_248	10719229	A chimeric receptor containing the ATD of the GABAB R1a subunit encompassing all of the ATD except the last 40 amino acids immediately upstream of the first TMD (termed aN550) bound a GABAB receptor photoaffinity ligand, while a construct fused 60 amino acids upstream of the first TMD (termed aN530) did not bind the photoaffinity label [ 23].	bind
43219	8	9412	5	13	NULL	NULL	NULL	statement 7	GP		does not bind					photoaffinity label	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_180_s_248	10719229	A chimeric receptor containing the ATD of the GABAB R1a subunit encompassing all of the ATD except the last 40 amino acids immediately upstream of the first TMD (termed aN550) bound a GABAB receptor photoaffinity ligand, while a construct fused 60 amino acids upstream of the first TMD (termed aN530) did not bind the photoaffinity label [ 23].	bind
39632	1	9412	7	10	NULL	0	NULL	chimeric receptor	NULL		contains	NULL				GABAB	NULL		ATD R1a subunit 		NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_180_s_248	10719229	A chimeric receptor containing the ATD of the GABAB R1a subunit encompassing all of the ATD except the last 40 amino acids immediately upstream of the first TMD (termed aN550) bound a GABAB receptor photoaffinity ligand, while a construct fused 60 amino acids upstream of the first TMD (termed aN530) did not bind the photoaffinity label [ 23].	bind
39707	2	9412	7	NULL	NULL	0	NULL	chimeric receptor	NULL		does not have	NULL				ATD	NULL		 last 40 amino acid upstream of first TMD		NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_180_s_248	10719229	A chimeric receptor containing the ATD of the GABAB R1a subunit encompassing all of the ATD except the last 40 amino acids immediately upstream of the first TMD (termed aN550) bound a GABAB receptor photoaffinity ligand, while a construct fused 60 amino acids upstream of the first TMD (termed aN530) did not bind the photoaffinity label [ 23].	bind
39708	4	9412	7	NULL	NULL	0	NULL	aN550	NULL		bind	NULL				GABAB receptor photoaffinity ligand	NULL				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_180_s_248	10719229	A chimeric receptor containing the ATD of the GABAB R1a subunit encompassing all of the ATD except the last 40 amino acids immediately upstream of the first TMD (termed aN550) bound a GABAB receptor photoaffinity ligand, while a construct fused 60 amino acids upstream of the first TMD (termed aN530) did not bind the photoaffinity label [ 23].	bind
39709	4	9412	7	NULL	NULL	0	NULL	chimeric receptor	NULL		contains	NULL					NULL		60 amino acids upstream of the first TMD		NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_180_s_248	10719229	A chimeric receptor containing the ATD of the GABAB R1a subunit encompassing all of the ATD except the last 40 amino acids immediately upstream of the first TMD (termed aN550) bound a GABAB receptor photoaffinity ligand, while a construct fused 60 amino acids upstream of the first TMD (termed aN530) did not bind the photoaffinity label [ 23].	bind
39710	5	9412	7	NULL	NULL	0	NULL	chimeric receptor	NULL		is	NULL				aN530	NULL				NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_180_s_248	10719229	A chimeric receptor containing the ATD of the GABAB R1a subunit encompassing all of the ATD except the last 40 amino acids immediately upstream of the first TMD (termed aN550) bound a GABAB receptor photoaffinity ligand, while a construct fused 60 amino acids upstream of the first TMD (termed aN530) did not bind the photoaffinity label [ 23].	bind
39711	6	9412	7	NULL	NULL	0	NULL	aN530	NULL		does not bind	NULL				GABAB receptor photoaffinity ligand	NULL				NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_180_s_248	10719229	A chimeric receptor containing the ATD of the GABAB R1a subunit encompassing all of the ATD except the last 40 amino acids immediately upstream of the first TMD (termed aN550) bound a GABAB receptor photoaffinity ligand, while a construct fused 60 amino acids upstream of the first TMD (termed aN530) did not bind the photoaffinity label [ 23].	bind
39712	3	9412	7	NULL	NULL	0	NULL	chimeric receptor	NULL		is	NULL				aN550	NULL				NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_180_s_248	10719229	A chimeric receptor containing the ATD of the GABAB R1a subunit encompassing all of the ATD except the last 40 amino acids immediately upstream of the first TMD (termed aN550) bound a GABAB receptor photoaffinity ligand, while a construct fused 60 amino acids upstream of the first TMD (termed aN530) did not bind the photoaffinity label [ 23].	bind
43077	1	9413	5	13	NULL	NULL	NULL	IP3R	GP		is substituted into			2318-2328		RyR	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_73_0_437_s_305	15189149	A chimeric RyR substitution of residues  2318-2328 of IP3R into RyR retained FKBP12 binding, although binding of native IP3R to FKBP12 could not be demonstrated.	bind
43082	2	9413	5	13	NULL	NULL	NULL	chimeric RyR	GP		bind					FKBP12	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_73_0_437_s_305	15189149	A chimeric RyR substitution of residues  2318-2328 of IP3R into RyR retained FKBP12 binding, although binding of native IP3R to FKBP12 could not be demonstrated.	bind
43083	3	9413	5	13	NULL	NULL	NULL	IP3R	GP	native	does not bind					FKBP12	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_73_0_437_s_305	15189149	A chimeric RyR substitution of residues  2318-2328 of IP3R into RyR retained FKBP12 binding, although binding of native IP3R to FKBP12 could not be demonstrated.	bind
39713	1	9413	7	NULL	NULL	0	NULL	chimeric RyR	NULL		substituted with	NULL				IP3R	NULL		 residues 2318-2328		NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_437_s_305	15189149	A chimeric RyR substitution of residues  2318-2328 of IP3R into RyR retained FKBP12 binding, although binding of native IP3R to FKBP12 could not be demonstrated.	bind
39714	2	9413	7	NULL	NULL	0	NULL	chimeric RyR	NULL		bind	NULL				FKBP12	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_437_s_305	15189149	A chimeric RyR substitution of residues  2318-2328 of IP3R into RyR retained FKBP12 binding, although binding of native IP3R to FKBP12 could not be demonstrated.	bind
39715	3	9413	7	NULL	NULL	0	NULL	IP3R	NULL	native	does not bind	NULL				FKBP12	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_437_s_305	15189149	A chimeric RyR substitution of residues  2318-2328 of IP3R into RyR retained FKBP12 binding, although binding of native IP3R to FKBP12 could not be demonstrated.	bind
43195	1	9414	5	13	NULL	NULL	NULL	chimeric STAT5 protein	GP		consists of					STAT5A	GP		first 545 amino acids		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_33936_s_105	9852045	A chimeric STAT5 protein containing the first 545 amino acids of STAT5A and the COOH terminus of STAT5B (AB) did not bind to the APRE probe behaving like STAT5A ( lanes 2 and  8), and the complementary chimera with the NH2-terminal 545 amino acids of STAT5B fused to the COOH terminus of STAT5A (5BA) had the recognition property of STAT5B, that is, it bound well to APRE probe ( lanes 4 and  6).	bind
43196	2	9414	5	13	NULL	NULL	NULL	chimeric STAT5 protein	GP		consists of					STAT5B	GP		COOH terminus		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_33936_s_105	9852045	A chimeric STAT5 protein containing the first 545 amino acids of STAT5A and the COOH terminus of STAT5B (AB) did not bind to the APRE probe behaving like STAT5A ( lanes 2 and  8), and the complementary chimera with the NH2-terminal 545 amino acids of STAT5B fused to the COOH terminus of STAT5A (5BA) had the recognition property of STAT5B, that is, it bound well to APRE probe ( lanes 4 and  6).	bind
43197	3	9414	5	13	NULL	NULL	NULL	APRE probe	GP		behave like					STAT5A	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_33936_s_105	9852045	A chimeric STAT5 protein containing the first 545 amino acids of STAT5A and the COOH terminus of STAT5B (AB) did not bind to the APRE probe behaving like STAT5A ( lanes 2 and  8), and the complementary chimera with the NH2-terminal 545 amino acids of STAT5B fused to the COOH terminus of STAT5A (5BA) had the recognition property of STAT5B, that is, it bound well to APRE probe ( lanes 4 and  6).	bind
43198	4	9414	5	13	NULL	NULL	NULL	statement 1	GP		does not bind					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_33936_s_105	9852045	A chimeric STAT5 protein containing the first 545 amino acids of STAT5A and the COOH terminus of STAT5B (AB) did not bind to the APRE probe behaving like STAT5A ( lanes 2 and  8), and the complementary chimera with the NH2-terminal 545 amino acids of STAT5B fused to the COOH terminus of STAT5A (5BA) had the recognition property of STAT5B, that is, it bound well to APRE probe ( lanes 4 and  6).	bind
43199	5	9414	5	13	NULL	NULL	NULL	statement 2	GP		does not bind					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_33936_s_105	9852045	A chimeric STAT5 protein containing the first 545 amino acids of STAT5A and the COOH terminus of STAT5B (AB) did not bind to the APRE probe behaving like STAT5A ( lanes 2 and  8), and the complementary chimera with the NH2-terminal 545 amino acids of STAT5B fused to the COOH terminus of STAT5A (5BA) had the recognition property of STAT5B, that is, it bound well to APRE probe ( lanes 4 and  6).	bind
43200	6	9414	5	13	NULL	NULL	NULL	STAT5B	GP		fused to			NH2-terminal 545 amino acids		STAT5A	GP		COOH terminus		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_33936_s_105	9852045	A chimeric STAT5 protein containing the first 545 amino acids of STAT5A and the COOH terminus of STAT5B (AB) did not bind to the APRE probe behaving like STAT5A ( lanes 2 and  8), and the complementary chimera with the NH2-terminal 545 amino acids of STAT5B fused to the COOH terminus of STAT5A (5BA) had the recognition property of STAT5B, that is, it bound well to APRE probe ( lanes 4 and  6).	bind
43201	7	9414	5	13	NULL	NULL	NULL	statement 6	GP		is					complementary chimera	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_33936_s_105	9852045	A chimeric STAT5 protein containing the first 545 amino acids of STAT5A and the COOH terminus of STAT5B (AB) did not bind to the APRE probe behaving like STAT5A ( lanes 2 and  8), and the complementary chimera with the NH2-terminal 545 amino acids of STAT5B fused to the COOH terminus of STAT5A (5BA) had the recognition property of STAT5B, that is, it bound well to APRE probe ( lanes 4 and  6).	bind
43202	8	9414	5	13	NULL	NULL	NULL	statement 7	GP		contains					STAT5B	GP	recognition property of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_33936_s_105	9852045	A chimeric STAT5 protein containing the first 545 amino acids of STAT5A and the COOH terminus of STAT5B (AB) did not bind to the APRE probe behaving like STAT5A ( lanes 2 and  8), and the complementary chimera with the NH2-terminal 545 amino acids of STAT5B fused to the COOH terminus of STAT5A (5BA) had the recognition property of STAT5B, that is, it bound well to APRE probe ( lanes 4 and  6).	bind
43203	9	9414	5	13	NULL	NULL	NULL	statement 7	GP		bind					APRE probe	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_33936_s_105	9852045	A chimeric STAT5 protein containing the first 545 amino acids of STAT5A and the COOH terminus of STAT5B (AB) did not bind to the APRE probe behaving like STAT5A ( lanes 2 and  8), and the complementary chimera with the NH2-terminal 545 amino acids of STAT5B fused to the COOH terminus of STAT5A (5BA) had the recognition property of STAT5B, that is, it bound well to APRE probe ( lanes 4 and  6).	bind
39716	1	9414	7	NULL	NULL	0	NULL	chimeric STAT5 protein 	NULL		contains	NULL				STAT5A	NULL		first 545 amino acids 		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_33936_s_105	9852045	A chimeric STAT5 protein containing the first 545 amino acids of STAT5A and the COOH terminus of STAT5B (AB) did not bind to the APRE probe behaving like STAT5A ( lanes 2 and  8), and the complementary chimera with the NH2-terminal 545 amino acids of STAT5B fused to the COOH terminus of STAT5A (5BA) had the recognition property of STAT5B, that is, it bound well to APRE probe ( lanes 4 and  6).	bind
39717	2	9414	7	NULL	NULL	0	NULL	chimeric STAT5 protein	NULL		contains	NULL				STAT5B	NULL		COOH terminus of		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_51_33936_s_105	9852045	A chimeric STAT5 protein containing the first 545 amino acids of STAT5A and the COOH terminus of STAT5B (AB) did not bind to the APRE probe behaving like STAT5A ( lanes 2 and  8), and the complementary chimera with the NH2-terminal 545 amino acids of STAT5B fused to the COOH terminus of STAT5A (5BA) had the recognition property of STAT5B, that is, it bound well to APRE probe ( lanes 4 and  6).	bind
39718	3	9414	7	NULL	NULL	0	NULL	chimeric STAT5 protein	NULL		does not bind	NULL				APRE probe	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_51_33936_s_105	9852045	A chimeric STAT5 protein containing the first 545 amino acids of STAT5A and the COOH terminus of STAT5B (AB) did not bind to the APRE probe behaving like STAT5A ( lanes 2 and  8), and the complementary chimera with the NH2-terminal 545 amino acids of STAT5B fused to the COOH terminus of STAT5A (5BA) had the recognition property of STAT5B, that is, it bound well to APRE probe ( lanes 4 and  6).	bind
39719	4	9414	7	NULL	NULL	0	NULL	chimeric STAT5 protein	NULL		behave like	NULL				STAT5A	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_51_33936_s_105	9852045	A chimeric STAT5 protein containing the first 545 amino acids of STAT5A and the COOH terminus of STAT5B (AB) did not bind to the APRE probe behaving like STAT5A ( lanes 2 and  8), and the complementary chimera with the NH2-terminal 545 amino acids of STAT5B fused to the COOH terminus of STAT5A (5BA) had the recognition property of STAT5B, that is, it bound well to APRE probe ( lanes 4 and  6).	bind
39720	5	9414	7	NULL	NULL	0	NULL	chimera	NULL		contains	NULL				STAT5B	NULL		NH2-terminal 545 amino acids of 		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_51_33936_s_105	9852045	A chimeric STAT5 protein containing the first 545 amino acids of STAT5A and the COOH terminus of STAT5B (AB) did not bind to the APRE probe behaving like STAT5A ( lanes 2 and  8), and the complementary chimera with the NH2-terminal 545 amino acids of STAT5B fused to the COOH terminus of STAT5A (5BA) had the recognition property of STAT5B, that is, it bound well to APRE probe ( lanes 4 and  6).	bind
39721	6	9414	7	NULL	NULL	0	NULL	chimera	NULL		contains	NULL				STAT5A	NULL		COOH terminus of		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_51_33936_s_105	9852045	A chimeric STAT5 protein containing the first 545 amino acids of STAT5A and the COOH terminus of STAT5B (AB) did not bind to the APRE probe behaving like STAT5A ( lanes 2 and  8), and the complementary chimera with the NH2-terminal 545 amino acids of STAT5B fused to the COOH terminus of STAT5A (5BA) had the recognition property of STAT5B, that is, it bound well to APRE probe ( lanes 4 and  6).	bind
39722	8	9414	7	NULL	NULL	0	NULL	chimera	NULL		bind	NULL				APRE probe	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_33936_s_105	9852045	A chimeric STAT5 protein containing the first 545 amino acids of STAT5A and the COOH terminus of STAT5B (AB) did not bind to the APRE probe behaving like STAT5A ( lanes 2 and  8), and the complementary chimera with the NH2-terminal 545 amino acids of STAT5B fused to the COOH terminus of STAT5A (5BA) had the recognition property of STAT5B, that is, it bound well to APRE probe ( lanes 4 and  6).	bind
39723	7	9414	7	NULL	NULL	0	NULL	chimera	NULL		behave like	NULL				STAT5B	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_51_33936_s_105	9852045	A chimeric STAT5 protein containing the first 545 amino acids of STAT5A and the COOH terminus of STAT5B (AB) did not bind to the APRE probe behaving like STAT5A ( lanes 2 and  8), and the complementary chimera with the NH2-terminal 545 amino acids of STAT5B fused to the COOH terminus of STAT5A (5BA) had the recognition property of STAT5B, that is, it bound well to APRE probe ( lanes 4 and  6).	bind
43204	1	9415	5	13	NULL	NULL	NULL	chimeric tetramer	GP		is composed of					ubiquitins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34983_s_8	9857030	A chimeric tetramer composed of three ubiquitins and one histidine-tagged NEDD8 binds to the 26 S proteasome with an affinity similar to that of tetraubiquitin.	bind
43205	2	9415	5	13	NULL	NULL	NULL	chimeric tetramer	GP		is composed of					NEDD8	GP	histidine-tagged			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34983_s_8	9857030	A chimeric tetramer composed of three ubiquitins and one histidine-tagged NEDD8 binds to the 26 S proteasome with an affinity similar to that of tetraubiquitin.	bind
43206	3	9415	5	13	NULL	NULL	NULL	statement 1	GP		bind					26 S proteasome	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34983_s_8	9857030	A chimeric tetramer composed of three ubiquitins and one histidine-tagged NEDD8 binds to the 26 S proteasome with an affinity similar to that of tetraubiquitin.	bind
43207	4	9415	5	13	NULL	NULL	NULL	statement 2	GP		bind					26 S proteasome	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34983_s_8	9857030	A chimeric tetramer composed of three ubiquitins and one histidine-tagged NEDD8 binds to the 26 S proteasome with an affinity similar to that of tetraubiquitin.	bind
43208	5	9415	5	13	NULL	NULL	NULL	statement 1	GP		bind					tetraubiquitin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34983_s_8	9857030	A chimeric tetramer composed of three ubiquitins and one histidine-tagged NEDD8 binds to the 26 S proteasome with an affinity similar to that of tetraubiquitin.	bind
43209	6	9415	5	13	NULL	NULL	NULL	statement 2	GP		bind					tetraubiquitin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34983_s_8	9857030	A chimeric tetramer composed of three ubiquitins and one histidine-tagged NEDD8 binds to the 26 S proteasome with an affinity similar to that of tetraubiquitin.	bind
43210	7	9415	5	13	NULL	NULL	NULL	statement 3	Process		similar affinity to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34983_s_8	9857030	A chimeric tetramer composed of three ubiquitins and one histidine-tagged NEDD8 binds to the 26 S proteasome with an affinity similar to that of tetraubiquitin.	bind
43211	8	9415	5	13	NULL	NULL	NULL	statement 4	Process		similar affinity to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34983_s_8	9857030	A chimeric tetramer composed of three ubiquitins and one histidine-tagged NEDD8 binds to the 26 S proteasome with an affinity similar to that of tetraubiquitin.	bind
39725	1	9415	7	10	NULL	0	NULL	chimeric tetramer	NULL		is composed of	NULL				NEDD8	NULL	histidine tagged			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34983_s_8	9857030	A chimeric tetramer composed of three ubiquitins and one histidine-tagged NEDD8 binds to the 26 S proteasome with an affinity similar to that of tetraubiquitin.	bind
39726	4	9415	7	NULL	NULL	0	NULL	statement 3	NULL		binds to	NULL				26 S proteasome	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34983_s_8	9857030	A chimeric tetramer composed of three ubiquitins and one histidine-tagged NEDD8 binds to the 26 S proteasome with an affinity similar to that of tetraubiquitin.	bind
39727	5	9415	7	NULL	NULL	0	NULL	tetraubiquitin	NULL		bind	NULL				26 S proteasome	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34983_s_8	9857030	A chimeric tetramer composed of three ubiquitins and one histidine-tagged NEDD8 binds to the 26 S proteasome with an affinity similar to that of tetraubiquitin.	bind
46959	2	9415	7	NULL	NULL	0	NULL	chimeric tetramer	NULL		is composed of	NULL				three ubiquitins 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34983_s_8	9857030	A chimeric tetramer composed of three ubiquitins and one histidine-tagged NEDD8 binds to the 26 S proteasome with an affinity similar to that of tetraubiquitin.	bind
46960	3	9415	7	NULL	NULL	0	NULL	statement 1	NULL		occur along with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34983_s_8	9857030	A chimeric tetramer composed of three ubiquitins and one histidine-tagged NEDD8 binds to the 26 S proteasome with an affinity similar to that of tetraubiquitin.	bind
46961	6	9415	7	NULL	NULL	0	NULL	statement 4	NULL	affinity of	is similar to	NULL				statement 5	NULL	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34983_s_8	9857030	A chimeric tetramer composed of three ubiquitins and one histidine-tagged NEDD8 binds to the 26 S proteasome with an affinity similar to that of tetraubiquitin.	bind
41065	1	9416	5	13	NULL	NULL	NULL	PAX3-FKHR	GP		is a type of					chimeric transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_23259_s_23	10770948	A chimeric transcription factor PAX3-FKHR, produced by this t(2;13)(q35;q14) chromosomal translocation in alveolar rhabdomyosarcoma binds to the NCAM promoter through its Pax3 homeodomain recognition helix.	bind
41066	2	9416	5	13	NULL	NULL	NULL	PAX3-FKHR	GP		produced by							chromosomal translocation of		t(2;13)(q35;q14)	NULL	alveolar rhabdomyosarcoma 	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_23259_s_23	10770948	A chimeric transcription factor PAX3-FKHR, produced by this t(2;13)(q35;q14) chromosomal translocation in alveolar rhabdomyosarcoma binds to the NCAM promoter through its Pax3 homeodomain recognition helix.	bind
41067	3	9416	5	13	NULL	NULL	NULL	PAX3-FKHR	GP		bind			Pax3 homeodomain recognition helix		NCAM 	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_23259_s_23	10770948	A chimeric transcription factor PAX3-FKHR, produced by this t(2;13)(q35;q14) chromosomal translocation in alveolar rhabdomyosarcoma binds to the NCAM promoter through its Pax3 homeodomain recognition helix.	bind
39728	1	9416	7	10	NULL	0	NULL	PAX3-FKHR	NULL		is produced by	NULL				t(2;13)(q35;q14) 	NULL	chromosomal translocation of			NULL	alveolar rhabdomyosarcoma	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_23259_s_23	10770948	A chimeric transcription factor PAX3-FKHR, produced by this t(2;13)(q35;q14) chromosomal translocation in alveolar rhabdomyosarcoma binds to the NCAM promoter through its Pax3 homeodomain recognition helix.	bind
39729	2	9416	7	NULL	NULL	0	NULL	chimeric transcription factor PAX3-FKHR	NULL		binds to	NULL		Pax3 homeodomain recognition helix		NCAM	NULL			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_30_23259_s_23	10770948	A chimeric transcription factor PAX3-FKHR, produced by this t(2;13)(q35;q14) chromosomal translocation in alveolar rhabdomyosarcoma binds to the NCAM promoter through its Pax3 homeodomain recognition helix.	bind
46830	3	9416	7	10	NULL	0	NULL	PAX3-FKHR	NULL		is a type of 	NULL				chimeric transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_30_23259_s_23	10770948	A chimeric transcription factor PAX3-FKHR, produced by this t(2;13)(q35;q14) chromosomal translocation in alveolar rhabdomyosarcoma binds to the NCAM promoter through its Pax3 homeodomain recognition helix.	bind
41069	1	9417	5	13	NULL	NULL	NULL	chimeric virus	Organism		does not bind					Z-DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_12_6974_s_5	12777633	A chimeric virus incorporating a  related protein that does not bind Z-DNA is not pathogenic, but a mutation  that creates Z-DNA binding makes a lethal virus.	bind
41071	2	9417	5	13	NULL	NULL	NULL	statement 1	Organism		is not					pathogenic	Organism				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_12_6974_s_5	12777633	A chimeric virus incorporating a  related protein that does not bind Z-DNA is not pathogenic, but a mutation  that creates Z-DNA binding makes a lethal virus.	bind
41072	3	9417	5	13	NULL	NULL	NULL	chimeric virus	Organism	mutant	bind					Z-DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_12_6974_s_5	12777633	A chimeric virus incorporating a  related protein that does not bind Z-DNA is not pathogenic, but a mutation  that creates Z-DNA binding makes a lethal virus.	bind
41073	4	9417	5	13	NULL	NULL	NULL	statement 3	Organism		is a type of 					lethal virus	Organism				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_12_6974_s_5	12777633	A chimeric virus incorporating a  related protein that does not bind Z-DNA is not pathogenic, but a mutation  that creates Z-DNA binding makes a lethal virus.	bind
39730	1	9417	7	NULL	NULL	0	NULL	chimeric virus	NULL		does not bind	NULL				Z-DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_100_12_6974_s_5	12777633	A chimeric virus incorporating a  related protein that does not bind Z-DNA is not pathogenic, but a mutation  that creates Z-DNA binding makes a lethal virus.	bind
39731	2	9417	7	NULL	NULL	0	NULL	statement 1	NULL		is not	NULL				pathogenic	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_100_12_6974_s_5	12777633	A chimeric virus incorporating a  related protein that does not bind Z-DNA is not pathogenic, but a mutation  that creates Z-DNA binding makes a lethal virus.	bind
39732	3	9417	7	NULL	NULL	0	NULL	chimeric virus	NULL	mutated	binds	NULL				Z-DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_100_12_6974_s_5	12777633	A chimeric virus incorporating a  related protein that does not bind Z-DNA is not pathogenic, but a mutation  that creates Z-DNA binding makes a lethal virus.	bind
39733	4	9417	7	NULL	NULL	0	NULL	statement 3	NULL		is a type of	NULL				lethal virus	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_100_12_6974_s_5	12777633	A chimeric virus incorporating a  related protein that does not bind Z-DNA is not pathogenic, but a mutation  that creates Z-DNA binding makes a lethal virus.	bind
41074	1	9418	5	13	NULL	NULL	NULL	(IRS) 2/FRS3 adapter	GP		is a type of					chimerical insulin receptor substrate	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1763_4_366_s_191	16697063	A chimerical insulin receptor substrate (IRS) 2/FRS3 adapter supports insulin-dependent  MAPK/ERK activation and neuritogenesis and is dependent upon the integrity of the  Grb2 and Shp2 binding sites of FRS3	bind
41075	2	9418	5	13	NULL	NULL	NULL	(IRS) 2/FRS3 adapter	GP		supports					MAPK/ERK	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1763_4_366_s_191	16697063	A chimerical insulin receptor substrate (IRS) 2/FRS3 adapter supports insulin-dependent  MAPK/ERK activation and neuritogenesis and is dependent upon the integrity of the  Grb2 and Shp2 binding sites of FRS3	bind
41076	3	9418	5	13	NULL	NULL	NULL	MAPK/ERK	GP	activation of	is dependent on					insulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1763_4_366_s_191	16697063	A chimerical insulin receptor substrate (IRS) 2/FRS3 adapter supports insulin-dependent  MAPK/ERK activation and neuritogenesis and is dependent upon the integrity of the  Grb2 and Shp2 binding sites of FRS3	bind
41078	4	9418	5	13	NULL	NULL	NULL	(IRS) 2/FRS3 adapter	GP		supports					neuritogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1763_4_366_s_191	16697063	A chimerical insulin receptor substrate (IRS) 2/FRS3 adapter supports insulin-dependent  MAPK/ERK activation and neuritogenesis and is dependent upon the integrity of the  Grb2 and Shp2 binding sites of FRS3	bind
41079	5	9418	5	13	NULL	NULL	NULL	(IRS) 2/FRS3 adapter	GP		is dependent on					FRS3	GP	integrity of	Shp2 binding sites		NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1763_4_366_s_191	16697063	A chimerical insulin receptor substrate (IRS) 2/FRS3 adapter supports insulin-dependent  MAPK/ERK activation and neuritogenesis and is dependent upon the integrity of the  Grb2 and Shp2 binding sites of FRS3	bind
41081	6	9418	5	13	NULL	NULL	NULL	(IRS) 2/FRS3 adapter	GP		is dependent on					FRS3	GP	integrity of	Grb2 binding sites		NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1763_4_366_s_191	16697063	A chimerical insulin receptor substrate (IRS) 2/FRS3 adapter supports insulin-dependent  MAPK/ERK activation and neuritogenesis and is dependent upon the integrity of the  Grb2 and Shp2 binding sites of FRS3	bind
39734	1	9418	7	NULL	NULL	0	NULL	MAPK/ERK 	NULL	activation of	depends on	NULL				insulin	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1763_4_366_s_191	16697063	A chimerical insulin receptor substrate (IRS) 2/FRS3 adapter supports insulin-dependent  MAPK/ERK activation and neuritogenesis and is dependent upon the integrity of the  Grb2 and Shp2 binding sites of FRS3	bind
39735	2	9418	7	10	NULL	0	NULL	(IRS) 2/FRS3			supports					statement 1					NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1763_4_366_s_191	16697063	A chimerical insulin receptor substrate (IRS) 2/FRS3 adapter supports insulin-dependent  MAPK/ERK activation and neuritogenesis and is dependent upon the integrity of the  Grb2 and Shp2 binding sites of FRS3	bind
39736	3	9418	7	NULL	NULL	0	NULL	neuritogenesis	NULL		depends on	NULL				insulin	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1763_4_366_s_191	16697063	A chimerical insulin receptor substrate (IRS) 2/FRS3 adapter supports insulin-dependent  MAPK/ERK activation and neuritogenesis and is dependent upon the integrity of the  Grb2 and Shp2 binding sites of FRS3	bind
39737	4	9418	7	10	NULL	0	NULL	(IRS) 2/FRS3			supports					statement 3					NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1763_4_366_s_191	16697063	A chimerical insulin receptor substrate (IRS) 2/FRS3 adapter supports insulin-dependent  MAPK/ERK activation and neuritogenesis and is dependent upon the integrity of the  Grb2 and Shp2 binding sites of FRS3	bind
39738	5	9418	7	10	NULL	0	NULL	(IRS) 2/FRS3			is dependent on					FRS3		integrity of	Grb2 binding site		NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1763_4_366_s_191	16697063	A chimerical insulin receptor substrate (IRS) 2/FRS3 adapter supports insulin-dependent  MAPK/ERK activation and neuritogenesis and is dependent upon the integrity of the  Grb2 and Shp2 binding sites of FRS3	bind
39739	6	9418	7	10	NULL	0	NULL	(IRS) 2/FRS3			is dependent on					FRS3		integrity of	Shp2 binding site		NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1763_4_366_s_191	16697063	A chimerical insulin receptor substrate (IRS) 2/FRS3 adapter supports insulin-dependent  MAPK/ERK activation and neuritogenesis and is dependent upon the integrity of the  Grb2 and Shp2 binding sites of FRS3	bind
56711	7	9418	7	10	NULL	0	NULL	(IRS) 2/FRS3			is a type of					chimeric insulin receptor substrate					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1763_4_366_s_191	16697063	A chimerical insulin receptor substrate (IRS) 2/FRS3 adapter supports insulin-dependent  MAPK/ERK activation and neuritogenesis and is dependent upon the integrity of the  Grb2 and Shp2 binding sites of FRS3	bind
41082	1	9419	5	13	NULL	NULL	NULL	CBP	GP		bind					IL-10	NucleicAcid	proximal		promoter	NULL	in situ in LPS-stimulated primary macrophages	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_218	16835236	A ChIP analysis was performed on stimulated cells, and this assay verified that CBP binds to the proximal IL-10 promoter  in situ in LPS-stimulated primary macrophages ( Fig. 6 C), although the kinetics of CBP association appeared to be slightly different from that of p50 ( Fig. 6 C).	bind
39742	1	9419	7	NULL	NULL	0	NULL	CBP	NULL		binds to	NULL				IL-10	NULL	proximal		promoter	NULL	in situ in LPS-stimulated primary macrophages	0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_218	16835236	A ChIP analysis was performed on stimulated cells, and this assay verified that CBP binds to the proximal IL-10 promoter  in situ in LPS-stimulated primary macrophages ( Fig. 6 C), although the kinetics of CBP association appeared to be slightly different from that of p50 ( Fig. 6 C).	bind
41050	1	9420	5	13	NULL	NULL	NULL	SREBP-1	GP		bind					LGK	NucleicAcid			SREs of promoter	NULL	primary hepatocytes	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_29_30823_s_280	15123649	A ChIP assay using primary hepatocytes showed the increased binding of SREBP-1 to SREs of LGK promoter.	bind
39745	1	9420	7	NULL	NULL	0	NULL	SREBP-1 	NULL		bind	NULL				LGK	NULL			SREs in the promoter	NULL	primary hepatocytes	0	NULL	NULL	NULL	gw70_jbiolchem_279_29_30823_s_280	15123649	A ChIP assay using primary hepatocytes showed the increased binding of SREBP-1 to SREs of LGK promoter.	bind
41051	1	9421	5	13	NULL	NULL	NULL	Smad4	GP		bind					Ihh gene 	GP			GC-rich motifs within -285/-123 region	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18544_s_162	14981086	A ChIP assay was carried out to confirm that Smad4 binds to GC-rich motifs within the -285/-123 region of the  Ihh gene upon BMP7 stimulation  in vivo.	bind
41052	2	9421	5	13	NULL	NULL	NULL	BMP7	GP	stimulation of	leads to					statement 1	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18544_s_162	14981086	A ChIP assay was carried out to confirm that Smad4 binds to GC-rich motifs within the -285/-123 region of the  Ihh gene upon BMP7 stimulation  in vivo.	bind
39746	1	9421	7	NULL	NULL	0	NULL	Smad4 	NULL		binds to	NULL				Ihh gene	NULL			GC-rich motifs within the -285/-123 region	NULL	in vivo	0	NULL	NULL	NULL	gw70_jbiolchem_279_18_18544_s_162	14981086	A ChIP assay was carried out to confirm that Smad4 binds to GC-rich motifs within the -285/-123 region of the  Ihh gene upon BMP7 stimulation  in vivo.	bind
39747	2	9421	7	NULL	NULL	0	NULL	statement 1	NULL		occurs upon	NULL				BMP7 	NULL	stimulation of			NULL	in vivo	0	NULL	NULL	NULL	gw70_jbiolchem_279_18_18544_s_162	14981086	A ChIP assay was carried out to confirm that Smad4 binds to GC-rich motifs within the -285/-123 region of the  Ihh gene upon BMP7 stimulation  in vivo.	bind
41053	1	9423	5	13	NULL	NULL	NULL	cholera toxin	Chemical		bind			B-subunit variant		ganglioside GM1	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_3_1527_s_583	12595472	A cholera toxin B-subunit variant that binds ganglioside GM1 but fails to induce toxicity.	bind
41054	2	9423	5	13	NULL	NULL	NULL	statement 1	Process		does not induce					toxicity	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_71_3_1527_s_583	12595472	A cholera toxin B-subunit variant that binds ganglioside GM1 but fails to induce toxicity.	bind
39748	1	9423	7	NULL	NULL	0	NULL	cholera toxin 	NULL		binds	NULL		B-subunit variant		ganglioside GM1	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_71_3_1527_s_583	12595472	A cholera toxin B-subunit variant that binds ganglioside GM1 but fails to induce toxicity.	bind
39749	2	9423	7	NULL	NULL	0	NULL	statement 1	NULL		fails to induce	NULL				toxicity	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_71_3_1527_s_583	12595472	A cholera toxin B-subunit variant that binds ganglioside GM1 but fails to induce toxicity.	bind
41085	1	9424	5	13	NULL	NULL	NULL	mcl-1	GP		bind									SIE motif of promoter	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_mol-cell-biol_23_6_12612065_s_5	12612065	A chromatin immunoprecipitation  assay further confirmed that PU.1 binds to the mcl-1 promoter region containing  the SIE motif in vivo.	bind
39750	1	9424	7	10	NULL	0	NULL	 PU.1			binds to					 mcl-1				 SIE motif of promoter	NULL	in vivo	NULL	NULL	NULL	NULL	abs-batch0650-0679_mol-cell-biol_23_6_12612065_s_5	12612065	A chromatin immunoprecipitation  assay further confirmed that PU.1 binds to the mcl-1 promoter region containing  the SIE motif in vivo.	bind
41088	1	9426	5	13	NULL	NULL	NULL	Mitf	GP		bind					p21 Cip1	NucleicAcid			promoter	NULL	mel melanoma cells	NULL	NULL	NULL	NULL	gw70_nature_433_7027_764_s_49	15716956	A chromatin immunoprecipitation assay (ChIP) from 501mel  melanoma cells, which express both Mitf and p21Cip1, or melan-a melanocytes, using an anti-Mitf antibody and polymerase chain reaction  (PCR) primers spanning the  p21 Cip1 E2 element confirmed Mitf binding to the  p21 Cip1 promoter  in vivo ( Fig. 2e).	bind
41089	2	9426	5	13	NULL	NULL	NULL	mel melanoma cells	Cell		express					Mitf	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_433_7027_764_s_49	15716956	A chromatin immunoprecipitation assay (ChIP) from 501mel  melanoma cells, which express both Mitf and p21Cip1, or melan-a melanocytes, using an anti-Mitf antibody and polymerase chain reaction  (PCR) primers spanning the  p21 Cip1 E2 element confirmed Mitf binding to the  p21 Cip1 promoter  in vivo ( Fig. 2e).	bind
41090	3	9426	5	13	NULL	NULL	NULL	Mitf	GP		bind					p21 Cip1	NucleicAcid			promoter	NULL	melan-a melanocytes	NULL	NULL	NULL	NULL	gw70_nature_433_7027_764_s_49	15716956	A chromatin immunoprecipitation assay (ChIP) from 501mel  melanoma cells, which express both Mitf and p21Cip1, or melan-a melanocytes, using an anti-Mitf antibody and polymerase chain reaction  (PCR) primers spanning the  p21 Cip1 E2 element confirmed Mitf binding to the  p21 Cip1 promoter  in vivo ( Fig. 2e).	bind
41091	4	9426	5	13	NULL	NULL	NULL	mel melanoma cells	Cell		express					p21Cip1	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_433_7027_764_s_49	15716956	A chromatin immunoprecipitation assay (ChIP) from 501mel  melanoma cells, which express both Mitf and p21Cip1, or melan-a melanocytes, using an anti-Mitf antibody and polymerase chain reaction  (PCR) primers spanning the  p21 Cip1 E2 element confirmed Mitf binding to the  p21 Cip1 promoter  in vivo ( Fig. 2e).	bind
39755	1	9426	7	NULL	NULL	0	NULL	Mitf	NULL		bind	NULL				p21 Cip1	NULL			promoter	NULL	in vivo melanoma cells	NULL	NULL	NULL	NULL	gw70_nature_433_7027_764_s_49	15716956	A chromatin immunoprecipitation assay (ChIP) from 501mel  melanoma cells, which express both Mitf and p21Cip1, or melan-a melanocytes, using an anti-Mitf antibody and polymerase chain reaction  (PCR) primers spanning the  p21 Cip1 E2 element confirmed Mitf binding to the  p21 Cip1 promoter  in vivo ( Fig. 2e).	bind
39756	2	9426	7	NULL	NULL	0	NULL	melanoma cells	NULL		express	NULL				Mitf 	NULL				NULL		0	NULL	NULL	NULL	gw70_nature_433_7027_764_s_49	15716956	A chromatin immunoprecipitation assay (ChIP) from 501mel  melanoma cells, which express both Mitf and p21Cip1, or melan-a melanocytes, using an anti-Mitf antibody and polymerase chain reaction  (PCR) primers spanning the  p21 Cip1 E2 element confirmed Mitf binding to the  p21 Cip1 promoter  in vivo ( Fig. 2e).	bind
39757	3	9426	7	NULL	NULL	0	NULL	melanoma cells	NULL		express	NULL				p21Cip1	NULL				NULL		0	NULL	NULL	NULL	gw70_nature_433_7027_764_s_49	15716956	A chromatin immunoprecipitation assay (ChIP) from 501mel  melanoma cells, which express both Mitf and p21Cip1, or melan-a melanocytes, using an anti-Mitf antibody and polymerase chain reaction  (PCR) primers spanning the  p21 Cip1 E2 element confirmed Mitf binding to the  p21 Cip1 promoter  in vivo ( Fig. 2e).	bind
39758	4	9426	7	NULL	NULL	0	NULL	Mitf	NULL		bind	NULL				p21 Cip1	NULL			promoter	NULL	in vivo  melan-a melanocytes	0	NULL	NULL	NULL	gw70_nature_433_7027_764_s_49	15716956	A chromatin immunoprecipitation assay (ChIP) from 501mel  melanoma cells, which express both Mitf and p21Cip1, or melan-a melanocytes, using an anti-Mitf antibody and polymerase chain reaction  (PCR) primers spanning the  p21 Cip1 E2 element confirmed Mitf binding to the  p21 Cip1 promoter  in vivo ( Fig. 2e).	bind
41092	1	9427	5	13	NULL	NULL	NULL	Rgt1	GP		bind					HXT1	GP			promoter	NULL	cells grown on galactose	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_36_26144_s_115	16844691	A chromatin immunoprecipitation assay confirms that Rgt1 binds to the  HXT1 promoter in cells grown on galactose but not glucose ( Fig. 6 A).	bind
41095	2	9427	5	13	NULL	NULL	NULL	Rgt1	GP		does not bind					HXT1	GP			promoter	NULL	cells grown on glucose	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_36_26144_s_115	16844691	A chromatin immunoprecipitation assay confirms that Rgt1 binds to the  HXT1 promoter in cells grown on galactose but not glucose ( Fig. 6 A).	bind
39759	1	9427	7	NULL	NULL	0	NULL	Rgt1	NULL		binds to	NULL				HXT1	NULL			promoter	NULL	cells grown on galactose 	0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26144_s_115	16844691	A chromatin immunoprecipitation assay confirms that Rgt1 binds to the  HXT1 promoter in cells grown on galactose but not glucose ( Fig. 6 A).	bind
39760	2	9427	7	NULL	NULL	0	NULL	Rgt1	NULL		does not bind	NULL				HXT1	NULL			promoter	NULL	cells grown on glucose	0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26144_s_115	16844691	A chromatin immunoprecipitation assay confirms that Rgt1 binds to the  HXT1 promoter in cells grown on galactose but not glucose ( Fig. 6 A).	bind
41096	1	9428	5	13	NULL	NULL	NULL	mcl-1	NucleicAcid		contains				promoter					SIE motif	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_6_1896_s_5	12612065	A chromatin immunoprecipitation assay further confirmed that PU.1 binds to the  mcl-1 promoter region containing the SIE motif in vivo.	bind
41097	2	9428	5	NULL	NULL	0	NULL	PU.1	NULL		bind	NULL				statement 1	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_molcellbiol_23_6_1896_s_5	12612065	A chromatin immunoprecipitation assay further confirmed that PU.1 binds to the  mcl-1 promoter region containing the SIE motif in vivo.	bind
41098	1	9429	5	13	NULL	NULL	NULL	E2F-1	GP		bind					Apaf-1	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_j-biol-chem_277_42_12149244_s_8	12149244	A chromatin immunoprecipitation assay revealed that  E2F-1 bound to Apaf-1 promoter upon E2F-1 overexpression, suggesting that  Apaf-1 is under transcriptional regulation of E2F-1.	bind
41100	2	9429	5	13	NULL	NULL	NULL	E2F-1	GP	overexpression of	leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_j-biol-chem_277_42_12149244_s_8	12149244	A chromatin immunoprecipitation assay revealed that  E2F-1 bound to Apaf-1 promoter upon E2F-1 overexpression, suggesting that  Apaf-1 is under transcriptional regulation of E2F-1.	bind
41102	3	9429	5	13	NULL	NULL	NULL	E2F-1	GP		regulates		transcriptionally			Apaf-1	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_j-biol-chem_277_42_12149244_s_8	12149244	A chromatin immunoprecipitation assay revealed that  E2F-1 bound to Apaf-1 promoter upon E2F-1 overexpression, suggesting that  Apaf-1 is under transcriptional regulation of E2F-1.	bind
41103	4	9429	5	13	NULL	NULL	NULL	statement 1	Process		suggest					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_j-biol-chem_277_42_12149244_s_8	12149244	A chromatin immunoprecipitation assay revealed that  E2F-1 bound to Apaf-1 promoter upon E2F-1 overexpression, suggesting that  Apaf-1 is under transcriptional regulation of E2F-1.	bind
39761	1	9429	7	NULL	NULL	0	NULL	E2F-1	NULL		bind	NULL				Apaf-1	NULL			promoter	NULL		0	NULL	NULL	NULL	abs-batch0570-0579_j-biol-chem_277_42_12149244_s_8	12149244	A chromatin immunoprecipitation assay revealed that  E2F-1 bound to Apaf-1 promoter upon E2F-1 overexpression, suggesting that  Apaf-1 is under transcriptional regulation of E2F-1.	bind
39762	2	9429	7	NULL	NULL	0	NULL	statement 1	NULL		occurs upon	NULL				E2F-1	NULL	overexpression of			NULL		0	NULL	NULL	NULL	abs-batch0570-0579_j-biol-chem_277_42_12149244_s_8	12149244	A chromatin immunoprecipitation assay revealed that  E2F-1 bound to Apaf-1 promoter upon E2F-1 overexpression, suggesting that  Apaf-1 is under transcriptional regulation of E2F-1.	bind
39763	3	9429	7	NULL	NULL	0	NULL	E2F-1	NULL		regulates	NULL				Apaf-1	NULL	transcription of			NULL		0	NULL	NULL	NULL	abs-batch0570-0579_j-biol-chem_277_42_12149244_s_8	12149244	A chromatin immunoprecipitation assay revealed that  E2F-1 bound to Apaf-1 promoter upon E2F-1 overexpression, suggesting that  Apaf-1 is under transcriptional regulation of E2F-1.	bind
39764	4	9429	7	NULL	NULL	0	NULL	statement 1	NULL		suggests	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	abs-batch0570-0579_j-biol-chem_277_42_12149244_s_8	12149244	A chromatin immunoprecipitation assay revealed that  E2F-1 bound to Apaf-1 promoter upon E2F-1 overexpression, suggesting that  Apaf-1 is under transcriptional regulation of E2F-1.	bind
41104	1	9430	5	13	NULL	NULL	NULL	SREBP-1	GP		bind					LGK	NucleicAcid			SREs of promoter	NULL	primary hepatocytes	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_29_30823_s_10	15123649	A chromatin immunoprecipitation assay using primary hepatocytes showed increased binding of SREBP-1 to SREs of the LGK promoter by insulin.	bind
41105	2	9430	5	13	NULL	NULL	NULL	insulin	GP		increase					statement 1	Process				NULL	primary hepatocytes	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_29_30823_s_10	15123649	A chromatin immunoprecipitation assay using primary hepatocytes showed increased binding of SREBP-1 to SREs of the LGK promoter by insulin.	bind
39765	1	9430	7	NULL	NULL	0	NULL	SREBP-1 	NULL		bind	NULL				LGK	NULL			SREs in the promoter	NULL	primary hepatocytes	0	NULL	NULL	NULL	gw70_jbiolchem_279_29_30823_s_10	15123649	A chromatin immunoprecipitation assay using primary hepatocytes showed increased binding of SREBP-1 to SREs of the LGK promoter by insulin.	bind
39766	2	9430	7	NULL	NULL	0	NULL	insulin	NULL		increase	NULL				statement 1	NULL				NULL	primary hepatocytes	0	NULL	NULL	NULL	gw70_jbiolchem_279_29_30823_s_10	15123649	A chromatin immunoprecipitation assay using primary hepatocytes showed increased binding of SREBP-1 to SREs of the LGK promoter by insulin.	bind
41106	1	9431	5	13	NULL	NULL	NULL	DNA fragments	NucleicAcid	Drosophila	bind					Engrailed protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_20_7097_s_220	15870192	A chromatin immunoprecipitation procedure also has been used to identify DNA binding sites; 203  Drosophila DNA fragments that bind the Engrailed protein were localized in intergenic (53%) or intronic (47%) regions ( ).	bind
41107	2	9431	5	13	NULL	NULL	NULL	statement 1	GP		is localized in									intergenic regions	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_20_7097_s_220	15870192	A chromatin immunoprecipitation procedure also has been used to identify DNA binding sites; 203  Drosophila DNA fragments that bind the Engrailed protein were localized in intergenic (53%) or intronic (47%) regions ( ).	bind
41108	3	9431	5	13	NULL	NULL	NULL	statement 1	GP		is localized in									intronic regions	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_20_7097_s_220	15870192	A chromatin immunoprecipitation procedure also has been used to identify DNA binding sites; 203  Drosophila DNA fragments that bind the Engrailed protein were localized in intergenic (53%) or intronic (47%) regions ( ).	bind
41109	4	9431	5	13	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_20_7097_s_220	15870192	A chromatin immunoprecipitation procedure also has been used to identify DNA binding sites; 203  Drosophila DNA fragments that bind the Engrailed protein were localized in intergenic (53%) or intronic (47%) regions ( ).	bind
39767	1	9431	7	NULL	NULL	0	NULL	DNA fragments 	NULL	Drosophila	bind	NULL				Engrailed protein	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_20_7097_s_220	15870192	A chromatin immunoprecipitation procedure also has been used to identify DNA binding sites; 203  Drosophila DNA fragments that bind the Engrailed protein were localized in intergenic (53%) or intronic (47%) regions ( ).	bind
39768	2	9431	7	10	NULL	0	NULL	DNA fragments 		Drosophila	is localized in									intergenic region	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_20_7097_s_220	15870192	A chromatin immunoprecipitation procedure also has been used to identify DNA binding sites; 203  Drosophila DNA fragments that bind the Engrailed protein were localized in intergenic (53%) or intronic (47%) regions ( ).	bind
39769	3	9431	7	10	NULL	0	NULL	DNA fragments 		Drosophila	is localized in									intronic region	NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_20_7097_s_220	15870192	A chromatin immunoprecipitation procedure also has been used to identify DNA binding sites; 203  Drosophila DNA fragments that bind the Engrailed protein were localized in intergenic (53%) or intronic (47%) regions ( ).	bind
56715	4	9431	7	10	NULL	0	NULL	statement 2			is an alternative to					statement 3					NULL		0	NULL	NULL	NULL	gw70_pnas_102_20_7097_s_220	15870192	A chromatin immunoprecipitation procedure also has been used to identify DNA binding sites; 203  Drosophila DNA fragments that bind the Engrailed protein were localized in intergenic (53%) or intronic (47%) regions ( ).	bind
41110	1	9432	5	13	NULL	NULL	NULL	Rox1p	GP		bind					PIS1	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_38646_s_103	12890676	A circular permutation assay was used to determine whether DNA bending occurred when  Rox1p binds the  PIS1 promoter.	bind
39770	1	9432	7	NULL	NULL	0	NULL	Rox1p	NULL		binds	NULL				 PIS1	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_40_38646_s_103	12890676	A circular permutation assay was used to determine whether DNA bending occurred when  Rox1p binds the  PIS1 promoter.	bind
41111	1	9433	5	13	NULL	NULL	NULL	circulating IgG	GP		bind					beta-adrenoceptor	GP	myocardium			NULL	Chagas disease	NULL	NULL	NULL	NULL	gw60_infectimmun_68_9_5114_s_197	10948133	A circulating IgG in Chagas disease which binds to beta-adrenoceptor of myocardium and modulates their activity.	bind
41112	2	9433	5	13	NULL	NULL	NULL	statement 1	Process		modulates					beta-adrenoceptor	GP	activity of			NULL	Chagas disease	NULL	NULL	NULL	NULL	gw60_infectimmun_68_9_5114_s_197	10948133	A circulating IgG in Chagas disease which binds to beta-adrenoceptor of myocardium and modulates their activity.	bind
39771	1	9433	7	10	NULL	0	NULL	circulating IgG			binds to					beta-adrenoceptor		myocardium			NULL	Chagas disease	NULL	NULL	NULL	NULL	gw60_infectimmun_68_9_5114_s_197	10948133	A circulating IgG in Chagas disease which binds to beta-adrenoceptor of myocardium and modulates their activity.	bind
39772	2	9433	7	10	NULL	0	NULL	statement 1			modulates					beta-adrenoceptor		activity of			NULL	Chagas disease	NULL	NULL	NULL	NULL	gw60_infectimmun_68_9_5114_s_197	10948133	A circulating IgG in Chagas disease which binds to beta-adrenoceptor of myocardium and modulates their activity.	bind
41113	1	9436	5	13	NULL	NULL	NULL	caveolins	GP		is a type of					cellular proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_12_7791_s_16	16299268	A class of cellular proteins named caveolins bind cholesterol at a 1:1 ratio and are involved in transport of de novo-synthesized cholesterol from the ER to the plasma membrane.	bind
41114	2	9436	5	13	NULL	NULL	NULL	caveolins	GP		bind					cholesterol	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_12_7791_s_16	16299268	A class of cellular proteins named caveolins bind cholesterol at a 1:1 ratio and are involved in transport of de novo-synthesized cholesterol from the ER to the plasma membrane.	bind
41115	3	9436	5	13	NULL	NULL	NULL	cholesterol	Chemical	de novo-synthesized	is transported to					plasma membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_12_7791_s_16	16299268	A class of cellular proteins named caveolins bind cholesterol at a 1:1 ratio and are involved in transport of de novo-synthesized cholesterol from the ER to the plasma membrane.	bind
41116	4	9436	5	13	NULL	NULL	NULL	cholesterol	Chemical	de novo-synthesized	is transported from					ER	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_12_7791_s_16	16299268	A class of cellular proteins named caveolins bind cholesterol at a 1:1 ratio and are involved in transport of de novo-synthesized cholesterol from the ER to the plasma membrane.	bind
41117	5	9436	5	13	NULL	NULL	NULL	statement 3	Process		occurs after					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_12_7791_s_16	16299268	A class of cellular proteins named caveolins bind cholesterol at a 1:1 ratio and are involved in transport of de novo-synthesized cholesterol from the ER to the plasma membrane.	bind
56716	6	9436	5	13	NULL	NULL	NULL	caveolins	GP		is involved in					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_12_7791_s_16	16299268	A class of cellular proteins named caveolins bind cholesterol at a 1:1 ratio and are involved in transport of de novo-synthesized cholesterol from the ER to the plasma membrane.	bind
39889	1	9436	7	NULL	NULL	0	NULL	caveolins 	NULL		bind	NULL				cholesterol	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_12_7791_s_16	16299268	A class of cellular proteins named caveolins bind cholesterol at a 1:1 ratio and are involved in transport of de novo-synthesized cholesterol from the ER to the plasma membrane.	bind
39890	2	9436	7	10	NULL	0	NULL	cholesterol 	NULL	de novo-synthesized	move from	NULL				ER	NULL				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_12_7791_s_16	16299268	A class of cellular proteins named caveolins bind cholesterol at a 1:1 ratio and are involved in transport of de novo-synthesized cholesterol from the ER to the plasma membrane.	bind
39891	3	9436	7	10	NULL	0	NULL	cholesterol 	NULL	de novo-synthesized 	move to	NULL				plasma membrane	NULL				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_12_7791_s_16	16299268	A class of cellular proteins named caveolins bind cholesterol at a 1:1 ratio and are involved in transport of de novo-synthesized cholesterol from the ER to the plasma membrane.	bind
39892	4	9436	7	NULL	NULL	0	NULL	statement 3	NULL		occurs after	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_12_7791_s_16	16299268	A class of cellular proteins named caveolins bind cholesterol at a 1:1 ratio and are involved in transport of de novo-synthesized cholesterol from the ER to the plasma membrane.	bind
39893	5	9436	7	NULL	NULL	0	NULL	caveolins	NULL		is involved in	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_12_7791_s_16	16299268	A class of cellular proteins named caveolins bind cholesterol at a 1:1 ratio and are involved in transport of de novo-synthesized cholesterol from the ER to the plasma membrane.	bind
39894	6	9436	7	NULL	NULL	0	NULL	caveolins	NULL		is a type of	NULL				cellular proteins	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_12_7791_s_16	16299268	A class of cellular proteins named caveolins bind cholesterol at a 1:1 ratio and are involved in transport of de novo-synthesized cholesterol from the ER to the plasma membrane.	bind
41118	1	9437	5	13	NULL	NULL	NULL	GDP dissociation inhibitors	GP		is critical for					Rab proteins	GP	role of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20470_s_16	8702787	A class of molecules which appear to be critical for the role of Rab proteins are GDP dissociation inhibitors, which bind Rabs that are prenylated (doubly geranylgeranylated near the C terminus) in a specific manner and deliver them to their respective membranes, as well as retrieving them from these locations ( 11).	bind
41119	2	9437	5	13	NULL	NULL	NULL	GDP dissociation inhibitors	GP		bind					Rabs	GP	prenylated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20470_s_16	8702787	A class of molecules which appear to be critical for the role of Rab proteins are GDP dissociation inhibitors, which bind Rabs that are prenylated (doubly geranylgeranylated near the C terminus) in a specific manner and deliver them to their respective membranes, as well as retrieving them from these locations ( 11).	bind
41121	3	9437	5	13	NULL	NULL	NULL	Rabs	GP	prenylated	is delivered to					membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20470_s_16	8702787	A class of molecules which appear to be critical for the role of Rab proteins are GDP dissociation inhibitors, which bind Rabs that are prenylated (doubly geranylgeranylated near the C terminus) in a specific manner and deliver them to their respective membranes, as well as retrieving them from these locations ( 11).	bind
41122	4	9437	5	13	NULL	NULL	NULL	statement 2	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20470_s_16	8702787	A class of molecules which appear to be critical for the role of Rab proteins are GDP dissociation inhibitors, which bind Rabs that are prenylated (doubly geranylgeranylated near the C terminus) in a specific manner and deliver them to their respective membranes, as well as retrieving them from these locations ( 11).	bind
41124	5	9437	5	13	NULL	NULL	NULL	Rabs	GP	prenylated	is retrieved from					membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20470_s_16	8702787	A class of molecules which appear to be critical for the role of Rab proteins are GDP dissociation inhibitors, which bind Rabs that are prenylated (doubly geranylgeranylated near the C terminus) in a specific manner and deliver them to their respective membranes, as well as retrieving them from these locations ( 11).	bind
41125	6	9437	5	13	NULL	NULL	NULL	statement 2	Process		leads to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20470_s_16	8702787	A class of molecules which appear to be critical for the role of Rab proteins are GDP dissociation inhibitors, which bind Rabs that are prenylated (doubly geranylgeranylated near the C terminus) in a specific manner and deliver them to their respective membranes, as well as retrieving them from these locations ( 11).	bind
39896	2	9437	7	NULL	NULL	0	NULL	geranylgeranylation	NULL		is a type of	NULL	specifically			prenylation	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20470_s_16	8702787	A class of molecules which appear to be critical for the role of Rab proteins are GDP dissociation inhibitors, which bind Rabs that are prenylated (doubly geranylgeranylated near the C terminus) in a specific manner and deliver them to their respective membranes, as well as retrieving them from these locations ( 11).	bind
39897	3	9437	7	NULL	NULL	0	NULL	Rab	NULL		move to	NULL				membranes	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_34_20470_s_16	8702787	A class of molecules which appear to be critical for the role of Rab proteins are GDP dissociation inhibitors, which bind Rabs that are prenylated (doubly geranylgeranylated near the C terminus) in a specific manner and deliver them to their respective membranes, as well as retrieving them from these locations ( 11).	bind
39898	4	9437	7	NULL	NULL	0	NULL	statement 1	NULL		facilitate	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20470_s_16	8702787	A class of molecules which appear to be critical for the role of Rab proteins are GDP dissociation inhibitors, which bind Rabs that are prenylated (doubly geranylgeranylated near the C terminus) in a specific manner and deliver them to their respective membranes, as well as retrieving them from these locations ( 11).	bind
39900	1	9437	7	NULL	NULL	0	NULL	GDP dissociation inhibitors	NULL		bind	NULL				Rab proteins 	NULL	prenylated	C terminus		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20470_s_16	8702787	A class of molecules which appear to be critical for the role of Rab proteins are GDP dissociation inhibitors, which bind Rabs that are prenylated (doubly geranylgeranylated near the C terminus) in a specific manner and deliver them to their respective membranes, as well as retrieving them from these locations ( 11).	bind
39902	5	9437	7	NULL	NULL	0	NULL	Rab	NULL		retreive from	NULL				membranes	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20470_s_16	8702787	A class of molecules which appear to be critical for the role of Rab proteins are GDP dissociation inhibitors, which bind Rabs that are prenylated (doubly geranylgeranylated near the C terminus) in a specific manner and deliver them to their respective membranes, as well as retrieving them from these locations ( 11).	bind
39903	6	9437	7	10	NULL	0	NULL	statement 2	NULL		facilitate	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_34_20470_s_16	8702787	A class of molecules which appear to be critical for the role of Rab proteins are GDP dissociation inhibitors, which bind Rabs that are prenylated (doubly geranylgeranylated near the C terminus) in a specific manner and deliver them to their respective membranes, as well as retrieving them from these locations ( 11).	bind
41126	1	9438	5	13	NULL	NULL	NULL	Lip-1	GP		bind					Lyn	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7887_s_90	10713104	A clear association was seen between Lip-1 or Lip-2 and Lyn, with no appreciable binding of Lyn to GST alone (Fig.  1,  B and  C).	bind
41127	2	9438	5	13	NULL	NULL	NULL	Lip-2	GP		bind					Lyn	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7887_s_90	10713104	A clear association was seen between Lip-1 or Lip-2 and Lyn, with no appreciable binding of Lyn to GST alone (Fig.  1,  B and  C).	bind
41128	3	9438	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7887_s_90	10713104	A clear association was seen between Lip-1 or Lip-2 and Lyn, with no appreciable binding of Lyn to GST alone (Fig.  1,  B and  C).	bind
39914	1	9438	7	NULL	NULL	0	NULL	Lip-1	NULL		bind	NULL				Lyn	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_11_7887_s_90	10713104	A clear association was seen between Lip-1 or Lip-2 and Lyn, with no appreciable binding of Lyn to GST alone (Fig.  1,  B and  C).	bind
39917	2	9438	7	NULL	NULL	0	NULL	Lip-2	NULL		bind	NULL				Lyn	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_11_7887_s_90	10713104	A clear association was seen between Lip-1 or Lip-2 and Lyn, with no appreciable binding of Lyn to GST alone (Fig.  1,  B and  C).	bind
39918	3	9438	7	10	NULL	0	NULL	statement 1			is an alternative to					statement 2    					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7887_s_90	10713104	A clear association was seen between Lip-1 or Lip-2 and Lyn, with no appreciable binding of Lyn to GST alone (Fig.  1,  B and  C).	bind
41130	1	9439	5	13	NULL	NULL	NULL	RACK1	GP		undergoes					phosphorylation	Process		tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20346_s_320	11279199	A clear correlation exists between enhanced tyrosine phosphorylation of RACK1 and enhanced binding of RACK1 to Src (Figs.  3,  4, and  6).	bind
41131	2	9439	5	13	NULL	NULL	NULL	RACK1	GP		bind					Src	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20346_s_320	11279199	A clear correlation exists between enhanced tyrosine phosphorylation of RACK1 and enhanced binding of RACK1 to Src (Figs.  3,  4, and  6).	bind
41132	3	9439	5	13	NULL	NULL	NULL	statement 1	Process	enhanced	correlates with					statement 2	Process	enhanced			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20346_s_320	11279199	A clear correlation exists between enhanced tyrosine phosphorylation of RACK1 and enhanced binding of RACK1 to Src (Figs.  3,  4, and  6).	bind
39922	1	9439	7	NULL	NULL	0	NULL	RACK1	NULL		bind	NULL				Src	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_23_20346_s_320	11279199	A clear correlation exists between enhanced tyrosine phosphorylation of RACK1 and enhanced binding of RACK1 to Src (Figs.  3,  4, and  6).	bind
39923	2	9439	7	10	NULL	0	NULL	RACK1			undergoes							phosphorylation of 	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20346_s_320	11279199	A clear correlation exists between enhanced tyrosine phosphorylation of RACK1 and enhanced binding of RACK1 to Src (Figs.  3,  4, and  6).	bind
56720	3	9439	7	10	NULL	0	NULL	statement 1		enhanced	correlates with					statement 2		enhanced			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_23_20346_s_320	11279199	A clear correlation exists between enhanced tyrosine phosphorylation of RACK1 and enhanced binding of RACK1 to Src (Figs.  3,  4, and  6).	bind
41133	1	9441	5	13	NULL	NULL	NULL	CSN	GP		cooperates with					Ub - 26S proteasome system	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_7_1630_s_30	11285227	A clear example of CSN and Ub - 26S proteasome system cooperation is the transcription factor c-Jun, which also binds to CSN5/Jab1 ( Claret  et al., 1996).	bind
41134	2	9441	5	13	NULL	NULL	NULL	c-Jun	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_7_1630_s_30	11285227	A clear example of CSN and Ub - 26S proteasome system cooperation is the transcription factor c-Jun, which also binds to CSN5/Jab1 ( Claret  et al., 1996).	bind
41135	3	9441	5	13	NULL	NULL	NULL	c-Jun	GP		bind					CSN5/Jab1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_7_1630_s_30	11285227	A clear example of CSN and Ub - 26S proteasome system cooperation is the transcription factor c-Jun, which also binds to CSN5/Jab1 ( Claret  et al., 1996).	bind
41136	4	9441	5	13	NULL	NULL	NULL	c-Jun	GP		is an example of					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_7_1630_s_30	11285227	A clear example of CSN and Ub - 26S proteasome system cooperation is the transcription factor c-Jun, which also binds to CSN5/Jab1 ( Claret  et al., 1996).	bind
39924	1	9441	7	NULL	NULL	0	NULL	c-Jun	NULL		binds to	NULL				CSN5/Jab1	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_7_1630_s_30	11285227	A clear example of CSN and Ub - 26S proteasome system cooperation is the transcription factor c-Jun, which also binds to CSN5/Jab1 ( Claret  et al., 1996).	bind
39925	2	9441	7	NULL	NULL	0	NULL	c-Jun	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_7_1630_s_30	11285227	A clear example of CSN and Ub - 26S proteasome system cooperation is the transcription factor c-Jun, which also binds to CSN5/Jab1 ( Claret  et al., 1996).	bind
41264	1	9442	5	13	NULL	NULL	NULL	enzyme	GP		is directed to					site of action	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_26_23874_s_307	12684515	A clear function of the cell wall  binding domain of a peptidoglycan hydrolase is to direct the enzyme to its  site of action, to the poles of the cell in the case of AcmA.	bind
41265	2	9442	5	13	NULL	NULL	NULL	statement 1	GP		function of		clear			peptidoglycan hydrolase	GP		cell wall binding domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_26_23874_s_307	12684515	A clear function of the cell wall  binding domain of a peptidoglycan hydrolase is to direct the enzyme to its  site of action, to the poles of the cell in the case of AcmA.	bind
41266	3	9442	5	13	NULL	NULL	NULL	enzyme	GP		is directed to					cell	Cell	poles of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_26_23874_s_307	12684515	A clear function of the cell wall  binding domain of a peptidoglycan hydrolase is to direct the enzyme to its  site of action, to the poles of the cell in the case of AcmA.	bind
41267	4	9442	5	13	NULL	NULL	NULL	statement 3	Process		function of		clear			AcmA	GP		cell wall binding domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_26_23874_s_307	12684515	A clear function of the cell wall  binding domain of a peptidoglycan hydrolase is to direct the enzyme to its  site of action, to the poles of the cell in the case of AcmA.	bind
39926	1	9442	7	NULL	NULL	0	NULL	enzyme	NULL		move to	NULL				site of action	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_26_23874_s_307	12684515	A clear function of the cell wall  binding domain of a peptidoglycan hydrolase is to direct the enzyme to its  site of action, to the poles of the cell in the case of AcmA.	bind
39927	2	9442	7	NULL	NULL	0	NULL	peptidoglycan hydrolase	NULL		direct	NULL		cell wall binding domain 		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_26_23874_s_307	12684515	A clear function of the cell wall  binding domain of a peptidoglycan hydrolase is to direct the enzyme to its  site of action, to the poles of the cell in the case of AcmA.	bind
39928	3	9442	7	NULL	NULL	0	NULL	AcmA	NULL		move to	NULL				poles of the cell	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_26_23874_s_307	12684515	A clear function of the cell wall  binding domain of a peptidoglycan hydrolase is to direct the enzyme to its  site of action, to the poles of the cell in the case of AcmA.	bind
39929	4	9442	7	NULL	NULL	0	NULL	peptidoglycan hydrolase	NULL		direct	NULL		cell wall binding domain 		statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_26_23874_s_307	12684515	A clear function of the cell wall  binding domain of a peptidoglycan hydrolase is to direct the enzyme to its  site of action, to the poles of the cell in the case of AcmA.	bind
41137	1	9443	5	13	NULL	NULL	NULL	TG	GP		bind		tightly			GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_14_7744_s_111	10869438	A clear rationale for the tight binding of GTP by TG would be to keep the crosslinking activity of the enzyme in check as long as the red cell is to remain in the circulation.	bind
39930	1	9443	7	NULL	NULL	0	NULL	TG	NULL		bind	NULL	tightly			GTP	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_14_7744_s_111	10869438	A clear rationale for the tight binding of GTP by TG would be to keep the crosslinking activity of the enzyme in check as long as the red cell is to remain in the circulation.	bind
41138	1	9445	5	13	NULL	NULL	NULL	MAGE-A4 	GP	cleaved form of	bind					Miz-1	GP				NULL	human cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15505_s_1	14739298	A cleaved form of MAGE-A4 binds to Miz-1 and induces apoptosis in human cells.	bind
41139	2	9445	5	13	NULL	NULL	NULL	statement 1	Process		induce					apoptosis	Process				NULL	human cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15505_s_1	14739298	A cleaved form of MAGE-A4 binds to Miz-1 and induces apoptosis in human cells.	bind
39947	1	9445	7	10	NULL	0	NULL	MAGE-A4		cleaved form of	binds to					Miz-1					NULL	human cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15505_s_1	14739298	A cleaved form of MAGE-A4 binds to Miz-1 and induces apoptosis in human cells.	bind
39948	2	9445	7	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL				apoptosis	NULL				NULL	human cells	0	NULL	NULL	NULL	gw70_jbiolchem_279_15_15505_s_1	14739298	A cleaved form of MAGE-A4 binds to Miz-1 and induces apoptosis in human cells.	bind
41268	1	9447	5	13	NULL	NULL	NULL	cleft	GP		extends from					protomer	GP	center of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_47_48487_s_39	15337754	A cleft extends from the center of the protomer to the central pore of the pentamer, and several residues along the boundaries of this cleft have been shown to be critical for the binding of CRP to C1q, including Asp-112 and Tyr-175 ( ,  ).	bind
41269	2	9447	5	13	NULL	NULL	NULL	cleft	GP		extends to					pentamer	GP	central pore of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_47_48487_s_39	15337754	A cleft extends from the center of the protomer to the central pore of the pentamer, and several residues along the boundaries of this cleft have been shown to be critical for the binding of CRP to C1q, including Asp-112 and Tyr-175 ( ,  ).	bind
41270	3	9447	5	13	NULL	NULL	NULL	CRP	GP		bind					C1q	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_47_48487_s_39	15337754	A cleft extends from the center of the protomer to the central pore of the pentamer, and several residues along the boundaries of this cleft have been shown to be critical for the binding of CRP to C1q, including Asp-112 and Tyr-175 ( ,  ).	bind
41271	4	9447	5	13	NULL	NULL	NULL				is critical for			Asp-112		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_47_48487_s_39	15337754	A cleft extends from the center of the protomer to the central pore of the pentamer, and several residues along the boundaries of this cleft have been shown to be critical for the binding of CRP to C1q, including Asp-112 and Tyr-175 ( ,  ).	bind
41272	5	9447	5	13	NULL	NULL	NULL				is critical for			Tyr-175		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_47_48487_s_39	15337754	A cleft extends from the center of the protomer to the central pore of the pentamer, and several residues along the boundaries of this cleft have been shown to be critical for the binding of CRP to C1q, including Asp-112 and Tyr-175 ( ,  ).	bind
41273	6	9447	5	13	NULL	NULL	NULL	statement 5	Process		occurs after					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_47_48487_s_39	15337754	A cleft extends from the center of the protomer to the central pore of the pentamer, and several residues along the boundaries of this cleft have been shown to be critical for the binding of CRP to C1q, including Asp-112 and Tyr-175 ( ,  ).	bind
39949	1	9447	7	NULL	NULL	0	NULL	CRP	NULL		bind	NULL				C1q	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_48487_s_39	15337754	A cleft extends from the center of the protomer to the central pore of the pentamer, and several residues along the boundaries of this cleft have been shown to be critical for the binding of CRP to C1q, including Asp-112 and Tyr-175 ( ,  ).	bind
39950	2	9447	7	NULL	NULL	0	NULL		NULL		is critical for	NULL		Asp-112		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_48487_s_39	15337754	A cleft extends from the center of the protomer to the central pore of the pentamer, and several residues along the boundaries of this cleft have been shown to be critical for the binding of CRP to C1q, including Asp-112 and Tyr-175 ( ,  ).	bind
39951	3	9447	7	NULL	NULL	0	NULL		NULL		is critical for	NULL		 Tyr-175		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_48487_s_39	15337754	A cleft extends from the center of the protomer to the central pore of the pentamer, and several residues along the boundaries of this cleft have been shown to be critical for the binding of CRP to C1q, including Asp-112 and Tyr-175 ( ,  ).	bind
39952	4	9447	7	NULL	NULL	0	NULL	cleft	NULL		extend from	NULL				protomer	NULL	center of the			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_48487_s_39	15337754	A cleft extends from the center of the protomer to the central pore of the pentamer, and several residues along the boundaries of this cleft have been shown to be critical for the binding of CRP to C1q, including Asp-112 and Tyr-175 ( ,  ).	bind
39953	5	9447	7	NULL	NULL	0	NULL	cleft 	NULL		extend to	NULL				pentamer	NULL	central pore of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_48487_s_39	15337754	A cleft extends from the center of the protomer to the central pore of the pentamer, and several residues along the boundaries of this cleft have been shown to be critical for the binding of CRP to C1q, including Asp-112 and Tyr-175 ( ,  ).	bind
39961	6	9447	7	NULL	NULL	0	NULL	statement 5	NULL		occurs after	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_48487_s_39	15337754	A cleft extends from the center of the protomer to the central pore of the pentamer, and several residues along the boundaries of this cleft have been shown to be critical for the binding of CRP to C1q, including Asp-112 and Tyr-175 ( ,  ).	bind
41160	1	9448	5	13	NULL	NULL	NULL	Vi polysaccharide	Chemical	conjugate of	bind					exotoxin A	Chemical	nontoxic;; recombinant;; Pseudomonas aeruginosa			NULL	Vietnamese children	NULL	NULL	NULL	NULL	gw70_clinmicrobiolrev_14_4_872_s_545	11585789	A clinical trial of a conjugate of the Vi polysaccharide bound to nontoxic recombinant  Pseudomonas aeruginosa exotoxin A in Vietnamese children aged 2 to 5 years found the vaccine to be safe and immunogenic ( ).	bind
39962	1	9448	7	10	NULL	0	NULL	Vi polysaccharide		conjugate of	bind					exotoxin A		nontoxic;; recombinant;; Pseudomonas aeruginosa 			NULL	vietnamese children	NULL	NULL	NULL	NULL	gw70_clinmicrobiolrev_14_4_872_s_545	11585789	A clinical trial of a conjugate of the Vi polysaccharide bound to nontoxic recombinant  Pseudomonas aeruginosa exotoxin A in Vietnamese children aged 2 to 5 years found the vaccine to be safe and immunogenic ( ).	bind
41162	1	9450	5	13	NULL	NULL	NULL	AFC2	GP		is a type of					Clk/ty (LAMMER-type) kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_51_36428_s_470	10593939	A Clk/ty (LAMMER-type) kinase (AFC2) binds and phosphorylates all four SR proteins.	bind
41163	2	9450	5	13	NULL	NULL	NULL	AFC2	GP		bind					SR proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_51_36428_s_470	10593939	A Clk/ty (LAMMER-type) kinase (AFC2) binds and phosphorylates all four SR proteins.	bind
41164	3	9450	5	13	NULL	NULL	NULL	statement 1	GP		phosphorylate					SR proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_51_36428_s_470	10593939	A Clk/ty (LAMMER-type) kinase (AFC2) binds and phosphorylates all four SR proteins.	bind
39963	1	9450	7	NULL	NULL	0	NULL	AFC2	NULL		bind	NULL				SR proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_51_36428_s_470	10593939	A Clk/ty (LAMMER-type) kinase (AFC2) binds and phosphorylates all four SR proteins.	bind
39964	2	9450	7	NULL	NULL	0	NULL	AFC2	NULL		phosphorylates	NULL				SR proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_51_36428_s_470	10593939	A Clk/ty (LAMMER-type) kinase (AFC2) binds and phosphorylates all four SR proteins.	bind
39965	3	9450	7	NULL	NULL	0	NULL	AFC2	NULL		is	NULL				Clk/ty (LAMMER-type) kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_51_36428_s_470	10593939	A Clk/ty (LAMMER-type) kinase (AFC2) binds and phosphorylates all four SR proteins.	bind
41166	1	9451	5	13	NULL	NULL	NULL	mAb 12G5	GP		bind					CXCR4 coreceptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1587_2_258_s_36	12084468	A close correlation has been found, over a concentration range of 0.1-1000 ng/ml, between the AMD3100 concentrations required to inhibit (i) HIV-1 NL4-3 replication, (ii) monoclonal antibody (mAb 12G5) binding to the CXCR4 coreceptor, and (iii) SDF-1-induced signal transduction (Ca2+ flux), suggesting an intimate relationship between these three parameters [ 29 and  30].	bind
41167	2	9451	5	13	NULL	NULL	NULL	SDF-1	GP		induce					Ca2+ flux	Process	signal transduction of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1587_2_258_s_36	12084468	A close correlation has been found, over a concentration range of 0.1-1000 ng/ml, between the AMD3100 concentrations required to inhibit (i) HIV-1 NL4-3 replication, (ii) monoclonal antibody (mAb 12G5) binding to the CXCR4 coreceptor, and (iii) SDF-1-induced signal transduction (Ca2+ flux), suggesting an intimate relationship between these three parameters [ 29 and  30].	bind
41168	3	9451	5	13	NULL	NULL	NULL	AMD3100	Chemical		inhibit					HIV-1 NL4-3	Organism	replication of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1587_2_258_s_36	12084468	A close correlation has been found, over a concentration range of 0.1-1000 ng/ml, between the AMD3100 concentrations required to inhibit (i) HIV-1 NL4-3 replication, (ii) monoclonal antibody (mAb 12G5) binding to the CXCR4 coreceptor, and (iii) SDF-1-induced signal transduction (Ca2+ flux), suggesting an intimate relationship between these three parameters [ 29 and  30].	bind
41169	4	9451	5	13	NULL	NULL	NULL	AMD3100	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1587_2_258_s_36	12084468	A close correlation has been found, over a concentration range of 0.1-1000 ng/ml, between the AMD3100 concentrations required to inhibit (i) HIV-1 NL4-3 replication, (ii) monoclonal antibody (mAb 12G5) binding to the CXCR4 coreceptor, and (iii) SDF-1-induced signal transduction (Ca2+ flux), suggesting an intimate relationship between these three parameters [ 29 and  30].	bind
41170	5	9451	5	13	NULL	NULL	NULL	AMD3100	Chemical		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1587_2_258_s_36	12084468	A close correlation has been found, over a concentration range of 0.1-1000 ng/ml, between the AMD3100 concentrations required to inhibit (i) HIV-1 NL4-3 replication, (ii) monoclonal antibody (mAb 12G5) binding to the CXCR4 coreceptor, and (iii) SDF-1-induced signal transduction (Ca2+ flux), suggesting an intimate relationship between these three parameters [ 29 and  30].	bind
39966	1	9451	7	NULL	NULL	0	NULL	mAb 12G5	NULL		bind	NULL				CXCR4 coreceptor	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1587_2_258_s_36	12084468	A close correlation has been found, over a concentration range of 0.1-1000 ng/ml, between the AMD3100 concentrations required to inhibit (i) HIV-1 NL4-3 replication, (ii) monoclonal antibody (mAb 12G5) binding to the CXCR4 coreceptor, and (iii) SDF-1-induced signal transduction (Ca2+ flux), suggesting an intimate relationship between these three parameters [ 29 and  30].	bind
39967	2	9451	7	NULL	NULL	0	NULL	SDF-1	NULL		induce	NULL				Ca2+ flux	NULL	signal transduction of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1587_2_258_s_36	12084468	A close correlation has been found, over a concentration range of 0.1-1000 ng/ml, between the AMD3100 concentrations required to inhibit (i) HIV-1 NL4-3 replication, (ii) monoclonal antibody (mAb 12G5) binding to the CXCR4 coreceptor, and (iii) SDF-1-induced signal transduction (Ca2+ flux), suggesting an intimate relationship between these three parameters [ 29 and  30].	bind
39968	3	9451	7	NULL	NULL	0	NULL	AMD3100	NULL		inhibit	NULL				HIV-1 NL4-3 	NULL	replication of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1587_2_258_s_36	12084468	A close correlation has been found, over a concentration range of 0.1-1000 ng/ml, between the AMD3100 concentrations required to inhibit (i) HIV-1 NL4-3 replication, (ii) monoclonal antibody (mAb 12G5) binding to the CXCR4 coreceptor, and (iii) SDF-1-induced signal transduction (Ca2+ flux), suggesting an intimate relationship between these three parameters [ 29 and  30].	bind
39969	4	9451	7	NULL	NULL	0	NULL	AMD3100	NULL		inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1587_2_258_s_36	12084468	A close correlation has been found, over a concentration range of 0.1-1000 ng/ml, between the AMD3100 concentrations required to inhibit (i) HIV-1 NL4-3 replication, (ii) monoclonal antibody (mAb 12G5) binding to the CXCR4 coreceptor, and (iii) SDF-1-induced signal transduction (Ca2+ flux), suggesting an intimate relationship between these three parameters [ 29 and  30].	bind
39970	5	9451	7	NULL	NULL	0	NULL	AMD3100	NULL		inhibit	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1587_2_258_s_36	12084468	A close correlation has been found, over a concentration range of 0.1-1000 ng/ml, between the AMD3100 concentrations required to inhibit (i) HIV-1 NL4-3 replication, (ii) monoclonal antibody (mAb 12G5) binding to the CXCR4 coreceptor, and (iii) SDF-1-induced signal transduction (Ca2+ flux), suggesting an intimate relationship between these three parameters [ 29 and  30].	bind
41171	1	9453	5	13	NULL	NULL	NULL	Xylanase	GP	A. niger	is located in				XIP-I binding site	family 11 xylanases	GP		conserved "`thumb"` hairpin loop		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_46_44035_s_10	12207016	A close inspection of the three-dimensional structure of  A. niger xylanase suggests that the binding site of XIP-I is located at the conserved "`thumb"` hairpin loop of family 11 xylanases.	bind
39978	1	9453	7	NULL	NULL	0	NULL	xylanase	NULL	 A. niger	is located in the	NULL		XIP- binding site		family 11 xylanases	NULL		conserved "`thumb"` hairpin loop 		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_46_44035_s_10	12207016	A close inspection of the three-dimensional structure of  A. niger xylanase suggests that the binding site of XIP-I is located at the conserved "`thumb"` hairpin loop of family 11 xylanases.	bind
41172	1	9454	5	13	NULL	NULL	NULL	topo I	GP		bind					plasmid DNA	NucleicAcid	relaxed form of			NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_3_789_s_59	12565850	A close up on the DNA-enzyme complexes shown in   Figs. 1D-F demonstrates the binding of topo I to a relaxed form of the plasmid DNA.	bind
39979	1	9454	7	NULL	NULL	0	NULL	topo I	NULL		bind	NULL				plasmid DNA	NULL	relaxed form of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_3_789_s_59	12565850	A close up on the DNA-enzyme complexes shown in   Figs. 1D-F demonstrates the binding of topo I to a relaxed form of the plasmid DNA.	bind
41174	1	9457	5	13	NULL	NULL	NULL	Ank1	GP	muscle	bind					obscurin	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_mol-biol-evol_23_1_16135777_s_6	16135777	A closely related sequence in a muscle Ank1  product binds the cytoskeletal muscle proteins obscurin and titin.	bind
41175	2	9457	5	13	NULL	NULL	NULL	Ank1	GP	muscle	bind					titin	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_mol-biol-evol_23_1_16135777_s_6	16135777	A closely related sequence in a muscle Ank1  product binds the cytoskeletal muscle proteins obscurin and titin.	bind
41176	3	9457	5	13	NULL	NULL	NULL	titin	GP		is a type of					cytoskeletal muscle proteins	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_mol-biol-evol_23_1_16135777_s_6	16135777	A closely related sequence in a muscle Ank1  product binds the cytoskeletal muscle proteins obscurin and titin.	bind
41177	4	9457	5	13	NULL	NULL	NULL	obscurin	GP		is a type of					cytoskeletal muscle proteins	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_mol-biol-evol_23_1_16135777_s_6	16135777	A closely related sequence in a muscle Ank1  product binds the cytoskeletal muscle proteins obscurin and titin.	bind
39987	1	9457	7	NULL	NULL	0	NULL	Ank1 product	NULL	muscle	bind	NULL				obscurin	NULL				NULL		0	NULL	NULL	NULL	abs-batch0580-0599_mol-biol-evol_23_1_16135777_s_6	16135777	A closely related sequence in a muscle Ank1  product binds the cytoskeletal muscle proteins obscurin and titin.	bind
39988	2	9457	7	NULL	NULL	0	NULL	Ank1 product	NULL	muscle	bind	NULL				titin	NULL				NULL		0	NULL	NULL	NULL	abs-batch0580-0599_mol-biol-evol_23_1_16135777_s_6	16135777	A closely related sequence in a muscle Ank1  product binds the cytoskeletal muscle proteins obscurin and titin.	bind
39989	3	9457	7	NULL	NULL	0	NULL	obscurin	NULL		is a type of	NULL				cytoskeletal muscle proteins	NULL				NULL		0	NULL	NULL	NULL	abs-batch0580-0599_mol-biol-evol_23_1_16135777_s_6	16135777	A closely related sequence in a muscle Ank1  product binds the cytoskeletal muscle proteins obscurin and titin.	bind
39990	4	9457	7	NULL	NULL	0	NULL	titin	NULL		is a type of	NULL				cytoskeletal muscle protein	NULL				NULL		0	NULL	NULL	NULL	abs-batch0580-0599_mol-biol-evol_23_1_16135777_s_6	16135777	A closely related sequence in a muscle Ank1  product binds the cytoskeletal muscle proteins obscurin and titin.	bind
41276	1	9458	5	13	NULL	NULL	NULL	Sos	GP		bind					Grb2	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_10_5533_s_213	10318918	A closer analysis of NS5A class II motif revealed a complete conservation of the Grb2 N-SH3-binding consensus sequence (PXXPXR), which mediates Sos binding to Grb2.	bind
56721	1	9458	5	13	NULL	NULL	NULL	Grb2	GP		mediates			N-SH3-binding consensus sequence (PXXPXR)		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_10_5533_s_213	10318918	A closer analysis of NS5A class II motif revealed a complete conservation of the Grb2 N-SH3-binding consensus sequence (PXXPXR), which mediates Sos binding to Grb2.	bind
39991	1	9458	7	NULL	NULL	0	NULL	Sos binding	NULL		bind	NULL				Grb2	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_10_5533_s_213	10318918	A closer analysis of NS5A class II motif revealed a complete conservation of the Grb2 N-SH3-binding consensus sequence (PXXPXR), which mediates Sos binding to Grb2.	bind
39992	2	9458	7	NULL	NULL	0	NULL	 Grb2	NULL		mediates	NULL		conserved N-SH3-binding consensus sequence (PXXPXR)		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_10_5533_s_213	10318918	A closer analysis of NS5A class II motif revealed a complete conservation of the Grb2 N-SH3-binding consensus sequence (PXXPXR), which mediates Sos binding to Grb2.	bind
41278	1	9459	5	13	NULL	NULL	NULL	zyxin	GP	human	comprise of									alpha-actinin binding site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13410_s_162	10224105	A closer analysis of the sequence comprising the alpha-actinin binding site of human zyxin showed that it consists of a 10 amino acids submotif occurring twice in tandem (Fig.  5 b).	bind
39994	1	9459	7	10	NULL	0	NULL	zyxin  		human	comprise of									alpha-actinin binding site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13410_s_162	10224105	A closer analysis of the sequence comprising the alpha-actinin binding site of human zyxin showed that it consists of a 10 amino acids submotif occurring twice in tandem (Fig.  5 b).	bind
41279	1	9460	5	13	NULL	NULL	NULL	ATP/ADP	Chemical		bind					D1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32784_s_247	12807884	A closer examination of   Fig. 7 B revealed that  ATP/ADP binding to D1 does confer a slightly increased protection to the p58  N-D1-linker subcomplex.	bind
41280	2	9460	5	13	NULL	NULL	NULL	statement 1	Process		confer					p58 N-D1-linker subcomplex	GP	increased protection to			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32784_s_247	12807884	A closer examination of   Fig. 7 B revealed that  ATP/ADP binding to D1 does confer a slightly increased protection to the p58  N-D1-linker subcomplex.	bind
39995	1	9460	7	NULL	NULL	0	NULL	ATP/ADP	NULL		bind	NULL				D1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32784_s_247	12807884	A closer examination of   Fig. 7 B revealed that  ATP/ADP binding to D1 does confer a slightly increased protection to the p58  N-D1-linker subcomplex.	bind
39996	2	9460	7	NULL	NULL	0	NULL	statement 1	NULL		increase	NULL				p58 N-D1-linker subcomplex	NULL	protection to			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32784_s_247	12807884	A closer examination of   Fig. 7 B revealed that  ATP/ADP binding to D1 does confer a slightly increased protection to the p58  N-D1-linker subcomplex.	bind
41281	1	9462	5	10	NULL	0	NULL				overlaps			Sp1 site						SF-1 binding element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17987_s_127	10364248	A closer examination of this sequence revealed a potential Sp1 site, which is overlapping the SF-1 binding element to create an "`Sp1"`FF1 motif (see Fig.  5 B,  probe 2).	bind
41282	2	9462	5	13	NULL	NULL	NULL	statement 1	GP		creates									`Sp1`FF1 motif	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17987_s_127	10364248	A closer examination of this sequence revealed a potential Sp1 site, which is overlapping the SF-1 binding element to create an "`Sp1"`FF1 motif (see Fig.  5 B,  probe 2).	bind
40008	1	9462	7	NULL	NULL	0	NULL		NULL		overlaps with	NULL		Sp1 site			NULL			SF-1 binding element	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_17987_s_127	10364248	A closer examination of this sequence revealed a potential Sp1 site, which is overlapping the SF-1 binding element to create an "`Sp1"`FF1 motif (see Fig.  5 B,  probe 2).	bind
40009	2	9462	7	10	NULL	0	NULL	statement 1			create					"`Sp1"`FF1 motif					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17987_s_127	10364248	A closer examination of this sequence revealed a potential Sp1 site, which is overlapping the SF-1 binding element to create an "`Sp1"`FF1 motif (see Fig.  5 B,  probe 2).	bind
41283	1	9463	5	13	NULL	NULL	NULL	hs43	GP		bind		low affinity;;may		ATTG motif in promoter	D-Onecut	GP				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_97_1_57_s_225	11025207	A closer inspection of the  hs43 promoter reveals sequences containing the ATTG motif that may favor low affinity binding to D-Onecut.	bind
40010	1	9463	7	NULL	NULL	0	NULL	hs43	NULL		bind	NULL	low affinity		promoter containing ATTG motif 	D-Onecut	NULL				NULL		0	NULL	NULL	NULL	gw60_mechdev_97_1_57_s_225	11025207	A closer inspection of the  hs43 promoter reveals sequences containing the ATTG motif that may favor low affinity binding to D-Onecut.	bind
41769	1	9464	5	13	NULL	NULL	NULL	YfjB	GP		is a type of					NAD kinases	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
41770	2	9464	5	13	NULL	NULL	NULL	NadK	GP		is a type of					NAD kinases	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
41771	3	9464	5	13	NULL	NULL	NULL	Mfnk	GP		is a type of					NADH kinases	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
41772	4	9464	5	13	NULL	NULL	NULL	Ppnk	GP		is a type of					NADH kinases	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
41774	6	9464	5	13	NULL	NULL	NULL	Utr1p	GP		is a type of					NADH kinases	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
41775	7	9464	5	13	NULL	NULL	NULL	Yef1p	GP		is a type of					NADH kinases	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
41776	8	9464	5	13	NULL	NULL	NULL	Pos5p	GP		is a type of					NADH kinases	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
41777	11	9464	5	13	NULL	NULL	NULL	Ppnk-NAD	GP		participate in			Tyr-202		statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
41778	10	9464	5	13	NULL	NULL	NULL	Ppnk-NAD	GP		participate in			Ser-205		statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
41779	5	9464	5	13	NULL	NULL	NULL	Ppnk-NAD	GP		participate in			Asp-189		statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
56722	9	9464	5	13	NULL	NULL	NULL	NAD+	Chemical		bind			nicotinamide ring		Ppnk	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
40015	1	9464	7	NULL	NULL	0	NULL	NAD+	NULL		bind	NULL		 nicotinamide ring		Ppnk	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
40016	2	9464	7	NULL	NULL	0	NULL	Ppnk	NULL		participate in	NULL		Tyr-202		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
40017	3	9464	7	NULL	NULL	0	NULL	Ppnk	NULL		participate in	NULL		Ser-205		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
40018	4	9464	7	NULL	NULL	0	NULL	Ppnk	NULL		participate in	NULL		 Asp-189		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
40021	5	9464	7	NULL	NULL	0	NULL	Ppnk	NULL		is a type of	NULL				NADH kinases	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
48777	6	9464	7	NULL	NULL	0	NULL	YfjB	NULL		is a type of	NULL				NAD kinases	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
48778	7	9464	7	NULL	NULL	0	NULL	NadK	NULL		is a type of	NULL				NAD kinases	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
48779	8	9464	7	NULL	NULL	0	NULL	Mfnk	NULL		is a type of	NULL				NADH kinases	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
48780	9	9464	7	NULL	NULL	0	NULL	Utr1p	NULL		is a type of	NULL				NADH kinases	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
48781	10	9464	7	NULL	NULL	0	NULL	Yef1p	NULL		is a type of	NULL				NADH kinases	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
48782	11	9464	7	NULL	NULL	0	NULL	Pos5p	NULL		is a type of	NULL				NADH kinases	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_24104_s_112	15855156	A closer inspection of the primary structures of the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p), particularly with respect to the residues (Tyr-202, Ser-205, and Asp-189) participating in the binding of the nicotinamide ring of NAD+ in Ppnk-NAD ( Fig. 1 D), indicated that a residue corresponding to Gly-187 in Ppnk apparently differed between the NAD kinases (YfjB and NadK) and the NADH kinases (Mfnk, Ppnk, Utr1p, Yef1p, and Pos5p).	bind
41284	1	9465	5	13	NULL	NULL	NULL	Hop protein	GP		bind			TPR1 domain		Hsp70	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_43_40799_s_287	12145316	A clue can be provided by the Hop protein itself, which binds Hsp70 exclusively through its TPR1 domain and Hsp90 exclusively through its TPR2A domain.	bind
41285	2	9465	5	13	NULL	NULL	NULL	Hop protein	GP		bind			TPR2A domain		Hsp90	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_43_40799_s_287	12145316	A clue can be provided by the Hop protein itself, which binds Hsp70 exclusively through its TPR1 domain and Hsp90 exclusively through its TPR2A domain.	bind
40022	1	9465	7	NULL	NULL	0	NULL	Hop protein	NULL		bind	NULL		TPR1 domain		Hsp70	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_43_40799_s_287	12145316	A clue can be provided by the Hop protein itself, which binds Hsp70 exclusively through its TPR1 domain and Hsp90 exclusively through its TPR2A domain.	bind
40023	2	9465	7	NULL	NULL	0	NULL	Hop protein	NULL		bind	NULL		TPR2A domain		Hsp90	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_43_40799_s_287	12145316	A clue can be provided by the Hop protein itself, which binds Hsp70 exclusively through its TPR1 domain and Hsp90 exclusively through its TPR2A domain.	bind
41286	1	9466	5	13	NULL	NULL	NULL	ATP	Chemical		bind					Smc1/Smc3 heads	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_74_0_595_s_455	15952899	A clue is the finding  that hydrolysis of ATP bound to Smc1/Smc3 heads has an essential role in loading  cohesin onto chromosomes or even onto individual chromatids.	bind
41287	2	9466	5	13	NULL	NULL	NULL	cohesin	GP		loaded onto					chromosomes	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_74_0_595_s_455	15952899	A clue is the finding  that hydrolysis of ATP bound to Smc1/Smc3 heads has an essential role in loading  cohesin onto chromosomes or even onto individual chromatids.	bind
41288	3	9466	5	13	NULL	NULL	NULL	cohesin	GP		loaded onto					chromatids	Chromosome	individual			NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_74_0_595_s_455	15952899	A clue is the finding  that hydrolysis of ATP bound to Smc1/Smc3 heads has an essential role in loading  cohesin onto chromosomes or even onto individual chromatids.	bind
41289	4	9466	5	13	NULL	NULL	NULL	statement 1	Process	hydrolysis of	plays a role in		essential			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_74_0_595_s_455	15952899	A clue is the finding  that hydrolysis of ATP bound to Smc1/Smc3 heads has an essential role in loading  cohesin onto chromosomes or even onto individual chromatids.	bind
41290	5	9466	5	13	NULL	NULL	NULL	statement 1	Process	hydrolysis of	plays a role in		essential			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_74_0_595_s_455	15952899	A clue is the finding  that hydrolysis of ATP bound to Smc1/Smc3 heads has an essential role in loading  cohesin onto chromosomes or even onto individual chromatids.	bind
40024	1	9466	7	NULL	NULL	0	NULL	Smc1/Smc3 heads	NULL		bind	NULL				ATP	NULL				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_74_0_595_s_455	15952899	A clue is the finding  that hydrolysis of ATP bound to Smc1/Smc3 heads has an essential role in loading  cohesin onto chromosomes or even onto individual chromatids.	bind
40025	2	9466	7	NULL	NULL	0	NULL	cohesin	NULL		loaded onto	NULL				chromosomes	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_74_0_595_s_455	15952899	A clue is the finding  that hydrolysis of ATP bound to Smc1/Smc3 heads has an essential role in loading  cohesin onto chromosomes or even onto individual chromatids.	bind
40026	3	9466	7	10	NULL	0	NULL	statement 1	NULL	hydrolysis of	plays a role in	NULL	essential			statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_74_0_595_s_455	15952899	A clue is the finding  that hydrolysis of ATP bound to Smc1/Smc3 heads has an essential role in loading  cohesin onto chromosomes or even onto individual chromatids.	bind
40027	4	9466	7	NULL	NULL	0	NULL	cohesin	NULL		loaded onto	NULL				individual chromatids	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_74_0_595_s_455	15952899	A clue is the finding  that hydrolysis of ATP bound to Smc1/Smc3 heads has an essential role in loading  cohesin onto chromosomes or even onto individual chromatids.	bind
40028	5	9466	7	10	NULL	0	NULL	statement 1	NULL	hydrolysis of	plays a role in	NULL	essential			statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_74_0_595_s_455	15952899	A clue is the finding  that hydrolysis of ATP bound to Smc1/Smc3 heads has an essential role in loading  cohesin onto chromosomes or even onto individual chromatids.	bind
41291	1	9467	5	13	NULL	NULL	NULL	IGF-IR	GP		bind			Tyr950		IRS-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12423_s_296	10212216	A clue may be given by reports that the interactions of the IGF-IR with IRS-1 and Shc, although both centered at Tyr950, differ in the requirements for the surrounding amino acids ( 50,  63) and that IRS-1 may also bind directly to the tyrosine kinase domain ( 50).	bind
41292	2	9467	5	13	NULL	NULL	NULL	IGF-IR	GP		bind			Tyr950		Shc	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12423_s_296	10212216	A clue may be given by reports that the interactions of the IGF-IR with IRS-1 and Shc, although both centered at Tyr950, differ in the requirements for the surrounding amino acids ( 50,  63) and that IRS-1 may also bind directly to the tyrosine kinase domain ( 50).	bind
41293	3	9467	5	13	NULL	NULL	NULL	IGF-IR	GP		bind		directly;;may	tyrosine kinase domain		IRS-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12423_s_296	10212216	A clue may be given by reports that the interactions of the IGF-IR with IRS-1 and Shc, although both centered at Tyr950, differ in the requirements for the surrounding amino acids ( 50,  63) and that IRS-1 may also bind directly to the tyrosine kinase domain ( 50).	bind
40029	1	9467	7	10	NULL	0	NULL	IGF-IR			interacts with			Tyr950		IRS-1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12423_s_296	10212216	A clue may be given by reports that the interactions of the IGF-IR with IRS-1 and Shc, although both centered at Tyr950, differ in the requirements for the surrounding amino acids ( 50,  63) and that IRS-1 may also bind directly to the tyrosine kinase domain ( 50).	bind
40030	2	9467	7	10	NULL	0	NULL	IGF-IR			bind			Tyr950		Shc					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12423_s_296	10212216	A clue may be given by reports that the interactions of the IGF-IR with IRS-1 and Shc, although both centered at Tyr950, differ in the requirements for the surrounding amino acids ( 50,  63) and that IRS-1 may also bind directly to the tyrosine kinase domain ( 50).	bind
40033	5	9467	7	10	NULL	0	NULL	IGF-IR			bind		directly;; may	tyrosine kinase domain		IRS-1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12423_s_296	10212216	A clue may be given by reports that the interactions of the IGF-IR with IRS-1 and Shc, although both centered at Tyr950, differ in the requirements for the surrounding amino acids ( 50,  63) and that IRS-1 may also bind directly to the tyrosine kinase domain ( 50).	bind
41294	1	9468	5	13	NULL	NULL	NULL	caspase-3	GP		bind					XIAP	GP		BIR2		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_3_645_s_194	15650747	A clue that the conserved IBM interacting groove may be important for executioner  caspase inhibition is seen in the structure of caspase-3 bound to XIAP BIR2.	bind
41295	2	9468	5	13	NULL	NULL	NULL			conserved	may be important for			IBM interacting groove		statement 1	Process	inhibition of			NULL		NULL	NULL	NULL	NULL	gw70_embo_24_3_645_s_194	15650747	A clue that the conserved IBM interacting groove may be important for executioner  caspase inhibition is seen in the structure of caspase-3 bound to XIAP BIR2.	bind
40036	1	9468	7	10	NULL	0	NULL	caspase-3			bind					XIAP 			BIR2		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_3_645_s_194	15650747	A clue that the conserved IBM interacting groove may be important for executioner  caspase inhibition is seen in the structure of caspase-3 bound to XIAP BIR2.	bind
40037	2	9468	7	10	NULL	0	NULL			conserved	important for		may be	IBM interacting groove		statement 1		inhibition of			NULL		NULL	NULL	NULL	NULL	gw70_embo_24_3_645_s_194	15650747	A clue that the conserved IBM interacting groove may be important for executioner  caspase inhibition is seen in the structure of caspase-3 bound to XIAP BIR2.	bind
41297	1	9469	5	13	NULL	NULL	NULL	FC	GP		bind					Arn1p	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_5_952_s_31	15719020	A clue to the identity of the FC receptor comes from kinetic studies of FC binding  to Arn1p.	bind
40038	1	9469	7	NULL	NULL	0	NULL	FC receptor	NULL		bind	NULL				 Arn1p	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_5_952_s_31	15719020	A clue to the identity of the FC receptor comes from kinetic studies of FC binding  to Arn1p.	bind
41298	1	9470	5	13	NULL	NULL	NULL	separin	GP		splits					sister chromatids	Chromosome				NULL		NULL	NULL	NULL	NULL	gw60_science_288_5470_1379_s_185	10827941	A clue to the mechanism by which separin splits sister chromatids was the observation that in budding yeast (contrary to most other eukaryotic cells) most Scc1 remains bound to chromosomes until the metaphase-to-anaphase transition ( 48).	bind
41299	2	9470	5	13	NULL	NULL	NULL	Scc1	GP		bind					chromosomes	Chromosome				NULL	budding yeast	NULL	NULL	NULL	NULL	gw60_science_288_5470_1379_s_185	10827941	A clue to the mechanism by which separin splits sister chromatids was the observation that in budding yeast (contrary to most other eukaryotic cells) most Scc1 remains bound to chromosomes until the metaphase-to-anaphase transition ( 48).	bind
41300	3	9470	5	13	NULL	NULL	NULL	statement 2	Process		until					metaphase-to-anaphase transition 	Process				NULL	budding yeast	NULL	NULL	NULL	NULL	gw60_science_288_5470_1379_s_185	10827941	A clue to the mechanism by which separin splits sister chromatids was the observation that in budding yeast (contrary to most other eukaryotic cells) most Scc1 remains bound to chromosomes until the metaphase-to-anaphase transition ( 48).	bind
41301	4	9470	5	13	NULL	NULL	NULL	statement 2	Process		infers					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_288_5470_1379_s_185	10827941	A clue to the mechanism by which separin splits sister chromatids was the observation that in budding yeast (contrary to most other eukaryotic cells) most Scc1 remains bound to chromosomes until the metaphase-to-anaphase transition ( 48).	bind
40039	1	9470	7	NULL	NULL	0	NULL	separin	NULL		splits	NULL				sister chromatids	NULL				NULL	budding yeast	0	NULL	NULL	NULL	gw60_science_288_5470_1379_s_185	10827941	A clue to the mechanism by which separin splits sister chromatids was the observation that in budding yeast (contrary to most other eukaryotic cells) most Scc1 remains bound to chromosomes until the metaphase-to-anaphase transition ( 48).	bind
40040	2	9470	7	NULL	NULL	0	NULL	Scc1	NULL		bind	NULL				chromosomes	NULL				NULL	budding yeast	NULL	NULL	NULL	NULL	gw60_science_288_5470_1379_s_185	10827941	A clue to the mechanism by which separin splits sister chromatids was the observation that in budding yeast (contrary to most other eukaryotic cells) most Scc1 remains bound to chromosomes until the metaphase-to-anaphase transition ( 48).	bind
40041	3	9470	7	NULL	NULL	0	NULL	chromosomes	NULL		transit from	NULL				metaphase	NULL				NULL	budding yeast	NULL	NULL	NULL	NULL	gw60_science_288_5470_1379_s_185	10827941	A clue to the mechanism by which separin splits sister chromatids was the observation that in budding yeast (contrary to most other eukaryotic cells) most Scc1 remains bound to chromosomes until the metaphase-to-anaphase transition ( 48).	bind
40042	4	9470	7	NULL	NULL	0	NULL	chromosomes	NULL		transit to	NULL				anaphase	NULL				NULL	budding yeast	NULL	NULL	NULL	NULL	gw60_science_288_5470_1379_s_185	10827941	A clue to the mechanism by which separin splits sister chromatids was the observation that in budding yeast (contrary to most other eukaryotic cells) most Scc1 remains bound to chromosomes until the metaphase-to-anaphase transition ( 48).	bind
40043	5	9470	7	NULL	NULL	0	NULL	statement 4	NULL		occurs after	NULL				statement 3	NULL				NULL	budding yeast	NULL	NULL	NULL	NULL	gw60_science_288_5470_1379_s_185	10827941	A clue to the mechanism by which separin splits sister chromatids was the observation that in budding yeast (contrary to most other eukaryotic cells) most Scc1 remains bound to chromosomes until the metaphase-to-anaphase transition ( 48).	bind
40044	6	9470	7	NULL	NULL	0	NULL	statement 1	NULL		occur until	NULL				statement 5	NULL				NULL	budding yeast	NULL	NULL	NULL	NULL	gw60_science_288_5470_1379_s_185	10827941	A clue to the mechanism by which separin splits sister chromatids was the observation that in budding yeast (contrary to most other eukaryotic cells) most Scc1 remains bound to chromosomes until the metaphase-to-anaphase transition ( 48).	bind
41302	1	9471	5	13	NULL	NULL	NULL	Raf-1	GP	endogenous	bind					ERK5	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_44_31588_s_4	10531364	A clue to the mechanism of action of Raf-1 on ERK5 comes from the observation that endogenous Raf-1 binds to endogenous ERK5, suggesting the involvement of regulatory protein-protein interactions.	bind
41303	2	9471	5	13	NULL	NULL	NULL	statement 1	Process		suggest					regulatory protein-protein interactions	Process	involvement of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_44_31588_s_4	10531364	A clue to the mechanism of action of Raf-1 on ERK5 comes from the observation that endogenous Raf-1 binds to endogenous ERK5, suggesting the involvement of regulatory protein-protein interactions.	bind
40194	1	9471	7	NULL	NULL	0	NULL	Raf-1	NULL	endogenous	binds to	NULL				ERK5	NULL	endogenous			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_44_31588_s_4	10531364	A clue to the mechanism of action of Raf-1 on ERK5 comes from the observation that endogenous Raf-1 binds to endogenous ERK5, suggesting the involvement of regulatory protein-protein interactions.	bind
40195	2	9471	7	NULL	NULL	0	NULL	statement 1	NULL		suggests	NULL				regulatory protein-protein interactions	NULL	involvement of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_44_31588_s_4	10531364	A clue to the mechanism of action of Raf-1 on ERK5 comes from the observation that endogenous Raf-1 binds to endogenous ERK5, suggesting the involvement of regulatory protein-protein interactions.	bind
41304	1	9472	5	13	NULL	NULL	NULL	EDG-1	GP		overexpressed in					HEK293 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
41305	3	9472	5	13	NULL	NULL	NULL	statement 2	Process		induce					P-cadherins	GP	upregulation of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
41306	4	9472	5	13	NULL	NULL	NULL	statement 2	Process		induce					E-cadherins	GP	upregulation of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
41307	2	9472	5	13	NULL	NULL	NULL	SPP	Chemical		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
41308	5	9472	5	13	NULL	NULL	NULL	cell-cell aggregates	Process		is compacted					tightly 					NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
41309	6	9472	5	13	NULL	NULL	NULL	statement 5	Process		contains					architecture		organized;;network-like			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
41310	7	9472	5	13	NULL	NULL	NULL	statement 5	Process		contains					adherens junctions	CellComponent	well-developed			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
41311	8	9472	5	13	NULL	NULL	NULL	statement 3	Process		results in					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
41312	9	9472	5	13	NULL	NULL	NULL	statement 3	Process		results in					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
41313	10	9472	5	13	NULL	NULL	NULL	statement 4	Process		results in					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
41314	11	9472	5	13	NULL	NULL	NULL	statement 4	Process		results in					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
40196	1	9472	7	10	NULL	0	NULL	SPP			bind					statement 10					NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
40197	2	9472	7	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL				P-cadherins	NULL	upregulation of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
40198	3	9472	7	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL				E-cadherins	NULL	upregulation of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
40199	4	9472	7	NULL	NULL	0	NULL	statement 2	NULL		result in	NULL				cell-cell aggregates	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
40200	5	9472	7	NULL	NULL	0	NULL	statement 3	NULL		result in	NULL				cell-cell aggregates	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
40206	6	9472	7	NULL	NULL	0	NULL	statement 4	NULL		result in	NULL				 organized network-like architecture	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
40208	7	9472	7	10	NULL	0	NULL	statement 5	NULL		result in	NULL				network-like architecture	NULL	organized 			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
40211	8	9472	7	10	NULL	0	NULL	statement 4	NULL		result in	NULL				adherens junctions	NULL	well-developed 			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
40212	9	9472	7	10	NULL	0	NULL	statement 5	NULL		result in	NULL				adherens junctions	NULL	well-developed			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
56723	10	9472	7	10	NULL	0	NULL	EDG-1			overexpressed in					HEK293 cells					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_85	10760461	A clue to the potential physiological function of EDG-1 emerged from the discovery that binding of SPP to EDG-1 overexpressed in HEK293 cells induced up-regulation of P- and E-cadherins, resulting in a distinct morphology of tightly compacted cell-cell aggregates with an organized, network-like architecture and well-developed adherens junctions [ 49].	bind
41315	1	9473	5	13	NULL	NULL	NULL	F-actin	GP		bind					dystrophin	GP		cluster of basic repeats		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_1_153_s_372	10189375	A cluster of basic repeats in  the dystrophin rod domain binds F-actin through an electrostatic interaction.	bind
41317	2	9473	5	13	NULL	NULL	NULL	statement 1	Process		occurs through					electrostatic interaction	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_1_153_s_372	10189375	A cluster of basic repeats in  the dystrophin rod domain binds F-actin through an electrostatic interaction.	bind
40213	1	9473	7	NULL	NULL	0	NULL	dystrophin	NULL		binds	NULL		basic repeats in rod domain		F-actin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_1_153_s_372	10189375	A cluster of basic repeats in  the dystrophin rod domain binds F-actin through an electrostatic interaction.	bind
40214	2	9473	7	NULL	NULL	0	NULL	statement 1	NULL		occurs through	NULL				electrostatic interactions	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_1_153_s_372	10189375	A cluster of basic repeats in  the dystrophin rod domain binds F-actin through an electrostatic interaction.	bind
41318	1	9475	5	13	NULL	NULL	NULL	DnaA protein molecules	GP		bind					DnaA	GP			recognition sites in oriC	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_9796_s_9	15642730	A cluster of multiple DnaA protein molecules binds to DnaA recognition sites in the unique origin ( oriC) (  -  ).	bind
41319	2	9475	5	13	NULL	NULL	NULL	oriC	NucleicAcid		is					unique origin	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_9796_s_9	15642730	A cluster of multiple DnaA protein molecules binds to DnaA recognition sites in the unique origin ( oriC) (  -  ).	bind
56724	2	9475	5	13	NULL	NULL	NULL	oriC	NucleicAcid		is					unique origin	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_9796_s_9	15642730	A cluster of multiple DnaA protein molecules binds to DnaA recognition sites in the unique origin ( oriC) (  -  ).	bind
56725	2	9475	5	13	NULL	NULL	NULL	oriC	NucleicAcid		is					unique origin	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_9796_s_9	15642730	A cluster of multiple DnaA protein molecules binds to DnaA recognition sites in the unique origin ( oriC) (  -  ).	bind
40218	1	9475	7	NULL	NULL	0	NULL	DnaA protein molecules	NULL		bind	NULL				oriC	NULL		DnaA recognition site		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_11_9796_s_9	15642730	A cluster of multiple DnaA protein molecules binds to DnaA recognition sites in the unique origin ( oriC) (  -  ).	bind
41320	1	9476	5	13	NULL	NULL	NULL	p21	GP		bind			cluster of serine and threonine residues in C-terminal domain		PCNA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_15_11529_s_123	10753973	A cluster of serine and threonine residues is present within the C-terminal domain of p21 that binds to PCNA, and a "`motif"` search identified three of these residues as lying within possible consensus phosphorylation sites.	bind
40221	1	9476	7	NULL	NULL	0	NULL	p21	NULL		binds to	NULL		cluster of serine and threonine residues in C-terminal domain		PCNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_15_11529_s_123	10753973	A cluster of serine and threonine residues is present within the C-terminal domain of p21 that binds to PCNA, and a "`motif"` search identified three of these residues as lying within possible consensus phosphorylation sites.	bind
41322	1	9478	5	13	NULL	NULL	NULL	CNS-enriched factor	GP		bind					NF-kappa B	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_oncogene_10_2_7838536_s_1	7838536	A CNS-enriched factor that binds to NF-kappa B and is required for interaction with HIV-1 tat..	bind
41323	2	9478	5	13	NULL	NULL	NULL	statement 1	GP		is required for					HIV-1 tat	GP	interaction with			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_oncogene_10_2_7838536_s_1	7838536	A CNS-enriched factor that binds to NF-kappa B and is required for interaction with HIV-1 tat..	bind
40252	1	9478	7	NULL	NULL	0	NULL	CNS-enriched factor	NULL		binds to	NULL				NF-kappa B	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_oncogene_10_2_7838536_s_1	7838536	A CNS-enriched factor that binds to NF-kappa B and is required for interaction with HIV-1 tat..	bind
40253	2	9478	7	NULL	NULL	0	NULL	statement 1	NULL		is required for	NULL				HIV-1 tat	NULL	interaction of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_oncogene_10_2_7838536_s_1	7838536	A CNS-enriched factor that binds to NF-kappa B and is required for interaction with HIV-1 tat..	bind
41329	1	9479	5	13	NULL	NULL	NULL	heparin	Chemical		bind					basic fibroblast growth factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_13_12598_s_26	14707146	A co-crystal structure is available for heparin bound to the cytokine basic fibroblast growth factor ( ), but the features governing protein-GAG recognition are still relatively uncharacterized.	bind
41330	2	9479	5	13	NULL	NULL	NULL	basic fibroblast growth factor	GP		is a type of					cytokine	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_13_12598_s_26	14707146	A co-crystal structure is available for heparin bound to the cytokine basic fibroblast growth factor ( ), but the features governing protein-GAG recognition are still relatively uncharacterized.	bind
40254	1	9479	7	10	NULL	0	NULL	heparin	NULL		bind	NULL				basic fibroblast growth factor	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_13_12598_s_26	14707146	A co-crystal structure is available for heparin bound to the cytokine basic fibroblast growth factor ( ), but the features governing protein-GAG recognition are still relatively uncharacterized.	bind
46842	2	9479	7	10	NULL	0	NULL	basic fibroblast growth factor	NULL		is a type of 	NULL				cytokine	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12598_s_26	14707146	A co-crystal structure is available for heparin bound to the cytokine basic fibroblast growth factor ( ), but the features governing protein-GAG recognition are still relatively uncharacterized.	bind
41331	1	9480	5	13	NULL	NULL	NULL	peptide aldehyde inhibitor	GP		bind		covalently			Pre3	GP		terminal threonines		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25200_s_275	9312134	A co-crystallized peptide aldehyde inhibitor was found covalently bound to the terminal threonines of Pre3, Pup1, and Pre2.	bind
41332	2	9480	5	13	NULL	NULL	NULL	peptide aldehyde inhibitor	GP		bind		covalently			Pre2	GP		terminal threonines		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25200_s_275	9312134	A co-crystallized peptide aldehyde inhibitor was found covalently bound to the terminal threonines of Pre3, Pup1, and Pre2.	bind
41333	3	9480	5	13	NULL	NULL	NULL	peptide aldehyde inhibitor	GP		bind		covalently			Pup1	GP		terminal threonines		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25200_s_275	9312134	A co-crystallized peptide aldehyde inhibitor was found covalently bound to the terminal threonines of Pre3, Pup1, and Pre2.	bind
40255	1	9480	7	NULL	NULL	0	NULL	peptide aldehyde inhibitor	NULL		bind	NULL	covalently			Pre3	NULL		 terminal threonine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25200_s_275	9312134	A co-crystallized peptide aldehyde inhibitor was found covalently bound to the terminal threonines of Pre3, Pup1, and Pre2.	bind
40256	2	9480	7	NULL	NULL	0	NULL	peptide aldehyde inhibitor	NULL		bind	NULL	covalently			Pup1	NULL		terminal threonine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25200_s_275	9312134	A co-crystallized peptide aldehyde inhibitor was found covalently bound to the terminal threonines of Pre3, Pup1, and Pre2.	bind
40257	3	9480	7	NULL	NULL	0	NULL	peptide aldehyde inhibitor	NULL		bind	NULL	covalently			Pre2	NULL		terminal threonine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_40_25200_s_275	9312134	A co-crystallized peptide aldehyde inhibitor was found covalently bound to the terminal threonines of Pre3, Pup1, and Pre2.	bind
41334	1	9482	5	13	NULL	NULL	NULL	EGL-1	GP		bind		stably			CED-9	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_cell-death-differ_10_12_12894216_s_4	12894216	A coexpression system to  produce CED-9 in complex with proapoptotic EGL-1 enabled us to show that  the binding of EGL-1 to CED-9 is extremely stable, raising the melting  temperature (T(M)) of CED-9 by 25 degrees C, and that the binding surface  of CED-9 extends beyond the BH3-binding region and reaches the BH4 domain.	bind
41335	2	9482	5	13	NULL	NULL	NULL	CED-9	GP	binding surface of	extends beyond								BH3-binding region		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_cell-death-differ_10_12_12894216_s_4	12894216	A coexpression system to  produce CED-9 in complex with proapoptotic EGL-1 enabled us to show that  the binding of EGL-1 to CED-9 is extremely stable, raising the melting  temperature (T(M)) of CED-9 by 25 degrees C, and that the binding surface  of CED-9 extends beyond the BH3-binding region and reaches the BH4 domain.	bind
41336	3	9482	5	13	NULL	NULL	NULL	CED-9	GP	binding surface of	reaches								BH4 domain		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_cell-death-differ_10_12_12894216_s_4	12894216	A coexpression system to  produce CED-9 in complex with proapoptotic EGL-1 enabled us to show that  the binding of EGL-1 to CED-9 is extremely stable, raising the melting  temperature (T(M)) of CED-9 by 25 degrees C, and that the binding surface  of CED-9 extends beyond the BH3-binding region and reaches the BH4 domain.	bind
40260	1	9482	7	NULL	NULL	0	NULL	EGL-1	NULL		bind	NULL				CED-9	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_cell-death-differ_10_12_12894216_s_4	12894216	A coexpression system to  produce CED-9 in complex with proapoptotic EGL-1 enabled us to show that  the binding of EGL-1 to CED-9 is extremely stable, raising the melting  temperature (T(M)) of CED-9 by 25 degrees C, and that the binding surface  of CED-9 extends beyond the BH3-binding region and reaches the BH4 domain.	bind
40263	2	9482	7	10	NULL	0	NULL	CED-9		binding surface of	extends beyond								BH3-binding region		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_cell-death-differ_10_12_12894216_s_4	12894216	A coexpression system to  produce CED-9 in complex with proapoptotic EGL-1 enabled us to show that  the binding of EGL-1 to CED-9 is extremely stable, raising the melting  temperature (T(M)) of CED-9 by 25 degrees C, and that the binding surface  of CED-9 extends beyond the BH3-binding region and reaches the BH4 domain.	bind
40264	3	9482	7	10	NULL	0	NULL	CED-9		binding surface of	reaches								BH4 domain		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_cell-death-differ_10_12_12894216_s_4	12894216	A coexpression system to  produce CED-9 in complex with proapoptotic EGL-1 enabled us to show that  the binding of EGL-1 to CED-9 is extremely stable, raising the melting  temperature (T(M)) of CED-9 by 25 degrees C, and that the binding surface  of CED-9 extends beyond the BH3-binding region and reaches the BH4 domain.	bind
41337	1	9483	5	13	NULL	NULL	NULL	mod(mdg4)	Chemical		bind					su(Hw)	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_3_271_s_75	11825869	A cofactor, mod(mdg4), binds to su(Hw) and is essential for its enhancer-blocking activity (see below; Gerasimova et al. 1995  ).	bind
41338	2	9483	5	13	NULL	NULL	NULL	mod(mdg4)	Chemical		exhibits					enhancer-blocking activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_3_271_s_75	11825869	A cofactor, mod(mdg4), binds to su(Hw) and is essential for its enhancer-blocking activity (see below; Gerasimova et al. 1995  ).	bind
41339	3	9483	5	13	NULL	NULL	NULL	mod(mdg4)	Chemical		is a type of					cofactor	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_3_271_s_75	11825869	A cofactor, mod(mdg4), binds to su(Hw) and is essential for its enhancer-blocking activity (see below; Gerasimova et al. 1995  ).	bind
46843	4	9483	5	13	NULL	NULL	NULL	statement 1	Process		is essential for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_3_271_s_75	11825869	A cofactor, mod(mdg4), binds to su(Hw) and is essential for its enhancer-blocking activity (see below; Gerasimova et al. 1995  ).	bind
40275	1	9483	7	NULL	NULL	0	NULL	mdg4	NULL		binds to	NULL				su(Hw)	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_3_271_s_75	11825869	A cofactor, mod(mdg4), binds to su(Hw) and is essential for its enhancer-blocking activity (see below; Gerasimova et al. 1995  ).	bind
40276	2	9483	7	10	NULL	0	NULL	mod(mdg4)	NULL		exhibits	NULL				enhancer-blocking activity	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_3_271_s_75	11825869	A cofactor, mod(mdg4), binds to su(Hw) and is essential for its enhancer-blocking activity (see below; Gerasimova et al. 1995  ).	bind
40277	3	9483	7	NULL	NULL	0	NULL	mdg4	NULL		is a type of	NULL				cofactor mod	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_16_3_271_s_75	11825869	A cofactor, mod(mdg4), binds to su(Hw) and is essential for its enhancer-blocking activity (see below; Gerasimova et al. 1995  ).	bind
46844	4	9483	7	10	NULL	0	NULL	statement 1	NULL		is essential for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_16_3_271_s_75	11825869	A cofactor, mod(mdg4), binds to su(Hw) and is essential for its enhancer-blocking activity (see below; Gerasimova et al. 1995  ).	bind
41340	1	9486	5	13	NULL	NULL	NULL	p34	GP		bind					22 S dynein	GP	Paramecium			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_20048_s_173	11274140	A cold-labeled p29 fraction was added at increasing concentrations to compete with binding of p34 to  Paramecium 22 S dynein.	bind
40278	1	9486	7	NULL	NULL	0	NULL	 p34	NULL		bind	NULL				22 S dynein	NULL	Paramecium			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_23_20048_s_173	11274140	A cold-labeled p29 fraction was added at increasing concentrations to compete with binding of p34 to  Paramecium 22 S dynein.	bind
40279	2	9486	7	NULL	NULL	0	NULL	p29 fraction	NULL	cold-labeled	bind	NULL				22 S dynein	NULL	Paramecium			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_23_20048_s_173	11274140	A cold-labeled p29 fraction was added at increasing concentrations to compete with binding of p34 to  Paramecium 22 S dynein.	bind
40280	3	9486	7	NULL	NULL	0	NULL	statement 2	NULL		compete with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_23_20048_s_173	11274140	A cold-labeled p29 fraction was added at increasing concentrations to compete with binding of p34 to  Paramecium 22 S dynein.	bind
41341	1	9487	5	13	NULL	NULL	NULL	fibromodulin	GP		is a type of					collagen binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_genomeres_9_5_449_s_341	10330124	A collagen binding 59 kD protein (fibromodulin) is structurally related to the small interstitial proteoglycans PG S1 and PG S2 (decorin).	bind
41342	2	9487	5	13	NULL	NULL	NULL	fibromodulin	GP		is related to					PG S1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genomeres_9_5_449_s_341	10330124	A collagen binding 59 kD protein (fibromodulin) is structurally related to the small interstitial proteoglycans PG S1 and PG S2 (decorin).	bind
41343	3	9487	5	13	NULL	NULL	NULL	fibromodulin	GP		is related to					PG S2	GP				NULL		NULL	NULL	NULL	NULL	gw60_genomeres_9_5_449_s_341	10330124	A collagen binding 59 kD protein (fibromodulin) is structurally related to the small interstitial proteoglycans PG S1 and PG S2 (decorin).	bind
41344	4	9487	5	13	NULL	NULL	NULL	PG S1	GP		is a type of					small interstitial proteoglycans	GP				NULL		NULL	NULL	NULL	NULL	gw60_genomeres_9_5_449_s_341	10330124	A collagen binding 59 kD protein (fibromodulin) is structurally related to the small interstitial proteoglycans PG S1 and PG S2 (decorin).	bind
41345	5	9487	5	13	NULL	NULL	NULL	PG S2	GP		is a type of					small interstitial proteoglycans	GP				NULL		NULL	NULL	NULL	NULL	gw60_genomeres_9_5_449_s_341	10330124	A collagen binding 59 kD protein (fibromodulin) is structurally related to the small interstitial proteoglycans PG S1 and PG S2 (decorin).	bind
41346	6	9487	5	13	NULL	NULL	NULL	PG S2	GP		is					decorin	GP				NULL		NULL	NULL	NULL	NULL	gw60_genomeres_9_5_449_s_341	10330124	A collagen binding 59 kD protein (fibromodulin) is structurally related to the small interstitial proteoglycans PG S1 and PG S2 (decorin).	bind
40281	1	9487	7	NULL	NULL	0	NULL	fibromodulin	NULL		bind	NULL				collagen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genomeres_9_5_449_s_341	10330124	A collagen binding 59 kD protein (fibromodulin) is structurally related to the small interstitial proteoglycans PG S1 and PG S2 (decorin).	bind
40282	2	9487	7	NULL	NULL	0	NULL	fibromodulin	NULL		is a type of	NULL				59 kD protein	NULL				NULL		0	NULL	NULL	NULL	gw60_genomeres_9_5_449_s_341	10330124	A collagen binding 59 kD protein (fibromodulin) is structurally related to the small interstitial proteoglycans PG S1 and PG S2 (decorin).	bind
40283	3	9487	7	NULL	NULL	0	NULL	fibromodulin	NULL		is related to	NULL				PG S1	NULL				NULL		0	NULL	NULL	NULL	gw60_genomeres_9_5_449_s_341	10330124	A collagen binding 59 kD protein (fibromodulin) is structurally related to the small interstitial proteoglycans PG S1 and PG S2 (decorin).	bind
40284	4	9487	7	NULL	NULL	0	NULL	fibromodulin	NULL		is related to	NULL				PG S2	NULL				NULL		0	NULL	NULL	NULL	gw60_genomeres_9_5_449_s_341	10330124	A collagen binding 59 kD protein (fibromodulin) is structurally related to the small interstitial proteoglycans PG S1 and PG S2 (decorin).	bind
40286	5	9487	7	NULL	NULL	0	NULL	PG S1	NULL		is a type of	NULL				small interstitial proteoglycans	NULL				NULL		0	NULL	NULL	NULL	gw60_genomeres_9_5_449_s_341	10330124	A collagen binding 59 kD protein (fibromodulin) is structurally related to the small interstitial proteoglycans PG S1 and PG S2 (decorin).	bind
40287	6	9487	7	NULL	NULL	0	NULL	PG S2	NULL		is a type of	NULL				small interstitial proteoglycans	NULL				NULL		0	NULL	NULL	NULL	gw60_genomeres_9_5_449_s_341	10330124	A collagen binding 59 kD protein (fibromodulin) is structurally related to the small interstitial proteoglycans PG S1 and PG S2 (decorin).	bind
40288	7	9487	7	NULL	NULL	0	NULL	PG S2	NULL		is 	NULL				decorin	NULL				NULL		0	NULL	NULL	NULL	gw60_genomeres_9_5_449_s_341	10330124	A collagen binding 59 kD protein (fibromodulin) is structurally related to the small interstitial proteoglycans PG S1 and PG S2 (decorin).	bind
41349	1	9489	5	13	NULL	NULL	NULL	ShcB	GP		bind			Tyr499		TrkA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_29_26046_s_210	12006576	A combination mutation of S8 and S9 also significantly reduced the binding of ShcB to TrkA (Fig.  2 B,  top panel,  lane 6), which confirmed that Tyr499 is the binding site of ShcB to TrkA.	bind
41350	2	9489	5	13	NULL	NULL	NULL			mutant	reduce		significantly	S8		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_29_26046_s_210	12006576	A combination mutation of S8 and S9 also significantly reduced the binding of ShcB to TrkA (Fig.  2 B,  top panel,  lane 6), which confirmed that Tyr499 is the binding site of ShcB to TrkA.	bind
41351	3	9489	5	13	NULL	NULL	NULL			mutant	reduce		significantly	S9		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_29_26046_s_210	12006576	A combination mutation of S8 and S9 also significantly reduced the binding of ShcB to TrkA (Fig.  2 B,  top panel,  lane 6), which confirmed that Tyr499 is the binding site of ShcB to TrkA.	bind
40300	1	9489	7	NULL	NULL	0	NULL	ShcB 	NULL		bind	NULL		Tyr499		TrkA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26046_s_210	12006576	A combination mutation of S8 and S9 also significantly reduced the binding of ShcB to TrkA (Fig.  2 B,  top panel,  lane 6), which confirmed that Tyr499 is the binding site of ShcB to TrkA.	bind
40301	2	9489	7	NULL	NULL	0	NULL	 S8	NULL	mutation of	reduce	NULL	significantly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26046_s_210	12006576	A combination mutation of S8 and S9 also significantly reduced the binding of ShcB to TrkA (Fig.  2 B,  top panel,  lane 6), which confirmed that Tyr499 is the binding site of ShcB to TrkA.	bind
40302	3	9489	7	NULL	NULL	0	NULL	S9	NULL	mutation of	reduce	NULL	significantly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26046_s_210	12006576	A combination mutation of S8 and S9 also significantly reduced the binding of ShcB to TrkA (Fig.  2 B,  top panel,  lane 6), which confirmed that Tyr499 is the binding site of ShcB to TrkA.	bind
41352	1	9490	5	13	NULL	NULL	NULL	DNA complex	NucleicAcid	ATP-induced	consists		predominantly			NFAT-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13205_s_210	10224077	A combination of anti-NFAT-1 and anti-NFAT-2 strongly prevented DNA binding, indicating that the ATP-induced DNA complex predominantly consisted of NFAT-1 and NFAT-2.	bind
41353	2	9490	5	13	NULL	NULL	NULL	DNA complex	NucleicAcid	ATP-induced	consists		predominantly			NFAT-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13205_s_210	10224077	A combination of anti-NFAT-1 and anti-NFAT-2 strongly prevented DNA binding, indicating that the ATP-induced DNA complex predominantly consisted of NFAT-1 and NFAT-2.	bind
40303	1	9490	7	NULL	NULL	0	NULL	anti-NFAT-1 	NULL		prevents	NULL	strongly			DNA	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_19_13205_s_210	10224077	A combination of anti-NFAT-1 and anti-NFAT-2 strongly prevented DNA binding, indicating that the ATP-induced DNA complex predominantly consisted of NFAT-1 and NFAT-2.	bind
40304	2	9490	7	NULL	NULL	0	NULL	anti-NFAT-2	NULL		prevents	NULL	strongly			DNA	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_19_13205_s_210	10224077	A combination of anti-NFAT-1 and anti-NFAT-2 strongly prevented DNA binding, indicating that the ATP-induced DNA complex predominantly consisted of NFAT-1 and NFAT-2.	bind
40305	3	9490	7	NULL	NULL	0	NULL	statement 1	NULL		occur in combination with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_19_13205_s_210	10224077	A combination of anti-NFAT-1 and anti-NFAT-2 strongly prevented DNA binding, indicating that the ATP-induced DNA complex predominantly consisted of NFAT-1 and NFAT-2.	bind
40306	4	9490	7	NULL	NULL	0	NULL	ATP	NULL		induce	NULL				DNA complex	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_19_13205_s_210	10224077	A combination of anti-NFAT-1 and anti-NFAT-2 strongly prevented DNA binding, indicating that the ATP-induced DNA complex predominantly consisted of NFAT-1 and NFAT-2.	bind
40307	5	9490	7	NULL	NULL	0	NULL	statement 4	NULL		consist of	NULL				NFAT-1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_19_13205_s_210	10224077	A combination of anti-NFAT-1 and anti-NFAT-2 strongly prevented DNA binding, indicating that the ATP-induced DNA complex predominantly consisted of NFAT-1 and NFAT-2.	bind
40308	6	9490	7	NULL	NULL	0	NULL	statement 4	NULL		consist of	NULL				NFAT-2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_19_13205_s_210	10224077	A combination of anti-NFAT-1 and anti-NFAT-2 strongly prevented DNA binding, indicating that the ATP-induced DNA complex predominantly consisted of NFAT-1 and NFAT-2.	bind
41355	2	9492	5	13	NULL	NULL	NULL	secretory vesicles	CellComponent	small	depart from					trans-Golgi compartments	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_17_16868_s_23	15718243	A combination of mucin granules released at a very low rate and/or small secretory vesicles departing from the  trans-Golgi compartments might mediate constitutive mucin secretion ( ,  ).	bind
41356	3	9492	5	13	NULL	NULL	NULL	statement 2	Process		mediate					mucin	GP	constitutive secretion of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_17_16868_s_23	15718243	A combination of mucin granules released at a very low rate and/or small secretory vesicles departing from the  trans-Golgi compartments might mediate constitutive mucin secretion ( ,  ).	bind
56758	1	9492	5	13	NULL	NULL	NULL	mucin granules	CellComponent		mediate		might			mucin	GP	secretion of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_17_16868_s_23	15718243	A combination of mucin granules released at a very low rate and/or small secretory vesicles departing from the  trans-Golgi compartments might mediate constitutive mucin secretion ( ,  ).	bind
56762	4	9492	5	13	NULL	NULL	NULL	statement 1	Process		occur in combination of					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_17_16868_s_23	15718243	A combination of mucin granules released at a very low rate and/or small secretory vesicles departing from the  trans-Golgi compartments might mediate constitutive mucin secretion ( ,  ).	bind
56780	5	9492	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_17_16868_s_23	15718243	A combination of mucin granules released at a very low rate and/or small secretory vesicles departing from the  trans-Golgi compartments might mediate constitutive mucin secretion ( ,  ).	bind
40323	1	9492	7	NULL	NULL	0	NULL	mucin granules	NULL		mediate	NULL	might			mucin	NULL	secretion of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_17_16868_s_23	15718243	A combination of mucin granules released at a very low rate and/or small secretory vesicles departing from the  trans-Golgi compartments might mediate constitutive mucin secretion ( ,  ).	bind
40324	2	9492	7	NULL	NULL	0	NULL	small secretory vesicles	NULL		depart from	NULL				trans-Golgi compartments	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_17_16868_s_23	15718243	A combination of mucin granules released at a very low rate and/or small secretory vesicles departing from the  trans-Golgi compartments might mediate constitutive mucin secretion ( ,  ).	bind
40325	3	9492	7	NULL	NULL	0	NULL	statement 2	NULL		mediate	NULL	might			mucin	NULL	secretion of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_17_16868_s_23	15718243	A combination of mucin granules released at a very low rate and/or small secretory vesicles departing from the  trans-Golgi compartments might mediate constitutive mucin secretion ( ,  ).	bind
40326	4	9492	7	NULL	NULL	0	NULL	statement 1	NULL		occur in combination with	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_17_16868_s_23	15718243	A combination of mucin granules released at a very low rate and/or small secretory vesicles departing from the  trans-Golgi compartments might mediate constitutive mucin secretion ( ,  ).	bind
40327	5	9492	7	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_17_16868_s_23	15718243	A combination of mucin granules released at a very low rate and/or small secretory vesicles departing from the  trans-Golgi compartments might mediate constitutive mucin secretion ( ,  ).	bind
41357	1	9493	5	13	NULL	NULL	NULL	GST-AGS3	GP		bind					Galphai	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_9_6767_s_97	11756403	A combination of the inactive GPR truncation peptides (GPR 1-15 and GPR 15-28) did not inhibit binding of GST-AGS3 to Galphai.	bind
41358	2	9493	5	13	NULL	NULL	NULL	GPR	GP		does not inhibit			1-15		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_9_6767_s_97	11756403	A combination of the inactive GPR truncation peptides (GPR 1-15 and GPR 15-28) did not inhibit binding of GST-AGS3 to Galphai.	bind
41359	3	9493	5	13	NULL	NULL	NULL	GPR	GP		does not inhibit			15-28		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_9_6767_s_97	11756403	A combination of the inactive GPR truncation peptides (GPR 1-15 and GPR 15-28) did not inhibit binding of GST-AGS3 to Galphai.	bind
41360	4	9493	5	13	NULL	NULL	NULL	GPR	GP	inactive 	is			1-15		GPR truncation peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_9_6767_s_97	11756403	A combination of the inactive GPR truncation peptides (GPR 1-15 and GPR 15-28) did not inhibit binding of GST-AGS3 to Galphai.	bind
41361	5	9493	5	13	NULL	NULL	NULL	GPR	GP	inactive	is			15-28		GPR truncation peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_9_6767_s_97	11756403	A combination of the inactive GPR truncation peptides (GPR 1-15 and GPR 15-28) did not inhibit binding of GST-AGS3 to Galphai.	bind
40328	1	9493	7	NULL	NULL	0	NULL	GST-AGS3	NULL		bind	NULL				Galphai	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_9_6767_s_97	11756403	A combination of the inactive GPR truncation peptides (GPR 1-15 and GPR 15-28) did not inhibit binding of GST-AGS3 to Galphai.	bind
40329	2	9493	7	NULL	NULL	0	NULL	GPR 1-15	NULL	inactive	does not inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_9_6767_s_97	11756403	A combination of the inactive GPR truncation peptides (GPR 1-15 and GPR 15-28) did not inhibit binding of GST-AGS3 to Galphai.	bind
40330	3	9493	7	NULL	NULL	0	NULL	GPR 15-28	NULL	inactive	does not inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_9_6767_s_97	11756403	A combination of the inactive GPR truncation peptides (GPR 1-15 and GPR 15-28) did not inhibit binding of GST-AGS3 to Galphai.	bind
40331	4	9493	7	NULL	NULL	0	NULL	GPR 1-15	NULL		is a type of	NULL				GPR truncation peptides	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_9_6767_s_97	11756403	A combination of the inactive GPR truncation peptides (GPR 1-15 and GPR 15-28) did not inhibit binding of GST-AGS3 to Galphai.	bind
40332	5	9493	7	NULL	NULL	0	NULL	GPR 15-28	NULL		is a type of	NULL				GPR truncation peptides	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_9_6767_s_97	11756403	A combination of the inactive GPR truncation peptides (GPR 1-15 and GPR 15-28) did not inhibit binding of GST-AGS3 to Galphai.	bind
41362	1	9494	5	13	NULL	NULL	NULL			combined mutation	decrease		selectively	Y13L/S14Q		IL8R2	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8228_s_13	8626516	A combined  mutation Y13L/S14Q selectively decreased binding to IL8R2.	bind
40333	1	9494	7	10	NULL	0	NULL		NULL	combined mutation	decrease	NULL	selectively	Y13L/S14Q		IL8R2	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8228_s_13	8626516	A combined  mutation Y13L/S14Q selectively decreased binding to IL8R2.	bind
41602	1	9495	5	13	NULL	NULL	NULL	Smad3	GP		bind					p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_14_2114_s_51	9679056	A combined amino- and carboxy-terminal truncation (210-342) bound to p300 comparably as well as the 2-342 and 210-425 molecules, indicating that the carboxyl and amino termini of Smad3 can only negatively regulate binding of Smad3 to p300 when the other terminus is still present.	bind
41616	2	9495	5	13	NULL	NULL	NULL	Smad3	GP	truncated	bind			2-342		p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_14_2114_s_51	9679056	A combined amino- and carboxy-terminal truncation (210-342) bound to p300 comparably as well as the 2-342 and 210-425 molecules, indicating that the carboxyl and amino termini of Smad3 can only negatively regulate binding of Smad3 to p300 when the other terminus is still present.	bind
41617	3	9495	5	13	NULL	NULL	NULL	Smad3	GP	truncated	bind			210-425		p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_14_2114_s_51	9679056	A combined amino- and carboxy-terminal truncation (210-342) bound to p300 comparably as well as the 2-342 and 210-425 molecules, indicating that the carboxyl and amino termini of Smad3 can only negatively regulate binding of Smad3 to p300 when the other terminus is still present.	bind
41618	4	9495	5	13	NULL	NULL	NULL	Smad3	GP	truncated	bind			210-342		p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_14_2114_s_51	9679056	A combined amino- and carboxy-terminal truncation (210-342) bound to p300 comparably as well as the 2-342 and 210-425 molecules, indicating that the carboxyl and amino termini of Smad3 can only negatively regulate binding of Smad3 to p300 when the other terminus is still present.	bind
41619	5	9495	5	13	NULL	NULL	NULL	Smad3	GP	truncated	is			210-342		combined amino- and carboxy-terminal truncation of Smad3	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_14_2114_s_51	9679056	A combined amino- and carboxy-terminal truncation (210-342) bound to p300 comparably as well as the 2-342 and 210-425 molecules, indicating that the carboxyl and amino termini of Smad3 can only negatively regulate binding of Smad3 to p300 when the other terminus is still present.	bind
41620	6	9495	5	13	NULL	NULL	NULL	Smad3	GP		regulates		negatively	carboxyl & amino termini		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_14_2114_s_51	9679056	A combined amino- and carboxy-terminal truncation (210-342) bound to p300 comparably as well as the 2-342 and 210-425 molecules, indicating that the carboxyl and amino termini of Smad3 can only negatively regulate binding of Smad3 to p300 when the other terminus is still present.	bind
40334	1	9495	7	NULL	NULL	0	NULL	 Smad3	NULL		bind	NULL				p300	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_14_2114_s_51	9679056	A combined amino- and carboxy-terminal truncation (210-342) bound to p300 comparably as well as the 2-342 and 210-425 molecules, indicating that the carboxyl and amino termini of Smad3 can only negatively regulate binding of Smad3 to p300 when the other terminus is still present.	bind
40335	2	9495	7	10	NULL	0	NULL	Smad3	NULL	truncated	bind	NULL		amino- and carboxy-terminal		p300	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_14_2114_s_51	9679056	A combined amino- and carboxy-terminal truncation (210-342) bound to p300 comparably as well as the 2-342 and 210-425 molecules, indicating that the carboxyl and amino termini of Smad3 can only negatively regulate binding of Smad3 to p300 when the other terminus is still present.	bind
40336	3	9495	7	10	NULL	0	NULL	Smad3	NULL	truncated	bind	NULL		 2-342 molecule		p300	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_14_2114_s_51	9679056	A combined amino- and carboxy-terminal truncation (210-342) bound to p300 comparably as well as the 2-342 and 210-425 molecules, indicating that the carboxyl and amino termini of Smad3 can only negatively regulate binding of Smad3 to p300 when the other terminus is still present.	bind
40337	4	9495	7	10	NULL	0	NULL	Smad3	NULL	truncated	bind	NULL		210-425 molecule		p300	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_14_2114_s_51	9679056	A combined amino- and carboxy-terminal truncation (210-342) bound to p300 comparably as well as the 2-342 and 210-425 molecules, indicating that the carboxyl and amino termini of Smad3 can only negatively regulate binding of Smad3 to p300 when the other terminus is still present.	bind
40338	5	9495	7	NULL	NULL	0	NULL	Smad3	NULL		regulate	NULL	negatively	 carboxyl and amino termini		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_14_2114_s_51	9679056	A combined amino- and carboxy-terminal truncation (210-342) bound to p300 comparably as well as the 2-342 and 210-425 molecules, indicating that the carboxyl and amino termini of Smad3 can only negatively regulate binding of Smad3 to p300 when the other terminus is still present.	bind
41363	1	9496	5	13	NULL	NULL	NULL	67 kDa protein	GP		is a type of					calmodulin binding protein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
41364	2	9496	5	13	NULL	NULL	NULL	67 kDa protein	GP		is present in					oesophagus	OrganismPart	membrane fractions of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
41365	3	9496	5	13	NULL	NULL	NULL	67 kDa protein	GP		is present in					stomach	OrganismPart	membrane fractions of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
41366	4	9496	5	13	NULL	NULL	NULL	67 kDa protein	GP		is present in					proximal small intestine	OrganismPart	membrane fractions of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
41367	5	9496	5	13	NULL	NULL	NULL	67 kDa protein	GP		is present in					distal small intestine	OrganismPart	membrane fractions of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
41368	6	9496	5	13	NULL	NULL	NULL	67 kDa protein	GP		is present in					colon	OrganismPart	membrane fractions of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
41369	7	9496	5	13	NULL	NULL	NULL	67 kDa protein	GP		is present in					oesophagus	OrganismPart	cytosolic fractions of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
41370	8	9496	5	13	NULL	NULL	NULL	67 kDa protein	GP		is present in					stomach	OrganismPart	cytosolic fractions of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
41371	9	9496	5	13	NULL	NULL	NULL	67 kDa protein	GP		is present in					proximal small intestine	OrganismPart	cytosolic fractions of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
41372	10	9496	5	13	NULL	NULL	NULL	67 kDa protein	GP		is present in					distal small intestine	OrganismPart	cytosolic fractions of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
41373	11	9496	5	13	NULL	NULL	NULL	67 kDa protein	GP		is present in					colon	GP	cytosolic fractions of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
40339	1	9496	7	NULL	NULL	0	NULL	 67 kDa protein	NULL		is found in	NULL				 oesophagus	NULL	membrane fractions of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
40340	2	9496	7	NULL	NULL	0	NULL	67kDa  protein	NULL		is found in	NULL				stomach	NULL	membrane fractions of 			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
40341	3	9496	7	NULL	NULL	0	NULL	67 kDa  protein	NULL		is found in	NULL				colon	NULL	membrane fractions of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
40342	4	9496	7	NULL	NULL	0	NULL	67kDa  protein	NULL		is found in	NULL				proximal small intestine	NULL	membrane fractions of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
40343	5	9496	7	NULL	NULL	0	NULL	67kDa  protein	NULL		is found in	NULL				distal small intestine	NULL	membrane fractions of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
40344	6	9496	7	NULL	NULL	0	NULL	67kDa  protein	NULL		is found in	NULL				stomach	NULL	cytosolic fractions of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
46968	7	9496	7	NULL	NULL	0	NULL	67 kDa  protein	NULL		is found in	NULL				 oesophagus	NULL	cytosolic fractions of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
46969	8	9496	7	NULL	NULL	0	NULL	67kDa  protein	NULL		is found in	NULL				proximal small intestine	NULL	cytosolic fractions of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
46970	9	9496	7	NULL	NULL	0	NULL	67kDa  protein	NULL		is found in	NULL				distal small intestine	NULL	cytosolic fractions of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
46971	10	9496	7	NULL	NULL	0	NULL	67kDa  protein	NULL		is found in	NULL				colon	NULL	cytosolic fractions of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
46972	11	9496	7	NULL	NULL	0	NULL	67kDa  protein	NULL		is a type of	NULL				calmodulin binding protein	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_gut_32_10_1955165_s_4	1955165	A common  calmodulin binding protein of 67 kDa was found in membrane and cytosolic  fractions of oesophagus, stomach, proximal and distal small intestine,  and colon from all four species.	bind
41670	1	9497	5	13	NULL	NULL	NULL	PEA-15	GP		is similar to			ERK-binding surface		Tube	GP		ERK-binding surface		NULL		NULL	NULL	NULL	NULL	gw60_embo_21_23_6494_s_138	12456656	A common binding surface in the death motif mediates diverse protein - protein interactions   A comparison of the ERK-binding surface of PEA-15 with that observed for Tube DD in the crystal structure of the Tube - Pelle DD complex ( Xiao  et al., 1999) revealed an unexpected similarity in the binding motifs of Tube and PEA-15 (Figure  6).	bind
40345	1	9497	7	NULL	NULL	0	NULL	PEA-15	NULL		is similar to	NULL		ERK-binding surface		Tube	NULL		binding motifs of		NULL		0	NULL	NULL	NULL	gw60_embo_21_23_6494_s_138	12456656	A common binding surface in the death motif mediates diverse protein - protein interactions   A comparison of the ERK-binding surface of PEA-15 with that observed for Tube DD in the crystal structure of the Tube - Pelle DD complex ( Xiao  et al., 1999) revealed an unexpected similarity in the binding motifs of Tube and PEA-15 (Figure  6).	bind
41374	1	9498	5	13	NULL	NULL	NULL	Hsc70	GP		plays a role in					TfR	GP	externalization of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_13_9910_s_263	11133993	A common explanation of the role of Hsc70 in TfR externalization is that after many rounds of endocytic cycles, along with changes in the cytoplasm during cell maturation, partial unfolding of the TfR cytoplasmic domain would expose the hydrophobic sequence that would bind Hsc70.	bind
41375	2	9498	5	13	NULL	NULL	NULL	TfR	GP		is exposed by			hydrophobic sequence		TfR	GP	partial unfolding of	cytoplasmic domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_13_9910_s_263	11133993	A common explanation of the role of Hsc70 in TfR externalization is that after many rounds of endocytic cycles, along with changes in the cytoplasm during cell maturation, partial unfolding of the TfR cytoplasmic domain would expose the hydrophobic sequence that would bind Hsc70.	bind
41376	3	9498	5	13	NULL	NULL	NULL	statement 2	GP		bind					Hsc70	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_13_9910_s_263	11133993	A common explanation of the role of Hsc70 in TfR externalization is that after many rounds of endocytic cycles, along with changes in the cytoplasm during cell maturation, partial unfolding of the TfR cytoplasmic domain would expose the hydrophobic sequence that would bind Hsc70.	bind
41377	4	9498	5	13	NULL	NULL	NULL	statement 3	Process		occurs during					cell maturation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_13_9910_s_263	11133993	A common explanation of the role of Hsc70 in TfR externalization is that after many rounds of endocytic cycles, along with changes in the cytoplasm during cell maturation, partial unfolding of the TfR cytoplasmic domain would expose the hydrophobic sequence that would bind Hsc70.	bind
41378	5	9498	5	13	NULL	NULL	NULL	statement 4	Process		along with					cytoplasm	CellComponent	changes in			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_13_9910_s_263	11133993	A common explanation of the role of Hsc70 in TfR externalization is that after many rounds of endocytic cycles, along with changes in the cytoplasm during cell maturation, partial unfolding of the TfR cytoplasmic domain would expose the hydrophobic sequence that would bind Hsc70.	bind
41379	6	9498	5	13	NULL	NULL	NULL	statement 3	Process		occurs after					endocytic cycles	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_13_9910_s_263	11133993	A common explanation of the role of Hsc70 in TfR externalization is that after many rounds of endocytic cycles, along with changes in the cytoplasm during cell maturation, partial unfolding of the TfR cytoplasmic domain would expose the hydrophobic sequence that would bind Hsc70.	bind
40346	5	9498	7	NULL	NULL	0	NULL	statement 4	NULL		bind	NULL				Hsc 70	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_13_9910_s_263	11133993	A common explanation of the role of Hsc70 in TfR externalization is that after many rounds of endocytic cycles, along with changes in the cytoplasm during cell maturation, partial unfolding of the TfR cytoplasmic domain would expose the hydrophobic sequence that would bind Hsc70.	bind
48783	1	9498	7	NULL	NULL	0	NULL	Hsc70	NULL		plays a role in	NULL				TfR	NULL	externalization of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_13_9910_s_263	11133993	A common explanation of the role of Hsc70 in TfR externalization is that after many rounds of endocytic cycles, along with changes in the cytoplasm during cell maturation, partial unfolding of the TfR cytoplasmic domain would expose the hydrophobic sequence that would bind Hsc70.	bind
48784	2	9498	7	NULL	NULL	0	NULL	statement 1	NULL		occurs after	NULL				endocytic cycles	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_13_9910_s_263	11133993	A common explanation of the role of Hsc70 in TfR externalization is that after many rounds of endocytic cycles, along with changes in the cytoplasm during cell maturation, partial unfolding of the TfR cytoplasmic domain would expose the hydrophobic sequence that would bind Hsc70.	bind
48785	3	9498	7	NULL	NULL	0	NULL	statement 1	NULL		occurs during	NULL				cell maturation	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_13_9910_s_263	11133993	A common explanation of the role of Hsc70 in TfR externalization is that after many rounds of endocytic cycles, along with changes in the cytoplasm during cell maturation, partial unfolding of the TfR cytoplasmic domain would expose the hydrophobic sequence that would bind Hsc70.	bind
48786	4	9498	7	NULL	NULL	0	NULL	TfR 	NULL	partial unfolding of 	expose	NULL		cytoplasmic domain		hydrophobic sequence	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_13_9910_s_263	11133993	A common explanation of the role of Hsc70 in TfR externalization is that after many rounds of endocytic cycles, along with changes in the cytoplasm during cell maturation, partial unfolding of the TfR cytoplasmic domain would expose the hydrophobic sequence that would bind Hsc70.	bind
41380	1	9499	5	13	NULL	NULL	NULL	Ran	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40163_s_102	11024021	A common feature of nuclear transport receptors belonging to the importin beta family is their ability to specifically interact with the GTP-bound form of the small GTPase Ran.	bind
41381	2	9499	5	13	NULL	NULL	NULL	Ran	GP		is a type of					small GTPase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40163_s_102	11024021	A common feature of nuclear transport receptors belonging to the importin beta family is their ability to specifically interact with the GTP-bound form of the small GTPase Ran.	bind
41382	3	9499	5	13	NULL	NULL	NULL	nuclear transport receptors	GP		belong to					importin beta family	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40163_s_102	11024021	A common feature of nuclear transport receptors belonging to the importin beta family is their ability to specifically interact with the GTP-bound form of the small GTPase Ran.	bind
41383	4	9499	5	13	NULL	NULL	NULL	nuclear transport receptor	GP		interact with					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40163_s_102	11024021	A common feature of nuclear transport receptors belonging to the importin beta family is their ability to specifically interact with the GTP-bound form of the small GTPase Ran.	bind
40347	1	9499	7	10	NULL	0	NULL	GTP	NULL		bind	NULL				Ran	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40163_s_102	11024021	A common feature of nuclear transport receptors belonging to the importin beta family is their ability to specifically interact with the GTP-bound form of the small GTPase Ran.	bind
40348	2	9499	7	NULL	NULL	0	NULL	nuclear transport receptors 	NULL		belongs to	NULL				importin beta family	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_51_40163_s_102	11024021	A common feature of nuclear transport receptors belonging to the importin beta family is their ability to specifically interact with the GTP-bound form of the small GTPase Ran.	bind
40349	3	9499	7	NULL	NULL	0	NULL	Ran	NULL		is a type of	NULL				small GTPase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_51_40163_s_102	11024021	A common feature of nuclear transport receptors belonging to the importin beta family is their ability to specifically interact with the GTP-bound form of the small GTPase Ran.	bind
46845	4	9499	7	10	NULL	0	NULL	nuclear transport receptors	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_51_40163_s_102	11024021	A common feature of nuclear transport receptors belonging to the importin beta family is their ability to specifically interact with the GTP-bound form of the small GTPase Ran.	bind
41384	1	9500	5	13	NULL	NULL	NULL	b12	GP		bind					gp120	GP				NULL	clade B isolates	NULL	NULL	NULL	NULL	gw60_science_293_5532_1155_s_132	11498595	A common feature of these neutralization escape variants is the mutation of a proline at position 369, which strongly reduces b12 binding to gp120 in clade B isolates ( 50).	bind
41386	2	9500	5	13	NULL	NULL	NULL			mutation of	reduce		strongly	proline 369		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_293_5532_1155_s_132	11498595	A common feature of these neutralization escape variants is the mutation of a proline at position 369, which strongly reduces b12 binding to gp120 in clade B isolates ( 50).	bind
40350	1	9500	7	NULL	NULL	0	NULL	b12	NULL		bind	NULL				gp120	NULL				NULL	clade B isolates	0	NULL	NULL	NULL	gw60_science_293_5532_1155_s_132	11498595	A common feature of these neutralization escape variants is the mutation of a proline at position 369, which strongly reduces b12 binding to gp120 in clade B isolates ( 50).	bind
40351	2	9500	7	NULL	NULL	0	NULL		NULL	mutation of	reduce	NULL	strongly	proline 369		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_science_293_5532_1155_s_132	11498595	A common feature of these neutralization escape variants is the mutation of a proline at position 369, which strongly reduces b12 binding to gp120 in clade B isolates ( 50).	bind
41387	1	9502	5	13	NULL	NULL	NULL	MSL proteins	GP		bind					roX RNAs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_269_1_18_s_105	15081354	A common point of confusion arises from the fact that MSL proteins bind to both  roX RNAs and  roX genes.	bind
41388	2	9502	5	13	NULL	NULL	NULL	MSL proteins	GP		bind					roX genes	GP				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_269_1_18_s_105	15081354	A common point of confusion arises from the fact that MSL proteins bind to both  roX RNAs and  roX genes.	bind
40352	1	9502	7	NULL	NULL	0	NULL	MSL protein	NULL		bind	NULL				roX RNAs	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_269_1_18_s_105	15081354	A common point of confusion arises from the fact that MSL proteins bind to both  roX RNAs and  roX genes.	bind
40353	2	9502	7	NULL	NULL	0	NULL	MSL protein	NULL		bind	NULL				 roX gene	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_269_1_18_s_105	15081354	A common point of confusion arises from the fact that MSL proteins bind to both  roX RNAs and  roX genes.	bind
41389	1	9503	5	13	NULL	NULL	NULL	P-gp	GP		bind					vinblastine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_58_3_624_s_104	10953057	A common property of these modulators is the ability to reduce the maximal binding capacity of P-gp for [3]vinblastine (Fig.  1).	bind
40354	1	9503	7	NULL	NULL	0	NULL	P-gp	NULL		bind	NULL				vinblastine	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_3_624_s_104	10953057	A common property of these modulators is the ability to reduce the maximal binding capacity of P-gp for [3]vinblastine (Fig.  1).	bind
41391	1	9504	5	13	NULL	NULL	NULL	p300	GP		bind					Cdk protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_57	10330164	A common region of p300 binds to Cdk, TFIIB, and E1A proteins.	bind
41392	2	9504	5	13	NULL	NULL	NULL	p300	GP		bind					TFIIB protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_57	10330164	A common region of p300 binds to Cdk, TFIIB, and E1A proteins.	bind
41393	3	9504	5	13	NULL	NULL	NULL	p300	GP		bind					E1A protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_57	10330164	A common region of p300 binds to Cdk, TFIIB, and E1A proteins.	bind
40355	1	9504	7	NULL	NULL	0	NULL	p300	NULL		binds to	NULL				Cdk protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_57	10330164	A common region of p300 binds to Cdk, TFIIB, and E1A proteins.	bind
40356	2	9504	7	NULL	NULL	0	NULL	p300	NULL		binds to	NULL				TFIIB protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_57	10330164	A common region of p300 binds to Cdk, TFIIB, and E1A proteins.	bind
40357	3	9504	7	NULL	NULL	0	NULL	p300	NULL		binds to	NULL				E1A protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4241_s_57	10330164	A common region of p300 binds to Cdk, TFIIB, and E1A proteins.	bind
41394	1	9506	5	13	NULL	NULL	NULL	virulence factors	GP		bind					secretion chaperones	GP	bacterial			NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_mol-cell_21_5_16507363_s_1	16507363	A common structural motif in the binding of virulence factors to bacterial secretion chaperones..	bind
40358	1	9506	7	10	NULL	0	NULL	virulence factors	NULL		bind	NULL				secretion chaperones	NULL	bacterial 			NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_mol-cell_21_5_16507363_s_1	16507363	A common structural motif in the binding of virulence factors to bacterial secretion chaperones..	bind
41395	1	9507	5	13	NULL	NULL	NULL	[35]-GTP gammaS	GP		bind					Gq alpha	GP				NULL	CHO-m2m3 membranes	NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_7_1340_s_80	12711635	A comparable increase in [35]-GTP gammaS binding to Gq alpha was observed in CHO-m2m3 membranes and MCh stimulated this response with similar potencies in the two preparations (pEC50 values: CHO-m3, 4.49 plus-or-minus 0.34; CHO-m2m3, 4.29 plus-or-minus 0.37).	bind
40359	1	9507	7	NULL	NULL	0	NULL	[35]-GTP gammaS	NULL		bind	NULL				Gq alpha	NULL				NULL	CHO-m2m3 membranes	0	NULL	NULL	NULL	gw60_brjpharmacol_138_7_1340_s_80	12711635	A comparable increase in [35]-GTP gammaS binding to Gq alpha was observed in CHO-m2m3 membranes and MCh stimulated this response with similar potencies in the two preparations (pEC50 values: CHO-m3, 4.49 plus-or-minus 0.34; CHO-m2m3, 4.29 plus-or-minus 0.37).	bind
41397	1	9508	5	13	NULL	NULL	NULL	RecA	GP	mutation of	bind			K72R		ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31397_s_313	8537414	A comparable mutation in the conserved ATP  binding site of the RecA protein (RecA K72R) creates an altered protein  that binds, but does not hydrolyze ATP( 38) .	bind
41399	2	9508	5	13	NULL	NULL	NULL	statement 1	Process		does not hydrolyze					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31397_s_313	8537414	A comparable mutation in the conserved ATP  binding site of the RecA protein (RecA K72R) creates an altered protein  that binds, but does not hydrolyze ATP( 38) .	bind
40360	1	9508	7	10	NULL	0	NULL	RecA		 mutation of	bind			K72R		ATP					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31397_s_313	8537414	A comparable mutation in the conserved ATP  binding site of the RecA protein (RecA K72R) creates an altered protein  that binds, but does not hydrolyze ATP( 38) .	bind
40361	2	9508	7	NULL	NULL	0	NULL	statement 1	NULL		does not hydrolyse	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31397_s_313	8537414	A comparable mutation in the conserved ATP  binding site of the RecA protein (RecA K72R) creates an altered protein  that binds, but does not hydrolyze ATP( 38) .	bind
41400	1	9509	5	13	NULL	NULL	NULL	p53	GP		bind					PCNA gene	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44009_s_229	12947108	A comparable, yet distinct, profile of p53 binding to the PCNA gene was observed in the ChIP assay.	bind
40362	1	9509	7	NULL	NULL	0	NULL	p53	NULL		bind	NULL				PCNA gene	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_45_44009_s_229	12947108	A comparable, yet distinct, profile of p53 binding to the PCNA gene was observed in the ChIP assay.	bind
41674	1	9510	5	13	NULL	NULL	NULL	E2 protein	GP		bind		high affinity;;sequence-specific			DNA	NucleicAcid			A-tract structure of the core region	NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8490_s_4	11438706	A comparative analysis of E2-DNA conformations with respect to other structural and biochemical studies demonstrates that ( i) the A-tract structure of the core region, which is not contacted by the protein, is critical for the formation of the high-affinity sequence-specific protein-DNA complex, and ( ii) differential binding affinity is regulated by the intrinsic structure and deformability encoded in the base sequence of the DNA target.	bind
42380	2	9510	5	13	NULL	NULL	NULL				is critical for				A-tract structure of the core region	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8490_s_4	11438706	A comparative analysis of E2-DNA conformations with respect to other structural and biochemical studies demonstrates that ( i) the A-tract structure of the core region, which is not contacted by the protein, is critical for the formation of the high-affinity sequence-specific protein-DNA complex, and ( ii) differential binding affinity is regulated by the intrinsic structure and deformability encoded in the base sequence of the DNA target.	bind
40363	1	9510	7	10	NULL	0	NULL	E2 protein			complex with		high affinity;;sequence specific			DNA				A-tract structure of the core region	NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8490_s_4	11438706	A comparative analysis of E2-DNA conformations with respect to other structural and biochemical studies demonstrates that ( i) the A-tract structure of the core region, which is not contacted by the protein, is critical for the formation of the high-affinity sequence-specific protein-DNA complex, and ( ii) differential binding affinity is regulated by the intrinsic structure and deformability encoded in the base sequence of the DNA target.	bind
40364	2	9510	7	10	NULL	0	NULL	A-tract structure			is critical for			core region		statement 1					NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8490_s_4	11438706	A comparative analysis of E2-DNA conformations with respect to other structural and biochemical studies demonstrates that ( i) the A-tract structure of the core region, which is not contacted by the protein, is critical for the formation of the high-affinity sequence-specific protein-DNA complex, and ( ii) differential binding affinity is regulated by the intrinsic structure and deformability encoded in the base sequence of the DNA target.	bind
41401	1	9512	5	13	NULL	NULL	NULL	MBD proteins	GP	multiple	bind					hypermethylated genes	GP	cancer-associated			NULL	human cancer cell lines	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4243_s_33	16052033	A comparative study in human cancer cell lines using a chromatin immunoprecipitation (ChIP) assay combined with a CpG island microarray also suggests some specificities, since some cancer-associated hypermethylated genes are bound by multiple MBD proteins while others are associated with a single MBD protein ( ).	bind
56789	2	9512	5	13	NULL	NULL	NULL	MBD protein	GP	single	bind					hypermethylated genes	GP	cancer-associated			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4243_s_33	16052033	A comparative study in human cancer cell lines using a chromatin immunoprecipitation (ChIP) assay combined with a CpG island microarray also suggests some specificities, since some cancer-associated hypermethylated genes are bound by multiple MBD proteins while others are associated with a single MBD protein ( ).	bind
40440	1	9512	7	10	NULL	0	NULL	MBD proteins		multiple	bind					hypermethylated genes 		cancer-associated 			NULL	human cancer cell lines	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4243_s_33	16052033	A comparative study in human cancer cell lines using a chromatin immunoprecipitation (ChIP) assay combined with a CpG island microarray also suggests some specificities, since some cancer-associated hypermethylated genes are bound by multiple MBD proteins while others are associated with a single MBD protein ( ).	bind
40442	2	9512	7	10	NULL	0	NULL	MBD protein		single	bind					hypermethylated genes		cancer-associated 			NULL	human cancer cell lines	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4243_s_33	16052033	A comparative study in human cancer cell lines using a chromatin immunoprecipitation (ChIP) assay combined with a CpG island microarray also suggests some specificities, since some cancer-associated hypermethylated genes are bound by multiple MBD proteins while others are associated with a single MBD protein ( ).	bind
41402	1	9513	5	13	NULL	NULL	NULL	Azide	Chemical		bind					amine oxidases	GP	copper-containing			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_45_29_16846222_s_1	16846222	A Comparative Study of the Binding and Inhibition of Four Copper-Containing Amine Oxidases by Azide:	bind
41403	2	9513	5	13	NULL	NULL	NULL	statement 1	Chemical		inhibit					amine oxidases	GP	copper-containing			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_45_29_16846222_s_1	16846222	A Comparative Study of the Binding and Inhibition of Four Copper-Containing Amine Oxidases by Azide:	bind
40452	1	9513	7	10	NULL	0	NULL	Azide			bind					Amine Oxidase		Copper-Containing 			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_45_29_16846222_s_1	16846222	A Comparative Study of the Binding and Inhibition of Four Copper-Containing Amine Oxidases by Azide:	bind
40453	2	9513	7	10	NULL	0	NULL	statement 1			inhibit					Amine Oxidase		Copper-Containing			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_biochemistry_45_29_16846222_s_1	16846222	A Comparative Study of the Binding and Inhibition of Four Copper-Containing Amine Oxidases by Azide:	bind
41404	1	9514	5	13	NULL	NULL	NULL	MT1	GP		bind					MMP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11201_s_44	11790786	A comparative study of these compounds on the activation of pro-MMP-2 in cells expressing MT1-MMP shows that, when compared with marimastat, significantly higher dithiol concentrations are required for active MT1-MMP binding and enhancement of pro-MMP-2 activation in the presence of TIMP-2.	bind
41405	2	9514	5	13	NULL	NULL	NULL	marimastat	Chemical		is required for					MT1-MMP	GP	binding of active			NULL	cells expressing MT1-MMP	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11201_s_44	11790786	A comparative study of these compounds on the activation of pro-MMP-2 in cells expressing MT1-MMP shows that, when compared with marimastat, significantly higher dithiol concentrations are required for active MT1-MMP binding and enhancement of pro-MMP-2 activation in the presence of TIMP-2.	bind
41406	3	9514	5	13	NULL	NULL	NULL	marimastat	Chemical		is required for					pro-MMP-2	GP	enhancement of;;activation of			NULL	cells expressing MT1-MMP	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11201_s_44	11790786	A comparative study of these compounds on the activation of pro-MMP-2 in cells expressing MT1-MMP shows that, when compared with marimastat, significantly higher dithiol concentrations are required for active MT1-MMP binding and enhancement of pro-MMP-2 activation in the presence of TIMP-2.	bind
41407	4	9514	5	13	NULL	NULL	NULL	statement 3	Process		in the presence of					TIMP-2	GP				NULL	cells expressing MT1-MMP	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11201_s_44	11790786	A comparative study of these compounds on the activation of pro-MMP-2 in cells expressing MT1-MMP shows that, when compared with marimastat, significantly higher dithiol concentrations are required for active MT1-MMP binding and enhancement of pro-MMP-2 activation in the presence of TIMP-2.	bind
41408	5	9514	5	13	NULL	NULL	NULL	dithiol	Chemical		is required for					MT1-MMP	GP	binding of active			NULL	cells expressing MT1-MMP	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11201_s_44	11790786	A comparative study of these compounds on the activation of pro-MMP-2 in cells expressing MT1-MMP shows that, when compared with marimastat, significantly higher dithiol concentrations are required for active MT1-MMP binding and enhancement of pro-MMP-2 activation in the presence of TIMP-2.	bind
41409	6	9514	5	13	NULL	NULL	NULL	dithiol	Chemical		is required for					pro-MMP-2	GP	enhancement of;;activation of			NULL	cells expressing MT1-MMP	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11201_s_44	11790786	A comparative study of these compounds on the activation of pro-MMP-2 in cells expressing MT1-MMP shows that, when compared with marimastat, significantly higher dithiol concentrations are required for active MT1-MMP binding and enhancement of pro-MMP-2 activation in the presence of TIMP-2.	bind
41410	7	9514	5	13	NULL	NULL	NULL	statement 6	Process		in the presence of					TIMP-2	GP				NULL	cells expressing MT1-MMP	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11201_s_44	11790786	A comparative study of these compounds on the activation of pro-MMP-2 in cells expressing MT1-MMP shows that, when compared with marimastat, significantly higher dithiol concentrations are required for active MT1-MMP binding and enhancement of pro-MMP-2 activation in the presence of TIMP-2.	bind
40455	1	9514	7	10	NULL	0	NULL	MT1			bind					MMP					NULL	cells expressing MT1-MMP 	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11201_s_44	11790786	A comparative study of these compounds on the activation of pro-MMP-2 in cells expressing MT1-MMP shows that, when compared with marimastat, significantly higher dithiol concentrations are required for active MT1-MMP binding and enhancement of pro-MMP-2 activation in the presence of TIMP-2.	bind
40457	2	9514	7	10	NULL	0	NULL	marimastat			is required for					statement 1		active			NULL	cells expressing MT1-MMP	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11201_s_44	11790786	A comparative study of these compounds on the activation of pro-MMP-2 in cells expressing MT1-MMP shows that, when compared with marimastat, significantly higher dithiol concentrations are required for active MT1-MMP binding and enhancement of pro-MMP-2 activation in the presence of TIMP-2.	bind
40458	3	9514	7	10	NULL	0	NULL	dithiol 			is required for					statement 1		active			NULL	cells expressing MT1-MMP	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11201_s_44	11790786	A comparative study of these compounds on the activation of pro-MMP-2 in cells expressing MT1-MMP shows that, when compared with marimastat, significantly higher dithiol concentrations are required for active MT1-MMP binding and enhancement of pro-MMP-2 activation in the presence of TIMP-2.	bind
40459	4	9514	7	10	NULL	0	NULL	 marimastat			is required for					pro-MMP-2		enhancement of;;activation of			NULL	cells expressing MT1-MMP	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11201_s_44	11790786	A comparative study of these compounds on the activation of pro-MMP-2 in cells expressing MT1-MMP shows that, when compared with marimastat, significantly higher dithiol concentrations are required for active MT1-MMP binding and enhancement of pro-MMP-2 activation in the presence of TIMP-2.	bind
40460	5	9514	7	10	NULL	0	NULL	dithiol			is required for					pro-MMP-2		enhancement of;;activation of			NULL	cells expressing MT1-MMP	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11201_s_44	11790786	A comparative study of these compounds on the activation of pro-MMP-2 in cells expressing MT1-MMP shows that, when compared with marimastat, significantly higher dithiol concentrations are required for active MT1-MMP binding and enhancement of pro-MMP-2 activation in the presence of TIMP-2.	bind
40461	6	9514	7	10	NULL	0	NULL	statement 4			in presence of					TIMP-2 					NULL	cells expressing MT1-MMP	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11201_s_44	11790786	A comparative study of these compounds on the activation of pro-MMP-2 in cells expressing MT1-MMP shows that, when compared with marimastat, significantly higher dithiol concentrations are required for active MT1-MMP binding and enhancement of pro-MMP-2 activation in the presence of TIMP-2.	bind
40462	7	9514	7	10	NULL	0	NULL	statement 5			in presence of					TIMP-2 					NULL	cells expressing MT1-MMP	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11201_s_44	11790786	A comparative study of these compounds on the activation of pro-MMP-2 in cells expressing MT1-MMP shows that, when compared with marimastat, significantly higher dithiol concentrations are required for active MT1-MMP binding and enhancement of pro-MMP-2 activation in the presence of TIMP-2.	bind
41411	1	9515	5	13	NULL	NULL	NULL	TPP+	GP		bind					EmrE	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_22_23_6175_s_72	14633977	A comparison between projection maps of native EmrE and TPP+-bound EmrE suggest only a minor conformational change between the two structures  (  et al).	bind
40463	1	9515	7	NULL	NULL	0	NULL	TPP+	NULL		bind	NULL				EmrE	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_22_23_6175_s_72	14633977	A comparison between projection maps of native EmrE and TPP+-bound EmrE suggest only a minor conformational change between the two structures  (  et al).	bind
41412	1	9516	5	13	NULL	NULL	NULL	FhuA	GP		is a type of					outer membrane receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13966_s_169	11805094	A comparison between the binding modes of the outer membrane receptor FhuA and the periplasmic protein FhuD for albomycin is shown in Fig.  5.	bind
41413	2	9516	5	13	NULL	NULL	NULL	FhuA	GP		bind					albomycin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13966_s_169	11805094	A comparison between the binding modes of the outer membrane receptor FhuA and the periplasmic protein FhuD for albomycin is shown in Fig.  5.	bind
41414	3	9516	5	13	NULL	NULL	NULL	FhuD	GP		is a type of					periplasmic protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13966_s_169	11805094	A comparison between the binding modes of the outer membrane receptor FhuA and the periplasmic protein FhuD for albomycin is shown in Fig.  5.	bind
41415	4	9516	5	13	NULL	NULL	NULL	FhuD	GP		bind					albomycin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13966_s_169	11805094	A comparison between the binding modes of the outer membrane receptor FhuA and the periplasmic protein FhuD for albomycin is shown in Fig.  5.	bind
40464	1	9516	7	NULL	NULL	0	NULL	FhuA	NULL		bind	NULL				albomycin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13966_s_169	11805094	A comparison between the binding modes of the outer membrane receptor FhuA and the periplasmic protein FhuD for albomycin is shown in Fig.  5.	bind
40465	2	9516	7	NULL	NULL	0	NULL	FhuD	NULL		bind	NULL				albomycin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13966_s_169	11805094	A comparison between the binding modes of the outer membrane receptor FhuA and the periplasmic protein FhuD for albomycin is shown in Fig.  5.	bind
40466	3	9516	7	NULL	NULL	0	NULL	FhuA	NULL		is a type of	NULL				outer membrane receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13966_s_169	11805094	A comparison between the binding modes of the outer membrane receptor FhuA and the periplasmic protein FhuD for albomycin is shown in Fig.  5.	bind
40467	4	9516	7	NULL	NULL	0	NULL	FhuD	NULL		is a type of	NULL				 periplasmic protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13966_s_169	11805094	A comparison between the binding modes of the outer membrane receptor FhuA and the periplasmic protein FhuD for albomycin is shown in Fig.  5.	bind
41416	1	9518	5	13	NULL	NULL	NULL	moesin	GP	WT	bind					GST-C-moesin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12803_s_219	10212266	A comparison of  lanes 1 and  3 shows that PIP2 does not change binding between WT moesin and GST-C-moesin.	bind
41417	2	9518	5	13	NULL	NULL	NULL	PIP2	Chemical		does not change					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_18_12803_s_219	10212266	A comparison of  lanes 1 and  3 shows that PIP2 does not change binding between WT moesin and GST-C-moesin.	bind
40468	1	9518	7	NULL	NULL	0	NULL	WT moesin	NULL		bind	NULL				GST-C-moesin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_18_12803_s_219	10212266	A comparison of  lanes 1 and  3 shows that PIP2 does not change binding between WT moesin and GST-C-moesin.	bind
40469	2	9518	7	NULL	NULL	0	NULL	PIP2	NULL		does not change	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_18_12803_s_219	10212266	A comparison of  lanes 1 and  3 shows that PIP2 does not change binding between WT moesin and GST-C-moesin.	bind
42433	1	9519	5	13	NULL	NULL	NULL	126-base pair probe	NucleicAcid		is					alpha-Pal	GP			high affinity site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34703_s_159	9856992	A comparison of alpha-Pal or Max, or both, binding activity using the 126-base pair probe shows that at low concentrations, neither factor alone can form stable complexes with the alpha-Pal high affinity site.	bind
42436	2	9519	5	13	NULL	NULL	NULL	alpha-Pal	GP		does not complex with					126-base pair probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34703_s_159	9856992	A comparison of alpha-Pal or Max, or both, binding activity using the 126-base pair probe shows that at low concentrations, neither factor alone can form stable complexes with the alpha-Pal high affinity site.	bind
42439	3	9519	5	13	NULL	NULL	NULL	Max	GP		does not complex with					126-base pair probe	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34703_s_159	9856992	A comparison of alpha-Pal or Max, or both, binding activity using the 126-base pair probe shows that at low concentrations, neither factor alone can form stable complexes with the alpha-Pal high affinity site.	bind
40471	1	9519	7	NULL	NULL	0	NULL	126-base pair probe	NULL		is	NULL				alpha-Pal	NULL			high affinity site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34703_s_159	9856992	A comparison of alpha-Pal or Max, or both, binding activity using the 126-base pair probe shows that at low concentrations, neither factor alone can form stable complexes with the alpha-Pal high affinity site.	bind
40472	2	9519	7	NULL	NULL	0	NULL	alpha-Pal	NULL		does not complex with	NULL				126-base pair probe	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34703_s_159	9856992	A comparison of alpha-Pal or Max, or both, binding activity using the 126-base pair probe shows that at low concentrations, neither factor alone can form stable complexes with the alpha-Pal high affinity site.	bind
40757	3	9519	7	NULL	NULL	0	NULL	Max	NULL		does not complex with	NULL				126-base pair probe	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34703_s_159	9856992	A comparison of alpha-Pal or Max, or both, binding activity using the 126-base pair probe shows that at low concentrations, neither factor alone can form stable complexes with the alpha-Pal high affinity site.	bind
41418	1	9520	5	13	NULL	NULL	NULL	Arf	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1664_1_9_s_75	15238254	A comparison of Arf bound to GDP and to a nonhydrolyzable GTP analog revealed a unique  conformational switching mechanism in which GTP binding to Arf triggers the exposure  of the proteins' membrane anchor--a myristoylated amino-terminal  -helix ( Fig. 1B) [ 34].	bind
41419	2	9520	5	13	NULL	NULL	NULL	Arf	GP		bind					GTP analog	Chemical	nonhydrolyzable			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1664_1_9_s_75	15238254	A comparison of Arf bound to GDP and to a nonhydrolyzable GTP analog revealed a unique  conformational switching mechanism in which GTP binding to Arf triggers the exposure  of the proteins' membrane anchor--a myristoylated amino-terminal  -helix ( Fig. 1B) [ 34].	bind
41420	3	9520	5	13	NULL	NULL	NULL	GTP	Chemical		bind					Arf	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1664_1_9_s_75	15238254	A comparison of Arf bound to GDP and to a nonhydrolyzable GTP analog revealed a unique  conformational switching mechanism in which GTP binding to Arf triggers the exposure  of the proteins' membrane anchor--a myristoylated amino-terminal  -helix ( Fig. 1B) [ 34].	bind
41421	4	9520	5	13	NULL	NULL	NULL	myristoylated amino-terminal -helix	GP		is a type of 					proteins' membrane anchor	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1664_1_9_s_75	15238254	A comparison of Arf bound to GDP and to a nonhydrolyzable GTP analog revealed a unique  conformational switching mechanism in which GTP binding to Arf triggers the exposure  of the proteins' membrane anchor--a myristoylated amino-terminal  -helix ( Fig. 1B) [ 34].	bind
41422	5	9520	5	13	NULL	NULL	NULL	statement 3	Process		trigger					statement 4	GP	exposure of			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1664_1_9_s_75	15238254	A comparison of Arf bound to GDP and to a nonhydrolyzable GTP analog revealed a unique  conformational switching mechanism in which GTP binding to Arf triggers the exposure  of the proteins' membrane anchor--a myristoylated amino-terminal  -helix ( Fig. 1B) [ 34].	bind
40473	1	9520	7	NULL	NULL	0	NULL	Arf 	NULL		bind	NULL				GDP	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1664_1_9_s_75	15238254	A comparison of Arf bound to GDP and to a nonhydrolyzable GTP analog revealed a unique  conformational switching mechanism in which GTP binding to Arf triggers the exposure  of the proteins' membrane anchor--a myristoylated amino-terminal  -helix ( Fig. 1B) [ 34].	bind
40474	2	9520	7	NULL	NULL	0	NULL	Arf	NULL		bind	NULL				nonhydrolyzable GTP analog	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1664_1_9_s_75	15238254	A comparison of Arf bound to GDP and to a nonhydrolyzable GTP analog revealed a unique  conformational switching mechanism in which GTP binding to Arf triggers the exposure  of the proteins' membrane anchor--a myristoylated amino-terminal  -helix ( Fig. 1B) [ 34].	bind
40476	3	9520	7	NULL	NULL	0	NULL	Arf	NULL		bind	NULL				GTP	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1664_1_9_s_75	15238254	A comparison of Arf bound to GDP and to a nonhydrolyzable GTP analog revealed a unique  conformational switching mechanism in which GTP binding to Arf triggers the exposure  of the proteins' membrane anchor--a myristoylated amino-terminal  -helix ( Fig. 1B) [ 34].	bind
40479	4	9520	7	NULL	NULL	0	NULL	statement 3	NULL		triggers	NULL				myristoylated amino-terminal -helix 	NULL	exposure of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1664_1_9_s_75	15238254	A comparison of Arf bound to GDP and to a nonhydrolyzable GTP analog revealed a unique  conformational switching mechanism in which GTP binding to Arf triggers the exposure  of the proteins' membrane anchor--a myristoylated amino-terminal  -helix ( Fig. 1B) [ 34].	bind
40480	5	9520	7	NULL	NULL	0	NULL	myristoylated amino-terminal -helix 	NULL		is a type of	NULL				proteins' membrane anchor	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1664_1_9_s_75	15238254	A comparison of Arf bound to GDP and to a nonhydrolyzable GTP analog revealed a unique  conformational switching mechanism in which GTP binding to Arf triggers the exposure  of the proteins' membrane anchor--a myristoylated amino-terminal  -helix ( Fig. 1B) [ 34].	bind
40483	6	9520	7	NULL	NULL	0	NULL	statement 1	NULL		compared with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1664_1_9_s_75	15238254	A comparison of Arf bound to GDP and to a nonhydrolyzable GTP analog revealed a unique  conformational switching mechanism in which GTP binding to Arf triggers the exposure  of the proteins' membrane anchor--a myristoylated amino-terminal  -helix ( Fig. 1B) [ 34].	bind
40484	7	9520	7	NULL	NULL	0	NULL	statement 6	NULL		reveals	NULL				unique conformational switching mechanism	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1664_1_9_s_75	15238254	A comparison of Arf bound to GDP and to a nonhydrolyzable GTP analog revealed a unique  conformational switching mechanism in which GTP binding to Arf triggers the exposure  of the proteins' membrane anchor--a myristoylated amino-terminal  -helix ( Fig. 1B) [ 34].	bind
41423	1	9521	5	13	NULL	NULL	NULL	GAD65	GP		interact with		distinctly			PLP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1645_1_63_s_232	12535612	A comparison of binding and formation constants between GAD65 and GAD67 reveals that  the two isoforms interact distinctly with the cofactor PLP.	bind
41424	2	9521	5	13	NULL	NULL	NULL	GAD67	GP		interact with		distinctly			PLP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1645_1_63_s_232	12535612	A comparison of binding and formation constants between GAD65 and GAD67 reveals that  the two isoforms interact distinctly with the cofactor PLP.	bind
41425	3	9521	5	13	NULL	NULL	NULL	PLP	Chemical		is a type of					cofactor	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1645_1_63_s_232	12535612	A comparison of binding and formation constants between GAD65 and GAD67 reveals that  the two isoforms interact distinctly with the cofactor PLP.	bind
40612	1	9521	7	NULL	NULL	0	NULL	GAD65	NULL		interacts with	NULL	distinctly			PLP	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1645_1_63_s_232	12535612	A comparison of binding and formation constants between GAD65 and GAD67 reveals that  the two isoforms interact distinctly with the cofactor PLP.	bind
40613	2	9521	7	NULL	NULL	0	NULL	GAD67	NULL		interacts with	NULL	distinctly			PLP	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1645_1_63_s_232	12535612	A comparison of binding and formation constants between GAD65 and GAD67 reveals that  the two isoforms interact distinctly with the cofactor PLP.	bind
56798	3	9521	7	10	NULL	0	NULL	PLP			is a type of					cofactor					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1645_1_63_s_232	12535612	A comparison of binding and formation constants between GAD65 and GAD67 reveals that  the two isoforms interact distinctly with the cofactor PLP.	bind
41427	1	9523	5	13	NULL	NULL	NULL	DDT	Chemical		bind					EcTS	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_10_981_s_83	11590022	A comparison of DDT bound to EcTS to the antifolate ZD1694 bound to EcTS and hTS is shown in   Fig. 2 .	bind
41428	2	9523	5	13	NULL	NULL	NULL	ZD1694	Chemical		is a type of					antifolate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_10_981_s_83	11590022	A comparison of DDT bound to EcTS to the antifolate ZD1694 bound to EcTS and hTS is shown in   Fig. 2 .	bind
41429	3	9523	5	13	NULL	NULL	NULL	ZD1694	Chemical		bind					EcTS	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_10_981_s_83	11590022	A comparison of DDT bound to EcTS to the antifolate ZD1694 bound to EcTS and hTS is shown in   Fig. 2 .	bind
41430	4	9523	5	13	NULL	NULL	NULL	ZD1694	Chemical		bind					hTS	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_10_981_s_83	11590022	A comparison of DDT bound to EcTS to the antifolate ZD1694 bound to EcTS and hTS is shown in   Fig. 2 .	bind
40614	1	9523	7	NULL	NULL	0	NULL	DDT	NULL		bind	NULL				EcTS	NULL				NULL		0	NULL	NULL	NULL	gw60_chembiol_8_10_981_s_83	11590022	A comparison of DDT bound to EcTS to the antifolate ZD1694 bound to EcTS and hTS is shown in   Fig. 2 .	bind
40615	2	9523	7	10	NULL	0	NULL	ZD1694	NULL		bind	NULL				EcTS	NULL				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_10_981_s_83	11590022	A comparison of DDT bound to EcTS to the antifolate ZD1694 bound to EcTS and hTS is shown in   Fig. 2 .	bind
40616	3	9523	7	10	NULL	0	NULL	ZD1694	NULL		bind	NULL				hTS	NULL				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_10_981_s_83	11590022	A comparison of DDT bound to EcTS to the antifolate ZD1694 bound to EcTS and hTS is shown in   Fig. 2 .	bind
46865	4	9523	7	10	NULL	0	NULL	ZD1694	NULL		is a type of 	NULL				antifolate	NULL				NULL		0	NULL	NULL	NULL	gw60_chembiol_8_10_981_s_83	11590022	A comparison of DDT bound to EcTS to the antifolate ZD1694 bound to EcTS and hTS is shown in   Fig. 2 .	bind
41431	1	9524	5	13	NULL	NULL	NULL	flap endonuclease	GP		bind					pseudoY substrates	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_13_8542_s_9	12084915	A comparison of flap endonuclease binding to pseudoY substrates and duplexes with a single-stranded 5' overhang suggests a better model for 5' nuclease-DNA binding.	bind
41432	2	9524	5	13	NULL	NULL	NULL	flap endonuclease	GP		bind					duplexes	NucleicAcid			single-stranded 5' overhang	NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_13_8542_s_9	12084915	A comparison of flap endonuclease binding to pseudoY substrates and duplexes with a single-stranded 5' overhang suggests a better model for 5' nuclease-DNA binding.	bind
41433	3	9524	5	13	NULL	NULL	NULL	statement 1	Process		suggests					5' nuclease DNA	NucleicAcid	binding of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_13_8542_s_9	12084915	A comparison of flap endonuclease binding to pseudoY substrates and duplexes with a single-stranded 5' overhang suggests a better model for 5' nuclease-DNA binding.	bind
41434	4	9524	5	13	NULL	NULL	NULL	statement 1	Process		suggests					5' nuclease DNA	NucleicAcid	binding of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_13_8542_s_9	12084915	A comparison of flap endonuclease binding to pseudoY substrates and duplexes with a single-stranded 5' overhang suggests a better model for 5' nuclease-DNA binding.	bind
40617	1	9524	7	NULL	NULL	0	NULL	flap endonuclease	NULL		bind	NULL				pseudoY substrates	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_13_8542_s_9	12084915	A comparison of flap endonuclease binding to pseudoY substrates and duplexes with a single-stranded 5' overhang suggests a better model for 5' nuclease-DNA binding.	bind
40618	2	9524	7	NULL	NULL	0	NULL	flap endonuclease	NULL		bind	NULL				duplex	NULL			single-stranded 5' overhang	NULL		0	NULL	NULL	NULL	gw60_pnas_99_13_8542_s_9	12084915	A comparison of flap endonuclease binding to pseudoY substrates and duplexes with a single-stranded 5' overhang suggests a better model for 5' nuclease-DNA binding.	bind
40619	3	9524	7	NULL	NULL	0	NULL	statement 1	NULL		suggests	NULL				5'nuclease-DNA	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_pnas_99_13_8542_s_9	12084915	A comparison of flap endonuclease binding to pseudoY substrates and duplexes with a single-stranded 5' overhang suggests a better model for 5' nuclease-DNA binding.	bind
40620	4	9524	7	NULL	NULL	0	NULL	statement 2	NULL		suggests	NULL				5' nuclease-DNA	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_pnas_99_13_8542_s_9	12084915	A comparison of flap endonuclease binding to pseudoY substrates and duplexes with a single-stranded 5' overhang suggests a better model for 5' nuclease-DNA binding.	bind
41436	1	9525	5	13	NULL	NULL	NULL	Ugi	GP	[13C,15]	bind					Ung	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_34_21408_s_299	9261156	A comparison of free [15]Ugi (Fig.  9 A) to [13C,15]Ugi bound to Ung (Fig.  9 B) indicates that significant structural change of Ugi occurred as a consequence of complex formation.	bind
41437	2	9525	5	13	NULL	NULL	NULL	statement 1	Process		leads to					Ugi	GP	structural change of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_34_21408_s_299	9261156	A comparison of free [15]Ugi (Fig.  9 A) to [13C,15]Ugi bound to Ung (Fig.  9 B) indicates that significant structural change of Ugi occurred as a consequence of complex formation.	bind
56799	3	9525	5	13	NULL	NULL	NULL	Ugi	GP	free	bind					Ung	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_34_21408_s_299	9261156	A comparison of free [15]Ugi (Fig.  9 A) to [13C,15]Ugi bound to Ung (Fig.  9 B) indicates that significant structural change of Ugi occurred as a consequence of complex formation.	bind
40621	1	9525	7	10	NULL	0	NULL	Ugi	NULL	free	bind	NULL				Ung	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_34_21408_s_299	9261156	A comparison of free [15]Ugi (Fig.  9 A) to [13C,15]Ugi bound to Ung (Fig.  9 B) indicates that significant structural change of Ugi occurred as a consequence of complex formation.	bind
40622	2	9525	7	10	NULL	0	NULL	Ugi 	NULL	[13C,15]	bind	NULL				Ung	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_34_21408_s_299	9261156	A comparison of free [15]Ugi (Fig.  9 A) to [13C,15]Ugi bound to Ung (Fig.  9 B) indicates that significant structural change of Ugi occurred as a consequence of complex formation.	bind
40623	3	9525	7	10	NULL	0	NULL	statement 1			leads to					Ugi		structural change of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_34_21408_s_299	9261156	A comparison of free [15]Ugi (Fig.  9 A) to [13C,15]Ugi bound to Ung (Fig.  9 B) indicates that significant structural change of Ugi occurred as a consequence of complex formation.	bind
41438	1	9526	5	13	NULL	NULL	NULL	GST-FinO	GP		bind					FinP	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_15_10356_s_74	10187824	A comparison of GST-FinO binding affinities to FinP, SLI (nucleotides 1-34, Fig.  1) and SLII (nucleotides 35-79), which were transcribed from PCR-generated templates, is shown in Fig.  3.	bind
41439	2	9526	5	13	NULL	NULL	NULL	GST-FinO	GP		bind					SLI	NucleicAcid			nucleotides 1-34	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_15_10356_s_74	10187824	A comparison of GST-FinO binding affinities to FinP, SLI (nucleotides 1-34, Fig.  1) and SLII (nucleotides 35-79), which were transcribed from PCR-generated templates, is shown in Fig.  3.	bind
41440	3	9526	5	13	NULL	NULL	NULL	GST-FinO	GP		bind					SLII	NucleicAcid			nucleotides 35-79	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_15_10356_s_74	10187824	A comparison of GST-FinO binding affinities to FinP, SLI (nucleotides 1-34, Fig.  1) and SLII (nucleotides 35-79), which were transcribed from PCR-generated templates, is shown in Fig.  3.	bind
40625	1	9526	7	NULL	NULL	0	NULL	GST-FinO	NULL		bind	NULL				FinP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_15_10356_s_74	10187824	A comparison of GST-FinO binding affinities to FinP, SLI (nucleotides 1-34, Fig.  1) and SLII (nucleotides 35-79), which were transcribed from PCR-generated templates, is shown in Fig.  3.	bind
40626	2	9526	7	NULL	NULL	0	NULL	GST-FinO	NULL		bind	NULL				SL1	NULL			nucleotides 1-34	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_15_10356_s_74	10187824	A comparison of GST-FinO binding affinities to FinP, SLI (nucleotides 1-34, Fig.  1) and SLII (nucleotides 35-79), which were transcribed from PCR-generated templates, is shown in Fig.  3.	bind
40627	3	9526	7	NULL	NULL	0	NULL	GST-FinO	NULL		bind	NULL				SLII	NULL			nucleotides 35-79	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_15_10356_s_74	10187824	A comparison of GST-FinO binding affinities to FinP, SLI (nucleotides 1-34, Fig.  1) and SLII (nucleotides 35-79), which were transcribed from PCR-generated templates, is shown in Fig.  3.	bind
41441	1	9527	5	13	NULL	NULL	NULL	HIV-1 RT	GP		bind		effectively			ATP	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_plos-pathog_2_2_16485036_s_10	16485036	A comparison of HIV-1 and  HIV-2 RT shows that there are numerous differences in the putative ATP  binding sites that could explain why HIV-1 RT binds ATP more effectively.	bind
40628	1	9527	7	NULL	NULL	0	NULL	 HIV-1 RT	NULL		binds	NULL	effectively			ATP	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_plos-pathog_2_2_16485036_s_10	16485036	A comparison of HIV-1 and  HIV-2 RT shows that there are numerous differences in the putative ATP  binding sites that could explain why HIV-1 RT binds ATP more effectively.	bind
41442	1	9528	5	13	NULL	NULL	NULL	hMSH2	GP		bind					hMSH6	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_36_27851_s_79	10878012	A comparison of hMSH2-hMSH6 binding affinity suggests G/T   +CA > mG/T > mG/C   G/C.	bind
42417	2	9528	5	NULL	NULL	0	NULL		NULL	binding affinity of	greater than	NULL			G/T +CA		NULL	binding affinity of		mG/T	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27851_s_79	10878012	A comparison of hMSH2-hMSH6 binding affinity suggests G/T   +CA > mG/T > mG/C   G/C.	bind
42418	3	9528	5	13	NULL	NULL	NULL	statement 2	Process	binding affinity of	greater than							binding affinity of		mG/C	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_36_27851_s_79	10878012	A comparison of hMSH2-hMSH6 binding affinity suggests G/T   +CA > mG/T > mG/C   G/C.	bind
40630	1	9528	7	NULL	NULL	0	NULL	hMSH2	NULL		bind	NULL				hMSH6	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27851_s_79	10878012	A comparison of hMSH2-hMSH6 binding affinity suggests G/T   +CA > mG/T > mG/C   G/C.	bind
40631	2	9528	7	10	NULL	0	NULL			binding affinity of	is greater than				G/T +CA			binding affinity of		 mG/T	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_36_27851_s_79	10878012	A comparison of hMSH2-hMSH6 binding affinity suggests G/T   +CA > mG/T > mG/C   G/C.	bind
40632	3	9528	7	10	NULL	0	NULL	statement 2		binding affinity of	is greater than							binding affinity of		mG/C G/C	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_36_27851_s_79	10878012	A comparison of hMSH2-hMSH6 binding affinity suggests G/T   +CA > mG/T > mG/C   G/C.	bind
41443	1	9529	5	13	NULL	NULL	NULL	MARCKS	GP		bind			PSD		G-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_22351_s_162	11294839	A Comparison of MARCKS PSD Binding to F- and G-actin Reveals Localizing Interactions between MARCKS and F-actin-- Binding of the N-terminal PSD peptide to F-actin is increased relative to G-actin by a factor of less than 2 (Fig.  5 A,  inset).	bind
41444	2	9529	5	13	NULL	NULL	NULL	MARCKS	GP		bind			PSD		F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_22351_s_162	11294839	A Comparison of MARCKS PSD Binding to F- and G-actin Reveals Localizing Interactions between MARCKS and F-actin-- Binding of the N-terminal PSD peptide to F-actin is increased relative to G-actin by a factor of less than 2 (Fig.  5 A,  inset).	bind
41445	3	9529	5	13	NULL	NULL	NULL	PSD peptide	GP		bind			N-terminal		F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_22351_s_162	11294839	A Comparison of MARCKS PSD Binding to F- and G-actin Reveals Localizing Interactions between MARCKS and F-actin-- Binding of the N-terminal PSD peptide to F-actin is increased relative to G-actin by a factor of less than 2 (Fig.  5 A,  inset).	bind
41446	4	9529	5	13	NULL	NULL	NULL	PSD peptide	GP		bind			N-terminal		G-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_22351_s_162	11294839	A Comparison of MARCKS PSD Binding to F- and G-actin Reveals Localizing Interactions between MARCKS and F-actin-- Binding of the N-terminal PSD peptide to F-actin is increased relative to G-actin by a factor of less than 2 (Fig.  5 A,  inset).	bind
41447	5	9529	5	13	NULL	NULL	NULL	statement 3	Process		is relative to		increased			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_22351_s_162	11294839	A Comparison of MARCKS PSD Binding to F- and G-actin Reveals Localizing Interactions between MARCKS and F-actin-- Binding of the N-terminal PSD peptide to F-actin is increased relative to G-actin by a factor of less than 2 (Fig.  5 A,  inset).	bind
40635	1	9529	7	10	NULL	0	NULL	MARCKS 	NULL		bind	NULL		PSD		F-actin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_22351_s_162	11294839	A Comparison of MARCKS PSD Binding to F- and G-actin Reveals Localizing Interactions between MARCKS and F-actin-- Binding of the N-terminal PSD peptide to F-actin is increased relative to G-actin by a factor of less than 2 (Fig.  5 A,  inset).	bind
40636	2	9529	7	10	NULL	0	NULL	MARCKS	NULL		bind	NULL		PSD		G-actin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_22351_s_162	11294839	A Comparison of MARCKS PSD Binding to F- and G-actin Reveals Localizing Interactions between MARCKS and F-actin-- Binding of the N-terminal PSD peptide to F-actin is increased relative to G-actin by a factor of less than 2 (Fig.  5 A,  inset).	bind
40637	3	9529	7	NULL	NULL	0	NULL	PSD peptide	NULL		bind	NULL		N-terminal		F-actin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_25_22351_s_162	11294839	A Comparison of MARCKS PSD Binding to F- and G-actin Reveals Localizing Interactions between MARCKS and F-actin-- Binding of the N-terminal PSD peptide to F-actin is increased relative to G-actin by a factor of less than 2 (Fig.  5 A,  inset).	bind
40638	4	9529	7	NULL	NULL	0	NULL	PSD peptide	NULL		bind	NULL		N-terminal 		G-actin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_25_22351_s_162	11294839	A Comparison of MARCKS PSD Binding to F- and G-actin Reveals Localizing Interactions between MARCKS and F-actin-- Binding of the N-terminal PSD peptide to F-actin is increased relative to G-actin by a factor of less than 2 (Fig.  5 A,  inset).	bind
40639	5	9529	7	NULL	NULL	0	NULL	statement 3	NULL	binding of	is increased than	NULL				statement 4	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_25_22351_s_162	11294839	A Comparison of MARCKS PSD Binding to F- and G-actin Reveals Localizing Interactions between MARCKS and F-actin-- Binding of the N-terminal PSD peptide to F-actin is increased relative to G-actin by a factor of less than 2 (Fig.  5 A,  inset).	bind
41448	1	9530	5	13	NULL	NULL	NULL	p42Ets-1	GP		bind					DNA sequences	NucleicAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_oncogene_22_57_14668797_s_5	14668797	A comparison of optimal DNA-binding sites shows that  p42Ets-1 binds to more various DNA sequences than p51Ets-1; p42Ets-1 recognizes  the same optimal consensus sequence as p51Ets-1, but also many variations  of it, mainly at base -1, which is located just prior to the GGAA/T core  sequence.	bind
41449	2	9530	5	13	NULL	NULL	NULL	p51Ets-1	GP		bind					DNA sequences	NucleicAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_oncogene_22_57_14668797_s_5	14668797	A comparison of optimal DNA-binding sites shows that  p42Ets-1 binds to more various DNA sequences than p51Ets-1; p42Ets-1 recognizes  the same optimal consensus sequence as p51Ets-1, but also many variations  of it, mainly at base -1, which is located just prior to the GGAA/T core  sequence.	bind
40640	1	9530	7	10	NULL	0	NULL	p42Ets-1			binds to					consensus DNA sequence				 	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_oncogene_22_57_14668797_s_5	14668797	A comparison of optimal DNA-binding sites shows that  p42Ets-1 binds to more various DNA sequences than p51Ets-1; p42Ets-1 recognizes  the same optimal consensus sequence as p51Ets-1, but also many variations  of it, mainly at base -1, which is located just prior to the GGAA/T core  sequence.	bind
40641	2	9530	7	10	NULL	0	NULL	p51Ets-1			bind					consensus DNA sequence					NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_oncogene_22_57_14668797_s_5	14668797	A comparison of optimal DNA-binding sites shows that  p42Ets-1 binds to more various DNA sequences than p51Ets-1; p42Ets-1 recognizes  the same optimal consensus sequence as p51Ets-1, but also many variations  of it, mainly at base -1, which is located just prior to the GGAA/T core  sequence.	bind
41731	1	9531	5	13	NULL	NULL	NULL	Hsp90	GP		bind			Lys-40		PP5	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_43_40799_s_242	12145316	A comparison of our CyP40 mutational analysis data (Fig.  4) with that for PP5 ( 29) demonstrated complete concordance with the relative extent of Hsp90 binding to PP5, in that the status of nonbinding residues Lys-32, Lys-97, and Arg-101 (CyP40 residues Lys-227, Lys-308, and Arg-312, respectively), partial binders Arg-74 and Ile-63 (CyP40 residues Lys-285 and Ser-274, respectively), and the full binder Lys-40 (CyP40 residue Lys-235) was the same.	bind
42427	2	9531	5	13	NULL	NULL	NULL	PP5	GP		is not involved in			Lys-32		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_43_40799_s_242	12145316	A comparison of our CyP40 mutational analysis data (Fig.  4) with that for PP5 ( 29) demonstrated complete concordance with the relative extent of Hsp90 binding to PP5, in that the status of nonbinding residues Lys-32, Lys-97, and Arg-101 (CyP40 residues Lys-227, Lys-308, and Arg-312, respectively), partial binders Arg-74 and Ile-63 (CyP40 residues Lys-285 and Ser-274, respectively), and the full binder Lys-40 (CyP40 residue Lys-235) was the same.	bind
42428	3	9531	5	13	NULL	NULL	NULL	PP5	GP		is not involved in			Lys-97		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_43_40799_s_242	12145316	A comparison of our CyP40 mutational analysis data (Fig.  4) with that for PP5 ( 29) demonstrated complete concordance with the relative extent of Hsp90 binding to PP5, in that the status of nonbinding residues Lys-32, Lys-97, and Arg-101 (CyP40 residues Lys-227, Lys-308, and Arg-312, respectively), partial binders Arg-74 and Ile-63 (CyP40 residues Lys-285 and Ser-274, respectively), and the full binder Lys-40 (CyP40 residue Lys-235) was the same.	bind
42429	4	9531	5	13	NULL	NULL	NULL	PP5	GP		is not involved in			Arg-101		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_43_40799_s_242	12145316	A comparison of our CyP40 mutational analysis data (Fig.  4) with that for PP5 ( 29) demonstrated complete concordance with the relative extent of Hsp90 binding to PP5, in that the status of nonbinding residues Lys-32, Lys-97, and Arg-101 (CyP40 residues Lys-227, Lys-308, and Arg-312, respectively), partial binders Arg-74 and Ile-63 (CyP40 residues Lys-285 and Ser-274, respectively), and the full binder Lys-40 (CyP40 residue Lys-235) was the same.	bind
42430	5	9531	5	13	NULL	NULL	NULL	PP5	GP		is involved in		partially	Arg-74		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_43_40799_s_242	12145316	A comparison of our CyP40 mutational analysis data (Fig.  4) with that for PP5 ( 29) demonstrated complete concordance with the relative extent of Hsp90 binding to PP5, in that the status of nonbinding residues Lys-32, Lys-97, and Arg-101 (CyP40 residues Lys-227, Lys-308, and Arg-312, respectively), partial binders Arg-74 and Ile-63 (CyP40 residues Lys-285 and Ser-274, respectively), and the full binder Lys-40 (CyP40 residue Lys-235) was the same.	bind
42431	6	9531	5	13	NULL	NULL	NULL	PP5	GP		is involved in		partially	Ile-63		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_43_40799_s_242	12145316	A comparison of our CyP40 mutational analysis data (Fig.  4) with that for PP5 ( 29) demonstrated complete concordance with the relative extent of Hsp90 binding to PP5, in that the status of nonbinding residues Lys-32, Lys-97, and Arg-101 (CyP40 residues Lys-227, Lys-308, and Arg-312, respectively), partial binders Arg-74 and Ile-63 (CyP40 residues Lys-285 and Ser-274, respectively), and the full binder Lys-40 (CyP40 residue Lys-235) was the same.	bind
40643	1	9531	7	NULL	NULL	0	NULL	Hsp90	NULL		bind	NULL		Lys-40		PP5	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_43_40799_s_242	12145316	A comparison of our CyP40 mutational analysis data (Fig.  4) with that for PP5 ( 29) demonstrated complete concordance with the relative extent of Hsp90 binding to PP5, in that the status of nonbinding residues Lys-32, Lys-97, and Arg-101 (CyP40 residues Lys-227, Lys-308, and Arg-312, respectively), partial binders Arg-74 and Ile-63 (CyP40 residues Lys-285 and Ser-274, respectively), and the full binder Lys-40 (CyP40 residue Lys-235) was the same.	bind
40644	2	9531	7	NULL	NULL	0	NULL	PP5	NULL		is not involved in	NULL		Lys-32		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_43_40799_s_242	12145316	A comparison of our CyP40 mutational analysis data (Fig.  4) with that for PP5 ( 29) demonstrated complete concordance with the relative extent of Hsp90 binding to PP5, in that the status of nonbinding residues Lys-32, Lys-97, and Arg-101 (CyP40 residues Lys-227, Lys-308, and Arg-312, respectively), partial binders Arg-74 and Ile-63 (CyP40 residues Lys-285 and Ser-274, respectively), and the full binder Lys-40 (CyP40 residue Lys-235) was the same.	bind
40645	3	9531	7	NULL	NULL	0	NULL	PP5	NULL		is not involved in	NULL		Lys-97		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_43_40799_s_242	12145316	A comparison of our CyP40 mutational analysis data (Fig.  4) with that for PP5 ( 29) demonstrated complete concordance with the relative extent of Hsp90 binding to PP5, in that the status of nonbinding residues Lys-32, Lys-97, and Arg-101 (CyP40 residues Lys-227, Lys-308, and Arg-312, respectively), partial binders Arg-74 and Ile-63 (CyP40 residues Lys-285 and Ser-274, respectively), and the full binder Lys-40 (CyP40 residue Lys-235) was the same.	bind
40646	4	9531	7	NULL	NULL	0	NULL	PP5	NULL		is not involved in	NULL		 Arg-101		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_43_40799_s_242	12145316	A comparison of our CyP40 mutational analysis data (Fig.  4) with that for PP5 ( 29) demonstrated complete concordance with the relative extent of Hsp90 binding to PP5, in that the status of nonbinding residues Lys-32, Lys-97, and Arg-101 (CyP40 residues Lys-227, Lys-308, and Arg-312, respectively), partial binders Arg-74 and Ile-63 (CyP40 residues Lys-285 and Ser-274, respectively), and the full binder Lys-40 (CyP40 residue Lys-235) was the same.	bind
40647	5	9531	7	NULL	NULL	0	NULL	PP5	NULL		is involved in	NULL	partially	Arg-74		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_43_40799_s_242	12145316	A comparison of our CyP40 mutational analysis data (Fig.  4) with that for PP5 ( 29) demonstrated complete concordance with the relative extent of Hsp90 binding to PP5, in that the status of nonbinding residues Lys-32, Lys-97, and Arg-101 (CyP40 residues Lys-227, Lys-308, and Arg-312, respectively), partial binders Arg-74 and Ile-63 (CyP40 residues Lys-285 and Ser-274, respectively), and the full binder Lys-40 (CyP40 residue Lys-235) was the same.	bind
40648	6	9531	7	NULL	NULL	0	NULL	PP5	NULL		is involved in	NULL	partially	Ile-63		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_43_40799_s_242	12145316	A comparison of our CyP40 mutational analysis data (Fig.  4) with that for PP5 ( 29) demonstrated complete concordance with the relative extent of Hsp90 binding to PP5, in that the status of nonbinding residues Lys-32, Lys-97, and Arg-101 (CyP40 residues Lys-227, Lys-308, and Arg-312, respectively), partial binders Arg-74 and Ile-63 (CyP40 residues Lys-285 and Ser-274, respectively), and the full binder Lys-40 (CyP40 residue Lys-235) was the same.	bind
41453	1	9532	5	13	NULL	NULL	NULL	p47	GP		bind			C terminus		p97	GP		ND1		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_5_1030_s_68	14988733	A comparison of p47 C bound to p97 ND1 with the solution structure of p47 UBX ( Figure 2A,  Table II) shows differences in the N-terminal part, which may be due to the shorter fragment  used for the solution structure determination (282 370).	bind
40649	1	9532	7	10	NULL	0	NULL	 p47	NULL		binds to	NULL		 C terminus		p97 	NULL		ND1		NULL		NULL	NULL	NULL	NULL	gw70_embo_23_5_1030_s_68	14988733	A comparison of p47 C bound to p97 ND1 with the solution structure of p47 UBX ( Figure 2A,  Table II) shows differences in the N-terminal part, which may be due to the shorter fragment  used for the solution structure determination (282 370).	bind
41454	1	9533	5	13	NULL	NULL	NULL	R1	GP		bind					AMA1	GP	recombinant;;P. falciparum			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6981_s_151	16177378	A comparison of R1 binding to recombinant AMA1 from four different lines of  P. falciparum demonstrated that R1 recognizes AMA1 from the D10 line of  P. falciparum, as well as 3D7  PfAMA1, the form of the antigen used for panning.	bind
41455	2	9533	5	13	NULL	NULL	NULL	R1	GP		recognizes					AMA1	GP	D10 line of P. falciparum			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6981_s_151	16177378	A comparison of R1 binding to recombinant AMA1 from four different lines of  P. falciparum demonstrated that R1 recognizes AMA1 from the D10 line of  P. falciparum, as well as 3D7  PfAMA1, the form of the antigen used for panning.	bind
41456	3	9533	5	13	NULL	NULL	NULL	R1	GP		recognizes					AMA1	GP	3D7;; P. falciparum			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6981_s_151	16177378	A comparison of R1 binding to recombinant AMA1 from four different lines of  P. falciparum demonstrated that R1 recognizes AMA1 from the D10 line of  P. falciparum, as well as 3D7  PfAMA1, the form of the antigen used for panning.	bind
40650	1	9533	7	10	NULL	0	NULL	R1	NULL		bind	NULL				AMA1	NULL	recombinant;; P. falciparum			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6981_s_151	16177378	A comparison of R1 binding to recombinant AMA1 from four different lines of  P. falciparum demonstrated that R1 recognizes AMA1 from the D10 line of  P. falciparum, as well as 3D7  PfAMA1, the form of the antigen used for panning.	bind
40651	2	9533	7	10	NULL	0	NULL	R1	NULL		recognizes	NULL				AMA1	NULL	D10 line of P. falciparum			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6981_s_151	16177378	A comparison of R1 binding to recombinant AMA1 from four different lines of  P. falciparum demonstrated that R1 recognizes AMA1 from the D10 line of  P. falciparum, as well as 3D7  PfAMA1, the form of the antigen used for panning.	bind
40652	3	9533	7	10	NULL	0	NULL	R1	NULL		recognizes	NULL				AMA1	NULL	3D7;; P. falciparum			NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_73_10_6981_s_151	16177378	A comparison of R1 binding to recombinant AMA1 from four different lines of  P. falciparum demonstrated that R1 recognizes AMA1 from the D10 line of  P. falciparum, as well as 3D7  PfAMA1, the form of the antigen used for panning.	bind
41459	1	9534	5	13	NULL	NULL	NULL	SAP	GP		bind					laminin	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2143_s_118	8999915	A comparison of SAP binding to human and mouse laminin indicates that SAP binding to human laminin is lower than SAP binding to mouse laminin (Fig.  3 A).	bind
41460	2	9534	5	13	NULL	NULL	NULL	SAP	GP		bind					laminin	GP	mouse			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2143_s_118	8999915	A comparison of SAP binding to human and mouse laminin indicates that SAP binding to human laminin is lower than SAP binding to mouse laminin (Fig.  3 A).	bind
41461	3	9534	5	13	NULL	NULL	NULL	statement 1	Process		lower than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2143_s_118	8999915	A comparison of SAP binding to human and mouse laminin indicates that SAP binding to human laminin is lower than SAP binding to mouse laminin (Fig.  3 A).	bind
40653	1	9534	7	NULL	NULL	0	NULL	SAP	NULL		bind	NULL				laminin	NULL	human			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_4_2143_s_118	8999915	A comparison of SAP binding to human and mouse laminin indicates that SAP binding to human laminin is lower than SAP binding to mouse laminin (Fig.  3 A).	bind
40654	2	9534	7	NULL	NULL	0	NULL	SAP	NULL		bind	NULL				laminin	NULL	mouse			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_4_2143_s_118	8999915	A comparison of SAP binding to human and mouse laminin indicates that SAP binding to human laminin is lower than SAP binding to mouse laminin (Fig.  3 A).	bind
40655	3	9534	7	NULL	NULL	0	NULL	statement 1	NULL	binding of	is lower than	NULL				statement 2	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_4_2143_s_118	8999915	A comparison of SAP binding to human and mouse laminin indicates that SAP binding to human laminin is lower than SAP binding to mouse laminin (Fig.  3 A).	bind
41462	1	9535	5	13	NULL	NULL	NULL	SHC	GP		bind			PTB domain		substrates	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_9_1134_s_41	8805372	A comparison of SHC and NUMB PTB domains shows that amino acids critical for the binding of the SHC PTB domain to tyrosine-phosphorylated substrates are conserved in the mNUMB protein    [24-26]   (  Figure 1c).	bind
41463	2	9535	5	13	NULL	NULL	NULL	SHC	GP		is conserved in			amino acid PTB domain		mNUMB protein	GP		amino acid PTB domain		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_9_1134_s_41	8805372	A comparison of SHC and NUMB PTB domains shows that amino acids critical for the binding of the SHC PTB domain to tyrosine-phosphorylated substrates are conserved in the mNUMB protein    [24-26]   (  Figure 1c).	bind
56903	3	9535	5	13	NULL	NULL	NULL	mNUMB protein	GP		bind			PTB domain		substrates	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_9_1134_s_41	8805372	A comparison of SHC and NUMB PTB domains shows that amino acids critical for the binding of the SHC PTB domain to tyrosine-phosphorylated substrates are conserved in the mNUMB protein    [24-26]   (  Figure 1c).	bind
40656	1	9535	7	NULL	NULL	0	NULL	SHC	NULL		bind	NULL		PTB domain		substrates	NULL	phosphorylated	tyrosine		NULL		0	NULL	NULL	NULL	gw60_currbiol_6_9_1134_s_41	8805372	A comparison of SHC and NUMB PTB domains shows that amino acids critical for the binding of the SHC PTB domain to tyrosine-phosphorylated substrates are conserved in the mNUMB protein    [24-26]   (  Figure 1c).	bind
40657	2	9535	7	NULL	NULL	0	NULL	mNUMB protein	NULL		bind	NULL		PTB domain		substrates	NULL	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_9_1134_s_41	8805372	A comparison of SHC and NUMB PTB domains shows that amino acids critical for the binding of the SHC PTB domain to tyrosine-phosphorylated substrates are conserved in the mNUMB protein    [24-26]   (  Figure 1c).	bind
40658	3	9535	7	NULL	NULL	0	NULL	SHC	NULL		is conserved in	NULL		aminoacid PTB domain		mNUMB protein	NULL		aminoacid PTB domain		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_9_1134_s_41	8805372	A comparison of SHC and NUMB PTB domains shows that amino acids critical for the binding of the SHC PTB domain to tyrosine-phosphorylated substrates are conserved in the mNUMB protein    [24-26]   (  Figure 1c).	bind
41464	1	9536	5	13	NULL	NULL	NULL	T1E	GP		bind					ErbB1	GP		Domain I		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_39114_s_169	12869572	A Comparison of T1E Binding to ErbB1 Domain I and ErbB3 Domain I -- T1E is unique in its properties since it can bind both to ErbB1 and ErbB3.	bind
41465	2	9536	5	13	NULL	NULL	NULL	T1E	GP		bind					ErbB3	GP		Domain I		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_39114_s_169	12869572	A Comparison of T1E Binding to ErbB1 Domain I and ErbB3 Domain I -- T1E is unique in its properties since it can bind both to ErbB1 and ErbB3.	bind
40659	1	9536	7	NULL	NULL	0	NULL	 T1E	NULL		bind	NULL				 ErbB1	NULL		Domain I		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_40_39114_s_169	12869572	A Comparison of T1E Binding to ErbB1 Domain I and ErbB3 Domain I -- T1E is unique in its properties since it can bind both to ErbB1 and ErbB3.	bind
40660	2	9536	7	NULL	NULL	0	NULL	T1E	NULL		bind	NULL				ErbB3	NULL		Domain I		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_40_39114_s_169	12869572	A Comparison of T1E Binding to ErbB1 Domain I and ErbB3 Domain I -- T1E is unique in its properties since it can bind both to ErbB1 and ErbB3.	bind
41466	1	9537	5	13	NULL	NULL	NULL	holo-Tf	GP		bind					TfR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_22_16618_s_203	10748106	A comparison of Tf binding to TfR1 and TfR2-alpha cells found that the affinity of holo-Tf for TfR2-alpha was substantially lower than for TfR1.	bind
41467	2	9537	5	13	NULL	NULL	NULL	holo-Tf	GP		bind					TfR2-alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_22_16618_s_203	10748106	A comparison of Tf binding to TfR1 and TfR2-alpha cells found that the affinity of holo-Tf for TfR2-alpha was substantially lower than for TfR1.	bind
41468	3	9537	5	13	NULL	NULL	NULL	statement 2	Process		lower than		substantially			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_22_16618_s_203	10748106	A comparison of Tf binding to TfR1 and TfR2-alpha cells found that the affinity of holo-Tf for TfR2-alpha was substantially lower than for TfR1.	bind
40661	1	9537	7	10	NULL	0	NULL	holo-Tf			bind					TfR1-alpha cells					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_22_16618_s_203	10748106	A comparison of Tf binding to TfR1 and TfR2-alpha cells found that the affinity of holo-Tf for TfR2-alpha was substantially lower than for TfR1.	bind
40662	2	9537	7	10	NULL	0	NULL	holo-Tf			bind					TfR2-alpha cells					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_22_16618_s_203	10748106	A comparison of Tf binding to TfR1 and TfR2-alpha cells found that the affinity of holo-Tf for TfR2-alpha was substantially lower than for TfR1.	bind
40664	3	9537	7	10	NULL	0	NULL	statement 2		affinity of 	is lower than		substantially			statement 3		affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_22_16618_s_203	10748106	A comparison of Tf binding to TfR1 and TfR2-alpha cells found that the affinity of holo-Tf for TfR2-alpha was substantially lower than for TfR1.	bind
41469	1	9538	5	13	NULL	NULL	NULL	ASA-BZ-photolabeled peptides 	GP	H. contortus	bind		weakly	N-terminal 63-103		tubulin	GP	mammalian			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_15_8575_s_247	8621485	A comparison of the  amino acid sequence of ASA-BZ-photolabeled peptides (N-terminal  63-103) of  H. contortus  to bovine or human beta-tubulin  show two different amino acid residues (Ala    Gln and  Leu    Ile) that could confer weaker binding of BZ to  mammalian tubulin.	bind
40665	1	9538	7	10	NULL	0	NULL	ASA-BZ-photolabeled peptides 		H. contortus	bind		weakly	N-terminal 63-103		tubulin		mammalian			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_15_8575_s_247	8621485	A comparison of the  amino acid sequence of ASA-BZ-photolabeled peptides (N-terminal  63-103) of  H. contortus  to bovine or human beta-tubulin  show two different amino acid residues (Ala    Gln and  Leu    Ile) that could confer weaker binding of BZ to  mammalian tubulin.	bind
41470	1	9539	5	13	NULL	NULL	NULL	scFv	GP	bivalent	bind					BSA-A-trisaccharide	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2059_s_144	11679577	A comparison of the  K D values for bivalent scFv binding with BSA-A-trisaccharide  versus monovalent trisaccharide binding to scFv indicated that the avidity gain afforded by bivalency was ~75-fold for the L(103H)I and L(103H)V mutants.	bind
41471	2	9539	5	13	NULL	NULL	NULL	trisaccharide	Chemical	monovalent	bind					scFv	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2059_s_144	11679577	A comparison of the  K D values for bivalent scFv binding with BSA-A-trisaccharide  versus monovalent trisaccharide binding to scFv indicated that the avidity gain afforded by bivalency was ~75-fold for the L(103H)I and L(103H)V mutants.	bind
41704	3	9539	5	13	NULL	NULL	NULL	scFv	GP	bivalent;;mutant	increase			L(103H)I		statement 1	Process	avidity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2059_s_144	11679577	A comparison of the  K D values for bivalent scFv binding with BSA-A-trisaccharide  versus monovalent trisaccharide binding to scFv indicated that the avidity gain afforded by bivalency was ~75-fold for the L(103H)I and L(103H)V mutants.	bind
41705	4	9539	5	13	NULL	NULL	NULL	scFv	GP	bivalent;;mutant	increase			L(103H)V		statement 1	Process	avidity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2059_s_144	11679577	A comparison of the  K D values for bivalent scFv binding with BSA-A-trisaccharide  versus monovalent trisaccharide binding to scFv indicated that the avidity gain afforded by bivalency was ~75-fold for the L(103H)I and L(103H)V mutants.	bind
40670	1	9539	7	10	NULL	0	NULL	scFv		bivalent 	bind					BSA-A-trisaccharide					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2059_s_144	11679577	A comparison of the  K D values for bivalent scFv binding with BSA-A-trisaccharide  versus monovalent trisaccharide binding to scFv indicated that the avidity gain afforded by bivalency was ~75-fold for the L(103H)I and L(103H)V mutants.	bind
40671	2	9539	7	10	NULL	0	NULL	scFv			bind					 trisaccharide		monovalent			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2059_s_144	11679577	A comparison of the  K D values for bivalent scFv binding with BSA-A-trisaccharide  versus monovalent trisaccharide binding to scFv indicated that the avidity gain afforded by bivalency was ~75-fold for the L(103H)I and L(103H)V mutants.	bind
40672	3	9539	7	10	NULL	0	NULL	scFv		bivalent;;mutant	increase			L(103H)I		statement 1		avidity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2059_s_144	11679577	A comparison of the  K D values for bivalent scFv binding with BSA-A-trisaccharide  versus monovalent trisaccharide binding to scFv indicated that the avidity gain afforded by bivalency was ~75-fold for the L(103H)I and L(103H)V mutants.	bind
40673	4	9539	7	10	NULL	0	NULL	scFv		bivalent;;mutant	increase			 L(103H)V		statement 1		avidity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2059_s_144	11679577	A comparison of the  K D values for bivalent scFv binding with BSA-A-trisaccharide  versus monovalent trisaccharide binding to scFv indicated that the avidity gain afforded by bivalency was ~75-fold for the L(103H)I and L(103H)V mutants.	bind
41474	1	9541	5	13	NULL	NULL	NULL	cyt 	GP		bind		exclusively	b6 subunit		complex	GP	all pigments of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1506_1_55_s_226	11418097	A comparison of the absorbance spectra and the pigment analyses of all protein-containing fractions obtained from anion exchange HPLC indicates that the cyt  b6 subunit exclusively binds all pigments of the complex.	bind
40677	1	9541	7	NULL	NULL	0	NULL	cyt	NULL		binds	NULL	exclusively	b6 subunit		complex	NULL	pigments of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1506_1_55_s_226	11418097	A comparison of the absorbance spectra and the pigment analyses of all protein-containing fractions obtained from anion exchange HPLC indicates that the cyt  b6 subunit exclusively binds all pigments of the complex.	bind
41722	1	9543	5	13	NULL	NULL	NULL	CheY	GP		is involved in			amino acid side chains		metal	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_febslett_441_2_242_s_165	9883892	A comparison of the amino acid side chains involved in metal binding between CheY and PhoB reveals that they are identical except for the substitution of a glutamate residue at position 9 of PhoB which corresponds to Asp-12 of CheY [ 15,  32].	bind
41725	2	9543	5	13	NULL	NULL	NULL	PhoB	GP		is involved in			amino acid side chains		metal	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_febslett_441_2_242_s_165	9883892	A comparison of the amino acid side chains involved in metal binding between CheY and PhoB reveals that they are identical except for the substitution of a glutamate residue at position 9 of PhoB which corresponds to Asp-12 of CheY [ 15,  32].	bind
41726	3	9543	5	13	NULL	NULL	NULL	statement 1	Process		is identical to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_441_2_242_s_165	9883892	A comparison of the amino acid side chains involved in metal binding between CheY and PhoB reveals that they are identical except for the substitution of a glutamate residue at position 9 of PhoB which corresponds to Asp-12 of CheY [ 15,  32].	bind
41729	4	9543	5	13	NULL	NULL	NULL	PhoB	GP	substitution of	corresponds to			glutamate residue at position 9		CheY	GP		Asp-12		NULL		NULL	NULL	NULL	NULL	gw60_febslett_441_2_242_s_165	9883892	A comparison of the amino acid side chains involved in metal binding between CheY and PhoB reveals that they are identical except for the substitution of a glutamate residue at position 9 of PhoB which corresponds to Asp-12 of CheY [ 15,  32].	bind
41730	5	9543	5	13	NULL	NULL	NULL	statement 4	Process		is an exception for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_441_2_242_s_165	9883892	A comparison of the amino acid side chains involved in metal binding between CheY and PhoB reveals that they are identical except for the substitution of a glutamate residue at position 9 of PhoB which corresponds to Asp-12 of CheY [ 15,  32].	bind
40680	1	9543	7	NULL	NULL	0	NULL	CheY	NULL		bind	NULL		amino acid side chain		metal	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_441_2_242_s_165	9883892	A comparison of the amino acid side chains involved in metal binding between CheY and PhoB reveals that they are identical except for the substitution of a glutamate residue at position 9 of PhoB which corresponds to Asp-12 of CheY [ 15,  32].	bind
40681	2	9543	7	NULL	NULL	0	NULL	PhoB	NULL		bind	NULL		amino acid side chain		metal	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_441_2_242_s_165	9883892	A comparison of the amino acid side chains involved in metal binding between CheY and PhoB reveals that they are identical except for the substitution of a glutamate residue at position 9 of PhoB which corresponds to Asp-12 of CheY [ 15,  32].	bind
40682	3	9543	7	NULL	NULL	0	NULL	PhoB	NULL		differs as	NULL		glutamate residue at position 9		CheY	NULL		Asp-12		NULL		NULL	NULL	NULL	NULL	gw60_febslett_441_2_242_s_165	9883892	A comparison of the amino acid side chains involved in metal binding between CheY and PhoB reveals that they are identical except for the substitution of a glutamate residue at position 9 of PhoB which corresponds to Asp-12 of CheY [ 15,  32].	bind
40683	4	9543	7	NULL	NULL	0	NULL	statement 1	NULL	binding of	is similar to	NULL				statement 2	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_febslett_441_2_242_s_165	9883892	A comparison of the amino acid side chains involved in metal binding between CheY and PhoB reveals that they are identical except for the substitution of a glutamate residue at position 9 of PhoB which corresponds to Asp-12 of CheY [ 15,  32].	bind
40684	5	9543	7	NULL	NULL	0	NULL	statement 4	NULL		ocurs in exception with	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_441_2_242_s_165	9883892	A comparison of the amino acid side chains involved in metal binding between CheY and PhoB reveals that they are identical except for the substitution of a glutamate residue at position 9 of PhoB which corresponds to Asp-12 of CheY [ 15,  32].	bind
41484	1	9545	5	13	NULL	NULL	NULL	E.coli helicases	GP	binding activity of	is similar to					Pseudomonas sp. helicases	GP	binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_12_3262_s_95	11406602	A comparison of the binding activity of the  E. coliand  Pseudomonas sp. helicases by surface plasmon resonance (SPR) analysis (Figure  3H) produced similar results.	bind
41682	1	9545	7	10	NULL	0	NULL	E.coli helicases	NULL	binding activity of	is similar to	NULL				Pseudomonas sp. helicases	NULL	binding activity of 			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_12_3262_s_95	11406602	A comparison of the binding activity of the  E. coliand  Pseudomonas sp. helicases by surface plasmon resonance (SPR) analysis (Figure  3H) produced similar results.	bind
41485	1	9548	5	13	NULL	NULL	NULL	naphthalene	Chemical		bind					NDO	GP		active site		NULL		NULL	NULL	NULL	NULL	gw70_science_299_5609_1039_s_55	12586937	A comparison of the binding of  naphthalene and indole ( 22) in the active site of NDO shows that they bind similarly (fig. S4).	bind
41486	2	9548	5	13	NULL	NULL	NULL	indole	Chemical		bind					NDO	GP		active site		NULL		NULL	NULL	NULL	NULL	gw70_science_299_5609_1039_s_55	12586937	A comparison of the binding of  naphthalene and indole ( 22) in the active site of NDO shows that they bind similarly (fig. S4).	bind
41487	3	9548	5	13	NULL	NULL	NULL	statement 1	Process		similar to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_science_299_5609_1039_s_55	12586937	A comparison of the binding of  naphthalene and indole ( 22) in the active site of NDO shows that they bind similarly (fig. S4).	bind
41683	1	9548	7	NULL	NULL	0	NULL	naphthalene 	NULL		bind	NULL				NDO	NULL		active site		NULL		0	NULL	NULL	NULL	gw70_science_299_5609_1039_s_55	12586937	A comparison of the binding of  naphthalene and indole ( 22) in the active site of NDO shows that they bind similarly (fig. S4).	bind
41684	2	9548	7	NULL	NULL	0	NULL	 indole	NULL		bind	NULL				NDO	NULL		active site		NULL		0	NULL	NULL	NULL	gw70_science_299_5609_1039_s_55	12586937	A comparison of the binding of  naphthalene and indole ( 22) in the active site of NDO shows that they bind similarly (fig. S4).	bind
41685	3	9548	7	NULL	NULL	0	NULL	statement 1	NULL		is similar to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_science_299_5609_1039_s_55	12586937	A comparison of the binding of  naphthalene and indole ( 22) in the active site of NDO shows that they bind similarly (fig. S4).	bind
41488	1	9549	5	13	NULL	NULL	NULL	P12a peptide	GP		bind					protein 4.1	GP		30-kDa domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_715_s_111	7822301	A comparison of the binding of  peptides P12a and P12m to the 30-kDa domain of protein 4.1 indicated  that the substitution of alanine (RYMYAAAGTYHT) for RHK completely  abolished the association of the 30-kDa domain of protein 4.1 with  peptide P12a (data not shown).	bind
41489	2	9549	5	13	NULL	NULL	NULL	P12m peptide	GP		bind					protein 4.1	GP		30-kDa domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_715_s_111	7822301	A comparison of the binding of  peptides P12a and P12m to the 30-kDa domain of protein 4.1 indicated  that the substitution of alanine (RYMYAAAGTYHT) for RHK completely  abolished the association of the 30-kDa domain of protein 4.1 with  peptide P12a (data not shown).	bind
41490	3	9549	5	13	NULL	NULL	NULL	alanine	AminoAcid		is substituted for			RYMYAAAGTYHT		RHK	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_715_s_111	7822301	A comparison of the binding of  peptides P12a and P12m to the 30-kDa domain of protein 4.1 indicated  that the substitution of alanine (RYMYAAAGTYHT) for RHK completely  abolished the association of the 30-kDa domain of protein 4.1 with  peptide P12a (data not shown).	bind
41491	4	9549	5	13	NULL	NULL	NULL	statement 3	Process		abolishes		completely			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_715_s_111	7822301	A comparison of the binding of  peptides P12a and P12m to the 30-kDa domain of protein 4.1 indicated  that the substitution of alanine (RYMYAAAGTYHT) for RHK completely  abolished the association of the 30-kDa domain of protein 4.1 with  peptide P12a (data not shown).	bind
40761	1	9549	7	NULL	NULL	0	NULL	P12a peptide	NULL		bind	NULL				protein 4.1	NULL		30-kDa domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_2_715_s_111	7822301	A comparison of the binding of  peptides P12a and P12m to the 30-kDa domain of protein 4.1 indicated  that the substitution of alanine (RYMYAAAGTYHT) for RHK completely  abolished the association of the 30-kDa domain of protein 4.1 with  peptide P12a (data not shown).	bind
40762	2	9549	7	NULL	NULL	0	NULL	P12m peptide	NULL		bind	NULL				protein 4.1	NULL		30-kDa domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_2_715_s_111	7822301	A comparison of the binding of  peptides P12a and P12m to the 30-kDa domain of protein 4.1 indicated  that the substitution of alanine (RYMYAAAGTYHT) for RHK completely  abolished the association of the 30-kDa domain of protein 4.1 with  peptide P12a (data not shown).	bind
40763	3	9549	7	NULL	NULL	0	NULL		NULL		substituted with	NULL		RHK		Alanine	NULL		RYMYAAAGTYHT		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_2_715_s_111	7822301	A comparison of the binding of  peptides P12a and P12m to the 30-kDa domain of protein 4.1 indicated  that the substitution of alanine (RYMYAAAGTYHT) for RHK completely  abolished the association of the 30-kDa domain of protein 4.1 with  peptide P12a (data not shown).	bind
40764	4	9549	7	NULL	NULL	0	NULL	statement 3	NULL		abolishes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_2_715_s_111	7822301	A comparison of the binding of  peptides P12a and P12m to the 30-kDa domain of protein 4.1 indicated  that the substitution of alanine (RYMYAAAGTYHT) for RHK completely  abolished the association of the 30-kDa domain of protein 4.1 with  peptide P12a (data not shown).	bind
41493	1	9550	5	13	NULL	NULL	NULL	L1 sequence	GP		bind					RTP dimers	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_12_8771_s_121	11124956	A comparison of the binding profiles of L1 with L1 core supports the conclusion that the complete L1 sequence bound to two dimers RTP.	bind
40765	1	9550	7	10	NULL	0	NULL	L1 sequence			bind					dimers RTP					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_12_8771_s_121	11124956	A comparison of the binding profiles of L1 with L1 core supports the conclusion that the complete L1 sequence bound to two dimers RTP.	bind
41494	1	9551	5	13	NULL	NULL	NULL	AP-1	GP		bind					CD-MPR	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_22_23542_s_40	15044437	A comparison of the binding properties of AP-1 and GGA1 to the CD-MPR revealed subtle but essential differences.	bind
41495	2	9551	5	13	NULL	NULL	NULL	GGA1	GP		bind					CD-MPR	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_22_23542_s_40	15044437	A comparison of the binding properties of AP-1 and GGA1 to the CD-MPR revealed subtle but essential differences.	bind
40766	1	9551	7	NULL	NULL	0	NULL	AP-1	NULL		bind	NULL				CD-MPR	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_22_23542_s_40	15044437	A comparison of the binding properties of AP-1 and GGA1 to the CD-MPR revealed subtle but essential differences.	bind
40767	2	9551	7	NULL	NULL	0	NULL	 GGA1	NULL		bind	NULL				CD-MPR	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_22_23542_s_40	15044437	A comparison of the binding properties of AP-1 and GGA1 to the CD-MPR revealed subtle but essential differences.	bind
41497	1	9553	5	13	NULL	NULL	NULL				bind			Y782F		ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3446_s_212	9920889	A comparison of the chemical quench and pulse-chase results indicates that Y782F binds two ATP with a high commitment for catalysis, just as the wild type enzyme.	bind
41498	2	9553	5	13	NULL	NULL	NULL	statement 1	Process		commitment for		high			catalysis	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3446_s_212	9920889	A comparison of the chemical quench and pulse-chase results indicates that Y782F binds two ATP with a high commitment for catalysis, just as the wild type enzyme.	bind
40774	1	9553	7	NULL	NULL	0	NULL		NULL		binds	NULL		 Y782F		ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3446_s_212	9920889	A comparison of the chemical quench and pulse-chase results indicates that Y782F binds two ATP with a high commitment for catalysis, just as the wild type enzyme.	bind
40775	2	9553	7	10	NULL	0	NULL	statement 1	NULL		commitment for	NULL	high 			catalysis	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3446_s_212	9920889	A comparison of the chemical quench and pulse-chase results indicates that Y782F binds two ATP with a high commitment for catalysis, just as the wild type enzyme.	bind
41500	1	9554	5	13	NULL	NULL	NULL	U1-A	GP		bind			N-terminal RRM		U1	GP		SLII		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_17_3057_s_240	16096647	A comparison of the cocrystals of the N-terminal RRM of U1-A and U2-B"` bound  to U1 SLII and U2 SLIV, respectively, indicates that snRNA discrimination by U1-A  and U2-B"` is the result of the formation of a different network of multiple  hydrogen-bonding interactions between the RNA and protein (  et al;   et al).	bind
41501	2	9554	5	13	NULL	NULL	NULL	U2-B	GP		bind			N-terminal RRM		U2	GP		SLIV		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_17_3057_s_240	16096647	A comparison of the cocrystals of the N-terminal RRM of U1-A and U2-B"` bound  to U1 SLII and U2 SLIV, respectively, indicates that snRNA discrimination by U1-A  and U2-B"` is the result of the formation of a different network of multiple  hydrogen-bonding interactions between the RNA and protein (  et al;   et al).	bind
41502	3	9554	5	13	NULL	NULL	NULL	U1-A	GP		discriminates					snRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_17_3057_s_240	16096647	A comparison of the cocrystals of the N-terminal RRM of U1-A and U2-B"` bound  to U1 SLII and U2 SLIV, respectively, indicates that snRNA discrimination by U1-A  and U2-B"` is the result of the formation of a different network of multiple  hydrogen-bonding interactions between the RNA and protein (  et al;   et al).	bind
41503	4	9554	5	13	NULL	NULL	NULL	U2-B	GP		discriminates					snRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_17_3057_s_240	16096647	A comparison of the cocrystals of the N-terminal RRM of U1-A and U2-B"` bound  to U1 SLII and U2 SLIV, respectively, indicates that snRNA discrimination by U1-A  and U2-B"` is the result of the formation of a different network of multiple  hydrogen-bonding interactions between the RNA and protein (  et al;   et al).	bind
41504	5	9554	5	13	NULL	NULL	NULL	RNA	NucleicAcid		interact with					protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_17_3057_s_240	16096647	A comparison of the cocrystals of the N-terminal RRM of U1-A and U2-B"` bound  to U1 SLII and U2 SLIV, respectively, indicates that snRNA discrimination by U1-A  and U2-B"` is the result of the formation of a different network of multiple  hydrogen-bonding interactions between the RNA and protein (  et al;   et al).	bind
41505	6	9554	5	13	NULL	NULL	NULL	statement 5	Process		forms					multiple hydrogen-bonding interactions	Process	different network of			NULL		NULL	NULL	NULL	NULL	gw70_embo_24_17_3057_s_240	16096647	A comparison of the cocrystals of the N-terminal RRM of U1-A and U2-B"` bound  to U1 SLII and U2 SLIV, respectively, indicates that snRNA discrimination by U1-A  and U2-B"` is the result of the formation of a different network of multiple  hydrogen-bonding interactions between the RNA and protein (  et al;   et al).	bind
41506	7	9554	5	13	NULL	NULL	NULL	statement 6	Process		results in					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_17_3057_s_240	16096647	A comparison of the cocrystals of the N-terminal RRM of U1-A and U2-B"` bound  to U1 SLII and U2 SLIV, respectively, indicates that snRNA discrimination by U1-A  and U2-B"` is the result of the formation of a different network of multiple  hydrogen-bonding interactions between the RNA and protein (  et al;   et al).	bind
41507	8	9554	5	13	NULL	NULL	NULL	statement 6	Process		results in					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_17_3057_s_240	16096647	A comparison of the cocrystals of the N-terminal RRM of U1-A and U2-B"` bound  to U1 SLII and U2 SLIV, respectively, indicates that snRNA discrimination by U1-A  and U2-B"` is the result of the formation of a different network of multiple  hydrogen-bonding interactions between the RNA and protein (  et al;   et al).	bind
40776	1	9554	7	NULL	NULL	0	NULL	U1-A	NULL		bind	NULL		N-terminal RRM		 U1 SLII	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_17_3057_s_240	16096647	A comparison of the cocrystals of the N-terminal RRM of U1-A and U2-B"` bound  to U1 SLII and U2 SLIV, respectively, indicates that snRNA discrimination by U1-A  and U2-B"` is the result of the formation of a different network of multiple  hydrogen-bonding interactions between the RNA and protein (  et al;   et al).	bind
40777	2	9554	7	NULL	NULL	0	NULL	U2-B	NULL		bind	NULL		N-terminal RRM		U2 SLIV	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_17_3057_s_240	16096647	A comparison of the cocrystals of the N-terminal RRM of U1-A and U2-B"` bound  to U1 SLII and U2 SLIV, respectively, indicates that snRNA discrimination by U1-A  and U2-B"` is the result of the formation of a different network of multiple  hydrogen-bonding interactions between the RNA and protein (  et al;   et al).	bind
40779	7	9554	7	NULL	NULL	0	NULL	statement 3	NULL		is the result of	NULL				multiple hydrogen-bonding interactions 	NULL				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_17_3057_s_240	16096647	A comparison of the cocrystals of the N-terminal RRM of U1-A and U2-B"` bound  to U1 SLII and U2 SLIV, respectively, indicates that snRNA discrimination by U1-A  and U2-B"` is the result of the formation of a different network of multiple  hydrogen-bonding interactions between the RNA and protein (  et al;   et al).	bind
40780	8	9554	7	NULL	NULL	0	NULL	statement 4	NULL		is the result of	NULL				multiple hydrogen-bonding interactions 	NULL				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_17_3057_s_240	16096647	A comparison of the cocrystals of the N-terminal RRM of U1-A and U2-B"` bound  to U1 SLII and U2 SLIV, respectively, indicates that snRNA discrimination by U1-A  and U2-B"` is the result of the formation of a different network of multiple  hydrogen-bonding interactions between the RNA and protein (  et al;   et al).	bind
40781	3	9554	7	NULL	NULL	0	NULL	U1-A	NULL		discriminates	NULL				snRNA	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_17_3057_s_240	16096647	A comparison of the cocrystals of the N-terminal RRM of U1-A and U2-B"` bound  to U1 SLII and U2 SLIV, respectively, indicates that snRNA discrimination by U1-A  and U2-B"` is the result of the formation of a different network of multiple  hydrogen-bonding interactions between the RNA and protein (  et al;   et al).	bind
40782	4	9554	7	NULL	NULL	0	NULL	U2-B	NULL		discriminates	NULL				snRNA	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_17_3057_s_240	16096647	A comparison of the cocrystals of the N-terminal RRM of U1-A and U2-B"` bound  to U1 SLII and U2 SLIV, respectively, indicates that snRNA discrimination by U1-A  and U2-B"` is the result of the formation of a different network of multiple  hydrogen-bonding interactions between the RNA and protein (  et al;   et al).	bind
40783	5	9554	7	NULL	NULL	0	NULL	statement 1	NULL		indicates	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_17_3057_s_240	16096647	A comparison of the cocrystals of the N-terminal RRM of U1-A and U2-B"` bound  to U1 SLII and U2 SLIV, respectively, indicates that snRNA discrimination by U1-A  and U2-B"` is the result of the formation of a different network of multiple  hydrogen-bonding interactions between the RNA and protein (  et al;   et al).	bind
40786	6	9554	7	NULL	NULL	0	NULL	statement 2	NULL		indicates	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_17_3057_s_240	16096647	A comparison of the cocrystals of the N-terminal RRM of U1-A and U2-B"` bound  to U1 SLII and U2 SLIV, respectively, indicates that snRNA discrimination by U1-A  and U2-B"` is the result of the formation of a different network of multiple  hydrogen-bonding interactions between the RNA and protein (  et al;   et al).	bind
41508	1	9555	5	13	NULL	NULL	NULL	SptP	GP		bind					Rac1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_6_1449_s_173	11163217	A comparison of the crystal structure of the SptP monomer with that of SptP bound to Rac1 reveals marked structural changes.	bind
40788	1	9555	7	NULL	NULL	0	NULL	SptP	NULL		bind	NULL				Rac1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_6_6_1449_s_173	11163217	A comparison of the crystal structure of the SptP monomer with that of SptP bound to Rac1 reveals marked structural changes.	bind
41509	1	9556	5	13	NULL	NULL	NULL	CFR	GP		bind					FGFs	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5167_s_244	9030584	A comparison of the crystal structures for FGFR and CFR bound to FGFs will aid in the elucidation of the role(s) of CFR in FGF action.	bind
46866	2	9556	5	13	NULL	NULL	NULL	FGF	GP		bind					FGFR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5167_s_244	9030584	A comparison of the crystal structures for FGFR and CFR bound to FGFs will aid in the elucidation of the role(s) of CFR in FGF action.	bind
40789	1	9556	7	NULL	NULL	0	NULL	FGFs	NULL		bind	NULL				FGFR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_5167_s_244	9030584	A comparison of the crystal structures for FGFR and CFR bound to FGFs will aid in the elucidation of the role(s) of CFR in FGF action.	bind
40790	2	9556	7	NULL	NULL	0	NULL	FGFs	NULL		bind	NULL				CFR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_5167_s_244	9030584	A comparison of the crystal structures for FGFR and CFR bound to FGFs will aid in the elucidation of the role(s) of CFR in FGF action.	bind
41510	1	9557	5	13	NULL	NULL	NULL	C/EBP	GP		is a type of					bZip protein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_nucleic-acids-res_23_20_7479080_s_1	7479080	A comparison of the different DNA binding specificities of the bZip proteins C/EBP and GCN4..	bind
41511	2	9557	5	13	NULL	NULL	NULL	GCN4	GP		is a type of					bZip protein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_nucleic-acids-res_23_20_7479080_s_1	7479080	A comparison of the different DNA binding specificities of the bZip proteins C/EBP and GCN4..	bind
41512	3	9557	5	13	NULL	NULL	NULL	C/EBP	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_nucleic-acids-res_23_20_7479080_s_1	7479080	A comparison of the different DNA binding specificities of the bZip proteins C/EBP and GCN4..	bind
41513	4	9557	5	13	NULL	NULL	NULL	GCN4	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_nucleic-acids-res_23_20_7479080_s_1	7479080	A comparison of the different DNA binding specificities of the bZip proteins C/EBP and GCN4..	bind
40791	1	9557	7	NULL	NULL	0	NULL	C/EBP	NULL		binds	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_nucleic-acids-res_23_20_7479080_s_1	7479080	A comparison of the different DNA binding specificities of the bZip proteins C/EBP and GCN4..	bind
40792	2	9557	7	NULL	NULL	0	NULL	GCN4	NULL		binds	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_nucleic-acids-res_23_20_7479080_s_1	7479080	A comparison of the different DNA binding specificities of the bZip proteins C/EBP and GCN4..	bind
40793	3	9557	7	NULL	NULL	0	NULL	 C/EBP 	NULL		is a type of	NULL				bZip proteins	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_nucleic-acids-res_23_20_7479080_s_1	7479080	A comparison of the different DNA binding specificities of the bZip proteins C/EBP and GCN4..	bind
40794	4	9557	7	NULL	NULL	0	NULL	GCN4	NULL		is a type of	NULL				bZip proteins	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_nucleic-acids-res_23_20_7479080_s_1	7479080	A comparison of the different DNA binding specificities of the bZip proteins C/EBP and GCN4..	bind
41514	1	9558	5	13	NULL	NULL	NULL	aflatoxin	Chemical		bind					DNA	NucleicAcid	liver			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_cancer-res_52_2_1728400_s_9	1728400	A comparison of the dose-dependent residual levels of aflatoxin  binding to liver DNA with the amount of aflatoxin-N7-guanine excreted  in urine showed a correlation coefficient of 0.98.	bind
40795	1	9558	7	NULL	NULL	0	NULL	aflatoxin	NULL		bind	NULL				liver DNA	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_cancer-res_52_2_1728400_s_9	1728400	A comparison of the dose-dependent residual levels of aflatoxin  binding to liver DNA with the amount of aflatoxin-N7-guanine excreted  in urine showed a correlation coefficient of 0.98.	bind
41516	1	9560	5	13	NULL	NULL	NULL	FKBP12	GP		bind					FK506	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_96_3_425_s_172	10025408	A Comparison of the FKBP12 - FK506  and FKBP12 - TbetaR-I Complexes A surface representation of FKBP12 bound to FK506 is shown  to the left (Wilson et al., 1995   ).	bind
41517	2	9560	5	13	NULL	NULL	NULL	FKBP12	GP		bind					TbetaR-I	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_96_3_425_s_172	10025408	A Comparison of the FKBP12 - FK506  and FKBP12 - TbetaR-I Complexes A surface representation of FKBP12 bound to FK506 is shown  to the left (Wilson et al., 1995   ).	bind
40797	1	9560	7	NULL	NULL	0	NULL	FKBP12	NULL		complex with	NULL				FK506	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cell_96_3_425_s_172	10025408	A Comparison of the FKBP12 - FK506  and FKBP12 - TbetaR-I Complexes A surface representation of FKBP12 bound to FK506 is shown  to the left (Wilson et al., 1995   ).	bind
40798	2	9560	7	NULL	NULL	0	NULL	FKBP12	NULL		complex with	NULL				TbetaR-I	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_96_3_425_s_172	10025408	A Comparison of the FKBP12 - FK506  and FKBP12 - TbetaR-I Complexes A surface representation of FKBP12 bound to FK506 is shown  to the left (Wilson et al., 1995   ).	bind
41518	1	9561	5	13	NULL	NULL	NULL	P450s	GP		is involved in					trichothecene biosynthetic pathway	Process				NULL		NULL	NULL	NULL	NULL	gw70_applenvironmicrob_70_4_2044_s_235	15066795	A comparison of the heme-binding motifs of several different P450s involved in the trichothecene biosynthetic pathway from  F. sporotrichioides and  F. graminearum shows the conservation of residues in this 20-amino-acid region.	bind
41519	2	9561	5	13	NULL	NULL	NULL	P450s	GP	F. sporotrichioides	conserved in			heme-binding motif		P450s	GP	F. graminearum	heme-binding motif		NULL		NULL	NULL	NULL	NULL	gw70_applenvironmicrob_70_4_2044_s_235	15066795	A comparison of the heme-binding motifs of several different P450s involved in the trichothecene biosynthetic pathway from  F. sporotrichioides and  F. graminearum shows the conservation of residues in this 20-amino-acid region.	bind
40800	1	9561	7	10	NULL	0	NULL	P450s			is involved in			 heme-binding motif		trichothecene biosynthetic pathway					NULL		NULL	NULL	NULL	NULL	gw70_applenvironmicrob_70_4_2044_s_235	15066795	A comparison of the heme-binding motifs of several different P450s involved in the trichothecene biosynthetic pathway from  F. sporotrichioides and  F. graminearum shows the conservation of residues in this 20-amino-acid region.	bind
40802	2	9561	7	10	NULL	0	NULL	P450s		F. sporotrichioides	is conserved with			20-amino-acid region heme-binding motif		P450s		 F. graminearum 	20-amino-acid region heme-binding motif		NULL		NULL	NULL	NULL	NULL	gw70_applenvironmicrob_70_4_2044_s_235	15066795	A comparison of the heme-binding motifs of several different P450s involved in the trichothecene biosynthetic pathway from  F. sporotrichioides and  F. graminearum shows the conservation of residues in this 20-amino-acid region.	bind
41710	1	9562	5	13	NULL	NULL	NULL	Fim3	GP		is a type of					fimbrial subunit	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_5_2256_s_10	9573115	A comparison of the heparin binding regions of Fim2 with homologous regions of Fim3 and FimX, two closely related but antigenically distinct fimbrial subunits, showed that basic amino acids and tyrosines are generally conserved.	bind
41711	2	9562	5	13	NULL	NULL	NULL	FimX	GP		is a type of					fimbrial subunit	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_5_2256_s_10	9573115	A comparison of the heparin binding regions of Fim2 with homologous regions of Fim3 and FimX, two closely related but antigenically distinct fimbrial subunits, showed that basic amino acids and tyrosines are generally conserved.	bind
41712	3	9562	5	13	NULL	NULL	NULL	Fim3	GP		is related to		closely			FimX	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_5_2256_s_10	9573115	A comparison of the heparin binding regions of Fim2 with homologous regions of Fim3 and FimX, two closely related but antigenically distinct fimbrial subunits, showed that basic amino acids and tyrosines are generally conserved.	bind
41713	4	9562	5	13	NULL	NULL	NULL	Fim3	GP		is distinct from		antigenically			FimX	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_5_2256_s_10	9573115	A comparison of the heparin binding regions of Fim2 with homologous regions of Fim3 and FimX, two closely related but antigenically distinct fimbrial subunits, showed that basic amino acids and tyrosines are generally conserved.	bind
41716	5	9562	5	13	NULL	NULL	NULL	Fim2	GP		is conserved in			basic amino acids in heparin binding regions		Fim3	GP		heparin binding regions		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_5_2256_s_10	9573115	A comparison of the heparin binding regions of Fim2 with homologous regions of Fim3 and FimX, two closely related but antigenically distinct fimbrial subunits, showed that basic amino acids and tyrosines are generally conserved.	bind
41717	6	9562	5	13	NULL	NULL	NULL	Fim2	GP		is conserved in			basic amino acids in heparin binding regions		FimX	GP		heparin binding regions		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_5_2256_s_10	9573115	A comparison of the heparin binding regions of Fim2 with homologous regions of Fim3 and FimX, two closely related but antigenically distinct fimbrial subunits, showed that basic amino acids and tyrosines are generally conserved.	bind
41718	7	9562	5	13	NULL	NULL	NULL	Fim2	GP		is conserved in			tyrosines in heparin binding regions		Fim3	GP		heparin binding regions		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_5_2256_s_10	9573115	A comparison of the heparin binding regions of Fim2 with homologous regions of Fim3 and FimX, two closely related but antigenically distinct fimbrial subunits, showed that basic amino acids and tyrosines are generally conserved.	bind
41719	8	9562	5	13	NULL	NULL	NULL	Fim2	GP		is conserved in			tyrosines in heparin binding regions		FimX	GP		heparin binding regions		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_5_2256_s_10	9573115	A comparison of the heparin binding regions of Fim2 with homologous regions of Fim3 and FimX, two closely related but antigenically distinct fimbrial subunits, showed that basic amino acids and tyrosines are generally conserved.	bind
40821	1	9562	7	NULL	NULL	0	NULL	Fim2	NULL		is conserved with	NULL		basic amino acid in heparin binding region		Fim3	NULL		basic amino acid in heparin binding region		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_5_2256_s_10	9573115	A comparison of the heparin binding regions of Fim2 with homologous regions of Fim3 and FimX, two closely related but antigenically distinct fimbrial subunits, showed that basic amino acids and tyrosines are generally conserved.	bind
40822	2	9562	7	NULL	NULL	0	NULL	Fim2	NULL		is conserved with	NULL		basic amino acid in heparin binding region 		FimX	NULL		basic amino acid in heparin binding region 		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_5_2256_s_10	9573115	A comparison of the heparin binding regions of Fim2 with homologous regions of Fim3 and FimX, two closely related but antigenically distinct fimbrial subunits, showed that basic amino acids and tyrosines are generally conserved.	bind
46962	3	9562	7	NULL	NULL	0	NULL	Fim2	NULL		is conserved with	NULL		tyrosine in heparin binding region		Fim3	NULL		tyrosine in heparin binding region		NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_5_2256_s_10	9573115	A comparison of the heparin binding regions of Fim2 with homologous regions of Fim3 and FimX, two closely related but antigenically distinct fimbrial subunits, showed that basic amino acids and tyrosines are generally conserved.	bind
46963	4	9562	7	NULL	NULL	0	NULL	Fim2	NULL		is conserved with	NULL		tyrosine in heparin binding region		FimX	NULL		tyrosine in heparin binding region		NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_5_2256_s_10	9573115	A comparison of the heparin binding regions of Fim2 with homologous regions of Fim3 and FimX, two closely related but antigenically distinct fimbrial subunits, showed that basic amino acids and tyrosines are generally conserved.	bind
46964	5	9562	7	NULL	NULL	0	NULL	Fim3	NULL		is a type of	NULL				fimbrial subunit	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_5_2256_s_10	9573115	A comparison of the heparin binding regions of Fim2 with homologous regions of Fim3 and FimX, two closely related but antigenically distinct fimbrial subunits, showed that basic amino acids and tyrosines are generally conserved.	bind
46965	6	9562	7	NULL	NULL	0	NULL	FimX	NULL		is a type of	NULL				fimbrial subunit	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_5_2256_s_10	9573115	A comparison of the heparin binding regions of Fim2 with homologous regions of Fim3 and FimX, two closely related but antigenically distinct fimbrial subunits, showed that basic amino acids and tyrosines are generally conserved.	bind
46966	7	9562	7	NULL	NULL	0	NULL	Fim3	NULL		related to	NULL	closely			FimX	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_5_2256_s_10	9573115	A comparison of the heparin binding regions of Fim2 with homologous regions of Fim3 and FimX, two closely related but antigenically distinct fimbrial subunits, showed that basic amino acids and tyrosines are generally conserved.	bind
46967	8	9562	7	NULL	NULL	0	NULL	Fim3	NULL		is distinct from	NULL	antigenically			FimX	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_5_2256_s_10	9573115	A comparison of the heparin binding regions of Fim2 with homologous regions of Fim3 and FimX, two closely related but antigenically distinct fimbrial subunits, showed that basic amino acids and tyrosines are generally conserved.	bind
41521	1	9564	5	13	NULL	NULL	NULL	H3	GP	hyperacetylated	bind					betaA-globin DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_37_34810_s_175	11435438	A comparison of the hybridization signal intensities of the three probes in the input and acetylated H3-immunoprecipitated DNA fractions showed that hyperacetylated H3 was bound to betaA-globin and epsilon-globin DNA but not to vitellogenin DNA.	bind
41522	2	9564	5	13	NULL	NULL	NULL	H3	GP	hyperacetylated	bind					epsilon-globin DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_37_34810_s_175	11435438	A comparison of the hybridization signal intensities of the three probes in the input and acetylated H3-immunoprecipitated DNA fractions showed that hyperacetylated H3 was bound to betaA-globin and epsilon-globin DNA but not to vitellogenin DNA.	bind
41523	3	9564	5	13	NULL	NULL	NULL	H3	GP	hyperacetylated	does not bind					vitellogenin DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_37_34810_s_175	11435438	A comparison of the hybridization signal intensities of the three probes in the input and acetylated H3-immunoprecipitated DNA fractions showed that hyperacetylated H3 was bound to betaA-globin and epsilon-globin DNA but not to vitellogenin DNA.	bind
40829	1	9564	7	10	NULL	0	NULL	betaA-globin 			bind					H3		 hyperacetylated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_37_34810_s_175	11435438	A comparison of the hybridization signal intensities of the three probes in the input and acetylated H3-immunoprecipitated DNA fractions showed that hyperacetylated H3 was bound to betaA-globin and epsilon-globin DNA but not to vitellogenin DNA.	bind
40831	2	9564	7	10	NULL	0	NULL	H3		hyperacetylated 	bind					epsilon-globin DNA					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_37_34810_s_175	11435438	A comparison of the hybridization signal intensities of the three probes in the input and acetylated H3-immunoprecipitated DNA fractions showed that hyperacetylated H3 was bound to betaA-globin and epsilon-globin DNA but not to vitellogenin DNA.	bind
40832	3	9564	7	10	NULL	0	NULL	H3		hyperacetylated 	does not bind					vitellogenin DNA					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_37_34810_s_175	11435438	A comparison of the hybridization signal intensities of the three probes in the input and acetylated H3-immunoprecipitated DNA fractions showed that hyperacetylated H3 was bound to betaA-globin and epsilon-globin DNA but not to vitellogenin DNA.	bind
41524	1	9565	5	13	NULL	NULL	NULL	MMP-2C	GP		complex with			inhibitor binding pocket		SC-74020	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1598_1_10_s_274	12147339	A comparison of the inhibitor binding pocket of the MMP-2C solution structure (magenta) and the MMP-8 crystal structure (purple) complexed to SC-74020.	bind
41525	2	9565	5	13	NULL	NULL	NULL	MMP-8	GP		complex with			inhibitor binding pocket		SC-74020	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1598_1_10_s_274	12147339	A comparison of the inhibitor binding pocket of the MMP-2C solution structure (magenta) and the MMP-8 crystal structure (purple) complexed to SC-74020.	bind
40833	1	9565	7	NULL	NULL	0	NULL	MMP-2C	NULL		complex with	NULL		inhibitor binding pocket		SC-74020	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1598_1_10_s_274	12147339	A comparison of the inhibitor binding pocket of the MMP-2C solution structure (magenta) and the MMP-8 crystal structure (purple) complexed to SC-74020.	bind
40834	2	9565	7	NULL	NULL	0	NULL	MMP-8 	NULL		complex with	NULL		inhibitor binding pocket		SC-74020	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1598_1_10_s_274	12147339	A comparison of the inhibitor binding pocket of the MMP-2C solution structure (magenta) and the MMP-8 crystal structure (purple) complexed to SC-74020.	bind
41751	1	9566	5	13	NULL	NULL	NULL	QacR	GP		is a type of					repressor protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_611	12456787	A comparison of the ligand-binding domains of the QacR repressor and BmrR activator proteins reveals that although that of QacR is completely helical in nature ( ), whereas BmrR is predominantly beta-sheet ( ), the two proteins have notable similarities, including the aromatic, hydrophobic, and negatively charged residues that line their binding pockets as well as the crucial role played by tyrosines (see below).	bind
41752	2	9566	5	13	NULL	NULL	NULL	BmrR	GP		is a type of					activator protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_611	12456787	A comparison of the ligand-binding domains of the QacR repressor and BmrR activator proteins reveals that although that of QacR is completely helical in nature ( ), whereas BmrR is predominantly beta-sheet ( ), the two proteins have notable similarities, including the aromatic, hydrophobic, and negatively charged residues that line their binding pockets as well as the crucial role played by tyrosines (see below).	bind
41754	3	9566	5	13	NULL	NULL	NULL	QacR	GP		exhibits			ligand-binding domain		helical structure	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_611	12456787	A comparison of the ligand-binding domains of the QacR repressor and BmrR activator proteins reveals that although that of QacR is completely helical in nature ( ), whereas BmrR is predominantly beta-sheet ( ), the two proteins have notable similarities, including the aromatic, hydrophobic, and negatively charged residues that line their binding pockets as well as the crucial role played by tyrosines (see below).	bind
41760	4	9566	5	13	NULL	NULL	NULL	BmrR	GP		exhibits			ligand-binding domain		beta-sheet structure	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_611	12456787	A comparison of the ligand-binding domains of the QacR repressor and BmrR activator proteins reveals that although that of QacR is completely helical in nature ( ), whereas BmrR is predominantly beta-sheet ( ), the two proteins have notable similarities, including the aromatic, hydrophobic, and negatively charged residues that line their binding pockets as well as the crucial role played by tyrosines (see below).	bind
41761	5	9566	5	13	NULL	NULL	NULL	QacR	GP		is similar to			aromatic;;hydrophobic;;negatively charged residues		BmrR	GP		aromatic;;hydrophobic;;negatively charged residues		NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_611	12456787	A comparison of the ligand-binding domains of the QacR repressor and BmrR activator proteins reveals that although that of QacR is completely helical in nature ( ), whereas BmrR is predominantly beta-sheet ( ), the two proteins have notable similarities, including the aromatic, hydrophobic, and negatively charged residues that line their binding pockets as well as the crucial role played by tyrosines (see below).	bind
41681	1	9566	7	10	NULL	0	NULL	QacR	NULL		is similar to	NULL		aromatic;;hydrophobic;;negatively charged residues		BmrR	NULL		aromatic;;hydrophobic;;negatively charged residues		NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_611	12456787	A comparison of the ligand-binding domains of the QacR repressor and BmrR activator proteins reveals that although that of QacR is completely helical in nature ( ), whereas BmrR is predominantly beta-sheet ( ), the two proteins have notable similarities, including the aromatic, hydrophobic, and negatively charged residues that line their binding pockets as well as the crucial role played by tyrosines (see below).	bind
48097	2	9566	7	10	NULL	0	NULL	QacR	NULL		is a type of	NULL				repressor	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_611	12456787	A comparison of the ligand-binding domains of the QacR repressor and BmrR activator proteins reveals that although that of QacR is completely helical in nature ( ), whereas BmrR is predominantly beta-sheet ( ), the two proteins have notable similarities, including the aromatic, hydrophobic, and negatively charged residues that line their binding pockets as well as the crucial role played by tyrosines (see below).	bind
48098	3	9566	7	10	NULL	0	NULL	BmrR	NULL		is a type of	NULL				activator	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_611	12456787	A comparison of the ligand-binding domains of the QacR repressor and BmrR activator proteins reveals that although that of QacR is completely helical in nature ( ), whereas BmrR is predominantly beta-sheet ( ), the two proteins have notable similarities, including the aromatic, hydrophobic, and negatively charged residues that line their binding pockets as well as the crucial role played by tyrosines (see below).	bind
48099	4	9566	7	10	NULL	0	NULL	QacR	NULL		exhibit	NULL		ligand-binding domain		helical structure	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_611	12456787	A comparison of the ligand-binding domains of the QacR repressor and BmrR activator proteins reveals that although that of QacR is completely helical in nature ( ), whereas BmrR is predominantly beta-sheet ( ), the two proteins have notable similarities, including the aromatic, hydrophobic, and negatively charged residues that line their binding pockets as well as the crucial role played by tyrosines (see below).	bind
48100	5	9566	7	10	NULL	0	NULL	BmrR	NULL		exhibit	NULL		ligand-binding domain		beta-sheet	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_611	12456787	A comparison of the ligand-binding domains of the QacR repressor and BmrR activator proteins reveals that although that of QacR is completely helical in nature ( ), whereas BmrR is predominantly beta-sheet ( ), the two proteins have notable similarities, including the aromatic, hydrophobic, and negatively charged residues that line their binding pockets as well as the crucial role played by tyrosines (see below).	bind
41526	1	9568	5	13	NULL	NULL	NULL	v -src	GP		bind					Cx43	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_5_1033_s_271	10085299	A comparison of the loss of v -src binding to Cx43 and its  functional effect on channel gating	bind
41527	2	9568	5	13	NULL	NULL	NULL	statement 1	Process	loss of	effect					channel gating	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_5_1033_s_271	10085299	A comparison of the loss of v -src binding to Cx43 and its  functional effect on channel gating	bind
40840	1	9568	7	NULL	NULL	0	NULL	v -src	NULL		does not bind	NULL				Cx43	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_144_5_1033_s_271	10085299	A comparison of the loss of v -src binding to Cx43 and its  functional effect on channel gating	bind
40841	2	9568	7	10	NULL	0	NULL	statement 1		loss of 	effect					channel gating					NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_5_1033_s_271	10085299	A comparison of the loss of v -src binding to Cx43 and its  functional effect on channel gating	bind
41534	1	9570	5	13	NULL	NULL	NULL	formate	Chemical		bind					apo-MhFbpA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_12_3903_s_179	15175304	A comparison of the MhFbpAFeCO3 and formate-bound apo-MhFbpA structures reveals that anion-bound MhFbpA positions all of the iron-binding protein ligands within 0.5  Ang  of their positions in the ferric ion-bound state.	bind
41535	2	9570	5	13	NULL	NULL	NULL	FeCO3	Chemical		bind					MhFbpA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_12_3903_s_179	15175304	A comparison of the MhFbpAFeCO3 and formate-bound apo-MhFbpA structures reveals that anion-bound MhFbpA positions all of the iron-binding protein ligands within 0.5  Ang  of their positions in the ferric ion-bound state.	bind
40843	1	9570	7	NULL	NULL	0	NULL	formate	NULL		bind	NULL				apo-MhFbpA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_12_3903_s_179	15175304	A comparison of the MhFbpAFeCO3 and formate-bound apo-MhFbpA structures reveals that anion-bound MhFbpA positions all of the iron-binding protein ligands within 0.5  Ang  of their positions in the ferric ion-bound state.	bind
40844	2	9570	7	NULL	NULL	0	NULL	FeCO3	NULL		bind	NULL				MhFbpA 	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_12_3903_s_179	15175304	A comparison of the MhFbpAFeCO3 and formate-bound apo-MhFbpA structures reveals that anion-bound MhFbpA positions all of the iron-binding protein ligands within 0.5  Ang  of their positions in the ferric ion-bound state.	bind
41742	1	9571	5	13	NULL	NULL	NULL	USH-F9	GP		is similar to			NF binding faces		C32H	GP		NF binding faces		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_38_35720_s_327	12110675	A comparison of the NF binding faces of USH-F9 and C32H shows that, with the exception of the two aromatics, the binding faces are otherwise largely unperturbed.	bind
41743	2	9571	5	13	NULL	NULL	NULL	USH-F9	GP		differs from			aromatics		USH-F9	GP		NF binding face		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_38_35720_s_327	12110675	A comparison of the NF binding faces of USH-F9 and C32H shows that, with the exception of the two aromatics, the binding faces are otherwise largely unperturbed.	bind
41694	1	9571	7	NULL	NULL	0	NULL	USH-F9	NULL		is similar to	NULL		NF binding face		C32H	NULL		NF binding face		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_38_35720_s_327	12110675	A comparison of the NF binding faces of USH-F9 and C32H shows that, with the exception of the two aromatics, the binding faces are otherwise largely unperturbed.	bind
41695	2	9571	7	NULL	NULL	0	NULL	USH-F9	NULL		differs 	NULL		aromatics		C32H	NULL		aromatics		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_38_35720_s_327	12110675	A comparison of the NF binding faces of USH-F9 and C32H shows that, with the exception of the two aromatics, the binding faces are otherwise largely unperturbed.	bind
41537	1	9572	5	13	NULL	NULL	NULL	SSB1	GP		bind					ssDNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3270_s_157	11470885	A comparison of the NTD with itself gave a DALI score of 24, while a comparison of the NTD with an SSB1 structure bound to ssDNA gave a DALI score of 4.1, with a root mean square difference (r.m.s.d.) in the average alpha carbon positions of 3.9  Ang .	bind
40845	1	9572	7	NULL	NULL	0	NULL	SSB1	NULL		bind	NULL				ssDNA	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_15_3270_s_157	11470885	A comparison of the NTD with itself gave a DALI score of 24, while a comparison of the NTD with an SSB1 structure bound to ssDNA gave a DALI score of 4.1, with a root mean square difference (r.m.s.d.) in the average alpha carbon positions of 3.9  Ang .	bind
41538	1	9573	5	13	NULL	NULL	NULL	scFv clones	GP		bind		irreversibly			CRA I	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20436_s_158	12668670	A comparison of the peptide-MCA cleaving activity  (Glu-Ala-Arg-MCA substrate) and irreversible CRA  I binding by the scFv  clones indicated a strong correlation ( p < 0.005,   r2 = 0.77) ( Fig.  4 B), confirming the functional importance of superior  nucleophilic reactivity.	bind
41540	2	9573	5	13	NULL	NULL	NULL	statement 1	Process		confirms					superior nucleophilic reactivity	Process	importance of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_22_20436_s_158	12668670	A comparison of the peptide-MCA cleaving activity  (Glu-Ala-Arg-MCA substrate) and irreversible CRA  I binding by the scFv  clones indicated a strong correlation ( p < 0.005,   r2 = 0.77) ( Fig.  4 B), confirming the functional importance of superior  nucleophilic reactivity.	bind
40846	1	9573	7	NULL	NULL	0	NULL	scFv clones	NULL		bind	NULL	irreversibly			 CRA I	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_22_20436_s_158	12668670	A comparison of the peptide-MCA cleaving activity  (Glu-Ala-Arg-MCA substrate) and irreversible CRA  I binding by the scFv  clones indicated a strong correlation ( p < 0.005,   r2 = 0.77) ( Fig.  4 B), confirming the functional importance of superior  nucleophilic reactivity.	bind
40848	2	9573	7	NULL	NULL	0	NULL	statement 1	NULL		confirms	NULL				superior nucleophilic reactivity	NULL	importance of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_22_20436_s_158	12668670	A comparison of the peptide-MCA cleaving activity  (Glu-Ala-Arg-MCA substrate) and irreversible CRA  I binding by the scFv  clones indicated a strong correlation ( p < 0.005,   r2 = 0.77) ( Fig.  4 B), confirming the functional importance of superior  nucleophilic reactivity.	bind
41541	1	9574	5	13	NULL	NULL	NULL	PU.1	GP		bind					oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_898_s_240	7822329	A comparison of the percentage of each oligonucleotide bound to  PU.1 indicated that PU.1 bound to the Vkappa19 pyrimidine-rich motif  with the same affinity as to the SV40 PU box, which contains a strong  binding site for PU.1, and that it had a 4 times weaker affinity to the  pyrimidine-rich motif of the V101 promoter.	bind
41542	2	9574	5	13	NULL	NULL	NULL	PU.1	GP		bind					Vkappa19	GP			pyrimidine-rich motif	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_898_s_240	7822329	A comparison of the percentage of each oligonucleotide bound to  PU.1 indicated that PU.1 bound to the Vkappa19 pyrimidine-rich motif  with the same affinity as to the SV40 PU box, which contains a strong  binding site for PU.1, and that it had a 4 times weaker affinity to the  pyrimidine-rich motif of the V101 promoter.	bind
41543	3	9574	5	13	NULL	NULL	NULL	PU.1	GP		bind					SV40	NucleicAcid			PU box	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_898_s_240	7822329	A comparison of the percentage of each oligonucleotide bound to  PU.1 indicated that PU.1 bound to the Vkappa19 pyrimidine-rich motif  with the same affinity as to the SV40 PU box, which contains a strong  binding site for PU.1, and that it had a 4 times weaker affinity to the  pyrimidine-rich motif of the V101 promoter.	bind
41544	4	9574	5	13	NULL	NULL	NULL	statement 2	Process		same affinity as					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_898_s_240	7822329	A comparison of the percentage of each oligonucleotide bound to  PU.1 indicated that PU.1 bound to the Vkappa19 pyrimidine-rich motif  with the same affinity as to the SV40 PU box, which contains a strong  binding site for PU.1, and that it had a 4 times weaker affinity to the  pyrimidine-rich motif of the V101 promoter.	bind
41545	5	9574	5	13	NULL	NULL	NULL	SV40	NucleicAcid		contains				PU box	PU.1	GP		strong binding site for		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_898_s_240	7822329	A comparison of the percentage of each oligonucleotide bound to  PU.1 indicated that PU.1 bound to the Vkappa19 pyrimidine-rich motif  with the same affinity as to the SV40 PU box, which contains a strong  binding site for PU.1, and that it had a 4 times weaker affinity to the  pyrimidine-rich motif of the V101 promoter.	bind
41546	6	9574	5	13	NULL	NULL	NULL	PU.1	GP		bind					V101	NucleicAcid			pyrimidine-rich motif of promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_898_s_240	7822329	A comparison of the percentage of each oligonucleotide bound to  PU.1 indicated that PU.1 bound to the Vkappa19 pyrimidine-rich motif  with the same affinity as to the SV40 PU box, which contains a strong  binding site for PU.1, and that it had a 4 times weaker affinity to the  pyrimidine-rich motif of the V101 promoter.	bind
41547	7	9574	5	13	NULL	NULL	NULL	statement 2	Process		weaker affinity to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_898_s_240	7822329	A comparison of the percentage of each oligonucleotide bound to  PU.1 indicated that PU.1 bound to the Vkappa19 pyrimidine-rich motif  with the same affinity as to the SV40 PU box, which contains a strong  binding site for PU.1, and that it had a 4 times weaker affinity to the  pyrimidine-rich motif of the V101 promoter.	bind
40849	1	9574	7	NULL	NULL	0	NULL	oligonucleotide	NULL		bind	NULL				PU.1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_2_898_s_240	7822329	A comparison of the percentage of each oligonucleotide bound to  PU.1 indicated that PU.1 bound to the Vkappa19 pyrimidine-rich motif  with the same affinity as to the SV40 PU box, which contains a strong  binding site for PU.1, and that it had a 4 times weaker affinity to the  pyrimidine-rich motif of the V101 promoter.	bind
40850	2	9574	7	NULL	NULL	0	NULL	PU.1	NULL		bind	NULL				 Vkappa19	NULL			pyrimidine-rich motif	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_2_898_s_240	7822329	A comparison of the percentage of each oligonucleotide bound to  PU.1 indicated that PU.1 bound to the Vkappa19 pyrimidine-rich motif  with the same affinity as to the SV40 PU box, which contains a strong  binding site for PU.1, and that it had a 4 times weaker affinity to the  pyrimidine-rich motif of the V101 promoter.	bind
40851	3	9574	7	NULL	NULL	0	NULL	 PU.1	NULL		bind	NULL				 SV40 	NULL			PU box	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_2_898_s_240	7822329	A comparison of the percentage of each oligonucleotide bound to  PU.1 indicated that PU.1 bound to the Vkappa19 pyrimidine-rich motif  with the same affinity as to the SV40 PU box, which contains a strong  binding site for PU.1, and that it had a 4 times weaker affinity to the  pyrimidine-rich motif of the V101 promoter.	bind
40852	4	9574	7	NULL	NULL	0	NULL	statement 2	NULL	affinity of	is same as	NULL				statement 3	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_2_898_s_240	7822329	A comparison of the percentage of each oligonucleotide bound to  PU.1 indicated that PU.1 bound to the Vkappa19 pyrimidine-rich motif  with the same affinity as to the SV40 PU box, which contains a strong  binding site for PU.1, and that it had a 4 times weaker affinity to the  pyrimidine-rich motif of the V101 promoter.	bind
40853	5	9574	7	10	NULL	0	NULL	 SV40 			contains				PU box	PU.1			strong binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_898_s_240	7822329	A comparison of the percentage of each oligonucleotide bound to  PU.1 indicated that PU.1 bound to the Vkappa19 pyrimidine-rich motif  with the same affinity as to the SV40 PU box, which contains a strong  binding site for PU.1, and that it had a 4 times weaker affinity to the  pyrimidine-rich motif of the V101 promoter.	bind
40854	6	9574	7	NULL	NULL	0	NULL	PU.1	NULL		affinity for	NULL	weaker			V101	NULL			pyrimidine-rich motif in the promotoer	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_2_898_s_240	7822329	A comparison of the percentage of each oligonucleotide bound to  PU.1 indicated that PU.1 bound to the Vkappa19 pyrimidine-rich motif  with the same affinity as to the SV40 PU box, which contains a strong  binding site for PU.1, and that it had a 4 times weaker affinity to the  pyrimidine-rich motif of the V101 promoter.	bind
43537	1	9575	5	13	NULL	NULL	NULL	apoA-I	GP	recombinant;;pro form of	bind					phospholipid transfer protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
43538	2	9575	5	13	NULL	NULL	NULL	apoA-I	GP	recombinant;;mature form of	bind					phospholipid transfer protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
43539	3	9575	5	13	NULL	NULL	NULL	apoA-I	GP	human;;plasma	bind					phospholipid transfer protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
43540	4	9575	5	13	NULL	NULL	NULL	apoA-I	GP	recombinant;;pro form of	has ability to					self-associate	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
43541	5	9575	5	13	NULL	NULL	NULL	apoA-I	GP	recombinant;;mature form of	has ability to					self-associate	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
43542	6	9575	5	13	NULL	NULL	NULL	apoA-I	GP	human;;plasma	has ability to					self-associate	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
43543	7	9575	5	13	NULL	NULL	NULL	apoA-I	GP	recombinant;;pro form of	bind					lipid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
43544	8	9575	5	13	NULL	NULL	NULL	apoA-I	GP	recombinant;;mature form of	bind					lipid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
43545	9	9575	5	13	NULL	NULL	NULL	apoA-I	GP	human;;plasma	bind					lipid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
43546	10	9575	5	13	NULL	NULL	NULL	apoA-I	GP	recombinant;;pro form of	activates					lecithin: cholesterolacyltransferase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
43547	11	9575	5	13	NULL	NULL	NULL	apoA-I	GP	recombinant;;mature form of	activates					lecithin: cholesterolacyltransferase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
43548	12	9575	5	13	NULL	NULL	NULL	apoA-I	GP	human;;plasma	activates					lecithin: cholesterolacyltransferase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
40855	1	9575	7	NULL	NULL	0	NULL	pro apoA-I	NULL	recombinant	associate with	NULL				pro apoA-I	NULL	recombinant			NULL		0	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
40856	2	9575	7	NULL	NULL	0	NULL	pro apoA-I	NULL	recombinant	bind	NULL				lipids	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
40857	3	9575	7	NULL	NULL	0	NULL	pro apoA-I	NULL	recombinant	activates	NULL				lecithin: cholesterolacyltransferase	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
40858	4	9575	7	NULL	NULL	0	NULL	pro apoA-I	NULL	recombinant	bind	NULL				phospholipid transfer protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
40859	5	9575	7	NULL	NULL	0	NULL	mature apoA-I	NULL	recombinant	associate with	NULL				mature apoA-I	NULL	recombinant			NULL		0	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
40860	6	9575	7	NULL	NULL	0	NULL	mature apoA-I	NULL	recombinant	bind	NULL				lipids	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
40861	7	9575	7	NULL	NULL	0	NULL	mature apoA-I	NULL	recombinant	activates	NULL				lecithin: cholesterolacyltransferase	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
40862	8	9575	7	NULL	NULL	0	NULL	mature apoA-I	NULL	recombinant	bind	NULL				phospholipid transfer protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
40863	9	9575	7	NULL	NULL	0	NULL	apoA-I	NULL	human plasma	associate with	NULL				apoA-I	NULL	human plasma			NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
40864	10	9575	7	NULL	NULL	0	NULL	apoA-I	NULL	human plasma	bind	NULL				lipids	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
40865	11	9575	7	NULL	NULL	0	NULL	apoA-I	NULL	human plasma	activates	NULL				lecithin: cholesterolacyltransferase	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
40867	12	9575	7	NULL	NULL	0	NULL	apoA-I	NULL	human plasma	bind	NULL				phospholipid transfer protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_41_11_1872_s_4	11060357	A comparison of the properties of the pro- and mature forms of recombinant apoA-I and human plasma apoA-I showed no difference between all three in their secondary structure, their ability to self-associate, lipid-binding capacity, lecithin: cholesterolacyltransferase  activation, and binding to the phospholipid transfer protein.	bind
41709	1	9576	5	13	NULL	NULL	NULL	RNAP	GP		bind					pRM	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_1_216_s_49	10613884	A comparison of the pseudo-first-order rate constants ( kobs) for the binding of RNAP to the pRM promoter in the context of the different deletions is graphically shown in Fig.  2a, and the values for  kobs for each promoter deletion mutant are given in Table  1.	bind
40868	1	9576	7	NULL	NULL	0	NULL	RNAP 	NULL		bind	NULL				pRM	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_1_216_s_49	10613884	A comparison of the pseudo-first-order rate constants ( kobs) for the binding of RNAP to the pRM promoter in the context of the different deletions is graphically shown in Fig.  2a, and the values for  kobs for each promoter deletion mutant are given in Table  1.	bind
41706	1	9577	5	13	NULL	NULL	NULL	ezrin	GP		is homologous to			RII binding motif		MAP2	GP		RII binding motif		NULL		NULL	NULL	NULL	NULL	gw60_embo_16_1_35_s_89	9009265	A comparison of the region spanning the RII binding motif of ezrin with analogous regions from MAP2, HT-31 and AKAP79 (Figure  6B) shows significant homologies throughout the sequence.	bind
41707	2	9577	5	13	NULL	NULL	NULL	ezrin	GP		is homologous to			RII binding motif		HT-31	GP		RII binding motif		NULL		NULL	NULL	NULL	NULL	gw60_embo_16_1_35_s_89	9009265	A comparison of the region spanning the RII binding motif of ezrin with analogous regions from MAP2, HT-31 and AKAP79 (Figure  6B) shows significant homologies throughout the sequence.	bind
41708	3	9577	5	13	NULL	NULL	NULL	ezrin	GP		is homologous to			RII binding motif		AKAP79	GP		RII binding motif		NULL		NULL	NULL	NULL	NULL	gw60_embo_16_1_35_s_89	9009265	A comparison of the region spanning the RII binding motif of ezrin with analogous regions from MAP2, HT-31 and AKAP79 (Figure  6B) shows significant homologies throughout the sequence.	bind
41700	1	9577	7	NULL	NULL	0	NULL	ezrin	NULL		is homologous to	NULL		RII binding motif		MAP2	NULL		RII binding motif		NULL		0	NULL	NULL	NULL	gw60_embo_16_1_35_s_89	9009265	A comparison of the region spanning the RII binding motif of ezrin with analogous regions from MAP2, HT-31 and AKAP79 (Figure  6B) shows significant homologies throughout the sequence.	bind
41701	2	9577	7	NULL	NULL	0	NULL	ezrin	NULL		is homologous to	NULL		RII binding motif		HT-31	NULL		RII binding motif		NULL		0	NULL	NULL	NULL	gw60_embo_16_1_35_s_89	9009265	A comparison of the region spanning the RII binding motif of ezrin with analogous regions from MAP2, HT-31 and AKAP79 (Figure  6B) shows significant homologies throughout the sequence.	bind
41702	3	9577	7	NULL	NULL	0	NULL	ezrin	NULL		is homologous to	NULL		RII binding motif		AKAP79	NULL		RII binding motif		NULL		0	NULL	NULL	NULL	gw60_embo_16_1_35_s_89	9009265	A comparison of the region spanning the RII binding motif of ezrin with analogous regions from MAP2, HT-31 and AKAP79 (Figure  6B) shows significant homologies throughout the sequence.	bind
42703	1	9578	5	13	NULL	NULL	NULL	WASP	GP		bind		preferentially			Cdc42	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_47_36999_s_106	10950951	A comparison of the relative amounts of active Rac and active Cdc42 with the total amounts of the GTPases (Fig.  1 A) is consistent with WASP preferentially binding Cdc42 over Rac ( 12,  23).	bind
42704	2	9578	5	13	NULL	NULL	NULL	WASP	GP		bind					Rac	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_47_36999_s_106	10950951	A comparison of the relative amounts of active Rac and active Cdc42 with the total amounts of the GTPases (Fig.  1 A) is consistent with WASP preferentially binding Cdc42 over Rac ( 12,  23).	bind
40869	1	9578	7	NULL	NULL	0	NULL	WASP	NULL		bind	NULL	preferentially			Cdc42	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_47_36999_s_106	10950951	A comparison of the relative amounts of active Rac and active Cdc42 with the total amounts of the GTPases (Fig.  1 A) is consistent with WASP preferentially binding Cdc42 over Rac ( 12,  23).	bind
40870	2	9578	7	NULL	NULL	0	NULL	WASP	NULL		bind	NULL				Rac	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_47_36999_s_106	10950951	A comparison of the relative amounts of active Rac and active Cdc42 with the total amounts of the GTPases (Fig.  1 A) is consistent with WASP preferentially binding Cdc42 over Rac ( 12,  23).	bind
42706	1	9579	5	13	NULL	NULL	NULL	SarR	GP		bind					sar	NucleicAcid			P1 promoter	NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_2_885_s_217	11159982	A comparison of the relative binding of SarR and SarA to the  sar P1 promoter is of interest.	bind
42707	2	9579	5	13	NULL	NULL	NULL	SarA	GP		bind					sar	NucleicAcid			P1 promoter	NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_2_885_s_217	11159982	A comparison of the relative binding of SarR and SarA to the  sar P1 promoter is of interest.	bind
40871	1	9579	7	10	NULL	0	NULL	SarR	NULL		bind	NULL				sar 	NULL			P1 promoter	NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_2_885_s_217	11159982	A comparison of the relative binding of SarR and SarA to the  sar P1 promoter is of interest.	bind
40872	2	9579	7	10	NULL	0	NULL	SarA	NULL		bind	NULL				sar	NULL			P1 promoter	NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_2_885_s_217	11159982	A comparison of the relative binding of SarR and SarA to the  sar P1 promoter is of interest.	bind
42791	1	9582	5	13	NULL	NULL	NULL			mutation of	does not effect		grossly	D140A		alpha4beta7	GP	structure of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_33_25652_s_232	10837471	A comparison of the staining obtained with mAbs to at least two different epitopes on the alpha4 chain (B5G10, B5E2, and HP1/2) ( 76), three different epitopes on the beta7 chain (Fib21, Fib30, and Fib504) ( 65), and an antibody that recognizes cell-surface beta7 chain only in the context of alpha4beta7 (ACT-1) ( 60,  77) showed that the binding of these mAbs was unaffected and confirmed that the D140A mutation did not grossly affect the structure of alpha4beta7 (Fig.  5 A).	bind
40882	1	9582	7	10	NULL	0	NULL			mutation of	does not affect			D140A		alpha4beta7		structure of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_33_25652_s_232	10837471	A comparison of the staining obtained with mAbs to at least two different epitopes on the alpha4 chain (B5G10, B5E2, and HP1/2) ( 76), three different epitopes on the beta7 chain (Fib21, Fib30, and Fib504) ( 65), and an antibody that recognizes cell-surface beta7 chain only in the context of alpha4beta7 (ACT-1) ( 60,  77) showed that the binding of these mAbs was unaffected and confirmed that the D140A mutation did not grossly affect the structure of alpha4beta7 (Fig.  5 A).	bind
43255	1	9583	5	13	NULL	NULL	NULL	GP2	GP		bind					A2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21443_s_197	11287414	A comparison of the structure of GP2 bound to A2 with the structure of A2I2L/V5L shows that the leucine points in the same direction as valine in molecule 1, but the side chain points away from the hydrophobic pocket (Fig.  3 A).	bind
40883	1	9583	7	NULL	NULL	0	NULL	GP2	NULL		bind	NULL				A2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_24_21443_s_197	11287414	A comparison of the structure of GP2 bound to A2 with the structure of A2I2L/V5L shows that the leucine points in the same direction as valine in molecule 1, but the side chain points away from the hydrophobic pocket (Fig.  3 A).	bind
43257	1	9584	5	13	NULL	NULL	NULL	ADP	Chemical		bind					SCS	GP	E.coli			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_16_11058_s_152	16481318	A comparison of the structure of GTP bound to pig GTP-specific SCS with the structure of ADP bound to  E. coli SCS ( ) indicates which interactions lead to specificity for the guanine base.	bind
43258	2	9584	5	13	NULL	NULL	NULL	GTP	Chemical		bind					GTP-specific SCS	GP	pig			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_16_11058_s_152	16481318	A comparison of the structure of GTP bound to pig GTP-specific SCS with the structure of ADP bound to  E. coli SCS ( ) indicates which interactions lead to specificity for the guanine base.	bind
40913	1	9584	7	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				GTP-specific SCS 	NULL	pig			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_16_11058_s_152	16481318	A comparison of the structure of GTP bound to pig GTP-specific SCS with the structure of ADP bound to  E. coli SCS ( ) indicates which interactions lead to specificity for the guanine base.	bind
40914	2	9584	7	NULL	NULL	0	NULL	ADP	NULL		bind	NULL				SCS	NULL	E.coli			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_16_11058_s_152	16481318	A comparison of the structure of GTP bound to pig GTP-specific SCS with the structure of ADP bound to  E. coli SCS ( ) indicates which interactions lead to specificity for the guanine base.	bind
43260	1	9585	5	13	NULL	NULL	NULL	Arf1	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_20_0_87_s_187	15473836	A comparison of the structures  of Arf1 bound to GDP or a nonhydrolyzable analog of GTP shown in identical orientation.	bind
43261	2	9585	5	13	NULL	NULL	NULL	Arf1	GP		bind					GTP	Chemical	nonhydrolyzable analog of 			NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_20_0_87_s_187	15473836	A comparison of the structures  of Arf1 bound to GDP or a nonhydrolyzable analog of GTP shown in identical orientation.	bind
40915	1	9585	7	NULL	NULL	0	NULL	 Arf1	NULL		bind	NULL				GDP	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevcelldevbiol_20_0_87_s_187	15473836	A comparison of the structures  of Arf1 bound to GDP or a nonhydrolyzable analog of GTP shown in identical orientation.	bind
40917	2	9585	7	NULL	NULL	0	NULL	Arf1	NULL		bind	NULL				GTP	NULL	 nonhydrolyzable analog of 			NULL		0	NULL	NULL	NULL	gw70_annurevcelldevbiol_20_0_87_s_187	15473836	A comparison of the structures  of Arf1 bound to GDP or a nonhydrolyzable analog of GTP shown in identical orientation.	bind
43263	1	9586	5	13	NULL	NULL	NULL	syntaxin 1	GP		bind					Munc18-1	GP	rat			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_1_32_s_176	12506202	A comparison of the syntaxin-bound Munc18-1 structure from rat ( ) with the syntaxin-free Munc18 structure from squid ( ) suggests that syntaxin 1 binding to Munc18-1 also does not cause a conformational change; thus, syntaxin binding generally does not induce an allosteric signal in SM proteins.	bind
43264	2	9586	5	13	NULL	NULL	NULL	statement 1	Process		does not cause					conformational change	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_1_32_s_176	12506202	A comparison of the syntaxin-bound Munc18-1 structure from rat ( ) with the syntaxin-free Munc18 structure from squid ( ) suggests that syntaxin 1 binding to Munc18-1 also does not cause a conformational change; thus, syntaxin binding generally does not induce an allosteric signal in SM proteins.	bind
43265	3	9586	5	13	NULL	NULL	NULL	statement 1	Process		does not induce					SM proteins	GP	allosteric signal			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_1_32_s_176	12506202	A comparison of the syntaxin-bound Munc18-1 structure from rat ( ) with the syntaxin-free Munc18 structure from squid ( ) suggests that syntaxin 1 binding to Munc18-1 also does not cause a conformational change; thus, syntaxin binding generally does not induce an allosteric signal in SM proteins.	bind
40918	1	9586	7	NULL	NULL	0	NULL	syntaxin	NULL		bind	NULL				Munc18-1	NULL	rat			NULL		0	NULL	NULL	NULL	gw70_pnas_100_1_32_s_176	12506202	A comparison of the syntaxin-bound Munc18-1 structure from rat ( ) with the syntaxin-free Munc18 structure from squid ( ) suggests that syntaxin 1 binding to Munc18-1 also does not cause a conformational change; thus, syntaxin binding generally does not induce an allosteric signal in SM proteins.	bind
40920	2	9586	7	NULL	NULL	0	NULL	statement 1	NULL		does not cause	NULL				conformational change	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_100_1_32_s_176	12506202	A comparison of the syntaxin-bound Munc18-1 structure from rat ( ) with the syntaxin-free Munc18 structure from squid ( ) suggests that syntaxin 1 binding to Munc18-1 also does not cause a conformational change; thus, syntaxin binding generally does not induce an allosteric signal in SM proteins.	bind
40921	3	9586	7	NULL	NULL	0	NULL	statement 1	NULL		does not induce	NULL				SM protein	NULL	allosteric signal in			NULL		0	NULL	NULL	NULL	gw70_pnas_100_1_32_s_176	12506202	A comparison of the syntaxin-bound Munc18-1 structure from rat ( ) with the syntaxin-free Munc18 structure from squid ( ) suggests that syntaxin 1 binding to Munc18-1 also does not cause a conformational change; thus, syntaxin binding generally does not induce an allosteric signal in SM proteins.	bind
43266	1	9588	5	13	NULL	NULL	NULL	TGase 2 enzyme	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_7180_s_317	14645372	A comparison of the TGase 2 enzyme structure recently reported bound to GDP ( ) with that of the current structures of TGase 3 indicates that although there is only a 48% sequence identity between these enzymes, there is only a 1.33  Ang  root mean square deviation relating the structures of their Calpha atoms ( Fig. 7,  A and  B).	bind
40924	1	9588	7	NULL	NULL	0	NULL	TGase 2 enzyme	NULL		bind	NULL				GDP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_7180_s_317	14645372	A comparison of the TGase 2 enzyme structure recently reported bound to GDP ( ) with that of the current structures of TGase 3 indicates that although there is only a 48% sequence identity between these enzymes, there is only a 1.33  Ang  root mean square deviation relating the structures of their Calpha atoms ( Fig. 7,  A and  B).	bind
43550	1	9589	5	13	NULL	NULL	NULL	B-FABP	GP	human	interact with			Phe104		lipid hydrocarbon tail	Chemical		double bond		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_35_27045_s_6	10854433	A comparison of the three-dimensional structures and binding properties of human B-FABP with other homologous FABPs, indicates that the binding specificity is in part the result of nonconserved amino acid Phe104, which interacts with double bonds present in the lipid hydrocarbon tail.	bind
43551	2	9589	5	13	NULL	NULL	NULL	B-FABP	GP		is a type of			Phe104		nonconserved amino acid	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_35_27045_s_6	10854433	A comparison of the three-dimensional structures and binding properties of human B-FABP with other homologous FABPs, indicates that the binding specificity is in part the result of nonconserved amino acid Phe104, which interacts with double bonds present in the lipid hydrocarbon tail.	bind
40926	1	9589	7	NULL	NULL	0	NULL	B-FABP 	NULL	human	interacts with	NULL		nonconserved amino acid Phe104		lipid hydrocarbon tail	NULL		double bond		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_27045_s_6	10854433	A comparison of the three-dimensional structures and binding properties of human B-FABP with other homologous FABPs, indicates that the binding specificity is in part the result of nonconserved amino acid Phe104, which interacts with double bonds present in the lipid hydrocarbon tail.	bind
56920	2	9589	7	10	NULL	0	NULL	B-FABP			is a type of			Phe104		nonconserved amino acid					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_27045_s_6	10854433	A comparison of the three-dimensional structures and binding properties of human B-FABP with other homologous FABPs, indicates that the binding specificity is in part the result of nonconserved amino acid Phe104, which interacts with double bonds present in the lipid hydrocarbon tail.	bind
43278	1	9590	5	13	NULL	NULL	NULL	topo VI-A' dimer	GP	structure of	is different from					DNA topoisomerase I	GP	E. coli;;structure of	DNA-binding core		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6177_s_163	10545127	A comparison of the topo VI-A' dimer with the known structures of the DNA-binding and cleavage cores of  E.coli DNA topoisomerase I and yeast topoisomerase II shows that the overall structures are very different (Figure  5).	bind
43279	2	9590	5	13	NULL	NULL	NULL	topo VI-A' dimer	GP	structure of	is different from					DNA topoisomerase I	GP	E. coli;;structure of	cleavage core		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6177_s_163	10545127	A comparison of the topo VI-A' dimer with the known structures of the DNA-binding and cleavage cores of  E.coli DNA topoisomerase I and yeast topoisomerase II shows that the overall structures are very different (Figure  5).	bind
43280	3	9590	5	13	NULL	NULL	NULL	topo VI-A' dimer	GP	structure of	is different from					topoisomerase II	GP	yeast;;structure of	DNA-binding core		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6177_s_163	10545127	A comparison of the topo VI-A' dimer with the known structures of the DNA-binding and cleavage cores of  E.coli DNA topoisomerase I and yeast topoisomerase II shows that the overall structures are very different (Figure  5).	bind
43281	4	9590	5	13	NULL	NULL	NULL	topo VI-A' dimer	GP	structure of	is different from					topoisomerase II	GP	yeast;;structure of	cleavage core		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6177_s_163	10545127	A comparison of the topo VI-A' dimer with the known structures of the DNA-binding and cleavage cores of  E.coli DNA topoisomerase I and yeast topoisomerase II shows that the overall structures are very different (Figure  5).	bind
40929	1	9590	7	10	NULL	0	NULL	topo VI-A' dimer	NULL	structure of	is different from	NULL				DNA topoisomerase I	NULL	structure of;;E.coli	DNA-binding core		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6177_s_163	10545127	A comparison of the topo VI-A' dimer with the known structures of the DNA-binding and cleavage cores of  E.coli DNA topoisomerase I and yeast topoisomerase II shows that the overall structures are very different (Figure  5).	bind
40930	2	9590	7	10	NULL	0	NULL	topo VI-A' dimer	NULL	structure of	is different from	NULL				DNA topoisomerase I	NULL	E.coli;;structure of	cleavage core		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6177_s_163	10545127	A comparison of the topo VI-A' dimer with the known structures of the DNA-binding and cleavage cores of  E.coli DNA topoisomerase I and yeast topoisomerase II shows that the overall structures are very different (Figure  5).	bind
47516	3	9590	7	10	NULL	0	NULL	topo VI-A' dimer	NULL	structure of	is different from	NULL				topoisomerase II	NULL	structure of;;yeast	DNA-binding core		NULL		0	NULL	NULL	NULL	gw60_embo_18_21_6177_s_163	10545127	A comparison of the topo VI-A' dimer with the known structures of the DNA-binding and cleavage cores of  E.coli DNA topoisomerase I and yeast topoisomerase II shows that the overall structures are very different (Figure  5).	bind
47517	4	9590	7	10	NULL	0	NULL	topo VI-A' dimer	NULL	structure of	is different from	NULL				topoisomerase II 	NULL	structure of;;yeast	cleavage core		NULL		0	NULL	NULL	NULL	gw60_embo_18_21_6177_s_163	10545127	A comparison of the topo VI-A' dimer with the known structures of the DNA-binding and cleavage cores of  E.coli DNA topoisomerase I and yeast topoisomerase II shows that the overall structures are very different (Figure  5).	bind
43277	1	9591	5	13	NULL	NULL	NULL	AcpS	GP		bind				3'5''-ADP CoA binding pocket				Sfp binding site		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_20_5281_s_102	11032795	A comparison of the two (out of three) AcpS protomers with the two domain structures of Sfp indicates that the 3'5''-ADP CoA binding pocket of AcpS superimposes with the Sfp binding site.	bind
40933	1	9591	7	NULL	NULL	0	NULL	Sfp	NULL		bind	NULL		Sfp binding site		AcpS protomers	NULL		3'5''-ADP CoA binding pocket		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_20_5281_s_102	11032795	A comparison of the two (out of three) AcpS protomers with the two domain structures of Sfp indicates that the 3'5''-ADP CoA binding pocket of AcpS superimposes with the Sfp binding site.	bind
43282	1	9592	5	13	NULL	NULL	NULL	CD46	GP		differ from		substantially	virus-binding surface		CD4	GP	human	virus-binding surface		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_11_2911_s_44	10357804	A comparison of the virus-binding surface of CD46 with those reported for human CD4 and human intercellular cell adhesion molecule-1 (ICAM-1) reveals a substantial difference in their virus recognition modes.	bind
43283	2	9592	5	13	NULL	NULL	NULL	ICAM-1	GP		is					intercellular cell adhesion molecule-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_11_2911_s_44	10357804	A comparison of the virus-binding surface of CD46 with those reported for human CD4 and human intercellular cell adhesion molecule-1 (ICAM-1) reveals a substantial difference in their virus recognition modes.	bind
43284	3	9592	5	13	NULL	NULL	NULL	CD46	GP		differ from		substantially	virus-binding surface		ICAM-1	GP	human	virus-binding surface		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_11_2911_s_44	10357804	A comparison of the virus-binding surface of CD46 with those reported for human CD4 and human intercellular cell adhesion molecule-1 (ICAM-1) reveals a substantial difference in their virus recognition modes.	bind
40997	1	9592	7	10	NULL	0	NULL	CD46	NULL		differs with	NULL		virus-binding surface		CD4	NULL	human	virus-binding surface		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_11_2911_s_44	10357804	A comparison of the virus-binding surface of CD46 with those reported for human CD4 and human intercellular cell adhesion molecule-1 (ICAM-1) reveals a substantial difference in their virus recognition modes.	bind
40998	2	9592	7	10	NULL	0	NULL	CD46	NULL		differs with	NULL		virus-binding surface		ICAM-1	NULL	human	virus-binding surface		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_11_2911_s_44	10357804	A comparison of the virus-binding surface of CD46 with those reported for human CD4 and human intercellular cell adhesion molecule-1 (ICAM-1) reveals a substantial difference in their virus recognition modes.	bind
40999	3	9592	7	NULL	NULL	0	NULL	ICAM-1	NULL		is	NULL				intercellular cell adhesion molecule-1	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_18_11_2911_s_44	10357804	A comparison of the virus-binding surface of CD46 with those reported for human CD4 and human intercellular cell adhesion molecule-1 (ICAM-1) reveals a substantial difference in their virus recognition modes.	bind
43415	1	9593	5	13	NULL	NULL	NULL	SRP54	GP		bind		high affinity			GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_5_703_s_72	9182758	A comparison of these results with the apparent Kd values  for GTP binding to SRP54 (2 muM) and SR  (10 muM) that were determined  by photoaffinity labeling of purified SRP and SR (Miller et al., 1993    Miller et al., 1995   ) reveals that SRP54 and SR  bind GTP  with substantially higher affinity in the context of a translocation reaction.	bind
43416	2	9593	5	13	NULL	NULL	NULL	SR	GP		bind		high affinity			GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_5_703_s_72	9182758	A comparison of these results with the apparent Kd values  for GTP binding to SRP54 (2 muM) and SR  (10 muM) that were determined  by photoaffinity labeling of purified SRP and SR (Miller et al., 1993    Miller et al., 1995   ) reveals that SRP54 and SR  bind GTP  with substantially higher affinity in the context of a translocation reaction.	bind
43417	3	9593	5	13	NULL	NULL	NULL	statement 1	Process		in context of					translocation reaction	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_5_703_s_72	9182758	A comparison of these results with the apparent Kd values  for GTP binding to SRP54 (2 muM) and SR  (10 muM) that were determined  by photoaffinity labeling of purified SRP and SR (Miller et al., 1993    Miller et al., 1995   ) reveals that SRP54 and SR  bind GTP  with substantially higher affinity in the context of a translocation reaction.	bind
43418	4	9593	5	13	NULL	NULL	NULL	statement 2	Process		in context of					translocation reaction	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_5_703_s_72	9182758	A comparison of these results with the apparent Kd values  for GTP binding to SRP54 (2 muM) and SR  (10 muM) that were determined  by photoaffinity labeling of purified SRP and SR (Miller et al., 1993    Miller et al., 1995   ) reveals that SRP54 and SR  bind GTP  with substantially higher affinity in the context of a translocation reaction.	bind
40934	1	9593	7	NULL	NULL	0	NULL	 GTP	NULL		bind	NULL	high affinity			SRP54	NULL	purified			NULL		NULL	NULL	NULL	NULL	gw60_cell_89_5_703_s_72	9182758	A comparison of these results with the apparent Kd values  for GTP binding to SRP54 (2 muM) and SR  (10 muM) that were determined  by photoaffinity labeling of purified SRP and SR (Miller et al., 1993    Miller et al., 1995   ) reveals that SRP54 and SR  bind GTP  with substantially higher affinity in the context of a translocation reaction.	bind
40935	2	9593	7	NULL	NULL	0	NULL	GTP	NULL		bind	NULL	high affinity			SR	NULL	purified			NULL		NULL	NULL	NULL	NULL	gw60_cell_89_5_703_s_72	9182758	A comparison of these results with the apparent Kd values  for GTP binding to SRP54 (2 muM) and SR  (10 muM) that were determined  by photoaffinity labeling of purified SRP and SR (Miller et al., 1993    Miller et al., 1995   ) reveals that SRP54 and SR  bind GTP  with substantially higher affinity in the context of a translocation reaction.	bind
40940	3	9593	7	NULL	NULL	0	NULL	statement 1	NULL		occurs in the context of	NULL				translocation reaction	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_89_5_703_s_72	9182758	A comparison of these results with the apparent Kd values  for GTP binding to SRP54 (2 muM) and SR  (10 muM) that were determined  by photoaffinity labeling of purified SRP and SR (Miller et al., 1993    Miller et al., 1995   ) reveals that SRP54 and SR  bind GTP  with substantially higher affinity in the context of a translocation reaction.	bind
40941	4	9593	7	NULL	NULL	0	NULL	statement 2	NULL		occurs in the context of	NULL				translocation reaction	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_89_5_703_s_72	9182758	A comparison of these results with the apparent Kd values  for GTP binding to SRP54 (2 muM) and SR  (10 muM) that were determined  by photoaffinity labeling of purified SRP and SR (Miller et al., 1993    Miller et al., 1995   ) reveals that SRP54 and SR  bind GTP  with substantially higher affinity in the context of a translocation reaction.	bind
43285	1	9594	5	13	NULL	NULL	NULL	HCK	GP		accommodate		easily	binding site		emodin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29618_s_130	10882732	A comparison of these structures with that of the CK2-emodin complex reveals that the binding site of HCK can easily accommodate emodin, but possibly the binding is not so tight because the entrance of the cavity is not blocked after the binding of the inhibitor.	bind
43419	2	9594	5	13	NULL	NULL	NULL	HCK	GP	cavity of 	is not blocked after					inhibitor	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29618_s_130	10882732	A comparison of these structures with that of the CK2-emodin complex reveals that the binding site of HCK can easily accommodate emodin, but possibly the binding is not so tight because the entrance of the cavity is not blocked after the binding of the inhibitor.	bind
43421	3	9594	5	13	NULL	NULL	NULL	statement 2	Process		causes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29618_s_130	10882732	A comparison of these structures with that of the CK2-emodin complex reveals that the binding site of HCK can easily accommodate emodin, but possibly the binding is not so tight because the entrance of the cavity is not blocked after the binding of the inhibitor.	bind
40944	1	9594	7	NULL	NULL	0	NULL	CK2	NULL		complex with	NULL				emodin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29618_s_130	10882732	A comparison of these structures with that of the CK2-emodin complex reveals that the binding site of HCK can easily accommodate emodin, but possibly the binding is not so tight because the entrance of the cavity is not blocked after the binding of the inhibitor.	bind
40945	2	9594	7	NULL	NULL	0	NULL	HCK	NULL		bind	NULL	may weakly			emodin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29618_s_130	10882732	A comparison of these structures with that of the CK2-emodin complex reveals that the binding site of HCK can easily accommodate emodin, but possibly the binding is not so tight because the entrance of the cavity is not blocked after the binding of the inhibitor.	bind
40949	3	9594	7	NULL	NULL	0	NULL	inhibitor	NULL	binding of	does not block	NULL				HCK	NULL		cavity of		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29618_s_130	10882732	A comparison of these structures with that of the CK2-emodin complex reveals that the binding site of HCK can easily accommodate emodin, but possibly the binding is not so tight because the entrance of the cavity is not blocked after the binding of the inhibitor.	bind
40958	4	9594	7	NULL	NULL	0	NULL	statement 2	NULL		because of	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29618_s_130	10882732	A comparison of these structures with that of the CK2-emodin complex reveals that the binding site of HCK can easily accommodate emodin, but possibly the binding is not so tight because the entrance of the cavity is not blocked after the binding of the inhibitor.	bind
43422	1	9596	5	13	NULL	NULL	NULL	Sox2	GP		bind					Oct1	GP		POUS domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1449_s_253	14559893	A comparison of these two ternary complexes is of considerable interest since the separation between the Sox2 and Oct1 binding sites in the two complexes differ by three base pairs, and thus sheds light on multiple modes of interaction between Sox2 and the POUS domain of Oct1.	bind
40959	1	9596	7	NULL	NULL	0	NULL	Sox2	NULL		bind	NULL				Oct1	NULL		POUS domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_2_1449_s_253	14559893	A comparison of these two ternary complexes is of considerable interest since the separation between the Sox2 and Oct1 binding sites in the two complexes differ by three base pairs, and thus sheds light on multiple modes of interaction between Sox2 and the POUS domain of Oct1.	bind
43423	1	9597	5	13	NULL	NULL	NULL	thrombin receptor antibody 1809	GP		bind					WT5	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_27_16435_s_83	7608215	A comparison of thrombin receptor  antibody 1809 binding to WT5  versus  HEL cells ( 8,  24) also yielded an estimate of 5    10   receptors/cell for WT5.	bind
43424	2	9597	5	13	NULL	NULL	NULL	thrombin receptor antibody 1809	GP		bind					HEL cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_27_16435_s_83	7608215	A comparison of thrombin receptor  antibody 1809 binding to WT5  versus  HEL cells ( 8,  24) also yielded an estimate of 5    10   receptors/cell for WT5.	bind
40960	1	9597	7	NULL	NULL	0	NULL	thrombin receptor antibody 1809	NULL		bind	NULL				WT5 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_27_16435_s_83	7608215	A comparison of thrombin receptor  antibody 1809 binding to WT5  versus  HEL cells ( 8,  24) also yielded an estimate of 5    10   receptors/cell for WT5.	bind
40961	2	9597	7	NULL	NULL	0	NULL	thrombin receptor antibody 1809	NULL		bind	NULL				HEL cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_27_16435_s_83	7608215	A comparison of thrombin receptor  antibody 1809 binding to WT5  versus  HEL cells ( 8,  24) also yielded an estimate of 5    10   receptors/cell for WT5.	bind
43427	1	9598	5	13	NULL	NULL	NULL	importin-beta	GP		wraps around			HEAT repeats		importin-alpha	GP		helical importin-beta binding domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_9011_s_257	10722750	A comparison of two independent structures of importin-beta ( 51) indicates that HEAT repeat domain of importin-beta is flexible, thereby permitting conformational changes that allow the tandem HEAT repeats of importin-beta to wrap around the helical importin-beta binding domain of importin-alpha ( 51).	bind
43428	2	9598	5	13	NULL	NULL	NULL	importin-beta	GP	flexibility of 	permit 			HEAT repeats		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_9011_s_257	10722750	A comparison of two independent structures of importin-beta ( 51) indicates that HEAT repeat domain of importin-beta is flexible, thereby permitting conformational changes that allow the tandem HEAT repeats of importin-beta to wrap around the helical importin-beta binding domain of importin-alpha ( 51).	bind
40962	1	9598	7	NULL	NULL	0	NULL	importin-beta	NULL		wrap around	NULL		tandem HEAT repeats 		importin-alpha 	NULL		helical importin-beta binding domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_12_9011_s_257	10722750	A comparison of two independent structures of importin-beta ( 51) indicates that HEAT repeat domain of importin-beta is flexible, thereby permitting conformational changes that allow the tandem HEAT repeats of importin-beta to wrap around the helical importin-beta binding domain of importin-alpha ( 51).	bind
40963	2	9598	7	NULL	NULL	0	NULL	importin-beta	NULL	flexibility of	permit	NULL		HEAT repeat domain		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_12_9011_s_257	10722750	A comparison of two independent structures of importin-beta ( 51) indicates that HEAT repeat domain of importin-beta is flexible, thereby permitting conformational changes that allow the tandem HEAT repeats of importin-beta to wrap around the helical importin-beta binding domain of importin-alpha ( 51).	bind
43429	1	9599	5	13	NULL	NULL	NULL	lck-GFP	GP		does not alter					D10	Cell	proliferation of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_6_809_s_49	12479826	A comparison of wild-type and transduced D10 T cells shows that lck-GFP does not alter D10 proliferation over a range of conalbumin concentrations (Supplemental Figure S1B at  http://www.immunity.	bind
40964	1	9599	7	NULL	NULL	0	NULL	lck-GFP	NULL		does not alter	NULL				D10 T cells	NULL	proliferation of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_6_809_s_49	12479826	A comparison of wild-type and transduced D10 T cells shows that lck-GFP does not alter D10 proliferation over a range of conalbumin concentrations (Supplemental Figure S1B at  http://www.immunity.	bind
43431	1	9600	5	13	NULL	NULL	NULL	RF-X 	GP		bind					DRA	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_nucleic-acids-res_19_6_1903200_s_10	1903200	A comparison of X box basepair positions important for RF-X binding to  DRA with sequences conserved between X boxes of other class II alpha chain  genes suggests that high affinity RF-X binding is important for a high  level of expression and may explain differences in the levels of class  II expression of different class II alpha chains.	bind
43435	2	9600	5	13	NULL	NULL	NULL	DRA	GP		is important for				X box basepair positions	statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_nucleic-acids-res_19_6_1903200_s_10	1903200	A comparison of X box basepair positions important for RF-X binding to  DRA with sequences conserved between X boxes of other class II alpha chain  genes suggests that high affinity RF-X binding is important for a high  level of expression and may explain differences in the levels of class  II expression of different class II alpha chains.	bind
40965	1	9600	7	NULL	NULL	0	NULL	RF-X	NULL		bind	NULL				DRA	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_nucleic-acids-res_19_6_1903200_s_10	1903200	A comparison of X box basepair positions important for RF-X binding to  DRA with sequences conserved between X boxes of other class II alpha chain  genes suggests that high affinity RF-X binding is important for a high  level of expression and may explain differences in the levels of class  II expression of different class II alpha chains.	bind
40967	2	9600	7	10	NULL	0	NULL	RF-X	NULL		is important for	NULL			X box basepair positions	statement 1	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_nucleic-acids-res_19_6_1903200_s_10	1903200	A comparison of X box basepair positions important for RF-X binding to  DRA with sequences conserved between X boxes of other class II alpha chain  genes suggests that high affinity RF-X binding is important for a high  level of expression and may explain differences in the levels of class  II expression of different class II alpha chains.	bind
33857	1	9801	6	11	NULL	NULL	NULL	eglin-C	GP		bind					subtilisin	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_2_638_s_109	14733955	A corresponding part of eglin-C bound to subtilisin [ 24] is shown in magenta.	bind
40968	1	9801	7	11	NULL	NULL	NULL	 eglin-C 	GP		bind					subtilisin	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_2_638_s_109	14733955	A corresponding part of eglin-C bound to subtilisin [ 24] is shown in magenta.	bind
33858	1	9802	6	11	NULL	NULL	NULL	AT4	GP		bind		specifically			Ang IV	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_289_2_1075_s_223	10215690	A corresponding receptor, AT4, which specifically bound Ang IV, was thereafter identified in various tissues, including brain, heart, kidney, thymus, and adrenal from multiple species  .	bind
33859	2	9802	6	11	NULL	NULL	NULL	AT4	GP		is expressed in					brain	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_289_2_1075_s_223	10215690	A corresponding receptor, AT4, which specifically bound Ang IV, was thereafter identified in various tissues, including brain, heart, kidney, thymus, and adrenal from multiple species  .	bind
33860	3	9802	6	11	NULL	NULL	NULL	AT4	GP		is expressed in					kidney	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_289_2_1075_s_223	10215690	A corresponding receptor, AT4, which specifically bound Ang IV, was thereafter identified in various tissues, including brain, heart, kidney, thymus, and adrenal from multiple species  .	bind
33861	4	9802	6	11	NULL	NULL	NULL	AT4	GP		is expressed in					heart	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_289_2_1075_s_223	10215690	A corresponding receptor, AT4, which specifically bound Ang IV, was thereafter identified in various tissues, including brain, heart, kidney, thymus, and adrenal from multiple species  .	bind
33862	5	9802	6	11	NULL	NULL	NULL	AT4	GP		is expressed in					thymus	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_289_2_1075_s_223	10215690	A corresponding receptor, AT4, which specifically bound Ang IV, was thereafter identified in various tissues, including brain, heart, kidney, thymus, and adrenal from multiple species  .	bind
33863	6	9802	6	11	NULL	NULL	NULL	AT4	GP		is expressed in					adrenal	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_289_2_1075_s_223	10215690	A corresponding receptor, AT4, which specifically bound Ang IV, was thereafter identified in various tissues, including brain, heart, kidney, thymus, and adrenal from multiple species  .	bind
48890	7	9802	6	11	NULL	NULL	NULL	AT4	GP		is a type of					receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_289_2_1075_s_223	10215690	A corresponding receptor, AT4, which specifically bound Ang IV, was thereafter identified in various tissues, including brain, heart, kidney, thymus, and adrenal from multiple species  .	bind
40969	1	9802	7	11	NULL	NULL	NULL	AT4 receptor	GP		bind		specifically			Ang IV	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_289_2_1075_s_223	10215690	A corresponding receptor, AT4, which specifically bound Ang IV, was thereafter identified in various tissues, including brain, heart, kidney, thymus, and adrenal from multiple species  .	bind
48891	2	9802	7	11	NULL	NULL	NULL	AT4 receptor	GP		is expressed in					brain	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_289_2_1075_s_223	10215690	A corresponding receptor, AT4, which specifically bound Ang IV, was thereafter identified in various tissues, including brain, heart, kidney, thymus, and adrenal from multiple species  .	bind
48893	3	9802	7	11	NULL	NULL	NULL	AT4 receptor	GP		is expressed in					heart	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_289_2_1075_s_223	10215690	A corresponding receptor, AT4, which specifically bound Ang IV, was thereafter identified in various tissues, including brain, heart, kidney, thymus, and adrenal from multiple species  .	bind
48894	4	9802	7	11	NULL	NULL	NULL	AT4 receptor	GP		is expressed in					kidney	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_289_2_1075_s_223	10215690	A corresponding receptor, AT4, which specifically bound Ang IV, was thereafter identified in various tissues, including brain, heart, kidney, thymus, and adrenal from multiple species  .	bind
48895	5	9802	7	11	NULL	NULL	NULL	AT4 receptor	GP		is expressed in					thymus	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_289_2_1075_s_223	10215690	A corresponding receptor, AT4, which specifically bound Ang IV, was thereafter identified in various tissues, including brain, heart, kidney, thymus, and adrenal from multiple species  .	bind
48896	6	9802	7	11	NULL	NULL	NULL	AT4 receptor	GP		is expressed in					adrenal	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_289_2_1075_s_223	10215690	A corresponding receptor, AT4, which specifically bound Ang IV, was thereafter identified in various tissues, including brain, heart, kidney, thymus, and adrenal from multiple species  .	bind
33864	1	9803	6	11	NULL	NULL	NULL	accessory factor	GP		bind					gAF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_43_39885_s_124	11518712	A corresponding segment with a block mutation that prevents accessory factor binding to gAF2 does not promote complex formation ( open triangles).	bind
48897	2	9803	6	11	NULL	NULL	NULL	block mutation	Process		prevents					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_43_39885_s_124	11518712	A corresponding segment with a block mutation that prevents accessory factor binding to gAF2 does not promote complex formation ( open triangles).	bind
48898	3	9803	6	11	NULL	NULL	NULL	statement 2	Process		does not promote					complex	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_43_39885_s_124	11518712	A corresponding segment with a block mutation that prevents accessory factor binding to gAF2 does not promote complex formation ( open triangles).	bind
40970	1	9803	7	11	NULL	NULL	NULL	accessory factor 	GP		bind					gAF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_43_39885_s_124	11518712	A corresponding segment with a block mutation that prevents accessory factor binding to gAF2 does not promote complex formation ( open triangles).	bind
40971	2	9803	7	11	NULL	NULL	NULL	block mutation	Process		prevents					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_43_39885_s_124	11518712	A corresponding segment with a block mutation that prevents accessory factor binding to gAF2 does not promote complex formation ( open triangles).	bind
40972	3	9803	7	11	NULL	NULL	NULL	statement 2	Process		does not promote					complex	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_43_39885_s_124	11518712	A corresponding segment with a block mutation that prevents accessory factor binding to gAF2 does not promote complex formation ( open triangles).	bind
33866	1	9805	6	11	NULL	NULL	NULL	ATP	Chemical		bind					type IIA topoisomerases	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_24_8531_s_11	16321962	A coumarin, novobiocin, competitively inhibits ATP binding to type IIA topoisomerases ( ).	bind
33867	2	9805	6	11	NULL	NULL	NULL	novobiocin	Chemical		is a type of					coumarin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_24_8531_s_11	16321962	A coumarin, novobiocin, competitively inhibits ATP binding to type IIA topoisomerases ( ).	bind
33868	3	9805	6	11	NULL	NULL	NULL	novobiocin	Chemical		inhibits		competitively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_24_8531_s_11	16321962	A coumarin, novobiocin, competitively inhibits ATP binding to type IIA topoisomerases ( ).	bind
40974	1	9805	7	11	NULL	NULL	NULL	ATP	Chemical		bind					type IIA topoisomerases	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_24_8531_s_11	16321962	A coumarin, novobiocin, competitively inhibits ATP binding to type IIA topoisomerases ( ).	bind
40975	2	9805	7	11	NULL	NULL	NULL	novobiocin	Chemical		is a type of					coumarin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_24_8531_s_11	16321962	A coumarin, novobiocin, competitively inhibits ATP binding to type IIA topoisomerases ( ).	bind
40976	3	9805	7	11	NULL	NULL	NULL	novobiocin	Chemical		inhibits		competitively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_24_8531_s_11	16321962	A coumarin, novobiocin, competitively inhibits ATP binding to type IIA topoisomerases ( ).	bind
33869	1	9807	6	11	NULL	NULL	NULL	RyR2	GP		bind					FKBP12.6	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37941_s_174	16157601	A CPVT-linked RyR2 mutant in the central region (S2246L) also displays normal RyR2-FKBP12.6 binding ( ).	bind
33870	2	9807	6	11	NULL	NULL	NULL	RyR2	GP	mutant	bind			S2246L		FKBP12.6	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37941_s_174	16157601	A CPVT-linked RyR2 mutant in the central region (S2246L) also displays normal RyR2-FKBP12.6 binding ( ).	bind
40978	1	9807	7	11	NULL	NULL	NULL	CPVT-linked RyR2 	GP	mutant	bind		normally	central region S2246L		FKBP12.6	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37941_s_174	16157601	A CPVT-linked RyR2 mutant in the central region (S2246L) also displays normal RyR2-FKBP12.6 binding ( ).	bind
33871	1	9808	6	11	NULL	NULL	NULL	Brk	GP		represses					D-h	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_development_131_11_2681_s_305	15128656	A CRE in the D- h repression element is required for repression   Given the genetic evidence that Brk represses D- h expression and that Brk binds the CMB element in vitro, the most straightforward hypothesis is that Brk acts directly through the CMB in vivo to repress D- h expression.	bind
33872	2	9808	6	11	NULL	NULL	NULL	Brk	GP		bind									CMB element	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_131_11_2681_s_305	15128656	A CRE in the D- h repression element is required for repression   Given the genetic evidence that Brk represses D- h expression and that Brk binds the CMB element in vitro, the most straightforward hypothesis is that Brk acts directly through the CMB in vivo to repress D- h expression.	bind
33873	3	9808	6	11	NULL	NULL	NULL	Brk	GP		acts through		directly							CMB	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_development_131_11_2681_s_305	15128656	A CRE in the D- h repression element is required for repression   Given the genetic evidence that Brk represses D- h expression and that Brk binds the CMB element in vitro, the most straightforward hypothesis is that Brk acts directly through the CMB in vivo to repress D- h expression.	bind
33874	4	9808	6	11	NULL	NULL	NULL	statement 3	Process		leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_131_11_2681_s_305	15128656	A CRE in the D- h repression element is required for repression   Given the genetic evidence that Brk represses D- h expression and that Brk binds the CMB element in vitro, the most straightforward hypothesis is that Brk acts directly through the CMB in vivo to repress D- h expression.	bind
40979	1	9808	7	11	NULL	NULL	NULL	Brk	GP		binds									CMB element	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_development_131_11_2681_s_305	15128656	A CRE in the D- h repression element is required for repression   Given the genetic evidence that Brk represses D- h expression and that Brk binds the CMB element in vitro, the most straightforward hypothesis is that Brk acts directly through the CMB in vivo to repress D- h expression.	bind
40980	2	9808	7	11	NULL	NULL	NULL	Brk	GP		acts through		directly							CMB	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_development_131_11_2681_s_305	15128656	A CRE in the D- h repression element is required for repression   Given the genetic evidence that Brk represses D- h expression and that Brk binds the CMB element in vitro, the most straightforward hypothesis is that Brk acts directly through the CMB in vivo to repress D- h expression.	bind
40981	3	9808	7	11	NULL	NULL	NULL	Brk	GP		repress					D- h	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_development_131_11_2681_s_305	15128656	A CRE in the D- h repression element is required for repression   Given the genetic evidence that Brk represses D- h expression and that Brk binds the CMB element in vitro, the most straightforward hypothesis is that Brk acts directly through the CMB in vivo to repress D- h expression.	bind
40982	4	9808	7	11	NULL	NULL	NULL	statement 3	Process		occur through					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_131_11_2681_s_305	15128656	A CRE in the D- h repression element is required for repression   Given the genetic evidence that Brk represses D- h expression and that Brk binds the CMB element in vitro, the most straightforward hypothesis is that Brk acts directly through the CMB in vivo to repress D- h expression.	bind
33875	1	9809	6	11	NULL	NULL	NULL	statement 3	Process		bind					CREB1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5329_s_30	15964791	A CRE-like element in the 5''-flanking region of the MuSK gene binds to CREB1 to inhibit the MuSK promoter activity.	bind
33876	2	9809	6	11	NULL	NULL	NULL	statement 1	Process		inhibits					MuSK	GP	activity of 		promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5329_s_30	15964791	A CRE-like element in the 5''-flanking region of the MuSK gene binds to CREB1 to inhibit the MuSK promoter activity.	bind
56787	3	9809	6	11	NULL	NULL	NULL				is present in				CRE element	MuSK gene	GP			5''-flanking region	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5329_s_30	15964791	A CRE-like element in the 5''-flanking region of the MuSK gene binds to CREB1 to inhibit the MuSK promoter activity.	bind
40984	1	9809	7	11	NULL	NULL	NULL	 CREB1	GP		binds					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5329_s_30	15964791	A CRE-like element in the 5''-flanking region of the MuSK gene binds to CREB1 to inhibit the MuSK promoter activity.	bind
40985	2	9809	7	11	NULL	NULL	NULL	statement 1	Process		inhibit					MuSK	GP	activity of		promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5329_s_30	15964791	A CRE-like element in the 5''-flanking region of the MuSK gene binds to CREB1 to inhibit the MuSK promoter activity.	bind
56788	3	9809	7	11	NULL	NULL	NULL				is present in				CRE element	MuSK gene	GP			5''-flanking region	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5329_s_30	15964791	A CRE-like element in the 5''-flanking region of the MuSK gene binds to CREB1 to inhibit the MuSK promoter activity.	bind
33945	1	9810	6	11	NULL	NULL	NULL	CREB	GP		bind			B-ZIP domain		oligonucleotide	NucleicAcid			CRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_967_s_149	9447994	A CREB B-ZIP homodimer retarded the mobility of the radiolabeled double-stranded 25-bp oligonucleotide probe containing a single consensus CRE (Fig.  3A, lane 2), and an equimolar concentration of A-CREB (lane 3) effectively inhibited binding of the CREB B-ZIP domain to the CRE-containing oligonucleotide.	bind
33946	2	9810	6	11	NULL	NULL	NULL	A-CREB	GP		inhibits		effectively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_967_s_149	9447994	A CREB B-ZIP homodimer retarded the mobility of the radiolabeled double-stranded 25-bp oligonucleotide probe containing a single consensus CRE (Fig.  3A, lane 2), and an equimolar concentration of A-CREB (lane 3) effectively inhibited binding of the CREB B-ZIP domain to the CRE-containing oligonucleotide.	bind
40986	1	9810	7	11	NULL	NULL	NULL	CREB	GP		bind			B-ZIP domain		oligonucleotide	NucleicAcid			CRE	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_967_s_149	9447994	A CREB B-ZIP homodimer retarded the mobility of the radiolabeled double-stranded 25-bp oligonucleotide probe containing a single consensus CRE (Fig.  3A, lane 2), and an equimolar concentration of A-CREB (lane 3) effectively inhibited binding of the CREB B-ZIP domain to the CRE-containing oligonucleotide.	bind
40987	2	9810	7	11	NULL	NULL	NULL	A-CREB 	GP		inhibits		effectively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_2_967_s_149	9447994	A CREB B-ZIP homodimer retarded the mobility of the radiolabeled double-stranded 25-bp oligonucleotide probe containing a single consensus CRE (Fig.  3A, lane 2), and an equimolar concentration of A-CREB (lane 3) effectively inhibited binding of the CREB B-ZIP domain to the CRE-containing oligonucleotide.	bind
33877	1	9811	6	11	NULL	NULL	NULL	CREB Family Member	GP		bind					BDNF	GP			CRE	NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_4_709_s_282	9581763	A CREB Family Member Binds to the  BDNF-CRE and Mediates  BDNF Transcription	bind
33878	2	9811	6	11	NULL	NULL	NULL	statement 1	Process		mediates					BDNF	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_4_709_s_282	9581763	A CREB Family Member Binds to the  BDNF-CRE and Mediates  BDNF Transcription	bind
40988	1	9811	7	11	NULL	NULL	NULL	CREB Family Member 	GP		binds to					BDNF	GP			CRE	NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_4_709_s_282	9581763	A CREB Family Member Binds to the  BDNF-CRE and Mediates  BDNF Transcription	bind
40989	2	9811	7	11	NULL	NULL	NULL	statement 1	Process		mediates					BDNF	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_20_4_709_s_282	9581763	A CREB Family Member Binds to the  BDNF-CRE and Mediates  BDNF Transcription	bind
33879	1	9812	6	11	NULL	NULL	NULL	Ren-1c	GP		contains				enhancer					CREB/cAMP-response element modulator protein binding site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_35_32489_s_251	11432851	A CREB/cAMP-response element modulator protein binding site within the  Ren-1c enhancer located at  2.6 kb is critical for the enhancer function.	bind
33880	2	9812	6	11	NULL	NULL	NULL	Ren-1c	GP		is critical for				CREB/cAMP-response element modulator protein binding site	Ren-1c	GP	function of 		enhancer	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_35_32489_s_251	11432851	A CREB/cAMP-response element modulator protein binding site within the  Ren-1c enhancer located at  2.6 kb is critical for the enhancer function.	bind
40990	1	9812	7	11	NULL	NULL	NULL	Ren-1c	GP		contains				enhancer					CREB/cAMP-response element modulator protein binding site 	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_35_32489_s_251	11432851	A CREB/cAMP-response element modulator protein binding site within the  Ren-1c enhancer located at  2.6 kb is critical for the enhancer function.	bind
40991	2	9812	7	11	NULL	NULL	NULL	Ren-1c	GP		is critical for				CREB/cAMP-response element modulator protein binding site 	Ren-1c	GP	function of		enhancer	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_35_32489_s_251	11432851	A CREB/cAMP-response element modulator protein binding site within the  Ren-1c enhancer located at  2.6 kb is critical for the enhancer function.	bind
33881	1	9813	6	11	NULL	NULL	NULL	CREB/CREM family protein	GP		bind					A3 AR	GP	partial;;mouse		CRE site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_62_5_1167_s_211	12391281	A CREB/CREM family protein binds the partial CRE of the mouse A3 AR promoter.	bind
40992	1	9813	7	11	NULL	NULL	NULL	CREB/CREM family protein	GP		bind					A3 AR	GP	partial;;mouse		CRE site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_62_5_1167_s_211	12391281	A CREB/CREM family protein binds the partial CRE of the mouse A3 AR promoter.	bind
34721	1	9815	6	11	NULL	NULL	NULL	Abl	GP		bind			SH3 domain					proline in the SH2-CD linker		NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_27_s_174	12887890	A critical component of the c-Abl regulatory mechanism is shared with Src kinases: the Abl SH3 domain binds to a single proline (Pro242 in type Ib/IV c-Abl) in the SH2-CD linker that is conserved in Src family members.	bind
34972	2	9815	6	11	NULL	NULL	NULL				is conserved in			SH2-CD linker		Src family members	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_27_s_174	12887890	A critical component of the c-Abl regulatory mechanism is shared with Src kinases: the Abl SH3 domain binds to a single proline (Pro242 in type Ib/IV c-Abl) in the SH2-CD linker that is conserved in Src family members.	bind
40995	1	9815	7	11	NULL	NULL	NULL	Abl	GP		binds to			SH3 domain					Proline in SH2-CD linker		NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_27_s_174	12887890	A critical component of the c-Abl regulatory mechanism is shared with Src kinases: the Abl SH3 domain binds to a single proline (Pro242 in type Ib/IV c-Abl) in the SH2-CD linker that is conserved in Src family members.	bind
40996	2	9815	7	11	NULL	NULL	NULL				is conserved in			SH2-CD linker		Src family members	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_27_s_174	12887890	A critical component of the c-Abl regulatory mechanism is shared with Src kinases: the Abl SH3 domain binds to a single proline (Pro242 in type Ib/IV c-Abl) in the SH2-CD linker that is conserved in Src family members.	bind
34064	1	9816	6	11	NULL	NULL	NULL	SecA	GP		bind					chaperone-precursor complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_66_0_199_s_212	9242906	A critical cytoplasmic component of the  translocase is SecA, which binds to the chaperone-precursor complex and to SecY,  dependent on the presence of anionic phospholipids in the membrane ( 98).	bind
34066	2	9816	6	11	NULL	NULL	NULL	SecA	GP		bind					SecY	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_66_0_199_s_212	9242906	A critical cytoplasmic component of the  translocase is SecA, which binds to the chaperone-precursor complex and to SecY,  dependent on the presence of anionic phospholipids in the membrane ( 98).	bind
34718	3	9816	6	11	NULL	NULL	NULL	statement 1	Process		is dependent on					anionic phospholipids	Chemical	presence of			NULL	membrane	NULL	NULL	NULL	NULL	gw70_annurevbiochem_66_0_199_s_212	9242906	A critical cytoplasmic component of the  translocase is SecA, which binds to the chaperone-precursor complex and to SecY,  dependent on the presence of anionic phospholipids in the membrane ( 98).	bind
34719	4	9816	6	11	NULL	NULL	NULL	statement 2	Process		is dependent on					anionic phospholipids	Chemical	presence of			NULL	membrane	NULL	NULL	NULL	NULL	gw70_annurevbiochem_66_0_199_s_212	9242906	A critical cytoplasmic component of the  translocase is SecA, which binds to the chaperone-precursor complex and to SecY,  dependent on the presence of anionic phospholipids in the membrane ( 98).	bind
34720	5	9816	6	11	NULL	NULL	NULL	SecA	GP		is a critical cytoplasmic component of					translocase	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_66_0_199_s_212	9242906	A critical cytoplasmic component of the  translocase is SecA, which binds to the chaperone-precursor complex and to SecY,  dependent on the presence of anionic phospholipids in the membrane ( 98).	bind
41055	1	9816	7	11	NULL	NULL	NULL	SecA	GP		is a critical cytoplasmic component of					translocase 	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_66_0_199_s_212	9242906	A critical cytoplasmic component of the  translocase is SecA, which binds to the chaperone-precursor complex and to SecY,  dependent on the presence of anionic phospholipids in the membrane ( 98).	bind
41056	2	9816	7	11	NULL	NULL	NULL	chaperone	GP		complex with					precursor	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_66_0_199_s_212	9242906	A critical cytoplasmic component of the  translocase is SecA, which binds to the chaperone-precursor complex and to SecY,  dependent on the presence of anionic phospholipids in the membrane ( 98).	bind
41057	3	9816	7	11	NULL	NULL	NULL	SecA	GP		binds to					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_66_0_199_s_212	9242906	A critical cytoplasmic component of the  translocase is SecA, which binds to the chaperone-precursor complex and to SecY,  dependent on the presence of anionic phospholipids in the membrane ( 98).	bind
41058	4	9816	7	11	NULL	NULL	NULL	SecA	GP		binds to					SecY	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_66_0_199_s_212	9242906	A critical cytoplasmic component of the  translocase is SecA, which binds to the chaperone-precursor complex and to SecY,  dependent on the presence of anionic phospholipids in the membrane ( 98).	bind
41059	5	9816	7	11	NULL	NULL	NULL	statement 3	Process		depends on					anionic phospholipids	Chemical				NULL	in the membrane	NULL	NULL	NULL	NULL	gw70_annurevbiochem_66_0_199_s_212	9242906	A critical cytoplasmic component of the  translocase is SecA, which binds to the chaperone-precursor complex and to SecY,  dependent on the presence of anionic phospholipids in the membrane ( 98).	bind
41060	6	9816	7	11	NULL	NULL	NULL	statement 4	Process		depends on					anionic phospholipids	Chemical				NULL	in the membrane	NULL	NULL	NULL	NULL	gw70_annurevbiochem_66_0_199_s_212	9242906	A critical cytoplasmic component of the  translocase is SecA, which binds to the chaperone-precursor complex and to SecY,  dependent on the presence of anionic phospholipids in the membrane ( 98).	bind
34068	1	9817	6	11	NULL	NULL	NULL	DnaA protein	GP	Escherichia coli	bind		cooperatively			Plasmid RK2	NucleicAcid			Replication Origin	NULL		NULL	NULL	NULL	NULL	gw60_embo_17_15_4511_s_752	9687517	A Critical DnaA Box Directs the Cooperative Binding of the Escherichia coli DnaA Protein to the Plasmid RK2 Replication Origin.	bind
34069	2	9817	6	11	NULL	NULL	NULL				directs				DnaA Box	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_15_4511_s_752	9687517	A Critical DnaA Box Directs the Cooperative Binding of the Escherichia coli DnaA Protein to the Plasmid RK2 Replication Origin.	bind
41061	1	9817	7	11	NULL	NULL	NULL	DnaA Protein	GP	 Escherichia coli	bind		cooperatively			Plasmid RK2	NucleicAcid			Replication Origin	NULL		NULL	NULL	NULL	NULL	gw60_embo_17_15_4511_s_752	9687517	A Critical DnaA Box Directs the Cooperative Binding of the Escherichia coli DnaA Protein to the Plasmid RK2 Replication Origin.	bind
41062	2	9817	7	11	NULL	NULL	NULL				directs				DnaA Box	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_15_4511_s_752	9687517	A Critical DnaA Box Directs the Cooperative Binding of the Escherichia coli DnaA Protein to the Plasmid RK2 Replication Origin.	bind
34071	1	9819	6	11	NULL	NULL	NULL	IL-4	GP		bind					IL-4R	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_9_1_13_s_14	9697832	A critical event in the activation of IL-4 responsive genes involves the phosphorylation and nuclear translocation of the signal transducer and activator of transcription Stat6, which is specifically activated by binding of IL-4 to the IL-4R (  Hou et al. 1994  ; Ryan et al. 1996  ).	bind
34072	2	9819	6	11	NULL	NULL	NULL	Stat	GP		is					signal transducer and activator of transcription	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_9_1_13_s_14	9697832	A critical event in the activation of IL-4 responsive genes involves the phosphorylation and nuclear translocation of the signal transducer and activator of transcription Stat6, which is specifically activated by binding of IL-4 to the IL-4R (  Hou et al. 1994  ; Ryan et al. 1996  ).	bind
34074	3	9819	6	11	NULL	NULL	NULL	IL-4 responsive genes	GP	activation of	involves					Stat6	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_9_1_13_s_14	9697832	A critical event in the activation of IL-4 responsive genes involves the phosphorylation and nuclear translocation of the signal transducer and activator of transcription Stat6, which is specifically activated by binding of IL-4 to the IL-4R (  Hou et al. 1994  ; Ryan et al. 1996  ).	bind
34075	4	9819	6	11	NULL	NULL	NULL	IL-4 responsive genes	GP	activation of	involves					Stat6	GP	nuclear translocation of 			NULL		NULL	NULL	NULL	NULL	gw60_immunity_9_1_13_s_14	9697832	A critical event in the activation of IL-4 responsive genes involves the phosphorylation and nuclear translocation of the signal transducer and activator of transcription Stat6, which is specifically activated by binding of IL-4 to the IL-4R (  Hou et al. 1994  ; Ryan et al. 1996  ).	bind
34077	5	9819	6	11	NULL	NULL	NULL	statement 1	Process		activates					Stat6	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_9_1_13_s_14	9697832	A critical event in the activation of IL-4 responsive genes involves the phosphorylation and nuclear translocation of the signal transducer and activator of transcription Stat6, which is specifically activated by binding of IL-4 to the IL-4R (  Hou et al. 1994  ; Ryan et al. 1996  ).	bind
41063	1	9819	7	11	NULL	NULL	NULL	IL-4 responsive genes	GP	activation of 	involves					Stat6	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_9_1_13_s_14	9697832	A critical event in the activation of IL-4 responsive genes involves the phosphorylation and nuclear translocation of the signal transducer and activator of transcription Stat6, which is specifically activated by binding of IL-4 to the IL-4R (  Hou et al. 1994  ; Ryan et al. 1996  ).	bind
41064	2	9819	7	11	NULL	NULL	NULL	IL-4 responsive genes	GP	activation of	involves					Stat6	GP	nuclear translocation of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_9_1_13_s_14	9697832	A critical event in the activation of IL-4 responsive genes involves the phosphorylation and nuclear translocation of the signal transducer and activator of transcription Stat6, which is specifically activated by binding of IL-4 to the IL-4R (  Hou et al. 1994  ; Ryan et al. 1996  ).	bind
41068	3	9819	7	11	NULL	NULL	NULL	IL-4	GP		bind					IL-4R	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_9_1_13_s_14	9697832	A critical event in the activation of IL-4 responsive genes involves the phosphorylation and nuclear translocation of the signal transducer and activator of transcription Stat6, which is specifically activated by binding of IL-4 to the IL-4R (  Hou et al. 1994  ; Ryan et al. 1996  ).	bind
41077	4	9819	7	11	NULL	NULL	NULL	statement 3	Process		activates		specifically			Stat6	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_9_1_13_s_14	9697832	A critical event in the activation of IL-4 responsive genes involves the phosphorylation and nuclear translocation of the signal transducer and activator of transcription Stat6, which is specifically activated by binding of IL-4 to the IL-4R (  Hou et al. 1994  ; Ryan et al. 1996  ).	bind
41080	5	9819	7	11	NULL	NULL	NULL	Stat6	GP		is					signal transducer and activator of transcription 6	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_9_1_13_s_14	9697832	A critical event in the activation of IL-4 responsive genes involves the phosphorylation and nuclear translocation of the signal transducer and activator of transcription Stat6, which is specifically activated by binding of IL-4 to the IL-4R (  Hou et al. 1994  ; Ryan et al. 1996  ).	bind
49560	1	9820	6	11	NULL	NULL	NULL	dATP	Chemical		bind					CTX II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17869_s_199	10364232	A critical examination of the observed intramolecular NOEs between the sugar and the adenine ring (in the dATP molecule bound to CTX II) shows that intramolecular NOEs (between H8 proton of the adenine ring and the H1'', H2'', H2''', H4'' of the deoxy ribose sugar) are quite similar to that expected for the  anti conformation (of the nucleotide).	bind
49547	1	9820	7	11	NULL	NULL	NULL	dATP molecule	Chemical		bind					CTXII	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_17869_s_199	10364232	A critical examination of the observed intramolecular NOEs between the sugar and the adenine ring (in the dATP molecule bound to CTX II) shows that intramolecular NOEs (between H8 proton of the adenine ring and the H1'', H2'', H2''', H4'' of the deoxy ribose sugar) are quite similar to that expected for the  anti conformation (of the nucleotide).	bind
34080	1	9822	6	11	NULL	NULL	NULL	TR	GP		bind					TH-inducible genes	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_50_41222_s_35	16236718	A critical parameter for the dual function model is TR binding to TH-inducible genes  in vivo.	bind
41094	1	9822	7	11	NULL	NULL	NULL	TR	GP		bind					TH-inducible genes	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_50_41222_s_35	16236718	A critical parameter for the dual function model is TR binding to TH-inducible genes  in vivo.	bind
34084	1	9823	6	11	NULL	NULL	NULL	Crm1	GP		bind					target proteins	GP		leucine-rich NES sequences		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7273_s_159	10982844	A critical regulatory event in nucleocytoplasmic transport is the binding of a nuclear export receptor such as Crm1 to the leucine-rich NES sequences of target proteins.	bind
34086	2	9823	6	11	NULL	NULL	NULL	Crm1	GP		is a type of					nuclear export receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7273_s_159	10982844	A critical regulatory event in nucleocytoplasmic transport is the binding of a nuclear export receptor such as Crm1 to the leucine-rich NES sequences of target proteins.	bind
34088	3	9823	6	11	NULL	NULL	NULL	statement 1	Process		is a regulatory event in		critical			nucleocytoplasmic transport	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7273_s_159	10982844	A critical regulatory event in nucleocytoplasmic transport is the binding of a nuclear export receptor such as Crm1 to the leucine-rich NES sequences of target proteins.	bind
41099	1	9823	7	11	NULL	NULL	NULL	Crm1	GP		bind					target proteins	GP		leucine-rich NES sequences 		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7273_s_159	10982844	A critical regulatory event in nucleocytoplasmic transport is the binding of a nuclear export receptor such as Crm1 to the leucine-rich NES sequences of target proteins.	bind
41101	2	9823	7	11	NULL	NULL	NULL	Crm1	GP		is a type of					nuclear export receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7273_s_159	10982844	A critical regulatory event in nucleocytoplasmic transport is the binding of a nuclear export receptor such as Crm1 to the leucine-rich NES sequences of target proteins.	bind
41120	3	9823	7	11	NULL	NULL	NULL	statement 1	Process		regulates					nucleocytoplasmic transport	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7273_s_159	10982844	A critical regulatory event in nucleocytoplasmic transport is the binding of a nuclear export receptor such as Crm1 to the leucine-rich NES sequences of target proteins.	bind
34089	1	9824	6	11	NULL	NULL	NULL	PP1	GP		bind			threonine 340		c-SrcP	GP	mouse	ATP-binding pocket		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_1_59_s_175	16267045	A critical residue for PP1 to fit into the ATP binding pocket of mouse c-SrcP is threonine 340 (corresponding to v-Src threonine 338).	bind
41123	1	9824	7	11	NULL	NULL	NULL	PP1	GP		fits into the			threonine 340		c-SrcP	GP	mouse	ATP binding pocket		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_1_59_s_175	16267045	A critical residue for PP1 to fit into the ATP binding pocket of mouse c-SrcP is threonine 340 (corresponding to v-Src threonine 338).	bind
41129	2	9824	7	11	NULL	NULL	NULL	c-SrcP	GP		corresponds to			threonine 340 		v-Src 	GP		threonine 338		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_1_59_s_175	16267045	A critical residue for PP1 to fit into the ATP binding pocket of mouse c-SrcP is threonine 340 (corresponding to v-Src threonine 338).	bind
34090	1	9825	6	11	NULL	NULL	NULL	VWF	GP		bind					glycoprotein Ib-IX	GP	platelet			NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_blood_106_6_15941906_s_1	15941906	A critical role for 14-3-3zeta protein in regulating the VWF binding function of platelet glycoprotein Ib-IX and its therapeutic implications..	bind
34091	2	9825	6	11	NULL	NULL	NULL	14-3-3 zeta protein	GP		regulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_blood_106_6_15941906_s_1	15941906	A critical role for 14-3-3zeta protein in regulating the VWF binding function of platelet glycoprotein Ib-IX and its therapeutic implications..	bind
41140	1	9825	7	11	NULL	NULL	NULL	VWF	GP		bind					glycoprotein Ib-IX	GP	platelet			NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_blood_106_6_15941906_s_1	15941906	A critical role for 14-3-3zeta protein in regulating the VWF binding function of platelet glycoprotein Ib-IX and its therapeutic implications..	bind
41141	2	9825	7	11	NULL	NULL	NULL	14-3-3zeta protein	GP		regulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_blood_106_6_15941906_s_1	15941906	A critical role for 14-3-3zeta protein in regulating the VWF binding function of platelet glycoprotein Ib-IX and its therapeutic implications..	bind
34157	1	9826	6	11	NULL	NULL	NULL	Cbl	GP		bind			phosphotyrosine-binding domain		Syk	GP		phosphotyrosine 323		NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_20_0_669_s_1334	11861615	A critical role for Cbl phosphotyrosine-binding domain binding to Syk phosphotyrosine  323.	bind
41142	1	9826	7	11	NULL	NULL	NULL	Cbl	GP		bind			phosphotyrosine-binding domain		Syk	GP		phosphotyrosine 323		NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_20_0_669_s_1334	11861615	A critical role for Cbl phosphotyrosine-binding domain binding to Syk phosphotyrosine  323.	bind
34158	1	9829	6	11	NULL	NULL	NULL	TAT protein	GP		bind									TAR element	NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_retrovirology_2_1_16293193_s_3	16293193	A critical step in the production of new HIV virions involves  the TAT protein binding to the TAR element.	bind
34159	2	9829	6	11	NULL	NULL	NULL	HIV virions	Organism	production of	involves					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_retrovirology_2_1_16293193_s_3	16293193	A critical step in the production of new HIV virions involves  the TAT protein binding to the TAR element.	bind
41143	1	9829	7	11	NULL	NULL	NULL	TAT protein	GP		bind									TAR element	NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_retrovirology_2_1_16293193_s_3	16293193	A critical step in the production of new HIV virions involves  the TAT protein binding to the TAR element.	bind
41144	2	9829	7	11	NULL	NULL	NULL	new HIV virions	Organism	production of	involves					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_retrovirology_2_1_16293193_s_3	16293193	A critical step in the production of new HIV virions involves  the TAT protein binding to the TAR element.	bind
34160	1	9830	6	11	NULL	NULL	NULL	METS	GP		bind		selectively			c-Myc	GP			Ets site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_109_2_169_s_255	12007404	A critical test of the ability of METS to discriminate between monomeric sites in cell cycle-regulatory genes and composite elements in cell type-specific genes was provided by ChIP assays, which clearly established selective binding of METS to Ets sites in the  c-Myc,  Cdc2, and  p54 promoters, but not to the composite AP-1/Ets site in the  SR-A promoter in terminally differentiated macrophages.	bind
34161	2	9830	6	11	NULL	NULL	NULL	METS	GP		bind		selectively			p54	GP			Ets site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_109_2_169_s_255	12007404	A critical test of the ability of METS to discriminate between monomeric sites in cell cycle-regulatory genes and composite elements in cell type-specific genes was provided by ChIP assays, which clearly established selective binding of METS to Ets sites in the  c-Myc,  Cdc2, and  p54 promoters, but not to the composite AP-1/Ets site in the  SR-A promoter in terminally differentiated macrophages.	bind
34162	3	9830	6	11	NULL	NULL	NULL	METS	GP		bind		selectively			Cdc2	GP			Ets site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_109_2_169_s_255	12007404	A critical test of the ability of METS to discriminate between monomeric sites in cell cycle-regulatory genes and composite elements in cell type-specific genes was provided by ChIP assays, which clearly established selective binding of METS to Ets sites in the  c-Myc,  Cdc2, and  p54 promoters, but not to the composite AP-1/Ets site in the  SR-A promoter in terminally differentiated macrophages.	bind
34163	4	9830	6	11	NULL	NULL	NULL	METS	GP		does not bind					SR-A	GP			composite AP-1/Ets site of promoter	NULL	terminally differentiated macrophages	NULL	NULL	NULL	NULL	gw60_cell_109_2_169_s_255	12007404	A critical test of the ability of METS to discriminate between monomeric sites in cell cycle-regulatory genes and composite elements in cell type-specific genes was provided by ChIP assays, which clearly established selective binding of METS to Ets sites in the  c-Myc,  Cdc2, and  p54 promoters, but not to the composite AP-1/Ets site in the  SR-A promoter in terminally differentiated macrophages.	bind
41145	1	9830	7	11	NULL	NULL	NULL	 METS	GP		bind		selectively			c-Myc	GP			Ets sites in the promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_109_2_169_s_255	12007404	A critical test of the ability of METS to discriminate between monomeric sites in cell cycle-regulatory genes and composite elements in cell type-specific genes was provided by ChIP assays, which clearly established selective binding of METS to Ets sites in the  c-Myc,  Cdc2, and  p54 promoters, but not to the composite AP-1/Ets site in the  SR-A promoter in terminally differentiated macrophages.	bind
41146	2	9830	7	11	NULL	NULL	NULL	METS	GP		bind		selectively			Cdc2	GP			Ets sites in the promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_109_2_169_s_255	12007404	A critical test of the ability of METS to discriminate between monomeric sites in cell cycle-regulatory genes and composite elements in cell type-specific genes was provided by ChIP assays, which clearly established selective binding of METS to Ets sites in the  c-Myc,  Cdc2, and  p54 promoters, but not to the composite AP-1/Ets site in the  SR-A promoter in terminally differentiated macrophages.	bind
41147	3	9830	7	11	NULL	NULL	NULL	METS	GP		bind		selectively			p54	GP			Ets sites in the promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_109_2_169_s_255	12007404	A critical test of the ability of METS to discriminate between monomeric sites in cell cycle-regulatory genes and composite elements in cell type-specific genes was provided by ChIP assays, which clearly established selective binding of METS to Ets sites in the  c-Myc,  Cdc2, and  p54 promoters, but not to the composite AP-1/Ets site in the  SR-A promoter in terminally differentiated macrophages.	bind
41148	4	9830	7	11	NULL	NULL	NULL	METS	GP		does not bind					SR-A	GP			composite AP-1/Ets site in the promoter	NULL	terminally differentiated macrophages	NULL	NULL	NULL	NULL	gw60_cell_109_2_169_s_255	12007404	A critical test of the ability of METS to discriminate between monomeric sites in cell cycle-regulatory genes and composite elements in cell type-specific genes was provided by ChIP assays, which clearly established selective binding of METS to Ets sites in the  c-Myc,  Cdc2, and  p54 promoters, but not to the composite AP-1/Ets site in the  SR-A promoter in terminally differentiated macrophages.	bind
34164	1	9831	6	11	NULL	NULL	NULL	apolipoprotein	Chemical		bind			B domain		LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_271	9012650	A cross-species comparison of the apolipoprotein B domain that binds to the LDL receptor.	bind
41149	1	9831	7	11	NULL	NULL	NULL	 apolipoprotein 	Chemical		binds to			B domain		LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_149_s_271	9012650	A cross-species comparison of the apolipoprotein B domain that binds to the LDL receptor.	bind
34715	1	9832	6	11	NULL	NULL	NULL	CRP-cyclic AMP complex	GP		bind					dorf	NucleicAcid	stronger		CRP recognition site	NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-bacteriol_179_9_9139892_s_12	9139892	A CRP  recognition site is associated with each promoter in the crp-dorf intergenic  region; binding of the CRP-cyclic AMP complex to the stronger dorf CRP  recognition site activates transcription from the dorf promoter and represses  transcription from the crp promoter.	bind
34716	2	9832	6	11	NULL	NULL	NULL	statement 1	Process		activates 					dorf 	NucleicAcid	transcription of		promoter	NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-bacteriol_179_9_9139892_s_12	9139892	A CRP  recognition site is associated with each promoter in the crp-dorf intergenic  region; binding of the CRP-cyclic AMP complex to the stronger dorf CRP  recognition site activates transcription from the dorf promoter and represses  transcription from the crp promoter.	bind
34717	3	9832	6	11	NULL	NULL	NULL	statement 1	Process		represses					crp	GP	transcription of		promoter	NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-bacteriol_179_9_9139892_s_12	9139892	A CRP  recognition site is associated with each promoter in the crp-dorf intergenic  region; binding of the CRP-cyclic AMP complex to the stronger dorf CRP  recognition site activates transcription from the dorf promoter and represses  transcription from the crp promoter.	bind
41150	1	9832	7	11	NULL	NULL	NULL	 CRP-cyclic AMP complex 	GP		bind					dorf	NucleicAcid	stronger		CRP recognition site	NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-bacteriol_179_9_9139892_s_12	9139892	A CRP  recognition site is associated with each promoter in the crp-dorf intergenic  region; binding of the CRP-cyclic AMP complex to the stronger dorf CRP  recognition site activates transcription from the dorf promoter and represses  transcription from the crp promoter.	bind
41151	2	9832	7	11	NULL	NULL	NULL	statement 1	Process		activates					dorf	NucleicAcid	transcription of		promoter	NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-bacteriol_179_9_9139892_s_12	9139892	A CRP  recognition site is associated with each promoter in the crp-dorf intergenic  region; binding of the CRP-cyclic AMP complex to the stronger dorf CRP  recognition site activates transcription from the dorf promoter and represses  transcription from the crp promoter.	bind
41152	3	9832	7	11	NULL	NULL	NULL	statement 1	Process		repress					crp	GP	transcription of		promoter	NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-bacteriol_179_9_9139892_s_12	9139892	A CRP  recognition site is associated with each promoter in the crp-dorf intergenic  region; binding of the CRP-cyclic AMP complex to the stronger dorf CRP  recognition site activates transcription from the dorf promoter and represses  transcription from the crp promoter.	bind
34165	1	9833	6	11	NULL	NULL	NULL	SWI5	GP		encodes					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_5_687_s_34	8625407	A crucial role in directing mother cell - specific  HO expression  has been established for the transcription factor encoded by  SWI5 (Nasmyth, 1993   ).	bind
34166	2	9833	6	11	NULL	NULL	NULL	SWI5	GP		directs					HO	GP	expression of;; mother cell-specific			NULL		NULL	NULL	NULL	NULL	gw60_cell_84_5_687_s_34	8625407	A crucial role in directing mother cell - specific  HO expression  has been established for the transcription factor encoded by  SWI5 (Nasmyth, 1993   ).	bind
41153	1	9833	7	11	NULL	NULL	NULL	SWI5 	GP		encodes					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_5_687_s_34	8625407	A crucial role in directing mother cell - specific  HO expression  has been established for the transcription factor encoded by  SWI5 (Nasmyth, 1993   ).	bind
56897	2	9833	7	11	NULL	NULL	NULL	SWI5	GP		directs					HO	GP	expression of;; mother cell-specific			NULL		NULL	NULL	NULL	NULL	gw60_cell_84_5_687_s_34	8625407	A crucial role in directing mother cell - specific  HO expression  has been established for the transcription factor encoded by  SWI5 (Nasmyth, 1993   ).	bind
34208	1	9835	6	11	NULL	NULL	NULL	Adk	GP	B.stearothermophilus	bind					Ap5A plus magnesium	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_4_1073_s_184	11842120	A crystal structure of  B.stearothermophilus Adk bound to Ap5A plus magnesium or manganese showed that the Asp and Arg side chains both form hydrogen bonds to a water molecule within the octahedral coordination sphere of the metal ion ( 18).	bind
34211	2	9835	6	11	NULL	NULL	NULL	Adk	GP	B.stearothermophilus	bind					Ap5A plus manganese	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_4_1073_s_184	11842120	A crystal structure of  B.stearothermophilus Adk bound to Ap5A plus magnesium or manganese showed that the Asp and Arg side chains both form hydrogen bonds to a water molecule within the octahedral coordination sphere of the metal ion ( 18).	bind
34213	3	9835	6	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_4_1073_s_184	11842120	A crystal structure of  B.stearothermophilus Adk bound to Ap5A plus magnesium or manganese showed that the Asp and Arg side chains both form hydrogen bonds to a water molecule within the octahedral coordination sphere of the metal ion ( 18).	bind
34217	4	9835	6	11	NULL	NULL	NULL				form hydrogen bonds with			Asp side chains		water molecule	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_4_1073_s_184	11842120	A crystal structure of  B.stearothermophilus Adk bound to Ap5A plus magnesium or manganese showed that the Asp and Arg side chains both form hydrogen bonds to a water molecule within the octahedral coordination sphere of the metal ion ( 18).	bind
34218	5	9835	6	11	NULL	NULL	NULL				form hydrogen bonds with			Arg side chains		water molecule	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_4_1073_s_184	11842120	A crystal structure of  B.stearothermophilus Adk bound to Ap5A plus magnesium or manganese showed that the Asp and Arg side chains both form hydrogen bonds to a water molecule within the octahedral coordination sphere of the metal ion ( 18).	bind
41154	1	9835	7	11	NULL	NULL	NULL	Adk	GP	B.stearothermophilus 	bind					Ap5A plus magnesium	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_4_1073_s_184	11842120	A crystal structure of  B.stearothermophilus Adk bound to Ap5A plus magnesium or manganese showed that the Asp and Arg side chains both form hydrogen bonds to a water molecule within the octahedral coordination sphere of the metal ion ( 18).	bind
41155	2	9835	7	11	NULL	NULL	NULL	Adk	GP	B.stearothermophilus 	bind					Ap5A plus manganese	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_4_1073_s_184	11842120	A crystal structure of  B.stearothermophilus Adk bound to Ap5A plus magnesium or manganese showed that the Asp and Arg side chains both form hydrogen bonds to a water molecule within the octahedral coordination sphere of the metal ion ( 18).	bind
41156	3	9835	7	11	NULL	NULL	NULL	Ap5A	Chemical		forms hydrogen bond with			Asp side chain		water molecule	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_4_1073_s_184	11842120	A crystal structure of  B.stearothermophilus Adk bound to Ap5A plus magnesium or manganese showed that the Asp and Arg side chains both form hydrogen bonds to a water molecule within the octahedral coordination sphere of the metal ion ( 18).	bind
41157	4	9835	7	11	NULL	NULL	NULL	Ap5A	Chemical		forms hydrogen bond with			Arg side chain		water molecule	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_4_1073_s_184	11842120	A crystal structure of  B.stearothermophilus Adk bound to Ap5A plus magnesium or manganese showed that the Asp and Arg side chains both form hydrogen bonds to a water molecule within the octahedral coordination sphere of the metal ion ( 18).	bind
48905	5	9835	7	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_4_1073_s_184	11842120	A crystal structure of  B.stearothermophilus Adk bound to Ap5A plus magnesium or manganese showed that the Asp and Arg side chains both form hydrogen bonds to a water molecule within the octahedral coordination sphere of the metal ion ( 18).	bind
34220	1	9836	6	11	NULL	NULL	NULL	HMGB1	GP		bind			domain A		DNA duplex	NucleicAcid	cisplatin-modified			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_47_43589_s_242	11568187	A crystal structure of HMGB1 domain A bound to a cisplatin-modified DNA duplex revealed the intercalation of a single phenylalanine residue into the hydrophobic wedge created in the minor groove across from the platinum-induced d(GpG) cross-link, with its binding extending mainly to 3' side of the adduct ( 58).	bind
41161	1	9836	7	11	NULL	NULL	NULL	HMGB1	GP		bind			domain A		 DNA duplex	NucleicAcid	cisplatin-modified			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_47_43589_s_242	11568187	A crystal structure of HMGB1 domain A bound to a cisplatin-modified DNA duplex revealed the intercalation of a single phenylalanine residue into the hydrophobic wedge created in the minor groove across from the platinum-induced d(GpG) cross-link, with its binding extending mainly to 3' side of the adduct ( 58).	bind
41165	2	9836	7	11	NULL	NULL	NULL	statement 1	Process		reveals							intercalation of	 phenylalanine residue		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_47_43589_s_242	11568187	A crystal structure of HMGB1 domain A bound to a cisplatin-modified DNA duplex revealed the intercalation of a single phenylalanine residue into the hydrophobic wedge created in the minor groove across from the platinum-induced d(GpG) cross-link, with its binding extending mainly to 3' side of the adduct ( 58).	bind
41173	3	9836	7	11	NULL	NULL	NULL	statement 2	Process		occurs in					minor groove	NucleicAcid	hydrophobic wedge of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_47_43589_s_242	11568187	A crystal structure of HMGB1 domain A bound to a cisplatin-modified DNA duplex revealed the intercalation of a single phenylalanine residue into the hydrophobic wedge created in the minor groove across from the platinum-induced d(GpG) cross-link, with its binding extending mainly to 3' side of the adduct ( 58).	bind
41178	4	9836	7	11	NULL	NULL	NULL	platinum	Chemical		induce					d(GpG) cross-link	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_47_43589_s_242	11568187	A crystal structure of HMGB1 domain A bound to a cisplatin-modified DNA duplex revealed the intercalation of a single phenylalanine residue into the hydrophobic wedge created in the minor groove across from the platinum-induced d(GpG) cross-link, with its binding extending mainly to 3' side of the adduct ( 58).	bind
41179	5	9836	7	11	NULL	NULL	NULL	statement 3	Process		occurs from					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_47_43589_s_242	11568187	A crystal structure of HMGB1 domain A bound to a cisplatin-modified DNA duplex revealed the intercalation of a single phenylalanine residue into the hydrophobic wedge created in the minor groove across from the platinum-induced d(GpG) cross-link, with its binding extending mainly to 3' side of the adduct ( 58).	bind
41180	6	9836	7	11	NULL	NULL	NULL	statement 5	Process		extend to					adduct	Process			3' side of 	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_47_43589_s_242	11568187	A crystal structure of HMGB1 domain A bound to a cisplatin-modified DNA duplex revealed the intercalation of a single phenylalanine residue into the hydrophobic wedge created in the minor groove across from the platinum-induced d(GpG) cross-link, with its binding extending mainly to 3' side of the adduct ( 58).	bind
34224	1	9837	6	11	NULL	NULL	NULL	IleRS	NucleicAcid		bind					tRNAIle	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_23978_s_23	15845536	A crystal structure of IleRS bound to tRNAIle showed that the 3''-end of the tRNA approaches the editing domain, suggesting a plausible structural mechanism in which the flexible 3''-end of misaminoacylated Val-tRNAIle translocates across the enzyme surface from the Rossmann fold domain into the distant editing active site ( ).	bind
34712	2	9837	6	11	NULL	NULL	NULL	Val-tRNAIle 	NucleicAcid	3''-end of;;misaminoacylated	translocates from								Rossmann fold domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_23978_s_23	15845536	A crystal structure of IleRS bound to tRNAIle showed that the 3''-end of the tRNA approaches the editing domain, suggesting a plausible structural mechanism in which the flexible 3''-end of misaminoacylated Val-tRNAIle translocates across the enzyme surface from the Rossmann fold domain into the distant editing active site ( ).	bind
34713	3	9837	6	11	NULL	NULL	NULL	Val-tRNAIle	NucleicAcid	3''-end of;;misaminoacylated	translocates to					distant editing active site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_23978_s_23	15845536	A crystal structure of IleRS bound to tRNAIle showed that the 3''-end of the tRNA approaches the editing domain, suggesting a plausible structural mechanism in which the flexible 3''-end of misaminoacylated Val-tRNAIle translocates across the enzyme surface from the Rossmann fold domain into the distant editing active site ( ).	bind
34714	4	9837	6	11	NULL	NULL	NULL	statement 3	Process		occurs after					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_23978_s_23	15845536	A crystal structure of IleRS bound to tRNAIle showed that the 3''-end of the tRNA approaches the editing domain, suggesting a plausible structural mechanism in which the flexible 3''-end of misaminoacylated Val-tRNAIle translocates across the enzyme surface from the Rossmann fold domain into the distant editing active site ( ).	bind
41181	1	9837	7	11	NULL	NULL	NULL	IleRS	NucleicAcid		bind					tRNAIle	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_23978_s_23	15845536	A crystal structure of IleRS bound to tRNAIle showed that the 3''-end of the tRNA approaches the editing domain, suggesting a plausible structural mechanism in which the flexible 3''-end of misaminoacylated Val-tRNAIle translocates across the enzyme surface from the Rossmann fold domain into the distant editing active site ( ).	bind
41182	2	9837	7	11	NULL	NULL	NULL	tRNA	NucleicAcid	3'' end of	approaches					editing domain	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_23978_s_23	15845536	A crystal structure of IleRS bound to tRNAIle showed that the 3''-end of the tRNA approaches the editing domain, suggesting a plausible structural mechanism in which the flexible 3''-end of misaminoacylated Val-tRNAIle translocates across the enzyme surface from the Rossmann fold domain into the distant editing active site ( ).	bind
41183	3	9837	7	11	NULL	NULL	NULL	Val-tRNAIle	NucleicAcid	3" end of;;misaminoacylated	translocates across					enzyme surface	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_23978_s_23	15845536	A crystal structure of IleRS bound to tRNAIle showed that the 3''-end of the tRNA approaches the editing domain, suggesting a plausible structural mechanism in which the flexible 3''-end of misaminoacylated Val-tRNAIle translocates across the enzyme surface from the Rossmann fold domain into the distant editing active site ( ).	bind
41184	4	9837	7	11	NULL	NULL	NULL	statement 3	NucleicAcid		translocates from								Rossmann fold domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_23978_s_23	15845536	A crystal structure of IleRS bound to tRNAIle showed that the 3''-end of the tRNA approaches the editing domain, suggesting a plausible structural mechanism in which the flexible 3''-end of misaminoacylated Val-tRNAIle translocates across the enzyme surface from the Rossmann fold domain into the distant editing active site ( ).	bind
41185	5	9837	7	11	NULL	NULL	NULL	statement 4	NucleicAcid		translocates to					distant editing active site	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_23978_s_23	15845536	A crystal structure of IleRS bound to tRNAIle showed that the 3''-end of the tRNA approaches the editing domain, suggesting a plausible structural mechanism in which the flexible 3''-end of misaminoacylated Val-tRNAIle translocates across the enzyme surface from the Rossmann fold domain into the distant editing active site ( ).	bind
34225	1	9838	6	11	NULL	NULL	NULL	SK	GP		plays a role in			beta domain		Pg substrate	GP	processing of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_16_9168_s_72	12878727	A crystal structure of Pg substrate bound to the SK - plasmin complex  has not been obtained, but previous studies have indicated that the SK beta  domain plays a central role in processing Pg substrate  ( ,   ,   ).	bind
41187	1	9838	7	11	NULL	NULL	NULL	SK 	GP		plays a role in			beta domain		Pg substrate	GP	processing of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_16_9168_s_72	12878727	A crystal structure of Pg substrate bound to the SK - plasmin complex  has not been obtained, but previous studies have indicated that the SK beta  domain plays a central role in processing Pg substrate  ( ,   ,   ).	bind
34229	1	9839	6	11	NULL	NULL	NULL				bind			alpha2-I domain		collagen like peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_13_9985_s_28	11098050	A crystal structure of the alpha2-I domain reveals binding of a collagen-like peptide to a groove in the surface of the "`top"` face of the domain ( 12).	bind
41188	1	9839	7	11	NULL	NULL	NULL				bind			alpha2-I domain 		collagen-like peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_13_9985_s_28	11098050	A crystal structure of the alpha2-I domain reveals binding of a collagen-like peptide to a groove in the surface of the "`top"` face of the domain ( 12).	bind
34241	1	9840	6	11	NULL	NULL	NULL	gp43	GP		bind			C-terminal 		gp45	GP	bacteriophage RB69	hydrophobic pocket		NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8368_s_242	11459977	A crystal structure of the C-terminal peptide of gp43 bound to gp45 of bacteriophage RB69 shows that the peptide binds away from the subunit interface in a hydrophobic pocket close to the interdomain connecting loop ( 9).	bind
48970	2	9840	6	11	NULL	NULL	NULL				occurs close to			hydrophobic pocket					interdomain connecting loop		NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8368_s_242	11459977	A crystal structure of the C-terminal peptide of gp43 bound to gp45 of bacteriophage RB69 shows that the peptide binds away from the subunit interface in a hydrophobic pocket close to the interdomain connecting loop ( 9).	bind
48971	3	9840	6	11	NULL	NULL	NULL	statement 1	Process		occurs away from								subunit interface		NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8368_s_242	11459977	A crystal structure of the C-terminal peptide of gp43 bound to gp45 of bacteriophage RB69 shows that the peptide binds away from the subunit interface in a hydrophobic pocket close to the interdomain connecting loop ( 9).	bind
41189	1	9840	7	11	NULL	NULL	NULL	gp43	GP		bind			C-terminal peptide of		gp45	GP	bacteriophage RB69	hydrophobic pocket		NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8368_s_242	11459977	A crystal structure of the C-terminal peptide of gp43 bound to gp45 of bacteriophage RB69 shows that the peptide binds away from the subunit interface in a hydrophobic pocket close to the interdomain connecting loop ( 9).	bind
41190	2	9840	7	11	NULL	NULL	NULL	statement 1	Process		occurs away from					 			subunit interface		NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8368_s_242	11459977	A crystal structure of the C-terminal peptide of gp43 bound to gp45 of bacteriophage RB69 shows that the peptide binds away from the subunit interface in a hydrophobic pocket close to the interdomain connecting loop ( 9).	bind
41191	3	9840	7	11	NULL	NULL	NULL				occurs close to			hydrophobic pocket					interdomain connecting loop		NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_15_8368_s_242	11459977	A crystal structure of the C-terminal peptide of gp43 bound to gp45 of bacteriophage RB69 shows that the peptide binds away from the subunit interface in a hydrophobic pocket close to the interdomain connecting loop ( 9).	bind
34242	1	9841	6	11	NULL	NULL	NULL	NF-kappaB p50/p65 heterodimer	GP		bind					Ig-kappaB DNA target	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24392_s_36	10825175	A crystal structure of the NF-kappaB p50/p65 heterodimer bound to the Ig-kappaB DNA target has been completed ( 11).	bind
41198	1	9841	7	11	NULL	NULL	NULL	NF-kappaB p50/p65 heterodimer	GP		bind					Ig-kappaB DNA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24392_s_36	10825175	A crystal structure of the NF-kappaB p50/p65 heterodimer bound to the Ig-kappaB DNA target has been completed ( 11).	bind
34243	1	9842	6	11	NULL	NULL	NULL	A1	GP		bind			RBD		telomeric repeat DNA	NucleicAcid			d(TTAGGG)2	NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_72_0_291_s_334	12626338	A crystal structure of the two RBDs of A1 bound to the telomeric repeat DNA d(TTAGGG)2 shows that an A1 protein dimer forms a four-RNP-domain surface, which binds two DNAs  or four copies of the element ( 156).	bind
34711	2	9842	6	11	NULL	NULL	NULL	A1 protein dimer	GP		forms a 					four-RNP-domain surface	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_72_0_291_s_334	12626338	A crystal structure of the two RBDs of A1 bound to the telomeric repeat DNA d(TTAGGG)2 shows that an A1 protein dimer forms a four-RNP-domain surface, which binds two DNAs  or four copies of the element ( 156).	bind
41199	1	9842	7	11	NULL	NULL	NULL	A1	GP		bind			RBDs		telomeric repeat DNA 	NucleicAcid			d(TTAGGG)2	NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_72_0_291_s_334	12626338	A crystal structure of the two RBDs of A1 bound to the telomeric repeat DNA d(TTAGGG)2 shows that an A1 protein dimer forms a four-RNP-domain surface, which binds two DNAs  or four copies of the element ( 156).	bind
41200	2	9842	7	11	NULL	NULL	NULL	A1 protein dimer	GP		forms					RNP-domain surface	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_72_0_291_s_334	12626338	A crystal structure of the two RBDs of A1 bound to the telomeric repeat DNA d(TTAGGG)2 shows that an A1 protein dimer forms a four-RNP-domain surface, which binds two DNAs  or four copies of the element ( 156).	bind
34244	1	9843	6	11	NULL	NULL	NULL	PP2A	GP		bind					AR	GP		DBD-hinge-LBD region		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_295	15684382	A crystallographic analysis will be required to determine how the AF-1 phosphorylation sites are spatially positioned relative to the DBD-hinge-LBD region where PP2A binds AR.	bind
41202	1	9843	7	11	NULL	NULL	NULL	PP2A	GP		binds					AR	GP		DBD-hinge-LBD region		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_295	15684382	A crystallographic analysis will be required to determine how the AF-1 phosphorylation sites are spatially positioned relative to the DBD-hinge-LBD region where PP2A binds AR.	bind
34245	1	9845	6	11	NULL	NULL	NULL	water molecule	Chemical		bind					Csp3	GP		arginine		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_7_6_423_s_109	10873833	A crystallographic water molecule is observed binding to the conserved arginine for Csp3, Csp7 and Csp8.	bind
34252	2	9845	6	11	NULL	NULL	NULL	water molecule	Chemical		bind					Csp7	GP		arginine		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_7_6_423_s_109	10873833	A crystallographic water molecule is observed binding to the conserved arginine for Csp3, Csp7 and Csp8.	bind
34253	3	9845	6	11	NULL	NULL	NULL	water molecule	Chemical		bind					Csp8	GP		arginine		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_7_6_423_s_109	10873833	A crystallographic water molecule is observed binding to the conserved arginine for Csp3, Csp7 and Csp8.	bind
41203	1	9845	7	11	NULL	NULL	NULL	water molecule	Chemical		binds					Csp3	GP		arginine		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_7_6_423_s_109	10873833	A crystallographic water molecule is observed binding to the conserved arginine for Csp3, Csp7 and Csp8.	bind
41204	2	9845	7	11	NULL	NULL	NULL	water molecule	Chemical		binds					Csp7	GP		arginine		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_7_6_423_s_109	10873833	A crystallographic water molecule is observed binding to the conserved arginine for Csp3, Csp7 and Csp8.	bind
41205	3	9845	7	11	NULL	NULL	NULL	water molecule	Chemical		binds					Csp8	GP		arginine		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_7_6_423_s_109	10873833	A crystallographic water molecule is observed binding to the conserved arginine for Csp3, Csp7 and Csp8.	bind
34254	1	9847	6	11	NULL	NULL	NULL	HRGP	GP		bind					TSP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_107_1_45_s_80	11134179	A CSVTCG-containing peptide from the third type 1 repeat had similar inhibitory activity, but mutated peptides with substitution of alanine for the cysteine residues in the CSVTCG motif did not inhibit HRGP binding to TSP-1.	bind
34255	2	9847	6	11	NULL	NULL	NULL	alanine	AminoAcid		is substituted to					cysteine	AminoAcid		CSVTCG motif		NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_107_1_45_s_80	11134179	A CSVTCG-containing peptide from the third type 1 repeat had similar inhibitory activity, but mutated peptides with substitution of alanine for the cysteine residues in the CSVTCG motif did not inhibit HRGP binding to TSP-1.	bind
34256	3	9847	6	11	NULL	NULL	NULL	statement 2	Process		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_107_1_45_s_80	11134179	A CSVTCG-containing peptide from the third type 1 repeat had similar inhibitory activity, but mutated peptides with substitution of alanine for the cysteine residues in the CSVTCG motif did not inhibit HRGP binding to TSP-1.	bind
34257	4	9847	6	11	NULL	NULL	NULL	CSVTCG-containing peptide	AminoAcid		inhibits			third type 1 repeat		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_107_1_45_s_80	11134179	A CSVTCG-containing peptide from the third type 1 repeat had similar inhibitory activity, but mutated peptides with substitution of alanine for the cysteine residues in the CSVTCG motif did not inhibit HRGP binding to TSP-1.	bind
41210	1	9847	7	11	NULL	NULL	NULL	HRGP	GP		bind					TSP-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_107_1_45_s_80	11134179	A CSVTCG-containing peptide from the third type 1 repeat had similar inhibitory activity, but mutated peptides with substitution of alanine for the cysteine residues in the CSVTCG motif did not inhibit HRGP binding to TSP-1.	bind
41211	2	9847	7	11	NULL	NULL	NULL	CSVTCG-containing peptide	AminoAcid		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_107_1_45_s_80	11134179	A CSVTCG-containing peptide from the third type 1 repeat had similar inhibitory activity, but mutated peptides with substitution of alanine for the cysteine residues in the CSVTCG motif did not inhibit HRGP binding to TSP-1.	bind
41212	4	9847	7	11	NULL	NULL	NULL	statement 3	Process		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_107_1_45_s_80	11134179	A CSVTCG-containing peptide from the third type 1 repeat had similar inhibitory activity, but mutated peptides with substitution of alanine for the cysteine residues in the CSVTCG motif did not inhibit HRGP binding to TSP-1.	bind
41213	5	9847	7	11	NULL	NULL	NULL	third type 1 repeat	AminoAcid		contains					CSVTCG-containing peptide 	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_107_1_45_s_80	11134179	A CSVTCG-containing peptide from the third type 1 repeat had similar inhibitory activity, but mutated peptides with substitution of alanine for the cysteine residues in the CSVTCG motif did not inhibit HRGP binding to TSP-1.	bind
48972	3	9847	7	11	NULL	NULL	NULL	alanine	AminoAcid		is substituted to					cysteine	AminoAcid		CSVTCG motif		NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_107_1_45_s_80	11134179	A CSVTCG-containing peptide from the third type 1 repeat had similar inhibitory activity, but mutated peptides with substitution of alanine for the cysteine residues in the CSVTCG motif did not inhibit HRGP binding to TSP-1.	bind
34258	1	9848	6	11	NULL	NULL	NULL	CtBP dimer	GP		bind					Knirps	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_49_40757_s_142	16186109	A CtBP dimer binding to Knirps would be expected to produce a complex of only  150 kDa; therefore, we tested for the presence of additional proteins using antibodies to candidate proteins.	bind
41214	1	9848	7	11	NULL	NULL	NULL	CtBP dimer	GP		bind					Knirps	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_49_40757_s_142	16186109	A CtBP dimer binding to Knirps would be expected to produce a complex of only  150 kDa; therefore, we tested for the presence of additional proteins using antibodies to candidate proteins.	bind
34259	1	9849	6	11	NULL	NULL	NULL	CTD peptide	AminoAcid	phosphorylated 	bind			S5-repeats		GTase	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1577_2_308_s_93	12213660	A CTD peptide carrying as few as two S5-phosphorylated repeats is sufficient to bind to and stimulate the GTase, whereas peptides phosphorylated at S2 allow GTase binding but no stimulation [ 57].	bind
34260	2	9849	6	11	NULL	NULL	NULL	statement 1	Process		stimulate					GTase	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1577_2_308_s_93	12213660	A CTD peptide carrying as few as two S5-phosphorylated repeats is sufficient to bind to and stimulate the GTase, whereas peptides phosphorylated at S2 allow GTase binding but no stimulation [ 57].	bind
34261	3	9849	6	11	NULL	NULL	NULL	CTD peptide	AminoAcid	phosphorylated	bind			S2 repeats		GTase	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1577_2_308_s_93	12213660	A CTD peptide carrying as few as two S5-phosphorylated repeats is sufficient to bind to and stimulate the GTase, whereas peptides phosphorylated at S2 allow GTase binding but no stimulation [ 57].	bind
34262	4	9849	6	11	NULL	NULL	NULL	statement 3	Process		does not stimulate					GTase	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1577_2_308_s_93	12213660	A CTD peptide carrying as few as two S5-phosphorylated repeats is sufficient to bind to and stimulate the GTase, whereas peptides phosphorylated at S2 allow GTase binding but no stimulation [ 57].	bind
41215	1	9849	7	11	NULL	NULL	NULL	CTD peptide	AminoAcid	phosphorylated	bind			S5-repeats		GTase	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1577_2_308_s_93	12213660	A CTD peptide carrying as few as two S5-phosphorylated repeats is sufficient to bind to and stimulate the GTase, whereas peptides phosphorylated at S2 allow GTase binding but no stimulation [ 57].	bind
41216	2	9849	7	11	NULL	NULL	NULL	statement 1	Process		stimulate					GTase	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1577_2_308_s_93	12213660	A CTD peptide carrying as few as two S5-phosphorylated repeats is sufficient to bind to and stimulate the GTase, whereas peptides phosphorylated at S2 allow GTase binding but no stimulation [ 57].	bind
41217	3	9849	7	11	NULL	NULL	NULL	CTD peptide	AminoAcid	phosphorylated	bind			S2 repeats		GTase	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1577_2_308_s_93	12213660	A CTD peptide carrying as few as two S5-phosphorylated repeats is sufficient to bind to and stimulate the GTase, whereas peptides phosphorylated at S2 allow GTase binding but no stimulation [ 57].	bind
41218	4	9849	7	11	NULL	NULL	NULL	statement 3	Process		does not stimulate					GTase	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1577_2_308_s_93	12213660	A CTD peptide carrying as few as two S5-phosphorylated repeats is sufficient to bind to and stimulate the GTase, whereas peptides phosphorylated at S2 allow GTase binding but no stimulation [ 57].	bind
34263	1	9850	6	11	NULL	NULL	NULL	CTLA-4Ig	GP		bind					B7-1	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-exp-med_184_5_8920853_s_11	8920853	A CTLA-4Ig fusion protein  which binds to both B7-1 and B7-2 was shown to completely block the rescue  of thymocytes from glucocorticoid-induced cell death.	bind
34264	2	9850	6	11	NULL	NULL	NULL	CTLA-4Ig	GP		bind					B7-2	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-exp-med_184_5_8920853_s_11	8920853	A CTLA-4Ig fusion protein  which binds to both B7-1 and B7-2 was shown to completely block the rescue  of thymocytes from glucocorticoid-induced cell death.	bind
34265	3	9850	6	11	NULL	NULL	NULL	thymocytes	Cell		is rescued from					statement 6	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-exp-med_184_5_8920853_s_11	8920853	A CTLA-4Ig fusion protein  which binds to both B7-1 and B7-2 was shown to completely block the rescue  of thymocytes from glucocorticoid-induced cell death.	bind
34266	4	9850	6	11	NULL	NULL	NULL	CTLA-4Ig	GP		blocks		completely			statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-exp-med_184_5_8920853_s_11	8920853	A CTLA-4Ig fusion protein  which binds to both B7-1 and B7-2 was shown to completely block the rescue  of thymocytes from glucocorticoid-induced cell death.	bind
48973	5	9850	6	11	NULL	NULL	NULL	CTLA-4Ig	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-exp-med_184_5_8920853_s_11	8920853	A CTLA-4Ig fusion protein  which binds to both B7-1 and B7-2 was shown to completely block the rescue  of thymocytes from glucocorticoid-induced cell death.	bind
48975	6	9850	6	11	NULL	NULL	NULL	glucocorticoid	Chemical		induce					cell death	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-exp-med_184_5_8920853_s_11	8920853	A CTLA-4Ig fusion protein  which binds to both B7-1 and B7-2 was shown to completely block the rescue  of thymocytes from glucocorticoid-induced cell death.	bind
41219	1	9850	7	11	NULL	NULL	NULL	CTLA-4Ig	GP		binds to					 B7-1	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-exp-med_184_5_8920853_s_11	8920853	A CTLA-4Ig fusion protein  which binds to both B7-1 and B7-2 was shown to completely block the rescue  of thymocytes from glucocorticoid-induced cell death.	bind
41220	2	9850	7	11	NULL	NULL	NULL	CTLA-4Ig	GP		binds to					B7-2	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-exp-med_184_5_8920853_s_11	8920853	A CTLA-4Ig fusion protein  which binds to both B7-1 and B7-2 was shown to completely block the rescue  of thymocytes from glucocorticoid-induced cell death.	bind
41221	3	9850	7	11	NULL	NULL	NULL	glucocorticoid	Chemical		induce					cell death	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-exp-med_184_5_8920853_s_11	8920853	A CTLA-4Ig fusion protein  which binds to both B7-1 and B7-2 was shown to completely block the rescue  of thymocytes from glucocorticoid-induced cell death.	bind
41222	4	9850	7	11	NULL	NULL	NULL	thymocytes	Cell		is rescued from					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-exp-med_184_5_8920853_s_11	8920853	A CTLA-4Ig fusion protein  which binds to both B7-1 and B7-2 was shown to completely block the rescue  of thymocytes from glucocorticoid-induced cell death.	bind
41223	5	9850	7	11	NULL	NULL	NULL	CTLA-4Ig	GP		block		completely			statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-exp-med_184_5_8920853_s_11	8920853	A CTLA-4Ig fusion protein  which binds to both B7-1 and B7-2 was shown to completely block the rescue  of thymocytes from glucocorticoid-induced cell death.	bind
48974	6	9850	7	11	NULL	NULL	NULL	CTLA-4Ig 	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-exp-med_184_5_8920853_s_11	8920853	A CTLA-4Ig fusion protein  which binds to both B7-1 and B7-2 was shown to completely block the rescue  of thymocytes from glucocorticoid-induced cell death.	bind
34706	1	9851	6	11	NULL	NULL	NULL	Chl a	Chemical		is in close contact with					Chl b	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_471_1_89_s_8	10760519	A current 3.4  Ang  structural model of Lhcb1 monomer of the LHCII trimer [  9] includes three membrane spanning helices binding 12 chlorophyll (Chl) molecules with Chl  a in close contact with Chl  b for rapid energy transfer and two crossed lutein molecules possibly quenching Chl  a triplet states.	bind
34707	2	9851	6	11	NULL	NULL	NULL	Lhcb1 monomer	GP		bind			membrane spanning helices		Chl molecules	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_471_1_89_s_8	10760519	A current 3.4  Ang  structural model of Lhcb1 monomer of the LHCII trimer [  9] includes three membrane spanning helices binding 12 chlorophyll (Chl) molecules with Chl  a in close contact with Chl  b for rapid energy transfer and two crossed lutein molecules possibly quenching Chl  a triplet states.	bind
34708	3	9851	6	11	NULL	NULL	NULL	Chl	Chemical		is					chlorophyll	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_471_1_89_s_8	10760519	A current 3.4  Ang  structural model of Lhcb1 monomer of the LHCII trimer [  9] includes three membrane spanning helices binding 12 chlorophyll (Chl) molecules with Chl  a in close contact with Chl  b for rapid energy transfer and two crossed lutein molecules possibly quenching Chl  a triplet states.	bind
34709	4	9851	6	11	NULL	NULL	NULL	statement 1	Process		is needed for					energy transfer	Process	rapid			NULL		NULL	NULL	NULL	NULL	gw60_febslett_471_1_89_s_8	10760519	A current 3.4  Ang  structural model of Lhcb1 monomer of the LHCII trimer [  9] includes three membrane spanning helices binding 12 chlorophyll (Chl) molecules with Chl  a in close contact with Chl  b for rapid energy transfer and two crossed lutein molecules possibly quenching Chl  a triplet states.	bind
34710	5	9851	6	11	NULL	NULL	NULL	leutin molecules	Chemical		quench					Chl a	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_471_1_89_s_8	10760519	A current 3.4  Ang  structural model of Lhcb1 monomer of the LHCII trimer [  9] includes three membrane spanning helices binding 12 chlorophyll (Chl) molecules with Chl  a in close contact with Chl  b for rapid energy transfer and two crossed lutein molecules possibly quenching Chl  a triplet states.	bind
41225	2	9851	7	11	NULL	NULL	NULL	Lhcb1 monomer	GP		bind			membrane spanning helices		Chl molecules	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_471_1_89_s_8	10760519	A current 3.4  Ang  structural model of Lhcb1 monomer of the LHCII trimer [  9] includes three membrane spanning helices binding 12 chlorophyll (Chl) molecules with Chl  a in close contact with Chl  b for rapid energy transfer and two crossed lutein molecules possibly quenching Chl  a triplet states.	bind
41226	3	9851	7	11	NULL	NULL	NULL	Chl a	Chemical		is in close contact with					Chl b	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_471_1_89_s_8	10760519	A current 3.4  Ang  structural model of Lhcb1 monomer of the LHCII trimer [  9] includes three membrane spanning helices binding 12 chlorophyll (Chl) molecules with Chl  a in close contact with Chl  b for rapid energy transfer and two crossed lutein molecules possibly quenching Chl  a triplet states.	bind
41227	4	9851	7	11	NULL	NULL	NULL	statement 3	Process		is needed for					energy transfer	Process	rapid			NULL		NULL	NULL	NULL	NULL	gw60_febslett_471_1_89_s_8	10760519	A current 3.4  Ang  structural model of Lhcb1 monomer of the LHCII trimer [  9] includes three membrane spanning helices binding 12 chlorophyll (Chl) molecules with Chl  a in close contact with Chl  b for rapid energy transfer and two crossed lutein molecules possibly quenching Chl  a triplet states.	bind
41228	5	9851	7	11	NULL	NULL	NULL	lutein molecules	Chemical		quench					Chl a 	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_471_1_89_s_8	10760519	A current 3.4  Ang  structural model of Lhcb1 monomer of the LHCII trimer [  9] includes three membrane spanning helices binding 12 chlorophyll (Chl) molecules with Chl  a in close contact with Chl  b for rapid energy transfer and two crossed lutein molecules possibly quenching Chl  a triplet states.	bind
41230	1	9851	7	11	NULL	NULL	NULL	Chl molecules	Chemical		is					chlorophyll	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_471_1_89_s_8	10760519	A current 3.4  Ang  structural model of Lhcb1 monomer of the LHCII trimer [  9] includes three membrane spanning helices binding 12 chlorophyll (Chl) molecules with Chl  a in close contact with Chl  b for rapid energy transfer and two crossed lutein molecules possibly quenching Chl  a triplet states.	bind
34267	1	9852	6	11	NULL	NULL	NULL	CREB	GP		is					cyclic-AMP response element binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_7_s_193	10719210	A current cellular theory of depression outlined by Duman et al. [ 21] implicates the cyclic-AMP response element binding protein (CREB) transcription factor as an intracellular target of long but not short term antidepressant treatment.	bind
34268	2	9852	6	11	NULL	NULL	NULL	CREB	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_7_s_193	10719210	A current cellular theory of depression outlined by Duman et al. [ 21] implicates the cyclic-AMP response element binding protein (CREB) transcription factor as an intracellular target of long but not short term antidepressant treatment.	bind
34269	3	9852	6	11	NULL	NULL	NULL	CREB 	GP		is a target for		intracellular			antidepressant treatment	MedicalFinding	long term			NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_7_s_193	10719210	A current cellular theory of depression outlined by Duman et al. [ 21] implicates the cyclic-AMP response element binding protein (CREB) transcription factor as an intracellular target of long but not short term antidepressant treatment.	bind
48976	4	9852	6	11	NULL	NULL	NULL	CREB	GP		is not a target for					antidepressant treatment	MedicalFinding	short term			NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_7_s_193	10719210	A current cellular theory of depression outlined by Duman et al. [ 21] implicates the cyclic-AMP response element binding protein (CREB) transcription factor as an intracellular target of long but not short term antidepressant treatment.	bind
41232	1	9852	7	11	NULL	NULL	NULL	CREB	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_7_s_193	10719210	A current cellular theory of depression outlined by Duman et al. [ 21] implicates the cyclic-AMP response element binding protein (CREB) transcription factor as an intracellular target of long but not short term antidepressant treatment.	bind
41233	2	9852	7	11	NULL	NULL	NULL	CREB	GP		is					cyclic-AMP response element binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_7_s_193	10719210	A current cellular theory of depression outlined by Duman et al. [ 21] implicates the cyclic-AMP response element binding protein (CREB) transcription factor as an intracellular target of long but not short term antidepressant treatment.	bind
41235	3	9852	7	11	NULL	NULL	NULL	CREB	GP		is a target for		intracellular			antidepressant treatment	MedicalFinding	long term			NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_7_s_193	10719210	A current cellular theory of depression outlined by Duman et al. [ 21] implicates the cyclic-AMP response element binding protein (CREB) transcription factor as an intracellular target of long but not short term antidepressant treatment.	bind
41236	4	9852	7	11	NULL	NULL	NULL	CREB	GP		is not a target for					antidepressant treatment	MedicalFinding	short term			NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_76_1_7_s_193	10719210	A current cellular theory of depression outlined by Duman et al. [ 21] implicates the cyclic-AMP response element binding protein (CREB) transcription factor as an intracellular target of long but not short term antidepressant treatment.	bind
34270	1	9853	6	11	NULL	NULL	NULL	Sir1p	GP		bind					HMR-E	GP				NULL	chromatin	NULL	NULL	NULL	NULL	gw60_genesdev_15_2_147_s_45	11157772	A current model for silencing  HMR posits that Sir1p binds to the  HMR-E silencer in chromatin through interactions with the ORC that is bound directly to the silencer ACS.	bind
34271	2	9853	6	11	NULL	NULL	NULL	ORC	GP		bind		directly			ACS	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_2_147_s_45	11157772	A current model for silencing  HMR posits that Sir1p binds to the  HMR-E silencer in chromatin through interactions with the ORC that is bound directly to the silencer ACS.	bind
34272	3	9853	6	11	NULL	NULL	NULL	Sir1p	GP		interacts with					ORC	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_2_147_s_45	11157772	A current model for silencing  HMR posits that Sir1p binds to the  HMR-E silencer in chromatin through interactions with the ORC that is bound directly to the silencer ACS.	bind
48977	4	9853	6	11	NULL	NULL	NULL	statement 1	Process		occurs through					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_2_147_s_45	11157772	A current model for silencing  HMR posits that Sir1p binds to the  HMR-E silencer in chromatin through interactions with the ORC that is bound directly to the silencer ACS.	bind
48978	5	9853	6	11	NULL	NULL	NULL	HMR-E	GP		is a type of					silencer	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_2_147_s_45	11157772	A current model for silencing  HMR posits that Sir1p binds to the  HMR-E silencer in chromatin through interactions with the ORC that is bound directly to the silencer ACS.	bind
48979	6	9853	6	11	NULL	NULL	NULL	ACS	GP		is a type of					silencer	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_2_147_s_45	11157772	A current model for silencing  HMR posits that Sir1p binds to the  HMR-E silencer in chromatin through interactions with the ORC that is bound directly to the silencer ACS.	bind
41239	1	9853	7	11	NULL	NULL	NULL	 Sir1p	GP		binds to					HMR-E	GP				NULL	chromatin	NULL	NULL	NULL	NULL	gw60_genesdev_15_2_147_s_45	11157772	A current model for silencing  HMR posits that Sir1p binds to the  HMR-E silencer in chromatin through interactions with the ORC that is bound directly to the silencer ACS.	bind
41240	2	9853	7	11	NULL	NULL	NULL	ORC 	GP		bind		directly			ACS	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_2_147_s_45	11157772	A current model for silencing  HMR posits that Sir1p binds to the  HMR-E silencer in chromatin through interactions with the ORC that is bound directly to the silencer ACS.	bind
41241	3	9853	7	11	NULL	NULL	NULL	Sir1p	GP		interacts with					ORC	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_2_147_s_45	11157772	A current model for silencing  HMR posits that Sir1p binds to the  HMR-E silencer in chromatin through interactions with the ORC that is bound directly to the silencer ACS.	bind
48980	4	9853	7	11	NULL	NULL	NULL	statement 1	Process		occurs through					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_2_147_s_45	11157772	A current model for silencing  HMR posits that Sir1p binds to the  HMR-E silencer in chromatin through interactions with the ORC that is bound directly to the silencer ACS.	bind
48981	5	9853	7	11	NULL	NULL	NULL	HMR-E	GP		is a type of					silencer	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_2_147_s_45	11157772	A current model for silencing  HMR posits that Sir1p binds to the  HMR-E silencer in chromatin through interactions with the ORC that is bound directly to the silencer ACS.	bind
48982	6	9853	7	11	NULL	NULL	NULL	ACS	GP		is a type of					silencer	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_2_147_s_45	11157772	A current model for silencing  HMR posits that Sir1p binds to the  HMR-E silencer in chromatin through interactions with the ORC that is bound directly to the silencer ACS.	bind
34273	1	9854	6	11	NULL	NULL	NULL	Cdc13p	GP	telomere-associated	bind					Est1p	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_curr-opin-cell-biol_15_3_12787768_s_5	12787768	A current model for telomerase regulation is that  telomere-associated Cdc13p binds Est1p, thereby recruiting telomerase.	bind
34312	2	9854	6	11	NULL	NULL	NULL	statement 1	Process		recruits					telomerase	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_curr-opin-cell-biol_15_3_12787768_s_5	12787768	A current model for telomerase regulation is that  telomere-associated Cdc13p binds Est1p, thereby recruiting telomerase.	bind
41243	1	9854	7	11	NULL	NULL	NULL	Cdc13p	GP	telomere-associated	binds					Est1p	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_curr-opin-cell-biol_15_3_12787768_s_5	12787768	A current model for telomerase regulation is that  telomere-associated Cdc13p binds Est1p, thereby recruiting telomerase.	bind
41244	2	9854	7	11	NULL	NULL	NULL	statement 1	Process		recruits					telomerase	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_curr-opin-cell-biol_15_3_12787768_s_5	12787768	A current model for telomerase regulation is that  telomere-associated Cdc13p binds Est1p, thereby recruiting telomerase.	bind
34314	1	9855	6	11	NULL	NULL	NULL	FNBP	GP		bind					FN	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_10_5586_s_289	16988233	A current model for the function of these FNBPs suggested that the binding of FNBP with multiple FNs resulted in the localization of integrin binding sites, which induce the clustering of integrins in the membrane of host cells ( ).	bind
34315	2	9855	6	11	NULL	NULL	NULL	statement 1	Process		resulted in							localization of	integrin binding sites		NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_10_5586_s_289	16988233	A current model for the function of these FNBPs suggested that the binding of FNBP with multiple FNs resulted in the localization of integrin binding sites, which induce the clustering of integrins in the membrane of host cells ( ).	bind
34322	3	9855	6	11	NULL	NULL	NULL	statement 2	Process		induce					integrins	GP	clustering of			NULL	membrane of host cells	NULL	NULL	NULL	NULL	gw70_infectimmun_74_10_5586_s_289	16988233	A current model for the function of these FNBPs suggested that the binding of FNBP with multiple FNs resulted in the localization of integrin binding sites, which induce the clustering of integrins in the membrane of host cells ( ).	bind
41246	1	9855	7	11	NULL	NULL	NULL	FNBP	GP		bind					FNs	GP				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_10_5586_s_289	16988233	A current model for the function of these FNBPs suggested that the binding of FNBP with multiple FNs resulted in the localization of integrin binding sites, which induce the clustering of integrins in the membrane of host cells ( ).	bind
41248	2	9855	7	11	NULL	NULL	NULL	statement 1	Process		results in							 localization of	integrin binding sites		NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_10_5586_s_289	16988233	A current model for the function of these FNBPs suggested that the binding of FNBP with multiple FNs resulted in the localization of integrin binding sites, which induce the clustering of integrins in the membrane of host cells ( ).	bind
41250	3	9855	7	11	NULL	NULL	NULL	statement 2	Process		induce					integrins	GP	clustering of 			NULL	membrane of host cells	NULL	NULL	NULL	NULL	gw70_infectimmun_74_10_5586_s_289	16988233	A current model for the function of these FNBPs suggested that the binding of FNBP with multiple FNs resulted in the localization of integrin binding sites, which induce the clustering of integrins in the membrane of host cells ( ).	bind
34330	1	9856	6	11	NULL	NULL	NULL	GRK	GP		bind					agonist-occupied receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_13266_s_155	8662816	A current model of homologous desensitization of G protein-coupled receptors proposes rapid, agonist-dependent translocation to the plasma membrane of a GRK, which binds and phosphorylates the agonist-occupied receptor ( 2).	bind
34705	2	9856	6	11	NULL	NULL	NULL	statement 1	Process		phosphorylates					agonist-occupied receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_13266_s_155	8662816	A current model of homologous desensitization of G protein-coupled receptors proposes rapid, agonist-dependent translocation to the plasma membrane of a GRK, which binds and phosphorylates the agonist-occupied receptor ( 2).	bind
48983	3	9856	6	11	NULL	NULL	NULL	GRK	GP		translocates to					plasma membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_13266_s_155	8662816	A current model of homologous desensitization of G protein-coupled receptors proposes rapid, agonist-dependent translocation to the plasma membrane of a GRK, which binds and phosphorylates the agonist-occupied receptor ( 2).	bind
48984	4	9856	6	11	NULL	NULL	NULL	statement 3	Process		is dependent on					agonist	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_13266_s_155	8662816	A current model of homologous desensitization of G protein-coupled receptors proposes rapid, agonist-dependent translocation to the plasma membrane of a GRK, which binds and phosphorylates the agonist-occupied receptor ( 2).	bind
41556	1	9856	7	11	NULL	NULL	NULL	GRK	GP		translocates to					plasma membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_13266_s_155	8662816	A current model of homologous desensitization of G protein-coupled receptors proposes rapid, agonist-dependent translocation to the plasma membrane of a GRK, which binds and phosphorylates the agonist-occupied receptor ( 2).	bind
41557	2	9856	7	11	NULL	NULL	NULL	statement 1	Process		is dependent on					agonist	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_13266_s_155	8662816	A current model of homologous desensitization of G protein-coupled receptors proposes rapid, agonist-dependent translocation to the plasma membrane of a GRK, which binds and phosphorylates the agonist-occupied receptor ( 2).	bind
41558	3	9856	7	11	NULL	NULL	NULL	GRK	GP		binds					agonist-occupied receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_13266_s_155	8662816	A current model of homologous desensitization of G protein-coupled receptors proposes rapid, agonist-dependent translocation to the plasma membrane of a GRK, which binds and phosphorylates the agonist-occupied receptor ( 2).	bind
41559	4	9856	7	11	NULL	NULL	NULL	statement 3	Process		phosphorylates					agonist-occupied receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_13266_s_155	8662816	A current model of homologous desensitization of G protein-coupled receptors proposes rapid, agonist-dependent translocation to the plasma membrane of a GRK, which binds and phosphorylates the agonist-occupied receptor ( 2).	bind
34334	1	9860	6	11	NULL	NULL	NULL	ATP	Chemical		bind		preferentially			M2S structural state	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_6_2944_s_163	9501195	A cycle is easily established if ATP binds preferentially to the M2S structural state, which would occur if the transition from M1S to M2S is coupled to a product-release step or is faster than the rate of ADP release.	bind
41563	1	9860	7	11	NULL	NULL	NULL	ATP	Chemical		binds		preferentially			M2S structural state	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_6_2944_s_163	9501195	A cycle is easily established if ATP binds preferentially to the M2S structural state, which would occur if the transition from M1S to M2S is coupled to a product-release step or is faster than the rate of ADP release.	bind
34343	1	9861	6	11	NULL	NULL	NULL	myosin crossbridges	GP		bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_102_5_683_s_10	11007486	A cycle of actin - myosin interactions is thought to occur  as follows (Lymn and Taylor, 1971   ;  Spudich, 1994   ): the myosin  crossbridge binds to ATP, and then releases its attached actin filament.	bind
34346	2	9861	6	11	NULL	NULL	NULL	statement 1	Process		releases					actin filament	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_102_5_683_s_10	11007486	A cycle of actin - myosin interactions is thought to occur  as follows (Lymn and Taylor, 1971   ;  Spudich, 1994   ): the myosin  crossbridge binds to ATP, and then releases its attached actin filament.	bind
41568	1	9861	7	11	NULL	NULL	NULL	myosin crossbridge	GP		binds to					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_102_5_683_s_10	11007486	A cycle of actin - myosin interactions is thought to occur  as follows (Lymn and Taylor, 1971   ;  Spudich, 1994   ): the myosin  crossbridge binds to ATP, and then releases its attached actin filament.	bind
41569	2	9861	7	11	NULL	NULL	NULL	statement 1	Process		release					actin filament	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_102_5_683_s_10	11007486	A cycle of actin - myosin interactions is thought to occur  as follows (Lymn and Taylor, 1971   ;  Spudich, 1994   ): the myosin  crossbridge binds to ATP, and then releases its attached actin filament.	bind
34352	3	9862	6	11	NULL	NULL	NULL	statement 1	GP		bind					CREB1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5329_s_5	15964791	A cyclic AMP response element (CRE)-like element in the 5''-flanking region of the MuSK gene binds to CREB1	bind
34353	2	9862	6	11	NULL	NULL	NULL	CRE	GP		is					cyclic-AMP response element	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5329_s_5	15964791	A cyclic AMP response element (CRE)-like element in the 5''-flanking region of the MuSK gene binds to CREB1	bind
56901	1	9862	6	11	NULL	NULL	NULL	MuSK gene	GP		is present in				CRE-like element	MuSK gene	GP	5''-flanking region of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5329_s_5	15964791	A cyclic AMP response element (CRE)-like element in the 5''-flanking region of the MuSK gene binds to CREB1	bind
41572	3	9862	7	11	NULL	NULL	NULL	statement 1	GP		binds to					CREB1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5329_s_5	15964791	A cyclic AMP response element (CRE)-like element in the 5''-flanking region of the MuSK gene binds to CREB1	bind
41573	2	9862	7	11	NULL	NULL	NULL	CRE	GP		is					cyclic AMP response element 	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5329_s_5	15964791	A cyclic AMP response element (CRE)-like element in the 5''-flanking region of the MuSK gene binds to CREB1	bind
56902	1	9862	7	11	NULL	NULL	NULL	MuSK gene	GP		is present in				CRE-like element	MuSK gene	GP	5''-flanking region of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_13_5329_s_5	15964791	A cyclic AMP response element (CRE)-like element in the 5''-flanking region of the MuSK gene binds to CREB1	bind
34356	1	9863	6	11	NULL	NULL	NULL	anti-alpha5 mAb	GP		bind					alpha5beta1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_25664_s_5	9748233	A cyclic peptide containing this sequence (*CRRETAWAC*) had little effect on the binding of most anti-alpha5 and anti-beta1 mAbs to alpha5beta1 but completely blocked binding of the anti-alpha5 mAb 16 in a directly competitive manner.	bind
34357	2	9863	6	11	NULL	NULL	NULL	anti-beta1 mAb	GP		bind					alpha5beta1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_25664_s_5	9748233	A cyclic peptide containing this sequence (*CRRETAWAC*) had little effect on the binding of most anti-alpha5 and anti-beta1 mAbs to alpha5beta1 but completely blocked binding of the anti-alpha5 mAb 16 in a directly competitive manner.	bind
34703	3	9863	6	11	NULL	NULL	NULL	cyclic peptide	GP		has little effect on			CRRETAWAC		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_25664_s_5	9748233	A cyclic peptide containing this sequence (*CRRETAWAC*) had little effect on the binding of most anti-alpha5 and anti-beta1 mAbs to alpha5beta1 but completely blocked binding of the anti-alpha5 mAb 16 in a directly competitive manner.	bind
34704	4	9863	6	11	NULL	NULL	NULL	cyclic peptide	GP		has little effect on			CRRETAWAC		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_25664_s_5	9748233	A cyclic peptide containing this sequence (*CRRETAWAC*) had little effect on the binding of most anti-alpha5 and anti-beta1 mAbs to alpha5beta1 but completely blocked binding of the anti-alpha5 mAb 16 in a directly competitive manner.	bind
48985	5	9863	6	11	NULL	NULL	NULL	anti-alpha5 mAb 16	GP		bind					alpha5beta1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_25664_s_5	9748233	A cyclic peptide containing this sequence (*CRRETAWAC*) had little effect on the binding of most anti-alpha5 and anti-beta1 mAbs to alpha5beta1 but completely blocked binding of the anti-alpha5 mAb 16 in a directly competitive manner.	bind
48986	6	9863	6	11	NULL	NULL	NULL	cyclic peptide	GP		block		directly;;competitively	CRRETAWAC		statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_25664_s_5	9748233	A cyclic peptide containing this sequence (*CRRETAWAC*) had little effect on the binding of most anti-alpha5 and anti-beta1 mAbs to alpha5beta1 but completely blocked binding of the anti-alpha5 mAb 16 in a directly competitive manner.	bind
41576	1	9863	7	11	NULL	NULL	NULL	anti-alpha5 mAb	GP		bind					alpha5beta1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_25664_s_5	9748233	A cyclic peptide containing this sequence (*CRRETAWAC*) had little effect on the binding of most anti-alpha5 and anti-beta1 mAbs to alpha5beta1 but completely blocked binding of the anti-alpha5 mAb 16 in a directly competitive manner.	bind
41577	2	9863	7	11	NULL	NULL	NULL	anti-beta1 mAb	GP		bind					alpha5beta1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_25664_s_5	9748233	A cyclic peptide containing this sequence (*CRRETAWAC*) had little effect on the binding of most anti-alpha5 and anti-beta1 mAbs to alpha5beta1 but completely blocked binding of the anti-alpha5 mAb 16 in a directly competitive manner.	bind
41578	3	9863	7	11	NULL	NULL	NULL	cyclic peptide 	GP		little effect on			CRRETAWAC		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_25664_s_5	9748233	A cyclic peptide containing this sequence (*CRRETAWAC*) had little effect on the binding of most anti-alpha5 and anti-beta1 mAbs to alpha5beta1 but completely blocked binding of the anti-alpha5 mAb 16 in a directly competitive manner.	bind
41579	4	9863	7	11	NULL	NULL	NULL	cyclic peptide 	GP		little effect on			CRRETAWAC		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_25664_s_5	9748233	A cyclic peptide containing this sequence (*CRRETAWAC*) had little effect on the binding of most anti-alpha5 and anti-beta1 mAbs to alpha5beta1 but completely blocked binding of the anti-alpha5 mAb 16 in a directly competitive manner.	bind
41580	5	9863	7	11	NULL	NULL	NULL	anti-alpha5 mAb 16	GP		bind					alpha5beta1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_25664_s_5	9748233	A cyclic peptide containing this sequence (*CRRETAWAC*) had little effect on the binding of most anti-alpha5 and anti-beta1 mAbs to alpha5beta1 but completely blocked binding of the anti-alpha5 mAb 16 in a directly competitive manner.	bind
41585	6	9863	7	11	NULL	NULL	NULL	cyclic peptide	GP		block		directly;;competitively	CRRETAWAC		statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_40_25664_s_5	9748233	A cyclic peptide containing this sequence (*CRRETAWAC*) had little effect on the binding of most anti-alpha5 and anti-beta1 mAbs to alpha5beta1 but completely blocked binding of the anti-alpha5 mAb 16 in a directly competitive manner.	bind
34359	1	9865	6	11	NULL	NULL	NULL	thrombospondin 1	GP		bind					CD36 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_34_35159_s_145	15192113	A Cys-Ser-Val-Thr-Cys-Gly motif that is suggested to mediate thrombospondin 1 binding to the CD36 receptor ( ) is present at an identical location within TSR4 of human and mouse ADAMTS7B.	bind
34360	2	9865	6	11	NULL	NULL	NULL				mediate			Cys-Ser-Val-Thr-Cys-Gly motif		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_34_35159_s_145	15192113	A Cys-Ser-Val-Thr-Cys-Gly motif that is suggested to mediate thrombospondin 1 binding to the CD36 receptor ( ) is present at an identical location within TSR4 of human and mouse ADAMTS7B.	bind
41603	1	9865	7	11	NULL	NULL	NULL	 thrombospondin 1 	GP		bind					CD36 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_34_35159_s_145	15192113	A Cys-Ser-Val-Thr-Cys-Gly motif that is suggested to mediate thrombospondin 1 binding to the CD36 receptor ( ) is present at an identical location within TSR4 of human and mouse ADAMTS7B.	bind
41604	2	9865	7	11	NULL	NULL	NULL				mediate			Cys-Ser-Val-Thr-Cys-Gly motif		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_34_35159_s_145	15192113	A Cys-Ser-Val-Thr-Cys-Gly motif that is suggested to mediate thrombospondin 1 binding to the CD36 receptor ( ) is present at an identical location within TSR4 of human and mouse ADAMTS7B.	bind
41606	3	9865	7	11	NULL	NULL	NULL				is present			Cys-Ser-Val-Thr-Cys-Gly motif		ADAMTS7B	GP	human	within TSR4 		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_34_35159_s_145	15192113	A Cys-Ser-Val-Thr-Cys-Gly motif that is suggested to mediate thrombospondin 1 binding to the CD36 receptor ( ) is present at an identical location within TSR4 of human and mouse ADAMTS7B.	bind
41607	4	9865	7	11	NULL	NULL	NULL				is present 			Cys-Ser-Val-Thr-Cys-Gly motif		ADAMTS7B	GP	mouse	within TSR4 		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_34_35159_s_145	15192113	A Cys-Ser-Val-Thr-Cys-Gly motif that is suggested to mediate thrombospondin 1 binding to the CD36 receptor ( ) is present at an identical location within TSR4 of human and mouse ADAMTS7B.	bind
34361	1	9866	6	11	NULL	NULL	NULL	CD4 tail	GP		bind			cysteine motif		p56 lck	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_289_5483_1349_s_16	10958781	A cysteine motif present in the CD4 tail binds src-family kinase p56 lck ( 8), and Lck appears to be responsible for phosphorylating CD3zeta, the earliest known event in T cell signaling ( 9).	bind
34362	2	9866	6	11	NULL	NULL	NULL	p56 lck	GP		is a type of					src-family kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_289_5483_1349_s_16	10958781	A cysteine motif present in the CD4 tail binds src-family kinase p56 lck ( 8), and Lck appears to be responsible for phosphorylating CD3zeta, the earliest known event in T cell signaling ( 9).	bind
34363	3	9866	6	11	NULL	NULL	NULL	lck	GP		phosphorylates					CD3zeta	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_289_5483_1349_s_16	10958781	A cysteine motif present in the CD4 tail binds src-family kinase p56 lck ( 8), and Lck appears to be responsible for phosphorylating CD3zeta, the earliest known event in T cell signaling ( 9).	bind
34374	4	9866	6	11	NULL	NULL	NULL	statement 3	Process		is involved in					T cell signaling	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_289_5483_1349_s_16	10958781	A cysteine motif present in the CD4 tail binds src-family kinase p56 lck ( 8), and Lck appears to be responsible for phosphorylating CD3zeta, the earliest known event in T cell signaling ( 9).	bind
41608	1	9866	7	11	NULL	NULL	NULL	CD4 tail	GP		binds			cysteine motif 		p56 lck	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_289_5483_1349_s_16	10958781	A cysteine motif present in the CD4 tail binds src-family kinase p56 lck ( 8), and Lck appears to be responsible for phosphorylating CD3zeta, the earliest known event in T cell signaling ( 9).	bind
41609	2	9866	7	11	NULL	NULL	NULL	p56 lck	GP		is a type of					src-family kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_289_5483_1349_s_16	10958781	A cysteine motif present in the CD4 tail binds src-family kinase p56 lck ( 8), and Lck appears to be responsible for phosphorylating CD3zeta, the earliest known event in T cell signaling ( 9).	bind
41610	3	9866	7	11	NULL	NULL	NULL	Lck	GP		phosphorylate					CD3zeta	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_289_5483_1349_s_16	10958781	A cysteine motif present in the CD4 tail binds src-family kinase p56 lck ( 8), and Lck appears to be responsible for phosphorylating CD3zeta, the earliest known event in T cell signaling ( 9).	bind
41613	4	9866	7	11	NULL	NULL	NULL	statement 3	Process		is involved in					T cell signaling	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_289_5483_1349_s_16	10958781	A cysteine motif present in the CD4 tail binds src-family kinase p56 lck ( 8), and Lck appears to be responsible for phosphorylating CD3zeta, the earliest known event in T cell signaling ( 9).	bind
34701	1	9867	6	11	NULL	NULL	NULL	hCG analog	GP		bind			S138C in the beta-subunit COOH terminus		LHR	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_43_44442_s_376	15304493	A cysteine residue that had been added to the beta-subunit COOH terminus of a bifunctional hCG analog ( i.e. CFC101 - 114,) S138Cthat binds LHR and FSHR was found to become cross-linked to cysteines  added to the alpha-subunit during heterodimer synthesis in COS-7 cells.	bind
34702	2	9867	6	11	NULL	NULL	NULL				bind			S138C in the beta-subunit COOH terminus		FSHR	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_43_44442_s_376	15304493	A cysteine residue that had been added to the beta-subunit COOH terminus of a bifunctional hCG analog ( i.e. CFC101 - 114,) S138Cthat binds LHR and FSHR was found to become cross-linked to cysteines  added to the alpha-subunit during heterodimer synthesis in COS-7 cells.	bind
41614	1	9867	7	11	NULL	NULL	NULL	hCG analog	GP		binds			S138C in the beta-subunit COOH terminus		LHR	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_43_44442_s_376	15304493	A cysteine residue that had been added to the beta-subunit COOH terminus of a bifunctional hCG analog ( i.e. CFC101 - 114,) S138Cthat binds LHR and FSHR was found to become cross-linked to cysteines  added to the alpha-subunit during heterodimer synthesis in COS-7 cells.	bind
41615	2	9867	7	11	NULL	NULL	NULL	hCG analog	GP		binds			S138C in the beta-subunit COOH terminus		FSHR	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_43_44442_s_376	15304493	A cysteine residue that had been added to the beta-subunit COOH terminus of a bifunctional hCG analog ( i.e. CFC101 - 114,) S138Cthat binds LHR and FSHR was found to become cross-linked to cysteines  added to the alpha-subunit during heterodimer synthesis in COS-7 cells.	bind
41622	3	9867	7	11	NULL	NULL	NULL				crosslinked to			S138C					cysteines in alpha-subunit		NULL	COS-7 cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_43_44442_s_376	15304493	A cysteine residue that had been added to the beta-subunit COOH terminus of a bifunctional hCG analog ( i.e. CFC101 - 114,) S138Cthat binds LHR and FSHR was found to become cross-linked to cysteines  added to the alpha-subunit during heterodimer synthesis in COS-7 cells.	bind
41624	4	9867	7	11	NULL	NULL	NULL				added to			cysteines					alpha-subunit		NULL	COS-7 cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_43_44442_s_376	15304493	A cysteine residue that had been added to the beta-subunit COOH terminus of a bifunctional hCG analog ( i.e. CFC101 - 114,) S138Cthat binds LHR and FSHR was found to become cross-linked to cysteines  added to the alpha-subunit during heterodimer synthesis in COS-7 cells.	bind
41626	5	9867	7	11	NULL	NULL	NULL	statement 4	Process		occurs during					heterodimer synthesis	Process				NULL	COS-7 cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_43_44442_s_376	15304493	A cysteine residue that had been added to the beta-subunit COOH terminus of a bifunctional hCG analog ( i.e. CFC101 - 114,) S138Cthat binds LHR and FSHR was found to become cross-linked to cysteines  added to the alpha-subunit during heterodimer synthesis in COS-7 cells.	bind
34378	1	9868	6	11	NULL	NULL	NULL	ADAM12	GP		bind			cysteine rich domain		syndecan	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_43_32929_s_282	16945929	A cysteine-rich domain of ADAM12 binds syndecan that promotes mesenchymal cell spreading through integrin beta1 ( ).	bind
34379	2	9868	6	11	NULL	NULL	NULL	statement 1	Process		promotes					mesenchymal cell	Cell	spreading of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_43_32929_s_282	16945929	A cysteine-rich domain of ADAM12 binds syndecan that promotes mesenchymal cell spreading through integrin beta1 ( ).	bind
34381	3	9868	6	11	NULL	NULL	NULL	statement 2	Process		occurs through					integrin beta1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_43_32929_s_282	16945929	A cysteine-rich domain of ADAM12 binds syndecan that promotes mesenchymal cell spreading through integrin beta1 ( ).	bind
41627	1	9868	7	11	NULL	NULL	NULL	ADAM12	GP		binds			cysteine-rich domain		 syndecan	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_43_32929_s_282	16945929	A cysteine-rich domain of ADAM12 binds syndecan that promotes mesenchymal cell spreading through integrin beta1 ( ).	bind
41628	2	9868	7	11	NULL	NULL	NULL	statement 1	Process		promotes					mesenchymal cell 	Cell	spreading of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_43_32929_s_282	16945929	A cysteine-rich domain of ADAM12 binds syndecan that promotes mesenchymal cell spreading through integrin beta1 ( ).	bind
41629	3	9868	7	11	NULL	NULL	NULL	statement 2	Process		occurs through					integrin beta1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_43_32929_s_282	16945929	A cysteine-rich domain of ADAM12 binds syndecan that promotes mesenchymal cell spreading through integrin beta1 ( ).	bind
34384	1	9869	6	11	NULL	NULL	NULL	IkappaB kinase	GP	cytokine responsive	activates					NF-kappaB	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5523_s_476	9710636	A cytokine-responsive IkappaB kinase that activates the transcription factor NF-kappaB.	bind
34385	2	9869	6	11	NULL	NULL	NULL	NF-kappaB	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5523_s_476	9710636	A cytokine-responsive IkappaB kinase that activates the transcription factor NF-kappaB.	bind
41630	1	9869	7	11	NULL	NULL	NULL	IkappaB kinase	GP	cytokine-responsive	activates					NF-kappaB	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5523_s_476	9710636	A cytokine-responsive IkappaB kinase that activates the transcription factor NF-kappaB.	bind
41631	2	9869	7	11	NULL	NULL	NULL	NF-kappaB	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5523_s_476	9710636	A cytokine-responsive IkappaB kinase that activates the transcription factor NF-kappaB.	bind
34394	1	9870	6	11	NULL	NULL	NULL	cytolysin	Chemical	Salmonella	is required for					survival	Process				NULL	macrophages	NULL	NULL	NULL	NULL	gw60_infectimmun_69_2_706_s_326	11159958	A cytolysin encoded by  Salmonella is required for survival within macrophages.	bind
41633	2	9870	7	11	NULL	NULL	NULL	cytolysin	Chemical	Salmonella	is required for					survival	Process				NULL	macrophages	NULL	NULL	NULL	NULL	gw60_infectimmun_69_2_706_s_326	11159958	A cytolysin encoded by  Salmonella is required for survival within macrophages.	bind
34395	1	9871	6	11	NULL	NULL	NULL	chaperonin	GP	cytoplasmic	catalyzes					beta-actin	GP	folding of 			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_4_621_s_380	11106732	A cytoplasmic chaperonin that catalyzes beta-actin folding.	bind
41634	1	9871	7	11	NULL	NULL	NULL	chaperonin 	GP	cytoplasmic	catalyzes					beta-actin	GP	folding of			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_4_621_s_380	11106732	A cytoplasmic chaperonin that catalyzes beta-actin folding.	bind
34396	1	9872	6	11	NULL	NULL	NULL	serine protein kinase	GP	cytoplasmic	bind					FANCA	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_481_s_495	9759495	A cytoplasmic serine protein kinase binds and may regulate the Fanconi anemia protein FANCA.	bind
34397	2	9872	6	11	NULL	NULL	NULL	FANCA	GP		is					Fanconi anemia protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_481_s_495	9759495	A cytoplasmic serine protein kinase binds and may regulate the Fanconi anemia protein FANCA.	bind
34398	3	9872	6	11	NULL	NULL	NULL	statement 1	Process		regulates		may			FANCA	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_481_s_495	9759495	A cytoplasmic serine protein kinase binds and may regulate the Fanconi anemia protein FANCA.	bind
41635	1	9872	7	11	NULL	NULL	NULL	serine protein kinase	GP	cytoplasmic	binds					FANCA protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_481_s_495	9759495	A cytoplasmic serine protein kinase binds and may regulate the Fanconi anemia protein FANCA.	bind
41636	2	9872	7	11	NULL	NULL	NULL	statement 1	Process		regulate		may			FANCA protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_481_s_495	9759495	A cytoplasmic serine protein kinase binds and may regulate the Fanconi anemia protein FANCA.	bind
41637	3	9872	7	11	NULL	NULL	NULL	FANCA	GP		is					Fanconi anemia	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_481_s_495	9759495	A cytoplasmic serine protein kinase binds and may regulate the Fanconi anemia protein FANCA.	bind
34399	1	9873	6	11	NULL	NULL	NULL	tropomyosin	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2101_s_384	10595939	A cytoskeletal protein that binds to the end of erythrocyte tropomyosin and inhibits tropomyosin binding to actin.	bind
34400	2	9873	6	11	NULL	NULL	NULL	cytoskeletal protein	GP		bind					erythrocyte tropomyosin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2101_s_384	10595939	A cytoskeletal protein that binds to the end of erythrocyte tropomyosin and inhibits tropomyosin binding to actin.	bind
34401	3	9873	6	11	NULL	NULL	NULL	statement 2	Process		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2101_s_384	10595939	A cytoskeletal protein that binds to the end of erythrocyte tropomyosin and inhibits tropomyosin binding to actin.	bind
41638	1	9873	7	11	NULL	NULL	NULL	cytoskeletal protein	GP		binds to					erythrocyte tropomyosin 	GP		end of		NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2101_s_384	10595939	A cytoskeletal protein that binds to the end of erythrocyte tropomyosin and inhibits tropomyosin binding to actin.	bind
41639	2	9873	7	11	NULL	NULL	NULL	tropomyosin	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2101_s_384	10595939	A cytoskeletal protein that binds to the end of erythrocyte tropomyosin and inhibits tropomyosin binding to actin.	bind
41640	3	9873	7	11	NULL	NULL	NULL	statement 1	Process		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_155_6_2101_s_384	10595939	A cytoskeletal protein that binds to the end of erythrocyte tropomyosin and inhibits tropomyosin binding to actin.	bind
34691	1	9874	6	11	NULL	NULL	NULL	cytosolic PGES	GP		is					CPGES	GP				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_73_1_36_s_25	15744024	A cytosolic PGES (CPGES), also known as cytosolic PTGES or PTGES3, identical to p23, a ubiquitous chaperone protein weakly bound to the steroid hormone receptor/hsp90 complex [ ,  ], was characterized and found coupled to COX1 for immediate production of PGE2 [ ].	bind
34698	2	9874	6	11	NULL	NULL	NULL	CPGES	GP		is coupled to					COX1	GP				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_73_1_36_s_25	15744024	A cytosolic PGES (CPGES), also known as cytosolic PTGES or PTGES3, identical to p23, a ubiquitous chaperone protein weakly bound to the steroid hormone receptor/hsp90 complex [ ,  ], was characterized and found coupled to COX1 for immediate production of PGE2 [ ].	bind
34699	3	9874	6	11	NULL	NULL	NULL	statement 2	Process		leads to					PGE2	GP	production of			NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_73_1_36_s_25	15744024	A cytosolic PGES (CPGES), also known as cytosolic PTGES or PTGES3, identical to p23, a ubiquitous chaperone protein weakly bound to the steroid hormone receptor/hsp90 complex [ ,  ], was characterized and found coupled to COX1 for immediate production of PGE2 [ ].	bind
34700	4	9874	6	11	NULL	NULL	NULL	CPGES	GP		is identical to					p23	GP				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_73_1_36_s_25	15744024	A cytosolic PGES (CPGES), also known as cytosolic PTGES or PTGES3, identical to p23, a ubiquitous chaperone protein weakly bound to the steroid hormone receptor/hsp90 complex [ ,  ], was characterized and found coupled to COX1 for immediate production of PGE2 [ ].	bind
48997	5	9874	6	11	NULL	NULL	NULL	CPGES	GP		is					PTGES3	GP				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_73_1_36_s_25	15744024	A cytosolic PGES (CPGES), also known as cytosolic PTGES or PTGES3, identical to p23, a ubiquitous chaperone protein weakly bound to the steroid hormone receptor/hsp90 complex [ ,  ], was characterized and found coupled to COX1 for immediate production of PGE2 [ ].	bind
48998	6	9874	6	11	NULL	NULL	NULL	CPGES	GP		is					cytosolic PTGES	GP				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_73_1_36_s_25	15744024	A cytosolic PGES (CPGES), also known as cytosolic PTGES or PTGES3, identical to p23, a ubiquitous chaperone protein weakly bound to the steroid hormone receptor/hsp90 complex [ ,  ], was characterized and found coupled to COX1 for immediate production of PGE2 [ ].	bind
48999	7	9874	6	11	NULL	NULL	NULL	p23	GP		is a type of					ubiquitous chaperone protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_73_1_36_s_25	15744024	A cytosolic PGES (CPGES), also known as cytosolic PTGES or PTGES3, identical to p23, a ubiquitous chaperone protein weakly bound to the steroid hormone receptor/hsp90 complex [ ,  ], was characterized and found coupled to COX1 for immediate production of PGE2 [ ].	bind
49000	8	9874	6	11	NULL	NULL	NULL	p23	GP		bind		weakly			steroid hormone receptor/hsp90 complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_73_1_36_s_25	15744024	A cytosolic PGES (CPGES), also known as cytosolic PTGES or PTGES3, identical to p23, a ubiquitous chaperone protein weakly bound to the steroid hormone receptor/hsp90 complex [ ,  ], was characterized and found coupled to COX1 for immediate production of PGE2 [ ].	bind
41641	1	9874	7	11	NULL	NULL	NULL	CPGES	GP		is					cytosolic PTGES	GP				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_73_1_36_s_25	15744024	A cytosolic PGES (CPGES), also known as cytosolic PTGES or PTGES3, identical to p23, a ubiquitous chaperone protein weakly bound to the steroid hormone receptor/hsp90 complex [ ,  ], was characterized and found coupled to COX1 for immediate production of PGE2 [ ].	bind
41642	2	9874	7	11	NULL	NULL	NULL	CPGES	GP		is					PTGES3	GP				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_73_1_36_s_25	15744024	A cytosolic PGES (CPGES), also known as cytosolic PTGES or PTGES3, identical to p23, a ubiquitous chaperone protein weakly bound to the steroid hormone receptor/hsp90 complex [ ,  ], was characterized and found coupled to COX1 for immediate production of PGE2 [ ].	bind
41643	3	9874	7	11	NULL	NULL	NULL	CPGES	GP		is identical to					p23	GP				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_73_1_36_s_25	15744024	A cytosolic PGES (CPGES), also known as cytosolic PTGES or PTGES3, identical to p23, a ubiquitous chaperone protein weakly bound to the steroid hormone receptor/hsp90 complex [ ,  ], was characterized and found coupled to COX1 for immediate production of PGE2 [ ].	bind
41644	4	9874	7	11	NULL	NULL	NULL	CPGES	GP		is					cytosolic PGES	GP				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_73_1_36_s_25	15744024	A cytosolic PGES (CPGES), also known as cytosolic PTGES or PTGES3, identical to p23, a ubiquitous chaperone protein weakly bound to the steroid hormone receptor/hsp90 complex [ ,  ], was characterized and found coupled to COX1 for immediate production of PGE2 [ ].	bind
41645	5	9874	7	11	NULL	NULL	NULL	p23	GP		is a type of					ubiquitous chaperone protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_73_1_36_s_25	15744024	A cytosolic PGES (CPGES), also known as cytosolic PTGES or PTGES3, identical to p23, a ubiquitous chaperone protein weakly bound to the steroid hormone receptor/hsp90 complex [ ,  ], was characterized and found coupled to COX1 for immediate production of PGE2 [ ].	bind
41646	6	9874	7	11	NULL	NULL	NULL	p23	GP		bind		weakly			steroid hormone receptor/hsp90 complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_73_1_36_s_25	15744024	A cytosolic PGES (CPGES), also known as cytosolic PTGES or PTGES3, identical to p23, a ubiquitous chaperone protein weakly bound to the steroid hormone receptor/hsp90 complex [ ,  ], was characterized and found coupled to COX1 for immediate production of PGE2 [ ].	bind
41647	7	9874	7	11	NULL	NULL	NULL	CPGES	GP		coupled to					COX1	GP				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_73_1_36_s_25	15744024	A cytosolic PGES (CPGES), also known as cytosolic PTGES or PTGES3, identical to p23, a ubiquitous chaperone protein weakly bound to the steroid hormone receptor/hsp90 complex [ ,  ], was characterized and found coupled to COX1 for immediate production of PGE2 [ ].	bind
41648	8	9874	7	11	NULL	NULL	NULL	statement 7	Process		leads to					PGE2	GP	immediate production of			NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_73_1_36_s_25	15744024	A cytosolic PGES (CPGES), also known as cytosolic PTGES or PTGES3, identical to p23, a ubiquitous chaperone protein weakly bound to the steroid hormone receptor/hsp90 complex [ ,  ], was characterized and found coupled to COX1 for immediate production of PGE2 [ ].	bind
34402	1	9875	6	11	NULL	NULL	NULL	cytosolic protein factor	GP		bind		specifically			H-ferritin	GP			3''-UTR	NULL	THP-1 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_42_30209_s_6	10514512	A cytosolic protein factor from THP-1 cells was found to specifically bind to H-ferritin 3''-UTR.	bind
41649	1	9875	7	11	NULL	NULL	NULL	cytosolic protein factor	GP		bind		specifically			H-ferritin	GP			 3''-UTR	NULL	THP-1 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_42_30209_s_6	10514512	A cytosolic protein factor from THP-1 cells was found to specifically bind to H-ferritin 3''-UTR.	bind
34403	1	9876	6	11	NULL	NULL	NULL	cytotoxic mAb	GP		bind					ErbB-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_9_1307_s_342	15124022	A cytotoxic mAb that binds to ErbB-2, a member of the EGFR family, and induced apoptosis has been reported ( ).	bind
34404	2	9876	6	11	NULL	NULL	NULL	ErbB-2	GP		is a member of					EGFR family	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_9_1307_s_342	15124022	A cytotoxic mAb that binds to ErbB-2, a member of the EGFR family, and induced apoptosis has been reported ( ).	bind
49001	3	9876	6	11	NULL	NULL	NULL	statement 1	Process		induces					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_9_1307_s_342	15124022	A cytotoxic mAb that binds to ErbB-2, a member of the EGFR family, and induced apoptosis has been reported ( ).	bind
41650	1	9876	7	11	NULL	NULL	NULL	cytotoxic mAb	GP		binds to					ErbB-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_9_1307_s_342	15124022	A cytotoxic mAb that binds to ErbB-2, a member of the EGFR family, and induced apoptosis has been reported ( ).	bind
41651	2	9876	7	11	NULL	NULL	NULL	statement 1	Process		induce					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_9_1307_s_342	15124022	A cytotoxic mAb that binds to ErbB-2, a member of the EGFR family, and induced apoptosis has been reported ( ).	bind
41652	3	9876	7	11	NULL	NULL	NULL	ErbB-2	GP		is a member of					EGFR family	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_113_9_1307_s_342	15124022	A cytotoxic mAb that binds to ErbB-2, a member of the EGFR family, and induced apoptosis has been reported ( ).	bind
34405	1	9877	6	11	NULL	NULL	NULL	SEB	GP		bind					Daudi cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_immunity_5_2_137_s_73	8769477	A cytotoxicity assay was used to determine whether 1B2 Fab fragments could inhibit the 2C-mediated recognition of SEB, SEC1, and SEC3 bound to Daudi cells.	bind
34406	2	9877	6	11	NULL	NULL	NULL	SEC1	GP		bind					Daudi cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_immunity_5_2_137_s_73	8769477	A cytotoxicity assay was used to determine whether 1B2 Fab fragments could inhibit the 2C-mediated recognition of SEB, SEC1, and SEC3 bound to Daudi cells.	bind
34407	3	9877	6	11	NULL	NULL	NULL	SEC3	GP		bind					Daudi cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_immunity_5_2_137_s_73	8769477	A cytotoxicity assay was used to determine whether 1B2 Fab fragments could inhibit the 2C-mediated recognition of SEB, SEC1, and SEC3 bound to Daudi cells.	bind
41653	1	9877	7	11	NULL	NULL	NULL	SEB	GP		bind					Daudi cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_immunity_5_2_137_s_73	8769477	A cytotoxicity assay was used to determine whether 1B2 Fab fragments could inhibit the 2C-mediated recognition of SEB, SEC1, and SEC3 bound to Daudi cells.	bind
41654	2	9877	7	11	NULL	NULL	NULL	SEC1	GP		bind					Daudi cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_immunity_5_2_137_s_73	8769477	A cytotoxicity assay was used to determine whether 1B2 Fab fragments could inhibit the 2C-mediated recognition of SEB, SEC1, and SEC3 bound to Daudi cells.	bind
41655	3	9877	7	11	NULL	NULL	NULL	SEC3	Cell		bind					Daudi cells	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_5_2_137_s_73	8769477	A cytotoxicity assay was used to determine whether 1B2 Fab fragments could inhibit the 2C-mediated recognition of SEB, SEC1, and SEC3 bound to Daudi cells.	bind
34642	1	9878	6	11	NULL	NULL	NULL	D1 receptor	GP		does not bind			S198A		dopamine	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_44_37225_s_190	16115864	A D1 receptor generated with two of these serines, Ser198 and Ser199, substituted with alanine (D1(S198A/S199A)) did not bind dopamine or SCH 23390, but we determined that it did bind (+)BTC.	bind
34643	2	9878	6	11	NULL	NULL	NULL	D1 receptor	GP		does not bind			S199A		dopamine	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_44_37225_s_190	16115864	A D1 receptor generated with two of these serines, Ser198 and Ser199, substituted with alanine (D1(S198A/S199A)) did not bind dopamine or SCH 23390, but we determined that it did bind (+)BTC.	bind
34644	3	9878	6	11	NULL	NULL	NULL	D1 receptor	GP		does not bind			S198A		SCH 23390	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_44_37225_s_190	16115864	A D1 receptor generated with two of these serines, Ser198 and Ser199, substituted with alanine (D1(S198A/S199A)) did not bind dopamine or SCH 23390, but we determined that it did bind (+)BTC.	bind
34645	4	9878	6	11	NULL	NULL	NULL	D1 receptor	GP		does not bind			S199A		SCH 23390	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_44_37225_s_190	16115864	A D1 receptor generated with two of these serines, Ser198 and Ser199, substituted with alanine (D1(S198A/S199A)) did not bind dopamine or SCH 23390, but we determined that it did bind (+)BTC.	bind
34646	5	9878	6	11	NULL	NULL	NULL	D1 receptor	GP		bind			S198A		BTC	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_44_37225_s_190	16115864	A D1 receptor generated with two of these serines, Ser198 and Ser199, substituted with alanine (D1(S198A/S199A)) did not bind dopamine or SCH 23390, but we determined that it did bind (+)BTC.	bind
34647	6	9878	6	11	NULL	NULL	NULL	D1 receptor	GP		bind			S199A		BTC	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_44_37225_s_190	16115864	A D1 receptor generated with two of these serines, Ser198 and Ser199, substituted with alanine (D1(S198A/S199A)) did not bind dopamine or SCH 23390, but we determined that it did bind (+)BTC.	bind
34648	7	9878	6	11	NULL	NULL	NULL	S198A	AminoAcid		is					serine198 substituted with alanine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_44_37225_s_190	16115864	A D1 receptor generated with two of these serines, Ser198 and Ser199, substituted with alanine (D1(S198A/S199A)) did not bind dopamine or SCH 23390, but we determined that it did bind (+)BTC.	bind
34690	8	9878	6	11	NULL	NULL	NULL	S199A	AminoAcid		is					serine199 substituted with alanine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_44_37225_s_190	16115864	A D1 receptor generated with two of these serines, Ser198 and Ser199, substituted with alanine (D1(S198A/S199A)) did not bind dopamine or SCH 23390, but we determined that it did bind (+)BTC.	bind
41659	1	9878	7	11	NULL	NULL	NULL	D1 receptor	GP		does not bind			S198A/S199A		dopamine	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_44_37225_s_190	16115864	A D1 receptor generated with two of these serines, Ser198 and Ser199, substituted with alanine (D1(S198A/S199A)) did not bind dopamine or SCH 23390, but we determined that it did bind (+)BTC.	bind
41660	2	9878	7	11	NULL	NULL	NULL	D1 receptor	GP		does not bind			S198A/S199A		SCH 23390	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_44_37225_s_190	16115864	A D1 receptor generated with two of these serines, Ser198 and Ser199, substituted with alanine (D1(S198A/S199A)) did not bind dopamine or SCH 23390, but we determined that it did bind (+)BTC.	bind
41661	3	9878	7	11	NULL	NULL	NULL	D1 receptor	GP		bind			S198A/S199A		BTC	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_44_37225_s_190	16115864	A D1 receptor generated with two of these serines, Ser198 and Ser199, substituted with alanine (D1(S198A/S199A)) did not bind dopamine or SCH 23390, but we determined that it did bind (+)BTC.	bind
49548	4	9878	7	11	NULL	NULL	NULL	S198A	AminoAcid		is					serine198 substituted with alanine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_44_37225_s_190	16115864	A D1 receptor generated with two of these serines, Ser198 and Ser199, substituted with alanine (D1(S198A/S199A)) did not bind dopamine or SCH 23390, but we determined that it did bind (+)BTC.	bind
49549	5	9878	7	11	NULL	NULL	NULL	S199A	AminoAcid		is					serine199 substituted with alanine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_44_37225_s_190	16115864	A D1 receptor generated with two of these serines, Ser198 and Ser199, substituted with alanine (D1(S198A/S199A)) did not bind dopamine or SCH 23390, but we determined that it did bind (+)BTC.	bind
34408	1	9879	6	11	NULL	NULL	NULL	FYB	GP		bind					FYN	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbpathogenesis_27_4_231_s_116	10502464	A Da Silva, Z Li, C De Vera, E Canto, P Findell and CE Rudd, Cloning of a novel  T-cell protein FYB that binds FYN and SH2-domain-containing leukocyte protein 76  and modulates interleukin 2 production.	bind
34409	2	9879	6	11	NULL	NULL	NULL	leukocyte protein 76	GP		contains								SH2 domain		NULL		NULL	NULL	NULL	NULL	gw70_microbpathogenesis_27_4_231_s_116	10502464	A Da Silva, Z Li, C De Vera, E Canto, P Findell and CE Rudd, Cloning of a novel  T-cell protein FYB that binds FYN and SH2-domain-containing leukocyte protein 76  and modulates interleukin 2 production.	bind
34410	3	9879	6	11	NULL	NULL	NULL	statement 5	Process		modulates					interleukin 2	GP	production of			NULL		NULL	NULL	NULL	NULL	gw70_microbpathogenesis_27_4_231_s_116	10502464	A Da Silva, Z Li, C De Vera, E Canto, P Findell and CE Rudd, Cloning of a novel  T-cell protein FYB that binds FYN and SH2-domain-containing leukocyte protein 76  and modulates interleukin 2 production.	bind
49002	4	9879	6	11	NULL	NULL	NULL	FYB	GP		is a type of					novel T-cell protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbpathogenesis_27_4_231_s_116	10502464	A Da Silva, Z Li, C De Vera, E Canto, P Findell and CE Rudd, Cloning of a novel  T-cell protein FYB that binds FYN and SH2-domain-containing leukocyte protein 76  and modulates interleukin 2 production.	bind
49532	5	9879	6	11	NULL	NULL	NULL	FYB	GP		bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbpathogenesis_27_4_231_s_116	10502464	A Da Silva, Z Li, C De Vera, E Canto, P Findell and CE Rudd, Cloning of a novel  T-cell protein FYB that binds FYN and SH2-domain-containing leukocyte protein 76  and modulates interleukin 2 production.	bind
41662	1	9879	7	11	NULL	NULL	NULL	FYB	GP		binds					FYN	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbpathogenesis_27_4_231_s_116	10502464	A Da Silva, Z Li, C De Vera, E Canto, P Findell and CE Rudd, Cloning of a novel  T-cell protein FYB that binds FYN and SH2-domain-containing leukocyte protein 76  and modulates interleukin 2 production.	bind
41663	5	9879	7	11	NULL	NULL	NULL	FYB	GP		binds					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbpathogenesis_27_4_231_s_116	10502464	A Da Silva, Z Li, C De Vera, E Canto, P Findell and CE Rudd, Cloning of a novel  T-cell protein FYB that binds FYN and SH2-domain-containing leukocyte protein 76  and modulates interleukin 2 production.	bind
41664	3	9879	7	11	NULL	NULL	NULL	FYB	GP		modulates					interleukin 2	GP	production of			NULL		NULL	NULL	NULL	NULL	gw70_microbpathogenesis_27_4_231_s_116	10502464	A Da Silva, Z Li, C De Vera, E Canto, P Findell and CE Rudd, Cloning of a novel  T-cell protein FYB that binds FYN and SH2-domain-containing leukocyte protein 76  and modulates interleukin 2 production.	bind
41665	4	9879	7	11	NULL	NULL	NULL	FYB	GP		is a type of					novel T-cell protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbpathogenesis_27_4_231_s_116	10502464	A Da Silva, Z Li, C De Vera, E Canto, P Findell and CE Rudd, Cloning of a novel  T-cell protein FYB that binds FYN and SH2-domain-containing leukocyte protein 76  and modulates interleukin 2 production.	bind
49533	2	9879	7	11	NULL	NULL	NULL	 leukocyte protein 76	GP		contains								SH2 domain		NULL		NULL	NULL	NULL	NULL	gw70_microbpathogenesis_27_4_231_s_116	10502464	A Da Silva, Z Li, C De Vera, E Canto, P Findell and CE Rudd, Cloning of a novel  T-cell protein FYB that binds FYN and SH2-domain-containing leukocyte protein 76  and modulates interleukin 2 production.	bind
34635	1	9880	6	11	NULL	NULL	NULL	Daam1	GP		bind			C-terminal fragment		Dsh	GP		PDZ domain		NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_155_s_198	16212491	A Daam1 C-terminal fragment binds the Dsh PDZ and DEP domains, the N-terminal part  of Daam1 binds RhoA, and Daam1 is required for Fz-mediated Rho activation in  Xenopus ( Habas et al. 2001), which makes Daam1 a good candidate to recruit Rho to the sites of Dsh localization.	bind
34636	2	9880	6	11	NULL	NULL	NULL	Daam1	GP		bind			C-terminal fragment		Dsh	GP		DEP domain		NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_155_s_198	16212491	A Daam1 C-terminal fragment binds the Dsh PDZ and DEP domains, the N-terminal part  of Daam1 binds RhoA, and Daam1 is required for Fz-mediated Rho activation in  Xenopus ( Habas et al. 2001), which makes Daam1 a good candidate to recruit Rho to the sites of Dsh localization.	bind
34637	3	9880	6	11	NULL	NULL	NULL	Daam1	GP		bind			N-terminal part		RhoA	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_155_s_198	16212491	A Daam1 C-terminal fragment binds the Dsh PDZ and DEP domains, the N-terminal part  of Daam1 binds RhoA, and Daam1 is required for Fz-mediated Rho activation in  Xenopus ( Habas et al. 2001), which makes Daam1 a good candidate to recruit Rho to the sites of Dsh localization.	bind
34638	4	9880	6	11	NULL	NULL	NULL	Rho	GP	activation of	is mediated by					Fz	GP				NULL	Xenopus	NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_155_s_198	16212491	A Daam1 C-terminal fragment binds the Dsh PDZ and DEP domains, the N-terminal part  of Daam1 binds RhoA, and Daam1 is required for Fz-mediated Rho activation in  Xenopus ( Habas et al. 2001), which makes Daam1 a good candidate to recruit Rho to the sites of Dsh localization.	bind
34639	5	9880	6	11	NULL	NULL	NULL	Daam1	GP		is required for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_155_s_198	16212491	A Daam1 C-terminal fragment binds the Dsh PDZ and DEP domains, the N-terminal part  of Daam1 binds RhoA, and Daam1 is required for Fz-mediated Rho activation in  Xenopus ( Habas et al. 2001), which makes Daam1 a good candidate to recruit Rho to the sites of Dsh localization.	bind
34640	6	9880	6	11	NULL	NULL	NULL	Rho	GP		is recruited to					Dsh localization	GP	sites of 			NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_155_s_198	16212491	A Daam1 C-terminal fragment binds the Dsh PDZ and DEP domains, the N-terminal part  of Daam1 binds RhoA, and Daam1 is required for Fz-mediated Rho activation in  Xenopus ( Habas et al. 2001), which makes Daam1 a good candidate to recruit Rho to the sites of Dsh localization.	bind
34641	7	9880	6	11	NULL	NULL	NULL	Daam1	GP		plays a role in					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_155_s_198	16212491	A Daam1 C-terminal fragment binds the Dsh PDZ and DEP domains, the N-terminal part  of Daam1 binds RhoA, and Daam1 is required for Fz-mediated Rho activation in  Xenopus ( Habas et al. 2001), which makes Daam1 a good candidate to recruit Rho to the sites of Dsh localization.	bind
41666	1	9880	7	11	NULL	NULL	NULL	Daam1	GP		binds			C-terminal fragment		Dsh	GP		 PDZ domain		NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_155_s_198	16212491	A Daam1 C-terminal fragment binds the Dsh PDZ and DEP domains, the N-terminal part  of Daam1 binds RhoA, and Daam1 is required for Fz-mediated Rho activation in  Xenopus ( Habas et al. 2001), which makes Daam1 a good candidate to recruit Rho to the sites of Dsh localization.	bind
41667	2	9880	7	11	NULL	NULL	NULL	Daam1	GP		binds			C-terminal fragment		Dsh	GP		DEP domain		NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_155_s_198	16212491	A Daam1 C-terminal fragment binds the Dsh PDZ and DEP domains, the N-terminal part  of Daam1 binds RhoA, and Daam1 is required for Fz-mediated Rho activation in  Xenopus ( Habas et al. 2001), which makes Daam1 a good candidate to recruit Rho to the sites of Dsh localization.	bind
41668	3	9880	7	11	NULL	NULL	NULL	Daam1	GP		binds			N-terminal part		RhoA	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_155_s_198	16212491	A Daam1 C-terminal fragment binds the Dsh PDZ and DEP domains, the N-terminal part  of Daam1 binds RhoA, and Daam1 is required for Fz-mediated Rho activation in  Xenopus ( Habas et al. 2001), which makes Daam1 a good candidate to recruit Rho to the sites of Dsh localization.	bind
41669	4	9880	7	11	NULL	NULL	NULL	Fz	GP		mediates					Rho	GP	activation of			NULL	Xenopus	NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_155_s_198	16212491	A Daam1 C-terminal fragment binds the Dsh PDZ and DEP domains, the N-terminal part  of Daam1 binds RhoA, and Daam1 is required for Fz-mediated Rho activation in  Xenopus ( Habas et al. 2001), which makes Daam1 a good candidate to recruit Rho to the sites of Dsh localization.	bind
41671	5	9880	7	11	NULL	NULL	NULL	Daam1	GP		is required for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_155_s_198	16212491	A Daam1 C-terminal fragment binds the Dsh PDZ and DEP domains, the N-terminal part  of Daam1 binds RhoA, and Daam1 is required for Fz-mediated Rho activation in  Xenopus ( Habas et al. 2001), which makes Daam1 a good candidate to recruit Rho to the sites of Dsh localization.	bind
41672	6	9880	7	11	NULL	NULL	NULL	Daam1	GP		recruit					Rho	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_155_s_198	16212491	A Daam1 C-terminal fragment binds the Dsh PDZ and DEP domains, the N-terminal part  of Daam1 binds RhoA, and Daam1 is required for Fz-mediated Rho activation in  Xenopus ( Habas et al. 2001), which makes Daam1 a good candidate to recruit Rho to the sites of Dsh localization.	bind
41673	7	9880	7	11	NULL	NULL	NULL	statement 6	Process		occur at					Dsh localization	GP	sites of			NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_21_0_155_s_198	16212491	A Daam1 C-terminal fragment binds the Dsh PDZ and DEP domains, the N-terminal part  of Daam1 binds RhoA, and Daam1 is required for Fz-mediated Rho activation in  Xenopus ( Habas et al. 2001), which makes Daam1 a good candidate to recruit Rho to the sites of Dsh localization.	bind
34411	1	9882	6	11	NULL	NULL	NULL	lectin	Chemical	peroxidase-labeled;;peanut	bind		specifically			distal tubule cells	Cell	human			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_in-vitro-cell-dev-biol_26_5_2161826_s_8	2161826	A dark-brown reaction  product was observed in these cells when stained by the immunoperoxidase  method with peroxidase-labeled peanut lectin (Arachis hypogaea), which  binds specifically to human distal tubule and collecting duct cells.	bind
34412	2	9882	6	11	NULL	NULL	NULL	lectin	Chemical	peroxidase-labeled;;peanut	is					Arachis hypogaea	Organism				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_in-vitro-cell-dev-biol_26_5_2161826_s_8	2161826	A dark-brown reaction  product was observed in these cells when stained by the immunoperoxidase  method with peroxidase-labeled peanut lectin (Arachis hypogaea), which  binds specifically to human distal tubule and collecting duct cells.	bind
34492	3	9882	6	11	NULL	NULL	NULL	lectin	Chemical	peroxidase-labeled;;peanut	bind		specifically			collecting duct cells	Cell	human			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_in-vitro-cell-dev-biol_26_5_2161826_s_8	2161826	A dark-brown reaction  product was observed in these cells when stained by the immunoperoxidase  method with peroxidase-labeled peanut lectin (Arachis hypogaea), which  binds specifically to human distal tubule and collecting duct cells.	bind
41720	1	9882	7	11	NULL	NULL	NULL	lectin	Chemical	peroxidase-labeled;;peanut	bind		specifically			distal tubule	Cell	human			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_in-vitro-cell-dev-biol_26_5_2161826_s_8	2161826	A dark-brown reaction  product was observed in these cells when stained by the immunoperoxidase  method with peroxidase-labeled peanut lectin (Arachis hypogaea), which  binds specifically to human distal tubule and collecting duct cells.	bind
41721	2	9882	7	11	NULL	NULL	NULL	lectin	Chemical	peroxidase-labeled;;peanut	bind		specifically			collecting duct cells	Cell	human			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_in-vitro-cell-dev-biol_26_5_2161826_s_8	2161826	A dark-brown reaction  product was observed in these cells when stained by the immunoperoxidase  method with peroxidase-labeled peanut lectin (Arachis hypogaea), which  binds specifically to human distal tubule and collecting duct cells.	bind
41723	3	9882	7	11	NULL	NULL	NULL	lectin	Chemical	peroxidase-labeled;;peanut	is					Arachis hypogaea	Organism				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_in-vitro-cell-dev-biol_26_5_2161826_s_8	2161826	A dark-brown reaction  product was observed in these cells when stained by the immunoperoxidase  method with peroxidase-labeled peanut lectin (Arachis hypogaea), which  binds specifically to human distal tubule and collecting duct cells.	bind
34493	1	9884	6	11	NULL	NULL	NULL	RTP	GP		is					replication terminator protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_430_7002_913_s_49	15286659	A database search revealed that tCdt1 most closely resembles bacterial replication  terminator protein (RTP), which binds to bacterial replicative helicase, DnaB 21.	bind
34494	2	9884	6	11	NULL	NULL	NULL	tCdt1	GP		resembles					RTP	GP	bacterial			NULL		NULL	NULL	NULL	NULL	gw70_nature_430_7002_913_s_49	15286659	A database search revealed that tCdt1 most closely resembles bacterial replication  terminator protein (RTP), which binds to bacterial replicative helicase, DnaB 21.	bind
34495	3	9884	6	11	NULL	NULL	NULL	DnaB	GP		is a type of					replicative helicase	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_430_7002_913_s_49	15286659	A database search revealed that tCdt1 most closely resembles bacterial replication  terminator protein (RTP), which binds to bacterial replicative helicase, DnaB 21.	bind
34496	4	9884	6	11	NULL	NULL	NULL	RTP	GP	bacterial	bind					DnaB	GP	bacterial			NULL		NULL	NULL	NULL	NULL	gw70_nature_430_7002_913_s_49	15286659	A database search revealed that tCdt1 most closely resembles bacterial replication  terminator protein (RTP), which binds to bacterial replicative helicase, DnaB 21.	bind
41732	1	9884	7	11	NULL	NULL	NULL	RTP	GP	bacterial	binds to					DnaB	GP	bacterial			NULL		NULL	NULL	NULL	NULL	gw70_nature_430_7002_913_s_49	15286659	A database search revealed that tCdt1 most closely resembles bacterial replication  terminator protein (RTP), which binds to bacterial replicative helicase, DnaB 21.	bind
41733	2	9884	7	11	NULL	NULL	NULL	RTP	GP		is					replication terminator protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_430_7002_913_s_49	15286659	A database search revealed that tCdt1 most closely resembles bacterial replication  terminator protein (RTP), which binds to bacterial replicative helicase, DnaB 21.	bind
41734	3	9884	7	11	NULL	NULL	NULL	DnaB	GP		is a type of					replicative helicase	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_430_7002_913_s_49	15286659	A database search revealed that tCdt1 most closely resembles bacterial replication  terminator protein (RTP), which binds to bacterial replicative helicase, DnaB 21.	bind
41735	4	9884	7	11	NULL	NULL	NULL	tCdt1	GP		resembles					RTP	GP	bacterial			NULL		NULL	NULL	NULL	NULL	gw70_nature_430_7002_913_s_49	15286659	A database search revealed that tCdt1 most closely resembles bacterial replication  terminator protein (RTP), which binds to bacterial replicative helicase, DnaB 21.	bind
34497	1	9885	6	11	NULL	NULL	NULL	DBE probe	GP	mutant	does not bind				YY1 core recognition sequence	GST-YY1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_3_339_s_131	12176321	A DBE probe containing a mutation within the YY1 core recognition sequence was not bound by GST-YY1.	bind
41736	1	9885	7	11	NULL	NULL	NULL	DBE probe	GP	mutant	does not bind			 	YY1 core recognition sequence	GST-YY1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_110_3_339_s_131	12176321	A DBE probe containing a mutation within the YY1 core recognition sequence was not bound by GST-YY1.	bind
34498	1	9886	6	11	NULL	NULL	NULL	MCP	GP		is present on					spermatozoa	Cell	acrosome-reacted; human			NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_71_4_1374_s_299	15215199	A decade ago, Anderson and colleagues [ ] demonstrated that MCP on acrosome-reacted human spermatozoa specifically bound dimeric C3b and implicated this association in the adhesion of sperm and oocyte.	bind
34499	2	9886	6	11	NULL	NULL	NULL	MCP	GP		bind		specifically			dimeric C3b	GP				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_71_4_1374_s_299	15215199	A decade ago, Anderson and colleagues [ ] demonstrated that MCP on acrosome-reacted human spermatozoa specifically bound dimeric C3b and implicated this association in the adhesion of sperm and oocyte.	bind
34500	3	9886	6	11	NULL	NULL	NULL	statement 2	Process		plays a role in					sperm	Cell	adhesion of 			NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_71_4_1374_s_299	15215199	A decade ago, Anderson and colleagues [ ] demonstrated that MCP on acrosome-reacted human spermatozoa specifically bound dimeric C3b and implicated this association in the adhesion of sperm and oocyte.	bind
34501	4	9886	6	11	NULL	NULL	NULL	statement 2	Process		plays a role in					oocyte	Cell	adhesion of			NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_71_4_1374_s_299	15215199	A decade ago, Anderson and colleagues [ ] demonstrated that MCP on acrosome-reacted human spermatozoa specifically bound dimeric C3b and implicated this association in the adhesion of sperm and oocyte.	bind
41756	1	9886	7	11	NULL	NULL	NULL	 MCP	GP		bind		specifically			dimeric C3b	GP				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_71_4_1374_s_299	15215199	A decade ago, Anderson and colleagues [ ] demonstrated that MCP on acrosome-reacted human spermatozoa specifically bound dimeric C3b and implicated this association in the adhesion of sperm and oocyte.	bind
41759	2	9886	7	11	NULL	NULL	NULL	statement 1	Process		plays a role in					sperm	Cell	adhesion of			NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_71_4_1374_s_299	15215199	A decade ago, Anderson and colleagues [ ] demonstrated that MCP on acrosome-reacted human spermatozoa specifically bound dimeric C3b and implicated this association in the adhesion of sperm and oocyte.	bind
41784	3	9886	7	11	NULL	NULL	NULL	statement 1	Process		plays a role in					oocyte	Cell	adhesion of			NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_71_4_1374_s_299	15215199	A decade ago, Anderson and colleagues [ ] demonstrated that MCP on acrosome-reacted human spermatozoa specifically bound dimeric C3b and implicated this association in the adhesion of sperm and oocyte.	bind
49003	4	9886	7	11	NULL	NULL	NULL	MCP	GP		is present on					spermatozoa	Cell	acrosome-reacted;;human			NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_71_4_1374_s_299	15215199	A decade ago, Anderson and colleagues [ ] demonstrated that MCP on acrosome-reacted human spermatozoa specifically bound dimeric C3b and implicated this association in the adhesion of sperm and oocyte.	bind
41790	1	9887	7	NULL	NULL	0	NULL	HUVEC	NULL		produce	NULL				 essential complement factors	NULL				NULL		0	NULL	NULL	NULL	gw70_femsimmunolmedmic_36_1_55_s_146	12727366	A decade ago, we demonstrated that HUVEC produce the essential complement factors  for the binding of C3b and the terminal complement complex to co-cultured particulate  complement activators of the alternative pathway like agarose beads [  32].	bind
41793	2	9887	7	NULL	NULL	0	NULL	statement 1	NULL		is required for	NULL				C3b	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw70_femsimmunolmedmic_36_1_55_s_146	12727366	A decade ago, we demonstrated that HUVEC produce the essential complement factors  for the binding of C3b and the terminal complement complex to co-cultured particulate  complement activators of the alternative pathway like agarose beads [  32].	bind
41797	3	9887	7	NULL	NULL	0	NULL	HUVEC	NULL		produce	NULL				terminal complement complex	NULL				NULL		0	NULL	NULL	NULL	gw70_femsimmunolmedmic_36_1_55_s_146	12727366	A decade ago, we demonstrated that HUVEC produce the essential complement factors  for the binding of C3b and the terminal complement complex to co-cultured particulate  complement activators of the alternative pathway like agarose beads [  32].	bind
34503	1	9888	6	11	NULL	NULL	NULL	Cu	Chemical		bind					apo-CuZnSOD	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_20_0_291_s_136	10940336	A decline in GSH levels in a cell impairs the subsequent binding of Cu to apo-CuZnSOD  ( 126) or the delivery of Cu to the cytosolic enzymes ( 119).	bind
34504	2	9888	6	11	NULL	NULL	NULL	GSH levels	GP	decline of	impairs					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_20_0_291_s_136	10940336	A decline in GSH levels in a cell impairs the subsequent binding of Cu to apo-CuZnSOD  ( 126) or the delivery of Cu to the cytosolic enzymes ( 119).	bind
34505	3	9888	6	11	NULL	NULL	NULL	Cu	Chemical		is delivered to					cytosolic enzymes	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_20_0_291_s_136	10940336	A decline in GSH levels in a cell impairs the subsequent binding of Cu to apo-CuZnSOD  ( 126) or the delivery of Cu to the cytosolic enzymes ( 119).	bind
34506	4	9888	6	11	NULL	NULL	NULL	GSH levels	GP	decline of	impairs					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_20_0_291_s_136	10940336	A decline in GSH levels in a cell impairs the subsequent binding of Cu to apo-CuZnSOD  ( 126) or the delivery of Cu to the cytosolic enzymes ( 119).	bind
41802	1	9888	7	11	NULL	NULL	NULL	Cu	Chemical		bind					apo-CuZnSOD	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_20_0_291_s_136	10940336	A decline in GSH levels in a cell impairs the subsequent binding of Cu to apo-CuZnSOD  ( 126) or the delivery of Cu to the cytosolic enzymes ( 119).	bind
41803	2	9888	7	11	NULL	NULL	NULL	Cu	Chemical		delivered to					cytosolic enzymes	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_20_0_291_s_136	10940336	A decline in GSH levels in a cell impairs the subsequent binding of Cu to apo-CuZnSOD  ( 126) or the delivery of Cu to the cytosolic enzymes ( 119).	bind
41805	3	9888	7	11	NULL	NULL	NULL	GSH levels	GP	decline in	impairs					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_20_0_291_s_136	10940336	A decline in GSH levels in a cell impairs the subsequent binding of Cu to apo-CuZnSOD  ( 126) or the delivery of Cu to the cytosolic enzymes ( 119).	bind
41808	4	9888	7	11	NULL	NULL	NULL	GSH levels	GP	decline in	impairs 					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_20_0_291_s_136	10940336	A decline in GSH levels in a cell impairs the subsequent binding of Cu to apo-CuZnSOD  ( 126) or the delivery of Cu to the cytosolic enzymes ( 119).	bind
34633	1	9889	6	11	NULL	NULL	NULL	hamartin	GP	protein levels of	is decreased in					myrAkt cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_14_12361_s_69	12517744	A decline in the protein levels of the tuberin binding partner hamartin was also observed in myrAkt cells, and this decline was consistently accompanied by the appearance of a faster migrating species in hamartin immunoblots, suggesting the generation of a hamartin degradation product in cells with activated Akt.	bind
34634	2	9889	6	11	NULL	NULL	NULL	hamartin	GP		bind					tuberin	GP				NULL	myrAkt cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_278_14_12361_s_69	12517744	A decline in the protein levels of the tuberin binding partner hamartin was also observed in myrAkt cells, and this decline was consistently accompanied by the appearance of a faster migrating species in hamartin immunoblots, suggesting the generation of a hamartin degradation product in cells with activated Akt.	bind
41809	1	9889	7	11	NULL	NULL	NULL	hamartin	GP		bind					tuberin	GP				NULL	myrAkt cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_278_14_12361_s_69	12517744	A decline in the protein levels of the tuberin binding partner hamartin was also observed in myrAkt cells, and this decline was consistently accompanied by the appearance of a faster migrating species in hamartin immunoblots, suggesting the generation of a hamartin degradation product in cells with activated Akt.	bind
41810	2	9889	7	11	NULL	NULL	NULL	hamartin	GP	protein levels of	is decreased in					myrAkt cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_14_12361_s_69	12517744	A decline in the protein levels of the tuberin binding partner hamartin was also observed in myrAkt cells, and this decline was consistently accompanied by the appearance of a faster migrating species in hamartin immunoblots, suggesting the generation of a hamartin degradation product in cells with activated Akt.	bind
34630	1	9890	6	11	NULL	NULL	NULL	GCN4 gamma1 chimera	GP		folds into					homotypic coiled-coil dimers	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6762_s_205	10581249	A decrease in binding affinity of the recombinant gamma1 chains and the chimeric GCN4 fusion proteins compared with native laminin-1 may be explained in terms of different coiled-coil structures in these molecules: the GCN4 gamma1 chimera folds into homotypic coiled-coil dimers and the gamma1 deltaN95AE fragments into a mixture of different oligomers, whereas the coiled-coil domain of native laminin-1 is a heterotrimer composed of alpha1, beta1 and gamma1 chains.	bind
34631	2	9890	6	11	NULL	NULL	NULL				folds into			gamma1 deltaN95AE fragments		oligomers	Chemical	mixture of different			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6762_s_205	10581249	A decrease in binding affinity of the recombinant gamma1 chains and the chimeric GCN4 fusion proteins compared with native laminin-1 may be explained in terms of different coiled-coil structures in these molecules: the GCN4 gamma1 chimera folds into homotypic coiled-coil dimers and the gamma1 deltaN95AE fragments into a mixture of different oligomers, whereas the coiled-coil domain of native laminin-1 is a heterotrimer composed of alpha1, beta1 and gamma1 chains.	bind
34632	3	9890	6	11	NULL	NULL	NULL	laminin-1 	GP	native	is composed of			coiled coil domain					alpha1;; beta1;; gamma1		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6762_s_205	10581249	A decrease in binding affinity of the recombinant gamma1 chains and the chimeric GCN4 fusion proteins compared with native laminin-1 may be explained in terms of different coiled-coil structures in these molecules: the GCN4 gamma1 chimera folds into homotypic coiled-coil dimers and the gamma1 deltaN95AE fragments into a mixture of different oligomers, whereas the coiled-coil domain of native laminin-1 is a heterotrimer composed of alpha1, beta1 and gamma1 chains.	bind
41811	1	9890	7	11	NULL	NULL	NULL	GCN4 gamma1 chimera 	GP		folds into					 homotypic coiled-coil dimers	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6762_s_205	10581249	A decrease in binding affinity of the recombinant gamma1 chains and the chimeric GCN4 fusion proteins compared with native laminin-1 may be explained in terms of different coiled-coil structures in these molecules: the GCN4 gamma1 chimera folds into homotypic coiled-coil dimers and the gamma1 deltaN95AE fragments into a mixture of different oligomers, whereas the coiled-coil domain of native laminin-1 is a heterotrimer composed of alpha1, beta1 and gamma1 chains.	bind
41812	2	9890	7	11	NULL	NULL	NULL				folds into			gamma1 deltaN95AE fragments		oligomers	Chemical	mixture of different			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6762_s_205	10581249	A decrease in binding affinity of the recombinant gamma1 chains and the chimeric GCN4 fusion proteins compared with native laminin-1 may be explained in terms of different coiled-coil structures in these molecules: the GCN4 gamma1 chimera folds into homotypic coiled-coil dimers and the gamma1 deltaN95AE fragments into a mixture of different oligomers, whereas the coiled-coil domain of native laminin-1 is a heterotrimer composed of alpha1, beta1 and gamma1 chains.	bind
41813	3	9890	7	11	NULL	NULL	NULL	laminin-1	GP	native	is composed of			coiled-coil domain					alpha1;;beta1;;gamma1		NULL		NULL	NULL	NULL	NULL	gw60_embo_18_23_6762_s_205	10581249	A decrease in binding affinity of the recombinant gamma1 chains and the chimeric GCN4 fusion proteins compared with native laminin-1 may be explained in terms of different coiled-coil structures in these molecules: the GCN4 gamma1 chimera folds into homotypic coiled-coil dimers and the gamma1 deltaN95AE fragments into a mixture of different oligomers, whereas the coiled-coil domain of native laminin-1 is a heterotrimer composed of alpha1, beta1 and gamma1 chains.	bind
34621	1	9891	6	11	NULL	NULL	NULL	cyclin D2 levels	GP	decrease in	results in		might			RB	GP	decreased phosphorylation of 			NULL	WEHI-231 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
34622	2	9891	6	11	NULL	NULL	NULL	cyclin D2 levels	GP	decrease in	results in		might			p107	GP	decreased phosphorylation of			NULL	WEHI-231 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
34623	3	9891	6	11	NULL	NULL	NULL	cyclin D2 levels	GP	decrease in	results in		might			p130	GP	decreased phosphorylation of			NULL	WEHI-231 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
34624	4	9891	6	11	NULL	NULL	NULL	RB	GP		is a type of					pocket protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
34625	5	9891	6	11	NULL	NULL	NULL	p107	GP		is a type of					pocket protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
34626	6	9891	6	11	NULL	NULL	NULL	p130	GP		is a type of					pocket protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
34627	7	9891	6	11	NULL	NULL	NULL	RB	GP		bind					E2F	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
34628	8	9891	6	11	NULL	NULL	NULL	p107	GP		bind					E2F	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
34629	9	9891	6	11	NULL	NULL	NULL	p130	GP		bind					E2F	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
34973	10	9891	6	11	NULL	NULL	NULL	statement 1	Process		results in					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
34974	11	9891	6	11	NULL	NULL	NULL	statement 2	Process		results in					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
34975	12	9891	6	11	NULL	NULL	NULL	statement 3	Process		results in					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
34976	13	9891	6	11	NULL	NULL	NULL	WEHI-231 cells	Cell		are blocked at					G1-phase restriction point	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
34977	14	9891	6	11	NULL	NULL	NULL	statement 10	Process		leads to					statement 13	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
34978	15	9891	6	11	NULL	NULL	NULL	statement 11	Process		leads to					statement 13	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
34979	16	9891	6	11	NULL	NULL	NULL	statement 12	Process		leads to					statement 13	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
56922	17	9891	6	11	NULL	NULL	NULL	E2F	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
56923	18	9891	6	11	NULL	NULL	NULL	statement 14	Process		inhibits					WEHI-231 cells	Cell	S-phase entry of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
56924	19	9891	6	11	NULL	NULL	NULL	statement 15	Process		inhibits					WEHI-231 cells	Cell	S-phase entry of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
56925	20	9891	6	11	NULL	NULL	NULL	statement 16	Process		inhibits					WEHI-231 cells	Cell	S-phase entry of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
41818	1	9891	7	11	NULL	NULL	NULL	cyclin D2 levels	GP	decrease in	decrease		may			RB	GP	phosphorylation of			NULL	WEHI-231 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
41819	2	9891	7	11	NULL	NULL	NULL	cyclin D2 levels	GP	decrease in	decrease		may			p107	GP	phosphorylation of			NULL	WEHI-231 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
41820	3	9891	7	11	NULL	NULL	NULL	cyclin D2 levels	GP	decrease in	decrease		may			p130	GP	phosphorylation of			NULL	WEHI-231 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
41821	7	9891	7	11	NULL	NULL	NULL	RB	GP		bind					E2F	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
41822	10	9891	7	11	NULL	NULL	NULL	WEHI-231 cells	Cell		are blocked at					G1-phase restriction point	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
41823	11	9891	7	11	NULL	NULL	NULL	statement 16	Process		leads to					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
41824	13	9891	7	11	NULL	NULL	NULL	statement 20	Process		inhibits					WEHI-231 cells	Cell	S-phase entry of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
50232	4	9891	7	11	NULL	NULL	NULL	RB	GP		is a type of					pocket protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
50233	5	9891	7	11	NULL	NULL	NULL	p107	GP		is a type of					pocket protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
50234	6	9891	7	11	NULL	NULL	NULL	p130	GP		is a type of					pocket protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
50235	8	9891	7	11	NULL	NULL	NULL	p107	GP		bind					E2F	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
50236	9	9891	7	11	NULL	NULL	NULL	p130	GP		bind					E2F	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
50239	12	9891	7	11	NULL	NULL	NULL	statement 17	Process		leads to					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
50240	14	9891	7	11	NULL	NULL	NULL	statement 11	Process		inhibits					WEHI-231 cells	Cell	S-phase entry of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
50241	15	9891	7	11	NULL	NULL	NULL	statement 12	Process		inhibits					WEHI-231 cells	Cell	S-phase entry of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
50243	16	9891	7	11	NULL	NULL	NULL	statement 1	Process		result in					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
50244	17	9891	7	11	NULL	NULL	NULL	statement 2	Process		result in					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
50245	18	9891	7	11	NULL	NULL	NULL	statement 3	Process		result in					statement 9	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
50247	19	9891	7	11	NULL	NULL	NULL	E2F	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
56921	20	9891	7	11	NULL	NULL	NULL	statement 18	Process		leads to					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_19_12650_s_253	9139721	A decrease in cyclin D2 levels in WEHI-231 cells might result in decreased phosphorylation of RB, p107, and p130, a consequent continued binding of these pocket proteins to E2F transcription factors blockading cells at the G1-phase restriction point and inhibiting their entry into S-phase ( 93,  95).	bind
34518	1	9892	6	11	NULL	NULL	NULL	Sp100	GP		bind					NB	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2687_s_421	11909962	A decrease in ETS-1 levels would shift the equilibrium toward Sp100 bound to NBs (Fig.  8).	bind
41825	1	9892	7	11	NULL	NULL	NULL	Sp100	GP		bind					NBs	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_8_2687_s_421	11909962	A decrease in ETS-1 levels would shift the equilibrium toward Sp100 bound to NBs (Fig.  8).	bind
34519	1	9893	6	11	NULL	NULL	NULL	PCBP1	GP		bind					66 nt fragment	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_2_639_s_160	12527772	A decrease in mobility of the radiolabelled 292 - 358 fragment was also observed and this would imply that PCBP1 binds to a 66 nt fragment.	bind
41827	1	9893	7	11	NULL	NULL	NULL	PCBP1	GP		binds to					66 nt fragment	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_2_639_s_160	12527772	A decrease in mobility of the radiolabelled 292 - 358 fragment was also observed and this would imply that PCBP1 binds to a 66 nt fragment.	bind
34520	1	9894	6	11	NULL	NULL	NULL	alpha-actinin	GP	phosphorylated	bind					actin filament	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_31_28676_s_342	11369769	A decrease in the binding affinity of phosphorylated alpha-actinin for actin filaments may at least partially explain the disparity between the two alpha-actinin populations.	bind
41828	1	9894	7	11	NULL	NULL	NULL	alpha-actinin	GP	phosphorylated	bind					actin filaments	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_31_28676_s_342	11369769	A decrease in the binding affinity of phosphorylated alpha-actinin for actin filaments may at least partially explain the disparity between the two alpha-actinin populations.	bind
41829	2	9894	7	11	NULL	NULL	NULL	alpha-actinin	GP	disparity between	decrease		may			statement 1	Process	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_31_28676_s_342	11369769	A decrease in the binding affinity of phosphorylated alpha-actinin for actin filaments may at least partially explain the disparity between the two alpha-actinin populations.	bind
34530	1	9895	6	11	NULL	NULL	NULL	villin	GP	phosphorylated	bind					actin filaments	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36163_s_102	11500485	A decrease in the binding affinity of phosphorylated villin for actin filaments may partially explain the redistribution of tyrosine phosphorylated villin  in vivo.	bind
56926	2	9895	6	11	NULL	NULL	NULL	villin	GP	redistribution of;;phosphorylated 	decrease		may	tyrosine		statement 1	Process	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36163_s_102	11500485	A decrease in the binding affinity of phosphorylated villin for actin filaments may partially explain the redistribution of tyrosine phosphorylated villin  in vivo.	bind
41830	1	9895	7	11	NULL	NULL	NULL	villin	GP	phosphorylated	bind					actin filaments	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36163_s_102	11500485	A decrease in the binding affinity of phosphorylated villin for actin filaments may partially explain the redistribution of tyrosine phosphorylated villin  in vivo.	bind
41831	2	9895	7	11	NULL	NULL	NULL	 villin	GP	redistribution of;;phosphorylated 	decrease		may	tyrosine		statement 1	Process	binding affinity of			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_39_36163_s_102	11500485	A decrease in the binding affinity of phosphorylated villin for actin filaments may partially explain the redistribution of tyrosine phosphorylated villin  in vivo.	bind
34533	1	9896	6	11	NULL	NULL	NULL	p52	GP		bind					skp2 gene	GP	proximal		promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_16_3801_s_219	16902410	A decrease in the binding of p52 to the proximal   skp2 gene promoter was observed ( Figure 7F).	bind
41832	1	9896	7	11	NULL	NULL	NULL	 p52	GP		bind					skp2 gene	GP	proximal		promoter	NULL		NULL	NULL	NULL	NULL	gw70_embo_25_16_3801_s_219	16902410	A decrease in the binding of p52 to the proximal   skp2 gene promoter was observed ( Figure 7F).	bind
42295	1	9897	6	11	NULL	NULL	NULL	tc	Chemical		bind					TetR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_6936_s_183	9054381	A decrease in the equilibrium binding constant of tc to TetR can be caused by a decrease in the association rate constant, an increase in the dissociation rate constant, or both.	bind
41833	1	9897	7	11	NULL	NULL	NULL	tc	Chemical		bind					TetR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_6936_s_183	9054381	A decrease in the equilibrium binding constant of tc to TetR can be caused by a decrease in the association rate constant, an increase in the dissociation rate constant, or both.	bind
34535	1	9898	6	11	NULL	NULL	NULL	CSS	AminoAcid		bind					SCS	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_27_25901_s_212	15888455	A decrease in the GSH/GSSG ratio induced the inhibition of CSS and SCS binding, whereas SSC and SSS binding was not affected ( Fig. 3).	bind
34537	2	9898	6	11	NULL	NULL	NULL	GSH/GSSG ratio	QuantityOrMeasure	decrease in	induces					statement 1	Process	inhibiton of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_27_25901_s_212	15888455	A decrease in the GSH/GSSG ratio induced the inhibition of CSS and SCS binding, whereas SSC and SSS binding was not affected ( Fig. 3).	bind
34538	3	9898	6	11	NULL	NULL	NULL	SSC	AminoAcid		bind					SSS	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_27_25901_s_212	15888455	A decrease in the GSH/GSSG ratio induced the inhibition of CSS and SCS binding, whereas SSC and SSS binding was not affected ( Fig. 3).	bind
34540	4	9898	6	11	NULL	NULL	NULL	GSH/GSSG ratio	QuantityOrMeasure	decrease in	does not affect					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_27_25901_s_212	15888455	A decrease in the GSH/GSSG ratio induced the inhibition of CSS and SCS binding, whereas SSC and SSS binding was not affected ( Fig. 3).	bind
41839	1	9898	7	11	NULL	NULL	NULL	CSS	AminoAcid		bind					SCS	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_27_25901_s_212	15888455	A decrease in the GSH/GSSG ratio induced the inhibition of CSS and SCS binding, whereas SSC and SSS binding was not affected ( Fig. 3).	bind
41840	2	9898	7	11	NULL	NULL	NULL	SSC	AminoAcid		bind					SSS	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_27_25901_s_212	15888455	A decrease in the GSH/GSSG ratio induced the inhibition of CSS and SCS binding, whereas SSC and SSS binding was not affected ( Fig. 3).	bind
41841	3	9898	7	11	NULL	NULL	NULL	GSH/GSSG ratio	QuantityOrMeasure	decrease in	induce					statement 1	Process	inhibition of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_27_25901_s_212	15888455	A decrease in the GSH/GSSG ratio induced the inhibition of CSS and SCS binding, whereas SSC and SSS binding was not affected ( Fig. 3).	bind
41842	4	9898	7	11	NULL	NULL	NULL	GSH/GSSG ratio	QuantityOrMeasure	decrease in	does not affect					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_27_25901_s_212	15888455	A decrease in the GSH/GSSG ratio induced the inhibition of CSS and SCS binding, whereas SSC and SSS binding was not affected ( Fig. 3).	bind
34541	1	9899	6	11	NULL	NULL	NULL	actin	GP		bind					myosin IIA	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_1_121_s_184	16606694	A decrease of actin and myosin IIA binding was seen after treatment with 100 muM of the general protein tyrosine kinase inhibitor genistein (unpublished data), but the observed effects were most likely nonspecific because of the inhibition of all tyrosine kinases and an impairment of NK cell functions.	bind
34542	2	9899	6	11	NULL	NULL	NULL	genistein	Chemical		decreases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_1_121_s_184	16606694	A decrease of actin and myosin IIA binding was seen after treatment with 100 muM of the general protein tyrosine kinase inhibitor genistein (unpublished data), but the observed effects were most likely nonspecific because of the inhibition of all tyrosine kinases and an impairment of NK cell functions.	bind
49004	3	9899	6	11	NULL	NULL	NULL	genistein	Chemical		is a type of					protein tyrosine kinase inhibitor	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_1_121_s_184	16606694	A decrease of actin and myosin IIA binding was seen after treatment with 100 muM of the general protein tyrosine kinase inhibitor genistein (unpublished data), but the observed effects were most likely nonspecific because of the inhibition of all tyrosine kinases and an impairment of NK cell functions.	bind
41843	1	9899	7	11	NULL	NULL	NULL	actin	GP		bind					myosin IIA	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_1_121_s_184	16606694	A decrease of actin and myosin IIA binding was seen after treatment with 100 muM of the general protein tyrosine kinase inhibitor genistein (unpublished data), but the observed effects were most likely nonspecific because of the inhibition of all tyrosine kinases and an impairment of NK cell functions.	bind
41844	2	9899	7	11	NULL	NULL	NULL	genistein	Chemical		decrease					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_1_121_s_184	16606694	A decrease of actin and myosin IIA binding was seen after treatment with 100 muM of the general protein tyrosine kinase inhibitor genistein (unpublished data), but the observed effects were most likely nonspecific because of the inhibition of all tyrosine kinases and an impairment of NK cell functions.	bind
41845	3	9899	7	11	NULL	NULL	NULL	genistein	Chemical		is a type of					protein tyrosine kinase inhibitor	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_1_121_s_184	16606694	A decrease of actin and myosin IIA binding was seen after treatment with 100 muM of the general protein tyrosine kinase inhibitor genistein (unpublished data), but the observed effects were most likely nonspecific because of the inhibition of all tyrosine kinases and an impairment of NK cell functions.	bind
34543	1	9900	6	11	NULL	NULL	NULL	GAPDH	GP		bind					F-actin	GP	skeletal muscle			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_5_821_s_212	8620602	A decrease of ATP concentration has been reported to favor the binding of GAPDH to skeletal muscle F-actin 38  or to tubulin, 39  whereas Mg2+ seems to enhance GAPDH binding to the thin filament from beef muscle.	bind
34544	2	9900	6	11	NULL	NULL	NULL	GAPDH	GP		bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_5_821_s_212	8620602	A decrease of ATP concentration has been reported to favor the binding of GAPDH to skeletal muscle F-actin 38  or to tubulin, 39  whereas Mg2+ seems to enhance GAPDH binding to the thin filament from beef muscle.	bind
34545	3	9900	6	11	NULL	NULL	NULL	ATP concentration	Chemical	decrease of	favors					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_5_821_s_212	8620602	A decrease of ATP concentration has been reported to favor the binding of GAPDH to skeletal muscle F-actin 38  or to tubulin, 39  whereas Mg2+ seems to enhance GAPDH binding to the thin filament from beef muscle.	bind
34546	4	9900	6	11	NULL	NULL	NULL	ATP concentration	Chemical	decrease of	favors					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_5_821_s_212	8620602	A decrease of ATP concentration has been reported to favor the binding of GAPDH to skeletal muscle F-actin 38  or to tubulin, 39  whereas Mg2+ seems to enhance GAPDH binding to the thin filament from beef muscle.	bind
34547	5	9900	6	11	NULL	NULL	NULL	GAPDH	GP		bind					thin filament	GP	beef			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_5_821_s_212	8620602	A decrease of ATP concentration has been reported to favor the binding of GAPDH to skeletal muscle F-actin 38  or to tubulin, 39  whereas Mg2+ seems to enhance GAPDH binding to the thin filament from beef muscle.	bind
34548	6	9900	6	11	NULL	NULL	NULL	Mg2+	Chemical		enhances					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_5_821_s_212	8620602	A decrease of ATP concentration has been reported to favor the binding of GAPDH to skeletal muscle F-actin 38  or to tubulin, 39  whereas Mg2+ seems to enhance GAPDH binding to the thin filament from beef muscle.	bind
41848	1	9900	7	11	NULL	NULL	NULL	GAPDH	GP		bind					F-actin	GP	skeletal muscle			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_5_821_s_212	8620602	A decrease of ATP concentration has been reported to favor the binding of GAPDH to skeletal muscle F-actin 38  or to tubulin, 39  whereas Mg2+ seems to enhance GAPDH binding to the thin filament from beef muscle.	bind
41849	2	9900	7	11	NULL	NULL	NULL	GAPDH	GP		bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_5_821_s_212	8620602	A decrease of ATP concentration has been reported to favor the binding of GAPDH to skeletal muscle F-actin 38  or to tubulin, 39  whereas Mg2+ seems to enhance GAPDH binding to the thin filament from beef muscle.	bind
41850	3	9900	7	11	NULL	NULL	NULL	ATP	Chemical	decrease in	favors					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_5_821_s_212	8620602	A decrease of ATP concentration has been reported to favor the binding of GAPDH to skeletal muscle F-actin 38  or to tubulin, 39  whereas Mg2+ seems to enhance GAPDH binding to the thin filament from beef muscle.	bind
41851	4	9900	7	11	NULL	NULL	NULL	ATP	Chemical	decrease in	favors					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_5_821_s_212	8620602	A decrease of ATP concentration has been reported to favor the binding of GAPDH to skeletal muscle F-actin 38  or to tubulin, 39  whereas Mg2+ seems to enhance GAPDH binding to the thin filament from beef muscle.	bind
41852	5	9900	7	11	NULL	NULL	NULL	GAPDH	GP		bind					thin filament	GP	beef muscle			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_5_821_s_212	8620602	A decrease of ATP concentration has been reported to favor the binding of GAPDH to skeletal muscle F-actin 38  or to tubulin, 39  whereas Mg2+ seems to enhance GAPDH binding to the thin filament from beef muscle.	bind
41853	6	9900	7	11	NULL	NULL	NULL	Mg2+	Chemical		enhance					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_78_5_821_s_212	8620602	A decrease of ATP concentration has been reported to favor the binding of GAPDH to skeletal muscle F-actin 38  or to tubulin, 39  whereas Mg2+ seems to enhance GAPDH binding to the thin filament from beef muscle.	bind
34549	1	9901	6	11	NULL	NULL	NULL	SRF + SAP-1 complex	GP		bind					c-fos	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_98_1_78_s_50	8690807	A decreased binding of the SRF + SAP-1 complex to the  c-fos promotor, would probably lead to  a decreased transcription of the  c-fos gene, followed by a subsequent decrease of the DNA-binding of AP-1 to the  c-fos  promotor.	bind
34550	2	9901	6	11	NULL	NULL	NULL	statement 1	Process	decrease in	decreases					c-fos gene	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_98_1_78_s_50	8690807	A decreased binding of the SRF + SAP-1 complex to the  c-fos promotor, would probably lead to  a decreased transcription of the  c-fos gene, followed by a subsequent decrease of the DNA-binding of AP-1 to the  c-fos  promotor.	bind
34551	3	9901	6	11	NULL	NULL	NULL	AP-1	GP		bind					c-fos	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_98_1_78_s_50	8690807	A decreased binding of the SRF + SAP-1 complex to the  c-fos promotor, would probably lead to  a decreased transcription of the  c-fos gene, followed by a subsequent decrease of the DNA-binding of AP-1 to the  c-fos  promotor.	bind
34552	4	9901	6	11	NULL	NULL	NULL	statement 2	Process		leads to					statement 3	Process	decrease in			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_98_1_78_s_50	8690807	A decreased binding of the SRF + SAP-1 complex to the  c-fos promotor, would probably lead to  a decreased transcription of the  c-fos gene, followed by a subsequent decrease of the DNA-binding of AP-1 to the  c-fos  promotor.	bind
41854	1	9901	7	11	NULL	NULL	NULL	SRF + SAP-1 complex	GP		bind					c-fos	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_98_1_78_s_50	8690807	A decreased binding of the SRF + SAP-1 complex to the  c-fos promotor, would probably lead to  a decreased transcription of the  c-fos gene, followed by a subsequent decrease of the DNA-binding of AP-1 to the  c-fos  promotor.	bind
41855	2	9901	7	11	NULL	NULL	NULL	statement 1	Process		lead to					c-fos gene	GP	 transcription of 			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_98_1_78_s_50	8690807	A decreased binding of the SRF + SAP-1 complex to the  c-fos promotor, would probably lead to  a decreased transcription of the  c-fos gene, followed by a subsequent decrease of the DNA-binding of AP-1 to the  c-fos  promotor.	bind
41857	3	9901	7	11	NULL	NULL	NULL	AP-1	GP		bind					c-fos	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_98_1_78_s_50	8690807	A decreased binding of the SRF + SAP-1 complex to the  c-fos promotor, would probably lead to  a decreased transcription of the  c-fos gene, followed by a subsequent decrease of the DNA-binding of AP-1 to the  c-fos  promotor.	bind
41861	4	9901	7	11	NULL	NULL	NULL	statement 1	Process	decrease of	lead to					statement 2	Process	decrease of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_98_1_78_s_50	8690807	A decreased binding of the SRF + SAP-1 complex to the  c-fos promotor, would probably lead to  a decreased transcription of the  c-fos gene, followed by a subsequent decrease of the DNA-binding of AP-1 to the  c-fos  promotor.	bind
41862	5	9901	7	11	NULL	NULL	NULL	statement 2	Process	decrease of	lead to					statement 3	Process	decrease of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_98_1_78_s_50	8690807	A decreased binding of the SRF + SAP-1 complex to the  c-fos promotor, would probably lead to  a decreased transcription of the  c-fos gene, followed by a subsequent decrease of the DNA-binding of AP-1 to the  c-fos  promotor.	bind
34980	1	9902	6	11	NULL	NULL	NULL			positively charged	bind		likely	pocket S2					aspartic acid located N terminal to the cleavage site		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_1_302_s_10	14694194	A deep and positively charged pocket (S2) and a neighboring shallow surface (S3) likely bind to aspartic acid and glycine residues in the substrate located two (P2) and three (P3) residues N terminal to the cleavage site, respectively.	bind
34981	2	9902	6	11	NULL	NULL	NULL			positively charged	bind		likely	pocket S2					glycine residues N terminal to the cleavage site		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_1_302_s_10	14694194	A deep and positively charged pocket (S2) and a neighboring shallow surface (S3) likely bind to aspartic acid and glycine residues in the substrate located two (P2) and three (P3) residues N terminal to the cleavage site, respectively.	bind
34982	3	9902	6	11	NULL	NULL	NULL				bind		likely	shallow surface S3					aspartic acid located N terminal to the cleavage site		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_1_302_s_10	14694194	A deep and positively charged pocket (S2) and a neighboring shallow surface (S3) likely bind to aspartic acid and glycine residues in the substrate located two (P2) and three (P3) residues N terminal to the cleavage site, respectively.	bind
34983	4	9902	6	11	NULL	NULL	NULL				bind		likely	shallow surface S3					glycine residues N terminal to the cleavage site		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_1_302_s_10	14694194	A deep and positively charged pocket (S2) and a neighboring shallow surface (S3) likely bind to aspartic acid and glycine residues in the substrate located two (P2) and three (P3) residues N terminal to the cleavage site, respectively.	bind
41863	1	9902	7	11	NULL	NULL	NULL			positively charged	bind			S2 pocket					aspartic acid located N terminal to the cleavage site		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_1_302_s_10	14694194	A deep and positively charged pocket (S2) and a neighboring shallow surface (S3) likely bind to aspartic acid and glycine residues in the substrate located two (P2) and three (P3) residues N terminal to the cleavage site, respectively.	bind
41864	2	9902	7	11	NULL	NULL	NULL			positively charged	bind			S2 pocket					glycine located N terminal to the cleavage site		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_1_302_s_10	14694194	A deep and positively charged pocket (S2) and a neighboring shallow surface (S3) likely bind to aspartic acid and glycine residues in the substrate located two (P2) and three (P3) residues N terminal to the cleavage site, respectively.	bind
41865	3	9902	7	11	NULL	NULL	NULL				bind			shallow surface S3					aspartic acid located N terminal to the cleavage site		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_1_302_s_10	14694194	A deep and positively charged pocket (S2) and a neighboring shallow surface (S3) likely bind to aspartic acid and glycine residues in the substrate located two (P2) and three (P3) residues N terminal to the cleavage site, respectively.	bind
41866	4	9902	7	11	NULL	NULL	NULL				bind			shallow surface S3					glycine located N terminal to the cleavage site		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_1_302_s_10	14694194	A deep and positively charged pocket (S2) and a neighboring shallow surface (S3) likely bind to aspartic acid and glycine residues in the substrate located two (P2) and three (P3) residues N terminal to the cleavage site, respectively.	bind
34553	1	9904	6	11	NULL	NULL	NULL	CPF	GP		bind							unphosphorylated	CTD		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_8_1030_s_334	12704082	A defect in binding of CPF to unphosphorylated CTD may trigger a very specific removal of Pta1.	bind
34554	2	9904	6	11	NULL	NULL	NULL	statement 1	Process	defect in	trigger		may			Pta1	GP	removal of			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_8_1030_s_334	12704082	A defect in binding of CPF to unphosphorylated CTD may trigger a very specific removal of Pta1.	bind
41873	1	9904	7	11	NULL	NULL	NULL	CPF	GP		bind							unphosphorylated 	CTD		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_8_1030_s_334	12704082	A defect in binding of CPF to unphosphorylated CTD may trigger a very specific removal of Pta1.	bind
41874	2	9904	7	11	NULL	NULL	NULL	statement 1	Process	defect in	trigger					Pta1	GP	removal of			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_8_1030_s_334	12704082	A defect in binding of CPF to unphosphorylated CTD may trigger a very specific removal of Pta1.	bind
34618	1	9905	6	11	NULL	NULL	NULL	mucin	GP	deficiency in production of	compromise		may			intestinal barrier	OrganismPart	function of			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_3_353_s_29	12663492	A deficiency in mucin production, or altered mucin structure and lectin binding, could also compromise intestinal barrier function ( , ).	bind
34619	2	9905	6	11	NULL	NULL	NULL	mucin	GP	altered;;structure of	compromise		may			intestinal barrier	OrganismPart	function of			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_3_353_s_29	12663492	A deficiency in mucin production, or altered mucin structure and lectin binding, could also compromise intestinal barrier function ( , ).	bind
34620	3	9905	6	11	NULL	NULL	NULL	lectin	GP	binding of	compromise		may			intestinal barrier	OrganismPart	function of			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_3_353_s_29	12663492	A deficiency in mucin production, or altered mucin structure and lectin binding, could also compromise intestinal barrier function ( , ).	bind
41905	1	9905	7	11	NULL	NULL	NULL	mucin	GP	deficiency in production of	compromise		may			intestinal barrier	OrganismPart	function of			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_3_353_s_29	12663492	A deficiency in mucin production, or altered mucin structure and lectin binding, could also compromise intestinal barrier function ( , ).	bind
41906	2	9905	7	11	NULL	NULL	NULL	mucin	GP	altered;;structure of	compromise		may			intestinal barrier	OrganismPart	function of			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_3_353_s_29	12663492	A deficiency in mucin production, or altered mucin structure and lectin binding, could also compromise intestinal barrier function ( , ).	bind
41907	3	9905	7	11	NULL	NULL	NULL	lectin	GP	binding of	compromise		may			intestinal barrier	OrganismPart	function of			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_3_353_s_29	12663492	A deficiency in mucin production, or altered mucin structure and lectin binding, could also compromise intestinal barrier function ( , ).	bind
34555	1	9906	6	11	NULL	NULL	NULL	GAG chain	NucleicAcid		bind			pentasaccharide sequence		antithrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_25_15487_s_13	9624135	A defined pentasaccharide sequence in the GAG chain binds antithrombin and thus strongly promotes its function as an inhibitor of the serine proteases acting within the coagulation cascade ( 2).	bind
34556	2	9906	6	11	NULL	NULL	NULL	antithrombin	GP		functions as					serine proteases	GP	inhibitor of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_25_15487_s_13	9624135	A defined pentasaccharide sequence in the GAG chain binds antithrombin and thus strongly promotes its function as an inhibitor of the serine proteases acting within the coagulation cascade ( 2).	bind
34557	3	9906	6	11	NULL	NULL	NULL	statement 2	Process		occurs within					coagulation cascade	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_25_15487_s_13	9624135	A defined pentasaccharide sequence in the GAG chain binds antithrombin and thus strongly promotes its function as an inhibitor of the serine proteases acting within the coagulation cascade ( 2).	bind
34558	4	9906	6	11	NULL	NULL	NULL	statement 1	Process		promotes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_25_15487_s_13	9624135	A defined pentasaccharide sequence in the GAG chain binds antithrombin and thus strongly promotes its function as an inhibitor of the serine proteases acting within the coagulation cascade ( 2).	bind
41875	1	9906	7	11	NULL	NULL	NULL	GAG chain	NucleicAcid		binds			pentasaccharide sequence 		antithrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_25_15487_s_13	9624135	A defined pentasaccharide sequence in the GAG chain binds antithrombin and thus strongly promotes its function as an inhibitor of the serine proteases acting within the coagulation cascade ( 2).	bind
41876	2	9906	7	11	NULL	NULL	NULL	statement 1	Process		promotes					antithrombin	GP	function of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_25_15487_s_13	9624135	A defined pentasaccharide sequence in the GAG chain binds antithrombin and thus strongly promotes its function as an inhibitor of the serine proteases acting within the coagulation cascade ( 2).	bind
41877	3	9906	7	11	NULL	NULL	NULL	antithrombin	GP		functions as					serine proteases	GP	inhibitor of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_25_15487_s_13	9624135	A defined pentasaccharide sequence in the GAG chain binds antithrombin and thus strongly promotes its function as an inhibitor of the serine proteases acting within the coagulation cascade ( 2).	bind
41878	4	9906	7	11	NULL	NULL	NULL	statement 3	Process		occurs within					coagulation cascade	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_25_15487_s_13	9624135	A defined pentasaccharide sequence in the GAG chain binds antithrombin and thus strongly promotes its function as an inhibitor of the serine proteases acting within the coagulation cascade ( 2).	bind
34559	1	9907	6	11	NULL	NULL	NULL	Ran GTPase	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3011_s_112	14681208	A defining characteristic of karyopherins that function in nuclear export is that cargo binding requires the GTP-bound form of the Ran GTPase (Lei and Silver 2002 ).	bind
34560	2	9907	6	11	NULL	NULL	NULL	karyopherins	GP		function in					nuclear export	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3011_s_112	14681208	A defining characteristic of karyopherins that function in nuclear export is that cargo binding requires the GTP-bound form of the Ran GTPase (Lei and Silver 2002 ).	bind
34561	3	9907	6	11	NULL	NULL	NULL	cargo	GP	binding of	requires					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3011_s_112	14681208	A defining characteristic of karyopherins that function in nuclear export is that cargo binding requires the GTP-bound form of the Ran GTPase (Lei and Silver 2002 ).	bind
41879	1	9907	7	11	NULL	NULL	NULL	karyopherins	GP		function in					nuclear export	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3011_s_112	14681208	A defining characteristic of karyopherins that function in nuclear export is that cargo binding requires the GTP-bound form of the Ran GTPase (Lei and Silver 2002 ).	bind
41880	3	9907	7	11	NULL	NULL	NULL	cargo	GP	binding of	requires					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3011_s_112	14681208	A defining characteristic of karyopherins that function in nuclear export is that cargo binding requires the GTP-bound form of the Ran GTPase (Lei and Silver 2002 ).	bind
41881	2	9907	7	11	NULL	NULL	NULL	GTP	Chemical		bind					Ran GTPase	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3011_s_112	14681208	A defining characteristic of karyopherins that function in nuclear export is that cargo binding requires the GTP-bound form of the Ran GTPase (Lei and Silver 2002 ).	bind
34562	1	9908	6	11	NULL	NULL	NULL	karyopherins	GP		function in					nuclear export	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3011_s_29	14681208	A defining characteristic of karyopherins that function in nuclear export is that nuclear cargo binding requires the GTP-bound form of the Ran GTPase, whereas cytoplasmic hydrolysis of Ran-GTP to Ran-GDP induces cargo release.	bind
34563	2	9908	6	11	NULL	NULL	NULL	GTP	Chemical		bind					Ran GTPase	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3011_s_29	14681208	A defining characteristic of karyopherins that function in nuclear export is that nuclear cargo binding requires the GTP-bound form of the Ran GTPase, whereas cytoplasmic hydrolysis of Ran-GTP to Ran-GDP induces cargo release.	bind
34564	3	9908	6	11	NULL	NULL	NULL	cargo	GP	binding of;;nuclear	requires					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3011_s_29	14681208	A defining characteristic of karyopherins that function in nuclear export is that nuclear cargo binding requires the GTP-bound form of the Ran GTPase, whereas cytoplasmic hydrolysis of Ran-GTP to Ran-GDP induces cargo release.	bind
34565	4	9908	6	11	NULL	NULL	NULL	Ran-GTP	Chemical		is hydrolysed to					Ran-GDP	Chemical				NULL	cytoplasm	NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3011_s_29	14681208	A defining characteristic of karyopherins that function in nuclear export is that nuclear cargo binding requires the GTP-bound form of the Ran GTPase, whereas cytoplasmic hydrolysis of Ran-GTP to Ran-GDP induces cargo release.	bind
34566	5	9908	6	11	NULL	NULL	NULL	statement 4	Process		induces					cargo release	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3011_s_29	14681208	A defining characteristic of karyopherins that function in nuclear export is that nuclear cargo binding requires the GTP-bound form of the Ran GTPase, whereas cytoplasmic hydrolysis of Ran-GTP to Ran-GDP induces cargo release.	bind
41882	1	9908	7	11	NULL	NULL	NULL	karyopherins 	GP		function in					nuclear export	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3011_s_29	14681208	A defining characteristic of karyopherins that function in nuclear export is that nuclear cargo binding requires the GTP-bound form of the Ran GTPase, whereas cytoplasmic hydrolysis of Ran-GTP to Ran-GDP induces cargo release.	bind
41883	2	9908	7	11	NULL	NULL	NULL	GTP	Chemical		bind					Ran GTPase	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3011_s_29	14681208	A defining characteristic of karyopherins that function in nuclear export is that nuclear cargo binding requires the GTP-bound form of the Ran GTPase, whereas cytoplasmic hydrolysis of Ran-GTP to Ran-GDP induces cargo release.	bind
41884	3	9908	7	11	NULL	NULL	NULL	cargo	GP	binding of;;nuclear	requires					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3011_s_29	14681208	A defining characteristic of karyopherins that function in nuclear export is that nuclear cargo binding requires the GTP-bound form of the Ran GTPase, whereas cytoplasmic hydrolysis of Ran-GTP to Ran-GDP induces cargo release.	bind
41885	4	9908	7	11	NULL	NULL	NULL	Ran-GTP	Chemical		hydrolyse to					Ran-GDP	Chemical				NULL	cytoplasm	NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3011_s_29	14681208	A defining characteristic of karyopherins that function in nuclear export is that nuclear cargo binding requires the GTP-bound form of the Ran GTPase, whereas cytoplasmic hydrolysis of Ran-GTP to Ran-GDP induces cargo release.	bind
41886	5	9908	7	11	NULL	NULL	NULL	statement 4	Process		induce					cargo release	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_24_3011_s_29	14681208	A defining characteristic of karyopherins that function in nuclear export is that nuclear cargo binding requires the GTP-bound form of the Ran GTPase, whereas cytoplasmic hydrolysis of Ran-GTP to Ran-GDP induces cargo release.	bind
34567	1	9909	6	11	NULL	NULL	NULL	mAspAT	GP	refolding	bind					groEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_3_1138_s_402	7836372	A definitive answer to the question of why refolding mAspAT binds  more tightly to groEL than its homologous isozymic counterpart awaits  an analysis of the structure of the complex between groEL and its  passenger protein.	bind
34569	3	9909	6	11	NULL	NULL	NULL	statement 1	Process	affinity of	is higher than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_3_1138_s_402	7836372	A definitive answer to the question of why refolding mAspAT binds  more tightly to groEL than its homologous isozymic counterpart awaits  an analysis of the structure of the complex between groEL and its  passenger protein.	bind
49534	2	9909	6	11	NULL	NULL	NULL	mAspAT	GP		bind					GroEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_3_1138_s_402	7836372	A definitive answer to the question of why refolding mAspAT binds  more tightly to groEL than its homologous isozymic counterpart awaits  an analysis of the structure of the complex between groEL and its  passenger protein.	bind
41887	1	9909	7	11	NULL	NULL	NULL	mAspAT	GP	refolding	bind		tightly			groEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_3_1138_s_402	7836372	A definitive answer to the question of why refolding mAspAT binds  more tightly to groEL than its homologous isozymic counterpart awaits  an analysis of the structure of the complex between groEL and its  passenger protein.	bind
49550	2	9909	7	11	NULL	NULL	NULL	 mAspAT	GP		bind					groEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_3_1138_s_402	7836372	A definitive answer to the question of why refolding mAspAT binds  more tightly to groEL than its homologous isozymic counterpart awaits  an analysis of the structure of the complex between groEL and its  passenger protein.	bind
49551	3	9909	7	11	NULL	NULL	NULL	statement 1	Process	affinity of	is higher than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_3_1138_s_402	7836372	A definitive answer to the question of why refolding mAspAT binds  more tightly to groEL than its homologous isozymic counterpart awaits  an analysis of the structure of the complex between groEL and its  passenger protein.	bind
42296	1	9910	6	11	NULL	NULL	NULL	ERK2	GP		undergoes			Tyr185		phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40817_s_215	11524422	A definitive correlation between Tyr185 phosphorylation, changes in enzyme structure, and ATP binding must necessarily await a crystal structure of [Tyr(P)185]ERK2.	bind
42299	1	9910	7	11	NULL	NULL	NULL	ERK2	GP		undergoes			Tyr185		phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40817_s_215	11524422	A definitive correlation between Tyr185 phosphorylation, changes in enzyme structure, and ATP binding must necessarily await a crystal structure of [Tyr(P)185]ERK2.	bind
34570	1	9912	6	11	NULL	NULL	NULL	COP1	GP		bind			coiled coil domain		SPA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_41_38173_s_129	11461903	A deletion derivative of COP1 lacking the coiled-coil domain (COP1-deltacc) did not exhibit any detectable interaction with SPA1, indicating that the coiled-coil domain of COP1 is necessary for the SPA1 binding activity of COP1.	bind
34572	2	9912	6	11	NULL	NULL	NULL	COP1-deltacc	GP		is					deletion derivative of COP1 lacking the coiled-coil domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_41_38173_s_129	11461903	A deletion derivative of COP1 lacking the coiled-coil domain (COP1-deltacc) did not exhibit any detectable interaction with SPA1, indicating that the coiled-coil domain of COP1 is necessary for the SPA1 binding activity of COP1.	bind
34573	3	9912	6	11	NULL	NULL	NULL	COP1-deltacc	GP		does not interact with					SPA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_41_38173_s_129	11461903	A deletion derivative of COP1 lacking the coiled-coil domain (COP1-deltacc) did not exhibit any detectable interaction with SPA1, indicating that the coiled-coil domain of COP1 is necessary for the SPA1 binding activity of COP1.	bind
41890	1	9912	7	11	NULL	NULL	NULL	COP1-deltacc	GP		does not interact with					SPA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_41_38173_s_129	11461903	A deletion derivative of COP1 lacking the coiled-coil domain (COP1-deltacc) did not exhibit any detectable interaction with SPA1, indicating that the coiled-coil domain of COP1 is necessary for the SPA1 binding activity of COP1.	bind
41891	2	9912	7	11	NULL	NULL	NULL	COP1-deltacc	GP		is					deletion derivative lacking coiled-coil domain COP1 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_41_38173_s_129	11461903	A deletion derivative of COP1 lacking the coiled-coil domain (COP1-deltacc) did not exhibit any detectable interaction with SPA1, indicating that the coiled-coil domain of COP1 is necessary for the SPA1 binding activity of COP1.	bind
41892	3	9912	7	11	NULL	NULL	NULL	COP1	GP		bind			coiled-coil domain		SPA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_41_38173_s_129	11461903	A deletion derivative of COP1 lacking the coiled-coil domain (COP1-deltacc) did not exhibit any detectable interaction with SPA1, indicating that the coiled-coil domain of COP1 is necessary for the SPA1 binding activity of COP1.	bind
34615	1	9913	6	11	NULL	NULL	NULL	PDGF	GP		is					platelet-derived growth factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2395_s_328	9409207	A deletion in the extracellular domain of the alpha platelet-derived growth factor (PDGF) receptor differentially impairs PDGF-AA and PDGF-BB binding affinities.	bind
34616	2	9913	6	11	NULL	NULL	NULL	PDGF alpha receptor	GP	deletion of	impairs		differentially	extracellular domain		PDGF-AA	GP	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2395_s_328	9409207	A deletion in the extracellular domain of the alpha platelet-derived growth factor (PDGF) receptor differentially impairs PDGF-AA and PDGF-BB binding affinities.	bind
34617	3	9913	6	11	NULL	NULL	NULL	PDGF alpha receptor	GP	deletion of	impairs		differentially	extracellular domain		PDGF-BB	GP	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2395_s_328	9409207	A deletion in the extracellular domain of the alpha platelet-derived growth factor (PDGF) receptor differentially impairs PDGF-AA and PDGF-BB binding affinities.	bind
41893	1	9913	7	11	NULL	NULL	NULL	alpha PDGF receptor	GP	deletion in	impairs		differentially	 extracellular domain 		PDGF-AA	GP	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2395_s_328	9409207	A deletion in the extracellular domain of the alpha platelet-derived growth factor (PDGF) receptor differentially impairs PDGF-AA and PDGF-BB binding affinities.	bind
41894	2	9913	7	11	NULL	NULL	NULL	alpha PDGF receptor	GP	deletion in	impairs		differentially	extracellular domain		PDGF-BB	GP	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2395_s_328	9409207	A deletion in the extracellular domain of the alpha platelet-derived growth factor (PDGF) receptor differentially impairs PDGF-AA and PDGF-BB binding affinities.	bind
41895	3	9913	7	11	NULL	NULL	NULL	PDGF	GP		is					platelet-derived growth factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_11_2395_s_328	9409207	A deletion in the extracellular domain of the alpha platelet-derived growth factor (PDGF) receptor differentially impairs PDGF-AA and PDGF-BB binding affinities.	bind
34611	1	9914	6	11	NULL	NULL	NULL	Scd1	GP		bind					Klp5/6	GP				NULL		NULL	NULL	NULL	NULL	gw70_genetics_165_2_477_s_8	14573463	A deletion in the Scd1 C terminus, which contains the PB1 domain, prevented Scd1 binding to Klp5/6 and caused a growth defect in Klp5/6 mutant cells that is indistinguishable from that induced by  scd1delta.	bind
34612	2	9914	6	11	NULL	NULL	NULL	Scd1	GP		contains			C terminus					PB1 domain		NULL		NULL	NULL	NULL	NULL	gw70_genetics_165_2_477_s_8	14573463	A deletion in the Scd1 C terminus, which contains the PB1 domain, prevented Scd1 binding to Klp5/6 and caused a growth defect in Klp5/6 mutant cells that is indistinguishable from that induced by  scd1delta.	bind
34613	3	9914	6	11	NULL	NULL	NULL	Scd1	GP	deletion of	prevents			C terminus		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_genetics_165_2_477_s_8	14573463	A deletion in the Scd1 C terminus, which contains the PB1 domain, prevented Scd1 binding to Klp5/6 and caused a growth defect in Klp5/6 mutant cells that is indistinguishable from that induced by  scd1delta.	bind
34614	4	9914	6	11	NULL	NULL	NULL	Scd1	GP	deletion of	causes			C terminus		Klp5/6 mutant cells	Cell	growth defect in			NULL		NULL	NULL	NULL	NULL	gw70_genetics_165_2_477_s_8	14573463	A deletion in the Scd1 C terminus, which contains the PB1 domain, prevented Scd1 binding to Klp5/6 and caused a growth defect in Klp5/6 mutant cells that is indistinguishable from that induced by  scd1delta.	bind
49005	5	9914	6	11	NULL	NULL	NULL	scd1delta	GP		induces					growth defect	Process				NULL	Klp5/6 mutant cells	NULL	NULL	NULL	NULL	gw70_genetics_165_2_477_s_8	14573463	A deletion in the Scd1 C terminus, which contains the PB1 domain, prevented Scd1 binding to Klp5/6 and caused a growth defect in Klp5/6 mutant cells that is indistinguishable from that induced by  scd1delta.	bind
41896	1	9914	7	11	NULL	NULL	NULL	Scd1	GP		bind					Klp5/6	Cell				NULL		NULL	NULL	NULL	NULL	gw70_genetics_165_2_477_s_8	14573463	A deletion in the Scd1 C terminus, which contains the PB1 domain, prevented Scd1 binding to Klp5/6 and caused a growth defect in Klp5/6 mutant cells that is indistinguishable from that induced by  scd1delta.	bind
41897	2	9914	7	11	NULL	NULL	NULL	 Scd1	GP		contains			C terminus					PB1 domain		NULL		NULL	NULL	NULL	NULL	gw70_genetics_165_2_477_s_8	14573463	A deletion in the Scd1 C terminus, which contains the PB1 domain, prevented Scd1 binding to Klp5/6 and caused a growth defect in Klp5/6 mutant cells that is indistinguishable from that induced by  scd1delta.	bind
41898	3	9914	7	11	NULL	NULL	NULL	Scd1	GP	deletion of	prevents 			C terminus		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_genetics_165_2_477_s_8	14573463	A deletion in the Scd1 C terminus, which contains the PB1 domain, prevented Scd1 binding to Klp5/6 and caused a growth defect in Klp5/6 mutant cells that is indistinguishable from that induced by  scd1delta.	bind
41899	4	9914	7	11	NULL	NULL	NULL	statement 3	Process		cause					Klp5/6 mutant cells	Cell	growth defect in			NULL		NULL	NULL	NULL	NULL	gw70_genetics_165_2_477_s_8	14573463	A deletion in the Scd1 C terminus, which contains the PB1 domain, prevented Scd1 binding to Klp5/6 and caused a growth defect in Klp5/6 mutant cells that is indistinguishable from that induced by  scd1delta.	bind
41900	5	9914	7	11	NULL	NULL	NULL	scd1delta	GP		induce					growth defect	Process				NULL	Klp5/6 mutant cells	NULL	NULL	NULL	NULL	gw70_genetics_165_2_477_s_8	14573463	A deletion in the Scd1 C terminus, which contains the PB1 domain, prevented Scd1 binding to Klp5/6 and caused a growth defect in Klp5/6 mutant cells that is indistinguishable from that induced by  scd1delta.	bind
34609	1	9915	6	11	NULL	NULL	NULL	G protein	GP		bind					FPR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_39_27934_s_152	10488141	A deletion including three threonine and one serine residue, delta330-336, caused a significant decrease in G protein coupling, supporting previously obtained results showing that a synthetic peptide corresponding to amino acids 322-336 inhibits binding of G protein to FPR (Fig.  1 A) ( 5,  6).	bind
34610	2	9915	6	11	NULL	NULL	NULL	synthetic peptide	Chemical		inhibits			amino acids 322-336		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_39_27934_s_152	10488141	A deletion including three threonine and one serine residue, delta330-336, caused a significant decrease in G protein coupling, supporting previously obtained results showing that a synthetic peptide corresponding to amino acids 322-336 inhibits binding of G protein to FPR (Fig.  1 A) ( 5,  6).	bind
49007	3	9915	6	11	NULL	NULL	NULL	delta330-336	AminoAcid		includes					threonine and serine residue	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_39_27934_s_152	10488141	A deletion including three threonine and one serine residue, delta330-336, caused a significant decrease in G protein coupling, supporting previously obtained results showing that a synthetic peptide corresponding to amino acids 322-336 inhibits binding of G protein to FPR (Fig.  1 A) ( 5,  6).	bind
49008	4	9915	6	11	NULL	NULL	NULL	statement 3	Process		decreases					G protein coupling	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_39_27934_s_152	10488141	A deletion including three threonine and one serine residue, delta330-336, caused a significant decrease in G protein coupling, supporting previously obtained results showing that a synthetic peptide corresponding to amino acids 322-336 inhibits binding of G protein to FPR (Fig.  1 A) ( 5,  6).	bind
49009	5	9915	6	11	NULL	NULL	NULL	statement 4	Process		supports					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_39_27934_s_152	10488141	A deletion including three threonine and one serine residue, delta330-336, caused a significant decrease in G protein coupling, supporting previously obtained results showing that a synthetic peptide corresponding to amino acids 322-336 inhibits binding of G protein to FPR (Fig.  1 A) ( 5,  6).	bind
41901	1	9915	7	11	NULL	NULL	NULL	G protein	GP		bind					FPR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_39_27934_s_152	10488141	A deletion including three threonine and one serine residue, delta330-336, caused a significant decrease in G protein coupling, supporting previously obtained results showing that a synthetic peptide corresponding to amino acids 322-336 inhibits binding of G protein to FPR (Fig.  1 A) ( 5,  6).	bind
41902	2	9915	7	11	NULL	NULL	NULL	synthetic peptide	Chemical		inhibits			amino acids 322-336		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_39_27934_s_152	10488141	A deletion including three threonine and one serine residue, delta330-336, caused a significant decrease in G protein coupling, supporting previously obtained results showing that a synthetic peptide corresponding to amino acids 322-336 inhibits binding of G protein to FPR (Fig.  1 A) ( 5,  6).	bind
41903	4	9915	7	11	NULL	NULL	NULL	statement 3	Process		decrease					G protein coupling	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_39_27934_s_152	10488141	A deletion including three threonine and one serine residue, delta330-336, caused a significant decrease in G protein coupling, supporting previously obtained results showing that a synthetic peptide corresponding to amino acids 322-336 inhibits binding of G protein to FPR (Fig.  1 A) ( 5,  6).	bind
41904	5	9915	7	11	NULL	NULL	NULL	statement 4	Process		support					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_39_27934_s_152	10488141	A deletion including three threonine and one serine residue, delta330-336, caused a significant decrease in G protein coupling, supporting previously obtained results showing that a synthetic peptide corresponding to amino acids 322-336 inhibits binding of G protein to FPR (Fig.  1 A) ( 5,  6).	bind
49006	3	9915	7	11	NULL	NULL	NULL	delta330-336	AminoAcid		includes					threonine and serine residue	AminoAcid	deletion of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_39_27934_s_152	10488141	A deletion including three threonine and one serine residue, delta330-336, caused a significant decrease in G protein coupling, supporting previously obtained results showing that a synthetic peptide corresponding to amino acids 322-336 inhibits binding of G protein to FPR (Fig.  1 A) ( 5,  6).	bind
34605	1	9916	6	11	NULL	NULL	NULL				bind			central armadillo repeat region		cadherin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_23_16_6567_s_3	12878698	A deletion mutant betacatdeltaARM consists of the N- and  C-terminal domains of wild-type beta-catenin that contain, respectively,  alpha-catenin and postsynaptic density-95 (PSD-95)/discs large (Dlg)/zona  occludens-1 (ZO-1) (PDZ) binding sites but lacks the central armadillo repeat  region that binds cadherins and other proteins.	bind
41981	1	9916	7	11	NULL	NULL	NULL	 			binds			central armadillo repeat region		cadherins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_23_16_6567_s_3	12878698	A deletion mutant betacatdeltaARM consists of the N- and  C-terminal domains of wild-type beta-catenin that contain, respectively,  alpha-catenin and postsynaptic density-95 (PSD-95)/discs large (Dlg)/zona  occludens-1 (ZO-1) (PDZ) binding sites but lacks the central armadillo repeat  region that binds cadherins and other proteins.	bind
34606	1	9919	6	11	NULL	NULL	NULL	c-Abl	GP	deletion mutant	does not bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_741_s_6	10629029	A deletion mutant of c-Abl that does not bind to p53 is also incapable of activating p53 DNA binding.	bind
34607	2	9919	6	11	NULL	NULL	NULL	p53	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_741_s_6	10629029	A deletion mutant of c-Abl that does not bind to p53 is also incapable of activating p53 DNA binding.	bind
34608	3	9919	6	11	NULL	NULL	NULL	c-Abl	GP	deletion mutant	does not activate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_741_s_6	10629029	A deletion mutant of c-Abl that does not bind to p53 is also incapable of activating p53 DNA binding.	bind
41985	1	9919	7	11	NULL	NULL	NULL	 c-Abl	GP	deletion mutant	does not bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_741_s_6	10629029	A deletion mutant of c-Abl that does not bind to p53 is also incapable of activating p53 DNA binding.	bind
41986	2	9919	7	11	NULL	NULL	NULL	p53	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_741_s_6	10629029	A deletion mutant of c-Abl that does not bind to p53 is also incapable of activating p53 DNA binding.	bind
41987	3	9919	7	11	NULL	NULL	NULL	c-Abl	GP	deletion mutant	does not activate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_741_s_6	10629029	A deletion mutant of c-Abl that does not bind to p53 is also incapable of activating p53 DNA binding.	bind
34601	1	9920	6	11	NULL	NULL	NULL	E4BdeltaU	GP		bind					VCP	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_659_s_143	14749733	A deletion mutant of E4B that  lacks the COOH-terminal U-box domain (E4BdeltaU) also bound to VCP, whereas a mutant that lacks the NH2-terminal domain (E4BdeltaN) did not.	bind
34602	2	9920	6	11	NULL	NULL	NULL	E4BdeltaN	GP		does not bind					VCP	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_659_s_143	14749733	A deletion mutant of E4B that  lacks the COOH-terminal U-box domain (E4BdeltaU) also bound to VCP, whereas a mutant that lacks the NH2-terminal domain (E4BdeltaN) did not.	bind
34603	3	9920	6	11	NULL	NULL	NULL	E4BdeltaU	GP		is					E4B that lacks the COOH-terminal U-box domain	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_659_s_143	14749733	A deletion mutant of E4B that  lacks the COOH-terminal U-box domain (E4BdeltaU) also bound to VCP, whereas a mutant that lacks the NH2-terminal domain (E4BdeltaN) did not.	bind
34604	4	9920	6	11	NULL	NULL	NULL	E4BdeltaN	GP		is					E4B that lacks the NH2-terminal domain	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_659_s_143	14749733	A deletion mutant of E4B that  lacks the COOH-terminal U-box domain (E4BdeltaU) also bound to VCP, whereas a mutant that lacks the NH2-terminal domain (E4BdeltaN) did not.	bind
41988	1	9920	7	11	NULL	NULL	NULL	E4BdeltaU	GP		is					E4B that lacks the COOH-terminal U-box domain	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_659_s_143	14749733	A deletion mutant of E4B that  lacks the COOH-terminal U-box domain (E4BdeltaU) also bound to VCP, whereas a mutant that lacks the NH2-terminal domain (E4BdeltaN) did not.	bind
41989	2	9920	7	11	NULL	NULL	NULL	E4BdeltaU	GP		bind					VCP	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_659_s_143	14749733	A deletion mutant of E4B that  lacks the COOH-terminal U-box domain (E4BdeltaU) also bound to VCP, whereas a mutant that lacks the NH2-terminal domain (E4BdeltaN) did not.	bind
41990	3	9920	7	11	NULL	NULL	NULL	E4BdeltaN	GP		is					E4B that lacks the NH2-terminal domain	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_659_s_143	14749733	A deletion mutant of E4B that  lacks the COOH-terminal U-box domain (E4BdeltaU) also bound to VCP, whereas a mutant that lacks the NH2-terminal domain (E4BdeltaN) did not.	bind
41991	4	9920	7	11	NULL	NULL	NULL	E4BdeltaN	GP		does not bind					VCP	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_659_s_143	14749733	A deletion mutant of E4B that  lacks the COOH-terminal U-box domain (E4BdeltaU) also bound to VCP, whereas a mutant that lacks the NH2-terminal domain (E4BdeltaN) did not.	bind
34724	1	9922	6	11	NULL	NULL	NULL	Dc 63	AminoAcid		does not bind					Ab P2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_3_525_s_192	10069801	A deletion mutant with a truncation of the C-terminal 63 amino acids (Dc 63) does not bind to Ab P2.	bind
49010	2	9922	6	11	NULL	NULL	NULL	Dc 63	AminoAcid		is					deletion mutant with truncation of C-terminal 63 amino acids	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_3_525_s_192	10069801	A deletion mutant with a truncation of the C-terminal 63 amino acids (Dc 63) does not bind to Ab P2.	bind
41993	1	9922	7	11	NULL	NULL	NULL	Dc 63	AminoAcid		does not bind					Ab P2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_3_525_s_192	10069801	A deletion mutant with a truncation of the C-terminal 63 amino acids (Dc 63) does not bind to Ab P2.	bind
41994	2	9922	7	11	NULL	NULL	NULL	Dc 63	AminoAcid		is					deletion mutant with truncation of C-terminal 63 amino acids	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_3_525_s_192	10069801	A deletion mutant with a truncation of the C-terminal 63 amino acids (Dc 63) does not bind to Ab P2.	bind
34725	1	9923	6	11	NULL	NULL	NULL	Ssdp1	GP	mouse;; deletion of	does not bind			amino acid residues 1 to 121		Ldb1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_22_14320_s_126	12381786	A deletion of amino acid residues 1 to 121 from mouse Ssdp1 (see Fig.  1 B) yielded a protein that did not bind Ldb1 after cotransfection into cultured cells and was also unable to synergize with Xlim1 and Ldb1 in axis induction (data not shown).	bind
34726	2	9923	6	11	NULL	NULL	NULL	Xlim1	GP		plays a role in					axis 	Process	induction of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_22_14320_s_126	12381786	A deletion of amino acid residues 1 to 121 from mouse Ssdp1 (see Fig.  1 B) yielded a protein that did not bind Ldb1 after cotransfection into cultured cells and was also unable to synergize with Xlim1 and Ldb1 in axis induction (data not shown).	bind
34727	3	9923	6	11	NULL	NULL	NULL	Ldb1	GP		plays a role in					axis	Process	induction of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_22_14320_s_126	12381786	A deletion of amino acid residues 1 to 121 from mouse Ssdp1 (see Fig.  1 B) yielded a protein that did not bind Ldb1 after cotransfection into cultured cells and was also unable to synergize with Xlim1 and Ldb1 in axis induction (data not shown).	bind
34856	4	9923	6	11	NULL	NULL	NULL	Ssdp1	GP	mouse;; deletion of	does not synergize with			amino acid residues 1 to 121		Xlim1	GP				NULL	statement 2	NULL	NULL	NULL	NULL	gw60_pnas_99_22_14320_s_126	12381786	A deletion of amino acid residues 1 to 121 from mouse Ssdp1 (see Fig.  1 B) yielded a protein that did not bind Ldb1 after cotransfection into cultured cells and was also unable to synergize with Xlim1 and Ldb1 in axis induction (data not shown).	bind
34857	5	9923	6	11	NULL	NULL	NULL	Ssdp1	GP	mouse;; deletion of	does not synergize with			amino acid residues 1 to 121		Ldb1	GP				NULL	statement 3	NULL	NULL	NULL	NULL	gw60_pnas_99_22_14320_s_126	12381786	A deletion of amino acid residues 1 to 121 from mouse Ssdp1 (see Fig.  1 B) yielded a protein that did not bind Ldb1 after cotransfection into cultured cells and was also unable to synergize with Xlim1 and Ldb1 in axis induction (data not shown).	bind
41997	1	9923	7	11	NULL	NULL	NULL	Ssdp1	GP	mouse;;deletion of	does not bind			amino acid residues 1 to 121 		Ldb1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_22_14320_s_126	12381786	A deletion of amino acid residues 1 to 121 from mouse Ssdp1 (see Fig.  1 B) yielded a protein that did not bind Ldb1 after cotransfection into cultured cells and was also unable to synergize with Xlim1 and Ldb1 in axis induction (data not shown).	bind
41998	2	9923	7	11	NULL	NULL	NULL	Xlim1	GP		plays a role in					axis	Process	induction of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_22_14320_s_126	12381786	A deletion of amino acid residues 1 to 121 from mouse Ssdp1 (see Fig.  1 B) yielded a protein that did not bind Ldb1 after cotransfection into cultured cells and was also unable to synergize with Xlim1 and Ldb1 in axis induction (data not shown).	bind
41999	3	9923	7	11	NULL	NULL	NULL	Ldb1	GP		plays a role in					axis	Process	induction of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_22_14320_s_126	12381786	A deletion of amino acid residues 1 to 121 from mouse Ssdp1 (see Fig.  1 B) yielded a protein that did not bind Ldb1 after cotransfection into cultured cells and was also unable to synergize with Xlim1 and Ldb1 in axis induction (data not shown).	bind
42000	4	9923	7	11	NULL	NULL	NULL	Ssdp1	GP	mouse;;deletion of	does not syngergize with			amino acid residues 1 to 121 		Xlim1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_22_14320_s_126	12381786	A deletion of amino acid residues 1 to 121 from mouse Ssdp1 (see Fig.  1 B) yielded a protein that did not bind Ldb1 after cotransfection into cultured cells and was also unable to synergize with Xlim1 and Ldb1 in axis induction (data not shown).	bind
42001	5	9923	7	11	NULL	NULL	NULL	Ssdp1	GP	mouse;;deletion of	does not syngergize with			amino acid residues 1 to 121 		Ldb1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_22_14320_s_126	12381786	A deletion of amino acid residues 1 to 121 from mouse Ssdp1 (see Fig.  1 B) yielded a protein that did not bind Ldb1 after cotransfection into cultured cells and was also unable to synergize with Xlim1 and Ldb1 in axis induction (data not shown).	bind
34858	1	9924	6	11	NULL	NULL	NULL			deletion of	plays a role in		may	delta140 - 142		RNA	NucleicAcid	binding of			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4368_s_188	16077031	A deletion of residues delta140 - 142 (RRE), which we suspected might play a role in RNA binding due to the similarity of this region with the RNA-binding motif of lambda N protein and HIV Tat, indeed abolished both binding of the L18:pre-5S complex ( Figure 5) and enzyme activity	bind
34859	2	9924	6	11	NULL	NULL	NULL	RRE	AminoAcid		is					residues delta140 - 142	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4368_s_188	16077031	A deletion of residues delta140 - 142 (RRE), which we suspected might play a role in RNA binding due to the similarity of this region with the RNA-binding motif of lambda N protein and HIV Tat, indeed abolished both binding of the L18:pre-5S complex ( Figure 5) and enzyme activity	bind
34860	3	9924	6	11	NULL	NULL	NULL				is similar to			RRE		lambda N protein	GP		RNA binding motif		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4368_s_188	16077031	A deletion of residues delta140 - 142 (RRE), which we suspected might play a role in RNA binding due to the similarity of this region with the RNA-binding motif of lambda N protein and HIV Tat, indeed abolished both binding of the L18:pre-5S complex ( Figure 5) and enzyme activity	bind
34861	4	9924	6	11	NULL	NULL	NULL				is similar to			RRE		HIV Tat	GP		RNA-binding motif		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4368_s_188	16077031	A deletion of residues delta140 - 142 (RRE), which we suspected might play a role in RNA binding due to the similarity of this region with the RNA-binding motif of lambda N protein and HIV Tat, indeed abolished both binding of the L18:pre-5S complex ( Figure 5) and enzyme activity	bind
34862	5	9924	6	11	NULL	NULL	NULL				abolishes			RRE		L18:pre-5S complex	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4368_s_188	16077031	A deletion of residues delta140 - 142 (RRE), which we suspected might play a role in RNA binding due to the similarity of this region with the RNA-binding motif of lambda N protein and HIV Tat, indeed abolished both binding of the L18:pre-5S complex ( Figure 5) and enzyme activity	bind
34863	6	9924	6	11	NULL	NULL	NULL				abolishes			RRE		enzyme	GP	activity of 			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4368_s_188	16077031	A deletion of residues delta140 - 142 (RRE), which we suspected might play a role in RNA binding due to the similarity of this region with the RNA-binding motif of lambda N protein and HIV Tat, indeed abolished both binding of the L18:pre-5S complex ( Figure 5) and enzyme activity	bind
42002	1	9924	7	11	NULL	NULL	NULL			deletion of	plays a role in			 delta140 - 142		RNA	NucleicAcid	binding of			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4368_s_188	16077031	A deletion of residues delta140 - 142 (RRE), which we suspected might play a role in RNA binding due to the similarity of this region with the RNA-binding motif of lambda N protein and HIV Tat, indeed abolished both binding of the L18:pre-5S complex ( Figure 5) and enzyme activity	bind
42003	2	9924	7	11	NULL	NULL	NULL				is similar to			delta140 - 142		lambda N protein	GP		RNA-binding motif		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4368_s_188	16077031	A deletion of residues delta140 - 142 (RRE), which we suspected might play a role in RNA binding due to the similarity of this region with the RNA-binding motif of lambda N protein and HIV Tat, indeed abolished both binding of the L18:pre-5S complex ( Figure 5) and enzyme activity	bind
42004	3	9924	7	11	NULL	NULL	NULL				is similar to			delta140 - 142		HIV Tat	GP		RNA-binding motif		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4368_s_188	16077031	A deletion of residues delta140 - 142 (RRE), which we suspected might play a role in RNA binding due to the similarity of this region with the RNA-binding motif of lambda N protein and HIV Tat, indeed abolished both binding of the L18:pre-5S complex ( Figure 5) and enzyme activity	bind
42005	4	9924	7	11	NULL	NULL	NULL				abolishes			delta140 - 142		L18:pre-5S complex	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4368_s_188	16077031	A deletion of residues delta140 - 142 (RRE), which we suspected might play a role in RNA binding due to the similarity of this region with the RNA-binding motif of lambda N protein and HIV Tat, indeed abolished both binding of the L18:pre-5S complex ( Figure 5) and enzyme activity	bind
42006	5	9924	7	11	NULL	NULL	NULL				abolishes			delta140 - 142		enzyme	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4368_s_188	16077031	A deletion of residues delta140 - 142 (RRE), which we suspected might play a role in RNA binding due to the similarity of this region with the RNA-binding motif of lambda N protein and HIV Tat, indeed abolished both binding of the L18:pre-5S complex ( Figure 5) and enzyme activity	bind
49814	6	9924	7	11	NULL	NULL	NULL	RRE	AminoAcid		is					residues delta140-142	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4368_s_188	16077031	A deletion of residues delta140 - 142 (RRE), which we suspected might play a role in RNA binding due to the similarity of this region with the RNA-binding motif of lambda N protein and HIV Tat, indeed abolished both binding of the L18:pre-5S complex ( Figure 5) and enzyme activity	bind
34864	1	9925	6	11	NULL	NULL	NULL	pG180DS2	NucleicAcid		eliminates					preS	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8382_s_211	9525948	A deletion of the second domain and the N-terminal half of the third domain (pG180DS2) eliminated preS binding but showed carboxypeptidase activity (Figs.  4 and  5).	bind
34865	2	9925	6	11	NULL	NULL	NULL	pG180DS2	NucleicAcid		shows					carboxypeptidase activity 	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8382_s_211	9525948	A deletion of the second domain and the N-terminal half of the third domain (pG180DS2) eliminated preS binding but showed carboxypeptidase activity (Figs.  4 and  5).	bind
34866	3	9925	6	11	NULL	NULL	NULL	pG180DS2	NucleicAcid		is					deletion of the second domain and the N-terminal half of the third domain	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8382_s_211	9525948	A deletion of the second domain and the N-terminal half of the third domain (pG180DS2) eliminated preS binding but showed carboxypeptidase activity (Figs.  4 and  5).	bind
42086	1	9925	7	11	NULL	NULL	NULL	pG180DS2	NucleicAcid		eliminates					preS	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8382_s_211	9525948	A deletion of the second domain and the N-terminal half of the third domain (pG180DS2) eliminated preS binding but showed carboxypeptidase activity (Figs.  4 and  5).	bind
42087	2	9925	7	11	NULL	NULL	NULL	pG180DS2	NucleicAcid		shows 					carboxypeptidase activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8382_s_211	9525948	A deletion of the second domain and the N-terminal half of the third domain (pG180DS2) eliminated preS binding but showed carboxypeptidase activity (Figs.  4 and  5).	bind
42088	3	9925	7	11	NULL	NULL	NULL	pG180DS2	NucleicAcid		is					deletion of the second domain and the N-terminal half of the third domain	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8382_s_211	9525948	A deletion of the second domain and the N-terminal half of the third domain (pG180DS2) eliminated preS binding but showed carboxypeptidase activity (Figs.  4 and  5).	bind
34728	1	9926	6	11	NULL	NULL	NULL	PTEN	GP		bind					PDZ domain-containing proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6211_s_43	15988030	A deltaPDZB mutant was created with 3' primers bearing TKV/TVD mutations to disrupt PTEN's binding to PDZ domain-containing proteins.	bind
34729	2	9926	6	11	NULL	NULL	NULL	deltaPDZB	GP	mutant	disrupts			TKV/TVD		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6211_s_43	15988030	A deltaPDZB mutant was created with 3' primers bearing TKV/TVD mutations to disrupt PTEN's binding to PDZ domain-containing proteins.	bind
42089	1	9926	7	11	NULL	NULL	NULL	PTEN's	GP		bind					PDZ domain-containing proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6211_s_43	15988030	A deltaPDZB mutant was created with 3' primers bearing TKV/TVD mutations to disrupt PTEN's binding to PDZ domain-containing proteins.	bind
42090	2	9926	7	11	NULL	NULL	NULL	deltaPDZB	GP	mutant	disrupts			TKV/TVD		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_14_6211_s_43	15988030	A deltaPDZB mutant was created with 3' primers bearing TKV/TVD mutations to disrupt PTEN's binding to PDZ domain-containing proteins.	bind
34730	1	9928	6	11	NULL	NULL	NULL	beta1D construct	GP		bind					talin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6104_s_173	9497328	A densitometric analysis of the Coomassie Blue-stained proteins indicated that the beta1D construct bound 9 times more talin, and the beta7 construct bound 8.4 times more filamin than the beta1A model protein (Fig.  8).	bind
34731	2	9928	6	11	NULL	NULL	NULL	beta7 construct	GP		bind					filamin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6104_s_173	9497328	A densitometric analysis of the Coomassie Blue-stained proteins indicated that the beta1D construct bound 9 times more talin, and the beta7 construct bound 8.4 times more filamin than the beta1A model protein (Fig.  8).	bind
34732	3	9928	6	11	NULL	NULL	NULL	beta1A model protein	GP		bind					filamin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6104_s_173	9497328	A densitometric analysis of the Coomassie Blue-stained proteins indicated that the beta1D construct bound 9 times more talin, and the beta7 construct bound 8.4 times more filamin than the beta1A model protein (Fig.  8).	bind
34733	4	9928	6	11	NULL	NULL	NULL	statement 2	Process	affinity of	is more than					statement 3	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6104_s_173	9497328	A densitometric analysis of the Coomassie Blue-stained proteins indicated that the beta1D construct bound 9 times more talin, and the beta7 construct bound 8.4 times more filamin than the beta1A model protein (Fig.  8).	bind
49011	5	9928	6	11	NULL	NULL	NULL	beta1A model protein	GP		bind					talin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6104_s_173	9497328	A densitometric analysis of the Coomassie Blue-stained proteins indicated that the beta1D construct bound 9 times more talin, and the beta7 construct bound 8.4 times more filamin than the beta1A model protein (Fig.  8).	bind
49012	6	9928	6	11	NULL	NULL	NULL	statement 1	Process	affinity of	is more than					statement 5	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6104_s_173	9497328	A densitometric analysis of the Coomassie Blue-stained proteins indicated that the beta1D construct bound 9 times more talin, and the beta7 construct bound 8.4 times more filamin than the beta1A model protein (Fig.  8).	bind
42093	1	9928	7	11	NULL	NULL	NULL	beta1D construct	GP		bind					talin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6104_s_173	9497328	A densitometric analysis of the Coomassie Blue-stained proteins indicated that the beta1D construct bound 9 times more talin, and the beta7 construct bound 8.4 times more filamin than the beta1A model protein (Fig.  8).	bind
42094	2	9928	7	11	NULL	NULL	NULL	beta7 construct	GP		bind					filamin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6104_s_173	9497328	A densitometric analysis of the Coomassie Blue-stained proteins indicated that the beta1D construct bound 9 times more talin, and the beta7 construct bound 8.4 times more filamin than the beta1A model protein (Fig.  8).	bind
42095	3	9928	7	11	NULL	NULL	NULL	beta1A model protein	GP		bind					talin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6104_s_173	9497328	A densitometric analysis of the Coomassie Blue-stained proteins indicated that the beta1D construct bound 9 times more talin, and the beta7 construct bound 8.4 times more filamin than the beta1A model protein (Fig.  8).	bind
42096	4	9928	7	11	NULL	NULL	NULL	beta1A model protein	GP		bind					filamin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6104_s_173	9497328	A densitometric analysis of the Coomassie Blue-stained proteins indicated that the beta1D construct bound 9 times more talin, and the beta7 construct bound 8.4 times more filamin than the beta1A model protein (Fig.  8).	bind
42097	5	9928	7	11	NULL	NULL	NULL	statement 1	Process	binding of	is more than					statement 3	Process	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6104_s_173	9497328	A densitometric analysis of the Coomassie Blue-stained proteins indicated that the beta1D construct bound 9 times more talin, and the beta7 construct bound 8.4 times more filamin than the beta1A model protein (Fig.  8).	bind
42098	6	9928	7	11	NULL	NULL	NULL	statement 2	Process	binding of	is more than					statement 4	Process	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6104_s_173	9497328	A densitometric analysis of the Coomassie Blue-stained proteins indicated that the beta1D construct bound 9 times more talin, and the beta7 construct bound 8.4 times more filamin than the beta1A model protein (Fig.  8).	bind
34734	1	9929	6	11	NULL	NULL	NULL	Miz-1	GP		bind					AdML	Organism			promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_16_18_5672_s_86	9312026	A derivative of the AdML promoter which contains a mutated start site (kind gift of B.Roeder) was poorly transactivated by Miz-1, suggesting that binding of Miz-1 to the AdML promoter is required for activation (Figure  3B).	bind
34735	2	9929	6	11	NULL	NULL	NULL	statement 1	Process		is required for					AdML	Organism	activation of		promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_16_18_5672_s_86	9312026	A derivative of the AdML promoter which contains a mutated start site (kind gift of B.Roeder) was poorly transactivated by Miz-1, suggesting that binding of Miz-1 to the AdML promoter is required for activation (Figure  3B).	bind
42099	1	9929	7	11	NULL	NULL	NULL	 Miz-1	GP		bind					AdML	Organism			promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_16_18_5672_s_86	9312026	A derivative of the AdML promoter which contains a mutated start site (kind gift of B.Roeder) was poorly transactivated by Miz-1, suggesting that binding of Miz-1 to the AdML promoter is required for activation (Figure  3B).	bind
42100	2	9929	7	11	NULL	NULL	NULL	statement 1	Process		is required for					AdML	Organism	activation of		promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_16_18_5672_s_86	9312026	A derivative of the AdML promoter which contains a mutated start site (kind gift of B.Roeder) was poorly transactivated by Miz-1, suggesting that binding of Miz-1 to the AdML promoter is required for activation (Figure  3B).	bind
34867	1	9930	6	11	NULL	NULL	NULL	Desrt polypeptide	GP	recombinant	bind			amino acids 255-451 including the ARID domain		oligonucleotide	NucleicAcid			(TAA)9 repeat 	NULL		NULL	NULL	NULL	NULL	gw60_genomeres_11_8_1327_s_31	11483573	A Desrt recombinant polypeptide spanning amino acids 255-451 including the ARID domain binds a (TAA)9 repeat oligonucleotide that can be competed in a dose-dependent manner with excess unlabeled oligonucleotide (Complex C1) (Fig.  2B).	bind
42102	1	9930	7	11	NULL	NULL	NULL	Desrt polypeptide	GP	recombinant	binds			spanning amino acids 255-451 including the ARID domain		oligonucleotide	NucleicAcid			(TAA)9 repeat 	NULL		NULL	NULL	NULL	NULL	gw60_genomeres_11_8_1327_s_31	11483573	A Desrt recombinant polypeptide spanning amino acids 255-451 including the ARID domain binds a (TAA)9 repeat oligonucleotide that can be competed in a dose-dependent manner with excess unlabeled oligonucleotide (Complex C1) (Fig.  2B).	bind
34736	1	9931	6	11	NULL	NULL	NULL	ATVA	GP	mutant	bind		normally		destruction box	XDRP1	GP				NULL	egg extracts	NULL	NULL	NULL	NULL	gw60_embo_18_18_5009_s_180	10487753	A destruction-box mutant ATVA bound to XDRP1 normally in egg extracts (lane 4).	bind
42105	1	9931	7	11	NULL	NULL	NULL	ATVA	GP	mutant	bind		normally		destruction-box	XDRP1	GP				NULL	egg extracts	NULL	NULL	NULL	NULL	gw60_embo_18_18_5009_s_180	10487753	A destruction-box mutant ATVA bound to XDRP1 normally in egg extracts (lane 4).	bind
34737	1	9932	6	11	NULL	NULL	NULL	JIP-1	GP		bind					apoER2	GP		tail		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_33_25616_s_118	10827173	A detailed account of the binding properties of JIP-1 and JIP-2 to the apoER2 tail and the importance of the alternatively spliced insert is given in the accompanying paper by Stockinger  et al. ( 38).	bind
34738	2	9932	6	11	NULL	NULL	NULL	JIP-2	GP		bind					apoER2	GP		tail		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_33_25616_s_118	10827173	A detailed account of the binding properties of JIP-1 and JIP-2 to the apoER2 tail and the importance of the alternatively spliced insert is given in the accompanying paper by Stockinger  et al. ( 38).	bind
42106	1	9932	7	11	NULL	NULL	NULL	 JIP-1	GP		bind					apoER2	GP		tail		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_33_25616_s_118	10827173	A detailed account of the binding properties of JIP-1 and JIP-2 to the apoER2 tail and the importance of the alternatively spliced insert is given in the accompanying paper by Stockinger  et al. ( 38).	bind
42107	2	9932	7	11	NULL	NULL	NULL	JIP-2	GP		bind					apoER2	GP		tail		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_33_25616_s_118	10827173	A detailed account of the binding properties of JIP-1 and JIP-2 to the apoER2 tail and the importance of the alternatively spliced insert is given in the accompanying paper by Stockinger  et al. ( 38).	bind
34739	1	9933	6	11	NULL	NULL	NULL	ATP	Chemical		bind					Hsp90	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18608_s_211	9228028	A detailed analysis of ATP binding to Hsp90 seems to be required in comparison to Hsp70 to identify potential steps in the interaction with partner proteins and steroid receptors that may require ATP binding to Hsp90.	bind
34740	2	9933	6	11	NULL	NULL	NULL	ATP	Chemical		bind					Hsp70	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18608_s_211	9228028	A detailed analysis of ATP binding to Hsp90 seems to be required in comparison to Hsp70 to identify potential steps in the interaction with partner proteins and steroid receptors that may require ATP binding to Hsp90.	bind
49015	3	9933	6	11	NULL	NULL	NULL	steroid receptors	GP		require		may			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18608_s_211	9228028	A detailed analysis of ATP binding to Hsp90 seems to be required in comparison to Hsp70 to identify potential steps in the interaction with partner proteins and steroid receptors that may require ATP binding to Hsp90.	bind
42108	1	9933	7	11	NULL	NULL	NULL	ATP	Chemical		bind					Hsp90	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18608_s_211	9228028	A detailed analysis of ATP binding to Hsp90 seems to be required in comparison to Hsp70 to identify potential steps in the interaction with partner proteins and steroid receptors that may require ATP binding to Hsp90.	bind
42109	2	9933	7	11	NULL	NULL	NULL	ATP	Chemical		bind					Hsp70	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18608_s_211	9228028	A detailed analysis of ATP binding to Hsp90 seems to be required in comparison to Hsp70 to identify potential steps in the interaction with partner proteins and steroid receptors that may require ATP binding to Hsp90.	bind
42110	3	9933	7	11	NULL	NULL	NULL	steroid receptors	GP		require		may			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18608_s_211	9228028	A detailed analysis of ATP binding to Hsp90 seems to be required in comparison to Hsp70 to identify potential steps in the interaction with partner proteins and steroid receptors that may require ATP binding to Hsp90.	bind
34741	1	9934	6	11	NULL	NULL	NULL	Munc13-1	GP		bind					synaptobrevin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2520_s_155	8999968	A detailed analysis of Munc13-1 immunoprecipitation experiments and cosedimentation assays showed that in addition to syntaxin, Munc13-1 also binds synaptobrevin, SNAP25, and to a lesser extent, synaptotagmin (Figs.  4,  5,  6).	bind
34742	2	9934	6	11	NULL	NULL	NULL	Munc13-1	GP		bind					Syntaxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2520_s_155	8999968	A detailed analysis of Munc13-1 immunoprecipitation experiments and cosedimentation assays showed that in addition to syntaxin, Munc13-1 also binds synaptobrevin, SNAP25, and to a lesser extent, synaptotagmin (Figs.  4,  5,  6).	bind
34743	3	9934	6	11	NULL	NULL	NULL	Munc13-1	GP		bind					SNAP25	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2520_s_155	8999968	A detailed analysis of Munc13-1 immunoprecipitation experiments and cosedimentation assays showed that in addition to syntaxin, Munc13-1 also binds synaptobrevin, SNAP25, and to a lesser extent, synaptotagmin (Figs.  4,  5,  6).	bind
34744	4	9934	6	11	NULL	NULL	NULL	Munc13-1	GP		bind					synaptotagmin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2520_s_155	8999968	A detailed analysis of Munc13-1 immunoprecipitation experiments and cosedimentation assays showed that in addition to syntaxin, Munc13-1 also binds synaptobrevin, SNAP25, and to a lesser extent, synaptotagmin (Figs.  4,  5,  6).	bind
42111	1	9934	7	11	NULL	NULL	NULL	Munc13-1	GP		binds					syntaxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2520_s_155	8999968	A detailed analysis of Munc13-1 immunoprecipitation experiments and cosedimentation assays showed that in addition to syntaxin, Munc13-1 also binds synaptobrevin, SNAP25, and to a lesser extent, synaptotagmin (Figs.  4,  5,  6).	bind
42112	2	9934	7	11	NULL	NULL	NULL	Munc13-1	GP		binds					synaptobrevin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2520_s_155	8999968	A detailed analysis of Munc13-1 immunoprecipitation experiments and cosedimentation assays showed that in addition to syntaxin, Munc13-1 also binds synaptobrevin, SNAP25, and to a lesser extent, synaptotagmin (Figs.  4,  5,  6).	bind
42114	3	9934	7	11	NULL	NULL	NULL	 Munc13-1 	GP		binds					SNAP25	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2520_s_155	8999968	A detailed analysis of Munc13-1 immunoprecipitation experiments and cosedimentation assays showed that in addition to syntaxin, Munc13-1 also binds synaptobrevin, SNAP25, and to a lesser extent, synaptotagmin (Figs.  4,  5,  6).	bind
42116	4	9934	7	11	NULL	NULL	NULL	Munc13-1	GP		binds					synaptotagmin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2520_s_155	8999968	A detailed analysis of Munc13-1 immunoprecipitation experiments and cosedimentation assays showed that in addition to syntaxin, Munc13-1 also binds synaptobrevin, SNAP25, and to a lesser extent, synaptotagmin (Figs.  4,  5,  6).	bind
34745	1	9935	6	11	NULL	NULL	NULL	NFAT factor	GP		bind					HIV-1 clade	Organism			enhancer	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_51_52949_s_337	15466412	A detailed analysis of the binding of the NFAT factor to the different HIV-1 clade enhancers was also undertaken.	bind
42121	1	9935	7	11	NULL	NULL	NULL	NFAT factor	GP		bind					HIV-1 clade 	Organism			enhancer	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_51_52949_s_337	15466412	A detailed analysis of the binding of the NFAT factor to the different HIV-1 clade enhancers was also undertaken.	bind
34934	2	9937	6	11	NULL	NULL	NULL	FAD	Chemical		accommodate		might	QR1 binding site		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_7_3177_s_201	10706635	A detailed analysis of the FAD contacts suggests then the binding site of the human and mouse QR1 might accommodate a certain degree of bending of the isoalloxazine around its central axis; in these two enzymes, the shortest van der Waals contacts occur at the center of the isoallozaxine ring and relax to longer contacts toward the extremes.	bind
34936	1	9937	6	11	NULL	NULL	NULL	isoalloxazine	Chemical		bends around					central axis	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_7_3177_s_201	10706635	A detailed analysis of the FAD contacts suggests then the binding site of the human and mouse QR1 might accommodate a certain degree of bending of the isoalloxazine around its central axis; in these two enzymes, the shortest van der Waals contacts occur at the center of the isoallozaxine ring and relax to longer contacts toward the extremes.	bind
35093	3	9937	6	11	NULL	NULL	NULL	FAD	Chemical		bind					QR1	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_7_3177_s_201	10706635	A detailed analysis of the FAD contacts suggests then the binding site of the human and mouse QR1 might accommodate a certain degree of bending of the isoalloxazine around its central axis; in these two enzymes, the shortest van der Waals contacts occur at the center of the isoallozaxine ring and relax to longer contacts toward the extremes.	bind
35094	4	9937	6	11	NULL	NULL	NULL	FAD	Chemical		bind					QR1	GP	mouse			NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_7_3177_s_201	10706635	A detailed analysis of the FAD contacts suggests then the binding site of the human and mouse QR1 might accommodate a certain degree of bending of the isoalloxazine around its central axis; in these two enzymes, the shortest van der Waals contacts occur at the center of the isoallozaxine ring and relax to longer contacts toward the extremes.	bind
42130	1	9937	7	11	NULL	NULL	NULL	QR1	GP	 human	bind					FAD	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_7_3177_s_201	10706635	A detailed analysis of the FAD contacts suggests then the binding site of the human and mouse QR1 might accommodate a certain degree of bending of the isoalloxazine around its central axis; in these two enzymes, the shortest van der Waals contacts occur at the center of the isoallozaxine ring and relax to longer contacts toward the extremes.	bind
42132	2	9937	7	11	NULL	NULL	NULL	QR1	GP	mouse	bind					FAD	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_7_3177_s_201	10706635	A detailed analysis of the FAD contacts suggests then the binding site of the human and mouse QR1 might accommodate a certain degree of bending of the isoalloxazine around its central axis; in these two enzymes, the shortest van der Waals contacts occur at the center of the isoallozaxine ring and relax to longer contacts toward the extremes.	bind
42133	4	9937	7	11	NULL	NULL	NULL	FAD	Chemical		accomodate		might	QR1 binding site		statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_7_3177_s_201	10706635	A detailed analysis of the FAD contacts suggests then the binding site of the human and mouse QR1 might accommodate a certain degree of bending of the isoalloxazine around its central axis; in these two enzymes, the shortest van der Waals contacts occur at the center of the isoallozaxine ring and relax to longer contacts toward the extremes.	bind
49018	3	9937	7	11	NULL	NULL	NULL	isoallozaxine	Chemical		bends around					central axis	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_7_3177_s_201	10706635	A detailed analysis of the FAD contacts suggests then the binding site of the human and mouse QR1 might accommodate a certain degree of bending of the isoalloxazine around its central axis; in these two enzymes, the shortest van der Waals contacts occur at the center of the isoallozaxine ring and relax to longer contacts toward the extremes.	bind
34937	1	9938	6	11	NULL	NULL	NULL	T3R heterodimer	GP		bind					9- cis RXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27919_s_26	8910392	A detailed analysis of the human ppTRH gene promoter recently demonstrated that both the binding of T3Rs as heterodimers with the 9- cis-retinoic acid receptors (RXR) to the element that contains a single TRE half-site located 60 bp upstream of the TSS and the binding of T3R monomers to the two TRE half-sites positioning downstream of the TSS were required to exhibit full-inhibition of the human ppTRH gene promoter by T3 ( 7).	bind
34938	2	9938	6	11	NULL	NULL	NULL	RXR	GP		is					9- cis-retinoic acid receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27919_s_26	8910392	A detailed analysis of the human ppTRH gene promoter recently demonstrated that both the binding of T3Rs as heterodimers with the 9- cis-retinoic acid receptors (RXR) to the element that contains a single TRE half-site located 60 bp upstream of the TSS and the binding of T3R monomers to the two TRE half-sites positioning downstream of the TSS were required to exhibit full-inhibition of the human ppTRH gene promoter by T3 ( 7).	bind
34939	3	9938	6	11	NULL	NULL	NULL	statement 1	GP		bind					statement 8	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27919_s_26	8910392	A detailed analysis of the human ppTRH gene promoter recently demonstrated that both the binding of T3Rs as heterodimers with the 9- cis-retinoic acid receptors (RXR) to the element that contains a single TRE half-site located 60 bp upstream of the TSS and the binding of T3R monomers to the two TRE half-sites positioning downstream of the TSS were required to exhibit full-inhibition of the human ppTRH gene promoter by T3 ( 7).	bind
34940	4	9938	6	11	NULL	NULL	NULL	T3R monomers	GP		bind					statement 9	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27919_s_26	8910392	A detailed analysis of the human ppTRH gene promoter recently demonstrated that both the binding of T3Rs as heterodimers with the 9- cis-retinoic acid receptors (RXR) to the element that contains a single TRE half-site located 60 bp upstream of the TSS and the binding of T3R monomers to the two TRE half-sites positioning downstream of the TSS were required to exhibit full-inhibition of the human ppTRH gene promoter by T3 ( 7).	bind
34941	5	9938	6	11	NULL	NULL	NULL	T3	GP		inhibit					ppTRH gene	GP	human		promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27919_s_26	8910392	A detailed analysis of the human ppTRH gene promoter recently demonstrated that both the binding of T3Rs as heterodimers with the 9- cis-retinoic acid receptors (RXR) to the element that contains a single TRE half-site located 60 bp upstream of the TSS and the binding of T3R monomers to the two TRE half-sites positioning downstream of the TSS were required to exhibit full-inhibition of the human ppTRH gene promoter by T3 ( 7).	bind
49016	6	9938	6	11	NULL	NULL	NULL	statement 3	Process		is required for					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27919_s_26	8910392	A detailed analysis of the human ppTRH gene promoter recently demonstrated that both the binding of T3Rs as heterodimers with the 9- cis-retinoic acid receptors (RXR) to the element that contains a single TRE half-site located 60 bp upstream of the TSS and the binding of T3R monomers to the two TRE half-sites positioning downstream of the TSS were required to exhibit full-inhibition of the human ppTRH gene promoter by T3 ( 7).	bind
49017	7	9938	6	11	NULL	NULL	NULL	statement 4	Process		is required for					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27919_s_26	8910392	A detailed analysis of the human ppTRH gene promoter recently demonstrated that both the binding of T3Rs as heterodimers with the 9- cis-retinoic acid receptors (RXR) to the element that contains a single TRE half-site located 60 bp upstream of the TSS and the binding of T3R monomers to the two TRE half-sites positioning downstream of the TSS were required to exhibit full-inhibition of the human ppTRH gene promoter by T3 ( 7).	bind
56927	8	9938	6	11	NULL	NULL	NULL				is located				TRE half site			upstream of		TSS	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27919_s_26	8910392	A detailed analysis of the human ppTRH gene promoter recently demonstrated that both the binding of T3Rs as heterodimers with the 9- cis-retinoic acid receptors (RXR) to the element that contains a single TRE half-site located 60 bp upstream of the TSS and the binding of T3R monomers to the two TRE half-sites positioning downstream of the TSS were required to exhibit full-inhibition of the human ppTRH gene promoter by T3 ( 7).	bind
56928	9	9938	6	11	NULL	NULL	NULL				is located				TRE half site			downstream of		TSS	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27919_s_26	8910392	A detailed analysis of the human ppTRH gene promoter recently demonstrated that both the binding of T3Rs as heterodimers with the 9- cis-retinoic acid receptors (RXR) to the element that contains a single TRE half-site located 60 bp upstream of the TSS and the binding of T3R monomers to the two TRE half-sites positioning downstream of the TSS were required to exhibit full-inhibition of the human ppTRH gene promoter by T3 ( 7).	bind
42135	1	9938	7	11	NULL	NULL	NULL	T3R heterodimer	GP		bind					RXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27919_s_26	8910392	A detailed analysis of the human ppTRH gene promoter recently demonstrated that both the binding of T3Rs as heterodimers with the 9- cis-retinoic acid receptors (RXR) to the element that contains a single TRE half-site located 60 bp upstream of the TSS and the binding of T3R monomers to the two TRE half-sites positioning downstream of the TSS were required to exhibit full-inhibition of the human ppTRH gene promoter by T3 ( 7).	bind
42136	2	9938	7	11	NULL	NULL	NULL	statement 1	GP		bind					statement 8	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27919_s_26	8910392	A detailed analysis of the human ppTRH gene promoter recently demonstrated that both the binding of T3Rs as heterodimers with the 9- cis-retinoic acid receptors (RXR) to the element that contains a single TRE half-site located 60 bp upstream of the TSS and the binding of T3R monomers to the two TRE half-sites positioning downstream of the TSS were required to exhibit full-inhibition of the human ppTRH gene promoter by T3 ( 7).	bind
42137	3	9938	7	11	NULL	NULL	NULL	T3R monomer	GP		bind					statement 9	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27919_s_26	8910392	A detailed analysis of the human ppTRH gene promoter recently demonstrated that both the binding of T3Rs as heterodimers with the 9- cis-retinoic acid receptors (RXR) to the element that contains a single TRE half-site located 60 bp upstream of the TSS and the binding of T3R monomers to the two TRE half-sites positioning downstream of the TSS were required to exhibit full-inhibition of the human ppTRH gene promoter by T3 ( 7).	bind
42138	4	9938	7	11	NULL	NULL	NULL	T3	GP		inhibit					ppTRH gene	GP	human		promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27919_s_26	8910392	A detailed analysis of the human ppTRH gene promoter recently demonstrated that both the binding of T3Rs as heterodimers with the 9- cis-retinoic acid receptors (RXR) to the element that contains a single TRE half-site located 60 bp upstream of the TSS and the binding of T3R monomers to the two TRE half-sites positioning downstream of the TSS were required to exhibit full-inhibition of the human ppTRH gene promoter by T3 ( 7).	bind
42139	5	9938	7	11	NULL	NULL	NULL	statement 2	Process		is required for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27919_s_26	8910392	A detailed analysis of the human ppTRH gene promoter recently demonstrated that both the binding of T3Rs as heterodimers with the 9- cis-retinoic acid receptors (RXR) to the element that contains a single TRE half-site located 60 bp upstream of the TSS and the binding of T3R monomers to the two TRE half-sites positioning downstream of the TSS were required to exhibit full-inhibition of the human ppTRH gene promoter by T3 ( 7).	bind
42140	6	9938	7	11	NULL	NULL	NULL	statement 3	Process		is required for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27919_s_26	8910392	A detailed analysis of the human ppTRH gene promoter recently demonstrated that both the binding of T3Rs as heterodimers with the 9- cis-retinoic acid receptors (RXR) to the element that contains a single TRE half-site located 60 bp upstream of the TSS and the binding of T3R monomers to the two TRE half-sites positioning downstream of the TSS were required to exhibit full-inhibition of the human ppTRH gene promoter by T3 ( 7).	bind
42141	7	9938	7	11	NULL	NULL	NULL	RXR	GP		is					 9- cis-retinoic acid receptors 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27919_s_26	8910392	A detailed analysis of the human ppTRH gene promoter recently demonstrated that both the binding of T3Rs as heterodimers with the 9- cis-retinoic acid receptors (RXR) to the element that contains a single TRE half-site located 60 bp upstream of the TSS and the binding of T3R monomers to the two TRE half-sites positioning downstream of the TSS were required to exhibit full-inhibition of the human ppTRH gene promoter by T3 ( 7).	bind
56929	8	9938	7	11	NULL	NULL	NULL				is located				TRE half site			upstream of		TSS	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27919_s_26	8910392	A detailed analysis of the human ppTRH gene promoter recently demonstrated that both the binding of T3Rs as heterodimers with the 9- cis-retinoic acid receptors (RXR) to the element that contains a single TRE half-site located 60 bp upstream of the TSS and the binding of T3R monomers to the two TRE half-sites positioning downstream of the TSS were required to exhibit full-inhibition of the human ppTRH gene promoter by T3 ( 7).	bind
56930	9	9938	7	11	NULL	NULL	NULL				is located				TRE half site			downstream of		TSS	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27919_s_26	8910392	A detailed analysis of the human ppTRH gene promoter recently demonstrated that both the binding of T3Rs as heterodimers with the 9- cis-retinoic acid receptors (RXR) to the element that contains a single TRE half-site located 60 bp upstream of the TSS and the binding of T3R monomers to the two TRE half-sites positioning downstream of the TSS were required to exhibit full-inhibition of the human ppTRH gene promoter by T3 ( 7).	bind
34748	1	9939	6	11	NULL	NULL	NULL	TBP	GP		bind					C7 variant	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_14623_s_149	11278275	A detailed analysis of the kinetics of TBP binding the C7 variant is in progress and will be published elsewhere.	bind
42142	1	9939	7	11	NULL	NULL	NULL	TBP	GP		bind					C7 variant	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_14623_s_149	11278275	A detailed analysis of the kinetics of TBP binding the C7 variant is in progress and will be published elsewhere.	bind
34749	1	9940	6	11	NULL	NULL	NULL	HSP90	GP		bind							isolated	CS domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_16_16511_s_154	14761955	A detailed analysis of the peaks that disappear in the spectra of intact Sgt1 upon binding of HSP90 reveals that these signals correspond very closely to those affected by binding of HSP90 to the isolated CS domain ( cf.  Fig. 1 B).	bind
49019	2	9940	6	11	NULL	NULL	NULL	HSP90	GP		bind					Sgt1	GP	intact			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_16_16511_s_154	14761955	A detailed analysis of the peaks that disappear in the spectra of intact Sgt1 upon binding of HSP90 reveals that these signals correspond very closely to those affected by binding of HSP90 to the isolated CS domain ( cf.  Fig. 1 B).	bind
42143	1	9940	7	11	NULL	NULL	NULL	HSP90	GP		bind					Sgt1	GP	intact			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_16_16511_s_154	14761955	A detailed analysis of the peaks that disappear in the spectra of intact Sgt1 upon binding of HSP90 reveals that these signals correspond very closely to those affected by binding of HSP90 to the isolated CS domain ( cf.  Fig. 1 B).	bind
42144	2	9940	7	11	NULL	NULL	NULL	HSP90	GP		bind							isolated	CS domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_16_16511_s_154	14761955	A detailed analysis of the peaks that disappear in the spectra of intact Sgt1 upon binding of HSP90 reveals that these signals correspond very closely to those affected by binding of HSP90 to the isolated CS domain ( cf.  Fig. 1 B).	bind
34942	1	9941	6	11	NULL	NULL	NULL	RBCS	GP		is  					ribulose 1,5-bisphosphate carboxylase small subunit	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
34943	2	9941	6	11	NULL	NULL	NULL	CAB	GP		is					chlorophyll a/b binding proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
34944	3	9941	6	11	NULL	NULL	NULL	LRE	GP		is					light responsive elements	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
34945	4	9941	6	11	NULL	NULL	NULL	G	GP		is a type of					LRE	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
34946	5	9941	6	11	NULL	NULL	NULL	GATA	GP		is a type of					LRE	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
34947	6	9941	6	11	NULL	NULL	NULL	GT1	GP		is a type of					LRE	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
34948	7	9941	6	11	NULL	NULL	NULL	Z-box	GP		is a type of					LRE	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
34949	8	9941	6	11	NULL	NULL	NULL	G	GP		is critical for					transcriptional activity	Process	light-controlled			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
34950	9	9941	6	11	NULL	NULL	NULL	GATA	GP		is critical for					transcriptional activity	Process	light-controlled			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
34951	10	9941	6	11	NULL	NULL	NULL	GT1	GP		is critical for					transcriptional activity	Process	light-controlled			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
34952	11	9941	6	11	NULL	NULL	NULL	Z-box	GP		is critical for					transcriptional activity	Process	light-controlled			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
42145	1	9941	7	11	NULL	NULL	NULL	RBCS gene	GP		contains									G	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
42146	2	9941	7	11	NULL	NULL	NULL	RBCS gene	GP		contains									GATA	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
42147	3	9941	7	11	NULL	NULL	NULL	RBCS gene	GP		contains									GT1	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
42148	4	9941	7	11	NULL	NULL	NULL	RBCS gene	GP		contains									Z-box	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
42149	5	9941	7	11	NULL	NULL	NULL	CAB gene	GP		contains									G	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
42150	6	9941	7	11	NULL	NULL	NULL	CAB gene	GP		contains									GATA	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
42151	7	9941	7	11	NULL	NULL	NULL	CAB gene	GP		contains									GT1	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
42152	8	9941	7	11	NULL	NULL	NULL	CAB gene	GP		contains									Z-box	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
42153	9	9941	7	11	NULL	NULL	NULL	G	GP		is a type of					LREs	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
42154	10	9941	7	11	NULL	NULL	NULL	GATA	GP		is a type of					LREs	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
42155	11	9941	7	11	NULL	NULL	NULL	GT1	GP		is a type of					LREs	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
42156	12	9941	7	11	NULL	NULL	NULL	Z-box	GP		is a type of					LREs	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
42157	13	9941	7	11	NULL	NULL	NULL	RBCS	GP		is					ribulose 1,5-bisphosphate carboxylase small subunit	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
42158	14	9941	7	11	NULL	NULL	NULL	CAB	GP		is					chlorophyll a/b binding proteins 	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
42159	15	9941	7	11	NULL	NULL	NULL	CAB	GP		is a type of					nuclear-encoded photosynthesis related genes	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5256_s_23	12954761	A detailed analysis of the promoter of some of these genes, such as ribulose 1,5-bisphosphate carboxylase small subunit ( RBCS) and nuclear-encoded photosynthesis related genes for chlorophyll a/b binding proteins ( CAB) revealed the presence of several light responsive elements (LREs), such as G, GATA, GT1 and Z-box that are critical for light-controlled transcriptional activity ( 23 -  28).	bind
34750	1	9942	6	NULL	NULL	0	NULL	BaCRASP-1	NULL		bind	NULL	strongly			FHL-1/reconectin	NULL				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_infect-immun_69_12_11705962_s_10	11705962	A detailed comparison  reveals overlapping and even identical binding profiles for BaCRASP-1  (27.5 kDa), BbCRASP-1 (25.9 kDa), and BbCRASP-2 (23.2 kDa), which bind  FHL-1/reconectin strongly and interact weakly with factor H.	bind
34751	2	9942	6	NULL	NULL	0	NULL	BbCRASP-1	NULL		bind	NULL	strongly			FHL-1/reconectin	NULL				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_infect-immun_69_12_11705962_s_10	11705962	A detailed comparison  reveals overlapping and even identical binding profiles for BaCRASP-1  (27.5 kDa), BbCRASP-1 (25.9 kDa), and BbCRASP-2 (23.2 kDa), which bind  FHL-1/reconectin strongly and interact weakly with factor H.	bind
34752	3	9942	6	NULL	NULL	0	NULL	BbCRASP-2	NULL		bind	NULL	strongly			FHL-1/reconectin	NULL				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_infect-immun_69_12_11705962_s_10	11705962	A detailed comparison  reveals overlapping and even identical binding profiles for BaCRASP-1  (27.5 kDa), BbCRASP-1 (25.9 kDa), and BbCRASP-2 (23.2 kDa), which bind  FHL-1/reconectin strongly and interact weakly with factor H.	bind
34753	4	9942	6	10	NULL	0	NULL	BaCRASP-1	NULL		interacts with	NULL	weakly 			factor H	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_infect-immun_69_12_11705962_s_10	11705962	A detailed comparison  reveals overlapping and even identical binding profiles for BaCRASP-1  (27.5 kDa), BbCRASP-1 (25.9 kDa), and BbCRASP-2 (23.2 kDa), which bind  FHL-1/reconectin strongly and interact weakly with factor H.	bind
34754	5	9942	6	10	NULL	0	NULL	BbCRASP-1	NULL		interacts with	NULL	weakly			factor H	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_infect-immun_69_12_11705962_s_10	11705962	A detailed comparison  reveals overlapping and even identical binding profiles for BaCRASP-1  (27.5 kDa), BbCRASP-1 (25.9 kDa), and BbCRASP-2 (23.2 kDa), which bind  FHL-1/reconectin strongly and interact weakly with factor H.	bind
34755	6	9942	6	10	NULL	0	NULL	BbCRASP-2	NULL		interacts with	NULL	weakly			factor H	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_infect-immun_69_12_11705962_s_10	11705962	A detailed comparison  reveals overlapping and even identical binding profiles for BaCRASP-1  (27.5 kDa), BbCRASP-1 (25.9 kDa), and BbCRASP-2 (23.2 kDa), which bind  FHL-1/reconectin strongly and interact weakly with factor H.	bind
42160	1	9942	7	NULL	NULL	0	NULL	BaCRASP-1 	NULL		bind	NULL	strongly			FHL-1/reconectin 	NULL				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_infect-immun_69_12_11705962_s_10	11705962	A detailed comparison  reveals overlapping and even identical binding profiles for BaCRASP-1  (27.5 kDa), BbCRASP-1 (25.9 kDa), and BbCRASP-2 (23.2 kDa), which bind  FHL-1/reconectin strongly and interact weakly with factor H.	bind
42161	2	9942	7	NULL	NULL	0	NULL	BbCRASP-1	NULL		bind	NULL	strongly			FHL-1/reconectin 	NULL				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_infect-immun_69_12_11705962_s_10	11705962	A detailed comparison  reveals overlapping and even identical binding profiles for BaCRASP-1  (27.5 kDa), BbCRASP-1 (25.9 kDa), and BbCRASP-2 (23.2 kDa), which bind  FHL-1/reconectin strongly and interact weakly with factor H.	bind
42162	3	9942	7	NULL	NULL	0	NULL	 BbCRASP-2 	NULL		bind	NULL	strongly			FHL-1/reconectin 	NULL				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_infect-immun_69_12_11705962_s_10	11705962	A detailed comparison  reveals overlapping and even identical binding profiles for BaCRASP-1  (27.5 kDa), BbCRASP-1 (25.9 kDa), and BbCRASP-2 (23.2 kDa), which bind  FHL-1/reconectin strongly and interact weakly with factor H.	bind
42163	4	9942	7	10	NULL	0	NULL	BaCRASP-1	NULL		interacts with	NULL	weakly			factor H	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_infect-immun_69_12_11705962_s_10	11705962	A detailed comparison  reveals overlapping and even identical binding profiles for BaCRASP-1  (27.5 kDa), BbCRASP-1 (25.9 kDa), and BbCRASP-2 (23.2 kDa), which bind  FHL-1/reconectin strongly and interact weakly with factor H.	bind
42164	5	9942	7	10	NULL	0	NULL	BbCRASP-1	NULL		interacts with	NULL	weakly			factor H	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_infect-immun_69_12_11705962_s_10	11705962	A detailed comparison  reveals overlapping and even identical binding profiles for BaCRASP-1  (27.5 kDa), BbCRASP-1 (25.9 kDa), and BbCRASP-2 (23.2 kDa), which bind  FHL-1/reconectin strongly and interact weakly with factor H.	bind
42165	6	9942	7	10	NULL	0	NULL	BbCRASP-2	NULL		interacts with	NULL	weakly			factor H	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_infect-immun_69_12_11705962_s_10	11705962	A detailed comparison  reveals overlapping and even identical binding profiles for BaCRASP-1  (27.5 kDa), BbCRASP-1 (25.9 kDa), and BbCRASP-2 (23.2 kDa), which bind  FHL-1/reconectin strongly and interact weakly with factor H.	bind
34757	1	9944	6	11	NULL	NULL	NULL	c-Cbl	GP		bind					E2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_17_15341_s_268	12588869	A detailed comparison of the free EL5 RING finger domain with the E2-bound form of c-Cbl suggested that the side-chain conformations (chi1) of the Trp residues in both molecules are different (Fig.  3).	bind
42168	1	9944	7	11	NULL	NULL	NULL	E2	GP		bind					c-Cbl	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_17_15341_s_268	12588869	A detailed comparison of the free EL5 RING finger domain with the E2-bound form of c-Cbl suggested that the side-chain conformations (chi1) of the Trp residues in both molecules are different (Fig.  3).	bind
42169	2	9944	7	11	NULL	NULL	NULL	free EL5	GP	side-chain conformations of	differs from			Trp residues in RING finger domain		statement 1	GP	side-chain conformations of	Trp residues		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_17_15341_s_268	12588869	A detailed comparison of the free EL5 RING finger domain with the E2-bound form of c-Cbl suggested that the side-chain conformations (chi1) of the Trp residues in both molecules are different (Fig.  3).	bind
34758	1	9945	6	11	NULL	NULL	NULL	TIMP-2	GP		bind					N-MMP-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_34_21736_s_7	9705310	A detailed comparison of the N-TIMP-2 structure with that of TIMP-1 bound to N-MMP-3 (Gomis-Ruth, F.-X., Maskos, K., Betz, M., Bergner, A., Huber, R., Suzuki, K., Yoshida, N., Nagase, H., Brew, K., Bourne, G. P., Bartunik, H. & Bode, W. (1997)  Nature 389, 77-80) revealed that the core beta-barrels are very similar in topology but that the loop connecting beta-strands CD (P67-C72) would need to undergo a large conformational change for TIMP-2 to bind in a similar manner to TIMP-1.	bind
49670	2	9945	6	11	NULL	NULL	NULL	TIMP-1	GP		bind					N-MMP-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_34_21736_s_7	9705310	A detailed comparison of the N-TIMP-2 structure with that of TIMP-1 bound to N-MMP-3 (Gomis-Ruth, F.-X., Maskos, K., Betz, M., Bergner, A., Huber, R., Suzuki, K., Yoshida, N., Nagase, H., Brew, K., Bourne, G. P., Bartunik, H. & Bode, W. (1997)  Nature 389, 77-80) revealed that the core beta-barrels are very similar in topology but that the loop connecting beta-strands CD (P67-C72) would need to undergo a large conformational change for TIMP-2 to bind in a similar manner to TIMP-1.	bind
49671	3	9945	6	11	NULL	NULL	NULL	TIMP-1	GP		is similar to			core beta-barrels		TIMP-2	GP		core beta-barrels		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_34_21736_s_7	9705310	A detailed comparison of the N-TIMP-2 structure with that of TIMP-1 bound to N-MMP-3 (Gomis-Ruth, F.-X., Maskos, K., Betz, M., Bergner, A., Huber, R., Suzuki, K., Yoshida, N., Nagase, H., Brew, K., Bourne, G. P., Bartunik, H. & Bode, W. (1997)  Nature 389, 77-80) revealed that the core beta-barrels are very similar in topology but that the loop connecting beta-strands CD (P67-C72) would need to undergo a large conformational change for TIMP-2 to bind in a similar manner to TIMP-1.	bind
42170	1	9945	7	11	NULL	NULL	NULL	 TIMP-1	GP		bind					N-MMP-3 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_34_21736_s_7	9705310	A detailed comparison of the N-TIMP-2 structure with that of TIMP-1 bound to N-MMP-3 (Gomis-Ruth, F.-X., Maskos, K., Betz, M., Bergner, A., Huber, R., Suzuki, K., Yoshida, N., Nagase, H., Brew, K., Bourne, G. P., Bartunik, H. & Bode, W. (1997)  Nature 389, 77-80) revealed that the core beta-barrels are very similar in topology but that the loop connecting beta-strands CD (P67-C72) would need to undergo a large conformational change for TIMP-2 to bind in a similar manner to TIMP-1.	bind
42171	2	9945	7	11	NULL	NULL	NULL	TIMP-2	GP		bind					N-MMP-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_34_21736_s_7	9705310	A detailed comparison of the N-TIMP-2 structure with that of TIMP-1 bound to N-MMP-3 (Gomis-Ruth, F.-X., Maskos, K., Betz, M., Bergner, A., Huber, R., Suzuki, K., Yoshida, N., Nagase, H., Brew, K., Bourne, G. P., Bartunik, H. & Bode, W. (1997)  Nature 389, 77-80) revealed that the core beta-barrels are very similar in topology but that the loop connecting beta-strands CD (P67-C72) would need to undergo a large conformational change for TIMP-2 to bind in a similar manner to TIMP-1.	bind
42172	3	9945	7	11	NULL	NULL	NULL	TIMP-1	GP		is similar to			core beta-barrels		N-TIMP-2	GP		core beta-barrels		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_34_21736_s_7	9705310	A detailed comparison of the N-TIMP-2 structure with that of TIMP-1 bound to N-MMP-3 (Gomis-Ruth, F.-X., Maskos, K., Betz, M., Bergner, A., Huber, R., Suzuki, K., Yoshida, N., Nagase, H., Brew, K., Bourne, G. P., Bartunik, H. & Bode, W. (1997)  Nature 389, 77-80) revealed that the core beta-barrels are very similar in topology but that the loop connecting beta-strands CD (P67-C72) would need to undergo a large conformational change for TIMP-2 to bind in a similar manner to TIMP-1.	bind
34953	1	9947	6	11	NULL	NULL	NULL	N-Oct-3	GP		bind			POU domain		AADC	GP	neuronal		promoter	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1513_s_35	15767276	A detailed compilation of the available POU/DNA complex structures, as well as a combination of molecular modeling, DNA footprinting and electrophoretic mobility shift assay (EMSA) have enabled us to (i) uncover a new mode of homodimerization adopted by the N-Oct-3 POU domain bound to the respective neuronal AADC and CRH gene promoters, (ii) demonstrate that this pattern is induced by a novel structural motif, the NORE (N-Oct-3 responsive element) and (iii) understand how the same structural motif can also induce the formation of a heterodimer in association with HNF-3beta DBD.	bind
34954	2	9947	6	11	NULL	NULL	NULL	N-Oct-3	GP		bind			POU domain		CRH 	GP	neuronal		promoter	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1513_s_35	15767276	A detailed compilation of the available POU/DNA complex structures, as well as a combination of molecular modeling, DNA footprinting and electrophoretic mobility shift assay (EMSA) have enabled us to (i) uncover a new mode of homodimerization adopted by the N-Oct-3 POU domain bound to the respective neuronal AADC and CRH gene promoters, (ii) demonstrate that this pattern is induced by a novel structural motif, the NORE (N-Oct-3 responsive element) and (iii) understand how the same structural motif can also induce the formation of a heterodimer in association with HNF-3beta DBD.	bind
34955	3	9947	6	11	NULL	NULL	NULL	NORE	GP		is					N-Oct-3 responsive element	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1513_s_35	15767276	A detailed compilation of the available POU/DNA complex structures, as well as a combination of molecular modeling, DNA footprinting and electrophoretic mobility shift assay (EMSA) have enabled us to (i) uncover a new mode of homodimerization adopted by the N-Oct-3 POU domain bound to the respective neuronal AADC and CRH gene promoters, (ii) demonstrate that this pattern is induced by a novel structural motif, the NORE (N-Oct-3 responsive element) and (iii) understand how the same structural motif can also induce the formation of a heterodimer in association with HNF-3beta DBD.	bind
35095	4	9947	6	11	NULL	NULL	NULL	statement 1	GP		undergoes					homodimerization	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1513_s_35	15767276	A detailed compilation of the available POU/DNA complex structures, as well as a combination of molecular modeling, DNA footprinting and electrophoretic mobility shift assay (EMSA) have enabled us to (i) uncover a new mode of homodimerization adopted by the N-Oct-3 POU domain bound to the respective neuronal AADC and CRH gene promoters, (ii) demonstrate that this pattern is induced by a novel structural motif, the NORE (N-Oct-3 responsive element) and (iii) understand how the same structural motif can also induce the formation of a heterodimer in association with HNF-3beta DBD.	bind
35096	5	9947	6	11	NULL	NULL	NULL	statement 2	GP		undergoes					homodimerization	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1513_s_35	15767276	A detailed compilation of the available POU/DNA complex structures, as well as a combination of molecular modeling, DNA footprinting and electrophoretic mobility shift assay (EMSA) have enabled us to (i) uncover a new mode of homodimerization adopted by the N-Oct-3 POU domain bound to the respective neuronal AADC and CRH gene promoters, (ii) demonstrate that this pattern is induced by a novel structural motif, the NORE (N-Oct-3 responsive element) and (iii) understand how the same structural motif can also induce the formation of a heterodimer in association with HNF-3beta DBD.	bind
35097	6	9947	6	11	NULL	NULL	NULL	statement 4	Process		is induced by									NORE	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1513_s_35	15767276	A detailed compilation of the available POU/DNA complex structures, as well as a combination of molecular modeling, DNA footprinting and electrophoretic mobility shift assay (EMSA) have enabled us to (i) uncover a new mode of homodimerization adopted by the N-Oct-3 POU domain bound to the respective neuronal AADC and CRH gene promoters, (ii) demonstrate that this pattern is induced by a novel structural motif, the NORE (N-Oct-3 responsive element) and (iii) understand how the same structural motif can also induce the formation of a heterodimer in association with HNF-3beta DBD.	bind
35098	7	9947	6	11	NULL	NULL	NULL	statement 5	Process		is induced by									NORE	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1513_s_35	15767276	A detailed compilation of the available POU/DNA complex structures, as well as a combination of molecular modeling, DNA footprinting and electrophoretic mobility shift assay (EMSA) have enabled us to (i) uncover a new mode of homodimerization adopted by the N-Oct-3 POU domain bound to the respective neuronal AADC and CRH gene promoters, (ii) demonstrate that this pattern is induced by a novel structural motif, the NORE (N-Oct-3 responsive element) and (iii) understand how the same structural motif can also induce the formation of a heterodimer in association with HNF-3beta DBD.	bind
35099	8	9947	6	11	NULL	NULL	NULL	N-Oct-3	GP		forms heterodimer with			POU domain		HNF-3 beta	GP		DBD		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1513_s_35	15767276	A detailed compilation of the available POU/DNA complex structures, as well as a combination of molecular modeling, DNA footprinting and electrophoretic mobility shift assay (EMSA) have enabled us to (i) uncover a new mode of homodimerization adopted by the N-Oct-3 POU domain bound to the respective neuronal AADC and CRH gene promoters, (ii) demonstrate that this pattern is induced by a novel structural motif, the NORE (N-Oct-3 responsive element) and (iii) understand how the same structural motif can also induce the formation of a heterodimer in association with HNF-3beta DBD.	bind
35100	9	9947	6	11	NULL	NULL	NULL	statement 8	Process		is induced by									NORE	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1513_s_35	15767276	A detailed compilation of the available POU/DNA complex structures, as well as a combination of molecular modeling, DNA footprinting and electrophoretic mobility shift assay (EMSA) have enabled us to (i) uncover a new mode of homodimerization adopted by the N-Oct-3 POU domain bound to the respective neuronal AADC and CRH gene promoters, (ii) demonstrate that this pattern is induced by a novel structural motif, the NORE (N-Oct-3 responsive element) and (iii) understand how the same structural motif can also induce the formation of a heterodimer in association with HNF-3beta DBD.	bind
42177	1	9947	7	11	NULL	NULL	NULL	N-Oct-3	GP		bind			POU domain		AADC gene	GP	neuronal		promoter	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1513_s_35	15767276	A detailed compilation of the available POU/DNA complex structures, as well as a combination of molecular modeling, DNA footprinting and electrophoretic mobility shift assay (EMSA) have enabled us to (i) uncover a new mode of homodimerization adopted by the N-Oct-3 POU domain bound to the respective neuronal AADC and CRH gene promoters, (ii) demonstrate that this pattern is induced by a novel structural motif, the NORE (N-Oct-3 responsive element) and (iii) understand how the same structural motif can also induce the formation of a heterodimer in association with HNF-3beta DBD.	bind
42178	2	9947	7	11	NULL	NULL	NULL	N-Oct-3	GP		bind			POU domain		CRH gene	GP	neuronal		promoter	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1513_s_35	15767276	A detailed compilation of the available POU/DNA complex structures, as well as a combination of molecular modeling, DNA footprinting and electrophoretic mobility shift assay (EMSA) have enabled us to (i) uncover a new mode of homodimerization adopted by the N-Oct-3 POU domain bound to the respective neuronal AADC and CRH gene promoters, (ii) demonstrate that this pattern is induced by a novel structural motif, the NORE (N-Oct-3 responsive element) and (iii) understand how the same structural motif can also induce the formation of a heterodimer in association with HNF-3beta DBD.	bind
42179	3	9947	7	11	NULL	NULL	NULL	statement 1	Process		undergoes					homodimerization	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1513_s_35	15767276	A detailed compilation of the available POU/DNA complex structures, as well as a combination of molecular modeling, DNA footprinting and electrophoretic mobility shift assay (EMSA) have enabled us to (i) uncover a new mode of homodimerization adopted by the N-Oct-3 POU domain bound to the respective neuronal AADC and CRH gene promoters, (ii) demonstrate that this pattern is induced by a novel structural motif, the NORE (N-Oct-3 responsive element) and (iii) understand how the same structural motif can also induce the formation of a heterodimer in association with HNF-3beta DBD.	bind
42180	4	9947	7	11	NULL	NULL	NULL	statement 2	Process		undergoes					homodimerization	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1513_s_35	15767276	A detailed compilation of the available POU/DNA complex structures, as well as a combination of molecular modeling, DNA footprinting and electrophoretic mobility shift assay (EMSA) have enabled us to (i) uncover a new mode of homodimerization adopted by the N-Oct-3 POU domain bound to the respective neuronal AADC and CRH gene promoters, (ii) demonstrate that this pattern is induced by a novel structural motif, the NORE (N-Oct-3 responsive element) and (iii) understand how the same structural motif can also induce the formation of a heterodimer in association with HNF-3beta DBD.	bind
42181	5	9947	7	11	NULL	NULL	NULL	NORE	GP		is					N-Oct-3 responsive element	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1513_s_35	15767276	A detailed compilation of the available POU/DNA complex structures, as well as a combination of molecular modeling, DNA footprinting and electrophoretic mobility shift assay (EMSA) have enabled us to (i) uncover a new mode of homodimerization adopted by the N-Oct-3 POU domain bound to the respective neuronal AADC and CRH gene promoters, (ii) demonstrate that this pattern is induced by a novel structural motif, the NORE (N-Oct-3 responsive element) and (iii) understand how the same structural motif can also induce the formation of a heterodimer in association with HNF-3beta DBD.	bind
42182	6	9947	7	11	NULL	NULL	NULL	statement 3	GP		is induced by									NORE	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1513_s_35	15767276	A detailed compilation of the available POU/DNA complex structures, as well as a combination of molecular modeling, DNA footprinting and electrophoretic mobility shift assay (EMSA) have enabled us to (i) uncover a new mode of homodimerization adopted by the N-Oct-3 POU domain bound to the respective neuronal AADC and CRH gene promoters, (ii) demonstrate that this pattern is induced by a novel structural motif, the NORE (N-Oct-3 responsive element) and (iii) understand how the same structural motif can also induce the formation of a heterodimer in association with HNF-3beta DBD.	bind
42183	7	9947	7	11	NULL	NULL	NULL	N-Oct-3	GP		heterodimerizes with			POU domain		HNF-3beta	GP		DBD		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1513_s_35	15767276	A detailed compilation of the available POU/DNA complex structures, as well as a combination of molecular modeling, DNA footprinting and electrophoretic mobility shift assay (EMSA) have enabled us to (i) uncover a new mode of homodimerization adopted by the N-Oct-3 POU domain bound to the respective neuronal AADC and CRH gene promoters, (ii) demonstrate that this pattern is induced by a novel structural motif, the NORE (N-Oct-3 responsive element) and (iii) understand how the same structural motif can also induce the formation of a heterodimer in association with HNF-3beta DBD.	bind
42184	8	9947	7	11	NULL	NULL	NULL	NORE	GP		induce					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1513_s_35	15767276	A detailed compilation of the available POU/DNA complex structures, as well as a combination of molecular modeling, DNA footprinting and electrophoretic mobility shift assay (EMSA) have enabled us to (i) uncover a new mode of homodimerization adopted by the N-Oct-3 POU domain bound to the respective neuronal AADC and CRH gene promoters, (ii) demonstrate that this pattern is induced by a novel structural motif, the NORE (N-Oct-3 responsive element) and (iii) understand how the same structural motif can also induce the formation of a heterodimer in association with HNF-3beta DBD.	bind
49021	9	9947	7	11	NULL	NULL	NULL	statement 4	GP		is induced by									NORE	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1513_s_35	15767276	A detailed compilation of the available POU/DNA complex structures, as well as a combination of molecular modeling, DNA footprinting and electrophoretic mobility shift assay (EMSA) have enabled us to (i) uncover a new mode of homodimerization adopted by the N-Oct-3 POU domain bound to the respective neuronal AADC and CRH gene promoters, (ii) demonstrate that this pattern is induced by a novel structural motif, the NORE (N-Oct-3 responsive element) and (iii) understand how the same structural motif can also induce the formation of a heterodimer in association with HNF-3beta DBD.	bind
34956	1	9948	6	11	NULL	NULL	NULL	v-Ha-Ras 	GP		exists as					isomeric conformers	GP	population of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30363_s_437	10887184	A detailed kinetic analysis of the v-Ha-Ras-RBD interaction is presented in a separate paper,2 where we show v-Ha-Ras exists as a population of isomeric conformers and that A85K-RBD binds a greater proportion of these conformers than wt-RBD, giving rise to the difference in Ras saturation levels.	bind
34957	2	9948	6	11	NULL	NULL	NULL			wt	bind			RBD		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30363_s_437	10887184	A detailed kinetic analysis of the v-Ha-Ras-RBD interaction is presented in a separate paper,2 where we show v-Ha-Ras exists as a population of isomeric conformers and that A85K-RBD binds a greater proportion of these conformers than wt-RBD, giving rise to the difference in Ras saturation levels.	bind
34958	3	9948	6	11	NULL	NULL	NULL				bind			A85K-RBD		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30363_s_437	10887184	A detailed kinetic analysis of the v-Ha-Ras-RBD interaction is presented in a separate paper,2 where we show v-Ha-Ras exists as a population of isomeric conformers and that A85K-RBD binds a greater proportion of these conformers than wt-RBD, giving rise to the difference in Ras saturation levels.	bind
34959	4	9948	6	11	NULL	NULL	NULL	statement 3	Process	affinity of	is more than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30363_s_437	10887184	A detailed kinetic analysis of the v-Ha-Ras-RBD interaction is presented in a separate paper,2 where we show v-Ha-Ras exists as a population of isomeric conformers and that A85K-RBD binds a greater proportion of these conformers than wt-RBD, giving rise to the difference in Ras saturation levels.	bind
34960	5	9948	6	11	NULL	NULL	NULL	statement 4	Process		leads to					Ras	GP	difference in;;saturation levels of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30363_s_437	10887184	A detailed kinetic analysis of the v-Ha-Ras-RBD interaction is presented in a separate paper,2 where we show v-Ha-Ras exists as a population of isomeric conformers and that A85K-RBD binds a greater proportion of these conformers than wt-RBD, giving rise to the difference in Ras saturation levels.	bind
42305	2	9948	7	11	NULL	NULL	NULL				bind			A85K-RBD 		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30363_s_437	10887184	A detailed kinetic analysis of the v-Ha-Ras-RBD interaction is presented in a separate paper,2 where we show v-Ha-Ras exists as a population of isomeric conformers and that A85K-RBD binds a greater proportion of these conformers than wt-RBD, giving rise to the difference in Ras saturation levels.	bind
42306	3	9948	7	11	NULL	NULL	NULL			wt	bind			RBD		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30363_s_437	10887184	A detailed kinetic analysis of the v-Ha-Ras-RBD interaction is presented in a separate paper,2 where we show v-Ha-Ras exists as a population of isomeric conformers and that A85K-RBD binds a greater proportion of these conformers than wt-RBD, giving rise to the difference in Ras saturation levels.	bind
42307	4	9948	7	11	NULL	NULL	NULL	statement 1	Process	affinity of	is greater than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30363_s_437	10887184	A detailed kinetic analysis of the v-Ha-Ras-RBD interaction is presented in a separate paper,2 where we show v-Ha-Ras exists as a population of isomeric conformers and that A85K-RBD binds a greater proportion of these conformers than wt-RBD, giving rise to the difference in Ras saturation levels.	bind
49022	1	9948	7	11	NULL	NULL	NULL	v-Ha-Ras	GP		exists as					isomeric conformers	GP	population of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30363_s_437	10887184	A detailed kinetic analysis of the v-Ha-Ras-RBD interaction is presented in a separate paper,2 where we show v-Ha-Ras exists as a population of isomeric conformers and that A85K-RBD binds a greater proportion of these conformers than wt-RBD, giving rise to the difference in Ras saturation levels.	bind
49023	5	9948	7	11	NULL	NULL	NULL	statement 4	Process		leads to					Ras	GP	difference in;;saturation levels of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30363_s_437	10887184	A detailed kinetic analysis of the v-Ha-Ras-RBD interaction is presented in a separate paper,2 where we show v-Ha-Ras exists as a population of isomeric conformers and that A85K-RBD binds a greater proportion of these conformers than wt-RBD, giving rise to the difference in Ras saturation levels.	bind
34760	1	9949	6	11	NULL	NULL	NULL	nitrite	Chemical		bind					(P8+)FeIII(H2O)2	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_inorg-chem_45_16_16878967_s_7	16878967	A detailed kinetic studied revealed that nitrite binds to (P8+)FeIII(H2O)2  according to a dissociative mechanism, whereas nitrite binding to (P8+)FeIII(OH)(H2O)  at higher pH follows an associative mechanism, similar to that reported  for the binding of NO to these complexes.	bind
34761	2	9949	6	11	NULL	NULL	NULL	statement 1	Process		follows					dissociative mechanism	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_inorg-chem_45_16_16878967_s_7	16878967	A detailed kinetic studied revealed that nitrite binds to (P8+)FeIII(H2O)2  according to a dissociative mechanism, whereas nitrite binding to (P8+)FeIII(OH)(H2O)  at higher pH follows an associative mechanism, similar to that reported  for the binding of NO to these complexes.	bind
34762	3	9949	6	11	NULL	NULL	NULL	nitrite	Chemical		bind					(P8+)FeIII(OH)(H2O)	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_inorg-chem_45_16_16878967_s_7	16878967	A detailed kinetic studied revealed that nitrite binds to (P8+)FeIII(H2O)2  according to a dissociative mechanism, whereas nitrite binding to (P8+)FeIII(OH)(H2O)  at higher pH follows an associative mechanism, similar to that reported  for the binding of NO to these complexes.	bind
34763	4	9949	6	11	NULL	NULL	NULL	statement 3	Process		follows					associative mechanism	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_inorg-chem_45_16_16878967_s_7	16878967	A detailed kinetic studied revealed that nitrite binds to (P8+)FeIII(H2O)2  according to a dissociative mechanism, whereas nitrite binding to (P8+)FeIII(OH)(H2O)  at higher pH follows an associative mechanism, similar to that reported  for the binding of NO to these complexes.	bind
49024	5	9949	6	11	NULL	NULL	NULL	statement 3	Process		occurs at					pH	QuantityOrMeasure	higher			NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_inorg-chem_45_16_16878967_s_7	16878967	A detailed kinetic studied revealed that nitrite binds to (P8+)FeIII(H2O)2  according to a dissociative mechanism, whereas nitrite binding to (P8+)FeIII(OH)(H2O)  at higher pH follows an associative mechanism, similar to that reported  for the binding of NO to these complexes.	bind
49025	6	9949	6	11	NULL	NULL	NULL	NO	Chemical		bind					(P8+)FeIII(H2O)2	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_inorg-chem_45_16_16878967_s_7	16878967	A detailed kinetic studied revealed that nitrite binds to (P8+)FeIII(H2O)2  according to a dissociative mechanism, whereas nitrite binding to (P8+)FeIII(OH)(H2O)  at higher pH follows an associative mechanism, similar to that reported  for the binding of NO to these complexes.	bind
49026	7	9949	6	11	NULL	NULL	NULL	NO	Chemical		bind					(P8+)FeIII(OH)(H2O)	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_inorg-chem_45_16_16878967_s_7	16878967	A detailed kinetic studied revealed that nitrite binds to (P8+)FeIII(H2O)2  according to a dissociative mechanism, whereas nitrite binding to (P8+)FeIII(OH)(H2O)  at higher pH follows an associative mechanism, similar to that reported  for the binding of NO to these complexes.	bind
49027	8	9949	6	11	NULL	NULL	NULL	statement 1	Process		is similar to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_inorg-chem_45_16_16878967_s_7	16878967	A detailed kinetic studied revealed that nitrite binds to (P8+)FeIII(H2O)2  according to a dissociative mechanism, whereas nitrite binding to (P8+)FeIII(OH)(H2O)  at higher pH follows an associative mechanism, similar to that reported  for the binding of NO to these complexes.	bind
49028	9	9949	6	11	NULL	NULL	NULL	statement 3	Process		is similar to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_inorg-chem_45_16_16878967_s_7	16878967	A detailed kinetic studied revealed that nitrite binds to (P8+)FeIII(H2O)2  according to a dissociative mechanism, whereas nitrite binding to (P8+)FeIII(OH)(H2O)  at higher pH follows an associative mechanism, similar to that reported  for the binding of NO to these complexes.	bind
42185	1	9949	7	11	NULL	NULL	NULL	nitrite	Chemical		binds to					(P8+)FeIII(H2O)2	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_inorg-chem_45_16_16878967_s_7	16878967	A detailed kinetic studied revealed that nitrite binds to (P8+)FeIII(H2O)2  according to a dissociative mechanism, whereas nitrite binding to (P8+)FeIII(OH)(H2O)  at higher pH follows an associative mechanism, similar to that reported  for the binding of NO to these complexes.	bind
42186	2	9949	7	11	NULL	NULL	NULL	statement 1	Process		follows					dissociative mechanism	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_inorg-chem_45_16_16878967_s_7	16878967	A detailed kinetic studied revealed that nitrite binds to (P8+)FeIII(H2O)2  according to a dissociative mechanism, whereas nitrite binding to (P8+)FeIII(OH)(H2O)  at higher pH follows an associative mechanism, similar to that reported  for the binding of NO to these complexes.	bind
42187	3	9949	7	11	NULL	NULL	NULL	nitrite	Chemical		binds to					(P8+)FeIII(OH)(H2O)	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_inorg-chem_45_16_16878967_s_7	16878967	A detailed kinetic studied revealed that nitrite binds to (P8+)FeIII(H2O)2  according to a dissociative mechanism, whereas nitrite binding to (P8+)FeIII(OH)(H2O)  at higher pH follows an associative mechanism, similar to that reported  for the binding of NO to these complexes.	bind
42188	4	9949	7	11	NULL	NULL	NULL	statement 3	Process		occurs at					pH	QuantityOrMeasure	higher			NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_inorg-chem_45_16_16878967_s_7	16878967	A detailed kinetic studied revealed that nitrite binds to (P8+)FeIII(H2O)2  according to a dissociative mechanism, whereas nitrite binding to (P8+)FeIII(OH)(H2O)  at higher pH follows an associative mechanism, similar to that reported  for the binding of NO to these complexes.	bind
42189	5	9949	7	11	NULL	NULL	NULL	statement 3	Process		follows					associative mechanism	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_inorg-chem_45_16_16878967_s_7	16878967	A detailed kinetic studied revealed that nitrite binds to (P8+)FeIII(H2O)2  according to a dissociative mechanism, whereas nitrite binding to (P8+)FeIII(OH)(H2O)  at higher pH follows an associative mechanism, similar to that reported  for the binding of NO to these complexes.	bind
42190	6	9949	7	11	NULL	NULL	NULL	NO	Chemical		bind					 (P8+)FeIII(H2O)2	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_inorg-chem_45_16_16878967_s_7	16878967	A detailed kinetic studied revealed that nitrite binds to (P8+)FeIII(H2O)2  according to a dissociative mechanism, whereas nitrite binding to (P8+)FeIII(OH)(H2O)  at higher pH follows an associative mechanism, similar to that reported  for the binding of NO to these complexes.	bind
42191	7	9949	7	11	NULL	NULL	NULL	NO	Chemical		bind					(P8+)FeIII(OH)(H2O)	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_inorg-chem_45_16_16878967_s_7	16878967	A detailed kinetic studied revealed that nitrite binds to (P8+)FeIII(H2O)2  according to a dissociative mechanism, whereas nitrite binding to (P8+)FeIII(OH)(H2O)  at higher pH follows an associative mechanism, similar to that reported  for the binding of NO to these complexes.	bind
42192	8	9949	7	11	NULL	NULL	NULL	statement 1	Process		is similar to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_inorg-chem_45_16_16878967_s_7	16878967	A detailed kinetic studied revealed that nitrite binds to (P8+)FeIII(H2O)2  according to a dissociative mechanism, whereas nitrite binding to (P8+)FeIII(OH)(H2O)  at higher pH follows an associative mechanism, similar to that reported  for the binding of NO to these complexes.	bind
42193	9	9949	7	11	NULL	NULL	NULL	statement 3	Process		is similar to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_inorg-chem_45_16_16878967_s_7	16878967	A detailed kinetic studied revealed that nitrite binds to (P8+)FeIII(H2O)2  according to a dissociative mechanism, whereas nitrite binding to (P8+)FeIII(OH)(H2O)  at higher pH follows an associative mechanism, similar to that reported  for the binding of NO to these complexes.	bind
35086	1	9951	6	11	NULL	NULL	NULL	N-moesin	GP		is a type of					ERM protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35087	2	9951	6	11	NULL	NULL	NULL	N-ezrin	GP		is a type of					ERM protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35088	3	9951	6	11	NULL	NULL	NULL				bind			aa 487-503		N-moesin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35089	4	9951	6	11	NULL	NULL	NULL				bind			aa 487-503		N-ezrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35435	5	9951	6	11	NULL	NULL	NULL	N-moesin	GP		bind								S487A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35437	6	9951	6	11	NULL	NULL	NULL	statement 5	Process	affinity of	is less than					statement 3	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35438	7	9951	6	11	NULL	NULL	NULL	N-moesin	GP		bind								S489A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35440	8	9951	6	11	NULL	NULL	NULL	statement 7	Process	affinity of	is less than					statement 3	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35441	9	9951	6	11	NULL	NULL	NULL	N-moesin	GP		bind								S496A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35442	10	9951	6	11	NULL	NULL	NULL	statement 9	Process	affinity of	is less than					statement 3	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35444	11	9951	6	11	NULL	NULL	NULL	N-moesin	GP		bind								T497A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35445	12	9951	6	11	NULL	NULL	NULL	statement 11	Process	affinity of	is less than					statement 3	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35447	13	9951	6	11	NULL	NULL	NULL	N-ezrin	GP		bind								S487A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35448	14	9951	6	11	NULL	NULL	NULL	statement 13	Process	affinity of	is less than					statement 4	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35449	15	9951	6	11	NULL	NULL	NULL	N-ezrin	GP		bind								S489A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35451	16	9951	6	11	NULL	NULL	NULL	statement 15	Process	affinity of	is less than					statement 4	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35453	17	9951	6	11	NULL	NULL	NULL	N-ezrin	GP		bind								S496A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35454	18	9951	6	11	NULL	NULL	NULL	statement 17	Process	affinity of	is less than					statement 4	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35455	19	9951	6	11	NULL	NULL	NULL	N-ezrin	GP		bind								T497A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35456	20	9951	6	11	NULL	NULL	NULL	statement 19	Process	affinity of	is less than					statement 4	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35457	21	9951	6	11	NULL	NULL	NULL	N-ezrin	GP		bind								R493A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35458	22	9951	6	11	NULL	NULL	NULL	N-moesin	GP		bind								R493A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35459	23	9951	6	11	NULL	NULL	NULL	N-ezrin	GP		bind								S503A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
35461	24	9951	6	11	NULL	NULL	NULL	N-moesin	GP		bind								S503A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
42311	1	9951	7	11	NULL	NULL	NULL				bind			aa 487-503 		N-moesin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
42312	2	9951	7	11	NULL	NULL	NULL				bind			aa 487-503 		N-ezrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
42313	3	9951	7	11	NULL	NULL	NULL	N-moesin	GP		bind							point mutant	S487A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
42314	4	9951	7	11	NULL	NULL	NULL	N-moesin	GP		bind							point mutant	S489A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
42315	5	9951	7	11	NULL	NULL	NULL	N-moesin	GP		bind							point mutant	 S496A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
42316	6	9951	7	11	NULL	NULL	NULL	N-moesin	GP		bind							point mutant	T497A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
42317	7	9951	7	11	NULL	NULL	NULL	N-ezrin	GP		bind							point mutant	S487A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
42318	8	9951	7	11	NULL	NULL	NULL	N-ezrin	GP		bind							point mutant	S489A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
42319	9	9951	7	11	NULL	NULL	NULL	N-ezrin	GP		bind							point mutant	S496A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
42320	10	9951	7	11	NULL	NULL	NULL	N-ezrin	GP		bind							point mutant	T497A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
42321	11	9951	7	11	NULL	NULL	NULL	N-ezrin	GP		bind							point mutant	R493A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
42322	12	9951	7	11	NULL	NULL	NULL	N-ezrin	GP		bind							point mutant	S503A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
57602	13	9951	7	11	NULL	NULL	NULL	N-moesin	GP		bind							point mutant	R493A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
57603	14	9951	7	11	NULL	NULL	NULL	N-moesin	GP		bind							point mutant	S503A		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
57604	15	9951	7	11	NULL	NULL	NULL	statement 3	Process	affinity of	is lesser than					statement 1	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
57605	16	9951	7	11	NULL	NULL	NULL	statement 4	Process	affinity of	is lesser than					statement 1	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
57606	17	9951	7	11	NULL	NULL	NULL	statement 5	Process	affinity of	is lesser than					statement 1	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
57607	18	9951	7	11	NULL	NULL	NULL	statement 6	Process	affinity of	is lesser than					statement 1	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
57608	19	9951	7	11	NULL	NULL	NULL	statement 7	Process	affinity of	is lesser than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
57609	20	9951	7	11	NULL	NULL	NULL	statement 8	Process	affinity of	is lesser than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
57610	21	9951	7	11	NULL	NULL	NULL	statement 9	Process	affinity of	is lesser than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
57611	22	9951	7	11	NULL	NULL	NULL	statement 10	Process	affinity of	is lesser than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
57612	23	9951	7	11	NULL	NULL	NULL	N-moesin	GP		is a type of					ERM protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
57613	24	9951	7	11	NULL	NULL	NULL	N-ezrin	GP		is a type of					ERM protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10400_s_229	11784723	A detailed mutational analysis of this region (residues 487-503) showed that binding of N-moesin and N-ezrin to S487A, S489A, S496A, and T497A point mutations was reduced, whereas R493A and S503A mutants bound both ERM proteins at levels comparable with those of the wild type protein (Fig.  7,  A-C).	bind
34772	1	9952	6	11	NULL	NULL	NULL	Sir2 proteins	GP		mediates					nicotinamide	Chemical	clevage of 			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_23_8563_s_14	15150415	A detailed structural understanding of how the Sir2 proteins mediate nicotinamide cleavage and ADP-ribose transfer to acetate has been hampered by the difficulty in trapping a Sir2 protein bound to a form of NAD+ containing an ordered nicotinamide group ( ,  ,  ,  ).	bind
49030	2	9952	6	11	NULL	NULL	NULL	ADP-ribose	Chemical		is transfered to					acetate	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_23_8563_s_14	15150415	A detailed structural understanding of how the Sir2 proteins mediate nicotinamide cleavage and ADP-ribose transfer to acetate has been hampered by the difficulty in trapping a Sir2 protein bound to a form of NAD+ containing an ordered nicotinamide group ( ,  ,  ,  ).	bind
49031	3	9952	6	11	NULL	NULL	NULL	Sir2 proteins	GP		mediate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_23_8563_s_14	15150415	A detailed structural understanding of how the Sir2 proteins mediate nicotinamide cleavage and ADP-ribose transfer to acetate has been hampered by the difficulty in trapping a Sir2 protein bound to a form of NAD+ containing an ordered nicotinamide group ( ,  ,  ,  ).	bind
49032	4	9952	6	11	NULL	NULL	NULL	NAD+	Chemical		contains					nicotinamide group	Chemical	ordered			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_23_8563_s_14	15150415	A detailed structural understanding of how the Sir2 proteins mediate nicotinamide cleavage and ADP-ribose transfer to acetate has been hampered by the difficulty in trapping a Sir2 protein bound to a form of NAD+ containing an ordered nicotinamide group ( ,  ,  ,  ).	bind
49033	5	9952	6	11	NULL	NULL	NULL	Sir2 protein	GP		bind					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_23_8563_s_14	15150415	A detailed structural understanding of how the Sir2 proteins mediate nicotinamide cleavage and ADP-ribose transfer to acetate has been hampered by the difficulty in trapping a Sir2 protein bound to a form of NAD+ containing an ordered nicotinamide group ( ,  ,  ,  ).	bind
42323	1	9952	7	11	NULL	NULL	NULL	 Sir2 proteins	GP		mediate					nicotinamide	Chemical	cleavage of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_23_8563_s_14	15150415	A detailed structural understanding of how the Sir2 proteins mediate nicotinamide cleavage and ADP-ribose transfer to acetate has been hampered by the difficulty in trapping a Sir2 protein bound to a form of NAD+ containing an ordered nicotinamide group ( ,  ,  ,  ).	bind
42324	2	9952	7	11	NULL	NULL	NULL	 ADP-ribose	Chemical		is transfered to					acetate	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_23_8563_s_14	15150415	A detailed structural understanding of how the Sir2 proteins mediate nicotinamide cleavage and ADP-ribose transfer to acetate has been hampered by the difficulty in trapping a Sir2 protein bound to a form of NAD+ containing an ordered nicotinamide group ( ,  ,  ,  ).	bind
42325	3	9952	7	11	NULL	NULL	NULL	Sir2 proteins	GP		mediate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_23_8563_s_14	15150415	A detailed structural understanding of how the Sir2 proteins mediate nicotinamide cleavage and ADP-ribose transfer to acetate has been hampered by the difficulty in trapping a Sir2 protein bound to a form of NAD+ containing an ordered nicotinamide group ( ,  ,  ,  ).	bind
42326	5	9952	7	11	NULL	NULL	NULL	Sir2 protein	GP		bind					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_23_8563_s_14	15150415	A detailed structural understanding of how the Sir2 proteins mediate nicotinamide cleavage and ADP-ribose transfer to acetate has been hampered by the difficulty in trapping a Sir2 protein bound to a form of NAD+ containing an ordered nicotinamide group ( ,  ,  ,  ).	bind
49029	4	9952	7	11	NULL	NULL	NULL	NAD+	Chemical		contains					nicotinamide group	Chemical	ordered			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_23_8563_s_14	15150415	A detailed structural understanding of how the Sir2 proteins mediate nicotinamide cleavage and ADP-ribose transfer to acetate has been hampered by the difficulty in trapping a Sir2 protein bound to a form of NAD+ containing an ordered nicotinamide group ( ,  ,  ,  ).	bind
34773	1	9953	6	11	NULL	NULL	NULL	Cak1p	GP		bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_9_2545_s_366	9725911	A detailed study of the ATP-binding properties of Cak1p will be published elsewhere (Enke, Holmes, Kaldis, and Solomon).	bind
42327	1	9953	7	11	NULL	NULL	NULL	Cak1p	GP		bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_9_2545_s_366	9725911	A detailed study of the ATP-binding properties of Cak1p will be published elsewhere (Enke, Holmes, Kaldis, and Solomon).	bind
35090	1	9954	6	11	NULL	NULL	NULL	GM	GP		bind					Hsp90	GP		N-terminal ADP/ATP binding site		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_3_289_s_51	11306353	A detailed study of the mode of binding of GM (Protein Data Bank code 1YET), RD (code 1BGQ) and ADP (code 1AMW) to the Hsp90 N-terminal ADP/ATP binding site revealed several important factors to be considered in designing a molecule that would interact with this pocket: (1) a key interaction between the inhibitor and the Asp93/Ser52 at the base of the pocket, (2) interactions at the top involving Lys112, Lys58 and hydrogen acceptor functionalities on the inhibitor, (3) a hydrophobic pocket that lies midway in the binding site and that is constituted by Met98, Val150, Leu107, Leu103, Phe138 and Val186 (the amino acid numbering as in human Hsp90  ).	bind
35091	2	9954	6	11	NULL	NULL	NULL	RD	GP		bind					Hsp90	GP		N-terminal ADP/ATP binding site		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_3_289_s_51	11306353	A detailed study of the mode of binding of GM (Protein Data Bank code 1YET), RD (code 1BGQ) and ADP (code 1AMW) to the Hsp90 N-terminal ADP/ATP binding site revealed several important factors to be considered in designing a molecule that would interact with this pocket: (1) a key interaction between the inhibitor and the Asp93/Ser52 at the base of the pocket, (2) interactions at the top involving Lys112, Lys58 and hydrogen acceptor functionalities on the inhibitor, (3) a hydrophobic pocket that lies midway in the binding site and that is constituted by Met98, Val150, Leu107, Leu103, Phe138 and Val186 (the amino acid numbering as in human Hsp90  ).	bind
35092	3	9954	6	11	NULL	NULL	NULL	ADP	Chemical		bind					Hsp90	GP		N-terminal ADP/ATP binding site		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_3_289_s_51	11306353	A detailed study of the mode of binding of GM (Protein Data Bank code 1YET), RD (code 1BGQ) and ADP (code 1AMW) to the Hsp90 N-terminal ADP/ATP binding site revealed several important factors to be considered in designing a molecule that would interact with this pocket: (1) a key interaction between the inhibitor and the Asp93/Ser52 at the base of the pocket, (2) interactions at the top involving Lys112, Lys58 and hydrogen acceptor functionalities on the inhibitor, (3) a hydrophobic pocket that lies midway in the binding site and that is constituted by Met98, Val150, Leu107, Leu103, Phe138 and Val186 (the amino acid numbering as in human Hsp90  ).	bind
35466	4	9954	6	11	NULL	NULL	NULL	Hsp90	GP	human	constitute			Met98;; Val150;; Leu107;; Leu103;; Phe138;; Val186		HSP90	GP		hydrophobic pocket in N-terminal ADP/ATP binding site		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_3_289_s_51	11306353	A detailed study of the mode of binding of GM (Protein Data Bank code 1YET), RD (code 1BGQ) and ADP (code 1AMW) to the Hsp90 N-terminal ADP/ATP binding site revealed several important factors to be considered in designing a molecule that would interact with this pocket: (1) a key interaction between the inhibitor and the Asp93/Ser52 at the base of the pocket, (2) interactions at the top involving Lys112, Lys58 and hydrogen acceptor functionalities on the inhibitor, (3) a hydrophobic pocket that lies midway in the binding site and that is constituted by Met98, Val150, Leu107, Leu103, Phe138 and Val186 (the amino acid numbering as in human Hsp90  ).	bind
42328	1	9954	7	11	NULL	NULL	NULL	GM	GP		bind					 Hsp90	GP		N-terminal ADP/ATP binding site		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_3_289_s_51	11306353	A detailed study of the mode of binding of GM (Protein Data Bank code 1YET), RD (code 1BGQ) and ADP (code 1AMW) to the Hsp90 N-terminal ADP/ATP binding site revealed several important factors to be considered in designing a molecule that would interact with this pocket: (1) a key interaction between the inhibitor and the Asp93/Ser52 at the base of the pocket, (2) interactions at the top involving Lys112, Lys58 and hydrogen acceptor functionalities on the inhibitor, (3) a hydrophobic pocket that lies midway in the binding site and that is constituted by Met98, Val150, Leu107, Leu103, Phe138 and Val186 (the amino acid numbering as in human Hsp90  ).	bind
42329	2	9954	7	11	NULL	NULL	NULL	RD	GP		bind					Hsp90	GP		N-terminal ADP/ATP binding site		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_3_289_s_51	11306353	A detailed study of the mode of binding of GM (Protein Data Bank code 1YET), RD (code 1BGQ) and ADP (code 1AMW) to the Hsp90 N-terminal ADP/ATP binding site revealed several important factors to be considered in designing a molecule that would interact with this pocket: (1) a key interaction between the inhibitor and the Asp93/Ser52 at the base of the pocket, (2) interactions at the top involving Lys112, Lys58 and hydrogen acceptor functionalities on the inhibitor, (3) a hydrophobic pocket that lies midway in the binding site and that is constituted by Met98, Val150, Leu107, Leu103, Phe138 and Val186 (the amino acid numbering as in human Hsp90  ).	bind
42330	3	9954	7	11	NULL	NULL	NULL	ADP	Chemical		bind					Hsp90	GP		N-terminal ADP/ATP binding site		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_3_289_s_51	11306353	A detailed study of the mode of binding of GM (Protein Data Bank code 1YET), RD (code 1BGQ) and ADP (code 1AMW) to the Hsp90 N-terminal ADP/ATP binding site revealed several important factors to be considered in designing a molecule that would interact with this pocket: (1) a key interaction between the inhibitor and the Asp93/Ser52 at the base of the pocket, (2) interactions at the top involving Lys112, Lys58 and hydrogen acceptor functionalities on the inhibitor, (3) a hydrophobic pocket that lies midway in the binding site and that is constituted by Met98, Val150, Leu107, Leu103, Phe138 and Val186 (the amino acid numbering as in human Hsp90  ).	bind
42344	4	9954	7	11	NULL	NULL	NULL	Hsp90	GP	human	constitute			Met98;;Val150;;Leu107;;Leu103;;Phe138;;Val186		Hsp90	GP		hydrophobic pocket in N-terminal ADP/ATPbinding site		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_3_289_s_51	11306353	A detailed study of the mode of binding of GM (Protein Data Bank code 1YET), RD (code 1BGQ) and ADP (code 1AMW) to the Hsp90 N-terminal ADP/ATP binding site revealed several important factors to be considered in designing a molecule that would interact with this pocket: (1) a key interaction between the inhibitor and the Asp93/Ser52 at the base of the pocket, (2) interactions at the top involving Lys112, Lys58 and hydrogen acceptor functionalities on the inhibitor, (3) a hydrophobic pocket that lies midway in the binding site and that is constituted by Met98, Val150, Leu107, Leu103, Phe138 and Val186 (the amino acid numbering as in human Hsp90  ).	bind
34774	1	9955	6	11	NULL	NULL	NULL	E.coli	Organism	P-fimbriated	bind					uroepithelial cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_microbesinfect_8_3_938_s_47	16460984	A detailed study using a different inhibitor of GlcCer synthase,  N-butyl deoxynojirimycin (an N-butylated amino sugar-like compound), also blockaded  P-fimbriated  E. coli binding to human uroepithelial cells   [15].	bind
34775	2	9955	6	11	NULL	NULL	NULL	N-butyl deoxynojirimycin	Chemical		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_microbesinfect_8_3_938_s_47	16460984	A detailed study using a different inhibitor of GlcCer synthase,  N-butyl deoxynojirimycin (an N-butylated amino sugar-like compound), also blockaded  P-fimbriated  E. coli binding to human uroepithelial cells   [15].	bind
34776	3	9955	6	11	NULL	NULL	NULL	N-butyl deoxynojirimycin	Chemical		is an					N-butylated amino sugar-like compound	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_microbesinfect_8_3_938_s_47	16460984	A detailed study using a different inhibitor of GlcCer synthase,  N-butyl deoxynojirimycin (an N-butylated amino sugar-like compound), also blockaded  P-fimbriated  E. coli binding to human uroepithelial cells   [15].	bind
49034	4	9955	6	11	NULL	NULL	NULL	N-butyl deoxynojirimycin	Chemical		is an inhibitor of					GlcCer synthase	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbesinfect_8_3_938_s_47	16460984	A detailed study using a different inhibitor of GlcCer synthase,  N-butyl deoxynojirimycin (an N-butylated amino sugar-like compound), also blockaded  P-fimbriated  E. coli binding to human uroepithelial cells   [15].	bind
42354	1	9955	7	11	NULL	NULL	NULL	E. coli	Organism	P-fimbriated	bind					uroepithelial cells	Cell	human			NULL		NULL	NULL	NULL	NULL	gw70_microbesinfect_8_3_938_s_47	16460984	A detailed study using a different inhibitor of GlcCer synthase,  N-butyl deoxynojirimycin (an N-butylated amino sugar-like compound), also blockaded  P-fimbriated  E. coli binding to human uroepithelial cells   [15].	bind
42355	2	9955	7	11	NULL	NULL	NULL	N-butyl deoxynojirimycin	Chemical		is an inhibitor of					GlcCer synthase	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbesinfect_8_3_938_s_47	16460984	A detailed study using a different inhibitor of GlcCer synthase,  N-butyl deoxynojirimycin (an N-butylated amino sugar-like compound), also blockaded  P-fimbriated  E. coli binding to human uroepithelial cells   [15].	bind
42356	3	9955	7	11	NULL	NULL	NULL	N-butyl deoxynojirimycin	Chemical		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_microbesinfect_8_3_938_s_47	16460984	A detailed study using a different inhibitor of GlcCer synthase,  N-butyl deoxynojirimycin (an N-butylated amino sugar-like compound), also blockaded  P-fimbriated  E. coli binding to human uroepithelial cells   [15].	bind
42357	4	9955	7	11	NULL	NULL	NULL	N-butyl deoxynojirimycin	Chemical		is					N-butylated amino sugar-like compound	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_microbesinfect_8_3_938_s_47	16460984	A detailed study using a different inhibitor of GlcCer synthase,  N-butyl deoxynojirimycin (an N-butylated amino sugar-like compound), also blockaded  P-fimbriated  E. coli binding to human uroepithelial cells   [15].	bind
34777	1	9956	6	11	NULL	NULL	NULL	PYY	GP	125I-labeled	is an agonist of		potent	3-36		Y2	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_115_4_1035_s_148	12453477	A detailed Y2-binding study of  Schwarzer et al. (1998) demonstrated that [125]PYY 3-36 is a potent Y2 agonist with much less affinities for Y1, Y4 and Y5 receptors, indicating that this ligand may bind mainly to Y2 receptors.	bind
34778	2	9956	6	11	NULL	NULL	NULL	PYY 	GP	125I-labeled	bind		mainly;;may	3-36		Y2 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_115_4_1035_s_148	12453477	A detailed Y2-binding study of  Schwarzer et al. (1998) demonstrated that [125]PYY 3-36 is a potent Y2 agonist with much less affinities for Y1, Y4 and Y5 receptors, indicating that this ligand may bind mainly to Y2 receptors.	bind
34779	3	9956	6	11	NULL	NULL	NULL	PYY	GP	125I-labeled	affinity for		less	3-36		Y1 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_115_4_1035_s_148	12453477	A detailed Y2-binding study of  Schwarzer et al. (1998) demonstrated that [125]PYY 3-36 is a potent Y2 agonist with much less affinities for Y1, Y4 and Y5 receptors, indicating that this ligand may bind mainly to Y2 receptors.	bind
34780	4	9956	6	11	NULL	NULL	NULL	PYY	GP	125I-labeled	affinity for		less	3-36		Y4 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_115_4_1035_s_148	12453477	A detailed Y2-binding study of  Schwarzer et al. (1998) demonstrated that [125]PYY 3-36 is a potent Y2 agonist with much less affinities for Y1, Y4 and Y5 receptors, indicating that this ligand may bind mainly to Y2 receptors.	bind
34781	5	9956	6	11	NULL	NULL	NULL	PYY	GP	125I-labeled	affinity for		less	3-36		Y5 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_115_4_1035_s_148	12453477	A detailed Y2-binding study of  Schwarzer et al. (1998) demonstrated that [125]PYY 3-36 is a potent Y2 agonist with much less affinities for Y1, Y4 and Y5 receptors, indicating that this ligand may bind mainly to Y2 receptors.	bind
42358	1	9956	7	11	NULL	NULL	NULL	PYY	GP	125I-labeled	is an agonist of		potent	3-36		Y2	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_115_4_1035_s_148	12453477	A detailed Y2-binding study of  Schwarzer et al. (1998) demonstrated that [125]PYY 3-36 is a potent Y2 agonist with much less affinities for Y1, Y4 and Y5 receptors, indicating that this ligand may bind mainly to Y2 receptors.	bind
42359	2	9956	7	11	NULL	NULL	NULL	PYY	GP	125I-labeled	affinity for		less	3-36		Y1 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_115_4_1035_s_148	12453477	A detailed Y2-binding study of  Schwarzer et al. (1998) demonstrated that [125]PYY 3-36 is a potent Y2 agonist with much less affinities for Y1, Y4 and Y5 receptors, indicating that this ligand may bind mainly to Y2 receptors.	bind
42360	3	9956	7	11	NULL	NULL	NULL	PYY	GP	125I-labeled	affinity for		less	3-36		Y4 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_115_4_1035_s_148	12453477	A detailed Y2-binding study of  Schwarzer et al. (1998) demonstrated that [125]PYY 3-36 is a potent Y2 agonist with much less affinities for Y1, Y4 and Y5 receptors, indicating that this ligand may bind mainly to Y2 receptors.	bind
42362	4	9956	7	11	NULL	NULL	NULL	PYY	GP	125I-labeled	affinity for		less	3-36		Y5 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_115_4_1035_s_148	12453477	A detailed Y2-binding study of  Schwarzer et al. (1998) demonstrated that [125]PYY 3-36 is a potent Y2 agonist with much less affinities for Y1, Y4 and Y5 receptors, indicating that this ligand may bind mainly to Y2 receptors.	bind
42363	5	9956	7	11	NULL	NULL	NULL	PYY	GP	125I-labeled	bind		mainly;;may	3-36		Y2 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_115_4_1035_s_148	12453477	A detailed Y2-binding study of  Schwarzer et al. (1998) demonstrated that [125]PYY 3-36 is a potent Y2 agonist with much less affinities for Y1, Y4 and Y5 receptors, indicating that this ligand may bind mainly to Y2 receptors.	bind
34782	1	9957	6	11	NULL	NULL	NULL	ARF	GP		bind					GST-NCS-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_7_6047_s_106	15576365	A detectable signal was observed only for ARF1 binding to GST-NCS-1 in the presence  of free Ca2+.	bind
34783	2	9957	6	11	NULL	NULL	NULL	statement 1	Process		in the presence of					Ca2+	Chemical	free			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_7_6047_s_106	15576365	A detectable signal was observed only for ARF1 binding to GST-NCS-1 in the presence  of free Ca2+.	bind
42372	1	9957	7	11	NULL	NULL	NULL	 ARF1	GP		binds					GST-NCS-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_7_6047_s_106	15576365	A detectable signal was observed only for ARF1 binding to GST-NCS-1 in the presence  of free Ca2+.	bind
42373	2	9957	7	11	NULL	NULL	NULL	statement 1	Process		in the presence of					Ca2+	Chemical	free			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_7_6047_s_106	15576365	A detectable signal was observed only for ARF1 binding to GST-NCS-1 in the presence  of free Ca2+.	bind
34784	1	9959	6	11	NULL	NULL	NULL	determinant linked to CLA	GP		bind					E-selectin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_22_12899_s_25	14566059	A determinant linked to cutaneous lymphocyte-associated antigen (CLA) ( ) binds to E-selectin to assist lymphocyte trafficking to skin.	bind
34785	2	9959	6	11	NULL	NULL	NULL	CLA	GP		is					cutaneous lymphocyte-associated antigen	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_22_12899_s_25	14566059	A determinant linked to cutaneous lymphocyte-associated antigen (CLA) ( ) binds to E-selectin to assist lymphocyte trafficking to skin.	bind
34786	3	9959	6	11	NULL	NULL	NULL	lymphocyte	Cell		is trafficked to					skin	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_22_12899_s_25	14566059	A determinant linked to cutaneous lymphocyte-associated antigen (CLA) ( ) binds to E-selectin to assist lymphocyte trafficking to skin.	bind
49535	4	9959	6	11	NULL	NULL	NULL	statement 1	Process		assist					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_22_12899_s_25	14566059	A determinant linked to cutaneous lymphocyte-associated antigen (CLA) ( ) binds to E-selectin to assist lymphocyte trafficking to skin.	bind
42376	1	9959	7	11	NULL	NULL	NULL	 determinant linked to CLA	GP		binds to					E-selectin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_22_12899_s_25	14566059	A determinant linked to cutaneous lymphocyte-associated antigen (CLA) ( ) binds to E-selectin to assist lymphocyte trafficking to skin.	bind
42377	2	9959	7	11	NULL	NULL	NULL	lymphocyte	Cell		is trafficked to					skin	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_22_12899_s_25	14566059	A determinant linked to cutaneous lymphocyte-associated antigen (CLA) ( ) binds to E-selectin to assist lymphocyte trafficking to skin.	bind
42378	3	9959	7	11	NULL	NULL	NULL	statement 1	Process		assist					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_22_12899_s_25	14566059	A determinant linked to cutaneous lymphocyte-associated antigen (CLA) ( ) binds to E-selectin to assist lymphocyte trafficking to skin.	bind
42379	4	9959	7	11	NULL	NULL	NULL	CLA	GP		is					cutaneous lymphocyte-associated antigen	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_22_12899_s_25	14566059	A determinant linked to cutaneous lymphocyte-associated antigen (CLA) ( ) binds to E-selectin to assist lymphocyte trafficking to skin.	bind
34962	1	9960	6	11	NULL	NULL	NULL	DGK-zeta	GP	mutant	mimics							phosphorylation of	MARCKS domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7289_s_12	16055737	A DGK-zeta mutant that mimics phosphorylation of the MARCKS domain was unable to bind an activated Rac1 mutant (Rac1V12) and phorbol myristate acetate-induced protein kinase C activation inhibited the interaction of DGK-zeta with Rac1V12, suggesting protein kinase C-mediated phosphorylation of the MARCKS domain negatively regulates DGK-zeta binding to active Rac1.	bind
34963	2	9960	6	11	NULL	NULL	NULL	DGK-zeta	GP	mutant	does not bind					Rac1	GP	activated;; mutant			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7289_s_12	16055737	A DGK-zeta mutant that mimics phosphorylation of the MARCKS domain was unable to bind an activated Rac1 mutant (Rac1V12) and phorbol myristate acetate-induced protein kinase C activation inhibited the interaction of DGK-zeta with Rac1V12, suggesting protein kinase C-mediated phosphorylation of the MARCKS domain negatively regulates DGK-zeta binding to active Rac1.	bind
34964	3	9960	6	11	NULL	NULL	NULL	DGK-zeta	GP		interacts with					Rac1V12	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7289_s_12	16055737	A DGK-zeta mutant that mimics phosphorylation of the MARCKS domain was unable to bind an activated Rac1 mutant (Rac1V12) and phorbol myristate acetate-induced protein kinase C activation inhibited the interaction of DGK-zeta with Rac1V12, suggesting protein kinase C-mediated phosphorylation of the MARCKS domain negatively regulates DGK-zeta binding to active Rac1.	bind
34965	4	9960	6	11	NULL	NULL	NULL	protein kinase C	GP	activation of	is induced by					phorbol myristate acetate	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7289_s_12	16055737	A DGK-zeta mutant that mimics phosphorylation of the MARCKS domain was unable to bind an activated Rac1 mutant (Rac1V12) and phorbol myristate acetate-induced protein kinase C activation inhibited the interaction of DGK-zeta with Rac1V12, suggesting protein kinase C-mediated phosphorylation of the MARCKS domain negatively regulates DGK-zeta binding to active Rac1.	bind
34966	5	9960	6	11	NULL	NULL	NULL	statement 4	Process		inhibits					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7289_s_12	16055737	A DGK-zeta mutant that mimics phosphorylation of the MARCKS domain was unable to bind an activated Rac1 mutant (Rac1V12) and phorbol myristate acetate-induced protein kinase C activation inhibited the interaction of DGK-zeta with Rac1V12, suggesting protein kinase C-mediated phosphorylation of the MARCKS domain negatively regulates DGK-zeta binding to active Rac1.	bind
34967	6	9960	6	11	NULL	NULL	NULL			phosphorylation of	is mediated by			MARCKS domain		protein kinase C	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7289_s_12	16055737	A DGK-zeta mutant that mimics phosphorylation of the MARCKS domain was unable to bind an activated Rac1 mutant (Rac1V12) and phorbol myristate acetate-induced protein kinase C activation inhibited the interaction of DGK-zeta with Rac1V12, suggesting protein kinase C-mediated phosphorylation of the MARCKS domain negatively regulates DGK-zeta binding to active Rac1.	bind
34968	7	9960	6	11	NULL	NULL	NULL	DGK-zeta	GP		bind					Rac1	GP	active			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7289_s_12	16055737	A DGK-zeta mutant that mimics phosphorylation of the MARCKS domain was unable to bind an activated Rac1 mutant (Rac1V12) and phorbol myristate acetate-induced protein kinase C activation inhibited the interaction of DGK-zeta with Rac1V12, suggesting protein kinase C-mediated phosphorylation of the MARCKS domain negatively regulates DGK-zeta binding to active Rac1.	bind
34969	8	9960	6	11	NULL	NULL	NULL	statement 6	Process		regulates		negatively			statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7289_s_12	16055737	A DGK-zeta mutant that mimics phosphorylation of the MARCKS domain was unable to bind an activated Rac1 mutant (Rac1V12) and phorbol myristate acetate-induced protein kinase C activation inhibited the interaction of DGK-zeta with Rac1V12, suggesting protein kinase C-mediated phosphorylation of the MARCKS domain negatively regulates DGK-zeta binding to active Rac1.	bind
49035	9	9960	6	11	NULL	NULL	NULL	Rac1V12	GP		is					activated Rac1 mutant	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7289_s_12	16055737	A DGK-zeta mutant that mimics phosphorylation of the MARCKS domain was unable to bind an activated Rac1 mutant (Rac1V12) and phorbol myristate acetate-induced protein kinase C activation inhibited the interaction of DGK-zeta with Rac1V12, suggesting protein kinase C-mediated phosphorylation of the MARCKS domain negatively regulates DGK-zeta binding to active Rac1.	bind
42381	1	9960	7	11	NULL	NULL	NULL	DGK-zeta	GP	mutant	mimics							phosphorylation of	MARCKS domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7289_s_12	16055737	A DGK-zeta mutant that mimics phosphorylation of the MARCKS domain was unable to bind an activated Rac1 mutant (Rac1V12) and phorbol myristate acetate-induced protein kinase C activation inhibited the interaction of DGK-zeta with Rac1V12, suggesting protein kinase C-mediated phosphorylation of the MARCKS domain negatively regulates DGK-zeta binding to active Rac1.	bind
42382	2	9960	7	11	NULL	NULL	NULL	statement 1	GP		does not bind					Rac1	GP	activated;;mutant			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7289_s_12	16055737	A DGK-zeta mutant that mimics phosphorylation of the MARCKS domain was unable to bind an activated Rac1 mutant (Rac1V12) and phorbol myristate acetate-induced protein kinase C activation inhibited the interaction of DGK-zeta with Rac1V12, suggesting protein kinase C-mediated phosphorylation of the MARCKS domain negatively regulates DGK-zeta binding to active Rac1.	bind
42383	3	9960	7	11	NULL	NULL	NULL	phorbol myristate acetate	Chemical		induce					protein kinase C 	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7289_s_12	16055737	A DGK-zeta mutant that mimics phosphorylation of the MARCKS domain was unable to bind an activated Rac1 mutant (Rac1V12) and phorbol myristate acetate-induced protein kinase C activation inhibited the interaction of DGK-zeta with Rac1V12, suggesting protein kinase C-mediated phosphorylation of the MARCKS domain negatively regulates DGK-zeta binding to active Rac1.	bind
42384	4	9960	7	11	NULL	NULL	NULL	DGK-zeta	GP		interacts with					Rac1V12	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7289_s_12	16055737	A DGK-zeta mutant that mimics phosphorylation of the MARCKS domain was unable to bind an activated Rac1 mutant (Rac1V12) and phorbol myristate acetate-induced protein kinase C activation inhibited the interaction of DGK-zeta with Rac1V12, suggesting protein kinase C-mediated phosphorylation of the MARCKS domain negatively regulates DGK-zeta binding to active Rac1.	bind
42385	5	9960	7	11	NULL	NULL	NULL	statement 3	Process		inhibits					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7289_s_12	16055737	A DGK-zeta mutant that mimics phosphorylation of the MARCKS domain was unable to bind an activated Rac1 mutant (Rac1V12) and phorbol myristate acetate-induced protein kinase C activation inhibited the interaction of DGK-zeta with Rac1V12, suggesting protein kinase C-mediated phosphorylation of the MARCKS domain negatively regulates DGK-zeta binding to active Rac1.	bind
42386	6	9960	7	11	NULL	NULL	NULL	 protein kinase C	GP		mediates							phosphorylation of	MARCKS domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7289_s_12	16055737	A DGK-zeta mutant that mimics phosphorylation of the MARCKS domain was unable to bind an activated Rac1 mutant (Rac1V12) and phorbol myristate acetate-induced protein kinase C activation inhibited the interaction of DGK-zeta with Rac1V12, suggesting protein kinase C-mediated phosphorylation of the MARCKS domain negatively regulates DGK-zeta binding to active Rac1.	bind
42387	7	9960	7	11	NULL	NULL	NULL	DGK-zeta	GP		bind					Rac1	GP	active			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7289_s_12	16055737	A DGK-zeta mutant that mimics phosphorylation of the MARCKS domain was unable to bind an activated Rac1 mutant (Rac1V12) and phorbol myristate acetate-induced protein kinase C activation inhibited the interaction of DGK-zeta with Rac1V12, suggesting protein kinase C-mediated phosphorylation of the MARCKS domain negatively regulates DGK-zeta binding to active Rac1.	bind
42388	8	9960	7	11	NULL	NULL	NULL	statement 6	Process		regulates		negatively			statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7289_s_12	16055737	A DGK-zeta mutant that mimics phosphorylation of the MARCKS domain was unable to bind an activated Rac1 mutant (Rac1V12) and phorbol myristate acetate-induced protein kinase C activation inhibited the interaction of DGK-zeta with Rac1V12, suggesting protein kinase C-mediated phosphorylation of the MARCKS domain negatively regulates DGK-zeta binding to active Rac1.	bind
42389	9	9960	7	11	NULL	NULL	NULL	statement 5	Process		suggests					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7289_s_12	16055737	A DGK-zeta mutant that mimics phosphorylation of the MARCKS domain was unable to bind an activated Rac1 mutant (Rac1V12) and phorbol myristate acetate-induced protein kinase C activation inhibited the interaction of DGK-zeta with Rac1V12, suggesting protein kinase C-mediated phosphorylation of the MARCKS domain negatively regulates DGK-zeta binding to active Rac1.	bind
42390	10	9960	7	11	NULL	NULL	NULL	Rac1V12	GP		is					activated Rac1 mutant	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7289_s_12	16055737	A DGK-zeta mutant that mimics phosphorylation of the MARCKS domain was unable to bind an activated Rac1 mutant (Rac1V12) and phorbol myristate acetate-induced protein kinase C activation inhibited the interaction of DGK-zeta with Rac1V12, suggesting protein kinase C-mediated phosphorylation of the MARCKS domain negatively regulates DGK-zeta binding to active Rac1.	bind
34970	1	9961	6	11	NULL	NULL	NULL	C-Raf1	GP		bind					Nef	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_25_15727_s_111	9624170	A Di-aspartic Acid Motif Is Critical for C-Raf1 Binding to Nef-- Since the carboxyl-terminal end of the Nef sequence deleted from the GST-delta41Nef fusion protein above, Leu-His-Pro-Val-Ser-Leu-His-Gly-Met-Asp-Asp-Pro-Glu (amino acids 165-177), also contains the highly conserved pair of aspartic acid residues (positions 174 and 175), we investigated the contributions of this pair of acidic residues to binding of the c-Raf1 protein  in vitro.	bind
34971	2	9961	6	11	NULL	NULL	NULL				is critical for			Di-aspartic Acid Motif 		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_25_15727_s_111	9624170	A Di-aspartic Acid Motif Is Critical for C-Raf1 Binding to Nef-- Since the carboxyl-terminal end of the Nef sequence deleted from the GST-delta41Nef fusion protein above, Leu-His-Pro-Val-Ser-Leu-His-Gly-Met-Asp-Asp-Pro-Glu (amino acids 165-177), also contains the highly conserved pair of aspartic acid residues (positions 174 and 175), we investigated the contributions of this pair of acidic residues to binding of the c-Raf1 protein  in vitro.	bind
42391	1	9961	7	11	NULL	NULL	NULL	C-Raf1	GP		bind					Nef	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_25_15727_s_111	9624170	A Di-aspartic Acid Motif Is Critical for C-Raf1 Binding to Nef-- Since the carboxyl-terminal end of the Nef sequence deleted from the GST-delta41Nef fusion protein above, Leu-His-Pro-Val-Ser-Leu-His-Gly-Met-Asp-Asp-Pro-Glu (amino acids 165-177), also contains the highly conserved pair of aspartic acid residues (positions 174 and 175), we investigated the contributions of this pair of acidic residues to binding of the c-Raf1 protein  in vitro.	bind
42392	2	9961	7	11	NULL	NULL	NULL	Nef	GP		is critical for			Di-aspartic Acid Motif		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_25_15727_s_111	9624170	A Di-aspartic Acid Motif Is Critical for C-Raf1 Binding to Nef-- Since the carboxyl-terminal end of the Nef sequence deleted from the GST-delta41Nef fusion protein above, Leu-His-Pro-Val-Ser-Leu-His-Gly-Met-Asp-Asp-Pro-Glu (amino acids 165-177), also contains the highly conserved pair of aspartic acid residues (positions 174 and 175), we investigated the contributions of this pair of acidic residues to binding of the c-Raf1 protein  in vitro.	bind
34787	1	9962	6	11	NULL	NULL	NULL	DAB p3S5	GP		bind								KDR domain 1		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_19_14321_s_185	10799512	A diabody, DAB p3S5, which binds to KDR domain 1, was used in all ELISA to demonstrate the functional expression of the variant proteins and to normalize the amounts of protein added in the assay.	bind
49036	2	9962	6	11	NULL	NULL	NULL	DAB p3S5	GP		is a type of					diabody	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_19_14321_s_185	10799512	A diabody, DAB p3S5, which binds to KDR domain 1, was used in all ELISA to demonstrate the functional expression of the variant proteins and to normalize the amounts of protein added in the assay.	bind
42398	1	9962	7	11	NULL	NULL	NULL	DAB p3S5	GP		binds to								KDR domain 1		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_19_14321_s_185	10799512	A diabody, DAB p3S5, which binds to KDR domain 1, was used in all ELISA to demonstrate the functional expression of the variant proteins and to normalize the amounts of protein added in the assay.	bind
42399	2	9962	7	11	NULL	NULL	NULL	DAB p3S5	GP		is a type of					diabody	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_19_14321_s_185	10799512	A diabody, DAB p3S5, which binds to KDR domain 1, was used in all ELISA to demonstrate the functional expression of the variant proteins and to normalize the amounts of protein added in the assay.	bind
34788	1	9964	6	11	NULL	NULL	NULL	cortisol	Chemical		bind					hCBG	GP	native			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-mol-model-(online)_9_3_12733052_s_14	12733052	A difference accessible surface area (DASA) study revealed that cortisol  binds with the native hCBG more tightly than aldosterone.	bind
34789	2	9964	6	11	NULL	NULL	NULL	aldosterone	Chemical		bind					hCBG	GP	native			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-mol-model-(online)_9_3_12733052_s_14	12733052	A difference accessible surface area (DASA) study revealed that cortisol  binds with the native hCBG more tightly than aldosterone.	bind
34790	3	9964	6	11	NULL	NULL	NULL	statement 1	Process		more tightly than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-mol-model-(online)_9_3_12733052_s_14	12733052	A difference accessible surface area (DASA) study revealed that cortisol  binds with the native hCBG more tightly than aldosterone.	bind
42401	1	9964	7	11	NULL	NULL	NULL	cortisol	Chemical		binds					hCBG	GP	native			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-mol-model-(online)_9_3_12733052_s_14	12733052	A difference accessible surface area (DASA) study revealed that cortisol  binds with the native hCBG more tightly than aldosterone.	bind
42402	2	9964	7	11	NULL	NULL	NULL	aldosterone	Chemical		binds					hCBG	GP	native			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-mol-model-(online)_9_3_12733052_s_14	12733052	A difference accessible surface area (DASA) study revealed that cortisol  binds with the native hCBG more tightly than aldosterone.	bind
42403	3	9964	7	11	NULL	NULL	NULL	statement 1	Process		more tightly than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-mol-model-(online)_9_3_12733052_s_14	12733052	A difference accessible surface area (DASA) study revealed that cortisol  binds with the native hCBG more tightly than aldosterone.	bind
34791	1	9965	6	11	NULL	NULL	NULL	MTSET	Chemical		plays a role in					CFT	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1608_s_195	10636852	A difference between the effects of the reagents on binding and transport is that the reaction of MTSET with Cys-90 or Cys-306 decreased the  K d of [3]CFT binding, whereas it increased the  Vmax of DA uptake.	bind
34792	2	9965	6	11	NULL	NULL	NULL	MTSET	Chemical		plays a role in					DA 	Chemical	uptake of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1608_s_195	10636852	A difference between the effects of the reagents on binding and transport is that the reaction of MTSET with Cys-90 or Cys-306 decreased the  K d of [3]CFT binding, whereas it increased the  Vmax of DA uptake.	bind
42407	1	9965	7	11	NULL	NULL	NULL	MTSET	Chemical		plays a role in					CFT	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1608_s_195	10636852	A difference between the effects of the reagents on binding and transport is that the reaction of MTSET with Cys-90 or Cys-306 decreased the  K d of [3]CFT binding, whereas it increased the  Vmax of DA uptake.	bind
42408	2	9965	7	11	NULL	NULL	NULL	MTSET	Chemical		plays a role in					DA	Chemical	uptake of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_3_1608_s_195	10636852	A difference between the effects of the reagents on binding and transport is that the reaction of MTSET with Cys-90 or Cys-306 decreased the  K d of [3]CFT binding, whereas it increased the  Vmax of DA uptake.	bind
34793	1	9966	6	11	NULL	NULL	NULL	band 3 tetramers	GP		promotes					cytoskeleton	CellComponent	binding of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_20_11771_s_113	11573011	A difference between the manner in which BS3 and DIDS act on band 3 is that the former shifts the band 3 population toward tetramers ( 25), which promotes cytoskeleton binding through band 3 binding with ankyrin, whereas the latter shifts the population of band 3 to dimers, which weakens cytoskeleton binding ( 26).	bind
34794	2	9966	6	11	NULL	NULL	NULL	band 3	GP		bind					ankyrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_20_11771_s_113	11573011	A difference between the manner in which BS3 and DIDS act on band 3 is that the former shifts the band 3 population toward tetramers ( 25), which promotes cytoskeleton binding through band 3 binding with ankyrin, whereas the latter shifts the population of band 3 to dimers, which weakens cytoskeleton binding ( 26).	bind
34795	3	9966	6	11	NULL	NULL	NULL	statement 1	Process		occurs through					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_20_11771_s_113	11573011	A difference between the manner in which BS3 and DIDS act on band 3 is that the former shifts the band 3 population toward tetramers ( 25), which promotes cytoskeleton binding through band 3 binding with ankyrin, whereas the latter shifts the population of band 3 to dimers, which weakens cytoskeleton binding ( 26).	bind
34796	4	9966	6	11	NULL	NULL	NULL	BS3	Chemical		increases 					band-3 tetramers	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_20_11771_s_113	11573011	A difference between the manner in which BS3 and DIDS act on band 3 is that the former shifts the band 3 population toward tetramers ( 25), which promotes cytoskeleton binding through band 3 binding with ankyrin, whereas the latter shifts the population of band 3 to dimers, which weakens cytoskeleton binding ( 26).	bind
34797	5	9966	6	11	NULL	NULL	NULL	DIDS	Chemical		promotes					band-3 dimers	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_20_11771_s_113	11573011	A difference between the manner in which BS3 and DIDS act on band 3 is that the former shifts the band 3 population toward tetramers ( 25), which promotes cytoskeleton binding through band 3 binding with ankyrin, whereas the latter shifts the population of band 3 to dimers, which weakens cytoskeleton binding ( 26).	bind
34798	6	9966	6	11	NULL	NULL	NULL	band 3 dimers	GP		weakens					cytoskeleton	CellComponent	binding of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_20_11771_s_113	11573011	A difference between the manner in which BS3 and DIDS act on band 3 is that the former shifts the band 3 population toward tetramers ( 25), which promotes cytoskeleton binding through band 3 binding with ankyrin, whereas the latter shifts the population of band 3 to dimers, which weakens cytoskeleton binding ( 26).	bind
42414	1	9966	7	11	NULL	NULL	NULL	band 3 tetramers	GP		promotes					cytoskeleton	CellComponent	binding of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_20_11771_s_113	11573011	A difference between the manner in which BS3 and DIDS act on band 3 is that the former shifts the band 3 population toward tetramers ( 25), which promotes cytoskeleton binding through band 3 binding with ankyrin, whereas the latter shifts the population of band 3 to dimers, which weakens cytoskeleton binding ( 26).	bind
42416	2	9966	7	11	NULL	NULL	NULL	band 3	GP		bind					ankyrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_20_11771_s_113	11573011	A difference between the manner in which BS3 and DIDS act on band 3 is that the former shifts the band 3 population toward tetramers ( 25), which promotes cytoskeleton binding through band 3 binding with ankyrin, whereas the latter shifts the population of band 3 to dimers, which weakens cytoskeleton binding ( 26).	bind
49044	3	9966	7	11	NULL	NULL	NULL	statement 1	Process		occurs through					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_20_11771_s_113	11573011	A difference between the manner in which BS3 and DIDS act on band 3 is that the former shifts the band 3 population toward tetramers ( 25), which promotes cytoskeleton binding through band 3 binding with ankyrin, whereas the latter shifts the population of band 3 to dimers, which weakens cytoskeleton binding ( 26).	bind
49045	4	9966	7	11	NULL	NULL	NULL	BS3	Chemical		increases					band-3 tetramers	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_20_11771_s_113	11573011	A difference between the manner in which BS3 and DIDS act on band 3 is that the former shifts the band 3 population toward tetramers ( 25), which promotes cytoskeleton binding through band 3 binding with ankyrin, whereas the latter shifts the population of band 3 to dimers, which weakens cytoskeleton binding ( 26).	bind
49046	5	9966	7	11	NULL	NULL	NULL	DIDS	Chemical		promotes					band-3 dimers	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_20_11771_s_113	11573011	A difference between the manner in which BS3 and DIDS act on band 3 is that the former shifts the band 3 population toward tetramers ( 25), which promotes cytoskeleton binding through band 3 binding with ankyrin, whereas the latter shifts the population of band 3 to dimers, which weakens cytoskeleton binding ( 26).	bind
49047	6	9966	7	11	NULL	NULL	NULL	band 3 dimers	GP		weakens					cytoskeleton	CellComponent	binding of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_20_11771_s_113	11573011	A difference between the manner in which BS3 and DIDS act on band 3 is that the former shifts the band 3 population toward tetramers ( 25), which promotes cytoskeleton binding through band 3 binding with ankyrin, whereas the latter shifts the population of band 3 to dimers, which weakens cytoskeleton binding ( 26).	bind
34799	1	9968	6	11	NULL	NULL	NULL	NGF	GP		bind					p75	GP				NULL	KA-treated adult animals	NULL	NULL	NULL	NULL	gw60_brainres_853_2_174_s_249	10640615	A difference between these two situations may be that in KA-treated adult animals, NGF binding to p75 produces cell death, whereas in developing animals, NGF promotes cell survival.	bind
34800	2	9968	6	11	NULL	NULL	NULL	statement 1	Process		produces					cell death	Process				NULL	KA-treated adult animals	NULL	NULL	NULL	NULL	gw60_brainres_853_2_174_s_249	10640615	A difference between these two situations may be that in KA-treated adult animals, NGF binding to p75 produces cell death, whereas in developing animals, NGF promotes cell survival.	bind
34801	3	9968	6	11	NULL	NULL	NULL	NGF	GP		promotes					cell survival	Process				NULL	developing animals	NULL	NULL	NULL	NULL	gw60_brainres_853_2_174_s_249	10640615	A difference between these two situations may be that in KA-treated adult animals, NGF binding to p75 produces cell death, whereas in developing animals, NGF promotes cell survival.	bind
42422	1	9968	7	11	NULL	NULL	NULL	NGF	GP		bind					p75	GP				NULL	KA-treated adult animals	NULL	NULL	NULL	NULL	gw60_brainres_853_2_174_s_249	10640615	A difference between these two situations may be that in KA-treated adult animals, NGF binding to p75 produces cell death, whereas in developing animals, NGF promotes cell survival.	bind
42423	2	9968	7	11	NULL	NULL	NULL	statement 1	Process		produces					cell death	Process				NULL	KA-treated adult animals	NULL	NULL	NULL	NULL	gw60_brainres_853_2_174_s_249	10640615	A difference between these two situations may be that in KA-treated adult animals, NGF binding to p75 produces cell death, whereas in developing animals, NGF promotes cell survival.	bind
42425	3	9968	7	11	NULL	NULL	NULL	NGF	GP		promotes					cell survival	Process				NULL	developing animals	NULL	NULL	NULL	NULL	gw60_brainres_853_2_174_s_249	10640615	A difference between these two situations may be that in KA-treated adult animals, NGF binding to p75 produces cell death, whereas in developing animals, NGF promotes cell survival.	bind
34813	1	9969	6	11	NULL	NULL	NULL	Ku proteins	GP		constitute					DNA-PK	GP				NULL	mammalian cells	NULL	NULL	NULL	NULL	gw60_genetics_148_3_975_s_324	9539418	A difference between yeast and mammalian cells is that in mammalian cells, the Ku proteins constitute the DNA-binding moiety of a larger complex, the DNA-dependent protein kinase (DNA-PK).	bind
49048	2	9969	6	11	NULL	NULL	NULL	DNA-PK	GP		is					DNA-dependent protein kinase 	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_148_3_975_s_324	9539418	A difference between yeast and mammalian cells is that in mammalian cells, the Ku proteins constitute the DNA-binding moiety of a larger complex, the DNA-dependent protein kinase (DNA-PK).	bind
49049	3	9969	6	11	NULL	NULL	NULL	DNA-PK	GP		is a type of					DNA-binding moiety of a larger complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_148_3_975_s_324	9539418	A difference between yeast and mammalian cells is that in mammalian cells, the Ku proteins constitute the DNA-binding moiety of a larger complex, the DNA-dependent protein kinase (DNA-PK).	bind
42466	1	9969	7	11	NULL	NULL	NULL	 Ku proteins	GP		constitute					DNA-PK	GP				NULL	mammalian cells	NULL	NULL	NULL	NULL	gw60_genetics_148_3_975_s_324	9539418	A difference between yeast and mammalian cells is that in mammalian cells, the Ku proteins constitute the DNA-binding moiety of a larger complex, the DNA-dependent protein kinase (DNA-PK).	bind
42467	2	9969	7	11	NULL	NULL	NULL	DNA-PK	GP		is					DNA-dependent protein kinase 	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_148_3_975_s_324	9539418	A difference between yeast and mammalian cells is that in mammalian cells, the Ku proteins constitute the DNA-binding moiety of a larger complex, the DNA-dependent protein kinase (DNA-PK).	bind
42468	3	9969	7	11	NULL	NULL	NULL	DNA-PK	GP		is a type of					DNA-binding moiety of a larger complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_148_3_975_s_324	9539418	A difference between yeast and mammalian cells is that in mammalian cells, the Ku proteins constitute the DNA-binding moiety of a larger complex, the DNA-dependent protein kinase (DNA-PK).	bind
34814	1	9970	6	11	NULL	NULL	NULL	CTD peptide	AminoAcid		bind					CID molecule	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_nature_430_6996_223_s_146	15241417	A difference Fourier for the peptide-soaked crystal was calculated  with phases from the CID model and identified strong density for the CTD peptide  bound to one CID molecule (chain B).	bind
42469	1	9970	7	11	NULL	NULL	NULL	CTD peptide	AminoAcid		bind					CID molecule	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_nature_430_6996_223_s_146	15241417	A difference Fourier for the peptide-soaked crystal was calculated  with phases from the CID model and identified strong density for the CTD peptide  bound to one CID molecule (chain B).	bind
34815	1	9971	6	11	NULL	NULL	NULL	VWF	GP		bind					rHPA-2a	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_121	12775575	A difference in affinity of VWF for rHPA-2a and rHPA-2b was also seen in the presence of 0.1 mug/mL botrocetin, where VWF bound with a Kd,app of 2.49 and 7.47 nmol/L to rHPA-2a and rHPA-2b, respectively (mean of 2 experiments), which could be confirmed with HPA-2a2a and HPA-2b2b platelets ( P<0.05) when anti-GPIbalpha moAb 27C11 was used as a reference to normalize for GPIbalpha numbers ( Figure 6).	bind
34816	2	9971	6	11	NULL	NULL	NULL	VWF	GP		bind					rHPA-2b	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_121	12775575	A difference in affinity of VWF for rHPA-2a and rHPA-2b was also seen in the presence of 0.1 mug/mL botrocetin, where VWF bound with a Kd,app of 2.49 and 7.47 nmol/L to rHPA-2a and rHPA-2b, respectively (mean of 2 experiments), which could be confirmed with HPA-2a2a and HPA-2b2b platelets ( P<0.05) when anti-GPIbalpha moAb 27C11 was used as a reference to normalize for GPIbalpha numbers ( Figure 6).	bind
34817	3	9971	6	11	NULL	NULL	NULL	statement 1	Process		occurs in presence of					botrocetin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_121	12775575	A difference in affinity of VWF for rHPA-2a and rHPA-2b was also seen in the presence of 0.1 mug/mL botrocetin, where VWF bound with a Kd,app of 2.49 and 7.47 nmol/L to rHPA-2a and rHPA-2b, respectively (mean of 2 experiments), which could be confirmed with HPA-2a2a and HPA-2b2b platelets ( P<0.05) when anti-GPIbalpha moAb 27C11 was used as a reference to normalize for GPIbalpha numbers ( Figure 6).	bind
34818	4	9971	6	11	NULL	NULL	NULL	statement 2	Process		occurs in presence of					botrocetin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_121	12775575	A difference in affinity of VWF for rHPA-2a and rHPA-2b was also seen in the presence of 0.1 mug/mL botrocetin, where VWF bound with a Kd,app of 2.49 and 7.47 nmol/L to rHPA-2a and rHPA-2b, respectively (mean of 2 experiments), which could be confirmed with HPA-2a2a and HPA-2b2b platelets ( P<0.05) when anti-GPIbalpha moAb 27C11 was used as a reference to normalize for GPIbalpha numbers ( Figure 6).	bind
42470	1	9971	7	11	NULL	NULL	NULL	VWF	GP		bind					rHPA-2a	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_121	12775575	A difference in affinity of VWF for rHPA-2a and rHPA-2b was also seen in the presence of 0.1 mug/mL botrocetin, where VWF bound with a Kd,app of 2.49 and 7.47 nmol/L to rHPA-2a and rHPA-2b, respectively (mean of 2 experiments), which could be confirmed with HPA-2a2a and HPA-2b2b platelets ( P<0.05) when anti-GPIbalpha moAb 27C11 was used as a reference to normalize for GPIbalpha numbers ( Figure 6).	bind
42471	2	9971	7	11	NULL	NULL	NULL	VWF	GP		bind					rHPA-2b	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_121	12775575	A difference in affinity of VWF for rHPA-2a and rHPA-2b was also seen in the presence of 0.1 mug/mL botrocetin, where VWF bound with a Kd,app of 2.49 and 7.47 nmol/L to rHPA-2a and rHPA-2b, respectively (mean of 2 experiments), which could be confirmed with HPA-2a2a and HPA-2b2b platelets ( P<0.05) when anti-GPIbalpha moAb 27C11 was used as a reference to normalize for GPIbalpha numbers ( Figure 6).	bind
42472	3	9971	7	11	NULL	NULL	NULL	statement 1	Process		in presence of					 botrocetin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_121	12775575	A difference in affinity of VWF for rHPA-2a and rHPA-2b was also seen in the presence of 0.1 mug/mL botrocetin, where VWF bound with a Kd,app of 2.49 and 7.47 nmol/L to rHPA-2a and rHPA-2b, respectively (mean of 2 experiments), which could be confirmed with HPA-2a2a and HPA-2b2b platelets ( P<0.05) when anti-GPIbalpha moAb 27C11 was used as a reference to normalize for GPIbalpha numbers ( Figure 6).	bind
42473	4	9971	7	11	NULL	NULL	NULL	statement 2	Process		in presence of					botrocetin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_7_1302_s_121	12775575	A difference in affinity of VWF for rHPA-2a and rHPA-2b was also seen in the presence of 0.1 mug/mL botrocetin, where VWF bound with a Kd,app of 2.49 and 7.47 nmol/L to rHPA-2a and rHPA-2b, respectively (mean of 2 experiments), which could be confirmed with HPA-2a2a and HPA-2b2b platelets ( P<0.05) when anti-GPIbalpha moAb 27C11 was used as a reference to normalize for GPIbalpha numbers ( Figure 6).	bind
42476	1	9972	7	NULL	NULL	0	NULL	Grb7	NULL		bind	NULL		SH2 domain		 HER 1-2 receptor	NULL	activated			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_21_12502_s_187	8647858	A difference in binding  selectivity between the Grb7 and Grb14 SH2 domains was more evident  when binding to the activated HER 1-2 receptor (an EGFR/ErbB2  chimera containing the intracellular domain of ErbB2) was investigated.	bind
42477	2	9972	7	NULL	NULL	0	NULL	Grb14 	NULL		bind	NULL		SH2 domain		HER 1-2 receptor	NULL	activated			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_21_12502_s_187	8647858	A difference in binding  selectivity between the Grb7 and Grb14 SH2 domains was more evident  when binding to the activated HER 1-2 receptor (an EGFR/ErbB2  chimera containing the intracellular domain of ErbB2) was investigated.	bind
42478	3	9972	7	10	NULL	0	NULL	HER 1-2 receptor	NULL		is	NULL				EGFR/ErbB2 chimera containing intracellular domain of ErbB2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_21_12502_s_187	8647858	A difference in binding  selectivity between the Grb7 and Grb14 SH2 domains was more evident  when binding to the activated HER 1-2 receptor (an EGFR/ErbB2  chimera containing the intracellular domain of ErbB2) was investigated.	bind
34821	1	9973	6	11	NULL	NULL	NULL	alpha-fetoprotein	GP	serum	bind					lectin	GP	lentil			NULL	hepatocellular carcinomas	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27810_s_18	8910378	A difference in the binding pattern of serum alpha-fetoprotein with lentil lectin between hepatocellular carcinomas and benign liver diseases has been reported ( 15,  16,  17).	bind
34822	2	9973	6	11	NULL	NULL	NULL	alpha-fetoprotein	GP	serum	bind					lectin	GP	lentil			NULL	benign liver diseases	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27810_s_18	8910378	A difference in the binding pattern of serum alpha-fetoprotein with lentil lectin between hepatocellular carcinomas and benign liver diseases has been reported ( 15,  16,  17).	bind
42479	1	9973	7	11	NULL	NULL	NULL	alpha-fetoprotein	GP	serum	bind					lectin	GP	lentil			NULL	hepatocellular carcinomas	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27810_s_18	8910378	A difference in the binding pattern of serum alpha-fetoprotein with lentil lectin between hepatocellular carcinomas and benign liver diseases has been reported ( 15,  16,  17).	bind
42480	2	9973	7	11	NULL	NULL	NULL	alpha-fetoprotein	GP	serum	bind					lectin	GP	lentil			NULL	benign liver diseases	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_44_27810_s_18	8910378	A difference in the binding pattern of serum alpha-fetoprotein with lentil lectin between hepatocellular carcinomas and benign liver diseases has been reported ( 15,  16,  17).	bind
34823	1	9974	6	11	NULL	NULL	NULL	dI	GP	isolated form of 	bind					NAD+/NADH	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_19490_s_308	10747934	A difference in the NAD+/NADH binding properties of dI in its isolated form and in the complete, membrane-bound protein was also inferred from a steady-state kinetic analysis ( 7).	bind
34824	2	9974	6	11	NULL	NULL	NULL	dI	GP	membrane-bound	bind					NAD+/NADH	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_19490_s_308	10747934	A difference in the NAD+/NADH binding properties of dI in its isolated form and in the complete, membrane-bound protein was also inferred from a steady-state kinetic analysis ( 7).	bind
42481	1	9974	7	11	NULL	NULL	NULL	NAD+/NADH	Chemical		bind					dI	GP	isolated form			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_19490_s_308	10747934	A difference in the NAD+/NADH binding properties of dI in its isolated form and in the complete, membrane-bound protein was also inferred from a steady-state kinetic analysis ( 7).	bind
42483	2	9974	7	11	NULL	NULL	NULL	NAD+/NADH	Chemical		bind					dI	GP	membrane-bound			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_19490_s_308	10747934	A difference in the NAD+/NADH binding properties of dI in its isolated form and in the complete, membrane-bound protein was also inferred from a steady-state kinetic analysis ( 7).	bind
34825	1	9976	6	11	NULL	NULL	NULL	tFR	GP		bind					FAD	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23303_s_294	9287340	A difference spectrum between free FAD and tFR-bound FAD exhibits negative peaks at 490, 460, and 356 nm and a positive peak at 396 nm (Fig.  3,  curve C).	bind
42486	1	9976	7	11	NULL	NULL	NULL	 tFR	GP		bind					FAD	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_37_23303_s_294	9287340	A difference spectrum between free FAD and tFR-bound FAD exhibits negative peaks at 490, 460, and 356 nm and a positive peak at 396 nm (Fig.  3,  curve C).	bind
34826	1	9977	6	11	NULL	NULL	NULL	G-actin	GP	clevage of	diminishes			DNase-I-binding loop		actin	GP	rate of;; polymerization of 			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1478_1_138_s_98	10719182	A difference was observed in the rate of the polymerization-induced change: with intact actin, the maximum   n value was reached within 10-15 min, whereas with subtilisin-cleaved actin it took 25-30 min, in agreement with earlier observations showing that cleavage of G-actin within the DNase-I-binding loop diminishes the rate of actin polymerization [ 31 and  32].	bind
49052	2	9977	6	11	NULL	NULL	NULL	subtilisin	GP		cleaves					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1478_1_138_s_98	10719182	A difference was observed in the rate of the polymerization-induced change: with intact actin, the maximum   n value was reached within 10-15 min, whereas with subtilisin-cleaved actin it took 25-30 min, in agreement with earlier observations showing that cleavage of G-actin within the DNase-I-binding loop diminishes the rate of actin polymerization [ 31 and  32].	bind
42487	1	9977	7	11	NULL	NULL	NULL	subtilisin	GP		cleaves					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1478_1_138_s_98	10719182	A difference was observed in the rate of the polymerization-induced change: with intact actin, the maximum   n value was reached within 10-15 min, whereas with subtilisin-cleaved actin it took 25-30 min, in agreement with earlier observations showing that cleavage of G-actin within the DNase-I-binding loop diminishes the rate of actin polymerization [ 31 and  32].	bind
42488	2	9977	7	11	NULL	NULL	NULL	G-actin	GP	cleavage of	diminish			DNase-I-binding loop		actin	GP	 rate of;;polymerization of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1478_1_138_s_98	10719182	A difference was observed in the rate of the polymerization-induced change: with intact actin, the maximum   n value was reached within 10-15 min, whereas with subtilisin-cleaved actin it took 25-30 min, in agreement with earlier observations showing that cleavage of G-actin within the DNase-I-binding loop diminishes the rate of actin polymerization [ 31 and  32].	bind
34827	1	9978	6	11	NULL	NULL	NULL	MAGE-3 peptide	GP		bind					HLA-A29	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_21_12463_s_226	8647853	A different and  more complex situation was observed for the MAGE-3 peptide binding by  HLA-A29.	bind
42489	1	9978	7	11	NULL	NULL	NULL	HLA-A29	GP		bind					MAGE-3 peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_21_12463_s_226	8647853	A different and  more complex situation was observed for the MAGE-3 peptide binding by  HLA-A29.	bind
34828	1	9979	6	11	NULL	NULL	NULL	p22 phox	GP		bind			residues 176-195		p47 phox	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_300	11733522	A different approach to the identification of interaction domains in p22 phox was introduced by Kanegasaki and co-workers ( 44) who showed that a peptide corresponding to residues 176-195 of p22 phox inhibited SDS-induced NADPH oxidase activation in a cell-free system, albeit with a rather high IC50 (36 muM); the peptide also bound p47 phox in the presence of SDS.	bind
34829	2	9979	6	11	NULL	NULL	NULL	statement 1	Process		in the presence of					SDS	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_300	11733522	A different approach to the identification of interaction domains in p22 phox was introduced by Kanegasaki and co-workers ( 44) who showed that a peptide corresponding to residues 176-195 of p22 phox inhibited SDS-induced NADPH oxidase activation in a cell-free system, albeit with a rather high IC50 (36 muM); the peptide also bound p47 phox in the presence of SDS.	bind
34830	3	9979	6	11	NULL	NULL	NULL	SDS	Chemical		induces					NADPH oxidase	GP	activation of 			NULL	cell-free system	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_300	11733522	A different approach to the identification of interaction domains in p22 phox was introduced by Kanegasaki and co-workers ( 44) who showed that a peptide corresponding to residues 176-195 of p22 phox inhibited SDS-induced NADPH oxidase activation in a cell-free system, albeit with a rather high IC50 (36 muM); the peptide also bound p47 phox in the presence of SDS.	bind
34831	4	9979	6	11	NULL	NULL	NULL	p22 phox	GP		inhibits			residues 176-195		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_300	11733522	A different approach to the identification of interaction domains in p22 phox was introduced by Kanegasaki and co-workers ( 44) who showed that a peptide corresponding to residues 176-195 of p22 phox inhibited SDS-induced NADPH oxidase activation in a cell-free system, albeit with a rather high IC50 (36 muM); the peptide also bound p47 phox in the presence of SDS.	bind
42490	1	9979	7	11	NULL	NULL	NULL	 SDS	Chemical		induce					NADPH oxidase 	GP	activation of			NULL	cell-free system	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_300	11733522	A different approach to the identification of interaction domains in p22 phox was introduced by Kanegasaki and co-workers ( 44) who showed that a peptide corresponding to residues 176-195 of p22 phox inhibited SDS-induced NADPH oxidase activation in a cell-free system, albeit with a rather high IC50 (36 muM); the peptide also bound p47 phox in the presence of SDS.	bind
42491	2	9979	7	11	NULL	NULL	NULL	p22 phox peptide	GP		inhibits			residues 176-195 		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_300	11733522	A different approach to the identification of interaction domains in p22 phox was introduced by Kanegasaki and co-workers ( 44) who showed that a peptide corresponding to residues 176-195 of p22 phox inhibited SDS-induced NADPH oxidase activation in a cell-free system, albeit with a rather high IC50 (36 muM); the peptide also bound p47 phox in the presence of SDS.	bind
42492	3	9979	7	11	NULL	NULL	NULL	p22 phox peptide	GP		bind			residues 176-195 		p47phox	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_300	11733522	A different approach to the identification of interaction domains in p22 phox was introduced by Kanegasaki and co-workers ( 44) who showed that a peptide corresponding to residues 176-195 of p22 phox inhibited SDS-induced NADPH oxidase activation in a cell-free system, albeit with a rather high IC50 (36 muM); the peptide also bound p47 phox in the presence of SDS.	bind
42493	4	9979	7	11	NULL	NULL	NULL	statement 3	Process		in the presence of					SDS	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_10_8421_s_300	11733522	A different approach to the identification of interaction domains in p22 phox was introduced by Kanegasaki and co-workers ( 44) who showed that a peptide corresponding to residues 176-195 of p22 phox inhibited SDS-induced NADPH oxidase activation in a cell-free system, albeit with a rather high IC50 (36 muM); the peptide also bound p47 phox in the presence of SDS.	bind
34832	1	9980	6	11	NULL	NULL	NULL	O2	Chemical		bind					Hb	GP	human;;adult			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_47_29859_s_11	8939926	A different behavior has been observed for O2 binding to human adult Hb, which displays some kinetic heterogeneity ( 3,  4,  5,  6).	bind
42494	1	9980	7	11	NULL	NULL	NULL	O2	Chemical		bind					Hb	GP	human;;adult			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_47_29859_s_11	8939926	A different behavior has been observed for O2 binding to human adult Hb, which displays some kinetic heterogeneity ( 3,  4,  5,  6).	bind
49061	1	9981	6	11	NULL	NULL	NULL	ligand	Chemical	endogenous	replaces					Fe(III) L116K CooAP	Chemical		Pro2		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_33616_s_155	12121986	A Different Endogenous Ligand Replaces Pro2 in Fe(III) L116K CooAP-- Given the close proximity of the position 116 residue to the heme and the unusually high aerobic DNA binding activity of L116K CooA, we expected that Fe(III) L116K would be structurally perturbed around the heme center and that this perturbation might be revealed by electronic absorption spectroscopy.	bind
49062	2	9981	6	11	NULL	NULL	NULL	CooA	Chemical		bind		aerobic	L116K		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_33616_s_155	12121986	A Different Endogenous Ligand Replaces Pro2 in Fe(III) L116K CooAP-- Given the close proximity of the position 116 residue to the heme and the unusually high aerobic DNA binding activity of L116K CooA, we expected that Fe(III) L116K would be structurally perturbed around the heme center and that this perturbation might be revealed by electronic absorption spectroscopy.	bind
42584	1	9981	7	11	NULL	NULL	NULL	ligand	Chemical	endogenous	replaces					Fe(III) L116K CooAP	Chemical		Pro2		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_33616_s_155	12121986	A Different Endogenous Ligand Replaces Pro2 in Fe(III) L116K CooAP-- Given the close proximity of the position 116 residue to the heme and the unusually high aerobic DNA binding activity of L116K CooA, we expected that Fe(III) L116K would be structurally perturbed around the heme center and that this perturbation might be revealed by electronic absorption spectroscopy.	bind
42585	2	9981	7	11	NULL	NULL	NULL	CooA	Chemical		bind		aerobic	L116K		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_33616_s_155	12121986	A Different Endogenous Ligand Replaces Pro2 in Fe(III) L116K CooAP-- Given the close proximity of the position 116 residue to the heme and the unusually high aerobic DNA binding activity of L116K CooA, we expected that Fe(III) L116K would be structurally perturbed around the heme center and that this perturbation might be revealed by electronic absorption spectroscopy.	bind
34833	1	9982	6	11	NULL	NULL	NULL	initiation factor 4E	GP		bind					5' RNA cap	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_12_3875_s_308	11739787	A different labeling was observed with antibodies to initiation factor 4E, a protein that binds to the 5' RNA cap and mediates ribosome binding (Sonenberg  et al., 1978  ).	bind
34834	2	9982	6	11	NULL	NULL	NULL	statement 1	Process		mediates					ribosome	CellComponent	binding of 			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_12_3875_s_308	11739787	A different labeling was observed with antibodies to initiation factor 4E, a protein that binds to the 5' RNA cap and mediates ribosome binding (Sonenberg  et al., 1978  ).	bind
42587	1	9982	7	11	NULL	NULL	NULL	initiation factor 4E	GP		bind					5' RNA cap	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_12_3875_s_308	11739787	A different labeling was observed with antibodies to initiation factor 4E, a protein that binds to the 5' RNA cap and mediates ribosome binding (Sonenberg  et al., 1978  ).	bind
42588	2	9982	7	11	NULL	NULL	NULL	statement 1	Process		mediates					ribosome	CellComponent	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_12_3875_s_308	11739787	A different labeling was observed with antibodies to initiation factor 4E, a protein that binds to the 5' RNA cap and mediates ribosome binding (Sonenberg  et al., 1978  ).	bind
34984	1	9983	6	11	NULL	NULL	NULL	p12I	GP	 cytoplasm facing region	bind					calcineurin	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_4_1117_s_125	14623298	A different region of p12I, presumably facing the cytoplasm, binds calcineurin; however, the SPSLPLT sequence  in this region is a relatively poor PxIxIT motif since it contains an internal proline  and since substitution of the essential threonine with alanine does not impair binding  of p12I to calcineurin [  40].	bind
34985	2	9983	6	11	NULL	NULL	NULL	p12I	GP		is a type of		relatively	SPSLPLT sequence				poor	PxIxIT motif		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_4_1117_s_125	14623298	A different region of p12I, presumably facing the cytoplasm, binds calcineurin; however, the SPSLPLT sequence  in this region is a relatively poor PxIxIT motif since it contains an internal proline  and since substitution of the essential threonine with alanine does not impair binding  of p12I to calcineurin [  40].	bind
34986	3	9983	6	11	NULL	NULL	NULL				is substituted with			threonine in PxIxIT motif					alanine in PxIxIT motif		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_4_1117_s_125	14623298	A different region of p12I, presumably facing the cytoplasm, binds calcineurin; however, the SPSLPLT sequence  in this region is a relatively poor PxIxIT motif since it contains an internal proline  and since substitution of the essential threonine with alanine does not impair binding  of p12I to calcineurin [  40].	bind
34987	4	9983	6	11	NULL	NULL	NULL	statement 3	Process		does not impair					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_4_1117_s_125	14623298	A different region of p12I, presumably facing the cytoplasm, binds calcineurin; however, the SPSLPLT sequence  in this region is a relatively poor PxIxIT motif since it contains an internal proline  and since substitution of the essential threonine with alanine does not impair binding  of p12I to calcineurin [  40].	bind
42589	1	9983	7	11	NULL	NULL	NULL	 p12I 	GP	cytoplasm facing region	binds					calcineurin	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_4_1117_s_125	14623298	A different region of p12I, presumably facing the cytoplasm, binds calcineurin; however, the SPSLPLT sequence  in this region is a relatively poor PxIxIT motif since it contains an internal proline  and since substitution of the essential threonine with alanine does not impair binding  of p12I to calcineurin [  40].	bind
42590	2	9983	7	11	NULL	NULL	NULL	p12I	GP		is a type of			SPSLPLT sequence					PxIxIT motif		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_4_1117_s_125	14623298	A different region of p12I, presumably facing the cytoplasm, binds calcineurin; however, the SPSLPLT sequence  in this region is a relatively poor PxIxIT motif since it contains an internal proline  and since substitution of the essential threonine with alanine does not impair binding  of p12I to calcineurin [  40].	bind
42591	3	9983	7	11	NULL	NULL	NULL	statement 2	Process		is because of 					internal proline residue	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_4_1117_s_125	14623298	A different region of p12I, presumably facing the cytoplasm, binds calcineurin; however, the SPSLPLT sequence  in this region is a relatively poor PxIxIT motif since it contains an internal proline  and since substitution of the essential threonine with alanine does not impair binding  of p12I to calcineurin [  40].	bind
42592	4	9983	7	11	NULL	NULL	NULL				is substituted with			threonine in PxIxIT motif					alanine in PxIxIT motif		NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_4_1117_s_125	14623298	A different region of p12I, presumably facing the cytoplasm, binds calcineurin; however, the SPSLPLT sequence  in this region is a relatively poor PxIxIT motif since it contains an internal proline  and since substitution of the essential threonine with alanine does not impair binding  of p12I to calcineurin [  40].	bind
42593	5	9983	7	11	NULL	NULL	NULL	statement 4	Process		does not impair					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_4_1117_s_125	14623298	A different region of p12I, presumably facing the cytoplasm, binds calcineurin; however, the SPSLPLT sequence  in this region is a relatively poor PxIxIT motif since it contains an internal proline  and since substitution of the essential threonine with alanine does not impair binding  of p12I to calcineurin [  40].	bind
34835	1	9984	6	11	NULL	NULL	NULL	PlexB	GP		bind					RhoA	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_1_39_s_6	11604137	A different region of PlexB binds to RhoA.	bind
42594	1	9984	7	11	NULL	NULL	NULL	PlexB	GP		binds to					RhoA	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_1_39_s_6	11604137	A different region of PlexB binds to RhoA.	bind
34988	1	9985	6	11	NULL	NULL	NULL	V1ROSS proteins	GP		bind					calmodulin	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16574744_s_8	16574744	A different series of soluble receptor analogs,  named vasopressin receptor 1 elements on a soluble scaffold (V1ROSS) proteins,  consist of the third intracellular loop and/or the C-terminal segment  of the hV1R receptor juxtaposed on the surface of the MBP. V1ROSS proteins  bind calmodulin and a truncated, phosphorylation-independent form of arrestin2  more tightly than the corresponding linear fusion proteins.	bind
34989	2	9985	6	11	NULL	NULL	NULL	V1ROSS proteins	GP		bind					arrestin2	GP	truncated;; phosphorylation-independent form of			NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16574744_s_8	16574744	A different series of soluble receptor analogs,  named vasopressin receptor 1 elements on a soluble scaffold (V1ROSS) proteins,  consist of the third intracellular loop and/or the C-terminal segment  of the hV1R receptor juxtaposed on the surface of the MBP. V1ROSS proteins  bind calmodulin and a truncated, phosphorylation-independent form of arrestin2  more tightly than the corresponding linear fusion proteins.	bind
34990	3	9985	6	11	NULL	NULL	NULL	V1ROSS proteins	GP		bind					arrestin2	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16574744_s_8	16574744	A different series of soluble receptor analogs,  named vasopressin receptor 1 elements on a soluble scaffold (V1ROSS) proteins,  consist of the third intracellular loop and/or the C-terminal segment  of the hV1R receptor juxtaposed on the surface of the MBP. V1ROSS proteins  bind calmodulin and a truncated, phosphorylation-independent form of arrestin2  more tightly than the corresponding linear fusion proteins.	bind
34991	4	9985	6	11	NULL	NULL	NULL	statement 1	Process	affinity of	is more than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16574744_s_8	16574744	A different series of soluble receptor analogs,  named vasopressin receptor 1 elements on a soluble scaffold (V1ROSS) proteins,  consist of the third intracellular loop and/or the C-terminal segment  of the hV1R receptor juxtaposed on the surface of the MBP. V1ROSS proteins  bind calmodulin and a truncated, phosphorylation-independent form of arrestin2  more tightly than the corresponding linear fusion proteins.	bind
34992	5	9985	6	11	NULL	NULL	NULL	V1ROSS	GP		is					vasopressin receptor 1 elements on a soluble scaffold	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16574744_s_8	16574744	A different series of soluble receptor analogs,  named vasopressin receptor 1 elements on a soluble scaffold (V1ROSS) proteins,  consist of the third intracellular loop and/or the C-terminal segment  of the hV1R receptor juxtaposed on the surface of the MBP. V1ROSS proteins  bind calmodulin and a truncated, phosphorylation-independent form of arrestin2  more tightly than the corresponding linear fusion proteins.	bind
34993	6	9985	6	11	NULL	NULL	NULL	V1ROSS protein	GP		is a type of					receptor analog	GP	soluble			NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16574744_s_8	16574744	A different series of soluble receptor analogs,  named vasopressin receptor 1 elements on a soluble scaffold (V1ROSS) proteins,  consist of the third intracellular loop and/or the C-terminal segment  of the hV1R receptor juxtaposed on the surface of the MBP. V1ROSS proteins  bind calmodulin and a truncated, phosphorylation-independent form of arrestin2  more tightly than the corresponding linear fusion proteins.	bind
34994	7	9985	6	11	NULL	NULL	NULL	V1ROSS proteins	GP		consists of					hV1R receptor	GP		third intracellular loop		NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16574744_s_8	16574744	A different series of soluble receptor analogs,  named vasopressin receptor 1 elements on a soluble scaffold (V1ROSS) proteins,  consist of the third intracellular loop and/or the C-terminal segment  of the hV1R receptor juxtaposed on the surface of the MBP. V1ROSS proteins  bind calmodulin and a truncated, phosphorylation-independent form of arrestin2  more tightly than the corresponding linear fusion proteins.	bind
34995	8	9985	6	11	NULL	NULL	NULL	V1ROSS protein	GP		consists of					hV1R receptor juxtaposed on the surface of the MBP	GP		C-terminal segment		NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16574744_s_8	16574744	A different series of soluble receptor analogs,  named vasopressin receptor 1 elements on a soluble scaffold (V1ROSS) proteins,  consist of the third intracellular loop and/or the C-terminal segment  of the hV1R receptor juxtaposed on the surface of the MBP. V1ROSS proteins  bind calmodulin and a truncated, phosphorylation-independent form of arrestin2  more tightly than the corresponding linear fusion proteins.	bind
42595	1	9985	7	11	NULL	NULL	NULL	vasopressin receptor 1 elements	GP		present on					V1ROSS proteins	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16574744_s_8	16574744	A different series of soluble receptor analogs,  named vasopressin receptor 1 elements on a soluble scaffold (V1ROSS) proteins,  consist of the third intracellular loop and/or the C-terminal segment  of the hV1R receptor juxtaposed on the surface of the MBP. V1ROSS proteins  bind calmodulin and a truncated, phosphorylation-independent form of arrestin2  more tightly than the corresponding linear fusion proteins.	bind
42596	2	9985	7	11	NULL	NULL	NULL	statement 1	Process		consist of					hV1R receptor	GP		third intracellular loop		NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16574744_s_8	16574744	A different series of soluble receptor analogs,  named vasopressin receptor 1 elements on a soluble scaffold (V1ROSS) proteins,  consist of the third intracellular loop and/or the C-terminal segment  of the hV1R receptor juxtaposed on the surface of the MBP. V1ROSS proteins  bind calmodulin and a truncated, phosphorylation-independent form of arrestin2  more tightly than the corresponding linear fusion proteins.	bind
42597	3	9985	7	11	NULL	NULL	NULL	statement 1	Process		consist of					hV1R receptor	GP		C-terminal segment 		NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16574744_s_8	16574744	A different series of soluble receptor analogs,  named vasopressin receptor 1 elements on a soluble scaffold (V1ROSS) proteins,  consist of the third intracellular loop and/or the C-terminal segment  of the hV1R receptor juxtaposed on the surface of the MBP. V1ROSS proteins  bind calmodulin and a truncated, phosphorylation-independent form of arrestin2  more tightly than the corresponding linear fusion proteins.	bind
42598	4	9985	7	11	NULL	NULL	NULL	statement 2	Process		 juxtaposed on					MBP	GP	surface of			NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16574744_s_8	16574744	A different series of soluble receptor analogs,  named vasopressin receptor 1 elements on a soluble scaffold (V1ROSS) proteins,  consist of the third intracellular loop and/or the C-terminal segment  of the hV1R receptor juxtaposed on the surface of the MBP. V1ROSS proteins  bind calmodulin and a truncated, phosphorylation-independent form of arrestin2  more tightly than the corresponding linear fusion proteins.	bind
42599	5	9985	7	11	NULL	NULL	NULL	statement 3	Process		juxtaposed on					MBP	GP	surface of			NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16574744_s_8	16574744	A different series of soluble receptor analogs,  named vasopressin receptor 1 elements on a soluble scaffold (V1ROSS) proteins,  consist of the third intracellular loop and/or the C-terminal segment  of the hV1R receptor juxtaposed on the surface of the MBP. V1ROSS proteins  bind calmodulin and a truncated, phosphorylation-independent form of arrestin2  more tightly than the corresponding linear fusion proteins.	bind
42600	6	9985	7	11	NULL	NULL	NULL	V1ROSS proteins	GP		bind					calmodulin 	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16574744_s_8	16574744	A different series of soluble receptor analogs,  named vasopressin receptor 1 elements on a soluble scaffold (V1ROSS) proteins,  consist of the third intracellular loop and/or the C-terminal segment  of the hV1R receptor juxtaposed on the surface of the MBP. V1ROSS proteins  bind calmodulin and a truncated, phosphorylation-independent form of arrestin2  more tightly than the corresponding linear fusion proteins.	bind
42601	7	9985	7	11	NULL	NULL	NULL	V1ROSS proteins	GP		bind					arrestin2	GP	truncated;;phosphorylation-independent form of 			NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16574744_s_8	16574744	A different series of soluble receptor analogs,  named vasopressin receptor 1 elements on a soluble scaffold (V1ROSS) proteins,  consist of the third intracellular loop and/or the C-terminal segment  of the hV1R receptor juxtaposed on the surface of the MBP. V1ROSS proteins  bind calmodulin and a truncated, phosphorylation-independent form of arrestin2  more tightly than the corresponding linear fusion proteins.	bind
42602	8	9985	7	11	NULL	NULL	NULL	V1ROSS proteins	GP		bind					linear fusion protein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16574744_s_8	16574744	A different series of soluble receptor analogs,  named vasopressin receptor 1 elements on a soluble scaffold (V1ROSS) proteins,  consist of the third intracellular loop and/or the C-terminal segment  of the hV1R receptor juxtaposed on the surface of the MBP. V1ROSS proteins  bind calmodulin and a truncated, phosphorylation-independent form of arrestin2  more tightly than the corresponding linear fusion proteins.	bind
42603	9	9985	7	11	NULL	NULL	NULL	statement 6	Process		is more tight than					statement 8	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16574744_s_8	16574744	A different series of soluble receptor analogs,  named vasopressin receptor 1 elements on a soluble scaffold (V1ROSS) proteins,  consist of the third intracellular loop and/or the C-terminal segment  of the hV1R receptor juxtaposed on the surface of the MBP. V1ROSS proteins  bind calmodulin and a truncated, phosphorylation-independent form of arrestin2  more tightly than the corresponding linear fusion proteins.	bind
42604	10	9985	7	11	NULL	NULL	NULL	statement 7	Process		is more tight than					statement 8	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16574744_s_8	16574744	A different series of soluble receptor analogs,  named vasopressin receptor 1 elements on a soluble scaffold (V1ROSS) proteins,  consist of the third intracellular loop and/or the C-terminal segment  of the hV1R receptor juxtaposed on the surface of the MBP. V1ROSS proteins  bind calmodulin and a truncated, phosphorylation-independent form of arrestin2  more tightly than the corresponding linear fusion proteins.	bind
42605	11	9985	7	11	NULL	NULL	NULL	V1ROSS proteins	GP		is a type of					soluble scaffold proteins	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-pharmacol_70_1_16574744_s_8	16574744	A different series of soluble receptor analogs,  named vasopressin receptor 1 elements on a soluble scaffold (V1ROSS) proteins,  consist of the third intracellular loop and/or the C-terminal segment  of the hV1R receptor juxtaposed on the surface of the MBP. V1ROSS proteins  bind calmodulin and a truncated, phosphorylation-independent form of arrestin2  more tightly than the corresponding linear fusion proteins.	bind
34836	1	9987	6	11	NULL	NULL	NULL	[BeF3]ADP	Chemical		bind					NS3h	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_26_23311_s_155	12660239	A different type of fluorimetric titration was conducted to confirm that  [BeF3]ADP binding to NS3h indeed reduces its affinity for ssDNA.	bind
34837	2	9987	6	11	NULL	NULL	NULL	NS3h	GP		has affinity for					ssDNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_26_23311_s_155	12660239	A different type of fluorimetric titration was conducted to confirm that  [BeF3]ADP binding to NS3h indeed reduces its affinity for ssDNA.	bind
34838	3	9987	6	11	NULL	NULL	NULL	statement 1	Process		reduces					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_26_23311_s_155	12660239	A different type of fluorimetric titration was conducted to confirm that  [BeF3]ADP binding to NS3h indeed reduces its affinity for ssDNA.	bind
42606	1	9987	7	11	NULL	NULL	NULL	 [BeF3]ADP	Chemical		bind					NS3h	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_26_23311_s_155	12660239	A different type of fluorimetric titration was conducted to confirm that  [BeF3]ADP binding to NS3h indeed reduces its affinity for ssDNA.	bind
42607	2	9987	7	11	NULL	NULL	NULL	NS3h	GP		affinity for					ssDNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_26_23311_s_155	12660239	A different type of fluorimetric titration was conducted to confirm that  [BeF3]ADP binding to NS3h indeed reduces its affinity for ssDNA.	bind
42608	3	9987	7	11	NULL	NULL	NULL	statement 1	Process		reduces					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_26_23311_s_155	12660239	A different type of fluorimetric titration was conducted to confirm that  [BeF3]ADP binding to NS3h indeed reduces its affinity for ssDNA.	bind
34839	1	9989	6	11	NULL	NULL	NULL	O2	Chemical		bind					deoxyhemoglobin	GP				NULL	erythrocytes	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_30_18709_s_86	9668042	A Diffusion Model for Reaction of Free NO with RBCs-- Hartridge and Roughton ( 8) reported in 1927 that reaction (binding) of O2 with deoxyhemoglobin occurs much more slowly when the deoxyhemoglobin is contained within erythrocytes than when free in solution.	bind
34840	2	9989	6	11	NULL	NULL	NULL	O2	Chemical		bind					erythrocytes	Cell	free			NULL	solution	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_30_18709_s_86	9668042	A Diffusion Model for Reaction of Free NO with RBCs-- Hartridge and Roughton ( 8) reported in 1927 that reaction (binding) of O2 with deoxyhemoglobin occurs much more slowly when the deoxyhemoglobin is contained within erythrocytes than when free in solution.	bind
34841	3	9989	6	11	NULL	NULL	NULL	statement 1	Process		slower than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_30_18709_s_86	9668042	A Diffusion Model for Reaction of Free NO with RBCs-- Hartridge and Roughton ( 8) reported in 1927 that reaction (binding) of O2 with deoxyhemoglobin occurs much more slowly when the deoxyhemoglobin is contained within erythrocytes than when free in solution.	bind
57124	4	9989	6	11	NULL	NULL	NULL	NO	Chemical	free	reacts with					RBCs	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_30_18709_s_86	9668042	A Diffusion Model for Reaction of Free NO with RBCs-- Hartridge and Roughton ( 8) reported in 1927 that reaction (binding) of O2 with deoxyhemoglobin occurs much more slowly when the deoxyhemoglobin is contained within erythrocytes than when free in solution.	bind
42609	1	9989	7	11	NULL	NULL	NULL	NO 	Chemical	free	reacts with					RBCs	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_30_18709_s_86	9668042	A Diffusion Model for Reaction of Free NO with RBCs-- Hartridge and Roughton ( 8) reported in 1927 that reaction (binding) of O2 with deoxyhemoglobin occurs much more slowly when the deoxyhemoglobin is contained within erythrocytes than when free in solution.	bind
42610	2	9989	7	11	NULL	NULL	NULL	O2	Chemical		binds					deoxyhemoglobin	GP				NULL	erythrocytes	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_30_18709_s_86	9668042	A Diffusion Model for Reaction of Free NO with RBCs-- Hartridge and Roughton ( 8) reported in 1927 that reaction (binding) of O2 with deoxyhemoglobin occurs much more slowly when the deoxyhemoglobin is contained within erythrocytes than when free in solution.	bind
42611	3	9989	7	11	NULL	NULL	NULL	O2	Chemical		binds					deoxyhemoglobin	GP	free			NULL	solution	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_30_18709_s_86	9668042	A Diffusion Model for Reaction of Free NO with RBCs-- Hartridge and Roughton ( 8) reported in 1927 that reaction (binding) of O2 with deoxyhemoglobin occurs much more slowly when the deoxyhemoglobin is contained within erythrocytes than when free in solution.	bind
42612	4	9989	7	11	NULL	NULL	NULL	statement 2	Process		is slower than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_30_18709_s_86	9668042	A Diffusion Model for Reaction of Free NO with RBCs-- Hartridge and Roughton ( 8) reported in 1927 that reaction (binding) of O2 with deoxyhemoglobin occurs much more slowly when the deoxyhemoglobin is contained within erythrocytes than when free in solution.	bind
34842	1	9991	6	11	NULL	NULL	NULL	FGF-2	GP		bind					SOS	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_26_16382_s_150	9195945	A dimer formed by simultaneous binding of two FGF-2s to one SOS would thus be a head to head dimer where FGF-2 molecules are  trans to the SOS ligand (Fig.  4 A), with SOS presenting two anionic surfaces for binding.	bind
42614	1	9991	7	11	NULL	NULL	NULL	FGF-2	GP		bind					SOS	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_26_16382_s_150	9195945	A dimer formed by simultaneous binding of two FGF-2s to one SOS would thus be a head to head dimer where FGF-2 molecules are  trans to the SOS ligand (Fig.  4 A), with SOS presenting two anionic surfaces for binding.	bind
35078	1	9992	6	11	NULL	NULL	NULL	E2	GP		bind							proximal		E2 BS12	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3522_s_418	10652347	A dimer of E1 is first recruited to the E1-binding site by cooperative interactions with E2 bound to proximal E2 BS12 ( 13) or distal BS11.2 Sequences in the E1 palindrome are critical for dimer binding.	bind
35079	2	9992	6	11	NULL	NULL	NULL	E2	GP		bind							distal		BS11.2 Sequences in E1 palindrome	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3522_s_418	10652347	A dimer of E1 is first recruited to the E1-binding site by cooperative interactions with E2 bound to proximal E2 BS12 ( 13) or distal BS11.2 Sequences in the E1 palindrome are critical for dimer binding.	bind
35080	3	9992	6	11	NULL	NULL	NULL	E1 dimer	GP		is recruited to									E1-binding site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3522_s_418	10652347	A dimer of E1 is first recruited to the E1-binding site by cooperative interactions with E2 bound to proximal E2 BS12 ( 13) or distal BS11.2 Sequences in the E1 palindrome are critical for dimer binding.	bind
35081	4	9992	6	11	NULL	NULL	NULL	E1 dimer	GP		interacts with		cooperatively			statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3522_s_418	10652347	A dimer of E1 is first recruited to the E1-binding site by cooperative interactions with E2 bound to proximal E2 BS12 ( 13) or distal BS11.2 Sequences in the E1 palindrome are critical for dimer binding.	bind
35082	5	9992	6	11	NULL	NULL	NULL	E1 dimer	GP		interacts with		cooperatively			statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3522_s_418	10652347	A dimer of E1 is first recruited to the E1-binding site by cooperative interactions with E2 bound to proximal E2 BS12 ( 13) or distal BS11.2 Sequences in the E1 palindrome are critical for dimer binding.	bind
35083	6	9992	6	11	NULL	NULL	NULL	statement 3	Process		occurs via					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3522_s_418	10652347	A dimer of E1 is first recruited to the E1-binding site by cooperative interactions with E2 bound to proximal E2 BS12 ( 13) or distal BS11.2 Sequences in the E1 palindrome are critical for dimer binding.	bind
35084	7	9992	6	11	NULL	NULL	NULL	statement 3	Process		occurs via					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3522_s_418	10652347	A dimer of E1 is first recruited to the E1-binding site by cooperative interactions with E2 bound to proximal E2 BS12 ( 13) or distal BS11.2 Sequences in the E1 palindrome are critical for dimer binding.	bind
35085	8	9992	6	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3522_s_418	10652347	A dimer of E1 is first recruited to the E1-binding site by cooperative interactions with E2 bound to proximal E2 BS12 ( 13) or distal BS11.2 Sequences in the E1 palindrome are critical for dimer binding.	bind
42619	1	9992	7	11	NULL	NULL	NULL	E1 dimer	GP		recruits to									E1-binding site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3522_s_418	10652347	A dimer of E1 is first recruited to the E1-binding site by cooperative interactions with E2 bound to proximal E2 BS12 ( 13) or distal BS11.2 Sequences in the E1 palindrome are critical for dimer binding.	bind
42622	2	9992	7	11	NULL	NULL	NULL	E2	GP		bind							proximal		E2 BS12	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3522_s_418	10652347	A dimer of E1 is first recruited to the E1-binding site by cooperative interactions with E2 bound to proximal E2 BS12 ( 13) or distal BS11.2 Sequences in the E1 palindrome are critical for dimer binding.	bind
42623	3	9992	7	11	NULL	NULL	NULL	E2	GP		bind							distal		BS11.2 sequences in E1 palindrome	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3522_s_418	10652347	A dimer of E1 is first recruited to the E1-binding site by cooperative interactions with E2 bound to proximal E2 BS12 ( 13) or distal BS11.2 Sequences in the E1 palindrome are critical for dimer binding.	bind
42624	4	9992	7	11	NULL	NULL	NULL	E1 dimer	GP		interacts with		cooperatively			statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3522_s_418	10652347	A dimer of E1 is first recruited to the E1-binding site by cooperative interactions with E2 bound to proximal E2 BS12 ( 13) or distal BS11.2 Sequences in the E1 palindrome are critical for dimer binding.	bind
42637	5	9992	7	11	NULL	NULL	NULL	E1 dimer	GP		interacts with		cooperatively			statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3522_s_418	10652347	A dimer of E1 is first recruited to the E1-binding site by cooperative interactions with E2 bound to proximal E2 BS12 ( 13) or distal BS11.2 Sequences in the E1 palindrome are critical for dimer binding.	bind
42638	6	9992	7	11	NULL	NULL	NULL	statement 1	Process		occurs via					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3522_s_418	10652347	A dimer of E1 is first recruited to the E1-binding site by cooperative interactions with E2 bound to proximal E2 BS12 ( 13) or distal BS11.2 Sequences in the E1 palindrome are critical for dimer binding.	bind
49148	7	9992	7	11	NULL	NULL	NULL	statement 1	Process		occurs via					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3522_s_418	10652347	A dimer of E1 is first recruited to the E1-binding site by cooperative interactions with E2 bound to proximal E2 BS12 ( 13) or distal BS11.2 Sequences in the E1 palindrome are critical for dimer binding.	bind
57125	8	9992	7	11	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3522_s_418	10652347	A dimer of E1 is first recruited to the E1-binding site by cooperative interactions with E2 bound to proximal E2 BS12 ( 13) or distal BS11.2 Sequences in the E1 palindrome are critical for dimer binding.	bind
34843	1	9993	6	11	NULL	NULL	NULL	EBNA1 dimer	GP		bind									18 bp binding site	NULL		NULL	NULL	NULL	NULL	gw60_cell_84_5_791_s_66	8625416	A Dimer of EBNA1 Bound to Its  18 bp Binding Site	bind
42639	1	9993	7	11	NULL	NULL	NULL	 EBNA1 dimer	GP		bind									18 bp Binding Site	NULL		NULL	NULL	NULL	NULL	gw60_cell_84_5_791_s_66	8625416	A Dimer of EBNA1 Bound to Its  18 bp Binding Site	bind
34844	1	9994	6	11	NULL	NULL	NULL	EBNA1 dimer	GP		bind									18 bp recognition site	NULL		NULL	NULL	NULL	NULL	gw60_cell_84_5_791_s_201	8625416	A dimer of EBNA1 bound to its 18 bp recognition site cannot  function as an origin.	bind
34845	2	9994	6	11	NULL	NULL	NULL	EBNA1 dimer	GP		does not function as 					origin	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_5_791_s_201	8625416	A dimer of EBNA1 bound to its 18 bp recognition site cannot  function as an origin.	bind
42640	1	9994	7	11	NULL	NULL	NULL	EBNA1 dimer	GP		bind									18 bp recognition site	NULL		NULL	NULL	NULL	NULL	gw60_cell_84_5_791_s_201	8625416	A dimer of EBNA1 bound to its 18 bp recognition site cannot  function as an origin.	bind
42641	2	9994	7	11	NULL	NULL	NULL	statement 1	GP		does not function as					origin	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_cell_84_5_791_s_201	8625416	A dimer of EBNA1 bound to its 18 bp recognition site cannot  function as an origin.	bind
34846	1	9995	6	11	NULL	NULL	NULL	PICK1 dimer	GP		bind					PKC receptor subunit	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_6_919_s_131	10727702	A dimer of PICK1 could bind to both PKC  and AMPA receptor subunits, bringing active PKC  into intimate contact with the AMPA receptor.	bind
34847	2	9995	6	11	NULL	NULL	NULL	PICK1 dimer	GP		bind					AMPA receptor subunit	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_6_919_s_131	10727702	A dimer of PICK1 could bind to both PKC  and AMPA receptor subunits, bringing active PKC  into intimate contact with the AMPA receptor.	bind
34848	3	9995	6	11	NULL	NULL	NULL	PKC	GP	active	contact with		intimate			AMPA receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_6_919_s_131	10727702	A dimer of PICK1 could bind to both PKC  and AMPA receptor subunits, bringing active PKC  into intimate contact with the AMPA receptor.	bind
34849	4	9995	6	11	NULL	NULL	NULL	statement 1	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_6_919_s_131	10727702	A dimer of PICK1 could bind to both PKC  and AMPA receptor subunits, bringing active PKC  into intimate contact with the AMPA receptor.	bind
34850	5	9995	6	11	NULL	NULL	NULL	statement 2	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_6_919_s_131	10727702	A dimer of PICK1 could bind to both PKC  and AMPA receptor subunits, bringing active PKC  into intimate contact with the AMPA receptor.	bind
42642	1	9995	7	11	NULL	NULL	NULL	PICK1 dimer	GP		bind					PKC receptor subunit	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_6_919_s_131	10727702	A dimer of PICK1 could bind to both PKC  and AMPA receptor subunits, bringing active PKC  into intimate contact with the AMPA receptor.	bind
42643	2	9995	7	11	NULL	NULL	NULL	PICK1 dimer	GP		bind					AMPA receptor subunit	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_6_919_s_131	10727702	A dimer of PICK1 could bind to both PKC  and AMPA receptor subunits, bringing active PKC  into intimate contact with the AMPA receptor.	bind
42644	3	9995	7	11	NULL	NULL	NULL	PKC	GP	active	contact with		intimate			AMPA receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_6_919_s_131	10727702	A dimer of PICK1 could bind to both PKC  and AMPA receptor subunits, bringing active PKC  into intimate contact with the AMPA receptor.	bind
42645	4	9995	7	11	NULL	NULL	NULL	statement 1	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_6_919_s_131	10727702	A dimer of PICK1 could bind to both PKC  and AMPA receptor subunits, bringing active PKC  into intimate contact with the AMPA receptor.	bind
42646	5	9995	7	11	NULL	NULL	NULL	statement 2	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_6_919_s_131	10727702	A dimer of PICK1 could bind to both PKC  and AMPA receptor subunits, bringing active PKC  into intimate contact with the AMPA receptor.	bind
34851	1	9996	6	11	NULL	NULL	NULL	SRF dimer	GP		bind									SRE at 300 in promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12202_s_38	9770464	A dimer of SRF and one molecule of Elk-1 (also known as TCF, ternary complex factor) bind to the serum response element (SRE) centered at  300 in the promoter ( 27).	bind
34852	2	9996	6	11	NULL	NULL	NULL	Elk-1	GP		is a synonym of					TCF	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12202_s_38	9770464	A dimer of SRF and one molecule of Elk-1 (also known as TCF, ternary complex factor) bind to the serum response element (SRE) centered at  300 in the promoter ( 27).	bind
34853	3	9996	6	11	NULL	NULL	NULL	TCF	GP		is					ternary complex factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12202_s_38	9770464	A dimer of SRF and one molecule of Elk-1 (also known as TCF, ternary complex factor) bind to the serum response element (SRE) centered at  300 in the promoter ( 27).	bind
34854	4	9996	6	11	NULL	NULL	NULL	Elk-1	GP		bind									SRE at 300 in promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12202_s_38	9770464	A dimer of SRF and one molecule of Elk-1 (also known as TCF, ternary complex factor) bind to the serum response element (SRE) centered at  300 in the promoter ( 27).	bind
34855	5	9996	6	11	NULL	NULL	NULL	SRE	GP		is					serum response element	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12202_s_38	9770464	A dimer of SRF and one molecule of Elk-1 (also known as TCF, ternary complex factor) bind to the serum response element (SRE) centered at  300 in the promoter ( 27).	bind
42647	1	9996	7	11	NULL	NULL	NULL	SRF dimer	GP		bind									SRE at 300 in the promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12202_s_38	9770464	A dimer of SRF and one molecule of Elk-1 (also known as TCF, ternary complex factor) bind to the serum response element (SRE) centered at  300 in the promoter ( 27).	bind
42648	2	9996	7	11	NULL	NULL	NULL	Elk-1 	GP		bind									SRE at 300 in the promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12202_s_38	9770464	A dimer of SRF and one molecule of Elk-1 (also known as TCF, ternary complex factor) bind to the serum response element (SRE) centered at  300 in the promoter ( 27).	bind
42649	3	9996	7	11	NULL	NULL	NULL	Elk-1 	GP		is a synonym of					TCF	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12202_s_38	9770464	A dimer of SRF and one molecule of Elk-1 (also known as TCF, ternary complex factor) bind to the serum response element (SRE) centered at  300 in the promoter ( 27).	bind
42650	4	9996	7	11	NULL	NULL	NULL	TCF	GP		is					ternary complex factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12202_s_38	9770464	A dimer of SRF and one molecule of Elk-1 (also known as TCF, ternary complex factor) bind to the serum response element (SRE) centered at  300 in the promoter ( 27).	bind
42651	5	9996	7	11	NULL	NULL	NULL	SRE	GP		is					serum response element	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12202_s_38	9770464	A dimer of SRF and one molecule of Elk-1 (also known as TCF, ternary complex factor) bind to the serum response element (SRE) centered at  300 in the promoter ( 27).	bind
34996	1	9997	6	11	NULL	NULL	NULL	IscA	GP		is a type of					FeS cluster biosynthesis protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_22_0_457_s_1112	16824008	A dimer of the FeS cluster biosynthesis protein IscA from cyanobacteria  binds a [2Fe2] cluster between two protomers and transfers it to [2Fe2] and [4Fe4]  apo proteins.	bind
34997	2	9997	6	11	NULL	NULL	NULL	IscA dimer	GP	cyanobacteria	bind					[2Fe2] cluster 	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_22_0_457_s_1112	16824008	A dimer of the FeS cluster biosynthesis protein IscA from cyanobacteria  binds a [2Fe2] cluster between two protomers and transfers it to [2Fe2] and [4Fe4]  apo proteins.	bind
34998	3	9997	6	11	NULL	NULL	NULL	[2Fe2] cluster 	Chemical		is transfered to					[2Fe2] apo protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_22_0_457_s_1112	16824008	A dimer of the FeS cluster biosynthesis protein IscA from cyanobacteria  binds a [2Fe2] cluster between two protomers and transfers it to [2Fe2] and [4Fe4]  apo proteins.	bind
34999	4	9997	6	11	NULL	NULL	NULL	[2Fe2] cluster	Chemical		is transfered to					[4Fe4] apo protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_22_0_457_s_1112	16824008	A dimer of the FeS cluster biosynthesis protein IscA from cyanobacteria  binds a [2Fe2] cluster between two protomers and transfers it to [2Fe2] and [4Fe4]  apo proteins.	bind
35000	5	9997	6	11	NULL	NULL	NULL	statement 3	Process		occurs simultaneously with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_22_0_457_s_1112	16824008	A dimer of the FeS cluster biosynthesis protein IscA from cyanobacteria  binds a [2Fe2] cluster between two protomers and transfers it to [2Fe2] and [4Fe4]  apo proteins.	bind
35001	6	9997	6	11	NULL	NULL	NULL	statement 2	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_22_0_457_s_1112	16824008	A dimer of the FeS cluster biosynthesis protein IscA from cyanobacteria  binds a [2Fe2] cluster between two protomers and transfers it to [2Fe2] and [4Fe4]  apo proteins.	bind
35002	7	9997	6	11	NULL	NULL	NULL	statement 2	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_22_0_457_s_1112	16824008	A dimer of the FeS cluster biosynthesis protein IscA from cyanobacteria  binds a [2Fe2] cluster between two protomers and transfers it to [2Fe2] and [4Fe4]  apo proteins.	bind
42652	1	9997	7	11	NULL	NULL	NULL	IscA dimer	GP	cyanobacteria	binds					[2Fe2] cluster	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_22_0_457_s_1112	16824008	A dimer of the FeS cluster biosynthesis protein IscA from cyanobacteria  binds a [2Fe2] cluster between two protomers and transfers it to [2Fe2] and [4Fe4]  apo proteins.	bind
42653	2	9997	7	11	NULL	NULL	NULL	[2Fe2] cluster 	Chemical		is transfered to					[2Fe2] apo protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_22_0_457_s_1112	16824008	A dimer of the FeS cluster biosynthesis protein IscA from cyanobacteria  binds a [2Fe2] cluster between two protomers and transfers it to [2Fe2] and [4Fe4]  apo proteins.	bind
42654	3	9997	7	11	NULL	NULL	NULL	[2Fe2] cluster	Chemical		is transfered to					[4Fe4] apo protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_22_0_457_s_1112	16824008	A dimer of the FeS cluster biosynthesis protein IscA from cyanobacteria  binds a [2Fe2] cluster between two protomers and transfers it to [2Fe2] and [4Fe4]  apo proteins.	bind
42655	4	9997	7	11	NULL	NULL	NULL	IscA	GP		is a type of					FeS cluster biosynthesis protein 	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_22_0_457_s_1112	16824008	A dimer of the FeS cluster biosynthesis protein IscA from cyanobacteria  binds a [2Fe2] cluster between two protomers and transfers it to [2Fe2] and [4Fe4]  apo proteins.	bind
49149	5	9997	7	11	NULL	NULL	NULL	statement 2	Process		occurs simultaneously with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_22_0_457_s_1112	16824008	A dimer of the FeS cluster biosynthesis protein IscA from cyanobacteria  binds a [2Fe2] cluster between two protomers and transfers it to [2Fe2] and [4Fe4]  apo proteins.	bind
49150	6	9997	7	11	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_22_0_457_s_1112	16824008	A dimer of the FeS cluster biosynthesis protein IscA from cyanobacteria  binds a [2Fe2] cluster between two protomers and transfers it to [2Fe2] and [4Fe4]  apo proteins.	bind
49151	7	9997	7	11	NULL	NULL	NULL	statement 1	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_22_0_457_s_1112	16824008	A dimer of the FeS cluster biosynthesis protein IscA from cyanobacteria  binds a [2Fe2] cluster between two protomers and transfers it to [2Fe2] and [4Fe4]  apo proteins.	bind
35003	1	10000	6	11	NULL	NULL	NULL	importin	GP		bind								NLS		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_2_89_s_20	9427645	A dimeric receptor comprising importin    (that binds the NLS) and importin    (that mediates translocation) imports proteins bearing the classical NLS motif, which contains basic residues      [1-4,15]  .	bind
35004	2	10000	6	11	NULL	NULL	NULL	importin	GP		mediates					translocation	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_2_89_s_20	9427645	A dimeric receptor comprising importin    (that binds the NLS) and importin    (that mediates translocation) imports proteins bearing the classical NLS motif, which contains basic residues      [1-4,15]  .	bind
35005	3	10000	6	11	NULL	NULL	NULL	dimeric receptor	GP		comprise					statement 1 & statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_2_89_s_20	9427645	A dimeric receptor comprising importin    (that binds the NLS) and importin    (that mediates translocation) imports proteins bearing the classical NLS motif, which contains basic residues      [1-4,15]  .	bind
35006	4	10000	6	11	NULL	NULL	NULL	statement 3	Process		imports 					proteins 	GP		classical NLS motif		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_2_89_s_20	9427645	A dimeric receptor comprising importin    (that binds the NLS) and importin    (that mediates translocation) imports proteins bearing the classical NLS motif, which contains basic residues      [1-4,15]  .	bind
35007	5	10000	6	11	NULL	NULL	NULL				contains			classical NLS motif		basic residues	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_2_89_s_20	9427645	A dimeric receptor comprising importin    (that binds the NLS) and importin    (that mediates translocation) imports proteins bearing the classical NLS motif, which contains basic residues      [1-4,15]  .	bind
42656	3	10000	7	11	NULL	NULL	NULL	dimeric receptor	GP		comprise					statement 1 & statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_2_89_s_20	9427645	A dimeric receptor comprising importin    (that binds the NLS) and importin    (that mediates translocation) imports proteins bearing the classical NLS motif, which contains basic residues      [1-4,15]  .	bind
42657	1	10000	7	11	NULL	NULL	NULL	importin	GP		binds								NLS		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_2_89_s_20	9427645	A dimeric receptor comprising importin    (that binds the NLS) and importin    (that mediates translocation) imports proteins bearing the classical NLS motif, which contains basic residues      [1-4,15]  .	bind
42658	2	10000	7	11	NULL	NULL	NULL	importin	GP		mediates					translocation	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_2_89_s_20	9427645	A dimeric receptor comprising importin    (that binds the NLS) and importin    (that mediates translocation) imports proteins bearing the classical NLS motif, which contains basic residues      [1-4,15]  .	bind
42660	4	10000	7	11	NULL	NULL	NULL	statement 3	Process		imports					proteins	GP		 classical NLS motif		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_2_89_s_20	9427645	A dimeric receptor comprising importin    (that binds the NLS) and importin    (that mediates translocation) imports proteins bearing the classical NLS motif, which contains basic residues      [1-4,15]  .	bind
42661	5	10000	7	11	NULL	NULL	NULL				contains			classical NLS motif		basic residues	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_2_89_s_20	9427645	A dimeric receptor comprising importin    (that binds the NLS) and importin    (that mediates translocation) imports proteins bearing the classical NLS motif, which contains basic residues      [1-4,15]  .	bind
35008	1	10001	6	11	NULL	NULL	NULL	p85	GP		bind					IRS-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_11_2569_s_169	8647950	A diminished binding of p85 to IRS-1 containing the Gly  Arg  substitution could be due to an effect of the mutation on the  tertiary structure of IRS-1.	bind
35009	2	10001	6	11	NULL	NULL	NULL	IRS-1	GP		effects			Gly Arg substitution		IRS-1	GP	tertiary structure of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_11_2569_s_169	8647950	A diminished binding of p85 to IRS-1 containing the Gly  Arg  substitution could be due to an effect of the mutation on the  tertiary structure of IRS-1.	bind
35010	3	10001	6	11	NULL	NULL	NULL	p85	GP		bind					IRS-1	GP		Gly Arg substitution		NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_11_2569_s_169	8647950	A diminished binding of p85 to IRS-1 containing the Gly  Arg  substitution could be due to an effect of the mutation on the  tertiary structure of IRS-1.	bind
35011	4	10001	6	11	NULL	NULL	NULL	statement 1	Process	affinity of	is less than					statement 3	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_11_2569_s_169	8647950	A diminished binding of p85 to IRS-1 containing the Gly  Arg  substitution could be due to an effect of the mutation on the  tertiary structure of IRS-1.	bind
35012	5	10001	6	11	NULL	NULL	NULL	statement 4	Process		could be due to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_11_2569_s_169	8647950	A diminished binding of p85 to IRS-1 containing the Gly  Arg  substitution could be due to an effect of the mutation on the  tertiary structure of IRS-1.	bind
42662	1	10001	7	11	NULL	NULL	NULL	IRS-1	GP		substituted with			Gly		IRS-1	GP		Arg		NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_11_2569_s_169	8647950	A diminished binding of p85 to IRS-1 containing the Gly  Arg  substitution could be due to an effect of the mutation on the  tertiary structure of IRS-1.	bind
42663	2	10001	7	11	NULL	NULL	NULL	p85	GP		bind					IRS-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_11_2569_s_169	8647950	A diminished binding of p85 to IRS-1 containing the Gly  Arg  substitution could be due to an effect of the mutation on the  tertiary structure of IRS-1.	bind
57614	3	10001	7	11	NULL	NULL	NULL	p85	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_11_2569_s_169	8647950	A diminished binding of p85 to IRS-1 containing the Gly  Arg  substitution could be due to an effect of the mutation on the  tertiary structure of IRS-1.	bind
57615	4	10001	7	11	NULL	NULL	NULL	statement 3	Process	affinity of	is lesser than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_11_2569_s_169	8647950	A diminished binding of p85 to IRS-1 containing the Gly  Arg  substitution could be due to an effect of the mutation on the  tertiary structure of IRS-1.	bind
57616	5	10001	7	11	NULL	NULL	NULL	mutation	Process		effect					IRS-1	GP	tertiary structure of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_11_2569_s_169	8647950	A diminished binding of p85 to IRS-1 containing the Gly  Arg  substitution could be due to an effect of the mutation on the  tertiary structure of IRS-1.	bind
57617	6	10001	7	11	NULL	NULL	NULL	statement 4	Process		because of					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_11_2569_s_169	8647950	A diminished binding of p85 to IRS-1 containing the Gly  Arg  substitution could be due to an effect of the mutation on the  tertiary structure of IRS-1.	bind
35013	1	10002	6	11	NULL	NULL	NULL	UBR1	GP		bind					N-degron	AminoAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7120_s_256	16055722	A dipeptide bearing type 1 or type 2 N-degron competitively inhibits the in vitro binding of UBR1 and UBR2 to N-degron ( ,  ).	bind
35014	2	10002	6	11	NULL	NULL	NULL	UBR2	GP		bind					N-degron	AminoAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7120_s_256	16055722	A dipeptide bearing type 1 or type 2 N-degron competitively inhibits the in vitro binding of UBR1 and UBR2 to N-degron ( ,  ).	bind
35015	3	10002	6	11	NULL	NULL	NULL	dipeptide bearing type 1 N-degron	AminoAcid		inhibits		competitively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7120_s_256	16055722	A dipeptide bearing type 1 or type 2 N-degron competitively inhibits the in vitro binding of UBR1 and UBR2 to N-degron ( ,  ).	bind
35016	4	10002	6	11	NULL	NULL	NULL	dipeptide bearing type 1 N-degron	AminoAcid		inhibits		competitively			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7120_s_256	16055722	A dipeptide bearing type 1 or type 2 N-degron competitively inhibits the in vitro binding of UBR1 and UBR2 to N-degron ( ,  ).	bind
35017	5	10002	6	11	NULL	NULL	NULL	dipeptide bearing type 2 N-degron	AminoAcid		inhibits		competitively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7120_s_256	16055722	A dipeptide bearing type 1 or type 2 N-degron competitively inhibits the in vitro binding of UBR1 and UBR2 to N-degron ( ,  ).	bind
35018	6	10002	6	11	NULL	NULL	NULL	dipeptide bearing type 2 N-degron	AminoAcid		inhibits		competitively			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7120_s_256	16055722	A dipeptide bearing type 1 or type 2 N-degron competitively inhibits the in vitro binding of UBR1 and UBR2 to N-degron ( ,  ).	bind
35019	7	10002	6	11	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7120_s_256	16055722	A dipeptide bearing type 1 or type 2 N-degron competitively inhibits the in vitro binding of UBR1 and UBR2 to N-degron ( ,  ).	bind
35020	8	10002	6	11	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7120_s_256	16055722	A dipeptide bearing type 1 or type 2 N-degron competitively inhibits the in vitro binding of UBR1 and UBR2 to N-degron ( ,  ).	bind
42664	1	10002	7	11	NULL	NULL	NULL	 UBR1	GP		bind					N-degron	AminoAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7120_s_256	16055722	A dipeptide bearing type 1 or type 2 N-degron competitively inhibits the in vitro binding of UBR1 and UBR2 to N-degron ( ,  ).	bind
42665	2	10002	7	11	NULL	NULL	NULL	UBR2	GP		bind					N-degron	AminoAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7120_s_256	16055722	A dipeptide bearing type 1 or type 2 N-degron competitively inhibits the in vitro binding of UBR1 and UBR2 to N-degron ( ,  ).	bind
42666	3	10002	7	11	NULL	NULL	NULL	dipeptide bearing type 1 N-degron 	AminoAcid		inhibits		competitively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7120_s_256	16055722	A dipeptide bearing type 1 or type 2 N-degron competitively inhibits the in vitro binding of UBR1 and UBR2 to N-degron ( ,  ).	bind
42667	4	10002	7	11	NULL	NULL	NULL	dipeptide bearing type 1 N-degron 	AminoAcid		inhibits		competitively			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7120_s_256	16055722	A dipeptide bearing type 1 or type 2 N-degron competitively inhibits the in vitro binding of UBR1 and UBR2 to N-degron ( ,  ).	bind
42668	5	10002	7	11	NULL	NULL	NULL	dipeptide bearing type 2 N-degron 	AminoAcid		inhibits		competitively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7120_s_256	16055722	A dipeptide bearing type 1 or type 2 N-degron competitively inhibits the in vitro binding of UBR1 and UBR2 to N-degron ( ,  ).	bind
42669	6	10002	7	11	NULL	NULL	NULL	dipeptide bearing type 2 N-degron 	AminoAcid		inhibits		competitively			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7120_s_256	16055722	A dipeptide bearing type 1 or type 2 N-degron competitively inhibits the in vitro binding of UBR1 and UBR2 to N-degron ( ,  ).	bind
49152	7	10002	7	11	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7120_s_256	16055722	A dipeptide bearing type 1 or type 2 N-degron competitively inhibits the in vitro binding of UBR1 and UBR2 to N-degron ( ,  ).	bind
49153	8	10002	7	11	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_16_7120_s_256	16055722	A dipeptide bearing type 1 or type 2 N-degron competitively inhibits the in vitro binding of UBR1 and UBR2 to N-degron ( ,  ).	bind
35074	1	10003	6	11	NULL	NULL	NULL	DP IV	GP		is a type of					aminopeptidase	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_9_5063_s_8	12690074	A dipeptide mimicking inhibitor complexed to the active site discloses key determinants for substrate recognition, including a Glu-Glu motif that distinguishes DP IV as an aminopeptidase and an oxyanion trap that binds and activates the P2-carbonyl oxygen necessary for efficient postproline cleavage.	bind
35075	2	10003	6	11	NULL	NULL	NULL	oxyanion trap	Chemical		bind					P2-carbonyl oxygen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_9_5063_s_8	12690074	A dipeptide mimicking inhibitor complexed to the active site discloses key determinants for substrate recognition, including a Glu-Glu motif that distinguishes DP IV as an aminopeptidase and an oxyanion trap that binds and activates the P2-carbonyl oxygen necessary for efficient postproline cleavage.	bind
35076	3	10003	6	11	NULL	NULL	NULL	statement 2	Process		activates					P2-carbonyl oxygen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_9_5063_s_8	12690074	A dipeptide mimicking inhibitor complexed to the active site discloses key determinants for substrate recognition, including a Glu-Glu motif that distinguishes DP IV as an aminopeptidase and an oxyanion trap that binds and activates the P2-carbonyl oxygen necessary for efficient postproline cleavage.	bind
35077	4	10003	6	11	NULL	NULL	NULL	statement 3	Process		is necessary for					postproline	AminoAcid	efficient cleavage of 			NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_9_5063_s_8	12690074	A dipeptide mimicking inhibitor complexed to the active site discloses key determinants for substrate recognition, including a Glu-Glu motif that distinguishes DP IV as an aminopeptidase and an oxyanion trap that binds and activates the P2-carbonyl oxygen necessary for efficient postproline cleavage.	bind
42678	1	10003	7	11	NULL	NULL	NULL	oxyanion trap	Chemical		binds					P2-carbonyl oxygen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_9_5063_s_8	12690074	A dipeptide mimicking inhibitor complexed to the active site discloses key determinants for substrate recognition, including a Glu-Glu motif that distinguishes DP IV as an aminopeptidase and an oxyanion trap that binds and activates the P2-carbonyl oxygen necessary for efficient postproline cleavage.	bind
42679	2	10003	7	11	NULL	NULL	NULL	statement 1	Process		activates					P2-carbonyl oxygen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_9_5063_s_8	12690074	A dipeptide mimicking inhibitor complexed to the active site discloses key determinants for substrate recognition, including a Glu-Glu motif that distinguishes DP IV as an aminopeptidase and an oxyanion trap that binds and activates the P2-carbonyl oxygen necessary for efficient postproline cleavage.	bind
42680	3	10003	7	11	NULL	NULL	NULL	statement 2	Process		is necessary for					postproline	AminoAcid	efficient cleavage of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_9_5063_s_8	12690074	A dipeptide mimicking inhibitor complexed to the active site discloses key determinants for substrate recognition, including a Glu-Glu motif that distinguishes DP IV as an aminopeptidase and an oxyanion trap that binds and activates the P2-carbonyl oxygen necessary for efficient postproline cleavage.	bind
42685	4	10003	7	11	NULL	NULL	NULL	DP IV	GP		is a type of					aminopeptidase	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_9_5063_s_8	12690074	A dipeptide mimicking inhibitor complexed to the active site discloses key determinants for substrate recognition, including a Glu-Glu motif that distinguishes DP IV as an aminopeptidase and an oxyanion trap that binds and activates the P2-carbonyl oxygen necessary for efficient postproline cleavage.	bind
35023	1	10005	6	11	NULL	NULL	NULL	She2p	GP		bind		directly			She3p	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_19_20_5514_s_247	11032818	A direct  ASH1 RNA-independent binding of She2p and She3p is suggested by our  in vitro pulldown experiments.	bind
35024	2	10005	6	11	NULL	NULL	NULL	statement 1	Process		is independent of					ASH1 RNA	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_19_20_5514_s_247	11032818	A direct  ASH1 RNA-independent binding of She2p and She3p is suggested by our  in vitro pulldown experiments.	bind
42721	1	10005	7	11	NULL	NULL	NULL	She2p	GP		bind		directly			She3p	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_19_20_5514_s_247	11032818	A direct  ASH1 RNA-independent binding of She2p and She3p is suggested by our  in vitro pulldown experiments.	bind
42722	2	10005	7	11	NULL	NULL	NULL	statement 1	Process		is independent of					ASH1 RNA	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_19_20_5514_s_247	11032818	A direct  ASH1 RNA-independent binding of She2p and She3p is suggested by our  in vitro pulldown experiments.	bind
35025	1	10006	6	11	NULL	NULL	NULL	DAG	Chemical	PC-derived	activates		directly			Raf-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_36_21299_s_17	7673165	A direct activation of  Raf-1 by PC-derived DAG may also be possible since the enzyme contains  a cysteine finger in the regulatory domain similar to the DAG binding  motifs of PKC and DAG kinase( 20) .	bind
35026	2	10006	6	11	NULL	NULL	NULL	DAG	Chemical	PC-derived	is similar to			cysteine finger in the regulatory domain		PKC kinase	GP		DAG binding motif		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_36_21299_s_17	7673165	A direct activation of  Raf-1 by PC-derived DAG may also be possible since the enzyme contains  a cysteine finger in the regulatory domain similar to the DAG binding  motifs of PKC and DAG kinase( 20) .	bind
35027	3	10006	6	11	NULL	NULL	NULL	DAG	Chemical	PC-derived	is similar to			cysteine finger in the regulatory domain		DAG kinase	GP		DAG binding motif		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_36_21299_s_17	7673165	A direct activation of  Raf-1 by PC-derived DAG may also be possible since the enzyme contains  a cysteine finger in the regulatory domain similar to the DAG binding  motifs of PKC and DAG kinase( 20) .	bind
35029	4	10006	6	11	NULL	NULL	NULL	statement 1	Process		occurs due to		may			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_36_21299_s_17	7673165	A direct activation of  Raf-1 by PC-derived DAG may also be possible since the enzyme contains  a cysteine finger in the regulatory domain similar to the DAG binding  motifs of PKC and DAG kinase( 20) .	bind
35030	5	10006	6	11	NULL	NULL	NULL	statement 1	Process		occurs due to		may			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_36_21299_s_17	7673165	A direct activation of  Raf-1 by PC-derived DAG may also be possible since the enzyme contains  a cysteine finger in the regulatory domain similar to the DAG binding  motifs of PKC and DAG kinase( 20) .	bind
42725	1	10006	7	11	NULL	NULL	NULL	DAG 	Chemical	PC-derived	activates		directly			Raf-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_36_21299_s_17	7673165	A direct activation of  Raf-1 by PC-derived DAG may also be possible since the enzyme contains  a cysteine finger in the regulatory domain similar to the DAG binding  motifs of PKC and DAG kinase( 20) .	bind
42726	2	10006	7	11	NULL	NULL	NULL	 DAG 	Chemical	PC-derived	is similar to			cysteine finger in the regulatory domain		PKC kinase	GP		DAG binding motif		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_36_21299_s_17	7673165	A direct activation of  Raf-1 by PC-derived DAG may also be possible since the enzyme contains  a cysteine finger in the regulatory domain similar to the DAG binding  motifs of PKC and DAG kinase( 20) .	bind
42727	3	10006	7	11	NULL	NULL	NULL	DAG	Chemical	PC-derived	is similar to			cysteine finger in the regulatory domain		DAG kinase	GP		DAG binding motifs		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_36_21299_s_17	7673165	A direct activation of  Raf-1 by PC-derived DAG may also be possible since the enzyme contains  a cysteine finger in the regulatory domain similar to the DAG binding  motifs of PKC and DAG kinase( 20) .	bind
42728	4	10006	7	11	NULL	NULL	NULL	statement 1	Process		occurs due to		may			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_36_21299_s_17	7673165	A direct activation of  Raf-1 by PC-derived DAG may also be possible since the enzyme contains  a cysteine finger in the regulatory domain similar to the DAG binding  motifs of PKC and DAG kinase( 20) .	bind
49330	5	10006	7	11	NULL	NULL	NULL	statement 1	Process		occurs due to		may			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_36_21299_s_17	7673165	A direct activation of  Raf-1 by PC-derived DAG may also be possible since the enzyme contains  a cysteine finger in the regulatory domain similar to the DAG binding  motifs of PKC and DAG kinase( 20) .	bind
49556	1	10007	6	11	NULL	NULL	NULL			mutant	effects			Gly-294		L-serine	AminoAcid	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_21_17844_s_104	11278587	A direct analysis of L-serine binding by equilibrium dialysis was performed to look at the effect of mutating Gly-294 on serine binding (Fig.  5).	bind
42729	1	10007	7	11	NULL	NULL	NULL			mutant	effect			Gly-294		L-serine	AminoAcid	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_21_17844_s_104	11278587	A direct analysis of L-serine binding by equilibrium dialysis was performed to look at the effect of mutating Gly-294 on serine binding (Fig.  5).	bind
49561	1	10008	6	11	NULL	NULL	NULL	vitronectin	GP		bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1545_1_289_s_131	11342054	A direct assay was used to measure vitronectin binding to heparin-coated microtiter plates.	bind
42730	1	10008	7	11	NULL	NULL	NULL	vitronectin	GP		bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1545_1_289_s_131	11342054	A direct assay was used to measure vitronectin binding to heparin-coated microtiter plates.	bind
35031	1	10009	6	11	NULL	NULL	NULL	DEDD	GP	FLAG-tagged;; in vitro translated	bind					ubiquitin	GP				NULL		NULL	NULL	NULL	NULL	gw70_amjpathol_164_2_395_s_168	14742246	A direct binding assay of FLAG-tagged,  in vitro translated, DEDD shows binding of DEDD, but not the dominant-negative derivative  of FADD (DN-FADD), to ubiquitin Sepharose (Ubi-Seph).	bind
35032	2	10009	6	11	NULL	NULL	NULL	DN-FADD	GP		does not bind					ubiquitin	GP				NULL		NULL	NULL	NULL	NULL	gw70_amjpathol_164_2_395_s_168	14742246	A direct binding assay of FLAG-tagged,  in vitro translated, DEDD shows binding of DEDD, but not the dominant-negative derivative  of FADD (DN-FADD), to ubiquitin Sepharose (Ubi-Seph).	bind
35033	3	10009	6	11	NULL	NULL	NULL	DN-FADD	GP		is					dominant-negative derivative of FADD	GP				NULL		NULL	NULL	NULL	NULL	gw70_amjpathol_164_2_395_s_168	14742246	A direct binding assay of FLAG-tagged,  in vitro translated, DEDD shows binding of DEDD, but not the dominant-negative derivative  of FADD (DN-FADD), to ubiquitin Sepharose (Ubi-Seph).	bind
42731	1	10009	7	11	NULL	NULL	NULL	DEDD	GP	FLAG-tagged;;in vitro translated	bind					ubiquitin	GP				NULL		NULL	NULL	NULL	NULL	gw70_amjpathol_164_2_395_s_168	14742246	A direct binding assay of FLAG-tagged,  in vitro translated, DEDD shows binding of DEDD, but not the dominant-negative derivative  of FADD (DN-FADD), to ubiquitin Sepharose (Ubi-Seph).	bind
42732	2	10009	7	11	NULL	NULL	NULL	DN-FADD	GP		does not bind					ubiquitin	GP				NULL		NULL	NULL	NULL	NULL	gw70_amjpathol_164_2_395_s_168	14742246	A direct binding assay of FLAG-tagged,  in vitro translated, DEDD shows binding of DEDD, but not the dominant-negative derivative  of FADD (DN-FADD), to ubiquitin Sepharose (Ubi-Seph).	bind
42733	3	10009	7	11	NULL	NULL	NULL	DN-FADD	GP		is					dominant-negative derivative of FADD 	GP				NULL		NULL	NULL	NULL	NULL	gw70_amjpathol_164_2_395_s_168	14742246	A direct binding assay of FLAG-tagged,  in vitro translated, DEDD shows binding of DEDD, but not the dominant-negative derivative  of FADD (DN-FADD), to ubiquitin Sepharose (Ubi-Seph).	bind
57238	1	10010	6	10	NULL	0	NULL	Rdr1p			does not bind		directly			PDR5					NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_3_583_s_419	16959962	A direct binding of Rdr1p to  PDR5 has not been demonstrated, and the mode of binding (e.g., monomer or heterodimer)  of Yrm1p (in orange) is not known.	bind
42735	1	10010	7	NULL	NULL	0	NULL	Rdr1p	NULL		does not bind	NULL	directly			PDR5	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_3_583_s_419	16959962	A direct binding of Rdr1p to  PDR5 has not been demonstrated, and the mode of binding (e.g., monomer or heterodimer)  of Yrm1p (in orange) is not known.	bind
35034	1	10011	6	11	NULL	NULL	NULL	125I-FX	GP		bind		directly			sTF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3622_s_405	11723140	A direct binding plot for binding of 125I-FX to sTF is presented in Fig.  9 A and the  K d(app) obtained from this plot for binding of FX to sTF was 500  plus-or-minus  100 nM.	bind
42736	1	10011	7	11	NULL	NULL	NULL	125I-FX	GP		bind		directly			sTF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3622_s_405	11723140	A direct binding plot for binding of 125I-FX to sTF is presented in Fig.  9 A and the  K d(app) obtained from this plot for binding of FX to sTF was 500  plus-or-minus  100 nM.	bind
35035	1	10012	6	11	NULL	NULL	NULL	Phab B7	GP		has affinity for		high			B7 clone	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_19_5571_s_194	11544219	A direct comparison by ELISA of the binding properties of Phab B7 and Phab B9 also revealed a higher affinity of the B7 clone (Fig.  3).	bind
35036	2	10012	6	11	NULL	NULL	NULL	Phab B9	GP		has affinity for		high			B7 clone	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_19_5571_s_194	11544219	A direct comparison by ELISA of the binding properties of Phab B7 and Phab B9 also revealed a higher affinity of the B7 clone (Fig.  3).	bind
42737	1	10012	7	11	NULL	NULL	NULL	B7 clone	GP		affinity for		high			Phab B7	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_19_5571_s_194	11544219	A direct comparison by ELISA of the binding properties of Phab B7 and Phab B9 also revealed a higher affinity of the B7 clone (Fig.  3).	bind
42738	2	10012	7	11	NULL	NULL	NULL	B7 clone	GP		affinity for		high			Phab B9	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_19_5571_s_194	11544219	A direct comparison by ELISA of the binding properties of Phab B7 and Phab B9 also revealed a higher affinity of the B7 clone (Fig.  3).	bind
35037	1	10013	6	11	NULL	NULL	NULL	FKBP12	GP		bind		may			RyR	GP	cardiac			NULL	intact cells	NULL	NULL	NULL	NULL	gw60_circulationres_88_2_134_s_38	11157663	A direct comparison of control and FKBP12.6-overexpressing cells was therefore valid, because although in vitro experiments indicate that cardiac RyRs are poor substrates for FKBP12, 14 15  binding of FKBP12 to cardiac RyRs in intact cells has not been ruled out.	bind
35038	2	10013	6	3	NULL	0	NULL	RyR	GP	cardiac	substrate for		poor			FKBP12	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulationres_88_2_134_s_38	11157663	A direct comparison of control and FKBP12.6-overexpressing cells was therefore valid, because although in vitro experiments indicate that cardiac RyRs are poor substrates for FKBP12, 14 15  binding of FKBP12 to cardiac RyRs in intact cells has not been ruled out.	bind
42739	1	10013	7	3	NULL	0	NULL	RyRs	GP	cardiac	substrate for		poor			FKBP12	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_circulationres_88_2_134_s_38	11157663	A direct comparison of control and FKBP12.6-overexpressing cells was therefore valid, because although in vitro experiments indicate that cardiac RyRs are poor substrates for FKBP12, 14 15  binding of FKBP12 to cardiac RyRs in intact cells has not been ruled out.	bind
42742	4	10013	7	3	NULL	0	NULL	FKBP12	GP		bind		may			RyRs	GP	cardiac			NULL	intact cells	NULL	NULL	NULL	NULL	gw60_circulationres_88_2_134_s_38	11157663	A direct comparison of control and FKBP12.6-overexpressing cells was therefore valid, because although in vitro experiments indicate that cardiac RyRs are poor substrates for FKBP12, 14 15  binding of FKBP12 to cardiac RyRs in intact cells has not been ruled out.	bind
35039	1	10014	6	3	NULL	0	NULL	PLD	GP		bind					PC vesicles	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_50_35367_s_189	10585404	A direct comparison of PLD binding to PC and PS vesicles in the absence or presence of Ba2+ emphasizes this behavior	bind
35040	2	10014	6	3	NULL	0	NULL	PLD	GP		bind					PS vesicles	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_50_35367_s_189	10585404	A direct comparison of PLD binding to PC and PS vesicles in the absence or presence of Ba2+ emphasizes this behavior	bind
42743	1	10014	7	3	NULL	0	NULL	 PLD	GP		bind					PC vesicles	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_50_35367_s_189	10585404	A direct comparison of PLD binding to PC and PS vesicles in the absence or presence of Ba2+ emphasizes this behavior	bind
42744	2	10014	7	3	NULL	0	NULL	PLD	GP		bind					PS vesicles	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_50_35367_s_189	10585404	A direct comparison of PLD binding to PC and PS vesicles in the absence or presence of Ba2+ emphasizes this behavior	bind
35041	1	10015	6	3	NULL	0	NULL	ATP	Chemical		bind					Kir6.2	GP		C terminus		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_19_19097_s_173	15760904	A direct competition for binding between ATP and PIP2 at the C terminus of Kir6.2 has been reported ( ).	bind
35042	2	10015	6	3	NULL	0	NULL	PIP2	Chemical		bind					Kir6.2	GP		C terminus		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_19_19097_s_173	15760904	A direct competition for binding between ATP and PIP2 at the C terminus of Kir6.2 has been reported ( ).	bind
35043	3	10015	6	3	NULL	0	NULL	statement 1	Process		competes		directly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_19_19097_s_173	15760904	A direct competition for binding between ATP and PIP2 at the C terminus of Kir6.2 has been reported ( ).	bind
42745	1	10015	7	3	NULL	0	NULL	ATP 	Chemical		bind					Kir6.2	GP		 C terminus		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_19_19097_s_173	15760904	A direct competition for binding between ATP and PIP2 at the C terminus of Kir6.2 has been reported ( ).	bind
42746	2	10015	7	3	NULL	0	NULL	PIP2	Chemical		bind					Kir6.2	GP		C terminus		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_19_19097_s_173	15760904	A direct competition for binding between ATP and PIP2 at the C terminus of Kir6.2 has been reported ( ).	bind
42747	3	10015	7	3	NULL	0	NULL	statement 1	Process		competes with		directly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_19_19097_s_173	15760904	A direct competition for binding between ATP and PIP2 at the C terminus of Kir6.2 has been reported ( ).	bind
35044	1	10016	6	3	NULL	0	NULL	Vpu	GP		bind					beta-TrCP	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_280_5371_1880_s_89	9632380	A direct connection between Vpu and the proteasome was established by the demonstration that Vpu binds to a protein termed beta-TrCP, which in turn binds to the proteasome targeting factor Skp1p ( Fig. 3).	bind
35045	2	10016	6	3	NULL	0	NULL	statement 1	Process		bind					Skp1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_280_5371_1880_s_89	9632380	A direct connection between Vpu and the proteasome was established by the demonstration that Vpu binds to a protein termed beta-TrCP, which in turn binds to the proteasome targeting factor Skp1p ( Fig. 3).	bind
35046	3	10016	6	3	NULL	0	NULL	Skp1p	GP		is a type of					proteasome targeting factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_280_5371_1880_s_89	9632380	A direct connection between Vpu and the proteasome was established by the demonstration that Vpu binds to a protein termed beta-TrCP, which in turn binds to the proteasome targeting factor Skp1p ( Fig. 3).	bind
42748	1	10016	7	3	NULL	0	NULL	Vpu	GP		binds					beta-TrCP	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_280_5371_1880_s_89	9632380	A direct connection between Vpu and the proteasome was established by the demonstration that Vpu binds to a protein termed beta-TrCP, which in turn binds to the proteasome targeting factor Skp1p ( Fig. 3).	bind
42749	2	10016	7	3	NULL	0	NULL	statement 1	Process		binds					Skp1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_280_5371_1880_s_89	9632380	A direct connection between Vpu and the proteasome was established by the demonstration that Vpu binds to a protein termed beta-TrCP, which in turn binds to the proteasome targeting factor Skp1p ( Fig. 3).	bind
42750	3	10016	7	3	NULL	0	NULL	Skp1p	GP		is a type of					proteasome targeting factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_280_5371_1880_s_89	9632380	A direct connection between Vpu and the proteasome was established by the demonstration that Vpu binds to a protein termed beta-TrCP, which in turn binds to the proteasome targeting factor Skp1p ( Fig. 3).	bind
35047	1	10017	6	3	NULL	0	NULL	vitronectin	GP		bind					PAI-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5112_s_197	9030577	A direct consequence of vitronectin binding to PAI-1 is that the half-life of the active conformation of the serpin is increased 2-3-fold ( 17-19).	bind
35048	2	10017	6	3	NULL	0	NULL	statement 1	Process		increases					serpin	GP	half life of;; active conformation of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5112_s_197	9030577	A direct consequence of vitronectin binding to PAI-1 is that the half-life of the active conformation of the serpin is increased 2-3-fold ( 17-19).	bind
42751	1	10017	7	3	NULL	0	NULL	 vitronectin	GP		bind					PAI-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5112_s_197	9030577	A direct consequence of vitronectin binding to PAI-1 is that the half-life of the active conformation of the serpin is increased 2-3-fold ( 17-19).	bind
42752	2	10017	7	3	NULL	0	NULL	statement 1	Process		increase					serpin	GP	half-life of;;active conformation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_5112_s_197	9030577	A direct consequence of vitronectin binding to PAI-1 is that the half-life of the active conformation of the serpin is increased 2-3-fold ( 17-19).	bind
35049	1	10018	6	11	NULL	NULL	NULL	PV IgG	GP		bind					KC	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29466_s_350	10899159	A direct evidence of activation of second messenger systems in response to PV IgG binding to KC have been obtained in the studies showing changes with phospholipase C, inositol 1,4,5-trisphosphate, transmembrane flux and intracellular levels of Ca2+, intracellular cAMP/cGMP ratios, and activity and intracellular location of protein kinase C (reviewed in Refs.	bind
35070	2	10018	6	11	NULL	NULL	NULL	Ca2+	Chemical		is a type of					second messenger	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29466_s_350	10899159	A direct evidence of activation of second messenger systems in response to PV IgG binding to KC have been obtained in the studies showing changes with phospholipase C, inositol 1,4,5-trisphosphate, transmembrane flux and intracellular levels of Ca2+, intracellular cAMP/cGMP ratios, and activity and intracellular location of protein kinase C (reviewed in Refs.	bind
35071	3	10018	6	11	NULL	NULL	NULL	cAMP/cGMP	Chemical		is a type of					second messenger	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29466_s_350	10899159	A direct evidence of activation of second messenger systems in response to PV IgG binding to KC have been obtained in the studies showing changes with phospholipase C, inositol 1,4,5-trisphosphate, transmembrane flux and intracellular levels of Ca2+, intracellular cAMP/cGMP ratios, and activity and intracellular location of protein kinase C (reviewed in Refs.	bind
35072	4	10018	6	11	NULL	NULL	NULL	Ca2+	Chemical	activation of	occurs in response to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29466_s_350	10899159	A direct evidence of activation of second messenger systems in response to PV IgG binding to KC have been obtained in the studies showing changes with phospholipase C, inositol 1,4,5-trisphosphate, transmembrane flux and intracellular levels of Ca2+, intracellular cAMP/cGMP ratios, and activity and intracellular location of protein kinase C (reviewed in Refs.	bind
35073	5	10018	6	11	NULL	NULL	NULL	cAMP/cGMP	Chemical	activation of	occurs in response to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29466_s_350	10899159	A direct evidence of activation of second messenger systems in response to PV IgG binding to KC have been obtained in the studies showing changes with phospholipase C, inositol 1,4,5-trisphosphate, transmembrane flux and intracellular levels of Ca2+, intracellular cAMP/cGMP ratios, and activity and intracellular location of protein kinase C (reviewed in Refs.	bind
42753	1	10018	7	11	NULL	NULL	NULL	PV IgG	GP		bind					KC	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29466_s_350	10899159	A direct evidence of activation of second messenger systems in response to PV IgG binding to KC have been obtained in the studies showing changes with phospholipase C, inositol 1,4,5-trisphosphate, transmembrane flux and intracellular levels of Ca2+, intracellular cAMP/cGMP ratios, and activity and intracellular location of protein kinase C (reviewed in Refs.	bind
42754	2	10018	7	11	NULL	NULL	NULL	statement 1	Process		activates					second messenger systems	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29466_s_350	10899159	A direct evidence of activation of second messenger systems in response to PV IgG binding to KC have been obtained in the studies showing changes with phospholipase C, inositol 1,4,5-trisphosphate, transmembrane flux and intracellular levels of Ca2+, intracellular cAMP/cGMP ratios, and activity and intracellular location of protein kinase C (reviewed in Refs.	bind
42755	3	10018	7	11	NULL	NULL	NULL	statement 1	GP		activates					phospholipase C	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29466_s_350	10899159	A direct evidence of activation of second messenger systems in response to PV IgG binding to KC have been obtained in the studies showing changes with phospholipase C, inositol 1,4,5-trisphosphate, transmembrane flux and intracellular levels of Ca2+, intracellular cAMP/cGMP ratios, and activity and intracellular location of protein kinase C (reviewed in Refs.	bind
42756	4	10018	7	11	NULL	NULL	NULL	statement 1	GP		activates					inositol 1,4,5-trisphosphate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29466_s_350	10899159	A direct evidence of activation of second messenger systems in response to PV IgG binding to KC have been obtained in the studies showing changes with phospholipase C, inositol 1,4,5-trisphosphate, transmembrane flux and intracellular levels of Ca2+, intracellular cAMP/cGMP ratios, and activity and intracellular location of protein kinase C (reviewed in Refs.	bind
42757	5	10018	7	11	NULL	NULL	NULL	statement 1	GP		activates					Ca2+	Chemical	transmembrane flux of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29466_s_350	10899159	A direct evidence of activation of second messenger systems in response to PV IgG binding to KC have been obtained in the studies showing changes with phospholipase C, inositol 1,4,5-trisphosphate, transmembrane flux and intracellular levels of Ca2+, intracellular cAMP/cGMP ratios, and activity and intracellular location of protein kinase C (reviewed in Refs.	bind
42758	6	10018	7	11	NULL	NULL	NULL	statement 1	GP		activates					Ca2+	Chemical	intracellular levels of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29466_s_350	10899159	A direct evidence of activation of second messenger systems in response to PV IgG binding to KC have been obtained in the studies showing changes with phospholipase C, inositol 1,4,5-trisphosphate, transmembrane flux and intracellular levels of Ca2+, intracellular cAMP/cGMP ratios, and activity and intracellular location of protein kinase C (reviewed in Refs.	bind
42759	7	10018	7	11	NULL	NULL	NULL	statement 1	GP		activates					cAMP/cGMP	Chemical	intracellular ratios of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29466_s_350	10899159	A direct evidence of activation of second messenger systems in response to PV IgG binding to KC have been obtained in the studies showing changes with phospholipase C, inositol 1,4,5-trisphosphate, transmembrane flux and intracellular levels of Ca2+, intracellular cAMP/cGMP ratios, and activity and intracellular location of protein kinase C (reviewed in Refs.	bind
42760	8	10018	7	11	NULL	NULL	NULL	statement 1	GP		activates					protein kinase C	GP	intracellular location of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29466_s_350	10899159	A direct evidence of activation of second messenger systems in response to PV IgG binding to KC have been obtained in the studies showing changes with phospholipase C, inositol 1,4,5-trisphosphate, transmembrane flux and intracellular levels of Ca2+, intracellular cAMP/cGMP ratios, and activity and intracellular location of protein kinase C (reviewed in Refs.	bind
42761	9	10018	7	11	NULL	NULL	NULL	statement 1	GP		activates					protein kinase C	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_38_29466_s_350	10899159	A direct evidence of activation of second messenger systems in response to PV IgG binding to KC have been obtained in the studies showing changes with phospholipase C, inositol 1,4,5-trisphosphate, transmembrane flux and intracellular levels of Ca2+, intracellular cAMP/cGMP ratios, and activity and intracellular location of protein kinase C (reviewed in Refs.	bind
35050	1	10019	6	11	NULL	NULL	NULL	apo E	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_232	7600129	A direct inhibition of apo E binding to the LDL receptor by apo CIII cannot be excluded.	bind
35051	2	10019	6	11	NULL	NULL	NULL	apo CIII	GP		inhibits		directly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_232	7600129	A direct inhibition of apo E binding to the LDL receptor by apo CIII cannot be excluded.	bind
42762	1	10019	7	11	NULL	NULL	NULL	apo E	GP		bind					LDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_232	7600129	A direct inhibition of apo E binding to the LDL receptor by apo CIII cannot be excluded.	bind
42763	2	10019	7	11	NULL	NULL	NULL	apo CIII	GP		inhibits		directly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_7_963_s_232	7600129	A direct inhibition of apo E binding to the LDL receptor by apo CIII cannot be excluded.	bind
35052	1	10020	6	11	NULL	NULL	NULL	CHIP	GP		interacts with		directly			AR	GP		NH2-terminal conserved motif		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_29_30643_s_248	15107424	A direct interaction between CHIP and the AR NH2-terminal conserved motif was confirmed in mammalian two-hybrid and GST affinity matrix binding assays, supporting the initial identification of CHIP in a yeast two-hybrid screen as a  bona fide AR-interacting protein.	bind
42764	1	10020	7	11	NULL	NULL	NULL	CHIP	GP		interacts with		directly			 AR	GP		NH2-terminal conserved motif		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_29_30643_s_248	15107424	A direct interaction between CHIP and the AR NH2-terminal conserved motif was confirmed in mammalian two-hybrid and GST affinity matrix binding assays, supporting the initial identification of CHIP in a yeast two-hybrid screen as a  bona fide AR-interacting protein.	bind
35053	1	10021	6	11	NULL	NULL	NULL	Swi5	GP		interacts 		directly			SWI/SNF	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_94	16705163	A direct interaction between Swi5 and SWI/SNF has been demonstrated in vitro ( ), and a  swi5 mutation eliminates SWI/SNF binding to  HO in vivo ( ).	bind
35054	2	10021	6	11	NULL	NULL	NULL	SWI/SNF	GP		bind					HO	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_94	16705163	A direct interaction between Swi5 and SWI/SNF has been demonstrated in vitro ( ), and a  swi5 mutation eliminates SWI/SNF binding to  HO in vivo ( ).	bind
35055	3	10021	6	11	NULL	NULL	NULL	Swi5	GP	mutant	eliminates					statement 2	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_94	16705163	A direct interaction between Swi5 and SWI/SNF has been demonstrated in vitro ( ), and a  swi5 mutation eliminates SWI/SNF binding to  HO in vivo ( ).	bind
42765	1	10021	7	11	NULL	NULL	NULL	Swi5 	GP		interacts with		directly			SWI/SNF	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_94	16705163	A direct interaction between Swi5 and SWI/SNF has been demonstrated in vitro ( ), and a  swi5 mutation eliminates SWI/SNF binding to  HO in vivo ( ).	bind
42766	2	10021	7	11	NULL	NULL	NULL	SWI/SNF	GP		bind					HO	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_94	16705163	A direct interaction between Swi5 and SWI/SNF has been demonstrated in vitro ( ), and a  swi5 mutation eliminates SWI/SNF binding to  HO in vivo ( ).	bind
42767	3	10021	7	11	NULL	NULL	NULL	swi5	GP	mutant	eliminates					statement 2	Process				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_11_4095_s_94	16705163	A direct interaction between Swi5 and SWI/SNF has been demonstrated in vitro ( ), and a  swi5 mutation eliminates SWI/SNF binding to  HO in vivo ( ).	bind
35056	1	10022	6	11	NULL	NULL	NULL	gp32	GP		interacts with		directly	core domain		gp59	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25236_s_47	11309384	A direct interaction between the core domain of gp32 and gp59 could destabilize the gp32-ssDNA interaction, which when followed by gp59 oligomer formation and binding to the helicase, results in displacement of gp32 from the DNA and loading of gp41 in its place.	bind
35057	2	10022	6	11	NULL	NULL	NULL	gp32	GP		interacts with					ssDNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25236_s_47	11309384	A direct interaction between the core domain of gp32 and gp59 could destabilize the gp32-ssDNA interaction, which when followed by gp59 oligomer formation and binding to the helicase, results in displacement of gp32 from the DNA and loading of gp41 in its place.	bind
35058	3	10022	6	11	NULL	NULL	NULL	statement 1	Process		destabilize					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25236_s_47	11309384	A direct interaction between the core domain of gp32 and gp59 could destabilize the gp32-ssDNA interaction, which when followed by gp59 oligomer formation and binding to the helicase, results in displacement of gp32 from the DNA and loading of gp41 in its place.	bind
35059	4	10022	6	11	NULL	NULL	NULL	gp59	GP		bind					helicase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25236_s_47	11309384	A direct interaction between the core domain of gp32 and gp59 could destabilize the gp32-ssDNA interaction, which when followed by gp59 oligomer formation and binding to the helicase, results in displacement of gp32 from the DNA and loading of gp41 in its place.	bind
35060	5	10022	6	11	NULL	NULL	NULL	statement 3	Process		is followed by					gp59 oligomer	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25236_s_47	11309384	A direct interaction between the core domain of gp32 and gp59 could destabilize the gp32-ssDNA interaction, which when followed by gp59 oligomer formation and binding to the helicase, results in displacement of gp32 from the DNA and loading of gp41 in its place.	bind
35061	6	10022	6	11	NULL	NULL	NULL	statement 3	Process		is followed by					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25236_s_47	11309384	A direct interaction between the core domain of gp32 and gp59 could destabilize the gp32-ssDNA interaction, which when followed by gp59 oligomer formation and binding to the helicase, results in displacement of gp32 from the DNA and loading of gp41 in its place.	bind
35062	7	10022	6	11	NULL	NULL	NULL	gp32	GP		is replaced by					gp41	GP				NULL	 in DNA	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25236_s_47	11309384	A direct interaction between the core domain of gp32 and gp59 could destabilize the gp32-ssDNA interaction, which when followed by gp59 oligomer formation and binding to the helicase, results in displacement of gp32 from the DNA and loading of gp41 in its place.	bind
35063	8	10022	6	11	NULL	NULL	NULL	statement 4	Process		results in					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25236_s_47	11309384	A direct interaction between the core domain of gp32 and gp59 could destabilize the gp32-ssDNA interaction, which when followed by gp59 oligomer formation and binding to the helicase, results in displacement of gp32 from the DNA and loading of gp41 in its place.	bind
42768	1	10022	7	11	NULL	NULL	NULL	gp32	GP		interacts with		directly	core domain		gp59	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25236_s_47	11309384	A direct interaction between the core domain of gp32 and gp59 could destabilize the gp32-ssDNA interaction, which when followed by gp59 oligomer formation and binding to the helicase, results in displacement of gp32 from the DNA and loading of gp41 in its place.	bind
42769	2	10022	7	11	NULL	NULL	NULL	gp32	GP		interacts with					ssDNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25236_s_47	11309384	A direct interaction between the core domain of gp32 and gp59 could destabilize the gp32-ssDNA interaction, which when followed by gp59 oligomer formation and binding to the helicase, results in displacement of gp32 from the DNA and loading of gp41 in its place.	bind
42770	3	10022	7	11	NULL	NULL	NULL	statement 1	Process		destabilize					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25236_s_47	11309384	A direct interaction between the core domain of gp32 and gp59 could destabilize the gp32-ssDNA interaction, which when followed by gp59 oligomer formation and binding to the helicase, results in displacement of gp32 from the DNA and loading of gp41 in its place.	bind
42771	4	10022	7	11	NULL	NULL	NULL	gp59	GP		forms					oligomer	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25236_s_47	11309384	A direct interaction between the core domain of gp32 and gp59 could destabilize the gp32-ssDNA interaction, which when followed by gp59 oligomer formation and binding to the helicase, results in displacement of gp32 from the DNA and loading of gp41 in its place.	bind
42772	5	10022	7	11	NULL	NULL	NULL	gp59	GP		bind					helicase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25236_s_47	11309384	A direct interaction between the core domain of gp32 and gp59 could destabilize the gp32-ssDNA interaction, which when followed by gp59 oligomer formation and binding to the helicase, results in displacement of gp32 from the DNA and loading of gp41 in its place.	bind
42773	6	10022	7	11	NULL	NULL	NULL	statement 3	Process		is followed by					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25236_s_47	11309384	A direct interaction between the core domain of gp32 and gp59 could destabilize the gp32-ssDNA interaction, which when followed by gp59 oligomer formation and binding to the helicase, results in displacement of gp32 from the DNA and loading of gp41 in its place.	bind
42774	7	10022	7	11	NULL	NULL	NULL	gp32	GP		is replaced by					gp41	GP				NULL	DNA	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25236_s_47	11309384	A direct interaction between the core domain of gp32 and gp59 could destabilize the gp32-ssDNA interaction, which when followed by gp59 oligomer formation and binding to the helicase, results in displacement of gp32 from the DNA and loading of gp41 in its place.	bind
42775	8	10022	7	11	NULL	NULL	NULL	statement 5	Process		results in					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25236_s_47	11309384	A direct interaction between the core domain of gp32 and gp59 could destabilize the gp32-ssDNA interaction, which when followed by gp59 oligomer formation and binding to the helicase, results in displacement of gp32 from the DNA and loading of gp41 in its place.	bind
35064	1	10023	6	11	NULL	NULL	NULL	Mot1	GP		interacts with		directly	DNA binding surface		TBP	GP		DNA binding surface		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_15_13216_s_478	12571241	A direct interaction between the DNA-binding surfaces of Mot1 and TBP can explain why the Mot1.TBP binary complex does not bind DNA.	bind
35065	2	10023	6	11	NULL	NULL	NULL	Mot1.TBP binary complex	GP		does not bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_15_13216_s_478	12571241	A direct interaction between the DNA-binding surfaces of Mot1 and TBP can explain why the Mot1.TBP binary complex does not bind DNA.	bind
42778	1	10023	7	11	NULL	NULL	NULL	Mot1	GP		interacts with		directly	DNA-binding surface		TBP	GP		DNA-binding surface		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_15_13216_s_478	12571241	A direct interaction between the DNA-binding surfaces of Mot1 and TBP can explain why the Mot1.TBP binary complex does not bind DNA.	bind
42779	2	10023	7	11	NULL	NULL	NULL	Mot1.TBP binary complex	GP		does not bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_15_13216_s_478	12571241	A direct interaction between the DNA-binding surfaces of Mot1 and TBP can explain why the Mot1.TBP binary complex does not bind DNA.	bind
35066	1	10024	6	11	NULL	NULL	NULL	Fir1p	GP	35S-labeled;;in vitro translated	bind			amino acids 173 - 876		GST-Sin1p	GP		N-terminus		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_26_9808_s_61	16788068	A direct interaction between the two proteins was confirmed by showing that 35S-labeled,  in vitro translated Fir1p (amino acids 173 - 876) bound GST-Sin1p fusion proteins derived from the N terminus of the protein, whereas GST alone did not bind ( Fig. 2).	bind
35067	2	10024	6	11	NULL	NULL	NULL	Fir1p	GP	35S-labeled;;in vitro translated	does not bind			amino acids 173 - 876		GST	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_26_9808_s_61	16788068	A direct interaction between the two proteins was confirmed by showing that 35S-labeled,  in vitro translated Fir1p (amino acids 173 - 876) bound GST-Sin1p fusion proteins derived from the N terminus of the protein, whereas GST alone did not bind ( Fig. 2).	bind
49331	3	10024	6	11	NULL	NULL	NULL	GST-Sin1p	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_26_9808_s_61	16788068	A direct interaction between the two proteins was confirmed by showing that 35S-labeled,  in vitro translated Fir1p (amino acids 173 - 876) bound GST-Sin1p fusion proteins derived from the N terminus of the protein, whereas GST alone did not bind ( Fig. 2).	bind
42781	1	10024	7	11	NULL	NULL	NULL	Fir1p	GP	35S-labeled;;in vitro translated	bind			amino acids 173 - 876		GST-Sin1p	GP	N-terminus			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_26_9808_s_61	16788068	A direct interaction between the two proteins was confirmed by showing that 35S-labeled,  in vitro translated Fir1p (amino acids 173 - 876) bound GST-Sin1p fusion proteins derived from the N terminus of the protein, whereas GST alone did not bind ( Fig. 2).	bind
49332	2	10024	7	11	NULL	NULL	NULL	Fir1p	GP	35S-labeled;;in vitro translated	does not bind			amino acids 173 - 876		GST	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_26_9808_s_61	16788068	A direct interaction between the two proteins was confirmed by showing that 35S-labeled,  in vitro translated Fir1p (amino acids 173 - 876) bound GST-Sin1p fusion proteins derived from the N terminus of the protein, whereas GST alone did not bind ( Fig. 2).	bind
49334	3	10024	7	11	NULL	NULL	NULL	GST-Sin1p	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_26_9808_s_61	16788068	A direct interaction between the two proteins was confirmed by showing that 35S-labeled,  in vitro translated Fir1p (amino acids 173 - 876) bound GST-Sin1p fusion proteins derived from the N terminus of the protein, whereas GST alone did not bind ( Fig. 2).	bind
35068	1	10025	6	11	NULL	NULL	NULL	GTP	Chemical		bind					Cdc42p	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_20_5657_s_203	11598009	A direct interaction of Cla4p with the GTP-bound form of Cdc42p was shown by overlay and two-hybrid assays ( Cvrckova   et al., 1995;  Richman  et al., 1999).	bind
35069	2	10025	6	11	NULL	NULL	NULL	Cla4p	GP		interacts with		directly			statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_20_5657_s_203	11598009	A direct interaction of Cla4p with the GTP-bound form of Cdc42p was shown by overlay and two-hybrid assays ( Cvrckova   et al., 1995;  Richman  et al., 1999).	bind
42782	2	10025	7	11	NULL	NULL	NULL	Cla4p	GP		interacts with		directly			statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_20_5657_s_203	11598009	A direct interaction of Cla4p with the GTP-bound form of Cdc42p was shown by overlay and two-hybrid assays ( Cvrckova   et al., 1995;  Richman  et al., 1999).	bind
42783	1	10025	7	11	NULL	NULL	NULL	GTP	Chemical		bind					Cdc42p	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_20_5657_s_203	11598009	A direct interaction of Cla4p with the GTP-bound form of Cdc42p was shown by overlay and two-hybrid assays ( Cvrckova   et al., 1995;  Richman  et al., 1999).	bind
35498	1	10026	6	11	NULL	NULL	NULL	QacR	GP		bind					IR1 DNA	NucleicAcid			operator	NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
35519	2	10026	6	11	NULL	NULL	NULL	benzalkonium	Chemical		is a type of					QacA substrate	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
35520	3	10026	6	11	NULL	NULL	NULL	dequalinium	Chemical		is a type of					QacA substrate	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
35521	4	10026	6	11	NULL	NULL	NULL	ethidium bromide	Chemical		is a type of					QacA substrate	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
35522	5	10026	6	11	NULL	NULL	NULL	chlorhexidine	Chemical		is a type of					QacA substrate	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
35523	6	10026	6	11	NULL	NULL	NULL	rhodamine 6G	Chemical		is a type of					QacA substrate	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
35524	7	10026	6	11	NULL	NULL	NULL	QacR	GP		acts as a					sensor molecule	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
35525	8	10026	6	11	NULL	NULL	NULL	QacR	GP		facilitate					transcription	Process	increase in			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
35526	9	10026	6	11	NULL	NULL	NULL	statement 8	Process		occurs in response to					toxic compounds	Chemical	presence of			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
35527	10	10026	6	11	NULL	NULL	NULL	benzalkonium	Chemical		disrupts					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
35529	11	10026	6	11	NULL	NULL	NULL	dequalinium	Chemical		disrupts					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
35530	12	10026	6	11	NULL	NULL	NULL	ethidium bromide	Chemical		disrupts					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
35531	13	10026	6	11	NULL	NULL	NULL	chlorhexidine	Chemical		disrupts					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
35532	14	10026	6	11	NULL	NULL	NULL	rhodamine 6G	Chemical		disrupts					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
49335	15	10026	6	11	NULL	NULL	NULL	TetR	GP		acts as					sensor molecule 	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
49336	16	10026	6	11	NULL	NULL	NULL	ligand-bound QacR	GP		does not bind					DNA	NucleicAcid			operator	NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
57239	17	10026	6	11	NULL	NULL	NULL	TetR	GP		acts as					sensor molecule	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
42784	1	10026	7	11	NULL	NULL	NULL	QacR	GP		bind					IR1  DNA	NucleicAcid			operator	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
42785	2	10026	7	11	NULL	NULL	NULL	benzalkonium	Chemical		disrupts					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
42786	3	10026	7	11	NULL	NULL	NULL	dequalinium	Chemical		disrupts					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
42787	4	10026	7	11	NULL	NULL	NULL	ethidium bromide	Chemical		disrupts					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
42788	5	10026	7	11	NULL	NULL	NULL	chlorhexidine	Chemical		disrupts					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
42789	6	10026	7	11	NULL	NULL	NULL	rhodamine 6G	Chemical		disrupts					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
42790	7	10026	7	11	NULL	NULL	NULL	QacR	GP		acts as a					sensor molecule	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
42792	8	10026	7	11	NULL	NULL	NULL	TetR	GP		acts as a					sensor molecule	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
42794	10	10026	7	11	NULL	NULL	NULL	statement 7	Process		facilitate					transcription	Process	increase in			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
42795	11	10026	7	11	NULL	NULL	NULL	statement 10	Process		occurs in response to					toxic compounds	Chemical	presence of			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
42796	12	10026	7	11	NULL	NULL	NULL	ligand-bound QacR	GP		does not bind					DNA	NucleicAcid			operator	NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
42797	13	10026	7	11	NULL	NULL	NULL	benzalkonium	Chemical		is a type of					QacA substrate	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
42798	14	10026	7	11	NULL	NULL	NULL	dequalinium	Chemical		is a type of					QacA substrate	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
42799	15	10026	7	11	NULL	NULL	NULL	ethidium bromide	Chemical		is a type of					QacA substrate	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
42800	16	10026	7	11	NULL	NULL	NULL	chlorhexidine	Chemical		is a type of					QacA substrate	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
42801	17	10026	7	11	NULL	NULL	NULL	 rhodamine 6G	Chemical		is a type of					QacA substrate	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_66_4_671_s_514	12456787	A direct interaction of QacR with these inducing compounds was subsequently confirmed by the binding of QacR to IR1 operator DNA that had been disrupted in vitro by the separate addition of eight structurally diverse QacA substrates, including benzalkonium, dequalinium, ethidium bromide, chlorhexidine, and rhodamine 6G ( ) Thus, like TetR, QacR acts as a sensor molecule that can facilitate increases in transcription in response to the presence of toxic compounds because the ligand-bound form of this protein is incapable of binding operator DNA (Fig.  10A).	bind
35101	1	10028	6	11	NULL	NULL	NULL	YC-1	GP		bind					heme-depleted enzyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_53_1_123_s_8	9443939	A direct interaction of YC-1 with the heme group can be ruled out because YC-1 did not change the Soret absorption of basal or stimulated sGC and, in addition, still bound to the heme-depleted enzyme.	bind
35102	2	10028	6	11	NULL	NULL	NULL	YC-1	GP		does not interact with		directly			heme group	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_53_1_123_s_8	9443939	A direct interaction of YC-1 with the heme group can be ruled out because YC-1 did not change the Soret absorption of basal or stimulated sGC and, in addition, still bound to the heme-depleted enzyme.	bind
42802	1	10028	7	11	NULL	NULL	NULL	 YC-1 	GP		bind					heme-depleted enzyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_53_1_123_s_8	9443939	A direct interaction of YC-1 with the heme group can be ruled out because YC-1 did not change the Soret absorption of basal or stimulated sGC and, in addition, still bound to the heme-depleted enzyme.	bind
42803	2	10028	7	11	NULL	NULL	NULL	YC-1	GP		does not interact with		directly			heme group	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_53_1_123_s_8	9443939	A direct interaction of YC-1 with the heme group can be ruled out because YC-1 did not change the Soret absorption of basal or stimulated sGC and, in addition, still bound to the heme-depleted enzyme.	bind
35103	1	10029	6	11	NULL	NULL	NULL	E(Z)	GP	Drosophila	bind		directly			ESC	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_159_3_1135_s_362	11729158	A direct link between E(Z) and histone deacetylation is suggested by the finding that the Drosophila E(Z) binds directly to ESC ( J ONES et al. 1998   ;	bind
49337	2	10029	6	11	NULL	NULL	NULL	E(Z)	GP		linked to		directly			histone	GP	deacetylation of			NULL		NULL	NULL	NULL	NULL	gw60_genetics_159_3_1135_s_362	11729158	A direct link between E(Z) and histone deacetylation is suggested by the finding that the Drosophila E(Z) binds directly to ESC ( J ONES et al. 1998   ;	bind
49338	3	10029	6	11	NULL	NULL	NULL	statement 1	Process		suggest					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_genetics_159_3_1135_s_362	11729158	A direct link between E(Z) and histone deacetylation is suggested by the finding that the Drosophila E(Z) binds directly to ESC ( J ONES et al. 1998   ;	bind
42804	1	10029	7	11	NULL	NULL	NULL	E(Z)	GP	Drosophila	binds		directly			ESC	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_159_3_1135_s_362	11729158	A direct link between E(Z) and histone deacetylation is suggested by the finding that the Drosophila E(Z) binds directly to ESC ( J ONES et al. 1998   ;	bind
42805	2	10029	7	11	NULL	NULL	NULL	 E(Z) 	GP		linked to		directly			histone	GP	deacetylation of			NULL		NULL	NULL	NULL	NULL	gw60_genetics_159_3_1135_s_362	11729158	A direct link between E(Z) and histone deacetylation is suggested by the finding that the Drosophila E(Z) binds directly to ESC ( J ONES et al. 1998   ;	bind
42806	3	10029	7	11	NULL	NULL	NULL	statement 1	Process		suggests					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_genetics_159_3_1135_s_362	11729158	A direct link between E(Z) and histone deacetylation is suggested by the finding that the Drosophila E(Z) binds directly to ESC ( J ONES et al. 1998   ;	bind
35104	1	10030	6	11	NULL	NULL	NULL	protein 4.1	GP		bind					p55	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5360_s_146	7890649	A direct measure of the protein 4.1  binding to p55 was obtained by determining the amount of  GPC-3-saturated protein 4.1 bound to p55-saturated alkali-stripped  membranes.	bind
42807	1	10030	7	11	NULL	NULL	NULL	protein 4.1	GP		bind					p55	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5360_s_146	7890649	A direct measure of the protein 4.1  binding to p55 was obtained by determining the amount of  GPC-3-saturated protein 4.1 bound to p55-saturated alkali-stripped  membranes.	bind
35534	1	10031	6	11	NULL	NULL	NULL	IL-1ra analogs	GP		bind					IL-1R AcP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_38_22460_s_212	7673234	A direct measurement of binding of the IL-1ra analogs  to the IL-1R AcP is not possible because the accessory protein does not  bind IL-1 ligands except in the presence of the Type I  IL-1R( 37) .	bind
35535	2	10031	6	11	NULL	NULL	NULL	accessory protein	GP		bind					IL-1 ligands	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_38_22460_s_212	7673234	A direct measurement of binding of the IL-1ra analogs  to the IL-1R AcP is not possible because the accessory protein does not  bind IL-1 ligands except in the presence of the Type I  IL-1R( 37) .	bind
35536	3	10031	6	11	NULL	NULL	NULL	statement 2	Process		in presence of		only			Type I IL-1R	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_38_22460_s_212	7673234	A direct measurement of binding of the IL-1ra analogs  to the IL-1R AcP is not possible because the accessory protein does not  bind IL-1 ligands except in the presence of the Type I  IL-1R( 37) .	bind
42808	1	10031	7	11	NULL	NULL	NULL	IL-1ra analogs	GP		bind					IL-1R AcP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_38_22460_s_212	7673234	A direct measurement of binding of the IL-1ra analogs  to the IL-1R AcP is not possible because the accessory protein does not  bind IL-1 ligands except in the presence of the Type I  IL-1R( 37) .	bind
42809	2	10031	7	11	NULL	NULL	NULL	accessory protein	GP		bind					IL-1 ligands	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_38_22460_s_212	7673234	A direct measurement of binding of the IL-1ra analogs  to the IL-1R AcP is not possible because the accessory protein does not  bind IL-1 ligands except in the presence of the Type I  IL-1R( 37) .	bind
42810	3	10031	7	11	NULL	NULL	NULL	statement 2	Process		in the presence of 		only			Type I IL-1R	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_38_22460_s_212	7673234	A direct measurement of binding of the IL-1ra analogs  to the IL-1R AcP is not possible because the accessory protein does not  bind IL-1 ligands except in the presence of the Type I  IL-1R( 37) .	bind
35105	1	10032	6	11	NULL	NULL	NULL	myosin Ia	GP		bind					post-TGN vesicles	GP	ALPK1-carrying			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_27_25637_s_122	15883161	A direct overlap between ALPK1-labeled vesicular structures and myo1A-YFP staining is shown in  Fig. 4 H, strongly suggesting that myosin Ia binds to ALPK1-carrying post-TGN vesicles.	bind
42811	1	10032	7	11	NULL	NULL	NULL	myosin Ia	GP		binds to					post-TGN vesicles	GP	ALPK1-carrying			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_27_25637_s_122	15883161	A direct overlap between ALPK1-labeled vesicular structures and myo1A-YFP staining is shown in  Fig. 4 H, strongly suggesting that myosin Ia binds to ALPK1-carrying post-TGN vesicles.	bind
35106	1	10033	6	11	NULL	NULL	NULL	Cbl-N	GP	unphosphorylated	bind					ZAP-70	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24063_s_113	8798643	A direct phosphotyrosine-dependent binding between unphosphorylated Cbl-N and tyrosine-phosphorylated ZAP-70 strongly suggests the presence of a hitherto unidentified PTB domain within the transforming N-terminal region of Cbl, functionally analogous to PTB domains identified within the Shc adapter protein ( 31,  32,  33) and subsequently in insulin receptor substrate 1 ( 25).	bind
35107	2	10033	6	11	NULL	NULL	NULL	statement 1	Process		depends on		directly	PTB domain within N-terminal region		phosphotyrosine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24063_s_113	8798643	A direct phosphotyrosine-dependent binding between unphosphorylated Cbl-N and tyrosine-phosphorylated ZAP-70 strongly suggests the presence of a hitherto unidentified PTB domain within the transforming N-terminal region of Cbl, functionally analogous to PTB domains identified within the Shc adapter protein ( 31,  32,  33) and subsequently in insulin receptor substrate 1 ( 25).	bind
35108	3	10033	6	11	NULL	NULL	NULL			unidentified	is present within			PTB domain		Cbl	GP		N-terminal region		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24063_s_113	8798643	A direct phosphotyrosine-dependent binding between unphosphorylated Cbl-N and tyrosine-phosphorylated ZAP-70 strongly suggests the presence of a hitherto unidentified PTB domain within the transforming N-terminal region of Cbl, functionally analogous to PTB domains identified within the Shc adapter protein ( 31,  32,  33) and subsequently in insulin receptor substrate 1 ( 25).	bind
57242	4	10033	6	11	NULL	NULL	NULL	statement 1	Process		suggest		strongly			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24063_s_113	8798643	A direct phosphotyrosine-dependent binding between unphosphorylated Cbl-N and tyrosine-phosphorylated ZAP-70 strongly suggests the presence of a hitherto unidentified PTB domain within the transforming N-terminal region of Cbl, functionally analogous to PTB domains identified within the Shc adapter protein ( 31,  32,  33) and subsequently in insulin receptor substrate 1 ( 25).	bind
57243	5	10033	6	11	NULL	NULL	NULL	statement 3	Process		is analogous to		functionally			Shc	GP		PTB domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24063_s_113	8798643	A direct phosphotyrosine-dependent binding between unphosphorylated Cbl-N and tyrosine-phosphorylated ZAP-70 strongly suggests the presence of a hitherto unidentified PTB domain within the transforming N-terminal region of Cbl, functionally analogous to PTB domains identified within the Shc adapter protein ( 31,  32,  33) and subsequently in insulin receptor substrate 1 ( 25).	bind
57244	6	10033	6	11	NULL	NULL	NULL	statement 3	Process		is analogous to		functionally			insulin receptor substrate 1	GP		PTB domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24063_s_113	8798643	A direct phosphotyrosine-dependent binding between unphosphorylated Cbl-N and tyrosine-phosphorylated ZAP-70 strongly suggests the presence of a hitherto unidentified PTB domain within the transforming N-terminal region of Cbl, functionally analogous to PTB domains identified within the Shc adapter protein ( 31,  32,  33) and subsequently in insulin receptor substrate 1 ( 25).	bind
57245	7	10033	6	11	NULL	NULL	NULL	Shc	GP		is a type of					adapter protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24063_s_113	8798643	A direct phosphotyrosine-dependent binding between unphosphorylated Cbl-N and tyrosine-phosphorylated ZAP-70 strongly suggests the presence of a hitherto unidentified PTB domain within the transforming N-terminal region of Cbl, functionally analogous to PTB domains identified within the Shc adapter protein ( 31,  32,  33) and subsequently in insulin receptor substrate 1 ( 25).	bind
42812	1	10033	7	11	NULL	NULL	NULL	Cbl-N	GP	unphosphorylated 	bind					 ZAP-70	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24063_s_113	8798643	A direct phosphotyrosine-dependent binding between unphosphorylated Cbl-N and tyrosine-phosphorylated ZAP-70 strongly suggests the presence of a hitherto unidentified PTB domain within the transforming N-terminal region of Cbl, functionally analogous to PTB domains identified within the Shc adapter protein ( 31,  32,  33) and subsequently in insulin receptor substrate 1 ( 25).	bind
42813	2	10033	7	11	NULL	NULL	NULL	statement 1	Process		depends on		directly			phosphotyrosine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24063_s_113	8798643	A direct phosphotyrosine-dependent binding between unphosphorylated Cbl-N and tyrosine-phosphorylated ZAP-70 strongly suggests the presence of a hitherto unidentified PTB domain within the transforming N-terminal region of Cbl, functionally analogous to PTB domains identified within the Shc adapter protein ( 31,  32,  33) and subsequently in insulin receptor substrate 1 ( 25).	bind
42814	3	10033	7	11	NULL	NULL	NULL	statement 1	Process		suggests		strongly			statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24063_s_113	8798643	A direct phosphotyrosine-dependent binding between unphosphorylated Cbl-N and tyrosine-phosphorylated ZAP-70 strongly suggests the presence of a hitherto unidentified PTB domain within the transforming N-terminal region of Cbl, functionally analogous to PTB domains identified within the Shc adapter protein ( 31,  32,  33) and subsequently in insulin receptor substrate 1 ( 25).	bind
42815	4	10033	7	11	NULL	NULL	NULL	statement 7	Process		is analogous to		functionally			Shc	GP		PTB domains		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24063_s_113	8798643	A direct phosphotyrosine-dependent binding between unphosphorylated Cbl-N and tyrosine-phosphorylated ZAP-70 strongly suggests the presence of a hitherto unidentified PTB domain within the transforming N-terminal region of Cbl, functionally analogous to PTB domains identified within the Shc adapter protein ( 31,  32,  33) and subsequently in insulin receptor substrate 1 ( 25).	bind
42816	5	10033	7	11	NULL	NULL	NULL	statement 7	Process		is analogous to		functionally			insulin receptor substrate 1	GP		PTB domains		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24063_s_113	8798643	A direct phosphotyrosine-dependent binding between unphosphorylated Cbl-N and tyrosine-phosphorylated ZAP-70 strongly suggests the presence of a hitherto unidentified PTB domain within the transforming N-terminal region of Cbl, functionally analogous to PTB domains identified within the Shc adapter protein ( 31,  32,  33) and subsequently in insulin receptor substrate 1 ( 25).	bind
57240	6	10033	7	11	NULL	NULL	NULL	Shc	GP		is a type of					adapter protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24063_s_113	8798643	A direct phosphotyrosine-dependent binding between unphosphorylated Cbl-N and tyrosine-phosphorylated ZAP-70 strongly suggests the presence of a hitherto unidentified PTB domain within the transforming N-terminal region of Cbl, functionally analogous to PTB domains identified within the Shc adapter protein ( 31,  32,  33) and subsequently in insulin receptor substrate 1 ( 25).	bind
57241	7	10033	7	11	NULL	NULL	NULL			unidentified	is present within			PTB domain		Cbl	GP		N-terminal region		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_24063_s_113	8798643	A direct phosphotyrosine-dependent binding between unphosphorylated Cbl-N and tyrosine-phosphorylated ZAP-70 strongly suggests the presence of a hitherto unidentified PTB domain within the transforming N-terminal region of Cbl, functionally analogous to PTB domains identified within the Shc adapter protein ( 31,  32,  33) and subsequently in insulin receptor substrate 1 ( 25).	bind
35109	1	10034	6	11	NULL	NULL	NULL	PDGFrbeta	GP		bind					integrin beta3 subunit	GP		extracellular domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_41_39882_s_292	12881526	A direct physical association between these two cell surface receptors likely plays a role in this cooperation, as the PDGFrbeta binds the extracellular domain of the integrin beta3 subunit in a manner that is independent of PDGFrbeta activation ( ).	bind
35110	2	10034	6	11	NULL	NULL	NULL	statement 1	Process		is independent of					PDGFrbeta	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_41_39882_s_292	12881526	A direct physical association between these two cell surface receptors likely plays a role in this cooperation, as the PDGFrbeta binds the extracellular domain of the integrin beta3 subunit in a manner that is independent of PDGFrbeta activation ( ).	bind
42817	1	10034	7	11	NULL	NULL	NULL	PDGFrbeta	GP		binds					integrin beta3 subunit 	GP		extracellular domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_41_39882_s_292	12881526	A direct physical association between these two cell surface receptors likely plays a role in this cooperation, as the PDGFrbeta binds the extracellular domain of the integrin beta3 subunit in a manner that is independent of PDGFrbeta activation ( ).	bind
42818	2	10034	7	11	NULL	NULL	NULL	statement 1	Process		is independent of					PDGFrbeta	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_41_39882_s_292	12881526	A direct physical association between these two cell surface receptors likely plays a role in this cooperation, as the PDGFrbeta binds the extracellular domain of the integrin beta3 subunit in a manner that is independent of PDGFrbeta activation ( ).	bind
35111	1	10035	6	11	NULL	NULL	NULL	OxyR	GP		bind					ahpC	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_7_2674_s_141	16547055	A direct regulation of  ahpC by OxyR was confirmed by DNA binding of OxyR to the  ahpC promoter region by using an electrophoretic mobility shift assay (Fig.  2C).	bind
35112	2	10035	6	11	NULL	NULL	NULL	OxyR	GP		regulates		directly			ahpC	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_7_2674_s_141	16547055	A direct regulation of  ahpC by OxyR was confirmed by DNA binding of OxyR to the  ahpC promoter region by using an electrophoretic mobility shift assay (Fig.  2C).	bind
42819	1	10035	7	11	NULL	NULL	NULL	OxyR 	GP		bind					ahpC	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_7_2674_s_141	16547055	A direct regulation of  ahpC by OxyR was confirmed by DNA binding of OxyR to the  ahpC promoter region by using an electrophoretic mobility shift assay (Fig.  2C).	bind
42820	2	10035	7	11	NULL	NULL	NULL	OxyR	GP		regulates		directly			ahpC	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_188_7_2674_s_141	16547055	A direct regulation of  ahpC by OxyR was confirmed by DNA binding of OxyR to the  ahpC promoter region by using an electrophoretic mobility shift assay (Fig.  2C).	bind
35537	1	10036	6	11	NULL	NULL	NULL	RFX	GP		belongs to			RFX5 subunit		methyl-DNA-binding proteins	GP	family of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_38914_s_214	16166088	A direct role for DNA methylation in the function of RFX may be possible because (i) the RFX5 subunit of RFX belongs to a family of methyl-DNA-binding proteins; (ii) C residue methylation is known not to inhibit the binding of RFX5 to a collagen gene promoter ( ); and (iii) RFX protects the methylation of the C residue immediately adjacent to its previously described  HLA-DRA promoter binding site ( Fig. 4,  E - G).	bind
35538	2	10036	6	11	NULL	NULL	NULL	RFX5	GP		bind					collagen gene	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_38914_s_214	16166088	A direct role for DNA methylation in the function of RFX may be possible because (i) the RFX5 subunit of RFX belongs to a family of methyl-DNA-binding proteins; (ii) C residue methylation is known not to inhibit the binding of RFX5 to a collagen gene promoter ( ); and (iii) RFX protects the methylation of the C residue immediately adjacent to its previously described  HLA-DRA promoter binding site ( Fig. 4,  E - G).	bind
35539	3	10036	6	11	NULL	NULL	NULL			methylation of	does not inhibit			C residue		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_38914_s_214	16166088	A direct role for DNA methylation in the function of RFX may be possible because (i) the RFX5 subunit of RFX belongs to a family of methyl-DNA-binding proteins; (ii) C residue methylation is known not to inhibit the binding of RFX5 to a collagen gene promoter ( ); and (iii) RFX protects the methylation of the C residue immediately adjacent to its previously described  HLA-DRA promoter binding site ( Fig. 4,  E - G).	bind
35543	4	10036	6	11	NULL	NULL	NULL	RFX	GP		protects							methylation of	C residue		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_38914_s_214	16166088	A direct role for DNA methylation in the function of RFX may be possible because (i) the RFX5 subunit of RFX belongs to a family of methyl-DNA-binding proteins; (ii) C residue methylation is known not to inhibit the binding of RFX5 to a collagen gene promoter ( ); and (iii) RFX protects the methylation of the C residue immediately adjacent to its previously described  HLA-DRA promoter binding site ( Fig. 4,  E - G).	bind
36454	5	10036	6	11	NULL	NULL	NULL	statement 4	Process		occurs					HLA-DR5	GP	adjacent to		promoter binding site	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_38914_s_214	16166088	A direct role for DNA methylation in the function of RFX may be possible because (i) the RFX5 subunit of RFX belongs to a family of methyl-DNA-binding proteins; (ii) C residue methylation is known not to inhibit the binding of RFX5 to a collagen gene promoter ( ); and (iii) RFX protects the methylation of the C residue immediately adjacent to its previously described  HLA-DRA promoter binding site ( Fig. 4,  E - G).	bind
42821	1	10036	7	11	NULL	NULL	NULL	RFX	GP		belongs to			 RFX5 subunit		methyl-DNA-binding proteins	GP	family of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_38914_s_214	16166088	A direct role for DNA methylation in the function of RFX may be possible because (i) the RFX5 subunit of RFX belongs to a family of methyl-DNA-binding proteins; (ii) C residue methylation is known not to inhibit the binding of RFX5 to a collagen gene promoter ( ); and (iii) RFX protects the methylation of the C residue immediately adjacent to its previously described  HLA-DRA promoter binding site ( Fig. 4,  E - G).	bind
42822	2	10036	7	11	NULL	NULL	NULL	RFX5	GP		bind					collagen gene	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_38914_s_214	16166088	A direct role for DNA methylation in the function of RFX may be possible because (i) the RFX5 subunit of RFX belongs to a family of methyl-DNA-binding proteins; (ii) C residue methylation is known not to inhibit the binding of RFX5 to a collagen gene promoter ( ); and (iii) RFX protects the methylation of the C residue immediately adjacent to its previously described  HLA-DRA promoter binding site ( Fig. 4,  E - G).	bind
42823	3	10036	7	11	NULL	NULL	NULL			methylation of	does not inhibit			C residue		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_38914_s_214	16166088	A direct role for DNA methylation in the function of RFX may be possible because (i) the RFX5 subunit of RFX belongs to a family of methyl-DNA-binding proteins; (ii) C residue methylation is known not to inhibit the binding of RFX5 to a collagen gene promoter ( ); and (iii) RFX protects the methylation of the C residue immediately adjacent to its previously described  HLA-DRA promoter binding site ( Fig. 4,  E - G).	bind
42824	4	10036	7	11	NULL	NULL	NULL	RFX	GP		protects							methylation of 	C residue		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_38914_s_214	16166088	A direct role for DNA methylation in the function of RFX may be possible because (i) the RFX5 subunit of RFX belongs to a family of methyl-DNA-binding proteins; (ii) C residue methylation is known not to inhibit the binding of RFX5 to a collagen gene promoter ( ); and (iii) RFX protects the methylation of the C residue immediately adjacent to its previously described  HLA-DRA promoter binding site ( Fig. 4,  E - G).	bind
42825	5	10036	7	11	NULL	NULL	NULL	statement 4	Process		occurs					HLA-DRA 	GP	adjacent to		promoter binding site	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_38914_s_214	16166088	A direct role for DNA methylation in the function of RFX may be possible because (i) the RFX5 subunit of RFX belongs to a family of methyl-DNA-binding proteins; (ii) C residue methylation is known not to inhibit the binding of RFX5 to a collagen gene promoter ( ); and (iii) RFX protects the methylation of the C residue immediately adjacent to its previously described  HLA-DRA promoter binding site ( Fig. 4,  E - G).	bind
35113	1	10037	6	11	NULL	NULL	NULL	AP1	GP		bind					AP3	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_2_135_s_93	11832239	A direct role of AP1 in regulating  AP3 is further supported by the finding that AP1 binds to the  AP3 promoter and that the binding site is required for normal activity of this promoter   (Hill et al., 1998  ; Tilly et al., 1998  ).	bind
35114	2	10037	6	11	NULL	NULL	NULL	AP3	GP		is required for				AP1 binding site of promoter	AP3 	GP	normal activity of 		promoter	NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_2_135_s_93	11832239	A direct role of AP1 in regulating  AP3 is further supported by the finding that AP1 binds to the  AP3 promoter and that the binding site is required for normal activity of this promoter   (Hill et al., 1998  ; Tilly et al., 1998  ).	bind
42826	1	10037	7	11	NULL	NULL	NULL	 AP1	GP		binds to					AP3	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_2_135_s_93	11832239	A direct role of AP1 in regulating  AP3 is further supported by the finding that AP1 binds to the  AP3 promoter and that the binding site is required for normal activity of this promoter   (Hill et al., 1998  ; Tilly et al., 1998  ).	bind
42827	2	10037	7	11	NULL	NULL	NULL	AP3	GP		is required for				AP1 binding site of promoter	AP3	GP	normal activity of		 promoter	NULL		NULL	NULL	NULL	NULL	gw60_devcell_2_2_135_s_93	11832239	A direct role of AP1 in regulating  AP3 is further supported by the finding that AP1 binds to the  AP3 promoter and that the binding site is required for normal activity of this promoter   (Hill et al., 1998  ; Tilly et al., 1998  ).	bind
35115	1	10038	6	11	NULL	NULL	NULL	STAT1	GP		interacts with					p48	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_20070_s_171	9242679	A directed yeast two-hybrid transcription system detected interaction of STAT1 with p48 ( 31), and  in vitro mixing of crude lysates from cells overexpressing STAT1 and p48 showed apparent complex binding to DNA (38).	bind
49514	2	10038	6	11	NULL	NULL	NULL	statement 1	GP		bind					DNA	NucleicAcid				NULL	in vitro,crude lysates from cells overexpressing STAT1 and p48	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_20070_s_171	9242679	A directed yeast two-hybrid transcription system detected interaction of STAT1 with p48 ( 31), and  in vitro mixing of crude lysates from cells overexpressing STAT1 and p48 showed apparent complex binding to DNA (38).	bind
42828	1	10038	7	11	NULL	NULL	NULL	STAT1	GP		interacts with					p48	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_20070_s_171	9242679	A directed yeast two-hybrid transcription system detected interaction of STAT1 with p48 ( 31), and  in vitro mixing of crude lysates from cells overexpressing STAT1 and p48 showed apparent complex binding to DNA (38).	bind
42829	2	10038	7	11	NULL	NULL	NULL	statement 1	GP		bind					DNA	NucleicAcid				NULL	in vitro,crude lysates from cells overexpressing STAT1 and p48	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_20070_s_171	9242679	A directed yeast two-hybrid transcription system detected interaction of STAT1 with p48 ( 31), and  in vitro mixing of crude lysates from cells overexpressing STAT1 and p48 showed apparent complex binding to DNA (38).	bind
35116	1	10039	6	11	NULL	NULL	NULL	mPR	GP	recombinant	bind					progesterone	Chemical				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_annurevphysiol_67_0_335_s_302	15709962	A discrepancy was observed in the steroid- binding specificity in that recombinant  mPR in vitro bound progesterone only, whereas mPR expressed on the surface of breast  cancer cells responded to both progesterone and 20 S.	bind
35117	2	10039	6	11	NULL	NULL	NULL	mPR	GP		expressed on					breast cancer cells	Cell	surface of 			NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_67_0_335_s_302	15709962	A discrepancy was observed in the steroid- binding specificity in that recombinant  mPR in vitro bound progesterone only, whereas mPR expressed on the surface of breast  cancer cells responded to both progesterone and 20 S.	bind
35118	3	10039	6	11	NULL	NULL	NULL	statement 2	Cell		responds to					progesterone	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_67_0_335_s_302	15709962	A discrepancy was observed in the steroid- binding specificity in that recombinant  mPR in vitro bound progesterone only, whereas mPR expressed on the surface of breast  cancer cells responded to both progesterone and 20 S.	bind
35119	4	10039	6	11	NULL	NULL	NULL	statement 2	Cell		responds to					20 S	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_67_0_335_s_302	15709962	A discrepancy was observed in the steroid- binding specificity in that recombinant  mPR in vitro bound progesterone only, whereas mPR expressed on the surface of breast  cancer cells responded to both progesterone and 20 S.	bind
42830	1	10039	7	11	NULL	NULL	NULL	mPR	GP	recombinant	bind					progesterone	Chemical				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_annurevphysiol_67_0_335_s_302	15709962	A discrepancy was observed in the steroid- binding specificity in that recombinant  mPR in vitro bound progesterone only, whereas mPR expressed on the surface of breast  cancer cells responded to both progesterone and 20 S.	bind
42831	2	10039	7	11	NULL	NULL	NULL	mPR	GP		expressed on					breast cancer cells 	Cell	surface of			NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_67_0_335_s_302	15709962	A discrepancy was observed in the steroid- binding specificity in that recombinant  mPR in vitro bound progesterone only, whereas mPR expressed on the surface of breast  cancer cells responded to both progesterone and 20 S.	bind
42832	3	10039	7	11	NULL	NULL	NULL	statement 2	Cell		respond to					progesterone	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_67_0_335_s_302	15709962	A discrepancy was observed in the steroid- binding specificity in that recombinant  mPR in vitro bound progesterone only, whereas mPR expressed on the surface of breast  cancer cells responded to both progesterone and 20 S.	bind
42833	4	10039	7	11	NULL	NULL	NULL	statement 2	Cell		respond to					20 S	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_67_0_335_s_302	15709962	A discrepancy was observed in the steroid- binding specificity in that recombinant  mPR in vitro bound progesterone only, whereas mPR expressed on the surface of breast  cancer cells responded to both progesterone and 20 S.	bind
35590	1	10040	6	11	NULL	NULL	NULL	P2	CellComponent		bind					Pex1p	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
35591	2	10040	6	11	NULL	NULL	NULL	P2	CellComponent		bind					Pex6p	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
35592	3	10040	6	11	NULL	NULL	NULL	P2	CellComponent		bind					PI(4)P-bp	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
35593	4	10040	6	11	NULL	NULL	NULL	P2	CellComponent		bind					PI(4,5)P2-bp	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
35594	5	10040	6	11	NULL	NULL	NULL	Pex1p	GP		is a type of					membrane protein	GP	detergent insoluble			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
35595	6	10040	6	11	NULL	NULL	NULL	Pex6p	GP		is a type of					membrane protein	GP	detergent insoluble			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
35596	7	10040	6	11	NULL	NULL	NULL	PI(4)P-bp	GP		is a type of					membrane protein	GP	detergent insoluble			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
35597	8	10040	6	11	NULL	NULL	NULL	PI(4,5)P2-bp	GP		is a type of					membrane protein	GP	detergent insoluble			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
35598	9	10040	6	11	NULL	NULL	NULL	P1	CellComponent		associates with					Pex1p	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
35599	10	10040	6	11	NULL	NULL	NULL	P1	CellComponent		associates with					PI(4)P-bp	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
35600	11	10040	6	11	NULL	NULL	NULL	P1	CellComponent		associates with					PI(4,5)P2-bp	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
35601	12	10040	6	11	NULL	NULL	NULL	P1	CellComponent		associates with					GTP-bp	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
42834	1	10040	7	11	NULL	NULL	NULL	P1	CellComponent		associate with					Pex1p	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
42835	2	10040	7	11	NULL	NULL	NULL	Pex1p	GP		is a type of					 membrane protein	GP	 detergent-insoluble			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
42836	3	10040	7	11	NULL	NULL	NULL	PI(4)P-bp	GP		is a type of					 membrane protein	GP	detergent-insoluble			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
42837	4	10040	7	11	NULL	NULL	NULL	PI(4,5)P2-bp	GP		is a type of					 membrane protein	GP	detergent-insoluble			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
42838	5	10040	7	11	NULL	NULL	NULL	GTP-bp	GP		is a type of					 membrane protein	GP	detergent-insoluble			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
42839	6	10040	7	11	NULL	NULL	NULL	P2	CellComponent		bind					Pex1p	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
49861	7	10040	7	11	NULL	NULL	NULL	P1	CellComponent		associate with					PI(4)P-bp	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
49862	8	10040	7	11	NULL	NULL	NULL	P1	CellComponent		associate with					PI(4,5)P2-bp	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
49863	9	10040	7	11	NULL	NULL	NULL	P1	CellComponent		associate with					GTP-bp	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
49864	10	10040	7	11	NULL	NULL	NULL	P2	CellComponent		bind					Pex6p	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
49865	11	10040	7	11	NULL	NULL	NULL	P2	CellComponent		bind					PI(4)P-bp	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
49866	12	10040	7	11	NULL	NULL	NULL	P2	CellComponent		bind					PI(4,5)P2-bp	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_5_761_s_129	15738267	A discrete group of detergent-insoluble membrane proteins, including the P1-associated forms of Pex1p, PI(4)P-bp, PI(4,5)P2-bp, and GTP-bp ( Fig. 4 A) and the P2-bound forms of Pex1p, Pex6p, PI(4)P-bp, and PI(4,5)P2-bp ( Fig. 4 B), floated to the low-density fractions 5 - 9 and peaked in fraction 7 of the gradient.	bind
35120	1	10041	6	11	NULL	NULL	NULL	BACE	GP		bind					GGA protein	GP		VHS domain		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-cell-sci_117_pt-22_15466887_s_4	15466887	A DISLL sequence near the BACE  C-terminus mediates binding of BACE to the VHS domains of Golgi-localized  gamma-ear-containing ARF-binding (GGA) proteins, which are involved in  the sorting of proteins to endosomes.	bind
35121	2	10041	6	11	NULL	NULL	NULL	GGA	GP		is 					Golgi-localized gamma-ear-containing ARF-binding proteins	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-cell-sci_117_pt-22_15466887_s_4	15466887	A DISLL sequence near the BACE  C-terminus mediates binding of BACE to the VHS domains of Golgi-localized  gamma-ear-containing ARF-binding (GGA) proteins, which are involved in  the sorting of proteins to endosomes.	bind
35122	3	10041	6	11	NULL	NULL	NULL	BACE	GP		mediates			DISLL sequence near C terminus		statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-cell-sci_117_pt-22_15466887_s_4	15466887	A DISLL sequence near the BACE  C-terminus mediates binding of BACE to the VHS domains of Golgi-localized  gamma-ear-containing ARF-binding (GGA) proteins, which are involved in  the sorting of proteins to endosomes.	bind
49515	4	10041	6	11	NULL	NULL	NULL	proteins	GP		sorted to					endosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-cell-sci_117_pt-22_15466887_s_4	15466887	A DISLL sequence near the BACE  C-terminus mediates binding of BACE to the VHS domains of Golgi-localized  gamma-ear-containing ARF-binding (GGA) proteins, which are involved in  the sorting of proteins to endosomes.	bind
49516	5	10041	6	11	NULL	NULL	NULL	GGA	GP		is involved in					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-cell-sci_117_pt-22_15466887_s_4	15466887	A DISLL sequence near the BACE  C-terminus mediates binding of BACE to the VHS domains of Golgi-localized  gamma-ear-containing ARF-binding (GGA) proteins, which are involved in  the sorting of proteins to endosomes.	bind
42861	1	10041	7	11	NULL	NULL	NULL	BACE	GP		bind					GGA proteins	GP		VHS domain		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-cell-sci_117_pt-22_15466887_s_4	15466887	A DISLL sequence near the BACE  C-terminus mediates binding of BACE to the VHS domains of Golgi-localized  gamma-ear-containing ARF-binding (GGA) proteins, which are involved in  the sorting of proteins to endosomes.	bind
42862	2	10041	7	11	NULL	NULL	NULL	BACE	GP		mediates			DISLL sequence near C-terminus		statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-cell-sci_117_pt-22_15466887_s_4	15466887	A DISLL sequence near the BACE  C-terminus mediates binding of BACE to the VHS domains of Golgi-localized  gamma-ear-containing ARF-binding (GGA) proteins, which are involved in  the sorting of proteins to endosomes.	bind
42863	4	10041	7	11	NULL	NULL	NULL	GGA	GP		is involved in					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-cell-sci_117_pt-22_15466887_s_4	15466887	A DISLL sequence near the BACE  C-terminus mediates binding of BACE to the VHS domains of Golgi-localized  gamma-ear-containing ARF-binding (GGA) proteins, which are involved in  the sorting of proteins to endosomes.	bind
42864	3	10041	7	11	NULL	NULL	NULL	proteins	GP		sorted to					endosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-cell-sci_117_pt-22_15466887_s_4	15466887	A DISLL sequence near the BACE  C-terminus mediates binding of BACE to the VHS domains of Golgi-localized  gamma-ear-containing ARF-binding (GGA) proteins, which are involved in  the sorting of proteins to endosomes.	bind
42865	5	10041	7	11	NULL	NULL	NULL	GGA	GP		is					Golgi-localized gamma-ear-containing ARF-binding proteins	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-cell-sci_117_pt-22_15466887_s_4	15466887	A DISLL sequence near the BACE  C-terminus mediates binding of BACE to the VHS domains of Golgi-localized  gamma-ear-containing ARF-binding (GGA) proteins, which are involved in  the sorting of proteins to endosomes.	bind
35138	1	10042	6	11	NULL	NULL	NULL	Lp(a)	GP		bind					TRL particles	GP	larger			NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_42_12_2058_s_11	11734579	A disproportionate amount of Lp[a was bound to the larger TRL particles.	bind
42866	1	10042	7	11	NULL	NULL	NULL	Lp[a	GP		bind					TRL particles	GP	larger			NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_42_12_2058_s_11	11734579	A disproportionate amount of Lp[a was bound to the larger TRL particles.	bind
35139	1	10043	6	11	NULL	NULL	NULL	LRP-2	GP	radiolabeled	bind					SVS-II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_9_5557_s_136	10026171	A dissociation constant ( K d) of 10.4  plus-or-minus  4.9 nM ( n = 6) was determined for the binding of radiolabeled LRP-2 to SVS-II from the best fit of the data to a single class of binding sites model.	bind
42867	1	10043	7	11	NULL	NULL	NULL	 LRP-2	GP	radiolabeled 	bind					SVS-II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_9_5557_s_136	10026171	A dissociation constant ( K d) of 10.4  plus-or-minus  4.9 nM ( n = 6) was determined for the binding of radiolabeled LRP-2 to SVS-II from the best fit of the data to a single class of binding sites model.	bind
35140	1	10044	6	11	NULL	NULL	NULL	LTP-like basic protein	GP	Oat	bind					oleic acid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_structure_3_2_189_s_149	7735835	A dissociation constant of 3.5x10-6 M has been reported for the binding of oleic acid by an LTP-like basic protein from oat  [13]  .	bind
42868	1	10044	7	11	NULL	NULL	NULL	LTP-like basic protein 	GP	Oat	bind					oleic acid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_structure_3_2_189_s_149	7735835	A dissociation constant of 3.5x10-6 M has been reported for the binding of oleic acid by an LTP-like basic protein from oat  [13]  .	bind
35141	1	10045	6	11	NULL	NULL	NULL	CD36	GP		bind					HDL	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_40_30794_s_245	10896940	A dissociation of efflux from binding is also indicated by the finding that CD36 can bind HDL but it does not facilitate cholesterol efflux ( 7).	bind
35142	2	10045	6	11	NULL	NULL	NULL	CD36	GP		does not facilitate					cholesterol efflux	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_40_30794_s_245	10896940	A dissociation of efflux from binding is also indicated by the finding that CD36 can bind HDL but it does not facilitate cholesterol efflux ( 7).	bind
42869	1	10045	7	11	NULL	NULL	NULL	CD36	GP		bind					HDL	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_40_30794_s_245	10896940	A dissociation of efflux from binding is also indicated by the finding that CD36 can bind HDL but it does not facilitate cholesterol efflux ( 7).	bind
42870	2	10045	7	11	NULL	NULL	NULL	CD36	GP		does not facilitate					cholesterol efflux	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_40_30794_s_245	10896940	A dissociation of efflux from binding is also indicated by the finding that CD36 can bind HDL but it does not facilitate cholesterol efflux ( 7).	bind
35143	1	10046	6	11	NULL	NULL	NULL	glucose oxidase	GP		oxidizes					hydrogen peroxide	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_anal-chem_75_5_12641231_s_8	12641231	A distinct current increase following the oxidation  of hydrogen peroxide produced by the enzymatic reaction of glucose oxidase  was observed, which indicates that the capture proteins could actually  bind the target proteins.	bind
42871	1	10046	7	11	NULL	NULL	NULL	glucose oxidase	GP		oxidizes					hydrogen peroxide	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_anal-chem_75_5_12641231_s_8	12641231	A distinct current increase following the oxidation  of hydrogen peroxide produced by the enzymatic reaction of glucose oxidase  was observed, which indicates that the capture proteins could actually  bind the target proteins.	bind
35144	1	10047	6	11	NULL	NULL	NULL	anti-galactan monoclonal antibody	GP		bind					beta-(1 6)-galactosyl ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8209_s_85	8626513	A distinct difference can be seen on the one hand between the  anti-galactan monoclonal antibodies binding to  beta-(1 6)-galactosyl ligands and on the other hand the  anti-dextran monoclonal antibodies binding to alpha-(1 6)-glucosyl  ligands (  Table 6 and   Table 7 and   Fig. 5 and  Fig. 6 ).	bind
35145	2	10047	6	11	NULL	NULL	NULL	anti-dextran monoclonal antibody	GP		bind					alpha-(1 6)-glucosyl ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8209_s_85	8626513	A distinct difference can be seen on the one hand between the  anti-galactan monoclonal antibodies binding to  beta-(1 6)-galactosyl ligands and on the other hand the  anti-dextran monoclonal antibodies binding to alpha-(1 6)-glucosyl  ligands (  Table 6 and   Table 7 and   Fig. 5 and  Fig. 6 ).	bind
42872	1	10047	7	11	NULL	NULL	NULL	anti-galactan monoclonal antibodies	GP		bind					beta-(1 6)-galactosyl ligands 	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8209_s_85	8626513	A distinct difference can be seen on the one hand between the  anti-galactan monoclonal antibodies binding to  beta-(1 6)-galactosyl ligands and on the other hand the  anti-dextran monoclonal antibodies binding to alpha-(1 6)-glucosyl  ligands (  Table 6 and   Table 7 and   Fig. 5 and  Fig. 6 ).	bind
42873	2	10047	7	11	NULL	NULL	NULL	anti-dextran monoclonal antibodies	GP		bind					alpha-(1 6)-glucosyl ligands	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8209_s_85	8626513	A distinct difference can be seen on the one hand between the  anti-galactan monoclonal antibodies binding to  beta-(1 6)-galactosyl ligands and on the other hand the  anti-dextran monoclonal antibodies binding to alpha-(1 6)-glucosyl  ligands (  Table 6 and   Table 7 and   Fig. 5 and  Fig. 6 ).	bind
35152	1	10048	6	11	NULL	NULL	NULL	Exo III	GP		bind					MutY	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_25_22605_s_407	11960995	A distinct feature of Exo III, is that, unlike Endo IV and MutM, it does not bind to the DNA duplex under the conditions used; however, Exo III does bind to the MutY.	bind
35153	2	10048	6	11	NULL	NULL	NULL	Endo IV	GP		bind					DNA duplex	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_25_22605_s_407	11960995	A distinct feature of Exo III, is that, unlike Endo IV and MutM, it does not bind to the DNA duplex under the conditions used; however, Exo III does bind to the MutY.	bind
35154	3	10048	6	11	NULL	NULL	NULL	MutM	GP		bind					DNA duplex	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_25_22605_s_407	11960995	A distinct feature of Exo III, is that, unlike Endo IV and MutM, it does not bind to the DNA duplex under the conditions used; however, Exo III does bind to the MutY.	bind
35155	4	10048	6	11	NULL	NULL	NULL	Exo III	GP		does not bind					DNA duplex	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_25_22605_s_407	11960995	A distinct feature of Exo III, is that, unlike Endo IV and MutM, it does not bind to the DNA duplex under the conditions used; however, Exo III does bind to the MutY.	bind
42874	1	10048	7	11	NULL	NULL	NULL	 Exo III	GP		does not bind					DNA duplex	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_25_22605_s_407	11960995	A distinct feature of Exo III, is that, unlike Endo IV and MutM, it does not bind to the DNA duplex under the conditions used; however, Exo III does bind to the MutY.	bind
42875	2	10048	7	11	NULL	NULL	NULL	Endo IV	GP		bind					DNA duplex	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_25_22605_s_407	11960995	A distinct feature of Exo III, is that, unlike Endo IV and MutM, it does not bind to the DNA duplex under the conditions used; however, Exo III does bind to the MutY.	bind
42876	3	10048	7	11	NULL	NULL	NULL	MutM	GP		bind					DNA duplex	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_25_22605_s_407	11960995	A distinct feature of Exo III, is that, unlike Endo IV and MutM, it does not bind to the DNA duplex under the conditions used; however, Exo III does bind to the MutY.	bind
42877	4	10048	7	11	NULL	NULL	NULL	Exo III	GP		bind					MutY	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_25_22605_s_407	11960995	A distinct feature of Exo III, is that, unlike Endo IV and MutM, it does not bind to the DNA duplex under the conditions used; however, Exo III does bind to the MutY.	bind
35156	2	10049	6	11	NULL	NULL	NULL	statement 1	GP		bind		cooperatively			cAMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21500_s_352	16728394	A distinct finding was that the PKA holoenzyme associated RI subunit-bound cAMP with positive cooperativity, because of intrachain interaction between the A and B sites.	bind
35157	3	10049	6	11	NULL	NULL	NULL				interacts with			A site					B site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21500_s_352	16728394	A distinct finding was that the PKA holoenzyme associated RI subunit-bound cAMP with positive cooperativity, because of intrachain interaction between the A and B sites.	bind
49517	1	10049	6	11	NULL	NULL	NULL	RI subunit	GP		is associated with					PKA holoenzyme	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21500_s_352	16728394	A distinct finding was that the PKA holoenzyme associated RI subunit-bound cAMP with positive cooperativity, because of intrachain interaction between the A and B sites.	bind
49518	4	10049	6	11	NULL	NULL	NULL	statement 3	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21500_s_352	16728394	A distinct finding was that the PKA holoenzyme associated RI subunit-bound cAMP with positive cooperativity, because of intrachain interaction between the A and B sites.	bind
42878	1	10049	7	11	NULL	NULL	NULL	RI subunit	GP		is associated with					PKA holoenzyme	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21500_s_352	16728394	A distinct finding was that the PKA holoenzyme associated RI subunit-bound cAMP with positive cooperativity, because of intrachain interaction between the A and B sites.	bind
42879	2	10049	7	11	NULL	NULL	NULL	statement 1	GP		bind		cooperatively			cAMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21500_s_352	16728394	A distinct finding was that the PKA holoenzyme associated RI subunit-bound cAMP with positive cooperativity, because of intrachain interaction between the A and B sites.	bind
42881	3	10049	7	11	NULL	NULL	NULL				interacts with			A site					B site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21500_s_352	16728394	A distinct finding was that the PKA holoenzyme associated RI subunit-bound cAMP with positive cooperativity, because of intrachain interaction between the A and B sites.	bind
42882	4	10049	7	11	NULL	NULL	NULL	statement 3	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21500_s_352	16728394	A distinct finding was that the PKA holoenzyme associated RI subunit-bound cAMP with positive cooperativity, because of intrachain interaction between the A and B sites.	bind
35158	1	10050	6	11	NULL	NULL	NULL	Mac-1 positive cells	Cell		bind		specifically			G-CSF	GP				NULL	peripheral blood of mice	NULL	NULL	NULL	NULL	gw60_jclininvest_102_3_483_s_139	9691084	A distinct Mac-1 positive population of  cells that specifically bound G-CSF was detected in the peripheral blood of mice of each genotype (Fig.  2 B); the slight increase in G-CSF binding seen with Wt/Mt or Mt/Mt cells was a  consistent finding.	bind
35159	2	10050	6	11	NULL	NULL	NULL	G-CSF	GP	binding of	increased in					Wt/Mt cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_3_483_s_139	9691084	A distinct Mac-1 positive population of  cells that specifically bound G-CSF was detected in the peripheral blood of mice of each genotype (Fig.  2 B); the slight increase in G-CSF binding seen with Wt/Mt or Mt/Mt cells was a  consistent finding.	bind
35160	3	10050	6	11	NULL	NULL	NULL	G-CSF	GP	binding of	is increased in					Mt/Mt cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_3_483_s_139	9691084	A distinct Mac-1 positive population of  cells that specifically bound G-CSF was detected in the peripheral blood of mice of each genotype (Fig.  2 B); the slight increase in G-CSF binding seen with Wt/Mt or Mt/Mt cells was a  consistent finding.	bind
42883	1	10050	7	11	NULL	NULL	NULL	Mac-1 positive cells	Cell		bind		specifically			G-CSF	GP				NULL	peripheral blood of mice 	NULL	NULL	NULL	NULL	gw60_jclininvest_102_3_483_s_139	9691084	A distinct Mac-1 positive population of  cells that specifically bound G-CSF was detected in the peripheral blood of mice of each genotype (Fig.  2 B); the slight increase in G-CSF binding seen with Wt/Mt or Mt/Mt cells was a  consistent finding.	bind
42897	2	10050	7	11	NULL	NULL	NULL	G-CSF	GP	binding of	increased in					Wt/Mt cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_3_483_s_139	9691084	A distinct Mac-1 positive population of  cells that specifically bound G-CSF was detected in the peripheral blood of mice of each genotype (Fig.  2 B); the slight increase in G-CSF binding seen with Wt/Mt or Mt/Mt cells was a  consistent finding.	bind
42898	3	10050	7	11	NULL	NULL	NULL	G-CSF	GP	binding of	increased in					Mt/Mt cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_3_483_s_139	9691084	A distinct Mac-1 positive population of  cells that specifically bound G-CSF was detected in the peripheral blood of mice of each genotype (Fig.  2 B); the slight increase in G-CSF binding seen with Wt/Mt or Mt/Mt cells was a  consistent finding.	bind
35161	1	10051	6	11	NULL	NULL	NULL	transcription factor	GP	distinct negative	bind		may							GT elements	NULL	root cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_51_32593_s_83	8955086	A distinct negative transcription factor may bind to GT elements, resulting in transcription repression in root cells.	bind
35162	2	10051	6	11	NULL	NULL	NULL	statement 1	Process		results in					transcription	Process	repression of			NULL	root cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_51_32593_s_83	8955086	A distinct negative transcription factor may bind to GT elements, resulting in transcription repression in root cells.	bind
42899	1	10051	7	11	NULL	NULL	NULL	transcription factor	GP	distinct negative	bind		may							GT elements	NULL	root cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_51_32593_s_83	8955086	A distinct negative transcription factor may bind to GT elements, resulting in transcription repression in root cells.	bind
42900	2	10051	7	11	NULL	NULL	NULL	statement 1	Process		results in					transcription	Process	repression of			NULL	root cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_51_32593_s_83	8955086	A distinct negative transcription factor may bind to GT elements, resulting in transcription repression in root cells.	bind
35163	1	10052	6	11	NULL	NULL	NULL	PKG-I	GP		bind			NH2-terminal leucine-zipper domain		MYPT1	GP		COOH-terminal leucine-zipper domain		NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_68_0_345_s_361	16460276	A distinct PKG-specific mechanism  involves binding of the NH2-terminal leucine-zipper domain of PKG-I  to the COOH-terminal leucine-zipper domain  of MYPT1.	bind
49519	2	10052	6	11	NULL	NULL	NULL	PKG-specific mechanism	GP		involves					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_68_0_345_s_361	16460276	A distinct PKG-specific mechanism  involves binding of the NH2-terminal leucine-zipper domain of PKG-I  to the COOH-terminal leucine-zipper domain  of MYPT1.	bind
42901	1	10052	7	11	NULL	NULL	NULL	PKG-I	GP		binds to			NH2-terminal leucine-zipper domain		MYPT1	GP		COOH-terminal leucine-zipper domain		NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_68_0_345_s_361	16460276	A distinct PKG-specific mechanism  involves binding of the NH2-terminal leucine-zipper domain of PKG-I  to the COOH-terminal leucine-zipper domain  of MYPT1.	bind
42902	2	10052	7	11	NULL	NULL	NULL	PKG-specific mechanism	GP		involves					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_68_0_345_s_361	16460276	A distinct PKG-specific mechanism  involves binding of the NH2-terminal leucine-zipper domain of PKG-I  to the COOH-terminal leucine-zipper domain  of MYPT1.	bind
35164	1	10053	6	11	NULL	NULL	NULL	GRH	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_gene_307_0_77_s_30	12706890	A distinct regulatory element, the upstream regulatory element (URE), is bound by the Grainyhead (GRH) transcription factor (   Hayashi et al., 1999).	bind
35165	2	10053	6	11	NULL	NULL	NULL	GRH	GP		is					Grainyhead	GP				NULL		NULL	NULL	NULL	NULL	gw60_gene_307_0_77_s_30	12706890	A distinct regulatory element, the upstream regulatory element (URE), is bound by the Grainyhead (GRH) transcription factor (   Hayashi et al., 1999).	bind
35166	3	10053	6	11	NULL	NULL	NULL	GRH	GP		bind									URE	NULL		NULL	NULL	NULL	NULL	gw60_gene_307_0_77_s_30	12706890	A distinct regulatory element, the upstream regulatory element (URE), is bound by the Grainyhead (GRH) transcription factor (   Hayashi et al., 1999).	bind
35167	4	10053	6	11	NULL	NULL	NULL	URE	NucleicAcid		is					upstream regulatory element	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_gene_307_0_77_s_30	12706890	A distinct regulatory element, the upstream regulatory element (URE), is bound by the Grainyhead (GRH) transcription factor (   Hayashi et al., 1999).	bind
42903	1	10053	7	11	NULL	NULL	NULL	GRH	GP		bind									URE	NULL		NULL	NULL	NULL	NULL	gw60_gene_307_0_77_s_30	12706890	A distinct regulatory element, the upstream regulatory element (URE), is bound by the Grainyhead (GRH) transcription factor (   Hayashi et al., 1999).	bind
42904	2	10053	7	11	NULL	NULL	NULL	GRH	GP		is					Grainyhead	GP				NULL		NULL	NULL	NULL	NULL	gw60_gene_307_0_77_s_30	12706890	A distinct regulatory element, the upstream regulatory element (URE), is bound by the Grainyhead (GRH) transcription factor (   Hayashi et al., 1999).	bind
42905	3	10053	7	11	NULL	NULL	NULL	URE	NucleicAcid		is					upstream regulatory element	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_gene_307_0_77_s_30	12706890	A distinct regulatory element, the upstream regulatory element (URE), is bound by the Grainyhead (GRH) transcription factor (   Hayashi et al., 1999).	bind
49520	4	10053	7	11	NULL	NULL	NULL	GRH	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_gene_307_0_77_s_30	12706890	A distinct regulatory element, the upstream regulatory element (URE), is bound by the Grainyhead (GRH) transcription factor (   Hayashi et al., 1999).	bind
35168	1	10054	6	11	NULL	NULL	NULL	GLD-3	GP		bind					GLD-2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_101_13_4407_s_42	15070731	A distinct RNA-binding protein, GLD-3 ( ), binds to GLD-2 and stimulates its polyadenylation activity  in vitro ( ).	bind
35169	2	10054	6	11	NULL	NULL	NULL	GLD-3	GP		is a type of					RNA-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_13_4407_s_42	15070731	A distinct RNA-binding protein, GLD-3 ( ), binds to GLD-2 and stimulates its polyadenylation activity  in vitro ( ).	bind
35170	3	10054	6	11	NULL	NULL	NULL	statement 1	Process		stimulates					GLD-2	GP	polyadenylation activity of			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_101_13_4407_s_42	15070731	A distinct RNA-binding protein, GLD-3 ( ), binds to GLD-2 and stimulates its polyadenylation activity  in vitro ( ).	bind
42906	1	10054	7	11	NULL	NULL	NULL	GLD-3 	GP		binds to					GLD-2	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_101_13_4407_s_42	15070731	A distinct RNA-binding protein, GLD-3 ( ), binds to GLD-2 and stimulates its polyadenylation activity  in vitro ( ).	bind
42907	2	10054	7	11	NULL	NULL	NULL	statement 1	Process		stimulates					GLD-2	GP	polyadenylation activity of			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_101_13_4407_s_42	15070731	A distinct RNA-binding protein, GLD-3 ( ), binds to GLD-2 and stimulates its polyadenylation activity  in vitro ( ).	bind
42908	3	10054	7	11	NULL	NULL	NULL	GLD-3 	GP		is a type of					RNA-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_13_4407_s_42	15070731	A distinct RNA-binding protein, GLD-3 ( ), binds to GLD-2 and stimulates its polyadenylation activity  in vitro ( ).	bind
35171	1	10055	6	11	NULL	NULL	NULL	Grb2	GP		bind		constitutively			HPK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27804_s_203	9346925	A distinction between Grb2 and Nck binding to HPK1 is that the interaction of HPK1 with Grb2 appears constitutive, whereas its association with Nck is stimulated by EGF stimulation (Figs.  5 A and  6).	bind
35172	2	10055	6	11	NULL	NULL	NULL	Nck	GP		bind					HPK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27804_s_203	9346925	A distinction between Grb2 and Nck binding to HPK1 is that the interaction of HPK1 with Grb2 appears constitutive, whereas its association with Nck is stimulated by EGF stimulation (Figs.  5 A and  6).	bind
35173	3	10055	6	11	NULL	NULL	NULL	statement 2	Process		is stimulated by					EGF	GP	stimulation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27804_s_203	9346925	A distinction between Grb2 and Nck binding to HPK1 is that the interaction of HPK1 with Grb2 appears constitutive, whereas its association with Nck is stimulated by EGF stimulation (Figs.  5 A and  6).	bind
42909	1	10055	7	11	NULL	NULL	NULL	Grb2	GP		binds		constitutively			HPK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27804_s_203	9346925	A distinction between Grb2 and Nck binding to HPK1 is that the interaction of HPK1 with Grb2 appears constitutive, whereas its association with Nck is stimulated by EGF stimulation (Figs.  5 A and  6).	bind
42910	2	10055	7	11	NULL	NULL	NULL	Nck	GP		binds					HPK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27804_s_203	9346925	A distinction between Grb2 and Nck binding to HPK1 is that the interaction of HPK1 with Grb2 appears constitutive, whereas its association with Nck is stimulated by EGF stimulation (Figs.  5 A and  6).	bind
42912	3	10055	7	11	NULL	NULL	NULL	EGF	GP	stimulation of	stimulates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27804_s_203	9346925	A distinction between Grb2 and Nck binding to HPK1 is that the interaction of HPK1 with Grb2 appears constitutive, whereas its association with Nck is stimulated by EGF stimulation (Figs.  5 A and  6).	bind
35174	1	10056	6	11	NULL	NULL	NULL	IGFBP-6	GP		bind		high affinity			IGF-II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14587_s_214	10329650	A distinctive feature of IGFBP-6 compared with IGFBPs 1-5 is its high binding affinity for IGF-II and its marked preferential binding of IGF-II relative to IGF-I.	bind
49558	2	10056	6	11	NULL	NULL	NULL	IGFBP-6	GP		bind					IGF-I	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14587_s_214	10329650	A distinctive feature of IGFBP-6 compared with IGFBPs 1-5 is its high binding affinity for IGF-II and its marked preferential binding of IGF-II relative to IGF-I.	bind
49559	3	10056	6	11	NULL	NULL	NULL	statement 1	Process		is more preferential than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14587_s_214	10329650	A distinctive feature of IGFBP-6 compared with IGFBPs 1-5 is its high binding affinity for IGF-II and its marked preferential binding of IGF-II relative to IGF-I.	bind
42913	1	10056	7	11	NULL	NULL	NULL	IGFBP-6	GP		bind		high affinity			IGF-II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14587_s_214	10329650	A distinctive feature of IGFBP-6 compared with IGFBPs 1-5 is its high binding affinity for IGF-II and its marked preferential binding of IGF-II relative to IGF-I.	bind
42914	2	10056	7	11	NULL	NULL	NULL	IGFBP-6	GP		bind					IGF-I	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14587_s_214	10329650	A distinctive feature of IGFBP-6 compared with IGFBPs 1-5 is its high binding affinity for IGF-II and its marked preferential binding of IGF-II relative to IGF-I.	bind
42915	3	10056	7	11	NULL	NULL	NULL	statement 1	Process		is preferred over					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14587_s_214	10329650	A distinctive feature of IGFBP-6 compared with IGFBPs 1-5 is its high binding affinity for IGF-II and its marked preferential binding of IGF-II relative to IGF-I.	bind
42916	4	10056	7	11	NULL	NULL	NULL	IGFBP-1	GP		bind					IGF-II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14587_s_214	10329650	A distinctive feature of IGFBP-6 compared with IGFBPs 1-5 is its high binding affinity for IGF-II and its marked preferential binding of IGF-II relative to IGF-I.	bind
42917	5	10056	7	11	NULL	NULL	NULL	IGFBP-2	GP		bind					IGF-II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14587_s_214	10329650	A distinctive feature of IGFBP-6 compared with IGFBPs 1-5 is its high binding affinity for IGF-II and its marked preferential binding of IGF-II relative to IGF-I.	bind
42918	6	10056	7	11	NULL	NULL	NULL	IGFBP-3	GP		bind					IGF-II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14587_s_214	10329650	A distinctive feature of IGFBP-6 compared with IGFBPs 1-5 is its high binding affinity for IGF-II and its marked preferential binding of IGF-II relative to IGF-I.	bind
42919	7	10056	7	11	NULL	NULL	NULL	IGFBP-4	GP		bind					IGF-II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14587_s_214	10329650	A distinctive feature of IGFBP-6 compared with IGFBPs 1-5 is its high binding affinity for IGF-II and its marked preferential binding of IGF-II relative to IGF-I.	bind
42920	8	10056	7	11	NULL	NULL	NULL	IGFBP-5	GP		bind					IGF-II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14587_s_214	10329650	A distinctive feature of IGFBP-6 compared with IGFBPs 1-5 is its high binding affinity for IGF-II and its marked preferential binding of IGF-II relative to IGF-I.	bind
42921	9	10056	7	11	NULL	NULL	NULL	statement 1	Process	binding affinity of	is higher than					statement 4	Process	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14587_s_214	10329650	A distinctive feature of IGFBP-6 compared with IGFBPs 1-5 is its high binding affinity for IGF-II and its marked preferential binding of IGF-II relative to IGF-I.	bind
42922	10	10056	7	11	NULL	NULL	NULL	statement 1	Process	binding affinity of	is higher than					statement 5	Process	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14587_s_214	10329650	A distinctive feature of IGFBP-6 compared with IGFBPs 1-5 is its high binding affinity for IGF-II and its marked preferential binding of IGF-II relative to IGF-I.	bind
42923	11	10056	7	11	NULL	NULL	NULL	statement 1	Process	binding affinity of	is higher than					statement 6	Process	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14587_s_214	10329650	A distinctive feature of IGFBP-6 compared with IGFBPs 1-5 is its high binding affinity for IGF-II and its marked preferential binding of IGF-II relative to IGF-I.	bind
42924	12	10056	7	11	NULL	NULL	NULL	statement 1	Process	binding affinity of	is higher than					statement 7	Process	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14587_s_214	10329650	A distinctive feature of IGFBP-6 compared with IGFBPs 1-5 is its high binding affinity for IGF-II and its marked preferential binding of IGF-II relative to IGF-I.	bind
42925	13	10056	7	11	NULL	NULL	NULL	statement 1	Process	binding affinity of	is higher than					statement 8	Process	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14587_s_214	10329650	A distinctive feature of IGFBP-6 compared with IGFBPs 1-5 is its high binding affinity for IGF-II and its marked preferential binding of IGF-II relative to IGF-I.	bind
35175	1	10057	6	11	NULL	NULL	NULL	RdgC	GP		bind					plasmid DNA	NucleicAcid	circular			NULL		NULL	NULL	NULL	NULL	gw70_embo_22_3_735_s_75	12554673	A distributive mode of binding is also supported by the fact that  RdgC binds circular plasmid DNA and uniformly protects linear duplex DNA from attack  by hydroxyl radicals (data not shown).	bind
35176	2	10057	6	11	NULL	NULL	NULL	hydroxyl radicals	Chemical		attack					duplex DNA	NucleicAcid	linear			NULL		NULL	NULL	NULL	NULL	gw70_embo_22_3_735_s_75	12554673	A distributive mode of binding is also supported by the fact that  RdgC binds circular plasmid DNA and uniformly protects linear duplex DNA from attack  by hydroxyl radicals (data not shown).	bind
35177	3	10057	6	11	NULL	NULL	NULL	statement 1	Process		protects		uniformly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_22_3_735_s_75	12554673	A distributive mode of binding is also supported by the fact that  RdgC binds circular plasmid DNA and uniformly protects linear duplex DNA from attack  by hydroxyl radicals (data not shown).	bind
42926	1	10057	7	11	NULL	NULL	NULL	 RdgC 	GP		binds					plasmid DNA	NucleicAcid	circular			NULL		NULL	NULL	NULL	NULL	gw70_embo_22_3_735_s_75	12554673	A distributive mode of binding is also supported by the fact that  RdgC binds circular plasmid DNA and uniformly protects linear duplex DNA from attack  by hydroxyl radicals (data not shown).	bind
42927	2	10057	7	11	NULL	NULL	NULL	hydroxyl radicals	Chemical		attack					duplex DNA	NucleicAcid	linear			NULL		NULL	NULL	NULL	NULL	gw70_embo_22_3_735_s_75	12554673	A distributive mode of binding is also supported by the fact that  RdgC binds circular plasmid DNA and uniformly protects linear duplex DNA from attack  by hydroxyl radicals (data not shown).	bind
42928	3	10057	7	11	NULL	NULL	NULL	statement 1	Process		protects		uniformly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_22_3_735_s_75	12554673	A distributive mode of binding is also supported by the fact that  RdgC binds circular plasmid DNA and uniformly protects linear duplex DNA from attack  by hydroxyl radicals (data not shown).	bind
35183	1	10059	6	11	NULL	NULL	NULL	AP20187	Chemical		is a type of					divalent Fv ligand	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_19_16466_s_67	12637514	A divalent Fv ligand, AP20187, binds to Fv with high affinity but not to endogenous FKBP, thus minimizing the interference from endogenous FKBP and allowing for the effective dimerization of Fv fusion proteins.	bind
35184	2	10059	6	11	NULL	NULL	NULL	AP20187	Chemical		bind		high affinity			Fv	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_19_16466_s_67	12637514	A divalent Fv ligand, AP20187, binds to Fv with high affinity but not to endogenous FKBP, thus minimizing the interference from endogenous FKBP and allowing for the effective dimerization of Fv fusion proteins.	bind
35186	3	10059	6	11	NULL	NULL	NULL	AP20187	Chemical		does not bind					FKBP	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_19_16466_s_67	12637514	A divalent Fv ligand, AP20187, binds to Fv with high affinity but not to endogenous FKBP, thus minimizing the interference from endogenous FKBP and allowing for the effective dimerization of Fv fusion proteins.	bind
35602	4	10059	6	11	NULL	NULL	NULL	statement 2	Process		allows					Fv fusion proteins	GP	effective;;dimerization of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_19_16466_s_67	12637514	A divalent Fv ligand, AP20187, binds to Fv with high affinity but not to endogenous FKBP, thus minimizing the interference from endogenous FKBP and allowing for the effective dimerization of Fv fusion proteins.	bind
49521	5	10059	6	11	NULL	NULL	NULL	statement 2	Process		minimize					FKBP	GP	interference from;;endogenous			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_19_16466_s_67	12637514	A divalent Fv ligand, AP20187, binds to Fv with high affinity but not to endogenous FKBP, thus minimizing the interference from endogenous FKBP and allowing for the effective dimerization of Fv fusion proteins.	bind
42929	1	10059	7	11	NULL	NULL	NULL	AP20187	Chemical		binds to		high affinity			Fv	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_19_16466_s_67	12637514	A divalent Fv ligand, AP20187, binds to Fv with high affinity but not to endogenous FKBP, thus minimizing the interference from endogenous FKBP and allowing for the effective dimerization of Fv fusion proteins.	bind
42930	2	10059	7	11	NULL	NULL	NULL	AP20187	Chemical		does not bind					FKBP	GP	endogenous			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_19_16466_s_67	12637514	A divalent Fv ligand, AP20187, binds to Fv with high affinity but not to endogenous FKBP, thus minimizing the interference from endogenous FKBP and allowing for the effective dimerization of Fv fusion proteins.	bind
42931	3	10059	7	11	NULL	NULL	NULL	statement 1	Process		minimize					 FKBP	GP	interference from;;endogenous			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_19_16466_s_67	12637514	A divalent Fv ligand, AP20187, binds to Fv with high affinity but not to endogenous FKBP, thus minimizing the interference from endogenous FKBP and allowing for the effective dimerization of Fv fusion proteins.	bind
42932	4	10059	7	11	NULL	NULL	NULL	statement 1	Process		allows					Fv fusion proteins	GP	effective;;dimerization of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_19_16466_s_67	12637514	A divalent Fv ligand, AP20187, binds to Fv with high affinity but not to endogenous FKBP, thus minimizing the interference from endogenous FKBP and allowing for the effective dimerization of Fv fusion proteins.	bind
57267	5	10059	7	11	NULL	NULL	NULL	AP20187	Process		is a type of					divalent Fv ligand	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_19_16466_s_67	12637514	A divalent Fv ligand, AP20187, binds to Fv with high affinity but not to endogenous FKBP, thus minimizing the interference from endogenous FKBP and allowing for the effective dimerization of Fv fusion proteins.	bind
35190	1	10060	6	11	NULL	NULL	NULL	IL-6	GP		induces					STAT3-LUC	GP	expression of			NULL	293T cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_3_692_s_68	14975756	A DN-STAT3 significantly inhibited IL-6- or LIF-induced STAT3-LUC expression in  a dose-dependent fashion in 293T cells as described previously [ 27].	bind
35191	2	10060	6	11	NULL	NULL	NULL	LIF	GP		induces					STAT3-LUC	GP	expression of			NULL	293T cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_3_692_s_68	14975756	A DN-STAT3 significantly inhibited IL-6- or LIF-induced STAT3-LUC expression in  a dose-dependent fashion in 293T cells as described previously [ 27].	bind
35194	3	10060	6	11	NULL	NULL	NULL	DN-STAT3	GP		inhibits		significantly;;dose dependently			statement 1	Process				NULL	293T cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_3_692_s_68	14975756	A DN-STAT3 significantly inhibited IL-6- or LIF-induced STAT3-LUC expression in  a dose-dependent fashion in 293T cells as described previously [ 27].	bind
35195	4	10060	6	11	NULL	NULL	NULL	DN-STAT3	GP		inhibits		significantly;;dose dependently			statement 2	Process				NULL	293T cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_3_692_s_68	14975756	A DN-STAT3 significantly inhibited IL-6- or LIF-induced STAT3-LUC expression in  a dose-dependent fashion in 293T cells as described previously [ 27].	bind
42933	3	10060	7	11	NULL	NULL	NULL	DN-STAT3	GP		inhibits		significantly;;dose dependently			statement 1	Process				NULL	293T cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_3_692_s_68	14975756	A DN-STAT3 significantly inhibited IL-6- or LIF-induced STAT3-LUC expression in  a dose-dependent fashion in 293T cells as described previously [ 27].	bind
42934	2	10060	7	11	NULL	NULL	NULL	LIF	GP		induce					 STAT3-LUC	GP	expression of			NULL	293T cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_3_692_s_68	14975756	A DN-STAT3 significantly inhibited IL-6- or LIF-induced STAT3-LUC expression in  a dose-dependent fashion in 293T cells as described previously [ 27].	bind
42935	4	10060	7	11	NULL	NULL	NULL	DN-STAT3	GP		inhibits		significantly;;dose dependently			statement 2	Process				NULL	293T cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_3_692_s_68	14975756	A DN-STAT3 significantly inhibited IL-6- or LIF-induced STAT3-LUC expression in  a dose-dependent fashion in 293T cells as described previously [ 27].	bind
49522	1	10060	7	11	NULL	NULL	NULL	IL-6	GP		induces					STAT3-LUC	GP	expression of			NULL	293T cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_315_3_692_s_68	14975756	A DN-STAT3 significantly inhibited IL-6- or LIF-induced STAT3-LUC expression in  a dose-dependent fashion in 293T cells as described previously [ 27].	bind
35603	3	10061	6	11	NULL	NULL	NULL	statement 1	Chemical		bind		cooperatively							CD28RE-TRE Sequence	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_1_552_s_110	9417115	A DNA Affinity-purified Multicomponent Complex from Ionomycin/PMA-and Anti-CD28 mAb-stimulated Jurkat T-cells Binds Cooperatively to the CD28RE-TRE Sequence-- A DNA-binding protein complex was isolated from ionomycin/PMA/anti-CD28 mAb-stimulated Jurkat T-cells by DNA affinity chromatography (Fig.  2).	bind
35604	4	10061	6	11	NULL	NULL	NULL	statement 2	GP		bind		cooperatively							CD28RE-TRE Sequence	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_1_552_s_110	9417115	A DNA Affinity-purified Multicomponent Complex from Ionomycin/PMA-and Anti-CD28 mAb-stimulated Jurkat T-cells Binds Cooperatively to the CD28RE-TRE Sequence-- A DNA-binding protein complex was isolated from ionomycin/PMA/anti-CD28 mAb-stimulated Jurkat T-cells by DNA affinity chromatography (Fig.  2).	bind
57317	1	10061	6	11	NULL	NULL	NULL	Ionomycin/PMA	Chemical		stimulates					Jurkat T-cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_1_552_s_110	9417115	A DNA Affinity-purified Multicomponent Complex from Ionomycin/PMA-and Anti-CD28 mAb-stimulated Jurkat T-cells Binds Cooperatively to the CD28RE-TRE Sequence-- A DNA-binding protein complex was isolated from ionomycin/PMA/anti-CD28 mAb-stimulated Jurkat T-cells by DNA affinity chromatography (Fig.  2).	bind
57318	2	10061	6	11	NULL	NULL	NULL	Anti-CD28 mAb	GP		stimulates					Jurkat T-cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_1_552_s_110	9417115	A DNA Affinity-purified Multicomponent Complex from Ionomycin/PMA-and Anti-CD28 mAb-stimulated Jurkat T-cells Binds Cooperatively to the CD28RE-TRE Sequence-- A DNA-binding protein complex was isolated from ionomycin/PMA/anti-CD28 mAb-stimulated Jurkat T-cells by DNA affinity chromatography (Fig.  2).	bind
42936	1	10061	7	11	NULL	NULL	NULL	Ionomycin/PMA mAb	GP		stimulate					Jurkat T-cells 	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_1_552_s_110	9417115	A DNA Affinity-purified Multicomponent Complex from Ionomycin/PMA-and Anti-CD28 mAb-stimulated Jurkat T-cells Binds Cooperatively to the CD28RE-TRE Sequence-- A DNA-binding protein complex was isolated from ionomycin/PMA/anti-CD28 mAb-stimulated Jurkat T-cells by DNA affinity chromatography (Fig.  2).	bind
42937	2	10061	7	11	NULL	NULL	NULL	Anti-CD28 mAb	GP		stimulate					Jurkat T-cells 	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_1_552_s_110	9417115	A DNA Affinity-purified Multicomponent Complex from Ionomycin/PMA-and Anti-CD28 mAb-stimulated Jurkat T-cells Binds Cooperatively to the CD28RE-TRE Sequence-- A DNA-binding protein complex was isolated from ionomycin/PMA/anti-CD28 mAb-stimulated Jurkat T-cells by DNA affinity chromatography (Fig.  2).	bind
42938	3	10061	7	11	NULL	NULL	NULL	statement 1	Chemical		bind		cooperatively							CD28RE-TRE Sequence	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_1_552_s_110	9417115	A DNA Affinity-purified Multicomponent Complex from Ionomycin/PMA-and Anti-CD28 mAb-stimulated Jurkat T-cells Binds Cooperatively to the CD28RE-TRE Sequence-- A DNA-binding protein complex was isolated from ionomycin/PMA/anti-CD28 mAb-stimulated Jurkat T-cells by DNA affinity chromatography (Fig.  2).	bind
42939	4	10061	7	11	NULL	NULL	NULL	statement 2	GP		bind		cooperatively							CD28RE-TRE Sequence	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_1_552_s_110	9417115	A DNA Affinity-purified Multicomponent Complex from Ionomycin/PMA-and Anti-CD28 mAb-stimulated Jurkat T-cells Binds Cooperatively to the CD28RE-TRE Sequence-- A DNA-binding protein complex was isolated from ionomycin/PMA/anti-CD28 mAb-stimulated Jurkat T-cells by DNA affinity chromatography (Fig.  2).	bind
35198	1	10062	6	11	NULL	NULL	NULL	AP-1	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_63_3_607_s_178	12606768	A DNA binding activity of AP-1 and SP-1 was determined by gel mobility shift assay as described under  Materials and Methods.	bind
35199	2	10062	6	11	NULL	NULL	NULL	SP-1	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_63_3_607_s_178	12606768	A DNA binding activity of AP-1 and SP-1 was determined by gel mobility shift assay as described under  Materials and Methods.	bind
42940	1	10062	7	11	NULL	NULL	NULL	AP-1	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_63_3_607_s_178	12606768	A DNA binding activity of AP-1 and SP-1 was determined by gel mobility shift assay as described under  Materials and Methods.	bind
42941	2	10062	7	11	NULL	NULL	NULL	SP-1	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_63_3_607_s_178	12606768	A DNA binding activity of AP-1 and SP-1 was determined by gel mobility shift assay as described under  Materials and Methods.	bind
35205	1	10064	6	11	NULL	NULL	NULL	sod	GP	B. fragilis	bind		could		promoter	OxyR protein	GP	P. gingivalis			NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_microbiology_152_pt-4_16549660_s_11	16549660	A DNA fragment  including the B. fragilis sod promoter region could bind the P. gingivalis  OxyR protein; however, a putative OxyR binding sequence within the DNA  fragment was 14 bases distant from a putative -35 box of its promoter.	bind
42944	1	10064	7	11	NULL	NULL	NULL	sod	GP	B. fragilis	bind		could		promoter	OxyR protein	GP	P. gingivalis			NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_microbiology_152_pt-4_16549660_s_11	16549660	A DNA fragment  including the B. fragilis sod promoter region could bind the P. gingivalis  OxyR protein; however, a putative OxyR binding sequence within the DNA  fragment was 14 bases distant from a putative -35 box of its promoter.	bind
42945	2	10064	7	11	NULL	NULL	NULL	OxyR	GP		is present at				putative binding sequence within the DNA fragment	OxyR	GP			14 bases distant from a putative -35 box of promoter	NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_microbiology_152_pt-4_16549660_s_11	16549660	A DNA fragment  including the B. fragilis sod promoter region could bind the P. gingivalis  OxyR protein; however, a putative OxyR binding sequence within the DNA  fragment was 14 bases distant from a putative -35 box of its promoter.	bind
35605	1	10067	6	11	NULL	NULL	NULL	tissue-type plasminogen activator gene	GP	human	cooperate in				cAMP-responsive element of promoter	basal expression	Process				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_94_1_79_s_515	10842061	A DNA motif related to the cAMP-responsive element and an exon- located activator protein-2 binding site in the human tissue-type plasminogen activator gene promoter cooperate in basal expression and convey activation by phorbol ester and cAMP.	bind
35606	2	10067	6	11	NULL	NULL	NULL	tissue-type plasminogen activator gene	GP	human	cooperate in				exon- located activator protein-2 binding site of promoter	basal expression	Process				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_94_1_79_s_515	10842061	A DNA motif related to the cAMP-responsive element and an exon- located activator protein-2 binding site in the human tissue-type plasminogen activator gene promoter cooperate in basal expression and convey activation by phorbol ester and cAMP.	bind
35607	3	10067	6	11	NULL	NULL	NULL	tissue-type plasminogen activator gene	GP	human	is activated by				cAMP-responsive element of promoter	phorbol ester	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_94_1_79_s_515	10842061	A DNA motif related to the cAMP-responsive element and an exon- located activator protein-2 binding site in the human tissue-type plasminogen activator gene promoter cooperate in basal expression and convey activation by phorbol ester and cAMP.	bind
35608	4	10067	6	11	NULL	NULL	NULL	tissue-type plasminogen activator gene	GP	human	is activated by				cAMP-responsive element of promoter	cAMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_94_1_79_s_515	10842061	A DNA motif related to the cAMP-responsive element and an exon- located activator protein-2 binding site in the human tissue-type plasminogen activator gene promoter cooperate in basal expression and convey activation by phorbol ester and cAMP.	bind
35609	5	10067	6	11	NULL	NULL	NULL	tissue-type plasminogen activator gene	GP	human	is activated by				exon- located activator protein-2 binding site of promoter	phorbol ester	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_94_1_79_s_515	10842061	A DNA motif related to the cAMP-responsive element and an exon- located activator protein-2 binding site in the human tissue-type plasminogen activator gene promoter cooperate in basal expression and convey activation by phorbol ester and cAMP.	bind
35610	6	10067	6	11	NULL	NULL	NULL	tissue-type plasminogen activator gene	GP	human	is activated by				exon- located activator protein-2 binding site of promoter	cAMP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_94_1_79_s_515	10842061	A DNA motif related to the cAMP-responsive element and an exon- located activator protein-2 binding site in the human tissue-type plasminogen activator gene promoter cooperate in basal expression and convey activation by phorbol ester and cAMP.	bind
42946	1	10067	7	11	NULL	NULL	NULL	tissue-type plasminogen activator gene	GP	human	cooperate in				DNA motif related to the cAMP-responsive element in the promoter	basal expression	Process				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_94_1_79_s_515	10842061	A DNA motif related to the cAMP-responsive element and an exon- located activator protein-2 binding site in the human tissue-type plasminogen activator gene promoter cooperate in basal expression and convey activation by phorbol ester and cAMP.	bind
42947	2	10067	7	11	NULL	NULL	NULL	tissue-type plasminogen activator gene	GP	human	cooperate in				 exon- located activator protein-2 binding site in the promoter	basal expression	Process				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_94_1_79_s_515	10842061	A DNA motif related to the cAMP-responsive element and an exon- located activator protein-2 binding site in the human tissue-type plasminogen activator gene promoter cooperate in basal expression and convey activation by phorbol ester and cAMP.	bind
42948	3	10067	7	11	NULL	NULL	NULL	phorbol ester	Chemical		activates					tissue-type plasminogen activator gene	GP	 human		DNA motif related to the cAMP-responsive element in the promoter	NULL		NULL	NULL	NULL	NULL	gw60_mechdev_94_1_79_s_515	10842061	A DNA motif related to the cAMP-responsive element and an exon- located activator protein-2 binding site in the human tissue-type plasminogen activator gene promoter cooperate in basal expression and convey activation by phorbol ester and cAMP.	bind
42949	4	10067	7	11	NULL	NULL	NULL	phorbol ester	Chemical		activates					tissue-type plasminogen activator gene	GP	human		exon- located activator protein-2 binding site in the promoter	NULL		NULL	NULL	NULL	NULL	gw60_mechdev_94_1_79_s_515	10842061	A DNA motif related to the cAMP-responsive element and an exon- located activator protein-2 binding site in the human tissue-type plasminogen activator gene promoter cooperate in basal expression and convey activation by phorbol ester and cAMP.	bind
42950	5	10067	7	11	NULL	NULL	NULL	cAMP	Chemical		activates					tissue-type plasminogen activator gene	GP	human		DNA motif related to the cAMP-responsive element in the promoter	NULL		NULL	NULL	NULL	NULL	gw60_mechdev_94_1_79_s_515	10842061	A DNA motif related to the cAMP-responsive element and an exon- located activator protein-2 binding site in the human tissue-type plasminogen activator gene promoter cooperate in basal expression and convey activation by phorbol ester and cAMP.	bind
42951	6	10067	7	11	NULL	NULL	NULL	cAMP	Chemical		activates					tissue-type plasminogen activator gene	GP	human		exon- located activator protein-2 binding site	NULL		NULL	NULL	NULL	NULL	gw60_mechdev_94_1_79_s_515	10842061	A DNA motif related to the cAMP-responsive element and an exon- located activator protein-2 binding site in the human tissue-type plasminogen activator gene promoter cooperate in basal expression and convey activation by phorbol ester and cAMP.	bind
35212	1	10068	6	11	NULL	NULL	NULL	BMP-7	GP		does not activate					2GC(MUT)-luc	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18544_s_171	14981086	A DNA pulldown assay was carried out to examine whether lack of activation of 2GC(MUT)-luc by BMP7 is caused by lack of Smad4 binding to GC-1, GC-2, GC-3, and GC-pal motifs ( Fig. 3 B).	bind
35213	2	10068	6	11	NULL	NULL	NULL	Smad4	GP		does not bind									GC-1	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18544_s_171	14981086	A DNA pulldown assay was carried out to examine whether lack of activation of 2GC(MUT)-luc by BMP7 is caused by lack of Smad4 binding to GC-1, GC-2, GC-3, and GC-pal motifs ( Fig. 3 B).	bind
35214	3	10068	6	11	NULL	NULL	NULL	Smad4	GP		does not bind									GC-2	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18544_s_171	14981086	A DNA pulldown assay was carried out to examine whether lack of activation of 2GC(MUT)-luc by BMP7 is caused by lack of Smad4 binding to GC-1, GC-2, GC-3, and GC-pal motifs ( Fig. 3 B).	bind
35215	4	10068	6	11	NULL	NULL	NULL	Smad4	GP		does not bind									GC-3	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18544_s_171	14981086	A DNA pulldown assay was carried out to examine whether lack of activation of 2GC(MUT)-luc by BMP7 is caused by lack of Smad4 binding to GC-1, GC-2, GC-3, and GC-pal motifs ( Fig. 3 B).	bind
35216	5	10068	6	11	NULL	NULL	NULL	Smad4	GP		does not bind									GC-pal motif	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18544_s_171	14981086	A DNA pulldown assay was carried out to examine whether lack of activation of 2GC(MUT)-luc by BMP7 is caused by lack of Smad4 binding to GC-1, GC-2, GC-3, and GC-pal motifs ( Fig. 3 B).	bind
42952	1	10068	7	11	NULL	NULL	NULL	Smad4 	GP		does not bind									GC-1 motifs	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18544_s_171	14981086	A DNA pulldown assay was carried out to examine whether lack of activation of 2GC(MUT)-luc by BMP7 is caused by lack of Smad4 binding to GC-1, GC-2, GC-3, and GC-pal motifs ( Fig. 3 B).	bind
42953	2	10068	7	11	NULL	NULL	NULL	Smad4	GP		does not bind									GC-2 motifs	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18544_s_171	14981086	A DNA pulldown assay was carried out to examine whether lack of activation of 2GC(MUT)-luc by BMP7 is caused by lack of Smad4 binding to GC-1, GC-2, GC-3, and GC-pal motifs ( Fig. 3 B).	bind
42954	3	10068	7	11	NULL	NULL	NULL	Smad4	GP		does not bind									GC-3 motifs	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18544_s_171	14981086	A DNA pulldown assay was carried out to examine whether lack of activation of 2GC(MUT)-luc by BMP7 is caused by lack of Smad4 binding to GC-1, GC-2, GC-3, and GC-pal motifs ( Fig. 3 B).	bind
42955	4	10068	7	11	NULL	NULL	NULL	Smad4	GP		does not bind									GC-pal motifs	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18544_s_171	14981086	A DNA pulldown assay was carried out to examine whether lack of activation of 2GC(MUT)-luc by BMP7 is caused by lack of Smad4 binding to GC-1, GC-2, GC-3, and GC-pal motifs ( Fig. 3 B).	bind
42956	5	10068	7	11	NULL	NULL	NULL	BMP7	GP		does not activate					 2GC(MUT)-luc	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18544_s_171	14981086	A DNA pulldown assay was carried out to examine whether lack of activation of 2GC(MUT)-luc by BMP7 is caused by lack of Smad4 binding to GC-1, GC-2, GC-3, and GC-pal motifs ( Fig. 3 B).	bind
35217	1	10069	6	11	NULL	NULL	NULL	chromosome	Chromosome	DNA segment of;;E. coli	bind				replication terminus region	XerC	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_new-biol_3_8_1931824_s_6	1931824	A DNA segment (dif)  from the replication terminus region of the E. coli chromosome binds XerC  and acts as a substrate for XerC-mediated site-specific recombination  when inserted into multicopy plasmids.	bind
35218	2	10069	6	11	NULL	NULL	NULL	XerC	GP		mediates					recombination	Process	site-specific			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_new-biol_3_8_1931824_s_6	1931824	A DNA segment (dif)  from the replication terminus region of the E. coli chromosome binds XerC  and acts as a substrate for XerC-mediated site-specific recombination  when inserted into multicopy plasmids.	bind
35225	3	10069	6	11	NULL	NULL	NULL	chromosome	Chromosome	DNA segment of;;E. coli	acts as a substrate for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_new-biol_3_8_1931824_s_6	1931824	A DNA segment (dif)  from the replication terminus region of the E. coli chromosome binds XerC  and acts as a substrate for XerC-mediated site-specific recombination  when inserted into multicopy plasmids.	bind
35226	4	10069	6	11	NULL	NULL	NULL	statement 2	Process		occurs when inserted into					multicopy plasmids	NucleicAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_new-biol_3_8_1931824_s_6	1931824	A DNA segment (dif)  from the replication terminus region of the E. coli chromosome binds XerC  and acts as a substrate for XerC-mediated site-specific recombination  when inserted into multicopy plasmids.	bind
42961	1	10069	7	11	NULL	NULL	NULL	chromosome	Chromosome	DNA segment of;;E. coli	binds				replication terminus region of 	XerC	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_new-biol_3_8_1931824_s_6	1931824	A DNA segment (dif)  from the replication terminus region of the E. coli chromosome binds XerC  and acts as a substrate for XerC-mediated site-specific recombination  when inserted into multicopy plasmids.	bind
42962	2	10069	7	11	NULL	NULL	NULL	XerC	GP		mediate					recombination	Process	site-specific			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_new-biol_3_8_1931824_s_6	1931824	A DNA segment (dif)  from the replication terminus region of the E. coli chromosome binds XerC  and acts as a substrate for XerC-mediated site-specific recombination  when inserted into multicopy plasmids.	bind
42963	3	10069	7	11	NULL	NULL	NULL	chromosome	Chromosome	DNA segment of;;E. coli	acts as a substrate for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_new-biol_3_8_1931824_s_6	1931824	A DNA segment (dif)  from the replication terminus region of the E. coli chromosome binds XerC  and acts as a substrate for XerC-mediated site-specific recombination  when inserted into multicopy plasmids.	bind
35227	1	10070	6	11	NULL	NULL	NULL	MOP3-MOP4 heterodimer	GP		bind					DNA	NucleicAcid			CACGTGA element	NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_proc-natl-acad-sci-u-s-a_95_10_9576906_s_4	9576906	A DNA selection protocol revealed  that the MOP3-MOP4 heterodimer bound a CACGTGA-containing DNA element.	bind
42964	1	10070	7	11	NULL	NULL	NULL	MOP3-MOP4 heterodimer	GP		bind					DNA	NucleicAcid			CACGTGA element	NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_proc-natl-acad-sci-u-s-a_95_10_9576906_s_4	9576906	A DNA selection protocol revealed  that the MOP3-MOP4 heterodimer bound a CACGTGA-containing DNA element.	bind
35228	1	10071	6	11	NULL	NULL	NULL	DNA-binding protein	GP	Candida albicans	bind							Saccharomyces cerevisiae		RPG box	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_17_5273_s_336	10464197	A DNA-binding protein from  Candida albicans that binds to the RPG box of  Saccharomyces cerevisiae and the telomeric repeat sequence of  C. albicans.	bind
35230	2	10071	6	11	NULL	NULL	NULL	DNA-binding protein	GP	Candida albicans	bind							C.albicans		telomeric repeat sequence	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_17_5273_s_336	10464197	A DNA-binding protein from  Candida albicans that binds to the RPG box of  Saccharomyces cerevisiae and the telomeric repeat sequence of  C. albicans.	bind
42965	1	10071	7	11	NULL	NULL	NULL	DNA-binding protein	GP	 Candida albicans	binds to							Saccharomyces cerevisiae		RPG box	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_17_5273_s_336	10464197	A DNA-binding protein from  Candida albicans that binds to the RPG box of  Saccharomyces cerevisiae and the telomeric repeat sequence of  C. albicans.	bind
42966	2	10071	7	11	NULL	NULL	NULL	DNA-binding protein	GP	Candida albicans	binds to							C. albicans		telomeric repeat sequence 	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_17_5273_s_336	10464197	A DNA-binding protein from  Candida albicans that binds to the RPG box of  Saccharomyces cerevisiae and the telomeric repeat sequence of  C. albicans.	bind
35611	1	10072	6	11	NULL	NULL	NULL	RAG1	GP		bind					RSS	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5584_s_310	12488446	A DNA-induced Conformational Change in RAG1--  It has been proposed previously that RAG2 can induce a conformational change in RAG1  that facilitates binding of RAG1 to the RSS and perhaps also the appropriate folding of the RAG1 DDE active site ( ,  ,  ).	bind
35612	2	10072	6	11	NULL	NULL	NULL	RAG2	GP		induces					RAG1	GP	conformational change in			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5584_s_310	12488446	A DNA-induced Conformational Change in RAG1--  It has been proposed previously that RAG2 can induce a conformational change in RAG1  that facilitates binding of RAG1 to the RSS and perhaps also the appropriate folding of the RAG1 DDE active site ( ,  ,  ).	bind
35613	3	10072	6	11	NULL	NULL	NULL	statement 2	Process		facilitates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5584_s_310	12488446	A DNA-induced Conformational Change in RAG1--  It has been proposed previously that RAG2 can induce a conformational change in RAG1  that facilitates binding of RAG1 to the RSS and perhaps also the appropriate folding of the RAG1 DDE active site ( ,  ,  ).	bind
35614	4	10072	6	11	NULL	NULL	NULL	statement 2	Process		facilitates		perhaps			RAG1	GP	folding of	DDE active site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5584_s_310	12488446	A DNA-induced Conformational Change in RAG1--  It has been proposed previously that RAG2 can induce a conformational change in RAG1  that facilitates binding of RAG1 to the RSS and perhaps also the appropriate folding of the RAG1 DDE active site ( ,  ,  ).	bind
49525	5	10072	6	11	NULL	NULL	NULL	DNA	NucleicAcid		induce					RAG1	GP	\tconformational change in 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5584_s_310	12488446	A DNA-induced Conformational Change in RAG1--  It has been proposed previously that RAG2 can induce a conformational change in RAG1  that facilitates binding of RAG1 to the RSS and perhaps also the appropriate folding of the RAG1 DDE active site ( ,  ,  ).	bind
42967	1	10072	7	11	NULL	NULL	NULL	RAG2	GP		induce					RAG1	GP	conformational change in 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5584_s_310	12488446	A DNA-induced Conformational Change in RAG1--  It has been proposed previously that RAG2 can induce a conformational change in RAG1  that facilitates binding of RAG1 to the RSS and perhaps also the appropriate folding of the RAG1 DDE active site ( ,  ,  ).	bind
42968	2	10072	7	11	NULL	NULL	NULL	RAG1	GP		bind					RSS	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5584_s_310	12488446	A DNA-induced Conformational Change in RAG1--  It has been proposed previously that RAG2 can induce a conformational change in RAG1  that facilitates binding of RAG1 to the RSS and perhaps also the appropriate folding of the RAG1 DDE active site ( ,  ,  ).	bind
42969	3	10072	7	11	NULL	NULL	NULL	statement 1	Process		facilitate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5584_s_310	12488446	A DNA-induced Conformational Change in RAG1--  It has been proposed previously that RAG2 can induce a conformational change in RAG1  that facilitates binding of RAG1 to the RSS and perhaps also the appropriate folding of the RAG1 DDE active site ( ,  ,  ).	bind
42970	4	10072	7	11	NULL	NULL	NULL	statement 1	Process		facilitate					RAG1	GP	folding of	DDE active site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5584_s_310	12488446	A DNA-induced Conformational Change in RAG1--  It has been proposed previously that RAG2 can induce a conformational change in RAG1  that facilitates binding of RAG1 to the RSS and perhaps also the appropriate folding of the RAG1 DDE active site ( ,  ,  ).	bind
42971	5	10072	7	11	NULL	NULL	NULL	DNA	NucleicAcid		induce					RAG1	GP	conformational change in			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_5584_s_310	12488446	A DNA-induced Conformational Change in RAG1--  It has been proposed previously that RAG2 can induce a conformational change in RAG1  that facilitates binding of RAG1 to the RSS and perhaps also the appropriate folding of the RAG1 DDE active site ( ,  ,  ).	bind
35259	1	10074	6	11	NULL	NULL	NULL	Sc/Da	GP		bind									E1	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_13_2036_s_123	9649507	A DNase footprint assay indicated that Sc/Da bound to E1, but not to the N box (not shown).	bind
35261	2	10074	6	11	NULL	NULL	NULL	Sc/Da	GP		does not bind									N box	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_13_2036_s_123	9649507	A DNase footprint assay indicated that Sc/Da bound to E1, but not to the N box (not shown).	bind
42972	1	10074	7	11	NULL	NULL	NULL	Sc/Da	GP		bind									E1	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_13_2036_s_123	9649507	A DNase footprint assay indicated that Sc/Da bound to E1, but not to the N box (not shown).	bind
42973	2	10074	7	11	NULL	NULL	NULL	Sc/Da	GP		does not bind									N box	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_13_2036_s_123	9649507	A DNase footprint assay indicated that Sc/Da bound to E1, but not to the N box (not shown).	bind
35263	1	10075	6	11	NULL	NULL	NULL	OmpR	GP		bind		may;; directly			ssrA	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_3_771_s_175	10633113	A DNase I protection assay was used to determine if OmpR binds directly to the  ssrA promoter region.	bind
42974	1	10075	7	11	NULL	NULL	NULL	OmpR	GP		binds		may;;directly			ssrA	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_3_771_s_175	10633113	A DNase I protection assay was used to determine if OmpR binds directly to the  ssrA promoter region.	bind
35269	1	10076	6	11	NULL	NULL	NULL	cullin	GP		bind		selectively	DOC domain		Skp1-Fbx29	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_47_43824_s_232	11568188	A DOC domain-containing cullin selectively binds Skp1{middle dot}Fbx29 to form an SCF-like complex          PNAS,                       December 24, 2002;  99(26):  16601 - 16606.	bind
36456	2	10076	6	11	NULL	NULL	NULL	statement 1	Process		forms					SCF-like complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_47_43824_s_232	11568188	A DOC domain-containing cullin selectively binds Skp1{middle dot}Fbx29 to form an SCF-like complex          PNAS,                       December 24, 2002;  99(26):  16601 - 16606.	bind
42982	1	10076	7	11	NULL	NULL	NULL	cullin	GP		binds		selectively	DOC domain		Skp1-Fbx29	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_47_43824_s_232	11568188	A DOC domain-containing cullin selectively binds Skp1{middle dot}Fbx29 to form an SCF-like complex          PNAS,                       December 24, 2002;  99(26):  16601 - 16606.	bind
42983	2	10076	7	11	NULL	NULL	NULL	statement 1	Process		forms					SCF-like complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_47_43824_s_232	11568188	A DOC domain-containing cullin selectively binds Skp1{middle dot}Fbx29 to form an SCF-like complex          PNAS,                       December 24, 2002;  99(26):  16601 - 16606.	bind
35274	1	10078	6	11	NULL	NULL	NULL	p130CAS	GP		bind			SH3 domain		FAK	GP		PR1		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_8_6802_s_319	15557280	A docking molecule p130CAS binds to PR1 of FAK through its SH3 domain ( ).	bind
42984	1	10078	7	11	NULL	NULL	NULL	p130CAS	GP		binds to			 SH3 domain		FAK	GP		PR1		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_8_6802_s_319	15557280	A docking molecule p130CAS binds to PR1 of FAK through its SH3 domain ( ).	bind
35275	1	10079	6	11	NULL	NULL	NULL	Ras-Rac pathway	GP		mediates					cell transformation	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_3834	10066831	A domain containing the Cdc42/Rac interactive binding (CRIB) region of p65PAK inhibits transcriptional activation and cell transformation mediated by the Ras-Rac pathway.	bind
35276	2	10079	6	11	NULL	NULL	NULL	Ras-Rac pathway	GP		mediates					transcriptional activation	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_3834	10066831	A domain containing the Cdc42/Rac interactive binding (CRIB) region of p65PAK inhibits transcriptional activation and cell transformation mediated by the Ras-Rac pathway.	bind
35277	3	10079	6	11	NULL	NULL	NULL	p65PAK	GP		inhibits			CRIB 		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_3834	10066831	A domain containing the Cdc42/Rac interactive binding (CRIB) region of p65PAK inhibits transcriptional activation and cell transformation mediated by the Ras-Rac pathway.	bind
35278	4	10079	6	11	NULL	NULL	NULL	CRIB	GP		is					Cdc42/Rac interactive binding 	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_3834	10066831	A domain containing the Cdc42/Rac interactive binding (CRIB) region of p65PAK inhibits transcriptional activation and cell transformation mediated by the Ras-Rac pathway.	bind
35280	5	10079	6	11	NULL	NULL	NULL	p65PAK	GP		inhibits			CRIB		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_3834	10066831	A domain containing the Cdc42/Rac interactive binding (CRIB) region of p65PAK inhibits transcriptional activation and cell transformation mediated by the Ras-Rac pathway.	bind
42985	1	10079	7	11	NULL	NULL	NULL	p65PAK	GP		inhibits			CRIB region		statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_3834	10066831	A domain containing the Cdc42/Rac interactive binding (CRIB) region of p65PAK inhibits transcriptional activation and cell transformation mediated by the Ras-Rac pathway.	bind
42986	2	10079	7	11	NULL	NULL	NULL	Ras-Rac pathway	GP		mediates					cell transformation	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_3834	10066831	A domain containing the Cdc42/Rac interactive binding (CRIB) region of p65PAK inhibits transcriptional activation and cell transformation mediated by the Ras-Rac pathway.	bind
42987	3	10079	7	11	NULL	NULL	NULL	p65PAK	GP		inhibits			CRIB region		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_3834	10066831	A domain containing the Cdc42/Rac interactive binding (CRIB) region of p65PAK inhibits transcriptional activation and cell transformation mediated by the Ras-Rac pathway.	bind
42988	4	10079	7	11	NULL	NULL	NULL	CRIB region 	GP		is					Cdc42/Rac interactive binding region	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_3834	10066831	A domain containing the Cdc42/Rac interactive binding (CRIB) region of p65PAK inhibits transcriptional activation and cell transformation mediated by the Ras-Rac pathway.	bind
49526	5	10079	7	11	NULL	NULL	NULL	Ras-Rac pathway	GP		mediates					transcriptional activation	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_3834	10066831	A domain containing the Cdc42/Rac interactive binding (CRIB) region of p65PAK inhibits transcriptional activation and cell transformation mediated by the Ras-Rac pathway.	bind
35281	1	10081	6	11	NULL	NULL	NULL	p21	GP		bind					PCNA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_20865_s_18	16731526	A domain of p21 binds and inactivates PCNA ( ,  ).	bind
35282	2	10081	6	11	NULL	NULL	NULL	statement 1	Process		inactivates					PCNA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_20865_s_18	16731526	A domain of p21 binds and inactivates PCNA ( ,  ).	bind
42989	1	10081	7	11	NULL	NULL	NULL	p21	GP		binds					PCNA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_20865_s_18	16731526	A domain of p21 binds and inactivates PCNA ( ,  ).	bind
42990	2	10081	7	11	NULL	NULL	NULL	statement 1	Process		inactivates					PCNA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_20865_s_18	16731526	A domain of p21 binds and inactivates PCNA ( ,  ).	bind
35615	1	10082	6	11	NULL	NULL	NULL	BTX	Chemical		bind					Na+ channel	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_2_404_s_35	10419561	A domain-interface allosteric model of BTX binding, similar to the domain-interface model of Ca2+-channel drug binding (interface of D3-S6 and D4-S6; Hockerman et al., 1997  ), was proposed for BTX binding to the Na+ channel, with its dimethylpyrrolidone carboxylic acid group directed toward D1-S6 and its steroid moiety toward D4-S6.	bind
35616	2	10082	6	11	NULL	NULL	NULL	BTX	Chemical		is directed towards			dimethylpyrrolidone carboxylic acid group					D1-S6		NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_2_404_s_35	10419561	A domain-interface allosteric model of BTX binding, similar to the domain-interface model of Ca2+-channel drug binding (interface of D3-S6 and D4-S6; Hockerman et al., 1997  ), was proposed for BTX binding to the Na+ channel, with its dimethylpyrrolidone carboxylic acid group directed toward D1-S6 and its steroid moiety toward D4-S6.	bind
36457	3	10082	6	11	NULL	NULL	NULL	BTX	Chemical		is directed towards			steroid moiety					D4-S6		NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_2_404_s_35	10419561	A domain-interface allosteric model of BTX binding, similar to the domain-interface model of Ca2+-channel drug binding (interface of D3-S6 and D4-S6; Hockerman et al., 1997  ), was proposed for BTX binding to the Na+ channel, with its dimethylpyrrolidone carboxylic acid group directed toward D1-S6 and its steroid moiety toward D4-S6.	bind
36458	4	10082	6	11	NULL	NULL	NULL	statement 2	Process		occurs simultaneously with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_2_404_s_35	10419561	A domain-interface allosteric model of BTX binding, similar to the domain-interface model of Ca2+-channel drug binding (interface of D3-S6 and D4-S6; Hockerman et al., 1997  ), was proposed for BTX binding to the Na+ channel, with its dimethylpyrrolidone carboxylic acid group directed toward D1-S6 and its steroid moiety toward D4-S6.	bind
36459	5	10082	6	11	NULL	NULL	NULL	statement 3	Process		occurs simultaneously with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_2_404_s_35	10419561	A domain-interface allosteric model of BTX binding, similar to the domain-interface model of Ca2+-channel drug binding (interface of D3-S6 and D4-S6; Hockerman et al., 1997  ), was proposed for BTX binding to the Na+ channel, with its dimethylpyrrolidone carboxylic acid group directed toward D1-S6 and its steroid moiety toward D4-S6.	bind
42991	1	10082	7	11	NULL	NULL	NULL	BTX	Chemical		bind					Na+ channel	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_2_404_s_35	10419561	A domain-interface allosteric model of BTX binding, similar to the domain-interface model of Ca2+-channel drug binding (interface of D3-S6 and D4-S6; Hockerman et al., 1997  ), was proposed for BTX binding to the Na+ channel, with its dimethylpyrrolidone carboxylic acid group directed toward D1-S6 and its steroid moiety toward D4-S6.	bind
42992	2	10082	7	11	NULL	NULL	NULL	BTX	Chemical		directed towards			dimethylpyrrolidone carboxylic acid group 					D1-S6 		NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_2_404_s_35	10419561	A domain-interface allosteric model of BTX binding, similar to the domain-interface model of Ca2+-channel drug binding (interface of D3-S6 and D4-S6; Hockerman et al., 1997  ), was proposed for BTX binding to the Na+ channel, with its dimethylpyrrolidone carboxylic acid group directed toward D1-S6 and its steroid moiety toward D4-S6.	bind
42993	3	10082	7	11	NULL	NULL	NULL	BTX	Chemical		directed towards			steroid moiety					D4-S6		NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_2_404_s_35	10419561	A domain-interface allosteric model of BTX binding, similar to the domain-interface model of Ca2+-channel drug binding (interface of D3-S6 and D4-S6; Hockerman et al., 1997  ), was proposed for BTX binding to the Na+ channel, with its dimethylpyrrolidone carboxylic acid group directed toward D1-S6 and its steroid moiety toward D4-S6.	bind
49527	4	10082	7	11	NULL	NULL	NULL	statement 2	Process		occurs simultaneously with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_2_404_s_35	10419561	A domain-interface allosteric model of BTX binding, similar to the domain-interface model of Ca2+-channel drug binding (interface of D3-S6 and D4-S6; Hockerman et al., 1997  ), was proposed for BTX binding to the Na+ channel, with its dimethylpyrrolidone carboxylic acid group directed toward D1-S6 and its steroid moiety toward D4-S6.	bind
49528	5	10082	7	11	NULL	NULL	NULL	statement 3	Process		occurs simultaneously with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_2_404_s_35	10419561	A domain-interface allosteric model of BTX binding, similar to the domain-interface model of Ca2+-channel drug binding (interface of D3-S6 and D4-S6; Hockerman et al., 1997  ), was proposed for BTX binding to the Na+ channel, with its dimethylpyrrolidone carboxylic acid group directed toward D1-S6 and its steroid moiety toward D4-S6.	bind
35344	1	10085	6	11	NULL	NULL	NULL	Ikaros gene	GP	dominant mutant	leads to					leukemia	MedicalFinding	development of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_1_131_s_505	12871645	A dominant mutation in the Ikaros gene leads to rapid development of leukemia and lymphoma.	bind
35345	2	10085	6	11	NULL	NULL	NULL	Ikaros gene	GP	dominant mutant	leads to					lymphoma	MedicalFinding	development of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_1_131_s_505	12871645	A dominant mutation in the Ikaros gene leads to rapid development of leukemia and lymphoma.	bind
43004	1	10085	7	11	NULL	NULL	NULL	Ikaros gene	GP	dominant mutant	leads to					leukemia	MedicalFinding	rapid development of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_1_131_s_505	12871645	A dominant mutation in the Ikaros gene leads to rapid development of leukemia and lymphoma.	bind
43005	2	10085	7	11	NULL	NULL	NULL	Ikaros gene	GP	dominant mutant	leads to					lymphoma	MedicalFinding	rapid development of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_1_131_s_505	12871645	A dominant mutation in the Ikaros gene leads to rapid development of leukemia and lymphoma.	bind
35346	1	10086	6	11	NULL	NULL	NULL	CK1epsilon	GP		bind					dsh	GP		PDZ domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_183	11524435	A dominant negative dsh mutant (Xdd1) that lacks the putative CK1epsilon binding domain (PDZ domain) fails to block the ability of CK1epsilon to stimulate wnt signaling in vivo ( Sokol, 1996), a result inconsistent with a model in which CK1epsilon mediates wnt signaling by binding to the PDZ domain of dsh.	bind
35347	2	10086	6	11	NULL	NULL	NULL	CK1epsilon	GP		mediates					wnt signaling	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_183	11524435	A dominant negative dsh mutant (Xdd1) that lacks the putative CK1epsilon binding domain (PDZ domain) fails to block the ability of CK1epsilon to stimulate wnt signaling in vivo ( Sokol, 1996), a result inconsistent with a model in which CK1epsilon mediates wnt signaling by binding to the PDZ domain of dsh.	bind
35348	3	10086	6	11	NULL	NULL	NULL	statement 1	Process		occurs via					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_183	11524435	A dominant negative dsh mutant (Xdd1) that lacks the putative CK1epsilon binding domain (PDZ domain) fails to block the ability of CK1epsilon to stimulate wnt signaling in vivo ( Sokol, 1996), a result inconsistent with a model in which CK1epsilon mediates wnt signaling by binding to the PDZ domain of dsh.	bind
35617	4	10086	6	11	NULL	NULL	NULL	Xdd1	GP		is a type of					dominant negative dsh mutant	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_183	11524435	A dominant negative dsh mutant (Xdd1) that lacks the putative CK1epsilon binding domain (PDZ domain) fails to block the ability of CK1epsilon to stimulate wnt signaling in vivo ( Sokol, 1996), a result inconsistent with a model in which CK1epsilon mediates wnt signaling by binding to the PDZ domain of dsh.	bind
35618	5	10086	6	11	NULL	NULL	NULL	Xdd1	GP		lacks							putative	PDZ domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_183	11524435	A dominant negative dsh mutant (Xdd1) that lacks the putative CK1epsilon binding domain (PDZ domain) fails to block the ability of CK1epsilon to stimulate wnt signaling in vivo ( Sokol, 1996), a result inconsistent with a model in which CK1epsilon mediates wnt signaling by binding to the PDZ domain of dsh.	bind
35619	6	10086	6	11	NULL	NULL	NULL	CK1epsilon binding domain	GP		is					PDZ domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_183	11524435	A dominant negative dsh mutant (Xdd1) that lacks the putative CK1epsilon binding domain (PDZ domain) fails to block the ability of CK1epsilon to stimulate wnt signaling in vivo ( Sokol, 1996), a result inconsistent with a model in which CK1epsilon mediates wnt signaling by binding to the PDZ domain of dsh.	bind
35620	7	10086	6	11	NULL	NULL	NULL	statement 5	Process		fails to block					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_183	11524435	A dominant negative dsh mutant (Xdd1) that lacks the putative CK1epsilon binding domain (PDZ domain) fails to block the ability of CK1epsilon to stimulate wnt signaling in vivo ( Sokol, 1996), a result inconsistent with a model in which CK1epsilon mediates wnt signaling by binding to the PDZ domain of dsh.	bind
49529	8	10086	6	11	NULL	NULL	NULL	CK1epsilon	GP		stimulates					wnt signaling	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_183	11524435	A dominant negative dsh mutant (Xdd1) that lacks the putative CK1epsilon binding domain (PDZ domain) fails to block the ability of CK1epsilon to stimulate wnt signaling in vivo ( Sokol, 1996), a result inconsistent with a model in which CK1epsilon mediates wnt signaling by binding to the PDZ domain of dsh.	bind
43007	1	10086	7	11	NULL	NULL	NULL	CK1epsilon	GP		stimulate					wnt signaling	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_183	11524435	A dominant negative dsh mutant (Xdd1) that lacks the putative CK1epsilon binding domain (PDZ domain) fails to block the ability of CK1epsilon to stimulate wnt signaling in vivo ( Sokol, 1996), a result inconsistent with a model in which CK1epsilon mediates wnt signaling by binding to the PDZ domain of dsh.	bind
43008	2	10086	7	11	NULL	NULL	NULL	CK1epsilon 	GP		mediates					wnt signaling	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_183	11524435	A dominant negative dsh mutant (Xdd1) that lacks the putative CK1epsilon binding domain (PDZ domain) fails to block the ability of CK1epsilon to stimulate wnt signaling in vivo ( Sokol, 1996), a result inconsistent with a model in which CK1epsilon mediates wnt signaling by binding to the PDZ domain of dsh.	bind
43024	3	10086	7	11	NULL	NULL	NULL	Xdd1	GP		lacks							putative	 PDZ domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_183	11524435	A dominant negative dsh mutant (Xdd1) that lacks the putative CK1epsilon binding domain (PDZ domain) fails to block the ability of CK1epsilon to stimulate wnt signaling in vivo ( Sokol, 1996), a result inconsistent with a model in which CK1epsilon mediates wnt signaling by binding to the PDZ domain of dsh.	bind
43027	4	10086	7	11	NULL	NULL	NULL	statement 3	Process		fails to block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_183	11524435	A dominant negative dsh mutant (Xdd1) that lacks the putative CK1epsilon binding domain (PDZ domain) fails to block the ability of CK1epsilon to stimulate wnt signaling in vivo ( Sokol, 1996), a result inconsistent with a model in which CK1epsilon mediates wnt signaling by binding to the PDZ domain of dsh.	bind
43028	5	10086	7	11	NULL	NULL	NULL	CK1epsilon	GP		bind					dsh	GP		PDZ domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_183	11524435	A dominant negative dsh mutant (Xdd1) that lacks the putative CK1epsilon binding domain (PDZ domain) fails to block the ability of CK1epsilon to stimulate wnt signaling in vivo ( Sokol, 1996), a result inconsistent with a model in which CK1epsilon mediates wnt signaling by binding to the PDZ domain of dsh.	bind
43029	6	10086	7	11	NULL	NULL	NULL	statement 2	Process		occurs via					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_183	11524435	A dominant negative dsh mutant (Xdd1) that lacks the putative CK1epsilon binding domain (PDZ domain) fails to block the ability of CK1epsilon to stimulate wnt signaling in vivo ( Sokol, 1996), a result inconsistent with a model in which CK1epsilon mediates wnt signaling by binding to the PDZ domain of dsh.	bind
43030	7	10086	7	11	NULL	NULL	NULL	Xdd1	GP		is a type of					dominant negative dsh mutant	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_183	11524435	A dominant negative dsh mutant (Xdd1) that lacks the putative CK1epsilon binding domain (PDZ domain) fails to block the ability of CK1epsilon to stimulate wnt signaling in vivo ( Sokol, 1996), a result inconsistent with a model in which CK1epsilon mediates wnt signaling by binding to the PDZ domain of dsh.	bind
49530	8	10086	7	11	NULL	NULL	NULL	CK1epsilon binding domain	GP		is					PDZ domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_183	11524435	A dominant negative dsh mutant (Xdd1) that lacks the putative CK1epsilon binding domain (PDZ domain) fails to block the ability of CK1epsilon to stimulate wnt signaling in vivo ( Sokol, 1996), a result inconsistent with a model in which CK1epsilon mediates wnt signaling by binding to the PDZ domain of dsh.	bind
35349	1	10087	6	11	NULL	NULL	NULL	peroxisome proliferator-activated receptor-gamma	GP	dominant negative;; knock-in mouse	exhibits					metabolic syndrome	MedicalFinding	features of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_17_17118_s_1	15716267	A dominant negative peroxisome proliferator-activated receptor-gamma knock-in mouse exhibits features of the metabolic syndrome.	bind
43031	1	10087	7	11	NULL	NULL	NULL	peroxisome proliferator-activated receptor-gamma 	GP	dominant negative;;knock-in mouse	exhibits					metabolic syndrome	MedicalFinding	features of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_17_17118_s_1	15716267	A dominant negative peroxisome proliferator-activated receptor-gamma knock-in mouse exhibits features of the metabolic syndrome.	bind
35621	1	10088	6	11	NULL	NULL	NULL	CD27	GP		induces					NF-kappaB	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13353_s_111	9582383	A Dominant Negative TRAF2 or TRAF5 Block NF-kappa B Activation Induced by CD27-- To determine whether TRAF2 and TRAF5 are involved in NF-kappaB activation by CD27, we tested whether N-terminal truncated mutants of TRAF2 and TRAF5 would act as dominant negative mutants based on previous results that showed that the zinc binding domain of TRAF2 and TRAF5 is required for NF-kappaB activation ( 9,  12).	bind
35622	2	10088	6	11	NULL	NULL	NULL	TRAF2	GP		is required for			zinc binding domain		NF-kappaB	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13353_s_111	9582383	A Dominant Negative TRAF2 or TRAF5 Block NF-kappa B Activation Induced by CD27-- To determine whether TRAF2 and TRAF5 are involved in NF-kappaB activation by CD27, we tested whether N-terminal truncated mutants of TRAF2 and TRAF5 would act as dominant negative mutants based on previous results that showed that the zinc binding domain of TRAF2 and TRAF5 is required for NF-kappaB activation ( 9,  12).	bind
35623	3	10088	6	11	NULL	NULL	NULL	TRAF5	GP		is required for			zinc binding domain		NF-kappaB	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13353_s_111	9582383	A Dominant Negative TRAF2 or TRAF5 Block NF-kappa B Activation Induced by CD27-- To determine whether TRAF2 and TRAF5 are involved in NF-kappaB activation by CD27, we tested whether N-terminal truncated mutants of TRAF2 and TRAF5 would act as dominant negative mutants based on previous results that showed that the zinc binding domain of TRAF2 and TRAF5 is required for NF-kappaB activation ( 9,  12).	bind
35624	4	10088	6	11	NULL	NULL	NULL	TRAF2	GP	dominant-negative	blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13353_s_111	9582383	A Dominant Negative TRAF2 or TRAF5 Block NF-kappa B Activation Induced by CD27-- To determine whether TRAF2 and TRAF5 are involved in NF-kappaB activation by CD27, we tested whether N-terminal truncated mutants of TRAF2 and TRAF5 would act as dominant negative mutants based on previous results that showed that the zinc binding domain of TRAF2 and TRAF5 is required for NF-kappaB activation ( 9,  12).	bind
35625	5	10088	6	11	NULL	NULL	NULL	TRAF5	GP	dominant-negative	blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13353_s_111	9582383	A Dominant Negative TRAF2 or TRAF5 Block NF-kappa B Activation Induced by CD27-- To determine whether TRAF2 and TRAF5 are involved in NF-kappaB activation by CD27, we tested whether N-terminal truncated mutants of TRAF2 and TRAF5 would act as dominant negative mutants based on previous results that showed that the zinc binding domain of TRAF2 and TRAF5 is required for NF-kappaB activation ( 9,  12).	bind
43033	1	10088	7	11	NULL	NULL	NULL	TRAF2	GP		is required for			zinc binding domain 		NF-kappaB	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13353_s_111	9582383	A Dominant Negative TRAF2 or TRAF5 Block NF-kappa B Activation Induced by CD27-- To determine whether TRAF2 and TRAF5 are involved in NF-kappaB activation by CD27, we tested whether N-terminal truncated mutants of TRAF2 and TRAF5 would act as dominant negative mutants based on previous results that showed that the zinc binding domain of TRAF2 and TRAF5 is required for NF-kappaB activation ( 9,  12).	bind
43034	2	10088	7	11	NULL	NULL	NULL	TRAF5	GP		is required for			zinc binding domain 		NF-kappaB	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13353_s_111	9582383	A Dominant Negative TRAF2 or TRAF5 Block NF-kappa B Activation Induced by CD27-- To determine whether TRAF2 and TRAF5 are involved in NF-kappaB activation by CD27, we tested whether N-terminal truncated mutants of TRAF2 and TRAF5 would act as dominant negative mutants based on previous results that showed that the zinc binding domain of TRAF2 and TRAF5 is required for NF-kappaB activation ( 9,  12).	bind
43035	3	10088	7	11	NULL	NULL	NULL	CD27	GP		induce					NF-kappaB	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13353_s_111	9582383	A Dominant Negative TRAF2 or TRAF5 Block NF-kappa B Activation Induced by CD27-- To determine whether TRAF2 and TRAF5 are involved in NF-kappaB activation by CD27, we tested whether N-terminal truncated mutants of TRAF2 and TRAF5 would act as dominant negative mutants based on previous results that showed that the zinc binding domain of TRAF2 and TRAF5 is required for NF-kappaB activation ( 9,  12).	bind
43036	4	10088	7	11	NULL	NULL	NULL	TRAF2	GP	dominant-negative	blocks					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13353_s_111	9582383	A Dominant Negative TRAF2 or TRAF5 Block NF-kappa B Activation Induced by CD27-- To determine whether TRAF2 and TRAF5 are involved in NF-kappaB activation by CD27, we tested whether N-terminal truncated mutants of TRAF2 and TRAF5 would act as dominant negative mutants based on previous results that showed that the zinc binding domain of TRAF2 and TRAF5 is required for NF-kappaB activation ( 9,  12).	bind
43037	5	10088	7	11	NULL	NULL	NULL	TRAF5	GP	dominant-negative	blocks					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13353_s_111	9582383	A Dominant Negative TRAF2 or TRAF5 Block NF-kappa B Activation Induced by CD27-- To determine whether TRAF2 and TRAF5 are involved in NF-kappaB activation by CD27, we tested whether N-terminal truncated mutants of TRAF2 and TRAF5 would act as dominant negative mutants based on previous results that showed that the zinc binding domain of TRAF2 and TRAF5 is required for NF-kappaB activation ( 9,  12).	bind
35350	1	10089	6	11	NULL	NULL	NULL	FADD-DN	GP		lacks								death effector domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25783_s_84	9325306	A dominant negative version of FADD (FADD-DN) that lacks the death effector domain and is therefore unable to recruit FLICE inhibits cell death induced by all three receptors (CD95, TNFR1, and DR3).	bind
35351	2	10089	6	11	NULL	NULL	NULL	FADD-DN	GP		is unable to recruit					FLICE	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25783_s_84	9325306	A dominant negative version of FADD (FADD-DN) that lacks the death effector domain and is therefore unable to recruit FLICE inhibits cell death induced by all three receptors (CD95, TNFR1, and DR3).	bind
36460	3	10089	6	11	NULL	NULL	NULL	FADD-DN	GP		inhibits					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25783_s_84	9325306	A dominant negative version of FADD (FADD-DN) that lacks the death effector domain and is therefore unable to recruit FLICE inhibits cell death induced by all three receptors (CD95, TNFR1, and DR3).	bind
36461	4	10089	6	11	NULL	NULL	NULL	cell death	Process		is induced by					CD95	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25783_s_84	9325306	A dominant negative version of FADD (FADD-DN) that lacks the death effector domain and is therefore unable to recruit FLICE inhibits cell death induced by all three receptors (CD95, TNFR1, and DR3).	bind
36462	5	10089	6	11	NULL	NULL	NULL	cell death	Process		is induced by					TNFR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25783_s_84	9325306	A dominant negative version of FADD (FADD-DN) that lacks the death effector domain and is therefore unable to recruit FLICE inhibits cell death induced by all three receptors (CD95, TNFR1, and DR3).	bind
36463	6	10089	6	11	NULL	NULL	NULL	cell death 	Process		is induced by					DR3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25783_s_84	9325306	A dominant negative version of FADD (FADD-DN) that lacks the death effector domain and is therefore unable to recruit FLICE inhibits cell death induced by all three receptors (CD95, TNFR1, and DR3).	bind
49536	7	10089	6	11	NULL	NULL	NULL	FADD-DN	GP		inhibits					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25783_s_84	9325306	A dominant negative version of FADD (FADD-DN) that lacks the death effector domain and is therefore unable to recruit FLICE inhibits cell death induced by all three receptors (CD95, TNFR1, and DR3).	bind
49537	8	10089	6	11	NULL	NULL	NULL	FADD-DN	GP		inhibits					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25783_s_84	9325306	A dominant negative version of FADD (FADD-DN) that lacks the death effector domain and is therefore unable to recruit FLICE inhibits cell death induced by all three receptors (CD95, TNFR1, and DR3).	bind
57319	9	10089	6	11	NULL	NULL	NULL	FADD-DN	GP		is					dominant negative mutant of FADD	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25783_s_84	9325306	A dominant negative version of FADD (FADD-DN) that lacks the death effector domain and is therefore unable to recruit FLICE inhibits cell death induced by all three receptors (CD95, TNFR1, and DR3).	bind
43038	1	10089	7	11	NULL	NULL	NULL	FADD-DN	GP		lacks								death effector domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25783_s_84	9325306	A dominant negative version of FADD (FADD-DN) that lacks the death effector domain and is therefore unable to recruit FLICE inhibits cell death induced by all three receptors (CD95, TNFR1, and DR3).	bind
43039	2	10089	7	11	NULL	NULL	NULL	statement 1	Process		is unable to recruit					FLICE	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25783_s_84	9325306	A dominant negative version of FADD (FADD-DN) that lacks the death effector domain and is therefore unable to recruit FLICE inhibits cell death induced by all three receptors (CD95, TNFR1, and DR3).	bind
43040	3	10089	7	11	NULL	NULL	NULL	cell death	Process		induced by					CD95	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25783_s_84	9325306	A dominant negative version of FADD (FADD-DN) that lacks the death effector domain and is therefore unable to recruit FLICE inhibits cell death induced by all three receptors (CD95, TNFR1, and DR3).	bind
43061	4	10089	7	11	NULL	NULL	NULL	cell death	Process		induced by					TNFR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25783_s_84	9325306	A dominant negative version of FADD (FADD-DN) that lacks the death effector domain and is therefore unable to recruit FLICE inhibits cell death induced by all three receptors (CD95, TNFR1, and DR3).	bind
43062	5	10089	7	11	NULL	NULL	NULL	cell death	Process		induced by					DR3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25783_s_84	9325306	A dominant negative version of FADD (FADD-DN) that lacks the death effector domain and is therefore unable to recruit FLICE inhibits cell death induced by all three receptors (CD95, TNFR1, and DR3).	bind
43063	6	10089	7	11	NULL	NULL	NULL	FADD-DN	GP		inhibits					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25783_s_84	9325306	A dominant negative version of FADD (FADD-DN) that lacks the death effector domain and is therefore unable to recruit FLICE inhibits cell death induced by all three receptors (CD95, TNFR1, and DR3).	bind
43064	7	10089	7	11	NULL	NULL	NULL	FADD-DN	GP		inhibits					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25783_s_84	9325306	A dominant negative version of FADD (FADD-DN) that lacks the death effector domain and is therefore unable to recruit FLICE inhibits cell death induced by all three receptors (CD95, TNFR1, and DR3).	bind
43065	8	10089	7	11	NULL	NULL	NULL	FADD-DN	GP		inhibits					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25783_s_84	9325306	A dominant negative version of FADD (FADD-DN) that lacks the death effector domain and is therefore unable to recruit FLICE inhibits cell death induced by all three receptors (CD95, TNFR1, and DR3).	bind
43066	9	10089	7	11	NULL	NULL	NULL	FADD-DN	GP		is					dominant negative mutant of FADD	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25783_s_84	9325306	A dominant negative version of FADD (FADD-DN) that lacks the death effector domain and is therefore unable to recruit FLICE inhibits cell death induced by all three receptors (CD95, TNFR1, and DR3).	bind
35352	1	10090	6	11	NULL	NULL	NULL	N17Cdc42	GP		does not bind					WASP	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_1_70_s_45	8805223	A dominant-negative form of Cdc42 (N17Cdc42) also failed to bind WASP, suggesting that WASP specifically recognized the GTP-bound conformation of Cdc42.	bind
35353	2	10090	6	11	NULL	NULL	NULL	dominant-negative form of Cdc42	GP		is					N17Cdc42	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_1_70_s_45	8805223	A dominant-negative form of Cdc42 (N17Cdc42) also failed to bind WASP, suggesting that WASP specifically recognized the GTP-bound conformation of Cdc42.	bind
35354	3	10090	6	11	NULL	NULL	NULL	Cdc42	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_1_70_s_45	8805223	A dominant-negative form of Cdc42 (N17Cdc42) also failed to bind WASP, suggesting that WASP specifically recognized the GTP-bound conformation of Cdc42.	bind
35355	4	10090	6	11	NULL	NULL	NULL	WASP	GP		recognizes		specifically			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_1_70_s_45	8805223	A dominant-negative form of Cdc42 (N17Cdc42) also failed to bind WASP, suggesting that WASP specifically recognized the GTP-bound conformation of Cdc42.	bind
43067	1	10090	7	11	NULL	NULL	NULL	N17Cdc42	GP		fails to bind					WASP	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_1_70_s_45	8805223	A dominant-negative form of Cdc42 (N17Cdc42) also failed to bind WASP, suggesting that WASP specifically recognized the GTP-bound conformation of Cdc42.	bind
43068	2	10090	7	11	NULL	NULL	NULL	Cdc42	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_1_70_s_45	8805223	A dominant-negative form of Cdc42 (N17Cdc42) also failed to bind WASP, suggesting that WASP specifically recognized the GTP-bound conformation of Cdc42.	bind
43069	3	10090	7	11	NULL	NULL	NULL	WASP	GP		recognize		specifically			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_1_70_s_45	8805223	A dominant-negative form of Cdc42 (N17Cdc42) also failed to bind WASP, suggesting that WASP specifically recognized the GTP-bound conformation of Cdc42.	bind
43070	4	10090	7	11	NULL	NULL	NULL	dominant-negative form of Cdc42	GP		is					N17Cdc42	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_1_70_s_45	8805223	A dominant-negative form of Cdc42 (N17Cdc42) also failed to bind WASP, suggesting that WASP specifically recognized the GTP-bound conformation of Cdc42.	bind
35356	1	10091	6	11	NULL	NULL	NULL	Ras	GP	dominant-negative mutant	bind		tightly	S17N		Ras-GEF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_46_27880_s_188	7499262	A dominant-negative mutant  Ras(S17N), which binds to Ras-GEFs tightly to prevent its action toward  endogenous Ras, has been utilized widely to evaluate whether Ras is  essential for a particular signal transduction pathway (Feig and  Cooper, 1988).	bind
43078	1	10091	7	11	NULL	NULL	NULL	Ras	GP	\tdominant-negative mutant	binds to		tightly	S17N		Ras-GEFs	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_46_27880_s_188	7499262	A dominant-negative mutant  Ras(S17N), which binds to Ras-GEFs tightly to prevent its action toward  endogenous Ras, has been utilized widely to evaluate whether Ras is  essential for a particular signal transduction pathway (Feig and  Cooper, 1988).	bind
35357	1	10092	6	11	NULL	NULL	NULL	cyclin D1	GP	dominant-negative mutant	bind			T156A		Cdk4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2251_s_309	10022912	A dominant-negative mutant of cyclin D1 (T156A) can still bind to cdk4, but the complex is not imported into the nucleus ( 14), suggesting that a conformational state is recognized by such a carrier protein.	bind
49552	2	10092	6	11	NULL	NULL	NULL	statement 1	Process		is not imported into					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2251_s_309	10022912	A dominant-negative mutant of cyclin D1 (T156A) can still bind to cdk4, but the complex is not imported into the nucleus ( 14), suggesting that a conformational state is recognized by such a carrier protein.	bind
43084	1	10092	7	11	NULL	NULL	NULL	cyclin D1	GP	dominant-negative mutant 	bind			T156A		cdk4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2251_s_309	10022912	A dominant-negative mutant of cyclin D1 (T156A) can still bind to cdk4, but the complex is not imported into the nucleus ( 14), suggesting that a conformational state is recognized by such a carrier protein.	bind
43085	2	10092	7	11	NULL	NULL	NULL	statement 1	Process		is not imported into					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2251_s_309	10022912	A dominant-negative mutant of cyclin D1 (T156A) can still bind to cdk4, but the complex is not imported into the nucleus ( 14), suggesting that a conformational state is recognized by such a carrier protein.	bind
35358	1	10094	6	11	NULL	NULL	NULL	Rab11	GP	\tdominant-negative mutant	bind		constitutively	S25N		GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_6065_s_365	16880518	A dominant-negative Rab11 mutant, Rab11 (S25N), which constitutively binds GDP, and blocks endosomal trafficking ( ) was coexpressed with GFP-GLUT4 and HA-72-5ptase (Fig.  8C).	bind
35359	2	10094	6	11	NULL	NULL	NULL	statement 1	Process		blocks					endosomal trafficking	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_6065_s_365	16880518	A dominant-negative Rab11 mutant, Rab11 (S25N), which constitutively binds GDP, and blocks endosomal trafficking ( ) was coexpressed with GFP-GLUT4 and HA-72-5ptase (Fig.  8C).	bind
43088	1	10094	7	11	NULL	NULL	NULL	Rab11	GP	\tdominant-negative mutant	binds		constitutively	S25N		GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_6065_s_365	16880518	A dominant-negative Rab11 mutant, Rab11 (S25N), which constitutively binds GDP, and blocks endosomal trafficking ( ) was coexpressed with GFP-GLUT4 and HA-72-5ptase (Fig.  8C).	bind
43089	2	10094	7	11	NULL	NULL	NULL	statement 1	Process		blocks					endosomal trafficking	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_6065_s_365	16880518	A dominant-negative Rab11 mutant, Rab11 (S25N), which constitutively binds GDP, and blocks endosomal trafficking ( ) was coexpressed with GFP-GLUT4 and HA-72-5ptase (Fig.  8C).	bind
35626	1	10095	6	11	NULL	NULL	NULL	TRAF2	GP		bind					CD40	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_4_379_s_173	9133417	A dominant-negative TRAF3, which has the potential to displace the binding of both TRAF3 and TRAF2 to CD40 (  Cheng et al. 1995  ; Rothe et al. 1995  ), was previously shown to inhibit CD40-mediated expression of CD23 but not of ICAM-1 ( Cheng et al. 1995  ).	bind
35627	2	10095	6	11	NULL	NULL	NULL	TRAF3	GP		bind					CD40	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_4_379_s_173	9133417	A dominant-negative TRAF3, which has the potential to displace the binding of both TRAF3 and TRAF2 to CD40 (  Cheng et al. 1995  ; Rothe et al. 1995  ), was previously shown to inhibit CD40-mediated expression of CD23 but not of ICAM-1 ( Cheng et al. 1995  ).	bind
35628	3	10095	6	11	NULL	NULL	NULL	TRAF3	GP	dominant-negative	displaces					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_4_379_s_173	9133417	A dominant-negative TRAF3, which has the potential to displace the binding of both TRAF3 and TRAF2 to CD40 (  Cheng et al. 1995  ; Rothe et al. 1995  ), was previously shown to inhibit CD40-mediated expression of CD23 but not of ICAM-1 ( Cheng et al. 1995  ).	bind
35629	4	10095	6	11	NULL	NULL	NULL	TRAF3	GP	dominant-negative	displaces					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_4_379_s_173	9133417	A dominant-negative TRAF3, which has the potential to displace the binding of both TRAF3 and TRAF2 to CD40 (  Cheng et al. 1995  ; Rothe et al. 1995  ), was previously shown to inhibit CD40-mediated expression of CD23 but not of ICAM-1 ( Cheng et al. 1995  ).	bind
35630	5	10095	6	11	NULL	NULL	NULL	CD23	GP	expression of	is mediated by					CD40	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_4_379_s_173	9133417	A dominant-negative TRAF3, which has the potential to displace the binding of both TRAF3 and TRAF2 to CD40 (  Cheng et al. 1995  ; Rothe et al. 1995  ), was previously shown to inhibit CD40-mediated expression of CD23 but not of ICAM-1 ( Cheng et al. 1995  ).	bind
35631	6	10095	6	11	NULL	NULL	NULL	TRAF3	GP	dominant-negative	inhibits					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_4_379_s_173	9133417	A dominant-negative TRAF3, which has the potential to displace the binding of both TRAF3 and TRAF2 to CD40 (  Cheng et al. 1995  ; Rothe et al. 1995  ), was previously shown to inhibit CD40-mediated expression of CD23 but not of ICAM-1 ( Cheng et al. 1995  ).	bind
35632	7	10095	6	11	NULL	NULL	NULL	TRAF3	GP	dominant-negative	does not inhibit					ICAM-1	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_4_379_s_173	9133417	A dominant-negative TRAF3, which has the potential to displace the binding of both TRAF3 and TRAF2 to CD40 (  Cheng et al. 1995  ; Rothe et al. 1995  ), was previously shown to inhibit CD40-mediated expression of CD23 but not of ICAM-1 ( Cheng et al. 1995  ).	bind
43091	1	10095	7	11	NULL	NULL	NULL	TRAF3 	GP		bind					CD40	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_4_379_s_173	9133417	A dominant-negative TRAF3, which has the potential to displace the binding of both TRAF3 and TRAF2 to CD40 (  Cheng et al. 1995  ; Rothe et al. 1995  ), was previously shown to inhibit CD40-mediated expression of CD23 but not of ICAM-1 ( Cheng et al. 1995  ).	bind
43092	2	10095	7	11	NULL	NULL	NULL	TRAF2	GP		bind					CD40	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_4_379_s_173	9133417	A dominant-negative TRAF3, which has the potential to displace the binding of both TRAF3 and TRAF2 to CD40 (  Cheng et al. 1995  ; Rothe et al. 1995  ), was previously shown to inhibit CD40-mediated expression of CD23 but not of ICAM-1 ( Cheng et al. 1995  ).	bind
43093	3	10095	7	11	NULL	NULL	NULL	TRAF3	GP	dominant-negative	displace					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_4_379_s_173	9133417	A dominant-negative TRAF3, which has the potential to displace the binding of both TRAF3 and TRAF2 to CD40 (  Cheng et al. 1995  ; Rothe et al. 1995  ), was previously shown to inhibit CD40-mediated expression of CD23 but not of ICAM-1 ( Cheng et al. 1995  ).	bind
43094	4	10095	7	11	NULL	NULL	NULL	TRAF3	GP	dominant-negative	displace					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_4_379_s_173	9133417	A dominant-negative TRAF3, which has the potential to displace the binding of both TRAF3 and TRAF2 to CD40 (  Cheng et al. 1995  ; Rothe et al. 1995  ), was previously shown to inhibit CD40-mediated expression of CD23 but not of ICAM-1 ( Cheng et al. 1995  ).	bind
43095	5	10095	7	11	NULL	NULL	NULL	CD23	GP	expression of	is mediated by					CD40	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_4_379_s_173	9133417	A dominant-negative TRAF3, which has the potential to displace the binding of both TRAF3 and TRAF2 to CD40 (  Cheng et al. 1995  ; Rothe et al. 1995  ), was previously shown to inhibit CD40-mediated expression of CD23 but not of ICAM-1 ( Cheng et al. 1995  ).	bind
43097	6	10095	7	11	NULL	NULL	NULL	TRAF3	GP	dominant-negative	inhibits					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_4_379_s_173	9133417	A dominant-negative TRAF3, which has the potential to displace the binding of both TRAF3 and TRAF2 to CD40 (  Cheng et al. 1995  ; Rothe et al. 1995  ), was previously shown to inhibit CD40-mediated expression of CD23 but not of ICAM-1 ( Cheng et al. 1995  ).	bind
43099	7	10095	7	11	NULL	NULL	NULL	TRAF3	GP	dominant-negative	does not inhibit					ICAM-1	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_4_379_s_173	9133417	A dominant-negative TRAF3, which has the potential to displace the binding of both TRAF3 and TRAF2 to CD40 (  Cheng et al. 1995  ; Rothe et al. 1995  ), was previously shown to inhibit CD40-mediated expression of CD23 but not of ICAM-1 ( Cheng et al. 1995  ).	bind
35360	1	10096	6	11	NULL	NULL	NULL	CD80Fc	GP		bind					CD152-Fc	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10149_s_144	15598660	A dose response exhibiting greater decrease in the percentage of binding of CD80Fc to CD152-Fc was observed with increasing concentrations of CD80-CAP1 ( Fig. 4 B).	bind
35361	2	10096	6	11	NULL	NULL	NULL	CD80-CAP1	GP	increasing concentrations of	decreases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10149_s_144	15598660	A dose response exhibiting greater decrease in the percentage of binding of CD80Fc to CD152-Fc was observed with increasing concentrations of CD80-CAP1 ( Fig. 4 B).	bind
43101	1	10096	7	11	NULL	NULL	NULL	CD80Fc	GP		binds					CD152-Fc	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10149_s_144	15598660	A dose response exhibiting greater decrease in the percentage of binding of CD80Fc to CD152-Fc was observed with increasing concentrations of CD80-CAP1 ( Fig. 4 B).	bind
49553	2	10096	7	11	NULL	NULL	NULL	CD80-CAP1	GP	increasing concentrations of	decreases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10149_s_144	15598660	A dose response exhibiting greater decrease in the percentage of binding of CD80Fc to CD152-Fc was observed with increasing concentrations of CD80-CAP1 ( Fig. 4 B).	bind
35362	1	10097	6	11	NULL	NULL	NULL	tra-1	GP		interacts with		dose-sensitively			ehn-3	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_131_17_4333_s_229	15294864	A dose sensitive interaction between  tra-1 and  ehn-3   In constructing  tra-1(e1099); ehn-3(q689), we found that  tra-1 is a dominant enhancer of the  ehn-3 gonadogenesis defects.	bind
35364	3	10097	6	11	NULL	NULL	NULL	tra-1	GP		is an enhancer of		dominant			ehn-3	GP	gonadogenesis defects of			NULL		NULL	NULL	NULL	NULL	gw70_development_131_17_4333_s_229	15294864	A dose sensitive interaction between  tra-1 and  ehn-3   In constructing  tra-1(e1099); ehn-3(q689), we found that  tra-1 is a dominant enhancer of the  ehn-3 gonadogenesis defects.	bind
43102	1	10097	7	11	NULL	NULL	NULL	tra-1 	GP		interacts with		dose-sensitively			ehn-3	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_131_17_4333_s_229	15294864	A dose sensitive interaction between  tra-1 and  ehn-3   In constructing  tra-1(e1099); ehn-3(q689), we found that  tra-1 is a dominant enhancer of the  ehn-3 gonadogenesis defects.	bind
43103	2	10097	7	11	NULL	NULL	NULL	tra-1	GP		is an enhancer of		dominant			ehn-3	GP	gonadogenesis defects of			NULL		NULL	NULL	NULL	NULL	gw70_development_131_17_4333_s_229	15294864	A dose sensitive interaction between  tra-1 and  ehn-3   In constructing  tra-1(e1099); ehn-3(q689), we found that  tra-1 is a dominant enhancer of the  ehn-3 gonadogenesis defects.	bind
35365	1	10098	6	11	NULL	NULL	NULL	H-kininogen	GP	biotinylated	bind		dose dependently			EA.hy926 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_13040_s_154	8662673	A dose-dependent binding of biotinylated H-kininogen to EA.hy926 cells was observed at concentrations of  10 nM.	bind
43104	1	10098	7	11	NULL	NULL	NULL	H-kininogen	GP	biotinylated	bind		dose-dependently			EA.hy926 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_22_13040_s_154	8662673	A dose-dependent binding of biotinylated H-kininogen to EA.hy926 cells was observed at concentrations of  10 nM.	bind
35366	1	10100	6	11	NULL	NULL	NULL	nuclear factor	GP		bind		high affinity			Glut3	GP	mouse;; unlabeled		bp 149 to 124	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27474_s_182	9765277	A dose-dependent displacement of the band shifts with the unlabeled bp  149 to  124 region of the mouse Glut 3 established a relatively high affinity binding of nuclear factor(s) to this region (Fig.  3 C).	bind
43105	1	10100	7	11	NULL	NULL	NULL	nuclear factors	GP		bind		high affinity			Glut 3 	GP	mouse;;unlabeled		bp 149 to 124	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27474_s_182	9765277	A dose-dependent displacement of the band shifts with the unlabeled bp  149 to  124 region of the mouse Glut 3 established a relatively high affinity binding of nuclear factor(s) to this region (Fig.  3 C).	bind
35367	1	10101	6	11	NULL	NULL	NULL	HSP90	GP		bind		dose dependently			eNOS	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_11_9339_s_154	12519764	A dose-dependent increase in HSP90 binding to eNOS also was observed at high Ca2+ concentration.	bind
35368	2	10101	6	11	NULL	NULL	NULL	statement 1	Process		in the presence of					Ca2+ 	Chemical	high concentrations of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_11_9339_s_154	12519764	A dose-dependent increase in HSP90 binding to eNOS also was observed at high Ca2+ concentration.	bind
43107	1	10101	7	11	NULL	NULL	NULL	HSP90	GP		bind		dose-dependently			eNOS	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_11_9339_s_154	12519764	A dose-dependent increase in HSP90 binding to eNOS also was observed at high Ca2+ concentration.	bind
43108	2	10101	7	11	NULL	NULL	NULL	statement 1	Process		 in the presence of					Ca2+	Chemical	high concentrations of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_11_9339_s_154	12519764	A dose-dependent increase in HSP90 binding to eNOS also was observed at high Ca2+ concentration.	bind
35369	1	10102	6	11	NULL	NULL	NULL	anti - HSP-65	GP		bind					HSP-65	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_505_s_108	10073950	A dose-dependent inhibition of anti - HSP-65 binding to HSP-65 - coated plates was evident.	bind
43109	1	10102	7	11	NULL	NULL	NULL	anti - HSP-65	GP		bind					HSP-65	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_505_s_108	10073950	A dose-dependent inhibition of anti - HSP-65 binding to HSP-65 - coated plates was evident.	bind
35370	1	10103	6	11	NULL	NULL	NULL	CRP	GP		bind					E-LDL	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2348_s_143	10521363	A dose-dependent inhibition of CRP binding to E-LDL was observed, indicating that CRP interacted with its classical ligand 25 26  within the degraded LDL particles.	bind
35371	2	10103	6	11	NULL	NULL	NULL	CRP	GP		interacts with					classical ligand	Chemical				NULL	degraded LDL particle	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2348_s_143	10521363	A dose-dependent inhibition of CRP binding to E-LDL was observed, indicating that CRP interacted with its classical ligand 25 26  within the degraded LDL particles.	bind
43111	1	10103	7	11	NULL	NULL	NULL	CRP	GP		bind					E-LDL	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2348_s_143	10521363	A dose-dependent inhibition of CRP binding to E-LDL was observed, indicating that CRP interacted with its classical ligand 25 26  within the degraded LDL particles.	bind
43112	2	10103	7	11	NULL	NULL	NULL	CRP	GP		interacts with					classical ligand	Chemical				NULL	degraded LDL particles	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2348_s_143	10521363	A dose-dependent inhibition of CRP binding to E-LDL was observed, indicating that CRP interacted with its classical ligand 25 26  within the degraded LDL particles.	bind
35372	1	10104	6	11	NULL	NULL	NULL	sMT1	Chemical		bind					M4 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_63_1_26_s_170	12488533	A dose-dependent inhibition was also observed for the binding of sMT1 to the M4 receptor with an IC50 of 5.5 muM.	bind
43114	1	10104	7	11	NULL	NULL	NULL	sMT1	Chemical		bind					M4 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_63_1_26_s_170	12488533	A dose-dependent inhibition was also observed for the binding of sMT1 to the M4 receptor with an IC50 of 5.5 muM.	bind
35373	1	10105	6	11	NULL	NULL	NULL	ScKar2p	GP		bind					GST-63Jp	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6923_s_355	10958688	A dose-dependent stimulation of  ScKar2p binding to GST-63Jp was observed (Fig.  7), and a significant amount of  ScSls1p remained bound to the glutathione pellet.	bind
43115	1	10105	7	11	NULL	NULL	NULL	ScKar2p	GP		bind					GST-63Jp	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6923_s_355	10958688	A dose-dependent stimulation of  ScKar2p binding to GST-63Jp was observed (Fig.  7), and a significant amount of  ScSls1p remained bound to the glutathione pellet.	bind
35374	1	10106	6	11	NULL	NULL	NULL	NAP	GP		bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28531_s_101	15123709	A dot blot assay performed with spotted tubulin indicated NAP binding to tubulin ( Fig. 2 B).	bind
43117	1	10106	7	11	NULL	NULL	NULL	NAP	GP		bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28531_s_101	15123709	A dot blot assay performed with spotted tubulin indicated NAP binding to tubulin ( Fig. 2 B).	bind
35375	1	10107	6	11	NULL	NULL	NULL	fibronectin	GP		bind					chlamydial EB	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3935_s_40	12065538	A dot blot assay was used to test binding of fibronectin to chlamydial EB.	bind
43118	1	10107	7	11	NULL	NULL	NULL	fibronectin	GP		bind					chlamydial EB	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_7_3935_s_40	12065538	A dot blot assay was used to test binding of fibronectin to chlamydial EB.	bind
35376	1	10108	6	11	NULL	NULL	NULL	RhoG	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_nature_424_6947_461_s_41	12879077	A dot-blot assay using GTP-gammaS- or GDP-loaded purified GST RhoG as a probe showed that the GTP-bound form of RhoG  directly interacted with Elmo ( Fig. 1c).	bind
35377	2	10108	6	11	NULL	NULL	NULL	statement 1	GP		interacts with		directly			Elmo	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_424_6947_461_s_41	12879077	A dot-blot assay using GTP-gammaS- or GDP-loaded purified GST RhoG as a probe showed that the GTP-bound form of RhoG  directly interacted with Elmo ( Fig. 1c).	bind
43119	1	10108	7	11	NULL	NULL	NULL	RhoG	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_nature_424_6947_461_s_41	12879077	A dot-blot assay using GTP-gammaS- or GDP-loaded purified GST RhoG as a probe showed that the GTP-bound form of RhoG  directly interacted with Elmo ( Fig. 1c).	bind
43120	2	10108	7	11	NULL	NULL	NULL	statement 1	GP		interacts with		directly			Elmo	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_424_6947_461_s_41	12879077	A dot-blot assay using GTP-gammaS- or GDP-loaded purified GST RhoG as a probe showed that the GTP-bound form of RhoG  directly interacted with Elmo ( Fig. 1c).	bind
35378	1	10109	6	11	NULL	NULL	NULL	Cdk2	GP		bind		indirectly			p21	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_32_29282_s_139	15964852	A double deletion mutant lacking the CDK-binding site and cy1 (p21 deltacy1, CDK) could also bind Cdk2 NFG, indicating that indirect binding of Cdk2 to p21 does not absolutely require cy1.	bind
35379	2	10109	6	11	NULL	NULL	NULL	statement 1	Process		does not require					cy1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_32_29282_s_139	15964852	A double deletion mutant lacking the CDK-binding site and cy1 (p21 deltacy1, CDK) could also bind Cdk2 NFG, indicating that indirect binding of Cdk2 to p21 does not absolutely require cy1.	bind
35380	3	10109	6	11	NULL	NULL	NULL	p21 deltacy1, CDK	GP	double deletion mutant	lacks								\tCDK-binding site;;CDK		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_32_29282_s_139	15964852	A double deletion mutant lacking the CDK-binding site and cy1 (p21 deltacy1, CDK) could also bind Cdk2 NFG, indicating that indirect binding of Cdk2 to p21 does not absolutely require cy1.	bind
35381	4	10109	6	11	NULL	NULL	NULL	p21 deltacy1, CDK	GP	double deletion mutant	bind					Cdk2 NFG	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_32_29282_s_139	15964852	A double deletion mutant lacking the CDK-binding site and cy1 (p21 deltacy1, CDK) could also bind Cdk2 NFG, indicating that indirect binding of Cdk2 to p21 does not absolutely require cy1.	bind
57320	5	10109	6	11	NULL	NULL	NULL	statement 4	Process		indicates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_32_29282_s_139	15964852	A double deletion mutant lacking the CDK-binding site and cy1 (p21 deltacy1, CDK) could also bind Cdk2 NFG, indicating that indirect binding of Cdk2 to p21 does not absolutely require cy1.	bind
43121	1	10109	7	11	NULL	NULL	NULL	Cdk2	GP		bind		indirectly			p21	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_32_29282_s_139	15964852	A double deletion mutant lacking the CDK-binding site and cy1 (p21 deltacy1, CDK) could also bind Cdk2 NFG, indicating that indirect binding of Cdk2 to p21 does not absolutely require cy1.	bind
43122	2	10109	7	11	NULL	NULL	NULL	statement 1	Process		does not require					cy1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_32_29282_s_139	15964852	A double deletion mutant lacking the CDK-binding site and cy1 (p21 deltacy1, CDK) could also bind Cdk2 NFG, indicating that indirect binding of Cdk2 to p21 does not absolutely require cy1.	bind
43123	3	10109	7	11	NULL	NULL	NULL	p21 deltacy1, CDK	GP	double deletion mutant	lacks								CDK-binding site;;CDK		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_32_29282_s_139	15964852	A double deletion mutant lacking the CDK-binding site and cy1 (p21 deltacy1, CDK) could also bind Cdk2 NFG, indicating that indirect binding of Cdk2 to p21 does not absolutely require cy1.	bind
43125	4	10109	7	11	NULL	NULL	NULL	p21 deltacy1, CDK	GP	double deletion mutant	bind					Cdk2 NFG	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_32_29282_s_139	15964852	A double deletion mutant lacking the CDK-binding site and cy1 (p21 deltacy1, CDK) could also bind Cdk2 NFG, indicating that indirect binding of Cdk2 to p21 does not absolutely require cy1.	bind
57321	5	10109	7	11	NULL	NULL	NULL	statement 4	Process		indicates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_32_29282_s_139	15964852	A double deletion mutant lacking the CDK-binding site and cy1 (p21 deltacy1, CDK) could also bind Cdk2 NFG, indicating that indirect binding of Cdk2 to p21 does not absolutely require cy1.	bind
35633	1	10110	6	11	NULL	NULL	NULL	Id3/1	GP		is replaced by			aspartic acid		Id1	GP		tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19785_s_190	9242638	A double mutant (Fig.  6,  line 11), created by altering the aspartic acid and histidine residues of Id3/1 to the complementary tyrosine and glycine residues of Id1, resulted in almost full binding to MyoD, increased binding to Myf-5, and weak binding to MRF4/Myf-6.	bind
35634	2	10110	6	11	NULL	NULL	NULL	Id3/1	GP		is replaced by			histidine		Id1	GP		glycine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19785_s_190	9242638	A double mutant (Fig.  6,  line 11), created by altering the aspartic acid and histidine residues of Id3/1 to the complementary tyrosine and glycine residues of Id1, resulted in almost full binding to MyoD, increased binding to Myf-5, and weak binding to MRF4/Myf-6.	bind
35635	3	10110	6	11	NULL	NULL	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19785_s_190	9242638	A double mutant (Fig.  6,  line 11), created by altering the aspartic acid and histidine residues of Id3/1 to the complementary tyrosine and glycine residues of Id1, resulted in almost full binding to MyoD, increased binding to Myf-5, and weak binding to MRF4/Myf-6.	bind
35636	4	10110	6	11	NULL	NULL	NULL	Id3/1	GP	double mutant	is created by					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19785_s_190	9242638	A double mutant (Fig.  6,  line 11), created by altering the aspartic acid and histidine residues of Id3/1 to the complementary tyrosine and glycine residues of Id1, resulted in almost full binding to MyoD, increased binding to Myf-5, and weak binding to MRF4/Myf-6.	bind
35637	5	10110	6	11	NULL	NULL	NULL	Id3/1	GP	double mutant	bind					MyoD	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19785_s_190	9242638	A double mutant (Fig.  6,  line 11), created by altering the aspartic acid and histidine residues of Id3/1 to the complementary tyrosine and glycine residues of Id1, resulted in almost full binding to MyoD, increased binding to Myf-5, and weak binding to MRF4/Myf-6.	bind
35638	6	10110	6	11	NULL	NULL	NULL	Id3/1	GP	double mutant	bind		increased			Myf5	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19785_s_190	9242638	A double mutant (Fig.  6,  line 11), created by altering the aspartic acid and histidine residues of Id3/1 to the complementary tyrosine and glycine residues of Id1, resulted in almost full binding to MyoD, increased binding to Myf-5, and weak binding to MRF4/Myf-6.	bind
35639	7	10110	6	11	NULL	NULL	NULL	Id3/1	GP	double mutant	bind		weak			MRF4/Myf-6	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19785_s_190	9242638	A double mutant (Fig.  6,  line 11), created by altering the aspartic acid and histidine residues of Id3/1 to the complementary tyrosine and glycine residues of Id1, resulted in almost full binding to MyoD, increased binding to Myf-5, and weak binding to MRF4/Myf-6.	bind
43126	1	10110	7	11	NULL	NULL	NULL	 Id3/1 	GP		is replaced by			aspartic acid residue		Id1	GP		tyrosine  residue		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19785_s_190	9242638	A double mutant (Fig.  6,  line 11), created by altering the aspartic acid and histidine residues of Id3/1 to the complementary tyrosine and glycine residues of Id1, resulted in almost full binding to MyoD, increased binding to Myf-5, and weak binding to MRF4/Myf-6.	bind
43127	4	10110	7	11	NULL	NULL	NULL	statement 3	Process		creates					Id3/1	GP	double mutant			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19785_s_190	9242638	A double mutant (Fig.  6,  line 11), created by altering the aspartic acid and histidine residues of Id3/1 to the complementary tyrosine and glycine residues of Id1, resulted in almost full binding to MyoD, increased binding to Myf-5, and weak binding to MRF4/Myf-6.	bind
43129	5	10110	7	11	NULL	NULL	NULL	Id3/1	GP	double mutant	bind					 MyoD	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19785_s_190	9242638	A double mutant (Fig.  6,  line 11), created by altering the aspartic acid and histidine residues of Id3/1 to the complementary tyrosine and glycine residues of Id1, resulted in almost full binding to MyoD, increased binding to Myf-5, and weak binding to MRF4/Myf-6.	bind
50213	2	10110	7	11	NULL	NULL	NULL	Id3/1	GP		is replaced by			histidine residue		Id1	GP		glycine residue		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19785_s_190	9242638	A double mutant (Fig.  6,  line 11), created by altering the aspartic acid and histidine residues of Id3/1 to the complementary tyrosine and glycine residues of Id1, resulted in almost full binding to MyoD, increased binding to Myf-5, and weak binding to MRF4/Myf-6.	bind
50214	3	10110	7	11	NULL	NULL	NULL	statement 1	Process		occur simultaneously with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19785_s_190	9242638	A double mutant (Fig.  6,  line 11), created by altering the aspartic acid and histidine residues of Id3/1 to the complementary tyrosine and glycine residues of Id1, resulted in almost full binding to MyoD, increased binding to Myf-5, and weak binding to MRF4/Myf-6.	bind
50215	6	10110	7	11	NULL	NULL	NULL	Id3/1	GP	double mutant	bind		increased			Myf-5	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19785_s_190	9242638	A double mutant (Fig.  6,  line 11), created by altering the aspartic acid and histidine residues of Id3/1 to the complementary tyrosine and glycine residues of Id1, resulted in almost full binding to MyoD, increased binding to Myf-5, and weak binding to MRF4/Myf-6.	bind
50216	7	10110	7	11	NULL	NULL	NULL	Id3/1	GP	double mutant	bind		weakly			MRF4/Myf-6	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19785_s_190	9242638	A double mutant (Fig.  6,  line 11), created by altering the aspartic acid and histidine residues of Id3/1 to the complementary tyrosine and glycine residues of Id1, resulted in almost full binding to MyoD, increased binding to Myf-5, and weak binding to MRF4/Myf-6.	bind
35382	1	10111	6	11	NULL	NULL	NULL			double mutant	bind			D150K;; D182K		Cu(I)	Chemical	wild type			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_40_34113_s_214	16091356	A double mutant containing D150K and D182K substitutions was purified and found to exhibit wild type Cu(I) and Cu(II) binding and was not further pursued (data not shown).	bind
35383	2	10111	6	11	NULL	NULL	NULL			double mutant	bind			D150K;; D182K		Cu(II)	Chemical	wild type			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_40_34113_s_214	16091356	A double mutant containing D150K and D182K substitutions was purified and found to exhibit wild type Cu(I) and Cu(II) binding and was not further pursued (data not shown).	bind
43130	1	10111	7	11	NULL	NULL	NULL			double mutant	bind			D150K;;D182K		 Cu(I)	Chemical	wild type			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_40_34113_s_214	16091356	A double mutant containing D150K and D182K substitutions was purified and found to exhibit wild type Cu(I) and Cu(II) binding and was not further pursued (data not shown).	bind
43131	2	10111	7	11	NULL	NULL	NULL			double mutant	bind			D150K;; D182K		Cu(II)	Chemical	wild type			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_40_34113_s_214	16091356	A double mutant containing D150K and D182K substitutions was purified and found to exhibit wild type Cu(I) and Cu(II) binding and was not further pursued (data not shown).	bind
43135	1	10112	7	10	NULL	0	NULL	fnbA genes	NULL	S. aureus	is required for	NULL				fibronectin 	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_13_3999_s_200	11395464	A double mutant of  S. aureus lacking both genes for fibronectin binding ( fnbA and  fnbB) was constructed ( 5).	bind
43136	2	10112	7	10	NULL	0	NULL	fnbB genes	NULL	S. aureus	is required for	NULL				fibronectin	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_13_3999_s_200	11395464	A double mutant of  S. aureus lacking both genes for fibronectin binding ( fnbA and  fnbB) was constructed ( 5).	bind
35384	1	10113	6	11	NULL	NULL	NULL	E6	GP		bind					BRCA1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_39_33165_s_187	15983032	A double point mutation that disrupts both zinc finger domains of E6-(C66,136G) abrogated the binding of E6 to BRCA1.	bind
35385	3	10113	6	11	NULL	NULL	NULL	statement 2	Process		abrogates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_39_33165_s_187	15983032	A double point mutation that disrupts both zinc finger domains of E6-(C66,136G) abrogated the binding of E6 to BRCA1.	bind
49557	2	10113	6	11	NULL	NULL	NULL			double point mutation	disrupts					E6	GP		\tzinc finger domains C66,136G		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_39_33165_s_187	15983032	A double point mutation that disrupts both zinc finger domains of E6-(C66,136G) abrogated the binding of E6 to BRCA1.	bind
43137	1	10113	7	11	NULL	NULL	NULL	E6 	GP		bind					BRCA1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_39_33165_s_187	15983032	A double point mutation that disrupts both zinc finger domains of E6-(C66,136G) abrogated the binding of E6 to BRCA1.	bind
43138	2	10113	7	11	NULL	NULL	NULL			double point mutation	disrupts					E6	GP		zinc finger domains C66,136G		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_39_33165_s_187	15983032	A double point mutation that disrupts both zinc finger domains of E6-(C66,136G) abrogated the binding of E6 to BRCA1.	bind
43139	3	10113	7	11	NULL	NULL	NULL	statement 2	Process		abrogates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_39_33165_s_187	15983032	A double point mutation that disrupts both zinc finger domains of E6-(C66,136G) abrogated the binding of E6 to BRCA1.	bind
35387	1	10114	6	11	NULL	NULL	NULL	IF2	GP		bind					fAA-tRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_3_1891_s_117	8999877	A double reciprocal plot of 1/ r, where  r is the fraction of IF2 bound with fAA-tRNA against [1/fAA-tRNA free is shown on Fig.  5.	bind
43140	1	10114	7	11	NULL	NULL	NULL	IF2	GP		bind					 fAA-tRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_3_1891_s_117	8999877	A double reciprocal plot of 1/ r, where  r is the fraction of IF2 bound with fAA-tRNA against [1/fAA-tRNA free is shown on Fig.  5.	bind
35388	1	10115	6	11	NULL	NULL	NULL	fibrinogen	GP		bind								G708N		NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_53	12730600	A double reciprocal plot of fibrinogen binding to G708N revealed a dissociation constant ( Kd) of 180 nM, similar to the  Kd's of 81 nM and 178 nM for fibrinogen binding to ADP-stimulated and epinephrine-stimulated platelets, respectively (  20).	bind
35389	4	10115	6	11	NULL	NULL	NULL	fibrinogen	GP		bind					statement 2	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_53	12730600	A double reciprocal plot of fibrinogen binding to G708N revealed a dissociation constant ( Kd) of 180 nM, similar to the  Kd's of 81 nM and 178 nM for fibrinogen binding to ADP-stimulated and epinephrine-stimulated platelets, respectively (  20).	bind
35390	5	10115	6	11	NULL	NULL	NULL	fibrinogen	GP		bind					statement 3	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_53	12730600	A double reciprocal plot of fibrinogen binding to G708N revealed a dissociation constant ( Kd) of 180 nM, similar to the  Kd's of 81 nM and 178 nM for fibrinogen binding to ADP-stimulated and epinephrine-stimulated platelets, respectively (  20).	bind
49583	2	10115	6	11	NULL	NULL	NULL	platelets	OrganismPart		is stimulated by					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_53	12730600	A double reciprocal plot of fibrinogen binding to G708N revealed a dissociation constant ( Kd) of 180 nM, similar to the  Kd's of 81 nM and 178 nM for fibrinogen binding to ADP-stimulated and epinephrine-stimulated platelets, respectively (  20).	bind
49584	3	10115	6	11	NULL	NULL	NULL	platelets	OrganismPart		is stimulated by					epinephrine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_53	12730600	A double reciprocal plot of fibrinogen binding to G708N revealed a dissociation constant ( Kd) of 180 nM, similar to the  Kd's of 81 nM and 178 nM for fibrinogen binding to ADP-stimulated and epinephrine-stimulated platelets, respectively (  20).	bind
43141	1	10115	7	11	NULL	NULL	NULL	fibrinogen	GP		bind								G708N		NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_53	12730600	A double reciprocal plot of fibrinogen binding to G708N revealed a dissociation constant ( Kd) of 180 nM, similar to the  Kd's of 81 nM and 178 nM for fibrinogen binding to ADP-stimulated and epinephrine-stimulated platelets, respectively (  20).	bind
43142	2	10115	7	11	NULL	NULL	NULL	platelets	OrganismPart		is stimulated by					ADP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_53	12730600	A double reciprocal plot of fibrinogen binding to G708N revealed a dissociation constant ( Kd) of 180 nM, similar to the  Kd's of 81 nM and 178 nM for fibrinogen binding to ADP-stimulated and epinephrine-stimulated platelets, respectively (  20).	bind
43143	3	10115	7	11	NULL	NULL	NULL	platelets	OrganismPart		is stimulated by					epinephrine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_53	12730600	A double reciprocal plot of fibrinogen binding to G708N revealed a dissociation constant ( Kd) of 180 nM, similar to the  Kd's of 81 nM and 178 nM for fibrinogen binding to ADP-stimulated and epinephrine-stimulated platelets, respectively (  20).	bind
43144	4	10115	7	11	NULL	NULL	NULL	statement 2	OrganismPart		binds					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_53	12730600	A double reciprocal plot of fibrinogen binding to G708N revealed a dissociation constant ( Kd) of 180 nM, similar to the  Kd's of 81 nM and 178 nM for fibrinogen binding to ADP-stimulated and epinephrine-stimulated platelets, respectively (  20).	bind
43145	5	10115	7	11	NULL	NULL	NULL	statement 3	OrganismPart		binds					fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_300_5620_795_s_53	12730600	A double reciprocal plot of fibrinogen binding to G708N revealed a dissociation constant ( Kd) of 180 nM, similar to the  Kd's of 81 nM and 178 nM for fibrinogen binding to ADP-stimulated and epinephrine-stimulated platelets, respectively (  20).	bind
35391	1	10116	6	11	NULL	NULL	NULL	K88ab adhesin	GP		bind					pSTf	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2336_s_110	11953368	A double-reciprocal plot of this binding data was used to determine that the dissociation constant for the binding of K88ab adhesin to pSTf is 75 muM.	bind
43146	1	10116	7	11	NULL	NULL	NULL	K88ab adhesin	GP		bind					pSTf	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2336_s_110	11953368	A double-reciprocal plot of this binding data was used to determine that the dissociation constant for the binding of K88ab adhesin to pSTf is 75 muM.	bind
35392	1	10118	6	11	NULL	NULL	NULL	HOXC11	GP		bind					CE-LPH1-24 probe	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13297_s_150	9582375	A double-stranded oligonucleotide covering this vector sequence, referred to as BSK-17 in Fig.  1, was able to compete for HOXC11 binding to the CE-LPH1-24 probe in EMSA analysis (Fig.  5,  lane 9).	bind
49588	2	10118	6	11	NULL	NULL	NULL	BSK-17	GP		bind					HOXC11	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13297_s_150	9582375	A double-stranded oligonucleotide covering this vector sequence, referred to as BSK-17 in Fig.  1, was able to compete for HOXC11 binding to the CE-LPH1-24 probe in EMSA analysis (Fig.  5,  lane 9).	bind
49589	3	10118	6	11	NULL	NULL	NULL	statement 2	Process		competes with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13297_s_150	9582375	A double-stranded oligonucleotide covering this vector sequence, referred to as BSK-17 in Fig.  1, was able to compete for HOXC11 binding to the CE-LPH1-24 probe in EMSA analysis (Fig.  5,  lane 9).	bind
43147	1	10118	7	11	NULL	NULL	NULL	 HOXC11	GP		bind					CE-LPH1-24 probe	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13297_s_150	9582375	A double-stranded oligonucleotide covering this vector sequence, referred to as BSK-17 in Fig.  1, was able to compete for HOXC11 binding to the CE-LPH1-24 probe in EMSA analysis (Fig.  5,  lane 9).	bind
43148	2	10118	7	11	NULL	NULL	NULL	BSK-17	GP		bind					HOXC11	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13297_s_150	9582375	A double-stranded oligonucleotide covering this vector sequence, referred to as BSK-17 in Fig.  1, was able to compete for HOXC11 binding to the CE-LPH1-24 probe in EMSA analysis (Fig.  5,  lane 9).	bind
49587	3	10118	7	11	NULL	NULL	NULL	statement 2	Process		competes with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13297_s_150	9582375	A double-stranded oligonucleotide covering this vector sequence, referred to as BSK-17 in Fig.  1, was able to compete for HOXC11 binding to the CE-LPH1-24 probe in EMSA analysis (Fig.  5,  lane 9).	bind
35393	1	10120	6	11	NULL	NULL	NULL	U11	GP		bind		efficiently			NRS	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_37_38201_s_154	15252020	A downstream G-rich region is required for efficient U11 binding to the NRS.	bind
35394	2	10120	6	11	NULL	NULL	NULL				is required for				G-rich region	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_37_38201_s_154	15252020	A downstream G-rich region is required for efficient U11 binding to the NRS.	bind
43149	1	10120	7	11	NULL	NULL	NULL	U11	GP		bind					NRS	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_37_38201_s_154	15252020	A downstream G-rich region is required for efficient U11 binding to the NRS.	bind
43150	2	10120	7	11	NULL	NULL	NULL				is required for				G-rich region	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_37_38201_s_154	15252020	A downstream G-rich region is required for efficient U11 binding to the NRS.	bind
35395	1	10121	6	11	NULL	NULL	NULL	atf1/gad7 genes	GP		encodes for					heterodimeric bZIP transcriptional activator	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6426_s_28	10938120	A downstream target of the MAPK, a heterodimeric bZIP transcriptional activator encoded by the  atf1/gad7 and the  pcr1 genes, is required to derepress  fbp1 transcription ( 22,  50,  55,  63).	bind
35396	2	10121	6	11	NULL	NULL	NULL	pcr1 gene	GP		encodes for					heterodimeric bZIP transcriptional activator	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6426_s_28	10938120	A downstream target of the MAPK, a heterodimeric bZIP transcriptional activator encoded by the  atf1/gad7 and the  pcr1 genes, is required to derepress  fbp1 transcription ( 22,  50,  55,  63).	bind
35397	3	10121	6	11	NULL	NULL	NULL	downstream target of the MAPK	GP		is a type of					heterodimeric bZIP transcriptional activator	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6426_s_28	10938120	A downstream target of the MAPK, a heterodimeric bZIP transcriptional activator encoded by the  atf1/gad7 and the  pcr1 genes, is required to derepress  fbp1 transcription ( 22,  50,  55,  63).	bind
35398	4	10121	6	11	NULL	NULL	NULL	downstream target of the MAPK	GP		derepress					fbp1	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6426_s_28	10938120	A downstream target of the MAPK, a heterodimeric bZIP transcriptional activator encoded by the  atf1/gad7 and the  pcr1 genes, is required to derepress  fbp1 transcription ( 22,  50,  55,  63).	bind
43151	1	10121	7	11	NULL	NULL	NULL	atf1/gad7 genes	GP		encodes					MAPK	GP	downstream target of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6426_s_28	10938120	A downstream target of the MAPK, a heterodimeric bZIP transcriptional activator encoded by the  atf1/gad7 and the  pcr1 genes, is required to derepress  fbp1 transcription ( 22,  50,  55,  63).	bind
43152	2	10121	7	11	NULL	NULL	NULL	pcr1 genes	GP		encodes					MAPK	GP	downstream target of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6426_s_28	10938120	A downstream target of the MAPK, a heterodimeric bZIP transcriptional activator encoded by the  atf1/gad7 and the  pcr1 genes, is required to derepress  fbp1 transcription ( 22,  50,  55,  63).	bind
43153	3	10121	7	11	NULL	NULL	NULL	downstream target of MAPK	GP		is a type of					heterodimeric bZIP transcriptional activator	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6426_s_28	10938120	A downstream target of the MAPK, a heterodimeric bZIP transcriptional activator encoded by the  atf1/gad7 and the  pcr1 genes, is required to derepress  fbp1 transcription ( 22,  50,  55,  63).	bind
43154	4	10121	7	11	NULL	NULL	NULL	downstream target of MAPK	GP		derepress					fbp1	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6426_s_28	10938120	A downstream target of the MAPK, a heterodimeric bZIP transcriptional activator encoded by the  atf1/gad7 and the  pcr1 genes, is required to derepress  fbp1 transcription ( 22,  50,  55,  63).	bind
35399	1	10122	6	11	NULL	NULL	NULL	DR-1	GP		bind					HNF-4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_44_4_686_s_187	12562861	A DR-1 also binds HNF-4 ( ).	bind
43155	1	10122	7	11	NULL	NULL	NULL	 DR-1	GP		binds					HNF-4 	GP				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_44_4_686_s_187	12562861	A DR-1 also binds HNF-4 ( ).	bind
35400	1	10124	6	11	NULL	NULL	NULL	ezrin	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_867_s_328	11238445	A dramatic increase in ezrin binding to actin suggests that ezrin is likely to be the PIP2 regulator of membrane - cytoskeletal linkage.	bind
35401	2	10124	6	11	NULL	NULL	NULL	ezrin	GP		is 					membrane - cytoskeletal linkage	CellComponent	PIP2 regulator of 			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_867_s_328	11238445	A dramatic increase in ezrin binding to actin suggests that ezrin is likely to be the PIP2 regulator of membrane - cytoskeletal linkage.	bind
35402	3	10124	6	11	NULL	NULL	NULL	statement 1	Process	increase in	suggests					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_867_s_328	11238445	A dramatic increase in ezrin binding to actin suggests that ezrin is likely to be the PIP2 regulator of membrane - cytoskeletal linkage.	bind
43156	1	10124	7	11	NULL	NULL	NULL	ezrin	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_867_s_328	11238445	A dramatic increase in ezrin binding to actin suggests that ezrin is likely to be the PIP2 regulator of membrane - cytoskeletal linkage.	bind
43157	2	10124	7	11	NULL	NULL	NULL	ezrin	GP		likey to be the					membrane - cytoskeletal linkage	CellComponent	PIP2 regulator of 			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_5_867_s_328	11238445	A dramatic increase in ezrin binding to actin suggests that ezrin is likely to be the PIP2 regulator of membrane - cytoskeletal linkage.	bind
35640	1	10126	6	11	NULL	NULL	NULL	BUDeR	Chemical		inhibits					AP1-like	GP				NULL	HEK cell line	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_13_8630_s_187	10085100	A dramatic inhibition of  cis-acting transcription factor AP1-like-, gamma-interferon activation sequence-, and especially NF-kappaB-DNA binding by the GCs DEX and BUDeR, temporally correlating to a reduction in cyclooxygenase-2 message synthesis, has recently been demonstrated in HEK cell lines ( 14).	bind
35641	2	10126	6	11	NULL	NULL	NULL	BUDeR	Chemical		inhibits					gamma-interferon activation sequence-	NucleicAcid				NULL	HEK cell line	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_13_8630_s_187	10085100	A dramatic inhibition of  cis-acting transcription factor AP1-like-, gamma-interferon activation sequence-, and especially NF-kappaB-DNA binding by the GCs DEX and BUDeR, temporally correlating to a reduction in cyclooxygenase-2 message synthesis, has recently been demonstrated in HEK cell lines ( 14).	bind
35642	3	10126	6	11	NULL	NULL	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL	HEK cell line	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_13_8630_s_187	10085100	A dramatic inhibition of  cis-acting transcription factor AP1-like-, gamma-interferon activation sequence-, and especially NF-kappaB-DNA binding by the GCs DEX and BUDeR, temporally correlating to a reduction in cyclooxygenase-2 message synthesis, has recently been demonstrated in HEK cell lines ( 14).	bind
35643	4	10126	6	11	NULL	NULL	NULL	BUDeR	Chemical		inhibits					statement 3	Process				NULL	HEK cell line	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_13_8630_s_187	10085100	A dramatic inhibition of  cis-acting transcription factor AP1-like-, gamma-interferon activation sequence-, and especially NF-kappaB-DNA binding by the GCs DEX and BUDeR, temporally correlating to a reduction in cyclooxygenase-2 message synthesis, has recently been demonstrated in HEK cell lines ( 14).	bind
35644	5	10126	6	11	NULL	NULL	NULL	GCs DEX	Chemical		inhibits					AP1-like	GP				NULL	HEK cell line	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_13_8630_s_187	10085100	A dramatic inhibition of  cis-acting transcription factor AP1-like-, gamma-interferon activation sequence-, and especially NF-kappaB-DNA binding by the GCs DEX and BUDeR, temporally correlating to a reduction in cyclooxygenase-2 message synthesis, has recently been demonstrated in HEK cell lines ( 14).	bind
35645	6	10126	6	11	NULL	NULL	NULL	GCs DEX	Chemical		inhibits					gamma-interferon activation sequence	NucleicAcid				NULL	HEK cell line	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_13_8630_s_187	10085100	A dramatic inhibition of  cis-acting transcription factor AP1-like-, gamma-interferon activation sequence-, and especially NF-kappaB-DNA binding by the GCs DEX and BUDeR, temporally correlating to a reduction in cyclooxygenase-2 message synthesis, has recently been demonstrated in HEK cell lines ( 14).	bind
35646	7	10126	6	11	NULL	NULL	NULL	GCs DEX	Chemical		inhibits					statement 3	Process				NULL	HEK cell line	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_13_8630_s_187	10085100	A dramatic inhibition of  cis-acting transcription factor AP1-like-, gamma-interferon activation sequence-, and especially NF-kappaB-DNA binding by the GCs DEX and BUDeR, temporally correlating to a reduction in cyclooxygenase-2 message synthesis, has recently been demonstrated in HEK cell lines ( 14).	bind
35647	8	10126	6	11	NULL	NULL	NULL	AP1	GP		is a type of					cis-acting transcription factor	GP				NULL	HEK cell line	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_13_8630_s_187	10085100	A dramatic inhibition of  cis-acting transcription factor AP1-like-, gamma-interferon activation sequence-, and especially NF-kappaB-DNA binding by the GCs DEX and BUDeR, temporally correlating to a reduction in cyclooxygenase-2 message synthesis, has recently been demonstrated in HEK cell lines ( 14).	bind
43268	1	10126	7	11	NULL	NULL	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL	HEK cell lines	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_13_8630_s_187	10085100	A dramatic inhibition of  cis-acting transcription factor AP1-like-, gamma-interferon activation sequence-, and especially NF-kappaB-DNA binding by the GCs DEX and BUDeR, temporally correlating to a reduction in cyclooxygenase-2 message synthesis, has recently been demonstrated in HEK cell lines ( 14).	bind
43286	2	10126	7	11	NULL	NULL	NULL	GCs DEX	Chemical		inhibit					statement 1	Process				NULL	HEK cell lines	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_13_8630_s_187	10085100	A dramatic inhibition of  cis-acting transcription factor AP1-like-, gamma-interferon activation sequence-, and especially NF-kappaB-DNA binding by the GCs DEX and BUDeR, temporally correlating to a reduction in cyclooxygenase-2 message synthesis, has recently been demonstrated in HEK cell lines ( 14).	bind
43287	3	10126	7	11	NULL	NULL	NULL	BUDeR	Chemical		inhibit					statement 1	Process				NULL	HEK cell lines	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_13_8630_s_187	10085100	A dramatic inhibition of  cis-acting transcription factor AP1-like-, gamma-interferon activation sequence-, and especially NF-kappaB-DNA binding by the GCs DEX and BUDeR, temporally correlating to a reduction in cyclooxygenase-2 message synthesis, has recently been demonstrated in HEK cell lines ( 14).	bind
43288	4	10126	7	11	NULL	NULL	NULL	statement 2	Process		correlates to		temporally			cyclooxygenase-2 message 	GP	reduction of;;synthesis of			NULL	HEK cell lines	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_13_8630_s_187	10085100	A dramatic inhibition of  cis-acting transcription factor AP1-like-, gamma-interferon activation sequence-, and especially NF-kappaB-DNA binding by the GCs DEX and BUDeR, temporally correlating to a reduction in cyclooxygenase-2 message synthesis, has recently been demonstrated in HEK cell lines ( 14).	bind
43289	5	10126	7	11	NULL	NULL	NULL	statement 3	Process		correlates to		temporally			cyclooxygenase-2 message 	GP	reduction of;;synthesis of			NULL	HEK cell lines	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_13_8630_s_187	10085100	A dramatic inhibition of  cis-acting transcription factor AP1-like-, gamma-interferon activation sequence-, and especially NF-kappaB-DNA binding by the GCs DEX and BUDeR, temporally correlating to a reduction in cyclooxygenase-2 message synthesis, has recently been demonstrated in HEK cell lines ( 14).	bind
35648	1	10127	6	11	NULL	NULL	NULL	fusion protein	GP		contains					hCLCA2	GP		beta4-binding motif		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49406_s_45	14512419	A dramatic inhibition of metastasis of MDA-MB-231 breast cancer cells by a fusion protein containing the beta4-binding motif of hCLCA2 further advances the role of the beta4/CLCA adhesion in pulmonary metastasis.	bind
35649	2	10127	6	11	NULL	NULL	NULL	statement 1	Process		inhibits					MDA-MB-231	Cell	metastasis of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49406_s_45	14512419	A dramatic inhibition of metastasis of MDA-MB-231 breast cancer cells by a fusion protein containing the beta4-binding motif of hCLCA2 further advances the role of the beta4/CLCA adhesion in pulmonary metastasis.	bind
35650	3	10127	6	11	NULL	NULL	NULL	MDA-MB-231	Cell		is a type of					breast cancer cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49406_s_45	14512419	A dramatic inhibition of metastasis of MDA-MB-231 breast cancer cells by a fusion protein containing the beta4-binding motif of hCLCA2 further advances the role of the beta4/CLCA adhesion in pulmonary metastasis.	bind
35651	4	10127	6	11	NULL	NULL	NULL	beta4/CLCA	GP	adhesion of	plays a role in					pulmonary metastasis	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49406_s_45	14512419	A dramatic inhibition of metastasis of MDA-MB-231 breast cancer cells by a fusion protein containing the beta4-binding motif of hCLCA2 further advances the role of the beta4/CLCA adhesion in pulmonary metastasis.	bind
43269	1	10127	7	11	NULL	NULL	NULL	fusion protein 	GP		contains					hCLCA2	GP		beta4-binding motif		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49406_s_45	14512419	A dramatic inhibition of metastasis of MDA-MB-231 breast cancer cells by a fusion protein containing the beta4-binding motif of hCLCA2 further advances the role of the beta4/CLCA adhesion in pulmonary metastasis.	bind
43270	2	10127	7	11	NULL	NULL	NULL	statement 1	Process		inhibits					MDA-MB-231	Cell	 metastasis of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49406_s_45	14512419	A dramatic inhibition of metastasis of MDA-MB-231 breast cancer cells by a fusion protein containing the beta4-binding motif of hCLCA2 further advances the role of the beta4/CLCA adhesion in pulmonary metastasis.	bind
43273	3	10127	7	11	NULL	NULL	NULL	beta4/CLCA 	GP	adhesion of	plays a role in					pulmonary metastasis	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49406_s_45	14512419	A dramatic inhibition of metastasis of MDA-MB-231 breast cancer cells by a fusion protein containing the beta4-binding motif of hCLCA2 further advances the role of the beta4/CLCA adhesion in pulmonary metastasis.	bind
49592	4	10127	7	11	NULL	NULL	NULL	MDA-MB-231	Cell		is a type of					breast cancer cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49406_s_45	14512419	A dramatic inhibition of metastasis of MDA-MB-231 breast cancer cells by a fusion protein containing the beta4-binding motif of hCLCA2 further advances the role of the beta4/CLCA adhesion in pulmonary metastasis.	bind
35403	1	10128	6	11	NULL	NULL	NULL	MLCK-FIP	GP		bind					calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_156_3_543_s_91	11815633	A dramatic loss of FRET was seen immediately after ionomycin treatment ( Fig. 2 B), indicated by a shift from red to green or blue, showing that MLCK-FIP bound calmodulin and was therefore activated.	bind
49595	2	10128	6	11	NULL	NULL	NULL	statement 1	Process		activates					MLCK-FIP	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_156_3_543_s_91	11815633	A dramatic loss of FRET was seen immediately after ionomycin treatment ( Fig. 2 B), indicated by a shift from red to green or blue, showing that MLCK-FIP bound calmodulin and was therefore activated.	bind
43293	1	10128	7	11	NULL	NULL	NULL	MLCK-FIP	GP		bind					calmodulin 	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_156_3_543_s_91	11815633	A dramatic loss of FRET was seen immediately after ionomycin treatment ( Fig. 2 B), indicated by a shift from red to green or blue, showing that MLCK-FIP bound calmodulin and was therefore activated.	bind
43294	2	10128	7	11	NULL	NULL	NULL	statement 1	GP		activates					MLCK-FIP 	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_156_3_543_s_91	11815633	A dramatic loss of FRET was seen immediately after ionomycin treatment ( Fig. 2 B), indicated by a shift from red to green or blue, showing that MLCK-FIP bound calmodulin and was therefore activated.	bind
35775	1	10130	6	11	NULL	NULL	NULL	GATA factor family member	GP	Drosophila	bind					Adh	GP			regulatory sequences	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_5_2901_s_369	9566909	A Drosophila GATA factor family member that binds to Adh regulatory sequences is expressed in the developing fat body.	bind
35776	2	10130	6	11	NULL	NULL	NULL	GATA family member	GP	Drosophila	is expressed in					developing fat body	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_5_2901_s_369	9566909	A Drosophila GATA factor family member that binds to Adh regulatory sequences is expressed in the developing fat body.	bind
43295	1	10130	7	11	NULL	NULL	NULL	GATA factor family	GP	Drosophila	bind					Adh	GP			regulatory sequences	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_5_2901_s_369	9566909	A Drosophila GATA factor family member that binds to Adh regulatory sequences is expressed in the developing fat body.	bind
43296	2	10130	7	11	NULL	NULL	NULL	statement 1	GP		is expressed in					developing fat body	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_5_2901_s_369	9566909	A Drosophila GATA factor family member that binds to Adh regulatory sequences is expressed in the developing fat body.	bind
35777	1	10132	6	11	NULL	NULL	NULL	adenomatous polyposis coli	GP	Drosophila homolog	downregulates					beta-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_311_s_156	11057903	A Drosophila homolog of the tumor suppressor gene adenomatous polyposis coli down-regulates beta-catenin but its zygotic expression is not essential for the regulation of Armadillo.	bind
35778	2	10132	6	11	NULL	NULL	NULL	adenomatous polyposis coli	Organism		is a type of					tumor suppressor gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_311_s_156	11057903	A Drosophila homolog of the tumor suppressor gene adenomatous polyposis coli down-regulates beta-catenin but its zygotic expression is not essential for the regulation of Armadillo.	bind
35779	3	10132	6	11	NULL	NULL	NULL	adenomatous polyposis coli	GP	Drosophila homolog;;zygotic expression of	is not essential for					Armadillo	Organism	regulation of			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_311_s_156	11057903	A Drosophila homolog of the tumor suppressor gene adenomatous polyposis coli down-regulates beta-catenin but its zygotic expression is not essential for the regulation of Armadillo.	bind
43297	1	10132	7	11	NULL	NULL	NULL	adenomatous polyposis coli	GP	Drosophila homolog of	down-regulates					beta-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_311_s_156	11057903	A Drosophila homolog of the tumor suppressor gene adenomatous polyposis coli down-regulates beta-catenin but its zygotic expression is not essential for the regulation of Armadillo.	bind
43298	2	10132	7	11	NULL	NULL	NULL	adenomatous polyposis coli 	GP	zygotic expression of;;Drosophila homolog	is not essential for					Armadillo	Organism	 regulation of			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_311_s_156	11057903	A Drosophila homolog of the tumor suppressor gene adenomatous polyposis coli down-regulates beta-catenin but its zygotic expression is not essential for the regulation of Armadillo.	bind
43299	3	10132	7	11	NULL	NULL	NULL	adenomatous polyposis coli	GP		is a type of					 tumor suppressor gene 	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_311_s_156	11057903	A Drosophila homolog of the tumor suppressor gene adenomatous polyposis coli down-regulates beta-catenin but its zygotic expression is not essential for the regulation of Armadillo.	bind
35780	1	10133	6	11	NULL	NULL	NULL	TRAF	GP		is					TNF-receptor-associated factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_9_s_409	12110163	A Drosophila TNF-receptor-associated factor (TRAF) binds the ste20 kinase Misshapen and activates Jun kinase.	bind
35781	2	10133	6	11	NULL	NULL	NULL	TRAF	GP	Drosophila	bind					misshapen	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_9_s_409	12110163	A Drosophila TNF-receptor-associated factor (TRAF) binds the ste20 kinase Misshapen and activates Jun kinase.	bind
35782	3	10133	6	11	NULL	NULL	NULL	Misshapen	GP		is a type of					ste20 kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_9_s_409	12110163	A Drosophila TNF-receptor-associated factor (TRAF) binds the ste20 kinase Misshapen and activates Jun kinase.	bind
35783	4	10133	6	11	NULL	NULL	NULL	statement 2	GP		activates					Jun kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_9_s_409	12110163	A Drosophila TNF-receptor-associated factor (TRAF) binds the ste20 kinase Misshapen and activates Jun kinase.	bind
43300	1	10133	7	11	NULL	NULL	NULL	TRAF	GP	Drosophila	binds					Misshapen 	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_9_s_409	12110163	A Drosophila TNF-receptor-associated factor (TRAF) binds the ste20 kinase Misshapen and activates Jun kinase.	bind
43301	2	10133	7	11	NULL	NULL	NULL	statement 1	GP		activates					Jun kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_9_s_409	12110163	A Drosophila TNF-receptor-associated factor (TRAF) binds the ste20 kinase Misshapen and activates Jun kinase.	bind
43302	3	10133	7	11	NULL	NULL	NULL	TRAF	GP		is					TNF-receptor-associated factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_9_s_409	12110163	A Drosophila TNF-receptor-associated factor (TRAF) binds the ste20 kinase Misshapen and activates Jun kinase.	bind
49598	4	10133	7	11	NULL	NULL	NULL	Misshapen	GP		is a type of					ste20 kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_9_s_409	12110163	A Drosophila TNF-receptor-associated factor (TRAF) binds the ste20 kinase Misshapen and activates Jun kinase.	bind
35784	1	10134	6	11	NULL	NULL	NULL	DSB	NucleicAcid		occurs in					loop DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_18_4075_s_285	12235392	A DSB that occurs in loop DNA is first bound by Ku70/Ku86 that then recruits DNA-PKcs and possibly other proteins to the ends.	bind
35785	2	10134	6	11	NULL	NULL	NULL	DSB	NucleicAcid		bind					Ku70/Ku86	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_18_4075_s_285	12235392	A DSB that occurs in loop DNA is first bound by Ku70/Ku86 that then recruits DNA-PKcs and possibly other proteins to the ends.	bind
36100	3	10134	6	11	NULL	NULL	NULL	DNA-PKcs	NucleicAcid		are recruited to					DNA ends	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_18_4075_s_285	12235392	A DSB that occurs in loop DNA is first bound by Ku70/Ku86 that then recruits DNA-PKcs and possibly other proteins to the ends.	bind
36101	4	10134	6	11	NULL	NULL	NULL	DSB	NucleicAcid		recruits					DNA-PKcs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_18_4075_s_285	12235392	A DSB that occurs in loop DNA is first bound by Ku70/Ku86 that then recruits DNA-PKcs and possibly other proteins to the ends.	bind
36102	5	10134	6	11	NULL	NULL	NULL	statement 4	Process		occurs after					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_18_4075_s_285	12235392	A DSB that occurs in loop DNA is first bound by Ku70/Ku86 that then recruits DNA-PKcs and possibly other proteins to the ends.	bind
43303	1	10134	7	11	NULL	NULL	NULL	DSB	NucleicAcid		occurs in					loop DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_18_4075_s_285	12235392	A DSB that occurs in loop DNA is first bound by Ku70/Ku86 that then recruits DNA-PKcs and possibly other proteins to the ends.	bind
43304	2	10134	7	11	NULL	NULL	NULL	statement 1	NucleicAcid		bind					Ku70/Ku86	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_18_4075_s_285	12235392	A DSB that occurs in loop DNA is first bound by Ku70/Ku86 that then recruits DNA-PKcs and possibly other proteins to the ends.	bind
43305	3	10134	7	11	NULL	NULL	NULL	statement 2	NucleicAcid		recruits					DNA-PKcs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_18_4075_s_285	12235392	A DSB that occurs in loop DNA is first bound by Ku70/Ku86 that then recruits DNA-PKcs and possibly other proteins to the ends.	bind
43306	4	10134	7	11	NULL	NULL	NULL	DNA-PKcs \t	NucleicAcid		is recruited to					DNA ends	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_18_4075_s_285	12235392	A DSB that occurs in loop DNA is first bound by Ku70/Ku86 that then recruits DNA-PKcs and possibly other proteins to the ends.	bind
35786	1	10135	6	11	NULL	NULL	NULL	Dazl protein	GP		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2479_s_4	11410654	A dual approach was taken to understand the RNA-binding specificity of the Dazl protein: (i) traditional SELEX and (ii) a novel tri-hybrid screen.	bind
43307	1	10135	7	11	NULL	NULL	NULL	Dazl protein	GP		bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_12_2479_s_4	11410654	A dual approach was taken to understand the RNA-binding specificity of the Dazl protein: (i) traditional SELEX and (ii) a novel tri-hybrid screen.	bind
35787	1	10136	6	11	NULL	NULL	NULL	FHL2	GP		bind					alpha-integrin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_358	15117962	A dual binding of FHL2 and FHL3 to both alpha- and beta-integrin chains might provide a stronger connection of the receptor to the cell interior than only a single interaction.	bind
35788	2	10136	6	11	NULL	NULL	NULL	FHL3	GP		bind					alpha-integrin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_358	15117962	A dual binding of FHL2 and FHL3 to both alpha- and beta-integrin chains might provide a stronger connection of the receptor to the cell interior than only a single interaction.	bind
35789	3	10136	6	11	NULL	NULL	NULL	FHL2			bind					beta-integrin					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_358	15117962	A dual binding of FHL2 and FHL3 to both alpha- and beta-integrin chains might provide a stronger connection of the receptor to the cell interior than only a single interaction.	bind
35790	4	10136	6	11	NULL	NULL	NULL	FHL3	GP		bind					beta-integrin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_358	15117962	A dual binding of FHL2 and FHL3 to both alpha- and beta-integrin chains might provide a stronger connection of the receptor to the cell interior than only a single interaction.	bind
43308	1	10136	7	11	NULL	NULL	NULL	FHL2	GP		bind					alpha-integrin chain	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_358	15117962	A dual binding of FHL2 and FHL3 to both alpha- and beta-integrin chains might provide a stronger connection of the receptor to the cell interior than only a single interaction.	bind
43309	2	10136	7	11	NULL	NULL	NULL	FHL3	GP		bind					beta-integrin chain	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_358	15117962	A dual binding of FHL2 and FHL3 to both alpha- and beta-integrin chains might provide a stronger connection of the receptor to the cell interior than only a single interaction.	bind
50228	3	10136	7	11	NULL	NULL	NULL	FHL2	GP		bind					beta-integrin chain	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_358	15117962	A dual binding of FHL2 and FHL3 to both alpha- and beta-integrin chains might provide a stronger connection of the receptor to the cell interior than only a single interaction.	bind
50229	4	10136	7	11	NULL	NULL	NULL	FHL3	GP		bind					alpha-integrin chain	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28641_s_358	15117962	A dual binding of FHL2 and FHL3 to both alpha- and beta-integrin chains might provide a stronger connection of the receptor to the cell interior than only a single interaction.	bind
35791	1	10137	6	11	NULL	NULL	NULL	Id2	GP		is linked to					pRb	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_16_15836_s_20	15691830	A dual connection links Id2 and pRb: when overexpressed, Id2 overrides the tumor suppressor function of RB, allowing binding of E2F to its target genes, promoting entry into S phase and cell proliferation ( ).	bind
35792	2	10137	6	11	NULL	NULL	NULL	Id2	GP	overexpressed	overrides					RB	GP	\ttumor suppressor function of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_16_15836_s_20	15691830	A dual connection links Id2 and pRb: when overexpressed, Id2 overrides the tumor suppressor function of RB, allowing binding of E2F to its target genes, promoting entry into S phase and cell proliferation ( ).	bind
35793	3	10137	6	11	NULL	NULL	NULL	E2F	GP		bind					target genes	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_16_15836_s_20	15691830	A dual connection links Id2 and pRb: when overexpressed, Id2 overrides the tumor suppressor function of RB, allowing binding of E2F to its target genes, promoting entry into S phase and cell proliferation ( ).	bind
35794	4	10137	6	11	NULL	NULL	NULL	statement 2	Process		allows					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_16_15836_s_20	15691830	A dual connection links Id2 and pRb: when overexpressed, Id2 overrides the tumor suppressor function of RB, allowing binding of E2F to its target genes, promoting entry into S phase and cell proliferation ( ).	bind
35795	5	10137	6	11	NULL	NULL	NULL	statement 4	Process		promotes					S phase	Process	entry into			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_16_15836_s_20	15691830	A dual connection links Id2 and pRb: when overexpressed, Id2 overrides the tumor suppressor function of RB, allowing binding of E2F to its target genes, promoting entry into S phase and cell proliferation ( ).	bind
35796	6	10137	6	11	NULL	NULL	NULL	statement 4	Process		promotes					cell	Cell	proliferation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_16_15836_s_20	15691830	A dual connection links Id2 and pRb: when overexpressed, Id2 overrides the tumor suppressor function of RB, allowing binding of E2F to its target genes, promoting entry into S phase and cell proliferation ( ).	bind
43313	1	10137	7	NULL	NULL	0	NULL	 Id2	NULL		links to	NULL				pRb	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_16_15836_s_20	15691830	A dual connection links Id2 and pRb: when overexpressed, Id2 overrides the tumor suppressor function of RB, allowing binding of E2F to its target genes, promoting entry into S phase and cell proliferation ( ).	bind
43314	2	10137	7	NULL	NULL	0	NULL	Id2	NULL	overexpression of	overrides	NULL				RB	NULL	tumor suppressor function of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_16_15836_s_20	15691830	A dual connection links Id2 and pRb: when overexpressed, Id2 overrides the tumor suppressor function of RB, allowing binding of E2F to its target genes, promoting entry into S phase and cell proliferation ( ).	bind
43315	3	10137	7	NULL	NULL	0	NULL	E2F	NULL		bind	NULL				target genes	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_16_15836_s_20	15691830	A dual connection links Id2 and pRb: when overexpressed, Id2 overrides the tumor suppressor function of RB, allowing binding of E2F to its target genes, promoting entry into S phase and cell proliferation ( ).	bind
43316	4	10137	7	NULL	NULL	0	NULL	statement 2	NULL		allows	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_16_15836_s_20	15691830	A dual connection links Id2 and pRb: when overexpressed, Id2 overrides the tumor suppressor function of RB, allowing binding of E2F to its target genes, promoting entry into S phase and cell proliferation ( ).	bind
43317	5	10137	7	NULL	NULL	0	NULL	statement 4	NULL		promotes	NULL				S phase	NULL	entry into			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_16_15836_s_20	15691830	A dual connection links Id2 and pRb: when overexpressed, Id2 overrides the tumor suppressor function of RB, allowing binding of E2F to its target genes, promoting entry into S phase and cell proliferation ( ).	bind
43318	6	10137	7	10	NULL	0	NULL	statement 4			promotes					cell		proliferation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_16_15836_s_20	15691830	A dual connection links Id2 and pRb: when overexpressed, Id2 overrides the tumor suppressor function of RB, allowing binding of E2F to its target genes, promoting entry into S phase and cell proliferation ( ).	bind
35797	1	10139	6	11	NULL	NULL	NULL	Dyn2 dimer	GP		bind			PRD		SNX9	GP		SH3		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_42694_s_241	15299020	A Dyn2 dimer is bound  to SNX9 through a PRD-SH3 interaction.	bind
43319	1	10139	7	NULL	NULL	0	NULL	Dyn2 dimer	NULL		bind	NULL		PRD		SNX9	NULL		SH3		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_41_42694_s_241	15299020	A Dyn2 dimer is bound  to SNX9 through a PRD-SH3 interaction.	bind
35799	1	10140	6	11	NULL	NULL	NULL	bilirubin	Chemical		bind					serum albumin	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_73_s_170	7814422	A Dynamic Model for Bilirubin Binding to Human Serum Albumin.	bind
43320	1	10140	7	NULL	NULL	0	NULL	Bilirubin	NULL		bind	NULL				Serum Albumin	NULL	human			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_73_s_170	7814422	A Dynamic Model for Bilirubin Binding to Human Serum Albumin.	bind
35800	1	10141	6	11	NULL	NULL	NULL	dyn	GP	mutant	bind		reduced affinity	K44A		GTP	Chemical				NULL	podosomes in BHK-RSV cells	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3301_s_27	15872089	A dynamin mutant (dynK44A), which binds GTP with reduced affinity (Damke  et al., 1994 ; Warnock  et al., 1995 ), affected actin stress fiber formation and cell shape (Damke  et al., 1994 ) and delayed actin turnover at podosomes in BHK-RSV cells (Ochoa  et al., 2000 ).	bind
35801	2	10141	6	11	NULL	NULL	NULL	statement 1	Process		affects					actin stress fiber	GP	formation of			NULL	podosomes in BHK-RSV cells	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3301_s_27	15872089	A dynamin mutant (dynK44A), which binds GTP with reduced affinity (Damke  et al., 1994 ; Warnock  et al., 1995 ), affected actin stress fiber formation and cell shape (Damke  et al., 1994 ) and delayed actin turnover at podosomes in BHK-RSV cells (Ochoa  et al., 2000 ).	bind
35802	3	10141	6	11	NULL	NULL	NULL	statement 1	Process		affects					cell shape	Cell				NULL	podosomes in BHK-RSV cells	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3301_s_27	15872089	A dynamin mutant (dynK44A), which binds GTP with reduced affinity (Damke  et al., 1994 ; Warnock  et al., 1995 ), affected actin stress fiber formation and cell shape (Damke  et al., 1994 ) and delayed actin turnover at podosomes in BHK-RSV cells (Ochoa  et al., 2000 ).	bind
35803	4	10141	6	11	NULL	NULL	NULL	statement 1	Process		delays					actin turnover	GP				NULL	podosomes in BHK-RSV cells	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3301_s_27	15872089	A dynamin mutant (dynK44A), which binds GTP with reduced affinity (Damke  et al., 1994 ; Warnock  et al., 1995 ), affected actin stress fiber formation and cell shape (Damke  et al., 1994 ) and delayed actin turnover at podosomes in BHK-RSV cells (Ochoa  et al., 2000 ).	bind
43321	1	10141	7	10	NULL	0	NULL	dyn		mutant	binds		reduced affinity	K44A		GTP					NULL	podosomes in BHK-RSV cells	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3301_s_27	15872089	A dynamin mutant (dynK44A), which binds GTP with reduced affinity (Damke  et al., 1994 ; Warnock  et al., 1995 ), affected actin stress fiber formation and cell shape (Damke  et al., 1994 ) and delayed actin turnover at podosomes in BHK-RSV cells (Ochoa  et al., 2000 ).	bind
43322	2	10141	7	10	NULL	0	NULL	statement 1			affects					actin stress fiber		formation of			NULL	podosomes in BHK-RSV cells	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3301_s_27	15872089	A dynamin mutant (dynK44A), which binds GTP with reduced affinity (Damke  et al., 1994 ; Warnock  et al., 1995 ), affected actin stress fiber formation and cell shape (Damke  et al., 1994 ) and delayed actin turnover at podosomes in BHK-RSV cells (Ochoa  et al., 2000 ).	bind
43323	3	10141	7	10	NULL	0	NULL	statement 1			affects					cell shape					NULL	podosomes in BHK-RSV cells	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3301_s_27	15872089	A dynamin mutant (dynK44A), which binds GTP with reduced affinity (Damke  et al., 1994 ; Warnock  et al., 1995 ), affected actin stress fiber formation and cell shape (Damke  et al., 1994 ) and delayed actin turnover at podosomes in BHK-RSV cells (Ochoa  et al., 2000 ).	bind
43324	4	10141	7	10	NULL	0	NULL	statement 1			delays					actin turnover					NULL	podosomes in BHK-RSV cells	NULL	NULL	NULL	NULL	gw70_molbiolcell_16_7_3301_s_27	15872089	A dynamin mutant (dynK44A), which binds GTP with reduced affinity (Damke  et al., 1994 ; Warnock  et al., 1995 ), affected actin stress fiber formation and cell shape (Damke  et al., 1994 ) and delayed actin turnover at podosomes in BHK-RSV cells (Ochoa  et al., 2000 ).	bind
43325	5	10141	7	NULL	NULL	0	NULL	dynK44A	NULL		is	NULL				dynamin mutant	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_7_3301_s_27	15872089	A dynamin mutant (dynK44A), which binds GTP with reduced affinity (Damke  et al., 1994 ; Warnock  et al., 1995 ), affected actin stress fiber formation and cell shape (Damke  et al., 1994 ) and delayed actin turnover at podosomes in BHK-RSV cells (Ochoa  et al., 2000 ).	bind
35804	1	10143	6	11	NULL	NULL	NULL	nuclear protein of 130 kDa	GP	eukaryotic	bind							bacterial		cAMP responsive element	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochim-biophys-acta_1089_2_1647212_s_1	1647212	A eukaryotic nuclear protein of 130 kDa binds to a bacterial cAMP responsive element..	bind
43328	1	10143	7	10	NULL	0	NULL	nuclear protein of 130 kDa	NULL	eukaryotic	binds to	NULL					NULL	bacterial		cAMP responsive element	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochim-biophys-acta_1089_2_1647212_s_1	1647212	A eukaryotic nuclear protein of 130 kDa binds to a bacterial cAMP responsive element..	bind
35805	1	10144	6	11	NULL	NULL	NULL	eRF-1	GP		bind					PP2A	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_73_1_68_s_290	10581399	A eukaryotic translational release factor (eRF-1) binds to PP2A and localizes the phosphatase to ribosomes  [ 2.	bind
35806	2	10144	6	11	NULL	NULL	NULL	eRF-1	GP		is					eukaryotic translational release factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_73_1_68_s_290	10581399	A eukaryotic translational release factor (eRF-1) binds to PP2A and localizes the phosphatase to ribosomes  [ 2.	bind
35807	3	10144	6	11	NULL	NULL	NULL	phosphatase	GP		is localized to					ribosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_73_1_68_s_290	10581399	A eukaryotic translational release factor (eRF-1) binds to PP2A and localizes the phosphatase to ribosomes  [ 2.	bind
35808	4	10144	6	11	NULL	NULL	NULL	statement 1	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_brainresmolbrainres_73_1_68_s_290	10581399	A eukaryotic translational release factor (eRF-1) binds to PP2A and localizes the phosphatase to ribosomes  [ 2.	bind
43329	1	10144	7	NULL	NULL	0	NULL	eRF-1	NULL		binds to	NULL				PP2A	NULL				NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_73_1_68_s_290	10581399	A eukaryotic translational release factor (eRF-1) binds to PP2A and localizes the phosphatase to ribosomes  [ 2.	bind
43330	2	10144	7	NULL	NULL	0	NULL	phosphatases	NULL		localize to	NULL				ribosomes	NULL				NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_73_1_68_s_290	10581399	A eukaryotic translational release factor (eRF-1) binds to PP2A and localizes the phosphatase to ribosomes  [ 2.	bind
43331	3	10144	7	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_73_1_68_s_290	10581399	A eukaryotic translational release factor (eRF-1) binds to PP2A and localizes the phosphatase to ribosomes  [ 2.	bind
43332	4	10144	7	NULL	NULL	0	NULL	eRF-1	NULL		is	NULL				eukaryotic translational release factor	NULL				NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_73_1_68_s_290	10581399	A eukaryotic translational release factor (eRF-1) binds to PP2A and localizes the phosphatase to ribosomes  [ 2.	bind
35809	1	10145	6	11	NULL	NULL	NULL	Lipoprotein(a)	Chemical		bind					platelets	CellComponent	human			NULL		NULL	NULL	NULL	NULL	gw60_atherosclerosis_140_1_155_s_161	9733226	A Ezratty, DI Simon and J Loscalzo, Lipoprotein(a) binds to human platelets and attenuates plasminogen binding and activation.	bind
35810	2	10145	6	11	NULL	NULL	NULL	statement 1	Process		attenuates					plasminogen	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_atherosclerosis_140_1_155_s_161	9733226	A Ezratty, DI Simon and J Loscalzo, Lipoprotein(a) binds to human platelets and attenuates plasminogen binding and activation.	bind
35811	3	10145	6	11	NULL	NULL	NULL	statement 1	Process		attenuates					plasminogen	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_atherosclerosis_140_1_155_s_161	9733226	A Ezratty, DI Simon and J Loscalzo, Lipoprotein(a) binds to human platelets and attenuates plasminogen binding and activation.	bind
43333	1	10145	7	NULL	NULL	0	NULL	Lipoprotein	NULL		binds to	NULL				platelets	NULL	human			NULL		0	NULL	NULL	NULL	gw60_atherosclerosis_140_1_155_s_161	9733226	A Ezratty, DI Simon and J Loscalzo, Lipoprotein(a) binds to human platelets and attenuates plasminogen binding and activation.	bind
43334	2	10145	7	NULL	NULL	0	NULL	statement 1	NULL		attenuates	NULL				plasminogen	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_atherosclerosis_140_1_155_s_161	9733226	A Ezratty, DI Simon and J Loscalzo, Lipoprotein(a) binds to human platelets and attenuates plasminogen binding and activation.	bind
43335	3	10145	7	NULL	NULL	0	NULL	statement 1	NULL		attenuates	NULL				plasminogen	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_atherosclerosis_140_1_155_s_161	9733226	A Ezratty, DI Simon and J Loscalzo, Lipoprotein(a) binds to human platelets and attenuates plasminogen binding and activation.	bind
35812	1	10147	6	11	NULL	NULL	NULL	NIF	GP	125I-labeled	bind							recombinant	I-domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18769_s_109	11880366	A facile binding assay for quantifying NIF binding to the recombinant I-domains was developed by measuring the binding of 125I-NIF to the recombinant I-domains captured onto glutathione-Sepharose.	bind
44004	1	10147	7	10	NULL	0	NULL	NIF	NULL	125I-labeled	bind	NULL					NULL	recombinant	I-domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18769_s_109	11880366	A facile binding assay for quantifying NIF binding to the recombinant I-domains was developed by measuring the binding of 125I-NIF to the recombinant I-domains captured onto glutathione-Sepharose.	bind
35813	1	10148	6	11	NULL	NULL	NULL	DSC	ResearchActivity		bind		specifically							MCB cis-element	NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_6_1577_s_11	9614195	A factor complex that specifically binds to the MCB  cis-element was initially identified in budding yeast by gel shift assay and called DSC (Lowndes  et al., 1991  ).	bind
35814	2	10148	6	11	NULL	NULL	NULL	DSC	ResearchActivity		is identified in					budding yeast	Organism				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_6_1577_s_11	9614195	A factor complex that specifically binds to the MCB  cis-element was initially identified in budding yeast by gel shift assay and called DSC (Lowndes  et al., 1991  ).	bind
44005	1	10148	7	10	NULL	0	NULL	DSC	NULL		bind	NULL	specifically				NULL			MCB cis-element	NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_6_1577_s_11	9614195	A factor complex that specifically binds to the MCB  cis-element was initially identified in budding yeast by gel shift assay and called DSC (Lowndes  et al., 1991  ).	bind
49602	2	10148	7	10	NULL	0	NULL	DSC	NULL		is identified in	NULL				budding yeast	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_6_1577_s_11	9614195	A factor complex that specifically binds to the MCB  cis-element was initially identified in budding yeast by gel shift assay and called DSC (Lowndes  et al., 1991  ).	bind
35816	1	10150	6	11	NULL	NULL	NULL	factor VIII	GP		bind					von Willebrand factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_nature_402_6760_439_s_174	10586887	A factor VIII neutralizing monoclonal antibody and a human inhibitor alloantibody recognizing epitopes in the C2 domain inhibit factor VIII binding to von Willebrand factor and to phosphatidylserine.	bind
35817	2	10150	6	11	NULL	NULL	NULL	factor VIII neutralizing monoclonal antibody	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nature_402_6760_439_s_174	10586887	A factor VIII neutralizing monoclonal antibody and a human inhibitor alloantibody recognizing epitopes in the C2 domain inhibit factor VIII binding to von Willebrand factor and to phosphatidylserine.	bind
35818	3	10150	6	11	NULL	NULL	NULL	factor VIII	GP		bind					phosphatidylserine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_nature_402_6760_439_s_174	10586887	A factor VIII neutralizing monoclonal antibody and a human inhibitor alloantibody recognizing epitopes in the C2 domain inhibit factor VIII binding to von Willebrand factor and to phosphatidylserine.	bind
35819	4	10150	6	11	NULL	NULL	NULL	factor VIII neutralizing monoclonal antibody	GP		inhibits					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_nature_402_6760_439_s_174	10586887	A factor VIII neutralizing monoclonal antibody and a human inhibitor alloantibody recognizing epitopes in the C2 domain inhibit factor VIII binding to von Willebrand factor and to phosphatidylserine.	bind
35820	5	10150	6	11	NULL	NULL	NULL	inhibitor alloantibody	GP	human	recognize							epitopes in	C2 domain		NULL		NULL	NULL	NULL	NULL	gw60_nature_402_6760_439_s_174	10586887	A factor VIII neutralizing monoclonal antibody and a human inhibitor alloantibody recognizing epitopes in the C2 domain inhibit factor VIII binding to von Willebrand factor and to phosphatidylserine.	bind
35821	6	10150	6	11	NULL	NULL	NULL	statement 5	Process		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nature_402_6760_439_s_174	10586887	A factor VIII neutralizing monoclonal antibody and a human inhibitor alloantibody recognizing epitopes in the C2 domain inhibit factor VIII binding to von Willebrand factor and to phosphatidylserine.	bind
35822	7	10150	6	11	NULL	NULL	NULL	statement 5	Process		inhibits					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_nature_402_6760_439_s_174	10586887	A factor VIII neutralizing monoclonal antibody and a human inhibitor alloantibody recognizing epitopes in the C2 domain inhibit factor VIII binding to von Willebrand factor and to phosphatidylserine.	bind
44010	1	10150	7	NULL	NULL	0	NULL	factor VIII	NULL		bind	NULL				von Willebrand factor 	NULL				NULL		0	NULL	NULL	NULL	gw60_nature_402_6760_439_s_174	10586887	A factor VIII neutralizing monoclonal antibody and a human inhibitor alloantibody recognizing epitopes in the C2 domain inhibit factor VIII binding to von Willebrand factor and to phosphatidylserine.	bind
44012	2	10150	7	NULL	NULL	0	NULL	factor VIII	NULL		bind	NULL				phosphatidylserine	NULL				NULL		0	NULL	NULL	NULL	gw60_nature_402_6760_439_s_174	10586887	A factor VIII neutralizing monoclonal antibody and a human inhibitor alloantibody recognizing epitopes in the C2 domain inhibit factor VIII binding to von Willebrand factor and to phosphatidylserine.	bind
44018	3	10150	7	NULL	NULL	0	NULL	inhibitor alloantibody	NULL	human	recognize	NULL					NULL	epitopes in	 C2 domain		NULL		NULL	NULL	NULL	NULL	gw60_nature_402_6760_439_s_174	10586887	A factor VIII neutralizing monoclonal antibody and a human inhibitor alloantibody recognizing epitopes in the C2 domain inhibit factor VIII binding to von Willebrand factor and to phosphatidylserine.	bind
44020	4	10150	7	NULL	NULL	0	NULL	statement 3	NULL		inhibit	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nature_402_6760_439_s_174	10586887	A factor VIII neutralizing monoclonal antibody and a human inhibitor alloantibody recognizing epitopes in the C2 domain inhibit factor VIII binding to von Willebrand factor and to phosphatidylserine.	bind
44021	5	10150	7	NULL	NULL	0	NULL	statement 3	NULL		inhibit	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nature_402_6760_439_s_174	10586887	A factor VIII neutralizing monoclonal antibody and a human inhibitor alloantibody recognizing epitopes in the C2 domain inhibit factor VIII binding to von Willebrand factor and to phosphatidylserine.	bind
44023	7	10150	7	NULL	NULL	0	NULL	factor VIII neutralizing monoclonal antibody	NULL		inhibit	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nature_402_6760_439_s_174	10586887	A factor VIII neutralizing monoclonal antibody and a human inhibitor alloantibody recognizing epitopes in the C2 domain inhibit factor VIII binding to von Willebrand factor and to phosphatidylserine.	bind
50242	6	10150	7	NULL	NULL	0	NULL	factor VIII neutralizing monoclonal antibody	NULL		inhibit	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nature_402_6760_439_s_174	10586887	A factor VIII neutralizing monoclonal antibody and a human inhibitor alloantibody recognizing epitopes in the C2 domain inhibit factor VIII binding to von Willebrand factor and to phosphatidylserine.	bind
35823	1	10151	6	11	NULL	NULL	NULL	U2AF	GP		is required for					U2 snRNP	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_7_1010_s_534	9531538	A factor, U2AF, is required for U2 snRNP binding and splicing complex assembly.	bind
35824	2	10151	6	11	NULL	NULL	NULL	U2AF	GP		is required for					splicing complex	GP	assembly of			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_7_1010_s_534	9531538	A factor, U2AF, is required for U2 snRNP binding and splicing complex assembly.	bind
44024	1	10151	7	NULL	NULL	0	NULL	U2AF factor	NULL		is required for	NULL				U2 snRNP	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_genesdev_12_7_1010_s_534	9531538	A factor, U2AF, is required for U2 snRNP binding and splicing complex assembly.	bind
44025	2	10151	7	NULL	NULL	0	NULL	U2AF  factor	NULL		is required for	NULL				splicing complex	NULL	assembly of			NULL		0	NULL	NULL	NULL	gw60_genesdev_12_7_1010_s_534	9531538	A factor, U2AF, is required for U2 snRNP binding and splicing complex assembly.	bind
35825	1	10152	6	11	NULL	NULL	NULL	Xa7	GP	Xanthomonas oryzae pv. oryzae	bind					DNA	NucleicAcid			AT-rich 	NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_60_0_425_s_224	16753033	A family  member from  Xanthomonas oryzae pv.  oryzae, Xa7, binds AT-rich DNA ( 134), but specific host DNA binding sites have not been identified.	bind
44026	1	10152	7	10	NULL	0	NULL	Xa7	NULL	Xanthomonas oryzae pv. oryzae	binds	NULL				DNA	NULL			AT-rich	NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_60_0_425_s_224	16753033	A family  member from  Xanthomonas oryzae pv.  oryzae, Xa7, binds AT-rich DNA ( 134), but specific host DNA binding sites have not been identified.	bind
35826	1	10154	6	11	NULL	NULL	NULL	MBD	GP		is a					methyl-CpG-binding domain	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_397_s_22	16415179	A family of DNA binding proteins harboring a methyl-CpG-binding domain (MBD) recognizes and binds to methylated CpG sequences ( ).	bind
35827	2	10154	6	11	NULL	NULL	NULL	DNA-binding protein	GP		bind			MBD				methylated		CpG sequences	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_397_s_22	16415179	A family of DNA binding proteins harboring a methyl-CpG-binding domain (MBD) recognizes and binds to methylated CpG sequences ( ).	bind
35828	3	10154	6	11	NULL	NULL	NULL	DNA-binding protein	GP		recognizes			MBD				methylated		CpG sequences	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_397_s_22	16415179	A family of DNA binding proteins harboring a methyl-CpG-binding domain (MBD) recognizes and binds to methylated CpG sequences ( ).	bind
44031	1	10154	7	10	NULL	0	NULL	DNA-binding protein			recognizes			MBD				methylated		CpG sequences	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_397_s_22	16415179	A family of DNA binding proteins harboring a methyl-CpG-binding domain (MBD) recognizes and binds to methylated CpG sequences ( ).	bind
44033	2	10154	7	10	NULL	0	NULL	DNA-binding protein			binds			MBD				methylated		CpG sequences	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_397_s_22	16415179	A family of DNA binding proteins harboring a methyl-CpG-binding domain (MBD) recognizes and binds to methylated CpG sequences ( ).	bind
44035	3	10154	7	NULL	NULL	0	NULL	MBD	NULL		is	NULL				methyl-CpG-binding domain	NULL				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_397_s_22	16415179	A family of DNA binding proteins harboring a methyl-CpG-binding domain (MBD) recognizes and binds to methylated CpG sequences ( ).	bind
35829	1	10155	6	11	NULL	NULL	NULL	lymphoid Ig-like receptor	GP	human	bind					MHC class I molecules	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiophysbiomol_32_0_93_s_389	12471063	A family of human  lymphoid and myeloid Ig-like receptors, some of which bind to MHC class I molecules.	bind
35830	2	10155	6	11	NULL	NULL	NULL	myeloid Ig-like receptor	GP	human	bind					MHC class I molecules	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiophysbiomol_32_0_93_s_389	12471063	A family of human  lymphoid and myeloid Ig-like receptors, some of which bind to MHC class I molecules.	bind
44037	1	10155	7	NULL	NULL	0	NULL	lymphoid Ig-like receptors	NULL	human	binds to	NULL				MHC class I  molecules	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevbiophysbiomol_32_0_93_s_389	12471063	A family of human  lymphoid and myeloid Ig-like receptors, some of which bind to MHC class I molecules.	bind
44038	2	10155	7	NULL	NULL	0	NULL	myeloid Ig-like receptors	NULL	human	binds to	NULL				MHC class I  molecules	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevbiophysbiomol_32_0_93_s_389	12471063	A family of human  lymphoid and myeloid Ig-like receptors, some of which bind to MHC class I molecules.	bind
35831	1	10157	6	11	NULL	NULL	NULL	LIM	GP		is a type of					homeodomain protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4161_s_417	12874135	A family of LIM domain-associated cofactors confer transcriptional synergism between LIM and Otx homeodomain proteins.	bind
35832	2	10157	6	11	NULL	NULL	NULL	Otx	GP		is a type of					homeodomain protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4161_s_417	12874135	A family of LIM domain-associated cofactors confer transcriptional synergism between LIM and Otx homeodomain proteins.	bind
35833	3	10157	6	11	NULL	NULL	NULL	LIM	GP		synergizes with		transcriptionaly			Otx	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4161_s_417	12874135	A family of LIM domain-associated cofactors confer transcriptional synergism between LIM and Otx homeodomain proteins.	bind
35834	4	10157	6	11	NULL	NULL	NULL	LIM domain-associated cofactors	GP		confer					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4161_s_417	12874135	A family of LIM domain-associated cofactors confer transcriptional synergism between LIM and Otx homeodomain proteins.	bind
44039	1	10157	7	10	NULL	0	NULL	LIM	NULL		synergize with	NULL	transcriptionally			Otx	NULL				NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4161_s_417	12874135	A family of LIM domain-associated cofactors confer transcriptional synergism between LIM and Otx homeodomain proteins.	bind
44040	2	10157	7	10	NULL	0	NULL	LIM domain-associated cofactors	NULL		confer	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_development_130_17_4161_s_417	12874135	A family of LIM domain-associated cofactors confer transcriptional synergism between LIM and Otx homeodomain proteins.	bind
49662	3	10157	7	10	NULL	0	NULL	LIM	NULL		is a type of	NULL				homeodomain protein	NULL				NULL		0	NULL	NULL	NULL	gw60_development_130_17_4161_s_417	12874135	A family of LIM domain-associated cofactors confer transcriptional synergism between LIM and Otx homeodomain proteins.	bind
49663	4	10157	7	10	NULL	0	NULL	Otx	NULL		is a type of	NULL				homeodomain protein	NULL				NULL		0	NULL	NULL	NULL	gw60_development_130_17_4161_s_417	12874135	A family of LIM domain-associated cofactors confer transcriptional synergism between LIM and Otx homeodomain proteins.	bind
35835	1	10159	6	11	NULL	NULL	NULL	Na+/H+ exchanger regulatory factor	GP		bind								C terminus (D(SST)- X-L)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_6_3729_s_139	10660517	A family of PDZ-binding domain proteins, including the Na+/H+ exchanger regulatory factor ( 65) and ezrin-binding protein 50 ( 66), bind to the C terminus (D(SST)- X-L) (Fig.  2).	bind
35836	2	10159	6	11	NULL	NULL	NULL	ezrin-binding protein 50	GP		bind								C terminus (D(SST)- X-L)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_6_3729_s_139	10660517	A family of PDZ-binding domain proteins, including the Na+/H+ exchanger regulatory factor ( 65) and ezrin-binding protein 50 ( 66), bind to the C terminus (D(SST)- X-L) (Fig.  2).	bind
35837	3	10159	6	11	NULL	NULL	NULL	Na+/H+ exchanger regulatory factor	GP		is a type of					PDZ-binding domain protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_6_3729_s_139	10660517	A family of PDZ-binding domain proteins, including the Na+/H+ exchanger regulatory factor ( 65) and ezrin-binding protein 50 ( 66), bind to the C terminus (D(SST)- X-L) (Fig.  2).	bind
35838	4	10159	6	11	NULL	NULL	NULL	ezrin-binding protein 50	GP		is a type of					PDZ-binding domain protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_6_3729_s_139	10660517	A family of PDZ-binding domain proteins, including the Na+/H+ exchanger regulatory factor ( 65) and ezrin-binding protein 50 ( 66), bind to the C terminus (D(SST)- X-L) (Fig.  2).	bind
44042	1	10159	7	NULL	NULL	0	NULL	Na+/H+ exchanger regulatory factor	NULL		bind	NULL					NULL		C terminus  (D(SST)- X-L)		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_6_3729_s_139	10660517	A family of PDZ-binding domain proteins, including the Na+/H+ exchanger regulatory factor ( 65) and ezrin-binding protein 50 ( 66), bind to the C terminus (D(SST)- X-L) (Fig.  2).	bind
44043	2	10159	7	NULL	NULL	0	NULL	ezrin-binding protein	NULL		bind	NULL					NULL		C terminus  (D(SST)- X-L)		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_6_3729_s_139	10660517	A family of PDZ-binding domain proteins, including the Na+/H+ exchanger regulatory factor ( 65) and ezrin-binding protein 50 ( 66), bind to the C terminus (D(SST)- X-L) (Fig.  2).	bind
44044	3	10159	7	NULL	NULL	0	NULL	Na+/H+ exchanger regulatory factor	NULL		is a type of	NULL				PDZ-binding domain proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_6_3729_s_139	10660517	A family of PDZ-binding domain proteins, including the Na+/H+ exchanger regulatory factor ( 65) and ezrin-binding protein 50 ( 66), bind to the C terminus (D(SST)- X-L) (Fig.  2).	bind
44045	4	10159	7	NULL	NULL	0	NULL	ezrin-binding protein	NULL		is a type of	NULL				PDZ-binding domain proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_6_3729_s_139	10660517	A family of PDZ-binding domain proteins, including the Na+/H+ exchanger regulatory factor ( 65) and ezrin-binding protein 50 ( 66), bind to the C terminus (D(SST)- X-L) (Fig.  2).	bind
35839	1	10160	6	11	NULL	NULL	NULL	von Hippel-Lindau tumor suppressor protein	GP		bind					HIF-1alpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_26_23111_s_20	11943784	A family of prolyl hydroxylase enzymes regulates the binding of von Hippel-Lindau tumor suppressor protein to HIF-1alpha by hydroxylating key proline residues on the HIF-1alpha protein ( 17-20).	bind
35840	2	10160	6	11	NULL	NULL	NULL	family of prolyl hydroxylase enzymes	GP		regulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_26_23111_s_20	11943784	A family of prolyl hydroxylase enzymes regulates the binding of von Hippel-Lindau tumor suppressor protein to HIF-1alpha by hydroxylating key proline residues on the HIF-1alpha protein ( 17-20).	bind
35841	3	10160	6	11	NULL	NULL	NULL	family of prolyl hydroxylase enzymes	GP		hydroxylate					HIF-1alpha protein	GP		proline residues		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_26_23111_s_20	11943784	A family of prolyl hydroxylase enzymes regulates the binding of von Hippel-Lindau tumor suppressor protein to HIF-1alpha by hydroxylating key proline residues on the HIF-1alpha protein ( 17-20).	bind
35842	4	10160	6	11	NULL	NULL	NULL	statement 2	Process		occurs by					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_26_23111_s_20	11943784	A family of prolyl hydroxylase enzymes regulates the binding of von Hippel-Lindau tumor suppressor protein to HIF-1alpha by hydroxylating key proline residues on the HIF-1alpha protein ( 17-20).	bind
44046	1	10160	7	NULL	NULL	0	NULL	von Hippel-Lindau tumor suppressor protein	NULL		bind	NULL				HIF-1alpha	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23111_s_20	11943784	A family of prolyl hydroxylase enzymes regulates the binding of von Hippel-Lindau tumor suppressor protein to HIF-1alpha by hydroxylating key proline residues on the HIF-1alpha protein ( 17-20).	bind
44047	2	10160	7	NULL	NULL	0	NULL	statement 1	NULL		occurs upon	NULL				HIF-1alpha protein	NULL	hydroxylation of	key proline residues		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23111_s_20	11943784	A family of prolyl hydroxylase enzymes regulates the binding of von Hippel-Lindau tumor suppressor protein to HIF-1alpha by hydroxylating key proline residues on the HIF-1alpha protein ( 17-20).	bind
44048	3	10160	7	NULL	NULL	0	NULL	prolyl hydroxylase enzymes	NULL		regulate	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23111_s_20	11943784	A family of prolyl hydroxylase enzymes regulates the binding of von Hippel-Lindau tumor suppressor protein to HIF-1alpha by hydroxylating key proline residues on the HIF-1alpha protein ( 17-20).	bind
35843	1	10161	6	11	NULL	NULL	NULL	IGFBPs	GP		bind					IGF-I	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_endocrinology_138_11_9348216_s_2	9348216	A family of six insulin-like growth factor binding proteins (IGFBPs) bind  IGF-I and modulate its biological activity.	bind
35844	2	10161	6	11	NULL	NULL	NULL	statement 1	GP		modulates					IGF-I	GP	biological activity of			NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_endocrinology_138_11_9348216_s_2	9348216	A family of six insulin-like growth factor binding proteins (IGFBPs) bind  IGF-I and modulate its biological activity.	bind
35845	3	10161	6	11	NULL	NULL	NULL	IGFBP	GP		is					insulin-like growth factor binding protein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_endocrinology_138_11_9348216_s_2	9348216	A family of six insulin-like growth factor binding proteins (IGFBPs) bind  IGF-I and modulate its biological activity.	bind
44049	1	10161	7	NULL	NULL	0	NULL	IGFBPs	NULL		bind	NULL				IGF-I	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_endocrinology_138_11_9348216_s_2	9348216	A family of six insulin-like growth factor binding proteins (IGFBPs) bind  IGF-I and modulate its biological activity.	bind
44050	2	10161	7	NULL	NULL	0	NULL	statement 1	NULL		modulate	NULL				IGF-I	NULL	biological activity of			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_endocrinology_138_11_9348216_s_2	9348216	A family of six insulin-like growth factor binding proteins (IGFBPs) bind  IGF-I and modulate its biological activity.	bind
44051	3	10161	7	NULL	NULL	0	NULL	IGFBPs	NULL		is	NULL				insulin-like growth factor binding proteins	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_endocrinology_138_11_9348216_s_2	9348216	A family of six insulin-like growth factor binding proteins (IGFBPs) bind  IGF-I and modulate its biological activity.	bind
35846	1	10162	6	11	NULL	NULL	NULL	AKAP	GP		is a type of					anchoring protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_512_1_91_s_8	11852058	A family of these anchoring proteins (AKAP) bind both cAMP-dependent PK (PKA) and PPs targeting them to specific cellular membranes [ 7,   8 and   9].	bind
35847	2	10162	6	11	NULL	NULL	NULL	AKAP	GP		bind					PKA	GP	cAMP-dependent			NULL		NULL	NULL	NULL	NULL	gw60_febslett_512_1_91_s_8	11852058	A family of these anchoring proteins (AKAP) bind both cAMP-dependent PK (PKA) and PPs targeting them to specific cellular membranes [ 7,   8 and   9].	bind
35848	3	10162	6	11	NULL	NULL	NULL	AKAP	GP		bind					PP	GP	cAMP-dependent			NULL		NULL	NULL	NULL	NULL	gw60_febslett_512_1_91_s_8	11852058	A family of these anchoring proteins (AKAP) bind both cAMP-dependent PK (PKA) and PPs targeting them to specific cellular membranes [ 7,   8 and   9].	bind
44052	1	10162	7	NULL	NULL	0	NULL	AKAP	NULL		bind	NULL				PKA	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_512_1_91_s_8	11852058	A family of these anchoring proteins (AKAP) bind both cAMP-dependent PK (PKA) and PPs targeting them to specific cellular membranes [ 7,   8 and   9].	bind
44053	2	10162	7	NULL	NULL	0	NULL	AKAP	NULL		bind	NULL				PPs	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_512_1_91_s_8	11852058	A family of these anchoring proteins (AKAP) bind both cAMP-dependent PK (PKA) and PPs targeting them to specific cellular membranes [ 7,   8 and   9].	bind
44054	3	10162	7	11	NULL	NULL	NULL	PKA	GP		targeted to					cellular membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_febslett_512_1_91_s_8	11852058	A family of these anchoring proteins (AKAP) bind both cAMP-dependent PK (PKA) and PPs targeting them to specific cellular membranes [ 7,   8 and   9].	bind
44055	4	10162	7	11	NULL	NULL	NULL	PPs	GP		targeted to					cellular membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_febslett_512_1_91_s_8	11852058	A family of these anchoring proteins (AKAP) bind both cAMP-dependent PK (PKA) and PPs targeting them to specific cellular membranes [ 7,   8 and   9].	bind
44056	5	10162	7	11	NULL	NULL	NULL	statement 1	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_512_1_91_s_8	11852058	A family of these anchoring proteins (AKAP) bind both cAMP-dependent PK (PKA) and PPs targeting them to specific cellular membranes [ 7,   8 and   9].	bind
44057	6	10162	7	11	NULL	NULL	NULL	statement 2	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_512_1_91_s_8	11852058	A family of these anchoring proteins (AKAP) bind both cAMP-dependent PK (PKA) and PPs targeting them to specific cellular membranes [ 7,   8 and   9].	bind
44058	7	10162	7	NULL	NULL	0	NULL	AKAP	NULL		is a type of	NULL				anchoring proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_512_1_91_s_8	11852058	A family of these anchoring proteins (AKAP) bind both cAMP-dependent PK (PKA) and PPs targeting them to specific cellular membranes [ 7,   8 and   9].	bind
44059	8	10162	7	11	NULL	NULL	NULL	PKA	GP		is					cAMP-dependent PK	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_512_1_91_s_8	11852058	A family of these anchoring proteins (AKAP) bind both cAMP-dependent PK (PKA) and PPs targeting them to specific cellular membranes [ 7,   8 and   9].	bind
35849	1	10163	6	NULL	NULL	0	NULL	family of ubiquitin-like proteins	NULL		bind	NULL				Hsp70-like Stch	NULL		ATPase domain		NULL		0	NULL	NULL	NULL	abs-batch0720-0739_febs-lett_467_2-3_10675567_s_1	10675567	A family of ubiquitin-like proteins binds the ATPase domain of Hsp70-like Stch..	bind
44060	1	10163	7	NULL	NULL	0	NULL	ubiquitin-like proteins	NULL		binds	NULL				Hsp70-like Stch	NULL		ATPase domain		NULL		0	NULL	NULL	NULL	abs-batch0720-0739_febs-lett_467_2-3_10675567_s_1	10675567	A family of ubiquitin-like proteins binds the ATPase domain of Hsp70-like Stch..	bind
35850	1	10165	6	11	NULL	NULL	NULL	Crk	GP		bind					focal adhesion proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_43_35953_s_168	16123042	A far Western analysis was used to determine whether disruption of the interaction by ADP-ribosylation with focal adhesion proteins could be attributed to direct inhibition of Crk binding to the focal adhesion proteins.	bind
44061	1	10165	7	NULL	NULL	0	NULL	Crk	NULL		bind	NULL				focal adhesion proteins	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_43_35953_s_168	16123042	A far Western analysis was used to determine whether disruption of the interaction by ADP-ribosylation with focal adhesion proteins could be attributed to direct inhibition of Crk binding to the focal adhesion proteins.	bind
35851	1	10167	6	11	NULL	NULL	NULL	virus	Organism		bind					host cell membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_68_0_863_s_88	10872468	A fascinating aspect of viral infection   is that in most cases, binding of the virus to the host cell membrane and fusion   of the viral membrane with this membrane are carried out by a single protein   referred to as the viral fusion protein.	bind
35853	2	10167	6	11	NULL	NULL	NULL	viral fusion protein	GP		carries out					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_68_0_863_s_88	10872468	A fascinating aspect of viral infection   is that in most cases, binding of the virus to the host cell membrane and fusion   of the viral membrane with this membrane are carried out by a single protein   referred to as the viral fusion protein.	bind
35855	3	10167	6	11	NULL	NULL	NULL	viral cell membrane	CellComponent		fused with					host cell membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_68_0_863_s_88	10872468	A fascinating aspect of viral infection   is that in most cases, binding of the virus to the host cell membrane and fusion   of the viral membrane with this membrane are carried out by a single protein   referred to as the viral fusion protein.	bind
35856	4	10167	6	11	NULL	NULL	NULL	viral fusion protein	GP		carries out					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_68_0_863_s_88	10872468	A fascinating aspect of viral infection   is that in most cases, binding of the virus to the host cell membrane and fusion   of the viral membrane with this membrane are carried out by a single protein   referred to as the viral fusion protein.	bind
44076	1	10167	7	NULL	NULL	0	NULL	virus	NULL		bind	NULL				host cell membrane	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_68_0_863_s_88	10872468	A fascinating aspect of viral infection   is that in most cases, binding of the virus to the host cell membrane and fusion   of the viral membrane with this membrane are carried out by a single protein   referred to as the viral fusion protein.	bind
44078	2	10167	7	NULL	NULL	0	NULL	viral membrane	NULL		fuse with	NULL				host cell membrane	NULL				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_68_0_863_s_88	10872468	A fascinating aspect of viral infection   is that in most cases, binding of the virus to the host cell membrane and fusion   of the viral membrane with this membrane are carried out by a single protein   referred to as the viral fusion protein.	bind
44081	3	10167	7	NULL	NULL	0	NULL	viral fusion protein	NULL		carries out	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_68_0_863_s_88	10872468	A fascinating aspect of viral infection   is that in most cases, binding of the virus to the host cell membrane and fusion   of the viral membrane with this membrane are carried out by a single protein   referred to as the viral fusion protein.	bind
49664	4	10167	7	10	NULL	0	NULL	viral fusion protein	NULL		carries out	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_68_0_863_s_88	10872468	A fascinating aspect of viral infection   is that in most cases, binding of the virus to the host cell membrane and fusion   of the viral membrane with this membrane are carried out by a single protein   referred to as the viral fusion protein.	bind
35857	1	10169	6	11	NULL	NULL	NULL	BASI	GP		bind					AMY2	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1696_2_145_s_201	14871655	A fast and tight simple two-step mechanism was determined for the binding of BASI  to AMY2 [ 85].	bind
44085	1	10169	7	NULL	NULL	0	NULL	BASI	NULL		bind	NULL				AMY2	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1696_2_145_s_201	14871655	A fast and tight simple two-step mechanism was determined for the binding of BASI  to AMY2 [ 85].	bind
35859	1	10170	6	11	NULL	NULL	NULL	Pi	Chemical		bind					mIPS	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_12_11475_s_107	15653679	A fast exchange analysis (deltanuobs - deltanuo = ( Eodeltab)/( KD +  Lo), where (deltanuobs - deltanuo) was the difference in line width for free Pi at a given concentration and Pi when enzyme was present,  Eo was the total enzyme concentration, and  Lo was the total Pi concentration) was used to estimate the enzyme bound line width, deltab, and  KD for Pi binding to recombinant mIPS.	bind
44088	1	10170	7	NULL	NULL	0	NULL	Pi	NULL		bind	NULL				mIPS	NULL	recombinant			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_12_11475_s_107	15653679	A fast exchange analysis (deltanuobs - deltanuo = ( Eodeltab)/( KD +  Lo), where (deltanuobs - deltanuo) was the difference in line width for free Pi at a given concentration and Pi when enzyme was present,  Eo was the total enzyme concentration, and  Lo was the total Pi concentration) was used to estimate the enzyme bound line width, deltab, and  KD for Pi binding to recombinant mIPS.	bind
36300	1	10171	6	11	NULL	NULL	NULL	LRDD	AminoAcid		is similar to		significantly	intermediate region		ankyrin	GP		spectrin binding domain		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1478_2_280_s_114	10825539	A FastA search of the GenBank database using the full-length LRDD (753 aa) revealed that the intermediate region of LRDD shows significant similarity with the spectrin binding domain of ankyrins.	bind
44091	1	10171	7	10	NULL	0	NULL	LRDD	NULL		is similar to	NULL	significantly	intermediate region		ankyrins	NULL		spectrin binding domain		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1478_2_280_s_114	10825539	A FastA search of the GenBank database using the full-length LRDD (753 aa) revealed that the intermediate region of LRDD shows significant similarity with the spectrin binding domain of ankyrins.	bind
35874	1	10172	6	11	NULL	NULL	NULL	ARF	GP		is					ADP-ribosylation factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_8	15657398	A favored current model for how this coupling is achieved, known as the priming complex model ( ), proposes that the activated (GTP-bound) form of an ADP ribosylation factor (ARF) - like small GTPase promotes the binding of coat proteins onto the cytoplasmic domain of transmembrane cargo proteins to form a key intermediate that drives both cargo sorting and vesicle formation.	bind
35875	2	10172	6	11	NULL	NULL	NULL	GTP	Chemical		bind					ARF	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_8	15657398	A favored current model for how this coupling is achieved, known as the priming complex model ( ), proposes that the activated (GTP-bound) form of an ADP ribosylation factor (ARF) - like small GTPase promotes the binding of coat proteins onto the cytoplasmic domain of transmembrane cargo proteins to form a key intermediate that drives both cargo sorting and vesicle formation.	bind
35877	3	10172	6	11	NULL	NULL	NULL	ARF	GP		is a type of					small GTPase	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_8	15657398	A favored current model for how this coupling is achieved, known as the priming complex model ( ), proposes that the activated (GTP-bound) form of an ADP ribosylation factor (ARF) - like small GTPase promotes the binding of coat proteins onto the cytoplasmic domain of transmembrane cargo proteins to form a key intermediate that drives both cargo sorting and vesicle formation.	bind
35879	4	10172	6	11	NULL	NULL	NULL	coat proteins	GP		bind					transmembrane cargo proteins	GP		cytoplasmic domain		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_8	15657398	A favored current model for how this coupling is achieved, known as the priming complex model ( ), proposes that the activated (GTP-bound) form of an ADP ribosylation factor (ARF) - like small GTPase promotes the binding of coat proteins onto the cytoplasmic domain of transmembrane cargo proteins to form a key intermediate that drives both cargo sorting and vesicle formation.	bind
35881	5	10172	6	11	NULL	NULL	NULL	statement 2	Process		promotes					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_8	15657398	A favored current model for how this coupling is achieved, known as the priming complex model ( ), proposes that the activated (GTP-bound) form of an ADP ribosylation factor (ARF) - like small GTPase promotes the binding of coat proteins onto the cytoplasmic domain of transmembrane cargo proteins to form a key intermediate that drives both cargo sorting and vesicle formation.	bind
35887	6	10172	6	11	NULL	NULL	NULL	statement 4	Process		forms 					intermediate	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_8	15657398	A favored current model for how this coupling is achieved, known as the priming complex model ( ), proposes that the activated (GTP-bound) form of an ADP ribosylation factor (ARF) - like small GTPase promotes the binding of coat proteins onto the cytoplasmic domain of transmembrane cargo proteins to form a key intermediate that drives both cargo sorting and vesicle formation.	bind
35889	7	10172	6	11	NULL	NULL	NULL	statement 6	Process		plays a role in					cargo sorting	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_8	15657398	A favored current model for how this coupling is achieved, known as the priming complex model ( ), proposes that the activated (GTP-bound) form of an ADP ribosylation factor (ARF) - like small GTPase promotes the binding of coat proteins onto the cytoplasmic domain of transmembrane cargo proteins to form a key intermediate that drives both cargo sorting and vesicle formation.	bind
35891	8	10172	6	11	NULL	NULL	NULL	statement 6	Process		plays a role in					vesicle formation	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_8	15657398	A favored current model for how this coupling is achieved, known as the priming complex model ( ), proposes that the activated (GTP-bound) form of an ADP ribosylation factor (ARF) - like small GTPase promotes the binding of coat proteins onto the cytoplasmic domain of transmembrane cargo proteins to form a key intermediate that drives both cargo sorting and vesicle formation.	bind
44096	1	10172	7	NULL	NULL	0	NULL	coat proteins	NULL		bind	NULL				transmembrane cargo proteins	NULL		cytoplasmic domain		NULL		0	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_8	15657398	A favored current model for how this coupling is achieved, known as the priming complex model ( ), proposes that the activated (GTP-bound) form of an ADP ribosylation factor (ARF) - like small GTPase promotes the binding of coat proteins onto the cytoplasmic domain of transmembrane cargo proteins to form a key intermediate that drives both cargo sorting and vesicle formation.	bind
44098	2	10172	7	NULL	NULL	0	NULL	ARF	NULL	activated	promotes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_8	15657398	A favored current model for how this coupling is achieved, known as the priming complex model ( ), proposes that the activated (GTP-bound) form of an ADP ribosylation factor (ARF) - like small GTPase promotes the binding of coat proteins onto the cytoplasmic domain of transmembrane cargo proteins to form a key intermediate that drives both cargo sorting and vesicle formation.	bind
44100	3	10172	7	NULL	NULL	0	NULL	small GTPase	NULL		promotes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_8	15657398	A favored current model for how this coupling is achieved, known as the priming complex model ( ), proposes that the activated (GTP-bound) form of an ADP ribosylation factor (ARF) - like small GTPase promotes the binding of coat proteins onto the cytoplasmic domain of transmembrane cargo proteins to form a key intermediate that drives both cargo sorting and vesicle formation.	bind
44101	4	10172	7	NULL	NULL	0	NULL	statement 1	NULL		forms	NULL				key intermediate	NULL				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_8	15657398	A favored current model for how this coupling is achieved, known as the priming complex model ( ), proposes that the activated (GTP-bound) form of an ADP ribosylation factor (ARF) - like small GTPase promotes the binding of coat proteins onto the cytoplasmic domain of transmembrane cargo proteins to form a key intermediate that drives both cargo sorting and vesicle formation.	bind
44115	5	10172	7	NULL	NULL	0	NULL	statement 4	NULL		drives	NULL				cargo sorting	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_8	15657398	A favored current model for how this coupling is achieved, known as the priming complex model ( ), proposes that the activated (GTP-bound) form of an ADP ribosylation factor (ARF) - like small GTPase promotes the binding of coat proteins onto the cytoplasmic domain of transmembrane cargo proteins to form a key intermediate that drives both cargo sorting and vesicle formation.	bind
44116	6	10172	7	NULL	NULL	0	NULL	statement 4	NULL		drives	NULL				vesicle formation	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_8	15657398	A favored current model for how this coupling is achieved, known as the priming complex model ( ), proposes that the activated (GTP-bound) form of an ADP ribosylation factor (ARF) - like small GTPase promotes the binding of coat proteins onto the cytoplasmic domain of transmembrane cargo proteins to form a key intermediate that drives both cargo sorting and vesicle formation.	bind
44119	7	10172	7	NULL	NULL	0	NULL	ARF	NULL	activated	is	NULL				ADP ribosylation factor	NULL	GTP-bound form of			NULL		0	NULL	NULL	NULL	gw70_cellbiol_168_2_281_s_8	15657398	A favored current model for how this coupling is achieved, known as the priming complex model ( ), proposes that the activated (GTP-bound) form of an ADP ribosylation factor (ARF) - like small GTPase promotes the binding of coat proteins onto the cytoplasmic domain of transmembrane cargo proteins to form a key intermediate that drives both cargo sorting and vesicle formation.	bind
35895	1	10173	6	11	NULL	NULL	NULL	RepA initiator	GP		does not bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_5_533_s_140	12586394	A feature of Rep initiators is that, opposite to DnaA (see above), they do not  bind ATP.	bind
35896	2	10173	6	11	NULL	NULL	NULL	DnaA	GP		bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_5_533_s_140	12586394	A feature of Rep initiators is that, opposite to DnaA (see above), they do not  bind ATP.	bind
44127	1	10173	7	NULL	NULL	0	NULL	Rep initiators	NULL		does not bind	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_5_533_s_140	12586394	A feature of Rep initiators is that, opposite to DnaA (see above), they do not  bind ATP.	bind
44128	2	10173	7	NULL	NULL	0	NULL	DnaA	NULL		bind	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_5_533_s_140	12586394	A feature of Rep initiators is that, opposite to DnaA (see above), they do not  bind ATP.	bind
35899	1	10175	6	11	NULL	NULL	NULL	vWF	GP		bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_1_425_s_162	11756664	A feature that clearly distinguishes collagen-bound from self-assembled VWF multimers is the stability of interaction with the surface, because homotypic VWF interactions are reversible in a few minutes whereas VWF binding to collagen is apparently irreversible on a comparable time scale.	bind
35901	2	10175	6	11	NULL	NULL	NULL	vWF	GP		interacts with					vWF	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_1_425_s_162	11756664	A feature that clearly distinguishes collagen-bound from self-assembled VWF multimers is the stability of interaction with the surface, because homotypic VWF interactions are reversible in a few minutes whereas VWF binding to collagen is apparently irreversible on a comparable time scale.	bind
35912	3	10175	6	11	NULL	NULL	NULL	statement 1	Process		is reversible as compared to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_1_425_s_162	11756664	A feature that clearly distinguishes collagen-bound from self-assembled VWF multimers is the stability of interaction with the surface, because homotypic VWF interactions are reversible in a few minutes whereas VWF binding to collagen is apparently irreversible on a comparable time scale.	bind
44129	1	10175	7	NULL	NULL	0	NULL	VWF	NULL		bind	NULL				collagen	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_1_425_s_162	11756664	A feature that clearly distinguishes collagen-bound from self-assembled VWF multimers is the stability of interaction with the surface, because homotypic VWF interactions are reversible in a few minutes whereas VWF binding to collagen is apparently irreversible on a comparable time scale.	bind
44130	2	10175	7	10	NULL	0	NULL	vWF	NULL		interacts with	NULL				vWF	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_1_425_s_162	11756664	A feature that clearly distinguishes collagen-bound from self-assembled VWF multimers is the stability of interaction with the surface, because homotypic VWF interactions are reversible in a few minutes whereas VWF binding to collagen is apparently irreversible on a comparable time scale.	bind
44131	3	10175	7	10	NULL	0	NULL	statement 1	NULL		\tis reversible as compared to	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_1_425_s_162	11756664	A feature that clearly distinguishes collagen-bound from self-assembled VWF multimers is the stability of interaction with the surface, because homotypic VWF interactions are reversible in a few minutes whereas VWF binding to collagen is apparently irreversible on a comparable time scale.	bind
35965	1	10177	6	11	NULL	NULL	NULL	LDL	Chemical	plasma	bind					PBE-94	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_110_9_2268712_s_2	2268712	A few alternatives of the binding of healthy patients plasma low density  lipoproteins (LDL) with anion exchanger PBE-94 were revealed.	bind
44134	1	10177	7	NULL	NULL	0	NULL	LDL	NULL	plasma	bind	NULL				PBE-94	NULL				NULL		0	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_110_9_2268712_s_2	2268712	A few alternatives of the binding of healthy patients plasma low density  lipoproteins (LDL) with anion exchanger PBE-94 were revealed.	bind
35966	1	10178	6	11	NULL	NULL	NULL	nuclear factor I	GP		bind					alpha1(I) collagen	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
35967	2	10178	6	11	NULL	NULL	NULL	statement 1	Process		activate					alpha1(I) collagen	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
35968	3	10178	6	11	NULL	NULL	NULL	Sp1	GP		bind					alpha2(I) collagen	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
35969	4	10178	6	11	NULL	NULL	NULL	statement 3	Process		activate					alpha2(I) collagen	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
35970	5	10178	6	11	NULL	NULL	NULL	nuclear factor I	GP		bind					alpha2(I) collagen	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
35971	6	10178	6	11	NULL	NULL	NULL	statement 5	Process		activate					alpha2(I) collagen	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
35972	7	10178	6	11	NULL	NULL	NULL	Sp1	GP		bind					alpha1(I) collagen	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
35973	8	10178	6	11	NULL	NULL	NULL	statement 7	Process		activates					alpha1(I) collagen	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
35975	9	10178	6	11	NULL	NULL	NULL	Sp1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
35977	10	10178	6	11	NULL	NULL	NULL	nuclear factor I	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
44135	1	10178	7	NULL	NULL	0	NULL	nuclear factor I 	NULL		bind	NULL				alpha1 collagen	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
44136	2	10178	7	NULL	NULL	0	NULL	 nuclear factor I	NULL		bind	NULL				alpha2 collagen	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
44137	3	10178	7	NULL	NULL	0	NULL	statement 1	NULL		activate	NULL				alpha1 collagen	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
44138	4	10178	7	NULL	NULL	0	NULL	statement 2	NULL		activate	NULL				alpha2 collagen	NULL			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
44139	5	10178	7	NULL	NULL	0	NULL	 Sp1	NULL		bind	NULL				alpha1 collagen	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
44140	6	10178	7	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				alpha2 collagen	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
44141	7	10178	7	NULL	NULL	0	NULL	statement 5	NULL		activate	NULL				alpha1 collagen	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
44142	8	10178	7	NULL	NULL	0	NULL	statement 6	NULL		activate	NULL				alpha2 collagen	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
49665	9	10178	7	10	NULL	0	NULL	Sp1	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
49666	10	10178	7	10	NULL	0	NULL	nuclear factor I	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_15_15639_s_19	14722113	A few common transcription factors such as nuclear factor I and Sp1 are known to bind and activate both the alpha1(I) ( ) and the alpha2(I) collagen promoters ( - ).	bind
35979	1	10180	6	11	NULL	NULL	NULL	adenovirus	Organism		bind					vimentin	GP				NULL	HeLa cells	NULL	NULL	NULL	NULL	gw60_infectimmun_68_4_1787_s_278	10722565	A few examples of this have been observed, including the deleterious effects of adenovirus and human papillomavirus binding to vimentin and cytokeratins in HeLa cells and human keratinocytes, respectively ( 6,  47).	bind
35980	2	10180	6	11	NULL	NULL	NULL	papillomavirus	Organism	human	bind					cytokeratin	GP				NULL	human keratinocytes	NULL	NULL	NULL	NULL	gw60_infectimmun_68_4_1787_s_278	10722565	A few examples of this have been observed, including the deleterious effects of adenovirus and human papillomavirus binding to vimentin and cytokeratins in HeLa cells and human keratinocytes, respectively ( 6,  47).	bind
44143	1	10180	7	NULL	NULL	0	NULL	adenovirus	NULL		bind	NULL				vimentin	NULL				NULL	HeLa cells	NULL	NULL	NULL	NULL	gw60_infectimmun_68_4_1787_s_278	10722565	A few examples of this have been observed, including the deleterious effects of adenovirus and human papillomavirus binding to vimentin and cytokeratins in HeLa cells and human keratinocytes, respectively ( 6,  47).	bind
44150	2	10180	7	10	NULL	0	NULL	papillomavirus	NULL	human	bind	NULL				cytokeratins	NULL				NULL	human keratinocytes	NULL	NULL	NULL	NULL	gw60_infectimmun_68_4_1787_s_278	10722565	A few examples of this have been observed, including the deleterious effects of adenovirus and human papillomavirus binding to vimentin and cytokeratins in HeLa cells and human keratinocytes, respectively ( 6,  47).	bind
36103	1	10181	6	11	NULL	NULL	NULL	E1 tetramers	GP		bind					E2	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_69_0_961_s_611	10966480	A few molecules of kinase can rapidly inactivate the multiple E1 tetramers bound  to E2, and it has been proposed that the tightly bound kinase dimer may move by a  "`hand-over-hand"` mechanism around the surface of the E2 core, thereby encountering  (and phosphorylating) the E1  subunits, a process facilitated by the flexible linkers  in the E2p chain ( 147).	bind
37214	2	10181	6	11	NULL	NULL	NULL	kinase	GP		inactivate		rapidly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_69_0_961_s_611	10966480	A few molecules of kinase can rapidly inactivate the multiple E1 tetramers bound  to E2, and it has been proposed that the tightly bound kinase dimer may move by a  "`hand-over-hand"` mechanism around the surface of the E2 core, thereby encountering  (and phosphorylating) the E1  subunits, a process facilitated by the flexible linkers  in the E2p chain ( 147).	bind
37215	3	10181	6	11	NULL	NULL	NULL	kinase dimer	GP		bind		tightly			E2 core	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_69_0_961_s_611	10966480	A few molecules of kinase can rapidly inactivate the multiple E1 tetramers bound  to E2, and it has been proposed that the tightly bound kinase dimer may move by a  "`hand-over-hand"` mechanism around the surface of the E2 core, thereby encountering  (and phosphorylating) the E1  subunits, a process facilitated by the flexible linkers  in the E2p chain ( 147).	bind
37216	5	10181	6	11	NULL	NULL	NULL	statement 4	Process		encounter					E1 subunit	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_69_0_961_s_611	10966480	A few molecules of kinase can rapidly inactivate the multiple E1 tetramers bound  to E2, and it has been proposed that the tightly bound kinase dimer may move by a  "`hand-over-hand"` mechanism around the surface of the E2 core, thereby encountering  (and phosphorylating) the E1  subunits, a process facilitated by the flexible linkers  in the E2p chain ( 147).	bind
37217	6	10181	6	11	NULL	NULL	NULL	statement 5	GP		phosphorylates					E1 subunit	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_69_0_961_s_611	10966480	A few molecules of kinase can rapidly inactivate the multiple E1 tetramers bound  to E2, and it has been proposed that the tightly bound kinase dimer may move by a  "`hand-over-hand"` mechanism around the surface of the E2 core, thereby encountering  (and phosphorylating) the E1  subunits, a process facilitated by the flexible linkers  in the E2p chain ( 147).	bind
37305	4	10181	6	11	NULL	NULL	NULL	statement 3	GP		move around					E2 core	GP	surface of			NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_69_0_961_s_611	10966480	A few molecules of kinase can rapidly inactivate the multiple E1 tetramers bound  to E2, and it has been proposed that the tightly bound kinase dimer may move by a  "`hand-over-hand"` mechanism around the surface of the E2 core, thereby encountering  (and phosphorylating) the E1  subunits, a process facilitated by the flexible linkers  in the E2p chain ( 147).	bind
57479	7	10181	6	11	NULL	NULL	NULL	E2p chain	GP		facilitates			flexible linkers		statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_69_0_961_s_611	10966480	A few molecules of kinase can rapidly inactivate the multiple E1 tetramers bound  to E2, and it has been proposed that the tightly bound kinase dimer may move by a  "`hand-over-hand"` mechanism around the surface of the E2 core, thereby encountering  (and phosphorylating) the E1  subunits, a process facilitated by the flexible linkers  in the E2p chain ( 147).	bind
44151	1	10181	7	10	NULL	0	NULL	E1 tetramers			bind					E2					NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_69_0_961_s_611	10966480	A few molecules of kinase can rapidly inactivate the multiple E1 tetramers bound  to E2, and it has been proposed that the tightly bound kinase dimer may move by a  "`hand-over-hand"` mechanism around the surface of the E2 core, thereby encountering  (and phosphorylating) the E1  subunits, a process facilitated by the flexible linkers  in the E2p chain ( 147).	bind
44152	2	10181	7	NULL	NULL	0	NULL	kinase	NULL		inactivate	NULL	rapidly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_69_0_961_s_611	10966480	A few molecules of kinase can rapidly inactivate the multiple E1 tetramers bound  to E2, and it has been proposed that the tightly bound kinase dimer may move by a  "`hand-over-hand"` mechanism around the surface of the E2 core, thereby encountering  (and phosphorylating) the E1  subunits, a process facilitated by the flexible linkers  in the E2p chain ( 147).	bind
44153	3	10181	7	NULL	NULL	0	NULL	kinase dimer	NULL		bind	NULL	tightly			E2 core	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_69_0_961_s_611	10966480	A few molecules of kinase can rapidly inactivate the multiple E1 tetramers bound  to E2, and it has been proposed that the tightly bound kinase dimer may move by a  "`hand-over-hand"` mechanism around the surface of the E2 core, thereby encountering  (and phosphorylating) the E1  subunits, a process facilitated by the flexible linkers  in the E2p chain ( 147).	bind
44154	4	10181	7	NULL	NULL	0	NULL	statement 3	NULL		move around	NULL				E2 core	NULL	surface of			NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_69_0_961_s_611	10966480	A few molecules of kinase can rapidly inactivate the multiple E1 tetramers bound  to E2, and it has been proposed that the tightly bound kinase dimer may move by a  "`hand-over-hand"` mechanism around the surface of the E2 core, thereby encountering  (and phosphorylating) the E1  subunits, a process facilitated by the flexible linkers  in the E2p chain ( 147).	bind
44155	6	10181	7	10	NULL	0	NULL	statement 5			phosphorylate					E1 subunits					NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_69_0_961_s_611	10966480	A few molecules of kinase can rapidly inactivate the multiple E1 tetramers bound  to E2, and it has been proposed that the tightly bound kinase dimer may move by a  "`hand-over-hand"` mechanism around the surface of the E2 core, thereby encountering  (and phosphorylating) the E1  subunits, a process facilitated by the flexible linkers  in the E2p chain ( 147).	bind
44156	7	10181	7	10	NULL	0	NULL	E2p chain			facilitate			flexible linkers		statement 6					NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_69_0_961_s_611	10966480	A few molecules of kinase can rapidly inactivate the multiple E1 tetramers bound  to E2, and it has been proposed that the tightly bound kinase dimer may move by a  "`hand-over-hand"` mechanism around the surface of the E2 core, thereby encountering  (and phosphorylating) the E1  subunits, a process facilitated by the flexible linkers  in the E2p chain ( 147).	bind
44157	5	10181	7	10	NULL	0	NULL	statement 4			encounter					E1 subunits					NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_69_0_961_s_611	10966480	A few molecules of kinase can rapidly inactivate the multiple E1 tetramers bound  to E2, and it has been proposed that the tightly bound kinase dimer may move by a  "`hand-over-hand"` mechanism around the surface of the E2 core, thereby encountering  (and phosphorylating) the E1  subunits, a process facilitated by the flexible linkers  in the E2p chain ( 147).	bind
35981	1	10182	6	11	NULL	NULL	NULL	HFE	GP		bind					transferrin receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_2_205_s_210	12594948	A few perform unrelated functions, however, such as HFE, which binds to the transferrin receptor and regulates iron homeostasis  (Feder et al., 1998  ).	bind
35982	2	10182	6	11	NULL	NULL	NULL	statement 1	Process		regulates					iron	Chemical	homeostasis of 			NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_2_205_s_210	12594948	A few perform unrelated functions, however, such as HFE, which binds to the transferrin receptor and regulates iron homeostasis  (Feder et al., 1998  ).	bind
44158	1	10182	7	NULL	NULL	0	NULL	HFE	NULL		binds to	NULL				transferrin receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_18_2_205_s_210	12594948	A few perform unrelated functions, however, such as HFE, which binds to the transferrin receptor and regulates iron homeostasis  (Feder et al., 1998  ).	bind
44159	2	10182	7	10	NULL	0	NULL	statement 1	NULL		regulates	NULL				iron	NULL	homeostasis of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_2_205_s_210	12594948	A few perform unrelated functions, however, such as HFE, which binds to the transferrin receptor and regulates iron homeostasis  (Feder et al., 1998  ).	bind
35983	1	10183	6	11	NULL	NULL	NULL	RPL3	GP		is 					ribosomal protein L3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2066_s_294	10688653	A few ribosomal protein genes, including  RPL3 (encoding ribosomal protein L3), have no site for Rap1 but have a single Abf1-binding site instead ( 3,  6,  8).	bind
35984	2	10183	6	11	NULL	NULL	NULL	RPL3	GP		have no site for					Rap1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2066_s_294	10688653	A few ribosomal protein genes, including  RPL3 (encoding ribosomal protein L3), have no site for Rap1 but have a single Abf1-binding site instead ( 3,  6,  8).	bind
35985	3	10183	6	11	NULL	NULL	NULL	RPL3	GP		have 							single		Abf1-binding site	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2066_s_294	10688653	A few ribosomal protein genes, including  RPL3 (encoding ribosomal protein L3), have no site for Rap1 but have a single Abf1-binding site instead ( 3,  6,  8).	bind
44160	1	10183	7	10	NULL	0	NULL	RPL3 	NULL		contains	NULL					NULL			Abf1-binding site	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2066_s_294	10688653	A few ribosomal protein genes, including  RPL3 (encoding ribosomal protein L3), have no site for Rap1 but have a single Abf1-binding site instead ( 3,  6,  8).	bind
44161	2	10183	7	NULL	NULL	0	NULL	RPL3	NULL		is	NULL				encoding ribosomal protein L3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2066_s_294	10688653	A few ribosomal protein genes, including  RPL3 (encoding ribosomal protein L3), have no site for Rap1 but have a single Abf1-binding site instead ( 3,  6,  8).	bind
44162	3	10183	7	10	NULL	0	NULL	RPL3	NULL		have no site for	NULL				Rap1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2066_s_294	10688653	A few ribosomal protein genes, including  RPL3 (encoding ribosomal protein L3), have no site for Rap1 but have a single Abf1-binding site instead ( 3,  6,  8).	bind
35989	1	10185	6	11	NULL	NULL	NULL	EBP2	GP	human	bind		specifically			EBNA1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4934_s_18	15923612	A few years ago, we identified a previously uncharacterized cellular protein that we called EBNA1 binding protein 2 (EBP2) from a two-hybrid screening for human proteins that specifically bind EBNA1 ( ).	bind
35990	2	10185	6	11	NULL	NULL	NULL	EBP2	GP		is					EBNA1 binding protein 2 	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4934_s_18	15923612	A few years ago, we identified a previously uncharacterized cellular protein that we called EBNA1 binding protein 2 (EBP2) from a two-hybrid screening for human proteins that specifically bind EBNA1 ( ).	bind
44164	1	10185	7	10	NULL	0	NULL	EBP2	NULL	human	bind	NULL	specifically			EBNA1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_4934_s_18	15923612	A few years ago, we identified a previously uncharacterized cellular protein that we called EBNA1 binding protein 2 (EBP2) from a two-hybrid screening for human proteins that specifically bind EBNA1 ( ).	bind
44165	2	10185	7	NULL	NULL	0	NULL	EBP2	NULL		is	NULL				EBNA1 binding protein 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_12_4934_s_18	15923612	A few years ago, we identified a previously uncharacterized cellular protein that we called EBNA1 binding protein 2 (EBP2) from a two-hybrid screening for human proteins that specifically bind EBNA1 ( ).	bind
35992	1	10186	6	11	NULL	NULL	NULL	FAP	GP	M. avium	bind		may			fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_3_1_37_s_37	11226852	A fibronectin attachment protein (FAP) has been described on  M. avium and it has been hypothesized that FAP would bind fibronectin that could work as a bridge between the bacterial and the mucosal cell.	bind
35993	2	10186	6	11	NULL	NULL	NULL	FAP	GP		is					fibronectin attachment protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_3_1_37_s_37	11226852	A fibronectin attachment protein (FAP) has been described on  M. avium and it has been hypothesized that FAP would bind fibronectin that could work as a bridge between the bacterial and the mucosal cell.	bind
36301	3	10186	6	11	NULL	NULL	NULL	bacterial cell	Organism		bridge between					mucosal cell	Cell				NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_3_1_37_s_37	11226852	A fibronectin attachment protein (FAP) has been described on  M. avium and it has been hypothesized that FAP would bind fibronectin that could work as a bridge between the bacterial and the mucosal cell.	bind
36302	4	10186	6	11	NULL	NULL	NULL	statement 1	Process		leads to		may			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_3_1_37_s_37	11226852	A fibronectin attachment protein (FAP) has been described on  M. avium and it has been hypothesized that FAP would bind fibronectin that could work as a bridge between the bacterial and the mucosal cell.	bind
44166	1	10186	7	10	NULL	0	NULL	FAP		M. avium	bind		may			fibronectin					NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_3_1_37_s_37	11226852	A fibronectin attachment protein (FAP) has been described on  M. avium and it has been hypothesized that FAP would bind fibronectin that could work as a bridge between the bacterial and the mucosal cell.	bind
44167	2	10186	7	NULL	NULL	0	NULL	FAP	NULL		is	NULL				fibronectin attachment protein	NULL				NULL		0	NULL	NULL	NULL	gw60_microbesinfect_3_1_37_s_37	11226852	A fibronectin attachment protein (FAP) has been described on  M. avium and it has been hypothesized that FAP would bind fibronectin that could work as a bridge between the bacterial and the mucosal cell.	bind
44182	3	10186	7	NULL	NULL	0	NULL	bacterial cell	NULL		bridge between	NULL				mucosal cell	NULL				NULL		0	NULL	NULL	NULL	gw60_microbesinfect_3_1_37_s_37	11226852	A fibronectin attachment protein (FAP) has been described on  M. avium and it has been hypothesized that FAP would bind fibronectin that could work as a bridge between the bacterial and the mucosal cell.	bind
44183	4	10186	7	10	NULL	0	NULL	statement 1			leads to		may			statement 3					NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_3_1_37_s_37	11226852	A fibronectin attachment protein (FAP) has been described on  M. avium and it has been hypothesized that FAP would bind fibronectin that could work as a bridge between the bacterial and the mucosal cell.	bind
35994	1	10187	6	11	NULL	NULL	NULL	fibronectin-binding protein	GP	Streptococcus equi	bind					collagen	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_biochem-biophys-res-commun_340_2_16376297_s_1	16376297	A fibronectin-binding protein from Streptococcus equi binds collagen and modulates cell-mediated collagen gel contraction..	bind
35995	2	10187	6	11	NULL	NULL	NULL	cell	Cell		mediates					collagen gel 	GP	contraction of			NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_biochem-biophys-res-commun_340_2_16376297_s_1	16376297	A fibronectin-binding protein from Streptococcus equi binds collagen and modulates cell-mediated collagen gel contraction..	bind
49667	3	10187	6	11	NULL	NULL	NULL	statement 1	Process		modulates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_biochem-biophys-res-commun_340_2_16376297_s_1	16376297	A fibronectin-binding protein from Streptococcus equi binds collagen and modulates cell-mediated collagen gel contraction..	bind
44184	1	10187	7	NULL	NULL	0	NULL	fibronectin-binding protein	NULL	Streptococcus equi	binds	NULL				collagen	NULL				NULL		0	NULL	NULL	NULL	abs-batch0570-0579_biochem-biophys-res-commun_340_2_16376297_s_1	16376297	A fibronectin-binding protein from Streptococcus equi binds collagen and modulates cell-mediated collagen gel contraction..	bind
44185	2	10187	7	NULL	NULL	0	NULL	cell	NULL		mediates	NULL				collagen gel 	NULL	contraction of			NULL		0	NULL	NULL	NULL	abs-batch0570-0579_biochem-biophys-res-commun_340_2_16376297_s_1	16376297	A fibronectin-binding protein from Streptococcus equi binds collagen and modulates cell-mediated collagen gel contraction..	bind
44186	3	10187	7	NULL	NULL	0	NULL	statement 1	NULL		modulates	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	abs-batch0570-0579_biochem-biophys-res-commun_340_2_16376297_s_1	16376297	A fibronectin-binding protein from Streptococcus equi binds collagen and modulates cell-mediated collagen gel contraction..	bind
35997	1	10189	6	11	NULL	NULL	NULL	HGFSF	GP	wt	bind					heparin	Chemical	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_3_125_s_280	9443912	A figure showing BIAcore analysis of wt-HGFSF and HP1 binding to immobilised heparin is published with this paper on the internet.	bind
35999	2	10189	6	11	NULL	NULL	NULL	HP1	GP		bind					heparin	Chemical	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_3_125_s_280	9443912	A figure showing BIAcore analysis of wt-HGFSF and HP1 binding to immobilised heparin is published with this paper on the internet.	bind
44188	1	10189	7	NULL	NULL	0	NULL	HGFSF	NULL	wt	bind	NULL				heparin	NULL	immobilized			NULL		0	NULL	NULL	NULL	gw60_currbiol_8_3_125_s_280	9443912	A figure showing BIAcore analysis of wt-HGFSF and HP1 binding to immobilised heparin is published with this paper on the internet.	bind
44189	2	10189	7	NULL	NULL	0	NULL	HP1	NULL		bind	NULL				heparin	NULL	immobilized			NULL		0	NULL	NULL	NULL	gw60_currbiol_8_3_125_s_280	9443912	A figure showing BIAcore analysis of wt-HGFSF and HP1 binding to immobilised heparin is published with this paper on the internet.	bind
36016	1	10190	6	11	NULL	NULL	NULL	[125]E r-1	GP		bind					p143	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1445_s_184	10749941	A filled arrowhead indicates [125]E r-1 binding to p143.	bind
44190	1	10190	7	NULL	NULL	0	NULL	[125]E r-1	NULL		bind	NULL				p143	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1445_s_184	10749941	A filled arrowhead indicates [125]E r-1 binding to p143.	bind
36017	1	10191	6	11	NULL	NULL	NULL	AnCOB protein extract	GP		bind		tightly			AnCOB precursor	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_17_8994_s_130	9256423	A filter binding assay (Fig.  4) showed that the AnCOB protein extract bound tightly to the AnCOB precursor ( Kd = 3 nM) and very poorly to a precursor containing the AnOX2 intron.	bind
36018	2	10191	6	11	NULL	NULL	NULL	AnCOB protein extract	GP		bind		poorly			AnOX2 intron precursor	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_17_8994_s_130	9256423	A filter binding assay (Fig.  4) showed that the AnCOB protein extract bound tightly to the AnCOB precursor ( Kd = 3 nM) and very poorly to a precursor containing the AnOX2 intron.	bind
44191	1	10191	7	NULL	NULL	0	NULL	AnCOB protein extract	NULL		bind	NULL	tightly			AnCOB precursor	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_94_17_8994_s_130	9256423	A filter binding assay (Fig.  4) showed that the AnCOB protein extract bound tightly to the AnCOB precursor ( Kd = 3 nM) and very poorly to a precursor containing the AnOX2 intron.	bind
44192	2	10191	7	10	NULL	0	NULL	 AnCOB protein extract			bind		poorly			 AnOX2 intron precursor					NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_17_8994_s_130	9256423	A filter binding assay (Fig.  4) showed that the AnCOB protein extract bound tightly to the AnCOB precursor ( Kd = 3 nM) and very poorly to a precursor containing the AnOX2 intron.	bind
36020	1	10192	6	11	NULL	NULL	NULL	ATP	Chemical		bind					MutL	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_97_1_85_s_224	10199405	A filter binding assay using  - and  -32P-labeled  ATP that allows quantitation of the amounts of ATP and ADP bound  to MutL was employed to study the dynamics of nucleotide - protein interaction and  the rate-limiting step of ATP hydrolysis (see Experimental Procedures).	bind
36021	2	10192	6	11	NULL	NULL	NULL	ADP	Chemical		bind					MutL	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_97_1_85_s_224	10199405	A filter binding assay using  - and  -32P-labeled  ATP that allows quantitation of the amounts of ATP and ADP bound  to MutL was employed to study the dynamics of nucleotide - protein interaction and  the rate-limiting step of ATP hydrolysis (see Experimental Procedures).	bind
44198	1	10192	7	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				MutL	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_97_1_85_s_224	10199405	A filter binding assay using  - and  -32P-labeled  ATP that allows quantitation of the amounts of ATP and ADP bound  to MutL was employed to study the dynamics of nucleotide - protein interaction and  the rate-limiting step of ATP hydrolysis (see Experimental Procedures).	bind
44199	2	10192	7	NULL	NULL	0	NULL	ADP	NULL		bind	NULL				MutL	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_97_1_85_s_224	10199405	A filter binding assay using  - and  -32P-labeled  ATP that allows quantitation of the amounts of ATP and ADP bound  to MutL was employed to study the dynamics of nucleotide - protein interaction and  the rate-limiting step of ATP hydrolysis (see Experimental Procedures).	bind
36022	1	10193	6	11	NULL	NULL	NULL	4.5 RNA	NucleicAcid		bind					Ffh	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_180_2_271_s_102	10556722	A filter binding assay using purified Ffh and EF-G (1-91) confirmed in this study that the binding affinity of 4.5 RNA for Ffh and EF-G is quite different.	bind
36023	2	10193	6	11	NULL	NULL	NULL	4.5 RNA	NucleicAcid		bind					EF-G	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_180_2_271_s_102	10556722	A filter binding assay using purified Ffh and EF-G (1-91) confirmed in this study that the binding affinity of 4.5 RNA for Ffh and EF-G is quite different.	bind
49669	3	10193	6	11	NULL	NULL	NULL	statement 1	Process	affinity of	is different from					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_180_2_271_s_102	10556722	A filter binding assay using purified Ffh and EF-G (1-91) confirmed in this study that the binding affinity of 4.5 RNA for Ffh and EF-G is quite different.	bind
44200	1	10193	7	NULL	NULL	0	NULL	Ffh	NULL	purified	bind	NULL				4.5RNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_180_2_271_s_102	10556722	A filter binding assay using purified Ffh and EF-G (1-91) confirmed in this study that the binding affinity of 4.5 RNA for Ffh and EF-G is quite different.	bind
44201	2	10193	7	NULL	NULL	0	NULL	EF-G	NULL	purified	bind	NULL				4.5RNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_180_2_271_s_102	10556722	A filter binding assay using purified Ffh and EF-G (1-91) confirmed in this study that the binding affinity of 4.5 RNA for Ffh and EF-G is quite different.	bind
44202	3	10193	7	10	NULL	0	NULL	statement 1	NULL	affinity of	is different from	NULL				statement 2	NULL	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_180_2_271_s_102	10556722	A filter binding assay using purified Ffh and EF-G (1-91) confirmed in this study that the binding affinity of 4.5 RNA for Ffh and EF-G is quite different.	bind
36024	1	10194	6	11	NULL	NULL	NULL	trp repressor	GP		bind		specifically			DNA	NucleicAcid			operator	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_nucleic-acids-res_15_13_3299270_s_2	3299270	A filter binding assay was developed that allows measurement of specific  binding of trp repressor to operator DNA.	bind
44205	1	10194	7	NULL	NULL	0	NULL	trp repressor	NULL		bind	NULL	specifically			DNA	NULL			operator	NULL		0	NULL	NULL	NULL	abs-batch0650-0679_nucleic-acids-res_15_13_3299270_s_2	3299270	A filter binding assay was developed that allows measurement of specific  binding of trp repressor to operator DNA.	bind
36026	1	10196	6	11	NULL	NULL	NULL	VDR/RXR heterodimer	GP		bind					TRPV6 gene	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-endocrinol_20_6_16574738_s_11	16574738	A final  ChIP assay revealed that VDR/RXR heterodimer binding to the TRPV6 gene  was accompanied by both the recruitment of steroid receptor coactivator  1 as well as a broad change in histone 4 acetylation.	bind
36027	2	10196	6	11	NULL	NULL	NULL	statement 1	Process		occurs by					steroid receptor coactivator 1	GP	recruitment of			NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-endocrinol_20_6_16574738_s_11	16574738	A final  ChIP assay revealed that VDR/RXR heterodimer binding to the TRPV6 gene  was accompanied by both the recruitment of steroid receptor coactivator  1 as well as a broad change in histone 4 acetylation.	bind
36028	3	10196	6	11	NULL	NULL	NULL	statement 1	Process		occurs by					histone 4	GP	change in acetylation of			NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-endocrinol_20_6_16574738_s_11	16574738	A final  ChIP assay revealed that VDR/RXR heterodimer binding to the TRPV6 gene  was accompanied by both the recruitment of steroid receptor coactivator  1 as well as a broad change in histone 4 acetylation.	bind
36030	4	10196	6	11	NULL	NULL	NULL	statement 2	Process		occurs simultaneously with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_mol-endocrinol_20_6_16574738_s_11	16574738	A final  ChIP assay revealed that VDR/RXR heterodimer binding to the TRPV6 gene  was accompanied by both the recruitment of steroid receptor coactivator  1 as well as a broad change in histone 4 acetylation.	bind
44206	1	10196	7	NULL	NULL	0	NULL	VDR/RXR heterodimer	NULL		bind	NULL				TRPV6 gene	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_mol-endocrinol_20_6_16574738_s_11	16574738	A final  ChIP assay revealed that VDR/RXR heterodimer binding to the TRPV6 gene  was accompanied by both the recruitment of steroid receptor coactivator  1 as well as a broad change in histone 4 acetylation.	bind
44207	2	10196	7	NULL	NULL	0	NULL	statement 1	NULL		recruits	NULL				steroid receptor coactivator 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_mol-endocrinol_20_6_16574738_s_11	16574738	A final  ChIP assay revealed that VDR/RXR heterodimer binding to the TRPV6 gene  was accompanied by both the recruitment of steroid receptor coactivator  1 as well as a broad change in histone 4 acetylation.	bind
44208	3	10196	7	NULL	NULL	0	NULL	statement 1	NULL		changes	NULL				histone 4	NULL	acetylation of			NULL		0	NULL	NULL	NULL	abs-batch0700-0719_mol-endocrinol_20_6_16574738_s_11	16574738	A final  ChIP assay revealed that VDR/RXR heterodimer binding to the TRPV6 gene  was accompanied by both the recruitment of steroid receptor coactivator  1 as well as a broad change in histone 4 acetylation.	bind
57480	4	10196	7	10	NULL	0	NULL	statement 2			occurs simultaneously with					statement 3					NULL		0	NULL	NULL	NULL	abs-batch0700-0719_mol-endocrinol_20_6_16574738_s_11	16574738	A final  ChIP assay revealed that VDR/RXR heterodimer binding to the TRPV6 gene  was accompanied by both the recruitment of steroid receptor coactivator  1 as well as a broad change in histone 4 acetylation.	bind
36031	1	10197	6	11	NULL	NULL	NULL	Rab11-FIP1	GP		bind					Rab11a	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
36032	2	10197	6	11	NULL	NULL	NULL	Rab11-FIP1	GP		bind					Rab11b	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
36033	3	10197	6	11	NULL	NULL	NULL	Rab11-FIP1	GP		bind					Rab25	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
36034	4	10197	6	11	NULL	NULL	NULL	Rab11-FIP2	GP		bind					Rab11a	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
36036	5	10197	6	11	NULL	NULL	NULL	Rab11-FIP2	GP		bind					Rab11b	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
36038	6	10197	6	11	NULL	NULL	NULL	Rab11-FIP2	GP		bind					Rab25	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
36039	7	10197	6	11	NULL	NULL	NULL	Rab11-FIP3	GP		bind					Rab11a	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
36040	8	10197	6	11	NULL	NULL	NULL	Rab11-FIP3	GP		bind					Rab11b	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
36041	9	10197	6	11	NULL	NULL	NULL	Rab11-FIP3	GP		bind					Rab25	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
36043	10	10197	6	11	NULL	NULL	NULL	pp75/Rip11	GP		bind					Rab11a	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
36044	11	10197	6	11	NULL	NULL	NULL	pp75/Rip11	GP		bind					Rab11b	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
36046	12	10197	6	11	NULL	NULL	NULL	pp75/Rip11	GP		bind					Rab25	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
44209	1	10197	7	NULL	NULL	0	NULL	Rab11-FIP1	NULL		bind	NULL				Rab11a	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
44210	2	10197	7	NULL	NULL	0	NULL	Rab11-FIP1	NULL		bind	NULL				Rab11b	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
44211	3	10197	7	NULL	NULL	0	NULL	Rab11-FIP1	NULL		bind	NULL				Rab25	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
44261	4	10197	7	NULL	NULL	0	NULL	Rab11-FIP2	NULL		bind	NULL				Rab11a	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
44262	5	10197	7	NULL	NULL	0	NULL	Rab11-FIP2	NULL		bind	NULL				Rab11b	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
44263	6	10197	7	NULL	NULL	0	NULL	Rab11-FIP2	NULL		bind	NULL				Rab25	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
44264	7	10197	7	NULL	NULL	0	NULL	Rab11-FIP3	NULL		bind	NULL				Rab11a	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
44265	8	10197	7	NULL	NULL	0	NULL	Rab11-FIP3	NULL		bind	NULL				Rab11b	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
44266	9	10197	7	NULL	NULL	0	NULL	Rab11-FIP3	NULL		bind	NULL				Rab25	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
44271	10	10197	7	NULL	NULL	0	NULL	pp75/Rip11	NULL		bind	NULL				Rab11a	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
44272	11	10197	7	NULL	NULL	0	NULL	pp75/Rip11	NULL		bind	NULL				Rab11b	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
44273	12	10197	7	NULL	NULL	0	NULL	pp75/Rip11	NULL		bind	NULL				Rab25	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39067_s_343	11495908	A final explanation is that Rab11-FIP1, Rab11-FIP2, Rab11-FIP3, and pp75/Rip11 all bind Rab11a, Rab11b, or Rab25, but their binding may be reserved for different functions oriented in time.	bind
36050	1	10200	6	11	NULL	NULL	NULL	intimin-alpha	GP		contains		may			host cell surface receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2876_s_44	11704679	A final line of evidence that suggests that intimin may have a host cell surface receptor other than Tir comes from mutational analysis of the host cell binding domain of intimin-alpha.	bind
49668	2	10200	6	11	NULL	NULL	NULL	intimin	GP		contains					Tir	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2876_s_44	11704679	A final line of evidence that suggests that intimin may have a host cell surface receptor other than Tir comes from mutational analysis of the host cell binding domain of intimin-alpha.	bind
44276	1	10200	7	10	NULL	0	NULL	intimin-alpha	NULL		contains	NULL	may			host cell surface receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2876_s_44	11704679	A final line of evidence that suggests that intimin may have a host cell surface receptor other than Tir comes from mutational analysis of the host cell binding domain of intimin-alpha.	bind
44277	2	10200	7	NULL	NULL	0	NULL	intimin	NULL		contains	NULL				Tir	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2876_s_44	11704679	A final line of evidence that suggests that intimin may have a host cell surface receptor other than Tir comes from mutational analysis of the host cell binding domain of intimin-alpha.	bind
43388	1	10201	5	11	NULL	NULL	NULL	md130	Organism	mutation	does not affect		possibly			VA	MedicalProcedure	binding of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_5_2479_s_204	10051668	A final possibility is that the  md130 mutation does not affect VA binding; rather, it could indirectly decrease VA efficacy by counteracting the effect of VA binding or regulate the process disrupted by VAs.	bind
43389	2	10201	5	11	NULL	NULL	NULL	md130	Organism	mutation	counteracts		possibly			VA	MedicalProcedure	effect of;;binding of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_5_2479_s_204	10051668	A final possibility is that the  md130 mutation does not affect VA binding; rather, it could indirectly decrease VA efficacy by counteracting the effect of VA binding or regulate the process disrupted by VAs.	bind
43390	3	10201	5	11	NULL	NULL	NULL	md130	Organism	mutation	decrease		indirectly;;possibly			VA	MedicalProcedure	efficacy of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_5_2479_s_204	10051668	A final possibility is that the  md130 mutation does not affect VA binding; rather, it could indirectly decrease VA efficacy by counteracting the effect of VA binding or regulate the process disrupted by VAs.	bind
43393	4	10201	5	11	NULL	NULL	NULL	statement 2	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_5_2479_s_204	10051668	A final possibility is that the  md130 mutation does not affect VA binding; rather, it could indirectly decrease VA efficacy by counteracting the effect of VA binding or regulate the process disrupted by VAs.	bind
36330	1	10201	6	10	NULL	0	NULL	md130		mutation of	does not affect		possibly			VA		binding of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_5_2479_s_204	10051668	A final possibility is that the  md130 mutation does not affect VA binding; rather, it could indirectly decrease VA efficacy by counteracting the effect of VA binding or regulate the process disrupted by VAs.	bind
57481	2	10201	6	10	NULL	0	NULL	md130		mutation of	counteracts		possibly			VA		effect of;;binding of			NULL		0	NULL	NULL	NULL	gw60_pnas_96_5_2479_s_204	10051668	A final possibility is that the  md130 mutation does not affect VA binding; rather, it could indirectly decrease VA efficacy by counteracting the effect of VA binding or regulate the process disrupted by VAs.	bind
57482	3	10201	6	10	NULL	0	NULL	md130		mutation of	decrease		indirectly;;possibly \t			VA		efficacy of			NULL		0	NULL	NULL	NULL	gw60_pnas_96_5_2479_s_204	10051668	A final possibility is that the  md130 mutation does not affect VA binding; rather, it could indirectly decrease VA efficacy by counteracting the effect of VA binding or regulate the process disrupted by VAs.	bind
57483	4	10201	6	10	NULL	0	NULL	statement 2			leads to					statement 3					NULL		0	NULL	NULL	NULL	gw60_pnas_96_5_2479_s_204	10051668	A final possibility is that the  md130 mutation does not affect VA binding; rather, it could indirectly decrease VA efficacy by counteracting the effect of VA binding or regulate the process disrupted by VAs.	bind
43395	1	10202	5	11	NULL	NULL	NULL				bind			HisRS-related domain		tRNA	NucleicAcid	uncharged			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_22_22820_s_37	15010461	A final proposed role for the extreme carboxyl terminus of Gcn2p is to facilitate binding of the HisRS-related domain to uncharged tRNA ( ).	bind
43396	2	10202	5	11	NULL	NULL	NULL	Gcn2p	GP		facilitates		possibly	carboxyl terminus		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_22_22820_s_37	15010461	A final proposed role for the extreme carboxyl terminus of Gcn2p is to facilitate binding of the HisRS-related domain to uncharged tRNA ( ).	bind
36361	1	10202	6	NULL	NULL	0	NULL		NULL		bind	NULL		HisRS-related domain		tRNA	NULL	uncharged			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_22_22820_s_37	15010461	A final proposed role for the extreme carboxyl terminus of Gcn2p is to facilitate binding of the HisRS-related domain to uncharged tRNA ( ).	bind
36362	2	10202	6	10	NULL	0	NULL	Gcn2p			facilitate		possibly	carboxyl terminus		statement 1					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_22_22820_s_37	15010461	A final proposed role for the extreme carboxyl terminus of Gcn2p is to facilitate binding of the HisRS-related domain to uncharged tRNA ( ).	bind
43397	1	10203	5	NULL	NULL	0	NULL	SAP97	NULL		is important for	NULL		GK domain		presynaptic effects	NULL	transducing			NULL		0	NULL	NULL	NULL	gw70_jneurosci_26_8_2343_s_358	16495462	A final region of SAP97 found to be important for transducing its presynaptic effects is the GK domain, which binds members of the GK associated protein/SAP90/PSD-95-associated protein (GKAP/SAPAP) family (Kim et al., 1997 ; Takeuchi et al., 1997 ) and SPAR/SPAL, an actin binding protein with RapGAP activity (Pak et al., 2001 ; Roy et al., 2002 ).	bind
43440	2	10203	5	NULL	NULL	0	NULL	SAP97	NULL		bind	NULL		GK domain		GKAP/SAPAP family	NULL	members of			NULL		0	NULL	NULL	NULL	gw70_jneurosci_26_8_2343_s_358	16495462	A final region of SAP97 found to be important for transducing its presynaptic effects is the GK domain, which binds members of the GK associated protein/SAP90/PSD-95-associated protein (GKAP/SAPAP) family (Kim et al., 1997 ; Takeuchi et al., 1997 ) and SPAR/SPAL, an actin binding protein with RapGAP activity (Pak et al., 2001 ; Roy et al., 2002 ).	bind
43441	3	10203	5	NULL	NULL	0	NULL	GKAP/SAPAP family	NULL		is	NULL				GK associated protein/SAP90/PSD-95-associated protein family	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_26_8_2343_s_358	16495462	A final region of SAP97 found to be important for transducing its presynaptic effects is the GK domain, which binds members of the GK associated protein/SAP90/PSD-95-associated protein (GKAP/SAPAP) family (Kim et al., 1997 ; Takeuchi et al., 1997 ) and SPAR/SPAL, an actin binding protein with RapGAP activity (Pak et al., 2001 ; Roy et al., 2002 ).	bind
43442	4	10203	5	NULL	NULL	0	NULL	SPAR/SPAL	NULL		is a type of	NULL				actin binding protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_26_8_2343_s_358	16495462	A final region of SAP97 found to be important for transducing its presynaptic effects is the GK domain, which binds members of the GK associated protein/SAP90/PSD-95-associated protein (GKAP/SAPAP) family (Kim et al., 1997 ; Takeuchi et al., 1997 ) and SPAR/SPAL, an actin binding protein with RapGAP activity (Pak et al., 2001 ; Roy et al., 2002 ).	bind
43443	5	10203	5	10	NULL	0	NULL	SPAR/SPAL			contains					RapGAP activity					NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_26_8_2343_s_358	16495462	A final region of SAP97 found to be important for transducing its presynaptic effects is the GK domain, which binds members of the GK associated protein/SAP90/PSD-95-associated protein (GKAP/SAPAP) family (Kim et al., 1997 ; Takeuchi et al., 1997 ) and SPAR/SPAL, an actin binding protein with RapGAP activity (Pak et al., 2001 ; Roy et al., 2002 ).	bind
43444	6	10203	5	NULL	NULL	0	NULL	SAP97	NULL		bind	NULL		GK domain		SPAR/SPAL	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_26_8_2343_s_358	16495462	A final region of SAP97 found to be important for transducing its presynaptic effects is the GK domain, which binds members of the GK associated protein/SAP90/PSD-95-associated protein (GKAP/SAPAP) family (Kim et al., 1997 ; Takeuchi et al., 1997 ) and SPAR/SPAL, an actin binding protein with RapGAP activity (Pak et al., 2001 ; Roy et al., 2002 ).	bind
36428	1	10203	6	NULL	NULL	0	NULL	SAP97	NULL		bind	NULL		GK domain		GKAP/SAPAP family	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_26_8_2343_s_358	16495462	A final region of SAP97 found to be important for transducing its presynaptic effects is the GK domain, which binds members of the GK associated protein/SAP90/PSD-95-associated protein (GKAP/SAPAP) family (Kim et al., 1997 ; Takeuchi et al., 1997 ) and SPAR/SPAL, an actin binding protein with RapGAP activity (Pak et al., 2001 ; Roy et al., 2002 ).	bind
36429	2	10203	6	10	NULL	0	NULL	GKAP/SAPAP family			is					GK associated protein/SAP90/PSD-95-associated protein family					NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_26_8_2343_s_358	16495462	A final region of SAP97 found to be important for transducing its presynaptic effects is the GK domain, which binds members of the GK associated protein/SAP90/PSD-95-associated protein (GKAP/SAPAP) family (Kim et al., 1997 ; Takeuchi et al., 1997 ) and SPAR/SPAL, an actin binding protein with RapGAP activity (Pak et al., 2001 ; Roy et al., 2002 ).	bind
36431	4	10203	6	NULL	NULL	0	NULL	SAP97	NULL		bind	NULL		GK domain		SPAR/SPAL	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_26_8_2343_s_358	16495462	A final region of SAP97 found to be important for transducing its presynaptic effects is the GK domain, which binds members of the GK associated protein/SAP90/PSD-95-associated protein (GKAP/SAPAP) family (Kim et al., 1997 ; Takeuchi et al., 1997 ) and SPAR/SPAL, an actin binding protein with RapGAP activity (Pak et al., 2001 ; Roy et al., 2002 ).	bind
36433	5	10203	6	NULL	NULL	0	NULL	SPAR/SPAL	NULL		is a type of	NULL				actin binding protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_26_8_2343_s_358	16495462	A final region of SAP97 found to be important for transducing its presynaptic effects is the GK domain, which binds members of the GK associated protein/SAP90/PSD-95-associated protein (GKAP/SAPAP) family (Kim et al., 1997 ; Takeuchi et al., 1997 ) and SPAR/SPAL, an actin binding protein with RapGAP activity (Pak et al., 2001 ; Roy et al., 2002 ).	bind
36434	6	10203	6	10	NULL	0	NULL	SPAR/SPAL			contains					RapGAP activity					NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_26_8_2343_s_358	16495462	A final region of SAP97 found to be important for transducing its presynaptic effects is the GK domain, which binds members of the GK associated protein/SAP90/PSD-95-associated protein (GKAP/SAPAP) family (Kim et al., 1997 ; Takeuchi et al., 1997 ) and SPAR/SPAL, an actin binding protein with RapGAP activity (Pak et al., 2001 ; Roy et al., 2002 ).	bind
36435	3	10203	6	10	NULL	0	NULL	SAP97			is important for			GK domain		presynaptic effects		transducing			NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_26_8_2343_s_358	16495462	A final region of SAP97 found to be important for transducing its presynaptic effects is the GK domain, which binds members of the GK associated protein/SAP90/PSD-95-associated protein (GKAP/SAPAP) family (Kim et al., 1997 ; Takeuchi et al., 1997 ) and SPAR/SPAL, an actin binding protein with RapGAP activity (Pak et al., 2001 ; Roy et al., 2002 ).	bind
43445	1	10204	5	11	NULL	NULL	NULL	enzymes	GP	mutant	bind					TP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_13_11289_s_471	12522214	A final support for the interpretation that mutant enzymes bind TP in a nonproductive mode is obtained by examination of the catalytic competence of the enzyme-TP covalent complexes of individual mutant enzymes.	bind
36387	1	10204	6	NULL	NULL	0	NULL	enzymes	NULL	mutant	bind	NULL				TP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_13_11289_s_471	12522214	A final support for the interpretation that mutant enzymes bind TP in a nonproductive mode is obtained by examination of the catalytic competence of the enzyme-TP covalent complexes of individual mutant enzymes.	bind
43447	1	10206	5	11	NULL	NULL	NULL	LexA	GP	E. coli	bind		differentially							SOS box	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_8_2201_s_316	9555905	A finding of an equal affinity of DinR for each DinR box would contrast dramatically with the finding that  E. coli uses differential binding of LexA to its SOS box to regulate damage-inducible gene expression.	bind
43448	2	10206	5	11	NULL	NULL	NULL	statement 1	GP		regulates					damage-inducible gene	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_8_2201_s_316	9555905	A finding of an equal affinity of DinR for each DinR box would contrast dramatically with the finding that  E. coli uses differential binding of LexA to its SOS box to regulate damage-inducible gene expression.	bind
43449	3	10206	5	11	NULL	NULL	NULL	DinR	GP		affinity to									DinR box	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_8_2201_s_316	9555905	A finding of an equal affinity of DinR for each DinR box would contrast dramatically with the finding that  E. coli uses differential binding of LexA to its SOS box to regulate damage-inducible gene expression.	bind
36388	1	10206	6	NULL	NULL	0	NULL	LexA	NULL	E.coli	bind	NULL	differentially				NULL			SOS box	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_8_2201_s_316	9555905	A finding of an equal affinity of DinR for each DinR box would contrast dramatically with the finding that  E. coli uses differential binding of LexA to its SOS box to regulate damage-inducible gene expression.	bind
36389	2	10206	6	10	NULL	0	NULL	statement 1	NULL		regulates	NULL				damage-inducible gene	NULL	expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_8_2201_s_316	9555905	A finding of an equal affinity of DinR for each DinR box would contrast dramatically with the finding that  E. coli uses differential binding of LexA to its SOS box to regulate damage-inducible gene expression.	bind
36390	3	10206	6	NULL	NULL	0	NULL	DinR	NULL		has affinity for	NULL					NULL			DinR box	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_8_2201_s_316	9555905	A finding of an equal affinity of DinR for each DinR box would contrast dramatically with the finding that  E. coli uses differential binding of LexA to its SOS box to regulate damage-inducible gene expression.	bind
43453	1	10207	5	11	NULL	NULL	NULL	AHR	GP		bind									DREs	NULL		NULL	NULL	NULL	NULL	gw60_annurevcelldevbiol_12_0_55_s_116	8970722	A finding with great impact on how we think of AHR signaling was  the determination that the AHR bound to DREs as part of a  heterodimeric complex ( Elferink et al 1990,  Reyes et al 1992,  Dolwick et al 1993b).	bind
43454	2	10207	5	11	NULL	NULL	NULL	statement 1	GP		is a part of					heterodimeric complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_annurevcelldevbiol_12_0_55_s_116	8970722	A finding with great impact on how we think of AHR signaling was  the determination that the AHR bound to DREs as part of a  heterodimeric complex ( Elferink et al 1990,  Reyes et al 1992,  Dolwick et al 1993b).	bind
36391	1	10207	6	NULL	NULL	0	NULL	AHR 	NULL		is part of the	NULL				heterodimeric complex	NULL				NULL		NULL	NULL	NULL	NULL	gw60_annurevcelldevbiol_12_0_55_s_116	8970722	A finding with great impact on how we think of AHR signaling was  the determination that the AHR bound to DREs as part of a  heterodimeric complex ( Elferink et al 1990,  Reyes et al 1992,  Dolwick et al 1993b).	bind
36392	2	10207	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL					NULL			DRE	NULL		0	NULL	NULL	NULL	gw60_annurevcelldevbiol_12_0_55_s_116	8970722	A finding with great impact on how we think of AHR signaling was  the determination that the AHR bound to DREs as part of a  heterodimeric complex ( Elferink et al 1990,  Reyes et al 1992,  Dolwick et al 1993b).	bind
43455	1	10209	5	11	NULL	NULL	NULL	finger protein	GP		similar to		structurally			TFIIIA	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_1_58_s_493	11782445	A finger protein structurally similar to TFIIIA that binds exclusively to 5S RNA in  Xenopus.	bind
43456	2	10209	5	11	NULL	NULL	NULL	statement 1	GP		bind		exclusively			5S RNA	NucleicAcid	Xenopus			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_1_58_s_493	11782445	A finger protein structurally similar to TFIIIA that binds exclusively to 5S RNA in  Xenopus.	bind
36393	1	10209	6	10	NULL	0	NULL	finger protein	NULL		is similar to	NULL	structurally			TFIIIA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_1_58_s_493	11782445	A finger protein structurally similar to TFIIIA that binds exclusively to 5S RNA in  Xenopus.	bind
36394	2	10209	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL	exclusively			5S RNA	NULL	Xenopus			NULL		0	NULL	NULL	NULL	gw60_genesdev_16_1_58_s_493	11782445	A finger protein structurally similar to TFIIIA that binds exclusively to 5S RNA in  Xenopus.	bind
43457	1	10210	5	11	NULL	NULL	NULL	Nck	GP		bind					TCR-CD3	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_109_7_901_s_186	12110186	A first approach to investigate whether Nck binding to TCR-CD3 plays an important role in TCR-CD3 signaling was to study the activation potency of Nck-CD3  interaction-inducing (OKT3) and noninducing (JOVI.1) antibodies described above     (Figure 5C).	bind
36395	1	10210	6	NULL	NULL	0	NULL	Nck	NULL		bind	NULL				TCR-CD3	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_109_7_901_s_186	12110186	A first approach to investigate whether Nck binding to TCR-CD3 plays an important role in TCR-CD3 signaling was to study the activation potency of Nck-CD3  interaction-inducing (OKT3) and noninducing (JOVI.1) antibodies described above     (Figure 5C).	bind
43458	1	10211	5	11	NULL	NULL	NULL	Sm proteins	GP	canonical 	bind					U1 snRNAs	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_12_3451_s_157	10369684	A first complex contains the canonical Sm proteins which bind to the U1, U2, U4 and U5 snRNAs.	bind
43460	2	10211	5	11	NULL	NULL	NULL	Sm proteins	GP	canonical 	bind					U2 snRNAs	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_12_3451_s_157	10369684	A first complex contains the canonical Sm proteins which bind to the U1, U2, U4 and U5 snRNAs.	bind
43461	3	10211	5	11	NULL	NULL	NULL	Sm proteins	GP	canonical 	bind					U4 snRNAs	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_12_3451_s_157	10369684	A first complex contains the canonical Sm proteins which bind to the U1, U2, U4 and U5 snRNAs.	bind
43463	4	10211	5	11	NULL	NULL	NULL	Sm proteins	GP	canonical 	bind					U5 snRNAs	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_12_3451_s_157	10369684	A first complex contains the canonical Sm proteins which bind to the U1, U2, U4 and U5 snRNAs.	bind
36396	1	10211	6	10	NULL	0	NULL	Sm proteins	NULL	canonical 	bind	NULL				U1 snRNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_12_3451_s_157	10369684	A first complex contains the canonical Sm proteins which bind to the U1, U2, U4 and U5 snRNAs.	bind
36397	2	10211	6	10	NULL	0	NULL	Sm proteins	NULL	canonical 	bind	NULL				U2 snRNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_12_3451_s_157	10369684	A first complex contains the canonical Sm proteins which bind to the U1, U2, U4 and U5 snRNAs.	bind
36398	3	10211	6	10	NULL	0	NULL	Sm proteins	NULL	canonical 	bind	NULL				U4 snRNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_12_3451_s_157	10369684	A first complex contains the canonical Sm proteins which bind to the U1, U2, U4 and U5 snRNAs.	bind
36399	4	10211	6	10	NULL	0	NULL	Sm proteins	NULL	canonical 	bind	NULL				U5 snRNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_12_3451_s_157	10369684	A first complex contains the canonical Sm proteins which bind to the U1, U2, U4 and U5 snRNAs.	bind
43464	1	10213	5	11	NULL	NULL	NULL	single-chain flavohemoglobins	GP		consists of								C-terminal FAD binding domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_11_2424_s_12	10835341	A first group, occurring in bacteria and fungi, includes single-chain flavohemoglobins, which consist of an N-terminal heme-containing domain displaying a conventional globin fold, and a C-terminal FAD or NADP+ binding domain structurally related to ferredoxin NADP+ reductase ( Ermler  et al., 1995).	bind
43465	2	10213	5	11	NULL	NULL	NULL	single-chain flavohemoglobins	GP		consists of								C-terminal FAD binding domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_11_2424_s_12	10835341	A first group, occurring in bacteria and fungi, includes single-chain flavohemoglobins, which consist of an N-terminal heme-containing domain displaying a conventional globin fold, and a C-terminal FAD or NADP+ binding domain structurally related to ferredoxin NADP+ reductase ( Ermler  et al., 1995).	bind
43467	3	10213	5	11	NULL	NULL	NULL	single-chain flavohemoglobins	GP		displays			N-terminal heme-containing domain 		globin fold	GP	conventional 			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_11_2424_s_12	10835341	A first group, occurring in bacteria and fungi, includes single-chain flavohemoglobins, which consist of an N-terminal heme-containing domain displaying a conventional globin fold, and a C-terminal FAD or NADP+ binding domain structurally related to ferredoxin NADP+ reductase ( Ermler  et al., 1995).	bind
43468	4	10213	5	11	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_11_2424_s_12	10835341	A first group, occurring in bacteria and fungi, includes single-chain flavohemoglobins, which consist of an N-terminal heme-containing domain displaying a conventional globin fold, and a C-terminal FAD or NADP+ binding domain structurally related to ferredoxin NADP+ reductase ( Ermler  et al., 1995).	bind
43469	5	10213	5	11	NULL	NULL	NULL	statement 4	Process		is related to		structurally			ferredoxin NADP+ reductase	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_11_2424_s_12	10835341	A first group, occurring in bacteria and fungi, includes single-chain flavohemoglobins, which consist of an N-terminal heme-containing domain displaying a conventional globin fold, and a C-terminal FAD or NADP+ binding domain structurally related to ferredoxin NADP+ reductase ( Ermler  et al., 1995).	bind
36437	1	10213	6	10	NULL	0	NULL	single-chain flavohemoglobins			displays a			N-terminal heme-containing domain		globin fold		conventional			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_11_2424_s_12	10835341	A first group, occurring in bacteria and fungi, includes single-chain flavohemoglobins, which consist of an N-terminal heme-containing domain displaying a conventional globin fold, and a C-terminal FAD or NADP+ binding domain structurally related to ferredoxin NADP+ reductase ( Ermler  et al., 1995).	bind
36438	2	10213	6	10	NULL	0	NULL	single-chain flavohemoglobins			consists of								C-terminal FAD binding domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_11_2424_s_12	10835341	A first group, occurring in bacteria and fungi, includes single-chain flavohemoglobins, which consist of an N-terminal heme-containing domain displaying a conventional globin fold, and a C-terminal FAD or NADP+ binding domain structurally related to ferredoxin NADP+ reductase ( Ermler  et al., 1995).	bind
36439	3	10213	6	10	NULL	0	NULL	single-chain flavohemoglobins			consists of								NADP+ binding domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_11_2424_s_12	10835341	A first group, occurring in bacteria and fungi, includes single-chain flavohemoglobins, which consist of an N-terminal heme-containing domain displaying a conventional globin fold, and a C-terminal FAD or NADP+ binding domain structurally related to ferredoxin NADP+ reductase ( Ermler  et al., 1995).	bind
36440	4	10213	6	10	NULL	0	NULL	statement 2			is an alternative to					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_embo_19_11_2424_s_12	10835341	A first group, occurring in bacteria and fungi, includes single-chain flavohemoglobins, which consist of an N-terminal heme-containing domain displaying a conventional globin fold, and a C-terminal FAD or NADP+ binding domain structurally related to ferredoxin NADP+ reductase ( Ermler  et al., 1995).	bind
57484	5	10213	6	10	NULL	0	NULL	statement 4			is related to		structurally			ferredoxin NADP+ reductase					NULL		NULL	NULL	NULL	NULL	gw60_embo_19_11_2424_s_12	10835341	A first group, occurring in bacteria and fungi, includes single-chain flavohemoglobins, which consist of an N-terminal heme-containing domain displaying a conventional globin fold, and a C-terminal FAD or NADP+ binding domain structurally related to ferredoxin NADP+ reductase ( Ermler  et al., 1995).	bind
43470	1	10214	5	11	NULL	NULL	NULL	citrate synthase	GP	heat-denatured	bind					Hsp25	GP	mammalian			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_18_11032_s_166	9556585	A first indication that sHsps may collaborate with other chaperones in the refolding of bound denatured proteins came from the observation that the refolding of heat-denatured citrate synthase bound to mammalian Hsp25, can be activated by Hsp70, even without ATP ( 4).	bind
43471	2	10214	5	11	NULL	NULL	NULL	Hsp70	GP		activates					statement 1	Process	refolding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_18_11032_s_166	9556585	A first indication that sHsps may collaborate with other chaperones in the refolding of bound denatured proteins came from the observation that the refolding of heat-denatured citrate synthase bound to mammalian Hsp25, can be activated by Hsp70, even without ATP ( 4).	bind
43472	3	10214	5	11	NULL	NULL	NULL	ATP	Chemical		is not required for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_18_11032_s_166	9556585	A first indication that sHsps may collaborate with other chaperones in the refolding of bound denatured proteins came from the observation that the refolding of heat-denatured citrate synthase bound to mammalian Hsp25, can be activated by Hsp70, even without ATP ( 4).	bind
43475	6	10214	5	11	NULL	NULL	NULL	statement 4	Process		leads to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_18_11032_s_166	9556585	A first indication that sHsps may collaborate with other chaperones in the refolding of bound denatured proteins came from the observation that the refolding of heat-denatured citrate synthase bound to mammalian Hsp25, can be activated by Hsp70, even without ATP ( 4).	bind
36400	1	10214	6	NULL	NULL	0	NULL	citrate synthase	NULL	heat denatured	bind	NULL				Hsp25	NULL	mammalian			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_18_11032_s_166	9556585	A first indication that sHsps may collaborate with other chaperones in the refolding of bound denatured proteins came from the observation that the refolding of heat-denatured citrate synthase bound to mammalian Hsp25, can be activated by Hsp70, even without ATP ( 4).	bind
36401	2	10214	6	10	NULL	0	NULL	Hsp70			activates					statement 1		refolding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_18_11032_s_166	9556585	A first indication that sHsps may collaborate with other chaperones in the refolding of bound denatured proteins came from the observation that the refolding of heat-denatured citrate synthase bound to mammalian Hsp25, can be activated by Hsp70, even without ATP ( 4).	bind
36402	3	10214	6	NULL	NULL	0	NULL	statement 2	NULL		occurs without	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_18_11032_s_166	9556585	A first indication that sHsps may collaborate with other chaperones in the refolding of bound denatured proteins came from the observation that the refolding of heat-denatured citrate synthase bound to mammalian Hsp25, can be activated by Hsp70, even without ATP ( 4).	bind
43476	1	10215	5	11	NULL	NULL	NULL	Hsp40	GP		bind					unfolded proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_51_36757_s_226	10593983	A first possibility is that binding of Hsp40 to unfolded proteins is essential for their delivery to Hsp70 and that this capacity is lost in the Hsp40 mutants.	bind
43477	2	10215	5	11	NULL	NULL	NULL	unfolded proteins	GP		are delivered to					Hsp70	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_51_36757_s_226	10593983	A first possibility is that binding of Hsp40 to unfolded proteins is essential for their delivery to Hsp70 and that this capacity is lost in the Hsp40 mutants.	bind
43478	3	10215	5	11	NULL	NULL	NULL	statement 1	Process		is essential for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_51_36757_s_226	10593983	A first possibility is that binding of Hsp40 to unfolded proteins is essential for their delivery to Hsp70 and that this capacity is lost in the Hsp40 mutants.	bind
43479	4	10215	5	11	NULL	NULL	NULL	Hsp40	GP	mutant	does not bind					unfolded proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_51_36757_s_226	10593983	A first possibility is that binding of Hsp40 to unfolded proteins is essential for their delivery to Hsp70 and that this capacity is lost in the Hsp40 mutants.	bind
36403	1	10215	6	NULL	NULL	0	NULL	Hsp40	NULL		bind	NULL				unfolded proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_51_36757_s_226	10593983	A first possibility is that binding of Hsp40 to unfolded proteins is essential for their delivery to Hsp70 and that this capacity is lost in the Hsp40 mutants.	bind
36441	2	10215	6	NULL	NULL	0	NULL	unfolded proteins	NULL		are delivered to	NULL				Hsp70	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_51_36757_s_226	10593983	A first possibility is that binding of Hsp40 to unfolded proteins is essential for their delivery to Hsp70 and that this capacity is lost in the Hsp40 mutants.	bind
36442	3	10215	6	NULL	NULL	0	NULL	statement 1	NULL		is essential for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_51_36757_s_226	10593983	A first possibility is that binding of Hsp40 to unfolded proteins is essential for their delivery to Hsp70 and that this capacity is lost in the Hsp40 mutants.	bind
36443	4	10215	6	NULL	NULL	0	NULL	Hsp40	NULL	mutant	does not bind	NULL				unfolded proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_51_36757_s_226	10593983	A first possibility is that binding of Hsp40 to unfolded proteins is essential for their delivery to Hsp70 and that this capacity is lost in the Hsp40 mutants.	bind
43481	1	10217	5	11	NULL	NULL	NULL	Mad2	GP		bind					Cdc20	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_10_4584_s_28	15269280	A first series of studies showed that Mad2 binds to Cdc20 and thereby inhibits APC/Cdc20 ubiquitination activity (Li  et al., 1997 ; Fang  et al., 1998 ; Hwang  et al., 1998 ; Kim  et al., 1998 ).	bind
43482	2	10217	5	11	NULL	NULL	NULL	statement 1	Process		inhibits					APC/Cdc20	GP	ubiquitination of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_10_4584_s_28	15269280	A first series of studies showed that Mad2 binds to Cdc20 and thereby inhibits APC/Cdc20 ubiquitination activity (Li  et al., 1997 ; Fang  et al., 1998 ; Hwang  et al., 1998 ; Kim  et al., 1998 ).	bind
36404	1	10217	6	NULL	NULL	0	NULL	Mad2	NULL		bind	NULL				Cdc20	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_10_4584_s_28	15269280	A first series of studies showed that Mad2 binds to Cdc20 and thereby inhibits APC/Cdc20 ubiquitination activity (Li  et al., 1997 ; Fang  et al., 1998 ; Hwang  et al., 1998 ; Kim  et al., 1998 ).	bind
36405	2	10217	6	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				APC/Cdc20	NULL	ubiquitination of			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_10_4584_s_28	15269280	A first series of studies showed that Mad2 binds to Cdc20 and thereby inhibits APC/Cdc20 ubiquitination activity (Li  et al., 1997 ; Fang  et al., 1998 ; Hwang  et al., 1998 ; Kim  et al., 1998 ).	bind
43483	1	10218	5	NULL	NULL	0	NULL	Cre	NULL		mediate	NULL				DNA recombination	NULL	site-specific			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_13_2764_s_2	12087159	A first step in Cre-mediated site-specific DNA recombination is binding to the two 13 bp repeats of the 34 bp site  loxP.	bind
48408	2	10218	5	10	NULL	0	NULL	Cre	NULL		bind	NULL				loxP	NULL			13 bp repeats of the 34 bp site 	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_13_2764_s_2	12087159	A first step in Cre-mediated site-specific DNA recombination is binding to the two 13 bp repeats of the 34 bp site  loxP.	bind
36406	1	10218	6	10	NULL	0	NULL	Cre	NULL		mediates	NULL				DNA recombination	NULL	site-specific			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_13_2764_s_2	12087159	A first step in Cre-mediated site-specific DNA recombination is binding to the two 13 bp repeats of the 34 bp site  loxP.	bind
48409	2	10218	6	10	NULL	0	NULL	Cre	NULL		bind	NULL				loxP	NULL			13 bp repeats of the 34 bp site	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_13_2764_s_2	12087159	A first step in Cre-mediated site-specific DNA recombination is binding to the two 13 bp repeats of the 34 bp site  loxP.	bind
43487	1	10219	5	11	NULL	NULL	NULL	top1	GP	reconstituted;;human	lacks							whole	linker domain		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_9_871_s_216	11564555	A first work on reconstituted human top1 showed that the lack of the whole linker domain decreased DNA binding and cleavage levels with CPT  [34]  .	bind
43488	2	10219	5	11	NULL	NULL	NULL	statement 1	Process		decrease					DNA	NucleicAcid	binding of			NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_9_871_s_216	11564555	A first work on reconstituted human top1 showed that the lack of the whole linker domain decreased DNA binding and cleavage levels with CPT  [34]  .	bind
43489	3	10219	5	11	NULL	NULL	NULL	statement 1	Process		decrease					CPT	Chemical	cleavage levels with			NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_9_871_s_216	11564555	A first work on reconstituted human top1 showed that the lack of the whole linker domain decreased DNA binding and cleavage levels with CPT  [34]  .	bind
36444	1	10219	6	NULL	NULL	0	NULL	top1	NULL	human	bind	NULL		linker domain		DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_chembiol_8_9_871_s_216	11564555	A first work on reconstituted human top1 showed that the lack of the whole linker domain decreased DNA binding and cleavage levels with CPT  [34]  .	bind
36445	2	10219	6	NULL	NULL	0	NULL	top1	NULL	human;; lack of	decreases 	NULL		linker domain		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_chembiol_8_9_871_s_216	11564555	A first work on reconstituted human top1 showed that the lack of the whole linker domain decreased DNA binding and cleavage levels with CPT  [34]  .	bind
36446	3	10219	6	NULL	NULL	0	NULL	top1	NULL	human;; lack of	decreases	NULL		linker domain		CPT	NULL	clevage levels with			NULL		0	NULL	NULL	NULL	gw60_chembiol_8_9_871_s_216	11564555	A first work on reconstituted human top1 showed that the lack of the whole linker domain decreased DNA binding and cleavage levels with CPT  [34]  .	bind
43490	1	10220	5	11	NULL	NULL	NULL	F-actin	GP		bind		weakly			vimentin	GP		tail domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_41_30393_s_126	16901892	A fit of the binding curve using nonlinear regression (supplemental Fig. S1) yielded an equilibrium dissociation constant,  kd, of  13.8 muM, indicative of weak binding between F-actin and the tail domain of vimentin.	bind
36407	1	10220	6	NULL	NULL	0	NULL	F-actin	NULL		bind	NULL	weakly			vimentin	NULL		tail domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_41_30393_s_126	16901892	A fit of the binding curve using nonlinear regression (supplemental Fig. S1) yielded an equilibrium dissociation constant,  kd, of  13.8 muM, indicative of weak binding between F-actin and the tail domain of vimentin.	bind
43491	1	10221	5	NULL	NULL	0	NULL	Ffh	NULL		bind	NULL				FtsY	NULL				NULL		0	NULL	NULL	NULL	gw60_science_288_5471_1640_s_49	10834842	A fit of the data to the equation  kobs =  kon[protein] +  koff gave values of  kon = 5.6 ( plus-or-minus 0.6) x 102 M 1 s 1 and 9.2 ( plus-or-minus 0.7) x 104 M 1 s 1 for the binding of Ffh and the Ffh/4.5 S RNP, respectively, to FtsY.	bind
43492	2	10221	5	NULL	NULL	0	NULL	Ffh/4.5 S RNP	NULL		bind	NULL				FtsY	NULL				NULL		0	NULL	NULL	NULL	gw60_science_288_5471_1640_s_49	10834842	A fit of the data to the equation  kobs =  kon[protein] +  koff gave values of  kon = 5.6 ( plus-or-minus 0.6) x 102 M 1 s 1 and 9.2 ( plus-or-minus 0.7) x 104 M 1 s 1 for the binding of Ffh and the Ffh/4.5 S RNP, respectively, to FtsY.	bind
36408	1	10221	6	NULL	NULL	0	NULL	Ffh	NULL		bind	NULL				FtsY	NULL				NULL		0	NULL	NULL	NULL	gw60_science_288_5471_1640_s_49	10834842	A fit of the data to the equation  kobs =  kon[protein] +  koff gave values of  kon = 5.6 ( plus-or-minus 0.6) x 102 M 1 s 1 and 9.2 ( plus-or-minus 0.7) x 104 M 1 s 1 for the binding of Ffh and the Ffh/4.5 S RNP, respectively, to FtsY.	bind
36409	2	10221	6	NULL	NULL	0	NULL	Ffh/4.5 S RNP	NULL		bind	NULL				FtsY	NULL				NULL		0	NULL	NULL	NULL	gw60_science_288_5471_1640_s_49	10834842	A fit of the data to the equation  kobs =  kon[protein] +  koff gave values of  kon = 5.6 ( plus-or-minus 0.6) x 102 M 1 s 1 and 9.2 ( plus-or-minus 0.7) x 104 M 1 s 1 for the binding of Ffh and the Ffh/4.5 S RNP, respectively, to FtsY.	bind
43493	1	10222	5	11	NULL	NULL	NULL	sV(HIgR)-Fc	GP		bind		saturable			gD	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_26_15700_s_175	9861033	A fixed amount of sV(HIgR)-Fc (10 nM), giving saturable binding to gD in  A, was mixed with increasing amounts of IgGs from the indicated antibodies and then allowed to react with gD, preimmobilized to microwells.	bind
48549	1	10222	6	NULL	NULL	0	NULL	sV(HIgR)-Fc	NULL		bind	NULL				gD	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_26_15700_s_175	9861033	A fixed amount of sV(HIgR)-Fc (10 nM), giving saturable binding to gD in  A, was mixed with increasing amounts of IgGs from the indicated antibodies and then allowed to react with gD, preimmobilized to microwells.	bind
43494	1	10223	5	11	NULL	NULL	NULL	Mant-ATP 	Chemical		bind					CDK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_13_8746_s_248	10085115	A fixed concentration of CDK2 (0.2 muM) ( open symbols) and phosphorylated CDK2 ( closed symbols) were titrated with increasing concentrations of ATP ( ,  ) and ADP (  , ).  b, Mant-ATP and Mant-ADP binding to CDK2 and phosphorylated CDK2.	bind
43497	2	10223	5	11	NULL	NULL	NULL	Mant-ADP	Chemical		bind					CDK2	GP	phosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_13_8746_s_248	10085115	A fixed concentration of CDK2 (0.2 muM) ( open symbols) and phosphorylated CDK2 ( closed symbols) were titrated with increasing concentrations of ATP ( ,  ) and ADP (  , ).  b, Mant-ATP and Mant-ADP binding to CDK2 and phosphorylated CDK2.	bind
36410	1	10223	6	NULL	NULL	0	NULL	Mant-ATP	NULL		bind	NULL				CDK2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_13_8746_s_248	10085115	A fixed concentration of CDK2 (0.2 muM) ( open symbols) and phosphorylated CDK2 ( closed symbols) were titrated with increasing concentrations of ATP ( ,  ) and ADP (  , ).  b, Mant-ATP and Mant-ADP binding to CDK2 and phosphorylated CDK2.	bind
36411	2	10223	6	NULL	NULL	0	NULL	Mant-ADP	NULL		bind	NULL				CDK2	NULL	phosphorylated			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_13_8746_s_248	10085115	A fixed concentration of CDK2 (0.2 muM) ( open symbols) and phosphorylated CDK2 ( closed symbols) were titrated with increasing concentrations of ATP ( ,  ) and ADP (  , ).  b, Mant-ATP and Mant-ADP binding to CDK2 and phosphorylated CDK2.	bind
43553	1	10224	5	11	NULL	NULL	NULL	netrin1 gene	GP	zebrafish	requires				floor plate enhancer	Cyclops	Organism	signaling of			NULL		NULL	NULL	NULL	NULL	gw60_development_130_14_3331_s_465	12783802	A floor plate enhancer of the zebrafish netrin1 gene requires Cyclops (Nodal) signalling and the winged helix transcription factor FoxA2.	bind
43554	2	10224	5	11	NULL	NULL	NULL	netrin1 gene	GP	zebrafish	requires				floor plate enhancer	FoxA2	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_130_14_3331_s_465	12783802	A floor plate enhancer of the zebrafish netrin1 gene requires Cyclops (Nodal) signalling and the winged helix transcription factor FoxA2.	bind
43555	3	10224	5	11	NULL	NULL	NULL	FoxA2	GP		is a type of					winged helix transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_development_130_14_3331_s_465	12783802	A floor plate enhancer of the zebrafish netrin1 gene requires Cyclops (Nodal) signalling and the winged helix transcription factor FoxA2.	bind
36412	1	10224	6	NULL	NULL	0	NULL	netrin1 gene	NULL	zebrafish	requires	NULL			floor plate enhancer	FoxA2	NULL				NULL		0	NULL	NULL	NULL	gw60_development_130_14_3331_s_465	12783802	A floor plate enhancer of the zebrafish netrin1 gene requires Cyclops (Nodal) signalling and the winged helix transcription factor FoxA2.	bind
36413	2	10224	6	NULL	NULL	0	NULL	FoxA2	NULL		is a type of	NULL				winged helix transcription factor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_development_130_14_3331_s_465	12783802	A floor plate enhancer of the zebrafish netrin1 gene requires Cyclops (Nodal) signalling and the winged helix transcription factor FoxA2.	bind
36414	3	10224	6	NULL	NULL	0	NULL	netrin1 gene	NULL	zebrafish	requires	NULL			floor plate enhancer	Cyclops (Nodal)	NULL	signaling of			NULL		0	NULL	NULL	NULL	gw60_development_130_14_3331_s_465	12783802	A floor plate enhancer of the zebrafish netrin1 gene requires Cyclops (Nodal) signalling and the winged helix transcription factor FoxA2.	bind
43498	1	10225	5	11	NULL	NULL	NULL	LPS	Chemical	E. coli	bind					PBMs	Cell	porcine			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_4_1421_s_122	9529062	A flow cytometric assay was developed to monitor LPS binding to porcine PBMs. Density gradient-isolated cells were incubated with FITC-labelled  E. coli LPS in the presence of autologous serum, and binding to PBMs was characterized by flow cytometry.	bind
36415	1	10225	6	10	NULL	0	NULL	LPS	NULL	E.coli	bind	NULL				PBM	NULL	porcine			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_4_1421_s_122	9529062	A flow cytometric assay was developed to monitor LPS binding to porcine PBMs. Density gradient-isolated cells were incubated with FITC-labelled  E. coli LPS in the presence of autologous serum, and binding to PBMs was characterized by flow cytometry.	bind
43558	1	10226	5	11	NULL	NULL	NULL	methotrexate	Chemical	fluorescein	bind					DHFR	GP	reconstituted			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_pnas_96_10_5394_s_5	10318894	A fluorescence assay also is described, based on stoichiometric binding of fluorescein-methotrexate to reconstituted DHFR  in vivo.	bind
36416	1	10226	6	10	NULL	0	NULL	methotrexate	NULL	fluorescein	bind	NULL				DHFR	NULL	reconstituted			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_pnas_96_10_5394_s_5	10318894	A fluorescence assay also is described, based on stoichiometric binding of fluorescein-methotrexate to reconstituted DHFR  in vivo.	bind
43560	1	10227	5	11	NULL	NULL	NULL	synaptotagmin	GP		penetrates into		directly	Ca2+-binding loop 3 of the C2A domain		lipid bilayers	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_49_32966_s_225	9830048	A fluorescence study revealed that Ca2+-binding loop 3 of the C2A domain of synaptotagmin directly penetrates into lipid bilayers, potentially providing movement or force to trigger neuronal exocytosis ( 37).	bind
43561	2	10227	5	11	NULL	NULL	NULL	statement 1	Process		trigger		potentially			neuronal exocytosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_49_32966_s_225	9830048	A fluorescence study revealed that Ca2+-binding loop 3 of the C2A domain of synaptotagmin directly penetrates into lipid bilayers, potentially providing movement or force to trigger neuronal exocytosis ( 37).	bind
36417	1	10227	6	NULL	NULL	0	NULL	synaptotagmin	NULL		penetrates	NULL	directly	Ca2+-binding loop 3 of the C2A domain		lipid bilayers	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32966_s_225	9830048	A fluorescence study revealed that Ca2+-binding loop 3 of the C2A domain of synaptotagmin directly penetrates into lipid bilayers, potentially providing movement or force to trigger neuronal exocytosis ( 37).	bind
36418	2	10227	6	NULL	NULL	0	NULL	statement 1	NULL		triggers	NULL				neuronal exocytosis	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32966_s_225	9830048	A fluorescence study revealed that Ca2+-binding loop 3 of the C2A domain of synaptotagmin directly penetrates into lipid bilayers, potentially providing movement or force to trigger neuronal exocytosis ( 37).	bind
43563	1	10229	5	11	NULL	NULL	NULL	cyclopamine	Chemical	fluorescent derivative of	bind					Smo-expressing cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_21_2743_s_63	12414725	A fluorescent derivative of cyclopamine binds Smo-expressing cells.	bind
36419	1	10229	6	NULL	NULL	0	NULL	cyclopamine	NULL	fluorescent derivative of	bind	NULL				Smo-expressing cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_21_2743_s_63	12414725	A fluorescent derivative of cyclopamine binds Smo-expressing cells.	bind
43565	1	10230	5	11	NULL	NULL	NULL	cyclopamine	Chemical	fluorescent derivative of	bind		specifically			Smo-expressing cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_21_2743_s_54	12414725	A fluorescent derivative of cyclopamine specifically binds Smo-expressing cells	bind
36420	1	10230	6	NULL	NULL	0	NULL	cyclopamine	NULL	fluorescent derivative of	bind	NULL	specifically			Smo-expressing cells	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_16_21_2743_s_54	12414725	A fluorescent derivative of cyclopamine specifically binds Smo-expressing cells	bind
48726	1	10232	5	11	NULL	NULL	NULL	nuclear proteins	GP	unfractionated testis cells	bind									RE region	NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_68_6_2267_s_214	12606375	A footprint was formed over the RE region by the binding of nuclear proteins derived from unfractionated testis cells and from an enriched population of pachytene primary spermatocytes.	bind
48727	2	10232	5	11	NULL	NULL	NULL	nuclear proteins	GP	pachytene primary spermatocytes	bind									RE region	NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_68_6_2267_s_214	12606375	A footprint was formed over the RE region by the binding of nuclear proteins derived from unfractionated testis cells and from an enriched population of pachytene primary spermatocytes.	bind
36449	1	10232	6	NULL	NULL	0	NULL	nuclear proteins	NULL	unfractionated testis cells 	bind	NULL					NULL			RE region	NULL		0	NULL	NULL	NULL	gw70_biolreprod_68_6_2267_s_214	12606375	A footprint was formed over the RE region by the binding of nuclear proteins derived from unfractionated testis cells and from an enriched population of pachytene primary spermatocytes.	bind
36450	2	10232	6	10	NULL	0	NULL	nuclear proteins		pachytene primary spermatocytes	bind									RE region	NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_68_6_2267_s_214	12606375	A footprint was formed over the RE region by the binding of nuclear proteins derived from unfractionated testis cells and from an enriched population of pachytene primary spermatocytes.	bind
43573	1	10233	5	11	NULL	NULL	NULL	ADP	Chemical		bind		weakly			acto-Myo9b	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_38957_s_257	16179355	A forced fit to the observed rates gave an approximate estimate of  KAD of 156 muM, indicating that ADP bound weakly to acto-Myo9b (data not shown).	bind
36421	1	10233	6	NULL	NULL	0	NULL	ADP	NULL		bind	NULL	weakly			acto-Myo9b	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_47_38957_s_257	16179355	A forced fit to the observed rates gave an approximate estimate of  KAD of 156 muM, indicating that ADP bound weakly to acto-Myo9b (data not shown).	bind
43574	1	10234	5	11	NULL	NULL	NULL	UNC-13S	GP		does not bind					DAG	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_2_335_s_277	10571228	A form of UNC-13S that does not bind DAG shifts the dose-response curve for phorbol-induced hypersensitivity to aldicarb, suggesting that neurons contain a second low-affinity phorbol receptor that regulates acetylcholine release.	bind
43577	3	10234	5	11	NULL	NULL	NULL	neurons	Cell		contains					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_2_335_s_277	10571228	A form of UNC-13S that does not bind DAG shifts the dose-response curve for phorbol-induced hypersensitivity to aldicarb, suggesting that neurons contain a second low-affinity phorbol receptor that regulates acetylcholine release.	bind
43578	2	10234	5	11	NULL	NULL	NULL	phorbol receptor	GP	low-affinity	regulates					acetylcholine	Chemical	release of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_2_335_s_277	10571228	A form of UNC-13S that does not bind DAG shifts the dose-response curve for phorbol-induced hypersensitivity to aldicarb, suggesting that neurons contain a second low-affinity phorbol receptor that regulates acetylcholine release.	bind
36451	1	10234	6	NULL	NULL	0	NULL	UNC-13S	NULL		does not bind	NULL				DAG	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_24_2_335_s_277	10571228	A form of UNC-13S that does not bind DAG shifts the dose-response curve for phorbol-induced hypersensitivity to aldicarb, suggesting that neurons contain a second low-affinity phorbol receptor that regulates acetylcholine release.	bind
36452	2	10234	6	NULL	NULL	0	NULL	neurons	NULL		contain	NULL				phorbol receptor	NULL	second low affinity			NULL		0	NULL	NULL	NULL	gw60_neuron_24_2_335_s_277	10571228	A form of UNC-13S that does not bind DAG shifts the dose-response curve for phorbol-induced hypersensitivity to aldicarb, suggesting that neurons contain a second low-affinity phorbol receptor that regulates acetylcholine release.	bind
36453	3	10234	6	NULL	NULL	0	NULL	statement 2	NULL		regulates	NULL				acetylcholine	NULL	release of 			NULL		0	NULL	NULL	NULL	gw60_neuron_24_2_335_s_277	10571228	A form of UNC-13S that does not bind DAG shifts the dose-response curve for phorbol-induced hypersensitivity to aldicarb, suggesting that neurons contain a second low-affinity phorbol receptor that regulates acetylcholine release.	bind
43582	1	10236	5	11	NULL	NULL	NULL	Daam1	GP		is a type of					Formin-Homology Protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_843_s_83	11779461	A Formin-Homology (FH) Protein Daam1 that Binds  to Dvl	bind
43583	2	10236	5	11	NULL	NULL	NULL	Daam1	GP		bind					Dvl	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_843_s_83	11779461	A Formin-Homology (FH) Protein Daam1 that Binds  to Dvl	bind
48426	3	10236	5	11	NULL	NULL	NULL	FH	GP		is					Formin-Homology	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_107_7_843_s_83	11779461	A Formin-Homology (FH) Protein Daam1 that Binds  to Dvl	bind
36422	1	10236	6	NULL	NULL	0	NULL	Daam1	NULL		bind	NULL				Dvl	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_107_7_843_s_83	11779461	A Formin-Homology (FH) Protein Daam1 that Binds  to Dvl	bind
36423	2	10236	6	NULL	NULL	0	NULL	Daam1	NULL		is a type of	NULL				FH protein	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_107_7_843_s_83	11779461	A Formin-Homology (FH) Protein Daam1 that Binds  to Dvl	bind
36424	3	10236	6	NULL	NULL	0	NULL	FH	NULL		is	NULL				Formin-Homology	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_107_7_843_s_83	11779461	A Formin-Homology (FH) Protein Daam1 that Binds  to Dvl	bind
43584	1	10237	5	11	NULL	NULL	NULL	FoTFdeltaN	GP		is					FoTF mutant lacking N-terminal half 	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_4_1175_s_114	15657123	A FoTF mutant lacking the N-terminal half of the protein (FoTFdeltaN) did not bind to TSWV RNA ( Fig. 2 C).	bind
43585	2	10237	5	11	NULL	NULL	NULL	FoTFdeltaN	GP		does not bind					TSWV RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_4_1175_s_114	15657123	A FoTF mutant lacking the N-terminal half of the protein (FoTFdeltaN) did not bind to TSWV RNA ( Fig. 2 C).	bind
36425	1	10237	6	NULL	NULL	0	NULL	FoTFdeltaN	NULL		does not bind	NULL				TSWV RNA	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_4_1175_s_114	15657123	A FoTF mutant lacking the N-terminal half of the protein (FoTFdeltaN) did not bind to TSWV RNA ( Fig. 2 C).	bind
36426	2	10237	6	10	NULL	0	NULL	FoTFdeltaN	NULL		is	NULL				FoTF mutant lacking the N-terminal half	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_4_1175_s_114	15657123	A FoTF mutant lacking the N-terminal half of the protein (FoTFdeltaN) did not bind to TSWV RNA ( Fig. 2 C).	bind
43586	1	10238	5	11	NULL	NULL	NULL	E1A	GP		bind					Rb-family proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_15_9966_s_7	12119420	A four amino acid E1A deletion that eliminates binding to Rb-family proteins blocked both repression of TNF-alpha-induced transcription and sensitization to apoptosis.	bind
43587	2	10238	5	11	NULL	NULL	NULL	E1A	GP	four amino acid deletion	eliminate					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_15_9966_s_7	12119420	A four amino acid E1A deletion that eliminates binding to Rb-family proteins blocked both repression of TNF-alpha-induced transcription and sensitization to apoptosis.	bind
43588	3	10238	5	11	NULL	NULL	NULL	TNF-alpha	GP		induce					transcription	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_15_9966_s_7	12119420	A four amino acid E1A deletion that eliminates binding to Rb-family proteins blocked both repression of TNF-alpha-induced transcription and sensitization to apoptosis.	bind
43589	4	10238	5	11	NULL	NULL	NULL	statement 2	Process		block					statement 3	Process	repression of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_15_9966_s_7	12119420	A four amino acid E1A deletion that eliminates binding to Rb-family proteins blocked both repression of TNF-alpha-induced transcription and sensitization to apoptosis.	bind
43591	5	10238	5	11	NULL	NULL	NULL	statement 2	Process		block					apoptosis	Process	sensitization to			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_15_9966_s_7	12119420	A four amino acid E1A deletion that eliminates binding to Rb-family proteins blocked both repression of TNF-alpha-induced transcription and sensitization to apoptosis.	bind
36464	1	10238	6	NULL	NULL	0	NULL	E1A	NULL		bind	NULL				Rb-family proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_15_9966_s_7	12119420	A four amino acid E1A deletion that eliminates binding to Rb-family proteins blocked both repression of TNF-alpha-induced transcription and sensitization to apoptosis.	bind
36465	2	10238	6	10	NULL	0	NULL	E1A		four amino acids deletion of	eliminates					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_15_9966_s_7	12119420	A four amino acid E1A deletion that eliminates binding to Rb-family proteins blocked both repression of TNF-alpha-induced transcription and sensitization to apoptosis.	bind
36466	3	10238	6	NULL	NULL	0	NULL	TNF-alpha	NULL		induces	NULL				transcription	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_15_9966_s_7	12119420	A four amino acid E1A deletion that eliminates binding to Rb-family proteins blocked both repression of TNF-alpha-induced transcription and sensitization to apoptosis.	bind
36467	4	10238	6	10	NULL	0	NULL	statement 2			blocks					statement 3		repression of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_15_9966_s_7	12119420	A four amino acid E1A deletion that eliminates binding to Rb-family proteins blocked both repression of TNF-alpha-induced transcription and sensitization to apoptosis.	bind
36468	5	10238	6	10	NULL	0	NULL	statement 2			blocks					apoptosis		sensitization to			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_15_9966_s_7	12119420	A four amino acid E1A deletion that eliminates binding to Rb-family proteins blocked both repression of TNF-alpha-induced transcription and sensitization to apoptosis.	bind
43592	1	10239	5	11	NULL	NULL	NULL	Bmp2C2	GP		is					fourth Bmp2 DNA region	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_development_131_18_4581_s_165	15342482	A fourth  Bmp2 DNA region,  Bmp2C2, was also bound by the A13-DBD peptide; however, 2- to 4-fold higher concentrations of A13-DBD were required to affect its electrophoretic mobility ( Fig. 2C).	bind
43593	2	10239	5	11	NULL	NULL	NULL	Bmp2C2	GP		bind					A13-DBD peptide	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_development_131_18_4581_s_165	15342482	A fourth  Bmp2 DNA region,  Bmp2C2, was also bound by the A13-DBD peptide; however, 2- to 4-fold higher concentrations of A13-DBD were required to affect its electrophoretic mobility ( Fig. 2C).	bind
36469	1	10239	6	NULL	NULL	0	NULL	Bmp2C2	NULL		bind	NULL				A13DBD peptide	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_18_4581_s_165	15342482	A fourth  Bmp2 DNA region,  Bmp2C2, was also bound by the A13-DBD peptide; however, 2- to 4-fold higher concentrations of A13-DBD were required to affect its electrophoretic mobility ( Fig. 2C).	bind
36470	2	10239	6	NULL	NULL	0	NULL	Bmp2C2	NULL		is	NULL				fourth Bmp2 DNA region	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_18_4581_s_165	15342482	A fourth  Bmp2 DNA region,  Bmp2C2, was also bound by the A13-DBD peptide; however, 2- to 4-fold higher concentrations of A13-DBD were required to affect its electrophoretic mobility ( Fig. 2C).	bind
43599	1	10241	5	11	NULL	NULL	NULL	GATA-4	GP		is a type of					zinc finger binding proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_100_2_263_s_12	11165483	A fourth family of transcriptional regulators, the zinc finger binding proteins GATA-4, -5 and -6, are expressed very early in the cardiac program.	bind
43600	2	10241	5	11	NULL	NULL	NULL	GATA-4	GP		is a member of					transcriptional regulators family	GP				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_100_2_263_s_12	11165483	A fourth family of transcriptional regulators, the zinc finger binding proteins GATA-4, -5 and -6, are expressed very early in the cardiac program.	bind
43601	3	10241	5	11	NULL	NULL	NULL	GATA-4	GP		is expressed in		very early			cardiac program	MedicalProcedure				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_100_2_263_s_12	11165483	A fourth family of transcriptional regulators, the zinc finger binding proteins GATA-4, -5 and -6, are expressed very early in the cardiac program.	bind
43602	4	10241	5	11	NULL	NULL	NULL	GATA-5	GP		is a type of					zinc finger binding proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_100_2_263_s_12	11165483	A fourth family of transcriptional regulators, the zinc finger binding proteins GATA-4, -5 and -6, are expressed very early in the cardiac program.	bind
43603	5	10241	5	11	NULL	NULL	NULL	GATA-5	GP		is a member of					transcriptional regulators family	GP				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_100_2_263_s_12	11165483	A fourth family of transcriptional regulators, the zinc finger binding proteins GATA-4, -5 and -6, are expressed very early in the cardiac program.	bind
43604	6	10241	5	11	NULL	NULL	NULL	GATA-5	GP		is expressed in		very early			cardiac program	MedicalProcedure				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_100_2_263_s_12	11165483	A fourth family of transcriptional regulators, the zinc finger binding proteins GATA-4, -5 and -6, are expressed very early in the cardiac program.	bind
43605	7	10241	5	11	NULL	NULL	NULL	GATA-6	GP		is a type of					zinc finger binding proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_100_2_263_s_12	11165483	A fourth family of transcriptional regulators, the zinc finger binding proteins GATA-4, -5 and -6, are expressed very early in the cardiac program.	bind
43606	8	10241	5	11	NULL	NULL	NULL	GATA-6	GP		is a member of					transcriptional regulators family	GP				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_100_2_263_s_12	11165483	A fourth family of transcriptional regulators, the zinc finger binding proteins GATA-4, -5 and -6, are expressed very early in the cardiac program.	bind
43607	9	10241	5	11	NULL	NULL	NULL	GATA-6	GP		is expressed in		very early			cardiac program	MedicalProcedure				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_100_2_263_s_12	11165483	A fourth family of transcriptional regulators, the zinc finger binding proteins GATA-4, -5 and -6, are expressed very early in the cardiac program.	bind
36471	1	10241	6	NULL	NULL	0	NULL	GATA-4	NULL		is a type of	NULL				zinc finger binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_mechdev_100_2_263_s_12	11165483	A fourth family of transcriptional regulators, the zinc finger binding proteins GATA-4, -5 and -6, are expressed very early in the cardiac program.	bind
36472	2	10241	6	NULL	NULL	0	NULL	GATA-5	NULL		is a type of	NULL				zinc finger binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_mechdev_100_2_263_s_12	11165483	A fourth family of transcriptional regulators, the zinc finger binding proteins GATA-4, -5 and -6, are expressed very early in the cardiac program.	bind
36473	3	10241	6	NULL	NULL	0	NULL	GATA-6	NULL		is a type of	NULL				zinc finger binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_mechdev_100_2_263_s_12	11165483	A fourth family of transcriptional regulators, the zinc finger binding proteins GATA-4, -5 and -6, are expressed very early in the cardiac program.	bind
36474	4	10241	6	NULL	NULL	0	NULL	GATA-4	NULL		is a type of	NULL				transcriptional regulator	NULL				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_100_2_263_s_12	11165483	A fourth family of transcriptional regulators, the zinc finger binding proteins GATA-4, -5 and -6, are expressed very early in the cardiac program.	bind
36475	5	10241	6	NULL	NULL	0	NULL	GATA-5	NULL		is a type of	NULL				transcriptional regulator	NULL				NULL		0	NULL	NULL	NULL	gw60_mechdev_100_2_263_s_12	11165483	A fourth family of transcriptional regulators, the zinc finger binding proteins GATA-4, -5 and -6, are expressed very early in the cardiac program.	bind
36476	6	10241	6	NULL	NULL	0	NULL	GATA-6	NULL		is a type of	NULL				transcriptional regulator	NULL				NULL		0	NULL	NULL	NULL	gw60_mechdev_100_2_263_s_12	11165483	A fourth family of transcriptional regulators, the zinc finger binding proteins GATA-4, -5 and -6, are expressed very early in the cardiac program.	bind
36477	7	10241	6	10	NULL	0	NULL	GATA-4	NULL		is expressed 	NULL	early			cardiac program	NULL				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_100_2_263_s_12	11165483	A fourth family of transcriptional regulators, the zinc finger binding proteins GATA-4, -5 and -6, are expressed very early in the cardiac program.	bind
36478	8	10241	6	10	NULL	0	NULL	GATA-5	NULL		is expressed	NULL	early			cardiac program	NULL				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_100_2_263_s_12	11165483	A fourth family of transcriptional regulators, the zinc finger binding proteins GATA-4, -5 and -6, are expressed very early in the cardiac program.	bind
36479	9	10241	6	10	NULL	0	NULL	GATA-6	NULL		is expressed	NULL	early			cardiac program	NULL				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_100_2_263_s_12	11165483	A fourth family of transcriptional regulators, the zinc finger binding proteins GATA-4, -5 and -6, are expressed very early in the cardiac program.	bind
43594	1	10242	5	11	NULL	NULL	NULL	CBP	GP		is					CREB binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_6_704_s_259	10189358	A fourth gene encodes a nuclear protein, CREB binding protein (CBP), that can bind to phosphorylated CREB to serve as a cofactor in the regulation of transcription of target genes.	bind
43595	2	10242	5	11	NULL	NULL	NULL	CBP	GP		is a type of					nuclear protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_6_704_s_259	10189358	A fourth gene encodes a nuclear protein, CREB binding protein (CBP), that can bind to phosphorylated CREB to serve as a cofactor in the regulation of transcription of target genes.	bind
43596	3	10242	5	11	NULL	NULL	NULL	CBP	GP		bind					CREB	GP	phosphorylated			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_6_704_s_259	10189358	A fourth gene encodes a nuclear protein, CREB binding protein (CBP), that can bind to phosphorylated CREB to serve as a cofactor in the regulation of transcription of target genes.	bind
43597	4	10242	5	11	NULL	NULL	NULL	statement 3	GP		serve as					cofactor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_6_704_s_259	10189358	A fourth gene encodes a nuclear protein, CREB binding protein (CBP), that can bind to phosphorylated CREB to serve as a cofactor in the regulation of transcription of target genes.	bind
43598	5	10242	5	11	NULL	NULL	NULL	statement 4	Process		during					target genes	GP	regulation of;; transcription of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_6_704_s_259	10189358	A fourth gene encodes a nuclear protein, CREB binding protein (CBP), that can bind to phosphorylated CREB to serve as a cofactor in the regulation of transcription of target genes.	bind
36480	1	10242	6	NULL	NULL	0	NULL	CBP	NULL		is 	NULL				CREB binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_6_704_s_259	10189358	A fourth gene encodes a nuclear protein, CREB binding protein (CBP), that can bind to phosphorylated CREB to serve as a cofactor in the regulation of transcription of target genes.	bind
36481	2	10242	6	NULL	NULL	0	NULL	CBP	NULL		bind	NULL				CREB	NULL	phosphorylated			NULL		0	NULL	NULL	NULL	gw60_circulationres_84_6_704_s_259	10189358	A fourth gene encodes a nuclear protein, CREB binding protein (CBP), that can bind to phosphorylated CREB to serve as a cofactor in the regulation of transcription of target genes.	bind
36482	3	10242	6	NULL	NULL	0	NULL	CBP	NULL		acts as a cofactor for	NULL				target genes	NULL	regulation of;; transcription of			NULL		0	NULL	NULL	NULL	gw60_circulationres_84_6_704_s_259	10189358	A fourth gene encodes a nuclear protein, CREB binding protein (CBP), that can bind to phosphorylated CREB to serve as a cofactor in the regulation of transcription of target genes.	bind
36483	4	10242	6	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_84_6_704_s_259	10189358	A fourth gene encodes a nuclear protein, CREB binding protein (CBP), that can bind to phosphorylated CREB to serve as a cofactor in the regulation of transcription of target genes.	bind
57485	5	10242	6	10	NULL	0	NULL	CBP			is a type of					nuclear protein					NULL		0	NULL	NULL	NULL	gw60_circulationres_84_6_704_s_259	10189358	A fourth gene encodes a nuclear protein, CREB binding protein (CBP), that can bind to phosphorylated CREB to serve as a cofactor in the regulation of transcription of target genes.	bind
43608	1	10243	5	11	NULL	NULL	NULL	HBO1	GP		is					histone acetyltransferase bound to ORC	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_2_435_s_255	10839822	A fourth human MYST protein is HBO1 (histone acetyltransferase bound  to ORC), which was discovered in a two-hybrid screen on the basis of its interaction with the ORC1 subunit of the origin recognition complex (ORC) ( ).	bind
43609	2	10243	5	11	NULL	NULL	NULL	HBO1	GP		is a type of					MYST protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_2_435_s_255	10839822	A fourth human MYST protein is HBO1 (histone acetyltransferase bound  to ORC), which was discovered in a two-hybrid screen on the basis of its interaction with the ORC1 subunit of the origin recognition complex (ORC) ( ).	bind
43610	3	10243	5	11	NULL	NULL	NULL	HBO1	GP	human	interact with					ORC	GP		ORC1 subunit		NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_2_435_s_255	10839822	A fourth human MYST protein is HBO1 (histone acetyltransferase bound  to ORC), which was discovered in a two-hybrid screen on the basis of its interaction with the ORC1 subunit of the origin recognition complex (ORC) ( ).	bind
43611	4	10243	5	11	NULL	NULL	NULL	ORC	GP		is					origin recognition complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_2_435_s_255	10839822	A fourth human MYST protein is HBO1 (histone acetyltransferase bound  to ORC), which was discovered in a two-hybrid screen on the basis of its interaction with the ORC1 subunit of the origin recognition complex (ORC) ( ).	bind
36484	1	10243	6	10	NULL	0	NULL	HBO1	NULL		is a type of	NULL				MYST protein	NULL				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_2_435_s_255	10839822	A fourth human MYST protein is HBO1 (histone acetyltransferase bound  to ORC), which was discovered in a two-hybrid screen on the basis of its interaction with the ORC1 subunit of the origin recognition complex (ORC) ( ).	bind
36485	2	10243	6	10	NULL	0	NULL	HBO1	NULL	human	bind	NULL				ORC	NULL		ORC1 subunit		NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_2_435_s_255	10839822	A fourth human MYST protein is HBO1 (histone acetyltransferase bound  to ORC), which was discovered in a two-hybrid screen on the basis of its interaction with the ORC1 subunit of the origin recognition complex (ORC) ( ).	bind
36486	3	10243	6	NULL	NULL	0	NULL	ORC	NULL		is	NULL				origin recognition complex	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_2_435_s_255	10839822	A fourth human MYST protein is HBO1 (histone acetyltransferase bound  to ORC), which was discovered in a two-hybrid screen on the basis of its interaction with the ORC1 subunit of the origin recognition complex (ORC) ( ).	bind
48427	4	10243	6	10	NULL	0	NULL	HBO1	NULL		is	NULL				histone acetyltransferase bound to ORC	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_2_435_s_255	10839822	A fourth human MYST protein is HBO1 (histone acetyltransferase bound  to ORC), which was discovered in a two-hybrid screen on the basis of its interaction with the ORC1 subunit of the origin recognition complex (ORC) ( ).	bind
43612	1	10245	5	11	NULL	NULL	NULL	growth factors	GP		bind					cell-membrane receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_31_18456_s_225	8702490	A fourth hypothesis invokes differences in the binding of growth factors to their cell-membrane receptors, which in several instances requires the presence of heparan sulfate, leading to a change in cell proliferation ( 36).	bind
43613	2	10245	5	11	NULL	NULL	NULL	statement 1	Process		requires					heparan sulfate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_31_18456_s_225	8702490	A fourth hypothesis invokes differences in the binding of growth factors to their cell-membrane receptors, which in several instances requires the presence of heparan sulfate, leading to a change in cell proliferation ( 36).	bind
43614	3	10245	5	11	NULL	NULL	NULL	statement 2	Process		leads to					cell proliferation	Process	change in			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_31_18456_s_225	8702490	A fourth hypothesis invokes differences in the binding of growth factors to their cell-membrane receptors, which in several instances requires the presence of heparan sulfate, leading to a change in cell proliferation ( 36).	bind
36487	1	10245	6	NULL	NULL	0	NULL	growth factors	NULL		bind	NULL				cell membrane receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_31_18456_s_225	8702490	A fourth hypothesis invokes differences in the binding of growth factors to their cell-membrane receptors, which in several instances requires the presence of heparan sulfate, leading to a change in cell proliferation ( 36).	bind
36488	2	10245	6	NULL	NULL	0	NULL	statement 1	NULL		requires	NULL				heparan sulfate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_31_18456_s_225	8702490	A fourth hypothesis invokes differences in the binding of growth factors to their cell-membrane receptors, which in several instances requires the presence of heparan sulfate, leading to a change in cell proliferation ( 36).	bind
36489	3	10245	6	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				cell proliferation	NULL	change in			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_31_18456_s_225	8702490	A fourth hypothesis invokes differences in the binding of growth factors to their cell-membrane receptors, which in several instances requires the presence of heparan sulfate, leading to a change in cell proliferation ( 36).	bind
43615	1	10246	5	11	NULL	NULL	NULL	TM1	GP		is					transmembrane one	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32016_s_58	8943250	A fourth mutation that converted a leucine to a serine in transmembrane one (TM1 L-S) destroyed the binding of iodinated Orphanin FQ.	bind
48728	2	10246	5	11	NULL	NULL	NULL	TM1	GP		is converted to			leucine		TM1	GP		serine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32016_s_58	8943250	A fourth mutation that converted a leucine to a serine in transmembrane one (TM1 L-S) destroyed the binding of iodinated Orphanin FQ.	bind
48729	3	10246	5	11	NULL	NULL	NULL	TM1	GP		bind					Orphanin FQ	GP	iodinated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32016_s_58	8943250	A fourth mutation that converted a leucine to a serine in transmembrane one (TM1 L-S) destroyed the binding of iodinated Orphanin FQ.	bind
48730	4	10246	5	11	NULL	NULL	NULL	statement 2	Process		destroys					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32016_s_58	8943250	A fourth mutation that converted a leucine to a serine in transmembrane one (TM1 L-S) destroyed the binding of iodinated Orphanin FQ.	bind
36490	1	10246	6	NULL	NULL	0	NULL	TM1	NULL		is	NULL				transmembrane one	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_50_32016_s_58	8943250	A fourth mutation that converted a leucine to a serine in transmembrane one (TM1 L-S) destroyed the binding of iodinated Orphanin FQ.	bind
36491	2	10246	6	NULL	NULL	0	NULL	TM-1	NULL		is converted to	NULL		leucine		TM-1	NULL		serine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_50_32016_s_58	8943250	A fourth mutation that converted a leucine to a serine in transmembrane one (TM1 L-S) destroyed the binding of iodinated Orphanin FQ.	bind
36492	3	10246	6	NULL	NULL	0	NULL	TM1	NULL		bind	NULL				Orphanin FQ	NULL	iodinated			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_50_32016_s_58	8943250	A fourth mutation that converted a leucine to a serine in transmembrane one (TM1 L-S) destroyed the binding of iodinated Orphanin FQ.	bind
36493	4	10246	6	NULL	NULL	0	NULL	statement 2	NULL		destroys	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_50_32016_s_58	8943250	A fourth mutation that converted a leucine to a serine in transmembrane one (TM1 L-S) destroyed the binding of iodinated Orphanin FQ.	bind
43616	1	10247	5	11	NULL	NULL	NULL	anti- Candida antibodies	GP		bind					Candida	Organism				NULL	lavage fluid	NULL	NULL	NULL	NULL	gw60_infectimmun_70_10_5790_s_200	12228309	A fourth possibility is that, due to infection with  Candida, anti- Candida antibodies could be bound by  Candida in the lavage fluid and removed during processing for the soluble fraction.	bind
36494	1	10247	6	NULL	NULL	0	NULL	anti- Candida antibodies	NULL		bind	NULL				Candida	NULL				NULL	lavage fluid	0	NULL	NULL	NULL	gw60_infectimmun_70_10_5790_s_200	12228309	A fourth possibility is that, due to infection with  Candida, anti- Candida antibodies could be bound by  Candida in the lavage fluid and removed during processing for the soluble fraction.	bind
43623	1	10249	5	11	NULL	NULL	NULL	Jak3 probe	GP		bind					CD3zeta	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_25378_s_170	11349123	A fraction (~1/150) of Jak3 probe bound to CD3zeta ( lane 4).	bind
36496	1	10249	6	NULL	NULL	0	NULL	Jak3 probe	NULL		bind	NULL				CD3zeta	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_27_25378_s_170	11349123	A fraction (~1/150) of Jak3 probe bound to CD3zeta ( lane 4).	bind
43624	1	10250	5	11	NULL	NULL	NULL	CDK7	GP		bind					XPD	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_14_3749_s_36	11447116	A fraction of CDK7 is also bound to XPD (Figure  1A), which is found along with CAK in TFIIH.	bind
43627	2	10250	5	11	NULL	NULL	NULL	XPD	GP		is found in					TFIIH	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_14_3749_s_36	11447116	A fraction of CDK7 is also bound to XPD (Figure  1A), which is found along with CAK in TFIIH.	bind
43628	3	10250	5	11	NULL	NULL	NULL	CAK	GP		is found in					TFIIH	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_14_3749_s_36	11447116	A fraction of CDK7 is also bound to XPD (Figure  1A), which is found along with CAK in TFIIH.	bind
36497	1	10250	6	NULL	NULL	0	NULL	CDK7	NULL		bind	NULL				XPD	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_14_3749_s_36	11447116	A fraction of CDK7 is also bound to XPD (Figure  1A), which is found along with CAK in TFIIH.	bind
37016	2	10250	6	NULL	NULL	0	NULL	XPD	NULL		is found in	NULL				TFIIH	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_14_3749_s_36	11447116	A fraction of CDK7 is also bound to XPD (Figure  1A), which is found along with CAK in TFIIH.	bind
37017	3	10250	6	NULL	NULL	0	NULL	CAK	NULL		is found in	NULL				TFIIH	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_14_3749_s_36	11447116	A fraction of CDK7 is also bound to XPD (Figure  1A), which is found along with CAK in TFIIH.	bind
43630	1	10251	5	11	NULL	NULL	NULL	LS-Rg	GP		bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_science_261_5120_7687382_s_6	7687382	A fraction of commercial  heparin bound to LS-Rg and LS-Rg bound to heparin-agarose, both in a calcium-dependent  manner.	bind
43631	2	10251	5	11	NULL	NULL	NULL	statement 1	Process		is dependent on					calcium	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_science_261_5120_7687382_s_6	7687382	A fraction of commercial  heparin bound to LS-Rg and LS-Rg bound to heparin-agarose, both in a calcium-dependent  manner.	bind
36498	1	10251	6	NULL	NULL	0	NULL	heparin	NULL		bind	NULL				LS-Rg	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_science_261_5120_7687382_s_6	7687382	A fraction of commercial  heparin bound to LS-Rg and LS-Rg bound to heparin-agarose, both in a calcium-dependent  manner.	bind
36499	2	10251	6	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				calcium	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_science_261_5120_7687382_s_6	7687382	A fraction of commercial  heparin bound to LS-Rg and LS-Rg bound to heparin-agarose, both in a calcium-dependent  manner.	bind
43634	1	10252	5	11	NULL	NULL	NULL	CREB polypeptide	GP		bind					GST-KIX	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_2_3_353_s_105	9774973	A fraction of each CREB polypeptide bound to GST-KIX resin is shown.	bind
36500	1	10252	6	NULL	NULL	0	NULL	CREB polypeptide	NULL		bind	NULL				GST-KIX	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_2_3_353_s_105	9774973	A fraction of each CREB polypeptide bound to GST-KIX resin is shown.	bind
43635	1	10253	5	11	NULL	NULL	NULL	mtHsp70	GP		bind		transiently			Tim44	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_5_941_s_14	11230118	A fraction of mtHsp70 transiently binds to the inner membrane protein Tim44 in an ATP-sensitive manner ( Kronidou  et al., 1994;  Rassow  et al., 1994;  Schneider  et al., 1994;  von Ahsen  et al., 1995;  Ungermann  et al., 1996).	bind
43636	2	10253	5	11	NULL	NULL	NULL	Tim44	GP		is a type of					inner membrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_5_941_s_14	11230118	A fraction of mtHsp70 transiently binds to the inner membrane protein Tim44 in an ATP-sensitive manner ( Kronidou  et al., 1994;  Rassow  et al., 1994;  Schneider  et al., 1994;  von Ahsen  et al., 1995;  Ungermann  et al., 1996).	bind
43637	3	10253	5	11	NULL	NULL	NULL	statement 1	Process		is sensitive to					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_5_941_s_14	11230118	A fraction of mtHsp70 transiently binds to the inner membrane protein Tim44 in an ATP-sensitive manner ( Kronidou  et al., 1994;  Rassow  et al., 1994;  Schneider  et al., 1994;  von Ahsen  et al., 1995;  Ungermann  et al., 1996).	bind
36501	1	10253	6	NULL	NULL	0	NULL	Tim44	NULL		is a type of	NULL				inner membrane protein	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_5_941_s_14	11230118	A fraction of mtHsp70 transiently binds to the inner membrane protein Tim44 in an ATP-sensitive manner ( Kronidou  et al., 1994;  Rassow  et al., 1994;  Schneider  et al., 1994;  von Ahsen  et al., 1995;  Ungermann  et al., 1996).	bind
36502	2	10253	6	NULL	NULL	0	NULL	mtHsp70	NULL		bind	NULL	transiently			Tim44	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_5_941_s_14	11230118	A fraction of mtHsp70 transiently binds to the inner membrane protein Tim44 in an ATP-sensitive manner ( Kronidou  et al., 1994;  Rassow  et al., 1994;  Schneider  et al., 1994;  von Ahsen  et al., 1995;  Ungermann  et al., 1996).	bind
36503	3	10253	6	NULL	NULL	0	NULL	statement 1	NULL		is sensitive to	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_5_941_s_14	11230118	A fraction of mtHsp70 transiently binds to the inner membrane protein Tim44 in an ATP-sensitive manner ( Kronidou  et al., 1994;  Rassow  et al., 1994;  Schneider  et al., 1994;  von Ahsen  et al., 1995;  Ungermann  et al., 1996).	bind
43639	1	10254	5	11	NULL	NULL	NULL	Smc3 fragment	GP		does not bind			251-968		chitin matrix	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_6_765_s_238	12654244	A fraction of Smc3's central aa 251-968 fragment was not bound to the chitin matrix, presumably because a portion of the Smc1/Smc3 heterodimer is not bound to Scc1 (see   Figure 3C).	bind
43641	2	10254	5	11	NULL	NULL	NULL	Smc1/Smc3 heterodimer	GP		does not bind					Scc1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_6_765_s_238	12654244	A fraction of Smc3's central aa 251-968 fragment was not bound to the chitin matrix, presumably because a portion of the Smc1/Smc3 heterodimer is not bound to Scc1 (see   Figure 3C).	bind
43642	3	10254	5	11	NULL	NULL	NULL	statement 2	Process		leads to		possibly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_6_765_s_238	12654244	A fraction of Smc3's central aa 251-968 fragment was not bound to the chitin matrix, presumably because a portion of the Smc1/Smc3 heterodimer is not bound to Scc1 (see   Figure 3C).	bind
36504	1	10254	6	NULL	NULL	0	NULL	Smc1/Smc3 heterodimer	NULL		does not bind	NULL				Scc1	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_112_6_765_s_238	12654244	A fraction of Smc3's central aa 251-968 fragment was not bound to the chitin matrix, presumably because a portion of the Smc1/Smc3 heterodimer is not bound to Scc1 (see   Figure 3C).	bind
36505	2	10254	6	10	NULL	0	NULL	Smc3 fragment			does not bind			251-968		chitin					NULL		NULL	NULL	NULL	NULL	gw60_cell_112_6_765_s_238	12654244	A fraction of Smc3's central aa 251-968 fragment was not bound to the chitin matrix, presumably because a portion of the Smc1/Smc3 heterodimer is not bound to Scc1 (see   Figure 3C).	bind
48428	3	10254	6	10	NULL	0	NULL	statement 1	NULL		leads to	NULL	possibly			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_112_6_765_s_238	12654244	A fraction of Smc3's central aa 251-968 fragment was not bound to the chitin matrix, presumably because a portion of the Smc1/Smc3 heterodimer is not bound to Scc1 (see   Figure 3C).	bind
43644	1	10255	5	11	NULL	NULL	NULL	U2 snRNA	NucleicAcid		bind					Cus1p	GP				NULL	splicing extracts	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2176_s_157	10688664	A fraction of U2 snRNA is bound to Cus1p in splicing extracts.	bind
36506	1	10255	6	NULL	NULL	0	NULL	U2 snRNA	NULL		bind	NULL				Cus1p	NULL				NULL	splicing extracts	0	NULL	NULL	NULL	gw60_molcellbiol_20_6_2176_s_157	10688664	A fraction of U2 snRNA is bound to Cus1p in splicing extracts.	bind
43646	1	10256	5	11	NULL	NULL	NULL	U3 fragment	GP		bind			3' domain		U3-55k	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_18_3462_s_193	10982864	A fragment consisting of the entire 3' domain of U3 was bound by U3-55k  in vivo (Fig.  4, 3' Domain, lanes 1 - 3), but as expected U3-55k did not interact with a sub-fragment consisting of the Box C''/D motif (composed of U3 Box C'', Box D and flanking stems; Fig.  4, lanes 7 - 9).	bind
43648	2	10256	5	11	NULL	NULL	NULL	U3-55k	GP		does not interact with					sub-fragment	AminoAcid		Box C''/D motif		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_18_3462_s_193	10982864	A fragment consisting of the entire 3' domain of U3 was bound by U3-55k  in vivo (Fig.  4, 3' Domain, lanes 1 - 3), but as expected U3-55k did not interact with a sub-fragment consisting of the Box C''/D motif (composed of U3 Box C'', Box D and flanking stems; Fig.  4, lanes 7 - 9).	bind
43650	3	10256	5	11	NULL	NULL	NULL	sub-fragment	AminoAcid		is composed of			Box C''/D motif					U3 Box C''		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_18_3462_s_193	10982864	A fragment consisting of the entire 3' domain of U3 was bound by U3-55k  in vivo (Fig.  4, 3' Domain, lanes 1 - 3), but as expected U3-55k did not interact with a sub-fragment consisting of the Box C''/D motif (composed of U3 Box C'', Box D and flanking stems; Fig.  4, lanes 7 - 9).	bind
43653	4	10256	5	11	NULL	NULL	NULL	sub-fragment	AminoAcid		is composed of			Box C''/D motif					Box D		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_18_3462_s_193	10982864	A fragment consisting of the entire 3' domain of U3 was bound by U3-55k  in vivo (Fig.  4, 3' Domain, lanes 1 - 3), but as expected U3-55k did not interact with a sub-fragment consisting of the Box C''/D motif (composed of U3 Box C'', Box D and flanking stems; Fig.  4, lanes 7 - 9).	bind
43654	5	10256	5	11	NULL	NULL	NULL	sub-fragment	AminoAcid		is composed of			Box C''/D motif					flanking stems		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_18_3462_s_193	10982864	A fragment consisting of the entire 3' domain of U3 was bound by U3-55k  in vivo (Fig.  4, 3' Domain, lanes 1 - 3), but as expected U3-55k did not interact with a sub-fragment consisting of the Box C''/D motif (composed of U3 Box C'', Box D and flanking stems; Fig.  4, lanes 7 - 9).	bind
36507	1	10256	6	NULL	NULL	0	NULL	U3	NULL		bind	NULL		3' domain		U3-55k	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_nucleicacidsres_28_18_3462_s_193	10982864	A fragment consisting of the entire 3' domain of U3 was bound by U3-55k  in vivo (Fig.  4, 3' Domain, lanes 1 - 3), but as expected U3-55k did not interact with a sub-fragment consisting of the Box C''/D motif (composed of U3 Box C'', Box D and flanking stems; Fig.  4, lanes 7 - 9).	bind
36508	2	10256	6	10	NULL	0	NULL	U3-55k			does not interact with					sub-fragment			Box C''/D motif		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_18_3462_s_193	10982864	A fragment consisting of the entire 3' domain of U3 was bound by U3-55k  in vivo (Fig.  4, 3' Domain, lanes 1 - 3), but as expected U3-55k did not interact with a sub-fragment consisting of the Box C''/D motif (composed of U3 Box C'', Box D and flanking stems; Fig.  4, lanes 7 - 9).	bind
48430	3	10256	6	10	NULL	0	NULL	sub-fragment			is composed of			Box C''/D motif					U3 Box C''		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_18_3462_s_193	10982864	A fragment consisting of the entire 3' domain of U3 was bound by U3-55k  in vivo (Fig.  4, 3' Domain, lanes 1 - 3), but as expected U3-55k did not interact with a sub-fragment consisting of the Box C''/D motif (composed of U3 Box C'', Box D and flanking stems; Fig.  4, lanes 7 - 9).	bind
48431	4	10256	6	10	NULL	0	NULL	sub-fragment			is composed of			Box C''/D motif					Box D		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_18_3462_s_193	10982864	A fragment consisting of the entire 3' domain of U3 was bound by U3-55k  in vivo (Fig.  4, 3' Domain, lanes 1 - 3), but as expected U3-55k did not interact with a sub-fragment consisting of the Box C''/D motif (composed of U3 Box C'', Box D and flanking stems; Fig.  4, lanes 7 - 9).	bind
48432	5	10256	6	10	NULL	0	NULL	sub-fragment			is composed of			Box C''/D motif					flanking stem		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_18_3462_s_193	10982864	A fragment consisting of the entire 3' domain of U3 was bound by U3-55k  in vivo (Fig.  4, 3' Domain, lanes 1 - 3), but as expected U3-55k did not interact with a sub-fragment consisting of the Box C''/D motif (composed of U3 Box C'', Box D and flanking stems; Fig.  4, lanes 7 - 9).	bind
44241	1	10257	5	11	NULL	NULL	NULL	fragment	GP		contains					ATP-DnaA	GP			box b	NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
44242	2	10257	5	11	NULL	NULL	NULL	fragment	GP		contains					ATP-DnaA	GP			box c	NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
44243	3	10257	5	11	NULL	NULL	NULL	fragment	GP		does not contain					DnaA	GP			box 1	NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
44244	4	10257	5	11	NULL	NULL	NULL	fragment	GP		does not contain					DnaA	GP			box 2	NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
44245	5	10257	5	11	NULL	NULL	NULL	statement 1	GP		does not bind					ATP-DnaA protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
44246	6	10257	5	11	NULL	NULL	NULL	statement 2	GP		does not bind					ATP-DnaA protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
44247	7	10257	5	11	NULL	NULL	NULL	statement 3	GP		does not bind					ATP-DnaA protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
44248	8	10257	5	11	NULL	NULL	NULL	statement 4	GP		does not bind					ATP-DnaA protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
44249	9	10257	5	11	NULL	NULL	NULL	statement 1	GP		does not bind					ADP-DnaA protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
44250	10	10257	5	11	NULL	NULL	NULL	statement 2	GP		does not bind					ADP-DnaA protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
44251	11	10257	5	11	NULL	NULL	NULL	statement 3	GP		does not bind					ADP-DnaA protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
44252	12	10257	5	11	NULL	NULL	NULL	statement 4	GP		does not bind					ADP-DnaA protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
37018	1	10257	6	NULL	NULL	0	NULL	fragment containing ATP-DnaA box b	NULL		does not bind	NULL				ATP-DnaA protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
37019	2	10257	6	NULL	NULL	0	NULL	fragment containing ATP-DnaA box c	NULL		does not bind	NULL				ATP-DnaA protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
48550	3	10257	6	NULL	NULL	0	NULL	statement 1	NULL		occurs simultaneously with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
48551	4	10257	6	NULL	NULL	0	NULL	fragment containing ATP-DnaA box b	NULL		does not bind	NULL				ATP-DnaA protein	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
48552	5	10257	6	NULL	NULL	0	NULL	fragment containing ATP-DnaA box c	NULL		does not bind	NULL				ADP-DnaA protein	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
48553	6	10257	6	NULL	NULL	0	NULL	statement 4	NULL		occurs simultaneously with	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
48554	7	10257	6	NULL	NULL	0	NULL	fragment without DnaA box1	NULL		does not bind	NULL				ATP-DnaA protein	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
48555	8	10257	6	NULL	NULL	0	NULL	fragment without DnaA box 2	NULL		does not bind	NULL				ATP-DnaA protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
48556	9	10257	6	NULL	NULL	0	NULL	statement 7	NULL		occurs simultaneously with	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
48557	10	10257	6	NULL	NULL	0	NULL	fragment containing ATP-DnaA box b	NULL		does not bind	NULL				ADP-DnaA protein	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
48558	11	10257	6	NULL	NULL	0	NULL	fragment containing ATP-DnaA box c	NULL		does not bind	NULL				ADP-DnaA protein	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
48559	12	10257	6	NULL	NULL	0	NULL	statement 10	NULL		occurs simultaneously with	NULL				statement 11	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_6169_s_113	10545126	A fragment containing ATP-DnaA box b and ATP-DnaA box c, but without DnaA boxes 1 and 2, did not show any binding of ATP- and ADP-DnaA protein.	bind
43657	1	10258	5	11	NULL	NULL	NULL	fragment containing part of coil X	GP		does not bind					p115	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_14_10196_s_84	10744704	A fragment containing part of coil X ( lane 3), a fragment containing coil II ( lane 5), and GST alone ( lane 1) did not bind p115.	bind
43659	2	10258	5	11	NULL	NULL	NULL	fragment containing coil II 	GP		does not bind					p115	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_14_10196_s_84	10744704	A fragment containing part of coil X ( lane 3), a fragment containing coil II ( lane 5), and GST alone ( lane 1) did not bind p115.	bind
43660	3	10258	5	11	NULL	NULL	NULL	GST	GP		does not bind					p115	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_14_10196_s_84	10744704	A fragment containing part of coil X ( lane 3), a fragment containing coil II ( lane 5), and GST alone ( lane 1) did not bind p115.	bind
36509	1	10258	6	NULL	NULL	0	NULL	fragment containing part of coil X	NULL		does not bind	NULL				p115	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10196_s_84	10744704	A fragment containing part of coil X ( lane 3), a fragment containing coil II ( lane 5), and GST alone ( lane 1) did not bind p115.	bind
36510	2	10258	6	NULL	NULL	0	NULL	fragment containing coil II	NULL		does not bind	NULL				p115	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10196_s_84	10744704	A fragment containing part of coil X ( lane 3), a fragment containing coil II ( lane 5), and GST alone ( lane 1) did not bind p115.	bind
36511	3	10258	6	NULL	NULL	0	NULL	GST	NULL		does not bind	NULL				p115	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10196_s_84	10744704	A fragment containing part of coil X ( lane 3), a fragment containing coil II ( lane 5), and GST alone ( lane 1) did not bind p115.	bind
43661	1	10259	5	11	NULL	NULL	NULL	AP53	Organism		is					PAM-expressing group A streptococcal strain	Organism				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_38_24420_s_66	9733732	A fragment encompassing K1-K3 bound to the PAM-expressing group A streptococcal strain AP53, whereas fragments containing K4 alone or K5 and the proteinase domain (m-Pg) showed almost no binding to this strain (Fig.  2,  A-C).	bind
43662	2	10259	5	11	NULL	NULL	NULL	fragment	AminoAcid		encompass								K1-K3		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_38_24420_s_66	9733732	A fragment encompassing K1-K3 bound to the PAM-expressing group A streptococcal strain AP53, whereas fragments containing K4 alone or K5 and the proteinase domain (m-Pg) showed almost no binding to this strain (Fig.  2,  A-C).	bind
43663	3	10259	5	11	NULL	NULL	NULL	statement 2	AminoAcid		bind					AP53	Organism				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_38_24420_s_66	9733732	A fragment encompassing K1-K3 bound to the PAM-expressing group A streptococcal strain AP53, whereas fragments containing K4 alone or K5 and the proteinase domain (m-Pg) showed almost no binding to this strain (Fig.  2,  A-C).	bind
43664	4	10259	5	11	NULL	NULL	NULL	fragment	AminoAcid		contains								K4		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_38_24420_s_66	9733732	A fragment encompassing K1-K3 bound to the PAM-expressing group A streptococcal strain AP53, whereas fragments containing K4 alone or K5 and the proteinase domain (m-Pg) showed almost no binding to this strain (Fig.  2,  A-C).	bind
43665	5	10259	5	11	NULL	NULL	NULL	statement 4	AminoAcid		does not bind					AP53	Organism				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_38_24420_s_66	9733732	A fragment encompassing K1-K3 bound to the PAM-expressing group A streptococcal strain AP53, whereas fragments containing K4 alone or K5 and the proteinase domain (m-Pg) showed almost no binding to this strain (Fig.  2,  A-C).	bind
43667	6	10259	5	11	NULL	NULL	NULL	fragment	AminoAcid		contains								K5		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_38_24420_s_66	9733732	A fragment encompassing K1-K3 bound to the PAM-expressing group A streptococcal strain AP53, whereas fragments containing K4 alone or K5 and the proteinase domain (m-Pg) showed almost no binding to this strain (Fig.  2,  A-C).	bind
43669	7	10259	5	11	NULL	NULL	NULL	statement 6	AminoAcid		does not bind					AP53	Organism				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_38_24420_s_66	9733732	A fragment encompassing K1-K3 bound to the PAM-expressing group A streptococcal strain AP53, whereas fragments containing K4 alone or K5 and the proteinase domain (m-Pg) showed almost no binding to this strain (Fig.  2,  A-C).	bind
43670	8	10259	5	11	NULL	NULL	NULL	fragment	AminoAcid		contains								m-Pg		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_38_24420_s_66	9733732	A fragment encompassing K1-K3 bound to the PAM-expressing group A streptococcal strain AP53, whereas fragments containing K4 alone or K5 and the proteinase domain (m-Pg) showed almost no binding to this strain (Fig.  2,  A-C).	bind
43672	9	10259	5	11	NULL	NULL	NULL	m-Pg	GP		is					proteinase domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_38_24420_s_66	9733732	A fragment encompassing K1-K3 bound to the PAM-expressing group A streptococcal strain AP53, whereas fragments containing K4 alone or K5 and the proteinase domain (m-Pg) showed almost no binding to this strain (Fig.  2,  A-C).	bind
43673	10	10259	5	11	NULL	NULL	NULL	statement 8	AminoAcid		does not bind					AP53	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_38_24420_s_66	9733732	A fragment encompassing K1-K3 bound to the PAM-expressing group A streptococcal strain AP53, whereas fragments containing K4 alone or K5 and the proteinase domain (m-Pg) showed almost no binding to this strain (Fig.  2,  A-C).	bind
36512	1	10259	6	NULL	NULL	0	NULL		NULL		bind	NULL		K1-K3		AP53	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_38_24420_s_66	9733732	A fragment encompassing K1-K3 bound to the PAM-expressing group A streptococcal strain AP53, whereas fragments containing K4 alone or K5 and the proteinase domain (m-Pg) showed almost no binding to this strain (Fig.  2,  A-C).	bind
36513	2	10259	6	NULL	NULL	0	NULL	AP53	NULL		is	NULL				PAM-expressing group A streptococcal strain	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_38_24420_s_66	9733732	A fragment encompassing K1-K3 bound to the PAM-expressing group A streptococcal strain AP53, whereas fragments containing K4 alone or K5 and the proteinase domain (m-Pg) showed almost no binding to this strain (Fig.  2,  A-C).	bind
36514	3	10259	6	NULL	NULL	0	NULL		NULL		does not bind	NULL		K4		AP53	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_38_24420_s_66	9733732	A fragment encompassing K1-K3 bound to the PAM-expressing group A streptococcal strain AP53, whereas fragments containing K4 alone or K5 and the proteinase domain (m-Pg) showed almost no binding to this strain (Fig.  2,  A-C).	bind
36515	4	10259	6	NULL	NULL	0	NULL		NULL		does not bind	NULL		K5		AP53	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_38_24420_s_66	9733732	A fragment encompassing K1-K3 bound to the PAM-expressing group A streptococcal strain AP53, whereas fragments containing K4 alone or K5 and the proteinase domain (m-Pg) showed almost no binding to this strain (Fig.  2,  A-C).	bind
36516	5	10259	6	NULL	NULL	0	NULL		NULL		does not bind	NULL		proteinase domain		AP53	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_38_24420_s_66	9733732	A fragment encompassing K1-K3 bound to the PAM-expressing group A streptococcal strain AP53, whereas fragments containing K4 alone or K5 and the proteinase domain (m-Pg) showed almost no binding to this strain (Fig.  2,  A-C).	bind
43674	2	10260	5	11	NULL	NULL	NULL	p3RIZrdeltaNBam construct	GP		bind			1272-1706		PR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_26_15933_s_153	9632640	A fragment encompassing residues 900 to 1272 (construct p3RIZrBB) did not bind to GST-PR, but a fragment encoding residues 1272 to the end codon 1706 (construct p3RIZrdeltaNBam) retained full PR binding activity.	bind
43677	1	10260	5	11	NULL	NULL	NULL	p3RIZrBB construct	GP		does not bind			900-1272		GST-PR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_26_15933_s_153	9632640	A fragment encompassing residues 900 to 1272 (construct p3RIZrBB) did not bind to GST-PR, but a fragment encoding residues 1272 to the end codon 1706 (construct p3RIZrdeltaNBam) retained full PR binding activity.	bind
37022	1	10260	6	NULL	NULL	0	NULL	construct p3RIZrBB	NULL		does not bind	NULL		900-1272		GST-PR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_26_15933_s_153	9632640	A fragment encompassing residues 900 to 1272 (construct p3RIZrBB) did not bind to GST-PR, but a fragment encoding residues 1272 to the end codon 1706 (construct p3RIZrdeltaNBam) retained full PR binding activity.	bind
37023	2	10260	6	NULL	NULL	0	NULL	construct p3RIZrdeltaNBam	NULL		bind	NULL		1272-1706		PR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_26_15933_s_153	9632640	A fragment encompassing residues 900 to 1272 (construct p3RIZrBB) did not bind to GST-PR, but a fragment encoding residues 1272 to the end codon 1706 (construct p3RIZrdeltaNBam) retained full PR binding activity.	bind
43683	1	10262	5	11	NULL	NULL	NULL	Smad1	GP	mutant	bind			C86-465		calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41430_s_178	11007779	A fragment lacking the amino-terminal 86 residues (Smad1(C86-465)) still bound calmodulin, while deleting nine more amino acids (Smad1(C95-465)) eliminated calmodulin binding (Fig.  2,  A and  B).	bind
43684	2	10262	5	11	NULL	NULL	NULL	Smad1	GP	mutant	does not bind			C95-465		calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41430_s_178	11007779	A fragment lacking the amino-terminal 86 residues (Smad1(C86-465)) still bound calmodulin, while deleting nine more amino acids (Smad1(C95-465)) eliminated calmodulin binding (Fig.  2,  A and  B).	bind
36517	1	10262	6	10	NULL	0	NULL	Smad1	NULL	mutant	bind	NULL		C86-485		calmodulin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41430_s_178	11007779	A fragment lacking the amino-terminal 86 residues (Smad1(C86-465)) still bound calmodulin, while deleting nine more amino acids (Smad1(C95-465)) eliminated calmodulin binding (Fig.  2,  A and  B).	bind
36518	2	10262	6	10	NULL	0	NULL	Smad1	NULL	mutant	does not bind	NULL		C95-465		calmodulin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41430_s_178	11007779	A fragment lacking the amino-terminal 86 residues (Smad1(C86-465)) still bound calmodulin, while deleting nine more amino acids (Smad1(C95-465)) eliminated calmodulin binding (Fig.  2,  A and  B).	bind
43685	1	10263	5	11	NULL	NULL	NULL	APC fragment	GP		contains								beta-catenin-binding repeat 7;;SAMP repeat		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_10_2270_s_57	10811618	A fragment of APC containing beta-catenin-binding repeat 7 and the third SAMP repeat bound equally well to the Axin-RGS and p38 proteins (Figure  2A).	bind
43686	2	10263	5	11	NULL	NULL	NULL	statement 1	GP		bind					Axin-RGS	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_10_2270_s_57	10811618	A fragment of APC containing beta-catenin-binding repeat 7 and the third SAMP repeat bound equally well to the Axin-RGS and p38 proteins (Figure  2A).	bind
43687	3	10263	5	11	NULL	NULL	NULL	statement 1	GP		bind					p38 proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_10_2270_s_57	10811618	A fragment of APC containing beta-catenin-binding repeat 7 and the third SAMP repeat bound equally well to the Axin-RGS and p38 proteins (Figure  2A).	bind
36519	2	10263	6	10	NULL	0	NULL	statement 1			bind					Axin-RGS					NULL		NULL	NULL	NULL	NULL	gw60_embo_19_10_2270_s_57	10811618	A fragment of APC containing beta-catenin-binding repeat 7 and the third SAMP repeat bound equally well to the Axin-RGS and p38 proteins (Figure  2A).	bind
36520	3	10263	6	10	NULL	0	NULL	statement 1			bind					p38 proteins					NULL		NULL	NULL	NULL	NULL	gw60_embo_19_10_2270_s_57	10811618	A fragment of APC containing beta-catenin-binding repeat 7 and the third SAMP repeat bound equally well to the Axin-RGS and p38 proteins (Figure  2A).	bind
57486	1	10263	6	10	NULL	0	NULL	APC fragment			contains								\tbeta-catenin-binding repeat 7;;SAMP repeat		NULL		0	NULL	NULL	NULL	gw60_embo_19_10_2270_s_57	10811618	A fragment of APC containing beta-catenin-binding repeat 7 and the third SAMP repeat bound equally well to the Axin-RGS and p38 proteins (Figure  2A).	bind
43688	1	10264	5	11	NULL	NULL	NULL	CKIIbeta fragment	GP		does not bind					Mos	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_17_9136_s_94	9256448	A fragment of CKIIbeta that does not bind to Mos, CKIIbeta1-160, had no effect ( 7).	bind
36521	1	10264	6	10	NULL	0	NULL	CKIIbeta fragment			does not bind					Mos					NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_17_9136_s_94	9256448	A fragment of CKIIbeta that does not bind to Mos, CKIIbeta1-160, had no effect ( 7).	bind
44235	1	10265	5	11	NULL	NULL	NULL	hCASK fragment	GP		contains							intact	SH3 domain;;GUK domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41192_s_221	10993877	A fragment of hCASK containing the intact SH3 and GUK domains ( SH3GUK) does not bind the hCASK SH3 domain, again suggesting that SH3-GUK interactions in  cis are inhibitory to similar interactions in  trans.	bind
44239	3	10265	5	11	NULL	NULL	NULL	statement 1	GP		does not bind					hCASK	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41192_s_221	10993877	A fragment of hCASK containing the intact SH3 and GUK domains ( SH3GUK) does not bind the hCASK SH3 domain, again suggesting that SH3-GUK interactions in  cis are inhibitory to similar interactions in  trans.	bind
57487	2	10265	5	11	NULL	NULL	NULL	SH3GUK	GP		is					intact SH3 and GUK domains	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41192_s_221	10993877	A fragment of hCASK containing the intact SH3 and GUK domains ( SH3GUK) does not bind the hCASK SH3 domain, again suggesting that SH3-GUK interactions in  cis are inhibitory to similar interactions in  trans.	bind
37024	1	10265	6	NULL	NULL	0	NULL	hCASK	NULL		does not bind	NULL		SH3GUK		hCASK	NULL		SH3 domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41192_s_221	10993877	A fragment of hCASK containing the intact SH3 and GUK domains ( SH3GUK) does not bind the hCASK SH3 domain, again suggesting that SH3-GUK interactions in  cis are inhibitory to similar interactions in  trans.	bind
37025	2	10265	6	NULL	NULL	0	NULL	SH3GUK	NULL		is 	NULL				intact SH3 and GUK domains	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41192_s_221	10993877	A fragment of hCASK containing the intact SH3 and GUK domains ( SH3GUK) does not bind the hCASK SH3 domain, again suggesting that SH3-GUK interactions in  cis are inhibitory to similar interactions in  trans.	bind
43690	1	10266	5	11	NULL	NULL	NULL	hEST1A fragment	GP		contains			630-1388					TPR repeats;;PIN domain		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_8_698_s_80	12699629	A fragment of hEST1A (spanning aa 630-1388) that contained the TPR repeats and PIN domain did not bind DNA (Figure S2A).	bind
43691	2	10266	5	11	NULL	NULL	NULL	statement 1	GP		does not bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_8_698_s_80	12699629	A fragment of hEST1A (spanning aa 630-1388) that contained the TPR repeats and PIN domain did not bind DNA (Figure S2A).	bind
36522	1	10266	6	10	NULL	0	NULL	hEST1A	NULL		contains	NULL		aa 630-1388			NULL		TPR repeats;; PIN domain		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_8_698_s_80	12699629	A fragment of hEST1A (spanning aa 630-1388) that contained the TPR repeats and PIN domain did not bind DNA (Figure S2A).	bind
36523	2	10266	6	10	NULL	0	NULL	statement 1	NULL		does not bind	NULL				DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_8_698_s_80	12699629	A fragment of hEST1A (spanning aa 630-1388) that contained the TPR repeats and PIN domain did not bind DNA (Figure S2A).	bind
43692	1	10267	5	11	NULL	NULL	NULL	MASP-1 fragment	GP		comprise								CUB-1;;EGF		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_28_25894_s_173	11337510	A fragment of MASP-1 comprising the CUB-1 and EGF modules ( 13) bound to MBP-A, demonstrating that either or both of these domains form part of the binding site.	bind
43693	2	10267	5	11	NULL	NULL	NULL	statement 1	GP		bind					MBP-A	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_28_25894_s_173	11337510	A fragment of MASP-1 comprising the CUB-1 and EGF modules ( 13) bound to MBP-A, demonstrating that either or both of these domains form part of the binding site.	bind
36524	1	10267	6	NULL	NULL	0	NULL	MASP-1	NULL		bind	NULL		CUB-1;; EGF		MBP-A	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_28_25894_s_173	11337510	A fragment of MASP-1 comprising the CUB-1 and EGF modules ( 13) bound to MBP-A, demonstrating that either or both of these domains form part of the binding site.	bind
44226	1	10268	5	11	NULL	NULL	NULL	N-WASP fragment	GP		include								basic region		NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_70_0_649_s_269	11395419	A fragment of N-WASP including this basic region and GBD binds PIP2-containing vesicles, and deletion or point mutations reducing the positive charge of the basic region reduce PIP2 binding ( 66,  86).	bind
44227	2	10268	5	11	NULL	NULL	NULL	N-WASP fragment	GP		include								GBD		NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_70_0_649_s_269	11395419	A fragment of N-WASP including this basic region and GBD binds PIP2-containing vesicles, and deletion or point mutations reducing the positive charge of the basic region reduce PIP2 binding ( 66,  86).	bind
44228	3	10268	5	11	NULL	NULL	NULL	vesicles	CellComponent		contains					PIP2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_70_0_649_s_269	11395419	A fragment of N-WASP including this basic region and GBD binds PIP2-containing vesicles, and deletion or point mutations reducing the positive charge of the basic region reduce PIP2 binding ( 66,  86).	bind
44229	4	10268	5	11	NULL	NULL	NULL	statement 1	GP		bind					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_70_0_649_s_269	11395419	A fragment of N-WASP including this basic region and GBD binds PIP2-containing vesicles, and deletion or point mutations reducing the positive charge of the basic region reduce PIP2 binding ( 66,  86).	bind
44230	5	10268	5	11	NULL	NULL	NULL	statement 2	GP		bind					statement 3	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_70_0_649_s_269	11395419	A fragment of N-WASP including this basic region and GBD binds PIP2-containing vesicles, and deletion or point mutations reducing the positive charge of the basic region reduce PIP2 binding ( 66,  86).	bind
44231	6	10268	5	11	NULL	NULL	NULL	N-WASP	GP	deletion mutation of	reduce							positive charge of	basic region		NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_70_0_649_s_269	11395419	A fragment of N-WASP including this basic region and GBD binds PIP2-containing vesicles, and deletion or point mutations reducing the positive charge of the basic region reduce PIP2 binding ( 66,  86).	bind
44232	7	10268	5	11	NULL	NULL	NULL	N-WASP fragment	GP	point mutation of	reduce							positive charge of	basic region		NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_70_0_649_s_269	11395419	A fragment of N-WASP including this basic region and GBD binds PIP2-containing vesicles, and deletion or point mutations reducing the positive charge of the basic region reduce PIP2 binding ( 66,  86).	bind
44233	8	10268	5	11	NULL	NULL	NULL	statement 6	Process		reduce					PIP2	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_70_0_649_s_269	11395419	A fragment of N-WASP including this basic region and GBD binds PIP2-containing vesicles, and deletion or point mutations reducing the positive charge of the basic region reduce PIP2 binding ( 66,  86).	bind
44234	9	10268	5	11	NULL	NULL	NULL	statement 7	Process		reduce					PIP2	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_70_0_649_s_269	11395419	A fragment of N-WASP including this basic region and GBD binds PIP2-containing vesicles, and deletion or point mutations reducing the positive charge of the basic region reduce PIP2 binding ( 66,  86).	bind
37026	1	10268	6	NULL	NULL	0	NULL	N-WASP	NULL		bind	NULL		basic region		PIP2-containing vesicles	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_70_0_649_s_269	11395419	A fragment of N-WASP including this basic region and GBD binds PIP2-containing vesicles, and deletion or point mutations reducing the positive charge of the basic region reduce PIP2 binding ( 66,  86).	bind
37027	2	10268	6	NULL	NULL	0	NULL	N-WASP	NULL		bind	NULL		GBD		PIP2-containing vesicles	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_70_0_649_s_269	11395419	A fragment of N-WASP including this basic region and GBD binds PIP2-containing vesicles, and deletion or point mutations reducing the positive charge of the basic region reduce PIP2 binding ( 66,  86).	bind
37028	3	10268	6	NULL	NULL	0	NULL	statement 1	NULL		is simultaneous with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_70_0_649_s_269	11395419	A fragment of N-WASP including this basic region and GBD binds PIP2-containing vesicles, and deletion or point mutations reducing the positive charge of the basic region reduce PIP2 binding ( 66,  86).	bind
37029	4	10268	6	NULL	NULL	0	NULL	N-WASP	NULL	deletion of	reduces	NULL		basic region		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_70_0_649_s_269	11395419	A fragment of N-WASP including this basic region and GBD binds PIP2-containing vesicles, and deletion or point mutations reducing the positive charge of the basic region reduce PIP2 binding ( 66,  86).	bind
48569	5	10268	6	NULL	NULL	0	NULL	N-WASP	NULL	mutant	reduces	NULL					NULL	positive charge on	basic region		NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_70_0_649_s_269	11395419	A fragment of N-WASP including this basic region and GBD binds PIP2-containing vesicles, and deletion or point mutations reducing the positive charge of the basic region reduce PIP2 binding ( 66,  86).	bind
48570	6	10268	6	NULL	NULL	0	NULL	statement 5	NULL		reduces	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_70_0_649_s_269	11395419	A fragment of N-WASP including this basic region and GBD binds PIP2-containing vesicles, and deletion or point mutations reducing the positive charge of the basic region reduce PIP2 binding ( 66,  86).	bind
43694	1	10270	5	11	NULL	NULL	NULL	PEX5 fragment	GP		contains							little more than	PTS1-binding domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_147_4_761_s_184	10562279	A fragment of PEX5 containing little more than the PTS1-binding domain of PEX5 retained full binding to PEX12.	bind
43696	2	10270	5	11	NULL	NULL	NULL	statement 1	GP		bind					PEX12	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_147_4_761_s_184	10562279	A fragment of PEX5 containing little more than the PTS1-binding domain of PEX5 retained full binding to PEX12.	bind
36525	1	10270	6	10	NULL	0	NULL	PEX5 fragment			contains								PTS1-binding domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_147_4_761_s_184	10562279	A fragment of PEX5 containing little more than the PTS1-binding domain of PEX5 retained full binding to PEX12.	bind
57488	2	10270	6	10	NULL	0	NULL	statement 1			bind					PEX12					NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_4_761_s_184	10562279	A fragment of PEX5 containing little more than the PTS1-binding domain of PEX5 retained full binding to PEX12.	bind
43697	1	10271	5	11	NULL	NULL	NULL	Raf kinase fragment	GP		bind		preferentially			GTP-Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_29_22037_s_224	10801823	A fragment of Raf kinase that binds preferentially to GTP-Ras was used as an affinity reagent to isolate active Ha-Ras proteins from stimulated cells.	bind
36526	1	10271	6	NULL	NULL	0	NULL	fragment of Raf kinase	NULL		bind	NULL	preferentially			GTP-Ras	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_29_22037_s_224	10801823	A fragment of Raf kinase that binds preferentially to GTP-Ras was used as an affinity reagent to isolate active Ha-Ras proteins from stimulated cells.	bind
44217	1	10272	5	11	NULL	NULL	NULL	T antigen fragment	GP		express								J domain		NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_2_179_s_505	12040123	A fragment of T antigen that expresses the J domain and pRB-binding motif (N1 to 121) is sufficient to induce pancreatic and hepatic tumors as well as full-length T antigen, suggesting that binding to p53 is not required to induce tumors in these systems ( 7,  241).	bind
44218	2	10272	5	11	NULL	NULL	NULL	T antigen fragment	GP		express								pRB-binding motif (N1 to 121)		NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_2_179_s_505	12040123	A fragment of T antigen that expresses the J domain and pRB-binding motif (N1 to 121) is sufficient to induce pancreatic and hepatic tumors as well as full-length T antigen, suggesting that binding to p53 is not required to induce tumors in these systems ( 7,  241).	bind
44219	3	10272	5	11	NULL	NULL	NULL	statement 1	Process		induce					pancreatic tumor	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_2_179_s_505	12040123	A fragment of T antigen that expresses the J domain and pRB-binding motif (N1 to 121) is sufficient to induce pancreatic and hepatic tumors as well as full-length T antigen, suggesting that binding to p53 is not required to induce tumors in these systems ( 7,  241).	bind
44220	4	10272	5	11	NULL	NULL	NULL	statement 2	Process		induce					pancreatic tumor	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_2_179_s_505	12040123	A fragment of T antigen that expresses the J domain and pRB-binding motif (N1 to 121) is sufficient to induce pancreatic and hepatic tumors as well as full-length T antigen, suggesting that binding to p53 is not required to induce tumors in these systems ( 7,  241).	bind
44221	5	10272	5	11	NULL	NULL	NULL	statement 1	Process		induce					hepatic tumor	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_2_179_s_505	12040123	A fragment of T antigen that expresses the J domain and pRB-binding motif (N1 to 121) is sufficient to induce pancreatic and hepatic tumors as well as full-length T antigen, suggesting that binding to p53 is not required to induce tumors in these systems ( 7,  241).	bind
44222	6	10272	5	11	NULL	NULL	NULL	statement 2	Process		induce					hepatic tumor	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_2_179_s_505	12040123	A fragment of T antigen that expresses the J domain and pRB-binding motif (N1 to 121) is sufficient to induce pancreatic and hepatic tumors as well as full-length T antigen, suggesting that binding to p53 is not required to induce tumors in these systems ( 7,  241).	bind
48560	1	10272	6	NULL	NULL	0	NULL	fragment of T antigen	NULL		expresses	NULL					NULL		J domain		NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_2_179_s_505	12040123	A fragment of T antigen that expresses the J domain and pRB-binding motif (N1 to 121) is sufficient to induce pancreatic and hepatic tumors as well as full-length T antigen, suggesting that binding to p53 is not required to induce tumors in these systems ( 7,  241).	bind
48561	2	10272	6	NULL	NULL	0	NULL	fragment of T antigen	NULL		expresses	NULL					NULL		pRB-binding motif (N1-121)		NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_2_179_s_505	12040123	A fragment of T antigen that expresses the J domain and pRB-binding motif (N1 to 121) is sufficient to induce pancreatic and hepatic tumors as well as full-length T antigen, suggesting that binding to p53 is not required to induce tumors in these systems ( 7,  241).	bind
48562	3	10272	6	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL				pancreatic tumors	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_2_179_s_505	12040123	A fragment of T antigen that expresses the J domain and pRB-binding motif (N1 to 121) is sufficient to induce pancreatic and hepatic tumors as well as full-length T antigen, suggesting that binding to p53 is not required to induce tumors in these systems ( 7,  241).	bind
48563	4	10272	6	NULL	NULL	0	NULL	statement 2	NULL		induce	NULL				pancreatic tumors	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_2_179_s_505	12040123	A fragment of T antigen that expresses the J domain and pRB-binding motif (N1 to 121) is sufficient to induce pancreatic and hepatic tumors as well as full-length T antigen, suggesting that binding to p53 is not required to induce tumors in these systems ( 7,  241).	bind
48564	5	10272	6	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL				hepatic tumors	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_2_179_s_505	12040123	A fragment of T antigen that expresses the J domain and pRB-binding motif (N1 to 121) is sufficient to induce pancreatic and hepatic tumors as well as full-length T antigen, suggesting that binding to p53 is not required to induce tumors in these systems ( 7,  241).	bind
48565	6	10272	6	NULL	NULL	0	NULL	statement 2	NULL		induce	NULL				hepatic tumors	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_2_179_s_505	12040123	A fragment of T antigen that expresses the J domain and pRB-binding motif (N1 to 121) is sufficient to induce pancreatic and hepatic tumors as well as full-length T antigen, suggesting that binding to p53 is not required to induce tumors in these systems ( 7,  241).	bind
44196	1	10273	5	11	NULL	NULL	NULL	Nt-TPR9	GP		is					N terminus to the end of TPR9	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_142	16880507	A fragment of Tfc4 extending from the N terminus to the end of TPR9 (Nt-TPR9) binds to Brf1 with reduced affinity relative to the two independent Brf1 binding sites (Nt-TPR5 and TPR6-9) contained within this region ( ).	bind
44212	2	10273	5	11	NULL	NULL	NULL	Tfc4 fragment	GP		bind			Nt-TPR9		Brf1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_142	16880507	A fragment of Tfc4 extending from the N terminus to the end of TPR9 (Nt-TPR9) binds to Brf1 with reduced affinity relative to the two independent Brf1 binding sites (Nt-TPR5 and TPR6-9) contained within this region ( ).	bind
44213	3	10273	5	11	NULL	NULL	NULL	Tfc4	GP		bind			Nt-TPR5		Brf1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_142	16880507	A fragment of Tfc4 extending from the N terminus to the end of TPR9 (Nt-TPR9) binds to Brf1 with reduced affinity relative to the two independent Brf1 binding sites (Nt-TPR5 and TPR6-9) contained within this region ( ).	bind
44214	4	10273	5	11	NULL	NULL	NULL	Tfc4	GP		bind			TPR6-9		Brf1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_142	16880507	A fragment of Tfc4 extending from the N terminus to the end of TPR9 (Nt-TPR9) binds to Brf1 with reduced affinity relative to the two independent Brf1 binding sites (Nt-TPR5 and TPR6-9) contained within this region ( ).	bind
44215	5	10273	5	11	NULL	NULL	NULL	statement 2	Process	affinity of	is lower than					statement 3	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_142	16880507	A fragment of Tfc4 extending from the N terminus to the end of TPR9 (Nt-TPR9) binds to Brf1 with reduced affinity relative to the two independent Brf1 binding sites (Nt-TPR5 and TPR6-9) contained within this region ( ).	bind
44216	6	10273	5	11	NULL	NULL	NULL	statement 2	Process	affinity of	is lower than					statement 4	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_142	16880507	A fragment of Tfc4 extending from the N terminus to the end of TPR9 (Nt-TPR9) binds to Brf1 with reduced affinity relative to the two independent Brf1 binding sites (Nt-TPR5 and TPR6-9) contained within this region ( ).	bind
37030	1	10273	6	NULL	NULL	0	NULL	Nt-TPR9	NULL		is	NULL				N terminus to the end of TPR9	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_142	16880507	A fragment of Tfc4 extending from the N terminus to the end of TPR9 (Nt-TPR9) binds to Brf1 with reduced affinity relative to the two independent Brf1 binding sites (Nt-TPR5 and TPR6-9) contained within this region ( ).	bind
37031	2	10273	6	NULL	NULL	0	NULL	Tfc4	NULL		bind	NULL		Nt-TPR9		Brf1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_142	16880507	A fragment of Tfc4 extending from the N terminus to the end of TPR9 (Nt-TPR9) binds to Brf1 with reduced affinity relative to the two independent Brf1 binding sites (Nt-TPR5 and TPR6-9) contained within this region ( ).	bind
37032	3	10273	6	NULL	NULL	0	NULL	Tfc4	NULL		bind	NULL		Nt-TPR5		Brf1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_142	16880507	A fragment of Tfc4 extending from the N terminus to the end of TPR9 (Nt-TPR9) binds to Brf1 with reduced affinity relative to the two independent Brf1 binding sites (Nt-TPR5 and TPR6-9) contained within this region ( ).	bind
37033	4	10273	6	NULL	NULL	0	NULL	Tfc4	NULL		bind	NULL		TPR6-9		Brf1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_142	16880507	A fragment of Tfc4 extending from the N terminus to the end of TPR9 (Nt-TPR9) binds to Brf1 with reduced affinity relative to the two independent Brf1 binding sites (Nt-TPR5 and TPR6-9) contained within this region ( ).	bind
37034	5	10273	6	NULL	NULL	0	NULL	statement 2	NULL	affinity of	is lower than	NULL				statement 3	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_142	16880507	A fragment of Tfc4 extending from the N terminus to the end of TPR9 (Nt-TPR9) binds to Brf1 with reduced affinity relative to the two independent Brf1 binding sites (Nt-TPR5 and TPR6-9) contained within this region ( ).	bind
37035	6	10273	6	NULL	NULL	0	NULL	statement 2	NULL	affinity of	is lower than	NULL				statement 4	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_142	16880507	A fragment of Tfc4 extending from the N terminus to the end of TPR9 (Nt-TPR9) binds to Brf1 with reduced affinity relative to the two independent Brf1 binding sites (Nt-TPR5 and TPR6-9) contained within this region ( ).	bind
43705	1	10274	5	11	NULL	NULL	NULL	Rb protein fragment	GP		bind					MCM7	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_9_1007_s_52	15879550	A fragment of the Rb protein that binds MCM7 and inhibits helicase activity (Sterner et al. 1998 ) blocks unwinding, as do neutralizing antibodies to CDC45, which functions as a cofactor for the MCM complex (Pacek and Walter 2004 ).	bind
43706	2	10274	5	11	NULL	NULL	NULL	statement 1	Process		inhibit					helicase	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_9_1007_s_52	15879550	A fragment of the Rb protein that binds MCM7 and inhibits helicase activity (Sterner et al. 1998 ) blocks unwinding, as do neutralizing antibodies to CDC45, which functions as a cofactor for the MCM complex (Pacek and Walter 2004 ).	bind
43708	3	10274	5	11	NULL	NULL	NULL	statement 2	Process		block					unwinding	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_9_1007_s_52	15879550	A fragment of the Rb protein that binds MCM7 and inhibits helicase activity (Sterner et al. 1998 ) blocks unwinding, as do neutralizing antibodies to CDC45, which functions as a cofactor for the MCM complex (Pacek and Walter 2004 ).	bind
43710	4	10274	5	11	NULL	NULL	NULL	CDC45	GP		acts as a 					cofactor	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_9_1007_s_52	15879550	A fragment of the Rb protein that binds MCM7 and inhibits helicase activity (Sterner et al. 1998 ) blocks unwinding, as do neutralizing antibodies to CDC45, which functions as a cofactor for the MCM complex (Pacek and Walter 2004 ).	bind
48433	5	10274	5	11	NULL	NULL	NULL	statement 4	Process		occurs in					MCM complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_9_1007_s_52	15879550	A fragment of the Rb protein that binds MCM7 and inhibits helicase activity (Sterner et al. 1998 ) blocks unwinding, as do neutralizing antibodies to CDC45, which functions as a cofactor for the MCM complex (Pacek and Walter 2004 ).	bind
36578	1	10274	6	NULL	NULL	0	NULL	fragment of Rb protein	NULL		bind	NULL				MCM7	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_9_1007_s_52	15879550	A fragment of the Rb protein that binds MCM7 and inhibits helicase activity (Sterner et al. 1998 ) blocks unwinding, as do neutralizing antibodies to CDC45, which functions as a cofactor for the MCM complex (Pacek and Walter 2004 ).	bind
36579	2	10274	6	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				helicase	NULL	activity of			NULL		0	NULL	NULL	NULL	gw70_genesdev_19_9_1007_s_52	15879550	A fragment of the Rb protein that binds MCM7 and inhibits helicase activity (Sterner et al. 1998 ) blocks unwinding, as do neutralizing antibodies to CDC45, which functions as a cofactor for the MCM complex (Pacek and Walter 2004 ).	bind
36580	3	10274	6	NULL	NULL	0	NULL	statement 1	NULL		blocks	NULL				DNA unwinding activity	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_9_1007_s_52	15879550	A fragment of the Rb protein that binds MCM7 and inhibits helicase activity (Sterner et al. 1998 ) blocks unwinding, as do neutralizing antibodies to CDC45, which functions as a cofactor for the MCM complex (Pacek and Walter 2004 ).	bind
36581	4	10274	6	10	NULL	0	NULL	CDC45	NULL		acts as a 	NULL				cofactor	NULL				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_9_1007_s_52	15879550	A fragment of the Rb protein that binds MCM7 and inhibits helicase activity (Sterner et al. 1998 ) blocks unwinding, as do neutralizing antibodies to CDC45, which functions as a cofactor for the MCM complex (Pacek and Walter 2004 ).	bind
48434	5	10274	6	10	NULL	0	NULL	statement 4	NULL		occurs in	NULL				MCM complex	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_9_1007_s_52	15879550	A fragment of the Rb protein that binds MCM7 and inhibits helicase activity (Sterner et al. 1998 ) blocks unwinding, as do neutralizing antibodies to CDC45, which functions as a cofactor for the MCM complex (Pacek and Walter 2004 ).	bind
43701	1	10275	5	11	NULL	NULL	NULL				contains			reductase domain fragment				only	FMN domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_10_8827_s_255	14681230	A fragment of the reductase domain containing only the FMN domain could bind caveolin-1, suggesting that the FMN domain itself is essential for the caveolin-1 interaction.	bind
43702	2	10275	5	11	NULL	NULL	NULL	statement 1	GP		bind					caveolin-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_10_8827_s_255	14681230	A fragment of the reductase domain containing only the FMN domain could bind caveolin-1, suggesting that the FMN domain itself is essential for the caveolin-1 interaction.	bind
43703	3	10275	5	11	NULL	NULL	NULL				is essential for			FMN domain		caveolin-1	GP	interaction of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_10_8827_s_255	14681230	A fragment of the reductase domain containing only the FMN domain could bind caveolin-1, suggesting that the FMN domain itself is essential for the caveolin-1 interaction.	bind
36582	1	10275	6	10	NULL	0	NULL	reductase domain fragment	NULL		contains	NULL					NULL		FMN domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_10_8827_s_255	14681230	A fragment of the reductase domain containing only the FMN domain could bind caveolin-1, suggesting that the FMN domain itself is essential for the caveolin-1 interaction.	bind
36583	3	10275	6	10	NULL	0	NULL		NULL		is essential for	NULL		FMN domain		caveolin-1	NULL	interaction of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_10_8827_s_255	14681230	A fragment of the reductase domain containing only the FMN domain could bind caveolin-1, suggesting that the FMN domain itself is essential for the caveolin-1 interaction.	bind
48435	2	10275	6	10	NULL	0	NULL	statement 1	NULL		bind	NULL				caveolin-1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_10_8827_s_255	14681230	A fragment of the reductase domain containing only the FMN domain could bind caveolin-1, suggesting that the FMN domain itself is essential for the caveolin-1 interaction.	bind
43725	1	10276	5	11	NULL	NULL	NULL	free peptide	AminoAcid	amino acid sequence of	is identical to					phage	Organism				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7075_s_41	16423833	A free peptide with identical amino acid sequence to that displayed by the phage was able to inhibit binding of the phage to SC, suggesting that the peptide alone was sufficient for binding.	bind
43726	2	10276	5	11	NULL	NULL	NULL	phage	Organism		bind					SC	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7075_s_41	16423833	A free peptide with identical amino acid sequence to that displayed by the phage was able to inhibit binding of the phage to SC, suggesting that the peptide alone was sufficient for binding.	bind
43727	3	10276	5	11	NULL	NULL	NULL	statement 1	Process		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7075_s_41	16423833	A free peptide with identical amino acid sequence to that displayed by the phage was able to inhibit binding of the phage to SC, suggesting that the peptide alone was sufficient for binding.	bind
36584	1	10276	6	NULL	NULL	0	NULL	phage	NULL		bind	NULL				SC	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7075_s_41	16423833	A free peptide with identical amino acid sequence to that displayed by the phage was able to inhibit binding of the phage to SC, suggesting that the peptide alone was sufficient for binding.	bind
36585	2	10276	6	10	NULL	0	NULL	free peptide	NULL	amino acid sequence of 	is identical to	NULL				phage	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7075_s_41	16423833	A free peptide with identical amino acid sequence to that displayed by the phage was able to inhibit binding of the phage to SC, suggesting that the peptide alone was sufficient for binding.	bind
36586	3	10276	6	NULL	NULL	0	NULL	statement 2	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7075_s_41	16423833	A free peptide with identical amino acid sequence to that displayed by the phage was able to inhibit binding of the phage to SC, suggesting that the peptide alone was sufficient for binding.	bind
43730	1	10277	5	11	NULL	NULL	NULL	oligosaccharide	Chemical	core 	is attached to		freshly			glycoprotein	GP	unfolded			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
43731	2	10277	5	11	NULL	NULL	NULL	statement 1	GP		is trimmed by					glucosidases I	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
43732	3	10277	5	11	NULL	NULL	NULL	statement 1	GP		is trimmed by					glucosidases II	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
43733	4	10277	5	11	NULL	NULL	NULL	glycoprotein	GP		bind					CNX	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
43734	5	10277	5	11	NULL	NULL	NULL	glycoprotein	GP		bind					CRT	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
43735	6	10277	5	11	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
43736	7	10277	5	11	NULL	NULL	NULL	statement 2	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
43737	8	10277	5	11	NULL	NULL	NULL	statement 2	Process		leads to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
43738	9	10277	5	11	NULL	NULL	NULL	statement 3	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
43739	10	10277	5	11	NULL	NULL	NULL	statement 3	Process		leads to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
43740	11	10277	5	11	NULL	NULL	NULL	statement 4	GP		bind					ERp57	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
43741	12	10277	5	11	NULL	NULL	NULL	statement 5	GP		bind					ERp57	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
37036	1	10277	6	10	NULL	0	NULL	oligosaccharide		core	is attached to		freshly			glycoprotein		unfolded			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
37037	2	10277	6	NULL	NULL	0	NULL	glucosidases I	NULL		trims	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
37038	3	10277	6	NULL	NULL	0	NULL	glucosidase II	NULL		trims	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
37039	4	10277	6	NULL	NULL	0	NULL	glycoprotein	NULL		bind	NULL				CNX	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
37040	5	10277	6	NULL	NULL	0	NULL	glycoprotein	NULL		bind	NULL				CRT	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
37041	6	10277	6	NULL	NULL	0	NULL	statement 4	NULL		is an alternative to	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
37042	7	10277	6	NULL	NULL	0	NULL	statement 6	NULL		occurs after	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
37043	8	10277	6	NULL	NULL	0	NULL	statement 6	NULL		occurs after	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
37044	9	10277	6	NULL	NULL	0	NULL	statement 4	NULL		bind	NULL				ERp57	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
37045	10	10277	6	NULL	NULL	0	NULL	statement 5	NULL		bind	NULL				ERp57	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_14_13607_s_22	14732712	A freshly attached core oligosaccharide of an unfolded glycoprotein is first trimmed by glucosidases I and II, after which the glycoprotein becomes bound to CNX or CRT, this being followed by binding of the complex to ERp57 ( ,  ).	bind
43742	1	10278	5	11	NULL	NULL	NULL	Rab proteins	GP	mutant	bind		preferentially	S21N		GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_devcell_1_1_73_s_45	11703925	A full-length human RIN1 prey fusion protein  (Han et al., 1997  ) was tested for interaction with bait fusion proteins consisting of wild-type Vps21p and Rab5A, as well as mutant versions of the Rab proteins that preferentially bind GDP (S21N and S34N, respectively).	bind
43743	2	10278	5	11	NULL	NULL	NULL	Rab proteins	GP	mutant	bind		preferentially	S34N		GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_devcell_1_1_73_s_45	11703925	A full-length human RIN1 prey fusion protein  (Han et al., 1997  ) was tested for interaction with bait fusion proteins consisting of wild-type Vps21p and Rab5A, as well as mutant versions of the Rab proteins that preferentially bind GDP (S21N and S34N, respectively).	bind
36587	1	10278	6	NULL	NULL	0	NULL	Rab protein	NULL	mutant	bind	NULL	preferentially	S21N		GDP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_devcell_1_1_73_s_45	11703925	A full-length human RIN1 prey fusion protein  (Han et al., 1997  ) was tested for interaction with bait fusion proteins consisting of wild-type Vps21p and Rab5A, as well as mutant versions of the Rab proteins that preferentially bind GDP (S21N and S34N, respectively).	bind
36588	2	10278	6	NULL	NULL	0	NULL	Rab protein	NULL	mutant	bind	NULL	preferentially	S34N		GDP	NULL				NULL		0	NULL	NULL	NULL	gw60_devcell_1_1_73_s_45	11703925	A full-length human RIN1 prey fusion protein  (Han et al., 1997  ) was tested for interaction with bait fusion proteins consisting of wild-type Vps21p and Rab5A, as well as mutant versions of the Rab proteins that preferentially bind GDP (S21N and S34N, respectively).	bind
43744	1	10279	5	11	NULL	NULL	NULL	MBP	GP		is					maltose binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_5_1225_s_15	11844750	A fuller understanding of how these binding proteins function in transport was realized following our recent observation in the maltose transport system that the periplasmic maltose binding protein (MBP) becomes tightly bound to the membrane transporter (MalFGK2, a complex of MalF, MalG, and two MalK proteins) in the presumed catalytic transition state for ATP hydrolysis ( 22).	bind
43745	2	10279	5	11	NULL	NULL	NULL	MalFGK2	GP		is a type of					membrane transporter	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_5_1225_s_15	11844750	A fuller understanding of how these binding proteins function in transport was realized following our recent observation in the maltose transport system that the periplasmic maltose binding protein (MBP) becomes tightly bound to the membrane transporter (MalFGK2, a complex of MalF, MalG, and two MalK proteins) in the presumed catalytic transition state for ATP hydrolysis ( 22).	bind
43746	3	10279	5	11	NULL	NULL	NULL	MalFGK2	GP		contains					MalF proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_5_1225_s_15	11844750	A fuller understanding of how these binding proteins function in transport was realized following our recent observation in the maltose transport system that the periplasmic maltose binding protein (MBP) becomes tightly bound to the membrane transporter (MalFGK2, a complex of MalF, MalG, and two MalK proteins) in the presumed catalytic transition state for ATP hydrolysis ( 22).	bind
43747	6	10279	5	11	NULL	NULL	NULL	MBP	GP	periplasmic	bind		tightly			MalFGK2	GP				NULL	maltose transport system	NULL	NULL	NULL	NULL	gw60_jbacteriol_184_5_1225_s_15	11844750	A fuller understanding of how these binding proteins function in transport was realized following our recent observation in the maltose transport system that the periplasmic maltose binding protein (MBP) becomes tightly bound to the membrane transporter (MalFGK2, a complex of MalF, MalG, and two MalK proteins) in the presumed catalytic transition state for ATP hydrolysis ( 22).	bind
43812	4	10279	5	11	NULL	NULL	NULL	MalFGK2	GP		contains					MalG proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_5_1225_s_15	11844750	A fuller understanding of how these binding proteins function in transport was realized following our recent observation in the maltose transport system that the periplasmic maltose binding protein (MBP) becomes tightly bound to the membrane transporter (MalFGK2, a complex of MalF, MalG, and two MalK proteins) in the presumed catalytic transition state for ATP hydrolysis ( 22).	bind
43813	5	10279	5	11	NULL	NULL	NULL	MalFGK2	GP		contains					MalK proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_5_1225_s_15	11844750	A fuller understanding of how these binding proteins function in transport was realized following our recent observation in the maltose transport system that the periplasmic maltose binding protein (MBP) becomes tightly bound to the membrane transporter (MalFGK2, a complex of MalF, MalG, and two MalK proteins) in the presumed catalytic transition state for ATP hydrolysis ( 22).	bind
37046	1	10279	6	NULL	NULL	0	NULL	MBP	NULL		is	NULL				maltose binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_5_1225_s_15	11844750	A fuller understanding of how these binding proteins function in transport was realized following our recent observation in the maltose transport system that the periplasmic maltose binding protein (MBP) becomes tightly bound to the membrane transporter (MalFGK2, a complex of MalF, MalG, and two MalK proteins) in the presumed catalytic transition state for ATP hydrolysis ( 22).	bind
37047	2	10279	6	10	NULL	0	NULL	MBP		periplasmic	bind		tightly			MalFGK2					NULL	maltose transport system	NULL	NULL	NULL	NULL	gw60_jbacteriol_184_5_1225_s_15	11844750	A fuller understanding of how these binding proteins function in transport was realized following our recent observation in the maltose transport system that the periplasmic maltose binding protein (MBP) becomes tightly bound to the membrane transporter (MalFGK2, a complex of MalF, MalG, and two MalK proteins) in the presumed catalytic transition state for ATP hydrolysis ( 22).	bind
37048	3	10279	6	NULL	NULL	0	NULL	MalFGK2	NULL		is a type of	NULL				membrane transporter	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_5_1225_s_15	11844750	A fuller understanding of how these binding proteins function in transport was realized following our recent observation in the maltose transport system that the periplasmic maltose binding protein (MBP) becomes tightly bound to the membrane transporter (MalFGK2, a complex of MalF, MalG, and two MalK proteins) in the presumed catalytic transition state for ATP hydrolysis ( 22).	bind
37049	4	10279	6	NULL	NULL	0	NULL	statement 2	NULL		occurs in the	NULL				catalytic transition state	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_5_1225_s_15	11844750	A fuller understanding of how these binding proteins function in transport was realized following our recent observation in the maltose transport system that the periplasmic maltose binding protein (MBP) becomes tightly bound to the membrane transporter (MalFGK2, a complex of MalF, MalG, and two MalK proteins) in the presumed catalytic transition state for ATP hydrolysis ( 22).	bind
37050	5	10279	6	NULL	NULL	0	NULL	statement 4	NULL		occurs for	NULL				ATP	NULL	hydrolysis of			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_5_1225_s_15	11844750	A fuller understanding of how these binding proteins function in transport was realized following our recent observation in the maltose transport system that the periplasmic maltose binding protein (MBP) becomes tightly bound to the membrane transporter (MalFGK2, a complex of MalF, MalG, and two MalK proteins) in the presumed catalytic transition state for ATP hydrolysis ( 22).	bind
48571	6	10279	6	NULL	NULL	0	NULL	MalFGK2	NULL		is	NULL				a complex of MalF, MalG, and two MalK proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_5_1225_s_15	11844750	A fuller understanding of how these binding proteins function in transport was realized following our recent observation in the maltose transport system that the periplasmic maltose binding protein (MBP) becomes tightly bound to the membrane transporter (MalFGK2, a complex of MalF, MalG, and two MalK proteins) in the presumed catalytic transition state for ATP hydrolysis ( 22).	bind
43749	1	10280	5	11	NULL	NULL	NULL	TMs	GP		bind		cooperatively			F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_36_22409_s_14	9278391	A function common to all TMs is cooperative binding to F-actin ( 2).	bind
36589	1	10280	6	NULL	NULL	0	NULL	TM	NULL		bind	NULL	cooperatively			F-actin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_36_22409_s_14	9278391	A function common to all TMs is cooperative binding to F-actin ( 2).	bind
43750	1	10281	5	11	NULL	NULL	NULL	DnaJ	GP		bind					DnaK	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_5_2139_s_259	7836443	A Function for the QKRAA Amino Acid Motif: Mediating Binding of DnaJ to DnaK .	bind
48436	2	10281	5	11	NULL	NULL	NULL				mediates			QKRAA Amino Acid Motif		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_5_2139_s_259	7836443	A Function for the QKRAA Amino Acid Motif: Mediating Binding of DnaJ to DnaK .	bind
36590	1	10281	6	NULL	NULL	0	NULL	DnaJ	NULL		bind	NULL				DnaK	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_5_2139_s_259	7836443	A Function for the QKRAA Amino Acid Motif: Mediating Binding of DnaJ to DnaK .	bind
36591	2	10281	6	NULL	NULL	0	NULL		NULL		mediates	NULL		QKRAA amino acid motif		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_5_2139_s_259	7836443	A Function for the QKRAA Amino Acid Motif: Mediating Binding of DnaJ to DnaK .	bind
43753	1	10282	5	11	NULL	NULL	NULL				inhibit			R subunit		kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_12_6687_s_190	9618473	A function for the R subunit apart from kinase inhibition is also suggested by the finding that the cAMP binding domain of RII shares extensive homology with the bacterial catabolite activator protein (CAP) ( 28).	bind
43754	2	10282	5	11	NULL	NULL	NULL	RII	GP		is homologous to		extensively	cAMP binding domain		CAP	GP	bacterial			NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_12_6687_s_190	9618473	A function for the R subunit apart from kinase inhibition is also suggested by the finding that the cAMP binding domain of RII shares extensive homology with the bacterial catabolite activator protein (CAP) ( 28).	bind
43755	3	10282	5	11	NULL	NULL	NULL	CAP	GP		is					catabolite activator protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_12_6687_s_190	9618473	A function for the R subunit apart from kinase inhibition is also suggested by the finding that the cAMP binding domain of RII shares extensive homology with the bacterial catabolite activator protein (CAP) ( 28).	bind
36592	1	10282	6	NULL	NULL	0	NULL	RII	NULL		is homologous to	NULL	extensively	cAMP binding domain		CAP	NULL	bacterial			NULL		0	NULL	NULL	NULL	gw60_pnas_95_12_6687_s_190	9618473	A function for the R subunit apart from kinase inhibition is also suggested by the finding that the cAMP binding domain of RII shares extensive homology with the bacterial catabolite activator protein (CAP) ( 28).	bind
36593	2	10282	6	NULL	NULL	0	NULL	CAP	NULL		is	NULL				catabolite activator protein	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_12_6687_s_190	9618473	A function for the R subunit apart from kinase inhibition is also suggested by the finding that the cAMP binding domain of RII shares extensive homology with the bacterial catabolite activator protein (CAP) ( 28).	bind
36594	3	10282	6	NULL	NULL	0	NULL	R subunit	NULL		functions in	NULL				kinase	NULL	inhibiton of			NULL		0	NULL	NULL	NULL	gw60_pnas_95_12_6687_s_190	9618473	A function for the R subunit apart from kinase inhibition is also suggested by the finding that the cAMP binding domain of RII shares extensive homology with the bacterial catabolite activator protein (CAP) ( 28).	bind
43751	1	10283	5	11	NULL	NULL	NULL	sperm	Cell	free-swimming;;acrosome-reacted;;mouse	does not bind					eggs	Cell	ZP-encased			NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_66_6_1585_s_344	12021035	A function for the ZP3 binding sites on the plasma membrane overlying the acrosome is evident from the fact that free-swimming, acrosome-reacted mouse sperm cannot bind to ZP-encased eggs [ 7.	bind
36595	1	10283	6	10	NULL	0	NULL	sperm	NULL	free swimming;; acrosome-reacted;; mouse	does not bind	NULL				eggs	NULL	ZP-encased			NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_66_6_1585_s_344	12021035	A function for the ZP3 binding sites on the plasma membrane overlying the acrosome is evident from the fact that free-swimming, acrosome-reacted mouse sperm cannot bind to ZP-encased eggs [ 7.	bind
43756	1	10284	5	11	NULL	NULL	NULL	APP	GP	transmembrane	serve as		directly			cell adhesion molecule	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1613_s_216	8576160	A functional  collagen binding site of APP is of great importance, since  transmembrane APP could serve directly as a cell adhesion molecule, and  the secreted forms might be involved in the regulation of cell  interactions.	bind
43758	2	10284	5	11	NULL	NULL	NULL	APP	GP	secreted	is involved in		might be			cell interactions	Process	regulation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_3_1613_s_216	8576160	A functional  collagen binding site of APP is of great importance, since  transmembrane APP could serve directly as a cell adhesion molecule, and  the secreted forms might be involved in the regulation of cell  interactions.	bind
36596	1	10284	6	NULL	NULL	0	NULL	APP	NULL	transmembrane	serves as a	NULL				cell adhesion molecule	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_3_1613_s_216	8576160	A functional  collagen binding site of APP is of great importance, since  transmembrane APP could serve directly as a cell adhesion molecule, and  the secreted forms might be involved in the regulation of cell  interactions.	bind
36597	2	10284	6	NULL	NULL	0	NULL	APP	NULL	secreted form of	is involved in	NULL	might			cell interactions	NULL	regulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_3_1613_s_216	8576160	A functional  collagen binding site of APP is of great importance, since  transmembrane APP could serve directly as a cell adhesion molecule, and  the secreted forms might be involved in the regulation of cell  interactions.	bind
43759	1	10285	5	11	NULL	NULL	NULL	c-myb gene	GP	functional	is required for					hepatic hematopoiesis	Process	normal;;murine;;fetal			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9203_s_519	11094072	A functional c-myb gene is required for normal murine fetal hepatic hematopoiesis.	bind
36598	1	10285	6	10	NULL	0	NULL	c-myb gene	NULL	functional	is required for	NULL				hepatic hematopoiesis	NULL	normal;; murine;; fetal			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9203_s_519	11094072	A functional c-myb gene is required for normal murine fetal hepatic hematopoiesis.	bind
43761	1	10287	5	11	NULL	NULL	NULL	FnBP fragment	GP	functional	bind					Hsp60	GP	epithelial cell membrane			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_11_6321_s_127	11035741	A functional fragment of FnBP binds to Hsp60 from epithelial cell membrane fractions.	bind
36599	1	10287	6	10	NULL	0	NULL	FnBP fragment	NULL	functional	bind	NULL				Hsp60	NULL	epithelial cell membrane 			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_11_6321_s_127	11035741	A functional fragment of FnBP binds to Hsp60 from epithelial cell membrane fractions.	bind
43762	1	10288	5	11	NULL	NULL	NULL	E2	Chemical		bind					Bmp6 gene	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_35_25509_s_17	16798745	A functional relationship between E2 and BMP-6 was further suggested by E2 binding to the  Bmp6 gene promotor ( ) and by increased BMP-6 immunostaining in bone marrow of mice treated with E2 ( ).	bind
36600	1	10288	6	NULL	NULL	0	NULL	E2	NULL		bind	NULL				Bmp6 gene	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_35_25509_s_17	16798745	A functional relationship between E2 and BMP-6 was further suggested by E2 binding to the  Bmp6 gene promotor ( ) and by increased BMP-6 immunostaining in bone marrow of mice treated with E2 ( ).	bind
43764	1	10289	5	11	NULL	NULL	NULL	Eps15	GP	human	bind			DPF repeats		AP-2	GP		alpha-adaptin subunit		NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_23_9638_s_315	9822725	A functional role for the DPF motif is suggested by a recent study that demonstrates that the binding of human Eps15 to the alpha-adaptin subunit of AP-2 is mediated by a portion of Eps15 that contains four of these DPF repeats (Benmerah et al., 1996  ).	bind
36601	1	10289	6	10	NULL	0	NULL	Eps15		human	bind			DPF repeats		AP-2			alpha-adaptin subunit		NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_23_9638_s_315	9822725	A functional role for the DPF motif is suggested by a recent study that demonstrates that the binding of human Eps15 to the alpha-adaptin subunit of AP-2 is mediated by a portion of Eps15 that contains four of these DPF repeats (Benmerah et al., 1996  ).	bind
43765	1	10290	5	11	NULL	NULL	NULL	SRP	GP		bind		tightly			RNCs	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_1_103_s_279	9436994	A functional signal sequence would be required to trigger tight binding of SRP to the RNCs (Walter  et al., 1981  ).	bind
36603	1	10290	6	10	NULL	0	NULL	SRP	NULL		bind	NULL	tightly			RNC	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_1_103_s_279	9436994	A functional signal sequence would be required to trigger tight binding of SRP to the RNCs (Walter  et al., 1981  ).	bind
43767	1	10291	5	11	NULL	NULL	NULL			functional	is present in				STAT6-binding site	I gene	GP			proximal promoter region	NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10800_s_213	10485906	A functional STAT6-binding site is present in the proximal promoter region of the I  gene, and binding of activated STAT6 to this site is essential for IL-4-induced gene expression ( 44).	bind
43768	2	10291	5	11	NULL	NULL	NULL	STAT6	GP	activated	bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10800_s_213	10485906	A functional STAT6-binding site is present in the proximal promoter region of the I  gene, and binding of activated STAT6 to this site is essential for IL-4-induced gene expression ( 44).	bind
43769	3	10291	5	11	NULL	NULL	NULL	IL-4	GP		induce					gene	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10800_s_213	10485906	A functional STAT6-binding site is present in the proximal promoter region of the I  gene, and binding of activated STAT6 to this site is essential for IL-4-induced gene expression ( 44).	bind
43770	4	10291	5	11	NULL	NULL	NULL	statement 2	GP		is essential for					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_19_10800_s_213	10485906	A functional STAT6-binding site is present in the proximal promoter region of the I  gene, and binding of activated STAT6 to this site is essential for IL-4-induced gene expression ( 44).	bind
36604	1	10291	6	NULL	NULL	0	NULL	STAT6	NULL	activated	bind	NULL				I gene	NULL	functional		STAT6-binding site of promoter	NULL		0	NULL	NULL	NULL	gw60_pnas_96_19_10800_s_213	10485906	A functional STAT6-binding site is present in the proximal promoter region of the I  gene, and binding of activated STAT6 to this site is essential for IL-4-induced gene expression ( 44).	bind
36605	2	10291	6	NULL	NULL	0	NULL	IL-4	NULL		induces	NULL				I gene	NULL	expression of			NULL		0	NULL	NULL	NULL	gw60_pnas_96_19_10800_s_213	10485906	A functional STAT6-binding site is present in the proximal promoter region of the I  gene, and binding of activated STAT6 to this site is essential for IL-4-induced gene expression ( 44).	bind
36606	3	10291	6	NULL	NULL	0	NULL	statement 1	NULL		is essential for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_19_10800_s_213	10485906	A functional STAT6-binding site is present in the proximal promoter region of the I  gene, and binding of activated STAT6 to this site is essential for IL-4-induced gene expression ( 44).	bind
43771	1	10292	5	11	NULL	NULL	NULL				bind			p40 Subunit		ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_20_11607_s_99	9751713	A Functional Walker A Motif Is Required for ATP Binding to the p40 Subunit.	bind
43772	2	10292	5	11	NULL	NULL	NULL			functional	is required for			walker a motif		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_20_11607_s_99	9751713	A Functional Walker A Motif Is Required for ATP Binding to the p40 Subunit.	bind
36607	1	10292	6	10	NULL	0	NULL	ATP			bind								p40 subunit		NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_20_11607_s_99	9751713	A Functional Walker A Motif Is Required for ATP Binding to the p40 Subunit.	bind
36608	2	10292	6	NULL	NULL	0	NULL		NULL	functional	is required for	NULL		Walker A Motif		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_20_11607_s_99	9751713	A Functional Walker A Motif Is Required for ATP Binding to the p40 Subunit.	bind
43773	1	10293	5	11	NULL	NULL	NULL	synthetic peptide	GP	functional;;discontinuous;;branched	is derived from					HIV-1 gp120	GP		C3/C4 domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_16_10_2599_s_532	9184207	A functional, discontinuous HIV-1 gp120 C3/C4 domain-derived, branched, synthetic peptide that binds to CD4 and inhibits MIP-1{alpha} chemokine binding.	bind
43774	2	10293	5	11	NULL	NULL	NULL	statement 1	GP		bind					CD4	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_10_2599_s_532	9184207	A functional, discontinuous HIV-1 gp120 C3/C4 domain-derived, branched, synthetic peptide that binds to CD4 and inhibits MIP-1{alpha} chemokine binding.	bind
43775	3	10293	5	11	NULL	NULL	NULL	statement 2	GP		inhibit					MIP-1{alpha}	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_embo_16_10_2599_s_532	9184207	A functional, discontinuous HIV-1 gp120 C3/C4 domain-derived, branched, synthetic peptide that binds to CD4 and inhibits MIP-1{alpha} chemokine binding.	bind
43776	4	10293	5	11	NULL	NULL	NULL	MIP-1{alpha}	GP		is a type of					chemokine	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_10_2599_s_532	9184207	A functional, discontinuous HIV-1 gp120 C3/C4 domain-derived, branched, synthetic peptide that binds to CD4 and inhibits MIP-1{alpha} chemokine binding.	bind
37051	1	10293	6	10	NULL	0	NULL	synthetic peptide	NULL	\tfunctional;;discontinuous;;branched \t	is derived from	NULL				HIV-1 gp120	NULL		C3/C4 domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_16_10_2599_s_532	9184207	A functional, discontinuous HIV-1 gp120 C3/C4 domain-derived, branched, synthetic peptide that binds to CD4 and inhibits MIP-1{alpha} chemokine binding.	bind
37052	2	10293	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				CD4	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_10_2599_s_532	9184207	A functional, discontinuous HIV-1 gp120 C3/C4 domain-derived, branched, synthetic peptide that binds to CD4 and inhibits MIP-1{alpha} chemokine binding.	bind
37053	3	10293	6	10	NULL	0	NULL	statement 1	NULL		inhibits	NULL				MIP-1{alpha}	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_embo_16_10_2599_s_532	9184207	A functional, discontinuous HIV-1 gp120 C3/C4 domain-derived, branched, synthetic peptide that binds to CD4 and inhibits MIP-1{alpha} chemokine binding.	bind
48437	4	10293	6	10	NULL	0	NULL	MIP-1{alpha}	NULL		is a type of	NULL				chemokine	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_10_2599_s_532	9184207	A functional, discontinuous HIV-1 gp120 C3/C4 domain-derived, branched, synthetic peptide that binds to CD4 and inhibits MIP-1{alpha} chemokine binding.	bind
43777	1	10294	5	11	NULL	NULL	NULL	RFX	GP		bind		cooperative			NF-Y	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_19_0_331_s_1106	11244040	A functionally essential domain of RFX5 mediates activation of  MHC class II promoters by promoting cooperative binding between RFX and NF-Y.	bind
43778	2	10294	5	11	NULL	NULL	NULL	RFX5	GP	functional	mediate			essential domain		MHC class II	GP	activation of		promoter	NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_19_0_331_s_1106	11244040	A functionally essential domain of RFX5 mediates activation of  MHC class II promoters by promoting cooperative binding between RFX and NF-Y.	bind
43779	3	10294	5	11	NULL	NULL	NULL	RFX5	GP	functional	promotes			essential domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_19_0_331_s_1106	11244040	A functionally essential domain of RFX5 mediates activation of  MHC class II promoters by promoting cooperative binding between RFX and NF-Y.	bind
43780	4	10294	5	11	NULL	NULL	NULL	statement 3	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_19_0_331_s_1106	11244040	A functionally essential domain of RFX5 mediates activation of  MHC class II promoters by promoting cooperative binding between RFX and NF-Y.	bind
36609	1	10294	6	NULL	NULL	0	NULL	RFX	NULL		bind	NULL	cooperatively			NF-Y	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_19_0_331_s_1106	11244040	A functionally essential domain of RFX5 mediates activation of  MHC class II promoters by promoting cooperative binding between RFX and NF-Y.	bind
36611	2	10294	6	NULL	NULL	0	NULL	RFX5	NULL	functional	mediates	NULL		essential domain		MHC class II	NULL	activation of		promoter	NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_19_0_331_s_1106	11244040	A functionally essential domain of RFX5 mediates activation of  MHC class II promoters by promoting cooperative binding between RFX and NF-Y.	bind
36613	3	10294	6	NULL	NULL	0	NULL	statement 2	NULL		occurs by promoting	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_19_0_331_s_1106	11244040	A functionally essential domain of RFX5 mediates activation of  MHC class II promoters by promoting cooperative binding between RFX and NF-Y.	bind
48438	4	10294	6	10	NULL	0	NULL	statement 3	NULL		leads to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_19_0_331_s_1106	11244040	A functionally essential domain of RFX5 mediates activation of  MHC class II promoters by promoting cooperative binding between RFX and NF-Y.	bind
43781	1	10297	5	11	NULL	NULL	NULL	RAG protein	GP		bind									SEs	NULL		NULL	NULL	NULL	NULL	gw60_cell_89_1_43_s_206	9094713	A fundamental difference, therefore, appears to exist in RAG  protein binding to one versus two SEs.	bind
36616	1	10297	6	NULL	NULL	0	NULL	RAG protein	NULL		bind	NULL				SE	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_89_1_43_s_206	9094713	A fundamental difference, therefore, appears to exist in RAG  protein binding to one versus two SEs.	bind
43782	1	10298	5	11	NULL	NULL	NULL	transducin	Process		bind					rhodopsin dimers	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_18_12896_s_371	16500896	A fundamental observation gleaned from docking the three-dimensional structures of rhodopsin and transducin is that transducin binds to rhodopsin dimers in such a way that one molecule of rhodopsin binds transducin and the other serves as a docking platform ( ).	bind
37054	1	10298	6	10	NULL	0	NULL	rhodopsin dimers			bind					transducin					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_18_12896_s_371	16500896	A fundamental observation gleaned from docking the three-dimensional structures of rhodopsin and transducin is that transducin binds to rhodopsin dimers in such a way that one molecule of rhodopsin binds transducin and the other serves as a docking platform ( ).	bind
43785	1	10299	5	11	NULL	NULL	NULL	GBR-hydroxy	Chemical		is released into		slowly			bloodstream	Process				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_301_3_1190_s_204	12023554	A fundamental premise of the present study is that the effects of GBR-decanoate are mediated by a slow release of GBR-hydroxy into the bloodstream, with subsequent pseudo-irreversible binding of GBR-hydroxy to DAT sites in the brain (Lewis et al., 1999  ).	bind
43786	2	10299	5	11	NULL	NULL	NULL	GBR-decanoate	Chemical	effects of	is mediated by					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_301_3_1190_s_204	12023554	A fundamental premise of the present study is that the effects of GBR-decanoate are mediated by a slow release of GBR-hydroxy into the bloodstream, with subsequent pseudo-irreversible binding of GBR-hydroxy to DAT sites in the brain (Lewis et al., 1999  ).	bind
43787	3	10299	5	11	NULL	NULL	NULL	GBR-hydroxy	Chemical		bind		pseudo-irreversible			DAT sites	GP				NULL	brain	NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_301_3_1190_s_204	12023554	A fundamental premise of the present study is that the effects of GBR-decanoate are mediated by a slow release of GBR-hydroxy into the bloodstream, with subsequent pseudo-irreversible binding of GBR-hydroxy to DAT sites in the brain (Lewis et al., 1999  ).	bind
43788	4	10299	5	11	NULL	NULL	NULL	statement 1	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_301_3_1190_s_204	12023554	A fundamental premise of the present study is that the effects of GBR-decanoate are mediated by a slow release of GBR-hydroxy into the bloodstream, with subsequent pseudo-irreversible binding of GBR-hydroxy to DAT sites in the brain (Lewis et al., 1999  ).	bind
48566	1	10299	6	NULL	NULL	0	NULL	GBR-hydroxy	NULL		is released into	NULL	slowly			bloodstream	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_301_3_1190_s_204	12023554	A fundamental premise of the present study is that the effects of GBR-decanoate are mediated by a slow release of GBR-hydroxy into the bloodstream, with subsequent pseudo-irreversible binding of GBR-hydroxy to DAT sites in the brain (Lewis et al., 1999  ).	bind
48567	2	10299	6	10	NULL	0	NULL	GBR-hydroxy			bind		pseudo-irreversibly			DAT sites					NULL	brain	NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_301_3_1190_s_204	12023554	A fundamental premise of the present study is that the effects of GBR-decanoate are mediated by a slow release of GBR-hydroxy into the bloodstream, with subsequent pseudo-irreversible binding of GBR-hydroxy to DAT sites in the brain (Lewis et al., 1999  ).	bind
48568	3	10299	6	NULL	NULL	0	NULL	GBR-decanoate	NULL	effects of	is mediated by	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_301_3_1190_s_204	12023554	A fundamental premise of the present study is that the effects of GBR-decanoate are mediated by a slow release of GBR-hydroxy into the bloodstream, with subsequent pseudo-irreversible binding of GBR-hydroxy to DAT sites in the brain (Lewis et al., 1999  ).	bind
43814	1	10300	5	11	NULL	NULL	NULL	linker histones	GP	recognition of	is a fundamental step in					chromatin	Chromosome	assembly of;;native			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_25817_s_2	8824211	A fundamental step in the assembly of native chromatin is the specific recognition and binding of linker histones to the nucleoprotein subunit known as the nucleosome.	bind
43815	2	10300	5	11	NULL	NULL	NULL	linker histones	GP		bind					nucleoprotein subunit	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_25817_s_2	8824211	A fundamental step in the assembly of native chromatin is the specific recognition and binding of linker histones to the nucleoprotein subunit known as the nucleosome.	bind
43816	3	10300	5	11	NULL	NULL	NULL	nucleoprotein subunit	GP		is known as					nucleosome	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_25817_s_2	8824211	A fundamental step in the assembly of native chromatin is the specific recognition and binding of linker histones to the nucleoprotein subunit known as the nucleosome.	bind
43817	4	10300	5	11	NULL	NULL	NULL	statement 2	Process		is a fundamental step in					chromatin	Chromosome	assembly of;;native			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_25817_s_2	8824211	A fundamental step in the assembly of native chromatin is the specific recognition and binding of linker histones to the nucleoprotein subunit known as the nucleosome.	bind
36618	1	10300	6	NULL	NULL	0	NULL	nucleosome	NULL		is the	NULL				nucleoprotein subunit	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_42_25817_s_2	8824211	A fundamental step in the assembly of native chromatin is the specific recognition and binding of linker histones to the nucleoprotein subunit known as the nucleosome.	bind
36620	2	10300	6	NULL	NULL	0	NULL	linker histones	NULL		recognize	NULL				nucleosome	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_42_25817_s_2	8824211	A fundamental step in the assembly of native chromatin is the specific recognition and binding of linker histones to the nucleoprotein subunit known as the nucleosome.	bind
36622	3	10300	6	NULL	NULL	0	NULL	linker histones	NULL		bind	NULL				nucleosomes	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_42_25817_s_2	8824211	A fundamental step in the assembly of native chromatin is the specific recognition and binding of linker histones to the nucleoprotein subunit known as the nucleosome.	bind
36623	4	10300	6	NULL	NULL	0	NULL	statement 2	NULL		occurs simultaneously with	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_42_25817_s_2	8824211	A fundamental step in the assembly of native chromatin is the specific recognition and binding of linker histones to the nucleoprotein subunit known as the nucleosome.	bind
36625	5	10300	6	NULL	NULL	0	NULL	statement 4	NULL		is the fundamental step for	NULL				chromatin	NULL	assembly of;; native			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_42_25817_s_2	8824211	A fundamental step in the assembly of native chromatin is the specific recognition and binding of linker histones to the nucleoprotein subunit known as the nucleosome.	bind
43818	1	10301	5	11	NULL	NULL	NULL	p300	GP	highly purified	bind		strongly			GST-VP16	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_3_551_s_145	11030335	A further analysis with very highly purified p300 showed very strong binding to GST-VP16 and more moderate binding to GST-SP1 but no detectable binding to GST-CTF1 or GST alone (  Figure 7C).	bind
43819	2	10301	5	11	NULL	NULL	NULL	p300	GP	highly purified	bind		moderatley			GST-SP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_3_551_s_145	11030335	A further analysis with very highly purified p300 showed very strong binding to GST-VP16 and more moderate binding to GST-SP1 but no detectable binding to GST-CTF1 or GST alone (  Figure 7C).	bind
43820	3	10301	5	11	NULL	NULL	NULL	p300	GP	highly purified	does not bind					GST-CTF1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_3_551_s_145	11030335	A further analysis with very highly purified p300 showed very strong binding to GST-VP16 and more moderate binding to GST-SP1 but no detectable binding to GST-CTF1 or GST alone (  Figure 7C).	bind
43821	4	10301	5	11	NULL	NULL	NULL	p300	GP	highly purified	does not bind					GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_3_551_s_145	11030335	A further analysis with very highly purified p300 showed very strong binding to GST-VP16 and more moderate binding to GST-SP1 but no detectable binding to GST-CTF1 or GST alone (  Figure 7C).	bind
36680	1	10301	6	NULL	NULL	0	NULL	p300	NULL	highly purified	bind	NULL	very strongly			GST-VP16	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_6_3_551_s_145	11030335	A further analysis with very highly purified p300 showed very strong binding to GST-VP16 and more moderate binding to GST-SP1 but no detectable binding to GST-CTF1 or GST alone (  Figure 7C).	bind
36681	2	10301	6	NULL	NULL	0	NULL	p300	NULL	highly purified	bind	NULL	moderately			GST-SP1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_6_3_551_s_145	11030335	A further analysis with very highly purified p300 showed very strong binding to GST-VP16 and more moderate binding to GST-SP1 but no detectable binding to GST-CTF1 or GST alone (  Figure 7C).	bind
36682	3	10301	6	NULL	NULL	0	NULL	p300	NULL	highly purified	does not bind	NULL				GST-CTF1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_6_3_551_s_145	11030335	A further analysis with very highly purified p300 showed very strong binding to GST-VP16 and more moderate binding to GST-SP1 but no detectable binding to GST-CTF1 or GST alone (  Figure 7C).	bind
36689	4	10301	6	NULL	NULL	0	NULL	p300	NULL	highly purified	does not bind	NULL				GST	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_6_3_551_s_145	11030335	A further analysis with very highly purified p300 showed very strong binding to GST-VP16 and more moderate binding to GST-SP1 but no detectable binding to GST-CTF1 or GST alone (  Figure 7C).	bind
43827	1	10302	5	11	NULL	NULL	NULL	pol delta	GP		interact with					PCNA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_27_24340_s_172	11986310	A further argument against the third subunit being the mediator of the interaction between pol delta and PCNA is the observation that deletion of the PCNA-binding motif of Pol32 in  S. cerevisiae did not significantly affect the processivity of PCNA-dependent DNA synthesis by pol delta ( 54).	bind
43828	2	10302	5	11	NULL	NULL	NULL	pol delta	GP		synthesizes					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_27_24340_s_172	11986310	A further argument against the third subunit being the mediator of the interaction between pol delta and PCNA is the observation that deletion of the PCNA-binding motif of Pol32 in  S. cerevisiae did not significantly affect the processivity of PCNA-dependent DNA synthesis by pol delta ( 54).	bind
43829	3	10302	5	11	NULL	NULL	NULL	statement 2	Process		is dependent on					PCNA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_27_24340_s_172	11986310	A further argument against the third subunit being the mediator of the interaction between pol delta and PCNA is the observation that deletion of the PCNA-binding motif of Pol32 in  S. cerevisiae did not significantly affect the processivity of PCNA-dependent DNA synthesis by pol delta ( 54).	bind
43830	4	10302	5	11	NULL	NULL	NULL	Pol32	GP	S. cerevisiae;;deletion mutant	does not affect		significantly	PCNA-binding motif		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_27_24340_s_172	11986310	A further argument against the third subunit being the mediator of the interaction between pol delta and PCNA is the observation that deletion of the PCNA-binding motif of Pol32 in  S. cerevisiae did not significantly affect the processivity of PCNA-dependent DNA synthesis by pol delta ( 54).	bind
37056	1	10302	6	NULL	NULL	0	NULL	Poldelta	NULL		synthesizes	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24340_s_172	11986310	A further argument against the third subunit being the mediator of the interaction between pol delta and PCNA is the observation that deletion of the PCNA-binding motif of Pol32 in  S. cerevisiae did not significantly affect the processivity of PCNA-dependent DNA synthesis by pol delta ( 54).	bind
37057	2	10302	6	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				PCNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24340_s_172	11986310	A further argument against the third subunit being the mediator of the interaction between pol delta and PCNA is the observation that deletion of the PCNA-binding motif of Pol32 in  S. cerevisiae did not significantly affect the processivity of PCNA-dependent DNA synthesis by pol delta ( 54).	bind
37058	3	10302	6	10	NULL	0	NULL	Pol32		S. cerevisiae;;deletion mutant	did not affect		significantly	PCNA-binding motif		statement 2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_27_24340_s_172	11986310	A further argument against the third subunit being the mediator of the interaction between pol delta and PCNA is the observation that deletion of the PCNA-binding motif of Pol32 in  S. cerevisiae did not significantly affect the processivity of PCNA-dependent DNA synthesis by pol delta ( 54).	bind
48572	4	10302	6	10	NULL	0	NULL	pol delta	NULL		interacts with	NULL				PCNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24340_s_172	11986310	A further argument against the third subunit being the mediator of the interaction between pol delta and PCNA is the observation that deletion of the PCNA-binding motif of Pol32 in  S. cerevisiae did not significantly affect the processivity of PCNA-dependent DNA synthesis by pol delta ( 54).	bind
43831	1	10303	5	11	NULL	NULL	NULL	FGF-2 monomer	GP		bind		covalently			heparin oligosaccharide	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_227	10816596	A further argument in favor of the bridging hypothesis rather than the FGF dimerization model, is the finding by Pye and Gallagher ( 37) that a conjugate of an FGF-2 monomer covalently bound to a heparin oligosaccharide showed mitogenic activity.	bind
43832	2	10303	5	11	NULL	NULL	NULL	FGF-2 monomer	GP	conjugate of	shows					mitogenic activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_227	10816596	A further argument in favor of the bridging hypothesis rather than the FGF dimerization model, is the finding by Pye and Gallagher ( 37) that a conjugate of an FGF-2 monomer covalently bound to a heparin oligosaccharide showed mitogenic activity.	bind
36690	1	10303	6	NULL	NULL	0	NULL	FGF-2 monomer 	NULL		bind	NULL	covalently			heparin oligosaccharide	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_227	10816596	A further argument in favor of the bridging hypothesis rather than the FGF dimerization model, is the finding by Pye and Gallagher ( 37) that a conjugate of an FGF-2 monomer covalently bound to a heparin oligosaccharide showed mitogenic activity.	bind
48573	2	10303	6	10	NULL	0	NULL	FGF-2 monomer	NULL	conjugate of	shows	NULL				mitogenic activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24653_s_227	10816596	A further argument in favor of the bridging hypothesis rather than the FGF dimerization model, is the finding by Pye and Gallagher ( 37) that a conjugate of an FGF-2 monomer covalently bound to a heparin oligosaccharide showed mitogenic activity.	bind
43833	1	10306	5	11	NULL	NULL	NULL	Munc13-1	GP		bind					syntaxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_138_7_1191_s_281	12711617	A further complication arises if it can be confirmed that Munc13-1 binding to syntaxin is not affected by phorbol esters (see Rhee  et al., 2002  , p. 131).	bind
36856	1	10306	6	NULL	NULL	0	NULL	Munc13-1	NULL		bind	NULL				syntaxin	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_138_7_1191_s_281	12711617	A further complication arises if it can be confirmed that Munc13-1 binding to syntaxin is not affected by phorbol esters (see Rhee  et al., 2002  , p. 131).	bind
43834	1	10307	5	11	NULL	NULL	NULL	p20	GP		bind					eIF4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_16_4798_s_245	9707439	A further conclusion from this study is that p20 binding to eIF4E involves some, but not all, of the surface residues bound by 4G-BD4EHis6.	bind
43835	2	10307	5	11	NULL	NULL	NULL	surface residues	AminoAcid		is bound by					4G-BD4EHis6	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_16_4798_s_245	9707439	A further conclusion from this study is that p20 binding to eIF4E involves some, but not all, of the surface residues bound by 4G-BD4EHis6.	bind
43836	3	10307	5	11	NULL	NULL	NULL	statement 1	Process		involves					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_16_4798_s_245	9707439	A further conclusion from this study is that p20 binding to eIF4E involves some, but not all, of the surface residues bound by 4G-BD4EHis6.	bind
36858	1	10307	6	NULL	NULL	0	NULL	p20	NULL		bind	NULL				eIF4E	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_17_16_4798_s_245	9707439	A further conclusion from this study is that p20 binding to eIF4E involves some, but not all, of the surface residues bound by 4G-BD4EHis6.	bind
36860	2	10307	6	10	NULL	0	NULL	surface residues	NULL		bind	NULL				4G-BD4EHis6	NULL				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_16_4798_s_245	9707439	A further conclusion from this study is that p20 binding to eIF4E involves some, but not all, of the surface residues bound by 4G-BD4EHis6.	bind
48574	3	10307	6	10	NULL	0	NULL	statement 1	NULL		involves	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_17_16_4798_s_245	9707439	A further conclusion from this study is that p20 binding to eIF4E involves some, but not all, of the surface residues bound by 4G-BD4EHis6.	bind
43837	2	10308	5	11	NULL	NULL	NULL	statement 1	Process		leads to					EGR1.DNA complex	NucleicAcid	prevalence of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_23999_s_187	8798634	A further confirmation that the prevalence of the EGR1.DNA complex was due to the higher binding affinity of EGR1 compared with TBP came from studies in which TFIIA was included.	bind
49539	1	10308	5	11	NULL	NULL	NULL	EGR1	GP	binding of	has high affinity to					TBP	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_39_23999_s_187	8798634	A further confirmation that the prevalence of the EGR1.DNA complex was due to the higher binding affinity of EGR1 compared with TBP came from studies in which TFIIA was included.	bind
37059	1	10308	6	NULL	NULL	0	NULL	EGR1	NULL	binding of	has high affinity to	NULL				TBP	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_39_23999_s_187	8798634	A further confirmation that the prevalence of the EGR1.DNA complex was due to the higher binding affinity of EGR1 compared with TBP came from studies in which TFIIA was included.	bind
49540	2	10308	6	10	NULL	0	NULL	statement 1	NULL		leads to	NULL				EGR1.DNA complex	NULL	prevalence of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_39_23999_s_187	8798634	A further confirmation that the prevalence of the EGR1.DNA complex was due to the higher binding affinity of EGR1 compared with TBP came from studies in which TFIIA was included.	bind
43838	1	10309	5	11	NULL	NULL	NULL	M-cyclin	GP		bind			N-terminus		cdk2	GP		T-loop		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_12_2877_s_193	10856233	A further consequence of the position of M-cyclin bound to cdk2 is that almost half of the cdk2 T-loop is buried within the interface pincered between the N-terminus of M-cyclin and the PSTAIRE helix (Figure  2C).	bind
43840	3	10309	5	11	NULL	NULL	NULL	cdk2	GP		bind			T-loop		M-cyclin	GP		PSTAIRE helix		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_12_2877_s_193	10856233	A further consequence of the position of M-cyclin bound to cdk2 is that almost half of the cdk2 T-loop is buried within the interface pincered between the N-terminus of M-cyclin and the PSTAIRE helix (Figure  2C).	bind
36861	1	10309	6	NULL	NULL	0	NULL	M-cyclin	NULL		bind	NULL		N-terminus		Cdk2	NULL		T loop		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_12_2877_s_193	10856233	A further consequence of the position of M-cyclin bound to cdk2 is that almost half of the cdk2 T-loop is buried within the interface pincered between the N-terminus of M-cyclin and the PSTAIRE helix (Figure  2C).	bind
36862	2	10309	6	NULL	NULL	0	NULL	M-cyclin	NULL		bind	NULL		PSTAIRE helix		Cdk2	NULL		T-loop		NULL		0	NULL	NULL	NULL	gw60_embo_19_12_2877_s_193	10856233	A further consequence of the position of M-cyclin bound to cdk2 is that almost half of the cdk2 T-loop is buried within the interface pincered between the N-terminus of M-cyclin and the PSTAIRE helix (Figure  2C).	bind
46392	1	10310	5	11	NULL	NULL	NULL	CTB	Chemical	immunoreactive	bind					GM1	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1260_s_104	11854209	A further construct, pMGJ913, containing a polylinker sequence encoding 13 residues inserted into the  HincII site formed immunoreactive CTB that also bound to GM1 (not shown) and was found to be halo negative by RPIHA.	bind
36863	1	10310	6	NULL	NULL	0	NULL	CTB	NULL	immunoreactive	bind	NULL				GM1	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_3_1260_s_104	11854209	A further construct, pMGJ913, containing a polylinker sequence encoding 13 residues inserted into the  HincII site formed immunoreactive CTB that also bound to GM1 (not shown) and was found to be halo negative by RPIHA.	bind
43841	1	10312	5	11	NULL	NULL	NULL	ASF/SF2	GP		does not inhibit			RS domain		IIIa-MS2I	GP	splicing of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12579_s_155	11801589	A further dissection of ASF/SF2 demonstrated that the ASF/SF2-RS domain did not inhibit IIIa-MS2I splicing (Fig.  5,  lanes 9-12), whereas the MS2 fusion protein encoding for ASF/SF2-RBD2 inhibited IIIa-MS2I splicing ~5-fold (Fig.  5,  lanes 5-8).	bind
43842	2	10312	5	11	NULL	NULL	NULL	MS2	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12579_s_155	11801589	A further dissection of ASF/SF2 demonstrated that the ASF/SF2-RS domain did not inhibit IIIa-MS2I splicing (Fig.  5,  lanes 9-12), whereas the MS2 fusion protein encoding for ASF/SF2-RBD2 inhibited IIIa-MS2I splicing ~5-fold (Fig.  5,  lanes 5-8).	bind
43843	3	10312	5	11	NULL	NULL	NULL	MS2	GP		encodes					ASF/SF2-RBD2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12579_s_155	11801589	A further dissection of ASF/SF2 demonstrated that the ASF/SF2-RS domain did not inhibit IIIa-MS2I splicing (Fig.  5,  lanes 9-12), whereas the MS2 fusion protein encoding for ASF/SF2-RBD2 inhibited IIIa-MS2I splicing ~5-fold (Fig.  5,  lanes 5-8).	bind
43844	4	10312	5	11	NULL	NULL	NULL	MS2	GP		inhibit					IIIa-MS2I	GP	splicing of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12579_s_155	11801589	A further dissection of ASF/SF2 demonstrated that the ASF/SF2-RS domain did not inhibit IIIa-MS2I splicing (Fig.  5,  lanes 9-12), whereas the MS2 fusion protein encoding for ASF/SF2-RBD2 inhibited IIIa-MS2I splicing ~5-fold (Fig.  5,  lanes 5-8).	bind
36864	1	10312	6	10	NULL	0	NULL	ASF/SF2	NULL		did not inhibit	NULL		RS domain		IIIa-MS2I	NULL	splicing of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12579_s_155	11801589	A further dissection of ASF/SF2 demonstrated that the ASF/SF2-RS domain did not inhibit IIIa-MS2I splicing (Fig.  5,  lanes 9-12), whereas the MS2 fusion protein encoding for ASF/SF2-RBD2 inhibited IIIa-MS2I splicing ~5-fold (Fig.  5,  lanes 5-8).	bind
36865	2	10312	6	10	NULL	0	NULL	MS2			encodes for					ASF/SF2-RBD2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12579_s_155	11801589	A further dissection of ASF/SF2 demonstrated that the ASF/SF2-RS domain did not inhibit IIIa-MS2I splicing (Fig.  5,  lanes 9-12), whereas the MS2 fusion protein encoding for ASF/SF2-RBD2 inhibited IIIa-MS2I splicing ~5-fold (Fig.  5,  lanes 5-8).	bind
36866	3	10312	6	NULL	NULL	0	NULL	statement 2	NULL		inhibits	NULL				IIIa-MS2I	NULL	splicing of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12579_s_155	11801589	A further dissection of ASF/SF2 demonstrated that the ASF/SF2-RS domain did not inhibit IIIa-MS2I splicing (Fig.  5,  lanes 9-12), whereas the MS2 fusion protein encoding for ASF/SF2-RBD2 inhibited IIIa-MS2I splicing ~5-fold (Fig.  5,  lanes 5-8).	bind
57489	4	10312	6	10	NULL	0	NULL	MS2			is a type of					fusion protein					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12579_s_155	11801589	A further dissection of ASF/SF2 demonstrated that the ASF/SF2-RS domain did not inhibit IIIa-MS2I splicing (Fig.  5,  lanes 9-12), whereas the MS2 fusion protein encoding for ASF/SF2-RBD2 inhibited IIIa-MS2I splicing ~5-fold (Fig.  5,  lanes 5-8).	bind
43845	1	10313	5	11	NULL	NULL	NULL	Keap1	GP		is a type of					Skp1-like BTB-adaptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1579_s_254	16478980	A further downstream regulated interaction is demonstrated between the Skp1-like BTB-adaptor, Keap1, that binds its substrate, the transcription factor Nrf2, but no longer binds the Cul3 scaffold under stress conditions.	bind
43846	2	10313	5	11	NULL	NULL	NULL	Keap1	GP		bind					Nrf2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1579_s_254	16478980	A further downstream regulated interaction is demonstrated between the Skp1-like BTB-adaptor, Keap1, that binds its substrate, the transcription factor Nrf2, but no longer binds the Cul3 scaffold under stress conditions.	bind
43847	3	10313	5	11	NULL	NULL	NULL	Nrf2	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1579_s_254	16478980	A further downstream regulated interaction is demonstrated between the Skp1-like BTB-adaptor, Keap1, that binds its substrate, the transcription factor Nrf2, but no longer binds the Cul3 scaffold under stress conditions.	bind
43848	4	10313	5	11	NULL	NULL	NULL	Keap1	GP		does not bind					Cul3	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1579_s_254	16478980	A further downstream regulated interaction is demonstrated between the Skp1-like BTB-adaptor, Keap1, that binds its substrate, the transcription factor Nrf2, but no longer binds the Cul3 scaffold under stress conditions.	bind
43849	5	10313	5	11	NULL	NULL	NULL	statement 4	Process		in the presence of					stress	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1579_s_254	16478980	A further downstream regulated interaction is demonstrated between the Skp1-like BTB-adaptor, Keap1, that binds its substrate, the transcription factor Nrf2, but no longer binds the Cul3 scaffold under stress conditions.	bind
48705	6	10313	5	11	NULL	NULL	NULL	statement 2	Process		occurs under					stress	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1579_s_254	16478980	A further downstream regulated interaction is demonstrated between the Skp1-like BTB-adaptor, Keap1, that binds its substrate, the transcription factor Nrf2, but no longer binds the Cul3 scaffold under stress conditions.	bind
36867	1	10313	6	NULL	NULL	0	NULL	Keap1	NULL		is a type of	NULL				Skp1-like BTB-adaptor	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1579_s_254	16478980	A further downstream regulated interaction is demonstrated between the Skp1-like BTB-adaptor, Keap1, that binds its substrate, the transcription factor Nrf2, but no longer binds the Cul3 scaffold under stress conditions.	bind
36868	2	10313	6	NULL	NULL	0	NULL	Keap1	NULL		bind	NULL				Nrf2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1579_s_254	16478980	A further downstream regulated interaction is demonstrated between the Skp1-like BTB-adaptor, Keap1, that binds its substrate, the transcription factor Nrf2, but no longer binds the Cul3 scaffold under stress conditions.	bind
36869	3	10313	6	NULL	NULL	0	NULL	Nrf2	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1579_s_254	16478980	A further downstream regulated interaction is demonstrated between the Skp1-like BTB-adaptor, Keap1, that binds its substrate, the transcription factor Nrf2, but no longer binds the Cul3 scaffold under stress conditions.	bind
36870	4	10313	6	NULL	NULL	0	NULL	Keap1	NULL		does not bind	NULL				Cul3 	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1579_s_254	16478980	A further downstream regulated interaction is demonstrated between the Skp1-like BTB-adaptor, Keap1, that binds its substrate, the transcription factor Nrf2, but no longer binds the Cul3 scaffold under stress conditions.	bind
36871	5	10313	6	NULL	NULL	0	NULL	Cul3	NULL		is a type of	NULL				scaffold protein	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1579_s_254	16478980	A further downstream regulated interaction is demonstrated between the Skp1-like BTB-adaptor, Keap1, that binds its substrate, the transcription factor Nrf2, but no longer binds the Cul3 scaffold under stress conditions.	bind
36872	6	10313	6	NULL	NULL	0	NULL	statement 2	NULL		occurs under	NULL				stress	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1579_s_254	16478980	A further downstream regulated interaction is demonstrated between the Skp1-like BTB-adaptor, Keap1, that binds its substrate, the transcription factor Nrf2, but no longer binds the Cul3 scaffold under stress conditions.	bind
36873	7	10313	6	NULL	NULL	0	NULL	statement 4	NULL		occurs under	NULL				stress	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1579_s_254	16478980	A further downstream regulated interaction is demonstrated between the Skp1-like BTB-adaptor, Keap1, that binds its substrate, the transcription factor Nrf2, but no longer binds the Cul3 scaffold under stress conditions.	bind
44177	1	10315	5	11	NULL	NULL	NULL	hNK1	GP	double mutant	shows			P112D;M291		Zn2+	Chemical	increased affinity for			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_58_2_263_s_72	10908293	A further increase in Zn2+ affinity was observed in the double mutants [P112D;M291]-hNK1 (Fig.  2A) and [P112H;M291]-hNK1 where Zn2+ inhibited 125I-BH-Substance P binding with  Ki values of 33  plus-or-minus  12 muM and 41  plus-or-minus  8 muM, respectively.	bind
44178	2	10315	5	11	NULL	NULL	NULL	hNK1	GP	double mutant	shows			P112H;M291		Zn2+	Chemical	increased affinity for			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_58_2_263_s_72	10908293	A further increase in Zn2+ affinity was observed in the double mutants [P112D;M291]-hNK1 (Fig.  2A) and [P112H;M291]-hNK1 where Zn2+ inhibited 125I-BH-Substance P binding with  Ki values of 33  plus-or-minus  12 muM and 41  plus-or-minus  8 muM, respectively.	bind
44179	3	10315	5	11	NULL	NULL	NULL	Zn2+	Chemical		inhibit					125I-BH-Substance P	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_58_2_263_s_72	10908293	A further increase in Zn2+ affinity was observed in the double mutants [P112D;M291]-hNK1 (Fig.  2A) and [P112H;M291]-hNK1 where Zn2+ inhibited 125I-BH-Substance P binding with  Ki values of 33  plus-or-minus  12 muM and 41  plus-or-minus  8 muM, respectively.	bind
36874	1	10315	6	NULL	NULL	0	NULL	Zn2+	NULL		inhibits	NULL				substance P	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_2_263_s_72	10908293	A further increase in Zn2+ affinity was observed in the double mutants [P112D;M291]-hNK1 (Fig.  2A) and [P112H;M291]-hNK1 where Zn2+ inhibited 125I-BH-Substance P binding with  Ki values of 33  plus-or-minus  12 muM and 41  plus-or-minus  8 muM, respectively.	bind
48706	2	10315	6	10	NULL	0	NULL	hNK1	NULL	double mutant	shows 	NULL		P112D;M291		Zn2+	NULL	increased affinity for			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_58_2_263_s_72	10908293	A further increase in Zn2+ affinity was observed in the double mutants [P112D;M291]-hNK1 (Fig.  2A) and [P112H;M291]-hNK1 where Zn2+ inhibited 125I-BH-Substance P binding with  Ki values of 33  plus-or-minus  12 muM and 41  plus-or-minus  8 muM, respectively.	bind
48707	3	10315	6	10	NULL	0	NULL	hNK1	NULL	double mutant	shows	NULL		P112H;M291		Zn2+	NULL	increased affinity for			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_2_263_s_72	10908293	A further increase in Zn2+ affinity was observed in the double mutants [P112D;M291]-hNK1 (Fig.  2A) and [P112H;M291]-hNK1 where Zn2+ inhibited 125I-BH-Substance P binding with  Ki values of 33  plus-or-minus  12 muM and 41  plus-or-minus  8 muM, respectively.	bind
43850	1	10316	5	11	NULL	NULL	NULL	Cdc24	GP		bind					Bud1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_9_4463_s_153	9114012	A further indication of the residues that are important for binding of Cdc24 to Bud1 comes from analysis of the Bud1T35A mutant.	bind
36875	1	10316	6	NULL	NULL	0	NULL	Cdc24	NULL		bind	NULL				Bud1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_94_9_4463_s_153	9114012	A further indication of the residues that are important for binding of Cdc24 to Bud1 comes from analysis of the Bud1T35A mutant.	bind
43851	1	10317	5	11	NULL	NULL	NULL	STAT-1	GP		bind					TNFR1-TRADD	GP				NULL		NULL	NULL	NULL	NULL	gw60_diabetes_51_6_1805_s_207	12031968	A further interaction between the two cytokines  signaling pathways ( 58) is through binding of STAT-1 to the TNFR1-TRADD signaling complex, which favors the formation of the DISC required for induction of apoptosis.	bind
43852	2	10317	5	11	NULL	NULL	NULL	TNFR1-TRADD	GP		is a type of					signaling complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_diabetes_51_6_1805_s_207	12031968	A further interaction between the two cytokines  signaling pathways ( 58) is through binding of STAT-1 to the TNFR1-TRADD signaling complex, which favors the formation of the DISC required for induction of apoptosis.	bind
43853	3	10317	5	11	NULL	NULL	NULL	statement 1	Process		favors					DISC	GP	formation of			NULL		NULL	NULL	NULL	NULL	gw60_diabetes_51_6_1805_s_207	12031968	A further interaction between the two cytokines  signaling pathways ( 58) is through binding of STAT-1 to the TNFR1-TRADD signaling complex, which favors the formation of the DISC required for induction of apoptosis.	bind
43854	4	10317	5	11	NULL	NULL	NULL	DISC	GP	formation of	is required for					apoptosis	Process	induction of			NULL		NULL	NULL	NULL	NULL	gw60_diabetes_51_6_1805_s_207	12031968	A further interaction between the two cytokines  signaling pathways ( 58) is through binding of STAT-1 to the TNFR1-TRADD signaling complex, which favors the formation of the DISC required for induction of apoptosis.	bind
36935	1	10317	6	10	NULL	0	NULL	STAT-1	NULL		bind	NULL				TNFR1-TRADD 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_diabetes_51_6_1805_s_207	12031968	A further interaction between the two cytokines  signaling pathways ( 58) is through binding of STAT-1 to the TNFR1-TRADD signaling complex, which favors the formation of the DISC required for induction of apoptosis.	bind
36936	2	10317	6	NULL	NULL	0	NULL	statement 1	NULL		favours 	NULL				DISC	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_diabetes_51_6_1805_s_207	12031968	A further interaction between the two cytokines  signaling pathways ( 58) is through binding of STAT-1 to the TNFR1-TRADD signaling complex, which favors the formation of the DISC required for induction of apoptosis.	bind
36937	3	10317	6	10	NULL	0	NULL	DISC	NULL	formation of	is required for	NULL				apoptosis	NULL	induction of			NULL		NULL	NULL	NULL	NULL	gw60_diabetes_51_6_1805_s_207	12031968	A further interaction between the two cytokines  signaling pathways ( 58) is through binding of STAT-1 to the TNFR1-TRADD signaling complex, which favors the formation of the DISC required for induction of apoptosis.	bind
48708	4	10317	6	10	NULL	0	NULL	TNFR1-TRADD	NULL		is a type of	NULL				signaling complex	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_51_6_1805_s_207	12031968	A further interaction between the two cytokines  signaling pathways ( 58) is through binding of STAT-1 to the TNFR1-TRADD signaling complex, which favors the formation of the DISC required for induction of apoptosis.	bind
43855	1	10318	5	11	NULL	NULL	NULL				interact with			Asn111					Asn295		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_7_4245_s_171	9020140	A further interesting but more speculative implication of the present study is that the interaction between Asn111 and Asn295 may be fundamental in determining the apparent peptide binding selectivity of AT1 and AT2 receptors.	bind
43856	4	10318	5	11	NULL	NULL	NULL	statement 1	Process		determines					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_7_4245_s_171	9020140	A further interesting but more speculative implication of the present study is that the interaction between Asn111 and Asn295 may be fundamental in determining the apparent peptide binding selectivity of AT1 and AT2 receptors.	bind
43857	5	10318	5	11	NULL	NULL	NULL	statement 1	Process		determines					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_7_4245_s_171	9020140	A further interesting but more speculative implication of the present study is that the interaction between Asn111 and Asn295 may be fundamental in determining the apparent peptide binding selectivity of AT1 and AT2 receptors.	bind
43858	2	10318	5	11	NULL	NULL	NULL	AT1 receptors	GP		bind		selectively			peptides	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_7_4245_s_171	9020140	A further interesting but more speculative implication of the present study is that the interaction between Asn111 and Asn295 may be fundamental in determining the apparent peptide binding selectivity of AT1 and AT2 receptors.	bind
43859	3	10318	5	11	NULL	NULL	NULL	AT2 receptors	GP		bind		selectively			peptides	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_7_4245_s_171	9020140	A further interesting but more speculative implication of the present study is that the interaction between Asn111 and Asn295 may be fundamental in determining the apparent peptide binding selectivity of AT1 and AT2 receptors.	bind
36942	1	10318	6	NULL	NULL	0	NULL		NULL		interacts with	NULL		Asn111			NULL		Asn295		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_7_4245_s_171	9020140	A further interesting but more speculative implication of the present study is that the interaction between Asn111 and Asn295 may be fundamental in determining the apparent peptide binding selectivity of AT1 and AT2 receptors.	bind
37875	2	10318	6	10	NULL	0	NULL	AT1 receptor	NULL		bind	NULL				peptide	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_7_4245_s_171	9020140	A further interesting but more speculative implication of the present study is that the interaction between Asn111 and Asn295 may be fundamental in determining the apparent peptide binding selectivity of AT1 and AT2 receptors.	bind
37876	3	10318	6	10	NULL	0	NULL	AT2 receptor	NULL		bind	NULL				peptide	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_7_4245_s_171	9020140	A further interesting but more speculative implication of the present study is that the interaction between Asn111 and Asn295 may be fundamental in determining the apparent peptide binding selectivity of AT1 and AT2 receptors.	bind
48709	4	10318	6	10	NULL	0	NULL	statement 1	NULL		determines	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_7_4245_s_171	9020140	A further interesting but more speculative implication of the present study is that the interaction between Asn111 and Asn295 may be fundamental in determining the apparent peptide binding selectivity of AT1 and AT2 receptors.	bind
48710	5	10318	6	10	NULL	0	NULL	statement 1	NULL		determines	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_7_4245_s_171	9020140	A further interesting but more speculative implication of the present study is that the interaction between Asn111 and Asn295 may be fundamental in determining the apparent peptide binding selectivity of AT1 and AT2 receptors.	bind
43860	1	10319	5	11	NULL	NULL	NULL	HIV-1	Organism		bind					Candida	Organism				NULL		NULL	NULL	NULL	NULL	gw70_femsimmunolmedmic_37_1_77_s_16	12770763	A further objective was to assess  whether HIV-1 binding to  Candida has an effect on fungal adhesion to human endo- or epithelial cells, representing  targets of mucosal or systemic infection, respectively.	bind
48721	2	10319	5	11	NULL	NULL	NULL	epithelial cells	Cell	human	are targets for					systemic infection	Process				NULL		NULL	NULL	NULL	NULL	gw70_femsimmunolmedmic_37_1_77_s_16	12770763	A further objective was to assess  whether HIV-1 binding to  Candida has an effect on fungal adhesion to human endo- or epithelial cells, representing  targets of mucosal or systemic infection, respectively.	bind
48722	3	10319	5	11	NULL	NULL	NULL	endothelial cells	Cell	human	are targets for					mucosal infection	Process				NULL		NULL	NULL	NULL	NULL	gw70_femsimmunolmedmic_37_1_77_s_16	12770763	A further objective was to assess  whether HIV-1 binding to  Candida has an effect on fungal adhesion to human endo- or epithelial cells, representing  targets of mucosal or systemic infection, respectively.	bind
36948	1	10319	6	NULL	NULL	0	NULL	HIV-1	NULL		bind	NULL				Candida	NULL				NULL		0	NULL	NULL	NULL	gw70_femsimmunolmedmic_37_1_77_s_16	12770763	A further objective was to assess  whether HIV-1 binding to  Candida has an effect on fungal adhesion to human endo- or epithelial cells, representing  targets of mucosal or systemic infection, respectively.	bind
36949	2	10319	6	NULL	NULL	0	NULL	endothelial cells	NULL	human	are targets for	NULL				mucosal infection	NULL				NULL		0	NULL	NULL	NULL	gw70_femsimmunolmedmic_37_1_77_s_16	12770763	A further objective was to assess  whether HIV-1 binding to  Candida has an effect on fungal adhesion to human endo- or epithelial cells, representing  targets of mucosal or systemic infection, respectively.	bind
36950	3	10319	6	10	NULL	0	NULL	epithelial cells		human	are targets for					systemic infection					NULL		NULL	NULL	NULL	NULL	gw70_femsimmunolmedmic_37_1_77_s_16	12770763	A further objective was to assess  whether HIV-1 binding to  Candida has an effect on fungal adhesion to human endo- or epithelial cells, representing  targets of mucosal or systemic infection, respectively.	bind
43861	1	10320	5	11	NULL	NULL	NULL	Rac	GP		bind					GTP	Chemical				NULL	platelets	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_39474_s_388	16195235	A further possibility is that a basal level of GTP-bound form of Rac is present in platelets and is sufficient to lead to initiation of lamellipodia formation.	bind
43862	2	10320	5	11	NULL	NULL	NULL	statement 1	Process		leads to		possibly			lamellipodia	MedicalFinding	initiation of;; formation of			NULL	platelets	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_39474_s_388	16195235	A further possibility is that a basal level of GTP-bound form of Rac is present in platelets and is sufficient to lead to initiation of lamellipodia formation.	bind
37112	1	10320	6	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				Rac	NULL				NULL	platelets	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_39474_s_388	16195235	A further possibility is that a basal level of GTP-bound form of Rac is present in platelets and is sufficient to lead to initiation of lamellipodia formation.	bind
37113	2	10320	6	10	NULL	0	NULL	statement 1			leads to		possibly			lamellipodia		initiation of;; formation of 			NULL	platelets	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_39474_s_388	16195235	A further possibility is that a basal level of GTP-bound form of Rac is present in platelets and is sufficient to lead to initiation of lamellipodia formation.	bind
43864	1	10321	5	11	NULL	NULL	NULL	LAP2	GP		bind					BAF	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_7_1754_s_287	11285238	A further prediction from our work is that the stoichiometry of LAP2 - BAF complexes varies as a function of the LAP2 concentration, and that binding between LAP2 and BAF might not follow simple first-order kinetics.	bind
37114	1	10321	6	NULL	NULL	0	NULL	LAP2	NULL		bind	NULL				BAF	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_7_1754_s_287	11285238	A further prediction from our work is that the stoichiometry of LAP2 - BAF complexes varies as a function of the LAP2 concentration, and that binding between LAP2 and BAF might not follow simple first-order kinetics.	bind
43866	1	10323	5	11	NULL	NULL	NULL	VCAM-1	GP		promotes		potentially			inflammation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_42_30041_s_317	10514490	A further recent study suggested an important role for VCAM-1 in promoting inflammation in asthma by demonstrating that inhibition of binding of VCAM-1 to its ligand VLA-4 markedly inhibited lymphocyte and eosinophil infiltration in an animal model of allergen-induced inflammation ( 30).	bind
43867	2	10323	5	11	NULL	NULL	NULL	VCAM-1	GP		bind					VLA-4 ligand	GP				NULL	animal model of allergen-induced inflammation	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_42_30041_s_317	10514490	A further recent study suggested an important role for VCAM-1 in promoting inflammation in asthma by demonstrating that inhibition of binding of VCAM-1 to its ligand VLA-4 markedly inhibited lymphocyte and eosinophil infiltration in an animal model of allergen-induced inflammation ( 30).	bind
43868	3	10323	5	11	NULL	NULL	NULL	statement 1	Process		occurs during					asthma	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_42_30041_s_317	10514490	A further recent study suggested an important role for VCAM-1 in promoting inflammation in asthma by demonstrating that inhibition of binding of VCAM-1 to its ligand VLA-4 markedly inhibited lymphocyte and eosinophil infiltration in an animal model of allergen-induced inflammation ( 30).	bind
43869	4	10323	5	11	NULL	NULL	NULL	statement 2	Process	inhibition of	inhibit					lymphocyte	Cell	infiltration of			NULL	animal model of allergen-induced inflammation	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_42_30041_s_317	10514490	A further recent study suggested an important role for VCAM-1 in promoting inflammation in asthma by demonstrating that inhibition of binding of VCAM-1 to its ligand VLA-4 markedly inhibited lymphocyte and eosinophil infiltration in an animal model of allergen-induced inflammation ( 30).	bind
43870	5	10323	5	11	NULL	NULL	NULL	statement 2	Process	inhibition of	inhibit					eosinophil	Cell	infiltration of			NULL	animal model of allergen-induced inflammation	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_42_30041_s_317	10514490	A further recent study suggested an important role for VCAM-1 in promoting inflammation in asthma by demonstrating that inhibition of binding of VCAM-1 to its ligand VLA-4 markedly inhibited lymphocyte and eosinophil infiltration in an animal model of allergen-induced inflammation ( 30).	bind
37118	1	10323	6	10	NULL	0	NULL	VCAM-1			bind					VLA-4 ligand					NULL	\tanimal model of allergen-induced inflammation	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_42_30041_s_317	10514490	A further recent study suggested an important role for VCAM-1 in promoting inflammation in asthma by demonstrating that inhibition of binding of VCAM-1 to its ligand VLA-4 markedly inhibited lymphocyte and eosinophil infiltration in an animal model of allergen-induced inflammation ( 30).	bind
37119	2	10323	6	NULL	NULL	0	NULL	VCAM-1	NULL		promotes	NULL				inflammation	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_42_30041_s_317	10514490	A further recent study suggested an important role for VCAM-1 in promoting inflammation in asthma by demonstrating that inhibition of binding of VCAM-1 to its ligand VLA-4 markedly inhibited lymphocyte and eosinophil infiltration in an animal model of allergen-induced inflammation ( 30).	bind
37120	3	10323	6	NULL	NULL	0	NULL	statement 2	NULL		occurs during	NULL				Asthma	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_42_30041_s_317	10514490	A further recent study suggested an important role for VCAM-1 in promoting inflammation in asthma by demonstrating that inhibition of binding of VCAM-1 to its ligand VLA-4 markedly inhibited lymphocyte and eosinophil infiltration in an animal model of allergen-induced inflammation ( 30).	bind
37121	4	10323	6	NULL	NULL	0	NULL	statement 1	NULL	inhibition of	inhibits	NULL				lymphocyte	NULL	infiltration of			NULL	animal model of allergen-induced inflammation	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_42_30041_s_317	10514490	A further recent study suggested an important role for VCAM-1 in promoting inflammation in asthma by demonstrating that inhibition of binding of VCAM-1 to its ligand VLA-4 markedly inhibited lymphocyte and eosinophil infiltration in an animal model of allergen-induced inflammation ( 30).	bind
37122	5	10323	6	NULL	NULL	0	NULL	statement 1	NULL	inhibition of	inhibits	NULL				eosinophil	NULL	infiltration of 			NULL	animal model of allergen-induced inflammation	0	NULL	NULL	NULL	gw60_jbiolchem_274_42_30041_s_317	10514490	A further recent study suggested an important role for VCAM-1 in promoting inflammation in asthma by demonstrating that inhibition of binding of VCAM-1 to its ligand VLA-4 markedly inhibited lymphocyte and eosinophil infiltration in an animal model of allergen-induced inflammation ( 30).	bind
43871	1	10324	5	11	NULL	NULL	NULL	PLA2R	GP		bind					PLA2	GP	nonglycosylated forms of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_13_8780_s_53	16452473	A further relevant feature of this family of receptors is that some of them interact with other proteins through their CTLD in a sugar independent fashion, as it is the case for PLA2R that binds nonglycosylated forms of PLA2 ( ).	bind
37123	1	10324	6	NULL	NULL	0	NULL	PLA2R	NULL		bind	NULL				PLA2	NULL	nonglycosylated			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_13_8780_s_53	16452473	A further relevant feature of this family of receptors is that some of them interact with other proteins through their CTLD in a sugar independent fashion, as it is the case for PLA2R that binds nonglycosylated forms of PLA2 ( ).	bind
43877	1	10325	5	11	NULL	NULL	NULL	synthetic peptide	AminoAcid		is derived from			1399 - 1410		LN-1	GP	murine	LG4		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44168_s_28	12947106	A further report shows binding of syndecan-1 from human submandibular gland cells and mouse melanoma cells B16F10 to a synthetic peptide corresponding to residues 1399 - 1410 derived from the LG4 sequence of murine LN-1 and LN-2 ( ).	bind
43878	2	10325	5	11	NULL	NULL	NULL	synthetic peptide	AminoAcid		is derived from			1399 - 1410		LN-2	GP	murine	LG4		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44168_s_28	12947106	A further report shows binding of syndecan-1 from human submandibular gland cells and mouse melanoma cells B16F10 to a synthetic peptide corresponding to residues 1399 - 1410 derived from the LG4 sequence of murine LN-1 and LN-2 ( ).	bind
43879	3	10325	5	11	NULL	NULL	NULL	syndecan-1	GP	human;;submandibular gland cells	bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44168_s_28	12947106	A further report shows binding of syndecan-1 from human submandibular gland cells and mouse melanoma cells B16F10 to a synthetic peptide corresponding to residues 1399 - 1410 derived from the LG4 sequence of murine LN-1 and LN-2 ( ).	bind
43880	4	10325	5	11	NULL	NULL	NULL	syndecan-1	GP	human;;submandibular gland cells	bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44168_s_28	12947106	A further report shows binding of syndecan-1 from human submandibular gland cells and mouse melanoma cells B16F10 to a synthetic peptide corresponding to residues 1399 - 1410 derived from the LG4 sequence of murine LN-1 and LN-2 ( ).	bind
43881	5	10325	5	11	NULL	NULL	NULL	syndecan-1	GP	B16F10	bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44168_s_28	12947106	A further report shows binding of syndecan-1 from human submandibular gland cells and mouse melanoma cells B16F10 to a synthetic peptide corresponding to residues 1399 - 1410 derived from the LG4 sequence of murine LN-1 and LN-2 ( ).	bind
43882	6	10325	5	11	NULL	NULL	NULL	syndecan-1	GP	B16F10	bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44168_s_28	12947106	A further report shows binding of syndecan-1 from human submandibular gland cells and mouse melanoma cells B16F10 to a synthetic peptide corresponding to residues 1399 - 1410 derived from the LG4 sequence of murine LN-1 and LN-2 ( ).	bind
43883	7	10325	5	11	NULL	NULL	NULL	B16F10	Cell		is a type of					mouse melanoma cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44168_s_28	12947106	A further report shows binding of syndecan-1 from human submandibular gland cells and mouse melanoma cells B16F10 to a synthetic peptide corresponding to residues 1399 - 1410 derived from the LG4 sequence of murine LN-1 and LN-2 ( ).	bind
37883	1	10325	6	10	NULL	0	NULL	synthetic peptide	NULL		is derived from	NULL		residues 1399 - 1410		LN-1	NULL	murine	LG4 sequence		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44168_s_28	12947106	A further report shows binding of syndecan-1 from human submandibular gland cells and mouse melanoma cells B16F10 to a synthetic peptide corresponding to residues 1399 - 1410 derived from the LG4 sequence of murine LN-1 and LN-2 ( ).	bind
37884	2	10325	6	10	NULL	0	NULL	synthetic peptide	NULL		is derived from	NULL		residues 1399 - 1410		LN2	NULL	murine	LG-4 sequence		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44168_s_28	12947106	A further report shows binding of syndecan-1 from human submandibular gland cells and mouse melanoma cells B16F10 to a synthetic peptide corresponding to residues 1399 - 1410 derived from the LG4 sequence of murine LN-1 and LN-2 ( ).	bind
37885	3	10325	6	10	NULL	0	NULL	syndecan-1	NULL	human;; submandibular gland cells	bind	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44168_s_28	12947106	A further report shows binding of syndecan-1 from human submandibular gland cells and mouse melanoma cells B16F10 to a synthetic peptide corresponding to residues 1399 - 1410 derived from the LG4 sequence of murine LN-1 and LN-2 ( ).	bind
49562	4	10325	6	10	NULL	0	NULL	syndecan-1	NULL	human;; submandibular gland cells	bind	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_45_44168_s_28	12947106	A further report shows binding of syndecan-1 from human submandibular gland cells and mouse melanoma cells B16F10 to a synthetic peptide corresponding to residues 1399 - 1410 derived from the LG4 sequence of murine LN-1 and LN-2 ( ).	bind
49563	5	10325	6	10	NULL	0	NULL	syndecan-1	NULL	B16F10	bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_45_44168_s_28	12947106	A further report shows binding of syndecan-1 from human submandibular gland cells and mouse melanoma cells B16F10 to a synthetic peptide corresponding to residues 1399 - 1410 derived from the LG4 sequence of murine LN-1 and LN-2 ( ).	bind
49564	6	10325	6	10	NULL	0	NULL	syndecan-1	NULL	B16F10	bind	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_45_44168_s_28	12947106	A further report shows binding of syndecan-1 from human submandibular gland cells and mouse melanoma cells B16F10 to a synthetic peptide corresponding to residues 1399 - 1410 derived from the LG4 sequence of murine LN-1 and LN-2 ( ).	bind
49565	7	10325	6	10	NULL	0	NULL	B16F10	NULL		is a type of	NULL				mouse melanoma cells	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_45_44168_s_28	12947106	A further report shows binding of syndecan-1 from human submandibular gland cells and mouse melanoma cells B16F10 to a synthetic peptide corresponding to residues 1399 - 1410 derived from the LG4 sequence of murine LN-1 and LN-2 ( ).	bind
43884	1	10327	5	11	NULL	NULL	NULL	Rap1/Krev-1	GP		is a type of					Ras-related protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_1928_s_273	10022880	A further twist is that the Ras-related protein Rap1/Krev-1 binds to p120 Ras-GAP with high affinity but is not a substrate ( 27).	bind
43885	2	10327	5	11	NULL	NULL	NULL	Rap1/Krev-1	GP		bind		high affinity			p120 Ras-GAP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_1928_s_273	10022880	A further twist is that the Ras-related protein Rap1/Krev-1 binds to p120 Ras-GAP with high affinity but is not a substrate ( 27).	bind
37124	1	10327	6	NULL	NULL	0	NULL	Rap1/Krev-1	NULL		bind	NULL	high affinity			p120 Ras-GAP	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_1928_s_273	10022880	A further twist is that the Ras-related protein Rap1/Krev-1 binds to p120 Ras-GAP with high affinity but is not a substrate ( 27).	bind
37125	2	10327	6	10	NULL	0	NULL	Rap1/Krev-1	NULL		is a type of	NULL				Ras related protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_1928_s_273	10022880	A further twist is that the Ras-related protein Rap1/Krev-1 binds to p120 Ras-GAP with high affinity but is not a substrate ( 27).	bind
43887	1	10328	5	11	NULL	NULL	NULL	LTC4	GP		bind		potentially			G protein-coupled receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_53_4_750_s_204	9547367	A further, but unlikely, hypothesis is that LTC4 binds to a G protein-coupled receptor (different from that of LTD4) but behaves as an antagonist, thus being unable to activate GTPase and displaying a GTP-insensitive binding.	bind
43888	2	10328	5	11	NULL	NULL	NULL	LTC4	GP		acts as					antagonist	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_53_4_750_s_204	9547367	A further, but unlikely, hypothesis is that LTC4 binds to a G protein-coupled receptor (different from that of LTD4) but behaves as an antagonist, thus being unable to activate GTPase and displaying a GTP-insensitive binding.	bind
43890	3	10328	5	11	NULL	NULL	NULL	LTC4	GP		does not activate					GTPase	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_53_4_750_s_204	9547367	A further, but unlikely, hypothesis is that LTC4 binds to a G protein-coupled receptor (different from that of LTD4) but behaves as an antagonist, thus being unable to activate GTPase and displaying a GTP-insensitive binding.	bind
43891	4	10328	5	11	NULL	NULL	NULL	statement 1	Process		is insensitive to					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_53_4_750_s_204	9547367	A further, but unlikely, hypothesis is that LTC4 binds to a G protein-coupled receptor (different from that of LTD4) but behaves as an antagonist, thus being unable to activate GTPase and displaying a GTP-insensitive binding.	bind
37126	1	10328	6	NULL	NULL	0	NULL	LTC4	NULL		bind	NULL				G protein-coupled receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_53_4_750_s_204	9547367	A further, but unlikely, hypothesis is that LTC4 binds to a G protein-coupled receptor (different from that of LTD4) but behaves as an antagonist, thus being unable to activate GTPase and displaying a GTP-insensitive binding.	bind
37127	2	10328	6	NULL	NULL	0	NULL	LTC4	NULL		does not activate	NULL				GTPase	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_53_4_750_s_204	9547367	A further, but unlikely, hypothesis is that LTC4 binds to a G protein-coupled receptor (different from that of LTD4) but behaves as an antagonist, thus being unable to activate GTPase and displaying a GTP-insensitive binding.	bind
37128	3	10328	6	NULL	NULL	0	NULL	LTC4	NULL		behaves as an	NULL				antagonist	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_53_4_750_s_204	9547367	A further, but unlikely, hypothesis is that LTC4 binds to a G protein-coupled receptor (different from that of LTD4) but behaves as an antagonist, thus being unable to activate GTPase and displaying a GTP-insensitive binding.	bind
37129	4	10328	6	10	NULL	0	NULL	statement 1	NULL		is insensitive to	NULL				GTP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_53_4_750_s_204	9547367	A further, but unlikely, hypothesis is that LTC4 binds to a G protein-coupled receptor (different from that of LTD4) but behaves as an antagonist, thus being unable to activate GTPase and displaying a GTP-insensitive binding.	bind
43892	1	10329	5	11	NULL	NULL	NULL				forms			N-terminal domain		thioredoxin	GP	fusion protein with			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_52_14530265_s_6	14530265	A fusion  protein of the N-terminal domain and thioredoxin binds tightly to MTs  at low salt, consistent with the increased affinity of motor domain constructs  (which contain the N-terminal domain) being due to the additional binding  of the N-terminal domain to the microtubule.	bind
43894	2	10329	5	11	NULL	NULL	NULL	statement 1	GP		bind		tightly			MTs	CellComponent				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_52_14530265_s_6	14530265	A fusion  protein of the N-terminal domain and thioredoxin binds tightly to MTs  at low salt, consistent with the increased affinity of motor domain constructs  (which contain the N-terminal domain) being due to the additional binding  of the N-terminal domain to the microtubule.	bind
43895	3	10329	5	11	NULL	NULL	NULL	statement 2	Process		in the presence of					salt	Chemical	low			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_52_14530265_s_6	14530265	A fusion  protein of the N-terminal domain and thioredoxin binds tightly to MTs  at low salt, consistent with the increased affinity of motor domain constructs  (which contain the N-terminal domain) being due to the additional binding  of the N-terminal domain to the microtubule.	bind
43901	4	10329	5	11	NULL	NULL	NULL				bind			N-terminal domain		microtubule	CellComponent				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_52_14530265_s_6	14530265	A fusion  protein of the N-terminal domain and thioredoxin binds tightly to MTs  at low salt, consistent with the increased affinity of motor domain constructs  (which contain the N-terminal domain) being due to the additional binding  of the N-terminal domain to the microtubule.	bind
37886	1	10329	6	NULL	NULL	0	NULL		NULL		forms	NULL		N-terminal domain		thioredoxin	NULL	fusion protein with			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_52_14530265_s_6	14530265	A fusion  protein of the N-terminal domain and thioredoxin binds tightly to MTs  at low salt, consistent with the increased affinity of motor domain constructs  (which contain the N-terminal domain) being due to the additional binding  of the N-terminal domain to the microtubule.	bind
37887	2	10329	6	10	NULL	0	NULL	statement 1			bind		tightly			MTs					NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_52_14530265_s_6	14530265	A fusion  protein of the N-terminal domain and thioredoxin binds tightly to MTs  at low salt, consistent with the increased affinity of motor domain constructs  (which contain the N-terminal domain) being due to the additional binding  of the N-terminal domain to the microtubule.	bind
38141	3	10329	6	NULL	NULL	0	NULL		NULL		bind	NULL		N-terminal domain		microtubule	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_52_14530265_s_6	14530265	A fusion  protein of the N-terminal domain and thioredoxin binds tightly to MTs  at low salt, consistent with the increased affinity of motor domain constructs  (which contain the N-terminal domain) being due to the additional binding  of the N-terminal domain to the microtubule.	bind
57490	4	10329	6	10	NULL	0	NULL	statement 2			in the presence of					salt		low			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_278_52_14530265_s_6	14530265	A fusion  protein of the N-terminal domain and thioredoxin binds tightly to MTs  at low salt, consistent with the increased affinity of motor domain constructs  (which contain the N-terminal domain) being due to the additional binding  of the N-terminal domain to the microtubule.	bind
43902	1	10330	5	11	NULL	NULL	NULL	GST-kendrin	GP		does not bind			coiled-coil		calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_11_5919_s_72	10823944	A fusion between GST and a coiled-coil region of kendrin does not bind calmodulin, nor does GST alone.	bind
43903	2	10330	5	11	NULL	NULL	NULL	GST-kendrin	GP		is a type of			coiled-coil		fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_11_5919_s_72	10823944	A fusion between GST and a coiled-coil region of kendrin does not bind calmodulin, nor does GST alone.	bind
37130	1	10330	6	NULL	NULL	0	NULL	GST	NULL		fuses	NULL				kendrin	NULL		coiled-coil region		NULL		0	NULL	NULL	NULL	gw60_pnas_97_11_5919_s_72	10823944	A fusion between GST and a coiled-coil region of kendrin does not bind calmodulin, nor does GST alone.	bind
37131	2	10330	6	NULL	NULL	0	NULL	statement 1	NULL		does not bind	NULL				calmodulin	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_11_5919_s_72	10823944	A fusion between GST and a coiled-coil region of kendrin does not bind calmodulin, nor does GST alone.	bind
37132	3	10330	6	10	NULL	0	NULL	GST	NULL		does not bind	NULL				calmodulin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_11_5919_s_72	10823944	A fusion between GST and a coiled-coil region of kendrin does not bind calmodulin, nor does GST alone.	bind
43909	2	10340	5	11	NULL	NULL	NULL	pCTLA4-Ig	GP		contains					pCTLA4	GP	extracellular regions of			NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-immunol_165_6_10975832_s_6	10975832	A fusion protein constructed from the extracellular  regions of pCTLA4 and the constant regions of human IgG1 (pCTLA4-Ig) bound  porcine CD86 with equivalent affinity to that of hCTLA4-Ig.	bind
43910	3	10340	5	11	NULL	NULL	NULL	pCTLA4-Ig	GP		contains					IgG1	GP	human	constant regions		NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-immunol_165_6_10975832_s_6	10975832	A fusion protein constructed from the extracellular  regions of pCTLA4 and the constant regions of human IgG1 (pCTLA4-Ig) bound  porcine CD86 with equivalent affinity to that of hCTLA4-Ig.	bind
43911	1	10340	5	11	NULL	NULL	NULL	pCTLA4-Ig	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-immunol_165_6_10975832_s_6	10975832	A fusion protein constructed from the extracellular  regions of pCTLA4 and the constant regions of human IgG1 (pCTLA4-Ig) bound  porcine CD86 with equivalent affinity to that of hCTLA4-Ig.	bind
43912	4	10340	5	11	NULL	NULL	NULL	pCTLA4-Ig	GP		bind					CD86	GP	porcine			NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-immunol_165_6_10975832_s_6	10975832	A fusion protein constructed from the extracellular  regions of pCTLA4 and the constant regions of human IgG1 (pCTLA4-Ig) bound  porcine CD86 with equivalent affinity to that of hCTLA4-Ig.	bind
43913	5	10340	5	11	NULL	NULL	NULL	hCTLA4-Ig	GP		bind					CD86	GP	porcine			NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-immunol_165_6_10975832_s_6	10975832	A fusion protein constructed from the extracellular  regions of pCTLA4 and the constant regions of human IgG1 (pCTLA4-Ig) bound  porcine CD86 with equivalent affinity to that of hCTLA4-Ig.	bind
43914	6	10340	5	11	NULL	NULL	NULL	statement 4	Process		equal affinity to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-immunol_165_6_10975832_s_6	10975832	A fusion protein constructed from the extracellular  regions of pCTLA4 and the constant regions of human IgG1 (pCTLA4-Ig) bound  porcine CD86 with equivalent affinity to that of hCTLA4-Ig.	bind
37133	1	10340	6	NULL	NULL	0	NULL	pCTLA4	NULL		forms fusion protein with	NULL		extracellular region		IgG1	NULL	human	constant region		NULL		0	NULL	NULL	NULL	abs-batch0680-0699_j-immunol_165_6_10975832_s_6	10975832	A fusion protein constructed from the extracellular  regions of pCTLA4 and the constant regions of human IgG1 (pCTLA4-Ig) bound  porcine CD86 with equivalent affinity to that of hCTLA4-Ig.	bind
37134	2	10340	6	10	NULL	0	NULL	pCTLA4-Ig	NULL		bind	NULL				CD86	NULL	porcine			NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-immunol_165_6_10975832_s_6	10975832	A fusion protein constructed from the extracellular  regions of pCTLA4 and the constant regions of human IgG1 (pCTLA4-Ig) bound  porcine CD86 with equivalent affinity to that of hCTLA4-Ig.	bind
37135	3	10340	6	NULL	NULL	0	NULL	hCTLA4-Ig	NULL		bind	NULL				CD86	NULL	porcine			NULL		0	NULL	NULL	NULL	abs-batch0680-0699_j-immunol_165_6_10975832_s_6	10975832	A fusion protein constructed from the extracellular  regions of pCTLA4 and the constant regions of human IgG1 (pCTLA4-Ig) bound  porcine CD86 with equivalent affinity to that of hCTLA4-Ig.	bind
37136	4	10340	6	NULL	NULL	0	NULL	statement 2	NULL	affinity of	is equal to	NULL				statement 3	NULL	affinity of			NULL		0	NULL	NULL	NULL	abs-batch0680-0699_j-immunol_165_6_10975832_s_6	10975832	A fusion protein constructed from the extracellular  regions of pCTLA4 and the constant regions of human IgG1 (pCTLA4-Ig) bound  porcine CD86 with equivalent affinity to that of hCTLA4-Ig.	bind
57496	5	10340	6	10	NULL	0	NULL	pCTLA4-Ig			is					statement 1					NULL		0	NULL	NULL	NULL	abs-batch0680-0699_j-immunol_165_6_10975832_s_6	10975832	A fusion protein constructed from the extracellular  regions of pCTLA4 and the constant regions of human IgG1 (pCTLA4-Ig) bound  porcine CD86 with equivalent affinity to that of hCTLA4-Ig.	bind
43916	1	10341	5	11	NULL	NULL	NULL	fusion protein	GP		contains								Pro-1 region		NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_274_15_10187839_s_5	10187839	A fusion protein containing  the Pro-1 region showed promiscuous binding to SH3 domains of several  proteins in vitro, whereas a Pro-2 fusion bound preferentially to domains  derived from kinases.	bind
43917	2	10341	5	11	NULL	NULL	NULL	statement 1	GP		bind		promiscuous			protein	GP		SH3 domain		NULL	in vitro	NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_274_15_10187839_s_5	10187839	A fusion protein containing  the Pro-1 region showed promiscuous binding to SH3 domains of several  proteins in vitro, whereas a Pro-2 fusion bound preferentially to domains  derived from kinases.	bind
43919	3	10341	5	11	NULL	NULL	NULL	fusion protein	GP		contains								Pro-2 region		NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_274_15_10187839_s_5	10187839	A fusion protein containing  the Pro-1 region showed promiscuous binding to SH3 domains of several  proteins in vitro, whereas a Pro-2 fusion bound preferentially to domains  derived from kinases.	bind
43920	4	10341	5	10	NULL	0	NULL	statement 3	NULL		bind	NULL	preferentially				NULL		kinase domain		NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_274_15_10187839_s_5	10187839	A fusion protein containing  the Pro-1 region showed promiscuous binding to SH3 domains of several  proteins in vitro, whereas a Pro-2 fusion bound preferentially to domains  derived from kinases.	bind
37553	1	10341	6	NULL	NULL	0	NULL	Pro-1 fusion protein	NULL		bind	NULL	promiscuous				NULL		SH3 domain		NULL	in vitro	NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_274_15_10187839_s_5	10187839	A fusion protein containing  the Pro-1 region showed promiscuous binding to SH3 domains of several  proteins in vitro, whereas a Pro-2 fusion bound preferentially to domains  derived from kinases.	bind
37554	2	10341	6	10	NULL	0	NULL	Pro-2 fusion protein	NULL		bind	NULL	preferentially				NULL		kinase domain		NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_274_15_10187839_s_5	10187839	A fusion protein containing  the Pro-1 region showed promiscuous binding to SH3 domains of several  proteins in vitro, whereas a Pro-2 fusion bound preferentially to domains  derived from kinases.	bind
43922	1	10342	5	11	NULL	NULL	NULL	fusion protein	GP		contains					Lyn	GP		SH2 domain;;SH3 domain		NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_eur-j-immunol_27_1_9022035_s_7	9022035	A fusion protein containing Src homology 2 (SH2) and SH3 domains  of Lyn bound Syk from lysates of nonactivated RBL cells; an increased  binding was observed when lysates from Ag- or pervanadate-activated cells  were used.	bind
43924	3	10342	5	11	NULL	NULL	NULL	statement 1	GP		bind					Syk	GP				NULL	lysates of nonactivated RBL cells	NULL	NULL	NULL	NULL	abs-batch0620-0649_eur-j-immunol_27_1_9022035_s_7	9022035	A fusion protein containing Src homology 2 (SH2) and SH3 domains  of Lyn bound Syk from lysates of nonactivated RBL cells; an increased  binding was observed when lysates from Ag- or pervanadate-activated cells  were used.	bind
43927	5	10342	5	11	NULL	NULL	NULL	statement 1	GP		bind		increased			Syk	GP				NULL	lysates from Ag activated cells	NULL	NULL	NULL	NULL	abs-batch0620-0649_eur-j-immunol_27_1_9022035_s_7	9022035	A fusion protein containing Src homology 2 (SH2) and SH3 domains  of Lyn bound Syk from lysates of nonactivated RBL cells; an increased  binding was observed when lysates from Ag- or pervanadate-activated cells  were used.	bind
43929	4	10342	5	11	NULL	NULL	NULL	statement 1	GP		bind		increased			Syk	GP				NULL	lysates from pervanadate activated cells	NULL	NULL	NULL	NULL	abs-batch0620-0649_eur-j-immunol_27_1_9022035_s_7	9022035	A fusion protein containing Src homology 2 (SH2) and SH3 domains  of Lyn bound Syk from lysates of nonactivated RBL cells; an increased  binding was observed when lysates from Ag- or pervanadate-activated cells  were used.	bind
57497	2	10342	5	11	NULL	NULL	NULL	SH2	GP		is					Src homology 2	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_eur-j-immunol_27_1_9022035_s_7	9022035	A fusion protein containing Src homology 2 (SH2) and SH3 domains  of Lyn bound Syk from lysates of nonactivated RBL cells; an increased  binding was observed when lysates from Ag- or pervanadate-activated cells  were used.	bind
37624	1	10342	6	NULL	NULL	0	NULL	Src homology 2	NULL		is	NULL				SH2	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_eur-j-immunol_27_1_9022035_s_7	9022035	A fusion protein containing Src homology 2 (SH2) and SH3 domains  of Lyn bound Syk from lysates of nonactivated RBL cells; an increased  binding was observed when lysates from Ag- or pervanadate-activated cells  were used.	bind
38041	2	10342	6	10	NULL	0	NULL	Lyn			forms 			SH2 domain;;SH3 domains		fusion protein					NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_eur-j-immunol_27_1_9022035_s_7	9022035	A fusion protein containing Src homology 2 (SH2) and SH3 domains  of Lyn bound Syk from lysates of nonactivated RBL cells; an increased  binding was observed when lysates from Ag- or pervanadate-activated cells  were used.	bind
38042	3	10342	6	NULL	NULL	0	NULL	statement 2	NULL		bind	NULL				Syk	NULL				NULL	lysates of nonactivated RBL cells	0	NULL	NULL	NULL	abs-batch0620-0649_eur-j-immunol_27_1_9022035_s_7	9022035	A fusion protein containing Src homology 2 (SH2) and SH3 domains  of Lyn bound Syk from lysates of nonactivated RBL cells; an increased  binding was observed when lysates from Ag- or pervanadate-activated cells  were used.	bind
38043	4	10342	6	NULL	NULL	0	NULL	statement 2	NULL		bind	NULL				Syk	NULL				NULL	lysates from Ag- or pervanadate-activated cells	0	NULL	NULL	NULL	abs-batch0620-0649_eur-j-immunol_27_1_9022035_s_7	9022035	A fusion protein containing Src homology 2 (SH2) and SH3 domains  of Lyn bound Syk from lysates of nonactivated RBL cells; an increased  binding was observed when lysates from Ag- or pervanadate-activated cells  were used.	bind
38044	5	10342	6	NULL	NULL	0	NULL	statement 3	NULL		is greater than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_eur-j-immunol_27_1_9022035_s_7	9022035	A fusion protein containing Src homology 2 (SH2) and SH3 domains  of Lyn bound Syk from lysates of nonactivated RBL cells; an increased  binding was observed when lysates from Ag- or pervanadate-activated cells  were used.	bind
43932	1	10344	5	11	NULL	NULL	NULL	fusion protein	GP		contains					mGluR 7A	GP		COOH-terminal		NULL		NULL	NULL	NULL	NULL	gw60_science_286_5442_1180_s_42	10550060	A fusion protein encompassing the 27 COOH-terminal amino acids of mGluR 7A (C27; see  Fig. 1A) failed to bind calmodulin, but fusion constructs N38 and N25 containing the common NH2-terminal fragments ( Fig. 1A) both bound calmodulin ( 12).	bind
43933	2	10344	5	11	NULL	NULL	NULL	statement 1	GP		does not bind					calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5442_1180_s_42	10550060	A fusion protein encompassing the 27 COOH-terminal amino acids of mGluR 7A (C27; see  Fig. 1A) failed to bind calmodulin, but fusion constructs N38 and N25 containing the common NH2-terminal fragments ( Fig. 1A) both bound calmodulin ( 12).	bind
43934	3	10344	5	11	NULL	NULL	NULL	N38	GP		is a type of					fusion construct	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5442_1180_s_42	10550060	A fusion protein encompassing the 27 COOH-terminal amino acids of mGluR 7A (C27; see  Fig. 1A) failed to bind calmodulin, but fusion constructs N38 and N25 containing the common NH2-terminal fragments ( Fig. 1A) both bound calmodulin ( 12).	bind
43935	4	10344	5	11	NULL	NULL	NULL	N25	GP		is a type of					fusion construct	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5442_1180_s_42	10550060	A fusion protein encompassing the 27 COOH-terminal amino acids of mGluR 7A (C27; see  Fig. 1A) failed to bind calmodulin, but fusion constructs N38 and N25 containing the common NH2-terminal fragments ( Fig. 1A) both bound calmodulin ( 12).	bind
43936	5	10344	5	11	NULL	NULL	NULL	N38	GP		bind			N-terminal		calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5442_1180_s_42	10550060	A fusion protein encompassing the 27 COOH-terminal amino acids of mGluR 7A (C27; see  Fig. 1A) failed to bind calmodulin, but fusion constructs N38 and N25 containing the common NH2-terminal fragments ( Fig. 1A) both bound calmodulin ( 12).	bind
43937	6	10344	5	11	NULL	NULL	NULL	N25	GP		bind			N-terminal		calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5442_1180_s_42	10550060	A fusion protein encompassing the 27 COOH-terminal amino acids of mGluR 7A (C27; see  Fig. 1A) failed to bind calmodulin, but fusion constructs N38 and N25 containing the common NH2-terminal fragments ( Fig. 1A) both bound calmodulin ( 12).	bind
37137	1	10344	6	NULL	NULL	0	NULL	mGluR 7A	NULL		forms	NULL		COOH-terminal amino acids		fusion protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5442_1180_s_42	10550060	A fusion protein encompassing the 27 COOH-terminal amino acids of mGluR 7A (C27; see  Fig. 1A) failed to bind calmodulin, but fusion constructs N38 and N25 containing the common NH2-terminal fragments ( Fig. 1A) both bound calmodulin ( 12).	bind
38036	2	10344	6	NULL	NULL	0	NULL	statement 1	NULL		does not bind	NULL				calmodulin	NULL				NULL		0	NULL	NULL	NULL	gw60_science_286_5442_1180_s_42	10550060	A fusion protein encompassing the 27 COOH-terminal amino acids of mGluR 7A (C27; see  Fig. 1A) failed to bind calmodulin, but fusion constructs N38 and N25 containing the common NH2-terminal fragments ( Fig. 1A) both bound calmodulin ( 12).	bind
38037	3	10344	6	NULL	NULL	0	NULL	mGluR 7A	NULL		forms	NULL		NH2-terminal fragments		N38 fusion protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_286_5442_1180_s_42	10550060	A fusion protein encompassing the 27 COOH-terminal amino acids of mGluR 7A (C27; see  Fig. 1A) failed to bind calmodulin, but fusion constructs N38 and N25 containing the common NH2-terminal fragments ( Fig. 1A) both bound calmodulin ( 12).	bind
38038	4	10344	6	NULL	NULL	0	NULL	statement 3	NULL		bind	NULL				calmodulin	NULL				NULL		0	NULL	NULL	NULL	gw60_science_286_5442_1180_s_42	10550060	A fusion protein encompassing the 27 COOH-terminal amino acids of mGluR 7A (C27; see  Fig. 1A) failed to bind calmodulin, but fusion constructs N38 and N25 containing the common NH2-terminal fragments ( Fig. 1A) both bound calmodulin ( 12).	bind
38039	5	10344	6	NULL	NULL	0	NULL	mGluR 7A	NULL		forms	NULL		NH2-terminal fragments		N25 fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_science_286_5442_1180_s_42	10550060	A fusion protein encompassing the 27 COOH-terminal amino acids of mGluR 7A (C27; see  Fig. 1A) failed to bind calmodulin, but fusion constructs N38 and N25 containing the common NH2-terminal fragments ( Fig. 1A) both bound calmodulin ( 12).	bind
38040	6	10344	6	NULL	NULL	0	NULL	statement 5	NULL		bind	NULL				calmodulin	NULL				NULL		0	NULL	NULL	NULL	gw60_science_286_5442_1180_s_42	10550060	A fusion protein encompassing the 27 COOH-terminal amino acids of mGluR 7A (C27; see  Fig. 1A) failed to bind calmodulin, but fusion constructs N38 and N25 containing the common NH2-terminal fragments ( Fig. 1A) both bound calmodulin ( 12).	bind
44180	1	10345	5	11	NULL	NULL	NULL	fusion protein	GP		is formed by							chromosomal translocation of		t(2;13)	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_20_11719_s_104	7744814	A fusion protein formed by the t(2;13) chromosomal  translocation resulting in alveolar rhabdomyosarcoma shares DNA binding  properties with Pax3, since it includes the intact Pax3 paired and  homeodomains.	bind
44181	2	10345	5	11	NULL	NULL	NULL			chromosomal translocation of	results in				t(2;13)	alveolar rhabdomyosarcoma	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_20_11719_s_104	7744814	A fusion protein formed by the t(2;13) chromosomal  translocation resulting in alveolar rhabdomyosarcoma shares DNA binding  properties with Pax3, since it includes the intact Pax3 paired and  homeodomains.	bind
44193	3	10345	5	11	NULL	NULL	NULL	PAX3	GP		exhibits					DNA binding activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_20_11719_s_104	7744814	A fusion protein formed by the t(2;13) chromosomal  translocation resulting in alveolar rhabdomyosarcoma shares DNA binding  properties with Pax3, since it includes the intact Pax3 paired and  homeodomains.	bind
44194	4	10345	5	11	NULL	NULL	NULL	statement 1	Process		shares					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_20_11719_s_104	7744814	A fusion protein formed by the t(2;13) chromosomal  translocation resulting in alveolar rhabdomyosarcoma shares DNA binding  properties with Pax3, since it includes the intact Pax3 paired and  homeodomains.	bind
44195	5	10345	5	11	NULL	NULL	NULL	statement 1	Process		includes					Pax3	GP		paired;;homeodomain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_20_11719_s_104	7744814	A fusion protein formed by the t(2;13) chromosomal  translocation resulting in alveolar rhabdomyosarcoma shares DNA binding  properties with Pax3, since it includes the intact Pax3 paired and  homeodomains.	bind
38045	1	10345	6	10	NULL	0	NULL		NULL	chromosomal translocation of	results in	NULL			t(2;13) 	alveolar rhabdomyosarcoma	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_20_11719_s_104	7744814	A fusion protein formed by the t(2;13) chromosomal  translocation resulting in alveolar rhabdomyosarcoma shares DNA binding  properties with Pax3, since it includes the intact Pax3 paired and  homeodomains.	bind
38046	2	10345	6	10	NULL	0	NULL		NULL	chromosomal translocation of	forms	NULL			t(2;13) 	fusion protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_20_11719_s_104	7744814	A fusion protein formed by the t(2;13) chromosomal  translocation resulting in alveolar rhabdomyosarcoma shares DNA binding  properties with Pax3, since it includes the intact Pax3 paired and  homeodomains.	bind
38047	3	10345	6	10	NULL	0	NULL	statement 2			includes					Pax3			paired;;homeodomains		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_20_11719_s_104	7744814	A fusion protein formed by the t(2;13) chromosomal  translocation resulting in alveolar rhabdomyosarcoma shares DNA binding  properties with Pax3, since it includes the intact Pax3 paired and  homeodomains.	bind
38048	4	10345	6	NULL	NULL	0	NULL	Pax3	NULL		exhibits	NULL				DNA binding activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_20_11719_s_104	7744814	A fusion protein formed by the t(2;13) chromosomal  translocation resulting in alveolar rhabdomyosarcoma shares DNA binding  properties with Pax3, since it includes the intact Pax3 paired and  homeodomains.	bind
38049	5	10345	6	NULL	NULL	0	NULL	statement 2	NULL		shares	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_20_11719_s_104	7744814	A fusion protein formed by the t(2;13) chromosomal  translocation resulting in alveolar rhabdomyosarcoma shares DNA binding  properties with Pax3, since it includes the intact Pax3 paired and  homeodomains.	bind
43938	1	10346	5	11	NULL	NULL	NULL	pCS7299	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7293_s_194	11705900	A fusion protein lacking the last 94 amino acids of EibA (pCS7299) failed to bind IgG Fc (Fig.  5A, lane 5) and failed to form large bands, appearing instead as a monomer-sized band recognized by anti-MBP (Fig.  5B, lane 5).	bind
43939	2	10346	5	11	NULL	NULL	NULL	pCS7299	GP		lacks					EibA	GP		last 94 amino acids of		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7293_s_194	11705900	A fusion protein lacking the last 94 amino acids of EibA (pCS7299) failed to bind IgG Fc (Fig.  5A, lane 5) and failed to form large bands, appearing instead as a monomer-sized band recognized by anti-MBP (Fig.  5B, lane 5).	bind
43940	3	10346	5	11	NULL	NULL	NULL	pCS7299	GP		does not bind					IgG Fc	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7293_s_194	11705900	A fusion protein lacking the last 94 amino acids of EibA (pCS7299) failed to bind IgG Fc (Fig.  5A, lane 5) and failed to form large bands, appearing instead as a monomer-sized band recognized by anti-MBP (Fig.  5B, lane 5).	bind
38050	1	10346	6	NULL	NULL	0	NULL	pCS7299	NULL		is a 	NULL				fusion protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7293_s_194	11705900	A fusion protein lacking the last 94 amino acids of EibA (pCS7299) failed to bind IgG Fc (Fig.  5A, lane 5) and failed to form large bands, appearing instead as a monomer-sized band recognized by anti-MBP (Fig.  5B, lane 5).	bind
38051	2	10346	6	NULL	NULL	0	NULL	statement 1	NULL		does not bind	NULL				IgG Fc	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7293_s_194	11705900	A fusion protein lacking the last 94 amino acids of EibA (pCS7299) failed to bind IgG Fc (Fig.  5A, lane 5) and failed to form large bands, appearing instead as a monomer-sized band recognized by anti-MBP (Fig.  5B, lane 5).	bind
38897	3	10346	6	NULL	NULL	0	NULL	pCS7299	NULL		lacks	NULL				EibA	NULL		last 94 amino acids of		NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7293_s_194	11705900	A fusion protein lacking the last 94 amino acids of EibA (pCS7299) failed to bind IgG Fc (Fig.  5A, lane 5) and failed to form large bands, appearing instead as a monomer-sized band recognized by anti-MBP (Fig.  5B, lane 5).	bind
43980	1	10347	5	11	NULL	NULL	NULL	alpha-catenin	GP		forms fusion protein with			beta-catenin-binding domain		formin-1	GP		actin polymerization domain		NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_nat-cell-biol_6_1_14647292_s_6	14647292	A fusion protein of the beta-catenin-binding  domain of alpha-catenin with the actin polymerization domains of formin-1  rescues formation of adherens junctions and associated actin cables in  alpha-catenin-null keratinocytes.	bind
43982	2	10347	5	11	NULL	NULL	NULL	statement 1	Process		rescues					adherens junctions	Cell	formation of			NULL	alpha-catenin-null keratinocytes	NULL	NULL	NULL	NULL	abs-batch0680-0699_nat-cell-biol_6_1_14647292_s_6	14647292	A fusion protein of the beta-catenin-binding  domain of alpha-catenin with the actin polymerization domains of formin-1  rescues formation of adherens junctions and associated actin cables in  alpha-catenin-null keratinocytes.	bind
43984	3	10347	5	11	NULL	NULL	NULL	statement 1	Process		rescues					actin cables	CellComponent	associated			NULL	alpha-catenin-null keratinocytes	NULL	NULL	NULL	NULL	abs-batch0680-0699_nat-cell-biol_6_1_14647292_s_6	14647292	A fusion protein of the beta-catenin-binding  domain of alpha-catenin with the actin polymerization domains of formin-1  rescues formation of adherens junctions and associated actin cables in  alpha-catenin-null keratinocytes.	bind
38052	1	10347	6	NULL	NULL	0	NULL	alpha-catenin	NULL		forms fusion protein with	NULL		beta-catenin-binding domain		formin-1	NULL		actin polymerization domain		NULL		0	NULL	NULL	NULL	abs-batch0680-0699_nat-cell-biol_6_1_14647292_s_6	14647292	A fusion protein of the beta-catenin-binding  domain of alpha-catenin with the actin polymerization domains of formin-1  rescues formation of adherens junctions and associated actin cables in  alpha-catenin-null keratinocytes.	bind
38053	2	10347	6	NULL	NULL	0	NULL	statement 1	NULL		rescues	NULL				adherens junctions	NULL	formation of			NULL	alpha-catenin-null keratinocytes	NULL	NULL	NULL	NULL	abs-batch0680-0699_nat-cell-biol_6_1_14647292_s_6	14647292	A fusion protein of the beta-catenin-binding  domain of alpha-catenin with the actin polymerization domains of formin-1  rescues formation of adherens junctions and associated actin cables in  alpha-catenin-null keratinocytes.	bind
38054	3	10347	6	NULL	NULL	0	NULL	statement 1	NULL		rescues	NULL				associated actin cables	NULL	formation of			NULL	alpha-catenin-null keratinocytes	0	NULL	NULL	NULL	abs-batch0680-0699_nat-cell-biol_6_1_14647292_s_6	14647292	A fusion protein of the beta-catenin-binding  domain of alpha-catenin with the actin polymerization domains of formin-1  rescues formation of adherens junctions and associated actin cables in  alpha-catenin-null keratinocytes.	bind
43986	1	10348	5	11	NULL	NULL	NULL	Nx1alpha-1	GP		is					neurexin Ialpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34716_s_171	9856994	A fusion protein of the entire extracellular sequence of neurexin Ialpha (Nx1alpha-1) efficiently bound neurexophilin 1 with enrichment of the processed form (Fig.  3, compare  lanes 3 and  4).	bind
43988	2	10348	5	11	NULL	NULL	NULL	Nx1alpha-1	GP		bind		efficiently	extracellular sequence		neurexophilin 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34716_s_171	9856994	A fusion protein of the entire extracellular sequence of neurexin Ialpha (Nx1alpha-1) efficiently bound neurexophilin 1 with enrichment of the processed form (Fig.  3, compare  lanes 3 and  4).	bind
37548	1	10348	6	NULL	NULL	0	NULL	neurexin Ialpha 	NULL		bind	NULL	efficiently	extracellular sequence		neurexophilin 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34716_s_171	9856994	A fusion protein of the entire extracellular sequence of neurexin Ialpha (Nx1alpha-1) efficiently bound neurexophilin 1 with enrichment of the processed form (Fig.  3, compare  lanes 3 and  4).	bind
37549	2	10348	6	NULL	NULL	0	NULL	Nx1alpha-1	NULL		is	NULL				neurexin Ialpha	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34716_s_171	9856994	A fusion protein of the entire extracellular sequence of neurexin Ialpha (Nx1alpha-1) efficiently bound neurexophilin 1 with enrichment of the processed form (Fig.  3, compare  lanes 3 and  4).	bind
37550	1	10349	6	NULL	NULL	0	NULL		NULL		forms fusion protein with	NULL		N-terminal domain		thioredoxin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_52_52315_s_6	14530265	A fusion protein of the N-terminal domain and thioredoxin binds tightly to MTs at low salt, consistent with the increased affinity of motor domain constructs (which contain the N-terminal domain) being due to the additional binding of the N-terminal domain to the microtubule.	bind
37551	2	10349	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL	tightly			MT	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_52_52315_s_6	14530265	A fusion protein of the N-terminal domain and thioredoxin binds tightly to MTs at low salt, consistent with the increased affinity of motor domain constructs (which contain the N-terminal domain) being due to the additional binding of the N-terminal domain to the microtubule.	bind
37552	3	10349	6	NULL	NULL	0	NULL		NULL		bind	NULL		N-terminal domain		microtubule	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_52_52315_s_6	14530265	A fusion protein of the N-terminal domain and thioredoxin binds tightly to MTs at low salt, consistent with the increased affinity of motor domain constructs (which contain the N-terminal domain) being due to the additional binding of the N-terminal domain to the microtubule.	bind
43989	1	10351	5	11	NULL	NULL	NULL	Man-R	GP		is replaced with			transmembrane domain		IgG1	GP	human	constant region		NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_5_2089_s_15	9482843	A fusion protein produced by replacing the transmembrane domain of the Man-R with the constant region of human IgG1 also binds both S4GGnM-BSA and Man-BSA.	bind
43990	2	10351	5	11	NULL	NULL	NULL	statement 1	Process		forms					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_5_2089_s_15	9482843	A fusion protein produced by replacing the transmembrane domain of the Man-R with the constant region of human IgG1 also binds both S4GGnM-BSA and Man-BSA.	bind
43991	3	10351	5	11	NULL	NULL	NULL	statement 2	GP		bind					S4GGnM-BSA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_5_2089_s_15	9482843	A fusion protein produced by replacing the transmembrane domain of the Man-R with the constant region of human IgG1 also binds both S4GGnM-BSA and Man-BSA.	bind
43992	4	10351	5	11	NULL	NULL	NULL	statement 2	GP		bind					Man-BSA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_5_2089_s_15	9482843	A fusion protein produced by replacing the transmembrane domain of the Man-R with the constant region of human IgG1 also binds both S4GGnM-BSA and Man-BSA.	bind
38055	1	10351	6	NULL	NULL	0	NULL	Man-R	NULL		is replaced by	NULL		transmembrane domain		IgG1	NULL	human	constant region		NULL		0	NULL	NULL	NULL	gw60_pnas_95_5_2089_s_15	9482843	A fusion protein produced by replacing the transmembrane domain of the Man-R with the constant region of human IgG1 also binds both S4GGnM-BSA and Man-BSA.	bind
38056	2	10351	6	NULL	NULL	0	NULL	statement 1	NULL		forms a 	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_5_2089_s_15	9482843	A fusion protein produced by replacing the transmembrane domain of the Man-R with the constant region of human IgG1 also binds both S4GGnM-BSA and Man-BSA.	bind
38057	3	10351	6	NULL	NULL	0	NULL	statement 2	NULL		bind	NULL				S4GGnM-BSA	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_5_2089_s_15	9482843	A fusion protein produced by replacing the transmembrane domain of the Man-R with the constant region of human IgG1 also binds both S4GGnM-BSA and Man-BSA.	bind
38058	4	10351	6	NULL	NULL	0	NULL	statement 2	NULL		bind	NULL				Man-BSA	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_5_2089_s_15	9482843	A fusion protein produced by replacing the transmembrane domain of the Man-R with the constant region of human IgG1 also binds both S4GGnM-BSA and Man-BSA.	bind
43993	1	10352	5	11	NULL	NULL	NULL	CaM	GP		bind					KCNQ2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_22_18_7991_s_247	12223552	A fusion protein that decreases CaM binding to KCNQ2 reduces channel activity	bind
37555	1	10352	6	NULL	NULL	0	NULL	CaM	NULL		bind	NULL				KCNQ2	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_22_18_7991_s_247	12223552	A fusion protein that decreases CaM binding to KCNQ2 reduces channel activity	bind
43996	1	10353	5	11	NULL	NULL	NULL	pDC2252	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7293_s_193	11705900	A fusion protein which retained only the last 92 amino acids of EibA (pDC2252) failed to bind IgG Fc (Fig.  5A, lane 4) but was still able to form bands larger than 200 kDa (recognized by anti-MBP) (Fig.  5B, lane 4).	bind
43997	2	10353	5	11	NULL	NULL	NULL	pDC2252	GP		retains					EibA	GP		last 92 amino acids of		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7293_s_193	11705900	A fusion protein which retained only the last 92 amino acids of EibA (pDC2252) failed to bind IgG Fc (Fig.  5A, lane 4) but was still able to form bands larger than 200 kDa (recognized by anti-MBP) (Fig.  5B, lane 4).	bind
43998	3	10353	5	11	NULL	NULL	NULL	pDC2252	GP		does not bind					IgG Fc	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7293_s_193	11705900	A fusion protein which retained only the last 92 amino acids of EibA (pDC2252) failed to bind IgG Fc (Fig.  5A, lane 4) but was still able to form bands larger than 200 kDa (recognized by anti-MBP) (Fig.  5B, lane 4).	bind
38059	1	10353	6	10	NULL	0	NULL	pDC2252	NULL		retains	NULL				EibA	NULL		last 92 amino acids of		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_12_7293_s_193	11705900	A fusion protein which retained only the last 92 amino acids of EibA (pDC2252) failed to bind IgG Fc (Fig.  5A, lane 4) but was still able to form bands larger than 200 kDa (recognized by anti-MBP) (Fig.  5B, lane 4).	bind
38060	2	10353	6	NULL	NULL	0	NULL	statement 1	NULL		does not bind	NULL				IgG Fc	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7293_s_193	11705900	A fusion protein which retained only the last 92 amino acids of EibA (pDC2252) failed to bind IgG Fc (Fig.  5A, lane 4) but was still able to form bands larger than 200 kDa (recognized by anti-MBP) (Fig.  5B, lane 4).	bind
57498	3	10353	6	10	NULL	0	NULL	pDC2252			is a type of					fusion protein					NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7293_s_193	11705900	A fusion protein which retained only the last 92 amino acids of EibA (pDC2252) failed to bind IgG Fc (Fig.  5A, lane 4) but was still able to form bands larger than 200 kDa (recognized by anti-MBP) (Fig.  5B, lane 4).	bind
43999	1	10354	5	11	NULL	NULL	NULL	amino-terminal domain	AminoAcid		is					ALCAM V2CCC Rg	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_29_17390_s_164	8663238	A fusion protein without the amino-terminal domain (ALCAM V2CCC Rg) bound very weakly to CD6 in an ELISA (Fig.  3 B), but binding to CD6 expressing cells was not detectable.	bind
44000	2	10354	5	11	NULL	NULL	NULL	fusion protein	GP	lacking	bind		weakly	amino terminal domain		CD6	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_29_17390_s_164	8663238	A fusion protein without the amino-terminal domain (ALCAM V2CCC Rg) bound very weakly to CD6 in an ELISA (Fig.  3 B), but binding to CD6 expressing cells was not detectable.	bind
38061	1	10354	6	NULL	NULL	0	NULL	fusion protein	NULL	lacking	bind	NULL	very weakly	amino-terminal domain		CD6	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_29_17390_s_164	8663238	A fusion protein without the amino-terminal domain (ALCAM V2CCC Rg) bound very weakly to CD6 in an ELISA (Fig.  3 B), but binding to CD6 expressing cells was not detectable.	bind
38062	2	10354	6	NULL	NULL	0	NULL	amino-terminal domain	NULL		is	NULL				ALCAM V2CCC Rg	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_29_17390_s_164	8663238	A fusion protein without the amino-terminal domain (ALCAM V2CCC Rg) bound very weakly to CD6 in an ELISA (Fig.  3 B), but binding to CD6 expressing cells was not detectable.	bind
44008	1	10359	5	11	NULL	NULL	NULL	RGS11	GP		bind			G protein gamma subunit-like domain					Gbeta5 subunits		NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_46_0_151_s_1125	16402902	A G protein  gamma subunit-like domain shared between RGS11 and other RGS proteins specifies binding  to Gbeta5 subunits.	bind
48712	2	10359	5	11	NULL	NULL	NULL	RGS proteins	GP		bind			G protein gamma subunit-like domain					Gbeta5 subunit		NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_46_0_151_s_1125	16402902	A G protein  gamma subunit-like domain shared between RGS11 and other RGS proteins specifies binding  to Gbeta5 subunits.	bind
38063	1	10359	6	10	NULL	0	NULL	RGS11 			bind			G protein gamma subunit-like domain					Gbeta5 subunit		NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_46_0_151_s_1125	16402902	A G protein  gamma subunit-like domain shared between RGS11 and other RGS proteins specifies binding  to Gbeta5 subunits.	bind
48713	2	10359	6	10	NULL	0	NULL	RGS proteins			bind			G protein gamma subunit-like domain					Gbeta5 subunit		NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_46_0_151_s_1125	16402902	A G protein  gamma subunit-like domain shared between RGS11 and other RGS proteins specifies binding  to Gbeta5 subunits.	bind
44011	1	10360	5	11	NULL	NULL	NULL	GTP	Chemical		bind					G protein	GP		alpha subunit		NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_5_1947_s_14	10051575	A G protein becomes activated upon the receptor-stimulated binding of GTP to its alpha subunit and continues to modulate the activity of the effector until bound GTP is hydrolyzed (reviewed in refs.	bind
44013	2	10360	5	11	NULL	NULL	NULL	receptor	GP		stimulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_5_1947_s_14	10051575	A G protein becomes activated upon the receptor-stimulated binding of GTP to its alpha subunit and continues to modulate the activity of the effector until bound GTP is hydrolyzed (reviewed in refs.	bind
44014	3	10360	5	11	NULL	NULL	NULL	statement 1	Process		activates					G protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_5_1947_s_14	10051575	A G protein becomes activated upon the receptor-stimulated binding of GTP to its alpha subunit and continues to modulate the activity of the effector until bound GTP is hydrolyzed (reviewed in refs.	bind
44015	4	10360	5	11	NULL	NULL	NULL	statement 3	Process		modulates					effector	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_5_1947_s_14	10051575	A G protein becomes activated upon the receptor-stimulated binding of GTP to its alpha subunit and continues to modulate the activity of the effector until bound GTP is hydrolyzed (reviewed in refs.	bind
44017	5	10360	5	11	NULL	NULL	NULL	statement 4	Process		occurs until					statement 1	Process	hydrolysis of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_5_1947_s_14	10051575	A G protein becomes activated upon the receptor-stimulated binding of GTP to its alpha subunit and continues to modulate the activity of the effector until bound GTP is hydrolyzed (reviewed in refs.	bind
38064	1	10360	6	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				G protein	NULL		alpha subunit		NULL		0	NULL	NULL	NULL	gw60_pnas_96_5_1947_s_14	10051575	A G protein becomes activated upon the receptor-stimulated binding of GTP to its alpha subunit and continues to modulate the activity of the effector until bound GTP is hydrolyzed (reviewed in refs.	bind
38065	2	10360	6	NULL	NULL	0	NULL	statement 1	NULL		is stimulated by	NULL				receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_5_1947_s_14	10051575	A G protein becomes activated upon the receptor-stimulated binding of GTP to its alpha subunit and continues to modulate the activity of the effector until bound GTP is hydrolyzed (reviewed in refs.	bind
38066	3	10360	6	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				G protein	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_5_1947_s_14	10051575	A G protein becomes activated upon the receptor-stimulated binding of GTP to its alpha subunit and continues to modulate the activity of the effector until bound GTP is hydrolyzed (reviewed in refs.	bind
38142	4	10360	6	NULL	NULL	0	NULL	G protein	NULL		modulates	NULL				effector	NULL	activity of 			NULL		0	NULL	NULL	NULL	gw60_pnas_96_5_1947_s_14	10051575	A G protein becomes activated upon the receptor-stimulated binding of GTP to its alpha subunit and continues to modulate the activity of the effector until bound GTP is hydrolyzed (reviewed in refs.	bind
38143	5	10360	6	NULL	NULL	0	NULL	statement 4	NULL		occurs until	NULL				statement 1	NULL	hydrolysis of			NULL		0	NULL	NULL	NULL	gw60_pnas_96_5_1947_s_14	10051575	A G protein becomes activated upon the receptor-stimulated binding of GTP to its alpha subunit and continues to modulate the activity of the effector until bound GTP is hydrolyzed (reviewed in refs.	bind
44171	1	10364	5	11	NULL	NULL	NULL	G protein	GP		uses					GTP	Chemical	binding energy of			NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_66_0_639_s_288	9242920	A G protein uses the binding energy of GTP to stabilize the switch regions to produce  a conformation that permits its association with effector.	bind
44172	2	10364	5	11	NULL	NULL	NULL	statement 1	GP		stabilize									switch regions	NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_66_0_639_s_288	9242920	A G protein uses the binding energy of GTP to stabilize the switch regions to produce  a conformation that permits its association with effector.	bind
44174	3	10364	5	11	NULL	NULL	NULL	G protein	GP		associate with					effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_66_0_639_s_288	9242920	A G protein uses the binding energy of GTP to stabilize the switch regions to produce  a conformation that permits its association with effector.	bind
38067	1	10364	6	NULL	NULL	0	NULL	G protein	NULL		associates with	NULL				effector	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_66_0_639_s_288	9242920	A G protein uses the binding energy of GTP to stabilize the switch regions to produce  a conformation that permits its association with effector.	bind
38130	2	10364	6	NULL	NULL	0	NULL	statement 1	NULL		uses	NULL				GTP	NULL	binding energy of 			NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_66_0_639_s_288	9242920	A G protein uses the binding energy of GTP to stabilize the switch regions to produce  a conformation that permits its association with effector.	bind
44068	1	10365	5	11	NULL	NULL	NULL	ss telomeric DNA	NucleicAcid		bind					POT1a N	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_21_5180_s_87	17053789	A G to C substitution at position 10 of the telomeric substrate abolished ss telomeric  DNA binding to both POT1a N and POT1b N, supporting previous results indicating that  this 3' terminal G10 residue is of critical importance for human POT1 binding  to telomeres (  et al).	bind
44069	2	10365	5	11	NULL	NULL	NULL	ss telomeric DNA	NucleicAcid		bind					POT1b N	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_21_5180_s_87	17053789	A G to C substitution at position 10 of the telomeric substrate abolished ss telomeric  DNA binding to both POT1a N and POT1b N, supporting previous results indicating that  this 3' terminal G10 residue is of critical importance for human POT1 binding  to telomeres (  et al).	bind
44070	3	10365	5	11	NULL	NULL	NULL	telomeric substrate	GP		is substituted to			G10		telomeric substrate	GP		C		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_21_5180_s_87	17053789	A G to C substitution at position 10 of the telomeric substrate abolished ss telomeric  DNA binding to both POT1a N and POT1b N, supporting previous results indicating that  this 3' terminal G10 residue is of critical importance for human POT1 binding  to telomeres (  et al).	bind
44071	4	10365	5	11	NULL	NULL	NULL	statement 3	Process		abolishes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_21_5180_s_87	17053789	A G to C substitution at position 10 of the telomeric substrate abolished ss telomeric  DNA binding to both POT1a N and POT1b N, supporting previous results indicating that  this 3' terminal G10 residue is of critical importance for human POT1 binding  to telomeres (  et al).	bind
44072	5	10365	5	11	NULL	NULL	NULL	statement 3	Process		abolishes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_21_5180_s_87	17053789	A G to C substitution at position 10 of the telomeric substrate abolished ss telomeric  DNA binding to both POT1a N and POT1b N, supporting previous results indicating that  this 3' terminal G10 residue is of critical importance for human POT1 binding  to telomeres (  et al).	bind
44074	6	10365	5	11	NULL	NULL	NULL	POT1	GP	human	bind					telomeres	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_21_5180_s_87	17053789	A G to C substitution at position 10 of the telomeric substrate abolished ss telomeric  DNA binding to both POT1a N and POT1b N, supporting previous results indicating that  this 3' terminal G10 residue is of critical importance for human POT1 binding  to telomeres (  et al).	bind
44075	7	10365	5	11	NULL	NULL	NULL	POT1	GP	human	is important for		critical	3' terminal G10 residue		statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_21_5180_s_87	17053789	A G to C substitution at position 10 of the telomeric substrate abolished ss telomeric  DNA binding to both POT1a N and POT1b N, supporting previous results indicating that  this 3' terminal G10 residue is of critical importance for human POT1 binding  to telomeres (  et al).	bind
38131	1	10365	6	NULL	NULL	0	NULL	ss telomeric DNA	NULL		bind	NULL				POT1a	NULL		N terminus		NULL		0	NULL	NULL	NULL	gw70_embo_25_21_5180_s_87	17053789	A G to C substitution at position 10 of the telomeric substrate abolished ss telomeric  DNA binding to both POT1a N and POT1b N, supporting previous results indicating that  this 3' terminal G10 residue is of critical importance for human POT1 binding  to telomeres (  et al).	bind
38132	2	10365	6	NULL	NULL	0	NULL	ss telomeric DNA	NULL		bind	NULL				POT1b	NULL		N terminus		NULL		0	NULL	NULL	NULL	gw70_embo_25_21_5180_s_87	17053789	A G to C substitution at position 10 of the telomeric substrate abolished ss telomeric  DNA binding to both POT1a N and POT1b N, supporting previous results indicating that  this 3' terminal G10 residue is of critical importance for human POT1 binding  to telomeres (  et al).	bind
38133	3	10365	6	NULL	NULL	0	NULL	telomeric substrate	NULL		is substituted by	NULL		G10 residue		telomeric substrate	NULL		C10 residue		NULL		0	NULL	NULL	NULL	gw70_embo_25_21_5180_s_87	17053789	A G to C substitution at position 10 of the telomeric substrate abolished ss telomeric  DNA binding to both POT1a N and POT1b N, supporting previous results indicating that  this 3' terminal G10 residue is of critical importance for human POT1 binding  to telomeres (  et al).	bind
38134	4	10365	6	NULL	NULL	0	NULL	statement 3	NULL		abolishes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_25_21_5180_s_87	17053789	A G to C substitution at position 10 of the telomeric substrate abolished ss telomeric  DNA binding to both POT1a N and POT1b N, supporting previous results indicating that  this 3' terminal G10 residue is of critical importance for human POT1 binding  to telomeres (  et al).	bind
38135	5	10365	6	NULL	NULL	0	NULL	statement 3	NULL		abolishes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_25_21_5180_s_87	17053789	A G to C substitution at position 10 of the telomeric substrate abolished ss telomeric  DNA binding to both POT1a N and POT1b N, supporting previous results indicating that  this 3' terminal G10 residue is of critical importance for human POT1 binding  to telomeres (  et al).	bind
57499	6	10365	6	10	NULL	0	NULL	POT1		human	bind					telomeres					NULL		0	NULL	NULL	NULL	gw70_embo_25_21_5180_s_87	17053789	A G to C substitution at position 10 of the telomeric substrate abolished ss telomeric  DNA binding to both POT1a N and POT1b N, supporting previous results indicating that  this 3' terminal G10 residue is of critical importance for human POT1 binding  to telomeres (  et al).	bind
57500	7	10365	6	10	NULL	0	NULL	POT1		human	is important for		critical	3' terminal G10 residue		statement 6					NULL		0	NULL	NULL	NULL	gw70_embo_25_21_5180_s_87	17053789	A G to C substitution at position 10 of the telomeric substrate abolished ss telomeric  DNA binding to both POT1a N and POT1b N, supporting previous results indicating that  this 3' terminal G10 residue is of critical importance for human POT1 binding  to telomeres (  et al).	bind
44066	1	10366	5	11	NULL	NULL	NULL	U11	GP		bind									NRS	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_37_38201_s_133	15252020	A G-rich Downstream Element Promotes U11 Binding to the NRS --	bind
44067	2	10366	5	11	NULL	NULL	NULL				promotes				G-rich downstream element	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_37_38201_s_133	15252020	A G-rich Downstream Element Promotes U11 Binding to the NRS --	bind
38136	1	10366	6	10	NULL	0	NULL	U11			bind									NRS	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_37_38201_s_133	15252020	A G-rich Downstream Element Promotes U11 Binding to the NRS --	bind
38137	2	10366	6	NULL	NULL	0	NULL		NULL		promotes	NULL			G-rich downstream element	statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_37_38201_s_133	15252020	A G-rich Downstream Element Promotes U11 Binding to the NRS --	bind
44032	1	10368	5	11	NULL	NULL	NULL	EFTu ternary-complex	GP		bind					ribosome	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_3_460_s_612	12209000	A G-to-A mutation at base 530 reduced EFTu ternary-complex binding to the ribosome ( 156).	bind
44034	2	10368	5	11	NULL	NULL	NULL	EFTu ternary-complex	GP	mutant	reduces			G-to-A at base 530		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_3_460_s_612	12209000	A G-to-A mutation at base 530 reduced EFTu ternary-complex binding to the ribosome ( 156).	bind
38138	1	10368	6	NULL	NULL	0	NULL	EFTu ternary-complex	NULL		bind	NULL				ribosome	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_3_460_s_612	12209000	A G-to-A mutation at base 530 reduced EFTu ternary-complex binding to the ribosome ( 156).	bind
38139	2	10368	6	NULL	NULL	0	NULL		NULL	mutant	reduces	NULL		G to A		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_3_460_s_612	12209000	A G-to-A mutation at base 530 reduced EFTu ternary-complex binding to the ribosome ( 156).	bind
44063	1	10369	5	11	NULL	NULL	NULL	trans-acting factor(s)	GP	G0 growth arrest-specific	bind					C/EBP mRNA	NucleicAcid			3''-UTR	NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_304_2_344_s_61	12711321	A G0 growth arrest-specific trans-acting factor(s) binds the C/EBP  mRNA 3''-UTR.	bind
38140	1	10369	6	10	NULL	0	NULL	trans-acting factor	NULL	G0 growth arrest-specific	bind	NULL				C/EBP mRNA	NULL			3''-UTR	NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_304_2_344_s_61	12711321	A G0 growth arrest-specific trans-acting factor(s) binds the C/EBP  mRNA 3''-UTR.	bind
44064	1	10370	5	11	NULL	NULL	NULL	G3deltaEGF	GP		is					G3 construct lacking EGF-like motifs	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_14178_s_27	11297534	A G3 construct lacking the EGF-like motifs (G3deltaEGF) binds to the astrocytoma cell surface.	bind
44065	2	10370	5	11	NULL	NULL	NULL	G3deltaEGF	GP		bind					astrocytoma	MedicalFinding	cell surface			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_14178_s_27	11297534	A G3 construct lacking the EGF-like motifs (G3deltaEGF) binds to the astrocytoma cell surface.	bind
37557	1	10370	6	10	NULL	0	NULL	G3deltaEGF	NULL		is	NULL				G3 construct lacking the EGF-like motifs	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_14178_s_27	11297534	A G3 construct lacking the EGF-like motifs (G3deltaEGF) binds to the astrocytoma cell surface.	bind
37558	2	10370	6	10	NULL	0	NULL	G3deltaEGF	NULL		bind	NULL				astrocytoma	NULL	cell surface			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_14178_s_27	11297534	A G3 construct lacking the EGF-like motifs (G3deltaEGF) binds to the astrocytoma cell surface.	bind
44077	1	10372	5	11	NULL	NULL	NULL	GATA-4	GP	deletion mutant	lacks			carboxyl-terminal					ZF1		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_8_5760_s_213	12480945	A GATA-4 carboxyl-terminal deletion mutant lacking the ZF1 and ZF2 regions did not bind RXR (Fig.  5 B).	bind
44079	2	10372	5	11	NULL	NULL	NULL	GATA-4	GP	deletion mutant	lacks			carboxyl-terminal					ZF2		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_8_5760_s_213	12480945	A GATA-4 carboxyl-terminal deletion mutant lacking the ZF1 and ZF2 regions did not bind RXR (Fig.  5 B).	bind
44080	3	10372	5	11	NULL	NULL	NULL	statement 1	GP		does not bind					RXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_8_5760_s_213	12480945	A GATA-4 carboxyl-terminal deletion mutant lacking the ZF1 and ZF2 regions did not bind RXR (Fig.  5 B).	bind
44082	4	10372	5	11	NULL	NULL	NULL	statement 2	GP		does not bind					RXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_8_5760_s_213	12480945	A GATA-4 carboxyl-terminal deletion mutant lacking the ZF1 and ZF2 regions did not bind RXR (Fig.  5 B).	bind
37559	1	10372	6	NULL	NULL	0	NULL	GATA-4	NULL	deletion mutant	lacks	NULL		carboxy terminal			NULL		ZF1 region		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_8_5760_s_213	12480945	A GATA-4 carboxyl-terminal deletion mutant lacking the ZF1 and ZF2 regions did not bind RXR (Fig.  5 B).	bind
37560	2	10372	6	NULL	NULL	0	NULL	GATA-4	NULL	deletion mutant	lacks	NULL		carboxyl-terminal			NULL		ZF2 region		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_8_5760_s_213	12480945	A GATA-4 carboxyl-terminal deletion mutant lacking the ZF1 and ZF2 regions did not bind RXR (Fig.  5 B).	bind
37561	3	10372	6	NULL	NULL	0	NULL	statement 1	NULL		does not bind	NULL				RXR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_8_5760_s_213	12480945	A GATA-4 carboxyl-terminal deletion mutant lacking the ZF1 and ZF2 regions did not bind RXR (Fig.  5 B).	bind
37562	4	10372	6	NULL	NULL	0	NULL	statement 2	NULL		does not bind	NULL				RXR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_8_5760_s_213	12480945	A GATA-4 carboxyl-terminal deletion mutant lacking the ZF1 and ZF2 regions did not bind RXR (Fig.  5 B).	bind
44083	1	10373	5	11	NULL	NULL	NULL	TFIIB	GP		bind					TBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_9_6260_s_23	11096089	A GC-rich sequence upstream from TATA (the BRE) can enhance TFIIB binding to the TBP.	bind
44084	2	10373	5	11	NULL	NULL	NULL	BRE	NucleicAcid		is					GC-rich sequence upstream from TATA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_9_6260_s_23	11096089	A GC-rich sequence upstream from TATA (the BRE) can enhance TFIIB binding to the TBP.	bind
44086	3	10373	5	11	NULL	NULL	NULL	TFIIB	GP		enhance				BRE	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_9_6260_s_23	11096089	A GC-rich sequence upstream from TATA (the BRE) can enhance TFIIB binding to the TBP.	bind
37563	1	10373	6	NULL	NULL	0	NULL	TFIIB	NULL		bind	NULL				TBP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_9_6260_s_23	11096089	A GC-rich sequence upstream from TATA (the BRE) can enhance TFIIB binding to the TBP.	bind
37564	2	10373	6	10	NULL	0	NULL	BRE	NULL		is	NULL				GC-rich sequence upstream from TATA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_9_6260_s_23	11096089	A GC-rich sequence upstream from TATA (the BRE) can enhance TFIIB binding to the TBP.	bind
37565	3	10373	6	10	NULL	0	NULL	TFIIB	NULL		enhance	NULL			BRE	statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_9_6260_s_23	11096089	A GC-rich sequence upstream from TATA (the BRE) can enhance TFIIB binding to the TBP.	bind
44087	1	10375	5	11	NULL	NULL	NULL	tRNA	NucleicAcid		bind								HisRS-like domains		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_16_16514_s_30	15722345	A GCN2 dimer is shown as a pair of  medium gray ribbons with tRNA bound to the HisRS-like domains.	bind
37566	1	10375	6	NULL	NULL	0	NULL	tRNA	NULL		bind	NULL					NULL		HisRS-like domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_16_16514_s_30	15722345	A GCN2 dimer is shown as a pair of  medium gray ribbons with tRNA bound to the HisRS-like domains.	bind
44089	1	10376	5	11	NULL	NULL	NULL	tRNA	NucleicAcid		bind								HisRS-like domains		NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_244	16153175	A Gcn2p dimer is  shown as a pair of blue ribbons with tRNA bound to the HisRS-like domains and activating  the kinase function.	bind
44090	2	10376	5	11	NULL	NULL	NULL	Gcn2p dimer	GP		activates					kinase	GP	function of			NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_244	16153175	A Gcn2p dimer is  shown as a pair of blue ribbons with tRNA bound to the HisRS-like domains and activating  the kinase function.	bind
37567	1	10376	6	NULL	NULL	0	NULL	tRNA	NULL		bind	NULL					NULL		HisRS-like domain		NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_244	16153175	A Gcn2p dimer is  shown as a pair of blue ribbons with tRNA bound to the HisRS-like domains and activating  the kinase function.	bind
37568	2	10376	6	10	NULL	0	NULL	Gcn2p dimer	NULL		activates	NULL				kinase	NULL	function of			NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_59_0_407_s_244	16153175	A Gcn2p dimer is  shown as a pair of blue ribbons with tRNA bound to the HisRS-like domains and activating  the kinase function.	bind
44092	1	10378	5	11	NULL	NULL	NULL	Rab1	GP		bind					GDP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_937_s_509	11739406	A GDP-bound form of Rab1 inhibits protein export from the endoplasmic reticulum and transport between Golgi compartments.	bind
44093	2	10378	5	11	NULL	NULL	NULL	protein	GP		is exported from					endoplasmic reticulum	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_937_s_509	11739406	A GDP-bound form of Rab1 inhibits protein export from the endoplasmic reticulum and transport between Golgi compartments.	bind
44094	3	10378	5	11	NULL	NULL	NULL	protein	GP		is transported between					Golgi compartments	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_937_s_509	11739406	A GDP-bound form of Rab1 inhibits protein export from the endoplasmic reticulum and transport between Golgi compartments.	bind
44095	4	10378	5	11	NULL	NULL	NULL	statement 1	Process		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_937_s_509	11739406	A GDP-bound form of Rab1 inhibits protein export from the endoplasmic reticulum and transport between Golgi compartments.	bind
44097	5	10378	5	11	NULL	NULL	NULL	statement 1	Process		inhibit					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_155_6_937_s_509	11739406	A GDP-bound form of Rab1 inhibits protein export from the endoplasmic reticulum and transport between Golgi compartments.	bind
37569	1	10378	6	NULL	NULL	0	NULL	GDP	NULL		bind	NULL				Rab1	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_6_937_s_509	11739406	A GDP-bound form of Rab1 inhibits protein export from the endoplasmic reticulum and transport between Golgi compartments.	bind
37570	2	10378	6	NULL	NULL	0	NULL	endoplasmic reticulum	NULL		exports	NULL				proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_6_937_s_509	11739406	A GDP-bound form of Rab1 inhibits protein export from the endoplasmic reticulum and transport between Golgi compartments.	bind
37571	3	10378	6	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_6_937_s_509	11739406	A GDP-bound form of Rab1 inhibits protein export from the endoplasmic reticulum and transport between Golgi compartments.	bind
37572	4	10378	6	NULL	NULL	0	NULL	protein	NULL		is transported between	NULL				golgi compartments	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_6_937_s_509	11739406	A GDP-bound form of Rab1 inhibits protein export from the endoplasmic reticulum and transport between Golgi compartments.	bind
37573	5	10378	6	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_6_937_s_509	11739406	A GDP-bound form of Rab1 inhibits protein export from the endoplasmic reticulum and transport between Golgi compartments.	bind
44099	1	10380	5	11	NULL	NULL	NULL	NAC	GP		bind					nac	GP	E. coli		promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_5_1166_s_199	9495755	A gel mobility shift assay (Fig.  5) confirms that NAC binds to the  E. coli nac promoter region, consistent with the argument that the  E. coli nac gene is autogenously regulated, just like that from  K. aerogenes.	bind
44102	2	10380	5	11	NULL	NULL	NULL	nac gene	GP	E. coli	is regulated					autogenously	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_5_1166_s_199	9495755	A gel mobility shift assay (Fig.  5) confirms that NAC binds to the  E. coli nac promoter region, consistent with the argument that the  E. coli nac gene is autogenously regulated, just like that from  K. aerogenes.	bind
44103	3	10380	5	11	NULL	NULL	NULL	nac gene	GP	K. aerogenes	is regulated					autogenously	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_5_1166_s_199	9495755	A gel mobility shift assay (Fig.  5) confirms that NAC binds to the  E. coli nac promoter region, consistent with the argument that the  E. coli nac gene is autogenously regulated, just like that from  K. aerogenes.	bind
37574	1	10380	6	10	NULL	0	NULL	NAC			bind					nac		E.coli		promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_5_1166_s_199	9495755	A gel mobility shift assay (Fig.  5) confirms that NAC binds to the  E. coli nac promoter region, consistent with the argument that the  E. coli nac gene is autogenously regulated, just like that from  K. aerogenes.	bind
37575	2	10380	6	NULL	NULL	0	NULL	statement 1	NULL		confirms	NULL				nac gene	NULL	autogeneous regulation of;; E.coli			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_5_1166_s_199	9495755	A gel mobility shift assay (Fig.  5) confirms that NAC binds to the  E. coli nac promoter region, consistent with the argument that the  E. coli nac gene is autogenously regulated, just like that from  K. aerogenes.	bind
37576	3	10380	6	NULL	NULL	0	NULL	nac gene	NULL	K. aerogenes	is 	NULL				autogenously regulated	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_5_1166_s_199	9495755	A gel mobility shift assay (Fig.  5) confirms that NAC binds to the  E. coli nac promoter region, consistent with the argument that the  E. coli nac gene is autogenously regulated, just like that from  K. aerogenes.	bind
44104	1	10381	5	11	NULL	NULL	NULL	Oct3/4	GP		bind									enhancer	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_8_2699_s_11	12665572	A gel mobility shift assay demonstrated cooperative binding of Oct3/4 and Sox2 to the enhancer sequence.	bind
44105	2	10381	5	11	NULL	NULL	NULL	Sox2	GP		bind									enhancer	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_8_2699_s_11	12665572	A gel mobility shift assay demonstrated cooperative binding of Oct3/4 and Sox2 to the enhancer sequence.	bind
57501	3	10381	5	11	NULL	NULL	NULL	statement 1	Process		occurs in cooperation with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_8_2699_s_11	12665572	A gel mobility shift assay demonstrated cooperative binding of Oct3/4 and Sox2 to the enhancer sequence.	bind
37577	1	10381	6	NULL	NULL	0	NULL	Oct3/4	NULL		bind	NULL					NULL			enhancer	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_8_2699_s_11	12665572	A gel mobility shift assay demonstrated cooperative binding of Oct3/4 and Sox2 to the enhancer sequence.	bind
37578	2	10381	6	NULL	NULL	0	NULL	Sox2	NULL		bind	NULL					NULL			enhancer	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_8_2699_s_11	12665572	A gel mobility shift assay demonstrated cooperative binding of Oct3/4 and Sox2 to the enhancer sequence.	bind
37579	3	10381	6	NULL	NULL	0	NULL	statement 1	NULL		acts in cooperation with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_8_2699_s_11	12665572	A gel mobility shift assay demonstrated cooperative binding of Oct3/4 and Sox2 to the enhancer sequence.	bind
44106	1	10382	5	11	NULL	NULL	NULL	BF-1 protein	GP	WT	bind		high affinity			S2 double-stranded oligonucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6201_s_175	10938097	A gel mobility shift assay demonstrates high-affinity binding of the WT BF-1 protein to the S2 double-stranded oligonucleotide (lane 1).	bind
37580	1	10382	6	NULL	NULL	0	NULL	BF-1 protein	NULL	wild type	bind	NULL	high affinity			S2 double-stranded oligonucleotide	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6201_s_175	10938097	A gel mobility shift assay demonstrates high-affinity binding of the WT BF-1 protein to the S2 double-stranded oligonucleotide (lane 1).	bind
44107	1	10383	5	11	NULL	NULL	NULL	KKLF protein	GP	recombinant	bind					CLC-K1	GP			GA element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7319_s_8	10982849	A gel mobility shift assay revealed sequence-specific binding of recombinant KKLF and MAZ proteins to the CLC-K1 GA element, and the fine-mutation assay clarified that the consensus sequence for the KKLF binding site was GGGGNGGNG.	bind
44108	2	10383	5	11	NULL	NULL	NULL	MAZ protein	GP	recombinant	bind					CLC-K1	GP			GA element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7319_s_8	10982849	A gel mobility shift assay revealed sequence-specific binding of recombinant KKLF and MAZ proteins to the CLC-K1 GA element, and the fine-mutation assay clarified that the consensus sequence for the KKLF binding site was GGGGNGGNG.	bind
44109	3	10383	5	11	NULL	NULL	NULL	KKLF binding site	GP		is									GGGGNGGNG	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7319_s_8	10982849	A gel mobility shift assay revealed sequence-specific binding of recombinant KKLF and MAZ proteins to the CLC-K1 GA element, and the fine-mutation assay clarified that the consensus sequence for the KKLF binding site was GGGGNGGNG.	bind
37581	1	10383	6	NULL	NULL	0	NULL	KKLF protein	NULL	recombinant	bind	NULL	sequence specifically				NULL			CLC-K1GA element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7319_s_8	10982849	A gel mobility shift assay revealed sequence-specific binding of recombinant KKLF and MAZ proteins to the CLC-K1 GA element, and the fine-mutation assay clarified that the consensus sequence for the KKLF binding site was GGGGNGGNG.	bind
37582	2	10383	6	NULL	NULL	0	NULL	MAZ protein	NULL	recombinant	bind	NULL	sequence specifically				NULL			CLC-K1GA element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7319_s_8	10982849	A gel mobility shift assay revealed sequence-specific binding of recombinant KKLF and MAZ proteins to the CLC-K1 GA element, and the fine-mutation assay clarified that the consensus sequence for the KKLF binding site was GGGGNGGNG.	bind
37583	3	10383	6	10	NULL	0	NULL	KKLF binding site 			is									GGGGNGGNG	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_19_7319_s_8	10982849	A gel mobility shift assay revealed sequence-specific binding of recombinant KKLF and MAZ proteins to the CLC-K1 GA element, and the fine-mutation assay clarified that the consensus sequence for the KKLF binding site was GGGGNGGNG.	bind
44110	1	10384	5	11	NULL	NULL	NULL	protein	GP		bind					citB	GP			dyad symmetry sequence in promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_13_3304_s_214	9642180	A gel mobility shift assay showed that a protein(s) binds to the dyad symmetry sequence in the  citB promoter region ( 15).	bind
37584	1	10384	6	NULL	NULL	0	NULL	protein	NULL		bind	NULL				citB	NULL			dyad symmetry sequence of promoter	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_13_3304_s_214	9642180	A gel mobility shift assay showed that a protein(s) binds to the dyad symmetry sequence in the  citB promoter region ( 15).	bind
44111	1	10385	5	11	NULL	NULL	NULL	Tead4 protein	GP		bind		sequence specifically							CE	NULL		NULL	NULL	NULL	NULL	gw70_development_132_21_4719_s_136	16207754	A gel mobility shift assay showed that Tead4 and Tead2 proteins bound to CE in a sequence-specific manner, as shown by competition with an excess amount of unlabeled CE oligonucleotide ( Fig. 4A, lanes 2, 3, 10, 11).	bind
44112	2	10385	5	11	NULL	NULL	NULL	Tead2 protein	GP		bind		sequence specifically							CE	NULL		NULL	NULL	NULL	NULL	gw70_development_132_21_4719_s_136	16207754	A gel mobility shift assay showed that Tead4 and Tead2 proteins bound to CE in a sequence-specific manner, as shown by competition with an excess amount of unlabeled CE oligonucleotide ( Fig. 4A, lanes 2, 3, 10, 11).	bind
48723	3	10385	5	11	NULL	NULL	NULL	CE oligonucleotide	NucleicAcid	unlabeled	bind									CE	NULL		NULL	NULL	NULL	NULL	gw70_development_132_21_4719_s_136	16207754	A gel mobility shift assay showed that Tead4 and Tead2 proteins bound to CE in a sequence-specific manner, as shown by competition with an excess amount of unlabeled CE oligonucleotide ( Fig. 4A, lanes 2, 3, 10, 11).	bind
48724	4	10385	5	11	NULL	NULL	NULL	statement 1	Process		competes with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_132_21_4719_s_136	16207754	A gel mobility shift assay showed that Tead4 and Tead2 proteins bound to CE in a sequence-specific manner, as shown by competition with an excess amount of unlabeled CE oligonucleotide ( Fig. 4A, lanes 2, 3, 10, 11).	bind
48725	5	10385	5	11	NULL	NULL	NULL	statement 2	Process		competes with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_development_132_21_4719_s_136	16207754	A gel mobility shift assay showed that Tead4 and Tead2 proteins bound to CE in a sequence-specific manner, as shown by competition with an excess amount of unlabeled CE oligonucleotide ( Fig. 4A, lanes 2, 3, 10, 11).	bind
37585	1	10385	6	NULL	NULL	0	NULL	Tead4 protein	NULL		bind	NULL	sequence specifically				NULL			CE	NULL		0	NULL	NULL	NULL	gw70_development_132_21_4719_s_136	16207754	A gel mobility shift assay showed that Tead4 and Tead2 proteins bound to CE in a sequence-specific manner, as shown by competition with an excess amount of unlabeled CE oligonucleotide ( Fig. 4A, lanes 2, 3, 10, 11).	bind
37586	2	10385	6	NULL	NULL	0	NULL	Tead2 protein	NULL		bind	NULL	sequence specifically				NULL			CE	NULL		0	NULL	NULL	NULL	gw70_development_132_21_4719_s_136	16207754	A gel mobility shift assay showed that Tead4 and Tead2 proteins bound to CE in a sequence-specific manner, as shown by competition with an excess amount of unlabeled CE oligonucleotide ( Fig. 4A, lanes 2, 3, 10, 11).	bind
37603	3	10385	6	NULL	NULL	0	NULL	CE oligonucleotide	NULL	unlabeled	bind	NULL					NULL			CE	NULL		0	NULL	NULL	NULL	gw70_development_132_21_4719_s_136	16207754	A gel mobility shift assay showed that Tead4 and Tead2 proteins bound to CE in a sequence-specific manner, as shown by competition with an excess amount of unlabeled CE oligonucleotide ( Fig. 4A, lanes 2, 3, 10, 11).	bind
37604	4	10385	6	NULL	NULL	0	NULL	statement 1	NULL		competes	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_development_132_21_4719_s_136	16207754	A gel mobility shift assay showed that Tead4 and Tead2 proteins bound to CE in a sequence-specific manner, as shown by competition with an excess amount of unlabeled CE oligonucleotide ( Fig. 4A, lanes 2, 3, 10, 11).	bind
37605	5	10385	6	NULL	NULL	0	NULL	statement 2	NULL		competes	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_development_132_21_4719_s_136	16207754	A gel mobility shift assay showed that Tead4 and Tead2 proteins bound to CE in a sequence-specific manner, as shown by competition with an excess amount of unlabeled CE oligonucleotide ( Fig. 4A, lanes 2, 3, 10, 11).	bind
44113	1	10386	5	11	NULL	NULL	NULL	NREB	GP	endogenous	bind					renin gene	GP	rat			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_9_1059_s_6	10325243	A gel mobility shift assay showed that transfected NRE TFD blocked endogenous NREB binding with the rat renin gene.	bind
44114	2	10386	5	11	NULL	NULL	NULL	NRE	GP	transfected	block			TFD		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_9_1059_s_6	10325243	A gel mobility shift assay showed that transfected NRE TFD blocked endogenous NREB binding with the rat renin gene.	bind
37606	1	10386	6	NULL	NULL	0	NULL	NREB	NULL	endogenous	bind	NULL				renin gene	NULL	rat			NULL		0	NULL	NULL	NULL	gw60_circulationres_84_9_1059_s_6	10325243	A gel mobility shift assay showed that transfected NRE TFD blocked endogenous NREB binding with the rat renin gene.	bind
37607	2	10386	6	10	NULL	0	NULL	NRE	NULL	transfected	blocks	NULL		TFD		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_9_1059_s_6	10325243	A gel mobility shift assay showed that transfected NRE TFD blocked endogenous NREB binding with the rat renin gene.	bind
44117	1	10390	5	11	NULL	NULL	NULL	U1 snRNP	GP	purified	bind					tau	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_4036_s_34	10805746	A gel mobility shift assay with purified U1 snRNP preparations demonstrates a significantly higher level of U1 snRNP binding to the mutant tau than to the wild-type tau pre-mRNA.	bind
44118	2	10390	5	11	NULL	NULL	NULL	U1 snRNP	GP		bind					tau pre-mRNA	NucleicAcid	wild-type			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_4036_s_34	10805746	A gel mobility shift assay with purified U1 snRNP preparations demonstrates a significantly higher level of U1 snRNP binding to the mutant tau than to the wild-type tau pre-mRNA.	bind
44120	3	10390	5	11	NULL	NULL	NULL	statement 1	Process		higher level than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_4036_s_34	10805746	A gel mobility shift assay with purified U1 snRNP preparations demonstrates a significantly higher level of U1 snRNP binding to the mutant tau than to the wild-type tau pre-mRNA.	bind
37610	1	10390	6	NULL	NULL	0	NULL	tau pre-mRNA	NULL	wild type	bind	NULL				U1 snRNP	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_11_4036_s_34	10805746	A gel mobility shift assay with purified U1 snRNP preparations demonstrates a significantly higher level of U1 snRNP binding to the mutant tau than to the wild-type tau pre-mRNA.	bind
37611	2	10390	6	NULL	NULL	0	NULL	tau pre-mRNA	NULL	mutant	bind	NULL				U1 snRNP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_11_4036_s_34	10805746	A gel mobility shift assay with purified U1 snRNP preparations demonstrates a significantly higher level of U1 snRNP binding to the mutant tau than to the wild-type tau pre-mRNA.	bind
37612	3	10390	6	NULL	NULL	0	NULL	statement 2	NULL	affinity of	is higher than	NULL				statement 1	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_11_4036_s_34	10805746	A gel mobility shift assay with purified U1 snRNP preparations demonstrates a significantly higher level of U1 snRNP binding to the mutant tau than to the wild-type tau pre-mRNA.	bind
44121	1	10393	5	11	NULL	NULL	NULL	muR1.1 RNA	NucleicAcid		bind					RNase III	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_34_13_3708_s_131	16896014	A gel shift assay ( Figure 2B) reveals that muR1.1 RNA binds RNase III to form a complex with a measured apparent dissociation constant ( ) of 205 nM ( Figure 2C).	bind
37613	1	10393	6	NULL	NULL	0	NULL	muR1.1 RNA	NULL		forms a complex with	NULL				RNase III	NULL				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_34_13_3708_s_131	16896014	A gel shift assay ( Figure 2B) reveals that muR1.1 RNA binds RNase III to form a complex with a measured apparent dissociation constant ( ) of 205 nM ( Figure 2C).	bind
44122	1	10395	5	11	NULL	NULL	NULL	ASF/SF2	GP	recombinant	bind									purine-rich element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4001_s_214	12024014	A gel shift assay performed with the purine-rich element and the CE9.7 RNA reveals that recombinant ASF/SF2 binds to the purine-rich element (Fig.  7B, lanes 2 to 5).	bind
37614	1	10395	6	NULL	NULL	0	NULL	ASF/SF2	NULL	recombinant	bind	NULL					NULL			purine-rich element	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_12_4001_s_214	12024014	A gel shift assay performed with the purine-rich element and the CE9.7 RNA reveals that recombinant ASF/SF2 binds to the purine-rich element (Fig.  7B, lanes 2 to 5).	bind
44123	1	10397	5	11	NULL	NULL	NULL	Zalpha nuclease	GP	purified	bind					Z-DNA	NucleicAcid	radioactive			NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_24_12875_s_111	9371768	A gel-mobility shift assay with a radioactive Z-DNA probe and the purified Zalpha nuclease confirms that the Zalpha nuclease binds Z-DNA with a similar affinity to that of the Zalpha domain itself (data not shown).	bind
44124	2	10397	5	11	NULL	NULL	NULL				bind			Zalpha domain		Z-DNA	NucleicAcid	radioactive			NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_24_12875_s_111	9371768	A gel-mobility shift assay with a radioactive Z-DNA probe and the purified Zalpha nuclease confirms that the Zalpha nuclease binds Z-DNA with a similar affinity to that of the Zalpha domain itself (data not shown).	bind
44125	3	10397	5	11	NULL	NULL	NULL	statement 1	Process		similar affinity to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_24_12875_s_111	9371768	A gel-mobility shift assay with a radioactive Z-DNA probe and the purified Zalpha nuclease confirms that the Zalpha nuclease binds Z-DNA with a similar affinity to that of the Zalpha domain itself (data not shown).	bind
37615	1	10397	6	10	NULL	0	NULL	Zalpha nuclease		purified	bind					Z-DNA		radioactive			NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_24_12875_s_111	9371768	A gel-mobility shift assay with a radioactive Z-DNA probe and the purified Zalpha nuclease confirms that the Zalpha nuclease binds Z-DNA with a similar affinity to that of the Zalpha domain itself (data not shown).	bind
37616	2	10397	6	NULL	NULL	0	NULL	Zalpha nuclease	NULL		bind	NULL					NULL		Zalpha domain
\n		NULL		0	NULL	NULL	NULL	gw60_pnas_94_24_12875_s_111	9371768	A gel-mobility shift assay with a radioactive Z-DNA probe and the purified Zalpha nuclease confirms that the Zalpha nuclease binds Z-DNA with a similar affinity to that of the Zalpha domain itself (data not shown).	bind
37617	3	10397	6	NULL	NULL	0	NULL	statement 1	NULL	affinity of	is equal to	NULL				statement 2	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_pnas_94_24_12875_s_111	9371768	A gel-mobility shift assay with a radioactive Z-DNA probe and the purified Zalpha nuclease confirms that the Zalpha nuclease binds Z-DNA with a similar affinity to that of the Zalpha domain itself (data not shown).	bind
44126	1	10398	5	11	NULL	NULL	NULL	Hoxc8	GP		bind					OPN	GP			promoter	NULL	in vitro	NULL	NULL	NULL	NULL	gw70_pnas_102_7_2420_s_123	15699330	A gel-shift assay was performed to demonstrate that Hoxc8 binds to the  OPN promoter  in vitro ( ).	bind
37618	1	10398	6	NULL	NULL	0	NULL	Hoxc8	NULL		bind	NULL				OPN	NULL			promoter	NULL	in vitro	0	NULL	NULL	NULL	gw70_pnas_102_7_2420_s_123	15699330	A gel-shift assay was performed to demonstrate that Hoxc8 binds to the  OPN promoter  in vitro ( ).	bind
44168	1	10400	5	11	NULL	NULL	NULL	tetO sequence	GP		bind					tetO	GP				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1328_s_26	16087738	A gene that is placed under the control of a minimal promoter in which all activating sequences have been removed and replaced by the  tetO sequence will be expressed in cells producing tTA, which in the absence of tetracycline binds to  tetO to allow transcription.	bind
44169	2	10400	5	11	NULL	NULL	NULL	statement 3	Process		allows					transcription	Process				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1328_s_26	16087738	A gene that is placed under the control of a minimal promoter in which all activating sequences have been removed and replaced by the  tetO sequence will be expressed in cells producing tTA, which in the absence of tetracycline binds to  tetO to allow transcription.	bind
44170	3	10400	5	11	NULL	NULL	NULL	statement 1	Process		in the absence of					tetracycline	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1328_s_26	16087738	A gene that is placed under the control of a minimal promoter in which all activating sequences have been removed and replaced by the  tetO sequence will be expressed in cells producing tTA, which in the absence of tetracycline binds to  tetO to allow transcription.	bind
37941	1	10400	6	NULL	NULL	0	NULL	tetO sequence 	NULL		bind	NULL				tetO	NULL				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1328_s_26	16087738	A gene that is placed under the control of a minimal promoter in which all activating sequences have been removed and replaced by the  tetO sequence will be expressed in cells producing tTA, which in the absence of tetracycline binds to  tetO to allow transcription.	bind
37942	2	10400	6	NULL	NULL	0	NULL	statement 1	NULL		occurs in absence of	NULL				tetracyclin	NULL				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1328_s_26	16087738	A gene that is placed under the control of a minimal promoter in which all activating sequences have been removed and replaced by the  tetO sequence will be expressed in cells producing tTA, which in the absence of tetracycline binds to  tetO to allow transcription.	bind
37943	3	10400	6	NULL	NULL	0	NULL	statement 2	NULL		allows	NULL				transcription	NULL				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1328_s_26	16087738	A gene that is placed under the control of a minimal promoter in which all activating sequences have been removed and replaced by the  tetO sequence will be expressed in cells producing tTA, which in the absence of tetracycline binds to  tetO to allow transcription.	bind
38144	1	10401	6	13	NULL	NULL	NULL	GTP S	Chemical		bind					membrane G proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_40_6_826_s_20	11369036	A general agonist action was investigated by assessing the ability of SKF83959 to stimulate [35]guanosine-5''- O-(3-thio)triphosphate ([35]GTP S) binding to membrane G proteins (  Wang and   Panchalingam).	bind
38145	2	10401	6	13	NULL	NULL	NULL	GTP S	Chemical		is					guanosine-5''- O-(3-thio)triphosphate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_40_6_826_s_20	11369036	A general agonist action was investigated by assessing the ability of SKF83959 to stimulate [35]guanosine-5''- O-(3-thio)triphosphate ([35]GTP S) binding to membrane G proteins (  Wang and   Panchalingam).	bind
44307	1	10401	7	10	NULL	0	NULL	GTP S			bind					membrane G proteins					NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_40_6_826_s_20	11369036	A general agonist action was investigated by assessing the ability of SKF83959 to stimulate [35]guanosine-5''- O-(3-thio)triphosphate ([35]GTP S) binding to membrane G proteins (  Wang and   Panchalingam).	bind
44309	3	10401	7	10	NULL	0	NULL	GTP S			is					guanosine-5''- O-(3-thio)triphosphate					NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_40_6_826_s_20	11369036	A general agonist action was investigated by assessing the ability of SKF83959 to stimulate [35]guanosine-5''- O-(3-thio)triphosphate ([35]GTP S) binding to membrane G proteins (  Wang and   Panchalingam).	bind
38147	1	10402	6	13	NULL	NULL	NULL	PBCV-1 capping enzyme	GP	Chlorella virus	bind		directly			target RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_21_12226_s_26	9770468	A general mechanism for RNA guanylylation, proposed on the basis of the crystal structure of  Chlorella virus PBCV-1 capping enzyme ( 37), suggested direct binding to target RNAs.	bind
44310	1	10402	7	NULL	NULL	0	NULL	 PBCV-1 capping enzyme	NULL	Chlorella virus	bind	NULL	directly			RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_21_12226_s_26	9770468	A general mechanism for RNA guanylylation, proposed on the basis of the crystal structure of  Chlorella virus PBCV-1 capping enzyme ( 37), suggested direct binding to target RNAs.	bind
38384	2	10403	6	13	NULL	NULL	NULL	MeCP2	GP		bind					DNA	NucleicAcid	methylated			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
38385	3	10403	6	13	NULL	NULL	NULL	MeCP2	GP		recruits					SIN3 histone deacetylase- containing complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
38386	4	10403	6	13	NULL	NULL	NULL	statement 3	Process		occurs after					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
38387	5	10403	6	13	NULL	NULL	NULL	MBD2	GP		interacts with					NuRD/Mi2 deacetylase complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
38389	7	10403	6	13	NULL	NULL	NULL	MBD3	GP		interacts with					NuRD/Mi2 deacetylase complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
38390	8	10403	6	13	NULL	NULL	NULL	MBD1	GP	transcriptional repression of	is dependent on					deacetylase	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
50178	1	10403	6	13	NULL	NULL	NULL	MBD proteins	GP		bind							methylated		CpG	NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
50179	6	10403	6	13	NULL	NULL	NULL	MBD proteins	GP		bind							methylated		CpG	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
50180	9	10403	6	13	NULL	NULL	NULL	MBD proteins	GP		function in					transcription	Process	repression of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
50181	10	10403	6	13	NULL	NULL	NULL	MBD proteins	GP		is associated with					histone deacetylases	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
44311	1	10403	7	NULL	NULL	0	NULL	MBD proteins	NULL		bind	NULL					NULL	methylated		CpG	NULL	in vitro	0	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
44312	2	10403	7	10	NULL	0	NULL	MBD proteins	NULL		bind	NULL					NULL	methylated		CpG	NULL	in vivo	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
44313	3	10403	7	NULL	NULL	0	NULL	MBD proteins	NULL		function in	NULL				transcription	NULL	repression of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
44314	4	10403	7	10	NULL	0	NULL	MBD proteins	NULL		is associated with	NULL				histone deacetylases	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
44316	6	10403	7	10	NULL	0	NULL	MBD proteins	NULL		bind	NULL				DNA	NULL	methylated			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
44317	7	10403	7	NULL	NULL	0	NULL	MeCP2 	NULL		recruits	NULL				SIN3 histone deacetylase- containing complex	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
44318	8	10403	7	NULL	NULL	0	NULL	statement 7	NULL		occurs upon	NULL				statement 6	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
44319	9	10403	7	NULL	NULL	0	NULL	MBD2	NULL		interacts with	NULL				NuRD/Mi2 deacetylase complex	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
44320	10	10403	7	NULL	NULL	0	NULL	MBD3	NULL		interacts with	NULL				NuRD/Mi2 deacetylase complex	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
44321	11	10403	7	NULL	NULL	0	NULL	MBD1	NULL	transcriptional repression of	depends on	NULL				deacetylase	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_18_5291_s_20	12954765	A general notion is that MBD proteins bind methylated CpG  in vitro and  in vivo, function in transcriptional repression and are associated with histone deacetylases: when bound to methylated DNA, MeCP2 recruits the SIN3 histone deacetylase- containing complex, while MBD2 and MBD3 interact with the NuRD/Mi2 deacetylase complex ( 11) and MBD1 transcriptional repression has been shown to be deacetylase-dependent ( 12).	bind
38148	1	10404	6	13	NULL	NULL	NULL	ZBP-89	GP		bind									GC-rich region	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_19955_s_385	9685330	A general scheme has emerged; ZBP-89 binds to a GC-rich region that is within the first 200 base pairs downstream of the transcriptional start site of the gene.	bind
50182	2	10404	6	10	NULL	0	NULL		NULL		is located	NULL			GC-rich region		NULL	downstream of 		transcriptional start site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_19955_s_385	9685330	A general scheme has emerged; ZBP-89 binds to a GC-rich region that is within the first 200 base pairs downstream of the transcriptional start site of the gene.	bind
44322	1	10404	7	10	NULL	0	NULL	ZBP-89	NULL		binds to	NULL					NULL			GC-rich region	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_19955_s_385	9685330	A general scheme has emerged; ZBP-89 binds to a GC-rich region that is within the first 200 base pairs downstream of the transcriptional start site of the gene.	bind
50183	1	10404	7	10	NULL	0	NULL		NULL		is located	NULL			GC-rich region		NULL	downstream of		transcriptional start site	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_19955_s_385	9685330	A general scheme has emerged; ZBP-89 binds to a GC-rich region that is within the first 200 base pairs downstream of the transcriptional start site of the gene.	bind
38391	1	10405	6	13	NULL	NULL	NULL	IGF	GP		bind					IGF-1R	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_14_3638_s_118	11447105	A general trend established from comparing IGFs binding to IGF-1R, IGF-2R, IR and IGFBPs was that the residues that bind to the type 1 receptor appear to overlap those that bind to the insulin receptor, whereas those that bind to type 2 receptor overlap those that interact with IGF-binding proteins.	bind
38392	2	10405	6	13	NULL	NULL	NULL	IGF	GP		bind					IGF-2R	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_14_3638_s_118	11447105	A general trend established from comparing IGFs binding to IGF-1R, IGF-2R, IR and IGFBPs was that the residues that bind to the type 1 receptor appear to overlap those that bind to the insulin receptor, whereas those that bind to type 2 receptor overlap those that interact with IGF-binding proteins.	bind
38393	3	10405	6	13	NULL	NULL	NULL	IGF	GP		bind					IR	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_14_3638_s_118	11447105	A general trend established from comparing IGFs binding to IGF-1R, IGF-2R, IR and IGFBPs was that the residues that bind to the type 1 receptor appear to overlap those that bind to the insulin receptor, whereas those that bind to type 2 receptor overlap those that interact with IGF-binding proteins.	bind
38394	4	10405	6	13	NULL	NULL	NULL	IGF	GP		bind					IGFBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_14_3638_s_118	11447105	A general trend established from comparing IGFs binding to IGF-1R, IGF-2R, IR and IGFBPs was that the residues that bind to the type 1 receptor appear to overlap those that bind to the insulin receptor, whereas those that bind to type 2 receptor overlap those that interact with IGF-binding proteins.	bind
44323	1	10405	7	NULL	NULL	0	NULL	IGFs	NULL		bind	NULL				IGF-1R	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_14_3638_s_118	11447105	A general trend established from comparing IGFs binding to IGF-1R, IGF-2R, IR and IGFBPs was that the residues that bind to the type 1 receptor appear to overlap those that bind to the insulin receptor, whereas those that bind to type 2 receptor overlap those that interact with IGF-binding proteins.	bind
44324	2	10405	7	NULL	NULL	0	NULL	IGFs	NULL		bind	NULL				IGF-2R	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_14_3638_s_118	11447105	A general trend established from comparing IGFs binding to IGF-1R, IGF-2R, IR and IGFBPs was that the residues that bind to the type 1 receptor appear to overlap those that bind to the insulin receptor, whereas those that bind to type 2 receptor overlap those that interact with IGF-binding proteins.	bind
44325	3	10405	7	NULL	NULL	0	NULL	IGFs	NULL		bind	NULL				IR	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_14_3638_s_118	11447105	A general trend established from comparing IGFs binding to IGF-1R, IGF-2R, IR and IGFBPs was that the residues that bind to the type 1 receptor appear to overlap those that bind to the insulin receptor, whereas those that bind to type 2 receptor overlap those that interact with IGF-binding proteins.	bind
44326	4	10405	7	NULL	NULL	0	NULL	IGFs	NULL		bind	NULL				IGFBPs	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_14_3638_s_118	11447105	A general trend established from comparing IGFs binding to IGF-1R, IGF-2R, IR and IGFBPs was that the residues that bind to the type 1 receptor appear to overlap those that bind to the insulin receptor, whereas those that bind to type 2 receptor overlap those that interact with IGF-binding proteins.	bind
48851	5	10405	7	NULL	NULL	0	NULL	type 1 receptor	NULL	binding of	overlap with	NULL		 residues 		insulin receptor	NULL	binding of	residues		NULL		0	NULL	NULL	NULL	gw60_embo_20_14_3638_s_118	11447105	A general trend established from comparing IGFs binding to IGF-1R, IGF-2R, IR and IGFBPs was that the residues that bind to the type 1 receptor appear to overlap those that bind to the insulin receptor, whereas those that bind to type 2 receptor overlap those that interact with IGF-binding proteins.	bind
48852	6	10405	7	NULL	NULL	0	NULL	type 2 receptor	NULL	binding of	overlap with	NULL		residues		IGF-binding proteins	NULL	interaction of	residues		NULL		0	NULL	NULL	NULL	gw60_embo_20_14_3638_s_118	11447105	A general trend established from comparing IGFs binding to IGF-1R, IGF-2R, IR and IGFBPs was that the residues that bind to the type 1 receptor appear to overlap those that bind to the insulin receptor, whereas those that bind to type 2 receptor overlap those that interact with IGF-binding proteins.	bind
38149	1	10406	6	13	NULL	NULL	NULL	TR	GP		bind					TH/bZIP	GP			TRE	NULL	tails of untreated, premetamorphic tadpoles	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_50_41222_s_140	16236718	A generality based on the above data is that the level of TR binding to the TH/bZIP TRE in tails and intestines of untreated, premetamorphic tadpoles was at or marginally above background levels, based on signal from exon 5 and control antibody.	bind
38150	2	10406	6	13	NULL	NULL	NULL	TR	GP		bind					TH/bZIP	GP			TRE	NULL	intestines of untreated, premetamorphic tadpoles	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_50_41222_s_140	16236718	A generality based on the above data is that the level of TR binding to the TH/bZIP TRE in tails and intestines of untreated, premetamorphic tadpoles was at or marginally above background levels, based on signal from exon 5 and control antibody.	bind
44327	1	10406	7	NULL	NULL	0	NULL	TR	NULL		bind	NULL				TH/bZIP	NULL			TRE	NULL	tails of untreated premetamorphic tadpoles	0	NULL	NULL	NULL	gw70_jbiolchem_280_50_41222_s_140	16236718	A generality based on the above data is that the level of TR binding to the TH/bZIP TRE in tails and intestines of untreated, premetamorphic tadpoles was at or marginally above background levels, based on signal from exon 5 and control antibody.	bind
44328	2	10406	7	NULL	NULL	0	NULL	TR	NULL		bind	NULL				TH/bZIP	NULL			TRE	NULL	intestines of untreated premetamorphic tadpoles	0	NULL	NULL	NULL	gw70_jbiolchem_280_50_41222_s_140	16236718	A generality based on the above data is that the level of TR binding to the TH/bZIP TRE in tails and intestines of untreated, premetamorphic tadpoles was at or marginally above background levels, based on signal from exon 5 and control antibody.	bind
38151	1	10407	6	13	NULL	NULL	NULL	clusterin	GP		bind					PEX deposits	OrganismPart				NULL	ocular tissues of PEX eyes	NULL	NULL	NULL	NULL	abs-batch0650-0679_invest-ophthalmol-vis-sci_47_5_16639006_s_9	16639006	A generally  decreased immunoreactivity, but a prominent binding of clusterin to all  PEX deposits, could be observed in ocular tissues of PEX eyes.	bind
44329	1	10407	7	NULL	NULL	0	NULL	clusterin	NULL		bind	NULL				PEX deposits	NULL				NULL	ocular tissues of PEX eyes	0	NULL	NULL	NULL	abs-batch0650-0679_invest-ophthalmol-vis-sci_47_5_16639006_s_9	16639006	A generally  decreased immunoreactivity, but a prominent binding of clusterin to all  PEX deposits, could be observed in ocular tissues of PEX eyes.	bind
38152	1	10408	6	13	NULL	NULL	NULL	Pumilio homolog	GP	Drosophila	bind		specifically			fem-3	GP			PME regulatory element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2189_s_25	10022905	A genetic screen for recessive mutations that cause failure of the sperm-oocyte switch identified six  mog (for masculinization of the germ line) genes ( 18,  19), while a yeast three-hybrid screen for PME-binding proteins yielded FBF (for  fem-3 binding factor), a homolog of  Drosophila Pumilio that binds specifically to the  fem-3 PME regulatory element ( 46).	bind
50184	2	10408	6	13	NULL	NULL	NULL	PME	GP		bind					FBF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2189_s_25	10022905	A genetic screen for recessive mutations that cause failure of the sperm-oocyte switch identified six  mog (for masculinization of the germ line) genes ( 18,  19), while a yeast three-hybrid screen for PME-binding proteins yielded FBF (for  fem-3 binding factor), a homolog of  Drosophila Pumilio that binds specifically to the  fem-3 PME regulatory element ( 46).	bind
50185	3	10408	6	13	NULL	NULL	NULL	FBF	GP		is					fem-3 binding factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2189_s_25	10022905	A genetic screen for recessive mutations that cause failure of the sperm-oocyte switch identified six  mog (for masculinization of the germ line) genes ( 18,  19), while a yeast three-hybrid screen for PME-binding proteins yielded FBF (for  fem-3 binding factor), a homolog of  Drosophila Pumilio that binds specifically to the  fem-3 PME regulatory element ( 46).	bind
44360	1	10408	7	NULL	NULL	0	NULL	PME	NULL		bind	NULL				FBF	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2189_s_25	10022905	A genetic screen for recessive mutations that cause failure of the sperm-oocyte switch identified six  mog (for masculinization of the germ line) genes ( 18,  19), while a yeast three-hybrid screen for PME-binding proteins yielded FBF (for  fem-3 binding factor), a homolog of  Drosophila Pumilio that binds specifically to the  fem-3 PME regulatory element ( 46).	bind
44361	2	10408	7	NULL	NULL	0	NULL	Pumilio homolog 	NULL	Drosophila	bind	NULL	specifically			fem-3	NULL			PME regulatory element	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2189_s_25	10022905	A genetic screen for recessive mutations that cause failure of the sperm-oocyte switch identified six  mog (for masculinization of the germ line) genes ( 18,  19), while a yeast three-hybrid screen for PME-binding proteins yielded FBF (for  fem-3 binding factor), a homolog of  Drosophila Pumilio that binds specifically to the  fem-3 PME regulatory element ( 46).	bind
44362	3	10408	7	NULL	NULL	0	NULL	FBF	NULL		is	NULL				fem-3 binding factor	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2189_s_25	10022905	A genetic screen for recessive mutations that cause failure of the sperm-oocyte switch identified six  mog (for masculinization of the germ line) genes ( 18,  19), while a yeast three-hybrid screen for PME-binding proteins yielded FBF (for  fem-3 binding factor), a homolog of  Drosophila Pumilio that binds specifically to the  fem-3 PME regulatory element ( 46).	bind
38153	1	10409	6	13	NULL	NULL	NULL	COUP-TFII	GP		bind									GIRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_40_28385_s_5	10497199	A genetic screen in yeast has allowed us to identify a novel transcriptional factor binding to the GlRE,  i.e. the chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII).	bind
38154	2	10409	6	13	NULL	NULL	NULL	COUP-TFII	GP		is					chicken ovalbumin upstream promoter-transcription factor II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_40_28385_s_5	10497199	A genetic screen in yeast has allowed us to identify a novel transcriptional factor binding to the GlRE,  i.e. the chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII).	bind
50186	3	10409	6	13	NULL	NULL	NULL	COUP-TFII \t	GP		is a type of					novel transcriptional factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_40_28385_s_5	10497199	A genetic screen in yeast has allowed us to identify a novel transcriptional factor binding to the GlRE,  i.e. the chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII).	bind
44363	1	10409	7	NULL	NULL	0	NULL	COUP-TFII	NULL		bind	NULL					NULL			GlRE	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_40_28385_s_5	10497199	A genetic screen in yeast has allowed us to identify a novel transcriptional factor binding to the GlRE,  i.e. the chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII).	bind
44364	2	10409	7	10	NULL	0	NULL	COUP-TFII	NULL		is	NULL				chicken ovalbumin upstream promoter-transcription factor II	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_40_28385_s_5	10497199	A genetic screen in yeast has allowed us to identify a novel transcriptional factor binding to the GlRE,  i.e. the chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII).	bind
44365	3	10409	7	NULL	NULL	0	NULL	COUP-TFII	NULL		is a type of	NULL				novel transcriptional factor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_40_28385_s_5	10497199	A genetic screen in yeast has allowed us to identify a novel transcriptional factor binding to the GlRE,  i.e. the chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII).	bind
38155	1	10410	6	13	NULL	NULL	NULL	cellular proteins	GP		bind					RRS	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_pnas_98_26_14991_s_90	11734633	A Genetic Screen to Identify Cellular Proteins That Bind to the RRS  in Vivo.	bind
44366	1	10410	7	NULL	NULL	0	NULL	Cellular Proteins	NULL		bind	NULL				RRS	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_pnas_98_26_14991_s_90	11734633	A Genetic Screen to Identify Cellular Proteins That Bind to the RRS  in Vivo.	bind
38395	1	10412	6	13	NULL	NULL	NULL	GFP-beta-CaMKII	GP		does not bind					calmodulin	GP		A303R		NULL		NULL	NULL	NULL	NULL	gw60_science_284_5411_162_s_151	10102820	A GFP-beta-CaMKII deficient in calmodulin binding (A303R) bound effectively to F-actin and failed to dissociate after an increase in Ca2+ concentration ( Fig. 4E,  n = 16).	bind
38396	2	10412	6	13	NULL	NULL	NULL	GFP-beta-CaMKII	GP		bind		effectively			F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5411_162_s_151	10102820	A GFP-beta-CaMKII deficient in calmodulin binding (A303R) bound effectively to F-actin and failed to dissociate after an increase in Ca2+ concentration ( Fig. 4E,  n = 16).	bind
38397	3	10412	6	13	NULL	NULL	NULL	Ca2+	Chemical	increase in;;concentration of	does not dissociate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5411_162_s_151	10102820	A GFP-beta-CaMKII deficient in calmodulin binding (A303R) bound effectively to F-actin and failed to dissociate after an increase in Ca2+ concentration ( Fig. 4E,  n = 16).	bind
44367	1	10412	7	10	NULL	0	NULL	GFP-beta-CaMKII	NULL		does not bind	NULL				calmodulin	NULL		A303R		NULL		NULL	NULL	NULL	NULL	gw60_science_284_5411_162_s_151	10102820	A GFP-beta-CaMKII deficient in calmodulin binding (A303R) bound effectively to F-actin and failed to dissociate after an increase in Ca2+ concentration ( Fig. 4E,  n = 16).	bind
44368	2	10412	7	NULL	NULL	0	NULL	GFP-beta-CaMKII	NULL		bind	NULL	effectively			F-actin	NULL				NULL		0	NULL	NULL	NULL	gw60_science_284_5411_162_s_151	10102820	A GFP-beta-CaMKII deficient in calmodulin binding (A303R) bound effectively to F-actin and failed to dissociate after an increase in Ca2+ concentration ( Fig. 4E,  n = 16).	bind
44369	3	10412	7	10	NULL	0	NULL	Ca2+	NULL	increase in;;concentration of	does not dissociate	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_284_5411_162_s_151	10102820	A GFP-beta-CaMKII deficient in calmodulin binding (A303R) bound effectively to F-actin and failed to dissociate after an increase in Ca2+ concentration ( Fig. 4E,  n = 16).	bind
38156	1	10413	6	13	NULL	NULL	NULL	GHS	GP		bind					GHS-R	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40441_s_314	11546772	A GHS-R homologue identified in the pufferfish shares 58% identity to human GHS-R and is activated by GHRP-6 and nonpeptidyl GHSs ( 17), suggesting that GHS binding to the GHS-R is not species-specific.	bind
50187	2	10413	6	13	NULL	NULL	NULL	GHS-R homologue	GP	pufferfish	is similar to					GHS-R	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40441_s_314	11546772	A GHS-R homologue identified in the pufferfish shares 58% identity to human GHS-R and is activated by GHRP-6 and nonpeptidyl GHSs ( 17), suggesting that GHS binding to the GHS-R is not species-specific.	bind
50188	3	10413	6	13	NULL	NULL	NULL	GHRP-6	GP		activates					GHS-R homologue	GP	pufferfish			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40441_s_314	11546772	A GHS-R homologue identified in the pufferfish shares 58% identity to human GHS-R and is activated by GHRP-6 and nonpeptidyl GHSs ( 17), suggesting that GHS binding to the GHS-R is not species-specific.	bind
50189	4	10413	6	13	NULL	NULL	NULL	nonpeptidyl GHSs	GP		activates					GHS-R homologue	GP	pufferfish			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40441_s_314	11546772	A GHS-R homologue identified in the pufferfish shares 58% identity to human GHS-R and is activated by GHRP-6 and nonpeptidyl GHSs ( 17), suggesting that GHS binding to the GHS-R is not species-specific.	bind
44370	1	10413	7	NULL	NULL	0	NULL	GHS-R homologue	NULL	pufferfish	is similar to	NULL				GHS-R	NULL	human			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40441_s_314	11546772	A GHS-R homologue identified in the pufferfish shares 58% identity to human GHS-R and is activated by GHRP-6 and nonpeptidyl GHSs ( 17), suggesting that GHS binding to the GHS-R is not species-specific.	bind
44371	2	10413	7	NULL	NULL	0	NULL	GHRP-6	NULL		activates	NULL				GHS-R homologue	NULL	pufferfish			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40441_s_314	11546772	A GHS-R homologue identified in the pufferfish shares 58% identity to human GHS-R and is activated by GHRP-6 and nonpeptidyl GHSs ( 17), suggesting that GHS binding to the GHS-R is not species-specific.	bind
44372	3	10413	7	NULL	NULL	0	NULL	nonpeptidyl GHSs	NULL		activates	NULL				GHS-R homologue	NULL	pufferfish			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_44_40441_s_314	11546772	A GHS-R homologue identified in the pufferfish shares 58% identity to human GHS-R and is activated by GHRP-6 and nonpeptidyl GHSs ( 17), suggesting that GHS binding to the GHS-R is not species-specific.	bind
44373	4	10413	7	NULL	NULL	0	NULL	GHS	NULL		bind	NULL	non species-specific			GHS-R	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_44_40441_s_314	11546772	A GHS-R homologue identified in the pufferfish shares 58% identity to human GHS-R and is activated by GHRP-6 and nonpeptidyl GHSs ( 17), suggesting that GHS binding to the GHS-R is not species-specific.	bind
38398	1	10417	6	13	NULL	NULL	NULL	S2- InsP3R-1	GP		forms fusion protein with			amino acids 1574-1765					glycine-rich motif Gly-Tyr-Gly-Glu-Lys-Gly		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_281_25_16621795_s_4	16621795	A glutathione  S-transferase fusion protein encompassing amino acids 1574-1765 of the  S2- InsP3R-1 and including the glycine-rich motif Gly-Tyr-Gly-Glu-Lys-Gly  bound ATP specifically as measured by fluorescent trinitrophenyl-ATP binding.	bind
38399	2	10417	6	13	NULL	NULL	NULL	statement 1	GP		bind		specifically			ATP	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_281_25_16621795_s_4	16621795	A glutathione  S-transferase fusion protein encompassing amino acids 1574-1765 of the  S2- InsP3R-1 and including the glycine-rich motif Gly-Tyr-Gly-Glu-Lys-Gly  bound ATP specifically as measured by fluorescent trinitrophenyl-ATP binding.	bind
44375	1	10417	7	NULL	NULL	0	NULL	glutathione S-transferase  protein	NULL		encompass	NULL				S2- InsP3R-1	NULL		amino acids 1574-1765		NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_281_25_16621795_s_4	16621795	A glutathione  S-transferase fusion protein encompassing amino acids 1574-1765 of the  S2- InsP3R-1 and including the glycine-rich motif Gly-Tyr-Gly-Glu-Lys-Gly  bound ATP specifically as measured by fluorescent trinitrophenyl-ATP binding.	bind
44376	2	10417	7	NULL	NULL	0	NULL	glutathione S-transferase  protein	NULL		encompass	NULL					NULL		glycine-rich motif Gly-Tyr-Gly-Glu-Lys-Gly		NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_281_25_16621795_s_4	16621795	A glutathione  S-transferase fusion protein encompassing amino acids 1574-1765 of the  S2- InsP3R-1 and including the glycine-rich motif Gly-Tyr-Gly-Glu-Lys-Gly  bound ATP specifically as measured by fluorescent trinitrophenyl-ATP binding.	bind
44377	3	10417	7	NULL	NULL	0	NULL	statement 1	NULL		occur along with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_281_25_16621795_s_4	16621795	A glutathione  S-transferase fusion protein encompassing amino acids 1574-1765 of the  S2- InsP3R-1 and including the glycine-rich motif Gly-Tyr-Gly-Glu-Lys-Gly  bound ATP specifically as measured by fluorescent trinitrophenyl-ATP binding.	bind
44378	4	10417	7	NULL	NULL	0	NULL	statement 3	NULL		bind	NULL	specifically			ATP	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_281_25_16621795_s_4	16621795	A glutathione  S-transferase fusion protein encompassing amino acids 1574-1765 of the  S2- InsP3R-1 and including the glycine-rich motif Gly-Tyr-Gly-Glu-Lys-Gly  bound ATP specifically as measured by fluorescent trinitrophenyl-ATP binding.	bind
44379	5	10417	7	NULL	NULL	0	NULL	glutathione S-transferase protein	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_281_25_16621795_s_4	16621795	A glutathione  S-transferase fusion protein encompassing amino acids 1574-1765 of the  S2- InsP3R-1 and including the glycine-rich motif Gly-Tyr-Gly-Glu-Lys-Gly  bound ATP specifically as measured by fluorescent trinitrophenyl-ATP binding.	bind
38157	1	10420	6	13	NULL	NULL	NULL	S2(-) InsP(3)R-1	GP		forms fusion protein with			amino acids 1574-1765					glycine-rich motif Gly-Tyr-Gly-Glu-Lys-Gly		NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_j-biol-chem_281_25_16621795_s_4	16621795	A glutathione S-transferase fusion protein encompassing amino acids 1574-1765  of the S2(-) InsP(3)R-1 and including the glycine-rich motif Gly-Tyr-Gly-Glu-Lys-Gly  bound ATP specifically as measured by fluorescent trinitrophenyl-ATP binding.	bind
38158	2	10420	6	13	NULL	NULL	NULL	statement 1	GP		bind		specifically			ATP	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_j-biol-chem_281_25_16621795_s_4	16621795	A glutathione S-transferase fusion protein encompassing amino acids 1574-1765  of the S2(-) InsP(3)R-1 and including the glycine-rich motif Gly-Tyr-Gly-Glu-Lys-Gly  bound ATP specifically as measured by fluorescent trinitrophenyl-ATP binding.	bind
38400	1	10422	6	13	NULL	NULL	NULL	Glycosulfopeptide	GP		bind			C2-O-sLex at Thr-57		P-selectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39569_s_135	10978329	A Glycosulfopeptide with C2-O-sLex at Thr-57 but Not at Thr-44 Binds to P-selectin--  wo isomeric 35SO3-labeled glycosulfopeptides containing three TyrSO3 residues and a C2-O-sLex at either Thr-57 (3-GSP-6) or Thr-44 (3-GSP-6'') were chromatographed on an affinity column containing sPS at a coupling density of 6.5 mg/ml (Fig.  3).	bind
38401	2	10422	6	13	NULL	NULL	NULL	Glycosulfopeptide	GP		does not bind			C2-O-sLex at Thr-44		P-selectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39569_s_135	10978329	A Glycosulfopeptide with C2-O-sLex at Thr-57 but Not at Thr-44 Binds to P-selectin--  wo isomeric 35SO3-labeled glycosulfopeptides containing three TyrSO3 residues and a C2-O-sLex at either Thr-57 (3-GSP-6) or Thr-44 (3-GSP-6'') were chromatographed on an affinity column containing sPS at a coupling density of 6.5 mg/ml (Fig.  3).	bind
44385	1	10422	7	10	NULL	0	NULL	Glycosulfopeptide	NULL		bind	NULL		C2-O-sLex at Thr-57		P-selectin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39569_s_135	10978329	A Glycosulfopeptide with C2-O-sLex at Thr-57 but Not at Thr-44 Binds to P-selectin--  wo isomeric 35SO3-labeled glycosulfopeptides containing three TyrSO3 residues and a C2-O-sLex at either Thr-57 (3-GSP-6) or Thr-44 (3-GSP-6'') were chromatographed on an affinity column containing sPS at a coupling density of 6.5 mg/ml (Fig.  3).	bind
44386	2	10422	7	10	NULL	0	NULL	Glycosulfopeptide	NULL		does not bind	NULL		C2-O-sLex at Thr-44		P-selectin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_50_39569_s_135	10978329	A Glycosulfopeptide with C2-O-sLex at Thr-57 but Not at Thr-44 Binds to P-selectin--  wo isomeric 35SO3-labeled glycosulfopeptides containing three TyrSO3 residues and a C2-O-sLex at either Thr-57 (3-GSP-6) or Thr-44 (3-GSP-6'') were chromatographed on an affinity column containing sPS at a coupling density of 6.5 mg/ml (Fig.  3).	bind
38159	1	10425	6	13	NULL	NULL	NULL	betaIII spectrin	GP		bind					dynactin	GP		Arp1 subunit 		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_172_5_655_s_154	16505164	A Golgi-associated spectrin isoform, betaIII spectrin, was found to bind to the Arp1 subunit of dynactin ( ,  ), whereas ZW10 binds to the dynamitin subunit ( ).	bind
38160	2	10425	6	13	NULL	NULL	NULL	ZW10	GP		bind					dynactin	GP		dynamitin subunit		NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_172_5_655_s_154	16505164	A Golgi-associated spectrin isoform, betaIII spectrin, was found to bind to the Arp1 subunit of dynactin ( ,  ), whereas ZW10 binds to the dynamitin subunit ( ).	bind
38161	3	10425	6	13	NULL	NULL	NULL	betaIII spectrin	GP		is a type of					Golgi-associated spectrin isoform	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_172_5_655_s_154	16505164	A Golgi-associated spectrin isoform, betaIII spectrin, was found to bind to the Arp1 subunit of dynactin ( ,  ), whereas ZW10 binds to the dynamitin subunit ( ).	bind
44387	1	10425	7	NULL	NULL	0	NULL	betaIII spectrin	NULL		bind	NULL				dynactin	NULL		Arp1 subunit		NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_5_655_s_154	16505164	A Golgi-associated spectrin isoform, betaIII spectrin, was found to bind to the Arp1 subunit of dynactin ( ,  ), whereas ZW10 binds to the dynamitin subunit ( ).	bind
44388	2	10425	7	NULL	NULL	0	NULL	ZW10	NULL		binds to	NULL				dynactin	NULL		dynamitin subunit		NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_5_655_s_154	16505164	A Golgi-associated spectrin isoform, betaIII spectrin, was found to bind to the Arp1 subunit of dynactin ( ,  ), whereas ZW10 binds to the dynamitin subunit ( ).	bind
44389	3	10425	7	NULL	NULL	0	NULL	betaIII spectrin	NULL		is a type of	NULL				Golgi-associated spectrin isoform	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_5_655_s_154	16505164	A Golgi-associated spectrin isoform, betaIII spectrin, was found to bind to the Arp1 subunit of dynactin ( ,  ), whereas ZW10 binds to the dynamitin subunit ( ).	bind
38453	1	10426	6	13	NULL	NULL	NULL	titin	GP		bind			N2A domain		Capn3	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_24_9127_s_286	14645524	A good candidate for this Capn3 inhibition is its giant partner, titin, possibly through the N2A domain, which binds Capn3 but is not cleaved by it ( ).	bind
38899	2	10426	6	13	NULL	NULL	NULL	titin	GP		is not cleaved by					Capn3	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_24_9127_s_286	14645524	A good candidate for this Capn3 inhibition is its giant partner, titin, possibly through the N2A domain, which binds Capn3 but is not cleaved by it ( ).	bind
44390	1	10426	7	10	NULL	0	NULL	 Capn3	NULL		binds	NULL				titin	NULL		N2A domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_24_9127_s_286	14645524	A good candidate for this Capn3 inhibition is its giant partner, titin, possibly through the N2A domain, which binds Capn3 but is not cleaved by it ( ).	bind
44391	2	10426	7	NULL	NULL	0	NULL	Capn3	NULL		does not cleave	NULL				titin	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_24_9127_s_286	14645524	A good candidate for this Capn3 inhibition is its giant partner, titin, possibly through the N2A domain, which binds Capn3 but is not cleaved by it ( ).	bind
38456	1	10428	6	13	NULL	NULL	NULL	MAP kinase phosphatase	GP		bind					ERK2	GP	mutant	loop L16;; D316N		NULL	yeast	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37885_s_246	16148006	A good correlation was found between the strength of MAP kinase phosphatase binding to ERK2 mutations at the loop L16 (D316N, D319N, D319E, E320A, and E320Q) in yeast and ERK2 cytosolic retention in COS-7 cells (compare  Fig. 4 and  TABLE ONE).	bind
38457	2	10428	6	13	NULL	NULL	NULL	MAP kinase phosphatase	GP		bind					ERK2	GP	mutant	loop L16;; D319N		NULL	yeast	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37885_s_246	16148006	A good correlation was found between the strength of MAP kinase phosphatase binding to ERK2 mutations at the loop L16 (D316N, D319N, D319E, E320A, and E320Q) in yeast and ERK2 cytosolic retention in COS-7 cells (compare  Fig. 4 and  TABLE ONE).	bind
38458	3	10428	6	13	NULL	NULL	NULL	MAP kinase phosphatase	GP		bind					ERK2	GP	mutant	loop L16;; D319E		NULL	Yeast	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37885_s_246	16148006	A good correlation was found between the strength of MAP kinase phosphatase binding to ERK2 mutations at the loop L16 (D316N, D319N, D319E, E320A, and E320Q) in yeast and ERK2 cytosolic retention in COS-7 cells (compare  Fig. 4 and  TABLE ONE).	bind
38459	4	10428	6	13	NULL	NULL	NULL	MAP kinase phosphatase	GP		bind					ERK2	GP	mutant	loop L16;; E320A		NULL	yeast	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37885_s_246	16148006	A good correlation was found between the strength of MAP kinase phosphatase binding to ERK2 mutations at the loop L16 (D316N, D319N, D319E, E320A, and E320Q) in yeast and ERK2 cytosolic retention in COS-7 cells (compare  Fig. 4 and  TABLE ONE).	bind
38461	5	10428	6	13	NULL	NULL	NULL	MAP kinase phosphatase	GP		bind					ERK2	GP	mutant	loop L16;; E320Q		NULL	yeast	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37885_s_246	16148006	A good correlation was found between the strength of MAP kinase phosphatase binding to ERK2 mutations at the loop L16 (D316N, D319N, D319E, E320A, and E320Q) in yeast and ERK2 cytosolic retention in COS-7 cells (compare  Fig. 4 and  TABLE ONE).	bind
44392	1	10428	7	10	NULL	0	NULL	MAP kinase phosphatase			bind					ERK2		mutation of	loop L16;;D316N		NULL	yeast	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37885_s_246	16148006	A good correlation was found between the strength of MAP kinase phosphatase binding to ERK2 mutations at the loop L16 (D316N, D319N, D319E, E320A, and E320Q) in yeast and ERK2 cytosolic retention in COS-7 cells (compare  Fig. 4 and  TABLE ONE).	bind
44393	2	10428	7	10	NULL	0	NULL	MAP kinase phosphatase			bind					ERK2		mutation of	loop L16;;D319N 		NULL	yeast	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37885_s_246	16148006	A good correlation was found between the strength of MAP kinase phosphatase binding to ERK2 mutations at the loop L16 (D316N, D319N, D319E, E320A, and E320Q) in yeast and ERK2 cytosolic retention in COS-7 cells (compare  Fig. 4 and  TABLE ONE).	bind
44394	3	10428	7	10	NULL	0	NULL	MAP kinase phosphatase			bind					ERK2		mutation of	loop L16;;D319E		NULL	yeast	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37885_s_246	16148006	A good correlation was found between the strength of MAP kinase phosphatase binding to ERK2 mutations at the loop L16 (D316N, D319N, D319E, E320A, and E320Q) in yeast and ERK2 cytosolic retention in COS-7 cells (compare  Fig. 4 and  TABLE ONE).	bind
44395	4	10428	7	10	NULL	0	NULL	MAP kinase phosphatase			bind					ERK2		mutation of	loop L16;;E320A		NULL	yeast	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37885_s_246	16148006	A good correlation was found between the strength of MAP kinase phosphatase binding to ERK2 mutations at the loop L16 (D316N, D319N, D319E, E320A, and E320Q) in yeast and ERK2 cytosolic retention in COS-7 cells (compare  Fig. 4 and  TABLE ONE).	bind
44396	5	10428	7	10	NULL	0	NULL	MAP kinase phosphatase			bind					ERK2		mutation of	loop L16;;E320Q		NULL	yeast	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37885_s_246	16148006	A good correlation was found between the strength of MAP kinase phosphatase binding to ERK2 mutations at the loop L16 (D316N, D319N, D319E, E320A, and E320Q) in yeast and ERK2 cytosolic retention in COS-7 cells (compare  Fig. 4 and  TABLE ONE).	bind
38466	1	10429	6	13	NULL	NULL	NULL	hMR	GP	mutant	bind					aldosterone	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_12_3317_s_111	9628869	A good correlation was observed between the decrease in the binding affinity of the mutant hMRs for aldosterone and the decrease in their transactivation capacity.	bind
38467	2	10429	6	13	NULL	NULL	NULL	statement 1	Process	decrease in	corelates with					hMRs	GP	decrease in;;transactivation of			NULL		NULL	NULL	NULL	NULL	gw60_embo_17_12_3317_s_111	9628869	A good correlation was observed between the decrease in the binding affinity of the mutant hMRs for aldosterone and the decrease in their transactivation capacity.	bind
44397	1	10429	7	NULL	NULL	0	NULL	hMRs	NULL	mutant	bind	NULL				aldosterone	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_17_12_3317_s_111	9628869	A good correlation was observed between the decrease in the binding affinity of the mutant hMRs for aldosterone and the decrease in their transactivation capacity.	bind
44398	2	10429	7	10	NULL	0	NULL	statement 1	NULL	decrease in	corelates with	NULL				hMRs	NULL	decrease in;;transactivation of			NULL		NULL	NULL	NULL	NULL	gw60_embo_17_12_3317_s_111	9628869	A good correlation was observed between the decrease in the binding affinity of the mutant hMRs for aldosterone and the decrease in their transactivation capacity.	bind
38163	1	10430	6	13	NULL	NULL	NULL	Ste5	GP		bind					Ste11	GP				NULL	yeast	NULL	NULL	NULL	NULL	gw70_annurevpharmacol_42_0_283_s_438	11807174	A good example derives from the mating  pathway in yeast, where the Ste5 scaffold protein binds the MAPKKK Ste11, the MAPKK  Ste7, and the MAPK Fus3.	bind
38164	2	10430	6	13	NULL	NULL	NULL	Ste5	GP		is a type of					scaffold protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_42_0_283_s_438	11807174	A good example derives from the mating  pathway in yeast, where the Ste5 scaffold protein binds the MAPKKK Ste11, the MAPKK  Ste7, and the MAPK Fus3.	bind
38165	3	10430	6	13	NULL	NULL	NULL	Ste5	GP		bind					Ste7	GP				NULL	yeast	NULL	NULL	NULL	NULL	gw70_annurevpharmacol_42_0_283_s_438	11807174	A good example derives from the mating  pathway in yeast, where the Ste5 scaffold protein binds the MAPKKK Ste11, the MAPKK  Ste7, and the MAPK Fus3.	bind
38166	4	10430	6	13	NULL	NULL	NULL	Ste7	GP		is a type of					MAPKK	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_42_0_283_s_438	11807174	A good example derives from the mating  pathway in yeast, where the Ste5 scaffold protein binds the MAPKKK Ste11, the MAPKK  Ste7, and the MAPK Fus3.	bind
38167	5	10430	6	13	NULL	NULL	NULL	Ste11	GP		is a type of					MAPKKK	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_42_0_283_s_438	11807174	A good example derives from the mating  pathway in yeast, where the Ste5 scaffold protein binds the MAPKKK Ste11, the MAPKK  Ste7, and the MAPK Fus3.	bind
38168	6	10430	6	13	NULL	NULL	NULL	Ste5	GP		bind					Fus3	GP				NULL	yeast	NULL	NULL	NULL	NULL	gw70_annurevpharmacol_42_0_283_s_438	11807174	A good example derives from the mating  pathway in yeast, where the Ste5 scaffold protein binds the MAPKKK Ste11, the MAPKK  Ste7, and the MAPK Fus3.	bind
38169	7	10430	6	13	NULL	NULL	NULL	Fus3	GP		is a type of					MAPK	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_42_0_283_s_438	11807174	A good example derives from the mating  pathway in yeast, where the Ste5 scaffold protein binds the MAPKKK Ste11, the MAPKK  Ste7, and the MAPK Fus3.	bind
44399	1	10430	7	10	NULL	0	NULL	Ste5	NULL		binds	NULL				Ste11	NULL				NULL	yeast	NULL	NULL	NULL	NULL	gw70_annurevpharmacol_42_0_283_s_438	11807174	A good example derives from the mating  pathway in yeast, where the Ste5 scaffold protein binds the MAPKKK Ste11, the MAPKK  Ste7, and the MAPK Fus3.	bind
44400	2	10430	7	10	NULL	0	NULL	Ste5 	NULL		binds	NULL				Ste7	NULL				NULL	yeast	NULL	NULL	NULL	NULL	gw70_annurevpharmacol_42_0_283_s_438	11807174	A good example derives from the mating  pathway in yeast, where the Ste5 scaffold protein binds the MAPKKK Ste11, the MAPKK  Ste7, and the MAPK Fus3.	bind
44401	3	10430	7	10	NULL	0	NULL	Ste5	NULL		binds	NULL				Fus3	NULL				NULL	yeast	NULL	NULL	NULL	NULL	gw70_annurevpharmacol_42_0_283_s_438	11807174	A good example derives from the mating  pathway in yeast, where the Ste5 scaffold protein binds the MAPKKK Ste11, the MAPKK  Ste7, and the MAPK Fus3.	bind
44637	4	10430	7	NULL	NULL	0	NULL	Ste5	NULL		is a type of	NULL				scaffold protein	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevpharmacol_42_0_283_s_438	11807174	A good example derives from the mating  pathway in yeast, where the Ste5 scaffold protein binds the MAPKKK Ste11, the MAPKK  Ste7, and the MAPK Fus3.	bind
50190	5	10430	7	10	NULL	0	NULL	Ste11	NULL		is a type of	NULL				MAPKKK	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevpharmacol_42_0_283_s_438	11807174	A good example derives from the mating  pathway in yeast, where the Ste5 scaffold protein binds the MAPKKK Ste11, the MAPKK  Ste7, and the MAPK Fus3.	bind
50191	6	10430	7	10	NULL	0	NULL	Ste7	NULL		is a type of	NULL				MAPKK	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevpharmacol_42_0_283_s_438	11807174	A good example derives from the mating  pathway in yeast, where the Ste5 scaffold protein binds the MAPKKK Ste11, the MAPKK  Ste7, and the MAPK Fus3.	bind
50192	7	10430	7	10	NULL	0	NULL	Fus3	NULL		is a type of	NULL				MAPK	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevpharmacol_42_0_283_s_438	11807174	A good example derives from the mating  pathway in yeast, where the Ste5 scaffold protein binds the MAPKKK Ste11, the MAPKK  Ste7, and the MAPK Fus3.	bind
38170	1	10431	6	13	NULL	NULL	NULL	Rabenosyn-5	GP		bind					Rab5	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_2_153_s_77	12586059	A good example is Rabenosyn-5, which can bind to both Rab5 and Rab4 via distinct binding sites.	bind
38171	2	10431	6	13	NULL	NULL	NULL	Rabenosyn-5	GP		bind					Rab4	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_2_153_s_77	12586059	A good example is Rabenosyn-5, which can bind to both Rab5 and Rab4 via distinct binding sites.	bind
38172	3	10431	6	13	NULL	NULL	NULL	statement 1	Process	binding site of	is distinct from					statement 2	Process	binding site of			NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_2_153_s_77	12586059	A good example is Rabenosyn-5, which can bind to both Rab5 and Rab4 via distinct binding sites.	bind
44638	1	10431	7	NULL	NULL	0	NULL	Rabenosyn-5	NULL		bind	NULL				Rab5	NULL				NULL		0	NULL	NULL	NULL	gw60_devcell_4_2_153_s_77	12586059	A good example is Rabenosyn-5, which can bind to both Rab5 and Rab4 via distinct binding sites.	bind
44639	2	10431	7	NULL	NULL	0	NULL	Rabenosyn-5	NULL		bind	NULL				Rab4	NULL				NULL		0	NULL	NULL	NULL	gw60_devcell_4_2_153_s_77	12586059	A good example is Rabenosyn-5, which can bind to both Rab5 and Rab4 via distinct binding sites.	bind
44640	3	10431	7	NULL	NULL	0	NULL	statement 1	NULL	binding site of	is different from	NULL				statement 2	NULL	binding site of			NULL		0	NULL	NULL	NULL	gw60_devcell_4_2_153_s_77	12586059	A good example is Rabenosyn-5, which can bind to both Rab5 and Rab4 via distinct binding sites.	bind
38173	1	10432	6	13	NULL	NULL	NULL	FMOC- l-leucine	Chemical		is a type of					partial PPAR agonist	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_65_0_261_s_178	12518001	A good example of this is given  by the partial PPAR  agonist FMOC- l-leucine, which binds and activates PPAR  with weaker affinity compared with full  agonists ( 78).	bind
38174	2	10432	6	13	NULL	NULL	NULL	FMOC- l-leucine	Chemical		bind					PPAR	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_65_0_261_s_178	12518001	A good example of this is given  by the partial PPAR  agonist FMOC- l-leucine, which binds and activates PPAR  with weaker affinity compared with full  agonists ( 78).	bind
38175	3	10432	6	13	NULL	NULL	NULL	FMOC- l-leucine	Chemical		activates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_65_0_261_s_178	12518001	A good example of this is given  by the partial PPAR  agonist FMOC- l-leucine, which binds and activates PPAR  with weaker affinity compared with full  agonists ( 78).	bind
44641	1	10432	7	10	NULL	0	NULL	FMOC- l-leucine	NULL		bind	NULL				PPAR	NULL				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_65_0_261_s_178	12518001	A good example of this is given  by the partial PPAR  agonist FMOC- l-leucine, which binds and activates PPAR  with weaker affinity compared with full  agonists ( 78).	bind
44642	2	10432	7	NULL	NULL	0	NULL	FMOC- l-leucine	NULL		activates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevphysiol_65_0_261_s_178	12518001	A good example of this is given  by the partial PPAR  agonist FMOC- l-leucine, which binds and activates PPAR  with weaker affinity compared with full  agonists ( 78).	bind
44643	3	10432	7	NULL	NULL	0	NULL	FMOC- l-leucine	NULL		is a type of	NULL				partial PPAR agonist	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevphysiol_65_0_261_s_178	12518001	A good example of this is given  by the partial PPAR  agonist FMOC- l-leucine, which binds and activates PPAR  with weaker affinity compared with full  agonists ( 78).	bind
38193	1	10434	6	13	NULL	NULL	NULL	HSPG	GP	GPI-anchored;;melanoma cells	facilitates					fibronectin	GP	adhesion to 			NULL		NULL	NULL	NULL	NULL	gw60_gene_206_2_255_s_166	9469940	A GPI-anchored HSPG from melanoma cells has been shown to facilitate adhesion to fibronection (  Drake et al., 1992) and bind members of the heparin binding growth factor family (  Brunner et al., 1991).	bind
38195	2	10434	6	13	NULL	NULL	NULL	HSPG	GP	GPI-anchored;;melanoma cells	bind					members of the heparin binding growth factor family	GP				NULL		NULL	NULL	NULL	NULL	gw60_gene_206_2_255_s_166	9469940	A GPI-anchored HSPG from melanoma cells has been shown to facilitate adhesion to fibronection (  Drake et al., 1992) and bind members of the heparin binding growth factor family (  Brunner et al., 1991).	bind
44644	1	10434	7	NULL	NULL	0	NULL	HSPG	NULL	GPI-anchored;; melanoma cells	facilitate	NULL				fibronection	NULL	adhesion to			NULL		NULL	NULL	NULL	NULL	gw60_gene_206_2_255_s_166	9469940	A GPI-anchored HSPG from melanoma cells has been shown to facilitate adhesion to fibronection (  Drake et al., 1992) and bind members of the heparin binding growth factor family (  Brunner et al., 1991).	bind
44645	2	10434	7	NULL	NULL	0	NULL	HSPG	NULL	GPI-anchored;;melanoma cells	bind	NULL				heparin binding growth factor family	NULL				NULL		NULL	NULL	NULL	NULL	gw60_gene_206_2_255_s_166	9469940	A GPI-anchored HSPG from melanoma cells has been shown to facilitate adhesion to fibronection (  Drake et al., 1992) and bind members of the heparin binding growth factor family (  Brunner et al., 1991).	bind
38196	1	10436	6	13	NULL	NULL	NULL	Grb2	GP		bind					proline-rich ligands	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_10_5533_s_146	10318918	A Grb2 mutant containing a point mutation in the N-terminal SH3 domain (W36K), which renders Grb2 unable to bind proline-rich ligands ( 23), exerted significant diminished binding to NS5A (Fig.  3 B Right, lane 4).	bind
38197	2	10436	6	13	NULL	NULL	NULL	Grb2 	GP	mutant	abolishes			N-terminal SH3 domain (W36K)		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_10_5533_s_146	10318918	A Grb2 mutant containing a point mutation in the N-terminal SH3 domain (W36K), which renders Grb2 unable to bind proline-rich ligands ( 23), exerted significant diminished binding to NS5A (Fig.  3 B Right, lane 4).	bind
38198	3	10436	6	13	NULL	NULL	NULL	Grb2	GP		bind								NS5A		NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_10_5533_s_146	10318918	A Grb2 mutant containing a point mutation in the N-terminal SH3 domain (W36K), which renders Grb2 unable to bind proline-rich ligands ( 23), exerted significant diminished binding to NS5A (Fig.  3 B Right, lane 4).	bind
38199	4	10436	6	13	NULL	NULL	NULL	Grb2	GP	mutant	diminishes			N-terminal SH3 domain (W36K)		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_10_5533_s_146	10318918	A Grb2 mutant containing a point mutation in the N-terminal SH3 domain (W36K), which renders Grb2 unable to bind proline-rich ligands ( 23), exerted significant diminished binding to NS5A (Fig.  3 B Right, lane 4).	bind
44648	1	10436	7	10	NULL	0	NULL	Grb2	NULL	point mutation of	does not bind	NULL		N-terminal SH3 domain (W36K)		proline-rich ligands	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_10_5533_s_146	10318918	A Grb2 mutant containing a point mutation in the N-terminal SH3 domain (W36K), which renders Grb2 unable to bind proline-rich ligands ( 23), exerted significant diminished binding to NS5A (Fig.  3 B Right, lane 4).	bind
44649	2	10436	7	10	NULL	0	NULL	Grb2	NULL	point mutation of	diminishes	NULL		N-terminal SH3 domain (W36K)		NS5A	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_10_5533_s_146	10318918	A Grb2 mutant containing a point mutation in the N-terminal SH3 domain (W36K), which renders Grb2 unable to bind proline-rich ligands ( 23), exerted significant diminished binding to NS5A (Fig.  3 B Right, lane 4).	bind
38471	1	10437	6	13	NULL	NULL	NULL	WGA	GP		is a type of					lectin	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
38472	2	10437	6	13	NULL	NULL	NULL	LCA	GP		is a type of					lectin	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
38474	3	10437	6	13	NULL	NULL	NULL	AChE	GP		bind					LCA	GP				NULL	ANCT	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
38475	4	10437	6	13	NULL	NULL	NULL	AChE	GP		bind					WGA	GP				NULL	ANCT	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
38477	5	10437	6	13	NULL	NULL	NULL	AChE	GP		bind					LCA	GP				NULL	AC	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
38478	6	10437	6	13	NULL	NULL	NULL	AChE	GP		bind					WGA	GP				NULL	AC	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
38481	7	10437	6	13	NULL	NULL	NULL	AChE	GP		bind					LCA	GP				NULL	LCC	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
38482	8	10437	6	13	NULL	NULL	NULL	AChE	GP		bind					WGA	GP				NULL	LCC	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
38483	9	10437	6	13	NULL	NULL	NULL	AChE	GP		bind					LCA	GP				NULL	SCC	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
38487	10	10437	6	13	NULL	NULL	NULL	AChE	GP		bind					WGA	GP				NULL	SCC	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
44650	1	10437	7	NULL	NULL	0	NULL	AChE	NULL		bind	NULL				LCA	NULL				NULL	ANCT	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
44651	2	10437	7	NULL	NULL	0	NULL	AChE	NULL		bind	NULL				LCA	NULL				NULL	AC	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
44652	3	10437	7	NULL	NULL	0	NULL	AChE	NULL		bind	NULL				LCA	NULL				NULL	LCC	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
44653	4	10437	7	NULL	NULL	0	NULL	AChE	NULL		bind	NULL				LCA	NULL				NULL	SCC	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
44654	5	10437	7	NULL	NULL	0	NULL	AChE	NULL		bind	NULL				WGA	NULL				NULL	ANCT	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
44655	6	10437	7	NULL	NULL	0	NULL	AChE	NULL		bind	NULL				WGA	NULL				NULL	AC	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
44656	7	10437	7	NULL	NULL	0	NULL	AChE	NULL		bind	NULL				WGA	NULL				NULL	LCC	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
44657	8	10437	7	NULL	NULL	0	NULL	AChE	NULL		bind	NULL				WGA	NULL				NULL	SCC	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
50299	9	10437	7	10	NULL	0	NULL	LCA	NULL		is a type of	NULL				lectin	NULL				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
50301	10	10437	7	10	NULL	0	NULL	WGA	NULL		is a type of	NULL				lectin	NULL				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_3_429_s_148	16272577	A great fraction (85-100%) of AChE activity in ANCT, AC, LCC and SCC was bound by LCA and WGA, and no statistically significant differences in the percentage of binding between the above lectins and AChE in the various types of lung samples were observed ( Figure 2).	bind
38200	1	10438	6	13	NULL	NULL	NULL	curcumin-treated cells	Cell		bind					annexin probe	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_11_2155_s_134	15271854	A greater number of curcumin-treated cells than control cells bound the annexin probe, giving them a brilliant green fluorescence at the cell surface.	bind
44658	1	10438	7	10	NULL	0	NULL	curcumin-treated cells	NULL		bind	NULL				annexin probe	NULL				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_25_11_2155_s_134	15271854	A greater number of curcumin-treated cells than control cells bound the annexin probe, giving them a brilliant green fluorescence at the cell surface.	bind
38202	1	10439	6	13	NULL	NULL	NULL	apoE	GP		bind					VLDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_42_6_959_s_241	11369804	A greater number of peptide molecules compared with apoE (increased ligand-binding domains relative to one apoE) could bind VLDL; thus more Ac-hE18A-NH2-VLDL is taken up than VLDL itself.	bind
38204	2	10439	6	13	NULL	NULL	NULL	peptide molecules	GP		bind					VLDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_42_6_959_s_241	11369804	A greater number of peptide molecules compared with apoE (increased ligand-binding domains relative to one apoE) could bind VLDL; thus more Ac-hE18A-NH2-VLDL is taken up than VLDL itself.	bind
38205	3	10439	6	13	NULL	NULL	NULL	statement 2	Process		is greater than					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_42_6_959_s_241	11369804	A greater number of peptide molecules compared with apoE (increased ligand-binding domains relative to one apoE) could bind VLDL; thus more Ac-hE18A-NH2-VLDL is taken up than VLDL itself.	bind
38206	4	10439	6	13	NULL	NULL	NULL	statement 2	Process		results in					Ac-hE18A-NH2-VLDL	GP	uptake of 			NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_42_6_959_s_241	11369804	A greater number of peptide molecules compared with apoE (increased ligand-binding domains relative to one apoE) could bind VLDL; thus more Ac-hE18A-NH2-VLDL is taken up than VLDL itself.	bind
38209	5	10439	6	13	NULL	NULL	NULL	statement 2	Process		results in					VLDL	GP	uptake of 			NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_42_6_959_s_241	11369804	A greater number of peptide molecules compared with apoE (increased ligand-binding domains relative to one apoE) could bind VLDL; thus more Ac-hE18A-NH2-VLDL is taken up than VLDL itself.	bind
38210	6	10439	6	13	NULL	NULL	NULL	statement 4	Process		is more than					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_42_6_959_s_241	11369804	A greater number of peptide molecules compared with apoE (increased ligand-binding domains relative to one apoE) could bind VLDL; thus more Ac-hE18A-NH2-VLDL is taken up than VLDL itself.	bind
44659	1	10439	7	NULL	NULL	0	NULL	peptide molecules 	NULL		bind	NULL				VLDL	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_42_6_959_s_241	11369804	A greater number of peptide molecules compared with apoE (increased ligand-binding domains relative to one apoE) could bind VLDL; thus more Ac-hE18A-NH2-VLDL is taken up than VLDL itself.	bind
44660	2	10439	7	NULL	NULL	0	NULL	apoE	NULL		bind	NULL				VLDL	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_42_6_959_s_241	11369804	A greater number of peptide molecules compared with apoE (increased ligand-binding domains relative to one apoE) could bind VLDL; thus more Ac-hE18A-NH2-VLDL is taken up than VLDL itself.	bind
44661	3	10439	7	NULL	NULL	0	NULL	Ac-hE18A-NH2-VLDL	NULL	uptake of	is more than	NULL				VLDL	NULL	uptake of			NULL		0	NULL	NULL	NULL	gw60_jlipidres_42_6_959_s_241	11369804	A greater number of peptide molecules compared with apoE (increased ligand-binding domains relative to one apoE) could bind VLDL; thus more Ac-hE18A-NH2-VLDL is taken up than VLDL itself.	bind
44662	4	10439	7	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_42_6_959_s_241	11369804	A greater number of peptide molecules compared with apoE (increased ligand-binding domains relative to one apoE) could bind VLDL; thus more Ac-hE18A-NH2-VLDL is taken up than VLDL itself.	bind
44663	5	10439	7	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_42_6_959_s_241	11369804	A greater number of peptide molecules compared with apoE (increased ligand-binding domains relative to one apoE) could bind VLDL; thus more Ac-hE18A-NH2-VLDL is taken up than VLDL itself.	bind
38213	1	10440	6	13	NULL	NULL	NULL	postsynaptic gephyrins	GP		bind					GlyR	GP				NULL	transfected neurons	NULL	NULL	NULL	NULL	gw70_jneurosci_24_6_1398_s_6	14960612	A green fluorescent protein (GFP)-tagged gephyrin-binding loop of the GlyR beta subunit (GFP::betaL) was used as a surrogate for full-length receptors to characterize the GlyR binding capacity of postsynaptic gephyrins in transfected neurons.	bind
44666	1	10440	7	10	NULL	0	NULL	GlyR	NULL		bind	NULL				postsynaptic gephyrins	NULL				NULL	transfected neurons	NULL	NULL	NULL	NULL	gw70_jneurosci_24_6_1398_s_6	14960612	A green fluorescent protein (GFP)-tagged gephyrin-binding loop of the GlyR beta subunit (GFP::betaL) was used as a surrogate for full-length receptors to characterize the GlyR binding capacity of postsynaptic gephyrins in transfected neurons.	bind
38214	1	10441	6	13	NULL	NULL	NULL	DsrA	GP		bind		putative;; direct			target mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_18_6179_s_169	15342588	A grey dashed line to the right of DsrA shows putative direct DsrA  binding to other target mRNAs.	bind
44935	1	10441	7	10	NULL	0	NULL	DsrA	NULL		bind	NULL	direct;;putative			target mRNA	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_18_6179_s_169	15342588	A grey dashed line to the right of DsrA shows putative direct DsrA  binding to other target mRNAs.	bind
38216	1	10442	6	13	NULL	NULL	NULL	PHO	GP		bind					GRH	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_4_1434_s_253	16449654	A GRH-PHO complex was clearly observed, along with a concomitant decrease in the unbound probe DNA, indicating that binding of PHO to GRH increases its affinity for DNA (Fig.  6A).	bind
38217	2	10442	6	13	NULL	NULL	NULL	PHO	GP		has affinity for					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_4_1434_s_253	16449654	A GRH-PHO complex was clearly observed, along with a concomitant decrease in the unbound probe DNA, indicating that binding of PHO to GRH increases its affinity for DNA (Fig.  6A).	bind
38218	3	10442	6	13	NULL	NULL	NULL	statement 1	Process		increases					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_4_1434_s_253	16449654	A GRH-PHO complex was clearly observed, along with a concomitant decrease in the unbound probe DNA, indicating that binding of PHO to GRH increases its affinity for DNA (Fig.  6A).	bind
44936	1	10442	7	NULL	NULL	0	NULL	PHO	NULL		bind	NULL				GRH	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_4_1434_s_253	16449654	A GRH-PHO complex was clearly observed, along with a concomitant decrease in the unbound probe DNA, indicating that binding of PHO to GRH increases its affinity for DNA (Fig.  6A).	bind
44937	2	10442	7	NULL	NULL	0	NULL	GRH	NULL		has affinity for	NULL				DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_4_1434_s_253	16449654	A GRH-PHO complex was clearly observed, along with a concomitant decrease in the unbound probe DNA, indicating that binding of PHO to GRH increases its affinity for DNA (Fig.  6A).	bind
44938	3	10442	7	NULL	NULL	0	NULL	statement 1	NULL		increase	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_4_1434_s_253	16449654	A GRH-PHO complex was clearly observed, along with a concomitant decrease in the unbound probe DNA, indicating that binding of PHO to GRH increases its affinity for DNA (Fig.  6A).	bind
38219	1	10445	6	13	NULL	NULL	NULL	Shh	GP	mouse	does not bind		biochemically			Smo	GP	mouse			NULL		NULL	NULL	NULL	NULL	gw60_science_274_5291_1304_s_26	8966601	A group led by Arnon Rosenthal, a molecular neurobiologist at San Francisco's Genentech Inc., reports in  Nature that mouse Shh doesn't bind biochemically to cells producing the mouse version of Smo, but does bind to cells making mouse Ptc.	bind
38220	2	10445	6	13	NULL	NULL	NULL	Shh	GP	mouse	bind		biochemically			Ptc	GP	mouse			NULL		NULL	NULL	NULL	NULL	gw60_science_274_5291_1304_s_26	8966601	A group led by Arnon Rosenthal, a molecular neurobiologist at San Francisco's Genentech Inc., reports in  Nature that mouse Shh doesn't bind biochemically to cells producing the mouse version of Smo, but does bind to cells making mouse Ptc.	bind
44940	1	10445	7	10	NULL	0	NULL	Shh		mouse	does not bind		biochemically			Smo		mouse			NULL		NULL	NULL	NULL	NULL	gw60_science_274_5291_1304_s_26	8966601	A group led by Arnon Rosenthal, a molecular neurobiologist at San Francisco's Genentech Inc., reports in  Nature that mouse Shh doesn't bind biochemically to cells producing the mouse version of Smo, but does bind to cells making mouse Ptc.	bind
44942	2	10445	7	10	NULL	0	NULL	Shh			bind					Ptc		mouse			NULL		NULL	NULL	NULL	NULL	gw60_science_274_5291_1304_s_26	8966601	A group led by Arnon Rosenthal, a molecular neurobiologist at San Francisco's Genentech Inc., reports in  Nature that mouse Shh doesn't bind biochemically to cells producing the mouse version of Smo, but does bind to cells making mouse Ptc.	bind
38221	1	10446	6	13	NULL	NULL	NULL	Yap1p	GP		bind					Xpo1p	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_20805_s_31	11303030	A group of conserved cysteine residues adjacent to the NES is required for regulated localization of Yap1p, and oxidation of these cysteines disrupts binding of Yap1p to Xpo1p  in vitro ( 4).	bind
38238	2	10446	6	13	NULL	NULL	NULL				is required for			conserved cysteine residues adjacent to the NES		Yap1p	GP	regulated localization of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_20805_s_31	11303030	A group of conserved cysteine residues adjacent to the NES is required for regulated localization of Yap1p, and oxidation of these cysteines disrupts binding of Yap1p to Xpo1p  in vitro ( 4).	bind
38240	3	10446	6	13	NULL	NULL	NULL			oxidation of	disrupts			conserved cysteine residues adjacent to the NES		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_20805_s_31	11303030	A group of conserved cysteine residues adjacent to the NES is required for regulated localization of Yap1p, and oxidation of these cysteines disrupts binding of Yap1p to Xpo1p  in vitro ( 4).	bind
44943	1	10446	7	NULL	NULL	0	NULL	Yap1p	NULL		bind	NULL				Xpo1p	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_276_24_20805_s_31	11303030	A group of conserved cysteine residues adjacent to the NES is required for regulated localization of Yap1p, and oxidation of these cysteines disrupts binding of Yap1p to Xpo1p  in vitro ( 4).	bind
44944	2	10446	7	NULL	NULL	0	NULL		NULL	group of	is adjacent to	NULL		conserved cysteine residues			NULL		NES		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_24_20805_s_31	11303030	A group of conserved cysteine residues adjacent to the NES is required for regulated localization of Yap1p, and oxidation of these cysteines disrupts binding of Yap1p to Xpo1p  in vitro ( 4).	bind
44945	3	10446	7	NULL	NULL	0	NULL	statement 2	NULL		is required for	NULL				Yap1p	NULL	regulated localization of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_20805_s_31	11303030	A group of conserved cysteine residues adjacent to the NES is required for regulated localization of Yap1p, and oxidation of these cysteines disrupts binding of Yap1p to Xpo1p  in vitro ( 4).	bind
44946	4	10446	7	NULL	NULL	0	NULL	statement 2	NULL	oxidation of	disrupts	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_24_20805_s_31	11303030	A group of conserved cysteine residues adjacent to the NES is required for regulated localization of Yap1p, and oxidation of these cysteines disrupts binding of Yap1p to Xpo1p  in vitro ( 4).	bind
38242	1	10447	6	13	NULL	NULL	NULL	MBD	GP		is					methyl-CpG binding domain protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_40_37936_s_32	12151392	A group of the methyl-CpG binding domain proteins (MBDs) bind preferentially to methylated CpGs ( 27-30), and several of these MBD proteins associate with histone deacetylases or Mi-2, a member of the SWI2/SNF2 family of ATP-dependent chromatin-remodeling proteins ( 31-34).	bind
38243	2	10447	6	13	NULL	NULL	NULL	MBD	GP		bind		preferentially					methylated		CpGs	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_40_37936_s_32	12151392	A group of the methyl-CpG binding domain proteins (MBDs) bind preferentially to methylated CpGs ( 27-30), and several of these MBD proteins associate with histone deacetylases or Mi-2, a member of the SWI2/SNF2 family of ATP-dependent chromatin-remodeling proteins ( 31-34).	bind
38245	3	10447	6	13	NULL	NULL	NULL	MBD proteins	GP		associates with					histone deacetylases	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_40_37936_s_32	12151392	A group of the methyl-CpG binding domain proteins (MBDs) bind preferentially to methylated CpGs ( 27-30), and several of these MBD proteins associate with histone deacetylases or Mi-2, a member of the SWI2/SNF2 family of ATP-dependent chromatin-remodeling proteins ( 31-34).	bind
38246	4	10447	6	13	NULL	NULL	NULL	MBD proteins	GP		associate with					Mi-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_40_37936_s_32	12151392	A group of the methyl-CpG binding domain proteins (MBDs) bind preferentially to methylated CpGs ( 27-30), and several of these MBD proteins associate with histone deacetylases or Mi-2, a member of the SWI2/SNF2 family of ATP-dependent chromatin-remodeling proteins ( 31-34).	bind
38322	5	10447	6	13	NULL	NULL	NULL	Mi-2	GP		is a member of					SWI2/SNF2 family of ATP-dependent chromatin-remodeling protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_40_37936_s_32	12151392	A group of the methyl-CpG binding domain proteins (MBDs) bind preferentially to methylated CpGs ( 27-30), and several of these MBD proteins associate with histone deacetylases or Mi-2, a member of the SWI2/SNF2 family of ATP-dependent chromatin-remodeling proteins ( 31-34).	bind
44947	1	10447	7	10	NULL	0	NULL	MBDs	NULL		bind	NULL	preferentially				NULL	methylated		CpGs	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_40_37936_s_32	12151392	A group of the methyl-CpG binding domain proteins (MBDs) bind preferentially to methylated CpGs ( 27-30), and several of these MBD proteins associate with histone deacetylases or Mi-2, a member of the SWI2/SNF2 family of ATP-dependent chromatin-remodeling proteins ( 31-34).	bind
44948	2	10447	7	NULL	NULL	0	NULL	MBD proteins	NULL		associate with	NULL				histone deacetylases	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37936_s_32	12151392	A group of the methyl-CpG binding domain proteins (MBDs) bind preferentially to methylated CpGs ( 27-30), and several of these MBD proteins associate with histone deacetylases or Mi-2, a member of the SWI2/SNF2 family of ATP-dependent chromatin-remodeling proteins ( 31-34).	bind
44949	4	10447	7	10	NULL	0	NULL	Mi-2	NULL		is a member of	NULL				SWI2/SNF2 family of ATP-dependent chromatin-remodeling proteins	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_40_37936_s_32	12151392	A group of the methyl-CpG binding domain proteins (MBDs) bind preferentially to methylated CpGs ( 27-30), and several of these MBD proteins associate with histone deacetylases or Mi-2, a member of the SWI2/SNF2 family of ATP-dependent chromatin-remodeling proteins ( 31-34).	bind
44951	5	10447	7	NULL	NULL	0	NULL	MBDs	NULL		is	NULL				methyl-CpG binding domain proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37936_s_32	12151392	A group of the methyl-CpG binding domain proteins (MBDs) bind preferentially to methylated CpGs ( 27-30), and several of these MBD proteins associate with histone deacetylases or Mi-2, a member of the SWI2/SNF2 family of ATP-dependent chromatin-remodeling proteins ( 31-34).	bind
44952	6	10447	7	NULL	NULL	0	NULL	MBD proteins	NULL		associate with	NULL				Mi-2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37936_s_32	12151392	A group of the methyl-CpG binding domain proteins (MBDs) bind preferentially to methylated CpGs ( 27-30), and several of these MBD proteins associate with histone deacetylases or Mi-2, a member of the SWI2/SNF2 family of ATP-dependent chromatin-remodeling proteins ( 31-34).	bind
38323	1	10448	6	13	NULL	NULL	NULL	NGF	GP		mediates					survival effect	Process				NULL	neurons	NULL	NULL	NULL	NULL	gw60_neuroscience_107_2_353_s_215	11731109	A growing body of data accumulates concerning the survival effect mediated by NGF in neurons.	bind
44953	1	10448	7	NULL	NULL	0	NULL	NGF	NULL		mediates	NULL				survival effect	NULL				NULL	in neurons	0	NULL	NULL	NULL	gw60_neuroscience_107_2_353_s_215	11731109	A growing body of data accumulates concerning the survival effect mediated by NGF in neurons.	bind
38324	1	10449	6	13	NULL	NULL	NULL	transcription factor	GP		bind									cis-elements	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_259	15718508	A growing body of evidence in all cell types indicates that the binding of transcription factors to  cis-elements and subsequent gene transcription are profoundly affected by the chromatin structure.	bind
38325	2	10449	6	13	NULL	NULL	NULL	statement 1	Process		leads to					gene transcription	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_259	15718508	A growing body of evidence in all cell types indicates that the binding of transcription factors to  cis-elements and subsequent gene transcription are profoundly affected by the chromatin structure.	bind
38326	3	10449	6	13	NULL	NULL	NULL	statement 1	Process		is affected by		profoundly			chromatin structure	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_259	15718508	A growing body of evidence in all cell types indicates that the binding of transcription factors to  cis-elements and subsequent gene transcription are profoundly affected by the chromatin structure.	bind
38327	4	10449	6	13	NULL	NULL	NULL	statement 2	Process		is affected by		profoundly			chromatin structure	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_259	15718508	A growing body of evidence in all cell types indicates that the binding of transcription factors to  cis-elements and subsequent gene transcription are profoundly affected by the chromatin structure.	bind
44954	1	10449	7	10	NULL	0	NULL	 transcription factors 			bind									cis-elements	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_259	15718508	A growing body of evidence in all cell types indicates that the binding of transcription factors to  cis-elements and subsequent gene transcription are profoundly affected by the chromatin structure.	bind
44955	2	10449	7	10	NULL	0	NULL	statement 1	NULL		leads to	NULL				gene transcription	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_259	15718508	A growing body of evidence in all cell types indicates that the binding of transcription factors to  cis-elements and subsequent gene transcription are profoundly affected by the chromatin structure.	bind
44956	3	10449	7	10	NULL	0	NULL	statement 1	NULL		is affected by	NULL	profoundly			chromatin structure	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_259	15718508	A growing body of evidence in all cell types indicates that the binding of transcription factors to  cis-elements and subsequent gene transcription are profoundly affected by the chromatin structure.	bind
50193	4	10449	7	10	NULL	0	NULL	statement 2	NULL		is affected by	NULL	profoundly			chromatin structure	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_96_3_280_s_259	15718508	A growing body of evidence in all cell types indicates that the binding of transcription factors to  cis-elements and subsequent gene transcription are profoundly affected by the chromatin structure.	bind
38328	1	10450	6	13	NULL	NULL	NULL	HSP47	GP		is a type of					collagen binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9637_s_245	9545296	A growing body of evidence is accumulating that suggests a key role for the collagen binding protein HSP47 in the biosynthesis of procollagen ( 36).	bind
38329	2	10450	6	13	NULL	NULL	NULL	HSP47	GP		plays a role in					procollagen	GP	biosynthesis of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9637_s_245	9545296	A growing body of evidence is accumulating that suggests a key role for the collagen binding protein HSP47 in the biosynthesis of procollagen ( 36).	bind
44957	1	10450	7	NULL	NULL	0	NULL	HSP47	NULL		plays a role in	NULL				procollagen	NULL	biosynthesis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9637_s_245	9545296	A growing body of evidence is accumulating that suggests a key role for the collagen binding protein HSP47 in the biosynthesis of procollagen ( 36).	bind
44958	2	10450	7	NULL	NULL	0	NULL	HSP47	NULL		is a type of	NULL				collagen binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9637_s_245	9545296	A growing body of evidence is accumulating that suggests a key role for the collagen binding protein HSP47 in the biosynthesis of procollagen ( 36).	bind
38330	1	10451	6	13	NULL	NULL	NULL	IGFBP4	GP		is					insulin-like growth factor binding protein 4	GP				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
38331	2	10451	6	13	NULL	NULL	NULL	IGFBP5	GP		is					insulin-like growth factor binding protein 5	GP				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
38332	3	10451	6	13	NULL	NULL	NULL	IGFBP-4	GP		is derived from					granulosa cell	Cell				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
38333	4	10451	6	13	NULL	NULL	NULL	IGFBP5	GP		is derived from					granulosa cell	Cell				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
38334	5	10451	6	13	NULL	NULL	NULL	IGFBP4	GP		possess					antigonadotropic role	Process				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
38335	6	10451	6	13	NULL	NULL	NULL	statement 5	Process		occurs during					ovarian folliculogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
38336	7	10451	6	13	NULL	NULL	NULL	IGFBP4	GP		possess					atretogenic role	Process				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
38337	8	10451	6	13	NULL	NULL	NULL	statement 7	Process		occurs during					ovarian folliculogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
38338	9	10451	6	13	NULL	NULL	NULL	IGFBP5	GP		possess					antigonadotropic role	Process				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
38339	10	10451	6	13	NULL	NULL	NULL	statement 9	Process		occurs during					ovarian folliculogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
38340	11	10451	6	13	NULL	NULL	NULL	IGFBP5	GP		possess					atretogenic role	Process				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
38341	12	10451	6	13	NULL	NULL	NULL	statement 11	Process		occurs during					ovarian folliculogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
44959	1	10451	7	NULL	NULL	0	NULL	IGFBP4	NULL		is derived from	NULL				granulosa cell	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
44960	2	10451	7	NULL	NULL	0	NULL	IGFBP5	NULL		is derived from	NULL				granulosa cell	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
44961	3	10451	7	NULL	NULL	0	NULL	statement 1	NULL		possess	NULL				antigonadotropic role	NULL				NULL		0	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
44962	4	10451	7	NULL	NULL	0	NULL	statement 1	NULL		possess	NULL				atretogenic role	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
44963	5	10451	7	NULL	NULL	0	NULL	statement 2	NULL		possess	NULL				antigonadotropic role	NULL				NULL		0	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
44964	6	10451	7	NULL	NULL	0	NULL	statement 2	NULL		possess	NULL				atretogenic role	NULL				NULL		0	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
44965	7	10451	7	NULL	NULL	0	NULL	statement 3	NULL		during	NULL				ovarian folliculogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
44966	8	10451	7	NULL	NULL	0	NULL	statement 4	NULL		during	NULL				ovarian folliculogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
44967	9	10451	7	NULL	NULL	0	NULL	statement 5	NULL		during	NULL				ovarian folliculogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
44968	10	10451	7	NULL	NULL	0	NULL	statement 6	NULL		during	NULL				ovarian folliculogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
44969	11	10451	7	NULL	NULL	0	NULL	IGFBP	NULL		is	NULL				insulin-like growth factor binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_biolreprod_67_3_1003_s_2	12193414	A growing body of information suggests antigonadotropic and atretogenic roles for granulosa cell-derived insulin-like growth factor binding proteins (IGFBPs) 4 and 5 during ovarian folliculogenesis.	bind
38342	1	10452	6	13	NULL	NULL	NULL	human immunodeficiency virus	Organism		bind					DC-SIGN	GP				NULL		NULL	NULL	NULL	NULL	gw70_amjpathol_164_5_1587_s_29	15111305	A growing list of pathogens is bound by DC-SIGN,  including human immunodeficiency virus,  Mycobacterium tuberculosis,   Leishmania amastigotes,   and Dengue virus.	bind
38343	2	10452	6	13	NULL	NULL	NULL	Mycobacterium tuberculosis	Organism		bind					DC-SIGN	GP				NULL		NULL	NULL	NULL	NULL	gw70_amjpathol_164_5_1587_s_29	15111305	A growing list of pathogens is bound by DC-SIGN,  including human immunodeficiency virus,  Mycobacterium tuberculosis,   Leishmania amastigotes,   and Dengue virus.	bind
38344	3	10452	6	13	NULL	NULL	NULL	Leishmania amastigotes	Organism		bind					DC-SIGN	GP				NULL		NULL	NULL	NULL	NULL	gw70_amjpathol_164_5_1587_s_29	15111305	A growing list of pathogens is bound by DC-SIGN,  including human immunodeficiency virus,  Mycobacterium tuberculosis,   Leishmania amastigotes,   and Dengue virus.	bind
38345	4	10452	6	13	NULL	NULL	NULL	Dengue virus	Organism		bind					DC-SIGN	GP				NULL		NULL	NULL	NULL	NULL	gw70_amjpathol_164_5_1587_s_29	15111305	A growing list of pathogens is bound by DC-SIGN,  including human immunodeficiency virus,  Mycobacterium tuberculosis,   Leishmania amastigotes,   and Dengue virus.	bind
44970	1	10452	7	NULL	NULL	0	NULL	DC-SIGN	NULL		bind	NULL				human immunodeficiency virus	NULL				NULL		0	NULL	NULL	NULL	gw70_amjpathol_164_5_1587_s_29	15111305	A growing list of pathogens is bound by DC-SIGN,  including human immunodeficiency virus,  Mycobacterium tuberculosis,   Leishmania amastigotes,   and Dengue virus.	bind
44971	2	10452	7	NULL	NULL	0	NULL	DC-SIGN	NULL		bind	NULL				Mycobacterium tuberculosis	NULL				NULL		0	NULL	NULL	NULL	gw70_amjpathol_164_5_1587_s_29	15111305	A growing list of pathogens is bound by DC-SIGN,  including human immunodeficiency virus,  Mycobacterium tuberculosis,   Leishmania amastigotes,   and Dengue virus.	bind
44972	3	10452	7	NULL	NULL	0	NULL	DC-SIGN	NULL		bind	NULL				Leishmania amastigotes	NULL				NULL		0	NULL	NULL	NULL	gw70_amjpathol_164_5_1587_s_29	15111305	A growing list of pathogens is bound by DC-SIGN,  including human immunodeficiency virus,  Mycobacterium tuberculosis,   Leishmania amastigotes,   and Dengue virus.	bind
44973	4	10452	7	NULL	NULL	0	NULL	DC-SIGN	NULL		bind	NULL				Dengue virus	NULL				NULL		0	NULL	NULL	NULL	gw70_amjpathol_164_5_1587_s_29	15111305	A growing list of pathogens is bound by DC-SIGN,  including human immunodeficiency virus,  Mycobacterium tuberculosis,   Leishmania amastigotes,   and Dengue virus.	bind
38358	1	10454	6	13	NULL	NULL	NULL	GLUT1	GP		is a type of					glucose transporter	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38359	2	10454	6	13	NULL	NULL	NULL	GLUT1	GP		is a type of					membrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38360	3	10454	6	13	NULL	NULL	NULL	transmembrane Semaphorin-F	GP		is a type of					membrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38361	4	10454	6	13	NULL	NULL	NULL	neurophilin-1	GP		is a type of					membrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38362	5	10454	6	13	NULL	NULL	NULL	syndecan-4	GP		is a type of					membrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38363	6	10454	6	13	NULL	NULL	NULL	tyrosinase-related protein-1	GP		is a type of					membrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38364	7	10454	6	13	NULL	NULL	NULL	alpha5 integrin	GP		is a type of					membrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38365	8	10454	6	13	NULL	NULL	NULL	alpha6 integrin	GP		is a type of					membrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38366	9	10454	6	13	NULL	NULL	NULL	type III transforming growth factor-beta receptor	GP		is a type of					membrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38367	10	10454	6	13	NULL	NULL	NULL	insulin-like growth factor 1 receptor	GP		is a type of					membrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38368	11	10454	6	13	NULL	NULL	NULL	megalin	GP		is a type of					membrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38369	12	10454	6	13	NULL	NULL	NULL	5T4 antigen	GP		is a type of					membrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38370	13	10454	6	13	NULL	NULL	NULL	beta1-adrenergic receptor	GP		is a type of					membrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38371	14	10454	6	13	NULL	NULL	NULL	GIPC	GP		bind			PDZ domain		GLUT1	GP		C-terminus		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38372	15	10454	6	13	NULL	NULL	NULL	GIPC	GP		bind			PDZ domain		transmembrane Semaphorin-F	GP		C-termini		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38373	16	10454	6	13	NULL	NULL	NULL	GIPC	GP		bind			PDZ domain		neurophilin-1	GP		C-termini		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38374	17	10454	6	13	NULL	NULL	NULL	GIPC	GP		bind			PDZ domain		syndecan-4	GP		C-termini		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38375	18	10454	6	13	NULL	NULL	NULL	GIPC	GP		bind			PDZ domain		tyrosinase-related protein-1	GP		C-termini		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38376	19	10454	6	13	NULL	NULL	NULL	GIPC	GP		bind			PDZ domain		alpha5 integrin	GP		C-termini		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38377	20	10454	6	13	NULL	NULL	NULL	GIPC	GP		bind			PDZ domain		alpha6 integrin	GP		C-termini		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38378	21	10454	6	13	NULL	NULL	NULL	GIPC	GP		bind			PDZ domain		type III transforming growth factor-beta receptor	GP		C-termini		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38379	22	10454	6	13	NULL	NULL	NULL	GIPC	GP		bind			PDZ domain		insulin-like growth factor 1 receptor	GP		C-termini		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38380	23	10454	6	13	NULL	NULL	NULL	GIPC	GP		bind			PDZ domain		megalin	GP		C-termini		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38381	24	10454	6	13	NULL	NULL	NULL	GIPC	GP		bind			PDZ domain		5T4 antigen	GP		C-termini		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38382	25	10454	6	13	NULL	NULL	NULL	GIPC	GP		bind			PDZ domain		beta1-adrenergic receptor	GP		C-termini		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
44974	1	10454	7	NULL	NULL	0	NULL	GLUT1	NULL		bind	NULL		C terminus		GIPC	NULL		PDZ domain 		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
44975	2	10454	7	NULL	NULL	0	NULL	Semaphorin-F	NULL		bind	NULL		C-terminus		GIPC	NULL		PDZ domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
44994	3	10454	7	NULL	NULL	0	NULL	neurophilin-1	NULL		bind	NULL		C terminus		GIPC	NULL		PDZ domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
44997	4	10454	7	NULL	NULL	0	NULL	syndecan-4 	NULL		bind	NULL		C terminus		GIPC	NULL		PDZ domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
44998	5	10454	7	NULL	NULL	0	NULL	tyrosinase-related protein-1	NULL		bind	NULL		C terminus		GIPC	NULL		PDZ domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
45001	6	10454	7	NULL	NULL	0	NULL	integrin	NULL		bind	NULL		alpha5 subunit		GIPC	NULL		PDZ domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
45003	7	10454	7	NULL	NULL	0	NULL	integrin	NULL		bind	NULL		alpha6 subunit		GIPC	NULL		PDZ domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
45004	8	10454	7	NULL	NULL	0	NULL	type III transforming growth factor-beta receptor	NULL		bind	NULL		C terminus		GIPC	NULL		PDZ domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
45007	9	10454	7	NULL	NULL	0	NULL	insulin-like growth factor 1 receptor 	NULL		bind	NULL		C terminus		GIPC	NULL		PDZ domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
45049	10	10454	7	NULL	NULL	0	NULL	megalin	NULL		bind	NULL		C terminus		GIPC	NULL		PDZ domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
45050	11	10454	7	NULL	NULL	0	NULL	5T4 antigen	NULL		bind	NULL		C terminus		GIPC	NULL		PDZ domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
45051	12	10454	7	NULL	NULL	0	NULL	beta1-adrenergic receptor	NULL		bind	NULL		C terminus		GIPC	NULL		PDZ domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
45052	13	10454	7	NULL	NULL	0	NULL	GLUT1	NULL		is a type of	NULL				glucose transporter	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
50286	14	10454	7	NULL	NULL	0	NULL	GLUT1 	NULL		is a type of	NULL				membrane protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
50287	15	10454	7	NULL	NULL	0	NULL	Semaphorin-F	NULL		is a type of	NULL				transmembrane protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
50288	16	10454	7	NULL	NULL	0	NULL	neurophilin-1	NULL		is a type of	NULL				membrane protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
50289	17	10454	7	NULL	NULL	0	NULL	syndecan-4	NULL		is a type of	NULL				membrane protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
50290	18	10454	7	NULL	NULL	0	NULL	 tyrosinase-related protein-1	NULL		is a type of	NULL				membrane protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
50291	19	10454	7	NULL	NULL	0	NULL	 integrin	NULL		is a type of	NULL				membrane protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
50292	20	10454	7	NULL	NULL	0	NULL	type III transforming growth factor-beta receptor	NULL		is a type of	NULL				membrane protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
50293	21	10454	7	NULL	NULL	0	NULL	insulin-like growth factor 1 receptor 	NULL		is a type of	NULL				membrane protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
50294	22	10454	7	NULL	NULL	0	NULL	megalin	NULL		is a type of	NULL				membrane protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
50295	23	10454	7	NULL	NULL	0	NULL	5T4 antigen	NULL		is a type of	NULL				membrane protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
50296	24	10454	7	NULL	NULL	0	NULL	beta1-adrenergic receptor	NULL		is a type of	NULL				membrane protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_49348_s_269	14507927	A growing number of membrane proteins that bind to the PDZ domain of GIPC through their C termini include the glucose transporter GLUT1 ( ), transmembrane Semaphorin-F ( ), neurophilin-1 ( ), syndecan-4 ( ), tyrosinase-related protein-1 ( ), the alpha5 and alpha6 subunits of integrin ( ), the type III transforming growth factor-beta receptor ( ), the insulin-like growth factor 1 receptor ( ), megalin ( ), the 5T4 antigen ( ), and the beta1-adrenergic receptor ( ).	bind
38348	1	10455	6	13	NULL	NULL	NULL	epidermal growth factor	GP		is a type of					growth factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
38349	2	10455	6	13	NULL	NULL	NULL	Bmi-1	GP		is a type of					polycomb group repressor	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
38350	3	10455	6	13	NULL	NULL	NULL	Bmi-1	GP		control					hTERT	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
38351	4	10455	6	13	NULL	NULL	NULL	protein	GP		bind					hTERT	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
38352	5	10455	6	13	NULL	NULL	NULL	statement 3	Process		occurs via					statement 4	Process	regulation of			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
38353	6	10455	6	13	NULL	NULL	NULL	epidermal growth factor	GP		is a type of					putative hTERT regulator	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
38354	7	10455	6	13	NULL	NULL	NULL	Bmi-1	GP		is a type of					putative hTERT regulator	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
38355	8	10455	6	13	NULL	NULL	NULL	stress-activated protein kinase signaling pathway	Process		is a type of					putative hTERT regulator	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
38356	9	10455	6	13	NULL	NULL	NULL	protein kinases	GP		are involved in					mitogen-activated protein kinase signaling pathway	Process				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
38357	10	10455	6	13	NULL	NULL	NULL	statement 9	GP		is a type of					putative hTERT regulator	GP				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
45055	1	10455	7	NULL	NULL	0	NULL	epidermal growth factor	NULL		is a type of	NULL				growth factor	NULL				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
45056	2	10455	7	NULL	NULL	0	NULL	epidermal growth factor	NULL		is a type of	NULL				putative hTERT regulator	NULL				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
45058	3	10455	7	NULL	NULL	0	NULL	protein kinases	NULL		involved in	NULL				mitogen-activated protein kinase signaling pathway	NULL				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
45059	4	10455	7	NULL	NULL	0	NULL	statement 3	NULL		is a type of	NULL				putative hTERT regulator	NULL				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
45062	5	10455	7	NULL	NULL	0	NULL	protein kinases	NULL		involved in	NULL				stress-activated protein kinase signaling pathway	NULL				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
45064	6	10455	7	NULL	NULL	0	NULL	statement 5	NULL		is a type of	NULL				putative hTERT regulator	NULL				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
45066	7	10455	7	NULL	NULL	0	NULL	Bmi-1	NULL		is a type of	NULL				oncogenic Polycomb group repressor 	NULL				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
45067	8	10455	7	NULL	NULL	0	NULL	Bmi-1	NULL		control	NULL				hTERT	NULL	transcription of			NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
45068	9	10455	7	NULL	NULL	0	NULL	proteins	NULL		bind	NULL				hTERT	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
45069	10	10455	7	NULL	NULL	0	NULL	statement 8	NULL		occur through	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1167_s_181	12807729	A growing number of protein factors are being added to the list of putative  hTERT regulators, including growth factors (e.g. epidermal growth factor) ( ), protein kinases involved in the mitogen-activated protein kinase signaling pathway ( , ) and the stress-activated protein kinase signaling pathway ( ), and an oncogenic, Polycomb group repressor Bmi-1 ( ), which appear to control the  hTERT transcription through the regulation of known or unknown proteins binding to the  hTERT promoter.	bind
38346	1	10457	6	13	NULL	NULL	NULL	growth factor receptor-bound protein 2	GP		bind			SH3 domain		SOS	GP				NULL		NULL	NULL	NULL	NULL	gw70_jimmunol_177_1_147_s_166	16785509	A growth factor receptor-bound protein 2 binds to a guanine nucleotide-exchange factor SOS through the SH3 domain.	bind
38347	2	10457	6	13	NULL	NULL	NULL	SOS	GP		is a type of					guanine nucleotide-exchange factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jimmunol_177_1_147_s_166	16785509	A growth factor receptor-bound protein 2 binds to a guanine nucleotide-exchange factor SOS through the SH3 domain.	bind
45071	1	10457	7	NULL	NULL	0	NULL	growth factor receptor-bound protein 2	NULL		bind	NULL		SH3 domain		SOS	NULL				NULL		0	NULL	NULL	NULL	gw70_jimmunol_177_1_147_s_166	16785509	A growth factor receptor-bound protein 2 binds to a guanine nucleotide-exchange factor SOS through the SH3 domain.	bind
45072	2	10457	7	NULL	NULL	0	NULL	SOS	NULL		is a type of	NULL				guanine nucleotide-exchange factor	NULL				NULL		0	NULL	NULL	NULL	gw70_jimmunol_177_1_147_s_166	16785509	A growth factor receptor-bound protein 2 binds to a guanine nucleotide-exchange factor SOS through the SH3 domain.	bind
39060	1	10458	6	13	NULL	NULL	NULL	NR2B	GP		is expressed in					COS7 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_11_4189_s_239	10341223	A GST fusion containing only the PDZ domain of MALS-2 [GST:MALS-2(PDZ)] binds NR2B expressed in COS7 cells, whereas an MALS-2 construct containing only the unique N-terminal region [GST:MALS-2(N70)] is inactive (Fig.  9 A).	bind
39061	2	10458	6	13	NULL	NULL	NULL	GST-fusion protein	GP		contains					MALS-2	GP		PDZ domain		NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_11_4189_s_239	10341223	A GST fusion containing only the PDZ domain of MALS-2 [GST:MALS-2(PDZ)] binds NR2B expressed in COS7 cells, whereas an MALS-2 construct containing only the unique N-terminal region [GST:MALS-2(N70)] is inactive (Fig.  9 A).	bind
39062	3	10458	6	13	NULL	NULL	NULL	statement 2	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_11_4189_s_239	10341223	A GST fusion containing only the PDZ domain of MALS-2 [GST:MALS-2(PDZ)] binds NR2B expressed in COS7 cells, whereas an MALS-2 construct containing only the unique N-terminal region [GST:MALS-2(N70)] is inactive (Fig.  9 A).	bind
39063	4	10458	6	13	NULL	NULL	NULL	GST:MALS-2(PDZ)	GP		is					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_11_4189_s_239	10341223	A GST fusion containing only the PDZ domain of MALS-2 [GST:MALS-2(PDZ)] binds NR2B expressed in COS7 cells, whereas an MALS-2 construct containing only the unique N-terminal region [GST:MALS-2(N70)] is inactive (Fig.  9 A).	bind
39064	5	10458	6	13	NULL	NULL	NULL	MALS-2 construct	GP		contains							unique	N-terminal region		NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_11_4189_s_239	10341223	A GST fusion containing only the PDZ domain of MALS-2 [GST:MALS-2(PDZ)] binds NR2B expressed in COS7 cells, whereas an MALS-2 construct containing only the unique N-terminal region [GST:MALS-2(N70)] is inactive (Fig.  9 A).	bind
39065	6	10458	6	13	NULL	NULL	NULL	GST:MALS-2(N70)	GP		is					statement 5	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_11_4189_s_239	10341223	A GST fusion containing only the PDZ domain of MALS-2 [GST:MALS-2(PDZ)] binds NR2B expressed in COS7 cells, whereas an MALS-2 construct containing only the unique N-terminal region [GST:MALS-2(N70)] is inactive (Fig.  9 A).	bind
39066	7	10458	6	13	NULL	NULL	NULL	statement 5	GP		is					inactive					NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_11_4189_s_239	10341223	A GST fusion containing only the PDZ domain of MALS-2 [GST:MALS-2(PDZ)] binds NR2B expressed in COS7 cells, whereas an MALS-2 construct containing only the unique N-terminal region [GST:MALS-2(N70)] is inactive (Fig.  9 A).	bind
45073	1	10458	7	NULL	NULL	0	NULL	NR2B	NULL		is expressed in	NULL				COS7 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_11_4189_s_239	10341223	A GST fusion containing only the PDZ domain of MALS-2 [GST:MALS-2(PDZ)] binds NR2B expressed in COS7 cells, whereas an MALS-2 construct containing only the unique N-terminal region [GST:MALS-2(N70)] is inactive (Fig.  9 A).	bind
45074	2	10458	7	NULL	NULL	0	NULL	GST:MALS-2(PDZ)	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_11_4189_s_239	10341223	A GST fusion containing only the PDZ domain of MALS-2 [GST:MALS-2(PDZ)] binds NR2B expressed in COS7 cells, whereas an MALS-2 construct containing only the unique N-terminal region [GST:MALS-2(N70)] is inactive (Fig.  9 A).	bind
45076	3	10458	7	NULL	NULL	0	NULL	GST:MALS-2(N70)	NULL		contains	NULL				MALS-2 construct	NULL		unique N-terminal region 		NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_11_4189_s_239	10341223	A GST fusion containing only the PDZ domain of MALS-2 [GST:MALS-2(PDZ)] binds NR2B expressed in COS7 cells, whereas an MALS-2 construct containing only the unique N-terminal region [GST:MALS-2(N70)] is inactive (Fig.  9 A).	bind
45077	4	10458	7	NULL	NULL	0	NULL	statement 3	NULL		is a type of	NULL				inactive construct	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_11_4189_s_239	10341223	A GST fusion containing only the PDZ domain of MALS-2 [GST:MALS-2(PDZ)] binds NR2B expressed in COS7 cells, whereas an MALS-2 construct containing only the unique N-terminal region [GST:MALS-2(N70)] is inactive (Fig.  9 A).	bind
45078	5	10458	7	NULL	NULL	0	NULL	GST:MALS-2(PDZ)	NULL		contains	NULL				MALS-2	NULL		PDZ domain		NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_11_4189_s_239	10341223	A GST fusion containing only the PDZ domain of MALS-2 [GST:MALS-2(PDZ)] binds NR2B expressed in COS7 cells, whereas an MALS-2 construct containing only the unique N-terminal region [GST:MALS-2(N70)] is inactive (Fig.  9 A).	bind
38498	1	10459	6	13	NULL	NULL	NULL	deltakinase MEK5	GP		bind					ERK5	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_6_2065_s_55	16507987	A GST fusion of MEK5 residues 18 to 165 (deltakinase MEK5) that includes the PB1 domain, but not the kinase domain binds ERK5 (Fig.  1A).	bind
39067	2	10459	6	13	NULL	NULL	NULL	deltakinase MEK5	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_6_2065_s_55	16507987	A GST fusion of MEK5 residues 18 to 165 (deltakinase MEK5) that includes the PB1 domain, but not the kinase domain binds ERK5 (Fig.  1A).	bind
39068	3	10459	6	13	NULL	NULL	NULL	deltakinase MEK5	GP		includes								PB1 domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_6_2065_s_55	16507987	A GST fusion of MEK5 residues 18 to 165 (deltakinase MEK5) that includes the PB1 domain, but not the kinase domain binds ERK5 (Fig.  1A).	bind
39069	4	10459	6	13	NULL	NULL	NULL	deltakinase MEK5	GP		does not include								kinase domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_6_2065_s_55	16507987	A GST fusion of MEK5 residues 18 to 165 (deltakinase MEK5) that includes the PB1 domain, but not the kinase domain binds ERK5 (Fig.  1A).	bind
50194	1	10459	6	13	NULL	NULL	NULL	deltakinase MEK5	GP		contains					MEK5	GP		18-165		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_6_2065_s_55	16507987	A GST fusion of MEK5 residues 18 to 165 (deltakinase MEK5) that includes the PB1 domain, but not the kinase domain binds ERK5 (Fig.  1A).	bind
45079	1	10459	7	NULL	NULL	0	NULL	deltakinase MEK5	NULL		contains	NULL				MEK5 residues	NULL		18-165		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_6_2065_s_55	16507987	A GST fusion of MEK5 residues 18 to 165 (deltakinase MEK5) that includes the PB1 domain, but not the kinase domain binds ERK5 (Fig.  1A).	bind
45080	2	10459	7	NULL	NULL	0	NULL	deltakinase MEK5	NULL		contains	NULL					NULL		PB1 domain		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_6_2065_s_55	16507987	A GST fusion of MEK5 residues 18 to 165 (deltakinase MEK5) that includes the PB1 domain, but not the kinase domain binds ERK5 (Fig.  1A).	bind
45082	3	10459	7	10	NULL	0	NULL	deltakinase MEK5	NULL		does not contain	NULL					NULL		kinase domain		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_6_2065_s_55	16507987	A GST fusion of MEK5 residues 18 to 165 (deltakinase MEK5) that includes the PB1 domain, but not the kinase domain binds ERK5 (Fig.  1A).	bind
45084	4	10459	7	10	NULL	0	NULL	deltakinase MEK5	NULL		binds	NULL				ERK5	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_6_2065_s_55	16507987	A GST fusion of MEK5 residues 18 to 165 (deltakinase MEK5) that includes the PB1 domain, but not the kinase domain binds ERK5 (Fig.  1A).	bind
45085	5	10459	7	10	NULL	0	NULL	deltakinase MEK5	NULL		is a type of	NULL				GST fusion protein	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_6_2065_s_55	16507987	A GST fusion of MEK5 residues 18 to 165 (deltakinase MEK5) that includes the PB1 domain, but not the kinase domain binds ERK5 (Fig.  1A).	bind
38512	2	10460	6	13	NULL	NULL	NULL	statement 1	GP		bind					Axin-RGS	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_10_2270_s_71	10811618	A GST fusion of the 25 amino acid APC SAMP3 repeat alone bound to Axin-RGS as well as the longest fragment tested (Figure  2B).	bind
50195	1	10460	6	13	NULL	NULL	NULL	GST fusion protein	GP		contains					APC	GP		SAMP3 repeat 		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_10_2270_s_71	10811618	A GST fusion of the 25 amino acid APC SAMP3 repeat alone bound to Axin-RGS as well as the longest fragment tested (Figure  2B).	bind
45086	1	10460	7	10	NULL	0	NULL	GST fusion protein			contains					APC			SAMP3 repeat		NULL		NULL	NULL	NULL	NULL	gw60_embo_19_10_2270_s_71	10811618	A GST fusion of the 25 amino acid APC SAMP3 repeat alone bound to Axin-RGS as well as the longest fragment tested (Figure  2B).	bind
45087	2	10460	7	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				Axin-RGS	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_19_10_2270_s_71	10811618	A GST fusion of the 25 amino acid APC SAMP3 repeat alone bound to Axin-RGS as well as the longest fragment tested (Figure  2B).	bind
39070	1	10461	6	13	NULL	NULL	NULL	amphiphysin 1	GP		bind			first 150 amino acids		amphiphysin 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5378_821_s_65	9694653	A GST fusion protein comprising the first 150 amino acids of amphiphysin 1 bound to both amphiphysins 1 and 2 in an overlay assay ( Fig. 2B), indicating that dimerization is mediated by this coiled-coil region of amphiphysin; this suggests the possibility that both heterodimers and homodimers are present.	bind
39071	2	10461	6	13	NULL	NULL	NULL	statement 1	Process		is					homodimerization	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5378_821_s_65	9694653	A GST fusion protein comprising the first 150 amino acids of amphiphysin 1 bound to both amphiphysins 1 and 2 in an overlay assay ( Fig. 2B), indicating that dimerization is mediated by this coiled-coil region of amphiphysin; this suggests the possibility that both heterodimers and homodimers are present.	bind
39072	3	10461	6	13	NULL	NULL	NULL	amphiphysin 1	GP		bind			first 150 amino acids		amphiphysin 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5378_821_s_65	9694653	A GST fusion protein comprising the first 150 amino acids of amphiphysin 1 bound to both amphiphysins 1 and 2 in an overlay assay ( Fig. 2B), indicating that dimerization is mediated by this coiled-coil region of amphiphysin; this suggests the possibility that both heterodimers and homodimers are present.	bind
39073	4	10461	6	13	NULL	NULL	NULL	amphiphysin	GP		mediates			coiled-coil region		amphiphysin	GP	dimerization of			NULL		NULL	NULL	NULL	NULL	gw60_science_281_5378_821_s_65	9694653	A GST fusion protein comprising the first 150 amino acids of amphiphysin 1 bound to both amphiphysins 1 and 2 in an overlay assay ( Fig. 2B), indicating that dimerization is mediated by this coiled-coil region of amphiphysin; this suggests the possibility that both heterodimers and homodimers are present.	bind
40395	5	10461	6	13	NULL	NULL	NULL	statement 3	Process		is					heterodimerization	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5378_821_s_65	9694653	A GST fusion protein comprising the first 150 amino acids of amphiphysin 1 bound to both amphiphysins 1 and 2 in an overlay assay ( Fig. 2B), indicating that dimerization is mediated by this coiled-coil region of amphiphysin; this suggests the possibility that both heterodimers and homodimers are present.	bind
45088	1	10461	7	NULL	NULL	0	NULL	GST fusion protein	NULL		comprise	NULL				amphiphysin 1	NULL		first 150 amino acids		NULL		0	NULL	NULL	NULL	gw60_science_281_5378_821_s_65	9694653	A GST fusion protein comprising the first 150 amino acids of amphiphysin 1 bound to both amphiphysins 1 and 2 in an overlay assay ( Fig. 2B), indicating that dimerization is mediated by this coiled-coil region of amphiphysin; this suggests the possibility that both heterodimers and homodimers are present.	bind
45089	2	10461	7	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				amphiphysin 1	NULL				NULL		0	NULL	NULL	NULL	gw60_science_281_5378_821_s_65	9694653	A GST fusion protein comprising the first 150 amino acids of amphiphysin 1 bound to both amphiphysins 1 and 2 in an overlay assay ( Fig. 2B), indicating that dimerization is mediated by this coiled-coil region of amphiphysin; this suggests the possibility that both heterodimers and homodimers are present.	bind
45090	3	10461	7	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				amphiphysin 2	NULL				NULL		0	NULL	NULL	NULL	gw60_science_281_5378_821_s_65	9694653	A GST fusion protein comprising the first 150 amino acids of amphiphysin 1 bound to both amphiphysins 1 and 2 in an overlay assay ( Fig. 2B), indicating that dimerization is mediated by this coiled-coil region of amphiphysin; this suggests the possibility that both heterodimers and homodimers are present.	bind
45091	4	10461	7	10	NULL	0	NULL	amphiphysin			mediates			coiled-coil region		amphiphysin 		dimerization of			NULL		NULL	NULL	NULL	NULL	gw60_science_281_5378_821_s_65	9694653	A GST fusion protein comprising the first 150 amino acids of amphiphysin 1 bound to both amphiphysins 1 and 2 in an overlay assay ( Fig. 2B), indicating that dimerization is mediated by this coiled-coil region of amphiphysin; this suggests the possibility that both heterodimers and homodimers are present.	bind
45092	5	10461	7	NULL	NULL	0	NULL	statement 2	NULL		indicate	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_science_281_5378_821_s_65	9694653	A GST fusion protein comprising the first 150 amino acids of amphiphysin 1 bound to both amphiphysins 1 and 2 in an overlay assay ( Fig. 2B), indicating that dimerization is mediated by this coiled-coil region of amphiphysin; this suggests the possibility that both heterodimers and homodimers are present.	bind
45093	6	10461	7	NULL	NULL	0	NULL	statement 3	NULL		indicate	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_science_281_5378_821_s_65	9694653	A GST fusion protein comprising the first 150 amino acids of amphiphysin 1 bound to both amphiphysins 1 and 2 in an overlay assay ( Fig. 2B), indicating that dimerization is mediated by this coiled-coil region of amphiphysin; this suggests the possibility that both heterodimers and homodimers are present.	bind
45094	7	10461	7	NULL	NULL	0	NULL	statement 5	NULL		suggests	NULL				homodimers	NULL	possibility of			NULL		0	NULL	NULL	NULL	gw60_science_281_5378_821_s_65	9694653	A GST fusion protein comprising the first 150 amino acids of amphiphysin 1 bound to both amphiphysins 1 and 2 in an overlay assay ( Fig. 2B), indicating that dimerization is mediated by this coiled-coil region of amphiphysin; this suggests the possibility that both heterodimers and homodimers are present.	bind
45095	8	10461	7	NULL	NULL	0	NULL	statement 6	NULL		suggests	NULL				heterodimers	NULL	possibility of			NULL		0	NULL	NULL	NULL	gw60_science_281_5378_821_s_65	9694653	A GST fusion protein comprising the first 150 amino acids of amphiphysin 1 bound to both amphiphysins 1 and 2 in an overlay assay ( Fig. 2B), indicating that dimerization is mediated by this coiled-coil region of amphiphysin; this suggests the possibility that both heterodimers and homodimers are present.	bind
38516	3	10462	6	13	NULL	NULL	NULL	GST-DN	GP		bind		efficiently			LIS1	GP				NULL	brain homogenates	NULL	NULL	NULL	NULL	gw60_neuron_28_3_665_s_113	11163258	A GST fusion protein containing amino acids 88-156 of mNudE (GST-DN) efficiently bound LIS1 from brain homogenates (  Figure 2B), suggesting that the LIS1 binding domain lies between amino acids 90 and 156.	bind
38517	4	10462	6	10	NULL	0	NULL		NULL		lies between	NULL		LIS1 binding domain			NULL		amino acids 90 and 156		NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_3_665_s_113	11163258	A GST fusion protein containing amino acids 88-156 of mNudE (GST-DN) efficiently bound LIS1 from brain homogenates (  Figure 2B), suggesting that the LIS1 binding domain lies between amino acids 90 and 156.	bind
50196	1	10462	6	13	NULL	NULL	NULL	GST fusion protein	GP		contains					mNudE	GP		amino acids 88-156		NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_3_665_s_113	11163258	A GST fusion protein containing amino acids 88-156 of mNudE (GST-DN) efficiently bound LIS1 from brain homogenates (  Figure 2B), suggesting that the LIS1 binding domain lies between amino acids 90 and 156.	bind
50197	2	10462	6	13	NULL	NULL	NULL	GST-DN	GP		is					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_3_665_s_113	11163258	A GST fusion protein containing amino acids 88-156 of mNudE (GST-DN) efficiently bound LIS1 from brain homogenates (  Figure 2B), suggesting that the LIS1 binding domain lies between amino acids 90 and 156.	bind
45136	1	10462	7	NULL	NULL	0	NULL	GST fusion protein	NULL		contains	NULL				mNudE	NULL		amino acids 88-156		NULL		0	NULL	NULL	NULL	gw60_neuron_28_3_665_s_113	11163258	A GST fusion protein containing amino acids 88-156 of mNudE (GST-DN) efficiently bound LIS1 from brain homogenates (  Figure 2B), suggesting that the LIS1 binding domain lies between amino acids 90 and 156.	bind
45137	2	10462	7	10	NULL	0	NULL	GST-DN	NULL		bind	NULL	efficiently			LIS1	NULL				NULL	brain homogenates	NULL	NULL	NULL	NULL	gw60_neuron_28_3_665_s_113	11163258	A GST fusion protein containing amino acids 88-156 of mNudE (GST-DN) efficiently bound LIS1 from brain homogenates (  Figure 2B), suggesting that the LIS1 binding domain lies between amino acids 90 and 156.	bind
45138	3	10462	7	NULL	NULL	0	NULL	GST-DN	NULL		is	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_3_665_s_113	11163258	A GST fusion protein containing amino acids 88-156 of mNudE (GST-DN) efficiently bound LIS1 from brain homogenates (  Figure 2B), suggesting that the LIS1 binding domain lies between amino acids 90 and 156.	bind
45139	4	10462	7	10	NULL	0	NULL		NULL		lies between	NULL		LIS1 binding domain			NULL		amino acids 90 and 156		NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_3_665_s_113	11163258	A GST fusion protein containing amino acids 88-156 of mNudE (GST-DN) efficiently bound LIS1 from brain homogenates (  Figure 2B), suggesting that the LIS1 binding domain lies between amino acids 90 and 156.	bind
39074	1	10463	6	13	NULL	NULL	NULL	GST-fusion protein	GP		contains					Grb2	GP	full length			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27804_s_120	9346925	A GST fusion protein containing full-length Grb2 bound HPK1 more tightly than either SH3 domain alone, indicating that the two SH3 domains of Grb2 may bind HPK1 in a bidentate fashion, as suggested by the two-hybrid analysis.	bind
39075	2	10463	6	13	NULL	NULL	NULL	statement 1	GP		bind					HPK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27804_s_120	9346925	A GST fusion protein containing full-length Grb2 bound HPK1 more tightly than either SH3 domain alone, indicating that the two SH3 domains of Grb2 may bind HPK1 in a bidentate fashion, as suggested by the two-hybrid analysis.	bind
39076	3	10463	6	13	NULL	NULL	NULL	Grb2	GP		bind			SH3 domain		HPK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27804_s_120	9346925	A GST fusion protein containing full-length Grb2 bound HPK1 more tightly than either SH3 domain alone, indicating that the two SH3 domains of Grb2 may bind HPK1 in a bidentate fashion, as suggested by the two-hybrid analysis.	bind
39077	4	10463	6	13	NULL	NULL	NULL	statement 2	Process		is tighter than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27804_s_120	9346925	A GST fusion protein containing full-length Grb2 bound HPK1 more tightly than either SH3 domain alone, indicating that the two SH3 domains of Grb2 may bind HPK1 in a bidentate fashion, as suggested by the two-hybrid analysis.	bind
39078	5	10463	6	13	NULL	NULL	NULL	statement 3	Process		occurs in a 					bidentate fashion	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27804_s_120	9346925	A GST fusion protein containing full-length Grb2 bound HPK1 more tightly than either SH3 domain alone, indicating that the two SH3 domains of Grb2 may bind HPK1 in a bidentate fashion, as suggested by the two-hybrid analysis.	bind
45140	1	10463	7	NULL	NULL	0	NULL	GST fusion protein	NULL		contains	NULL				Grb2	NULL	full-length			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27804_s_120	9346925	A GST fusion protein containing full-length Grb2 bound HPK1 more tightly than either SH3 domain alone, indicating that the two SH3 domains of Grb2 may bind HPK1 in a bidentate fashion, as suggested by the two-hybrid analysis.	bind
45141	2	10463	7	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL	tightly			HPK1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27804_s_120	9346925	A GST fusion protein containing full-length Grb2 bound HPK1 more tightly than either SH3 domain alone, indicating that the two SH3 domains of Grb2 may bind HPK1 in a bidentate fashion, as suggested by the two-hybrid analysis.	bind
45142	3	10463	7	10	NULL	0	NULL	Grb2	NULL		bind	NULL		SH3 domain		HPK1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27804_s_120	9346925	A GST fusion protein containing full-length Grb2 bound HPK1 more tightly than either SH3 domain alone, indicating that the two SH3 domains of Grb2 may bind HPK1 in a bidentate fashion, as suggested by the two-hybrid analysis.	bind
45143	4	10463	7	NULL	NULL	0	NULL	statement 2	NULL		occurs more tightly than	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27804_s_120	9346925	A GST fusion protein containing full-length Grb2 bound HPK1 more tightly than either SH3 domain alone, indicating that the two SH3 domains of Grb2 may bind HPK1 in a bidentate fashion, as suggested by the two-hybrid analysis.	bind
45144	5	10463	7	10	NULL	0	NULL	statement 3	NULL		occur in a	NULL				bidentate fashion	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27804_s_120	9346925	A GST fusion protein containing full-length Grb2 bound HPK1 more tightly than either SH3 domain alone, indicating that the two SH3 domains of Grb2 may bind HPK1 in a bidentate fashion, as suggested by the two-hybrid analysis.	bind
38523	1	10464	6	13	NULL	NULL	NULL	GST fusion protein	GP		contains					CasL	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_13_6_2147_s_126	12058076	A GST fusion protein containing the CasL SH3 domain (Figure  2, lane 5) also bound efficiently to FAK, whereas GST alone failed to bind FAK (Figure  2, lane 2).	bind
38525	2	10464	6	13	NULL	NULL	NULL	statement 1	GP		bind		efficiently			FAK	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_13_6_2147_s_126	12058076	A GST fusion protein containing the CasL SH3 domain (Figure  2, lane 5) also bound efficiently to FAK, whereas GST alone failed to bind FAK (Figure  2, lane 2).	bind
38527	3	10464	6	13	NULL	NULL	NULL	GST 	GP		did not bind					FAK	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_13_6_2147_s_126	12058076	A GST fusion protein containing the CasL SH3 domain (Figure  2, lane 5) also bound efficiently to FAK, whereas GST alone failed to bind FAK (Figure  2, lane 2).	bind
45145	1	10464	7	NULL	NULL	0	NULL	GST fusion protein	NULL		contains	NULL				CasL	NULL		SH3 domain		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_13_6_2147_s_126	12058076	A GST fusion protein containing the CasL SH3 domain (Figure  2, lane 5) also bound efficiently to FAK, whereas GST alone failed to bind FAK (Figure  2, lane 2).	bind
45146	2	10464	7	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL	efficiently			FAK	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_13_6_2147_s_126	12058076	A GST fusion protein containing the CasL SH3 domain (Figure  2, lane 5) also bound efficiently to FAK, whereas GST alone failed to bind FAK (Figure  2, lane 2).	bind
45147	3	10464	7	NULL	NULL	0	NULL	GST	NULL		does not bind	NULL				FAK	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_13_6_2147_s_126	12058076	A GST fusion protein containing the CasL SH3 domain (Figure  2, lane 5) also bound efficiently to FAK, whereas GST alone failed to bind FAK (Figure  2, lane 2).	bind
38530	1	10465	6	13	NULL	NULL	NULL	Grb2	GP		bind			SH2 domain		LAT	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9149_s_319	11094067	A GST fusion protein containing the SH2 domain of Grb2, which is known to bind to LAT, served as a positive control ( 73).	bind
45149	1	10465	7	10	NULL	0	NULL	Grb2	NULL		bind	NULL		SH2 domain		LAT	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9149_s_319	11094067	A GST fusion protein containing the SH2 domain of Grb2, which is known to bind to LAT, served as a positive control ( 73).	bind
38545	1	10466	6	10	NULL	0	NULL		NULL		contains	NULL		236-amino acid region of the cytoplasmic tail of beta subunit			NULL		four tyrosine residues		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_26_16189_s_9	9195918	A GST fusion protein encoding a 236-amino acid region of the cytoplasmic tail of the beta subunit, which contained four tyrosine residues, bound to hck and fyn.	bind
38546	2	10466	6	13	NULL	NULL	NULL	statement 1	GP		bind					hck	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_26_16189_s_9	9195918	A GST fusion protein encoding a 236-amino acid region of the cytoplasmic tail of the beta subunit, which contained four tyrosine residues, bound to hck and fyn.	bind
38548	3	10466	6	13	NULL	NULL	NULL	statement 1	GP		bind					Fyn	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_26_16189_s_9	9195918	A GST fusion protein encoding a 236-amino acid region of the cytoplasmic tail of the beta subunit, which contained four tyrosine residues, bound to hck and fyn.	bind
45150	1	10466	7	NULL	NULL	0	NULL		NULL		contains	NULL		236-amino acid region of the cytoplasmic tail of the beta subunit			NULL		four tyrosine residues		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_26_16189_s_9	9195918	A GST fusion protein encoding a 236-amino acid region of the cytoplasmic tail of the beta subunit, which contained four tyrosine residues, bound to hck and fyn.	bind
45151	2	10466	7	NULL	NULL	0	NULL	GST fusion protein	NULL		encode	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_26_16189_s_9	9195918	A GST fusion protein encoding a 236-amino acid region of the cytoplasmic tail of the beta subunit, which contained four tyrosine residues, bound to hck and fyn.	bind
45152	3	10466	7	NULL	NULL	0	NULL	statement 2	NULL		bind	NULL				hck	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_26_16189_s_9	9195918	A GST fusion protein encoding a 236-amino acid region of the cytoplasmic tail of the beta subunit, which contained four tyrosine residues, bound to hck and fyn.	bind
45153	4	10466	7	NULL	NULL	0	NULL	statement 2	NULL		bind	NULL				fyn	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_26_16189_s_9	9195918	A GST fusion protein encoding a 236-amino acid region of the cytoplasmic tail of the beta subunit, which contained four tyrosine residues, bound to hck and fyn.	bind
38553	1	10468	6	13	NULL	NULL	NULL	Homer	GP	Drosophila	bind					mGluR5	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_4_707_s_172	9808458	A GST fusion protein of  Drosophila Homer also bound mGluR5 (data not shown).	bind
50198	2	10468	6	13	NULL	NULL	NULL	Homer	GP	Drosophila	is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_21_4_707_s_172	9808458	A GST fusion protein of  Drosophila Homer also bound mGluR5 (data not shown).	bind
45154	1	10468	7	NULL	NULL	0	NULL	Homer	NULL	Drosophila	bind	NULL				mGluR5	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_21_4_707_s_172	9808458	A GST fusion protein of  Drosophila Homer also bound mGluR5 (data not shown).	bind
45155	2	10468	7	NULL	NULL	0	NULL	Homer	NULL	Drosophila	is a type of	NULL				GST fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_21_4_707_s_172	9808458	A GST fusion protein of  Drosophila Homer also bound mGluR5 (data not shown).	bind
39079	1	10469	6	13	NULL	NULL	NULL	Erk	GP		is a type of					Tyr(P)-containing protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_17_11693_s_165	10206983	A GST fusion protein of HePTP lacking this region (GST-deltaN) failed to bind any Tyr(P)-containing proteins, Erk, or p38 (Fig.  5 a) in lysates of Jurkat T cells.	bind
39080	2	10469	6	13	NULL	NULL	NULL	p38	GP		is a type of					Tyr(P)-containing protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_17_11693_s_165	10206983	A GST fusion protein of HePTP lacking this region (GST-deltaN) failed to bind any Tyr(P)-containing proteins, Erk, or p38 (Fig.  5 a) in lysates of Jurkat T cells.	bind
39081	3	10469	6	13	NULL	NULL	NULL	HePTP	GP		lacks								GST-deltaN		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_17_11693_s_165	10206983	A GST fusion protein of HePTP lacking this region (GST-deltaN) failed to bind any Tyr(P)-containing proteins, Erk, or p38 (Fig.  5 a) in lysates of Jurkat T cells.	bind
39082	4	10469	6	13	NULL	NULL	NULL	statement 3	GP		does not bind					Erk	GP				NULL	lysates of Jurkat T cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_17_11693_s_165	10206983	A GST fusion protein of HePTP lacking this region (GST-deltaN) failed to bind any Tyr(P)-containing proteins, Erk, or p38 (Fig.  5 a) in lysates of Jurkat T cells.	bind
39083	5	10469	6	13	NULL	NULL	NULL	statement 3	GP		does not bind					p38	GP				NULL	lysates of Jurkat T cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_17_11693_s_165	10206983	A GST fusion protein of HePTP lacking this region (GST-deltaN) failed to bind any Tyr(P)-containing proteins, Erk, or p38 (Fig.  5 a) in lysates of Jurkat T cells.	bind
50199	6	10469	6	13	NULL	NULL	NULL	HePTP	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_17_11693_s_165	10206983	A GST fusion protein of HePTP lacking this region (GST-deltaN) failed to bind any Tyr(P)-containing proteins, Erk, or p38 (Fig.  5 a) in lysates of Jurkat T cells.	bind
45156	1	10469	7	NULL	NULL	0	NULL	HePTP	NULL		lacks	NULL					NULL		GST-deltaN		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11693_s_165	10206983	A GST fusion protein of HePTP lacking this region (GST-deltaN) failed to bind any Tyr(P)-containing proteins, Erk, or p38 (Fig.  5 a) in lysates of Jurkat T cells.	bind
45157	2	10469	7	NULL	NULL	0	NULL	statement 1	NULL		does not bind	NULL				Erk	NULL				NULL	lysates of Jurkat T cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_17_11693_s_165	10206983	A GST fusion protein of HePTP lacking this region (GST-deltaN) failed to bind any Tyr(P)-containing proteins, Erk, or p38 (Fig.  5 a) in lysates of Jurkat T cells.	bind
45158	3	10469	7	NULL	NULL	0	NULL	statement 1	NULL		does not bind	NULL				p38	NULL				NULL	lysates of Jurkat T cells	0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11693_s_165	10206983	A GST fusion protein of HePTP lacking this region (GST-deltaN) failed to bind any Tyr(P)-containing proteins, Erk, or p38 (Fig.  5 a) in lysates of Jurkat T cells.	bind
45159	4	10469	7	NULL	NULL	0	NULL	Erk	NULL		is a type of	NULL				Tyr(P)-containing protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11693_s_165	10206983	A GST fusion protein of HePTP lacking this region (GST-deltaN) failed to bind any Tyr(P)-containing proteins, Erk, or p38 (Fig.  5 a) in lysates of Jurkat T cells.	bind
45160	5	10469	7	NULL	NULL	0	NULL	p38	NULL		is a type of	NULL				Tyr(P)-containing protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11693_s_165	10206983	A GST fusion protein of HePTP lacking this region (GST-deltaN) failed to bind any Tyr(P)-containing proteins, Erk, or p38 (Fig.  5 a) in lysates of Jurkat T cells.	bind
45161	6	10469	7	NULL	NULL	0	NULL	 HePTP	NULL		is a type of	NULL				GST fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11693_s_165	10206983	A GST fusion protein of HePTP lacking this region (GST-deltaN) failed to bind any Tyr(P)-containing proteins, Erk, or p38 (Fig.  5 a) in lysates of Jurkat T cells.	bind
39084	1	10470	6	13	NULL	NULL	NULL	GST-DIL	GP		bind					MBP-mADIP-F	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_178	12446711	A GST fusion protein of the DIL domain of afadin (GST-DIL) bound to an MBP-fusion protein of the region of ADIP containing the all three coiled-coil domains (aa 121-436) (MBP-mADIP-F) immobilized on amylose resin beads.	bind
50203	2	10470	6	13	NULL	NULL	NULL	MBP-mADIP-F	GP		is a type of					MBP-fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_178	12446711	A GST fusion protein of the DIL domain of afadin (GST-DIL) bound to an MBP-fusion protein of the region of ADIP containing the all three coiled-coil domains (aa 121-436) (MBP-mADIP-F) immobilized on amylose resin beads.	bind
50204	3	10470	6	13	NULL	NULL	NULL	MBP-mADIP-F	GP		contains					ADIP	GP		coiled-coil domains (aa 121-436)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_178	12446711	A GST fusion protein of the DIL domain of afadin (GST-DIL) bound to an MBP-fusion protein of the region of ADIP containing the all three coiled-coil domains (aa 121-436) (MBP-mADIP-F) immobilized on amylose resin beads.	bind
50205	4	10470	6	13	NULL	NULL	NULL	GST-DIL	GP		is a type of					GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_178	12446711	A GST fusion protein of the DIL domain of afadin (GST-DIL) bound to an MBP-fusion protein of the region of ADIP containing the all three coiled-coil domains (aa 121-436) (MBP-mADIP-F) immobilized on amylose resin beads.	bind
50206	5	10470	6	13	NULL	NULL	NULL	GST-DIL	GP		contains					afadin	GP		DIL domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_178	12446711	A GST fusion protein of the DIL domain of afadin (GST-DIL) bound to an MBP-fusion protein of the region of ADIP containing the all three coiled-coil domains (aa 121-436) (MBP-mADIP-F) immobilized on amylose resin beads.	bind
45162	1	10470	7	NULL	NULL	0	NULL	GST-DIL	NULL		bind	NULL				MBP-mADIP-F	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_178	12446711	A GST fusion protein of the DIL domain of afadin (GST-DIL) bound to an MBP-fusion protein of the region of ADIP containing the all three coiled-coil domains (aa 121-436) (MBP-mADIP-F) immobilized on amylose resin beads.	bind
45163	2	10470	7	10	NULL	0	NULL	GST-DIL	NULL		is a type of	NULL				GST fusion protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_178	12446711	A GST fusion protein of the DIL domain of afadin (GST-DIL) bound to an MBP-fusion protein of the region of ADIP containing the all three coiled-coil domains (aa 121-436) (MBP-mADIP-F) immobilized on amylose resin beads.	bind
45164	3	10470	7	10	NULL	0	NULL	MBP-mADIP-F	NULL		is a type of	NULL				MBP-fusion protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_178	12446711	A GST fusion protein of the DIL domain of afadin (GST-DIL) bound to an MBP-fusion protein of the region of ADIP containing the all three coiled-coil domains (aa 121-436) (MBP-mADIP-F) immobilized on amylose resin beads.	bind
45165	4	10470	7	10	NULL	0	NULL	MBP-mADIP-F	NULL		contains	NULL				ADIP	NULL		coiled-coil domains (aa 121-436)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_178	12446711	A GST fusion protein of the DIL domain of afadin (GST-DIL) bound to an MBP-fusion protein of the region of ADIP containing the all three coiled-coil domains (aa 121-436) (MBP-mADIP-F) immobilized on amylose resin beads.	bind
50202	5	10470	7	10	NULL	0	NULL	GST-DIL	NULL		contains	NULL				afadin	NULL		DIL domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_6_4103_s_178	12446711	A GST fusion protein of the DIL domain of afadin (GST-DIL) bound to an MBP-fusion protein of the region of ADIP containing the all three coiled-coil domains (aa 121-436) (MBP-mADIP-F) immobilized on amylose resin beads.	bind
38645	1	10471	6	13	NULL	NULL	NULL	RLIP76	GP		bind		specifically	RalBD		Ral	GP	activated form of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_5_2486_s_74	9566869	A GST fusion protein of the RalBD of RLIP76 binds specifically to the activated form of Ral.	bind
50207	2	10471	6	13	NULL	NULL	NULL	RLIP76	GP		is a type of			RalBD		GST fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_5_2486_s_74	9566869	A GST fusion protein of the RalBD of RLIP76 binds specifically to the activated form of Ral.	bind
45170	1	10471	7	NULL	NULL	0	NULL	RLIP76	NULL		bind	NULL	specifically	RalBD		Ral	NULL	activated			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_5_2486_s_74	9566869	A GST fusion protein of the RalBD of RLIP76 binds specifically to the activated form of Ral.	bind
45171	2	10471	7	NULL	NULL	0	NULL	RLIP76	NULL		is a type of	NULL		RalBD		GST fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_5_2486_s_74	9566869	A GST fusion protein of the RalBD of RLIP76 binds specifically to the activated form of Ral.	bind
38646	1	10472	6	13	NULL	NULL	NULL	CED-4	GP		bind					E1B 19K	GP				NULL	yeast	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_10_6052_s_134	9742122	A GST fusion protein system was employed to confirm the binding specificity of CED-4 with E1B 19K in yeast.	bind
45172	1	10472	7	NULL	NULL	0	NULL	CED-4	NULL		bind	NULL				 E1B 19K	NULL				NULL	yeast	0	NULL	NULL	NULL	gw60_molcellbiol_18_10_6052_s_134	9742122	A GST fusion protein system was employed to confirm the binding specificity of CED-4 with E1B 19K in yeast.	bind
38647	1	10473	6	13	NULL	NULL	NULL	DPAK	GP		bind			N-terminal CRIB domain		RacA	GP	Drosophila			NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_982	10066831	A GST fusion to the DPAK N-terminal CRIB domain bound to  Drosophila RacA (DRacA) and Cdc42p (Dcdc42) and human Rac1 and Cdc42p (data not shown) in an overlay assay ( 199).	bind
38648	2	10473	6	13	NULL	NULL	NULL	DRacA	GP		is					Drosophila RacA	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_982	10066831	A GST fusion to the DPAK N-terminal CRIB domain bound to  Drosophila RacA (DRacA) and Cdc42p (Dcdc42) and human Rac1 and Cdc42p (data not shown) in an overlay assay ( 199).	bind
38649	3	10473	6	13	NULL	NULL	NULL	DPAK	GP		bind			N-terminal CRIB domain		Cdc42p	GP	Drosophila			NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_982	10066831	A GST fusion to the DPAK N-terminal CRIB domain bound to  Drosophila RacA (DRacA) and Cdc42p (Dcdc42) and human Rac1 and Cdc42p (data not shown) in an overlay assay ( 199).	bind
38650	4	10473	6	13	NULL	NULL	NULL	Dcdc42	GP		is					Drosophila Cdc42p	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_982	10066831	A GST fusion to the DPAK N-terminal CRIB domain bound to  Drosophila RacA (DRacA) and Cdc42p (Dcdc42) and human Rac1 and Cdc42p (data not shown) in an overlay assay ( 199).	bind
38651	5	10473	6	13	NULL	NULL	NULL	DPAK	GP		bind			N-terminal CRIB domain		Rac1	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_982	10066831	A GST fusion to the DPAK N-terminal CRIB domain bound to  Drosophila RacA (DRacA) and Cdc42p (Dcdc42) and human Rac1 and Cdc42p (data not shown) in an overlay assay ( 199).	bind
38652	6	10473	6	13	NULL	NULL	NULL	DPAK	GP		bind			N-terminal CRIB domain		Cdc42p	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_982	10066831	A GST fusion to the DPAK N-terminal CRIB domain bound to  Drosophila RacA (DRacA) and Cdc42p (Dcdc42) and human Rac1 and Cdc42p (data not shown) in an overlay assay ( 199).	bind
45173	1	10473	7	NULL	NULL	0	NULL	DPAK	NULL		bind	NULL		N-terminal CRIB domain		DRacA	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_982	10066831	A GST fusion to the DPAK N-terminal CRIB domain bound to  Drosophila RacA (DRacA) and Cdc42p (Dcdc42) and human Rac1 and Cdc42p (data not shown) in an overlay assay ( 199).	bind
45174	2	10473	7	NULL	NULL	0	NULL	DPAK	NULL		bind	NULL		N-terminal CRIB domain		Dcdc42	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_982	10066831	A GST fusion to the DPAK N-terminal CRIB domain bound to  Drosophila RacA (DRacA) and Cdc42p (Dcdc42) and human Rac1 and Cdc42p (data not shown) in an overlay assay ( 199).	bind
45175	3	10473	7	NULL	NULL	0	NULL	DPAK	NULL		bind	NULL		N-terminal CRIB domain		Rac1	NULL	human			NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_982	10066831	A GST fusion to the DPAK N-terminal CRIB domain bound to  Drosophila RacA (DRacA) and Cdc42p (Dcdc42) and human Rac1 and Cdc42p (data not shown) in an overlay assay ( 199).	bind
45176	4	10473	7	NULL	NULL	0	NULL	DPAK	NULL		bind	NULL		N-terminal CRIB domain		Cdc42p	NULL	human			NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_982	10066831	A GST fusion to the DPAK N-terminal CRIB domain bound to  Drosophila RacA (DRacA) and Cdc42p (Dcdc42) and human Rac1 and Cdc42p (data not shown) in an overlay assay ( 199).	bind
45177	5	10473	7	10	NULL	0	NULL	DRacA			is					Drosophila RacA					NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_982	10066831	A GST fusion to the DPAK N-terminal CRIB domain bound to  Drosophila RacA (DRacA) and Cdc42p (Dcdc42) and human Rac1 and Cdc42p (data not shown) in an overlay assay ( 199).	bind
45178	6	10473	7	10	NULL	0	NULL	Dcdc42			is					Drosophila Cdc42p					NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_982	10066831	A GST fusion to the DPAK N-terminal CRIB domain bound to  Drosophila RacA (DRacA) and Cdc42p (Dcdc42) and human Rac1 and Cdc42p (data not shown) in an overlay assay ( 199).	bind
38653	1	10474	6	13	NULL	NULL	NULL	Sp1-F	GP		bind					huntington	GP	transfected			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_5_1277_s_151	11839795	A GST pull down assay showed that Sp1-F and Sp1-C bound to transfected huntingtin, whereas Sp1-P or Sp1-N did not (Fig.  1C).	bind
38654	2	10474	6	13	NULL	NULL	NULL	Sp1-C	GP		bind					huntington	GP	transfected			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_5_1277_s_151	11839795	A GST pull down assay showed that Sp1-F and Sp1-C bound to transfected huntingtin, whereas Sp1-P or Sp1-N did not (Fig.  1C).	bind
38655	3	10474	6	13	NULL	NULL	NULL	Sp1-P	GP		does not bind					huntington	GP	transfected			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_5_1277_s_151	11839795	A GST pull down assay showed that Sp1-F and Sp1-C bound to transfected huntingtin, whereas Sp1-P or Sp1-N did not (Fig.  1C).	bind
38656	4	10474	6	13	NULL	NULL	NULL	Sp1-N	GP		does not bind					huntington	GP	transfected			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_5_1277_s_151	11839795	A GST pull down assay showed that Sp1-F and Sp1-C bound to transfected huntingtin, whereas Sp1-P or Sp1-N did not (Fig.  1C).	bind
45180	1	10474	7	NULL	NULL	0	NULL	Sp1-F	NULL		bind	NULL				 huntingtin	NULL	transfected			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_5_1277_s_151	11839795	A GST pull down assay showed that Sp1-F and Sp1-C bound to transfected huntingtin, whereas Sp1-P or Sp1-N did not (Fig.  1C).	bind
45181	2	10474	7	NULL	NULL	0	NULL	Sp1-C	NULL		bind	NULL				huntingtin	NULL	transfected			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_5_1277_s_151	11839795	A GST pull down assay showed that Sp1-F and Sp1-C bound to transfected huntingtin, whereas Sp1-P or Sp1-N did not (Fig.  1C).	bind
45182	3	10474	7	NULL	NULL	0	NULL	Sp1-P	NULL		does not bind	NULL				huntingtin	NULL	transfected			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_5_1277_s_151	11839795	A GST pull down assay showed that Sp1-F and Sp1-C bound to transfected huntingtin, whereas Sp1-P or Sp1-N did not (Fig.  1C).	bind
45183	4	10474	7	NULL	NULL	0	NULL	Sp1-N	NULL		does not bind	NULL				huntingtin	NULL	transfected			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_5_1277_s_151	11839795	A GST pull down assay showed that Sp1-F and Sp1-C bound to transfected huntingtin, whereas Sp1-P or Sp1-N did not (Fig.  1C).	bind
38657	1	10475	6	13	NULL	NULL	NULL	HCF	GP		bind					ZF	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2446_s_183	10871379	A GST pull-down assay (Fig.  4B) and a mammalian two-hybrid assay (Fig.  4C) were performed to examine the effects of these mutations on the  in vitro as well as  in vivo binding of HCF by ZF.	bind
38658	2	10475	6	13	NULL	NULL	NULL	HCF	GP		bind					ZF	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2446_s_183	10871379	A GST pull-down assay (Fig.  4B) and a mammalian two-hybrid assay (Fig.  4C) were performed to examine the effects of these mutations on the  in vitro as well as  in vivo binding of HCF by ZF.	bind
45184	1	10475	7	10	NULL	0	NULL	ZF	NULL		bind	NULL				HCF	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2446_s_183	10871379	A GST pull-down assay (Fig.  4B) and a mammalian two-hybrid assay (Fig.  4C) were performed to examine the effects of these mutations on the  in vitro as well as  in vivo binding of HCF by ZF.	bind
50208	2	10475	7	10	NULL	0	NULL	ZF	NULL		bind	NULL				HCF	NULL				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2446_s_183	10871379	A GST pull-down assay (Fig.  4B) and a mammalian two-hybrid assay (Fig.  4C) were performed to examine the effects of these mutations on the  in vitro as well as  in vivo binding of HCF by ZF.	bind
38659	1	10476	6	13	NULL	NULL	NULL	bZIP	GP	radiolabeled	bind								gst-DBD		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_50_41421_s_113	16223730	A GST pull-down assay demonstrating binding of radiolabled bZIP or IE2 probe to gst-DBD  with the indicated substitutions at Arg232 and Arg235 is shown.	bind
38660	2	10476	6	13	NULL	NULL	NULL	IE2 probe	GP		bind								gst-DBD		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_50_41421_s_113	16223730	A GST pull-down assay demonstrating binding of radiolabled bZIP or IE2 probe to gst-DBD  with the indicated substitutions at Arg232 and Arg235 is shown.	bind
45185	1	10476	7	10	NULL	0	NULL	bZIP		radiolabeled 	bind								gst-DBD		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_50_41421_s_113	16223730	A GST pull-down assay demonstrating binding of radiolabled bZIP or IE2 probe to gst-DBD  with the indicated substitutions at Arg232 and Arg235 is shown.	bind
45187	2	10476	7	10	NULL	0	NULL	IE2 probe			bind								gst-DBD		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_50_41421_s_113	16223730	A GST pull-down assay demonstrating binding of radiolabled bZIP or IE2 probe to gst-DBD  with the indicated substitutions at Arg232 and Arg235 is shown.	bind
38661	1	10477	6	13	NULL	NULL	NULL	His6-KRAB-A	GP	35S-labeled	bind		specifically			GST-pVHL19	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_22_8_1857_s_106	12682018	A GST pull-down assay result further demonstrated that the 35S-labeled His6-KRAB-A specifically bound to the GST - pVHL19 fusion protein, but not to GST alone (Figure  2F), indicating a physical association  in vitro.	bind
50209	2	10477	6	13	NULL	NULL	NULL	GST-pVHL19	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_8_1857_s_106	12682018	A GST pull-down assay result further demonstrated that the 35S-labeled His6-KRAB-A specifically bound to the GST - pVHL19 fusion protein, but not to GST alone (Figure  2F), indicating a physical association  in vitro.	bind
50210	3	10477	6	13	NULL	NULL	NULL	His6-KRAB-A \t	GP	35S-labeled	does not bind					GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_8_1857_s_106	12682018	A GST pull-down assay result further demonstrated that the 35S-labeled His6-KRAB-A specifically bound to the GST - pVHL19 fusion protein, but not to GST alone (Figure  2F), indicating a physical association  in vitro.	bind
45189	1	10477	7	NULL	NULL	0	NULL	His6-KRAB-A	NULL	 35S-labeled	bind	NULL	specifically			GST - pVHL19	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_embo_22_8_1857_s_106	12682018	A GST pull-down assay result further demonstrated that the 35S-labeled His6-KRAB-A specifically bound to the GST - pVHL19 fusion protein, but not to GST alone (Figure  2F), indicating a physical association  in vitro.	bind
45190	2	10477	7	NULL	NULL	0	NULL	His6-KRAB-A	NULL	35S-labeled	does not bind	NULL	 			GST	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_22_8_1857_s_106	12682018	A GST pull-down assay result further demonstrated that the 35S-labeled His6-KRAB-A specifically bound to the GST - pVHL19 fusion protein, but not to GST alone (Figure  2F), indicating a physical association  in vitro.	bind
45191	3	10477	7	NULL	NULL	0	NULL	GST - pVHL19	NULL		is a type of	NULL				GST fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_22_8_1857_s_106	12682018	A GST pull-down assay result further demonstrated that the 35S-labeled His6-KRAB-A specifically bound to the GST - pVHL19 fusion protein, but not to GST alone (Figure  2F), indicating a physical association  in vitro.	bind
39087	1	10479	6	13	NULL	NULL	NULL	N-CoR	GP		bind		directly	ID1		ERalpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_233	12738788	A GST pull-down assay showed both  GST-ID1-2 derived from N-CoR and SMRT directly bound to ERalpha in the  presence of OHT ( Fig.  6 B).	bind
39088	2	10479	6	13	NULL	NULL	NULL	N-CoR	GP		bind		directly	ID2		ERalpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_233	12738788	A GST pull-down assay showed both  GST-ID1-2 derived from N-CoR and SMRT directly bound to ERalpha in the  presence of OHT ( Fig.  6 B).	bind
39089	3	10479	6	13	NULL	NULL	NULL	SMRT	GP		bind		directly	ID1		ERalpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_233	12738788	A GST pull-down assay showed both  GST-ID1-2 derived from N-CoR and SMRT directly bound to ERalpha in the  presence of OHT ( Fig.  6 B).	bind
39090	4	10479	6	13	NULL	NULL	NULL	SMRT	GP		bind		directly	ID2		ERalpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_233	12738788	A GST pull-down assay showed both  GST-ID1-2 derived from N-CoR and SMRT directly bound to ERalpha in the  presence of OHT ( Fig.  6 B).	bind
39091	5	10479	6	13	NULL	NULL	NULL	statement 1	Process		occurs in presence of					OHT	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_233	12738788	A GST pull-down assay showed both  GST-ID1-2 derived from N-CoR and SMRT directly bound to ERalpha in the  presence of OHT ( Fig.  6 B).	bind
39092	6	10479	6	13	NULL	NULL	NULL	statement 2	Process		occurs in presence of					OHT	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_233	12738788	A GST pull-down assay showed both  GST-ID1-2 derived from N-CoR and SMRT directly bound to ERalpha in the  presence of OHT ( Fig.  6 B).	bind
39093	7	10479	6	13	NULL	NULL	NULL	statement 3	Process		occurs in presence of					OHT	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_233	12738788	A GST pull-down assay showed both  GST-ID1-2 derived from N-CoR and SMRT directly bound to ERalpha in the  presence of OHT ( Fig.  6 B).	bind
39094	8	10479	6	13	NULL	NULL	NULL	statement 4	Process		occurs in presence of					OHT	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_233	12738788	A GST pull-down assay showed both  GST-ID1-2 derived from N-CoR and SMRT directly bound to ERalpha in the  presence of OHT ( Fig.  6 B).	bind
45192	1	10479	7	10	NULL	0	NULL	N-CoR			bind		directly	ID1		ERalpha					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_233	12738788	A GST pull-down assay showed both  GST-ID1-2 derived from N-CoR and SMRT directly bound to ERalpha in the  presence of OHT ( Fig.  6 B).	bind
45193	2	10479	7	10	NULL	0	NULL	N-CoR			bind		directly	ID2		ERalpha					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_233	12738788	A GST pull-down assay showed both  GST-ID1-2 derived from N-CoR and SMRT directly bound to ERalpha in the  presence of OHT ( Fig.  6 B).	bind
45194	3	10479	7	10	NULL	0	NULL	SMRT			bind		directly	ID1		ERalpha					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_233	12738788	A GST pull-down assay showed both  GST-ID1-2 derived from N-CoR and SMRT directly bound to ERalpha in the  presence of OHT ( Fig.  6 B).	bind
45195	4	10479	7	10	NULL	0	NULL	SMRT			bind		directly	ID2		ERalpha					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_233	12738788	A GST pull-down assay showed both  GST-ID1-2 derived from N-CoR and SMRT directly bound to ERalpha in the  presence of OHT ( Fig.  6 B).	bind
45196	5	10479	7	10	NULL	0	NULL	statement 1			in the presence of					OHT					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_233	12738788	A GST pull-down assay showed both  GST-ID1-2 derived from N-CoR and SMRT directly bound to ERalpha in the  presence of OHT ( Fig.  6 B).	bind
57618	6	10479	7	10	NULL	0	NULL	statement 2			in the presence of					OHT					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_233	12738788	A GST pull-down assay showed both  GST-ID1-2 derived from N-CoR and SMRT directly bound to ERalpha in the  presence of OHT ( Fig.  6 B).	bind
57619	7	10479	7	10	NULL	0	NULL	statement 3			in the presence of					OHT					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_233	12738788	A GST pull-down assay showed both  GST-ID1-2 derived from N-CoR and SMRT directly bound to ERalpha in the  presence of OHT ( Fig.  6 B).	bind
57620	8	10479	7	10	NULL	0	NULL	statement 4			in the presence of					statement 8					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_233	12738788	A GST pull-down assay showed both  GST-ID1-2 derived from N-CoR and SMRT directly bound to ERalpha in the  presence of OHT ( Fig.  6 B).	bind
38913	1	10480	6	13	NULL	NULL	NULL	FOXO1	GP	in vitro-translated	bind					GST-mPXR	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_18_7931_s_210	15340055	A GST pull-down assay showed that in vitro-translated FOXO1 bound to GST-mPXR, which was increased by the specific PXR activator pregnenolone PCN (Fig.  6a).	bind
38914	2	10480	6	13	NULL	NULL	NULL	PCN	Chemical		increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_18_7931_s_210	15340055	A GST pull-down assay showed that in vitro-translated FOXO1 bound to GST-mPXR, which was increased by the specific PXR activator pregnenolone PCN (Fig.  6a).	bind
38915	3	10480	6	13	NULL	NULL	NULL	PCN	Chemical		is a type of					PXR activator	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_18_7931_s_210	15340055	A GST pull-down assay showed that in vitro-translated FOXO1 bound to GST-mPXR, which was increased by the specific PXR activator pregnenolone PCN (Fig.  6a).	bind
50211	4	10480	6	13	NULL	NULL	NULL	PCN	Chemical		is					pregnenolone	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_18_7931_s_210	15340055	A GST pull-down assay showed that in vitro-translated FOXO1 bound to GST-mPXR, which was increased by the specific PXR activator pregnenolone PCN (Fig.  6a).	bind
45197	1	10480	7	NULL	NULL	0	NULL	FOXO1	NULL	in vitro-translated	bind	NULL				GST-mPXR	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_18_7931_s_210	15340055	A GST pull-down assay showed that in vitro-translated FOXO1 bound to GST-mPXR, which was increased by the specific PXR activator pregnenolone PCN (Fig.  6a).	bind
45198	2	10480	7	10	NULL	0	NULL	PCN	NULL		increase	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_18_7931_s_210	15340055	A GST pull-down assay showed that in vitro-translated FOXO1 bound to GST-mPXR, which was increased by the specific PXR activator pregnenolone PCN (Fig.  6a).	bind
45199	3	10480	7	10	NULL	0	NULL	PCN	NULL		is a type of	NULL				PXR activator	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_18_7931_s_210	15340055	A GST pull-down assay showed that in vitro-translated FOXO1 bound to GST-mPXR, which was increased by the specific PXR activator pregnenolone PCN (Fig.  6a).	bind
50212	4	10480	7	10	NULL	0	NULL	PCN	NULL		is	NULL				pregnenolone	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_18_7931_s_210	15340055	A GST pull-down assay showed that in vitro-translated FOXO1 bound to GST-mPXR, which was increased by the specific PXR activator pregnenolone PCN (Fig.  6a).	bind
38916	1	10481	6	13	NULL	NULL	NULL	TaWIN1	GP		bind		specifically;;directly			GST-WPK4	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31695_s_84	10918058	A GST pull-down assay showed that TaWIN1 specifically binds GST-WPK4 but not GST-K75D  in vitro, indicating a direct interaction between WPK4 and TaWIN1 Fig.  2 C).	bind
38917	2	10481	6	13	NULL	NULL	NULL	TaWIN1	GP		does not bind								GST-K75D		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31695_s_84	10918058	A GST pull-down assay showed that TaWIN1 specifically binds GST-WPK4 but not GST-K75D  in vitro, indicating a direct interaction between WPK4 and TaWIN1 Fig.  2 C).	bind
45202	1	10481	7	NULL	NULL	0	NULL	TaWIN1	NULL		bind	NULL	specifically;;directly			GST-WPK4	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31695_s_84	10918058	A GST pull-down assay showed that TaWIN1 specifically binds GST-WPK4 but not GST-K75D  in vitro, indicating a direct interaction between WPK4 and TaWIN1 Fig.  2 C).	bind
45203	2	10481	7	NULL	NULL	0	NULL	TaWIN1 	NULL		does not bind	NULL					NULL		GST-K75D		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_31695_s_84	10918058	A GST pull-down assay showed that TaWIN1 specifically binds GST-WPK4 but not GST-K75D  in vitro, indicating a direct interaction between WPK4 and TaWIN1 Fig.  2 C).	bind
39095	1	10482	6	13	NULL	NULL	NULL	SRC-1	GP		is a type of					AF-2 coactivator	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
39096	2	10482	6	13	NULL	NULL	NULL	TRAP220	GP		is a type of					AF-2 coactivator	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
39097	3	10482	6	13	NULL	NULL	NULL	TRRAP	GP		is a type of					AF-2 coactivator	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
39098	4	10482	6	13	NULL	NULL	NULL	ERalpha(GAL-DEF)	GP		bind		directly			SRC-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
39099	5	10482	6	13	NULL	NULL	NULL	ERalpha(GAL-DEF)	GP		bind		directly			TRAP220	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
39100	6	10482	6	13	NULL	NULL	NULL	ERalpha(GAL-DEF)	GP		bind		directly			TRRAP	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
39101	7	10482	6	13	NULL	NULL	NULL	E2	Chemical		induces					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
39102	8	10482	6	13	NULL	NULL	NULL	E2	Chemical		induces					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
39103	9	10482	6	13	NULL	NULL	NULL	E2	Chemical		induces					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
39104	10	10482	6	13	NULL	NULL	NULL	BBP	Chemical		abrogates					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
39105	11	10482	6	13	NULL	NULL	NULL	BBP	Chemical		abrogates					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
39106	12	10482	6	13	NULL	NULL	NULL	BBP	Chemical		abrogates					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
39107	13	10482	6	13	NULL	NULL	NULL	OHT	Chemical		abrogates					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
39108	14	10482	6	13	NULL	NULL	NULL	OHT	Chemical		abrogates					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
39109	15	10482	6	13	NULL	NULL	NULL	OHT	Chemical		abrogates					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
45207	1	10482	7	NULL	NULL	0	NULL	ERalpha	NULL		bind	NULL	directly			SRC-1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
45223	2	10482	7	NULL	NULL	0	NULL	ERalpha	NULL		bind	NULL	directly			TRAP220	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
45225	3	10482	7	NULL	NULL	0	NULL	ERalpha	NULL		bind	NULL	directly			TRRAP	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
45228	4	10482	7	NULL	NULL	0	NULL	E2	NULL		induce	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
45229	5	10482	7	NULL	NULL	0	NULL	E2	NULL		induce	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
45230	6	10482	7	NULL	NULL	0	NULL	E2	NULL		induce	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
45236	7	10482	7	NULL	NULL	0	NULL	statement 2	NULL		is an alternative to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
45240	8	10482	7	NULL	NULL	0	NULL	BBP 	NULL		abrogates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
45242	9	10482	7	NULL	NULL	0	NULL	BBP	NULL		abrogates	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
45244	10	10482	7	NULL	NULL	0	NULL	BBP	NULL		abrogates	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
45245	11	10482	7	NULL	NULL	0	NULL	OHT	NULL		abrogates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
45248	12	10482	7	NULL	NULL	0	NULL	OHT	NULL		abrogates	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
45249	13	10482	7	NULL	NULL	0	NULL	OHT	NULL		abrogates	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
45251	14	10482	7	NULL	NULL	0	NULL	ERalpha	NULL		is	NULL				GAL-DEF	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
45252	15	10482	7	NULL	NULL	0	NULL	SRC-1	NULL		is a type of	NULL				AF-2 coactivator	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
45253	16	10482	7	NULL	NULL	0	NULL	TRAP220	NULL		is a type of	NULL				AF-2 coactivator	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
45255	17	10482	7	NULL	NULL	0	NULL	TRRAP	NULL		is a type of	NULL				AF-2 coactivator	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26704_s_171	12738788	A GST pull-down assay showed that whereas E2 induced the direct  binding of ERalpha(GAL-DEF) to AF-2 coactivators SRC-1, TRAP220, or TRRAP,  BBP and OHT abrogated the interaction between GAL-DEF and AF-2 coactivators  ( Fig. 3 C).	bind
38918	1	10483	6	13	NULL	NULL	NULL	cdr2	GP		bind					c-Myc	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_13_16_2087_s_45	10465786	A GST pull-down assay was used to examine the in vitro binding of cdr2 and c-Myc.	bind
45261	1	10483	7	NULL	NULL	0	NULL	cdr2	NULL		bind	NULL				c-Myc	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_genesdev_13_16_2087_s_45	10465786	A GST pull-down assay was used to examine the in vitro binding of cdr2 and c-Myc.	bind
38919	1	10484	6	13	NULL	NULL	NULL	CtBP protein	GP	GAL4-tagged	bind					GST-MLL	GP	immobilized	R/MT		NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_14_8342_s_108	12829790	A GST pull-down assay with various, immobilized GST-MLL RD  proteins incubated with GAL4-tagged CtBP protein expressed by transient  transfection demonstrated that CtBP binds to both MLL(R/MT) and MLL(RD1) but  not to GST alone or to MLL(RD2) ( Fig.  4 A).	bind
38920	2	10484	6	13	NULL	NULL	NULL	CtBP protein	GP	GAL4-tagged	bind					GST-MLL	GP	immobilized	RD1		NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_14_8342_s_108	12829790	A GST pull-down assay with various, immobilized GST-MLL RD  proteins incubated with GAL4-tagged CtBP protein expressed by transient  transfection demonstrated that CtBP binds to both MLL(R/MT) and MLL(RD1) but  not to GST alone or to MLL(RD2) ( Fig.  4 A).	bind
38921	3	10484	6	13	NULL	NULL	NULL	CtBP protein	GP	GAL4-tagged	does not bind					GST-MLL	GP	immobilized	RD2		NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_14_8342_s_108	12829790	A GST pull-down assay with various, immobilized GST-MLL RD  proteins incubated with GAL4-tagged CtBP protein expressed by transient  transfection demonstrated that CtBP binds to both MLL(R/MT) and MLL(RD1) but  not to GST alone or to MLL(RD2) ( Fig.  4 A).	bind
50217	4	10484	6	13	NULL	NULL	NULL	CtBP protein	GP	GAL4-tagged	does not bind					GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_14_8342_s_108	12829790	A GST pull-down assay with various, immobilized GST-MLL RD  proteins incubated with GAL4-tagged CtBP protein expressed by transient  transfection demonstrated that CtBP binds to both MLL(R/MT) and MLL(RD1) but  not to GST alone or to MLL(RD2) ( Fig.  4 A).	bind
45278	1	10484	7	10	NULL	0	NULL	CtBP protein	NULL	GAL4-tagged	bind	NULL				GST-MLL	NULL	immobilized	R/MT		NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_14_8342_s_108	12829790	A GST pull-down assay with various, immobilized GST-MLL RD  proteins incubated with GAL4-tagged CtBP protein expressed by transient  transfection demonstrated that CtBP binds to both MLL(R/MT) and MLL(RD1) but  not to GST alone or to MLL(RD2) ( Fig.  4 A).	bind
45282	2	10484	7	10	NULL	0	NULL	CtBP protein	NULL	GAL4-tagged	bind	NULL				GST-MLL	NULL	immobilized	RD1		NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_14_8342_s_108	12829790	A GST pull-down assay with various, immobilized GST-MLL RD  proteins incubated with GAL4-tagged CtBP protein expressed by transient  transfection demonstrated that CtBP binds to both MLL(R/MT) and MLL(RD1) but  not to GST alone or to MLL(RD2) ( Fig.  4 A).	bind
45285	3	10484	7	NULL	NULL	0	NULL	CtBP protein	NULL	GAL4-tagged	does not bind	NULL				GST	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_100_14_8342_s_108	12829790	A GST pull-down assay with various, immobilized GST-MLL RD  proteins incubated with GAL4-tagged CtBP protein expressed by transient  transfection demonstrated that CtBP binds to both MLL(R/MT) and MLL(RD1) but  not to GST alone or to MLL(RD2) ( Fig.  4 A).	bind
45286	4	10484	7	10	NULL	0	NULL	CtBP protein	NULL	GAL4-tagged	does not bind	NULL				GST-MLL	NULL	immobilized	RD2		NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_14_8342_s_108	12829790	A GST pull-down assay with various, immobilized GST-MLL RD  proteins incubated with GAL4-tagged CtBP protein expressed by transient  transfection demonstrated that CtBP binds to both MLL(R/MT) and MLL(RD1) but  not to GST alone or to MLL(RD2) ( Fig.  4 A).	bind
39110	1	10486	6	13	NULL	NULL	NULL	gp185ErbB-2	GP		bind					GST-clone 52	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_20_7735_s_124	11003669	A GST-clone 52 fusion protein readily bound constitutively active gp185ErbB-2 (Fig.  1B) solubilized from NIH-ErbB-2 transfectants ( 17), whereas no ErbB-2 binding to GST beads (Fig.  1B) and GST-clone 52 beads incubated with NIH 3T3 lysates (data not shown) was observed.	bind
39113	2	10486	6	13	NULL	NULL	NULL	ErbB-2	GP		does not bind					GST-clone 52	GP				NULL	NIH 3T3 lysates	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_20_7735_s_124	11003669	A GST-clone 52 fusion protein readily bound constitutively active gp185ErbB-2 (Fig.  1B) solubilized from NIH-ErbB-2 transfectants ( 17), whereas no ErbB-2 binding to GST beads (Fig.  1B) and GST-clone 52 beads incubated with NIH 3T3 lysates (data not shown) was observed.	bind
50218	3	10486	6	13	NULL	NULL	NULL	GST-clone 52	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_20_7735_s_124	11003669	A GST-clone 52 fusion protein readily bound constitutively active gp185ErbB-2 (Fig.  1B) solubilized from NIH-ErbB-2 transfectants ( 17), whereas no ErbB-2 binding to GST beads (Fig.  1B) and GST-clone 52 beads incubated with NIH 3T3 lysates (data not shown) was observed.	bind
50219	4	10486	6	13	NULL	NULL	NULL	ErbB-2	GP		does not bind					GST	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_20_7735_s_124	11003669	A GST-clone 52 fusion protein readily bound constitutively active gp185ErbB-2 (Fig.  1B) solubilized from NIH-ErbB-2 transfectants ( 17), whereas no ErbB-2 binding to GST beads (Fig.  1B) and GST-clone 52 beads incubated with NIH 3T3 lysates (data not shown) was observed.	bind
45368	2	10486	7	NULL	NULL	0	NULL	GST-clone 52 protein	NULL		bind	NULL	readily			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_20_7735_s_124	11003669	A GST-clone 52 fusion protein readily bound constitutively active gp185ErbB-2 (Fig.  1B) solubilized from NIH-ErbB-2 transfectants ( 17), whereas no ErbB-2 binding to GST beads (Fig.  1B) and GST-clone 52 beads incubated with NIH 3T3 lysates (data not shown) was observed.	bind
45369	1	10486	7	NULL	NULL	0	NULL	gp185ErbB-2	NULL		is solubilized from	NULL				NIH-ErbB-2 transfectants	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_20_7735_s_124	11003669	A GST-clone 52 fusion protein readily bound constitutively active gp185ErbB-2 (Fig.  1B) solubilized from NIH-ErbB-2 transfectants ( 17), whereas no ErbB-2 binding to GST beads (Fig.  1B) and GST-clone 52 beads incubated with NIH 3T3 lysates (data not shown) was observed.	bind
45370	3	10486	7	10	NULL	0	NULL	 ErbB-2	NULL		does not bind	NULL				GST	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_20_7735_s_124	11003669	A GST-clone 52 fusion protein readily bound constitutively active gp185ErbB-2 (Fig.  1B) solubilized from NIH-ErbB-2 transfectants ( 17), whereas no ErbB-2 binding to GST beads (Fig.  1B) and GST-clone 52 beads incubated with NIH 3T3 lysates (data not shown) was observed.	bind
45371	4	10486	7	NULL	NULL	0	NULL	ErbB-2	NULL		does not bind	NULL				GST-clone 52	NULL				NULL	NIH 3T3 lysates 	0	NULL	NULL	NULL	gw60_molcellbiol_20_20_7735_s_124	11003669	A GST-clone 52 fusion protein readily bound constitutively active gp185ErbB-2 (Fig.  1B) solubilized from NIH-ErbB-2 transfectants ( 17), whereas no ErbB-2 binding to GST beads (Fig.  1B) and GST-clone 52 beads incubated with NIH 3T3 lysates (data not shown) was observed.	bind
45372	5	10486	7	NULL	NULL	0	NULL	GST-clone 52	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_20_7735_s_124	11003669	A GST-clone 52 fusion protein readily bound constitutively active gp185ErbB-2 (Fig.  1B) solubilized from NIH-ErbB-2 transfectants ( 17), whereas no ErbB-2 binding to GST beads (Fig.  1B) and GST-clone 52 beads incubated with NIH 3T3 lysates (data not shown) was observed.	bind
38929	1	10487	6	13	NULL	NULL	NULL	GST-CRIB	GP	immobilized	bind					GFP-Cdc42	GP				NULL	yeast lysates	NULL	NULL	NULL	NULL	gw70_pnas_103_11_4116_s_152	16537494	A GST-CRIB fusion protein immobilized on glutathione beads was incubated with yeast lysates; bound GFP-Cdc42.	bind
50220	2	10487	6	13	NULL	NULL	NULL	GST-CRIB	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_11_4116_s_152	16537494	A GST-CRIB fusion protein immobilized on glutathione beads was incubated with yeast lysates; bound GFP-Cdc42.	bind
45373	1	10487	7	NULL	NULL	0	NULL	GST-CRIB protein	NULL	immobilized	bind	NULL				GFP-Cdc42	NULL				NULL	yeast lysates	0	NULL	NULL	NULL	gw70_pnas_103_11_4116_s_152	16537494	A GST-CRIB fusion protein immobilized on glutathione beads was incubated with yeast lysates; bound GFP-Cdc42.	bind
45374	2	10487	7	NULL	NULL	0	NULL	GST-CRIB protein	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_11_4116_s_152	16537494	A GST-CRIB fusion protein immobilized on glutathione beads was incubated with yeast lysates; bound GFP-Cdc42.	bind
38930	1	10488	6	13	NULL	NULL	NULL	GST-Ebp1	GP		encodes								amino acids 293 - 372		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_8_2168_s_197	12682367	A GST-Ebp1 fusion protein encoding amino acids 293 - 372 (encompassing the HDAC2 binding domain) bound HDAC enzymatic activity as well as full-length Ebp1.	bind
38931	2	10488	6	13	NULL	NULL	NULL	GST-Ebp1	GP		encompasses								HDAC2 binding domain		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_8_2168_s_197	12682367	A GST-Ebp1 fusion protein encoding amino acids 293 - 372 (encompassing the HDAC2 binding domain) bound HDAC enzymatic activity as well as full-length Ebp1.	bind
38932	3	10488	6	13	NULL	NULL	NULL	GST-Ebp1	GP		bind					HDAC	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_8_2168_s_197	12682367	A GST-Ebp1 fusion protein encoding amino acids 293 - 372 (encompassing the HDAC2 binding domain) bound HDAC enzymatic activity as well as full-length Ebp1.	bind
38933	4	10488	6	13	NULL	NULL	NULL	GST-Ebp1	GP		bind					Ebp1	GP	full length			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_8_2168_s_197	12682367	A GST-Ebp1 fusion protein encoding amino acids 293 - 372 (encompassing the HDAC2 binding domain) bound HDAC enzymatic activity as well as full-length Ebp1.	bind
50221	5	10488	6	13	NULL	NULL	NULL	GST-Ebp1 	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_8_2168_s_197	12682367	A GST-Ebp1 fusion protein encoding amino acids 293 - 372 (encompassing the HDAC2 binding domain) bound HDAC enzymatic activity as well as full-length Ebp1.	bind
45375	1	10488	7	NULL	NULL	0	NULL	GST-Ebp1	NULL		encode	NULL					NULL		amino acids 293 - 372		NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_8_2168_s_197	12682367	A GST-Ebp1 fusion protein encoding amino acids 293 - 372 (encompassing the HDAC2 binding domain) bound HDAC enzymatic activity as well as full-length Ebp1.	bind
45376	2	10488	7	10	NULL	0	NULL	statement 1			encompass								HDAC2 binding domain		NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_8_2168_s_197	12682367	A GST-Ebp1 fusion protein encoding amino acids 293 - 372 (encompassing the HDAC2 binding domain) bound HDAC enzymatic activity as well as full-length Ebp1.	bind
45377	3	10488	7	NULL	NULL	0	NULL	statement 2	NULL		bind	NULL				HDAC	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_8_2168_s_197	12682367	A GST-Ebp1 fusion protein encoding amino acids 293 - 372 (encompassing the HDAC2 binding domain) bound HDAC enzymatic activity as well as full-length Ebp1.	bind
45378	4	10488	7	NULL	NULL	0	NULL	statement 2	NULL		bind	NULL				Ebp1	NULL	full-length			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_8_2168_s_197	12682367	A GST-Ebp1 fusion protein encoding amino acids 293 - 372 (encompassing the HDAC2 binding domain) bound HDAC enzymatic activity as well as full-length Ebp1.	bind
45379	5	10488	7	NULL	NULL	0	NULL	GST-Ebp1 	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_8_2168_s_197	12682367	A GST-Ebp1 fusion protein encoding amino acids 293 - 372 (encompassing the HDAC2 binding domain) bound HDAC enzymatic activity as well as full-length Ebp1.	bind
39114	1	10489	6	13	NULL	NULL	NULL	GST-fusion protein	GP		contains					l-afadin	GP		PDZ domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_3_539_s_153	10225955	A GST-fusion protein  of the PDZ domain of l-afadin (GST-l-afadin-PDZ)  bound to a Myc-tagged protein of the cytoplasmic region  of nectin-1 (Myc-nectin-1-CP) immobilized on protein  A-Sepharose beads through the anti-Myc mAb (Fig.  2 A).	bind
39115	2	10489	6	13	NULL	NULL	NULL	statement 1	GP		is					GST-1-afadin-PDZ	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_3_539_s_153	10225955	A GST-fusion protein  of the PDZ domain of l-afadin (GST-l-afadin-PDZ)  bound to a Myc-tagged protein of the cytoplasmic region  of nectin-1 (Myc-nectin-1-CP) immobilized on protein  A-Sepharose beads through the anti-Myc mAb (Fig.  2 A).	bind
39116	3	10489	6	13	NULL	NULL	NULL	nectin-1	GP	Myc-tagged	is			cytoplasmic region		Myc-nectin-1-CP	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_3_539_s_153	10225955	A GST-fusion protein  of the PDZ domain of l-afadin (GST-l-afadin-PDZ)  bound to a Myc-tagged protein of the cytoplasmic region  of nectin-1 (Myc-nectin-1-CP) immobilized on protein  A-Sepharose beads through the anti-Myc mAb (Fig.  2 A).	bind
39117	4	10489	6	13	NULL	NULL	NULL	GST-l-afadin-PDZ	GP		bind					Myc-nectin-1-CP	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_3_539_s_153	10225955	A GST-fusion protein  of the PDZ domain of l-afadin (GST-l-afadin-PDZ)  bound to a Myc-tagged protein of the cytoplasmic region  of nectin-1 (Myc-nectin-1-CP) immobilized on protein  A-Sepharose beads through the anti-Myc mAb (Fig.  2 A).	bind
45380	1	10489	7	NULL	NULL	0	NULL	GST-l-afadin-PDZ	NULL		bind	NULL				Myc-nectin-1-CP	NULL	immobilized			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_3_539_s_153	10225955	A GST-fusion protein  of the PDZ domain of l-afadin (GST-l-afadin-PDZ)  bound to a Myc-tagged protein of the cytoplasmic region  of nectin-1 (Myc-nectin-1-CP) immobilized on protein  A-Sepharose beads through the anti-Myc mAb (Fig.  2 A).	bind
45381	2	10489	7	NULL	NULL	0	NULL	GST-l-afadin-PDZ	NULL		is	NULL				l-afadin 	NULL		PDZ domain		NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_3_539_s_153	10225955	A GST-fusion protein  of the PDZ domain of l-afadin (GST-l-afadin-PDZ)  bound to a Myc-tagged protein of the cytoplasmic region  of nectin-1 (Myc-nectin-1-CP) immobilized on protein  A-Sepharose beads through the anti-Myc mAb (Fig.  2 A).	bind
45382	3	10489	7	NULL	NULL	0	NULL	statement 2	NULL		is a type of	NULL				GST-fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_3_539_s_153	10225955	A GST-fusion protein  of the PDZ domain of l-afadin (GST-l-afadin-PDZ)  bound to a Myc-tagged protein of the cytoplasmic region  of nectin-1 (Myc-nectin-1-CP) immobilized on protein  A-Sepharose beads through the anti-Myc mAb (Fig.  2 A).	bind
45383	4	10489	7	NULL	NULL	0	NULL	Myc-nectin-1-CP	NULL		is	NULL				nectin-1	NULL		cytoplasmic region of		NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_3_539_s_153	10225955	A GST-fusion protein  of the PDZ domain of l-afadin (GST-l-afadin-PDZ)  bound to a Myc-tagged protein of the cytoplasmic region  of nectin-1 (Myc-nectin-1-CP) immobilized on protein  A-Sepharose beads through the anti-Myc mAb (Fig.  2 A).	bind
45384	5	10489	7	NULL	NULL	0	NULL	statement 4	NULL		is a type of	NULL				Myc-tagged protein 	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_3_539_s_153	10225955	A GST-fusion protein  of the PDZ domain of l-afadin (GST-l-afadin-PDZ)  bound to a Myc-tagged protein of the cytoplasmic region  of nectin-1 (Myc-nectin-1-CP) immobilized on protein  A-Sepharose beads through the anti-Myc mAb (Fig.  2 A).	bind
38934	1	10490	6	13	NULL	NULL	NULL	GST-fusion protein	GP		carry					hSet2/HYPB	GP		residues 1,884 - 2,061		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_49_17636_s_30	16314571	A GST-fusion protein carrying residues 1,884 - 2,061 of hSet2/HYPB, containing a WW domain and a putative SRI domain, was expressed in and purified from bacterial cells (see  Supporting Text, which is published as  supporting information on the PNAS web site, for detailed procedures); far-Western blotting (performed as described in ref.  ) confirmed that this fusion protein binds the PCTD.	bind
38935	2	10490	6	13	NULL	NULL	NULL	GST-fusion protein	GP		contains								WW domain		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_49_17636_s_30	16314571	A GST-fusion protein carrying residues 1,884 - 2,061 of hSet2/HYPB, containing a WW domain and a putative SRI domain, was expressed in and purified from bacterial cells (see  Supporting Text, which is published as  supporting information on the PNAS web site, for detailed procedures); far-Western blotting (performed as described in ref.  ) confirmed that this fusion protein binds the PCTD.	bind
38936	3	10490	6	13	NULL	NULL	NULL	GST-fusion protein	GP		contains							putative	SRI domain		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_49_17636_s_30	16314571	A GST-fusion protein carrying residues 1,884 - 2,061 of hSet2/HYPB, containing a WW domain and a putative SRI domain, was expressed in and purified from bacterial cells (see  Supporting Text, which is published as  supporting information on the PNAS web site, for detailed procedures); far-Western blotting (performed as described in ref.  ) confirmed that this fusion protein binds the PCTD.	bind
38937	4	10490	6	13	NULL	NULL	NULL	GST-fusion protein	GP		bind					PCTD	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_49_17636_s_30	16314571	A GST-fusion protein carrying residues 1,884 - 2,061 of hSet2/HYPB, containing a WW domain and a putative SRI domain, was expressed in and purified from bacterial cells (see  Supporting Text, which is published as  supporting information on the PNAS web site, for detailed procedures); far-Western blotting (performed as described in ref.  ) confirmed that this fusion protein binds the PCTD.	bind
45385	1	10490	7	NULL	NULL	0	NULL	GST-fusion protein	NULL		contains	NULL				hSet2/HYPB	NULL		residues 1,884 - 2,061		NULL		0	NULL	NULL	NULL	gw70_pnas_102_49_17636_s_30	16314571	A GST-fusion protein carrying residues 1,884 - 2,061 of hSet2/HYPB, containing a WW domain and a putative SRI domain, was expressed in and purified from bacterial cells (see  Supporting Text, which is published as  supporting information on the PNAS web site, for detailed procedures); far-Western blotting (performed as described in ref.  ) confirmed that this fusion protein binds the PCTD.	bind
45572	2	10490	7	10	NULL	0	NULL	GST-fusion protein			contains								WW domain		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_49_17636_s_30	16314571	A GST-fusion protein carrying residues 1,884 - 2,061 of hSet2/HYPB, containing a WW domain and a putative SRI domain, was expressed in and purified from bacterial cells (see  Supporting Text, which is published as  supporting information on the PNAS web site, for detailed procedures); far-Western blotting (performed as described in ref.  ) confirmed that this fusion protein binds the PCTD.	bind
45573	3	10490	7	10	NULL	0	NULL	GST-fusion protein			contains							putative	SRI domain		NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_49_17636_s_30	16314571	A GST-fusion protein carrying residues 1,884 - 2,061 of hSet2/HYPB, containing a WW domain and a putative SRI domain, was expressed in and purified from bacterial cells (see  Supporting Text, which is published as  supporting information on the PNAS web site, for detailed procedures); far-Western blotting (performed as described in ref.  ) confirmed that this fusion protein binds the PCTD.	bind
45575	5	10490	7	NULL	NULL	0	NULL	statement 1	NULL		occur along  with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_49_17636_s_30	16314571	A GST-fusion protein carrying residues 1,884 - 2,061 of hSet2/HYPB, containing a WW domain and a putative SRI domain, was expressed in and purified from bacterial cells (see  Supporting Text, which is published as  supporting information on the PNAS web site, for detailed procedures); far-Western blotting (performed as described in ref.  ) confirmed that this fusion protein binds the PCTD.	bind
45576	6	10490	7	NULL	NULL	0	NULL	statement 1	NULL		occur along with	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_49_17636_s_30	16314571	A GST-fusion protein carrying residues 1,884 - 2,061 of hSet2/HYPB, containing a WW domain and a putative SRI domain, was expressed in and purified from bacterial cells (see  Supporting Text, which is published as  supporting information on the PNAS web site, for detailed procedures); far-Western blotting (performed as described in ref.  ) confirmed that this fusion protein binds the PCTD.	bind
45577	7	10490	7	NULL	NULL	0	NULL	GST-fusion protein	NULL		bind	NULL				PCTD	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_49_17636_s_30	16314571	A GST-fusion protein carrying residues 1,884 - 2,061 of hSet2/HYPB, containing a WW domain and a putative SRI domain, was expressed in and purified from bacterial cells (see  Supporting Text, which is published as  supporting information on the PNAS web site, for detailed procedures); far-Western blotting (performed as described in ref.  ) confirmed that this fusion protein binds the PCTD.	bind
38939	1	10492	6	13	NULL	NULL	NULL	GST-Fyn SH2	GP		bind		directly			Syk	GP				NULL	Jurkat-TAg cells transfected with H902-tagged Syk	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8867_s_219	9535867	A GST-Fyn SH2 fusion protein directly bound to Syk as demonstrated by Far-Western blotting of cell lysates from Jurkat-TAg cells transfected with H902-tagged Syk or with an empty vector (pME18S) (Fig.  8 A,  top panel).	bind
50222	2	10492	6	13	NULL	NULL	NULL	GST-Fyn SH2	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8867_s_219	9535867	A GST-Fyn SH2 fusion protein directly bound to Syk as demonstrated by Far-Western blotting of cell lysates from Jurkat-TAg cells transfected with H902-tagged Syk or with an empty vector (pME18S) (Fig.  8 A,  top panel).	bind
45585	1	10492	7	10	NULL	0	NULL	GST-Fyn SH2	NULL		bind	NULL	directly			Syk	NULL				NULL	Jurkat-TAg cell lysates transfected with H902-tagged Syk	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8867_s_219	9535867	A GST-Fyn SH2 fusion protein directly bound to Syk as demonstrated by Far-Western blotting of cell lysates from Jurkat-TAg cells transfected with H902-tagged Syk or with an empty vector (pME18S) (Fig.  8 A,  top panel).	bind
45586	2	10492	7	10	NULL	0	NULL	GST-Fyn SH2	NULL		is a type of	NULL				fusion protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_15_8867_s_219	9535867	A GST-Fyn SH2 fusion protein directly bound to Syk as demonstrated by Far-Western blotting of cell lysates from Jurkat-TAg cells transfected with H902-tagged Syk or with an empty vector (pME18S) (Fig.  8 A,  top panel).	bind
38940	1	10494	6	13	NULL	NULL	NULL	NS1 protein	GP	35S-labeled	bind					GST-Neb1 protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_1_7_991_s_57	9651582	A GST-Neb1 fusion protein was bound to glutathione agarose beads, and the ability of a 35S-labeled NS1 protein to bind to the GST-Neb1 protein was determined (  Figure 1B).	bind
45587	1	10494	7	NULL	NULL	0	NULL	NS1 protein	NULL	35S-labeled 	bind	NULL				GST-Neb1 protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_1_7_991_s_57	9651582	A GST-Neb1 fusion protein was bound to glutathione agarose beads, and the ability of a 35S-labeled NS1 protein to bind to the GST-Neb1 protein was determined (  Figure 1B).	bind
38941	1	10495	6	13	NULL	NULL	NULL	GST-PFD	GP		bind		specifically			gD260t	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_26_9323_s_241	15972328	A GST-PFD fusion protein specifically bound gD260t or longer forms of gD.	bind
38942	2	10495	6	13	NULL	NULL	NULL	GST-PFD	GP		bind		specifically			gD	GP	longer forms of 			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_26_9323_s_241	15972328	A GST-PFD fusion protein specifically bound gD260t or longer forms of gD.	bind
50223	3	10495	6	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_26_9323_s_241	15972328	A GST-PFD fusion protein specifically bound gD260t or longer forms of gD.	bind
50224	4	10495	6	13	NULL	NULL	NULL	GST-PFD	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_26_9323_s_241	15972328	A GST-PFD fusion protein specifically bound gD260t or longer forms of gD.	bind
45588	1	10495	7	NULL	NULL	0	NULL	GST-PFD	NULL		bind	NULL	specifically			gD260t	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_26_9323_s_241	15972328	A GST-PFD fusion protein specifically bound gD260t or longer forms of gD.	bind
45589	2	10495	7	10	NULL	0	NULL	GST-PFD			bind		specifically			gD		longer forms of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_26_9323_s_241	15972328	A GST-PFD fusion protein specifically bound gD260t or longer forms of gD.	bind
45590	3	10495	7	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_26_9323_s_241	15972328	A GST-PFD fusion protein specifically bound gD260t or longer forms of gD.	bind
45591	4	10495	7	NULL	NULL	0	NULL	GST-PFD	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_26_9323_s_241	15972328	A GST-PFD fusion protein specifically bound gD260t or longer forms of gD.	bind
38943	1	10496	6	13	NULL	NULL	NULL	GST-syntenin	GP		bind					GST-syndecan-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_19933_s_125	10770943	A GST-syntenin fusion protein binds also to GST-syndecan-2 fusion proteins that have been fractionated by SDS-PAGE and blotted on nitrocellulose membranes ( 2).	bind
50225	2	10496	6	13	NULL	NULL	NULL	GST-syntenin	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_19933_s_125	10770943	A GST-syntenin fusion protein binds also to GST-syndecan-2 fusion proteins that have been fractionated by SDS-PAGE and blotted on nitrocellulose membranes ( 2).	bind
50226	3	10496	6	13	NULL	NULL	NULL	GST-syndecan-2	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_19933_s_125	10770943	A GST-syntenin fusion protein binds also to GST-syndecan-2 fusion proteins that have been fractionated by SDS-PAGE and blotted on nitrocellulose membranes ( 2).	bind
45592	1	10496	7	NULL	NULL	0	NULL	GST-syntenin	NULL		bind	NULL				GST-syndecan-2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_26_19933_s_125	10770943	A GST-syntenin fusion protein binds also to GST-syndecan-2 fusion proteins that have been fractionated by SDS-PAGE and blotted on nitrocellulose membranes ( 2).	bind
45593	2	10496	7	NULL	NULL	0	NULL	GST-syntenin	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_26_19933_s_125	10770943	A GST-syntenin fusion protein binds also to GST-syndecan-2 fusion proteins that have been fractionated by SDS-PAGE and blotted on nitrocellulose membranes ( 2).	bind
45594	3	10496	7	NULL	NULL	0	NULL	GST-syndecan-2	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_26_19933_s_125	10770943	A GST-syntenin fusion protein binds also to GST-syndecan-2 fusion proteins that have been fractionated by SDS-PAGE and blotted on nitrocellulose membranes ( 2).	bind
38944	1	10497	6	13	NULL	NULL	NULL	GST-TAP20	GP		bind		specifically			beta5 integrin	GP	detergent-solubilized			NULL	ECV cells	NULL	NULL	NULL	NULL	gw60_cellbiol_147_5_1073_s_251	10579726	A GST-TAP20 fusion protein coprecipitated specifically with detergent-solubilized beta5 integrin from ECV cells, and thus the binding of TAP20 to beta5 integrin does not depend on the existence of alphav.	bind
38945	2	10497	6	13	NULL	NULL	NULL	statement 1	Process		does not depend on					alphav	GP	existence of 			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_147_5_1073_s_251	10579726	A GST-TAP20 fusion protein coprecipitated specifically with detergent-solubilized beta5 integrin from ECV cells, and thus the binding of TAP20 to beta5 integrin does not depend on the existence of alphav.	bind
50227	3	10497	6	13	NULL	NULL	NULL	GST-TAP20	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_147_5_1073_s_251	10579726	A GST-TAP20 fusion protein coprecipitated specifically with detergent-solubilized beta5 integrin from ECV cells, and thus the binding of TAP20 to beta5 integrin does not depend on the existence of alphav.	bind
45595	1	10497	7	10	NULL	0	NULL	GST-TAP20			bind		specifically			beta5 integrin		detergent-solubilized			NULL	ECV cells	NULL	NULL	NULL	NULL	gw60_cellbiol_147_5_1073_s_251	10579726	A GST-TAP20 fusion protein coprecipitated specifically with detergent-solubilized beta5 integrin from ECV cells, and thus the binding of TAP20 to beta5 integrin does not depend on the existence of alphav.	bind
45596	2	10497	7	NULL	NULL	0	NULL	statement 1	NULL		does not depend on	NULL				alphav	NULL	existence of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_5_1073_s_251	10579726	A GST-TAP20 fusion protein coprecipitated specifically with detergent-solubilized beta5 integrin from ECV cells, and thus the binding of TAP20 to beta5 integrin does not depend on the existence of alphav.	bind
45597	3	10497	7	NULL	NULL	0	NULL	GST-TAP20	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_5_1073_s_251	10579726	A GST-TAP20 fusion protein coprecipitated specifically with detergent-solubilized beta5 integrin from ECV cells, and thus the binding of TAP20 to beta5 integrin does not depend on the existence of alphav.	bind
39118	1	10498	6	13	NULL	NULL	NULL	adenosine 3'',5''-monophosphate	Chemical	basal	regulates					surfactant protein A2 gene	GP	human			NULL	alveolar type II cells	NULL	NULL	NULL	NULL	gw70_annurevphysiol_62_0_875_s_1384	10845115	A GT box element is essential for basal and cyclic  adenosine 3'',5''-monophosphate regulation of the  human surfactant protein A2 gene in alveolar type II cells: evidence for the binding of lung nuclear proteins  distinct from Sp1.	bind
39119	3	10498	6	13	NULL	NULL	NULL				is essential for				GT box element	statement 1	Process				NULL	alveolar type II cells	NULL	NULL	NULL	NULL	gw70_annurevphysiol_62_0_875_s_1384	10845115	A GT box element is essential for basal and cyclic  adenosine 3'',5''-monophosphate regulation of the  human surfactant protein A2 gene in alveolar type II cells: evidence for the binding of lung nuclear proteins  distinct from Sp1.	bind
50762	2	10498	6	13	NULL	NULL	NULL	adenosine 3'',5''-monophosphate	Chemical	cyclic	regulates					surfactant protein A2 gene	GP	human			NULL	alveolar type II cells	NULL	NULL	NULL	NULL	gw70_annurevphysiol_62_0_875_s_1384	10845115	A GT box element is essential for basal and cyclic  adenosine 3'',5''-monophosphate regulation of the  human surfactant protein A2 gene in alveolar type II cells: evidence for the binding of lung nuclear proteins  distinct from Sp1.	bind
50763	4	10498	6	13	NULL	NULL	NULL				is essential for				GT box element	statement 2	Process				NULL	alveolar type II cells	NULL	NULL	NULL	NULL	gw70_annurevphysiol_62_0_875_s_1384	10845115	A GT box element is essential for basal and cyclic  adenosine 3'',5''-monophosphate regulation of the  human surfactant protein A2 gene in alveolar type II cells: evidence for the binding of lung nuclear proteins  distinct from Sp1.	bind
50764	5	10498	6	13	NULL	NULL	NULL	lung nuclear proteins	GP	binding of	is distinct from					Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_62_0_875_s_1384	10845115	A GT box element is essential for basal and cyclic  adenosine 3'',5''-monophosphate regulation of the  human surfactant protein A2 gene in alveolar type II cells: evidence for the binding of lung nuclear proteins  distinct from Sp1.	bind
45598	1	10498	7	NULL	NULL	0	NULL	adenosine 3'',5''-monophosphate	NULL	basal	regulates	NULL				surfactant protein A2 gene	NULL	human			NULL	 alveolar type II cells	0	NULL	NULL	NULL	gw70_annurevphysiol_62_0_875_s_1384	10845115	A GT box element is essential for basal and cyclic  adenosine 3'',5''-monophosphate regulation of the  human surfactant protein A2 gene in alveolar type II cells: evidence for the binding of lung nuclear proteins  distinct from Sp1.	bind
45599	2	10498	7	NULL	NULL	0	NULL	adenosine 3'',5''-monophosphate	NULL	cyclic	regulates	NULL				surfactant protein A2 gene	NULL	human			NULL	alveolar type II cells	0	NULL	NULL	NULL	gw70_annurevphysiol_62_0_875_s_1384	10845115	A GT box element is essential for basal and cyclic  adenosine 3'',5''-monophosphate regulation of the  human surfactant protein A2 gene in alveolar type II cells: evidence for the binding of lung nuclear proteins  distinct from Sp1.	bind
45600	3	10498	7	10	NULL	0	NULL				is essential for				GT box element	statement 1					NULL	alveolar type II cells	NULL	NULL	NULL	NULL	gw70_annurevphysiol_62_0_875_s_1384	10845115	A GT box element is essential for basal and cyclic  adenosine 3'',5''-monophosphate regulation of the  human surfactant protein A2 gene in alveolar type II cells: evidence for the binding of lung nuclear proteins  distinct from Sp1.	bind
45601	4	10498	7	10	NULL	0	NULL				is essential for				GT box element	statement 2					NULL	alveolar type II cells	NULL	NULL	NULL	NULL	gw70_annurevphysiol_62_0_875_s_1384	10845115	A GT box element is essential for basal and cyclic  adenosine 3'',5''-monophosphate regulation of the  human surfactant protein A2 gene in alveolar type II cells: evidence for the binding of lung nuclear proteins  distinct from Sp1.	bind
45602	5	10498	7	NULL	NULL	0	NULL	lung nuclear proteins	NULL	binding of	is distinct from	NULL				Sp1	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevphysiol_62_0_875_s_1384	10845115	A GT box element is essential for basal and cyclic  adenosine 3'',5''-monophosphate regulation of the  human surfactant protein A2 gene in alveolar type II cells: evidence for the binding of lung nuclear proteins  distinct from Sp1.	bind
38946	1	10502	6	13	NULL	NULL	NULL	Ran	GP	yeast	bind			G21V		GTP	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_31_0_277_s_295	9442897	A GTP-bound form of yeast Ran (G21V;  146), as well as mutations in  YRB1 ( 147), and in  RNA1 ( 25,  95), block nuclear protein import and the appearance of poly	bind
38947	2	10502	6	13	NULL	NULL	NULL	RNA1	GP	mutant	blocks					nuclear protein	GP	import of			NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_31_0_277_s_295	9442897	A GTP-bound form of yeast Ran (G21V;  146), as well as mutations in  YRB1 ( 147), and in  RNA1 ( 25,  95), block nuclear protein import and the appearance of poly	bind
38948	3	10502	6	13	NULL	NULL	NULL	YRB1	GP	mutant	blocks					nuclear protein	GP	import of			NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_31_0_277_s_295	9442897	A GTP-bound form of yeast Ran (G21V;  146), as well as mutations in  YRB1 ( 147), and in  RNA1 ( 25,  95), block nuclear protein import and the appearance of poly	bind
38949	4	10502	6	13	NULL	NULL	NULL	statement 1	Process		blocks					nuclear protein	GP	import of			NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_31_0_277_s_295	9442897	A GTP-bound form of yeast Ran (G21V;  146), as well as mutations in  YRB1 ( 147), and in  RNA1 ( 25,  95), block nuclear protein import and the appearance of poly	bind
46219	1	10502	7	10	NULL	0	NULL	GTP	NULL		bind	NULL				Ran	NULL	yeast	G21V		NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_31_0_277_s_295	9442897	A GTP-bound form of yeast Ran (G21V;  146), as well as mutations in  YRB1 ( 147), and in  RNA1 ( 25,  95), block nuclear protein import and the appearance of poly	bind
46220	2	10502	7	10	NULL	0	NULL	statement 1	NULL		block	NULL				nuclear protein	NULL	import of			NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_31_0_277_s_295	9442897	A GTP-bound form of yeast Ran (G21V;  146), as well as mutations in  YRB1 ( 147), and in  RNA1 ( 25,  95), block nuclear protein import and the appearance of poly	bind
46221	3	10502	7	10	NULL	0	NULL	YRB1	NULL	mutant	block	NULL				nuclear protein	NULL	import of			NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_31_0_277_s_295	9442897	A GTP-bound form of yeast Ran (G21V;  146), as well as mutations in  YRB1 ( 147), and in  RNA1 ( 25,  95), block nuclear protein import and the appearance of poly	bind
46222	4	10502	7	10	NULL	0	NULL	RNA1	NULL	mutant	block	NULL				nuclear protein	NULL	import of			NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_31_0_277_s_295	9442897	A GTP-bound form of yeast Ran (G21V;  146), as well as mutations in  YRB1 ( 147), and in  RNA1 ( 25,  95), block nuclear protein import and the appearance of poly	bind
38950	1	10503	6	13	NULL	NULL	NULL	GBD	GP		is					GTPase-binding domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35761_s_28	11459849	A GTPase-binding domain (GBD) binds Cdc42, a Rho family GTPase ( 14).	bind
38951	2	10503	6	13	NULL	NULL	NULL				bind			GBD		Cdc42	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35761_s_28	11459849	A GTPase-binding domain (GBD) binds Cdc42, a Rho family GTPase ( 14).	bind
38952	3	10503	6	13	NULL	NULL	NULL	Cdc42	GP		is a type of					Rho family GTPase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35761_s_28	11459849	A GTPase-binding domain (GBD) binds Cdc42, a Rho family GTPase ( 14).	bind
46223	1	10503	7	NULL	NULL	0	NULL		NULL		binds	NULL		GBD		Cdc42	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_38_35761_s_28	11459849	A GTPase-binding domain (GBD) binds Cdc42, a Rho family GTPase ( 14).	bind
46224	2	10503	7	10	NULL	0	NULL	GBD	NULL		is	NULL				GTPase-binding domain	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35761_s_28	11459849	A GTPase-binding domain (GBD) binds Cdc42, a Rho family GTPase ( 14).	bind
46225	3	10503	7	NULL	NULL	0	NULL	Cdc42	NULL		is a type of	NULL				Rho family GTPase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_38_35761_s_28	11459849	A GTPase-binding domain (GBD) binds Cdc42, a Rho family GTPase ( 14).	bind
38953	1	10504	6	13	NULL	NULL	NULL	guanine nucleotide exchange factor for Ras	GP		bind					GRB2	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_18_2295_s_824	9308960	A guanine nucleotide exchange factor for Ras that binds to GRB2.	bind
46227	1	10504	7	10	NULL	0	NULL	guanine nucleotide exchange factor for Ras	NULL		bind	NULL				GRB2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_18_2295_s_824	9308960	A guanine nucleotide exchange factor for Ras that binds to GRB2.	bind
38954	1	10506	6	13	NULL	NULL	NULL	UNC-18	GP		bind					Ce syntaxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_12_4772_s_93	10366611	A half-maximal binding (ED50) of UNC-18 to  Ce syntaxin occurred at 0.08 muM.	bind
46228	1	10506	7	NULL	NULL	0	NULL	UNC-18 	NULL		bind	NULL				Ce syntaxin	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_12_4772_s_93	10366611	A half-maximal binding (ED50) of UNC-18 to  Ce syntaxin occurred at 0.08 muM.	bind
38955	1	10507	6	13	NULL	NULL	NULL	dopamine	Chemical		bind					NCS	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_33878_s_136	12107162	A Hanes plot ([substrate concentration] nH V 1 versus [substrate concentration] nH), where  nH = 1.8, also produced a linear function confirming the positive cooperativity of dopamine binding to NCS at a saturating level of 4-HPAA. Varying the concentration of 4-HPAA from 0.2 to 1.3 mM at a saturating level (280 muM) of dopamine produced hyperbolic saturation kinetics, indicating the lack of cooperativity in the binding of 4-HPAA to purified NCS.	bind
38956	2	10507	6	13	NULL	NULL	NULL	4-HPAA	GP		bind					NCS	GP	purified			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_33878_s_136	12107162	A Hanes plot ([substrate concentration] nH V 1 versus [substrate concentration] nH), where  nH = 1.8, also produced a linear function confirming the positive cooperativity of dopamine binding to NCS at a saturating level of 4-HPAA. Varying the concentration of 4-HPAA from 0.2 to 1.3 mM at a saturating level (280 muM) of dopamine produced hyperbolic saturation kinetics, indicating the lack of cooperativity in the binding of 4-HPAA to purified NCS.	bind
46229	1	10507	7	NULL	NULL	0	NULL	dopamine	NULL		bind	NULL				NCS	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_37_33878_s_136	12107162	A Hanes plot ([substrate concentration] nH V 1 versus [substrate concentration] nH), where  nH = 1.8, also produced a linear function confirming the positive cooperativity of dopamine binding to NCS at a saturating level of 4-HPAA. Varying the concentration of 4-HPAA from 0.2 to 1.3 mM at a saturating level (280 muM) of dopamine produced hyperbolic saturation kinetics, indicating the lack of cooperativity in the binding of 4-HPAA to purified NCS.	bind
46230	2	10507	7	NULL	NULL	0	NULL	 4-HPAA	NULL		bind	NULL				NCS	NULL	purified			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_37_33878_s_136	12107162	A Hanes plot ([substrate concentration] nH V 1 versus [substrate concentration] nH), where  nH = 1.8, also produced a linear function confirming the positive cooperativity of dopamine binding to NCS at a saturating level of 4-HPAA. Varying the concentration of 4-HPAA from 0.2 to 1.3 mM at a saturating level (280 muM) of dopamine produced hyperbolic saturation kinetics, indicating the lack of cooperativity in the binding of 4-HPAA to purified NCS.	bind
39120	1	10508	6	13	NULL	NULL	NULL	PRT1 - TIF34 - TIF35 subcomplex	GP		does not bind					TIF32-delta5-His	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5886_s_198	12411506	A hc plasmid with  PRT1,  TIF34 and  TIF35 did not suppress the Slg -  phenotype of hc  TIF32-delta5-His (Figure  5D, sector 3 versus 5), in agreement with the fact that the PRT1 - TIF34 - TIF35 subcomplex does not bind to TIF32-delta5-His.	bind
46231	1	10508	7	NULL	NULL	0	NULL	PRT1 - TIF34 - TIF35 subcomplex	NULL		does not bind	NULL				TIF32-delta5-His	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5886_s_198	12411506	A hc plasmid with  PRT1,  TIF34 and  TIF35 did not suppress the Slg -  phenotype of hc  TIF32-delta5-His (Figure  5D, sector 3 versus 5), in agreement with the fact that the PRT1 - TIF34 - TIF35 subcomplex does not bind to TIF32-delta5-His.	bind
38958	1	10509	6	13	NULL	NULL	NULL	head-to-tail monomer of Fu	GP		bind					Cos2	Cell				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_23_10397_s_86	15542847	A head-to-tail monomer of Fu binds Cos2.	bind
46232	1	10509	7	10	NULL	0	NULL	 head-to-tail monomer of Fu	NULL		bind	NULL				Cos2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_23_10397_s_86	15542847	A head-to-tail monomer of Fu binds Cos2.	bind
38959	1	10510	6	13	NULL	NULL	NULL	HSF1	GP	human	regulates			heat shock-responsive domain				function of	transcription activation domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_4949_s_450	9710578	A heat shock-responsive domain of human HSF1 that regulates transcription activation domain function.	bind
46233	1	10510	7	NULL	NULL	0	NULL	 HSF1	NULL	human	regulates	NULL		heat shock-responsive domain			NULL	function of	transcription activation domain		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_9_4949_s_450	9710578	A heat shock-responsive domain of human HSF1 that regulates transcription activation domain function.	bind
50815	1	10512	6	13	NULL	NULL	NULL	helicase	GP		catalyse					43 nucleotide DNA fragment	NucleicAcid	displacement of 			NULL		NULL	NULL	NULL	NULL	gw70_yeast_22_16_1269_s_255	16358299	A helicase that binds and translocates 5   3  will catalyse displacement of the 43 nucleotide DNA fragment.	bind
46234	1	10512	7	NULL	NULL	0	NULL	helicase	NULL		catalyse	NULL				43 nucleotide DNA fragment	NULL	displacement of			NULL		0	NULL	NULL	NULL	gw70_yeast_22_16_1269_s_255	16358299	A helicase that binds and translocates 5   3  will catalyse displacement of the 43 nucleotide DNA fragment.	bind
38962	1	10513	6	13	NULL	NULL	NULL	helix-loop-helix zipper protein	GP		forms a complex with		sequence specifically			Myc	GP				NULL		NULL	NULL	NULL	NULL	gw60_gene_216_1_155_s_181	9714786	A helix-loop-helix zipper protein that forms a sequence specific DNA binding complex with Myc.	bind
46235	1	10513	7	10	NULL	0	NULL	helix-loop-helix zipper protein	NULL		forms complex with	NULL	sequence specifically			Myc 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_gene_216_1_155_s_181	9714786	A helix-loop-helix zipper protein that forms a sequence specific DNA binding complex with Myc.	bind
38964	1	10514	6	13	NULL	NULL	NULL	basic fibroblast growth factor	GP		is a type of					angiogenic protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_82_3_321_s_307	9486660	A heparin binding angiogenic protein -- basic fibroblast growth factor -- is stored within basement membrane.	bind
38965	2	10514	6	13	NULL	NULL	NULL	basic fibroblast growth factor	GP		bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_82_3_321_s_307	9486660	A heparin binding angiogenic protein -- basic fibroblast growth factor -- is stored within basement membrane.	bind
38966	3	10514	6	13	NULL	NULL	NULL	basic fibroblast growth factor	GP		is stored within					basement membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_82_3_321_s_307	9486660	A heparin binding angiogenic protein -- basic fibroblast growth factor -- is stored within basement membrane.	bind
46237	1	10514	7	10	NULL	0	NULL	basic fibroblast growth factor	NULL		is a type of	NULL				angiogenic protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_82_3_321_s_307	9486660	A heparin binding angiogenic protein -- basic fibroblast growth factor -- is stored within basement membrane.	bind
46238	2	10514	7	NULL	NULL	0	NULL	basic fibroblast growth factor	NULL		is stored within	NULL				basement membrane	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_82_3_321_s_307	9486660	A heparin binding angiogenic protein -- basic fibroblast growth factor -- is stored within basement membrane.	bind
50230	3	10514	7	10	NULL	0	NULL	\tbasic fibroblast growth factor	NULL		bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_82_3_321_s_307	9486660	A heparin binding angiogenic protein -- basic fibroblast growth factor -- is stored within basement membrane.	bind
38967	1	10515	6	13	NULL	NULL	NULL	heparin	Chemical		bind					gp120	GP		V3 loop		NULL		NULL	NULL	NULL	NULL	gw70_neuroscience_128_1_143_s_285	15450361	A heparin site on gp120 for initial binding  is consistent with work showing that heparin binds to the V3 loop of gp120 to block  HIV-1 infectivity (  Harrop and Rider, 1998;   Rider, 1997).	bind
38969	2	10515	6	13	NULL	NULL	NULL	statement 1	Process		block					HIV-1	Organism	infectivity of			NULL		NULL	NULL	NULL	NULL	gw70_neuroscience_128_1_143_s_285	15450361	A heparin site on gp120 for initial binding  is consistent with work showing that heparin binds to the V3 loop of gp120 to block  HIV-1 infectivity (  Harrop and Rider, 1998;   Rider, 1997).	bind
46239	1	10515	7	NULL	NULL	0	NULL	heparin	NULL		bind	NULL				gp120	NULL		V3 loop		NULL		0	NULL	NULL	NULL	gw70_neuroscience_128_1_143_s_285	15450361	A heparin site on gp120 for initial binding  is consistent with work showing that heparin binds to the V3 loop of gp120 to block  HIV-1 infectivity (  Harrop and Rider, 1998;   Rider, 1997).	bind
46240	2	10515	7	10	NULL	0	NULL	statement 1			block					HIV-1		infectivity of			NULL		NULL	NULL	NULL	NULL	gw70_neuroscience_128_1_143_s_285	15450361	A heparin site on gp120 for initial binding  is consistent with work showing that heparin binds to the V3 loop of gp120 to block  HIV-1 infectivity (  Harrop and Rider, 1998;   Rider, 1997).	bind
39124	1	10516	6	13	NULL	NULL	NULL	Cyr61	GP	mutant	does not bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24953_s_9	10821835	A heparin-binding defective mutant of Cyr61 was unable to mediate fibroblast adhesion through integrin alpha6beta1 but still mediated endothelial cell adhesion through integrin alphaVbeta3, indicating that endothelial cell adhesion through integrin alphaVbeta3 is independent of the heparin-binding activity of Cyr61.	bind
39125	2	10516	6	13	NULL	NULL	NULL	statement 1	Process		does not mediate					fibroblast	Cell	adhesion of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24953_s_9	10821835	A heparin-binding defective mutant of Cyr61 was unable to mediate fibroblast adhesion through integrin alpha6beta1 but still mediated endothelial cell adhesion through integrin alphaVbeta3, indicating that endothelial cell adhesion through integrin alphaVbeta3 is independent of the heparin-binding activity of Cyr61.	bind
39126	3	10516	6	13	NULL	NULL	NULL	statement 2	Process		occurs through					integrin alpha6beta1 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24953_s_9	10821835	A heparin-binding defective mutant of Cyr61 was unable to mediate fibroblast adhesion through integrin alpha6beta1 but still mediated endothelial cell adhesion through integrin alphaVbeta3, indicating that endothelial cell adhesion through integrin alphaVbeta3 is independent of the heparin-binding activity of Cyr61.	bind
39127	4	10516	6	13	NULL	NULL	NULL	statement 1	Process		mediates					endothelial cells	Cell	adhesion of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24953_s_9	10821835	A heparin-binding defective mutant of Cyr61 was unable to mediate fibroblast adhesion through integrin alpha6beta1 but still mediated endothelial cell adhesion through integrin alphaVbeta3, indicating that endothelial cell adhesion through integrin alphaVbeta3 is independent of the heparin-binding activity of Cyr61.	bind
39128	5	10516	6	13	NULL	NULL	NULL	statement 4	Process		occurs through					integrin alphaVbeta3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24953_s_9	10821835	A heparin-binding defective mutant of Cyr61 was unable to mediate fibroblast adhesion through integrin alpha6beta1 but still mediated endothelial cell adhesion through integrin alphaVbeta3, indicating that endothelial cell adhesion through integrin alphaVbeta3 is independent of the heparin-binding activity of Cyr61.	bind
39129	6	10516	6	13	NULL	NULL	NULL	statement 5	Process		is independent of					Cyr61	GP	heparin-binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24953_s_9	10821835	A heparin-binding defective mutant of Cyr61 was unable to mediate fibroblast adhesion through integrin alpha6beta1 but still mediated endothelial cell adhesion through integrin alphaVbeta3, indicating that endothelial cell adhesion through integrin alphaVbeta3 is independent of the heparin-binding activity of Cyr61.	bind
48699	1	10516	7	NULL	NULL	0	NULL	fibroblast	NULL	adhesion of	occur through	NULL				integrin alpha6beta1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24953_s_9	10821835	A heparin-binding defective mutant of Cyr61 was unable to mediate fibroblast adhesion through integrin alpha6beta1 but still mediated endothelial cell adhesion through integrin alphaVbeta3, indicating that endothelial cell adhesion through integrin alphaVbeta3 is independent of the heparin-binding activity of Cyr61.	bind
48700	2	10516	7	10	NULL	0	NULL	statement 6	NULL		does not mediate	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24953_s_9	10821835	A heparin-binding defective mutant of Cyr61 was unable to mediate fibroblast adhesion through integrin alpha6beta1 but still mediated endothelial cell adhesion through integrin alphaVbeta3, indicating that endothelial cell adhesion through integrin alphaVbeta3 is independent of the heparin-binding activity of Cyr61.	bind
48701	3	10516	7	NULL	NULL	0	NULL	endothelial cell	NULL	adhesion of	occur through	NULL				integrin alphaVbeta3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24953_s_9	10821835	A heparin-binding defective mutant of Cyr61 was unable to mediate fibroblast adhesion through integrin alpha6beta1 but still mediated endothelial cell adhesion through integrin alphaVbeta3, indicating that endothelial cell adhesion through integrin alphaVbeta3 is independent of the heparin-binding activity of Cyr61.	bind
48702	4	10516	7	10	NULL	0	NULL	statement 6	NULL		mediate	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24953_s_9	10821835	A heparin-binding defective mutant of Cyr61 was unable to mediate fibroblast adhesion through integrin alpha6beta1 but still mediated endothelial cell adhesion through integrin alphaVbeta3, indicating that endothelial cell adhesion through integrin alphaVbeta3 is independent of the heparin-binding activity of Cyr61.	bind
48703	5	10516	7	NULL	NULL	0	NULL	statement 4	NULL		is independent of	NULL				Cyr61	NULL	heparin-binding activity of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24953_s_9	10821835	A heparin-binding defective mutant of Cyr61 was unable to mediate fibroblast adhesion through integrin alpha6beta1 but still mediated endothelial cell adhesion through integrin alphaVbeta3, indicating that endothelial cell adhesion through integrin alphaVbeta3 is independent of the heparin-binding activity of Cyr61.	bind
50231	6	10516	7	10	NULL	0	NULL	Cyr61	NULL	mutant	does not bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24953_s_9	10821835	A heparin-binding defective mutant of Cyr61 was unable to mediate fibroblast adhesion through integrin alpha6beta1 but still mediated endothelial cell adhesion through integrin alphaVbeta3, indicating that endothelial cell adhesion through integrin alphaVbeta3 is independent of the heparin-binding activity of Cyr61.	bind
38974	1	10517	6	13	NULL	NULL	NULL	HEPES molecule	GP		bind							putative	K domain in the lysine-binding pocket		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_20_5543_s_37	11597998	A HEPES molecule is bound to each of the K domains in the putative lysine-binding pocket, as in the 1bht structure ( Ultsch  et al., 1998).	bind
48704	1	10517	7	10	NULL	0	NULL	HEPES molecule	NULL		bind	NULL					NULL	putative	K domains in lysine-binding pocket		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_20_5543_s_37	11597998	A HEPES molecule is bound to each of the K domains in the putative lysine-binding pocket, as in the 1bht structure ( Ultsch  et al., 1998).	bind
38975	1	10518	6	13	NULL	NULL	NULL	MRP8 (S100A8)	GP		forms heterocomplex with					MRP14 (S100A9)	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_6_3692_s_321	11349032	A heterocomplex formed by the calcium-binding proteins MRP8 (S100A8) and MRP14 (S100A9) binds unsaturated fatty acids with high affinity.	bind
38976	2	10518	6	13	NULL	NULL	NULL	statement 1	GP		bind		high affinity			fatty acids	Chemical	unsaturated			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_6_3692_s_321	11349032	A heterocomplex formed by the calcium-binding proteins MRP8 (S100A8) and MRP14 (S100A9) binds unsaturated fatty acids with high affinity.	bind
38977	3	10518	6	13	NULL	NULL	NULL	MRP8	GP		is a type of					calcium binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_6_3692_s_321	11349032	A heterocomplex formed by the calcium-binding proteins MRP8 (S100A8) and MRP14 (S100A9) binds unsaturated fatty acids with high affinity.	bind
38978	4	10518	6	13	NULL	NULL	NULL	MRP14	GP		is a type of					calcium binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_6_3692_s_321	11349032	A heterocomplex formed by the calcium-binding proteins MRP8 (S100A8) and MRP14 (S100A9) binds unsaturated fatty acids with high affinity.	bind
48731	1	10518	7	10	NULL	0	NULL	 MRP8(S100A8)			forms heterocomplex with					MRP14(S100A9)					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_6_3692_s_321	11349032	A heterocomplex formed by the calcium-binding proteins MRP8 (S100A8) and MRP14 (S100A9) binds unsaturated fatty acids with high affinity.	bind
48733	2	10518	7	10	NULL	0	NULL	statement 1			bind		high affinity			 fatty acids		unsaturated			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_6_3692_s_321	11349032	A heterocomplex formed by the calcium-binding proteins MRP8 (S100A8) and MRP14 (S100A9) binds unsaturated fatty acids with high affinity.	bind
48735	3	10518	7	10	NULL	0	NULL	MRP8			is a type of					calcium binding protein					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_6_3692_s_321	11349032	A heterocomplex formed by the calcium-binding proteins MRP8 (S100A8) and MRP14 (S100A9) binds unsaturated fatty acids with high affinity.	bind
48736	4	10518	7	10	NULL	0	NULL	 MRP14 			is a type of					calcium binding protein					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_6_3692_s_321	11349032	A heterocomplex formed by the calcium-binding proteins MRP8 (S100A8) and MRP14 (S100A9) binds unsaturated fatty acids with high affinity.	bind
38979	1	10519	6	13	NULL	NULL	NULL	p50 subunit	GP		forms heterodimer with					p65 subunit	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_7_2927_s_17	9096323	A heterodimer composed of a p50 subunit bound to a p65 (Rel A) subunit is the common dimer.	bind
38980	2	10519	6	13	NULL	NULL	NULL	p65	GP		is					Rel A	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_7_2927_s_17	9096323	A heterodimer composed of a p50 subunit bound to a p65 (Rel A) subunit is the common dimer.	bind
48737	1	10519	7	10	NULL	0	NULL	p50 subunit 	NULL		forms heterodimer with	NULL				p65 subunit	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_7_2927_s_17	9096323	A heterodimer composed of a p50 subunit bound to a p65 (Rel A) subunit is the common dimer.	bind
48739	2	10519	7	10	NULL	0	NULL	p65 subunit	NULL		is	NULL				RelA subunit	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_7_2927_s_17	9096323	A heterodimer composed of a p50 subunit bound to a p65 (Rel A) subunit is the common dimer.	bind
38981	1	10520	6	13	NULL	NULL	NULL	STE12	GP		forms heterodimer with					TEC1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_23_7008_s_19	9384580	A heterodimer composed of STE12 and TEC1 binds to a filamentation response element (FRE), which may regulate expression of genes necessary for pseudohyphal differentiation (Laloux  et al., 1994  ; Mosch  et al., 1996  ; Madhani and Fink, 1997  ).	bind
38982	2	10520	6	13	NULL	NULL	NULL	statement 1	GP		bind									FRE	NULL		NULL	NULL	NULL	NULL	gw60_embo_16_23_7008_s_19	9384580	A heterodimer composed of STE12 and TEC1 binds to a filamentation response element (FRE), which may regulate expression of genes necessary for pseudohyphal differentiation (Laloux  et al., 1994  ; Mosch  et al., 1996  ; Madhani and Fink, 1997  ).	bind
38983	3	10520	6	13	NULL	NULL	NULL	FRE	NucleicAcid		is					filamentation response element	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_23_7008_s_19	9384580	A heterodimer composed of STE12 and TEC1 binds to a filamentation response element (FRE), which may regulate expression of genes necessary for pseudohyphal differentiation (Laloux  et al., 1994  ; Mosch  et al., 1996  ; Madhani and Fink, 1997  ).	bind
38985	4	10520	6	13	NULL	NULL	NULL	statement 2	Process		regulates		may			pseudohyphal differentiation genes	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_embo_16_23_7008_s_19	9384580	A heterodimer composed of STE12 and TEC1 binds to a filamentation response element (FRE), which may regulate expression of genes necessary for pseudohyphal differentiation (Laloux  et al., 1994  ; Mosch  et al., 1996  ; Madhani and Fink, 1997  ).	bind
48740	1	10520	7	NULL	NULL	0	NULL	STE12 	NULL		heterodimerizes with	NULL				TEC1	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_23_7008_s_19	9384580	A heterodimer composed of STE12 and TEC1 binds to a filamentation response element (FRE), which may regulate expression of genes necessary for pseudohyphal differentiation (Laloux  et al., 1994  ; Mosch  et al., 1996  ; Madhani and Fink, 1997  ).	bind
48741	2	10520	7	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL					NULL			FRE	NULL		0	NULL	NULL	NULL	gw60_embo_16_23_7008_s_19	9384580	A heterodimer composed of STE12 and TEC1 binds to a filamentation response element (FRE), which may regulate expression of genes necessary for pseudohyphal differentiation (Laloux  et al., 1994  ; Mosch  et al., 1996  ; Madhani and Fink, 1997  ).	bind
48742	3	10520	7	10	NULL	0	NULL	statement 2			regulate		may			pseudohyphal differentiation genes		expression of			NULL		NULL	NULL	NULL	NULL	gw60_embo_16_23_7008_s_19	9384580	A heterodimer composed of STE12 and TEC1 binds to a filamentation response element (FRE), which may regulate expression of genes necessary for pseudohyphal differentiation (Laloux  et al., 1994  ; Mosch  et al., 1996  ; Madhani and Fink, 1997  ).	bind
48743	4	10520	7	NULL	NULL	0	NULL	FRE	NULL		is	NULL				filamentation response element	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_23_7008_s_19	9384580	A heterodimer composed of STE12 and TEC1 binds to a filamentation response element (FRE), which may regulate expression of genes necessary for pseudohyphal differentiation (Laloux  et al., 1994  ; Mosch  et al., 1996  ; Madhani and Fink, 1997  ).	bind
39022	1	10521	6	13	NULL	NULL	NULL	USF-1/USF-2 heterodimer	GP		bind								HO HLH site		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jneurosci_23_3_807_s_256	12574409	A heterodimer of USF-1/USF-2 can bind the HO HLH site  in vitro (Lanigan and Russo, 1997  ).	bind
48744	1	10521	7	10	NULL	0	NULL	USF-1/USF-2 heterodimer			bind								HO HLH site		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jneurosci_23_3_807_s_256	12574409	A heterodimer of USF-1/USF-2 can bind the HO HLH site  in vitro (Lanigan and Russo, 1997  ).	bind
39023	1	10522	6	13	NULL	NULL	NULL	GlnRS	GP	E.coli	bind					tRNAGln transcript	NucleicAcid	yeast			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_23_16508_s_147	10347214	A heterologous RNA binding domain enhances binding of  E. coli GlnRS  to a transcript of yeast tRNAGln.	bind
50237	2	10522	6	13	NULL	NULL	NULL				enhances			heterologous RNA binding domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_23_16508_s_147	10347214	A heterologous RNA binding domain enhances binding of  E. coli GlnRS  to a transcript of yeast tRNAGln.	bind
48746	1	10522	7	NULL	NULL	0	NULL	GlnRS 	NULL	E.coli	bind	NULL				tRNAGln transcript	NULL	yeast			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_23_16508_s_147	10347214	A heterologous RNA binding domain enhances binding of  E. coli GlnRS  to a transcript of yeast tRNAGln.	bind
48747	2	10522	7	NULL	NULL	0	NULL		NULL		enhance	NULL		heterologous RNA binding domain		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_23_16508_s_147	10347214	A heterologous RNA binding domain enhances binding of  E. coli GlnRS  to a transcript of yeast tRNAGln.	bind
39024	1	10523	6	13	NULL	NULL	NULL	YRNYPT hexapeptide sequence	GP		is based on					CbpA	GP		R1/R2 region		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_22_15464_s_358	16597618	A hexapeptide (YRNYPT) sequence based on the R1/R2 region of CbpA was found to bind human SIgA by a similar peptide mapping approach.	bind
39025	2	10523	6	13	NULL	NULL	NULL	statement 1	GP		bind					SIgA	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_22_15464_s_358	16597618	A hexapeptide (YRNYPT) sequence based on the R1/R2 region of CbpA was found to bind human SIgA by a similar peptide mapping approach.	bind
48748	1	10523	7	NULL	NULL	0	NULL	YRNYPT hexapeptide	NULL		bind	NULL				SIgA	NULL	human			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_22_15464_s_358	16597618	A hexapeptide (YRNYPT) sequence based on the R1/R2 region of CbpA was found to bind human SIgA by a similar peptide mapping approach.	bind
48749	2	10523	7	NULL	NULL	0	NULL	YRNYPT hexapeptide	NULL		is based on	NULL				CbpA	NULL		R1/R2 region of		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_22_15464_s_358	16597618	A hexapeptide (YRNYPT) sequence based on the R1/R2 region of CbpA was found to bind human SIgA by a similar peptide mapping approach.	bind
39026	1	10524	6	13	NULL	NULL	NULL	BS-I-B4	GP		bind					endothelial cells	Cell	pig;; aortic			NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_1_19_s_106	12890473	A hexapeptide mimetic of Gal- 1,3-Gal was found by screening the hexapeptide library with the lectin BS-I-B4, which can block the binding of BS-I-B4 to pig aortic endothelial cells [ 7.	bind
39027	2	10524	6	13	NULL	NULL	NULL	hexapeptide mimetic of Gal- 1,3-Gal	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_1_19_s_106	12890473	A hexapeptide mimetic of Gal- 1,3-Gal was found by screening the hexapeptide library with the lectin BS-I-B4, which can block the binding of BS-I-B4 to pig aortic endothelial cells [ 7.	bind
48750	1	10524	7	10	NULL	0	NULL	BS-I-B4	NULL		bind	NULL				endothelial cells	NULL	pig;;aortic			NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_1_19_s_106	12890473	A hexapeptide mimetic of Gal- 1,3-Gal was found by screening the hexapeptide library with the lectin BS-I-B4, which can block the binding of BS-I-B4 to pig aortic endothelial cells [ 7.	bind
48752	2	10524	7	10	NULL	0	NULL	hexapeptide mimetic of Gal- 1,3-Gal	NULL		block	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_308_1_19_s_106	12890473	A hexapeptide mimetic of Gal- 1,3-Gal was found by screening the hexapeptide library with the lectin BS-I-B4, which can block the binding of BS-I-B4 to pig aortic endothelial cells [ 7.	bind
39130	1	10525	6	13	NULL	NULL	NULL	hIGFBP-3 	GP		is substituted with			Arg75;;Leu77		hIGFBP-3	GP		Ala75;;Ala77		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10489_s_287	11784719	A hIGFBP-3 mutant with alanine substitutions at only two of the six positions, Arg75 and Leu77, also exhibited markedly decreased binding of both IGF-I and IGF-II.	bind
39132	2	10525	6	13	NULL	NULL	NULL	statement 1	Process		bind		decreased			IGF-I	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10489_s_287	11784719	A hIGFBP-3 mutant with alanine substitutions at only two of the six positions, Arg75 and Leu77, also exhibited markedly decreased binding of both IGF-I and IGF-II.	bind
39133	3	10525	6	13	NULL	NULL	NULL	statement 1	Process		bind		decreased			IGF-II	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10489_s_287	11784719	A hIGFBP-3 mutant with alanine substitutions at only two of the six positions, Arg75 and Leu77, also exhibited markedly decreased binding of both IGF-I and IGF-II.	bind
48753	1	10525	7	10	NULL	0	NULL	hIGFBP-3			is substituted with			 Arg75;;Leu77		hIGFBP-3			Ala75;;Ala77		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10489_s_287	11784719	A hIGFBP-3 mutant with alanine substitutions at only two of the six positions, Arg75 and Leu77, also exhibited markedly decreased binding of both IGF-I and IGF-II.	bind
48754	2	10525	7	10	NULL	0	NULL	statement 1			bind		decreased			IGF-I					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10489_s_287	11784719	A hIGFBP-3 mutant with alanine substitutions at only two of the six positions, Arg75 and Leu77, also exhibited markedly decreased binding of both IGF-I and IGF-II.	bind
48755	3	10525	7	10	NULL	0	NULL	statement 1			bind		decreased			IGF-II					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10489_s_287	11784719	A hIGFBP-3 mutant with alanine substitutions at only two of the six positions, Arg75 and Leu77, also exhibited markedly decreased binding of both IGF-I and IGF-II.	bind
39028	1	10526	6	13	NULL	NULL	NULL	bis-ANS	Chemical		bind		weakly			LPL	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37183_s_152	12855707	A high  Ki value represents a weak binding of bis-ANS to LPL.	bind
48757	1	10526	7	NULL	NULL	0	NULL	bis-ANS	NULL		bind	NULL	weakly			LPL	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_39_37183_s_152	12855707	A high  Ki value represents a weak binding of bis-ANS to LPL.	bind
39029	1	10527	6	13	NULL	NULL	NULL	ATP	Chemical		bind					P2X7 receptor	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37344_s_193	12869560	A high (low to submicromolar) and a low (>100 muM) affinity state for ATP binding to the human P2X7 receptor have been demonstrated ( ).	bind
48758	1	10527	7	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				P2X7 receptor	NULL	human			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_39_37344_s_193	12869560	A high (low to submicromolar) and a low (>100 muM) affinity state for ATP binding to the human P2X7 receptor have been demonstrated ( ).	bind
39030	1	10528	6	13	NULL	NULL	NULL	GBS	Organism		bind					mAb S9	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_27_24740_s_37	12700231	A high affinity (IC50 = 23  muM) peptide ligand, FDTGAFDPDWPAC, competitively inhibited  binding of GBS not only to mAb S9 but also to polyclonal anti-GBS antibodies.	bind
39031	2	10528	6	13	NULL	NULL	NULL	GBS	Organism		bind					anti-GBS antibody	GP	polyclonal			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_27_24740_s_37	12700231	A high affinity (IC50 = 23  muM) peptide ligand, FDTGAFDPDWPAC, competitively inhibited  binding of GBS not only to mAb S9 but also to polyclonal anti-GBS antibodies.	bind
39032	3	10528	6	13	NULL	NULL	NULL	FDTGAFDPDWPAC	GP		inhibits		competitively			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_27_24740_s_37	12700231	A high affinity (IC50 = 23  muM) peptide ligand, FDTGAFDPDWPAC, competitively inhibited  binding of GBS not only to mAb S9 but also to polyclonal anti-GBS antibodies.	bind
39033	4	10528	6	13	NULL	NULL	NULL	FDTGAFDPDWPAC	GP		inhibits		competitively			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_27_24740_s_37	12700231	A high affinity (IC50 = 23  muM) peptide ligand, FDTGAFDPDWPAC, competitively inhibited  binding of GBS not only to mAb S9 but also to polyclonal anti-GBS antibodies.	bind
50238	5	10528	6	13	NULL	NULL	NULL	FDTGAFDPDWPAC	GP		is a type of					peptide ligand	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_27_24740_s_37	12700231	A high affinity (IC50 = 23  muM) peptide ligand, FDTGAFDPDWPAC, competitively inhibited  binding of GBS not only to mAb S9 but also to polyclonal anti-GBS antibodies.	bind
48759	1	10528	7	NULL	NULL	0	NULL	GBS	NULL		bind	NULL				mAb S9 	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_27_24740_s_37	12700231	A high affinity (IC50 = 23  muM) peptide ligand, FDTGAFDPDWPAC, competitively inhibited  binding of GBS not only to mAb S9 but also to polyclonal anti-GBS antibodies.	bind
48760	2	10528	7	NULL	NULL	0	NULL	GBS	NULL		bind	NULL				polyclonal anti-GBS antibodies	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_27_24740_s_37	12700231	A high affinity (IC50 = 23  muM) peptide ligand, FDTGAFDPDWPAC, competitively inhibited  binding of GBS not only to mAb S9 but also to polyclonal anti-GBS antibodies.	bind
48761	3	10528	7	NULL	NULL	0	NULL	FDTGAFDPDWPAC 	NULL		inhibit	NULL	competitively			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_27_24740_s_37	12700231	A high affinity (IC50 = 23  muM) peptide ligand, FDTGAFDPDWPAC, competitively inhibited  binding of GBS not only to mAb S9 but also to polyclonal anti-GBS antibodies.	bind
48762	4	10528	7	NULL	NULL	0	NULL	FDTGAFDPDWPAC 	NULL		inhibit	NULL	competitively			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_27_24740_s_37	12700231	A high affinity (IC50 = 23  muM) peptide ligand, FDTGAFDPDWPAC, competitively inhibited  binding of GBS not only to mAb S9 but also to polyclonal anti-GBS antibodies.	bind
48763	5	10528	7	NULL	NULL	0	NULL	FDTGAFDPDWPAC	NULL		is a type of	NULL				peptide ligand	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_27_24740_s_37	12700231	A high affinity (IC50 = 23  muM) peptide ligand, FDTGAFDPDWPAC, competitively inhibited  binding of GBS not only to mAb S9 but also to polyclonal anti-GBS antibodies.	bind
39034	1	10529	6	13	NULL	NULL	NULL	PKC	GP		bind		high affinity			Btk	GP		PH domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_20_13033_s_39	9148913	A high affinity binding between PKC and the Btk PH domain was demonstrated by this assay.	bind
48764	1	10529	7	NULL	NULL	0	NULL	 PKC	NULL		bind	NULL	high affinity			Btk	NULL		PH domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_20_13033_s_39	9148913	A high affinity binding between PKC and the Btk PH domain was demonstrated by this assay.	bind
39035	1	10530	6	13	NULL	NULL	NULL	ANS	Chemical		bind					BSP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_19480_s_166	15757902	A high affinity-binding site for ANS at or near the promiscuous H-site of hGST P1 - 1 has also been reported ( ,  ), in agreement with the competitive binding between ANS and BSP ( ).	bind
59040	1	10530	7	NULL	NULL	0	NULL	ANS			bind					BSP					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19480_s_166	15757902	A high affinity-binding site for ANS at or near the promiscuous H-site of hGST P1 - 1 has also been reported ( ,  ), in agreement with the competitive binding between ANS and BSP ( ).	bind
39036	1	10531	6	13	NULL	NULL	NULL	LDL	GP		bind					LDL receptor	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_atherosclerosis_132_1_19_s_299	9247355	A high capacity, stable line for evaluating the binding of LDL to the human LDL receptor.	bind
48765	1	10531	7	NULL	NULL	0	NULL	LDL	NULL		bind	NULL				LDL receptor	NULL	human			NULL		0	NULL	NULL	NULL	gw60_atherosclerosis_132_1_19_s_299	9247355	A high capacity, stable line for evaluating the binding of LDL to the human LDL receptor.	bind
39136	1	10532	6	13	NULL	NULL	NULL	coumarin	Chemical		is a type of					CYP2A5/CYP2G1 substrates	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0560-0569_drug-metab-dispos_34_1_16221755_s_4	16221755	A high covalent binding of 2,6-diClPh-(14)C-MeSO(2) in olfactory  mucosa S9 fraction was observed, and the CYP2A5/CYP2G1 substrates coumarin  and dichlobenil significantly decreased the binding, whereas the CYP2E1  substrate chlorzoxazone had no effects.	bind
39137	2	10532	6	13	NULL	NULL	NULL	dichlobenil	Chemical		is a type of					CYP2A5/CYP2G1 substrates	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0560-0569_drug-metab-dispos_34_1_16221755_s_4	16221755	A high covalent binding of 2,6-diClPh-(14)C-MeSO(2) in olfactory  mucosa S9 fraction was observed, and the CYP2A5/CYP2G1 substrates coumarin  and dichlobenil significantly decreased the binding, whereas the CYP2E1  substrate chlorzoxazone had no effects.	bind
39138	3	10532	6	13	NULL	NULL	NULL	chlorzoxazone	Chemical		is a type of					CYP2E1 substrate	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0560-0569_drug-metab-dispos_34_1_16221755_s_4	16221755	A high covalent binding of 2,6-diClPh-(14)C-MeSO(2) in olfactory  mucosa S9 fraction was observed, and the CYP2A5/CYP2G1 substrates coumarin  and dichlobenil significantly decreased the binding, whereas the CYP2E1  substrate chlorzoxazone had no effects.	bind
39139	4	10532	6	13	NULL	NULL	NULL	coumarin	Chemical		decreases					2,6-diClPh-(14)C-MeSO(2)	Chemical	covalent binding of			NULL	olfactory mucosa S9 fraction	NULL	NULL	NULL	NULL	abs-batch0560-0569_drug-metab-dispos_34_1_16221755_s_4	16221755	A high covalent binding of 2,6-diClPh-(14)C-MeSO(2) in olfactory  mucosa S9 fraction was observed, and the CYP2A5/CYP2G1 substrates coumarin  and dichlobenil significantly decreased the binding, whereas the CYP2E1  substrate chlorzoxazone had no effects.	bind
39140	5	10532	6	13	NULL	NULL	NULL	dichlobenil	Chemical		decreases					2,6-diClPh-(14)C-MeSO(2)	Chemical	covalent binding of			NULL	olfactory mucosa S9 fraction	NULL	NULL	NULL	NULL	abs-batch0560-0569_drug-metab-dispos_34_1_16221755_s_4	16221755	A high covalent binding of 2,6-diClPh-(14)C-MeSO(2) in olfactory  mucosa S9 fraction was observed, and the CYP2A5/CYP2G1 substrates coumarin  and dichlobenil significantly decreased the binding, whereas the CYP2E1  substrate chlorzoxazone had no effects.	bind
39141	6	10532	6	13	NULL	NULL	NULL	chlorzoxazone	Chemical		has no effect in					2,6-diClPh-(14)C-MeSO(2)	Chemical	covalent binding of			NULL	olfactory mucosa S9 fraction	NULL	NULL	NULL	NULL	abs-batch0560-0569_drug-metab-dispos_34_1_16221755_s_4	16221755	A high covalent binding of 2,6-diClPh-(14)C-MeSO(2) in olfactory  mucosa S9 fraction was observed, and the CYP2A5/CYP2G1 substrates coumarin  and dichlobenil significantly decreased the binding, whereas the CYP2E1  substrate chlorzoxazone had no effects.	bind
48767	1	10532	7	10	NULL	0	NULL	coumarin			decrease					 2,6-diClPh-(14)C-MeSO(2)		covalent binding of			NULL	 olfactory mucosa S9 fraction	NULL	NULL	NULL	NULL	abs-batch0560-0569_drug-metab-dispos_34_1_16221755_s_4	16221755	A high covalent binding of 2,6-diClPh-(14)C-MeSO(2) in olfactory  mucosa S9 fraction was observed, and the CYP2A5/CYP2G1 substrates coumarin  and dichlobenil significantly decreased the binding, whereas the CYP2E1  substrate chlorzoxazone had no effects.	bind
48768	2	10532	7	10	NULL	0	NULL	dichlobenil 			decrease					2,6-diClPh-(14)C-MeSO(2)		covalent binding of			NULL	olfactory mucosa S9 fraction	NULL	NULL	NULL	NULL	abs-batch0560-0569_drug-metab-dispos_34_1_16221755_s_4	16221755	A high covalent binding of 2,6-diClPh-(14)C-MeSO(2) in olfactory  mucosa S9 fraction was observed, and the CYP2A5/CYP2G1 substrates coumarin  and dichlobenil significantly decreased the binding, whereas the CYP2E1  substrate chlorzoxazone had no effects.	bind
48769	3	10532	7	10	NULL	0	NULL	chlorzoxazone			does not effect					2,6-diClPh-(14)C-MeSO(2)		covalent binding of 			NULL	olfactory mucosa S9 fraction	NULL	NULL	NULL	NULL	abs-batch0560-0569_drug-metab-dispos_34_1_16221755_s_4	16221755	A high covalent binding of 2,6-diClPh-(14)C-MeSO(2) in olfactory  mucosa S9 fraction was observed, and the CYP2A5/CYP2G1 substrates coumarin  and dichlobenil significantly decreased the binding, whereas the CYP2E1  substrate chlorzoxazone had no effects.	bind
48770	5	10532	7	NULL	NULL	0	NULL	coumarin	NULL		is a type of	NULL				CYP2A5/CYP2G1 substrates	NULL				NULL		0	NULL	NULL	NULL	abs-batch0560-0569_drug-metab-dispos_34_1_16221755_s_4	16221755	A high covalent binding of 2,6-diClPh-(14)C-MeSO(2) in olfactory  mucosa S9 fraction was observed, and the CYP2A5/CYP2G1 substrates coumarin  and dichlobenil significantly decreased the binding, whereas the CYP2E1  substrate chlorzoxazone had no effects.	bind
48771	6	10532	7	NULL	NULL	0	NULL	dichlobenil	NULL		is a type of	NULL				CYP2A5/CYP2G1 substrates	NULL				NULL		0	NULL	NULL	NULL	abs-batch0560-0569_drug-metab-dispos_34_1_16221755_s_4	16221755	A high covalent binding of 2,6-diClPh-(14)C-MeSO(2) in olfactory  mucosa S9 fraction was observed, and the CYP2A5/CYP2G1 substrates coumarin  and dichlobenil significantly decreased the binding, whereas the CYP2E1  substrate chlorzoxazone had no effects.	bind
48772	4	10532	7	10	NULL	0	NULL	chlorzoxazone			is a type of					CYP2E1 substrate					NULL		NULL	NULL	NULL	NULL	abs-batch0560-0569_drug-metab-dispos_34_1_16221755_s_4	16221755	A high covalent binding of 2,6-diClPh-(14)C-MeSO(2) in olfactory  mucosa S9 fraction was observed, and the CYP2A5/CYP2G1 substrates coumarin  and dichlobenil significantly decreased the binding, whereas the CYP2E1  substrate chlorzoxazone had no effects.	bind
39037	1	10534	6	13	NULL	NULL	NULL	MURA	GP		does not bind					Mu5 transposon	NucleicAcid	inactive	divergent left TIR		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genetics_160_2_697_s_410	11861572	A high degree of conservation in this predicted binding site is thought to be required for MURA binding because MURA fails to bind  in vitro to the divergent left TIR of the apparently inactive  Mu5 transposon ( B ENITO and WALBOT 1997   ).	bind
48787	1	10534	7	NULL	NULL	0	NULL	MURA 	NULL		does not bind	NULL				Mu5 transposon	NULL	inactive	divergent left TIR		NULL	in vitro	0	NULL	NULL	NULL	gw60_genetics_160_2_697_s_410	11861572	A high degree of conservation in this predicted binding site is thought to be required for MURA binding because MURA fails to bind  in vitro to the divergent left TIR of the apparently inactive  Mu5 transposon ( B ENITO and WALBOT 1997   ).	bind
39142	1	10535	6	13	NULL	NULL	NULL	HDL	GP		bind					SR-BI	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_29_20344_s_187	10400657	A high degree of correlation between HDL binding and CE-selective uptake is seen over the entire range of HDL binding (Fig.  2), indicating a tight correspondence between HDL binding to SR-BI and the subsequent transfer of HDL-CE into the cell.	bind
39143	2	10535	6	13	NULL	NULL	NULL	HDL-CE	GP		is transfered to					cell	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_29_20344_s_187	10400657	A high degree of correlation between HDL binding and CE-selective uptake is seen over the entire range of HDL binding (Fig.  2), indicating a tight correspondence between HDL binding to SR-BI and the subsequent transfer of HDL-CE into the cell.	bind
39144	3	10535	6	13	NULL	NULL	NULL	statement 1	Process		correlates with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_29_20344_s_187	10400657	A high degree of correlation between HDL binding and CE-selective uptake is seen over the entire range of HDL binding (Fig.  2), indicating a tight correspondence between HDL binding to SR-BI and the subsequent transfer of HDL-CE into the cell.	bind
48788	1	10535	7	NULL	NULL	0	NULL	HDL	NULL		bind	NULL				SR-BI	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_29_20344_s_187	10400657	A high degree of correlation between HDL binding and CE-selective uptake is seen over the entire range of HDL binding (Fig.  2), indicating a tight correspondence between HDL binding to SR-BI and the subsequent transfer of HDL-CE into the cell.	bind
48789	2	10535	7	NULL	NULL	0	NULL	HDL-CE	NULL		transfers to	NULL				cell	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_29_20344_s_187	10400657	A high degree of correlation between HDL binding and CE-selective uptake is seen over the entire range of HDL binding (Fig.  2), indicating a tight correspondence between HDL binding to SR-BI and the subsequent transfer of HDL-CE into the cell.	bind
48790	3	10535	7	NULL	NULL	0	NULL	statement 1	NULL		corresponds to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_29_20344_s_187	10400657	A high degree of correlation between HDL binding and CE-selective uptake is seen over the entire range of HDL binding (Fig.  2), indicating a tight correspondence between HDL binding to SR-BI and the subsequent transfer of HDL-CE into the cell.	bind
39147	1	10537	6	13	NULL	NULL	NULL	mGlu2 receptor	GP		is localized on					cell body of golgi cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_40_2_163_s_6	11114394	A high density of [3](2S,2'R,3'R)-2-(2'',3''-dicarboxycyclopropyl)glycine ([3]DCG-IV) binding sites were detected in the granular layer of the rat cerebellum, matching the localization of mGlu2 receptor on cell bodies and axon terminals of Golgi cells (  Mutel et al., 1998).	bind
39148	2	10537	6	13	NULL	NULL	NULL	mGlu2 receptor	GP		is localized on					axon terminals of golgi cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_40_2_163_s_6	11114394	A high density of [3](2S,2'R,3'R)-2-(2'',3''-dicarboxycyclopropyl)glycine ([3]DCG-IV) binding sites were detected in the granular layer of the rat cerebellum, matching the localization of mGlu2 receptor on cell bodies and axon terminals of Golgi cells (  Mutel et al., 1998).	bind
48791	1	10537	7	10	NULL	0	NULL	granular layer	NULL	 rat;;cerebellum	contains	NULL					NULL		(2S,2'R,3'R)-2-(2'',3''-dicarboxycyclopropyl)glycine DCG-IV) binding site		NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_40_2_163_s_6	11114394	A high density of [3](2S,2'R,3'R)-2-(2'',3''-dicarboxycyclopropyl)glycine ([3]DCG-IV) binding sites were detected in the granular layer of the rat cerebellum, matching the localization of mGlu2 receptor on cell bodies and axon terminals of Golgi cells (  Mutel et al., 1998).	bind
50297	2	10537	7	10	NULL	0	NULL	mGlu2 receptor	NULL		localize on	NULL				cell body on golgi cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_40_2_163_s_6	11114394	A high density of [3](2S,2'R,3'R)-2-(2'',3''-dicarboxycyclopropyl)glycine ([3]DCG-IV) binding sites were detected in the granular layer of the rat cerebellum, matching the localization of mGlu2 receptor on cell bodies and axon terminals of Golgi cells (  Mutel et al., 1998).	bind
50298	3	10537	7	10	NULL	0	NULL	mGlu2 receptor	NULL		localize on	NULL				axon terminals of Golgi cells	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_40_2_163_s_6	11114394	A high density of [3](2S,2'R,3'R)-2-(2'',3''-dicarboxycyclopropyl)glycine ([3]DCG-IV) binding sites were detected in the granular layer of the rat cerebellum, matching the localization of mGlu2 receptor on cell bodies and axon terminals of Golgi cells (  Mutel et al., 1998).	bind
39038	1	10539	6	13	NULL	NULL	NULL	high mobility group protein	GP		bind							long		CAG repeat tracts	NULL	Saccharomyces cerevisiae	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_23_15735_s_1	16603770	A high mobility group protein binds to long CAG repeat tracts and establishes their chromatin organization in Saccharomyces cerevisiae.	bind
39151	2	10539	6	13	NULL	NULL	NULL	statement 1	Process		establishes					chromatin	Chromosome	organization of		long CAG repeat tracts	NULL	Saccharomyces cerevisiae	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_23_15735_s_1	16603770	A high mobility group protein binds to long CAG repeat tracts and establishes their chromatin organization in Saccharomyces cerevisiae.	bind
48794	1	10539	7	10	NULL	0	NULL	high mobility group protein 	NULL		bind	NULL					NULL	long 		CAG repeat tracts	NULL	Saccharomyces cerevisiae	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_23_15735_s_1	16603770	A high mobility group protein binds to long CAG repeat tracts and establishes their chromatin organization in Saccharomyces cerevisiae.	bind
48795	2	10539	7	10	NULL	0	NULL	statement 1	NULL		establishes	NULL				chromatin 	NULL	organization of		long CAG repeat tracts	NULL	Saccharomyces cerevisiae	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_23_15735_s_1	16603770	A high mobility group protein binds to long CAG repeat tracts and establishes their chromatin organization in Saccharomyces cerevisiae.	bind
39039	1	10541	6	13	NULL	NULL	NULL	insulin-like growth factor II messenger RNA	NucleicAcid		acts as a marker for					anaplasia	Process				NULL	meningiomas	NULL	NULL	NULL	NULL	gw60_amjpathol_161_2_665_s_210	12163391	A high ratio of insulin-like growth factor II/insulin-like growth factor binding protein 2 messenger RNA as a marker for anaplasia in meningiomas.	bind
39040	2	10541	6	13	NULL	NULL	NULL	insulin-like growth factor binding protein 2 messenger RNA	NucleicAcid		acts as a marker for					anaplasia	Process				NULL	meningiomas	NULL	NULL	NULL	NULL	gw60_amjpathol_161_2_665_s_210	12163391	A high ratio of insulin-like growth factor II/insulin-like growth factor binding protein 2 messenger RNA as a marker for anaplasia in meningiomas.	bind
48796	1	10541	7	NULL	NULL	0	NULL	 insulin-like growth factor II/insulin-like growth factor binding protein 2 messenger RNA	NULL	high ratio of	marker for	NULL				anaplasia	NULL				NULL	meningiomas	0	NULL	NULL	NULL	gw60_amjpathol_161_2_665_s_210	12163391	A high ratio of insulin-like growth factor II/insulin-like growth factor binding protein 2 messenger RNA as a marker for anaplasia in meningiomas.	bind
39041	1	10542	6	13	NULL	NULL	NULL	FADD-DD	GP		bind					Fas-DD	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_46_36217_s_132	10952991	A high salt concentration virtually abolished the binding affinity of FADD-DD for Fas-DD.	bind
50246	2	10542	6	13	NULL	NULL	NULL	salt	Chemical	high concentration of	abolishes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_46_36217_s_132	10952991	A high salt concentration virtually abolished the binding affinity of FADD-DD for Fas-DD.	bind
48797	1	10542	7	10	NULL	0	NULL	FADD-DD	NULL		bind	NULL				Fas-DD	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_46_36217_s_132	10952991	A high salt concentration virtually abolished the binding affinity of FADD-DD for Fas-DD.	bind
48798	2	10542	7	10	NULL	0	NULL	salt	NULL	high concentration of	abolishes	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_46_36217_s_132	10952991	A high salt concentration virtually abolished the binding affinity of FADD-DD for Fas-DD.	bind
39042	1	10543	6	13	NULL	NULL	NULL	Sir1p	GP		bind					HMR a	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_15_1817_s_90	12897051	A high-affinity ORC-binding site contributes to silencing of and efficient  Sir1p binding to  HMR  a.	bind
39043	2	10543	6	13	NULL	NULL	NULL			high-affinity	contributes to				ORC-binding site	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_15_1817_s_90	12897051	A high-affinity ORC-binding site contributes to silencing of and efficient  Sir1p binding to  HMR  a.	bind
39044	3	10543	6	13	NULL	NULL	NULL			high-affinity	contributes to				ORC-binding site	statement 1	Process	silencing of 			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_15_1817_s_90	12897051	A high-affinity ORC-binding site contributes to silencing of and efficient  Sir1p binding to  HMR  a.	bind
48799	1	10543	7	NULL	NULL	0	NULL	Sir1p	NULL		bind	NULL				HMR a	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_17_15_1817_s_90	12897051	A high-affinity ORC-binding site contributes to silencing of and efficient  Sir1p binding to  HMR  a.	bind
48800	2	10543	7	10	NULL	0	NULL		NULL	high-affinity	silence	NULL			ORC-binding site	statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_15_1817_s_90	12897051	A high-affinity ORC-binding site contributes to silencing of and efficient  Sir1p binding to  HMR  a.	bind
48801	3	10543	7	10	NULL	0	NULL		NULL	high affinity 	contributes to	NULL	efficiently		ORC-binding site	statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_15_1817_s_90	12897051	A high-affinity ORC-binding site contributes to silencing of and efficient  Sir1p binding to  HMR  a.	bind
39152	1	10545	6	13	NULL	NULL	NULL	high-fat diet	Food		does not increase					IBAT	OrganismPart	growth of 			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_am-j-physiol_253_5-pt-2_3688276_s_4	3688276	A high-fat diet, fed isoenergetically  to the low-fat diet, did not increase the growth of IBAT and decreased  specific GDP binding in both strains.	bind
39153	2	10545	6	13	NULL	NULL	NULL	high-fat diet	Food		decreases					GDP	Chemical	specific;; binding of 			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_am-j-physiol_253_5-pt-2_3688276_s_4	3688276	A high-fat diet, fed isoenergetically  to the low-fat diet, did not increase the growth of IBAT and decreased  specific GDP binding in both strains.	bind
48802	1	10545	7	NULL	NULL	0	NULL	high-fat diet	NULL		does not increase	NULL				IBAT	NULL	growth of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_am-j-physiol_253_5-pt-2_3688276_s_4	3688276	A high-fat diet, fed isoenergetically  to the low-fat diet, did not increase the growth of IBAT and decreased  specific GDP binding in both strains.	bind
48803	2	10545	7	10	NULL	0	NULL	high-fat diet	NULL		decrease	NULL				GDP	NULL	specific;;binding of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_am-j-physiol_253_5-pt-2_3688276_s_4	3688276	A high-fat diet, fed isoenergetically  to the low-fat diet, did not increase the growth of IBAT and decreased  specific GDP binding in both strains.	bind
39154	1	10546	6	13	NULL	NULL	NULL	SmpB	GP		bind			OB fold		tmRNA	NucleicAcid	Aquifex aeolicus	elbow region of the TLD		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_11_3529_s_29	15972795	A high-resolution crystal structure of a complex containing SmpB and the TLD of tmRNA from  Aquifex aeolicus ( ) reveals that one side of the OB fold in SmpB binds to the elbow region of the TLD and stabilizes its D-loop in an extended conformation.	bind
39155	2	10546	6	13	NULL	NULL	NULL	statement 1	Process		stabilizes					tmRNA	NucleicAcid	Aquifex aeolicus	D-loop		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_11_3529_s_29	15972795	A high-resolution crystal structure of a complex containing SmpB and the TLD of tmRNA from  Aquifex aeolicus ( ) reveals that one side of the OB fold in SmpB binds to the elbow region of the TLD and stabilizes its D-loop in an extended conformation.	bind
48804	1	10546	7	NULL	NULL	0	NULL	SmpB	NULL		complex with	NULL				tmRNA	NULL	Aquifex aeolicus	TLD		NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_11_3529_s_29	15972795	A high-resolution crystal structure of a complex containing SmpB and the TLD of tmRNA from  Aquifex aeolicus ( ) reveals that one side of the OB fold in SmpB binds to the elbow region of the TLD and stabilizes its D-loop in an extended conformation.	bind
48805	2	10546	7	10	NULL	0	NULL	SmpB			bind			OB fold		tmRNA		Aquifex aeolicus	elbow region of TLD		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_11_3529_s_29	15972795	A high-resolution crystal structure of a complex containing SmpB and the TLD of tmRNA from  Aquifex aeolicus ( ) reveals that one side of the OB fold in SmpB binds to the elbow region of the TLD and stabilizes its D-loop in an extended conformation.	bind
48806	3	10546	7	10	NULL	0	NULL	statement 1			stabilizes					tmRNA		Aquifex aeolicus	D-loop		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_11_3529_s_29	15972795	A high-resolution crystal structure of a complex containing SmpB and the TLD of tmRNA from  Aquifex aeolicus ( ) reveals that one side of the OB fold in SmpB binds to the elbow region of the TLD and stabilizes its D-loop in an extended conformation.	bind
39045	1	10548	6	13	NULL	NULL	NULL	small molecules	Chemical		bind					Bcl-XL	GP		hydrophobic BH3-binding groove		NULL		NULL	NULL	NULL	NULL	gw70_nature_435_7042_677_s_28	15902208	A high-throughput NMR-based method for lead compound discovery called 'SAR by  NMR'' 20 was used to screen a chemical library to identify small molecules that bind to the  hydrophobic BH3-binding groove of Bcl-XL.	bind
48807	1	10548	7	NULL	NULL	0	NULL	small molecules	NULL		bind	NULL				Bcl-XL	NULL		hydrophobic BH3-binding groove		NULL		0	NULL	NULL	NULL	gw70_nature_435_7042_677_s_28	15902208	A high-throughput NMR-based method for lead compound discovery called 'SAR by  NMR'' 20 was used to screen a chemical library to identify small molecules that bind to the  hydrophobic BH3-binding groove of Bcl-XL.	bind
39046	1	10549	6	13	NULL	NULL	NULL	gp120	GP		is a type of					human immunodeficiency virus envelope glycoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30443_s_106	9804811	A higher affinity ( K D 40-400 nM) has been reported for the binding of the human immunodeficiency virus envelope glycoprotein gp120 to its cell surface receptor CD4 ( 23).	bind
39047	2	10549	6	13	NULL	NULL	NULL	CD4	GP		is a type of					cell surface receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30443_s_106	9804811	A higher affinity ( K D 40-400 nM) has been reported for the binding of the human immunodeficiency virus envelope glycoprotein gp120 to its cell surface receptor CD4 ( 23).	bind
39048	3	10549	6	13	NULL	NULL	NULL	gp120	GP		bind		high affinity			CD4	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30443_s_106	9804811	A higher affinity ( K D 40-400 nM) has been reported for the binding of the human immunodeficiency virus envelope glycoprotein gp120 to its cell surface receptor CD4 ( 23).	bind
48808	1	10549	7	NULL	NULL	0	NULL	gp120	NULL		bind	NULL	high affinity			CD4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30443_s_106	9804811	A higher affinity ( K D 40-400 nM) has been reported for the binding of the human immunodeficiency virus envelope glycoprotein gp120 to its cell surface receptor CD4 ( 23).	bind
48809	2	10549	7	NULL	NULL	0	NULL	gp120	NULL		is a type of	NULL				human immunodeficiency virus envelope glycoprotein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_46_30443_s_106	9804811	A higher affinity ( K D 40-400 nM) has been reported for the binding of the human immunodeficiency virus envelope glycoprotein gp120 to its cell surface receptor CD4 ( 23).	bind
48810	3	10549	7	NULL	NULL	0	NULL	CD4	NULL		is a type of	NULL				cell surface receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_46_30443_s_106	9804811	A higher affinity ( K D 40-400 nM) has been reported for the binding of the human immunodeficiency virus envelope glycoprotein gp120 to its cell surface receptor CD4 ( 23).	bind
39049	1	10550	6	13	NULL	NULL	NULL	PD 158771	Chemical		bind		preferentially			D2L receptors	GP		D2 high affinity agonist binding site		NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_7_1197_s_292	10760362	A higher affinity was achieved when the D2L receptors were labeled with DA agonist [3]N-0437, suggesting that PD 158771 binds preferentially to the D2 high affinity agonist binding site.	bind
48811	1	10550	7	NULL	NULL	0	NULL	PD 158771	NULL		bind	NULL	preferentially			D2L receptor	NULL		D2 high affinity agonist binding site		NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_7_1197_s_292	10760362	A higher affinity was achieved when the D2L receptors were labeled with DA agonist [3]N-0437, suggesting that PD 158771 binds preferentially to the D2 high affinity agonist binding site.	bind
39156	1	10552	6	13	NULL	NULL	NULL	RMK	GP		bind		irreversibly			liver macromolecules	GP	mouse			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_mutat-res_119_1_6337321_s_5	6337321	A higher percentage  of RMK and MK became irreversibly bound to mouse-liver macromolecules  than to rat-liver macromolecules when incubated at 37 degrees C in the  presence of reduced nicotinamide adenine dinucleotide phosphate.	bind
39157	2	10552	6	13	NULL	NULL	NULL	MK	GP		bind		irreversibly			liver macromolecules	GP	mouse			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_mutat-res_119_1_6337321_s_5	6337321	A higher percentage  of RMK and MK became irreversibly bound to mouse-liver macromolecules  than to rat-liver macromolecules when incubated at 37 degrees C in the  presence of reduced nicotinamide adenine dinucleotide phosphate.	bind
39158	3	10552	6	13	NULL	NULL	NULL	RMK	GP		bind		irreversibly			liver macromolecules	GP	rat			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_mutat-res_119_1_6337321_s_5	6337321	A higher percentage  of RMK and MK became irreversibly bound to mouse-liver macromolecules  than to rat-liver macromolecules when incubated at 37 degrees C in the  presence of reduced nicotinamide adenine dinucleotide phosphate.	bind
39159	4	10552	6	13	NULL	NULL	NULL	MK	GP		bind		irreversibly			liver macromolecules	GP	rat			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_mutat-res_119_1_6337321_s_5	6337321	A higher percentage  of RMK and MK became irreversibly bound to mouse-liver macromolecules  than to rat-liver macromolecules when incubated at 37 degrees C in the  presence of reduced nicotinamide adenine dinucleotide phosphate.	bind
39160	5	10552	6	13	NULL	NULL	NULL	statement 1	Process		is greater than					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_mutat-res_119_1_6337321_s_5	6337321	A higher percentage  of RMK and MK became irreversibly bound to mouse-liver macromolecules  than to rat-liver macromolecules when incubated at 37 degrees C in the  presence of reduced nicotinamide adenine dinucleotide phosphate.	bind
39161	6	10552	6	13	NULL	NULL	NULL	statement 5	Process		occurs in presence of					nicotinamide adenine dinucleotide phosphate	Chemical	reduced			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_mutat-res_119_1_6337321_s_5	6337321	A higher percentage  of RMK and MK became irreversibly bound to mouse-liver macromolecules  than to rat-liver macromolecules when incubated at 37 degrees C in the  presence of reduced nicotinamide adenine dinucleotide phosphate.	bind
39162	7	10552	6	13	NULL	NULL	NULL	statement 2	Process		is greater than					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_mutat-res_119_1_6337321_s_5	6337321	A higher percentage  of RMK and MK became irreversibly bound to mouse-liver macromolecules  than to rat-liver macromolecules when incubated at 37 degrees C in the  presence of reduced nicotinamide adenine dinucleotide phosphate.	bind
39163	8	10552	6	13	NULL	NULL	NULL	statement 7	Process		occurs in presence of					nicotinamide adenine dinucleotide phosphate	Chemical	reduced			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_mutat-res_119_1_6337321_s_5	6337321	A higher percentage  of RMK and MK became irreversibly bound to mouse-liver macromolecules  than to rat-liver macromolecules when incubated at 37 degrees C in the  presence of reduced nicotinamide adenine dinucleotide phosphate.	bind
48813	1	10552	7	NULL	NULL	0	NULL	RMK 	NULL		bind	NULL	irreversibly			macromolecules	NULL	mouse-liver			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_mutat-res_119_1_6337321_s_5	6337321	A higher percentage  of RMK and MK became irreversibly bound to mouse-liver macromolecules  than to rat-liver macromolecules when incubated at 37 degrees C in the  presence of reduced nicotinamide adenine dinucleotide phosphate.	bind
48814	2	10552	7	NULL	NULL	0	NULL	MK	NULL		bind	NULL	irreversibly			macromolecules	NULL	mouse-liver			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_mutat-res_119_1_6337321_s_5	6337321	A higher percentage  of RMK and MK became irreversibly bound to mouse-liver macromolecules  than to rat-liver macromolecules when incubated at 37 degrees C in the  presence of reduced nicotinamide adenine dinucleotide phosphate.	bind
48815	3	10552	7	NULL	NULL	0	NULL	RMK	NULL		bind	NULL	irreversibly			macromolecules	NULL	rat-liver			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_mutat-res_119_1_6337321_s_5	6337321	A higher percentage  of RMK and MK became irreversibly bound to mouse-liver macromolecules  than to rat-liver macromolecules when incubated at 37 degrees C in the  presence of reduced nicotinamide adenine dinucleotide phosphate.	bind
48816	4	10552	7	NULL	NULL	0	NULL	MK	NULL		bind	NULL	irreversibly			macromolecules	NULL	rat-liver			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_mutat-res_119_1_6337321_s_5	6337321	A higher percentage  of RMK and MK became irreversibly bound to mouse-liver macromolecules  than to rat-liver macromolecules when incubated at 37 degrees C in the  presence of reduced nicotinamide adenine dinucleotide phosphate.	bind
48817	6	10552	7	10	NULL	0	NULL	statement 5			in presence of					nicotinamide adenine dinucleotide phosphate		reduced			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_mutat-res_119_1_6337321_s_5	6337321	A higher percentage  of RMK and MK became irreversibly bound to mouse-liver macromolecules  than to rat-liver macromolecules when incubated at 37 degrees C in the  presence of reduced nicotinamide adenine dinucleotide phosphate.	bind
48818	8	10552	7	10	NULL	0	NULL	statement 7			in presence of					nicotinamide adenine dinucleotide phosphate		reduced			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_mutat-res_119_1_6337321_s_5	6337321	A higher percentage  of RMK and MK became irreversibly bound to mouse-liver macromolecules  than to rat-liver macromolecules when incubated at 37 degrees C in the  presence of reduced nicotinamide adenine dinucleotide phosphate.	bind
48821	5	10552	7	10	NULL	0	NULL	statement 1		affinity of	is higher than					statement 3		affinity of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_mutat-res_119_1_6337321_s_5	6337321	A higher percentage  of RMK and MK became irreversibly bound to mouse-liver macromolecules  than to rat-liver macromolecules when incubated at 37 degrees C in the  presence of reduced nicotinamide adenine dinucleotide phosphate.	bind
48822	7	10552	7	10	NULL	0	NULL	statement 2		affinity of	is higher than					statement 4		affinity of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_mutat-res_119_1_6337321_s_5	6337321	A higher percentage  of RMK and MK became irreversibly bound to mouse-liver macromolecules  than to rat-liver macromolecules when incubated at 37 degrees C in the  presence of reduced nicotinamide adenine dinucleotide phosphate.	bind
39050	1	10553	6	13	NULL	NULL	NULL	Notch	GP		bind		cooperatively			RBP-jkappa	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_8_5106_s_394	16365048	A higher probability of activation could result from Notch binding to RBP-jkappa cooperatively when two RBP-jkappa molecules are properly positioned in proximity to each other.	bind
48823	1	10553	7	NULL	NULL	0	NULL	Notch	NULL		bind	NULL	cooperatively			RBP-jkappa	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_8_5106_s_394	16365048	A higher probability of activation could result from Notch binding to RBP-jkappa cooperatively when two RBP-jkappa molecules are properly positioned in proximity to each other.	bind
39051	1	10554	6	13	NULL	NULL	NULL	PACS-1	GP		is					phosphofurin acidic cluster sorting protein-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_21_2677_s_120	11069884	A highly conserved acidic cluster (AC) in the amino-proximal third of Nef (EEEE65) binds PACS-1 (phosphofurin acidic cluster sorting protein-1), the first identified member of a new family of coat proteins.	bind
39052	2	10554	6	13	NULL	NULL	NULL	PACS-1	GP		is a type of					coat protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_21_2677_s_120	11069884	A highly conserved acidic cluster (AC) in the amino-proximal third of Nef (EEEE65) binds PACS-1 (phosphofurin acidic cluster sorting protein-1), the first identified member of a new family of coat proteins.	bind
39053	3	10554	6	13	NULL	NULL	NULL	Nef	GP		bind			EEEE65		PACS-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_21_2677_s_120	11069884	A highly conserved acidic cluster (AC) in the amino-proximal third of Nef (EEEE65) binds PACS-1 (phosphofurin acidic cluster sorting protein-1), the first identified member of a new family of coat proteins.	bind
39054	4	10554	6	13	NULL	NULL	NULL	AC	GP		is 					acidic cluster	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_21_2677_s_120	11069884	A highly conserved acidic cluster (AC) in the amino-proximal third of Nef (EEEE65) binds PACS-1 (phosphofurin acidic cluster sorting protein-1), the first identified member of a new family of coat proteins.	bind
39055	5	10554	6	13	NULL	NULL	NULL	EEEE65	GP		is					highly conserved acidic cluster in the amino-proximal third	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_21_2677_s_120	11069884	A highly conserved acidic cluster (AC) in the amino-proximal third of Nef (EEEE65) binds PACS-1 (phosphofurin acidic cluster sorting protein-1), the first identified member of a new family of coat proteins.	bind
48827	1	10554	7	NULL	NULL	0	NULL	Nef	NULL		bind	NULL		amino-proximal EEEE65		PACS-1	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_14_21_2677_s_120	11069884	A highly conserved acidic cluster (AC) in the amino-proximal third of Nef (EEEE65) binds PACS-1 (phosphofurin acidic cluster sorting protein-1), the first identified member of a new family of coat proteins.	bind
48828	2	10554	7	NULL	NULL	0	NULL	Nef	NULL		is a type of	NULL		amino-proximal EEEE65		AC	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_14_21_2677_s_120	11069884	A highly conserved acidic cluster (AC) in the amino-proximal third of Nef (EEEE65) binds PACS-1 (phosphofurin acidic cluster sorting protein-1), the first identified member of a new family of coat proteins.	bind
48829	3	10554	7	NULL	NULL	0	NULL	AC	NULL		is	NULL				acidic cluster	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_14_21_2677_s_120	11069884	A highly conserved acidic cluster (AC) in the amino-proximal third of Nef (EEEE65) binds PACS-1 (phosphofurin acidic cluster sorting protein-1), the first identified member of a new family of coat proteins.	bind
48830	4	10554	7	NULL	NULL	0	NULL	PACS-1	NULL		is	NULL				phosphofurin acidic cluster sorting protein-1	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_14_21_2677_s_120	11069884	A highly conserved acidic cluster (AC) in the amino-proximal third of Nef (EEEE65) binds PACS-1 (phosphofurin acidic cluster sorting protein-1), the first identified member of a new family of coat proteins.	bind
48831	5	10554	7	NULL	NULL	0	NULL	PACS-1	NULL		is a type of	NULL				coat protein	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_14_21_2677_s_120	11069884	A highly conserved acidic cluster (AC) in the amino-proximal third of Nef (EEEE65) binds PACS-1 (phosphofurin acidic cluster sorting protein-1), the first identified member of a new family of coat proteins.	bind
39056	1	10556	6	13	NULL	NULL	NULL	HIV-1	Organism		bind			sulfate motif		CCR5	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_39493_s_1	16157597	A highly conserved arginine in gp120 governs HIV-1 binding to both syndecans and CCR5 via sulfated motifs.	bind
39057	2	10556	6	13	NULL	NULL	NULL	HIV-1	Organism		bind			sulfate motif		syndecan	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_39493_s_1	16157597	A highly conserved arginine in gp120 governs HIV-1 binding to both syndecans and CCR5 via sulfated motifs.	bind
39058	3	10556	6	13	NULL	NULL	NULL	gp120	GP	highly conserved	governs			arginine		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_39493_s_1	16157597	A highly conserved arginine in gp120 governs HIV-1 binding to both syndecans and CCR5 via sulfated motifs.	bind
39059	4	10556	6	13	NULL	NULL	NULL	gp120	GP	highly conserved	governs			arginine		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_39493_s_1	16157597	A highly conserved arginine in gp120 governs HIV-1 binding to both syndecans and CCR5 via sulfated motifs.	bind
48832	1	10556	7	NULL	NULL	0	NULL	HIV-1	NULL		bind	NULL		sulfated motif		syndecans	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_47_39493_s_1	16157597	A highly conserved arginine in gp120 governs HIV-1 binding to both syndecans and CCR5 via sulfated motifs.	bind
48833	2	10556	7	NULL	NULL	0	NULL	HIV-1	NULL		bind	NULL		sulfated motif		CCR5	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_47_39493_s_1	16157597	A highly conserved arginine in gp120 governs HIV-1 binding to both syndecans and CCR5 via sulfated motifs.	bind
48834	3	10556	7	10	NULL	0	NULL	gp120	NULL	highly conserved 	governs	NULL		arginine		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_39493_s_1	16157597	A highly conserved arginine in gp120 governs HIV-1 binding to both syndecans and CCR5 via sulfated motifs.	bind
48835	4	10556	7	10	NULL	0	NULL	gp120	NULL	highly conserved	governs	NULL		arginine		statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_39493_s_1	16157597	A highly conserved arginine in gp120 governs HIV-1 binding to both syndecans and CCR5 via sulfated motifs.	bind
39164	1	10558	6	13	NULL	NULL	NULL	HIV-1	Organism		bind					Syndecan	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_39493_s_146	16157597	A Highly Conserved Arginine in gp120 Mediates HIV-1 Binding to Syndecans --	bind
39165	2	10558	6	13	NULL	NULL	NULL	gp120	GP	highly conserved	mediates			arginine		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_39493_s_146	16157597	A Highly Conserved Arginine in gp120 Mediates HIV-1 Binding to Syndecans --	bind
48836	1	10558	7	NULL	NULL	0	NULL	HIV-1 	NULL		bind	NULL				Syndecans	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_47_39493_s_146	16157597	A Highly Conserved Arginine in gp120 Mediates HIV-1 Binding to Syndecans --	bind
48837	2	10558	7	10	NULL	0	NULL	gp120	NULL	highly conserved	mediates	NULL		Arginine		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_47_39493_s_146	16157597	A Highly Conserved Arginine in gp120 Mediates HIV-1 Binding to Syndecans --	bind
39844	1	10559	6	13	NULL	NULL	NULL	Rel/FkappaB family	GP	transcriptionally active	bind									CK1 element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_24_14020_s_203	8662845	A highly conserved CK1/CK2 DNA sequence is present in this region and may be important in this activity, since a concatamer of this sequence has been shown to inhibit the basal transcription of a heterologous promoter and proteins from the transcriptionally active Rel/FkappaB family bind to the CK1 element ( 31).	bind
48838	1	10559	7	NULL	NULL	0	NULL		NULL	concatamer of	inhibit	NULL		highly conserved CK1/CK2 DNA sequence		heterologous promoter	NULL	basal transcription of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_24_14020_s_203	8662845	A highly conserved CK1/CK2 DNA sequence is present in this region and may be important in this activity, since a concatamer of this sequence has been shown to inhibit the basal transcription of a heterologous promoter and proteins from the transcriptionally active Rel/FkappaB family bind to the CK1 element ( 31).	bind
48840	2	10559	7	10	NULL	0	NULL	Rel/FkappaB family	NULL	transcriptionally active	bind	NULL					NULL			CK1 element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_24_14020_s_203	8662845	A highly conserved CK1/CK2 DNA sequence is present in this region and may be important in this activity, since a concatamer of this sequence has been shown to inhibit the basal transcription of a heterologous promoter and proteins from the transcriptionally active Rel/FkappaB family bind to the CK1 element ( 31).	bind
39212	1	10560	6	13	NULL	NULL	NULL	S-layer proteins	GP	L. acidophilus	bind			C-terminus		cell wall	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_68_12_5943_s_20	12450814	A highly conserved domain was recently shown to mediate the binding of the S-layer protein subunits to the cell wall in the C-terminal part of the  L. acidophilus group S-layer proteins ( 49).	bind
48841	1	10560	7	NULL	NULL	0	NULL	S-layer protein	NULL	L. acidophilus	bind	NULL		 C-terminal subunit		cell wall	NULL				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_68_12_5943_s_20	12450814	A highly conserved domain was recently shown to mediate the binding of the S-layer protein subunits to the cell wall in the C-terminal part of the  L. acidophilus group S-layer proteins ( 49).	bind
39307	1	10561	6	13	NULL	NULL	NULL	SGT1	GP	eukaryotic	bind		specifically			HSP90	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_embo-j_25_9_16619029_s_2	16619029	A highly conserved eukaryotic protein SGT1 binds specifically to the molecular  chaperone, HSP90.	bind
39309	2	10561	6	13	NULL	NULL	NULL	HSP90	GP		is a type of					molecular chaperone	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_embo-j_25_9_16619029_s_2	16619029	A highly conserved eukaryotic protein SGT1 binds specifically to the molecular  chaperone, HSP90.	bind
48853	1	10561	7	10	NULL	0	NULL	 SGT1		eukaryotic	bind		specifically			HSP90					NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_embo-j_25_9_16619029_s_2	16619029	A highly conserved eukaryotic protein SGT1 binds specifically to the molecular  chaperone, HSP90.	bind
48855	2	10561	7	10	NULL	0	NULL	HSP90			is a type of					molecular chaperone					NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_embo-j_25_9_16619029_s_2	16619029	A highly conserved eukaryotic protein SGT1 binds specifically to the molecular  chaperone, HSP90.	bind
39845	1	10562	6	13	NULL	NULL	NULL	PKR kinase	GP	cellular	bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_7_4419_s_250	9020165	A highly conserved lysine residue (Fig.  2) established as essential for the R-motif mediated RNA-binding activity of the cellular PKR kinase and the viral E3L protein ( 29,  30,  33) was substituted with glutamic acid in either any one, or all three, of the R copies in the ADAR splice variants.	bind
39846	2	10562	6	13	NULL	NULL	NULL	E3L protein	GP	viral	bind					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_7_4419_s_250	9020165	A highly conserved lysine residue (Fig.  2) established as essential for the R-motif mediated RNA-binding activity of the cellular PKR kinase and the viral E3L protein ( 29,  30,  33) was substituted with glutamic acid in either any one, or all three, of the R copies in the ADAR splice variants.	bind
39847	3	10562	6	13	NULL	NULL	NULL				mediates			conserved lysine residue in R motif		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_7_4419_s_250	9020165	A highly conserved lysine residue (Fig.  2) established as essential for the R-motif mediated RNA-binding activity of the cellular PKR kinase and the viral E3L protein ( 29,  30,  33) was substituted with glutamic acid in either any one, or all three, of the R copies in the ADAR splice variants.	bind
39848	4	10562	6	13	NULL	NULL	NULL				mediates			conserved lysine residue in R motif		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_7_4419_s_250	9020165	A highly conserved lysine residue (Fig.  2) established as essential for the R-motif mediated RNA-binding activity of the cellular PKR kinase and the viral E3L protein ( 29,  30,  33) was substituted with glutamic acid in either any one, or all three, of the R copies in the ADAR splice variants.	bind
48856	1	10562	7	NULL	NULL	0	NULL	PKR kinase	NULL	cellular	bind	NULL				RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_7_4419_s_250	9020165	A highly conserved lysine residue (Fig.  2) established as essential for the R-motif mediated RNA-binding activity of the cellular PKR kinase and the viral E3L protein ( 29,  30,  33) was substituted with glutamic acid in either any one, or all three, of the R copies in the ADAR splice variants.	bind
48857	2	10562	7	10	NULL	0	NULL	E3L protein	NULL	 viral	bind	NULL				RNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_7_4419_s_250	9020165	A highly conserved lysine residue (Fig.  2) established as essential for the R-motif mediated RNA-binding activity of the cellular PKR kinase and the viral E3L protein ( 29,  30,  33) was substituted with glutamic acid in either any one, or all three, of the R copies in the ADAR splice variants.	bind
48858	3	10562	7	NULL	NULL	0	NULL		NULL		mediates	NULL		 R-motif		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_7_4419_s_250	9020165	A highly conserved lysine residue (Fig.  2) established as essential for the R-motif mediated RNA-binding activity of the cellular PKR kinase and the viral E3L protein ( 29,  30,  33) was substituted with glutamic acid in either any one, or all three, of the R copies in the ADAR splice variants.	bind
48859	4	10562	7	NULL	NULL	0	NULL		NULL		mediates	NULL		R-motif		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_7_4419_s_250	9020165	A highly conserved lysine residue (Fig.  2) established as essential for the R-motif mediated RNA-binding activity of the cellular PKR kinase and the viral E3L protein ( 29,  30,  33) was substituted with glutamic acid in either any one, or all three, of the R copies in the ADAR splice variants.	bind
48860	5	10562	7	NULL	NULL	0	NULL		NULL		is required for	NULL		highly conserved lysine residue		statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_7_4419_s_250	9020165	A highly conserved lysine residue (Fig.  2) established as essential for the R-motif mediated RNA-binding activity of the cellular PKR kinase and the viral E3L protein ( 29,  30,  33) was substituted with glutamic acid in either any one, or all three, of the R copies in the ADAR splice variants.	bind
48861	6	10562	7	NULL	NULL	0	NULL		NULL		is required for	NULL		highly conserved lysine residue		statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_7_4419_s_250	9020165	A highly conserved lysine residue (Fig.  2) established as essential for the R-motif mediated RNA-binding activity of the cellular PKR kinase and the viral E3L protein ( 29,  30,  33) was substituted with glutamic acid in either any one, or all three, of the R copies in the ADAR splice variants.	bind
39310	1	10563	6	13	NULL	NULL	NULL	antigen 85 complex proteins	GP	recombinant	bind					fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_8_4521_s_145	9988684	A highly conserved motif among the antigen 85 complex proteins, FEWYYQ, was identified as an important sequence in the binding of recombinant 85 complex proteins to fibronectin ( 12).	bind
39311	2	10563	6	13	NULL	NULL	NULL	antigen 85 complex protein	GP		is important for			FEWYYQ		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_8_4521_s_145	9988684	A highly conserved motif among the antigen 85 complex proteins, FEWYYQ, was identified as an important sequence in the binding of recombinant 85 complex proteins to fibronectin ( 12).	bind
48862	1	10563	7	NULL	NULL	0	NULL	 antigen 85 complex protein	NULL	recombinant	bind	NULL				fibronectin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_8_4521_s_145	9988684	A highly conserved motif among the antigen 85 complex proteins, FEWYYQ, was identified as an important sequence in the binding of recombinant 85 complex proteins to fibronectin ( 12).	bind
48863	2	10563	7	NULL	NULL	0	NULL	antigen 85 complex protein	NULL		is required for	NULL		FEWYYQ		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_8_4521_s_145	9988684	A highly conserved motif among the antigen 85 complex proteins, FEWYYQ, was identified as an important sequence in the binding of recombinant 85 complex proteins to fibronectin ( 12).	bind
39312	1	10564	6	13	NULL	NULL	NULL	ETV6-NTRK3	GP		bind			NTRK3 C-terminal sequence		insulin receptor substrate-1	GP		phosphotyrosine binding domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_6225_s_1	14668342	A highly conserved NTRK3 C-terminal sequence in the ETV6-NTRK3 oncoprotein binds the phosphotyrosine binding domain of insulin receptor substrate-1: an essential interaction for transformation.	bind
50257	2	10564	6	13	NULL	NULL	NULL	statement 1	Process		is essential for					transformation	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_6225_s_1	14668342	A highly conserved NTRK3 C-terminal sequence in the ETV6-NTRK3 oncoprotein binds the phosphotyrosine binding domain of insulin receptor substrate-1: an essential interaction for transformation.	bind
50258	3	10564	6	13	NULL	NULL	NULL	ETV6-NTRK3	GP		is a type of					oncoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_6225_s_1	14668342	A highly conserved NTRK3 C-terminal sequence in the ETV6-NTRK3 oncoprotein binds the phosphotyrosine binding domain of insulin receptor substrate-1: an essential interaction for transformation.	bind
48864	1	10564	7	NULL	NULL	0	NULL	ETV6-NTRK3	NULL		bind	NULL		highly conserved NTRK3 C-terminal sequence		insulin receptor substrate-1	NULL		 phosphotyrosine binding domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_6225_s_1	14668342	A highly conserved NTRK3 C-terminal sequence in the ETV6-NTRK3 oncoprotein binds the phosphotyrosine binding domain of insulin receptor substrate-1: an essential interaction for transformation.	bind
48865	2	10564	7	NULL	NULL	0	NULL	statement 1	NULL		is essential for	NULL				transformation	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6225_s_1	14668342	A highly conserved NTRK3 C-terminal sequence in the ETV6-NTRK3 oncoprotein binds the phosphotyrosine binding domain of insulin receptor substrate-1: an essential interaction for transformation.	bind
48866	3	10564	7	NULL	NULL	0	NULL	ETV6-NTRK3	NULL		is a type of	NULL				oncoprotein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6225_s_1	14668342	A highly conserved NTRK3 C-terminal sequence in the ETV6-NTRK3 oncoprotein binds the phosphotyrosine binding domain of insulin receptor substrate-1: an essential interaction for transformation.	bind
39313	1	10566	6	13	NULL	NULL	NULL	RyR2	GP		is					cardiac muscle RyR	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37941_s_150	16157601	A highly homologous protein (FKBP12.6) binds to the cardiac muscle RyR (known as RyR2) and stabilizes RyR2 in a similar manner ( ,  ).	bind
39314	2	10566	6	13	NULL	NULL	NULL	FKBP12.6	GP		bind					RyR2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37941_s_150	16157601	A highly homologous protein (FKBP12.6) binds to the cardiac muscle RyR (known as RyR2) and stabilizes RyR2 in a similar manner ( ,  ).	bind
39315	3	10566	6	13	NULL	NULL	NULL	statement 2	Process		stabilizes					RyR2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37941_s_150	16157601	A highly homologous protein (FKBP12.6) binds to the cardiac muscle RyR (known as RyR2) and stabilizes RyR2 in a similar manner ( ,  ).	bind
48867	1	10566	7	10	NULL	0	NULL	FKBP12.6	NULL		bind	NULL				RyR	NULL	cardiac muscle			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37941_s_150	16157601	A highly homologous protein (FKBP12.6) binds to the cardiac muscle RyR (known as RyR2) and stabilizes RyR2 in a similar manner ( ,  ).	bind
48868	2	10566	7	NULL	NULL	0	NULL	statement 1	NULL		stabilizes	NULL				RyR2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_45_37941_s_150	16157601	A highly homologous protein (FKBP12.6) binds to the cardiac muscle RyR (known as RyR2) and stabilizes RyR2 in a similar manner ( ,  ).	bind
48869	3	10566	7	10	NULL	0	NULL	cardiac muscle RyR	NULL		is	NULL				RyR2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37941_s_150	16157601	A highly homologous protein (FKBP12.6) binds to the cardiac muscle RyR (known as RyR2) and stabilizes RyR2 in a similar manner ( ,  ).	bind
39316	1	10567	6	13	NULL	NULL	NULL	Mcm4	GP	highly phosphorylated	accumulates on					chromatin	Chromosome				NULL	Xenopus egg extracts	NULL	NULL	NULL	NULL	gw70_genesdev_19_19_2295_s_85	16204181	A highly phosphorylated form of Mcm4 has been described and shown to accumulate on chromatin at the G1/S transition in  Xenopus egg extracts independently of Cdk2 activity (Pereverzeva et al. 2000 ).	bind
39317	2	10567	6	13	NULL	NULL	NULL	statement 1	Process		occurs during					G1/S transition	Process				NULL	Xenopus egg extracts	NULL	NULL	NULL	NULL	gw70_genesdev_19_19_2295_s_85	16204181	A highly phosphorylated form of Mcm4 has been described and shown to accumulate on chromatin at the G1/S transition in  Xenopus egg extracts independently of Cdk2 activity (Pereverzeva et al. 2000 ).	bind
39318	3	10567	6	13	NULL	NULL	NULL	statement 1	Process		is independent of					Cdk2	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_19_2295_s_85	16204181	A highly phosphorylated form of Mcm4 has been described and shown to accumulate on chromatin at the G1/S transition in  Xenopus egg extracts independently of Cdk2 activity (Pereverzeva et al. 2000 ).	bind
48870	1	10567	7	10	NULL	0	NULL	Mcm4	NULL	highly phosphorylated	accumulate on	NULL				chromatin	NULL				NULL	Xenopus egg extracts	NULL	NULL	NULL	NULL	gw70_genesdev_19_19_2295_s_85	16204181	A highly phosphorylated form of Mcm4 has been described and shown to accumulate on chromatin at the G1/S transition in  Xenopus egg extracts independently of Cdk2 activity (Pereverzeva et al. 2000 ).	bind
48871	2	10567	7	10	NULL	0	NULL	statement 1	NULL		is independent of	NULL				Cdk2 	NULL	activity of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_19_2295_s_85	16204181	A highly phosphorylated form of Mcm4 has been described and shown to accumulate on chromatin at the G1/S transition in  Xenopus egg extracts independently of Cdk2 activity (Pereverzeva et al. 2000 ).	bind
50259	3	10567	7	10	NULL	0	NULL	statement 1	NULL		occurs during	NULL				G1/S transition	NULL				NULL	Xenopus egg extracts	0	NULL	NULL	NULL	gw70_genesdev_19_19_2295_s_85	16204181	A highly phosphorylated form of Mcm4 has been described and shown to accumulate on chromatin at the G1/S transition in  Xenopus egg extracts independently of Cdk2 activity (Pereverzeva et al. 2000 ).	bind
39319	1	10568	6	13	NULL	NULL	NULL	CsrA	GP		bind					CsrB	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_18_5130_s_34	12193630	A highly repeated sequence element that is located in the loops of predicted CsrB hairpins and is related to the sequences involved in  glgCAP recognition sites ( 6) probably mediates the binding of CsrA to CsrB.	bind
39320	2	10568	6	13	NULL	NULL	NULL	CsrB hairpins	GP		mediates		probably		repeated sequence element	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_18_5130_s_34	12193630	A highly repeated sequence element that is located in the loops of predicted CsrB hairpins and is related to the sequences involved in  glgCAP recognition sites ( 6) probably mediates the binding of CsrA to CsrB.	bind
48872	1	10568	7	NULL	NULL	0	NULL	CsrA	NULL		bind	NULL				CsrB	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_18_5130_s_34	12193630	A highly repeated sequence element that is located in the loops of predicted CsrB hairpins and is related to the sequences involved in  glgCAP recognition sites ( 6) probably mediates the binding of CsrA to CsrB.	bind
48873	2	10568	7	NULL	NULL	0	NULL	CsrB hairpins	NULL		is related to	NULL			highly repeated sequence element in loops of	glgCAP	NULL		sequences involved in recognition site of		NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_18_5130_s_34	12193630	A highly repeated sequence element that is located in the loops of predicted CsrB hairpins and is related to the sequences involved in  glgCAP recognition sites ( 6) probably mediates the binding of CsrA to CsrB.	bind
48874	3	10568	7	NULL	NULL	0	NULL	statement 2	NULL		mediate	NULL	may			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_18_5130_s_34	12193630	A highly repeated sequence element that is located in the loops of predicted CsrB hairpins and is related to the sequences involved in  glgCAP recognition sites ( 6) probably mediates the binding of CsrA to CsrB.	bind
39849	1	10569	6	13	NULL	NULL	NULL	SecA subunit	GP		is a type of					ATPase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_20_15526_s_265	10809785	A highly similar model was proposed for the preprotein translocase of  E. coli, where the ATP-bound form of the SecA subunit, an ATPase, is membrane-embedded, while hydrolysis triggers release into the cytoplasm ( 31).	bind
39850	2	10569	6	13	NULL	NULL	NULL	ATP	Chemical		bind					preprotein translocase	GP	E. coli	SecA subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_20_15526_s_265	10809785	A highly similar model was proposed for the preprotein translocase of  E. coli, where the ATP-bound form of the SecA subunit, an ATPase, is membrane-embedded, while hydrolysis triggers release into the cytoplasm ( 31).	bind
39851	3	10569	6	13	NULL	NULL	NULL	preprotein translocase	GP	E. coli	is embedded in			SecA subunit		membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_20_15526_s_265	10809785	A highly similar model was proposed for the preprotein translocase of  E. coli, where the ATP-bound form of the SecA subunit, an ATPase, is membrane-embedded, while hydrolysis triggers release into the cytoplasm ( 31).	bind
39852	4	10569	6	13	NULL	NULL	NULL	preprotein translocase	GP	E. coli	is released into 			SecA subunit		cytoplasm	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_20_15526_s_265	10809785	A highly similar model was proposed for the preprotein translocase of  E. coli, where the ATP-bound form of the SecA subunit, an ATPase, is membrane-embedded, while hydrolysis triggers release into the cytoplasm ( 31).	bind
39853	5	10569	6	13	NULL	NULL	NULL	hydrolysis	Process		triggers					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_20_15526_s_265	10809785	A highly similar model was proposed for the preprotein translocase of  E. coli, where the ATP-bound form of the SecA subunit, an ATPase, is membrane-embedded, while hydrolysis triggers release into the cytoplasm ( 31).	bind
48875	1	10569	7	10	NULL	0	NULL	ATP	NULL		bind	NULL				preprotein translocase	NULL	E. coli	SecA subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_20_15526_s_265	10809785	A highly similar model was proposed for the preprotein translocase of  E. coli, where the ATP-bound form of the SecA subunit, an ATPase, is membrane-embedded, while hydrolysis triggers release into the cytoplasm ( 31).	bind
48876	2	10569	7	10	NULL	0	NULL	SecA subunit	NULL		is a type of	NULL				ATPase	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_20_15526_s_265	10809785	A highly similar model was proposed for the preprotein translocase of  E. coli, where the ATP-bound form of the SecA subunit, an ATPase, is membrane-embedded, while hydrolysis triggers release into the cytoplasm ( 31).	bind
48877	3	10569	7	10	NULL	0	NULL	preprotein translocase	NULL	E. coli	is embedded in	NULL		SecA subunit		membrane	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_20_15526_s_265	10809785	A highly similar model was proposed for the preprotein translocase of  E. coli, where the ATP-bound form of the SecA subunit, an ATPase, is membrane-embedded, while hydrolysis triggers release into the cytoplasm ( 31).	bind
48878	4	10569	7	10	NULL	0	NULL	preprotein translocase	NULL	E. coli	is released into	NULL		SecA subunit		cytoplasm	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_20_15526_s_265	10809785	A highly similar model was proposed for the preprotein translocase of  E. coli, where the ATP-bound form of the SecA subunit, an ATPase, is membrane-embedded, while hydrolysis triggers release into the cytoplasm ( 31).	bind
50260	5	10569	7	10	NULL	0	NULL	hydrolysis	NULL		triggers	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_20_15526_s_265	10809785	A highly similar model was proposed for the preprotein translocase of  E. coli, where the ATP-bound form of the SecA subunit, an ATPase, is membrane-embedded, while hydrolysis triggers release into the cytoplasm ( 31).	bind
39321	1	10570	6	13	NULL	NULL	NULL	streptococcal M protein family	GP		bind			variable region		C4BP	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_6_837_s_529	12818164	A highly variable region in members of the streptococcal M protein family binds the human complement regulator C4BP.	bind
39322	2	10570	6	13	NULL	NULL	NULL	C4BP	GP		is a type of					complement regulator	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_6_837_s_529	12818164	A highly variable region in members of the streptococcal M protein family binds the human complement regulator C4BP.	bind
48879	1	10570	7	NULL	NULL	0	NULL	streptococcal M protein family	NULL		bind	NULL		highly variable region		C4BP	NULL	human			NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_6_837_s_529	12818164	A highly variable region in members of the streptococcal M protein family binds the human complement regulator C4BP.	bind
48880	2	10570	7	NULL	NULL	0	NULL	C4BP	NULL		is a type of	NULL				complement regulator	NULL				NULL		NULL	NULL	NULL	NULL	gw60_immunity_18_6_837_s_529	12818164	A highly variable region in members of the streptococcal M protein family binds the human complement regulator C4BP.	bind
39323	1	10571	6	13	NULL	NULL	NULL	Protamine	GP		bind					RyR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_7_2213_s_122	10888663	A Hill coefficient of >4 in a three-parameter Hill equation [f = (a x xb)/(cb + xb)] fit indicates that more than four molecules of protamine must bind to the RyR to induce block.	bind
39324	2	10571	6	13	NULL	NULL	NULL	statement 1	Process		induce					block	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_7_2213_s_122	10888663	A Hill coefficient of >4 in a three-parameter Hill equation [f = (a x xb)/(cb + xb)] fit indicates that more than four molecules of protamine must bind to the RyR to induce block.	bind
48881	1	10571	7	NULL	NULL	0	NULL	protamine	NULL		bind	NULL				RyR	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_7_2213_s_122	10888663	A Hill coefficient of >4 in a three-parameter Hill equation [f = (a x xb)/(cb + xb)] fit indicates that more than four molecules of protamine must bind to the RyR to induce block.	bind
48882	2	10571	7	NULL	NULL	0	NULL	statement 1	NULL		induce 	NULL				block	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_7_2213_s_122	10888663	A Hill coefficient of >4 in a three-parameter Hill equation [f = (a x xb)/(cb + xb)] fit indicates that more than four molecules of protamine must bind to the RyR to induce block.	bind
39325	1	10572	6	13	NULL	NULL	NULL	UmuD``C	GP		bind					M13 DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_18_10767_s_9	8631887	A Hill coefficient,  n  =  3, characterizes the binding of UmuD``C to M13 DNA and to  a 600 nucleotide DNA oligomer, suggesting that at least three protein  complexes may interact cooperatively when binding to DNA.	bind
39326	2	10572	6	13	NULL	NULL	NULL	UmuD``C	GP		bind					DNA oligomer	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_18_10767_s_9	8631887	A Hill coefficient,  n  =  3, characterizes the binding of UmuD``C to M13 DNA and to  a 600 nucleotide DNA oligomer, suggesting that at least three protein  complexes may interact cooperatively when binding to DNA.	bind
48883	1	10572	7	NULL	NULL	0	NULL	UmuD``C 	NULL		bind	NULL				M13 DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_18_10767_s_9	8631887	A Hill coefficient,  n  =  3, characterizes the binding of UmuD``C to M13 DNA and to  a 600 nucleotide DNA oligomer, suggesting that at least three protein  complexes may interact cooperatively when binding to DNA.	bind
48884	2	10572	7	10	NULL	0	NULL	UmuD``C	NULL		bind	NULL				DNA oligomer	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_18_10767_s_9	8631887	A Hill coefficient,  n  =  3, characterizes the binding of UmuD``C to M13 DNA and to  a 600 nucleotide DNA oligomer, suggesting that at least three protein  complexes may interact cooperatively when binding to DNA.	bind
39327	1	10576	6	13	NULL	NULL	NULL	CycT1	GP		bind			histidine-rich sequence in C terminus				unphosphorylated	CTD		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_6_748_s_34	12651893	A histidine-rich sequence in the C terminus of CycT1 then binds the unphosphorylated CTD.	bind
48892	1	10576	7	NULL	NULL	0	NULL	CycT1	NULL		bind	NULL		histidine-rich sequence in the C terminus			NULL	unphosphorylated	CTD		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_6_748_s_34	12651893	A histidine-rich sequence in the C terminus of CycT1 then binds the unphosphorylated CTD.	bind
39854	1	10577	6	13	NULL	NULL	NULL	phorbol ester	Chemical		bind					Munc13-1	GP		C1 domain		NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_2_335_s_167	10571228	A histidine-to-lysine substitution at this position abolished phorbol ester binding to the C1 domain of Munc13-1 ( Betz et al. 1998  ), and other substitutions at this position abolished phorbol ester binding to protein kinase C  ( Kazanietz et al. 1995b  ).	bind
39855	2	10577	6	13	NULL	NULL	NULL	phorbol ester	Chemical		bind					protein kinase C	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_2_335_s_167	10571228	A histidine-to-lysine substitution at this position abolished phorbol ester binding to the C1 domain of Munc13-1 ( Betz et al. 1998  ), and other substitutions at this position abolished phorbol ester binding to protein kinase C  ( Kazanietz et al. 1995b  ).	bind
39856	3	10577	6	13	NULL	NULL	NULL	histidine	AminoAcid		is substituted with					lysine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_2_335_s_167	10571228	A histidine-to-lysine substitution at this position abolished phorbol ester binding to the C1 domain of Munc13-1 ( Betz et al. 1998  ), and other substitutions at this position abolished phorbol ester binding to protein kinase C  ( Kazanietz et al. 1995b  ).	bind
39857	4	10577	6	13	NULL	NULL	NULL	statement 3	Process		abolishes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_2_335_s_167	10571228	A histidine-to-lysine substitution at this position abolished phorbol ester binding to the C1 domain of Munc13-1 ( Betz et al. 1998  ), and other substitutions at this position abolished phorbol ester binding to protein kinase C  ( Kazanietz et al. 1995b  ).	bind
48899	1	10577	7	NULL	NULL	0	NULL	phorbol ester	NULL		bind	NULL				Munc13-1	NULL		C1 domain		NULL		0	NULL	NULL	NULL	gw60_neuron_24_2_335_s_167	10571228	A histidine-to-lysine substitution at this position abolished phorbol ester binding to the C1 domain of Munc13-1 ( Betz et al. 1998  ), and other substitutions at this position abolished phorbol ester binding to protein kinase C  ( Kazanietz et al. 1995b  ).	bind
48900	4	10577	7	10	NULL	0	NULL	statement 2	NULL		abolishes	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_24_2_335_s_167	10571228	A histidine-to-lysine substitution at this position abolished phorbol ester binding to the C1 domain of Munc13-1 ( Betz et al. 1998  ), and other substitutions at this position abolished phorbol ester binding to protein kinase C  ( Kazanietz et al. 1995b  ).	bind
48901	3	10577	7	NULL	NULL	0	NULL	phorbol ester	NULL		bind	NULL				protein kinase C	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_24_2_335_s_167	10571228	A histidine-to-lysine substitution at this position abolished phorbol ester binding to the C1 domain of Munc13-1 ( Betz et al. 1998  ), and other substitutions at this position abolished phorbol ester binding to protein kinase C  ( Kazanietz et al. 1995b  ).	bind
50261	2	10577	7	10	NULL	0	NULL	histidine	NULL		is substituted to	NULL				lysine	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_24_2_335_s_167	10571228	A histidine-to-lysine substitution at this position abolished phorbol ester binding to the C1 domain of Munc13-1 ( Betz et al. 1998  ), and other substitutions at this position abolished phorbol ester binding to protein kinase C  ( Kazanietz et al. 1995b  ).	bind
39328	1	10579	6	13	NULL	NULL	NULL			homeotic mutation;;trithorax	impedes			SET domain		histone	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_nature_426_6962_78_s_252	14603321	A homeotic  mutation in the trithorax SET domain impedes histone binding.	bind
48903	1	10579	7	10	NULL	0	NULL		NULL	homeotic mutation;;trithorax	impede	NULL		SET domain		histone	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw70_nature_426_6962_78_s_252	14603321	A homeotic  mutation in the trithorax SET domain impedes histone binding.	bind
39329	1	10581	6	13	NULL	NULL	NULL	MPP11	GP	ribosome-associated fraction of	does not bind					Id1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_29_10064_s_117	16002468	A homolog of Id1 was not detected, suggesting that the ribosome-associated fraction of MPP11 was not bound to this transcription factor (see Introduction).	bind
39330	2	10581	6	13	NULL	NULL	NULL	Id1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_29_10064_s_117	16002468	A homolog of Id1 was not detected, suggesting that the ribosome-associated fraction of MPP11 was not bound to this transcription factor (see Introduction).	bind
48906	1	10581	7	NULL	NULL	0	NULL	MPP11	NULL	ribosome-associated fraction of	does not bind	NULL				Id1	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_29_10064_s_117	16002468	A homolog of Id1 was not detected, suggesting that the ribosome-associated fraction of MPP11 was not bound to this transcription factor (see Introduction).	bind
50262	2	10581	7	10	NULL	0	NULL	Id1	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_29_10064_s_117	16002468	A homolog of Id1 was not detected, suggesting that the ribosome-associated fraction of MPP11 was not bound to this transcription factor (see Introduction).	bind
39331	1	10582	6	13	NULL	NULL	NULL	MarR 	GP		is a type of					repressor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_16_5131_s_67	10438794	A homologous MarR repressor binds salicylate and controls the expression of a global regulator, MarA, in  E. coli ( 14-16,  19).	bind
39332	2	10582	6	13	NULL	NULL	NULL	MarR	GP	homologous	bind					salicylate	Chemical				NULL	E.coli	NULL	NULL	NULL	NULL	gw60_jbacteriol_181_16_5131_s_67	10438794	A homologous MarR repressor binds salicylate and controls the expression of a global regulator, MarA, in  E. coli ( 14-16,  19).	bind
39333	3	10582	6	13	NULL	NULL	NULL	MarA	GP		is a type of					regulator	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_16_5131_s_67	10438794	A homologous MarR repressor binds salicylate and controls the expression of a global regulator, MarA, in  E. coli ( 14-16,  19).	bind
39334	4	10582	6	13	NULL	NULL	NULL	statement 1	Process		controls					MarA	GP	expression of			NULL	E.coli	NULL	NULL	NULL	NULL	gw60_jbacteriol_181_16_5131_s_67	10438794	A homologous MarR repressor binds salicylate and controls the expression of a global regulator, MarA, in  E. coli ( 14-16,  19).	bind
48907	1	10582	7	10	NULL	0	NULL	MarR	NULL	homologous	bind	NULL				salicylate	NULL				NULL	E.coli	NULL	NULL	NULL	NULL	gw60_jbacteriol_181_16_5131_s_67	10438794	A homologous MarR repressor binds salicylate and controls the expression of a global regulator, MarA, in  E. coli ( 14-16,  19).	bind
48908	2	10582	7	NULL	NULL	0	NULL	statement 1	NULL		controls	NULL				MarA	NULL	expression of			NULL	E.coli	0	NULL	NULL	NULL	gw60_jbacteriol_181_16_5131_s_67	10438794	A homologous MarR repressor binds salicylate and controls the expression of a global regulator, MarA, in  E. coli ( 14-16,  19).	bind
48909	3	10582	7	NULL	NULL	0	NULL	MarR	NULL		is a type of	NULL				repressor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_16_5131_s_67	10438794	A homologous MarR repressor binds salicylate and controls the expression of a global regulator, MarA, in  E. coli ( 14-16,  19).	bind
48910	4	10582	7	NULL	NULL	0	NULL	MarA	NULL		is a type of	NULL				global regulator	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_16_5131_s_67	10438794	A homologous MarR repressor binds salicylate and controls the expression of a global regulator, MarA, in  E. coli ( 14-16,  19).	bind
39335	1	10583	6	13	NULL	NULL	NULL	VirB	GP	Agrobacterium tumefaciens homologue	is essential for					Brucella suis	Organism	intracellular survival of 			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_2_865_s_237	11159979	A homologue of the  Agrobacterium tumefaciens VirB and  Bordetella pertussis Ptl type IV secretion systems is essential for intracellular survival of  Brucella suis.	bind
39336	2	10583	6	13	NULL	NULL	NULL	Ptl type IV secretion system	Process	Bordetella pertussis	is essential for					Brucella suis	Organism	intracellular survival of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_69_2_865_s_237	11159979	A homologue of the  Agrobacterium tumefaciens VirB and  Bordetella pertussis Ptl type IV secretion systems is essential for intracellular survival of  Brucella suis.	bind
48911	1	10583	7	NULL	NULL	0	NULL	VirB	NULL	Agrobacterium tumefaciens homologue	is essential for	NULL				Brucella suis	NULL	intracellular survival of			NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_2_865_s_237	11159979	A homologue of the  Agrobacterium tumefaciens VirB and  Bordetella pertussis Ptl type IV secretion systems is essential for intracellular survival of  Brucella suis.	bind
48912	2	10583	7	NULL	NULL	0	NULL	Ptl type IV secretion systems	NULL	Bordetella pertussis	is essential for	NULL				Brucella suis	NULL	 intracellular survival of			NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_2_865_s_237	11159979	A homologue of the  Agrobacterium tumefaciens VirB and  Bordetella pertussis Ptl type IV secretion systems is essential for intracellular survival of  Brucella suis.	bind
39337	1	10584	6	13	NULL	NULL	NULL	progesterone	Chemical		bind					PR	GP		LBD		NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_63_5_1012_s_224	12695529	A homology model was created for the LBD of GR based on the X-ray crystal structure  of the progesterone bound LBD of PR (Williams and Sigler, 1998 ).	bind
48913	1	10584	7	NULL	NULL	0	NULL	progesterone 	NULL		bind	NULL				PR	NULL		LBD		NULL		0	NULL	NULL	NULL	gw70_molpharmacol_63_5_1012_s_224	12695529	A homology model was created for the LBD of GR based on the X-ray crystal structure  of the progesterone bound LBD of PR (Williams and Sigler, 1998 ).	bind
39352	1	10587	6	13	NULL	NULL	NULL	homopyrimidine third strand	NucleicAcid		contains					cytosine	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7295_s_33	7706270	A homopyrimidine third strand  containing cytosine and/or thymine binds to the purine strand in a  parallel orientation.	bind
39353	2	10587	6	13	NULL	NULL	NULL	homopyrimidine third strand	NucleicAcid		contains					thymine	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7295_s_33	7706270	A homopyrimidine third strand  containing cytosine and/or thymine binds to the purine strand in a  parallel orientation.	bind
39354	3	10587	6	13	NULL	NULL	NULL	statement 1	NucleicAcid		bind					purine strand	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7295_s_33	7706270	A homopyrimidine third strand  containing cytosine and/or thymine binds to the purine strand in a  parallel orientation.	bind
39355	4	10587	6	13	NULL	NULL	NULL	statement 2	NucleicAcid		bind					purine strand	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7295_s_33	7706270	A homopyrimidine third strand  containing cytosine and/or thymine binds to the purine strand in a  parallel orientation.	bind
39356	5	10587	6	13	NULL	NULL	NULL	statement 3	Process		occurs in					parallel orientation					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7295_s_33	7706270	A homopyrimidine third strand  containing cytosine and/or thymine binds to the purine strand in a  parallel orientation.	bind
39357	6	10587	6	13	NULL	NULL	NULL	statement 4	Process		occurs in					parallel orientation					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7295_s_33	7706270	A homopyrimidine third strand  containing cytosine and/or thymine binds to the purine strand in a  parallel orientation.	bind
48915	3	10587	7	10	NULL	0	NULL	statement 1	NULL		bind	NULL				purine strand	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7295_s_33	7706270	A homopyrimidine third strand  containing cytosine and/or thymine binds to the purine strand in a  parallel orientation.	bind
48916	5	10587	7	10	NULL	0	NULL	statement 3	NULL		occurs in	NULL				parallel orientation	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7295_s_33	7706270	A homopyrimidine third strand  containing cytosine and/or thymine binds to the purine strand in a  parallel orientation.	bind
48917	4	10587	7	10	NULL	0	NULL	statement 2	NULL		bind	NULL				purine strand	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7295_s_33	7706270	A homopyrimidine third strand  containing cytosine and/or thymine binds to the purine strand in a  parallel orientation.	bind
48918	6	10587	7	10	NULL	0	NULL	statement 4	NULL		occurs in	NULL				parallel orientation	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_13_7295_s_33	7706270	A homopyrimidine third strand  containing cytosine and/or thymine binds to the purine strand in a  parallel orientation.	bind
50263	1	10587	7	10	NULL	0	NULL	\thomopyrimidine third strand	NULL		contains	NULL				cytosine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_13_7295_s_33	7706270	A homopyrimidine third strand  containing cytosine and/or thymine binds to the purine strand in a  parallel orientation.	bind
50264	2	10587	7	10	NULL	0	NULL	homopyrimidine third strand	NULL		contains	NULL				thymine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_13_7295_s_33	7706270	A homopyrimidine third strand  containing cytosine and/or thymine binds to the purine strand in a  parallel orientation.	bind
39358	1	10588	6	13	NULL	NULL	NULL	RARs	GP		is a type of					retinoid receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_469_1_118_s_9	10708768	A HRE located between nucleotides -352 and -320 in the HIV long terminal repeat (LTR) binds retinoid receptors (RARs and RXRs) [  11 and   12].	bind
39359	2	10588	6	13	NULL	NULL	NULL	RXRs	GP		is a type of					retinoid receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_469_1_118_s_9	10708768	A HRE located between nucleotides -352 and -320 in the HIV long terminal repeat (LTR) binds retinoid receptors (RARs and RXRs) [  11 and   12].	bind
39360	3	10588	6	13	NULL	NULL	NULL	LTR	NucleicAcid		is					long terminal repeat	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_febslett_469_1_118_s_9	10708768	A HRE located between nucleotides -352 and -320 in the HIV long terminal repeat (LTR) binds retinoid receptors (RARs and RXRs) [  11 and   12].	bind
39361	4	10588	6	13	NULL	NULL	NULL	HIV LTR	NucleicAcid		bind				HRE (-352 to -320)	RAR	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_469_1_118_s_9	10708768	A HRE located between nucleotides -352 and -320 in the HIV long terminal repeat (LTR) binds retinoid receptors (RARs and RXRs) [  11 and   12].	bind
39362	5	10588	6	13	NULL	NULL	NULL	HIV LTR	NucleicAcid		bind				HRE (-352 to -320)	RXR	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_469_1_118_s_9	10708768	A HRE located between nucleotides -352 and -320 in the HIV long terminal repeat (LTR) binds retinoid receptors (RARs and RXRs) [  11 and   12].	bind
48920	2	10588	7	10	NULL	0	NULL	HIV LTR	NULL		bind	NULL			HRE (-352 to -320)	RARs	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_469_1_118_s_9	10708768	A HRE located between nucleotides -352 and -320 in the HIV long terminal repeat (LTR) binds retinoid receptors (RARs and RXRs) [  11 and   12].	bind
48921	3	10588	7	10	NULL	0	NULL	HIV LTR	NULL		bind	NULL			HRE (-352 to -320)	RXRs	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_469_1_118_s_9	10708768	A HRE located between nucleotides -352 and -320 in the HIV long terminal repeat (LTR) binds retinoid receptors (RARs and RXRs) [  11 and   12].	bind
48922	4	10588	7	NULL	NULL	0	NULL	RARs	NULL		is a type of	NULL				retinoid receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_469_1_118_s_9	10708768	A HRE located between nucleotides -352 and -320 in the HIV long terminal repeat (LTR) binds retinoid receptors (RARs and RXRs) [  11 and   12].	bind
48923	5	10588	7	NULL	NULL	0	NULL	RXRs	NULL		is a type of	NULL				retinoid receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_469_1_118_s_9	10708768	A HRE located between nucleotides -352 and -320 in the HIV long terminal repeat (LTR) binds retinoid receptors (RARs and RXRs) [  11 and   12].	bind
48924	1	10588	7	10	NULL	0	NULL	LTR			is					Long terminal repeat					NULL		NULL	NULL	NULL	NULL	gw60_febslett_469_1_118_s_9	10708768	A HRE located between nucleotides -352 and -320 in the HIV long terminal repeat (LTR) binds retinoid receptors (RARs and RXRs) [  11 and   12].	bind
39858	1	10589	6	13	NULL	NULL	NULL	HS species	Chemical		bind					FGF ligand	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_19	11786412	A HS species that binds both FGF ligand and RTK will act as a stimulator, whereas a HS that only binds FGF ligand will act as an inhibitor of signaling by sequestering the growth factor.	bind
39859	2	10589	6	13	NULL	NULL	NULL	HS species	Chemical		bind					RTK	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_19	11786412	A HS species that binds both FGF ligand and RTK will act as a stimulator, whereas a HS that only binds FGF ligand will act as an inhibitor of signaling by sequestering the growth factor.	bind
48925	1	10589	7	NULL	NULL	0	NULL	HS species	NULL		bind	NULL				FGF ligand	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_19	11786412	A HS species that binds both FGF ligand and RTK will act as a stimulator, whereas a HS that only binds FGF ligand will act as an inhibitor of signaling by sequestering the growth factor.	bind
48926	2	10589	7	NULL	NULL	0	NULL	HS species	NULL		bind	NULL				RTK	NULL				NULL		0	NULL	NULL	NULL	gw60_amjpathol_160_1_185_s_19	11786412	A HS species that binds both FGF ligand and RTK will act as a stimulator, whereas a HS that only binds FGF ligand will act as an inhibitor of signaling by sequestering the growth factor.	bind
39363	1	10591	6	13	NULL	NULL	NULL	endothelial cell membrane protein	GP	human	bind					Staphylococcus aureus	Organism				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_infectimmun_67_11_6130_s_584	10531276	A human endothelial cell membrane protein that binds  Staphylococcus aureus in vitro.	bind
48933	1	10591	7	NULL	NULL	0	NULL	endothelial cell membrane protein	NULL	human	bind	NULL				Staphylococcus aureus	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_infectimmun_67_11_6130_s_584	10531276	A human endothelial cell membrane protein that binds  Staphylococcus aureus in vitro.	bind
39860	1	10592	6	13	NULL	NULL	NULL	immunoglobulin G1 antibody	GP	human	bind		avidly			MUC1	GP	tumor-associated			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-pathol_160_5_12000712_s_1	12000712	A human immunoglobulin G1 antibody originating from an in vitro-selected Fab phage antibody binds avidly to tumor-associated MUC1 and is efficiently internalized..	bind
39861	2	10592	6	13	NULL	NULL	NULL	immunoglobulin G1 antibody	GP	human	originates from					Fab phage antibody	GP	in vitro-selected			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-pathol_160_5_12000712_s_1	12000712	A human immunoglobulin G1 antibody originating from an in vitro-selected Fab phage antibody binds avidly to tumor-associated MUC1 and is efficiently internalized..	bind
50265	3	10592	6	13	NULL	NULL	NULL	statement 1	Process		undergoes					internalization	Process	efficient			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-pathol_160_5_12000712_s_1	12000712	A human immunoglobulin G1 antibody originating from an in vitro-selected Fab phage antibody binds avidly to tumor-associated MUC1 and is efficiently internalized..	bind
48934	1	10592	7	10	NULL	0	NULL	immunoglobulin G1 antibody	NULL	human	originate from	NULL				Fab phage antibody	NULL	in vitro-selected 			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-pathol_160_5_12000712_s_1	12000712	A human immunoglobulin G1 antibody originating from an in vitro-selected Fab phage antibody binds avidly to tumor-associated MUC1 and is efficiently internalized..	bind
48935	2	10592	7	10	NULL	0	NULL	statement 1	NULL		bind	NULL	avidly			MUC1	NULL	tumor-associated			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-pathol_160_5_12000712_s_1	12000712	A human immunoglobulin G1 antibody originating from an in vitro-selected Fab phage antibody binds avidly to tumor-associated MUC1 and is efficiently internalized..	bind
48936	3	10592	7	10	NULL	0	NULL	statement 2	NULL		undergoes	NULL				internalization	NULL	efficient			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-pathol_160_5_12000712_s_1	12000712	A human immunoglobulin G1 antibody originating from an in vitro-selected Fab phage antibody binds avidly to tumor-associated MUC1 and is efficiently internalized..	bind
39364	1	10593	6	13	NULL	NULL	NULL	Rabin8	GP	human	bind					Rab8	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_methods-enzymol_403_1_16473595_s_5	16473595	A human protein (Rabin8) and its rat equivalent (Rabin3)  were found to bind Rab8 and function as nucleotide exchange factors for  Rab8 but not for Rab3A and Rab5.	bind
39365	2	10593	6	13	NULL	NULL	NULL	Rabin3	GP	rat	bind					Rab8	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_methods-enzymol_403_1_16473595_s_5	16473595	A human protein (Rabin8) and its rat equivalent (Rabin3)  were found to bind Rab8 and function as nucleotide exchange factors for  Rab8 but not for Rab3A and Rab5.	bind
39366	3	10593	6	13	NULL	NULL	NULL	statement 1	GP		function as					Rab8	GP	nucleotide exchange factor for			NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_methods-enzymol_403_1_16473595_s_5	16473595	A human protein (Rabin8) and its rat equivalent (Rabin3)  were found to bind Rab8 and function as nucleotide exchange factors for  Rab8 but not for Rab3A and Rab5.	bind
39367	4	10593	6	13	NULL	NULL	NULL	statement 2	GP		function as					Rab8	GP	nucleotide exchange factor for			NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_methods-enzymol_403_1_16473595_s_5	16473595	A human protein (Rabin8) and its rat equivalent (Rabin3)  were found to bind Rab8 and function as nucleotide exchange factors for  Rab8 but not for Rab3A and Rab5.	bind
39368	5	10593	6	13	NULL	NULL	NULL	statement 1	GP		does not function as					Rab3A	GP	nucleotide exchange factor for			NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_methods-enzymol_403_1_16473595_s_5	16473595	A human protein (Rabin8) and its rat equivalent (Rabin3)  were found to bind Rab8 and function as nucleotide exchange factors for  Rab8 but not for Rab3A and Rab5.	bind
39369	6	10593	6	13	NULL	NULL	NULL	statement 1	GP		does not function as					Rab5	GP	nucleotide exchange factor for			NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_methods-enzymol_403_1_16473595_s_5	16473595	A human protein (Rabin8) and its rat equivalent (Rabin3)  were found to bind Rab8 and function as nucleotide exchange factors for  Rab8 but not for Rab3A and Rab5.	bind
39370	7	10593	6	13	NULL	NULL	NULL	statement 2	GP		does not function as					Rab3A	GP	nucleotide exchange factor for			NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_methods-enzymol_403_1_16473595_s_5	16473595	A human protein (Rabin8) and its rat equivalent (Rabin3)  were found to bind Rab8 and function as nucleotide exchange factors for  Rab8 but not for Rab3A and Rab5.	bind
39371	8	10593	6	13	NULL	NULL	NULL	statement 2	GP		does not function as					Rab5	GP	nucleotide exchange factor for			NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_methods-enzymol_403_1_16473595_s_5	16473595	A human protein (Rabin8) and its rat equivalent (Rabin3)  were found to bind Rab8 and function as nucleotide exchange factors for  Rab8 but not for Rab3A and Rab5.	bind
48937	1	10593	7	NULL	NULL	0	NULL	Rabin8	NULL	human	bind	NULL				Rab8	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_methods-enzymol_403_1_16473595_s_5	16473595	A human protein (Rabin8) and its rat equivalent (Rabin3)  were found to bind Rab8 and function as nucleotide exchange factors for  Rab8 but not for Rab3A and Rab5.	bind
48938	2	10593	7	NULL	NULL	0	NULL	Rabin3	NULL	rat	bind	NULL				Rab8	NULL				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_methods-enzymol_403_1_16473595_s_5	16473595	A human protein (Rabin8) and its rat equivalent (Rabin3)  were found to bind Rab8 and function as nucleotide exchange factors for  Rab8 but not for Rab3A and Rab5.	bind
48939	3	10593	7	NULL	NULL	0	NULL	statement 1	NULL		function as	NULL				Rab8	NULL	nucleotide exchange factors for			NULL		0	NULL	NULL	NULL	abs-batch0600-0619_methods-enzymol_403_1_16473595_s_5	16473595	A human protein (Rabin8) and its rat equivalent (Rabin3)  were found to bind Rab8 and function as nucleotide exchange factors for  Rab8 but not for Rab3A and Rab5.	bind
48940	4	10593	7	NULL	NULL	0	NULL	statement 2	NULL		function as	NULL				Rab8	NULL	nucleotide exchange factors for			NULL		0	NULL	NULL	NULL	abs-batch0600-0619_methods-enzymol_403_1_16473595_s_5	16473595	A human protein (Rabin8) and its rat equivalent (Rabin3)  were found to bind Rab8 and function as nucleotide exchange factors for  Rab8 but not for Rab3A and Rab5.	bind
48941	5	10593	7	NULL	NULL	0	NULL	statement 1	NULL		does not function as	NULL				Rab3A	NULL	nucleotide exchange factors for			NULL		0	NULL	NULL	NULL	abs-batch0600-0619_methods-enzymol_403_1_16473595_s_5	16473595	A human protein (Rabin8) and its rat equivalent (Rabin3)  were found to bind Rab8 and function as nucleotide exchange factors for  Rab8 but not for Rab3A and Rab5.	bind
48942	6	10593	7	NULL	NULL	0	NULL	statement 2	NULL		does not function as	NULL				Rab3A	NULL	nucleotide exchange factors for			NULL		0	NULL	NULL	NULL	abs-batch0600-0619_methods-enzymol_403_1_16473595_s_5	16473595	A human protein (Rabin8) and its rat equivalent (Rabin3)  were found to bind Rab8 and function as nucleotide exchange factors for  Rab8 but not for Rab3A and Rab5.	bind
48943	7	10593	7	NULL	NULL	0	NULL	statement 1	NULL		does not function as	NULL				Rab5	NULL	nucleotide exchange factors for			NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_methods-enzymol_403_1_16473595_s_5	16473595	A human protein (Rabin8) and its rat equivalent (Rabin3)  were found to bind Rab8 and function as nucleotide exchange factors for  Rab8 but not for Rab3A and Rab5.	bind
48944	8	10593	7	NULL	NULL	0	NULL	statement 2	NULL		does not function as	NULL				Rab5	NULL	nucleotide exchange factors for			NULL		0	NULL	NULL	NULL	abs-batch0600-0619_methods-enzymol_403_1_16473595_s_5	16473595	A human protein (Rabin8) and its rat equivalent (Rabin3)  were found to bind Rab8 and function as nucleotide exchange factors for  Rab8 but not for Rab3A and Rab5.	bind
39387	1	10594	6	13	NULL	NULL	NULL	protein	GP	human	contains								cold shock domain		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_269_19_8188694_s_1	8188694	A human protein containing a "`cold"` shock domain binds specifically to H-DNA upstream from the human gamma-globin genes..	bind
39388	2	10594	6	13	NULL	NULL	NULL	statement 1	GP		bind		specifically			gamma globin genes	GP	human		H-DNA upstream from	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_269_19_8188694_s_1	8188694	A human protein containing a "`cold"` shock domain binds specifically to H-DNA upstream from the human gamma-globin genes..	bind
48945	1	10594	7	10	NULL	0	NULL	protein		human	bind		specifically	cold shock domain		H-DNA				upstream from the human gamma-globin genes	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_269_19_8188694_s_1	8188694	A human protein containing a "`cold"` shock domain binds specifically to H-DNA upstream from the human gamma-globin genes..	bind
39389	1	10595	6	13	NULL	NULL	NULL	protein	GP	human	interferes with					ras	GP	function of			NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_6_773_s_409	9208849	A human protein selected for interference with ras function interacts directly with ras and competes with raf1.	bind
39390	2	10595	6	13	NULL	NULL	NULL	statement 1	GP		interacts		directly			ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_6_773_s_409	9208849	A human protein selected for interference with ras function interacts directly with ras and competes with raf1.	bind
39391	3	10595	6	13	NULL	NULL	NULL	statement 1	GP		competes with					raf1	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_6_6_773_s_409	9208849	A human protein selected for interference with ras function interacts directly with ras and competes with raf1.	bind
48946	1	10595	7	NULL	NULL	0	NULL	 protein	NULL	human	interferes with	NULL				 ras 	NULL	function of			NULL		0	NULL	NULL	NULL	gw60_immunity_6_6_773_s_409	9208849	A human protein selected for interference with ras function interacts directly with ras and competes with raf1.	bind
48947	2	10595	7	NULL	NULL	0	NULL	statement 1	NULL		interacts with	NULL	directly			ras	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_6_6_773_s_409	9208849	A human protein selected for interference with ras function interacts directly with ras and competes with raf1.	bind
48948	3	10595	7	NULL	NULL	0	NULL	statement 1	NULL		compete with	NULL				raf1	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_6_6_773_s_409	9208849	A human protein selected for interference with ras function interacts directly with ras and competes with raf1.	bind
39392	1	10596	6	13	NULL	NULL	NULL	AMP	Chemical		bind								C1 subunit		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_19737_s_246	15767255	A hybrid tetramer of FBPase that constrains AMP binding to subunits C1 and C2, however, exhibits noncooperative inhibition, even though it undergoes a quaternary transition ( ).	bind
39393	2	10596	6	13	NULL	NULL	NULL	AMP	Chemical		bind								C2 subunit		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_19737_s_246	15767255	A hybrid tetramer of FBPase that constrains AMP binding to subunits C1 and C2, however, exhibits noncooperative inhibition, even though it undergoes a quaternary transition ( ).	bind
39394	3	10596	6	13	NULL	NULL	NULL	FBPase	GP	hybrid tetramer	constrains					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_19737_s_246	15767255	A hybrid tetramer of FBPase that constrains AMP binding to subunits C1 and C2, however, exhibits noncooperative inhibition, even though it undergoes a quaternary transition ( ).	bind
39395	4	10596	6	13	NULL	NULL	NULL	FBPase	GP	hybrid tetramer	constrains					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_19737_s_246	15767255	A hybrid tetramer of FBPase that constrains AMP binding to subunits C1 and C2, however, exhibits noncooperative inhibition, even though it undergoes a quaternary transition ( ).	bind
39399	5	10596	6	13	NULL	NULL	NULL	FBPase	GP	hybrid tetramer	undergoes a					quaternary transition	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_19737_s_246	15767255	A hybrid tetramer of FBPase that constrains AMP binding to subunits C1 and C2, however, exhibits noncooperative inhibition, even though it undergoes a quaternary transition ( ).	bind
48949	1	10596	7	NULL	NULL	0	NULL	AMP	NULL		bind	NULL					NULL		C1 subunit		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19737_s_246	15767255	A hybrid tetramer of FBPase that constrains AMP binding to subunits C1 and C2, however, exhibits noncooperative inhibition, even though it undergoes a quaternary transition ( ).	bind
48950	2	10596	7	NULL	NULL	0	NULL	AMP	NULL		bind	NULL					NULL		C2 subunit		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19737_s_246	15767255	A hybrid tetramer of FBPase that constrains AMP binding to subunits C1 and C2, however, exhibits noncooperative inhibition, even though it undergoes a quaternary transition ( ).	bind
48951	3	10596	7	NULL	NULL	0	NULL	FBPase	NULL	 hybrid tetramer of	constrains	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19737_s_246	15767255	A hybrid tetramer of FBPase that constrains AMP binding to subunits C1 and C2, however, exhibits noncooperative inhibition, even though it undergoes a quaternary transition ( ).	bind
48952	4	10596	7	NULL	NULL	0	NULL	FBPase	NULL	hybrid tetramer of	constrains	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19737_s_246	15767255	A hybrid tetramer of FBPase that constrains AMP binding to subunits C1 and C2, however, exhibits noncooperative inhibition, even though it undergoes a quaternary transition ( ).	bind
48953	5	10596	7	NULL	NULL	0	NULL	FBPase	NULL	hybrid tetramer of 	undergoes	NULL				quaternary transition	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19737_s_246	15767255	A hybrid tetramer of FBPase that constrains AMP binding to subunits C1 and C2, however, exhibits noncooperative inhibition, even though it undergoes a quaternary transition ( ).	bind
39862	1	10598	6	13	NULL	NULL	NULL	IkappaBalpha	GP		forms			SRR		IkappaBbeta	GP	hybrid protein with			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_7_3048_s_222	15024091	A hydrid IkappaB protein containing the SRR of IkappaBalpha and the rest of IkappaBbeta binds poorly with kappaB-Ras (lane 3).	bind
39863	2	10598	6	13	NULL	NULL	NULL	statement 1	GP		bind		poorly			kappaB-Ras	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_7_3048_s_222	15024091	A hydrid IkappaB protein containing the SRR of IkappaBalpha and the rest of IkappaBbeta binds poorly with kappaB-Ras (lane 3).	bind
48955	2	10598	7	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL	poorly			kappaB-Ras	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_7_3048_s_222	15024091	A hydrid IkappaB protein containing the SRR of IkappaBalpha and the rest of IkappaBbeta binds poorly with kappaB-Ras (lane 3).	bind
48956	1	10598	7	10	NULL	0	NULL	IkappaBalpha	NULL		forms	NULL		SRR		IkappaBbeta	NULL	hybrid protein with			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_7_3048_s_222	15024091	A hydrid IkappaB protein containing the SRR of IkappaBalpha and the rest of IkappaBbeta binds poorly with kappaB-Ras (lane 3).	bind
39400	1	10599	6	13	NULL	NULL	NULL	FKBP12-rapamycin	GP		bind					TOR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_46_27531_s_160	7499212	A hydrophobic  substitution of an FKBP12 acidic surface residue, D48V, had only a  minor 2-4-fold effect on FKBP12-rapamycin binding to TOR1 or TOR2 ( Fig. 5,  A  and  B).	bind
39401	2	10599	6	13	NULL	NULL	NULL	FKBP12-rapamycin	GP		bind					TOR2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_46_27531_s_160	7499212	A hydrophobic  substitution of an FKBP12 acidic surface residue, D48V, had only a  minor 2-4-fold effect on FKBP12-rapamycin binding to TOR1 or TOR2 ( Fig. 5,  A  and  B).	bind
39864	3	10599	6	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_46_27531_s_160	7499212	A hydrophobic  substitution of an FKBP12 acidic surface residue, D48V, had only a  minor 2-4-fold effect on FKBP12-rapamycin binding to TOR1 or TOR2 ( Fig. 5,  A  and  B).	bind
39865	4	10599	6	13	NULL	NULL	NULL	FKBP12	GP	hydrophobic substitution of 	effects		minor	acidic surface residue;; D48V		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_46_27531_s_160	7499212	A hydrophobic  substitution of an FKBP12 acidic surface residue, D48V, had only a  minor 2-4-fold effect on FKBP12-rapamycin binding to TOR1 or TOR2 ( Fig. 5,  A  and  B).	bind
39866	5	10599	6	13	NULL	NULL	NULL	FKBP12	GP	hydrophobic substitution of	effects		minor	acidic surface residue;; D48V		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_46_27531_s_160	7499212	A hydrophobic  substitution of an FKBP12 acidic surface residue, D48V, had only a  minor 2-4-fold effect on FKBP12-rapamycin binding to TOR1 or TOR2 ( Fig. 5,  A  and  B).	bind
48957	1	10599	7	NULL	NULL	0	NULL	FKBP12-rapamycin	NULL		bind	NULL				TOR1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_46_27531_s_160	7499212	A hydrophobic  substitution of an FKBP12 acidic surface residue, D48V, had only a  minor 2-4-fold effect on FKBP12-rapamycin binding to TOR1 or TOR2 ( Fig. 5,  A  and  B).	bind
48958	2	10599	7	NULL	NULL	0	NULL	FKBP12-rapamycin	NULL		bind	NULL				TOR2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_46_27531_s_160	7499212	A hydrophobic  substitution of an FKBP12 acidic surface residue, D48V, had only a  minor 2-4-fold effect on FKBP12-rapamycin binding to TOR1 or TOR2 ( Fig. 5,  A  and  B).	bind
48959	3	10599	7	10	NULL	0	NULL	FKBP12	NULL	hydrophobic substitution of	effects	NULL	minor	acidic surface residue;;D48V		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_46_27531_s_160	7499212	A hydrophobic  substitution of an FKBP12 acidic surface residue, D48V, had only a  minor 2-4-fold effect on FKBP12-rapamycin binding to TOR1 or TOR2 ( Fig. 5,  A  and  B).	bind
48960	4	10599	7	10	NULL	0	NULL	 FKBP12	NULL	hydrophobic substitution of	effects	NULL	minor	acidic surface residue;;D48V		statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_46_27531_s_160	7499212	A hydrophobic  substitution of an FKBP12 acidic surface residue, D48V, had only a  minor 2-4-fold effect on FKBP12-rapamycin binding to TOR1 or TOR2 ( Fig. 5,  A  and  B).	bind
57695	5	10599	7	10	NULL	0	NULL	statement 1			is an alternative to					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_46_27531_s_160	7499212	A hydrophobic  substitution of an FKBP12 acidic surface residue, D48V, had only a  minor 2-4-fold effect on FKBP12-rapamycin binding to TOR1 or TOR2 ( Fig. 5,  A  and  B).	bind
39402	1	10600	6	13	NULL	NULL	NULL	Cdc42	GP	geranylgeranyl moiety of	bind					membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_19_15776_s_223	11278313	A hydrophobic pocket in rhoGDI surrounds the membrane-binding geranylgeranyl moiety of Cdc42, thus leading to membrane release.	bind
39403	2	10600	6	13	NULL	NULL	NULL	rhoGDI	GP		surrounds			hydrophobic pocket		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_19_15776_s_223	11278313	A hydrophobic pocket in rhoGDI surrounds the membrane-binding geranylgeranyl moiety of Cdc42, thus leading to membrane release.	bind
39404	3	10600	6	13	NULL	NULL	NULL	statement 2	Process		leads to					membrane	CellComponent	release of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_19_15776_s_223	11278313	A hydrophobic pocket in rhoGDI surrounds the membrane-binding geranylgeranyl moiety of Cdc42, thus leading to membrane release.	bind
48961	2	10600	7	NULL	NULL	0	NULL	rhoGDI	NULL		surrounds	NULL		hydrophobic pocket		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_19_15776_s_223	11278313	A hydrophobic pocket in rhoGDI surrounds the membrane-binding geranylgeranyl moiety of Cdc42, thus leading to membrane release.	bind
48962	1	10600	7	NULL	NULL	0	NULL	Cdc42	NULL	geranylgeranyl moiety of	bind	NULL				membrane	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_19_15776_s_223	11278313	A hydrophobic pocket in rhoGDI surrounds the membrane-binding geranylgeranyl moiety of Cdc42, thus leading to membrane release.	bind
48963	3	10600	7	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				membrane	NULL	release of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_19_15776_s_223	11278313	A hydrophobic pocket in rhoGDI surrounds the membrane-binding geranylgeranyl moiety of Cdc42, thus leading to membrane release.	bind
47133	1	10601	5	13	NULL	NULL	NULL	IRS1	GP		bind			-6 to -8 residues N-terminal to the phosphotyrosine					NP XpY motifs		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_6_4962_s_110	14607833	A hydrophobic residue at position -5 and a proline at -2 are crucial for the Shc PTB domain, but the amino acids from -6 to -8 residues N-terminal to the phosphotyrosine are important for IRS1 binding to the NP XpY motifs.	bind
39867	1	10601	6	NULL	NULL	0	NULL	IRS1	NULL		bind	NULL		\t-6 to -8 residues N-terminal to phosphotyrosine \t		Shc	NULL		NP XpY motifs		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_6_4962_s_110	14607833	A hydrophobic residue at position -5 and a proline at -2 are crucial for the Shc PTB domain, but the amino acids from -6 to -8 residues N-terminal to the phosphotyrosine are important for IRS1 binding to the NP XpY motifs.	bind
47135	1	10602	5	13	NULL	NULL	NULL	HslU	GP		bind			hydrophobic surface of the short terminal helix		HslV	GP			hydrophobic pocket of promoter	NULL		NULL	NULL	NULL	NULL	gw60_cell_103_4_633_s_128	11106733	A hydrophobic surface of  the short terminal helix of HslU binds a hydrophobic pocket of a  neighboring HslV protomer.	bind
39405	1	10602	6	NULL	NULL	0	NULL	HslU	NULL		bind	NULL		hydrophobic surface of the short terminal helix		HslV	NULL			hydrophobic pocket of promoter	NULL		0	NULL	NULL	NULL	gw60_cell_103_4_633_s_128	11106733	A hydrophobic surface of  the short terminal helix of HslU binds a hydrophobic pocket of a  neighboring HslV protomer.	bind
47136	1	10603	5	13	NULL	NULL	NULL	thrombin	GP		bind					FpA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18875_s_189	11901150	A hydrophobic/aromatic residue fills systematically the aryl binding site as documented in the crystal structures of thrombin bound to FpA ( 8,  9) or PAR1 ( 17).	bind
47137	2	10603	5	13	NULL	NULL	NULL	thrombin	GP		bind					PAR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18875_s_189	11901150	A hydrophobic/aromatic residue fills systematically the aryl binding site as documented in the crystal structures of thrombin bound to FpA ( 8,  9) or PAR1 ( 17).	bind
47138	3	10603	5	13	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18875_s_189	11901150	A hydrophobic/aromatic residue fills systematically the aryl binding site as documented in the crystal structures of thrombin bound to FpA ( 8,  9) or PAR1 ( 17).	bind
47139	4	10603	5	NULL	NULL	0	NULL		NULL		fills	NULL	systematically	hydrophobic/aromatic residue			NULL		aryl binding site		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18875_s_189	11901150	A hydrophobic/aromatic residue fills systematically the aryl binding site as documented in the crystal structures of thrombin bound to FpA ( 8,  9) or PAR1 ( 17).	bind
39406	1	10603	6	NULL	NULL	0	NULL	thrombin	NULL		bind	NULL				FpA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18875_s_189	11901150	A hydrophobic/aromatic residue fills systematically the aryl binding site as documented in the crystal structures of thrombin bound to FpA ( 8,  9) or PAR1 ( 17).	bind
39407	2	10603	6	NULL	NULL	0	NULL	thrombin	NULL		bind	NULL				PAR1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18875_s_189	11901150	A hydrophobic/aromatic residue fills systematically the aryl binding site as documented in the crystal structures of thrombin bound to FpA ( 8,  9) or PAR1 ( 17).	bind
39408	3	10603	6	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18875_s_189	11901150	A hydrophobic/aromatic residue fills systematically the aryl binding site as documented in the crystal structures of thrombin bound to FpA ( 8,  9) or PAR1 ( 17).	bind
39409	4	10603	6	NULL	NULL	0	NULL		NULL		fills	NULL	systematically	hydrophobic/aromatic residue			NULL		aryl binding site		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18875_s_189	11901150	A hydrophobic/aromatic residue fills systematically the aryl binding site as documented in the crystal structures of thrombin bound to FpA ( 8,  9) or PAR1 ( 17).	bind
47140	1	10604	5	13	NULL	NULL	NULL	TF	GP		bind					cell cycle genes	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_21_7988_s_238	16702552	A hypergeometric distribution was used to estimate the statistical significance of the binding specificity of the given TF to the cell cycle genes.	bind
39410	1	10604	6	NULL	NULL	0	NULL	TF	NULL		bind	NULL				cell cycle genes	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_21_7988_s_238	16702552	A hypergeometric distribution was used to estimate the statistical significance of the binding specificity of the given TF to the cell cycle genes.	bind
47141	1	10605	5	13	NULL	NULL	NULL	CbbR	GP	binding of	introduces					CBR	NucleicAcid	DNA bend within			NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiolrev_21_2_135_s_284	9348665	A hypersensitive site ( Fig. 4) observed in a DNase I footprint suggested that binding of CbbR introduces a DNA bend within the CBR [ 146].	bind
39412	1	10605	6	10	NULL	0	NULL	CbbR	NULL	binding of	introduces 	NULL				CBR	NULL	DNA bend within			NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiolrev_21_2_135_s_284	9348665	A hypersensitive site ( Fig. 4) observed in a DNase I footprint suggested that binding of CbbR introduces a DNA bend within the CBR [ 146].	bind
47142	1	10606	5	13	NULL	NULL	NULL	titin/connectin	GP		bind					actinin	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-muscle-res-cell-motil_26_6-8_16465475_s_5	16465475	A hypertrophic cardiomyopathy-associated titin/connectin  mutation (Arg740Leu) was found to increase the binding to actinin, while  other dilated cardiomyopathy-associated titin/connectin mutations (Ala743Val  and Val54Met) decreased the binding to actinin and Tcap/telethonin, respectively.	bind
47143	3	10606	5	13	NULL	NULL	NULL	statement 2	Process		increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-muscle-res-cell-motil_26_6-8_16465475_s_5	16465475	A hypertrophic cardiomyopathy-associated titin/connectin  mutation (Arg740Leu) was found to increase the binding to actinin, while  other dilated cardiomyopathy-associated titin/connectin mutations (Ala743Val  and Val54Met) decreased the binding to actinin and Tcap/telethonin, respectively.	bind
47144	2	10606	5	13	NULL	NULL	NULL	titin/connectin	GP	mutant	is associated with			Arg740Leu		hypertrophic cardiomyopathy	MedicalFinding				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-muscle-res-cell-motil_26_6-8_16465475_s_5	16465475	A hypertrophic cardiomyopathy-associated titin/connectin  mutation (Arg740Leu) was found to increase the binding to actinin, while  other dilated cardiomyopathy-associated titin/connectin mutations (Ala743Val  and Val54Met) decreased the binding to actinin and Tcap/telethonin, respectively.	bind
47145	5	10606	5	13	NULL	NULL	NULL	statement 4	Process		decreases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-muscle-res-cell-motil_26_6-8_16465475_s_5	16465475	A hypertrophic cardiomyopathy-associated titin/connectin  mutation (Arg740Leu) was found to increase the binding to actinin, while  other dilated cardiomyopathy-associated titin/connectin mutations (Ala743Val  and Val54Met) decreased the binding to actinin and Tcap/telethonin, respectively.	bind
47146	4	10606	5	13	NULL	NULL	NULL	titin/connectin	GP	mutant	is associated with			Ala743Val		dilated cardiomyopathy	MedicalFinding				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-muscle-res-cell-motil_26_6-8_16465475_s_5	16465475	A hypertrophic cardiomyopathy-associated titin/connectin  mutation (Arg740Leu) was found to increase the binding to actinin, while  other dilated cardiomyopathy-associated titin/connectin mutations (Ala743Val  and Val54Met) decreased the binding to actinin and Tcap/telethonin, respectively.	bind
47147	6	10606	5	13	NULL	NULL	NULL	titin/connectin	GP	mutant	is associated with			Val54Met		dilated cardiomyopathy	MedicalFinding				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-muscle-res-cell-motil_26_6-8_16465475_s_5	16465475	A hypertrophic cardiomyopathy-associated titin/connectin  mutation (Arg740Leu) was found to increase the binding to actinin, while  other dilated cardiomyopathy-associated titin/connectin mutations (Ala743Val  and Val54Met) decreased the binding to actinin and Tcap/telethonin, respectively.	bind
47148	7	10606	5	13	NULL	NULL	NULL	titin/connectin	GP		bind					Tcap/telethonin	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-muscle-res-cell-motil_26_6-8_16465475_s_5	16465475	A hypertrophic cardiomyopathy-associated titin/connectin  mutation (Arg740Leu) was found to increase the binding to actinin, while  other dilated cardiomyopathy-associated titin/connectin mutations (Ala743Val  and Val54Met) decreased the binding to actinin and Tcap/telethonin, respectively.	bind
57598	8	10606	5	13	NULL	NULL	NULL	statement 6	Process		decreases					statement 7	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-muscle-res-cell-motil_26_6-8_16465475_s_5	16465475	A hypertrophic cardiomyopathy-associated titin/connectin  mutation (Arg740Leu) was found to increase the binding to actinin, while  other dilated cardiomyopathy-associated titin/connectin mutations (Ala743Val  and Val54Met) decreased the binding to actinin and Tcap/telethonin, respectively.	bind
39869	1	10606	6	NULL	NULL	0	NULL	titin/connectin	NULL		bind	NULL				actinin	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-muscle-res-cell-motil_26_6-8_16465475_s_5	16465475	A hypertrophic cardiomyopathy-associated titin/connectin  mutation (Arg740Leu) was found to increase the binding to actinin, while  other dilated cardiomyopathy-associated titin/connectin mutations (Ala743Val  and Val54Met) decreased the binding to actinin and Tcap/telethonin, respectively.	bind
39870	2	10606	6	10	NULL	0	NULL	titin/connectin		mutant	increases			Arg740Leu		statement 1					NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-muscle-res-cell-motil_26_6-8_16465475_s_5	16465475	A hypertrophic cardiomyopathy-associated titin/connectin  mutation (Arg740Leu) was found to increase the binding to actinin, while  other dilated cardiomyopathy-associated titin/connectin mutations (Ala743Val  and Val54Met) decreased the binding to actinin and Tcap/telethonin, respectively.	bind
39871	3	10606	6	10	NULL	0	NULL	titin/connectin		mutant	decreases			Ala743Val		statement 1					NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-muscle-res-cell-motil_26_6-8_16465475_s_5	16465475	A hypertrophic cardiomyopathy-associated titin/connectin  mutation (Arg740Leu) was found to increase the binding to actinin, while  other dilated cardiomyopathy-associated titin/connectin mutations (Ala743Val  and Val54Met) decreased the binding to actinin and Tcap/telethonin, respectively.	bind
39872	4	10606	6	NULL	NULL	0	NULL	titin/connectin	NULL		bind	NULL				Tcap/telethonin	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-muscle-res-cell-motil_26_6-8_16465475_s_5	16465475	A hypertrophic cardiomyopathy-associated titin/connectin  mutation (Arg740Leu) was found to increase the binding to actinin, while  other dilated cardiomyopathy-associated titin/connectin mutations (Ala743Val  and Val54Met) decreased the binding to actinin and Tcap/telethonin, respectively.	bind
39873	5	10606	6	10	NULL	0	NULL	titin/connectin		mutant	decreases			Val54Met		statement 4					NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-muscle-res-cell-motil_26_6-8_16465475_s_5	16465475	A hypertrophic cardiomyopathy-associated titin/connectin  mutation (Arg740Leu) was found to increase the binding to actinin, while  other dilated cardiomyopathy-associated titin/connectin mutations (Ala743Val  and Val54Met) decreased the binding to actinin and Tcap/telethonin, respectively.	bind
40396	6	10606	6	10	NULL	0	NULL	statement 2	NULL		is associated with	NULL				hypertrophic cardiomyopathy	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-muscle-res-cell-motil_26_6-8_16465475_s_5	16465475	A hypertrophic cardiomyopathy-associated titin/connectin  mutation (Arg740Leu) was found to increase the binding to actinin, while  other dilated cardiomyopathy-associated titin/connectin mutations (Ala743Val  and Val54Met) decreased the binding to actinin and Tcap/telethonin, respectively.	bind
40397	7	10606	6	10	NULL	0	NULL	statement 3	NULL		is associated with	NULL				 dilated cardiomyopathy	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-muscle-res-cell-motil_26_6-8_16465475_s_5	16465475	A hypertrophic cardiomyopathy-associated titin/connectin  mutation (Arg740Leu) was found to increase the binding to actinin, while  other dilated cardiomyopathy-associated titin/connectin mutations (Ala743Val  and Val54Met) decreased the binding to actinin and Tcap/telethonin, respectively.	bind
40398	8	10606	6	10	NULL	0	NULL	statement 5	NULL		is associated with	NULL				dilated cardiomyopathy	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-muscle-res-cell-motil_26_6-8_16465475_s_5	16465475	A hypertrophic cardiomyopathy-associated titin/connectin  mutation (Arg740Leu) was found to increase the binding to actinin, while  other dilated cardiomyopathy-associated titin/connectin mutations (Ala743Val  and Val54Met) decreased the binding to actinin and Tcap/telethonin, respectively.	bind
47149	1	10607	5	13	NULL	NULL	NULL	Mks1p	GP	hypophosphorylated;;inactive	bind					Rtg2p	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_mol-cell_12_2_14536080_s_6	14536080	A hypophosphorylated form of Mks1p bound to Rtg2p is inactive.	bind
39415	1	10607	6	10	NULL	0	NULL	Mks1p	NULL	hypophosphorylated;; inactive	bind	NULL				Rtg2p	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_mol-cell_12_2_14536080_s_6	14536080	A hypophosphorylated form of Mks1p bound to Rtg2p is inactive.	bind
47150	1	10608	5	13	NULL	NULL	NULL	DnaA protein	GP		bind		possibly							DnaA boxes	NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_4_355_s_548	12413665	A hypothesis has been formulated [   and   ] that postulates that initially all newly synthesized DnaA protein is bound to DnaA  boxes around the chromosome.	bind
47151	2	10608	5	13	NULL	NULL	NULL	statement 1	Process		occurs around		possibly			chromosome	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_4_355_s_548	12413665	A hypothesis has been formulated [   and   ] that postulates that initially all newly synthesized DnaA protein is bound to DnaA  boxes around the chromosome.	bind
39418	1	10608	6	NULL	NULL	0	NULL	DnaA protein	NULL		bind	NULL					NULL			DnaA box	NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_4_355_s_548	12413665	A hypothesis has been formulated [   and   ] that postulates that initially all newly synthesized DnaA protein is bound to DnaA  boxes around the chromosome.	bind
39419	2	10608	6	NULL	NULL	0	NULL	statement 1	NULL		occurs around the	NULL				chromosome	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_4_355_s_548	12413665	A hypothesis has been formulated [   and   ] that postulates that initially all newly synthesized DnaA protein is bound to DnaA  boxes around the chromosome.	bind
47154	1	10610	5	13	NULL	NULL	NULL	IGF-I	GP		bind					IGF-I receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8189_s_311	9079636	A hypothetical explanation for this difference is that IGF-I binds to the IGF-I receptor and induces a conformational change by simultaneously bridging the high and low affinity sites ( 42).	bind
47155	2	10610	5	13	NULL	NULL	NULL	statement 1	Process		induces					conformational change	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8189_s_311	9079636	A hypothetical explanation for this difference is that IGF-I binds to the IGF-I receptor and induces a conformational change by simultaneously bridging the high and low affinity sites ( 42).	bind
39422	1	10610	6	NULL	NULL	0	NULL	IGF-I	NULL		bind	NULL				IGF-I receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_13_8189_s_311	9079636	A hypothetical explanation for this difference is that IGF-I binds to the IGF-I receptor and induces a conformational change by simultaneously bridging the high and low affinity sites ( 42).	bind
49999	2	10610	6	10	NULL	0	NULL	statement 1	NULL		induce	NULL				conformational change	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_13_8189_s_311	9079636	A hypothetical explanation for this difference is that IGF-I binds to the IGF-I receptor and induces a conformational change by simultaneously bridging the high and low affinity sites ( 42).	bind
47160	1	10611	5	13	NULL	NULL	NULL	Hfq	GP		bind					rpoS mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_3_373_s_288	12208995	A hypothetical model consistent with all data available would be that Hfq bound to  rpoS mRNA recruits DsrA into a ternary complex (in which secondary structures of  rpoS mRNA and/or of DsrA could also be altered) and thereby facilitate translational stimulation by DsrA.	bind
47161	2	10611	5	13	NULL	NULL	NULL	DsrA	GP		is recruited to					ternary complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_3_373_s_288	12208995	A hypothetical model consistent with all data available would be that Hfq bound to  rpoS mRNA recruits DsrA into a ternary complex (in which secondary structures of  rpoS mRNA and/or of DsrA could also be altered) and thereby facilitate translational stimulation by DsrA.	bind
47162	3	10611	5	13	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_3_373_s_288	12208995	A hypothetical model consistent with all data available would be that Hfq bound to  rpoS mRNA recruits DsrA into a ternary complex (in which secondary structures of  rpoS mRNA and/or of DsrA could also be altered) and thereby facilitate translational stimulation by DsrA.	bind
47163	4	10611	5	13	NULL	NULL	NULL	statement 2	Process		alters		may			rpoS mRNA	NucleicAcid	secondary structure of			NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_3_373_s_288	12208995	A hypothetical model consistent with all data available would be that Hfq bound to  rpoS mRNA recruits DsrA into a ternary complex (in which secondary structures of  rpoS mRNA and/or of DsrA could also be altered) and thereby facilitate translational stimulation by DsrA.	bind
47164	5	10611	5	13	NULL	NULL	NULL	statement 2	Process		alters		may			DsrA	GP	secondary structure of			NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_3_373_s_288	12208995	A hypothetical model consistent with all data available would be that Hfq bound to  rpoS mRNA recruits DsrA into a ternary complex (in which secondary structures of  rpoS mRNA and/or of DsrA could also be altered) and thereby facilitate translational stimulation by DsrA.	bind
47165	6	10611	5	13	NULL	NULL	NULL	DsrA	GP		carries out					translational stimulation	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_3_373_s_288	12208995	A hypothetical model consistent with all data available would be that Hfq bound to  rpoS mRNA recruits DsrA into a ternary complex (in which secondary structures of  rpoS mRNA and/or of DsrA could also be altered) and thereby facilitate translational stimulation by DsrA.	bind
47166	7	10611	5	13	NULL	NULL	NULL	statement 3	Process		facilitates		potentially			statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_3_373_s_288	12208995	A hypothetical model consistent with all data available would be that Hfq bound to  rpoS mRNA recruits DsrA into a ternary complex (in which secondary structures of  rpoS mRNA and/or of DsrA could also be altered) and thereby facilitate translational stimulation by DsrA.	bind
39423	1	10611	6	NULL	NULL	0	NULL	Hfq	NULL		bind	NULL				rpoS mRNA	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_3_373_s_288	12208995	A hypothetical model consistent with all data available would be that Hfq bound to  rpoS mRNA recruits DsrA into a ternary complex (in which secondary structures of  rpoS mRNA and/or of DsrA could also be altered) and thereby facilitate translational stimulation by DsrA.	bind
39424	2	10611	6	NULL	NULL	0	NULL	statement 1	NULL		recruits	NULL				DsrA	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_3_373_s_288	12208995	A hypothetical model consistent with all data available would be that Hfq bound to  rpoS mRNA recruits DsrA into a ternary complex (in which secondary structures of  rpoS mRNA and/or of DsrA could also be altered) and thereby facilitate translational stimulation by DsrA.	bind
39426	3	10611	6	NULL	NULL	0	NULL	DsrA	NULL		is recruited into	NULL				ternary complex	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_3_373_s_288	12208995	A hypothetical model consistent with all data available would be that Hfq bound to  rpoS mRNA recruits DsrA into a ternary complex (in which secondary structures of  rpoS mRNA and/or of DsrA could also be altered) and thereby facilitate translational stimulation by DsrA.	bind
39428	4	10611	6	NULL	NULL	0	NULL	DsrA	NULL		carries out	NULL				translational stimulation	NULL				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_3_373_s_288	12208995	A hypothetical model consistent with all data available would be that Hfq bound to  rpoS mRNA recruits DsrA into a ternary complex (in which secondary structures of  rpoS mRNA and/or of DsrA could also be altered) and thereby facilitate translational stimulation by DsrA.	bind
39430	5	10611	6	NULL	NULL	0	NULL	statement 2	NULL		facilitates	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_3_373_s_288	12208995	A hypothetical model consistent with all data available would be that Hfq bound to  rpoS mRNA recruits DsrA into a ternary complex (in which secondary structures of  rpoS mRNA and/or of DsrA could also be altered) and thereby facilitate translational stimulation by DsrA.	bind
39432	6	10611	6	NULL	NULL	0	NULL	statement 2	NULL		alters	NULL	could			rpoS mRNA	NULL	secondary structure of 			NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_3_373_s_288	12208995	A hypothetical model consistent with all data available would be that Hfq bound to  rpoS mRNA recruits DsrA into a ternary complex (in which secondary structures of  rpoS mRNA and/or of DsrA could also be altered) and thereby facilitate translational stimulation by DsrA.	bind
39434	7	10611	6	NULL	NULL	0	NULL	statement 2	NULL		alters	NULL	could			DsrA	NULL	secondary structure of			NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_66_3_373_s_288	12208995	A hypothetical model consistent with all data available would be that Hfq bound to  rpoS mRNA recruits DsrA into a ternary complex (in which secondary structures of  rpoS mRNA and/or of DsrA could also be altered) and thereby facilitate translational stimulation by DsrA.	bind
47167	3	10612	5	13	NULL	NULL	NULL	statement 1	Process		influences		possibly			integrin affinity	Process	modulation of			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_6_1799_s_286	10359597	A hypothetical scheme of how the GTP-binding cycles of Ras and R-Ras could influence integrin affinity modulation.	bind
47168	4	10612	5	13	NULL	NULL	NULL	statement 2	Process		influences		possibly			integrin affinity	Process	modulation of			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_6_1799_s_286	10359597	A hypothetical scheme of how the GTP-binding cycles of Ras and R-Ras could influence integrin affinity modulation.	bind
50000	1	10612	5	13	NULL	NULL	NULL	Ras	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_6_1799_s_286	10359597	A hypothetical scheme of how the GTP-binding cycles of Ras and R-Ras could influence integrin affinity modulation.	bind
50001	2	10612	5	13	NULL	NULL	NULL	R-Ras	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_6_1799_s_286	10359597	A hypothetical scheme of how the GTP-binding cycles of Ras and R-Ras could influence integrin affinity modulation.	bind
39470	1	10612	6	NULL	NULL	0	NULL	Ras	NULL		bind	NULL				GTP	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_6_1799_s_286	10359597	A hypothetical scheme of how the GTP-binding cycles of Ras and R-Ras could influence integrin affinity modulation.	bind
39471	2	10612	6	NULL	NULL	0	NULL	R-Ras	NULL		bind	NULL				GTP	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_6_1799_s_286	10359597	A hypothetical scheme of how the GTP-binding cycles of Ras and R-Ras could influence integrin affinity modulation.	bind
39472	3	10612	6	NULL	NULL	0	NULL	statement 1	NULL		influence	NULL	may			integrin affinity	NULL	modulation of 			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_6_1799_s_286	10359597	A hypothetical scheme of how the GTP-binding cycles of Ras and R-Ras could influence integrin affinity modulation.	bind
39473	4	10612	6	NULL	NULL	0	NULL	statement 2	NULL		influence	NULL	may			integrin affinity	NULL	modulation of			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_6_1799_s_286	10359597	A hypothetical scheme of how the GTP-binding cycles of Ras and R-Ras could influence integrin affinity modulation.	bind
47169	1	10613	5	13	NULL	NULL	NULL	hypoxia-inducible factor	GP		bind					VEGF	GP			enhancer	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_77_3_638_s_127	7641334	A hypoxia-inducible factor binds to the VEGF enhancer.	bind
39474	1	10613	6	NULL	NULL	0	NULL	hypoxia-inducible factor	NULL		bind	NULL				VEGF	NULL			enhancer	NULL		0	NULL	NULL	NULL	gw60_circulationres_77_3_638_s_127	7641334	A hypoxia-inducible factor binds to the VEGF enhancer.	bind
47170	1	10615	5	13	NULL	NULL	NULL	transcription factor	GP		bind							sequences resembling		interferon- activation site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_966_s_142	7822337	A Jak-type kinase  probably mediates IL-4-stimulated tyrosine phosphorylation of a  transcription factor that binds to sequences resembling the  interferon-   activation site and increases transcriptional activity  in reporter gene assays( 46 ,  47 ,  48 ) .	bind
47171	2	10615	5	13	NULL	NULL	NULL	statement 1	GP		increases					transcriptional activity	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_966_s_142	7822337	A Jak-type kinase  probably mediates IL-4-stimulated tyrosine phosphorylation of a  transcription factor that binds to sequences resembling the  interferon-   activation site and increases transcriptional activity  in reporter gene assays( 46 ,  47 ,  48 ) .	bind
47172	3	10615	5	13	NULL	NULL	NULL	IL-4	GP		stimulate					statement 1	Process	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_966_s_142	7822337	A Jak-type kinase  probably mediates IL-4-stimulated tyrosine phosphorylation of a  transcription factor that binds to sequences resembling the  interferon-   activation site and increases transcriptional activity  in reporter gene assays( 46 ,  47 ,  48 ) .	bind
47173	4	10615	5	13	NULL	NULL	NULL	Jak-type kinase	GP		mediates		probably			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_966_s_142	7822337	A Jak-type kinase  probably mediates IL-4-stimulated tyrosine phosphorylation of a  transcription factor that binds to sequences resembling the  interferon-   activation site and increases transcriptional activity  in reporter gene assays( 46 ,  47 ,  48 ) .	bind
50758	1	10615	6	10	NULL	0	NULL	transcription factor	NULL		bind	NULL					NULL	sequence resembling		interferon- activation site	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_2_966_s_142	7822337	A Jak-type kinase  probably mediates IL-4-stimulated tyrosine phosphorylation of a  transcription factor that binds to sequences resembling the  interferon-   activation site and increases transcriptional activity  in reporter gene assays( 46 ,  47 ,  48 ) .	bind
50759	2	10615	6	10	NULL	0	NULL	IL-4	NULL		stimulates	NULL				transcription factor	NULL	phosphorylation of	Tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_2_966_s_142	7822337	A Jak-type kinase  probably mediates IL-4-stimulated tyrosine phosphorylation of a  transcription factor that binds to sequences resembling the  interferon-   activation site and increases transcriptional activity  in reporter gene assays( 46 ,  47 ,  48 ) .	bind
50760	3	10615	6	10	NULL	0	NULL	Jak-type kinase	NULL		mediates	NULL	probably			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_2_966_s_142	7822337	A Jak-type kinase  probably mediates IL-4-stimulated tyrosine phosphorylation of a  transcription factor that binds to sequences resembling the  interferon-   activation site and increases transcriptional activity  in reporter gene assays( 46 ,  47 ,  48 ) .	bind
47205	1	10616	5	13	NULL	NULL	NULL	DNS-SsrA peptide	GP		bind					ClpA hexamer	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12221_s_181	15657062	A Job plot based on the method of continuous variations ( ) of DNS-SsrA peptide binding to ClpA6 shows a maximum at a molar ratio of protein to peptide of 0.45, indicating that approximately 1 mol of DNS-SsrA peptide binds to the 1 mol of ClpA hexamer ( Fig. 5 A).	bind
39475	1	10616	6	NULL	NULL	0	NULL	DNS-SsrA peptide	NULL		bind	NULL				ClpA hexamer	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_13_12221_s_181	15657062	A Job plot based on the method of continuous variations ( ) of DNS-SsrA peptide binding to ClpA6 shows a maximum at a molar ratio of protein to peptide of 0.45, indicating that approximately 1 mol of DNS-SsrA peptide binds to the 1 mol of ClpA hexamer ( Fig. 5 A).	bind
47206	1	10617	5	13	NULL	NULL	NULL	NAD+	Chemical		bind					IPS	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_12_11475_s_53	15653679	A Jobin y Van Fluoromax 3 spectrofluorimeter was used to monitor the binding of NAD+ to IPS and IPS mutants ( 1 muM in 10 mM EDTA with 10 mM KH2PO4, pH 7).	bind
47207	2	10617	5	13	NULL	NULL	NULL	NAD+	Chemical		bind					IPS	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_12_11475_s_53	15653679	A Jobin y Van Fluoromax 3 spectrofluorimeter was used to monitor the binding of NAD+ to IPS and IPS mutants ( 1 muM in 10 mM EDTA with 10 mM KH2PO4, pH 7).	bind
39515	1	10617	6	NULL	NULL	0	NULL	NAD+	NULL		bind	NULL				IPS	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_12_11475_s_53	15653679	A Jobin y Van Fluoromax 3 spectrofluorimeter was used to monitor the binding of NAD+ to IPS and IPS mutants ( 1 muM in 10 mM EDTA with 10 mM KH2PO4, pH 7).	bind
39516	2	10617	6	NULL	NULL	0	NULL	NAD+	NULL		bind	NULL				IPS	NULL	mutant			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_12_11475_s_53	15653679	A Jobin y Van Fluoromax 3 spectrofluorimeter was used to monitor the binding of NAD+ to IPS and IPS mutants ( 1 muM in 10 mM EDTA with 10 mM KH2PO4, pH 7).	bind
47208	1	10618	5	13	NULL	NULL	NULL	insulin receptor	GP	mutant	lacks			K1018A		tyrosine kinase activity					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_207	10821852	A K1018A mutant of the insulin receptor lacking tyrosine kinase activity does not bind to SOCS-3 (row 2).	bind
47209	2	10618	5	13	NULL	NULL	NULL	insulin receptor	GP	mutant	does not bind			K1018A		SOCS-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_207	10821852	A K1018A mutant of the insulin receptor lacking tyrosine kinase activity does not bind to SOCS-3 (row 2).	bind
39517	1	10618	6	NULL	NULL	0	NULL	insulin receptor	NULL	mutant	lacks	NULL		K1018A		tyrosine kinase activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_207	10821852	A K1018A mutant of the insulin receptor lacking tyrosine kinase activity does not bind to SOCS-3 (row 2).	bind
39518	2	10618	6	10	NULL	0	NULL	insulin receptor		mutant	does not bind			K1018A		SOCS-3					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15985_s_207	10821852	A K1018A mutant of the insulin receptor lacking tyrosine kinase activity does not bind to SOCS-3 (row 2).	bind
47210	1	10619	5	13	NULL	NULL	NULL				is substituted in			K215R		Isw2p	GP	putative	ATP-binding pocket		NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_8_942_s_106	15833917	A K215R substitution in the putative ATP-binding pocket of Isw2p reduces ATPase activity to background levels without affecting Isw2 complex integrity (Gelbart et al. 2001 ; Fitzgerald et al. 2004 ).	bind
47211	2	10619	5	13	NULL	NULL	NULL	statement 1	Process		reduces					ATPase 	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_8_942_s_106	15833917	A K215R substitution in the putative ATP-binding pocket of Isw2p reduces ATPase activity to background levels without affecting Isw2 complex integrity (Gelbart et al. 2001 ; Fitzgerald et al. 2004 ).	bind
47212	3	10619	5	13	NULL	NULL	NULL	statement 2	Process		does not affect					Isw2 complex	GP	integrity of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_8_942_s_106	15833917	A K215R substitution in the putative ATP-binding pocket of Isw2p reduces ATPase activity to background levels without affecting Isw2 complex integrity (Gelbart et al. 2001 ; Fitzgerald et al. 2004 ).	bind
39874	1	10619	6	10	NULL	0	NULL	Isw2p		mutant;; putative	reduces			K215R ;; ATP-binding pocket		ATPase 		activity of 			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_8_942_s_106	15833917	A K215R substitution in the putative ATP-binding pocket of Isw2p reduces ATPase activity to background levels without affecting Isw2 complex integrity (Gelbart et al. 2001 ; Fitzgerald et al. 2004 ).	bind
39875	2	10619	6	NULL	NULL	0	NULL	Isw2p	NULL	mutant;; putative	does not affect	NULL		K215R ;; ATP-binding pocket		Isw2 complex	NULL	integrity of			NULL		0	NULL	NULL	NULL	gw70_genesdev_19_8_942_s_106	15833917	A K215R substitution in the putative ATP-binding pocket of Isw2p reduces ATPase activity to background levels without affecting Isw2 complex integrity (Gelbart et al. 2001 ; Fitzgerald et al. 2004 ).	bind
47213	1	10620	5	13	NULL	NULL	NULL	XPD	GP	canonical	is mutated in			GKS/T ATP binding motif					K48R		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_21_7355_s_27	11585917	A K48R mutation in the canonical GKS/T ATP binding motif of XPD or the Rad3 homolog abolishes repair but does not compromise transcription ( 43,  66).	bind
47214	2	10620	5	13	NULL	NULL	NULL	statement 1	Process		abolishes					repair	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_21_7355_s_27	11585917	A K48R mutation in the canonical GKS/T ATP binding motif of XPD or the Rad3 homolog abolishes repair but does not compromise transcription ( 43,  66).	bind
47215	3	10620	5	13	NULL	NULL	NULL	statement 1	Process		does not compromise					transcription	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_21_7355_s_27	11585917	A K48R mutation in the canonical GKS/T ATP binding motif of XPD or the Rad3 homolog abolishes repair but does not compromise transcription ( 43,  66).	bind
47216	4	10620	5	13	NULL	NULL	NULL	Rad3 homolog	GP	canonical	is mutated in			GKS/T ATP binding motif					K48R		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_21_7355_s_27	11585917	A K48R mutation in the canonical GKS/T ATP binding motif of XPD or the Rad3 homolog abolishes repair but does not compromise transcription ( 43,  66).	bind
47217	5	10620	5	13	NULL	NULL	NULL	statement 4	Process		abolishes					repair	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_21_7355_s_27	11585917	A K48R mutation in the canonical GKS/T ATP binding motif of XPD or the Rad3 homolog abolishes repair but does not compromise transcription ( 43,  66).	bind
47218	6	10620	5	13	NULL	NULL	NULL	statement 4	Process		does not compromise					transcription	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_21_7355_s_27	11585917	A K48R mutation in the canonical GKS/T ATP binding motif of XPD or the Rad3 homolog abolishes repair but does not compromise transcription ( 43,  66).	bind
39876	1	10620	6	NULL	NULL	0	NULL	XPD	NULL	mutant	abolishes	NULL		K48R;; GKS/T ATP binding motif		repair	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_21_7355_s_27	11585917	A K48R mutation in the canonical GKS/T ATP binding motif of XPD or the Rad3 homolog abolishes repair but does not compromise transcription ( 43,  66).	bind
39877	2	10620	6	NULL	NULL	0	NULL	rad3 homolog	NULL	mutant	abolishes	NULL		K48R;; GKS/T ATP binding motif		repair	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_21_7355_s_27	11585917	A K48R mutation in the canonical GKS/T ATP binding motif of XPD or the Rad3 homolog abolishes repair but does not compromise transcription ( 43,  66).	bind
39878	3	10620	6	NULL	NULL	0	NULL	XPD	NULL	mutant	has no effect on	NULL		K48R;; GKS/T ATP binding motif		transcription	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_21_7355_s_27	11585917	A K48R mutation in the canonical GKS/T ATP binding motif of XPD or the Rad3 homolog abolishes repair but does not compromise transcription ( 43,  66).	bind
39879	4	10620	6	NULL	NULL	0	NULL	rad3 homolog	NULL	mutant	has no effect on	NULL		K48R;; GKS/T ATP binding motif		transcription	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_21_7355_s_27	11585917	A K48R mutation in the canonical GKS/T ATP binding motif of XPD or the Rad3 homolog abolishes repair but does not compromise transcription ( 43,  66).	bind
47220	1	10621	5	13	NULL	NULL	NULL	serine proteinase/serpin complex	GP		bind					very-low-density lipoprotein receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_atherosclerosis_141_2_191_s_493	9862168	A Kasza, HH Petersen, CW Heegaard, K Oka, A Christensen, A Dubin, L Chan and PA. Andreasen, Specificity of serine proteinase/serpin complex binding to very-low-density lipoprotein receptor and  2-macroglobulin receptor/low-density-lipoprotein-receptor-related protein.	bind
47223	2	10621	5	13	NULL	NULL	NULL	serine proteinase/serpin complex	GP		bind					2-macroglobulin receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_atherosclerosis_141_2_191_s_493	9862168	A Kasza, HH Petersen, CW Heegaard, K Oka, A Christensen, A Dubin, L Chan and PA. Andreasen, Specificity of serine proteinase/serpin complex binding to very-low-density lipoprotein receptor and  2-macroglobulin receptor/low-density-lipoprotein-receptor-related protein.	bind
47224	3	10621	5	13	NULL	NULL	NULL	2-macroglobulin receptor	GP		is a type of					low-density-lipoprotein-receptor-related protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_atherosclerosis_141_2_191_s_493	9862168	A Kasza, HH Petersen, CW Heegaard, K Oka, A Christensen, A Dubin, L Chan and PA. Andreasen, Specificity of serine proteinase/serpin complex binding to very-low-density lipoprotein receptor and  2-macroglobulin receptor/low-density-lipoprotein-receptor-related protein.	bind
39519	1	10621	6	NULL	NULL	0	NULL	serine proteinase/serpin complex	NULL		bind	NULL				very-low-density lipoprotein receptor 	NULL				NULL		0	NULL	NULL	NULL	gw60_atherosclerosis_141_2_191_s_493	9862168	A Kasza, HH Petersen, CW Heegaard, K Oka, A Christensen, A Dubin, L Chan and PA. Andreasen, Specificity of serine proteinase/serpin complex binding to very-low-density lipoprotein receptor and  2-macroglobulin receptor/low-density-lipoprotein-receptor-related protein.	bind
39520	2	10621	6	NULL	NULL	0	NULL	serine proteinase/serpin complex	NULL		bind	NULL				2-macroglobulin receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_atherosclerosis_141_2_191_s_493	9862168	A Kasza, HH Petersen, CW Heegaard, K Oka, A Christensen, A Dubin, L Chan and PA. Andreasen, Specificity of serine proteinase/serpin complex binding to very-low-density lipoprotein receptor and  2-macroglobulin receptor/low-density-lipoprotein-receptor-related protein.	bind
39521	3	10621	6	NULL	NULL	0	NULL	2-macroglobulin receptor	NULL		is a type of	NULL				low-density-lipoprotein-receptor-related protein	NULL				NULL		0	NULL	NULL	NULL	gw60_atherosclerosis_141_2_191_s_493	9862168	A Kasza, HH Petersen, CW Heegaard, K Oka, A Christensen, A Dubin, L Chan and PA. Andreasen, Specificity of serine proteinase/serpin complex binding to very-low-density lipoprotein receptor and  2-macroglobulin receptor/low-density-lipoprotein-receptor-related protein.	bind
47225	1	10622	5	13	NULL	NULL	NULL	KEP1 protein	GP	truncated	bind			GSG domain		poly(U) homopolymeric RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_46_30122_s_185	9804767	A KEP1 truncation protein encompassing the entire GSG domain bound poly(U) homopolymeric RNA (Fig.  5 A, KEP:1-224).	bind
39522	1	10622	6	NULL	NULL	0	NULL	KEP1 protein	NULL	truncated	bind	NULL		GSG domain		poly(U) homopolymeric RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_46_30122_s_185	9804767	A KEP1 truncation protein encompassing the entire GSG domain bound poly(U) homopolymeric RNA (Fig.  5 A, KEP:1-224).	bind
47227	1	10623	5	13	NULL	NULL	NULL	ketoconazole molecule	Chemical		bind			imidazole nitrogen		heme iron	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_37_13682_s_63	16954191	A ketoconazole molecule with its imidazole nitrogen bound to the heme iron could unambiguously be modeled into electron density in all four molecules in the asymmetric unit ( Fig. 3).	bind
39557	1	10623	6	NULL	NULL	0	NULL	ketoconazole molecule	NULL		bind	NULL		imidazole nitrogen		heme iron	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_37_13682_s_63	16954191	A ketoconazole molecule with its imidazole nitrogen bound to the heme iron could unambiguously be modeled into electron density in all four molecules in the asymmetric unit ( Fig. 3).	bind
47228	1	10624	5	13	NULL	NULL	NULL	Vps10p	GP		is a type of					type I transmembrane receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_10_3242_s_21	11598206	A key component in the sorting and transport of vacuolar hydrolases is Vps10p, a type I transmembrane receptor that binds vacuolar hydrolases in the late-Golgi (Marcusson  et al., 1994  ; Cooper and Stevens, 1996  ).	bind
47229	2	10624	5	13	NULL	NULL	NULL	Vps10p	GP		bind					vacuolar hydrolases	GP				NULL	late-Golgi	NULL	NULL	NULL	NULL	gw60_molbiolcell_12_10_3242_s_21	11598206	A key component in the sorting and transport of vacuolar hydrolases is Vps10p, a type I transmembrane receptor that binds vacuolar hydrolases in the late-Golgi (Marcusson  et al., 1994  ; Cooper and Stevens, 1996  ).	bind
47230	3	10624	5	13	NULL	NULL	NULL	Vps10p	GP		plays a role in					vacuolar hydrolases	GP	sorting of			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_10_3242_s_21	11598206	A key component in the sorting and transport of vacuolar hydrolases is Vps10p, a type I transmembrane receptor that binds vacuolar hydrolases in the late-Golgi (Marcusson  et al., 1994  ; Cooper and Stevens, 1996  ).	bind
47232	4	10624	5	13	NULL	NULL	NULL	Vps10p	GP		plays a role in					vacuolar hydrolases	GP	transport of			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_10_3242_s_21	11598206	A key component in the sorting and transport of vacuolar hydrolases is Vps10p, a type I transmembrane receptor that binds vacuolar hydrolases in the late-Golgi (Marcusson  et al., 1994  ; Cooper and Stevens, 1996  ).	bind
39558	1	10624	6	NULL	NULL	0	NULL	Vps10p	NULL		is a type of	NULL				type I transmembrane receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_10_3242_s_21	11598206	A key component in the sorting and transport of vacuolar hydrolases is Vps10p, a type I transmembrane receptor that binds vacuolar hydrolases in the late-Golgi (Marcusson  et al., 1994  ; Cooper and Stevens, 1996  ).	bind
39559	2	10624	6	NULL	NULL	0	NULL	Vps10p	NULL		bind	NULL				vacuolar hydrolases	NULL				NULL	late golgi	0	NULL	NULL	NULL	gw60_molbiolcell_12_10_3242_s_21	11598206	A key component in the sorting and transport of vacuolar hydrolases is Vps10p, a type I transmembrane receptor that binds vacuolar hydrolases in the late-Golgi (Marcusson  et al., 1994  ; Cooper and Stevens, 1996  ).	bind
39560	3	10624	6	NULL	NULL	0	NULL	Vps10p	NULL		plays a role in	NULL				vacuolar hydrolases	NULL	sorting of			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_10_3242_s_21	11598206	A key component in the sorting and transport of vacuolar hydrolases is Vps10p, a type I transmembrane receptor that binds vacuolar hydrolases in the late-Golgi (Marcusson  et al., 1994  ; Cooper and Stevens, 1996  ).	bind
39561	4	10624	6	NULL	NULL	0	NULL	Vps10p	NULL		plays a role in	NULL				vacuolar hydrolases	NULL	transport of 			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_10_3242_s_21	11598206	A key component in the sorting and transport of vacuolar hydrolases is Vps10p, a type I transmembrane receptor that binds vacuolar hydrolases in the late-Golgi (Marcusson  et al., 1994  ; Cooper and Stevens, 1996  ).	bind
47233	1	10625	5	13	NULL	NULL	NULL	FRS2	GP		plays a role in					FGF signaling	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_3_1747_s_23	14593093	A key component of FGF signaling is the docking protein FRS2, which binds to the FGFRs and recruits several signal transducing molecules leading to the activation of the mitogen-activated protein kinase (MAPK) cascade and the PI3K-AKT antiapoptotic pathway (  -  ).	bind
47234	2	10625	5	13	NULL	NULL	NULL	FRS2	GP		bind					FGFRs	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_3_1747_s_23	14593093	A key component of FGF signaling is the docking protein FRS2, which binds to the FGFRs and recruits several signal transducing molecules leading to the activation of the mitogen-activated protein kinase (MAPK) cascade and the PI3K-AKT antiapoptotic pathway (  -  ).	bind
47235	3	10625	5	13	NULL	NULL	NULL	statement 2	GP		recruits					signal transducing molecules	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_3_1747_s_23	14593093	A key component of FGF signaling is the docking protein FRS2, which binds to the FGFRs and recruits several signal transducing molecules leading to the activation of the mitogen-activated protein kinase (MAPK) cascade and the PI3K-AKT antiapoptotic pathway (  -  ).	bind
47236	4	10625	5	13	NULL	NULL	NULL	statement 3	GP		leads to					MAPK cascade	Process	activation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_3_1747_s_23	14593093	A key component of FGF signaling is the docking protein FRS2, which binds to the FGFRs and recruits several signal transducing molecules leading to the activation of the mitogen-activated protein kinase (MAPK) cascade and the PI3K-AKT antiapoptotic pathway (  -  ).	bind
47239	5	10625	5	13	NULL	NULL	NULL	MAPK	GP		is					mitogen-activated protein kinase	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_3_1747_s_23	14593093	A key component of FGF signaling is the docking protein FRS2, which binds to the FGFRs and recruits several signal transducing molecules leading to the activation of the mitogen-activated protein kinase (MAPK) cascade and the PI3K-AKT antiapoptotic pathway (  -  ).	bind
47241	6	10625	5	13	NULL	NULL	NULL	statement 3	Process		leads to					PI3K-AKT antiapoptotic pathway	Process	activation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_3_1747_s_23	14593093	A key component of FGF signaling is the docking protein FRS2, which binds to the FGFRs and recruits several signal transducing molecules leading to the activation of the mitogen-activated protein kinase (MAPK) cascade and the PI3K-AKT antiapoptotic pathway (  -  ).	bind
47242	7	10625	5	13	NULL	NULL	NULL	FRS2	GP		is a type of					docking protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_3_1747_s_23	14593093	A key component of FGF signaling is the docking protein FRS2, which binds to the FGFRs and recruits several signal transducing molecules leading to the activation of the mitogen-activated protein kinase (MAPK) cascade and the PI3K-AKT antiapoptotic pathway (  -  ).	bind
39562	1	10625	6	NULL	NULL	0	NULL	FRS2	NULL		is a type of	NULL				docking protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_3_1747_s_23	14593093	A key component of FGF signaling is the docking protein FRS2, which binds to the FGFRs and recruits several signal transducing molecules leading to the activation of the mitogen-activated protein kinase (MAPK) cascade and the PI3K-AKT antiapoptotic pathway (  -  ).	bind
39563	2	10625	6	NULL	NULL	0	NULL	FRS2	NULL		bind	NULL				FGFR	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_3_1747_s_23	14593093	A key component of FGF signaling is the docking protein FRS2, which binds to the FGFRs and recruits several signal transducing molecules leading to the activation of the mitogen-activated protein kinase (MAPK) cascade and the PI3K-AKT antiapoptotic pathway (  -  ).	bind
39564	3	10625	6	NULL	NULL	0	NULL	FRS2	NULL		is a key component of	NULL				FGF signaling	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_3_1747_s_23	14593093	A key component of FGF signaling is the docking protein FRS2, which binds to the FGFRs and recruits several signal transducing molecules leading to the activation of the mitogen-activated protein kinase (MAPK) cascade and the PI3K-AKT antiapoptotic pathway (  -  ).	bind
39565	4	10625	6	NULL	NULL	0	NULL	statement 2	NULL		recruits	NULL				signal transducing molecules	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_3_1747_s_23	14593093	A key component of FGF signaling is the docking protein FRS2, which binds to the FGFRs and recruits several signal transducing molecules leading to the activation of the mitogen-activated protein kinase (MAPK) cascade and the PI3K-AKT antiapoptotic pathway (  -  ).	bind
39566	5	10625	6	NULL	NULL	0	NULL	statement 4	NULL		leads to	NULL				MAPK cascade	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_3_1747_s_23	14593093	A key component of FGF signaling is the docking protein FRS2, which binds to the FGFRs and recruits several signal transducing molecules leading to the activation of the mitogen-activated protein kinase (MAPK) cascade and the PI3K-AKT antiapoptotic pathway (  -  ).	bind
39567	6	10625	6	NULL	NULL	0	NULL	MAPK	NULL		is	NULL				mitogen-activated protein kinase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_3_1747_s_23	14593093	A key component of FGF signaling is the docking protein FRS2, which binds to the FGFRs and recruits several signal transducing molecules leading to the activation of the mitogen-activated protein kinase (MAPK) cascade and the PI3K-AKT antiapoptotic pathway (  -  ).	bind
39568	7	10625	6	NULL	NULL	0	NULL	statement 4	NULL		leads to	NULL				PI3K-AKT antiapoptotic pathway	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_3_1747_s_23	14593093	A key component of FGF signaling is the docking protein FRS2, which binds to the FGFRs and recruits several signal transducing molecules leading to the activation of the mitogen-activated protein kinase (MAPK) cascade and the PI3K-AKT antiapoptotic pathway (  -  ).	bind
47246	1	10626	5	13	NULL	NULL	NULL	SH2 domain	GP		is					Src homology 2 domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_19_11962_s_23	9565625	A key component of several signaling intermediates is the Src homology 2 (SH2) domain that binds tyrosine-phosphorylated proteins in a sequence-specific manner ( 12).	bind
47247	2	10626	5	13	NULL	NULL	NULL				bind		sequence specifically	SH2 domain		proteins	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_19_11962_s_23	9565625	A key component of several signaling intermediates is the Src homology 2 (SH2) domain that binds tyrosine-phosphorylated proteins in a sequence-specific manner ( 12).	bind
39569	1	10626	6	NULL	NULL	0	NULL		NULL		bind	NULL	sequence specifically	SH2 domain		protein	NULL	phosphorylated	tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_19_11962_s_23	9565625	A key component of several signaling intermediates is the Src homology 2 (SH2) domain that binds tyrosine-phosphorylated proteins in a sequence-specific manner ( 12).	bind
39570	2	10626	6	NULL	NULL	0	NULL	SH2	NULL		is	NULL				Src homology 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_19_11962_s_23	9565625	A key component of several signaling intermediates is the Src homology 2 (SH2) domain that binds tyrosine-phosphorylated proteins in a sequence-specific manner ( 12).	bind
47248	1	10627	5	13	NULL	NULL	NULL	CD154	GP		is a type of					T-cell - expressed CD40 ligand	GP				NULL		NULL	NULL	NULL	NULL	gw70_diabetes_55_1_27_s_10	16380473	A key costimulatory pathway involves the binding of the T-cell - expressed CD40 ligand (CD154) to CD40 on antigen-presenting cells ( ).	bind
47249	2	10627	5	13	NULL	NULL	NULL	CD154	GP		bind					CD40	GP				NULL	antigen-presenting cells	NULL	NULL	NULL	NULL	gw70_diabetes_55_1_27_s_10	16380473	A key costimulatory pathway involves the binding of the T-cell - expressed CD40 ligand (CD154) to CD40 on antigen-presenting cells ( ).	bind
50002	3	10627	5	13	NULL	NULL	NULL	costimulatory pathway	Process		involves					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_diabetes_55_1_27_s_10	16380473	A key costimulatory pathway involves the binding of the T-cell - expressed CD40 ligand (CD154) to CD40 on antigen-presenting cells ( ).	bind
39571	1	10627	6	10	NULL	0	NULL	CD154	NULL		is a type of	NULL				T-cell-expressed CD40 ligand	NULL				NULL		NULL	NULL	NULL	NULL	gw70_diabetes_55_1_27_s_10	16380473	A key costimulatory pathway involves the binding of the T-cell - expressed CD40 ligand (CD154) to CD40 on antigen-presenting cells ( ).	bind
39572	2	10627	6	NULL	NULL	0	NULL	CD154	NULL		bind	NULL				CD40	NULL				NULL	antigen presenting cells	0	NULL	NULL	NULL	gw70_diabetes_55_1_27_s_10	16380473	A key costimulatory pathway involves the binding of the T-cell - expressed CD40 ligand (CD154) to CD40 on antigen-presenting cells ( ).	bind
39573	3	10627	6	10	NULL	0	NULL	costimulatory pathway	NULL		involves	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_diabetes_55_1_27_s_10	16380473	A key costimulatory pathway involves the binding of the T-cell - expressed CD40 ligand (CD154) to CD40 on antigen-presenting cells ( ).	bind
47252	1	10629	5	13	NULL	NULL	NULL	PDZ proteins	GP		bind					ct-GluR2/3	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_3_873_s_247	11163273	A key feature of our model is that the binding of PDZ proteins to ct-GluR2/3 regulates the insertion of receptors.	bind
47253	2	10629	5	13	NULL	NULL	NULL	statement 1	Process		regulates					receptors	GP	insertion of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_28_3_873_s_247	11163273	A key feature of our model is that the binding of PDZ proteins to ct-GluR2/3 regulates the insertion of receptors.	bind
39575	1	10629	6	NULL	NULL	0	NULL	PDZ proteins	NULL		bind	NULL				ct-GluR2/3	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_28_3_873_s_247	11163273	A key feature of our model is that the binding of PDZ proteins to ct-GluR2/3 regulates the insertion of receptors.	bind
39576	2	10629	6	NULL	NULL	0	NULL	statement 1	NULL		regulates	NULL				receptors	NULL	insertion of 			NULL		0	NULL	NULL	NULL	gw60_neuron_28_3_873_s_247	11163273	A key feature of our model is that the binding of PDZ proteins to ct-GluR2/3 regulates the insertion of receptors.	bind
47254	1	10630	5	13	NULL	NULL	NULL	Atr	GP		bind					stalled replication forks	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_45507_s_163	14525986	A key feature of our studies is the observation that Cut5 is essential for the binding of both Atr and Pol alpha to stalled replication forks, two fundamental events in checkpoint activation.	bind
47255	2	10630	5	13	NULL	NULL	NULL	Cut5	GP		is essential for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_45507_s_163	14525986	A key feature of our studies is the observation that Cut5 is essential for the binding of both Atr and Pol alpha to stalled replication forks, two fundamental events in checkpoint activation.	bind
47256	3	10630	5	13	NULL	NULL	NULL	statement 1	Process		is a fundamental step in					checkpoint activation 	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_45507_s_163	14525986	A key feature of our studies is the observation that Cut5 is essential for the binding of both Atr and Pol alpha to stalled replication forks, two fundamental events in checkpoint activation.	bind
47257	4	10630	5	13	NULL	NULL	NULL	Pol alpha	GP		bind					stalled replication forks	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_45507_s_163	14525986	A key feature of our studies is the observation that Cut5 is essential for the binding of both Atr and Pol alpha to stalled replication forks, two fundamental events in checkpoint activation.	bind
47258	5	10630	5	13	NULL	NULL	NULL	Cut5	GP		is essential for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_45507_s_163	14525986	A key feature of our studies is the observation that Cut5 is essential for the binding of both Atr and Pol alpha to stalled replication forks, two fundamental events in checkpoint activation.	bind
47259	6	10630	5	13	NULL	NULL	NULL	statement 4	Process		is a fundamental step in					checkpoint activation	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_45507_s_163	14525986	A key feature of our studies is the observation that Cut5 is essential for the binding of both Atr and Pol alpha to stalled replication forks, two fundamental events in checkpoint activation.	bind
39577	1	10630	6	NULL	NULL	0	NULL	Atr	NULL		bind	NULL				replication fork	NULL	stalled			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_45507_s_163	14525986	A key feature of our studies is the observation that Cut5 is essential for the binding of both Atr and Pol alpha to stalled replication forks, two fundamental events in checkpoint activation.	bind
39578	2	10630	6	NULL	NULL	0	NULL	Pol alpha	NULL		bind	NULL				replication fork	NULL	stalled			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_45507_s_163	14525986	A key feature of our studies is the observation that Cut5 is essential for the binding of both Atr and Pol alpha to stalled replication forks, two fundamental events in checkpoint activation.	bind
39579	3	10630	6	10	NULL	0	NULL	statement 1			is a fundamental step in					checkpoint activation					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_45507_s_163	14525986	A key feature of our studies is the observation that Cut5 is essential for the binding of both Atr and Pol alpha to stalled replication forks, two fundamental events in checkpoint activation.	bind
39580	4	10630	6	10	NULL	0	NULL	statement 2			is a fundamental step in					checkpoint activation					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_45507_s_163	14525986	A key feature of our studies is the observation that Cut5 is essential for the binding of both Atr and Pol alpha to stalled replication forks, two fundamental events in checkpoint activation.	bind
39581	5	10630	6	NULL	NULL	0	NULL	Cut5	NULL		is essential for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_45507_s_163	14525986	A key feature of our studies is the observation that Cut5 is essential for the binding of both Atr and Pol alpha to stalled replication forks, two fundamental events in checkpoint activation.	bind
39582	6	10630	6	NULL	NULL	0	NULL	Cut5	NULL		is essential for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_45507_s_163	14525986	A key feature of our studies is the observation that Cut5 is essential for the binding of both Atr and Pol alpha to stalled replication forks, two fundamental events in checkpoint activation.	bind
47260	1	10631	5	13	NULL	NULL	NULL	T cell	Cell		express					CD4	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_5_548_s_14	8805272	A key feature of the activation process is that the T cell can distinguish an MHC-bound ligand from other ligands because the T cell expresses cell-surface molecules, CD4 and CD8, which can bind directly to MHC proteins in domains distinct from their peptide-binding sites.	bind
47261	2	10631	5	13	NULL	NULL	NULL	CD4	GP		is a type of					cell-surface molecules	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_5_548_s_14	8805272	A key feature of the activation process is that the T cell can distinguish an MHC-bound ligand from other ligands because the T cell expresses cell-surface molecules, CD4 and CD8, which can bind directly to MHC proteins in domains distinct from their peptide-binding sites.	bind
47262	3	10631	5	13	NULL	NULL	NULL	CD4	GP		bind		directly			MHC proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_5_548_s_14	8805272	A key feature of the activation process is that the T cell can distinguish an MHC-bound ligand from other ligands because the T cell expresses cell-surface molecules, CD4 and CD8, which can bind directly to MHC proteins in domains distinct from their peptide-binding sites.	bind
47263	4	10631	5	13	NULL	NULL	NULL	T cells	Cell		express					CD8	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_5_548_s_14	8805272	A key feature of the activation process is that the T cell can distinguish an MHC-bound ligand from other ligands because the T cell expresses cell-surface molecules, CD4 and CD8, which can bind directly to MHC proteins in domains distinct from their peptide-binding sites.	bind
47264	5	10631	5	13	NULL	NULL	NULL	CD8	GP		is a type of					cell-surface molecules	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_5_548_s_14	8805272	A key feature of the activation process is that the T cell can distinguish an MHC-bound ligand from other ligands because the T cell expresses cell-surface molecules, CD4 and CD8, which can bind directly to MHC proteins in domains distinct from their peptide-binding sites.	bind
47265	6	10631	5	13	NULL	NULL	NULL	CD8	GP		bind		directly			MHC proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_6_5_548_s_14	8805272	A key feature of the activation process is that the T cell can distinguish an MHC-bound ligand from other ligands because the T cell expresses cell-surface molecules, CD4 and CD8, which can bind directly to MHC proteins in domains distinct from their peptide-binding sites.	bind
39583	1	10631	6	NULL	NULL	0	NULL	T cell	NULL		express	NULL				CD4	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_6_5_548_s_14	8805272	A key feature of the activation process is that the T cell can distinguish an MHC-bound ligand from other ligands because the T cell expresses cell-surface molecules, CD4 and CD8, which can bind directly to MHC proteins in domains distinct from their peptide-binding sites.	bind
39584	2	10631	6	NULL	NULL	0	NULL	T cell	NULL		express	NULL				CD8	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_6_5_548_s_14	8805272	A key feature of the activation process is that the T cell can distinguish an MHC-bound ligand from other ligands because the T cell expresses cell-surface molecules, CD4 and CD8, which can bind directly to MHC proteins in domains distinct from their peptide-binding sites.	bind
39585	3	10631	6	NULL	NULL	0	NULL	CD4 	NULL		is a type of	NULL				cell-surface molecule	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_6_5_548_s_14	8805272	A key feature of the activation process is that the T cell can distinguish an MHC-bound ligand from other ligands because the T cell expresses cell-surface molecules, CD4 and CD8, which can bind directly to MHC proteins in domains distinct from their peptide-binding sites.	bind
39586	4	10631	6	NULL	NULL	0	NULL	CD8	NULL		is a type of	NULL				cell surface receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_6_5_548_s_14	8805272	A key feature of the activation process is that the T cell can distinguish an MHC-bound ligand from other ligands because the T cell expresses cell-surface molecules, CD4 and CD8, which can bind directly to MHC proteins in domains distinct from their peptide-binding sites.	bind
39587	5	10631	6	NULL	NULL	0	NULL	CD4	NULL		bind	NULL	directly			MHC proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_6_5_548_s_14	8805272	A key feature of the activation process is that the T cell can distinguish an MHC-bound ligand from other ligands because the T cell expresses cell-surface molecules, CD4 and CD8, which can bind directly to MHC proteins in domains distinct from their peptide-binding sites.	bind
39588	6	10631	6	NULL	NULL	0	NULL	CD8	NULL		bind	NULL	directly			MHC proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_6_5_548_s_14	8805272	A key feature of the activation process is that the T cell can distinguish an MHC-bound ligand from other ligands because the T cell expresses cell-surface molecules, CD4 and CD8, which can bind directly to MHC proteins in domains distinct from their peptide-binding sites.	bind
47266	1	10632	5	13	NULL	NULL	NULL	EHD2	GP	acidic;;putative	 linked to		might be	Arp2/3 complex binding motif		actin cytoskeleton	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_11_10593_s_411	14676205	A key finding presented here is that at least two distinct motifs are present in the C terminus of EHD2 that might link this protein to the actin cytoskeleton, an acidic and putative Arp2/3 complex binding motif and the EH domain itself which binds the novel CH domain-containing protein EHBP1 (Figs.  6 and  10).	bind
47267	2	10632	5	13	NULL	NULL	NULL	EHD2	GP		 linked to		might be	EH domain		actin cytoskeleton	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_11_10593_s_411	14676205	A key finding presented here is that at least two distinct motifs are present in the C terminus of EHD2 that might link this protein to the actin cytoskeleton, an acidic and putative Arp2/3 complex binding motif and the EH domain itself which binds the novel CH domain-containing protein EHBP1 (Figs.  6 and  10).	bind
47268	3	10632	5	13	NULL	NULL	NULL				bind			EH domain		EHBP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_11_10593_s_411	14676205	A key finding presented here is that at least two distinct motifs are present in the C terminus of EHD2 that might link this protein to the actin cytoskeleton, an acidic and putative Arp2/3 complex binding motif and the EH domain itself which binds the novel CH domain-containing protein EHBP1 (Figs.  6 and  10).	bind
47269	4	10632	5	13	NULL	NULL	NULL	EHBP1	GP		is a type of					CH domain-containing protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_11_10593_s_411	14676205	A key finding presented here is that at least two distinct motifs are present in the C terminus of EHD2 that might link this protein to the actin cytoskeleton, an acidic and putative Arp2/3 complex binding motif and the EH domain itself which binds the novel CH domain-containing protein EHBP1 (Figs.  6 and  10).	bind
39880	1	10632	6	NULL	NULL	0	NULL	EHD2 protein	NULL	acidic;; putative	linked to	NULL	might be	Arp2/3 complex binding motif in C-terminus		actin cytoskeleton	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_11_10593_s_411	14676205	A key finding presented here is that at least two distinct motifs are present in the C terminus of EHD2 that might link this protein to the actin cytoskeleton, an acidic and putative Arp2/3 complex binding motif and the EH domain itself which binds the novel CH domain-containing protein EHBP1 (Figs.  6 and  10).	bind
39881	2	10632	6	NULL	NULL	0	NULL	EHD2	NULL		linked to	NULL	might be	EH domain in C terminus		actin cytoskeleton	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_11_10593_s_411	14676205	A key finding presented here is that at least two distinct motifs are present in the C terminus of EHD2 that might link this protein to the actin cytoskeleton, an acidic and putative Arp2/3 complex binding motif and the EH domain itself which binds the novel CH domain-containing protein EHBP1 (Figs.  6 and  10).	bind
39882	3	10632	6	NULL	NULL	0	NULL	EHBP1	NULL		is a type of	NULL				CH domain-containing protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_11_10593_s_411	14676205	A key finding presented here is that at least two distinct motifs are present in the C terminus of EHD2 that might link this protein to the actin cytoskeleton, an acidic and putative Arp2/3 complex binding motif and the EH domain itself which binds the novel CH domain-containing protein EHBP1 (Figs.  6 and  10).	bind
39883	4	10632	6	NULL	NULL	0	NULL		NULL		bind	NULL		EH domain		EHBP1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_11_10593_s_411	14676205	A key finding presented here is that at least two distinct motifs are present in the C terminus of EHD2 that might link this protein to the actin cytoskeleton, an acidic and putative Arp2/3 complex binding motif and the EH domain itself which binds the novel CH domain-containing protein EHBP1 (Figs.  6 and  10).	bind
47270	1	10633	5	13	NULL	NULL	NULL	Ca2+	Chemical		mediates					feedback regulation	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_6_1097_s_16	11754840	A key mediator of the Ca2+-mediated feedback regulation is calmodulin   (Porter et al., 1995  ; Scott et al., 1997  ); however, there are only a few signaling proteins known to function in  Drosophila phototransduction that bind to calmodulin.	bind
50003	2	10633	5	13	NULL	NULL	NULL	calmodulin	GP		key mediator of					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_6_1097_s_16	11754840	A key mediator of the Ca2+-mediated feedback regulation is calmodulin   (Porter et al., 1995  ; Scott et al., 1997  ); however, there are only a few signaling proteins known to function in  Drosophila phototransduction that bind to calmodulin.	bind
50005	3	10633	5	13	NULL	NULL	NULL	signaling proteins	GP		function in					 phototransduction 	Process	Drosophila			NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_6_1097_s_16	11754840	A key mediator of the Ca2+-mediated feedback regulation is calmodulin   (Porter et al., 1995  ; Scott et al., 1997  ); however, there are only a few signaling proteins known to function in  Drosophila phototransduction that bind to calmodulin.	bind
50006	4	10633	5	13	NULL	NULL	NULL	statement 3	GP		bind					calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_6_1097_s_16	11754840	A key mediator of the Ca2+-mediated feedback regulation is calmodulin   (Porter et al., 1995  ; Scott et al., 1997  ); however, there are only a few signaling proteins known to function in  Drosophila phototransduction that bind to calmodulin.	bind
39589	1	10633	6	10	NULL	0	NULL	Ca2+	NULL		mediates	NULL				feedback regulation	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_6_1097_s_16	11754840	A key mediator of the Ca2+-mediated feedback regulation is calmodulin   (Porter et al., 1995  ; Scott et al., 1997  ); however, there are only a few signaling proteins known to function in  Drosophila phototransduction that bind to calmodulin.	bind
50004	2	10633	6	10	NULL	0	NULL	calmodulin	NULL		key mediator of	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_32_6_1097_s_16	11754840	A key mediator of the Ca2+-mediated feedback regulation is calmodulin   (Porter et al., 1995  ; Scott et al., 1997  ); however, there are only a few signaling proteins known to function in  Drosophila phototransduction that bind to calmodulin.	bind
50007	3	10633	6	10	NULL	0	NULL	signaling proteins	NULL		function in	NULL				phototransduction	NULL	Drosophila			NULL		0	NULL	NULL	NULL	gw60_neuron_32_6_1097_s_16	11754840	A key mediator of the Ca2+-mediated feedback regulation is calmodulin   (Porter et al., 1995  ; Scott et al., 1997  ); however, there are only a few signaling proteins known to function in  Drosophila phototransduction that bind to calmodulin.	bind
50008	4	10633	6	10	NULL	0	NULL	statement 3	NULL		bind	NULL				calmodulin	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_32_6_1097_s_16	11754840	A key mediator of the Ca2+-mediated feedback regulation is calmodulin   (Porter et al., 1995  ; Scott et al., 1997  ); however, there are only a few signaling proteins known to function in  Drosophila phototransduction that bind to calmodulin.	bind
47271	1	10634	5	13	NULL	NULL	NULL	TGFalpha	GP		is a type of					mitogenic peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_33181_s_243	9407106	A key mitogenic peptide involved in squamous epithelial proliferation is TGFalpha, which is believed to be more physiologically relevant in these tissues than epidermal growth factor, although both bind the same epidermal growth factor receptor ( 30,  44).	bind
47272	2	10634	5	13	NULL	NULL	NULL	TGFalpha	GP		is involved in					squamous epithelium	OrganismPart	proliferation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_33181_s_243	9407106	A key mitogenic peptide involved in squamous epithelial proliferation is TGFalpha, which is believed to be more physiologically relevant in these tissues than epidermal growth factor, although both bind the same epidermal growth factor receptor ( 30,  44).	bind
47275	3	10634	5	13	NULL	NULL	NULL	TGFalpha	GP		bind					epidermal growth factor receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_33181_s_243	9407106	A key mitogenic peptide involved in squamous epithelial proliferation is TGFalpha, which is believed to be more physiologically relevant in these tissues than epidermal growth factor, although both bind the same epidermal growth factor receptor ( 30,  44).	bind
47277	4	10634	5	13	NULL	NULL	NULL	epidermal growth factor	GP		bind					epidermal growth factor receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_33181_s_243	9407106	A key mitogenic peptide involved in squamous epithelial proliferation is TGFalpha, which is believed to be more physiologically relevant in these tissues than epidermal growth factor, although both bind the same epidermal growth factor receptor ( 30,  44).	bind
39590	1	10634	6	10	NULL	0	NULL	TGFalpha			plays a role in					squamous epithelial		proliferation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_33181_s_243	9407106	A key mitogenic peptide involved in squamous epithelial proliferation is TGFalpha, which is believed to be more physiologically relevant in these tissues than epidermal growth factor, although both bind the same epidermal growth factor receptor ( 30,  44).	bind
39884	2	10634	6	NULL	NULL	0	NULL	TGFalpha	NULL		bind	NULL				epidermal growth factor receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_33181_s_243	9407106	A key mitogenic peptide involved in squamous epithelial proliferation is TGFalpha, which is believed to be more physiologically relevant in these tissues than epidermal growth factor, although both bind the same epidermal growth factor receptor ( 30,  44).	bind
39885	3	10634	6	NULL	NULL	0	NULL	epidermal growth factor	NULL		bind	NULL				epidermal growth factor receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_33181_s_243	9407106	A key mitogenic peptide involved in squamous epithelial proliferation is TGFalpha, which is believed to be more physiologically relevant in these tissues than epidermal growth factor, although both bind the same epidermal growth factor receptor ( 30,  44).	bind
50009	4	10634	6	10	NULL	0	NULL	TGFalpha	NULL		is a type of	NULL				mitogenic peptide	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_33181_s_243	9407106	A key mitogenic peptide involved in squamous epithelial proliferation is TGFalpha, which is believed to be more physiologically relevant in these tissues than epidermal growth factor, although both bind the same epidermal growth factor receptor ( 30,  44).	bind
47282	1	10635	5	13	NULL	NULL	NULL	hHop	GP		forms chimera with							Drosophila	DP2		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_10_8906_s_187	15632128	A key observation in this study is that exchanging DP2 between hHop and dHop does not grossly affect Hsp70 binding; nonetheless, chimera I (hHop with  Drosophila DP2) fails to support GR activity, and the converse chimera J (dHop with human DP2) gains the ability to enhance GR activity.	bind
47283	2	10635	5	13	NULL	NULL	NULL	statement 1	Process		does not support					GR	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_10_8906_s_187	15632128	A key observation in this study is that exchanging DP2 between hHop and dHop does not grossly affect Hsp70 binding; nonetheless, chimera I (hHop with  Drosophila DP2) fails to support GR activity, and the converse chimera J (dHop with human DP2) gains the ability to enhance GR activity.	bind
47284	3	10635	5	13	NULL	NULL	NULL	dHop	GP		forms chimera with							human	DP2		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_10_8906_s_187	15632128	A key observation in this study is that exchanging DP2 between hHop and dHop does not grossly affect Hsp70 binding; nonetheless, chimera I (hHop with  Drosophila DP2) fails to support GR activity, and the converse chimera J (dHop with human DP2) gains the ability to enhance GR activity.	bind
47285	4	10635	5	13	NULL	NULL	NULL	statement 3	Process		enhance					GR	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_10_8906_s_187	15632128	A key observation in this study is that exchanging DP2 between hHop and dHop does not grossly affect Hsp70 binding; nonetheless, chimera I (hHop with  Drosophila DP2) fails to support GR activity, and the converse chimera J (dHop with human DP2) gains the ability to enhance GR activity.	bind
39983	1	10635	6	NULL	NULL	0	NULL	Hop	NULL	human	forms a chimeric protein with	NULL					NULL	Drosophila	DP2		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8906_s_187	15632128	A key observation in this study is that exchanging DP2 between hHop and dHop does not grossly affect Hsp70 binding; nonetheless, chimera I (hHop with  Drosophila DP2) fails to support GR activity, and the converse chimera J (dHop with human DP2) gains the ability to enhance GR activity.	bind
39984	2	10635	6	NULL	NULL	0	NULL	statement 1	NULL		does not support	NULL				GR	NULL	activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8906_s_187	15632128	A key observation in this study is that exchanging DP2 between hHop and dHop does not grossly affect Hsp70 binding; nonetheless, chimera I (hHop with  Drosophila DP2) fails to support GR activity, and the converse chimera J (dHop with human DP2) gains the ability to enhance GR activity.	bind
39985	3	10635	6	NULL	NULL	0	NULL	Hop	NULL	Drosophila	forms a chimeric protein with	NULL					NULL	human	DP2		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8906_s_187	15632128	A key observation in this study is that exchanging DP2 between hHop and dHop does not grossly affect Hsp70 binding; nonetheless, chimera I (hHop with  Drosophila DP2) fails to support GR activity, and the converse chimera J (dHop with human DP2) gains the ability to enhance GR activity.	bind
39986	4	10635	6	NULL	NULL	0	NULL	statement 3	NULL		enhances	NULL				GR	NULL	activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8906_s_187	15632128	A key observation in this study is that exchanging DP2 between hHop and dHop does not grossly affect Hsp70 binding; nonetheless, chimera I (hHop with  Drosophila DP2) fails to support GR activity, and the converse chimera J (dHop with human DP2) gains the ability to enhance GR activity.	bind
47286	1	10636	5	13	NULL	NULL	NULL	Rb protein	GP		is					retinoblastoma protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_15_6560_s_17	15254224	A key physiological substrate for Cdk4 and Cdk6 is the retinoblastoma (Rb) protein, which binds and inactivates the E2F-DP transcription complexes that are essential for S-phase entry.	bind
47287	2	10636	5	13	NULL	NULL	NULL	Rb protein	GP		is a physiological substrate for					Cdk4	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_15_6560_s_17	15254224	A key physiological substrate for Cdk4 and Cdk6 is the retinoblastoma (Rb) protein, which binds and inactivates the E2F-DP transcription complexes that are essential for S-phase entry.	bind
47288	3	10636	5	13	NULL	NULL	NULL	Rb protein	GP		is a physiological substrate for					Cdk6	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_15_6560_s_17	15254224	A key physiological substrate for Cdk4 and Cdk6 is the retinoblastoma (Rb) protein, which binds and inactivates the E2F-DP transcription complexes that are essential for S-phase entry.	bind
47290	4	10636	5	13	NULL	NULL	NULL	Rb protein	GP		bind					E2F-DP transcription complexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_15_6560_s_17	15254224	A key physiological substrate for Cdk4 and Cdk6 is the retinoblastoma (Rb) protein, which binds and inactivates the E2F-DP transcription complexes that are essential for S-phase entry.	bind
47291	5	10636	5	13	NULL	NULL	NULL	statement 4	Process		inactivates					E2F-DP transcription complexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_15_6560_s_17	15254224	A key physiological substrate for Cdk4 and Cdk6 is the retinoblastoma (Rb) protein, which binds and inactivates the E2F-DP transcription complexes that are essential for S-phase entry.	bind
47293	6	10636	5	13	NULL	NULL	NULL	E2F-DP transcription complexes	GP		is essential for					S-phase	Process	entry into			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_15_6560_s_17	15254224	A key physiological substrate for Cdk4 and Cdk6 is the retinoblastoma (Rb) protein, which binds and inactivates the E2F-DP transcription complexes that are essential for S-phase entry.	bind
39591	1	10636	6	NULL	NULL	0	NULL	Rb protein	NULL		is the physiological substrate for	NULL				Cdk4	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_15_6560_s_17	15254224	A key physiological substrate for Cdk4 and Cdk6 is the retinoblastoma (Rb) protein, which binds and inactivates the E2F-DP transcription complexes that are essential for S-phase entry.	bind
39592	2	10636	6	NULL	NULL	0	NULL	Rb protein	NULL		is the physiological substrate for	NULL				Cdk6	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_15_6560_s_17	15254224	A key physiological substrate for Cdk4 and Cdk6 is the retinoblastoma (Rb) protein, which binds and inactivates the E2F-DP transcription complexes that are essential for S-phase entry.	bind
39593	3	10636	6	NULL	NULL	0	NULL	Rb	NULL		is	NULL				retinoblastoma protein	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_15_6560_s_17	15254224	A key physiological substrate for Cdk4 and Cdk6 is the retinoblastoma (Rb) protein, which binds and inactivates the E2F-DP transcription complexes that are essential for S-phase entry.	bind
39594	4	10636	6	NULL	NULL	0	NULL	E2F-DP transcription complexes	NULL		are essential for	NULL				S-phase	NULL	entry into			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_15_6560_s_17	15254224	A key physiological substrate for Cdk4 and Cdk6 is the retinoblastoma (Rb) protein, which binds and inactivates the E2F-DP transcription complexes that are essential for S-phase entry.	bind
39595	5	10636	6	NULL	NULL	0	NULL	Rb protein	NULL		bind	NULL				E2F-DP transcription complexes	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_15_6560_s_17	15254224	A key physiological substrate for Cdk4 and Cdk6 is the retinoblastoma (Rb) protein, which binds and inactivates the E2F-DP transcription complexes that are essential for S-phase entry.	bind
39596	6	10636	6	NULL	NULL	0	NULL	Rb protein	NULL		inactivates	NULL				E2F-DP transcription complexes	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_15_6560_s_17	15254224	A key physiological substrate for Cdk4 and Cdk6 is the retinoblastoma (Rb) protein, which binds and inactivates the E2F-DP transcription complexes that are essential for S-phase entry.	bind
47294	1	10637	5	13	NULL	NULL	NULL	CcmE	GP		is a type of					heme chaperone	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_35_32591_s_24	11384983	A key player in the maturation pathway has been identified in the heme chaperone CcmE, which binds heme covalently at a single histidine residue and subsequently transfers it to apocytochrome  c ( 11).	bind
47295	2	10637	5	13	NULL	NULL	NULL	CcmE	GP		bind		covalently			heme	Chemical		histidine residue		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_35_32591_s_24	11384983	A key player in the maturation pathway has been identified in the heme chaperone CcmE, which binds heme covalently at a single histidine residue and subsequently transfers it to apocytochrome  c ( 11).	bind
47296	3	10637	5	13	NULL	NULL	NULL	heme	Chemical		is transfered to					apocytochrome c	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_35_32591_s_24	11384983	A key player in the maturation pathway has been identified in the heme chaperone CcmE, which binds heme covalently at a single histidine residue and subsequently transfers it to apocytochrome  c ( 11).	bind
47297	4	10637	5	13	NULL	NULL	NULL	statement 2	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_35_32591_s_24	11384983	A key player in the maturation pathway has been identified in the heme chaperone CcmE, which binds heme covalently at a single histidine residue and subsequently transfers it to apocytochrome  c ( 11).	bind
39597	1	10637	6	NULL	NULL	0	NULL	CcmE	NULL		is a type of	NULL				heme chaperone	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32591_s_24	11384983	A key player in the maturation pathway has been identified in the heme chaperone CcmE, which binds heme covalently at a single histidine residue and subsequently transfers it to apocytochrome  c ( 11).	bind
39598	2	10637	6	NULL	NULL	0	NULL	CcmE	NULL		bind	NULL	covalently			heme	NULL		histidine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32591_s_24	11384983	A key player in the maturation pathway has been identified in the heme chaperone CcmE, which binds heme covalently at a single histidine residue and subsequently transfers it to apocytochrome  c ( 11).	bind
39599	3	10637	6	NULL	NULL	0	NULL	heme	NULL		is transfered to	NULL				apocytochrome c	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32591_s_24	11384983	A key player in the maturation pathway has been identified in the heme chaperone CcmE, which binds heme covalently at a single histidine residue and subsequently transfers it to apocytochrome  c ( 11).	bind
39600	4	10637	6	NULL	NULL	0	NULL	CcmE	NULL		transfers	NULL				heme	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32591_s_24	11384983	A key player in the maturation pathway has been identified in the heme chaperone CcmE, which binds heme covalently at a single histidine residue and subsequently transfers it to apocytochrome  c ( 11).	bind
39601	5	10637	6	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32591_s_24	11384983	A key player in the maturation pathway has been identified in the heme chaperone CcmE, which binds heme covalently at a single histidine residue and subsequently transfers it to apocytochrome  c ( 11).	bind
47298	1	10638	5	13	NULL	NULL	NULL	v-Src	GP		mediates					STAT3	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2043_s_50	10688651	A key question, then, is how v-Src or activated c-Src mediates the activation of STAT3.	bind
47299	2	10638	5	13	NULL	NULL	NULL	c-Src	GP	activated	mediates					STAT3	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_2043_s_50	10688651	A key question, then, is how v-Src or activated c-Src mediates the activation of STAT3.	bind
39602	1	10638	6	NULL	NULL	0	NULL	v-Src	NULL		mediates	NULL				STAT3	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_6_2043_s_50	10688651	A key question, then, is how v-Src or activated c-Src mediates the activation of STAT3.	bind
39603	2	10638	6	NULL	NULL	0	NULL	c-Src	NULL	activated	mediates	NULL				STAT3	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_6_2043_s_50	10688651	A key question, then, is how v-Src or activated c-Src mediates the activation of STAT3.	bind
47300	1	10639	5	13	NULL	NULL	NULL	Fas	GP		bind					FasL	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_49_40599_s_18	16227629	A key signaling activity of Fas, which binds to Fas ligand (FasL), and of DR4 and DR5, which bind to Apo2L/TRAIL, is apoptosis induction.	bind
47301	2	10639	5	13	NULL	NULL	NULL	FasL	GP		is					Fas ligand	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_49_40599_s_18	16227629	A key signaling activity of Fas, which binds to Fas ligand (FasL), and of DR4 and DR5, which bind to Apo2L/TRAIL, is apoptosis induction.	bind
47302	3	10639	5	13	NULL	NULL	NULL	DR4	GP		bind					Apo2L/TRAIL	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_49_40599_s_18	16227629	A key signaling activity of Fas, which binds to Fas ligand (FasL), and of DR4 and DR5, which bind to Apo2L/TRAIL, is apoptosis induction.	bind
47303	4	10639	5	13	NULL	NULL	NULL	DR5	GP		bind					Apo2L/TRAIL	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_49_40599_s_18	16227629	A key signaling activity of Fas, which binds to Fas ligand (FasL), and of DR4 and DR5, which bind to Apo2L/TRAIL, is apoptosis induction.	bind
47304	5	10639	5	13	NULL	NULL	NULL	apoptosis	Process	induction of	is a key signaling activity of					Fas	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_49_40599_s_18	16227629	A key signaling activity of Fas, which binds to Fas ligand (FasL), and of DR4 and DR5, which bind to Apo2L/TRAIL, is apoptosis induction.	bind
47305	6	10639	5	13	NULL	NULL	NULL	apoptosis	Process	induction of	is a key signaling activity of					DR4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_49_40599_s_18	16227629	A key signaling activity of Fas, which binds to Fas ligand (FasL), and of DR4 and DR5, which bind to Apo2L/TRAIL, is apoptosis induction.	bind
47307	7	10639	5	13	NULL	NULL	NULL	apoptosis	Process	induction of	is a key signaling activity of					DR5	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_49_40599_s_18	16227629	A key signaling activity of Fas, which binds to Fas ligand (FasL), and of DR4 and DR5, which bind to Apo2L/TRAIL, is apoptosis induction.	bind
39604	1	10639	6	NULL	NULL	0	NULL	Fas	NULL		bind	NULL				FasL	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_49_40599_s_18	16227629	A key signaling activity of Fas, which binds to Fas ligand (FasL), and of DR4 and DR5, which bind to Apo2L/TRAIL, is apoptosis induction.	bind
39605	2	10639	6	NULL	NULL	0	NULL	DR4	NULL		bind	NULL				Apo2L/TRAIL	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_49_40599_s_18	16227629	A key signaling activity of Fas, which binds to Fas ligand (FasL), and of DR4 and DR5, which bind to Apo2L/TRAIL, is apoptosis induction.	bind
39606	3	10639	6	NULL	NULL	0	NULL	DR5	NULL		bind	NULL				Apo2L/TRAIL	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_49_40599_s_18	16227629	A key signaling activity of Fas, which binds to Fas ligand (FasL), and of DR4 and DR5, which bind to Apo2L/TRAIL, is apoptosis induction.	bind
39607	4	10639	6	NULL	NULL	0	NULL	Fas	NULL		plays a role in	NULL				apoptosis	NULL	induction of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_49_40599_s_18	16227629	A key signaling activity of Fas, which binds to Fas ligand (FasL), and of DR4 and DR5, which bind to Apo2L/TRAIL, is apoptosis induction.	bind
39608	5	10639	6	NULL	NULL	0	NULL	DR4	NULL		plays a role in	NULL				apoptosis	NULL	induction of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_49_40599_s_18	16227629	A key signaling activity of Fas, which binds to Fas ligand (FasL), and of DR4 and DR5, which bind to Apo2L/TRAIL, is apoptosis induction.	bind
39609	6	10639	6	NULL	NULL	0	NULL	DR5	NULL		plays a role in	NULL				apoptosis	NULL	induction of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_49_40599_s_18	16227629	A key signaling activity of Fas, which binds to Fas ligand (FasL), and of DR4 and DR5, which bind to Apo2L/TRAIL, is apoptosis induction.	bind
50010	7	10639	6	10	NULL	0	NULL	FasL	NULL		is	NULL				Fas ligand	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_49_40599_s_18	16227629	A key signaling activity of Fas, which binds to Fas ligand (FasL), and of DR4 and DR5, which bind to Apo2L/TRAIL, is apoptosis induction.	bind
47309	1	10640	5	13	NULL	NULL	NULL	MHC I	GP		bind					CD8	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_15_0_535_s_196	9143699	A key to understanding coreceptor expression by NK1 T cells is whether CD1 binds CD8  (as does MHC I), or CD4 (like MHC II), or neither.	bind
47310	2	10640	5	13	NULL	NULL	NULL	MHC II	GP		bind					CD4	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_15_0_535_s_196	9143699	A key to understanding coreceptor expression by NK1 T cells is whether CD1 binds CD8  (as does MHC I), or CD4 (like MHC II), or neither.	bind
39610	1	10640	6	NULL	NULL	0	NULL	MHC I	NULL		bind	NULL				CD8	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_15_0_535_s_196	9143699	A key to understanding coreceptor expression by NK1 T cells is whether CD1 binds CD8  (as does MHC I), or CD4 (like MHC II), or neither.	bind
39611	2	10640	6	NULL	NULL	0	NULL	MHC II	NULL		bind	NULL				CD4	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_15_0_535_s_196	9143699	A key to understanding coreceptor expression by NK1 T cells is whether CD1 binds CD8  (as does MHC I), or CD4 (like MHC II), or neither.	bind
47313	1	10641	5	13	NULL	NULL	NULL	p27	GP	mutant	bind			kinase		cyclins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_21_20620_s_214	15788393	A kinase contact mutant of p27, which still binds cyclins, does not inhibit cyclin E-cdk2 complexes but becomes phosphorylated and rapidly degraded.	bind
47314	2	10641	5	13	NULL	NULL	NULL	p27	GP	mutant	does not inhibit			kinase		cyclin E-cdk2 complexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_21_20620_s_214	15788393	A kinase contact mutant of p27, which still binds cyclins, does not inhibit cyclin E-cdk2 complexes but becomes phosphorylated and rapidly degraded.	bind
47316	3	10641	5	13	NULL	NULL	NULL	p27	GP	mutant	undergoes			kinase		phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_21_20620_s_214	15788393	A kinase contact mutant of p27, which still binds cyclins, does not inhibit cyclin E-cdk2 complexes but becomes phosphorylated and rapidly degraded.	bind
47318	4	10641	5	13	NULL	NULL	NULL	p27	GP	mutant	undergoes		rapidly	kinase		degradation	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_21_20620_s_214	15788393	A kinase contact mutant of p27, which still binds cyclins, does not inhibit cyclin E-cdk2 complexes but becomes phosphorylated and rapidly degraded.	bind
39612	1	10641	6	NULL	NULL	0	NULL	p27	NULL	mutant	bind	NULL		kinase		cyclin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_21_20620_s_214	15788393	A kinase contact mutant of p27, which still binds cyclins, does not inhibit cyclin E-cdk2 complexes but becomes phosphorylated and rapidly degraded.	bind
39613	2	10641	6	NULL	NULL	0	NULL	p27	NULL	mutant	does not inhibit	NULL		kinase		cyclin E-cdk2 complexes	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_21_20620_s_214	15788393	A kinase contact mutant of p27, which still binds cyclins, does not inhibit cyclin E-cdk2 complexes but becomes phosphorylated and rapidly degraded.	bind
39614	3	10641	6	10	NULL	0	NULL	p27	NULL	mutant	undergoes	NULL	rapidly	kinase		degradation	NULL	rapidly			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_21_20620_s_214	15788393	A kinase contact mutant of p27, which still binds cyclins, does not inhibit cyclin E-cdk2 complexes but becomes phosphorylated and rapidly degraded.	bind
39615	4	10641	6	10	NULL	0	NULL	p27	NULL	mutant	undergoes	NULL		kinase		phosphorylation	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_21_20620_s_214	15788393	A kinase contact mutant of p27, which still binds cyclins, does not inhibit cyclin E-cdk2 complexes but becomes phosphorylated and rapidly degraded.	bind
47321	1	10642	5	13	NULL	NULL	NULL	kinase	GP	human;;platelets	bind					RalA	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1763_9_948_s_132	16945434	A kinase from human platelets binds to recombinant RalA and RalB. 200  l GST-RalA-GDP  or GST-RalB-GDP or GST-cH-Ras-GDP bead suspension (1:1) was incubated with total  human platelet extract.	bind
47322	2	10642	5	13	NULL	NULL	NULL	kinase	GP	human;;platelets	bind					RalB	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1763_9_948_s_132	16945434	A kinase from human platelets binds to recombinant RalA and RalB. 200  l GST-RalA-GDP  or GST-RalB-GDP or GST-cH-Ras-GDP bead suspension (1:1) was incubated with total  human platelet extract.	bind
39616	1	10642	6	NULL	NULL	0	NULL	kinase 	NULL	 human;; platelets	bind	NULL				RalA	NULL	recombinant			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1763_9_948_s_132	16945434	A kinase from human platelets binds to recombinant RalA and RalB. 200  l GST-RalA-GDP  or GST-RalB-GDP or GST-cH-Ras-GDP bead suspension (1:1) was incubated with total  human platelet extract.	bind
39617	2	10642	6	NULL	NULL	0	NULL	kinase	NULL	human;; platelets	bind	NULL				RalB	NULL	recombinant			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1763_9_948_s_132	16945434	A kinase from human platelets binds to recombinant RalA and RalB. 200  l GST-RalA-GDP  or GST-RalB-GDP or GST-cH-Ras-GDP bead suspension (1:1) was incubated with total  human platelet extract.	bind
47324	1	10643	5	13	NULL	NULL	NULL	PHAS-I	GP		bind					eIF-4E	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_31_18531_s_266	7629182	A kinase that acted on both free  [H ]PHAS-I and [H ]PHAS-I  bound to eIF-4E eluted at relatively high concentrations of NaCl  (fraction 58).	bind
39618	1	10643	6	NULL	NULL	0	NULL	PHAS-I 	NULL		bind	NULL				eIF-4E	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_31_18531_s_266	7629182	A kinase that acted on both free  [H ]PHAS-I and [H ]PHAS-I  bound to eIF-4E eluted at relatively high concentrations of NaCl  (fraction 58).	bind
47325	1	10644	5	13	NULL	NULL	NULL	PDK1	GP		is a type of					kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_31_22033_s_140	10419529	A kinase, termed PDK1, that can phosphorylate Thr-308 only when Akt/PKB is bound to PIP3 has been purified and cloned.	bind
47327	2	10644	5	13	NULL	NULL	NULL	Akt/PKB	GP		bind					PIP3	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_31_22033_s_140	10419529	A kinase, termed PDK1, that can phosphorylate Thr-308 only when Akt/PKB is bound to PIP3 has been purified and cloned.	bind
47328	3	10644	5	13	NULL	NULL	NULL	PDK1	GP		phosphorylate								Thr-308		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_31_22033_s_140	10419529	A kinase, termed PDK1, that can phosphorylate Thr-308 only when Akt/PKB is bound to PIP3 has been purified and cloned.	bind
47332	4	10644	5	13	NULL	NULL	NULL	statement 3	Process		in the presence of		only			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_31_22033_s_140	10419529	A kinase, termed PDK1, that can phosphorylate Thr-308 only when Akt/PKB is bound to PIP3 has been purified and cloned.	bind
39775	1	10644	6	NULL	NULL	0	NULL	Akt/PKB	NULL		bind	NULL				PIP3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_31_22033_s_140	10419529	A kinase, termed PDK1, that can phosphorylate Thr-308 only when Akt/PKB is bound to PIP3 has been purified and cloned.	bind
39776	2	10644	6	NULL	NULL	0	NULL	PDK1	NULL		is a type of	NULL				kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_31_22033_s_140	10419529	A kinase, termed PDK1, that can phosphorylate Thr-308 only when Akt/PKB is bound to PIP3 has been purified and cloned.	bind
39777	3	10644	6	NULL	NULL	0	NULL	PDK1	NULL		phosphorylates	NULL					NULL		Thr-308		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_31_22033_s_140	10419529	A kinase, termed PDK1, that can phosphorylate Thr-308 only when Akt/PKB is bound to PIP3 has been purified and cloned.	bind
39778	4	10644	6	10	NULL	0	NULL	statement 3	NULL		occurs upon	NULL	only			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_31_22033_s_140	10419529	A kinase, termed PDK1, that can phosphorylate Thr-308 only when Akt/PKB is bound to PIP3 has been purified and cloned.	bind
47333	1	10647	5	13	NULL	NULL	NULL	Kidins220	GP		is localized to					plasma membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_281_27_16651260_s_5	16651260	A kinase-inactive mutant of PKD3 is only able to alter the localization  of Kidins220 at the plasma membrane when its C terminus has been substituted  by the PDZ-binding motif of PKD1 or PKD2.	bind
47334	2	10647	5	13	NULL	NULL	NULL	PKD3	GP		is substituted by			C terminus		PKD1	GP		PDZ-binding motif		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_281_27_16651260_s_5	16651260	A kinase-inactive mutant of PKD3 is only able to alter the localization  of Kidins220 at the plasma membrane when its C terminus has been substituted  by the PDZ-binding motif of PKD1 or PKD2.	bind
47336	3	10647	5	13	NULL	NULL	NULL	PKD3	GP		is substituted by			carboxyl terminus		PKD2	GP		PDZ-binding motif		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_281_27_16651260_s_5	16651260	A kinase-inactive mutant of PKD3 is only able to alter the localization  of Kidins220 at the plasma membrane when its C terminus has been substituted  by the PDZ-binding motif of PKD1 or PKD2.	bind
47338	4	10647	5	13	NULL	NULL	NULL	statement 2	Process		alters					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_281_27_16651260_s_5	16651260	A kinase-inactive mutant of PKD3 is only able to alter the localization  of Kidins220 at the plasma membrane when its C terminus has been substituted  by the PDZ-binding motif of PKD1 or PKD2.	bind
47339	5	10647	5	13	NULL	NULL	NULL	statement 3	Process		alters					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_281_27_16651260_s_5	16651260	A kinase-inactive mutant of PKD3 is only able to alter the localization  of Kidins220 at the plasma membrane when its C terminus has been substituted  by the PDZ-binding motif of PKD1 or PKD2.	bind
39886	1	10647	6	NULL	NULL	0	NULL	Kidins220	NULL		is localized at	NULL				plasma membrane	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_281_27_16651260_s_5	16651260	A kinase-inactive mutant of PKD3 is only able to alter the localization  of Kidins220 at the plasma membrane when its C terminus has been substituted  by the PDZ-binding motif of PKD1 or PKD2.	bind
39887	2	10647	6	NULL	NULL	0	NULL	PKD3	NULL		is substituted by	NULL		C-terminus		PKD1	NULL		PDZ-binding motif		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_281_27_16651260_s_5	16651260	A kinase-inactive mutant of PKD3 is only able to alter the localization  of Kidins220 at the plasma membrane when its C terminus has been substituted  by the PDZ-binding motif of PKD1 or PKD2.	bind
39888	3	10647	6	NULL	NULL	0	NULL	PKD3	NULL		is substituted by	NULL		C terminus		PKD2	NULL		PDZ-binding motif		NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_281_27_16651260_s_5	16651260	A kinase-inactive mutant of PKD3 is only able to alter the localization  of Kidins220 at the plasma membrane when its C terminus has been substituted  by the PDZ-binding motif of PKD1 or PKD2.	bind
39940	4	10647	6	NULL	NULL	0	NULL	statement 2	NULL		alters	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_281_27_16651260_s_5	16651260	A kinase-inactive mutant of PKD3 is only able to alter the localization  of Kidins220 at the plasma membrane when its C terminus has been substituted  by the PDZ-binding motif of PKD1 or PKD2.	bind
39941	5	10647	6	NULL	NULL	0	NULL	statement 3	NULL		alters	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_281_27_16651260_s_5	16651260	A kinase-inactive mutant of PKD3 is only able to alter the localization  of Kidins220 at the plasma membrane when its C terminus has been substituted  by the PDZ-binding motif of PKD1 or PKD2.	bind
47340	1	10648	5	13	NULL	NULL	NULL	kinectin isoform	GP		lacks							major portion of	kinesin-binding domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_34_32115_s_3	12773547	A kinectin isoform that lacks a major portion of the  kinesin-binding domain does not bind kinesin but interacts with another  resident of the endoplasmic reticulum, the translation elongation factor-1  delta (EF-1delta).	bind
47341	2	10648	5	13	NULL	NULL	NULL	statement 1	GP		does not bind					kinesin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_34_32115_s_3	12773547	A kinectin isoform that lacks a major portion of the  kinesin-binding domain does not bind kinesin but interacts with another  resident of the endoplasmic reticulum, the translation elongation factor-1  delta (EF-1delta).	bind
47342	3	10648	5	13	NULL	NULL	NULL	statement 1	GP		interacts with					EF-1delta	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_34_32115_s_3	12773547	A kinectin isoform that lacks a major portion of the  kinesin-binding domain does not bind kinesin but interacts with another  resident of the endoplasmic reticulum, the translation elongation factor-1  delta (EF-1delta).	bind
47343	4	10648	5	13	NULL	NULL	NULL	EF-1delta	GP		is					translation elongation factor-1 delta	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_34_32115_s_3	12773547	A kinectin isoform that lacks a major portion of the  kinesin-binding domain does not bind kinesin but interacts with another  resident of the endoplasmic reticulum, the translation elongation factor-1  delta (EF-1delta).	bind
47344	5	10648	5	13	NULL	NULL	NULL	EF-1delta	GP		resides in					endoplasmic reticulum	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_34_32115_s_3	12773547	A kinectin isoform that lacks a major portion of the  kinesin-binding domain does not bind kinesin but interacts with another  resident of the endoplasmic reticulum, the translation elongation factor-1  delta (EF-1delta).	bind
39779	5	10648	6	10	NULL	0	NULL	statement 1	NULL		does not bind	NULL				kinesin	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_34_32115_s_3	12773547	A kinectin isoform that lacks a major portion of the  kinesin-binding domain does not bind kinesin but interacts with another  resident of the endoplasmic reticulum, the translation elongation factor-1  delta (EF-1delta).	bind
39780	2	10648	6	10	NULL	0	NULL	statement 1	NULL		interacts with	NULL				translation EF-1delta	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_34_32115_s_3	12773547	A kinectin isoform that lacks a major portion of the  kinesin-binding domain does not bind kinesin but interacts with another  resident of the endoplasmic reticulum, the translation elongation factor-1  delta (EF-1delta).	bind
39781	3	10648	6	NULL	NULL	0	NULL	EF-1delta	NULL		is	NULL				elongation factor-1 delta	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_32115_s_3	12773547	A kinectin isoform that lacks a major portion of the  kinesin-binding domain does not bind kinesin but interacts with another  resident of the endoplasmic reticulum, the translation elongation factor-1  delta (EF-1delta).	bind
39782	4	10648	6	NULL	NULL	0	NULL	EF-1delta	NULL		resides in	NULL				endoplasmic reticulum	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_32115_s_3	12773547	A kinectin isoform that lacks a major portion of the  kinesin-binding domain does not bind kinesin but interacts with another  resident of the endoplasmic reticulum, the translation elongation factor-1  delta (EF-1delta).	bind
50011	1	10648	6	10	NULL	0	NULL	kinectin isoform	NULL		lacks	NULL					NULL	major portion of	kinesin-binding domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_32115_s_3	12773547	A kinectin isoform that lacks a major portion of the  kinesin-binding domain does not bind kinesin but interacts with another  resident of the endoplasmic reticulum, the translation elongation factor-1  delta (EF-1delta).	bind
47345	1	10650	5	13	NULL	NULL	NULL	Rabkinesin-6	GP		is a type of					kinesin-like protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_14_7933_s_190	10859366	A kinesin-like protein, termed Rabkinesin-6, has recently been identified that interacts with the GTP-bound forms of Rab6 ( 50).	bind
47346	2	10650	5	13	NULL	NULL	NULL	Rab6	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_14_7933_s_190	10859366	A kinesin-like protein, termed Rabkinesin-6, has recently been identified that interacts with the GTP-bound forms of Rab6 ( 50).	bind
47348	3	10650	5	13	NULL	NULL	NULL	Rabkinesin-6	GP		interacts with					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_14_7933_s_190	10859366	A kinesin-like protein, termed Rabkinesin-6, has recently been identified that interacts with the GTP-bound forms of Rab6 ( 50).	bind
39783	1	10650	6	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				Rab6	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_14_7933_s_190	10859366	A kinesin-like protein, termed Rabkinesin-6, has recently been identified that interacts with the GTP-bound forms of Rab6 ( 50).	bind
39784	2	10650	6	NULL	NULL	0	NULL	Rabkinesin-6	NULL		interacts with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_14_7933_s_190	10859366	A kinesin-like protein, termed Rabkinesin-6, has recently been identified that interacts with the GTP-bound forms of Rab6 ( 50).	bind
39785	3	10650	6	NULL	NULL	0	NULL	Rabkinesin-6	NULL		is a type of	NULL				kinesin-like protein	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_14_7933_s_190	10859366	A kinesin-like protein, termed Rabkinesin-6, has recently been identified that interacts with the GTP-bound forms of Rab6 ( 50).	bind
47379	1	10651	5	13	NULL	NULL	NULL	HNF-6	GP		bind									HNF-3beta site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_22_13552_s_287	9593691	A kinetic analysis of HNF-6 binding to the HNF-3beta site showed that this difference results from a strong effect of linker length on the docking ( kon of HNF-6beta 60-fold higherR than that of HNF-6alpha) without much influence on the stability of the complex ( koff of HNF-6beta 3-fold higherR than that of HNF-6alpha).	bind
39954	1	10651	6	NULL	NULL	0	NULL	HNF-6	NULL		bind	NULL					NULL			HNF-3beta site	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_22_13552_s_287	9593691	A kinetic analysis of HNF-6 binding to the HNF-3beta site showed that this difference results from a strong effect of linker length on the docking ( kon of HNF-6beta 60-fold higherR than that of HNF-6alpha) without much influence on the stability of the complex ( koff of HNF-6beta 3-fold higherR than that of HNF-6alpha).	bind
47380	1	10652	5	13	NULL	NULL	NULL	siglec-2	GP	mouse	bind					Neu5Gc	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_8633_s_10	10722703	A known evolutionary difference is the strong preference of mouse siglec-2 (CD22) for Neu5Gc, contrasting with human siglec-2, which binds Neu5Ac equally well.	bind
47381	2	10652	5	13	NULL	NULL	NULL	siglec-2	GP	human	bind					Neu5Ac	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_8633_s_10	10722703	A known evolutionary difference is the strong preference of mouse siglec-2 (CD22) for Neu5Gc, contrasting with human siglec-2, which binds Neu5Ac equally well.	bind
47382	3	10652	5	13	NULL	NULL	NULL	statement 1	Process	affinity of	is equal to					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_8633_s_10	10722703	A known evolutionary difference is the strong preference of mouse siglec-2 (CD22) for Neu5Gc, contrasting with human siglec-2, which binds Neu5Ac equally well.	bind
47383	4	10652	5	13	NULL	NULL	NULL	statement 1	Process		is prefered over					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_8633_s_10	10722703	A known evolutionary difference is the strong preference of mouse siglec-2 (CD22) for Neu5Gc, contrasting with human siglec-2, which binds Neu5Ac equally well.	bind
47387	5	10652	5	13	NULL	NULL	NULL	CD22	GP		is 					siglec-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_12_8633_s_10	10722703	A known evolutionary difference is the strong preference of mouse siglec-2 (CD22) for Neu5Gc, contrasting with human siglec-2, which binds Neu5Ac equally well.	bind
39831	1	10652	6	NULL	NULL	0	NULL	siglec-2	NULL		is	NULL				CD22	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_12_8633_s_10	10722703	A known evolutionary difference is the strong preference of mouse siglec-2 (CD22) for Neu5Gc, contrasting with human siglec-2, which binds Neu5Ac equally well.	bind
39832	2	10652	6	NULL	NULL	0	NULL	siglec-2	NULL	mouse	bind	NULL				Neu5Gc	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_12_8633_s_10	10722703	A known evolutionary difference is the strong preference of mouse siglec-2 (CD22) for Neu5Gc, contrasting with human siglec-2, which binds Neu5Ac equally well.	bind
39833	3	10652	6	NULL	NULL	0	NULL	siglec-2	NULL	human	bind	NULL				Neu5Ac	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_12_8633_s_10	10722703	A known evolutionary difference is the strong preference of mouse siglec-2 (CD22) for Neu5Gc, contrasting with human siglec-2, which binds Neu5Ac equally well.	bind
39834	4	10652	6	NULL	NULL	0	NULL	statement 2	NULL	affinity of	is equal to	NULL				statement 3	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_12_8633_s_10	10722703	A known evolutionary difference is the strong preference of mouse siglec-2 (CD22) for Neu5Gc, contrasting with human siglec-2, which binds Neu5Ac equally well.	bind
50012	5	10652	6	10	NULL	0	NULL	statement 2	NULL		is preferred over	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_12_8633_s_10	10722703	A known evolutionary difference is the strong preference of mouse siglec-2 (CD22) for Neu5Gc, contrasting with human siglec-2, which binds Neu5Ac equally well.	bind
47386	1	10653	5	13	NULL	NULL	NULL	TBC 1269	Chemical		is a type of					L-selectin antagonist	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_5_2_123_s_356	12650770	A known L-selectin antagonist, TBC 1269, not only inhibits RSV infectivity, but also inhibits annexin II-binding to its ligands, plasminogen and heparin indicating that the binding of annexin II to these three ligands is through a similar or closely associated site.	bind
47388	2	10653	5	13	NULL	NULL	NULL	TBC 1269	Chemical		inhibit					RSV 	Organism	infectivity of			NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_5_2_123_s_356	12650770	A known L-selectin antagonist, TBC 1269, not only inhibits RSV infectivity, but also inhibits annexin II-binding to its ligands, plasminogen and heparin indicating that the binding of annexin II to these three ligands is through a similar or closely associated site.	bind
47389	3	10653	5	13	NULL	NULL	NULL	annexin II	GP		bind					plasminogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_5_2_123_s_356	12650770	A known L-selectin antagonist, TBC 1269, not only inhibits RSV infectivity, but also inhibits annexin II-binding to its ligands, plasminogen and heparin indicating that the binding of annexin II to these three ligands is through a similar or closely associated site.	bind
47390	4	10653	5	13	NULL	NULL	NULL	annexin II	GP		bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_5_2_123_s_356	12650770	A known L-selectin antagonist, TBC 1269, not only inhibits RSV infectivity, but also inhibits annexin II-binding to its ligands, plasminogen and heparin indicating that the binding of annexin II to these three ligands is through a similar or closely associated site.	bind
47391	5	10653	5	13	NULL	NULL	NULL	TBC 1269	Chemical		inhibit					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_5_2_123_s_356	12650770	A known L-selectin antagonist, TBC 1269, not only inhibits RSV infectivity, but also inhibits annexin II-binding to its ligands, plasminogen and heparin indicating that the binding of annexin II to these three ligands is through a similar or closely associated site.	bind
47392	6	10653	5	13	NULL	NULL	NULL	TBC 1269	Chemical		inhibit					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_5_2_123_s_356	12650770	A known L-selectin antagonist, TBC 1269, not only inhibits RSV infectivity, but also inhibits annexin II-binding to its ligands, plasminogen and heparin indicating that the binding of annexin II to these three ligands is through a similar or closely associated site.	bind
47396	7	10653	5	13	NULL	NULL	NULL	plasminogen	GP		is a type of					ligand	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_5_2_123_s_356	12650770	A known L-selectin antagonist, TBC 1269, not only inhibits RSV infectivity, but also inhibits annexin II-binding to its ligands, plasminogen and heparin indicating that the binding of annexin II to these three ligands is through a similar or closely associated site.	bind
47397	8	10653	5	13	NULL	NULL	NULL	heparin	Chemical		is a type of					ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_5_2_123_s_356	12650770	A known L-selectin antagonist, TBC 1269, not only inhibits RSV infectivity, but also inhibits annexin II-binding to its ligands, plasminogen and heparin indicating that the binding of annexin II to these three ligands is through a similar or closely associated site.	bind
39955	1	10653	6	NULL	NULL	0	NULL	TBC 1269	NULL		is a type of	NULL				L-selectin antagonist	NULL				NULL		0	NULL	NULL	NULL	gw60_microbesinfect_5_2_123_s_356	12650770	A known L-selectin antagonist, TBC 1269, not only inhibits RSV infectivity, but also inhibits annexin II-binding to its ligands, plasminogen and heparin indicating that the binding of annexin II to these three ligands is through a similar or closely associated site.	bind
39956	2	10653	6	10	NULL	0	NULL	TBC 1269			inhibits					RSV		infectivity of			NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_5_2_123_s_356	12650770	A known L-selectin antagonist, TBC 1269, not only inhibits RSV infectivity, but also inhibits annexin II-binding to its ligands, plasminogen and heparin indicating that the binding of annexin II to these three ligands is through a similar or closely associated site.	bind
39957	3	10653	6	NULL	NULL	0	NULL	annexin II	NULL		bind	NULL				plasminogen	NULL				NULL		0	NULL	NULL	NULL	gw60_microbesinfect_5_2_123_s_356	12650770	A known L-selectin antagonist, TBC 1269, not only inhibits RSV infectivity, but also inhibits annexin II-binding to its ligands, plasminogen and heparin indicating that the binding of annexin II to these three ligands is through a similar or closely associated site.	bind
39958	4	10653	6	NULL	NULL	0	NULL	annexin II	NULL		bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_microbesinfect_5_2_123_s_356	12650770	A known L-selectin antagonist, TBC 1269, not only inhibits RSV infectivity, but also inhibits annexin II-binding to its ligands, plasminogen and heparin indicating that the binding of annexin II to these three ligands is through a similar or closely associated site.	bind
39959	5	10653	6	NULL	NULL	0	NULL	TBC 1269	NULL		inhibits	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_microbesinfect_5_2_123_s_356	12650770	A known L-selectin antagonist, TBC 1269, not only inhibits RSV infectivity, but also inhibits annexin II-binding to its ligands, plasminogen and heparin indicating that the binding of annexin II to these three ligands is through a similar or closely associated site.	bind
39960	6	10653	6	NULL	NULL	0	NULL	TBC 1269	NULL		inhibits	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_microbesinfect_5_2_123_s_356	12650770	A known L-selectin antagonist, TBC 1269, not only inhibits RSV infectivity, but also inhibits annexin II-binding to its ligands, plasminogen and heparin indicating that the binding of annexin II to these three ligands is through a similar or closely associated site.	bind
47398	1	10654	5	13	NULL	NULL	NULL	KRAB-ZFP	GP		bind		sequence specifically	C2H2 zinc fingers		DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18000_s_383	10748030	A KRAB-ZFP binds target gene DNA sequence-specifically through its array of C2H2 zinc fingers.	bind
39835	1	10654	6	NULL	NULL	0	NULL	KRAB-ZFP	NULL		bind	NULL	sequence specifically	C2H2 zinc fingers		DNA 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_24_18000_s_383	10748030	A KRAB-ZFP binds target gene DNA sequence-specifically through its array of C2H2 zinc fingers.	bind
47399	1	10655	5	13	NULL	NULL	NULL	I-RNA	NucleicAcid	yeast	bind		strongly			La antigen	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_36_27531_s_340	10856291	A La depletion/add-back approach was also employed by Das  et al. ( 50) during their studies on the inhibition of the HCV IRES-mediated translation by yeast I-RNA, which strongly binds human La antigen.	bind
47400	2	10655	5	13	NULL	NULL	NULL	IRES	NucleicAcid		mediates					HCV	Organism	translation of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_36_27531_s_340	10856291	A La depletion/add-back approach was also employed by Das  et al. ( 50) during their studies on the inhibition of the HCV IRES-mediated translation by yeast I-RNA, which strongly binds human La antigen.	bind
47401	3	10655	5	13	NULL	NULL	NULL	I-RNA	NucleicAcid	yeast	inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_36_27531_s_340	10856291	A La depletion/add-back approach was also employed by Das  et al. ( 50) during their studies on the inhibition of the HCV IRES-mediated translation by yeast I-RNA, which strongly binds human La antigen.	bind
39836	1	10655	6	NULL	NULL	0	NULL	I-RNA	NULL	yeast	bind	NULL	strongly			La antigen	NULL	human			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27531_s_340	10856291	A La depletion/add-back approach was also employed by Das  et al. ( 50) during their studies on the inhibition of the HCV IRES-mediated translation by yeast I-RNA, which strongly binds human La antigen.	bind
39837	2	10655	6	NULL	NULL	0	NULL	IRES	NULL		mediates	NULL				HCV	NULL	translation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27531_s_340	10856291	A La depletion/add-back approach was also employed by Das  et al. ( 50) during their studies on the inhibition of the HCV IRES-mediated translation by yeast I-RNA, which strongly binds human La antigen.	bind
39838	3	10655	6	NULL	NULL	0	NULL	I-RNA	NULL	yeast	inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27531_s_340	10856291	A La depletion/add-back approach was also employed by Das  et al. ( 50) during their studies on the inhibition of the HCV IRES-mediated translation by yeast I-RNA, which strongly binds human La antigen.	bind
47402	1	10656	5	13	NULL	NULL	NULL	Ad5 origin fragment	NucleicAcid	labeled	bind					GST-POU	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_6_3398_s_164	9013582	A labeled Ad5 origin fragment bound by GST-POU was immobilized on GA beads (Fig.  5 A).	bind
39839	1	10656	6	NULL	NULL	0	NULL	Ad5 origin fragment	NULL		bind	NULL				GST-POU	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_6_3398_s_164	9013582	A labeled Ad5 origin fragment bound by GST-POU was immobilized on GA beads (Fig.  5 A).	bind
47403	1	10657	5	13	NULL	NULL	NULL	oligonucleotide	NucleicAcid	mutant;;labeled	does not bind				PU.1 site (P106M)	PU.1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_13_9098_s_199	10085160	A labeled oligonucleotide mutated at the PU.1 site (P106M) did not bind PU.1 ( lane 8) and a labeled Sp1 mutant (S91M) did not bind Sp1 ( lane 9).	bind
47404	2	10657	5	13	NULL	NULL	NULL	Sp1	GP	mutant;;labeled	does not bind			S91M		Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_13_9098_s_199	10085160	A labeled oligonucleotide mutated at the PU.1 site (P106M) did not bind PU.1 ( lane 8) and a labeled Sp1 mutant (S91M) did not bind Sp1 ( lane 9).	bind
39840	1	10657	6	NULL	NULL	0	NULL	oligonucleotide	NULL	mutant	does not bind	NULL			PU.1 site (P106M)	PU.1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_13_9098_s_199	10085160	A labeled oligonucleotide mutated at the PU.1 site (P106M) did not bind PU.1 ( lane 8) and a labeled Sp1 mutant (S91M) did not bind Sp1 ( lane 9).	bind
39841	2	10657	6	10	NULL	0	NULL	Sp1	NULL	mutant;;labeled	does not bind	NULL		S91M		Sp1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_13_9098_s_199	10085160	A labeled oligonucleotide mutated at the PU.1 site (P106M) did not bind PU.1 ( lane 8) and a labeled Sp1 mutant (S91M) did not bind Sp1 ( lane 9).	bind
47405	1	10659	5	13	NULL	NULL	NULL	Hu HB-EGF	GP	recombinant;;mature	is identical to			63 to 148		HB-EGF	GP	mature;;monkey			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2344_s_51	11953369	A laboratory earlier reported that recombinant mature Hu HB-EGF (residues 63 to 148), which is identical to the mature Mk HB-EGF (except that Asn87 of human is replaced with Ser87 in the monkey [Fig.  1]), strongly inhibits the binding of radiolabeled DT to toxin receptor-bearing cells ( 26).	bind
47406	2	10659	5	13	NULL	NULL	NULL	cells	Cell		bear					toxin receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2344_s_51	11953369	A laboratory earlier reported that recombinant mature Hu HB-EGF (residues 63 to 148), which is identical to the mature Mk HB-EGF (except that Asn87 of human is replaced with Ser87 in the monkey [Fig.  1]), strongly inhibits the binding of radiolabeled DT to toxin receptor-bearing cells ( 26).	bind
47407	3	10659	5	13	NULL	NULL	NULL	DT	GP	radiolabeled	bind					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2344_s_51	11953369	A laboratory earlier reported that recombinant mature Hu HB-EGF (residues 63 to 148), which is identical to the mature Mk HB-EGF (except that Asn87 of human is replaced with Ser87 in the monkey [Fig.  1]), strongly inhibits the binding of radiolabeled DT to toxin receptor-bearing cells ( 26).	bind
47408	4	10659	5	13	NULL	NULL	NULL	statement 1	Process		inhibit		strongly			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2344_s_51	11953369	A laboratory earlier reported that recombinant mature Hu HB-EGF (residues 63 to 148), which is identical to the mature Mk HB-EGF (except that Asn87 of human is replaced with Ser87 in the monkey [Fig.  1]), strongly inhibits the binding of radiolabeled DT to toxin receptor-bearing cells ( 26).	bind
39971	1	10659	6	NULL	NULL	0	NULL	DT	NULL	radiolabeled	bind	NULL				toxin receptor-bearing cells	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2344_s_51	11953369	A laboratory earlier reported that recombinant mature Hu HB-EGF (residues 63 to 148), which is identical to the mature Mk HB-EGF (except that Asn87 of human is replaced with Ser87 in the monkey [Fig.  1]), strongly inhibits the binding of radiolabeled DT to toxin receptor-bearing cells ( 26).	bind
39973	2	10659	6	NULL	NULL	0	NULL	HB-EGF	NULL	recombinant;; mature;; human	inhibits	NULL	strongly	residues 63 to 148		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2344_s_51	11953369	A laboratory earlier reported that recombinant mature Hu HB-EGF (residues 63 to 148), which is identical to the mature Mk HB-EGF (except that Asn87 of human is replaced with Ser87 in the monkey [Fig.  1]), strongly inhibits the binding of radiolabeled DT to toxin receptor-bearing cells ( 26).	bind
39974	3	10659	6	NULL	NULL	0	NULL	HB-EGF	NULL	recombinant;; mature;; human	is identical to	NULL				HB-EGF	NULL	mature;; monkey			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2344_s_51	11953369	A laboratory earlier reported that recombinant mature Hu HB-EGF (residues 63 to 148), which is identical to the mature Mk HB-EGF (except that Asn87 of human is replaced with Ser87 in the monkey [Fig.  1]), strongly inhibits the binding of radiolabeled DT to toxin receptor-bearing cells ( 26).	bind
47409	1	10661	5	13	NULL	NULL	NULL	ephedrine	Chemical		bind					beta3-adrenoreceptors	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_clin-sci-(lond)_96_5_10209080_s_11	10209080	A lack  of binding of ephedrine to beta3-adrenoreceptors and the observed decrease  in urinary noradrenaline during ephedrine treatment suggest that the thermogenic  effect of ephedrine results from direct beta1-/beta2-adrenoreceptor agonism.	bind
47410	2	10661	5	13	NULL	NULL	NULL	statement 1	Process		occurs during					ephedrine	Chemical	treatment			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_clin-sci-(lond)_96_5_10209080_s_11	10209080	A lack  of binding of ephedrine to beta3-adrenoreceptors and the observed decrease  in urinary noradrenaline during ephedrine treatment suggest that the thermogenic  effect of ephedrine results from direct beta1-/beta2-adrenoreceptor agonism.	bind
47411	3	10661	5	13	NULL	NULL	NULL	ephedrine	Chemical	treatment with	decreases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_clin-sci-(lond)_96_5_10209080_s_11	10209080	A lack  of binding of ephedrine to beta3-adrenoreceptors and the observed decrease  in urinary noradrenaline during ephedrine treatment suggest that the thermogenic  effect of ephedrine results from direct beta1-/beta2-adrenoreceptor agonism.	bind
47412	4	10661	5	13	NULL	NULL	NULL	ephedrine	Chemical		possess					thermogenic effect					NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_clin-sci-(lond)_96_5_10209080_s_11	10209080	A lack  of binding of ephedrine to beta3-adrenoreceptors and the observed decrease  in urinary noradrenaline during ephedrine treatment suggest that the thermogenic  effect of ephedrine results from direct beta1-/beta2-adrenoreceptor agonism.	bind
47413	5	10661	5	13	NULL	NULL	NULL	statement 4	Process		results from					beta1-/beta2-adrenoreceptor agonism	Process	direct			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_clin-sci-(lond)_96_5_10209080_s_11	10209080	A lack  of binding of ephedrine to beta3-adrenoreceptors and the observed decrease  in urinary noradrenaline during ephedrine treatment suggest that the thermogenic  effect of ephedrine results from direct beta1-/beta2-adrenoreceptor agonism.	bind
39975	1	10661	6	NULL	NULL	0	NULL	ephedrine	NULL		bind	NULL				beta3-adrenoreceptors	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_clin-sci-(lond)_96_5_10209080_s_11	10209080	A lack  of binding of ephedrine to beta3-adrenoreceptors and the observed decrease  in urinary noradrenaline during ephedrine treatment suggest that the thermogenic  effect of ephedrine results from direct beta1-/beta2-adrenoreceptor agonism.	bind
39976	2	10661	6	NULL	NULL	0	NULL	ephedrine	NULL	treatment with	decreases	NULL				noradrenaline 	NULL	urinary			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_clin-sci-(lond)_96_5_10209080_s_11	10209080	A lack  of binding of ephedrine to beta3-adrenoreceptors and the observed decrease  in urinary noradrenaline during ephedrine treatment suggest that the thermogenic  effect of ephedrine results from direct beta1-/beta2-adrenoreceptor agonism.	bind
39977	3	10661	6	NULL	NULL	0	NULL	ephedrine	NULL	treatment with	decreases	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_clin-sci-(lond)_96_5_10209080_s_11	10209080	A lack  of binding of ephedrine to beta3-adrenoreceptors and the observed decrease  in urinary noradrenaline during ephedrine treatment suggest that the thermogenic  effect of ephedrine results from direct beta1-/beta2-adrenoreceptor agonism.	bind
39980	4	10661	6	10	NULL	0	NULL	ephedrine	NULL		possess	NULL				thermogenic effect	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_clin-sci-(lond)_96_5_10209080_s_11	10209080	A lack  of binding of ephedrine to beta3-adrenoreceptors and the observed decrease  in urinary noradrenaline during ephedrine treatment suggest that the thermogenic  effect of ephedrine results from direct beta1-/beta2-adrenoreceptor agonism.	bind
39981	5	10661	6	NULL	NULL	0	NULL	statement 4	NULL		results from	NULL				beta1-/beta2-adrenoreceptor agonism	NULL	direct			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_clin-sci-(lond)_96_5_10209080_s_11	10209080	A lack  of binding of ephedrine to beta3-adrenoreceptors and the observed decrease  in urinary noradrenaline during ephedrine treatment suggest that the thermogenic  effect of ephedrine results from direct beta1-/beta2-adrenoreceptor agonism.	bind
47416	1	10662	5	13	NULL	NULL	NULL	Mgat3 T37 gene	GP		express					GlcNAc-TIII activity	GP				NULL	LEC10 CHO cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_29_26300_s_228	11986323	A lack of a dominant-negative effect was confirmed by overexpressing a cDNA encoding the  Mgat3 T37 gene in LEC10 CHO cells, which express GlcNAc-TIII activity ( 3), due to a gain-of-function mutation that activates transcription of the endogenous  Mgat3 gene.	bind
47418	2	10662	5	13	NULL	NULL	NULL	function mutation	Process		activates					Mgat3 gene	GP	transcription of;;endogenous			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_29_26300_s_228	11986323	A lack of a dominant-negative effect was confirmed by overexpressing a cDNA encoding the  Mgat3 T37 gene in LEC10 CHO cells, which express GlcNAc-TIII activity ( 3), due to a gain-of-function mutation that activates transcription of the endogenous  Mgat3 gene.	bind
39982	1	10662	6	10	NULL	0	NULL	Mgat3 T37 gene	NULL		express	NULL				GlcNAc-TIII activity	NULL				NULL	LEC10 CHO cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_29_26300_s_228	11986323	A lack of a dominant-negative effect was confirmed by overexpressing a cDNA encoding the  Mgat3 T37 gene in LEC10 CHO cells, which express GlcNAc-TIII activity ( 3), due to a gain-of-function mutation that activates transcription of the endogenous  Mgat3 gene.	bind
50248	2	10662	6	10	NULL	0	NULL	function mutation	NULL		activates	NULL				Mgat3 gene	NULL	transcription of;; endogenous 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26300_s_228	11986323	A lack of a dominant-negative effect was confirmed by overexpressing a cDNA encoding the  Mgat3 T37 gene in LEC10 CHO cells, which express GlcNAc-TIII activity ( 3), due to a gain-of-function mutation that activates transcription of the endogenous  Mgat3 gene.	bind
47420	1	10663	5	13	NULL	NULL	NULL	actophorin	GP		does not bind					ADP-Pi filaments	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_22_15538_s_307	10336448	A lack of actophorin binding to ADP-Pi filaments and phalloidin-ADP filaments in pelleting assays establishes that the absence of a fluorescence signal is due to a lack of binding rather than failure of bound actophorin to induce a fluorescence change in pyrenyl ADP-Pi-actin filaments.	bind
47421	2	10663	5	13	NULL	NULL	NULL	actophorin	GP		does not bind					phalloidin-ADP filaments	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_22_15538_s_307	10336448	A lack of actophorin binding to ADP-Pi filaments and phalloidin-ADP filaments in pelleting assays establishes that the absence of a fluorescence signal is due to a lack of binding rather than failure of bound actophorin to induce a fluorescence change in pyrenyl ADP-Pi-actin filaments.	bind
39842	1	10663	6	NULL	NULL	0	NULL	actophorin	NULL		does not bind	NULL				ADP-pi filaments	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_22_15538_s_307	10336448	A lack of actophorin binding to ADP-Pi filaments and phalloidin-ADP filaments in pelleting assays establishes that the absence of a fluorescence signal is due to a lack of binding rather than failure of bound actophorin to induce a fluorescence change in pyrenyl ADP-Pi-actin filaments.	bind
39843	2	10663	6	NULL	NULL	0	NULL	actophorin	NULL		does not bind	NULL				phalloidin-ADP filaments	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_22_15538_s_307	10336448	A lack of actophorin binding to ADP-Pi filaments and phalloidin-ADP filaments in pelleting assays establishes that the absence of a fluorescence signal is due to a lack of binding rather than failure of bound actophorin to induce a fluorescence change in pyrenyl ADP-Pi-actin filaments.	bind
47423	1	10665	5	13	NULL	NULL	NULL	Sec9p/Sso1p	GP		bind					v-SNARE Sec22p	GP	ER-Golgi			NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_4_1643_s_163	10924463	A lack of specificity is seen in formation of the ternary complex, however, as Sec9p/Sso1p will bind to the ER-Golgi v-SNARE Sec22p ( D ASCHER et al. 1991   ;	bind
39997	1	10665	6	10	NULL	0	NULL	Sec9p/Sso1p	NULL		bind	NULL				v-SNARE Sec22p	NULL	ER-Golgi 			NULL		NULL	NULL	NULL	NULL	gw60_genetics_155_4_1643_s_163	10924463	A lack of specificity is seen in formation of the ternary complex, however, as Sec9p/Sso1p will bind to the ER-Golgi v-SNARE Sec22p ( D ASCHER et al. 1991   ;	bind
47424	1	10666	5	13	NULL	NULL	NULL	laminin	GP		bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_267_25_1387642_s_2	1387642	A laminin-binding peptide (peptide G), predicted from the cDNA sequence  for a 33-kDa protein related to the 67-kDa laminin receptor, specifically  inhibits binding of laminin to heparin and sulfatide.	bind
47425	2	10666	5	13	NULL	NULL	NULL	laminin	GP		bind					sulfatide	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_267_25_1387642_s_2	1387642	A laminin-binding peptide (peptide G), predicted from the cDNA sequence  for a 33-kDa protein related to the 67-kDa laminin receptor, specifically  inhibits binding of laminin to heparin and sulfatide.	bind
47426	3	10666	5	13	NULL	NULL	NULL	laminin-binding peptide	GP		inhibit		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_267_25_1387642_s_2	1387642	A laminin-binding peptide (peptide G), predicted from the cDNA sequence  for a 33-kDa protein related to the 67-kDa laminin receptor, specifically  inhibits binding of laminin to heparin and sulfatide.	bind
47427	4	10666	5	13	NULL	NULL	NULL	laminin-binding peptide	GP		inhibit		specifically			statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_267_25_1387642_s_2	1387642	A laminin-binding peptide (peptide G), predicted from the cDNA sequence  for a 33-kDa protein related to the 67-kDa laminin receptor, specifically  inhibits binding of laminin to heparin and sulfatide.	bind
50249	5	10666	5	13	NULL	NULL	NULL	peptide G	GP		is a type of					 laminin-binding peptide	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_267_25_1387642_s_2	1387642	A laminin-binding peptide (peptide G), predicted from the cDNA sequence  for a 33-kDa protein related to the 67-kDa laminin receptor, specifically  inhibits binding of laminin to heparin and sulfatide.	bind
40000	1	10666	6	NULL	NULL	0	NULL	laminin	NULL		bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_267_25_1387642_s_2	1387642	A laminin-binding peptide (peptide G), predicted from the cDNA sequence  for a 33-kDa protein related to the 67-kDa laminin receptor, specifically  inhibits binding of laminin to heparin and sulfatide.	bind
40001	2	10666	6	NULL	NULL	0	NULL	laminin	NULL		bind	NULL				sulfatide	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_267_25_1387642_s_2	1387642	A laminin-binding peptide (peptide G), predicted from the cDNA sequence  for a 33-kDa protein related to the 67-kDa laminin receptor, specifically  inhibits binding of laminin to heparin and sulfatide.	bind
40002	3	10666	6	10	NULL	0	NULL	laminin-binding peptide 	NULL		inhibits	NULL	specifically			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_267_25_1387642_s_2	1387642	A laminin-binding peptide (peptide G), predicted from the cDNA sequence  for a 33-kDa protein related to the 67-kDa laminin receptor, specifically  inhibits binding of laminin to heparin and sulfatide.	bind
40003	4	10666	6	10	NULL	0	NULL	laminin-binding peptide 	NULL		inhibits	NULL	specifically			statement 2	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_267_25_1387642_s_2	1387642	A laminin-binding peptide (peptide G), predicted from the cDNA sequence  for a 33-kDa protein related to the 67-kDa laminin receptor, specifically  inhibits binding of laminin to heparin and sulfatide.	bind
50250	5	10666	6	10	NULL	0	NULL	peptide G	NULL		is a type of	NULL				 laminin-binding peptide	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_267_25_1387642_s_2	1387642	A laminin-binding peptide (peptide G), predicted from the cDNA sequence  for a 33-kDa protein related to the 67-kDa laminin receptor, specifically  inhibits binding of laminin to heparin and sulfatide.	bind
47428	1	10667	5	13	NULL	NULL	NULL	ADAMTS4	GP	125I-labeled	bind					fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_31_32483_s_146	15161923	A large amount of 125I-labeled ADAMTS4 could bind to intact fibronectin-coated wells, whereas BSA-coated wells showed only back-ground binding.	bind
40007	1	10667	6	10	NULL	0	NULL	ADAMTS4		125I-labeled	bind					fibronectin					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_31_32483_s_146	15161923	A large amount of 125I-labeled ADAMTS4 could bind to intact fibronectin-coated wells, whereas BSA-coated wells showed only back-ground binding.	bind
47429	1	10668	5	13	NULL	NULL	NULL	IP(3)	Chemical		is					1,4,5-trisphosphate	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_biophys-j_89_2_15908571_s_2	15908571	A large amount of data and observations on inositol 1,4,5-trisphosphate  (IP(3)) binding to the IP(3) receptor/Ca(2+) channel, the steady-state  activity of the channel, and its inactivation by IP(3) can be explained  by assuming one activation and one inhibition module, both allosterically  operated by Ca(2+), IP(3), and ATP, and one adaptation element, driven  by IP(3), Ca(2+), and the interconversion between two possible conformations  of the receptor.	bind
47430	2	10668	5	13	NULL	NULL	NULL	IP(3)	Chemical		bind					IP(3) receptor/Ca(2+) channel	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_biophys-j_89_2_15908571_s_2	15908571	A large amount of data and observations on inositol 1,4,5-trisphosphate  (IP(3)) binding to the IP(3) receptor/Ca(2+) channel, the steady-state  activity of the channel, and its inactivation by IP(3) can be explained  by assuming one activation and one inhibition module, both allosterically  operated by Ca(2+), IP(3), and ATP, and one adaptation element, driven  by IP(3), Ca(2+), and the interconversion between two possible conformations  of the receptor.	bind
47431	3	10668	5	13	NULL	NULL	NULL	IP(3)	Chemical		inactivates					IP(3) receptor/Ca(2+) channel	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0580-0599_biophys-j_89_2_15908571_s_2	15908571	A large amount of data and observations on inositol 1,4,5-trisphosphate  (IP(3)) binding to the IP(3) receptor/Ca(2+) channel, the steady-state  activity of the channel, and its inactivation by IP(3) can be explained  by assuming one activation and one inhibition module, both allosterically  operated by Ca(2+), IP(3), and ATP, and one adaptation element, driven  by IP(3), Ca(2+), and the interconversion between two possible conformations  of the receptor.	bind
40399	1	10668	6	NULL	NULL	0	NULL	IP(3)	NULL		is	NULL				inositol 1,4,5-trisphosphate	NULL				NULL		0	NULL	NULL	NULL	abs-batch0580-0599_biophys-j_89_2_15908571_s_2	15908571	A large amount of data and observations on inositol 1,4,5-trisphosphate  (IP(3)) binding to the IP(3) receptor/Ca(2+) channel, the steady-state  activity of the channel, and its inactivation by IP(3) can be explained  by assuming one activation and one inhibition module, both allosterically  operated by Ca(2+), IP(3), and ATP, and one adaptation element, driven  by IP(3), Ca(2+), and the interconversion between two possible conformations  of the receptor.	bind
40400	2	10668	6	NULL	NULL	0	NULL	IP(3)	NULL		bind	NULL				IP(3) receptor/Ca(2+) channel	NULL				NULL		0	NULL	NULL	NULL	abs-batch0580-0599_biophys-j_89_2_15908571_s_2	15908571	A large amount of data and observations on inositol 1,4,5-trisphosphate  (IP(3)) binding to the IP(3) receptor/Ca(2+) channel, the steady-state  activity of the channel, and its inactivation by IP(3) can be explained  by assuming one activation and one inhibition module, both allosterically  operated by Ca(2+), IP(3), and ATP, and one adaptation element, driven  by IP(3), Ca(2+), and the interconversion between two possible conformations  of the receptor.	bind
40418	3	10668	6	NULL	NULL	0	NULL	IP(3)	NULL		inactivates	NULL				IP(3) receptor/Ca(2+) channel	NULL				NULL		0	NULL	NULL	NULL	abs-batch0580-0599_biophys-j_89_2_15908571_s_2	15908571	A large amount of data and observations on inositol 1,4,5-trisphosphate  (IP(3)) binding to the IP(3) receptor/Ca(2+) channel, the steady-state  activity of the channel, and its inactivation by IP(3) can be explained  by assuming one activation and one inhibition module, both allosterically  operated by Ca(2+), IP(3), and ATP, and one adaptation element, driven  by IP(3), Ca(2+), and the interconversion between two possible conformations  of the receptor.	bind
47432	1	10669	5	13	NULL	NULL	NULL	phosphate	Chemical		bind					L. casei TS	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-mol-biol_232_4_8371269_s_15	8371269	A large and a small P6(1)22 crystal form are observed for  both phosphate-bound and dUMP-bound L. casei TS.	bind
47433	2	10669	5	13	NULL	NULL	NULL	dUMP	Chemical		bind					L. casei TS	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-mol-biol_232_4_8371269_s_15	8371269	A large and a small P6(1)22 crystal form are observed for  both phosphate-bound and dUMP-bound L. casei TS.	bind
40012	1	10669	6	NULL	NULL	0	NULL	L. casei TS	NULL		bind	NULL				dUMP	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-mol-biol_232_4_8371269_s_15	8371269	A large and a small P6(1)22 crystal form are observed for  both phosphate-bound and dUMP-bound L. casei TS.	bind
40013	2	10669	6	NULL	NULL	0	NULL	L. casei TS	NULL		bind	NULL				phosphate	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-mol-biol_232_4_8371269_s_15	8371269	A large and a small P6(1)22 crystal form are observed for  both phosphate-bound and dUMP-bound L. casei TS.	bind
47434	1	10670	5	13	NULL	NULL	NULL	rhodopsin	GP		bind					arrestin	GP	visual			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_14_11703_s_180	11809770	A large conformational change has been suggested to occur when rhodopsin binds to visual arrestin, which could assemble many recognition elements to create a continuous receptor-binding surface ( 44).	bind
47435	2	10670	5	13	NULL	NULL	NULL	statement 1	GP		assemble					recognition elements	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_14_11703_s_180	11809770	A large conformational change has been suggested to occur when rhodopsin binds to visual arrestin, which could assemble many recognition elements to create a continuous receptor-binding surface ( 44).	bind
47436	3	10670	5	13	NULL	NULL	NULL	statement 2	Process		creates					receptor-binding surface	GP	continuous			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_14_11703_s_180	11809770	A large conformational change has been suggested to occur when rhodopsin binds to visual arrestin, which could assemble many recognition elements to create a continuous receptor-binding surface ( 44).	bind
40014	1	10670	6	NULL	NULL	0	NULL	rhodopsin	NULL		bind	NULL				arrestin	NULL	visual			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_14_11703_s_180	11809770	A large conformational change has been suggested to occur when rhodopsin binds to visual arrestin, which could assemble many recognition elements to create a continuous receptor-binding surface ( 44).	bind
40045	2	10670	6	NULL	NULL	0	NULL	statement 1	NULL		creates	NULL				conformational change	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_14_11703_s_180	11809770	A large conformational change has been suggested to occur when rhodopsin binds to visual arrestin, which could assemble many recognition elements to create a continuous receptor-binding surface ( 44).	bind
40046	3	10670	6	NULL	NULL	0	NULL	statement 2	NULL		creates	NULL				receptor-binding surface	NULL	continuous			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_14_11703_s_180	11809770	A large conformational change has been suggested to occur when rhodopsin binds to visual arrestin, which could assemble many recognition elements to create a continuous receptor-binding surface ( 44).	bind
40047	4	10670	6	NULL	NULL	0	NULL	statement 3	NULL		occurs via	NULL				recognition elements	NULL	assembly of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_14_11703_s_180	11809770	A large conformational change has been suggested to occur when rhodopsin binds to visual arrestin, which could assemble many recognition elements to create a continuous receptor-binding surface ( 44).	bind
47437	1	10671	5	13	NULL	NULL	NULL	Lin bone marrow cells	Cell		bind		specifically			Fc-FGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_2_241_s_44	12586067	A large fraction of Lin  bone marrow cells specifically binds the Fc-FGF fusion protein (B).	bind
47438	2	10671	5	13	NULL	NULL	NULL	Fc-FGF	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_2_241_s_44	12586067	A large fraction of Lin  bone marrow cells specifically binds the Fc-FGF fusion protein (B).	bind
40048	1	10671	6	10	NULL	0	NULL	Lin bone marrow cells	NULL		bind	NULL	specifically			Fc-FGF 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_devcell_4_2_241_s_44	12586067	A large fraction of Lin  bone marrow cells specifically binds the Fc-FGF fusion protein (B).	bind
50251	2	10671	6	10	NULL	0	NULL	Fc-FGF	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw60_devcell_4_2_241_s_44	12586067	A large fraction of Lin  bone marrow cells specifically binds the Fc-FGF fusion protein (B).	bind
47439	1	10672	5	13	NULL	NULL	NULL	DNA ligase IIIalpha	GP	mitochondrial	does not bind					XRCC1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_52_48978_s_258	11598119	A large fraction of the mtDNA ligase IIIalpha did not bind the XRCC1 column, suggesting that it may be associated with a protein that blocks this interaction.	bind
40050	1	10672	6	10	NULL	0	NULL	DNA ligase IIIalpha	NULL	mitochondrial 	does not bind	NULL				XRCC1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_52_48978_s_258	11598119	A large fraction of the mtDNA ligase IIIalpha did not bind the XRCC1 column, suggesting that it may be associated with a protein that blocks this interaction.	bind
48019	1	10673	5	13	NULL	NULL	NULL	8A6	GP		interacts with					CD36	GP		immunodominant domain (aa 155-183)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
48020	2	10673	5	13	NULL	NULL	NULL	statement 1	Process		blocks					CD36	GP	function of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
48021	3	10673	5	13	NULL	NULL	NULL	CD36 	GP		function in					TSP	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50765	4	10673	5	13	NULL	NULL	NULL	CD36	GP		function in					collagen	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50766	5	10673	5	13	NULL	NULL	NULL	CD36	GP		function in					malaria	MedicalFinding	cytoadhesion of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50767	6	10673	5	13	NULL	NULL	NULL	CD36	GP		function in					apoptotic cells	Cell	uptake of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50768	7	10673	5	13	NULL	NULL	NULL	CD36	GP		function in					Ox-LDL	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50769	8	10673	5	13	NULL	NULL	NULL	8A6	GP		is a type of					\tmonoclonal antibody against human CD36	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50770	9	10673	5	13	NULL	NULL	NULL	OKM5	GP		is a type of					monoclonal antibody against human CD36	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50771	10	10673	5	13	NULL	NULL	NULL	FA6-152	GP		is a type of					\tmonoclonal antibody against human CD36	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50772	11	10673	5	13	NULL	NULL	NULL	L103	GP		is a type of					monoclonal antibody against human CD36	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50773	12	10673	5	13	NULL	NULL	NULL	5F1	GP		is a type of					monoclonal antibody against human CD36	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50774	13	10673	5	13	NULL	NULL	NULL	Smphi	GP		is a type of					monoclonal antibody against human CD36	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50775	14	10673	5	13	NULL	NULL	NULL	ESIVC7	GP		is a type of					monoclonal antibody against human CD36	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50776	15	10673	5	13	NULL	NULL	NULL	10/5	GP		is a type of					monoclonal antibody against human CD36	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50777	16	10673	5	13	NULL	NULL	NULL	OKM5	GP		interacts with					CD36	GP		\timmunodominant domain (aa 155-183)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50778	17	10673	5	13	NULL	NULL	NULL	statement 16	Process		blocks					CD36	GP	function of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50779	18	10673	5	13	NULL	NULL	NULL	FA6-152	GP		interacts with					CD36	GP		immunodominant domain (aa 155-183)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50780	19	10673	5	13	NULL	NULL	NULL	statement 18	Process		blocks					CD36	GP	function of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50781	20	10673	5	13	NULL	NULL	NULL	L103	GP		interacts with					CD36	GP		immunodominant domain (aa 155-183)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50782	21	10673	5	13	NULL	NULL	NULL	statement 20	Process		blocks					CD36	GP	function of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50783	22	10673	5	13	NULL	NULL	NULL	5F1	GP		interacts with					CD36	GP		immunodominant domain (aa 155-183)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50784	23	10673	5	13	NULL	NULL	NULL	statement 22	Process		blocks					CD36	GP	function of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50785	24	10673	5	13	NULL	NULL	NULL	Smphi	GP		interacts with					CD36	GP		immunodominant domain (aa 155-183)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50786	25	10673	5	13	NULL	NULL	NULL	statement 24	Process		blocks					CD36	GP	function of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50787	26	10673	5	13	NULL	NULL	NULL	ESIVC7	GP		interacts with					CD36	GP		immunodominant domain (aa 155-183)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50788	27	10673	5	13	NULL	NULL	NULL	statement 26	Process		blocks					CD36	GP	function of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50789	28	10673	5	13	NULL	NULL	NULL	10/5	GP		interacts with					CD36	GP		immunodominant domain (aa 155-183)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50790	29	10673	5	13	NULL	NULL	NULL	statement 28	Process		blocks					CD36	GP	function of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
50791	30	10673	5	13	NULL	NULL	NULL	CD36	GP		function in					ROS	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40419	1	10673	6	NULL	NULL	0	NULL	CD36	NULL		function in	NULL				TSP	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40420	2	10673	6	NULL	NULL	0	NULL	CD36	NULL		functions in	NULL				collagen	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40421	3	10673	6	NULL	NULL	0	NULL	CD36	NULL		functions in	NULL				malaria	NULL	cytoadhesion of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40422	4	10673	6	NULL	NULL	0	NULL	CD36	NULL		functions in	NULL				apoptotic cells	NULL	uptake of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40423	5	10673	6	NULL	NULL	0	NULL	CD36	NULL		functions in	NULL				ROS	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40424	6	10673	6	NULL	NULL	0	NULL	CD36	NULL		functions in	NULL				Ox-LDL	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40425	7	10673	6	NULL	NULL	0	NULL	8A6	NULL		is a type of	NULL				monoclonal antibody against human CD36	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40426	8	10673	6	NULL	NULL	0	NULL	OKM5	NULL		is a type of	NULL				monoclonal antibody against human CD36	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40427	9	10673	6	NULL	NULL	0	NULL	FA6-152	NULL		is a type of	NULL				monoclonal antibody against human CD36	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40428	10	10673	6	NULL	NULL	0	NULL	L103	NULL		is a type of	NULL				monoclonal antibody against human CD36	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40429	11	10673	6	NULL	NULL	0	NULL	5F1	NULL		is a type of	NULL				monoclonal antibody against human CD36	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40430	12	10673	6	NULL	NULL	0	NULL	Smphi	NULL		is a type of	NULL				monoclonal antibody against human CD36	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40431	13	10673	6	NULL	NULL	0	NULL	ESIVC7	NULL		is a type of	NULL				monoclonal antibody against human CD36	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40432	14	10673	6	NULL	NULL	0	NULL	10/5	NULL		is a type of	NULL				monoclonal antibody against human CD36	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40433	15	10673	6	NULL	NULL	0	NULL	8A6	NULL		interacts with	NULL				CD36	NULL		immunodominant domain (aa 155-183)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40437	16	10673	6	NULL	NULL	0	NULL	statement 15	NULL		blocks	NULL				CD36	NULL	function of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40438	17	10673	6	NULL	NULL	0	NULL	OKM5	NULL		interacts with	NULL				CD36	NULL		immunodominant domain (aa 155-183)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40439	18	10673	6	NULL	NULL	0	NULL	statement 17	NULL		blocks	NULL				CD36	NULL	function of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40441	19	10673	6	NULL	NULL	0	NULL	FA6-152	NULL		interacts with	NULL				CD36	NULL		immunodominant domain (aa 155-183)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40443	20	10673	6	NULL	NULL	0	NULL	statement 19	NULL		blocks	NULL				CD36	NULL	function of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40444	21	10673	6	NULL	NULL	0	NULL	L103	NULL		interacts with	NULL				CD36	NULL		immunodominant domain (aa 155-183)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40445	22	10673	6	NULL	NULL	0	NULL	statement 21	NULL		blocks	NULL				CD36	NULL	function of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40446	23	10673	6	NULL	NULL	0	NULL	5F1	NULL		interacts with	NULL				CD36	NULL		immunodominant domain (aa 155-183)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40447	24	10673	6	NULL	NULL	0	NULL	statement 23	NULL		blocks	NULL				CD36	NULL	function of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40448	25	10673	6	NULL	NULL	0	NULL	Smphi	NULL		interacts with	NULL				CD36	NULL		immunodominant domain (aa 155-183)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40449	26	10673	6	NULL	NULL	0	NULL	statement 25	NULL		blocks	NULL				CD36	NULL	function of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40450	27	10673	6	NULL	NULL	0	NULL	ESIVC7	NULL		interacts with	NULL				CD36	NULL		immunodominant domain (aa 155-183)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40451	28	10673	6	NULL	NULL	0	NULL	statement 27	NULL		blocks	NULL				CD36	NULL	function of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40454	29	10673	6	NULL	NULL	0	NULL	10/5	NULL		interacts with	NULL				CD36	NULL		immunodominant domain (aa 155-183)		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
40456	30	10673	6	NULL	NULL	0	NULL	statement 29	NULL		blocks	NULL				CD36	NULL	function of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_34875_s_36	9857015	A large group of monoclonal antibodies raised in different laboratories against human CD36 ( e.g. 8A6, OKM5, FA6-152, L103, 5F1, Smphi, ESIVC7, and 10/5) have been shown to interact with an immunodominant domain spanning amino acids 155-183 ( 50,  51,  54) and to block numerous unrelated CD36 functions including TSP binding ( 52,  53), collagen binding ( 55), malaria cytoadhesion ( 56), uptake of apoptotic cells ( 44) and ROS ( 35), and Ox-LDL binding ( 25,  26).	bind
47440	1	10674	5	13	NULL	NULL	NULL	pericentrin B/kendrin	GP	large isoform	is homologous to					Spc110p	GP		calmodulin binding domain		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_8_3642_s_26	15146056	A large isoform (pericentrin B/kendrin; Flory and Davis, 2003 ) and another centrosome protein called AKAP450/GC-NAP share homology with the calmodulin binding domain of Spc110p (Flory  et al., 2000 ; Gillingham and Munro, 2000 ; Li  et al., 2001 ).	bind
47441	2	10674	5	13	NULL	NULL	NULL	AKAP450/GC-NAP	GP		is homologous to					Spc110p	GP		calmodulin binding domain		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_8_3642_s_26	15146056	A large isoform (pericentrin B/kendrin; Flory and Davis, 2003 ) and another centrosome protein called AKAP450/GC-NAP share homology with the calmodulin binding domain of Spc110p (Flory  et al., 2000 ; Gillingham and Munro, 2000 ; Li  et al., 2001 ).	bind
47442	3	10674	5	13	NULL	NULL	NULL	AKAP450/GC-NAP	GP		is a type of					centrosome protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_8_3642_s_26	15146056	A large isoform (pericentrin B/kendrin; Flory and Davis, 2003 ) and another centrosome protein called AKAP450/GC-NAP share homology with the calmodulin binding domain of Spc110p (Flory  et al., 2000 ; Gillingham and Munro, 2000 ; Li  et al., 2001 ).	bind
40051	1	10674	6	10	NULL	0	NULL	pericentrin B/kendrin	NULL	large isoform	is homologous to	NULL				Spc110p	NULL		calmodulin binding domain		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_8_3642_s_26	15146056	A large isoform (pericentrin B/kendrin; Flory and Davis, 2003 ) and another centrosome protein called AKAP450/GC-NAP share homology with the calmodulin binding domain of Spc110p (Flory  et al., 2000 ; Gillingham and Munro, 2000 ; Li  et al., 2001 ).	bind
40053	2	10674	6	NULL	NULL	0	NULL	AKAP450/GC-NAP	NULL		is a type of	NULL				centrosome protein	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3642_s_26	15146056	A large isoform (pericentrin B/kendrin; Flory and Davis, 2003 ) and another centrosome protein called AKAP450/GC-NAP share homology with the calmodulin binding domain of Spc110p (Flory  et al., 2000 ; Gillingham and Munro, 2000 ; Li  et al., 2001 ).	bind
40056	3	10674	6	NULL	NULL	0	NULL	AKAP450/GC-NAP	NULL		is homologous to	NULL				Spc110p	NULL		calmodulin binding domain		NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3642_s_26	15146056	A large isoform (pericentrin B/kendrin; Flory and Davis, 2003 ) and another centrosome protein called AKAP450/GC-NAP share homology with the calmodulin binding domain of Spc110p (Flory  et al., 2000 ; Gillingham and Munro, 2000 ; Li  et al., 2001 ).	bind
47445	1	10677	5	13	NULL	NULL	NULL	HCV peptide	GP		bind					HLA-A2	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_58_0_391_s_214	15487943	A large number of HCV epitopes have been identified either by predictive  algorithms for HCV peptide binding to common MHC molecules such as HLA-A2 ( 10, 16) or by mapping with virus-specific CD8+ T cell populations recovered from blood or  liver of infected individuals.	bind
47446	2	10677	5	13	NULL	NULL	NULL	HLA-A2	GP		is a type of					MHC molecule	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_58_0_391_s_214	15487943	A large number of HCV epitopes have been identified either by predictive  algorithms for HCV peptide binding to common MHC molecules such as HLA-A2 ( 10, 16) or by mapping with virus-specific CD8+ T cell populations recovered from blood or  liver of infected individuals.	bind
40411	1	10677	6	NULL	NULL	0	NULL	HCV peptide	NULL		bind	NULL				HLA-A2	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_58_0_391_s_214	15487943	A large number of HCV epitopes have been identified either by predictive  algorithms for HCV peptide binding to common MHC molecules such as HLA-A2 ( 10, 16) or by mapping with virus-specific CD8+ T cell populations recovered from blood or  liver of infected individuals.	bind
40412	2	10677	6	NULL	NULL	0	NULL	HLA-A2	NULL		is a type of	NULL				MHC molecules	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_58_0_391_s_214	15487943	A large number of HCV epitopes have been identified either by predictive  algorithms for HCV peptide binding to common MHC molecules such as HLA-A2 ( 10, 16) or by mapping with virus-specific CD8+ T cell populations recovered from blood or  liver of infected individuals.	bind
47447	1	10678	5	13	NULL	NULL	NULL	PcGs	GP		bind					neuronal differentiation genes	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_9_1123_s_157	16618801	A large number of neuronal differentiation genes are bound by PcGs (Table  1).	bind
40061	1	10678	6	10	NULL	0	NULL	PcGs	NULL		bind	NULL				 neuronal differentiation genes	NULL				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_20_9_1123_s_157	16618801	A large number of neuronal differentiation genes are bound by PcGs (Table  1).	bind
47448	1	10679	5	13	NULL	NULL	NULL	complexins	GP		bind					syntaxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_26_1_45_s_20	10798391	A large number of proteins have been identified which bind to SNARE proteins and have been implicated in regulating SNARE complex formation: complexins, Munc-13, Munc-18, syncollin, syntaphilin, and tomosyn bind to syntaxin; HRS-2 and snapin bind to SNAP-25; and VAP-33 binds to VAMP (   Skehel, 1995  ; Bean et al. 1997  ; Edwardson, 1997  ; Mochida et al., 2000).	bind
47449	2	10679	5	13	NULL	NULL	NULL	Munc-13	GP		bind					syntaxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_26_1_45_s_20	10798391	A large number of proteins have been identified which bind to SNARE proteins and have been implicated in regulating SNARE complex formation: complexins, Munc-13, Munc-18, syncollin, syntaphilin, and tomosyn bind to syntaxin; HRS-2 and snapin bind to SNAP-25; and VAP-33 binds to VAMP (   Skehel, 1995  ; Bean et al. 1997  ; Edwardson, 1997  ; Mochida et al., 2000).	bind
47450	3	10679	5	13	NULL	NULL	NULL	Munc-18	GP		bind					syntaxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_26_1_45_s_20	10798391	A large number of proteins have been identified which bind to SNARE proteins and have been implicated in regulating SNARE complex formation: complexins, Munc-13, Munc-18, syncollin, syntaphilin, and tomosyn bind to syntaxin; HRS-2 and snapin bind to SNAP-25; and VAP-33 binds to VAMP (   Skehel, 1995  ; Bean et al. 1997  ; Edwardson, 1997  ; Mochida et al., 2000).	bind
47451	4	10679	5	13	NULL	NULL	NULL	syncollin	GP		bind					syntaxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_26_1_45_s_20	10798391	A large number of proteins have been identified which bind to SNARE proteins and have been implicated in regulating SNARE complex formation: complexins, Munc-13, Munc-18, syncollin, syntaphilin, and tomosyn bind to syntaxin; HRS-2 and snapin bind to SNAP-25; and VAP-33 binds to VAMP (   Skehel, 1995  ; Bean et al. 1997  ; Edwardson, 1997  ; Mochida et al., 2000).	bind
47452	5	10679	5	13	NULL	NULL	NULL	syntaphilin	GP		bind					syntaxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_26_1_45_s_20	10798391	A large number of proteins have been identified which bind to SNARE proteins and have been implicated in regulating SNARE complex formation: complexins, Munc-13, Munc-18, syncollin, syntaphilin, and tomosyn bind to syntaxin; HRS-2 and snapin bind to SNAP-25; and VAP-33 binds to VAMP (   Skehel, 1995  ; Bean et al. 1997  ; Edwardson, 1997  ; Mochida et al., 2000).	bind
47453	6	10679	5	13	NULL	NULL	NULL	tomosyn	GP		bind					syntaxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_26_1_45_s_20	10798391	A large number of proteins have been identified which bind to SNARE proteins and have been implicated in regulating SNARE complex formation: complexins, Munc-13, Munc-18, syncollin, syntaphilin, and tomosyn bind to syntaxin; HRS-2 and snapin bind to SNAP-25; and VAP-33 binds to VAMP (   Skehel, 1995  ; Bean et al. 1997  ; Edwardson, 1997  ; Mochida et al., 2000).	bind
47454	7	10679	5	13	NULL	NULL	NULL	HRS-2	GP		bind					SNAP-25	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_26_1_45_s_20	10798391	A large number of proteins have been identified which bind to SNARE proteins and have been implicated in regulating SNARE complex formation: complexins, Munc-13, Munc-18, syncollin, syntaphilin, and tomosyn bind to syntaxin; HRS-2 and snapin bind to SNAP-25; and VAP-33 binds to VAMP (   Skehel, 1995  ; Bean et al. 1997  ; Edwardson, 1997  ; Mochida et al., 2000).	bind
47455	8	10679	5	13	NULL	NULL	NULL	snapin	GP		bind					SNAP-25	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_26_1_45_s_20	10798391	A large number of proteins have been identified which bind to SNARE proteins and have been implicated in regulating SNARE complex formation: complexins, Munc-13, Munc-18, syncollin, syntaphilin, and tomosyn bind to syntaxin; HRS-2 and snapin bind to SNAP-25; and VAP-33 binds to VAMP (   Skehel, 1995  ; Bean et al. 1997  ; Edwardson, 1997  ; Mochida et al., 2000).	bind
47456	9	10679	5	13	NULL	NULL	NULL	VAP-33	GP		bind					VAMP	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_26_1_45_s_20	10798391	A large number of proteins have been identified which bind to SNARE proteins and have been implicated in regulating SNARE complex formation: complexins, Munc-13, Munc-18, syncollin, syntaphilin, and tomosyn bind to syntaxin; HRS-2 and snapin bind to SNAP-25; and VAP-33 binds to VAMP (   Skehel, 1995  ; Bean et al. 1997  ; Edwardson, 1997  ; Mochida et al., 2000).	bind
40062	1	10679	6	NULL	NULL	0	NULL	complexins	NULL		bind	NULL				syntaxin	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_26_1_45_s_20	10798391	A large number of proteins have been identified which bind to SNARE proteins and have been implicated in regulating SNARE complex formation: complexins, Munc-13, Munc-18, syncollin, syntaphilin, and tomosyn bind to syntaxin; HRS-2 and snapin bind to SNAP-25; and VAP-33 binds to VAMP (   Skehel, 1995  ; Bean et al. 1997  ; Edwardson, 1997  ; Mochida et al., 2000).	bind
40063	2	10679	6	NULL	NULL	0	NULL	Munc-13	NULL		bind	NULL				syntaxin	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_26_1_45_s_20	10798391	A large number of proteins have been identified which bind to SNARE proteins and have been implicated in regulating SNARE complex formation: complexins, Munc-13, Munc-18, syncollin, syntaphilin, and tomosyn bind to syntaxin; HRS-2 and snapin bind to SNAP-25; and VAP-33 binds to VAMP (   Skehel, 1995  ; Bean et al. 1997  ; Edwardson, 1997  ; Mochida et al., 2000).	bind
40065	3	10679	6	NULL	NULL	0	NULL	Munc-18	NULL		bind	NULL				syntaxin	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_26_1_45_s_20	10798391	A large number of proteins have been identified which bind to SNARE proteins and have been implicated in regulating SNARE complex formation: complexins, Munc-13, Munc-18, syncollin, syntaphilin, and tomosyn bind to syntaxin; HRS-2 and snapin bind to SNAP-25; and VAP-33 binds to VAMP (   Skehel, 1995  ; Bean et al. 1997  ; Edwardson, 1997  ; Mochida et al., 2000).	bind
40067	4	10679	6	NULL	NULL	0	NULL	syncollin	NULL		bind	NULL				syntaxin	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_26_1_45_s_20	10798391	A large number of proteins have been identified which bind to SNARE proteins and have been implicated in regulating SNARE complex formation: complexins, Munc-13, Munc-18, syncollin, syntaphilin, and tomosyn bind to syntaxin; HRS-2 and snapin bind to SNAP-25; and VAP-33 binds to VAMP (   Skehel, 1995  ; Bean et al. 1997  ; Edwardson, 1997  ; Mochida et al., 2000).	bind
40069	5	10679	6	NULL	NULL	0	NULL	syntaphilin	NULL		bind	NULL				syntaxin	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_26_1_45_s_20	10798391	A large number of proteins have been identified which bind to SNARE proteins and have been implicated in regulating SNARE complex formation: complexins, Munc-13, Munc-18, syncollin, syntaphilin, and tomosyn bind to syntaxin; HRS-2 and snapin bind to SNAP-25; and VAP-33 binds to VAMP (   Skehel, 1995  ; Bean et al. 1997  ; Edwardson, 1997  ; Mochida et al., 2000).	bind
40070	6	10679	6	NULL	NULL	0	NULL	tomosyn	NULL		bind	NULL				syntaxin	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_26_1_45_s_20	10798391	A large number of proteins have been identified which bind to SNARE proteins and have been implicated in regulating SNARE complex formation: complexins, Munc-13, Munc-18, syncollin, syntaphilin, and tomosyn bind to syntaxin; HRS-2 and snapin bind to SNAP-25; and VAP-33 binds to VAMP (   Skehel, 1995  ; Bean et al. 1997  ; Edwardson, 1997  ; Mochida et al., 2000).	bind
40071	7	10679	6	NULL	NULL	0	NULL	HRS-2	NULL		bind	NULL				SNAP-25	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_26_1_45_s_20	10798391	A large number of proteins have been identified which bind to SNARE proteins and have been implicated in regulating SNARE complex formation: complexins, Munc-13, Munc-18, syncollin, syntaphilin, and tomosyn bind to syntaxin; HRS-2 and snapin bind to SNAP-25; and VAP-33 binds to VAMP (   Skehel, 1995  ; Bean et al. 1997  ; Edwardson, 1997  ; Mochida et al., 2000).	bind
40072	8	10679	6	NULL	NULL	0	NULL	snapin	NULL		bind	NULL				SNAP-25	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_26_1_45_s_20	10798391	A large number of proteins have been identified which bind to SNARE proteins and have been implicated in regulating SNARE complex formation: complexins, Munc-13, Munc-18, syncollin, syntaphilin, and tomosyn bind to syntaxin; HRS-2 and snapin bind to SNAP-25; and VAP-33 binds to VAMP (   Skehel, 1995  ; Bean et al. 1997  ; Edwardson, 1997  ; Mochida et al., 2000).	bind
40073	9	10679	6	NULL	NULL	0	NULL	VAP-33	NULL		bind	NULL				VAMP	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_26_1_45_s_20	10798391	A large number of proteins have been identified which bind to SNARE proteins and have been implicated in regulating SNARE complex formation: complexins, Munc-13, Munc-18, syncollin, syntaphilin, and tomosyn bind to syntaxin; HRS-2 and snapin bind to SNAP-25; and VAP-33 binds to VAMP (   Skehel, 1995  ; Bean et al. 1997  ; Edwardson, 1997  ; Mochida et al., 2000).	bind
47457	1	10680	5	13	NULL	NULL	NULL	vinca alkaloids	Chemical		bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_29_30731_s_20	15123603	A large number of structurally diverse compounds, including many unusual peptides and depsipeptides, interfere with the binding of vinca alkaloids to tubulin.	bind
47458	2	10680	5	13	NULL	NULL	NULL	depsipeptides	GP		interfere with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_29_30731_s_20	15123603	A large number of structurally diverse compounds, including many unusual peptides and depsipeptides, interfere with the binding of vinca alkaloids to tubulin.	bind
40076	1	10680	6	NULL	NULL	0	NULL	vinca alkaloids	NULL		bind	NULL				tubulin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_29_30731_s_20	15123603	A large number of structurally diverse compounds, including many unusual peptides and depsipeptides, interfere with the binding of vinca alkaloids to tubulin.	bind
40077	2	10680	6	NULL	NULL	0	NULL	depsipeptides	NULL		interferes with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_29_30731_s_20	15123603	A large number of structurally diverse compounds, including many unusual peptides and depsipeptides, interfere with the binding of vinca alkaloids to tubulin.	bind
47459	1	10681	5	13	NULL	NULL	NULL	Cds1	GP		preserves					genome	NucleicAcid	integrity of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_8_919_s_56	15805465	A large number of studies have established that Cds1 and Rad53 are required for survival of replication stress, and some have demonstrated physical links between these proteins and others involved in genome maintenance, but there have been few mechanistic insights into exactly how Cds1 and Rad53 function to preserve genome integrity.	bind
47460	2	10681	5	13	NULL	NULL	NULL	Rad53	GP		preserves					genome	NucleicAcid	integrity of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_8_919_s_56	15805465	A large number of studies have established that Cds1 and Rad53 are required for survival of replication stress, and some have demonstrated physical links between these proteins and others involved in genome maintenance, but there have been few mechanistic insights into exactly how Cds1 and Rad53 function to preserve genome integrity.	bind
47461	3	10681	5	13	NULL	NULL	NULL	Cds1	GP		is required for					replication stress	Process	survival of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_8_919_s_56	15805465	A large number of studies have established that Cds1 and Rad53 are required for survival of replication stress, and some have demonstrated physical links between these proteins and others involved in genome maintenance, but there have been few mechanistic insights into exactly how Cds1 and Rad53 function to preserve genome integrity.	bind
47462	4	10681	5	13	NULL	NULL	NULL	Rad53	GP		is required for					replication stress	Process	survival of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_8_919_s_56	15805465	A large number of studies have established that Cds1 and Rad53 are required for survival of replication stress, and some have demonstrated physical links between these proteins and others involved in genome maintenance, but there have been few mechanistic insights into exactly how Cds1 and Rad53 function to preserve genome integrity.	bind
40470	1	10681	6	NULL	NULL	0	NULL	Cds1	NULL		is required for	NULL				replication stress	NULL	survival of			NULL		0	NULL	NULL	NULL	gw70_genesdev_19_8_919_s_56	15805465	A large number of studies have established that Cds1 and Rad53 are required for survival of replication stress, and some have demonstrated physical links between these proteins and others involved in genome maintenance, but there have been few mechanistic insights into exactly how Cds1 and Rad53 function to preserve genome integrity.	bind
40475	2	10681	6	NULL	NULL	0	NULL	Rad53	NULL		are required for	NULL				replication stress	NULL	survival of			NULL		0	NULL	NULL	NULL	gw70_genesdev_19_8_919_s_56	15805465	A large number of studies have established that Cds1 and Rad53 are required for survival of replication stress, and some have demonstrated physical links between these proteins and others involved in genome maintenance, but there have been few mechanistic insights into exactly how Cds1 and Rad53 function to preserve genome integrity.	bind
40477	3	10681	6	10	NULL	0	NULL	Cds1			preserves					genome 		integrity of 			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_8_919_s_56	15805465	A large number of studies have established that Cds1 and Rad53 are required for survival of replication stress, and some have demonstrated physical links between these proteins and others involved in genome maintenance, but there have been few mechanistic insights into exactly how Cds1 and Rad53 function to preserve genome integrity.	bind
40478	4	10681	6	10	NULL	0	NULL	Rad53			preserves					genome 		integrity of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_8_919_s_56	15805465	A large number of studies have established that Cds1 and Rad53 are required for survival of replication stress, and some have demonstrated physical links between these proteins and others involved in genome maintenance, but there have been few mechanistic insights into exactly how Cds1 and Rad53 function to preserve genome integrity.	bind
47463	1	10682	5	13	NULL	NULL	NULL	cells	Cell	porin-treated	bind					annexin V	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_2_339_s_118	9889191	A large percentage of the porin-treated cells bound annexin V (Figure  2D).	bind
40078	1	10682	6	NULL	NULL	0	NULL	porin-treated cells	NULL		bind	NULL				annexin V	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_18_2_339_s_118	9889191	A large percentage of the porin-treated cells bound annexin V (Figure  2D).	bind
47464	1	10683	5	13	NULL	NULL	NULL	mPIP5KIbeta	GP		colocalize with					PI(4,5)P2 microdomains	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_17_17346_s_209	15741173	A large population of mPIP5KIbeta was colocalized with PI(4,5)P2 microdomains ( B) and syntaxin clusters ( C).	bind
47465	2	10683	5	13	NULL	NULL	NULL	mPIP5KIbeta	GP		colocalize with					syntaxin clusters	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_17_17346_s_209	15741173	A large population of mPIP5KIbeta was colocalized with PI(4,5)P2 microdomains ( B) and syntaxin clusters ( C).	bind
40080	1	10683	6	NULL	NULL	0	NULL	mPIP5KIbeta	NULL		colocalizes with	NULL				PI(4,5)P2 microdomains	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_17_17346_s_209	15741173	A large population of mPIP5KIbeta was colocalized with PI(4,5)P2 microdomains ( B) and syntaxin clusters ( C).	bind
40081	2	10683	6	NULL	NULL	0	NULL	mPIP5KIbeta	NULL		colocalizes with	NULL				syntaxin clusters	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_17_17346_s_209	15741173	A large population of mPIP5KIbeta was colocalized with PI(4,5)P2 microdomains ( B) and syntaxin clusters ( C).	bind
47466	1	10684	5	13	NULL	NULL	NULL	TSP-4 particles	GP		bind					collagen molecules	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_47_37110_s_202	10956668	A large proportion of all TSP-4 particles was bound to collagen molecules.	bind
40082	1	10684	6	NULL	NULL	0	NULL	TSP-4 particles	NULL		bind	NULL				collagen molecules	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_47_37110_s_202	10956668	A large proportion of all TSP-4 particles was bound to collagen molecules.	bind
47467	1	10685	5	13	NULL	NULL	NULL	B-Myb	GP		complexes with					p107	GP				NULL	cotransfected cells	NULL	NULL	NULL	NULL	abs-batch0517-0529_oncogene_21_52_12439743_s_5	12439743	A large proportion of B-Myb formed complexes with p107 in cotransfected  cells, however, B-Myb bound weakly to the related p130 protein and not  at all to pRb.	bind
47468	2	10685	5	13	NULL	NULL	NULL	B-Myb	GP		bind		weakly			p130 protein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_oncogene_21_52_12439743_s_5	12439743	A large proportion of B-Myb formed complexes with p107 in cotransfected  cells, however, B-Myb bound weakly to the related p130 protein and not  at all to pRb.	bind
47469	3	10685	5	13	NULL	NULL	NULL	B-Myb	GP		does not bind					pRb	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_oncogene_21_52_12439743_s_5	12439743	A large proportion of B-Myb formed complexes with p107 in cotransfected  cells, however, B-Myb bound weakly to the related p130 protein and not  at all to pRb.	bind
40084	1	10685	6	NULL	NULL	0	NULL	B-Myb	NULL		forms complexes with	NULL				p107	NULL				NULL	cotransfected cells	0	NULL	NULL	NULL	abs-batch0517-0529_oncogene_21_52_12439743_s_5	12439743	A large proportion of B-Myb formed complexes with p107 in cotransfected  cells, however, B-Myb bound weakly to the related p130 protein and not  at all to pRb.	bind
40085	2	10685	6	NULL	NULL	0	NULL	B-Myb	NULL		bind	NULL	weakly			p130 protein	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_oncogene_21_52_12439743_s_5	12439743	A large proportion of B-Myb formed complexes with p107 in cotransfected  cells, however, B-Myb bound weakly to the related p130 protein and not  at all to pRb.	bind
40086	3	10685	6	NULL	NULL	0	NULL	B-Myb	NULL		does not bind	NULL				pRb	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_oncogene_21_52_12439743_s_5	12439743	A large proportion of B-Myb formed complexes with p107 in cotransfected  cells, however, B-Myb bound weakly to the related p130 protein and not  at all to pRb.	bind
47507	1	10686	5	13	NULL	NULL	NULL	PLTP	GP		bind					apoA-I	GP				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_39_1_152_s_149	9469594	A large proportion of the applied PLTP activity (66%) bound to the apoA-I column, and could be recovered (84%) by elution with 0.5% CHAPS in PBS.	bind
40099	1	10686	6	NULL	NULL	0	NULL	PLTP	NULL		bind	NULL				apoA-I	NULL				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_1_152_s_149	9469594	A large proportion of the applied PLTP activity (66%) bound to the apoA-I column, and could be recovered (84%) by elution with 0.5% CHAPS in PBS.	bind
47508	1	10687	5	13	NULL	NULL	NULL	GABAA receptor subtype	GP	thalamus	does not bind			MUS binding sites		benzodiazepines	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_118_4_1033_s_209	12732248	A large proportion of [3]MUS binding sites in the thalamus is thought to be a part of the GABAA receptor subtype that does not bind benzodiazepines ( Unnerstal et al., 1981).	bind
40100	1	10687	6	10	NULL	0	NULL	GABAA receptor subtype	NULL	thalamus	does not bind	NULL		MUS binding sites		benzodiazepines	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_118_4_1033_s_209	12732248	A large proportion of [3]MUS binding sites in the thalamus is thought to be a part of the GABAA receptor subtype that does not bind benzodiazepines ( Unnerstal et al., 1981).	bind
47501	1	10688	5	13	NULL	NULL	NULL	Ypt7	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_1_148_s_209	15110766	A large protein complex containing vps39 and vps41 functions  as a downstream effector of the active, GTP-bound form of Ypt7, a rab GTPase required  for the fusion of vesicular intermediates with a vacuole [ 51].	bind
47502	2	10688	5	13	NULL	NULL	NULL	vps39	GP		is in complex with					vps41	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_1_148_s_209	15110766	A large protein complex containing vps39 and vps41 functions  as a downstream effector of the active, GTP-bound form of Ypt7, a rab GTPase required  for the fusion of vesicular intermediates with a vacuole [ 51].	bind
47503	3	10688	5	13	NULL	NULL	NULL	statement 2	Process		function as					statement 1	Process	downstream effector of;;active			NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_1_148_s_209	15110766	A large protein complex containing vps39 and vps41 functions  as a downstream effector of the active, GTP-bound form of Ypt7, a rab GTPase required  for the fusion of vesicular intermediates with a vacuole [ 51].	bind
47504	4	10688	5	13	NULL	NULL	NULL	Ypt7	GP		is a type of					rab GTPase	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_1_148_s_209	15110766	A large protein complex containing vps39 and vps41 functions  as a downstream effector of the active, GTP-bound form of Ypt7, a rab GTPase required  for the fusion of vesicular intermediates with a vacuole [ 51].	bind
47505	5	10688	5	13	NULL	NULL	NULL	vesicular intermediates	CellComponent		fuse with					vacuole	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_1_148_s_209	15110766	A large protein complex containing vps39 and vps41 functions  as a downstream effector of the active, GTP-bound form of Ypt7, a rab GTPase required  for the fusion of vesicular intermediates with a vacuole [ 51].	bind
50252	6	10688	5	13	NULL	NULL	NULL	Ypt7	GP		is required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_1_148_s_209	15110766	A large protein complex containing vps39 and vps41 functions  as a downstream effector of the active, GTP-bound form of Ypt7, a rab GTPase required  for the fusion of vesicular intermediates with a vacuole [ 51].	bind
40413	1	10688	6	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				Ypt7	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_1_148_s_209	15110766	A large protein complex containing vps39 and vps41 functions  as a downstream effector of the active, GTP-bound form of Ypt7, a rab GTPase required  for the fusion of vesicular intermediates with a vacuole [ 51].	bind
40414	2	10688	6	NULL	NULL	0	NULL	Ypt7	NULL		is a type of	NULL				rab GTPase	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_1_148_s_209	15110766	A large protein complex containing vps39 and vps41 functions  as a downstream effector of the active, GTP-bound form of Ypt7, a rab GTPase required  for the fusion of vesicular intermediates with a vacuole [ 51].	bind
40415	3	10688	6	10	NULL	0	NULL	vesicular intermediates	NULL		fuse with	NULL				vacuole	NULL				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_1_148_s_209	15110766	A large protein complex containing vps39 and vps41 functions  as a downstream effector of the active, GTP-bound form of Ypt7, a rab GTPase required  for the fusion of vesicular intermediates with a vacuole [ 51].	bind
40416	4	10688	6	NULL	NULL	0	NULL	vps39	NULL		forms a complex with	NULL				vps41	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_1_148_s_209	15110766	A large protein complex containing vps39 and vps41 functions  as a downstream effector of the active, GTP-bound form of Ypt7, a rab GTPase required  for the fusion of vesicular intermediates with a vacuole [ 51].	bind
40417	5	10688	6	NULL	NULL	0	NULL	statement 4	NULL		acts as 	NULL				statement 1	NULL	downstream effector of;; active			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_1_148_s_209	15110766	A large protein complex containing vps39 and vps41 functions  as a downstream effector of the active, GTP-bound form of Ypt7, a rab GTPase required  for the fusion of vesicular intermediates with a vacuole [ 51].	bind
50253	6	10688	6	10	NULL	0	NULL	Ypt7	NULL		is required for	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_1_148_s_209	15110766	A large protein complex containing vps39 and vps41 functions  as a downstream effector of the active, GTP-bound form of Ypt7, a rab GTPase required  for the fusion of vesicular intermediates with a vacuole [ 51].	bind
47509	1	10689	5	13	NULL	NULL	NULL	EB	Chemical		bind					CHO-18.4 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_3_1795_s_75	16495553	A large reduction in EB binding to CHO-18.4 cells was not observed, suggesting that the specific lack of heparan sulfate on the surface of CHO cells had little effect on the ability of EB to attach to host cells.	bind
47510	2	10689	5	13	NULL	NULL	NULL	CHO cells	Cell	surface of	lacks					heparan sulfate	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_3_1795_s_75	16495553	A large reduction in EB binding to CHO-18.4 cells was not observed, suggesting that the specific lack of heparan sulfate on the surface of CHO cells had little effect on the ability of EB to attach to host cells.	bind
47511	3	10689	5	13	NULL	NULL	NULL	statement 2	Process		has little effect on					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_infectimmun_74_3_1795_s_75	16495553	A large reduction in EB binding to CHO-18.4 cells was not observed, suggesting that the specific lack of heparan sulfate on the surface of CHO cells had little effect on the ability of EB to attach to host cells.	bind
40101	1	10689	6	NULL	NULL	0	NULL	EB	NULL		bind	NULL				CHO-18.4 cells	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_74_3_1795_s_75	16495553	A large reduction in EB binding to CHO-18.4 cells was not observed, suggesting that the specific lack of heparan sulfate on the surface of CHO cells had little effect on the ability of EB to attach to host cells.	bind
50254	2	10689	6	10	NULL	0	NULL	CHO cells	NULL	surface of	lack	NULL				 heparan sulfate	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_74_3_1795_s_75	16495553	A large reduction in EB binding to CHO-18.4 cells was not observed, suggesting that the specific lack of heparan sulfate on the surface of CHO cells had little effect on the ability of EB to attach to host cells.	bind
50255	3	10689	6	10	NULL	0	NULL	statement 2	NULL		has little effect on	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_74_3_1795_s_75	16495553	A large reduction in EB binding to CHO-18.4 cells was not observed, suggesting that the specific lack of heparan sulfate on the surface of CHO cells had little effect on the ability of EB to attach to host cells.	bind
47512	1	10690	5	13	NULL	NULL	NULL	p300	GP		bind					HIF-alpha 	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_11_9899_s_154	14701857	A larger decrease in O2 concentration is needed for a significant decrease in the activity of FIH, which allows binding of p300 to HIF-alpha and thus leads to maximal transcriptional activity.	bind
47513	2	10690	5	13	NULL	NULL	NULL	O2	Chemical	decrease in;;concentration of	is needed for					FIH	GP	decrease in;;activity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_11_9899_s_154	14701857	A larger decrease in O2 concentration is needed for a significant decrease in the activity of FIH, which allows binding of p300 to HIF-alpha and thus leads to maximal transcriptional activity.	bind
47514	3	10690	5	13	NULL	NULL	NULL	statement 2	Process		allows					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_11_9899_s_154	14701857	A larger decrease in O2 concentration is needed for a significant decrease in the activity of FIH, which allows binding of p300 to HIF-alpha and thus leads to maximal transcriptional activity.	bind
47515	4	10690	5	13	NULL	NULL	NULL	statement 3	Process		leads to					transcriptional activity	Process	maximal			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_11_9899_s_154	14701857	A larger decrease in O2 concentration is needed for a significant decrease in the activity of FIH, which allows binding of p300 to HIF-alpha and thus leads to maximal transcriptional activity.	bind
40172	1	10690	6	NULL	NULL	0	NULL	p300	NULL		bind	NULL				HIF-alpha	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_11_9899_s_154	14701857	A larger decrease in O2 concentration is needed for a significant decrease in the activity of FIH, which allows binding of p300 to HIF-alpha and thus leads to maximal transcriptional activity.	bind
40173	2	10690	6	NULL	NULL	0	NULL	O2 concentration	NULL	decrease in	is needed for	NULL				FIH	NULL	decrease in;; activity of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_11_9899_s_154	14701857	A larger decrease in O2 concentration is needed for a significant decrease in the activity of FIH, which allows binding of p300 to HIF-alpha and thus leads to maximal transcriptional activity.	bind
40174	3	10690	6	NULL	NULL	0	NULL	statement 2	NULL		allows	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_11_9899_s_154	14701857	A larger decrease in O2 concentration is needed for a significant decrease in the activity of FIH, which allows binding of p300 to HIF-alpha and thus leads to maximal transcriptional activity.	bind
40175	4	10690	6	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				transcriptional activity	NULL	maximal			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_11_9899_s_154	14701857	A larger decrease in O2 concentration is needed for a significant decrease in the activity of FIH, which allows binding of p300 to HIF-alpha and thus leads to maximal transcriptional activity.	bind
47574	1	10691	5	13	NULL	NULL	NULL	AML-1B	GP		is an isoform of					AML-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10647_s_236	9553127	A larger isoform of AML-1, AML-1B has an N-terminal extension ( 26); the AML-1B antiserum is specific to AML-1 members, and it has only weak binding to human AML-2 and AML-3 ( 27), which are other members of the AML family ( 28).	bind
47576	2	10691	5	13	NULL	NULL	NULL	AML-1B antiserum	GP		is specific to					AML-1 members	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10647_s_236	9553127	A larger isoform of AML-1, AML-1B has an N-terminal extension ( 26); the AML-1B antiserum is specific to AML-1 members, and it has only weak binding to human AML-2 and AML-3 ( 27), which are other members of the AML family ( 28).	bind
47577	3	10691	5	13	NULL	NULL	NULL	AML-1B antiserum	GP		bind		weakly			AML-2	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10647_s_236	9553127	A larger isoform of AML-1, AML-1B has an N-terminal extension ( 26); the AML-1B antiserum is specific to AML-1 members, and it has only weak binding to human AML-2 and AML-3 ( 27), which are other members of the AML family ( 28).	bind
47578	4	10691	5	13	NULL	NULL	NULL	AML-1B antiserum	GP		bind		weakly			AML-3	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10647_s_236	9553127	A larger isoform of AML-1, AML-1B has an N-terminal extension ( 26); the AML-1B antiserum is specific to AML-1 members, and it has only weak binding to human AML-2 and AML-3 ( 27), which are other members of the AML family ( 28).	bind
47579	5	10691	5	13	NULL	NULL	NULL	AML-2	GP		is a member of					AML family	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10647_s_236	9553127	A larger isoform of AML-1, AML-1B has an N-terminal extension ( 26); the AML-1B antiserum is specific to AML-1 members, and it has only weak binding to human AML-2 and AML-3 ( 27), which are other members of the AML family ( 28).	bind
47580	6	10691	5	13	NULL	NULL	NULL	AML-3	GP		is a member of					AML family	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10647_s_236	9553127	A larger isoform of AML-1, AML-1B has an N-terminal extension ( 26); the AML-1B antiserum is specific to AML-1 members, and it has only weak binding to human AML-2 and AML-3 ( 27), which are other members of the AML family ( 28).	bind
40481	1	10691	6	NULL	NULL	0	NULL	AML-1B antiserum	NULL		bind	NULL	weakly			AML-2	NULL	human			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_17_10647_s_236	9553127	A larger isoform of AML-1, AML-1B has an N-terminal extension ( 26); the AML-1B antiserum is specific to AML-1 members, and it has only weak binding to human AML-2 and AML-3 ( 27), which are other members of the AML family ( 28).	bind
40482	2	10691	6	NULL	NULL	0	NULL	AML-1B antiserum	NULL		bind	NULL	weakly			AML-3	NULL	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_17_10647_s_236	9553127	A larger isoform of AML-1, AML-1B has an N-terminal extension ( 26); the AML-1B antiserum is specific to AML-1 members, and it has only weak binding to human AML-2 and AML-3 ( 27), which are other members of the AML family ( 28).	bind
40485	3	10691	6	NULL	NULL	0	NULL	AML-1B	NULL		is an isoform of	NULL				AML-1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_17_10647_s_236	9553127	A larger isoform of AML-1, AML-1B has an N-terminal extension ( 26); the AML-1B antiserum is specific to AML-1 members, and it has only weak binding to human AML-2 and AML-3 ( 27), which are other members of the AML family ( 28).	bind
40486	4	10691	6	NULL	NULL	0	NULL	AML-2	NULL		is a member of	NULL				AML family	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_17_10647_s_236	9553127	A larger isoform of AML-1, AML-1B has an N-terminal extension ( 26); the AML-1B antiserum is specific to AML-1 members, and it has only weak binding to human AML-2 and AML-3 ( 27), which are other members of the AML family ( 28).	bind
40487	5	10691	6	NULL	NULL	0	NULL	AML-3	NULL		is a member of	NULL				AML family	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_17_10647_s_236	9553127	A larger isoform of AML-1, AML-1B has an N-terminal extension ( 26); the AML-1B antiserum is specific to AML-1 members, and it has only weak binding to human AML-2 and AML-3 ( 27), which are other members of the AML family ( 28).	bind
50256	6	10691	6	10	NULL	0	NULL	AML-1B antiserum	NULL		is specific to	NULL				AML-1 members	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_17_10647_s_236	9553127	A larger isoform of AML-1, AML-1B has an N-terminal extension ( 26); the AML-1B antiserum is specific to AML-1 members, and it has only weak binding to human AML-2 and AML-3 ( 27), which are other members of the AML family ( 28).	bind
47581	1	10694	5	13	NULL	NULL	NULL	UP1	GP		bind					TR2-6F	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_43_42300_s_96	12904298	A least squares superposition of Calphas from the structures of UP1 bound to TR2-6F and TR2 (d(TTAGGG)2) showed no significant differences (root mean square deviation = 0.23  Ang ).	bind
47582	2	10694	5	13	NULL	NULL	NULL	UP1	GP		bind					TR2	NucleicAcid			d(TTAGGG)2	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_43_42300_s_96	12904298	A least squares superposition of Calphas from the structures of UP1 bound to TR2-6F and TR2 (d(TTAGGG)2) showed no significant differences (root mean square deviation = 0.23  Ang ).	bind
40176	1	10694	6	NULL	NULL	0	NULL	UP1	NULL		bind	NULL				TR2-6F	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_43_42300_s_96	12904298	A least squares superposition of Calphas from the structures of UP1 bound to TR2-6F and TR2 (d(TTAGGG)2) showed no significant differences (root mean square deviation = 0.23  Ang ).	bind
40177	2	10694	6	NULL	NULL	0	NULL	UP1	NULL		bind	NULL				TR2	NULL			d(TTAGGG)2	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_43_42300_s_96	12904298	A least squares superposition of Calphas from the structures of UP1 bound to TR2-6F and TR2 (d(TTAGGG)2) showed no significant differences (root mean square deviation = 0.23  Ang ).	bind
47583	1	10697	5	13	NULL	NULL	NULL	RNP complex	GP		bind			L7Ae					C/D motif		NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_22_6524_s_216	14602911	A less rigid RNP complex with only one L7Ae bound to the C/D motif could account for the increased activity.	bind
40488	1	10697	6	NULL	NULL	0	NULL	RNP complex	NULL		bind	NULL		L7Ae			NULL		C/D motif		NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_22_6524_s_216	14602911	A less rigid RNP complex with only one L7Ae bound to the C/D motif could account for the increased activity.	bind
47585	1	10699	5	13	NULL	NULL	NULL	KCNQ1	GP		coordinates			leucine zipper motif in C-terminus		yotiao	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_43_0_441_s_177	12540747	A leucine zipper motif in the C-terminus of KCNQ1 coordinates the binding of a  targeting protein yotiao ( 85,  86), which in turn binds to and recruits PKA and protein phosphatase 1 (PP1) to the  channel.	bind
47586	2	10699	5	13	NULL	NULL	NULL	yotiao	GP		bind					PKA	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_43_0_441_s_177	12540747	A leucine zipper motif in the C-terminus of KCNQ1 coordinates the binding of a  targeting protein yotiao ( 85,  86), which in turn binds to and recruits PKA and protein phosphatase 1 (PP1) to the  channel.	bind
47587	3	10699	5	13	NULL	NULL	NULL	yotiao	GP		bind					PP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_43_0_441_s_177	12540747	A leucine zipper motif in the C-terminus of KCNQ1 coordinates the binding of a  targeting protein yotiao ( 85,  86), which in turn binds to and recruits PKA and protein phosphatase 1 (PP1) to the  channel.	bind
47588	4	10699	5	13	NULL	NULL	NULL	PP1	GP		is					protein phosphatase 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_43_0_441_s_177	12540747	A leucine zipper motif in the C-terminus of KCNQ1 coordinates the binding of a  targeting protein yotiao ( 85,  86), which in turn binds to and recruits PKA and protein phosphatase 1 (PP1) to the  channel.	bind
47589	5	10699	5	13	NULL	NULL	NULL	yotiao	GP		recruits					PKA	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_43_0_441_s_177	12540747	A leucine zipper motif in the C-terminus of KCNQ1 coordinates the binding of a  targeting protein yotiao ( 85,  86), which in turn binds to and recruits PKA and protein phosphatase 1 (PP1) to the  channel.	bind
47590	6	10699	5	13	NULL	NULL	NULL	yotiao	GP		recruits					PP1	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_43_0_441_s_177	12540747	A leucine zipper motif in the C-terminus of KCNQ1 coordinates the binding of a  targeting protein yotiao ( 85,  86), which in turn binds to and recruits PKA and protein phosphatase 1 (PP1) to the  channel.	bind
47591	7	10699	5	13	NULL	NULL	NULL	PKA	GP		is recruited to					channel	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_43_0_441_s_177	12540747	A leucine zipper motif in the C-terminus of KCNQ1 coordinates the binding of a  targeting protein yotiao ( 85,  86), which in turn binds to and recruits PKA and protein phosphatase 1 (PP1) to the  channel.	bind
47592	8	10699	5	13	NULL	NULL	NULL	PP1	GP		is recruited to					channel	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_43_0_441_s_177	12540747	A leucine zipper motif in the C-terminus of KCNQ1 coordinates the binding of a  targeting protein yotiao ( 85,  86), which in turn binds to and recruits PKA and protein phosphatase 1 (PP1) to the  channel.	bind
47593	9	10699	5	13	NULL	NULL	NULL	yotiao	GP		is a type of					targeting protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_43_0_441_s_177	12540747	A leucine zipper motif in the C-terminus of KCNQ1 coordinates the binding of a  targeting protein yotiao ( 85,  86), which in turn binds to and recruits PKA and protein phosphatase 1 (PP1) to the  channel.	bind
40489	1	10699	6	NULL	NULL	0	NULL	yotiao	NULL		bind	NULL				PKA	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevpharmacol_43_0_441_s_177	12540747	A leucine zipper motif in the C-terminus of KCNQ1 coordinates the binding of a  targeting protein yotiao ( 85,  86), which in turn binds to and recruits PKA and protein phosphatase 1 (PP1) to the  channel.	bind
40490	2	10699	6	NULL	NULL	0	NULL	yotiao	NULL		bind	NULL				PP1	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevpharmacol_43_0_441_s_177	12540747	A leucine zipper motif in the C-terminus of KCNQ1 coordinates the binding of a  targeting protein yotiao ( 85,  86), which in turn binds to and recruits PKA and protein phosphatase 1 (PP1) to the  channel.	bind
40491	3	10699	6	NULL	NULL	0	NULL	PP1	NULL		is	NULL				protein phosphatase 1	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevpharmacol_43_0_441_s_177	12540747	A leucine zipper motif in the C-terminus of KCNQ1 coordinates the binding of a  targeting protein yotiao ( 85,  86), which in turn binds to and recruits PKA and protein phosphatase 1 (PP1) to the  channel.	bind
40492	4	10699	6	NULL	NULL	0	NULL	yotiao	NULL		recruits	NULL				PKA	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevpharmacol_43_0_441_s_177	12540747	A leucine zipper motif in the C-terminus of KCNQ1 coordinates the binding of a  targeting protein yotiao ( 85,  86), which in turn binds to and recruits PKA and protein phosphatase 1 (PP1) to the  channel.	bind
40493	5	10699	6	NULL	NULL	0	NULL	PKA	NULL		is recruited to	NULL				channel	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevpharmacol_43_0_441_s_177	12540747	A leucine zipper motif in the C-terminus of KCNQ1 coordinates the binding of a  targeting protein yotiao ( 85,  86), which in turn binds to and recruits PKA and protein phosphatase 1 (PP1) to the  channel.	bind
40494	6	10699	6	NULL	NULL	0	NULL	PP1	NULL		is recruited to	NULL				channel	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevpharmacol_43_0_441_s_177	12540747	A leucine zipper motif in the C-terminus of KCNQ1 coordinates the binding of a  targeting protein yotiao ( 85,  86), which in turn binds to and recruits PKA and protein phosphatase 1 (PP1) to the  channel.	bind
40495	7	10699	6	NULL	NULL	0	NULL	yotiao	NULL		recruits	NULL				PP1	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevpharmacol_43_0_441_s_177	12540747	A leucine zipper motif in the C-terminus of KCNQ1 coordinates the binding of a  targeting protein yotiao ( 85,  86), which in turn binds to and recruits PKA and protein phosphatase 1 (PP1) to the  channel.	bind
40496	8	10699	6	NULL	NULL	0	NULL	yotiao	NULL		is a type of	NULL				targeting protein	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevpharmacol_43_0_441_s_177	12540747	A leucine zipper motif in the C-terminus of KCNQ1 coordinates the binding of a  targeting protein yotiao ( 85,  86), which in turn binds to and recruits PKA and protein phosphatase 1 (PP1) to the  channel.	bind
40497	9	10699	6	NULL	NULL	0	NULL	KCNQ1	NULL		coordinates	NULL		leucine zipper motif in C-terminus		yotiao	NULL	binding of			NULL		0	NULL	NULL	NULL	gw70_annurevpharmacol_43_0_441_s_177	12540747	A leucine zipper motif in the C-terminus of KCNQ1 coordinates the binding of a  targeting protein yotiao ( 85,  86), which in turn binds to and recruits PKA and protein phosphatase 1 (PP1) to the  channel.	bind
47594	1	10700	5	13	NULL	NULL	NULL	PAK	GP		is a type of					p21 GTPase-activated kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_34_26436_s_16	10840040	A leucine-rich motif that is repeated five times within the N terminus of paxillin binds a protein complex containing the p21 GTPase-activated kinase PAK, the adapter protein Nck, the guanine nucleotide exchange factor PIX, and the new multidomain ARF-GAP protein p95PKL (paxillin kinase linker) ( 11).	bind
47595	2	10700	5	13	NULL	NULL	NULL	Nck	GP		is a type of					adapter protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_34_26436_s_16	10840040	A leucine-rich motif that is repeated five times within the N terminus of paxillin binds a protein complex containing the p21 GTPase-activated kinase PAK, the adapter protein Nck, the guanine nucleotide exchange factor PIX, and the new multidomain ARF-GAP protein p95PKL (paxillin kinase linker) ( 11).	bind
47596	3	10700	5	13	NULL	NULL	NULL	PIX	GP		is a type of					guanine nucleotide exchange factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_34_26436_s_16	10840040	A leucine-rich motif that is repeated five times within the N terminus of paxillin binds a protein complex containing the p21 GTPase-activated kinase PAK, the adapter protein Nck, the guanine nucleotide exchange factor PIX, and the new multidomain ARF-GAP protein p95PKL (paxillin kinase linker) ( 11).	bind
47597	4	10700	5	13	NULL	NULL	NULL	p95PKL	GP		is					paxillin kinase linker	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_34_26436_s_16	10840040	A leucine-rich motif that is repeated five times within the N terminus of paxillin binds a protein complex containing the p21 GTPase-activated kinase PAK, the adapter protein Nck, the guanine nucleotide exchange factor PIX, and the new multidomain ARF-GAP protein p95PKL (paxillin kinase linker) ( 11).	bind
47598	5	10700	5	13	NULL	NULL	NULL	p95PKL	GP		is a type of					multidomain ARF-GAP protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_34_26436_s_16	10840040	A leucine-rich motif that is repeated five times within the N terminus of paxillin binds a protein complex containing the p21 GTPase-activated kinase PAK, the adapter protein Nck, the guanine nucleotide exchange factor PIX, and the new multidomain ARF-GAP protein p95PKL (paxillin kinase linker) ( 11).	bind
47599	6	10700	5	13	NULL	NULL	NULL	PAK	GP		is in complex with					Nck	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_34_26436_s_16	10840040	A leucine-rich motif that is repeated five times within the N terminus of paxillin binds a protein complex containing the p21 GTPase-activated kinase PAK, the adapter protein Nck, the guanine nucleotide exchange factor PIX, and the new multidomain ARF-GAP protein p95PKL (paxillin kinase linker) ( 11).	bind
47600	7	10700	5	13	NULL	NULL	NULL	statement 6	GP		is in complex with					PIX	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_34_26436_s_16	10840040	A leucine-rich motif that is repeated five times within the N terminus of paxillin binds a protein complex containing the p21 GTPase-activated kinase PAK, the adapter protein Nck, the guanine nucleotide exchange factor PIX, and the new multidomain ARF-GAP protein p95PKL (paxillin kinase linker) ( 11).	bind
47601	8	10700	5	13	NULL	NULL	NULL	statement 7	GP		is in complex with					p95PKL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_34_26436_s_16	10840040	A leucine-rich motif that is repeated five times within the N terminus of paxillin binds a protein complex containing the p21 GTPase-activated kinase PAK, the adapter protein Nck, the guanine nucleotide exchange factor PIX, and the new multidomain ARF-GAP protein p95PKL (paxillin kinase linker) ( 11).	bind
47602	9	10700	5	13	NULL	NULL	NULL	paxillin	GP		bind			leucine-rich motif within the N terminus		statement 8	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_34_26436_s_16	10840040	A leucine-rich motif that is repeated five times within the N terminus of paxillin binds a protein complex containing the p21 GTPase-activated kinase PAK, the adapter protein Nck, the guanine nucleotide exchange factor PIX, and the new multidomain ARF-GAP protein p95PKL (paxillin kinase linker) ( 11).	bind
40498	1	10700	6	NULL	NULL	0	NULL	PAK	NULL		is a type of	NULL				p21 GTPase-activated kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_34_26436_s_16	10840040	A leucine-rich motif that is repeated five times within the N terminus of paxillin binds a protein complex containing the p21 GTPase-activated kinase PAK, the adapter protein Nck, the guanine nucleotide exchange factor PIX, and the new multidomain ARF-GAP protein p95PKL (paxillin kinase linker) ( 11).	bind
40499	2	10700	6	NULL	NULL	0	NULL	Nck	NULL		is a type of	NULL				adapter protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_34_26436_s_16	10840040	A leucine-rich motif that is repeated five times within the N terminus of paxillin binds a protein complex containing the p21 GTPase-activated kinase PAK, the adapter protein Nck, the guanine nucleotide exchange factor PIX, and the new multidomain ARF-GAP protein p95PKL (paxillin kinase linker) ( 11).	bind
40500	3	10700	6	NULL	NULL	0	NULL	PIX	NULL		is a type of	NULL				guanine nucleotide exchange factor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_34_26436_s_16	10840040	A leucine-rich motif that is repeated five times within the N terminus of paxillin binds a protein complex containing the p21 GTPase-activated kinase PAK, the adapter protein Nck, the guanine nucleotide exchange factor PIX, and the new multidomain ARF-GAP protein p95PKL (paxillin kinase linker) ( 11).	bind
40501	4	10700	6	NULL	NULL	0	NULL	p95PKL	NULL		is a type of	NULL				multidomain ARF-GAP protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_34_26436_s_16	10840040	A leucine-rich motif that is repeated five times within the N terminus of paxillin binds a protein complex containing the p21 GTPase-activated kinase PAK, the adapter protein Nck, the guanine nucleotide exchange factor PIX, and the new multidomain ARF-GAP protein p95PKL (paxillin kinase linker) ( 11).	bind
40502	5	10700	6	NULL	NULL	0	NULL	PKL	NULL		is	NULL				paxillin kinase linker	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_34_26436_s_16	10840040	A leucine-rich motif that is repeated five times within the N terminus of paxillin binds a protein complex containing the p21 GTPase-activated kinase PAK, the adapter protein Nck, the guanine nucleotide exchange factor PIX, and the new multidomain ARF-GAP protein p95PKL (paxillin kinase linker) ( 11).	bind
40503	6	10700	6	NULL	NULL	0	NULL	PAK	NULL		forms a complex with	NULL				Nck	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_34_26436_s_16	10840040	A leucine-rich motif that is repeated five times within the N terminus of paxillin binds a protein complex containing the p21 GTPase-activated kinase PAK, the adapter protein Nck, the guanine nucleotide exchange factor PIX, and the new multidomain ARF-GAP protein p95PKL (paxillin kinase linker) ( 11).	bind
40504	7	10700	6	NULL	NULL	0	NULL	statement 6	NULL		forms a complex with	NULL				PIX	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_34_26436_s_16	10840040	A leucine-rich motif that is repeated five times within the N terminus of paxillin binds a protein complex containing the p21 GTPase-activated kinase PAK, the adapter protein Nck, the guanine nucleotide exchange factor PIX, and the new multidomain ARF-GAP protein p95PKL (paxillin kinase linker) ( 11).	bind
40505	8	10700	6	NULL	NULL	0	NULL	statement 7	NULL		forms a complex with	NULL				p95PKL	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_34_26436_s_16	10840040	A leucine-rich motif that is repeated five times within the N terminus of paxillin binds a protein complex containing the p21 GTPase-activated kinase PAK, the adapter protein Nck, the guanine nucleotide exchange factor PIX, and the new multidomain ARF-GAP protein p95PKL (paxillin kinase linker) ( 11).	bind
40506	9	10700	6	NULL	NULL	0	NULL	paxillin	NULL		bind	NULL		leucine-rich motif within N terminus		statement 8	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_34_26436_s_16	10840040	A leucine-rich motif that is repeated five times within the N terminus of paxillin binds a protein complex containing the p21 GTPase-activated kinase PAK, the adapter protein Nck, the guanine nucleotide exchange factor PIX, and the new multidomain ARF-GAP protein p95PKL (paxillin kinase linker) ( 11).	bind
47603	1	10701	5	13	NULL	NULL	NULL	NXF3	GP		is essential for			leucine-rich motif (296 to 302)		Crm1	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_397_s_202	11545741	A leucine-rich motif that mapped to around residues 296 to 302 in NXF3   (Figure 1A) was in fact found to be essential for both Crm1 binding and nuclear export mediated by the NXF3 protein    (Figures 2A and 4A).	bind
47604	2	10701	5	13	NULL	NULL	NULL	NXF3 protein	GP		mediate					nuclear export	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_397_s_202	11545741	A leucine-rich motif that mapped to around residues 296 to 302 in NXF3   (Figure 1A) was in fact found to be essential for both Crm1 binding and nuclear export mediated by the NXF3 protein    (Figures 2A and 4A).	bind
47605	3	10701	5	13	NULL	NULL	NULL	NXF3	GP		is essential for			leucine-rich motif (296 to 302)		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_397_s_202	11545741	A leucine-rich motif that mapped to around residues 296 to 302 in NXF3   (Figure 1A) was in fact found to be essential for both Crm1 binding and nuclear export mediated by the NXF3 protein    (Figures 2A and 4A).	bind
46902	1	10701	6	NULL	NULL	0	NULL	NXF3	NULL		is essential for	NULL		leucine rich motif;; 296-302		Crm1	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_2_397_s_202	11545741	A leucine-rich motif that mapped to around residues 296 to 302 in NXF3   (Figure 1A) was in fact found to be essential for both Crm1 binding and nuclear export mediated by the NXF3 protein    (Figures 2A and 4A).	bind
46903	2	10701	6	NULL	NULL	0	NULL	NXF3 protein	NULL		mediates	NULL				nuclear export	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_8_2_397_s_202	11545741	A leucine-rich motif that mapped to around residues 296 to 302 in NXF3   (Figure 1A) was in fact found to be essential for both Crm1 binding and nuclear export mediated by the NXF3 protein    (Figures 2A and 4A).	bind
46905	3	10701	6	NULL	NULL	0	NULL	NXF3	NULL		is essential for	NULL		leucine rich motif;; 296-302		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_8_2_397_s_202	11545741	A leucine-rich motif that mapped to around residues 296 to 302 in NXF3   (Figure 1A) was in fact found to be essential for both Crm1 binding and nuclear export mediated by the NXF3 protein    (Figures 2A and 4A).	bind
47606	1	10703	5	13	NULL	NULL	NULL	long chain fatty acyl-CoA thioesters	Chemical		bind					HNF-4	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34105_s_227	9852068	A ligand for COUP-TF has not yet been identified, but it has recently been reported that long chain fatty acyl-CoA thioesters bind HNF-4 and enhance its ability to dimerize and bind DNA ( 44).	bind
47607	2	10703	5	13	NULL	NULL	NULL	HNF-4	GP		undergoes					dimerization	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34105_s_227	9852068	A ligand for COUP-TF has not yet been identified, but it has recently been reported that long chain fatty acyl-CoA thioesters bind HNF-4 and enhance its ability to dimerize and bind DNA ( 44).	bind
47608	3	10703	5	13	NULL	NULL	NULL	HNF-4	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34105_s_227	9852068	A ligand for COUP-TF has not yet been identified, but it has recently been reported that long chain fatty acyl-CoA thioesters bind HNF-4 and enhance its ability to dimerize and bind DNA ( 44).	bind
47609	4	10703	5	13	NULL	NULL	NULL	statement 1	Process		enhance					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34105_s_227	9852068	A ligand for COUP-TF has not yet been identified, but it has recently been reported that long chain fatty acyl-CoA thioesters bind HNF-4 and enhance its ability to dimerize and bind DNA ( 44).	bind
47610	5	10703	5	13	NULL	NULL	NULL	statement 1	Process		enhance					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34105_s_227	9852068	A ligand for COUP-TF has not yet been identified, but it has recently been reported that long chain fatty acyl-CoA thioesters bind HNF-4 and enhance its ability to dimerize and bind DNA ( 44).	bind
46906	1	10703	6	NULL	NULL	0	NULL	long chain fatty acyl-CoA thioesters	NULL		bind	NULL				HNF4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_51_34105_s_227	9852068	A ligand for COUP-TF has not yet been identified, but it has recently been reported that long chain fatty acyl-CoA thioesters bind HNF-4 and enhance its ability to dimerize and bind DNA ( 44).	bind
46907	2	10703	6	NULL	NULL	0	NULL	HNF4	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_51_34105_s_227	9852068	A ligand for COUP-TF has not yet been identified, but it has recently been reported that long chain fatty acyl-CoA thioesters bind HNF-4 and enhance its ability to dimerize and bind DNA ( 44).	bind
46908	3	10703	6	10	NULL	0	NULL	HNF4	NULL		undergoes	NULL				dimerization	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34105_s_227	9852068	A ligand for COUP-TF has not yet been identified, but it has recently been reported that long chain fatty acyl-CoA thioesters bind HNF-4 and enhance its ability to dimerize and bind DNA ( 44).	bind
46909	4	10703	6	NULL	NULL	0	NULL	statement 1	NULL		enhances	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_51_34105_s_227	9852068	A ligand for COUP-TF has not yet been identified, but it has recently been reported that long chain fatty acyl-CoA thioesters bind HNF-4 and enhance its ability to dimerize and bind DNA ( 44).	bind
46910	5	10703	6	NULL	NULL	0	NULL	statement 1	NULL		enhances	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_51_34105_s_227	9852068	A ligand for COUP-TF has not yet been identified, but it has recently been reported that long chain fatty acyl-CoA thioesters bind HNF-4 and enhance its ability to dimerize and bind DNA ( 44).	bind
47611	1	10705	5	13	NULL	NULL	NULL	Rho1p	GP	yeast	bind		directly			Fks1p	GP	Candida homolog of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_53_38119_s_158	10608882	A ligand overlay assay with  Candida albicans Rho1p has shown that yeast Rho1p can directly bind to the  Candida homolog of Fks1p ( 39).	bind
46911	1	10705	6	10	NULL	0	NULL	Rho1p	NULL	yeast	bind	NULL	directly			Fks1p	NULL	Candida homolog			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_53_38119_s_158	10608882	A ligand overlay assay with  Candida albicans Rho1p has shown that yeast Rho1p can directly bind to the  Candida homolog of Fks1p ( 39).	bind
47612	1	10707	5	13	NULL	NULL	NULL	PILR-L ligand	GP		bind					PILR	GP	mouse			NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_23_0_225_s_497	15771571	A ligand, designated PILR-L, that binds both mouse PILR  and PILR  has been identified;  it is a small transmembrane-anchored cell surface protein with homology to the CD99  gene family ( 344).	bind
47613	2	10707	5	13	NULL	NULL	NULL	PILR-L ligand	GP		bind					PILR	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_23_0_225_s_497	15771571	A ligand, designated PILR-L, that binds both mouse PILR  and PILR  has been identified;  it is a small transmembrane-anchored cell surface protein with homology to the CD99  gene family ( 344).	bind
47614	3	10707	5	13	NULL	NULL	NULL	PILR-L ligand	GP		is a type of					small transmembrane-anchored cell surface protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_23_0_225_s_497	15771571	A ligand, designated PILR-L, that binds both mouse PILR  and PILR  has been identified;  it is a small transmembrane-anchored cell surface protein with homology to the CD99  gene family ( 344).	bind
47615	4	10707	5	13	NULL	NULL	NULL	PILR-L ligand	GP		has homology to					CD99 gene family	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_23_0_225_s_497	15771571	A ligand, designated PILR-L, that binds both mouse PILR  and PILR  has been identified;  it is a small transmembrane-anchored cell surface protein with homology to the CD99  gene family ( 344).	bind
46912	1	10707	6	NULL	NULL	0	NULL	PILR-L	NULL		bind	NULL				PILR	NULL	mouse			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_23_0_225_s_497	15771571	A ligand, designated PILR-L, that binds both mouse PILR  and PILR  has been identified;  it is a small transmembrane-anchored cell surface protein with homology to the CD99  gene family ( 344).	bind
46913	2	10707	6	NULL	NULL	0	NULL	PILR-L	NULL		bind	NULL				PILR	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_23_0_225_s_497	15771571	A ligand, designated PILR-L, that binds both mouse PILR  and PILR  has been identified;  it is a small transmembrane-anchored cell surface protein with homology to the CD99  gene family ( 344).	bind
46914	3	10707	6	NULL	NULL	0	NULL	PILR-L	NULL		is a type of 	NULL				small transmembrane-anchored cell surface protein	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_23_0_225_s_497	15771571	A ligand, designated PILR-L, that binds both mouse PILR  and PILR  has been identified;  it is a small transmembrane-anchored cell surface protein with homology to the CD99  gene family ( 344).	bind
46915	4	10707	6	NULL	NULL	0	NULL	PILR-L	NULL		has homology to	NULL				CD99 gene family	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_23_0_225_s_497	15771571	A ligand, designated PILR-L, that binds both mouse PILR  and PILR  has been identified;  it is a small transmembrane-anchored cell surface protein with homology to the CD99  gene family ( 344).	bind
47616	1	10709	5	13	NULL	NULL	NULL	Blimp-1	GP		is a member of					Groucho family of co-repressors	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_2_263_s_181	10637230	A likely candidate is Blimp-1, a member of the Groucho family of co-repressors that binds to the PRF site of the c- myc promoter and mediates repression (Lin  et al., 1997  ; Ren  et al., 1999)  .	bind
47617	2	10709	5	13	NULL	NULL	NULL	Blimp-1	GP		bind					c- myc	NucleicAcid			PRF site of promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_19_2_263_s_181	10637230	A likely candidate is Blimp-1, a member of the Groucho family of co-repressors that binds to the PRF site of the c- myc promoter and mediates repression (Lin  et al., 1997  ; Ren  et al., 1999)  .	bind
47618	3	10709	5	13	NULL	NULL	NULL	statement 2	Process		mediates					c-myc	GP	repression of 			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_2_263_s_181	10637230	A likely candidate is Blimp-1, a member of the Groucho family of co-repressors that binds to the PRF site of the c- myc promoter and mediates repression (Lin  et al., 1997  ; Ren  et al., 1999)  .	bind
46916	1	10709	6	NULL	NULL	0	NULL	Blimp-1	NULL		is a member of	NULL				Groucho family of co-repressors	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_19_2_263_s_181	10637230	A likely candidate is Blimp-1, a member of the Groucho family of co-repressors that binds to the PRF site of the c- myc promoter and mediates repression (Lin  et al., 1997  ; Ren  et al., 1999)  .	bind
46917	2	10709	6	NULL	NULL	0	NULL	Blimp-1	NULL		bind	NULL				c- myc	NULL			PRF site of promoter	NULL		0	NULL	NULL	NULL	gw60_embo_19_2_263_s_181	10637230	A likely candidate is Blimp-1, a member of the Groucho family of co-repressors that binds to the PRF site of the c- myc promoter and mediates repression (Lin  et al., 1997  ; Ren  et al., 1999)  .	bind
46918	3	10709	6	NULL	NULL	0	NULL	Blimp-1	NULL		mediates	NULL				c- myc	NULL	repression of		promoter	NULL		0	NULL	NULL	NULL	gw60_embo_19_2_263_s_181	10637230	A likely candidate is Blimp-1, a member of the Groucho family of co-repressors that binds to the PRF site of the c- myc promoter and mediates repression (Lin  et al., 1997  ; Ren  et al., 1999)  .	bind
47619	1	10710	5	13	NULL	NULL	NULL	Bax alpha	GP		bind					Bcl-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10587_s_251	15590655	A likely explanation for the lack of activity detected with the latter mutant could be that mutation of Lys-64 enhanced the binding of Bax alpha to Bcl-2 (Fig. S4), and Asp-33 is central for the activation of Bax by proteases during apoptosis ( ,  ).	bind
47620	2	10710	5	13	NULL	NULL	NULL			mutation of	enhance			Lys-64		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10587_s_251	15590655	A likely explanation for the lack of activity detected with the latter mutant could be that mutation of Lys-64 enhanced the binding of Bax alpha to Bcl-2 (Fig. S4), and Asp-33 is central for the activation of Bax by proteases during apoptosis ( ,  ).	bind
47621	3	10710	5	13	NULL	NULL	NULL	Bax	GP		is activated by					proteases	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10587_s_251	15590655	A likely explanation for the lack of activity detected with the latter mutant could be that mutation of Lys-64 enhanced the binding of Bax alpha to Bcl-2 (Fig. S4), and Asp-33 is central for the activation of Bax by proteases during apoptosis ( ,  ).	bind
47622	4	10710	5	13	NULL	NULL	NULL				is essential for			Asp-33		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10587_s_251	15590655	A likely explanation for the lack of activity detected with the latter mutant could be that mutation of Lys-64 enhanced the binding of Bax alpha to Bcl-2 (Fig. S4), and Asp-33 is central for the activation of Bax by proteases during apoptosis ( ,  ).	bind
47623	5	10710	5	13	NULL	NULL	NULL	statement 4	Process		occurs during					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10587_s_251	15590655	A likely explanation for the lack of activity detected with the latter mutant could be that mutation of Lys-64 enhanced the binding of Bax alpha to Bcl-2 (Fig. S4), and Asp-33 is central for the activation of Bax by proteases during apoptosis ( ,  ).	bind
46919	1	10710	6	NULL	NULL	0	NULL	Bax alpha	NULL		bind	NULL				Bcl-2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_11_10587_s_251	15590655	A likely explanation for the lack of activity detected with the latter mutant could be that mutation of Lys-64 enhanced the binding of Bax alpha to Bcl-2 (Fig. S4), and Asp-33 is central for the activation of Bax by proteases during apoptosis ( ,  ).	bind
46920	2	10710	6	NULL	NULL	0	NULL		NULL	mutation of	enhances	NULL		Lys-64		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_11_10587_s_251	15590655	A likely explanation for the lack of activity detected with the latter mutant could be that mutation of Lys-64 enhanced the binding of Bax alpha to Bcl-2 (Fig. S4), and Asp-33 is central for the activation of Bax by proteases during apoptosis ( ,  ).	bind
46921	4	10710	6	10	NULL	0	NULL		NULL		is essential for	NULL		Asp-33		statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_10587_s_251	15590655	A likely explanation for the lack of activity detected with the latter mutant could be that mutation of Lys-64 enhanced the binding of Bax alpha to Bcl-2 (Fig. S4), and Asp-33 is central for the activation of Bax by proteases during apoptosis ( ,  ).	bind
50302	3	10710	6	10	NULL	0	NULL	Bax	NULL		is activated by	NULL				proteases	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_11_10587_s_251	15590655	A likely explanation for the lack of activity detected with the latter mutant could be that mutation of Lys-64 enhanced the binding of Bax alpha to Bcl-2 (Fig. S4), and Asp-33 is central for the activation of Bax by proteases during apoptosis ( ,  ).	bind
50303	5	10710	6	10	NULL	0	NULL	statement 4	NULL		occur during	NULL				apoptosis	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_11_10587_s_251	15590655	A likely explanation for the lack of activity detected with the latter mutant could be that mutation of Lys-64 enhanced the binding of Bax alpha to Bcl-2 (Fig. S4), and Asp-33 is central for the activation of Bax by proteases during apoptosis ( ,  ).	bind
47624	1	10711	5	13	NULL	NULL	NULL	SET7/9	GP		exclude		sterically	residues in lysine binding channel					target lysine side chain with methyl group		NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_177_s_162	12887903	A likely explanation for their different product specificities is that residues in the lysine binding channel of SET7/9 sterically exclude the target lysine side chain with methyl group(s).	bind
46922	1	10711	6	10	NULL	0	NULL	SET7/9	NULL		exclude	NULL	sterically	residues in  lysine binding channel			NULL		lysine side chain with methyl group		NULL		NULL	NULL	NULL	NULL	gw60_molcell_12_1_177_s_162	12887903	A likely explanation for their different product specificities is that residues in the lysine binding channel of SET7/9 sterically exclude the target lysine side chain with methyl group(s).	bind
47625	1	10712	5	13	NULL	NULL	NULL	EcRE1	GP		bind					20E-EcRB11USPP1 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_7_4897_s_281	10373539	A likely explanation for these findings is that the EcRE1 binds the 20E-EcRB11USPP1 complex, and EcRE-like sequences 2 and 3 bind other transcription factors present in the cell extract.	bind
46923	1	10712	6	NULL	NULL	0	NULL	EcRE1 	NULL		bind	NULL				20E-EcRB11USPP1 complex	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4897_s_281	10373539	A likely explanation for these findings is that the EcRE1 binds the 20E-EcRB11USPP1 complex, and EcRE-like sequences 2 and 3 bind other transcription factors present in the cell extract.	bind
47626	1	10713	5	13	NULL	NULL	NULL	dIgA	GP		bind					pIgR	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_7_1787_s_46	9658171	A likely explanation for these results is that binding of dIgA to the pIgR leads to activation of a phosphatidyl inositol-specific phospholipase C (PLC).	bind
47627	2	10713	5	13	NULL	NULL	NULL	statement 1	Process		leads to					PLC	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_7_1787_s_46	9658171	A likely explanation for these results is that binding of dIgA to the pIgR leads to activation of a phosphatidyl inositol-specific phospholipase C (PLC).	bind
47628	3	10713	5	13	NULL	NULL	NULL	PLC	GP		is					phosphatidyl inositol-specific phospholipase C	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_7_1787_s_46	9658171	A likely explanation for these results is that binding of dIgA to the pIgR leads to activation of a phosphatidyl inositol-specific phospholipase C (PLC).	bind
46924	1	10713	6	NULL	NULL	0	NULL	dIgA	NULL		bind	NULL				pIgR	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_7_1787_s_46	9658171	A likely explanation for these results is that binding of dIgA to the pIgR leads to activation of a phosphatidyl inositol-specific phospholipase C (PLC).	bind
46925	2	10713	6	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				PLC	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_7_1787_s_46	9658171	A likely explanation for these results is that binding of dIgA to the pIgR leads to activation of a phosphatidyl inositol-specific phospholipase C (PLC).	bind
46926	3	10713	6	NULL	NULL	0	NULL	PLC	NULL		is	NULL				phosphatidyl inositol-specific phospholipase C	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_7_1787_s_46	9658171	A likely explanation for these results is that binding of dIgA to the pIgR leads to activation of a phosphatidyl inositol-specific phospholipase C (PLC).	bind
47629	1	10714	5	13	NULL	NULL	NULL	H-NS	GP		bind					donor DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_18_2224_s_270	16166383	A likely explanation for this apparent paradox, and supported by data presented here, is that H-NS binding to the donor DNA initiates unfolding, and then additional molecules of H-NS bind within the terminal inverted repeat, effectively locking in the unfolded conformation.	bind
47630	2	10714	5	13	NULL	NULL	NULL	statement 1	Process		initiates					unfolding	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_18_2224_s_270	16166383	A likely explanation for this apparent paradox, and supported by data presented here, is that H-NS binding to the donor DNA initiates unfolding, and then additional molecules of H-NS bind within the terminal inverted repeat, effectively locking in the unfolded conformation.	bind
47631	3	10714	5	13	NULL	NULL	NULL	H-NS	GP		bind									terminal inverted repeat	NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_18_2224_s_270	16166383	A likely explanation for this apparent paradox, and supported by data presented here, is that H-NS binding to the donor DNA initiates unfolding, and then additional molecules of H-NS bind within the terminal inverted repeat, effectively locking in the unfolded conformation.	bind
47632	4	10714	5	13	NULL	NULL	NULL	statement 3	Process		locks		effectively			unfolded conformation	Process				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_18_2224_s_270	16166383	A likely explanation for this apparent paradox, and supported by data presented here, is that H-NS binding to the donor DNA initiates unfolding, and then additional molecules of H-NS bind within the terminal inverted repeat, effectively locking in the unfolded conformation.	bind
46927	1	10714	6	NULL	NULL	0	NULL	H-NS	NULL		bind	NULL				donor DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_18_2224_s_270	16166383	A likely explanation for this apparent paradox, and supported by data presented here, is that H-NS binding to the donor DNA initiates unfolding, and then additional molecules of H-NS bind within the terminal inverted repeat, effectively locking in the unfolded conformation.	bind
46928	2	10714	6	NULL	NULL	0	NULL	statement 1	NULL		initiates	NULL				unfolding	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_18_2224_s_270	16166383	A likely explanation for this apparent paradox, and supported by data presented here, is that H-NS binding to the donor DNA initiates unfolding, and then additional molecules of H-NS bind within the terminal inverted repeat, effectively locking in the unfolded conformation.	bind
46929	3	10714	6	NULL	NULL	0	NULL	H-NS molecules	NULL		bind	NULL					NULL			terminal inverted repeat	NULL		0	NULL	NULL	NULL	gw70_genesdev_19_18_2224_s_270	16166383	A likely explanation for this apparent paradox, and supported by data presented here, is that H-NS binding to the donor DNA initiates unfolding, and then additional molecules of H-NS bind within the terminal inverted repeat, effectively locking in the unfolded conformation.	bind
50338	4	10714	6	10	NULL	0	NULL	statement 3	NULL		locks	NULL	effectively			unfolded conformation	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_18_2224_s_270	16166383	A likely explanation for this apparent paradox, and supported by data presented here, is that H-NS binding to the donor DNA initiates unfolding, and then additional molecules of H-NS bind within the terminal inverted repeat, effectively locking in the unfolded conformation.	bind
47633	1	10715	5	13	NULL	NULL	NULL	Src protein	GP		bind					PTP1B	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_26_24857_s_206	15866871	A likely explanation for this phenomenon is that Src proteins bound to PTP1B-trapping mutants are catalytically inactive because Tyr527 is phosphorylated, while Src proteins associated with the wild-type PTP1B are activated because of the removal of the inhibitory phosphate.	bind
47634	2	10715	5	13	NULL	NULL	NULL	Src proteins	GP		associate with					PTP1B	GP	wild-type			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_26_24857_s_206	15866871	A likely explanation for this phenomenon is that Src proteins bound to PTP1B-trapping mutants are catalytically inactive because Tyr527 is phosphorylated, while Src proteins associated with the wild-type PTP1B are activated because of the removal of the inhibitory phosphate.	bind
47635	3	10715	5	13	NULL	NULL	NULL	inhibitory phosphate	Chemical	removal of	makes					statement 2	Process	activated			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_26_24857_s_206	15866871	A likely explanation for this phenomenon is that Src proteins bound to PTP1B-trapping mutants are catalytically inactive because Tyr527 is phosphorylated, while Src proteins associated with the wild-type PTP1B are activated because of the removal of the inhibitory phosphate.	bind
47636	4	10715	5	13	NULL	NULL	NULL	Src protein	GP	phosphorylated	makes			Tyr527		statement 1	Process	catalytically inactive			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_26_24857_s_206	15866871	A likely explanation for this phenomenon is that Src proteins bound to PTP1B-trapping mutants are catalytically inactive because Tyr527 is phosphorylated, while Src proteins associated with the wild-type PTP1B are activated because of the removal of the inhibitory phosphate.	bind
46930	1	10715	6	NULL	NULL	0	NULL	Src protein	NULL		bind	NULL				PTP1B	NULL	mutant			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_26_24857_s_206	15866871	A likely explanation for this phenomenon is that Src proteins bound to PTP1B-trapping mutants are catalytically inactive because Tyr527 is phosphorylated, while Src proteins associated with the wild-type PTP1B are activated because of the removal of the inhibitory phosphate.	bind
46931	2	10715	6	NULL	NULL	0	NULL		NULL	phosphorylated	makes	NULL		Tyr527		Src	NULL	catalytically inactive			NULL	statement 1	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_26_24857_s_206	15866871	A likely explanation for this phenomenon is that Src proteins bound to PTP1B-trapping mutants are catalytically inactive because Tyr527 is phosphorylated, while Src proteins associated with the wild-type PTP1B are activated because of the removal of the inhibitory phosphate.	bind
46932	3	10715	6	NULL	NULL	0	NULL	Src protein	NULL		bind	NULL				PTP1B	NULL	wild type			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_26_24857_s_206	15866871	A likely explanation for this phenomenon is that Src proteins bound to PTP1B-trapping mutants are catalytically inactive because Tyr527 is phosphorylated, while Src proteins associated with the wild-type PTP1B are activated because of the removal of the inhibitory phosphate.	bind
46933	4	10715	6	NULL	NULL	0	NULL	phosphate	NULL	removal of;; inhibitory	makes	NULL				Src	NULL	active			NULL	statement 1	0	NULL	NULL	NULL	gw70_jbiolchem_280_26_24857_s_206	15866871	A likely explanation for this phenomenon is that Src proteins bound to PTP1B-trapping mutants are catalytically inactive because Tyr527 is phosphorylated, while Src proteins associated with the wild-type PTP1B are activated because of the removal of the inhibitory phosphate.	bind
47637	1	10717	5	13	NULL	NULL	NULL	IFNAR1/IFNAR2	GP		is a type of					membrane-anchored receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_11_6138_s_229	11344274	A likely explanation is that the  Kd of the soluble receptor for IFN-tau4 (70 nM) is sufficient for it to be detected in a binding assay but too high for it to compete effectively for ligand with the IFNAR1/IFNAR2 membrane-anchored receptor of MDBK cells, which binds IFN-tau with a  Kd of  0.3 nM (unpublished data).	bind
47638	2	10717	5	13	NULL	NULL	NULL	IFNAR1/IFNAR2	GP		bind					IFN-tau	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_11_6138_s_229	11344274	A likely explanation is that the  Kd of the soluble receptor for IFN-tau4 (70 nM) is sufficient for it to be detected in a binding assay but too high for it to compete effectively for ligand with the IFNAR1/IFNAR2 membrane-anchored receptor of MDBK cells, which binds IFN-tau with a  Kd of  0.3 nM (unpublished data).	bind
46934	1	10717	6	NULL	NULL	0	NULL	IFNAR1/IFNAR2	NULL		bind	NULL				IFN-tau	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_98_11_6138_s_229	11344274	A likely explanation is that the  Kd of the soluble receptor for IFN-tau4 (70 nM) is sufficient for it to be detected in a binding assay but too high for it to compete effectively for ligand with the IFNAR1/IFNAR2 membrane-anchored receptor of MDBK cells, which binds IFN-tau with a  Kd of  0.3 nM (unpublished data).	bind
46935	2	10717	6	NULL	NULL	0	NULL	IFNAR1/IFNAR2	NULL		is a type of 	NULL				membrane anchored receptor of MDBK cells	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_98_11_6138_s_229	11344274	A likely explanation is that the  Kd of the soluble receptor for IFN-tau4 (70 nM) is sufficient for it to be detected in a binding assay but too high for it to compete effectively for ligand with the IFNAR1/IFNAR2 membrane-anchored receptor of MDBK cells, which binds IFN-tau with a  Kd of  0.3 nM (unpublished data).	bind
47639	1	10718	5	13	NULL	NULL	NULL	phosphorylation	Process		inhibit		possibly			protein 4.1	GP	function of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_51_47869_s_234	11604393	A likely explanation is the inhibition of protein 4.1 function by phosphorylation, which reduces its ability to promote binding of F-actin to spectrin ( 40,  41).	bind
47640	2	10718	5	13	NULL	NULL	NULL	F-actin	GP		bind					spectrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_51_47869_s_234	11604393	A likely explanation is the inhibition of protein 4.1 function by phosphorylation, which reduces its ability to promote binding of F-actin to spectrin ( 40,  41).	bind
47641	3	10718	5	13	NULL	NULL	NULL	protein 4.1	GP		promotes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_51_47869_s_234	11604393	A likely explanation is the inhibition of protein 4.1 function by phosphorylation, which reduces its ability to promote binding of F-actin to spectrin ( 40,  41).	bind
47642	4	10718	5	13	NULL	NULL	NULL	statement 1	Process		reduces					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_51_47869_s_234	11604393	A likely explanation is the inhibition of protein 4.1 function by phosphorylation, which reduces its ability to promote binding of F-actin to spectrin ( 40,  41).	bind
46936	1	10718	6	NULL	NULL	0	NULL	F-actin	NULL		bind	NULL				spectrin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_47869_s_234	11604393	A likely explanation is the inhibition of protein 4.1 function by phosphorylation, which reduces its ability to promote binding of F-actin to spectrin ( 40,  41).	bind
46937	2	10718	6	NULL	NULL	0	NULL	protein 4.1	NULL	function of	is inhibited by	NULL				phosphorylation	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_47869_s_234	11604393	A likely explanation is the inhibition of protein 4.1 function by phosphorylation, which reduces its ability to promote binding of F-actin to spectrin ( 40,  41).	bind
46938	3	10718	6	NULL	NULL	0	NULL	protein 4.1	NULL		promotes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_47869_s_234	11604393	A likely explanation is the inhibition of protein 4.1 function by phosphorylation, which reduces its ability to promote binding of F-actin to spectrin ( 40,  41).	bind
46939	4	10718	6	NULL	NULL	0	NULL	statement 2	NULL		reduces	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_47869_s_234	11604393	A likely explanation is the inhibition of protein 4.1 function by phosphorylation, which reduces its ability to promote binding of F-actin to spectrin ( 40,  41).	bind
47643	1	10719	5	13	NULL	NULL	NULL	JIP-1	GP		bind					APP	GP				NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_25_15_3741_s_368	15829626	A likely explanation, supported by our results ( Fig. 3), is that JIP-1 binding to APP is competed off by proteins with higher affinity or more abundant than JIP-1 (e.g., Fe65) (Matsuda et al., 2001 ), or that in neurons, the phosphorylation of APP through the JIP-3-dependent pathway prevails and is distinct from that implicating JIP-1.	bind
47644	2	10719	5	13	NULL	NULL	NULL	APP	GP	phosphorylation of	occurs through					JIP-3-dependent pathway	Process				NULL	neurons	NULL	NULL	NULL	NULL	gw70_jneurosci_25_15_3741_s_368	15829626	A likely explanation, supported by our results ( Fig. 3), is that JIP-1 binding to APP is competed off by proteins with higher affinity or more abundant than JIP-1 (e.g., Fe65) (Matsuda et al., 2001 ), or that in neurons, the phosphorylation of APP through the JIP-3-dependent pathway prevails and is distinct from that implicating JIP-1.	bind
46940	1	10719	6	NULL	NULL	0	NULL	JIP-1	NULL		bind	NULL				APP	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_25_15_3741_s_368	15829626	A likely explanation, supported by our results ( Fig. 3), is that JIP-1 binding to APP is competed off by proteins with higher affinity or more abundant than JIP-1 (e.g., Fe65) (Matsuda et al., 2001 ), or that in neurons, the phosphorylation of APP through the JIP-3-dependent pathway prevails and is distinct from that implicating JIP-1.	bind
46941	2	10719	6	NULL	NULL	0	NULL	APP	NULL	phosphorylation of	occurs through	NULL				JIP-3-dependent pathway	NULL				NULL	neurons	NULL	NULL	NULL	NULL	gw70_jneurosci_25_15_3741_s_368	15829626	A likely explanation, supported by our results ( Fig. 3), is that JIP-1 binding to APP is competed off by proteins with higher affinity or more abundant than JIP-1 (e.g., Fe65) (Matsuda et al., 2001 ), or that in neurons, the phosphorylation of APP through the JIP-3-dependent pathway prevails and is distinct from that implicating JIP-1.	bind
47645	1	10720	5	13	NULL	NULL	NULL	regulatory proteins	GP		bind								terminal alpha rings		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18557_s_27	10764772	A likely mechanism for control of substrate access to the proteasome involves binding of regulatory proteins to its terminal alpha rings.	bind
50342	2	10720	5	13	NULL	NULL	NULL	substrate	GP		access to					proteasome	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18557_s_27	10764772	A likely mechanism for control of substrate access to the proteasome involves binding of regulatory proteins to its terminal alpha rings.	bind
50343	3	10720	5	13	NULL	NULL	NULL	statement 2	Process	control of	involves					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18557_s_27	10764772	A likely mechanism for control of substrate access to the proteasome involves binding of regulatory proteins to its terminal alpha rings.	bind
46942	1	10720	6	10	NULL	0	NULL	regulatory proteins	NULL		bind	NULL				alpha rings	NULL		terminal		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18557_s_27	10764772	A likely mechanism for control of substrate access to the proteasome involves binding of regulatory proteins to its terminal alpha rings.	bind
46973	2	10720	6	NULL	NULL	0	NULL	substrate	NULL		access to	NULL				proteasome	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_24_18557_s_27	10764772	A likely mechanism for control of substrate access to the proteasome involves binding of regulatory proteins to its terminal alpha rings.	bind
46974	3	10720	6	NULL	NULL	0	NULL	statement 2	NULL	control of	involves	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_24_18557_s_27	10764772	A likely mechanism for control of substrate access to the proteasome involves binding of regulatory proteins to its terminal alpha rings.	bind
50802	1	10721	5	13	NULL	NULL	NULL	Abeta	GP		is present in					membrane compartment	CellComponent	detergent-insoluble			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_36_27901_s_27	10846187	A likely possibility is that the earliest abnormality in beta-amyloidogenesis is the altered intracellular trafficking of the specific membrane domains, because i) a substantial fraction of Abeta is present in the detergent-insoluble membrane compartment, which is rich in cholesterol and sphingolipids, in cultured cells and rat brains ( 26,  27); ii) Abeta, generated from apically missorted APP in a cholesterol-dependent manner in Madin-Darby canine kidney cells, serves as a seed for Abeta fibrillogenesis ( 28); iii) GM1 ganglioside-bound Abeta is detected in Down's syndrome brains exhibiting exclusively diffuse plaques, the earliest stage of senile plaques ( 29); and iv) the addition of GM1-containing vesicles to Abeta solution dramatically accelerates Abeta fibril formation  in vitro ( 30).	bind
50803	2	10721	5	13	NULL	NULL	NULL	membrane compartment	CellComponent	detergent-insoluble	is rich in					cholesterol	Chemical				NULL	cultured cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_36_27901_s_27	10846187	A likely possibility is that the earliest abnormality in beta-amyloidogenesis is the altered intracellular trafficking of the specific membrane domains, because i) a substantial fraction of Abeta is present in the detergent-insoluble membrane compartment, which is rich in cholesterol and sphingolipids, in cultured cells and rat brains ( 26,  27); ii) Abeta, generated from apically missorted APP in a cholesterol-dependent manner in Madin-Darby canine kidney cells, serves as a seed for Abeta fibrillogenesis ( 28); iii) GM1 ganglioside-bound Abeta is detected in Down's syndrome brains exhibiting exclusively diffuse plaques, the earliest stage of senile plaques ( 29); and iv) the addition of GM1-containing vesicles to Abeta solution dramatically accelerates Abeta fibril formation  in vitro ( 30).	bind
50804	3	10721	5	13	NULL	NULL	NULL	membrane compartment	CellComponent	detergent-insoluble	is rich in					sphingolipids	Chemical				NULL	cultured cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_36_27901_s_27	10846187	A likely possibility is that the earliest abnormality in beta-amyloidogenesis is the altered intracellular trafficking of the specific membrane domains, because i) a substantial fraction of Abeta is present in the detergent-insoluble membrane compartment, which is rich in cholesterol and sphingolipids, in cultured cells and rat brains ( 26,  27); ii) Abeta, generated from apically missorted APP in a cholesterol-dependent manner in Madin-Darby canine kidney cells, serves as a seed for Abeta fibrillogenesis ( 28); iii) GM1 ganglioside-bound Abeta is detected in Down's syndrome brains exhibiting exclusively diffuse plaques, the earliest stage of senile plaques ( 29); and iv) the addition of GM1-containing vesicles to Abeta solution dramatically accelerates Abeta fibril formation  in vitro ( 30).	bind
50805	4	10721	5	13	NULL	NULL	NULL	membrane compartment	CellComponent	detergent-insoluble	is rich in					cholesterol	Chemical				NULL	rat brains	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_36_27901_s_27	10846187	A likely possibility is that the earliest abnormality in beta-amyloidogenesis is the altered intracellular trafficking of the specific membrane domains, because i) a substantial fraction of Abeta is present in the detergent-insoluble membrane compartment, which is rich in cholesterol and sphingolipids, in cultured cells and rat brains ( 26,  27); ii) Abeta, generated from apically missorted APP in a cholesterol-dependent manner in Madin-Darby canine kidney cells, serves as a seed for Abeta fibrillogenesis ( 28); iii) GM1 ganglioside-bound Abeta is detected in Down's syndrome brains exhibiting exclusively diffuse plaques, the earliest stage of senile plaques ( 29); and iv) the addition of GM1-containing vesicles to Abeta solution dramatically accelerates Abeta fibril formation  in vitro ( 30).	bind
50806	5	10721	5	13	NULL	NULL	NULL	membrane compartment	CellComponent	detergent-insoluble	is rich in					sphingolipids	Chemical				NULL	rat brains	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_36_27901_s_27	10846187	A likely possibility is that the earliest abnormality in beta-amyloidogenesis is the altered intracellular trafficking of the specific membrane domains, because i) a substantial fraction of Abeta is present in the detergent-insoluble membrane compartment, which is rich in cholesterol and sphingolipids, in cultured cells and rat brains ( 26,  27); ii) Abeta, generated from apically missorted APP in a cholesterol-dependent manner in Madin-Darby canine kidney cells, serves as a seed for Abeta fibrillogenesis ( 28); iii) GM1 ganglioside-bound Abeta is detected in Down's syndrome brains exhibiting exclusively diffuse plaques, the earliest stage of senile plaques ( 29); and iv) the addition of GM1-containing vesicles to Abeta solution dramatically accelerates Abeta fibril formation  in vitro ( 30).	bind
50807	6	10721	5	13	NULL	NULL	NULL	Abeta	GP		is generated from					APP	GP	apically missorted			NULL	Madin-Darby canine kidney cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_36_27901_s_27	10846187	A likely possibility is that the earliest abnormality in beta-amyloidogenesis is the altered intracellular trafficking of the specific membrane domains, because i) a substantial fraction of Abeta is present in the detergent-insoluble membrane compartment, which is rich in cholesterol and sphingolipids, in cultured cells and rat brains ( 26,  27); ii) Abeta, generated from apically missorted APP in a cholesterol-dependent manner in Madin-Darby canine kidney cells, serves as a seed for Abeta fibrillogenesis ( 28); iii) GM1 ganglioside-bound Abeta is detected in Down's syndrome brains exhibiting exclusively diffuse plaques, the earliest stage of senile plaques ( 29); and iv) the addition of GM1-containing vesicles to Abeta solution dramatically accelerates Abeta fibril formation  in vitro ( 30).	bind
50808	7	10721	5	13	NULL	NULL	NULL	statement 6	Process		is dependent on					cholesterol	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_36_27901_s_27	10846187	A likely possibility is that the earliest abnormality in beta-amyloidogenesis is the altered intracellular trafficking of the specific membrane domains, because i) a substantial fraction of Abeta is present in the detergent-insoluble membrane compartment, which is rich in cholesterol and sphingolipids, in cultured cells and rat brains ( 26,  27); ii) Abeta, generated from apically missorted APP in a cholesterol-dependent manner in Madin-Darby canine kidney cells, serves as a seed for Abeta fibrillogenesis ( 28); iii) GM1 ganglioside-bound Abeta is detected in Down's syndrome brains exhibiting exclusively diffuse plaques, the earliest stage of senile plaques ( 29); and iv) the addition of GM1-containing vesicles to Abeta solution dramatically accelerates Abeta fibril formation  in vitro ( 30).	bind
50809	8	10721	5	13	NULL	NULL	NULL	statement 6	Process		serves as a seed for					Abeta fibrillogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_36_27901_s_27	10846187	A likely possibility is that the earliest abnormality in beta-amyloidogenesis is the altered intracellular trafficking of the specific membrane domains, because i) a substantial fraction of Abeta is present in the detergent-insoluble membrane compartment, which is rich in cholesterol and sphingolipids, in cultured cells and rat brains ( 26,  27); ii) Abeta, generated from apically missorted APP in a cholesterol-dependent manner in Madin-Darby canine kidney cells, serves as a seed for Abeta fibrillogenesis ( 28); iii) GM1 ganglioside-bound Abeta is detected in Down's syndrome brains exhibiting exclusively diffuse plaques, the earliest stage of senile plaques ( 29); and iv) the addition of GM1-containing vesicles to Abeta solution dramatically accelerates Abeta fibril formation  in vitro ( 30).	bind
50810	9	10721	5	13	NULL	NULL	NULL	GM1 ganglioside	GP		bind					Abeta	GP				NULL	Down's syndrome brains exhibiting exclusively diffuse plaques	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_36_27901_s_27	10846187	A likely possibility is that the earliest abnormality in beta-amyloidogenesis is the altered intracellular trafficking of the specific membrane domains, because i) a substantial fraction of Abeta is present in the detergent-insoluble membrane compartment, which is rich in cholesterol and sphingolipids, in cultured cells and rat brains ( 26,  27); ii) Abeta, generated from apically missorted APP in a cholesterol-dependent manner in Madin-Darby canine kidney cells, serves as a seed for Abeta fibrillogenesis ( 28); iii) GM1 ganglioside-bound Abeta is detected in Down's syndrome brains exhibiting exclusively diffuse plaques, the earliest stage of senile plaques ( 29); and iv) the addition of GM1-containing vesicles to Abeta solution dramatically accelerates Abeta fibril formation  in vitro ( 30).	bind
50811	10	10721	5	13	NULL	NULL	NULL	GM1-containing vesicles	CellComponent		accelerates		dramatically			Abeta	GP	fibril formation of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_36_27901_s_27	10846187	A likely possibility is that the earliest abnormality in beta-amyloidogenesis is the altered intracellular trafficking of the specific membrane domains, because i) a substantial fraction of Abeta is present in the detergent-insoluble membrane compartment, which is rich in cholesterol and sphingolipids, in cultured cells and rat brains ( 26,  27); ii) Abeta, generated from apically missorted APP in a cholesterol-dependent manner in Madin-Darby canine kidney cells, serves as a seed for Abeta fibrillogenesis ( 28); iii) GM1 ganglioside-bound Abeta is detected in Down's syndrome brains exhibiting exclusively diffuse plaques, the earliest stage of senile plaques ( 29); and iv) the addition of GM1-containing vesicles to Abeta solution dramatically accelerates Abeta fibril formation  in vitro ( 30).	bind
47371	1	10721	6	NULL	NULL	0	NULL	Abeta	NULL		is present in	NULL				membrane compartment	NULL	detergent insoluble			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27901_s_27	10846187	A likely possibility is that the earliest abnormality in beta-amyloidogenesis is the altered intracellular trafficking of the specific membrane domains, because i) a substantial fraction of Abeta is present in the detergent-insoluble membrane compartment, which is rich in cholesterol and sphingolipids, in cultured cells and rat brains ( 26,  27); ii) Abeta, generated from apically missorted APP in a cholesterol-dependent manner in Madin-Darby canine kidney cells, serves as a seed for Abeta fibrillogenesis ( 28); iii) GM1 ganglioside-bound Abeta is detected in Down's syndrome brains exhibiting exclusively diffuse plaques, the earliest stage of senile plaques ( 29); and iv) the addition of GM1-containing vesicles to Abeta solution dramatically accelerates Abeta fibril formation  in vitro ( 30).	bind
47372	2	10721	6	NULL	NULL	0	NULL	membrane compartment	NULL	detergent insoluble	is rich in	NULL				cholesterol	NULL				NULL	cultured cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_36_27901_s_27	10846187	A likely possibility is that the earliest abnormality in beta-amyloidogenesis is the altered intracellular trafficking of the specific membrane domains, because i) a substantial fraction of Abeta is present in the detergent-insoluble membrane compartment, which is rich in cholesterol and sphingolipids, in cultured cells and rat brains ( 26,  27); ii) Abeta, generated from apically missorted APP in a cholesterol-dependent manner in Madin-Darby canine kidney cells, serves as a seed for Abeta fibrillogenesis ( 28); iii) GM1 ganglioside-bound Abeta is detected in Down's syndrome brains exhibiting exclusively diffuse plaques, the earliest stage of senile plaques ( 29); and iv) the addition of GM1-containing vesicles to Abeta solution dramatically accelerates Abeta fibril formation  in vitro ( 30).	bind
47373	3	10721	6	NULL	NULL	0	NULL	membrane compartment	NULL	detergent insoluble	is rich in	NULL				sphingolipids	NULL				NULL	cultured cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_36_27901_s_27	10846187	A likely possibility is that the earliest abnormality in beta-amyloidogenesis is the altered intracellular trafficking of the specific membrane domains, because i) a substantial fraction of Abeta is present in the detergent-insoluble membrane compartment, which is rich in cholesterol and sphingolipids, in cultured cells and rat brains ( 26,  27); ii) Abeta, generated from apically missorted APP in a cholesterol-dependent manner in Madin-Darby canine kidney cells, serves as a seed for Abeta fibrillogenesis ( 28); iii) GM1 ganglioside-bound Abeta is detected in Down's syndrome brains exhibiting exclusively diffuse plaques, the earliest stage of senile plaques ( 29); and iv) the addition of GM1-containing vesicles to Abeta solution dramatically accelerates Abeta fibril formation  in vitro ( 30).	bind
47374	4	10721	6	NULL	NULL	0	NULL	membrane compartment	NULL	detergent insoluble	is rich in	NULL				cholesterol	NULL				NULL	rat brains	0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27901_s_27	10846187	A likely possibility is that the earliest abnormality in beta-amyloidogenesis is the altered intracellular trafficking of the specific membrane domains, because i) a substantial fraction of Abeta is present in the detergent-insoluble membrane compartment, which is rich in cholesterol and sphingolipids, in cultured cells and rat brains ( 26,  27); ii) Abeta, generated from apically missorted APP in a cholesterol-dependent manner in Madin-Darby canine kidney cells, serves as a seed for Abeta fibrillogenesis ( 28); iii) GM1 ganglioside-bound Abeta is detected in Down's syndrome brains exhibiting exclusively diffuse plaques, the earliest stage of senile plaques ( 29); and iv) the addition of GM1-containing vesicles to Abeta solution dramatically accelerates Abeta fibril formation  in vitro ( 30).	bind
47375	5	10721	6	NULL	NULL	0	NULL	membrane compartment	NULL	detergent insoluble	is rich in	NULL				sphingolipids	NULL				NULL	rat brains	0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27901_s_27	10846187	A likely possibility is that the earliest abnormality in beta-amyloidogenesis is the altered intracellular trafficking of the specific membrane domains, because i) a substantial fraction of Abeta is present in the detergent-insoluble membrane compartment, which is rich in cholesterol and sphingolipids, in cultured cells and rat brains ( 26,  27); ii) Abeta, generated from apically missorted APP in a cholesterol-dependent manner in Madin-Darby canine kidney cells, serves as a seed for Abeta fibrillogenesis ( 28); iii) GM1 ganglioside-bound Abeta is detected in Down's syndrome brains exhibiting exclusively diffuse plaques, the earliest stage of senile plaques ( 29); and iv) the addition of GM1-containing vesicles to Abeta solution dramatically accelerates Abeta fibril formation  in vitro ( 30).	bind
47376	6	10721	6	NULL	NULL	0	NULL	APP	NULL	apically missorted	serves as a seed for	NULL				Abeta fibrillogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27901_s_27	10846187	A likely possibility is that the earliest abnormality in beta-amyloidogenesis is the altered intracellular trafficking of the specific membrane domains, because i) a substantial fraction of Abeta is present in the detergent-insoluble membrane compartment, which is rich in cholesterol and sphingolipids, in cultured cells and rat brains ( 26,  27); ii) Abeta, generated from apically missorted APP in a cholesterol-dependent manner in Madin-Darby canine kidney cells, serves as a seed for Abeta fibrillogenesis ( 28); iii) GM1 ganglioside-bound Abeta is detected in Down's syndrome brains exhibiting exclusively diffuse plaques, the earliest stage of senile plaques ( 29); and iv) the addition of GM1-containing vesicles to Abeta solution dramatically accelerates Abeta fibril formation  in vitro ( 30).	bind
47377	7	10721	6	NULL	NULL	0	NULL	GM1 ganglioside	NULL		bind	NULL				Abeta	NULL				NULL	Down's syndrome brains exhibiting exclusively diffuse plaques	0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27901_s_27	10846187	A likely possibility is that the earliest abnormality in beta-amyloidogenesis is the altered intracellular trafficking of the specific membrane domains, because i) a substantial fraction of Abeta is present in the detergent-insoluble membrane compartment, which is rich in cholesterol and sphingolipids, in cultured cells and rat brains ( 26,  27); ii) Abeta, generated from apically missorted APP in a cholesterol-dependent manner in Madin-Darby canine kidney cells, serves as a seed for Abeta fibrillogenesis ( 28); iii) GM1 ganglioside-bound Abeta is detected in Down's syndrome brains exhibiting exclusively diffuse plaques, the earliest stage of senile plaques ( 29); and iv) the addition of GM1-containing vesicles to Abeta solution dramatically accelerates Abeta fibril formation  in vitro ( 30).	bind
47378	8	10721	6	NULL	NULL	0	NULL	GM1-containing vesicles	NULL	addition of	accelerates	NULL				Abeta	NULL	fibril formation of			NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27901_s_27	10846187	A likely possibility is that the earliest abnormality in beta-amyloidogenesis is the altered intracellular trafficking of the specific membrane domains, because i) a substantial fraction of Abeta is present in the detergent-insoluble membrane compartment, which is rich in cholesterol and sphingolipids, in cultured cells and rat brains ( 26,  27); ii) Abeta, generated from apically missorted APP in a cholesterol-dependent manner in Madin-Darby canine kidney cells, serves as a seed for Abeta fibrillogenesis ( 28); iii) GM1 ganglioside-bound Abeta is detected in Down's syndrome brains exhibiting exclusively diffuse plaques, the earliest stage of senile plaques ( 29); and iv) the addition of GM1-containing vesicles to Abeta solution dramatically accelerates Abeta fibril formation  in vitro ( 30).	bind
47646	1	10722	5	13	NULL	NULL	NULL	AP-1	GP		suppress					ET-1	GP	expression of			NULL	EC	NULL	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_236	16357303	A likely role of BA/FXR-mediated inhibition of AP-1 activity in suppressing ET-1 expression in EC was further supported by results from ChIP assays in which CDCA treatment led to decreased binding of c-Jun to an AP-1 binding site in ET-1 promoter in RPAEC ( Figure 8C).	bind
47647	2	10722	5	13	NULL	NULL	NULL	c-Jun	GP		bind					ET-1	GP			AP-1 binding site in promoter	NULL	RPAEC	NULL	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_236	16357303	A likely role of BA/FXR-mediated inhibition of AP-1 activity in suppressing ET-1 expression in EC was further supported by results from ChIP assays in which CDCA treatment led to decreased binding of c-Jun to an AP-1 binding site in ET-1 promoter in RPAEC ( Figure 8C).	bind
50344	3	10722	5	13	NULL	NULL	NULL	BA/FXR	GP		mediates					statement 1	Process	inhibition of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_236	16357303	A likely role of BA/FXR-mediated inhibition of AP-1 activity in suppressing ET-1 expression in EC was further supported by results from ChIP assays in which CDCA treatment led to decreased binding of c-Jun to an AP-1 binding site in ET-1 promoter in RPAEC ( Figure 8C).	bind
50345	4	10722	5	13	NULL	NULL	NULL	CDCA	GP		decrease					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_236	16357303	A likely role of BA/FXR-mediated inhibition of AP-1 activity in suppressing ET-1 expression in EC was further supported by results from ChIP assays in which CDCA treatment led to decreased binding of c-Jun to an AP-1 binding site in ET-1 promoter in RPAEC ( Figure 8C).	bind
46975	1	10722	6	NULL	NULL	0	NULL	c-Jun	NULL		bind	NULL				ET-1	NULL			AP-1 binding site of promoter	NULL		0	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_236	16357303	A likely role of BA/FXR-mediated inhibition of AP-1 activity in suppressing ET-1 expression in EC was further supported by results from ChIP assays in which CDCA treatment led to decreased binding of c-Jun to an AP-1 binding site in ET-1 promoter in RPAEC ( Figure 8C).	bind
46976	2	10722	6	10	NULL	0	NULL	AP-1	NULL		suppress	NULL				ET-1	NULL	expression of			NULL	EC	NULL	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_236	16357303	A likely role of BA/FXR-mediated inhibition of AP-1 activity in suppressing ET-1 expression in EC was further supported by results from ChIP assays in which CDCA treatment led to decreased binding of c-Jun to an AP-1 binding site in ET-1 promoter in RPAEC ( Figure 8C).	bind
46977	3	10722	6	NULL	NULL	0	NULL	CDCA	NULL		decreases	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_236	16357303	A likely role of BA/FXR-mediated inhibition of AP-1 activity in suppressing ET-1 expression in EC was further supported by results from ChIP assays in which CDCA treatment led to decreased binding of c-Jun to an AP-1 binding site in ET-1 promoter in RPAEC ( Figure 8C).	bind
50347	4	10722	6	10	NULL	0	NULL	BA/FXR	NULL		mediates	NULL				statement 2	NULL	inhibition of			NULL		0	NULL	NULL	NULL	gw70_circulationres_98_2_192_s_236	16357303	A likely role of BA/FXR-mediated inhibition of AP-1 activity in suppressing ET-1 expression in EC was further supported by results from ChIP assays in which CDCA treatment led to decreased binding of c-Jun to an AP-1 binding site in ET-1 promoter in RPAEC ( Figure 8C).	bind
47648	1	10723	5	13	NULL	NULL	NULL	SR proteins	GP		bind					exon	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_6_2411_s_139	7852296	A likely scenario invokes interactions between the SR  proteins bound to one exon with the SR proteins bound to an adjoining  exon.	bind
46978	1	10723	6	NULL	NULL	0	NULL	SR protein	NULL		bind	NULL				exon	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_6_2411_s_139	7852296	A likely scenario invokes interactions between the SR  proteins bound to one exon with the SR proteins bound to an adjoining  exon.	bind
47649	1	10725	5	13	NULL	NULL	NULL	PhcA	GP		bind					P xpsR	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbacteriol_180_10_2736_s_216	9573161	A likely site centered around  77 was confirmed and further defined by analysis of the effects of mutations in the site on in vivo expression from P xpsR and in vitro binding of PhcA to P xpsR.	bind
46979	1	10725	6	NULL	NULL	0	NULL	PhcA	NULL		bind	NULL				P xpsR	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_jbacteriol_180_10_2736_s_216	9573161	A likely site centered around  77 was confirmed and further defined by analysis of the effects of mutations in the site on in vivo expression from P xpsR and in vitro binding of PhcA to P xpsR.	bind
47650	1	10726	5	13	NULL	NULL	NULL	FAD	Chemical		bind					AO monomers	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_786_s_303	12589070	A likely way to explain both observations is that FAD binding to AO monomers in the cytosol is a prerequisite to allow efficient translocation into peroxisomes.	bind
50348	2	10726	5	13	NULL	NULL	NULL	statement 1	GP		allows					peroxisomes	CellComponent	translocation into			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_14_2_786_s_303	12589070	A likely way to explain both observations is that FAD binding to AO monomers in the cytosol is a prerequisite to allow efficient translocation into peroxisomes.	bind
46980	1	10726	6	NULL	NULL	0	NULL	FAD	NULL		bind	NULL				AO monomers	NULL				NULL	cytosol	0	NULL	NULL	NULL	gw60_molbiolcell_14_2_786_s_303	12589070	A likely way to explain both observations is that FAD binding to AO monomers in the cytosol is a prerequisite to allow efficient translocation into peroxisomes.	bind
46981	2	10726	6	NULL	NULL	0	NULL	statement 1	NULL		allows	NULL				peroxisomes	NULL	translocation into			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_2_786_s_303	12589070	A likely way to explain both observations is that FAD binding to AO monomers in the cytosol is a prerequisite to allow efficient translocation into peroxisomes.	bind
47651	1	10727	5	13	NULL	NULL	NULL	Ajuba protein	GP		bind			LIM domain		Aurora-A	GP	human	N-terminal noncatalytic domain of 		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_47201_s_301	15316025	A LIM domain containing the protein Ajuba binds and activates human Aurora-A through the N-terminal noncatalytic domain of Aurora-A ( ).	bind
47652	2	10727	5	13	NULL	NULL	NULL	statement 1	Process		activates					Aurora-A	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_47201_s_301	15316025	A LIM domain containing the protein Ajuba binds and activates human Aurora-A through the N-terminal noncatalytic domain of Aurora-A ( ).	bind
46982	1	10727	6	NULL	NULL	0	NULL	Ajuba protein	NULL		bind	NULL		LIM domain		Aurora-A	NULL	human	N-terminal noncatalytic domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_45_47201_s_301	15316025	A LIM domain containing the protein Ajuba binds and activates human Aurora-A through the N-terminal noncatalytic domain of Aurora-A ( ).	bind
46983	2	10727	6	10	NULL	0	NULL	statement 1			activates					Aurora-A		human			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_47201_s_301	15316025	A LIM domain containing the protein Ajuba binds and activates human Aurora-A through the N-terminal noncatalytic domain of Aurora-A ( ).	bind
47653	1	10728	5	13	NULL	NULL	NULL	Translin/Trax	GP		bind					L-PK	GP			GRE	NULL	in vivo	NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1624_1_29_s_178	14642810	A limitation of our study,  however, is that we do not presently know the extent of Translin/Trax binding to  the L-PK GRE in vivo.	bind
46984	1	10728	6	NULL	NULL	0	NULL	Translin/Trax	NULL		bind	NULL				L-PK	NULL			GRE	NULL	in vivo	0	NULL	NULL	NULL	gw70_biochimbiophysacta_1624_1_29_s_178	14642810	A limitation of our study,  however, is that we do not presently know the extent of Translin/Trax binding to  the L-PK GRE in vivo.	bind
47654	1	10729	5	13	NULL	NULL	NULL	TF	GP		bind					VII variants	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_19875_s_84	9242651	A limitation of the competitive assay approach is the presence of substrate that could differentially affect TF binding by the VII variants.	bind
46985	1	10729	6	NULL	NULL	0	NULL	VII variants	NULL		bind	NULL				TF	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_32_19875_s_84	9242651	A limitation of the competitive assay approach is the presence of substrate that could differentially affect TF binding by the VII variants.	bind
47655	1	10730	5	13	NULL	NULL	NULL	HeLa cells	Cell		contains					RARalpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_8_4355_s_161	8626785	A limitation of these experiments was that  HeLa cells contain multiple retinoid receptors (RARalpha, RAR ,  RXRbeta),   and the ligand used in these studies (ATRA) can  activate both classes of receptors (it binds to RARs directly and can  be isomerized  in vivo  to 9- cis-RA, which binds to  RXRs).	bind
47656	2	10730	5	13	NULL	NULL	NULL	RARalpha	GP		is a type of					retinoid receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_8_4355_s_161	8626785	A limitation of these experiments was that  HeLa cells contain multiple retinoid receptors (RARalpha, RAR ,  RXRbeta),   and the ligand used in these studies (ATRA) can  activate both classes of receptors (it binds to RARs directly and can  be isomerized  in vivo  to 9- cis-RA, which binds to  RXRs).	bind
47657	3	10730	5	13	NULL	NULL	NULL	HeLa cells	Cell		contains					RAR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_8_4355_s_161	8626785	A limitation of these experiments was that  HeLa cells contain multiple retinoid receptors (RARalpha, RAR ,  RXRbeta),   and the ligand used in these studies (ATRA) can  activate both classes of receptors (it binds to RARs directly and can  be isomerized  in vivo  to 9- cis-RA, which binds to  RXRs).	bind
47658	4	10730	5	13	NULL	NULL	NULL	RAR	GP		is a type of					retinoid receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_8_4355_s_161	8626785	A limitation of these experiments was that  HeLa cells contain multiple retinoid receptors (RARalpha, RAR ,  RXRbeta),   and the ligand used in these studies (ATRA) can  activate both classes of receptors (it binds to RARs directly and can  be isomerized  in vivo  to 9- cis-RA, which binds to  RXRs).	bind
47659	5	10730	5	13	NULL	NULL	NULL	HeLa cells	Cell		contains					RXRbeta	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_8_4355_s_161	8626785	A limitation of these experiments was that  HeLa cells contain multiple retinoid receptors (RARalpha, RAR ,  RXRbeta),   and the ligand used in these studies (ATRA) can  activate both classes of receptors (it binds to RARs directly and can  be isomerized  in vivo  to 9- cis-RA, which binds to  RXRs).	bind
47660	6	10730	5	13	NULL	NULL	NULL	RXRbeta	GP		is a type of					retinoid receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_8_4355_s_161	8626785	A limitation of these experiments was that  HeLa cells contain multiple retinoid receptors (RARalpha, RAR ,  RXRbeta),   and the ligand used in these studies (ATRA) can  activate both classes of receptors (it binds to RARs directly and can  be isomerized  in vivo  to 9- cis-RA, which binds to  RXRs).	bind
47661	7	10730	5	13	NULL	NULL	NULL	ATRA ligand	GP		bind		directly			RARs	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_8_4355_s_161	8626785	A limitation of these experiments was that  HeLa cells contain multiple retinoid receptors (RARalpha, RAR ,  RXRbeta),   and the ligand used in these studies (ATRA) can  activate both classes of receptors (it binds to RARs directly and can  be isomerized  in vivo  to 9- cis-RA, which binds to  RXRs).	bind
47662	8	10730	5	13	NULL	NULL	NULL	ATRA ligand	GP		is isomerized to					9- cis-RA	Chemical				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_8_4355_s_161	8626785	A limitation of these experiments was that  HeLa cells contain multiple retinoid receptors (RARalpha, RAR ,  RXRbeta),   and the ligand used in these studies (ATRA) can  activate both classes of receptors (it binds to RARs directly and can  be isomerized  in vivo  to 9- cis-RA, which binds to  RXRs).	bind
47663	9	10730	5	13	NULL	NULL	NULL	9- cis-RA	Chemical		bind					RXRs	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_8_4355_s_161	8626785	A limitation of these experiments was that  HeLa cells contain multiple retinoid receptors (RARalpha, RAR ,  RXRbeta),   and the ligand used in these studies (ATRA) can  activate both classes of receptors (it binds to RARs directly and can  be isomerized  in vivo  to 9- cis-RA, which binds to  RXRs).	bind
46986	1	10730	6	NULL	NULL	0	NULL	HeLa cells	NULL		contains	NULL				RARalpha	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_8_4355_s_161	8626785	A limitation of these experiments was that  HeLa cells contain multiple retinoid receptors (RARalpha, RAR ,  RXRbeta),   and the ligand used in these studies (ATRA) can  activate both classes of receptors (it binds to RARs directly and can  be isomerized  in vivo  to 9- cis-RA, which binds to  RXRs).	bind
46987	2	10730	6	NULL	NULL	0	NULL	HeLa cells	NULL		contain	NULL				RAR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_8_4355_s_161	8626785	A limitation of these experiments was that  HeLa cells contain multiple retinoid receptors (RARalpha, RAR ,  RXRbeta),   and the ligand used in these studies (ATRA) can  activate both classes of receptors (it binds to RARs directly and can  be isomerized  in vivo  to 9- cis-RA, which binds to  RXRs).	bind
46988	3	10730	6	NULL	NULL	0	NULL	HeLa cells	NULL		contain	NULL				RXRbeta	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_8_4355_s_161	8626785	A limitation of these experiments was that  HeLa cells contain multiple retinoid receptors (RARalpha, RAR ,  RXRbeta),   and the ligand used in these studies (ATRA) can  activate both classes of receptors (it binds to RARs directly and can  be isomerized  in vivo  to 9- cis-RA, which binds to  RXRs).	bind
46989	4	10730	6	NULL	NULL	0	NULL	ATRA	NULL		bind	NULL	directly			RARs	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_8_4355_s_161	8626785	A limitation of these experiments was that  HeLa cells contain multiple retinoid receptors (RARalpha, RAR ,  RXRbeta),   and the ligand used in these studies (ATRA) can  activate both classes of receptors (it binds to RARs directly and can  be isomerized  in vivo  to 9- cis-RA, which binds to  RXRs).	bind
46990	5	10730	6	NULL	NULL	0	NULL	ATRA	NULL		is isomerized to	NULL				9- cis-RA	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_jbiolchem_271_8_4355_s_161	8626785	A limitation of these experiments was that  HeLa cells contain multiple retinoid receptors (RARalpha, RAR ,  RXRbeta),   and the ligand used in these studies (ATRA) can  activate both classes of receptors (it binds to RARs directly and can  be isomerized  in vivo  to 9- cis-RA, which binds to  RXRs).	bind
46991	6	10730	6	NULL	NULL	0	NULL	9- cis-RA	NULL		bind	NULL				RXRs	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_8_4355_s_161	8626785	A limitation of these experiments was that  HeLa cells contain multiple retinoid receptors (RARalpha, RAR ,  RXRbeta),   and the ligand used in these studies (ATRA) can  activate both classes of receptors (it binds to RARs directly and can  be isomerized  in vivo  to 9- cis-RA, which binds to  RXRs).	bind
50349	7	10730	6	10	NULL	0	NULL	RARalpha	NULL		is a type of	NULL				retinoid receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_8_4355_s_161	8626785	A limitation of these experiments was that  HeLa cells contain multiple retinoid receptors (RARalpha, RAR ,  RXRbeta),   and the ligand used in these studies (ATRA) can  activate both classes of receptors (it binds to RARs directly and can  be isomerized  in vivo  to 9- cis-RA, which binds to  RXRs).	bind
50350	8	10730	6	10	NULL	0	NULL	RAR	NULL		is a type of	NULL				retinoid receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_8_4355_s_161	8626785	A limitation of these experiments was that  HeLa cells contain multiple retinoid receptors (RARalpha, RAR ,  RXRbeta),   and the ligand used in these studies (ATRA) can  activate both classes of receptors (it binds to RARs directly and can  be isomerized  in vivo  to 9- cis-RA, which binds to  RXRs).	bind
50351	9	10730	6	10	NULL	0	NULL	RXRbeta	NULL		is a type of	NULL				retinoid receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_8_4355_s_161	8626785	A limitation of these experiments was that  HeLa cells contain multiple retinoid receptors (RARalpha, RAR ,  RXRbeta),   and the ligand used in these studies (ATRA) can  activate both classes of receptors (it binds to RARs directly and can  be isomerized  in vivo  to 9- cis-RA, which binds to  RXRs).	bind
47666	1	10732	5	13	NULL	NULL	NULL	Grb	GP		bind					dynamin	GP		proline-rich tail		NULL	in vivo	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1538_1_10_s_184	11341978	A limited number of these in vitro interactions occur in vivo, including binding of Grb2, amphiphysin, PLC  and src to dynamin's proline-rich tail and binding of    subunits of heterotrimeric G proteins to the PH domain.	bind
47667	2	10732	5	13	NULL	NULL	NULL	amphiphysin	GP		bind					dynamin	GP		proline-rich tail		NULL	in vivo	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1538_1_10_s_184	11341978	A limited number of these in vitro interactions occur in vivo, including binding of Grb2, amphiphysin, PLC  and src to dynamin's proline-rich tail and binding of    subunits of heterotrimeric G proteins to the PH domain.	bind
47668	3	10732	5	13	NULL	NULL	NULL	PLC 	GP		bind					dynamin	GP		proline-rich tail		NULL	in vivo	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1538_1_10_s_184	11341978	A limited number of these in vitro interactions occur in vivo, including binding of Grb2, amphiphysin, PLC  and src to dynamin's proline-rich tail and binding of    subunits of heterotrimeric G proteins to the PH domain.	bind
47669	4	10732	5	13	NULL	NULL	NULL	src	GP		bind					dynamin	GP		proline-rich tail		NULL	in vivo	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1538_1_10_s_184	11341978	A limited number of these in vitro interactions occur in vivo, including binding of Grb2, amphiphysin, PLC  and src to dynamin's proline-rich tail and binding of    subunits of heterotrimeric G proteins to the PH domain.	bind
47670	5	10732	5	13	NULL	NULL	NULL	 G protein	GP		bind			heterotrimeric					PH domain		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1538_1_10_s_184	11341978	A limited number of these in vitro interactions occur in vivo, including binding of Grb2, amphiphysin, PLC  and src to dynamin's proline-rich tail and binding of    subunits of heterotrimeric G proteins to the PH domain.	bind
46992	1	10732	6	NULL	NULL	0	NULL	Grb2	NULL		bind	NULL				dynamin	NULL		proline-rich tail		NULL	in vivo	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1538_1_10_s_184	11341978	A limited number of these in vitro interactions occur in vivo, including binding of Grb2, amphiphysin, PLC  and src to dynamin's proline-rich tail and binding of    subunits of heterotrimeric G proteins to the PH domain.	bind
46993	2	10732	6	NULL	NULL	0	NULL	amphiphysin	NULL		bind	NULL				dynamin	NULL		proline-rich tail		NULL	in vivo	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1538_1_10_s_184	11341978	A limited number of these in vitro interactions occur in vivo, including binding of Grb2, amphiphysin, PLC  and src to dynamin's proline-rich tail and binding of    subunits of heterotrimeric G proteins to the PH domain.	bind
46994	3	10732	6	NULL	NULL	0	NULL	PLC	NULL		bind	NULL				dynamin	NULL		proline-rich tail		NULL	in vivo	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1538_1_10_s_184	11341978	A limited number of these in vitro interactions occur in vivo, including binding of Grb2, amphiphysin, PLC  and src to dynamin's proline-rich tail and binding of    subunits of heterotrimeric G proteins to the PH domain.	bind
46995	4	10732	6	NULL	NULL	0	NULL	src	NULL		bind	NULL				dynamin	NULL		proline-rich tail		NULL	in vivo	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1538_1_10_s_184	11341978	A limited number of these in vitro interactions occur in vivo, including binding of Grb2, amphiphysin, PLC  and src to dynamin's proline-rich tail and binding of    subunits of heterotrimeric G proteins to the PH domain.	bind
46996	5	10732	6	10	NULL	0	NULL	G protein subunit	NULL		bind	NULL		heterotrimeric			NULL		PH domain		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1538_1_10_s_184	11341978	A limited number of these in vitro interactions occur in vivo, including binding of Grb2, amphiphysin, PLC  and src to dynamin's proline-rich tail and binding of    subunits of heterotrimeric G proteins to the PH domain.	bind
47671	1	10733	5	13	NULL	NULL	NULL				bind			SH2 domains		BCR	GP				NULL		NULL	NULL	NULL	NULL	gw60_structure_3_10_1075_s_379	8590002	A limited set of SH2 domains binds BCR through a high-affinity phosphotyrosine-independent interactions.	bind
47672	2	10733	5	13	NULL	NULL	NULL	statement 1	Process		is independent of					phosphotyrosine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_structure_3_10_1075_s_379	8590002	A limited set of SH2 domains binds BCR through a high-affinity phosphotyrosine-independent interactions.	bind
46997	1	10733	6	NULL	NULL	0	NULL		NULL		bind	NULL		SH2 domain		BCR	NULL				NULL		0	NULL	NULL	NULL	gw60_structure_3_10_1075_s_379	8590002	A limited set of SH2 domains binds BCR through a high-affinity phosphotyrosine-independent interactions.	bind
46998	2	10733	6	NULL	NULL	0	NULL	statement 1	NULL		is independent of	NULL				phosphotyrosine	NULL				NULL		0	NULL	NULL	NULL	gw60_structure_3_10_1075_s_379	8590002	A limited set of SH2 domains binds BCR through a high-affinity phosphotyrosine-independent interactions.	bind
47673	1	10734	5	13	NULL	NULL	NULL	pol I	GP		bind		low efficiency			Rrn3p	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_98_25_14334_s_242	11717393	A limiting amount of properly phosphorylated pol I would also explain why the  in vitro binding efficiency of pol I and Rrn3p was rather low although the interaction was strikingly stable.	bind
47003	1	10734	6	NULL	NULL	0	NULL	pol I	NULL		bind	NULL	low efficiency			Rrn3p	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_pnas_98_25_14334_s_242	11717393	A limiting amount of properly phosphorylated pol I would also explain why the  in vitro binding efficiency of pol I and Rrn3p was rather low although the interaction was strikingly stable.	bind
47674	1	10735	5	13	NULL	NULL	NULL	MyD88	GP		is a type of					adapter protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_19_17210_s_13	12618429	A linear activation sequence following engagement of the type I IL-1 receptor (IL-1RI) has been intensely studied and involves binding of the MyD88 and Tollip adapters to the IL-1 receptor chains ( ,  ) with subsequent recruitment of IL-1 receptor-associated kinase ( ,  ).	bind
47675	2	10735	5	13	NULL	NULL	NULL	Tollip	GP		is a type of					adapter protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_19_17210_s_13	12618429	A linear activation sequence following engagement of the type I IL-1 receptor (IL-1RI) has been intensely studied and involves binding of the MyD88 and Tollip adapters to the IL-1 receptor chains ( ,  ) with subsequent recruitment of IL-1 receptor-associated kinase ( ,  ).	bind
47676	3	10735	5	13	NULL	NULL	NULL	MyD88	GP		bind					IL-1 receptor chains	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_19_17210_s_13	12618429	A linear activation sequence following engagement of the type I IL-1 receptor (IL-1RI) has been intensely studied and involves binding of the MyD88 and Tollip adapters to the IL-1 receptor chains ( ,  ) with subsequent recruitment of IL-1 receptor-associated kinase ( ,  ).	bind
47677	4	10735	5	13	NULL	NULL	NULL	Tollip	GP		bind					IL-1 receptor chains	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_19_17210_s_13	12618429	A linear activation sequence following engagement of the type I IL-1 receptor (IL-1RI) has been intensely studied and involves binding of the MyD88 and Tollip adapters to the IL-1 receptor chains ( ,  ) with subsequent recruitment of IL-1 receptor-associated kinase ( ,  ).	bind
47678	5	10735	5	13	NULL	NULL	NULL	statement 3	Process		leads to					IL-1 receptor-associated kinase	GP	recruitment of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_19_17210_s_13	12618429	A linear activation sequence following engagement of the type I IL-1 receptor (IL-1RI) has been intensely studied and involves binding of the MyD88 and Tollip adapters to the IL-1 receptor chains ( ,  ) with subsequent recruitment of IL-1 receptor-associated kinase ( ,  ).	bind
47679	6	10735	5	13	NULL	NULL	NULL	statement 4	Process		leads to					IL-1 receptor-associated kinase	GP	recruitment of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_19_17210_s_13	12618429	A linear activation sequence following engagement of the type I IL-1 receptor (IL-1RI) has been intensely studied and involves binding of the MyD88 and Tollip adapters to the IL-1 receptor chains ( ,  ) with subsequent recruitment of IL-1 receptor-associated kinase ( ,  ).	bind
50352	7	10735	5	13	NULL	NULL	NULL	IL-1RI	GP		is					type I IL-1 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_19_17210_s_13	12618429	A linear activation sequence following engagement of the type I IL-1 receptor (IL-1RI) has been intensely studied and involves binding of the MyD88 and Tollip adapters to the IL-1 receptor chains ( ,  ) with subsequent recruitment of IL-1 receptor-associated kinase ( ,  ).	bind
47004	1	10735	6	NULL	NULL	0	NULL	MyD88	NULL		bind	NULL				IL-1 receptor chains	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_19_17210_s_13	12618429	A linear activation sequence following engagement of the type I IL-1 receptor (IL-1RI) has been intensely studied and involves binding of the MyD88 and Tollip adapters to the IL-1 receptor chains ( ,  ) with subsequent recruitment of IL-1 receptor-associated kinase ( ,  ).	bind
47005	2	10735	6	NULL	NULL	0	NULL	Tollip	NULL		bind	NULL				IL-1 receptor chains	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_19_17210_s_13	12618429	A linear activation sequence following engagement of the type I IL-1 receptor (IL-1RI) has been intensely studied and involves binding of the MyD88 and Tollip adapters to the IL-1 receptor chains ( ,  ) with subsequent recruitment of IL-1 receptor-associated kinase ( ,  ).	bind
47006	3	10735	6	NULL	NULL	0	NULL	Tollip	NULL		is a type of	NULL				adaptor	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_19_17210_s_13	12618429	A linear activation sequence following engagement of the type I IL-1 receptor (IL-1RI) has been intensely studied and involves binding of the MyD88 and Tollip adapters to the IL-1 receptor chains ( ,  ) with subsequent recruitment of IL-1 receptor-associated kinase ( ,  ).	bind
47007	4	10735	6	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				IL-1 receptor-associated kinase	NULL	recruitment of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_19_17210_s_13	12618429	A linear activation sequence following engagement of the type I IL-1 receptor (IL-1RI) has been intensely studied and involves binding of the MyD88 and Tollip adapters to the IL-1 receptor chains ( ,  ) with subsequent recruitment of IL-1 receptor-associated kinase ( ,  ).	bind
47009	5	10735	6	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				IL-1 receptor-associated kinase	NULL	recruitment of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_19_17210_s_13	12618429	A linear activation sequence following engagement of the type I IL-1 receptor (IL-1RI) has been intensely studied and involves binding of the MyD88 and Tollip adapters to the IL-1 receptor chains ( ,  ) with subsequent recruitment of IL-1 receptor-associated kinase ( ,  ).	bind
50353	6	10735	6	10	NULL	0	NULL	MyD88	NULL		is a type of	NULL				adapter	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_19_17210_s_13	12618429	A linear activation sequence following engagement of the type I IL-1 receptor (IL-1RI) has been intensely studied and involves binding of the MyD88 and Tollip adapters to the IL-1 receptor chains ( ,  ) with subsequent recruitment of IL-1 receptor-associated kinase ( ,  ).	bind
50354	7	10735	6	10	NULL	0	NULL	IL-1RI	NULL		is 	NULL				 type I IL-1 receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_19_17210_s_13	12618429	A linear activation sequence following engagement of the type I IL-1 receptor (IL-1RI) has been intensely studied and involves binding of the MyD88 and Tollip adapters to the IL-1 receptor chains ( ,  ) with subsequent recruitment of IL-1 receptor-associated kinase ( ,  ).	bind
47681	1	10738	5	13	NULL	NULL	NULL	PDTI	GP		bind					trypsin	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1621_2_170_s_193	12726993	A linear extrapolation to obtain 100% inhibition indicated that PDTI bound both  trypsins in a 1:1 molar ratio ( Fig. 2), whereas there was no obvious stoichiometry with chymotrypsin.	bind
47013	1	10738	6	NULL	NULL	0	NULL	PDTI	NULL		bind	NULL				trypsin	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1621_2_170_s_193	12726993	A linear extrapolation to obtain 100% inhibition indicated that PDTI bound both  trypsins in a 1:1 molar ratio ( Fig. 2), whereas there was no obvious stoichiometry with chymotrypsin.	bind
47682	1	10739	5	13	NULL	NULL	NULL	actin	GP		bind					mX-S1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_15_15071_s_300	15705568	A linear fit to the same data set (not shown) yielded an apparent second-order  rate constant of actin binding to the mX-S1.	bind
47015	1	10739	6	NULL	NULL	0	NULL	actin	NULL		bind	NULL				mX-S1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_15_15071_s_300	15705568	A linear fit to the same data set (not shown) yielded an apparent second-order  rate constant of actin binding to the mX-S1.	bind
47683	1	10740	5	13	NULL	NULL	NULL	MC-2 	GP		is derived from					IFN	GP		heparin-binding region		NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_74_0_385_s_322	15952892	A linear octapeptide,  MC-2, derived from the heparin-binding region of IFN , significantly prolonged skin  graft survival in an experimental rat model of skin transplantation when it was administered  directly into the graft via osmotic mini pumps ( 83).	bind
47684	2	10740	5	13	NULL	NULL	NULL	statement 1	Process		prolonged		significantly			skin graft	OrganismPart	survival of			NULL	experimental rat model	NULL	NULL	NULL	NULL	gw70_annurevbiochem_74_0_385_s_322	15952892	A linear octapeptide,  MC-2, derived from the heparin-binding region of IFN , significantly prolonged skin  graft survival in an experimental rat model of skin transplantation when it was administered  directly into the graft via osmotic mini pumps ( 83).	bind
50355	3	10740	5	13	NULL	NULL	NULL	MC-2	GP		is a type of					linear octapeptide	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_74_0_385_s_322	15952892	A linear octapeptide,  MC-2, derived from the heparin-binding region of IFN , significantly prolonged skin  graft survival in an experimental rat model of skin transplantation when it was administered  directly into the graft via osmotic mini pumps ( 83).	bind
47016	1	10740	6	NULL	NULL	0	NULL	MC-2	NULL		is a type of	NULL				linear octapeptide	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_74_0_385_s_322	15952892	A linear octapeptide,  MC-2, derived from the heparin-binding region of IFN , significantly prolonged skin  graft survival in an experimental rat model of skin transplantation when it was administered  directly into the graft via osmotic mini pumps ( 83).	bind
47017	2	10740	6	NULL	NULL	0	NULL	MC-2	NULL		is derived from	NULL				IFN	NULL		heparin-binding region		NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_74_0_385_s_322	15952892	A linear octapeptide,  MC-2, derived from the heparin-binding region of IFN , significantly prolonged skin  graft survival in an experimental rat model of skin transplantation when it was administered  directly into the graft via osmotic mini pumps ( 83).	bind
47020	3	10740	6	NULL	NULL	0	NULL	MC-2	NULL		prolonged	NULL				skin graft survival	NULL				NULL	experimental rat model of skin transplantation	0	NULL	NULL	NULL	gw70_annurevbiochem_74_0_385_s_322	15952892	A linear octapeptide,  MC-2, derived from the heparin-binding region of IFN , significantly prolonged skin  graft survival in an experimental rat model of skin transplantation when it was administered  directly into the graft via osmotic mini pumps ( 83).	bind
47685	1	10745	5	13	NULL	NULL	NULL	Arf	GP		bind					Golgi membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_28_16952_s_188	8663371	A link between Arf and PKC seems to be established by the observation that activation of the latter leads to enhanced binding of Arf and beta-COP to Golgi membranes ( 19).	bind
47686	2	10745	5	13	NULL	NULL	NULL	beta-COP	GP		bind					Golgi membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_28_16952_s_188	8663371	A link between Arf and PKC seems to be established by the observation that activation of the latter leads to enhanced binding of Arf and beta-COP to Golgi membranes ( 19).	bind
47687	3	10745	5	13	NULL	NULL	NULL	PKC	GP	activation of	enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_28_16952_s_188	8663371	A link between Arf and PKC seems to be established by the observation that activation of the latter leads to enhanced binding of Arf and beta-COP to Golgi membranes ( 19).	bind
47688	4	10745	5	13	NULL	NULL	NULL	PKC	GP	activation of	enhances					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_28_16952_s_188	8663371	A link between Arf and PKC seems to be established by the observation that activation of the latter leads to enhanced binding of Arf and beta-COP to Golgi membranes ( 19).	bind
47021	1	10745	6	NULL	NULL	0	NULL	Arf 	NULL		bind	NULL				Golgi membrane	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_28_16952_s_188	8663371	A link between Arf and PKC seems to be established by the observation that activation of the latter leads to enhanced binding of Arf and beta-COP to Golgi membranes ( 19).	bind
47022	2	10745	6	NULL	NULL	0	NULL	beta-COP	NULL		bind	NULL				Golgi membranes	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_28_16952_s_188	8663371	A link between Arf and PKC seems to be established by the observation that activation of the latter leads to enhanced binding of Arf and beta-COP to Golgi membranes ( 19).	bind
47023	3	10745	6	10	NULL	0	NULL	PKC		activation of	enhances					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_28_16952_s_188	8663371	A link between Arf and PKC seems to be established by the observation that activation of the latter leads to enhanced binding of Arf and beta-COP to Golgi membranes ( 19).	bind
47024	4	10745	6	10	NULL	0	NULL	PKC		activation of	enhances					statement 2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_28_16952_s_188	8663371	A link between Arf and PKC seems to be established by the observation that activation of the latter leads to enhanced binding of Arf and beta-COP to Golgi membranes ( 19).	bind
47736	1	10746	5	13	NULL	NULL	NULL	simian virus 40 large T antigen	GP		bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_7_2358_s_264	10713160	A link between p53 and CDF-1 is further supported by the recent observation that simian virus 40 large T antigen, which binds and inactivates p53, prevents CDF-1 from binding to CDE elements in WI-38 cells ( 63).	bind
47737	2	10746	5	13	NULL	NULL	NULL	statement 1	Process		inactivates					p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_7_2358_s_264	10713160	A link between p53 and CDF-1 is further supported by the recent observation that simian virus 40 large T antigen, which binds and inactivates p53, prevents CDF-1 from binding to CDE elements in WI-38 cells ( 63).	bind
47738	3	10746	5	13	NULL	NULL	NULL	CDF-1	GP		bind									CDE elements	NULL	WI-38 cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_7_2358_s_264	10713160	A link between p53 and CDF-1 is further supported by the recent observation that simian virus 40 large T antigen, which binds and inactivates p53, prevents CDF-1 from binding to CDE elements in WI-38 cells ( 63).	bind
47739	4	10746	5	13	NULL	NULL	NULL	simian virus 40 large T antigen	GP		prevents					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_7_2358_s_264	10713160	A link between p53 and CDF-1 is further supported by the recent observation that simian virus 40 large T antigen, which binds and inactivates p53, prevents CDF-1 from binding to CDE elements in WI-38 cells ( 63).	bind
47025	1	10746	6	NULL	NULL	0	NULL	simian virus 40 large T antigen	NULL		bind	NULL				p53	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_7_2358_s_264	10713160	A link between p53 and CDF-1 is further supported by the recent observation that simian virus 40 large T antigen, which binds and inactivates p53, prevents CDF-1 from binding to CDE elements in WI-38 cells ( 63).	bind
47026	2	10746	6	NULL	NULL	0	NULL	simian virus 40 large T antigen	NULL		inactivates	NULL				p53	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_7_2358_s_264	10713160	A link between p53 and CDF-1 is further supported by the recent observation that simian virus 40 large T antigen, which binds and inactivates p53, prevents CDF-1 from binding to CDE elements in WI-38 cells ( 63).	bind
47027	3	10746	6	NULL	NULL	0	NULL	CDF-1	NULL		bind	NULL					NULL			CDE element	NULL	WI-38 cells	0	NULL	NULL	NULL	gw60_molcellbiol_20_7_2358_s_264	10713160	A link between p53 and CDF-1 is further supported by the recent observation that simian virus 40 large T antigen, which binds and inactivates p53, prevents CDF-1 from binding to CDE elements in WI-38 cells ( 63).	bind
47031	4	10746	6	NULL	NULL	0	NULL	simian virus 40 large T antigen	NULL		prevents	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_7_2358_s_264	10713160	A link between p53 and CDF-1 is further supported by the recent observation that simian virus 40 large T antigen, which binds and inactivates p53, prevents CDF-1 from binding to CDE elements in WI-38 cells ( 63).	bind
47740	1	10747	5	13	NULL	NULL	NULL	IL-8	GP	native	bind					CXCR1 peptide	GP		N-domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_35_36175_s_117	15252057	A linkage scheme of native IL-8 binding to CXCR1 N-domain peptide.	bind
47034	1	10747	6	NULL	NULL	0	NULL	IL-8	NULL	native	bind	NULL				CXCR1	NULL		N-domain peptide		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_35_36175_s_117	15252057	A linkage scheme of native IL-8 binding to CXCR1 N-domain peptide.	bind
47741	1	10748	5	13	NULL	NULL	NULL				exits between			linker region		Vinexin	GP		second SH3 domain & third SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_13053_s_107	11825889	A Linker Region between the Second and Third SH3 Domains of Vinexin beta Is Necessary for Anchorage-independent ERK2 Activation-- The first and second SH3 domains of vinexin beta bind to vinculin, and the third SH3 domain binds to Sos.	bind
47742	2	10748	5	13	NULL	NULL	NULL	ERK2	GP	activation of	is independent of					anchorage	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_13053_s_107	11825889	A Linker Region between the Second and Third SH3 Domains of Vinexin beta Is Necessary for Anchorage-independent ERK2 Activation-- The first and second SH3 domains of vinexin beta bind to vinculin, and the third SH3 domain binds to Sos.	bind
47743	3	10748	5	13	NULL	NULL	NULL	statement 1	Process		is necessary for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_13053_s_107	11825889	A Linker Region between the Second and Third SH3 Domains of Vinexin beta Is Necessary for Anchorage-independent ERK2 Activation-- The first and second SH3 domains of vinexin beta bind to vinculin, and the third SH3 domain binds to Sos.	bind
47744	4	10748	5	13	NULL	NULL	NULL	vinexin beta	GP		bind			SH3 domain		vinculin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_13053_s_107	11825889	A Linker Region between the Second and Third SH3 Domains of Vinexin beta Is Necessary for Anchorage-independent ERK2 Activation-- The first and second SH3 domains of vinexin beta bind to vinculin, and the third SH3 domain binds to Sos.	bind
47745	5	10748	5	13	NULL	NULL	NULL	vinexin beta	GP		bind			SH3 domain		Sos	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_13053_s_107	11825889	A Linker Region between the Second and Third SH3 Domains of Vinexin beta Is Necessary for Anchorage-independent ERK2 Activation-- The first and second SH3 domains of vinexin beta bind to vinculin, and the third SH3 domain binds to Sos.	bind
47035	1	10748	6	NULL	NULL	0	NULL	vinexin beta	NULL		bind	NULL		first and second SH3 domain		vinculin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_13053_s_107	11825889	A Linker Region between the Second and Third SH3 Domains of Vinexin beta Is Necessary for Anchorage-independent ERK2 Activation-- The first and second SH3 domains of vinexin beta bind to vinculin, and the third SH3 domain binds to Sos.	bind
47036	2	10748	6	NULL	NULL	0	NULL	vinexin beta	NULL		bind	NULL		third SH3 domain		Sos	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_13053_s_107	11825889	A Linker Region between the Second and Third SH3 Domains of Vinexin beta Is Necessary for Anchorage-independent ERK2 Activation-- The first and second SH3 domains of vinexin beta bind to vinculin, and the third SH3 domain binds to Sos.	bind
47037	5	10748	6	10	NULL	0	NULL	statement 4	NULL		is necessary for	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_13053_s_107	11825889	A Linker Region between the Second and Third SH3 Domains of Vinexin beta Is Necessary for Anchorage-independent ERK2 Activation-- The first and second SH3 domains of vinexin beta bind to vinculin, and the third SH3 domain binds to Sos.	bind
47038	3	10748	6	NULL	NULL	0	NULL	ERK2	NULL	activation of	is independent of	NULL				anchorage	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_13053_s_107	11825889	A Linker Region between the Second and Third SH3 Domains of Vinexin beta Is Necessary for Anchorage-independent ERK2 Activation-- The first and second SH3 domains of vinexin beta bind to vinculin, and the third SH3 domain binds to Sos.	bind
50356	4	10748	6	10	NULL	0	NULL	linker region	NULL		exist between	NULL				Vinexin beta	NULL		Second and Third SH3 Domains		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_13053_s_107	11825889	A Linker Region between the Second and Third SH3 Domains of Vinexin beta Is Necessary for Anchorage-independent ERK2 Activation-- The first and second SH3 domains of vinexin beta bind to vinculin, and the third SH3 domain binds to Sos.	bind
47746	1	10749	5	13	NULL	NULL	NULL	Leu3p	GP		is a type of					Zinc Cluster Protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_24_15521_s_258	9182587	A Linker Region of the Yeast Zinc Cluster Protein Leu3p Specifies Binding to Everted Repeat DNA.	bind
47747	2	10749	5	13	NULL	NULL	NULL	Leu3p	GP	yeast	bind			linker region		everted repeat DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_24_15521_s_258	9182587	A Linker Region of the Yeast Zinc Cluster Protein Leu3p Specifies Binding to Everted Repeat DNA.	bind
47039	1	10749	6	10	NULL	0	NULL	Leu3p		yeast	bind			linker region		Everted Repeat DNA					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_24_15521_s_258	9182587	A Linker Region of the Yeast Zinc Cluster Protein Leu3p Specifies Binding to Everted Repeat DNA.	bind
47040	2	10749	6	NULL	NULL	0	NULL	Leu3p	NULL		is a type of	NULL				Zinc cluster protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_24_15521_s_258	9182587	A Linker Region of the Yeast Zinc Cluster Protein Leu3p Specifies Binding to Everted Repeat DNA.	bind
47748	1	10750	5	13	NULL	NULL	NULL	familial dysbetalipoproteinemia	MedicalFinding		is a type of					lipid disorder	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_181	7583549	A lipid disorder (familial dysbetalipoproteinemia) affecting apoE, the other ligand known to bind to the LDLR, results in a markedly reduced binding of apoE-containing VLDL remnants to the LDLR.	bind
47749	2	10750	5	13	NULL	NULL	NULL	apoE	GP		is a type of					ligand	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_181	7583549	A lipid disorder (familial dysbetalipoproteinemia) affecting apoE, the other ligand known to bind to the LDLR, results in a markedly reduced binding of apoE-containing VLDL remnants to the LDLR.	bind
47750	3	10750	5	13	NULL	NULL	NULL	apoE	GP		bind					LDLR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_181	7583549	A lipid disorder (familial dysbetalipoproteinemia) affecting apoE, the other ligand known to bind to the LDLR, results in a markedly reduced binding of apoE-containing VLDL remnants to the LDLR.	bind
47751	4	10750	5	13	NULL	NULL	NULL	VLDL remnants	GP	apoE-containing	bind					LDLR	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_181	7583549	A lipid disorder (familial dysbetalipoproteinemia) affecting apoE, the other ligand known to bind to the LDLR, results in a markedly reduced binding of apoE-containing VLDL remnants to the LDLR.	bind
47752	5	10750	5	13	NULL	NULL	NULL	familial dysbetalipoproteinemia	MedicalFinding		reduces		markedly			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_181	7583549	A lipid disorder (familial dysbetalipoproteinemia) affecting apoE, the other ligand known to bind to the LDLR, results in a markedly reduced binding of apoE-containing VLDL remnants to the LDLR.	bind
47041	1	10750	6	NULL	NULL	0	NULL	apoE	NULL		bind	NULL				LDLR	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_181	7583549	A lipid disorder (familial dysbetalipoproteinemia) affecting apoE, the other ligand known to bind to the LDLR, results in a markedly reduced binding of apoE-containing VLDL remnants to the LDLR.	bind
47042	2	10750	6	NULL	NULL	0	NULL	familial dysbetalipoproteinemia	NULL		is a type of	NULL				lipid disorder	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_181	7583549	A lipid disorder (familial dysbetalipoproteinemia) affecting apoE, the other ligand known to bind to the LDLR, results in a markedly reduced binding of apoE-containing VLDL remnants to the LDLR.	bind
47043	3	10750	6	NULL	NULL	0	NULL	VLDL remnants	NULL	apoE-containing	bind	NULL				LDLR	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_181	7583549	A lipid disorder (familial dysbetalipoproteinemia) affecting apoE, the other ligand known to bind to the LDLR, results in a markedly reduced binding of apoE-containing VLDL remnants to the LDLR.	bind
47044	4	10750	6	10	NULL	0	NULL	familial dysbetalipoproteinemia			reduces					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_181	7583549	A lipid disorder (familial dysbetalipoproteinemia) affecting apoE, the other ligand known to bind to the LDLR, results in a markedly reduced binding of apoE-containing VLDL remnants to the LDLR.	bind
50357	5	10750	6	10	NULL	0	NULL	apoE	NULL		is a type of	NULL				ligand	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_10_1719_s_181	7583549	A lipid disorder (familial dysbetalipoproteinemia) affecting apoE, the other ligand known to bind to the LDLR, results in a markedly reduced binding of apoE-containing VLDL remnants to the LDLR.	bind
47753	1	10751	5	13	NULL	NULL	NULL	LmB	GP		is a type of					lipoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2408_s_27	11953377	A lipoprotein, designated LmB, which binds to both Fn and laminin was cloned from GBS, but it was not shown to be involved in adherence or invasion of epithelial cells ( 23).	bind
47754	2	10751	5	13	NULL	NULL	NULL	LmB	GP		bind					Fn	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2408_s_27	11953377	A lipoprotein, designated LmB, which binds to both Fn and laminin was cloned from GBS, but it was not shown to be involved in adherence or invasion of epithelial cells ( 23).	bind
47755	3	10751	5	13	NULL	NULL	NULL	LmB	GP		bind					laminin	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2408_s_27	11953377	A lipoprotein, designated LmB, which binds to both Fn and laminin was cloned from GBS, but it was not shown to be involved in adherence or invasion of epithelial cells ( 23).	bind
47756	4	10751	5	13	NULL	NULL	NULL	LmB	GP		is not involved in					epithelial cells	Cell	adherence of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2408_s_27	11953377	A lipoprotein, designated LmB, which binds to both Fn and laminin was cloned from GBS, but it was not shown to be involved in adherence or invasion of epithelial cells ( 23).	bind
47757	5	10751	5	13	NULL	NULL	NULL	LmB	GP		is not involved in					epithelial cells	Cell	invasion of			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2408_s_27	11953377	A lipoprotein, designated LmB, which binds to both Fn and laminin was cloned from GBS, but it was not shown to be involved in adherence or invasion of epithelial cells ( 23).	bind
47045	1	10751	6	NULL	NULL	0	NULL	LmB	NULL		is a type of	NULL				lipoprotein	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2408_s_27	11953377	A lipoprotein, designated LmB, which binds to both Fn and laminin was cloned from GBS, but it was not shown to be involved in adherence or invasion of epithelial cells ( 23).	bind
47046	2	10751	6	NULL	NULL	0	NULL	LmB	NULL		bind	NULL				Fn	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2408_s_27	11953377	A lipoprotein, designated LmB, which binds to both Fn and laminin was cloned from GBS, but it was not shown to be involved in adherence or invasion of epithelial cells ( 23).	bind
47047	3	10751	6	NULL	NULL	0	NULL	LmB	NULL		bind	NULL				laminin	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_70_5_2408_s_27	11953377	A lipoprotein, designated LmB, which binds to both Fn and laminin was cloned from GBS, but it was not shown to be involved in adherence or invasion of epithelial cells ( 23).	bind
47048	4	10751	6	10	NULL	0	NULL	LmB	NULL		is not involved in	NULL				epithelial cells	NULL	adherence of 			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2408_s_27	11953377	A lipoprotein, designated LmB, which binds to both Fn and laminin was cloned from GBS, but it was not shown to be involved in adherence or invasion of epithelial cells ( 23).	bind
47049	5	10751	6	10	NULL	0	NULL	LmB	NULL		is not involved in	NULL				epithelial cells	NULL	invasion of 			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_5_2408_s_27	11953377	A lipoprotein, designated LmB, which binds to both Fn and laminin was cloned from GBS, but it was not shown to be involved in adherence or invasion of epithelial cells ( 23).	bind
50761	1	10752	5	13	NULL	NULL	NULL	fibulin-2 	GP		bind					gamma2-r	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_5_2814_s_55	9006922	A list of synthetic peptides from the N-terminus of domain IV of the gamma2 chain and their activities for competing fibulin-2 binding to gamma2-r    he activities shown were from the competition assays in Fig 4. ++, active at 200 mug/ml; +, active at 1 mg/ml;  , inactive even at 1 mg/ml.	bind
50814	1	10752	6	NULL	NULL	0	NULL	fibulin-2	NULL		bind	NULL				gamma2-r	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_5_2814_s_55	9006922	A list of synthetic peptides from the N-terminus of domain IV of the gamma2 chain and their activities for competing fibulin-2 binding to gamma2-r    he activities shown were from the competition assays in Fig 4. ++, active at 200 mug/ml; +, active at 1 mg/ml;  , inactive even at 1 mg/ml.	bind
47759	1	10753	5	13	NULL	NULL	NULL	calmodulin	GP		bind					IQGAP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_542_1_7_s_89	12729888	A localized increase in [Ca2+]i increases the binding of calmodulin to IQGAP1.	bind
47760	2	10753	5	13	NULL	NULL	NULL	Ca2+	Chemical	increase in	increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_542_1_7_s_89	12729888	A localized increase in [Ca2+]i increases the binding of calmodulin to IQGAP1.	bind
47050	1	10753	6	NULL	NULL	0	NULL	calmodulin	NULL		bind	NULL				IQGAP1	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_542_1_7_s_89	12729888	A localized increase in [Ca2+]i increases the binding of calmodulin to IQGAP1.	bind
47051	2	10753	6	NULL	NULL	0	NULL	[Ca2+]	NULL	increase in	increases	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_542_1_7_s_89	12729888	A localized increase in [Ca2+]i increases the binding of calmodulin to IQGAP1.	bind
47761	1	10754	5	13	NULL	NULL	NULL	TFIID subunit	GP		bind					TBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_23_17391_s_127	10751405	A logical explanation for these findings is that in the absence of TAFII145p another TFIID subunit binds to TBP and protects it from degradation.	bind
47762	2	10754	5	13	NULL	NULL	NULL	statement 1	Process		protects					TBP	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_23_17391_s_127	10751405	A logical explanation for these findings is that in the absence of TAFII145p another TFIID subunit binds to TBP and protects it from degradation.	bind
47763	3	10754	5	13	NULL	NULL	NULL	statement 1	Process		in the absence of					TAFII145p	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_23_17391_s_127	10751405	A logical explanation for these findings is that in the absence of TAFII145p another TFIID subunit binds to TBP and protects it from degradation.	bind
47052	1	10754	6	NULL	NULL	0	NULL	TFIID subunit	NULL		bind	NULL				TBP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_23_17391_s_127	10751405	A logical explanation for these findings is that in the absence of TAFII145p another TFIID subunit binds to TBP and protects it from degradation.	bind
47053	2	10754	6	NULL	NULL	0	NULL	statement 1	NULL		occurs in absence of	NULL				TAFII145p	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_23_17391_s_127	10751405	A logical explanation for these findings is that in the absence of TAFII145p another TFIID subunit binds to TBP and protects it from degradation.	bind
47054	3	10754	6	NULL	NULL	0	NULL	statement 1	NULL		protects	NULL				TBP	NULL	degradation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_23_17391_s_127	10751405	A logical explanation for these findings is that in the absence of TAFII145p another TFIID subunit binds to TBP and protects it from degradation.	bind
47764	1	10755	5	13	NULL	NULL	NULL	TFIID subunits	GP		bind					TBP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_23_17391_s_27	10751405	A logical explanation for these observations is that additional TFIID subunits bind to TBP in the absence of TAFII145p, and that the histone-like TAFIIs are more important for TFIID structure.	bind
47765	2	10755	5	13	NULL	NULL	NULL	statement 1	Process		in the absence of					TAFII145p	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_23_17391_s_27	10751405	A logical explanation for these observations is that additional TFIID subunits bind to TBP in the absence of TAFII145p, and that the histone-like TAFIIs are more important for TFIID structure.	bind
47766	3	10755	5	13	NULL	NULL	NULL	 TAFIIs	GP	histone-like	is important for					TFIID 	GP	structure of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_23_17391_s_27	10751405	A logical explanation for these observations is that additional TFIID subunits bind to TBP in the absence of TAFII145p, and that the histone-like TAFIIs are more important for TFIID structure.	bind
47055	1	10755	6	NULL	NULL	0	NULL	TFIID subunit	NULL		bind	NULL				TBP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_23_17391_s_27	10751405	A logical explanation for these observations is that additional TFIID subunits bind to TBP in the absence of TAFII145p, and that the histone-like TAFIIs are more important for TFIID structure.	bind
47056	2	10755	6	NULL	NULL	0	NULL	statement 1	NULL		occurs in absence of	NULL				TAFII145p	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_23_17391_s_27	10751405	A logical explanation for these observations is that additional TFIID subunits bind to TBP in the absence of TAFII145p, and that the histone-like TAFIIs are more important for TFIID structure.	bind
47057	3	10755	6	NULL	NULL	0	NULL	TAFIIs	NULL	histone-like	are important for	NULL				TFIID	NULL	structure of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_23_17391_s_27	10751405	A logical explanation for these observations is that additional TFIID subunits bind to TBP in the absence of TAFII145p, and that the histone-like TAFIIs are more important for TFIID structure.	bind
47767	1	10756	5	13	NULL	NULL	NULL	L1	GP		bind					PDP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_331	11842080	A logical explanation is that the native Ser-Leu residues of L1 do not allow the corresponding Glu55 side chain to be properly positioned for abetting binding of L1 to PDP1.	bind
47768	2	10756	5	13	NULL	NULL	NULL	L1	GP	native	does not allow			Ser-Leu residues				proper positioning of	Glu55 side chain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_331	11842080	A logical explanation is that the native Ser-Leu residues of L1 do not allow the corresponding Glu55 side chain to be properly positioned for abetting binding of L1 to PDP1.	bind
47769	3	10756	5	13	NULL	NULL	NULL			\t	abet			Glu55 side chain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_331	11842080	A logical explanation is that the native Ser-Leu residues of L1 do not allow the corresponding Glu55 side chain to be properly positioned for abetting binding of L1 to PDP1.	bind
47058	1	10756	6	NULL	NULL	0	NULL	L1	NULL		bind	NULL				PDP1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_331	11842080	A logical explanation is that the native Ser-Leu residues of L1 do not allow the corresponding Glu55 side chain to be properly positioned for abetting binding of L1 to PDP1.	bind
47059	2	10756	6	NULL	NULL	0	NULL	L1	NULL	native	do not allow	NULL		Ser-Leu residue			NULL	positioning of	Glu55 side chain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_331	11842080	A logical explanation is that the native Ser-Leu residues of L1 do not allow the corresponding Glu55 side chain to be properly positioned for abetting binding of L1 to PDP1.	bind
47060	3	10756	6	NULL	NULL	0	NULL		NULL		abett	NULL		Glu55 side chain		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_17_14976_s_331	11842080	A logical explanation is that the native Ser-Leu residues of L1 do not allow the corresponding Glu55 side chain to be properly positioned for abetting binding of L1 to PDP1.	bind
47770	1	10757	5	13	NULL	NULL	NULL	transcription factor	GP		bind							p53-regulated		promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_10_8261_s_256	12475992	A logical extension of these observations is that there may be a transcription factor that binds to p53-regulated promoters and establishes the open chromatin confirmation prior to p53 activation.	bind
47771	2	10757	5	13	NULL	NULL	NULL	statement 1	Process		establishes					open chromatin confirmation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_10_8261_s_256	12475992	A logical extension of these observations is that there may be a transcription factor that binds to p53-regulated promoters and establishes the open chromatin confirmation prior to p53 activation.	bind
47772	3	10757	5	13	NULL	NULL	NULL	statement 2	Process		occurs prior to					p53	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_10_8261_s_256	12475992	A logical extension of these observations is that there may be a transcription factor that binds to p53-regulated promoters and establishes the open chromatin confirmation prior to p53 activation.	bind
47062	1	10757	6	NULL	NULL	0	NULL	transcription factor	NULL		bind	NULL					NULL	p53-regulated		promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_10_8261_s_256	12475992	A logical extension of these observations is that there may be a transcription factor that binds to p53-regulated promoters and establishes the open chromatin confirmation prior to p53 activation.	bind
47063	2	10757	6	10	NULL	0	NULL	statement 1	NULL		establishes	NULL				open chromatin confirmation	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_10_8261_s_256	12475992	A logical extension of these observations is that there may be a transcription factor that binds to p53-regulated promoters and establishes the open chromatin confirmation prior to p53 activation.	bind
47064	3	10757	6	NULL	NULL	0	NULL	statement 2	NULL		occurs before	NULL				p53	NULL	activation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_10_8261_s_256	12475992	A logical extension of these observations is that there may be a transcription factor that binds to p53-regulated promoters and establishes the open chromatin confirmation prior to p53 activation.	bind
47773	1	10758	5	13	NULL	NULL	NULL	GroES	GP		bind					Gp31	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_34_0_439_s_175	11092834	A logical extrapolation of the results detailed above would be that the GroEL(E191G)  mutant protein spends more time in the closed state, thus disfavoring GroES and Gp31  binding.	bind
47774	2	10758	5	13	NULL	NULL	NULL	GroEL	GP	mutant	is present in			E191G		closed state					NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_34_0_439_s_175	11092834	A logical extrapolation of the results detailed above would be that the GroEL(E191G)  mutant protein spends more time in the closed state, thus disfavoring GroES and Gp31  binding.	bind
47775	3	10758	5	13	NULL	NULL	NULL	statement 2	Process		disfavor					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_34_0_439_s_175	11092834	A logical extrapolation of the results detailed above would be that the GroEL(E191G)  mutant protein spends more time in the closed state, thus disfavoring GroES and Gp31  binding.	bind
47065	1	10758	6	NULL	NULL	0	NULL	GroES	NULL		bind	NULL				Gp31	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevgenet_34_0_439_s_175	11092834	A logical extrapolation of the results detailed above would be that the GroEL(E191G)  mutant protein spends more time in the closed state, thus disfavoring GroES and Gp31  binding.	bind
47066	2	10758	6	NULL	NULL	0	NULL	GroEL protein	NULL	mutant	is in 	NULL		E191G		closed confirmation	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevgenet_34_0_439_s_175	11092834	A logical extrapolation of the results detailed above would be that the GroEL(E191G)  mutant protein spends more time in the closed state, thus disfavoring GroES and Gp31  binding.	bind
47067	3	10758	6	NULL	NULL	0	NULL	statement 2	NULL		disfavors	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevgenet_34_0_439_s_175	11092834	A logical extrapolation of the results detailed above would be that the GroEL(E191G)  mutant protein spends more time in the closed state, thus disfavoring GroES and Gp31  binding.	bind
47776	1	10759	5	13	NULL	NULL	NULL	p85	GP		bind		weakly	tyrosine 799;;tyrosine 1173		CKR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_21_17686_s_159	11278468	A long exposure of the blot showed trace evidence of p85 in CKR/F799 and CKR/F1173 but not in CKR/F2 (data not shown), suggesting that binding of p85 to CKR is not strong and both tyrosines 799 and 1173 may be acting as low affinity binding sites for p85.	bind
47273	1	10759	6	10	NULL	0	NULL	p85	NULL		bind	NULL	weakly	tyrosine 799;; tyrosine 1173		CKR	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_21_17686_s_159	11278468	A long exposure of the blot showed trace evidence of p85 in CKR/F799 and CKR/F1173 but not in CKR/F2 (data not shown), suggesting that binding of p85 to CKR is not strong and both tyrosines 799 and 1173 may be acting as low affinity binding sites for p85.	bind
47777	1	10760	5	13	NULL	NULL	NULL	GpIbalpha	GP		bind					thrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_301_5630_222_s_138	12855811	A long O-glycosylated mucin-like stalk (not drawn to scale) of the GpIbalpha receptor places its thrombin binding domain  45 nm away from the platelet membrane surface (  39); thus, platelet membranes that are about 100 nm apart could be linked together by binding interactions between GpIbalpha and thrombin.	bind
47778	2	10760	5	13	NULL	NULL	NULL	platelet membranes	CellComponent		is linked together by					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_301_5630_222_s_138	12855811	A long O-glycosylated mucin-like stalk (not drawn to scale) of the GpIbalpha receptor places its thrombin binding domain  45 nm away from the platelet membrane surface (  39); thus, platelet membranes that are about 100 nm apart could be linked together by binding interactions between GpIbalpha and thrombin.	bind
47779	3	10760	5	13	NULL	NULL	NULL	GpIbalpha receptor	GP		is placed away from			thrombin binding domain		platelet membrane surface	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_science_301_5630_222_s_138	12855811	A long O-glycosylated mucin-like stalk (not drawn to scale) of the GpIbalpha receptor places its thrombin binding domain  45 nm away from the platelet membrane surface (  39); thus, platelet membranes that are about 100 nm apart could be linked together by binding interactions between GpIbalpha and thrombin.	bind
47780	4	10760	5	13	NULL	NULL	NULL	GpIbalpha receptor	GP		is required for			O-glycosylated mucin-like stalk		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_301_5630_222_s_138	12855811	A long O-glycosylated mucin-like stalk (not drawn to scale) of the GpIbalpha receptor places its thrombin binding domain  45 nm away from the platelet membrane surface (  39); thus, platelet membranes that are about 100 nm apart could be linked together by binding interactions between GpIbalpha and thrombin.	bind
47068	1	10760	6	NULL	NULL	0	NULL	GpIbalpha	NULL		bind	NULL				thrombin	NULL				NULL		0	NULL	NULL	NULL	gw60_science_301_5630_222_s_138	12855811	A long O-glycosylated mucin-like stalk (not drawn to scale) of the GpIbalpha receptor places its thrombin binding domain  45 nm away from the platelet membrane surface (  39); thus, platelet membranes that are about 100 nm apart could be linked together by binding interactions between GpIbalpha and thrombin.	bind
47292	2	10760	6	NULL	NULL	0	NULL	statement 1	NULL		links	NULL				platelet membranes	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_301_5630_222_s_138	12855811	A long O-glycosylated mucin-like stalk (not drawn to scale) of the GpIbalpha receptor places its thrombin binding domain  45 nm away from the platelet membrane surface (  39); thus, platelet membranes that are about 100 nm apart could be linked together by binding interactions between GpIbalpha and thrombin.	bind
47306	3	10760	6	10	NULL	0	NULL	GpIbalpha receptor			is placed away from			thrombin binding domain		platelet membrane surface					NULL		NULL	NULL	NULL	NULL	gw60_science_301_5630_222_s_138	12855811	A long O-glycosylated mucin-like stalk (not drawn to scale) of the GpIbalpha receptor places its thrombin binding domain  45 nm away from the platelet membrane surface (  39); thus, platelet membranes that are about 100 nm apart could be linked together by binding interactions between GpIbalpha and thrombin.	bind
47308	4	10760	6	10	NULL	0	NULL	GpIbalpha			is required for			long O-glycosylated mucin-like stalk		statement 3					NULL		NULL	NULL	NULL	NULL	gw60_science_301_5630_222_s_138	12855811	A long O-glycosylated mucin-like stalk (not drawn to scale) of the GpIbalpha receptor places its thrombin binding domain  45 nm away from the platelet membrane surface (  39); thus, platelet membranes that are about 100 nm apart could be linked together by binding interactions between GpIbalpha and thrombin.	bind
47781	1	10761	5	13	NULL	NULL	NULL	antibodies	GP	conventional	lacks			VL		antigen-binding surface	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24774_s_21	11335716	A longer CDR3 increases the antigen-binding surface and partially compensates for the absence of the antigen-binding surface provided by the VL in conventional antibodies ( 3).	bind
47783	2	10761	5	13	NULL	NULL	NULL	CDR3	GP	longer	increases					antigen-binding surface	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24774_s_21	11335716	A longer CDR3 increases the antigen-binding surface and partially compensates for the absence of the antigen-binding surface provided by the VL in conventional antibodies ( 3).	bind
47784	3	10761	5	13	NULL	NULL	NULL	statement 2	Process		compensates for		partially			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24774_s_21	11335716	A longer CDR3 increases the antigen-binding surface and partially compensates for the absence of the antigen-binding surface provided by the VL in conventional antibodies ( 3).	bind
47311	1	10761	6	10	NULL	0	NULL	CDR3		longer	increases					antigen-binding surface					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24774_s_21	11335716	A longer CDR3 increases the antigen-binding surface and partially compensates for the absence of the antigen-binding surface provided by the VL in conventional antibodies ( 3).	bind
47312	2	10761	6	10	NULL	0	NULL	antigen binding surface			is absent in					VL					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24774_s_21	11335716	A longer CDR3 increases the antigen-binding surface and partially compensates for the absence of the antigen-binding surface provided by the VL in conventional antibodies ( 3).	bind
47315	3	10761	6	NULL	NULL	0	NULL	statement 1	NULL		compensates	NULL	partially			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_27_24774_s_21	11335716	A longer CDR3 increases the antigen-binding surface and partially compensates for the absence of the antigen-binding surface provided by the VL in conventional antibodies ( 3).	bind
47848	1	10762	5	13	NULL	NULL	NULL	Nef	GP		bind					Nef receptor	GP	putative			NULL		NULL	NULL	NULL	NULL	gw60_febslett_422_3_363_s_108	9498817	A longer preincubation period for fasudil hydrochloride was required than for M3, probably because fasudil hydrochloride taken up by cells was converted to an active form M3 during this period [ 10], and thereby impeded transduction of the apoptosis-inducing signal introduced by binding of Nef to a putative Nef receptor, a death-signalling receptor.	bind
47849	2	10762	5	13	NULL	NULL	NULL	Nef receptor	GP		is a type of					death-signalling receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_422_3_363_s_108	9498817	A longer preincubation period for fasudil hydrochloride was required than for M3, probably because fasudil hydrochloride taken up by cells was converted to an active form M3 during this period [ 10], and thereby impeded transduction of the apoptosis-inducing signal introduced by binding of Nef to a putative Nef receptor, a death-signalling receptor.	bind
47851	3	10762	5	13	NULL	NULL	NULL	statement 1	Process		introduces					apoptosis-inducing signal	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_422_3_363_s_108	9498817	A longer preincubation period for fasudil hydrochloride was required than for M3, probably because fasudil hydrochloride taken up by cells was converted to an active form M3 during this period [ 10], and thereby impeded transduction of the apoptosis-inducing signal introduced by binding of Nef to a putative Nef receptor, a death-signalling receptor.	bind
47852	4	10762	5	13	NULL	NULL	NULL	fasudil hydrochloride	Chemical		is converted to					M3	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_422_3_363_s_108	9498817	A longer preincubation period for fasudil hydrochloride was required than for M3, probably because fasudil hydrochloride taken up by cells was converted to an active form M3 during this period [ 10], and thereby impeded transduction of the apoptosis-inducing signal introduced by binding of Nef to a putative Nef receptor, a death-signalling receptor.	bind
47853	5	10762	5	13	NULL	NULL	NULL	statement 4	Process		impede					apoptosis-inducing signal	Process	transduction of			NULL		NULL	NULL	NULL	NULL	gw60_febslett_422_3_363_s_108	9498817	A longer preincubation period for fasudil hydrochloride was required than for M3, probably because fasudil hydrochloride taken up by cells was converted to an active form M3 during this period [ 10], and thereby impeded transduction of the apoptosis-inducing signal introduced by binding of Nef to a putative Nef receptor, a death-signalling receptor.	bind
47317	1	10762	6	NULL	NULL	0	NULL	fasudil hydrochloride	NULL		is converted to	NULL				M3	NULL	active 			NULL		0	NULL	NULL	NULL	gw60_febslett_422_3_363_s_108	9498817	A longer preincubation period for fasudil hydrochloride was required than for M3, probably because fasudil hydrochloride taken up by cells was converted to an active form M3 during this period [ 10], and thereby impeded transduction of the apoptosis-inducing signal introduced by binding of Nef to a putative Nef receptor, a death-signalling receptor.	bind
47319	2	10762	6	NULL	NULL	0	NULL	Nef	NULL		bind	NULL				Nef receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_422_3_363_s_108	9498817	A longer preincubation period for fasudil hydrochloride was required than for M3, probably because fasudil hydrochloride taken up by cells was converted to an active form M3 during this period [ 10], and thereby impeded transduction of the apoptosis-inducing signal introduced by binding of Nef to a putative Nef receptor, a death-signalling receptor.	bind
47320	3	10762	6	NULL	NULL	0	NULL	Nef receptor	NULL		is a type of	NULL				death-signalling receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_422_3_363_s_108	9498817	A longer preincubation period for fasudil hydrochloride was required than for M3, probably because fasudil hydrochloride taken up by cells was converted to an active form M3 during this period [ 10], and thereby impeded transduction of the apoptosis-inducing signal introduced by binding of Nef to a putative Nef receptor, a death-signalling receptor.	bind
47323	4	10762	6	NULL	NULL	0	NULL	statement 2	NULL		introduces	NULL				apoptosis-inducing signal	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_422_3_363_s_108	9498817	A longer preincubation period for fasudil hydrochloride was required than for M3, probably because fasudil hydrochloride taken up by cells was converted to an active form M3 during this period [ 10], and thereby impeded transduction of the apoptosis-inducing signal introduced by binding of Nef to a putative Nef receptor, a death-signalling receptor.	bind
47326	5	10762	6	NULL	NULL	0	NULL	statement 1	NULL		impedes	NULL				apoptosis-inducing signal	NULL	transduction of 			NULL		0	NULL	NULL	NULL	gw60_febslett_422_3_363_s_108	9498817	A longer preincubation period for fasudil hydrochloride was required than for M3, probably because fasudil hydrochloride taken up by cells was converted to an active form M3 during this period [ 10], and thereby impeded transduction of the apoptosis-inducing signal introduced by binding of Nef to a putative Nef receptor, a death-signalling receptor.	bind
47850	1	10763	5	NULL	NULL	0	NULL		NULL		bind	NULL		Lys			NULL		S-adenosylmethionine		NULL		0	NULL	NULL	NULL	abs-batch0740-0759_plant-cell_18_7_16731588_s_7	16731588	A loop involved in the binding  of Lys and S-adenosylmethionine provides an explanation for the synergistic  inhibition by these effectors.	bind
47069	1	10763	6	NULL	NULL	0	NULL		NULL		bind	NULL		Lys			NULL		S-adenosylmethionine		NULL		0	NULL	NULL	NULL	abs-batch0740-0759_plant-cell_18_7_16731588_s_7	16731588	A loop involved in the binding  of Lys and S-adenosylmethionine provides an explanation for the synergistic  inhibition by these effectors.	bind
47854	1	10764	5	13	NULL	NULL	NULL	Brf1	GP		bind					TFIIIC-DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_172	16880507	A loop region in repeat II of the TFIIB homology domain is important for Brf1 binding  to TFIIIC-DNA.	bind
47855	2	10764	5	13	NULL	NULL	NULL	TFIIB	GP		is important for			loop region in repeat II of homology domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_172	16880507	A loop region in repeat II of the TFIIB homology domain is important for Brf1 binding  to TFIIIC-DNA.	bind
47070	1	10764	6	NULL	NULL	0	NULL	Brf1	NULL		bind	NULL				TFIIIC-DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_172	16880507	A loop region in repeat II of the TFIIB homology domain is important for Brf1 binding  to TFIIIC-DNA.	bind
47071	2	10764	6	NULL	NULL	0	NULL	TFIIB	NULL		is important for	NULL		loop region in repeat II of homology domain		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_172	16880507	A loop region in repeat II of the TFIIB homology domain is important for Brf1 binding  to TFIIIC-DNA.	bind
47856	1	10765	5	NULL	NULL	0	NULL		NULL		bind	NULL		Arg-3500			NULL		Trp-4369		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_28_19732_s_250	16704977	A loop was proposed near the carboxyl-terminal end of apoB-100 ( ) that is stabilized by the binding of Arg-3500 to Trp-4369 ( ) and modulates the binding of the LDL receptor to the LDL receptor binding site (residues 3359-3369).	bind
47857	2	10765	5	13	NULL	NULL	NULL	statement 1	Process		stabilize					apoB-100	GP		loop near carboxyl-terminal end		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_28_19732_s_250	16704977	A loop was proposed near the carboxyl-terminal end of apoB-100 ( ) that is stabilized by the binding of Arg-3500 to Trp-4369 ( ) and modulates the binding of the LDL receptor to the LDL receptor binding site (residues 3359-3369).	bind
47858	3	10765	5	13	NULL	NULL	NULL	LDL receptor	GP		bind								LDL receptor binding site (3359-3369)		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_28_19732_s_250	16704977	A loop was proposed near the carboxyl-terminal end of apoB-100 ( ) that is stabilized by the binding of Arg-3500 to Trp-4369 ( ) and modulates the binding of the LDL receptor to the LDL receptor binding site (residues 3359-3369).	bind
47859	4	10765	5	13	NULL	NULL	NULL	apoB-100	GP	\t	modulates			loop near carboxyl-terminal end		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_28_19732_s_250	16704977	A loop was proposed near the carboxyl-terminal end of apoB-100 ( ) that is stabilized by the binding of Arg-3500 to Trp-4369 ( ) and modulates the binding of the LDL receptor to the LDL receptor binding site (residues 3359-3369).	bind
47072	1	10765	6	NULL	NULL	0	NULL		NULL		bind	NULL		Arg-3500			NULL		Trp-4369		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_28_19732_s_250	16704977	A loop was proposed near the carboxyl-terminal end of apoB-100 ( ) that is stabilized by the binding of Arg-3500 to Trp-4369 ( ) and modulates the binding of the LDL receptor to the LDL receptor binding site (residues 3359-3369).	bind
47073	2	10765	6	NULL	NULL	0	NULL	LDL receptor	NULL		bind	NULL					NULL		 LDL receptor binding site		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_28_19732_s_250	16704977	A loop was proposed near the carboxyl-terminal end of apoB-100 ( ) that is stabilized by the binding of Arg-3500 to Trp-4369 ( ) and modulates the binding of the LDL receptor to the LDL receptor binding site (residues 3359-3369).	bind
47074	3	10765	6	NULL	NULL	0	NULL	apoB-100	NULL		is stabilized by	NULL		loop near carboxyl-terminal end		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_28_19732_s_250	16704977	A loop was proposed near the carboxyl-terminal end of apoB-100 ( ) that is stabilized by the binding of Arg-3500 to Trp-4369 ( ) and modulates the binding of the LDL receptor to the LDL receptor binding site (residues 3359-3369).	bind
47075	4	10765	6	NULL	NULL	0	NULL	apoB-100	NULL		modulates	NULL		loop near carboxyl-terminal end		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_28_19732_s_250	16704977	A loop was proposed near the carboxyl-terminal end of apoB-100 ( ) that is stabilized by the binding of Arg-3500 to Trp-4369 ( ) and modulates the binding of the LDL receptor to the LDL receptor binding site (residues 3359-3369).	bind
47076	5	10765	6	NULL	NULL	0	NULL	LDL receptor binding site	NULL		resides between	NULL				residues 3359-3369	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_28_19732_s_250	16704977	A loop was proposed near the carboxyl-terminal end of apoB-100 ( ) that is stabilized by the binding of Arg-3500 to Trp-4369 ( ) and modulates the binding of the LDL receptor to the LDL receptor binding site (residues 3359-3369).	bind
47919	1	10766	5	13	NULL	NULL	NULL	Brf1	GP		bind					TFIIIC	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_345	16880507	A loss-of-function mutation in TPR7 (L469K) of Tfc4 was previously shown to decrease Brf1 (and Bdp1) binding to TFIIIC.	bind
47920	2	10766	5	13	NULL	NULL	NULL	Bdp1	GP		bind					TFIIIC	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_345	16880507	A loss-of-function mutation in TPR7 (L469K) of Tfc4 was previously shown to decrease Brf1 (and Bdp1) binding to TFIIIC.	bind
47921	3	10766	5	13	NULL	NULL	NULL	Tfc4	GP	mutant	decreases			TPR7 (L469K)		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_345	16880507	A loss-of-function mutation in TPR7 (L469K) of Tfc4 was previously shown to decrease Brf1 (and Bdp1) binding to TFIIIC.	bind
47922	4	10766	5	13	NULL	NULL	NULL	Tfc4	GP	mutant	decreases			TPR7 (L469K)		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_345	16880507	A loss-of-function mutation in TPR7 (L469K) of Tfc4 was previously shown to decrease Brf1 (and Bdp1) binding to TFIIIC.	bind
47119	1	10766	6	NULL	NULL	0	NULL	Brf1	NULL		bind	NULL				TFIIIC	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_345	16880507	A loss-of-function mutation in TPR7 (L469K) of Tfc4 was previously shown to decrease Brf1 (and Bdp1) binding to TFIIIC.	bind
47120	2	10766	6	NULL	NULL	0	NULL	Bdp1	NULL		bind	NULL				TFIIIC	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_345	16880507	A loss-of-function mutation in TPR7 (L469K) of Tfc4 was previously shown to decrease Brf1 (and Bdp1) binding to TFIIIC.	bind
47124	3	10766	6	NULL	NULL	0	NULL	Tfc4	NULL	mutant	decreases	NULL		L469K in TPR7		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_345	16880507	A loss-of-function mutation in TPR7 (L469K) of Tfc4 was previously shown to decrease Brf1 (and Bdp1) binding to TFIIIC.	bind
47125	4	10766	6	NULL	NULL	0	NULL	Tfc4	NULL	mutant	decreases	NULL		L469K in TPR7		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_345	16880507	A loss-of-function mutation in TPR7 (L469K) of Tfc4 was previously shown to decrease Brf1 (and Bdp1) binding to TFIIIC.	bind
47923	1	10767	5	13	NULL	NULL	NULL	NS1	Organism		bind		inefficient			NS2	Organism				NULL		NULL	NULL	NULL	NULL	gw70_femsimmunolmedmic_35_2_87_s_108	12628542	A low adsorption rate due to inefficient binding of NS1 and NS2 might also result  in failure to detect phage susceptibility.	bind
47126	1	10767	6	NULL	NULL	0	NULL	NS1	NULL		bind	NULL	inefficiently			NS2	NULL				NULL		0	NULL	NULL	NULL	gw70_femsimmunolmedmic_35_2_87_s_108	12628542	A low adsorption rate due to inefficient binding of NS1 and NS2 might also result  in failure to detect phage susceptibility.	bind
47924	1	10769	5	13	NULL	NULL	NULL	Fas	GP		bind		low affinity			UBC-FAP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_49_31037_s_224	8940097	A low binding affinity between Fas and UBC-FAP may explain our unsuccessful efforts to date to coprecipitate these proteins from cell lysates.	bind
47127	1	10769	6	NULL	NULL	0	NULL	Fas	NULL		bind	NULL	low affinity			UBC-FAP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_49_31037_s_224	8940097	A low binding affinity between Fas and UBC-FAP may explain our unsuccessful efforts to date to coprecipitate these proteins from cell lysates.	bind
47925	1	10770	5	13	NULL	NULL	NULL	APC	GP		bind					EPCR	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_20077_s_130	16709569	A low concentration of exogenous APC (3.3 nM) was used, and barrier protective effects of exogenous APC were blocked by both wild type PC and PC S360A, consistent with the expected role of zymogen PC as a competitive inhibitor for APC binding to EPCR.	bind
47926	2	10770	5	13	NULL	NULL	NULL	zymogen PC	GP		bind					EPCR	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_20077_s_130	16709569	A low concentration of exogenous APC (3.3 nM) was used, and barrier protective effects of exogenous APC were blocked by both wild type PC and PC S360A, consistent with the expected role of zymogen PC as a competitive inhibitor for APC binding to EPCR.	bind
47927	3	10770	5	13	NULL	NULL	NULL	APC	GP	exogenous	effects					barrier protective	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_20077_s_130	16709569	A low concentration of exogenous APC (3.3 nM) was used, and barrier protective effects of exogenous APC were blocked by both wild type PC and PC S360A, consistent with the expected role of zymogen PC as a competitive inhibitor for APC binding to EPCR.	bind
47928	4	10770	5	13	NULL	NULL	NULL	PC	GP	wild type	blocks					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_20077_s_130	16709569	A low concentration of exogenous APC (3.3 nM) was used, and barrier protective effects of exogenous APC were blocked by both wild type PC and PC S360A, consistent with the expected role of zymogen PC as a competitive inhibitor for APC binding to EPCR.	bind
47929	5	10770	5	13	NULL	NULL	NULL	PC	GP		blocks			S360A		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_20077_s_130	16709569	A low concentration of exogenous APC (3.3 nM) was used, and barrier protective effects of exogenous APC were blocked by both wild type PC and PC S360A, consistent with the expected role of zymogen PC as a competitive inhibitor for APC binding to EPCR.	bind
50358	6	10770	5	13	NULL	NULL	NULL	statement 1	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_20077_s_130	16709569	A low concentration of exogenous APC (3.3 nM) was used, and barrier protective effects of exogenous APC were blocked by both wild type PC and PC S360A, consistent with the expected role of zymogen PC as a competitive inhibitor for APC binding to EPCR.	bind
47274	1	10770	6	NULL	NULL	0	NULL	APC	NULL		bind	NULL				EPCR	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_29_20077_s_130	16709569	A low concentration of exogenous APC (3.3 nM) was used, and barrier protective effects of exogenous APC were blocked by both wild type PC and PC S360A, consistent with the expected role of zymogen PC as a competitive inhibitor for APC binding to EPCR.	bind
47276	2	10770	6	NULL	NULL	0	NULL	zymogen PC	NULL		bind	NULL				EPCR	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_29_20077_s_130	16709569	A low concentration of exogenous APC (3.3 nM) was used, and barrier protective effects of exogenous APC were blocked by both wild type PC and PC S360A, consistent with the expected role of zymogen PC as a competitive inhibitor for APC binding to EPCR.	bind
47278	3	10770	6	NULL	NULL	0	NULL	statement 1	NULL		competes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_29_20077_s_130	16709569	A low concentration of exogenous APC (3.3 nM) was used, and barrier protective effects of exogenous APC were blocked by both wild type PC and PC S360A, consistent with the expected role of zymogen PC as a competitive inhibitor for APC binding to EPCR.	bind
47279	4	10770	6	10	NULL	0	NULL	APC		exogenous	effects					barrier protective					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_29_20077_s_130	16709569	A low concentration of exogenous APC (3.3 nM) was used, and barrier protective effects of exogenous APC were blocked by both wild type PC and PC S360A, consistent with the expected role of zymogen PC as a competitive inhibitor for APC binding to EPCR.	bind
47280	5	10770	6	NULL	NULL	0	NULL	statement 4	NULL		is blocked by	NULL				PC	NULL	wild type			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_29_20077_s_130	16709569	A low concentration of exogenous APC (3.3 nM) was used, and barrier protective effects of exogenous APC were blocked by both wild type PC and PC S360A, consistent with the expected role of zymogen PC as a competitive inhibitor for APC binding to EPCR.	bind
47281	6	10770	6	NULL	NULL	0	NULL	statement 4	NULL		is blocked by	NULL				PC	NULL		S360A		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_29_20077_s_130	16709569	A low concentration of exogenous APC (3.3 nM) was used, and barrier protective effects of exogenous APC were blocked by both wild type PC and PC S360A, consistent with the expected role of zymogen PC as a competitive inhibitor for APC binding to EPCR.	bind
47930	1	10774	5	13	NULL	NULL	NULL				bind				CSL-binding site in the GC-rich domain	Notch 1	GP		ICD		NULL		NULL	NULL	NULL	NULL	gw70_development_130_24_6089_s_198	14597575	A low level of induction was also observed with Notch 1 ICD alone ( Fig. 6B), suggesting that the CSL-binding site in the GC-rich domain could bind Notch 1 ICD through CSL.	bind
57236	2	10774	5	13	NULL	NULL	NULL	statement 1	Process		occurs through					CSL	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_130_24_6089_s_198	14597575	A low level of induction was also observed with Notch 1 ICD alone ( Fig. 6B), suggesting that the CSL-binding site in the GC-rich domain could bind Notch 1 ICD through CSL.	bind
47128	1	10774	6	NULL	NULL	0	NULL	Notch 1	NULL		bind	NULL		ICD		CSL	NULL		CSL-binding site in the GC-rich domain		NULL		0	NULL	NULL	NULL	gw70_development_130_24_6089_s_198	14597575	A low level of induction was also observed with Notch 1 ICD alone ( Fig. 6B), suggesting that the CSL-binding site in the GC-rich domain could bind Notch 1 ICD through CSL.	bind
57237	2	10774	6	10	NULL	0	NULL	statement 1			occurs through					CSL					NULL		0	NULL	NULL	NULL	gw70_development_130_24_6089_s_198	14597575	A low level of induction was also observed with Notch 1 ICD alone ( Fig. 6B), suggesting that the CSL-binding site in the GC-rich domain could bind Notch 1 ICD through CSL.	bind
47932	1	10775	5	13	NULL	NULL	NULL	PP1	GP		bind					PNUTS	GP		309-401		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_16_13819_s_140	12574161	A low level of PP1 was found to bind to PNUTS-(309-401), but no binding was detected for PNUTS-(404-537), PNUTS-(590-872), and PNUTS-(724-872) or for two fragments with an internal deletion of residues 254-589.	bind
47933	2	10775	5	13	NULL	NULL	NULL	PP1	GP		does not bind					PNUTS	GP		404-537		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_16_13819_s_140	12574161	A low level of PP1 was found to bind to PNUTS-(309-401), but no binding was detected for PNUTS-(404-537), PNUTS-(590-872), and PNUTS-(724-872) or for two fragments with an internal deletion of residues 254-589.	bind
47934	3	10775	5	13	NULL	NULL	NULL	PP1	GP		does not bind					PNUTS	GP		590-872		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_16_13819_s_140	12574161	A low level of PP1 was found to bind to PNUTS-(309-401), but no binding was detected for PNUTS-(404-537), PNUTS-(590-872), and PNUTS-(724-872) or for two fragments with an internal deletion of residues 254-589.	bind
47935	4	10775	5	13	NULL	NULL	NULL	PP1	GP		does not bind					PNUTS	GP		724-872		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_16_13819_s_140	12574161	A low level of PP1 was found to bind to PNUTS-(309-401), but no binding was detected for PNUTS-(404-537), PNUTS-(590-872), and PNUTS-(724-872) or for two fragments with an internal deletion of residues 254-589.	bind
47129	1	10775	6	NULL	NULL	0	NULL	PP1	NULL		bind	NULL				PNUTS	NULL		309-401		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_16_13819_s_140	12574161	A low level of PP1 was found to bind to PNUTS-(309-401), but no binding was detected for PNUTS-(404-537), PNUTS-(590-872), and PNUTS-(724-872) or for two fragments with an internal deletion of residues 254-589.	bind
47130	2	10775	6	NULL	NULL	0	NULL	PP1	NULL		does not bind	NULL				PNUTS	NULL		404-537		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_16_13819_s_140	12574161	A low level of PP1 was found to bind to PNUTS-(309-401), but no binding was detected for PNUTS-(404-537), PNUTS-(590-872), and PNUTS-(724-872) or for two fragments with an internal deletion of residues 254-589.	bind
47131	3	10775	6	NULL	NULL	0	NULL	PP1	NULL		does not bind	NULL				PNUTS	NULL		724-872		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_16_13819_s_140	12574161	A low level of PP1 was found to bind to PNUTS-(309-401), but no binding was detected for PNUTS-(404-537), PNUTS-(590-872), and PNUTS-(724-872) or for two fragments with an internal deletion of residues 254-589.	bind
47132	4	10775	6	NULL	NULL	0	NULL	PP1	NULL		does not bind	NULL				PNUTS	NULL		590-872		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_16_13819_s_140	12574161	A low level of PP1 was found to bind to PNUTS-(309-401), but no binding was detected for PNUTS-(404-537), PNUTS-(590-872), and PNUTS-(724-872) or for two fragments with an internal deletion of residues 254-589.	bind
47936	1	10776	5	13	NULL	NULL	NULL	Sba1p	GP		bind					GR	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_4_422_s_76	10691735	A low level of Sba1p reproducibly remained bound to GR and MR after hormone addition, possibly indicating that p23 proteins might affect both holoreceptors and aporeceptors.	bind
47937	2	10776	5	13	NULL	NULL	NULL	Sba1p	GP		bind					MR	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_4_422_s_76	10691735	A low level of Sba1p reproducibly remained bound to GR and MR after hormone addition, possibly indicating that p23 proteins might affect both holoreceptors and aporeceptors.	bind
47938	3	10776	5	13	NULL	NULL	NULL	hormone	Chemical	addition of	retains					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_4_422_s_76	10691735	A low level of Sba1p reproducibly remained bound to GR and MR after hormone addition, possibly indicating that p23 proteins might affect both holoreceptors and aporeceptors.	bind
47939	4	10776	5	13	NULL	NULL	NULL	hormone	Chemical	addition of	retains					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_4_422_s_76	10691735	A low level of Sba1p reproducibly remained bound to GR and MR after hormone addition, possibly indicating that p23 proteins might affect both holoreceptors and aporeceptors.	bind
47940	5	10776	5	13	NULL	NULL	NULL	p23 proteins	GP		effect		might			holoreceptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_4_422_s_76	10691735	A low level of Sba1p reproducibly remained bound to GR and MR after hormone addition, possibly indicating that p23 proteins might affect both holoreceptors and aporeceptors.	bind
47941	6	10776	5	13	NULL	NULL	NULL	p23 proteins	GP		effect		might			aporeceptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_4_422_s_76	10691735	A low level of Sba1p reproducibly remained bound to GR and MR after hormone addition, possibly indicating that p23 proteins might affect both holoreceptors and aporeceptors.	bind
47152	1	10776	6	NULL	NULL	0	NULL	Sba1p	NULL		bind	NULL				GR	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_14_4_422_s_76	10691735	A low level of Sba1p reproducibly remained bound to GR and MR after hormone addition, possibly indicating that p23 proteins might affect both holoreceptors and aporeceptors.	bind
47153	2	10776	6	NULL	NULL	0	NULL	Sba1p	NULL		bind	NULL				MR	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_14_4_422_s_76	10691735	A low level of Sba1p reproducibly remained bound to GR and MR after hormone addition, possibly indicating that p23 proteins might affect both holoreceptors and aporeceptors.	bind
47156	3	10776	6	10	NULL	0	NULL	p23 protein			affect		might			holoreceptors					NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_4_422_s_76	10691735	A low level of Sba1p reproducibly remained bound to GR and MR after hormone addition, possibly indicating that p23 proteins might affect both holoreceptors and aporeceptors.	bind
47157	4	10776	6	10	NULL	0	NULL	p23 protein			affects		might			aporeceptors					NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_4_422_s_76	10691735	A low level of Sba1p reproducibly remained bound to GR and MR after hormone addition, possibly indicating that p23 proteins might affect both holoreceptors and aporeceptors.	bind
50359	5	10776	6	10	NULL	0	NULL	hormone	NULL	addition of	retains	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_14_4_422_s_76	10691735	A low level of Sba1p reproducibly remained bound to GR and MR after hormone addition, possibly indicating that p23 proteins might affect both holoreceptors and aporeceptors.	bind
50360	6	10776	6	10	NULL	0	NULL	hormone	NULL	addition of	retains	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_14_4_422_s_76	10691735	A low level of Sba1p reproducibly remained bound to GR and MR after hormone addition, possibly indicating that p23 proteins might affect both holoreceptors and aporeceptors.	bind
47942	1	10777	5	13	NULL	NULL	NULL	PapI	GP		is a type of					coregulatory protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_3_830_s_307	16959970	A low level of the coregulatory protein PapI, required for Pap pili expression ( ,  ,  ), increases the affinity of Lrp for  pap DNA hemimethylated at GATCdist but does not enhance binding of Lrp to  pap DNA fully methylated at GATCdist ( ).	bind
47943	2	10777	5	13	NULL	NULL	NULL	PapI	GP		is required for					Pap pili	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_3_830_s_307	16959970	A low level of the coregulatory protein PapI, required for Pap pili expression ( ,  ,  ), increases the affinity of Lrp for  pap DNA hemimethylated at GATCdist but does not enhance binding of Lrp to  pap DNA fully methylated at GATCdist ( ).	bind
47944	3	10777	5	13	NULL	NULL	NULL	Lrp	GP		shows affinity to					pap DNA	NucleicAcid	hemimethylated		GATCdist	NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_3_830_s_307	16959970	A low level of the coregulatory protein PapI, required for Pap pili expression ( ,  ,  ), increases the affinity of Lrp for  pap DNA hemimethylated at GATCdist but does not enhance binding of Lrp to  pap DNA fully methylated at GATCdist ( ).	bind
47945	4	10777	5	13	NULL	NULL	NULL	Lrp	GP		bind					pap DNA	NucleicAcid	fully methylated		GATCdist	NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_3_830_s_307	16959970	A low level of the coregulatory protein PapI, required for Pap pili expression ( ,  ,  ), increases the affinity of Lrp for  pap DNA hemimethylated at GATCdist but does not enhance binding of Lrp to  pap DNA fully methylated at GATCdist ( ).	bind
47946	5	10777	5	13	NULL	NULL	NULL	PapI	GP		increases					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_3_830_s_307	16959970	A low level of the coregulatory protein PapI, required for Pap pili expression ( ,  ,  ), increases the affinity of Lrp for  pap DNA hemimethylated at GATCdist but does not enhance binding of Lrp to  pap DNA fully methylated at GATCdist ( ).	bind
47947	6	10777	5	13	NULL	NULL	NULL	PapI	GP		does not enhance					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_3_830_s_307	16959970	A low level of the coregulatory protein PapI, required for Pap pili expression ( ,  ,  ), increases the affinity of Lrp for  pap DNA hemimethylated at GATCdist but does not enhance binding of Lrp to  pap DNA fully methylated at GATCdist ( ).	bind
47329	1	10777	6	NULL	NULL	0	NULL	PapI	NULL		is a type of	NULL				coregulatory protein	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_3_830_s_307	16959970	A low level of the coregulatory protein PapI, required for Pap pili expression ( ,  ,  ), increases the affinity of Lrp for  pap DNA hemimethylated at GATCdist but does not enhance binding of Lrp to  pap DNA fully methylated at GATCdist ( ).	bind
47330	2	10777	6	NULL	NULL	0	NULL	PapI	NULL		is required for	NULL				Pap pili	NULL	expression of 			NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_3_830_s_307	16959970	A low level of the coregulatory protein PapI, required for Pap pili expression ( ,  ,  ), increases the affinity of Lrp for  pap DNA hemimethylated at GATCdist but does not enhance binding of Lrp to  pap DNA fully methylated at GATCdist ( ).	bind
47331	3	10777	6	10	NULL	0	NULL	Lrp	NULL		shows affinity to	NULL				pap DNA	NULL	hemimethylated		GATCdist	NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_3_830_s_307	16959970	A low level of the coregulatory protein PapI, required for Pap pili expression ( ,  ,  ), increases the affinity of Lrp for  pap DNA hemimethylated at GATCdist but does not enhance binding of Lrp to  pap DNA fully methylated at GATCdist ( ).	bind
47335	4	10777	6	10	NULL	0	NULL	Lrp	NULL		shows affinity to	NULL				pap DNA	NULL	fully methylated		GATCdist	NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_3_830_s_307	16959970	A low level of the coregulatory protein PapI, required for Pap pili expression ( ,  ,  ), increases the affinity of Lrp for  pap DNA hemimethylated at GATCdist but does not enhance binding of Lrp to  pap DNA fully methylated at GATCdist ( ).	bind
47337	5	10777	6	10	NULL	0	NULL	PapI	NULL		increase	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_3_830_s_307	16959970	A low level of the coregulatory protein PapI, required for Pap pili expression ( ,  ,  ), increases the affinity of Lrp for  pap DNA hemimethylated at GATCdist but does not enhance binding of Lrp to  pap DNA fully methylated at GATCdist ( ).	bind
50361	6	10777	6	10	NULL	0	NULL	PapI	NULL		does not enhance	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_70_3_830_s_307	16959970	A low level of the coregulatory protein PapI, required for Pap pili expression ( ,  ,  ), increases the affinity of Lrp for  pap DNA hemimethylated at GATCdist but does not enhance binding of Lrp to  pap DNA fully methylated at GATCdist ( ).	bind
47948	1	10779	5	13	NULL	NULL	NULL	retinol binding protein	GP		bind					transthyretin	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_21_0_167_s_802	11375434	A low molar ratio of retinol binding protein to transthyretin  indicates vitamin A deficiency during inflammation: studies in rats and a posterior  analysis of vitamin A-supplemented children with measles.	bind
47949	2	10779	5	13	NULL	NULL	NULL	statement 1	Process		indicates					vitamin A	Chemical	deficiency of			NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_21_0_167_s_802	11375434	A low molar ratio of retinol binding protein to transthyretin  indicates vitamin A deficiency during inflammation: studies in rats and a posterior  analysis of vitamin A-supplemented children with measles.	bind
47950	3	10779	5	13	NULL	NULL	NULL	statement 2	GP		occurs during					inflammation	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_21_0_167_s_802	11375434	A low molar ratio of retinol binding protein to transthyretin  indicates vitamin A deficiency during inflammation: studies in rats and a posterior  analysis of vitamin A-supplemented children with measles.	bind
47174	1	10779	6	NULL	NULL	0	NULL	retinol binding protein	NULL		bind	NULL	low affinity			transthyretin	NULL				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_21_0_167_s_802	11375434	A low molar ratio of retinol binding protein to transthyretin  indicates vitamin A deficiency during inflammation: studies in rats and a posterior  analysis of vitamin A-supplemented children with measles.	bind
47175	2	10779	6	NULL	NULL	0	NULL	statement 1	NULL		indicates	NULL				vitamin A	NULL	deficiency of			NULL		0	NULL	NULL	NULL	gw70_annurevnutr_21_0_167_s_802	11375434	A low molar ratio of retinol binding protein to transthyretin  indicates vitamin A deficiency during inflammation: studies in rats and a posterior  analysis of vitamin A-supplemented children with measles.	bind
47176	3	10779	6	NULL	NULL	0	NULL	statement 2	NULL		occurs during 	NULL				inflammation	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevnutr_21_0_167_s_802	11375434	A low molar ratio of retinol binding protein to transthyretin  indicates vitamin A deficiency during inflammation: studies in rats and a posterior  analysis of vitamin A-supplemented children with measles.	bind
47951	1	10780	5	13	NULL	NULL	NULL	CXCL12	GP	labeled	bind					CXCR4	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_eur-cytokine-netw_17_1_16613763_s_7	16613763	A low molecular weight antagonist of CXCR4 prevented binding of labeled  CXCL12 to CXCR4 comparably to a neutralizing anti-CXCR4 antibody.	bind
47952	2	10780	5	13	NULL	NULL	NULL	CXCR4 antagonist	Chemical	low molecular weight	prevents					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_eur-cytokine-netw_17_1_16613763_s_7	16613763	A low molecular weight antagonist of CXCR4 prevented binding of labeled  CXCL12 to CXCR4 comparably to a neutralizing anti-CXCR4 antibody.	bind
47177	1	10780	6	NULL	NULL	0	NULL	CXCL12	NULL	labeled	bind	NULL				CXCR4	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_eur-cytokine-netw_17_1_16613763_s_7	16613763	A low molecular weight antagonist of CXCR4 prevented binding of labeled  CXCL12 to CXCR4 comparably to a neutralizing anti-CXCR4 antibody.	bind
47178	2	10780	6	NULL	NULL	0	NULL	CXCR4 antagonist	NULL	low molecular weight	prevents	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_eur-cytokine-netw_17_1_16613763_s_7	16613763	A low molecular weight antagonist of CXCR4 prevented binding of labeled  CXCL12 to CXCR4 comparably to a neutralizing anti-CXCR4 antibody.	bind
47953	1	10781	5	13	NULL	NULL	NULL	12 antenna Chls	Chemical	S. elongatus	bind					CP43	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_530_1_117_s_164	12387877	A low resolution (3.8  Ang ) X-ray crystal structure for this complex from  S. elongatus has been described [ 4, that included 12 antenna Chls bound to CP43 and 14 antenna Chls bound to CP47.	bind
47954	2	10781	5	13	NULL	NULL	NULL	14 antenna Chls	Chemical	S. elongatus	bind					CP47	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_530_1_117_s_164	12387877	A low resolution (3.8  Ang ) X-ray crystal structure for this complex from  S. elongatus has been described [ 4, that included 12 antenna Chls bound to CP43 and 14 antenna Chls bound to CP47.	bind
47179	1	10781	6	NULL	NULL	0	NULL	12 antenna Chls	NULL	S. elongatus	bind	NULL				CP43	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_530_1_117_s_164	12387877	A low resolution (3.8  Ang ) X-ray crystal structure for this complex from  S. elongatus has been described [ 4, that included 12 antenna Chls bound to CP43 and 14 antenna Chls bound to CP47.	bind
47180	2	10781	6	NULL	NULL	0	NULL	14 antenna Chls	NULL	S. elongatus	bind	NULL				CP47	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_530_1_117_s_164	12387877	A low resolution (3.8  Ang ) X-ray crystal structure for this complex from  S. elongatus has been described [ 4, that included 12 antenna Chls bound to CP43 and 14 antenna Chls bound to CP47.	bind
47958	1	10782	5	13	NULL	NULL	NULL	atherosclerosis	Process	low risk of	is observed in					APOB	GP	mutation of	LDL binding region		NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_7_693_s_20	10449689	A low risk of atherosclerosis is observed in  APOB mutations outside the LDL binding region and in cholesteryl ester transfer protein ( CETP) deficiency, whereas the impact of  APOAII deficiency on atherosclerosis has not been established 1  (Table 1  ).	bind
47959	2	10782	5	13	NULL	NULL	NULL	atherosclerosis	Process	low risk of	is observed in					CETP	GP	deficiency of			NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_7_693_s_20	10449689	A low risk of atherosclerosis is observed in  APOB mutations outside the LDL binding region and in cholesteryl ester transfer protein ( CETP) deficiency, whereas the impact of  APOAII deficiency on atherosclerosis has not been established 1  (Table 1  ).	bind
47960	3	10782	5	13	NULL	NULL	NULL	CETP	GP		is					cholesteryl ester transfer protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_100_7_693_s_20	10449689	A low risk of atherosclerosis is observed in  APOB mutations outside the LDL binding region and in cholesteryl ester transfer protein ( CETP) deficiency, whereas the impact of  APOAII deficiency on atherosclerosis has not been established 1  (Table 1  ).	bind
47349	1	10782	6	NULL	NULL	0	NULL	CETP	NULL		is	NULL				cholesteryl ester transfer protein	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_7_693_s_20	10449689	A low risk of atherosclerosis is observed in  APOB mutations outside the LDL binding region and in cholesteryl ester transfer protein ( CETP) deficiency, whereas the impact of  APOAII deficiency on atherosclerosis has not been established 1  (Table 1  ).	bind
47350	2	10782	6	NULL	NULL	0	NULL	CETP	NULL	deficiency of	causes risk of	NULL				atherosclerosis	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_7_693_s_20	10449689	A low risk of atherosclerosis is observed in  APOB mutations outside the LDL binding region and in cholesteryl ester transfer protein ( CETP) deficiency, whereas the impact of  APOAII deficiency on atherosclerosis has not been established 1  (Table 1  ).	bind
47351	3	10782	6	NULL	NULL	0	NULL	APOB	NULL	mutation of	causes risk of	NULL	low	LDL binding region		atherosclerosis	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_100_7_693_s_20	10449689	A low risk of atherosclerosis is observed in  APOB mutations outside the LDL binding region and in cholesteryl ester transfer protein ( CETP) deficiency, whereas the impact of  APOAII deficiency on atherosclerosis has not been established 1  (Table 1  ).	bind
47961	1	10783	5	13	NULL	NULL	NULL	seminal plasma	Chemical	human;;low-molecular-weight fraction of	activates					adenylyl cyclase	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5385_2027_s_405	9748162	A low-molecular-weight fraction of human seminal plasma activates adenylyl cyclase and induces caspase 3-independent apoptosis in prostatic epithelial cells by decreasing mitochondrial potential and Bcl-2/Bax ratio.	bind
47962	2	10783	5	13	NULL	NULL	NULL	apoptosis	GP		is independent of					caspase 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5385_2027_s_405	9748162	A low-molecular-weight fraction of human seminal plasma activates adenylyl cyclase and induces caspase 3-independent apoptosis in prostatic epithelial cells by decreasing mitochondrial potential and Bcl-2/Bax ratio.	bind
47963	3	10783	5	13	NULL	NULL	NULL	statement 1	Process		induces					statement 2	Process				NULL	prostatic epithelial cells	NULL	NULL	NULL	NULL	gw60_science_281_5385_2027_s_405	9748162	A low-molecular-weight fraction of human seminal plasma activates adenylyl cyclase and induces caspase 3-independent apoptosis in prostatic epithelial cells by decreasing mitochondrial potential and Bcl-2/Bax ratio.	bind
47964	4	10783	5	13	NULL	NULL	NULL	statement 3	Process		occurs by					mitochondrial potential	Process	decreasing			NULL		NULL	NULL	NULL	NULL	gw60_science_281_5385_2027_s_405	9748162	A low-molecular-weight fraction of human seminal plasma activates adenylyl cyclase and induces caspase 3-independent apoptosis in prostatic epithelial cells by decreasing mitochondrial potential and Bcl-2/Bax ratio.	bind
47965	5	10783	5	13	NULL	NULL	NULL	statement 3	Process		occurs by					Bcl-2/Bax ratio	GP	decreasing			NULL		NULL	NULL	NULL	NULL	gw60_science_281_5385_2027_s_405	9748162	A low-molecular-weight fraction of human seminal plasma activates adenylyl cyclase and induces caspase 3-independent apoptosis in prostatic epithelial cells by decreasing mitochondrial potential and Bcl-2/Bax ratio.	bind
47181	1	10783	6	NULL	NULL	0	NULL	seminal plasma	NULL	human;; low molecular weight fraction of	activates	NULL				adenylyl cyclase	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5385_2027_s_405	9748162	A low-molecular-weight fraction of human seminal plasma activates adenylyl cyclase and induces caspase 3-independent apoptosis in prostatic epithelial cells by decreasing mitochondrial potential and Bcl-2/Bax ratio.	bind
47182	2	10783	6	NULL	NULL	0	NULL	apoptosis	NULL		is independent of	NULL				caspase-3	NULL				NULL		0	NULL	NULL	NULL	gw60_science_281_5385_2027_s_405	9748162	A low-molecular-weight fraction of human seminal plasma activates adenylyl cyclase and induces caspase 3-independent apoptosis in prostatic epithelial cells by decreasing mitochondrial potential and Bcl-2/Bax ratio.	bind
47183	3	10783	6	NULL	NULL	0	NULL	statement 1	NULL		induces	NULL				statement 2	NULL				NULL	prostatic epithelial cells	0	NULL	NULL	NULL	gw60_science_281_5385_2027_s_405	9748162	A low-molecular-weight fraction of human seminal plasma activates adenylyl cyclase and induces caspase 3-independent apoptosis in prostatic epithelial cells by decreasing mitochondrial potential and Bcl-2/Bax ratio.	bind
47184	4	10783	6	NULL	NULL	0	NULL	statement 3	NULL		occurs by	NULL				mitochondrial potential	NULL	decreasing			NULL		0	NULL	NULL	NULL	gw60_science_281_5385_2027_s_405	9748162	A low-molecular-weight fraction of human seminal plasma activates adenylyl cyclase and induces caspase 3-independent apoptosis in prostatic epithelial cells by decreasing mitochondrial potential and Bcl-2/Bax ratio.	bind
47185	5	10783	6	NULL	NULL	0	NULL	statement 3	NULL		occurs by	NULL				Bcl-2/Bax ratio	NULL	decreasing			NULL		0	NULL	NULL	NULL	gw60_science_281_5385_2027_s_405	9748162	A low-molecular-weight fraction of human seminal plasma activates adenylyl cyclase and induces caspase 3-independent apoptosis in prostatic epithelial cells by decreasing mitochondrial potential and Bcl-2/Bax ratio.	bind
47966	1	10784	5	13	NULL	NULL	NULL	BD-Pdcd4	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_9_3894_s_68	15082783	A luciferase reporter becomes activated when the BD-Pdcd4 (wild-type or mutant) fusion protein binds to the AD-eIF4A fusion protein.	bind
47967	2	10784	5	13	NULL	NULL	NULL	AD-eIF4A	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_9_3894_s_68	15082783	A luciferase reporter becomes activated when the BD-Pdcd4 (wild-type or mutant) fusion protein binds to the AD-eIF4A fusion protein.	bind
47968	3	10784	5	13	NULL	NULL	NULL	BD-Pdcd4	GP	wild-type	bind					AD-eIF4A	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_9_3894_s_68	15082783	A luciferase reporter becomes activated when the BD-Pdcd4 (wild-type or mutant) fusion protein binds to the AD-eIF4A fusion protein.	bind
47969	4	10784	5	13	NULL	NULL	NULL	BD-Pdcd4	GP	mutant	bind					AD-eIF4A	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_9_3894_s_68	15082783	A luciferase reporter becomes activated when the BD-Pdcd4 (wild-type or mutant) fusion protein binds to the AD-eIF4A fusion protein.	bind
47970	5	10784	5	13	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_9_3894_s_68	15082783	A luciferase reporter becomes activated when the BD-Pdcd4 (wild-type or mutant) fusion protein binds to the AD-eIF4A fusion protein.	bind
47186	1	10784	6	10	NULL	0	NULL	BD-Pdcd4	NULL	wild type	bind	NULL				AD-eIF4A	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_9_3894_s_68	15082783	A luciferase reporter becomes activated when the BD-Pdcd4 (wild-type or mutant) fusion protein binds to the AD-eIF4A fusion protein.	bind
47187	2	10784	6	10	NULL	0	NULL	BD-Pdcd4 	NULL	mutant	bind	NULL				AD-eIF4A	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_9_3894_s_68	15082783	A luciferase reporter becomes activated when the BD-Pdcd4 (wild-type or mutant) fusion protein binds to the AD-eIF4A fusion protein.	bind
47188	3	10784	6	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_9_3894_s_68	15082783	A luciferase reporter becomes activated when the BD-Pdcd4 (wild-type or mutant) fusion protein binds to the AD-eIF4A fusion protein.	bind
50362	4	10784	6	10	NULL	0	NULL	BD-Pdcd4	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_9_3894_s_68	15082783	A luciferase reporter becomes activated when the BD-Pdcd4 (wild-type or mutant) fusion protein binds to the AD-eIF4A fusion protein.	bind
50363	5	10784	6	10	NULL	0	NULL	AD-eIF4A	NULL		is a type of	NULL				fusion protein	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_9_3894_s_68	15082783	A luciferase reporter becomes activated when the BD-Pdcd4 (wild-type or mutant) fusion protein binds to the AD-eIF4A fusion protein.	bind
47971	1	10785	5	13	NULL	NULL	NULL	HsCdc6	GP		forms complex with					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_8_2631_s_334	10436018	A Lys to Ala mutation within the highly conserved Walker A motif of GST-HsCdc6 strongly reduced ATP-binding activity, and GST alone did not bind to ATP (Figure  1), demonstrating that complex formation with ATP is an intrinsic function of HsCdc6.	bind
47972	2	10785	5	13	NULL	NULL	NULL	GST-HsCdc6	GP		bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_8_2631_s_334	10436018	A Lys to Ala mutation within the highly conserved Walker A motif of GST-HsCdc6 strongly reduced ATP-binding activity, and GST alone did not bind to ATP (Figure  1), demonstrating that complex formation with ATP is an intrinsic function of HsCdc6.	bind
47973	3	10785	5	13	NULL	NULL	NULL	GST-HsCdc6	GP		is mutated to			Lys in Walker A motif		GST-HsCdc6	GP		Ala in Walker A motif		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_8_2631_s_334	10436018	A Lys to Ala mutation within the highly conserved Walker A motif of GST-HsCdc6 strongly reduced ATP-binding activity, and GST alone did not bind to ATP (Figure  1), demonstrating that complex formation with ATP is an intrinsic function of HsCdc6.	bind
47974	4	10785	5	13	NULL	NULL	NULL	statement 3	Process		reduces		strongly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_8_2631_s_334	10436018	A Lys to Ala mutation within the highly conserved Walker A motif of GST-HsCdc6 strongly reduced ATP-binding activity, and GST alone did not bind to ATP (Figure  1), demonstrating that complex formation with ATP is an intrinsic function of HsCdc6.	bind
47975	5	10785	5	13	NULL	NULL	NULL	GST	GP		does not bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_8_2631_s_334	10436018	A Lys to Ala mutation within the highly conserved Walker A motif of GST-HsCdc6 strongly reduced ATP-binding activity, and GST alone did not bind to ATP (Figure  1), demonstrating that complex formation with ATP is an intrinsic function of HsCdc6.	bind
47189	1	10785	6	NULL	NULL	0	NULL	GST-HsCdc6	NULL		is mutated to	NULL		Lys;; Walker A motif		GST-HsCdc6	NULL		Ala;; Walker A motif		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_8_2631_s_334	10436018	A Lys to Ala mutation within the highly conserved Walker A motif of GST-HsCdc6 strongly reduced ATP-binding activity, and GST alone did not bind to ATP (Figure  1), demonstrating that complex formation with ATP is an intrinsic function of HsCdc6.	bind
47190	2	10785	6	NULL	NULL	0	NULL	GST-HsCdc6	NULL		bind	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_8_2631_s_334	10436018	A Lys to Ala mutation within the highly conserved Walker A motif of GST-HsCdc6 strongly reduced ATP-binding activity, and GST alone did not bind to ATP (Figure  1), demonstrating that complex formation with ATP is an intrinsic function of HsCdc6.	bind
47191	3	10785	6	NULL	NULL	0	NULL	statement 1	NULL		reduces	NULL	strongly			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_8_2631_s_334	10436018	A Lys to Ala mutation within the highly conserved Walker A motif of GST-HsCdc6 strongly reduced ATP-binding activity, and GST alone did not bind to ATP (Figure  1), demonstrating that complex formation with ATP is an intrinsic function of HsCdc6.	bind
47192	4	10785	6	NULL	NULL	0	NULL	GST	NULL		does not bind	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_8_2631_s_334	10436018	A Lys to Ala mutation within the highly conserved Walker A motif of GST-HsCdc6 strongly reduced ATP-binding activity, and GST alone did not bind to ATP (Figure  1), demonstrating that complex formation with ATP is an intrinsic function of HsCdc6.	bind
49689	1	10788	5	13	NULL	NULL	NULL	beta MHC	GP	human	is changed to			lysine at amino acid 184		beta MHC	GP	human	arginine at amino acid 184		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-cell-biol_137_1_9105042_s_5	9105042	A lysine to arginine  change at amino acid 184 in the consensus ATP binding sequence of human  beta MHC resulted in abnormal subcellular localization and disrupted both  thick and thin filament structure in transfected NRC.	bind
49690	2	10788	5	13	NULL	NULL	NULL	statement 1	Process		results in					beta MHC	GP	abnormal;;subcellular localization of;;human			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-cell-biol_137_1_9105042_s_5	9105042	A lysine to arginine  change at amino acid 184 in the consensus ATP binding sequence of human  beta MHC resulted in abnormal subcellular localization and disrupted both  thick and thin filament structure in transfected NRC.	bind
49691	3	10788	5	13	NULL	NULL	NULL	statement 1	Process		disrupts					thin filament	GP	structure of			NULL	transfected NRC	NULL	NULL	NULL	NULL	abs-batch0720-0739_j-cell-biol_137_1_9105042_s_5	9105042	A lysine to arginine  change at amino acid 184 in the consensus ATP binding sequence of human  beta MHC resulted in abnormal subcellular localization and disrupted both  thick and thin filament structure in transfected NRC.	bind
49692	4	10788	5	13	NULL	NULL	NULL	statement 1	Process		disrupts					thick filament	GP	structure of			NULL	transfected NRC	NULL	NULL	NULL	NULL	abs-batch0720-0739_j-cell-biol_137_1_9105042_s_5	9105042	A lysine to arginine  change at amino acid 184 in the consensus ATP binding sequence of human  beta MHC resulted in abnormal subcellular localization and disrupted both  thick and thin filament structure in transfected NRC.	bind
47193	1	10788	6	NULL	NULL	0	NULL	beta MHC	NULL	human	is changed to	NULL		lysine ;; amino acid 184		beta MHC	NULL	human	arginine;; amino acid 184		NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-cell-biol_137_1_9105042_s_5	9105042	A lysine to arginine  change at amino acid 184 in the consensus ATP binding sequence of human  beta MHC resulted in abnormal subcellular localization and disrupted both  thick and thin filament structure in transfected NRC.	bind
47194	2	10788	6	NULL	NULL	0	NULL	statement 1	NULL		results in abnormal	NULL				beta MHC	NULL	human;; subcellular localization of 			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-cell-biol_137_1_9105042_s_5	9105042	A lysine to arginine  change at amino acid 184 in the consensus ATP binding sequence of human  beta MHC resulted in abnormal subcellular localization and disrupted both  thick and thin filament structure in transfected NRC.	bind
47195	3	10788	6	NULL	NULL	0	NULL	statement 1	NULL		disrupts	NULL				thick filament	NULL	structure of			NULL	transfected NRC	0	NULL	NULL	NULL	abs-batch0720-0739_j-cell-biol_137_1_9105042_s_5	9105042	A lysine to arginine  change at amino acid 184 in the consensus ATP binding sequence of human  beta MHC resulted in abnormal subcellular localization and disrupted both  thick and thin filament structure in transfected NRC.	bind
47196	4	10788	6	NULL	NULL	0	NULL	statement 1	NULL		disrupts	NULL				thin filament	NULL	structure of			NULL	transfected NRC	0	NULL	NULL	NULL	abs-batch0720-0739_j-cell-biol_137_1_9105042_s_5	9105042	A lysine to arginine  change at amino acid 184 in the consensus ATP binding sequence of human  beta MHC resulted in abnormal subcellular localization and disrupted both  thick and thin filament structure in transfected NRC.	bind
49693	1	10790	5	13	NULL	NULL	NULL	NT-3	GP		bind					p75 receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_22_8915_s_398	11698603	A lysosomal pathway of NT-3 may be common to all neurotrophins and may involve binding to the p75 receptor ( U) or binding of NT-3 to trkC receptor ( Y) in the presence of the tyrosine kinase inhibitor K252a.	bind
49694	2	10790	5	13	NULL	NULL	NULL	statement 1	Process		in the presence of					K252a	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_22_8915_s_398	11698603	A lysosomal pathway of NT-3 may be common to all neurotrophins and may involve binding to the p75 receptor ( U) or binding of NT-3 to trkC receptor ( Y) in the presence of the tyrosine kinase inhibitor K252a.	bind
49695	3	10790	5	13	NULL	NULL	NULL	K252a	Chemical		is a type of					tyrosine kinase inhibitor	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_22_8915_s_398	11698603	A lysosomal pathway of NT-3 may be common to all neurotrophins and may involve binding to the p75 receptor ( U) or binding of NT-3 to trkC receptor ( Y) in the presence of the tyrosine kinase inhibitor K252a.	bind
49696	4	10790	5	13	NULL	NULL	NULL	NT-3	GP		bind					trkC receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_22_8915_s_398	11698603	A lysosomal pathway of NT-3 may be common to all neurotrophins and may involve binding to the p75 receptor ( U) or binding of NT-3 to trkC receptor ( Y) in the presence of the tyrosine kinase inhibitor K252a.	bind
49697	5	10790	5	13	NULL	NULL	NULL	statement 4	Process		in the presence of					K252a	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_22_8915_s_398	11698603	A lysosomal pathway of NT-3 may be common to all neurotrophins and may involve binding to the p75 receptor ( U) or binding of NT-3 to trkC receptor ( Y) in the presence of the tyrosine kinase inhibitor K252a.	bind
49698	6	10790	5	13	NULL	NULL	NULL	lysosomal pathway of NT-3	Process		involves		may			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_22_8915_s_398	11698603	A lysosomal pathway of NT-3 may be common to all neurotrophins and may involve binding to the p75 receptor ( U) or binding of NT-3 to trkC receptor ( Y) in the presence of the tyrosine kinase inhibitor K252a.	bind
49699	7	10790	5	13	NULL	NULL	NULL	lysosomal pathway of NT-3	Process		involves		may			statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_22_8915_s_398	11698603	A lysosomal pathway of NT-3 may be common to all neurotrophins and may involve binding to the p75 receptor ( U) or binding of NT-3 to trkC receptor ( Y) in the presence of the tyrosine kinase inhibitor K252a.	bind
49700	8	10790	5	13	NULL	NULL	NULL	lysosomal pathway of NT-3	Process		is common to					neurotrophins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_22_8915_s_398	11698603	A lysosomal pathway of NT-3 may be common to all neurotrophins and may involve binding to the p75 receptor ( U) or binding of NT-3 to trkC receptor ( Y) in the presence of the tyrosine kinase inhibitor K252a.	bind
47197	1	10790	6	10	NULL	0	NULL	NT-3	NULL		bind	NULL				p75 receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_22_8915_s_398	11698603	A lysosomal pathway of NT-3 may be common to all neurotrophins and may involve binding to the p75 receptor ( U) or binding of NT-3 to trkC receptor ( Y) in the presence of the tyrosine kinase inhibitor K252a.	bind
47198	2	10790	6	10	NULL	0	NULL	NT-3	NULL		bind	NULL				trkC receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_21_22_8915_s_398	11698603	A lysosomal pathway of NT-3 may be common to all neurotrophins and may involve binding to the p75 receptor ( U) or binding of NT-3 to trkC receptor ( Y) in the presence of the tyrosine kinase inhibitor K252a.	bind
47199	3	10790	6	NULL	NULL	0	NULL	lysosomal pathway of NT-3	NULL		is common to	NULL	may			neurotrophins	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_22_8915_s_398	11698603	A lysosomal pathway of NT-3 may be common to all neurotrophins and may involve binding to the p75 receptor ( U) or binding of NT-3 to trkC receptor ( Y) in the presence of the tyrosine kinase inhibitor K252a.	bind
47200	4	10790	6	NULL	NULL	0	NULL	statement 3	NULL		involve	NULL	may			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_22_8915_s_398	11698603	A lysosomal pathway of NT-3 may be common to all neurotrophins and may involve binding to the p75 receptor ( U) or binding of NT-3 to trkC receptor ( Y) in the presence of the tyrosine kinase inhibitor K252a.	bind
47201	5	10790	6	NULL	NULL	0	NULL	statement 3	NULL		involve	NULL	may			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_22_8915_s_398	11698603	A lysosomal pathway of NT-3 may be common to all neurotrophins and may involve binding to the p75 receptor ( U) or binding of NT-3 to trkC receptor ( Y) in the presence of the tyrosine kinase inhibitor K252a.	bind
47202	6	10790	6	NULL	NULL	0	NULL	statement 1	NULL		occurs in presence of	NULL				K252a	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_22_8915_s_398	11698603	A lysosomal pathway of NT-3 may be common to all neurotrophins and may involve binding to the p75 receptor ( U) or binding of NT-3 to trkC receptor ( Y) in the presence of the tyrosine kinase inhibitor K252a.	bind
47203	7	10790	6	NULL	NULL	0	NULL	statement 2	NULL		occurs in presence of	NULL				K252a	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_22_8915_s_398	11698603	A lysosomal pathway of NT-3 may be common to all neurotrophins and may involve binding to the p75 receptor ( U) or binding of NT-3 to trkC receptor ( Y) in the presence of the tyrosine kinase inhibitor K252a.	bind
47204	8	10790	6	NULL	NULL	0	NULL	K252a	NULL		is a type of	NULL				tyrosine kinase inhibitor	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_22_8915_s_398	11698603	A lysosomal pathway of NT-3 may be common to all neurotrophins and may involve binding to the p75 receptor ( U) or binding of NT-3 to trkC receptor ( Y) in the presence of the tyrosine kinase inhibitor K252a.	bind
49701	1	10791	5	13	NULL	NULL	NULL	TRA-2-10, IgG1	GP		is a type of					mAb against 2102ep	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_fertil-steril_58_3_1521662_s_2	1521662	A mAb (TRA-2-10, IgG1) to an embryonal carcinoma cell line (2102ep) that  recognizes an antigen termed membrane cofactor protein (CD 46, TLX antigen)  binds to human sperm after chemical induction of acrosomal loss by Ca2+  ionophore.	bind
49702	2	10791	5	13	NULL	NULL	NULL	2102ep	Cell		is a type of					embryonal carcinoma cell line	Cell				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_fertil-steril_58_3_1521662_s_2	1521662	A mAb (TRA-2-10, IgG1) to an embryonal carcinoma cell line (2102ep) that  recognizes an antigen termed membrane cofactor protein (CD 46, TLX antigen)  binds to human sperm after chemical induction of acrosomal loss by Ca2+  ionophore.	bind
49703	3	10791	5	13	NULL	NULL	NULL	CD 46	GP		is a type of					antigen	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_fertil-steril_58_3_1521662_s_2	1521662	A mAb (TRA-2-10, IgG1) to an embryonal carcinoma cell line (2102ep) that  recognizes an antigen termed membrane cofactor protein (CD 46, TLX antigen)  binds to human sperm after chemical induction of acrosomal loss by Ca2+  ionophore.	bind
49704	4	10791	5	13	NULL	NULL	NULL	CD 46	GP		is a type of					membrane cofactor protein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_fertil-steril_58_3_1521662_s_2	1521662	A mAb (TRA-2-10, IgG1) to an embryonal carcinoma cell line (2102ep) that  recognizes an antigen termed membrane cofactor protein (CD 46, TLX antigen)  binds to human sperm after chemical induction of acrosomal loss by Ca2+  ionophore.	bind
49705	5	10791	5	13	NULL	NULL	NULL	TRA-2-10, IgG1	GP		bind					sperm	Cell	human			NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_fertil-steril_58_3_1521662_s_2	1521662	A mAb (TRA-2-10, IgG1) to an embryonal carcinoma cell line (2102ep) that  recognizes an antigen termed membrane cofactor protein (CD 46, TLX antigen)  binds to human sperm after chemical induction of acrosomal loss by Ca2+  ionophore.	bind
49706	6	10791	5	13	NULL	NULL	NULL	Ca2+ ionophore	Chemical		induce		chemically			acrosome	CellComponent	loss of			NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_fertil-steril_58_3_1521662_s_2	1521662	A mAb (TRA-2-10, IgG1) to an embryonal carcinoma cell line (2102ep) that  recognizes an antigen termed membrane cofactor protein (CD 46, TLX antigen)  binds to human sperm after chemical induction of acrosomal loss by Ca2+  ionophore.	bind
49707	7	10791	5	13	NULL	NULL	NULL	statement 5	Process		occurs after					statement 6	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_fertil-steril_58_3_1521662_s_2	1521662	A mAb (TRA-2-10, IgG1) to an embryonal carcinoma cell line (2102ep) that  recognizes an antigen termed membrane cofactor protein (CD 46, TLX antigen)  binds to human sperm after chemical induction of acrosomal loss by Ca2+  ionophore.	bind
50812	8	10791	5	13	NULL	NULL	NULL	TLX antigen	GP		is a type of					antigen	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_fertil-steril_58_3_1521662_s_2	1521662	A mAb (TRA-2-10, IgG1) to an embryonal carcinoma cell line (2102ep) that  recognizes an antigen termed membrane cofactor protein (CD 46, TLX antigen)  binds to human sperm after chemical induction of acrosomal loss by Ca2+  ionophore.	bind
50813	9	10791	5	13	NULL	NULL	NULL	TLX antigen	GP		is a type of					membrane cofactor protein \t	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_fertil-steril_58_3_1521662_s_2	1521662	A mAb (TRA-2-10, IgG1) to an embryonal carcinoma cell line (2102ep) that  recognizes an antigen termed membrane cofactor protein (CD 46, TLX antigen)  binds to human sperm after chemical induction of acrosomal loss by Ca2+  ionophore.	bind
47352	1	10791	6	10	NULL	0	NULL	CD46 	NULL		is a type of	NULL				membrane cofactor protein	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_fertil-steril_58_3_1521662_s_2	1521662	A mAb (TRA-2-10, IgG1) to an embryonal carcinoma cell line (2102ep) that  recognizes an antigen termed membrane cofactor protein (CD 46, TLX antigen)  binds to human sperm after chemical induction of acrosomal loss by Ca2+  ionophore.	bind
47353	2	10791	6	10	NULL	0	NULL	TLX antigen 	NULL		is a type of	NULL				membrane cofactor protein	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_fertil-steril_58_3_1521662_s_2	1521662	A mAb (TRA-2-10, IgG1) to an embryonal carcinoma cell line (2102ep) that  recognizes an antigen termed membrane cofactor protein (CD 46, TLX antigen)  binds to human sperm after chemical induction of acrosomal loss by Ca2+  ionophore.	bind
47354	3	10791	6	NULL	NULL	0	NULL	CD 46	NULL		is a type of	NULL				antigen	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fertil-steril_58_3_1521662_s_2	1521662	A mAb (TRA-2-10, IgG1) to an embryonal carcinoma cell line (2102ep) that  recognizes an antigen termed membrane cofactor protein (CD 46, TLX antigen)  binds to human sperm after chemical induction of acrosomal loss by Ca2+  ionophore.	bind
47355	4	10791	6	NULL	NULL	0	NULL	TLX antigen	NULL		is a type of	NULL				antigen	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fertil-steril_58_3_1521662_s_2	1521662	A mAb (TRA-2-10, IgG1) to an embryonal carcinoma cell line (2102ep) that  recognizes an antigen termed membrane cofactor protein (CD 46, TLX antigen)  binds to human sperm after chemical induction of acrosomal loss by Ca2+  ionophore.	bind
47356	5	10791	6	NULL	NULL	0	NULL	TRA-2-10, IgG1	NULL		is a type of	NULL				mAb against 2101ep	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fertil-steril_58_3_1521662_s_2	1521662	A mAb (TRA-2-10, IgG1) to an embryonal carcinoma cell line (2102ep) that  recognizes an antigen termed membrane cofactor protein (CD 46, TLX antigen)  binds to human sperm after chemical induction of acrosomal loss by Ca2+  ionophore.	bind
47357	6	10791	6	NULL	NULL	0	NULL	2102ep	NULL		is a type of	NULL				embryonal carcinoma cell line	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fertil-steril_58_3_1521662_s_2	1521662	A mAb (TRA-2-10, IgG1) to an embryonal carcinoma cell line (2102ep) that  recognizes an antigen termed membrane cofactor protein (CD 46, TLX antigen)  binds to human sperm after chemical induction of acrosomal loss by Ca2+  ionophore.	bind
47362	7	10791	6	NULL	NULL	0	NULL	TRA-2-10, IgG1	NULL		bind	NULL				sperm	NULL	human			NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fertil-steril_58_3_1521662_s_2	1521662	A mAb (TRA-2-10, IgG1) to an embryonal carcinoma cell line (2102ep) that  recognizes an antigen termed membrane cofactor protein (CD 46, TLX antigen)  binds to human sperm after chemical induction of acrosomal loss by Ca2+  ionophore.	bind
47363	8	10791	6	10	NULL	0	NULL	Ca2+ ionophore	NULL		induces	NULL				acrosome	NULL	loss of			NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_fertil-steril_58_3_1521662_s_2	1521662	A mAb (TRA-2-10, IgG1) to an embryonal carcinoma cell line (2102ep) that  recognizes an antigen termed membrane cofactor protein (CD 46, TLX antigen)  binds to human sperm after chemical induction of acrosomal loss by Ca2+  ionophore.	bind
47364	9	10791	6	NULL	NULL	0	NULL	statement 7	NULL		occurs after	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fertil-steril_58_3_1521662_s_2	1521662	A mAb (TRA-2-10, IgG1) to an embryonal carcinoma cell line (2102ep) that  recognizes an antigen termed membrane cofactor protein (CD 46, TLX antigen)  binds to human sperm after chemical induction of acrosomal loss by Ca2+  ionophore.	bind
49708	1	10792	5	13	NULL	NULL	NULL	mAb against an alpha spectrin	GP		bind					230-kDa protein	GP				NULL	HeLa chromatin-associated protein extracts	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_32904_s_85	10551855	A mAb against an alpha spectrin, with specificity for mammalian nonerythroid alpha spectrin (Chemicon), bound to the 230-kDa protein from HeLa chromatin-associated protein extracts (Fig.  1,  lane 1); binding of this mAb to human erythroid spectrin (alpha and beta chains) (Fig.  1,  lane 2) was used as a control.	bind
49709	2	10792	5	13	NULL	NULL	NULL	mAb against an alpha spectrin	GP		is specific to					nonerythroid alpha spectrin	GP	mammalian			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_32904_s_85	10551855	A mAb against an alpha spectrin, with specificity for mammalian nonerythroid alpha spectrin (Chemicon), bound to the 230-kDa protein from HeLa chromatin-associated protein extracts (Fig.  1,  lane 1); binding of this mAb to human erythroid spectrin (alpha and beta chains) (Fig.  1,  lane 2) was used as a control.	bind
49710	3	10792	5	13	NULL	NULL	NULL	mAb against an alpha spectrin	GP		bind					erythroid spectrin	GP	human	alpha chain;;beta chain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_46_32904_s_85	10551855	A mAb against an alpha spectrin, with specificity for mammalian nonerythroid alpha spectrin (Chemicon), bound to the 230-kDa protein from HeLa chromatin-associated protein extracts (Fig.  1,  lane 1); binding of this mAb to human erythroid spectrin (alpha and beta chains) (Fig.  1,  lane 2) was used as a control.	bind
47365	1	10792	6	NULL	NULL	0	NULL	230-kDa protein	NULL		isolated from	NULL				HeLa chromatin-associated protein extracts	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_46_32904_s_85	10551855	A mAb against an alpha spectrin, with specificity for mammalian nonerythroid alpha spectrin (Chemicon), bound to the 230-kDa protein from HeLa chromatin-associated protein extracts (Fig.  1,  lane 1); binding of this mAb to human erythroid spectrin (alpha and beta chains) (Fig.  1,  lane 2) was used as a control.	bind
47366	2	10792	6	NULL	NULL	0	NULL	mAb against an alpha spectrin	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_46_32904_s_85	10551855	A mAb against an alpha spectrin, with specificity for mammalian nonerythroid alpha spectrin (Chemicon), bound to the 230-kDa protein from HeLa chromatin-associated protein extracts (Fig.  1,  lane 1); binding of this mAb to human erythroid spectrin (alpha and beta chains) (Fig.  1,  lane 2) was used as a control.	bind
47367	3	10792	6	NULL	NULL	0	NULL	mAb against alpha spectrin	NULL		bind	NULL				erythroid spectrin	NULL	human	alpha chain;; beta chain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_46_32904_s_85	10551855	A mAb against an alpha spectrin, with specificity for mammalian nonerythroid alpha spectrin (Chemicon), bound to the 230-kDa protein from HeLa chromatin-associated protein extracts (Fig.  1,  lane 1); binding of this mAb to human erythroid spectrin (alpha and beta chains) (Fig.  1,  lane 2) was used as a control.	bind
50374	4	10792	6	10	NULL	0	NULL	mAb against alpha spectrin	NULL		is specific to	NULL				nonerythroid alpha spectrin	NULL	mammalian			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_46_32904_s_85	10551855	A mAb against an alpha spectrin, with specificity for mammalian nonerythroid alpha spectrin (Chemicon), bound to the 230-kDa protein from HeLa chromatin-associated protein extracts (Fig.  1,  lane 1); binding of this mAb to human erythroid spectrin (alpha and beta chains) (Fig.  1,  lane 2) was used as a control.	bind
49711	1	10793	5	13	NULL	NULL	NULL	Fn	GP		bind			HBD		M. tuberculosis	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1287_s_161	11854212	A MAb specific to the HBD of Fn, but not to the CBD or GBD of Fn, decreased binding of Fn to  M. tuberculosis, suggesting that the HBD is the site on the Fn molecule responsible for Fn binding to  M. tuberculosis.	bind
47368	1	10793	6	NULL	NULL	0	NULL	Fn	NULL		bind	NULL		HBD		M. tuberculosis	NULL				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1287_s_161	11854212	A MAb specific to the HBD of Fn, but not to the CBD or GBD of Fn, decreased binding of Fn to  M. tuberculosis, suggesting that the HBD is the site on the Fn molecule responsible for Fn binding to  M. tuberculosis.	bind
49712	2	10795	5	13	NULL	NULL	NULL	MAGP-1	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_22_23045_s_233	15044481	A MAGP-1-binding site in exon 1 would be compatible with the studies of Jensen  et al. ( ), who showed positive MAGP-1 binding to a fibrillin-1 fragment encoding exons 1 - 11 but negative binding to fragments spanning this region but lacking exons 1 - 3.	bind
49713	3	10795	5	13	NULL	NULL	NULL	MAGP-1	GP		does not bind					fibrillin-1 fragment	GP	lacking		exons 1 - 3	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_22_23045_s_233	15044481	A MAGP-1-binding site in exon 1 would be compatible with the studies of Jensen  et al. ( ), who showed positive MAGP-1 binding to a fibrillin-1 fragment encoding exons 1 - 11 but negative binding to fragments spanning this region but lacking exons 1 - 3.	bind
50375	1	10795	5	13	NULL	NULL	NULL	 fibrillin-1 fragment 	GP		encode									exons 1-11	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_22_23045_s_233	15044481	A MAGP-1-binding site in exon 1 would be compatible with the studies of Jensen  et al. ( ), who showed positive MAGP-1 binding to a fibrillin-1 fragment encoding exons 1 - 11 but negative binding to fragments spanning this region but lacking exons 1 - 3.	bind
47219	1	10795	6	10	NULL	0	NULL	fibrillin-1 fragment	NULL		encodes	NULL					NULL			exons 1-11	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_22_23045_s_233	15044481	A MAGP-1-binding site in exon 1 would be compatible with the studies of Jensen  et al. ( ), who showed positive MAGP-1 binding to a fibrillin-1 fragment encoding exons 1 - 11 but negative binding to fragments spanning this region but lacking exons 1 - 3.	bind
47221	2	10795	6	NULL	NULL	0	NULL	MAGP-1 	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_22_23045_s_233	15044481	A MAGP-1-binding site in exon 1 would be compatible with the studies of Jensen  et al. ( ), who showed positive MAGP-1 binding to a fibrillin-1 fragment encoding exons 1 - 11 but negative binding to fragments spanning this region but lacking exons 1 - 3.	bind
47226	3	10795	6	NULL	NULL	0	NULL	MAGP-1	NULL		does not bind	NULL				fibrillin-1 fragment 	NULL	lacking		exons 1-3	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_22_23045_s_233	15044481	A MAGP-1-binding site in exon 1 would be compatible with the studies of Jensen  et al. ( ), who showed positive MAGP-1 binding to a fibrillin-1 fragment encoding exons 1 - 11 but negative binding to fragments spanning this region but lacking exons 1 - 3.	bind
49714	1	10796	5	13	NULL	NULL	NULL	PCNA	GP		bind					RF-C	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_3_1769_s_203	8999859	A main goal of this work was to begin characterizing the molecular interactions between RF-C and PCNA by first determining the region within PCNA that is bound by RF-C.	bind
47231	1	10796	6	NULL	NULL	0	NULL	PCNA	NULL		bind	NULL				RF-C	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_3_1769_s_203	8999859	A main goal of this work was to begin characterizing the molecular interactions between RF-C and PCNA by first determining the region within PCNA that is bound by RF-C.	bind
49715	1	10797	5	13	NULL	NULL	NULL	zinc finger protein	GP	maize	bind					zein gene	GP			prolamin box in promoter	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_1_28_s_291	10640273	A maize zinc finger protein binds the prolamin box in zein gene promoters and interacts with basic leucine zipper transcriptional activator Opaque2.	bind
49716	2	10797	5	13	NULL	NULL	NULL	zinc finger protein	GP	maize	interacts with					Opaque2	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_1_28_s_291	10640273	A maize zinc finger protein binds the prolamin box in zein gene promoters and interacts with basic leucine zipper transcriptional activator Opaque2.	bind
49717	3	10797	5	13	NULL	NULL	NULL	Opaque2	GP		is a type of					basic leucine zipper transcriptional activator	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_1_28_s_291	10640273	A maize zinc finger protein binds the prolamin box in zein gene promoters and interacts with basic leucine zipper transcriptional activator Opaque2.	bind
47237	1	10797	6	10	NULL	0	NULL	zinc finger protein	NULL	maize	bind	NULL				zein gene	NULL			prolamin box of promoter	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_1_28_s_291	10640273	A maize zinc finger protein binds the prolamin box in zein gene promoters and interacts with basic leucine zipper transcriptional activator Opaque2.	bind
47238	2	10797	6	NULL	NULL	0	NULL	zinc finger protein	NULL	maize	interacts with	NULL				Opaque2	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_14_1_28_s_291	10640273	A maize zinc finger protein binds the prolamin box in zein gene promoters and interacts with basic leucine zipper transcriptional activator Opaque2.	bind
47240	3	10797	6	NULL	NULL	0	NULL	opaque 2	NULL		is a type of	NULL				basic leucine zipper transcriptional activator	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_14_1_28_s_291	10640273	A maize zinc finger protein binds the prolamin box in zein gene promoters and interacts with basic leucine zipper transcriptional activator Opaque2.	bind
49718	1	10800	5	13	NULL	NULL	NULL	HP1	GP		is					heterochromatin protein 1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_112_5_599_s_31	12628181	A major advance came from the discovery that mammalian heterochromatin protein 1 (HP1) binds methylated histone H3 tails  (Bannister et al., 2001  ).	bind
49719	2	10800	5	13	NULL	NULL	NULL	HP1	GP	mammalian	bind					histone H3 tails	GP	methylated			NULL		NULL	NULL	NULL	NULL	gw60_cell_112_5_599_s_31	12628181	A major advance came from the discovery that mammalian heterochromatin protein 1 (HP1) binds methylated histone H3 tails  (Bannister et al., 2001  ).	bind
47243	1	10800	6	NULL	NULL	0	NULL	HP1	NULL	mammalian	bind	NULL				Histone H3 tail	NULL	methylated			NULL		0	NULL	NULL	NULL	gw60_cell_112_5_599_s_31	12628181	A major advance came from the discovery that mammalian heterochromatin protein 1 (HP1) binds methylated histone H3 tails  (Bannister et al., 2001  ).	bind
47245	2	10800	6	NULL	NULL	0	NULL	HP1	NULL		is	NULL				heterochromatin protein 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_112_5_599_s_31	12628181	A major advance came from the discovery that mammalian heterochromatin protein 1 (HP1) binds methylated histone H3 tails  (Bannister et al., 2001  ).	bind
49720	1	10801	5	13	NULL	NULL	NULL	CBF3	GP		is a type of					multi subunit complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_30_0_7_s_203	8982447	A major advance in centromere research was the biochemical identification of CBF3,  a multi subunit complex that specifically binds CDEIII DNA ( 63).	bind
49721	2	10801	5	13	NULL	NULL	NULL	CBF3	GP		bind		specifically			CDEIII DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_30_0_7_s_203	8982447	A major advance in centromere research was the biochemical identification of CBF3,  a multi subunit complex that specifically binds CDEIII DNA ( 63).	bind
37944	1	10801	6	10	NULL	0	NULL	CBF3	NULL		is a type of	NULL				multi subunit complex	NULL				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_30_0_7_s_203	8982447	A major advance in centromere research was the biochemical identification of CBF3,  a multi subunit complex that specifically binds CDEIII DNA ( 63).	bind
37945	2	10801	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL	specifically			CDEIII DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevgenet_30_0_7_s_203	8982447	A major advance in centromere research was the biochemical identification of CBF3,  a multi subunit complex that specifically binds CDEIII DNA ( 63).	bind
49722	1	10802	5	13	NULL	NULL	NULL	CaBP1	GP		bind					alpha11.2	GP		NT		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_33_29612_s_216	15980432	A major assumption is that CaBP1 is constitutively associated with the channel via the NT of alpha11.2, which is based on our findings that CaBP1 binds to the NT in the presence and absence of Ca2+ ( Fig. 3).	bind
49723	2	10802	5	13	NULL	NULL	NULL	CaBP1	GP		is associated with		may;;constitutively			channel	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_33_29612_s_216	15980432	A major assumption is that CaBP1 is constitutively associated with the channel via the NT of alpha11.2, which is based on our findings that CaBP1 binds to the NT in the presence and absence of Ca2+ ( Fig. 3).	bind
49724	3	10802	5	13	NULL	NULL	NULL	statement 2	Process		via					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_33_29612_s_216	15980432	A major assumption is that CaBP1 is constitutively associated with the channel via the NT of alpha11.2, which is based on our findings that CaBP1 binds to the NT in the presence and absence of Ca2+ ( Fig. 3).	bind
37946	1	10802	6	10	NULL	0	NULL	CaBP1	NULL		bind	NULL				alpha11.2	NULL		NT		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_33_29612_s_216	15980432	A major assumption is that CaBP1 is constitutively associated with the channel via the NT of alpha11.2, which is based on our findings that CaBP1 binds to the NT in the presence and absence of Ca2+ ( Fig. 3).	bind
40507	2	10802	6	NULL	NULL	0	NULL	CaBP1	NULL		associated with	NULL	may be;; constitutively			channel	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_33_29612_s_216	15980432	A major assumption is that CaBP1 is constitutively associated with the channel via the NT of alpha11.2, which is based on our findings that CaBP1 binds to the NT in the presence and absence of Ca2+ ( Fig. 3).	bind
40508	3	10802	6	NULL	NULL	0	NULL	statement 2	NULL		is because of	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_33_29612_s_216	15980432	A major assumption is that CaBP1 is constitutively associated with the channel via the NT of alpha11.2, which is based on our findings that CaBP1 binds to the NT in the presence and absence of Ca2+ ( Fig. 3).	bind
49725	1	10804	5	13	NULL	NULL	NULL	RhoGDI	GP		associate with		directly			Rho proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_18_12445_s_158	16517596	A major class of proteins that directly associates with Rho proteins in cells is termed RhoGDI, and its binding to Rho GTPases is via an interaction that is known to be prenylation-dependent ( ).	bind
49726	2	10804	5	13	NULL	NULL	NULL	RhoGDI	GP		bind					Rho GTPases	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_18_12445_s_158	16517596	A major class of proteins that directly associates with Rho proteins in cells is termed RhoGDI, and its binding to Rho GTPases is via an interaction that is known to be prenylation-dependent ( ).	bind
49727	3	10804	5	13	NULL	NULL	NULL	statement 2	Process		is dependent on					prenylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_18_12445_s_158	16517596	A major class of proteins that directly associates with Rho proteins in cells is termed RhoGDI, and its binding to Rho GTPases is via an interaction that is known to be prenylation-dependent ( ).	bind
40509	1	10804	6	NULL	NULL	0	NULL	RhoGDI	NULL		bind	NULL				RhoGTPase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_18_12445_s_158	16517596	A major class of proteins that directly associates with Rho proteins in cells is termed RhoGDI, and its binding to Rho GTPases is via an interaction that is known to be prenylation-dependent ( ).	bind
40510	2	10804	6	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				prenylation	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_18_12445_s_158	16517596	A major class of proteins that directly associates with Rho proteins in cells is termed RhoGDI, and its binding to Rho GTPases is via an interaction that is known to be prenylation-dependent ( ).	bind
50376	3	10804	6	10	NULL	0	NULL	RhoGDI	NULL		associate with	NULL	directly			Rho protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_18_12445_s_158	16517596	A major class of proteins that directly associates with Rho proteins in cells is termed RhoGDI, and its binding to Rho GTPases is via an interaction that is known to be prenylation-dependent ( ).	bind
49728	1	10805	5	13	NULL	NULL	NULL	CmtR	GP		bind					35-bp DNA fragment	NucleicAcid			degenerate 10 - 5-10 hyphenated-inverted repeat	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44560_s_99	12939264	A major complex was detected with P2 and P3 but not with P4 ( Fig. 1 D), confirming CmtR binding to sequences contained within a 35-bp DNA fragment that includes a degenerate 10 - 5-10 hyphenated-inverted repeat ( Fig. 1 E).	bind
40193	1	10805	6	NULL	NULL	0	NULL	CmtR	NULL		bind	NULL				35-bp DNA	NULL			hyphenated-inverted repeat	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_45_44560_s_99	12939264	A major complex was detected with P2 and P3 but not with P4 ( Fig. 1 D), confirming CmtR binding to sequences contained within a 35-bp DNA fragment that includes a degenerate 10 - 5-10 hyphenated-inverted repeat ( Fig. 1 E).	bind
50792	1	10806	5	13	NULL	NULL	NULL	Ras	GP		induce					ARF	GP				NULL		NULL	NULL	NULL	NULL	gw60_cancercell_1_1_19_s_63	12086884	A major component of the differential that couples the oppositely spinning wheels of proliferation and growth suppression is the ARF/Mdm-2/p53 tumor suppressor pathway ( Sherr, 2001  ); Ras, E1A, Myc, and E2F all induce ARF, an alternate product of the  INK4a locus which then binds and inactivates Mdm-2, a key part of the ubiquitin ligase that keeps p53 at bay ( Lowe, 1999  ).	bind
50793	2	10806	5	13	NULL	NULL	NULL	E1A	GP		induce					ARF	GP				NULL		NULL	NULL	NULL	NULL	gw60_cancercell_1_1_19_s_63	12086884	A major component of the differential that couples the oppositely spinning wheels of proliferation and growth suppression is the ARF/Mdm-2/p53 tumor suppressor pathway ( Sherr, 2001  ); Ras, E1A, Myc, and E2F all induce ARF, an alternate product of the  INK4a locus which then binds and inactivates Mdm-2, a key part of the ubiquitin ligase that keeps p53 at bay ( Lowe, 1999  ).	bind
50794	3	10806	5	13	NULL	NULL	NULL	Myc	GP		induce					ARF	GP				NULL		NULL	NULL	NULL	NULL	gw60_cancercell_1_1_19_s_63	12086884	A major component of the differential that couples the oppositely spinning wheels of proliferation and growth suppression is the ARF/Mdm-2/p53 tumor suppressor pathway ( Sherr, 2001  ); Ras, E1A, Myc, and E2F all induce ARF, an alternate product of the  INK4a locus which then binds and inactivates Mdm-2, a key part of the ubiquitin ligase that keeps p53 at bay ( Lowe, 1999  ).	bind
50795	4	10806	5	13	NULL	NULL	NULL	E2F 	GP		induce					ARF	GP				NULL		NULL	NULL	NULL	NULL	gw60_cancercell_1_1_19_s_63	12086884	A major component of the differential that couples the oppositely spinning wheels of proliferation and growth suppression is the ARF/Mdm-2/p53 tumor suppressor pathway ( Sherr, 2001  ); Ras, E1A, Myc, and E2F all induce ARF, an alternate product of the  INK4a locus which then binds and inactivates Mdm-2, a key part of the ubiquitin ligase that keeps p53 at bay ( Lowe, 1999  ).	bind
50796	5	10806	5	13	NULL	NULL	NULL	ARF	GP		is an alternate product of					INK4a locus	GP				NULL		NULL	NULL	NULL	NULL	gw60_cancercell_1_1_19_s_63	12086884	A major component of the differential that couples the oppositely spinning wheels of proliferation and growth suppression is the ARF/Mdm-2/p53 tumor suppressor pathway ( Sherr, 2001  ); Ras, E1A, Myc, and E2F all induce ARF, an alternate product of the  INK4a locus which then binds and inactivates Mdm-2, a key part of the ubiquitin ligase that keeps p53 at bay ( Lowe, 1999  ).	bind
50797	6	10806	5	13	NULL	NULL	NULL	ARF	GP	induced	bind					Mdm-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cancercell_1_1_19_s_63	12086884	A major component of the differential that couples the oppositely spinning wheels of proliferation and growth suppression is the ARF/Mdm-2/p53 tumor suppressor pathway ( Sherr, 2001  ); Ras, E1A, Myc, and E2F all induce ARF, an alternate product of the  INK4a locus which then binds and inactivates Mdm-2, a key part of the ubiquitin ligase that keeps p53 at bay ( Lowe, 1999  ).	bind
50798	7	10806	5	13	NULL	NULL	NULL	statement 6	Process		inactivates					Mdm-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cancercell_1_1_19_s_63	12086884	A major component of the differential that couples the oppositely spinning wheels of proliferation and growth suppression is the ARF/Mdm-2/p53 tumor suppressor pathway ( Sherr, 2001  ); Ras, E1A, Myc, and E2F all induce ARF, an alternate product of the  INK4a locus which then binds and inactivates Mdm-2, a key part of the ubiquitin ligase that keeps p53 at bay ( Lowe, 1999  ).	bind
50799	8	10806	5	13	NULL	NULL	NULL	Mdm-2	GP		is a part of					ubiquitin ligase	GP				NULL		NULL	NULL	NULL	NULL	gw60_cancercell_1_1_19_s_63	12086884	A major component of the differential that couples the oppositely spinning wheels of proliferation and growth suppression is the ARF/Mdm-2/p53 tumor suppressor pathway ( Sherr, 2001  ); Ras, E1A, Myc, and E2F all induce ARF, an alternate product of the  INK4a locus which then binds and inactivates Mdm-2, a key part of the ubiquitin ligase that keeps p53 at bay ( Lowe, 1999  ).	bind
40511	1	10806	6	NULL	NULL	0	NULL	Ras	NULL		induce	NULL				ARF	NULL				NULL		0	NULL	NULL	NULL	gw60_cancercell_1_1_19_s_63	12086884	A major component of the differential that couples the oppositely spinning wheels of proliferation and growth suppression is the ARF/Mdm-2/p53 tumor suppressor pathway ( Sherr, 2001  ); Ras, E1A, Myc, and E2F all induce ARF, an alternate product of the  INK4a locus which then binds and inactivates Mdm-2, a key part of the ubiquitin ligase that keeps p53 at bay ( Lowe, 1999  ).	bind
40512	2	10806	6	NULL	NULL	0	NULL	E1A	NULL		induce	NULL				ARF	NULL				NULL		0	NULL	NULL	NULL	gw60_cancercell_1_1_19_s_63	12086884	A major component of the differential that couples the oppositely spinning wheels of proliferation and growth suppression is the ARF/Mdm-2/p53 tumor suppressor pathway ( Sherr, 2001  ); Ras, E1A, Myc, and E2F all induce ARF, an alternate product of the  INK4a locus which then binds and inactivates Mdm-2, a key part of the ubiquitin ligase that keeps p53 at bay ( Lowe, 1999  ).	bind
40513	3	10806	6	NULL	NULL	0	NULL	Myc	NULL		induce	NULL				ARF	NULL				NULL		0	NULL	NULL	NULL	gw60_cancercell_1_1_19_s_63	12086884	A major component of the differential that couples the oppositely spinning wheels of proliferation and growth suppression is the ARF/Mdm-2/p53 tumor suppressor pathway ( Sherr, 2001  ); Ras, E1A, Myc, and E2F all induce ARF, an alternate product of the  INK4a locus which then binds and inactivates Mdm-2, a key part of the ubiquitin ligase that keeps p53 at bay ( Lowe, 1999  ).	bind
40514	4	10806	6	NULL	NULL	0	NULL	E2F	NULL		induce	NULL				ARF	NULL				NULL		0	NULL	NULL	NULL	gw60_cancercell_1_1_19_s_63	12086884	A major component of the differential that couples the oppositely spinning wheels of proliferation and growth suppression is the ARF/Mdm-2/p53 tumor suppressor pathway ( Sherr, 2001  ); Ras, E1A, Myc, and E2F all induce ARF, an alternate product of the  INK4a locus which then binds and inactivates Mdm-2, a key part of the ubiquitin ligase that keeps p53 at bay ( Lowe, 1999  ).	bind
40515	5	10806	6	NULL	NULL	0	NULL	ARF	NULL		is an alternate product of	NULL				INK4a locus	NULL				NULL		0	NULL	NULL	NULL	gw60_cancercell_1_1_19_s_63	12086884	A major component of the differential that couples the oppositely spinning wheels of proliferation and growth suppression is the ARF/Mdm-2/p53 tumor suppressor pathway ( Sherr, 2001  ); Ras, E1A, Myc, and E2F all induce ARF, an alternate product of the  INK4a locus which then binds and inactivates Mdm-2, a key part of the ubiquitin ligase that keeps p53 at bay ( Lowe, 1999  ).	bind
40516	6	10806	6	NULL	NULL	0	NULL	ARF	NULL	induced	bind	NULL				Mdm-2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cancercell_1_1_19_s_63	12086884	A major component of the differential that couples the oppositely spinning wheels of proliferation and growth suppression is the ARF/Mdm-2/p53 tumor suppressor pathway ( Sherr, 2001  ); Ras, E1A, Myc, and E2F all induce ARF, an alternate product of the  INK4a locus which then binds and inactivates Mdm-2, a key part of the ubiquitin ligase that keeps p53 at bay ( Lowe, 1999  ).	bind
40517	7	10806	6	10	NULL	0	NULL	statement 6			inactivates					Mdm-2					NULL		NULL	NULL	NULL	NULL	gw60_cancercell_1_1_19_s_63	12086884	A major component of the differential that couples the oppositely spinning wheels of proliferation and growth suppression is the ARF/Mdm-2/p53 tumor suppressor pathway ( Sherr, 2001  ); Ras, E1A, Myc, and E2F all induce ARF, an alternate product of the  INK4a locus which then binds and inactivates Mdm-2, a key part of the ubiquitin ligase that keeps p53 at bay ( Lowe, 1999  ).	bind
40518	8	10806	6	NULL	NULL	0	NULL	Mdm-2	NULL		is a key part of	NULL				ubiquitin ligase	NULL				NULL		0	NULL	NULL	NULL	gw60_cancercell_1_1_19_s_63	12086884	A major component of the differential that couples the oppositely spinning wheels of proliferation and growth suppression is the ARF/Mdm-2/p53 tumor suppressor pathway ( Sherr, 2001  ); Ras, E1A, Myc, and E2F all induce ARF, an alternate product of the  INK4a locus which then binds and inactivates Mdm-2, a key part of the ubiquitin ligase that keeps p53 at bay ( Lowe, 1999  ).	bind
49729	1	10807	5	13	NULL	NULL	NULL	HDL	GP		bind					SR-BI	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochemistry_39_1_10625497_s_3	10625497	A major component of the enhanced FC flux appears to occur independently  of HDL binding to SR-BI and may be due to changes in membrane lipid domains  resulting from SR-BI expression (1).	bind
49730	2	10807	5	13	NULL	NULL	NULL	FC flux	Process	enhanced	is independent of					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochemistry_39_1_10625497_s_3	10625497	A major component of the enhanced FC flux appears to occur independently  of HDL binding to SR-BI and may be due to changes in membrane lipid domains  resulting from SR-BI expression (1).	bind
49731	3	10807	5	13	NULL	NULL	NULL	SR-BI	GP	expression of	results in					membrane lipid domains	GP	chnages in			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochemistry_39_1_10625497_s_3	10625497	A major component of the enhanced FC flux appears to occur independently  of HDL binding to SR-BI and may be due to changes in membrane lipid domains  resulting from SR-BI expression (1).	bind
49732	4	10807	5	13	NULL	NULL	NULL	FC flux	Process	enhanced	occurs due to		may			statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochemistry_39_1_10625497_s_3	10625497	A major component of the enhanced FC flux appears to occur independently  of HDL binding to SR-BI and may be due to changes in membrane lipid domains  resulting from SR-BI expression (1).	bind
40259	1	10807	6	NULL	NULL	0	NULL	HDL	NULL		bind	NULL				SR-BI	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biochemistry_39_1_10625497_s_3	10625497	A major component of the enhanced FC flux appears to occur independently  of HDL binding to SR-BI and may be due to changes in membrane lipid domains  resulting from SR-BI expression (1).	bind
40266	2	10807	6	NULL	NULL	0	NULL	SR-BI	NULL	expression of	results in	NULL				membrane lipid domains	NULL	changes in			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biochemistry_39_1_10625497_s_3	10625497	A major component of the enhanced FC flux appears to occur independently  of HDL binding to SR-BI and may be due to changes in membrane lipid domains  resulting from SR-BI expression (1).	bind
40267	3	10807	6	10	NULL	0	NULL	FC flux	NULL	enhanced	is due to	NULL	may			statement 2	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochemistry_39_1_10625497_s_3	10625497	A major component of the enhanced FC flux appears to occur independently  of HDL binding to SR-BI and may be due to changes in membrane lipid domains  resulting from SR-BI expression (1).	bind
40268	4	10807	6	NULL	NULL	0	NULL	FC flux	NULL		is independent of	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biochemistry_39_1_10625497_s_3	10625497	A major component of the enhanced FC flux appears to occur independently  of HDL binding to SR-BI and may be due to changes in membrane lipid domains  resulting from SR-BI expression (1).	bind
49733	1	10808	5	13	NULL	NULL	NULL	MSH2	GP		is a component of		major			GT binding complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_46_36256_s_92	10954713	A major component of the GT binding complex is MSH2.	bind
40269	1	10808	6	10	NULL	0	NULL	MSH2			is a component of		major			GT binding complex					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_46_36256_s_92	10954713	A major component of the GT binding complex is MSH2.	bind
49734	1	10809	5	13	NULL	NULL	NULL	GDP	Chemical		bind					p21ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_structure_4_4_475_s_312	8740369	A major conceptional constraint on any activation model is imposed by the observation that the GEF reduces the binding affinity of GDP and GTP to p21ras by a similar amount.	bind
49735	2	10809	5	13	NULL	NULL	NULL	GTP	Chemical		bind					p21ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_structure_4_4_475_s_312	8740369	A major conceptional constraint on any activation model is imposed by the observation that the GEF reduces the binding affinity of GDP and GTP to p21ras by a similar amount.	bind
49736	3	10809	5	13	NULL	NULL	NULL	GEF	GP		reduces					statement 1	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_structure_4_4_475_s_312	8740369	A major conceptional constraint on any activation model is imposed by the observation that the GEF reduces the binding affinity of GDP and GTP to p21ras by a similar amount.	bind
49737	4	10809	5	13	NULL	NULL	NULL	GEF	GP		reduces					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_structure_4_4_475_s_312	8740369	A major conceptional constraint on any activation model is imposed by the observation that the GEF reduces the binding affinity of GDP and GTP to p21ras by a similar amount.	bind
40270	1	10809	6	NULL	NULL	0	NULL	GDP	NULL		bind	NULL				p21ras	NULL				NULL		0	NULL	NULL	NULL	gw60_structure_4_4_475_s_312	8740369	A major conceptional constraint on any activation model is imposed by the observation that the GEF reduces the binding affinity of GDP and GTP to p21ras by a similar amount.	bind
40271	2	10809	6	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				p21ras	NULL				NULL		0	NULL	NULL	NULL	gw60_structure_4_4_475_s_312	8740369	A major conceptional constraint on any activation model is imposed by the observation that the GEF reduces the binding affinity of GDP and GTP to p21ras by a similar amount.	bind
40272	3	10809	6	NULL	NULL	0	NULL	GEF	NULL		reduces	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_structure_4_4_475_s_312	8740369	A major conceptional constraint on any activation model is imposed by the observation that the GEF reduces the binding affinity of GDP and GTP to p21ras by a similar amount.	bind
40273	4	10809	6	NULL	NULL	0	NULL	GEF	NULL		reduces	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_structure_4_4_475_s_312	8740369	A major conceptional constraint on any activation model is imposed by the observation that the GEF reduces the binding affinity of GDP and GTP to p21ras by a similar amount.	bind
49765	1	10810	5	13	NULL	NULL	NULL	DnaA	NucleicAcid		bind									DnaA boxes	NULL	bacterial hosts	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18454_s_30	10749858	A major difference between replication initiation in plasmid RK2 (as well as most of the DnaA-dependent plasmids studied so far) and that of chromosomal origins, is the fact that in most cases this plasmid requires, in addition to the binding of DnaA to DnaA boxes in most bacterial hosts, the binding of a plasmid encoded replication initiation protein to the origin for the formation of an open complex ( 16).	bind
49767	2	10810	5	13	NULL	NULL	NULL	replication initiation protein	NucleicAcid		bind					origin	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18454_s_30	10749858	A major difference between replication initiation in plasmid RK2 (as well as most of the DnaA-dependent plasmids studied so far) and that of chromosomal origins, is the fact that in most cases this plasmid requires, in addition to the binding of DnaA to DnaA boxes in most bacterial hosts, the binding of a plasmid encoded replication initiation protein to the origin for the formation of an open complex ( 16).	bind
49768	3	10810	5	13	NULL	NULL	NULL	statement 2	Process		is required for					open complex	GP	formation of			NULL	plasmid RK2	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18454_s_30	10749858	A major difference between replication initiation in plasmid RK2 (as well as most of the DnaA-dependent plasmids studied so far) and that of chromosomal origins, is the fact that in most cases this plasmid requires, in addition to the binding of DnaA to DnaA boxes in most bacterial hosts, the binding of a plasmid encoded replication initiation protein to the origin for the formation of an open complex ( 16).	bind
49769	4	10810	5	13	NULL	NULL	NULL	statement 1	Process		is required for					open complex	GP	formation of			NULL	plasmid RK2	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18454_s_30	10749858	A major difference between replication initiation in plasmid RK2 (as well as most of the DnaA-dependent plasmids studied so far) and that of chromosomal origins, is the fact that in most cases this plasmid requires, in addition to the binding of DnaA to DnaA boxes in most bacterial hosts, the binding of a plasmid encoded replication initiation protein to the origin for the formation of an open complex ( 16).	bind
40519	1	10810	6	NULL	NULL	0	NULL	DnaA	NULL		bind	NULL					NULL			DnaA box	NULL	bacterial host	0	NULL	NULL	NULL	gw60_jbiolchem_275_24_18454_s_30	10749858	A major difference between replication initiation in plasmid RK2 (as well as most of the DnaA-dependent plasmids studied so far) and that of chromosomal origins, is the fact that in most cases this plasmid requires, in addition to the binding of DnaA to DnaA boxes in most bacterial hosts, the binding of a plasmid encoded replication initiation protein to the origin for the formation of an open complex ( 16).	bind
40520	2	10810	6	NULL	NULL	0	NULL	replication initiation protein	NULL		bind	NULL				origin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_24_18454_s_30	10749858	A major difference between replication initiation in plasmid RK2 (as well as most of the DnaA-dependent plasmids studied so far) and that of chromosomal origins, is the fact that in most cases this plasmid requires, in addition to the binding of DnaA to DnaA boxes in most bacterial hosts, the binding of a plasmid encoded replication initiation protein to the origin for the formation of an open complex ( 16).	bind
40521	3	10810	6	10	NULL	0	NULL	statement 2			is required for					open complex		formation of			NULL	plasmid RK2	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18454_s_30	10749858	A major difference between replication initiation in plasmid RK2 (as well as most of the DnaA-dependent plasmids studied so far) and that of chromosomal origins, is the fact that in most cases this plasmid requires, in addition to the binding of DnaA to DnaA boxes in most bacterial hosts, the binding of a plasmid encoded replication initiation protein to the origin for the formation of an open complex ( 16).	bind
50377	4	10810	6	10	NULL	0	NULL	statement 1			is required for					open complex		formation of			NULL	plasmid RK2	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_24_18454_s_30	10749858	A major difference between replication initiation in plasmid RK2 (as well as most of the DnaA-dependent plasmids studied so far) and that of chromosomal origins, is the fact that in most cases this plasmid requires, in addition to the binding of DnaA to DnaA boxes in most bacterial hosts, the binding of a plasmid encoded replication initiation protein to the origin for the formation of an open complex ( 16).	bind
49770	1	10811	5	13	NULL	NULL	NULL	Ars/A1 BCR	GP		bind					autoantigen	GP	natural			NULL		NULL	NULL	NULL	NULL	gw60_immunity_14_1_33_s_205	11163228	A major difference between the Ars/A1 mouse and the HEL/anti-HEL model is the affinity of the anergy-inducing autoantigen: while the affinity of the receptor for HEL is  2 nanomolar ( Goodnow et al. 1988  ), several lines of evidence suggest that the Ars/A1 BCR binds its natural autoantigen with an affinity that is >10,000-fold lower.	bind
40274	1	10811	6	NULL	NULL	0	NULL	Ars/A1 BCR	NULL		bind	NULL				autoantigen	NULL	natural			NULL		0	NULL	NULL	NULL	gw60_immunity_14_1_33_s_205	11163228	A major difference between the Ars/A1 mouse and the HEL/anti-HEL model is the affinity of the anergy-inducing autoantigen: while the affinity of the receptor for HEL is  2 nanomolar ( Goodnow et al. 1988  ), several lines of evidence suggest that the Ars/A1 BCR binds its natural autoantigen with an affinity that is >10,000-fold lower.	bind
49771	1	10812	5	13	NULL	NULL	NULL	LC8	GP		interacts with					LC8 targets	GP		glutamine		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_23_21981_s_157	15701632	A major difference between the binding groove of LC8 and the putative TcTex-1 groove is at the site on LC8 that interacts with the invariant glutamine in LC8 targets ( Fig. 3,  B and  C).	bind
40522	1	10812	6	10	NULL	0	NULL	LC8			interacts with					LC8 targets			glutamine		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_23_21981_s_157	15701632	A major difference between the binding groove of LC8 and the putative TcTex-1 groove is at the site on LC8 that interacts with the invariant glutamine in LC8 targets ( Fig. 3,  B and  C).	bind
49772	1	10814	5	13	NULL	NULL	NULL	RA	Chemical		bind			carboxylate group		CRABP-II	GP	positively charged	 amino acid residues		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_9_4518_s_174	7876220	A major factor in the  binding of RA to CRABP-II involves the electrostatic interactions  between the carboxylate group of all- trans-RA and positively  charge amino acid residues in the protein( 9 ) .	bind
40285	1	10814	6	NULL	NULL	0	NULL	RA	NULL		bind	NULL		carboxylate group 		CRABP-II	NULL	positively charged	amino acids		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_9_4518_s_174	7876220	A major factor in the  binding of RA to CRABP-II involves the electrostatic interactions  between the carboxylate group of all- trans-RA and positively  charge amino acid residues in the protein( 9 ) .	bind
49773	1	10815	5	13	NULL	NULL	NULL	THP-1 macrophages	Cell		is stimulated by					LIGHT	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_14_2121_s_200	16186421	A major finding in the present study was the noticeable upregulation of SR-A in LIGHT-stimulated THP-1 macrophages, as shown at both the mRNA and protein level, as well as the increased binding of acLDL to this scavenger receptor.	bind
49774	2	10815	5	13	NULL	NULL	NULL	SR-A	GP		is upregulated in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_14_2121_s_200	16186421	A major finding in the present study was the noticeable upregulation of SR-A in LIGHT-stimulated THP-1 macrophages, as shown at both the mRNA and protein level, as well as the increased binding of acLDL to this scavenger receptor.	bind
49775	3	10815	5	13	NULL	NULL	NULL	acLDL	GP		bind					SR-A	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_14_2121_s_200	16186421	A major finding in the present study was the noticeable upregulation of SR-A in LIGHT-stimulated THP-1 macrophages, as shown at both the mRNA and protein level, as well as the increased binding of acLDL to this scavenger receptor.	bind
49776	4	10815	5	13	NULL	NULL	NULL	SR-A	GP		is a type of					scavenger receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_14_2121_s_200	16186421	A major finding in the present study was the noticeable upregulation of SR-A in LIGHT-stimulated THP-1 macrophages, as shown at both the mRNA and protein level, as well as the increased binding of acLDL to this scavenger receptor.	bind
40289	1	10815	6	NULL	NULL	0	NULL	acLDL	NULL		bind	NULL				SR-A	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_14_2121_s_200	16186421	A major finding in the present study was the noticeable upregulation of SR-A in LIGHT-stimulated THP-1 macrophages, as shown at both the mRNA and protein level, as well as the increased binding of acLDL to this scavenger receptor.	bind
40290	2	10815	6	10	NULL	0	NULL	LIGHT	NULL		stimulate	NULL				THP-1 macrophages	NULL				NULL		NULL	NULL	NULL	NULL	gw70_circulation_112_14_2121_s_200	16186421	A major finding in the present study was the noticeable upregulation of SR-A in LIGHT-stimulated THP-1 macrophages, as shown at both the mRNA and protein level, as well as the increased binding of acLDL to this scavenger receptor.	bind
40291	3	10815	6	NULL	NULL	0	NULL	SR-A	NULL		is a type of	NULL				scavenger receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_112_14_2121_s_200	16186421	A major finding in the present study was the noticeable upregulation of SR-A in LIGHT-stimulated THP-1 macrophages, as shown at both the mRNA and protein level, as well as the increased binding of acLDL to this scavenger receptor.	bind
50378	4	10815	6	10	NULL	0	NULL	SR-A	NULL		is upregulated in	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_circulation_112_14_2121_s_200	16186421	A major finding in the present study was the noticeable upregulation of SR-A in LIGHT-stimulated THP-1 macrophages, as shown at both the mRNA and protein level, as well as the increased binding of acLDL to this scavenger receptor.	bind
49777	1	10816	5	13	NULL	NULL	NULL	mechanical stretch	ResearchActivity		activates					p38 MAPK	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_23_24852_s_292	15051723	A major finding of the present study was that mechanical stretch activated p38 MAPK and that the activation of the kinase was necessary for wall stretch-induced GATA-4 binding to BNP promoter both in the left ventricle and in the atria.	bind
49778	2	10816	5	13	NULL	NULL	NULL	GATA-4	GP		is induced by					wall stretch	ResearchActivity				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_23_24852_s_292	15051723	A major finding of the present study was that mechanical stretch activated p38 MAPK and that the activation of the kinase was necessary for wall stretch-induced GATA-4 binding to BNP promoter both in the left ventricle and in the atria.	bind
49779	3	10816	5	13	NULL	NULL	NULL	statement 2	GP		bind					BNP	NucleicAcid			promoter	NULL	left ventricle	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_23_24852_s_292	15051723	A major finding of the present study was that mechanical stretch activated p38 MAPK and that the activation of the kinase was necessary for wall stretch-induced GATA-4 binding to BNP promoter both in the left ventricle and in the atria.	bind
49780	4	10816	5	13	NULL	NULL	NULL	statement 1	Process		is necessary for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_23_24852_s_292	15051723	A major finding of the present study was that mechanical stretch activated p38 MAPK and that the activation of the kinase was necessary for wall stretch-induced GATA-4 binding to BNP promoter both in the left ventricle and in the atria.	bind
50379	5	10816	5	13	NULL	NULL	NULL	statement 2	GP		bind					BNP	NucleicAcid			promoter	NULL	atria	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_23_24852_s_292	15051723	A major finding of the present study was that mechanical stretch activated p38 MAPK and that the activation of the kinase was necessary for wall stretch-induced GATA-4 binding to BNP promoter both in the left ventricle and in the atria.	bind
50380	6	10816	5	13	NULL	NULL	NULL	statement 1	Process		is necessary for					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_23_24852_s_292	15051723	A major finding of the present study was that mechanical stretch activated p38 MAPK and that the activation of the kinase was necessary for wall stretch-induced GATA-4 binding to BNP promoter both in the left ventricle and in the atria.	bind
40292	1	10816	6	NULL	NULL	0	NULL	GATA-4	NULL		bind	NULL				BNP	NULL			promoter	NULL	left ventricle	0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24852_s_292	15051723	A major finding of the present study was that mechanical stretch activated p38 MAPK and that the activation of the kinase was necessary for wall stretch-induced GATA-4 binding to BNP promoter both in the left ventricle and in the atria.	bind
40294	2	10816	6	NULL	NULL	0	NULL	mechanical stretch	NULL		activates	NULL				p38 MAPK	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24852_s_292	15051723	A major finding of the present study was that mechanical stretch activated p38 MAPK and that the activation of the kinase was necessary for wall stretch-induced GATA-4 binding to BNP promoter both in the left ventricle and in the atria.	bind
40295	3	10816	6	NULL	NULL	0	NULL	GATA-4	NULL		bind	NULL				BNP	NULL			promoter	NULL	atria	0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24852_s_292	15051723	A major finding of the present study was that mechanical stretch activated p38 MAPK and that the activation of the kinase was necessary for wall stretch-induced GATA-4 binding to BNP promoter both in the left ventricle and in the atria.	bind
40296	4	10816	6	NULL	NULL	0	NULL	statement 1	NULL		is induced by	NULL				wall stretch	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24852_s_292	15051723	A major finding of the present study was that mechanical stretch activated p38 MAPK and that the activation of the kinase was necessary for wall stretch-induced GATA-4 binding to BNP promoter both in the left ventricle and in the atria.	bind
40297	5	10816	6	NULL	NULL	0	NULL	statement 3	NULL		is induced by	NULL				wall stretch	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24852_s_292	15051723	A major finding of the present study was that mechanical stretch activated p38 MAPK and that the activation of the kinase was necessary for wall stretch-induced GATA-4 binding to BNP promoter both in the left ventricle and in the atria.	bind
40298	6	10816	6	NULL	NULL	0	NULL	statement 2	NULL		is necessary for	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_23_24852_s_292	15051723	A major finding of the present study was that mechanical stretch activated p38 MAPK and that the activation of the kinase was necessary for wall stretch-induced GATA-4 binding to BNP promoter both in the left ventricle and in the atria.	bind
40299	7	10816	6	NULL	NULL	0	NULL	statement 2	NULL		is necessary for	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24852_s_292	15051723	A major finding of the present study was that mechanical stretch activated p38 MAPK and that the activation of the kinase was necessary for wall stretch-induced GATA-4 binding to BNP promoter both in the left ventricle and in the atria.	bind
49781	1	10817	5	13	NULL	NULL	NULL	RanGAP	GP		bind					RanBP2	GP	cytoplasmically oriented			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_645_s_38	10330396	A major fraction of RanGAP is bound to the cytoplasmically oriented nucleoporin RanBP2 due to its modification by the ubiquitin-related modifier SUMO-1 (Matunis  et al., 1996  ; Mahajan et al., 1997  ), and the remainder of  RanGAP is soluble in the cytoplasm.	bind
49782	2	10817	5	13	NULL	NULL	NULL	RanBP2	GP		is a type of					nucleoporin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_645_s_38	10330396	A major fraction of RanGAP is bound to the cytoplasmically oriented nucleoporin RanBP2 due to its modification by the ubiquitin-related modifier SUMO-1 (Matunis  et al., 1996  ; Mahajan et al., 1997  ), and the remainder of  RanGAP is soluble in the cytoplasm.	bind
49783	3	10817	5	13	NULL	NULL	NULL	RanBP2	GP		is modified by					SUMO-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_645_s_38	10330396	A major fraction of RanGAP is bound to the cytoplasmically oriented nucleoporin RanBP2 due to its modification by the ubiquitin-related modifier SUMO-1 (Matunis  et al., 1996  ; Mahajan et al., 1997  ), and the remainder of  RanGAP is soluble in the cytoplasm.	bind
49784	4	10817	5	13	NULL	NULL	NULL	SUMO-1	GP		is a type of					ubiquitin-related modifier	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_645_s_38	10330396	A major fraction of RanGAP is bound to the cytoplasmically oriented nucleoporin RanBP2 due to its modification by the ubiquitin-related modifier SUMO-1 (Matunis  et al., 1996  ; Mahajan et al., 1997  ), and the remainder of  RanGAP is soluble in the cytoplasm.	bind
49785	5	10817	5	13	NULL	NULL	NULL	statement 3	Process		leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_645_s_38	10330396	A major fraction of RanGAP is bound to the cytoplasmically oriented nucleoporin RanBP2 due to its modification by the ubiquitin-related modifier SUMO-1 (Matunis  et al., 1996  ; Mahajan et al., 1997  ), and the remainder of  RanGAP is soluble in the cytoplasm.	bind
49786	6	10817	5	13	NULL	NULL	NULL	RanGAP	GP		is soluble in					cytoplasm	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_645_s_38	10330396	A major fraction of RanGAP is bound to the cytoplasmically oriented nucleoporin RanBP2 due to its modification by the ubiquitin-related modifier SUMO-1 (Matunis  et al., 1996  ; Mahajan et al., 1997  ), and the remainder of  RanGAP is soluble in the cytoplasm.	bind
40528	1	10817	6	NULL	NULL	0	NULL	RanGAP	NULL		bind	NULL				RanBP2	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_4_645_s_38	10330396	A major fraction of RanGAP is bound to the cytoplasmically oriented nucleoporin RanBP2 due to its modification by the ubiquitin-related modifier SUMO-1 (Matunis  et al., 1996  ; Mahajan et al., 1997  ), and the remainder of  RanGAP is soluble in the cytoplasm.	bind
40529	2	10817	6	10	NULL	0	NULL	RanBP2			is a type of					cytoplasmically oriented nucleoporin					NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_145_4_645_s_38	10330396	A major fraction of RanGAP is bound to the cytoplasmically oriented nucleoporin RanBP2 due to its modification by the ubiquitin-related modifier SUMO-1 (Matunis  et al., 1996  ; Mahajan et al., 1997  ), and the remainder of  RanGAP is soluble in the cytoplasm.	bind
40530	3	10817	6	NULL	NULL	0	NULL	SUMO-1	NULL		is a type of	NULL				ubiquitin-related modifier	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_4_645_s_38	10330396	A major fraction of RanGAP is bound to the cytoplasmically oriented nucleoporin RanBP2 due to its modification by the ubiquitin-related modifier SUMO-1 (Matunis  et al., 1996  ; Mahajan et al., 1997  ), and the remainder of  RanGAP is soluble in the cytoplasm.	bind
40531	4	10817	6	NULL	NULL	0	NULL	SUMO-1	NULL		modifies	NULL				RanBP2	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_4_645_s_38	10330396	A major fraction of RanGAP is bound to the cytoplasmically oriented nucleoporin RanBP2 due to its modification by the ubiquitin-related modifier SUMO-1 (Matunis  et al., 1996  ; Mahajan et al., 1997  ), and the remainder of  RanGAP is soluble in the cytoplasm.	bind
40532	5	10817	6	NULL	NULL	0	NULL	statement 1	NULL		is because of	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_4_645_s_38	10330396	A major fraction of RanGAP is bound to the cytoplasmically oriented nucleoporin RanBP2 due to its modification by the ubiquitin-related modifier SUMO-1 (Matunis  et al., 1996  ; Mahajan et al., 1997  ), and the remainder of  RanGAP is soluble in the cytoplasm.	bind
40533	6	10817	6	NULL	NULL	0	NULL	RanGAP	NULL		is soluble in	NULL				cytoplasm	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_4_645_s_38	10330396	A major fraction of RanGAP is bound to the cytoplasmically oriented nucleoporin RanBP2 due to its modification by the ubiquitin-related modifier SUMO-1 (Matunis  et al., 1996  ; Mahajan et al., 1997  ), and the remainder of  RanGAP is soluble in the cytoplasm.	bind
49787	1	10818	5	13	NULL	NULL	NULL	trans-acting factor(s)	GP		bind									TCE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_37798_s_32	10954723	A major goal of our previous study ( 11) was to identify the  trans-acting factor(s) that bind to the TCE.	bind
40534	1	10818	6	NULL	NULL	0	NULL	trans-acting factor	NULL		bind	NULL					NULL			TCE	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_48_37798_s_32	10954723	A major goal of our previous study ( 11) was to identify the  trans-acting factor(s) that bind to the TCE.	bind
49788	1	10819	5	13	NULL	NULL	NULL	rhodopsin kinase	GP		phosphorylates					rhodopsin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_51_1_161_s_16	9016359	A major mechanism for quenching the visual transduction cascade is initiated by the rapid light-dependent phosphorylation of rhodopsin by the enzyme rhodopsin kinase, followed by the highly selective binding of the protein arrestin to P-Rh* ( 1).	bind
49789	2	10819	5	13	NULL	NULL	NULL	statement 1	Process		is dependent on					light					NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_51_1_161_s_16	9016359	A major mechanism for quenching the visual transduction cascade is initiated by the rapid light-dependent phosphorylation of rhodopsin by the enzyme rhodopsin kinase, followed by the highly selective binding of the protein arrestin to P-Rh* ( 1).	bind
49790	3	10819	5	13	NULL	NULL	NULL	arrestin	GP		bind		highly selective			P-Rh*	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_51_1_161_s_16	9016359	A major mechanism for quenching the visual transduction cascade is initiated by the rapid light-dependent phosphorylation of rhodopsin by the enzyme rhodopsin kinase, followed by the highly selective binding of the protein arrestin to P-Rh* ( 1).	bind
49791	4	10819	5	13	NULL	NULL	NULL	statement 1	Process		is followed by					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_51_1_161_s_16	9016359	A major mechanism for quenching the visual transduction cascade is initiated by the rapid light-dependent phosphorylation of rhodopsin by the enzyme rhodopsin kinase, followed by the highly selective binding of the protein arrestin to P-Rh* ( 1).	bind
49792	5	10819	5	13	NULL	NULL	NULL	statement 4	Process		quenches					visual transduction cascade	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_51_1_161_s_16	9016359	A major mechanism for quenching the visual transduction cascade is initiated by the rapid light-dependent phosphorylation of rhodopsin by the enzyme rhodopsin kinase, followed by the highly selective binding of the protein arrestin to P-Rh* ( 1).	bind
49793	6	10819	5	13	NULL	NULL	NULL	rhodopsin kinase	GP		is a type of					enzyme	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_51_1_161_s_16	9016359	A major mechanism for quenching the visual transduction cascade is initiated by the rapid light-dependent phosphorylation of rhodopsin by the enzyme rhodopsin kinase, followed by the highly selective binding of the protein arrestin to P-Rh* ( 1).	bind
40545	1	10819	6	10	NULL	0	NULL	protein arrestin	NULL		bind	NULL	highly selective			P-Rh*	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_51_1_161_s_16	9016359	A major mechanism for quenching the visual transduction cascade is initiated by the rapid light-dependent phosphorylation of rhodopsin by the enzyme rhodopsin kinase, followed by the highly selective binding of the protein arrestin to P-Rh* ( 1).	bind
40546	2	10819	6	NULL	NULL	0	NULL	rhodopsin kinase	NULL		is a type of	NULL				enzyme	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_51_1_161_s_16	9016359	A major mechanism for quenching the visual transduction cascade is initiated by the rapid light-dependent phosphorylation of rhodopsin by the enzyme rhodopsin kinase, followed by the highly selective binding of the protein arrestin to P-Rh* ( 1).	bind
40547	3	10819	6	NULL	NULL	0	NULL	rhodopsin kinase	NULL		phosphorylates	NULL				rhodopsin	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_51_1_161_s_16	9016359	A major mechanism for quenching the visual transduction cascade is initiated by the rapid light-dependent phosphorylation of rhodopsin by the enzyme rhodopsin kinase, followed by the highly selective binding of the protein arrestin to P-Rh* ( 1).	bind
40548	4	10819	6	NULL	NULL	0	NULL	statement 3	NULL		is dependent on	NULL				light	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_51_1_161_s_16	9016359	A major mechanism for quenching the visual transduction cascade is initiated by the rapid light-dependent phosphorylation of rhodopsin by the enzyme rhodopsin kinase, followed by the highly selective binding of the protein arrestin to P-Rh* ( 1).	bind
40549	5	10819	6	NULL	NULL	0	NULL	statement 4	NULL		quenches	NULL				visual transduction cascade	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_51_1_161_s_16	9016359	A major mechanism for quenching the visual transduction cascade is initiated by the rapid light-dependent phosphorylation of rhodopsin by the enzyme rhodopsin kinase, followed by the highly selective binding of the protein arrestin to P-Rh* ( 1).	bind
50381	6	10819	6	10	NULL	0	NULL	statement 1	NULL		follows	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_51_1_161_s_16	9016359	A major mechanism for quenching the visual transduction cascade is initiated by the rapid light-dependent phosphorylation of rhodopsin by the enzyme rhodopsin kinase, followed by the highly selective binding of the protein arrestin to P-Rh* ( 1).	bind
49794	1	10820	5	13	NULL	NULL	NULL	export cargo protein	GP		bind					CRM1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_1_201_s_146	12529437	A major mechanism of nuclear export involves binding of the export cargo protein to  the exportin CRM1.	bind
49795	2	10820	5	13	NULL	NULL	NULL	CRM1	GP		is a type of					exportin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_1_201_s_146	12529437	A major mechanism of nuclear export involves binding of the export cargo protein to  the exportin CRM1.	bind
40550	1	10820	6	NULL	NULL	0	NULL	export cargo protein	NULL		bind	NULL				CRM1	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_1_201_s_146	12529437	A major mechanism of nuclear export involves binding of the export cargo protein to  the exportin CRM1.	bind
40551	2	10820	6	NULL	NULL	0	NULL	CRM1	NULL		is a type of	NULL				exportin	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_1_201_s_146	12529437	A major mechanism of nuclear export involves binding of the export cargo protein to  the exportin CRM1.	bind
49796	1	10822	5	13	NULL	NULL	NULL	Mig1	GP		is a type of					zinc finger protein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_yeast_14_11_9730278_s_2	9730278	A major mediator of glucose repression in yeast is Mig1, a zinc finger  protein that binds to a GC-rich recognition sequence found upstream of  many glucose-repressible genes.	bind
49797	2	10822	5	13	NULL	NULL	NULL	Mig1	GP		mediates					glucose	Chemical	repression of			NULL	yeast	NULL	NULL	NULL	NULL	abs-batch0550-0559_yeast_14_11_9730278_s_2	9730278	A major mediator of glucose repression in yeast is Mig1, a zinc finger  protein that binds to a GC-rich recognition sequence found upstream of  many glucose-repressible genes.	bind
49798	3	10822	5	13	NULL	NULL	NULL	Mig1	GP	yeast	bind					glucose-repressible genes	GP			GC-rich recognition sequence	NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_yeast_14_11_9730278_s_2	9730278	A major mediator of glucose repression in yeast is Mig1, a zinc finger  protein that binds to a GC-rich recognition sequence found upstream of  many glucose-repressible genes.	bind
40552	1	10822	6	NULL	NULL	0	NULL	Mig1	NULL		is a type of	NULL				zinc finger protein	NULL				NULL		0	NULL	NULL	NULL	abs-batch0550-0559_yeast_14_11_9730278_s_2	9730278	A major mediator of glucose repression in yeast is Mig1, a zinc finger  protein that binds to a GC-rich recognition sequence found upstream of  many glucose-repressible genes.	bind
40553	2	10822	6	NULL	NULL	0	NULL	Mig1	NULL		bind	NULL				glucose-repressible gene	NULL			GC-rich recognition sequences	NULL		0	NULL	NULL	NULL	abs-batch0550-0559_yeast_14_11_9730278_s_2	9730278	A major mediator of glucose repression in yeast is Mig1, a zinc finger  protein that binds to a GC-rich recognition sequence found upstream of  many glucose-repressible genes.	bind
40554	3	10822	6	NULL	NULL	0	NULL	Mig1	NULL		mediates	NULL				glucose	NULL	repression of			NULL	yeast	0	NULL	NULL	NULL	abs-batch0550-0559_yeast_14_11_9730278_s_2	9730278	A major mediator of glucose repression in yeast is Mig1, a zinc finger  protein that binds to a GC-rich recognition sequence found upstream of  many glucose-repressible genes.	bind
49799	1	10823	5	13	NULL	NULL	NULL	CITED2	GP		does not bind					TAZ1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_4_3042_s_180	14594809	A major part of the HIF-1alpha binding surface consists of the alphaC helix on the backside of the molecule as viewed in  Fig. 7 A. CITED2 does not contact TAZ1 at all in this region.	bind
40555	1	10823	6	10	NULL	0	NULL	CITED2	NULL		does not bind	NULL				TAZ1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_4_3042_s_180	14594809	A major part of the HIF-1alpha binding surface consists of the alphaC helix on the backside of the molecule as viewed in  Fig. 7 A. CITED2 does not contact TAZ1 at all in this region.	bind
49800	1	10824	5	13	NULL	NULL	NULL	Gsp1p	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0560-0569_embo-j_14_21_7489726_s_4	7489726	A major protein  with the apparent size of 34 kDa co-purifies with the GTP-bound form of  Gsp1p.	bind
40556	1	10824	6	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				Gsp1p	NULL				NULL		0	NULL	NULL	NULL	abs-batch0560-0569_embo-j_14_21_7489726_s_4	7489726	A major protein  with the apparent size of 34 kDa co-purifies with the GTP-bound form of  Gsp1p.	bind
49801	1	10825	5	13	NULL	NULL	NULL	TFIID	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_4_1252_s_2	12582245	A major rate-limiting step in transcription initiation by RNA polymerase II is recognition and binding of the TATA element by the transcription factor TFIID.	bind
49802	2	10825	5	13	NULL	NULL	NULL	TFIID	GP		recognizes									TATA element	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_4_1252_s_2	12582245	A major rate-limiting step in transcription initiation by RNA polymerase II is recognition and binding of the TATA element by the transcription factor TFIID.	bind
49803	3	10825	5	13	NULL	NULL	NULL	TFIID	GP		bind									TATA element	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_4_1252_s_2	12582245	A major rate-limiting step in transcription initiation by RNA polymerase II is recognition and binding of the TATA element by the transcription factor TFIID.	bind
49804	4	10825	5	13	NULL	NULL	NULL	RNA polymerase II	GP		initiates					transcription	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_4_1252_s_2	12582245	A major rate-limiting step in transcription initiation by RNA polymerase II is recognition and binding of the TATA element by the transcription factor TFIID.	bind
49805	5	10825	5	13	NULL	NULL	NULL	statement 4	Process		via					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_4_1252_s_2	12582245	A major rate-limiting step in transcription initiation by RNA polymerase II is recognition and binding of the TATA element by the transcription factor TFIID.	bind
49806	6	10825	5	13	NULL	NULL	NULL	statement 4	Process		via					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_4_1252_s_2	12582245	A major rate-limiting step in transcription initiation by RNA polymerase II is recognition and binding of the TATA element by the transcription factor TFIID.	bind
40557	1	10825	6	NULL	NULL	0	NULL	TFIID	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_4_1252_s_2	12582245	A major rate-limiting step in transcription initiation by RNA polymerase II is recognition and binding of the TATA element by the transcription factor TFIID.	bind
40558	2	10825	6	NULL	NULL	0	NULL	TFIID	NULL		bind	NULL					NULL			TATA element	NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_4_1252_s_2	12582245	A major rate-limiting step in transcription initiation by RNA polymerase II is recognition and binding of the TATA element by the transcription factor TFIID.	bind
40559	3	10825	6	NULL	NULL	0	NULL	TFIID	NULL		recognizes	NULL					NULL			TATA element	NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_4_1252_s_2	12582245	A major rate-limiting step in transcription initiation by RNA polymerase II is recognition and binding of the TATA element by the transcription factor TFIID.	bind
40560	4	10825	6	NULL	NULL	0	NULL	RNA polymerase II	NULL		initiates	NULL				transcription	NULL				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_4_1252_s_2	12582245	A major rate-limiting step in transcription initiation by RNA polymerase II is recognition and binding of the TATA element by the transcription factor TFIID.	bind
40561	5	10825	6	NULL	NULL	0	NULL	statement 4	NULL		occurs via	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_4_1252_s_2	12582245	A major rate-limiting step in transcription initiation by RNA polymerase II is recognition and binding of the TATA element by the transcription factor TFIID.	bind
40562	6	10825	6	NULL	NULL	0	NULL	statement 4	NULL		occurs via	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_4_1252_s_2	12582245	A major rate-limiting step in transcription initiation by RNA polymerase II is recognition and binding of the TATA element by the transcription factor TFIID.	bind
49807	1	10826	5	13	NULL	NULL	NULL	RB	GP		regulates					G1/S transition	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_16_14230_s_78	12584188	A major regulator of G1/S transition is the RB, which binds to the E2F transcription factor, thereby converting E2F from a transcriptional activator to a transcriptional repressor.	bind
49808	2	10826	5	13	NULL	NULL	NULL	RB	GP		bind					E2F	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_16_14230_s_78	12584188	A major regulator of G1/S transition is the RB, which binds to the E2F transcription factor, thereby converting E2F from a transcriptional activator to a transcriptional repressor.	bind
49809	3	10826	5	13	NULL	NULL	NULL	E2F	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_16_14230_s_78	12584188	A major regulator of G1/S transition is the RB, which binds to the E2F transcription factor, thereby converting E2F from a transcriptional activator to a transcriptional repressor.	bind
49810	4	10826	5	13	NULL	NULL	NULL	transcriptional activator	GP		is converted to					transcriptional repressor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_16_14230_s_78	12584188	A major regulator of G1/S transition is the RB, which binds to the E2F transcription factor, thereby converting E2F from a transcriptional activator to a transcriptional repressor.	bind
49811	5	10826	5	13	NULL	NULL	NULL	E2F	GP		is a type of					transcriptional activator	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_16_14230_s_78	12584188	A major regulator of G1/S transition is the RB, which binds to the E2F transcription factor, thereby converting E2F from a transcriptional activator to a transcriptional repressor.	bind
49812	6	10826	5	13	NULL	NULL	NULL	statement 2	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_16_14230_s_78	12584188	A major regulator of G1/S transition is the RB, which binds to the E2F transcription factor, thereby converting E2F from a transcriptional activator to a transcriptional repressor.	bind
40563	1	10826	6	NULL	NULL	0	NULL	RB	NULL		bind	NULL				E2F	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_16_14230_s_78	12584188	A major regulator of G1/S transition is the RB, which binds to the E2F transcription factor, thereby converting E2F from a transcriptional activator to a transcriptional repressor.	bind
40564	2	10826	6	NULL	NULL	0	NULL	E2F	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_16_14230_s_78	12584188	A major regulator of G1/S transition is the RB, which binds to the E2F transcription factor, thereby converting E2F from a transcriptional activator to a transcriptional repressor.	bind
40565	3	10826	6	NULL	NULL	0	NULL	RB	NULL		regulates	NULL				G1/S transition	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_16_14230_s_78	12584188	A major regulator of G1/S transition is the RB, which binds to the E2F transcription factor, thereby converting E2F from a transcriptional activator to a transcriptional repressor.	bind
40566	4	10826	6	NULL	NULL	0	NULL	E2F	NULL		is converted to	NULL				transcriptional repressor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_16_14230_s_78	12584188	A major regulator of G1/S transition is the RB, which binds to the E2F transcription factor, thereby converting E2F from a transcriptional activator to a transcriptional repressor.	bind
40567	5	10826	6	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_16_14230_s_78	12584188	A major regulator of G1/S transition is the RB, which binds to the E2F transcription factor, thereby converting E2F from a transcriptional activator to a transcriptional repressor.	bind
40568	6	10826	6	NULL	NULL	0	NULL	E2F	NULL		is a type of	NULL				transcriptional activator	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_16_14230_s_78	12584188	A major regulator of G1/S transition is the RB, which binds to the E2F transcription factor, thereby converting E2F from a transcriptional activator to a transcriptional repressor.	bind
49815	1	10827	5	13	NULL	NULL	NULL	CmtR	GP		bind		specifically			111-bp P1 fragment	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44560_s_97	12939264	A major retarded complex (and several minor retarded complexes) was formed with increasing concentrations of CmtR with a concomitant decrease in the amount of free probe but no shift of nonspecific competitor DNA ( Fig. 1 D), demonstrating specific binding of CmtR to the 111-bp P1 fragment.	bind
40569	1	10827	6	10	NULL	0	NULL	CmtR	NULL		bind	NULL	specifically			111-bp P1 fragment	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_45_44560_s_97	12939264	A major retarded complex (and several minor retarded complexes) was formed with increasing concentrations of CmtR with a concomitant decrease in the amount of free probe but no shift of nonspecific competitor DNA ( Fig. 1 D), demonstrating specific binding of CmtR to the 111-bp P1 fragment.	bind
49816	1	10828	5	13	NULL	NULL	NULL	TBP	GP		is					TATA-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1627_2_101_s_3	12818428	A major route to the formation of the preinitiation complex (PIC) for class II transcription  involves the stepwise and ordered assembly of the general transcription factors (GTFs),  initiated by the sequence-specific binding of TATA-binding protein (TBP) (or TFIID)  to the TATA-element in the promoter [  1.	bind
49817	2	10828	5	13	NULL	NULL	NULL	TBP	GP		bind		sequence specifically							TATA-element in promoter	NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1627_2_101_s_3	12818428	A major route to the formation of the preinitiation complex (PIC) for class II transcription  involves the stepwise and ordered assembly of the general transcription factors (GTFs),  initiated by the sequence-specific binding of TATA-binding protein (TBP) (or TFIID)  to the TATA-element in the promoter [  1.	bind
49818	3	10828	5	13	NULL	NULL	NULL	TFIID	GP		bind		sequence specifically							TATA-element in promoter	NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1627_2_101_s_3	12818428	A major route to the formation of the preinitiation complex (PIC) for class II transcription  involves the stepwise and ordered assembly of the general transcription factors (GTFs),  initiated by the sequence-specific binding of TATA-binding protein (TBP) (or TFIID)  to the TATA-element in the promoter [  1.	bind
49819	4	10828	5	13	NULL	NULL	NULL	PIC	GP		is					preinitiation complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1627_2_101_s_3	12818428	A major route to the formation of the preinitiation complex (PIC) for class II transcription  involves the stepwise and ordered assembly of the general transcription factors (GTFs),  initiated by the sequence-specific binding of TATA-binding protein (TBP) (or TFIID)  to the TATA-element in the promoter [  1.	bind
49820	5	10828	5	13	NULL	NULL	NULL	GTFs	GP		is					general transcription factors	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1627_2_101_s_3	12818428	A major route to the formation of the preinitiation complex (PIC) for class II transcription  involves the stepwise and ordered assembly of the general transcription factors (GTFs),  initiated by the sequence-specific binding of TATA-binding protein (TBP) (or TFIID)  to the TATA-element in the promoter [  1.	bind
49821	6	10828	5	13	NULL	NULL	NULL	PIC	GP	formation of	involves					GTFs	GP	stepwise;;ordered assembly of			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1627_2_101_s_3	12818428	A major route to the formation of the preinitiation complex (PIC) for class II transcription  involves the stepwise and ordered assembly of the general transcription factors (GTFs),  initiated by the sequence-specific binding of TATA-binding protein (TBP) (or TFIID)  to the TATA-element in the promoter [  1.	bind
49822	7	10828	5	13	NULL	NULL	NULL	statement 2	Process		initiates					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1627_2_101_s_3	12818428	A major route to the formation of the preinitiation complex (PIC) for class II transcription  involves the stepwise and ordered assembly of the general transcription factors (GTFs),  initiated by the sequence-specific binding of TATA-binding protein (TBP) (or TFIID)  to the TATA-element in the promoter [  1.	bind
49823	8	10828	5	13	NULL	NULL	NULL	statement 3	Process		initiates					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1627_2_101_s_3	12818428	A major route to the formation of the preinitiation complex (PIC) for class II transcription  involves the stepwise and ordered assembly of the general transcription factors (GTFs),  initiated by the sequence-specific binding of TATA-binding protein (TBP) (or TFIID)  to the TATA-element in the promoter [  1.	bind
40570	1	10828	6	NULL	NULL	0	NULL	TBP	NULL		is	NULL				TATA-binding protein	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1627_2_101_s_3	12818428	A major route to the formation of the preinitiation complex (PIC) for class II transcription  involves the stepwise and ordered assembly of the general transcription factors (GTFs),  initiated by the sequence-specific binding of TATA-binding protein (TBP) (or TFIID)  to the TATA-element in the promoter [  1.	bind
40571	2	10828	6	NULL	NULL	0	NULL	TBP	NULL		bind	NULL	sequence specifically				NULL			TATA-element of promoter	NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1627_2_101_s_3	12818428	A major route to the formation of the preinitiation complex (PIC) for class II transcription  involves the stepwise and ordered assembly of the general transcription factors (GTFs),  initiated by the sequence-specific binding of TATA-binding protein (TBP) (or TFIID)  to the TATA-element in the promoter [  1.	bind
40572	3	10828	6	NULL	NULL	0	NULL	TFIID	NULL		bind	NULL	sequence specifically				NULL			TATA-element of promoter	NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1627_2_101_s_3	12818428	A major route to the formation of the preinitiation complex (PIC) for class II transcription  involves the stepwise and ordered assembly of the general transcription factors (GTFs),  initiated by the sequence-specific binding of TATA-binding protein (TBP) (or TFIID)  to the TATA-element in the promoter [  1.	bind
40573	4	10828	6	NULL	NULL	0	NULL	PIC	NULL		is	NULL				preinitiation complex	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1627_2_101_s_3	12818428	A major route to the formation of the preinitiation complex (PIC) for class II transcription  involves the stepwise and ordered assembly of the general transcription factors (GTFs),  initiated by the sequence-specific binding of TATA-binding protein (TBP) (or TFIID)  to the TATA-element in the promoter [  1.	bind
40574	5	10828	6	NULL	NULL	0	NULL	GTF	NULL		is	NULL				general transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1627_2_101_s_3	12818428	A major route to the formation of the preinitiation complex (PIC) for class II transcription  involves the stepwise and ordered assembly of the general transcription factors (GTFs),  initiated by the sequence-specific binding of TATA-binding protein (TBP) (or TFIID)  to the TATA-element in the promoter [  1.	bind
40575	6	10828	6	NULL	NULL	0	NULL	PIC	NULL	formation of	involves	NULL				GTF	NULL	assembly of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1627_2_101_s_3	12818428	A major route to the formation of the preinitiation complex (PIC) for class II transcription  involves the stepwise and ordered assembly of the general transcription factors (GTFs),  initiated by the sequence-specific binding of TATA-binding protein (TBP) (or TFIID)  to the TATA-element in the promoter [  1.	bind
40576	7	10828	6	NULL	NULL	0	NULL	statement 6	NULL		is initated by	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1627_2_101_s_3	12818428	A major route to the formation of the preinitiation complex (PIC) for class II transcription  involves the stepwise and ordered assembly of the general transcription factors (GTFs),  initiated by the sequence-specific binding of TATA-binding protein (TBP) (or TFIID)  to the TATA-element in the promoter [  1.	bind
40577	8	10828	6	NULL	NULL	0	NULL	statement 6	NULL		is initated by	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1627_2_101_s_3	12818428	A major route to the formation of the preinitiation complex (PIC) for class II transcription  involves the stepwise and ordered assembly of the general transcription factors (GTFs),  initiated by the sequence-specific binding of TATA-binding protein (TBP) (or TFIID)  to the TATA-element in the promoter [  1.	bind
49824	1	10829	5	13	NULL	NULL	NULL	Gab2	GP		is a type of					adapter	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_13_2331_s_244	15933714	A major SHP-2-binding protein is the adapter  Gab2 (  et al), which binds the SH3 domains of Grb2 and Gads (  et al).	bind
49825	2	10829	5	13	NULL	NULL	NULL	Gab2	GP		is a type of					SHP-2-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_13_2331_s_244	15933714	A major SHP-2-binding protein is the adapter  Gab2 (  et al), which binds the SH3 domains of Grb2 and Gads (  et al).	bind
49826	3	10829	5	13	NULL	NULL	NULL	Gab2	GP		bind					Grb2	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_13_2331_s_244	15933714	A major SHP-2-binding protein is the adapter  Gab2 (  et al), which binds the SH3 domains of Grb2 and Gads (  et al).	bind
49827	4	10829	5	13	NULL	NULL	NULL	Gab2	GP		bind					Gads	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_13_2331_s_244	15933714	A major SHP-2-binding protein is the adapter  Gab2 (  et al), which binds the SH3 domains of Grb2 and Gads (  et al).	bind
40578	1	10829	6	NULL	NULL	0	NULL	Gab2	NULL		bind	NULL				Grb2	NULL		SH3 domain		NULL		0	NULL	NULL	NULL	gw70_embo_24_13_2331_s_244	15933714	A major SHP-2-binding protein is the adapter  Gab2 (  et al), which binds the SH3 domains of Grb2 and Gads (  et al).	bind
40579	2	10829	6	NULL	NULL	0	NULL	Gab2	NULL		bind	NULL				Gads	NULL		SH3 domain		NULL		0	NULL	NULL	NULL	gw70_embo_24_13_2331_s_244	15933714	A major SHP-2-binding protein is the adapter  Gab2 (  et al), which binds the SH3 domains of Grb2 and Gads (  et al).	bind
40580	3	10829	6	NULL	NULL	0	NULL	Gab2	NULL		is a type of	NULL				adapter protein	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_24_13_2331_s_244	15933714	A major SHP-2-binding protein is the adapter  Gab2 (  et al), which binds the SH3 domains of Grb2 and Gads (  et al).	bind
40581	4	10829	6	10	NULL	0	NULL	Gab2	NULL		is a type of	NULL				SHP-2 binding protein	NULL				NULL		NULL	NULL	NULL	NULL	gw70_embo_24_13_2331_s_244	15933714	A major SHP-2-binding protein is the adapter  Gab2 (  et al), which binds the SH3 domains of Grb2 and Gads (  et al).	bind
49828	1	10830	5	13	NULL	NULL	NULL	11 S regulator	GP		bind					20 S proteasome	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_18_15800_s_215	12600991	A major structural change is induced upon binding of the 11 S regulator to the yeast 20 S proteasome.	bind
49829	2	10830	5	13	NULL	NULL	NULL	statement 1	Process		induce					structural change	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_18_15800_s_215	12600991	A major structural change is induced upon binding of the 11 S regulator to the yeast 20 S proteasome.	bind
40582	1	10830	6	10	NULL	0	NULL	11 S regulator	NULL		bind	NULL				20 S proteasome	NULL	Yeast			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_18_15800_s_215	12600991	A major structural change is induced upon binding of the 11 S regulator to the yeast 20 S proteasome.	bind
40583	2	10830	6	NULL	NULL	0	NULL	statement 1	NULL		induces	NULL				structural change	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_18_15800_s_215	12600991	A major structural change is induced upon binding of the 11 S regulator to the yeast 20 S proteasome.	bind
49830	1	10832	5	13	NULL	NULL	NULL	c-Erb Aalpha1	GP		bind									TREs	NULL	QM7 cells transiently transfected with the T3Ralpha expression vector	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_19_11392_s_123	8626694	A Major T3R-RXR Heterodimer Is Detected in HeLa Cells but  Not in QM7 MyoblastsIn EMSA experiments, we studied the c-Erb  Aalpha1 binding pattern to TREs using QM7 or HeLa cells transiently  transfected with the T3Ralpha  expression vector.	bind
49831	2	10832	5	13	NULL	NULL	NULL	c-Erb Aalpha1	GP		bind									TREs	NULL	HeLa cells transiently transfected with the T3Ralpha expression vector	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_19_11392_s_123	8626694	A Major T3R-RXR Heterodimer Is Detected in HeLa Cells but  Not in QM7 MyoblastsIn EMSA experiments, we studied the c-Erb  Aalpha1 binding pattern to TREs using QM7 or HeLa cells transiently  transfected with the T3Ralpha  expression vector.	bind
40584	1	10832	6	NULL	NULL	0	NULL	c-Erb Aalpha1	NULL		bind	NULL					NULL			TRE	NULL	QM7 transiently transfected with the T3Ralpha expression vector	0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11392_s_123	8626694	A Major T3R-RXR Heterodimer Is Detected in HeLa Cells but  Not in QM7 MyoblastsIn EMSA experiments, we studied the c-Erb  Aalpha1 binding pattern to TREs using QM7 or HeLa cells transiently  transfected with the T3Ralpha  expression vector.	bind
40585	2	10832	6	NULL	NULL	0	NULL	c-Erb Aalpha1	NULL		bind	NULL					NULL			TRE	NULL	HeLa cells transiently transfected with the T3Ralpha expression vector	0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11392_s_123	8626694	A Major T3R-RXR Heterodimer Is Detected in HeLa Cells but  Not in QM7 MyoblastsIn EMSA experiments, we studied the c-Erb  Aalpha1 binding pattern to TREs using QM7 or HeLa cells transiently  transfected with the T3Ralpha  expression vector.	bind
49832	1	10833	5	13	NULL	NULL	NULL	2H-TRE	GP		is					two thyroid hormone response element half-site motifs 	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_biochim-biophys-acta_1761_4_16647292_s_3	16647292	A major transcription start site was identified at -154 bp  relative to the ATG translation initiation codon, within a region containing  two thyroid hormone response element half-site motifs (2H-TRE). Binding  of thyroid hormone receptors alpha and beta1 to this element was demonstrated.	bind
49833	2	10833	5	13	NULL	NULL	NULL	thyroid hormone receptor alpha	GP		bind									2H-TRE	NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_biochim-biophys-acta_1761_4_16647292_s_3	16647292	A major transcription start site was identified at -154 bp  relative to the ATG translation initiation codon, within a region containing  two thyroid hormone response element half-site motifs (2H-TRE). Binding  of thyroid hormone receptors alpha and beta1 to this element was demonstrated.	bind
49834	3	10833	5	13	NULL	NULL	NULL	thyroid hormone receptor beta1	GP		bind									2H-TRE	NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_biochim-biophys-acta_1761_4_16647292_s_3	16647292	A major transcription start site was identified at -154 bp  relative to the ATG translation initiation codon, within a region containing  two thyroid hormone response element half-site motifs (2H-TRE). Binding  of thyroid hormone receptors alpha and beta1 to this element was demonstrated.	bind
40586	1	10833	6	NULL	NULL	0	NULL	2H-TRE	NULL		is	NULL				thyroid hormone response element half-site motif	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_biochim-biophys-acta_1761_4_16647292_s_3	16647292	A major transcription start site was identified at -154 bp  relative to the ATG translation initiation codon, within a region containing  two thyroid hormone response element half-site motifs (2H-TRE). Binding  of thyroid hormone receptors alpha and beta1 to this element was demonstrated.	bind
40587	2	10833	6	NULL	NULL	0	NULL	thyroid hormone receptor alpha	NULL		bind	NULL					NULL			2H-TRE	NULL		0	NULL	NULL	NULL	abs-batch0700-0719_biochim-biophys-acta_1761_4_16647292_s_3	16647292	A major transcription start site was identified at -154 bp  relative to the ATG translation initiation codon, within a region containing  two thyroid hormone response element half-site motifs (2H-TRE). Binding  of thyroid hormone receptors alpha and beta1 to this element was demonstrated.	bind
40588	3	10833	6	NULL	NULL	0	NULL	thyroid hormone receptor beta1	NULL		bind	NULL					NULL			2H-TRE	NULL		0	NULL	NULL	NULL	abs-batch0700-0719_biochim-biophys-acta_1761_4_16647292_s_3	16647292	A major transcription start site was identified at -154 bp  relative to the ATG translation initiation codon, within a region containing  two thyroid hormone response element half-site motifs (2H-TRE). Binding  of thyroid hormone receptors alpha and beta1 to this element was demonstrated.	bind
49835	1	10834	5	13	NULL	NULL	NULL	SCAP 	GP		bind					insig-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12753_s_248	12242332	A major unresolved question relates to the mechanism by which binding of SCAP to insig-1 or -2 leads to its retention in the ER.	bind
49836	2	10834	5	13	NULL	NULL	NULL	SCAP	GP		bind					insig-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12753_s_248	12242332	A major unresolved question relates to the mechanism by which binding of SCAP to insig-1 or -2 leads to its retention in the ER.	bind
49837	3	10834	5	13	NULL	NULL	NULL	SCAP	GP		is retained in					ER	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12753_s_248	12242332	A major unresolved question relates to the mechanism by which binding of SCAP to insig-1 or -2 leads to its retention in the ER.	bind
49838	4	10834	5	13	NULL	NULL	NULL	statement 1	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12753_s_248	12242332	A major unresolved question relates to the mechanism by which binding of SCAP to insig-1 or -2 leads to its retention in the ER.	bind
49839	5	10834	5	13	NULL	NULL	NULL	statement 2	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12753_s_248	12242332	A major unresolved question relates to the mechanism by which binding of SCAP to insig-1 or -2 leads to its retention in the ER.	bind
40589	1	10834	6	NULL	NULL	0	NULL	SCAP	NULL		bind	NULL				insig-1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_20_12753_s_248	12242332	A major unresolved question relates to the mechanism by which binding of SCAP to insig-1 or -2 leads to its retention in the ER.	bind
40590	2	10834	6	NULL	NULL	0	NULL	SCAP	NULL		bind	NULL				insig-2	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_20_12753_s_248	12242332	A major unresolved question relates to the mechanism by which binding of SCAP to insig-1 or -2 leads to its retention in the ER.	bind
40591	3	10834	6	NULL	NULL	0	NULL	SCAP	NULL		retains in	NULL				ER	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_20_12753_s_248	12242332	A major unresolved question relates to the mechanism by which binding of SCAP to insig-1 or -2 leads to its retention in the ER.	bind
40592	4	10834	6	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_20_12753_s_248	12242332	A major unresolved question relates to the mechanism by which binding of SCAP to insig-1 or -2 leads to its retention in the ER.	bind
40593	5	10834	6	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_20_12753_s_248	12242332	A major unresolved question relates to the mechanism by which binding of SCAP to insig-1 or -2 leads to its retention in the ER.	bind
49840	1	10837	5	13	NULL	NULL	NULL	maltose binding protein - Kap123p	GP		bind					H2A	GP		NLS		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_2_251_s_295	11309407	A maltose binding protein - Kap123p fusion also bound to the H2A and H2B NLSs and not to GST alone (data not shown).	bind
49841	2	10837	5	13	NULL	NULL	NULL	maltose binding protein - Kap123p	GP		bind					H2B	GP		NLS		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_2_251_s_295	11309407	A maltose binding protein - Kap123p fusion also bound to the H2A and H2B NLSs and not to GST alone (data not shown).	bind
49842	3	10837	5	13	NULL	NULL	NULL	maltose binding protein - Kap123p	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_2_251_s_295	11309407	A maltose binding protein - Kap123p fusion also bound to the H2A and H2B NLSs and not to GST alone (data not shown).	bind
40594	1	10837	6	10	NULL	0	NULL	maltose binding protein - Kap123p 			bind					H2A			NLS		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_2_251_s_295	11309407	A maltose binding protein - Kap123p fusion also bound to the H2A and H2B NLSs and not to GST alone (data not shown).	bind
40595	2	10837	6	10	NULL	0	NULL	maltose binding protein - Kap123p 			bind					H2B			NLS		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_2_251_s_295	11309407	A maltose binding protein - Kap123p fusion also bound to the H2A and H2B NLSs and not to GST alone (data not shown).	bind
40596	3	10837	6	10	NULL	0	NULL	maltose binding protein - Kap123p 			is a type of					fusion protein					NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_2_251_s_295	11309407	A maltose binding protein - Kap123p fusion also bound to the H2A and H2B NLSs and not to GST alone (data not shown).	bind
49843	1	10839	5	13	NULL	NULL	NULL	VP8*	GP		bind					TRAF2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_23_19889_s_134	11262403	A mammalian 2-hybrid analysis was also used to assess VP8* binding to TRAF2 (Fig.  2 B).	bind
40597	1	10839	6	NULL	NULL	0	NULL	VP8*	NULL		bind	NULL				TRAF2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_23_19889_s_134	11262403	A mammalian 2-hybrid analysis was also used to assess VP8* binding to TRAF2 (Fig.  2 B).	bind
49844	1	10840	5	13	NULL	NULL	NULL	Apaf-1	GP		is a type of					CED-4-related caspase adaptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_21_0_71_s_70	12414721	A mammalian CED-4-related caspase adaptor, called Apaf-1, was found ( 70), but unlike CED-4, which binds to CED-9, Apaf-1 did not bind to Bcl-2 (or its homologs)  ( 71).	bind
49845	2	10840	5	13	NULL	NULL	NULL	CED-4	GP		bind					CED-9	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_21_0_71_s_70	12414721	A mammalian CED-4-related caspase adaptor, called Apaf-1, was found ( 70), but unlike CED-4, which binds to CED-9, Apaf-1 did not bind to Bcl-2 (or its homologs)  ( 71).	bind
49846	3	10840	5	13	NULL	NULL	NULL	Apaf-1	GP	mammalian	does not bind					Bcl-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_21_0_71_s_70	12414721	A mammalian CED-4-related caspase adaptor, called Apaf-1, was found ( 70), but unlike CED-4, which binds to CED-9, Apaf-1 did not bind to Bcl-2 (or its homologs)  ( 71).	bind
40598	1	10840	6	NULL	NULL	0	NULL	Apaf-1	NULL		is a type of	NULL				CED-4-related caspase adaptor	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_21_0_71_s_70	12414721	A mammalian CED-4-related caspase adaptor, called Apaf-1, was found ( 70), but unlike CED-4, which binds to CED-9, Apaf-1 did not bind to Bcl-2 (or its homologs)  ( 71).	bind
40599	2	10840	6	NULL	NULL	0	NULL	CED-4	NULL		bind	NULL				CED-9	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_21_0_71_s_70	12414721	A mammalian CED-4-related caspase adaptor, called Apaf-1, was found ( 70), but unlike CED-4, which binds to CED-9, Apaf-1 did not bind to Bcl-2 (or its homologs)  ( 71).	bind
40600	3	10840	6	10	NULL	0	NULL	Apaf-1		mammalian	does not bind					Bcl2					NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_21_0_71_s_70	12414721	A mammalian CED-4-related caspase adaptor, called Apaf-1, was found ( 70), but unlike CED-4, which binds to CED-9, Apaf-1 did not bind to Bcl-2 (or its homologs)  ( 71).	bind
49847	1	10841	5	13	NULL	NULL	NULL	RAFT1	GP		is a type of					FKBP12-rapamycin binding protein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_genes-dev_10_3_8595879_s_4	8595879	A mammalian FKBP12-rapamycin binding  protein, RAFT1, shares 39% and 43% identity with TOR1 and TOR2 proteins,  respectively but has not been linked to rapamycin action in vivo.	bind
49848	2	10841	5	13	NULL	NULL	NULL	RAFT1	GP	mammalian	is not linked to					rapamycin	Chemical	action of			NULL	in vivo	NULL	NULL	NULL	NULL	abs-batch0517-0529_genes-dev_10_3_8595879_s_4	8595879	A mammalian FKBP12-rapamycin binding  protein, RAFT1, shares 39% and 43% identity with TOR1 and TOR2 proteins,  respectively but has not been linked to rapamycin action in vivo.	bind
50457	3	10841	5	13	NULL	NULL	NULL	RAFT1	GP		is similar to					TOR1 protein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_genes-dev_10_3_8595879_s_4	8595879	A mammalian FKBP12-rapamycin binding  protein, RAFT1, shares 39% and 43% identity with TOR1 and TOR2 proteins,  respectively but has not been linked to rapamycin action in vivo.	bind
50458	4	10841	5	13	NULL	NULL	NULL	RAFT1	GP		is similar to					TOR2 protein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_genes-dev_10_3_8595879_s_4	8595879	A mammalian FKBP12-rapamycin binding  protein, RAFT1, shares 39% and 43% identity with TOR1 and TOR2 proteins,  respectively but has not been linked to rapamycin action in vivo.	bind
40601	1	10841	6	NULL	NULL	0	NULL	RAFT1	NULL		is a type of	NULL				FKBP12-rapamycin binding protein	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_genes-dev_10_3_8595879_s_4	8595879	A mammalian FKBP12-rapamycin binding  protein, RAFT1, shares 39% and 43% identity with TOR1 and TOR2 proteins,  respectively but has not been linked to rapamycin action in vivo.	bind
40602	2	10841	6	10	NULL	0	NULL	RAFT1			is similar to					TOR1 protein					NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_genes-dev_10_3_8595879_s_4	8595879	A mammalian FKBP12-rapamycin binding  protein, RAFT1, shares 39% and 43% identity with TOR1 and TOR2 proteins,  respectively but has not been linked to rapamycin action in vivo.	bind
40603	3	10841	6	10	NULL	0	NULL	RAFT1			is similar to					TOR2 protein					NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_genes-dev_10_3_8595879_s_4	8595879	A mammalian FKBP12-rapamycin binding  protein, RAFT1, shares 39% and 43% identity with TOR1 and TOR2 proteins,  respectively but has not been linked to rapamycin action in vivo.	bind
40604	4	10841	6	10	NULL	0	NULL	RAFT1		mammalian	is not linked to					rapamycin		action of			NULL	in vivo	NULL	NULL	NULL	NULL	abs-batch0517-0529_genes-dev_10_3_8595879_s_4	8595879	A mammalian FKBP12-rapamycin binding  protein, RAFT1, shares 39% and 43% identity with TOR1 and TOR2 proteins,  respectively but has not been linked to rapamycin action in vivo.	bind
49849	1	10842	5	13	NULL	NULL	NULL	guanine nucleotides	NucleicAcid		bind					R-Ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18602_s_100	9228027	A mammalian GST-fusion R-Ras expression vector was introduced into COS7 cells and guanine nucleotides bound to R-Ras were examined (Fig.  3,  A and  B).	bind
40605	1	10842	6	NULL	NULL	0	NULL	guanine nucleotides	NULL		bind	NULL				R-Ras	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_30_18602_s_100	9228027	A mammalian GST-fusion R-Ras expression vector was introduced into COS7 cells and guanine nucleotides bound to R-Ras were examined (Fig.  3,  A and  B).	bind
49850	1	10843	5	13	NULL	NULL	NULL	MOB1	GP	mammalian homolog of yeast	is a member of					Striatin Family-Protein Phosphatase 2A Complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_45_31917_s_526	10542219	A Mammalian Homolog of Yeast MOB1 Is Both a Member and a Putative Substrate of Striatin Family-Protein Phosphatase 2A Complexes.	bind
49851	2	10843	5	13	NULL	NULL	NULL	MOB1	GP	mammalian homolog of yeast	is a substrate of		putative			Striatin Family-Protein Phosphatase 2A Complexes	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_45_31917_s_526	10542219	A Mammalian Homolog of Yeast MOB1 Is Both a Member and a Putative Substrate of Striatin Family-Protein Phosphatase 2A Complexes.	bind
40606	1	10843	6	NULL	NULL	0	NULL	MOB1	NULL	mammalian homolog to Yeast	is a member of	NULL				Striatin Family-Protein Phosphatase 2A Complexes	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_45_31917_s_526	10542219	A Mammalian Homolog of Yeast MOB1 Is Both a Member and a Putative Substrate of Striatin Family-Protein Phosphatase 2A Complexes.	bind
40607	2	10843	6	NULL	NULL	0	NULL	MOB1	NULL	mammalian homolog to Yeast	is a substrate for	NULL	putative			Striatin Family-Protein Phosphatase 2A Complexes	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_45_31917_s_526	10542219	A Mammalian Homolog of Yeast MOB1 Is Both a Member and a Putative Substrate of Striatin Family-Protein Phosphatase 2A Complexes.	bind
49852	1	10844	5	13	NULL	NULL	NULL	inscuteable	GP	mammalian partner of	bind					NuMA	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_437_7056_275_s_265	16094321	A mammalian Partner of inscuteable  binds NuMA and regulates mitotic spindle organization.	bind
49853	2	10844	5	13	NULL	NULL	NULL	statement 1	Process		regulates					mitotic spindle	CellComponent	organization of			NULL		NULL	NULL	NULL	NULL	gw70_nature_437_7056_275_s_265	16094321	A mammalian Partner of inscuteable  binds NuMA and regulates mitotic spindle organization.	bind
40608	1	10844	6	NULL	NULL	0	NULL	inscuteable	NULL	mammalian partner of	bind	NULL				NuMA	NULL				NULL		0	NULL	NULL	NULL	gw70_nature_437_7056_275_s_265	16094321	A mammalian Partner of inscuteable  binds NuMA and regulates mitotic spindle organization.	bind
40609	2	10844	6	10	NULL	0	NULL	statement 1	NULL		regulates	NULL				mitotic spindle 	NULL	organization of			NULL		NULL	NULL	NULL	NULL	gw70_nature_437_7056_275_s_265	16094321	A mammalian Partner of inscuteable  binds NuMA and regulates mitotic spindle organization.	bind
49854	1	10849	5	13	NULL	NULL	NULL	TORs	GP	mammalian homolog of yeast	bind					FKBP12	GP				NULL		NULL	NULL	NULL	NULL	gw60_clinmicrobiolrev_12_4_583_s_2282	10515904	A mammalian protein that binds to FKBP12 in a rapamycin-dependent fashion and is homologous to yeast TORs.	bind
49855	2	10849	5	13	NULL	NULL	NULL	statement 1	Process		is dependent on					rapamycin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_clinmicrobiolrev_12_4_583_s_2282	10515904	A mammalian protein that binds to FKBP12 in a rapamycin-dependent fashion and is homologous to yeast TORs.	bind
40610	1	10849	6	NULL	NULL	0	NULL	TOR	NULL	mammalian homolog to Yeast	bind	NULL				FKBP12	NULL				NULL		0	NULL	NULL	NULL	gw60_clinmicrobiolrev_12_4_583_s_2282	10515904	A mammalian protein that binds to FKBP12 in a rapamycin-dependent fashion and is homologous to yeast TORs.	bind
40611	2	10849	6	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				rapamycin	NULL				NULL		0	NULL	NULL	NULL	gw60_clinmicrobiolrev_12_4_583_s_2282	10515904	A mammalian protein that binds to FKBP12 in a rapamycin-dependent fashion and is homologous to yeast TORs.	bind
49856	1	10852	5	13	NULL	NULL	NULL	VHL peptide	GP	mammalian	bind					Elc1	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_16_9033_s_135	10430890	A Mammalian VHL Peptide Binds to Yeast Elc1 and Induces Formation of Two C-Terminal alpha-Helices.	bind
49857	2	10852	5	13	NULL	NULL	NULL	statement 1	Process		induces							formation of	C-Terminal alpha-Helices		NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_16_9033_s_135	10430890	A Mammalian VHL Peptide Binds to Yeast Elc1 and Induces Formation of Two C-Terminal alpha-Helices.	bind
41714	1	10852	6	NULL	NULL	0	NULL	VHL peptide	NULL	mammalian	bind	NULL				Elc1	NULL	Yeast			NULL		0	NULL	NULL	NULL	gw60_pnas_96_16_9033_s_135	10430890	A Mammalian VHL Peptide Binds to Yeast Elc1 and Induces Formation of Two C-Terminal alpha-Helices.	bind
41715	2	10852	6	NULL	NULL	0	NULL	statement 1	NULL		induces	NULL					NULL	formation of	two C-Terminal alpha-Helices		NULL		0	NULL	NULL	NULL	gw60_pnas_96_16_9033_s_135	10430890	A Mammalian VHL Peptide Binds to Yeast Elc1 and Induces Formation of Two C-Terminal alpha-Helices.	bind
49858	1	10853	5	13	NULL	NULL	NULL	N-linked glycopeptide	GP		contains					mannose 6-phosphate	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_156_5_8596035_s_1	8596035	A mannose 6-phosphate-containing N-linked glycopeptide derived from lysosomal acid lipase is bound to MHC class II in B lymphoblastoid cell lines..	bind
49859	2	10853	5	13	NULL	NULL	NULL	statement 1	GP		bind					MHC class II	GP				NULL	B lymphoblastoid cell lines	NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_156_5_8596035_s_1	8596035	A mannose 6-phosphate-containing N-linked glycopeptide derived from lysosomal acid lipase is bound to MHC class II in B lymphoblastoid cell lines..	bind
49860	3	10853	5	13	NULL	NULL	NULL	statement 1	GP		is derived from					lysosomal acid lipase	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_156_5_8596035_s_1	8596035	A mannose 6-phosphate-containing N-linked glycopeptide derived from lysosomal acid lipase is bound to MHC class II in B lymphoblastoid cell lines..	bind
41737	1	10853	6	NULL	NULL	0	NULL	N-linked glycopeptide	NULL		contains	NULL				mannose 6-phosphate	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_156_5_8596035_s_1	8596035	A mannose 6-phosphate-containing N-linked glycopeptide derived from lysosomal acid lipase is bound to MHC class II in B lymphoblastoid cell lines..	bind
41738	2	10853	6	10	NULL	0	NULL	statement 1	NULL		is derived from	NULL				lysosomal acid lipase	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_156_5_8596035_s_1	8596035	A mannose 6-phosphate-containing N-linked glycopeptide derived from lysosomal acid lipase is bound to MHC class II in B lymphoblastoid cell lines..	bind
41740	3	10853	6	10	NULL	0	NULL	statement 1	NULL		bind	NULL				MHC class II	NULL				NULL	B lymphoblastoid cell lines	NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_156_5_8596035_s_1	8596035	A mannose 6-phosphate-containing N-linked glycopeptide derived from lysosomal acid lipase is bound to MHC class II in B lymphoblastoid cell lines..	bind
49867	1	10857	5	13	NULL	NULL	NULL	3H-DHA	Chemical		bind					beta-adrenoceptors	GP	cortical			NULL	castrated animals	NULL	NULL	NULL	NULL	gw60_jneurosci_21_2_726_s_128	11160451	A marginally significant elevation in the binding of 3H-DHA to cortical beta-adrenoceptors (Fig.  5) was seen for the castrated animals ( F(1,30) = 3.293;  p < 0.08).	bind
41744	1	10857	6	10	NULL	0	NULL	3H-DHA			bind					beta-adrenoceptors		cortical			NULL	castrated animals	NULL	NULL	NULL	NULL	gw60_jneurosci_21_2_726_s_128	11160451	A marginally significant elevation in the binding of 3H-DHA to cortical beta-adrenoceptors (Fig.  5) was seen for the castrated animals ( F(1,30) = 3.293;  p < 0.08).	bind
49868	1	10858	5	13	NULL	NULL	NULL	Cdc27	GP		bind					Nup98	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_438_7070_1036_s_96	16355229	A marked decrease in Cdc27 and Cdh1 binding to Nup98 occurred in the first 10 min  after nocodazole release, a period when cellular securin started to decline ( Fig. 2g).	bind
49869	2	10858	5	13	NULL	NULL	NULL	Cdh1	GP		bind					Nup98	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_438_7070_1036_s_96	16355229	A marked decrease in Cdc27 and Cdh1 binding to Nup98 occurred in the first 10 min  after nocodazole release, a period when cellular securin started to decline ( Fig. 2g).	bind
49870	3	10858	5	13	NULL	NULL	NULL	nocodazole	Chemical	release of	decreases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_nature_438_7070_1036_s_96	16355229	A marked decrease in Cdc27 and Cdh1 binding to Nup98 occurred in the first 10 min  after nocodazole release, a period when cellular securin started to decline ( Fig. 2g).	bind
49871	4	10858	5	13	NULL	NULL	NULL	nocodazole	Chemical	release of	decreases					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_nature_438_7070_1036_s_96	16355229	A marked decrease in Cdc27 and Cdh1 binding to Nup98 occurred in the first 10 min  after nocodazole release, a period when cellular securin started to decline ( Fig. 2g).	bind
49872	5	10858	5	13	NULL	NULL	NULL	nocodazole	Chemical	release of	is related to					securin	GP	decline in;;cellular			NULL		NULL	NULL	NULL	NULL	gw70_nature_438_7070_1036_s_96	16355229	A marked decrease in Cdc27 and Cdh1 binding to Nup98 occurred in the first 10 min  after nocodazole release, a period when cellular securin started to decline ( Fig. 2g).	bind
41745	1	10858	6	NULL	NULL	0	NULL	Cdc27	NULL		bind	NULL				Nup98	NULL				NULL		0	NULL	NULL	NULL	gw70_nature_438_7070_1036_s_96	16355229	A marked decrease in Cdc27 and Cdh1 binding to Nup98 occurred in the first 10 min  after nocodazole release, a period when cellular securin started to decline ( Fig. 2g).	bind
41746	2	10858	6	NULL	NULL	0	NULL	Cdh1	NULL		bind	NULL				Nup98	NULL				NULL		0	NULL	NULL	NULL	gw70_nature_438_7070_1036_s_96	16355229	A marked decrease in Cdc27 and Cdh1 binding to Nup98 occurred in the first 10 min  after nocodazole release, a period when cellular securin started to decline ( Fig. 2g).	bind
50459	3	10858	6	10	NULL	0	NULL	nocodazole	NULL	release of	decrease	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_nature_438_7070_1036_s_96	16355229	A marked decrease in Cdc27 and Cdh1 binding to Nup98 occurred in the first 10 min  after nocodazole release, a period when cellular securin started to decline ( Fig. 2g).	bind
50460	4	10858	6	10	NULL	0	NULL	nocodazole	NULL	release of	decrease	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_nature_438_7070_1036_s_96	16355229	A marked decrease in Cdc27 and Cdh1 binding to Nup98 occurred in the first 10 min  after nocodazole release, a period when cellular securin started to decline ( Fig. 2g).	bind
49873	1	10859	5	13	NULL	NULL	NULL	Cdk4	GP		bind					p27	GP				NULL	Tet-p27 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25863_s_92	9325318	A marked increase in p27 levels led only to a small (less than 2-fold) increase in the amount of p27-bound Cdk4 in the Tet-p27 cells (Fig.  1 c), suggesting that most of the cyclin D-Cdk4 present in proliferating Mv1Lu cells is already bound to p27.	bind
49874	2	10859	5	13	NULL	NULL	NULL	p27	GP	increase in	leads to					statement 1	Process	increase in			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25863_s_92	9325318	A marked increase in p27 levels led only to a small (less than 2-fold) increase in the amount of p27-bound Cdk4 in the Tet-p27 cells (Fig.  1 c), suggesting that most of the cyclin D-Cdk4 present in proliferating Mv1Lu cells is already bound to p27.	bind
49876	3	10859	5	13	NULL	NULL	NULL	cyclin D-Cdk4	GP		bind					p27	GP				NULL	proliferating Mv1Lu cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25863_s_92	9325318	A marked increase in p27 levels led only to a small (less than 2-fold) increase in the amount of p27-bound Cdk4 in the Tet-p27 cells (Fig.  1 c), suggesting that most of the cyclin D-Cdk4 present in proliferating Mv1Lu cells is already bound to p27.	bind
41747	1	10859	6	NULL	NULL	0	NULL	p27	NULL		bind	NULL				Cdk4	NULL				NULL	Tet-p27 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25863_s_92	9325318	A marked increase in p27 levels led only to a small (less than 2-fold) increase in the amount of p27-bound Cdk4 in the Tet-p27 cells (Fig.  1 c), suggesting that most of the cyclin D-Cdk4 present in proliferating Mv1Lu cells is already bound to p27.	bind
41748	2	10859	6	NULL	NULL	0	NULL	cyclin D-Cdk4	NULL		bind	NULL				p27	NULL				NULL	proliferating Mv1Lu cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_41_25863_s_92	9325318	A marked increase in p27 levels led only to a small (less than 2-fold) increase in the amount of p27-bound Cdk4 in the Tet-p27 cells (Fig.  1 c), suggesting that most of the cyclin D-Cdk4 present in proliferating Mv1Lu cells is already bound to p27.	bind
42049	3	10859	6	NULL	NULL	0	NULL	p27	NULL	increase in	leads to	NULL				statement 1	NULL	small increase in			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_41_25863_s_92	9325318	A marked increase in p27 levels led only to a small (less than 2-fold) increase in the amount of p27-bound Cdk4 in the Tet-p27 cells (Fig.  1 c), suggesting that most of the cyclin D-Cdk4 present in proliferating Mv1Lu cells is already bound to p27.	bind
49877	1	10861	5	13	NULL	NULL	NULL	E-selectin/IgM	GP		bind					sulfated compounds	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_42_32642_s_204	10938267	A markedly different pattern of E-selectin/IgM binding to the sulfated compounds was observed compared with L-selectingM (Fig.  8 B).	bind
49878	2	10861	5	13	NULL	NULL	NULL	L-selectingM	GP		bind					sulfated compounds	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_42_32642_s_204	10938267	A markedly different pattern of E-selectin/IgM binding to the sulfated compounds was observed compared with L-selectingM (Fig.  8 B).	bind
41749	1	10861	6	NULL	NULL	0	NULL	E-selectin/IgM	NULL		bind	NULL				sulfated compounds	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_42_32642_s_204	10938267	A markedly different pattern of E-selectin/IgM binding to the sulfated compounds was observed compared with L-selectingM (Fig.  8 B).	bind
50461	2	10861	6	10	NULL	0	NULL	 L-selectingM	NULL		bind	NULL				sulfated compounds	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_42_32642_s_204	10938267	A markedly different pattern of E-selectin/IgM binding to the sulfated compounds was observed compared with L-selectingM (Fig.  8 B).	bind
49880	1	10862	5	13	NULL	NULL	NULL	cisplatin	Chemical		bind					transferrin	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_chembiochem_6_10_16196027_s_1	16196027	A mass spectrometric and molecular modelling study of cisplatin binding to transferrin..	bind
41750	1	10862	6	NULL	NULL	0	NULL	cisplatin	NULL		bind	NULL				transferrin	NULL				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_chembiochem_6_10_16196027_s_1	16196027	A mass spectrometric and molecular modelling study of cisplatin binding to transferrin..	bind
49881	1	10863	5	13	NULL	NULL	NULL	Ras	GP		bind					GTP	Chemical				NULL	sensory neurons	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_37_21751_s_98	7665594	A maximally effective  concentration of NGF (1 nM  or 26 ng/ml) was able to stimulate  GTP binding to Ras in both sensory and sympathetic neurons at all  stages examined.	bind
49882	2	10863	5	13	NULL	NULL	NULL	NGF	GP		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_37_21751_s_98	7665594	A maximally effective  concentration of NGF (1 nM  or 26 ng/ml) was able to stimulate  GTP binding to Ras in both sensory and sympathetic neurons at all  stages examined.	bind
50462	3	10863	5	13	NULL	NULL	NULL	Ras	GP		bind					GTP	Chemical				NULL	sympathetic neurons	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_37_21751_s_98	7665594	A maximally effective  concentration of NGF (1 nM  or 26 ng/ml) was able to stimulate  GTP binding to Ras in both sensory and sympathetic neurons at all  stages examined.	bind
50463	4	10863	5	13	NULL	NULL	NULL	NGF	GP		stimulates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_37_21751_s_98	7665594	A maximally effective  concentration of NGF (1 nM  or 26 ng/ml) was able to stimulate  GTP binding to Ras in both sensory and sympathetic neurons at all  stages examined.	bind
41753	1	10863	6	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				Ras	NULL				NULL	sensory neurons	0	NULL	NULL	NULL	gw60_jbiolchem_270_37_21751_s_98	7665594	A maximally effective  concentration of NGF (1 nM  or 26 ng/ml) was able to stimulate  GTP binding to Ras in both sensory and sympathetic neurons at all  stages examined.	bind
41755	2	10863	6	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				Ras	NULL				NULL	sympathetic neurons	0	NULL	NULL	NULL	gw60_jbiolchem_270_37_21751_s_98	7665594	A maximally effective  concentration of NGF (1 nM  or 26 ng/ml) was able to stimulate  GTP binding to Ras in both sensory and sympathetic neurons at all  stages examined.	bind
41757	3	10863	6	NULL	NULL	0	NULL	NGF	NULL		stimulates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_37_21751_s_98	7665594	A maximally effective  concentration of NGF (1 nM  or 26 ng/ml) was able to stimulate  GTP binding to Ras in both sensory and sympathetic neurons at all  stages examined.	bind
41758	4	10863	6	NULL	NULL	0	NULL	NGF	NULL		stimulates	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_37_21751_s_98	7665594	A maximally effective  concentration of NGF (1 nM  or 26 ng/ml) was able to stimulate  GTP binding to Ras in both sensory and sympathetic neurons at all  stages examined.	bind
49883	1	10864	5	13	NULL	NULL	NULL	eIF4G	GP		bind					eIF3	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_8_1659_s_203	16541103	A maximally effective concentration of insulin had little effect on the amount of  eIF4G bound to eIF3 after 1 min of incubation ( Figure 7A); however, the amount of eIF4G bound was increased more than two-fold after 3 min  ( Figure 7B).	bind
49884	2	10864	5	13	NULL	NULL	NULL	insulin	GP		increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_8_1659_s_203	16541103	A maximally effective concentration of insulin had little effect on the amount of  eIF4G bound to eIF3 after 1 min of incubation ( Figure 7A); however, the amount of eIF4G bound was increased more than two-fold after 3 min  ( Figure 7B).	bind
41763	1	10864	6	NULL	NULL	0	NULL	eIF4G	NULL		bind	NULL				eIF3	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_25_8_1659_s_203	16541103	A maximally effective concentration of insulin had little effect on the amount of  eIF4G bound to eIF3 after 1 min of incubation ( Figure 7A); however, the amount of eIF4G bound was increased more than two-fold after 3 min  ( Figure 7B).	bind
41765	2	10864	6	10	NULL	0	NULL	insulin	NULL		increases	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_8_1659_s_203	16541103	A maximally effective concentration of insulin had little effect on the amount of  eIF4G bound to eIF3 after 1 min of incubation ( Figure 7A); however, the amount of eIF4G bound was increased more than two-fold after 3 min  ( Figure 7B).	bind
49885	1	10865	5	13	NULL	NULL	NULL	E1	GP		bind					E2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_6921_s_356	14638692	A maximum  S* value of 81  plus-or-minus  1 S is reached which is 18.4 S below that with saturated binding of  E1 to  E2	bind
41783	1	10865	6	NULL	NULL	0	NULL	E1	NULL		bind	NULL				E2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6921_s_356	14638692	A maximum  S* value of 81  plus-or-minus  1 S is reached which is 18.4 S below that with saturated binding of  E1 to  E2	bind
49886	1	10867	5	13	NULL	NULL	NULL	water molecule	Chemical		bind					tyrosine-9	AminoAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-biophys-res-commun_280_3_11162605_s_8	11162605	A mechanism  involving a tyrosine-9-bound water molecule acting as a proton shuttle  is proposed for the Michael additions catalyzed by GST A4-4.	bind
49887	2	10867	5	13	NULL	NULL	NULL	statement 1	Process		acts as					proton shuttle	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-biophys-res-commun_280_3_11162605_s_8	11162605	A mechanism  involving a tyrosine-9-bound water molecule acting as a proton shuttle  is proposed for the Michael additions catalyzed by GST A4-4.	bind
41789	1	10867	6	10	NULL	0	NULL	tyrosine-9			bind					water molecule					NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-biophys-res-commun_280_3_11162605_s_8	11162605	A mechanism  involving a tyrosine-9-bound water molecule acting as a proton shuttle  is proposed for the Michael additions catalyzed by GST A4-4.	bind
50464	2	10867	6	10	NULL	0	NULL	statement 1	NULL		acts as a	NULL				proton shuttle	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biochem-biophys-res-commun_280_3_11162605_s_8	11162605	A mechanism  involving a tyrosine-9-bound water molecule acting as a proton shuttle  is proposed for the Michael additions catalyzed by GST A4-4.	bind
49888	1	10868	5	13	NULL	NULL	NULL	NC2	GP	heterodimeric 	bind			histone fold domains		TBP-promoter complexes	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_34_0_77_s_1658	11092823	A mechanism for  repression of class II gene transcription through specific binding of NC2 to TBP-promoter  complexes via heterodimeric histone fold domains.	bind
49889	2	10868	5	13	NULL	NULL	NULL	statement 1	Process		repress					class II gene	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_34_0_77_s_1658	11092823	A mechanism for  repression of class II gene transcription through specific binding of NC2 to TBP-promoter  complexes via heterodimeric histone fold domains.	bind
41796	1	10868	6	10	NULL	0	NULL	NC2		heterodimeric	bind			histone fold domains		TBP-promoter complex					NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_34_0_77_s_1658	11092823	A mechanism for  repression of class II gene transcription through specific binding of NC2 to TBP-promoter  complexes via heterodimeric histone fold domains.	bind
41798	2	10868	6	NULL	NULL	0	NULL	statement 1	NULL		represses	NULL				class II gene	NULL	transcription of 			NULL		0	NULL	NULL	NULL	gw70_annurevgenet_34_0_77_s_1658	11092823	A mechanism for  repression of class II gene transcription through specific binding of NC2 to TBP-promoter  complexes via heterodimeric histone fold domains.	bind
49890	1	10869	5	13	NULL	NULL	NULL	QacR dimers	GP		bind		cooperatively			IR1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_24_7102_s_219	11717268	A mechanism for cooperative binding of QacR dimers to IR1 that involved indirect interactions through the DNA would be consistent with all the results presented in this work.	bind
41799	1	10869	6	NULL	NULL	0	NULL	QacR dimers	NULL		bind	NULL	cooperatively			IR1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_24_7102_s_219	11717268	A mechanism for cooperative binding of QacR dimers to IR1 that involved indirect interactions through the DNA would be consistent with all the results presented in this work.	bind
49891	1	10876	5	13	NULL	NULL	NULL	BAR	GP		induce					SHP	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7027_s_28	12496277	A mechanism has been proposed whereby BAR induces the negative transcriptional regulator  SHP (small heterodimer partner), which in turn represses transcription factors that bind to the  CYP7A1 BAREs ( ,  ).	bind
49892	2	10876	5	13	NULL	NULL	NULL	SHP	GP		is					small heterodimer partner	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7027_s_28	12496277	A mechanism has been proposed whereby BAR induces the negative transcriptional regulator  SHP (small heterodimer partner), which in turn represses transcription factors that bind to the  CYP7A1 BAREs ( ,  ).	bind
49893	3	10876	5	13	NULL	NULL	NULL	SHP	GP		is a type of					negative transcriptional regulator	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7027_s_28	12496277	A mechanism has been proposed whereby BAR induces the negative transcriptional regulator  SHP (small heterodimer partner), which in turn represses transcription factors that bind to the  CYP7A1 BAREs ( ,  ).	bind
49894	4	10876	5	13	NULL	NULL	NULL	transcription factors	GP		bind					CYP7A1	GP			BAREs	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7027_s_28	12496277	A mechanism has been proposed whereby BAR induces the negative transcriptional regulator  SHP (small heterodimer partner), which in turn represses transcription factors that bind to the  CYP7A1 BAREs ( ,  ).	bind
49895	5	10876	5	13	NULL	NULL	NULL	SHP	GP		repress					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7027_s_28	12496277	A mechanism has been proposed whereby BAR induces the negative transcriptional regulator  SHP (small heterodimer partner), which in turn represses transcription factors that bind to the  CYP7A1 BAREs ( ,  ).	bind
49896	6	10876	5	13	NULL	NULL	NULL	statement 1	Process		leads to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7027_s_28	12496277	A mechanism has been proposed whereby BAR induces the negative transcriptional regulator  SHP (small heterodimer partner), which in turn represses transcription factors that bind to the  CYP7A1 BAREs ( ,  ).	bind
41834	1	10876	6	10	NULL	0	NULL	transcription factor	NULL		bind	NULL				CYP7A1	NULL			BARE	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7027_s_28	12496277	A mechanism has been proposed whereby BAR induces the negative transcriptional regulator  SHP (small heterodimer partner), which in turn represses transcription factors that bind to the  CYP7A1 BAREs ( ,  ).	bind
41835	2	10876	6	NULL	NULL	0	NULL	SHP	NULL		represses	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7027_s_28	12496277	A mechanism has been proposed whereby BAR induces the negative transcriptional regulator  SHP (small heterodimer partner), which in turn represses transcription factors that bind to the  CYP7A1 BAREs ( ,  ).	bind
41836	3	10876	6	10	NULL	0	NULL	SHP	NULL		is a type of	NULL				negative transcriptional regulator	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_9_7027_s_28	12496277	A mechanism has been proposed whereby BAR induces the negative transcriptional regulator  SHP (small heterodimer partner), which in turn represses transcription factors that bind to the  CYP7A1 BAREs ( ,  ).	bind
41837	4	10876	6	NULL	NULL	0	NULL	BAR	NULL		induces	NULL				SHP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7027_s_28	12496277	A mechanism has been proposed whereby BAR induces the negative transcriptional regulator  SHP (small heterodimer partner), which in turn represses transcription factors that bind to the  CYP7A1 BAREs ( ,  ).	bind
41838	5	10876	6	NULL	NULL	0	NULL	SHP	NULL		is	NULL				small heterodimer partner	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7027_s_28	12496277	A mechanism has been proposed whereby BAR induces the negative transcriptional regulator  SHP (small heterodimer partner), which in turn represses transcription factors that bind to the  CYP7A1 BAREs ( ,  ).	bind
50465	6	10876	6	10	NULL	0	NULL	statement 4	NULL		leads to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7027_s_28	12496277	A mechanism has been proposed whereby BAR induces the negative transcriptional regulator  SHP (small heterodimer partner), which in turn represses transcription factors that bind to the  CYP7A1 BAREs ( ,  ).	bind
49897	1	10878	5	13	NULL	NULL	NULL	KCNK3	GP		is a type of					channel	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_4_577_s_22	12437930	A mechanism is suggested by demonstration that (despite separation of retention and release motifs in the KCNK3 primary sequence) the channels bind beta-COP or 14-3-3beta in mutually exclusive fashion.	bind
49898	2	10878	5	13	NULL	NULL	NULL	KCNK3	GP		bind					beta-COP	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_4_577_s_22	12437930	A mechanism is suggested by demonstration that (despite separation of retention and release motifs in the KCNK3 primary sequence) the channels bind beta-COP or 14-3-3beta in mutually exclusive fashion.	bind
49899	3	10878	5	13	NULL	NULL	NULL	KCNK3	GP		bind					14-3-3beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_4_577_s_22	12437930	A mechanism is suggested by demonstration that (despite separation of retention and release motifs in the KCNK3 primary sequence) the channels bind beta-COP or 14-3-3beta in mutually exclusive fashion.	bind
49900	4	10878	5	13	NULL	NULL	NULL	statement 2	Process		mutually exclusive to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_4_577_s_22	12437930	A mechanism is suggested by demonstration that (despite separation of retention and release motifs in the KCNK3 primary sequence) the channels bind beta-COP or 14-3-3beta in mutually exclusive fashion.	bind
41856	1	10878	6	NULL	NULL	0	NULL	KCNK3	NULL		is a type of	NULL				channel	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_111_4_577_s_22	12437930	A mechanism is suggested by demonstration that (despite separation of retention and release motifs in the KCNK3 primary sequence) the channels bind beta-COP or 14-3-3beta in mutually exclusive fashion.	bind
41858	2	10878	6	NULL	NULL	0	NULL	KCNK3	NULL		bind	NULL				beta-COP	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_111_4_577_s_22	12437930	A mechanism is suggested by demonstration that (despite separation of retention and release motifs in the KCNK3 primary sequence) the channels bind beta-COP or 14-3-3beta in mutually exclusive fashion.	bind
41859	3	10878	6	NULL	NULL	0	NULL	KCNK3	NULL		bind	NULL				14-3-3beta	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_111_4_577_s_22	12437930	A mechanism is suggested by demonstration that (despite separation of retention and release motifs in the KCNK3 primary sequence) the channels bind beta-COP or 14-3-3beta in mutually exclusive fashion.	bind
41860	4	10878	6	NULL	NULL	0	NULL	statement 2	NULL		is independent of	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_111_4_577_s_22	12437930	A mechanism is suggested by demonstration that (despite separation of retention and release motifs in the KCNK3 primary sequence) the channels bind beta-COP or 14-3-3beta in mutually exclusive fashion.	bind
49901	1	10879	5	13	NULL	NULL	NULL	Spi-1	GP		bind			wHTH domain		IL1B	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_294_4_854_s_134	12061786	A mechanism of PTT was suggested in which the Spi-1 wHTH domain binds to the  IL1B promoter and physically interacts with IE2, which provides both TBP recruitment and acidic transactivation domains.	bind
49902	2	10879	5	13	NULL	NULL	NULL	Spi-1	GP		interacts with		physically	wHTH domain		IE2	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_294_4_854_s_134	12061786	A mechanism of PTT was suggested in which the Spi-1 wHTH domain binds to the  IL1B promoter and physically interacts with IE2, which provides both TBP recruitment and acidic transactivation domains.	bind
49903	3	10879	5	13	NULL	NULL	NULL	statement 2	Process		leads to					TBP	GP	recruitment of			NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_294_4_854_s_134	12061786	A mechanism of PTT was suggested in which the Spi-1 wHTH domain binds to the  IL1B promoter and physically interacts with IE2, which provides both TBP recruitment and acidic transactivation domains.	bind
50466	4	10879	5	13	NULL	NULL	NULL	statement 2	Process		leads to							acidic	transactivation domain		NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_294_4_854_s_134	12061786	A mechanism of PTT was suggested in which the Spi-1 wHTH domain binds to the  IL1B promoter and physically interacts with IE2, which provides both TBP recruitment and acidic transactivation domains.	bind
41908	1	10879	6	NULL	NULL	0	NULL	Spi-1	NULL		bind	NULL		wHTH domain		IL1B	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_294_4_854_s_134	12061786	A mechanism of PTT was suggested in which the Spi-1 wHTH domain binds to the  IL1B promoter and physically interacts with IE2, which provides both TBP recruitment and acidic transactivation domains.	bind
41909	2	10879	6	10	NULL	0	NULL	Spi-1	NULL		interacts with	NULL	physically	wHTH domain		IE2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_294_4_854_s_134	12061786	A mechanism of PTT was suggested in which the Spi-1 wHTH domain binds to the  IL1B promoter and physically interacts with IE2, which provides both TBP recruitment and acidic transactivation domains.	bind
41910	3	10879	6	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				TBP	NULL	recruitment of			NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_294_4_854_s_134	12061786	A mechanism of PTT was suggested in which the Spi-1 wHTH domain binds to the  IL1B promoter and physically interacts with IE2, which provides both TBP recruitment and acidic transactivation domains.	bind
41911	4	10879	6	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL					NULL	acidic	transactivation domain		NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_294_4_854_s_134	12061786	A mechanism of PTT was suggested in which the Spi-1 wHTH domain binds to the  IL1B promoter and physically interacts with IE2, which provides both TBP recruitment and acidic transactivation domains.	bind
49904	1	10880	5	13	NULL	NULL	NULL	OxyR 	GP		bind					mom	GP			GATC sites	NULL		NULL	NULL	NULL	NULL	gw60_genetics_152_1_31_s_435	10408954	A mechanism of this kind would be analogous to that described for  mom, with the difference that OxyR binds to GATC sites located upstream of the  mom promoter ( B OLKER and KAHMANN 1989   ).	bind
49905	2	10880	5	13	NULL	NULL	NULL				is located				GATC sites	mom	GP	upstream of		promoter	NULL		NULL	NULL	NULL	NULL	gw60_genetics_152_1_31_s_435	10408954	A mechanism of this kind would be analogous to that described for  mom, with the difference that OxyR binds to GATC sites located upstream of the  mom promoter ( B OLKER and KAHMANN 1989   ).	bind
41912	1	10880	6	10	NULL	0	NULL	OxyR	NULL		bind	NULL				mom	NULL			GATC sites 	NULL		NULL	NULL	NULL	NULL	gw60_genetics_152_1_31_s_435	10408954	A mechanism of this kind would be analogous to that described for  mom, with the difference that OxyR binds to GATC sites located upstream of the  mom promoter ( B OLKER and KAHMANN 1989   ).	bind
50467	2	10880	6	10	NULL	0	NULL		NULL		is located 	NULL			GATC sites	mom	NULL	upstream of		promoter	NULL		0	NULL	NULL	NULL	gw60_genetics_152_1_31_s_435	10408954	A mechanism of this kind would be analogous to that described for  mom, with the difference that OxyR binds to GATC sites located upstream of the  mom promoter ( B OLKER and KAHMANN 1989   ).	bind
49906	1	10881	5	13	NULL	NULL	NULL	Hsp70	GP		bind					HSF1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_17_12081_s_175	10207033	A mechanism that has been proposed for autoregulation or self-limiting expression of  Hsp70 is based on the observation that Hsp70 binds to HSF1 ( 20-22).	bind
41913	1	10881	6	NULL	NULL	0	NULL	Hsp70	NULL		bind	NULL				HSF1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_12081_s_175	10207033	A mechanism that has been proposed for autoregulation or self-limiting expression of  Hsp70 is based on the observation that Hsp70 binds to HSF1 ( 20-22).	bind
49907	1	10882	5	13	NULL	NULL	NULL	chaperone	GP		is involved in					Cxs	GP	membrane integration of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_7856_s_250	9525879	A mechanism that would explain this phenomenon is that a specific factor, such as a chaperone that normally is involved in the membrane integration of Cxs and, for example, binds to the Cx polypeptide sequence to aid in their correct positioning within the ER translocon (represented schematically in Fig.  8 C), is absent or not functional in the cell-free expression system.	bind
49908	2	10882	5	13	NULL	NULL	NULL	chaperone	GP		bind					Cx polypeptide sequence	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_7856_s_250	9525879	A mechanism that would explain this phenomenon is that a specific factor, such as a chaperone that normally is involved in the membrane integration of Cxs and, for example, binds to the Cx polypeptide sequence to aid in their correct positioning within the ER translocon (represented schematically in Fig.  8 C), is absent or not functional in the cell-free expression system.	bind
49909	3	10882	5	13	NULL	NULL	NULL	chaperone	GP		is positioned within					ER translocon	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_7856_s_250	9525879	A mechanism that would explain this phenomenon is that a specific factor, such as a chaperone that normally is involved in the membrane integration of Cxs and, for example, binds to the Cx polypeptide sequence to aid in their correct positioning within the ER translocon (represented schematically in Fig.  8 C), is absent or not functional in the cell-free expression system.	bind
49910	4	10882	5	13	NULL	NULL	NULL	statement 2	Process		aid in					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_7856_s_250	9525879	A mechanism that would explain this phenomenon is that a specific factor, such as a chaperone that normally is involved in the membrane integration of Cxs and, for example, binds to the Cx polypeptide sequence to aid in their correct positioning within the ER translocon (represented schematically in Fig.  8 C), is absent or not functional in the cell-free expression system.	bind
42050	1	10882	6	NULL	NULL	0	NULL	chaperone	NULL		is involved in	NULL				Cxs	NULL	membrane integration of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_7856_s_250	9525879	A mechanism that would explain this phenomenon is that a specific factor, such as a chaperone that normally is involved in the membrane integration of Cxs and, for example, binds to the Cx polypeptide sequence to aid in their correct positioning within the ER translocon (represented schematically in Fig.  8 C), is absent or not functional in the cell-free expression system.	bind
42051	2	10882	6	NULL	NULL	0	NULL	chaperone	NULL		is positioned within	NULL				ER translocon	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_7856_s_250	9525879	A mechanism that would explain this phenomenon is that a specific factor, such as a chaperone that normally is involved in the membrane integration of Cxs and, for example, binds to the Cx polypeptide sequence to aid in their correct positioning within the ER translocon (represented schematically in Fig.  8 C), is absent or not functional in the cell-free expression system.	bind
42052	3	10882	6	NULL	NULL	0	NULL	chaperone	NULL		bind	NULL				Cx polypeptide	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_7856_s_250	9525879	A mechanism that would explain this phenomenon is that a specific factor, such as a chaperone that normally is involved in the membrane integration of Cxs and, for example, binds to the Cx polypeptide sequence to aid in their correct positioning within the ER translocon (represented schematically in Fig.  8 C), is absent or not functional in the cell-free expression system.	bind
42053	4	10882	6	NULL	NULL	0	NULL	statement 3	NULL		aids in	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_7856_s_250	9525879	A mechanism that would explain this phenomenon is that a specific factor, such as a chaperone that normally is involved in the membrane integration of Cxs and, for example, binds to the Cx polypeptide sequence to aid in their correct positioning within the ER translocon (represented schematically in Fig.  8 C), is absent or not functional in the cell-free expression system.	bind
49911	1	10883	5	13	NULL	NULL	NULL	synaptobrevin	GP		bind			S1 domain		exosites	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_6_3459_s_133	9013591	A mechanism which could account for the present results is the promotion of an active conformation of TeNT induced by the binding of the S1 and S2 domains of synaptobrevin to exosites present on the toxin surface, as in the case of allosteric enzymes ( 36-38).	bind
49912	2	10883	5	13	NULL	NULL	NULL	exosites	Chemical		is present on					toxin	Chemical	surface of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_6_3459_s_133	9013591	A mechanism which could account for the present results is the promotion of an active conformation of TeNT induced by the binding of the S1 and S2 domains of synaptobrevin to exosites present on the toxin surface, as in the case of allosteric enzymes ( 36-38).	bind
49913	3	10883	5	13	NULL	NULL	NULL	synaptobrevin	GP		bind			S2 domain		exosites 	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_6_3459_s_133	9013591	A mechanism which could account for the present results is the promotion of an active conformation of TeNT induced by the binding of the S1 and S2 domains of synaptobrevin to exosites present on the toxin surface, as in the case of allosteric enzymes ( 36-38).	bind
49914	4	10883	5	13	NULL	NULL	NULL	statement 1	Process		induce					TeNT	GP	active conformation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_6_3459_s_133	9013591	A mechanism which could account for the present results is the promotion of an active conformation of TeNT induced by the binding of the S1 and S2 domains of synaptobrevin to exosites present on the toxin surface, as in the case of allosteric enzymes ( 36-38).	bind
49915	5	10883	5	13	NULL	NULL	NULL	statement 3	Process		induce					TeNT	GP	active conformation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_6_3459_s_133	9013591	A mechanism which could account for the present results is the promotion of an active conformation of TeNT induced by the binding of the S1 and S2 domains of synaptobrevin to exosites present on the toxin surface, as in the case of allosteric enzymes ( 36-38).	bind
41914	1	10883	6	10	NULL	0	NULL	exosite	NULL		is present on	NULL				toxin surface	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_6_3459_s_133	9013591	A mechanism which could account for the present results is the promotion of an active conformation of TeNT induced by the binding of the S1 and S2 domains of synaptobrevin to exosites present on the toxin surface, as in the case of allosteric enzymes ( 36-38).	bind
41915	2	10883	6	10	NULL	0	NULL	synaptobrevin	NULL		bind	NULL		S1 domain		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_6_3459_s_133	9013591	A mechanism which could account for the present results is the promotion of an active conformation of TeNT induced by the binding of the S1 and S2 domains of synaptobrevin to exosites present on the toxin surface, as in the case of allosteric enzymes ( 36-38).	bind
41916	4	10883	6	10	NULL	0	NULL	statement 2	NULL		induces	NULL				TeNT	NULL	active conformation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_6_3459_s_133	9013591	A mechanism which could account for the present results is the promotion of an active conformation of TeNT induced by the binding of the S1 and S2 domains of synaptobrevin to exosites present on the toxin surface, as in the case of allosteric enzymes ( 36-38).	bind
41917	5	10883	6	10	NULL	0	NULL	statement 3	NULL		induces	NULL				TeNT	NULL	active conformation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_6_3459_s_133	9013591	A mechanism which could account for the present results is the promotion of an active conformation of TeNT induced by the binding of the S1 and S2 domains of synaptobrevin to exosites present on the toxin surface, as in the case of allosteric enzymes ( 36-38).	bind
50468	3	10883	6	10	NULL	0	NULL	synaptobrevin	NULL		bind	NULL		S2 domain		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_6_3459_s_133	9013591	A mechanism which could account for the present results is the promotion of an active conformation of TeNT induced by the binding of the S1 and S2 domains of synaptobrevin to exosites present on the toxin surface, as in the case of allosteric enzymes ( 36-38).	bind
49916	1	10884	5	13	NULL	NULL	NULL	PKCs	GP	atypical	bind					p62	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35344_s_227	11445585	A mechanistic explanation to the roles of atypical PKCs in NF-kappaB activation has been provided by the findings that atypical PKCs bind to the scaffold protein p62 via protein complex formation with receptor interacting protein or TRAF6 in TNF-alpha- or IL-1beta-signaling, respectively ( 39,  81).	bind
49917	2	10884	5	13	NULL	NULL	NULL	p62	GP		is a type of					scaffold protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35344_s_227	11445585	A mechanistic explanation to the roles of atypical PKCs in NF-kappaB activation has been provided by the findings that atypical PKCs bind to the scaffold protein p62 via protein complex formation with receptor interacting protein or TRAF6 in TNF-alpha- or IL-1beta-signaling, respectively ( 39,  81).	bind
49918	3	10884	5	13	NULL	NULL	NULL	statement 1	Process		via					TRAF6	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35344_s_227	11445585	A mechanistic explanation to the roles of atypical PKCs in NF-kappaB activation has been provided by the findings that atypical PKCs bind to the scaffold protein p62 via protein complex formation with receptor interacting protein or TRAF6 in TNF-alpha- or IL-1beta-signaling, respectively ( 39,  81).	bind
49919	4	10884	5	13	NULL	NULL	NULL	statement 3	Process		occurs during					IL-1beta	GP	signaling of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35344_s_227	11445585	A mechanistic explanation to the roles of atypical PKCs in NF-kappaB activation has been provided by the findings that atypical PKCs bind to the scaffold protein p62 via protein complex formation with receptor interacting protein or TRAF6 in TNF-alpha- or IL-1beta-signaling, respectively ( 39,  81).	bind
42054	1	10884	6	NULL	NULL	0	NULL	PKC	NULL	atypical	bind	NULL				p62	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_38_35344_s_227	11445585	A mechanistic explanation to the roles of atypical PKCs in NF-kappaB activation has been provided by the findings that atypical PKCs bind to the scaffold protein p62 via protein complex formation with receptor interacting protein or TRAF6 in TNF-alpha- or IL-1beta-signaling, respectively ( 39,  81).	bind
42055	2	10884	6	NULL	NULL	0	NULL	p62	NULL		is a type of	NULL				scaffold protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_38_35344_s_227	11445585	A mechanistic explanation to the roles of atypical PKCs in NF-kappaB activation has been provided by the findings that atypical PKCs bind to the scaffold protein p62 via protein complex formation with receptor interacting protein or TRAF6 in TNF-alpha- or IL-1beta-signaling, respectively ( 39,  81).	bind
42057	3	10884	6	10	NULL	0	NULL	statement 1	NULL		occurs via	NULL				TRAF6	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35344_s_227	11445585	A mechanistic explanation to the roles of atypical PKCs in NF-kappaB activation has been provided by the findings that atypical PKCs bind to the scaffold protein p62 via protein complex formation with receptor interacting protein or TRAF6 in TNF-alpha- or IL-1beta-signaling, respectively ( 39,  81).	bind
42058	4	10884	6	10	NULL	0	NULL	statement 3	NULL		occurs during	NULL				IL-1beta	NULL	signaling of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_38_35344_s_227	11445585	A mechanistic explanation to the roles of atypical PKCs in NF-kappaB activation has been provided by the findings that atypical PKCs bind to the scaffold protein p62 via protein complex formation with receptor interacting protein or TRAF6 in TNF-alpha- or IL-1beta-signaling, respectively ( 39,  81).	bind
49922	1	10885	5	13	NULL	NULL	NULL	TFIID complex	GP		bind									promoter	NULL		NULL	NULL	NULL	NULL	gw60_embo_17_17_5103_s_13	9724646	A mechanistic study supported the hypothesis that PC4 facilitates binding of the TFIID complex to promoters (Kaiser  et al., 1995  ).	bind
49923	2	10885	5	13	NULL	NULL	NULL	PC4	GP		facilitates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_17_5103_s_13	9724646	A mechanistic study supported the hypothesis that PC4 facilitates binding of the TFIID complex to promoters (Kaiser  et al., 1995  ).	bind
41918	1	10885	6	NULL	NULL	0	NULL	TFIID complex	NULL		bind	NULL					NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_embo_17_17_5103_s_13	9724646	A mechanistic study supported the hypothesis that PC4 facilitates binding of the TFIID complex to promoters (Kaiser  et al., 1995  ).	bind
41919	2	10885	6	NULL	NULL	0	NULL	PC4	NULL		facilitates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_17_17_5103_s_13	9724646	A mechanistic study supported the hypothesis that PC4 facilitates binding of the TFIID complex to promoters (Kaiser  et al., 1995  ).	bind
49924	1	10886	5	13	NULL	NULL	NULL	CRF	GP		is					corticotropin-releasing factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_brainres_980_2_206_s_337	12867260	A member of the  corticotropin-releasing factor (CRF) neuropeptide family that is selectively bound  by type 2 CRF receptors.	bind
49925	2	10886	5	13	NULL	NULL	NULL	type 2 CRF receptors	GP		bind		selectively			member of CRF neuropeptide family	GP				NULL		NULL	NULL	NULL	NULL	gw70_brainres_980_2_206_s_337	12867260	A member of the  corticotropin-releasing factor (CRF) neuropeptide family that is selectively bound  by type 2 CRF receptors.	bind
41920	1	10886	6	NULL	NULL	0	NULL	CRF	NULL		is	NULL				corticotropin-releasing factor	NULL				NULL		0	NULL	NULL	NULL	gw70_brainres_980_2_206_s_337	12867260	A member of the  corticotropin-releasing factor (CRF) neuropeptide family that is selectively bound  by type 2 CRF receptors.	bind
41921	2	10886	6	NULL	NULL	0	NULL	member of CRF family	NULL		bind	NULL	selectively			type 2 CRF receptors	NULL				NULL		0	NULL	NULL	NULL	gw70_brainres_980_2_206_s_337	12867260	A member of the  corticotropin-releasing factor (CRF) neuropeptide family that is selectively bound  by type 2 CRF receptors.	bind
49926	1	10889	5	13	NULL	NULL	NULL	Meis1 homeodomain family member	GP		bind					CRS1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_7941_s_86	9525891	A member of the Meis1 homeodomain family binds CRS1.	bind
41922	1	10889	6	NULL	NULL	0	NULL	Meis1 homeodomain family member	NULL		bind	NULL				CRS1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_7941_s_86	9525891	A member of the Meis1 homeodomain family binds CRS1.	bind
49927	1	10890	5	13	NULL	NULL	NULL	AR	GP		is a member of					steroid hormone receptor family	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37853_s_12	16141201	A member of the steroid hormone receptor family, AR binds androgen and drives the transcription of androgen-responsive genes in a variety of tissues and cell types.	bind
49928	2	10890	5	13	NULL	NULL	NULL	AR	GP		bind					androgen	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37853_s_12	16141201	A member of the steroid hormone receptor family, AR binds androgen and drives the transcription of androgen-responsive genes in a variety of tissues and cell types.	bind
49929	3	10890	5	13	NULL	NULL	NULL	statement 2	Process		drives					androgen-responsive genes	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37853_s_12	16141201	A member of the steroid hormone receptor family, AR binds androgen and drives the transcription of androgen-responsive genes in a variety of tissues and cell types.	bind
41923	1	10890	6	NULL	NULL	0	NULL	AR	NULL		bind	NULL				androgen	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_45_37853_s_12	16141201	A member of the steroid hormone receptor family, AR binds androgen and drives the transcription of androgen-responsive genes in a variety of tissues and cell types.	bind
41924	2	10890	6	10	NULL	0	NULL	AR	NULL		is a member of	NULL				steroid hormone receptor family	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_45_37853_s_12	16141201	A member of the steroid hormone receptor family, AR binds androgen and drives the transcription of androgen-responsive genes in a variety of tissues and cell types.	bind
41925	3	10890	6	NULL	NULL	0	NULL	statement 1	NULL		drives	NULL				androgen responsive genes	NULL	transcription of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_45_37853_s_12	16141201	A member of the steroid hormone receptor family, AR binds androgen and drives the transcription of androgen-responsive genes in a variety of tissues and cell types.	bind
49930	1	10892	5	13	NULL	NULL	NULL	photoreceptor apoprotein	GP		bind		reversibly			riboflavin	Chemical	free			NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiolrev_25_5_503_s_203	11742688	A membrane protein that binds free riboflavin reversibly is a plausible photoreceptor apoprotein [  31].	bind
49931	2	10892	5	13	NULL	NULL	NULL	photoreceptor apoprotein	GP		is a type of					membrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiolrev_25_5_503_s_203	11742688	A membrane protein that binds free riboflavin reversibly is a plausible photoreceptor apoprotein [  31].	bind
41926	1	10892	6	NULL	NULL	0	NULL	photoreceptor apoprotein	NULL		bind	NULL	reversibly			riboflavin	NULL	free			NULL		0	NULL	NULL	NULL	gw60_femsmicrobiolrev_25_5_503_s_203	11742688	A membrane protein that binds free riboflavin reversibly is a plausible photoreceptor apoprotein [  31].	bind
41927	2	10892	6	NULL	NULL	0	NULL	photoreceptor apoprotein	NULL		is a type of	NULL				membrane protein	NULL				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiolrev_25_5_503_s_203	11742688	A membrane protein that binds free riboflavin reversibly is a plausible photoreceptor apoprotein [  31].	bind
49932	1	10893	5	13	NULL	NULL	NULL	E-cadherin protein	GP		bind					C3G	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_15_6690_s_57	15254236	A membrane was incubated with 200 nM GST-E-cadherin, and the E-cadherin protein bound to C3G on the membrane was detected by anti-E-cadherin antibody.	bind
41928	1	10893	6	NULL	NULL	0	NULL	E-cadherin protein	NULL		bind	NULL				C3G	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_15_6690_s_57	15254236	A membrane was incubated with 200 nM GST-E-cadherin, and the E-cadherin protein bound to C3G on the membrane was detected by anti-E-cadherin antibody.	bind
49933	1	10894	5	13	NULL	NULL	NULL	minireceptor	GP	membrane-anchored	does not bind					alpha2M	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6057_s_236	9497322	A membrane-anchored minireceptor that contained all eight class A repeats of cluster II but not the neighboring fourth epidermal growth factor repeat did not show binding to alpha2M ( 11).	bind
49934	2	10894	5	13	NULL	NULL	NULL	minireceptor	GP	membrane-anchored	contains								class A repeats of cluster II		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6057_s_236	9497322	A membrane-anchored minireceptor that contained all eight class A repeats of cluster II but not the neighboring fourth epidermal growth factor repeat did not show binding to alpha2M ( 11).	bind
49935	3	10894	5	13	NULL	NULL	NULL	minireceptor	GP	membrane-anchored	does not contain								fourth epidermal growth factor repeat		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_11_6057_s_236	9497322	A membrane-anchored minireceptor that contained all eight class A repeats of cluster II but not the neighboring fourth epidermal growth factor repeat did not show binding to alpha2M ( 11).	bind
42059	1	10894	6	NULL	NULL	0	NULL	minireceptor	NULL	membrane-anchored	contains	NULL					NULL		class A repeats of cluster II		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_11_6057_s_236	9497322	A membrane-anchored minireceptor that contained all eight class A repeats of cluster II but not the neighboring fourth epidermal growth factor repeat did not show binding to alpha2M ( 11).	bind
42060	2	10894	6	NULL	NULL	0	NULL	statement 1	NULL		does not bind	NULL				alpha2M	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_11_6057_s_236	9497322	A membrane-anchored minireceptor that contained all eight class A repeats of cluster II but not the neighboring fourth epidermal growth factor repeat did not show binding to alpha2M ( 11).	bind
42061	3	10894	6	NULL	NULL	0	NULL	minireceptor	NULL	membrane-anchored	does not contain	NULL					NULL		fourth epidermal growth factor repeat		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_11_6057_s_236	9497322	A membrane-anchored minireceptor that contained all eight class A repeats of cluster II but not the neighboring fourth epidermal growth factor repeat did not show binding to alpha2M ( 11).	bind
49936	1	10895	5	13	NULL	NULL	NULL	AZ-521	Cell		is a type of					human gastric cancer cell lines	Cell				NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_53_0_353_s_176	10547695	A membrane-bound 140-kDa   protein present in human gastric cancer cell lines (AZ-521 and AGS)   has been identified as a potential receptor for binding of VacA to   target cells because this protein was coimmunoprecipitated with   VacA by anti-VacA antibodies ( 177).	bind
49937	2	10895	5	13	NULL	NULL	NULL	AGS	Cell		is a type of					human gastric cancer cell lines	Cell				NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_53_0_353_s_176	10547695	A membrane-bound 140-kDa   protein present in human gastric cancer cell lines (AZ-521 and AGS)   has been identified as a potential receptor for binding of VacA to   target cells because this protein was coimmunoprecipitated with   VacA by anti-VacA antibodies ( 177).	bind
49938	3	10895	5	13	NULL	NULL	NULL	VacA	GP		bind					target cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_53_0_353_s_176	10547695	A membrane-bound 140-kDa   protein present in human gastric cancer cell lines (AZ-521 and AGS)   has been identified as a potential receptor for binding of VacA to   target cells because this protein was coimmunoprecipitated with   VacA by anti-VacA antibodies ( 177).	bind
49939	5	10895	5	13	NULL	NULL	NULL	statement 4	GP		is a receptor for		potentially			statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_53_0_353_s_176	10547695	A membrane-bound 140-kDa   protein present in human gastric cancer cell lines (AZ-521 and AGS)   has been identified as a potential receptor for binding of VacA to   target cells because this protein was coimmunoprecipitated with   VacA by anti-VacA antibodies ( 177).	bind
49940	6	10895	5	13	NULL	NULL	NULL	statement 4	GP		is present in					AZ-521	Cell				NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_53_0_353_s_176	10547695	A membrane-bound 140-kDa   protein present in human gastric cancer cell lines (AZ-521 and AGS)   has been identified as a potential receptor for binding of VacA to   target cells because this protein was coimmunoprecipitated with   VacA by anti-VacA antibodies ( 177).	bind
49941	7	10895	5	13	NULL	NULL	NULL	statement 4	GP		is present in					AGS	Cell				NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_53_0_353_s_176	10547695	A membrane-bound 140-kDa   protein present in human gastric cancer cell lines (AZ-521 and AGS)   has been identified as a potential receptor for binding of VacA to   target cells because this protein was coimmunoprecipitated with   VacA by anti-VacA antibodies ( 177).	bind
50472	4	10895	5	13	NULL	NULL	NULL	140-kDa protein	GP		bind					membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_53_0_353_s_176	10547695	A membrane-bound 140-kDa   protein present in human gastric cancer cell lines (AZ-521 and AGS)   has been identified as a potential receptor for binding of VacA to   target cells because this protein was coimmunoprecipitated with   VacA by anti-VacA antibodies ( 177).	bind
41929	1	10895	6	NULL	NULL	0	NULL	AZ-521	NULL		is a type of	NULL				gastric cancer cell line	NULL	human			NULL		0	NULL	NULL	NULL	gw60_annurevmicrobiol_53_0_353_s_176	10547695	A membrane-bound 140-kDa   protein present in human gastric cancer cell lines (AZ-521 and AGS)   has been identified as a potential receptor for binding of VacA to   target cells because this protein was coimmunoprecipitated with   VacA by anti-VacA antibodies ( 177).	bind
41930	2	10895	6	NULL	NULL	0	NULL	AGS	NULL		is a type of	NULL				gastric cancer cell line	NULL	human			NULL		0	NULL	NULL	NULL	gw60_annurevmicrobiol_53_0_353_s_176	10547695	A membrane-bound 140-kDa   protein present in human gastric cancer cell lines (AZ-521 and AGS)   has been identified as a potential receptor for binding of VacA to   target cells because this protein was coimmunoprecipitated with   VacA by anti-VacA antibodies ( 177).	bind
41931	3	10895	6	NULL	NULL	0	NULL	VacA	NULL		bind	NULL				target cells	NULL				NULL		0	NULL	NULL	NULL	gw60_annurevmicrobiol_53_0_353_s_176	10547695	A membrane-bound 140-kDa   protein present in human gastric cancer cell lines (AZ-521 and AGS)   has been identified as a potential receptor for binding of VacA to   target cells because this protein was coimmunoprecipitated with   VacA by anti-VacA antibodies ( 177).	bind
41932	5	10895	6	10	NULL	0	NULL	statement 4	NULL		acts as a receptor for	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_53_0_353_s_176	10547695	A membrane-bound 140-kDa   protein present in human gastric cancer cell lines (AZ-521 and AGS)   has been identified as a potential receptor for binding of VacA to   target cells because this protein was coimmunoprecipitated with   VacA by anti-VacA antibodies ( 177).	bind
41933	6	10895	6	10	NULL	0	NULL	statement 4	NULL		is present in	NULL				AZ-521	NULL				NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_53_0_353_s_176	10547695	A membrane-bound 140-kDa   protein present in human gastric cancer cell lines (AZ-521 and AGS)   has been identified as a potential receptor for binding of VacA to   target cells because this protein was coimmunoprecipitated with   VacA by anti-VacA antibodies ( 177).	bind
41934	7	10895	6	10	NULL	0	NULL	statement 4	NULL		is present in	NULL				AGS	NULL				NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_53_0_353_s_176	10547695	A membrane-bound 140-kDa   protein present in human gastric cancer cell lines (AZ-521 and AGS)   has been identified as a potential receptor for binding of VacA to   target cells because this protein was coimmunoprecipitated with   VacA by anti-VacA antibodies ( 177).	bind
50473	4	10895	6	10	NULL	0	NULL	140-kDa protein	NULL		bind	NULL				membrane	NULL				NULL		0	NULL	NULL	NULL	gw60_annurevmicrobiol_53_0_353_s_176	10547695	A membrane-bound 140-kDa   protein present in human gastric cancer cell lines (AZ-521 and AGS)   has been identified as a potential receptor for binding of VacA to   target cells because this protein was coimmunoprecipitated with   VacA by anti-VacA antibodies ( 177).	bind
49943	2	10897	5	13	NULL	NULL	NULL	metabolite of acetaminophen	Chemical		bind		covalently			56 kDa selenium binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_280_1_501_s_255	8996234	A metabolite of acetaminophen covalently binds to the 56 kDa selenium binding protein.	bind
41935	1	10897	6	NULL	NULL	0	NULL	acetaminophen metabolite	NULL		bind	NULL	covalently			56 kDa selenium binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_280_1_501_s_255	8996234	A metabolite of acetaminophen covalently binds to the 56 kDa selenium binding protein.	bind
49944	1	10898	5	13	NULL	NULL	NULL	VEGF	GP		bind					VEGF receptor	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_arch-pharm-res_28_11_16350854_s_4	16350854	A methanol extract and organic solvent (n-hexane,  ethyl acetate, n-butanol, aqueous) fractions from Rubus coreanus were  examined for their inhibitory effects on VEGF binding to the VEGF receptor.	bind
41936	1	10898	6	NULL	NULL	0	NULL	VEGF	NULL		bind	NULL				VEGF receptor	NULL				NULL		0	NULL	NULL	NULL	abs-batch0550-0559_arch-pharm-res_28_11_16350854_s_4	16350854	A methanol extract and organic solvent (n-hexane,  ethyl acetate, n-butanol, aqueous) fractions from Rubus coreanus were  examined for their inhibitory effects on VEGF binding to the VEGF receptor.	bind
49945	1	10900	5	13	NULL	NULL	NULL	antimycin A	Chemical	methoxy derivative of 	bind					Bcl-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_115_10_2648_s_174	16200198	A methoxy derivative of antimycin A binds to Bcl-2 with a  Kd of 0.82 muM ( ).	bind
41937	1	10900	6	10	NULL	0	NULL	antimycin A 	NULL	methoxy derivative of 	bind	NULL				Bcl-2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_115_10_2648_s_174	16200198	A methoxy derivative of antimycin A binds to Bcl-2 with a  Kd of 0.82 muM ( ).	bind
49946	1	10901	5	13	NULL	NULL	NULL	copper transport proteins	GP		bind		selectively	Mets motif peptide		Cu(I)	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_inorg-chem_44_26_16363848_s_1	16363848	A Mets motif peptide found in copper transport proteins selectively binds Cu(I) with methionine-only coordination..	bind
41938	1	10901	6	NULL	NULL	0	NULL	copper transport protein	NULL		bind	NULL	selectively	Mets motif peptide		Cu(I)	NULL				NULL		0	NULL	NULL	NULL	abs-batch0550-0559_inorg-chem_44_26_16363848_s_1	16363848	A Mets motif peptide found in copper transport proteins selectively binds Cu(I) with methionine-only coordination..	bind
49947	1	10902	5	13	NULL	NULL	NULL	GTP	Chemical	non-exchangeable	bind								alpha-subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
49948	2	10902	5	13	NULL	NULL	NULL	Mg2+ ion	Chemical		coordinates with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
49949	3	10902	5	13	NULL	NULL	NULL	statement 2	Process		is located near								alpha-beta dimerization interface		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
49950	4	10902	5	13	NULL	NULL	NULL	statement 2	Process		controls					statement 1	Process	stability of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
49951	5	10902	5	13	NULL	NULL	NULL	cation	Chemical		bind								beta-subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
49952	6	10902	5	13	NULL	NULL	NULL	statement 5	Process		is located near								beta-alpha axial interface		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
49953	7	10902	5	13	NULL	NULL	NULL	statement 5	Process		leads to					protofilament	CellComponent	formation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
49954	8	10902	5	13	NULL	NULL	NULL	nucleotide	NucleicAcid	exchangeable	bind								beta-subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
49955	9	10902	5	13	NULL	NULL	NULL	statement 8	Process		is located near								beta-alpha axial interface		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
49956	10	10902	5	13	NULL	NULL	NULL	statement 8	Process		leads to					protofilament	CellComponent	formation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
49957	11	10902	5	13	NULL	NULL	NULL	statement 5	Process		controls					microtubule	CellComponent	stability of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
49958	12	10902	5	13	NULL	NULL	NULL	statement 8	Process		controls					microtubule 	CellComponent	stability of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
42062	1	10902	6	10	NULL	0	NULL	GTP		non-exchangeable	bind								alpha-subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
42063	2	10902	6	10	NULL	0	NULL	Mg2+ ion			is coordinated with					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
42064	3	10902	6	10	NULL	0	NULL	statement 1			controls					statement 1		stability of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
50816	4	10902	6	NULL	NULL	0	NULL	statement 2	NULL		occurs near	NULL				alpha-beta dimerization interface	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
50817	5	10902	6	NULL	NULL	0	NULL	beta-subunit	NULL		bind	NULL				nucleotide	NULL	exchangeable			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
50818	6	10902	6	NULL	NULL	0	NULL	cation	NULL		bind	NULL				beta-subunit	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
50819	7	10902	6	NULL	NULL	0	NULL	statement 5	NULL		leads to	NULL				protofilament 	NULL	formation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
50820	8	10902	6	NULL	NULL	0	NULL	statement 6	NULL		leads to	NULL				protofilament	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
50821	9	10902	6	NULL	NULL	0	NULL	statement 5	NULL		occurs near	NULL				beta-alpha axial interface	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
50822	10	10902	6	NULL	NULL	0	NULL	statement 6	NULL		occurs near	NULL				beta-alpha axial interface	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
58413	11	10902	6	10	NULL	0	NULL	statement 5			controls					microtubule		stability of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
58414	12	10902	6	10	NULL	0	NULL	statement 6			controls					microtubule		stability of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_50_33803_s_14	9837970	A Mg2+ ion coordinated with non-exchangeable GTP bound to the alpha-subunit near the alpha-beta dimerization interface controls the stability of the heterodimer ( 1), whereas the cation and exchangeable nucleotide bound to the beta-subunit, near the beta-alpha axial interface leading to protofilament formation ( 2) control microtubule stability.	bind
49959	1	10903	5	13	NULL	NULL	NULL	FAT10	GP		is a type of					MHC-encoded ubiquitin-like protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_18_5509_s_431	9312010	A MHC-encoded ubiquitin-like protein (FAT10) binds noncovalently to the spindle assembly checkpoint protein MAD2.	bind
49960	2	10903	5	13	NULL	NULL	NULL	MAD2	GP		is a type of					spindle assembly checkpoint protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_18_5509_s_431	9312010	A MHC-encoded ubiquitin-like protein (FAT10) binds noncovalently to the spindle assembly checkpoint protein MAD2.	bind
49961	3	10903	5	13	NULL	NULL	NULL	FAT10	GP		bind		noncovalently			MAD2	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_18_5509_s_431	9312010	A MHC-encoded ubiquitin-like protein (FAT10) binds noncovalently to the spindle assembly checkpoint protein MAD2.	bind
41939	1	10903	6	NULL	NULL	0	NULL	FAT10	NULL		is a type of	NULL				MHC-encoded ubiquitin-like protein	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_18_5509_s_431	9312010	A MHC-encoded ubiquitin-like protein (FAT10) binds noncovalently to the spindle assembly checkpoint protein MAD2.	bind
41940	2	10903	6	NULL	NULL	0	NULL	MAD2	NULL		is a type of	NULL				spindle assembly checkpoint protein	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_18_5509_s_431	9312010	A MHC-encoded ubiquitin-like protein (FAT10) binds noncovalently to the spindle assembly checkpoint protein MAD2.	bind
41941	3	10903	6	NULL	NULL	0	NULL	FAT10	NULL		bind	NULL	noncovalently			MAD2	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_18_5509_s_431	9312010	A MHC-encoded ubiquitin-like protein (FAT10) binds noncovalently to the spindle assembly checkpoint protein MAD2.	bind
50474	1	10905	5	13	NULL	NULL	NULL	IscU	GP		bind					Hsc20	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_14_7790_s_63	10869428	A Microcal (Amherst, MA) Omega titration calorimeter was used to investigate the binding of IscU and Hsc20 by using procedures described previously ( 27).	bind
41942	1	10905	6	NULL	NULL	0	NULL	IScU	NULL		bind	NULL				Hsc20	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_14_7790_s_63	10869428	A Microcal (Amherst, MA) Omega titration calorimeter was used to investigate the binding of IscU and Hsc20 by using procedures described previously ( 27).	bind
50476	1	10906	5	13	NULL	NULL	NULL	IscU protein	GP		bind					Hsc66	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37582_s_63	12871959	A Microcal Omega microcalorimeter (Amherst, MA) was used to investigate the binding of IscU proteins to Hsc66 and Hsc20.	bind
50477	2	10906	5	13	NULL	NULL	NULL	IscU protein	GP		bind					Hsc20	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37582_s_63	12871959	A Microcal Omega microcalorimeter (Amherst, MA) was used to investigate the binding of IscU proteins to Hsc66 and Hsc20.	bind
41945	2	10906	6	NULL	NULL	0	NULL	IscU protein	NULL		bind	NULL				Hsc20	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_39_37582_s_63	12871959	A Microcal Omega microcalorimeter (Amherst, MA) was used to investigate the binding of IscU proteins to Hsc66 and Hsc20.	bind
50475	1	10906	6	10	NULL	0	NULL	IscU protein	NULL		bind	NULL				Hsc66	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37582_s_63	12871959	A Microcal Omega microcalorimeter (Amherst, MA) was used to investigate the binding of IscU proteins to Hsc66 and Hsc20.	bind
49962	1	10907	5	13	NULL	NULL	NULL	GtfI	GP		bind			GBD		alpha-1,3 glucan	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_24_8301_s_7	15576779	A microplate binding assay was developed to measure the binding affinity of recombinant GBDs. GBD of GtfI was shown to be capable of binding glucans with predominantly alpha-1,3 or alpha-1,6 links, as well as alternating alpha-1,3 and alpha-1,6 links (alternan).	bind
49963	2	10907	5	13	NULL	NULL	NULL	GtfI	GP		bind			GBD		alpha-1,6 glucan	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_24_8301_s_7	15576779	A microplate binding assay was developed to measure the binding affinity of recombinant GBDs. GBD of GtfI was shown to be capable of binding glucans with predominantly alpha-1,3 or alpha-1,6 links, as well as alternating alpha-1,3 and alpha-1,6 links (alternan).	bind
42065	1	10907	6	NULL	NULL	0	NULL	GtfI	NULL		bind	NULL	predominantly	GBD		alpha-1,3-glucans	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_24_8301_s_7	15576779	A microplate binding assay was developed to measure the binding affinity of recombinant GBDs. GBD of GtfI was shown to be capable of binding glucans with predominantly alpha-1,3 or alpha-1,6 links, as well as alternating alpha-1,3 and alpha-1,6 links (alternan).	bind
42066	2	10907	6	NULL	NULL	0	NULL	GtfI	NULL		bind	NULL	predominantly	GBD		alpha-1,6 glucan	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_24_8301_s_7	15576779	A microplate binding assay was developed to measure the binding affinity of recombinant GBDs. GBD of GtfI was shown to be capable of binding glucans with predominantly alpha-1,3 or alpha-1,6 links, as well as alternating alpha-1,3 and alpha-1,6 links (alternan).	bind
49964	1	10911	5	13	NULL	NULL	NULL				shows			G519A		peripheral accumulation	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1506_s_111	15014437	A milder mutation at G519 (G519A rather than G519R) showed peripheral accumulation  and MT binding similar to that of G519R (data not shown).	bind
49965	2	10911	5	13	NULL	NULL	NULL				bind			G519A		MT	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1506_s_111	15014437	A milder mutation at G519 (G519A rather than G519R) showed peripheral accumulation  and MT binding similar to that of G519R (data not shown).	bind
49966	3	10911	5	13	NULL	NULL	NULL				shows			G519R		peripheral accumulation	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1506_s_111	15014437	A milder mutation at G519 (G519A rather than G519R) showed peripheral accumulation  and MT binding similar to that of G519R (data not shown).	bind
49967	4	10911	5	13	NULL	NULL	NULL				bind			G519R		MT	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1506_s_111	15014437	A milder mutation at G519 (G519A rather than G519R) showed peripheral accumulation  and MT binding similar to that of G519R (data not shown).	bind
41946	1	10911	6	NULL	NULL	0	NULL		NULL		bind	NULL		G519A		MT	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_23_7_1506_s_111	15014437	A milder mutation at G519 (G519A rather than G519R) showed peripheral accumulation  and MT binding similar to that of G519R (data not shown).	bind
41947	2	10911	6	NULL	NULL	0	NULL		NULL		shows	NULL		G519A		peripheral accumulation	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_23_7_1506_s_111	15014437	A milder mutation at G519 (G519A rather than G519R) showed peripheral accumulation  and MT binding similar to that of G519R (data not shown).	bind
41948	3	10911	6	NULL	NULL	0	NULL		NULL		bind	NULL		G519R		MT	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_23_7_1506_s_111	15014437	A milder mutation at G519 (G519A rather than G519R) showed peripheral accumulation  and MT binding similar to that of G519R (data not shown).	bind
41949	4	10911	6	NULL	NULL	0	NULL		NULL		shows	NULL		G519R		peripheral accumulation	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_23_7_1506_s_111	15014437	A milder mutation at G519 (G519A rather than G519R) showed peripheral accumulation  and MT binding similar to that of G519R (data not shown).	bind
49968	1	10912	5	13	NULL	NULL	NULL	tRNAiMet	NucleicAcid	yeast	forms complex with		stably	acceptor stem		LysRS	GP	mammalian			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1762_s_175	11706011	A minihelix corresponding to a noncognate tRNA, the acceptor stem of yeast tRNAiMet, also formed a stable complex with LysRS with an apparent  K d of 1 muM (not shown), further exemplifying the general RNA binding potency of mammalian LysRS.	bind
42067	1	10912	6	10	NULL	0	NULL	tRNAiMet	NULL	yeast	forms a complex with	NULL	stably	acceptor stem		LysRS	NULL	mammalian			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_1762_s_175	11706011	A minihelix corresponding to a noncognate tRNA, the acceptor stem of yeast tRNAiMet, also formed a stable complex with LysRS with an apparent  K d of 1 muM (not shown), further exemplifying the general RNA binding potency of mammalian LysRS.	bind
49969	1	10913	5	13	NULL	NULL	NULL	Dal80p dimer	GP		bind		may			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_21_5682_s_4	9791119	A minimal Gln3p binding site consists of a single GATA sequence, whereas a Dal80p binding site consists of two GATA sequences in specific orientation, 15 to 35 bp apart, suggesting that Dal80p may bind to DNA as a dimer.	bind
50478	2	10913	5	13	NULL	NULL	NULL	Dal80p	GP		consist of				binding site					two GATA sequences	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_21_5682_s_4	9791119	A minimal Gln3p binding site consists of a single GATA sequence, whereas a Dal80p binding site consists of two GATA sequences in specific orientation, 15 to 35 bp apart, suggesting that Dal80p may bind to DNA as a dimer.	bind
41950	1	10913	6	10	NULL	0	NULL	Dal80p dimer	NULL		bind	NULL	may			DNA	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_21_5682_s_4	9791119	A minimal Gln3p binding site consists of a single GATA sequence, whereas a Dal80p binding site consists of two GATA sequences in specific orientation, 15 to 35 bp apart, suggesting that Dal80p may bind to DNA as a dimer.	bind
50479	2	10913	6	10	NULL	0	NULL	Dal80p	NULL		consist of	NULL			binding site		NULL			two GATA sequences	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_21_5682_s_4	9791119	A minimal Gln3p binding site consists of a single GATA sequence, whereas a Dal80p binding site consists of two GATA sequences in specific orientation, 15 to 35 bp apart, suggesting that Dal80p may bind to DNA as a dimer.	bind
49970	1	10914	5	13	NULL	NULL	NULL	ATP	Chemical		bind					ArsA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_23_16153_s_98	10347168	A minimal value can be calculated for the second-order association rate constant for the binding of ATP to the ArsA from ( kmax +  kmin)/ K d, yielding a value of 0.34 x 106M 1 s 1.	bind
41951	1	10914	6	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				ArsA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_23_16153_s_98	10347168	A minimal value can be calculated for the second-order association rate constant for the binding of ATP to the ArsA from ( kmax +  kmin)/ K d, yielding a value of 0.34 x 106M 1 s 1.	bind
49971	1	10915	5	13	NULL	NULL	NULL	C3d	GP		enhances			CR2 binding domain		immunity	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_adv-exp-med-biol_586_1_16893077_s_1	16893077	A minimum CR2 binding domain of C3d enhances immunity following vaccination..	bind
49972	2	10915	5	13	NULL	NULL	NULL	statement 1	Process		occurs following					vaccination	MedicalProcedure				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_adv-exp-med-biol_586_1_16893077_s_1	16893077	A minimum CR2 binding domain of C3d enhances immunity following vaccination..	bind
41952	1	10915	6	NULL	NULL	0	NULL	C3d	NULL		enhances	NULL		CR2 binding domain		immunity	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_adv-exp-med-biol_586_1_16893077_s_1	16893077	A minimum CR2 binding domain of C3d enhances immunity following vaccination..	bind
49973	1	10918	5	13	NULL	NULL	NULL	heparin	Chemical		bind					PF4	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_50_0_129_s_85	10073268	A minimum of 12 saccharide units ( 28), a minimum degree of sulfation ( 16,  29), and an optimal binding ratio of heparin and PF4 are required to form the HIT antigen  ( 30).	bind
41954	1	10918	6	NULL	NULL	0	NULL	heparin	NULL		bind	NULL				PF4	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevmed_50_0_129_s_85	10073268	A minimum of 12 saccharide units ( 28), a minimum degree of sulfation ( 16,  29), and an optimal binding ratio of heparin and PF4 are required to form the HIT antigen  ( 30).	bind
49974	1	10919	5	13	NULL	NULL	NULL	proteins	GP		is expressed in					retina	OrganismPart	Drosophila			NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_231_s_377	10611962	A minimum of 13 proteins expressed in the Drosophila retina bind directly to calmodulin.	bind
49975	2	10919	5	13	NULL	NULL	NULL	statement 1	GP		bind		directly			calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_231_s_377	10611962	A minimum of 13 proteins expressed in the Drosophila retina bind directly to calmodulin.	bind
41956	1	10919	6	NULL	NULL	0	NULL	proteins	NULL		expressed in	NULL				retina	NULL	Drosophila			NULL		0	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_231_s_377	10611962	A minimum of 13 proteins expressed in the Drosophila retina bind directly to calmodulin.	bind
41957	2	10919	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL	directly			calmodulin	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevcelldevbiol_15_0_231_s_377	10611962	A minimum of 13 proteins expressed in the Drosophila retina bind directly to calmodulin.	bind
49976	1	10920	5	13	NULL	NULL	NULL	gp120JR-FL/CD4 complex	GP	soluble	bind					CCR5	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_11_5762_s_158	10823934	A minimum of two sulfotyrosines in positions 10 and 14 were required for efficient inhibition of soluble gp120JR-FL/CD4 complex binding to CCR5.	bind
49977	2	10920	5	13	NULL	NULL	NULL				inhibit		effectively	sulfotyrosines in positions 10 and 14		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_11_5762_s_158	10823934	A minimum of two sulfotyrosines in positions 10 and 14 were required for efficient inhibition of soluble gp120JR-FL/CD4 complex binding to CCR5.	bind
41958	1	10920	6	NULL	NULL	0	NULL	gp120JR-FL/CD4 complex	NULL	soluble	bind	NULL				CCR5	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_11_5762_s_158	10823934	A minimum of two sulfotyrosines in positions 10 and 14 were required for efficient inhibition of soluble gp120JR-FL/CD4 complex binding to CCR5.	bind
41959	2	10920	6	NULL	NULL	0	NULL		NULL		are required for	NULL		two sulfotyrosines in positions 10 and 14		statement 1	NULL	inhibiton of			NULL		0	NULL	NULL	NULL	gw60_pnas_97_11_5762_s_158	10823934	A minimum of two sulfotyrosines in positions 10 and 14 were required for efficient inhibition of soluble gp120JR-FL/CD4 complex binding to CCR5.	bind
49978	1	10921	5	13	NULL	NULL	NULL	NTPi	NucleicAcid		is					initiating nucleotide	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
49979	2	10921	5	13	NULL	NULL	NULL	NTPi+1	Chemical		is					first NTP substrate	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
49980	3	10921	5	13	NULL	NULL	NULL	NTPi	NucleicAcid		bind								P-site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
49981	4	10921	5	13	NULL	NULL	NULL	NTPi+1	Chemical		bind								N-site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
49982	5	10921	5	13	NULL	NULL	NULL	BVDV	Organism		initiates					RNA	NucleicAcid	de novo synthesis of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
49983	6	10921	5	13	NULL	NULL	NULL	HCV RdRps	GP		initiates					RNA	NucleicAcid	de novo synthesis of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
49984	7	10921	5	13	NULL	NULL	NULL	statement 5	Process		involves					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
49985	8	10921	5	13	NULL	NULL	NULL	statement 5	Process		involves					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
49986	9	10921	5	13	NULL	NULL	NULL	statement 6	Process		involves					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
49987	10	10921	5	13	NULL	NULL	NULL	statement 6	Process		involves					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
41960	1	10921	6	NULL	NULL	0	NULL	NTPi	NULL		is	NULL				initiating nucleotide	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
41962	2	10921	6	NULL	NULL	0	NULL	NTPi+1	NULL		is	NULL				first NTP substrate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
41963	3	10921	6	NULL	NULL	0	NULL	NTPi	NULL		bind	NULL					NULL		P-site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
41964	4	10921	6	NULL	NULL	0	NULL	NTPi+1	NULL		bind	NULL					NULL		N-site		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
41966	5	10921	6	NULL	NULL	0	NULL	BVDV	NULL		initiates	NULL				RNA	NULL	de novo synthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
41968	6	10921	6	NULL	NULL	0	NULL	HCV RdRps	NULL		initiates	NULL				RNA	NULL	de novo synthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
41970	7	10921	6	NULL	NULL	0	NULL	statement 5	NULL		requires	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
41971	8	10921	6	NULL	NULL	0	NULL	statement 5	NULL		requires	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
41973	9	10921	6	NULL	NULL	0	NULL	statement 6	NULL		requires	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
41974	10	10921	6	NULL	NULL	0	NULL	statement 6	NULL		requires	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24991_s_173	16831816	A minimum requirement for  de novo initiation of RNA synthesis by BVDV and HCV RdRps involves binding of the initiating nucleotide (NTPi) to the P-site and binding of the first NTP substrate (NTPi+1) to the N-site.	bind
49988	1	10922	5	13	NULL	NULL	NULL	Msbp-4	GP		is a type of					minisatellite-binding protein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_267_17_1601895_s_2	1601895	A minisatellite-binding protein, Msbp-4, with a molecular mass of 35 kDa  has been purified from mouse tumor cells that binds to hypervariable Pc-1  and Pc-2 minisatellites.	bind
49989	2	10922	5	13	NULL	NULL	NULL	Pc-1	NucleicAcid		is a type of					hypervariable minisatellite	NucleicAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_267_17_1601895_s_2	1601895	A minisatellite-binding protein, Msbp-4, with a molecular mass of 35 kDa  has been purified from mouse tumor cells that binds to hypervariable Pc-1  and Pc-2 minisatellites.	bind
49990	3	10922	5	13	NULL	NULL	NULL	Pc-2	NucleicAcid		is a type of					hypervariable minisatellite	NucleicAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_267_17_1601895_s_2	1601895	A minisatellite-binding protein, Msbp-4, with a molecular mass of 35 kDa  has been purified from mouse tumor cells that binds to hypervariable Pc-1  and Pc-2 minisatellites.	bind
49991	4	10922	5	13	NULL	NULL	NULL	Msbp-4	GP		bind					Pc-1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_267_17_1601895_s_2	1601895	A minisatellite-binding protein, Msbp-4, with a molecular mass of 35 kDa  has been purified from mouse tumor cells that binds to hypervariable Pc-1  and Pc-2 minisatellites.	bind
49992	5	10922	5	13	NULL	NULL	NULL	Msbp-4	GP		bind					Pc-2	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_267_17_1601895_s_2	1601895	A minisatellite-binding protein, Msbp-4, with a molecular mass of 35 kDa  has been purified from mouse tumor cells that binds to hypervariable Pc-1  and Pc-2 minisatellites.	bind
41976	1	10922	6	NULL	NULL	0	NULL	Msbp-4	NULL		is a type of	NULL				minisatellite-binding protein	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_267_17_1601895_s_2	1601895	A minisatellite-binding protein, Msbp-4, with a molecular mass of 35 kDa  has been purified from mouse tumor cells that binds to hypervariable Pc-1  and Pc-2 minisatellites.	bind
41977	2	10922	6	NULL	NULL	0	NULL	Msbp-4	NULL		bind	NULL				Pc-1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_267_17_1601895_s_2	1601895	A minisatellite-binding protein, Msbp-4, with a molecular mass of 35 kDa  has been purified from mouse tumor cells that binds to hypervariable Pc-1  and Pc-2 minisatellites.	bind
41978	3	10922	6	NULL	NULL	0	NULL	Msbp-4	NULL		bind	NULL				Pc-2	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_267_17_1601895_s_2	1601895	A minisatellite-binding protein, Msbp-4, with a molecular mass of 35 kDa  has been purified from mouse tumor cells that binds to hypervariable Pc-1  and Pc-2 minisatellites.	bind
41979	4	10922	6	NULL	NULL	0	NULL	Pc-1	NULL		is a type of	NULL				hypervariable minisatellite	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_267_17_1601895_s_2	1601895	A minisatellite-binding protein, Msbp-4, with a molecular mass of 35 kDa  has been purified from mouse tumor cells that binds to hypervariable Pc-1  and Pc-2 minisatellites.	bind
41980	5	10922	6	NULL	NULL	0	NULL	Pc-2	NULL		is a type of	NULL				hypervariable minisatellite	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_267_17_1601895_s_2	1601895	A minisatellite-binding protein, Msbp-4, with a molecular mass of 35 kDa  has been purified from mouse tumor cells that binds to hypervariable Pc-1  and Pc-2 minisatellites.	bind
49993	1	10923	5	13	NULL	NULL	NULL	GST-GluR2	GP		bind					SAP97	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_31_19518_s_244	9677374	A minor amount of GST-GluR2 bound to SAP97 (Fig.  5,  lane 2), but GST-GluR2 binding was hardly detectable.	bind
41995	1	10923	6	NULL	NULL	0	NULL	GST-GluR2	NULL		bind	NULL				SAP97	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_31_19518_s_244	9677374	A minor amount of GST-GluR2 bound to SAP97 (Fig.  5,  lane 2), but GST-GluR2 binding was hardly detectable.	bind
49995	1	10925	5	13	NULL	NULL	NULL	PE2I	GP		bind					SERT	GP				NULL	cerebral area	NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_291_2_648_s_196	10525084	A minor binding of PE2I to the SERT can therefore not be excluded in this cerebral area.	bind
42007	1	10925	6	NULL	NULL	0	NULL	PE2I	NULL		bind	NULL				SERT	NULL				NULL	cerebral area	0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_2_648_s_196	10525084	A minor binding of PE2I to the SERT can therefore not be excluded in this cerebral area.	bind
49996	1	10926	5	13	NULL	NULL	NULL	minor protein	GP		is present in					type 1 fimbriae	CellComponent	tip of			NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_50_0_513_s_289	8905090	A minor protein at the tip of the type 1 fimbriae  possibly mediates the binding of  A. naeslundii T14V to  salivary proline-rich proteins ( 162).	bind
49997	2	10926	5	13	NULL	NULL	NULL			A. naeslundii	bind			T14V		proline-rich proteins	GP	salivary			NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_50_0_513_s_289	8905090	A minor protein at the tip of the type 1 fimbriae  possibly mediates the binding of  A. naeslundii T14V to  salivary proline-rich proteins ( 162).	bind
49998	3	10926	5	13	NULL	NULL	NULL	statement 1	Process		mediate		possibly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_50_0_513_s_289	8905090	A minor protein at the tip of the type 1 fimbriae  possibly mediates the binding of  A. naeslundii T14V to  salivary proline-rich proteins ( 162).	bind
42008	1	10926	6	NULL	NULL	0	NULL		NULL	A. naeslundii	bind	NULL		T14V		proline-rich proteins	NULL	salivary			NULL		0	NULL	NULL	NULL	gw60_annurevmicrobiol_50_0_513_s_289	8905090	A minor protein at the tip of the type 1 fimbriae  possibly mediates the binding of  A. naeslundii T14V to  salivary proline-rich proteins ( 162).	bind
42009	2	10926	6	10	NULL	0	NULL	minor protein	NULL		is present at	NULL				 type 1 fimbriae	NULL	tip of 			NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_50_0_513_s_289	8905090	A minor protein at the tip of the type 1 fimbriae  possibly mediates the binding of  A. naeslundii T14V to  salivary proline-rich proteins ( 162).	bind
42010	3	10926	6	10	NULL	0	NULL	statement 2			mediates		possibly			statement 1					NULL		NULL	NULL	NULL	NULL	gw60_annurevmicrobiol_50_0_513_s_289	8905090	A minor protein at the tip of the type 1 fimbriae  possibly mediates the binding of  A. naeslundii T14V to  salivary proline-rich proteins ( 162).	bind
50013	1	10927	5	13	NULL	NULL	NULL	colicin E9	GP		is a type of					DNase	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_3_1286_s_174	11830660	A mismatch of the binding site on only one of the two helices, as occurs when colicin E9 DNase binds to the noncognate ImmE2, causes the binding constant to fall by six orders of magnitude ( 23).	bind
50014	2	10927	5	13	NULL	NULL	NULL	colicin E9	GP		bind					ImmE2	GP	noncognate			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_3_1286_s_174	11830660	A mismatch of the binding site on only one of the two helices, as occurs when colicin E9 DNase binds to the noncognate ImmE2, causes the binding constant to fall by six orders of magnitude ( 23).	bind
42011	1	10927	6	10	NULL	0	NULL	colicin E9	NULL		bind	NULL				ImmE2	NULL	noncognate 			NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_3_1286_s_174	11830660	A mismatch of the binding site on only one of the two helices, as occurs when colicin E9 DNase binds to the noncognate ImmE2, causes the binding constant to fall by six orders of magnitude ( 23).	bind
42012	2	10927	6	NULL	NULL	0	NULL	colicin E9	NULL		is a type of	NULL				DNase	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_3_1286_s_174	11830660	A mismatch of the binding site on only one of the two helices, as occurs when colicin E9 DNase binds to the noncognate ImmE2, causes the binding constant to fall by six orders of magnitude ( 23).	bind
50015	1	10929	5	13	NULL	NULL	NULL	Ena	GP		bind					zyxin	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molbiolcell_9_8_2157_s_7	9693373	A missense mutation that resulted in an amino acid substitution in the EVH1 domain eliminated in vitro binding of Ena to the cytoskeletal protein zyxin, a previously reported binding partner of VASP.	bind
50016	2	10929	5	13	NULL	NULL	NULL	zyxin	GP		is a type of					cytoskeletal protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_8_2157_s_7	9693373	A missense mutation that resulted in an amino acid substitution in the EVH1 domain eliminated in vitro binding of Ena to the cytoskeletal protein zyxin, a previously reported binding partner of VASP.	bind
50017	3	10929	5	13	NULL	NULL	NULL	zyxin	GP		bind					VASP	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_8_2157_s_7	9693373	A missense mutation that resulted in an amino acid substitution in the EVH1 domain eliminated in vitro binding of Ena to the cytoskeletal protein zyxin, a previously reported binding partner of VASP.	bind
50018	4	10929	5	13	NULL	NULL	NULL			missense mutation in	eliminates			EVH1 domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_8_2157_s_7	9693373	A missense mutation that resulted in an amino acid substitution in the EVH1 domain eliminated in vitro binding of Ena to the cytoskeletal protein zyxin, a previously reported binding partner of VASP.	bind
42013	1	10929	6	NULL	NULL	0	NULL	Ena	NULL		bind	NULL				zyxin	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_molbiolcell_9_8_2157_s_7	9693373	A missense mutation that resulted in an amino acid substitution in the EVH1 domain eliminated in vitro binding of Ena to the cytoskeletal protein zyxin, a previously reported binding partner of VASP.	bind
42014	2	10929	6	NULL	NULL	0	NULL	zyxin	NULL		is a type of	NULL				cytoskeletal protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_8_2157_s_7	9693373	A missense mutation that resulted in an amino acid substitution in the EVH1 domain eliminated in vitro binding of Ena to the cytoskeletal protein zyxin, a previously reported binding partner of VASP.	bind
42015	3	10929	6	NULL	NULL	0	NULL	zyxin	NULL		bind	NULL				VASP	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_8_2157_s_7	9693373	A missense mutation that resulted in an amino acid substitution in the EVH1 domain eliminated in vitro binding of Ena to the cytoskeletal protein zyxin, a previously reported binding partner of VASP.	bind
42016	4	10929	6	NULL	NULL	0	NULL		NULL	mutant	eliminates	NULL		EVH1 domain		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_8_2157_s_7	9693373	A missense mutation that resulted in an amino acid substitution in the EVH1 domain eliminated in vitro binding of Ena to the cytoskeletal protein zyxin, a previously reported binding partner of VASP.	bind
50019	1	10930	5	13	NULL	NULL	NULL	RBP16	GP		is a type of					mitochondrial Y-box protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_7010_s_331	11564883	A mitochondrial Y-box protein in  Trypanosoma brucei, RBP16, which binds guide RNAs (gRNAs) specifically in vitro, has been shown to interact with gRNAs in vivo ( 28).	bind
50020	2	10930	5	13	NULL	NULL	NULL	RBP16	GP	Trypanosoma brucei	bind		specifically			gRNAs	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_7010_s_331	11564883	A mitochondrial Y-box protein in  Trypanosoma brucei, RBP16, which binds guide RNAs (gRNAs) specifically in vitro, has been shown to interact with gRNAs in vivo ( 28).	bind
50021	3	10930	5	13	NULL	NULL	NULL	RBP16	GP	Trypanosoma brucei	interacts with					gRNAs	NucleicAcid				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_7010_s_331	11564883	A mitochondrial Y-box protein in  Trypanosoma brucei, RBP16, which binds guide RNAs (gRNAs) specifically in vitro, has been shown to interact with gRNAs in vivo ( 28).	bind
50022	4	10930	5	13	NULL	NULL	NULL	gRNAs	NucleicAcid		is					guide RNAs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_7010_s_331	11564883	A mitochondrial Y-box protein in  Trypanosoma brucei, RBP16, which binds guide RNAs (gRNAs) specifically in vitro, has been shown to interact with gRNAs in vivo ( 28).	bind
42017	1	10930	6	NULL	NULL	0	NULL	RBP16	NULL		is a type of	NULL				mitochondrial Y-box protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_20_7010_s_331	11564883	A mitochondrial Y-box protein in  Trypanosoma brucei, RBP16, which binds guide RNAs (gRNAs) specifically in vitro, has been shown to interact with gRNAs in vivo ( 28).	bind
42018	2	10930	6	NULL	NULL	0	NULL	gRNA	NULL		is	NULL				guide RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_20_7010_s_331	11564883	A mitochondrial Y-box protein in  Trypanosoma brucei, RBP16, which binds guide RNAs (gRNAs) specifically in vitro, has been shown to interact with gRNAs in vivo ( 28).	bind
42019	3	10930	6	NULL	NULL	0	NULL	RBP16	NULL	Trypanosoma brucei	bind	NULL	specifically			gRNA	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_7010_s_331	11564883	A mitochondrial Y-box protein in  Trypanosoma brucei, RBP16, which binds guide RNAs (gRNAs) specifically in vitro, has been shown to interact with gRNAs in vivo ( 28).	bind
42020	4	10930	6	NULL	NULL	0	NULL	RBP16	NULL	Trypanosoma brucei	bind	NULL	specifically			gRNA	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_molcellbiol_21_20_7010_s_331	11564883	A mitochondrial Y-box protein in  Trypanosoma brucei, RBP16, which binds guide RNAs (gRNAs) specifically in vitro, has been shown to interact with gRNAs in vivo ( 28).	bind
50023	1	10931	5	13	NULL	NULL	NULL	mitogen	Chemical		activates					Protein Kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_699	9819386	A Mitogen-activated Protein Kinase-dependent Signaling Pathway in the Activation of Platelet Integrin alpha IIbbeta 3.	bind
50024	2	10931	5	13	NULL	NULL	NULL	signaling pathway	Process		depends on					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_699	9819386	A Mitogen-activated Protein Kinase-dependent Signaling Pathway in the Activation of Platelet Integrin alpha IIbbeta 3.	bind
50025	3	10931	5	13	NULL	NULL	NULL	statement 2	Process		activates					Integrin alpha IIbbeta 3	GP	platelet			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_699	9819386	A Mitogen-activated Protein Kinase-dependent Signaling Pathway in the Activation of Platelet Integrin alpha IIbbeta 3.	bind
42021	1	10931	6	10	NULL	0	NULL	Mitogen	NULL		activates	NULL				Protein Kinase	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_699	9819386	A Mitogen-activated Protein Kinase-dependent Signaling Pathway in the Activation of Platelet Integrin alpha IIbbeta 3.	bind
42022	2	10931	6	10	NULL	0	NULL	signaling pathway	NULL		depends on	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_699	9819386	A Mitogen-activated Protein Kinase-dependent Signaling Pathway in the Activation of Platelet Integrin alpha IIbbeta 3.	bind
50480	3	10931	6	10	NULL	0	NULL	statement 2	NULL		activates	NULL				Integrin alpha IIbbeta 3	NULL	platelet			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_699	9819386	A Mitogen-activated Protein Kinase-dependent Signaling Pathway in the Activation of Platelet Integrin alpha IIbbeta 3.	bind
50026	1	10932	5	13	NULL	NULL	NULL	mitotic kinesin-related protein	GP		bind					PP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5600_s_266	7890679	A Mitotic Kinesin-related Protein That Binds PP1.	bind
42023	1	10932	6	10	NULL	0	NULL	Mitotic Kinesin-related Protein	NULL		bind	NULL				PP1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_10_5600_s_266	7890679	A Mitotic Kinesin-related Protein That Binds PP1.	bind
50027	1	10933	5	13	NULL	NULL	NULL	aminopeptidase	GP	Manduca sexta	mixed with					alkaline phosphatase	GP				NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_97_s_513	11719073	A mixture of  Manduca sexta aminopeptidase and alkaline phosphatase enhances  Bacillus thuringiensis insecticidal Cry1A(c) toxin binding and 86Rb+-K+ leakage in vitro.	bind
50028	2	10933	5	13	NULL	NULL	NULL	statement 1	Process		enhances					Cry1A(c)	Chemical	Bacillus thuringiensis;;binding of			NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_97_s_513	11719073	A mixture of  Manduca sexta aminopeptidase and alkaline phosphatase enhances  Bacillus thuringiensis insecticidal Cry1A(c) toxin binding and 86Rb+-K+ leakage in vitro.	bind
50029	3	10933	5	13	NULL	NULL	NULL	Cry1A(c)	Chemical		is a type of					insecticidal toxin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_97_s_513	11719073	A mixture of  Manduca sexta aminopeptidase and alkaline phosphatase enhances  Bacillus thuringiensis insecticidal Cry1A(c) toxin binding and 86Rb+-K+ leakage in vitro.	bind
50030	4	10933	5	13	NULL	NULL	NULL	statement 1	Process		enhances					Rb+-K+	Chemical	leakage of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_97_s_513	11719073	A mixture of  Manduca sexta aminopeptidase and alkaline phosphatase enhances  Bacillus thuringiensis insecticidal Cry1A(c) toxin binding and 86Rb+-K+ leakage in vitro.	bind
42024	1	10933	6	NULL	NULL	0	NULL	aminopeptidase	NULL	Manduca sexta	forms a mixture with	NULL				alkaline phosphatase	NULL				NULL		0	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_97_s_513	11719073	A mixture of  Manduca sexta aminopeptidase and alkaline phosphatase enhances  Bacillus thuringiensis insecticidal Cry1A(c) toxin binding and 86Rb+-K+ leakage in vitro.	bind
42025	2	10933	6	NULL	NULL	0	NULL	statement 1	NULL		enhances	NULL				Rb+-K+	NULL	leakage of			NULL	in vitro	0	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_97_s_513	11719073	A mixture of  Manduca sexta aminopeptidase and alkaline phosphatase enhances  Bacillus thuringiensis insecticidal Cry1A(c) toxin binding and 86Rb+-K+ leakage in vitro.	bind
42026	3	10933	6	NULL	NULL	0	NULL	statement 1	NULL		enhances	NULL				Cry1A(c)	NULL	Bacillus thuringiensis;; binding of 			NULL		0	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_97_s_513	11719073	A mixture of  Manduca sexta aminopeptidase and alkaline phosphatase enhances  Bacillus thuringiensis insecticidal Cry1A(c) toxin binding and 86Rb+-K+ leakage in vitro.	bind
42027	4	10933	6	NULL	NULL	0	NULL	Cry1A(c)	NULL		is a type of	NULL				insecticidal toxin	NULL				NULL		0	NULL	NULL	NULL	gw60_insectbiochemmolbiol_32_1_97_s_513	11719073	A mixture of  Manduca sexta aminopeptidase and alkaline phosphatase enhances  Bacillus thuringiensis insecticidal Cry1A(c) toxin binding and 86Rb+-K+ leakage in vitro.	bind
50031	1	10934	5	13	NULL	NULL	NULL	aminopeptidase	GP	Manduca sexta	mixed with					phosphatase	GP				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_8_2995_s_526	9687463	A mixture of  Manduca sexta aminopeptidase and phosphatase enhances  Bacillus thuringiensis insecticidal Cry1A(c) toxin binding and 86Rb + efflux  in vitro.	bind
50032	2	10934	5	13	NULL	NULL	NULL	statement 1	Process		enhances					Cry1A(c)	Chemical	Bacillus thuringiensis;;binding of			NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_8_2995_s_526	9687463	A mixture of  Manduca sexta aminopeptidase and phosphatase enhances  Bacillus thuringiensis insecticidal Cry1A(c) toxin binding and 86Rb + efflux  in vitro.	bind
50033	3	10934	5	13	NULL	NULL	NULL	Cry1A(c)	Chemical		is a type of					insecticidal toxin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_8_2995_s_526	9687463	A mixture of  Manduca sexta aminopeptidase and phosphatase enhances  Bacillus thuringiensis insecticidal Cry1A(c) toxin binding and 86Rb + efflux  in vitro.	bind
50034	4	10934	5	13	NULL	NULL	NULL	statement 1	Process		enhances					Rb + efflux	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_applenvironmicrob_64_8_2995_s_526	9687463	A mixture of  Manduca sexta aminopeptidase and phosphatase enhances  Bacillus thuringiensis insecticidal Cry1A(c) toxin binding and 86Rb + efflux  in vitro.	bind
50035	1	10937	5	13	NULL	NULL	NULL	GST-EBP50	GP		bind					ezrin	GP		N-ERMAD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7621_s_233	11106646	A mixture of the two N-ERMADs used is shown in  lane L. B, competitive binding of GST-EBP50 ( EBP) and ezrin C-ERMAD ( EzC) or merlin C-ERMAD ( MrC) to ezrin N-ERMAD beads.	bind
50036	2	10937	5	13	NULL	NULL	NULL	ezrin	GP		bind			C-ERMAD		ezrin	GP		N-ERMAD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7621_s_233	11106646	A mixture of the two N-ERMADs used is shown in  lane L. B, competitive binding of GST-EBP50 ( EBP) and ezrin C-ERMAD ( EzC) or merlin C-ERMAD ( MrC) to ezrin N-ERMAD beads.	bind
50037	3	10937	5	13	NULL	NULL	NULL	merlin	GP		bind			C-ERMAD		ezrin	GP		N-ERMAD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7621_s_233	11106646	A mixture of the two N-ERMADs used is shown in  lane L. B, competitive binding of GST-EBP50 ( EBP) and ezrin C-ERMAD ( EzC) or merlin C-ERMAD ( MrC) to ezrin N-ERMAD beads.	bind
50038	4	10937	5	13	NULL	NULL	NULL	statement 1	Process		competes with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7621_s_233	11106646	A mixture of the two N-ERMADs used is shown in  lane L. B, competitive binding of GST-EBP50 ( EBP) and ezrin C-ERMAD ( EzC) or merlin C-ERMAD ( MrC) to ezrin N-ERMAD beads.	bind
50039	5	10937	5	13	NULL	NULL	NULL	statement 1	Process		competes with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7621_s_233	11106646	A mixture of the two N-ERMADs used is shown in  lane L. B, competitive binding of GST-EBP50 ( EBP) and ezrin C-ERMAD ( EzC) or merlin C-ERMAD ( MrC) to ezrin N-ERMAD beads.	bind
42068	1	10937	6	NULL	NULL	0	NULL	GST-EBP50	NULL		bind	NULL				ezrin	NULL		N-ERMAD		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_10_7621_s_233	11106646	A mixture of the two N-ERMADs used is shown in  lane L. B, competitive binding of GST-EBP50 ( EBP) and ezrin C-ERMAD ( EzC) or merlin C-ERMAD ( MrC) to ezrin N-ERMAD beads.	bind
42069	2	10937	6	NULL	NULL	0	NULL	ezrin	NULL		bind	NULL		C-ERMAD		ezrin	NULL		N-ERMAD		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_10_7621_s_233	11106646	A mixture of the two N-ERMADs used is shown in  lane L. B, competitive binding of GST-EBP50 ( EBP) and ezrin C-ERMAD ( EzC) or merlin C-ERMAD ( MrC) to ezrin N-ERMAD beads.	bind
42070	3	10937	6	NULL	NULL	0	NULL	statement 1	NULL		competes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_10_7621_s_233	11106646	A mixture of the two N-ERMADs used is shown in  lane L. B, competitive binding of GST-EBP50 ( EBP) and ezrin C-ERMAD ( EzC) or merlin C-ERMAD ( MrC) to ezrin N-ERMAD beads.	bind
42071	4	10937	6	NULL	NULL	0	NULL	merlin	NULL		bind	NULL		C-ERMAD		ezrin	NULL		N-ERMAD		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_10_7621_s_233	11106646	A mixture of the two N-ERMADs used is shown in  lane L. B, competitive binding of GST-EBP50 ( EBP) and ezrin C-ERMAD ( EzC) or merlin C-ERMAD ( MrC) to ezrin N-ERMAD beads.	bind
42072	5	10937	6	NULL	NULL	0	NULL	statement 1	NULL		competes	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_10_7621_s_233	11106646	A mixture of the two N-ERMADs used is shown in  lane L. B, competitive binding of GST-EBP50 ( EBP) and ezrin C-ERMAD ( EzC) or merlin C-ERMAD ( MrC) to ezrin N-ERMAD beads.	bind
50040	1	10939	5	13	NULL	NULL	NULL	Gal4p	GP		bind					episomal DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7612_s_183	10713069	A MN cleavage site with very similar characteristic has been recently described in the case of Gal4p binding to episomal DNA ( 43).	bind
42028	1	10939	6	NULL	NULL	0	NULL	Gal4p	NULL		bind	NULL				episomal DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_11_7612_s_183	10713069	A MN cleavage site with very similar characteristic has been recently described in the case of Gal4p binding to episomal DNA ( 43).	bind
50041	1	10941	5	13	NULL	NULL	NULL	TLF	GP		mediates					trypanosomes	Organism	lysis of			NULL		NULL	NULL	NULL	NULL	gw70_clinmicrobiolrev_12_1_112_s_162	9880477	A model ( ) has been proposed which recognizes three phases in the process of TLF-mediated lysis of trypanosomes: (i) binding of TLF to a trypanosome receptor, (ii) internalization by endocytosis, and (iii) lysosomal targeting.	bind
50042	2	10941	5	13	NULL	NULL	NULL	TLF	GP		bind					trypanosome receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_clinmicrobiolrev_12_1_112_s_162	9880477	A model ( ) has been proposed which recognizes three phases in the process of TLF-mediated lysis of trypanosomes: (i) binding of TLF to a trypanosome receptor, (ii) internalization by endocytosis, and (iii) lysosomal targeting.	bind
42029	1	10941	6	NULL	NULL	0	NULL	TLF	NULL		bind	NULL				trypanosome receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_clinmicrobiolrev_12_1_112_s_162	9880477	A model ( ) has been proposed which recognizes three phases in the process of TLF-mediated lysis of trypanosomes: (i) binding of TLF to a trypanosome receptor, (ii) internalization by endocytosis, and (iii) lysosomal targeting.	bind
50481	2	10941	6	10	NULL	0	NULL	TLF	NULL		mediates	NULL				trypanosomes	NULL	lysis of			NULL		0	NULL	NULL	NULL	gw70_clinmicrobiolrev_12_1_112_s_162	9880477	A model ( ) has been proposed which recognizes three phases in the process of TLF-mediated lysis of trypanosomes: (i) binding of TLF to a trypanosome receptor, (ii) internalization by endocytosis, and (iii) lysosomal targeting.	bind
50043	1	10943	5	13	NULL	NULL	NULL	PICK1	GP		bind					GluR2	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_52_18212_s_17	15608060	A model based on these findings proposes that PICK1 binds GluR2 after protein kinase C-mediated phosphorylation at Ser-880.	bind
50044	2	10943	5	13	NULL	NULL	NULL	protein kinase C	GP		mediates							phosphorylation	Ser-880		NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_52_18212_s_17	15608060	A model based on these findings proposes that PICK1 binds GluR2 after protein kinase C-mediated phosphorylation at Ser-880.	bind
50045	3	10943	5	13	NULL	NULL	NULL	statement 1	Process		occurs after					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_52_18212_s_17	15608060	A model based on these findings proposes that PICK1 binds GluR2 after protein kinase C-mediated phosphorylation at Ser-880.	bind
42030	1	10943	6	NULL	NULL	0	NULL	PICK1	NULL		bind	NULL				GluR2	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_52_18212_s_17	15608060	A model based on these findings proposes that PICK1 binds GluR2 after protein kinase C-mediated phosphorylation at Ser-880.	bind
42031	2	10943	6	NULL	NULL	0	NULL	protein kinase C	NULL		mediates	NULL					NULL	phosphorylation at	Ser-880		NULL		0	NULL	NULL	NULL	gw70_pnas_101_52_18212_s_17	15608060	A model based on these findings proposes that PICK1 binds GluR2 after protein kinase C-mediated phosphorylation at Ser-880.	bind
42032	3	10943	6	NULL	NULL	0	NULL	statement 1	NULL		occurs after	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_52_18212_s_17	15608060	A model based on these findings proposes that PICK1 binds GluR2 after protein kinase C-mediated phosphorylation at Ser-880.	bind
50046	1	10944	5	13	NULL	NULL	NULL	adducin tails	GP		bind					actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_7986_s_134	8626479	A model depicting binding  of adducin tails to actin and capping the barbed end of the actin  filament by adducin heads is shown in  Fig. 5 .	bind
50047	2	10944	5	13	NULL	NULL	NULL	adducin heads	GP		caps					actin filament	GP	barbed end of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_7986_s_134	8626479	A model depicting binding  of adducin tails to actin and capping the barbed end of the actin  filament by adducin heads is shown in  Fig. 5 .	bind
42033	1	10944	6	NULL	NULL	0	NULL	adducin tails	NULL		bind	NULL				actin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_7986_s_134	8626479	A model depicting binding  of adducin tails to actin and capping the barbed end of the actin  filament by adducin heads is shown in  Fig. 5 .	bind
50482	2	10944	6	10	NULL	0	NULL	adducin heads	NULL		caps	NULL				actin filaments	NULL	barbed end of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_7986_s_134	8626479	A model depicting binding  of adducin tails to actin and capping the barbed end of the actin  filament by adducin heads is shown in  Fig. 5 .	bind
50048	1	10945	5	13	NULL	NULL	NULL	PP2A	GP		interacts with					CK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_49_34669_s_217	10574932	A model depicting regulation of Sp1 binding by  PP2A  interacting with  CK2  at basal and MAPK-signaled activation of  eNOS  gene transcription.	bind
50049	2	10945	5	13	NULL	NULL	NULL	statement 1	Process		regulates					Sp1	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_49_34669_s_217	10574932	A model depicting regulation of Sp1 binding by  PP2A  interacting with  CK2  at basal and MAPK-signaled activation of  eNOS  gene transcription.	bind
50050	3	10945	5	13	NULL	NULL	NULL	eNOS gene	GP	activation of ;;transcription of	is signaled by					MAPK	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_49_34669_s_217	10574932	A model depicting regulation of Sp1 binding by  PP2A  interacting with  CK2  at basal and MAPK-signaled activation of  eNOS  gene transcription.	bind
42073	1	10945	6	NULL	NULL	0	NULL	PP2A	NULL		interacts with	NULL				CK2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_49_34669_s_217	10574932	A model depicting regulation of Sp1 binding by  PP2A  interacting with  CK2  at basal and MAPK-signaled activation of  eNOS  gene transcription.	bind
42074	2	10945	6	10	NULL	0	NULL	MAPK	NULL		signals	NULL				eNOS gene 	NULL	activation of;;transcription of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_49_34669_s_217	10574932	A model depicting regulation of Sp1 binding by  PP2A  interacting with  CK2  at basal and MAPK-signaled activation of  eNOS  gene transcription.	bind
42075	3	10945	6	NULL	NULL	0	NULL	statement 1	NULL		regulates	NULL				Sp1	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_49_34669_s_217	10574932	A model depicting regulation of Sp1 binding by  PP2A  interacting with  CK2  at basal and MAPK-signaled activation of  eNOS  gene transcription.	bind
50052	1	10946	5	13	NULL	NULL	NULL	Argos	GP		is a type of					epidermal growth factor-like negative regulator 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27734_s_213	9765311	A model depicting the way agonists and antagonists may cooperate to control function is offered by  Drosophila, in which the epidermal growth factor-like negative regulator Argos binds to the mammalian epidermal growth factor receptor homologue ( Drosophila EGF receptor or DER), thereby preventing its activation by Spitz.	bind
50053	2	10946	5	13	NULL	NULL	NULL	Argos	GP	Drosophila	bind					DER	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27734_s_213	9765311	A model depicting the way agonists and antagonists may cooperate to control function is offered by  Drosophila, in which the epidermal growth factor-like negative regulator Argos binds to the mammalian epidermal growth factor receptor homologue ( Drosophila EGF receptor or DER), thereby preventing its activation by Spitz.	bind
50054	3	10946	5	13	NULL	NULL	NULL	DER	GP		is					Drosophila EGF receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27734_s_213	9765311	A model depicting the way agonists and antagonists may cooperate to control function is offered by  Drosophila, in which the epidermal growth factor-like negative regulator Argos binds to the mammalian epidermal growth factor receptor homologue ( Drosophila EGF receptor or DER), thereby preventing its activation by Spitz.	bind
50055	4	10946	5	13	NULL	NULL	NULL	DER	GP		is a homolog of					mammalian epidermal growth factor receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27734_s_213	9765311	A model depicting the way agonists and antagonists may cooperate to control function is offered by  Drosophila, in which the epidermal growth factor-like negative regulator Argos binds to the mammalian epidermal growth factor receptor homologue ( Drosophila EGF receptor or DER), thereby preventing its activation by Spitz.	bind
50056	5	10946	5	13	NULL	NULL	NULL	Spitz	GP		activates					DER	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27734_s_213	9765311	A model depicting the way agonists and antagonists may cooperate to control function is offered by  Drosophila, in which the epidermal growth factor-like negative regulator Argos binds to the mammalian epidermal growth factor receptor homologue ( Drosophila EGF receptor or DER), thereby preventing its activation by Spitz.	bind
50057	6	10946	5	13	NULL	NULL	NULL	statement 2	Process		prevents					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27734_s_213	9765311	A model depicting the way agonists and antagonists may cooperate to control function is offered by  Drosophila, in which the epidermal growth factor-like negative regulator Argos binds to the mammalian epidermal growth factor receptor homologue ( Drosophila EGF receptor or DER), thereby preventing its activation by Spitz.	bind
42076	1	10946	6	NULL	NULL	0	NULL	Argos	NULL		is a type of	NULL				epidermal growth factor-like negative regulator	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27734_s_213	9765311	A model depicting the way agonists and antagonists may cooperate to control function is offered by  Drosophila, in which the epidermal growth factor-like negative regulator Argos binds to the mammalian epidermal growth factor receptor homologue ( Drosophila EGF receptor or DER), thereby preventing its activation by Spitz.	bind
42077	2	10946	6	NULL	NULL	0	NULL	Argos	NULL	Drosophila	bind	NULL				DER	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27734_s_213	9765311	A model depicting the way agonists and antagonists may cooperate to control function is offered by  Drosophila, in which the epidermal growth factor-like negative regulator Argos binds to the mammalian epidermal growth factor receptor homologue ( Drosophila EGF receptor or DER), thereby preventing its activation by Spitz.	bind
42078	3	10946	6	NULL	NULL	0	NULL	DER	NULL		is	NULL				Drosophila EGF receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27734_s_213	9765311	A model depicting the way agonists and antagonists may cooperate to control function is offered by  Drosophila, in which the epidermal growth factor-like negative regulator Argos binds to the mammalian epidermal growth factor receptor homologue ( Drosophila EGF receptor or DER), thereby preventing its activation by Spitz.	bind
42079	4	10946	6	10	NULL	0	NULL	DER	NULL		is a homolog of	NULL				mammalian epidermal growth factor receptor	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_42_27734_s_213	9765311	A model depicting the way agonists and antagonists may cooperate to control function is offered by  Drosophila, in which the epidermal growth factor-like negative regulator Argos binds to the mammalian epidermal growth factor receptor homologue ( Drosophila EGF receptor or DER), thereby preventing its activation by Spitz.	bind
42080	5	10946	6	NULL	NULL	0	NULL	Spitz	NULL		activates	NULL				DER	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27734_s_213	9765311	A model depicting the way agonists and antagonists may cooperate to control function is offered by  Drosophila, in which the epidermal growth factor-like negative regulator Argos binds to the mammalian epidermal growth factor receptor homologue ( Drosophila EGF receptor or DER), thereby preventing its activation by Spitz.	bind
42081	6	10946	6	NULL	NULL	0	NULL	statement 2	NULL		prevents	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27734_s_213	9765311	A model depicting the way agonists and antagonists may cooperate to control function is offered by  Drosophila, in which the epidermal growth factor-like negative regulator Argos binds to the mammalian epidermal growth factor receptor homologue ( Drosophila EGF receptor or DER), thereby preventing its activation by Spitz.	bind
50058	1	10947	5	13	NULL	NULL	NULL	TPL-2	GP		bind					LPS	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_biochem-j_393_pt-3_16229681_s_12	16229681	A model describing  TPL-2 binding with LPS is proposed.	bind
42034	1	10947	6	NULL	NULL	0	NULL	TPL-2	NULL		bind	NULL				LPS	NULL				NULL		0	NULL	NULL	NULL	abs-batch0570-0579_biochem-j_393_pt-3_16229681_s_12	16229681	A model describing  TPL-2 binding with LPS is proposed.	bind
50059	1	10948	5	13	NULL	NULL	NULL	transcription factor	GP		bind									Region A sequence	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_8_6153_s_218	11748224	A model describing transcription factor binding to the Region A sequence, and the effects of mutations in the CCAAT-box and addition of mithramycin ( M) on binding, is illustrated in Fig.  5 B where  R represents the putative repressor binding to the GC-box.	bind
50061	2	10948	5	13	NULL	NULL	NULL	repressor	GP	putative	bind									GC-box	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_8_6153_s_218	11748224	A model describing transcription factor binding to the Region A sequence, and the effects of mutations in the CCAAT-box and addition of mithramycin ( M) on binding, is illustrated in Fig.  5 B where  R represents the putative repressor binding to the GC-box.	bind
42035	1	10948	6	NULL	NULL	0	NULL	repressor	NULL	putative	bind	NULL					NULL			GC-box	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_8_6153_s_218	11748224	A model describing transcription factor binding to the Region A sequence, and the effects of mutations in the CCAAT-box and addition of mithramycin ( M) on binding, is illustrated in Fig.  5 B where  R represents the putative repressor binding to the GC-box.	bind
42036	2	10948	6	NULL	NULL	0	NULL	transcription factor	NULL		bind	NULL					NULL			region A sequence	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_8_6153_s_218	11748224	A model describing transcription factor binding to the Region A sequence, and the effects of mutations in the CCAAT-box and addition of mithramycin ( M) on binding, is illustrated in Fig.  5 B where  R represents the putative repressor binding to the GC-box.	bind
50062	1	10949	5	13	NULL	NULL	NULL	tRNAPhe	NucleicAcid		bind					GAPDH	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1432_2_222_s_169	10407144	A model exhibiting the binding of tRNAPhe to GAPDH is shown in  Fig. 4.	bind
42037	1	10949	6	NULL	NULL	0	NULL	tRNAPhe	NULL		bind	NULL				GAPDH	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1432_2_222_s_169	10407144	A model exhibiting the binding of tRNAPhe to GAPDH is shown in  Fig. 4.	bind
50063	1	10950	5	13	NULL	NULL	NULL	L5	GP		bind			amino-terminal domain		5 S rRNA	NucleicAcid				NULL	nucleoplasm	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_19_11571_s_108	8626719	A model for 5 S rRNA trafficking can be formulated  where the L5 amino-terminal domain binds to 5 S rRNA shortly after  transcription in the nucleoplasm and the RNP then localizes to the  nucleolus by virtue of interactions between a nucleolar component and  the carboxyl-terminal domain of L5.	bind
50064	2	10950	5	13	NULL	NULL	NULL	statement 1	Process		occurs after		shortly			transcription	Process				NULL	nucleoplasm	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_19_11571_s_108	8626719	A model for 5 S rRNA trafficking can be formulated  where the L5 amino-terminal domain binds to 5 S rRNA shortly after  transcription in the nucleoplasm and the RNP then localizes to the  nucleolus by virtue of interactions between a nucleolar component and  the carboxyl-terminal domain of L5.	bind
50065	3	10950	5	13	NULL	NULL	NULL	RNP	GP		localize to					nucleolus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_19_11571_s_108	8626719	A model for 5 S rRNA trafficking can be formulated  where the L5 amino-terminal domain binds to 5 S rRNA shortly after  transcription in the nucleoplasm and the RNP then localizes to the  nucleolus by virtue of interactions between a nucleolar component and  the carboxyl-terminal domain of L5.	bind
50066	4	10950	5	13	NULL	NULL	NULL	statement 1	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_19_11571_s_108	8626719	A model for 5 S rRNA trafficking can be formulated  where the L5 amino-terminal domain binds to 5 S rRNA shortly after  transcription in the nucleoplasm and the RNP then localizes to the  nucleolus by virtue of interactions between a nucleolar component and  the carboxyl-terminal domain of L5.	bind
50067	5	10950	5	13	NULL	NULL	NULL	nucleolar component	CellComponent		interacts with					L5	GP		carboxyl-terminal domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_19_11571_s_108	8626719	A model for 5 S rRNA trafficking can be formulated  where the L5 amino-terminal domain binds to 5 S rRNA shortly after  transcription in the nucleoplasm and the RNP then localizes to the  nucleolus by virtue of interactions between a nucleolar component and  the carboxyl-terminal domain of L5.	bind
42038	1	10950	6	NULL	NULL	0	NULL	L5	NULL		bind	NULL		amino-terminal domain		5S rRNA	NULL				NULL	nucleoplasm	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_19_11571_s_108	8626719	A model for 5 S rRNA trafficking can be formulated  where the L5 amino-terminal domain binds to 5 S rRNA shortly after  transcription in the nucleoplasm and the RNP then localizes to the  nucleolus by virtue of interactions between a nucleolar component and  the carboxyl-terminal domain of L5.	bind
42082	2	10950	6	10	NULL	0	NULL	statement 1	NULL		occurs after	NULL				transcription	NULL				NULL	nucleoplasm	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_19_11571_s_108	8626719	A model for 5 S rRNA trafficking can be formulated  where the L5 amino-terminal domain binds to 5 S rRNA shortly after  transcription in the nucleoplasm and the RNP then localizes to the  nucleolus by virtue of interactions between a nucleolar component and  the carboxyl-terminal domain of L5.	bind
42083	3	10950	6	NULL	NULL	0	NULL	RNP	NULL		localizes to	NULL				nucleolus	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11571_s_108	8626719	A model for 5 S rRNA trafficking can be formulated  where the L5 amino-terminal domain binds to 5 S rRNA shortly after  transcription in the nucleoplasm and the RNP then localizes to the  nucleolus by virtue of interactions between a nucleolar component and  the carboxyl-terminal domain of L5.	bind
42084	4	10950	6	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11571_s_108	8626719	A model for 5 S rRNA trafficking can be formulated  where the L5 amino-terminal domain binds to 5 S rRNA shortly after  transcription in the nucleoplasm and the RNP then localizes to the  nucleolus by virtue of interactions between a nucleolar component and  the carboxyl-terminal domain of L5.	bind
42569	5	10950	6	NULL	NULL	0	NULL	L5	NULL		bind	NULL		carboxyl-terminal domain		RNP	NULL		nucleolar component		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11571_s_108	8626719	A model for 5 S rRNA trafficking can be formulated  where the L5 amino-terminal domain binds to 5 S rRNA shortly after  transcription in the nucleoplasm and the RNP then localizes to the  nucleolus by virtue of interactions between a nucleolar component and  the carboxyl-terminal domain of L5.	bind
50068	1	10951	5	13	NULL	NULL	NULL	ANP	GP		bind								extracellular domain		NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_68_0_127_s_146	10872446	A model for activation of GC-A, then, is that ANP binding to the   extracellular domain and ATP binding to the kinase homology domain lead to a   conformational change relieving kinase homology domain inhibition of the   catalytic domain.	bind
50069	2	10951	5	13	NULL	NULL	NULL	ATP	Chemical		bind								kinase homology domain		NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_68_0_127_s_146	10872446	A model for activation of GC-A, then, is that ANP binding to the   extracellular domain and ATP binding to the kinase homology domain lead to a   conformational change relieving kinase homology domain inhibition of the   catalytic domain.	bind
50070	3	10951	5	13	NULL	NULL	NULL	statement 1	Process		leads to					conformational change	Process				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_68_0_127_s_146	10872446	A model for activation of GC-A, then, is that ANP binding to the   extracellular domain and ATP binding to the kinase homology domain lead to a   conformational change relieving kinase homology domain inhibition of the   catalytic domain.	bind
50071	4	10951	5	NULL	NULL	0	NULL		NULL		inhibits	NULL		kinase homology domain			NULL		catalytic domain		NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_68_0_127_s_146	10872446	A model for activation of GC-A, then, is that ANP binding to the   extracellular domain and ATP binding to the kinase homology domain lead to a   conformational change relieving kinase homology domain inhibition of the   catalytic domain.	bind
50072	5	10951	5	13	NULL	NULL	NULL	statement 3	Process		relieves					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_68_0_127_s_146	10872446	A model for activation of GC-A, then, is that ANP binding to the   extracellular domain and ATP binding to the kinase homology domain lead to a   conformational change relieving kinase homology domain inhibition of the   catalytic domain.	bind
50073	6	10951	5	13	NULL	NULL	NULL	statement 2	Process		leads to					conformational change	Process				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_68_0_127_s_146	10872446	A model for activation of GC-A, then, is that ANP binding to the   extracellular domain and ATP binding to the kinase homology domain lead to a   conformational change relieving kinase homology domain inhibition of the   catalytic domain.	bind
50074	7	10951	5	13	NULL	NULL	NULL	statement 6	Process		relieves					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_68_0_127_s_146	10872446	A model for activation of GC-A, then, is that ANP binding to the   extracellular domain and ATP binding to the kinase homology domain lead to a   conformational change relieving kinase homology domain inhibition of the   catalytic domain.	bind
42039	1	10951	6	NULL	NULL	0	NULL	ANP	NULL		bind	NULL					NULL		extracellular domain		NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_68_0_127_s_146	10872446	A model for activation of GC-A, then, is that ANP binding to the   extracellular domain and ATP binding to the kinase homology domain lead to a   conformational change relieving kinase homology domain inhibition of the   catalytic domain.	bind
42040	2	10951	6	NULL	NULL	0	NULL	ATP	NULL		bind	NULL					NULL		kinase homology domain		NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_68_0_127_s_146	10872446	A model for activation of GC-A, then, is that ANP binding to the   extracellular domain and ATP binding to the kinase homology domain lead to a   conformational change relieving kinase homology domain inhibition of the   catalytic domain.	bind
42041	3	10951	6	NULL	NULL	0	NULL		NULL		inhibits	NULL		kinase homology domain			NULL		catalytic domain		NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_68_0_127_s_146	10872446	A model for activation of GC-A, then, is that ANP binding to the   extracellular domain and ATP binding to the kinase homology domain lead to a   conformational change relieving kinase homology domain inhibition of the   catalytic domain.	bind
42042	4	10951	6	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				conformational change	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_68_0_127_s_146	10872446	A model for activation of GC-A, then, is that ANP binding to the   extracellular domain and ATP binding to the kinase homology domain lead to a   conformational change relieving kinase homology domain inhibition of the   catalytic domain.	bind
42043	5	10951	6	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				conformational change	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_68_0_127_s_146	10872446	A model for activation of GC-A, then, is that ANP binding to the   extracellular domain and ATP binding to the kinase homology domain lead to a   conformational change relieving kinase homology domain inhibition of the   catalytic domain.	bind
42044	6	10951	6	NULL	NULL	0	NULL	statement 4	NULL		relieves	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_68_0_127_s_146	10872446	A model for activation of GC-A, then, is that ANP binding to the   extracellular domain and ATP binding to the kinase homology domain lead to a   conformational change relieving kinase homology domain inhibition of the   catalytic domain.	bind
42045	7	10951	6	NULL	NULL	0	NULL	statement 5	NULL		relieves	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_68_0_127_s_146	10872446	A model for activation of GC-A, then, is that ANP binding to the   extracellular domain and ATP binding to the kinase homology domain lead to a   conformational change relieving kinase homology domain inhibition of the   catalytic domain.	bind
50075	1	10952	5	13	NULL	NULL	NULL	AGRP	GP		bind					MCRs	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_20_14100_s_146	10318826	A model for AGRP binding to the MCRs remains to be developed.	bind
42046	1	10952	6	NULL	NULL	0	NULL	AGRP	NULL		bind	NULL				MCR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_20_14100_s_146	10318826	A model for AGRP binding to the MCRs remains to be developed.	bind
50076	1	10953	5	13	NULL	NULL	NULL	DnaA monomers	GP		bind					oriC	NucleicAcid			DnaA box	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_48_44919_s_213	11551962	A Model for Assembly of the Prepriming Complex--  In this model (Fig.  6), DnaA monomers bound to each DnaA box in  oriC creates a structure recognized by the DnaB-DnaC complex.	bind
50077	2	10953	5	13	NULL	NULL	NULL	statement 1	GP		is recognized by					DnaB-DnaC complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_48_44919_s_213	11551962	A Model for Assembly of the Prepriming Complex--  In this model (Fig.  6), DnaA monomers bound to each DnaA box in  oriC creates a structure recognized by the DnaB-DnaC complex.	bind
42047	1	10953	6	NULL	NULL	0	NULL	DnaA monomers	NULL		bind	NULL				oriC	NULL			DnaA box	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_48_44919_s_213	11551962	A Model for Assembly of the Prepriming Complex--  In this model (Fig.  6), DnaA monomers bound to each DnaA box in  oriC creates a structure recognized by the DnaB-DnaC complex.	bind
42048	2	10953	6	NULL	NULL	0	NULL	statement 1	NULL		is recognized by	NULL				DnaB-DnaC complex	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_48_44919_s_213	11551962	A Model for Assembly of the Prepriming Complex--  In this model (Fig.  6), DnaA monomers bound to each DnaA box in  oriC creates a structure recognized by the DnaB-DnaC complex.	bind
50078	1	10954	5	13	NULL	NULL	NULL	EG	Chemical		bind					mOR-EG	GP				NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_25_7_1806_s_196	15716417	A model for binding of EG to mOR-EG and the orientation of amino acids in the binding  site.	bind
42085	1	10954	6	NULL	NULL	0	NULL	EG	NULL		bind	NULL				mOR-EG	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_25_7_1806_s_196	15716417	A model for binding of EG to mOR-EG and the orientation of amino acids in the binding  site.	bind
50079	1	10955	5	13	NULL	NULL	NULL	nitrite	Chemical		bind					NIR	GP	A. xylosoxidans			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_46_27458_s_343	7499203	A model for binding of nitrite to NIR from  A.  xylosoxidans  based on EXAFS studies ( 27 ) is not consistent  with our results.	bind
42128	1	10955	6	NULL	NULL	0	NULL	nitrite	NULL		bind	NULL				NIR	NULL	A. xylosoxidans			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_46_27458_s_343	7499203	A model for binding of nitrite to NIR from  A.  xylosoxidans  based on EXAFS studies ( 27 ) is not consistent  with our results.	bind
50080	1	10956	5	13	NULL	NULL	NULL	G9I peptide	GP		bind					Dd	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1151_s_304	14583622	A model for binding of peptides G9I and Q11I to Dd.	bind
50081	2	10956	5	13	NULL	NULL	NULL	Q11I peptide	GP		bind					Dd	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_2_1151_s_304	14583622	A model for binding of peptides G9I and Q11I to Dd.	bind
42129	1	10956	6	NULL	NULL	0	NULL	G9I peptide	NULL		bind	NULL				Dd	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_2_1151_s_304	14583622	A model for binding of peptides G9I and Q11I to Dd.	bind
42131	2	10956	6	NULL	NULL	0	NULL	Q11I peptide	NULL		bind	NULL				Dd	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_2_1151_s_304	14583622	A model for binding of peptides G9I and Q11I to Dd.	bind
50082	1	10957	5	13	NULL	NULL	NULL	S1P	GP		bind					S1P1	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_270_s_225	12069838	A model for binding of S1P to S1P1 indicates that the polar head group of the ligand is situated in a polar region of the receptor near the extracellular surface, while the fatty acid tail is inserted into the receptor within its transmembrane domains [  67].	bind
42195	1	10957	6	NULL	NULL	0	NULL	S1P	NULL		bind	NULL		polar head group;; fatty acid tail		S1P1	NULL		polar region;; transmembrane domain		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_270_s_225	12069838	A model for binding of S1P to S1P1 indicates that the polar head group of the ligand is situated in a polar region of the receptor near the extracellular surface, while the fatty acid tail is inserted into the receptor within its transmembrane domains [  67].	bind
50083	1	10959	5	13	NULL	NULL	NULL	thermolysin	GP		is a type of					metallopeptidase	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_41_39497_s_169	12888578	A model for catalysis based on the metallopeptidase thermolysin proposes that the internal glutamic acid polarizes the zinc-bound water molecule for a nucleophilic attack on the carbonyl carbon of the scissile peptide bond in the substrate ( ).	bind
50084	2	10959	5	13	NULL	NULL	NULL	water molecule	Chemical		bind					zinc	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_41_39497_s_169	12888578	A model for catalysis based on the metallopeptidase thermolysin proposes that the internal glutamic acid polarizes the zinc-bound water molecule for a nucleophilic attack on the carbonyl carbon of the scissile peptide bond in the substrate ( ).	bind
50085	3	10959	5	13	NULL	NULL	NULL			internal	polarize			glutamic acid		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_41_39497_s_169	12888578	A model for catalysis based on the metallopeptidase thermolysin proposes that the internal glutamic acid polarizes the zinc-bound water molecule for a nucleophilic attack on the carbonyl carbon of the scissile peptide bond in the substrate ( ).	bind
42196	1	10959	6	NULL	NULL	0	NULL	thermolysin	NULL		is a type of	NULL				metallopeptidase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_41_39497_s_169	12888578	A model for catalysis based on the metallopeptidase thermolysin proposes that the internal glutamic acid polarizes the zinc-bound water molecule for a nucleophilic attack on the carbonyl carbon of the scissile peptide bond in the substrate ( ).	bind
42197	2	10959	6	NULL	NULL	0	NULL	zinc	NULL		bind	NULL				water molecule	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_41_39497_s_169	12888578	A model for catalysis based on the metallopeptidase thermolysin proposes that the internal glutamic acid polarizes the zinc-bound water molecule for a nucleophilic attack on the carbonyl carbon of the scissile peptide bond in the substrate ( ).	bind
42198	3	10959	6	NULL	NULL	0	NULL		NULL	internal	polarizes	NULL		glutamic acid		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_41_39497_s_169	12888578	A model for catalysis based on the metallopeptidase thermolysin proposes that the internal glutamic acid polarizes the zinc-bound water molecule for a nucleophilic attack on the carbonyl carbon of the scissile peptide bond in the substrate ( ).	bind
50086	1	10960	5	13	NULL	NULL	NULL	ATP	Chemical		bind					Rho	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_41_26477_s_358	9756883	A Model for Catalysis-- Our model for the hydrolysis of three labeled ATP molecules bound to Rho when RNA and excess unlabeled ATP are added is shown in Scheme  1.	bind
42199	1	10960	6	NULL	NULL	0	NULL	ATP molecules	NULL		bind	NULL				Rho	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_41_26477_s_358	9756883	A Model for Catalysis-- Our model for the hydrolysis of three labeled ATP molecules bound to Rho when RNA and excess unlabeled ATP are added is shown in Scheme  1.	bind
50087	1	10961	5	13	NULL	NULL	NULL	GSH	GP		bind		covalently						Cys-32		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24798_s_92	10783391	A model for GSH covalently bound to Cys-32 as well as chemically reasonable water molecules and sulfate ions was built into sigmaA-weighted 2  F o    F c maps ( 30).	bind
50088	2	10961	5	13	NULL	NULL	NULL	GSH	GP		bind		covalently			water molecule	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24798_s_92	10783391	A model for GSH covalently bound to Cys-32 as well as chemically reasonable water molecules and sulfate ions was built into sigmaA-weighted 2  F o    F c maps ( 30).	bind
50089	3	10961	5	13	NULL	NULL	NULL	GSH	GP		bind		covalently			sulfate ions	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24798_s_92	10783391	A model for GSH covalently bound to Cys-32 as well as chemically reasonable water molecules and sulfate ions was built into sigmaA-weighted 2  F o    F c maps ( 30).	bind
42200	1	10961	6	NULL	NULL	0	NULL	GSH	NULL		bind	NULL	covalently				NULL		Cys-32		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24798_s_92	10783391	A model for GSH covalently bound to Cys-32 as well as chemically reasonable water molecules and sulfate ions was built into sigmaA-weighted 2  F o    F c maps ( 30).	bind
50524	2	10961	6	10	NULL	0	NULL	GSH	NULL		bind	NULL	covalently			water molecule	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24798_s_92	10783391	A model for GSH covalently bound to Cys-32 as well as chemically reasonable water molecules and sulfate ions was built into sigmaA-weighted 2  F o    F c maps ( 30).	bind
50526	3	10961	6	10	NULL	0	NULL	GSH	NULL		bind	NULL	covalently			sulfate ions	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24798_s_92	10783391	A model for GSH covalently bound to Cys-32 as well as chemically reasonable water molecules and sulfate ions was built into sigmaA-weighted 2  F o    F c maps ( 30).	bind
50090	1	10962	5	13	NULL	NULL	NULL	ISG15	GP		bind					UbE1L	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_29_27356_s_232	15917233	A Model For ISG15 Binding to UbE1L --	bind
42201	1	10962	6	NULL	NULL	0	NULL	ISG15	NULL		bind	NULL				UbE1L	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27356_s_232	15917233	A Model For ISG15 Binding to UbE1L --	bind
50091	1	10963	5	13	NULL	NULL	NULL	G-protein	GP		bind		directly	betagamma subunit		Ca2+ channel	GP		alpha1B		NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_13_4883_s_153	9634554	A model for membrane-delimited voltage-dependent inhibition in which the G-protein betagamma subunit binds directly to the alpha1B Ca2+ channel has recently received experimental support (De Waard et al., 1997  ; Zamponi et al., 1997  ).	bind
42202	1	10963	6	10	NULL	0	NULL	G-protein 	NULL		bind	NULL	directly	betagamma subunit		 Ca2+ channel	NULL		alpha1B		NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_13_4883_s_153	9634554	A model for membrane-delimited voltage-dependent inhibition in which the G-protein betagamma subunit binds directly to the alpha1B Ca2+ channel has recently received experimental support (De Waard et al., 1997  ; Zamponi et al., 1997  ).	bind
50092	1	10964	5	13	NULL	NULL	NULL	N-CAM	GP		bind		homophilic	Ig I		N-CAM	GP		Ig V		NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_5_2592_s_16	9482931	A model for N-CAM homophilic binding has been proposed in which the Ig domains bind in a pairwise antiparallel manner such that Ig I binds Ig V, Ig II binds Ig IV, and Ig III binds Ig III ( 3).	bind
50093	2	10964	5	13	NULL	NULL	NULL	N-CAM	GP		bind		homophilic	Ig II		N-CAM	GP		Ig IV		NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_5_2592_s_16	9482931	A model for N-CAM homophilic binding has been proposed in which the Ig domains bind in a pairwise antiparallel manner such that Ig I binds Ig V, Ig II binds Ig IV, and Ig III binds Ig III ( 3).	bind
50094	3	10964	5	13	NULL	NULL	NULL	N-CAM	GP		bind		homophilic	Ig III		N-CAM	GP		Ig III		NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_5_2592_s_16	9482931	A model for N-CAM homophilic binding has been proposed in which the Ig domains bind in a pairwise antiparallel manner such that Ig I binds Ig V, Ig II binds Ig IV, and Ig III binds Ig III ( 3).	bind
42203	1	10964	6	10	NULL	0	NULL	N-CAM	NULL		bind	NULL	homophilic	Ig I		N-CAM	NULL		Ig V		NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_5_2592_s_16	9482931	A model for N-CAM homophilic binding has been proposed in which the Ig domains bind in a pairwise antiparallel manner such that Ig I binds Ig V, Ig II binds Ig IV, and Ig III binds Ig III ( 3).	bind
42204	2	10964	6	10	NULL	0	NULL	N-CAM	NULL		bind	NULL	homophilic	Ig II		N-CAM	NULL		Ig IV		NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_5_2592_s_16	9482931	A model for N-CAM homophilic binding has been proposed in which the Ig domains bind in a pairwise antiparallel manner such that Ig I binds Ig V, Ig II binds Ig IV, and Ig III binds Ig III ( 3).	bind
42205	3	10964	6	10	NULL	0	NULL	N-CAM	NULL		bind	NULL	homophilic	Ig III		N-CAM	NULL		Ig III		NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_5_2592_s_16	9482931	A model for N-CAM homophilic binding has been proposed in which the Ig domains bind in a pairwise antiparallel manner such that Ig I binds Ig V, Ig II binds Ig IV, and Ig III binds Ig III ( 3).	bind
50095	1	10965	5	13	NULL	NULL	NULL	Rad52 protein	GP		bind					RPA-ssDNA complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_31663_s_300	12077133	A model for presynaptic complex formation by Rad51 and Rad52 proteins and  RPA. Rad52 protein binds to RPA-ssDNA complex ( a) to form a Rad52-RPA-ssDNA nucleoprotein co-complex ( b).	bind
50097	2	10965	5	13	NULL	NULL	NULL	statement 1	Process		forms					Rad52-RPA-ssDNA nucleoprotein co-complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_31663_s_300	12077133	A model for presynaptic complex formation by Rad51 and Rad52 proteins and  RPA. Rad52 protein binds to RPA-ssDNA complex ( a) to form a Rad52-RPA-ssDNA nucleoprotein co-complex ( b).	bind
42206	1	10965	6	NULL	NULL	0	NULL	Rad52 protein	NULL		bind	NULL				RPA-ssDNA complex	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_35_31663_s_300	12077133	A model for presynaptic complex formation by Rad51 and Rad52 proteins and  RPA. Rad52 protein binds to RPA-ssDNA complex ( a) to form a Rad52-RPA-ssDNA nucleoprotein co-complex ( b).	bind
42207	2	10965	6	NULL	NULL	0	NULL	statement 1	NULL		forms a 	NULL				Rad52-RPA-ssDNA nucleoprotein co-complex	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_35_31663_s_300	12077133	A model for presynaptic complex formation by Rad51 and Rad52 proteins and  RPA. Rad52 protein binds to RPA-ssDNA complex ( a) to form a Rad52-RPA-ssDNA nucleoprotein co-complex ( b).	bind
50098	1	10966	5	13	NULL	NULL	NULL	Bas1p/Bas2p	GP		regulates					adenine	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_23_4665_s_236	11095676	A model for promoter-specific adenine regulation of the Bas1p/Bas2p couple.	bind
50099	2	10966	5	13	NULL	NULL	NULL	statement 1	Process		is specific to					promoter	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_23_4665_s_236	11095676	A model for promoter-specific adenine regulation of the Bas1p/Bas2p couple.	bind
42208	1	10966	6	10	NULL	0	NULL	Bas1p/Bas2p couple	NULL		regulate	NULL				adenine 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_23_4665_s_236	11095676	A model for promoter-specific adenine regulation of the Bas1p/Bas2p couple.	bind
42209	2	10966	6	10	NULL	0	NULL	statement 1	NULL		is specific to	NULL				promoter	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_23_4665_s_236	11095676	A model for promoter-specific adenine regulation of the Bas1p/Bas2p couple.	bind
50100	1	10967	5	13	NULL	NULL	NULL	Rac1	GP		bind								IMD		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_240_s_202	15635447	A model for Rac1 binding  to the IMD can be readily derived by superimposing the IMD structure with the Rac1-arfaptin2  complex (  et al).	bind
42210	1	10967	6	10	NULL	0	NULL	Rac1	NULL		bind	NULL					NULL		IMD		NULL		NULL	NULL	NULL	NULL	gw70_embo_24_2_240_s_202	15635447	A model for Rac1 binding  to the IMD can be readily derived by superimposing the IMD structure with the Rac1-arfaptin2  complex (  et al).	bind
50101	1	10968	5	13	NULL	NULL	NULL	SDF-1	GP		bind					CXCR4	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_23_6996_s_193	9384579	A model for SDF-1 receptor [[ interactions        Based ]] on these results we propose a two site model for SDF-1 binding to CXCR4 (Figure  7).	bind
42211	1	10968	6	NULL	NULL	0	NULL	SDF-1	NULL		bind	NULL				CXCR4	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_23_6996_s_193	9384579	A model for SDF-1 receptor [[ interactions        Based ]] on these results we propose a two site model for SDF-1 binding to CXCR4 (Figure  7).	bind
50102	1	10969	5	13	NULL	NULL	NULL	Sm2DBD homodimer	GP		bind					target gene	GP				NULL		NULL	NULL	NULL	NULL	gw70_gene_366_2_303_s_48	16406405	A model for Sm2DBDs  bind to their target gene as a homodimer or heterodimer.	bind
50103	2	10969	5	13	NULL	NULL	NULL	Sm2DBD heterodimer	GP		bind					target gene	GP				NULL		NULL	NULL	NULL	NULL	gw70_gene_366_2_303_s_48	16406405	A model for Sm2DBDs  bind to their target gene as a homodimer or heterodimer.	bind
42213	1	10969	6	10	NULL	0	NULL	Sm2DBD homodimer	NULL		bind	NULL				target gene	NULL				NULL		NULL	NULL	NULL	NULL	gw70_gene_366_2_303_s_48	16406405	A model for Sm2DBDs  bind to their target gene as a homodimer or heterodimer.	bind
42214	2	10969	6	10	NULL	0	NULL	Sm2DBD heterodimer	NULL		bind	NULL				target gene	NULL				NULL		NULL	NULL	NULL	NULL	gw70_gene_366_2_303_s_48	16406405	A model for Sm2DBDs  bind to their target gene as a homodimer or heterodimer.	bind
50104	1	10970	5	13	NULL	NULL	NULL	Sm2DBD monomer	GP		bind					target gene	GP				NULL		NULL	NULL	NULL	NULL	gw70_gene_366_2_303_s_46	16406405	A model for Sm2DBDs bind to their target gene as monomer.	bind
42212	1	10970	6	10	NULL	0	NULL	Sm2DBD monomer	NULL		bind	NULL				target gene	NULL				NULL		NULL	NULL	NULL	NULL	gw70_gene_366_2_303_s_46	16406405	A model for Sm2DBDs bind to their target gene as monomer.	bind
50105	1	10971	5	13	NULL	NULL	NULL	TFIIB	GP		bind					TBP-DNA complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_1_34_s_302	9420329	A model for TFIIB binding to the TBP-DNA complex.	bind
42215	1	10971	6	NULL	NULL	0	NULL	TFIIB	NULL		bind	NULL				TBP-DNA complex	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_1_34_s_302	9420329	A model for TFIIB binding to the TBP-DNA complex.	bind
50106	1	10972	5	13	NULL	NULL	NULL	GATA-4	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13752_s_319	11827958	A model for the  MAPK  regulation of transcription factor GATA-4 binding to   BNP  gene promoter by hypertrophic agonists.	bind
50107	2	10972	5	13	NULL	NULL	NULL	GATA-4	GP		bind					BNP gene	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13752_s_319	11827958	A model for the  MAPK  regulation of transcription factor GATA-4 binding to   BNP  gene promoter by hypertrophic agonists.	bind
50108	3	10972	5	13	NULL	NULL	NULL	MAPK	GP		regulates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13752_s_319	11827958	A model for the  MAPK  regulation of transcription factor GATA-4 binding to   BNP  gene promoter by hypertrophic agonists.	bind
42216	1	10972	6	NULL	NULL	0	NULL	GATA-4	NULL		bind	NULL				BNP gene	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13752_s_319	11827958	A model for the  MAPK  regulation of transcription factor GATA-4 binding to   BNP  gene promoter by hypertrophic agonists.	bind
42217	2	10972	6	NULL	NULL	0	NULL	GATA-4	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13752_s_319	11827958	A model for the  MAPK  regulation of transcription factor GATA-4 binding to   BNP  gene promoter by hypertrophic agonists.	bind
42218	3	10972	6	NULL	NULL	0	NULL	statement 1	NULL		is regulated by	NULL				MAPK	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13752_s_319	11827958	A model for the  MAPK  regulation of transcription factor GATA-4 binding to   BNP  gene promoter by hypertrophic agonists.	bind
50109	1	10973	5	13	NULL	NULL	NULL	MT1-MMP	GP		bind			catalytic domain		TIMP-2	GP		N-terminus		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41415_s_26	10998420	A model for the activation of pro-MMP-2 has been proposed in which the catalytic domain of MT1-MMP binds to the N-terminal portion of TIMP-2, leaving the negatively charged C-terminal region of TIMP-2 available for the binding of the hemopexin-like domain of pro-MMP-2 ( 12,  34-38).	bind
50110	2	10973	5	13	NULL	NULL	NULL	TIMP-2	GP		bind			negatively charged C-terminus		pro-MMP-2	GP		hemopexin-like domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41415_s_26	10998420	A model for the activation of pro-MMP-2 has been proposed in which the catalytic domain of MT1-MMP binds to the N-terminal portion of TIMP-2, leaving the negatively charged C-terminal region of TIMP-2 available for the binding of the hemopexin-like domain of pro-MMP-2 ( 12,  34-38).	bind
42219	1	10973	6	NULL	NULL	0	NULL	MT1-MMP	NULL		bind	NULL		catalytic domain		TIMP-2	NULL		N-terminal 		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41415_s_26	10998420	A model for the activation of pro-MMP-2 has been proposed in which the catalytic domain of MT1-MMP binds to the N-terminal portion of TIMP-2, leaving the negatively charged C-terminal region of TIMP-2 available for the binding of the hemopexin-like domain of pro-MMP-2 ( 12,  34-38).	bind
42220	2	10973	6	NULL	NULL	0	NULL	pro-MMP-2	NULL		bind	NULL		hemopexin-like domain		TIMP-2	NULL		negatively charged C-terminal region		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41415_s_26	10998420	A model for the activation of pro-MMP-2 has been proposed in which the catalytic domain of MT1-MMP binds to the N-terminal portion of TIMP-2, leaving the negatively charged C-terminal region of TIMP-2 available for the binding of the hemopexin-like domain of pro-MMP-2 ( 12,  34-38).	bind
50111	1	10974	5	13	NULL	NULL	NULL	PS-I	GP		is a type of					reaction center	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_46_36250_s_149	10948201	A model for the binding of Fd to the PS-I reaction center is presented in Fig.  5.	bind
50112	2	10974	5	13	NULL	NULL	NULL	Fd	Chemical		bind					PS-I	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_46_36250_s_149	10948201	A model for the binding of Fd to the PS-I reaction center is presented in Fig.  5.	bind
42221	1	10974	6	NULL	NULL	0	NULL	Fd	NULL		bind	NULL				PS-I reaction center	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_46_36250_s_149	10948201	A model for the binding of Fd to the PS-I reaction center is presented in Fig.  5.	bind
50113	1	10975	5	13	NULL	NULL	NULL	unr	GP		bind					Apaf-1	GP			IRES	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_3_757_s_226	12667457	A Model for the Binding of unr and nPTB to the Apaf-1 IRES during Ribosome Recruitment	bind
50114	2	10975	5	13	NULL	NULL	NULL	statement 1	Process		occurs during					ribosome	CellComponent	recruitment of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_3_757_s_226	12667457	A Model for the Binding of unr and nPTB to the Apaf-1 IRES during Ribosome Recruitment	bind
50115	3	10975	5	13	NULL	NULL	NULL	nPTB	GP		bind					Apaf-1	GP			IRES	NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_3_757_s_226	12667457	A Model for the Binding of unr and nPTB to the Apaf-1 IRES during Ribosome Recruitment	bind
50116	4	10975	5	13	NULL	NULL	NULL	statement 3	Process		occurs during					ribosome	CellComponent	recruitment of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_3_757_s_226	12667457	A Model for the Binding of unr and nPTB to the Apaf-1 IRES during Ribosome Recruitment	bind
42222	1	10975	6	NULL	NULL	0	NULL	unr	NULL		bind	NULL				Apaf-1	NULL			IRES	NULL		0	NULL	NULL	NULL	gw60_molcell_11_3_757_s_226	12667457	A Model for the Binding of unr and nPTB to the Apaf-1 IRES during Ribosome Recruitment	bind
42223	2	10975	6	NULL	NULL	0	NULL	nPTB	NULL		bind	NULL				Apaf-1	NULL			IRES	NULL		0	NULL	NULL	NULL	gw60_molcell_11_3_757_s_226	12667457	A Model for the Binding of unr and nPTB to the Apaf-1 IRES during Ribosome Recruitment	bind
42224	3	10975	6	NULL	NULL	0	NULL	statement 1	NULL		occurs during	NULL				ribosome	NULL	recruitment of			NULL		0	NULL	NULL	NULL	gw60_molcell_11_3_757_s_226	12667457	A Model for the Binding of unr and nPTB to the Apaf-1 IRES during Ribosome Recruitment	bind
42225	4	10975	6	NULL	NULL	0	NULL	statement 2	NULL		occurs during	NULL				ribosome	NULL	recruitment of			NULL		0	NULL	NULL	NULL	gw60_molcell_11_3_757_s_226	12667457	A Model for the Binding of unr and nPTB to the Apaf-1 IRES during Ribosome Recruitment	bind
50117	1	10976	5	13	NULL	NULL	NULL	MDM2	GP		degrades					p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_7288_s_206	9819415	A model for the degradation of p53 by MDM2.	bind
42226	1	10976	6	NULL	NULL	0	NULL	MDM2	NULL		degrades	NULL				p53	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_7288_s_206	9819415	A model for the degradation of p53 by MDM2.	bind
50118	1	10977	5	13	NULL	NULL	NULL	METH	Chemical		induce					DA responses	Process				NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_24_9_2212_s_456	14999072	A model for the modulation by TNF-alpha of METH-induced DA responses.	bind
50119	2	10977	5	13	NULL	NULL	NULL	TNF-alpha	GP		modulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_24_9_2212_s_456	14999072	A model for the modulation by TNF-alpha of METH-induced DA responses.	bind
42227	1	10977	6	NULL	NULL	0	NULL	METH	NULL		induces	NULL				DA responses	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_24_9_2212_s_456	14999072	A model for the modulation by TNF-alpha of METH-induced DA responses.	bind
42228	2	10977	6	10	NULL	0	NULL	TNF-alpha	NULL		modulates	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_24_9_2212_s_456	14999072	A model for the modulation by TNF-alpha of METH-induced DA responses.	bind
50120	1	10978	5	13	NULL	NULL	NULL	m-xylene	Chemical		bind					XylR	GP		A domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_86_2_331_s_194	8706137	A Model for the Multimerization Cycle  of XylR at the UAS of the  Pu Promoter The series of events  that follow the release of intramolecular repression caused by  m-xylene binding to  the A domain of XylR are sketched in the figure as a  multimerization and demultimerization cycle driven by ATP.	bind
50121	2	10978	5	13	NULL	NULL	NULL	statement 1	Process		causes					intramolecular repression	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_86_2_331_s_194	8706137	A Model for the Multimerization Cycle  of XylR at the UAS of the  Pu Promoter The series of events  that follow the release of intramolecular repression caused by  m-xylene binding to  the A domain of XylR are sketched in the figure as a  multimerization and demultimerization cycle driven by ATP.	bind
42229	1	10978	6	NULL	NULL	0	NULL	m-xylene	NULL		bind	NULL				XylR	NULL		A domain		NULL		0	NULL	NULL	NULL	gw60_cell_86_2_331_s_194	8706137	A Model for the Multimerization Cycle  of XylR at the UAS of the  Pu Promoter The series of events  that follow the release of intramolecular repression caused by  m-xylene binding to  the A domain of XylR are sketched in the figure as a  multimerization and demultimerization cycle driven by ATP.	bind
50565	2	10978	6	10	NULL	0	NULL	statement 1	NULL		cause	NULL				intramolecular repression	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_86_2_331_s_194	8706137	A Model for the Multimerization Cycle  of XylR at the UAS of the  Pu Promoter The series of events  that follow the release of intramolecular repression caused by  m-xylene binding to  the A domain of XylR are sketched in the figure as a  multimerization and demultimerization cycle driven by ATP.	bind
50122	1	10979	5	13	NULL	NULL	NULL	PLC-delta1	GP		bind			pleckstrin homology domain		IP3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_34401_s_153	12097325	A model for the PIP2 head group was taken from the structure of the pleckstrin homology domain of PLC-delta1 bound to IP3 (Protein Data Bank code  1MAI) ( 65).	bind
42230	1	10979	6	NULL	NULL	0	NULL	PLC-delta1	NULL		bind	NULL		pleckstrin homology domain		IP3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_37_34401_s_153	12097325	A model for the PIP2 head group was taken from the structure of the pleckstrin homology domain of PLC-delta1 bound to IP3 (Protein Data Bank code  1MAI) ( 65).	bind
50123	1	10980	5	13	NULL	NULL	NULL	PAF	GP		bind					G protein-coupled seven transmembrane receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_5_3497_s_239	14617636	A model for the stimulation of separate pathways upon binding of PAF to its G protein-coupled  seven transmembrane receptor.	bind
42231	1	10980	6	NULL	NULL	0	NULL	PAF	NULL		bind	NULL				G protein-coupled seven transmembrane receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_5_3497_s_239	14617636	A model for the stimulation of separate pathways upon binding of PAF to its G protein-coupled  seven transmembrane receptor.	bind
50124	1	10981	5	13	NULL	NULL	NULL	Frq1	GP	yeast	bind					Ca2+	Chemical	N-myristoylated			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49589_s_15	14512421	A model for the three-dimensional structure of  N-myristoylated Ca2+-bound yeast Frq1, based on analysis by NMR, is nearly superimposable ( ).	bind
42232	1	10981	6	10	NULL	0	NULL	Ca2+	NULL	N-myristoylated	bind	NULL				Frq1	NULL	yeast			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_49_49589_s_15	14512421	A model for the three-dimensional structure of  N-myristoylated Ca2+-bound yeast Frq1, based on analysis by NMR, is nearly superimposable ( ).	bind
50126	1	10982	5	13	NULL	NULL	NULL	thrombin	GP		is a type of					serine protease	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1705_s_16	8601636	A model for thrombin receptor activation in which the  serine protease thrombin binds to an acidic hirudin-like domain and proteolytically cleaves the amino terminal exodomain of the thrombin receptor between Arg  41 and Ser42 ( 4)  has since been postulated.	bind
50127	2	10982	5	13	NULL	NULL	NULL	thrombin	GP		bind							acidic	hirudin-like domain		NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1705_s_16	8601636	A model for thrombin receptor activation in which the  serine protease thrombin binds to an acidic hirudin-like domain and proteolytically cleaves the amino terminal exodomain of the thrombin receptor between Arg  41 and Ser42 ( 4)  has since been postulated.	bind
50128	3	10982	5	13	NULL	NULL	NULL	statement 1	GP		cleaves		proteolytically			thrombin receptor	GP		amino terminal exodomain;;between Arg 41 and Ser42		NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_97_7_1705_s_16	8601636	A model for thrombin receptor activation in which the  serine protease thrombin binds to an acidic hirudin-like domain and proteolytically cleaves the amino terminal exodomain of the thrombin receptor between Arg  41 and Ser42 ( 4)  has since been postulated.	bind
42233	1	10982	6	NULL	NULL	0	NULL	thrombin	NULL		is a type of	NULL				serine protease	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_7_1705_s_16	8601636	A model for thrombin receptor activation in which the  serine protease thrombin binds to an acidic hirudin-like domain and proteolytically cleaves the amino terminal exodomain of the thrombin receptor between Arg  41 and Ser42 ( 4)  has since been postulated.	bind
42234	2	10982	6	NULL	NULL	0	NULL	thrombin	NULL		bind	NULL					NULL	acidic	hirudin-like domain 		NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_7_1705_s_16	8601636	A model for thrombin receptor activation in which the  serine protease thrombin binds to an acidic hirudin-like domain and proteolytically cleaves the amino terminal exodomain of the thrombin receptor between Arg  41 and Ser42 ( 4)  has since been postulated.	bind
42235	3	10982	6	NULL	NULL	0	NULL	thrombin	NULL		cleaves	NULL	proteolytically			thrombin receptor	NULL		amino terminal exodomain;; between Arg 41 and Ser42		NULL		0	NULL	NULL	NULL	gw60_jclininvest_97_7_1705_s_16	8601636	A model for thrombin receptor activation in which the  serine protease thrombin binds to an acidic hirudin-like domain and proteolytically cleaves the amino terminal exodomain of the thrombin receptor between Arg  41 and Ser42 ( 4)  has since been postulated.	bind
50133	1	10983	5	13	NULL	NULL	NULL	Gpb1/2	GP		bind					Gpa2	GP		N-terminus amino acids 1 - 45		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4557_s_321	16030250	A model governing how the kelch Gpb1/2 subunits control Gpa2 is that Gpb1/2 bind to the Gpa2 N-terminal region spanning amino acids 1 - 45 and occlude binding of the Gpr1 C-terminal tail to the first fifteen amino acids of Gpa2 ( Figure 9).	bind
50134	2	10983	5	13	NULL	NULL	NULL	Gpr1	GP		bind			C-terminal tail 		Gpa2	GP		first fifteen amino acids of		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4557_s_321	16030250	A model governing how the kelch Gpb1/2 subunits control Gpa2 is that Gpb1/2 bind to the Gpa2 N-terminal region spanning amino acids 1 - 45 and occlude binding of the Gpr1 C-terminal tail to the first fifteen amino acids of Gpa2 ( Figure 9).	bind
50135	3	10983	5	13	NULL	NULL	NULL	statement 1	Process		occlude					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4557_s_321	16030250	A model governing how the kelch Gpb1/2 subunits control Gpa2 is that Gpb1/2 bind to the Gpa2 N-terminal region spanning amino acids 1 - 45 and occlude binding of the Gpr1 C-terminal tail to the first fifteen amino acids of Gpa2 ( Figure 9).	bind
42236	1	10983	6	NULL	NULL	0	NULL	Gpb1/2	NULL		bind	NULL				Gpa2	NULL		N-terminal region;; amino acid 1 to 45		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4557_s_321	16030250	A model governing how the kelch Gpb1/2 subunits control Gpa2 is that Gpb1/2 bind to the Gpa2 N-terminal region spanning amino acids 1 - 45 and occlude binding of the Gpr1 C-terminal tail to the first fifteen amino acids of Gpa2 ( Figure 9).	bind
42237	2	10983	6	NULL	NULL	0	NULL	Gpr1	NULL		bind	NULL		C-terminal tail		Gpa2	NULL		first fifteen amino acid		NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4557_s_321	16030250	A model governing how the kelch Gpb1/2 subunits control Gpa2 is that Gpb1/2 bind to the Gpa2 N-terminal region spanning amino acids 1 - 45 and occlude binding of the Gpr1 C-terminal tail to the first fifteen amino acids of Gpa2 ( Figure 9).	bind
42238	3	10983	6	NULL	NULL	0	NULL	statement 1	NULL		occlude	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4557_s_321	16030250	A model governing how the kelch Gpb1/2 subunits control Gpa2 is that Gpb1/2 bind to the Gpa2 N-terminal region spanning amino acids 1 - 45 and occlude binding of the Gpr1 C-terminal tail to the first fifteen amino acids of Gpa2 ( Figure 9).	bind
50137	1	10984	5	13	NULL	NULL	NULL	MBP	GP	unfolded form of	bind					SecB	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_38247_s_29	12829711	A model has been proposed for the interaction of SecB and MBP: an unfolded form of MBP binds to SecB and is in equilibrium with unbound form.	bind
50138	2	10984	5	13	NULL	NULL	NULL	statement 1	Process		is in equilibrium with					MBP	GP	unbound form of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_38247_s_29	12829711	A model has been proposed for the interaction of SecB and MBP: an unfolded form of MBP binds to SecB and is in equilibrium with unbound form.	bind
42239	1	10984	6	NULL	NULL	0	NULL	SecB	NULL		interacts with	NULL				MBP	NULL	unfolded			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_40_38247_s_29	12829711	A model has been proposed for the interaction of SecB and MBP: an unfolded form of MBP binds to SecB and is in equilibrium with unbound form.	bind
58415	2	10984	6	10	NULL	0	NULL	statement 1			is in equilibrium with					MBP		unbound form of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_40_38247_s_29	12829711	A model has been proposed for the interaction of SecB and MBP: an unfolded form of MBP binds to SecB and is in equilibrium with unbound form.	bind
50129	1	10985	5	13	NULL	NULL	NULL	syndecan 4	GP		bind		low affinity						cysteine-rich domain		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_861_s_26	15574885	A model has been proposed in which initial low-affinity binding of the cysteine-rich domain by syndecan 4 triggers a conformational change of ADAM12- cys, allowing its binding to integrins (Iba  et al., 2000 ).	bind
50130	2	10985	5	13	NULL	NULL	NULL	statement 1	Process		triggers					ADAM12	GP	conformational change of	cys		NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_861_s_26	15574885	A model has been proposed in which initial low-affinity binding of the cysteine-rich domain by syndecan 4 triggers a conformational change of ADAM12- cys, allowing its binding to integrins (Iba  et al., 2000 ).	bind
50131	3	10985	5	13	NULL	NULL	NULL	ADAM12	GP		bind			cys		integrins 	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_861_s_26	15574885	A model has been proposed in which initial low-affinity binding of the cysteine-rich domain by syndecan 4 triggers a conformational change of ADAM12- cys, allowing its binding to integrins (Iba  et al., 2000 ).	bind
50132	4	10985	5	13	NULL	NULL	NULL	statement 2	Process		allows					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_2_861_s_26	15574885	A model has been proposed in which initial low-affinity binding of the cysteine-rich domain by syndecan 4 triggers a conformational change of ADAM12- cys, allowing its binding to integrins (Iba  et al., 2000 ).	bind
42240	1	10985	6	NULL	NULL	0	NULL		NULL		bind	NULL	low affinity	cysteine-rich domain		syndecan-4	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_2_861_s_26	15574885	A model has been proposed in which initial low-affinity binding of the cysteine-rich domain by syndecan 4 triggers a conformational change of ADAM12- cys, allowing its binding to integrins (Iba  et al., 2000 ).	bind
42241	2	10985	6	NULL	NULL	0	NULL	statement 1	NULL		triggers	NULL				ADAM12	NULL	conformational change of	Cys		NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_2_861_s_26	15574885	A model has been proposed in which initial low-affinity binding of the cysteine-rich domain by syndecan 4 triggers a conformational change of ADAM12- cys, allowing its binding to integrins (Iba  et al., 2000 ).	bind
42242	3	10985	6	NULL	NULL	0	NULL	ADAM12	NULL		bind	NULL		cys		integrin	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_2_861_s_26	15574885	A model has been proposed in which initial low-affinity binding of the cysteine-rich domain by syndecan 4 triggers a conformational change of ADAM12- cys, allowing its binding to integrins (Iba  et al., 2000 ).	bind
42243	4	10985	6	NULL	NULL	0	NULL	statement 2	NULL		leads to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_2_861_s_26	15574885	A model has been proposed in which initial low-affinity binding of the cysteine-rich domain by syndecan 4 triggers a conformational change of ADAM12- cys, allowing its binding to integrins (Iba  et al., 2000 ).	bind
50136	1	10986	5	13	NULL	NULL	NULL	SipA	GP		bind					actin monomers	GP	consecutive			NULL		NULL	NULL	NULL	NULL	gw60_annurevcelldevbiol_17_0_53_s_196	11687484	A model has been proposed in which SipA binds two consecutive actin monomers across the double-stranded right-handed helix in both of its faces ( Mitra et al. 2000) ( Figure 4).	bind
50572	2	10986	5	13	NULL	NULL	NULL	statement 1	Process		occur across					double-stranded right-handed helix	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_annurevcelldevbiol_17_0_53_s_196	11687484	A model has been proposed in which SipA binds two consecutive actin monomers across the double-stranded right-handed helix in both of its faces ( Mitra et al. 2000) ( Figure 4).	bind
42244	1	10986	6	NULL	NULL	0	NULL	SipA	NULL		bind	NULL				actin monomer	NULL				NULL		0	NULL	NULL	NULL	gw60_annurevcelldevbiol_17_0_53_s_196	11687484	A model has been proposed in which SipA binds two consecutive actin monomers across the double-stranded right-handed helix in both of its faces ( Mitra et al. 2000) ( Figure 4).	bind
42245	2	10986	6	10	NULL	0	NULL	statement 1	NULL		occurs across	NULL				double-stranded right-handed helix	NULL				NULL		NULL	NULL	NULL	NULL	gw60_annurevcelldevbiol_17_0_53_s_196	11687484	A model has been proposed in which SipA binds two consecutive actin monomers across the double-stranded right-handed helix in both of its faces ( Mitra et al. 2000) ( Figure 4).	bind
50139	1	10987	5	13	NULL	NULL	NULL	S1P	GP		bind					EDG receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_136	12069805	A model has been proposed that implicates LPPs in S1P signal termination at EDG receptors [ 1, whereby S1P binding to EDG receptors stimulates protein kinases, which then both transmit movement signals and phosphorylate and activate the putative signal terminator phosphatase [ 1.	bind
50140	2	10987	5	13	NULL	NULL	NULL	statement 1	Process		stimulates					protein kinases	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_136	12069805	A model has been proposed that implicates LPPs in S1P signal termination at EDG receptors [ 1, whereby S1P binding to EDG receptors stimulates protein kinases, which then both transmit movement signals and phosphorylate and activate the putative signal terminator phosphatase [ 1.	bind
50141	3	10987	5	13	NULL	NULL	NULL	statement 1	Process		transmit					movement signals	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_136	12069805	A model has been proposed that implicates LPPs in S1P signal termination at EDG receptors [ 1, whereby S1P binding to EDG receptors stimulates protein kinases, which then both transmit movement signals and phosphorylate and activate the putative signal terminator phosphatase [ 1.	bind
50142	4	10987	5	13	NULL	NULL	NULL	statement 1	Process		phosphorylates					signal terminator phosphatase	GP	putative			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_136	12069805	A model has been proposed that implicates LPPs in S1P signal termination at EDG receptors [ 1, whereby S1P binding to EDG receptors stimulates protein kinases, which then both transmit movement signals and phosphorylate and activate the putative signal terminator phosphatase [ 1.	bind
50143	5	10987	5	13	NULL	NULL	NULL	statement 1	Process		activates					signal terminator phosphatase	GP	putative			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_136	12069805	A model has been proposed that implicates LPPs in S1P signal termination at EDG receptors [ 1, whereby S1P binding to EDG receptors stimulates protein kinases, which then both transmit movement signals and phosphorylate and activate the putative signal terminator phosphatase [ 1.	bind
42246	1	10987	6	NULL	NULL	0	NULL	S1P	NULL		bind	NULL				EDG receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_136	12069805	A model has been proposed that implicates LPPs in S1P signal termination at EDG receptors [ 1, whereby S1P binding to EDG receptors stimulates protein kinases, which then both transmit movement signals and phosphorylate and activate the putative signal terminator phosphatase [ 1.	bind
42247	2	10987	6	NULL	NULL	0	NULL	statement 1	NULL		stimulates	NULL				protein kinases	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_136	12069805	A model has been proposed that implicates LPPs in S1P signal termination at EDG receptors [ 1, whereby S1P binding to EDG receptors stimulates protein kinases, which then both transmit movement signals and phosphorylate and activate the putative signal terminator phosphatase [ 1.	bind
42248	3	10987	6	10	NULL	0	NULL	statement 1	NULL		phosphorylates	NULL				signal terminator phosphatase	NULL	putative			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_136	12069805	A model has been proposed that implicates LPPs in S1P signal termination at EDG receptors [ 1, whereby S1P binding to EDG receptors stimulates protein kinases, which then both transmit movement signals and phosphorylate and activate the putative signal terminator phosphatase [ 1.	bind
42249	4	10987	6	10	NULL	0	NULL	statement 1	NULL		activates	NULL				signal terminator phosphatase	NULL	putative			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_136	12069805	A model has been proposed that implicates LPPs in S1P signal termination at EDG receptors [ 1, whereby S1P binding to EDG receptors stimulates protein kinases, which then both transmit movement signals and phosphorylate and activate the putative signal terminator phosphatase [ 1.	bind
42250	5	10987	6	10	NULL	0	NULL	statement 1	NULL		transmit	NULL				movement signals	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_136	12069805	A model has been proposed that implicates LPPs in S1P signal termination at EDG receptors [ 1, whereby S1P binding to EDG receptors stimulates protein kinases, which then both transmit movement signals and phosphorylate and activate the putative signal terminator phosphatase [ 1.	bind
50144	1	10989	5	13	NULL	NULL	NULL	FGF2	GP		complex with					FGFR1	GP		ligand binding domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_101_4_413_s_11	10830168	A model has emerged from the recent crystal structure of  FGF2 complexed with the ligand binding domain of FGFR1 to explain how  FGFs in concert with heparin induce FGFR dimerization and activation (Plotnikov et  al., 1999   ).	bind
50145	2	10989	5	13	NULL	NULL	NULL	FGFs	GP		induce					FGFR	GP	dimerization of			NULL		NULL	NULL	NULL	NULL	gw60_cell_101_4_413_s_11	10830168	A model has emerged from the recent crystal structure of  FGF2 complexed with the ligand binding domain of FGFR1 to explain how  FGFs in concert with heparin induce FGFR dimerization and activation (Plotnikov et  al., 1999   ).	bind
50146	3	10989	5	13	NULL	NULL	NULL	statement 2	Process		in concert with					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_101_4_413_s_11	10830168	A model has emerged from the recent crystal structure of  FGF2 complexed with the ligand binding domain of FGFR1 to explain how  FGFs in concert with heparin induce FGFR dimerization and activation (Plotnikov et  al., 1999   ).	bind
50147	4	10989	5	13	NULL	NULL	NULL	FGFs	GP		induce					FGFR	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_cell_101_4_413_s_11	10830168	A model has emerged from the recent crystal structure of  FGF2 complexed with the ligand binding domain of FGFR1 to explain how  FGFs in concert with heparin induce FGFR dimerization and activation (Plotnikov et  al., 1999   ).	bind
50148	5	10989	5	13	NULL	NULL	NULL	statement 4	Process		in concert with					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_101_4_413_s_11	10830168	A model has emerged from the recent crystal structure of  FGF2 complexed with the ligand binding domain of FGFR1 to explain how  FGFs in concert with heparin induce FGFR dimerization and activation (Plotnikov et  al., 1999   ).	bind
42251	1	10989	6	10	NULL	0	NULL	FGF2	NULL		complex with	NULL				FGFR1	NULL		ligand binding domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_101_4_413_s_11	10830168	A model has emerged from the recent crystal structure of  FGF2 complexed with the ligand binding domain of FGFR1 to explain how  FGFs in concert with heparin induce FGFR dimerization and activation (Plotnikov et  al., 1999   ).	bind
42252	2	10989	6	NULL	NULL	0	NULL	FGF	NULL		induce	NULL				FGFR	NULL	dimerization of			NULL		0	NULL	NULL	NULL	gw60_cell_101_4_413_s_11	10830168	A model has emerged from the recent crystal structure of  FGF2 complexed with the ligand binding domain of FGFR1 to explain how  FGFs in concert with heparin induce FGFR dimerization and activation (Plotnikov et  al., 1999   ).	bind
42253	3	10989	6	NULL	NULL	0	NULL	statement 2	NULL		occurs in concert with	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_101_4_413_s_11	10830168	A model has emerged from the recent crystal structure of  FGF2 complexed with the ligand binding domain of FGFR1 to explain how  FGFs in concert with heparin induce FGFR dimerization and activation (Plotnikov et  al., 1999   ).	bind
42254	4	10989	6	NULL	NULL	0	NULL	FGF	NULL		induce	NULL				FGFR	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_cell_101_4_413_s_11	10830168	A model has emerged from the recent crystal structure of  FGF2 complexed with the ligand binding domain of FGFR1 to explain how  FGFs in concert with heparin induce FGFR dimerization and activation (Plotnikov et  al., 1999   ).	bind
42255	5	10989	6	NULL	NULL	0	NULL	statement 4	NULL		occurs in concert with	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_101_4_413_s_11	10830168	A model has emerged from the recent crystal structure of  FGF2 complexed with the ligand binding domain of FGFR1 to explain how  FGFs in concert with heparin induce FGFR dimerization and activation (Plotnikov et  al., 1999   ).	bind
50149	1	10990	5	13	NULL	NULL	NULL	IkappaBbeta	GP	newly synthesized;;unphosphorylated	bind					NF-kappaB	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_234	9418895	A model has recently been proposed ( 65), in which after the stimulus-induced degradation of both IkappaBs, the binding of the newly synthesized unphosphorylated IkappaBbeta to NF-kappaB blocks the inhibitory effect of the newly synthesized IkappaBalpha.	bind
50150	2	10990	5	13	NULL	NULL	NULL	statement 1	Process		blocks					IkappaBalpha	GP	inhibitory effect of;;newly synthesized			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_234	9418895	A model has recently been proposed ( 65), in which after the stimulus-induced degradation of both IkappaBs, the binding of the newly synthesized unphosphorylated IkappaBbeta to NF-kappaB blocks the inhibitory effect of the newly synthesized IkappaBalpha.	bind
50151	3	10990	5	13	NULL	NULL	NULL	stimulus	Process		induce					IkappaBs	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_234	9418895	A model has recently been proposed ( 65), in which after the stimulus-induced degradation of both IkappaBs, the binding of the newly synthesized unphosphorylated IkappaBbeta to NF-kappaB blocks the inhibitory effect of the newly synthesized IkappaBalpha.	bind
50573	4	10990	5	13	NULL	NULL	NULL	statement 2	Process		occurs after					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_234	9418895	A model has recently been proposed ( 65), in which after the stimulus-induced degradation of both IkappaBs, the binding of the newly synthesized unphosphorylated IkappaBbeta to NF-kappaB blocks the inhibitory effect of the newly synthesized IkappaBalpha.	bind
42256	1	10990	6	NULL	NULL	0	NULL	IkappaBbeta	NULL	newly synthesized;; unphosphorylated	bind	NULL				NF-kappaB	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_234	9418895	A model has recently been proposed ( 65), in which after the stimulus-induced degradation of both IkappaBs, the binding of the newly synthesized unphosphorylated IkappaBbeta to NF-kappaB blocks the inhibitory effect of the newly synthesized IkappaBalpha.	bind
42257	2	10990	6	10	NULL	0	NULL	statement 1	NULL		blocks	NULL				IkappaBalpha	NULL	inhibitory effect of ;;newly synthesized			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_234	9418895	A model has recently been proposed ( 65), in which after the stimulus-induced degradation of both IkappaBs, the binding of the newly synthesized unphosphorylated IkappaBbeta to NF-kappaB blocks the inhibitory effect of the newly synthesized IkappaBalpha.	bind
42258	3	10990	6	10	NULL	0	NULL	stimulus	NULL		induce	NULL				IkappaBs	NULL	degradation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_234	9418895	A model has recently been proposed ( 65), in which after the stimulus-induced degradation of both IkappaBs, the binding of the newly synthesized unphosphorylated IkappaBbeta to NF-kappaB blocks the inhibitory effect of the newly synthesized IkappaBalpha.	bind
50574	4	10990	6	10	NULL	0	NULL	statement 2	NULL		occurs after	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_234	9418895	A model has recently been proposed ( 65), in which after the stimulus-induced degradation of both IkappaBs, the binding of the newly synthesized unphosphorylated IkappaBbeta to NF-kappaB blocks the inhibitory effect of the newly synthesized IkappaBalpha.	bind
50152	1	10991	5	13	NULL	NULL	NULL	SM	GP		bind					pre-mRNA	NucleicAcid			3' terminus	NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_15_8852_s_232	9671768	A model in which SM binds pre-mRNA at the 3' terminus is consistent with the negative effect of SM on intron-containing transcripts.	bind
50575	2	10991	5	13	NULL	NULL	NULL	SM	GP		effect		negatively			intron-containing transcripts	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_15_8852_s_232	9671768	A model in which SM binds pre-mRNA at the 3' terminus is consistent with the negative effect of SM on intron-containing transcripts.	bind
42259	1	10991	6	10	NULL	0	NULL	SM			bind					pre-mRNA				3' terminus	NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_15_8852_s_232	9671768	A model in which SM binds pre-mRNA at the 3' terminus is consistent with the negative effect of SM on intron-containing transcripts.	bind
42260	2	10991	6	10	NULL	0	NULL	SM 	NULL		effect	NULL	negatively			intron-containing transcripts	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_15_8852_s_232	9671768	A model in which SM binds pre-mRNA at the 3' terminus is consistent with the negative effect of SM on intron-containing transcripts.	bind
50153	1	10992	5	13	NULL	NULL	NULL	gp31	GP		bind					GroEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34075_s_344	9852065	A model in which the binding of gp31 to GroEL creates a larger folding cavity than when GroES is bound to GroEL could also explain the GroEL-gp31-specific requirement.	bind
50154	2	10992	5	13	NULL	NULL	NULL	GroES	GP		bind					GroEL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34075_s_344	9852065	A model in which the binding of gp31 to GroEL creates a larger folding cavity than when GroES is bound to GroEL could also explain the GroEL-gp31-specific requirement.	bind
50155	3	10992	5	13	NULL	NULL	NULL	statement 1	Process		creates					folding cavity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34075_s_344	9852065	A model in which the binding of gp31 to GroEL creates a larger folding cavity than when GroES is bound to GroEL could also explain the GroEL-gp31-specific requirement.	bind
50156	4	10992	5	13	NULL	NULL	NULL	statement 2	Process		creates					folding cavity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34075_s_344	9852065	A model in which the binding of gp31 to GroEL creates a larger folding cavity than when GroES is bound to GroEL could also explain the GroEL-gp31-specific requirement.	bind
50157	5	10992	5	13	NULL	NULL	NULL	statement 3	Process		is larger than					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34075_s_344	9852065	A model in which the binding of gp31 to GroEL creates a larger folding cavity than when GroES is bound to GroEL could also explain the GroEL-gp31-specific requirement.	bind
42261	1	10992	6	NULL	NULL	0	NULL	gp31	NULL		bind	NULL				GroEL	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_51_34075_s_344	9852065	A model in which the binding of gp31 to GroEL creates a larger folding cavity than when GroES is bound to GroEL could also explain the GroEL-gp31-specific requirement.	bind
42262	2	10992	6	NULL	NULL	0	NULL	GroES	NULL		bind	NULL				GroEL	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_51_34075_s_344	9852065	A model in which the binding of gp31 to GroEL creates a larger folding cavity than when GroES is bound to GroEL could also explain the GroEL-gp31-specific requirement.	bind
50576	3	10992	6	10	NULL	0	NULL	statement 1	NULL		creates	NULL				folding cavity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_51_34075_s_344	9852065	A model in which the binding of gp31 to GroEL creates a larger folding cavity than when GroES is bound to GroEL could also explain the GroEL-gp31-specific requirement.	bind
50577	4	10992	6	10	NULL	0	NULL	statement 2	NULL		creates	NULL				folding cavity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_51_34075_s_344	9852065	A model in which the binding of gp31 to GroEL creates a larger folding cavity than when GroES is bound to GroEL could also explain the GroEL-gp31-specific requirement.	bind
50578	5	10992	6	10	NULL	0	NULL	statement 3	NULL		is larger than	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_51_34075_s_344	9852065	A model in which the binding of gp31 to GroEL creates a larger folding cavity than when GroES is bound to GroEL could also explain the GroEL-gp31-specific requirement.	bind
50159	1	10994	5	13	NULL	NULL	NULL	Rac1	GP		bind			effector region		p67 phox	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18834_s_13	9228059	A model is discussed in which the Rac1 effector region binds to p67 phox, the C terminus binds to the membrane, and the insert region interacts with a different protein component, possibly cytochrome  b558.	bind
50160	2	10994	5	13	NULL	NULL	NULL	Rac1	GP		bind			C terminus		membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18834_s_13	9228059	A model is discussed in which the Rac1 effector region binds to p67 phox, the C terminus binds to the membrane, and the insert region interacts with a different protein component, possibly cytochrome  b558.	bind
50161	3	10994	5	13	NULL	NULL	NULL	Rac1	GP		interacts with		possibly	insert region		cytochrome b558	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18834_s_13	9228059	A model is discussed in which the Rac1 effector region binds to p67 phox, the C terminus binds to the membrane, and the insert region interacts with a different protein component, possibly cytochrome  b558.	bind
42263	1	10994	6	NULL	NULL	0	NULL	Rac1	NULL		bind	NULL		effector region		p67 phox	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_30_18834_s_13	9228059	A model is discussed in which the Rac1 effector region binds to p67 phox, the C terminus binds to the membrane, and the insert region interacts with a different protein component, possibly cytochrome  b558.	bind
42264	2	10994	6	NULL	NULL	0	NULL	Rac1	NULL		bind	NULL		C terminus		membrane	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_30_18834_s_13	9228059	A model is discussed in which the Rac1 effector region binds to p67 phox, the C terminus binds to the membrane, and the insert region interacts with a different protein component, possibly cytochrome  b558.	bind
42265	3	10994	6	NULL	NULL	0	NULL	Rac1	NULL		interacts with	NULL	possibly	insert region		cytochrome b558	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_30_18834_s_13	9228059	A model is discussed in which the Rac1 effector region binds to p67 phox, the C terminus binds to the membrane, and the insert region interacts with a different protein component, possibly cytochrome  b558.	bind
50162	1	10995	5	13	NULL	NULL	NULL	TSU	GP		bind		sequence specifically			extracts containing STAT1	GP				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_60_1_23_s_234	9858482	A model is proposed in  Figure 8 that takes into account the observed reduction in STAT1 translocation in TSU stable transfectants as well as the saturable and sequence-specific binding of TSU and small loop-loop model RNA to extracts containing STAT1.	bind
50163	2	10995	5	13	NULL	NULL	NULL	small loop-loop model RNA	NucleicAcid		bind		sequence specifically			extracts containing STAT1	GP				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_60_1_23_s_234	9858482	A model is proposed in  Figure 8 that takes into account the observed reduction in STAT1 translocation in TSU stable transfectants as well as the saturable and sequence-specific binding of TSU and small loop-loop model RNA to extracts containing STAT1.	bind
42501	1	10995	6	NULL	NULL	0	NULL	TSU	NULL		bind	NULL	sequence specifically			extracts containing STAT1	NULL				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_1_23_s_234	9858482	A model is proposed in  Figure 8 that takes into account the observed reduction in STAT1 translocation in TSU stable transfectants as well as the saturable and sequence-specific binding of TSU and small loop-loop model RNA to extracts containing STAT1.	bind
42502	2	10995	6	NULL	NULL	0	NULL	small loop-loop model RNA	NULL		bind	NULL	sequence specifically			extracts containing STAT1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_60_1_23_s_234	9858482	A model is proposed in  Figure 8 that takes into account the observed reduction in STAT1 translocation in TSU stable transfectants as well as the saturable and sequence-specific binding of TSU and small loop-loop model RNA to extracts containing STAT1.	bind
50164	1	10996	5	13	NULL	NULL	NULL	TorI	GP		bind					TorR	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_25_9423_s_32	15197250	A model is proposed in which binding of TorI to TorR could prevent RNA polymerase recruitment to the  torC promoter.	bind
50165	2	10996	5	13	NULL	NULL	NULL	RNA polymerase	GP		is recruited to					torC	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_25_9423_s_32	15197250	A model is proposed in which binding of TorI to TorR could prevent RNA polymerase recruitment to the  torC promoter.	bind
50166	3	10996	5	13	NULL	NULL	NULL	statement 1	Process		prevents					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_25_9423_s_32	15197250	A model is proposed in which binding of TorI to TorR could prevent RNA polymerase recruitment to the  torC promoter.	bind
42266	1	10996	6	NULL	NULL	0	NULL	TorI	NULL		bind	NULL				TorR	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_25_9423_s_32	15197250	A model is proposed in which binding of TorI to TorR could prevent RNA polymerase recruitment to the  torC promoter.	bind
42267	2	10996	6	NULL	NULL	0	NULL	RNA polymerase 	NULL		is recruited to	NULL				torC 	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_pnas_101_25_9423_s_32	15197250	A model is proposed in which binding of TorI to TorR could prevent RNA polymerase recruitment to the  torC promoter.	bind
42268	3	10996	6	NULL	NULL	0	NULL	statement 1	NULL		prevents	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_25_9423_s_32	15197250	A model is proposed in which binding of TorI to TorR could prevent RNA polymerase recruitment to the  torC promoter.	bind
50167	1	10997	5	13	NULL	NULL	NULL	RNA-2	NucleicAcid		bind		directly			RNA-1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5378_829_s_10	9694655	A model is proposed in which direct binding of RNA-2 to RNA-1 trans-activates sgRNA synthesis.	bind
50168	2	10997	5	13	NULL	NULL	NULL	statement 1	Process		trans-activates					sgRNA	NucleicAcid	synthesis of			NULL		NULL	NULL	NULL	NULL	gw60_science_281_5378_829_s_10	9694655	A model is proposed in which direct binding of RNA-2 to RNA-1 trans-activates sgRNA synthesis.	bind
42269	1	10997	6	NULL	NULL	0	NULL	RNA-2	NULL		bind	NULL	directly			RNA-1	NULL				NULL		0	NULL	NULL	NULL	gw60_science_281_5378_829_s_10	9694655	A model is proposed in which direct binding of RNA-2 to RNA-1 trans-activates sgRNA synthesis.	bind
42270	2	10997	6	10	NULL	0	NULL	statement 1	NULL		trans-activates	NULL				sgRNA	NULL	synthesis of			NULL		NULL	NULL	NULL	NULL	gw60_science_281_5378_829_s_10	9694655	A model is proposed in which direct binding of RNA-2 to RNA-1 trans-activates sgRNA synthesis.	bind
50169	1	10998	5	13	NULL	NULL	NULL	IF1	GP		bind					F1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_9927_s_48	15640141	A model is proposed where the rate of IF1 binding to F1 is controlled by changes in the conformation of the IF1 binding site on F1, which depends on the catalytic state of the enzyme.	bind
50170	2	10998	5	13	NULL	NULL	NULL	statement 1	Process	rate of	is controlled by					F1	GP	changes in conformation of	IF1 binding site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_9927_s_48	15640141	A model is proposed where the rate of IF1 binding to F1 is controlled by changes in the conformation of the IF1 binding site on F1, which depends on the catalytic state of the enzyme.	bind
50171	3	10998	5	13	NULL	NULL	NULL	F1	GP	changes in conformation of	depends on			IF1 binding site		enzyme	GP	catalytic state of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_11_9927_s_48	15640141	A model is proposed where the rate of IF1 binding to F1 is controlled by changes in the conformation of the IF1 binding site on F1, which depends on the catalytic state of the enzyme.	bind
42271	1	10998	6	NULL	NULL	0	NULL	IF1	NULL		bind	NULL				F1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_11_9927_s_48	15640141	A model is proposed where the rate of IF1 binding to F1 is controlled by changes in the conformation of the IF1 binding site on F1, which depends on the catalytic state of the enzyme.	bind
42503	2	10998	6	NULL	NULL	0	NULL	statement 1	NULL	rate of	is controlled by	NULL				F1	NULL	conformational changes of	IF1 binding site		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_11_9927_s_48	15640141	A model is proposed where the rate of IF1 binding to F1 is controlled by changes in the conformation of the IF1 binding site on F1, which depends on the catalytic state of the enzyme.	bind
42504	3	10998	6	NULL	NULL	0	NULL	F1	NULL	conformational change of	depends on	NULL		IF1 binding site		enzyme	NULL	catalytic state of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_11_9927_s_48	15640141	A model is proposed where the rate of IF1 binding to F1 is controlled by changes in the conformation of the IF1 binding site on F1, which depends on the catalytic state of the enzyme.	bind
50172	1	10999	5	13	NULL	NULL	NULL	RIP140	GP		bind			AF-2		holo-RARholo-RXR	GP		AF-2		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_44_31320_s_246	10531331	A model is proposed wherein RIP140 also binds to holo-RARholo-RXR in a 2:1 ratio through the AF-2 of both receptors (Fig.  7 A).	bind
42272	1	10999	6	NULL	NULL	0	NULL	RIP140	NULL		bind	NULL		AF-2		holo-RARholo-RXR	NULL		AF-2		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_44_31320_s_246	10531331	A model is proposed wherein RIP140 also binds to holo-RARholo-RXR in a 2:1 ratio through the AF-2 of both receptors (Fig.  7 A).	bind
50173	1	11000	5	10	NULL	NULL	NULL	LGL	Cell		bind					target cell	Cell				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_143_2_2544649_s_12	2544649	A model is proposed,  whereby subsequent to binding of LGL to target cell the large granules  fuse to the LGL plasma membrane and release the small vesicles into the  binding pocket.	bind
50174	2	11000	5	10	NULL	NULL	NULL	large granules	CellComponent		fuse to					LGL plasma membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_143_2_2544649_s_12	2544649	A model is proposed,  whereby subsequent to binding of LGL to target cell the large granules  fuse to the LGL plasma membrane and release the small vesicles into the  binding pocket.	bind
50175	4	11000	5	10	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_143_2_2544649_s_12	2544649	A model is proposed,  whereby subsequent to binding of LGL to target cell the large granules  fuse to the LGL plasma membrane and release the small vesicles into the  binding pocket.	bind
50176	3	11000	5	10	NULL	NULL	NULL	small vesicles	CellComponent		is released into								binding pocket		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_143_2_2544649_s_12	2544649	A model is proposed,  whereby subsequent to binding of LGL to target cell the large granules  fuse to the LGL plasma membrane and release the small vesicles into the  binding pocket.	bind
50177	5	11000	5	10	NULL	NULL	NULL	statement 2	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_143_2_2544649_s_12	2544649	A model is proposed,  whereby subsequent to binding of LGL to target cell the large granules  fuse to the LGL plasma membrane and release the small vesicles into the  binding pocket.	bind
42505	1	11000	6	10	NULL	NULL	NULL	LGL	Cell		bind					target cell	Cell				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_143_2_2544649_s_12	2544649	A model is proposed,  whereby subsequent to binding of LGL to target cell the large granules  fuse to the LGL plasma membrane and release the small vesicles into the  binding pocket.	bind
42506	2	11000	6	10	NULL	NULL	NULL	large granules	CellComponent		fuse to					LGL plasma membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_143_2_2544649_s_12	2544649	A model is proposed,  whereby subsequent to binding of LGL to target cell the large granules  fuse to the LGL plasma membrane and release the small vesicles into the  binding pocket.	bind
42507	3	11000	6	10	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_143_2_2544649_s_12	2544649	A model is proposed,  whereby subsequent to binding of LGL to target cell the large granules  fuse to the LGL plasma membrane and release the small vesicles into the  binding pocket.	bind
42508	4	11000	6	10	NULL	NULL	NULL	small vesicles	CellComponent		released into								binding pocket		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_143_2_2544649_s_12	2544649	A model is proposed,  whereby subsequent to binding of LGL to target cell the large granules  fuse to the LGL plasma membrane and release the small vesicles into the  binding pocket.	bind
42509	5	11000	6	10	NULL	NULL	NULL	statement 2	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_143_2_2544649_s_12	2544649	A model is proposed,  whereby subsequent to binding of LGL to target cell the large granules  fuse to the LGL plasma membrane and release the small vesicles into the  binding pocket.	bind
42510	1	11001	6	10	NULL	NULL	NULL	KAP	GP		interacts with					pCDK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_615_s_235	11463386	A model of a ternary pCDK2/cyclinA/KAP complex based on our pCDK2/KAPt structure and that of the pCDK2/cyclinA/peptide complex explains these results because it predicts that with the phosphorylated activation segment sequestered at the pCDK2/cyclin A interface, the interaction of KAP with pCDK2 would not interfere with the peptide substrate binding site of CDK2 or the RXL recruitment peptide site of cyclin A   (Figure 5).	bind
42511	2	11001	6	10	NULL	NULL	NULL	statement 1	Process		does not interfere					CDK2	GP		peptide substrate binding site		NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_615_s_235	11463386	A model of a ternary pCDK2/cyclinA/KAP complex based on our pCDK2/KAPt structure and that of the pCDK2/cyclinA/peptide complex explains these results because it predicts that with the phosphorylated activation segment sequestered at the pCDK2/cyclin A interface, the interaction of KAP with pCDK2 would not interfere with the peptide substrate binding site of CDK2 or the RXL recruitment peptide site of cyclin A   (Figure 5).	bind
42512	3	11001	6	10	NULL	NULL	NULL	statement 1	Process		does not interfere with					cyclin A	GP		RXL recruitment peptide site		NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_615_s_235	11463386	A model of a ternary pCDK2/cyclinA/KAP complex based on our pCDK2/KAPt structure and that of the pCDK2/cyclinA/peptide complex explains these results because it predicts that with the phosphorylated activation segment sequestered at the pCDK2/cyclin A interface, the interaction of KAP with pCDK2 would not interfere with the peptide substrate binding site of CDK2 or the RXL recruitment peptide site of cyclin A   (Figure 5).	bind
48987	1	11001	7	10	NULL	NULL	NULL	KAP	GP		interacts with					pCDK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_615_s_235	11463386	A model of a ternary pCDK2/cyclinA/KAP complex based on our pCDK2/KAPt structure and that of the pCDK2/cyclinA/peptide complex explains these results because it predicts that with the phosphorylated activation segment sequestered at the pCDK2/cyclin A interface, the interaction of KAP with pCDK2 would not interfere with the peptide substrate binding site of CDK2 or the RXL recruitment peptide site of cyclin A   (Figure 5).	bind
48988	2	11001	7	10	NULL	NULL	NULL	statement 1	Process		does not interfere with					CDK2 	GP		peptide substrate binding site 		NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_615_s_235	11463386	A model of a ternary pCDK2/cyclinA/KAP complex based on our pCDK2/KAPt structure and that of the pCDK2/cyclinA/peptide complex explains these results because it predicts that with the phosphorylated activation segment sequestered at the pCDK2/cyclin A interface, the interaction of KAP with pCDK2 would not interfere with the peptide substrate binding site of CDK2 or the RXL recruitment peptide site of cyclin A   (Figure 5).	bind
48989	3	11001	7	10	NULL	NULL	NULL	statement 1	Process		does not interfere with					cyclin A	GP		RXL recruitment peptide site		NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_615_s_235	11463386	A model of a ternary pCDK2/cyclinA/KAP complex based on our pCDK2/KAPt structure and that of the pCDK2/cyclinA/peptide complex explains these results because it predicts that with the phosphorylated activation segment sequestered at the pCDK2/cyclin A interface, the interaction of KAP with pCDK2 would not interfere with the peptide substrate binding site of CDK2 or the RXL recruitment peptide site of cyclin A   (Figure 5).	bind
42273	1	11002	6	10	NULL	NULL	NULL	anthrax toxin lethal factor	GP		bind					protective antigen	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_45_16409_s_1	16251269	A model of anthrax toxin lethal factor bound to protective antigen.	bind
48990	1	11002	7	10	NULL	NULL	NULL	anthrax toxin lethal factor	GP		bind					protective antigen	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_45_16409_s_1	16251269	A model of anthrax toxin lethal factor bound to protective antigen.	bind
42274	1	11004	6	10	NULL	NULL	NULL	apoA-I	GP		bind					ABCA1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7384_s_309	14660648	A model of apoA-I lipidation  by ABCA1 can be proposed assuming that 1) initial binding of apoA-I to ABCA1 is irreversible  or slowly reversible ( k1"`  k -  1); 2) lipidated apoA-I (alpha-LpA-I-like particles) dissociate rapidly ( k2) from ABCA1 without any detectable reassociation; and 3) this system contains no  other apolipoprotein that could compete for the binding of lipid-free apoA-I to ABCA1.	bind
42513	2	11004	6	10	NULL	NULL	NULL	apo A-I	GP	lipid-free	bind					ABCA1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7384_s_309	14660648	A model of apoA-I lipidation  by ABCA1 can be proposed assuming that 1) initial binding of apoA-I to ABCA1 is irreversible  or slowly reversible ( k1"`  k -  1); 2) lipidated apoA-I (alpha-LpA-I-like particles) dissociate rapidly ( k2) from ABCA1 without any detectable reassociation; and 3) this system contains no  other apolipoprotein that could compete for the binding of lipid-free apoA-I to ABCA1.	bind
42514	3	11004	6	10	NULL	NULL	NULL	lipidated apoA-I	GP		is					alpha-LpA-I-like particles	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7384_s_309	14660648	A model of apoA-I lipidation  by ABCA1 can be proposed assuming that 1) initial binding of apoA-I to ABCA1 is irreversible  or slowly reversible ( k1"`  k -  1); 2) lipidated apoA-I (alpha-LpA-I-like particles) dissociate rapidly ( k2) from ABCA1 without any detectable reassociation; and 3) this system contains no  other apolipoprotein that could compete for the binding of lipid-free apoA-I to ABCA1.	bind
42515	4	11004	6	10	NULL	NULL	NULL	apoA-I	GP	lipidated	dissociates from		rapidly			ABCA1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7384_s_309	14660648	A model of apoA-I lipidation  by ABCA1 can be proposed assuming that 1) initial binding of apoA-I to ABCA1 is irreversible  or slowly reversible ( k1"`  k -  1); 2) lipidated apoA-I (alpha-LpA-I-like particles) dissociate rapidly ( k2) from ABCA1 without any detectable reassociation; and 3) this system contains no  other apolipoprotein that could compete for the binding of lipid-free apoA-I to ABCA1.	bind
48991	1	11004	7	10	NULL	NULL	NULL	apoA-I	GP		bind					ABCA1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7384_s_309	14660648	A model of apoA-I lipidation  by ABCA1 can be proposed assuming that 1) initial binding of apoA-I to ABCA1 is irreversible  or slowly reversible ( k1"`  k -  1); 2) lipidated apoA-I (alpha-LpA-I-like particles) dissociate rapidly ( k2) from ABCA1 without any detectable reassociation; and 3) this system contains no  other apolipoprotein that could compete for the binding of lipid-free apoA-I to ABCA1.	bind
48992	2	11004	7	10	NULL	NULL	NULL	statement 1	Process		is a type of					irreversible reaction	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7384_s_309	14660648	A model of apoA-I lipidation  by ABCA1 can be proposed assuming that 1) initial binding of apoA-I to ABCA1 is irreversible  or slowly reversible ( k1"`  k -  1); 2) lipidated apoA-I (alpha-LpA-I-like particles) dissociate rapidly ( k2) from ABCA1 without any detectable reassociation; and 3) this system contains no  other apolipoprotein that could compete for the binding of lipid-free apoA-I to ABCA1.	bind
48993	3	11004	7	10	NULL	NULL	NULL	statement 1	Process		is a type of					slowly reversible reaction	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7384_s_309	14660648	A model of apoA-I lipidation  by ABCA1 can be proposed assuming that 1) initial binding of apoA-I to ABCA1 is irreversible  or slowly reversible ( k1"`  k -  1); 2) lipidated apoA-I (alpha-LpA-I-like particles) dissociate rapidly ( k2) from ABCA1 without any detectable reassociation; and 3) this system contains no  other apolipoprotein that could compete for the binding of lipid-free apoA-I to ABCA1.	bind
48994	4	11004	7	10	NULL	NULL	NULL	 apoA-I	GP	lipidated	dissociate from		rapidly			ABCA1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7384_s_309	14660648	A model of apoA-I lipidation  by ABCA1 can be proposed assuming that 1) initial binding of apoA-I to ABCA1 is irreversible  or slowly reversible ( k1"`  k -  1); 2) lipidated apoA-I (alpha-LpA-I-like particles) dissociate rapidly ( k2) from ABCA1 without any detectable reassociation; and 3) this system contains no  other apolipoprotein that could compete for the binding of lipid-free apoA-I to ABCA1.	bind
48995	5	11004	7	10	NULL	NULL	NULL	apoA-I 	GP	lipid-free 	bind					ABCA1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7384_s_309	14660648	A model of apoA-I lipidation  by ABCA1 can be proposed assuming that 1) initial binding of apoA-I to ABCA1 is irreversible  or slowly reversible ( k1"`  k -  1); 2) lipidated apoA-I (alpha-LpA-I-like particles) dissociate rapidly ( k2) from ABCA1 without any detectable reassociation; and 3) this system contains no  other apolipoprotein that could compete for the binding of lipid-free apoA-I to ABCA1.	bind
48996	6	11004	7	10	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7384_s_309	14660648	A model of apoA-I lipidation  by ABCA1 can be proposed assuming that 1) initial binding of apoA-I to ABCA1 is irreversible  or slowly reversible ( k1"`  k -  1); 2) lipidated apoA-I (alpha-LpA-I-like particles) dissociate rapidly ( k2) from ABCA1 without any detectable reassociation; and 3) this system contains no  other apolipoprotein that could compete for the binding of lipid-free apoA-I to ABCA1.	bind
49037	7	11004	7	10	NULL	NULL	NULL	statement 4	Process		does not					reassociate	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7384_s_309	14660648	A model of apoA-I lipidation  by ABCA1 can be proposed assuming that 1) initial binding of apoA-I to ABCA1 is irreversible  or slowly reversible ( k1"`  k -  1); 2) lipidated apoA-I (alpha-LpA-I-like particles) dissociate rapidly ( k2) from ABCA1 without any detectable reassociation; and 3) this system contains no  other apolipoprotein that could compete for the binding of lipid-free apoA-I to ABCA1.	bind
49039	8	11004	7	10	NULL	NULL	NULL	lipidated apoA-I	GP		is					alpha-LpA-I-like particles	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_7384_s_309	14660648	A model of apoA-I lipidation  by ABCA1 can be proposed assuming that 1) initial binding of apoA-I to ABCA1 is irreversible  or slowly reversible ( k1"`  k -  1); 2) lipidated apoA-I (alpha-LpA-I-like particles) dissociate rapidly ( k2) from ABCA1 without any detectable reassociation; and 3) this system contains no  other apolipoprotein that could compete for the binding of lipid-free apoA-I to ABCA1.	bind
42275	1	11005	6	10	NULL	NULL	NULL	Cry1Ac	GP		bind		bivalent;;sequentially			APN	GP	L. dispar			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_19_14423_s_291	10799525	A model of bivalent sequential binding of Cry1Ac to  L. dispar APN.	bind
49040	1	11005	7	10	NULL	NULL	NULL	Cry1Ac	GP		bind		bivalent;;sequentially			APN	GP	L. dispar 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_19_14423_s_291	10799525	A model of bivalent sequential binding of Cry1Ac to  L. dispar APN.	bind
42276	1	11006	6	10	NULL	NULL	NULL	calmodulin	GP	Ca(2+)-free	bind					myosin	GP	unconventional			NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_structure_4_12_8994973_s_1	8994973	A model of Ca(2+)-free calmodulin binding to unconventional myosins reveals how calmodulin acts as a regulatory switch..	bind
42278	2	11006	6	10	NULL	NULL	NULL	calmodulin	GP		acts as a					regulatory switch	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_structure_4_12_8994973_s_1	8994973	A model of Ca(2+)-free calmodulin binding to unconventional myosins reveals how calmodulin acts as a regulatory switch..	bind
42279	3	11006	6	10	NULL	NULL	NULL	statement 1	Process		reveals					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_structure_4_12_8994973_s_1	8994973	A model of Ca(2+)-free calmodulin binding to unconventional myosins reveals how calmodulin acts as a regulatory switch..	bind
49041	1	11006	7	10	NULL	NULL	NULL	calmodulin 	GP	Ca(2+)-free	bind					myosins	GP	unconventional			NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_structure_4_12_8994973_s_1	8994973	A model of Ca(2+)-free calmodulin binding to unconventional myosins reveals how calmodulin acts as a regulatory switch..	bind
49042	2	11006	7	10	NULL	NULL	NULL	calmodulin	GP		acts as a 					regular switch	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_structure_4_12_8994973_s_1	8994973	A model of Ca(2+)-free calmodulin binding to unconventional myosins reveals how calmodulin acts as a regulatory switch..	bind
49043	3	11006	7	10	NULL	NULL	NULL	statement 1	Process		reveals					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_structure_4_12_8994973_s_1	8994973	A model of Ca(2+)-free calmodulin binding to unconventional myosins reveals how calmodulin acts as a regulatory switch..	bind
42280	1	11009	6	10	NULL	NULL	NULL	calmodulin	GP		bind								IQ motif		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_6_4347_s_192	12446675	A model of calmodulin bound to an IQ motif has been constructed, using the crystal structure of the regulatory domain of scallop myosin ( ,  ).	bind
49050	1	11009	7	10	NULL	NULL	NULL	calmodulin	GP		bind								IQ motif		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_6_4347_s_192	12446675	A model of calmodulin bound to an IQ motif has been constructed, using the crystal structure of the regulatory domain of scallop myosin ( ,  ).	bind
42281	1	11011	6	10	NULL	NULL	NULL	cGMP	Chemical		bind					delta1-52PKG-Ibeta	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_5_2380_s_5	12591946	A model of cGMP binding to delta1-52PKG-Ibeta indicates that elongation of delta1-52PKG-Ibeta requires binding of cGMP to the low-affinity binding site of the R domain.	bind
42282	2	11011	6	10	NULL	NULL	NULL	cGMP	Chemical		bind							low affinity	binding site of the R domain		NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_5_2380_s_5	12591946	A model of cGMP binding to delta1-52PKG-Ibeta indicates that elongation of delta1-52PKG-Ibeta requires binding of cGMP to the low-affinity binding site of the R domain.	bind
42283	3	11011	6	10	NULL	NULL	NULL	statement 2	Process		is required for					delta1-52PKG-Ibeta	GP	elongation of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_5_2380_s_5	12591946	A model of cGMP binding to delta1-52PKG-Ibeta indicates that elongation of delta1-52PKG-Ibeta requires binding of cGMP to the low-affinity binding site of the R domain.	bind
49051	1	11011	7	10	NULL	NULL	NULL	cGMP 	Chemical		bind					delta1-52PKG-Ibeta	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_5_2380_s_5	12591946	A model of cGMP binding to delta1-52PKG-Ibeta indicates that elongation of delta1-52PKG-Ibeta requires binding of cGMP to the low-affinity binding site of the R domain.	bind
49053	2	11011	7	10	NULL	NULL	NULL	 cGMP	Chemical		bind							low-affinity	binding site of R domain		NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_5_2380_s_5	12591946	A model of cGMP binding to delta1-52PKG-Ibeta indicates that elongation of delta1-52PKG-Ibeta requires binding of cGMP to the low-affinity binding site of the R domain.	bind
49054	3	11011	7	10	NULL	NULL	NULL	delta1-52PKG-Ibeta	GP	elongation of	requires					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_100_5_2380_s_5	12591946	A model of cGMP binding to delta1-52PKG-Ibeta indicates that elongation of delta1-52PKG-Ibeta requires binding of cGMP to the low-affinity binding site of the R domain.	bind
42284	1	11012	6	10	NULL	NULL	NULL	dimeric ligand	GP		bind					monomeric receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_14_2_135_s_170	11239446	A Model of Dimeric Ligand Binding to Monomeric Receptors	bind
49055	1	11012	7	10	NULL	NULL	NULL	Dimeric Ligand 	GP		bind					monomeric receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_14_2_135_s_170	11239446	A Model of Dimeric Ligand Binding to Monomeric Receptors	bind
42285	1	11014	6	10	NULL	NULL	NULL	glutamine	AminoAcid		bind					GlnRS	GP				NULL		NULL	NULL	NULL	NULL	gw60_structure_6_4_439_s_35	9562563	A model of glutamine bound to GlnRS was proposed based on the observed positions of ATP and adenine 76 (A76) of the tRNA  [6  .	bind
49056	1	11014	7	10	NULL	NULL	NULL	glutamine 	AminoAcid		bind					GlnRS	GP				NULL		NULL	NULL	NULL	NULL	gw60_structure_6_4_439_s_35	9562563	A model of glutamine bound to GlnRS was proposed based on the observed positions of ATP and adenine 76 (A76) of the tRNA  [6  .	bind
42287	2	11015	6	10	NULL	NULL	NULL	mAb 2G12 Fab2	GP		bind					HIV-1 Env spike					NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_42_14943_s_125	16219699	A model of mAb 2G12 Fab2 bound to the HIV-1 Env spike.	bind
49060	1	11015	7	10	NULL	NULL	NULL	mAb 2G12 Fab2	GP		bind					HIV-1 Env spike					NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_42_14943_s_125	16219699	A model of mAb 2G12 Fab2 bound to the HIV-1 Env spike.	bind
42288	1	11016	6	10	NULL	NULL	NULL	tRNA	NucleicAcid	bipartite precursor	bind					hLa protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_2_367_s_245	11134326	A model of phosphorylation-regulated, bipartite precursor tRNA binding by the hLa protein.	bind
42289	2	11016	6	10	NULL	NULL	NULL	statement 1	Process		is regulated by					phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_2_367_s_245	11134326	A model of phosphorylation-regulated, bipartite precursor tRNA binding by the hLa protein.	bind
49063	1	11016	7	10	NULL	NULL	NULL	hLa protein	GP		bind					tRNA	NucleicAcid	bipartite precursor			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_2_367_s_245	11134326	A model of phosphorylation-regulated, bipartite precursor tRNA binding by the hLa protein.	bind
49064	2	11016	7	10	NULL	NULL	NULL	phosphorylation	Process		regulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_2_367_s_245	11134326	A model of phosphorylation-regulated, bipartite precursor tRNA binding by the hLa protein.	bind
42516	1	11017	6	10	NULL	NULL	NULL	Immunophilin	GP		bind			tetratricopeptide repeat domain		hsp90	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_32_18841_s_244	7642537	A Model of Protein Targeting Mediated by Immunophilins and Other Proteins That Bind to hsp90 via Tetratricopeptide Repeat Domains.	bind
49065	1	11017	7	10	NULL	NULL	NULL	Immunophilins	GP		bind			Tetratricopeptide Repeat Domains		hsp90	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_32_18841_s_244	7642537	A Model of Protein Targeting Mediated by Immunophilins and Other Proteins That Bind to hsp90 via Tetratricopeptide Repeat Domains.	bind
42517	1	11018	6	10	NULL	NULL	NULL	GTP	Chemical		bind					Galpha subunit	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_13_11115_s_336	12538649	A model of RGS4 regulation by the anionic phospholipid  PA. Agonist-induced stimulation of G-protein-coupled receptors enhances GTP binding  to Galpha subunits.	bind
42518	2	11018	6	10	NULL	NULL	NULL	PA	Chemical		is a type of					anionic phospholipid	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_13_11115_s_336	12538649	A model of RGS4 regulation by the anionic phospholipid  PA. Agonist-induced stimulation of G-protein-coupled receptors enhances GTP binding  to Galpha subunits.	bind
42519	3	11018	6	10	NULL	NULL	NULL	PA	Chemical		regulates					RGS4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_13_11115_s_336	12538649	A model of RGS4 regulation by the anionic phospholipid  PA. Agonist-induced stimulation of G-protein-coupled receptors enhances GTP binding  to Galpha subunits.	bind
42520	4	11018	6	10	NULL	NULL	NULL	agonist	Chemical		induces					G-protein-coupled receptors 	GP	stimulation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_13_11115_s_336	12538649	A model of RGS4 regulation by the anionic phospholipid  PA. Agonist-induced stimulation of G-protein-coupled receptors enhances GTP binding  to Galpha subunits.	bind
42521	5	11018	6	10	NULL	NULL	NULL	statement 4	Process		enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_13_11115_s_336	12538649	A model of RGS4 regulation by the anionic phospholipid  PA. Agonist-induced stimulation of G-protein-coupled receptors enhances GTP binding  to Galpha subunits.	bind
49066	1	11018	7	10	NULL	NULL	NULL	PA	Chemical		regulates					RGS4	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_13_11115_s_336	12538649	A model of RGS4 regulation by the anionic phospholipid  PA. Agonist-induced stimulation of G-protein-coupled receptors enhances GTP binding  to Galpha subunits.	bind
49067	2	11018	7	10	NULL	NULL	NULL	GTP	Chemical		bind					Galpha subunits	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_13_11115_s_336	12538649	A model of RGS4 regulation by the anionic phospholipid  PA. Agonist-induced stimulation of G-protein-coupled receptors enhances GTP binding  to Galpha subunits.	bind
49068	3	11018	7	10	NULL	NULL	NULL	Agonist	Chemical		induce					G-protein-coupled receptors	GP	stimulation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_13_11115_s_336	12538649	A model of RGS4 regulation by the anionic phospholipid  PA. Agonist-induced stimulation of G-protein-coupled receptors enhances GTP binding  to Galpha subunits.	bind
49069	4	11018	7	10	NULL	NULL	NULL	statement 3	Process		enhance					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_13_11115_s_336	12538649	A model of RGS4 regulation by the anionic phospholipid  PA. Agonist-induced stimulation of G-protein-coupled receptors enhances GTP binding  to Galpha subunits.	bind
50266	5	11018	7	10	NULL	NULL	NULL	PA	Chemical		is a type of					anionic phospholipid	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_13_11115_s_336	12538649	A model of RGS4 regulation by the anionic phospholipid  PA. Agonist-induced stimulation of G-protein-coupled receptors enhances GTP binding  to Galpha subunits.	bind
42294	1	11020	6	10	NULL	NULL	NULL	SecA	GP		bind					SecB	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_mol-microbiol_58_2_16194224_s_8	16194224	A model of SecB-SecA complex suggests that  the binding of SecA to SecB changes the conformation of the polypeptide  binding sites in the chaperone, enabling transfer of precursor polypeptides  from SecB to SecA.	bind
42297	2	11020	6	10	NULL	NULL	NULL	statement 1	Process		changes					chaperone	GP	conformation of	polypeptide binding site		NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_mol-microbiol_58_2_16194224_s_8	16194224	A model of SecB-SecA complex suggests that  the binding of SecA to SecB changes the conformation of the polypeptide  binding sites in the chaperone, enabling transfer of precursor polypeptides  from SecB to SecA.	bind
42298	3	11020	6	10	NULL	NULL	NULL	precursor polypeptides	AminoAcid		are transfered to					SecA	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_mol-microbiol_58_2_16194224_s_8	16194224	A model of SecB-SecA complex suggests that  the binding of SecA to SecB changes the conformation of the polypeptide  binding sites in the chaperone, enabling transfer of precursor polypeptides  from SecB to SecA.	bind
42300	4	11020	6	10	NULL	NULL	NULL	statement 2	Process		enables					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_mol-microbiol_58_2_16194224_s_8	16194224	A model of SecB-SecA complex suggests that  the binding of SecA to SecB changes the conformation of the polypeptide  binding sites in the chaperone, enabling transfer of precursor polypeptides  from SecB to SecA.	bind
50267	5	11020	6	10	NULL	NULL	NULL	precursor polypeptides \t	AminoAcid		is transfered from					SecB	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_mol-microbiol_58_2_16194224_s_8	16194224	A model of SecB-SecA complex suggests that  the binding of SecA to SecB changes the conformation of the polypeptide  binding sites in the chaperone, enabling transfer of precursor polypeptides  from SecB to SecA.	bind
50268	6	11020	6	10	NULL	NULL	NULL	statement 5	Process		occurs simultaneously with					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_mol-microbiol_58_2_16194224_s_8	16194224	A model of SecB-SecA complex suggests that  the binding of SecA to SecB changes the conformation of the polypeptide  binding sites in the chaperone, enabling transfer of precursor polypeptides  from SecB to SecA.	bind
49070	1	11020	7	10	NULL	NULL	NULL	SecA 	GP		bind					SecB	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_mol-microbiol_58_2_16194224_s_8	16194224	A model of SecB-SecA complex suggests that  the binding of SecA to SecB changes the conformation of the polypeptide  binding sites in the chaperone, enabling transfer of precursor polypeptides  from SecB to SecA.	bind
49071	2	11020	7	10	NULL	NULL	NULL	statement 1	Process		changes					chaperone	GP	conformation of	polypeptide binding sites		NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_mol-microbiol_58_2_16194224_s_8	16194224	A model of SecB-SecA complex suggests that  the binding of SecA to SecB changes the conformation of the polypeptide  binding sites in the chaperone, enabling transfer of precursor polypeptides  from SecB to SecA.	bind
49072	3	11020	7	10	NULL	NULL	NULL	precursor polypeptide	AminoAcid		transferred from					SecB	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_mol-microbiol_58_2_16194224_s_8	16194224	A model of SecB-SecA complex suggests that  the binding of SecA to SecB changes the conformation of the polypeptide  binding sites in the chaperone, enabling transfer of precursor polypeptides  from SecB to SecA.	bind
49073	4	11020	7	10	NULL	NULL	NULL	precursor polypeptide	AminoAcid		transferred to					SecA	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_mol-microbiol_58_2_16194224_s_8	16194224	A model of SecB-SecA complex suggests that  the binding of SecA to SecB changes the conformation of the polypeptide  binding sites in the chaperone, enabling transfer of precursor polypeptides  from SecB to SecA.	bind
49074	5	11020	7	10	NULL	NULL	NULL	statement 3	Process		occur simultaneously with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_mol-microbiol_58_2_16194224_s_8	16194224	A model of SecB-SecA complex suggests that  the binding of SecA to SecB changes the conformation of the polypeptide  binding sites in the chaperone, enabling transfer of precursor polypeptides  from SecB to SecA.	bind
49075	6	11020	7	10	NULL	NULL	NULL	statement 2	Process		enables					statement 5	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_mol-microbiol_58_2_16194224_s_8	16194224	A model of SecB-SecA complex suggests that  the binding of SecA to SecB changes the conformation of the polypeptide  binding sites in the chaperone, enabling transfer of precursor polypeptides  from SecB to SecA.	bind
42522	1	11021	6	10	NULL	NULL	NULL	DAG	Chemical		bind					UNC-13	GP				NULL	C. elegans	NULL	NULL	NULL	NULL	gw70_genetics_169_2_651_s_235	15489511	A model of the  C. elegans EGL-30 (Galphaq) pathway predicts that this is caused by increased synaptic vesicle priming, in part via DAG-mediated activation of the UNC-13 synaptic vesicle priming protein ( Figure 1A); however, a prior study suggests that UNC-13-mediated synaptic vesicle priming is not dependent on DAG binding to UNC-13, because eliminating the ability of UNC-13 to bind DAG does not significantly affect neurotransmitter release ( HEE et al.).	bind
42523	2	11021	6	10	NULL	NULL	NULL	statement 1	Process	elimination of	does not affect		significantly			neurotransmitter	Process	release of			NULL	C. elegans	NULL	NULL	NULL	NULL	gw70_genetics_169_2_651_s_235	15489511	A model of the  C. elegans EGL-30 (Galphaq) pathway predicts that this is caused by increased synaptic vesicle priming, in part via DAG-mediated activation of the UNC-13 synaptic vesicle priming protein ( Figure 1A); however, a prior study suggests that UNC-13-mediated synaptic vesicle priming is not dependent on DAG binding to UNC-13, because eliminating the ability of UNC-13 to bind DAG does not significantly affect neurotransmitter release ( HEE et al.).	bind
42540	3	11021	6	10	NULL	NULL	NULL	UNC-13	GP		mediates					synaptic vesicle	CellComponent	priming of 			NULL	C. elegans	NULL	NULL	NULL	NULL	gw70_genetics_169_2_651_s_235	15489511	A model of the  C. elegans EGL-30 (Galphaq) pathway predicts that this is caused by increased synaptic vesicle priming, in part via DAG-mediated activation of the UNC-13 synaptic vesicle priming protein ( Figure 1A); however, a prior study suggests that UNC-13-mediated synaptic vesicle priming is not dependent on DAG binding to UNC-13, because eliminating the ability of UNC-13 to bind DAG does not significantly affect neurotransmitter release ( HEE et al.).	bind
42541	4	11021	6	10	NULL	NULL	NULL	statement 1	Process		is independent of					statement 3	Process				NULL	C. elegans	NULL	NULL	NULL	NULL	gw70_genetics_169_2_651_s_235	15489511	A model of the  C. elegans EGL-30 (Galphaq) pathway predicts that this is caused by increased synaptic vesicle priming, in part via DAG-mediated activation of the UNC-13 synaptic vesicle priming protein ( Figure 1A); however, a prior study suggests that UNC-13-mediated synaptic vesicle priming is not dependent on DAG binding to UNC-13, because eliminating the ability of UNC-13 to bind DAG does not significantly affect neurotransmitter release ( HEE et al.).	bind
50269	5	11021	6	10	NULL	NULL	NULL	DAG	Chemical		mediate					UNC-13 synaptic vesicle priming protein 	GP	activation of			NULL	C. elegans	NULL	NULL	NULL	NULL	gw70_genetics_169_2_651_s_235	15489511	A model of the  C. elegans EGL-30 (Galphaq) pathway predicts that this is caused by increased synaptic vesicle priming, in part via DAG-mediated activation of the UNC-13 synaptic vesicle priming protein ( Figure 1A); however, a prior study suggests that UNC-13-mediated synaptic vesicle priming is not dependent on DAG binding to UNC-13, because eliminating the ability of UNC-13 to bind DAG does not significantly affect neurotransmitter release ( HEE et al.).	bind
49076	1	11021	7	10	NULL	NULL	NULL	DAG	Chemical		mediates					UNC-13 synaptic vesicle priming protein 	GP	activation of			NULL	C.elegans	NULL	NULL	NULL	NULL	gw70_genetics_169_2_651_s_235	15489511	A model of the  C. elegans EGL-30 (Galphaq) pathway predicts that this is caused by increased synaptic vesicle priming, in part via DAG-mediated activation of the UNC-13 synaptic vesicle priming protein ( Figure 1A); however, a prior study suggests that UNC-13-mediated synaptic vesicle priming is not dependent on DAG binding to UNC-13, because eliminating the ability of UNC-13 to bind DAG does not significantly affect neurotransmitter release ( HEE et al.).	bind
49078	3	11021	7	10	NULL	NULL	NULL	 DAG	Chemical		bind					UNC-13	GP				NULL	C.elegans	NULL	NULL	NULL	NULL	gw70_genetics_169_2_651_s_235	15489511	A model of the  C. elegans EGL-30 (Galphaq) pathway predicts that this is caused by increased synaptic vesicle priming, in part via DAG-mediated activation of the UNC-13 synaptic vesicle priming protein ( Figure 1A); however, a prior study suggests that UNC-13-mediated synaptic vesicle priming is not dependent on DAG binding to UNC-13, because eliminating the ability of UNC-13 to bind DAG does not significantly affect neurotransmitter release ( HEE et al.).	bind
49079	4	11021	7	10	NULL	NULL	NULL	UNC-13	GP		mediates					synaptic vesicle 	CellComponent	priming of			NULL	C.elegans	NULL	NULL	NULL	NULL	gw70_genetics_169_2_651_s_235	15489511	A model of the  C. elegans EGL-30 (Galphaq) pathway predicts that this is caused by increased synaptic vesicle priming, in part via DAG-mediated activation of the UNC-13 synaptic vesicle priming protein ( Figure 1A); however, a prior study suggests that UNC-13-mediated synaptic vesicle priming is not dependent on DAG binding to UNC-13, because eliminating the ability of UNC-13 to bind DAG does not significantly affect neurotransmitter release ( HEE et al.).	bind
49080	5	11021	7	10	NULL	NULL	NULL	statement 4	Process		does not depend on					statement 3	Process				NULL	C.elegans	NULL	NULL	NULL	NULL	gw70_genetics_169_2_651_s_235	15489511	A model of the  C. elegans EGL-30 (Galphaq) pathway predicts that this is caused by increased synaptic vesicle priming, in part via DAG-mediated activation of the UNC-13 synaptic vesicle priming protein ( Figure 1A); however, a prior study suggests that UNC-13-mediated synaptic vesicle priming is not dependent on DAG binding to UNC-13, because eliminating the ability of UNC-13 to bind DAG does not significantly affect neurotransmitter release ( HEE et al.).	bind
49081	6	11021	7	10	NULL	NULL	NULL	statement 3	Process	elimination of	does not affect					neurotransmitter	Chemical	release of			NULL	C.elegans	NULL	NULL	NULL	NULL	gw70_genetics_169_2_651_s_235	15489511	A model of the  C. elegans EGL-30 (Galphaq) pathway predicts that this is caused by increased synaptic vesicle priming, in part via DAG-mediated activation of the UNC-13 synaptic vesicle priming protein ( Figure 1A); however, a prior study suggests that UNC-13-mediated synaptic vesicle priming is not dependent on DAG binding to UNC-13, because eliminating the ability of UNC-13 to bind DAG does not significantly affect neurotransmitter release ( HEE et al.).	bind
42301	1	11022	6	10	NULL	NULL	NULL	AC1	GP		bind			C1 domain		Gsalpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_25_13414_s_36	9391039	A model of the AC1 C1/AC2 C2 heterodimer was used to predict a region on the AC1 C1 domain that binds Gsalpha ( 20).	bind
49082	1	11022	7	10	NULL	NULL	NULL	AC1	GP		bind			C1 domain		Gsalpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_25_13414_s_36	9391039	A model of the AC1 C1/AC2 C2 heterodimer was used to predict a region on the AC1 C1 domain that binds Gsalpha ( 20).	bind
42567	1	11023	6	10	NULL	NULL	NULL	CipA	GP		bind			type II dockerin		SdbA 	GP		cohesin domain		NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_1_124_s_378	15755956	A model of the attachment of CipA to the cell involving use of its type II dockerin binding to a cohesin domain in the SdbA cell surface protein was proposed by Beguin and Alzari ( ).	bind
42568	2	11023	6	10	NULL	NULL	NULL	SdbA	GP		is a type of					cell surface protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_1_124_s_378	15755956	A model of the attachment of CipA to the cell involving use of its type II dockerin binding to a cohesin domain in the SdbA cell surface protein was proposed by Beguin and Alzari ( ).	bind
49083	1	11023	7	10	NULL	NULL	NULL	CipA	GP		bind			type II dockerin		SdbA	GP		cohesin domain		NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_1_124_s_378	15755956	A model of the attachment of CipA to the cell involving use of its type II dockerin binding to a cohesin domain in the SdbA cell surface protein was proposed by Beguin and Alzari ( ).	bind
49084	2	11023	7	10	NULL	NULL	NULL	SdbA	GP		is a type of					cell surface protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_1_124_s_378	15755956	A model of the attachment of CipA to the cell involving use of its type II dockerin binding to a cohesin domain in the SdbA cell surface protein was proposed by Beguin and Alzari ( ).	bind
42302	1	11024	6	10	NULL	NULL	NULL	Galphai1	GP		bind			helical domain		RGS14	GP		GL		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_46772_s_171	15337739	A model of the Galphai1 helical domain that binds to RGS14-GL is shown in  Fig. 5 A.	bind
49085	1	11024	7	10	NULL	NULL	NULL	Galphai1	GP		bind			helical domain 		RGS14	GP		GL		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_46772_s_171	15337739	A model of the Galphai1 helical domain that binds to RGS14-GL is shown in  Fig. 5 A.	bind
42303	1	11025	6	10	NULL	NULL	NULL	tyrphostin A25	Chemical		bind					CyaC	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31754_s_162	16002394	A model of the most effective tyrphostin A25 bound to CyaC may be generated without creating steric clash by superposition of the tyrphostin on the CE of the CyaC.2-CE complex ( Fig. 4 C).	bind
49086	1	11025	7	10	NULL	NULL	NULL	tyrphostin A25	Chemical		bind					CyaC	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_36_31754_s_162	16002394	A model of the most effective tyrphostin A25 bound to CyaC may be generated without creating steric clash by superposition of the tyrphostin on the CE of the CyaC.2-CE complex ( Fig. 4 C).	bind
42304	1	11027	6	10	NULL	NULL	NULL	Rad9	GP		bind					FHA2	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5374_185_s_43	9687277	A model presents itself: Rad9 binds to FHA2 to mediate the Rad53 response during G1 or G2 while another protein, perhaps polymerase e, binds to FHA1 to mediate the Rad53 response during S phase (see the figure).	bind
42331	2	11027	6	10	NULL	NULL	NULL	polymerase e	GP		bind		may			FHA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5374_185_s_43	9687277	A model presents itself: Rad9 binds to FHA2 to mediate the Rad53 response during G1 or G2 while another protein, perhaps polymerase e, binds to FHA1 to mediate the Rad53 response during S phase (see the figure).	bind
42332	3	11027	6	10	NULL	NULL	NULL	statement 1	Process		mediates					Rad53	GP	response of 			NULL		NULL	NULL	NULL	NULL	gw60_science_281_5374_185_s_43	9687277	A model presents itself: Rad9 binds to FHA2 to mediate the Rad53 response during G1 or G2 while another protein, perhaps polymerase e, binds to FHA1 to mediate the Rad53 response during S phase (see the figure).	bind
42333	4	11027	6	10	NULL	NULL	NULL	statement 3	Process		occurs during					G1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5374_185_s_43	9687277	A model presents itself: Rad9 binds to FHA2 to mediate the Rad53 response during G1 or G2 while another protein, perhaps polymerase e, binds to FHA1 to mediate the Rad53 response during S phase (see the figure).	bind
42334	5	11027	6	10	NULL	NULL	NULL	statement 3	Process		occurs during					G2	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5374_185_s_43	9687277	A model presents itself: Rad9 binds to FHA2 to mediate the Rad53 response during G1 or G2 while another protein, perhaps polymerase e, binds to FHA1 to mediate the Rad53 response during S phase (see the figure).	bind
42336	6	11027	6	10	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5374_185_s_43	9687277	A model presents itself: Rad9 binds to FHA2 to mediate the Rad53 response during G1 or G2 while another protein, perhaps polymerase e, binds to FHA1 to mediate the Rad53 response during S phase (see the figure).	bind
42343	7	11027	6	10	NULL	NULL	NULL	statement 2	Process		mediates					Rad53	GP	response of			NULL		NULL	NULL	NULL	NULL	gw60_science_281_5374_185_s_43	9687277	A model presents itself: Rad9 binds to FHA2 to mediate the Rad53 response during G1 or G2 while another protein, perhaps polymerase e, binds to FHA1 to mediate the Rad53 response during S phase (see the figure).	bind
42345	8	11027	6	10	NULL	NULL	NULL	statement 7	Process		occurs during					S phase	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5374_185_s_43	9687277	A model presents itself: Rad9 binds to FHA2 to mediate the Rad53 response during G1 or G2 while another protein, perhaps polymerase e, binds to FHA1 to mediate the Rad53 response during S phase (see the figure).	bind
49087	1	11027	7	10	NULL	NULL	NULL	Rad9 	GP		bind					FHA2	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5374_185_s_43	9687277	A model presents itself: Rad9 binds to FHA2 to mediate the Rad53 response during G1 or G2 while another protein, perhaps polymerase e, binds to FHA1 to mediate the Rad53 response during S phase (see the figure).	bind
49088	2	11027	7	10	NULL	NULL	NULL	statement 1	Process		mediate					Rad53	GP	response of			NULL		NULL	NULL	NULL	NULL	gw60_science_281_5374_185_s_43	9687277	A model presents itself: Rad9 binds to FHA2 to mediate the Rad53 response during G1 or G2 while another protein, perhaps polymerase e, binds to FHA1 to mediate the Rad53 response during S phase (see the figure).	bind
49089	3	11027	7	10	NULL	NULL	NULL	statement 2	Process		occur during					G1 phase	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5374_185_s_43	9687277	A model presents itself: Rad9 binds to FHA2 to mediate the Rad53 response during G1 or G2 while another protein, perhaps polymerase e, binds to FHA1 to mediate the Rad53 response during S phase (see the figure).	bind
49090	4	11027	7	10	NULL	NULL	NULL	statement 2	Process		occur during					G2 phase	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5374_185_s_43	9687277	A model presents itself: Rad9 binds to FHA2 to mediate the Rad53 response during G1 or G2 while another protein, perhaps polymerase e, binds to FHA1 to mediate the Rad53 response during S phase (see the figure).	bind
49091	5	11027	7	10	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5374_185_s_43	9687277	A model presents itself: Rad9 binds to FHA2 to mediate the Rad53 response during G1 or G2 while another protein, perhaps polymerase e, binds to FHA1 to mediate the Rad53 response during S phase (see the figure).	bind
49092	6	11027	7	10	NULL	NULL	NULL	polymerase e	GP		bind					FHA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5374_185_s_43	9687277	A model presents itself: Rad9 binds to FHA2 to mediate the Rad53 response during G1 or G2 while another protein, perhaps polymerase e, binds to FHA1 to mediate the Rad53 response during S phase (see the figure).	bind
49093	7	11027	7	10	NULL	NULL	NULL	statement 6	Process		mediate					Rad53	GP	response of			NULL		NULL	NULL	NULL	NULL	gw60_science_281_5374_185_s_43	9687277	A model presents itself: Rad9 binds to FHA2 to mediate the Rad53 response during G1 or G2 while another protein, perhaps polymerase e, binds to FHA1 to mediate the Rad53 response during S phase (see the figure).	bind
49094	8	11027	7	10	NULL	NULL	NULL	statement 7	Process		occur during					S phase	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5374_185_s_43	9687277	A model presents itself: Rad9 binds to FHA2 to mediate the Rad53 response during G1 or G2 while another protein, perhaps polymerase e, binds to FHA1 to mediate the Rad53 response during S phase (see the figure).	bind
42542	1	11028	6	10	NULL	NULL	NULL	all- trans-retinoic acid receptor	GP		forms heterodimer with					9-cis-retinoic acid receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_13271_s_159	12540843	A model proposed for the interaction of SRC-1 with a heterodimer of the receptors for all- trans-retinoic acid and 9- cis-retinoic acid suggests that binding of tandem NR boxes occurs in a cooperative manner ( 26).	bind
42543	2	11028	6	10	NULL	NULL	NULL	SRC-1	GP		interacts with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_13271_s_159	12540843	A model proposed for the interaction of SRC-1 with a heterodimer of the receptors for all- trans-retinoic acid and 9- cis-retinoic acid suggests that binding of tandem NR boxes occurs in a cooperative manner ( 26).	bind
49095	1	11028	7	10	NULL	NULL	NULL	all- trans-retinoic acid receptor	GP		forms heterodimer with					9-cis-retinoic acid receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_13271_s_159	12540843	A model proposed for the interaction of SRC-1 with a heterodimer of the receptors for all- trans-retinoic acid and 9- cis-retinoic acid suggests that binding of tandem NR boxes occurs in a cooperative manner ( 26).	bind
49096	2	11028	7	10	NULL	NULL	NULL	SRC-1	GP		interacts with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_13271_s_159	12540843	A model proposed for the interaction of SRC-1 with a heterodimer of the receptors for all- trans-retinoic acid and 9- cis-retinoic acid suggests that binding of tandem NR boxes occurs in a cooperative manner ( 26).	bind
42349	1	11029	6	10	NULL	NULL	NULL	gelsolin	GP	activation of	leads to					actin cytoskeleton	CellComponent	changes in			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_103_3_347_s_257	9927495	A model showing how gelsolin activation leading to dynamic changes in the actin cytoskeleton may modify tissue injury in cerebral ischemia.	bind
42350	2	11029	6	10	NULL	NULL	NULL	statement 1	Process		modify		may			tissue injury	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_103_3_347_s_257	9927495	A model showing how gelsolin activation leading to dynamic changes in the actin cytoskeleton may modify tissue injury in cerebral ischemia.	bind
42351	3	11029	6	10	NULL	NULL	NULL	statement 2	Process		occurs during					cerebral ischemia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_103_3_347_s_257	9927495	A model showing how gelsolin activation leading to dynamic changes in the actin cytoskeleton may modify tissue injury in cerebral ischemia.	bind
49102	1	11029	7	10	NULL	NULL	NULL	gelsolin	GP	activation of	leads to					actin cytoskeleton	CellComponent	dynamic changes in			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_103_3_347_s_257	9927495	A model showing how gelsolin activation leading to dynamic changes in the actin cytoskeleton may modify tissue injury in cerebral ischemia.	bind
49103	2	11029	7	10	NULL	NULL	NULL	statement 1	Process		modify		may			tissue injury	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_103_3_347_s_257	9927495	A model showing how gelsolin activation leading to dynamic changes in the actin cytoskeleton may modify tissue injury in cerebral ischemia.	bind
57753	3	11029	7	10	NULL	NULL	NULL	statement 2	Process		occurs during					cerebral ischemia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_103_3_347_s_257	9927495	A model showing how gelsolin activation leading to dynamic changes in the actin cytoskeleton may modify tissue injury in cerebral ischemia.	bind
42353	1	11030	6	10	NULL	NULL	NULL	calmodulin	GP		bind					L-selectin	GP		cytoplasmic tail		NULL	resting cell 	NULL	NULL	NULL	NULL	gw60_cell_92_6_809_s_206	9529256	A model that is consistent with our current data  would suggest that calmodulin is already bound to the L-selectin cytoplasmic tail  in the resting cell and that removal of calmodulin through cell activation, or  experimentally with trifluoperazine, results in L-selectin shedding.	bind
42361	2	11030	6	10	NULL	NULL	NULL	calmodulin	GP	removal of	results in					L-selectin	GP	shedding of 			NULL		NULL	NULL	NULL	NULL	gw60_cell_92_6_809_s_206	9529256	A model that is consistent with our current data  would suggest that calmodulin is already bound to the L-selectin cytoplasmic tail  in the resting cell and that removal of calmodulin through cell activation, or  experimentally with trifluoperazine, results in L-selectin shedding.	bind
49104	1	11030	7	10	NULL	NULL	NULL	calmodulin	GP		bind					L-selectin	GP		cytoplasmic tail		NULL	resting cell	NULL	NULL	NULL	NULL	gw60_cell_92_6_809_s_206	9529256	A model that is consistent with our current data  would suggest that calmodulin is already bound to the L-selectin cytoplasmic tail  in the resting cell and that removal of calmodulin through cell activation, or  experimentally with trifluoperazine, results in L-selectin shedding.	bind
49105	2	11030	7	10	NULL	NULL	NULL	calmodulin	GP	removal of	result in					L-selectin	GP	shedding of			NULL		NULL	NULL	NULL	NULL	gw60_cell_92_6_809_s_206	9529256	A model that is consistent with our current data  would suggest that calmodulin is already bound to the L-selectin cytoplasmic tail  in the resting cell and that removal of calmodulin through cell activation, or  experimentally with trifluoperazine, results in L-selectin shedding.	bind
42364	1	11031	6	10	NULL	NULL	NULL	Shh	GP		bind					Ptc	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_12_4505_s_141	16537363	A model to explain our findings would be that binding of Shh to Ptc increases surface localization of Smo for activation of PI3-kinase and Akt.	bind
42365	2	11031	6	10	NULL	NULL	NULL	statement 1	Process		increases					Smo	GP	surface localization of 			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_12_4505_s_141	16537363	A model to explain our findings would be that binding of Shh to Ptc increases surface localization of Smo for activation of PI3-kinase and Akt.	bind
42366	3	11031	6	10	NULL	NULL	NULL	statement 2	Process		is needed for					PI3-kinase	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_12_4505_s_141	16537363	A model to explain our findings would be that binding of Shh to Ptc increases surface localization of Smo for activation of PI3-kinase and Akt.	bind
42367	4	11031	6	10	NULL	NULL	NULL	statement 2	Process		is needed for					Akt	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_12_4505_s_141	16537363	A model to explain our findings would be that binding of Shh to Ptc increases surface localization of Smo for activation of PI3-kinase and Akt.	bind
49106	1	11031	7	10	NULL	NULL	NULL	Shh	GP		bind					Ptc	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_12_4505_s_141	16537363	A model to explain our findings would be that binding of Shh to Ptc increases surface localization of Smo for activation of PI3-kinase and Akt.	bind
49109	2	11031	7	10	NULL	NULL	NULL	statement 1	Process		increase					Smo	GP	surface localization of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_12_4505_s_141	16537363	A model to explain our findings would be that binding of Shh to Ptc increases surface localization of Smo for activation of PI3-kinase and Akt.	bind
50270	3	11031	7	10	NULL	NULL	NULL	statement 2	Process		is needed for					PI3-kinase	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_12_4505_s_141	16537363	A model to explain our findings would be that binding of Shh to Ptc increases surface localization of Smo for activation of PI3-kinase and Akt.	bind
50271	4	11031	7	10	NULL	NULL	NULL	statement 2	Process		is needed for					Akt	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_12_4505_s_141	16537363	A model to explain our findings would be that binding of Shh to Ptc increases surface localization of Smo for activation of PI3-kinase and Akt.	bind
42368	1	11032	6	10	NULL	NULL	NULL	Ndd1p	GP		activates					CLB cluster genes	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_14_1789_s_293	12865300	A model to explain the mechanism for how CLB cluster genes are activated by  Ndd1p during G2 - M, based on the finding described in this report.	bind
42369	2	11032	6	10	NULL	NULL	NULL	statement 1	Process		occurs during					G2-M	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_14_1789_s_293	12865300	A model to explain the mechanism for how CLB cluster genes are activated by  Ndd1p during G2 - M, based on the finding described in this report.	bind
49111	1	11032	7	10	NULL	NULL	NULL	Ndd1p	GP		activates					CLB cluster genes	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_14_1789_s_293	12865300	A model to explain the mechanism for how CLB cluster genes are activated by  Ndd1p during G2 - M, based on the finding described in this report.	bind
49112	2	11032	7	10	NULL	NULL	NULL	statement 1	Process		occur during					G2-M phase	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_17_14_1789_s_293	12865300	A model to explain the mechanism for how CLB cluster genes are activated by  Ndd1p during G2 - M, based on the finding described in this report.	bind
42370	1	11033	6	10	NULL	NULL	NULL	PS	GP		bind					NCT	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37213_s_247	12857757	A model was proposed by Takasugi  et al. ( ), suggesting that PS binds to NCT and Aph-1, forms a stable high molecular weight complex, and then subsequently binds Pen-2, allowing for PS endoproteolysis and the final glycosylation of NCT.	bind
42371	2	11033	6	10	NULL	NULL	NULL	PS	GP		bind					Aph-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37213_s_247	12857757	A model was proposed by Takasugi  et al. ( ), suggesting that PS binds to NCT and Aph-1, forms a stable high molecular weight complex, and then subsequently binds Pen-2, allowing for PS endoproteolysis and the final glycosylation of NCT.	bind
42544	3	11033	6	10	NULL	NULL	NULL	statement 1	Process		bind					Pen-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37213_s_247	12857757	A model was proposed by Takasugi  et al. ( ), suggesting that PS binds to NCT and Aph-1, forms a stable high molecular weight complex, and then subsequently binds Pen-2, allowing for PS endoproteolysis and the final glycosylation of NCT.	bind
42545	4	11033	6	10	NULL	NULL	NULL	statement 2	Process		bind					Pen-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37213_s_247	12857757	A model was proposed by Takasugi  et al. ( ), suggesting that PS binds to NCT and Aph-1, forms a stable high molecular weight complex, and then subsequently binds Pen-2, allowing for PS endoproteolysis and the final glycosylation of NCT.	bind
42546	5	11033	6	10	NULL	NULL	NULL	statement 3	Process		allows for					PS	GP	endoproteolysis of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37213_s_247	12857757	A model was proposed by Takasugi  et al. ( ), suggesting that PS binds to NCT and Aph-1, forms a stable high molecular weight complex, and then subsequently binds Pen-2, allowing for PS endoproteolysis and the final glycosylation of NCT.	bind
42547	6	11033	6	10	NULL	NULL	NULL	statement 4	Process		allows for					PS	GP	endoproteolysis of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37213_s_247	12857757	A model was proposed by Takasugi  et al. ( ), suggesting that PS binds to NCT and Aph-1, forms a stable high molecular weight complex, and then subsequently binds Pen-2, allowing for PS endoproteolysis and the final glycosylation of NCT.	bind
42548	7	11033	6	10	NULL	NULL	NULL	statement 3	Process		allows for					NCT	GP	glycosylation of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37213_s_247	12857757	A model was proposed by Takasugi  et al. ( ), suggesting that PS binds to NCT and Aph-1, forms a stable high molecular weight complex, and then subsequently binds Pen-2, allowing for PS endoproteolysis and the final glycosylation of NCT.	bind
42549	8	11033	6	10	NULL	NULL	NULL	statement 4	Process		allows for					NCT	GP	glycosylation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37213_s_247	12857757	A model was proposed by Takasugi  et al. ( ), suggesting that PS binds to NCT and Aph-1, forms a stable high molecular weight complex, and then subsequently binds Pen-2, allowing for PS endoproteolysis and the final glycosylation of NCT.	bind
49113	1	11033	7	10	NULL	NULL	NULL	 PS	GP		bind					NCT	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37213_s_247	12857757	A model was proposed by Takasugi  et al. ( ), suggesting that PS binds to NCT and Aph-1, forms a stable high molecular weight complex, and then subsequently binds Pen-2, allowing for PS endoproteolysis and the final glycosylation of NCT.	bind
49114	2	11033	7	10	NULL	NULL	NULL	PS	GP		bind					Aph-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37213_s_247	12857757	A model was proposed by Takasugi  et al. ( ), suggesting that PS binds to NCT and Aph-1, forms a stable high molecular weight complex, and then subsequently binds Pen-2, allowing for PS endoproteolysis and the final glycosylation of NCT.	bind
49115	3	11033	7	10	NULL	NULL	NULL	statement 1	Process		forms					high molecular weight complex		stable			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37213_s_247	12857757	A model was proposed by Takasugi  et al. ( ), suggesting that PS binds to NCT and Aph-1, forms a stable high molecular weight complex, and then subsequently binds Pen-2, allowing for PS endoproteolysis and the final glycosylation of NCT.	bind
49116	4	11033	7	10	NULL	NULL	NULL	statement 2	Process		forms					high molecular weight complex		stable			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37213_s_247	12857757	A model was proposed by Takasugi  et al. ( ), suggesting that PS binds to NCT and Aph-1, forms a stable high molecular weight complex, and then subsequently binds Pen-2, allowing for PS endoproteolysis and the final glycosylation of NCT.	bind
49117	5	11033	7	10	NULL	NULL	NULL	statement 3	Process		bind					Pen-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37213_s_247	12857757	A model was proposed by Takasugi  et al. ( ), suggesting that PS binds to NCT and Aph-1, forms a stable high molecular weight complex, and then subsequently binds Pen-2, allowing for PS endoproteolysis and the final glycosylation of NCT.	bind
49118	6	11033	7	10	NULL	NULL	NULL	statement 4	Process		bind					Pen-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37213_s_247	12857757	A model was proposed by Takasugi  et al. ( ), suggesting that PS binds to NCT and Aph-1, forms a stable high molecular weight complex, and then subsequently binds Pen-2, allowing for PS endoproteolysis and the final glycosylation of NCT.	bind
49119	7	11033	7	10	NULL	NULL	NULL	statement 5	Process		allows					PS	GP	endoproteolysis of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37213_s_247	12857757	A model was proposed by Takasugi  et al. ( ), suggesting that PS binds to NCT and Aph-1, forms a stable high molecular weight complex, and then subsequently binds Pen-2, allowing for PS endoproteolysis and the final glycosylation of NCT.	bind
49120	8	11033	7	10	NULL	NULL	NULL	statement 6	Process		allows					PS	GP	endoproteolysis of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37213_s_247	12857757	A model was proposed by Takasugi  et al. ( ), suggesting that PS binds to NCT and Aph-1, forms a stable high molecular weight complex, and then subsequently binds Pen-2, allowing for PS endoproteolysis and the final glycosylation of NCT.	bind
49121	9	11033	7	10	NULL	NULL	NULL	statement 5	Process		glycosylates					NCT	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37213_s_247	12857757	A model was proposed by Takasugi  et al. ( ), suggesting that PS binds to NCT and Aph-1, forms a stable high molecular weight complex, and then subsequently binds Pen-2, allowing for PS endoproteolysis and the final glycosylation of NCT.	bind
49122	10	11033	7	10	NULL	NULL	NULL	statement 6	Process		glycosylates					NCT	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_39_37213_s_247	12857757	A model was proposed by Takasugi  et al. ( ), suggesting that PS binds to NCT and Aph-1, forms a stable high molecular weight complex, and then subsequently binds Pen-2, allowing for PS endoproteolysis and the final glycosylation of NCT.	bind
42393	1	11034	6	10	NULL	NULL	NULL	Toc 159	GP		bind					precursor protein	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_embo_23_3_520_s_43	14765117	A model was proposed in which Toc 159 binds to precursor proteins in the  cytosol and targets them to the membrane.	bind
42394	2	11034	6	10	NULL	NULL	NULL	precursor proteins	GP		are targeted to					membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_520_s_43	14765117	A model was proposed in which Toc 159 binds to precursor proteins in the  cytosol and targets them to the membrane.	bind
42395	3	11034	6	10	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_520_s_43	14765117	A model was proposed in which Toc 159 binds to precursor proteins in the  cytosol and targets them to the membrane.	bind
49123	1	11034	7	10	NULL	NULL	NULL	 Toc 159 	GP		bind					precursor proteins	GP				NULL	cytosol	NULL	NULL	NULL	NULL	gw70_embo_23_3_520_s_43	14765117	A model was proposed in which Toc 159 binds to precursor proteins in the  cytosol and targets them to the membrane.	bind
49124	2	11034	7	10	NULL	NULL	NULL	precursor proteins	GP		targeted to					membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_520_s_43	14765117	A model was proposed in which Toc 159 binds to precursor proteins in the  cytosol and targets them to the membrane.	bind
49125	3	11034	7	10	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_3_520_s_43	14765117	A model was proposed in which Toc 159 binds to precursor proteins in the  cytosol and targets them to the membrane.	bind
42396	1	11035	6	10	NULL	NULL	NULL	TRCF	GP		bind					RNA pol	GP	stalled			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_9_4882_s_21	7876261	A model was proposed whereby  the TRCF bound to a stalled RNA Pol, dissociated the stalled RNA  polymerase and the truncated transcript, and delivered the  A B   complex to the damage site.	bind
42397	2	11035	6	10	NULL	NULL	NULL	statement 1	Process		dissociates					RNA polymerase	GP	stalled			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_9_4882_s_21	7876261	A model was proposed whereby  the TRCF bound to a stalled RNA Pol, dissociated the stalled RNA  polymerase and the truncated transcript, and delivered the  A B   complex to the damage site.	bind
42404	3	11035	6	10	NULL	NULL	NULL	statement 1	Process		dissociates					transcript	NucleicAcid	truncated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_9_4882_s_21	7876261	A model was proposed whereby  the TRCF bound to a stalled RNA Pol, dissociated the stalled RNA  polymerase and the truncated transcript, and delivered the  A B   complex to the damage site.	bind
42405	4	11035	6	10	NULL	NULL	NULL	A B complex	GP		is delivered to					damage site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_9_4882_s_21	7876261	A model was proposed whereby  the TRCF bound to a stalled RNA Pol, dissociated the stalled RNA  polymerase and the truncated transcript, and delivered the  A B   complex to the damage site.	bind
42406	5	11035	6	10	NULL	NULL	NULL	statement 2	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_9_4882_s_21	7876261	A model was proposed whereby  the TRCF bound to a stalled RNA Pol, dissociated the stalled RNA  polymerase and the truncated transcript, and delivered the  A B   complex to the damage site.	bind
57754	6	11035	6	10	NULL	NULL	NULL	statement 3	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_9_4882_s_21	7876261	A model was proposed whereby  the TRCF bound to a stalled RNA Pol, dissociated the stalled RNA  polymerase and the truncated transcript, and delivered the  A B   complex to the damage site.	bind
49126	1	11035	7	10	NULL	NULL	NULL	 TRCF	GP		bind					RNA Pol	GP	stalled			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_9_4882_s_21	7876261	A model was proposed whereby  the TRCF bound to a stalled RNA Pol, dissociated the stalled RNA  polymerase and the truncated transcript, and delivered the  A B   complex to the damage site.	bind
49127	2	11035	7	10	NULL	NULL	NULL	statement 1	Process		dissociate					RNA polymerase	GP	stalled			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_9_4882_s_21	7876261	A model was proposed whereby  the TRCF bound to a stalled RNA Pol, dissociated the stalled RNA  polymerase and the truncated transcript, and delivered the  A B   complex to the damage site.	bind
49128	3	11035	7	10	NULL	NULL	NULL	statement 1	Process		dissociate					transcript	NucleicAcid	truncated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_9_4882_s_21	7876261	A model was proposed whereby  the TRCF bound to a stalled RNA Pol, dissociated the stalled RNA  polymerase and the truncated transcript, and delivered the  A B   complex to the damage site.	bind
49129	4	11035	7	10	NULL	NULL	NULL	A B complex	GP		delivered to					damage site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_9_4882_s_21	7876261	A model was proposed whereby  the TRCF bound to a stalled RNA Pol, dissociated the stalled RNA  polymerase and the truncated transcript, and delivered the  A B   complex to the damage site.	bind
49130	5	11035	7	10	NULL	NULL	NULL	statement 2	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_9_4882_s_21	7876261	A model was proposed whereby  the TRCF bound to a stalled RNA Pol, dissociated the stalled RNA  polymerase and the truncated transcript, and delivered the  A B   complex to the damage site.	bind
49131	6	11035	7	10	NULL	NULL	NULL	statement 3	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_9_4882_s_21	7876261	A model was proposed whereby  the TRCF bound to a stalled RNA Pol, dissociated the stalled RNA  polymerase and the truncated transcript, and delivered the  A B   complex to the damage site.	bind
42409	1	11036	6	10	NULL	NULL	NULL	RyR	GP		bind			C terminus		FKBP	GP		catalytic site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_7_5475_s_292	15591045	A model where the RyR C terminus binds the FKBP catalytic site while the N-terminal and/or central domain bind to disparate FKBP surface residues, is compatible with the three-dimensional image reconstruction of the RyR1-FKBP12 complex, which indicates that the FKBP12-binding site lies at the periphery of the cytoplasmic portion about 11 nm away from the putative channel pore ( ).	bind
42410	2	11036	6	10	NULL	NULL	NULL	RyR	GP		bind			N-terminus		FKBP surface residues	AminoAcid	disparate			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_7_5475_s_292	15591045	A model where the RyR C terminus binds the FKBP catalytic site while the N-terminal and/or central domain bind to disparate FKBP surface residues, is compatible with the three-dimensional image reconstruction of the RyR1-FKBP12 complex, which indicates that the FKBP12-binding site lies at the periphery of the cytoplasmic portion about 11 nm away from the putative channel pore ( ).	bind
42434	3	11036	6	10	NULL	NULL	NULL	RyR	GP		bind			central domain		FKBP surface residues	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_7_5475_s_292	15591045	A model where the RyR C terminus binds the FKBP catalytic site while the N-terminal and/or central domain bind to disparate FKBP surface residues, is compatible with the three-dimensional image reconstruction of the RyR1-FKBP12 complex, which indicates that the FKBP12-binding site lies at the periphery of the cytoplasmic portion about 11 nm away from the putative channel pore ( ).	bind
42435	4	11036	6	10	NULL	NULL	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_7_5475_s_292	15591045	A model where the RyR C terminus binds the FKBP catalytic site while the N-terminal and/or central domain bind to disparate FKBP surface residues, is compatible with the three-dimensional image reconstruction of the RyR1-FKBP12 complex, which indicates that the FKBP12-binding site lies at the periphery of the cytoplasmic portion about 11 nm away from the putative channel pore ( ).	bind
49132	1	11036	7	10	NULL	NULL	NULL	RyR	GP		bind			C terminus		FKBP	GP		catalytic site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_7_5475_s_292	15591045	A model where the RyR C terminus binds the FKBP catalytic site while the N-terminal and/or central domain bind to disparate FKBP surface residues, is compatible with the three-dimensional image reconstruction of the RyR1-FKBP12 complex, which indicates that the FKBP12-binding site lies at the periphery of the cytoplasmic portion about 11 nm away from the putative channel pore ( ).	bind
49133	2	11036	7	10	NULL	NULL	NULL	RyR	GP		bind			N-terminal domain		FKBP surface residues	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_7_5475_s_292	15591045	A model where the RyR C terminus binds the FKBP catalytic site while the N-terminal and/or central domain bind to disparate FKBP surface residues, is compatible with the three-dimensional image reconstruction of the RyR1-FKBP12 complex, which indicates that the FKBP12-binding site lies at the periphery of the cytoplasmic portion about 11 nm away from the putative channel pore ( ).	bind
49134	3	11036	7	10	NULL	NULL	NULL	RyR	GP		bind			central domain		FKBP surface residues	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_7_5475_s_292	15591045	A model where the RyR C terminus binds the FKBP catalytic site while the N-terminal and/or central domain bind to disparate FKBP surface residues, is compatible with the three-dimensional image reconstruction of the RyR1-FKBP12 complex, which indicates that the FKBP12-binding site lies at the periphery of the cytoplasmic portion about 11 nm away from the putative channel pore ( ).	bind
49135	4	11036	7	10	NULL	NULL	NULL	RyR1	GP		forms complex with					FKBP12	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_7_5475_s_292	15591045	A model where the RyR C terminus binds the FKBP catalytic site while the N-terminal and/or central domain bind to disparate FKBP surface residues, is compatible with the three-dimensional image reconstruction of the RyR1-FKBP12 complex, which indicates that the FKBP12-binding site lies at the periphery of the cytoplasmic portion about 11 nm away from the putative channel pore ( ).	bind
49136	5	11036	7	NULL	NULL	0	NULL		NULL		lies at	NULL		FKBP12-binding site			NULL	periphery of	cytoplasmic portion		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_7_5475_s_292	15591045	A model where the RyR C terminus binds the FKBP catalytic site while the N-terminal and/or central domain bind to disparate FKBP surface residues, is compatible with the three-dimensional image reconstruction of the RyR1-FKBP12 complex, which indicates that the FKBP12-binding site lies at the periphery of the cytoplasmic portion about 11 nm away from the putative channel pore ( ).	bind
42437	1	11037	6	10	NULL	NULL	NULL	LTA4	GP		bind					humLTA4H	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_39_33477_s_96	16024909	A modeled binding conformation of LTA4 to  humLTA4H is shown in  green.	bind
49137	1	11037	7	10	NULL	NULL	NULL	LTA4	GP		bind					humLTA4H	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_39_33477_s_96	16024909	A modeled binding conformation of LTA4 to  humLTA4H is shown in  green.	bind
42438	1	11038	6	10	NULL	NULL	NULL	p85-p110 dimer	GP		bind					IRS protein	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_1_419_s_192	11752399	A moderate decrease in the amount of p85 protein (either p85alpha or p85beta) may reduce these inhibitory effects and leaves the amount of p85-p110 dimer bound to tyrosine-phosphorylated IRS proteins almost unchanged.	bind
50272	2	11038	6	10	NULL	NULL	NULL	p85alpha	GP	decrease in	does not effect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_1_419_s_192	11752399	A moderate decrease in the amount of p85 protein (either p85alpha or p85beta) may reduce these inhibitory effects and leaves the amount of p85-p110 dimer bound to tyrosine-phosphorylated IRS proteins almost unchanged.	bind
50273	3	11038	6	10	NULL	NULL	NULL	p85beta \t	GP	decrease in	does not effect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_1_419_s_192	11752399	A moderate decrease in the amount of p85 protein (either p85alpha or p85beta) may reduce these inhibitory effects and leaves the amount of p85-p110 dimer bound to tyrosine-phosphorylated IRS proteins almost unchanged.	bind
49139	1	11038	7	10	NULL	NULL	NULL	p85-p110 dimer	GP		bind					IRS proteins	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_1_419_s_192	11752399	A moderate decrease in the amount of p85 protein (either p85alpha or p85beta) may reduce these inhibitory effects and leaves the amount of p85-p110 dimer bound to tyrosine-phosphorylated IRS proteins almost unchanged.	bind
49140	2	11038	7	10	NULL	NULL	NULL	p85alpha	GP	decrease in	does not affect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_1_419_s_192	11752399	A moderate decrease in the amount of p85 protein (either p85alpha or p85beta) may reduce these inhibitory effects and leaves the amount of p85-p110 dimer bound to tyrosine-phosphorylated IRS proteins almost unchanged.	bind
49141	3	11038	7	10	NULL	NULL	NULL	p85beta	GP	decrease in	does not affect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_1_419_s_192	11752399	A moderate decrease in the amount of p85 protein (either p85alpha or p85beta) may reduce these inhibitory effects and leaves the amount of p85-p110 dimer bound to tyrosine-phosphorylated IRS proteins almost unchanged.	bind
42440	1	11039	6	10	NULL	NULL	NULL	E2	GP	removal of;; bovine	increases			bilipoyl domain region		PDP	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_23_14130_s_239	9603912	A modest (40%) increase in PDP activity was observed using an E1-binding preparation of bovine E2 in which the bilipoyl domain region was selectively removed by collagenase treatment ( 11).	bind
67422	1	11039	7	10	NULL	0	NULL	E2	GP	removal of;; bovine	increases			bilipoyl domain region		PDP	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14130_s_239	9603912	A modest (40%) increase in PDP activity was observed using an E1-binding preparation of bovine E2 in which the bilipoyl domain region was selectively removed by collagenase treatment ( 11).	bind
42550	1	11040	6	10	NULL	NULL	NULL	C4BP	GP		bind					protein S	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_15099_s_264	11847209	A modest inhibitory effect of HPS 34 on the C4BP binding to protein S was found only when HPS 34 and protein S were preincubated using a large molar excess of the antibody, whereas no binding of HPS 34 to the C4BP-protein S complex was detected with surface plasmon resonance.	bind
42551	2	11040	6	10	NULL	NULL	NULL	HPS34	GP		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_15099_s_264	11847209	A modest inhibitory effect of HPS 34 on the C4BP binding to protein S was found only when HPS 34 and protein S were preincubated using a large molar excess of the antibody, whereas no binding of HPS 34 to the C4BP-protein S complex was detected with surface plasmon resonance.	bind
50274	3	11040	6	10	NULL	NULL	NULL	HPS 34	GP		does not bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_15099_s_264	11847209	A modest inhibitory effect of HPS 34 on the C4BP binding to protein S was found only when HPS 34 and protein S were preincubated using a large molar excess of the antibody, whereas no binding of HPS 34 to the C4BP-protein S complex was detected with surface plasmon resonance.	bind
49142	1	11040	7	10	NULL	NULL	NULL	C4BP	GP		bind					protein S	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_15099_s_264	11847209	A modest inhibitory effect of HPS 34 on the C4BP binding to protein S was found only when HPS 34 and protein S were preincubated using a large molar excess of the antibody, whereas no binding of HPS 34 to the C4BP-protein S complex was detected with surface plasmon resonance.	bind
49143	2	11040	7	10	NULL	NULL	NULL	HPS 34	GP		inhibit		modestly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_15099_s_264	11847209	A modest inhibitory effect of HPS 34 on the C4BP binding to protein S was found only when HPS 34 and protein S were preincubated using a large molar excess of the antibody, whereas no binding of HPS 34 to the C4BP-protein S complex was detected with surface plasmon resonance.	bind
49144	3	11040	7	10	NULL	NULL	NULL	HPS 34	GP		does not bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_15099_s_264	11847209	A modest inhibitory effect of HPS 34 on the C4BP binding to protein S was found only when HPS 34 and protein S were preincubated using a large molar excess of the antibody, whereas no binding of HPS 34 to the C4BP-protein S complex was detected with surface plasmon resonance.	bind
42441	1	11041	6	10	NULL	NULL	NULL	pre-mRNA	NucleicAcid		bind					U6 snRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2475_s_68	16688215	A modification at intron position +10 should therefore not interfere with pre-mRNA  binding to U6 snRNA or with spliceosome function.	bind
42442	2	11041	6	10	NULL	NULL	NULL			modification at	does not interfere				intron position +10	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2475_s_68	16688215	A modification at intron position +10 should therefore not interfere with pre-mRNA  binding to U6 snRNA or with spliceosome function.	bind
42443	3	11041	6	10	NULL	NULL	NULL			modification at	does not interfere with				intron position +10	spliceosome 	NucleicAcid	function of			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2475_s_68	16688215	A modification at intron position +10 should therefore not interfere with pre-mRNA  binding to U6 snRNA or with spliceosome function.	bind
49145	1	11041	7	10	NULL	NULL	NULL	pre-mRNA	NucleicAcid		bind					U6 snRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2475_s_68	16688215	A modification at intron position +10 should therefore not interfere with pre-mRNA  binding to U6 snRNA or with spliceosome function.	bind
49146	2	11041	7	10	NULL	NULL	NULL			modification of	does not interfere with				intron position +10 	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2475_s_68	16688215	A modification at intron position +10 should therefore not interfere with pre-mRNA  binding to U6 snRNA or with spliceosome function.	bind
49147	3	11041	7	10	NULL	NULL	NULL			modification of	does not interfere with				intron position +10 	spliceosome	Process	function of			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_11_2475_s_68	16688215	A modification at intron position +10 should therefore not interfere with pre-mRNA  binding to U6 snRNA or with spliceosome function.	bind
42444	1	11042	6	10	NULL	NULL	NULL	U11 snRNP	GP		bind					pre-mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_13_7_851_s_296	10197985	A modification of the RNase H protection assays described previously (Barabino et al. 1990  ; Eperon et al. 1993  ) was used to examine the binding of U11 and U12 snRNPs to pre-mRNA.	bind
42445	2	11042	6	10	NULL	NULL	NULL	U12 snRNP	GP		bind					pre-mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_13_7_851_s_296	10197985	A modification of the RNase H protection assays described previously (Barabino et al. 1990  ; Eperon et al. 1993  ) was used to examine the binding of U11 and U12 snRNPs to pre-mRNA.	bind
49195	1	11042	7	10	NULL	NULL	NULL	U11 snRNP	GP		bind					pre-mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_13_7_851_s_296	10197985	A modification of the RNase H protection assays described previously (Barabino et al. 1990  ; Eperon et al. 1993  ) was used to examine the binding of U11 and U12 snRNPs to pre-mRNA.	bind
49196	2	11042	7	10	NULL	NULL	NULL	U12 snRNP	GP		bind					pre-mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_13_7_851_s_296	10197985	A modification of the RNase H protection assays described previously (Barabino et al. 1990  ; Eperon et al. 1993  ) was used to examine the binding of U11 and U12 snRNPs to pre-mRNA.	bind
42446	1	11043	6	10	NULL	NULL	NULL	Cla4p	GP	GST-tagged	does not bind		specifically	CRIB domain		Cdc42p	GP	myc-tagged			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1239_s_106	11359919	A modification of this strategy was used for Cla4p because the GST-tagged Cla4p CRIB domain did not display specific binding to myc-tagged Cdc42p.	bind
49197	1	11043	7	10	NULL	NULL	NULL	 Cla4p	GP	 GST-tagged	does not bind		specifically	CRIB domain		Cdc42p	GP	myc-tagged			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_5_1239_s_106	11359919	A modification of this strategy was used for Cla4p because the GST-tagged Cla4p CRIB domain did not display specific binding to myc-tagged Cdc42p.	bind
42447	1	11044	6	10	NULL	NULL	NULL	afadin	GP		bind					p120ctn	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_24095_s_211	15857834	A modification or another protein(s) may be required for the efficient binding between afadin and p120ctn.	bind
49198	1	11044	7	10	NULL	NULL	NULL	afadin	GP		bind					p120ctn	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_24095_s_211	15857834	A modification or another protein(s) may be required for the efficient binding between afadin and p120ctn.	bind
42448	1	11045	6	10	NULL	NULL	NULL	CREB	GP		bind					mtDNA	NucleicAcid				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_pnas_102_39_13915_s_192	16169904	A modified  ChIP method was used for detection of  in vivo binding of CREB to mtDNA as described in  Materials and Methods.	bind
49199	1	11045	7	10	NULL	NULL	NULL	CREB 	GP		bind					mtDNA	NucleicAcid				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_pnas_102_39_13915_s_192	16169904	A modified  ChIP method was used for detection of  in vivo binding of CREB to mtDNA as described in  Materials and Methods.	bind
42449	1	11046	6	10	NULL	NULL	NULL	NP220	GP		bind		preferentially			dsDNA	NucleicAcid			cytidine cluster	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_21_12525_s_123	8647861	A modified  SAAB method employing the pK1 product showed that NP220 preferentially  binds to cytidine clusters in either strand of dsDNA.	bind
49200	1	11046	7	10	NULL	NULL	NULL	NP220	GP		bind		preferentially			dsDNA	NucleicAcid			cytidine clusters 	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_21_12525_s_123	8647861	A modified  SAAB method employing the pK1 product showed that NP220 preferentially  binds to cytidine clusters in either strand of dsDNA.	bind
42450	1	11047	6	10	NULL	NULL	NULL	ATP	Chemical		bind		tightly			CF(0)F(1)	GP	chloroplast	noncatalytic site		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_photosynth-res_88_1_16440137_s_2	16440137	A modified 'cold chase'' technique was used to study tight [(14)C]ADP and  [(14)C]ATP binding to noncatalytic sites of chloroplast ATP synthase (CF(0)F(1)).	bind
42451	2	11047	6	10	NULL	NULL	NULL	ADP	Chemical		bind		tightly			CF(0)F(1)	GP	chloroplast	noncatalytic site		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_photosynth-res_88_1_16440137_s_2	16440137	A modified 'cold chase'' technique was used to study tight [(14)C]ADP and  [(14)C]ATP binding to noncatalytic sites of chloroplast ATP synthase (CF(0)F(1)).	bind
50275	3	11047	6	10	NULL	NULL	NULL	CF(0)F(1)	GP		is a type of					ATP synthase	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_photosynth-res_88_1_16440137_s_2	16440137	A modified 'cold chase'' technique was used to study tight [(14)C]ADP and  [(14)C]ATP binding to noncatalytic sites of chloroplast ATP synthase (CF(0)F(1)).	bind
49201	1	11047	7	10	NULL	NULL	NULL	ADP	Chemical		bind		tightly			CF(0)F(1)	GP	chloroplast	noncatalytic site		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_photosynth-res_88_1_16440137_s_2	16440137	A modified 'cold chase'' technique was used to study tight [(14)C]ADP and  [(14)C]ATP binding to noncatalytic sites of chloroplast ATP synthase (CF(0)F(1)).	bind
49202	2	11047	7	10	NULL	NULL	NULL	ATP	Chemical		bind		tightly			CF(0)F(1)	GP	chloroplast	noncatalytic site		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_photosynth-res_88_1_16440137_s_2	16440137	A modified 'cold chase'' technique was used to study tight [(14)C]ADP and  [(14)C]ATP binding to noncatalytic sites of chloroplast ATP synthase (CF(0)F(1)).	bind
50276	3	11047	7	10	NULL	NULL	NULL	CF(0)F(1)	GP		is a type of					ATP synthase	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_photosynth-res_88_1_16440137_s_2	16440137	A modified 'cold chase'' technique was used to study tight [(14)C]ADP and  [(14)C]ATP binding to noncatalytic sites of chloroplast ATP synthase (CF(0)F(1)).	bind
42452	1	11048	6	10	NULL	NULL	NULL	Sub2p	GP		bind					RNA	NucleicAcid	nascent			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_13_2620_s_5	15192704	A modified chromatin immunoprecipitation assay that includes an RNase  step indicates that Sub2p is bound to nascent RNA, Yra1p is associated with both  RNA and DNA, and Hpr1p is associated with DNA.	bind
42453	2	11048	6	10	NULL	NULL	NULL	Yra1p	GP		associates with					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_13_2620_s_5	15192704	A modified chromatin immunoprecipitation assay that includes an RNase  step indicates that Sub2p is bound to nascent RNA, Yra1p is associated with both  RNA and DNA, and Hpr1p is associated with DNA.	bind
42454	3	11048	6	10	NULL	NULL	NULL	Yra1p	GP		associates with					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_13_2620_s_5	15192704	A modified chromatin immunoprecipitation assay that includes an RNase  step indicates that Sub2p is bound to nascent RNA, Yra1p is associated with both  RNA and DNA, and Hpr1p is associated with DNA.	bind
42455	4	11048	6	10	NULL	NULL	NULL	Hpr1p	GP		associates with					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_13_2620_s_5	15192704	A modified chromatin immunoprecipitation assay that includes an RNase  step indicates that Sub2p is bound to nascent RNA, Yra1p is associated with both  RNA and DNA, and Hpr1p is associated with DNA.	bind
49203	1	11048	7	10	NULL	NULL	NULL	 Sub2p	GP		bind					RNA	NucleicAcid	nascent			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_13_2620_s_5	15192704	A modified chromatin immunoprecipitation assay that includes an RNase  step indicates that Sub2p is bound to nascent RNA, Yra1p is associated with both  RNA and DNA, and Hpr1p is associated with DNA.	bind
49204	2	11048	7	10	NULL	NULL	NULL	Yra1p	GP		associate with					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_13_2620_s_5	15192704	A modified chromatin immunoprecipitation assay that includes an RNase  step indicates that Sub2p is bound to nascent RNA, Yra1p is associated with both  RNA and DNA, and Hpr1p is associated with DNA.	bind
49205	3	11048	7	10	NULL	NULL	NULL	Yra1p	GP		associate with					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_13_2620_s_5	15192704	A modified chromatin immunoprecipitation assay that includes an RNase  step indicates that Sub2p is bound to nascent RNA, Yra1p is associated with both  RNA and DNA, and Hpr1p is associated with DNA.	bind
49206	4	11048	7	10	NULL	NULL	NULL	Hpr1p	GP		associate with					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_13_2620_s_5	15192704	A modified chromatin immunoprecipitation assay that includes an RNase  step indicates that Sub2p is bound to nascent RNA, Yra1p is associated with both  RNA and DNA, and Hpr1p is associated with DNA.	bind
42456	1	11049	6	10	NULL	NULL	NULL	DPPIV	GP		bind					FN	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_27_24600_s_67	12716896	A modified enzyme-linked  immunosorbent assay (ELISA) was used to measure the binding of DPPIV to FN  fusion proteins.	bind
57755	2	11049	6	10	NULL	NULL	NULL	FN	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_27_24600_s_67	12716896	A modified enzyme-linked  immunosorbent assay (ELISA) was used to measure the binding of DPPIV to FN  fusion proteins.	bind
49207	1	11049	7	10	NULL	NULL	NULL	DPPIV	GP		bind					FN	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_27_24600_s_67	12716896	A modified enzyme-linked  immunosorbent assay (ELISA) was used to measure the binding of DPPIV to FN  fusion proteins.	bind
49208	2	11049	7	10	NULL	NULL	NULL	FN	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_27_24600_s_67	12716896	A modified enzyme-linked  immunosorbent assay (ELISA) was used to measure the binding of DPPIV to FN  fusion proteins.	bind
42552	2	11050	6	10	NULL	NULL	NULL	ER HBD	GP		is					estrogen receptor hormone-binding domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13280_s_27	9582373	A modified estrogen receptor hormone-binding domain (ER HBD) containing a point mutation rendering the HBD unable to bind estrogen while retaining affinity for the synthetic ligand 4-hydroxytamoxifen (4-OH-tamoxifen) has been used to conditionally regulate heterologous proteins ( 29,  30).	bind
42553	3	11050	6	10	NULL	NULL	NULL	ER	GP	point mutant	does not bind			HBD		estrogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13280_s_27	9582373	A modified estrogen receptor hormone-binding domain (ER HBD) containing a point mutation rendering the HBD unable to bind estrogen while retaining affinity for the synthetic ligand 4-hydroxytamoxifen (4-OH-tamoxifen) has been used to conditionally regulate heterologous proteins ( 29,  30).	bind
42555	1	11050	6	10	NULL	NULL	NULL	4-OH-tamoxifen	Chemical		is					4-hydroxytamoxifen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13280_s_27	9582373	A modified estrogen receptor hormone-binding domain (ER HBD) containing a point mutation rendering the HBD unable to bind estrogen while retaining affinity for the synthetic ligand 4-hydroxytamoxifen (4-OH-tamoxifen) has been used to conditionally regulate heterologous proteins ( 29,  30).	bind
42556	5	11050	6	10	NULL	NULL	NULL	4-OH-tamoxifen	Chemical		is a type of					synthetic ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13280_s_27	9582373	A modified estrogen receptor hormone-binding domain (ER HBD) containing a point mutation rendering the HBD unable to bind estrogen while retaining affinity for the synthetic ligand 4-hydroxytamoxifen (4-OH-tamoxifen) has been used to conditionally regulate heterologous proteins ( 29,  30).	bind
42557	4	11050	6	10	NULL	NULL	NULL	ER	GP	point mutant	has affinity for			HBD		4-OH-tamoxifen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13280_s_27	9582373	A modified estrogen receptor hormone-binding domain (ER HBD) containing a point mutation rendering the HBD unable to bind estrogen while retaining affinity for the synthetic ligand 4-hydroxytamoxifen (4-OH-tamoxifen) has been used to conditionally regulate heterologous proteins ( 29,  30).	bind
49209	1	11050	7	10	NULL	NULL	NULL	ER	GP	point mutant	does not bind			HBD		estrogen	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13280_s_27	9582373	A modified estrogen receptor hormone-binding domain (ER HBD) containing a point mutation rendering the HBD unable to bind estrogen while retaining affinity for the synthetic ligand 4-hydroxytamoxifen (4-OH-tamoxifen) has been used to conditionally regulate heterologous proteins ( 29,  30).	bind
49211	3	11050	7	10	NULL	NULL	NULL	ER HBD	GP		is 					estrogen receptor hormone-binding domain	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13280_s_27	9582373	A modified estrogen receptor hormone-binding domain (ER HBD) containing a point mutation rendering the HBD unable to bind estrogen while retaining affinity for the synthetic ligand 4-hydroxytamoxifen (4-OH-tamoxifen) has been used to conditionally regulate heterologous proteins ( 29,  30).	bind
49212	4	11050	7	10	NULL	NULL	NULL	4-OH-tamoxifen	Chemical		is					 4-hydroxytamoxifen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13280_s_27	9582373	A modified estrogen receptor hormone-binding domain (ER HBD) containing a point mutation rendering the HBD unable to bind estrogen while retaining affinity for the synthetic ligand 4-hydroxytamoxifen (4-OH-tamoxifen) has been used to conditionally regulate heterologous proteins ( 29,  30).	bind
49213	5	11050	7	10	NULL	NULL	NULL	4-OH-tamoxifen	Chemical		is a type of					synthetic ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_21_13280_s_27	9582373	A modified estrogen receptor hormone-binding domain (ER HBD) containing a point mutation rendering the HBD unable to bind estrogen while retaining affinity for the synthetic ligand 4-hydroxytamoxifen (4-OH-tamoxifen) has been used to conditionally regulate heterologous proteins ( 29,  30).	bind
67423	2	11050	7	10	NULL	0	NULL	ER	GP	point mutant	has affinity for			HBD		4-OH-tamoxifen	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_21_13280_s_27	9582373	A modified estrogen receptor hormone-binding domain (ER HBD) containing a point mutation rendering the HBD unable to bind estrogen while retaining affinity for the synthetic ligand 4-hydroxytamoxifen (4-OH-tamoxifen) has been used to conditionally regulate heterologous proteins ( 29,  30).	bind
42458	1	11051	6	10	NULL	NULL	NULL	IgE Ab	GP		bind					Der p 2	GP	natural;; mite			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_43_26893_s_97	9341122	A modified monoclonal RAST measured IgE Ab binding to natural mite Der p 2 and rDer p 2 (D1S) (data not shown).	bind
42459	2	11051	6	10	NULL	NULL	NULL	IgE Ab	GP		bind					rDes p 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_43_26893_s_97	9341122	A modified monoclonal RAST measured IgE Ab binding to natural mite Der p 2 and rDer p 2 (D1S) (data not shown).	bind
49217	1	11051	7	10	NULL	NULL	NULL	 IgE Ab 	GP		bind					Der p 2	GP	natural;;mite			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_43_26893_s_97	9341122	A modified monoclonal RAST measured IgE Ab binding to natural mite Der p 2 and rDer p 2 (D1S) (data not shown).	bind
49218	2	11051	7	10	NULL	NULL	NULL	IgE Ab	GP		bind					rDer p 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_43_26893_s_97	9341122	A modified monoclonal RAST measured IgE Ab binding to natural mite Der p 2 and rDer p 2 (D1S) (data not shown).	bind
42460	1	11052	6	10	NULL	NULL	NULL	hPL	GP		bind					hPRLR	GP		ECD		NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-mol-biol_358_3_16546209_s_4	16546209	A modified surface plasmon resonance method was developed to measure  the kinetics for hPL and hGH binding to the hPRLR ECD, with and without  Zn2+ and showed that hPL has about a tenfold higher affinity for the hPRLR  ECD1 than hGH.	bind
42461	2	11052	6	10	NULL	NULL	NULL	hGH	GP		bind					hPRLR	GP		ECD		NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-mol-biol_358_3_16546209_s_4	16546209	A modified surface plasmon resonance method was developed to measure  the kinetics for hPL and hGH binding to the hPRLR ECD, with and without  Zn2+ and showed that hPL has about a tenfold higher affinity for the hPRLR  ECD1 than hGH.	bind
42462	3	11052	6	10	NULL	NULL	NULL	hPL	GP		has affinity for					hPRLR	GP		ECD1		NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-mol-biol_358_3_16546209_s_4	16546209	A modified surface plasmon resonance method was developed to measure  the kinetics for hPL and hGH binding to the hPRLR ECD, with and without  Zn2+ and showed that hPL has about a tenfold higher affinity for the hPRLR  ECD1 than hGH.	bind
42463	4	11052	6	10	NULL	NULL	NULL	hGH	GP		has affinity for					hPRLR	GP		ECD1		NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-mol-biol_358_3_16546209_s_4	16546209	A modified surface plasmon resonance method was developed to measure  the kinetics for hPL and hGH binding to the hPRLR ECD, with and without  Zn2+ and showed that hPL has about a tenfold higher affinity for the hPRLR  ECD1 than hGH.	bind
42464	5	11052	6	10	NULL	NULL	NULL	statement 3	Process		is higher than					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-mol-biol_358_3_16546209_s_4	16546209	A modified surface plasmon resonance method was developed to measure  the kinetics for hPL and hGH binding to the hPRLR ECD, with and without  Zn2+ and showed that hPL has about a tenfold higher affinity for the hPRLR  ECD1 than hGH.	bind
49219	1	11052	7	10	NULL	NULL	NULL	hPL	GP		bind					 hPRLR	GP		ECD1		NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-mol-biol_358_3_16546209_s_4	16546209	A modified surface plasmon resonance method was developed to measure  the kinetics for hPL and hGH binding to the hPRLR ECD, with and without  Zn2+ and showed that hPL has about a tenfold higher affinity for the hPRLR  ECD1 than hGH.	bind
49220	2	11052	7	10	NULL	NULL	NULL	hGH	GP		bind					hPRLR	GP		ECD1		NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-mol-biol_358_3_16546209_s_4	16546209	A modified surface plasmon resonance method was developed to measure  the kinetics for hPL and hGH binding to the hPRLR ECD, with and without  Zn2+ and showed that hPL has about a tenfold higher affinity for the hPRLR  ECD1 than hGH.	bind
49221	3	11052	7	10	NULL	NULL	NULL	statement 1	Process	affinity of	is higher than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-mol-biol_358_3_16546209_s_4	16546209	A modified surface plasmon resonance method was developed to measure  the kinetics for hPL and hGH binding to the hPRLR ECD, with and without  Zn2+ and showed that hPL has about a tenfold higher affinity for the hPRLR  ECD1 than hGH.	bind
42465	1	11053	6	10	NULL	NULL	NULL	agonist	Chemical		bind					V1 vascular vasopressin receptor	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_41_0_175_s_970	11264455	A molecular  model of agonist and nonpeptide antagonist binding to the human V1 vascular vasopressin receptor.	bind
42495	2	11053	6	10	NULL	NULL	NULL	nonpeptide antagonist	Chemical		bind					V1 vascular vasopressin receptor	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_41_0_175_s_970	11264455	A molecular  model of agonist and nonpeptide antagonist binding to the human V1 vascular vasopressin receptor.	bind
49222	1	11053	7	10	NULL	NULL	NULL	agonist	Chemical		bind					 V1 vascular vasopressin receptor	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_41_0_175_s_970	11264455	A molecular  model of agonist and nonpeptide antagonist binding to the human V1 vascular vasopressin receptor.	bind
49223	2	11053	7	10	NULL	NULL	NULL	nonpeptide antagonist	Chemical		bind					V1 vascular vasopressin receptor	GP	human			NULL		NULL	NULL	NULL	NULL	gw70_annurevpharmacol_41_0_175_s_970	11264455	A molecular  model of agonist and nonpeptide antagonist binding to the human V1 vascular vasopressin receptor.	bind
42496	1	11054	6	10	NULL	NULL	NULL	Fab ligand	GP		bind					Integrin alpha IIbbeta 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_28_16660_s_187	7542651	A Molecular Basis for Affinity Modulation of Fab Ligand Binding to Integrin alpha IIbbeta 3.	bind
49224	1	11054	7	10	NULL	NULL	NULL	Fab Ligand 	GP		bind					Integrin alpha IIbbeta 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_28_16660_s_187	7542651	A Molecular Basis for Affinity Modulation of Fab Ligand Binding to Integrin alpha IIbbeta 3.	bind
42498	1	11055	6	10	NULL	NULL	NULL	HERG	GP	mutant	causes					long QT syndrome	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_2_146_s_201	9933245	A molecular basis for cardiac arrhythmia:  HERG mutations cause long QT syndrome.	bind
49225	1	11055	7	10	NULL	NULL	NULL	HERG 	GP	mutant	cause					long QT syndrome	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_2_146_s_201	9933245	A molecular basis for cardiac arrhythmia:  HERG mutations cause long QT syndrome.	bind
42558	1	11056	6	10	NULL	NULL	NULL	calmodulin 	GP		bind					MOR	GP		intracellular i3 loop		NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_308_2_512_s_296	14600246	A molecular basis for the lasting regulation of basal MOR activity was suggested by our observation that calmodulin binds to the intracellular i3 loop of MOR in competition with G proteins, thereby suppressing inherent basal G protein coupling by MOR in untreated tissue (Wang et al., 1999 , 2000 , 2001b ).	bind
42559	2	11056	6	10	NULL	NULL	NULL	G protein	GP	inherent basal	couple with					MOR	GP				NULL	untreated tissue	NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_308_2_512_s_296	14600246	A molecular basis for the lasting regulation of basal MOR activity was suggested by our observation that calmodulin binds to the intracellular i3 loop of MOR in competition with G proteins, thereby suppressing inherent basal G protein coupling by MOR in untreated tissue (Wang et al., 1999 , 2000 , 2001b ).	bind
42560	3	11056	6	10	NULL	NULL	NULL	statement 1	Process		competes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_308_2_512_s_296	14600246	A molecular basis for the lasting regulation of basal MOR activity was suggested by our observation that calmodulin binds to the intracellular i3 loop of MOR in competition with G proteins, thereby suppressing inherent basal G protein coupling by MOR in untreated tissue (Wang et al., 1999 , 2000 , 2001b ).	bind
50278	4	11056	6	10	NULL	NULL	NULL	statement 3	Process		supress					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_308_2_512_s_296	14600246	A molecular basis for the lasting regulation of basal MOR activity was suggested by our observation that calmodulin binds to the intracellular i3 loop of MOR in competition with G proteins, thereby suppressing inherent basal G protein coupling by MOR in untreated tissue (Wang et al., 1999 , 2000 , 2001b ).	bind
49227	1	11056	7	10	NULL	NULL	NULL	 calmodulin	GP		bind					MOR	GP		intracellular i3 loop 		NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_308_2_512_s_296	14600246	A molecular basis for the lasting regulation of basal MOR activity was suggested by our observation that calmodulin binds to the intracellular i3 loop of MOR in competition with G proteins, thereby suppressing inherent basal G protein coupling by MOR in untreated tissue (Wang et al., 1999 , 2000 , 2001b ).	bind
49228	2	11056	7	10	NULL	NULL	NULL	MOR	GP		couple with					G protein	GP	 inherent basal			NULL	untreated tissue	NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_308_2_512_s_296	14600246	A molecular basis for the lasting regulation of basal MOR activity was suggested by our observation that calmodulin binds to the intracellular i3 loop of MOR in competition with G proteins, thereby suppressing inherent basal G protein coupling by MOR in untreated tissue (Wang et al., 1999 , 2000 , 2001b ).	bind
49229	3	11056	7	10	NULL	NULL	NULL	statement 1	Process		compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_308_2_512_s_296	14600246	A molecular basis for the lasting regulation of basal MOR activity was suggested by our observation that calmodulin binds to the intracellular i3 loop of MOR in competition with G proteins, thereby suppressing inherent basal G protein coupling by MOR in untreated tissue (Wang et al., 1999 , 2000 , 2001b ).	bind
49230	4	11056	7	10	NULL	NULL	NULL	statement 3	Process		suppress					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_308_2_512_s_296	14600246	A molecular basis for the lasting regulation of basal MOR activity was suggested by our observation that calmodulin binds to the intracellular i3 loop of MOR in competition with G proteins, thereby suppressing inherent basal G protein coupling by MOR in untreated tissue (Wang et al., 1999 , 2000 , 2001b ).	bind
42561	1	11057	6	10	NULL	NULL	NULL	single chain antibody	GP		is specific for					gp120	GP	highly conserved	CD4 binding site		NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_3_413_s_107	14499116	A molecular conjugate containing the effector domains of the  Pseudomonas exotoxin A linked to a single chain antibody with specificity for the highly conserved CD4 binding site of gp120 (3B3:N31H/Q100eY[dsFv]-PE) is able to kill cells productively infected with diverse CCR5- and CXCR4-tropic strains of HIV while sparing uninfected cells    (Bera et al., 1998  ; Goldstein et al., 2000  ; McHugh et al., 2002  ).	bind
42562	2	11057	6	10	NULL	NULL	NULL	exotoxin A	GP	pseudomonas	is linked to			effector domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_3_413_s_107	14499116	A molecular conjugate containing the effector domains of the  Pseudomonas exotoxin A linked to a single chain antibody with specificity for the highly conserved CD4 binding site of gp120 (3B3:N31H/Q100eY[dsFv]-PE) is able to kill cells productively infected with diverse CCR5- and CXCR4-tropic strains of HIV while sparing uninfected cells    (Bera et al., 1998  ; Goldstein et al., 2000  ; McHugh et al., 2002  ).	bind
42563	3	11057	6	10	NULL	NULL	NULL	HIV-CCR5 strain	Organism		infect					cells 	Cell				NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_3_413_s_107	14499116	A molecular conjugate containing the effector domains of the  Pseudomonas exotoxin A linked to a single chain antibody with specificity for the highly conserved CD4 binding site of gp120 (3B3:N31H/Q100eY[dsFv]-PE) is able to kill cells productively infected with diverse CCR5- and CXCR4-tropic strains of HIV while sparing uninfected cells    (Bera et al., 1998  ; Goldstein et al., 2000  ; McHugh et al., 2002  ).	bind
42564	4	11057	6	10	NULL	NULL	NULL	HIV-CXCR4 strain	Organism		infect					cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_3_413_s_107	14499116	A molecular conjugate containing the effector domains of the  Pseudomonas exotoxin A linked to a single chain antibody with specificity for the highly conserved CD4 binding site of gp120 (3B3:N31H/Q100eY[dsFv]-PE) is able to kill cells productively infected with diverse CCR5- and CXCR4-tropic strains of HIV while sparing uninfected cells    (Bera et al., 1998  ; Goldstein et al., 2000  ; McHugh et al., 2002  ).	bind
42565	5	11057	6	10	NULL	NULL	NULL	statement 2	Process		kills					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_3_413_s_107	14499116	A molecular conjugate containing the effector domains of the  Pseudomonas exotoxin A linked to a single chain antibody with specificity for the highly conserved CD4 binding site of gp120 (3B3:N31H/Q100eY[dsFv]-PE) is able to kill cells productively infected with diverse CCR5- and CXCR4-tropic strains of HIV while sparing uninfected cells    (Bera et al., 1998  ; Goldstein et al., 2000  ; McHugh et al., 2002  ).	bind
42566	6	11057	6	10	NULL	NULL	NULL	statement 2	Process		kills					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_3_413_s_107	14499116	A molecular conjugate containing the effector domains of the  Pseudomonas exotoxin A linked to a single chain antibody with specificity for the highly conserved CD4 binding site of gp120 (3B3:N31H/Q100eY[dsFv]-PE) is able to kill cells productively infected with diverse CCR5- and CXCR4-tropic strains of HIV while sparing uninfected cells    (Bera et al., 1998  ; Goldstein et al., 2000  ; McHugh et al., 2002  ).	bind
49231	1	11057	7	10	NULL	NULL	NULL	molecular conjugate			contains					exotoxin A	GP	Pseudomonas	 effector domains		NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_3_413_s_107	14499116	A molecular conjugate containing the effector domains of the  Pseudomonas exotoxin A linked to a single chain antibody with specificity for the highly conserved CD4 binding site of gp120 (3B3:N31H/Q100eY[dsFv]-PE) is able to kill cells productively infected with diverse CCR5- and CXCR4-tropic strains of HIV while sparing uninfected cells    (Bera et al., 1998  ; Goldstein et al., 2000  ; McHugh et al., 2002  ).	bind
49232	2	11057	7	10	NULL	NULL	NULL	statement 1	Process		linked to					single chain antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_3_413_s_107	14499116	A molecular conjugate containing the effector domains of the  Pseudomonas exotoxin A linked to a single chain antibody with specificity for the highly conserved CD4 binding site of gp120 (3B3:N31H/Q100eY[dsFv]-PE) is able to kill cells productively infected with diverse CCR5- and CXCR4-tropic strains of HIV while sparing uninfected cells    (Bera et al., 1998  ; Goldstein et al., 2000  ; McHugh et al., 2002  ).	bind
49233	3	11057	7	10	NULL	NULL	NULL	statement 2	Process		is specific for					gp120	GP		conserved CD4 binding site		NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_3_413_s_107	14499116	A molecular conjugate containing the effector domains of the  Pseudomonas exotoxin A linked to a single chain antibody with specificity for the highly conserved CD4 binding site of gp120 (3B3:N31H/Q100eY[dsFv]-PE) is able to kill cells productively infected with diverse CCR5- and CXCR4-tropic strains of HIV while sparing uninfected cells    (Bera et al., 1998  ; Goldstein et al., 2000  ; McHugh et al., 2002  ).	bind
49234	4	11057	7	10	NULL	NULL	NULL	cells	Cell		infected with					HIV CCR5-tropic strains 	Organism				NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_3_413_s_107	14499116	A molecular conjugate containing the effector domains of the  Pseudomonas exotoxin A linked to a single chain antibody with specificity for the highly conserved CD4 binding site of gp120 (3B3:N31H/Q100eY[dsFv]-PE) is able to kill cells productively infected with diverse CCR5- and CXCR4-tropic strains of HIV while sparing uninfected cells    (Bera et al., 1998  ; Goldstein et al., 2000  ; McHugh et al., 2002  ).	bind
49235	5	11057	7	10	NULL	NULL	NULL	cells	Cell		infected with					HIV CXCR4-tropic strains	Organism				NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_3_413_s_107	14499116	A molecular conjugate containing the effector domains of the  Pseudomonas exotoxin A linked to a single chain antibody with specificity for the highly conserved CD4 binding site of gp120 (3B3:N31H/Q100eY[dsFv]-PE) is able to kill cells productively infected with diverse CCR5- and CXCR4-tropic strains of HIV while sparing uninfected cells    (Bera et al., 1998  ; Goldstein et al., 2000  ; McHugh et al., 2002  ).	bind
49236	6	11057	7	10	NULL	NULL	NULL	statement 3	Process		kills					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_3_413_s_107	14499116	A molecular conjugate containing the effector domains of the  Pseudomonas exotoxin A linked to a single chain antibody with specificity for the highly conserved CD4 binding site of gp120 (3B3:N31H/Q100eY[dsFv]-PE) is able to kill cells productively infected with diverse CCR5- and CXCR4-tropic strains of HIV while sparing uninfected cells    (Bera et al., 1998  ; Goldstein et al., 2000  ; McHugh et al., 2002  ).	bind
49237	7	11057	7	10	NULL	NULL	NULL	statement 3	Process		kills					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_19_3_413_s_107	14499116	A molecular conjugate containing the effector domains of the  Pseudomonas exotoxin A linked to a single chain antibody with specificity for the highly conserved CD4 binding site of gp120 (3B3:N31H/Q100eY[dsFv]-PE) is able to kill cells productively infected with diverse CCR5- and CXCR4-tropic strains of HIV while sparing uninfected cells    (Bera et al., 1998  ; Goldstein et al., 2000  ; McHugh et al., 2002  ).	bind
42499	1	11058	6	10	NULL	NULL	NULL	YidC	GP		bind		directly			SecDF protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_6_769_s_65	15364957	A molecular interaction with the Sec translocase has been found; this interaction is likely due to a direct binding of YidC to the accessory SecDF proteins ( ).	bind
42500	2	11058	6	10	NULL	NULL	NULL	SecDF	GP		is a type of					accessory protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_6_769_s_65	15364957	A molecular interaction with the Sec translocase has been found; this interaction is likely due to a direct binding of YidC to the accessory SecDF proteins ( ).	bind
49238	1	11058	7	10	NULL	NULL	NULL	YidC	GP		bind		directly			SecDF protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_6_769_s_65	15364957	A molecular interaction with the Sec translocase has been found; this interaction is likely due to a direct binding of YidC to the accessory SecDF proteins ( ).	bind
50279	2	11058	7	10	NULL	NULL	NULL	SecDF 	GP		is a type of					accessory protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_6_769_s_65	15364957	A molecular interaction with the Sec translocase has been found; this interaction is likely due to a direct binding of YidC to the accessory SecDF proteins ( ).	bind
42570	1	11059	6	10	NULL	NULL	NULL	PDZ domain-containing proteins 	GP		bind					EphB2	GP		C-termini		NULL		NULL	NULL	NULL	NULL	gw60_neuron_26_2_417_s_5	10839360	A molecular link to fluid regulation is provided by demonstrating that PDZ domain-containing proteins that bind the C termini of EphB2 and B-ephrins can also recognize the cytoplasmic tails of anion exchangers and aquaporins.	bind
42571	2	11059	6	10	NULL	NULL	NULL	PDZ domain-containing proteins	GP		bind					B-ephrin	GP		C-termini		NULL		NULL	NULL	NULL	NULL	gw60_neuron_26_2_417_s_5	10839360	A molecular link to fluid regulation is provided by demonstrating that PDZ domain-containing proteins that bind the C termini of EphB2 and B-ephrins can also recognize the cytoplasmic tails of anion exchangers and aquaporins.	bind
42572	3	11059	6	10	NULL	NULL	NULL	PDZ domain-containing proteins	GP		recognize					anion exchangers	GP		cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_neuron_26_2_417_s_5	10839360	A molecular link to fluid regulation is provided by demonstrating that PDZ domain-containing proteins that bind the C termini of EphB2 and B-ephrins can also recognize the cytoplasmic tails of anion exchangers and aquaporins.	bind
42573	4	11059	6	10	NULL	NULL	NULL	PDZ domain-containing proteins	GP		recognize					aquaporins	GP		cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw60_neuron_26_2_417_s_5	10839360	A molecular link to fluid regulation is provided by demonstrating that PDZ domain-containing proteins that bind the C termini of EphB2 and B-ephrins can also recognize the cytoplasmic tails of anion exchangers and aquaporins.	bind
49239	1	11059	7	10	NULL	NULL	NULL	PDZ domain-containing proteins	GP		bind					EphB2	GP		C termini		NULL		NULL	NULL	NULL	NULL	gw60_neuron_26_2_417_s_5	10839360	A molecular link to fluid regulation is provided by demonstrating that PDZ domain-containing proteins that bind the C termini of EphB2 and B-ephrins can also recognize the cytoplasmic tails of anion exchangers and aquaporins.	bind
49240	2	11059	7	10	NULL	NULL	NULL	PDZ domain-containing proteins	GP		bind					B-ephrins	GP		C termini		NULL		NULL	NULL	NULL	NULL	gw60_neuron_26_2_417_s_5	10839360	A molecular link to fluid regulation is provided by demonstrating that PDZ domain-containing proteins that bind the C termini of EphB2 and B-ephrins can also recognize the cytoplasmic tails of anion exchangers and aquaporins.	bind
49241	3	11059	7	10	NULL	NULL	NULL	PDZ domain-containing proteins	GP		recognize					anion exchangers	GP		cytoplasmic tails 		NULL		NULL	NULL	NULL	NULL	gw60_neuron_26_2_417_s_5	10839360	A molecular link to fluid regulation is provided by demonstrating that PDZ domain-containing proteins that bind the C termini of EphB2 and B-ephrins can also recognize the cytoplasmic tails of anion exchangers and aquaporins.	bind
49242	4	11059	7	10	NULL	NULL	NULL	PDZ domain-containing proteins	GP		recognize					aquaporins	GP		cytoplasmic tails		NULL		NULL	NULL	NULL	NULL	gw60_neuron_26_2_417_s_5	10839360	A molecular link to fluid regulation is provided by demonstrating that PDZ domain-containing proteins that bind the C termini of EphB2 and B-ephrins can also recognize the cytoplasmic tails of anion exchangers and aquaporins.	bind
57859	1	11060	6	10	NULL	NULL	NULL	thrombin Met-SC(1 325) complex \t	GP		undergoes					dimerization	Process				NULL	solution	NULL	NULL	NULL	NULL	gw70_nature_425_6957_535_s_53	14523451	A molecular mass of 155   10 kDa was determined for the thrombin Met-SC(1 325) complex by using sedimentation equilibrium, indicating that the complex  dimerizes in solution.	bind
49243	1	11060	7	10	NULL	NULL	NULL	thrombin Met-SC(1 325) complex 	GP		undergoes					dimerization	Process				NULL	solution	NULL	NULL	NULL	NULL	gw70_nature_425_6957_535_s_53	14523451	A molecular mass of 155   10 kDa was determined for the thrombin Met-SC(1 325) complex by using sedimentation equilibrium, indicating that the complex  dimerizes in solution.	bind
42574	1	11061	6	10	NULL	NULL	NULL	imidazole group	Chemical		bind					Cu(II) ion	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_5_2042_s_237	10051591	A molecular model constructed for the Cu4[PrP(58-91)] complex showed that the four-copper atom cluster could be accommodated without strain at the corners of a distorted tetrahedron, with two imidazole groups bound to each Cu(II) ion at adjacent coordination sites.	bind
49244	1	11061	7	10	NULL	NULL	NULL	imidazole groups	Chemical		bind					Cu(II) ion	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_5_2042_s_237	10051591	A molecular model constructed for the Cu4[PrP(58-91)] complex showed that the four-copper atom cluster could be accommodated without strain at the corners of a distorted tetrahedron, with two imidazole groups bound to each Cu(II) ion at adjacent coordination sites.	bind
42575	1	11062	6	10	NULL	NULL	NULL	agonist	Chemical		bind					V1 vascular vasopressin receptor	GP	human			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-pharmacol-exp-ther_294_1_10871312_s_1	10871312	A molecular model of agonist and nonpeptide antagonist binding to the human V(1) vascular vasopressin receptor..	bind
42576	2	11062	6	10	NULL	NULL	NULL	nonpeptide antagonist	Chemical		bind					V1 vascular vasopressin receptor	GP	human			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-pharmacol-exp-ther_294_1_10871312_s_1	10871312	A molecular model of agonist and nonpeptide antagonist binding to the human V(1) vascular vasopressin receptor..	bind
49246	1	11062	7	10	NULL	NULL	NULL	agonist	Chemical		bind					V(1) vascular vasopressin receptor	GP	human			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-pharmacol-exp-ther_294_1_10871312_s_1	10871312	A molecular model of agonist and nonpeptide antagonist binding to the human V(1) vascular vasopressin receptor..	bind
49247	2	11062	7	10	NULL	NULL	NULL	nonpeptide antagonist	Chemical		bind					V(1) vascular vasopressin receptor	GP	human			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-pharmacol-exp-ther_294_1_10871312_s_1	10871312	A molecular model of agonist and nonpeptide antagonist binding to the human V(1) vascular vasopressin receptor..	bind
42577	1	11067	6	10	NULL	NULL	NULL	Sic1	GP		bind			inhibitory domain		Cdk2-cyclin A complex	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biochem-j_387_pt-3_15649124_s_6	15649124	A molecular model of the inhibitory domain of Sic1 bound to the Cdk2-cyclin  A complex suggested that the yeast inhibitor might productively interface  with the mammalian Cdk2-cyclin A complex.	bind
42578	2	11067	6	10	NULL	NULL	NULL	inhibitor	GP	yeast	interface with		might;;productively 			Cdk2-cyclin A complex	GP	mammalian			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biochem-j_387_pt-3_15649124_s_6	15649124	A molecular model of the inhibitory domain of Sic1 bound to the Cdk2-cyclin  A complex suggested that the yeast inhibitor might productively interface  with the mammalian Cdk2-cyclin A complex.	bind
49248	1	11067	7	10	NULL	NULL	NULL	Sic1	GP		bind			inhibitory domain		Cdk2-cyclin A complex	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biochem-j_387_pt-3_15649124_s_6	15649124	A molecular model of the inhibitory domain of Sic1 bound to the Cdk2-cyclin  A complex suggested that the yeast inhibitor might productively interface  with the mammalian Cdk2-cyclin A complex.	bind
49249	2	11067	7	10	NULL	NULL	NULL	 inhibitor	GP	yeast	interface with		may;;productively			Cdk2-cyclin A complex	GP	mammalian			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biochem-j_387_pt-3_15649124_s_6	15649124	A molecular model of the inhibitory domain of Sic1 bound to the Cdk2-cyclin  A complex suggested that the yeast inhibitor might productively interface  with the mammalian Cdk2-cyclin A complex.	bind
49250	3	11067	7	10	NULL	NULL	NULL	statement 1	Process		suggest					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biochem-j_387_pt-3_15649124_s_6	15649124	A molecular model of the inhibitory domain of Sic1 bound to the Cdk2-cyclin  A complex suggested that the yeast inhibitor might productively interface  with the mammalian Cdk2-cyclin A complex.	bind
42579	1	11068	6	10	NULL	NULL	NULL	anti-Abeta IgG 	GP		bind					Abeta fibrils	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_bioorg-med-chem-lett_16_4_16290147_s_6	16290147	A molecular surface coating with 3,6-diamino acridine  was able to inhibit 76+/-10% of the binding of an anti-Abeta IgG to Abeta  fibrils.	bind
42580	2	11068	6	10	NULL	NULL	NULL	3,6-diamino acridine 	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_bioorg-med-chem-lett_16_4_16290147_s_6	16290147	A molecular surface coating with 3,6-diamino acridine  was able to inhibit 76+/-10% of the binding of an anti-Abeta IgG to Abeta  fibrils.	bind
49251	1	11068	7	10	NULL	NULL	NULL	anti-Abeta IgG	GP		bind					Abeta fibrils	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_bioorg-med-chem-lett_16_4_16290147_s_6	16290147	A molecular surface coating with 3,6-diamino acridine  was able to inhibit 76+/-10% of the binding of an anti-Abeta IgG to Abeta  fibrils.	bind
49252	2	11068	7	10	NULL	NULL	NULL	 3,6-diamino acridine	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_bioorg-med-chem-lett_16_4_16290147_s_6	16290147	A molecular surface coating with 3,6-diamino acridine  was able to inhibit 76+/-10% of the binding of an anti-Abeta IgG to Abeta  fibrils.	bind
42581	1	11069	6	10	NULL	NULL	NULL	PPS	Chemical		is					3-(1-pyridino)-1-propanesulfonate	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_26_27511_s_151	15075327	A molecule of 3-(1-pyridino)-1-propanesulfonate (PPS) is bound to Stx2 in four of the five potential type 1 binding sites.	bind
42582	2	11069	6	10	NULL	NULL	NULL	PPS	Chemical		bind					Stx2	GP		type 1 binding site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_26_27511_s_151	15075327	A molecule of 3-(1-pyridino)-1-propanesulfonate (PPS) is bound to Stx2 in four of the five potential type 1 binding sites.	bind
49253	1	11069	7	10	NULL	NULL	NULL	PPS	Chemical		bind					Stx2	GP		type 1 binding site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_26_27511_s_151	15075327	A molecule of 3-(1-pyridino)-1-propanesulfonate (PPS) is bound to Stx2 in four of the five potential type 1 binding sites.	bind
49254	2	11069	7	10	NULL	NULL	NULL	PPS	Chemical		is					3-(1-pyridino)-1-propanesulfonate	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_26_27511_s_151	15075327	A molecule of 3-(1-pyridino)-1-propanesulfonate (PPS) is bound to Stx2 in four of the five potential type 1 binding sites.	bind
42583	1	11070	6	10	NULL	NULL	NULL	acetoacetyl-CoA	Chemical		bind					enoyl-CoA hydratase	GP				NULL		NULL	NULL	NULL	NULL	gw60_structure_6_8_957_s_107	9739087	A molecule of acetoacetyl-CoA, as it binds to enoyl-CoA hydratase  [17]  , is shown in ball-and-stick representation (green).	bind
49255	1	11070	7	10	NULL	NULL	NULL	acetoacetyl-CoA	Chemical		bind					enoyl-CoA hydratase	GP				NULL		NULL	NULL	NULL	NULL	gw60_structure_6_8_957_s_107	9739087	A molecule of acetoacetyl-CoA, as it binds to enoyl-CoA hydratase  [17]  , is shown in ball-and-stick representation (green).	bind
42845	1	11071	6	10	NULL	NULL	NULL	cAMP	Chemical		bind								B domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35521_s_201	16109722	A molecule of cAMP must first bind to the B domain, allowing cAMP binding to the A domain, which then causes the conformational changes directly responsible for C subunit activation.	bind
42846	2	11071	6	10	NULL	NULL	NULL	cAMP	Chemical		bind								A domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35521_s_201	16109722	A molecule of cAMP must first bind to the B domain, allowing cAMP binding to the A domain, which then causes the conformational changes directly responsible for C subunit activation.	bind
42847	3	11071	6	10	NULL	NULL	NULL	statement 1	Process		allows					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35521_s_201	16109722	A molecule of cAMP must first bind to the B domain, allowing cAMP binding to the A domain, which then causes the conformational changes directly responsible for C subunit activation.	bind
42848	4	11071	6	10	NULL	NULL	NULL	statement 2	Process		leads to					conformational changes	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35521_s_201	16109722	A molecule of cAMP must first bind to the B domain, allowing cAMP binding to the A domain, which then causes the conformational changes directly responsible for C subunit activation.	bind
42849	5	11071	6	10	NULL	NULL	NULL	statement 4	Process		is responsible for		directly			C subunit	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35521_s_201	16109722	A molecule of cAMP must first bind to the B domain, allowing cAMP binding to the A domain, which then causes the conformational changes directly responsible for C subunit activation.	bind
49256	1	11071	7	10	NULL	NULL	NULL	cAMP	Chemical		bind								B domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35521_s_201	16109722	A molecule of cAMP must first bind to the B domain, allowing cAMP binding to the A domain, which then causes the conformational changes directly responsible for C subunit activation.	bind
49257	2	11071	7	10	NULL	NULL	NULL	cAMP	Chemical		bind								A domain		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35521_s_201	16109722	A molecule of cAMP must first bind to the B domain, allowing cAMP binding to the A domain, which then causes the conformational changes directly responsible for C subunit activation.	bind
49258	3	11071	7	10	NULL	NULL	NULL	statement 1	Process		allows 					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35521_s_201	16109722	A molecule of cAMP must first bind to the B domain, allowing cAMP binding to the A domain, which then causes the conformational changes directly responsible for C subunit activation.	bind
49259	4	11071	7	10	NULL	NULL	NULL	statement 2	Process		cause					conformational changes	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35521_s_201	16109722	A molecule of cAMP must first bind to the B domain, allowing cAMP binding to the A domain, which then causes the conformational changes directly responsible for C subunit activation.	bind
49260	5	11071	7	10	NULL	NULL	NULL	statement 4	Process		leads to		directly			C subunit	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_42_35521_s_201	16109722	A molecule of cAMP must first bind to the B domain, allowing cAMP binding to the A domain, which then causes the conformational changes directly responsible for C subunit activation.	bind
42620	1	11072	6	10	NULL	NULL	NULL	CR1	GP	mouse	bind		less efficiency	SCR		C3b	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_153_2_8021513_s_6	8021513	A molecule that contains only the  first six SCRs of mouse CR1 also binds C3b, but with less efficiency.	bind
49261	1	11072	7	10	NULL	NULL	NULL	CR1	GP	mouse	bind		less efficiency	SCRs		C3b	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_153_2_8021513_s_6	8021513	A molecule that contains only the  first six SCRs of mouse CR1 also binds C3b, but with less efficiency.	bind
42621	1	11074	6	10	NULL	NULL	NULL	mAb2G5	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_97_6_755_s_32	10380927	A monoclonal  antibody, mAb2G5, which recognizes a region close to the ATP-binding cleft of the N-terminal  DnaK domain (Krska et al., 1993   ), coprecipitated DnaK and a wide variety  of newly synthesized polypeptides from the lysed spheroplasts (  Figure 1A, lane 3).	bind
42625	2	11074	6	10	NULL	NULL	NULL	mAb2G5	GP		recognizes								ATP-binding cleft of the N-terminal DnaK domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_97_6_755_s_32	10380927	A monoclonal  antibody, mAb2G5, which recognizes a region close to the ATP-binding cleft of the N-terminal  DnaK domain (Krska et al., 1993   ), coprecipitated DnaK and a wide variety  of newly synthesized polypeptides from the lysed spheroplasts (  Figure 1A, lane 3).	bind
42626	3	11074	6	10	NULL	NULL	NULL	mAb2G5	GP		bind					DnaK	GP				NULL	lysed spheroplasts	NULL	NULL	NULL	NULL	gw60_cell_97_6_755_s_32	10380927	A monoclonal  antibody, mAb2G5, which recognizes a region close to the ATP-binding cleft of the N-terminal  DnaK domain (Krska et al., 1993   ), coprecipitated DnaK and a wide variety  of newly synthesized polypeptides from the lysed spheroplasts (  Figure 1A, lane 3).	bind
49262	1	11074	7	10	NULL	NULL	NULL	mAb2G5	GP		recognizes							region close to	 ATP-binding cleft of the N-terminal DnaK domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_97_6_755_s_32	10380927	A monoclonal  antibody, mAb2G5, which recognizes a region close to the ATP-binding cleft of the N-terminal  DnaK domain (Krska et al., 1993   ), coprecipitated DnaK and a wide variety  of newly synthesized polypeptides from the lysed spheroplasts (  Figure 1A, lane 3).	bind
49263	2	11074	7	10	NULL	NULL	NULL	statement 1	Process		bind					DnaK	GP				NULL	lysed spheroplasts	NULL	NULL	NULL	NULL	gw60_cell_97_6_755_s_32	10380927	A monoclonal  antibody, mAb2G5, which recognizes a region close to the ATP-binding cleft of the N-terminal  DnaK domain (Krska et al., 1993   ), coprecipitated DnaK and a wide variety  of newly synthesized polypeptides from the lysed spheroplasts (  Figure 1A, lane 3).	bind
49264	3	11074	7	10	NULL	NULL	NULL	statement 1	Process		bind					polypeptides	AminoAcid	newly synthesized			NULL	lysed spheroplasts	NULL	NULL	NULL	NULL	gw60_cell_97_6_755_s_32	10380927	A monoclonal  antibody, mAb2G5, which recognizes a region close to the ATP-binding cleft of the N-terminal  DnaK domain (Krska et al., 1993   ), coprecipitated DnaK and a wide variety  of newly synthesized polypeptides from the lysed spheroplasts (  Figure 1A, lane 3).	bind
49265	4	11074	7	10	NULL	NULL	NULL	mAb2G5	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_97_6_755_s_32	10380927	A monoclonal  antibody, mAb2G5, which recognizes a region close to the ATP-binding cleft of the N-terminal  DnaK domain (Krska et al., 1993   ), coprecipitated DnaK and a wide variety  of newly synthesized polypeptides from the lysed spheroplasts (  Figure 1A, lane 3).	bind
42850	1	11075	6	10	NULL	NULL	NULL	C-19	GP		is a type of					polyclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5802_s_151	14597617	A monoclonal antibody (AB-1) whose epitope maps within amino acid residues 58 - 77 of human p21 near the CDK2 binding site and a polyclonal antibody (C-19) that binds to the C terminus of p21 and cannot recognize p21 bound to PCNA were used ( ).	bind
42851	2	11075	6	10	NULL	NULL	NULL	C-19	GP		bind					p21	GP		C terminus		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5802_s_151	14597617	A monoclonal antibody (AB-1) whose epitope maps within amino acid residues 58 - 77 of human p21 near the CDK2 binding site and a polyclonal antibody (C-19) that binds to the C terminus of p21 and cannot recognize p21 bound to PCNA were used ( ).	bind
50280	3	11075	6	10	NULL	NULL	NULL	p21	GP		bind					PCNA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5802_s_151	14597617	A monoclonal antibody (AB-1) whose epitope maps within amino acid residues 58 - 77 of human p21 near the CDK2 binding site and a polyclonal antibody (C-19) that binds to the C terminus of p21 and cannot recognize p21 bound to PCNA were used ( ).	bind
57860	4	11075	6	10	NULL	NULL	NULL	AB-1	GP		is a type of					monoclonal antibody \t	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5802_s_151	14597617	A monoclonal antibody (AB-1) whose epitope maps within amino acid residues 58 - 77 of human p21 near the CDK2 binding site and a polyclonal antibody (C-19) that binds to the C terminus of p21 and cannot recognize p21 bound to PCNA were used ( ).	bind
49266	1	11075	7	10	NULL	NULL	NULL	C-19	GP		bind					p21	GP		C terminus		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5802_s_151	14597617	A monoclonal antibody (AB-1) whose epitope maps within amino acid residues 58 - 77 of human p21 near the CDK2 binding site and a polyclonal antibody (C-19) that binds to the C terminus of p21 and cannot recognize p21 bound to PCNA were used ( ).	bind
49267	2	11075	7	10	NULL	NULL	NULL	p21	GP		bind					PCNA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5802_s_151	14597617	A monoclonal antibody (AB-1) whose epitope maps within amino acid residues 58 - 77 of human p21 near the CDK2 binding site and a polyclonal antibody (C-19) that binds to the C terminus of p21 and cannot recognize p21 bound to PCNA were used ( ).	bind
49268	3	11075	7	10	NULL	NULL	NULL	C-19	GP		is a type of					polyclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5802_s_151	14597617	A monoclonal antibody (AB-1) whose epitope maps within amino acid residues 58 - 77 of human p21 near the CDK2 binding site and a polyclonal antibody (C-19) that binds to the C terminus of p21 and cannot recognize p21 bound to PCNA were used ( ).	bind
49269	4	11075	7	10	NULL	NULL	NULL	AB-1	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5802_s_151	14597617	A monoclonal antibody (AB-1) whose epitope maps within amino acid residues 58 - 77 of human p21 near the CDK2 binding site and a polyclonal antibody (C-19) that binds to the C terminus of p21 and cannot recognize p21 bound to PCNA were used ( ).	bind
42852	1	11076	6	10	NULL	NULL	NULL	125I-Fn	GP		bind					M. tuberculosis	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1287_s_5	11854212	A monoclonal antibody (MAb) specific to the heparin binding domain (HBD) of Fn decreases 125I-Fn binding to  M. tuberculosis; whereas MAbs specific to either the cell binding domain (CBD) or the gelatin binding domain (GBD) have no effect on Fn binding to  M. tuberculosis.	bind
42853	2	11076	6	10	NULL	NULL	NULL	MAb	GP		is specific for					Fn	GP		HBD		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1287_s_5	11854212	A monoclonal antibody (MAb) specific to the heparin binding domain (HBD) of Fn decreases 125I-Fn binding to  M. tuberculosis; whereas MAbs specific to either the cell binding domain (CBD) or the gelatin binding domain (GBD) have no effect on Fn binding to  M. tuberculosis.	bind
42854	3	11076	6	10	NULL	NULL	NULL	statement 2	Process		decreases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1287_s_5	11854212	A monoclonal antibody (MAb) specific to the heparin binding domain (HBD) of Fn decreases 125I-Fn binding to  M. tuberculosis; whereas MAbs specific to either the cell binding domain (CBD) or the gelatin binding domain (GBD) have no effect on Fn binding to  M. tuberculosis.	bind
42855	4	11076	6	10	NULL	NULL	NULL	MAb	GP		is					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1287_s_5	11854212	A monoclonal antibody (MAb) specific to the heparin binding domain (HBD) of Fn decreases 125I-Fn binding to  M. tuberculosis; whereas MAbs specific to either the cell binding domain (CBD) or the gelatin binding domain (GBD) have no effect on Fn binding to  M. tuberculosis.	bind
42856	5	11076	6	10	NULL	NULL	NULL	HBD	AminoAcid		is					heparin binding domain	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1287_s_5	11854212	A monoclonal antibody (MAb) specific to the heparin binding domain (HBD) of Fn decreases 125I-Fn binding to  M. tuberculosis; whereas MAbs specific to either the cell binding domain (CBD) or the gelatin binding domain (GBD) have no effect on Fn binding to  M. tuberculosis.	bind
42857	6	11076	6	10	NULL	NULL	NULL	MAb	GP		is specific for					Fn	GP		CBD		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1287_s_5	11854212	A monoclonal antibody (MAb) specific to the heparin binding domain (HBD) of Fn decreases 125I-Fn binding to  M. tuberculosis; whereas MAbs specific to either the cell binding domain (CBD) or the gelatin binding domain (GBD) have no effect on Fn binding to  M. tuberculosis.	bind
42858	7	11076	6	10	NULL	NULL	NULL	MAb	GP		is specific for					Fn	GP		GBD		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1287_s_5	11854212	A monoclonal antibody (MAb) specific to the heparin binding domain (HBD) of Fn decreases 125I-Fn binding to  M. tuberculosis; whereas MAbs specific to either the cell binding domain (CBD) or the gelatin binding domain (GBD) have no effect on Fn binding to  M. tuberculosis.	bind
42859	8	11076	6	10	NULL	NULL	NULL	statement 6	Process		has no effect on					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1287_s_5	11854212	A monoclonal antibody (MAb) specific to the heparin binding domain (HBD) of Fn decreases 125I-Fn binding to  M. tuberculosis; whereas MAbs specific to either the cell binding domain (CBD) or the gelatin binding domain (GBD) have no effect on Fn binding to  M. tuberculosis.	bind
42860	9	11076	6	10	NULL	NULL	NULL	statement 7	Process		has no effect on					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1287_s_5	11854212	A monoclonal antibody (MAb) specific to the heparin binding domain (HBD) of Fn decreases 125I-Fn binding to  M. tuberculosis; whereas MAbs specific to either the cell binding domain (CBD) or the gelatin binding domain (GBD) have no effect on Fn binding to  M. tuberculosis.	bind
49270	1	11076	7	10	NULL	NULL	NULL	125I-Fn	GP		bind					M. tuberculosis	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1287_s_5	11854212	A monoclonal antibody (MAb) specific to the heparin binding domain (HBD) of Fn decreases 125I-Fn binding to  M. tuberculosis; whereas MAbs specific to either the cell binding domain (CBD) or the gelatin binding domain (GBD) have no effect on Fn binding to  M. tuberculosis.	bind
49271	2	11076	7	10	NULL	NULL	NULL	FnMAb	GP		decrease			HBD		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1287_s_5	11854212	A monoclonal antibody (MAb) specific to the heparin binding domain (HBD) of Fn decreases 125I-Fn binding to  M. tuberculosis; whereas MAbs specific to either the cell binding domain (CBD) or the gelatin binding domain (GBD) have no effect on Fn binding to  M. tuberculosis.	bind
49272	3	11076	7	10	NULL	NULL	NULL	Fn MAb	GP		does not affect			CBD		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1287_s_5	11854212	A monoclonal antibody (MAb) specific to the heparin binding domain (HBD) of Fn decreases 125I-Fn binding to  M. tuberculosis; whereas MAbs specific to either the cell binding domain (CBD) or the gelatin binding domain (GBD) have no effect on Fn binding to  M. tuberculosis.	bind
49273	4	11076	7	10	NULL	NULL	NULL	Fn MAb	GP		does not affect			GBD		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1287_s_5	11854212	A monoclonal antibody (MAb) specific to the heparin binding domain (HBD) of Fn decreases 125I-Fn binding to  M. tuberculosis; whereas MAbs specific to either the cell binding domain (CBD) or the gelatin binding domain (GBD) have no effect on Fn binding to  M. tuberculosis.	bind
49274	5	11076	7	10	NULL	NULL	NULL	MAb	GP		is					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1287_s_5	11854212	A monoclonal antibody (MAb) specific to the heparin binding domain (HBD) of Fn decreases 125I-Fn binding to  M. tuberculosis; whereas MAbs specific to either the cell binding domain (CBD) or the gelatin binding domain (GBD) have no effect on Fn binding to  M. tuberculosis.	bind
49275	6	11076	7	10	NULL	NULL	NULL	HBD	AminoAcid		is					heparin binding domain	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1287_s_5	11854212	A monoclonal antibody (MAb) specific to the heparin binding domain (HBD) of Fn decreases 125I-Fn binding to  M. tuberculosis; whereas MAbs specific to either the cell binding domain (CBD) or the gelatin binding domain (GBD) have no effect on Fn binding to  M. tuberculosis.	bind
49276	7	11076	7	10	NULL	NULL	NULL	CBD	AminoAcid		is 					cell binding domain	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1287_s_5	11854212	A monoclonal antibody (MAb) specific to the heparin binding domain (HBD) of Fn decreases 125I-Fn binding to  M. tuberculosis; whereas MAbs specific to either the cell binding domain (CBD) or the gelatin binding domain (GBD) have no effect on Fn binding to  M. tuberculosis.	bind
49277	8	11076	7	10	NULL	NULL	NULL	GBD	AminoAcid		is					gelatin binding domain	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_3_1287_s_5	11854212	A monoclonal antibody (MAb) specific to the heparin binding domain (HBD) of Fn decreases 125I-Fn binding to  M. tuberculosis; whereas MAbs specific to either the cell binding domain (CBD) or the gelatin binding domain (GBD) have no effect on Fn binding to  M. tuberculosis.	bind
42627	1	11077	6	10	NULL	NULL	NULL	MV	Organism		is					measles virus	Organism				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-virol_67_10_8371352_s_2	8371352	A monoclonal antibody (MCI20.6) which inhibited measles virus (MV) binding  to host cells was previously used to characterize a 57- to 67-kDa cell  surface glycoprotein as a potential MV receptor.	bind
42628	2	11077	6	10	NULL	NULL	NULL	MV	Organism		bind					host cells	Cell				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-virol_67_10_8371352_s_2	8371352	A monoclonal antibody (MCI20.6) which inhibited measles virus (MV) binding  to host cells was previously used to characterize a 57- to 67-kDa cell  surface glycoprotein as a potential MV receptor.	bind
42629	3	11077	6	10	NULL	NULL	NULL	MCI20.6	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-virol_67_10_8371352_s_2	8371352	A monoclonal antibody (MCI20.6) which inhibited measles virus (MV) binding  to host cells was previously used to characterize a 57- to 67-kDa cell  surface glycoprotein as a potential MV receptor.	bind
42630	4	11077	6	10	NULL	NULL	NULL	MCI20.6	GP		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-virol_67_10_8371352_s_2	8371352	A monoclonal antibody (MCI20.6) which inhibited measles virus (MV) binding  to host cells was previously used to characterize a 57- to 67-kDa cell  surface glycoprotein as a potential MV receptor.	bind
49278	1	11077	7	10	NULL	NULL	NULL	MV	Organism		bind					host cells	Cell				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-virol_67_10_8371352_s_2	8371352	A monoclonal antibody (MCI20.6) which inhibited measles virus (MV) binding  to host cells was previously used to characterize a 57- to 67-kDa cell  surface glycoprotein as a potential MV receptor.	bind
49279	2	11077	7	10	NULL	NULL	NULL	MCI20.6	GP		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-virol_67_10_8371352_s_2	8371352	A monoclonal antibody (MCI20.6) which inhibited measles virus (MV) binding  to host cells was previously used to characterize a 57- to 67-kDa cell  surface glycoprotein as a potential MV receptor.	bind
49281	4	11077	7	10	NULL	NULL	NULL	MCI20.6	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-virol_67_10_8371352_s_2	8371352	A monoclonal antibody (MCI20.6) which inhibited measles virus (MV) binding  to host cells was previously used to characterize a 57- to 67-kDa cell  surface glycoprotein as a potential MV receptor.	bind
49282	3	11077	7	10	NULL	NULL	NULL	MV	Organism		is 					measles virus	Organism				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-virol_67_10_8371352_s_2	8371352	A monoclonal antibody (MCI20.6) which inhibited measles virus (MV) binding  to host cells was previously used to characterize a 57- to 67-kDa cell  surface glycoprotein as a potential MV receptor.	bind
42631	1	11078	6	10	NULL	NULL	NULL	DR5	GP		is 					death receptor 5	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_clin-cancer-res_9_10-pt-1_14506165_s_3	14506165	A monoclonal antibody (TRA-8) has been developed that binds to  death receptor 5 (DR5), one of two death receptors bound by tumor necrosis  factor-related apoptosis-inducing ligand.	bind
42632	2	11078	6	10	NULL	NULL	NULL	TRA-8	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_clin-cancer-res_9_10-pt-1_14506165_s_3	14506165	A monoclonal antibody (TRA-8) has been developed that binds to  death receptor 5 (DR5), one of two death receptors bound by tumor necrosis  factor-related apoptosis-inducing ligand.	bind
42633	3	11078	6	10	NULL	NULL	NULL	TR-8	GP		bind					DR-5	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_clin-cancer-res_9_10-pt-1_14506165_s_3	14506165	A monoclonal antibody (TRA-8) has been developed that binds to  death receptor 5 (DR5), one of two death receptors bound by tumor necrosis  factor-related apoptosis-inducing ligand.	bind
42634	4	11078	6	10	NULL	NULL	NULL	DR-5	GP		bind					tumor necrosis factor-related apoptosis-inducing ligand	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_clin-cancer-res_9_10-pt-1_14506165_s_3	14506165	A monoclonal antibody (TRA-8) has been developed that binds to  death receptor 5 (DR5), one of two death receptors bound by tumor necrosis  factor-related apoptosis-inducing ligand.	bind
49283	1	11078	7	10	NULL	NULL	NULL	TRA-8	GP		bind					DR5	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_clin-cancer-res_9_10-pt-1_14506165_s_3	14506165	A monoclonal antibody (TRA-8) has been developed that binds to  death receptor 5 (DR5), one of two death receptors bound by tumor necrosis  factor-related apoptosis-inducing ligand.	bind
49284	2	11078	7	10	NULL	NULL	NULL	TRA-8	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_clin-cancer-res_9_10-pt-1_14506165_s_3	14506165	A monoclonal antibody (TRA-8) has been developed that binds to  death receptor 5 (DR5), one of two death receptors bound by tumor necrosis  factor-related apoptosis-inducing ligand.	bind
49285	3	11078	7	10	NULL	NULL	NULL	DR5	GP		is a type of					death receptor	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_clin-cancer-res_9_10-pt-1_14506165_s_3	14506165	A monoclonal antibody (TRA-8) has been developed that binds to  death receptor 5 (DR5), one of two death receptors bound by tumor necrosis  factor-related apoptosis-inducing ligand.	bind
49286	4	11078	7	10	NULL	NULL	NULL	tumor necrosis factor-related apoptosis-inducing ligand	GP		bind					DR5	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_clin-cancer-res_9_10-pt-1_14506165_s_3	14506165	A monoclonal antibody (TRA-8) has been developed that binds to  death receptor 5 (DR5), one of two death receptors bound by tumor necrosis  factor-related apoptosis-inducing ligand.	bind
42884	1	11080	6	10	NULL	NULL	NULL	CD24 	GP	substrate coated	elicits					neurite outgrowth	Process	negative influence on			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21656_s_135	11283023	A monoclonal antibody against CD24 and polyclonal antibodies against L1 were able to reduce or inhibit the negative influences on neurite outgrowth elicited by substrate-coated CD24 but not on poly-L-lysine (Fig.  3 A, compare CD24 + anti-CD24 and CD24 + anti-L1 with CD24 and PLL), whereas nonimmune IgG control antibodies had no effect (Fig.  3 A, compare CD24 + IgG with CD24), indicating that the L1 antibody binds to L1 at the cell surface of dorsal root ganglion neurons and masks it for binding to CD24 in trans-interaction.	bind
42885	2	11080	6	10	NULL	NULL	NULL	L1 antibody	GP		bind					L1	GP				NULL	cell surface of dorsal root ganglion neurons	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21656_s_135	11283023	A monoclonal antibody against CD24 and polyclonal antibodies against L1 were able to reduce or inhibit the negative influences on neurite outgrowth elicited by substrate-coated CD24 but not on poly-L-lysine (Fig.  3 A, compare CD24 + anti-CD24 and CD24 + anti-L1 with CD24 and PLL), whereas nonimmune IgG control antibodies had no effect (Fig.  3 A, compare CD24 + IgG with CD24), indicating that the L1 antibody binds to L1 at the cell surface of dorsal root ganglion neurons and masks it for binding to CD24 in trans-interaction.	bind
42886	3	11080	6	10	NULL	NULL	NULL	monoclonal antibody	GP		against					CD24	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21656_s_135	11283023	A monoclonal antibody against CD24 and polyclonal antibodies against L1 were able to reduce or inhibit the negative influences on neurite outgrowth elicited by substrate-coated CD24 but not on poly-L-lysine (Fig.  3 A, compare CD24 + anti-CD24 and CD24 + anti-L1 with CD24 and PLL), whereas nonimmune IgG control antibodies had no effect (Fig.  3 A, compare CD24 + IgG with CD24), indicating that the L1 antibody binds to L1 at the cell surface of dorsal root ganglion neurons and masks it for binding to CD24 in trans-interaction.	bind
42887	4	11080	6	10	NULL	NULL	NULL	statement 3	Process		reduce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21656_s_135	11283023	A monoclonal antibody against CD24 and polyclonal antibodies against L1 were able to reduce or inhibit the negative influences on neurite outgrowth elicited by substrate-coated CD24 but not on poly-L-lysine (Fig.  3 A, compare CD24 + anti-CD24 and CD24 + anti-L1 with CD24 and PLL), whereas nonimmune IgG control antibodies had no effect (Fig.  3 A, compare CD24 + IgG with CD24), indicating that the L1 antibody binds to L1 at the cell surface of dorsal root ganglion neurons and masks it for binding to CD24 in trans-interaction.	bind
42888	5	11080	6	10	NULL	NULL	NULL	Polyclonal antibodies	GP		against					L1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21656_s_135	11283023	A monoclonal antibody against CD24 and polyclonal antibodies against L1 were able to reduce or inhibit the negative influences on neurite outgrowth elicited by substrate-coated CD24 but not on poly-L-lysine (Fig.  3 A, compare CD24 + anti-CD24 and CD24 + anti-L1 with CD24 and PLL), whereas nonimmune IgG control antibodies had no effect (Fig.  3 A, compare CD24 + IgG with CD24), indicating that the L1 antibody binds to L1 at the cell surface of dorsal root ganglion neurons and masks it for binding to CD24 in trans-interaction.	bind
42889	6	11080	6	10	NULL	NULL	NULL	statement 5	Process		reduce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21656_s_135	11283023	A monoclonal antibody against CD24 and polyclonal antibodies against L1 were able to reduce or inhibit the negative influences on neurite outgrowth elicited by substrate-coated CD24 but not on poly-L-lysine (Fig.  3 A, compare CD24 + anti-CD24 and CD24 + anti-L1 with CD24 and PLL), whereas nonimmune IgG control antibodies had no effect (Fig.  3 A, compare CD24 + IgG with CD24), indicating that the L1 antibody binds to L1 at the cell surface of dorsal root ganglion neurons and masks it for binding to CD24 in trans-interaction.	bind
42890	7	11080	6	10	NULL	NULL	NULL	L1	GP		bind					CD24	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21656_s_135	11283023	A monoclonal antibody against CD24 and polyclonal antibodies against L1 were able to reduce or inhibit the negative influences on neurite outgrowth elicited by substrate-coated CD24 but not on poly-L-lysine (Fig.  3 A, compare CD24 + anti-CD24 and CD24 + anti-L1 with CD24 and PLL), whereas nonimmune IgG control antibodies had no effect (Fig.  3 A, compare CD24 + IgG with CD24), indicating that the L1 antibody binds to L1 at the cell surface of dorsal root ganglion neurons and masks it for binding to CD24 in trans-interaction.	bind
42891	8	11080	6	10	NULL	NULL	NULL	statement 2	Process		masks					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21656_s_135	11283023	A monoclonal antibody against CD24 and polyclonal antibodies against L1 were able to reduce or inhibit the negative influences on neurite outgrowth elicited by substrate-coated CD24 but not on poly-L-lysine (Fig.  3 A, compare CD24 + anti-CD24 and CD24 + anti-L1 with CD24 and PLL), whereas nonimmune IgG control antibodies had no effect (Fig.  3 A, compare CD24 + IgG with CD24), indicating that the L1 antibody binds to L1 at the cell surface of dorsal root ganglion neurons and masks it for binding to CD24 in trans-interaction.	bind
49287	1	11080	7	10	NULL	NULL	NULL	L1 antibody	GP		bind					L1	GP				NULL	cell surface of dorsal root ganglion neurons	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21656_s_135	11283023	A monoclonal antibody against CD24 and polyclonal antibodies against L1 were able to reduce or inhibit the negative influences on neurite outgrowth elicited by substrate-coated CD24 but not on poly-L-lysine (Fig.  3 A, compare CD24 + anti-CD24 and CD24 + anti-L1 with CD24 and PLL), whereas nonimmune IgG control antibodies had no effect (Fig.  3 A, compare CD24 + IgG with CD24), indicating that the L1 antibody binds to L1 at the cell surface of dorsal root ganglion neurons and masks it for binding to CD24 in trans-interaction.	bind
49288	2	11080	7	10	NULL	NULL	NULL	L1	GP		bind					CD24	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21656_s_135	11283023	A monoclonal antibody against CD24 and polyclonal antibodies against L1 were able to reduce or inhibit the negative influences on neurite outgrowth elicited by substrate-coated CD24 but not on poly-L-lysine (Fig.  3 A, compare CD24 + anti-CD24 and CD24 + anti-L1 with CD24 and PLL), whereas nonimmune IgG control antibodies had no effect (Fig.  3 A, compare CD24 + IgG with CD24), indicating that the L1 antibody binds to L1 at the cell surface of dorsal root ganglion neurons and masks it for binding to CD24 in trans-interaction.	bind
49289	3	11080	7	10	NULL	NULL	NULL	statement 1	Process		masks					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21656_s_135	11283023	A monoclonal antibody against CD24 and polyclonal antibodies against L1 were able to reduce or inhibit the negative influences on neurite outgrowth elicited by substrate-coated CD24 but not on poly-L-lysine (Fig.  3 A, compare CD24 + anti-CD24 and CD24 + anti-L1 with CD24 and PLL), whereas nonimmune IgG control antibodies had no effect (Fig.  3 A, compare CD24 + IgG with CD24), indicating that the L1 antibody binds to L1 at the cell surface of dorsal root ganglion neurons and masks it for binding to CD24 in trans-interaction.	bind
49290	4	11080	7	10	NULL	NULL	NULL	statement 2	Process		occurs in					trans-interaction	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_24_21656_s_135	11283023	A monoclonal antibody against CD24 and polyclonal antibodies against L1 were able to reduce or inhibit the negative influences on neurite outgrowth elicited by substrate-coated CD24 but not on poly-L-lysine (Fig.  3 A, compare CD24 + anti-CD24 and CD24 + anti-L1 with CD24 and PLL), whereas nonimmune IgG control antibodies had no effect (Fig.  3 A, compare CD24 + IgG with CD24), indicating that the L1 antibody binds to L1 at the cell surface of dorsal root ganglion neurons and masks it for binding to CD24 in trans-interaction.	bind
42892	1	11081	6	10	NULL	NULL	NULL	monoclonal antibody	GP		is directed against					GAF 	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_22_3_469_s_6	12554648	A monoclonal antibody directed against GAF A blocked cGMP binding, prevented  PDE5 activation and decreased basal activity, revealing that PDE5 in its non-activated  state has low intrinsic catalytic activity.	bind
42893	2	11081	6	10	NULL	NULL	NULL	statement 1	Process		blocks					cGMP	Chemical	binding of 			NULL		NULL	NULL	NULL	NULL	gw70_embo_22_3_469_s_6	12554648	A monoclonal antibody directed against GAF A blocked cGMP binding, prevented  PDE5 activation and decreased basal activity, revealing that PDE5 in its non-activated  state has low intrinsic catalytic activity.	bind
42894	3	11081	6	10	NULL	NULL	NULL	statement 1	Process		prevents					PDE5	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_embo_22_3_469_s_6	12554648	A monoclonal antibody directed against GAF A blocked cGMP binding, prevented  PDE5 activation and decreased basal activity, revealing that PDE5 in its non-activated  state has low intrinsic catalytic activity.	bind
42895	4	11081	6	10	NULL	NULL	NULL	PDE5	GP	non-activated	possess					catalytic activity	Process	low;; intrinsic			NULL		NULL	NULL	NULL	NULL	gw70_embo_22_3_469_s_6	12554648	A monoclonal antibody directed against GAF A blocked cGMP binding, prevented  PDE5 activation and decreased basal activity, revealing that PDE5 in its non-activated  state has low intrinsic catalytic activity.	bind
49291	1	11081	7	10	NULL	NULL	NULL	GAF A monoclonal antibody	GP		blocks					cGMP	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw70_embo_22_3_469_s_6	12554648	A monoclonal antibody directed against GAF A blocked cGMP binding, prevented  PDE5 activation and decreased basal activity, revealing that PDE5 in its non-activated  state has low intrinsic catalytic activity.	bind
49292	2	11081	7	10	NULL	NULL	NULL	GAF A monoclonal antibody	GP		prevents					PDE5	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_embo_22_3_469_s_6	12554648	A monoclonal antibody directed against GAF A blocked cGMP binding, prevented  PDE5 activation and decreased basal activity, revealing that PDE5 in its non-activated  state has low intrinsic catalytic activity.	bind
49294	3	11081	7	10	NULL	NULL	NULL	PDE5	GP	 non-activated	possess 					catalytic activity	Process	low;;intrinsic 			NULL		NULL	NULL	NULL	NULL	gw70_embo_22_3_469_s_6	12554648	A monoclonal antibody directed against GAF A blocked cGMP binding, prevented  PDE5 activation and decreased basal activity, revealing that PDE5 in its non-activated  state has low intrinsic catalytic activity.	bind
42670	1	11083	6	10	NULL	NULL	NULL	uPA	GP	human	bind					uPAR	GP	human			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol_277_3-pt-1_10484465_s_6	10484465	A monoclonal antibody that blocks  the binding of human uPA to human uPAR suppressed fibrin degradation by  human cells expressing human uPA but not murine uPA.	bind
42671	2	11083	6	10	NULL	NULL	NULL	cells	Cell	human	express					uPA	GP	human			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol_277_3-pt-1_10484465_s_6	10484465	A monoclonal antibody that blocks  the binding of human uPA to human uPAR suppressed fibrin degradation by  human cells expressing human uPA but not murine uPA.	bind
42672	3	11083	6	10	NULL	NULL	NULL	statement 2	Process		degrades					fibrin	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol_277_3-pt-1_10484465_s_6	10484465	A monoclonal antibody that blocks  the binding of human uPA to human uPAR suppressed fibrin degradation by  human cells expressing human uPA but not murine uPA.	bind
57867	4	11083	6	10	NULL	NULL	NULL	cells	Cell	human	express					uPA	GP	murine			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol_277_3-pt-1_10484465_s_6	10484465	A monoclonal antibody that blocks  the binding of human uPA to human uPAR suppressed fibrin degradation by  human cells expressing human uPA but not murine uPA.	bind
57868	5	11083	6	10	NULL	NULL	NULL	statement 4	Process		degrades					fibrin	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol_277_3-pt-1_10484465_s_6	10484465	A monoclonal antibody that blocks  the binding of human uPA to human uPAR suppressed fibrin degradation by  human cells expressing human uPA but not murine uPA.	bind
57869	6	11083	6	10	NULL	NULL	NULL	monoclonal antibody	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol_277_3-pt-1_10484465_s_6	10484465	A monoclonal antibody that blocks  the binding of human uPA to human uPAR suppressed fibrin degradation by  human cells expressing human uPA but not murine uPA.	bind
57870	7	11083	6	10	NULL	NULL	NULL	monoclonal antibody	GP		supress					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol_277_3-pt-1_10484465_s_6	10484465	A monoclonal antibody that blocks  the binding of human uPA to human uPAR suppressed fibrin degradation by  human cells expressing human uPA but not murine uPA.	bind
57871	8	11083	6	10	NULL	NULL	NULL	monoclonal antibody	GP		does not supress					statement 5	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol_277_3-pt-1_10484465_s_6	10484465	A monoclonal antibody that blocks  the binding of human uPA to human uPAR suppressed fibrin degradation by  human cells expressing human uPA but not murine uPA.	bind
49295	1	11083	7	10	NULL	NULL	NULL	 uPA 	GP	human	bind					uPAR	GP	human			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol_277_3-pt-1_10484465_s_6	10484465	A monoclonal antibody that blocks  the binding of human uPA to human uPAR suppressed fibrin degradation by  human cells expressing human uPA but not murine uPA.	bind
49296	2	11083	7	10	NULL	NULL	NULL	monoclonal antibody	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol_277_3-pt-1_10484465_s_6	10484465	A monoclonal antibody that blocks  the binding of human uPA to human uPAR suppressed fibrin degradation by  human cells expressing human uPA but not murine uPA.	bind
49297	3	11083	7	10	NULL	NULL	NULL	cells	Cell	human	express					uPA	GP	human			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol_277_3-pt-1_10484465_s_6	10484465	A monoclonal antibody that blocks  the binding of human uPA to human uPAR suppressed fibrin degradation by  human cells expressing human uPA but not murine uPA.	bind
49298	4	11083	7	10	NULL	NULL	NULL	cells	Cell	human	express					uPA	GP	murine			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol_277_3-pt-1_10484465_s_6	10484465	A monoclonal antibody that blocks  the binding of human uPA to human uPAR suppressed fibrin degradation by  human cells expressing human uPA but not murine uPA.	bind
49299	5	11083	7	10	NULL	NULL	NULL	statement 3	Process		degrades					fibrin	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol_277_3-pt-1_10484465_s_6	10484465	A monoclonal antibody that blocks  the binding of human uPA to human uPAR suppressed fibrin degradation by  human cells expressing human uPA but not murine uPA.	bind
49300	6	11083	7	10	NULL	NULL	NULL	statement 4	Process		degrades					fibrin	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol_277_3-pt-1_10484465_s_6	10484465	A monoclonal antibody that blocks  the binding of human uPA to human uPAR suppressed fibrin degradation by  human cells expressing human uPA but not murine uPA.	bind
49301	7	11083	7	10	NULL	NULL	NULL	monoclonal antibody	GP		suppress					statement 5	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol_277_3-pt-1_10484465_s_6	10484465	A monoclonal antibody that blocks  the binding of human uPA to human uPAR suppressed fibrin degradation by  human cells expressing human uPA but not murine uPA.	bind
49302	8	11083	7	10	NULL	NULL	NULL	monoclonal antibody	GP		does not suppress					statement 6	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol_277_3-pt-1_10484465_s_6	10484465	A monoclonal antibody that blocks  the binding of human uPA to human uPAR suppressed fibrin degradation by  human cells expressing human uPA but not murine uPA.	bind
42673	1	11084	6	10	NULL	NULL	NULL	MCP-1	GP		bind					CCR2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_9_858_s_198	15514167	A monoclonal antibody that blocks the binding of MCP-1 to CCR2 is being used in phase II trials for rheumatoid arthritis, and CCR5 antagonists that block HIV entry into cells are being used in advanced clinical trials as adjuvant treatments for AIDS.	bind
42681	2	11084	6	10	NULL	NULL	NULL	HIV	Organism		enters into					cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_9_858_s_198	15514167	A monoclonal antibody that blocks the binding of MCP-1 to CCR2 is being used in phase II trials for rheumatoid arthritis, and CCR5 antagonists that block HIV entry into cells are being used in advanced clinical trials as adjuvant treatments for AIDS.	bind
42682	3	11084	6	10	NULL	NULL	NULL	CCR5 antagonist	Chemical		blocks					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_9_858_s_198	15514167	A monoclonal antibody that blocks the binding of MCP-1 to CCR2 is being used in phase II trials for rheumatoid arthritis, and CCR5 antagonists that block HIV entry into cells are being used in advanced clinical trials as adjuvant treatments for AIDS.	bind
49303	1	11084	7	10	NULL	NULL	NULL	MCP-1 	GP		bind					CCR2	GP				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_9_858_s_198	15514167	A monoclonal antibody that blocks the binding of MCP-1 to CCR2 is being used in phase II trials for rheumatoid arthritis, and CCR5 antagonists that block HIV entry into cells are being used in advanced clinical trials as adjuvant treatments for AIDS.	bind
49304	2	11084	7	10	NULL	NULL	NULL	monoclonal antibody	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_9_858_s_198	15514167	A monoclonal antibody that blocks the binding of MCP-1 to CCR2 is being used in phase II trials for rheumatoid arthritis, and CCR5 antagonists that block HIV entry into cells are being used in advanced clinical trials as adjuvant treatments for AIDS.	bind
49305	3	11084	7	10	NULL	NULL	NULL	HIV	Organism		enter into					cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_9_858_s_198	15514167	A monoclonal antibody that blocks the binding of MCP-1 to CCR2 is being used in phase II trials for rheumatoid arthritis, and CCR5 antagonists that block HIV entry into cells are being used in advanced clinical trials as adjuvant treatments for AIDS.	bind
49306	4	11084	7	10	NULL	NULL	NULL	CCR5 antagonists	Chemical		block					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_9_858_s_198	15514167	A monoclonal antibody that blocks the binding of MCP-1 to CCR2 is being used in phase II trials for rheumatoid arthritis, and CCR5 antagonists that block HIV entry into cells are being used in advanced clinical trials as adjuvant treatments for AIDS.	bind
42683	1	11086	6	10	NULL	NULL	NULL	sperm	Cell	human	bind					oolemma	CellComponent	hamster			NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_795_s_308	12193387	A monoclonal antibody to human SP-10 inhibits in vitro the binding of human sperm to hamster oolemma but not to human zona pellucida.	bind
42684	2	11086	6	10	NULL	NULL	NULL	sperm	Cell	human	bind					zona pellucida	CellComponent	human			NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_795_s_308	12193387	A monoclonal antibody to human SP-10 inhibits in vitro the binding of human sperm to hamster oolemma but not to human zona pellucida.	bind
50281	3	11086	6	10	NULL	NULL	NULL	monoclonal antibody to SP-10	GP	human	inhibit					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_795_s_308	12193387	A monoclonal antibody to human SP-10 inhibits in vitro the binding of human sperm to hamster oolemma but not to human zona pellucida.	bind
50282	4	11086	6	10	NULL	NULL	NULL	monoclonal antibody to SP-10	GP	human	does not inhibit					statement 2	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_795_s_308	12193387	A monoclonal antibody to human SP-10 inhibits in vitro the binding of human sperm to hamster oolemma but not to human zona pellucida.	bind
49309	1	11086	7	10	NULL	NULL	NULL	sperm 	Cell	human	bind					oolemma	CellComponent	hamster			NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_795_s_308	12193387	A monoclonal antibody to human SP-10 inhibits in vitro the binding of human sperm to hamster oolemma but not to human zona pellucida.	bind
49310	2	11086	7	10	NULL	NULL	NULL	sperm	Cell	human	bind					zona pellucida	CellComponent	human			NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_795_s_308	12193387	A monoclonal antibody to human SP-10 inhibits in vitro the binding of human sperm to hamster oolemma but not to human zona pellucida.	bind
49311	3	11086	7	10	NULL	NULL	NULL	monoclonal antibody to SP-10	GP	human	inhibit					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_795_s_308	12193387	A monoclonal antibody to human SP-10 inhibits in vitro the binding of human sperm to hamster oolemma but not to human zona pellucida.	bind
49312	4	11086	7	10	NULL	NULL	NULL	monoclonal antibody to SP-10	GP	human	does not inhibit					statement 2	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_biolreprod_67_3_795_s_308	12193387	A monoclonal antibody to human SP-10 inhibits in vitro the binding of human sperm to hamster oolemma but not to human zona pellucida.	bind
42686	1	11088	6	10	NULL	NULL	NULL	CDK2	GP		bind					GST:SNR1	GP				NULL		NULL	NULL	NULL	NULL	gw70_genetics_168_1_199_s_209	15454538	A monoclonal antibody to the MYC epitope identified CDK2 bound to the GST:SNR1 fusion, but not GST alone.	bind
57872	2	11088	6	10	NULL	NULL	NULL	GST:SNR1	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_genetics_168_1_199_s_209	15454538	A monoclonal antibody to the MYC epitope identified CDK2 bound to the GST:SNR1 fusion, but not GST alone.	bind
49314	1	11088	7	10	NULL	NULL	NULL	 CDK2	GP		bind					GST:SNR1	GP				NULL		NULL	NULL	NULL	NULL	gw70_genetics_168_1_199_s_209	15454538	A monoclonal antibody to the MYC epitope identified CDK2 bound to the GST:SNR1 fusion, but not GST alone.	bind
57873	2	11088	7	10	NULL	NULL	NULL	GST:SNR1	GP		is a type of					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_genetics_168_1_199_s_209	15454538	A monoclonal antibody to the MYC epitope identified CDK2 bound to the GST:SNR1 fusion, but not GST alone.	bind
42687	1	11089	6	10	NULL	NULL	NULL	LPS	Chemical		bind					CD14	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_95	9784544	A monoclonal antibody, 26iC (10 mug/ml), which recognizes CD14 but does not block LPS binding to CD14, was used as a control.	bind
42688	2	11089	6	10	NULL	NULL	NULL	26iC	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_95	9784544	A monoclonal antibody, 26iC (10 mug/ml), which recognizes CD14 but does not block LPS binding to CD14, was used as a control.	bind
42689	3	11089	6	10	NULL	NULL	NULL	26iC	GP		recognizes					CD14	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_95	9784544	A monoclonal antibody, 26iC (10 mug/ml), which recognizes CD14 but does not block LPS binding to CD14, was used as a control.	bind
42690	4	11089	6	10	NULL	NULL	NULL	26iC	GP		does not block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_95	9784544	A monoclonal antibody, 26iC (10 mug/ml), which recognizes CD14 but does not block LPS binding to CD14, was used as a control.	bind
49317	1	11089	7	10	NULL	NULL	NULL	LPS	Chemical		bind					CD14	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_95	9784544	A monoclonal antibody, 26iC (10 mug/ml), which recognizes CD14 but does not block LPS binding to CD14, was used as a control.	bind
49318	2	11089	7	10	NULL	NULL	NULL	 26iC	GP		recognizes					CD14	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_95	9784544	A monoclonal antibody, 26iC (10 mug/ml), which recognizes CD14 but does not block LPS binding to CD14, was used as a control.	bind
49319	3	11089	7	10	NULL	NULL	NULL	 26iC	GP		does not block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_95	9784544	A monoclonal antibody, 26iC (10 mug/ml), which recognizes CD14 but does not block LPS binding to CD14, was used as a control.	bind
49320	4	11089	7	10	NULL	NULL	NULL	 26iC	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_11_5357_s_95	9784544	A monoclonal antibody, 26iC (10 mug/ml), which recognizes CD14 but does not block LPS binding to CD14, was used as a control.	bind
42691	1	11090	6	10	NULL	NULL	NULL	APC	GP		bind					EPCR	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_j-invest-dermatol_125_6_16354200_s_8	16354200	A monoclonal antibody, RCR252, which blocks APC binding  to EPCR, or a blocking antibody to PAR-1, abolished APC's effects on keratinocytes.	bind
42692	2	11090	6	10	NULL	NULL	NULL	RCR252	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_j-invest-dermatol_125_6_16354200_s_8	16354200	A monoclonal antibody, RCR252, which blocks APC binding  to EPCR, or a blocking antibody to PAR-1, abolished APC's effects on keratinocytes.	bind
42693	3	11090	6	10	NULL	NULL	NULL	RCR252	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_j-invest-dermatol_125_6_16354200_s_8	16354200	A monoclonal antibody, RCR252, which blocks APC binding  to EPCR, or a blocking antibody to PAR-1, abolished APC's effects on keratinocytes.	bind
42694	4	11090	6	10	NULL	NULL	NULL	APC	GP		effects					keratinocytes	Cell				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_j-invest-dermatol_125_6_16354200_s_8	16354200	A monoclonal antibody, RCR252, which blocks APC binding  to EPCR, or a blocking antibody to PAR-1, abolished APC's effects on keratinocytes.	bind
42695	5	11090	6	10	NULL	NULL	NULL	blocking antibody to PAR-1	GP		abolishes					statement 4	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_j-invest-dermatol_125_6_16354200_s_8	16354200	A monoclonal antibody, RCR252, which blocks APC binding  to EPCR, or a blocking antibody to PAR-1, abolished APC's effects on keratinocytes.	bind
49321	1	11090	7	10	NULL	NULL	NULL	APC	GP		bind					EPCR	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_j-invest-dermatol_125_6_16354200_s_8	16354200	A monoclonal antibody, RCR252, which blocks APC binding  to EPCR, or a blocking antibody to PAR-1, abolished APC's effects on keratinocytes.	bind
49322	2	11090	7	10	NULL	NULL	NULL	RCR252	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_j-invest-dermatol_125_6_16354200_s_8	16354200	A monoclonal antibody, RCR252, which blocks APC binding  to EPCR, or a blocking antibody to PAR-1, abolished APC's effects on keratinocytes.	bind
49323	3	11090	7	10	NULL	NULL	NULL	PAR-1 blocking antibody	GP		abolishes					APCs	GP	effect of			NULL	keratinocytes	NULL	NULL	NULL	NULL	abs-batch0550-0559_j-invest-dermatol_125_6_16354200_s_8	16354200	A monoclonal antibody, RCR252, which blocks APC binding  to EPCR, or a blocking antibody to PAR-1, abolished APC's effects on keratinocytes.	bind
49324	4	11090	7	10	NULL	NULL	NULL	RCR252	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_j-invest-dermatol_125_6_16354200_s_8	16354200	A monoclonal antibody, RCR252, which blocks APC binding  to EPCR, or a blocking antibody to PAR-1, abolished APC's effects on keratinocytes.	bind
42696	1	11091	6	10	NULL	NULL	NULL	TRA-8	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_cancer-gene-ther_13_2_16082379_s_4	16082379	A monoclonal antibody, TRA-8, specifically binds  to death receptor 5, one of two death receptors bound by tumor necrosis  factor-related apoptosis-inducing ligand (TRAIL).	bind
42697	2	11091	6	10	NULL	NULL	NULL	TRA-8	GP		bind		specifically			death receptor 5	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_cancer-gene-ther_13_2_16082379_s_4	16082379	A monoclonal antibody, TRA-8, specifically binds  to death receptor 5, one of two death receptors bound by tumor necrosis  factor-related apoptosis-inducing ligand (TRAIL).	bind
42698	3	11091	6	10	NULL	NULL	NULL	death receptor 5	GP		is a type of					death receptor	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_cancer-gene-ther_13_2_16082379_s_4	16082379	A monoclonal antibody, TRA-8, specifically binds  to death receptor 5, one of two death receptors bound by tumor necrosis  factor-related apoptosis-inducing ligand (TRAIL).	bind
42699	4	11091	6	10	NULL	NULL	NULL	death receptor 5	GP		bind					TRAIL	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_cancer-gene-ther_13_2_16082379_s_4	16082379	A monoclonal antibody, TRA-8, specifically binds  to death receptor 5, one of two death receptors bound by tumor necrosis  factor-related apoptosis-inducing ligand (TRAIL).	bind
42700	5	11091	6	10	NULL	NULL	NULL	TRAIL	GP		is					tumor necrosis factor-related apoptosis-inducing ligand	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_cancer-gene-ther_13_2_16082379_s_4	16082379	A monoclonal antibody, TRA-8, specifically binds  to death receptor 5, one of two death receptors bound by tumor necrosis  factor-related apoptosis-inducing ligand (TRAIL).	bind
49325	1	11091	7	10	NULL	NULL	NULL	TRA-8	GP		bind		specifically			death receptor 5	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_cancer-gene-ther_13_2_16082379_s_4	16082379	A monoclonal antibody, TRA-8, specifically binds  to death receptor 5, one of two death receptors bound by tumor necrosis  factor-related apoptosis-inducing ligand (TRAIL).	bind
49326	2	11091	7	10	NULL	NULL	NULL	TRAIL	GP		bind					death receptor 5	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_cancer-gene-ther_13_2_16082379_s_4	16082379	A monoclonal antibody, TRA-8, specifically binds  to death receptor 5, one of two death receptors bound by tumor necrosis  factor-related apoptosis-inducing ligand (TRAIL).	bind
49327	3	11091	7	10	NULL	NULL	NULL	TRA-8	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_cancer-gene-ther_13_2_16082379_s_4	16082379	A monoclonal antibody, TRA-8, specifically binds  to death receptor 5, one of two death receptors bound by tumor necrosis  factor-related apoptosis-inducing ligand (TRAIL).	bind
49328	4	11091	7	10	NULL	NULL	NULL	TRAIL	GP		is					tumor necrosis factor-related apoptosis-inducing ligand	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_cancer-gene-ther_13_2_16082379_s_4	16082379	A monoclonal antibody, TRA-8, specifically binds  to death receptor 5, one of two death receptors bound by tumor necrosis  factor-related apoptosis-inducing ligand (TRAIL).	bind
50283	5	11091	7	10	NULL	NULL	NULL	TRA-8	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_cancer-gene-ther_13_2_16082379_s_4	16082379	A monoclonal antibody, TRA-8, specifically binds  to death receptor 5, one of two death receptors bound by tumor necrosis  factor-related apoptosis-inducing ligand (TRAIL).	bind
42701	1	11092	6	10	NULL	NULL	NULL	nuclear proteins	GP	monocyte	bind					AP-2	GP	 Consensus Sequences			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_1_174_s_108	8995244	A Monocytic Nuclear Protein Binds to AP-2 Consensus Sequences	bind
49329	1	11092	7	10	NULL	NULL	NULL	Nuclear Protein	GP	Monocyte	bind					AP-2	GP	consensus sequence			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_1_174_s_108	8995244	A Monocytic Nuclear Protein Binds to AP-2 Consensus Sequences	bind
42702	1	11093	6	10	NULL	NULL	NULL	DnaA monomer	GP	E.coli	bind							stringent		DnaA box	NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiolrev_26_4_355_s_185	12413665	A monomer of  E. coli DnaA binds only to the stringent DnaA box.	bind
49339	1	11093	7	10	NULL	NULL	NULL	DnaA monomer	GP	E. coli	bind							stringent		DnaA box	NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiolrev_26_4_355_s_185	12413665	A monomer of  E. coli DnaA binds only to the stringent DnaA box.	bind
42780	1	11094	6	10	NULL	NULL	NULL	vancomysin monomer	GP		bind					disaccharide PG precursor	GP		dipeptidyl terminus		NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_5_511_s_376	12586393	A monomer of vancomycin binding the dipeptidyl  terminus of a disaccharide PG precursor (GlcNAc-MurNAc- -Ala- -Glu- -Lys- -Ala- -Ala) as it is delivered to the in vivo target site for transglycosylation by undecaprenyl  pyrophosphate (undecaprenol is depicted in red).	bind
42841	2	11094	6	10	NULL	NULL	NULL	disaccharide PG precursor	GP		is delivered to					target site					NULL	in vivo	NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_5_511_s_376	12586393	A monomer of vancomycin binding the dipeptidyl  terminus of a disaccharide PG precursor (GlcNAc-MurNAc- -Ala- -Glu- -Lys- -Ala- -Ala) as it is delivered to the in vivo target site for transglycosylation by undecaprenyl  pyrophosphate (undecaprenol is depicted in red).	bind
42842	3	11094	6	10	NULL	0	NULL	undecaprenyl pyrophosphate			catalyzes					disaccharide PG precursor		transglycosylation of 			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_5_511_s_376	12586393	A monomer of vancomycin binding the dipeptidyl  terminus of a disaccharide PG precursor (GlcNAc-MurNAc- -Ala- -Glu- -Lys- -Ala- -Ala) as it is delivered to the in vivo target site for transglycosylation by undecaprenyl  pyrophosphate (undecaprenol is depicted in red).	bind
42843	4	11094	6	10	NULL	NULL	NULL	statement 2	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_5_511_s_376	12586393	A monomer of vancomycin binding the dipeptidyl  terminus of a disaccharide PG precursor (GlcNAc-MurNAc- -Ala- -Glu- -Lys- -Ala- -Ala) as it is delivered to the in vivo target site for transglycosylation by undecaprenyl  pyrophosphate (undecaprenol is depicted in red).	bind
42844	5	11094	6	NULL	NULL	0	NULL	PG precursor	NULL		is	NULL				GlcNAc-MurNAc- -Ala- -Glu- -Lys- -Ala- -Ala	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_5_511_s_376	12586393	A monomer of vancomycin binding the dipeptidyl  terminus of a disaccharide PG precursor (GlcNAc-MurNAc- -Ala- -Glu- -Lys- -Ala- -Ala) as it is delivered to the in vivo target site for transglycosylation by undecaprenyl  pyrophosphate (undecaprenol is depicted in red).	bind
57874	6	11094	6	10	NULL	0	NULL	statement 1			leads to					statement 2					NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_5_511_s_376	12586393	A monomer of vancomycin binding the dipeptidyl  terminus of a disaccharide PG precursor (GlcNAc-MurNAc- -Ala- -Glu- -Lys- -Ala- -Ala) as it is delivered to the in vivo target site for transglycosylation by undecaprenyl  pyrophosphate (undecaprenol is depicted in red).	bind
49340	1	11094	7	NULL	NULL	0	NULL	vancomycin monomer	NULL		bind	NULL				disaccharide PG precursor	NULL		dipeptidyl terminus		NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_5_511_s_376	12586393	A monomer of vancomycin binding the dipeptidyl  terminus of a disaccharide PG precursor (GlcNAc-MurNAc- -Ala- -Glu- -Lys- -Ala- -Ala) as it is delivered to the in vivo target site for transglycosylation by undecaprenyl  pyrophosphate (undecaprenol is depicted in red).	bind
49341	2	11094	7	NULL	NULL	0	NULL	disaccharide PG precursor 	NULL		is	NULL				GlcNAc-MurNAc- -Ala- -Glu- -Lys- -Ala- -Ala	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_5_511_s_376	12586393	A monomer of vancomycin binding the dipeptidyl  terminus of a disaccharide PG precursor (GlcNAc-MurNAc- -Ala- -Glu- -Lys- -Ala- -Ala) as it is delivered to the in vivo target site for transglycosylation by undecaprenyl  pyrophosphate (undecaprenol is depicted in red).	bind
49342	3	11094	7	10	NULL	0	NULL	\tdisaccharide PG precursor			is delivered to					target site					NULL	in vivo	NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_5_511_s_376	12586393	A monomer of vancomycin binding the dipeptidyl  terminus of a disaccharide PG precursor (GlcNAc-MurNAc- -Ala- -Glu- -Lys- -Ala- -Ala) as it is delivered to the in vivo target site for transglycosylation by undecaprenyl  pyrophosphate (undecaprenol is depicted in red).	bind
49343	4	11094	7	10	NULL	0	NULL	undecaprenyl pyrophosphate			catalyzes					disaccharide PG precursor		transglycosylation of			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_5_511_s_376	12586393	A monomer of vancomycin binding the dipeptidyl  terminus of a disaccharide PG precursor (GlcNAc-MurNAc- -Ala- -Glu- -Lys- -Ala- -Ala) as it is delivered to the in vivo target site for transglycosylation by undecaprenyl  pyrophosphate (undecaprenol is depicted in red).	bind
49344	5	11094	7	10	NULL	0	NULL	statement 3			leads to					statement 4					NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_5_511_s_376	12586393	A monomer of vancomycin binding the dipeptidyl  terminus of a disaccharide PG precursor (GlcNAc-MurNAc- -Ala- -Glu- -Lys- -Ala- -Ala) as it is delivered to the in vivo target site for transglycosylation by undecaprenyl  pyrophosphate (undecaprenol is depicted in red).	bind
57875	6	11094	7	10	NULL	0	NULL	statement 1			leads to					statement 3					NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_5_511_s_376	12586393	A monomer of vancomycin binding the dipeptidyl  terminus of a disaccharide PG precursor (GlcNAc-MurNAc- -Ala- -Glu- -Lys- -Ala- -Ala) as it is delivered to the in vivo target site for transglycosylation by undecaprenyl  pyrophosphate (undecaprenol is depicted in red).	bind
42708	1	11096	6	10	NULL	NULL	NULL	Cu(I)	Chemical		bind					PDI	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_2_405_s_198	14592429	A mononuclear Cu(I) complex may either be linear (diagonal), trigonal, or tetragonal  coordinate; therefore in theory, the maximum Cu(I) bound to PDI is expected to be  2 mol/monomer.	bind
49345	1	11096	7	10	NULL	NULL	NULL	Cu(I)	Chemical		bind					PDI	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_2_405_s_198	14592429	A mononuclear Cu(I) complex may either be linear (diagonal), trigonal, or tetragonal  coordinate; therefore in theory, the maximum Cu(I) bound to PDI is expected to be  2 mol/monomer.	bind
42709	1	11097	6	10	NULL	NULL	NULL	ALG-2	GP		bind					annexin 7	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_22_20210_s_177	12601007	A more  recently identified ligand of annexin 11, namely the penta-EF-hand protein  ALG-2 (apoptosis-linked gene 2)  ( ) is expressed in the  nucleus ( ), though ALG-2  also binds annexin 7, peflin, and AIP1/Alix  ( ,   ).	bind
42710	2	11097	6	10	NULL	NULL	NULL	ALG-2	GP		bind					peflin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_22_20210_s_177	12601007	A more  recently identified ligand of annexin 11, namely the penta-EF-hand protein  ALG-2 (apoptosis-linked gene 2)  ( ) is expressed in the  nucleus ( ), though ALG-2  also binds annexin 7, peflin, and AIP1/Alix  ( ,   ).	bind
42711	3	11097	6	10	NULL	NULL	NULL	ALG-2	GP		bind					AIP1/Alix	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_22_20210_s_177	12601007	A more  recently identified ligand of annexin 11, namely the penta-EF-hand protein  ALG-2 (apoptosis-linked gene 2)  ( ) is expressed in the  nucleus ( ), though ALG-2  also binds annexin 7, peflin, and AIP1/Alix  ( ,   ).	bind
42712	4	11097	6	10	NULL	NULL	NULL	ALG-2	GP		is					apoptosis-linked gene 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_22_20210_s_177	12601007	A more  recently identified ligand of annexin 11, namely the penta-EF-hand protein  ALG-2 (apoptosis-linked gene 2)  ( ) is expressed in the  nucleus ( ), though ALG-2  also binds annexin 7, peflin, and AIP1/Alix  ( ,   ).	bind
42713	5	11097	6	10	NULL	NULL	NULL	ALG-2	GP		is expressed in					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_22_20210_s_177	12601007	A more  recently identified ligand of annexin 11, namely the penta-EF-hand protein  ALG-2 (apoptosis-linked gene 2)  ( ) is expressed in the  nucleus ( ), though ALG-2  also binds annexin 7, peflin, and AIP1/Alix  ( ,   ).	bind
42714	6	11097	6	10	NULL	NULL	NULL	ALG-2	GP		is a type of					penta-EF-hand protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_22_20210_s_177	12601007	A more  recently identified ligand of annexin 11, namely the penta-EF-hand protein  ALG-2 (apoptosis-linked gene 2)  ( ) is expressed in the  nucleus ( ), though ALG-2  also binds annexin 7, peflin, and AIP1/Alix  ( ,   ).	bind
42715	7	11097	6	10	NULL	NULL	NULL	ALG-2	GP		is ligand of					annexin 11	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_22_20210_s_177	12601007	A more  recently identified ligand of annexin 11, namely the penta-EF-hand protein  ALG-2 (apoptosis-linked gene 2)  ( ) is expressed in the  nucleus ( ), though ALG-2  also binds annexin 7, peflin, and AIP1/Alix  ( ,   ).	bind
49352	1	11097	7	10	NULL	NULL	NULL	ALG-2	GP		bind					annexin 11	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_22_20210_s_177	12601007	A more  recently identified ligand of annexin 11, namely the penta-EF-hand protein  ALG-2 (apoptosis-linked gene 2)  ( ) is expressed in the  nucleus ( ), though ALG-2  also binds annexin 7, peflin, and AIP1/Alix  ( ,   ).	bind
49353	2	11097	7	10	NULL	NULL	NULL	ALG-2	GP		is expressed in					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_22_20210_s_177	12601007	A more  recently identified ligand of annexin 11, namely the penta-EF-hand protein  ALG-2 (apoptosis-linked gene 2)  ( ) is expressed in the  nucleus ( ), though ALG-2  also binds annexin 7, peflin, and AIP1/Alix  ( ,   ).	bind
49354	3	11097	7	10	NULL	NULL	NULL	ALG-2	GP		bind					annexin 7	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_22_20210_s_177	12601007	A more  recently identified ligand of annexin 11, namely the penta-EF-hand protein  ALG-2 (apoptosis-linked gene 2)  ( ) is expressed in the  nucleus ( ), though ALG-2  also binds annexin 7, peflin, and AIP1/Alix  ( ,   ).	bind
49355	4	11097	7	10	NULL	NULL	NULL	ALG-2	GP		bind					peflin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_22_20210_s_177	12601007	A more  recently identified ligand of annexin 11, namely the penta-EF-hand protein  ALG-2 (apoptosis-linked gene 2)  ( ) is expressed in the  nucleus ( ), though ALG-2  also binds annexin 7, peflin, and AIP1/Alix  ( ,   ).	bind
49356	5	11097	7	10	NULL	NULL	NULL	ALG-2	GP		bind					AIP1/Alix 	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_22_20210_s_177	12601007	A more  recently identified ligand of annexin 11, namely the penta-EF-hand protein  ALG-2 (apoptosis-linked gene 2)  ( ) is expressed in the  nucleus ( ), though ALG-2  also binds annexin 7, peflin, and AIP1/Alix  ( ,   ).	bind
49357	6	11097	7	10	NULL	NULL	NULL	ALG-2	GP		is					apoptosis-linked gene 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_22_20210_s_177	12601007	A more  recently identified ligand of annexin 11, namely the penta-EF-hand protein  ALG-2 (apoptosis-linked gene 2)  ( ) is expressed in the  nucleus ( ), though ALG-2  also binds annexin 7, peflin, and AIP1/Alix  ( ,   ).	bind
49358	7	11097	7	10	NULL	NULL	NULL	ALG-2	GP		is a type of					 penta-EF-hand protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_22_20210_s_177	12601007	A more  recently identified ligand of annexin 11, namely the penta-EF-hand protein  ALG-2 (apoptosis-linked gene 2)  ( ) is expressed in the  nucleus ( ), though ALG-2  also binds annexin 7, peflin, and AIP1/Alix  ( ,   ).	bind
42716	1	11098	6	10	NULL	NULL	NULL	CTD peptide	AminoAcid		bind								CTD-binding domain		NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_12_1401_s_41	15964991	A more compact beta-spiral, only 100  Ang  long, and assuming only one beta-turn per repeat, was suggested based on a crystal structure of a CTD peptide bound to a CTD-binding domain ("`compact spiral"`) ( Fig. 1; Meinhart and Cramer 2004 ).	bind
49359	1	11098	7	10	NULL	NULL	NULL	CTD peptide	AminoAcid		bind								CTD-binding domain		NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_12_1401_s_41	15964991	A more compact beta-spiral, only 100  Ang  long, and assuming only one beta-turn per repeat, was suggested based on a crystal structure of a CTD peptide bound to a CTD-binding domain ("`compact spiral"`) ( Fig. 1; Meinhart and Cramer 2004 ).	bind
42717	1	11099	6	10	NULL	NULL	NULL	TnI	GP		interacts with					TnC	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12765_s_137	12239350	A more complex scenario would have the binding of TnT propagating along the polypeptide chain and increasing the interaction between TnI and TnC.	bind
57876	2	11099	6	10	NULL	NULL	NULL	TnT	GP	binding of	propagate along					polypeptide chain	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12765_s_137	12239350	A more complex scenario would have the binding of TnT propagating along the polypeptide chain and increasing the interaction between TnI and TnC.	bind
57877	3	11099	6	10	NULL	NULL	NULL	statement 2	Process		increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12765_s_137	12239350	A more complex scenario would have the binding of TnT propagating along the polypeptide chain and increasing the interaction between TnI and TnC.	bind
49360	1	11099	7	10	NULL	NULL	NULL	TnI	GP		interact with					TnC	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12765_s_137	12239350	A more complex scenario would have the binding of TnT propagating along the polypeptide chain and increasing the interaction between TnI and TnC.	bind
49361	2	11099	7	10	NULL	NULL	NULL	TnT	GP	binding of	propogate along					polypeptide chain	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12765_s_137	12239350	A more complex scenario would have the binding of TnT propagating along the polypeptide chain and increasing the interaction between TnI and TnC.	bind
49362	3	11099	7	10	NULL	NULL	NULL	statement 2	Process		increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_20_12765_s_137	12239350	A more complex scenario would have the binding of TnT propagating along the polypeptide chain and increasing the interaction between TnI and TnC.	bind
42718	1	11100	6	10	NULL	NULL	NULL	Bem1p	GP		is a type of					scaffold protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_20_0_559_s_75	15473852	A more complicated genetic screen identified a third component, Bem1p, a scaffold  protein that binds Cdc24p and Cdc42p ( Bose et al. 2001, Peterson et al. 1994, Zheng et al. 1995).	bind
42719	2	11100	6	10	NULL	NULL	NULL	Bem1p	GP		bind					Cdc24p	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_20_0_559_s_75	15473852	A more complicated genetic screen identified a third component, Bem1p, a scaffold  protein that binds Cdc24p and Cdc42p ( Bose et al. 2001, Peterson et al. 1994, Zheng et al. 1995).	bind
42720	3	11100	6	10	NULL	NULL	NULL	Bem1p	GP		bind					Cdc42p	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_20_0_559_s_75	15473852	A more complicated genetic screen identified a third component, Bem1p, a scaffold  protein that binds Cdc24p and Cdc42p ( Bose et al. 2001, Peterson et al. 1994, Zheng et al. 1995).	bind
49363	1	11100	7	10	NULL	NULL	NULL	Bem1p	GP		bind					Cdc24p	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_20_0_559_s_75	15473852	A more complicated genetic screen identified a third component, Bem1p, a scaffold  protein that binds Cdc24p and Cdc42p ( Bose et al. 2001, Peterson et al. 1994, Zheng et al. 1995).	bind
49364	2	11100	7	10	NULL	NULL	NULL	Bem1p	GP		bind					Cdc42p	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_20_0_559_s_75	15473852	A more complicated genetic screen identified a third component, Bem1p, a scaffold  protein that binds Cdc24p and Cdc42p ( Bose et al. 2001, Peterson et al. 1994, Zheng et al. 1995).	bind
49365	3	11100	7	10	NULL	NULL	NULL	Bem1p	GP		is a type of					scaffold protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_20_0_559_s_75	15473852	A more complicated genetic screen identified a third component, Bem1p, a scaffold  protein that binds Cdc24p and Cdc42p ( Bose et al. 2001, Peterson et al. 1994, Zheng et al. 1995).	bind
42975	1	11101	6	10	NULL	NULL	NULL	estradiol	GP		bind					SHBG	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_34_25920_s_105	10859323	A more detailed analysis (Fig.  3) revealed that the inhibitory effect of zinc on estradiol binding to SHBG could be detected at 10 muM ZnCl2 and increases progressively with increasing ZnCl2 concentrations.	bind
42976	2	11101	6	10	NULL	NULL	NULL	Zinc 	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_34_25920_s_105	10859323	A more detailed analysis (Fig.  3) revealed that the inhibitory effect of zinc on estradiol binding to SHBG could be detected at 10 muM ZnCl2 and increases progressively with increasing ZnCl2 concentrations.	bind
49366	1	11101	7	10	NULL	NULL	NULL	estradiol	GP		bind					SHBG	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_34_25920_s_105	10859323	A more detailed analysis (Fig.  3) revealed that the inhibitory effect of zinc on estradiol binding to SHBG could be detected at 10 muM ZnCl2 and increases progressively with increasing ZnCl2 concentrations.	bind
49367	2	11101	7	10	NULL	NULL	NULL	 zinc	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_34_25920_s_105	10859323	A more detailed analysis (Fig.  3) revealed that the inhibitory effect of zinc on estradiol binding to SHBG could be detected at 10 muM ZnCl2 and increases progressively with increasing ZnCl2 concentrations.	bind
42977	1	11102	6	10	NULL	NULL	NULL	Plk1	GP		bind		physically			p53	GP				NULL	cultured cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_6_2093_s_343	16507989	A more detailed analysis of the Plk1/p53 connection showed that Plk1 physically binds to p53 in cultured cells.	bind
49368	1	11102	7	10	NULL	NULL	NULL	Plk1	GP		bind		physically			p53	GP				NULL	cultured cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_6_2093_s_343	16507989	A more detailed analysis of the Plk1/p53 connection showed that Plk1 physically binds to p53 in cultured cells.	bind
43176	1	11103	6	10	NULL	NULL	NULL				bind		specifically	ADF-H domain		F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_1_393_s_227	10637315	A more detailed analysis showed that even the smallest fragment tested in the C-terminal truncation series, the ADF-H domain alone, still bound to F-actin in a specific, saturable manner, although the affinity of binding was reduced compared with the larger fragments (Figure  2B, right panel).	bind
49369	1	11103	7	10	NULL	NULL	NULL				bind		specific	ADF-H domain		F-actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_1_393_s_227	10637315	A more detailed analysis showed that even the smallest fragment tested in the C-terminal truncation series, the ADF-H domain alone, still bound to F-actin in a specific, saturable manner, although the affinity of binding was reduced compared with the larger fragments (Figure  2B, right panel).	bind
42978	1	11104	6	10	NULL	NULL	NULL	F2	NucleicAcid		bind					chimeric TRalpha	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_14_9048_s_180	9083030	A more detailed analysis was carried out by determining the affinities in the binding of F2 to the chimeric TRalphas.	bind
49371	1	11104	7	10	NULL	NULL	NULL	F2 	NucleicAcid		bind					chimeric TRalphas	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_14_9048_s_180	9083030	A more detailed analysis was carried out by determining the affinities in the binding of F2 to the chimeric TRalphas.	bind
43341	1	11105	6	10	NULL	NULL	NULL	LSP1	GP	human	bind			COOH terminal half		F-actin filaments	CellComponent				NULL	intact cells	NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1642_1_17_s_163	12972289	A more detailed study on human LSP1 identified at least three and possibly four  specific regions in the COOH-terminal half of human LSP1 that each individually can  function as an F-actin binding site [ 12], suggesting that binding of LSP1 to the F-actin filaments in intact cells involves  three or four binding sites.	bind
49372	1	11105	7	10	NULL	NULL	NULL	LSP1	GP	human	bind			COOH-terminal half 		F-actin filaments	CellComponent				NULL	intact cells	NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1642_1_17_s_163	12972289	A more detailed study on human LSP1 identified at least three and possibly four  specific regions in the COOH-terminal half of human LSP1 that each individually can  function as an F-actin binding site [ 12], suggesting that binding of LSP1 to the F-actin filaments in intact cells involves  three or four binding sites.	bind
42979	1	11107	6	10	NULL	NULL	NULL	Sir4	GP		stimulates					Sir2	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_16_6931_s_474	15282295	A more detailed understanding of the mechanism of Sir2 activity stimulation by Sir4 and Net1 binding will require a study of the structure of the entire Sir2 protein, both without ligands and in complex with its binding partners.	bind
42980	2	11107	6	10	NULL	NULL	NULL	Net1	GP	binding of	stimulates					Sir2	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_16_6931_s_474	15282295	A more detailed understanding of the mechanism of Sir2 activity stimulation by Sir4 and Net1 binding will require a study of the structure of the entire Sir2 protein, both without ligands and in complex with its binding partners.	bind
49375	1	11107	7	10	NULL	NULL	NULL	Sir4	GP		stimulate					Sir2	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_16_6931_s_474	15282295	A more detailed understanding of the mechanism of Sir2 activity stimulation by Sir4 and Net1 binding will require a study of the structure of the entire Sir2 protein, both without ligands and in complex with its binding partners.	bind
50284	2	11107	7	10	NULL	NULL	NULL	Net1	GP	binding of	stimulates					Sir2	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_16_6931_s_474	15282295	A more detailed understanding of the mechanism of Sir2 activity stimulation by Sir4 and Net1 binding will require a study of the structure of the entire Sir2 protein, both without ligands and in complex with its binding partners.	bind
42981	1	11108	6	10	NULL	NULL	NULL	7S NGF	GP		bind					NGF receptor	GP				NULL	embryonic chicken sensory ganglia	NULL	NULL	NULL	NULL	gw60_annrevneur_24_0_601_s_167	11283322	A more direct approach measured the binding of 7S NGF to the two specific NGF receptors that had just been identified on embryonic chicken sensory ganglia ( Sutter et al 1979).	bind
49376	1	11108	7	10	NULL	NULL	NULL	7S NGF	GP		bind					NGF receptors	GP				NULL	embryonic chicken sensory ganglia	NULL	NULL	NULL	NULL	gw60_annrevneur_24_0_601_s_167	11283322	A more direct approach measured the binding of 7S NGF to the two specific NGF receptors that had just been identified on embryonic chicken sensory ganglia ( Sutter et al 1979).	bind
43344	1	11110	6	10	NULL	NULL	NULL	mu			bind					DG	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24743_s_25	11328812	A more distantly related group of mu, nu, and PKD-2 isoforms binds DG but is Ca2+-insensitive and may or may not translocate depending on cell type ( 5-7).	bind
43345	2	11110	6	10	NULL	NULL	NULL	nu			bind					DG	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24743_s_25	11328812	A more distantly related group of mu, nu, and PKD-2 isoforms binds DG but is Ca2+-insensitive and may or may not translocate depending on cell type ( 5-7).	bind
43346	3	11110	6	10	NULL	NULL	NULL	PKD-2 isoforms	GP		bind					DG	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24743_s_25	11328812	A more distantly related group of mu, nu, and PKD-2 isoforms binds DG but is Ca2+-insensitive and may or may not translocate depending on cell type ( 5-7).	bind
57878	4	11110	6	10	NULL	NULL	NULL	statement 1	Process		is insensitive to					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24743_s_25	11328812	A more distantly related group of mu, nu, and PKD-2 isoforms binds DG but is Ca2+-insensitive and may or may not translocate depending on cell type ( 5-7).	bind
57879	5	11110	6	10	NULL	NULL	NULL	statement 2	Process		is insensitive to					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24743_s_25	11328812	A more distantly related group of mu, nu, and PKD-2 isoforms binds DG but is Ca2+-insensitive and may or may not translocate depending on cell type ( 5-7).	bind
57880	6	11110	6	10	NULL	NULL	NULL	statement 3	Process		is insensitive to					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24743_s_25	11328812	A more distantly related group of mu, nu, and PKD-2 isoforms binds DG but is Ca2+-insensitive and may or may not translocate depending on cell type ( 5-7).	bind
49377	1	11110	7	10	NULL	NULL	NULL	 mu			bind					DG	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24743_s_25	11328812	A more distantly related group of mu, nu, and PKD-2 isoforms binds DG but is Ca2+-insensitive and may or may not translocate depending on cell type ( 5-7).	bind
49378	2	11110	7	10	NULL	NULL	NULL	nu			bind					DG	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24743_s_25	11328812	A more distantly related group of mu, nu, and PKD-2 isoforms binds DG but is Ca2+-insensitive and may or may not translocate depending on cell type ( 5-7).	bind
49379	3	11110	7	10	NULL	NULL	NULL	PKD-2 isoforms	GP		bind					DG	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24743_s_25	11328812	A more distantly related group of mu, nu, and PKD-2 isoforms binds DG but is Ca2+-insensitive and may or may not translocate depending on cell type ( 5-7).	bind
49380	4	11110	7	10	NULL	NULL	NULL	statement 1	Process		is insensitive to					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24743_s_25	11328812	A more distantly related group of mu, nu, and PKD-2 isoforms binds DG but is Ca2+-insensitive and may or may not translocate depending on cell type ( 5-7).	bind
49381	5	11110	7	10	NULL	NULL	NULL	statement 2	Process		is insensitive to					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24743_s_25	11328812	A more distantly related group of mu, nu, and PKD-2 isoforms binds DG but is Ca2+-insensitive and may or may not translocate depending on cell type ( 5-7).	bind
49382	6	11110	7	10	NULL	NULL	NULL	statement 3	Process		is insensitive to					Ca2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_27_24743_s_25	11328812	A more distantly related group of mu, nu, and PKD-2 isoforms binds DG but is Ca2+-insensitive and may or may not translocate depending on cell type ( 5-7).	bind
43349	1	11111	6	10	NULL	NULL	NULL	mel-11	GP	worm	is homologous to					MYPT1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_40_37250_s_219	11486008	A more distantly related MYPT1 homologue termed  mel-11 is present in the worm and shares 35% amino acid identity with the higher vertebrate form ( 5,  28,  34,  41).	bind
49386	1	11111	7	10	NULL	NULL	NULL	mel-11	GP	worm	is homologous to					 MYPT1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_40_37250_s_219	11486008	A more distantly related MYPT1 homologue termed  mel-11 is present in the worm and shares 35% amino acid identity with the higher vertebrate form ( 5,  28,  34,  41).	bind
43352	1	11112	6	10	NULL	NULL	NULL	p120ctn	GP		bind					cadherin	GP		juxtamembrane site within the cytoplasmic domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_3_519_s_21	9971746	A more distantly related protein, p120ctn, also  contains a series of Arm repeats and binds to cadherin (Reynolds et al., 1992  , 1994  ; Shibamoto et al., 1995  ; Staddon et al., 1995  ) at a juxtamembrane site within the cytoplasmic domain of cadherin rather than the more distal  site where beta- and gamma-catenin bind (Ozawa and Kemler,  1998  ; Yap et al., 1998  ). p120ctn does not bind to alpha-catenin  (Daniel and Reynolds, 1995  ) and in nontransformed cells,  only small amounts bind to cadherin (Shibamoto et al.,  1995  ). .	bind
43356	2	11112	6	10	NULL	NULL	NULL	p120ctn	GP		contains								arm repeats		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_3_519_s_21	9971746	A more distantly related protein, p120ctn, also  contains a series of Arm repeats and binds to cadherin (Reynolds et al., 1992  , 1994  ; Shibamoto et al., 1995  ; Staddon et al., 1995  ) at a juxtamembrane site within the cytoplasmic domain of cadherin rather than the more distal  site where beta- and gamma-catenin bind (Ozawa and Kemler,  1998  ; Yap et al., 1998  ). p120ctn does not bind to alpha-catenin  (Daniel and Reynolds, 1995  ) and in nontransformed cells,  only small amounts bind to cadherin (Shibamoto et al.,  1995  ). .	bind
43359	3	11112	6	10	NULL	NULL	NULL	beta-catenin	GP		bind					cadherin	GP		distal site		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_3_519_s_21	9971746	A more distantly related protein, p120ctn, also  contains a series of Arm repeats and binds to cadherin (Reynolds et al., 1992  , 1994  ; Shibamoto et al., 1995  ; Staddon et al., 1995  ) at a juxtamembrane site within the cytoplasmic domain of cadherin rather than the more distal  site where beta- and gamma-catenin bind (Ozawa and Kemler,  1998  ; Yap et al., 1998  ). p120ctn does not bind to alpha-catenin  (Daniel and Reynolds, 1995  ) and in nontransformed cells,  only small amounts bind to cadherin (Shibamoto et al.,  1995  ). .	bind
43361	4	11112	6	10	NULL	NULL	NULL	gamma-catenin	GP		bind					cadherin	GP		distal site		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_3_519_s_21	9971746	A more distantly related protein, p120ctn, also  contains a series of Arm repeats and binds to cadherin (Reynolds et al., 1992  , 1994  ; Shibamoto et al., 1995  ; Staddon et al., 1995  ) at a juxtamembrane site within the cytoplasmic domain of cadherin rather than the more distal  site where beta- and gamma-catenin bind (Ozawa and Kemler,  1998  ; Yap et al., 1998  ). p120ctn does not bind to alpha-catenin  (Daniel and Reynolds, 1995  ) and in nontransformed cells,  only small amounts bind to cadherin (Shibamoto et al.,  1995  ). .	bind
43363	5	11112	6	10	NULL	NULL	NULL	p120ctn	GP		does not bind					alpha-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_3_519_s_21	9971746	A more distantly related protein, p120ctn, also  contains a series of Arm repeats and binds to cadherin (Reynolds et al., 1992  , 1994  ; Shibamoto et al., 1995  ; Staddon et al., 1995  ) at a juxtamembrane site within the cytoplasmic domain of cadherin rather than the more distal  site where beta- and gamma-catenin bind (Ozawa and Kemler,  1998  ; Yap et al., 1998  ). p120ctn does not bind to alpha-catenin  (Daniel and Reynolds, 1995  ) and in nontransformed cells,  only small amounts bind to cadherin (Shibamoto et al.,  1995  ). .	bind
43364	6	11112	6	10	NULL	NULL	NULL	p120ctn	GP	small amount	bind					cadherin	GP				NULL	nontransformed cells	NULL	NULL	NULL	NULL	gw60_cellbiol_144_3_519_s_21	9971746	A more distantly related protein, p120ctn, also  contains a series of Arm repeats and binds to cadherin (Reynolds et al., 1992  , 1994  ; Shibamoto et al., 1995  ; Staddon et al., 1995  ) at a juxtamembrane site within the cytoplasmic domain of cadherin rather than the more distal  site where beta- and gamma-catenin bind (Ozawa and Kemler,  1998  ; Yap et al., 1998  ). p120ctn does not bind to alpha-catenin  (Daniel and Reynolds, 1995  ) and in nontransformed cells,  only small amounts bind to cadherin (Shibamoto et al.,  1995  ). .	bind
49388	1	11112	7	10	NULL	NULL	NULL	p120ctn	GP		contains								series of Arm repeats		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_3_519_s_21	9971746	A more distantly related protein, p120ctn, also  contains a series of Arm repeats and binds to cadherin (Reynolds et al., 1992  , 1994  ; Shibamoto et al., 1995  ; Staddon et al., 1995  ) at a juxtamembrane site within the cytoplasmic domain of cadherin rather than the more distal  site where beta- and gamma-catenin bind (Ozawa and Kemler,  1998  ; Yap et al., 1998  ). p120ctn does not bind to alpha-catenin  (Daniel and Reynolds, 1995  ) and in nontransformed cells,  only small amounts bind to cadherin (Shibamoto et al.,  1995  ). .	bind
49389	2	11112	7	10	NULL	NULL	NULL	statement 1	Process		bind					cadherin	GP		juxtamembrane site within the cytoplasmic domain		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_3_519_s_21	9971746	A more distantly related protein, p120ctn, also  contains a series of Arm repeats and binds to cadherin (Reynolds et al., 1992  , 1994  ; Shibamoto et al., 1995  ; Staddon et al., 1995  ) at a juxtamembrane site within the cytoplasmic domain of cadherin rather than the more distal  site where beta- and gamma-catenin bind (Ozawa and Kemler,  1998  ; Yap et al., 1998  ). p120ctn does not bind to alpha-catenin  (Daniel and Reynolds, 1995  ) and in nontransformed cells,  only small amounts bind to cadherin (Shibamoto et al.,  1995  ). .	bind
49390	3	11112	7	10	NULL	NULL	NULL	beta-catenin	GP		bind					 cadherin	GP		distal site		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_3_519_s_21	9971746	A more distantly related protein, p120ctn, also  contains a series of Arm repeats and binds to cadherin (Reynolds et al., 1992  , 1994  ; Shibamoto et al., 1995  ; Staddon et al., 1995  ) at a juxtamembrane site within the cytoplasmic domain of cadherin rather than the more distal  site where beta- and gamma-catenin bind (Ozawa and Kemler,  1998  ; Yap et al., 1998  ). p120ctn does not bind to alpha-catenin  (Daniel and Reynolds, 1995  ) and in nontransformed cells,  only small amounts bind to cadherin (Shibamoto et al.,  1995  ). .	bind
49391	4	11112	7	10	NULL	NULL	NULL	gamma-catenin	GP		bind					cadherin	GP		distal site		NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_3_519_s_21	9971746	A more distantly related protein, p120ctn, also  contains a series of Arm repeats and binds to cadherin (Reynolds et al., 1992  , 1994  ; Shibamoto et al., 1995  ; Staddon et al., 1995  ) at a juxtamembrane site within the cytoplasmic domain of cadherin rather than the more distal  site where beta- and gamma-catenin bind (Ozawa and Kemler,  1998  ; Yap et al., 1998  ). p120ctn does not bind to alpha-catenin  (Daniel and Reynolds, 1995  ) and in nontransformed cells,  only small amounts bind to cadherin (Shibamoto et al.,  1995  ). .	bind
49392	5	11112	7	10	NULL	NULL	NULL	 p120ctn	GP		does not bind					alpha-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_144_3_519_s_21	9971746	A more distantly related protein, p120ctn, also  contains a series of Arm repeats and binds to cadherin (Reynolds et al., 1992  , 1994  ; Shibamoto et al., 1995  ; Staddon et al., 1995  ) at a juxtamembrane site within the cytoplasmic domain of cadherin rather than the more distal  site where beta- and gamma-catenin bind (Ozawa and Kemler,  1998  ; Yap et al., 1998  ). p120ctn does not bind to alpha-catenin  (Daniel and Reynolds, 1995  ) and in nontransformed cells,  only small amounts bind to cadherin (Shibamoto et al.,  1995  ). .	bind
49393	6	11112	7	10	NULL	NULL	NULL	 p120ctn	GP		bind					cadherin	GP				NULL	nontransformed cells	NULL	NULL	NULL	NULL	gw60_cellbiol_144_3_519_s_21	9971746	A more distantly related protein, p120ctn, also  contains a series of Arm repeats and binds to cadherin (Reynolds et al., 1992  , 1994  ; Shibamoto et al., 1995  ; Staddon et al., 1995  ) at a juxtamembrane site within the cytoplasmic domain of cadherin rather than the more distal  site where beta- and gamma-catenin bind (Ozawa and Kemler,  1998  ; Yap et al., 1998  ). p120ctn does not bind to alpha-catenin  (Daniel and Reynolds, 1995  ) and in nontransformed cells,  only small amounts bind to cadherin (Shibamoto et al.,  1995  ). .	bind
43633	1	11113	6	10	NULL	NULL	NULL	Pyk2	GP	double mutant	disrupts		completely			ASAP1	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_32_29560_s_157	12771146	A more dramatic effect was observed upon disruption of the first  proline-rich domain of Pyk2 (Pyk2-P717A), and binding of ASAP1 was completely  abolished in the corresponding double mutant.	bind
57881	1	11113	7	10	NULL	NULL	NULL	Pyk2	GP	double mutant	disrupts		completely			ASAP1	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_32_29560_s_157	12771146	A more dramatic effect was observed upon disruption of the first  proline-rich domain of Pyk2 (Pyk2-P717A), and binding of ASAP1 was completely  abolished in the corresponding double mutant.	bind
43158	1	11114	6	10	NULL	NULL	NULL	Nrd1	GP		bind					RNA	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_95_12_6699_s_201	9618475	A more empirical approach e.g., utilizing the selective  in vitro RNA-binding activity of Nrd1 may be necessary to identify the natural targets of Nrd1.	bind
49394	1	11114	7	10	NULL	NULL	NULL	Nrd1	GP		bind					RNA	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_95_12_6699_s_201	9618475	A more empirical approach e.g., utilizing the selective  in vitro RNA-binding activity of Nrd1 may be necessary to identify the natural targets of Nrd1.	bind
43159	1	11115	6	10	NULL	NULL	NULL	DDT	Chemical		bind					EcTS	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_10_981_s_148	11590022	A more extensive search of DDT conformational space than the 500 structures initially used may have more closely predicted the conformation of DDT bound to EcTS.	bind
49395	1	11115	7	10	NULL	NULL	NULL	DDT	Chemical		bind					EcTS	GP				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_8_10_981_s_148	11590022	A more extensive search of DDT conformational space than the 500 structures initially used may have more closely predicted the conformation of DDT bound to EcTS.	bind
43160	1	11116	6	10	NULL	NULL	NULL	CREB	GP		bind					TAT	GP			CRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_23_13716_s_184	8662719	A more extensive study ( 23) indicated that PKA phosphorylation significantly increased the binding of CREB to the tyrosine aminotransferase CRE (TATCRE) and other non-canonical sites, but had less of an effect on the canonical SSCRE.	bind
43161	2	11116	6	10	NULL	NULL	NULL	PKA	GP	phosphorylation of	increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_23_13716_s_184	8662719	A more extensive study ( 23) indicated that PKA phosphorylation significantly increased the binding of CREB to the tyrosine aminotransferase CRE (TATCRE) and other non-canonical sites, but had less of an effect on the canonical SSCRE.	bind
57882	3	11116	6	10	NULL	NULL	NULL	TAT	GP		is					tyrosine aminotransferase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_23_13716_s_184	8662719	A more extensive study ( 23) indicated that PKA phosphorylation significantly increased the binding of CREB to the tyrosine aminotransferase CRE (TATCRE) and other non-canonical sites, but had less of an effect on the canonical SSCRE.	bind
49396	1	11116	7	10	NULL	NULL	NULL	CREB	GP		bind					TAT	GP			CRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_23_13716_s_184	8662719	A more extensive study ( 23) indicated that PKA phosphorylation significantly increased the binding of CREB to the tyrosine aminotransferase CRE (TATCRE) and other non-canonical sites, but had less of an effect on the canonical SSCRE.	bind
49397	2	11116	7	10	NULL	NULL	NULL	PKA	GP	phosphorylation of	increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_23_13716_s_184	8662719	A more extensive study ( 23) indicated that PKA phosphorylation significantly increased the binding of CREB to the tyrosine aminotransferase CRE (TATCRE) and other non-canonical sites, but had less of an effect on the canonical SSCRE.	bind
49398	3	11116	7	10	NULL	NULL	NULL	PKA	GP	phosphorylation of	less effect on							canonical		SSCRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_23_13716_s_184	8662719	A more extensive study ( 23) indicated that PKA phosphorylation significantly increased the binding of CREB to the tyrosine aminotransferase CRE (TATCRE) and other non-canonical sites, but had less of an effect on the canonical SSCRE.	bind
57883	4	11116	7	10	NULL	NULL	NULL	TAT	GP		is					tyrosine aminotransferase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_23_13716_s_184	8662719	A more extensive study ( 23) indicated that PKA phosphorylation significantly increased the binding of CREB to the tyrosine aminotransferase CRE (TATCRE) and other non-canonical sites, but had less of an effect on the canonical SSCRE.	bind
43162	1	11117	6	10	NULL	NULL	NULL	Spo0A	GP		bind					spoIIG	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_1_200_s_181	14679239	A more important role for Spo0A binding to the  spoIIG promoter is illuminated by our model's prediction that the specific interactions between Spo0A and sigmaA that have been demonstrated genetically occur when sigmaA region 4 is located near a sequence centered between positions -33 and -32 of the  spoIIG promoter (Fig.  4B).	bind
43163	2	11117	6	10	NULL	NULL	NULL	Spo0A	GP		interacts with					sigmaA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_1_200_s_181	14679239	A more important role for Spo0A binding to the  spoIIG promoter is illuminated by our model's prediction that the specific interactions between Spo0A and sigmaA that have been demonstrated genetically occur when sigmaA region 4 is located near a sequence centered between positions -33 and -32 of the  spoIIG promoter (Fig.  4B).	bind
49399	1	11117	7	10	NULL	NULL	NULL	Spo0A	GP		bind					spoIIG	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_1_200_s_181	14679239	A more important role for Spo0A binding to the  spoIIG promoter is illuminated by our model's prediction that the specific interactions between Spo0A and sigmaA that have been demonstrated genetically occur when sigmaA region 4 is located near a sequence centered between positions -33 and -32 of the  spoIIG promoter (Fig.  4B).	bind
49400	2	11117	7	10	NULL	NULL	NULL	Spo0A	GP		interacts with					sigmaA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_1_200_s_181	14679239	A more important role for Spo0A binding to the  spoIIG promoter is illuminated by our model's prediction that the specific interactions between Spo0A and sigmaA that have been demonstrated genetically occur when sigmaA region 4 is located near a sequence centered between positions -33 and -32 of the  spoIIG promoter (Fig.  4B).	bind
43164	1	11118	6	10	NULL	NULL	NULL	synaptojanin	GP		bind					synaptojanin-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8710_s_178	9079704	A more interesting explanation may be that the binding of synaptojanin to the 40-kDa synaptojanin-binding protein excludes amphiphysin binding.	bind
43166	2	11118	6	10	NULL	NULL	NULL	statement 1	Process		excludes					amphiphysin	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8710_s_178	9079704	A more interesting explanation may be that the binding of synaptojanin to the 40-kDa synaptojanin-binding protein excludes amphiphysin binding.	bind
49402	1	11118	7	10	NULL	NULL	NULL	synaptojanin	GP		bind					synaptojanin-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_13_8710_s_178	9079704	A more interesting explanation may be that the binding of synaptojanin to the 40-kDa synaptojanin-binding protein excludes amphiphysin binding.	bind
67683	2	11118	7	10	NULL	0	NULL	statement 1	Process		excludes					amphiphysin	GP	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_13_8710_s_178	9079704	A more interesting explanation may be that the binding of synaptojanin to the 40-kDa synaptojanin-binding protein excludes amphiphysin binding.	bind
43167	1	11119	6	10	NULL	NULL	NULL	mu1	GP		bind					sigma3	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_5_979_s_156	11230122	A more likely difference between free and mu1-bound forms of sigma3 is disruption of the dimer interface.	bind
49403	1	11119	7	10	NULL	NULL	NULL	mu1	GP		bind					sigma3	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_5_979_s_156	11230122	A more likely difference between free and mu1-bound forms of sigma3 is disruption of the dimer interface.	bind
43168	1	11120	6	10	NULL	NULL	NULL	TFIID	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_22_3007_s_129	9367983	A more likely explanation is that other components of the in vitro transcription reactions (e.g., topoisomerase I) may modify the DNA-binding properties of TFIID and TFIIA, leading to enhanced interactions despite the reduced TATA-Inr spacing.	bind
43169	2	11120	6	10	NULL	NULL	NULL	TFIIA	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_22_3007_s_129	9367983	A more likely explanation is that other components of the in vitro transcription reactions (e.g., topoisomerase I) may modify the DNA-binding properties of TFIID and TFIIA, leading to enhanced interactions despite the reduced TATA-Inr spacing.	bind
43170	3	11120	6	10	NULL	NULL	NULL	topoisomerase  I	GP		is a component of 					transcription reaction	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_11_22_3007_s_129	9367983	A more likely explanation is that other components of the in vitro transcription reactions (e.g., topoisomerase I) may modify the DNA-binding properties of TFIID and TFIIA, leading to enhanced interactions despite the reduced TATA-Inr spacing.	bind
43171	4	11120	6	10	NULL	NULL	NULL	statement 3	Process		increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_22_3007_s_129	9367983	A more likely explanation is that other components of the in vitro transcription reactions (e.g., topoisomerase I) may modify the DNA-binding properties of TFIID and TFIIA, leading to enhanced interactions despite the reduced TATA-Inr spacing.	bind
43172	5	11120	6	10	NULL	NULL	NULL	statement 3	Process		increases					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_22_3007_s_129	9367983	A more likely explanation is that other components of the in vitro transcription reactions (e.g., topoisomerase I) may modify the DNA-binding properties of TFIID and TFIIA, leading to enhanced interactions despite the reduced TATA-Inr spacing.	bind
49404	1	11120	7	10	NULL	NULL	NULL	TFIID	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_22_3007_s_129	9367983	A more likely explanation is that other components of the in vitro transcription reactions (e.g., topoisomerase I) may modify the DNA-binding properties of TFIID and TFIIA, leading to enhanced interactions despite the reduced TATA-Inr spacing.	bind
49405	2	11120	7	10	NULL	NULL	NULL	TFIIA	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_22_3007_s_129	9367983	A more likely explanation is that other components of the in vitro transcription reactions (e.g., topoisomerase I) may modify the DNA-binding properties of TFIID and TFIIA, leading to enhanced interactions despite the reduced TATA-Inr spacing.	bind
49406	3	11120	7	10	NULL	NULL	NULL	topoisomerase I	GP		increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_22_3007_s_129	9367983	A more likely explanation is that other components of the in vitro transcription reactions (e.g., topoisomerase I) may modify the DNA-binding properties of TFIID and TFIIA, leading to enhanced interactions despite the reduced TATA-Inr spacing.	bind
49407	4	11120	7	10	NULL	NULL	NULL	topoisomerase I	GP		increase					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_11_22_3007_s_129	9367983	A more likely explanation is that other components of the in vitro transcription reactions (e.g., topoisomerase I) may modify the DNA-binding properties of TFIID and TFIIA, leading to enhanced interactions despite the reduced TATA-Inr spacing.	bind
49408	5	11120	7	10	NULL	NULL	NULL	topoisomerase I	GP		is a component of					transcription reactions	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genesdev_11_22_3007_s_129	9367983	A more likely explanation is that other components of the in vitro transcription reactions (e.g., topoisomerase I) may modify the DNA-binding properties of TFIID and TFIIA, leading to enhanced interactions despite the reduced TATA-Inr spacing.	bind
43173	1	11121	6	10	NULL	NULL	NULL				bind			Pro-Phe-Lys		OppA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_5_1215_s_192	9495761	A more likely explanation is that Pro-Phe-Lys binds preferentially to OppA rather than MppA.	bind
43174	2	11121	6	10	NULL	NULL	NULL				bind			Pro-Phe-Lys		MppA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_5_1215_s_192	9495761	A more likely explanation is that Pro-Phe-Lys binds preferentially to OppA rather than MppA.	bind
50285	3	11121	6	10	NULL	NULL	NULL	statement 1	Process		is preferred over					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_5_1215_s_192	9495761	A more likely explanation is that Pro-Phe-Lys binds preferentially to OppA rather than MppA.	bind
49410	1	11121	7	10	NULL	NULL	NULL				bind			Pro-Phe-Lys		OppA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_5_1215_s_192	9495761	A more likely explanation is that Pro-Phe-Lys binds preferentially to OppA rather than MppA.	bind
49411	2	11121	7	10	NULL	NULL	NULL				bind			Pro-Phe-Lys		MppA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_5_1215_s_192	9495761	A more likely explanation is that Pro-Phe-Lys binds preferentially to OppA rather than MppA.	bind
49412	3	11121	7	10	NULL	NULL	NULL	statement 1	Process		is preferred than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_5_1215_s_192	9495761	A more likely explanation is that Pro-Phe-Lys binds preferentially to OppA rather than MppA.	bind
43638	1	11122	6	10	NULL	NULL	NULL	NHP6A/B	GP		is required for					nucleoprotein complex	GP	assembly of;; repressive			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6804_s_164	11118215	A more likely function for NHP6A/B at the  CHA1 promoter is that these proteins are required either for assembly of a repressive nucleoprotein complex (e.g. nucleosome) or function as auxiliary co-repressors, facilitating the recruitment/binding of a repressive factor(s) working through chromatin (e.g. histone deacetylase activity).	bind
43640	2	11122	6	10	NULL	NULL	NULL	nucleosome	Chromosome		is a type of					nucleoprotein complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6804_s_164	11118215	A more likely function for NHP6A/B at the  CHA1 promoter is that these proteins are required either for assembly of a repressive nucleoprotein complex (e.g. nucleosome) or function as auxiliary co-repressors, facilitating the recruitment/binding of a repressive factor(s) working through chromatin (e.g. histone deacetylase activity).	bind
43643	3	11122	6	10	NULL	NULL	NULL	NHP6A/B	GP		function as					co-repressors	GP	auxiliary			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6804_s_164	11118215	A more likely function for NHP6A/B at the  CHA1 promoter is that these proteins are required either for assembly of a repressive nucleoprotein complex (e.g. nucleosome) or function as auxiliary co-repressors, facilitating the recruitment/binding of a repressive factor(s) working through chromatin (e.g. histone deacetylase activity).	bind
43645	4	11122	6	10	NULL	NULL	NULL	statement 3	Process		facilitates					repressive factor	GP	recruitment;; binding of			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6804_s_164	11118215	A more likely function for NHP6A/B at the  CHA1 promoter is that these proteins are required either for assembly of a repressive nucleoprotein complex (e.g. nucleosome) or function as auxiliary co-repressors, facilitating the recruitment/binding of a repressive factor(s) working through chromatin (e.g. histone deacetylase activity).	bind
49413	1	11122	7	10	NULL	NULL	NULL	NHP6A/B	GP		is required for					nucleoprotein complex	GP	assembly of;;repressive			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6804_s_164	11118215	A more likely function for NHP6A/B at the  CHA1 promoter is that these proteins are required either for assembly of a repressive nucleoprotein complex (e.g. nucleosome) or function as auxiliary co-repressors, facilitating the recruitment/binding of a repressive factor(s) working through chromatin (e.g. histone deacetylase activity).	bind
49414	2	11122	7	10	NULL	NULL	NULL	NHP6A/B	GP		function as					co-repressors	GP	auxiliary 			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6804_s_164	11118215	A more likely function for NHP6A/B at the  CHA1 promoter is that these proteins are required either for assembly of a repressive nucleoprotein complex (e.g. nucleosome) or function as auxiliary co-repressors, facilitating the recruitment/binding of a repressive factor(s) working through chromatin (e.g. histone deacetylase activity).	bind
49415	3	11122	7	10	NULL	NULL	NULL	NHP6A/B	GP		facilitate					repressive factors	GP	recruitment of;;binding of			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6804_s_164	11118215	A more likely function for NHP6A/B at the  CHA1 promoter is that these proteins are required either for assembly of a repressive nucleoprotein complex (e.g. nucleosome) or function as auxiliary co-repressors, facilitating the recruitment/binding of a repressive factor(s) working through chromatin (e.g. histone deacetylase activity).	bind
49417	5	11122	7	10	NULL	NULL	NULL	nucleosome	Chromosome		is a type of					nucleoprotein complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6804_s_164	11118215	A more likely function for NHP6A/B at the  CHA1 promoter is that these proteins are required either for assembly of a repressive nucleoprotein complex (e.g. nucleosome) or function as auxiliary co-repressors, facilitating the recruitment/binding of a repressive factor(s) working through chromatin (e.g. histone deacetylase activity).	bind
49418	4	11122	7	10	NULL	NULL	NULL	statement 2	Process		occur through					chromatin	Chromosome				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_24_6804_s_164	11118215	A more likely function for NHP6A/B at the  CHA1 promoter is that these proteins are required either for assembly of a repressive nucleoprotein complex (e.g. nucleosome) or function as auxiliary co-repressors, facilitating the recruitment/binding of a repressive factor(s) working through chromatin (e.g. histone deacetylase activity).	bind
43177	1	11123	6	10	NULL	NULL	NULL	Cdc42p	GP		bind					Ste20p	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_1_83_s_172	9009270	A more likely interpretation assumes that Cdc42p binding to Ste20p plays a role in polarized transport of components required for cell-cell adhesion in the tips of mating projections.	bind
43178	2	11123	6	10	NULL	NULL	NULL	components			are required for					cell-cell adhesion	Process				NULL	tips of mating projections	NULL	NULL	NULL	NULL	gw60_embo_16_1_83_s_172	9009270	A more likely interpretation assumes that Cdc42p binding to Ste20p plays a role in polarized transport of components required for cell-cell adhesion in the tips of mating projections.	bind
43179	3	11123	6	10	NULL	NULL	NULL	statement 1	Process		plays a role in					statement 2	Process	polarized;; transport of 			NULL		NULL	NULL	NULL	NULL	gw60_embo_16_1_83_s_172	9009270	A more likely interpretation assumes that Cdc42p binding to Ste20p plays a role in polarized transport of components required for cell-cell adhesion in the tips of mating projections.	bind
49419	1	11123	7	10	NULL	NULL	NULL	Cdc42p	GP		bind					Ste20p 	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_1_83_s_172	9009270	A more likely interpretation assumes that Cdc42p binding to Ste20p plays a role in polarized transport of components required for cell-cell adhesion in the tips of mating projections.	bind
49420	2	11123	7	10	NULL	NULL	NULL	statement 1	Process		plays a role in					components		polarized;;transport of			NULL		NULL	NULL	NULL	NULL	gw60_embo_16_1_83_s_172	9009270	A more likely interpretation assumes that Cdc42p binding to Ste20p plays a role in polarized transport of components required for cell-cell adhesion in the tips of mating projections.	bind
49421	3	11123	7	10	NULL	NULL	NULL	statement 2	Process		is required for					cell-cell adhesion	Process				NULL	tips of mating projections	NULL	NULL	NULL	NULL	gw60_embo_16_1_83_s_172	9009270	A more likely interpretation assumes that Cdc42p binding to Ste20p plays a role in polarized transport of components required for cell-cell adhesion in the tips of mating projections.	bind
43647	1	11124	6	10	NULL	NULL	NULL	gamma complex	GP		bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5131_s_200	10487764	A more likely possibility is that ATP binding is fast, but the gamma complex is not committed to hydrolyzing every ATP it binds (i.e. ATP dissociation competes effectively with ATP hydrolysis, when beta and DNA are absent).	bind
43649	2	11124	6	10	NULL	NULL	NULL	ATP	Chemical	dissociation of	competes with					ATP	Chemical	hydrolysis of			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5131_s_200	10487764	A more likely possibility is that ATP binding is fast, but the gamma complex is not committed to hydrolyzing every ATP it binds (i.e. ATP dissociation competes effectively with ATP hydrolysis, when beta and DNA are absent).	bind
43651	3	11124	6	10	NULL	NULL	NULL	statement 2	Process		occurs in absence of					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5131_s_200	10487764	A more likely possibility is that ATP binding is fast, but the gamma complex is not committed to hydrolyzing every ATP it binds (i.e. ATP dissociation competes effectively with ATP hydrolysis, when beta and DNA are absent).	bind
43652	4	11124	6	10	NULL	NULL	NULL	statement 2	Process		occurs in absence of					beta					NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5131_s_200	10487764	A more likely possibility is that ATP binding is fast, but the gamma complex is not committed to hydrolyzing every ATP it binds (i.e. ATP dissociation competes effectively with ATP hydrolysis, when beta and DNA are absent).	bind
49422	1	11124	7	10	NULL	NULL	NULL	ATP	Chemical	dissociation of	compete with		effectively			ATP	Chemical	hydrolysis of			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5131_s_200	10487764	A more likely possibility is that ATP binding is fast, but the gamma complex is not committed to hydrolyzing every ATP it binds (i.e. ATP dissociation competes effectively with ATP hydrolysis, when beta and DNA are absent).	bind
49423	2	11124	7	10	NULL	NULL	NULL	statement 1	Process		in absence of					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5131_s_200	10487764	A more likely possibility is that ATP binding is fast, but the gamma complex is not committed to hydrolyzing every ATP it binds (i.e. ATP dissociation competes effectively with ATP hydrolysis, when beta and DNA are absent).	bind
49424	3	11124	7	10	NULL	NULL	NULL	statement 1	Process		in absence of					beta					NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5131_s_200	10487764	A more likely possibility is that ATP binding is fast, but the gamma complex is not committed to hydrolyzing every ATP it binds (i.e. ATP dissociation competes effectively with ATP hydrolysis, when beta and DNA are absent).	bind
50304	4	11124	7	10	NULL	NULL	NULL	gamma complex	GP		bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_18_5131_s_200	10487764	A more likely possibility is that ATP binding is fast, but the gamma complex is not committed to hydrolyzing every ATP it binds (i.e. ATP dissociation competes effectively with ATP hydrolysis, when beta and DNA are absent).	bind
43181	1	11125	6	10	NULL	NULL	NULL	RRD proteins	GP	loss of	affects					PPH21	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_17_2138_s_250	12952889	A more likely possibility is that loss of the RRD proteins affects other  proteins in addition to PPH21 and PPH22.	bind
43182	2	11125	6	10	NULL	NULL	NULL	RRD proteins	GP	loss of	affects					PPH22	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_17_2138_s_250	12952889	A more likely possibility is that loss of the RRD proteins affects other  proteins in addition to PPH21 and PPH22.	bind
49426	1	11125	7	10	NULL	NULL	NULL	RRD proteins	GP	loss of	affects					 PPH21	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_17_2138_s_250	12952889	A more likely possibility is that loss of the RRD proteins affects other  proteins in addition to PPH21 and PPH22.	bind
49427	2	11125	7	10	NULL	NULL	NULL	RRD proteins	GP	loss of	affects					PPH22	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_17_2138_s_250	12952889	A more likely possibility is that loss of the RRD proteins affects other  proteins in addition to PPH21 and PPH22.	bind
43183	1	11126	6	10	NULL	NULL	NULL	E2	GP		contains								lipoyl domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_23_14130_s_238	9603912	A more likely prospect is that E1b, which is bound to an E2 containing two lipoyl domains, makes E1b a better substrate than free E1b for an unbound PDP, particularly when located next to a nonlipoylated L2.	bind
43184	2	11126	6	10	NULL	NULL	NULL	E1b	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_23_14130_s_238	9603912	A more likely prospect is that E1b, which is bound to an E2 containing two lipoyl domains, makes E1b a better substrate than free E1b for an unbound PDP, particularly when located next to a nonlipoylated L2.	bind
43655	3	11126	6	10	NULL	NULL	NULL	statement 2	Process		acts as a substrate for					PDP	GP	unbound			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_23_14130_s_238	9603912	A more likely prospect is that E1b, which is bound to an E2 containing two lipoyl domains, makes E1b a better substrate than free E1b for an unbound PDP, particularly when located next to a nonlipoylated L2.	bind
57884	4	11126	6	10	NULL	NULL	NULL	E1b	GP	free	is a substrate for					PDP	GP	unbound			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_23_14130_s_238	9603912	A more likely prospect is that E1b, which is bound to an E2 containing two lipoyl domains, makes E1b a better substrate than free E1b for an unbound PDP, particularly when located next to a nonlipoylated L2.	bind
57885	5	11126	6	10	NULL	NULL	NULL	statement 3	Process		better than					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_23_14130_s_238	9603912	A more likely prospect is that E1b, which is bound to an E2 containing two lipoyl domains, makes E1b a better substrate than free E1b for an unbound PDP, particularly when located next to a nonlipoylated L2.	bind
49428	1	11126	7	10	NULL	NULL	NULL	E2	GP		contains								lipoyl domains		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_23_14130_s_238	9603912	A more likely prospect is that E1b, which is bound to an E2 containing two lipoyl domains, makes E1b a better substrate than free E1b for an unbound PDP, particularly when located next to a nonlipoylated L2.	bind
49429	2	11126	7	10	NULL	NULL	NULL	E1b	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_23_14130_s_238	9603912	A more likely prospect is that E1b, which is bound to an E2 containing two lipoyl domains, makes E1b a better substrate than free E1b for an unbound PDP, particularly when located next to a nonlipoylated L2.	bind
49430	3	11126	7	10	NULL	NULL	NULL	statement 2	Process		substrate for					PDP	GP	unbound 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_23_14130_s_238	9603912	A more likely prospect is that E1b, which is bound to an E2 containing two lipoyl domains, makes E1b a better substrate than free E1b for an unbound PDP, particularly when located next to a nonlipoylated L2.	bind
49431	4	11126	7	10	NULL	NULL	NULL	E1b	GP	free	substrate for					PDP	GP	unbound			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_23_14130_s_238	9603912	A more likely prospect is that E1b, which is bound to an E2 containing two lipoyl domains, makes E1b a better substrate than free E1b for an unbound PDP, particularly when located next to a nonlipoylated L2.	bind
49432	5	11126	7	10	NULL	NULL	NULL	statement 3	Process		is better than					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_23_14130_s_238	9603912	A more likely prospect is that E1b, which is bound to an E2 containing two lipoyl domains, makes E1b a better substrate than free E1b for an unbound PDP, particularly when located next to a nonlipoylated L2.	bind
43185	1	11127	6	10	NULL	NULL	NULL	PtdIns-3,4,5-P3	Chemical		bind								PH domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_293_s_81	12419241	A more likely scenario is that after initial membrane translocation and activation via PtdIns-3,4,5-P3 binding to its PH domain, PKB dissociates from the plasma membrane, thus freeing its PH domain to interact with protein ligands such as TCL1.	bind
43666	2	11127	6	10	NULL	NULL	NULL	TCL1	GP		interacts with								PH domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_293_s_81	12419241	A more likely scenario is that after initial membrane translocation and activation via PtdIns-3,4,5-P3 binding to its PH domain, PKB dissociates from the plasma membrane, thus freeing its PH domain to interact with protein ligands such as TCL1.	bind
43668	3	11127	6	10	NULL	NULL	NULL	statement 1	Process		leads to					membrane	CellComponent	translocation of			NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_293_s_81	12419241	A more likely scenario is that after initial membrane translocation and activation via PtdIns-3,4,5-P3 binding to its PH domain, PKB dissociates from the plasma membrane, thus freeing its PH domain to interact with protein ligands such as TCL1.	bind
43671	4	11127	6	10	NULL	NULL	NULL	statement 1	Process		leads to					membrane	CellComponent	activation of			NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_293_s_81	12419241	A more likely scenario is that after initial membrane translocation and activation via PtdIns-3,4,5-P3 binding to its PH domain, PKB dissociates from the plasma membrane, thus freeing its PH domain to interact with protein ligands such as TCL1.	bind
43676	5	11127	6	10	NULL	NULL	NULL	PKB	GP		dissociates from					plasma membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_293_s_81	12419241	A more likely scenario is that after initial membrane translocation and activation via PtdIns-3,4,5-P3 binding to its PH domain, PKB dissociates from the plasma membrane, thus freeing its PH domain to interact with protein ligands such as TCL1.	bind
49434	1	11127	7	10	NULL	NULL	NULL	PKB	GP		translocates to					membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_293_s_81	12419241	A more likely scenario is that after initial membrane translocation and activation via PtdIns-3,4,5-P3 binding to its PH domain, PKB dissociates from the plasma membrane, thus freeing its PH domain to interact with protein ligands such as TCL1.	bind
49435	2	11127	7	10	NULL	NULL	NULL	PKB	GP		bind			PH domain		PtdIns-3,4,5-P3	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_293_s_81	12419241	A more likely scenario is that after initial membrane translocation and activation via PtdIns-3,4,5-P3 binding to its PH domain, PKB dissociates from the plasma membrane, thus freeing its PH domain to interact with protein ligands such as TCL1.	bind
49436	3	11127	7	10	NULL	NULL	NULL	statement 2	Process		leads to					PKB	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_293_s_81	12419241	A more likely scenario is that after initial membrane translocation and activation via PtdIns-3,4,5-P3 binding to its PH domain, PKB dissociates from the plasma membrane, thus freeing its PH domain to interact with protein ligands such as TCL1.	bind
49437	4	11127	7	10	NULL	NULL	NULL	PKB	GP		dissociates from					plasma membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_293_s_81	12419241	A more likely scenario is that after initial membrane translocation and activation via PtdIns-3,4,5-P3 binding to its PH domain, PKB dissociates from the plasma membrane, thus freeing its PH domain to interact with protein ligands such as TCL1.	bind
49438	5	11127	7	10	NULL	NULL	NULL	statement 4	Process		release					PKB	GP		PH domain		NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_293_s_81	12419241	A more likely scenario is that after initial membrane translocation and activation via PtdIns-3,4,5-P3 binding to its PH domain, PKB dissociates from the plasma membrane, thus freeing its PH domain to interact with protein ligands such as TCL1.	bind
49439	6	11127	7	10	NULL	NULL	NULL	PKB	GP		interacts with			PH domain		TCL1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_293_s_81	12419241	A more likely scenario is that after initial membrane translocation and activation via PtdIns-3,4,5-P3 binding to its PH domain, PKB dissociates from the plasma membrane, thus freeing its PH domain to interact with protein ligands such as TCL1.	bind
49440	7	11127	7	10	NULL	NULL	NULL	statement 4	Process		occurs after					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_293_s_81	12419241	A more likely scenario is that after initial membrane translocation and activation via PtdIns-3,4,5-P3 binding to its PH domain, PKB dissociates from the plasma membrane, thus freeing its PH domain to interact with protein ligands such as TCL1.	bind
49441	8	11127	7	10	NULL	NULL	NULL	statement 4	Process		occurs after					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_293_s_81	12419241	A more likely scenario is that after initial membrane translocation and activation via PtdIns-3,4,5-P3 binding to its PH domain, PKB dissociates from the plasma membrane, thus freeing its PH domain to interact with protein ligands such as TCL1.	bind
43186	1	11128	6	10	NULL	NULL	NULL	HDL	Chemical		bind					SR-BI	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_29993_s_244	11001950	A more parsimonious model is that KKB-1 blocks SR-BI-mediated [3]cholesterol efflux to HDL by blocking HDL binding to SR-BI.	bind
43187	2	11128	6	10	NULL	NULL	NULL	cholesterol	Chemical		effluxes					HDL	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_29993_s_244	11001950	A more parsimonious model is that KKB-1 blocks SR-BI-mediated [3]cholesterol efflux to HDL by blocking HDL binding to SR-BI.	bind
43188	3	11128	6	10	NULL	NULL	NULL	SR-BI	GP		mediates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_29993_s_244	11001950	A more parsimonious model is that KKB-1 blocks SR-BI-mediated [3]cholesterol efflux to HDL by blocking HDL binding to SR-BI.	bind
43189	4	11128	6	10	NULL	NULL	NULL	KKB-1	GP		blocks					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_29993_s_244	11001950	A more parsimonious model is that KKB-1 blocks SR-BI-mediated [3]cholesterol efflux to HDL by blocking HDL binding to SR-BI.	bind
43190	5	11128	6	10	NULL	NULL	NULL	statement 4	Process		occurs by blocking					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_29993_s_244	11001950	A more parsimonious model is that KKB-1 blocks SR-BI-mediated [3]cholesterol efflux to HDL by blocking HDL binding to SR-BI.	bind
49442	1	11128	7	10	NULL	NULL	NULL	HDL	Chemical		bind					SR-BI	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_29993_s_244	11001950	A more parsimonious model is that KKB-1 blocks SR-BI-mediated [3]cholesterol efflux to HDL by blocking HDL binding to SR-BI.	bind
49443	2	11128	7	10	NULL	NULL	NULL	cholesterol	Chemical		efflux to					HDL	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_29993_s_244	11001950	A more parsimonious model is that KKB-1 blocks SR-BI-mediated [3]cholesterol efflux to HDL by blocking HDL binding to SR-BI.	bind
49444	3	11128	7	10	NULL	NULL	NULL	SR-BI	GP		mediates					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_29993_s_244	11001950	A more parsimonious model is that KKB-1 blocks SR-BI-mediated [3]cholesterol efflux to HDL by blocking HDL binding to SR-BI.	bind
49445	4	11128	7	10	NULL	NULL	NULL	KKB-1 	GP		blocks					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_29993_s_244	11001950	A more parsimonious model is that KKB-1 blocks SR-BI-mediated [3]cholesterol efflux to HDL by blocking HDL binding to SR-BI.	bind
49446	5	11128	7	10	NULL	NULL	NULL	KKB-1 	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_29993_s_244	11001950	A more parsimonious model is that KKB-1 blocks SR-BI-mediated [3]cholesterol efflux to HDL by blocking HDL binding to SR-BI.	bind
49447	6	11128	7	10	NULL	NULL	NULL	statement 4	Process		occur by					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_29993_s_244	11001950	A more parsimonious model is that KKB-1 blocks SR-BI-mediated [3]cholesterol efflux to HDL by blocking HDL binding to SR-BI.	bind
43191	1	11133	6	10	NULL	NULL	NULL	GABA	Chemical		bind					hydra membranes	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_85_3_979_s_85	9639289	A more pronounced increase in [3]GABA binding to  Hydra membranes was apparent in the presence of general anaesthetics ( Fig. 1A).	bind
49453	1	11133	7	10	NULL	NULL	NULL	GABA	Chemical		bind					hydra membranes	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_85_3_979_s_85	9639289	A more pronounced increase in [3]GABA binding to  Hydra membranes was apparent in the presence of general anaesthetics ( Fig. 1A).	bind
43192	1	11134	6	10	NULL	NULL	NULL	guanine nucleotides	NucleicAcid		bind					Ras protein	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_46715_s_31	15339905	A more recent assay to analyze quantitatively the guanine nucleotides bound to the Ras proteins  in vivo was described by Taylor and Shalloway ( ) and exploits the known specificity of the interaction between Ras-GTP and the Ras-binding domain (RBD) of Raf-1 to detect activated Ras.	bind
43193	2	11134	6	10	NULL	NULL	NULL	Ras-GTP	GP		interacts with					Raf-1	GP		RBD		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_46715_s_31	15339905	A more recent assay to analyze quantitatively the guanine nucleotides bound to the Ras proteins  in vivo was described by Taylor and Shalloway ( ) and exploits the known specificity of the interaction between Ras-GTP and the Ras-binding domain (RBD) of Raf-1 to detect activated Ras.	bind
43194	3	11134	6	10	NULL	NULL	NULL	RBD	AminoAcid		is					Ras-binding domain	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_46715_s_31	15339905	A more recent assay to analyze quantitatively the guanine nucleotides bound to the Ras proteins  in vivo was described by Taylor and Shalloway ( ) and exploits the known specificity of the interaction between Ras-GTP and the Ras-binding domain (RBD) of Raf-1 to detect activated Ras.	bind
49455	1	11134	7	10	NULL	NULL	NULL	guanine nucleotides	NucleicAcid		bind					Ras proteins	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_46715_s_31	15339905	A more recent assay to analyze quantitatively the guanine nucleotides bound to the Ras proteins  in vivo was described by Taylor and Shalloway ( ) and exploits the known specificity of the interaction between Ras-GTP and the Ras-binding domain (RBD) of Raf-1 to detect activated Ras.	bind
49456	2	11134	7	10	NULL	NULL	NULL	Ras-GTP 	GP		interacts with					Raf-1	GP		RBD		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_46715_s_31	15339905	A more recent assay to analyze quantitatively the guanine nucleotides bound to the Ras proteins  in vivo was described by Taylor and Shalloway ( ) and exploits the known specificity of the interaction between Ras-GTP and the Ras-binding domain (RBD) of Raf-1 to detect activated Ras.	bind
49457	3	11134	7	10	NULL	NULL	NULL	RBD	AminoAcid		is					Ras-binding domain	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_46715_s_31	15339905	A more recent assay to analyze quantitatively the guanine nucleotides bound to the Ras proteins  in vivo was described by Taylor and Shalloway ( ) and exploits the known specificity of the interaction between Ras-GTP and the Ras-binding domain (RBD) of Raf-1 to detect activated Ras.	bind
49458	4	11134	7	10	NULL	NULL	NULL	statement 2	Process		detects					Ras	GP	activated			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_45_46715_s_31	15339905	A more recent assay to analyze quantitatively the guanine nucleotides bound to the Ras proteins  in vivo was described by Taylor and Shalloway ( ) and exploits the known specificity of the interaction between Ras-GTP and the Ras-binding domain (RBD) of Raf-1 to detect activated Ras.	bind
43220	1	11135	6	10	NULL	NULL	NULL	ARS1	GP		is assembled into					chromatin	Chromosome				NULL	in vitro chromatin assembly extract	NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_142_s_321	15020055	A more recent biochemical study of ORC and Abf1p binding to  ARS1 assembled into chromatin in an in vitro chromatin assembly extract confirms and extends  these findings [ 113].	bind
43221	2	11135	6	10	NULL	NULL	NULL	ORC	NucleicAcid		bind					statement 1	Process				NULL	in vitro chromatin assembly extract	NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_142_s_321	15020055	A more recent biochemical study of ORC and Abf1p binding to  ARS1 assembled into chromatin in an in vitro chromatin assembly extract confirms and extends  these findings [ 113].	bind
43222	3	11135	6	10	NULL	NULL	NULL	Abf1p	GP		bind					statement 1	Process				NULL	in vitro chromatin assembly extract	NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_142_s_321	15020055	A more recent biochemical study of ORC and Abf1p binding to  ARS1 assembled into chromatin in an in vitro chromatin assembly extract confirms and extends  these findings [ 113].	bind
49459	1	11135	7	10	NULL	NULL	NULL	ORC 	NucleicAcid		bind					ARS1	GP				NULL	in vitro chromatin assembly extract	NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_142_s_321	15020055	A more recent biochemical study of ORC and Abf1p binding to  ARS1 assembled into chromatin in an in vitro chromatin assembly extract confirms and extends  these findings [ 113].	bind
49460	2	11135	7	10	NULL	NULL	NULL	Abf1p	GP		bind					ARS1	GP				NULL	in vitro chromatin assembly extract	NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_142_s_321	15020055	A more recent biochemical study of ORC and Abf1p binding to  ARS1 assembled into chromatin in an in vitro chromatin assembly extract confirms and extends  these findings [ 113].	bind
49461	3	11135	7	10	NULL	NULL	NULL	ARS1	GP		assembled into					chromatin	Chromosome				NULL	in vitro chromatin assembly extract	NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_142_s_321	15020055	A more recent biochemical study of ORC and Abf1p binding to  ARS1 assembled into chromatin in an in vitro chromatin assembly extract confirms and extends  these findings [ 113].	bind
43975	1	11136	6	10	NULL	NULL	NULL	L-CPTI	GP		are critical for			first 18 N-terminal amino acid residues		malonyl-CoA	GP	inhibiton of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_14_9421_s_157	10092622	A more recent detailed deletion mutation analysis study of the 129 N-terminal amino acid residues of the yeast-expressed L-CPTI from our laboratory clearly demonstrated that residues critical for malonyl-CoA inhibition and binding of L-CPTI are located within the conserved first 18 N-terminal amino acid residues of the enzyme ( 14).	bind
43976	2	11136	6	10	NULL	NULL	NULL	L-CPTI	GP		are critical for			first 18 N-terminal amino acid residues		L-CPTI	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_14_9421_s_157	10092622	A more recent detailed deletion mutation analysis study of the 129 N-terminal amino acid residues of the yeast-expressed L-CPTI from our laboratory clearly demonstrated that residues critical for malonyl-CoA inhibition and binding of L-CPTI are located within the conserved first 18 N-terminal amino acid residues of the enzyme ( 14).	bind
50305	1	11136	7	10	NULL	NULL	NULL	L-CPTI	GP		are critical for			first 18 N-terminal amino acid residues		malonyl-CoA	GP	inhibiton of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_14_9421_s_157	10092622	A more recent detailed deletion mutation analysis study of the 129 N-terminal amino acid residues of the yeast-expressed L-CPTI from our laboratory clearly demonstrated that residues critical for malonyl-CoA inhibition and binding of L-CPTI are located within the conserved first 18 N-terminal amino acid residues of the enzyme ( 14).	bind
50306	2	11136	7	10	NULL	NULL	NULL	L-CPTI	GP		are critical for			first 18 N-terminal amino acid residues		L-CPTI	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_14_9421_s_157	10092622	A more recent detailed deletion mutation analysis study of the 129 N-terminal amino acid residues of the yeast-expressed L-CPTI from our laboratory clearly demonstrated that residues critical for malonyl-CoA inhibition and binding of L-CPTI are located within the conserved first 18 N-terminal amino acid residues of the enzyme ( 14).	bind
43223	1	11137	6	10	NULL	NULL	NULL	Sir2Tm	GP	wild type	bind					NAD+	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_75_0_435_s_472	16756498	A more recent structure of a ternary complex containing wild-type  Sir2Tm bound to NAD+ and acetylated peptide (K. Hoff, J. Avalos, K. Sens, and C. Wolberger, manuscript  submitted) provides further insights into the true nature of the Michaelis complex.	bind
43224	2	11137	6	10	NULL	NULL	NULL	Sir2Tm	GP	wild type	bind					peptide	AminoAcid	acetylated			NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_75_0_435_s_472	16756498	A more recent structure of a ternary complex containing wild-type  Sir2Tm bound to NAD+ and acetylated peptide (K. Hoff, J. Avalos, K. Sens, and C. Wolberger, manuscript  submitted) provides further insights into the true nature of the Michaelis complex.	bind
49465	1	11137	7	10	NULL	NULL	NULL	Sir2Tm	GP	wild-type	bind					NAD+	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_75_0_435_s_472	16756498	A more recent structure of a ternary complex containing wild-type  Sir2Tm bound to NAD+ and acetylated peptide (K. Hoff, J. Avalos, K. Sens, and C. Wolberger, manuscript  submitted) provides further insights into the true nature of the Michaelis complex.	bind
49466	2	11137	7	10	NULL	NULL	NULL	Sir2Tm	GP	wild-type	bind					peptide	AminoAcid	acetylated			NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_75_0_435_s_472	16756498	A more recent structure of a ternary complex containing wild-type  Sir2Tm bound to NAD+ and acetylated peptide (K. Hoff, J. Avalos, K. Sens, and C. Wolberger, manuscript  submitted) provides further insights into the true nature of the Michaelis complex.	bind
43225	1	11138	6	10	NULL	NULL	NULL	Oct-1	GP		does not bind					HIV-1	Organism			LTR	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4285_s_586	16061936	A more recent study contrasts with the latter one and demonstrates that Oct-1 and Oct-2 fail to bind the HIV-1 LTR, and that overexpression of Oct proteins has no effect on HIV-1 transcription or replication in primary human CD4+ T-cells ( ).	bind
43226	2	11138	6	10	NULL	NULL	NULL	Oct-2	GP		does not bind					HIV-1	Organism			LTR	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4285_s_586	16061936	A more recent study contrasts with the latter one and demonstrates that Oct-1 and Oct-2 fail to bind the HIV-1 LTR, and that overexpression of Oct proteins has no effect on HIV-1 transcription or replication in primary human CD4+ T-cells ( ).	bind
43227	3	11138	6	10	NULL	NULL	NULL	Oct proteins	GP	overexpression of	has no effect on					HIV-1	Organism	transcription of			NULL	primary human CD4+ T-cells	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4285_s_586	16061936	A more recent study contrasts with the latter one and demonstrates that Oct-1 and Oct-2 fail to bind the HIV-1 LTR, and that overexpression of Oct proteins has no effect on HIV-1 transcription or replication in primary human CD4+ T-cells ( ).	bind
43228	4	11138	6	10	NULL	NULL	NULL	Oct proteins	GP	overexpression of	has no effect on					HIV-1	Organism	replication of 			NULL	primary human CD4+ T-cells	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4285_s_586	16061936	A more recent study contrasts with the latter one and demonstrates that Oct-1 and Oct-2 fail to bind the HIV-1 LTR, and that overexpression of Oct proteins has no effect on HIV-1 transcription or replication in primary human CD4+ T-cells ( ).	bind
49467	1	11138	7	10	NULL	NULL	NULL	Oct-1 	GP		does not bind					HIV-1	Organism			LTR	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4285_s_586	16061936	A more recent study contrasts with the latter one and demonstrates that Oct-1 and Oct-2 fail to bind the HIV-1 LTR, and that overexpression of Oct proteins has no effect on HIV-1 transcription or replication in primary human CD4+ T-cells ( ).	bind
49468	2	11138	7	10	NULL	NULL	NULL	Oct-2	GP		does not bind					HIV-1	Organism			LTR	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4285_s_586	16061936	A more recent study contrasts with the latter one and demonstrates that Oct-1 and Oct-2 fail to bind the HIV-1 LTR, and that overexpression of Oct proteins has no effect on HIV-1 transcription or replication in primary human CD4+ T-cells ( ).	bind
49469	3	11138	7	10	NULL	NULL	NULL	Oct proteins	GP	overexpression of 	does not affect					HIV-1	Organism	transcription of			NULL	primary human CD4+ T-cells	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4285_s_586	16061936	A more recent study contrasts with the latter one and demonstrates that Oct-1 and Oct-2 fail to bind the HIV-1 LTR, and that overexpression of Oct proteins has no effect on HIV-1 transcription or replication in primary human CD4+ T-cells ( ).	bind
49470	4	11138	7	10	NULL	NULL	NULL	Oct proteins 	GP	overexpression of	does not affect					HIV-1	Organism	replication of			NULL	primary human CD4+ T-cells	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_13_4285_s_586	16061936	A more recent study contrasts with the latter one and demonstrates that Oct-1 and Oct-2 fail to bind the HIV-1 LTR, and that overexpression of Oct proteins has no effect on HIV-1 transcription or replication in primary human CD4+ T-cells ( ).	bind
43229	1	11139	6	10	NULL	NULL	NULL	BvgA	GP	phosphorylated	bind					bvgR	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_5_1648_s_26	15716435	A more recent study demonstrated that expression of BvgR is activated by the binding of phosphorylated BvgA to the  bvgR promoter ( ).	bind
43230	2	11139	6	10	NULL	NULL	NULL	BvgR	GP	expression of	is activated by					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_5_1648_s_26	15716435	A more recent study demonstrated that expression of BvgR is activated by the binding of phosphorylated BvgA to the  bvgR promoter ( ).	bind
49471	1	11139	7	10	NULL	NULL	NULL	BvgA	GP	phosphorylated 	bind					bvgR	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_5_1648_s_26	15716435	A more recent study demonstrated that expression of BvgR is activated by the binding of phosphorylated BvgA to the  bvgR promoter ( ).	bind
49472	2	11139	7	10	NULL	NULL	NULL	statement 1	Process		leads to					 BvgR 	GP	activation of;;expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_5_1648_s_26	15716435	A more recent study demonstrated that expression of BvgR is activated by the binding of phosphorylated BvgA to the  bvgR promoter ( ).	bind
43231	1	11140	6	10	NULL	NULL	NULL	aggrecan	GP		bind					hyaluronan	GP				NULL	bovine cartilage explants	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_9_6321_s_23	10692431	A more recent study demonstrated that the extent of tissue compression, with the concomitant changes in proteoglycan concentration and pH of the extracellular matrix, could influence the hyaluronan binding properties of aggrecan in bovine cartilage explants ( 14).	bind
43232	2	11140	6	10	NULL	NULL	NULL	proteoglycan	GP	change in concentration of	influence					statement 1	Process				NULL	bovine cartilage explants	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_9_6321_s_23	10692431	A more recent study demonstrated that the extent of tissue compression, with the concomitant changes in proteoglycan concentration and pH of the extracellular matrix, could influence the hyaluronan binding properties of aggrecan in bovine cartilage explants ( 14).	bind
43233	3	11140	6	10	NULL	NULL	NULL	extracellular matrix	CellComponent	change in pH of	influence		could			statement 1	Process				NULL	bovine cartilage explants	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_9_6321_s_23	10692431	A more recent study demonstrated that the extent of tissue compression, with the concomitant changes in proteoglycan concentration and pH of the extracellular matrix, could influence the hyaluronan binding properties of aggrecan in bovine cartilage explants ( 14).	bind
49473	1	11140	7	10	NULL	NULL	NULL	 aggrecan	GP		bind					hyaluronan	GP				NULL	bovine cartilage explants	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_9_6321_s_23	10692431	A more recent study demonstrated that the extent of tissue compression, with the concomitant changes in proteoglycan concentration and pH of the extracellular matrix, could influence the hyaluronan binding properties of aggrecan in bovine cartilage explants ( 14).	bind
50307	2	11140	7	10	NULL	NULL	NULL	proteoglycan	GP	change in concentration of	influence					statement 1	Process				NULL	bovine cartilage explants	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_9_6321_s_23	10692431	A more recent study demonstrated that the extent of tissue compression, with the concomitant changes in proteoglycan concentration and pH of the extracellular matrix, could influence the hyaluronan binding properties of aggrecan in bovine cartilage explants ( 14).	bind
50308	3	11140	7	10	NULL	NULL	NULL	extracellular matrix	CellComponent	change in pH of	influence					statement 1	Process				NULL	bovine cartilage explants	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_9_6321_s_23	10692431	A more recent study demonstrated that the extent of tissue compression, with the concomitant changes in proteoglycan concentration and pH of the extracellular matrix, could influence the hyaluronan binding properties of aggrecan in bovine cartilage explants ( 14).	bind
43234	1	11141	6	10	NULL	NULL	NULL	SDF-1	GP		in complex with					CXCR4 receptor	GP				NULL	surface of HeLa cells in vitro	NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
44278	2	11141	6	10	NULL	NULL	NULL	SDF-1	GP		in complex with					CXCR4 receptor	GP				NULL	primary lymphocytes in vitro	NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
44279	3	11141	6	10	NULL	NULL	NULL	SDF-1	GP		in complex with					CXCR4 receptor	GP				NULL	macrophages in vitro \t	NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
44976	4	11141	6	10	NULL	NULL	NULL	syndecan-4	GP		bind					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
44977	5	11141	6	10	NULL	NULL	NULL	syndecan-4	GP		bind					statement 2	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
44978	6	11141	6	10	NULL	NULL	NULL	syndecan-4	GP		bind					statement 3	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
44979	7	11141	6	10	NULL	NULL	NULL	syndecan-1	GP		does not bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
44980	8	11141	6	10	NULL	NULL	NULL	syndecan-1	GP		does not bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
44981	9	11141	6	10	NULL	NULL	NULL	syndecan-1	GP		does not bind					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
44982	10	11141	6	10	NULL	NULL	NULL	syndecan-2	GP		does not bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
44983	11	11141	6	10	NULL	NULL	NULL	syndecan-2	GP		does not bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
44984	12	11141	6	10	NULL	NULL	NULL	syndecan-2	GP		does not bind					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
44985	13	11141	6	10	NULL	NULL	NULL	betaglycan	GP		does not bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
67700	14	11141	6	10	NULL	0	NULL	betaglycan	GP		does not bind					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
67701	15	11141	6	10	NULL	0	NULL	betaglycan	GP		does not bind					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
67703	16	11141	6	10	NULL	0	NULL	CD44	GP		does not bind					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
67704	17	11141	6	10	NULL	0	NULL	CD44	GP		does not bind					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
67705	18	11141	6	10	NULL	0	NULL	CD44	GP		does not bind					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
49474	1	11141	7	10	NULL	NULL	NULL	SDF-1	GP		in complex with					CXCR4 receptor	GP				NULL	surface of HeLa cells in vitro	NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
49475	2	11141	7	10	NULL	NULL	NULL	 SDF-1	GP		in complex with					CXCR4 receptor 	GP				NULL	primary lymphocytes in vitro	NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
49476	3	11141	7	10	NULL	NULL	NULL	SDF-1	GP		in complex with					CXCR4 receptor	GP				NULL	macrophages in vitro	NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
49477	4	11141	7	10	NULL	NULL	NULL	syndecan-4	GP		bind					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
49478	5	11141	7	10	NULL	NULL	NULL	syndecan-4	GP		bind					statement 2	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
49479	6	11141	7	10	NULL	NULL	NULL	syndecan-4	GP		bind					statement 3	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
49480	7	11141	7	10	NULL	NULL	NULL	syndecan-1	GP		does not bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
49481	8	11141	7	10	NULL	NULL	NULL	syndecan-1	GP		does not bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
49482	9	11141	7	10	NULL	NULL	NULL	syndecan-1	GP		does not bind					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
49483	10	11141	7	10	NULL	NULL	NULL	syndecan-2	GP		does not bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
49484	11	11141	7	10	NULL	NULL	NULL	syndecan-2	GP		does not bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
49485	12	11141	7	10	NULL	NULL	NULL	syndecan-2	GP		does not bind					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
49486	13	11141	7	10	NULL	NULL	NULL	betaglycan	GP		does not bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
49487	14	11141	7	10	NULL	NULL	NULL	betaglycan	GP		does not bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
49488	15	11141	7	10	NULL	NULL	NULL	betaglycan	GP		does not bind					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
49489	16	11141	7	10	NULL	NULL	NULL	CD44	GP		does not bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
49490	17	11141	7	10	NULL	NULL	NULL	CD44	GP		does not bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
49491	18	11141	7	10	NULL	NULL	NULL	CD44	GP		does not bind					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_282_1_152_s_208	15936336	A more recent study has shown that syndecan-4 binds SDF-1 in a complex with the  CXCR4 receptor on the surface of HeLa cells, as well as on primary lymphocytes and  macrophages in vitro, while syndecan-1, syndecan-2, betaglycan, and CD44 did not  (  Hamon et al., 2004).	bind
43235	1	11142	6	10	NULL	NULL	NULL	heparin	GP		bind					HSV-1	Organism				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_24850_s_34	9312084	A more recent study implicated a variety of sulfate groups in the binding of heparin to HSV-1 ( 13).	bind
43236	2	11142	6	10	NULL	NULL	NULL	sulfate groups	Chemical		plays a role in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_24850_s_34	9312084	A more recent study implicated a variety of sulfate groups in the binding of heparin to HSV-1 ( 13).	bind
49492	1	11142	7	10	NULL	NULL	NULL	heparin	GP		bind					HSV-1	Organism				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_24850_s_34	9312084	A more recent study implicated a variety of sulfate groups in the binding of heparin to HSV-1 ( 13).	bind
49493	2	11142	7	10	NULL	NULL	NULL	sulfate groups	Chemical		is implicated in					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_24850_s_34	9312084	A more recent study implicated a variety of sulfate groups in the binding of heparin to HSV-1 ( 13).	bind
43237	1	11143	6	10	NULL	NULL	NULL	Sp1	GP		bind					Hmga2 gene	GP	proximal		promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_6_2296_s_307	14993269	A more recent study of the transcriptional inhibition of the  Hmga2 gene following TSA treatment has suggested that repression results from a decrease in Sp1 and Sp3 binding to the proximal promoter ( ).	bind
43238	2	11143	6	10	NULL	NULL	NULL	Sp3	GP		bind					Hmga2 gene	GP	proximal		promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_6_2296_s_307	14993269	A more recent study of the transcriptional inhibition of the  Hmga2 gene following TSA treatment has suggested that repression results from a decrease in Sp1 and Sp3 binding to the proximal promoter ( ).	bind
43239	3	11143	6	10	NULL	NULL	NULL	TSA	Chemical	treatment	inhibits					Hmga2 gene	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_6_2296_s_307	14993269	A more recent study of the transcriptional inhibition of the  Hmga2 gene following TSA treatment has suggested that repression results from a decrease in Sp1 and Sp3 binding to the proximal promoter ( ).	bind
43240	4	11143	6	10	NULL	NULL	NULL	statement 3	Process		occurs due to					statement 1	Process	decrease in			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_6_2296_s_307	14993269	A more recent study of the transcriptional inhibition of the  Hmga2 gene following TSA treatment has suggested that repression results from a decrease in Sp1 and Sp3 binding to the proximal promoter ( ).	bind
43241	5	11143	6	10	NULL	NULL	NULL	statement 3	Process		occurs due to					statement 2	Process	decrease in			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_6_2296_s_307	14993269	A more recent study of the transcriptional inhibition of the  Hmga2 gene following TSA treatment has suggested that repression results from a decrease in Sp1 and Sp3 binding to the proximal promoter ( ).	bind
49494	1	11143	7	10	NULL	NULL	NULL	Sp1	GP		bind					 Hmga2 gene	GP	proximal		promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_6_2296_s_307	14993269	A more recent study of the transcriptional inhibition of the  Hmga2 gene following TSA treatment has suggested that repression results from a decrease in Sp1 and Sp3 binding to the proximal promoter ( ).	bind
49495	2	11143	7	10	NULL	NULL	NULL	Sp3	GP		bind					Hmga2 gene	GP	proximal		promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_6_2296_s_307	14993269	A more recent study of the transcriptional inhibition of the  Hmga2 gene following TSA treatment has suggested that repression results from a decrease in Sp1 and Sp3 binding to the proximal promoter ( ).	bind
49496	4	11143	7	10	NULL	NULL	NULL	statement 3	Process	decrease in	results in					statement 1	Process	decrease in			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_6_2296_s_307	14993269	A more recent study of the transcriptional inhibition of the  Hmga2 gene following TSA treatment has suggested that repression results from a decrease in Sp1 and Sp3 binding to the proximal promoter ( ).	bind
50309	3	11143	7	10	NULL	NULL	NULL	TSA	Chemical	treatment	inhibits					Hmga2 gene	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_6_2296_s_307	14993269	A more recent study of the transcriptional inhibition of the  Hmga2 gene following TSA treatment has suggested that repression results from a decrease in Sp1 and Sp3 binding to the proximal promoter ( ).	bind
43242	1	11144	6	10	NULL	NULL	NULL	ERalpha	GP		does not bind					DR1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_135	11452016	A more recent study showed that neither ERalpha nor ERbeta bound to DR1 or DR4, irrespective of the presence or absence of RXR ( 122).	bind
43243	2	11144	6	10	NULL	NULL	NULL	ERalpha	GP		does not bind					DR4	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_135	11452016	A more recent study showed that neither ERalpha nor ERbeta bound to DR1 or DR4, irrespective of the presence or absence of RXR ( 122).	bind
43244	3	11144	6	10	NULL	NULL	NULL	ERbeta	GP		does not bind					DR1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_135	11452016	A more recent study showed that neither ERalpha nor ERbeta bound to DR1 or DR4, irrespective of the presence or absence of RXR ( 122).	bind
43245	4	11144	6	10	NULL	NULL	NULL	ERbeta	GP		does not bind					DR4	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_135	11452016	A more recent study showed that neither ERalpha nor ERbeta bound to DR1 or DR4, irrespective of the presence or absence of RXR ( 122).	bind
49498	1	11144	7	10	NULL	NULL	NULL	ERalpha	GP		does not bind					DR1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_135	11452016	A more recent study showed that neither ERalpha nor ERbeta bound to DR1 or DR4, irrespective of the presence or absence of RXR ( 122).	bind
49499	2	11144	7	10	NULL	NULL	NULL	ERalpha	GP		does not bind					DR4	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_135	11452016	A more recent study showed that neither ERalpha nor ERbeta bound to DR1 or DR4, irrespective of the presence or absence of RXR ( 122).	bind
49500	3	11144	7	10	NULL	NULL	NULL	ERbeta	GP		does not bind					DR1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_135	11452016	A more recent study showed that neither ERalpha nor ERbeta bound to DR1 or DR4, irrespective of the presence or absence of RXR ( 122).	bind
49501	4	11144	7	10	NULL	NULL	NULL	ERbeta	GP		does not bind					DR4	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_2905_s_135	11452016	A more recent study showed that neither ERalpha nor ERbeta bound to DR1 or DR4, irrespective of the presence or absence of RXR ( 122).	bind
43246	1	11145	6	10	NULL	NULL	NULL	p53	GP	mutant	bind			core domain		p73	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18817_s_330	11893750	A more recent work has reported that the core domain of mutant p53 can either bind to p73 or to p63 ( 42).	bind
43247	2	11145	6	10	NULL	NULL	NULL	p53	GP	mutant	bind			core domain		p63	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18817_s_330	11893750	A more recent work has reported that the core domain of mutant p53 can either bind to p73 or to p63 ( 42).	bind
43248	3	11145	6	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18817_s_330	11893750	A more recent work has reported that the core domain of mutant p53 can either bind to p73 or to p63 ( 42).	bind
49502	1	11145	7	10	NULL	NULL	NULL	p53	GP	mutant	bind 			core domain		p73	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18817_s_330	11893750	A more recent work has reported that the core domain of mutant p53 can either bind to p73 or to p63 ( 42).	bind
49503	2	11145	7	10	NULL	NULL	NULL	p53	GP	mutant	bind			core domain		p63	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18817_s_330	11893750	A more recent work has reported that the core domain of mutant p53 can either bind to p73 or to p63 ( 42).	bind
49504	3	11145	7	10	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18817_s_330	11893750	A more recent work has reported that the core domain of mutant p53 can either bind to p73 or to p63 ( 42).	bind
43249	1	11146	6	10	NULL	NULL	NULL	B2	GP		bind					E2	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_gene_305_2_205_s_210	12609741	A more rigorous examination of the sequence recognition characteristics of human Sp1 compared to B2 was performed by mutating critical nucleotides known to be important for B2 binding to E2.	bind
49505	1	11146	7	10	NULL	NULL	NULL	 B2	GP		bind					E2	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_gene_305_2_205_s_210	12609741	A more rigorous examination of the sequence recognition characteristics of human Sp1 compared to B2 was performed by mutating critical nucleotides known to be important for B2 binding to E2.	bind
43250	1	11147	6	10	NULL	NULL	NULL	tubulin	GP		bind					stathmin	GP		N-terminal extension of the core		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_10_6841_s_259	10702243	A more seducing hypothesis could be that tubulin binding to stathmin may occur in two different ways, an "`N way"` and a "`C way,"` in which either an N- or a C-terminal extension of the core would allow binding of stathmin to tubulin.	bind
50310	2	11147	6	10	NULL	NULL	NULL	tubulin	GP		bind					stathmin	GP		C-terminal extension of the core		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_10_6841_s_259	10702243	A more seducing hypothesis could be that tubulin binding to stathmin may occur in two different ways, an "`N way"` and a "`C way,"` in which either an N- or a C-terminal extension of the core would allow binding of stathmin to tubulin.	bind
49506	1	11147	7	10	NULL	NULL	NULL	tubulin	GP		bind					stathmin	GP		N-terminal extension of the core		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_10_6841_s_259	10702243	A more seducing hypothesis could be that tubulin binding to stathmin may occur in two different ways, an "`N way"` and a "`C way,"` in which either an N- or a C-terminal extension of the core would allow binding of stathmin to tubulin.	bind
49507	2	11147	7	10	NULL	NULL	NULL	tubulin 	GP		bind					stathmin	GP		C-terminal extension of the core		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_10_6841_s_259	10702243	A more seducing hypothesis could be that tubulin binding to stathmin may occur in two different ways, an "`N way"` and a "`C way,"` in which either an N- or a C-terminal extension of the core would allow binding of stathmin to tubulin.	bind
43251	1	11148	6	10	NULL	NULL	NULL	UmuD``C	GP		bind					M13 DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_18_10767_s_185	8631887	A more sensitive measurement for  the binding of UmuD``C to M13 DNA was performed using fluorescence  depolarization, see  e.g. Refs.	bind
49508	1	11148	7	10	NULL	NULL	NULL	UmuD``C	GP		bind					M13 DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_18_10767_s_185	8631887	A more sensitive measurement for  the binding of UmuD``C to M13 DNA was performed using fluorescence  depolarization, see  e.g. Refs.	bind
43252	1	11149	6	10	NULL	NULL	NULL	NGF	GP		bind					TrkA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_16_24_7950_s_215	8987823	A more slowly migrating band represents NGF bound to TrkA in an undefined oligomeric complex.	bind
49509	1	11149	7	10	NULL	NULL	NULL	NGF	GP		bind					TrkA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_16_24_7950_s_215	8987823	A more slowly migrating band represents NGF bound to TrkA in an undefined oligomeric complex.	bind
43342	1	11150	6	10	NULL	NULL	NULL	HIF-1	GP		is					hypoxia-inducible factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_3_329_s_204	10024307	A more specific mechanism of hypoxia-induced gene expression might involve the transcription factor hypoxia-inducible factor or HIF-1, which binds to identified hypoxia-sensitive elements in the promoter of several hypoxia-inducible genes.	bind
43343	2	11150	6	10	NULL	NULL	NULL	HIF-1	GP		bind					hypoxia-inducible genes	GP			hypoxia-sensitive element of promoter	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_3_329_s_204	10024307	A more specific mechanism of hypoxia-induced gene expression might involve the transcription factor hypoxia-inducible factor or HIF-1, which binds to identified hypoxia-sensitive elements in the promoter of several hypoxia-inducible genes.	bind
50311	3	11150	6	10	NULL	NULL	NULL	HIF-1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_3_329_s_204	10024307	A more specific mechanism of hypoxia-induced gene expression might involve the transcription factor hypoxia-inducible factor or HIF-1, which binds to identified hypoxia-sensitive elements in the promoter of several hypoxia-inducible genes.	bind
49511	1	11150	7	10	NULL	NULL	NULL	 HIF-1	GP		bind					hypoxia-inducible genes	GP			hypoxia-sensitive elements in the promoter	NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_3_329_s_204	10024307	A more specific mechanism of hypoxia-induced gene expression might involve the transcription factor hypoxia-inducible factor or HIF-1, which binds to identified hypoxia-sensitive elements in the promoter of several hypoxia-inducible genes.	bind
49512	2	11150	7	10	NULL	NULL	NULL	HIF-1	GP		is					hypoxia-inducible factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_3_329_s_204	10024307	A more specific mechanism of hypoxia-induced gene expression might involve the transcription factor hypoxia-inducible factor or HIF-1, which binds to identified hypoxia-sensitive elements in the promoter of several hypoxia-inducible genes.	bind
49513	3	11150	7	10	NULL	NULL	NULL	HIF-1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_84_3_329_s_204	10024307	A more specific mechanism of hypoxia-induced gene expression might involve the transcription factor hypoxia-inducible factor or HIF-1, which binds to identified hypoxia-sensitive elements in the promoter of several hypoxia-inducible genes.	bind
43253	1	11152	6	10	NULL	NULL	NULL	PFA	Chemical		bind					RT	GP		catalytic site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_38_27744_s_229	16829515	A more suitable explanation would be that PFA and the incoming dNTP bind to the catalytic site of RT but to different mechanistic forms of the enzyme in such a way that they do not compete with each other ( ).	bind
43254	2	11152	6	10	NULL	NULL	NULL	dNTP	Chemical		bind					RT	GP		catalytic site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_38_27744_s_229	16829515	A more suitable explanation would be that PFA and the incoming dNTP bind to the catalytic site of RT but to different mechanistic forms of the enzyme in such a way that they do not compete with each other ( ).	bind
51519	3	11152	6	10	NULL	NULL	NULL	statement 1	Process		does not compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_38_27744_s_229	16829515	A more suitable explanation would be that PFA and the incoming dNTP bind to the catalytic site of RT but to different mechanistic forms of the enzyme in such a way that they do not compete with each other ( ).	bind
49566	1	11152	7	10	NULL	NULL	NULL	PFA 	Chemical		bind					RT	GP		catalytic site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_38_27744_s_229	16829515	A more suitable explanation would be that PFA and the incoming dNTP bind to the catalytic site of RT but to different mechanistic forms of the enzyme in such a way that they do not compete with each other ( ).	bind
49567	2	11152	7	10	NULL	NULL	NULL	dNTP	Chemical		bind					RT	GP		catalytic site		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_38_27744_s_229	16829515	A more suitable explanation would be that PFA and the incoming dNTP bind to the catalytic site of RT but to different mechanistic forms of the enzyme in such a way that they do not compete with each other ( ).	bind
49568	3	11152	7	10	NULL	NULL	NULL	statement 1	Process		does not compete with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_38_27744_s_229	16829515	A more suitable explanation would be that PFA and the incoming dNTP bind to the catalytic site of RT but to different mechanistic forms of the enzyme in such a way that they do not compete with each other ( ).	bind
44280	1	11153	6	10	NULL	NULL	NULL	amphiphysin	GP		bind					clathrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5425_215_s_218	10398591	A motif L(L or I)(D, E, or N)(L or F)(D or E) (21) in the beta subunits of APs, the nonvisual arrestins, and amphiphysin (which also binds clathrin) is likely to account for the ability of these different proteins to bind clathrin.	bind
44281	2	11153	6	NULL	NULL	0	NULL	APs	NULL		is a type of	NULL				nonvisual arrestin	NULL				NULL		0	NULL	NULL	NULL	gw60_science_285_5425_215_s_218	10398591	A motif L(L or I)(D, E, or N)(L or F)(D or E) (21) in the beta subunits of APs, the nonvisual arrestins, and amphiphysin (which also binds clathrin) is likely to account for the ability of these different proteins to bind clathrin.	bind
44282	3	11153	6	NULL	NULL	0	NULL	APs	NULL		bind	NULL				clathrin	NULL				NULL		0	NULL	NULL	NULL	gw60_science_285_5425_215_s_218	10398591	A motif L(L or I)(D, E, or N)(L or F)(D or E) (21) in the beta subunits of APs, the nonvisual arrestins, and amphiphysin (which also binds clathrin) is likely to account for the ability of these different proteins to bind clathrin.	bind
44283	4	11153	6	NULL	NULL	0	NULL	amphiphysin	NULL		plays a role in	NULL		motif L in the beta subunit		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_science_285_5425_215_s_218	10398591	A motif L(L or I)(D, E, or N)(L or F)(D or E) (21) in the beta subunits of APs, the nonvisual arrestins, and amphiphysin (which also binds clathrin) is likely to account for the ability of these different proteins to bind clathrin.	bind
44284	5	11153	6	NULL	NULL	0	NULL	APs	NULL		plays a role in	NULL		motif L in the beta subunit		statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_science_285_5425_215_s_218	10398591	A motif L(L or I)(D, E, or N)(L or F)(D or E) (21) in the beta subunits of APs, the nonvisual arrestins, and amphiphysin (which also binds clathrin) is likely to account for the ability of these different proteins to bind clathrin.	bind
49569	1	11153	7	NULL	NULL	0	NULL	 APs	NULL		bind	NULL				clathrin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5425_215_s_218	10398591	A motif L(L or I)(D, E, or N)(L or F)(D or E) (21) in the beta subunits of APs, the nonvisual arrestins, and amphiphysin (which also binds clathrin) is likely to account for the ability of these different proteins to bind clathrin.	bind
49570	2	11153	7	NULL	NULL	0	NULL	 amphiphysin	NULL		bind	NULL				clathrin	NULL				NULL		0	NULL	NULL	NULL	gw60_science_285_5425_215_s_218	10398591	A motif L(L or I)(D, E, or N)(L or F)(D or E) (21) in the beta subunits of APs, the nonvisual arrestins, and amphiphysin (which also binds clathrin) is likely to account for the ability of these different proteins to bind clathrin.	bind
49571	3	11153	7	NULL	NULL	0	NULL	APs	NULL		is responsible for	NULL		motif L  in the beta subunits 		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_science_285_5425_215_s_218	10398591	A motif L(L or I)(D, E, or N)(L or F)(D or E) (21) in the beta subunits of APs, the nonvisual arrestins, and amphiphysin (which also binds clathrin) is likely to account for the ability of these different proteins to bind clathrin.	bind
49572	4	11153	7	NULL	NULL	0	NULL	APs	NULL		is required for	NULL		motifs I in the beta subunit		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_science_285_5425_215_s_218	10398591	A motif L(L or I)(D, E, or N)(L or F)(D or E) (21) in the beta subunits of APs, the nonvisual arrestins, and amphiphysin (which also binds clathrin) is likely to account for the ability of these different proteins to bind clathrin.	bind
49573	5	11153	7	NULL	NULL	0	NULL	statement 3	NULL		is an alternative to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_science_285_5425_215_s_218	10398591	A motif L(L or I)(D, E, or N)(L or F)(D or E) (21) in the beta subunits of APs, the nonvisual arrestins, and amphiphysin (which also binds clathrin) is likely to account for the ability of these different proteins to bind clathrin.	bind
49574	6	11153	7	NULL	NULL	0	NULL	APs	NULL		is required for	NULL		motif D in the beta subunits		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5425_215_s_218	10398591	A motif L(L or I)(D, E, or N)(L or F)(D or E) (21) in the beta subunits of APs, the nonvisual arrestins, and amphiphysin (which also binds clathrin) is likely to account for the ability of these different proteins to bind clathrin.	bind
49575	7	11153	7	NULL	NULL	0	NULL	APs	NULL		is required for	NULL		motif E in the beta subunit		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5425_215_s_218	10398591	A motif L(L or I)(D, E, or N)(L or F)(D or E) (21) in the beta subunits of APs, the nonvisual arrestins, and amphiphysin (which also binds clathrin) is likely to account for the ability of these different proteins to bind clathrin.	bind
49576	8	11153	7	NULL	NULL	0	NULL	AP	NULL		is required for	NULL		motif N in the beta subunit		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_science_285_5425_215_s_218	10398591	A motif L(L or I)(D, E, or N)(L or F)(D or E) (21) in the beta subunits of APs, the nonvisual arrestins, and amphiphysin (which also binds clathrin) is likely to account for the ability of these different proteins to bind clathrin.	bind
49577	9	11153	7	NULL	NULL	0	NULL	statement 6	NULL		is an alternative to	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_science_285_5425_215_s_218	10398591	A motif L(L or I)(D, E, or N)(L or F)(D or E) (21) in the beta subunits of APs, the nonvisual arrestins, and amphiphysin (which also binds clathrin) is likely to account for the ability of these different proteins to bind clathrin.	bind
49578	10	11153	7	NULL	NULL	0	NULL	statement 7	NULL		is an alternative to	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw60_science_285_5425_215_s_218	10398591	A motif L(L or I)(D, E, or N)(L or F)(D or E) (21) in the beta subunits of APs, the nonvisual arrestins, and amphiphysin (which also binds clathrin) is likely to account for the ability of these different proteins to bind clathrin.	bind
49579	11	11153	7	10	NULL	0	NULL	APs	NULL		is a type of	NULL				nonvisual arrestins	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5425_215_s_218	10398591	A motif L(L or I)(D, E, or N)(L or F)(D or E) (21) in the beta subunits of APs, the nonvisual arrestins, and amphiphysin (which also binds clathrin) is likely to account for the ability of these different proteins to bind clathrin.	bind
49581	13	11153	7	NULL	NULL	0	NULL	APs	NULL		is required for	NULL		motif F in the beta subunit		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_science_285_5425_215_s_218	10398591	A motif L(L or I)(D, E, or N)(L or F)(D or E) (21) in the beta subunits of APs, the nonvisual arrestins, and amphiphysin (which also binds clathrin) is likely to account for the ability of these different proteins to bind clathrin.	bind
49582	14	11153	7	NULL	NULL	0	NULL	statement 3	NULL		is an alternative to	NULL				statement 13	NULL				NULL		0	NULL	NULL	NULL	gw60_science_285_5425_215_s_218	10398591	A motif L(L or I)(D, E, or N)(L or F)(D or E) (21) in the beta subunits of APs, the nonvisual arrestins, and amphiphysin (which also binds clathrin) is likely to account for the ability of these different proteins to bind clathrin.	bind
43271	1	11154	6	10	NULL	NULL	NULL	E2F-1	GP		bind			\tY(X7)E(X3)DLF motif		Rb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_288	12944478	A motif with a similar format, described as Y(X7)E(X3)DLF, has been proposed to be involved in the binding of E2F-1 and NF-IL-6 (C/EBPbeta) to Rb ( 8).	bind
43272	2	11154	6	10	NULL	NULL	NULL	NF-IL-6 (C/EBPbeta)	GP		bind			\tY(X7)E(X3)DLF motif		Rb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_288	12944478	A motif with a similar format, described as Y(X7)E(X3)DLF, has been proposed to be involved in the binding of E2F-1 and NF-IL-6 (C/EBPbeta) to Rb ( 8).	bind
49585	1	11154	7	10	NULL	NULL	NULL	E2F-1 	GP		bind			\tY(X7)E(X3)DLF motif		Rb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_288	12944478	A motif with a similar format, described as Y(X7)E(X3)DLF, has been proposed to be involved in the binding of E2F-1 and NF-IL-6 (C/EBPbeta) to Rb ( 8).	bind
49586	2	11154	7	10	NULL	NULL	NULL	NF-IL-6 (C/EBPbeta)	GP		bind			\tY(X7)E(X3)DLF motif		Rb	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_18_6520_s_288	12944478	A motif with a similar format, described as Y(X7)E(X3)DLF, has been proposed to be involved in the binding of E2F-1 and NF-IL-6 (C/EBPbeta) to Rb ( 8).	bind
43274	1	11155	6	10	NULL	NULL	NULL	Cdk complex	GP		contains					cyclins A	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7488_s_299	14559997	A motif within the N terminus of Cdc25A confers binding of Cdc25A to Cdk complexes containing cyclins A and E but not B1 ( ).	bind
43275	2	11155	6	10	NULL	NULL	NULL	Cdk complex	GP		contains					cyclin E	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7488_s_299	14559997	A motif within the N terminus of Cdc25A confers binding of Cdc25A to Cdk complexes containing cyclins A and E but not B1 ( ).	bind
43276	3	11155	6	10	NULL	NULL	NULL	Cdk complex	GP		contain					cyclin B1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7488_s_299	14559997	A motif within the N terminus of Cdc25A confers binding of Cdc25A to Cdk complexes containing cyclins A and E but not B1 ( ).	bind
43695	4	11155	6	10	NULL	NULL	NULL	Cdc25A	GP		bind			motif within N terminus		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7488_s_299	14559997	A motif within the N terminus of Cdc25A confers binding of Cdc25A to Cdk complexes containing cyclins A and E but not B1 ( ).	bind
43698	5	11155	6	10	NULL	NULL	NULL	Cdc25A	GP		bind			motif within N terminus		statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7488_s_299	14559997	A motif within the N terminus of Cdc25A confers binding of Cdc25A to Cdk complexes containing cyclins A and E but not B1 ( ).	bind
51520	6	11155	6	10	NULL	NULL	NULL	Cdc25A	GP		does not bind			motif within N terminus		statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7488_s_299	14559997	A motif within the N terminus of Cdc25A confers binding of Cdc25A to Cdk complexes containing cyclins A and E but not B1 ( ).	bind
49593	1	11155	7	10	NULL	NULL	NULL	Cdk complex	GP		contains					cyclins A	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7488_s_299	14559997	A motif within the N terminus of Cdc25A confers binding of Cdc25A to Cdk complexes containing cyclins A and E but not B1 ( ).	bind
49594	2	11155	7	10	NULL	NULL	NULL	Cdk complex	GP		contains					cyclins E	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7488_s_299	14559997	A motif within the N terminus of Cdc25A confers binding of Cdc25A to Cdk complexes containing cyclins A and E but not B1 ( ).	bind
49596	3	11155	7	10	NULL	NULL	NULL	Cdk complex	GP		contains					cyclin B1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7488_s_299	14559997	A motif within the N terminus of Cdc25A confers binding of Cdc25A to Cdk complexes containing cyclins A and E but not B1 ( ).	bind
49597	4	11155	7	10	NULL	NULL	NULL	Cdc25A	GP		bind			motif within the N terminus		statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7488_s_299	14559997	A motif within the N terminus of Cdc25A confers binding of Cdc25A to Cdk complexes containing cyclins A and E but not B1 ( ).	bind
49599	5	11155	7	10	NULL	NULL	NULL	Cdc25A	GP		bind			motif within the N terminus		statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7488_s_299	14559997	A motif within the N terminus of Cdc25A confers binding of Cdc25A to Cdk complexes containing cyclins A and E but not B1 ( ).	bind
49600	6	11155	7	10	NULL	NULL	NULL	Cdc25A	GP		does not bind			motif within the N terminus		statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_21_7488_s_299	14559997	A motif within the N terminus of Cdc25A confers binding of Cdc25A to Cdk complexes containing cyclins A and E but not B1 ( ).	bind
43700	1	11157	6	10	NULL	NULL	NULL	fVII	GP	mouse	bind		tightly	targeting domain		tissue factor	GP	human			NULL	tumor cells	NULL	NULL	NULL	NULL	gw60_pnas_97_16_9221_s_155	10922073	A mouse fVII targeting domain was used for the experiments involving human tumor xenografts growing in SCID mice, because it binds tightly both to human tissue factor on the tumor cells and to mouse tissue factor on the mouse endothelial cells in the tumor vasculature.	bind
44287	2	11157	6	10	NULL	NULL	NULL	fVII	GP	mouse	bind		tightly	targeting domain		tissue factor	GP	mouse			NULL	mouse endothelial cells in the tumor vasculature	NULL	NULL	NULL	NULL	gw60_pnas_97_16_9221_s_155	10922073	A mouse fVII targeting domain was used for the experiments involving human tumor xenografts growing in SCID mice, because it binds tightly both to human tissue factor on the tumor cells and to mouse tissue factor on the mouse endothelial cells in the tumor vasculature.	bind
49601	1	11157	7	10	NULL	NULL	NULL	 fVII	GP	mouse	bind		tightly	targeting domain		tissue factor	GP	human			NULL	tumor cells	NULL	NULL	NULL	NULL	gw60_pnas_97_16_9221_s_155	10922073	A mouse fVII targeting domain was used for the experiments involving human tumor xenografts growing in SCID mice, because it binds tightly both to human tissue factor on the tumor cells and to mouse tissue factor on the mouse endothelial cells in the tumor vasculature.	bind
49603	2	11157	7	10	NULL	NULL	NULL	fVII	GP	mouse	bind		tightly	targeting domain		tissue factor	GP	mouse			NULL	mouse endothelial cells in the tumor vasculature	NULL	NULL	NULL	NULL	gw60_pnas_97_16_9221_s_155	10922073	A mouse fVII targeting domain was used for the experiments involving human tumor xenografts growing in SCID mice, because it binds tightly both to human tissue factor on the tumor cells and to mouse tissue factor on the mouse endothelial cells in the tumor vasculature.	bind
43707	1	11159	6	10	NULL	NULL	NULL	cGMP	Chemical		bind					PDE5	GP		GAF A domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_22_3_469_s_88	12554648	A mouse monoclonal antibody specifically blocks cGMP binding to the GAF A domain of PDE5   he previous studies showed that a short pre-incubation of PDE5 with cGMP on ice did not cause PDE5 phosphorylation, but was sufficient to induce PDE5 activation.	bind
43709	2	11159	6	10	NULL	NULL	NULL	monoclonal antibody	GP	mouse	blocks		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_3_469_s_88	12554648	A mouse monoclonal antibody specifically blocks cGMP binding to the GAF A domain of PDE5   he previous studies showed that a short pre-incubation of PDE5 with cGMP on ice did not cause PDE5 phosphorylation, but was sufficient to induce PDE5 activation.	bind
49604	1	11159	7	10	NULL	NULL	NULL	cGMP	Chemical		bind					PDE5	GP		GAF A domain		NULL		NULL	NULL	NULL	NULL	gw60_embo_22_3_469_s_88	12554648	A mouse monoclonal antibody specifically blocks cGMP binding to the GAF A domain of PDE5   he previous studies showed that a short pre-incubation of PDE5 with cGMP on ice did not cause PDE5 phosphorylation, but was sufficient to induce PDE5 activation.	bind
49605	2	11159	7	10	NULL	NULL	NULL	monoclonal antibody	GP	mouse	blocks		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_22_3_469_s_88	12554648	A mouse monoclonal antibody specifically blocks cGMP binding to the GAF A domain of PDE5   he previous studies showed that a short pre-incubation of PDE5 with cGMP on ice did not cause PDE5 phosphorylation, but was sufficient to induce PDE5 activation.	bind
44288	1	11162	6	NULL	NULL	0	NULL		NULL		bind	NULL	covalently	N of Lys216		retina	NULL		C-15		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1565_2_144_s_243	12409192	A movement of the side chain atoms may have been anticipated from the fact that N  of Lys216 (i.e. the Schiff base nitrogen) is covalently bound to C15 of the retinal ( Fig. 2A) and necessarily undergoes a significant movement in response to photoisomerization about the C13=C14 bond.	bind
51521	2	11162	6	10	NULL	NULL	NULL	N of Lys216	Chemical		is					Schiff base nitrogen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1565_2_144_s_243	12409192	A movement of the side chain atoms may have been anticipated from the fact that N  of Lys216 (i.e. the Schiff base nitrogen) is covalently bound to C15 of the retinal ( Fig. 2A) and necessarily undergoes a significant movement in response to photoisomerization about the C13=C14 bond.	bind
49606	1	11162	7	10	NULL	0	NULL		NULL		bind	NULL	covalently	N of Lys216		retinal 	NULL		C15		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1565_2_144_s_243	12409192	A movement of the side chain atoms may have been anticipated from the fact that N  of Lys216 (i.e. the Schiff base nitrogen) is covalently bound to C15 of the retinal ( Fig. 2A) and necessarily undergoes a significant movement in response to photoisomerization about the C13=C14 bond.	bind
49607	2	11162	7	10	NULL	NULL	NULL	N of Lys216	Chemical		is					Schiff base nitrogen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1565_2_144_s_243	12409192	A movement of the side chain atoms may have been anticipated from the fact that N  of Lys216 (i.e. the Schiff base nitrogen) is covalently bound to C15 of the retinal ( Fig. 2A) and necessarily undergoes a significant movement in response to photoisomerization about the C13=C14 bond.	bind
51522	1	11163	6	10	NULL	NULL	NULL	MTase	GP		is associated with					restriction endonuclease	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1491_s_270	11266551	A MTase not long ago associated with a restriction endonuclease may momentarily exist alone, before selective pressures swallow it as well.	bind
49608	1	11163	7	10	NULL	NULL	NULL	MTase	GP		is associated with					restriction endonuclease	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_7_1491_s_270	11266551	A MTase not long ago associated with a restriction endonuclease may momentarily exist alone, before selective pressures swallow it as well.	bind
43711	2	11164	6	10	NULL	NULL	NULL	TFIIIA	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_33_21352_s_172	9694896	A much different situation was found for TFIIIA binding to 5 S DNA assembled into a complete nucleosome.	bind
43712	1	11164	6	10	NULL	NULL	NULL	5S DNA	NucleicAcid		is assembled into					nucleosome	Chromosome				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_33_21352_s_172	9694896	A much different situation was found for TFIIIA binding to 5 S DNA assembled into a complete nucleosome.	bind
49609	2	11164	7	NULL	NULL	0	NULL	 TFIIIA	NULL		bind	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_33_21352_s_172	9694896	A much different situation was found for TFIIIA binding to 5 S DNA assembled into a complete nucleosome.	bind
49610	1	11164	7	10	NULL	NULL	NULL	5 S DNA	NucleicAcid		assemble into					nucleosome	Chromosome				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_33_21352_s_172	9694896	A much different situation was found for TFIIIA binding to 5 S DNA assembled into a complete nucleosome.	bind
44289	1	11165	6	10	NULL	NULL	NULL	GP63	GP	glycosylated	bind					ConA	GP	WT;;promastigotes			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_31_27968_s_185	12029085	A much higher level of glycosylated GP63 bound to ConA from WT promastigotes ( lane 1) than delta gpi8 cells ( lane 2).	bind
44290	2	11165	6	10	NULL	NULL	NULL	GP63	GP	glycosylated	bind					ConA	GP	delta gpi8 cells			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_31_27968_s_185	12029085	A much higher level of glycosylated GP63 bound to ConA from WT promastigotes ( lane 1) than delta gpi8 cells ( lane 2).	bind
44291	3	11165	6	10	NULL	NULL	NULL	statement 1	Process		is higher than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_31_27968_s_185	12029085	A much higher level of glycosylated GP63 bound to ConA from WT promastigotes ( lane 1) than delta gpi8 cells ( lane 2).	bind
49611	1	11165	7	10	NULL	NULL	NULL	GP63	GP	glycosylated	bind					ConA	GP	WT;;promastigotes			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_31_27968_s_185	12029085	A much higher level of glycosylated GP63 bound to ConA from WT promastigotes ( lane 1) than delta gpi8 cells ( lane 2).	bind
49612	2	11165	7	10	NULL	NULL	NULL	GP63	GP	glycosylated	bind					ConA	GP	 delta gpi8 cells 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_31_27968_s_185	12029085	A much higher level of glycosylated GP63 bound to ConA from WT promastigotes ( lane 1) than delta gpi8 cells ( lane 2).	bind
49613	3	11165	7	10	NULL	NULL	NULL	statement 1	Process		is higher than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_31_27968_s_185	12029085	A much higher level of glycosylated GP63 bound to ConA from WT promastigotes ( lane 1) than delta gpi8 cells ( lane 2).	bind
43713	1	11166	6	10	NULL	NULL	NULL	CDK2	GP		bind					p27	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_52_52052_s_70	14551212	A much smaller fraction of CDK2 was bound to p27.	bind
49614	1	11166	7	10	NULL	NULL	NULL	 CDK2 	GP		bind					p27	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_52_52052_s_70	14551212	A much smaller fraction of CDK2 was bound to p27.	bind
43714	1	11168	6	10	NULL	NULL	NULL	GTP	Chemical		bind					Rac	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_22_6527_s_87	9822598	A much weaker interaction was detected with the GTP-bound form of Rac, and no binding was observed with Rho.	bind
49616	1	11168	7	10	NULL	NULL	NULL	GTP	Chemical		bind					Rac	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_22_6527_s_87	9822598	A much weaker interaction was detected with the GTP-bound form of Rac, and no binding was observed with Rho.	bind
43715	1	11169	6	10	NULL	NULL	NULL	ORC	GP		is					origin recognition complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_4_3_238_s_10	7857395	A multi-protein origin recognition complex (ORC), which binds specifically to yeast replication origins, has been shown to play a key role in transcriptional silencing as well as in DNA replication      [2-6]  .	bind
43716	2	11169	6	10	NULL	NULL	NULL	ORC	GP		bind		specifically			replication origin	NucleicAcid	Yeast			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_4_3_238_s_10	7857395	A multi-protein origin recognition complex (ORC), which binds specifically to yeast replication origins, has been shown to play a key role in transcriptional silencing as well as in DNA replication      [2-6]  .	bind
43717	3	11169	6	10	NULL	NULL	NULL	statement 2	Process		plays a role in					transcription	Process	silencing of			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_4_3_238_s_10	7857395	A multi-protein origin recognition complex (ORC), which binds specifically to yeast replication origins, has been shown to play a key role in transcriptional silencing as well as in DNA replication      [2-6]  .	bind
43718	4	11169	6	10	NULL	NULL	NULL	ORC	GP		plays a role in					DNA 	NucleicAcid	replication of			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_4_3_238_s_10	7857395	A multi-protein origin recognition complex (ORC), which binds specifically to yeast replication origins, has been shown to play a key role in transcriptional silencing as well as in DNA replication      [2-6]  .	bind
49617	1	11169	7	10	NULL	NULL	NULL	ORC	GP		bind		specifically			 replication origins	NucleicAcid	yeast			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_4_3_238_s_10	7857395	A multi-protein origin recognition complex (ORC), which binds specifically to yeast replication origins, has been shown to play a key role in transcriptional silencing as well as in DNA replication      [2-6]  .	bind
49618	2	11169	7	10	NULL	NULL	NULL	statement 1	Process		play a key role in					transcription	Process	silencing of			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_4_3_238_s_10	7857395	A multi-protein origin recognition complex (ORC), which binds specifically to yeast replication origins, has been shown to play a key role in transcriptional silencing as well as in DNA replication      [2-6]  .	bind
49619	3	11169	7	10	NULL	NULL	NULL	statement 1	Process		play a key role in					DNA 	NucleicAcid	replication of			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_4_3_238_s_10	7857395	A multi-protein origin recognition complex (ORC), which binds specifically to yeast replication origins, has been shown to play a key role in transcriptional silencing as well as in DNA replication      [2-6]  .	bind
49620	4	11169	7	10	NULL	NULL	NULL	ORC	GP		is					origin recognition complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_4_3_238_s_10	7857395	A multi-protein origin recognition complex (ORC), which binds specifically to yeast replication origins, has been shown to play a key role in transcriptional silencing as well as in DNA replication      [2-6]  .	bind
43719	1	11170	6	10	NULL	NULL	NULL	CD28RC	GP		bind		cooperatively			CD28RE	NucleicAcid			TRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_1_552_s_105	9417115	A multicomponent affinity-purified complex (CD28RC) binds cooperatively to the CD28RE-TRE and makes extensive contacts with the CD28RE-TRE sequence.	bind
51523	2	11170	6	10	NULL	NULL	NULL	CD28RC	GP		is a type of					multicomponent affinity-purified complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_1_552_s_105	9417115	A multicomponent affinity-purified complex (CD28RC) binds cooperatively to the CD28RE-TRE and makes extensive contacts with the CD28RE-TRE sequence.	bind
49621	1	11170	7	10	NULL	NULL	NULL	CD28RC	GP		bind		cooperatively			CD28RE	GP			TRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_1_552_s_105	9417115	A multicomponent affinity-purified complex (CD28RC) binds cooperatively to the CD28RE-TRE and makes extensive contacts with the CD28RE-TRE sequence.	bind
49622	2	11170	7	10	NULL	NULL	NULL	statement 1	Process		contact with		extensively			CD28RE	NucleicAcid	sequence of		TRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_1_552_s_105	9417115	A multicomponent affinity-purified complex (CD28RC) binds cooperatively to the CD28RE-TRE and makes extensive contacts with the CD28RE-TRE sequence.	bind
49623	3	11170	7	10	NULL	NULL	NULL	CD28RC	GP		is a type of					multicomponent affinity-purified complex 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_1_552_s_105	9417115	A multicomponent affinity-purified complex (CD28RC) binds cooperatively to the CD28RE-TRE and makes extensive contacts with the CD28RE-TRE sequence.	bind
43720	1	11171	6	10	NULL	NULL	NULL	cyt bo3	GP		bind					ubiquinone-2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_25_16879_s_33	16624801	A multifrequency (9, 34, and 94 GHz) EPR study was performed with cyt  bo3 bound to ubiquinone-2 selectively labeled with 13C at either the 1- or the 4-carbonyl carbons ( ).	bind
49624	1	11171	7	10	NULL	NULL	NULL	cyt bo3	GP		bind					ubiquinone-2	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_25_16879_s_33	16624801	A multifrequency (9, 34, and 94 GHz) EPR study was performed with cyt  bo3 bound to ubiquinone-2 selectively labeled with 13C at either the 1- or the 4-carbonyl carbons ( ).	bind
43721	1	11172	6	10	NULL	NULL	NULL	Tek	GP		is required for			Tyr;; C-terminal		Grb2	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_43_30896_s_262	10521483	A multifunctional docking site, Tyr, is also present in the C-terminal tail of Tek, and this site is required for binding of Grb2 and Grb7 as well as phosphorylation of both Grb7 and p85.	bind
43722	2	11172	6	10	NULL	NULL	NULL	Tek	GP		is required for			Tyr;; C-terminal		Grb7	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_43_30896_s_262	10521483	A multifunctional docking site, Tyr, is also present in the C-terminal tail of Tek, and this site is required for binding of Grb2 and Grb7 as well as phosphorylation of both Grb7 and p85.	bind
43723	3	11172	6	10	NULL	NULL	NULL	Tek	GP		is required for			Tyr;; C-terminal		Grb7	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_43_30896_s_262	10521483	A multifunctional docking site, Tyr, is also present in the C-terminal tail of Tek, and this site is required for binding of Grb2 and Grb7 as well as phosphorylation of both Grb7 and p85.	bind
43724	4	11172	6	10	NULL	NULL	NULL	Tek	GP		is required for			Tyr;; C-terminal		p85	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_43_30896_s_262	10521483	A multifunctional docking site, Tyr, is also present in the C-terminal tail of Tek, and this site is required for binding of Grb2 and Grb7 as well as phosphorylation of both Grb7 and p85.	bind
51524	5	11172	6	10	NULL	NULL	NULL	Tek	GP		is a type of			Tyr;; C-terminal		multifunctional docking site	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_43_30896_s_262	10521483	A multifunctional docking site, Tyr, is also present in the C-terminal tail of Tek, and this site is required for binding of Grb2 and Grb7 as well as phosphorylation of both Grb7 and p85.	bind
49626	1	11172	7	10	NULL	NULL	NULL	Tek	GP		is required for			Tyr;; C-terminal		Grb2	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_43_30896_s_262	10521483	A multifunctional docking site, Tyr, is also present in the C-terminal tail of Tek, and this site is required for binding of Grb2 and Grb7 as well as phosphorylation of both Grb7 and p85.	bind
49627	2	11172	7	10	NULL	NULL	NULL	Tek	GP		is required for			Tyr;; C-terminal		Grb7	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_43_30896_s_262	10521483	A multifunctional docking site, Tyr, is also present in the C-terminal tail of Tek, and this site is required for binding of Grb2 and Grb7 as well as phosphorylation of both Grb7 and p85.	bind
49628	3	11172	7	10	NULL	NULL	NULL	Tek	GP		is required for			Tyr;; C-terminal		 Grb7	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_43_30896_s_262	10521483	A multifunctional docking site, Tyr, is also present in the C-terminal tail of Tek, and this site is required for binding of Grb2 and Grb7 as well as phosphorylation of both Grb7 and p85.	bind
49629	4	11172	7	10	NULL	NULL	NULL	Tek	GP		is required for			Tyr;; C-terminal		p85	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_43_30896_s_262	10521483	A multifunctional docking site, Tyr, is also present in the C-terminal tail of Tek, and this site is required for binding of Grb2 and Grb7 as well as phosphorylation of both Grb7 and p85.	bind
49630	5	11172	7	10	NULL	NULL	NULL	Tek	GP		is a type of			Tyr;; C-terminal		multifunctional docking site	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_43_30896_s_262	10521483	A multifunctional docking site, Tyr, is also present in the C-terminal tail of Tek, and this site is required for binding of Grb2 and Grb7 as well as phosphorylation of both Grb7 and p85.	bind
43800	1	11173	6	10	NULL	NULL	NULL	exportin 1	GP		is 					CRM1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8751_s_1	14612415	A multifunctional domain in human CRM1 (exportin 1) mediates RanBP3 binding and multimerization of human T-cell leukemia virus type 1 Rex protein.	bind
43801	2	11173	6	10	NULL	NULL	NULL	CRM1	GP	human	mediates					Rex protein	GP	multimerization of;;human T-cell leukemia virus type 1			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8751_s_1	14612415	A multifunctional domain in human CRM1 (exportin 1) mediates RanBP3 binding and multimerization of human T-cell leukemia virus type 1 Rex protein.	bind
43802	3	11173	6	10	NULL	NULL	NULL	CRM1	GP	human	mediates					RanBP3	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8751_s_1	14612415	A multifunctional domain in human CRM1 (exportin 1) mediates RanBP3 binding and multimerization of human T-cell leukemia virus type 1 Rex protein.	bind
49631	1	11173	7	10	NULL	NULL	NULL	CRM1	GP	human	mediates					RanBP3	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8751_s_1	14612415	A multifunctional domain in human CRM1 (exportin 1) mediates RanBP3 binding and multimerization of human T-cell leukemia virus type 1 Rex protein.	bind
49632	2	11173	7	10	NULL	NULL	NULL	CRM1	GP	human	mediates					Rex protein	GP	multimerization of;;human T-cell leukemia virus type 1			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8751_s_1	14612415	A multifunctional domain in human CRM1 (exportin 1) mediates RanBP3 binding and multimerization of human T-cell leukemia virus type 1 Rex protein.	bind
49633	3	11173	7	10	NULL	NULL	NULL	CRM1	GP		is 					exportin 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8751_s_1	14612415	A multifunctional domain in human CRM1 (exportin 1) mediates RanBP3 binding and multimerization of human T-cell leukemia virus type 1 Rex protein.	bind
43803	1	11174	6	10	NULL	NULL	NULL	alpha folate receptor	GP		is involved in					folate transport	Process	intracellular			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1288_s_21	11723236	A multigene family of high-affinity folate binding proteins (FBP) designated the alpha, beta, gamma folate receptors are thought to be involved in intracellular folate transport (Wagner, 1985  ; Kane et al., 1988  ; Henderson, 1990  ; Antony, 1996  ).	bind
43804	2	11174	6	10	NULL	NULL	NULL	beta folate receptor	GP		is involved in					folate transport	Process	intracellular			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1288_s_21	11723236	A multigene family of high-affinity folate binding proteins (FBP) designated the alpha, beta, gamma folate receptors are thought to be involved in intracellular folate transport (Wagner, 1985  ; Kane et al., 1988  ; Henderson, 1990  ; Antony, 1996  ).	bind
43805	3	11174	6	10	NULL	NULL	NULL	gamma folate receptor	GP		is involved in					folate transport	Process	intracellular			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1288_s_21	11723236	A multigene family of high-affinity folate binding proteins (FBP) designated the alpha, beta, gamma folate receptors are thought to be involved in intracellular folate transport (Wagner, 1985  ; Kane et al., 1988  ; Henderson, 1990  ; Antony, 1996  ).	bind
43806	4	11174	6	10	NULL	NULL	NULL	alpha folate receptor	GP		is a member of					folate binding protein family	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1288_s_21	11723236	A multigene family of high-affinity folate binding proteins (FBP) designated the alpha, beta, gamma folate receptors are thought to be involved in intracellular folate transport (Wagner, 1985  ; Kane et al., 1988  ; Henderson, 1990  ; Antony, 1996  ).	bind
43807	5	11174	6	10	NULL	NULL	NULL	FBP	GP		is					folate binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1288_s_21	11723236	A multigene family of high-affinity folate binding proteins (FBP) designated the alpha, beta, gamma folate receptors are thought to be involved in intracellular folate transport (Wagner, 1985  ; Kane et al., 1988  ; Henderson, 1990  ; Antony, 1996  ).	bind
43808	6	11174	6	10	NULL	NULL	NULL	beta folate receptor	GP		is a member of					folate binding protein family	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1288_s_21	11723236	A multigene family of high-affinity folate binding proteins (FBP) designated the alpha, beta, gamma folate receptors are thought to be involved in intracellular folate transport (Wagner, 1985  ; Kane et al., 1988  ; Henderson, 1990  ; Antony, 1996  ).	bind
43809	7	11174	6	10	NULL	NULL	NULL	gamma folate receptor	GP		is a member of					folate binding protein family	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1288_s_21	11723236	A multigene family of high-affinity folate binding proteins (FBP) designated the alpha, beta, gamma folate receptors are thought to be involved in intracellular folate transport (Wagner, 1985  ; Kane et al., 1988  ; Henderson, 1990  ; Antony, 1996  ).	bind
49634	1	11174	7	10	NULL	NULL	NULL	alpha folate receptor	GP		is involved in					 folate transport 	Process	intracellular			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1288_s_21	11723236	A multigene family of high-affinity folate binding proteins (FBP) designated the alpha, beta, gamma folate receptors are thought to be involved in intracellular folate transport (Wagner, 1985  ; Kane et al., 1988  ; Henderson, 1990  ; Antony, 1996  ).	bind
49635	2	11174	7	10	NULL	NULL	NULL	beta folate receptor	GP		is involved in					folate transport	Process	intracellular			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1288_s_21	11723236	A multigene family of high-affinity folate binding proteins (FBP) designated the alpha, beta, gamma folate receptors are thought to be involved in intracellular folate transport (Wagner, 1985  ; Kane et al., 1988  ; Henderson, 1990  ; Antony, 1996  ).	bind
49636	3	11174	7	10	NULL	NULL	NULL	gamma folate receptor	GP		is involved in					folate transport	Process	intracellular			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1288_s_21	11723236	A multigene family of high-affinity folate binding proteins (FBP) designated the alpha, beta, gamma folate receptors are thought to be involved in intracellular folate transport (Wagner, 1985  ; Kane et al., 1988  ; Henderson, 1990  ; Antony, 1996  ).	bind
49637	4	11174	7	10	NULL	NULL	NULL	alpha folate receptor	GP		is a member of					folate binding protein family	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1288_s_21	11723236	A multigene family of high-affinity folate binding proteins (FBP) designated the alpha, beta, gamma folate receptors are thought to be involved in intracellular folate transport (Wagner, 1985  ; Kane et al., 1988  ; Henderson, 1990  ; Antony, 1996  ).	bind
49638	5	11174	7	10	NULL	NULL	NULL	beta folate receptor	GP		is a member of					folate binding protein family	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1288_s_21	11723236	A multigene family of high-affinity folate binding proteins (FBP) designated the alpha, beta, gamma folate receptors are thought to be involved in intracellular folate transport (Wagner, 1985  ; Kane et al., 1988  ; Henderson, 1990  ; Antony, 1996  ).	bind
49639	6	11174	7	10	NULL	NULL	NULL	gamma folate receptor	GP		is a member of					folate binding protein family	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1288_s_21	11723236	A multigene family of high-affinity folate binding proteins (FBP) designated the alpha, beta, gamma folate receptors are thought to be involved in intracellular folate transport (Wagner, 1985  ; Kane et al., 1988  ; Henderson, 1990  ; Antony, 1996  ).	bind
49640	7	11174	7	10	NULL	NULL	NULL	FBP	GP		is					folate binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_60_6_1288_s_21	11723236	A multigene family of high-affinity folate binding proteins (FBP) designated the alpha, beta, gamma folate receptors are thought to be involved in intracellular folate transport (Wagner, 1985  ; Kane et al., 1988  ; Henderson, 1990  ; Antony, 1996  ).	bind
43810	1	11178	6	10	NULL	NULL	NULL	Skn7p	GP		does not bind									CDRE	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3473_s_255	11432834	A multipurpose Skn7p DNA-binding domain    Skn7pis a transcription factor and a DNA-binding protein, and although the CDRE was sufficient for the effect of Skn7p on Crz1p-dependent transcription, we were unable to detect Skn7p or Skn7p complex binding to the CDRE.	bind
43811	2	11178	6	10	NULL	NULL	NULL	Skn7p	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3473_s_255	11432834	A multipurpose Skn7p DNA-binding domain    Skn7pis a transcription factor and a DNA-binding protein, and although the CDRE was sufficient for the effect of Skn7p on Crz1p-dependent transcription, we were unable to detect Skn7p or Skn7p complex binding to the CDRE.	bind
44986	3	11178	6	10	NULL	NULL	NULL	Skn7p	GP		is a type of					DNA-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3473_s_255	11432834	A multipurpose Skn7p DNA-binding domain    Skn7pis a transcription factor and a DNA-binding protein, and although the CDRE was sufficient for the effect of Skn7p on Crz1p-dependent transcription, we were unable to detect Skn7p or Skn7p complex binding to the CDRE.	bind
44987	4	11178	6	10	NULL	NULL	NULL	transcription	Process		is dependent on					Crz1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3473_s_255	11432834	A multipurpose Skn7p DNA-binding domain    Skn7pis a transcription factor and a DNA-binding protein, and although the CDRE was sufficient for the effect of Skn7p on Crz1p-dependent transcription, we were unable to detect Skn7p or Skn7p complex binding to the CDRE.	bind
51525	5	11178	6	10	NULL	NULL	NULL	Skn7p	GP		effects					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3473_s_255	11432834	A multipurpose Skn7p DNA-binding domain    Skn7pis a transcription factor and a DNA-binding protein, and although the CDRE was sufficient for the effect of Skn7p on Crz1p-dependent transcription, we were unable to detect Skn7p or Skn7p complex binding to the CDRE.	bind
51526	6	11178	6	10	NULL	NULL	NULL				is sufficient for				CDRE	statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3473_s_255	11432834	A multipurpose Skn7p DNA-binding domain    Skn7pis a transcription factor and a DNA-binding protein, and although the CDRE was sufficient for the effect of Skn7p on Crz1p-dependent transcription, we were unable to detect Skn7p or Skn7p complex binding to the CDRE.	bind
49642	1	11178	7	10	NULL	NULL	NULL	 Skn7p	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3473_s_255	11432834	A multipurpose Skn7p DNA-binding domain    Skn7pis a transcription factor and a DNA-binding protein, and although the CDRE was sufficient for the effect of Skn7p on Crz1p-dependent transcription, we were unable to detect Skn7p or Skn7p complex binding to the CDRE.	bind
49643	2	11178	7	10	NULL	NULL	NULL	Skn7p	GP		is a type of					DNA-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3473_s_255	11432834	A multipurpose Skn7p DNA-binding domain    Skn7pis a transcription factor and a DNA-binding protein, and although the CDRE was sufficient for the effect of Skn7p on Crz1p-dependent transcription, we were unable to detect Skn7p or Skn7p complex binding to the CDRE.	bind
49644	3	11178	7	10	NULL	NULL	NULL	transcription	Process		depends on					Crz1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3473_s_255	11432834	A multipurpose Skn7p DNA-binding domain    Skn7pis a transcription factor and a DNA-binding protein, and although the CDRE was sufficient for the effect of Skn7p on Crz1p-dependent transcription, we were unable to detect Skn7p or Skn7p complex binding to the CDRE.	bind
49645	4	11178	7	10	NULL	NULL	NULL	Skn7p	GP		effect					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3473_s_255	11432834	A multipurpose Skn7p DNA-binding domain    Skn7pis a transcription factor and a DNA-binding protein, and although the CDRE was sufficient for the effect of Skn7p on Crz1p-dependent transcription, we were unable to detect Skn7p or Skn7p complex binding to the CDRE.	bind
49646	5	11178	7	10	NULL	NULL	NULL				is sufficient for				CDRE	statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3473_s_255	11432834	A multipurpose Skn7p DNA-binding domain    Skn7pis a transcription factor and a DNA-binding protein, and although the CDRE was sufficient for the effect of Skn7p on Crz1p-dependent transcription, we were unable to detect Skn7p or Skn7p complex binding to the CDRE.	bind
51527	6	11178	7	10	NULL	NULL	NULL	Skn7p	GP		does not bind									CDRE	NULL		NULL	NULL	NULL	NULL	gw60_embo_20_13_3473_s_255	11432834	A multipurpose Skn7p DNA-binding domain    Skn7pis a transcription factor and a DNA-binding protein, and although the CDRE was sufficient for the effect of Skn7p on Crz1p-dependent transcription, we were unable to detect Skn7p or Skn7p complex binding to the CDRE.	bind
43822	1	11179	6	10	NULL	NULL	NULL	FLNa	GP		bind					actin filament	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_37_32426_s_233	16030015	A multistep model for the regulation of the actin filament-binding of FLNa by CaM.	bind
43823	2	11179	6	10	NULL	NULL	NULL	CaM	GP		regulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_37_32426_s_233	16030015	A multistep model for the regulation of the actin filament-binding of FLNa by CaM.	bind
49647	1	11179	7	10	NULL	NULL	NULL	FLNa 	GP		bind					actin filament	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_37_32426_s_233	16030015	A multistep model for the regulation of the actin filament-binding of FLNa by CaM.	bind
49648	2	11179	7	10	NULL	NULL	NULL	CaM	GP		regulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_37_32426_s_233	16030015	A multistep model for the regulation of the actin filament-binding of FLNa by CaM.	bind
43824	1	11182	6	10	NULL	NULL	NULL	JIP-1	GP	murine	bind		specifically			JNK	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_277_5326_693_s_7	9235893	A murine cytoplasmic protein that binds specifically to JNK [the JNK interacting protein-1 (JIP-1)] was characterized and cloned.	bind
43825	2	11182	6	10	NULL	NULL	NULL	JIP-1	GP		is					JNK interacting protein-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_277_5326_693_s_7	9235893	A murine cytoplasmic protein that binds specifically to JNK [the JNK interacting protein-1 (JIP-1)] was characterized and cloned.	bind
43826	3	11182	6	10	NULL	NULL	NULL	JIP-1	GP		is a type of					cytoplasmic protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_277_5326_693_s_7	9235893	A murine cytoplasmic protein that binds specifically to JNK [the JNK interacting protein-1 (JIP-1)] was characterized and cloned.	bind
49649	1	11182	7	10	NULL	NULL	NULL	JIP-1	GP	murine	bind		specifically			 JNK	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_277_5326_693_s_7	9235893	A murine cytoplasmic protein that binds specifically to JNK [the JNK interacting protein-1 (JIP-1)] was characterized and cloned.	bind
49650	2	11182	7	10	NULL	NULL	NULL	JIP-1	GP		is a type of					cytoplasmic protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_277_5326_693_s_7	9235893	A murine cytoplasmic protein that binds specifically to JNK [the JNK interacting protein-1 (JIP-1)] was characterized and cloned.	bind
49651	3	11182	7	10	NULL	NULL	NULL	JIP-1	GP		is					JNK interacting protein-1 	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_277_5326_693_s_7	9235893	A murine cytoplasmic protein that binds specifically to JNK [the JNK interacting protein-1 (JIP-1)] was characterized and cloned.	bind
44292	1	11183	6	10	NULL	NULL	NULL	leukemia cell line	Cell	murine	is resistant to					E7010	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_jpn-j-cancer-res_92_7_11473728_s_6	11473728	A murine leukemia  cell line resistant to a sulfonamide antimitotic agent, E7010, which binds  to colchicine-binding sites on tubulin, was cross-resistant to the in  vitro growth-inhibitory effect of AM compounds.	bind
44293	2	11183	6	10	NULL	NULL	NULL	E7010	Chemical		is a type of					sulfonamide antimitotic agent	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_jpn-j-cancer-res_92_7_11473728_s_6	11473728	A murine leukemia  cell line resistant to a sulfonamide antimitotic agent, E7010, which binds  to colchicine-binding sites on tubulin, was cross-resistant to the in  vitro growth-inhibitory effect of AM compounds.	bind
44294	3	11183	6	10	NULL	NULL	NULL	leukemia cell line	Cell	murine	bind					tubulin	GP		colchicine binding site		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_jpn-j-cancer-res_92_7_11473728_s_6	11473728	A murine leukemia  cell line resistant to a sulfonamide antimitotic agent, E7010, which binds  to colchicine-binding sites on tubulin, was cross-resistant to the in  vitro growth-inhibitory effect of AM compounds.	bind
44295	4	11183	6	10	NULL	NULL	NULL	AM compounds	Chemical		inhibits					growth	Process				NULL	in vitro	NULL	NULL	NULL	NULL	abs-batch0650-0679_jpn-j-cancer-res_92_7_11473728_s_6	11473728	A murine leukemia  cell line resistant to a sulfonamide antimitotic agent, E7010, which binds  to colchicine-binding sites on tubulin, was cross-resistant to the in  vitro growth-inhibitory effect of AM compounds.	bind
44296	5	11183	6	10	NULL	NULL	NULL	leukemia cell line	Cell	murine	is cross-resistant to					statement 4	Process				NULL	in vitro	NULL	NULL	NULL	NULL	abs-batch0650-0679_jpn-j-cancer-res_92_7_11473728_s_6	11473728	A murine leukemia  cell line resistant to a sulfonamide antimitotic agent, E7010, which binds  to colchicine-binding sites on tubulin, was cross-resistant to the in  vitro growth-inhibitory effect of AM compounds.	bind
49652	1	11183	7	10	NULL	NULL	NULL	leukemia cell line	Cell	murine	resistant to					E7010	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_jpn-j-cancer-res_92_7_11473728_s_6	11473728	A murine leukemia  cell line resistant to a sulfonamide antimitotic agent, E7010, which binds  to colchicine-binding sites on tubulin, was cross-resistant to the in  vitro growth-inhibitory effect of AM compounds.	bind
49653	2	11183	7	10	NULL	NULL	NULL	statement 1	Process		bind					tubulin	GP		colchicine-binding site		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_jpn-j-cancer-res_92_7_11473728_s_6	11473728	A murine leukemia  cell line resistant to a sulfonamide antimitotic agent, E7010, which binds  to colchicine-binding sites on tubulin, was cross-resistant to the in  vitro growth-inhibitory effect of AM compounds.	bind
49654	3	11183	7	10	NULL	NULL	NULL	E7010	Chemical		is a type of					sulfonamide antimitotic agent	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_jpn-j-cancer-res_92_7_11473728_s_6	11473728	A murine leukemia  cell line resistant to a sulfonamide antimitotic agent, E7010, which binds  to colchicine-binding sites on tubulin, was cross-resistant to the in  vitro growth-inhibitory effect of AM compounds.	bind
49655	5	11183	7	10	NULL	NULL	NULL	statement 1	Process		cross-resistant to					statement 4	Process				NULL	in vitro	NULL	NULL	NULL	NULL	abs-batch0650-0679_jpn-j-cancer-res_92_7_11473728_s_6	11473728	A murine leukemia  cell line resistant to a sulfonamide antimitotic agent, E7010, which binds  to colchicine-binding sites on tubulin, was cross-resistant to the in  vitro growth-inhibitory effect of AM compounds.	bind
51528	4	11183	7	10	NULL	NULL	NULL	AM compounds	Chemical		inhibit					growth	Process				NULL	in vitro	NULL	NULL	NULL	NULL	abs-batch0650-0679_jpn-j-cancer-res_92_7_11473728_s_6	11473728	A murine leukemia  cell line resistant to a sulfonamide antimitotic agent, E7010, which binds  to colchicine-binding sites on tubulin, was cross-resistant to the in  vitro growth-inhibitory effect of AM compounds.	bind
43931	1	11184	6	10	NULL	NULL	NULL	laminin	GP		is a type of					non-collagenous protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_clinmicrobiolrev_13_3_470_s_4258	10885988	A murine nephritogenic monoclonal anti-DNA autoantibody binds directly to mouse laminin, the major non-collagenous protein component of the glomerular basement membrane.	bind
43941	2	11184	6	10	NULL	NULL	NULL	monoclonal anti-DNA autoantibody	GP	murine;; nephritogenic	bind		directly			laminin	GP	mouse			NULL		NULL	NULL	NULL	NULL	gw60_clinmicrobiolrev_13_3_470_s_4258	10885988	A murine nephritogenic monoclonal anti-DNA autoantibody binds directly to mouse laminin, the major non-collagenous protein component of the glomerular basement membrane.	bind
51529	3	11184	6	10	NULL	NULL	NULL	laminin	GP		is a component of					glomerular basement membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_clinmicrobiolrev_13_3_470_s_4258	10885988	A murine nephritogenic monoclonal anti-DNA autoantibody binds directly to mouse laminin, the major non-collagenous protein component of the glomerular basement membrane.	bind
49656	1	11184	7	10	NULL	NULL	NULL	monoclonal anti-DNA autoantibody 	GP	murine;;nephritogenic	bind		directly			laminin	GP	mouse			NULL		NULL	NULL	NULL	NULL	gw60_clinmicrobiolrev_13_3_470_s_4258	10885988	A murine nephritogenic monoclonal anti-DNA autoantibody binds directly to mouse laminin, the major non-collagenous protein component of the glomerular basement membrane.	bind
49657	2	11184	7	10	NULL	NULL	NULL	laminin	GP	mouse	is a type of					 non-collagenous protein 	GP				NULL		NULL	NULL	NULL	NULL	gw60_clinmicrobiolrev_13_3_470_s_4258	10885988	A murine nephritogenic monoclonal anti-DNA autoantibody binds directly to mouse laminin, the major non-collagenous protein component of the glomerular basement membrane.	bind
49658	3	11184	7	10	NULL	NULL	NULL	laminin	GP	mouse	is a component of					glomerular basement membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_clinmicrobiolrev_13_3_470_s_4258	10885988	A murine nephritogenic monoclonal anti-DNA autoantibody binds directly to mouse laminin, the major non-collagenous protein component of the glomerular basement membrane.	bind
44297	1	11185	6	10	NULL	NULL	NULL	actinin	GP		bind		may	C-terminal part of CH1 domain		actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_structure_6_11_1419_s_209	9817844	A mutagenesis study has identified residues within the C-terminal part of the   -actinin CH1 domain that may be involved in actin binding, as their substitution with alanine abolishes the interaction  [20]  .	bind
51530	2	11185	6	10	NULL	NULL	NULL	actinin	GP		is substituted with			C-terminal part of CH1 domain		alanine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_structure_6_11_1419_s_209	9817844	A mutagenesis study has identified residues within the C-terminal part of the   -actinin CH1 domain that may be involved in actin binding, as their substitution with alanine abolishes the interaction  [20]  .	bind
51531	3	11185	6	10	NULL	NULL	NULL	statement 2	Process		abolishes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_structure_6_11_1419_s_209	9817844	A mutagenesis study has identified residues within the C-terminal part of the   -actinin CH1 domain that may be involved in actin binding, as their substitution with alanine abolishes the interaction  [20]  .	bind
49659	1	11185	7	10	NULL	NULL	NULL	actinin	GP		bind		may	C-terminal part of CH1 domain		actin	GP				NULL		NULL	NULL	NULL	NULL	gw60_structure_6_11_1419_s_209	9817844	A mutagenesis study has identified residues within the C-terminal part of the   -actinin CH1 domain that may be involved in actin binding, as their substitution with alanine abolishes the interaction  [20]  .	bind
49660	3	11185	7	10	NULL	NULL	NULL	statement 2	Process		abolishes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_structure_6_11_1419_s_209	9817844	A mutagenesis study has identified residues within the C-terminal part of the   -actinin CH1 domain that may be involved in actin binding, as their substitution with alanine abolishes the interaction  [20]  .	bind
49661	2	11185	7	10	NULL	NULL	NULL	actinin	GP		is substituted with			C-terminal part of CH1 domain 		alanine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_structure_6_11_1419_s_209	9817844	A mutagenesis study has identified residues within the C-terminal part of the   -actinin CH1 domain that may be involved in actin binding, as their substitution with alanine abolishes the interaction  [20]  .	bind
43942	1	11186	6	10	NULL	NULL	NULL	E5 protein	GP	human papillomavirus type 16	bind					H+-ATPase	GP	vacuolar			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_virology_272_2_10873774_s_1	10873774	A mutagenic analysis of the E5 protein of human papillomavirus type 16 reveals that E5 binding to the vacuolar H+-ATPase is not sufficient for biological activity, using mammalian and yeast expression systems..	bind
43943	2	11186	6	10	NULL	NULL	NULL	statement 1	Process		is not sufficient for					biological activity	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_virology_272_2_10873774_s_1	10873774	A mutagenic analysis of the E5 protein of human papillomavirus type 16 reveals that E5 binding to the vacuolar H+-ATPase is not sufficient for biological activity, using mammalian and yeast expression systems..	bind
49672	1	11186	7	10	NULL	NULL	NULL	E5 protein	GP	human papillomavirus type 16	bind					H+-ATPase	GP	vacuolar			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_virology_272_2_10873774_s_1	10873774	A mutagenic analysis of the E5 protein of human papillomavirus type 16 reveals that E5 binding to the vacuolar H+-ATPase is not sufficient for biological activity, using mammalian and yeast expression systems..	bind
49673	2	11186	7	10	NULL	NULL	NULL	statement 1	Process		is not sufficient for					biological activity	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_virology_272_2_10873774_s_1	10873774	A mutagenic analysis of the E5 protein of human papillomavirus type 16 reveals that E5 binding to the vacuolar H+-ATPase is not sufficient for biological activity, using mammalian and yeast expression systems..	bind
44299	2	11187	6	10	NULL	NULL	NULL	statement 1	Process		is due to							disruption of		ISRE-like element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_14_9344_s_192	9083071	A mutant  194 to  244 bp sequence unable to bind the BID2 complex due to disruption of the ISRE-like element ( 19) also was unable to compete for TF1phox binding.	bind
44300	1	11187	6	10	NULL	NULL	NULL			mutant	does not bind				194 to 244 bp sequence	BID2 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_14_9344_s_192	9083071	A mutant  194 to  244 bp sequence unable to bind the BID2 complex due to disruption of the ISRE-like element ( 19) also was unable to compete for TF1phox binding.	bind
44301	3	11187	6	10	NULL	NULL	NULL	statement 1	Process		does not compete					TF1phox	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_14_9344_s_192	9083071	A mutant  194 to  244 bp sequence unable to bind the BID2 complex due to disruption of the ISRE-like element ( 19) also was unable to compete for TF1phox binding.	bind
49674	1	11187	7	10	NULL	NULL	NULL			mutant	does not bind				194 to 244 bp sequence	BID2 complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_14_9344_s_192	9083071	A mutant  194 to  244 bp sequence unable to bind the BID2 complex due to disruption of the ISRE-like element ( 19) also was unable to compete for TF1phox binding.	bind
49675	2	11187	7	10	NULL	NULL	NULL	statement 1	Process		due to							disruption of		ISRE-like element	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_14_9344_s_192	9083071	A mutant  194 to  244 bp sequence unable to bind the BID2 complex due to disruption of the ISRE-like element ( 19) also was unable to compete for TF1phox binding.	bind
49676	3	11187	7	10	NULL	NULL	NULL	statement 1	Process		does not compete with					TF1phox	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_14_9344_s_192	9083071	A mutant  194 to  244 bp sequence unable to bind the BID2 complex due to disruption of the ISRE-like element ( 19) also was unable to compete for TF1phox binding.	bind
43944	1	11188	6	10	NULL	NULL	NULL	B DNA	NucleicAcid	mutant	does not bind					myotrophin	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1589_3_247_s_274	12031792	A mutant  B DNA also did not show any binding to myotrophin.	bind
49677	1	11188	7	10	NULL	NULL	NULL	B DNA 	NucleicAcid	mutant	does not bind					myotrophin	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1589_3_247_s_274	12031792	A mutant  B DNA also did not show any binding to myotrophin.	bind
43945	1	11189	6	10	NULL	NULL	NULL	Mnk1	GP		bind					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_13_3465_s_9	10880459	A mutant adenovirus with a temperature-sensitive 100k protein that cannot inhibit cellular protein synthesis at restrictive temperature no longer blocks Mnk1 binding to eIF4G, or phosphorylation of eIF4E.	bind
43946	2	11189	6	10	NULL	NULL	NULL	100k protein	GP	mutant;; adenovirus	does not block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_13_3465_s_9	10880459	A mutant adenovirus with a temperature-sensitive 100k protein that cannot inhibit cellular protein synthesis at restrictive temperature no longer blocks Mnk1 binding to eIF4G, or phosphorylation of eIF4E.	bind
43947	3	11189	6	10	NULL	NULL	NULL	100k protein	GP	mutant;; adenovirus	does not block					eIF4E	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_13_3465_s_9	10880459	A mutant adenovirus with a temperature-sensitive 100k protein that cannot inhibit cellular protein synthesis at restrictive temperature no longer blocks Mnk1 binding to eIF4G, or phosphorylation of eIF4E.	bind
43948	4	11189	6	10	NULL	NULL	NULL	100k protein	GP	mutant;; adenovirus	is sensitive to					temperature					NULL		NULL	NULL	NULL	NULL	gw60_embo_19_13_3465_s_9	10880459	A mutant adenovirus with a temperature-sensitive 100k protein that cannot inhibit cellular protein synthesis at restrictive temperature no longer blocks Mnk1 binding to eIF4G, or phosphorylation of eIF4E.	bind
43949	5	11189	6	10	NULL	NULL	NULL	100k protein	GP	mutant;; adenovirus	does not inhibit					cellular proteins	GP	synthesis of			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_13_3465_s_9	10880459	A mutant adenovirus with a temperature-sensitive 100k protein that cannot inhibit cellular protein synthesis at restrictive temperature no longer blocks Mnk1 binding to eIF4G, or phosphorylation of eIF4E.	bind
49678	1	11189	7	10	NULL	NULL	NULL	Mnk1	GP		bind					eIF4G	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_13_3465_s_9	10880459	A mutant adenovirus with a temperature-sensitive 100k protein that cannot inhibit cellular protein synthesis at restrictive temperature no longer blocks Mnk1 binding to eIF4G, or phosphorylation of eIF4E.	bind
49679	2	11189	7	10	NULL	NULL	NULL	100k protein	GP	mutant;;adenovirus	does not inhibit					cellular proteins	GP	synthesis of			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_13_3465_s_9	10880459	A mutant adenovirus with a temperature-sensitive 100k protein that cannot inhibit cellular protein synthesis at restrictive temperature no longer blocks Mnk1 binding to eIF4G, or phosphorylation of eIF4E.	bind
49680	3	11189	7	10	NULL	NULL	NULL	100k protein	GP	mutant;;adenovirus	does not block					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_13_3465_s_9	10880459	A mutant adenovirus with a temperature-sensitive 100k protein that cannot inhibit cellular protein synthesis at restrictive temperature no longer blocks Mnk1 binding to eIF4G, or phosphorylation of eIF4E.	bind
49681	4	11189	7	10	NULL	NULL	NULL	100k protein	GP	mutant;;adenovirus	does not block					eIF4E	GP	phosphorylation of 			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_13_3465_s_9	10880459	A mutant adenovirus with a temperature-sensitive 100k protein that cannot inhibit cellular protein synthesis at restrictive temperature no longer blocks Mnk1 binding to eIF4G, or phosphorylation of eIF4E.	bind
51532	5	11189	7	10	NULL	NULL	NULL	100k protein	GP	mutant;;adenovirus	is sensitive to					temperature					NULL		NULL	NULL	NULL	NULL	gw60_embo_19_13_3465_s_9	10880459	A mutant adenovirus with a temperature-sensitive 100k protein that cannot inhibit cellular protein synthesis at restrictive temperature no longer blocks Mnk1 binding to eIF4G, or phosphorylation of eIF4E.	bind
44302	1	11190	6	10	NULL	NULL	NULL	alpha-TM DY competitor	NucleicAcid	mutant	does not bind					PTB	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_2699_s_256	10082536	A mutant alpha-TM DY competitor which does not bind PTB, DYdeltaPC ( 20), was virtually ineffective in activating splicing (Fig.  6, lanes 11 and 12), as was an alpha-actinin competitor RNA truncated at the  ClaI site in the spacer and which therefore lacks UCUU motifs (lanes 13 and 14).	bind
44303	2	11190	6	10	NULL	NULL	NULL	alpha-TM DY competitor	NucleicAcid	mutant	does not bind					DYdeltaPC	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_2699_s_256	10082536	A mutant alpha-TM DY competitor which does not bind PTB, DYdeltaPC ( 20), was virtually ineffective in activating splicing (Fig.  6, lanes 11 and 12), as was an alpha-actinin competitor RNA truncated at the  ClaI site in the spacer and which therefore lacks UCUU motifs (lanes 13 and 14).	bind
44304	3	11190	6	10	NULL	NULL	NULL	alpha-TM DY competitor	NucleicAcid	mutant	does not activate					splicing	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_2699_s_256	10082536	A mutant alpha-TM DY competitor which does not bind PTB, DYdeltaPC ( 20), was virtually ineffective in activating splicing (Fig.  6, lanes 11 and 12), as was an alpha-actinin competitor RNA truncated at the  ClaI site in the spacer and which therefore lacks UCUU motifs (lanes 13 and 14).	bind
44305	4	11190	6	10	NULL	NULL	NULL	alpha-actinin competitor RNA	NucleicAcid		is truncated at									ClaI site in the spacer 	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_2699_s_256	10082536	A mutant alpha-TM DY competitor which does not bind PTB, DYdeltaPC ( 20), was virtually ineffective in activating splicing (Fig.  6, lanes 11 and 12), as was an alpha-actinin competitor RNA truncated at the  ClaI site in the spacer and which therefore lacks UCUU motifs (lanes 13 and 14).	bind
44306	5	11190	6	10	NULL	NULL	NULL	statement 4	Process		lacks									UCUU motifs	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_2699_s_256	10082536	A mutant alpha-TM DY competitor which does not bind PTB, DYdeltaPC ( 20), was virtually ineffective in activating splicing (Fig.  6, lanes 11 and 12), as was an alpha-actinin competitor RNA truncated at the  ClaI site in the spacer and which therefore lacks UCUU motifs (lanes 13 and 14).	bind
51533	6	11190	6	10	NULL	NULL	NULL	alpha-TM DY competitor	NucleicAcid	mutant	is a type of					statement 4	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_2699_s_256	10082536	A mutant alpha-TM DY competitor which does not bind PTB, DYdeltaPC ( 20), was virtually ineffective in activating splicing (Fig.  6, lanes 11 and 12), as was an alpha-actinin competitor RNA truncated at the  ClaI site in the spacer and which therefore lacks UCUU motifs (lanes 13 and 14).	bind
49682	1	11190	7	10	NULL	NULL	NULL	alpha-TM DY competitor	NucleicAcid	mutant	does not bind					PTB	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_2699_s_256	10082536	A mutant alpha-TM DY competitor which does not bind PTB, DYdeltaPC ( 20), was virtually ineffective in activating splicing (Fig.  6, lanes 11 and 12), as was an alpha-actinin competitor RNA truncated at the  ClaI site in the spacer and which therefore lacks UCUU motifs (lanes 13 and 14).	bind
49683	2	11190	7	10	NULL	NULL	NULL	alpha-TM DY competitor	NucleicAcid	mutant	does not bind					DYdeltaPC	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_2699_s_256	10082536	A mutant alpha-TM DY competitor which does not bind PTB, DYdeltaPC ( 20), was virtually ineffective in activating splicing (Fig.  6, lanes 11 and 12), as was an alpha-actinin competitor RNA truncated at the  ClaI site in the spacer and which therefore lacks UCUU motifs (lanes 13 and 14).	bind
49684	3	11190	7	10	NULL	NULL	NULL	alpha-TM DY alpha-TM DY competitor	NucleicAcid	mutant	does not activate					splicing	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_2699_s_256	10082536	A mutant alpha-TM DY competitor which does not bind PTB, DYdeltaPC ( 20), was virtually ineffective in activating splicing (Fig.  6, lanes 11 and 12), as was an alpha-actinin competitor RNA truncated at the  ClaI site in the spacer and which therefore lacks UCUU motifs (lanes 13 and 14).	bind
51534	4	11190	7	10	NULL	NULL	NULL	alpha-actinin competitor RNA	NucleicAcid		is truncated at									ClaI site in the spacer	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_2699_s_256	10082536	A mutant alpha-TM DY competitor which does not bind PTB, DYdeltaPC ( 20), was virtually ineffective in activating splicing (Fig.  6, lanes 11 and 12), as was an alpha-actinin competitor RNA truncated at the  ClaI site in the spacer and which therefore lacks UCUU motifs (lanes 13 and 14).	bind
51535	5	11190	7	10	NULL	NULL	NULL	statement 4	Process		lacks									UCUU motifs	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_2699_s_256	10082536	A mutant alpha-TM DY competitor which does not bind PTB, DYdeltaPC ( 20), was virtually ineffective in activating splicing (Fig.  6, lanes 11 and 12), as was an alpha-actinin competitor RNA truncated at the  ClaI site in the spacer and which therefore lacks UCUU motifs (lanes 13 and 14).	bind
51536	6	11190	7	10	NULL	NULL	NULL	alpha-TM DY competitor	NucleicAcid	mutant	is a type of					statement 4	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_2699_s_256	10082536	A mutant alpha-TM DY competitor which does not bind PTB, DYdeltaPC ( 20), was virtually ineffective in activating splicing (Fig.  6, lanes 11 and 12), as was an alpha-actinin competitor RNA truncated at the  ClaI site in the spacer and which therefore lacks UCUU motifs (lanes 13 and 14).	bind
43950	2	11191	6	10	NULL	NULL	NULL	statement 1	Process		bind		noncovalently			apo(a)	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_502_s_19	12615683	A mutant apoB lacking Cys4326 still binds apo(a) noncovalently despite being unable to form the disulphide bond.	bind
43951	3	11191	6	10	NULL	NULL	NULL	statement 1	Process		does not form					disulphide bond					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_502_s_19	12615683	A mutant apoB lacking Cys4326 still binds apo(a) noncovalently despite being unable to form the disulphide bond.	bind
51537	1	11191	6	10	NULL	NULL	NULL	apoB	GP	mutant	lacks					Cys4326	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_502_s_19	12615683	A mutant apoB lacking Cys4326 still binds apo(a) noncovalently despite being unable to form the disulphide bond.	bind
49685	1	11191	7	10	NULL	NULL	NULL	apoB	GP	mutant	lacks					Cys4326 	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_502_s_19	12615683	A mutant apoB lacking Cys4326 still binds apo(a) noncovalently despite being unable to form the disulphide bond.	bind
49686	2	11191	7	10	NULL	NULL	NULL	statement 1	Process		bind		noncovalently			apo(a) 	GP				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_502_s_19	12615683	A mutant apoB lacking Cys4326 still binds apo(a) noncovalently despite being unable to form the disulphide bond.	bind
49687	3	11191	7	10	NULL	NULL	NULL	statement 1	Process		does not form					disulphide bond					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_23_3_502_s_19	12615683	A mutant apoB lacking Cys4326 still binds apo(a) noncovalently despite being unable to form the disulphide bond.	bind
43952	1	11192	6	10	NULL	NULL	NULL	 BAK peptide	AminoAcid	mutant	bind		decreased	R76A		BCL-XL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_39_24101_s_91	9305851	A mutant BAK R76A peptide demonstrated decreased binding to BCL-XL ( 17).	bind
49688	1	11192	7	10	NULL	NULL	NULL	BAK peptide	AminoAcid	mutant	bind		decreased	R76A		BCL-XL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_39_24101_s_91	9305851	A mutant BAK R76A peptide demonstrated decreased binding to BCL-XL ( 17).	bind
44988	1	11193	6	10	NULL	NULL	NULL	G-kinase	GP		regulates					c-Raf	GP		Ser43		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_7	9819386	A mutant c-Raf kinase with an Ala substitution for Ser43 was insensitive to inhibition by cGMP and G-kinase, and expression of this mutant kinase protected cells from inhibition of EGF-induced MAP kinase activity by cGMP and G-kinase, suggesting that Ser43 in c-Raf is the major target for regulation by G-kinase.	bind
44989	2	11193	6	10	NULL	NULL	NULL	EGF	GP		induces					MAP kinase 	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_7	9819386	A mutant c-Raf kinase with an Ala substitution for Ser43 was insensitive to inhibition by cGMP and G-kinase, and expression of this mutant kinase protected cells from inhibition of EGF-induced MAP kinase activity by cGMP and G-kinase, suggesting that Ser43 in c-Raf is the major target for regulation by G-kinase.	bind
44990	3	11193	6	10	NULL	NULL	NULL	cGMP	Chemical		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_7	9819386	A mutant c-Raf kinase with an Ala substitution for Ser43 was insensitive to inhibition by cGMP and G-kinase, and expression of this mutant kinase protected cells from inhibition of EGF-induced MAP kinase activity by cGMP and G-kinase, suggesting that Ser43 in c-Raf is the major target for regulation by G-kinase.	bind
44991	4	11193	6	10	NULL	NULL	NULL	G-kinase	GP		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_7	9819386	A mutant c-Raf kinase with an Ala substitution for Ser43 was insensitive to inhibition by cGMP and G-kinase, and expression of this mutant kinase protected cells from inhibition of EGF-induced MAP kinase activity by cGMP and G-kinase, suggesting that Ser43 in c-Raf is the major target for regulation by G-kinase.	bind
44992	5	11193	6	10	NULL	NULL	NULL	c-Raf	GP		is a type of					kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_7	9819386	A mutant c-Raf kinase with an Ala substitution for Ser43 was insensitive to inhibition by cGMP and G-kinase, and expression of this mutant kinase protected cells from inhibition of EGF-induced MAP kinase activity by cGMP and G-kinase, suggesting that Ser43 in c-Raf is the major target for regulation by G-kinase.	bind
44993	6	11193	6	10	NULL	NULL	NULL	c-Raf	GP		is substituted by			Ser43		c-Raf	GP		Ala		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_7	9819386	A mutant c-Raf kinase with an Ala substitution for Ser43 was insensitive to inhibition by cGMP and G-kinase, and expression of this mutant kinase protected cells from inhibition of EGF-induced MAP kinase activity by cGMP and G-kinase, suggesting that Ser43 in c-Raf is the major target for regulation by G-kinase.	bind
44995	7	11193	6	10	NULL	NULL	NULL	statement 6	Process		protects					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_7	9819386	A mutant c-Raf kinase with an Ala substitution for Ser43 was insensitive to inhibition by cGMP and G-kinase, and expression of this mutant kinase protected cells from inhibition of EGF-induced MAP kinase activity by cGMP and G-kinase, suggesting that Ser43 in c-Raf is the major target for regulation by G-kinase.	bind
44996	8	11193	6	10	NULL	NULL	NULL	statement 6	Process		protects					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_7	9819386	A mutant c-Raf kinase with an Ala substitution for Ser43 was insensitive to inhibition by cGMP and G-kinase, and expression of this mutant kinase protected cells from inhibition of EGF-induced MAP kinase activity by cGMP and G-kinase, suggesting that Ser43 in c-Raf is the major target for regulation by G-kinase.	bind
49738	1	11193	7	10	NULL	NULL	NULL	c-Raf kinase	GP		is substituted with			Ser43		c-Raf kinase	GP		Ala		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_7	9819386	A mutant c-Raf kinase with an Ala substitution for Ser43 was insensitive to inhibition by cGMP and G-kinase, and expression of this mutant kinase protected cells from inhibition of EGF-induced MAP kinase activity by cGMP and G-kinase, suggesting that Ser43 in c-Raf is the major target for regulation by G-kinase.	bind
49740	2	11193	7	10	NULL	NULL	NULL	EGF	GP		induce					MAP kinase	GP	activity of 			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_7	9819386	A mutant c-Raf kinase with an Ala substitution for Ser43 was insensitive to inhibition by cGMP and G-kinase, and expression of this mutant kinase protected cells from inhibition of EGF-induced MAP kinase activity by cGMP and G-kinase, suggesting that Ser43 in c-Raf is the major target for regulation by G-kinase.	bind
49741	3	11193	7	10	NULL	NULL	NULL	cGMP	Chemical		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_7	9819386	A mutant c-Raf kinase with an Ala substitution for Ser43 was insensitive to inhibition by cGMP and G-kinase, and expression of this mutant kinase protected cells from inhibition of EGF-induced MAP kinase activity by cGMP and G-kinase, suggesting that Ser43 in c-Raf is the major target for regulation by G-kinase.	bind
49742	4	11193	7	10	NULL	NULL	NULL	G-kinase	GP		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_7	9819386	A mutant c-Raf kinase with an Ala substitution for Ser43 was insensitive to inhibition by cGMP and G-kinase, and expression of this mutant kinase protected cells from inhibition of EGF-induced MAP kinase activity by cGMP and G-kinase, suggesting that Ser43 in c-Raf is the major target for regulation by G-kinase.	bind
49743	7	11193	7	10	NULL	NULL	NULL	G-kinase	GP		regulates					C-Raf	GP		Ser43		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_7	9819386	A mutant c-Raf kinase with an Ala substitution for Ser43 was insensitive to inhibition by cGMP and G-kinase, and expression of this mutant kinase protected cells from inhibition of EGF-induced MAP kinase activity by cGMP and G-kinase, suggesting that Ser43 in c-Raf is the major target for regulation by G-kinase.	bind
51756	5	11193	7	10	NULL	NULL	NULL	statement 1	Process		protect					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_7	9819386	A mutant c-Raf kinase with an Ala substitution for Ser43 was insensitive to inhibition by cGMP and G-kinase, and expression of this mutant kinase protected cells from inhibition of EGF-induced MAP kinase activity by cGMP and G-kinase, suggesting that Ser43 in c-Raf is the major target for regulation by G-kinase.	bind
51758	6	11193	7	10	NULL	NULL	NULL	statement 1	Process		protect					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6983_s_7	9819386	A mutant c-Raf kinase with an Ala substitution for Ser43 was insensitive to inhibition by cGMP and G-kinase, and expression of this mutant kinase protected cells from inhibition of EGF-induced MAP kinase activity by cGMP and G-kinase, suggesting that Ser43 in c-Raf is the major target for regulation by G-kinase.	bind
43955	1	11194	6	NULL	NULL	0	NULL		NULL		is changed to	NULL		Arg66			NULL		Glu		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_27_19237_s_285	10383431	A mutant carrying the combined change of Arg66 to Glu and His67 to Thr demonstrated decreased binding to C4b-Sepharose at physiological ionic strength.	bind
43956	2	11194	6	NULL	NULL	0	NULL		NULL		is changed to	NULL		His67			NULL		Thr		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_27_19237_s_285	10383431	A mutant carrying the combined change of Arg66 to Glu and His67 to Thr demonstrated decreased binding to C4b-Sepharose at physiological ionic strength.	bind
43957	3	11194	6	10	NULL	NULL	NULL	statement 1	Process		occurs in concert with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_27_19237_s_285	10383431	A mutant carrying the combined change of Arg66 to Glu and His67 to Thr demonstrated decreased binding to C4b-Sepharose at physiological ionic strength.	bind
43958	4	11194	6	10	NULL	NULL	NULL	statement 3	Process		bind		less avidly			C4b	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_27_19237_s_285	10383431	A mutant carrying the combined change of Arg66 to Glu and His67 to Thr demonstrated decreased binding to C4b-Sepharose at physiological ionic strength.	bind
51543	1	11194	7	10	NULL	0	NULL		NULL		is changed to	NULL		Arg66 			NULL		Glu 		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_27_19237_s_285	10383431	A mutant carrying the combined change of Arg66 to Glu and His67 to Thr demonstrated decreased binding to C4b-Sepharose at physiological ionic strength.	bind
51544	2	11194	7	10	NULL	0	NULL		NULL		is changed to	NULL		His67			NULL		Thr		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_27_19237_s_285	10383431	A mutant carrying the combined change of Arg66 to Glu and His67 to Thr demonstrated decreased binding to C4b-Sepharose at physiological ionic strength.	bind
51545	3	11194	7	10	NULL	NULL	NULL	statement 1	Process		occurs in concert with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_27_19237_s_285	10383431	A mutant carrying the combined change of Arg66 to Glu and His67 to Thr demonstrated decreased binding to C4b-Sepharose at physiological ionic strength.	bind
51546	4	11194	7	10	NULL	NULL	NULL	statement 3	Process		bind		less avidly			C4b	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_27_19237_s_285	10383431	A mutant carrying the combined change of Arg66 to Glu and His67 to Thr demonstrated decreased binding to C4b-Sepharose at physiological ionic strength.	bind
43959	1	11195	6	10	NULL	NULL	NULL	CD-R1	GP		is mutated to			C-tail tyrosine		CD-R1	GP		phenylalanine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7771_s_228	10713090	A mutant CD-R1 with both C-tail tyrosine residues mutated to phenylalanine failed to bind to Grb14, but the independent Y766F and Y776F receptor constructs bound to Grb14 with strength equal to the wild-type CD-R1.	bind
43960	2	11195	6	10	NULL	NULL	NULL	statement 1	Process		does not bind					Grb14	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7771_s_228	10713090	A mutant CD-R1 with both C-tail tyrosine residues mutated to phenylalanine failed to bind to Grb14, but the independent Y766F and Y776F receptor constructs bound to Grb14 with strength equal to the wild-type CD-R1.	bind
43961	3	11195	6	10	NULL	NULL	NULL	CD-R1	GP	wild type	bind					Grb14	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7771_s_228	10713090	A mutant CD-R1 with both C-tail tyrosine residues mutated to phenylalanine failed to bind to Grb14, but the independent Y766F and Y776F receptor constructs bound to Grb14 with strength equal to the wild-type CD-R1.	bind
43962	4	11195	6	10	NULL	NULL	NULL	receptor construct	AminoAcid		bind			Y766F		Grb14	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7771_s_228	10713090	A mutant CD-R1 with both C-tail tyrosine residues mutated to phenylalanine failed to bind to Grb14, but the independent Y766F and Y776F receptor constructs bound to Grb14 with strength equal to the wild-type CD-R1.	bind
43963	5	11195	6	10	NULL	NULL	NULL	receptor construct	AminoAcid		bind			Y776F		Grb14	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7771_s_228	10713090	A mutant CD-R1 with both C-tail tyrosine residues mutated to phenylalanine failed to bind to Grb14, but the independent Y766F and Y776F receptor constructs bound to Grb14 with strength equal to the wild-type CD-R1.	bind
43964	6	11195	6	10	NULL	NULL	NULL	statement 4	Process	affinity of	is equal to					statement 3	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7771_s_228	10713090	A mutant CD-R1 with both C-tail tyrosine residues mutated to phenylalanine failed to bind to Grb14, but the independent Y766F and Y776F receptor constructs bound to Grb14 with strength equal to the wild-type CD-R1.	bind
43965	7	11195	6	10	NULL	NULL	NULL	statement 5	Process	affinity of	is equal to					statement 3	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7771_s_228	10713090	A mutant CD-R1 with both C-tail tyrosine residues mutated to phenylalanine failed to bind to Grb14, but the independent Y766F and Y776F receptor constructs bound to Grb14 with strength equal to the wild-type CD-R1.	bind
49746	1	11195	7	10	NULL	NULL	NULL	statement 5	Process		does not bind					Grb14	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7771_s_228	10713090	A mutant CD-R1 with both C-tail tyrosine residues mutated to phenylalanine failed to bind to Grb14, but the independent Y766F and Y776F receptor constructs bound to Grb14 with strength equal to the wild-type CD-R1.	bind
49747	2	11195	7	10	NULL	NULL	NULL	receptor construct	AminoAcid		bind			Y766F		Grb14	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7771_s_228	10713090	A mutant CD-R1 with both C-tail tyrosine residues mutated to phenylalanine failed to bind to Grb14, but the independent Y766F and Y776F receptor constructs bound to Grb14 with strength equal to the wild-type CD-R1.	bind
49748	3	11195	7	10	NULL	NULL	NULL	receptor construct	AminoAcid		bind			Y776F		Grb14	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7771_s_228	10713090	A mutant CD-R1 with both C-tail tyrosine residues mutated to phenylalanine failed to bind to Grb14, but the independent Y766F and Y776F receptor constructs bound to Grb14 with strength equal to the wild-type CD-R1.	bind
49749	4	11195	7	10	NULL	NULL	NULL	CD-R1 receptor	GP	wild-type	bind					Grb14	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7771_s_228	10713090	A mutant CD-R1 with both C-tail tyrosine residues mutated to phenylalanine failed to bind to Grb14, but the independent Y766F and Y776F receptor constructs bound to Grb14 with strength equal to the wild-type CD-R1.	bind
51540	5	11195	7	10	NULL	NULL	NULL	CD-R1	GP		is mutated to			C-tail tyrosine		CD-R1	GP		phenylalanine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7771_s_228	10713090	A mutant CD-R1 with both C-tail tyrosine residues mutated to phenylalanine failed to bind to Grb14, but the independent Y766F and Y776F receptor constructs bound to Grb14 with strength equal to the wild-type CD-R1.	bind
51541	6	11195	7	10	NULL	NULL	NULL	statement 2	Process	affinity of	is equivalent to					statement 4	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7771_s_228	10713090	A mutant CD-R1 with both C-tail tyrosine residues mutated to phenylalanine failed to bind to Grb14, but the independent Y766F and Y776F receptor constructs bound to Grb14 with strength equal to the wild-type CD-R1.	bind
51542	7	11195	7	10	NULL	NULL	NULL	statement 3	Process	affinity of	is equivalent to					statement 4	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_11_7771_s_228	10713090	A mutant CD-R1 with both C-tail tyrosine residues mutated to phenylalanine failed to bind to Grb14, but the independent Y766F and Y776F receptor constructs bound to Grb14 with strength equal to the wild-type CD-R1.	bind
43966	1	11196	6	10	NULL	NULL	NULL	cholera toxin	GP	mutant	bind			 B subunit		GM1- ganglioside	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_4_905_s_623	9585410	A mutant cholera toxin B subunit that binds GM1- ganglioside but lacks immunomodulatory or toxic activity.	bind
43967	2	11196	6	10	NULL	NULL	NULL	statement 1	Process		lacks					immunomodulatory activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_4_905_s_623	9585410	A mutant cholera toxin B subunit that binds GM1- ganglioside but lacks immunomodulatory or toxic activity.	bind
43968	3	11196	6	10	NULL	NULL	NULL	statement 1	Process		lacks					toxic activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_4_905_s_623	9585410	A mutant cholera toxin B subunit that binds GM1- ganglioside but lacks immunomodulatory or toxic activity.	bind
49750	1	11196	7	10	NULL	NULL	NULL	cholera toxin	GP	mutant	bind			B subunit 		GM1- ganglioside	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_4_905_s_623	9585410	A mutant cholera toxin B subunit that binds GM1- ganglioside but lacks immunomodulatory or toxic activity.	bind
49751	2	11196	7	10	NULL	NULL	NULL	statement 1	Process		lacks					immunomodulatory activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_4_905_s_623	9585410	A mutant cholera toxin B subunit that binds GM1- ganglioside but lacks immunomodulatory or toxic activity.	bind
49752	3	11196	7	10	NULL	NULL	NULL	statement 1	Process		lacks					toxic activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_141_4_905_s_623	9585410	A mutant cholera toxin B subunit that binds GM1- ganglioside but lacks immunomodulatory or toxic activity.	bind
44330	1	11198	6	10	NULL	NULL	NULL	GATA-3	GP		bind									CIRE	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_31_28177_s_175	15941711	A mutant CIRE with 12 instead of 6 nucleotides separating the GATA-binding motifs can no longer inhibit binding of GATA-3 to the CIRE efficiently ( Fig. 5 B,  lane 3), and a mutant with an inverted 3' GATA-binding motif also cannot inhibit binding of CIRE to nuclear proteins of Th2 cells ( Fig. 5 B,  lane 4).	bind
44331	2	11198	6	10	NULL	NULL	NULL	nuclear proteins	GP		bind									CIRE	NULL	Th2 cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_31_28177_s_175	15941711	A mutant CIRE with 12 instead of 6 nucleotides separating the GATA-binding motifs can no longer inhibit binding of GATA-3 to the CIRE efficiently ( Fig. 5 B,  lane 3), and a mutant with an inverted 3' GATA-binding motif also cannot inhibit binding of CIRE to nuclear proteins of Th2 cells ( Fig. 5 B,  lane 4).	bind
44332	3	11198	6	10	NULL	NULL	NULL			mutant	does not inhibit		efficiently		CIRE	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_31_28177_s_175	15941711	A mutant CIRE with 12 instead of 6 nucleotides separating the GATA-binding motifs can no longer inhibit binding of GATA-3 to the CIRE efficiently ( Fig. 5 B,  lane 3), and a mutant with an inverted 3' GATA-binding motif also cannot inhibit binding of CIRE to nuclear proteins of Th2 cells ( Fig. 5 B,  lane 4).	bind
44333	4	11198	6	10	NULL	NULL	NULL			mutant	does not inhibit				inverted 3' GATA-binding motif 	statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_31_28177_s_175	15941711	A mutant CIRE with 12 instead of 6 nucleotides separating the GATA-binding motifs can no longer inhibit binding of GATA-3 to the CIRE efficiently ( Fig. 5 B,  lane 3), and a mutant with an inverted 3' GATA-binding motif also cannot inhibit binding of CIRE to nuclear proteins of Th2 cells ( Fig. 5 B,  lane 4).	bind
49753	1	11198	7	10	NULL	NULL	NULL	GATA-3	GP		bind									CIRE	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_31_28177_s_175	15941711	A mutant CIRE with 12 instead of 6 nucleotides separating the GATA-binding motifs can no longer inhibit binding of GATA-3 to the CIRE efficiently ( Fig. 5 B,  lane 3), and a mutant with an inverted 3' GATA-binding motif also cannot inhibit binding of CIRE to nuclear proteins of Th2 cells ( Fig. 5 B,  lane 4).	bind
49754	2	11198	7	10	NULL	NULL	NULL			mutant	does not inhibit		efficiently		CIRE	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_31_28177_s_175	15941711	A mutant CIRE with 12 instead of 6 nucleotides separating the GATA-binding motifs can no longer inhibit binding of GATA-3 to the CIRE efficiently ( Fig. 5 B,  lane 3), and a mutant with an inverted 3' GATA-binding motif also cannot inhibit binding of CIRE to nuclear proteins of Th2 cells ( Fig. 5 B,  lane 4).	bind
49755	3	11198	7	10	NULL	NULL	NULL				bind				CIRE	nuclear proteins	GP				NULL	Th2 cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_31_28177_s_175	15941711	A mutant CIRE with 12 instead of 6 nucleotides separating the GATA-binding motifs can no longer inhibit binding of GATA-3 to the CIRE efficiently ( Fig. 5 B,  lane 3), and a mutant with an inverted 3' GATA-binding motif also cannot inhibit binding of CIRE to nuclear proteins of Th2 cells ( Fig. 5 B,  lane 4).	bind
49756	4	11198	7	10	NULL	NULL	NULL			mutant	does not inhibit				inverted 3' GATA-binding motif	statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_31_28177_s_175	15941711	A mutant CIRE with 12 instead of 6 nucleotides separating the GATA-binding motifs can no longer inhibit binding of GATA-3 to the CIRE efficiently ( Fig. 5 B,  lane 3), and a mutant with an inverted 3' GATA-binding motif also cannot inhibit binding of CIRE to nuclear proteins of Th2 cells ( Fig. 5 B,  lane 4).	bind
43969	1	11199	6	10	NULL	NULL	NULL	DDB2	GP	mutant	does not bind					Cul-4A	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_6738_s_254	11564859	A mutant DDB2 (2RO) which does not bind Cul-4A did not exhibit any significant increase in ubiquitination by the coexpression of Cul-4A.	bind
43970	2	11199	6	10	NULL	NULL	NULL	DDB2	GP	mutant	is					2RO	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_6738_s_254	11564859	A mutant DDB2 (2RO) which does not bind Cul-4A did not exhibit any significant increase in ubiquitination by the coexpression of Cul-4A.	bind
43971	3	11199	6	10	NULL	NULL	NULL	DDB2	GP	mutant	is coexpressed with					Cul-4A	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_6738_s_254	11564859	A mutant DDB2 (2RO) which does not bind Cul-4A did not exhibit any significant increase in ubiquitination by the coexpression of Cul-4A.	bind
43972	4	11199	6	10	NULL	NULL	NULL	statement 3	Process		does not increase		significantly			ubiquitination	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_6738_s_254	11564859	A mutant DDB2 (2RO) which does not bind Cul-4A did not exhibit any significant increase in ubiquitination by the coexpression of Cul-4A.	bind
49757	1	11199	7	10	NULL	NULL	NULL	DDB2	GP	mutant	does not bind					Cul-4A	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_6738_s_254	11564859	A mutant DDB2 (2RO) which does not bind Cul-4A did not exhibit any significant increase in ubiquitination by the coexpression of Cul-4A.	bind
49758	2	11199	7	10	NULL	NULL	NULL	DDB2	GP	mutant	does not increase					ubiquitination	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_6738_s_254	11564859	A mutant DDB2 (2RO) which does not bind Cul-4A did not exhibit any significant increase in ubiquitination by the coexpression of Cul-4A.	bind
49759	3	11199	7	10	NULL	NULL	NULL	statement 2	Process		occur upon					Cul-4A	GP	coexpression of 			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_6738_s_254	11564859	A mutant DDB2 (2RO) which does not bind Cul-4A did not exhibit any significant increase in ubiquitination by the coexpression of Cul-4A.	bind
49760	4	11199	7	10	NULL	NULL	NULL	DDB2	GP	mutant	is					2RO	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_6738_s_254	11564859	A mutant DDB2 (2RO) which does not bind Cul-4A did not exhibit any significant increase in ubiquitination by the coexpression of Cul-4A.	bind
43973	1	11200	6	10	NULL	NULL	NULL	FnbA	GP	defective mutant	bind					Fn	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_6_2933_s_260	12010982	A mutant defective in both FnbA and FnbB ( 13) still shows residual binding to Fn ( 7), and it is possible that surface-associated Eap contributes to this binding.	bind
43974	2	11200	6	10	NULL	NULL	NULL	Eap	GP	surface associated	contributes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_6_2933_s_260	12010982	A mutant defective in both FnbA and FnbB ( 13) still shows residual binding to Fn ( 7), and it is possible that surface-associated Eap contributes to this binding.	bind
51538	3	11200	6	10	NULL	NULL	NULL	FnbB	GP	defective mutant	bind					Fn	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_6_2933_s_260	12010982	A mutant defective in both FnbA and FnbB ( 13) still shows residual binding to Fn ( 7), and it is possible that surface-associated Eap contributes to this binding.	bind
51539	4	11200	6	10	NULL	NULL	NULL	Eap	GP	surface associated	contribute to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_6_2933_s_260	12010982	A mutant defective in both FnbA and FnbB ( 13) still shows residual binding to Fn ( 7), and it is possible that surface-associated Eap contributes to this binding.	bind
49761	1	11200	7	10	NULL	NULL	NULL	FnbA	GP	defective mutant	bind					Fn	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_6_2933_s_260	12010982	A mutant defective in both FnbA and FnbB ( 13) still shows residual binding to Fn ( 7), and it is possible that surface-associated Eap contributes to this binding.	bind
49762	2	11200	7	10	NULL	NULL	NULL	FnbB	GP	defective mutant	bind					Fn	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_6_2933_s_260	12010982	A mutant defective in both FnbA and FnbB ( 13) still shows residual binding to Fn ( 7), and it is possible that surface-associated Eap contributes to this binding.	bind
49763	3	11200	7	10	NULL	NULL	NULL	Eap	GP	surface-associated	contribute to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_6_2933_s_260	12010982	A mutant defective in both FnbA and FnbB ( 13) still shows residual binding to Fn ( 7), and it is possible that surface-associated Eap contributes to this binding.	bind
49764	4	11200	7	10	NULL	NULL	NULL	Eap	GP	surface-associated	contribute to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_70_6_2933_s_260	12010982	A mutant defective in both FnbA and FnbB ( 13) still shows residual binding to Fn ( 7), and it is possible that surface-associated Eap contributes to this binding.	bind
44417	1	11201	5	10	NULL	NULL	NULL	Clock	GP	Drosophila	is a homolog of					Clock	GP	mammalian			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_7_1009_s_232	11163178	A mutant Drosophila homolog of mammalian  Clock disrupts circadian rhythms and transcription of  period and  timeless.	bind
44418	2	11201	5	10	NULL	NULL	NULL	statement 1	Process	mutant	disrupt					circadian rhythms	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_7_1009_s_232	11163178	A mutant Drosophila homolog of mammalian  Clock disrupts circadian rhythms and transcription of  period and  timeless.	bind
44419	3	11201	5	10	NULL	NULL	NULL	statement 1	Process	mutant	disrupt					period	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_7_1009_s_232	11163178	A mutant Drosophila homolog of mammalian  Clock disrupts circadian rhythms and transcription of  period and  timeless.	bind
44420	4	11201	5	10	NULL	NULL	NULL	statement 1	Process	mutant	disrupt					timeless	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_7_1009_s_232	11163178	A mutant Drosophila homolog of mammalian  Clock disrupts circadian rhythms and transcription of  period and  timeless.	bind
44334	1	11201	6	10	NULL	NULL	NULL	Clock	GP	Drosophila 	is a homolog of					Clock	GP	mammalian			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_7_1009_s_232	11163178	A mutant Drosophila homolog of mammalian  Clock disrupts circadian rhythms and transcription of  period and  timeless.	bind
44335	2	11201	6	10	NULL	NULL	NULL	statement 1	Process	mutant	disrupts					circadian rhythms	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_7_1009_s_232	11163178	A mutant Drosophila homolog of mammalian  Clock disrupts circadian rhythms and transcription of  period and  timeless.	bind
44336	3	11201	6	10	NULL	NULL	NULL	Clock	GP	mutant	disrupts					period	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_7_1009_s_232	11163178	A mutant Drosophila homolog of mammalian  Clock disrupts circadian rhythms and transcription of  period and  timeless.	bind
50850	4	11201	6	10	NULL	NULL	NULL	statement 1	Process	mutant	disrupts					timeless	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_cell_103_7_1009_s_232	11163178	A mutant Drosophila homolog of mammalian  Clock disrupts circadian rhythms and transcription of  period and  timeless.	bind
44421	1	11202	5	10	NULL	NULL	NULL	E1A	GP	mutant	does not bind				exon 2	CtBP	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10379_s_297	16287852	A mutant E1A exon 2 that no longerR binds to CtBP, however, had no effect on transcriptional activity of the  Hey1 promoter.	bind
44422	2	11202	5	10	NULL	NULL	NULL	E1A	GP	mutant	does not effect				exon 2	Hey1	GP	transcriptional activity of		promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10379_s_297	16287852	A mutant E1A exon 2 that no longerR binds to CtBP, however, had no effect on transcriptional activity of the  Hey1 promoter.	bind
44337	1	11202	6	10	NULL	NULL	NULL	E1A 	GP	mutant	does not bind				exon 2	CtBP	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10379_s_297	16287852	A mutant E1A exon 2 that no longerR binds to CtBP, however, had no effect on transcriptional activity of the  Hey1 promoter.	bind
44338	2	11202	6	10	NULL	NULL	NULL	E1A 	GP	mutant	has no effect on				exon 2	Hey1	GP	transcriptional activity of		promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_23_10379_s_297	16287852	A mutant E1A exon 2 that no longerR binds to CtBP, however, had no effect on transcriptional activity of the  Hey1 promoter.	bind
44423	1	11204	5	10	NULL	NULL	NULL	ABCA1	GP	mutant	bind			W590S		apoA-I	GP				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_45_2_287_s_8	14617740	A mutant form of ABCA1 (W590S) that avidly binds apoA-I but fails to promote cholesterol efflux released apoA-I with similar kinetics but without transfer of cholesterol to apoA-I.	bind
44424	2	11204	5	10	NULL	NULL	NULL	ABCA1	GP	mutant	does not promote			W590S		cholesterol efflux	Process				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_45_2_287_s_8	14617740	A mutant form of ABCA1 (W590S) that avidly binds apoA-I but fails to promote cholesterol efflux released apoA-I with similar kinetics but without transfer of cholesterol to apoA-I.	bind
44425	3	11204	5	10	NULL	NULL	NULL	ABCA1	GP	mutant	release			W590S		apoA-I	GP				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_45_2_287_s_8	14617740	A mutant form of ABCA1 (W590S) that avidly binds apoA-I but fails to promote cholesterol efflux released apoA-I with similar kinetics but without transfer of cholesterol to apoA-I.	bind
44426	4	11204	5	10	NULL	NULL	NULL	cholesterol	Chemical		is not transfered to					apoA-I	GP				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_45_2_287_s_8	14617740	A mutant form of ABCA1 (W590S) that avidly binds apoA-I but fails to promote cholesterol efflux released apoA-I with similar kinetics but without transfer of cholesterol to apoA-I.	bind
44427	5	11204	5	10	NULL	NULL	NULL	statement 3	Process		occurs simultaneously with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_45_2_287_s_8	14617740	A mutant form of ABCA1 (W590S) that avidly binds apoA-I but fails to promote cholesterol efflux released apoA-I with similar kinetics but without transfer of cholesterol to apoA-I.	bind
44339	1	11204	6	10	NULL	NULL	NULL	ABCA1	GP	mutant	bind		avidly	W590S		apoA-I	GP				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_45_2_287_s_8	14617740	A mutant form of ABCA1 (W590S) that avidly binds apoA-I but fails to promote cholesterol efflux released apoA-I with similar kinetics but without transfer of cholesterol to apoA-I.	bind
44340	2	11204	6	10	NULL	NULL	NULL	ABCA1	GP	mutant	does not promote			W590S		cholesterol efflux	Process				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_45_2_287_s_8	14617740	A mutant form of ABCA1 (W590S) that avidly binds apoA-I but fails to promote cholesterol efflux released apoA-I with similar kinetics but without transfer of cholesterol to apoA-I.	bind
44999	3	11204	6	10	NULL	NULL	NULL	ABCA1	GP	mutant	releases			W590S		apoA-I	GP				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_45_2_287_s_8	14617740	A mutant form of ABCA1 (W590S) that avidly binds apoA-I but fails to promote cholesterol efflux released apoA-I with similar kinetics but without transfer of cholesterol to apoA-I.	bind
45000	4	11204	6	10	NULL	NULL	NULL	cholesterol	Chemical		is not transfered to					apoA-I	GP				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_45_2_287_s_8	14617740	A mutant form of ABCA1 (W590S) that avidly binds apoA-I but fails to promote cholesterol efflux released apoA-I with similar kinetics but without transfer of cholesterol to apoA-I.	bind
45002	5	11204	6	10	NULL	NULL	NULL	statement 3	Process		occurs simultaneous with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_45_2_287_s_8	14617740	A mutant form of ABCA1 (W590S) that avidly binds apoA-I but fails to promote cholesterol efflux released apoA-I with similar kinetics but without transfer of cholesterol to apoA-I.	bind
44483	1	11205	5	10	NULL	NULL	NULL	Armadillo	GP	mutant	lacks								fifth Armadillo repeat		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_4_181_s_222	9501980	A mutant form of Armadillo lacking the fifth Armadillo repeat fails to bind to  Drosophila TCF (and therefore lacks signaling activity), but accumulates in embryonic nuclei in response to Wingless (Wnt) signaling   [34,40]  .	bind
44484	2	11205	5	10	NULL	NULL	NULL	statement 1	GP		does not bind					TCF	GP	Drosophila			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_4_181_s_222	9501980	A mutant form of Armadillo lacking the fifth Armadillo repeat fails to bind to  Drosophila TCF (and therefore lacks signaling activity), but accumulates in embryonic nuclei in response to Wingless (Wnt) signaling   [34,40]  .	bind
44485	3	11205	5	10	NULL	NULL	NULL	statement 1	GP		lacks					signaling activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_4_181_s_222	9501980	A mutant form of Armadillo lacking the fifth Armadillo repeat fails to bind to  Drosophila TCF (and therefore lacks signaling activity), but accumulates in embryonic nuclei in response to Wingless (Wnt) signaling   [34,40]  .	bind
44486	4	11205	5	10	NULL	NULL	NULL	statement 1	GP		accumulates in					nucleus	CellComponent	embryonic			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_4_181_s_222	9501980	A mutant form of Armadillo lacking the fifth Armadillo repeat fails to bind to  Drosophila TCF (and therefore lacks signaling activity), but accumulates in embryonic nuclei in response to Wingless (Wnt) signaling   [34,40]  .	bind
44487	5	11205	5	10	NULL	NULL	NULL	statement 4	Process		in response to					Wnt signaling	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_4_181_s_222	9501980	A mutant form of Armadillo lacking the fifth Armadillo repeat fails to bind to  Drosophila TCF (and therefore lacks signaling activity), but accumulates in embryonic nuclei in response to Wingless (Wnt) signaling   [34,40]  .	bind
44488	6	11205	5	10	NULL	NULL	NULL	Wnt signaling	Process		is					Wingless signaling	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_4_181_s_222	9501980	A mutant form of Armadillo lacking the fifth Armadillo repeat fails to bind to  Drosophila TCF (and therefore lacks signaling activity), but accumulates in embryonic nuclei in response to Wingless (Wnt) signaling   [34,40]  .	bind
44341	1	11205	6	10	NULL	NULL	NULL	Armadillo	GP	mutant;; lacking	does not bind			fifth repeat		TCF	GP	Drosophila			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_4_181_s_222	9501980	A mutant form of Armadillo lacking the fifth Armadillo repeat fails to bind to  Drosophila TCF (and therefore lacks signaling activity), but accumulates in embryonic nuclei in response to Wingless (Wnt) signaling   [34,40]  .	bind
44342	2	11205	6	10	NULL	NULL	NULL	Armadillo	GP	mutant;; lacking	accumulates in			fifth repeat		nuclei	CellComponent	embryonic			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_4_181_s_222	9501980	A mutant form of Armadillo lacking the fifth Armadillo repeat fails to bind to  Drosophila TCF (and therefore lacks signaling activity), but accumulates in embryonic nuclei in response to Wingless (Wnt) signaling   [34,40]  .	bind
44343	3	11205	6	10	NULL	NULL	NULL	statement 2	Process		occurs in response to					wnt signaling	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_4_181_s_222	9501980	A mutant form of Armadillo lacking the fifth Armadillo repeat fails to bind to  Drosophila TCF (and therefore lacks signaling activity), but accumulates in embryonic nuclei in response to Wingless (Wnt) signaling   [34,40]  .	bind
44344	4	11205	6	10	NULL	NULL	NULL	Wnt	GP		is					wingless	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_4_181_s_222	9501980	A mutant form of Armadillo lacking the fifth Armadillo repeat fails to bind to  Drosophila TCF (and therefore lacks signaling activity), but accumulates in embryonic nuclei in response to Wingless (Wnt) signaling   [34,40]  .	bind
44345	5	11205	6	10	NULL	NULL	NULL	Armadillo	GP	mutant;; lacking	lacks			fifth repeat		signaling activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_4_181_s_222	9501980	A mutant form of Armadillo lacking the fifth Armadillo repeat fails to bind to  Drosophila TCF (and therefore lacks signaling activity), but accumulates in embryonic nuclei in response to Wingless (Wnt) signaling   [34,40]  .	bind
44346	6	11205	6	10	NULL	NULL	NULL	statement 5	Process		is because of					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_4_181_s_222	9501980	A mutant form of Armadillo lacking the fifth Armadillo repeat fails to bind to  Drosophila TCF (and therefore lacks signaling activity), but accumulates in embryonic nuclei in response to Wingless (Wnt) signaling   [34,40]  .	bind
44489	1	11206	5	NULL	NULL	NULL	NULL	axin	GP	mutant	does not bind					GSK3beta	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_39037_s_251	11487578	A mutant form of axin that did not bind to GSK3beta nevertheless promoted the phosphorylation of APC fragments when coexpressed with them.	bind
44490	2	11206	5	NULL	NULL	NULL	NULL	axin	GP	mutant	promotes					APC fragments	AminoAcid	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_39037_s_251	11487578	A mutant form of axin that did not bind to GSK3beta nevertheless promoted the phosphorylation of APC fragments when coexpressed with them.	bind
44347	1	11206	6	NULL	NULL	0	NULL	axin	NULL	mutant	does not bind	NULL				GSK-3beta	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39037_s_251	11487578	A mutant form of axin that did not bind to GSK3beta nevertheless promoted the phosphorylation of APC fragments when coexpressed with them.	bind
44348	2	11206	6	NULL	NULL	0	NULL	axin	NULL	mutant	promotes	NULL				APC fragments	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39037_s_251	11487578	A mutant form of axin that did not bind to GSK3beta nevertheless promoted the phosphorylation of APC fragments when coexpressed with them.	bind
44491	1	11207	5	NULL	NULL	NULL	NULL	CBP	GP	mutant	contains							deletion in	p160 binding region (amino acids 2098 to 2163) 		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_1_39_s_48	11113179	A mutant form of CBP containing a deletion in the p160 binding region (amino acids 2098 to 2163) inhibited RAR-mediated transcription in microinjected cells ( 34).	bind
44492	2	11207	5	NULL	NULL	NULL	NULL	statement 1	Process		inhibit					transcription	Process				NULL	microinjected cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_1_39_s_48	11113179	A mutant form of CBP containing a deletion in the p160 binding region (amino acids 2098 to 2163) inhibited RAR-mediated transcription in microinjected cells ( 34).	bind
44493	3	11207	5	NULL	NULL	NULL	NULL	transcription	Process		mediated by					RAR	GP				NULL	microinjected cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_1_39_s_48	11113179	A mutant form of CBP containing a deletion in the p160 binding region (amino acids 2098 to 2163) inhibited RAR-mediated transcription in microinjected cells ( 34).	bind
45005	1	11207	6	10	NULL	0	NULL	RAR			mediates					transcription					NULL	microinjected cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_1_39_s_48	11113179	A mutant form of CBP containing a deletion in the p160 binding region (amino acids 2098 to 2163) inhibited RAR-mediated transcription in microinjected cells ( 34).	bind
45006	2	11207	6	10	NULL	0	NULL	CBP		mutant;; deletion of	inhibits			p160 binding region		statement 1					NULL	microinjected cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_1_39_s_48	11113179	A mutant form of CBP containing a deletion in the p160 binding region (amino acids 2098 to 2163) inhibited RAR-mediated transcription in microinjected cells ( 34).	bind
44495	1	11208	5	NULL	NULL	NULL	NULL	Importin alpha	GP	mutant	does not bind		efficiently	ED		NLS proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1526_s_118	15014441	A mutant form of Importin alpha that does not bind efficiently to NLS proteins, the ED mutant (  et al), did not change mobility in the presence of CKII and NLS peptides ( Supplementary Figure 1A).	bind
44349	1	11208	6	10	NULL	0	NULL	Importin alpha	NULL	mutant	does not bind	NULL	efficiently	ED		NLS proteins	NULL				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_7_1526_s_118	15014441	A mutant form of Importin alpha that does not bind efficiently to NLS proteins, the ED mutant (  et al), did not change mobility in the presence of CKII and NLS peptides ( Supplementary Figure 1A).	bind
44499	1	11209	5	NULL	NULL	NULL	NULL	NGF3T	GP		is a mutant of					NGF	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_38_23547_s_56	9295291	A mutant form of NGF (NGF3T) that does not bind p75NTR ( 21) was used to selectively activate TrkA and BDNF was used to selectively activate p75NTR.	bind
44500	2	11209	5	NULL	NULL	NULL	NULL	statement 1	Process		does not bind					p75NTR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_38_23547_s_56	9295291	A mutant form of NGF (NGF3T) that does not bind p75NTR ( 21) was used to selectively activate TrkA and BDNF was used to selectively activate p75NTR.	bind
44501	3	11209	5	NULL	NULL	NULL	NULL	statement 1	Process		activates		selectively			TrkA	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_38_23547_s_56	9295291	A mutant form of NGF (NGF3T) that does not bind p75NTR ( 21) was used to selectively activate TrkA and BDNF was used to selectively activate p75NTR.	bind
44502	4	11209	5	NULL	NULL	NULL	NULL	BDNF	GP		activates		selectively			p75NTR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_38_23547_s_56	9295291	A mutant form of NGF (NGF3T) that does not bind p75NTR ( 21) was used to selectively activate TrkA and BDNF was used to selectively activate p75NTR.	bind
44350	1	11209	6	10	NULL	0	NULL	NGF3T			is a mutant of					NGF					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_38_23547_s_56	9295291	A mutant form of NGF (NGF3T) that does not bind p75NTR ( 21) was used to selectively activate TrkA and BDNF was used to selectively activate p75NTR.	bind
44351	2	11209	6	NULL	NULL	0	NULL	NGF3T	NULL		does not bind	NULL				p75NTR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_38_23547_s_56	9295291	A mutant form of NGF (NGF3T) that does not bind p75NTR ( 21) was used to selectively activate TrkA and BDNF was used to selectively activate p75NTR.	bind
44352	3	11209	6	10	NULL	0	NULL	NGF3T			activate		selectively			TrkA					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_38_23547_s_56	9295291	A mutant form of NGF (NGF3T) that does not bind p75NTR ( 21) was used to selectively activate TrkA and BDNF was used to selectively activate p75NTR.	bind
44353	4	11209	6	NULL	NULL	0	NULL	BDNF	NULL		activates	NULL	selectively			p75NTR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_38_23547_s_56	9295291	A mutant form of NGF (NGF3T) that does not bind p75NTR ( 21) was used to selectively activate TrkA and BDNF was used to selectively activate p75NTR.	bind
44503	1	11210	5	NULL	NULL	NULL	NULL	NHERF	GP	mutant	does not bind					EGFR	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5470_s_29	15469991	A mutant form of NHERF that does not bind EGFR also enhances EGFR down-regulation, supporting the conclusion that NHERF functions to retain EGFR at the cell surface.	bind
44504	2	11210	5	NULL	NULL	NULL	NULL	NHERF	GP	mutant	enhance					EGFR	GP	down-regulation of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5470_s_29	15469991	A mutant form of NHERF that does not bind EGFR also enhances EGFR down-regulation, supporting the conclusion that NHERF functions to retain EGFR at the cell surface.	bind
44505	3	11210	5	NULL	NULL	NULL	NULL	NHERF	GP		retains					EGFR	GP				NULL	cell surface	NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5470_s_29	15469991	A mutant form of NHERF that does not bind EGFR also enhances EGFR down-regulation, supporting the conclusion that NHERF functions to retain EGFR at the cell surface.	bind
44354	1	11210	6	NULL	NULL	0	NULL	NHERF	NULL	mutant	does not bind	NULL				EGFR	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_12_5470_s_29	15469991	A mutant form of NHERF that does not bind EGFR also enhances EGFR down-regulation, supporting the conclusion that NHERF functions to retain EGFR at the cell surface.	bind
44355	2	11210	6	NULL	NULL	0	NULL	NHERF	NULL	mutant	enhances	NULL				EGFR	NULL	downregulation of			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5470_s_29	15469991	A mutant form of NHERF that does not bind EGFR also enhances EGFR down-regulation, supporting the conclusion that NHERF functions to retain EGFR at the cell surface.	bind
44356	3	11210	6	10	NULL	0	NULL	NHERF			retains					EGFR					NULL	cell surface	NULL	NULL	NULL	NULL	gw70_molbiolcell_15_12_5470_s_29	15469991	A mutant form of NHERF that does not bind EGFR also enhances EGFR down-regulation, supporting the conclusion that NHERF functions to retain EGFR at the cell surface.	bind
44506	1	11211	5	NULL	NULL	NULL	NULL	p120 ctn	GP	mutant	does not bind					cadherins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_15_11264_s_10	10753936	A mutant form of p120 ctn that fails to bind cadherins can still associate with RPTPmu.	bind
44507	2	11211	5	NULL	NULL	NULL	NULL	statement 1	Process		associate with					RPTPmu	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_15_11264_s_10	10753936	A mutant form of p120 ctn that fails to bind cadherins can still associate with RPTPmu.	bind
44358	1	11211	6	NULL	NULL	0	NULL	p120 ctn	NULL	mutant	does not bind	NULL				cadherin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_15_11264_s_10	10753936	A mutant form of p120 ctn that fails to bind cadherins can still associate with RPTPmu.	bind
44359	2	11211	6	NULL	NULL	0	NULL	p120 ctn	NULL	mutant	associates with	NULL				RPTPmu	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_15_11264_s_10	10753936	A mutant form of p120 ctn that fails to bind cadherins can still associate with RPTPmu.	bind
44508	1	11213	5	NULL	NULL	NULL	NULL	Pyk2	GP	mutant	does not bind			Y402F		Src	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14893_s_218	10329689	A mutant form of Pyk2 (Pyk2-Y402F) that is unable to bind and activate Src is impaired in its ability to induce association of Grb2 with Shc, binding of Crk to p130Cas and stimulation of the ERK and JNK cascades.	bind
44509	2	11213	5	NULL	NULL	NULL	NULL	statement 1	Process		does not activate					Src	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14893_s_218	10329689	A mutant form of Pyk2 (Pyk2-Y402F) that is unable to bind and activate Src is impaired in its ability to induce association of Grb2 with Shc, binding of Crk to p130Cas and stimulation of the ERK and JNK cascades.	bind
44510	3	11213	5	NULL	NULL	NULL	NULL	Grb2	GP		associate with					Shc	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14893_s_218	10329689	A mutant form of Pyk2 (Pyk2-Y402F) that is unable to bind and activate Src is impaired in its ability to induce association of Grb2 with Shc, binding of Crk to p130Cas and stimulation of the ERK and JNK cascades.	bind
44511	4	11213	5	NULL	NULL	NULL	NULL	Pyk2	GP	mutant	does not induce			Y402F		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14893_s_218	10329689	A mutant form of Pyk2 (Pyk2-Y402F) that is unable to bind and activate Src is impaired in its ability to induce association of Grb2 with Shc, binding of Crk to p130Cas and stimulation of the ERK and JNK cascades.	bind
44512	5	11213	5	NULL	NULL	NULL	NULL	Crk	GP		bind					p130Cas	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14893_s_218	10329689	A mutant form of Pyk2 (Pyk2-Y402F) that is unable to bind and activate Src is impaired in its ability to induce association of Grb2 with Shc, binding of Crk to p130Cas and stimulation of the ERK and JNK cascades.	bind
44513	6	11213	5	NULL	NULL	NULL	NULL	Pyk2	GP	mutant	does not induce			Y402F		statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14893_s_218	10329689	A mutant form of Pyk2 (Pyk2-Y402F) that is unable to bind and activate Src is impaired in its ability to induce association of Grb2 with Shc, binding of Crk to p130Cas and stimulation of the ERK and JNK cascades.	bind
44514	7	11213	5	NULL	NULL	NULL	NULL	Pyk2	GP	mutant	does not stimulate			Y402F		ERK cascade	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14893_s_218	10329689	A mutant form of Pyk2 (Pyk2-Y402F) that is unable to bind and activate Src is impaired in its ability to induce association of Grb2 with Shc, binding of Crk to p130Cas and stimulation of the ERK and JNK cascades.	bind
44515	8	11213	5	NULL	NULL	NULL	NULL	Pyk2	GP	mutant	does not stimulate			Y402F		JNK cascade	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14893_s_218	10329689	A mutant form of Pyk2 (Pyk2-Y402F) that is unable to bind and activate Src is impaired in its ability to induce association of Grb2 with Shc, binding of Crk to p130Cas and stimulation of the ERK and JNK cascades.	bind
44442	1	11213	6	NULL	NULL	0	NULL	Pyk2	NULL	mutant	does not bind	NULL		Y402F		Src	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_14893_s_218	10329689	A mutant form of Pyk2 (Pyk2-Y402F) that is unable to bind and activate Src is impaired in its ability to induce association of Grb2 with Shc, binding of Crk to p130Cas and stimulation of the ERK and JNK cascades.	bind
44443	2	11213	6	NULL	NULL	0	NULL	Pyk2	NULL	mutant	does not activate	NULL		Y402F		Src	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_14893_s_218	10329689	A mutant form of Pyk2 (Pyk2-Y402F) that is unable to bind and activate Src is impaired in its ability to induce association of Grb2 with Shc, binding of Crk to p130Cas and stimulation of the ERK and JNK cascades.	bind
44444	3	11213	6	NULL	NULL	0	NULL	Grb2	NULL		associates with	NULL				Shc	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_14893_s_218	10329689	A mutant form of Pyk2 (Pyk2-Y402F) that is unable to bind and activate Src is impaired in its ability to induce association of Grb2 with Shc, binding of Crk to p130Cas and stimulation of the ERK and JNK cascades.	bind
44445	4	11213	6	NULL	NULL	0	NULL	Pyk2	NULL	mutant	does not induce	NULL		Y402F		statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_14893_s_218	10329689	A mutant form of Pyk2 (Pyk2-Y402F) that is unable to bind and activate Src is impaired in its ability to induce association of Grb2 with Shc, binding of Crk to p130Cas and stimulation of the ERK and JNK cascades.	bind
44446	5	11213	6	NULL	NULL	0	NULL	Crk	NULL		bind	NULL				p130Cas	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_14893_s_218	10329689	A mutant form of Pyk2 (Pyk2-Y402F) that is unable to bind and activate Src is impaired in its ability to induce association of Grb2 with Shc, binding of Crk to p130Cas and stimulation of the ERK and JNK cascades.	bind
44447	6	11213	6	NULL	NULL	0	NULL	Pyk2	NULL	mutant	does not induce	NULL		Y402F		statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_14893_s_218	10329689	A mutant form of Pyk2 (Pyk2-Y402F) that is unable to bind and activate Src is impaired in its ability to induce association of Grb2 with Shc, binding of Crk to p130Cas and stimulation of the ERK and JNK cascades.	bind
44448	7	11213	6	NULL	NULL	0	NULL	Pyk2	NULL	mutant	does not induce	NULL		Y402F		ERK cascade	NULL	stimulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_14893_s_218	10329689	A mutant form of Pyk2 (Pyk2-Y402F) that is unable to bind and activate Src is impaired in its ability to induce association of Grb2 with Shc, binding of Crk to p130Cas and stimulation of the ERK and JNK cascades.	bind
44449	8	11213	6	NULL	NULL	0	NULL	Pyk2	NULL	mutant	does not induce	NULL		Y402F		JNK cascade	NULL	stimulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_14893_s_218	10329689	A mutant form of Pyk2 (Pyk2-Y402F) that is unable to bind and activate Src is impaired in its ability to induce association of Grb2 with Shc, binding of Crk to p130Cas and stimulation of the ERK and JNK cascades.	bind
44516	1	11214	5	NULL	NULL	NULL	NULL	deltap85	GP		is a mutant of					PI3-K	GP		p85 regulatory subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31515_s_145	9395488	A mutant form of the p85 regulatory subunit of PI3-K (deltap85) that fails to bind and activate the p110 catalytic subunit has been reported to act as a dominant negative mutant of this enzyme ( 34) and to abolish platelet-derived growth factor-induced activation of PKB in cotransfection experiments ( 5).	bind
44517	2	11214	5	NULL	NULL	NULL	NULL	deltap85 	GP		does not bind					p110	GP		catalytic subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31515_s_145	9395488	A mutant form of the p85 regulatory subunit of PI3-K (deltap85) that fails to bind and activate the p110 catalytic subunit has been reported to act as a dominant negative mutant of this enzyme ( 34) and to abolish platelet-derived growth factor-induced activation of PKB in cotransfection experiments ( 5).	bind
44518	3	11214	5	NULL	NULL	NULL	NULL	deltap85	GP		does not activate					p110	GP		catalytic subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31515_s_145	9395488	A mutant form of the p85 regulatory subunit of PI3-K (deltap85) that fails to bind and activate the p110 catalytic subunit has been reported to act as a dominant negative mutant of this enzyme ( 34) and to abolish platelet-derived growth factor-induced activation of PKB in cotransfection experiments ( 5).	bind
44519	4	11214	5	NULL	NULL	NULL	NULL	deltap85	GP		acts as					PI3-K	GP	dominant negative mutant of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31515_s_145	9395488	A mutant form of the p85 regulatory subunit of PI3-K (deltap85) that fails to bind and activate the p110 catalytic subunit has been reported to act as a dominant negative mutant of this enzyme ( 34) and to abolish platelet-derived growth factor-induced activation of PKB in cotransfection experiments ( 5).	bind
44520	5	11214	5	NULL	NULL	NULL	NULL	platelet-derived growth factor	GP		induce					PKB	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31515_s_145	9395488	A mutant form of the p85 regulatory subunit of PI3-K (deltap85) that fails to bind and activate the p110 catalytic subunit has been reported to act as a dominant negative mutant of this enzyme ( 34) and to abolish platelet-derived growth factor-induced activation of PKB in cotransfection experiments ( 5).	bind
44521	6	11214	5	NULL	NULL	NULL	NULL	deltap85	GP		abolishes					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31515_s_145	9395488	A mutant form of the p85 regulatory subunit of PI3-K (deltap85) that fails to bind and activate the p110 catalytic subunit has been reported to act as a dominant negative mutant of this enzyme ( 34) and to abolish platelet-derived growth factor-induced activation of PKB in cotransfection experiments ( 5).	bind
44450	1	11214	6	10	NULL	0	NULL	deltap85			is a mutant of					PI3-K			p85 regulatory subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31515_s_145	9395488	A mutant form of the p85 regulatory subunit of PI3-K (deltap85) that fails to bind and activate the p110 catalytic subunit has been reported to act as a dominant negative mutant of this enzyme ( 34) and to abolish platelet-derived growth factor-induced activation of PKB in cotransfection experiments ( 5).	bind
44451	2	11214	6	10	NULL	0	NULL	deltap85			does not bind					p110			catalytic subunit		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31515_s_145	9395488	A mutant form of the p85 regulatory subunit of PI3-K (deltap85) that fails to bind and activate the p110 catalytic subunit has been reported to act as a dominant negative mutant of this enzyme ( 34) and to abolish platelet-derived growth factor-induced activation of PKB in cotransfection experiments ( 5).	bind
44452	3	11214	6	10	NULL	0	NULL	platelet-derived growth factor			induces					PKB		activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31515_s_145	9395488	A mutant form of the p85 regulatory subunit of PI3-K (deltap85) that fails to bind and activate the p110 catalytic subunit has been reported to act as a dominant negative mutant of this enzyme ( 34) and to abolish platelet-derived growth factor-induced activation of PKB in cotransfection experiments ( 5).	bind
44453	4	11214	6	10	NULL	0	NULL	deltap85			abolishes					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_50_31515_s_145	9395488	A mutant form of the p85 regulatory subunit of PI3-K (deltap85) that fails to bind and activate the p110 catalytic subunit has been reported to act as a dominant negative mutant of this enzyme ( 34) and to abolish platelet-derived growth factor-induced activation of PKB in cotransfection experiments ( 5).	bind
50855	5	11214	6	10	NULL	0	NULL	deltap85	NULL		does not activate	NULL				p110	NULL		catalytic subuni		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31515_s_145	9395488	A mutant form of the p85 regulatory subunit of PI3-K (deltap85) that fails to bind and activate the p110 catalytic subunit has been reported to act as a dominant negative mutant of this enzyme ( 34) and to abolish platelet-derived growth factor-induced activation of PKB in cotransfection experiments ( 5).	bind
50856	6	11214	6	10	NULL	0	NULL	deltap85	NULL		acts as	NULL				PI3-K	NULL	 dominant negative mutant of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31515_s_145	9395488	A mutant form of the p85 regulatory subunit of PI3-K (deltap85) that fails to bind and activate the p110 catalytic subunit has been reported to act as a dominant negative mutant of this enzyme ( 34) and to abolish platelet-derived growth factor-induced activation of PKB in cotransfection experiments ( 5).	bind
44522	1	11216	5	NULL	NULL	NULL	NULL	Cyclin A1	GP		is a mutant of			E167A		Cyclin A1	GP		N-terminal Helix		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_15415_s_169	11278837	A Mutant in the N-terminal Helix of Cyclin A1, E167A, Can Bind to Cdc2 But Not to Cdk2-- Cyclin A binds to both Cdc2 and Cdk2.	bind
44523	2	11216	5	NULL	NULL	NULL	NULL	statement 1	Process		bind					Cdc2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_15415_s_169	11278837	A Mutant in the N-terminal Helix of Cyclin A1, E167A, Can Bind to Cdc2 But Not to Cdk2-- Cyclin A binds to both Cdc2 and Cdk2.	bind
44524	3	11216	5	NULL	NULL	NULL	NULL	statement 1	Process		does not bind					Cdk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_15415_s_169	11278837	A Mutant in the N-terminal Helix of Cyclin A1, E167A, Can Bind to Cdc2 But Not to Cdk2-- Cyclin A binds to both Cdc2 and Cdk2.	bind
44525	4	11216	5	NULL	NULL	NULL	NULL	Cyclin A	GP		bind					Cdc2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_15415_s_169	11278837	A Mutant in the N-terminal Helix of Cyclin A1, E167A, Can Bind to Cdc2 But Not to Cdk2-- Cyclin A binds to both Cdc2 and Cdk2.	bind
44526	5	11216	5	NULL	NULL	NULL	NULL	Cyclin A	GP		bind					Cdk2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_15415_s_169	11278837	A Mutant in the N-terminal Helix of Cyclin A1, E167A, Can Bind to Cdc2 But Not to Cdk2-- Cyclin A binds to both Cdc2 and Cdk2.	bind
44454	1	11216	6	NULL	NULL	0	NULL	Cyclin A1	NULL	mutant	bind	NULL		N-terminal helix;; E167A		Cdc2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_15415_s_169	11278837	A Mutant in the N-terminal Helix of Cyclin A1, E167A, Can Bind to Cdc2 But Not to Cdk2-- Cyclin A binds to both Cdc2 and Cdk2.	bind
44455	2	11216	6	10	NULL	0	NULL	Cyclin A1	NULL	mutant	does not bind	NULL		N-terminal helix;; E167A		Cdk2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_15415_s_169	11278837	A Mutant in the N-terminal Helix of Cyclin A1, E167A, Can Bind to Cdc2 But Not to Cdk2-- Cyclin A binds to both Cdc2 and Cdk2.	bind
44456	3	11216	6	10	NULL	0	NULL	Cyclin A	NULL		bind	NULL				Cdc2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_15415_s_169	11278837	A Mutant in the N-terminal Helix of Cyclin A1, E167A, Can Bind to Cdc2 But Not to Cdk2-- Cyclin A binds to both Cdc2 and Cdk2.	bind
50857	4	11216	6	10	NULL	0	NULL	Cyclin A	NULL		bind	NULL				Cdk2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_18_15415_s_169	11278837	A Mutant in the N-terminal Helix of Cyclin A1, E167A, Can Bind to Cdc2 But Not to Cdk2-- Cyclin A binds to both Cdc2 and Cdk2.	bind
44527	1	11217	5	NULL	NULL	NULL	NULL	ATF6	GP	mutant of	lacks			468-500					GLSs		NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_99_s_218	12110171	A mutant lacking the GLSs, ATF6( 468-500), bound and dissociated from BiP like wild-type ATF6   (Figure 5D).	bind
44528	2	11217	5	NULL	NULL	NULL	NULL	statement 1	Process		dissociates from					BiP	GP	wild-type			NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_99_s_218	12110171	A mutant lacking the GLSs, ATF6( 468-500), bound and dissociated from BiP like wild-type ATF6   (Figure 5D).	bind
46365	3	11217	5	NULL	NULL	NULL	NULL	ATF6	GP	wild-type	bind					BiP	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_99_s_218	12110171	A mutant lacking the GLSs, ATF6( 468-500), bound and dissociated from BiP like wild-type ATF6   (Figure 5D).	bind
46366	4	11217	5	NULL	NULL	NULL	NULL	statement 1	Process		is similar to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_99_s_218	12110171	A mutant lacking the GLSs, ATF6( 468-500), bound and dissociated from BiP like wild-type ATF6   (Figure 5D).	bind
46367	5	11217	5	NULL	NULL	NULL	NULL	ATF6	GP	wild type	dissociates from					BiP	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_99_s_218	12110171	A mutant lacking the GLSs, ATF6( 468-500), bound and dissociated from BiP like wild-type ATF6   (Figure 5D).	bind
46368	6	11217	5	NULL	NULL	NULL	NULL	ATF6	GP	mutation of	dissociates from			468-500		BiP	GP				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_99_s_218	12110171	A mutant lacking the GLSs, ATF6( 468-500), bound and dissociated from BiP like wild-type ATF6   (Figure 5D).	bind
46369	7	11217	5	NULL	NULL	NULL	NULL	statement 5	Process		is similar to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_99_s_218	12110171	A mutant lacking the GLSs, ATF6( 468-500), bound and dissociated from BiP like wild-type ATF6   (Figure 5D).	bind
44457	1	11217	6	NULL	NULL	0	NULL	ATF6	NULL	wild type	bind	NULL				BiP	NULL				NULL		0	NULL	NULL	NULL	gw60_devcell_3_1_99_s_218	12110171	A mutant lacking the GLSs, ATF6( 468-500), bound and dissociated from BiP like wild-type ATF6   (Figure 5D).	bind
44458	2	11217	6	NULL	NULL	0	NULL	ATF6	NULL	mutant of 	bind	NULL		468-500		BiP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_99_s_218	12110171	A mutant lacking the GLSs, ATF6( 468-500), bound and dissociated from BiP like wild-type ATF6   (Figure 5D).	bind
46354	3	11217	6	NULL	NULL	0	NULL	statement 1	NULL		is similar to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_devcell_3_1_99_s_218	12110171	A mutant lacking the GLSs, ATF6( 468-500), bound and dissociated from BiP like wild-type ATF6   (Figure 5D).	bind
46355	4	11217	6	NULL	NULL	0	NULL	ATF6	NULL	wild type	dissociates from	NULL				BiP	NULL				NULL		0	NULL	NULL	NULL	gw60_devcell_3_1_99_s_218	12110171	A mutant lacking the GLSs, ATF6( 468-500), bound and dissociated from BiP like wild-type ATF6   (Figure 5D).	bind
46356	5	11217	6	NULL	NULL	0	NULL	ATF6	NULL	mutant of	dissociates from	NULL		468-500		BiP	NULL				NULL		0	NULL	NULL	NULL	gw60_devcell_3_1_99_s_218	12110171	A mutant lacking the GLSs, ATF6( 468-500), bound and dissociated from BiP like wild-type ATF6   (Figure 5D).	bind
46357	6	11217	6	NULL	NULL	0	NULL	statement 4	NULL		is similar to	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_devcell_3_1_99_s_218	12110171	A mutant lacking the GLSs, ATF6( 468-500), bound and dissociated from BiP like wild-type ATF6   (Figure 5D).	bind
50858	7	11217	6	10	NULL	0	NULL	ATF6	NULL	mutant	lacks	NULL		468-500		GLSs	NULL				NULL		NULL	NULL	NULL	NULL	gw60_devcell_3_1_99_s_218	12110171	A mutant lacking the GLSs, ATF6( 468-500), bound and dissociated from BiP like wild-type ATF6   (Figure 5D).	bind
44627	1	11218	5	NULL	NULL	NULL	NULL			mutant	lacks					Fe(III) resistance genes	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803591_s_8	16803591	A mutant lacking the PmrA-regulated  Fe(III) resistance genes bound more Fe(III) than the wild-type strain  and was defective for survival in soil, suggesting that these PmrA-regulated  lipopolysaccharide modifications aid Salmonella's survival and spread  in non-host environments.	bind
44628	2	11218	5	NULL	NULL	NULL	NULL	Fe(III) resistance genes	GP		is regulated by					PmrA	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803591_s_8	16803591	A mutant lacking the PmrA-regulated  Fe(III) resistance genes bound more Fe(III) than the wild-type strain  and was defective for survival in soil, suggesting that these PmrA-regulated  lipopolysaccharide modifications aid Salmonella's survival and spread  in non-host environments.	bind
44629	3	11218	5	NULL	NULL	NULL	NULL	statement 1	Process		bind					Fe(III)	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803591_s_8	16803591	A mutant lacking the PmrA-regulated  Fe(III) resistance genes bound more Fe(III) than the wild-type strain  and was defective for survival in soil, suggesting that these PmrA-regulated  lipopolysaccharide modifications aid Salmonella's survival and spread  in non-host environments.	bind
44630	4	11218	5	NULL	NULL	NULL	NULL	strain		wild-type	bind					Fe(III)	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803591_s_8	16803591	A mutant lacking the PmrA-regulated  Fe(III) resistance genes bound more Fe(III) than the wild-type strain  and was defective for survival in soil, suggesting that these PmrA-regulated  lipopolysaccharide modifications aid Salmonella's survival and spread  in non-host environments.	bind
44631	5	11218	5	NULL	NULL	NULL	NULL	statement 3	Process	binding of	is more than					statement 4	Process	binding of			NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803591_s_8	16803591	A mutant lacking the PmrA-regulated  Fe(III) resistance genes bound more Fe(III) than the wild-type strain  and was defective for survival in soil, suggesting that these PmrA-regulated  lipopolysaccharide modifications aid Salmonella's survival and spread  in non-host environments.	bind
44632	6	11218	5	NULL	NULL	NULL	NULL	statement 1	Process		does not survive in					soil	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803591_s_8	16803591	A mutant lacking the PmrA-regulated  Fe(III) resistance genes bound more Fe(III) than the wild-type strain  and was defective for survival in soil, suggesting that these PmrA-regulated  lipopolysaccharide modifications aid Salmonella's survival and spread  in non-host environments.	bind
44633	7	11218	5	NULL	NULL	NULL	NULL	lipopolysaccharide	Chemical	modifications of	aid in					Salmonella	Organism	survival of			NULL	non-host environments	NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803591_s_8	16803591	A mutant lacking the PmrA-regulated  Fe(III) resistance genes bound more Fe(III) than the wild-type strain  and was defective for survival in soil, suggesting that these PmrA-regulated  lipopolysaccharide modifications aid Salmonella's survival and spread  in non-host environments.	bind
44634	8	11218	5	NULL	NULL	NULL	NULL	lipopolysaccharide	Chemical	modifications of	aid in					Salmonella	Organism	spreading of			NULL	non-host environments	NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803591_s_8	16803591	A mutant lacking the PmrA-regulated  Fe(III) resistance genes bound more Fe(III) than the wild-type strain  and was defective for survival in soil, suggesting that these PmrA-regulated  lipopolysaccharide modifications aid Salmonella's survival and spread  in non-host environments.	bind
44635	9	11218	5	NULL	NULL	NULL	NULL	lipopolysaccharide	Chemical	modifications of	is regulated by					PmrA	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803591_s_8	16803591	A mutant lacking the PmrA-regulated  Fe(III) resistance genes bound more Fe(III) than the wild-type strain  and was defective for survival in soil, suggesting that these PmrA-regulated  lipopolysaccharide modifications aid Salmonella's survival and spread  in non-host environments.	bind
45008	1	11218	6	10	NULL	0	NULL	PmrA	NULL		regulates	NULL				Fe(III) resistance gene	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803591_s_8	16803591	A mutant lacking the PmrA-regulated  Fe(III) resistance genes bound more Fe(III) than the wild-type strain  and was defective for survival in soil, suggesting that these PmrA-regulated  lipopolysaccharide modifications aid Salmonella's survival and spread  in non-host environments.	bind
45009	2	11218	6	10	NULL	0	NULL		NULL	mutant	lacks	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803591_s_8	16803591	A mutant lacking the PmrA-regulated  Fe(III) resistance genes bound more Fe(III) than the wild-type strain  and was defective for survival in soil, suggesting that these PmrA-regulated  lipopolysaccharide modifications aid Salmonella's survival and spread  in non-host environments.	bind
45010	4	11218	6	10	NULL	0	NULL	strain	NULL	wild-type	bind	NULL				Fe(III)	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803591_s_8	16803591	A mutant lacking the PmrA-regulated  Fe(III) resistance genes bound more Fe(III) than the wild-type strain  and was defective for survival in soil, suggesting that these PmrA-regulated  lipopolysaccharide modifications aid Salmonella's survival and spread  in non-host environments.	bind
45011	5	11218	6	10	NULL	0	NULL	PmrA	NULL		regulates	NULL				lipopolysaccharide	NULL	modification of 			NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803591_s_8	16803591	A mutant lacking the PmrA-regulated  Fe(III) resistance genes bound more Fe(III) than the wild-type strain  and was defective for survival in soil, suggesting that these PmrA-regulated  lipopolysaccharide modifications aid Salmonella's survival and spread  in non-host environments.	bind
45012	7	11218	6	10	NULL	0	NULL	statement 5	NULL		aids in	NULL				cell survival	NULL	salmonella			NULL	non-host environments	NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803591_s_8	16803591	A mutant lacking the PmrA-regulated  Fe(III) resistance genes bound more Fe(III) than the wild-type strain  and was defective for survival in soil, suggesting that these PmrA-regulated  lipopolysaccharide modifications aid Salmonella's survival and spread  in non-host environments.	bind
51052	6	11218	6	10	NULL	0	NULL	statement 3	NULL	binding of	is more than	NULL				statement 4	NULL	binding of			NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803591_s_8	16803591	A mutant lacking the PmrA-regulated  Fe(III) resistance genes bound more Fe(III) than the wild-type strain  and was defective for survival in soil, suggesting that these PmrA-regulated  lipopolysaccharide modifications aid Salmonella's survival and spread  in non-host environments.	bind
51053	3	11218	6	10	NULL	0	NULL	statement 2	NULL		bind	NULL				Fe(III)	NULL				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803591_s_8	16803591	A mutant lacking the PmrA-regulated  Fe(III) resistance genes bound more Fe(III) than the wild-type strain  and was defective for survival in soil, suggesting that these PmrA-regulated  lipopolysaccharide modifications aid Salmonella's survival and spread  in non-host environments.	bind
51054	8	11218	6	10	NULL	0	NULL	statement 5	NULL		aid in 	NULL				Salmonella	NULL	spreading of			NULL	non-host environments	0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803591_s_8	16803591	A mutant lacking the PmrA-regulated  Fe(III) resistance genes bound more Fe(III) than the wild-type strain  and was defective for survival in soil, suggesting that these PmrA-regulated  lipopolysaccharide modifications aid Salmonella's survival and spread  in non-host environments.	bind
44529	1	11219	5	NULL	NULL	NULL	NULL	estrogen receptor	GP	mutant	bind			LBD		tamoxifen	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_36_0_687_s_444	12429705	A mutant ligand-binding domain of the estrogen receptor (LBD), which binds tamoxifen  instead of estrogen ( 68), was fused to a dominant-negative CREB gene (S133A substitution).	bind
44530	2	11219	5	NULL	NULL	NULL	NULL	LBD	AminoAcid		is					ligand-binding domain	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_36_0_687_s_444	12429705	A mutant ligand-binding domain of the estrogen receptor (LBD), which binds tamoxifen  instead of estrogen ( 68), was fused to a dominant-negative CREB gene (S133A substitution).	bind
44459	1	11219	6	10	NULL	0	NULL	estrogen receptor		mutant	bind			LBD		tamoxifen					NULL		NULL	NULL	NULL	NULL	gw70_annurevgenet_36_0_687_s_444	12429705	A mutant ligand-binding domain of the estrogen receptor (LBD), which binds tamoxifen  instead of estrogen ( 68), was fused to a dominant-negative CREB gene (S133A substitution).	bind
44460	2	11219	6	NULL	NULL	0	NULL	LBD	NULL		is	NULL				ligand binding domain	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevgenet_36_0_687_s_444	12429705	A mutant ligand-binding domain of the estrogen receptor (LBD), which binds tamoxifen  instead of estrogen ( 68), was fused to a dominant-negative CREB gene (S133A substitution).	bind
44531	1	11220	5	NULL	NULL	NULL	NULL	mDab555	GP	mutant	is changed to			Tyr198		mDab555	GP	mutant	Phe		NULL		NULL	NULL	NULL	NULL	gw60_embo_16_1_121_s_173	9009273	A mutant mDab555, in which Tyr198 and 200 were both changed to Phe, was phosphorylated on tyrosine to a reduced extent when co-expressed with Src527F, and bound to the Src SH2 domain  in vitro (Figure  5A).	bind
44532	2	11220	5	NULL	NULL	NULL	NULL	mDab555	GP	mutant	is changed to			Tyr200		mDab555	GP	mutant	Phe		NULL		NULL	NULL	NULL	NULL	gw60_embo_16_1_121_s_173	9009273	A mutant mDab555, in which Tyr198 and 200 were both changed to Phe, was phosphorylated on tyrosine to a reduced extent when co-expressed with Src527F, and bound to the Src SH2 domain  in vitro (Figure  5A).	bind
44533	3	11220	5	NULL	NULL	NULL	NULL	Src	GP		phosphorylate		weakly	527F		statement 1	Process		tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_embo_16_1_121_s_173	9009273	A mutant mDab555, in which Tyr198 and 200 were both changed to Phe, was phosphorylated on tyrosine to a reduced extent when co-expressed with Src527F, and bound to the Src SH2 domain  in vitro (Figure  5A).	bind
44534	4	11220	5	NULL	NULL	NULL	NULL	Src	GP		phosphorylate		weakly	527F		statement 2	Process		tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_embo_16_1_121_s_173	9009273	A mutant mDab555, in which Tyr198 and 200 were both changed to Phe, was phosphorylated on tyrosine to a reduced extent when co-expressed with Src527F, and bound to the Src SH2 domain  in vitro (Figure  5A).	bind
44536	5	11220	5	NULL	NULL	NULL	NULL	statement 1	Process		bind					Src	GP		SH2 domain		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_16_1_121_s_173	9009273	A mutant mDab555, in which Tyr198 and 200 were both changed to Phe, was phosphorylated on tyrosine to a reduced extent when co-expressed with Src527F, and bound to the Src SH2 domain  in vitro (Figure  5A).	bind
44537	6	11220	5	NULL	NULL	NULL	NULL	statement 2	Process		bind					Src	GP		SH2 domain		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_16_1_121_s_173	9009273	A mutant mDab555, in which Tyr198 and 200 were both changed to Phe, was phosphorylated on tyrosine to a reduced extent when co-expressed with Src527F, and bound to the Src SH2 domain  in vitro (Figure  5A).	bind
45013	1	11220	6	10	NULL	0	NULL	mDab555		mutant	is changed to			Tyr198		mDab555		mutant	Phe		NULL		NULL	NULL	NULL	NULL	gw60_embo_16_1_121_s_173	9009273	A mutant mDab555, in which Tyr198 and 200 were both changed to Phe, was phosphorylated on tyrosine to a reduced extent when co-expressed with Src527F, and bound to the Src SH2 domain  in vitro (Figure  5A).	bind
45014	2	11220	6	10	NULL	0	NULL	mDab555		mutant	is changed to			Tyr200		mDab555		mutant	Phe		NULL		NULL	NULL	NULL	NULL	gw60_embo_16_1_121_s_173	9009273	A mutant mDab555, in which Tyr198 and 200 were both changed to Phe, was phosphorylated on tyrosine to a reduced extent when co-expressed with Src527F, and bound to the Src SH2 domain  in vitro (Figure  5A).	bind
45015	3	11220	6	10	NULL	0	NULL	statement 1	NULL		bind	NULL				Src	NULL		SH2 domain		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_16_1_121_s_173	9009273	A mutant mDab555, in which Tyr198 and 200 were both changed to Phe, was phosphorylated on tyrosine to a reduced extent when co-expressed with Src527F, and bound to the Src SH2 domain  in vitro (Figure  5A).	bind
51207	4	11220	6	10	NULL	0	NULL	statement 2			bind					Src			SH2 domain		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_embo_16_1_121_s_173	9009273	A mutant mDab555, in which Tyr198 and 200 were both changed to Phe, was phosphorylated on tyrosine to a reduced extent when co-expressed with Src527F, and bound to the Src SH2 domain  in vitro (Figure  5A).	bind
44541	1	11221	5	NULL	NULL	NULL	NULL	EbpS	GP	mutant;;S. aureus	bind					tropoelastin	GP	radiolabeled			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_1_243_s_41	11684686	A mutant of  S. aureus lacking EbpS exhibited decreased binding to radiolabeled tropoelastin, a defect that was restored by the presence of the wild-type  ebpS gene on a complementing plasmid.	bind
44542	2	11221	5	NULL	NULL	NULL	NULL	EbpS	GP	wild-type;;S. aureus	bind					tropoelastin	GP	radiolabeled			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_1_243_s_41	11684686	A mutant of  S. aureus lacking EbpS exhibited decreased binding to radiolabeled tropoelastin, a defect that was restored by the presence of the wild-type  ebpS gene on a complementing plasmid.	bind
60504	3	11221	5	NULL	NULL	NULL	NULL	statement 2	Process		lesser than					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_1_243_s_41	11684686	A mutant of  S. aureus lacking EbpS exhibited decreased binding to radiolabeled tropoelastin, a defect that was restored by the presence of the wild-type  ebpS gene on a complementing plasmid.	bind
44462	1	11221	6	NULL	NULL	0	NULL	EbpS	NULL	S.aureus;; mutant	bind	NULL				tropoelastin	NULL	radiolabeled			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_1_243_s_41	11684686	A mutant of  S. aureus lacking EbpS exhibited decreased binding to radiolabeled tropoelastin, a defect that was restored by the presence of the wild-type  ebpS gene on a complementing plasmid.	bind
44463	2	11221	6	10	NULL	0	NULL	EbpS	NULL	S.aureus;;wild-type	bind	NULL				tropoelastin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_1_243_s_41	11684686	A mutant of  S. aureus lacking EbpS exhibited decreased binding to radiolabeled tropoelastin, a defect that was restored by the presence of the wild-type  ebpS gene on a complementing plasmid.	bind
44464	3	11221	6	NULL	NULL	0	NULL	statement 2	NULL		is less than	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_1_243_s_41	11684686	A mutant of  S. aureus lacking EbpS exhibited decreased binding to radiolabeled tropoelastin, a defect that was restored by the presence of the wild-type  ebpS gene on a complementing plasmid.	bind
44543	1	11222	5	NULL	NULL	NULL	NULL	DSC1	GP	component of;;mutant	affect					cdt2+	GP	expression of			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_genetics_164_3_881_s_5	12871901	A mutant of a component of DSC1 affected  cdt2+ expression  in vivo, and a  cdt2+ promoter fragment containing MCB motifs bound DSC1  in vitro.	bind
44544	2	11222	5	NULL	NULL	NULL	NULL	cdt2+	GP		contains				promoter fragment					MCB motifs	NULL		NULL	NULL	NULL	NULL	gw60_genetics_164_3_881_s_5	12871901	A mutant of a component of DSC1 affected  cdt2+ expression  in vivo, and a  cdt2+ promoter fragment containing MCB motifs bound DSC1  in vitro.	bind
44545	3	11222	5	NULL	NULL	NULL	NULL	statement 2	Process		bind					DSC1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_genetics_164_3_881_s_5	12871901	A mutant of a component of DSC1 affected  cdt2+ expression  in vivo, and a  cdt2+ promoter fragment containing MCB motifs bound DSC1  in vitro.	bind
44465	1	11222	6	NULL	NULL	0	NULL	DSC1	NULL	mutant	affects	NULL				cdt2+	NULL	expression of			NULL	in vivo	0	NULL	NULL	NULL	gw60_genetics_164_3_881_s_5	12871901	A mutant of a component of DSC1 affected  cdt2+ expression  in vivo, and a  cdt2+ promoter fragment containing MCB motifs bound DSC1  in vitro.	bind
44466	2	11222	6	NULL	NULL	0	NULL	cdt2+	NULL		bind	NULL		MCB motif	promoter	DSC1	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_genetics_164_3_881_s_5	12871901	A mutant of a component of DSC1 affected  cdt2+ expression  in vivo, and a  cdt2+ promoter fragment containing MCB motifs bound DSC1  in vitro.	bind
44546	1	11223	5	NULL	NULL	NULL	NULL	E1A	GP	mutant	bind					Stat1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20406_s_183	10764778	A mutant of E1A that binds to Stat1 but not to CBP/p300 also down-regulates LMP2 transcription, whereas delta2-36, which binds to neither CBP/p300 nor Stat1, has no effect on the levels of LMP2 RNA in either U3A-701 or 2fTGH cells.	bind
44547	2	11223	5	NULL	NULL	NULL	NULL	E1A	GP	mutant	does not bind					CBP/p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20406_s_183	10764778	A mutant of E1A that binds to Stat1 but not to CBP/p300 also down-regulates LMP2 transcription, whereas delta2-36, which binds to neither CBP/p300 nor Stat1, has no effect on the levels of LMP2 RNA in either U3A-701 or 2fTGH cells.	bind
44548	3	11223	5	NULL	NULL	NULL	NULL	E1A	GP	mutant	downregulates					LMP2	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20406_s_183	10764778	A mutant of E1A that binds to Stat1 but not to CBP/p300 also down-regulates LMP2 transcription, whereas delta2-36, which binds to neither CBP/p300 nor Stat1, has no effect on the levels of LMP2 RNA in either U3A-701 or 2fTGH cells.	bind
44549	4	11223	5	NULL	NULL	NULL	NULL	delta2-36	GP		does not bind					CBP/p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20406_s_183	10764778	A mutant of E1A that binds to Stat1 but not to CBP/p300 also down-regulates LMP2 transcription, whereas delta2-36, which binds to neither CBP/p300 nor Stat1, has no effect on the levels of LMP2 RNA in either U3A-701 or 2fTGH cells.	bind
44550	5	11223	5	NULL	NULL	NULL	NULL	delta2-36	GP		does not bind					Stat1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20406_s_183	10764778	A mutant of E1A that binds to Stat1 but not to CBP/p300 also down-regulates LMP2 transcription, whereas delta2-36, which binds to neither CBP/p300 nor Stat1, has no effect on the levels of LMP2 RNA in either U3A-701 or 2fTGH cells.	bind
44551	6	11223	5	NULL	NULL	NULL	NULL	delta2-36	GP		does not effect					LMP2 RNA	NucleicAcid	levels of			NULL	U3A-701 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20406_s_183	10764778	A mutant of E1A that binds to Stat1 but not to CBP/p300 also down-regulates LMP2 transcription, whereas delta2-36, which binds to neither CBP/p300 nor Stat1, has no effect on the levels of LMP2 RNA in either U3A-701 or 2fTGH cells.	bind
44552	7	11223	5	NULL	NULL	NULL	NULL	delta2-36	GP		does not effect					LMP2 RNA	NucleicAcid	levels of			NULL	2fTGH cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20406_s_183	10764778	A mutant of E1A that binds to Stat1 but not to CBP/p300 also down-regulates LMP2 transcription, whereas delta2-36, which binds to neither CBP/p300 nor Stat1, has no effect on the levels of LMP2 RNA in either U3A-701 or 2fTGH cells.	bind
44553	8	11223	5	NULL	NULL	NULL	NULL	statement 6	Process		is an alternative to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20406_s_183	10764778	A mutant of E1A that binds to Stat1 but not to CBP/p300 also down-regulates LMP2 transcription, whereas delta2-36, which binds to neither CBP/p300 nor Stat1, has no effect on the levels of LMP2 RNA in either U3A-701 or 2fTGH cells.	bind
44467	1	11223	6	NULL	NULL	0	NULL	E1A	NULL	mutant	bind	NULL				Stat1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20406_s_183	10764778	A mutant of E1A that binds to Stat1 but not to CBP/p300 also down-regulates LMP2 transcription, whereas delta2-36, which binds to neither CBP/p300 nor Stat1, has no effect on the levels of LMP2 RNA in either U3A-701 or 2fTGH cells.	bind
44468	2	11223	6	NULL	NULL	0	NULL	E1A	NULL	mutant	does not bind	NULL				CBP/p300	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20406_s_183	10764778	A mutant of E1A that binds to Stat1 but not to CBP/p300 also down-regulates LMP2 transcription, whereas delta2-36, which binds to neither CBP/p300 nor Stat1, has no effect on the levels of LMP2 RNA in either U3A-701 or 2fTGH cells.	bind
44469	3	11223	6	NULL	NULL	0	NULL	E1A	NULL	mutant	downregulates	NULL				LMP2	NULL	transcription of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20406_s_183	10764778	A mutant of E1A that binds to Stat1 but not to CBP/p300 also down-regulates LMP2 transcription, whereas delta2-36, which binds to neither CBP/p300 nor Stat1, has no effect on the levels of LMP2 RNA in either U3A-701 or 2fTGH cells.	bind
45016	4	11223	6	NULL	NULL	0	NULL	delta2-36	NULL		does not bind	NULL				CBP/p300	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20406_s_183	10764778	A mutant of E1A that binds to Stat1 but not to CBP/p300 also down-regulates LMP2 transcription, whereas delta2-36, which binds to neither CBP/p300 nor Stat1, has no effect on the levels of LMP2 RNA in either U3A-701 or 2fTGH cells.	bind
45017	5	11223	6	NULL	NULL	0	NULL	delta2-36	NULL		does not bind	NULL				Stat1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20406_s_183	10764778	A mutant of E1A that binds to Stat1 but not to CBP/p300 also down-regulates LMP2 transcription, whereas delta2-36, which binds to neither CBP/p300 nor Stat1, has no effect on the levels of LMP2 RNA in either U3A-701 or 2fTGH cells.	bind
45018	6	11223	6	NULL	NULL	0	NULL	delta2-36	NULL		has no effect on	NULL				LMP2 RNA	NULL				NULL	U3A-701 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20406_s_183	10764778	A mutant of E1A that binds to Stat1 but not to CBP/p300 also down-regulates LMP2 transcription, whereas delta2-36, which binds to neither CBP/p300 nor Stat1, has no effect on the levels of LMP2 RNA in either U3A-701 or 2fTGH cells.	bind
45019	7	11223	6	NULL	NULL	0	NULL	delta2-36	NULL		has no effect on	NULL				LMP2 RNA	NULL				NULL	2fTGH cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20406_s_183	10764778	A mutant of E1A that binds to Stat1 but not to CBP/p300 also down-regulates LMP2 transcription, whereas delta2-36, which binds to neither CBP/p300 nor Stat1, has no effect on the levels of LMP2 RNA in either U3A-701 or 2fTGH cells.	bind
51209	8	11223	6	10	NULL	0	NULL	statement 6	NULL		is an alternative to	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20406_s_183	10764778	A mutant of E1A that binds to Stat1 but not to CBP/p300 also down-regulates LMP2 transcription, whereas delta2-36, which binds to neither CBP/p300 nor Stat1, has no effect on the levels of LMP2 RNA in either U3A-701 or 2fTGH cells.	bind
44554	1	11224	5	NULL	NULL	NULL	NULL	Skp2	GP	mutant	does not bind					Cul1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_20_5362_s_30	11032804	A mutant of Skp2 that fails to bind Cul1 is defective in these activities, suggesting that these activities of Skp2 represent SCF functions.	bind
45020	1	11224	6	NULL	NULL	0	NULL	Skp2	NULL	mutant	does not bind	NULL				Cul1	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_19_20_5362_s_30	11032804	A mutant of Skp2 that fails to bind Cul1 is defective in these activities, suggesting that these activities of Skp2 represent SCF functions.	bind
44557	1	11225	5	NULL	NULL	NULL	NULL	p47 phox	GP	mutant	does not bind			W193R;; N-terminal SH3 domain		p22 phox	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_24_23328_s_19	15824103	A mutant p47 phox carrying the W193R substitution in the N-terminal SH3 domain neither binds to p22 phox nor activates gp91 phox ( ,  ), and the substitution of Gln for Pro-156 in the PRR of p22 phox (P156Q), a mutation found in a patient with CGD ( ,  ), leads to a defective binding to p47 phox ( ,  ).	bind
44559	3	11225	5	NULL	NULL	NULL	NULL	p22 phox	GP	mutant	is found in			P156Q;; PRR 		CGD patients	GroupOfPeople				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_24_23328_s_19	15824103	A mutant p47 phox carrying the W193R substitution in the N-terminal SH3 domain neither binds to p22 phox nor activates gp91 phox ( ,  ), and the substitution of Gln for Pro-156 in the PRR of p22 phox (P156Q), a mutation found in a patient with CGD ( ,  ), leads to a defective binding to p47 phox ( ,  ).	bind
44560	4	11225	5	NULL	NULL	NULL	NULL	p22 phox	GP	mutant	does not bind			P156Q;; PRR		p47 phox	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_24_23328_s_19	15824103	A mutant p47 phox carrying the W193R substitution in the N-terminal SH3 domain neither binds to p22 phox nor activates gp91 phox ( ,  ), and the substitution of Gln for Pro-156 in the PRR of p22 phox (P156Q), a mutation found in a patient with CGD ( ,  ), leads to a defective binding to p47 phox ( ,  ).	bind
44589	2	11225	5	NULL	NULL	NULL	NULL	p47 phox	GP	mutant	does not activate			W193R;; N-terminal SH3 domain		gp91 phox	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_24_23328_s_19	15824103	A mutant p47 phox carrying the W193R substitution in the N-terminal SH3 domain neither binds to p22 phox nor activates gp91 phox ( ,  ), and the substitution of Gln for Pro-156 in the PRR of p22 phox (P156Q), a mutation found in a patient with CGD ( ,  ), leads to a defective binding to p47 phox ( ,  ).	bind
45021	1	11225	6	NULL	NULL	0	NULL	p47 phox	NULL	mutant	does not bind	NULL		W193R;; N-terminal SH3 domain		p22 phox	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_24_23328_s_19	15824103	A mutant p47 phox carrying the W193R substitution in the N-terminal SH3 domain neither binds to p22 phox nor activates gp91 phox ( ,  ), and the substitution of Gln for Pro-156 in the PRR of p22 phox (P156Q), a mutation found in a patient with CGD ( ,  ), leads to a defective binding to p47 phox ( ,  ).	bind
45022	2	11225	6	NULL	NULL	0	NULL	p47 phox	NULL	mutant	does not activate	NULL		W193R;; N-terminal SH3 domain		gp91 phox	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_24_23328_s_19	15824103	A mutant p47 phox carrying the W193R substitution in the N-terminal SH3 domain neither binds to p22 phox nor activates gp91 phox ( ,  ), and the substitution of Gln for Pro-156 in the PRR of p22 phox (P156Q), a mutation found in a patient with CGD ( ,  ), leads to a defective binding to p47 phox ( ,  ).	bind
45023	3	11225	6	10	NULL	0	NULL	p22 phox	NULL	mutant	is found in	NULL		P156Q;; PRR 		CGD patients	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_24_23328_s_19	15824103	A mutant p47 phox carrying the W193R substitution in the N-terminal SH3 domain neither binds to p22 phox nor activates gp91 phox ( ,  ), and the substitution of Gln for Pro-156 in the PRR of p22 phox (P156Q), a mutation found in a patient with CGD ( ,  ), leads to a defective binding to p47 phox ( ,  ).	bind
45024	4	11225	6	10	NULL	0	NULL	p22 phox	NULL	mutant	does not bind	NULL		P156Q;; PRR 		p47 phox	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_24_23328_s_19	15824103	A mutant p47 phox carrying the W193R substitution in the N-terminal SH3 domain neither binds to p22 phox nor activates gp91 phox ( ,  ), and the substitution of Gln for Pro-156 in the PRR of p22 phox (P156Q), a mutation found in a patient with CGD ( ,  ), leads to a defective binding to p47 phox ( ,  ).	bind
44591	1	11226	5	NULL	NULL	NULL	NULL	p53	GP	mutant	discriminates between					p53-responsive genes	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_321_s_399	11057904	A mutant p53 that discriminates between p53-responsive genes cannot induce apoptosis.	bind
44592	2	11226	5	NULL	NULL	NULL	NULL	statement 1	Process		does not induce					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_2_321_s_399	11057904	A mutant p53 that discriminates between p53-responsive genes cannot induce apoptosis.	bind
45025	1	11226	6	NULL	NULL	0	NULL	p53	NULL	mutant	does not induce	NULL				apoptosis	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_103_2_321_s_399	11057904	A mutant p53 that discriminates between p53-responsive genes cannot induce apoptosis.	bind
45026	2	11226	6	NULL	NULL	0	NULL	p53	NULL	mutant	discriminates between	NULL				p53-responsive genes	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_103_2_321_s_399	11057904	A mutant p53 that discriminates between p53-responsive genes cannot induce apoptosis.	bind
44593	1	11227	5	NULL	NULL	NULL	NULL	PCNA oligonucleotide	NucleicAcid	mutant	does not bind					p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_12_s_178	9858527	A mutant PCNA oligonucleotide that we showed previously does not bind p53 ( 70) did not compete effectively for binding with the wild-type PCNA probe (lanes 9 and 10).	bind
44636	2	11227	5	NULL	NULL	NULL	NULL	PCNA oligonucleotide	NucleicAcid	mutant	does not compete for		effectively			PCNA probe	NucleicAcid	binding with;;wild-type			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_12_s_178	9858527	A mutant PCNA oligonucleotide that we showed previously does not bind p53 ( 70) did not compete effectively for binding with the wild-type PCNA probe (lanes 9 and 10).	bind
45027	1	11227	6	NULL	NULL	0	NULL	PCNA oligonucleotide	NULL	mutant	does not bind	NULL				p53	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_12_s_178	9858527	A mutant PCNA oligonucleotide that we showed previously does not bind p53 ( 70) did not compete effectively for binding with the wild-type PCNA probe (lanes 9 and 10).	bind
51222	2	11227	6	10	NULL	0	NULL	PCNA oligonucleotide	NULL	mutant	does not compete with	NULL	effectively			PCNA probe	NULL	wild-type;;binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_12_s_178	9858527	A mutant PCNA oligonucleotide that we showed previously does not bind p53 ( 70) did not compete effectively for binding with the wild-type PCNA probe (lanes 9 and 10).	bind
44594	1	11228	5	NULL	NULL	NULL	NULL	p47(phox) peptide	AminoAcid	mutant	bind			319-337;;Ser328Glu		filamentous actin	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_febs-lett_580_1_16375898_s_8	16375898	A mutant peptide p47(phox)  (319-337, Ser328Glu) bound to filamentous actin more tightly than to monomer  actin.	bind
44595	2	11228	5	NULL	NULL	NULL	NULL	p47(phox) peptide	AminoAcid	mutant	bind			319-337;;Ser328Glu		monomer actin	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_febs-lett_580_1_16375898_s_8	16375898	A mutant peptide p47(phox)  (319-337, Ser328Glu) bound to filamentous actin more tightly than to monomer  actin.	bind
44596	3	11228	5	NULL	NULL	NULL	NULL	statement 1	Process		more tightly than					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_febs-lett_580_1_16375898_s_8	16375898	A mutant peptide p47(phox)  (319-337, Ser328Glu) bound to filamentous actin more tightly than to monomer  actin.	bind
45028	1	11228	6	10	NULL	0	NULL	p47(phox) 	NULL	mutant	bind	NULL		Ser328Glu		filamentous actin	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_febs-lett_580_1_16375898_s_8	16375898	A mutant peptide p47(phox)  (319-337, Ser328Glu) bound to filamentous actin more tightly than to monomer  actin.	bind
45029	2	11228	6	10	NULL	0	NULL	p47(phox)	NULL	mutant	bind	NULL		Ser328Glu		monomer actin	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0570-0579_febs-lett_580_1_16375898_s_8	16375898	A mutant peptide p47(phox)  (319-337, Ser328Glu) bound to filamentous actin more tightly than to monomer  actin.	bind
45030	3	11228	6	NULL	NULL	0	NULL	statement 1	NULL		is higher than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	abs-batch0570-0579_febs-lett_580_1_16375898_s_8	16375898	A mutant peptide p47(phox)  (319-337, Ser328Glu) bound to filamentous actin more tightly than to monomer  actin.	bind
44597	1	11230	5	NULL	NULL	NULL	NULL	NF- B DNA probe	NucleicAcid	mutant	does not bind					myotrophin	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1589_3_247_s_253	12031792	A mutant probe of NF- B DNA also did not show any binding to myotrophin.	bind
45031	1	11230	6	10	NULL	0	NULL	NF-B DNA probe		mutant	does not bind					myotrophin					NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1589_3_247_s_253	12031792	A mutant probe of NF- B DNA also did not show any binding to myotrophin.	bind
44603	1	11232	5	NULL	NULL	NULL	NULL	RNF4	GP	mutant	does not bind					PATZ	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3280_s_7	11719514	A mutant RNF4 that does not bind PATZ but enhances AR-dependent transcription is not influenced by PATZ, demonstrating that the repression by PATZ occurs only upon binding to RNF4.	bind
44604	2	11232	5	NULL	NULL	NULL	NULL	RNF4	GP	mutant	enhance					transcription	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3280_s_7	11719514	A mutant RNF4 that does not bind PATZ but enhances AR-dependent transcription is not influenced by PATZ, demonstrating that the repression by PATZ occurs only upon binding to RNF4.	bind
44605	3	11232	5	NULL	NULL	NULL	NULL	transcription	Process		is dependent on					AR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3280_s_7	11719514	A mutant RNF4 that does not bind PATZ but enhances AR-dependent transcription is not influenced by PATZ, demonstrating that the repression by PATZ occurs only upon binding to RNF4.	bind
44606	4	11232	5	NULL	NULL	NULL	NULL	statement 2	Process		is not influenced by					PATZ	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3280_s_7	11719514	A mutant RNF4 that does not bind PATZ but enhances AR-dependent transcription is not influenced by PATZ, demonstrating that the repression by PATZ occurs only upon binding to RNF4.	bind
44607	5	11232	5	NULL	NULL	NULL	NULL	PATZ	GP		repress					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3280_s_7	11719514	A mutant RNF4 that does not bind PATZ but enhances AR-dependent transcription is not influenced by PATZ, demonstrating that the repression by PATZ occurs only upon binding to RNF4.	bind
44608	6	11232	5	NULL	NULL	NULL	NULL	PATZ	GP		bind					RNF4	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3280_s_7	11719514	A mutant RNF4 that does not bind PATZ but enhances AR-dependent transcription is not influenced by PATZ, demonstrating that the repression by PATZ occurs only upon binding to RNF4.	bind
44609	7	11232	5	NULL	NULL	NULL	NULL	statement 6	Process		leads to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3280_s_7	11719514	A mutant RNF4 that does not bind PATZ but enhances AR-dependent transcription is not influenced by PATZ, demonstrating that the repression by PATZ occurs only upon binding to RNF4.	bind
45033	1	11232	6	NULL	NULL	0	NULL	RNF4	NULL	mutant	does not bind	NULL				PATZ	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_5_3280_s_7	11719514	A mutant RNF4 that does not bind PATZ but enhances AR-dependent transcription is not influenced by PATZ, demonstrating that the repression by PATZ occurs only upon binding to RNF4.	bind
45034	4	11232	6	NULL	NULL	0	NULL	RNF4	NULL	mutant	enhances	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_5_3280_s_7	11719514	A mutant RNF4 that does not bind PATZ but enhances AR-dependent transcription is not influenced by PATZ, demonstrating that the repression by PATZ occurs only upon binding to RNF4.	bind
52938	3	11232	6	10	NULL	0	NULL	statement 2	NULL		is not influenced by	NULL				PATZ	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_5_3280_s_7	11719514	A mutant RNF4 that does not bind PATZ but enhances AR-dependent transcription is not influenced by PATZ, demonstrating that the repression by PATZ occurs only upon binding to RNF4.	bind
52958	2	11232	6	NULL	NULL	0	NULL	transcription	NULL		is dependent on	NULL				AR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_5_3280_s_7	11719514	A mutant RNF4 that does not bind PATZ but enhances AR-dependent transcription is not influenced by PATZ, demonstrating that the repression by PATZ occurs only upon binding to RNF4.	bind
52959	5	11232	6	NULL	NULL	0	NULL	PATZ	NULL		bind	NULL				RNF4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_5_3280_s_7	11719514	A mutant RNF4 that does not bind PATZ but enhances AR-dependent transcription is not influenced by PATZ, demonstrating that the repression by PATZ occurs only upon binding to RNF4.	bind
52960	6	11232	6	NULL	NULL	0	NULL	PATZ	NULL		represses	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_5_3280_s_7	11719514	A mutant RNF4 that does not bind PATZ but enhances AR-dependent transcription is not influenced by PATZ, demonstrating that the repression by PATZ occurs only upon binding to RNF4.	bind
52961	7	11232	6	NULL	NULL	0	NULL	statement 6	NULL		occurs upon	NULL	only			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_5_3280_s_7	11719514	A mutant RNF4 that does not bind PATZ but enhances AR-dependent transcription is not influenced by PATZ, demonstrating that the repression by PATZ occurs only upon binding to RNF4.	bind
44610	1	11233	5	NULL	NULL	NULL	NULL	Ski protein	GP	mutant	retains					Smad4	GP	binding of	deltaS2/3		NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_357_s_152	12419246	A mutant Ski protein that retains binding to either Smad4 (deltaS2/3) or Smad2 (W274E) is able to repress activin signaling.	bind
44611	2	11233	5	NULL	NULL	NULL	NULL	Ski protein	GP	mutant	retains					Smad2	GP	binding of	W274E		NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_357_s_152	12419246	A mutant Ski protein that retains binding to either Smad4 (deltaS2/3) or Smad2 (W274E) is able to repress activin signaling.	bind
44612	3	11233	5	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_357_s_152	12419246	A mutant Ski protein that retains binding to either Smad4 (deltaS2/3) or Smad2 (W274E) is able to repress activin signaling.	bind
44613	4	11233	5	NULL	NULL	NULL	NULL	statement 1	Process		repress					activin	GP	signaling of			NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_357_s_152	12419246	A mutant Ski protein that retains binding to either Smad4 (deltaS2/3) or Smad2 (W274E) is able to repress activin signaling.	bind
44614	5	11233	5	NULL	NULL	NULL	NULL	statement 2	Process		repress					activin	GP	signaling of			NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_357_s_152	12419246	A mutant Ski protein that retains binding to either Smad4 (deltaS2/3) or Smad2 (W274E) is able to repress activin signaling.	bind
45035	1	11233	6	NULL	NULL	0	NULL	Ski protein	NULL	mutant	bind	NULL				Smad4	NULL		deltaS2/3		NULL		0	NULL	NULL	NULL	gw60_cell_111_3_357_s_152	12419246	A mutant Ski protein that retains binding to either Smad4 (deltaS2/3) or Smad2 (W274E) is able to repress activin signaling.	bind
45036	2	11233	6	NULL	NULL	0	NULL	Ski protein	NULL	mutant	bind	NULL				Smad2	NULL		W274E		NULL		0	NULL	NULL	NULL	gw60_cell_111_3_357_s_152	12419246	A mutant Ski protein that retains binding to either Smad4 (deltaS2/3) or Smad2 (W274E) is able to repress activin signaling.	bind
45037	3	11233	6	10	NULL	0	NULL	statement 1	NULL		repress	NULL				activin	NULL	signaling of			NULL		NULL	NULL	NULL	NULL	gw60_cell_111_3_357_s_152	12419246	A mutant Ski protein that retains binding to either Smad4 (deltaS2/3) or Smad2 (W274E) is able to repress activin signaling.	bind
51223	4	11233	6	10	NULL	0	NULL	statement 2	NULL		repress	NULL				activin	NULL	signaling of			NULL		0	NULL	NULL	NULL	gw60_cell_111_3_357_s_152	12419246	A mutant Ski protein that retains binding to either Smad4 (deltaS2/3) or Smad2 (W274E) is able to repress activin signaling.	bind
51224	5	11233	6	10	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_111_3_357_s_152	12419246	A mutant Ski protein that retains binding to either Smad4 (deltaS2/3) or Smad2 (W274E) is able to repress activin signaling.	bind
44851	1	11234	5	NULL	NULL	NULL	NULL	SR-BIdel509	GP		is a mutant of					SR-BI	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_34042_s_5	12119305	A mutant SR-BI (SR-BIdel509) that lacked only the leucine in the PDZ-interacting domain failed to interact with PDZK1  in vitro, while showing normal selective uptake function in nonpolarized cells.	bind
44852	2	11234	5	NULL	NULL	NULL	NULL	SR-BIdel509	GP		lacks					SR-BI	GP		leucine;;PDZ-interacting domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_34042_s_5	12119305	A mutant SR-BI (SR-BIdel509) that lacked only the leucine in the PDZ-interacting domain failed to interact with PDZK1  in vitro, while showing normal selective uptake function in nonpolarized cells.	bind
44853	3	11234	5	NULL	NULL	NULL	NULL	statement 2	Process		does not interact with					PDZK1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_34042_s_5	12119305	A mutant SR-BI (SR-BIdel509) that lacked only the leucine in the PDZ-interacting domain failed to interact with PDZK1  in vitro, while showing normal selective uptake function in nonpolarized cells.	bind
44854	4	11234	5	NULL	NULL	NULL	NULL	statement 2	Process		shows					selective uptake function	Process	normal			NULL	nonpolarized cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_34042_s_5	12119305	A mutant SR-BI (SR-BIdel509) that lacked only the leucine in the PDZ-interacting domain failed to interact with PDZK1  in vitro, while showing normal selective uptake function in nonpolarized cells.	bind
45038	1	11234	6	10	NULL	0	NULL	SR-BI		mutant;; lacking	does not interact with			leucine;; PDZ-interacting domain		PDZK1					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_37_34042_s_5	12119305	A mutant SR-BI (SR-BIdel509) that lacked only the leucine in the PDZ-interacting domain failed to interact with PDZK1  in vitro, while showing normal selective uptake function in nonpolarized cells.	bind
45039	2	11234	6	NULL	NULL	0	NULL	SR-BI	NULL	mutant;; lacking	displays	NULL		leucine;; PDZ-interacting domain		selective uptake	NULL				NULL	nonpolarized cells	0	NULL	NULL	NULL	gw60_jbiolchem_277_37_34042_s_5	12119305	A mutant SR-BI (SR-BIdel509) that lacked only the leucine in the PDZ-interacting domain failed to interact with PDZK1  in vitro, while showing normal selective uptake function in nonpolarized cells.	bind
44856	1	11235	5	NULL	NULL	NULL	NULL	ArpA	GP	mutant	does not bind					DNA target	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_2_326_s_370	15944459	A mutant strain deficient in ArpA or producing a mutant ArpA protein unable to bind to its target DNA overproduces streptomycin and forms aerial mycelia and spores earlier than the wild-type strain ( ,  ).	bind
44857	2	11235	5	NULL	NULL	NULL	NULL	ArpA	GP	mutant	overproduces					streptomycin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_2_326_s_370	15944459	A mutant strain deficient in ArpA or producing a mutant ArpA protein unable to bind to its target DNA overproduces streptomycin and forms aerial mycelia and spores earlier than the wild-type strain ( ,  ).	bind
44858	3	11235	5	NULL	NULL	NULL	NULL	ArpA	GP	mutant	forms					aerial mycelia	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_2_326_s_370	15944459	A mutant strain deficient in ArpA or producing a mutant ArpA protein unable to bind to its target DNA overproduces streptomycin and forms aerial mycelia and spores earlier than the wild-type strain ( ,  ).	bind
44859	4	11235	5	NULL	NULL	NULL	NULL	ArpA	GP	mutant	forms					spores	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_2_326_s_370	15944459	A mutant strain deficient in ArpA or producing a mutant ArpA protein unable to bind to its target DNA overproduces streptomycin and forms aerial mycelia and spores earlier than the wild-type strain ( ,  ).	bind
44861	5	11235	5	NULL	NULL	NULL	NULL	ArpA	GP	wild-type	forms					aerial mycelia	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_2_326_s_370	15944459	A mutant strain deficient in ArpA or producing a mutant ArpA protein unable to bind to its target DNA overproduces streptomycin and forms aerial mycelia and spores earlier than the wild-type strain ( ,  ).	bind
44862	6	11235	5	NULL	NULL	NULL	NULL	ArpA	GP	wild-type	forms					spores	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_2_326_s_370	15944459	A mutant strain deficient in ArpA or producing a mutant ArpA protein unable to bind to its target DNA overproduces streptomycin and forms aerial mycelia and spores earlier than the wild-type strain ( ,  ).	bind
44863	7	11235	5	NULL	NULL	NULL	NULL	statement 3	Process		occurs earlier than					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_2_326_s_370	15944459	A mutant strain deficient in ArpA or producing a mutant ArpA protein unable to bind to its target DNA overproduces streptomycin and forms aerial mycelia and spores earlier than the wild-type strain ( ,  ).	bind
44864	8	11235	5	NULL	NULL	NULL	NULL	statement 4	Process		occurs earlier than					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_2_326_s_370	15944459	A mutant strain deficient in ArpA or producing a mutant ArpA protein unable to bind to its target DNA overproduces streptomycin and forms aerial mycelia and spores earlier than the wild-type strain ( ,  ).	bind
45040	1	11235	6	NULL	NULL	0	NULL	ArpA	NULL	mutant	does not bind	NULL				target DNA	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_2_326_s_370	15944459	A mutant strain deficient in ArpA or producing a mutant ArpA protein unable to bind to its target DNA overproduces streptomycin and forms aerial mycelia and spores earlier than the wild-type strain ( ,  ).	bind
45041	2	11235	6	NULL	NULL	0	NULL	ArpA	NULL	mutant	overproduces	NULL				streptomycin	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_2_326_s_370	15944459	A mutant strain deficient in ArpA or producing a mutant ArpA protein unable to bind to its target DNA overproduces streptomycin and forms aerial mycelia and spores earlier than the wild-type strain ( ,  ).	bind
45042	3	11235	6	NULL	NULL	0	NULL	ArpA	NULL	mutant	forms	NULL				aerial mycelia	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_2_326_s_370	15944459	A mutant strain deficient in ArpA or producing a mutant ArpA protein unable to bind to its target DNA overproduces streptomycin and forms aerial mycelia and spores earlier than the wild-type strain ( ,  ).	bind
45043	4	11235	6	NULL	NULL	0	NULL	ArpA	NULL	wild type	forms	NULL				aerial mycelia	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_2_326_s_370	15944459	A mutant strain deficient in ArpA or producing a mutant ArpA protein unable to bind to its target DNA overproduces streptomycin and forms aerial mycelia and spores earlier than the wild-type strain ( ,  ).	bind
45044	5	11235	6	NULL	NULL	0	NULL	statement 3	NULL		is earlier than	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_2_326_s_370	15944459	A mutant strain deficient in ArpA or producing a mutant ArpA protein unable to bind to its target DNA overproduces streptomycin and forms aerial mycelia and spores earlier than the wild-type strain ( ,  ).	bind
45045	6	11235	6	NULL	NULL	0	NULL	ArpA	NULL	mutant	forms	NULL				spores	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_2_326_s_370	15944459	A mutant strain deficient in ArpA or producing a mutant ArpA protein unable to bind to its target DNA overproduces streptomycin and forms aerial mycelia and spores earlier than the wild-type strain ( ,  ).	bind
45046	7	11235	6	NULL	NULL	0	NULL	ArpA	NULL	wild type	forms	NULL				spores	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_2_326_s_370	15944459	A mutant strain deficient in ArpA or producing a mutant ArpA protein unable to bind to its target DNA overproduces streptomycin and forms aerial mycelia and spores earlier than the wild-type strain ( ,  ).	bind
45047	8	11235	6	NULL	NULL	0	NULL	statement 6	NULL		is earlier than	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_2_326_s_370	15944459	A mutant strain deficient in ArpA or producing a mutant ArpA protein unable to bind to its target DNA overproduces streptomycin and forms aerial mycelia and spores earlier than the wild-type strain ( ,  ).	bind
44870	1	11236	5	NULL	NULL	NULL	NULL	Tpr-Met protein	GP	mutant	does not bind			Tyr489 Phe		Grb2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_28_19649_s_190	10391903	A mutant Tpr-Met protein (Tyr489  Phe) that fails to bind to Grb2 has significantly impaired transforming activity.	bind
44871	2	11236	5	NULL	NULL	NULL	NULL	statement 1	Process		has impaired					transforming activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_28_19649_s_190	10391903	A mutant Tpr-Met protein (Tyr489  Phe) that fails to bind to Grb2 has significantly impaired transforming activity.	bind
45048	1	11236	6	NULL	NULL	0	NULL	Tpr-Met protein	NULL	mutant	does not bind	NULL				Grb2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_28_19649_s_190	10391903	A mutant Tpr-Met protein (Tyr489  Phe) that fails to bind to Grb2 has significantly impaired transforming activity.	bind
45053	2	11236	6	NULL	NULL	0	NULL	Tpr-Met protein	NULL	mutant	has impaired	NULL				transforming activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_28_19649_s_190	10391903	A mutant Tpr-Met protein (Tyr489  Phe) that fails to bind to Grb2 has significantly impaired transforming activity.	bind
44872	1	11237	5	NULL	NULL	NULL	NULL	Tpr-Met protein	GP	mutant	does not bind		selectively			Grb2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_20167_s_5	9242692	A mutant Tpr-Met protein that selectively fails to bind Grb2 has reduced transforming activity, implicating pathways downstream of Grb2 in Tpr-Met mediated cell transformation.	bind
44873	3	11237	5	NULL	NULL	NULL	NULL	Tpr-Met	GP		mediates					cell transformation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_20167_s_5	9242692	A mutant Tpr-Met protein that selectively fails to bind Grb2 has reduced transforming activity, implicating pathways downstream of Grb2 in Tpr-Met mediated cell transformation.	bind
44874	3	11237	5	NULL	NULL	NULL	NULL	statement 2	Process		implicates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_20167_s_5	9242692	A mutant Tpr-Met protein that selectively fails to bind Grb2 has reduced transforming activity, implicating pathways downstream of Grb2 in Tpr-Met mediated cell transformation.	bind
51225	2	11237	5	NULL	NULL	NULL	NULL	statement 1	Process		has reduced					transforming activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_32_20167_s_5	9242692	A mutant Tpr-Met protein that selectively fails to bind Grb2 has reduced transforming activity, implicating pathways downstream of Grb2 in Tpr-Met mediated cell transformation.	bind
45054	1	11237	6	NULL	NULL	0	NULL	Tpr-Met protein	NULL	mutant	does not bind	NULL	selectively			Grb2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_32_20167_s_5	9242692	A mutant Tpr-Met protein that selectively fails to bind Grb2 has reduced transforming activity, implicating pathways downstream of Grb2 in Tpr-Met mediated cell transformation.	bind
45057	2	11237	6	NULL	NULL	0	NULL	Tpr-Met 	NULL		mediates	NULL				cell transformation	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_32_20167_s_5	9242692	A mutant Tpr-Met protein that selectively fails to bind Grb2 has reduced transforming activity, implicating pathways downstream of Grb2 in Tpr-Met mediated cell transformation.	bind
45060	3	11237	6	NULL	NULL	0	NULL	Tpr-Met	NULL	mutant	has reduced	NULL				transforming activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_32_20167_s_5	9242692	A mutant Tpr-Met protein that selectively fails to bind Grb2 has reduced transforming activity, implicating pathways downstream of Grb2 in Tpr-Met mediated cell transformation.	bind
45061	4	11237	6	NULL	NULL	0	NULL	statement 3	NULL		implicates	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_32_20167_s_5	9242692	A mutant Tpr-Met protein that selectively fails to bind Grb2 has reduced transforming activity, implicating pathways downstream of Grb2 in Tpr-Met mediated cell transformation.	bind
46370	1	11238	5	NULL	NULL	NULL	NULL	Sp1	GP		bind					PKR	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
46371	2	11238	5	NULL	NULL	NULL	NULL	Sp3	GP		bind					PKR	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
46372	3	11238	5	NULL	NULL	NULL	NULL	Sp1	GP		activates					PKR	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
46373	4	11238	5	NULL	NULL	NULL	NULL	Sp3	GP		activates					PKR	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
46374	5	11238	5	NULL	NULL	NULL	NULL	statement 3	Process		is independent of					ISRE	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
46375	6	11238	5	NULL	NULL	NULL	NULL	statement 4	Process		is independent of					ISRE	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
46376	7	11238	5	NULL	NULL	NULL	NULL	Sp1	GP		recruits					TFIID	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
46377	8	11238	5	NULL	NULL	NULL	NULL	Sp1	GP		acts as					gene activator	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
46378	9	11238	5	NULL	NULL	NULL	NULL	statement 7	Process		leads to					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
46379	10	11238	5	NULL	NULL	NULL	NULL	TAF1	GP		interacts with					Sp1 protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
46380	11	11238	5	NULL	NULL	NULL	NULL	TAF1	GP		is					TBP-associated factor 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
46381	12	11238	5	NULL	NULL	NULL	NULL	TAF1	GP		activates					cyclin D1	GP			TATA-less promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
46382	13	11238	5	NULL	NULL	NULL	NULL	statement 12	Process		depends on					statement 11	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
45762	1	11238	6	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				PKR	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
45763	2	11238	6	NULL	NULL	0	NULL	Sp3	NULL		bind	NULL				PKR	NULL			promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
45764	3	11238	6	NULL	NULL	0	NULL	Sp1	NULL		activates	NULL				PKR	NULL	transcription of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
45765	4	11238	6	NULL	NULL	0	NULL	Sp3	NULL		activates	NULL				PKR	NULL	transcription of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
45766	5	11238	6	NULL	NULL	0	NULL	statement 3	NULL		is independent of	NULL					NULL			ISRE	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
45767	6	11238	6	NULL	NULL	0	NULL	statement 4	NULL		is independent of	NULL					NULL			ISRE	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
45768	7	11238	6	NULL	NULL	0	NULL	Sp1	NULL		recruits	NULL				TFIID	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
45769	8	11238	6	NULL	NULL	0	NULL	Sp1	NULL		acts as a 	NULL				gene activator	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
45770	9	11238	6	NULL	NULL	0	NULL	statement 8	NULL		is because of	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
45771	10	11238	6	NULL	NULL	0	NULL	TAF1	NULL		is	NULL				TBP-associated factor1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
45772	11	11238	6	NULL	NULL	0	NULL	TAF1	NULL		interacts with	NULL				Sp1 protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
45773	12	11238	6	10	NULL	0	NULL	TAF1	NULL		activates	NULL				cyclin D1	NULL			TATA-less promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
46358	13	11238	6	NULL	NULL	0	NULL	statement 12	NULL		depends on	NULL				statement 11	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_6_3244_s_331	16339759	A mutant with a nonfunctional ISRE, however, showed similar activity as the p503(WT) for both Sp1 and Sp3, further establishing that the binding of Sp1 and Sp3 to the  PKR promoter and basal transcriptional activation by these factors are independent of the ISRE. Sp1 has been shown to function as a gene activator by recruiting TFIID ( ), and the TBP-associated factor 1 (TAF1) activates the TATA-less cyclin D1 promoter by interacting with the Sp1 protein ( ).	bind
44875	1	11239	5	NULL	NULL	NULL	NULL			mutant	does not bind			Y205A		LDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_11_7018_s_66	10066756	A mutant with alanine at this position (Y205A) did not bind to LDL (Fig.  1).	bind
45063	1	11239	6	10	NULL	0	NULL		NULL	mutant	does not bind	NULL		Y205A		LDL	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_11_7018_s_66	10066756	A mutant with alanine at this position (Y205A) did not bind to LDL (Fig.  1).	bind
44876	1	11240	5	NULL	NULL	NULL	NULL	rIB2	GP		bind					p38	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4073_s_232	12024021	A mutant with the first 306 amino acids deleted, which eliminated rIB2 binding to p38 (rIB2-deltan306), failed to fully promote p38 activation when expressed alone or when coexpressed with Tiam1 (Fig.  7A, upper panel, lanes 5 and 8).	bind
44877	2	11240	5	NULL	NULL	NULL	NULL	rIB2-deltan306	GP		is formed from					rIB2	GP	deletion of	first 306 amino acids		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4073_s_232	12024021	A mutant with the first 306 amino acids deleted, which eliminated rIB2 binding to p38 (rIB2-deltan306), failed to fully promote p38 activation when expressed alone or when coexpressed with Tiam1 (Fig.  7A, upper panel, lanes 5 and 8).	bind
44878	3	11240	5	NULL	NULL	NULL	NULL	rIB2-deltan306	GP		eliminates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4073_s_232	12024021	A mutant with the first 306 amino acids deleted, which eliminated rIB2 binding to p38 (rIB2-deltan306), failed to fully promote p38 activation when expressed alone or when coexpressed with Tiam1 (Fig.  7A, upper panel, lanes 5 and 8).	bind
44879	4	11240	5	NULL	NULL	NULL	NULL	rIB2-deltan306	GP		does not promote		fully			p38	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4073_s_232	12024021	A mutant with the first 306 amino acids deleted, which eliminated rIB2 binding to p38 (rIB2-deltan306), failed to fully promote p38 activation when expressed alone or when coexpressed with Tiam1 (Fig.  7A, upper panel, lanes 5 and 8).	bind
45065	1	11240	6	NULL	NULL	0	NULL	rIB2	NULL		bind	NULL				p38	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_12_4073_s_232	12024021	A mutant with the first 306 amino acids deleted, which eliminated rIB2 binding to p38 (rIB2-deltan306), failed to fully promote p38 activation when expressed alone or when coexpressed with Tiam1 (Fig.  7A, upper panel, lanes 5 and 8).	bind
45070	2	11240	6	NULL	NULL	0	NULL	rIB2	NULL	mutant;;deletion of	failed to promote	NULL		first 306 amino acids		p38	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4073_s_232	12024021	A mutant with the first 306 amino acids deleted, which eliminated rIB2 binding to p38 (rIB2-deltan306), failed to fully promote p38 activation when expressed alone or when coexpressed with Tiam1 (Fig.  7A, upper panel, lanes 5 and 8).	bind
51241	3	11240	6	10	NULL	0	NULL	rIB2-deltan306			is formed from					 rIB2		deletion of	first 306 amino acids		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4073_s_232	12024021	A mutant with the first 306 amino acids deleted, which eliminated rIB2 binding to p38 (rIB2-deltan306), failed to fully promote p38 activation when expressed alone or when coexpressed with Tiam1 (Fig.  7A, upper panel, lanes 5 and 8).	bind
51242	4	11240	6	10	NULL	0	NULL	rIB2-deltan306	NULL		eliminates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_12_4073_s_232	12024021	A mutant with the first 306 amino acids deleted, which eliminated rIB2 binding to p38 (rIB2-deltan306), failed to fully promote p38 activation when expressed alone or when coexpressed with Tiam1 (Fig.  7A, upper panel, lanes 5 and 8).	bind
44885	1	11241	5	NULL	NULL	NULL	NULL	T	GP		bind					p130	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_8_3679_s_118	9108037	A mutant within the putative J-domain helix 3 does not impair T binding to p130, but prevents T-mediated alteration of its phosphorylation state, thus implying that an N-terminal region could influence cell cycle-dependent posttranslational modifications of p130 ( 29).	bind
44886	2	11241	5	NULL	NULL	NULL	NULL			mutant;;putative 	does not impair			J-domain helix 3		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_8_3679_s_118	9108037	A mutant within the putative J-domain helix 3 does not impair T binding to p130, but prevents T-mediated alteration of its phosphorylation state, thus implying that an N-terminal region could influence cell cycle-dependent posttranslational modifications of p130 ( 29).	bind
44887	3	11241	5	NULL	NULL	NULL	NULL	T	GP		mediate					p130	GP	alteration of phosphorylation state			NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_8_3679_s_118	9108037	A mutant within the putative J-domain helix 3 does not impair T binding to p130, but prevents T-mediated alteration of its phosphorylation state, thus implying that an N-terminal region could influence cell cycle-dependent posttranslational modifications of p130 ( 29).	bind
44888	4	11241	5	NULL	NULL	NULL	NULL	statement 2	Process		prevents					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_8_3679_s_118	9108037	A mutant within the putative J-domain helix 3 does not impair T binding to p130, but prevents T-mediated alteration of its phosphorylation state, thus implying that an N-terminal region could influence cell cycle-dependent posttranslational modifications of p130 ( 29).	bind
44889	5	11241	5	NULL	NULL	NULL	NULL	p130	GP	posttranslational modifications of	is dependent on					cell cycle	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_8_3679_s_118	9108037	A mutant within the putative J-domain helix 3 does not impair T binding to p130, but prevents T-mediated alteration of its phosphorylation state, thus implying that an N-terminal region could influence cell cycle-dependent posttranslational modifications of p130 ( 29).	bind
44890	6	11241	5	NULL	NULL	NULL	NULL	T	GP		influences			N-terminal region		statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_8_3679_s_118	9108037	A mutant within the putative J-domain helix 3 does not impair T binding to p130, but prevents T-mediated alteration of its phosphorylation state, thus implying that an N-terminal region could influence cell cycle-dependent posttranslational modifications of p130 ( 29).	bind
45075	1	11241	6	NULL	NULL	0	NULL	T 	NULL		bind	NULL				p130	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_94_8_3679_s_118	9108037	A mutant within the putative J-domain helix 3 does not impair T binding to p130, but prevents T-mediated alteration of its phosphorylation state, thus implying that an N-terminal region could influence cell cycle-dependent posttranslational modifications of p130 ( 29).	bind
45096	2	11241	6	NULL	NULL	0	NULL		NULL	mutant;; putative	does not impair	NULL		J-domain helix 3		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_94_8_3679_s_118	9108037	A mutant within the putative J-domain helix 3 does not impair T binding to p130, but prevents T-mediated alteration of its phosphorylation state, thus implying that an N-terminal region could influence cell cycle-dependent posttranslational modifications of p130 ( 29).	bind
45097	6	11241	6	10	NULL	0	NULL		NULL		influences	NULL		N-terminal region		statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_8_3679_s_118	9108037	A mutant within the putative J-domain helix 3 does not impair T binding to p130, but prevents T-mediated alteration of its phosphorylation state, thus implying that an N-terminal region could influence cell cycle-dependent posttranslational modifications of p130 ( 29).	bind
51243	3	11241	6	10	NULL	0	NULL	T	NULL		mediate	NULL				p130	NULL	alteration of  phosphorylation state			NULL		0	NULL	NULL	NULL	gw60_pnas_94_8_3679_s_118	9108037	A mutant within the putative J-domain helix 3 does not impair T binding to p130, but prevents T-mediated alteration of its phosphorylation state, thus implying that an N-terminal region could influence cell cycle-dependent posttranslational modifications of p130 ( 29).	bind
51244	4	11241	6	10	NULL	0	NULL	statement 2	NULL		prevents	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_94_8_3679_s_118	9108037	A mutant within the putative J-domain helix 3 does not impair T binding to p130, but prevents T-mediated alteration of its phosphorylation state, thus implying that an N-terminal region could influence cell cycle-dependent posttranslational modifications of p130 ( 29).	bind
51245	5	11241	6	10	NULL	NULL	NULL	p130		posttranslational modifications of	depends on					cell cycle					NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_8_3679_s_118	9108037	A mutant within the putative J-domain helix 3 does not impair T binding to p130, but prevents T-mediated alteration of its phosphorylation state, thus implying that an N-terminal region could influence cell cycle-dependent posttranslational modifications of p130 ( 29).	bind
44891	1	11242	5	NULL	NULL	NULL	NULL	RNA polymerase II	GP	mutant;;yeast	lacks								subunit Rpb9		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_26_24189_s_257	12692127	A mutant yeast RNA  polymerase II lacking subunit Rpb9 (RPIIdelta9) is significantly impaired in  its ability to respond to TFIIS-stimulated readthrough of elongation blocks,  although the mutant polymerase binds TFIIS as well as wild type polymerase  ( ).	bind
44892	2	11242	5	NULL	NULL	NULL	NULL	statement 1	Process		is					RPIIdelta9	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_26_24189_s_257	12692127	A mutant yeast RNA  polymerase II lacking subunit Rpb9 (RPIIdelta9) is significantly impaired in  its ability to respond to TFIIS-stimulated readthrough of elongation blocks,  although the mutant polymerase binds TFIIS as well as wild type polymerase  ( ).	bind
44893	3	11242	5	NULL	NULL	NULL	NULL	TFIIS	GP		stimulate					elongation blocks	NucleicAcid	readthrough of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_26_24189_s_257	12692127	A mutant yeast RNA  polymerase II lacking subunit Rpb9 (RPIIdelta9) is significantly impaired in  its ability to respond to TFIIS-stimulated readthrough of elongation blocks,  although the mutant polymerase binds TFIIS as well as wild type polymerase  ( ).	bind
44895	4	11242	5	NULL	NULL	NULL	NULL	RPIIdelta9	GP		impairs		significantly			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_26_24189_s_257	12692127	A mutant yeast RNA  polymerase II lacking subunit Rpb9 (RPIIdelta9) is significantly impaired in  its ability to respond to TFIIS-stimulated readthrough of elongation blocks,  although the mutant polymerase binds TFIIS as well as wild type polymerase  ( ).	bind
44896	6	11242	5	NULL	NULL	NULL	NULL	RPIIdelta9	GP		bind					TFIIS	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_26_24189_s_257	12692127	A mutant yeast RNA  polymerase II lacking subunit Rpb9 (RPIIdelta9) is significantly impaired in  its ability to respond to TFIIS-stimulated readthrough of elongation blocks,  although the mutant polymerase binds TFIIS as well as wild type polymerase  ( ).	bind
44897	5	11242	5	NULL	NULL	NULL	NULL	RNA polymerase II	GP	wild type	bind					TFIIS	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_26_24189_s_257	12692127	A mutant yeast RNA  polymerase II lacking subunit Rpb9 (RPIIdelta9) is significantly impaired in  its ability to respond to TFIIS-stimulated readthrough of elongation blocks,  although the mutant polymerase binds TFIIS as well as wild type polymerase  ( ).	bind
45098	1	11242	6	NULL	NULL	0	NULL	RNA polymerase II 	NULL	mutant;; yeast	lacks	NULL					NULL		Rpb9 subunit		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_26_24189_s_257	12692127	A mutant yeast RNA  polymerase II lacking subunit Rpb9 (RPIIdelta9) is significantly impaired in  its ability to respond to TFIIS-stimulated readthrough of elongation blocks,  although the mutant polymerase binds TFIIS as well as wild type polymerase  ( ).	bind
45099	2	11242	6	NULL	NULL	0	NULL	RNA polymerase II	NULL	yeast;; mutant	bind	NULL				TFIIS	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_26_24189_s_257	12692127	A mutant yeast RNA  polymerase II lacking subunit Rpb9 (RPIIdelta9) is significantly impaired in  its ability to respond to TFIIS-stimulated readthrough of elongation blocks,  although the mutant polymerase binds TFIIS as well as wild type polymerase  ( ).	bind
45100	3	11242	6	NULL	NULL	0	NULL	RNA polymerase II	NULL	yeast;; mutant	bind	NULL				polymerase	NULL	wild type			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_26_24189_s_257	12692127	A mutant yeast RNA  polymerase II lacking subunit Rpb9 (RPIIdelta9) is significantly impaired in  its ability to respond to TFIIS-stimulated readthrough of elongation blocks,  although the mutant polymerase binds TFIIS as well as wild type polymerase  ( ).	bind
45101	4	11242	6	NULL	NULL	0	NULL	TFIIS	NULL		stimulates	NULL				elongation blocks	NULL	readthrough of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_26_24189_s_257	12692127	A mutant yeast RNA  polymerase II lacking subunit Rpb9 (RPIIdelta9) is significantly impaired in  its ability to respond to TFIIS-stimulated readthrough of elongation blocks,  although the mutant polymerase binds TFIIS as well as wild type polymerase  ( ).	bind
45102	5	11242	6	NULL	NULL	0	NULL	RNA polymerase II	NULL	mutant;; yeast	impairs	NULL	significantly			statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_26_24189_s_257	12692127	A mutant yeast RNA  polymerase II lacking subunit Rpb9 (RPIIdelta9) is significantly impaired in  its ability to respond to TFIIS-stimulated readthrough of elongation blocks,  although the mutant polymerase binds TFIIS as well as wild type polymerase  ( ).	bind
51246	6	11242	6	10	NULL	0	NULL	RPIIdelta9	NULL		is	NULL				RNA polymerase II	NULL	mutant	lacking subunit Rpb9		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_26_24189_s_257	12692127	A mutant yeast RNA  polymerase II lacking subunit Rpb9 (RPIIdelta9) is significantly impaired in  its ability to respond to TFIIS-stimulated readthrough of elongation blocks,  although the mutant polymerase binds TFIIS as well as wild type polymerase  ( ).	bind
44898	1	11243	5	NULL	NULL	NULL	NULL	bcl-X  oligonucleotide	NucleicAcid	mutant	bind		less efficiently		HRE	PR	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_11_9831_s_216	14679196	A mutated  bcl-X HRE oligonucleotide binds less efficiently to PR.	bind
45103	1	11243	6	NULL	NULL	0	NULL	bcl-X oligonucleotide	NULL	mutant	bind	NULL	less efficiently		HRE	PR	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_11_9831_s_216	14679196	A mutated  bcl-X HRE oligonucleotide binds less efficiently to PR.	bind
44899	1	11244	5	NULL	NULL	NULL	NULL	nuclear proteins	GP		isolated from					HEK 293T cells	Cell	PKD2-transfected			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3423_s_129	10207066	A mutated AP-1 oligonucleotide failed to bind nuclear proteins isolated from PKD2-transfected HEK 293T cells.	bind
44900	2	11244	5	NULL	NULL	NULL	NULL	AP-1 oligonucleotide	NucleicAcid	mutant	does not bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3423_s_129	10207066	A mutated AP-1 oligonucleotide failed to bind nuclear proteins isolated from PKD2-transfected HEK 293T cells.	bind
45104	1	11244	6	NULL	NULL	0	NULL	nuclear proteins	NULL		isolated from	NULL				HEK 293T cells	NULL	PKD2-transfected			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3423_s_129	10207066	A mutated AP-1 oligonucleotide failed to bind nuclear proteins isolated from PKD2-transfected HEK 293T cells.	bind
45105	2	11244	6	NULL	NULL	0	NULL	AP-1 oligonucleotide	NULL	mutant	does not bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3423_s_129	10207066	A mutated AP-1 oligonucleotide failed to bind nuclear proteins isolated from PKD2-transfected HEK 293T cells.	bind
44901	1	11245	5	NULL	NULL	NULL	NULL	perlecan	GP	mutant	does not contain			domain I					GAG chains		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_15061_s_124	11847210	A mutated form of perlecan domain I containing no GAG chains did not bind PRELP (Fig.  3 B).	bind
44902	2	11245	5	NULL	NULL	NULL	NULL	statement 1	Process		does not bind					PRELP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_17_15061_s_124	11847210	A mutated form of perlecan domain I containing no GAG chains did not bind PRELP (Fig.  3 B).	bind
45106	1	11245	6	NULL	NULL	0	NULL	perlecan	NULL	mutant	does not contain	NULL		domain I			NULL		GAG chains		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_17_15061_s_124	11847210	A mutated form of perlecan domain I containing no GAG chains did not bind PRELP (Fig.  3 B).	bind
45107	2	11245	6	NULL	NULL	0	NULL	statement 1	NULL		does not bind	NULL				PRELP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_17_15061_s_124	11847210	A mutated form of perlecan domain I containing no GAG chains did not bind PRELP (Fig.  3 B).	bind
44903	1	11246	5	NULL	NULL	NULL	NULL	statement 1	Process		does not bind					JNK	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_95	9733513	A mutated JIP-1 molecule with an in-frame deletion of the JNK binding domain did not bind JNK but did bind MKK7, DLK, MLK3, and HPK1 ( Fig. 3A).	bind
44904	3	11246	5	NULL	NULL	NULL	NULL	statement 1	Process		bind					MKK7	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_95	9733513	A mutated JIP-1 molecule with an in-frame deletion of the JNK binding domain did not bind JNK but did bind MKK7, DLK, MLK3, and HPK1 ( Fig. 3A).	bind
44905	4	11246	5	NULL	NULL	NULL	NULL	statement 1	Process		bind					DLK	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_95	9733513	A mutated JIP-1 molecule with an in-frame deletion of the JNK binding domain did not bind JNK but did bind MKK7, DLK, MLK3, and HPK1 ( Fig. 3A).	bind
44906	5	11246	5	NULL	NULL	NULL	NULL	statement 1	Process		bind					MLK3	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_95	9733513	A mutated JIP-1 molecule with an in-frame deletion of the JNK binding domain did not bind JNK but did bind MKK7, DLK, MLK3, and HPK1 ( Fig. 3A).	bind
44907	6	11246	5	NULL	NULL	NULL	NULL	statement 1	Process		bind					HPK1	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_95	9733513	A mutated JIP-1 molecule with an in-frame deletion of the JNK binding domain did not bind JNK but did bind MKK7, DLK, MLK3, and HPK1 ( Fig. 3A).	bind
68149	1	11246	5	NULL	NULL	NULL	NULL	JIP-1	GP	deletion mutant	lacks					JNK binding domain	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_95	9733513	A mutated JIP-1 molecule with an in-frame deletion of the JNK binding domain did not bind JNK but did bind MKK7, DLK, MLK3, and HPK1 ( Fig. 3A).	bind
45108	1	11246	6	10	NULL	0	NULL	JIP-1 molecule	NULL	deletion mutant	does not bind	NULL		JNK binding domain		JNK	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_95	9733513	A mutated JIP-1 molecule with an in-frame deletion of the JNK binding domain did not bind JNK but did bind MKK7, DLK, MLK3, and HPK1 ( Fig. 3A).	bind
45109	2	11246	6	10	NULL	0	NULL	JIP-1 molecule	NULL	deletion mutant	bind	NULL		JNK binding domain		MKK7	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_95	9733513	A mutated JIP-1 molecule with an in-frame deletion of the JNK binding domain did not bind JNK but did bind MKK7, DLK, MLK3, and HPK1 ( Fig. 3A).	bind
45110	3	11246	6	10	NULL	0	NULL	JIP-1 molecule	NULL	deletion mutant	bind	NULL		JNK binding domain		DLK	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_95	9733513	A mutated JIP-1 molecule with an in-frame deletion of the JNK binding domain did not bind JNK but did bind MKK7, DLK, MLK3, and HPK1 ( Fig. 3A).	bind
45111	4	11246	6	10	NULL	0	NULL	JIP-1 molecule	NULL	deletion mutant	bind	NULL		JNK binding domain		MLK3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_95	9733513	A mutated JIP-1 molecule with an in-frame deletion of the JNK binding domain did not bind JNK but did bind MKK7, DLK, MLK3, and HPK1 ( Fig. 3A).	bind
45112	5	11246	6	10	NULL	0	NULL	JIP-1 molecule	NULL	deletion mutant	bind	NULL		JNK binding domain		HPK1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_science_281_5383_1671_s_95	9733513	A mutated JIP-1 molecule with an in-frame deletion of the JNK binding domain did not bind JNK but did bind MKK7, DLK, MLK3, and HPK1 ( Fig. 3A).	bind
44908	1	11247	5	NULL	NULL	NULL	NULL	Rb protein	GP	missense mutant	does not bind			C706F		E1A	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_21_11866_s_180	10518542	A mutated Rb protein carrying a C706F missense mutation which does not bind to oncoproteins E1A and large T antigen but does bind to c- myc and L- myc ( 18) also bound to GST-R-K (Fig.  6 C).	bind
44909	2	11247	5	NULL	NULL	NULL	NULL	E1A	GP		is a type of					oncoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_21_11866_s_180	10518542	A mutated Rb protein carrying a C706F missense mutation which does not bind to oncoproteins E1A and large T antigen but does bind to c- myc and L- myc ( 18) also bound to GST-R-K (Fig.  6 C).	bind
44910	3	11247	5	NULL	NULL	NULL	NULL	Rb protein	GP	missense mutant	does not bind			C706F		large T antigen	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_21_11866_s_180	10518542	A mutated Rb protein carrying a C706F missense mutation which does not bind to oncoproteins E1A and large T antigen but does bind to c- myc and L- myc ( 18) also bound to GST-R-K (Fig.  6 C).	bind
44911	4	11247	5	NULL	NULL	NULL	NULL	Rb protein	GP	missense mutant	bind			C706F		c- myc	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_21_11866_s_180	10518542	A mutated Rb protein carrying a C706F missense mutation which does not bind to oncoproteins E1A and large T antigen but does bind to c- myc and L- myc ( 18) also bound to GST-R-K (Fig.  6 C).	bind
44912	5	11247	5	NULL	NULL	NULL	NULL	Rb protein	GP	missense mutant	bind			C706F		L- myc	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_21_11866_s_180	10518542	A mutated Rb protein carrying a C706F missense mutation which does not bind to oncoproteins E1A and large T antigen but does bind to c- myc and L- myc ( 18) also bound to GST-R-K (Fig.  6 C).	bind
44913	6	11247	5	NULL	NULL	NULL	NULL	Rb protein	GP	missense mutant	bind			C706F		GST-R-K	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_21_11866_s_180	10518542	A mutated Rb protein carrying a C706F missense mutation which does not bind to oncoproteins E1A and large T antigen but does bind to c- myc and L- myc ( 18) also bound to GST-R-K (Fig.  6 C).	bind
45113	1	11247	6	10	NULL	0	NULL	Rb protein	NULL	missense mutant	does not bind	NULL		C706F		E1A 	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_21_11866_s_180	10518542	A mutated Rb protein carrying a C706F missense mutation which does not bind to oncoproteins E1A and large T antigen but does bind to c- myc and L- myc ( 18) also bound to GST-R-K (Fig.  6 C).	bind
45114	2	11247	6	10	NULL	0	NULL	Rb protein	NULL	missense mutant	does not bind	NULL		C706F		large T antigen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_21_11866_s_180	10518542	A mutated Rb protein carrying a C706F missense mutation which does not bind to oncoproteins E1A and large T antigen but does bind to c- myc and L- myc ( 18) also bound to GST-R-K (Fig.  6 C).	bind
45115	3	11247	6	10	NULL	0	NULL	Rb protein	NULL	missense mutant	bind	NULL		C706F		c-myc	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_21_11866_s_180	10518542	A mutated Rb protein carrying a C706F missense mutation which does not bind to oncoproteins E1A and large T antigen but does bind to c- myc and L- myc ( 18) also bound to GST-R-K (Fig.  6 C).	bind
45116	4	11247	6	10	NULL	0	NULL	Rb protein	NULL	missense mutant	bind	NULL		C706F		L-myc	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_21_11866_s_180	10518542	A mutated Rb protein carrying a C706F missense mutation which does not bind to oncoproteins E1A and large T antigen but does bind to c- myc and L- myc ( 18) also bound to GST-R-K (Fig.  6 C).	bind
45117	5	11247	6	10	NULL	0	NULL	Rb protein	NULL	missense mutant	bind	NULL		C706F		GST-R-K	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_96_21_11866_s_180	10518542	A mutated Rb protein carrying a C706F missense mutation which does not bind to oncoproteins E1A and large T antigen but does bind to c- myc and L- myc ( 18) also bound to GST-R-K (Fig.  6 C).	bind
45118	6	11247	6	NULL	NULL	0	NULL	E1A	NULL		is a type of	NULL				oncoprotein	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_21_11866_s_180	10518542	A mutated Rb protein carrying a C706F missense mutation which does not bind to oncoproteins E1A and large T antigen but does bind to c- myc and L- myc ( 18) also bound to GST-R-K (Fig.  6 C).	bind
44914	1	11248	5	NULL	NULL	NULL	NULL			mutant	does not bind				CGCT CAC CAGCCGC	LHX9	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_14_1839_s_169	12130543	A mutated sequence CGCT CAC CAGCCGC was no longer bound by LHX9.	bind
45119	1	11248	6	NULL	NULL	0	NULL		NULL	mutant	does not bind	NULL			CGCT CAC CAGCCGC	LHX9	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_16_14_1839_s_169	12130543	A mutated sequence CGCT CAC CAGCCGC was no longer bound by LHX9.	bind
44915	1	11249	5	NULL	NULL	NULL	NULL	DAT	GP	mutant	impairs			C terminus		CaMKIIalpha	GP	binding of			NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_neuron_51_4_16908408_s_7	16908408	A mutation  of the DAT C terminus impairing CaMKIIalpha binding also impaired amphetamine-induced  dopamine efflux.	bind
44916	2	11249	5	NULL	NULL	NULL	NULL	amphetamine	Chemical		induce					dopamine efflux	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_neuron_51_4_16908408_s_7	16908408	A mutation  of the DAT C terminus impairing CaMKIIalpha binding also impaired amphetamine-induced  dopamine efflux.	bind
44917	3	11249	5	NULL	NULL	NULL	NULL	DAT	GP	mutant	impairs			C terminus		statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_neuron_51_4_16908408_s_7	16908408	A mutation  of the DAT C terminus impairing CaMKIIalpha binding also impaired amphetamine-induced  dopamine efflux.	bind
45120	1	11249	6	NULL	NULL	0	NULL	amphetamine	NULL		induces	NULL				dopamine efflux	NULL				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_neuron_51_4_16908408_s_7	16908408	A mutation  of the DAT C terminus impairing CaMKIIalpha binding also impaired amphetamine-induced  dopamine efflux.	bind
45121	2	11249	6	NULL	NULL	0	NULL	DAT	NULL	mutant	impairs	NULL		C terminus		statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_neuron_51_4_16908408_s_7	16908408	A mutation  of the DAT C terminus impairing CaMKIIalpha binding also impaired amphetamine-induced  dopamine efflux.	bind
45122	3	11249	6	NULL	NULL	0	NULL	DAT	NULL	mutant	impairs	NULL		C terminus		CaMKIIalpha	NULL	binding of			NULL		0	NULL	NULL	NULL	abs-batch0740-0759_neuron_51_4_16908408_s_7	16908408	A mutation  of the DAT C terminus impairing CaMKIIalpha binding also impaired amphetamine-induced  dopamine efflux.	bind
44918	2	11250	5	NULL	NULL	NULL	NULL	Prp16	GP	mutant	inhibit			ATP-binding motif		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_8_441_s_9	9550699	A mutation ( prp16-1) near the ATP-binding motif of Prp16 inhibits both the RNA-dependent ATPase activity and the ATP-dependent RNA unwinding activity.	bind
44919	4	11250	5	NULL	NULL	NULL	NULL	Prp16	GP	mutant	inhibit			ATP-binding motif		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_8_441_s_9	9550699	A mutation ( prp16-1) near the ATP-binding motif of Prp16 inhibits both the RNA-dependent ATPase activity and the ATP-dependent RNA unwinding activity.	bind
45560	1	11250	5	NULL	NULL	NULL	NULL	ATPase activity	Process		is dependent on					RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_8_441_s_9	9550699	A mutation ( prp16-1) near the ATP-binding motif of Prp16 inhibits both the RNA-dependent ATPase activity and the ATP-dependent RNA unwinding activity.	bind
45561	3	11250	5	NULL	NULL	NULL	NULL	RNA unwinding activity	Process		is dependent on					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_8_8_441_s_9	9550699	A mutation ( prp16-1) near the ATP-binding motif of Prp16 inhibits both the RNA-dependent ATPase activity and the ATP-dependent RNA unwinding activity.	bind
45123	1	11250	6	NULL	NULL	0	NULL	ATPase activity	NULL		is dependent on	NULL				RNA	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_8_8_441_s_9	9550699	A mutation ( prp16-1) near the ATP-binding motif of Prp16 inhibits both the RNA-dependent ATPase activity and the ATP-dependent RNA unwinding activity.	bind
45124	2	11250	6	NULL	NULL	0	NULL	RNA unwinding activity	NULL		is dependent on	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_8_8_441_s_9	9550699	A mutation ( prp16-1) near the ATP-binding motif of Prp16 inhibits both the RNA-dependent ATPase activity and the ATP-dependent RNA unwinding activity.	bind
45125	3	11250	6	NULL	NULL	0	NULL	Prp16	NULL	mutant	inhibits	NULL		ATP-binding motif		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_8_8_441_s_9	9550699	A mutation ( prp16-1) near the ATP-binding motif of Prp16 inhibits both the RNA-dependent ATPase activity and the ATP-dependent RNA unwinding activity.	bind
45126	4	11250	6	NULL	NULL	0	NULL	Prp16	NULL	mutant	inhibits	NULL		ATP-binding motif		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_8_8_441_s_9	9550699	A mutation ( prp16-1) near the ATP-binding motif of Prp16 inhibits both the RNA-dependent ATPase activity and the ATP-dependent RNA unwinding activity.	bind
44920	1	11251	5	NULL	NULL	NULL	NULL	ERalpha537X	GP	mutant	increase					N-CoR	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_173	12482846	A Mutation (ERalpha537X) That Increases N-CoR Binding also Inhibits AF-1 Activity-- While SERMs show intriguing effects on ERalpha interactions with N-CoR, it is also clear that these interactions are relatively weak (see "`Discussion"`).	bind
44921	2	11251	5	NULL	NULL	NULL	NULL	ERalpha537X	GP	mutant	inhibit					AF-1 	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_173	12482846	A Mutation (ERalpha537X) That Increases N-CoR Binding also Inhibits AF-1 Activity-- While SERMs show intriguing effects on ERalpha interactions with N-CoR, it is also clear that these interactions are relatively weak (see "`Discussion"`).	bind
44922	3	11251	5	NULL	NULL	NULL	NULL	ERalpha	GP		interact with		weakly			N-CoR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_173	12482846	A Mutation (ERalpha537X) That Increases N-CoR Binding also Inhibits AF-1 Activity-- While SERMs show intriguing effects on ERalpha interactions with N-CoR, it is also clear that these interactions are relatively weak (see "`Discussion"`).	bind
45127	1	11251	6	NULL	NULL	0	NULL	ERalpha	NULL		interacts with	NULL	weakly			N-CoR	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_173	12482846	A Mutation (ERalpha537X) That Increases N-CoR Binding also Inhibits AF-1 Activity-- While SERMs show intriguing effects on ERalpha interactions with N-CoR, it is also clear that these interactions are relatively weak (see "`Discussion"`).	bind
45128	2	11251	6	NULL	NULL	0	NULL	ERalpha537X	NULL	mutant	increases	NULL				N-CoR	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_173	12482846	A Mutation (ERalpha537X) That Increases N-CoR Binding also Inhibits AF-1 Activity-- While SERMs show intriguing effects on ERalpha interactions with N-CoR, it is also clear that these interactions are relatively weak (see "`Discussion"`).	bind
45129	3	11251	6	NULL	NULL	0	NULL	ERalpha537X	NULL	mutant	inhibits	NULL				AF-1	NULL	activity of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_173	12482846	A Mutation (ERalpha537X) That Increases N-CoR Binding also Inhibits AF-1 Activity-- While SERMs show intriguing effects on ERalpha interactions with N-CoR, it is also clear that these interactions are relatively weak (see "`Discussion"`).	bind
44923	1	11252	5	NULL	NULL	NULL	NULL	N-CoR	GP		bind					SERMs	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_308	12482846	A mutation (L379R) that reduces and equalizes N-CoR binding with SERMs allows equivalent AF-1 activity at simple EREs and AP-1 sites in the presence of SERMs and increases ICI and raloxifene response at C3.	bind
44924	2	11252	5	NULL	NULL	NULL	NULL			mutant	reduces			L379R		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_308	12482846	A mutation (L379R) that reduces and equalizes N-CoR binding with SERMs allows equivalent AF-1 activity at simple EREs and AP-1 sites in the presence of SERMs and increases ICI and raloxifene response at C3.	bind
44925	3	11252	5	NULL	NULL	NULL	NULL			mutant	equalizes			L379R		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_308	12482846	A mutation (L379R) that reduces and equalizes N-CoR binding with SERMs allows equivalent AF-1 activity at simple EREs and AP-1 sites in the presence of SERMs and increases ICI and raloxifene response at C3.	bind
46383	4	11252	5	NULL	NULL	NULL	NULL			mutant	allows			L379R		AF-1	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_308	12482846	A mutation (L379R) that reduces and equalizes N-CoR binding with SERMs allows equivalent AF-1 activity at simple EREs and AP-1 sites in the presence of SERMs and increases ICI and raloxifene response at C3.	bind
46384	5	11252	5	NULL	NULL	NULL	NULL	statement 4	Process		occurs at									EREs	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_308	12482846	A mutation (L379R) that reduces and equalizes N-CoR binding with SERMs allows equivalent AF-1 activity at simple EREs and AP-1 sites in the presence of SERMs and increases ICI and raloxifene response at C3.	bind
46385	6	11252	5	NULL	NULL	NULL	NULL	statement 4	Process		occurs at									AP-1 sites	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_308	12482846	A mutation (L379R) that reduces and equalizes N-CoR binding with SERMs allows equivalent AF-1 activity at simple EREs and AP-1 sites in the presence of SERMs and increases ICI and raloxifene response at C3.	bind
46386	7	11252	5	NULL	NULL	NULL	NULL	statement 5	Process		is equivalent to					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_308	12482846	A mutation (L379R) that reduces and equalizes N-CoR binding with SERMs allows equivalent AF-1 activity at simple EREs and AP-1 sites in the presence of SERMs and increases ICI and raloxifene response at C3.	bind
46387	8	11252	5	NULL	NULL	NULL	NULL	statement 5	Process		in the presence of					SERMs	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_308	12482846	A mutation (L379R) that reduces and equalizes N-CoR binding with SERMs allows equivalent AF-1 activity at simple EREs and AP-1 sites in the presence of SERMs and increases ICI and raloxifene response at C3.	bind
46388	9	11252	5	NULL	NULL	NULL	NULL	statement 6	Process		in the presence of					SERMs	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_308	12482846	A mutation (L379R) that reduces and equalizes N-CoR binding with SERMs allows equivalent AF-1 activity at simple EREs and AP-1 sites in the presence of SERMs and increases ICI and raloxifene response at C3.	bind
45130	1	11252	6	NULL	NULL	0	NULL	N-CoR	NULL		bind	NULL				SERM	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_308	12482846	A mutation (L379R) that reduces and equalizes N-CoR binding with SERMs allows equivalent AF-1 activity at simple EREs and AP-1 sites in the presence of SERMs and increases ICI and raloxifene response at C3.	bind
45774	2	11252	6	NULL	NULL	0	NULL		NULL	mutant	reduces	NULL		L379R		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_308	12482846	A mutation (L379R) that reduces and equalizes N-CoR binding with SERMs allows equivalent AF-1 activity at simple EREs and AP-1 sites in the presence of SERMs and increases ICI and raloxifene response at C3.	bind
45775	3	11252	6	NULL	NULL	0	NULL		NULL	mutant	equalizes	NULL		L379R		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_308	12482846	A mutation (L379R) that reduces and equalizes N-CoR binding with SERMs allows equivalent AF-1 activity at simple EREs and AP-1 sites in the presence of SERMs and increases ICI and raloxifene response at C3.	bind
45777	4	11252	6	NULL	NULL	0	NULL		NULL	mutant	allows	NULL		L379R		AF-1	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_308	12482846	A mutation (L379R) that reduces and equalizes N-CoR binding with SERMs allows equivalent AF-1 activity at simple EREs and AP-1 sites in the presence of SERMs and increases ICI and raloxifene response at C3.	bind
45778	5	11252	6	NULL	NULL	0	NULL	statement 4	NULL		occurs at	NULL					NULL			ERE	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_308	12482846	A mutation (L379R) that reduces and equalizes N-CoR binding with SERMs allows equivalent AF-1 activity at simple EREs and AP-1 sites in the presence of SERMs and increases ICI and raloxifene response at C3.	bind
45779	6	11252	6	NULL	NULL	0	NULL	statement 4	NULL		occurs at	NULL					NULL			AP-1 site	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_308	12482846	A mutation (L379R) that reduces and equalizes N-CoR binding with SERMs allows equivalent AF-1 activity at simple EREs and AP-1 sites in the presence of SERMs and increases ICI and raloxifene response at C3.	bind
45780	7	11252	6	NULL	NULL	0	NULL	statement 5	NULL		occurs in presence of	NULL				SERM	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_308	12482846	A mutation (L379R) that reduces and equalizes N-CoR binding with SERMs allows equivalent AF-1 activity at simple EREs and AP-1 sites in the presence of SERMs and increases ICI and raloxifene response at C3.	bind
45781	8	11252	6	NULL	NULL	0	NULL	statement 6	NULL		occurs in presence of	NULL				SERM	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_6912_s_308	12482846	A mutation (L379R) that reduces and equalizes N-CoR binding with SERMs allows equivalent AF-1 activity at simple EREs and AP-1 sites in the presence of SERMs and increases ICI and raloxifene response at C3.	bind
45212	1	11253	5	NULL	NULL	NULL	NULL	Tfc4	GP		is mutated at					Tfc4	GP		L469K in TPR7		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_40	16880507	A mutation (L469K) in TPR7 of Tfc4, which affects the recruitment of Brf1, also inhibits the direct binding of Bdp1 to Tfc4 and decreases the affinity of Bdp1 for the TBP-Brf1-TFIIIC-DNA complex, suggesting that Brf1 and Bdp1 share an overlapping binding site in Tfc4 ( ).	bind
45213	2	11253	5	NULL	NULL	NULL	NULL	statement 1	Process		affect					Brf1	GP	recruitment of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_40	16880507	A mutation (L469K) in TPR7 of Tfc4, which affects the recruitment of Brf1, also inhibits the direct binding of Bdp1 to Tfc4 and decreases the affinity of Bdp1 for the TBP-Brf1-TFIIIC-DNA complex, suggesting that Brf1 and Bdp1 share an overlapping binding site in Tfc4 ( ).	bind
45214	3	11253	5	NULL	NULL	NULL	NULL	Bdp1	GP		bind		directly			Tfc4	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_40	16880507	A mutation (L469K) in TPR7 of Tfc4, which affects the recruitment of Brf1, also inhibits the direct binding of Bdp1 to Tfc4 and decreases the affinity of Bdp1 for the TBP-Brf1-TFIIIC-DNA complex, suggesting that Brf1 and Bdp1 share an overlapping binding site in Tfc4 ( ).	bind
45215	4	11253	5	NULL	NULL	NULL	NULL	statement 1	Process		inhibit					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_40	16880507	A mutation (L469K) in TPR7 of Tfc4, which affects the recruitment of Brf1, also inhibits the direct binding of Bdp1 to Tfc4 and decreases the affinity of Bdp1 for the TBP-Brf1-TFIIIC-DNA complex, suggesting that Brf1 and Bdp1 share an overlapping binding site in Tfc4 ( ).	bind
45216	5	11253	5	NULL	NULL	NULL	NULL	Bdp1	GP		shows affinity to					TBP-Brf1-TFIIIC-DNA complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_40	16880507	A mutation (L469K) in TPR7 of Tfc4, which affects the recruitment of Brf1, also inhibits the direct binding of Bdp1 to Tfc4 and decreases the affinity of Bdp1 for the TBP-Brf1-TFIIIC-DNA complex, suggesting that Brf1 and Bdp1 share an overlapping binding site in Tfc4 ( ).	bind
45217	6	11253	5	NULL	NULL	NULL	NULL	statement 1	Process		decrease					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_40	16880507	A mutation (L469K) in TPR7 of Tfc4, which affects the recruitment of Brf1, also inhibits the direct binding of Bdp1 to Tfc4 and decreases the affinity of Bdp1 for the TBP-Brf1-TFIIIC-DNA complex, suggesting that Brf1 and Bdp1 share an overlapping binding site in Tfc4 ( ).	bind
45218	7	11253	5	NULL	NULL	NULL	NULL	Brf1	GP		bind					Tfc4	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_40	16880507	A mutation (L469K) in TPR7 of Tfc4, which affects the recruitment of Brf1, also inhibits the direct binding of Bdp1 to Tfc4 and decreases the affinity of Bdp1 for the TBP-Brf1-TFIIIC-DNA complex, suggesting that Brf1 and Bdp1 share an overlapping binding site in Tfc4 ( ).	bind
45219	8	11253	5	NULL	NULL	NULL	NULL	statement 3	Process		overlaps			binding site		statement 7	Process		binding site		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_40	16880507	A mutation (L469K) in TPR7 of Tfc4, which affects the recruitment of Brf1, also inhibits the direct binding of Bdp1 to Tfc4 and decreases the affinity of Bdp1 for the TBP-Brf1-TFIIIC-DNA complex, suggesting that Brf1 and Bdp1 share an overlapping binding site in Tfc4 ( ).	bind
45782	1	11253	6	NULL	NULL	0	NULL	Bdp1	NULL		bind	NULL				Tfc4	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_40	16880507	A mutation (L469K) in TPR7 of Tfc4, which affects the recruitment of Brf1, also inhibits the direct binding of Bdp1 to Tfc4 and decreases the affinity of Bdp1 for the TBP-Brf1-TFIIIC-DNA complex, suggesting that Brf1 and Bdp1 share an overlapping binding site in Tfc4 ( ).	bind
45783	2	11253	6	NULL	NULL	0	NULL	Bdp1	NULL		has affinity for	NULL				TBP-Brf1-TFIIIC-DNA complex	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_40	16880507	A mutation (L469K) in TPR7 of Tfc4, which affects the recruitment of Brf1, also inhibits the direct binding of Bdp1 to Tfc4 and decreases the affinity of Bdp1 for the TBP-Brf1-TFIIIC-DNA complex, suggesting that Brf1 and Bdp1 share an overlapping binding site in Tfc4 ( ).	bind
45784	3	11253	6	NULL	NULL	0	NULL	Tcf4	NULL	mutant	affects	NULL		L469K in TPR7		Brf1	NULL	recruitment of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_40	16880507	A mutation (L469K) in TPR7 of Tfc4, which affects the recruitment of Brf1, also inhibits the direct binding of Bdp1 to Tfc4 and decreases the affinity of Bdp1 for the TBP-Brf1-TFIIIC-DNA complex, suggesting that Brf1 and Bdp1 share an overlapping binding site in Tfc4 ( ).	bind
45785	4	11253	6	NULL	NULL	0	NULL	Tfc4	NULL	mutant	inhibits	NULL		L469K in TPR7		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_40	16880507	A mutation (L469K) in TPR7 of Tfc4, which affects the recruitment of Brf1, also inhibits the direct binding of Bdp1 to Tfc4 and decreases the affinity of Bdp1 for the TBP-Brf1-TFIIIC-DNA complex, suggesting that Brf1 and Bdp1 share an overlapping binding site in Tfc4 ( ).	bind
45786	5	11253	6	NULL	NULL	0	NULL	Tfc4	NULL	mutant	decreases	NULL		L469K in TPR7		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_16_5946_s_40	16880507	A mutation (L469K) in TPR7 of Tfc4, which affects the recruitment of Brf1, also inhibits the direct binding of Bdp1 to Tfc4 and decreases the affinity of Bdp1 for the TBP-Brf1-TFIIIC-DNA complex, suggesting that Brf1 and Bdp1 share an overlapping binding site in Tfc4 ( ).	bind
45220	1	11254	5	NULL	NULL	NULL	NULL	NOXO1	GP		activates					ROS	GP	generation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_6_4737_s_146	14617635	A Mutation Affecting Lipid Binding Decreases the Ability of NOXO1 to Activate ROS Generation -- Cells were co-transfected with empty vector or plasmid encoding Nox1, NOXA1, plus either NOXO1 or NOXO1(R40Q).	bind
45221	2	11254	5	NULL	NULL	NULL	NULL	mutation 	Process		affect					lipid	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_6_4737_s_146	14617635	A Mutation Affecting Lipid Binding Decreases the Ability of NOXO1 to Activate ROS Generation -- Cells were co-transfected with empty vector or plasmid encoding Nox1, NOXA1, plus either NOXO1 or NOXO1(R40Q).	bind
45222	3	11254	5	NULL	NULL	NULL	NULL	statement 2	Process		decrease					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_6_4737_s_146	14617635	A Mutation Affecting Lipid Binding Decreases the Ability of NOXO1 to Activate ROS Generation -- Cells were co-transfected with empty vector or plasmid encoding Nox1, NOXA1, plus either NOXO1 or NOXO1(R40Q).	bind
45787	1	11254	6	NULL	NULL	0	NULL	NOXO1	NULL		activates	NULL				ROS	NULL	generation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_6_4737_s_146	14617635	A Mutation Affecting Lipid Binding Decreases the Ability of NOXO1 to Activate ROS Generation -- Cells were co-transfected with empty vector or plasmid encoding Nox1, NOXA1, plus either NOXO1 or NOXO1(R40Q).	bind
51247	2	11254	6	10	NULL	0	NULL	mutation 	NULL		affect	NULL				lipid	NULL	binding of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_6_4737_s_146	14617635	A Mutation Affecting Lipid Binding Decreases the Ability of NOXO1 to Activate ROS Generation -- Cells were co-transfected with empty vector or plasmid encoding Nox1, NOXA1, plus either NOXO1 or NOXO1(R40Q).	bind
51248	3	11254	6	10	NULL	0	NULL	statement 2	NULL		decrease	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_6_4737_s_146	14617635	A Mutation Affecting Lipid Binding Decreases the Ability of NOXO1 to Activate ROS Generation -- Cells were co-transfected with empty vector or plasmid encoding Nox1, NOXA1, plus either NOXO1 or NOXO1(R40Q).	bind
45224	1	11255	5	NULL	NULL	NULL	NULL	STAT1	GP		bind					STAT3	GP				NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_66_6_1719_s_9	15448191	A mutation analysis of the 5''- TTCATG GAA-3'' STAT1/3 element (palindrome underlined) was performed to determine nucleotide residues that are necessary for the binding of STAT1 and STAT3.	bind
45788	1	11255	6	NULL	NULL	0	NULL	STAT1	NULL		bind	NULL				STAT3	NULL				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_66_6_1719_s_9	15448191	A mutation analysis of the 5''- TTCATG GAA-3'' STAT1/3 element (palindrome underlined) was performed to determine nucleotide residues that are necessary for the binding of STAT1 and STAT3.	bind
45226	1	11256	5	NULL	NULL	NULL	NULL	apoE molecule	GP		bind					VLDL receptor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_46_8_1721_s_219	15863833	A mutation at arginine 145 (R145C) partially inhibited the binding of the apoE molecule to the VLDL receptor but completely prevented monoclonal antibody 1D7 from binding.	bind
45227	2	11256	5	NULL	NULL	NULL	NULL			mutant	inhibit		partially	R145C		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_46_8_1721_s_219	15863833	A mutation at arginine 145 (R145C) partially inhibited the binding of the apoE molecule to the VLDL receptor but completely prevented monoclonal antibody 1D7 from binding.	bind
45231	3	11256	5	NULL	NULL	NULL	NULL			mutant	prevents		completely	R145C		1D7	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_46_8_1721_s_219	15863833	A mutation at arginine 145 (R145C) partially inhibited the binding of the apoE molecule to the VLDL receptor but completely prevented monoclonal antibody 1D7 from binding.	bind
45232	4	11256	5	NULL	NULL	NULL	NULL	1D7	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_46_8_1721_s_219	15863833	A mutation at arginine 145 (R145C) partially inhibited the binding of the apoE molecule to the VLDL receptor but completely prevented monoclonal antibody 1D7 from binding.	bind
45789	1	11256	6	NULL	NULL	0	NULL	apoE molecule	NULL		bind	NULL				VLDL receptor	NULL				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_8_1721_s_219	15863833	A mutation at arginine 145 (R145C) partially inhibited the binding of the apoE molecule to the VLDL receptor but completely prevented monoclonal antibody 1D7 from binding.	bind
45790	2	11256	6	NULL	NULL	0	NULL		NULL	mutant	inhibits	NULL		arginine 145 (R145C)		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_8_1721_s_219	15863833	A mutation at arginine 145 (R145C) partially inhibited the binding of the apoE molecule to the VLDL receptor but completely prevented monoclonal antibody 1D7 from binding.	bind
45791	3	11256	6	NULL	NULL	0	NULL	1D7	NULL		is a type of	NULL				monoclonal antibody	NULL				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_8_1721_s_219	15863833	A mutation at arginine 145 (R145C) partially inhibited the binding of the apoE molecule to the VLDL receptor but completely prevented monoclonal antibody 1D7 from binding.	bind
45792	4	11256	6	NULL	NULL	0	NULL		NULL	mutant	prevents	NULL		arginine 145 (R145C)		statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_8_1721_s_219	15863833	A mutation at arginine 145 (R145C) partially inhibited the binding of the apoE molecule to the VLDL receptor but completely prevented monoclonal antibody 1D7 from binding.	bind
45233	1	11257	5	NULL	NULL	NULL	NULL	Pto	GP		bind					Pti1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_10_2257_s_310	10811617	A mutation at this residue increases the binding affinity of Pto for Pti1, while it reduces the interaction of Pto with Pti3 and Pti10.	bind
45234	2	11257	5	NULL	NULL	NULL	NULL	Pto	GP		interact with					Pti3	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_10_2257_s_310	10811617	A mutation at this residue increases the binding affinity of Pto for Pti1, while it reduces the interaction of Pto with Pti3 and Pti10.	bind
45235	3	11257	5	NULL	NULL	NULL	NULL	Pto	GP		interact with					Pti10	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_10_2257_s_310	10811617	A mutation at this residue increases the binding affinity of Pto for Pti1, while it reduces the interaction of Pto with Pti3 and Pti10.	bind
45794	1	11257	6	NULL	NULL	0	NULL	Pto	NULL		bind	NULL				Pti10	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_19_10_2257_s_310	10811617	A mutation at this residue increases the binding affinity of Pto for Pti1, while it reduces the interaction of Pto with Pti3 and Pti10.	bind
45795	2	11257	6	NULL	NULL	0	NULL	Pto	NULL		has affinity for	NULL				Pti1	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_19_10_2257_s_310	10811617	A mutation at this residue increases the binding affinity of Pto for Pti1, while it reduces the interaction of Pto with Pti3 and Pti10.	bind
45796	3	11257	6	NULL	NULL	0	NULL	Pto	NULL		bind	NULL				Pti3	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_19_10_2257_s_310	10811617	A mutation at this residue increases the binding affinity of Pto for Pti1, while it reduces the interaction of Pto with Pti3 and Pti10.	bind
45237	1	11258	5	NULL	NULL	NULL	NULL	FAK	GP	recombinant	bind					p85	GP		SH2 domain		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_26329_s_152	8824286	A mutation converting Tyr-397 to Phe abolished recombinant FAK binding to p85 or its SH2 domains  in vitro.	bind
45238	2	11258	5	NULL	NULL	0	NULL		NULL		is mutated to	NULL		Tyr-397			NULL		Phe		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_42_26329_s_152	8824286	A mutation converting Tyr-397 to Phe abolished recombinant FAK binding to p85 or its SH2 domains  in vitro.	bind
45239	3	11258	5	NULL	NULL	NULL	NULL	statement 2	Process		abolishes					statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_42_26329_s_152	8824286	A mutation converting Tyr-397 to Phe abolished recombinant FAK binding to p85 or its SH2 domains  in vitro.	bind
45797	1	11258	6	NULL	NULL	0	NULL	FAK	NULL	recombinant	bind	NULL				p85	NULL		SH2 domain		NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_271_42_26329_s_152	8824286	A mutation converting Tyr-397 to Phe abolished recombinant FAK binding to p85 or its SH2 domains  in vitro.	bind
45798	2	11258	6	NULL	NULL	0	NULL		NULL		is converted to	NULL		Tyr-397			NULL		Phe		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_42_26329_s_152	8824286	A mutation converting Tyr-397 to Phe abolished recombinant FAK binding to p85 or its SH2 domains  in vitro.	bind
45799	3	11258	6	NULL	NULL	0	NULL	statement 2	NULL		abolishes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_42_26329_s_152	8824286	A mutation converting Tyr-397 to Phe abolished recombinant FAK binding to p85 or its SH2 domains  in vitro.	bind
45246	1	11259	5	NULL	NULL	NULL	NULL	PAK	GP	activated	rescues					HUVEC	Cell				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_2_361_s_229	16247032	A mutation crippling the CRIB domain (H83/86L) did not impair the ability of activated PAK to rescue HUVEC from contact inhibition, indicating that this effect does not require Rac binding to PAK.	bind
45247	2	11259	5	NULL	NULL	NULL	NULL	HUVEC	Cell		is rescued from					contact inhibition	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_2_361_s_229	16247032	A mutation crippling the CRIB domain (H83/86L) did not impair the ability of activated PAK to rescue HUVEC from contact inhibition, indicating that this effect does not require Rac binding to PAK.	bind
45250	3	11259	5	NULL	NULL	NULL	NULL	Rac	GP		bind					PAK	GP				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_2_361_s_229	16247032	A mutation crippling the CRIB domain (H83/86L) did not impair the ability of activated PAK to rescue HUVEC from contact inhibition, indicating that this effect does not require Rac binding to PAK.	bind
45254	4	11259	5	NULL	NULL	NULL	NULL	PAK	GP	mutant	does not impair			 CRIB domain H83/86L		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_2_361_s_229	16247032	A mutation crippling the CRIB domain (H83/86L) did not impair the ability of activated PAK to rescue HUVEC from contact inhibition, indicating that this effect does not require Rac binding to PAK.	bind
45256	5	11259	5	NULL	NULL	NULL	NULL	statement 1	Process		does not require					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_2_361_s_229	16247032	A mutation crippling the CRIB domain (H83/86L) did not impair the ability of activated PAK to rescue HUVEC from contact inhibition, indicating that this effect does not require Rac binding to PAK.	bind
45800	1	11259	6	NULL	NULL	0	NULL	Rac	NULL		bind	NULL				PAK	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_171_2_361_s_229	16247032	A mutation crippling the CRIB domain (H83/86L) did not impair the ability of activated PAK to rescue HUVEC from contact inhibition, indicating that this effect does not require Rac binding to PAK.	bind
45801	3	11259	6	10	NULL	0	NULL	HUVEC	NULL		rescued from	NULL				contact inhibition	NULL				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_2_361_s_229	16247032	A mutation crippling the CRIB domain (H83/86L) did not impair the ability of activated PAK to rescue HUVEC from contact inhibition, indicating that this effect does not require Rac binding to PAK.	bind
45802	2	11259	6	10	NULL	0	NULL	PAK	NULL	activated	rescue	NULL				HUVEC	NULL				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_2_361_s_229	16247032	A mutation crippling the CRIB domain (H83/86L) did not impair the ability of activated PAK to rescue HUVEC from contact inhibition, indicating that this effect does not require Rac binding to PAK.	bind
45803	4	11259	6	10	NULL	0	NULL		NULL	mutant	does not impair	NULL		CRIB domain (H83/86L)		statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_2_361_s_229	16247032	A mutation crippling the CRIB domain (H83/86L) did not impair the ability of activated PAK to rescue HUVEC from contact inhibition, indicating that this effect does not require Rac binding to PAK.	bind
45804	5	11259	6	10	NULL	0	NULL	statement 2	NULL		does not require	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_171_2_361_s_229	16247032	A mutation crippling the CRIB domain (H83/86L) did not impair the ability of activated PAK to rescue HUVEC from contact inhibition, indicating that this effect does not require Rac binding to PAK.	bind
45257	1	11260	5	NULL	NULL	NULL	NULL	E7	GP		bind					RB	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_virology_204_2_7941347_s_10	7941347	A mutation either at amino acid 24 or 26 which is known to  disrupt the binding of E7 to RB, the retinoblastoma gene product, did  not strongly affect the nuclear localization of the fusion protein, suggesting  that the nuclear transportation of E7 is mostly independent of RB binding.	bind
45258	2	11260	5	NULL	NULL	NULL	NULL			mutation of	disrupt			amino acid 24		statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_virology_204_2_7941347_s_10	7941347	A mutation either at amino acid 24 or 26 which is known to  disrupt the binding of E7 to RB, the retinoblastoma gene product, did  not strongly affect the nuclear localization of the fusion protein, suggesting  that the nuclear transportation of E7 is mostly independent of RB binding.	bind
45259	3	11260	5	NULL	NULL	NULL	NULL			mutation of	disrupt			amino acid 26		statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_virology_204_2_7941347_s_10	7941347	A mutation either at amino acid 24 or 26 which is known to  disrupt the binding of E7 to RB, the retinoblastoma gene product, did  not strongly affect the nuclear localization of the fusion protein, suggesting  that the nuclear transportation of E7 is mostly independent of RB binding.	bind
45260	4	11260	5	NULL	NULL	NULL	NULL	RB	GP		is					retinoblastoma gene product	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_virology_204_2_7941347_s_10	7941347	A mutation either at amino acid 24 or 26 which is known to  disrupt the binding of E7 to RB, the retinoblastoma gene product, did  not strongly affect the nuclear localization of the fusion protein, suggesting  that the nuclear transportation of E7 is mostly independent of RB binding.	bind
45263	5	11260	5	NULL	NULL	NULL	NULL	E7	GP		is transported to					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_virology_204_2_7941347_s_10	7941347	A mutation either at amino acid 24 or 26 which is known to  disrupt the binding of E7 to RB, the retinoblastoma gene product, did  not strongly affect the nuclear localization of the fusion protein, suggesting  that the nuclear transportation of E7 is mostly independent of RB binding.	bind
45266	6	11260	5	NULL	NULL	NULL	NULL	statement 5	Process		is independent of					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_virology_204_2_7941347_s_10	7941347	A mutation either at amino acid 24 or 26 which is known to  disrupt the binding of E7 to RB, the retinoblastoma gene product, did  not strongly affect the nuclear localization of the fusion protein, suggesting  that the nuclear transportation of E7 is mostly independent of RB binding.	bind
45809	1	11260	6	NULL	NULL	0	NULL	E7	NULL		bind	NULL				RB	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_virology_204_2_7941347_s_10	7941347	A mutation either at amino acid 24 or 26 which is known to  disrupt the binding of E7 to RB, the retinoblastoma gene product, did  not strongly affect the nuclear localization of the fusion protein, suggesting  that the nuclear transportation of E7 is mostly independent of RB binding.	bind
45810	2	11260	6	NULL	NULL	0	NULL	RB	NULL		is 	NULL				retinoblastoma gene product	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_virology_204_2_7941347_s_10	7941347	A mutation either at amino acid 24 or 26 which is known to  disrupt the binding of E7 to RB, the retinoblastoma gene product, did  not strongly affect the nuclear localization of the fusion protein, suggesting  that the nuclear transportation of E7 is mostly independent of RB binding.	bind
45812	4	11260	6	NULL	NULL	0	NULL	E7	NULL		is transported to	NULL				nucleus	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_virology_204_2_7941347_s_10	7941347	A mutation either at amino acid 24 or 26 which is known to  disrupt the binding of E7 to RB, the retinoblastoma gene product, did  not strongly affect the nuclear localization of the fusion protein, suggesting  that the nuclear transportation of E7 is mostly independent of RB binding.	bind
45813	5	11260	6	NULL	NULL	0	NULL	statement 4	NULL		is independent of	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_virology_204_2_7941347_s_10	7941347	A mutation either at amino acid 24 or 26 which is known to  disrupt the binding of E7 to RB, the retinoblastoma gene product, did  not strongly affect the nuclear localization of the fusion protein, suggesting  that the nuclear transportation of E7 is mostly independent of RB binding.	bind
51251	6	11260	6	10	NULL	0	NULL		NULL	mutant	disrupt	NULL		amino acid 26		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_virology_204_2_7941347_s_10	7941347	A mutation either at amino acid 24 or 26 which is known to  disrupt the binding of E7 to RB, the retinoblastoma gene product, did  not strongly affect the nuclear localization of the fusion protein, suggesting  that the nuclear transportation of E7 is mostly independent of RB binding.	bind
45267	1	11261	5	NULL	NULL	NULL	NULL	Gem	GP	mouse	is mutated to			tryptophan 269		Gem	GP	mouse	glycine		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_651_s_186	14701738	A mutation from tryptophan to glycine at position 269 in mouse Gem (or the equivalent position 270 in human Gem) within the helix that binds calmodulin inhibits its binding.	bind
45268	2	11261	5	NULL	NULL	NULL	NULL	Gem	GP	mouse	bind			tryptophan 269		calmodulin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_651_s_186	14701738	A mutation from tryptophan to glycine at position 269 in mouse Gem (or the equivalent position 270 in human Gem) within the helix that binds calmodulin inhibits its binding.	bind
45269	3	11261	5	NULL	NULL	NULL	NULL	statement 1	Process		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_651_s_186	14701738	A mutation from tryptophan to glycine at position 269 in mouse Gem (or the equivalent position 270 in human Gem) within the helix that binds calmodulin inhibits its binding.	bind
45270	4	11261	5	NULL	NULL	NULL	NULL	Gem	GP	mouse	is equivalent to			tryptophan 269		Gem	GP	human	tryptophan 270		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_651_s_186	14701738	A mutation from tryptophan to glycine at position 269 in mouse Gem (or the equivalent position 270 in human Gem) within the helix that binds calmodulin inhibits its binding.	bind
45814	1	11261	6	NULL	NULL	0	NULL	Gem	NULL	mouse	bind	NULL		tryptophan 269		calmodulin	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_2_651_s_186	14701738	A mutation from tryptophan to glycine at position 269 in mouse Gem (or the equivalent position 270 in human Gem) within the helix that binds calmodulin inhibits its binding.	bind
45815	2	11261	6	NULL	NULL	0	NULL	Gem	NULL		is changed to	NULL		tryptophan 269		Gem	NULL		glycine 269		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_651_s_186	14701738	A mutation from tryptophan to glycine at position 269 in mouse Gem (or the equivalent position 270 in human Gem) within the helix that binds calmodulin inhibits its binding.	bind
45816	3	11261	6	10	NULL	0	NULL	statement 2	NULL		inhibit	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_2_651_s_186	14701738	A mutation from tryptophan to glycine at position 269 in mouse Gem (or the equivalent position 270 in human Gem) within the helix that binds calmodulin inhibits its binding.	bind
45817	4	11261	6	NULL	NULL	0	NULL	Gem	NULL	mouse	is equivalent to	NULL		tryptophan 269		Gem	NULL	human	tryptophan 270		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_2_651_s_186	14701738	A mutation from tryptophan to glycine at position 269 in mouse Gem (or the equivalent position 270 in human Gem) within the helix that binds calmodulin inhibits its binding.	bind
45271	1	11262	5	NULL	NULL	NULL	NULL	hns	GP		is a type of					global regulatory factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_22_2645_s_61	16291643	A mutation in  hns, a global regulatory factor that regulates many virulence factors, causes a threefold increase in  E. coli vesicle production (Horstman and Kuehn 2002 ).	bind
45272	2	11262	5	NULL	NULL	NULL	NULL	hns	GP		regulates					virulence factors	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_22_2645_s_61	16291643	A mutation in  hns, a global regulatory factor that regulates many virulence factors, causes a threefold increase in  E. coli vesicle production (Horstman and Kuehn 2002 ).	bind
45273	3	11262	5	NULL	NULL	NULL	NULL	hns	GP	mutant	increases					vesicle	CellComponent	E. coli;; production of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_22_2645_s_61	16291643	A mutation in  hns, a global regulatory factor that regulates many virulence factors, causes a threefold increase in  E. coli vesicle production (Horstman and Kuehn 2002 ).	bind
45818	1	11262	6	10	NULL	0	NULL	hns	NULL		is a type of	NULL				global regulatory factor	NULL				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_22_2645_s_61	16291643	A mutation in  hns, a global regulatory factor that regulates many virulence factors, causes a threefold increase in  E. coli vesicle production (Horstman and Kuehn 2002 ).	bind
45819	2	11262	6	NULL	NULL	0	NULL	statement 1	NULL		regulates	NULL				virulence factors	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_22_2645_s_61	16291643	A mutation in  hns, a global regulatory factor that regulates many virulence factors, causes a threefold increase in  E. coli vesicle production (Horstman and Kuehn 2002 ).	bind
45820	3	11262	6	10	NULL	0	NULL	hns	NULL	mutant	increases	NULL				vesicle	NULL	E.coli;;production of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_22_2645_s_61	16291643	A mutation in  hns, a global regulatory factor that regulates many virulence factors, causes a threefold increase in  E. coli vesicle production (Horstman and Kuehn 2002 ).	bind
45274	1	11263	5	NULL	NULL	NULL	NULL	HsdS	GP		bind					HsdM	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_2_412_s_344	10839821	A mutation in  hsdS may prevent binding of HsdS to HsdM or, as suggested by Weiserova and Firman ( ), the TRD may influence the precise positioning of HsdR, perhaps in response to the methylation state of the target sequence.	bind
45275	2	11263	5	NULL	NULL	NULL	NULL	hsdS	GP	mutant	prevents		may			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_2_412_s_344	10839821	A mutation in  hsdS may prevent binding of HsdS to HsdM or, as suggested by Weiserova and Firman ( ), the TRD may influence the precise positioning of HsdR, perhaps in response to the methylation state of the target sequence.	bind
45276	3	11263	5	NULL	NULL	NULL	NULL				influences			TRD		HsdR	GP	precise positioning of			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_2_412_s_344	10839821	A mutation in  hsdS may prevent binding of HsdS to HsdM or, as suggested by Weiserova and Firman ( ), the TRD may influence the precise positioning of HsdR, perhaps in response to the methylation state of the target sequence.	bind
45277	4	11263	5	NULL	NULL	NULL	NULL	statement 3	Process		occur in response to		may			target sequence	NucleicAcid	methylation state of			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_2_412_s_344	10839821	A mutation in  hsdS may prevent binding of HsdS to HsdM or, as suggested by Weiserova and Firman ( ), the TRD may influence the precise positioning of HsdR, perhaps in response to the methylation state of the target sequence.	bind
45821	1	11263	6	NULL	NULL	0	NULL	HsdS	NULL		bind	NULL				HsdM	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_2_412_s_344	10839821	A mutation in  hsdS may prevent binding of HsdS to HsdM or, as suggested by Weiserova and Firman ( ), the TRD may influence the precise positioning of HsdR, perhaps in response to the methylation state of the target sequence.	bind
45822	2	11263	6	NULL	NULL	0	NULL	hsdS	NULL	mutant	prevents	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_2_412_s_344	10839821	A mutation in  hsdS may prevent binding of HsdS to HsdM or, as suggested by Weiserova and Firman ( ), the TRD may influence the precise positioning of HsdR, perhaps in response to the methylation state of the target sequence.	bind
45823	3	11263	6	10	NULL	0	NULL				influences			TRD		HsdR		positioning of 			NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_2_412_s_344	10839821	A mutation in  hsdS may prevent binding of HsdS to HsdM or, as suggested by Weiserova and Firman ( ), the TRD may influence the precise positioning of HsdR, perhaps in response to the methylation state of the target sequence.	bind
45283	1	11266	5	NULL	NULL	NULL	NULL	actin	GP	Saccharomyces cerevisiae;;mutation of	causes			S14A		temperature-sensitive phenotype					NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_12_0_129_s_489	8970724	A mutation in an ATP-binding loop of  Saccharomyces cerevisiae actin (S14A) causes a temperature-sensitive phenotype.	bind
45284	2	11266	5	NULL	NULL	NULL	NULL	actin	GP	Saccharomyces cerevisiae;;mutation of	is present in			S14A		actin	GP	Saccharomyces cerevisiae;;mutant	ATP-binding loop		NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_12_0_129_s_489	8970724	A mutation in an ATP-binding loop of  Saccharomyces cerevisiae actin (S14A) causes a temperature-sensitive phenotype.	bind
45824	1	11266	6	10	NULL	0	NULL	actin	NULL	mutant;; Saccharomyces cerevisiae	causes a	NULL		ATP-binding loop;;S14A		temperature-sensitive phenotype	NULL				NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_12_0_129_s_489	8970724	A mutation in an ATP-binding loop of  Saccharomyces cerevisiae actin (S14A) causes a temperature-sensitive phenotype.	bind
45287	1	11268	5	NULL	NULL	NULL	NULL	Mcm4 protein	GP	mutation of	affect			ATP-binding motif		ssDNA1	NucleicAcid	 binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_45_42471_s_25	12207017	A mutation in an ATP-binding motif of the Mcm4 protein affected the ssDNA1 binding activity of the complex and led to moderate inhibition of the DNA helicase activity ( 9).	bind
45288	2	11268	5	NULL	NULL	NULL	NULL	statement 1	Process		leads to					DNA helicase activity	Process	moderate inhibition of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_45_42471_s_25	12207017	A mutation in an ATP-binding motif of the Mcm4 protein affected the ssDNA1 binding activity of the complex and led to moderate inhibition of the DNA helicase activity ( 9).	bind
45825	1	11268	6	NULL	NULL	0	NULL	Mcm4 protein	NULL	mutant	affects	NULL		ATP-binding motif		ssDNA1	NULL	binding activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_45_42471_s_25	12207017	A mutation in an ATP-binding motif of the Mcm4 protein affected the ssDNA1 binding activity of the complex and led to moderate inhibition of the DNA helicase activity ( 9).	bind
45826	2	11268	6	10	NULL	0	NULL	statement 1			leads to					DNA helicase activity		inhibiton of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_45_42471_s_25	12207017	A mutation in an ATP-binding motif of the Mcm4 protein affected the ssDNA1 binding activity of the complex and led to moderate inhibition of the DNA helicase activity ( 9).	bind
45289	1	11269	5	NULL	NULL	NULL	NULL	SULT1A1 probe	NucleicAcid	mutation of	does not change				EBS3	Elf1	GP	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_66_6_1690_s_237	15383623	A mutation in EBS3 of the  SULT1A1 probe did not change the binding affinity for Elf1 or Elk1, but compromised binding of the GABP heterodimer.	bind
45290	2	11269	5	NULL	NULL	NULL	NULL	SULT1A1 probe	NucleicAcid	mutation of	does not change				EBS3	Elk1	GP	binding affinity of			NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_66_6_1690_s_237	15383623	A mutation in EBS3 of the  SULT1A1 probe did not change the binding affinity for Elf1 or Elk1, but compromised binding of the GABP heterodimer.	bind
45291	3	11269	5	NULL	NULL	NULL	NULL	SULT1A1 probe	NucleicAcid	mutation of	compromises				EBS3	GABP heterodimer	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_66_6_1690_s_237	15383623	A mutation in EBS3 of the  SULT1A1 probe did not change the binding affinity for Elf1 or Elk1, but compromised binding of the GABP heterodimer.	bind
45827	1	11269	6	10	NULL	0	NULL	SULT1A1 probe		mutant	did not change				EBS3	Elf1		binding affinity of			NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_66_6_1690_s_237	15383623	A mutation in EBS3 of the  SULT1A1 probe did not change the binding affinity for Elf1 or Elk1, but compromised binding of the GABP heterodimer.	bind
45828	2	11269	6	10	NULL	0	NULL	SULT1A1 probe		mutant	did not change				EBS3	Elk1		binding affinity of			NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_66_6_1690_s_237	15383623	A mutation in EBS3 of the  SULT1A1 probe did not change the binding affinity for Elf1 or Elk1, but compromised binding of the GABP heterodimer.	bind
45829	3	11269	6	10	NULL	0	NULL	SULT1A1 probe		mutant	compromises				EBS3	GABP heterodimer		binding of			NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_66_6_1690_s_237	15383623	A mutation in EBS3 of the  SULT1A1 probe did not change the binding affinity for Elf1 or Elk1, but compromised binding of the GABP heterodimer.	bind
45292	1	11270	5	NULL	NULL	NULL	NULL	RNA polymerase holoenzyme	GP	Escherichia coli	bind					DNA	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_12_3019_s_873	9620948	A mutation in region 1.1 of sigma sigma 70 affects promoter DNA binding by Escherichia coli RNA polymerase holoenzyme.	bind
45293	2	11270	5	NULL	NULL	NULL	NULL	sigma 70	GP	mutant	affect			region 1.1		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_12_3019_s_873	9620948	A mutation in region 1.1 of sigma sigma 70 affects promoter DNA binding by Escherichia coli RNA polymerase holoenzyme.	bind
46136	1	11270	6	NULL	NULL	0	NULL	RNA polymerase holoenzyme	NULL	E. coli	bind	NULL				DNA	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_12_3019_s_873	9620948	A mutation in region 1.1 of sigma sigma 70 affects promoter DNA binding by Escherichia coli RNA polymerase holoenzyme.	bind
46137	2	11270	6	10	NULL	0	NULL	sigma70	NULL	mutant	affects	NULL		region 1.1		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_12_3019_s_873	9620948	A mutation in region 1.1 of sigma sigma 70 affects promoter DNA binding by Escherichia coli RNA polymerase holoenzyme.	bind
45294	1	11271	5	NULL	NULL	NULL	NULL	RNA polymerase holoenzyme	GP	E. coli	bind					DNA	NucleicAcid			promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_1_221_s_255	10613885	A mutation in region 1.1 of sigma70 affects promoter DNA binding by  E. coli RNA polymerase holoenzyme.	bind
45295	2	11271	5	NULL	NULL	NULL	NULL	sigma70	GP	mutant	affect				region 1.1	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_1_221_s_255	10613885	A mutation in region 1.1 of sigma70 affects promoter DNA binding by  E. coli RNA polymerase holoenzyme.	bind
45830	1	11272	6	NULL	NULL	0	NULL	RNA polymerase holoenzyme	NULL	Escherichia coli	bind	NULL				DNA 	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_1_162_s_548	11114913	A mutation in region 1.1 of sigma70 affects promoter DNA binding by  Escherichia coli RNA polymerase holoenzyme.	bind
45831	2	11272	6	NULL	NULL	0	NULL	sigma70	NULL	mutant	affects	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_1_162_s_548	11114913	A mutation in region 1.1 of sigma70 affects promoter DNA binding by  Escherichia coli RNA polymerase holoenzyme.	bind
45296	1	11274	5	NULL	NULL	NULL	NULL	complex			bind					single-stranded DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8003_s_26	10567526	A mutation in the ATP binding motifs of the Mcm4 protein affected the single-stranded DNA-binding activity of the complex, which moderately inhibited the DNA helicase activity.	bind
45297	2	11274	5	NULL	NULL	NULL	NULL	Mcm4 protein	GP	mutation in	affect			ATP binding motifs		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8003_s_26	10567526	A mutation in the ATP binding motifs of the Mcm4 protein affected the single-stranded DNA-binding activity of the complex, which moderately inhibited the DNA helicase activity.	bind
45298	3	11274	5	NULL	NULL	NULL	NULL	statement 2	Process		inhibit		moderatley			DNA helicase activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8003_s_26	10567526	A mutation in the ATP binding motifs of the Mcm4 protein affected the single-stranded DNA-binding activity of the complex, which moderately inhibited the DNA helicase activity.	bind
45832	1	11274	6	10	NULL	0	NULL	Mcm4 protein		mutant	affects			ATP-binding motif		complex		DNA binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_12_8003_s_26	10567526	A mutation in the ATP binding motifs of the Mcm4 protein affected the single-stranded DNA-binding activity of the complex, which moderately inhibited the DNA helicase activity.	bind
45833	2	11274	6	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL	moderately			DNA helicase activity	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_12_8003_s_26	10567526	A mutation in the ATP binding motifs of the Mcm4 protein affected the single-stranded DNA-binding activity of the complex, which moderately inhibited the DNA helicase activity.	bind
45299	2	11275	5	NULL	NULL	NULL	NULL	p38 subunit	GP	mutation of	does not alter			ATP binding site		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_20_11607_s_7	9751713	A mutation in the ATP binding site of the p38 subunit did not alter the replication activity of hRFC.	bind
58589	1	11275	5	NULL	NULL	NULL	NULL	hRFC	GP		activates					replication	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_20_11607_s_7	9751713	A mutation in the ATP binding site of the p38 subunit did not alter the replication activity of hRFC.	bind
45834	1	11275	6	10	NULL	0	NULL	hRFC			activates					replication					NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_20_11607_s_7	9751713	A mutation in the ATP binding site of the p38 subunit did not alter the replication activity of hRFC.	bind
45835	2	11275	6	10	NULL	0	NULL	p38 subunit		mutant	did not alter			ATP binding site		statement 1					NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_20_11607_s_7	9751713	A mutation in the ATP binding site of the p38 subunit did not alter the replication activity of hRFC.	bind
45302	1	11276	5	NULL	NULL	NULL	NULL	Rhp51	GP		interact with					Rad22	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1724_s_83	11292845	A mutation in the ATP-binding motifs of Rhp51 does not affect its interactions with Rad22 or itself   It has been reported that Rad51 binds to Rad52 and self-assembles ( 41).	bind
45303	2	11276	5	NULL	NULL	NULL	NULL	Rhp51	GP	mutation of	does not affect			ATP-binding motifs		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1724_s_83	11292845	A mutation in the ATP-binding motifs of Rhp51 does not affect its interactions with Rad22 or itself   It has been reported that Rad51 binds to Rad52 and self-assembles ( 41).	bind
45304	3	11276	5	NULL	NULL	NULL	NULL	Rhp51	GP		bind					Rhp51	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1724_s_83	11292845	A mutation in the ATP-binding motifs of Rhp51 does not affect its interactions with Rad22 or itself   It has been reported that Rad51 binds to Rad52 and self-assembles ( 41).	bind
45305	4	11276	5	NULL	NULL	NULL	NULL	Rhp51	GP	mutation of	does not affect			ATP-binding motifs		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1724_s_83	11292845	A mutation in the ATP-binding motifs of Rhp51 does not affect its interactions with Rad22 or itself   It has been reported that Rad51 binds to Rad52 and self-assembles ( 41).	bind
45306	5	11276	5	NULL	NULL	NULL	NULL	Rad51	GP		bind					Rad52	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1724_s_83	11292845	A mutation in the ATP-binding motifs of Rhp51 does not affect its interactions with Rad22 or itself   It has been reported that Rad51 binds to Rad52 and self-assembles ( 41).	bind
45307	6	11276	5	NULL	NULL	NULL	NULL	statement 5	Process		undergoes					self-assembling	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1724_s_83	11292845	A mutation in the ATP-binding motifs of Rhp51 does not affect its interactions with Rad22 or itself   It has been reported that Rad51 binds to Rad52 and self-assembles ( 41).	bind
45837	1	11276	6	10	NULL	0	NULL	Rhp51	NULL		interact with	NULL				Rad22	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1724_s_83	11292845	A mutation in the ATP-binding motifs of Rhp51 does not affect its interactions with Rad22 or itself   It has been reported that Rad51 binds to Rad52 and self-assembles ( 41).	bind
45838	2	11276	6	NULL	NULL	0	NULL		NULL	mutant	does not affect	NULL		ATP-binding motif		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1724_s_83	11292845	A mutation in the ATP-binding motifs of Rhp51 does not affect its interactions with Rad22 or itself   It has been reported that Rad51 binds to Rad52 and self-assembles ( 41).	bind
45839	5	11276	6	10	NULL	0	NULL	Rad51	NULL		bind	NULL				Rad52	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1724_s_83	11292845	A mutation in the ATP-binding motifs of Rhp51 does not affect its interactions with Rad22 or itself   It has been reported that Rad51 binds to Rad52 and self-assembles ( 41).	bind
45840	6	11276	6	10	NULL	0	NULL	statement 5	NULL		undergoes	NULL				self-assembling	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1724_s_83	11292845	A mutation in the ATP-binding motifs of Rhp51 does not affect its interactions with Rad22 or itself   It has been reported that Rad51 binds to Rad52 and self-assembles ( 41).	bind
51252	3	11276	6	10	NULL	0	NULL	Rhp51	NULL		bind	NULL				Rhp51	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1724_s_83	11292845	A mutation in the ATP-binding motifs of Rhp51 does not affect its interactions with Rad22 or itself   It has been reported that Rad51 binds to Rad52 and self-assembles ( 41).	bind
51253	4	11276	6	10	NULL	0	NULL	Rhp51	NULL	mutant	does not affect	NULL		ATP-binding motif		statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_8_1724_s_83	11292845	A mutation in the ATP-binding motifs of Rhp51 does not affect its interactions with Rad22 or itself   It has been reported that Rad51 binds to Rad52 and self-assembles ( 41).	bind
45308	1	11277	5	NULL	NULL	NULL	NULL	RecD subunit	GP	mutation of	reduces			consensus ATP-binding sequence		RecBCD enzyme	GP	processivity of;;Escherichia coli			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_13_7_890_s_415	10197988	A mutation in the consensus ATP-binding sequence of the RecD subunit reduces the processivity of the RecBCD enzyme from  Escherichia coli.	bind
45841	1	11277	6	10	NULL	0	NULL	RecD subunit	NULL	mutant	reduces	NULL		ATP-binding sequence		RecBCD enzyme	NULL	processivity of ;;Escherichia coli			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_13_7_890_s_415	10197988	A mutation in the consensus ATP-binding sequence of the RecD subunit reduces the processivity of the RecBCD enzyme from  Escherichia coli.	bind
45312	1	11279	5	NULL	NULL	NULL	NULL	Stat 3D	GP		is					mutation in the DNA binding region	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_12_9016_s_288	11114305	A mutation in the DNA binding region ( Stat 3D) as well as substitution of the STAT3 DNA binding region to STAT1 ( Stat 3/1 (D,Linker)) abolished IL-6 induction (Fig.  6).	bind
45313	2	11279	5	NULL	NULL	NULL	NULL	Stat 3D	GP		abolishes					IL-6	GP	induction of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_12_9016_s_288	11114305	A mutation in the DNA binding region ( Stat 3D) as well as substitution of the STAT3 DNA binding region to STAT1 ( Stat 3/1 (D,Linker)) abolished IL-6 induction (Fig.  6).	bind
45314	3	11279	5	NULL	NULL	NULL	NULL	STAT3	GP		is substituted to			DNA binding region		STAT1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_12_9016_s_288	11114305	A mutation in the DNA binding region ( Stat 3D) as well as substitution of the STAT3 DNA binding region to STAT1 ( Stat 3/1 (D,Linker)) abolished IL-6 induction (Fig.  6).	bind
45315	4	11279	5	NULL	NULL	NULL	NULL	statement 3	Process		abolishes					IL-6	GP	induction of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_12_9016_s_288	11114305	A mutation in the DNA binding region ( Stat 3D) as well as substitution of the STAT3 DNA binding region to STAT1 ( Stat 3/1 (D,Linker)) abolished IL-6 induction (Fig.  6).	bind
45842	1	11279	6	NULL	NULL	0	NULL	STAT 3D	NULL		abolishes	NULL		DNA binding region		IL-6	NULL	induction of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_12_9016_s_288	11114305	A mutation in the DNA binding region ( Stat 3D) as well as substitution of the STAT3 DNA binding region to STAT1 ( Stat 3/1 (D,Linker)) abolished IL-6 induction (Fig.  6).	bind
45843	2	11279	6	NULL	NULL	0	NULL	STAT3	NULL		is substituted by	NULL		DNA binding region		STAT1	NULL		Stat 3/1 (D,Linker)		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_12_9016_s_288	11114305	A mutation in the DNA binding region ( Stat 3D) as well as substitution of the STAT3 DNA binding region to STAT1 ( Stat 3/1 (D,Linker)) abolished IL-6 induction (Fig.  6).	bind
45844	3	11279	6	NULL	NULL	0	NULL	statement 2	NULL		abolishes	NULL				IL-6	NULL	induction of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_12_9016_s_288	11114305	A mutation in the DNA binding region ( Stat 3D) as well as substitution of the STAT3 DNA binding region to STAT1 ( Stat 3/1 (D,Linker)) abolished IL-6 induction (Fig.  6).	bind
51254	4	11279	6	10	NULL	0	NULL	Stat 3D	NULL		is	NULL				mutation in the DNA binding region	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_12_9016_s_288	11114305	A mutation in the DNA binding region ( Stat 3D) as well as substitution of the STAT3 DNA binding region to STAT1 ( Stat 3/1 (D,Linker)) abolished IL-6 induction (Fig.  6).	bind
46393	1	11280	5	NULL	NULL	NULL	NULL	TF	GP	mutant	abolishes				Egr-1 binding site in promoter	shear stress	Process	response to			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_281_s_158	9974408	A Mutation in the Egr-1 Binding Site in the TF Promoter Abolishes the Response to Shear Stress   To define more precisely the role of Sp1 and Egr-1 in shear stress  trans-activation of the TF promoter, we analyzed the effect of mutations in the overlapping Sp1/Egr-1 binding site that were known to abolish binding of Sp1 and Egr-1 in vitro.	bind
46394	2	11280	5	NULL	NULL	NULL	NULL	Sp1	GP		bind					Egr-1	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_281_s_158	9974408	A Mutation in the Egr-1 Binding Site in the TF Promoter Abolishes the Response to Shear Stress   To define more precisely the role of Sp1 and Egr-1 in shear stress  trans-activation of the TF promoter, we analyzed the effect of mutations in the overlapping Sp1/Egr-1 binding site that were known to abolish binding of Sp1 and Egr-1 in vitro.	bind
46395	3	11280	5	NULL	NULL	NULL	NULL			mutant	abolishes				overlapping Sp1/Egr-1 binding site	statement 2	Process				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_281_s_158	9974408	A Mutation in the Egr-1 Binding Site in the TF Promoter Abolishes the Response to Shear Stress   To define more precisely the role of Sp1 and Egr-1 in shear stress  trans-activation of the TF promoter, we analyzed the effect of mutations in the overlapping Sp1/Egr-1 binding site that were known to abolish binding of Sp1 and Egr-1 in vitro.	bind
46140	1	11280	6	NULL	NULL	0	NULL	TF	NULL	mutant	abolishes	NULL			egr-1 binding site of promoter	shear stress	NULL	response to			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_281_s_158	9974408	A Mutation in the Egr-1 Binding Site in the TF Promoter Abolishes the Response to Shear Stress   To define more precisely the role of Sp1 and Egr-1 in shear stress  trans-activation of the TF promoter, we analyzed the effect of mutations in the overlapping Sp1/Egr-1 binding site that were known to abolish binding of Sp1 and Egr-1 in vitro.	bind
46141	2	11280	6	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL				Egr-1	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_281_s_158	9974408	A Mutation in the Egr-1 Binding Site in the TF Promoter Abolishes the Response to Shear Stress   To define more precisely the role of Sp1 and Egr-1 in shear stress  trans-activation of the TF promoter, we analyzed the effect of mutations in the overlapping Sp1/Egr-1 binding site that were known to abolish binding of Sp1 and Egr-1 in vitro.	bind
46142	3	11280	6	10	NULL	0	NULL		NULL	mutant;;  	abolish	NULL			overlapping Sp1/Egr-1 binding site	statement 2	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_2_281_s_158	9974408	A Mutation in the Egr-1 Binding Site in the TF Promoter Abolishes the Response to Shear Stress   To define more precisely the role of Sp1 and Egr-1 in shear stress  trans-activation of the TF promoter, we analyzed the effect of mutations in the overlapping Sp1/Egr-1 binding site that were known to abolish binding of Sp1 and Egr-1 in vitro.	bind
45309	1	11281	5	NULL	NULL	NULL	NULL	cells	Cell		express					ABCA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_720_s_137	12615680	A mutation in the first intracellular ATP binding domain, however, also appears to impair apoA-I binding to ABCA1-expressing cells.	bind
45310	2	11281	5	NULL	NULL	NULL	NULL	apoA-I	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_720_s_137	12615680	A mutation in the first intracellular ATP binding domain, however, also appears to impair apoA-I binding to ABCA1-expressing cells.	bind
45311	3	11281	5	NULL	NULL	NULL	NULL			mutant	impairs			first intracellular ATP binding domain		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_720_s_137	12615680	A mutation in the first intracellular ATP binding domain, however, also appears to impair apoA-I binding to ABCA1-expressing cells.	bind
45845	1	11281	6	NULL	NULL	0	NULL	apoA-I	NULL		bind	NULL				ABCA1-expressing cells	NULL				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_720_s_137	12615680	A mutation in the first intracellular ATP binding domain, however, also appears to impair apoA-I binding to ABCA1-expressing cells.	bind
45846	2	11281	6	10	NULL	0	NULL		NULL	mutant	impairs	NULL		first intracellular ATP binding domain		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_23_5_720_s_137	12615680	A mutation in the first intracellular ATP binding domain, however, also appears to impair apoA-I binding to ABCA1-expressing cells.	bind
45316	1	11282	5	NULL	NULL	NULL	NULL	NADH:ubiquinone oxidoreductase complex	GP	mutant	increases			NADH-binding subunit		citrate	Chemical	biosynthesis of			NULL		NULL	NULL	NULL	NULL	gw70_annurevplantbiol_52_0_527_s_401	null	A mutation in the gene encoding the NADH-binding subunit of the NADH:ubiquinone  oxidoreductase complex increases citrate biosynthesis and causes a 30-fold increase  in the internal citrate under certain conditions ( 135).	bind
45317	2	11282	5	NULL	NULL	NULL	NULL	statement 1	Process		increases					citrate	Chemical	internal 			NULL		NULL	NULL	NULL	NULL	gw70_annurevplantbiol_52_0_527_s_401	null	A mutation in the gene encoding the NADH-binding subunit of the NADH:ubiquinone  oxidoreductase complex increases citrate biosynthesis and causes a 30-fold increase  in the internal citrate under certain conditions ( 135).	bind
45858	1	11282	6	NULL	NULL	0	NULL	NADH:ubiquinone oxidoreductase complex	NULL	mutant	increases	NULL		NADH-binding subunit		citrate	NULL	biosynthesis of			NULL		0	NULL	NULL	NULL	gw70_annurevplantbiol_52_0_527_s_401	null	A mutation in the gene encoding the NADH-binding subunit of the NADH:ubiquinone  oxidoreductase complex increases citrate biosynthesis and causes a 30-fold increase  in the internal citrate under certain conditions ( 135).	bind
45859	2	11282	6	10	NULL	0	NULL	statement 1			increases					citrate					NULL		NULL	NULL	NULL	NULL	gw70_annurevplantbiol_52_0_527_s_401	null	A mutation in the gene encoding the NADH-binding subunit of the NADH:ubiquinone  oxidoreductase complex increases citrate biosynthesis and causes a 30-fold increase  in the internal citrate under certain conditions ( 135).	bind
45318	1	11283	5	NULL	NULL	NULL	NULL	FtsZ	GP	B. subtilis;;mutant	supress			GTP binding site		minCD phenotype	GP	overexpression of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_18_5449_s_77	11514533	A mutation in the GTP binding site of  B. subtilis FtsZ suppresses the  minCD overexpression phenotype.	bind
45860	1	11283	6	10	NULL	0	NULL	FtsZ	NULL	B. subtilis;; mutation of	suppresses	NULL		GTP binding site		minCD phenotype	NULL	overexpression of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_18_5449_s_77	11514533	A mutation in the GTP binding site of  B. subtilis FtsZ suppresses the  minCD overexpression phenotype.	bind
45320	1	11284	5	NULL	NULL	NULL	NULL	eRF3	GP	mutation of	impairs			GTP-binding motifs		eRF1	GP	binding afbility of			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_279_44_15337765_s_7	15337765	A mutation in the GTP-binding  motifs of eRF3 impairs the eRF1-binding ability without altering the Pab1-  or Upf1-binding activity.	bind
45322	2	11284	5	NULL	NULL	NULL	NULL	statement 1	Process		occurs without altering					Pab1	GP	binding activity of			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_279_44_15337765_s_7	15337765	A mutation in the GTP-binding  motifs of eRF3 impairs the eRF1-binding ability without altering the Pab1-  or Upf1-binding activity.	bind
45324	3	11284	5	NULL	NULL	NULL	NULL	statement 1	Process		occurs without altering					 Upf1	GP	binding activity of			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_279_44_15337765_s_7	15337765	A mutation in the GTP-binding  motifs of eRF3 impairs the eRF1-binding ability without altering the Pab1-  or Upf1-binding activity.	bind
45861	1	11284	6	NULL	NULL	0	NULL	eRF3	NULL	mutant	impairs	NULL		GTP-binding motif		eRF1	NULL	binding ability of 			NULL		0	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_279_44_15337765_s_7	15337765	A mutation in the GTP-binding  motifs of eRF3 impairs the eRF1-binding ability without altering the Pab1-  or Upf1-binding activity.	bind
45862	2	11284	6	NULL	NULL	0	NULL	statement 1	NULL		occurs without altering	NULL				Pab1 	NULL	binding activity of			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_279_44_15337765_s_7	15337765	A mutation in the GTP-binding  motifs of eRF3 impairs the eRF1-binding ability without altering the Pab1-  or Upf1-binding activity.	bind
45863	3	11284	6	NULL	NULL	0	NULL	statement 1	NULL		occurs without altering	NULL				Upf1	NULL	binding activity of			NULL		0	NULL	NULL	NULL	abs-batch0517-0529_j-biol-chem_279_44_15337765_s_7	15337765	A mutation in the GTP-binding  motifs of eRF3 impairs the eRF1-binding ability without altering the Pab1-  or Upf1-binding activity.	bind
45325	1	11286	5	NULL	NULL	NULL	NULL	androgen receptor	GP	mutation of	affect			ligand binding domain		steroid	GP	binding characteristics of			NULL	human LNCaP cells	NULL	NULL	NULL	NULL	gw60_amjpathol_162_1_233_s_278	12507906	A mutation in the ligand binding domain of the androgen receptor of human LNCaP cells affects steroid binding characteristics and response to anti-androgens.	bind
45326	2	11286	5	NULL	NULL	NULL	NULL	androgen receptor	GP	mutation of	affect			ligand binding domain		anti-androgens	GP	response to			NULL	human LNCaP cells	NULL	NULL	NULL	NULL	gw60_amjpathol_162_1_233_s_278	12507906	A mutation in the ligand binding domain of the androgen receptor of human LNCaP cells affects steroid binding characteristics and response to anti-androgens.	bind
45864	1	11286	6	10	NULL	0	NULL	androgen receptor	NULL	mutant	affects	NULL		ligand binding domain		steroid	NULL	binding of;; characterstic of 			NULL	human LNCaP cells	NULL	NULL	NULL	NULL	gw60_amjpathol_162_1_233_s_278	12507906	A mutation in the ligand binding domain of the androgen receptor of human LNCaP cells affects steroid binding characteristics and response to anti-androgens.	bind
45865	2	11286	6	10	NULL	0	NULL	androgen receptor	NULL	mutant	affects	NULL		ligand binding domain		anti-androgens	NULL	response to			NULL	human LNCaP cells	NULL	NULL	NULL	NULL	gw60_amjpathol_162_1_233_s_278	12507906	A mutation in the ligand binding domain of the androgen receptor of human LNCaP cells affects steroid binding characteristics and response to anti-androgens.	bind
45327	1	11287	5	NULL	NULL	NULL	NULL	GCN2	GP	yeast	bind					tRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_8_1730_s_43	16601681	A mutation in the m2 motif of the HisRS domain in yeast GCN2 strongly decreased  the binding to tRNA, thus making the kinase unable to phosphorylate eIF2alpha in response to amino-acid deprivation (  et al).	bind
45328	2	11287	5	NULL	NULL	NULL	NULL	GCN2	GP	yeast;;mutant	decreases		strongly	m2 motif of HisRS domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_8_1730_s_43	16601681	A mutation in the m2 motif of the HisRS domain in yeast GCN2 strongly decreased  the binding to tRNA, thus making the kinase unable to phosphorylate eIF2alpha in response to amino-acid deprivation (  et al).	bind
45329	3	11287	5	NULL	NULL	NULL	NULL	GCN2	GP		does not phosphorylate					eIF2alpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_8_1730_s_43	16601681	A mutation in the m2 motif of the HisRS domain in yeast GCN2 strongly decreased  the binding to tRNA, thus making the kinase unable to phosphorylate eIF2alpha in response to amino-acid deprivation (  et al).	bind
45330	4	11287	5	NULL	NULL	NULL	NULL	statement 3	GP		in response to					amino-acid	AminoAcid	deprivation of			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_8_1730_s_43	16601681	A mutation in the m2 motif of the HisRS domain in yeast GCN2 strongly decreased  the binding to tRNA, thus making the kinase unable to phosphorylate eIF2alpha in response to amino-acid deprivation (  et al).	bind
45331	5	11287	5	NULL	NULL	NULL	NULL	statement 2	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_8_1730_s_43	16601681	A mutation in the m2 motif of the HisRS domain in yeast GCN2 strongly decreased  the binding to tRNA, thus making the kinase unable to phosphorylate eIF2alpha in response to amino-acid deprivation (  et al).	bind
51255	6	11287	5	NULL	NULL	NULL	NULL	GCN2	GP		is a type of					kinase	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_8_1730_s_43	16601681	A mutation in the m2 motif of the HisRS domain in yeast GCN2 strongly decreased  the binding to tRNA, thus making the kinase unable to phosphorylate eIF2alpha in response to amino-acid deprivation (  et al).	bind
46143	1	11287	6	NULL	NULL	0	NULL	GCN2	NULL	yeast	bind	NULL				tRNA	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_25_8_1730_s_43	16601681	A mutation in the m2 motif of the HisRS domain in yeast GCN2 strongly decreased  the binding to tRNA, thus making the kinase unable to phosphorylate eIF2alpha in response to amino-acid deprivation (  et al).	bind
46144	2	11287	6	NULL	NULL	0	NULL	GCN2	NULL	mutant;; yeast	decreases	NULL	strongly	m2 motif of HisRS domain		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_25_8_1730_s_43	16601681	A mutation in the m2 motif of the HisRS domain in yeast GCN2 strongly decreased  the binding to tRNA, thus making the kinase unable to phosphorylate eIF2alpha in response to amino-acid deprivation (  et al).	bind
46145	3	11287	6	NULL	NULL	0	NULL	GCN2	NULL		is a type of	NULL				kinase	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_25_8_1730_s_43	16601681	A mutation in the m2 motif of the HisRS domain in yeast GCN2 strongly decreased  the binding to tRNA, thus making the kinase unable to phosphorylate eIF2alpha in response to amino-acid deprivation (  et al).	bind
46146	4	11287	6	10	NULL	0	NULL	GCN2	NULL		does not phosphorylate	NULL				eIF2alpha	NULL				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_8_1730_s_43	16601681	A mutation in the m2 motif of the HisRS domain in yeast GCN2 strongly decreased  the binding to tRNA, thus making the kinase unable to phosphorylate eIF2alpha in response to amino-acid deprivation (  et al).	bind
46147	5	11287	6	10	NULL	0	NULL	statement 4	NULL		occurs in response to	NULL				amino-acid	NULL	deprivation of			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_8_1730_s_43	16601681	A mutation in the m2 motif of the HisRS domain in yeast GCN2 strongly decreased  the binding to tRNA, thus making the kinase unable to phosphorylate eIF2alpha in response to amino-acid deprivation (  et al).	bind
46148	6	11287	6	NULL	NULL	0	NULL	statement 2	NULL		abolishes	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_25_8_1730_s_43	16601681	A mutation in the m2 motif of the HisRS domain in yeast GCN2 strongly decreased  the binding to tRNA, thus making the kinase unable to phosphorylate eIF2alpha in response to amino-acid deprivation (  et al).	bind
45332	1	11288	5	NULL	NULL	NULL	NULL	MalY	GP	mutation of	results in			pyridoxal phosphate binding site		betaC-S lyase	GP	loss of;; activity of			NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_1_204_s_550	9529892	A mutation in the pyridoxal phosphate binding site of MalY was constructed that resulted in the loss of betaC-S lyase activity, even though the protein was still active as a  mal gene repressor.	bind
45333	2	11288	5	NULL	NULL	NULL	NULL	MalY	GP	mutant	is active as			pyridoxal phosphate binding site		mal gene repressor	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_1_204_s_550	9529892	A mutation in the pyridoxal phosphate binding site of MalY was constructed that resulted in the loss of betaC-S lyase activity, even though the protein was still active as a  mal gene repressor.	bind
45866	1	11288	6	NULL	NULL	0	NULL	MalY	NULL	mutant	results in	NULL		pyridoxal phosphate binding site		betaC-S lyase activity	NULL	loss of 			NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_1_204_s_550	9529892	A mutation in the pyridoxal phosphate binding site of MalY was constructed that resulted in the loss of betaC-S lyase activity, even though the protein was still active as a  mal gene repressor.	bind
51256	2	11288	6	10	NULL	0	NULL	MalY	NULL	mutant	is active as	NULL		pyridoxal phosphate binding site		mal gene repressor	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_62_1_204_s_550	9529892	A mutation in the pyridoxal phosphate binding site of MalY was constructed that resulted in the loss of betaC-S lyase activity, even though the protein was still active as a  mal gene repressor.	bind
45334	2	11289	5	NULL	NULL	NULL	NULL	Raf	GP	mutation of	prevents			Ras binding region		statement 1	Process				NULL	Sf9 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_38_23022_s_200	8798490	A mutation in the Ras binding region of Raf prevented the kinase activation of Raf induced by coexpression with Ras in Sf9 cells ( 25).	bind
45335	3	11289	5	NULL	NULL	NULL	NULL	statement 1	Process		induced by					Ras	GP	coexpression with			NULL	Sf9 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_38_23022_s_200	8798490	A mutation in the Ras binding region of Raf prevented the kinase activation of Raf induced by coexpression with Ras in Sf9 cells ( 25).	bind
51257	1	11289	5	NULL	NULL	NULL	NULL	kinase	GP		activates					Raf	GP				NULL	Sf9 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_38_23022_s_200	8798490	A mutation in the Ras binding region of Raf prevented the kinase activation of Raf induced by coexpression with Ras in Sf9 cells ( 25).	bind
46158	1	11289	6	10	NULL	0	NULL	kinase			activates					Raf					NULL	Sf9 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_38_23022_s_200	8798490	A mutation in the Ras binding region of Raf prevented the kinase activation of Raf induced by coexpression with Ras in Sf9 cells ( 25).	bind
46160	2	11289	6	NULL	NULL	0	NULL	statement 1	NULL		occurs after	NULL				Ras	NULL	coexpression with			NULL	Sf9 cells	0	NULL	NULL	NULL	gw60_jbiolchem_271_38_23022_s_200	8798490	A mutation in the Ras binding region of Raf prevented the kinase activation of Raf induced by coexpression with Ras in Sf9 cells ( 25).	bind
46162	3	11289	6	10	NULL	0	NULL	Raf		mutant	prevents			Ras binding region		statement 1					NULL	Sf9 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_38_23022_s_200	8798490	A mutation in the Ras binding region of Raf prevented the kinase activation of Raf induced by coexpression with Ras in Sf9 cells ( 25).	bind
45336	1	11290	5	NULL	NULL	NULL	NULL	p130Cas	GP	mutation of	reduces		significantly	SH3-binding motif		Src 	GP	kinase activity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_10_8837_s_376	12496276	A mutation in the SH3-binding motif of p130Cas causes significant reduction  in Src kinase activity ( ).	bind
45868	2	11290	6	10	NULL	0	NULL	p130Cas		mutant	reduces		significantly	SH3-binding motif		Src		kinase activity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_10_8837_s_376	12496276	A mutation in the SH3-binding motif of p130Cas causes significant reduction  in Src kinase activity ( ).	bind
45337	1	11291	5	NULL	NULL	NULL	NULL	STAT1	GP		bind					STAT3	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_278_5337_477_s_154	9334309	A mutation in the STAT DNA-binding sequence that disrupted the binding of STAT1 and STAT3 (Fig.  4D) blocked completely the ability of CNTF to activate GFAP promoter-driven reporter gene expression (Fig.  4C).	bind
45338	2	11291	5	NULL	NULL	NULL	NULL	STAT	GP	mutation of	disrupts			DNA-binding sequence		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_278_5337_477_s_154	9334309	A mutation in the STAT DNA-binding sequence that disrupted the binding of STAT1 and STAT3 (Fig.  4D) blocked completely the ability of CNTF to activate GFAP promoter-driven reporter gene expression (Fig.  4C).	bind
45339	3	11291	5	NULL	NULL	NULL	NULL	CNTF	GP		activates					GFAP 	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw60_science_278_5337_477_s_154	9334309	A mutation in the STAT DNA-binding sequence that disrupted the binding of STAT1 and STAT3 (Fig.  4D) blocked completely the ability of CNTF to activate GFAP promoter-driven reporter gene expression (Fig.  4C).	bind
45340	4	11291	5	NULL	NULL	NULL	NULL	STAT	GP	mutation of	block		completely	DNA-binding sequence		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_278_5337_477_s_154	9334309	A mutation in the STAT DNA-binding sequence that disrupted the binding of STAT1 and STAT3 (Fig.  4D) blocked completely the ability of CNTF to activate GFAP promoter-driven reporter gene expression (Fig.  4C).	bind
45869	1	11291	6	NULL	NULL	0	NULL	STAT1	NULL		bind	NULL				STAT3	NULL				NULL		0	NULL	NULL	NULL	gw60_science_278_5337_477_s_154	9334309	A mutation in the STAT DNA-binding sequence that disrupted the binding of STAT1 and STAT3 (Fig.  4D) blocked completely the ability of CNTF to activate GFAP promoter-driven reporter gene expression (Fig.  4C).	bind
45870	2	11291	6	10	NULL	0	NULL	STAT		mutant	disrupts			DNA-binding sequence	 	statement 1					NULL		NULL	NULL	NULL	NULL	gw60_science_278_5337_477_s_154	9334309	A mutation in the STAT DNA-binding sequence that disrupted the binding of STAT1 and STAT3 (Fig.  4D) blocked completely the ability of CNTF to activate GFAP promoter-driven reporter gene expression (Fig.  4C).	bind
45871	3	11291	6	NULL	NULL	0	NULL	CNTF	NULL		activates	NULL				GFAP	NULL			promoter	NULL		0	NULL	NULL	NULL	gw60_science_278_5337_477_s_154	9334309	A mutation in the STAT DNA-binding sequence that disrupted the binding of STAT1 and STAT3 (Fig.  4D) blocked completely the ability of CNTF to activate GFAP promoter-driven reporter gene expression (Fig.  4C).	bind
45872	4	11291	6	10	NULL	0	NULL	STAT		mutant	blocks		completely	DNA-binding sequence	 	statement 3					NULL		NULL	NULL	NULL	NULL	gw60_science_278_5337_477_s_154	9334309	A mutation in the STAT DNA-binding sequence that disrupted the binding of STAT1 and STAT3 (Fig.  4D) blocked completely the ability of CNTF to activate GFAP promoter-driven reporter gene expression (Fig.  4C).	bind
45341	1	11292	5	NULL	NULL	NULL	NULL	TFC3	GP	mutation of	decreases			tau138 subunit		TFIIIC-tRNA gene (DNA)	GP	binding affinity of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_1_s_28	9418847	A mutation in the tau138 subunit, encoded by  TFC3, decreased TFIIIC-tRNA gene (DNA) binding affinity and also affected 5S RNA synthesis in vitro ( 34).	bind
45342	2	11292	5	NULL	NULL	NULL	NULL	TFC3	GP	mutation of	affect			tau138 subunit		5S RNA	NucleicAcid	synthesis of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_1_s_28	9418847	A mutation in the tau138 subunit, encoded by  TFC3, decreased TFIIIC-tRNA gene (DNA) binding affinity and also affected 5S RNA synthesis in vitro ( 34).	bind
60554	3	11292	5	NULL	NULL	NULL	NULL	tau138 subunit	GP		is encoded by					TFC3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_1_s_28	9418847	A mutation in the tau138 subunit, encoded by  TFC3, decreased TFIIIC-tRNA gene (DNA) binding affinity and also affected 5S RNA synthesis in vitro ( 34).	bind
45875	1	11292	6	NULL	NULL	0	NULL	tau138 subunit	NULL		is encoded by	NULL				TFC3	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_1_s_28	9418847	A mutation in the tau138 subunit, encoded by  TFC3, decreased TFIIIC-tRNA gene (DNA) binding affinity and also affected 5S RNA synthesis in vitro ( 34).	bind
45876	2	11292	6	10	NULL	0	NULL		NULL	mutant	decreases	NULL		tau138 subunit		TFIIIC-tRNA gene	NULL	binding affinity of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_1_s_28	9418847	A mutation in the tau138 subunit, encoded by  TFC3, decreased TFIIIC-tRNA gene (DNA) binding affinity and also affected 5S RNA synthesis in vitro ( 34).	bind
45877	3	11292	6	10	NULL	0	NULL		NULL	mutant	affects	NULL		tau138 subunit		5S RNA	NULL	synthesis of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_1_s_28	9418847	A mutation in the tau138 subunit, encoded by  TFC3, decreased TFIIIC-tRNA gene (DNA) binding affinity and also affected 5S RNA synthesis in vitro ( 34).	bind
45343	1	11293	5	NULL	NULL	NULL	NULL	PRMT5 construct	GP	myc-tagged;;mutation of	leads to			S-adenosyl-L-methionine-binding motif I		enzymatic activity	Process	near complete loss of			NULL	COS-1 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_35_32971_s_9	11413150	A mutation introduced into the  S-adenosyl-L-methionine-binding motif I of a  myc-tagged PRMT5 construct in COS-1 cells led to a near complete loss of observed enzymatic activity.	bind
45878	1	11293	6	10	NULL	0	NULL	PRMT5 construct	NULL	Myc-tagged;; mutant	leads to	NULL		S-adenosyl-L-methionine-binding motif I		enzymatic activity	NULL	complete loss of			NULL	COS-1 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_35_32971_s_9	11413150	A mutation introduced into the  S-adenosyl-L-methionine-binding motif I of a  myc-tagged PRMT5 construct in COS-1 cells led to a near complete loss of observed enzymatic activity.	bind
45344	1	11294	5	NULL	NULL	NULL	NULL	mTOR	GP		bind					FKBP12-rapamycin complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_2_815_s_243	7822316	A mutation leading to a  reduction in the binding affinity of mTOR for the FKBP12-rapamycin  complex, with otherwise normal mTOR catalytic activity, would be  predicted to act in a dominant fashion in heterozygotes.	bind
45879	1	11294	6	NULL	NULL	0	NULL	mTOR	NULL		bind	NULL				FKBP12-rapamycin complex	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_2_815_s_243	7822316	A mutation leading to a  reduction in the binding affinity of mTOR for the FKBP12-rapamycin  complex, with otherwise normal mTOR catalytic activity, would be  predicted to act in a dominant fashion in heterozygotes.	bind
45347	1	11295	5	NULL	NULL	NULL	NULL	ST	GP		bind					PP2A	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_161	15684382	A mutation of a cysteine (C103S) that disrupts ST binding to PP2A ( ) resulted in a complete loss of PP2A binding to AR, even upon overexpression of the mutant ST (Fig.  3C).	bind
45348	2	11295	5	NULL	NULL	NULL	NULL			mutant	disrupts			C103S		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_161	15684382	A mutation of a cysteine (C103S) that disrupts ST binding to PP2A ( ) resulted in a complete loss of PP2A binding to AR, even upon overexpression of the mutant ST (Fig.  3C).	bind
45349	3	11295	5	NULL	NULL	NULL	NULL	PP2A	GP		bind					AR	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_161	15684382	A mutation of a cysteine (C103S) that disrupts ST binding to PP2A ( ) resulted in a complete loss of PP2A binding to AR, even upon overexpression of the mutant ST (Fig.  3C).	bind
45350	4	11295	5	NULL	NULL	NULL	NULL	statement 2	Process		results in					statement 3	Process	complete loss of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_161	15684382	A mutation of a cysteine (C103S) that disrupts ST binding to PP2A ( ) resulted in a complete loss of PP2A binding to AR, even upon overexpression of the mutant ST (Fig.  3C).	bind
45351	5	11295	5	NULL	NULL	NULL	NULL	ST	GP	overexpression of;;mutant	results in					statement 3	Process	complete loss of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_161	15684382	A mutation of a cysteine (C103S) that disrupts ST binding to PP2A ( ) resulted in a complete loss of PP2A binding to AR, even upon overexpression of the mutant ST (Fig.  3C).	bind
45880	1	11295	6	NULL	NULL	0	NULL	ST	NULL		bind	NULL				PP2A	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_161	15684382	A mutation of a cysteine (C103S) that disrupts ST binding to PP2A ( ) resulted in a complete loss of PP2A binding to AR, even upon overexpression of the mutant ST (Fig.  3C).	bind
45881	2	11295	6	NULL	NULL	0	NULL		NULL	mutant	disrupts	NULL		cysteine;; C103S		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_161	15684382	A mutation of a cysteine (C103S) that disrupts ST binding to PP2A ( ) resulted in a complete loss of PP2A binding to AR, even upon overexpression of the mutant ST (Fig.  3C).	bind
45882	3	11295	6	NULL	NULL	0	NULL	PP2A	NULL		bind	NULL				AR	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_161	15684382	A mutation of a cysteine (C103S) that disrupts ST binding to PP2A ( ) resulted in a complete loss of PP2A binding to AR, even upon overexpression of the mutant ST (Fig.  3C).	bind
45883	4	11295	6	NULL	NULL	0	NULL		NULL	mutant	results in	NULL		cysteine;; C103S		statement 3	NULL	complete loss of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_4_1298_s_161	15684382	A mutation of a cysteine (C103S) that disrupts ST binding to PP2A ( ) resulted in a complete loss of PP2A binding to AR, even upon overexpression of the mutant ST (Fig.  3C).	bind
45352	1	11296	5	NULL	NULL	NULL	NULL	ASK1	GP		bind					SOCS1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_9_5559_s_201	16407264	A mutation of ASK1 at Tyr-718 (ASK1-Y718F) diminished the binding to SOCS1 in both assays.	bind
45353	2	11296	5	NULL	NULL	NULL	NULL	ASK1	GP	mutant	diminishes			Y718F		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_9_5559_s_201	16407264	A mutation of ASK1 at Tyr-718 (ASK1-Y718F) diminished the binding to SOCS1 in both assays.	bind
45884	1	11296	6	NULL	NULL	0	NULL	ASK1	NULL		bind	NULL				SOCS1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_9_5559_s_201	16407264	A mutation of ASK1 at Tyr-718 (ASK1-Y718F) diminished the binding to SOCS1 in both assays.	bind
45885	2	11296	6	NULL	NULL	0	NULL	ASK1	NULL	mutant	diminishes	NULL		Tyr-718		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_9_5559_s_201	16407264	A mutation of ASK1 at Tyr-718 (ASK1-Y718F) diminished the binding to SOCS1 in both assays.	bind
45354	1	11297	5	NULL	NULL	NULL	NULL	glycine	AminoAcid		is mutated to			305		arginine	AminoAcid		305		NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1647_1_206_s_75	12686134	A mutation of glycine 305 to arginine will most probably affect cofactor binding  and potentially also the binding of the substrate serine, assuming that serine binds  to CBS in a similar fashion as the substrate analogue methionine in the complex structure  of OASS [  15].	bind
45355	2	11297	5	NULL	NULL	NULL	NULL	statement 1	Process		affect		probably			cofactor	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1647_1_206_s_75	12686134	A mutation of glycine 305 to arginine will most probably affect cofactor binding  and potentially also the binding of the substrate serine, assuming that serine binds  to CBS in a similar fashion as the substrate analogue methionine in the complex structure  of OASS [  15].	bind
45356	3	11297	5	NULL	NULL	NULL	NULL	statement 1	Process		affect		potentially			substrate serine	AminoAcid	binding of			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1647_1_206_s_75	12686134	A mutation of glycine 305 to arginine will most probably affect cofactor binding  and potentially also the binding of the substrate serine, assuming that serine binds  to CBS in a similar fashion as the substrate analogue methionine in the complex structure  of OASS [  15].	bind
45357	4	11297	5	NULL	NULL	NULL	NULL	serine	AminoAcid		bind		may			CBS	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1647_1_206_s_75	12686134	A mutation of glycine 305 to arginine will most probably affect cofactor binding  and potentially also the binding of the substrate serine, assuming that serine binds  to CBS in a similar fashion as the substrate analogue methionine in the complex structure  of OASS [  15].	bind
45886	1	11297	6	NULL	NULL	0	NULL	glycine	NULL		is mutated to	NULL				arginine	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1647_1_206_s_75	12686134	A mutation of glycine 305 to arginine will most probably affect cofactor binding  and potentially also the binding of the substrate serine, assuming that serine binds  to CBS in a similar fashion as the substrate analogue methionine in the complex structure  of OASS [  15].	bind
45887	2	11297	6	NULL	NULL	0	NULL	statement 1	NULL		affects	NULL	probably			cofactor	NULL	binding of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1647_1_206_s_75	12686134	A mutation of glycine 305 to arginine will most probably affect cofactor binding  and potentially also the binding of the substrate serine, assuming that serine binds  to CBS in a similar fashion as the substrate analogue methionine in the complex structure  of OASS [  15].	bind
45888	3	11297	6	NULL	NULL	0	NULL	statement 1	NULL		affects	NULL				substrate serine	NULL	binding of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1647_1_206_s_75	12686134	A mutation of glycine 305 to arginine will most probably affect cofactor binding  and potentially also the binding of the substrate serine, assuming that serine binds  to CBS in a similar fashion as the substrate analogue methionine in the complex structure  of OASS [  15].	bind
51274	4	11297	6	10	NULL	0	NULL	serine	NULL		bind	NULL				CBS	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1647_1_206_s_75	12686134	A mutation of glycine 305 to arginine will most probably affect cofactor binding  and potentially also the binding of the substrate serine, assuming that serine binds  to CBS in a similar fashion as the substrate analogue methionine in the complex structure  of OASS [  15].	bind
45360	1	11299	5	NULL	NULL	NULL	NULL	Rad27	GP	mutation of	eliminates					PCNA	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5373_s_38	10409728	A mutation of Rad27 eliminating PCNA binding had very little effect by itself but had major consequences via intragenic or intergenic interactions.	bind
45889	1	11299	6	NULL	NULL	0	NULL	Rad27	NULL	mutant	eliminates	NULL				PCNA	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5373_s_38	10409728	A mutation of Rad27 eliminating PCNA binding had very little effect by itself but had major consequences via intragenic or intergenic interactions.	bind
45361	1	11300	5	NULL	NULL	NULL	NULL	RG2	GP		is					E1A amino terminus	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_cell-growth-differ_7_10_8891337_s_11	8891337	A mutation of the E1A amino terminus  (RG2), which inhibits binding of p300 and related high molecular weight  proteins, reduced 12S repression by 40%.	bind
45362	2	11300	5	NULL	NULL	NULL	NULL	E1A	GP	mutation of	inhibit			RG2		p300	GP	binding of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_cell-growth-differ_7_10_8891337_s_11	8891337	A mutation of the E1A amino terminus  (RG2), which inhibits binding of p300 and related high molecular weight  proteins, reduced 12S repression by 40%.	bind
51275	3	11300	5	NULL	NULL	NULL	NULL	E1A	GP	mutant	reduce			amino terminus		12S	GP	repression of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_cell-growth-differ_7_10_8891337_s_11	8891337	A mutation of the E1A amino terminus  (RG2), which inhibits binding of p300 and related high molecular weight  proteins, reduced 12S repression by 40%.	bind
45890	1	11300	6	10	NULL	0	NULL	E1A	NULL	mutant	inhibits	NULL		amino terminus 		p300	NULL	binding of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_cell-growth-differ_7_10_8891337_s_11	8891337	A mutation of the E1A amino terminus  (RG2), which inhibits binding of p300 and related high molecular weight  proteins, reduced 12S repression by 40%.	bind
45891	2	11300	6	10	NULL	0	NULL	E1A	NULL	mutant	reduces	NULL		amino terminus		12S	NULL	repression of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_cell-growth-differ_7_10_8891337_s_11	8891337	A mutation of the E1A amino terminus  (RG2), which inhibits binding of p300 and related high molecular weight  proteins, reduced 12S repression by 40%.	bind
51276	3	11300	6	10	NULL	0	NULL	RG2	NULL		is	NULL				E1A amino terminus	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_cell-growth-differ_7_10_8891337_s_11	8891337	A mutation of the E1A amino terminus  (RG2), which inhibits binding of p300 and related high molecular weight  proteins, reduced 12S repression by 40%.	bind
45364	1	11301	5	NULL	NULL	NULL	NULL				is similar to			M875VPM878TLM881		Ctr1	GP	S. cerevisiae	copper-binding motifs		NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_13_3804_s_281	12813074	A mutation of the sequence motif M875VPM878TLM881, which is similar to the copper-binding motifs of Ctr1 and Ctr3 ( S.  cerevisiae) ( ,  ,  ) and Ctr4 ( S.  pombe) ( ), had no influence on copper resistance.	bind
45365	2	11301	5	NULL	NULL	NULL	NULL				is similar to			M875VPM878TLM881		Ctr3	GP	S. cerevisiae	copper-binding motifs		NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_13_3804_s_281	12813074	A mutation of the sequence motif M875VPM878TLM881, which is similar to the copper-binding motifs of Ctr1 and Ctr3 ( S.  cerevisiae) ( ,  ,  ) and Ctr4 ( S.  pombe) ( ), had no influence on copper resistance.	bind
45366	3	11301	5	NULL	NULL	NULL	NULL				is similar to			M875VPM878TLM881		Ctr4	GP	S. pombe	copper-binding motifs		NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_13_3804_s_281	12813074	A mutation of the sequence motif M875VPM878TLM881, which is similar to the copper-binding motifs of Ctr1 and Ctr3 ( S.  cerevisiae) ( ,  ,  ) and Ctr4 ( S.  pombe) ( ), had no influence on copper resistance.	bind
45367	4	11301	5	NULL	NULL	NULL	NULL			mutation of	does not influence			M875VPM878TLM881		copper resistance	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_13_3804_s_281	12813074	A mutation of the sequence motif M875VPM878TLM881, which is similar to the copper-binding motifs of Ctr1 and Ctr3 ( S.  cerevisiae) ( ,  ,  ) and Ctr4 ( S.  pombe) ( ), had no influence on copper resistance.	bind
45894	1	11301	6	10	NULL	0	NULL		NULL	mutant	does not influence	NULL		M875VPM878TLM881		copper resistance	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_13_3804_s_281	12813074	A mutation of the sequence motif M875VPM878TLM881, which is similar to the copper-binding motifs of Ctr1 and Ctr3 ( S.  cerevisiae) ( ,  ,  ) and Ctr4 ( S.  pombe) ( ), had no influence on copper resistance.	bind
45898	3	11301	6	10	NULL	0	NULL		NULL		is similar to	NULL		M875VPM878TLM881		Ctr1	NULL	S. cerevisiae	copper-binding motif		NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_13_3804_s_281	12813074	A mutation of the sequence motif M875VPM878TLM881, which is similar to the copper-binding motifs of Ctr1 and Ctr3 ( S.  cerevisiae) ( ,  ,  ) and Ctr4 ( S.  pombe) ( ), had no influence on copper resistance.	bind
45899	2	11301	6	10	NULL	0	NULL		NULL		is similar to	NULL		M875VPM878TLM881		Ctr4	NULL	 S. pombe	copper-binding motif		NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_13_3804_s_281	12813074	A mutation of the sequence motif M875VPM878TLM881, which is similar to the copper-binding motifs of Ctr1 and Ctr3 ( S.  cerevisiae) ( ,  ,  ) and Ctr4 ( S.  pombe) ( ), had no influence on copper resistance.	bind
45900	4	11301	6	10	NULL	0	NULL		NULL		is similar to	NULL		M875VPM878TLM881		Ctr3	NULL	S. cerevisiae	copper-binding motif		NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_13_3804_s_281	12813074	A mutation of the sequence motif M875VPM878TLM881, which is similar to the copper-binding motifs of Ctr1 and Ctr3 ( S.  cerevisiae) ( ,  ,  ) and Ctr4 ( S.  pombe) ( ), had no influence on copper resistance.	bind
45387	2	11303	5	NULL	NULL	NULL	NULL	Gab1	GP		interacts with					SHP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4109_s_8	9632795	A mutation of tyrosine 759, the SHP-2 binding site of gp130, abrogated the interactions of Gab1 with SHP-2 and PI-3 kinase as well as ERK2 activation.	bind
45388	3	11303	5	NULL	NULL	NULL	NULL	Gab1	GP		interacts with					PI-3 kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4109_s_8	9632795	A mutation of tyrosine 759, the SHP-2 binding site of gp130, abrogated the interactions of Gab1 with SHP-2 and PI-3 kinase as well as ERK2 activation.	bind
45389	4	11303	5	NULL	NULL	NULL	NULL	gp130	GP	mutation of	abrogates			tyrosine 759;;SHP-2 binding site		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4109_s_8	9632795	A mutation of tyrosine 759, the SHP-2 binding site of gp130, abrogated the interactions of Gab1 with SHP-2 and PI-3 kinase as well as ERK2 activation.	bind
45390	5	11303	5	NULL	NULL	NULL	NULL	gp130	GP	mutation of	abrogates			tyrosine 759;;SHP-2 binding site		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4109_s_8	9632795	A mutation of tyrosine 759, the SHP-2 binding site of gp130, abrogated the interactions of Gab1 with SHP-2 and PI-3 kinase as well as ERK2 activation.	bind
45391	1	11303	5	NULL	NULL	NULL	NULL	gp130	GP	mutation of	abrogates			tyrosine 759;;SHP-2 binding site		ERK2	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4109_s_8	9632795	A mutation of tyrosine 759, the SHP-2 binding site of gp130, abrogated the interactions of Gab1 with SHP-2 and PI-3 kinase as well as ERK2 activation.	bind
45906	1	11303	6	10	NULL	0	NULL	Gab1			interacts with					SHP-2					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4109_s_8	9632795	A mutation of tyrosine 759, the SHP-2 binding site of gp130, abrogated the interactions of Gab1 with SHP-2 and PI-3 kinase as well as ERK2 activation.	bind
45907	2	11303	6	10	NULL	0	NULL	Gab1			interacts with					PI-3 kinase					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4109_s_8	9632795	A mutation of tyrosine 759, the SHP-2 binding site of gp130, abrogated the interactions of Gab1 with SHP-2 and PI-3 kinase as well as ERK2 activation.	bind
45908	3	11303	6	10	NULL	0	NULL	gp130	NULL	mutant	abrogates	NULL		tyrosine 759;; the SHP-2 binding site		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4109_s_8	9632795	A mutation of tyrosine 759, the SHP-2 binding site of gp130, abrogated the interactions of Gab1 with SHP-2 and PI-3 kinase as well as ERK2 activation.	bind
45909	4	11303	6	10	NULL	0	NULL	gp130	NULL	mutant	abrogates	NULL		tyrosine 759;; the SHP-2 binding site		statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4109_s_8	9632795	A mutation of tyrosine 759, the SHP-2 binding site of gp130, abrogated the interactions of Gab1 with SHP-2 and PI-3 kinase as well as ERK2 activation.	bind
45910	5	11303	6	10	NULL	0	NULL	gp130	NULL	mutant	abrogates	NULL		tyrosine 759;;SHP-2 binding site		ERK2	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4109_s_8	9632795	A mutation of tyrosine 759, the SHP-2 binding site of gp130, abrogated the interactions of Gab1 with SHP-2 and PI-3 kinase as well as ERK2 activation.	bind
45392	1	11304	5	NULL	NULL	NULL	NULL			mutation of	abolishes		efficiently		GAS element	Stat3	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_517_s_217	11463377	A mutation on both GAS and AP1 elements efficiently abolished the binding of both Stat3 and c-Jun (  Figure 7e, panel II; compare wild type with DM lanes).	bind
45393	2	11304	5	NULL	NULL	NULL	NULL			mutation of	abolishes		efficiently		GAS element	Stat3	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_517_s_217	11463377	A mutation on both GAS and AP1 elements efficiently abolished the binding of both Stat3 and c-Jun (  Figure 7e, panel II; compare wild type with DM lanes).	bind
45394	3	11304	5	NULL	NULL	NULL	NULL			mutation of	abolishes		efficiently		AP1 element	c-Jun	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_517_s_217	11463377	A mutation on both GAS and AP1 elements efficiently abolished the binding of both Stat3 and c-Jun (  Figure 7e, panel II; compare wild type with DM lanes).	bind
45395	4	11304	5	NULL	NULL	NULL	NULL			mutation of	abolishes		efficiently		AP1 element	c-Jun	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_517_s_217	11463377	A mutation on both GAS and AP1 elements efficiently abolished the binding of both Stat3 and c-Jun (  Figure 7e, panel II; compare wild type with DM lanes).	bind
45912	1	11304	6	10	NULL	0	NULL			mutation of	abolishes		efficiently		GAS element	Stat3		binding of 			NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_517_s_217	11463377	A mutation on both GAS and AP1 elements efficiently abolished the binding of both Stat3 and c-Jun (  Figure 7e, panel II; compare wild type with DM lanes).	bind
45913	2	11304	6	10	NULL	0	NULL			mutation of	abolishes		efficiently		GAS element	c-Jun		binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_517_s_217	11463377	A mutation on both GAS and AP1 elements efficiently abolished the binding of both Stat3 and c-Jun (  Figure 7e, panel II; compare wild type with DM lanes).	bind
52954	3	11304	6	NULL	NULL	0	NULL		NULL	mutation of	abolishes	NULL	efficiently		AP1 element	Stat3	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_3_517_s_217	11463377	A mutation on both GAS and AP1 elements efficiently abolished the binding of both Stat3 and c-Jun (  Figure 7e, panel II; compare wild type with DM lanes).	bind
52955	4	11304	6	NULL	NULL	0	NULL		NULL	mutation of	abolishes	NULL	efficiently		AP1 element	c-Jun	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_molcell_7_3_517_s_217	11463377	A mutation on both GAS and AP1 elements efficiently abolished the binding of both Stat3 and c-Jun (  Figure 7e, panel II; compare wild type with DM lanes).	bind
46389	1	11305	5	NULL	NULL	NULL	NULL	ets	GP		bind									EBS	NULL		NULL	NULL	NULL	NULL	gw60_gene_307_0_87_s_118	12706891	A mutation that disrupted ets binding to the EBS but retained Sp1 binding at this site as well as disruption of both Sp1 and ets binding to the EBS resulted in comparable inhibition of the promoter activity suggesting that at the EBS the binding of ets alone contributes to the promoter activity.	bind
46390	2	11305	5	NULL	NULL	NULL	NULL	Sp1	GP		bind									EBS	NULL		NULL	NULL	NULL	NULL	gw60_gene_307_0_87_s_118	12706891	A mutation that disrupted ets binding to the EBS but retained Sp1 binding at this site as well as disruption of both Sp1 and ets binding to the EBS resulted in comparable inhibition of the promoter activity suggesting that at the EBS the binding of ets alone contributes to the promoter activity.	bind
46391	3	11305	5	NULL	NULL	NULL	NULL	statement 1	Process		promotes							activity of		promoter	NULL		NULL	NULL	NULL	NULL	gw60_gene_307_0_87_s_118	12706891	A mutation that disrupted ets binding to the EBS but retained Sp1 binding at this site as well as disruption of both Sp1 and ets binding to the EBS resulted in comparable inhibition of the promoter activity suggesting that at the EBS the binding of ets alone contributes to the promoter activity.	bind
45917	1	11305	6	NULL	NULL	0	NULL	ets	NULL		bind	NULL					NULL			EBS	NULL		NULL	NULL	NULL	NULL	gw60_gene_307_0_87_s_118	12706891	A mutation that disrupted ets binding to the EBS but retained Sp1 binding at this site as well as disruption of both Sp1 and ets binding to the EBS resulted in comparable inhibition of the promoter activity suggesting that at the EBS the binding of ets alone contributes to the promoter activity.	bind
45918	2	11305	6	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL					NULL			EBS	NULL		NULL	NULL	NULL	NULL	gw60_gene_307_0_87_s_118	12706891	A mutation that disrupted ets binding to the EBS but retained Sp1 binding at this site as well as disruption of both Sp1 and ets binding to the EBS resulted in comparable inhibition of the promoter activity suggesting that at the EBS the binding of ets alone contributes to the promoter activity.	bind
45919	3	11305	6	NULL	NULL	0	NULL	statement 1	NULL		contributes to	NULL					NULL	activity of		promoter	NULL		0	NULL	NULL	NULL	gw60_gene_307_0_87_s_118	12706891	A mutation that disrupted ets binding to the EBS but retained Sp1 binding at this site as well as disruption of both Sp1 and ets binding to the EBS resulted in comparable inhibition of the promoter activity suggesting that at the EBS the binding of ets alone contributes to the promoter activity.	bind
45396	1	11306	5	NULL	NULL	NULL	NULL	p53	GP		bind					MDR1	GP			HT site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_27716_s_7	11350951	A mutation that disrupted p53 binding to the MDR1 HT site blocked p53-mediated repression of the  MDR1 promoter in transfection assays.	bind
45397	2	11306	5	NULL	NULL	NULL	NULL	mutation	Process		disrupts					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_27716_s_7	11350951	A mutation that disrupted p53 binding to the MDR1 HT site blocked p53-mediated repression of the  MDR1 promoter in transfection assays.	bind
45398	3	11306	5	NULL	NULL	NULL	NULL	p53	GP		mediate					MDR1	GP	repression of		promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_27716_s_7	11350951	A mutation that disrupted p53 binding to the MDR1 HT site blocked p53-mediated repression of the  MDR1 promoter in transfection assays.	bind
45399	4	11306	5	NULL	NULL	NULL	NULL	statement 2	Process		block					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_27716_s_7	11350951	A mutation that disrupted p53 binding to the MDR1 HT site blocked p53-mediated repression of the  MDR1 promoter in transfection assays.	bind
45920	1	11306	6	NULL	NULL	0	NULL	p53	NULL		bind	NULL				MDR1	NULL			HT site	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_27716_s_7	11350951	A mutation that disrupted p53 binding to the MDR1 HT site blocked p53-mediated repression of the  MDR1 promoter in transfection assays.	bind
45921	2	11306	6	NULL	NULL	0	NULL	p53	NULL		mediates	NULL				MDR1	NULL	repression of		promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_27716_s_7	11350951	A mutation that disrupted p53 binding to the MDR1 HT site blocked p53-mediated repression of the  MDR1 promoter in transfection assays.	bind
51277	3	11306	6	10	NULL	0	NULL	mutation	NULL		disrupt	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_27716_s_7	11350951	A mutation that disrupted p53 binding to the MDR1 HT site blocked p53-mediated repression of the  MDR1 promoter in transfection assays.	bind
51278	4	11306	6	10	NULL	0	NULL	statement 3	NULL		block	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_27716_s_7	11350951	A mutation that disrupted p53 binding to the MDR1 HT site blocked p53-mediated repression of the  MDR1 promoter in transfection assays.	bind
45400	1	11307	5	NULL	NULL	NULL	NULL	NHERF	GP		bind			domain 2		GRK6A	GP	tail			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_24328_s_220	10446210	A mutation that reduces the binding of NHERF domain 2 to the GRK6A tail by approximately 4-fold reduces the efficiency with which GRK6A phosphorylates domain 2 by approximately 3-fold.	bind
45401	2	11307	5	NULL	NULL	NULL	NULL	GRK6A	GP		phosphorylate					NHERF	GP		domain 2		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_24328_s_220	10446210	A mutation that reduces the binding of NHERF domain 2 to the GRK6A tail by approximately 4-fold reduces the efficiency with which GRK6A phosphorylates domain 2 by approximately 3-fold.	bind
45402	3	11307	5	NULL	NULL	NULL	NULL	mutation	Process		reduces					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_24328_s_220	10446210	A mutation that reduces the binding of NHERF domain 2 to the GRK6A tail by approximately 4-fold reduces the efficiency with which GRK6A phosphorylates domain 2 by approximately 3-fold.	bind
45403	4	11307	5	NULL	NULL	NULL	NULL	statement 3	Process		reduces					statement 2	Process	efficiency of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_24328_s_220	10446210	A mutation that reduces the binding of NHERF domain 2 to the GRK6A tail by approximately 4-fold reduces the efficiency with which GRK6A phosphorylates domain 2 by approximately 3-fold.	bind
45922	1	11307	6	NULL	NULL	0	NULL	NHERF	NULL		bind	NULL		domain 2		GRK6A 	NULL		tail		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_34_24328_s_220	10446210	A mutation that reduces the binding of NHERF domain 2 to the GRK6A tail by approximately 4-fold reduces the efficiency with which GRK6A phosphorylates domain 2 by approximately 3-fold.	bind
45923	2	11307	6	10	NULL	0	NULL	GRK6A	NULL		phosphorylates	NULL				NHERF	NULL		domain 2		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_34_24328_s_220	10446210	A mutation that reduces the binding of NHERF domain 2 to the GRK6A tail by approximately 4-fold reduces the efficiency with which GRK6A phosphorylates domain 2 by approximately 3-fold.	bind
51279	3	11307	6	10	NULL	0	NULL	mutation 	NULL		reduces	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_34_24328_s_220	10446210	A mutation that reduces the binding of NHERF domain 2 to the GRK6A tail by approximately 4-fold reduces the efficiency with which GRK6A phosphorylates domain 2 by approximately 3-fold.	bind
51280	4	11307	6	10	NULL	0	NULL	statement 3	NULL		reduces	NULL				statement 2	NULL	efficiency of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_34_24328_s_220	10446210	A mutation that reduces the binding of NHERF domain 2 to the GRK6A tail by approximately 4-fold reduces the efficiency with which GRK6A phosphorylates domain 2 by approximately 3-fold.	bind
45404	1	11308	5	NULL	NULL	NULL	NULL	Sp1	GP		bind							proximal		GC box	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_3977_s_62	10330138	A mutation which disrupts both Sp1 and Egr-1 binding to the proximal GC box has been previously described ( 53).	bind
45405	2	11308	5	NULL	NULL	NULL	NULL	Egr-1	GP		bind							proximal		GC box	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_3977_s_62	10330138	A mutation which disrupts both Sp1 and Egr-1 binding to the proximal GC box has been previously described ( 53).	bind
45924	1	11308	6	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL					NULL	proximal		GC box	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_3977_s_62	10330138	A mutation which disrupts both Sp1 and Egr-1 binding to the proximal GC box has been previously described ( 53).	bind
45925	2	11308	6	NULL	NULL	0	NULL	Egr-1	NULL		bind	NULL					NULL	proximal		GC-box	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_3977_s_62	10330138	A mutation which disrupts both Sp1 and Egr-1 binding to the proximal GC box has been previously described ( 53).	bind
45406	1	11309	5	NULL	NULL	NULL	NULL	CtBP	GP		bind					HPC2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_777_s_381	9858600	A mutation within the 6-aa motif that mediates the binding between CtBP and HPC2 results in a significant but only small decrease in the repressing abilities of HPC2 (Fig.  9).	bind
45926	1	11309	6	NULL	NULL	0	NULL	CtBP	NULL		bind	NULL				HPC2	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_777_s_381	9858600	A mutation within the 6-aa motif that mediates the binding between CtBP and HPC2 results in a significant but only small decrease in the repressing abilities of HPC2 (Fig.  9).	bind
45408	1	11310	5	NULL	NULL	NULL	NULL	Sir2	GP		bind					Sir4	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_genesdev_16_12_1528_s_95	12080091	A mutation,  SIR2-H364Y, that disrupts both Sir2 NAD-dependent deacetylase and ADP-ribosyltransferase activities does not prevent binding of Sir2 to Sir4 in vivo (Tanny et al. 1999  ).	bind
45409	2	11310	5	NULL	NULL	NULL	NULL	SIR2	GP	mutant	disrupts			H364Y		Sir2 NAD-dependent deacetylase 	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_12_1528_s_95	12080091	A mutation,  SIR2-H364Y, that disrupts both Sir2 NAD-dependent deacetylase and ADP-ribosyltransferase activities does not prevent binding of Sir2 to Sir4 in vivo (Tanny et al. 1999  ).	bind
45410	3	11310	5	NULL	NULL	NULL	NULL	SIR2	GP	mutant	disrupts			H364Y		ADP-ribosyltransferase 	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_16_12_1528_s_95	12080091	A mutation,  SIR2-H364Y, that disrupts both Sir2 NAD-dependent deacetylase and ADP-ribosyltransferase activities does not prevent binding of Sir2 to Sir4 in vivo (Tanny et al. 1999  ).	bind
68150	4	11310	5	NULL	NULL	0	NULL	SIR2	GP	mutant	does not prevent			H364Y		statement 1	Process				NULL	in vivo	0	NULL	NULL	NULL	gw60_genesdev_16_12_1528_s_95	12080091	A mutation,  SIR2-H364Y, that disrupts both Sir2 NAD-dependent deacetylase and ADP-ribosyltransferase activities does not prevent binding of Sir2 to Sir4 in vivo (Tanny et al. 1999  ).	bind
45927	1	11310	6	NULL	NULL	0	NULL	Sir2	NULL		bind	NULL				Sir4	NULL				NULL	in vivo	0	NULL	NULL	NULL	gw60_genesdev_16_12_1528_s_95	12080091	A mutation,  SIR2-H364Y, that disrupts both Sir2 NAD-dependent deacetylase and ADP-ribosyltransferase activities does not prevent binding of Sir2 to Sir4 in vivo (Tanny et al. 1999  ).	bind
45928	2	11310	6	NULL	NULL	0	NULL	SIR2	NULL	mutant	disrupts	NULL		H364Y		Sir2 NAD-dependent deacetylase	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_genesdev_16_12_1528_s_95	12080091	A mutation,  SIR2-H364Y, that disrupts both Sir2 NAD-dependent deacetylase and ADP-ribosyltransferase activities does not prevent binding of Sir2 to Sir4 in vivo (Tanny et al. 1999  ).	bind
45929	3	11310	6	NULL	NULL	0	NULL	SIR2	NULL	mutant	disrupts	NULL		H364Y		ADP-ribosyltransferase	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_genesdev_16_12_1528_s_95	12080091	A mutation,  SIR2-H364Y, that disrupts both Sir2 NAD-dependent deacetylase and ADP-ribosyltransferase activities does not prevent binding of Sir2 to Sir4 in vivo (Tanny et al. 1999  ).	bind
45930	4	11310	6	10	NULL	0	NULL	SIR2		mutant	does not prevent			H364Y		statement 1					NULL	in vivo	NULL	NULL	NULL	NULL	gw60_genesdev_16_12_1528_s_95	12080091	A mutation,  SIR2-H364Y, that disrupts both Sir2 NAD-dependent deacetylase and ADP-ribosyltransferase activities does not prevent binding of Sir2 to Sir4 in vivo (Tanny et al. 1999  ).	bind
45412	1	11311	5	NULL	NULL	NULL	NULL	CREB	GP		bind									CRE	NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_55_6_1094_s_174	10347253	A mutational analysis (German and Wang, 1994  ; Eggers et al., 1998  ) and the overexpression of a dominant-negative CREB mutant (Eggers et al., 1998  ) have shown that the activation by cAMP of this promoter is mediated by CREB binding to the CRE.	bind
45931	1	11311	6	NULL	NULL	0	NULL	CREB	NULL		bind	NULL					NULL			CRE	NULL		0	NULL	NULL	NULL	gw60_molpharmacol_55_6_1094_s_174	10347253	A mutational analysis (German and Wang, 1994  ; Eggers et al., 1998  ) and the overexpression of a dominant-negative CREB mutant (Eggers et al., 1998  ) have shown that the activation by cAMP of this promoter is mediated by CREB binding to the CRE.	bind
45413	1	11312	5	NULL	NULL	NULL	NULL			single mutation of	reduces		significantly	D313A		eIF5A	GP	binding of	Lys		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28697_s_315	15100216	A mutational analysis of residues forming the NAD and spermidine binding sites revealed a single mutation (D313A) that significantly reduced eIF5A(Lys) binding ( ).	bind
45932	1	11312	6	10	NULL	0	NULL		NULL	mutant	reduces	NULL	significantly	D313A		eIF5A	NULL	binding of	Lys		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_27_28697_s_315	15100216	A mutational analysis of residues forming the NAD and spermidine binding sites revealed a single mutation (D313A) that significantly reduced eIF5A(Lys) binding ( ).	bind
45414	1	11314	5	NULL	NULL	NULL	NULL	enterotoxin B	GP	staphylococcal	bind					T cell receptor	GP		beta chain		NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_55_0_77_s_792	11544350	A mutational analysis of the binding of staphylococcal enterotoxins  B and C3 to the T cell receptor beta chain and major histocompatibility complex class  II.	bind
45415	2	11314	5	NULL	NULL	NULL	NULL	enterotoxin B	GP	staphylococcal	bind					major histocompatibility complex class II	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_55_0_77_s_792	11544350	A mutational analysis of the binding of staphylococcal enterotoxins  B and C3 to the T cell receptor beta chain and major histocompatibility complex class  II.	bind
45416	3	11314	5	NULL	NULL	NULL	NULL	enterotoxin C3	GP	staphylococcal	bind					T cell receptor	GP		beta chain		NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_55_0_77_s_792	11544350	A mutational analysis of the binding of staphylococcal enterotoxins  B and C3 to the T cell receptor beta chain and major histocompatibility complex class  II.	bind
45417	4	11314	5	NULL	NULL	NULL	NULL	enterotoxin C3	GP	staphylococcal	bind					major histocompatibility complex class II	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_55_0_77_s_792	11544350	A mutational analysis of the binding of staphylococcal enterotoxins  B and C3 to the T cell receptor beta chain and major histocompatibility complex class  II.	bind
45933	1	11314	6	NULL	NULL	0	NULL	enterotoxin B	NULL	Staphylococcal	bind	NULL				T cell receptor 	NULL		beta chain		NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_55_0_77_s_792	11544350	A mutational analysis of the binding of staphylococcal enterotoxins  B and C3 to the T cell receptor beta chain and major histocompatibility complex class  II.	bind
45934	2	11314	6	NULL	NULL	0	NULL	enterotoxin C3	NULL	Staphylococcal	bind	NULL				major histocompatibility complex class II	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_55_0_77_s_792	11544350	A mutational analysis of the binding of staphylococcal enterotoxins  B and C3 to the T cell receptor beta chain and major histocompatibility complex class  II.	bind
51459	3	11314	6	10	NULL	0	NULL	enterotoxins B	NULL	staphylococcal 	bind	NULL				major histocompatibility complex class II	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_55_0_77_s_792	11544350	A mutational analysis of the binding of staphylococcal enterotoxins  B and C3 to the T cell receptor beta chain and major histocompatibility complex class  II.	bind
51460	4	11314	6	10	NULL	0	NULL	enterotoxins C3	NULL	staphylococcal	bind	NULL				T cell receptor	NULL		beta chain		NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_55_0_77_s_792	11544350	A mutational analysis of the binding of staphylococcal enterotoxins  B and C3 to the T cell receptor beta chain and major histocompatibility complex class  II.	bind
45418	1	11316	5	NULL	NULL	NULL	NULL	Ras	GP		bind					Raf	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30363_s_35	10887184	A mutational analysis of the RBD binding site showed that Gln66, Lys84, and Arg89 are the major contributors to the binding affinity between Ras and Raf ( 1).	bind
45419	2	11316	5	NULL	NULL	NULL	NULL				contribute to		major	Gln66 in RBD binding site		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30363_s_35	10887184	A mutational analysis of the RBD binding site showed that Gln66, Lys84, and Arg89 are the major contributors to the binding affinity between Ras and Raf ( 1).	bind
45420	3	11316	5	NULL	NULL	NULL	NULL				contribute to		major	Lys84 in RBD binding site		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30363_s_35	10887184	A mutational analysis of the RBD binding site showed that Gln66, Lys84, and Arg89 are the major contributors to the binding affinity between Ras and Raf ( 1).	bind
45421	4	11316	5	NULL	NULL	NULL	NULL				contribute to		major	Arg89 in RBD binding site		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30363_s_35	10887184	A mutational analysis of the RBD binding site showed that Gln66, Lys84, and Arg89 are the major contributors to the binding affinity between Ras and Raf ( 1).	bind
45937	1	11316	6	NULL	NULL	0	NULL	Ras	NULL		bind	NULL				Raf	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_39_30363_s_35	10887184	A mutational analysis of the RBD binding site showed that Gln66, Lys84, and Arg89 are the major contributors to the binding affinity between Ras and Raf ( 1).	bind
45938	2	11316	6	NULL	NULL	0	NULL		NULL		contributes to	NULL		RBD binding site;; Gln66		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_39_30363_s_35	10887184	A mutational analysis of the RBD binding site showed that Gln66, Lys84, and Arg89 are the major contributors to the binding affinity between Ras and Raf ( 1).	bind
45939	3	11316	6	NULL	NULL	0	NULL		NULL		contributes to	NULL		RBD binding site;; Lys84		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_39_30363_s_35	10887184	A mutational analysis of the RBD binding site showed that Gln66, Lys84, and Arg89 are the major contributors to the binding affinity between Ras and Raf ( 1).	bind
45940	4	11316	6	NULL	NULL	0	NULL		NULL		contributes to	NULL		RBD binding site;; Arg89		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_39_30363_s_35	10887184	A mutational analysis of the RBD binding site showed that Gln66, Lys84, and Arg89 are the major contributors to the binding affinity between Ras and Raf ( 1).	bind
45422	1	11320	5	NULL	NULL	NULL	NULL	Cdc42p	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_23	10066831	A myriad of Cdc42p downstream effectors interact with the activated (GTP-bound) form of Cdc42p, thereby inducing a number of downstream events, including rearrangements of the actin cytoskeletal network and protein kinase-dependent induction of transcription, which are increasingly coming into view.	bind
45423	2	11320	5	NULL	NULL	NULL	NULL	Cdc42p downstream effectors	GP		interact with					statement 1	Process	activated			NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_23	10066831	A myriad of Cdc42p downstream effectors interact with the activated (GTP-bound) form of Cdc42p, thereby inducing a number of downstream events, including rearrangements of the actin cytoskeletal network and protein kinase-dependent induction of transcription, which are increasingly coming into view.	bind
45424	3	11320	5	NULL	NULL	NULL	NULL	statement 2	Process		induce					downstream events	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_23	10066831	A myriad of Cdc42p downstream effectors interact with the activated (GTP-bound) form of Cdc42p, thereby inducing a number of downstream events, including rearrangements of the actin cytoskeletal network and protein kinase-dependent induction of transcription, which are increasingly coming into view.	bind
45425	4	11320	5	NULL	NULL	NULL	NULL	downstream events	Process		include					actin cytoskeletal network	CellComponent	rearrangements of			NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_23	10066831	A myriad of Cdc42p downstream effectors interact with the activated (GTP-bound) form of Cdc42p, thereby inducing a number of downstream events, including rearrangements of the actin cytoskeletal network and protein kinase-dependent induction of transcription, which are increasingly coming into view.	bind
45426	5	11320	5	NULL	NULL	NULL	NULL	transcription	Process	induction of	is dependent on					protein kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_23	10066831	A myriad of Cdc42p downstream effectors interact with the activated (GTP-bound) form of Cdc42p, thereby inducing a number of downstream events, including rearrangements of the actin cytoskeletal network and protein kinase-dependent induction of transcription, which are increasingly coming into view.	bind
45427	6	11320	5	NULL	NULL	NULL	NULL	downstream events	Process		include					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_23	10066831	A myriad of Cdc42p downstream effectors interact with the activated (GTP-bound) form of Cdc42p, thereby inducing a number of downstream events, including rearrangements of the actin cytoskeletal network and protein kinase-dependent induction of transcription, which are increasingly coming into view.	bind
46093	1	11320	6	10	NULL	0	NULL	GTP	NULL		bind	NULL				Cdc42p	NULL				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_23	10066831	A myriad of Cdc42p downstream effectors interact with the activated (GTP-bound) form of Cdc42p, thereby inducing a number of downstream events, including rearrangements of the actin cytoskeletal network and protein kinase-dependent induction of transcription, which are increasingly coming into view.	bind
46094	2	11320	6	10	NULL	0	NULL	Cdc42p downstream effectors	NULL		interacts with	NULL				statement 1	NULL	activated			NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_23	10066831	A myriad of Cdc42p downstream effectors interact with the activated (GTP-bound) form of Cdc42p, thereby inducing a number of downstream events, including rearrangements of the actin cytoskeletal network and protein kinase-dependent induction of transcription, which are increasingly coming into view.	bind
46095	3	11320	6	NULL	NULL	0	NULL	statement 2	NULL		includes	NULL				actin cytoskeleton network	NULL	rearrangements of 			NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_23	10066831	A myriad of Cdc42p downstream effectors interact with the activated (GTP-bound) form of Cdc42p, thereby inducing a number of downstream events, including rearrangements of the actin cytoskeletal network and protein kinase-dependent induction of transcription, which are increasingly coming into view.	bind
46096	4	11320	6	NULL	NULL	0	NULL	transcription	NULL	induction of	is dependent on	NULL				protein kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_23	10066831	A myriad of Cdc42p downstream effectors interact with the activated (GTP-bound) form of Cdc42p, thereby inducing a number of downstream events, including rearrangements of the actin cytoskeletal network and protein kinase-dependent induction of transcription, which are increasingly coming into view.	bind
46098	5	11320	6	NULL	NULL	0	NULL	statement 2	NULL		induces	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_54_s_23	10066831	A myriad of Cdc42p downstream effectors interact with the activated (GTP-bound) form of Cdc42p, thereby inducing a number of downstream events, including rearrangements of the actin cytoskeletal network and protein kinase-dependent induction of transcription, which are increasingly coming into view.	bind
45428	1	11321	5	NULL	NULL	NULL	NULL	MC	GP		bind					MRD	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_3_926_s_28	11158572	A mystery has remained regarding the NADH requirement for binding of MC to MRD, because this cofactor would only be expected for the flavoreductase-mediated bioactivation of MC.	bind
45429	2	11321	5	NULL	NULL	NULL	NULL	flavoreductase	GP		mediates					MC	GP	bioactivation of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_3_926_s_28	11158572	A mystery has remained regarding the NADH requirement for binding of MC to MRD, because this cofactor would only be expected for the flavoreductase-mediated bioactivation of MC.	bind
45430	3	11321	5	NULL	NULL	NULL	NULL	NADH	Chemical		is required for		potentially			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_3_926_s_28	11158572	A mystery has remained regarding the NADH requirement for binding of MC to MRD, because this cofactor would only be expected for the flavoreductase-mediated bioactivation of MC.	bind
45941	1	11321	6	NULL	NULL	0	NULL	MC	NULL		bind	NULL				MRD	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_98_3_926_s_28	11158572	A mystery has remained regarding the NADH requirement for binding of MC to MRD, because this cofactor would only be expected for the flavoreductase-mediated bioactivation of MC.	bind
45431	1	11322	5	NULL	NULL	NULL	NULL	Hrd3p	GP	truncated	bind			N-terminal		Hrd1p	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_1827_s_214	16619026	A N-terminally  truncated form of Hrd3p still binds to Hrd1p and maintains it at wild-type levels,  although the function of the Hrd1p ligase complex is abolished (  et al and data not shown).	bind
45432	2	11322	5	NULL	NULL	NULL	NULL	Hrd3p	GP	truncated	abolishes			N-terminal		Hrd1p ligase complex	GP	function of			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_1827_s_214	16619026	A N-terminally  truncated form of Hrd3p still binds to Hrd1p and maintains it at wild-type levels,  although the function of the Hrd1p ligase complex is abolished (  et al and data not shown).	bind
45942	1	11322	6	NULL	NULL	0	NULL	Hrd3p	NULL	deletion of	bind	NULL		N-terminal		Hrd1p	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_25_9_1827_s_214	16619026	A N-terminally  truncated form of Hrd3p still binds to Hrd1p and maintains it at wild-type levels,  although the function of the Hrd1p ligase complex is abolished (  et al and data not shown).	bind
51461	2	11322	6	10	NULL	0	NULL	Hrd3p	NULL	deletion of	abolishes	NULL		N-terminal		Hrd1p ligase complex	NULL	function of			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_9_1827_s_214	16619026	A N-terminally  truncated form of Hrd3p still binds to Hrd1p and maintains it at wild-type levels,  although the function of the Hrd1p ligase complex is abolished (  et al and data not shown).	bind
45433	1	11323	5	NULL	NULL	NULL	NULL	ACh	Chemical		is					acetylcholine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_5_905_s_4	8630247	A nAChR normally binds acetylcholine (ACh) and undergoes a conformational change that opens a cation-selective channel for several milliseconds.	bind
45434	2	11323	5	NULL	NULL	NULL	NULL	nAChR	GP		bind					ACh	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_5_905_s_4	8630247	A nAChR normally binds acetylcholine (ACh) and undergoes a conformational change that opens a cation-selective channel for several milliseconds.	bind
45435	3	11323	5	NULL	NULL	NULL	NULL	nAChR	GP		undergoes					conformational change	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_5_905_s_4	8630247	A nAChR normally binds acetylcholine (ACh) and undergoes a conformational change that opens a cation-selective channel for several milliseconds.	bind
45436	4	11323	5	NULL	NULL	NULL	NULL	statement 2	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_5_905_s_4	8630247	A nAChR normally binds acetylcholine (ACh) and undergoes a conformational change that opens a cation-selective channel for several milliseconds.	bind
45437	5	11323	5	NULL	NULL	NULL	NULL	statement 3	Process		open					cation-selective channel	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_5_905_s_4	8630247	A nAChR normally binds acetylcholine (ACh) and undergoes a conformational change that opens a cation-selective channel for several milliseconds.	bind
45943	1	11323	6	NULL	NULL	0	NULL	nAChR	NULL		bind	NULL				ACh	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_16_5_905_s_4	8630247	A nAChR normally binds acetylcholine (ACh) and undergoes a conformational change that opens a cation-selective channel for several milliseconds.	bind
45944	2	11323	6	NULL	NULL	0	NULL	ACh	NULL		is	NULL				acetylcholine	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_16_5_905_s_4	8630247	A nAChR normally binds acetylcholine (ACh) and undergoes a conformational change that opens a cation-selective channel for several milliseconds.	bind
45945	3	11323	6	NULL	NULL	0	NULL	nAChR	NULL		undergoes a	NULL				conformational change	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_16_5_905_s_4	8630247	A nAChR normally binds acetylcholine (ACh) and undergoes a conformational change that opens a cation-selective channel for several milliseconds.	bind
45946	4	11323	6	10	NULL	0	NULL	statement 3	NULL		opens a	NULL				cation-selective channel	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuron_16_5_905_s_4	8630247	A nAChR normally binds acetylcholine (ACh) and undergoes a conformational change that opens a cation-selective channel for several milliseconds.	bind
51462	5	11323	6	10	NULL	0	NULL	statement 3	NULL		leads to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_16_5_905_s_4	8630247	A nAChR normally binds acetylcholine (ACh) and undergoes a conformational change that opens a cation-selective channel for several milliseconds.	bind
45438	1	11324	5	NULL	NULL	NULL	NULL	Spt5p	GP		bind			NGN - KOW region		Spt4p	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_17_3643_s_105	12202748	A natural corollary to the finding that an NGN - KOW region of Spt5p binds Spt4p is that their archaeal homologues, rpoE"` and NusG, may also associate.	bind
45439	2	11324	5	NULL	NULL	NULL	NULL	rpoE"	GP	archaeal	is a homolog of					Spt5p	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_17_3643_s_105	12202748	A natural corollary to the finding that an NGN - KOW region of Spt5p binds Spt4p is that their archaeal homologues, rpoE"` and NusG, may also associate.	bind
45440	3	11324	5	NULL	NULL	NULL	NULL	NusG	GP	archaeal	is a homolog of					Spt4p	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_17_3643_s_105	12202748	A natural corollary to the finding that an NGN - KOW region of Spt5p binds Spt4p is that their archaeal homologues, rpoE"` and NusG, may also associate.	bind
45441	4	11324	5	NULL	NULL	NULL	NULL	statement 2	Process		associate with		may			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_17_3643_s_105	12202748	A natural corollary to the finding that an NGN - KOW region of Spt5p binds Spt4p is that their archaeal homologues, rpoE"` and NusG, may also associate.	bind
45947	1	11324	6	NULL	NULL	0	NULL	Spt5p	NULL		bind	NULL		NGN - KOW region		Spt4p	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_17_3643_s_105	12202748	A natural corollary to the finding that an NGN - KOW region of Spt5p binds Spt4p is that their archaeal homologues, rpoE"` and NusG, may also associate.	bind
45948	2	11324	6	NULL	NULL	0	NULL	rpoE''	NULL	archaeal	is homologous to	NULL				Spt5p	NULL				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_17_3643_s_105	12202748	A natural corollary to the finding that an NGN - KOW region of Spt5p binds Spt4p is that their archaeal homologues, rpoE"` and NusG, may also associate.	bind
52956	3	11324	6	NULL	NULL	0	NULL	NusG	NULL	archaeal	is homologous to	NULL				Spt5p	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_17_3643_s_105	12202748	A natural corollary to the finding that an NGN - KOW region of Spt5p binds Spt4p is that their archaeal homologues, rpoE"` and NusG, may also associate.	bind
52957	4	11324	6	10	NULL	0	NULL	statement 2			associates with		may			statement 3					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_17_3643_s_105	12202748	A natural corollary to the finding that an NGN - KOW region of Spt5p binds Spt4p is that their archaeal homologues, rpoE"` and NusG, may also associate.	bind
45442	1	11325	5	NULL	NULL	NULL	NULL	cysteine protease virulence factor	GP	natural variant of;; group A Streptococcus	bind		preferentially	RGD motif		alphaV beta3	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_15_4461_s_442	12867455	A natural variant of the cysteine protease virulence factor of group A  Streptococcus with an arginine-glycine-aspartic acid (RGD) motif preferentially binds human integrins  alphaV beta3 and  alphaIIb beta3.	bind
45443	2	11325	5	NULL	NULL	NULL	NULL	alphaV beta3	GP		is a type of					integrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_15_4461_s_442	12867455	A natural variant of the cysteine protease virulence factor of group A  Streptococcus with an arginine-glycine-aspartic acid (RGD) motif preferentially binds human integrins  alphaV beta3 and  alphaIIb beta3.	bind
45444	3	11325	5	NULL	NULL	NULL	NULL	RGD motif	AminoAcid		is					arginine-glycine-aspartic acid motif 	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_15_4461_s_442	12867455	A natural variant of the cysteine protease virulence factor of group A  Streptococcus with an arginine-glycine-aspartic acid (RGD) motif preferentially binds human integrins  alphaV beta3 and  alphaIIb beta3.	bind
45445	4	11325	5	NULL	NULL	NULL	NULL	cysteine protease virulence factor	GP	natural variant of;; group A Streptococcus	bind		preferentially	RGD motif		alphaIIb beta3	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_15_4461_s_442	12867455	A natural variant of the cysteine protease virulence factor of group A  Streptococcus with an arginine-glycine-aspartic acid (RGD) motif preferentially binds human integrins  alphaV beta3 and  alphaIIb beta3.	bind
45446	5	11325	5	NULL	NULL	NULL	NULL	alphaIIb beta3	AminoAcid		is a type of					integrin	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_15_4461_s_442	12867455	A natural variant of the cysteine protease virulence factor of group A  Streptococcus with an arginine-glycine-aspartic acid (RGD) motif preferentially binds human integrins  alphaV beta3 and  alphaIIb beta3.	bind
45949	1	11325	6	10	NULL	0	NULL	cysteine protease virulence factor 		natural variant of;;group A Streptococcus	bind		preferentially	RGD motif		alphaV beta3		human			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_15_4461_s_442	12867455	A natural variant of the cysteine protease virulence factor of group A  Streptococcus with an arginine-glycine-aspartic acid (RGD) motif preferentially binds human integrins  alphaV beta3 and  alphaIIb beta3.	bind
45950	2	11325	6	10	NULL	0	NULL	cysteine protease virulence factor		natural variant of;;group A Streptococcus	bind		preferentially	RGD motif		alphaIIb beta3		human			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_15_4461_s_442	12867455	A natural variant of the cysteine protease virulence factor of group A  Streptococcus with an arginine-glycine-aspartic acid (RGD) motif preferentially binds human integrins  alphaV beta3 and  alphaIIb beta3.	bind
45951	3	11325	6	NULL	NULL	0	NULL	RGD	NULL		is	NULL				arginine-glycine-aspartic acid	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_185_15_4461_s_442	12867455	A natural variant of the cysteine protease virulence factor of group A  Streptococcus with an arginine-glycine-aspartic acid (RGD) motif preferentially binds human integrins  alphaV beta3 and  alphaIIb beta3.	bind
51463	4	11325	6	10	NULL	0	NULL	alphaV beta3	NULL		is a type of	NULL				integrin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_185_15_4461_s_442	12867455	A natural variant of the cysteine protease virulence factor of group A  Streptococcus with an arginine-glycine-aspartic acid (RGD) motif preferentially binds human integrins  alphaV beta3 and  alphaIIb beta3.	bind
51464	5	11325	6	10	NULL	0	NULL	alphaIIb beta3	NULL		is a type of	NULL				integrin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_185_15_4461_s_442	12867455	A natural variant of the cysteine protease virulence factor of group A  Streptococcus with an arginine-glycine-aspartic acid (RGD) motif preferentially binds human integrins  alphaV beta3 and  alphaIIb beta3.	bind
45447	1	11331	5	NULL	NULL	NULL	NULL	PR39	GP		is a type of					naturally occurring antibacterial peptide	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_9_877_s_153	11348996	A naturally occurring antibacterial peptide, PR39, which reversibly binds the 26S proteasome and blocks the degradation of IkappaBalpha by the ubiquitin-preoteasome pathway, suppresses VCAM-1 and ICAM-1 gene expression in TNF-alpha - activated human ECs and reduces the size of myocardial infarction in an in vivo mouse model of coronary ligature.	bind
45448	2	11331	5	NULL	NULL	NULL	NULL	PR39	GP		bind		reversibly			26S proteasome	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_9_877_s_153	11348996	A naturally occurring antibacterial peptide, PR39, which reversibly binds the 26S proteasome and blocks the degradation of IkappaBalpha by the ubiquitin-preoteasome pathway, suppresses VCAM-1 and ICAM-1 gene expression in TNF-alpha - activated human ECs and reduces the size of myocardial infarction in an in vivo mouse model of coronary ligature.	bind
45449	3	11331	5	NULL	NULL	NULL	NULL	statement 2	Process		block					IkappaBalpha	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_9_877_s_153	11348996	A naturally occurring antibacterial peptide, PR39, which reversibly binds the 26S proteasome and blocks the degradation of IkappaBalpha by the ubiquitin-preoteasome pathway, suppresses VCAM-1 and ICAM-1 gene expression in TNF-alpha - activated human ECs and reduces the size of myocardial infarction in an in vivo mouse model of coronary ligature.	bind
45450	4	11331	5	NULL	NULL	NULL	NULL	statement 3	Process		occurs by					ubiquitin-preoteasome pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_88_9_877_s_153	11348996	A naturally occurring antibacterial peptide, PR39, which reversibly binds the 26S proteasome and blocks the degradation of IkappaBalpha by the ubiquitin-preoteasome pathway, suppresses VCAM-1 and ICAM-1 gene expression in TNF-alpha - activated human ECs and reduces the size of myocardial infarction in an in vivo mouse model of coronary ligature.	bind
45451	5	11331	5	NULL	NULL	NULL	NULL	PR39	GP		supress					VCAM-1 gene	GP	expression of			NULL	TNF-alpha - activated human ECs	NULL	NULL	NULL	NULL	gw60_circulationres_88_9_877_s_153	11348996	A naturally occurring antibacterial peptide, PR39, which reversibly binds the 26S proteasome and blocks the degradation of IkappaBalpha by the ubiquitin-preoteasome pathway, suppresses VCAM-1 and ICAM-1 gene expression in TNF-alpha - activated human ECs and reduces the size of myocardial infarction in an in vivo mouse model of coronary ligature.	bind
45452	6	11331	5	NULL	NULL	NULL	NULL	PR39	GP		supress					ICAM-1 gene	GP	expression of			NULL	TNF-alpha - activated human ECs	NULL	NULL	NULL	NULL	gw60_circulationres_88_9_877_s_153	11348996	A naturally occurring antibacterial peptide, PR39, which reversibly binds the 26S proteasome and blocks the degradation of IkappaBalpha by the ubiquitin-preoteasome pathway, suppresses VCAM-1 and ICAM-1 gene expression in TNF-alpha - activated human ECs and reduces the size of myocardial infarction in an in vivo mouse model of coronary ligature.	bind
45453	7	11331	5	NULL	NULL	NULL	NULL	PR39	GP		reduces					myocardial infarction	MedicalFinding	size of			NULL	in vivo mouse model of coronary ligature	NULL	NULL	NULL	NULL	gw60_circulationres_88_9_877_s_153	11348996	A naturally occurring antibacterial peptide, PR39, which reversibly binds the 26S proteasome and blocks the degradation of IkappaBalpha by the ubiquitin-preoteasome pathway, suppresses VCAM-1 and ICAM-1 gene expression in TNF-alpha - activated human ECs and reduces the size of myocardial infarction in an in vivo mouse model of coronary ligature.	bind
45952	1	11331	6	NULL	NULL	0	NULL	PR39	NULL		is a type of	NULL				antibacterial peptide	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_88_9_877_s_153	11348996	A naturally occurring antibacterial peptide, PR39, which reversibly binds the 26S proteasome and blocks the degradation of IkappaBalpha by the ubiquitin-preoteasome pathway, suppresses VCAM-1 and ICAM-1 gene expression in TNF-alpha - activated human ECs and reduces the size of myocardial infarction in an in vivo mouse model of coronary ligature.	bind
45953	2	11331	6	NULL	NULL	0	NULL	PR39	NULL		bind	NULL	reversibly			26S proteasome	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_88_9_877_s_153	11348996	A naturally occurring antibacterial peptide, PR39, which reversibly binds the 26S proteasome and blocks the degradation of IkappaBalpha by the ubiquitin-preoteasome pathway, suppresses VCAM-1 and ICAM-1 gene expression in TNF-alpha - activated human ECs and reduces the size of myocardial infarction in an in vivo mouse model of coronary ligature.	bind
45954	3	11331	6	NULL	NULL	0	NULL	ubiquitin-preoteasome pathway	NULL		degrades	NULL				IkappaBalpha	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_88_9_877_s_153	11348996	A naturally occurring antibacterial peptide, PR39, which reversibly binds the 26S proteasome and blocks the degradation of IkappaBalpha by the ubiquitin-preoteasome pathway, suppresses VCAM-1 and ICAM-1 gene expression in TNF-alpha - activated human ECs and reduces the size of myocardial infarction in an in vivo mouse model of coronary ligature.	bind
45955	4	11331	6	NULL	NULL	0	NULL	statement 2	NULL		blocks	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_88_9_877_s_153	11348996	A naturally occurring antibacterial peptide, PR39, which reversibly binds the 26S proteasome and blocks the degradation of IkappaBalpha by the ubiquitin-preoteasome pathway, suppresses VCAM-1 and ICAM-1 gene expression in TNF-alpha - activated human ECs and reduces the size of myocardial infarction in an in vivo mouse model of coronary ligature.	bind
45958	5	11331	6	NULL	NULL	0	NULL	statement 2	NULL		suppresses	NULL				VCAM-1 gene	NULL	expression of			NULL	TNF-alpha - activated human ECs	0	NULL	NULL	NULL	gw60_circulationres_88_9_877_s_153	11348996	A naturally occurring antibacterial peptide, PR39, which reversibly binds the 26S proteasome and blocks the degradation of IkappaBalpha by the ubiquitin-preoteasome pathway, suppresses VCAM-1 and ICAM-1 gene expression in TNF-alpha - activated human ECs and reduces the size of myocardial infarction in an in vivo mouse model of coronary ligature.	bind
45959	6	11331	6	NULL	NULL	0	NULL	statement 2	NULL		suppresses	NULL				ICAM-1 gene	NULL	expression of			NULL	TNF-alpha - activated human ECs	NULL	NULL	NULL	NULL	gw60_circulationres_88_9_877_s_153	11348996	A naturally occurring antibacterial peptide, PR39, which reversibly binds the 26S proteasome and blocks the degradation of IkappaBalpha by the ubiquitin-preoteasome pathway, suppresses VCAM-1 and ICAM-1 gene expression in TNF-alpha - activated human ECs and reduces the size of myocardial infarction in an in vivo mouse model of coronary ligature.	bind
45960	7	11331	6	NULL	NULL	0	NULL	statement 2	NULL		reduces	NULL				myocardial infarction	NULL	size of			NULL	in vivo mouse model of coronary ligature	0	NULL	NULL	NULL	gw60_circulationres_88_9_877_s_153	11348996	A naturally occurring antibacterial peptide, PR39, which reversibly binds the 26S proteasome and blocks the degradation of IkappaBalpha by the ubiquitin-preoteasome pathway, suppresses VCAM-1 and ICAM-1 gene expression in TNF-alpha - activated human ECs and reduces the size of myocardial infarction in an in vivo mouse model of coronary ligature.	bind
45454	1	11332	5	NULL	NULL	NULL	NULL	parafibromin	GP	mutant	does not bind					PAF1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_5052_s_172	15923622	A naturally occurring loss-of-function mutant of parafibromin lacks PAF1 and RNAP  II binding activity.	bind
45455	2	11332	5	NULL	NULL	NULL	NULL	parafibromin	GP	mutant	does not bind					RNAP II	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_5052_s_172	15923622	A naturally occurring loss-of-function mutant of parafibromin lacks PAF1 and RNAP  II binding activity.	bind
45961	1	11332	6	NULL	NULL	0	NULL	parafibromin	NULL	mutant	does not bind	NULL				PAF1	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_12_5052_s_172	15923622	A naturally occurring loss-of-function mutant of parafibromin lacks PAF1 and RNAP  II binding activity.	bind
45962	2	11332	6	NULL	NULL	0	NULL	parafibromin	NULL	mutant	does not bind	NULL				RNAP II	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_12_5052_s_172	15923622	A naturally occurring loss-of-function mutant of parafibromin lacks PAF1 and RNAP  II binding activity.	bind
45456	1	11333	5	NULL	NULL	NULL	NULL	Fc gamma RIIA	GP		is mutated to			Q127		Fc gamma RIIA	GP		K127		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_3_1252_s_408	10678934	A naturally occurring mutation in Fc gamma RIIA: a Q to K127 change confers unique IgG binding properties to the R131 allelic form of the receptor.	bind
45458	3	11333	5	NULL	NULL	NULL	NULL	R131	GP		is an allelic form of					Fc gamma RIIA	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_3_1252_s_408	10678934	A naturally occurring mutation in Fc gamma RIIA: a Q to K127 change confers unique IgG binding properties to the R131 allelic form of the receptor.	bind
45459	2	11333	5	NULL	NULL	NULL	NULL	R131	GP		bind		uniquely			IgG	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_3_1252_s_408	10678934	A naturally occurring mutation in Fc gamma RIIA: a Q to K127 change confers unique IgG binding properties to the R131 allelic form of the receptor.	bind
45460	4	11333	5	NULL	NULL	NULL	NULL	statement 1	Process		confers					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_3_1252_s_408	10678934	A naturally occurring mutation in Fc gamma RIIA: a Q to K127 change confers unique IgG binding properties to the R131 allelic form of the receptor.	bind
46104	1	11333	6	10	NULL	0	NULL	Fc gamma RIIA	NULL		is changed to	NULL		Q127		Fc gamma RIIA	NULL		K127		NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_3_1252_s_408	10678934	A naturally occurring mutation in Fc gamma RIIA: a Q to K127 change confers unique IgG binding properties to the R131 allelic form of the receptor.	bind
46105	2	11333	6	10	NULL	0	NULL	IgG			bind		uniquely			R131					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_3_1252_s_408	10678934	A naturally occurring mutation in Fc gamma RIIA: a Q to K127 change confers unique IgG binding properties to the R131 allelic form of the receptor.	bind
46106	4	11333	6	10	NULL	0	NULL	statement 1			confers					statement 2					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_3_1252_s_408	10678934	A naturally occurring mutation in Fc gamma RIIA: a Q to K127 change confers unique IgG binding properties to the R131 allelic form of the receptor.	bind
60571	3	11333	6	10	NULL	0	NULL	R131			is an allelic form of					Fc gamma RIIA					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_3_1252_s_408	10678934	A naturally occurring mutation in Fc gamma RIIA: a Q to K127 change confers unique IgG binding properties to the R131 allelic form of the receptor.	bind
45461	1	11334	5	NULL	NULL	NULL	NULL	EC-SOD	GP		is substituted with			ECM-binding region;;Arg213		EC-SOD	GP		ECM-binding region;;Gly		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_21_22152_s_31	15044467	A naturally occurring mutation in the ECM-binding region of EC-SOD substitutes Arg213 for Gly ( Fig. 1) (  -  ).	bind
45963	1	11334	6	NULL	NULL	0	NULL	EC-SOD	NULL	mutant	is substituted with	NULL		ECM-binding region;; Arg213		EC-SOD	NULL	mutant	ECM-binding region;; Gly		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_21_22152_s_31	15044467	A naturally occurring mutation in the ECM-binding region of EC-SOD substitutes Arg213 for Gly ( Fig. 1) (  -  ).	bind
45463	1	11335	5	NULL	NULL	NULL	NULL	TM2	GP		is mutated to			Ala-73		TM2	GP		Val		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_38_36513_s_192	12837756	A naturally occurring mutation in TM2, Ala-73 to Val has been shown to be associated with an increase in CCR5 binding affinity to RANTES and increased sensitivity to the induction of chemotaxis by this ligand ( ,  ).	bind
45465	2	11335	5	NULL	NULL	NULL	NULL	CCR5	GP		bind					RANTES	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_38_36513_s_192	12837756	A naturally occurring mutation in TM2, Ala-73 to Val has been shown to be associated with an increase in CCR5 binding affinity to RANTES and increased sensitivity to the induction of chemotaxis by this ligand ( ,  ).	bind
45466	3	11335	5	NULL	NULL	NULL	NULL	statement 1	Process		is associated with					statement 2	Process	increase in			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_38_36513_s_192	12837756	A naturally occurring mutation in TM2, Ala-73 to Val has been shown to be associated with an increase in CCR5 binding affinity to RANTES and increased sensitivity to the induction of chemotaxis by this ligand ( ,  ).	bind
45467	4	11335	5	NULL	NULL	NULL	NULL	RANTES	GP		induce					chemotaxis	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_38_36513_s_192	12837756	A naturally occurring mutation in TM2, Ala-73 to Val has been shown to be associated with an increase in CCR5 binding affinity to RANTES and increased sensitivity to the induction of chemotaxis by this ligand ( ,  ).	bind
45468	5	11335	5	NULL	NULL	NULL	NULL	statement 1	Process		is associated with					statement 4	Process	increased sensitivity to			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_38_36513_s_192	12837756	A naturally occurring mutation in TM2, Ala-73 to Val has been shown to be associated with an increase in CCR5 binding affinity to RANTES and increased sensitivity to the induction of chemotaxis by this ligand ( ,  ).	bind
45964	1	11335	6	NULL	NULL	0	NULL	CCR5	NULL		has affinity for	NULL				RANTES	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_38_36513_s_192	12837756	A naturally occurring mutation in TM2, Ala-73 to Val has been shown to be associated with an increase in CCR5 binding affinity to RANTES and increased sensitivity to the induction of chemotaxis by this ligand ( ,  ).	bind
45965	2	11335	6	NULL	NULL	0	NULL	TM2	NULL		is mutated to	NULL		Ala-73		TM2	NULL		Val		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_38_36513_s_192	12837756	A naturally occurring mutation in TM2, Ala-73 to Val has been shown to be associated with an increase in CCR5 binding affinity to RANTES and increased sensitivity to the induction of chemotaxis by this ligand ( ,  ).	bind
45966	3	11335	6	NULL	NULL	0	NULL	statement 2	NULL		is associated with	NULL				statement 1	NULL	increase in			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_38_36513_s_192	12837756	A naturally occurring mutation in TM2, Ala-73 to Val has been shown to be associated with an increase in CCR5 binding affinity to RANTES and increased sensitivity to the induction of chemotaxis by this ligand ( ,  ).	bind
51465	4	11335	6	10	NULL	0	NULL	RANTES	NULL		induce	NULL				chemotaxis	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_38_36513_s_192	12837756	A naturally occurring mutation in TM2, Ala-73 to Val has been shown to be associated with an increase in CCR5 binding affinity to RANTES and increased sensitivity to the induction of chemotaxis by this ligand ( ,  ).	bind
51466	5	11335	6	10	NULL	0	NULL	statement 2	NULL		is associated with	NULL				statement 4	NULL	increased sensitivity to			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_38_36513_s_192	12837756	A naturally occurring mutation in TM2, Ala-73 to Val has been shown to be associated with an increase in CCR5 binding affinity to RANTES and increased sensitivity to the induction of chemotaxis by this ligand ( ,  ).	bind
45469	1	11336	5	NULL	NULL	NULL	NULL	FGF	GP		is					fibroblast growth factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_gene_230_1_69_s_323	10196476	A naturally occurring secreted form of fibroblast growth factor (FGF) receptor 1 binds basic FGF in preference over acidic FGF.	bind
45470	2	11336	5	NULL	NULL	NULL	NULL	fibroblast growth factor receptor 1	GP	naturally occurring;;secreted	bind					FGF	GP	basic			NULL		NULL	NULL	NULL	NULL	gw60_gene_230_1_69_s_323	10196476	A naturally occurring secreted form of fibroblast growth factor (FGF) receptor 1 binds basic FGF in preference over acidic FGF.	bind
45471	3	11336	5	NULL	NULL	NULL	NULL	fibroblast growth factor receptor 1	GP	naturally occurring;;secreted	bind					FGF	GP	acidic			NULL		NULL	NULL	NULL	NULL	gw60_gene_230_1_69_s_323	10196476	A naturally occurring secreted form of fibroblast growth factor (FGF) receptor 1 binds basic FGF in preference over acidic FGF.	bind
45472	4	11336	5	NULL	NULL	NULL	NULL	statement 2	Process		is prefered over					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_gene_230_1_69_s_323	10196476	A naturally occurring secreted form of fibroblast growth factor (FGF) receptor 1 binds basic FGF in preference over acidic FGF.	bind
45967	1	11336	6	NULL	NULL	0	NULL	FGF	NULL		is	NULL				fibroblast growth factor	NULL				NULL		0	NULL	NULL	NULL	gw60_gene_230_1_69_s_323	10196476	A naturally occurring secreted form of fibroblast growth factor (FGF) receptor 1 binds basic FGF in preference over acidic FGF.	bind
45968	2	11336	6	10	NULL	0	NULL	FGF receptor 1	NULL	naturally occuring;; secreted form	bind	NULL				FGF	NULL	basic			NULL		NULL	NULL	NULL	NULL	gw60_gene_230_1_69_s_323	10196476	A naturally occurring secreted form of fibroblast growth factor (FGF) receptor 1 binds basic FGF in preference over acidic FGF.	bind
45969	3	11336	6	10	NULL	0	NULL	FGF receptor 1	NULL	naturally occuring;; secreted form	bind	NULL				FGF	NULL	acidic			NULL		NULL	NULL	NULL	NULL	gw60_gene_230_1_69_s_323	10196476	A naturally occurring secreted form of fibroblast growth factor (FGF) receptor 1 binds basic FGF in preference over acidic FGF.	bind
45970	4	11336	6	NULL	NULL	0	NULL	statement 2	NULL		is more preferential than	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_gene_230_1_69_s_323	10196476	A naturally occurring secreted form of fibroblast growth factor (FGF) receptor 1 binds basic FGF in preference over acidic FGF.	bind
45473	1	11337	5	NULL	NULL	NULL	NULL	Tcf3	GP		bind					beta-catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_221	11524435	A nearly fivefold increase in the binding of Tcf3 to beta-catenin is seen when Tcf3 beads were preincubated with CK1epsilon.	bind
45474	2	11337	5	NULL	NULL	NULL	NULL	CK1epsilon	GP	presence of	increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_221	11524435	A nearly fivefold increase in the binding of Tcf3 to beta-catenin is seen when Tcf3 beads were preincubated with CK1epsilon.	bind
45971	1	11337	6	NULL	NULL	0	NULL	Tcf3	NULL		bind	NULL				beta-catenin	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_221	11524435	A nearly fivefold increase in the binding of Tcf3 to beta-catenin is seen when Tcf3 beads were preincubated with CK1epsilon.	bind
45973	2	11337	6	10	NULL	0	NULL	CK1epsilon	NULL	presence of	increase	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_5_983_s_221	11524435	A nearly fivefold increase in the binding of Tcf3 to beta-catenin is seen when Tcf3 beads were preincubated with CK1epsilon.	bind
45475	1	11338	5	NULL	NULL	NULL	NULL				bind				GC-box motif	Sp1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4293_s_232	12024040	A nearly perfect GC-box motif bound Sp1 and Sp3, as judged by electrophoretic mobility shift assays and supershifts with the appropriate antibodies (Fig.  7A).	bind
45476	2	11338	5	NULL	NULL	NULL	NULL				bind				GC-box motif	Sp3	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_12_4293_s_232	12024040	A nearly perfect GC-box motif bound Sp1 and Sp3, as judged by electrophoretic mobility shift assays and supershifts with the appropriate antibodies (Fig.  7A).	bind
45974	1	11338	6	NULL	NULL	0	NULL	Sp1	NULL		bind	NULL					NULL			GC-box 	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_12_4293_s_232	12024040	A nearly perfect GC-box motif bound Sp1 and Sp3, as judged by electrophoretic mobility shift assays and supershifts with the appropriate antibodies (Fig.  7A).	bind
45975	2	11338	6	NULL	NULL	0	NULL	Sp3	NULL		bind	NULL					NULL			GC-box	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_12_4293_s_232	12024040	A nearly perfect GC-box motif bound Sp1 and Sp3, as judged by electrophoretic mobility shift assays and supershifts with the appropriate antibodies (Fig.  7A).	bind
45477	1	11339	5	NULL	NULL	NULL	NULL	toxin A	GP		bind					enterocyte receptors	GP	luminal			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_98_3_641_s_23	8698855	A necessary  first step for enterotoxicity is binding of toxin A to luminal enterocyte receptors.	bind
45478	2	11339	5	NULL	NULL	NULL	NULL	statement 1	Process		is first step for		necessary			enterotoxicity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_98_3_641_s_23	8698855	A necessary  first step for enterotoxicity is binding of toxin A to luminal enterocyte receptors.	bind
45976	1	11339	6	NULL	NULL	0	NULL	toxin A	NULL		bind	NULL				enterocyte receptor	NULL	luminal			NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_3_641_s_23	8698855	A necessary  first step for enterotoxicity is binding of toxin A to luminal enterocyte receptors.	bind
45479	1	11340	5	NULL	NULL	NULL	NULL	CETP	GP		bind		stably			HDL	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_718_s_215	10073979	A necessary corollary to these findings is that the often-reported stable binding of CETP to HDL does not result in selective transfer from this lipoprotein fraction.	bind
45480	2	11340	5	NULL	NULL	NULL	NULL	statement 1	Process		does not result in					lipoprotein	GP	selective transfer from;;fraction of			NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_718_s_215	10073979	A necessary corollary to these findings is that the often-reported stable binding of CETP to HDL does not result in selective transfer from this lipoprotein fraction.	bind
51467	3	11340	5	NULL	NULL	NULL	NULL	HDL	GP		is a type of					lipoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_718_s_215	10073979	A necessary corollary to these findings is that the often-reported stable binding of CETP to HDL does not result in selective transfer from this lipoprotein fraction.	bind
45977	1	11340	6	10	NULL	0	NULL	CETP			bind		stable			HDL					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_718_s_215	10073979	A necessary corollary to these findings is that the often-reported stable binding of CETP to HDL does not result in selective transfer from this lipoprotein fraction.	bind
45978	2	11340	6	NULL	NULL	0	NULL	statement 1	NULL		does not result in	NULL				HDL	NULL	transfer from			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_718_s_215	10073979	A necessary corollary to these findings is that the often-reported stable binding of CETP to HDL does not result in selective transfer from this lipoprotein fraction.	bind
45979	3	11340	6	10	NULL	0	NULL	HDL	NULL		is a type of	NULL				lipoprotein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_3_718_s_215	10073979	A necessary corollary to these findings is that the often-reported stable binding of CETP to HDL does not result in selective transfer from this lipoprotein fraction.	bind
45481	1	11341	5	NULL	NULL	NULL	NULL	TRA-2	GP		bind		directly			FEM-3	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_34_12549_s_201	15306688	A negative arrow from TRA-2 to FEM-3 reflects the possibility  that TRA-2 directly binds and inhibits FEM-3 ( ).	bind
45482	2	11341	5	NULL	NULL	NULL	NULL	statement 1	Process		inhibit					FEM-3	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_34_12549_s_201	15306688	A negative arrow from TRA-2 to FEM-3 reflects the possibility  that TRA-2 directly binds and inhibits FEM-3 ( ).	bind
45980	1	11341	6	NULL	NULL	0	NULL	TRA-2	NULL		bind	NULL	directly			FEM-3	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_34_12549_s_201	15306688	A negative arrow from TRA-2 to FEM-3 reflects the possibility  that TRA-2 directly binds and inhibits FEM-3 ( ).	bind
45981	2	11341	6	NULL	NULL	0	NULL	TRA-2	NULL		inhibits	NULL				FEM-3	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_34_12549_s_201	15306688	A negative arrow from TRA-2 to FEM-3 reflects the possibility  that TRA-2 directly binds and inhibits FEM-3 ( ).	bind
45483	1	11342	5	NULL	NULL	NULL	NULL	CHO cells	Cell		is transfected with					P-selectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_14_1710_s_87	11015352	A negative control experiment using an isotype-matched control revealed that the binding of HL-60 cells to P-selectin - transfected CHO cells was hardly suppressed compared with results for S789G (Table  ).	bind
45484	2	11342	5	NULL	NULL	NULL	NULL	HL-60 cells	Cell		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulation_102_14_1710_s_87	11015352	A negative control experiment using an isotype-matched control revealed that the binding of HL-60 cells to P-selectin - transfected CHO cells was hardly suppressed compared with results for S789G (Table  ).	bind
45982	1	11342	6	NULL	NULL	0	NULL	P-selectin	NULL		is transfected to	NULL				CHO cells	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_14_1710_s_87	11015352	A negative control experiment using an isotype-matched control revealed that the binding of HL-60 cells to P-selectin - transfected CHO cells was hardly suppressed compared with results for S789G (Table  ).	bind
45983	2	11342	6	NULL	NULL	0	NULL	HL-60 cells	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_circulation_102_14_1710_s_87	11015352	A negative control experiment using an isotype-matched control revealed that the binding of HL-60 cells to P-selectin - transfected CHO cells was hardly suppressed compared with results for S789G (Table  ).	bind
45485	1	11343	5	NULL	NULL	NULL	NULL	Grb-2	GP		bind		low affinity			CD3-epsilon-ITAM	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_40_25310_s_176	9312149	A negative control in these experiments was the comparison with the low affinity binding of Grb-2 to CD3-epsilon-ITAM ( 37).	bind
45984	1	11343	6	NULL	NULL	0	NULL	Grb-2	NULL		bind	NULL	low affinity			CD3-epsilon-ITAM	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_40_25310_s_176	9312149	A negative control in these experiments was the comparison with the low affinity binding of Grb-2 to CD3-epsilon-ITAM ( 37).	bind
45487	1	11345	5	NULL	NULL	NULL	NULL	parathyroid hormone-related peptide gene	GP	human	bind				negative Vitamin D response DNA element	Vitamin D receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_27_16310_s_256	8663213	A Negative Vitamin D Response DNA Element in the Human Parathyroid Hormone-related Peptide Gene Binds to Vitamin D Receptor Along with Ku Antigen to Mediate Negative Gene Regulation by Vitamin D.   J. Biol.	bind
45488	2	11345	5	NULL	NULL	NULL	NULL	parathyroid hormone-related peptide gene	GP	human	bind				negative Vitamin D response DNA element	Ku Antigen	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_27_16310_s_256	8663213	A Negative Vitamin D Response DNA Element in the Human Parathyroid Hormone-related Peptide Gene Binds to Vitamin D Receptor Along with Ku Antigen to Mediate Negative Gene Regulation by Vitamin D.   J. Biol.	bind
45489	3	11345	5	NULL	NULL	NULL	NULL	Vitamin D	Chemical		mediate					negative gene regulation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_27_16310_s_256	8663213	A Negative Vitamin D Response DNA Element in the Human Parathyroid Hormone-related Peptide Gene Binds to Vitamin D Receptor Along with Ku Antigen to Mediate Negative Gene Regulation by Vitamin D.   J. Biol.	bind
45490	4	11345	5	NULL	NULL	NULL	NULL	statement 1	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_27_16310_s_256	8663213	A Negative Vitamin D Response DNA Element in the Human Parathyroid Hormone-related Peptide Gene Binds to Vitamin D Receptor Along with Ku Antigen to Mediate Negative Gene Regulation by Vitamin D.   J. Biol.	bind
45491	5	11345	5	NULL	NULL	NULL	NULL	statement 2	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_27_16310_s_256	8663213	A Negative Vitamin D Response DNA Element in the Human Parathyroid Hormone-related Peptide Gene Binds to Vitamin D Receptor Along with Ku Antigen to Mediate Negative Gene Regulation by Vitamin D.   J. Biol.	bind
45985	1	11345	6	NULL	NULL	0	NULL	Parathyroid Hormone-related Peptide Gene	NULL	human	bind	NULL			Vitamin D Response DNA Element	Vitamin D Receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_27_16310_s_256	8663213	A Negative Vitamin D Response DNA Element in the Human Parathyroid Hormone-related Peptide Gene Binds to Vitamin D Receptor Along with Ku Antigen to Mediate Negative Gene Regulation by Vitamin D.   J. Biol.	bind
45986	2	11345	6	10	NULL	0	NULL	Parathyroid Hormone-related Peptide Gene	NULL	human	bind	NULL			Vitamin D Response DNA Element	Ku antigen	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_27_16310_s_256	8663213	A Negative Vitamin D Response DNA Element in the Human Parathyroid Hormone-related Peptide Gene Binds to Vitamin D Receptor Along with Ku Antigen to Mediate Negative Gene Regulation by Vitamin D.   J. Biol.	bind
45987	5	11345	6	10	NULL	0	NULL	statement 2	NULL		mediates	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_27_16310_s_256	8663213	A Negative Vitamin D Response DNA Element in the Human Parathyroid Hormone-related Peptide Gene Binds to Vitamin D Receptor Along with Ku Antigen to Mediate Negative Gene Regulation by Vitamin D.   J. Biol.	bind
45988	3	11345	6	10	NULL	0	NULL	vitamin D 	NULL		causes	NULL				gene regulation	NULL	negative			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_27_16310_s_256	8663213	A Negative Vitamin D Response DNA Element in the Human Parathyroid Hormone-related Peptide Gene Binds to Vitamin D Receptor Along with Ku Antigen to Mediate Negative Gene Regulation by Vitamin D.   J. Biol.	bind
45989	4	11345	6	10	NULL	0	NULL	statement 1	NULL		mediates	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_27_16310_s_256	8663213	A Negative Vitamin D Response DNA Element in the Human Parathyroid Hormone-related Peptide Gene Binds to Vitamin D Receptor Along with Ku Antigen to Mediate Negative Gene Regulation by Vitamin D.   J. Biol.	bind
45492	1	11349	5	NULL	NULL	NULL	NULL	Pd(II) nanoparticle catalyst	Chemical	negatively charged	bind					PEI layer	Chemical	terminal cationic 			NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_j-am-chem-soc_125_37_16220946_s_4	16220946	A negatively charged Pd(II) nanoparticle catalyst  is bound to the terminal cationic PEI layer of the multilayer film and  initiates selective template metallization to form the helical Cu nanostructures.	bind
45493	2	11349	5	NULL	NULL	NULL	NULL	statement 1	Process		initiates					template metallization	Process	selective			NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_j-am-chem-soc_125_37_16220946_s_4	16220946	A negatively charged Pd(II) nanoparticle catalyst  is bound to the terminal cationic PEI layer of the multilayer film and  initiates selective template metallization to form the helical Cu nanostructures.	bind
45494	3	11349	5	NULL	NULL	NULL	NULL	statement 2	Process		forms					helical Cu nanostructures	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_j-am-chem-soc_125_37_16220946_s_4	16220946	A negatively charged Pd(II) nanoparticle catalyst  is bound to the terminal cationic PEI layer of the multilayer film and  initiates selective template metallization to form the helical Cu nanostructures.	bind
46107	1	11349	6	NULL	NULL	0	NULL	Pd(II) nanoparticle catalyst	NULL	negatively charged	bind	NULL				PEI layer	NULL	terminal cationic			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-am-chem-soc_125_37_16220946_s_4	16220946	A negatively charged Pd(II) nanoparticle catalyst  is bound to the terminal cationic PEI layer of the multilayer film and  initiates selective template metallization to form the helical Cu nanostructures.	bind
46108	2	11349	6	NULL	NULL	0	NULL	statement 1	NULL		initiates	NULL				template metallization	NULL				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-am-chem-soc_125_37_16220946_s_4	16220946	A negatively charged Pd(II) nanoparticle catalyst  is bound to the terminal cationic PEI layer of the multilayer film and  initiates selective template metallization to form the helical Cu nanostructures.	bind
46115	3	11349	6	10	NULL	0	NULL	statement 2	NULL		forms	NULL				helical Cu nanostructures	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_j-am-chem-soc_125_37_16220946_s_4	16220946	A negatively charged Pd(II) nanoparticle catalyst  is bound to the terminal cationic PEI layer of the multilayer film and  initiates selective template metallization to form the helical Cu nanostructures.	bind
45495	1	11350	5	NULL	NULL	NULL	NULL	PS	Chemical	negatively charged	bind		specifically			annexin V	GP	fluorescently labeled			NULL		NULL	NULL	NULL	NULL	gw60_febslett_477_1_1_s_22	10899301	A negatively charged PS can specifically bind fluorescently labeled annexin V, the most commonly used reagent for flow cytometric measurements of apoptosis [  11 and   12].	bind
45990	1	11350	6	NULL	NULL	0	NULL	PS	NULL	negatively charged	bind	NULL	specifically			annexin V	NULL	fluorescently labeled			NULL		0	NULL	NULL	NULL	gw60_febslett_477_1_1_s_22	10899301	A negatively charged PS can specifically bind fluorescently labeled annexin V, the most commonly used reagent for flow cytometric measurements of apoptosis [  11 and   12].	bind
45502	1	11352	5	NULL	NULL	NULL	NULL	hnRNP H	GP		bind									enhancer	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_21	12826680	A neurally enriched homologue of PTB  also greatly enhances the binding of hnRNP H and KH-type splicing-regulatory  protein to the enhancer ( ).	bind
45503	2	11352	5	NULL	NULL	NULL	NULL	KH-type splicing-regulatory protein	GP		bind									enhancer	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_21	12826680	A neurally enriched homologue of PTB  also greatly enhances the binding of hnRNP H and KH-type splicing-regulatory  protein to the enhancer ( ).	bind
45504	3	11352	5	NULL	NULL	NULL	NULL	PTB homolog	GP	neurally enriched	enhance		greatly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_21	12826680	A neurally enriched homologue of PTB  also greatly enhances the binding of hnRNP H and KH-type splicing-regulatory  protein to the enhancer ( ).	bind
45505	4	11352	5	NULL	NULL	NULL	NULL	PTB homolog	GP	neurally enriched	enhance		greatly			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_21	12826680	A neurally enriched homologue of PTB  also greatly enhances the binding of hnRNP H and KH-type splicing-regulatory  protein to the enhancer ( ).	bind
45991	1	11352	6	NULL	NULL	0	NULL	hnRNP H	NULL		bind	NULL					NULL			enhancer	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_21	12826680	A neurally enriched homologue of PTB  also greatly enhances the binding of hnRNP H and KH-type splicing-regulatory  protein to the enhancer ( ).	bind
45992	2	11352	6	NULL	NULL	0	NULL	KH-type splicing-regulatory protein	NULL		bind	NULL					NULL			enhancer	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_21	12826680	A neurally enriched homologue of PTB  also greatly enhances the binding of hnRNP H and KH-type splicing-regulatory  protein to the enhancer ( ).	bind
45993	3	11352	6	10	NULL	0	NULL	PTB homologue		neurally enriched	enhances		greatly			statement 1					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_21	12826680	A neurally enriched homologue of PTB  also greatly enhances the binding of hnRNP H and KH-type splicing-regulatory  protein to the enhancer ( ).	bind
45994	4	11352	6	10	NULL	0	NULL	PTB homologue		neurally enriched	enhances		greatly			statement 2					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32943_s_21	12826680	A neurally enriched homologue of PTB  also greatly enhances the binding of hnRNP H and KH-type splicing-regulatory  protein to the enhancer ( ).	bind
45506	1	11353	5	NULL	NULL	NULL	NULL	neurobeachin isoform	GP		does not bind					RII	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_20_23_8551_s_8	11102458	A neurobeachin isoform that does not bind RII, beige-like protein (BGL), is expressed in many tissues.	bind
45507	2	11353	5	NULL	NULL	NULL	NULL	neurobeachin isoform	GP		does not bind					BGL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_20_23_8551_s_8	11102458	A neurobeachin isoform that does not bind RII, beige-like protein (BGL), is expressed in many tissues.	bind
45508	3	11353	5	NULL	NULL	NULL	NULL	BGL	GP		is					beige-like protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_20_23_8551_s_8	11102458	A neurobeachin isoform that does not bind RII, beige-like protein (BGL), is expressed in many tissues.	bind
45995	1	11353	6	NULL	NULL	0	NULL	neurobeachin isoform	NULL		does not bind	NULL				RII	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_23_8551_s_8	11102458	A neurobeachin isoform that does not bind RII, beige-like protein (BGL), is expressed in many tissues.	bind
45996	2	11353	6	10	NULL	0	NULL	neurobeachin isoform	NULL		does not bind	NULL				BGL	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_20_23_8551_s_8	11102458	A neurobeachin isoform that does not bind RII, beige-like protein (BGL), is expressed in many tissues.	bind
45997	3	11353	6	NULL	NULL	0	NULL	BGL	NULL		is	NULL				beige-like protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_23_8551_s_8	11102458	A neurobeachin isoform that does not bind RII, beige-like protein (BGL), is expressed in many tissues.	bind
45511	1	11354	5	NULL	NULL	NULL	NULL	neuroligin	GP		is a type of					neuronal cell adhesion molecule	GP				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_22_3_757_s_22	11826105	A neuronal cell adhesion molecule, neuroligin, and a GDP/GTP exchange factor for rap1 bind to the second PDZ domain (PDZ1) (Hirao et al., 1998  ; Ohtsuka et al., 1999  ).	bind
45512	2	11354	5	NULL	NULL	NULL	NULL	neuroligin	GP		bind								PDZ1		NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_22_3_757_s_22	11826105	A neuronal cell adhesion molecule, neuroligin, and a GDP/GTP exchange factor for rap1 bind to the second PDZ domain (PDZ1) (Hirao et al., 1998  ; Ohtsuka et al., 1999  ).	bind
45513	3	11354	5	NULL	NULL	NULL	NULL	PDZ1	AminoAcid		is					second PDZ domain	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_22_3_757_s_22	11826105	A neuronal cell adhesion molecule, neuroligin, and a GDP/GTP exchange factor for rap1 bind to the second PDZ domain (PDZ1) (Hirao et al., 1998  ; Ohtsuka et al., 1999  ).	bind
45514	4	11354	5	NULL	NULL	NULL	NULL	GDP/GTP exchange factor for rap1	GP		bind								PDZ1		NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_22_3_757_s_22	11826105	A neuronal cell adhesion molecule, neuroligin, and a GDP/GTP exchange factor for rap1 bind to the second PDZ domain (PDZ1) (Hirao et al., 1998  ; Ohtsuka et al., 1999  ).	bind
45998	1	11354	6	NULL	NULL	0	NULL	neuroligin	NULL		is a type of	NULL				neuronal cell adhesion molecule	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_22_3_757_s_22	11826105	A neuronal cell adhesion molecule, neuroligin, and a GDP/GTP exchange factor for rap1 bind to the second PDZ domain (PDZ1) (Hirao et al., 1998  ; Ohtsuka et al., 1999  ).	bind
45999	2	11354	6	NULL	NULL	0	NULL	neuroligin	NULL		bind	NULL					NULL		PDZ1		NULL		0	NULL	NULL	NULL	gw60_jneurosci_22_3_757_s_22	11826105	A neuronal cell adhesion molecule, neuroligin, and a GDP/GTP exchange factor for rap1 bind to the second PDZ domain (PDZ1) (Hirao et al., 1998  ; Ohtsuka et al., 1999  ).	bind
46000	3	11354	6	NULL	NULL	0	NULL	GDP/GTP exchange factor for rap1	NULL		bind	NULL					NULL		PDZ1		NULL		0	NULL	NULL	NULL	gw60_jneurosci_22_3_757_s_22	11826105	A neuronal cell adhesion molecule, neuroligin, and a GDP/GTP exchange factor for rap1 bind to the second PDZ domain (PDZ1) (Hirao et al., 1998  ; Ohtsuka et al., 1999  ).	bind
46001	4	11354	6	NULL	NULL	0	NULL	PDZ1	NULL		is	NULL				second PDZ domain 	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_22_3_757_s_22	11826105	A neuronal cell adhesion molecule, neuroligin, and a GDP/GTP exchange factor for rap1 bind to the second PDZ domain (PDZ1) (Hirao et al., 1998  ; Ohtsuka et al., 1999  ).	bind
45515	1	11355	5	NULL	NULL	NULL	NULL	Hsp70	GP		bind					DC	Cell				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_3_353_s_64	12354387	A neutralizing anti-CD14 mAb (clone MY4) did not modulate Hsp70 binding to DC or macrophages   (Table 1), and Hsp70 did not bind to CD14-transfected cells   (Figure 2) .	bind
45516	2	11355	5	NULL	NULL	NULL	NULL	Hsp70	GP		bind					macrophages	Cell				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_3_353_s_64	12354387	A neutralizing anti-CD14 mAb (clone MY4) did not modulate Hsp70 binding to DC or macrophages   (Table 1), and Hsp70 did not bind to CD14-transfected cells   (Figure 2) .	bind
45517	3	11355	5	NULL	NULL	NULL	NULL	anti-CD14 mAb	GP	neutralizing	does not modulate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_3_353_s_64	12354387	A neutralizing anti-CD14 mAb (clone MY4) did not modulate Hsp70 binding to DC or macrophages   (Table 1), and Hsp70 did not bind to CD14-transfected cells   (Figure 2) .	bind
45518	4	11355	5	NULL	NULL	NULL	NULL	anti-CD14 mAb	GP	neutralizing	does not modulate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_3_353_s_64	12354387	A neutralizing anti-CD14 mAb (clone MY4) did not modulate Hsp70 binding to DC or macrophages   (Table 1), and Hsp70 did not bind to CD14-transfected cells   (Figure 2) .	bind
45519	5	11355	5	NULL	NULL	NULL	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_3_353_s_64	12354387	A neutralizing anti-CD14 mAb (clone MY4) did not modulate Hsp70 binding to DC or macrophages   (Table 1), and Hsp70 did not bind to CD14-transfected cells   (Figure 2) .	bind
45520	7	11355	5	NULL	NULL	NULL	NULL	Hsp70	GP		does not bind					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_3_353_s_64	12354387	A neutralizing anti-CD14 mAb (clone MY4) did not modulate Hsp70 binding to DC or macrophages   (Table 1), and Hsp70 did not bind to CD14-transfected cells   (Figure 2) .	bind
45521	6	11355	5	NULL	NULL	NULL	NULL	cells	Cell		is transfected with					CD14	GP				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_3_353_s_64	12354387	A neutralizing anti-CD14 mAb (clone MY4) did not modulate Hsp70 binding to DC or macrophages   (Table 1), and Hsp70 did not bind to CD14-transfected cells   (Figure 2) .	bind
46002	1	11355	6	NULL	NULL	0	NULL	Hsp70	NULL		bind	NULL				DC	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_17_3_353_s_64	12354387	A neutralizing anti-CD14 mAb (clone MY4) did not modulate Hsp70 binding to DC or macrophages   (Table 1), and Hsp70 did not bind to CD14-transfected cells   (Figure 2) .	bind
46003	2	11355	6	NULL	NULL	0	NULL	Hsp70	NULL		bind	NULL				macrophages	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_17_3_353_s_64	12354387	A neutralizing anti-CD14 mAb (clone MY4) did not modulate Hsp70 binding to DC or macrophages   (Table 1), and Hsp70 did not bind to CD14-transfected cells   (Figure 2) .	bind
46004	3	11355	6	NULL	NULL	0	NULL	anti-CD14 mAb	NULL	neutralizing	did not modulate	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_17_3_353_s_64	12354387	A neutralizing anti-CD14 mAb (clone MY4) did not modulate Hsp70 binding to DC or macrophages   (Table 1), and Hsp70 did not bind to CD14-transfected cells   (Figure 2) .	bind
46005	4	11355	6	NULL	NULL	0	NULL	anti-CD14 mAb	NULL	neutralizing	did not modulate	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_17_3_353_s_64	12354387	A neutralizing anti-CD14 mAb (clone MY4) did not modulate Hsp70 binding to DC or macrophages   (Table 1), and Hsp70 did not bind to CD14-transfected cells   (Figure 2) .	bind
46006	6	11355	6	10	NULL	0	NULL	Hsp70	NULL		does not bind	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw60_immunity_17_3_353_s_64	12354387	A neutralizing anti-CD14 mAb (clone MY4) did not modulate Hsp70 binding to DC or macrophages   (Table 1), and Hsp70 did not bind to CD14-transfected cells   (Figure 2) .	bind
51489	5	11355	6	10	NULL	0	NULL	cells	NULL		transfected with	NULL				CD14	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_17_3_353_s_64	12354387	A neutralizing anti-CD14 mAb (clone MY4) did not modulate Hsp70 binding to DC or macrophages   (Table 1), and Hsp70 did not bind to CD14-transfected cells   (Figure 2) .	bind
51490	7	11355	6	10	NULL	0	NULL	statement 3	NULL		is an alternative to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_immunity_17_3_353_s_64	12354387	A neutralizing anti-CD14 mAb (clone MY4) did not modulate Hsp70 binding to DC or macrophages   (Table 1), and Hsp70 did not bind to CD14-transfected cells   (Figure 2) .	bind
45522	1	11356	5	NULL	NULL	NULL	NULL	LDL	GP	Oxidized	bind					LOX-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_511_1_133_s_97	11821063	A neutralizing anti-LOX-1 monoclonal antibody, which inhibits binding of oxidized LDL to LOX-1, partly (by 72% of the LOX-1-dependent adhesion) but significantly inhibited adhesion of THP-1 cells to CHO-K1 cells stably expressing bovine LOX-1 (bLOX-1-CHO).	bind
45523	2	11356	5	NULL	NULL	NULL	NULL	anti-LOX-1	GP		is a type of					monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_511_1_133_s_97	11821063	A neutralizing anti-LOX-1 monoclonal antibody, which inhibits binding of oxidized LDL to LOX-1, partly (by 72% of the LOX-1-dependent adhesion) but significantly inhibited adhesion of THP-1 cells to CHO-K1 cells stably expressing bovine LOX-1 (bLOX-1-CHO).	bind
45524	3	11356	5	NULL	NULL	NULL	NULL	anti-LOX-1	GP	neutralizing	inhibit		partly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_511_1_133_s_97	11821063	A neutralizing anti-LOX-1 monoclonal antibody, which inhibits binding of oxidized LDL to LOX-1, partly (by 72% of the LOX-1-dependent adhesion) but significantly inhibited adhesion of THP-1 cells to CHO-K1 cells stably expressing bovine LOX-1 (bLOX-1-CHO).	bind
45525	4	11356	5	NULL	NULL	NULL	NULL	CHO-K1 cells	Cell		express		stably			LOX-1	GP	bovine			NULL		NULL	NULL	NULL	NULL	gw60_febslett_511_1_133_s_97	11821063	A neutralizing anti-LOX-1 monoclonal antibody, which inhibits binding of oxidized LDL to LOX-1, partly (by 72% of the LOX-1-dependent adhesion) but significantly inhibited adhesion of THP-1 cells to CHO-K1 cells stably expressing bovine LOX-1 (bLOX-1-CHO).	bind
45526	5	11356	5	NULL	NULL	NULL	NULL	bLOX-1-CHO	Cell		is					statement 4	Cell				NULL		NULL	NULL	NULL	NULL	gw60_febslett_511_1_133_s_97	11821063	A neutralizing anti-LOX-1 monoclonal antibody, which inhibits binding of oxidized LDL to LOX-1, partly (by 72% of the LOX-1-dependent adhesion) but significantly inhibited adhesion of THP-1 cells to CHO-K1 cells stably expressing bovine LOX-1 (bLOX-1-CHO).	bind
45527	6	11356	5	NULL	NULL	NULL	NULL	THP-1 cells	Cell		adhere to					bLOX-1-CHO	Cell				NULL		NULL	NULL	NULL	NULL	gw60_febslett_511_1_133_s_97	11821063	A neutralizing anti-LOX-1 monoclonal antibody, which inhibits binding of oxidized LDL to LOX-1, partly (by 72% of the LOX-1-dependent adhesion) but significantly inhibited adhesion of THP-1 cells to CHO-K1 cells stably expressing bovine LOX-1 (bLOX-1-CHO).	bind
45528	7	11356	5	NULL	NULL	NULL	NULL	anti-LOX-1	GP	neutralizing	inhibit		significantly			statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_511_1_133_s_97	11821063	A neutralizing anti-LOX-1 monoclonal antibody, which inhibits binding of oxidized LDL to LOX-1, partly (by 72% of the LOX-1-dependent adhesion) but significantly inhibited adhesion of THP-1 cells to CHO-K1 cells stably expressing bovine LOX-1 (bLOX-1-CHO).	bind
46007	1	11356	6	NULL	NULL	0	NULL	LDL	NULL	oxidized	bind	NULL				LOX-1	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_511_1_133_s_97	11821063	A neutralizing anti-LOX-1 monoclonal antibody, which inhibits binding of oxidized LDL to LOX-1, partly (by 72% of the LOX-1-dependent adhesion) but significantly inhibited adhesion of THP-1 cells to CHO-K1 cells stably expressing bovine LOX-1 (bLOX-1-CHO).	bind
46008	2	11356	6	10	NULL	0	NULL	anti-LOX-1	NULL	neutralizing	inhibits	NULL	partly			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_511_1_133_s_97	11821063	A neutralizing anti-LOX-1 monoclonal antibody, which inhibits binding of oxidized LDL to LOX-1, partly (by 72% of the LOX-1-dependent adhesion) but significantly inhibited adhesion of THP-1 cells to CHO-K1 cells stably expressing bovine LOX-1 (bLOX-1-CHO).	bind
46009	3	11356	6	NULL	NULL	0	NULL	THP-1 cells	NULL		adhers to	NULL				bLOX-1-CHO	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_511_1_133_s_97	11821063	A neutralizing anti-LOX-1 monoclonal antibody, which inhibits binding of oxidized LDL to LOX-1, partly (by 72% of the LOX-1-dependent adhesion) but significantly inhibited adhesion of THP-1 cells to CHO-K1 cells stably expressing bovine LOX-1 (bLOX-1-CHO).	bind
46010	4	11356	6	NULL	NULL	0	NULL	CHO-K1 cells	NULL		express 	NULL	stably			LOX-1	NULL	bovine			NULL		0	NULL	NULL	NULL	gw60_febslett_511_1_133_s_97	11821063	A neutralizing anti-LOX-1 monoclonal antibody, which inhibits binding of oxidized LDL to LOX-1, partly (by 72% of the LOX-1-dependent adhesion) but significantly inhibited adhesion of THP-1 cells to CHO-K1 cells stably expressing bovine LOX-1 (bLOX-1-CHO).	bind
46011	5	11356	6	NULL	NULL	0	NULL	bLOX-1-CHO	NULL		is	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_511_1_133_s_97	11821063	A neutralizing anti-LOX-1 monoclonal antibody, which inhibits binding of oxidized LDL to LOX-1, partly (by 72% of the LOX-1-dependent adhesion) but significantly inhibited adhesion of THP-1 cells to CHO-K1 cells stably expressing bovine LOX-1 (bLOX-1-CHO).	bind
51500	6	11356	6	10	NULL	0	NULL	 anti-LOX-1 	NULL	neutralizing 	inhibit	NULL	significantly			statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_511_1_133_s_97	11821063	A neutralizing anti-LOX-1 monoclonal antibody, which inhibits binding of oxidized LDL to LOX-1, partly (by 72% of the LOX-1-dependent adhesion) but significantly inhibited adhesion of THP-1 cells to CHO-K1 cells stably expressing bovine LOX-1 (bLOX-1-CHO).	bind
51501	7	11356	6	10	NULL	0	NULL	anti-LOX-1	NULL		is a type of	NULL				monoclonal antibody	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_511_1_133_s_97	11821063	A neutralizing anti-LOX-1 monoclonal antibody, which inhibits binding of oxidized LDL to LOX-1, partly (by 72% of the LOX-1-dependent adhesion) but significantly inhibited adhesion of THP-1 cells to CHO-K1 cells stably expressing bovine LOX-1 (bLOX-1-CHO).	bind
45529	1	11357	5	NULL	NULL	NULL	NULL	 antibody	GP	neutralizing	reacts with					gp42	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-virol_72_1_9420211_s_4	9420211	A neutralizing antibody  that reacts with gp42 inhibits virus-cell fusion and blocks binding of  gp42 to HLA class II; antibody to HLA class II can inhibit infection,  and B cells that lack HLA class II can only be infected if HLA class II  expression is restored.	bind
45530	2	11357	5	NULL	NULL	NULL	NULL	statement 1	Process		inhibit					virus-cell fusion	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-virol_72_1_9420211_s_4	9420211	A neutralizing antibody  that reacts with gp42 inhibits virus-cell fusion and blocks binding of  gp42 to HLA class II; antibody to HLA class II can inhibit infection,  and B cells that lack HLA class II can only be infected if HLA class II  expression is restored.	bind
45531	3	11357	5	NULL	NULL	NULL	NULL	gp42	GP		bind					HLA class II	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-virol_72_1_9420211_s_4	9420211	A neutralizing antibody  that reacts with gp42 inhibits virus-cell fusion and blocks binding of  gp42 to HLA class II; antibody to HLA class II can inhibit infection,  and B cells that lack HLA class II can only be infected if HLA class II  expression is restored.	bind
45532	4	11357	5	NULL	NULL	NULL	NULL	statement 1	Process		block					statement 3	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-virol_72_1_9420211_s_4	9420211	A neutralizing antibody  that reacts with gp42 inhibits virus-cell fusion and blocks binding of  gp42 to HLA class II; antibody to HLA class II can inhibit infection,  and B cells that lack HLA class II can only be infected if HLA class II  expression is restored.	bind
45533	5	11357	5	NULL	NULL	NULL	NULL	antibody to HLA class II	GP		inhibit					infection	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-virol_72_1_9420211_s_4	9420211	A neutralizing antibody  that reacts with gp42 inhibits virus-cell fusion and blocks binding of  gp42 to HLA class II; antibody to HLA class II can inhibit infection,  and B cells that lack HLA class II can only be infected if HLA class II  expression is restored.	bind
45534	6	11357	5	NULL	NULL	NULL	NULL	B cells	Cell		lacks					HLA class II	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-virol_72_1_9420211_s_4	9420211	A neutralizing antibody  that reacts with gp42 inhibits virus-cell fusion and blocks binding of  gp42 to HLA class II; antibody to HLA class II can inhibit infection,  and B cells that lack HLA class II can only be infected if HLA class II  expression is restored.	bind
45535	7	11357	5	NULL	NULL	NULL	NULL	statement 6	Process	infection of	occurs on		only			HLA class II	GP	restoration of;;expression of			NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-virol_72_1_9420211_s_4	9420211	A neutralizing antibody  that reacts with gp42 inhibits virus-cell fusion and blocks binding of  gp42 to HLA class II; antibody to HLA class II can inhibit infection,  and B cells that lack HLA class II can only be infected if HLA class II  expression is restored.	bind
46012	1	11357	6	NULL	NULL	0	NULL	gp42	NULL		bind	NULL				HLA class II	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_j-virol_72_1_9420211_s_4	9420211	A neutralizing antibody  that reacts with gp42 inhibits virus-cell fusion and blocks binding of  gp42 to HLA class II; antibody to HLA class II can inhibit infection,  and B cells that lack HLA class II can only be infected if HLA class II  expression is restored.	bind
46013	2	11357	6	NULL	NULL	0	NULL	neutralizing antibody	NULL		reacts with	NULL				gp42	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_j-virol_72_1_9420211_s_4	9420211	A neutralizing antibody  that reacts with gp42 inhibits virus-cell fusion and blocks binding of  gp42 to HLA class II; antibody to HLA class II can inhibit infection,  and B cells that lack HLA class II can only be infected if HLA class II  expression is restored.	bind
46014	3	11357	6	NULL	NULL	0	NULL	statement 2	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_j-virol_72_1_9420211_s_4	9420211	A neutralizing antibody  that reacts with gp42 inhibits virus-cell fusion and blocks binding of  gp42 to HLA class II; antibody to HLA class II can inhibit infection,  and B cells that lack HLA class II can only be infected if HLA class II  expression is restored.	bind
46015	4	11357	6	NULL	NULL	0	NULL	statement 2	NULL		inhibits	NULL				virus-cell fusion	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_j-virol_72_1_9420211_s_4	9420211	A neutralizing antibody  that reacts with gp42 inhibits virus-cell fusion and blocks binding of  gp42 to HLA class II; antibody to HLA class II can inhibit infection,  and B cells that lack HLA class II can only be infected if HLA class II  expression is restored.	bind
46016	5	11357	6	NULL	NULL	0	NULL	HLA class II antibody	NULL		inhibits	NULL				infection	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_j-virol_72_1_9420211_s_4	9420211	A neutralizing antibody  that reacts with gp42 inhibits virus-cell fusion and blocks binding of  gp42 to HLA class II; antibody to HLA class II can inhibit infection,  and B cells that lack HLA class II can only be infected if HLA class II  expression is restored.	bind
46017	6	11357	6	NULL	NULL	0	NULL	B cells	NULL		lack	NULL				HLA class II	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_j-virol_72_1_9420211_s_4	9420211	A neutralizing antibody  that reacts with gp42 inhibits virus-cell fusion and blocks binding of  gp42 to HLA class II; antibody to HLA class II can inhibit infection,  and B cells that lack HLA class II can only be infected if HLA class II  expression is restored.	bind
46018	7	11357	6	10	NULL	0	NULL	statement 6	NULL		occurs upon 	NULL				HLA class II	NULL	restoration of ;;expression of			NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_j-virol_72_1_9420211_s_4	9420211	A neutralizing antibody  that reacts with gp42 inhibits virus-cell fusion and blocks binding of  gp42 to HLA class II; antibody to HLA class II can inhibit infection,  and B cells that lack HLA class II can only be infected if HLA class II  expression is restored.	bind
45536	1	11358	5	NULL	NULL	NULL	NULL	C-IIIJ1	GP		bind									regulatory element J	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_222_s_26	9012660	A new activity designated C-IIIJ1 binds to the regulatory element J, and a minor activity as well as HNF-4 binds to the regulatory element I. 5 8  Finally, the proximal apoA-IV promoter consists of four regulatory elements located between nucleotides -22 and -274.	bind
45537	2	11358	5	NULL	NULL	NULL	NULL	HNF-4	GP		bind									regulatory element I	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_222_s_26	9012660	A new activity designated C-IIIJ1 binds to the regulatory element J, and a minor activity as well as HNF-4 binds to the regulatory element I. 5 8  Finally, the proximal apoA-IV promoter consists of four regulatory elements located between nucleotides -22 and -274.	bind
45538	3	11358	5	NULL	NULL	NULL	NULL	apoA-IV	GP	proximal	consists of				promoter					regulatory elements between nucleotides -22 and -274	NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_222_s_26	9012660	A new activity designated C-IIIJ1 binds to the regulatory element J, and a minor activity as well as HNF-4 binds to the regulatory element I. 5 8  Finally, the proximal apoA-IV promoter consists of four regulatory elements located between nucleotides -22 and -274.	bind
46019	1	11358	6	NULL	NULL	0	NULL	C-IIIJ1	NULL		bind	NULL					NULL			regulatory element J	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_222_s_26	9012660	A new activity designated C-IIIJ1 binds to the regulatory element J, and a minor activity as well as HNF-4 binds to the regulatory element I. 5 8  Finally, the proximal apoA-IV promoter consists of four regulatory elements located between nucleotides -22 and -274.	bind
46020	2	11358	6	NULL	NULL	0	NULL	HNF-4	NULL		bind	NULL					NULL			regulatory element I	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_222_s_26	9012660	A new activity designated C-IIIJ1 binds to the regulatory element J, and a minor activity as well as HNF-4 binds to the regulatory element I. 5 8  Finally, the proximal apoA-IV promoter consists of four regulatory elements located between nucleotides -22 and -274.	bind
46021	3	11358	6	NULL	NULL	0	NULL	apoA-IV	NULL	proximal	consists of	NULL			promoter		NULL			regulatory elements between nucleotides -22 and -274	NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_1_222_s_26	9012660	A new activity designated C-IIIJ1 binds to the regulatory element J, and a minor activity as well as HNF-4 binds to the regulatory element I. 5 8  Finally, the proximal apoA-IV promoter consists of four regulatory elements located between nucleotides -22 and -274.	bind
45539	1	11359	5	NULL	NULL	NULL	NULL	Ry	Chemical		bind					RyR1	GP				NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_69_2_532_s_145	16249374	A new and somewhat unexpected finding was that unlike XeC, its hydroxylated derivative XeD (9-OH XeC;  Fig. 3B), and related structures ArC and 7-OH-XeA (data not shown) enhanced [3]Ry binding to RyR1 with an EC50 value of 10.6  plus-or-minus  1.1 muM ( n = 6) for XeD, 7.5  plus-or-minus  0.9 muM for ArC ( n = 4), and 11.4  plus-or-minus  0.8 muM for 7-OH-XeA ( n = 4).	bind
45540	2	11359	5	NULL	NULL	NULL	NULL	XeC	Chemical		does not enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_69_2_532_s_145	16249374	A new and somewhat unexpected finding was that unlike XeC, its hydroxylated derivative XeD (9-OH XeC;  Fig. 3B), and related structures ArC and 7-OH-XeA (data not shown) enhanced [3]Ry binding to RyR1 with an EC50 value of 10.6  plus-or-minus  1.1 muM ( n = 6) for XeD, 7.5  plus-or-minus  0.9 muM for ArC ( n = 4), and 11.4  plus-or-minus  0.8 muM for 7-OH-XeA ( n = 4).	bind
45541	3	11359	5	NULL	NULL	NULL	NULL	9-OH XeC	Chemical		is hydroxylated derivative of					XeD	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_69_2_532_s_145	16249374	A new and somewhat unexpected finding was that unlike XeC, its hydroxylated derivative XeD (9-OH XeC;  Fig. 3B), and related structures ArC and 7-OH-XeA (data not shown) enhanced [3]Ry binding to RyR1 with an EC50 value of 10.6  plus-or-minus  1.1 muM ( n = 6) for XeD, 7.5  plus-or-minus  0.9 muM for ArC ( n = 4), and 11.4  plus-or-minus  0.8 muM for 7-OH-XeA ( n = 4).	bind
45542	4	11359	5	NULL	NULL	NULL	NULL	9-OH XeC	Chemical		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_69_2_532_s_145	16249374	A new and somewhat unexpected finding was that unlike XeC, its hydroxylated derivative XeD (9-OH XeC;  Fig. 3B), and related structures ArC and 7-OH-XeA (data not shown) enhanced [3]Ry binding to RyR1 with an EC50 value of 10.6  plus-or-minus  1.1 muM ( n = 6) for XeD, 7.5  plus-or-minus  0.9 muM for ArC ( n = 4), and 11.4  plus-or-minus  0.8 muM for 7-OH-XeA ( n = 4).	bind
45543	5	11359	5	NULL	NULL	NULL	NULL	ArC	Chemical		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_69_2_532_s_145	16249374	A new and somewhat unexpected finding was that unlike XeC, its hydroxylated derivative XeD (9-OH XeC;  Fig. 3B), and related structures ArC and 7-OH-XeA (data not shown) enhanced [3]Ry binding to RyR1 with an EC50 value of 10.6  plus-or-minus  1.1 muM ( n = 6) for XeD, 7.5  plus-or-minus  0.9 muM for ArC ( n = 4), and 11.4  plus-or-minus  0.8 muM for 7-OH-XeA ( n = 4).	bind
45544	6	11359	5	NULL	NULL	NULL	NULL	7-OH-XeA	Chemical		enhance					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_69_2_532_s_145	16249374	A new and somewhat unexpected finding was that unlike XeC, its hydroxylated derivative XeD (9-OH XeC;  Fig. 3B), and related structures ArC and 7-OH-XeA (data not shown) enhanced [3]Ry binding to RyR1 with an EC50 value of 10.6  plus-or-minus  1.1 muM ( n = 6) for XeD, 7.5  plus-or-minus  0.9 muM for ArC ( n = 4), and 11.4  plus-or-minus  0.8 muM for 7-OH-XeA ( n = 4).	bind
46022	1	11359	6	NULL	NULL	0	NULL	Ry	NULL		bind	NULL				RyR1	NULL				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_69_2_532_s_145	16249374	A new and somewhat unexpected finding was that unlike XeC, its hydroxylated derivative XeD (9-OH XeC;  Fig. 3B), and related structures ArC and 7-OH-XeA (data not shown) enhanced [3]Ry binding to RyR1 with an EC50 value of 10.6  plus-or-minus  1.1 muM ( n = 6) for XeD, 7.5  plus-or-minus  0.9 muM for ArC ( n = 4), and 11.4  plus-or-minus  0.8 muM for 7-OH-XeA ( n = 4).	bind
46023	2	11359	6	NULL	NULL	0	NULL	XeD	NULL		enhances	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_69_2_532_s_145	16249374	A new and somewhat unexpected finding was that unlike XeC, its hydroxylated derivative XeD (9-OH XeC;  Fig. 3B), and related structures ArC and 7-OH-XeA (data not shown) enhanced [3]Ry binding to RyR1 with an EC50 value of 10.6  plus-or-minus  1.1 muM ( n = 6) for XeD, 7.5  plus-or-minus  0.9 muM for ArC ( n = 4), and 11.4  plus-or-minus  0.8 muM for 7-OH-XeA ( n = 4).	bind
46024	3	11359	6	NULL	NULL	0	NULL	7-OH-XeA	NULL		enhances	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_69_2_532_s_145	16249374	A new and somewhat unexpected finding was that unlike XeC, its hydroxylated derivative XeD (9-OH XeC;  Fig. 3B), and related structures ArC and 7-OH-XeA (data not shown) enhanced [3]Ry binding to RyR1 with an EC50 value of 10.6  plus-or-minus  1.1 muM ( n = 6) for XeD, 7.5  plus-or-minus  0.9 muM for ArC ( n = 4), and 11.4  plus-or-minus  0.8 muM for 7-OH-XeA ( n = 4).	bind
46025	4	11359	6	NULL	NULL	0	NULL	XeC	NULL		does not enhance	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_69_2_532_s_145	16249374	A new and somewhat unexpected finding was that unlike XeC, its hydroxylated derivative XeD (9-OH XeC;  Fig. 3B), and related structures ArC and 7-OH-XeA (data not shown) enhanced [3]Ry binding to RyR1 with an EC50 value of 10.6  plus-or-minus  1.1 muM ( n = 6) for XeD, 7.5  plus-or-minus  0.9 muM for ArC ( n = 4), and 11.4  plus-or-minus  0.8 muM for 7-OH-XeA ( n = 4).	bind
51502	5	11359	6	10	NULL	0	NULL	ArC	NULL		enhance	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_69_2_532_s_145	16249374	A new and somewhat unexpected finding was that unlike XeC, its hydroxylated derivative XeD (9-OH XeC;  Fig. 3B), and related structures ArC and 7-OH-XeA (data not shown) enhanced [3]Ry binding to RyR1 with an EC50 value of 10.6  plus-or-minus  1.1 muM ( n = 6) for XeD, 7.5  plus-or-minus  0.9 muM for ArC ( n = 4), and 11.4  plus-or-minus  0.8 muM for 7-OH-XeA ( n = 4).	bind
51503	6	11359	6	10	NULL	0	NULL	9-OH XeC			is hydroxylated derivative of					XeD					NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_69_2_532_s_145	16249374	A new and somewhat unexpected finding was that unlike XeC, its hydroxylated derivative XeD (9-OH XeC;  Fig. 3B), and related structures ArC and 7-OH-XeA (data not shown) enhanced [3]Ry binding to RyR1 with an EC50 value of 10.6  plus-or-minus  1.1 muM ( n = 6) for XeD, 7.5  plus-or-minus  0.9 muM for ArC ( n = 4), and 11.4  plus-or-minus  0.8 muM for 7-OH-XeA ( n = 4).	bind
45545	1	11361	5	NULL	NULL	NULL	NULL	ATP	Chemical		bind					Ala	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_21_4134_s_225	15470502	A new ATP-binding mutant was constructed replacing Asn33 that chelates  Mg2+ and is essential for ATP binding with Ala ( Figure 3B).	bind
45546	2	11361	5	NULL	NULL	NULL	NULL	ATP-binding mutant \t	GP		chelates					Mg2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_21_4134_s_225	15470502	A new ATP-binding mutant was constructed replacing Asn33 that chelates  Mg2+ and is essential for ATP binding with Ala ( Figure 3B).	bind
45547	3	11361	5	NULL	NULL	NULL	NULL	Asn33	AminoAcid		is replaced in					ATP-binding mutant	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_21_4134_s_225	15470502	A new ATP-binding mutant was constructed replacing Asn33 that chelates  Mg2+ and is essential for ATP binding with Ala ( Figure 3B).	bind
45548	4	11361	5	NULL	NULL	NULL	NULL	statement 3	Process		is essential for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_21_4134_s_225	15470502	A new ATP-binding mutant was constructed replacing Asn33 that chelates  Mg2+ and is essential for ATP binding with Ala ( Figure 3B).	bind
46026	1	11361	6	10	NULL	0	NULL	ATP			bind					Ala					NULL		NULL	NULL	NULL	NULL	gw70_embo_23_21_4134_s_225	15470502	A new ATP-binding mutant was constructed replacing Asn33 that chelates  Mg2+ and is essential for ATP binding with Ala ( Figure 3B).	bind
46027	2	11361	6	NULL	NULL	0	NULL	ATP-binding mutant	NULL		is essential for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_23_21_4134_s_225	15470502	A new ATP-binding mutant was constructed replacing Asn33 that chelates  Mg2+ and is essential for ATP binding with Ala ( Figure 3B).	bind
46028	3	11361	6	NULL	NULL	0	NULL	ATP-binding mutant	NULL		chelates	NULL				Mg2+	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_23_21_4134_s_225	15470502	A new ATP-binding mutant was constructed replacing Asn33 that chelates  Mg2+ and is essential for ATP binding with Ala ( Figure 3B).	bind
51504	4	11361	6	10	NULL	0	NULL	Asn33	NULL		is replaced in	NULL				ATP-binding mutant	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_23_21_4134_s_225	15470502	A new ATP-binding mutant was constructed replacing Asn33 that chelates  Mg2+ and is essential for ATP binding with Ala ( Figure 3B).	bind
45549	1	11362	5	NULL	NULL	NULL	NULL	GLYT-1	GP		is a type of					glycine transporter	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_6128_s_22	12431995	A new C-terminal splice variant of the glycine transporter GLYT-1 bound to rho1 ( ), while the microtubule-associated protein 1B (MAP-1B) interacted with rho1 and rho2 and was co-localized with GABAC receptors in the retina ( ).	bind
45550	2	11362	5	NULL	NULL	NULL	NULL	GLYT-1	GP	splice variant of	bind			C-terminal		rho1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_6128_s_22	12431995	A new C-terminal splice variant of the glycine transporter GLYT-1 bound to rho1 ( ), while the microtubule-associated protein 1B (MAP-1B) interacted with rho1 and rho2 and was co-localized with GABAC receptors in the retina ( ).	bind
45551	3	11362	5	NULL	NULL	NULL	NULL	MAP-1B	GP		is					microtubule-associated protein 1B	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_6128_s_22	12431995	A new C-terminal splice variant of the glycine transporter GLYT-1 bound to rho1 ( ), while the microtubule-associated protein 1B (MAP-1B) interacted with rho1 and rho2 and was co-localized with GABAC receptors in the retina ( ).	bind
45552	4	11362	5	NULL	NULL	NULL	NULL	MAP-1B	GP		interacts with					rho1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_6128_s_22	12431995	A new C-terminal splice variant of the glycine transporter GLYT-1 bound to rho1 ( ), while the microtubule-associated protein 1B (MAP-1B) interacted with rho1 and rho2 and was co-localized with GABAC receptors in the retina ( ).	bind
45553	5	11362	5	NULL	NULL	NULL	NULL	MAP-1B	GP		interacts with					rho2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_6128_s_22	12431995	A new C-terminal splice variant of the glycine transporter GLYT-1 bound to rho1 ( ), while the microtubule-associated protein 1B (MAP-1B) interacted with rho1 and rho2 and was co-localized with GABAC receptors in the retina ( ).	bind
45554	6	11362	5	NULL	NULL	NULL	NULL	MAP-1B	GP		co-localizes with					GABAC receptors	GP				NULL	retina	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_6128_s_22	12431995	A new C-terminal splice variant of the glycine transporter GLYT-1 bound to rho1 ( ), while the microtubule-associated protein 1B (MAP-1B) interacted with rho1 and rho2 and was co-localized with GABAC receptors in the retina ( ).	bind
46029	1	11362	6	NULL	NULL	0	NULL	GLYT-1	NULL	splice variant	bind	NULL		C-terminal		rho1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_8_6128_s_22	12431995	A new C-terminal splice variant of the glycine transporter GLYT-1 bound to rho1 ( ), while the microtubule-associated protein 1B (MAP-1B) interacted with rho1 and rho2 and was co-localized with GABAC receptors in the retina ( ).	bind
46030	2	11362	6	10	NULL	0	NULL	MAP-1B			interacts with					rho1					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_6128_s_22	12431995	A new C-terminal splice variant of the glycine transporter GLYT-1 bound to rho1 ( ), while the microtubule-associated protein 1B (MAP-1B) interacted with rho1 and rho2 and was co-localized with GABAC receptors in the retina ( ).	bind
46031	3	11362	6	NULL	NULL	0	NULL	MAP-1B	NULL		interacts with	NULL				rho2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_8_6128_s_22	12431995	A new C-terminal splice variant of the glycine transporter GLYT-1 bound to rho1 ( ), while the microtubule-associated protein 1B (MAP-1B) interacted with rho1 and rho2 and was co-localized with GABAC receptors in the retina ( ).	bind
46032	4	11362	6	NULL	NULL	0	NULL	MAP-1B	NULL		is	NULL				microtubule-associated protein 1B	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_8_6128_s_22	12431995	A new C-terminal splice variant of the glycine transporter GLYT-1 bound to rho1 ( ), while the microtubule-associated protein 1B (MAP-1B) interacted with rho1 and rho2 and was co-localized with GABAC receptors in the retina ( ).	bind
46033	5	11362	6	10	NULL	0	NULL	MAP-1B	NULL		co-localized with	NULL				GABAC receptors	NULL				NULL	retina	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_6128_s_22	12431995	A new C-terminal splice variant of the glycine transporter GLYT-1 bound to rho1 ( ), while the microtubule-associated protein 1B (MAP-1B) interacted with rho1 and rho2 and was co-localized with GABAC receptors in the retina ( ).	bind
46034	6	11362	6	10	NULL	0	NULL	GLYT-1	NULL		is a type of	NULL				glycine transporter	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_8_6128_s_22	12431995	A new C-terminal splice variant of the glycine transporter GLYT-1 bound to rho1 ( ), while the microtubule-associated protein 1B (MAP-1B) interacted with rho1 and rho2 and was co-localized with GABAC receptors in the retina ( ).	bind
45555	1	11364	5	NULL	NULL	NULL	NULL	PR inhibitors	Chemical	symmetric	bind					HIV PR	GP				NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_4_725_s_147	11104817	A new direction was thus taken when it appeared that symmetric PR inhibitors could bind the HIV PR in an asymmetric fashion ( ,  ,  ).	bind
51505	2	11364	5	NULL	NULL	NULL	NULL	statement 1	Process		occurs in a					asymmetric fashion					NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_4_725_s_147	11104817	A new direction was thus taken when it appeared that symmetric PR inhibitors could bind the HIV PR in an asymmetric fashion ( ,  ,  ).	bind
46038	1	11364	6	10	NULL	0	NULL	PR inhibitors		symmetric	bind					HIV PR					NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_4_725_s_147	11104817	A new direction was thus taken when it appeared that symmetric PR inhibitors could bind the HIV PR in an asymmetric fashion ( ,  ,  ).	bind
46039	2	11364	6	NULL	NULL	0	NULL	statement 1	NULL		occurs in an	NULL				asymmetric fashion	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_64_4_725_s_147	11104817	A new direction was thus taken when it appeared that symmetric PR inhibitors could bind the HIV PR in an asymmetric fashion ( ,  ,  ).	bind
45556	1	11366	5	NULL	NULL	NULL	NULL	W600	Chemical		is					water molecule	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_24_16669_s_65	10358003	A new feature of the active site is a highly ordered (B = 21.9 Ang 2) water molecule (W600) bound to the O1G oxygen of the gamma-phosphate (Fig.  1 and Fig.  2 A).	bind
45557	2	11366	5	NULL	NULL	NULL	NULL	W600	Chemical		bind					O1G oxygen	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_24_16669_s_65	10358003	A new feature of the active site is a highly ordered (B = 21.9 Ang 2) water molecule (W600) bound to the O1G oxygen of the gamma-phosphate (Fig.  1 and Fig.  2 A).	bind
45558	3	11366	5	NULL	NULL	NULL	NULL	O1G oxygen	Chemical		is present in					gamma-phosphate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_24_16669_s_65	10358003	A new feature of the active site is a highly ordered (B = 21.9 Ang 2) water molecule (W600) bound to the O1G oxygen of the gamma-phosphate (Fig.  1 and Fig.  2 A).	bind
46040	1	11366	6	10	NULL	0	NULL	W600	NULL		bind	NULL				gamma-phosphate	NULL		O1G oxygen		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_24_16669_s_65	10358003	A new feature of the active site is a highly ordered (B = 21.9 Ang 2) water molecule (W600) bound to the O1G oxygen of the gamma-phosphate (Fig.  1 and Fig.  2 A).	bind
51506	2	11366	6	10	NULL	0	NULL	W600	NULL		is	NULL				water molecule	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_24_16669_s_65	10358003	A new feature of the active site is a highly ordered (B = 21.9 Ang 2) water molecule (W600) bound to the O1G oxygen of the gamma-phosphate (Fig.  1 and Fig.  2 A).	bind
45666	1	11370	5	NULL	NULL	NULL	NULL	O2	Chemical		bind		rapidly;;high affinity			heme	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_24_14100_s_144	9826660	A new round of catalysis then is initiated by O2 binding to heme (Eq.   3), which has been shown to occur very rapidly and with high affinity ( 27).	bind
45667	2	11370	5	NULL	NULL	NULL	NULL	statement 1	Process		initiates					catalysis	Process	new round of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_24_14100_s_144	9826660	A new round of catalysis then is initiated by O2 binding to heme (Eq.   3), which has been shown to occur very rapidly and with high affinity ( 27).	bind
46041	1	11370	6	10	NULL	0	NULL	O2	NULL		bind	NULL	rapidly;; high affinity			heme	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_24_14100_s_144	9826660	A new round of catalysis then is initiated by O2 binding to heme (Eq.   3), which has been shown to occur very rapidly and with high affinity ( 27).	bind
46042	2	11370	6	NULL	NULL	0	NULL	statement 1	NULL		initiates	NULL				catalysis	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_24_14100_s_144	9826660	A new round of catalysis then is initiated by O2 binding to heme (Eq.   3), which has been shown to occur very rapidly and with high affinity ( 27).	bind
45668	1	11371	5	NULL	NULL	NULL	NULL	colchicine	Chemical		bind					tubulin	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-med-chem_49_13_16789746_s_2	16789746	A new series of compounds in which the 2-amino-5-chlorophenyl ring of phenstatin  analogue 7 was replaced with a 2-amino-5-aryl thiophene was synthesized  and evaluated for antiproliferative activity and for inhibition of tubulin  polymerization and colchicine binding to tubulin.	bind
46043	1	11371	6	NULL	NULL	0	NULL	colchicine	NULL		bind	NULL				tubulin	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-med-chem_49_13_16789746_s_2	16789746	A new series of compounds in which the 2-amino-5-chlorophenyl ring of phenstatin  analogue 7 was replaced with a 2-amino-5-aryl thiophene was synthesized  and evaluated for antiproliferative activity and for inhibition of tubulin  polymerization and colchicine binding to tubulin.	bind
45669	1	11372	5	NULL	NULL	NULL	NULL	Nhp6	GP		bind					Gal4p	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_25_13732_s_143	11095729	A New Split-Ub-Based Screen Identifies Nhp6 as a Binding Partner of Gal4p and Tup1p.	bind
45670	2	11372	5	NULL	NULL	NULL	NULL	Nhp6	GP		bind					Tup1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_25_13732_s_143	11095729	A New Split-Ub-Based Screen Identifies Nhp6 as a Binding Partner of Gal4p and Tup1p.	bind
46044	1	11372	6	NULL	NULL	0	NULL	Nhp6	NULL		bind	NULL				Gal4p	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_25_13732_s_143	11095729	A New Split-Ub-Based Screen Identifies Nhp6 as a Binding Partner of Gal4p and Tup1p.	bind
46045	2	11372	6	NULL	NULL	0	NULL	Nhp6	NULL		bind	NULL				Tup1p	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_25_13732_s_143	11095729	A New Split-Ub-Based Screen Identifies Nhp6 as a Binding Partner of Gal4p and Tup1p.	bind
45671	1	11373	5	NULL	NULL	NULL	NULL				bind		specifically	cohesin domain		CipA	GP	Clostridium thermocellum	dockerin domain		NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_3_703_s_389	12533446	A new type of cohesin domain that specifically binds the dockerin domain of the  Clostridium thermocellum cellulosome integrating protein CipA.	bind
45672	2	11373	5	NULL	NULL	NULL	NULL	CipA	GP		is					cellulosome integrating protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_3_703_s_389	12533446	A new type of cohesin domain that specifically binds the dockerin domain of the  Clostridium thermocellum cellulosome integrating protein CipA.	bind
46046	1	11373	6	NULL	NULL	0	NULL	CipA	NULL	Clostridium thermocellum	bind	NULL	specifically	dockerin domain			NULL		cohesin domain		NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_3_703_s_389	12533446	A new type of cohesin domain that specifically binds the dockerin domain of the  Clostridium thermocellum cellulosome integrating protein CipA.	bind
46047	2	11373	6	10	NULL	0	NULL	CipA	NULL		is	NULL				cellulosome integrating protein	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_185_3_703_s_389	12533446	A new type of cohesin domain that specifically binds the dockerin domain of the  Clostridium thermocellum cellulosome integrating protein CipA.	bind
45673	1	11375	5	NULL	NULL	NULL	NULL	laccase	GP		bind					Ag surface	Chemical	thiol-coated			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_appl-spectrosc_60_7_16854262_s_3	16854262	A new, indirect way of monitoring laccase  bound to the thiol-coated Ag and Au surfaces is presented.	bind
45674	2	11375	5	NULL	NULL	NULL	NULL	laccase	GP		bind					Au surface	Chemical	thiol-coated			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_appl-spectrosc_60_7_16854262_s_3	16854262	A new, indirect way of monitoring laccase  bound to the thiol-coated Ag and Au surfaces is presented.	bind
46048	1	11375	6	NULL	NULL	0	NULL	laccase	NULL		bind	NULL				Ag surface	NULL	thiol-coated			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_appl-spectrosc_60_7_16854262_s_3	16854262	A new, indirect way of monitoring laccase  bound to the thiol-coated Ag and Au surfaces is presented.	bind
46049	2	11375	6	NULL	NULL	0	NULL	laccase	NULL		bind	NULL				Au surface	NULL	thiol-coated			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_appl-spectrosc_60_7_16854262_s_3	16854262	A new, indirect way of monitoring laccase  bound to the thiol-coated Ag and Au surfaces is presented.	bind
45675	1	11376	5	NULL	NULL	NULL	NULL	hGli2	GP		bind									TRE-2	NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_19_0_475_s_92	11244044	A newly identified protein, hGli2, binds to TRE-2 ( 51), and the binding of hGli2 to TRE-2 is essential for Tax-mediated  trans-activation of one copy of the 21-bp enhancer.	bind
45676	2	11376	5	NULL	NULL	NULL	NULL	Tax	GP		mediates							trans-activation of		21-bp enhancer	NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_19_0_475_s_92	11244044	A newly identified protein, hGli2, binds to TRE-2 ( 51), and the binding of hGli2 to TRE-2 is essential for Tax-mediated  trans-activation of one copy of the 21-bp enhancer.	bind
45678	3	11376	5	NULL	NULL	NULL	NULL	statement 1	Process		is essential for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_19_0_475_s_92	11244044	A newly identified protein, hGli2, binds to TRE-2 ( 51), and the binding of hGli2 to TRE-2 is essential for Tax-mediated  trans-activation of one copy of the 21-bp enhancer.	bind
46050	1	11376	6	10	NULL	0	NULL	hGli2	NULL		bind	NULL					NULL			TRE-2	NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_19_0_475_s_92	11244044	A newly identified protein, hGli2, binds to TRE-2 ( 51), and the binding of hGli2 to TRE-2 is essential for Tax-mediated  trans-activation of one copy of the 21-bp enhancer.	bind
46051	2	11376	6	10	NULL	0	NULL	Tax	NULL		mediates	NULL					NULL	transactivation of		21-bp enhancer	NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_19_0_475_s_92	11244044	A newly identified protein, hGli2, binds to TRE-2 ( 51), and the binding of hGli2 to TRE-2 is essential for Tax-mediated  trans-activation of one copy of the 21-bp enhancer.	bind
46052	3	11376	6	NULL	NULL	0	NULL	statement 1	NULL		is essential for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_19_0_475_s_92	11244044	A newly identified protein, hGli2, binds to TRE-2 ( 51), and the binding of hGli2 to TRE-2 is essential for Tax-mediated  trans-activation of one copy of the 21-bp enhancer.	bind
45680	1	11377	5	NULL	NULL	NULL	NULL	ACA	GP		is					agglutinin	GP	Amaranthus caudatus 			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_cancer-res_51_2_1985783_s_2	1985783	A newly isolated lectin, Amaranthus caudatus agglutinin (also called amaranthin  or ACA), which binds to the Thomsen-Friedenreich antigen (T-antigen) and  its sialylated variants, was used as a histochemical probe for proliferating  cells in sections of human colonic tissues.	bind
45681	2	11377	5	NULL	NULL	NULL	NULL	ACA	GP		is a type of					lectin	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_cancer-res_51_2_1985783_s_2	1985783	A newly isolated lectin, Amaranthus caudatus agglutinin (also called amaranthin  or ACA), which binds to the Thomsen-Friedenreich antigen (T-antigen) and  its sialylated variants, was used as a histochemical probe for proliferating  cells in sections of human colonic tissues.	bind
45682	3	11377	5	NULL	NULL	NULL	NULL	amaranthin	GP		is a synonym of					ACA	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_cancer-res_51_2_1985783_s_2	1985783	A newly isolated lectin, Amaranthus caudatus agglutinin (also called amaranthin  or ACA), which binds to the Thomsen-Friedenreich antigen (T-antigen) and  its sialylated variants, was used as a histochemical probe for proliferating  cells in sections of human colonic tissues.	bind
45683	4	11377	5	NULL	NULL	NULL	NULL	ACA	GP		bind					Thomsen-Friedenreich antigen	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_cancer-res_51_2_1985783_s_2	1985783	A newly isolated lectin, Amaranthus caudatus agglutinin (also called amaranthin  or ACA), which binds to the Thomsen-Friedenreich antigen (T-antigen) and  its sialylated variants, was used as a histochemical probe for proliferating  cells in sections of human colonic tissues.	bind
45684	5	11377	5	NULL	NULL	NULL	NULL	Thomsen-Friedenreich antigen	GP		is					T-antigen	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_cancer-res_51_2_1985783_s_2	1985783	A newly isolated lectin, Amaranthus caudatus agglutinin (also called amaranthin  or ACA), which binds to the Thomsen-Friedenreich antigen (T-antigen) and  its sialylated variants, was used as a histochemical probe for proliferating  cells in sections of human colonic tissues.	bind
45685	6	11377	5	NULL	NULL	NULL	NULL	ACA	GP		bind					Thomsen-Friedenreich antigen	GP	sialylated variants of			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_cancer-res_51_2_1985783_s_2	1985783	A newly isolated lectin, Amaranthus caudatus agglutinin (also called amaranthin  or ACA), which binds to the Thomsen-Friedenreich antigen (T-antigen) and  its sialylated variants, was used as a histochemical probe for proliferating  cells in sections of human colonic tissues.	bind
46117	1	11377	6	NULL	NULL	0	NULL	agglutinin	NULL		is	NULL				amaranthin	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_cancer-res_51_2_1985783_s_2	1985783	A newly isolated lectin, Amaranthus caudatus agglutinin (also called amaranthin  or ACA), which binds to the Thomsen-Friedenreich antigen (T-antigen) and  its sialylated variants, was used as a histochemical probe for proliferating  cells in sections of human colonic tissues.	bind
46118	2	11377	6	NULL	NULL	0	NULL	agglutinin	NULL		is	NULL				ACA	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_cancer-res_51_2_1985783_s_2	1985783	A newly isolated lectin, Amaranthus caudatus agglutinin (also called amaranthin  or ACA), which binds to the Thomsen-Friedenreich antigen (T-antigen) and  its sialylated variants, was used as a histochemical probe for proliferating  cells in sections of human colonic tissues.	bind
46119	3	11377	6	NULL	NULL	0	NULL	agglutinin	NULL		is a type of	NULL				lectin	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_cancer-res_51_2_1985783_s_2	1985783	A newly isolated lectin, Amaranthus caudatus agglutinin (also called amaranthin  or ACA), which binds to the Thomsen-Friedenreich antigen (T-antigen) and  its sialylated variants, was used as a histochemical probe for proliferating  cells in sections of human colonic tissues.	bind
46120	4	11377	6	NULL	NULL	0	NULL	agglutinin	NULL	Amaranthus caudatus	bind	NULL				T-antigen	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_cancer-res_51_2_1985783_s_2	1985783	A newly isolated lectin, Amaranthus caudatus agglutinin (also called amaranthin  or ACA), which binds to the Thomsen-Friedenreich antigen (T-antigen) and  its sialylated variants, was used as a histochemical probe for proliferating  cells in sections of human colonic tissues.	bind
46121	5	11377	6	NULL	NULL	0	NULL	T-antigen	NULL		is	NULL				Thomsen-Friedenreich antigen	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_cancer-res_51_2_1985783_s_2	1985783	A newly isolated lectin, Amaranthus caudatus agglutinin (also called amaranthin  or ACA), which binds to the Thomsen-Friedenreich antigen (T-antigen) and  its sialylated variants, was used as a histochemical probe for proliferating  cells in sections of human colonic tissues.	bind
46122	6	11377	6	NULL	NULL	0	NULL	agglutinin	NULL	Amaranthus caudatus	bind	NULL				T-antigen	NULL	sialyated			NULL		0	NULL	NULL	NULL	abs-batch0517-0529_cancer-res_51_2_1985783_s_2	1985783	A newly isolated lectin, Amaranthus caudatus agglutinin (also called amaranthin  or ACA), which binds to the Thomsen-Friedenreich antigen (T-antigen) and  its sialylated variants, was used as a histochemical probe for proliferating  cells in sections of human colonic tissues.	bind
45686	1	11380	5	NULL	NULL	NULL	NULL	RSK2	GP		is a type of					Ras-dependent protein kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_3_254_s_114	9662427	A NGF-inducible, Ras-dependent protein kinase, which was identified as RSK2, and catalyzes the phosphorylation of CREB (the cyclic AMP response element binding protein), was found to trigger this activation [ 22,   23].	bind
45687	2	11380	5	NULL	NULL	NULL	NULL	NGF	GP		induces					RSK2	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_3_254_s_114	9662427	A NGF-inducible, Ras-dependent protein kinase, which was identified as RSK2, and catalyzes the phosphorylation of CREB (the cyclic AMP response element binding protein), was found to trigger this activation [ 22,   23].	bind
45688	3	11380	5	NULL	NULL	NULL	NULL	RSK2	GP		catalyzes					CREB	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_3_254_s_114	9662427	A NGF-inducible, Ras-dependent protein kinase, which was identified as RSK2, and catalyzes the phosphorylation of CREB (the cyclic AMP response element binding protein), was found to trigger this activation [ 22,   23].	bind
45689	4	11380	5	NULL	NULL	NULL	NULL	CREB	GP		is					cyclic AMP response element binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_429_3_254_s_114	9662427	A NGF-inducible, Ras-dependent protein kinase, which was identified as RSK2, and catalyzes the phosphorylation of CREB (the cyclic AMP response element binding protein), was found to trigger this activation [ 22,   23].	bind
46053	1	11380	6	NULL	NULL	0	NULL	RSK2	NULL		catalyzes	NULL				CREB	NULL	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_febslett_429_3_254_s_114	9662427	A NGF-inducible, Ras-dependent protein kinase, which was identified as RSK2, and catalyzes the phosphorylation of CREB (the cyclic AMP response element binding protein), was found to trigger this activation [ 22,   23].	bind
46054	2	11380	6	NULL	NULL	0	NULL	RSK2	NULL		is a type of	NULL				Ras-dependent protein kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_429_3_254_s_114	9662427	A NGF-inducible, Ras-dependent protein kinase, which was identified as RSK2, and catalyzes the phosphorylation of CREB (the cyclic AMP response element binding protein), was found to trigger this activation [ 22,   23].	bind
46055	3	11380	6	NULL	NULL	0	NULL	NGF	NULL		induces	NULL				RSK2	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_429_3_254_s_114	9662427	A NGF-inducible, Ras-dependent protein kinase, which was identified as RSK2, and catalyzes the phosphorylation of CREB (the cyclic AMP response element binding protein), was found to trigger this activation [ 22,   23].	bind
46056	4	11380	6	NULL	NULL	0	NULL	CREB	NULL		is	NULL				cyclic AMP response element binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_429_3_254_s_114	9662427	A NGF-inducible, Ras-dependent protein kinase, which was identified as RSK2, and catalyzes the phosphorylation of CREB (the cyclic AMP response element binding protein), was found to trigger this activation [ 22,   23].	bind
45690	1	11381	5	NULL	NULL	NULL	NULL	junction peptide	AminoAcid	nonself	comprises of					ETV6 and AML1 	GP	residues of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_2_455_s_211	9664088	A nine  amino acid-long, nonself, junction peptide comprising four  ETV6 and five AML1 residues binds to HLA-A2.1 molecules  and induces in vitro CTL responses from both HLA-A2.1+  healthy donors and ALL-patients.	bind
45691	2	11381	5	NULL	NULL	NULL	NULL	statement 1			bind					HLA-A2.1 molecules	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_2_455_s_211	9664088	A nine  amino acid-long, nonself, junction peptide comprising four  ETV6 and five AML1 residues binds to HLA-A2.1 molecules  and induces in vitro CTL responses from both HLA-A2.1+  healthy donors and ALL-patients.	bind
45692	3	11381	5	NULL	NULL	NULL	NULL	statement 2	Process		induces					CTL responses	Process				NULL	in vitro in HLA-A2.1+ healthy donors	NULL	NULL	NULL	NULL	gw60_jclininvest_102_2_455_s_211	9664088	A nine  amino acid-long, nonself, junction peptide comprising four  ETV6 and five AML1 residues binds to HLA-A2.1 molecules  and induces in vitro CTL responses from both HLA-A2.1+  healthy donors and ALL-patients.	bind
45693	4	11381	5	NULL	NULL	NULL	NULL	statement 2	Process		induces					CTL responses	Process				NULL	in vitro in ALL-patients	NULL	NULL	NULL	NULL	gw60_jclininvest_102_2_455_s_211	9664088	A nine  amino acid-long, nonself, junction peptide comprising four  ETV6 and five AML1 residues binds to HLA-A2.1 molecules  and induces in vitro CTL responses from both HLA-A2.1+  healthy donors and ALL-patients.	bind
46127	1	11381	6	10	NULL	0	NULL	peptide			comprises of					 ETV6 and AML1		residues of			NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_102_2_455_s_211	9664088	A nine  amino acid-long, nonself, junction peptide comprising four  ETV6 and five AML1 residues binds to HLA-A2.1 molecules  and induces in vitro CTL responses from both HLA-A2.1+  healthy donors and ALL-patients.	bind
46128	2	11381	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				HLA-A2.1 molecules	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_102_2_455_s_211	9664088	A nine  amino acid-long, nonself, junction peptide comprising four  ETV6 and five AML1 residues binds to HLA-A2.1 molecules  and induces in vitro CTL responses from both HLA-A2.1+  healthy donors and ALL-patients.	bind
46129	3	11381	6	10	NULL	0	NULL	statement 2	NULL		induces	NULL				CTL responses	NULL				NULL	in vitro in HLA-A2.1+ healthy donors	NULL	NULL	NULL	NULL	gw60_jclininvest_102_2_455_s_211	9664088	A nine  amino acid-long, nonself, junction peptide comprising four  ETV6 and five AML1 residues binds to HLA-A2.1 molecules  and induces in vitro CTL responses from both HLA-A2.1+  healthy donors and ALL-patients.	bind
46130	4	11381	6	10	NULL	0	NULL	statement 2	NULL		induces	NULL				CTL responses	NULL				NULL	invitro in ALL-patients	NULL	NULL	NULL	NULL	gw60_jclininvest_102_2_455_s_211	9664088	A nine  amino acid-long, nonself, junction peptide comprising four  ETV6 and five AML1 residues binds to HLA-A2.1 molecules  and induces in vitro CTL responses from both HLA-A2.1+  healthy donors and ALL-patients.	bind
45694	2	11382	5	NULL	NULL	NULL	NULL	statement 1	AminoAcid		bind		strongly			HLA-A2 antigen	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_clin-cancer-res_7_11_11705846_s_4	11705846	A nine-amino acid peptide  derived from hTERT binds strongly to HLA-A2 antigen and elicits CTL responses  against a broad panel of hTERT+ tumors (but not hTERT+ hematopoietic progenitor  cells).	bind
45695	3	11382	5	NULL	NULL	NULL	NULL	statement 2	Process		elicits					CTL responses	Process				NULL	hTERT+ tumors	NULL	NULL	NULL	NULL	abs-batch0650-0679_clin-cancer-res_7_11_11705846_s_4	11705846	A nine-amino acid peptide  derived from hTERT binds strongly to HLA-A2 antigen and elicits CTL responses  against a broad panel of hTERT+ tumors (but not hTERT+ hematopoietic progenitor  cells).	bind
45696	4	11382	5	NULL	NULL	NULL	NULL	statement 2	Process		does not elicit					CTL responses	Process				NULL	hTERT+ hematopoietic progenitor cells	NULL	NULL	NULL	NULL	abs-batch0650-0679_clin-cancer-res_7_11_11705846_s_4	11705846	A nine-amino acid peptide  derived from hTERT binds strongly to HLA-A2 antigen and elicits CTL responses  against a broad panel of hTERT+ tumors (but not hTERT+ hematopoietic progenitor  cells).	bind
51508	1	11382	5	NULL	NULL	NULL	NULL	nine-amino acid peptide	AminoAcid		derived from					hTERT	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_clin-cancer-res_7_11_11705846_s_4	11705846	A nine-amino acid peptide  derived from hTERT binds strongly to HLA-A2 antigen and elicits CTL responses  against a broad panel of hTERT+ tumors (but not hTERT+ hematopoietic progenitor  cells).	bind
46057	1	11382	6	NULL	NULL	0	NULL	nine-amino acid peptide	NULL		is derived from	NULL				hTERT	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_clin-cancer-res_7_11_11705846_s_4	11705846	A nine-amino acid peptide  derived from hTERT binds strongly to HLA-A2 antigen and elicits CTL responses  against a broad panel of hTERT+ tumors (but not hTERT+ hematopoietic progenitor  cells).	bind
46058	2	11382	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL	strongly			HLA-A2 antigen	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_clin-cancer-res_7_11_11705846_s_4	11705846	A nine-amino acid peptide  derived from hTERT binds strongly to HLA-A2 antigen and elicits CTL responses  against a broad panel of hTERT+ tumors (but not hTERT+ hematopoietic progenitor  cells).	bind
46059	3	11382	6	10	NULL	0	NULL	statement 2	NULL		elicits	NULL				CTL responses	NULL				NULL	hTERT+ tumors	NULL	NULL	NULL	NULL	abs-batch0650-0679_clin-cancer-res_7_11_11705846_s_4	11705846	A nine-amino acid peptide  derived from hTERT binds strongly to HLA-A2 antigen and elicits CTL responses  against a broad panel of hTERT+ tumors (but not hTERT+ hematopoietic progenitor  cells).	bind
46060	4	11382	6	10	NULL	0	NULL	statement 2	NULL		does not elicit	NULL				CTL responses	NULL				NULL	hTERT+ hematopoietic progenitor cells	NULL	NULL	NULL	NULL	abs-batch0650-0679_clin-cancer-res_7_11_11705846_s_4	11705846	A nine-amino acid peptide  derived from hTERT binds strongly to HLA-A2 antigen and elicits CTL responses  against a broad panel of hTERT+ tumors (but not hTERT+ hematopoietic progenitor  cells).	bind
45697	1	11383	5	NULL	NULL	NULL	NULL	collagen	GP		bind					alpha2	GP		I-domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_44_31493_s_36	10531352	A nine-residue aspartate-containing peptide was obtained from the metalloproteinase that, when cyclized through the addition of terminal cysteines and oxidized to form a disulfide bond, was found to inhibit collagen binding to the alpha2 I-domain.	bind
45698	2	11383	5	NULL	NULL	NULL	NULL	aspartate-containing peptide	AminoAcid		is obtained from					metalloproteinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_44_31493_s_36	10531352	A nine-residue aspartate-containing peptide was obtained from the metalloproteinase that, when cyclized through the addition of terminal cysteines and oxidized to form a disulfide bond, was found to inhibit collagen binding to the alpha2 I-domain.	bind
45699	3	11383	5	NULL	NULL	NULL	NULL	statement 2	AminoAcid		is cyclized through					cysteines	AminoAcid	addition of;;terminal			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_44_31493_s_36	10531352	A nine-residue aspartate-containing peptide was obtained from the metalloproteinase that, when cyclized through the addition of terminal cysteines and oxidized to form a disulfide bond, was found to inhibit collagen binding to the alpha2 I-domain.	bind
45700	4	11383	5	NULL	NULL	NULL	NULL	statement 3	AminoAcid		undergoes					oxidation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_44_31493_s_36	10531352	A nine-residue aspartate-containing peptide was obtained from the metalloproteinase that, when cyclized through the addition of terminal cysteines and oxidized to form a disulfide bond, was found to inhibit collagen binding to the alpha2 I-domain.	bind
45701	5	11383	5	NULL	NULL	NULL	NULL	statement 4	AminoAcid		forms					disulfide bond					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_44_31493_s_36	10531352	A nine-residue aspartate-containing peptide was obtained from the metalloproteinase that, when cyclized through the addition of terminal cysteines and oxidized to form a disulfide bond, was found to inhibit collagen binding to the alpha2 I-domain.	bind
45702	6	11383	5	NULL	NULL	NULL	NULL	statement 5	Process		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_44_31493_s_36	10531352	A nine-residue aspartate-containing peptide was obtained from the metalloproteinase that, when cyclized through the addition of terminal cysteines and oxidized to form a disulfide bond, was found to inhibit collagen binding to the alpha2 I-domain.	bind
46061	1	11383	6	10	NULL	0	NULL	collagen			bind					alpha2			I-domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_44_31493_s_36	10531352	A nine-residue aspartate-containing peptide was obtained from the metalloproteinase that, when cyclized through the addition of terminal cysteines and oxidized to form a disulfide bond, was found to inhibit collagen binding to the alpha2 I-domain.	bind
46063	2	11383	6	NULL	NULL	0	NULL	aspartate-containing peptide	NULL		is derived from	NULL				metalloproteinase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_44_31493_s_36	10531352	A nine-residue aspartate-containing peptide was obtained from the metalloproteinase that, when cyclized through the addition of terminal cysteines and oxidized to form a disulfide bond, was found to inhibit collagen binding to the alpha2 I-domain.	bind
46064	6	11383	6	10	NULL	0	NULL	statement 5	NULL		inhibits	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_44_31493_s_36	10531352	A nine-residue aspartate-containing peptide was obtained from the metalloproteinase that, when cyclized through the addition of terminal cysteines and oxidized to form a disulfide bond, was found to inhibit collagen binding to the alpha2 I-domain.	bind
51509	3	11383	6	10	NULL	0	NULL	statement 2	NULL		is cyclized through	NULL				cysteines	NULL	addition of ;;terminal			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_44_31493_s_36	10531352	A nine-residue aspartate-containing peptide was obtained from the metalloproteinase that, when cyclized through the addition of terminal cysteines and oxidized to form a disulfide bond, was found to inhibit collagen binding to the alpha2 I-domain.	bind
51511	4	11383	6	10	NULL	0	NULL	statement 3	NULL		undergoes	NULL				oxidation	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_44_31493_s_36	10531352	A nine-residue aspartate-containing peptide was obtained from the metalloproteinase that, when cyclized through the addition of terminal cysteines and oxidized to form a disulfide bond, was found to inhibit collagen binding to the alpha2 I-domain.	bind
51512	5	11383	6	10	NULL	0	NULL	statement 4	NULL		forms	NULL				disulfide bond	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_44_31493_s_36	10531352	A nine-residue aspartate-containing peptide was obtained from the metalloproteinase that, when cyclized through the addition of terminal cysteines and oxidized to form a disulfide bond, was found to inhibit collagen binding to the alpha2 I-domain.	bind
45703	1	11384	5	NULL	NULL	NULL	NULL	LDL	GP	acetylated	bind					pBR322 plasmid DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_drug-deliv_10_3_12944143_s_6	12944143	A nitrocellulose  filter-binding assay revealed that acetylated LDL bound approximately  25% of the [3]-labeled pBR322 plasmid DNA bound by native LDL under the  same conditions.	bind
45704	2	11384	5	NULL	NULL	NULL	NULL	LDL	GP	native	bind					pBR322 plasmid DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_drug-deliv_10_3_12944143_s_6	12944143	A nitrocellulose  filter-binding assay revealed that acetylated LDL bound approximately  25% of the [3]-labeled pBR322 plasmid DNA bound by native LDL under the  same conditions.	bind
46065	1	11384	6	NULL	NULL	0	NULL	LDL	NULL	acetylated	bind	NULL				pBR322 plasmid DNA	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_drug-deliv_10_3_12944143_s_6	12944143	A nitrocellulose  filter-binding assay revealed that acetylated LDL bound approximately  25% of the [3]-labeled pBR322 plasmid DNA bound by native LDL under the  same conditions.	bind
46066	2	11384	6	NULL	NULL	0	NULL	LDL	NULL	native	bind	NULL				pBR322 plasmid DNA	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_drug-deliv_10_3_12944143_s_6	12944143	A nitrocellulose  filter-binding assay revealed that acetylated LDL bound approximately  25% of the [3]-labeled pBR322 plasmid DNA bound by native LDL under the  same conditions.	bind
45705	1	11385	5	NULL	NULL	NULL	NULL	coat protein	GP		bind					21 nucleotide RNA fragment	NucleicAcid	synthetic			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biomol-struct-dyn_1_2_6401118_s_3	6401118	A nitrocellulose filter retention assay is used  to demonstrate equimolar binding between the coat protein and a synthetic  21 nucleotide RNA fragment.	bind
46067	1	11385	6	10	NULL	0	NULL	coat protein	NULL		bind	NULL				21 nucleotide RNA fragment	NULL	synthetic 			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_j-biomol-struct-dyn_1_2_6401118_s_3	6401118	A nitrocellulose filter retention assay is used  to demonstrate equimolar binding between the coat protein and a synthetic  21 nucleotide RNA fragment.	bind
45706	1	11386	5	NULL	NULL	NULL	NULL	Chl	Chemical		bind					Chl aP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32174_s_182	8943272	A nitrogen-containing amino acid side chain in His, Asn, or Gln may act as the 5th ligand during the binding of Chl or Zn-phe to the Chl  aP ( 35).	bind
45707	2	11386	5	NULL	NULL	NULL	NULL	Zn-phe	Chemical		bind					Chl aP	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32174_s_182	8943272	A nitrogen-containing amino acid side chain in His, Asn, or Gln may act as the 5th ligand during the binding of Chl or Zn-phe to the Chl  aP ( 35).	bind
45708	3	11386	5	NULL	NULL	NULL	NULL	His	AminoAcid		acts as			nitrogen-containing amino acid side chain		statement 1	Process	ligand in			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32174_s_182	8943272	A nitrogen-containing amino acid side chain in His, Asn, or Gln may act as the 5th ligand during the binding of Chl or Zn-phe to the Chl  aP ( 35).	bind
45709	4	11386	5	NULL	NULL	NULL	NULL	His	AminoAcid		acts as			amino acid side chains		statement 2	Process	ligand in			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32174_s_182	8943272	A nitrogen-containing amino acid side chain in His, Asn, or Gln may act as the 5th ligand during the binding of Chl or Zn-phe to the Chl  aP ( 35).	bind
45710	5	11386	5	NULL	NULL	NULL	NULL	Asn	AminoAcid		acts as			nitrogen-containing amino acid side chain		statement 1	Process	ligand in			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32174_s_182	8943272	A nitrogen-containing amino acid side chain in His, Asn, or Gln may act as the 5th ligand during the binding of Chl or Zn-phe to the Chl  aP ( 35).	bind
45711	6	11386	5	NULL	NULL	NULL	NULL	Asn	AminoAcid		acts as			nitrogen-containing amino acid side chain		statement 2	Process	ligand in			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32174_s_182	8943272	A nitrogen-containing amino acid side chain in His, Asn, or Gln may act as the 5th ligand during the binding of Chl or Zn-phe to the Chl  aP ( 35).	bind
45712	7	11386	5	NULL	NULL	NULL	NULL	Gln	AminoAcid		acts as			nitrogen-containing amino acid side chain		statement 1	Process	ligand in			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32174_s_182	8943272	A nitrogen-containing amino acid side chain in His, Asn, or Gln may act as the 5th ligand during the binding of Chl or Zn-phe to the Chl  aP ( 35).	bind
45713	8	11386	5	NULL	NULL	NULL	NULL	Gln	AminoAcid		acts as			nitrogen-containing amino acid side chain		statement 2	Process	ligand in			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32174_s_182	8943272	A nitrogen-containing amino acid side chain in His, Asn, or Gln may act as the 5th ligand during the binding of Chl or Zn-phe to the Chl  aP ( 35).	bind
46068	1	11386	6	NULL	NULL	0	NULL	Chl	NULL		bind	NULL				Zn-phe	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32174_s_182	8943272	A nitrogen-containing amino acid side chain in His, Asn, or Gln may act as the 5th ligand during the binding of Chl or Zn-phe to the Chl  aP ( 35).	bind
46069	2	11386	6	NULL	NULL	0	NULL	Chl	NULL		bind	NULL				Chl aP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_50_32174_s_182	8943272	A nitrogen-containing amino acid side chain in His, Asn, or Gln may act as the 5th ligand during the binding of Chl or Zn-phe to the Chl  aP ( 35).	bind
52939	3	11386	6	10	NULL	0	NULL	His	NULL		acts as a ligand in	NULL		nitrogen-containing amino acid side chain		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_50_32174_s_182	8943272	A nitrogen-containing amino acid side chain in His, Asn, or Gln may act as the 5th ligand during the binding of Chl or Zn-phe to the Chl  aP ( 35).	bind
52949	4	11386	6	NULL	NULL	0	NULL	His	NULL		acts as a ligand in	NULL		nitrogen-containing amino acid side chain		statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_50_32174_s_182	8943272	A nitrogen-containing amino acid side chain in His, Asn, or Gln may act as the 5th ligand during the binding of Chl or Zn-phe to the Chl  aP ( 35).	bind
52950	5	11386	6	NULL	NULL	0	NULL	Asn	NULL		acts as a ligand in	NULL		nitrogen-containing amino acid side chain		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_50_32174_s_182	8943272	A nitrogen-containing amino acid side chain in His, Asn, or Gln may act as the 5th ligand during the binding of Chl or Zn-phe to the Chl  aP ( 35).	bind
52951	6	11386	6	NULL	NULL	0	NULL	Asn	NULL		acts as a ligand in	NULL		nitrogen-containing amino acid side chain		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_50_32174_s_182	8943272	A nitrogen-containing amino acid side chain in His, Asn, or Gln may act as the 5th ligand during the binding of Chl or Zn-phe to the Chl  aP ( 35).	bind
52952	7	11386	6	NULL	NULL	0	NULL	Gln	NULL		acts as a ligand in	NULL		nitrogen-containing amino acid side chain		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_50_32174_s_182	8943272	A nitrogen-containing amino acid side chain in His, Asn, or Gln may act as the 5th ligand during the binding of Chl or Zn-phe to the Chl  aP ( 35).	bind
52953	8	11386	6	NULL	NULL	0	NULL	Gln	NULL		acts as a ligand in	NULL		nitrogen-containing amino acid side chain		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_50_32174_s_182	8943272	A nitrogen-containing amino acid side chain in His, Asn, or Gln may act as the 5th ligand during the binding of Chl or Zn-phe to the Chl  aP ( 35).	bind
45714	1	11387	5	NULL	NULL	NULL	NULL	nod factor	Chemical	legume roots	bind					lectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_64_1_180_s_883	10704479	A nod factor binding lectin with apyrase activity from legume roots.	bind
45715	2	11387	5	NULL	NULL	NULL	NULL	statement 1	Process	legume roots	demonstrate					apyrase activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_64_1_180_s_883	10704479	A nod factor binding lectin with apyrase activity from legume roots.	bind
46070	1	11387	6	NULL	NULL	0	NULL	nod factor	NULL	legume roots	bind	NULL				lectin	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_64_1_180_s_883	10704479	A nod factor binding lectin with apyrase activity from legume roots.	bind
46071	2	11387	6	NULL	NULL	0	NULL	nod factor	NULL	legume roots	exhibits	NULL				apyrase activity	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_64_1_180_s_883	10704479	A nod factor binding lectin with apyrase activity from legume roots.	bind
45716	1	11388	5	NULL	NULL	NULL	NULL	CNQX	Chemical		is an antagonist of					non- N-methyl-D-aspartate ionotropic glutamate receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_2_429_s_101	10419564	A non- N-methyl-D-aspartate ionotropic glutamate receptor antagonist, CNQX, also displaced [3]MGA (30 nM) binding, with a  Ki value of 1.4 muM ( n = 3).	bind
45717	2	11388	5	NULL	NULL	NULL	NULL	CNQX	Chemical		displaces					MGA	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_2_429_s_101	10419564	A non- N-methyl-D-aspartate ionotropic glutamate receptor antagonist, CNQX, also displaced [3]MGA (30 nM) binding, with a  Ki value of 1.4 muM ( n = 3).	bind
46072	1	11388	6	10	NULL	0	NULL	CNQX	NULL		is an antagonist of	NULL				non- N-methyl-D-aspartate ionotropic glutamate receptor antagonist	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_56_2_429_s_101	10419564	A non- N-methyl-D-aspartate ionotropic glutamate receptor antagonist, CNQX, also displaced [3]MGA (30 nM) binding, with a  Ki value of 1.4 muM ( n = 3).	bind
46073	2	11388	6	NULL	NULL	0	NULL	CNQX	NULL		displaces	NULL				MGA	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_56_2_429_s_101	10419564	A non- N-methyl-D-aspartate ionotropic glutamate receptor antagonist, CNQX, also displaced [3]MGA (30 nM) binding, with a  Ki value of 1.4 muM ( n = 3).	bind
45719	1	11389	5	NULL	NULL	NULL	NULL	receptor	GP	non-native disulfide bond;;mutant	destabilize			C35A		receptor	GP	Ang II binding state of			NULL		NULL	NULL	NULL	NULL	gw60_febslett_484_2_133_s_182	11068047	A non-native disulfide bond thus formed in both C35A and C290A mutant receptors could destabilize the Ang II binding state of the receptor.	bind
45720	2	11389	5	NULL	NULL	NULL	NULL	receptor	GP	non-native disulfide bond;;mutant	destabilize			C290A		receptor	GP	Ang II binding state of			NULL		NULL	NULL	NULL	NULL	gw60_febslett_484_2_133_s_182	11068047	A non-native disulfide bond thus formed in both C35A and C290A mutant receptors could destabilize the Ang II binding state of the receptor.	bind
46074	1	11389	6	10	NULL	0	NULL	receptor	NULL	non-native disulfide bond;;mutant	destabilize	NULL		C35A		receptor	NULL	Ang II binding state of 			NULL		NULL	NULL	NULL	NULL	gw60_febslett_484_2_133_s_182	11068047	A non-native disulfide bond thus formed in both C35A and C290A mutant receptors could destabilize the Ang II binding state of the receptor.	bind
46075	2	11389	6	10	NULL	0	NULL	receptor	NULL	non-native disulfide bond;;mutant	destabilize	NULL		 C290A		receptor	NULL	Ang II binding state of			NULL		NULL	NULL	NULL	NULL	gw60_febslett_484_2_133_s_182	11068047	A non-native disulfide bond thus formed in both C35A and C290A mutant receptors could destabilize the Ang II binding state of the receptor.	bind
45721	1	11390	5	NULL	NULL	NULL	NULL	hamartin	GP	non-phosphorylatable;;alanine substitution mutant	does not interact with			T310		Plk1	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_hum-mol-genet_15_2_16339216_s_8	16339216	A non-phosphorylatable hamartin  mutant with an alanine substitution at residue T310 does not interact  with Plk1, whereas a non-phosphorylatable hamartin mutant at residue S332  in conjunction with alanine mutations at the other CDC2/cyclin B1 sites  (T417, S584 and T1047) does not impact hamartin binding to Plk1.	bind
45722	2	11390	5	NULL	NULL	NULL	NULL	hamartin	GP		bind					Plk1	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_hum-mol-genet_15_2_16339216_s_8	16339216	A non-phosphorylatable hamartin  mutant with an alanine substitution at residue T310 does not interact  with Plk1, whereas a non-phosphorylatable hamartin mutant at residue S332  in conjunction with alanine mutations at the other CDC2/cyclin B1 sites  (T417, S584 and T1047) does not impact hamartin binding to Plk1.	bind
45723	3	11390	5	NULL	NULL	NULL	NULL	hamartin	GP	non-phosphorylatable;;mutant	undergoes			S332				alanine mutations at	CDC2/cyclin B1 sites		NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_hum-mol-genet_15_2_16339216_s_8	16339216	A non-phosphorylatable hamartin  mutant with an alanine substitution at residue T310 does not interact  with Plk1, whereas a non-phosphorylatable hamartin mutant at residue S332  in conjunction with alanine mutations at the other CDC2/cyclin B1 sites  (T417, S584 and T1047) does not impact hamartin binding to Plk1.	bind
45724	4	11390	5	10	NULL	0	NULL		NULL	alanine mutations	constitute	NULL		CDC2/cyclin B1 sites			NULL		T417;;S584;;T1047		NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_hum-mol-genet_15_2_16339216_s_8	16339216	A non-phosphorylatable hamartin  mutant with an alanine substitution at residue T310 does not interact  with Plk1, whereas a non-phosphorylatable hamartin mutant at residue S332  in conjunction with alanine mutations at the other CDC2/cyclin B1 sites  (T417, S584 and T1047) does not impact hamartin binding to Plk1.	bind
45725	5	11390	5	NULL	NULL	NULL	NULL	statement 3	Process		does not impact					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_hum-mol-genet_15_2_16339216_s_8	16339216	A non-phosphorylatable hamartin  mutant with an alanine substitution at residue T310 does not interact  with Plk1, whereas a non-phosphorylatable hamartin mutant at residue S332  in conjunction with alanine mutations at the other CDC2/cyclin B1 sites  (T417, S584 and T1047) does not impact hamartin binding to Plk1.	bind
46131	1	11390	6	NULL	NULL	0	NULL	hamartin	NULL		is substituted by	NULL		alanine		hamartin	NULL		T310		NULL		0	NULL	NULL	NULL	abs-batch0600-0619_hum-mol-genet_15_2_16339216_s_8	16339216	A non-phosphorylatable hamartin  mutant with an alanine substitution at residue T310 does not interact  with Plk1, whereas a non-phosphorylatable hamartin mutant at residue S332  in conjunction with alanine mutations at the other CDC2/cyclin B1 sites  (T417, S584 and T1047) does not impact hamartin binding to Plk1.	bind
46132	2	11390	6	NULL	NULL	0	NULL	statement 1	NULL		does not bind	NULL				Plk1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_hum-mol-genet_15_2_16339216_s_8	16339216	A non-phosphorylatable hamartin  mutant with an alanine substitution at residue T310 does not interact  with Plk1, whereas a non-phosphorylatable hamartin mutant at residue S332  in conjunction with alanine mutations at the other CDC2/cyclin B1 sites  (T417, S584 and T1047) does not impact hamartin binding to Plk1.	bind
46133	3	11390	6	NULL	NULL	0	NULL	hamartin	NULL		bind	NULL				Plk1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_hum-mol-genet_15_2_16339216_s_8	16339216	A non-phosphorylatable hamartin  mutant with an alanine substitution at residue T310 does not interact  with Plk1, whereas a non-phosphorylatable hamartin mutant at residue S332  in conjunction with alanine mutations at the other CDC2/cyclin B1 sites  (T417, S584 and T1047) does not impact hamartin binding to Plk1.	bind
46134	4	11390	6	NULL	NULL	0	NULL	hamartin	NULL	mutant	acts in conjunction with	NULL		S332			NULL		T417;; S584;; T1047		NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_hum-mol-genet_15_2_16339216_s_8	16339216	A non-phosphorylatable hamartin  mutant with an alanine substitution at residue T310 does not interact  with Plk1, whereas a non-phosphorylatable hamartin mutant at residue S332  in conjunction with alanine mutations at the other CDC2/cyclin B1 sites  (T417, S584 and T1047) does not impact hamartin binding to Plk1.	bind
46135	5	11390	6	NULL	NULL	0	NULL	statement 4	NULL		does not impact	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_hum-mol-genet_15_2_16339216_s_8	16339216	A non-phosphorylatable hamartin  mutant with an alanine substitution at residue T310 does not interact  with Plk1, whereas a non-phosphorylatable hamartin mutant at residue S332  in conjunction with alanine mutations at the other CDC2/cyclin B1 sites  (T417, S584 and T1047) does not impact hamartin binding to Plk1.	bind
60572	1	11393	5	NULL	NULL	NULL	NULL	ss genomes \t	NucleicAcid		does not bind					protein A	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_12_3282_s_125	11406604	A non-specific binding of ss genomes or capsids to the protein A - Sepharose was, however, not detected (data not shown).	bind
60573	2	11393	5	NULL	NULL	NULL	NULL	capsids	GP		does not bind					protein A	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_12_3282_s_125	11406604	A non-specific binding of ss genomes or capsids to the protein A - Sepharose was, however, not detected (data not shown).	bind
46077	1	11393	6	NULL	NULL	0	NULL	ss genomes	NULL		does not bind	NULL				protein A	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_12_3282_s_125	11406604	A non-specific binding of ss genomes or capsids to the protein A - Sepharose was, however, not detected (data not shown).	bind
46078	2	11393	6	NULL	NULL	0	NULL	capsids	NULL		does not bind	NULL				protein A	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_20_12_3282_s_125	11406604	A non-specific binding of ss genomes or capsids to the protein A - Sepharose was, however, not detected (data not shown).	bind
45728	1	11394	5	NULL	NULL	NULL	NULL	F3	AminoAcid		bind					TR2	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_2_384_s_99	14521922	A non-specific protein (BSA,  1  g) failed to affect the binding of F3 to TR2 (data not shown).	bind
45729	2	11394	5	NULL	NULL	NULL	NULL	BSA	GP		does not affect					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_2_384_s_99	14521922	A non-specific protein (BSA,  1  g) failed to affect the binding of F3 to TR2 (data not shown).	bind
45730	3	11394	5	NULL	NULL	NULL	NULL	BSA	GP		is a type of					non-specific protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_2_384_s_99	14521922	A non-specific protein (BSA,  1  g) failed to affect the binding of F3 to TR2 (data not shown).	bind
46079	1	11394	6	NULL	NULL	0	NULL	F3	NULL		bind	NULL				TR2	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_2_384_s_99	14521922	A non-specific protein (BSA,  1  g) failed to affect the binding of F3 to TR2 (data not shown).	bind
46080	2	11394	6	10	NULL	0	NULL	BSA	NULL		does not affect	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_2_384_s_99	14521922	A non-specific protein (BSA,  1  g) failed to affect the binding of F3 to TR2 (data not shown).	bind
51513	3	11394	6	10	NULL	0	NULL	BSA	NULL		is a type of	NULL				non-specific protein	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_310_2_384_s_99	14521922	A non-specific protein (BSA,  1  g) failed to affect the binding of F3 to TR2 (data not shown).	bind
45731	1	11396	5	NULL	NULL	NULL	NULL	 LOS structures	Chemical	gonococcal	bind					Opa proteins	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_infect-immun_63_4_7890406_s_3	7890406	A noncompetitive inhibition assay used previously to determine  the carbohydrate structures recognized by the major hepatic asialoglycoprotein  receptor was modified to determine the gonococcal LOS structures that  bind Opa proteins (R. T. Lee, Targeted Diagn.	bind
46081	1	11396	6	NULL	NULL	0	NULL	LOS structures	NULL	gonococcal	bind	NULL				Opa proteins	NULL				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_infect-immun_63_4_7890406_s_3	7890406	A noncompetitive inhibition assay used previously to determine  the carbohydrate structures recognized by the major hepatic asialoglycoprotein  receptor was modified to determine the gonococcal LOS structures that  bind Opa proteins (R. T. Lee, Targeted Diagn.	bind
45732	1	11397	5	NULL	NULL	NULL	NULL	TSH	GP		bind		high affinity			TSHR	GP				NULL	293 human embryonal kidney cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33423_s_164	9837919	A nonessential role of galactose and sialic acid in function of TSHR shown in Lec8 cells is reminiscent of our previous finding ( 4,  40) of high affinity TSH binding to TSHR expressed in 293 human embryonal kidney cells.	bind
46082	1	11397	6	NULL	NULL	0	NULL	TSH	NULL		bind	NULL	high affinity			TSHR	NULL				NULL	293 human embryonal kidney cells	0	NULL	NULL	NULL	gw60_jbiolchem_273_50_33423_s_164	9837919	A nonessential role of galactose and sialic acid in function of TSHR shown in Lec8 cells is reminiscent of our previous finding ( 4,  40) of high affinity TSH binding to TSHR expressed in 293 human embryonal kidney cells.	bind
45733	1	11398	5	NULL	NULL	NULL	NULL	68-kDa alpha-L-fucosidase	GP	nonglycosylated	bind					sperm	Cell	Unio elongatulus;;plasma membrane of			NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_68_3_709_s_281	12604617	A nonglycosylated, 68-kDa alpha-L-fucosidase is bound to the mollusc bivalve  Unio elongatulus sperm plasma membrane and differs from a glycosylated 56-kDa form present in the seminal fluid.	bind
45734	2	11398	5	NULL	NULL	NULL	NULL	Unio elongatulus	Organism		is a type of	Organism				mollusc bivalve	Organism				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_68_3_709_s_281	12604617	A nonglycosylated, 68-kDa alpha-L-fucosidase is bound to the mollusc bivalve  Unio elongatulus sperm plasma membrane and differs from a glycosylated 56-kDa form present in the seminal fluid.	bind
45735	3	11398	5	NULL	NULL	NULL	NULL	56-kDa alpha-L-fucosidase		glycosylated	is present in					seminal fluid	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_68_3_709_s_281	12604617	A nonglycosylated, 68-kDa alpha-L-fucosidase is bound to the mollusc bivalve  Unio elongatulus sperm plasma membrane and differs from a glycosylated 56-kDa form present in the seminal fluid.	bind
45736	4	11398	5	NULL	NULL	NULL	NULL	statement 1	Process		differs from					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_68_3_709_s_281	12604617	A nonglycosylated, 68-kDa alpha-L-fucosidase is bound to the mollusc bivalve  Unio elongatulus sperm plasma membrane and differs from a glycosylated 56-kDa form present in the seminal fluid.	bind
46083	1	11398	6	NULL	NULL	0	NULL	alpha-L-fucosidase	NULL	nonglycoylated	bind	NULL				sperm plasma membrane	NULL	Unio elongatulus			NULL		0	NULL	NULL	NULL	gw60_biolreprod_68_3_709_s_281	12604617	A nonglycosylated, 68-kDa alpha-L-fucosidase is bound to the mollusc bivalve  Unio elongatulus sperm plasma membrane and differs from a glycosylated 56-kDa form present in the seminal fluid.	bind
46084	2	11398	6	10	NULL	0	NULL	Unio elongatulus	NULL		is a type of	NULL				mollusc bivalve	NULL				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_68_3_709_s_281	12604617	A nonglycosylated, 68-kDa alpha-L-fucosidase is bound to the mollusc bivalve  Unio elongatulus sperm plasma membrane and differs from a glycosylated 56-kDa form present in the seminal fluid.	bind
51514	3	11398	6	10	NULL	0	NULL	56-kDa alpha-L-fucosidase	NULL	glycosylated	is present in	NULL				seminal fluid	NULL				NULL		0	NULL	NULL	NULL	gw60_biolreprod_68_3_709_s_281	12604617	A nonglycosylated, 68-kDa alpha-L-fucosidase is bound to the mollusc bivalve  Unio elongatulus sperm plasma membrane and differs from a glycosylated 56-kDa form present in the seminal fluid.	bind
45737	1	11399	5	NULL	NULL	NULL	NULL	OFQ-R	GP		bind					G proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_51_5_816_s_10	9145920	A nonhydrolyzable GTP analog [guanosine-5 -(beta,gamma-imido)triphosphate] reduced the affinity of both OFQ ligands to their receptor without significant changes in the total binding capacity, indicating functional interactions between the OFQ-R and G proteins.	bind
45738	2	11399	5	NULL	NULL	NULL	NULL	OFQ ligands	GP		bind					receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_51_5_816_s_10	9145920	A nonhydrolyzable GTP analog [guanosine-5 -(beta,gamma-imido)triphosphate] reduced the affinity of both OFQ ligands to their receptor without significant changes in the total binding capacity, indicating functional interactions between the OFQ-R and G proteins.	bind
45739	3	11399	5	NULL	NULL	NULL	NULL	guanosine-5 -(beta,gamma-imido)triphosphate	Chemical		is an analog of					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_51_5_816_s_10	9145920	A nonhydrolyzable GTP analog [guanosine-5 -(beta,gamma-imido)triphosphate] reduced the affinity of both OFQ ligands to their receptor without significant changes in the total binding capacity, indicating functional interactions between the OFQ-R and G proteins.	bind
45740	4	11399	5	NULL	NULL	NULL	NULL	statement 3	Chemical		reduce					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_51_5_816_s_10	9145920	A nonhydrolyzable GTP analog [guanosine-5 -(beta,gamma-imido)triphosphate] reduced the affinity of both OFQ ligands to their receptor without significant changes in the total binding capacity, indicating functional interactions between the OFQ-R and G proteins.	bind
46085	1	11399	6	NULL	NULL	0	NULL	OFQ-R 	NULL		bind	NULL				G protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_51_5_816_s_10	9145920	A nonhydrolyzable GTP analog [guanosine-5 -(beta,gamma-imido)triphosphate] reduced the affinity of both OFQ ligands to their receptor without significant changes in the total binding capacity, indicating functional interactions between the OFQ-R and G proteins.	bind
46086	2	11399	6	10	NULL	0	NULL	guanosine-5 -(beta,gamma-imido)triphosphate	NULL		is a type of	NULL				GTP analog	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_51_5_816_s_10	9145920	A nonhydrolyzable GTP analog [guanosine-5 -(beta,gamma-imido)triphosphate] reduced the affinity of both OFQ ligands to their receptor without significant changes in the total binding capacity, indicating functional interactions between the OFQ-R and G proteins.	bind
46087	4	11399	6	10	NULL	0	NULL	statement 2	NULL		reduces	NULL				statement 3	NULL	affinity of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_51_5_816_s_10	9145920	A nonhydrolyzable GTP analog [guanosine-5 -(beta,gamma-imido)triphosphate] reduced the affinity of both OFQ ligands to their receptor without significant changes in the total binding capacity, indicating functional interactions between the OFQ-R and G proteins.	bind
51515	3	11399	6	10	NULL	0	NULL	OFQ ligands	NULL		bind	NULL				receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_51_5_816_s_10	9145920	A nonhydrolyzable GTP analog [guanosine-5 -(beta,gamma-imido)triphosphate] reduced the affinity of both OFQ ligands to their receptor without significant changes in the total binding capacity, indicating functional interactions between the OFQ-R and G proteins.	bind
45741	1	11400	5	NULL	NULL	NULL	NULL	Fl-APC	GP		bind					E-7 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_29_17491_s_176	8663475	A noninhibitory antibody (HPC2) was used to immobilize protein C. HPC2 is a calcium-independent, anti-human protein C IgG1 monoclonal antibody that also reacts with human APC. HPC2 does not inhibit Fl-APC binding to E-7 cells.	bind
45742	2	11400	5	NULL	NULL	NULL	NULL	HPC2	GP		does not inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_29_17491_s_176	8663475	A noninhibitory antibody (HPC2) was used to immobilize protein C. HPC2 is a calcium-independent, anti-human protein C IgG1 monoclonal antibody that also reacts with human APC. HPC2 does not inhibit Fl-APC binding to E-7 cells.	bind
45743	3	11400	5	NULL	NULL	NULL	NULL	HPC2	GP		is a type of					noninhibitory antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_29_17491_s_176	8663475	A noninhibitory antibody (HPC2) was used to immobilize protein C. HPC2 is a calcium-independent, anti-human protein C IgG1 monoclonal antibody that also reacts with human APC. HPC2 does not inhibit Fl-APC binding to E-7 cells.	bind
45744	4	11400	5	NULL	NULL	NULL	NULL	HPC2	GP		is a type of					anti-human protein C IgG1 monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_29_17491_s_176	8663475	A noninhibitory antibody (HPC2) was used to immobilize protein C. HPC2 is a calcium-independent, anti-human protein C IgG1 monoclonal antibody that also reacts with human APC. HPC2 does not inhibit Fl-APC binding to E-7 cells.	bind
45746	5	11400	5	NULL	NULL	NULL	NULL	HPC2	GP		is independent of					calcium	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_29_17491_s_176	8663475	A noninhibitory antibody (HPC2) was used to immobilize protein C. HPC2 is a calcium-independent, anti-human protein C IgG1 monoclonal antibody that also reacts with human APC. HPC2 does not inhibit Fl-APC binding to E-7 cells.	bind
45747	6	11400	5	NULL	NULL	NULL	NULL	HPC2	GP		reacts with					APC	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_29_17491_s_176	8663475	A noninhibitory antibody (HPC2) was used to immobilize protein C. HPC2 is a calcium-independent, anti-human protein C IgG1 monoclonal antibody that also reacts with human APC. HPC2 does not inhibit Fl-APC binding to E-7 cells.	bind
54087	7	11400	5	NULL	NULL	NULL	NULL	HPC2	GP		immobilize					protein C	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_29_17491_s_176	8663475	A noninhibitory antibody (HPC2) was used to immobilize protein C. HPC2 is a calcium-independent, anti-human protein C IgG1 monoclonal antibody that also reacts with human APC. HPC2 does not inhibit Fl-APC binding to E-7 cells.	bind
46088	1	11400	6	NULL	NULL	0	NULL	Fl-APC	NULL		bind	NULL				E-7 cells	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_29_17491_s_176	8663475	A noninhibitory antibody (HPC2) was used to immobilize protein C. HPC2 is a calcium-independent, anti-human protein C IgG1 monoclonal antibody that also reacts with human APC. HPC2 does not inhibit Fl-APC binding to E-7 cells.	bind
46089	2	11400	6	NULL	NULL	0	NULL	HPC2	NULL		does not inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_29_17491_s_176	8663475	A noninhibitory antibody (HPC2) was used to immobilize protein C. HPC2 is a calcium-independent, anti-human protein C IgG1 monoclonal antibody that also reacts with human APC. HPC2 does not inhibit Fl-APC binding to E-7 cells.	bind
46090	3	11400	6	NULL	NULL	0	NULL	HPC2	NULL		immobilize	NULL				protein C	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_29_17491_s_176	8663475	A noninhibitory antibody (HPC2) was used to immobilize protein C. HPC2 is a calcium-independent, anti-human protein C IgG1 monoclonal antibody that also reacts with human APC. HPC2 does not inhibit Fl-APC binding to E-7 cells.	bind
46091	4	11400	6	NULL	NULL	0	NULL	HPC2	NULL		is a type of	NULL				anti-human protein C IgG1 monoclonal antibody	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_29_17491_s_176	8663475	A noninhibitory antibody (HPC2) was used to immobilize protein C. HPC2 is a calcium-independent, anti-human protein C IgG1 monoclonal antibody that also reacts with human APC. HPC2 does not inhibit Fl-APC binding to E-7 cells.	bind
46092	5	11400	6	NULL	NULL	0	NULL	HPC2	NULL		is independent of	NULL				calcium	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_29_17491_s_176	8663475	A noninhibitory antibody (HPC2) was used to immobilize protein C. HPC2 is a calcium-independent, anti-human protein C IgG1 monoclonal antibody that also reacts with human APC. HPC2 does not inhibit Fl-APC binding to E-7 cells.	bind
51516	6	11400	6	10	NULL	0	NULL	HPC2	NULL		reacts with	NULL				APC	NULL	human			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_29_17491_s_176	8663475	A noninhibitory antibody (HPC2) was used to immobilize protein C. HPC2 is a calcium-independent, anti-human protein C IgG1 monoclonal antibody that also reacts with human APC. HPC2 does not inhibit Fl-APC binding to E-7 cells.	bind
51517	7	11400	6	10	NULL	0	NULL	HPC2	NULL		is a type of	NULL				noninhibitory antibody	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_29_17491_s_176	8663475	A noninhibitory antibody (HPC2) was used to immobilize protein C. HPC2 is a calcium-independent, anti-human protein C IgG1 monoclonal antibody that also reacts with human APC. HPC2 does not inhibit Fl-APC binding to E-7 cells.	bind
50823	1	11401	5	NULL	NULL	NULL	NULL	Nct1	NucleicAcid		is a type of					Nonprotein-Coding RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_73_4_840_s_119	15987823	A Nonprotein-Coding RNA (Nct1) Binds TSN	bind
50824	2	11401	5	NULL	NULL	NULL	NULL	Nct1	NucleicAcid		bind					TSN	GP				NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_73_4_840_s_119	15987823	A Nonprotein-Coding RNA (Nct1) Binds TSN	bind
47384	1	11401	6	NULL	NULL	0	NULL	Nct1	NULL		bind	NULL				TSN	NULL				NULL		0	NULL	NULL	NULL	gw70_biolreprod_73_4_840_s_119	15987823	A Nonprotein-Coding RNA (Nct1) Binds TSN	bind
47385	2	11401	6	10	NULL	0	NULL	Nct1			is a type of					Nonprotein-Coding RNA					NULL		NULL	NULL	NULL	NULL	gw70_biolreprod_73_4_840_s_119	15987823	A Nonprotein-Coding RNA (Nct1) Binds TSN	bind
50825	1	11403	5	NULL	NULL	NULL	NULL	Hm	Chemical		bind		high-affinity			P. gingivalis cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2528_s_291	12670977	A notable exception is the blocking of high-affinity Hm binding to  P. gingivalis cells by competition with PPIX ( ), indicating that in this case an alternative to the general mechanism is operative and a significant fraction of heme acquisition must be mediated by a process which can capture nonmetal porphyrins.	bind
50826	2	11403	5	NULL	NULL	NULL	NULL	PPIX	Chemical		bind					P. gingivalis cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2528_s_291	12670977	A notable exception is the blocking of high-affinity Hm binding to  P. gingivalis cells by competition with PPIX ( ), indicating that in this case an alternative to the general mechanism is operative and a significant fraction of heme acquisition must be mediated by a process which can capture nonmetal porphyrins.	bind
50827	3	11403	5	NULL	NULL	NULL	NULL	statement 1	Process		competes with					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2528_s_291	12670977	A notable exception is the blocking of high-affinity Hm binding to  P. gingivalis cells by competition with PPIX ( ), indicating that in this case an alternative to the general mechanism is operative and a significant fraction of heme acquisition must be mediated by a process which can capture nonmetal porphyrins.	bind
50828	4	11403	5	NULL	NULL	NULL	NULL	statement 2	Process		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2528_s_291	12670977	A notable exception is the blocking of high-affinity Hm binding to  P. gingivalis cells by competition with PPIX ( ), indicating that in this case an alternative to the general mechanism is operative and a significant fraction of heme acquisition must be mediated by a process which can capture nonmetal porphyrins.	bind
47393	1	11403	6	10	NULL	0	NULL	Hm			bind		high-affinity			P. gingivalis cells					NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2528_s_291	12670977	A notable exception is the blocking of high-affinity Hm binding to  P. gingivalis cells by competition with PPIX ( ), indicating that in this case an alternative to the general mechanism is operative and a significant fraction of heme acquisition must be mediated by a process which can capture nonmetal porphyrins.	bind
47394	2	11403	6	NULL	NULL	0	NULL	PPIX	NULL		bind	NULL				P. gingivalis cells	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_8_2528_s_291	12670977	A notable exception is the blocking of high-affinity Hm binding to  P. gingivalis cells by competition with PPIX ( ), indicating that in this case an alternative to the general mechanism is operative and a significant fraction of heme acquisition must be mediated by a process which can capture nonmetal porphyrins.	bind
47395	3	11403	6	NULL	NULL	0	NULL	statement 1	NULL		competes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_8_2528_s_291	12670977	A notable exception is the blocking of high-affinity Hm binding to  P. gingivalis cells by competition with PPIX ( ), indicating that in this case an alternative to the general mechanism is operative and a significant fraction of heme acquisition must be mediated by a process which can capture nonmetal porphyrins.	bind
54088	4	11403	6	10	NULL	0	NULL	statement 2			blocks					statement 1					NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_8_2528_s_291	12670977	A notable exception is the blocking of high-affinity Hm binding to  P. gingivalis cells by competition with PPIX ( ), indicating that in this case an alternative to the general mechanism is operative and a significant fraction of heme acquisition must be mediated by a process which can capture nonmetal porphyrins.	bind
50829	1	11405	5	NULL	NULL	NULL	NULL	Ag+	Chemical		acts as					SR Ca2+-releasing agent	Chemical	potent			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_7069_s_100	9054399	A notable exception is the effect of Ag+, which acts as a potent SR Ca2+-releasing agent at micromolar concentrations ( 4,  5), but decreases ryanodine binding by rapidly displacing bound ryanodine from its receptor ( 25).	bind
50830	2	11405	5	NULL	NULL	NULL	NULL	ryanodine	Chemical		bind					ryanodine receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_7069_s_100	9054399	A notable exception is the effect of Ag+, which acts as a potent SR Ca2+-releasing agent at micromolar concentrations ( 4,  5), but decreases ryanodine binding by rapidly displacing bound ryanodine from its receptor ( 25).	bind
50831	3	11405	5	NULL	NULL	NULL	NULL	ryanodine	Chemical		displaced from		rapidly			ryanodine receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_7069_s_100	9054399	A notable exception is the effect of Ag+, which acts as a potent SR Ca2+-releasing agent at micromolar concentrations ( 4,  5), but decreases ryanodine binding by rapidly displacing bound ryanodine from its receptor ( 25).	bind
50832	4	11405	5	NULL	NULL	NULL	NULL	Ag+	Chemical		decreases					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_7069_s_100	9054399	A notable exception is the effect of Ag+, which acts as a potent SR Ca2+-releasing agent at micromolar concentrations ( 4,  5), but decreases ryanodine binding by rapidly displacing bound ryanodine from its receptor ( 25).	bind
54091	5	11405	5	NULL	NULL	NULL	NULL	Ag+	Chemical		mediates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_11_7069_s_100	9054399	A notable exception is the effect of Ag+, which acts as a potent SR Ca2+-releasing agent at micromolar concentrations ( 4,  5), but decreases ryanodine binding by rapidly displacing bound ryanodine from its receptor ( 25).	bind
47414	1	11405	6	NULL	NULL	0	NULL	Ag+	NULL		acts as a 	NULL				SR Ca2+-releasing agent	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_11_7069_s_100	9054399	A notable exception is the effect of Ag+, which acts as a potent SR Ca2+-releasing agent at micromolar concentrations ( 4,  5), but decreases ryanodine binding by rapidly displacing bound ryanodine from its receptor ( 25).	bind
47415	2	11405	6	NULL	NULL	0	NULL	ryanodine	NULL		bind	NULL				ryanodine receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_11_7069_s_100	9054399	A notable exception is the effect of Ag+, which acts as a potent SR Ca2+-releasing agent at micromolar concentrations ( 4,  5), but decreases ryanodine binding by rapidly displacing bound ryanodine from its receptor ( 25).	bind
47417	3	11405	6	NULL	NULL	0	NULL	Ag+	NULL		decreases	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_11_7069_s_100	9054399	A notable exception is the effect of Ag+, which acts as a potent SR Ca2+-releasing agent at micromolar concentrations ( 4,  5), but decreases ryanodine binding by rapidly displacing bound ryanodine from its receptor ( 25).	bind
54089	4	11405	6	10	NULL	0	NULL	ryanodine			displaced from		rapidly			ryanodine receptor					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_11_7069_s_100	9054399	A notable exception is the effect of Ag+, which acts as a potent SR Ca2+-releasing agent at micromolar concentrations ( 4,  5), but decreases ryanodine binding by rapidly displacing bound ryanodine from its receptor ( 25).	bind
54090	5	11405	6	10	NULL	0	NULL	Ag+			mediates					statement 4					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_11_7069_s_100	9054399	A notable exception is the effect of Ag+, which acts as a potent SR Ca2+-releasing agent at micromolar concentrations ( 4,  5), but decreases ryanodine binding by rapidly displacing bound ryanodine from its receptor ( 25).	bind
50833	1	11406	5	NULL	NULL	NULL	NULL	vitronectin	GP		bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1545_1_289_s_4	11342054	A notable interaction is the binding of vitronectin to heparin, inhibiting its characteristic rate enhancement on the thrombin/antithrombin reaction [  1.	bind
50834	2	11406	5	NULL	NULL	NULL	NULL	thrombin	GP		bind					antithrombin	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1545_1_289_s_4	11342054	A notable interaction is the binding of vitronectin to heparin, inhibiting its characteristic rate enhancement on the thrombin/antithrombin reaction [  1.	bind
47419	1	11406	6	NULL	NULL	0	NULL	vitronectin	NULL		bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1545_1_289_s_4	11342054	A notable interaction is the binding of vitronectin to heparin, inhibiting its characteristic rate enhancement on the thrombin/antithrombin reaction [  1.	bind
47422	2	11406	6	NULL	NULL	0	NULL	thrombin	NULL		bind	NULL				antithrombin	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1545_1_289_s_4	11342054	A notable interaction is the binding of vitronectin to heparin, inhibiting its characteristic rate enhancement on the thrombin/antithrombin reaction [  1.	bind
50835	1	11407	5	NULL	NULL	NULL	NULL	u-PA 	GP		bind					VLDL-R	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20855_s_241	7657671	A noteworthy  difference was observed with monoclonal anti-PAI-1 antibody from  hybridoma clone 2, which markedly stimulated binding of u-PA PAI-1  to VLDL-R but inhibited its binding alpha MR/LRP  alpha-chain.	bind
50836	2	11407	5	NULL	NULL	NULL	NULL	u-PA	GP		bind					alpha MR/LRP	GP		alpha-chain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20855_s_241	7657671	A noteworthy  difference was observed with monoclonal anti-PAI-1 antibody from  hybridoma clone 2, which markedly stimulated binding of u-PA PAI-1  to VLDL-R but inhibited its binding alpha MR/LRP  alpha-chain.	bind
50837	3	11407	5	NULL	NULL	NULL	NULL	monoclonal anti-PAI-1 antibody	GP		stimulates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20855_s_241	7657671	A noteworthy  difference was observed with monoclonal anti-PAI-1 antibody from  hybridoma clone 2, which markedly stimulated binding of u-PA PAI-1  to VLDL-R but inhibited its binding alpha MR/LRP  alpha-chain.	bind
50838	4	11407	5	NULL	NULL	NULL	NULL	monoclonal anti-PAI-1 antibody	GP		inhibit					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20855_s_241	7657671	A noteworthy  difference was observed with monoclonal anti-PAI-1 antibody from  hybridoma clone 2, which markedly stimulated binding of u-PA PAI-1  to VLDL-R but inhibited its binding alpha MR/LRP  alpha-chain.	bind
54092	5	11407	5	NULL	NULL	NULL	NULL	PAI-1	GP		bind					VLDL-R	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20855_s_241	7657671	A noteworthy  difference was observed with monoclonal anti-PAI-1 antibody from  hybridoma clone 2, which markedly stimulated binding of u-PA PAI-1  to VLDL-R but inhibited its binding alpha MR/LRP  alpha-chain.	bind
54093	6	11407	5	NULL	NULL	NULL	NULL	PAI-1	GP		bind					alpha MR/LRP	GP		alpha-chain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20855_s_241	7657671	A noteworthy  difference was observed with monoclonal anti-PAI-1 antibody from  hybridoma clone 2, which markedly stimulated binding of u-PA PAI-1  to VLDL-R but inhibited its binding alpha MR/LRP  alpha-chain.	bind
54094	7	11407	5	NULL	NULL	NULL	NULL	monoclonal anti-PAI-1 antibody	GP		stimulate					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20855_s_241	7657671	A noteworthy  difference was observed with monoclonal anti-PAI-1 antibody from  hybridoma clone 2, which markedly stimulated binding of u-PA PAI-1  to VLDL-R but inhibited its binding alpha MR/LRP  alpha-chain.	bind
54095	8	11407	5	NULL	NULL	NULL	NULL	monoclonal anti-PAI-1 antibody	GP		inhibit					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20855_s_241	7657671	A noteworthy  difference was observed with monoclonal anti-PAI-1 antibody from  hybridoma clone 2, which markedly stimulated binding of u-PA PAI-1  to VLDL-R but inhibited its binding alpha MR/LRP  alpha-chain.	bind
47805	1	11407	6	NULL	NULL	0	NULL	u-PA	NULL		bind	NULL				VLDL-R	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20855_s_241	7657671	A noteworthy  difference was observed with monoclonal anti-PAI-1 antibody from  hybridoma clone 2, which markedly stimulated binding of u-PA PAI-1  to VLDL-R but inhibited its binding alpha MR/LRP  alpha-chain.	bind
47806	2	11407	6	NULL	NULL	0	NULL	PAI-1	NULL		bind	NULL				VLDL-R	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20855_s_241	7657671	A noteworthy  difference was observed with monoclonal anti-PAI-1 antibody from  hybridoma clone 2, which markedly stimulated binding of u-PA PAI-1  to VLDL-R but inhibited its binding alpha MR/LRP  alpha-chain.	bind
47807	3	11407	6	10	NULL	0	NULL	monoclonal anti-PAI-1 antibody			stimulates					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20855_s_241	7657671	A noteworthy  difference was observed with monoclonal anti-PAI-1 antibody from  hybridoma clone 2, which markedly stimulated binding of u-PA PAI-1  to VLDL-R but inhibited its binding alpha MR/LRP  alpha-chain.	bind
47808	4	11407	6	10	NULL	0	NULL	monoclonal anti-PAI-1 antibody			stimulates					statement 2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20855_s_241	7657671	A noteworthy  difference was observed with monoclonal anti-PAI-1 antibody from  hybridoma clone 2, which markedly stimulated binding of u-PA PAI-1  to VLDL-R but inhibited its binding alpha MR/LRP  alpha-chain.	bind
47809	5	11407	6	NULL	NULL	0	NULL	u-PA	NULL		bind	NULL				MR/LRP	NULL		alpha chain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20855_s_241	7657671	A noteworthy  difference was observed with monoclonal anti-PAI-1 antibody from  hybridoma clone 2, which markedly stimulated binding of u-PA PAI-1  to VLDL-R but inhibited its binding alpha MR/LRP  alpha-chain.	bind
47810	6	11407	6	NULL	NULL	0	NULL	PAI-1	NULL		bind	NULL				MR/LRP	NULL		alpha chain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20855_s_241	7657671	A noteworthy  difference was observed with monoclonal anti-PAI-1 antibody from  hybridoma clone 2, which markedly stimulated binding of u-PA PAI-1  to VLDL-R but inhibited its binding alpha MR/LRP  alpha-chain.	bind
47811	7	11407	6	10	NULL	0	NULL	monoclonal anti-PAI-1 antibody			inhibits					statement 5					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20855_s_241	7657671	A noteworthy  difference was observed with monoclonal anti-PAI-1 antibody from  hybridoma clone 2, which markedly stimulated binding of u-PA PAI-1  to VLDL-R but inhibited its binding alpha MR/LRP  alpha-chain.	bind
47812	8	11407	6	10	NULL	0	NULL	monoclonal anti-PAI-1 antibody			inhibits					statement 6					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20855_s_241	7657671	A noteworthy  difference was observed with monoclonal anti-PAI-1 antibody from  hybridoma clone 2, which markedly stimulated binding of u-PA PAI-1  to VLDL-R but inhibited its binding alpha MR/LRP  alpha-chain.	bind
50839	1	11409	5	NULL	NULL	NULL	NULL	96-kDa aminopeptidase	GP		is localized on					epithelial cell membranes	CellComponent	Bombyx mori;;midgut			NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-biochem-(tokyo)_139_2_16452310_s_1	16452310	A Novel 96-kDa Aminopeptidase Localized on Epithelial Cell Membranes of Bombyx mori Midgut, Which Binds to Cry1Ac Toxin of Bacillus thuringiensis..	bind
50840	2	11409	5	NULL	NULL	NULL	NULL	96-kDa aminopeptidase	GP		bind					Cry1Ac toxin	GP	Bacillus thuringiensis			NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-biochem-(tokyo)_139_2_16452310_s_1	16452310	A Novel 96-kDa Aminopeptidase Localized on Epithelial Cell Membranes of Bombyx mori Midgut, Which Binds to Cry1Ac Toxin of Bacillus thuringiensis..	bind
47474	1	11409	6	NULL	NULL	0	NULL	96-kDa Aminopeptidase	NULL		is localized on	NULL				Epithelial Cell Membranes	NULL	Bombyx mori;; Midgut			NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-biochem-(tokyo)_139_2_16452310_s_1	16452310	A Novel 96-kDa Aminopeptidase Localized on Epithelial Cell Membranes of Bombyx mori Midgut, Which Binds to Cry1Ac Toxin of Bacillus thuringiensis..	bind
47475	2	11409	6	NULL	NULL	0	NULL	96-kDa Aminopeptidase	NULL		bind	NULL				Cry1Ac Toxin	NULL	Bacillus thuringiensis			NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-biochem-(tokyo)_139_2_16452310_s_1	16452310	A Novel 96-kDa Aminopeptidase Localized on Epithelial Cell Membranes of Bombyx mori Midgut, Which Binds to Cry1Ac Toxin of Bacillus thuringiensis..	bind
50841	1	11410	5	NULL	NULL	NULL	NULL	Anti-beta 1 Integrin	GP		is a type of					Monoclonal Antibody	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25570_s_316	7592728	A Novel Activating Anti-beta 1 Integrin Monoclonal Antibody Binds to the Cysteine-rich Repeats in the beta 1 Chain.	bind
50842	2	11410	5	NULL	NULL	NULL	NULL	Anti-beta 1 Integrin	GP		bind								Cysteine-rich Repeats in beta 1 Chain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_43_25570_s_316	7592728	A Novel Activating Anti-beta 1 Integrin Monoclonal Antibody Binds to the Cysteine-rich Repeats in the beta 1 Chain.	bind
47476	1	11410	6	NULL	NULL	0	NULL	Anti-beta 1 Integrin	NULL		is a type of	NULL				monoclonal antibody	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_43_25570_s_316	7592728	A Novel Activating Anti-beta 1 Integrin Monoclonal Antibody Binds to the Cysteine-rich Repeats in the beta 1 Chain.	bind
47477	2	11410	6	NULL	NULL	0	NULL	Anti-beta 1 Integrin	NULL		bind	NULL					NULL		Cysteine-rich Repeats in the beta 1 Chain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_43_25570_s_316	7592728	A Novel Activating Anti-beta 1 Integrin Monoclonal Antibody Binds to the Cysteine-rich Repeats in the beta 1 Chain.	bind
50843	1	11411	5	NULL	NULL	NULL	NULL	Kinase adapter 1	GP	Caenorhabditis elegans	bind		avidly			Protein kinase C3	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevneur_21_0_279_s_427	9530498	A Novel Adapter Protein Employs a Phosphotyrosine Binding Domain and Exceptionally Basic N-terminal Domains to Capture and Localize an Atypical Protein Kinase C. CHARACTERIZATION OF CAENORHABDITIS ELEGANS C KINASE ADAPTER 1, A PROTEIN THAT AVIDLY BINDS PROTEIN KINASE C3.	bind
50844	2	11411	5	NULL	NULL	NULL	NULL	Adapter protein	GP		employs								phosphotyrosine binding domain;;basic N-terminal domains		NULL		NULL	NULL	NULL	NULL	gw60_annrevneur_21_0_279_s_427	9530498	A Novel Adapter Protein Employs a Phosphotyrosine Binding Domain and Exceptionally Basic N-terminal Domains to Capture and Localize an Atypical Protein Kinase C. CHARACTERIZATION OF CAENORHABDITIS ELEGANS C KINASE ADAPTER 1, A PROTEIN THAT AVIDLY BINDS PROTEIN KINASE C3.	bind
50845	3	11411	5	NULL	NULL	NULL	NULL	statement 2	Process		is required for					protein kinase C 	GP	localization of			NULL		NULL	NULL	NULL	NULL	gw60_annrevneur_21_0_279_s_427	9530498	A Novel Adapter Protein Employs a Phosphotyrosine Binding Domain and Exceptionally Basic N-terminal Domains to Capture and Localize an Atypical Protein Kinase C. CHARACTERIZATION OF CAENORHABDITIS ELEGANS C KINASE ADAPTER 1, A PROTEIN THAT AVIDLY BINDS PROTEIN KINASE C3.	bind
47813	1	11411	6	NULL	NULL	0	NULL	Kinase Adaptor 1	NULL	Caenorhabditis elegans	bind	NULL	avidly			Protein kinase C3	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevneur_21_0_279_s_427	9530498	A Novel Adapter Protein Employs a Phosphotyrosine Binding Domain and Exceptionally Basic N-terminal Domains to Capture and Localize an Atypical Protein Kinase C. CHARACTERIZATION OF CAENORHABDITIS ELEGANS C KINASE ADAPTER 1, A PROTEIN THAT AVIDLY BINDS PROTEIN KINASE C3.	bind
47814	2	11411	6	10	NULL	0	NULL	Adapter protein			employs								Phosphotyrosine Binding Domain;; Basic N-terminal Domain		NULL		NULL	NULL	NULL	NULL	gw60_annrevneur_21_0_279_s_427	9530498	A Novel Adapter Protein Employs a Phosphotyrosine Binding Domain and Exceptionally Basic N-terminal Domains to Capture and Localize an Atypical Protein Kinase C. CHARACTERIZATION OF CAENORHABDITIS ELEGANS C KINASE ADAPTER 1, A PROTEIN THAT AVIDLY BINDS PROTEIN KINASE C3.	bind
47815	3	11411	6	NULL	NULL	0	NULL	statement 2	NULL		is required for	NULL				protein kinase C	NULL	localization of 			NULL		0	NULL	NULL	NULL	gw60_annrevneur_21_0_279_s_427	9530498	A Novel Adapter Protein Employs a Phosphotyrosine Binding Domain and Exceptionally Basic N-terminal Domains to Capture and Localize an Atypical Protein Kinase C. CHARACTERIZATION OF CAENORHABDITIS ELEGANS C KINASE ADAPTER 1, A PROTEIN THAT AVIDLY BINDS PROTEIN KINASE C3.	bind
50846	1	11412	5	NULL	NULL	NULL	NULL	N2'' - Mad2	GP		bind					Mad1	GP				NULL	kinetochores	NULL	NULL	NULL	NULL	gw70_cellbiol_173_2_153_s_91	16636141	A novel and important extension of DeAntoni et al. (2005) was that the kinetochore localization of fluorescently labeled recombinant Mad2 injected into Ptk cells depends on its ability to dimerize with N2'' - Mad2 already bound to Mad1 at the kinetochores.	bind
50847	2	11412	5	NULL	NULL	NULL	NULL	Mad2	GP	recombinant	is localized in					kinetochore	CellComponent				NULL	Ptk cells	NULL	NULL	NULL	NULL	gw70_cellbiol_173_2_153_s_91	16636141	A novel and important extension of DeAntoni et al. (2005) was that the kinetochore localization of fluorescently labeled recombinant Mad2 injected into Ptk cells depends on its ability to dimerize with N2'' - Mad2 already bound to Mad1 at the kinetochores.	bind
50848	3	11412	5	NULL	NULL	NULL	NULL	Mad2	GP	recombinant	dimerize with					statement 1	Process				NULL	Ptk cells	NULL	NULL	NULL	NULL	gw70_cellbiol_173_2_153_s_91	16636141	A novel and important extension of DeAntoni et al. (2005) was that the kinetochore localization of fluorescently labeled recombinant Mad2 injected into Ptk cells depends on its ability to dimerize with N2'' - Mad2 already bound to Mad1 at the kinetochores.	bind
50849	4	11412	5	NULL	NULL	NULL	NULL	statement 2	Process		depends on					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_173_2_153_s_91	16636141	A novel and important extension of DeAntoni et al. (2005) was that the kinetochore localization of fluorescently labeled recombinant Mad2 injected into Ptk cells depends on its ability to dimerize with N2'' - Mad2 already bound to Mad1 at the kinetochores.	bind
47478	1	11412	6	NULL	NULL	0	NULL	N2'' - Mad2	NULL		bind	NULL				Mad1	NULL				NULL	kinetochores	0	NULL	NULL	NULL	gw70_cellbiol_173_2_153_s_91	16636141	A novel and important extension of DeAntoni et al. (2005) was that the kinetochore localization of fluorescently labeled recombinant Mad2 injected into Ptk cells depends on its ability to dimerize with N2'' - Mad2 already bound to Mad1 at the kinetochores.	bind
47479	2	11412	6	10	NULL	0	NULL	Mad2		recombinant	dimerizes with					statement 1					NULL	Ptk cells	NULL	NULL	NULL	NULL	gw70_cellbiol_173_2_153_s_91	16636141	A novel and important extension of DeAntoni et al. (2005) was that the kinetochore localization of fluorescently labeled recombinant Mad2 injected into Ptk cells depends on its ability to dimerize with N2'' - Mad2 already bound to Mad1 at the kinetochores.	bind
47480	3	11412	6	10	NULL	0	NULL	Mad2		recombinant	is localized on					kinetochore					NULL	Ptk cells	NULL	NULL	NULL	NULL	gw70_cellbiol_173_2_153_s_91	16636141	A novel and important extension of DeAntoni et al. (2005) was that the kinetochore localization of fluorescently labeled recombinant Mad2 injected into Ptk cells depends on its ability to dimerize with N2'' - Mad2 already bound to Mad1 at the kinetochores.	bind
47481	4	11412	6	NULL	NULL	0	NULL	statement 3	NULL		depends on	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_cellbiol_173_2_153_s_91	16636141	A novel and important extension of DeAntoni et al. (2005) was that the kinetochore localization of fluorescently labeled recombinant Mad2 injected into Ptk cells depends on its ability to dimerize with N2'' - Mad2 already bound to Mad1 at the kinetochores.	bind
50859	1	11415	5	NULL	NULL	NULL	NULL	BTB/POZ transcriptional repressor protein	GP	novel	interacts with					Fanconi anemia group C protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6550_s_590	10938130	A Novel BTB/POZ transcriptional repressor protein interacts with the Fanconi anemia group C protein and PLZF.	bind
50860	2	11415	5	NULL	NULL	NULL	NULL	BTB/POZ transcriptional repressor protein	GP	novel	interacts with					PLZF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_17_6550_s_590	10938130	A Novel BTB/POZ transcriptional repressor protein interacts with the Fanconi anemia group C protein and PLZF.	bind
47483	1	11415	6	NULL	NULL	0	NULL	BTB/POZ transcriptional repressor protein	NULL		interacts with	NULL				Fanconi anemia group C protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6550_s_590	10938130	A Novel BTB/POZ transcriptional repressor protein interacts with the Fanconi anemia group C protein and PLZF.	bind
47484	2	11415	6	NULL	NULL	0	NULL	BTB/POZ transcriptional repressor protein	NULL		interacts with	NULL				PLZF	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6550_s_590	10938130	A Novel BTB/POZ transcriptional repressor protein interacts with the Fanconi anemia group C protein and PLZF.	bind
50861	1	11416	5	NULL	NULL	NULL	NULL	factor VIII	GP		bind					von Willebrand factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_23_13826_s_259	7775440	A novel cause of mild/moderate hemophilia A: mutations scattered in the factor VIII C1 domain reduce factor VIII binding to von Willebrand factor.	bind
50862	2	11416	5	NULL	NULL	NULL	NULL	factor VIII	GP	mutant	reduces			C1 domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_23_13826_s_259	7775440	A novel cause of mild/moderate hemophilia A: mutations scattered in the factor VIII C1 domain reduce factor VIII binding to von Willebrand factor.	bind
50863	3	11416	5	NULL	NULL	NULL	NULL	statement 2	Process		causes					hemophilia A	GP	mild/moderate			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_23_13826_s_259	7775440	A novel cause of mild/moderate hemophilia A: mutations scattered in the factor VIII C1 domain reduce factor VIII binding to von Willebrand factor.	bind
47485	1	11416	6	NULL	NULL	0	NULL	factor VIII 	NULL		bind	NULL				von Willebrand factor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_23_13826_s_259	7775440	A novel cause of mild/moderate hemophilia A: mutations scattered in the factor VIII C1 domain reduce factor VIII binding to von Willebrand factor.	bind
47486	2	11416	6	NULL	NULL	0	NULL	factor VIII	NULL	mutant	reduce	NULL		C1 domain		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_23_13826_s_259	7775440	A novel cause of mild/moderate hemophilia A: mutations scattered in the factor VIII C1 domain reduce factor VIII binding to von Willebrand factor.	bind
47487	3	11416	6	NULL	NULL	0	NULL	statement 2	NULL		cause	NULL				hemophilia A	NULL	mild/moderate			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_23_13826_s_259	7775440	A novel cause of mild/moderate hemophilia A: mutations scattered in the factor VIII C1 domain reduce factor VIII binding to von Willebrand factor.	bind
50864	1	11417	5	NULL	NULL	NULL	NULL	MTBP	GP		is a type of					novel cellular protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_307_s_449	9759491	A Novel Cellular Protein (MTBP) Binds to MDM2 and Induces a G1 Arrest That Is Suppressed by MDM2.	bind
50865	2	11417	5	NULL	NULL	NULL	NULL	MTBP	GP		bind					MDM2	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_307_s_449	9759491	A Novel Cellular Protein (MTBP) Binds to MDM2 and Induces a G1 Arrest That Is Suppressed by MDM2.	bind
50866	3	11417	5	NULL	NULL	NULL	NULL	statement 2	Process		induce					G1 arrest	Process				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_307_s_449	9759491	A Novel Cellular Protein (MTBP) Binds to MDM2 and Induces a G1 Arrest That Is Suppressed by MDM2.	bind
50867	4	11417	5	NULL	NULL	NULL	NULL	MDM2	GP		suppress					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_307_s_449	9759491	A Novel Cellular Protein (MTBP) Binds to MDM2 and Induces a G1 Arrest That Is Suppressed by MDM2.	bind
47488	1	11417	6	NULL	NULL	0	NULL	MTBP	NULL		is a type of	NULL				cellular protein	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_67_0_307_s_449	9759491	A Novel Cellular Protein (MTBP) Binds to MDM2 and Induces a G1 Arrest That Is Suppressed by MDM2.	bind
47489	2	11417	6	NULL	NULL	0	NULL	MTBP	NULL		bind	NULL				MDM2	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_67_0_307_s_449	9759491	A Novel Cellular Protein (MTBP) Binds to MDM2 and Induces a G1 Arrest That Is Suppressed by MDM2.	bind
47490	3	11417	6	NULL	NULL	0	NULL	statement 2	NULL		induces 	NULL				G1 arrest	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_67_0_307_s_449	9759491	A Novel Cellular Protein (MTBP) Binds to MDM2 and Induces a G1 Arrest That Is Suppressed by MDM2.	bind
47491	4	11417	6	10	NULL	0	NULL	MDM2			suppress					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_307_s_449	9759491	A Novel Cellular Protein (MTBP) Binds to MDM2 and Induces a G1 Arrest That Is Suppressed by MDM2.	bind
50868	1	11418	5	NULL	NULL	NULL	NULL	DNA-binding protein	GP	plant-specific;;zinc-dependent	bind					A/T-rich DNA sequences	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_18_5484_s_511	9736626	A novel class of plant-specific zinc-dependent DNA-binding protein that binds to A/T-rich DNA sequences.	bind
47492	1	11418	6	10	NULL	0	NULL	DNA-binding protein		plant specific;; zinc dependent	bind					A/T-rich DNA sequences					NULL		NULL	NULL	NULL	NULL	gw60_embo_17_18_5484_s_511	9736626	A novel class of plant-specific zinc-dependent DNA-binding protein that binds to A/T-rich DNA sequences.	bind
50869	1	11420	5	NULL	NULL	NULL	NULL	SGT	GP		bind					CSP	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_31_6_987_s_34	11580898	A novel CSP binding partner termed SGT was identified.	bind
47493	1	11420	6	NULL	NULL	0	NULL	SGT	NULL		bind	NULL				CSP	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_31_6_987_s_34	11580898	A novel CSP binding partner termed SGT was identified.	bind
50870	1	11421	5	NULL	NULL	NULL	NULL	SHP1	GP	Rhodobacter sphaeroides	is a type of					novel cytochrome c	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_16050_s_15	10821858	A novel cytochrome  c, which transiently binds O2 during autooxidation, was discovered in the purple phototrophic bacterium  Rhodobacter sphaeroides and was designated SHP1	bind
50871	2	11421	5	NULL	NULL	NULL	NULL	SHP1	GP	Rhodobacter sphaeroides	bind		transiently			O2	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_16050_s_15	10821858	A novel cytochrome  c, which transiently binds O2 during autooxidation, was discovered in the purple phototrophic bacterium  Rhodobacter sphaeroides and was designated SHP1	bind
50872	3	11421	5	NULL	NULL	NULL	NULL	Rhodobacter sphaeroides	Organism		is a type of					purple phototrophic bacterium	Organism				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_16050_s_15	10821858	A novel cytochrome  c, which transiently binds O2 during autooxidation, was discovered in the purple phototrophic bacterium  Rhodobacter sphaeroides and was designated SHP1	bind
54096	4	11421	5	NULL	NULL	NULL	NULL	statement 2	Process		occur during					autooxidation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_16050_s_15	10821858	A novel cytochrome  c, which transiently binds O2 during autooxidation, was discovered in the purple phototrophic bacterium  Rhodobacter sphaeroides and was designated SHP1	bind
47496	1	11421	6	10	NULL	0	NULL	SHP1		Rhodobacter sphaeroides 	bind		transiently			O2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_16050_s_15	10821858	A novel cytochrome  c, which transiently binds O2 during autooxidation, was discovered in the purple phototrophic bacterium  Rhodobacter sphaeroides and was designated SHP1	bind
47497	2	11421	6	NULL	NULL	0	NULL	statement 1	NULL		occurs during	NULL				autooxidation	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_16050_s_15	10821858	A novel cytochrome  c, which transiently binds O2 during autooxidation, was discovered in the purple phototrophic bacterium  Rhodobacter sphaeroides and was designated SHP1	bind
47552	3	11421	6	NULL	NULL	0	NULL	Rhodobacter sphaeroides 	NULL		is a type of	NULL				purple photographic bacterium	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_16050_s_15	10821858	A novel cytochrome  c, which transiently binds O2 during autooxidation, was discovered in the purple phototrophic bacterium  Rhodobacter sphaeroides and was designated SHP1	bind
47553	4	11421	6	NULL	NULL	0	NULL	SHP1	NULL		is a type of	NULL				cytochrome c	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_16050_s_15	10821858	A novel cytochrome  c, which transiently binds O2 during autooxidation, was discovered in the purple phototrophic bacterium  Rhodobacter sphaeroides and was designated SHP1	bind
50873	1	11422	5	NULL	NULL	NULL	NULL	CIS	GP		is a type of					cytokine-indicible gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_12_3299_s_356	9843570	A novel cytokine-indicible gene CIS encodes an SH2-containing protein that binds to tyrosine-phosphorylated interleukin 3 and erythropoietin receptors.	bind
50874	2	11422	5	NULL	NULL	NULL	NULL	CIS	GP		encodes					SH2-containing protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_12_3299_s_356	9843570	A novel cytokine-indicible gene CIS encodes an SH2-containing protein that binds to tyrosine-phosphorylated interleukin 3 and erythropoietin receptors.	bind
50875	3	11422	5	NULL	NULL	NULL	NULL	statement 2	Process		bind					interleukin 3	GP	phosphorylated	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_12_3299_s_356	9843570	A novel cytokine-indicible gene CIS encodes an SH2-containing protein that binds to tyrosine-phosphorylated interleukin 3 and erythropoietin receptors.	bind
50876	4	11422	5	NULL	NULL	NULL	NULL	statement 2	Process		bind					erythropoietin receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_12_3299_s_356	9843570	A novel cytokine-indicible gene CIS encodes an SH2-containing protein that binds to tyrosine-phosphorylated interleukin 3 and erythropoietin receptors.	bind
47554	1	11422	6	NULL	NULL	0	NULL	CIS	NULL		is induced by	NULL				cytokine	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_12_3299_s_356	9843570	A novel cytokine-indicible gene CIS encodes an SH2-containing protein that binds to tyrosine-phosphorylated interleukin 3 and erythropoietin receptors.	bind
47555	2	11422	6	NULL	NULL	0	NULL	CIS	NULL		encodes	NULL				SH2-containing protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_12_3299_s_356	9843570	A novel cytokine-indicible gene CIS encodes an SH2-containing protein that binds to tyrosine-phosphorylated interleukin 3 and erythropoietin receptors.	bind
47556	3	11422	6	NULL	NULL	0	NULL	statement 2	NULL		bind	NULL				interleukin 3	NULL	phosphorylated	tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_12_3299_s_356	9843570	A novel cytokine-indicible gene CIS encodes an SH2-containing protein that binds to tyrosine-phosphorylated interleukin 3 and erythropoietin receptors.	bind
47557	4	11422	6	NULL	NULL	0	NULL	statement 2	NULL		bind	NULL				erythropoietin receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_12_3299_s_356	9843570	A novel cytokine-indicible gene CIS encodes an SH2-containing protein that binds to tyrosine-phosphorylated interleukin 3 and erythropoietin receptors.	bind
50877	1	11432	5	NULL	NULL	NULL	NULL	Rheb	GP		bind					mTOR effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_23433_s_88	15878852	A novel feature of the binding of Rheb to its effector mTOR, and one that contrasts with the interaction of other Ras-like GTPases with their known effectors, is that the Rheb-mTOR interaction does not require Rheb GTP charging ( ).	bind
50878	2	11432	5	NULL	NULL	NULL	NULL	statement 1	Process		does not require					Rheb GTP	GP	charging of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_23433_s_88	15878852	A novel feature of the binding of Rheb to its effector mTOR, and one that contrasts with the interaction of other Ras-like GTPases with their known effectors, is that the Rheb-mTOR interaction does not require Rheb GTP charging ( ).	bind
47816	1	11432	6	NULL	NULL	0	NULL	Rheb	NULL		bind	NULL				mTOR effector	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_25_23433_s_88	15878852	A novel feature of the binding of Rheb to its effector mTOR, and one that contrasts with the interaction of other Ras-like GTPases with their known effectors, is that the Rheb-mTOR interaction does not require Rheb GTP charging ( ).	bind
47817	2	11432	6	NULL	NULL	0	NULL	statement 1	NULL		does not require	NULL				Rheb G GTP	NULL	charging of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_25_23433_s_88	15878852	A novel feature of the binding of Rheb to its effector mTOR, and one that contrasts with the interaction of other Ras-like GTPases with their known effectors, is that the Rheb-mTOR interaction does not require Rheb GTP charging ( ).	bind
50879	1	11433	5	NULL	NULL	NULL	NULL	MAPK	GP		regulates		differentially			GATA-4	GP	binding activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_16_13752_s_281	11827958	A novel finding in our studies is the differential regulation of GATA-4 binding activity by MAPKs.	bind
47558	1	11433	6	NULL	NULL	0	NULL	MAPK	NULL		regulates	NULL	differentially			GATA-4	NULL	binding activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13752_s_281	11827958	A novel finding in our studies is the differential regulation of GATA-4 binding activity by MAPKs.	bind
50880	1	11434	5	NULL	NULL	NULL	NULL	grB	GP		bind					serglycin	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_2_623_s_322	16280358	A novel finding is that this is the critical mechanism of uptake when grB is bound to serglycin.	bind
47559	1	11434	6	NULL	NULL	0	NULL	grB	NULL		bind	NULL				serglycin	NULL				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_2_623_s_322	16280358	A novel finding is that this is the critical mechanism of uptake when grB is bound to serglycin.	bind
50881	1	11437	5	NULL	NULL	NULL	NULL	VEGF	GP		bind					VEGF receptor-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_2_171_s_417	12887919	A novel function for tissue inhibitor of metalloproteinases-3 (TIMP3): inhibition of angiogenesis by blockage of VEGF binding to VEGF receptor-2.	bind
50882	2	11437	5	NULL	NULL	NULL	NULL	TIMP3	GP		is					tissue inhibitor of metalloproteinases-3	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_2_171_s_417	12887919	A novel function for tissue inhibitor of metalloproteinases-3 (TIMP3): inhibition of angiogenesis by blockage of VEGF binding to VEGF receptor-2.	bind
50883	3	11437	5	NULL	NULL	NULL	NULL	TIMP3	GP		inhibits					angiogenesis	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_2_171_s_417	12887919	A novel function for tissue inhibitor of metalloproteinases-3 (TIMP3): inhibition of angiogenesis by blockage of VEGF binding to VEGF receptor-2.	bind
50884	4	11437	5	NULL	NULL	NULL	NULL	TIMP3	GP		blocks					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_2_171_s_417	12887919	A novel function for tissue inhibitor of metalloproteinases-3 (TIMP3): inhibition of angiogenesis by blockage of VEGF binding to VEGF receptor-2.	bind
50885	5	11437	5	NULL	NULL	NULL	NULL	statement 4	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_114_2_171_s_417	12887919	A novel function for tissue inhibitor of metalloproteinases-3 (TIMP3): inhibition of angiogenesis by blockage of VEGF binding to VEGF receptor-2.	bind
47561	1	11437	6	NULL	NULL	0	NULL	VEGF	NULL		bind	NULL				VEGF receptor-2	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_114_2_171_s_417	12887919	A novel function for tissue inhibitor of metalloproteinases-3 (TIMP3): inhibition of angiogenesis by blockage of VEGF binding to VEGF receptor-2.	bind
47562	2	11437	6	NULL	NULL	0	NULL	TIMP-3	NULL		blocks	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_114_2_171_s_417	12887919	A novel function for tissue inhibitor of metalloproteinases-3 (TIMP3): inhibition of angiogenesis by blockage of VEGF binding to VEGF receptor-2.	bind
47563	3	11437	6	NULL	NULL	0	NULL	statement 2	NULL		inhibits	NULL				angiogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_114_2_171_s_417	12887919	A novel function for tissue inhibitor of metalloproteinases-3 (TIMP3): inhibition of angiogenesis by blockage of VEGF binding to VEGF receptor-2.	bind
47564	4	11437	6	NULL	NULL	0	NULL	TIMP3	NULL		is	NULL				tissue inhibitor of metalloproteinases-3	NULL				NULL		0	NULL	NULL	NULL	gw60_cell_114_2_171_s_417	12887919	A novel function for tissue inhibitor of metalloproteinases-3 (TIMP3): inhibition of angiogenesis by blockage of VEGF binding to VEGF receptor-2.	bind
54097	5	11437	6	10	NULL	0	NULL	statement 2			leads to					statement 3					NULL		0	NULL	NULL	NULL	gw60_cell_114_2_171_s_417	12887919	A novel function for tissue inhibitor of metalloproteinases-3 (TIMP3): inhibition of angiogenesis by blockage of VEGF binding to VEGF receptor-2.	bind
50897	1	11439	5	NULL	NULL	NULL	NULL	frizzled wnt receptor gene	GP	human	is homologous to					frizzled wnt receptor gene	GP	Drosophila			NULL		NULL	NULL	NULL	NULL	gw70_annurevgenomicshum_1_0_461_s_1047	null	A novel human homologue of the  Drosophila frizzled wnt receptor gene binds wingless protein and is in the Williams syndrome  deletion at 7q11.	bind
50898	2	11439	5	NULL	NULL	NULL	NULL	frizzled wnt receptor gene	GP	human	bind					wingless protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenomicshum_1_0_461_s_1047	null	A novel human homologue of the  Drosophila frizzled wnt receptor gene binds wingless protein and is in the Williams syndrome  deletion at 7q11.	bind
50899	3	11439	5	NULL	NULL	NULL	NULL			deletion of	leads to				7q11	Williams syndrome	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw70_annurevgenomicshum_1_0_461_s_1047	null	A novel human homologue of the  Drosophila frizzled wnt receptor gene binds wingless protein and is in the Williams syndrome  deletion at 7q11.	bind
47565	1	11439	6	10	NULL	0	NULL	frizzled wnt receptor gene		human	is homologous to					frizzled wnt receptor gene		Drosophila			NULL		NULL	NULL	NULL	NULL	gw70_annurevgenomicshum_1_0_461_s_1047	null	A novel human homologue of the  Drosophila frizzled wnt receptor gene binds wingless protein and is in the Williams syndrome  deletion at 7q11.	bind
47566	2	11439	6	10	NULL	0	NULL	frizzled wnt receptor gene		human	bind					wingless protein					NULL		NULL	NULL	NULL	NULL	gw70_annurevgenomicshum_1_0_461_s_1047	null	A novel human homologue of the  Drosophila frizzled wnt receptor gene binds wingless protein and is in the Williams syndrome  deletion at 7q11.	bind
47567	3	11439	6	10	NULL	0	NULL			deletion of	leads to				7q11	Williams syndrome					NULL		NULL	NULL	NULL	NULL	gw70_annurevgenomicshum_1_0_461_s_1047	null	A novel human homologue of the  Drosophila frizzled wnt receptor gene binds wingless protein and is in the Williams syndrome  deletion at 7q11.	bind
50900	1	11443	5	NULL	NULL	NULL	NULL	Neisseria gonorrhoeae	Organism		is a type of					pathogen	Organism				NULL		NULL	NULL	NULL	NULL	gw60_vetmicrobiol_94_2_131_s_9	12781481	A novel mechanism for microbial exploitation of host factors was described in  Neisseria gonorrhoeae in which this pathogen bound heparin sulfate that directed the binding of vitronectin, which ultimately was used as a bridge to attach to host surfaces (  Duensing and Van Putten, 1998).	bind
50901	2	11443	5	NULL	NULL	NULL	NULL	Neisseria gonorrhoeae	Organism		bind					heparin sulfate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_vetmicrobiol_94_2_131_s_9	12781481	A novel mechanism for microbial exploitation of host factors was described in  Neisseria gonorrhoeae in which this pathogen bound heparin sulfate that directed the binding of vitronectin, which ultimately was used as a bridge to attach to host surfaces (  Duensing and Van Putten, 1998).	bind
50902	3	11443	5	NULL	NULL	NULL	NULL	statement 1	Process		directs					vitronectin	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_vetmicrobiol_94_2_131_s_9	12781481	A novel mechanism for microbial exploitation of host factors was described in  Neisseria gonorrhoeae in which this pathogen bound heparin sulfate that directed the binding of vitronectin, which ultimately was used as a bridge to attach to host surfaces (  Duensing and Van Putten, 1998).	bind
47820	1	11443	6	NULL	NULL	0	NULL	Neisseria gonorrhoeae	NULL		bind	NULL				heparin sulfate	NULL				NULL		0	NULL	NULL	NULL	gw60_vetmicrobiol_94_2_131_s_9	12781481	A novel mechanism for microbial exploitation of host factors was described in  Neisseria gonorrhoeae in which this pathogen bound heparin sulfate that directed the binding of vitronectin, which ultimately was used as a bridge to attach to host surfaces (  Duensing and Van Putten, 1998).	bind
47821	2	11443	6	NULL	NULL	0	NULL	statement 1	NULL		directed 	NULL				vitronectin	NULL	binding of 			NULL		0	NULL	NULL	NULL	gw60_vetmicrobiol_94_2_131_s_9	12781481	A novel mechanism for microbial exploitation of host factors was described in  Neisseria gonorrhoeae in which this pathogen bound heparin sulfate that directed the binding of vitronectin, which ultimately was used as a bridge to attach to host surfaces (  Duensing and Van Putten, 1998).	bind
58568	3	11443	6	10	NULL	0	NULL	Neisseria gonorrhoeae			is a type of					pathogen					NULL		0	NULL	NULL	NULL	gw60_vetmicrobiol_94_2_131_s_9	12781481	A novel mechanism for microbial exploitation of host factors was described in  Neisseria gonorrhoeae in which this pathogen bound heparin sulfate that directed the binding of vitronectin, which ultimately was used as a bridge to attach to host surfaces (  Duensing and Van Putten, 1998).	bind
50903	1	11445	5	NULL	NULL	NULL	NULL	S-nitrosoglutathione	Chemical		is a type of					NO releaser	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_11_3486_s_446	10348862	A novel mechanism for upregulation of the  Escherichia coli K-12  hmp (flavohaemoglobin) gene by the 'NO releaser'', S-nitrosoglutathione: nitrosation of homocysteine and modulation of MetR binding to the gly  hmp intergenic region.	bind
50904	2	11445	5	NULL	NULL	NULL	NULL	S-nitrosoglutathione	GP		upregulates					hmp gene	GP	Escherichia coli K-12			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_11_3486_s_446	10348862	A novel mechanism for upregulation of the  Escherichia coli K-12  hmp (flavohaemoglobin) gene by the 'NO releaser'', S-nitrosoglutathione: nitrosation of homocysteine and modulation of MetR binding to the gly  hmp intergenic region.	bind
50905	3	11445	5	NULL	NULL	NULL	NULL	hmp	GP		is					flavohaemoglobin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_11_3486_s_446	10348862	A novel mechanism for upregulation of the  Escherichia coli K-12  hmp (flavohaemoglobin) gene by the 'NO releaser'', S-nitrosoglutathione: nitrosation of homocysteine and modulation of MetR binding to the gly  hmp intergenic region.	bind
50907	4	11445	5	NULL	NULL	NULL	NULL	MetR	GP		bind									gly hmp intergenic region	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_11_3486_s_446	10348862	A novel mechanism for upregulation of the  Escherichia coli K-12  hmp (flavohaemoglobin) gene by the 'NO releaser'', S-nitrosoglutathione: nitrosation of homocysteine and modulation of MetR binding to the gly  hmp intergenic region.	bind
47846	1	11445	6	NULL	NULL	0	NULL	MetR	NULL		bind	NULL					NULL			gly hmp intergenic region	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_11_3486_s_446	10348862	A novel mechanism for upregulation of the  Escherichia coli K-12  hmp (flavohaemoglobin) gene by the 'NO releaser'', S-nitrosoglutathione: nitrosation of homocysteine and modulation of MetR binding to the gly  hmp intergenic region.	bind
47847	2	11445	6	NULL	NULL	0	NULL	S-nitrosoglutathione	NULL		is a type of	NULL				NO releaser	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_11_3486_s_446	10348862	A novel mechanism for upregulation of the  Escherichia coli K-12  hmp (flavohaemoglobin) gene by the 'NO releaser'', S-nitrosoglutathione: nitrosation of homocysteine and modulation of MetR binding to the gly  hmp intergenic region.	bind
47860	3	11445	6	NULL	NULL	0	NULL	S-nitrosoglutathione	NULL		upregulates	NULL				hmp gene	NULL	Escherichia coli K-12			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_11_3486_s_446	10348862	A novel mechanism for upregulation of the  Escherichia coli K-12  hmp (flavohaemoglobin) gene by the 'NO releaser'', S-nitrosoglutathione: nitrosation of homocysteine and modulation of MetR binding to the gly  hmp intergenic region.	bind
47861	4	11445	6	NULL	NULL	0	NULL	hmp	NULL		is	NULL				flavohaemoglobin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_11_3486_s_446	10348862	A novel mechanism for upregulation of the  Escherichia coli K-12  hmp (flavohaemoglobin) gene by the 'NO releaser'', S-nitrosoglutathione: nitrosation of homocysteine and modulation of MetR binding to the gly  hmp intergenic region.	bind
50909	1	11447	5	NULL	NULL	NULL	NULL	SHPS-1	GP		is a type of					membrane glycoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_17_0_875_s_917	10358776	A novel membrane glycoprotein, SHPS-1, that  binds the SH2-domain-containing protein tyrosine phosphatase SHP-2 in response to  mitogens and cell adhesion.	bind
50910	2	11447	5	NULL	NULL	NULL	NULL	SHPS-1	GP		bind					SHP-2	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_17_0_875_s_917	10358776	A novel membrane glycoprotein, SHPS-1, that  binds the SH2-domain-containing protein tyrosine phosphatase SHP-2 in response to  mitogens and cell adhesion.	bind
50911	3	11447	5	NULL	NULL	NULL	NULL	SHP-2	GP		is					SH2-domain-containing protein tyrosine phosphatase	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_17_0_875_s_917	10358776	A novel membrane glycoprotein, SHPS-1, that  binds the SH2-domain-containing protein tyrosine phosphatase SHP-2 in response to  mitogens and cell adhesion.	bind
50912	4	11447	5	NULL	NULL	NULL	NULL	statement 2	Process		in response to					mitogens	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_17_0_875_s_917	10358776	A novel membrane glycoprotein, SHPS-1, that  binds the SH2-domain-containing protein tyrosine phosphatase SHP-2 in response to  mitogens and cell adhesion.	bind
50913	5	11447	5	NULL	NULL	NULL	NULL	statement 2	Process		in response to					cell adhesion	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_17_0_875_s_917	10358776	A novel membrane glycoprotein, SHPS-1, that  binds the SH2-domain-containing protein tyrosine phosphatase SHP-2 in response to  mitogens and cell adhesion.	bind
47568	1	11447	6	10	NULL	0	NULL	SHPS-1			is a type of					membrane glycoprotein					NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_17_0_875_s_917	10358776	A novel membrane glycoprotein, SHPS-1, that  binds the SH2-domain-containing protein tyrosine phosphatase SHP-2 in response to  mitogens and cell adhesion.	bind
47569	2	11447	6	NULL	NULL	0	NULL	SHP-2	NULL		is	NULL				SH2-domain-containing protein tyrosine phosphatase	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_875_s_917	10358776	A novel membrane glycoprotein, SHPS-1, that  binds the SH2-domain-containing protein tyrosine phosphatase SHP-2 in response to  mitogens and cell adhesion.	bind
47570	3	11447	6	NULL	NULL	0	NULL	SHPS-1	NULL		bind	NULL				SHP-2	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_875_s_917	10358776	A novel membrane glycoprotein, SHPS-1, that  binds the SH2-domain-containing protein tyrosine phosphatase SHP-2 in response to  mitogens and cell adhesion.	bind
47571	4	11447	6	NULL	NULL	0	NULL	statement 3	NULL		occurs in response to	NULL				mitogen	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_875_s_917	10358776	A novel membrane glycoprotein, SHPS-1, that  binds the SH2-domain-containing protein tyrosine phosphatase SHP-2 in response to  mitogens and cell adhesion.	bind
47572	5	11447	6	NULL	NULL	0	NULL	statement 3	NULL		occurs in response to	NULL				cell adhesion	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_875_s_917	10358776	A novel membrane glycoprotein, SHPS-1, that  binds the SH2-domain-containing protein tyrosine phosphatase SHP-2 in response to  mitogens and cell adhesion.	bind
50914	1	11450	5	NULL	NULL	NULL	NULL	SW-480	Cell		is a type of					human colon carcinoma cell line	Cell				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6837_s_452	10958680	A novel mitogenic signaling pathway of bradykinin in the human colon carcinoma cell line SW-480 involves sequential activation of a Gq/11 protein, phosphatidylinositol 3-kinase beta, and [[ protein kinase C.  J. Biol. Chem.  273 ]] :32016-32022 [Abstract/ull Text].	bind
50915	2	11450	5	NULL	NULL	NULL	NULL	bradykinin	GP	mitogenic signaling pathway of	involves					Gq/11 protein	GP	sequential activation of			NULL	SW-480 cell line	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6837_s_452	10958680	A novel mitogenic signaling pathway of bradykinin in the human colon carcinoma cell line SW-480 involves sequential activation of a Gq/11 protein, phosphatidylinositol 3-kinase beta, and [[ protein kinase C.  J. Biol. Chem.  273 ]] :32016-32022 [Abstract/ull Text].	bind
50916	3	11450	5	NULL	NULL	NULL	NULL	bradykinin	GP	mitogenic signaling pathway of	involves					phosphatidylinositol 3-kinase beta	GP	sequential activation of			NULL	SW-480 cell line	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6837_s_452	10958680	A novel mitogenic signaling pathway of bradykinin in the human colon carcinoma cell line SW-480 involves sequential activation of a Gq/11 protein, phosphatidylinositol 3-kinase beta, and [[ protein kinase C.  J. Biol. Chem.  273 ]] :32016-32022 [Abstract/ull Text].	bind
50917	4	11450	5	NULL	NULL	NULL	NULL	bradykinin	GP	mitogenic signaling pathway of	involves					protein kinase C	GP	sequential activation of			NULL	SW-480 cell line	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6837_s_452	10958680	A novel mitogenic signaling pathway of bradykinin in the human colon carcinoma cell line SW-480 involves sequential activation of a Gq/11 protein, phosphatidylinositol 3-kinase beta, and [[ protein kinase C.  J. Biol. Chem.  273 ]] :32016-32022 [Abstract/ull Text].	bind
47573	1	11450	6	10	NULL	0	NULL	SW-480			is a type of					human colon carcinoma cell line					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6837_s_452	10958680	A novel mitogenic signaling pathway of bradykinin in the human colon carcinoma cell line SW-480 involves sequential activation of a Gq/11 protein, phosphatidylinositol 3-kinase beta, and [[ protein kinase C.  J. Biol. Chem.  273 ]] :32016-32022 [Abstract/ull Text].	bind
47689	2	11450	6	10	NULL	0	NULL	bradykinin 		mitogenic signaling pathway of	involves					Gq/11 protein		sequential activation of			NULL	SW-480 cell line	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6837_s_452	10958680	A novel mitogenic signaling pathway of bradykinin in the human colon carcinoma cell line SW-480 involves sequential activation of a Gq/11 protein, phosphatidylinositol 3-kinase beta, and [[ protein kinase C.  J. Biol. Chem.  273 ]] :32016-32022 [Abstract/ull Text].	bind
47690	3	11450	6	10	NULL	0	NULL	bradykinin		mitogenic signaling pathway of	involves					phosphatidylinositol 3-kinase beta		sequential activation of			NULL	SW-480 cell line	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6837_s_452	10958680	A novel mitogenic signaling pathway of bradykinin in the human colon carcinoma cell line SW-480 involves sequential activation of a Gq/11 protein, phosphatidylinositol 3-kinase beta, and [[ protein kinase C.  J. Biol. Chem.  273 ]] :32016-32022 [Abstract/ull Text].	bind
47691	4	11450	6	10	NULL	0	NULL	bradykinin 		mitogenic signaling pathway of	involves					protein kinase C		sequential activation of			NULL	SW-480 cell line	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_18_6837_s_452	10958680	A novel mitogenic signaling pathway of bradykinin in the human colon carcinoma cell line SW-480 involves sequential activation of a Gq/11 protein, phosphatidylinositol 3-kinase beta, and [[ protein kinase C.  J. Biol. Chem.  273 ]] :32016-32022 [Abstract/ull Text].	bind
50918	1	11451	5	NULL	NULL	NULL	NULL	MIBP	GP		is					muscle-specific beta1 integrin binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_4_861_s_332	10953009	A novel muscle-specific beta1 integrin binding protein (MIBP) that modulates myogenic differentiation.	bind
50919	2	11451	5	NULL	NULL	NULL	NULL	MIBP	GP		modulates					myogenic differentiation	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_150_4_861_s_332	10953009	A novel muscle-specific beta1 integrin binding protein (MIBP) that modulates myogenic differentiation.	bind
47692	1	11451	6	NULL	NULL	0	NULL	MIBP	NULL		modulates	NULL				myogenic differentiation	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_150_4_861_s_332	10953009	A novel muscle-specific beta1 integrin binding protein (MIBP) that modulates myogenic differentiation.	bind
47693	2	11451	6	NULL	NULL	0	NULL	MIBP	NULL		is	NULL				muscle-specific beta1 integrin binding protein	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_150_4_861_s_332	10953009	A novel muscle-specific beta1 integrin binding protein (MIBP) that modulates myogenic differentiation.	bind
50920	1	11452	5	NULL	NULL	NULL	NULL	cardiac ryanodine receptor gene	GP	human;;mutant	causes			R2401H in FKBP12.6 binding region		catecholaminergic polymorphic ventricular tachycardia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_int-j-cardiol_99_2_15749201_s_1	15749201	A novel mutation in FKBP12.6 binding region of the human cardiac ryanodine receptor gene (R2401H) in a Japanese patient with catecholaminergic polymorphic ventricular tachycardia..	bind
47694	1	11452	6	NULL	NULL	0	NULL	catecholaminergic polymorphic ventricular tachycardia	NULL		involves	NULL				cardiac ryanodine receptor gene	NULL	mutation of	R2401 in FKBP12.6 binding region		NULL		0	NULL	NULL	NULL	abs-batch0720-0739_int-j-cardiol_99_2_15749201_s_1	15749201	A novel mutation in FKBP12.6 binding region of the human cardiac ryanodine receptor gene (R2401H) in a Japanese patient with catecholaminergic polymorphic ventricular tachycardia..	bind
50921	1	11453	5	NULL	NULL	NULL	NULL	N-WASP	GP		is					neural Wiskott-Aldrich syndrome protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_7_534_s_487	12676083	A novel neural Wiskott-Aldrich syndrome protein (N-WASP) binding protein, WISH, induces Arp2/3 complex activation independent of Cdc42.	bind
50922	2	11453	5	NULL	NULL	NULL	NULL	WISH	GP		bind					N-WASP	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_7_534_s_487	12676083	A novel neural Wiskott-Aldrich syndrome protein (N-WASP) binding protein, WISH, induces Arp2/3 complex activation independent of Cdc42.	bind
50923	3	11453	5	NULL	NULL	NULL	NULL	WISH	GP		induces					Arp2/3 complex	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_7_534_s_487	12676083	A novel neural Wiskott-Aldrich syndrome protein (N-WASP) binding protein, WISH, induces Arp2/3 complex activation independent of Cdc42.	bind
50924	4	11453	5	NULL	NULL	NULL	NULL	statement 3	Process		is independent of					Cdc42	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_7_534_s_487	12676083	A novel neural Wiskott-Aldrich syndrome protein (N-WASP) binding protein, WISH, induces Arp2/3 complex activation independent of Cdc42.	bind
47695	1	11453	6	NULL	NULL	0	NULL	WISH	NULL		bind	NULL				N-WASP	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_13_7_534_s_487	12676083	A novel neural Wiskott-Aldrich syndrome protein (N-WASP) binding protein, WISH, induces Arp2/3 complex activation independent of Cdc42.	bind
47696	2	11453	6	NULL	NULL	0	NULL	N-WASP	NULL		is	NULL				neural Wiskott-Aldrich syndrome protein	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_13_7_534_s_487	12676083	A novel neural Wiskott-Aldrich syndrome protein (N-WASP) binding protein, WISH, induces Arp2/3 complex activation independent of Cdc42.	bind
47697	3	11453	6	NULL	NULL	0	NULL	WISH	NULL		induces	NULL				Arp2/3 complex	NULL	activation of			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_13_7_534_s_487	12676083	A novel neural Wiskott-Aldrich syndrome protein (N-WASP) binding protein, WISH, induces Arp2/3 complex activation independent of Cdc42.	bind
47698	4	11453	6	NULL	NULL	0	NULL	statement 3	NULL		is independent of	NULL				Cdc42	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_13_7_534_s_487	12676083	A novel neural Wiskott-Aldrich syndrome protein (N-WASP) binding protein, WISH, induces Arp2/3 complex activation independent of Cdc42.	bind
50926	1	11454	5	NULL	NULL	NULL	NULL	Noc/OFQ	GP		bind					receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_303_1_424_s_150	12235279	A novel nonpeptide Noc/OFQ antagonist JTC-801 was recently synthesized (Shinkai et al., 2000  ) and shown to inhibit [3]Noc/OFQ binding to the receptor ( Ki = 44.5 nM) and antagonize the suppression of Noc/OFQ on forskolin-induced cAMP formation (IC50 = 2.58 muM) in HeLa cells expressing human Noc/OFQ receptor (Yamada et al., 2002  ).	bind
50927	2	11454	5	NULL	NULL	NULL	NULL	JTC-801	Chemical		is an antagonist of					Noc/OFQ	GP				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_303_1_424_s_150	12235279	A novel nonpeptide Noc/OFQ antagonist JTC-801 was recently synthesized (Shinkai et al., 2000  ) and shown to inhibit [3]Noc/OFQ binding to the receptor ( Ki = 44.5 nM) and antagonize the suppression of Noc/OFQ on forskolin-induced cAMP formation (IC50 = 2.58 muM) in HeLa cells expressing human Noc/OFQ receptor (Yamada et al., 2002  ).	bind
50928	3	11454	5	NULL	NULL	NULL	NULL	JTC-801	Chemical		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_303_1_424_s_150	12235279	A novel nonpeptide Noc/OFQ antagonist JTC-801 was recently synthesized (Shinkai et al., 2000  ) and shown to inhibit [3]Noc/OFQ binding to the receptor ( Ki = 44.5 nM) and antagonize the suppression of Noc/OFQ on forskolin-induced cAMP formation (IC50 = 2.58 muM) in HeLa cells expressing human Noc/OFQ receptor (Yamada et al., 2002  ).	bind
50929	4	11454	5	NULL	NULL	NULL	NULL	forskolin	Chemical		induce					cAMP	Chemical	formation of			NULL	HeLa cells expressing human Noc/OFQ receptor	NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_303_1_424_s_150	12235279	A novel nonpeptide Noc/OFQ antagonist JTC-801 was recently synthesized (Shinkai et al., 2000  ) and shown to inhibit [3]Noc/OFQ binding to the receptor ( Ki = 44.5 nM) and antagonize the suppression of Noc/OFQ on forskolin-induced cAMP formation (IC50 = 2.58 muM) in HeLa cells expressing human Noc/OFQ receptor (Yamada et al., 2002  ).	bind
50930	5	11454	5	NULL	NULL	NULL	NULL	Noc/OFQ	GP		is supressed by					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_303_1_424_s_150	12235279	A novel nonpeptide Noc/OFQ antagonist JTC-801 was recently synthesized (Shinkai et al., 2000  ) and shown to inhibit [3]Noc/OFQ binding to the receptor ( Ki = 44.5 nM) and antagonize the suppression of Noc/OFQ on forskolin-induced cAMP formation (IC50 = 2.58 muM) in HeLa cells expressing human Noc/OFQ receptor (Yamada et al., 2002  ).	bind
50931	6	11454	5	NULL	NULL	NULL	NULL	JTC-801	Chemical		antagonize					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_303_1_424_s_150	12235279	A novel nonpeptide Noc/OFQ antagonist JTC-801 was recently synthesized (Shinkai et al., 2000  ) and shown to inhibit [3]Noc/OFQ binding to the receptor ( Ki = 44.5 nM) and antagonize the suppression of Noc/OFQ on forskolin-induced cAMP formation (IC50 = 2.58 muM) in HeLa cells expressing human Noc/OFQ receptor (Yamada et al., 2002  ).	bind
47699	1	11454	6	NULL	NULL	0	NULL	Noc/OFQ	NULL		bind	NULL				receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_303_1_424_s_150	12235279	A novel nonpeptide Noc/OFQ antagonist JTC-801 was recently synthesized (Shinkai et al., 2000  ) and shown to inhibit [3]Noc/OFQ binding to the receptor ( Ki = 44.5 nM) and antagonize the suppression of Noc/OFQ on forskolin-induced cAMP formation (IC50 = 2.58 muM) in HeLa cells expressing human Noc/OFQ receptor (Yamada et al., 2002  ).	bind
47700	2	11454	6	10	NULL	0	NULL	JTC-801			is an antagonist of					Noc/OFQ 					NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_303_1_424_s_150	12235279	A novel nonpeptide Noc/OFQ antagonist JTC-801 was recently synthesized (Shinkai et al., 2000  ) and shown to inhibit [3]Noc/OFQ binding to the receptor ( Ki = 44.5 nM) and antagonize the suppression of Noc/OFQ on forskolin-induced cAMP formation (IC50 = 2.58 muM) in HeLa cells expressing human Noc/OFQ receptor (Yamada et al., 2002  ).	bind
47701	3	11454	6	NULL	NULL	0	NULL	JTC-801	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_303_1_424_s_150	12235279	A novel nonpeptide Noc/OFQ antagonist JTC-801 was recently synthesized (Shinkai et al., 2000  ) and shown to inhibit [3]Noc/OFQ binding to the receptor ( Ki = 44.5 nM) and antagonize the suppression of Noc/OFQ on forskolin-induced cAMP formation (IC50 = 2.58 muM) in HeLa cells expressing human Noc/OFQ receptor (Yamada et al., 2002  ).	bind
47702	4	11454	6	NULL	NULL	0	NULL	forskolin	NULL		induces	NULL				cAMP	NULL	formation of			NULL	HeLa cells expressing human Noc/OFQ receptor	0	NULL	NULL	NULL	gw60_jpharmacolexpther_303_1_424_s_150	12235279	A novel nonpeptide Noc/OFQ antagonist JTC-801 was recently synthesized (Shinkai et al., 2000  ) and shown to inhibit [3]Noc/OFQ binding to the receptor ( Ki = 44.5 nM) and antagonize the suppression of Noc/OFQ on forskolin-induced cAMP formation (IC50 = 2.58 muM) in HeLa cells expressing human Noc/OFQ receptor (Yamada et al., 2002  ).	bind
47703	5	11454	6	NULL	NULL	0	NULL	Noc/OFQ	NULL		suppresses	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_303_1_424_s_150	12235279	A novel nonpeptide Noc/OFQ antagonist JTC-801 was recently synthesized (Shinkai et al., 2000  ) and shown to inhibit [3]Noc/OFQ binding to the receptor ( Ki = 44.5 nM) and antagonize the suppression of Noc/OFQ on forskolin-induced cAMP formation (IC50 = 2.58 muM) in HeLa cells expressing human Noc/OFQ receptor (Yamada et al., 2002  ).	bind
47704	6	11454	6	10	NULL	0	NULL	JTC-801			antagonizes					statement 5					NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_303_1_424_s_150	12235279	A novel nonpeptide Noc/OFQ antagonist JTC-801 was recently synthesized (Shinkai et al., 2000  ) and shown to inhibit [3]Noc/OFQ binding to the receptor ( Ki = 44.5 nM) and antagonize the suppression of Noc/OFQ on forskolin-induced cAMP formation (IC50 = 2.58 muM) in HeLa cells expressing human Noc/OFQ receptor (Yamada et al., 2002  ).	bind
50932	1	11456	5	NULL	NULL	NULL	NULL	ost	GP		is a type of					oncogene	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_4986_s_376	9710582	A novel oncogene, ost, encodes a guanine nucleotide exchange factor that potentially links Rho and Rac signaling pathways.	bind
50933	2	11456	5	NULL	NULL	NULL	NULL	ost	GP		encodes					guanine nucleotide exchange factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_4986_s_376	9710582	A novel oncogene, ost, encodes a guanine nucleotide exchange factor that potentially links Rho and Rac signaling pathways.	bind
50934	3	11456	5	NULL	NULL	NULL	NULL	Rho signaling pathway	Process		is linked to					Rac signaling pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_4986_s_376	9710582	A novel oncogene, ost, encodes a guanine nucleotide exchange factor that potentially links Rho and Rac signaling pathways.	bind
50935	4	11456	5	NULL	NULL	NULL	NULL	statement 2	Process		is required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_4986_s_376	9710582	A novel oncogene, ost, encodes a guanine nucleotide exchange factor that potentially links Rho and Rac signaling pathways.	bind
47705	1	11456	6	10	NULL	0	NULL	ost			encodes 					guanine nucleotide exchange factor					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_4986_s_376	9710582	A novel oncogene, ost, encodes a guanine nucleotide exchange factor that potentially links Rho and Rac signaling pathways.	bind
47706	2	11456	6	NULL	NULL	0	NULL	Rho signaling pathway	NULL		is linked to	NULL				Rac signaling pathway	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_9_4986_s_376	9710582	A novel oncogene, ost, encodes a guanine nucleotide exchange factor that potentially links Rho and Rac signaling pathways.	bind
47707	3	11456	6	10	NULL	0	NULL	guanine nucleotide exchange factor			is required for					statement 2					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_4986_s_376	9710582	A novel oncogene, ost, encodes a guanine nucleotide exchange factor that potentially links Rho and Rac signaling pathways.	bind
54118	4	11456	6	10	NULL	0	NULL	ost			is a type of					oncogene					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_9_4986_s_376	9710582	A novel oncogene, ost, encodes a guanine nucleotide exchange factor that potentially links Rho and Rac signaling pathways.	bind
50936	1	11462	5	NULL	NULL	NULL	NULL	Siah	GP	mammalian	is a homolog of					Sina	GP	Drosophila			NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_5_915_s_3	11389839	A novel pathway for  -catenin degradation was discovered involving mammalian homologs of  Drosophila Sina (Siah), which bind ubiquitin-conjugating enzymes, and Ebi, an F box protein that binds  -catenin independent of the phosphorylation sites recognized by  -TrCP.	bind
50937	2	11462	5	NULL	NULL	NULL	NULL	Siah	GP	mammalian	bind					ubiquitin-conjugating enzymes	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_5_915_s_3	11389839	A novel pathway for  -catenin degradation was discovered involving mammalian homologs of  Drosophila Sina (Siah), which bind ubiquitin-conjugating enzymes, and Ebi, an F box protein that binds  -catenin independent of the phosphorylation sites recognized by  -TrCP.	bind
50938	3	11462	5	NULL	NULL	NULL	NULL	Siah	GP	mammalian	bind					Ebi	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_5_915_s_3	11389839	A novel pathway for  -catenin degradation was discovered involving mammalian homologs of  Drosophila Sina (Siah), which bind ubiquitin-conjugating enzymes, and Ebi, an F box protein that binds  -catenin independent of the phosphorylation sites recognized by  -TrCP.	bind
50939	4	11462	5	NULL	NULL	NULL	NULL	Ebi	GP		is a type of					F box protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_5_915_s_3	11389839	A novel pathway for  -catenin degradation was discovered involving mammalian homologs of  Drosophila Sina (Siah), which bind ubiquitin-conjugating enzymes, and Ebi, an F box protein that binds  -catenin independent of the phosphorylation sites recognized by  -TrCP.	bind
50940	5	11462	5	NULL	NULL	NULL	NULL	Ebi	GP		bind					catenin	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_5_915_s_3	11389839	A novel pathway for  -catenin degradation was discovered involving mammalian homologs of  Drosophila Sina (Siah), which bind ubiquitin-conjugating enzymes, and Ebi, an F box protein that binds  -catenin independent of the phosphorylation sites recognized by  -TrCP.	bind
50941	6	11462	5	NULL	NULL	NULL	NULL	TrCP	GP		recognizes					phosphorylation sites	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_5_915_s_3	11389839	A novel pathway for  -catenin degradation was discovered involving mammalian homologs of  Drosophila Sina (Siah), which bind ubiquitin-conjugating enzymes, and Ebi, an F box protein that binds  -catenin independent of the phosphorylation sites recognized by  -TrCP.	bind
50942	7	11462	5	NULL	NULL	NULL	NULL	statement 5	Process		is independent of					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_5_915_s_3	11389839	A novel pathway for  -catenin degradation was discovered involving mammalian homologs of  Drosophila Sina (Siah), which bind ubiquitin-conjugating enzymes, and Ebi, an F box protein that binds  -catenin independent of the phosphorylation sites recognized by  -TrCP.	bind
47862	1	11462	6	10	NULL	0	NULL	Siah		mammalian	is a homolog of					Sina		Drosophila			NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_5_915_s_3	11389839	A novel pathway for  -catenin degradation was discovered involving mammalian homologs of  Drosophila Sina (Siah), which bind ubiquitin-conjugating enzymes, and Ebi, an F box protein that binds  -catenin independent of the phosphorylation sites recognized by  -TrCP.	bind
47863	2	11462	6	10	NULL	0	NULL	Siah		mammalian	bind					ubiquitin-conjugating enzyme					NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_5_915_s_3	11389839	A novel pathway for  -catenin degradation was discovered involving mammalian homologs of  Drosophila Sina (Siah), which bind ubiquitin-conjugating enzymes, and Ebi, an F box protein that binds  -catenin independent of the phosphorylation sites recognized by  -TrCP.	bind
47864	3	11462	6	10	NULL	0	NULL	Siah		 mammalian	bind					Ebi					NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_5_915_s_3	11389839	A novel pathway for  -catenin degradation was discovered involving mammalian homologs of  Drosophila Sina (Siah), which bind ubiquitin-conjugating enzymes, and Ebi, an F box protein that binds  -catenin independent of the phosphorylation sites recognized by  -TrCP.	bind
47865	4	11462	6	10	NULL	0	NULL	Ebi			bind					catenin					NULL		NULL	NULL	NULL	NULL	gw60_molcell_7_5_915_s_3	11389839	A novel pathway for  -catenin degradation was discovered involving mammalian homologs of  Drosophila Sina (Siah), which bind ubiquitin-conjugating enzymes, and Ebi, an F box protein that binds  -catenin independent of the phosphorylation sites recognized by  -TrCP.	bind
47866	5	11462	6	NULL	NULL	0	NULL		NULL		are recognized by	NULL		phosphorylation sites		TrCP	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_7_5_915_s_3	11389839	A novel pathway for  -catenin degradation was discovered involving mammalian homologs of  Drosophila Sina (Siah), which bind ubiquitin-conjugating enzymes, and Ebi, an F box protein that binds  -catenin independent of the phosphorylation sites recognized by  -TrCP.	bind
47867	6	11462	6	NULL	NULL	0	NULL	statement 4	NULL		is independent of	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_7_5_915_s_3	11389839	A novel pathway for  -catenin degradation was discovered involving mammalian homologs of  Drosophila Sina (Siah), which bind ubiquitin-conjugating enzymes, and Ebi, an F box protein that binds  -catenin independent of the phosphorylation sites recognized by  -TrCP.	bind
54119	7	11462	6	10	NULL	0	NULL	Ebi			is a type of					F box protein					NULL		0	NULL	NULL	NULL	gw60_molcell_7_5_915_s_3	11389839	A novel pathway for  -catenin degradation was discovered involving mammalian homologs of  Drosophila Sina (Siah), which bind ubiquitin-conjugating enzymes, and Ebi, an F box protein that binds  -catenin independent of the phosphorylation sites recognized by  -TrCP.	bind
50943	1	11464	5	NULL	NULL	NULL	NULL	ESX1	GP		is a type of					homeoprotein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_9_2376_s_337	9171351	A Novel PF/PN Motif Inhibits Nuclear Localization and DNA Binding Activity of the ESX1 Homeoprotein.	bind
50944	2	11464	5	NULL	NULL	NULL	NULL	ESX1	GP		is localized to					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_9_2376_s_337	9171351	A Novel PF/PN Motif Inhibits Nuclear Localization and DNA Binding Activity of the ESX1 Homeoprotein.	bind
50945	3	11464	5	NULL	NULL	NULL	NULL				inhibit			PF/PN motif		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_9_2376_s_337	9171351	A Novel PF/PN Motif Inhibits Nuclear Localization and DNA Binding Activity of the ESX1 Homeoprotein.	bind
50946	4	11464	5	NULL	NULL	NULL	NULL	ESX1	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_9_2376_s_337	9171351	A Novel PF/PN Motif Inhibits Nuclear Localization and DNA Binding Activity of the ESX1 Homeoprotein.	bind
50947	5	11464	5	NULL	NULL	NULL	NULL				inhibit			PF/PN motif		statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_9_2376_s_337	9171351	A Novel PF/PN Motif Inhibits Nuclear Localization and DNA Binding Activity of the ESX1 Homeoprotein.	bind
47708	1	11464	6	10	NULL	0	NULL	ESX1 			bind					DNA					NULL		NULL	NULL	NULL	NULL	gw60_embo_16_9_2376_s_337	9171351	A Novel PF/PN Motif Inhibits Nuclear Localization and DNA Binding Activity of the ESX1 Homeoprotein.	bind
47709	2	11464	6	10	NULL	0	NULL	ESX1			localizes to					nucleus					NULL		NULL	NULL	NULL	NULL	gw60_embo_16_9_2376_s_337	9171351	A Novel PF/PN Motif Inhibits Nuclear Localization and DNA Binding Activity of the ESX1 Homeoprotein.	bind
47710	3	11464	6	NULL	NULL	0	NULL		NULL		inhibits	NULL		PF/PN Motif		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_9_2376_s_337	9171351	A Novel PF/PN Motif Inhibits Nuclear Localization and DNA Binding Activity of the ESX1 Homeoprotein.	bind
47711	4	11464	6	NULL	NULL	0	NULL		NULL		inhibits	NULL		PF/PN Motif		statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_9_2376_s_337	9171351	A Novel PF/PN Motif Inhibits Nuclear Localization and DNA Binding Activity of the ESX1 Homeoprotein.	bind
54121	5	11464	6	10	NULL	0	NULL	ESX1			is a type of					homeoprotein					NULL		0	NULL	NULL	NULL	gw60_embo_16_9_2376_s_337	9171351	A Novel PF/PN Motif Inhibits Nuclear Localization and DNA Binding Activity of the ESX1 Homeoprotein.	bind
50948	1	11465	5	NULL	NULL	NULL	NULL	hINV gene	GP	activation of;;expression of	is dependent on					phorbol ester	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_19_17032_s_24	11864971	A novel PKC, Ras, MEKK1, MEK3/MEK6, p38 pathway has been shown to mediate phorbol ester-dependent activation of  hINV gene expression ( 28-30).	bind
50949	2	11465	5	NULL	NULL	NULL	NULL	PKC pathway	Process	novel	mediate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_19_17032_s_24	11864971	A novel PKC, Ras, MEKK1, MEK3/MEK6, p38 pathway has been shown to mediate phorbol ester-dependent activation of  hINV gene expression ( 28-30).	bind
50950	3	11465	5	NULL	NULL	NULL	NULL	Ras pathway	Process	novel	mediate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_19_17032_s_24	11864971	A novel PKC, Ras, MEKK1, MEK3/MEK6, p38 pathway has been shown to mediate phorbol ester-dependent activation of  hINV gene expression ( 28-30).	bind
50951	4	11465	5	NULL	NULL	NULL	NULL	MEKK1 pathway	Process	novel	mediate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_19_17032_s_24	11864971	A novel PKC, Ras, MEKK1, MEK3/MEK6, p38 pathway has been shown to mediate phorbol ester-dependent activation of  hINV gene expression ( 28-30).	bind
50952	5	11465	5	NULL	NULL	NULL	NULL	MEK3/MEK6 pathway	Process	novel	mediate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_19_17032_s_24	11864971	A novel PKC, Ras, MEKK1, MEK3/MEK6, p38 pathway has been shown to mediate phorbol ester-dependent activation of  hINV gene expression ( 28-30).	bind
50953	6	11465	5	NULL	NULL	NULL	NULL	p38 pathway	Process	novel	mediate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_19_17032_s_24	11864971	A novel PKC, Ras, MEKK1, MEK3/MEK6, p38 pathway has been shown to mediate phorbol ester-dependent activation of  hINV gene expression ( 28-30).	bind
47712	1	11465	6	10	NULL	0	NULL	hINV gene		activation of;;expression of	is dependent on					phorbol ester					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_19_17032_s_24	11864971	A novel PKC, Ras, MEKK1, MEK3/MEK6, p38 pathway has been shown to mediate phorbol ester-dependent activation of  hINV gene expression ( 28-30).	bind
47868	2	11465	6	NULL	NULL	0	NULL	PKC pathway	NULL	novel	mediates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_19_17032_s_24	11864971	A novel PKC, Ras, MEKK1, MEK3/MEK6, p38 pathway has been shown to mediate phorbol ester-dependent activation of  hINV gene expression ( 28-30).	bind
47869	3	11465	6	NULL	NULL	0	NULL	Ras pathway	NULL	novel	mediates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_19_17032_s_24	11864971	A novel PKC, Ras, MEKK1, MEK3/MEK6, p38 pathway has been shown to mediate phorbol ester-dependent activation of  hINV gene expression ( 28-30).	bind
47870	4	11465	6	NULL	NULL	0	NULL	MEKK1 pathway	NULL	novel	mediates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_19_17032_s_24	11864971	A novel PKC, Ras, MEKK1, MEK3/MEK6, p38 pathway has been shown to mediate phorbol ester-dependent activation of  hINV gene expression ( 28-30).	bind
47871	5	11465	6	NULL	NULL	0	NULL	MEK3/MEK6 pathway	NULL	novel	mediates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_19_17032_s_24	11864971	A novel PKC, Ras, MEKK1, MEK3/MEK6, p38 pathway has been shown to mediate phorbol ester-dependent activation of  hINV gene expression ( 28-30).	bind
47872	6	11465	6	NULL	NULL	0	NULL	p38 pathway	NULL	novel	mediates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_19_17032_s_24	11864971	A novel PKC, Ras, MEKK1, MEK3/MEK6, p38 pathway has been shown to mediate phorbol ester-dependent activation of  hINV gene expression ( 28-30).	bind
50954	1	11468	5	NULL	NULL	NULL	NULL	virus	Organism		induce					IFN-A genes	GP	transcription of			NULL		NULL	NULL	NULL	NULL	abs-batch0560-0569_nucleic-acids-res_23_24_8559665_s_1	8559665	A novel PRD I and TG binding activity involved in virus-induced transcription of IFN-A genes..	bind
50955	2	11468	5	NULL	NULL	NULL	NULL	PRD I	GP	binding activity of	involves					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0560-0569_nucleic-acids-res_23_24_8559665_s_1	8559665	A novel PRD I and TG binding activity involved in virus-induced transcription of IFN-A genes..	bind
50956	3	11468	5	NULL	NULL	NULL	NULL	TG	GP	binding activity of	involves					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0560-0569_nucleic-acids-res_23_24_8559665_s_1	8559665	A novel PRD I and TG binding activity involved in virus-induced transcription of IFN-A genes..	bind
47714	1	11468	6	NULL	NULL	0	NULL	virus	NULL		induces	NULL				IFN-A genes	NULL	transcription of			NULL		0	NULL	NULL	NULL	abs-batch0560-0569_nucleic-acids-res_23_24_8559665_s_1	8559665	A novel PRD I and TG binding activity involved in virus-induced transcription of IFN-A genes..	bind
47715	2	11468	6	NULL	NULL	0	NULL	PRD I	NULL	binding activity of	is involved in	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0560-0569_nucleic-acids-res_23_24_8559665_s_1	8559665	A novel PRD I and TG binding activity involved in virus-induced transcription of IFN-A genes..	bind
47716	3	11468	6	NULL	NULL	0	NULL	TG	NULL	binding activity of	is involved in	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0560-0569_nucleic-acids-res_23_24_8559665_s_1	8559665	A novel PRD I and TG binding activity involved in virus-induced transcription of IFN-A genes..	bind
50957	1	11469	5	NULL	NULL	NULL	NULL	RGPR-p117	GP		is a type of					regucalcin gene promoter region-related protein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0540-0549_int-j-mol-med_16_6_16273285_s_2	16273285	A novel protein RGPR-p117 was discovered as a regucalcin gene promoter  region-related protein that binds to the TTGGC motif using a yeast one-hybrid  system.	bind
50958	2	11469	5	NULL	NULL	NULL	NULL	RGPR-p117	GP		bind									TTGGC motif	NULL		NULL	NULL	NULL	NULL	abs-batch0540-0549_int-j-mol-med_16_6_16273285_s_2	16273285	A novel protein RGPR-p117 was discovered as a regucalcin gene promoter  region-related protein that binds to the TTGGC motif using a yeast one-hybrid  system.	bind
47717	1	11469	6	NULL	NULL	0	NULL	RGPR-p117 protein	NULL		is a type of	NULL				regucalcin gene promoter region-related protein	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_int-j-mol-med_16_6_16273285_s_2	16273285	A novel protein RGPR-p117 was discovered as a regucalcin gene promoter  region-related protein that binds to the TTGGC motif using a yeast one-hybrid  system.	bind
47718	2	11469	6	NULL	NULL	0	NULL	RGPR-p117 protein	NULL		bind	NULL					NULL			TTGGC motif	NULL		0	NULL	NULL	NULL	abs-batch0540-0549_int-j-mol-med_16_6_16273285_s_2	16273285	A novel protein RGPR-p117 was discovered as a regucalcin gene promoter  region-related protein that binds to the TTGGC motif using a yeast one-hybrid  system.	bind
50959	1	11473	5	NULL	NULL	NULL	NULL	Btf	GP		is					Bcl-2-associated transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4390_s_7	10330179	A novel protein, Btf (Bcl-2-associated transcription factor), that interacts with E1B 19K as well as with the antiapoptotic family members Bcl-2 and Bcl-xL but not with the proapoptotic protein Bax was identified.	bind
50960	2	11473	5	NULL	NULL	NULL	NULL	Btf	GP		interacts with					E1B 19K	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4390_s_7	10330179	A novel protein, Btf (Bcl-2-associated transcription factor), that interacts with E1B 19K as well as with the antiapoptotic family members Bcl-2 and Bcl-xL but not with the proapoptotic protein Bax was identified.	bind
50961	3	11473	5	NULL	NULL	NULL	NULL	Bcl-2	GP		is a member of					antiapoptotic family	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4390_s_7	10330179	A novel protein, Btf (Bcl-2-associated transcription factor), that interacts with E1B 19K as well as with the antiapoptotic family members Bcl-2 and Bcl-xL but not with the proapoptotic protein Bax was identified.	bind
50962	4	11473	5	NULL	NULL	NULL	NULL	Bcl-xL	GP		is a member of					antiapoptotic family	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4390_s_7	10330179	A novel protein, Btf (Bcl-2-associated transcription factor), that interacts with E1B 19K as well as with the antiapoptotic family members Bcl-2 and Bcl-xL but not with the proapoptotic protein Bax was identified.	bind
50963	5	11473	5	NULL	NULL	NULL	NULL	Btf	GP		interacts with					Bcl-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4390_s_7	10330179	A novel protein, Btf (Bcl-2-associated transcription factor), that interacts with E1B 19K as well as with the antiapoptotic family members Bcl-2 and Bcl-xL but not with the proapoptotic protein Bax was identified.	bind
50964	6	11473	5	NULL	NULL	NULL	NULL	Btf	GP		interacts with					Bcl-xL	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4390_s_7	10330179	A novel protein, Btf (Bcl-2-associated transcription factor), that interacts with E1B 19K as well as with the antiapoptotic family members Bcl-2 and Bcl-xL but not with the proapoptotic protein Bax was identified.	bind
50965	7	11473	5	NULL	NULL	NULL	NULL	Bax	GP		is a type of					proapoptotic protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4390_s_7	10330179	A novel protein, Btf (Bcl-2-associated transcription factor), that interacts with E1B 19K as well as with the antiapoptotic family members Bcl-2 and Bcl-xL but not with the proapoptotic protein Bax was identified.	bind
50966	8	11473	5	NULL	NULL	NULL	NULL	Btf	GP		does not interact with					Bax	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4390_s_7	10330179	A novel protein, Btf (Bcl-2-associated transcription factor), that interacts with E1B 19K as well as with the antiapoptotic family members Bcl-2 and Bcl-xL but not with the proapoptotic protein Bax was identified.	bind
47719	1	11473	6	NULL	NULL	0	NULL	Btf	NULL		is	NULL				Bcl-2-associated transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4390_s_7	10330179	A novel protein, Btf (Bcl-2-associated transcription factor), that interacts with E1B 19K as well as with the antiapoptotic family members Bcl-2 and Bcl-xL but not with the proapoptotic protein Bax was identified.	bind
47720	2	11473	6	10	NULL	0	NULL	Btf			interacts with					E1B 19K					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4390_s_7	10330179	A novel protein, Btf (Bcl-2-associated transcription factor), that interacts with E1B 19K as well as with the antiapoptotic family members Bcl-2 and Bcl-xL but not with the proapoptotic protein Bax was identified.	bind
47721	3	11473	6	10	NULL	0	NULL	Btf			interacts with					Bcl-2					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4390_s_7	10330179	A novel protein, Btf (Bcl-2-associated transcription factor), that interacts with E1B 19K as well as with the antiapoptotic family members Bcl-2 and Bcl-xL but not with the proapoptotic protein Bax was identified.	bind
47722	4	11473	6	10	NULL	0	NULL	Btf			interacts with					Bcl-xL					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4390_s_7	10330179	A novel protein, Btf (Bcl-2-associated transcription factor), that interacts with E1B 19K as well as with the antiapoptotic family members Bcl-2 and Bcl-xL but not with the proapoptotic protein Bax was identified.	bind
47723	5	11473	6	NULL	NULL	0	NULL	Bcl-2	NULL		is a type of	NULL				antiapoptotic family member	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4390_s_7	10330179	A novel protein, Btf (Bcl-2-associated transcription factor), that interacts with E1B 19K as well as with the antiapoptotic family members Bcl-2 and Bcl-xL but not with the proapoptotic protein Bax was identified.	bind
47724	6	11473	6	NULL	NULL	0	NULL	Bcl-xL	NULL		is a type of	NULL				antiapoptotic family member	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4390_s_7	10330179	A novel protein, Btf (Bcl-2-associated transcription factor), that interacts with E1B 19K as well as with the antiapoptotic family members Bcl-2 and Bcl-xL but not with the proapoptotic protein Bax was identified.	bind
47725	7	11473	6	10	NULL	0	NULL	Btf			does not interact with					Bax					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4390_s_7	10330179	A novel protein, Btf (Bcl-2-associated transcription factor), that interacts with E1B 19K as well as with the antiapoptotic family members Bcl-2 and Bcl-xL but not with the proapoptotic protein Bax was identified.	bind
47726	8	11473	6	NULL	NULL	0	NULL	Bax	NULL		is a type of	NULL				proapoptotic protein	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4390_s_7	10330179	A novel protein, Btf (Bcl-2-associated transcription factor), that interacts with E1B 19K as well as with the antiapoptotic family members Bcl-2 and Bcl-xL but not with the proapoptotic protein Bax was identified.	bind
50967	2	11474	5	NULL	NULL	NULL	NULL	chimeric T-cell receptors	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_clinmicrobiolrev_11_1_42_s_221	9457428	A novel protocol recently begun involves the redirection of the antigenic specificity of CD8-cell populations through the introduction of genes encoding chimeric T-cell receptors that bind HIV-1-infected cells.	bind
50968	1	11474	5	NULL	NULL	NULL	NULL	cells	Cell		infected by					HIV-1	Organism				NULL		NULL	NULL	NULL	NULL	gw60_clinmicrobiolrev_11_1_42_s_221	9457428	A novel protocol recently begun involves the redirection of the antigenic specificity of CD8-cell populations through the introduction of genes encoding chimeric T-cell receptors that bind HIV-1-infected cells.	bind
47727	2	11474	6	10	NULL	0	NULL	chimeric T-cell receptors			bind					HIV-1 infected cells					NULL		NULL	NULL	NULL	NULL	gw60_clinmicrobiolrev_11_1_42_s_221	9457428	A novel protocol recently begun involves the redirection of the antigenic specificity of CD8-cell populations through the introduction of genes encoding chimeric T-cell receptors that bind HIV-1-infected cells.	bind
58569	1	11474	6	10	NULL	0	NULL	cells			infected by					HIV					NULL		0	NULL	NULL	NULL	gw60_clinmicrobiolrev_11_1_42_s_221	9457428	A novel protocol recently begun involves the redirection of the antigenic specificity of CD8-cell populations through the introduction of genes encoding chimeric T-cell receptors that bind HIV-1-infected cells.	bind
50969	1	11475	5	NULL	NULL	NULL	NULL	MYT2	GP		is a type of					putative transcription factor protein	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_febs-lett_473_3_10818241_s_1	10818241	A novel putative transcription factor protein MYT2 that preferentially binds supercoiled DNA and induces DNA synthesis in quiescent cells..	bind
50970	2	11475	5	NULL	NULL	NULL	NULL	MYT2	GP		bind		preferentially			supercoiled DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_febs-lett_473_3_10818241_s_1	10818241	A novel putative transcription factor protein MYT2 that preferentially binds supercoiled DNA and induces DNA synthesis in quiescent cells..	bind
50971	3	11475	5	NULL	NULL	NULL	NULL	MYT2	GP		induce					DNA	NucleicAcid	synthesis of			NULL	quiescent cells	NULL	NULL	NULL	NULL	abs-batch0720-0739_febs-lett_473_3_10818241_s_1	10818241	A novel putative transcription factor protein MYT2 that preferentially binds supercoiled DNA and induces DNA synthesis in quiescent cells..	bind
47728	1	11475	6	NULL	NULL	0	NULL	MYT2 protein	NULL		is a type of	NULL				putative transcription factor	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_febs-lett_473_3_10818241_s_1	10818241	A novel putative transcription factor protein MYT2 that preferentially binds supercoiled DNA and induces DNA synthesis in quiescent cells..	bind
47729	2	11475	6	NULL	NULL	0	NULL	MYT2 protein	NULL		bind	NULL	preferentially			supercoiled DNA	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_febs-lett_473_3_10818241_s_1	10818241	A novel putative transcription factor protein MYT2 that preferentially binds supercoiled DNA and induces DNA synthesis in quiescent cells..	bind
47730	3	11475	6	NULL	NULL	0	NULL	MYT2 protein	NULL		induces	NULL				DNA	NULL	synthesis of			NULL	quiescent cells	0	NULL	NULL	NULL	abs-batch0720-0739_febs-lett_473_3_10818241_s_1	10818241	A novel putative transcription factor protein MYT2 that preferentially binds supercoiled DNA and induces DNA synthesis in quiescent cells..	bind
50972	1	11476	5	NULL	NULL	NULL	NULL	vitellogenin	GP	(DIG)-labeled	bind					ovarian membrane proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_2_655_s_7	12135911	A novel receptor-binding assay for vitellogenin was developed based on digoxigenin (DIG)-labeled vitellogenin tracer binding to ovarian membrane proteins immobilized in 96-well plates.	bind
47731	1	11476	6	10	NULL	0	NULL	vitellogenin tracer		(DIG)-labeled	bind					ovarian membrane proteins					NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_67_2_655_s_7	12135911	A novel receptor-binding assay for vitellogenin was developed based on digoxigenin (DIG)-labeled vitellogenin tracer binding to ovarian membrane proteins immobilized in 96-well plates.	bind
50973	1	11477	5	NULL	NULL	NULL	NULL	H+-V-ATPase	GP		bind					actin cytoskeleton	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_20_18499_s_1	12606563	A novel role for subunit C in mediating binding of the H+-V-ATPase to the actin cytoskeleton.	bind
50974	2	11477	5	NULL	NULL	NULL	NULL				mediate			subunit C		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_20_18499_s_1	12606563	A novel role for subunit C in mediating binding of the H+-V-ATPase to the actin cytoskeleton.	bind
47732	1	11477	6	NULL	NULL	0	NULL	H+-V-ATPase	NULL		bind	NULL				actin cytoskeleton	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_20_18499_s_1	12606563	A novel role for subunit C in mediating binding of the H+-V-ATPase to the actin cytoskeleton.	bind
47733	2	11477	6	NULL	NULL	0	NULL		NULL		mediates	NULL		subunit C		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_20_18499_s_1	12606563	A novel role for subunit C in mediating binding of the H+-V-ATPase to the actin cytoskeleton.	bind
50975	1	11478	5	NULL	NULL	NULL	NULL	Fen1/Rad27	GP		bind					PCNA	GP				NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_721_s_699	9759502	A Novel Role in DNA Metabolism for the Binding of Fen1/Rad27 to PCNA and Implications for Genetic Risk.	bind
50976	2	11478	5	NULL	NULL	NULL	NULL	statement 1	Process		plays a role in					DNA	NucleicAcid	metabolism of			NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_721_s_699	9759502	A Novel Role in DNA Metabolism for the Binding of Fen1/Rad27 to PCNA and Implications for Genetic Risk.	bind
47734	1	11478	6	NULL	NULL	0	NULL	Fen1/Rad27	NULL		bind	NULL				PCNA	NULL				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_67_0_721_s_699	9759502	A Novel Role in DNA Metabolism for the Binding of Fen1/Rad27 to PCNA and Implications for Genetic Risk.	bind
47735	2	11478	6	10	NULL	0	NULL	statement 1			plays a role in					DNA		metabolism of			NULL		NULL	NULL	NULL	NULL	gw60_annrevbiochem_67_0_721_s_699	9759502	A Novel Role in DNA Metabolism for the Binding of Fen1/Rad27 to PCNA and Implications for Genetic Risk.	bind
50977	1	11479	5	NULL	NULL	NULL	NULL	serine threonine kinase	GP	novel	bind					Ras-related RhoA GTPase	GP				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_3_195_s_180	10926869	A novel serine threonine kinase binding the Ras-related RhoA GTPase which translocate the kinase to peripheral membranes.	bind
50978	2	11479	5	NULL	NULL	NULL	NULL	serine threonine kinase	GP	novel	is translocated to					peripheral membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_3_195_s_180	10926869	A novel serine threonine kinase binding the Ras-related RhoA GTPase which translocate the kinase to peripheral membranes.	bind
50979	3	11479	5	NULL	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_3_195_s_180	10926869	A novel serine threonine kinase binding the Ras-related RhoA GTPase which translocate the kinase to peripheral membranes.	bind
47782	1	11479	6	NULL	NULL	0	NULL	serine threonine kinase	NULL		bind	NULL				Ras-related RhoA GTPase	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_3_195_s_180	10926869	A novel serine threonine kinase binding the Ras-related RhoA GTPase which translocate the kinase to peripheral membranes.	bind
47785	2	11479	6	10	NULL	0	NULL	serine threonine kinase			translocated to					peripheral membrane					NULL		NULL	NULL	NULL	NULL	gw60_circulationres_87_3_195_s_180	10926869	A novel serine threonine kinase binding the Ras-related RhoA GTPase which translocate the kinase to peripheral membranes.	bind
47786	3	11479	6	NULL	NULL	0	NULL	Ras-related RhoA GTPase	NULL		performs	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_87_3_195_s_180	10926869	A novel serine threonine kinase binding the Ras-related RhoA GTPase which translocate the kinase to peripheral membranes.	bind
50980	1	11490	5	NULL	NULL	NULL	NULL	shuttle protein	GP	novel	bind					RNA helicase A	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_160_2_177_s_569	12538639	A Novel Shuttle Protein Binds to RNA Helicase A and Activates the Retroviral Constitutive Transport Element.	bind
50981	2	11490	5	NULL	NULL	NULL	NULL	statement 1	Process		activates					retroviral constitutive transport element	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_160_2_177_s_569	12538639	A Novel Shuttle Protein Binds to RNA Helicase A and Activates the Retroviral Constitutive Transport Element.	bind
47787	1	11490	6	NULL	NULL	0	NULL	Shuttle Protein	NULL		bind	NULL				RNA Helicase A	NULL				NULL		0	NULL	NULL	NULL	gw60_cellbiol_160_2_177_s_569	12538639	A Novel Shuttle Protein Binds to RNA Helicase A and Activates the Retroviral Constitutive Transport Element.	bind
47788	2	11490	6	10	NULL	0	NULL	statement 1			activates					retroviral Constitutive Transport Element					NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_160_2_177_s_569	12538639	A Novel Shuttle Protein Binds to RNA Helicase A and Activates the Retroviral Constitutive Transport Element.	bind
50982	1	11491	5	NULL	NULL	NULL	NULL	EphA2	GP		is activated by					ligand	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1303_s_20	9430661	A novel Src homologous adapter protein, SLAP, also binds ligand-activated EphA2 ( 14).	bind
50983	2	11491	5	NULL	NULL	NULL	NULL	SLAP	GP		bind					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1303_s_20	9430661	A novel Src homologous adapter protein, SLAP, also binds ligand-activated EphA2 ( 14).	bind
50984	3	11491	5	NULL	NULL	NULL	NULL	SLAP	GP		is a type of					Src homologous adapter protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1303_s_20	9430661	A novel Src homologous adapter protein, SLAP, also binds ligand-activated EphA2 ( 14).	bind
47789	2	11491	6	10	NULL	0	NULL	SLAP			bind					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1303_s_20	9430661	A novel Src homologous adapter protein, SLAP, also binds ligand-activated EphA2 ( 14).	bind
47790	3	11491	6	10	NULL	0	NULL	SLAP			is a type of					Src homologous adapter protein					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1303_s_20	9430661	A novel Src homologous adapter protein, SLAP, also binds ligand-activated EphA2 ( 14).	bind
54122	1	11491	6	10	NULL	0	NULL	ligand			activates					EphA2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1303_s_20	9430661	A novel Src homologous adapter protein, SLAP, also binds ligand-activated EphA2 ( 14).	bind
50985	1	11492	5	NULL	NULL	NULL	NULL	GAKIN	GP		bind			stalk segment		hDlg	GP		GUK Domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_10_8395_s_110	12496241	A Novel Stalk Segment of GAKIN Binds to the GUK Domain of hDlg-- To map the hDlg-binding site within GAKIN, a series of truncated constructs of GAKIN were engineered and expressed in the rabbit reticulocyte transcription/translation system.	bind
47791	1	11492	6	NULL	NULL	0	NULL	GAKIN	NULL		bind	NULL		stalk segment		hDlg	NULL		GUK domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_10_8395_s_110	12496241	A Novel Stalk Segment of GAKIN Binds to the GUK Domain of hDlg-- To map the hDlg-binding site within GAKIN, a series of truncated constructs of GAKIN were engineered and expressed in the rabbit reticulocyte transcription/translation system.	bind
50986	1	11493	5	NULL	NULL	NULL	NULL	semaphorin	GP		is a type of					transmembrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nature_410_6825_174_s_254	11242070	A novel transmembrane semaphorin can bind c-src.	bind
50987	2	11493	5	NULL	NULL	NULL	NULL	semaphorin	GP		bind					c-src	GP				NULL		NULL	NULL	NULL	NULL	gw60_nature_410_6825_174_s_254	11242070	A novel transmembrane semaphorin can bind c-src.	bind
47792	1	11493	6	10	NULL	0	NULL	semaphorin			bind					c-src					NULL		NULL	NULL	NULL	NULL	gw60_nature_410_6825_174_s_254	11242070	A novel transmembrane semaphorin can bind c-src.	bind
54123	2	11493	6	10	NULL	0	NULL	semaphorin			is a type of					transmembrane protein					NULL		0	NULL	NULL	NULL	gw60_nature_410_6825_174_s_254	11242070	A novel transmembrane semaphorin can bind c-src.	bind
50988	1	11494	5	NULL	NULL	NULL	NULL	NSD1	GP		bind								holo-LBDs		NULL		NULL	NULL	NULL	NULL	gw60_embo_17_12_3398_s_7	9628876	A novel variant (FxxLL) of the NR box motif (LxxLL) is present in NID+L and is required for the binding of NSD1 to holo-LBDs.	bind
50989	2	11494	5	10	NULL	0	NULL				is a variant of				FxxLL					NR box motif LxxLL	NULL		NULL	NULL	NULL	NULL	gw60_embo_17_12_3398_s_7	9628876	A novel variant (FxxLL) of the NR box motif (LxxLL) is present in NID+L and is required for the binding of NSD1 to holo-LBDs.	bind
50990	3	11494	5	NULL	NULL	NULL	NULL	statement 2	Process		is present in					NID+L	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_12_3398_s_7	9628876	A novel variant (FxxLL) of the NR box motif (LxxLL) is present in NID+L and is required for the binding of NSD1 to holo-LBDs.	bind
50991	4	11494	5	NULL	NULL	NULL	NULL	statement 3	Process		is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_12_3398_s_7	9628876	A novel variant (FxxLL) of the NR box motif (LxxLL) is present in NID+L and is required for the binding of NSD1 to holo-LBDs.	bind
47793	1	11494	6	NULL	NULL	0	NULL	NSD1	NULL		bind	NULL					NULL		holo-LBD		NULL		0	NULL	NULL	NULL	gw60_embo_17_12_3398_s_7	9628876	A novel variant (FxxLL) of the NR box motif (LxxLL) is present in NID+L and is required for the binding of NSD1 to holo-LBDs.	bind
47794	2	11494	6	NULL	NULL	0	NULL		NULL		is a variant of	NULL			FxxLL		NULL			NR box motif LxxLL	NULL		0	NULL	NULL	NULL	gw60_embo_17_12_3398_s_7	9628876	A novel variant (FxxLL) of the NR box motif (LxxLL) is present in NID+L and is required for the binding of NSD1 to holo-LBDs.	bind
47795	3	11494	6	NULL	NULL	0	NULL	statement 2	NULL		is present in	NULL				NID+L	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_17_12_3398_s_7	9628876	A novel variant (FxxLL) of the NR box motif (LxxLL) is present in NID+L and is required for the binding of NSD1 to holo-LBDs.	bind
47796	4	11494	6	NULL	NULL	0	NULL		NULL		is required for	NULL			FxxLL	statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_17_12_3398_s_7	9628876	A novel variant (FxxLL) of the NR box motif (LxxLL) is present in NID+L and is required for the binding of NSD1 to holo-LBDs.	bind
50992	1	11495	5	NULL	NULL	NULL	NULL	WD repeat protein	GP		is a component of					methylosome	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6533_s_295	12192051	A novel WD repeat protein component of the methylosome binds Sm proteins.	bind
50993	2	11495	5	NULL	NULL	NULL	NULL	statement 1	Process		bind					Sm proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6533_s_295	12192051	A novel WD repeat protein component of the methylosome binds Sm proteins.	bind
47797	1	11495	6	10	NULL	0	NULL	WD repeat protein			is a component of					methylosome					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6533_s_295	12192051	A novel WD repeat protein component of the methylosome binds Sm proteins.	bind
47798	2	11495	6	10	NULL	0	NULL	statement 1			bind					Sm proteins					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_18_6533_s_295	12192051	A novel WD repeat protein component of the methylosome binds Sm proteins.	bind
50994	1	11497	5	NULL	NULL	NULL	NULL	bZIP protein	GP	yeast	bind									CRE motif	NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_14_0_459_s_608	9891790	A novel yeast bZIP protein binding to the CRE motif is a multicopy  suppressor for  cdc10 mutant of  Schizosaccharomyces pombe.	bind
50995	2	11497	5	NULL	NULL	NULL	NULL	statement 1	Process		is a suppressor for					cdc10	GP	mutant;;Schizosaccharomyces pombe			NULL		NULL	NULL	NULL	NULL	gw70_annurevcelldevbiol_14_0_459_s_608	9891790	A novel yeast bZIP protein binding to the CRE motif is a multicopy  suppressor for  cdc10 mutant of  Schizosaccharomyces pombe.	bind
47799	1	11497	6	NULL	NULL	0	NULL	bZIP protein	NULL	yeast	bind	NULL					NULL			CRE motif	NULL		0	NULL	NULL	NULL	gw70_annurevcelldevbiol_14_0_459_s_608	9891790	A novel yeast bZIP protein binding to the CRE motif is a multicopy  suppressor for  cdc10 mutant of  Schizosaccharomyces pombe.	bind
47800	2	11497	6	NULL	NULL	0	NULL	statement 1	NULL		is a suppressor for	NULL				cdc10 	NULL	Schizosaccharomyces pombe;; mutant			NULL		0	NULL	NULL	NULL	gw70_annurevcelldevbiol_14_0_459_s_608	9891790	A novel yeast bZIP protein binding to the CRE motif is a multicopy  suppressor for  cdc10 mutant of  Schizosaccharomyces pombe.	bind
50996	1	11499	5	NULL	NULL	NULL	NULL	blastopore lip-specific gene	GP	Xenopus laevis	is induced by					activin	GP				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_77_2_95_s_472	9831640	A novel, activin-inducible, blastopore lip-specific gene of  Xenopus laevis contains a fork head DNA-binding domain.	bind
54124	2	11499	5	NULL	NULL	NULL	NULL	blastopore lip-specific gene	GP	Xenopus laevis	contains								fork head DNA-binding domain		NULL		NULL	NULL	NULL	NULL	gw60_mechdev_77_2_95_s_472	9831640	A novel, activin-inducible, blastopore lip-specific gene of  Xenopus laevis contains a fork head DNA-binding domain.	bind
47801	1	11499	6	NULL	NULL	0	NULL	blastopore lip-specific gene	NULL	Xenopus laevis	is induced by	NULL				activin	NULL				NULL		NULL	NULL	NULL	NULL	gw60_mechdev_77_2_95_s_472	9831640	A novel, activin-inducible, blastopore lip-specific gene of  Xenopus laevis contains a fork head DNA-binding domain.	bind
47802	2	11499	6	NULL	NULL	0	NULL	blastopore lip-specific gene	NULL	Xenopus laevis	contains	NULL					NULL		fork head DNA-binding domain		NULL		0	NULL	NULL	NULL	gw60_mechdev_77_2_95_s_472	9831640	A novel, activin-inducible, blastopore lip-specific gene of  Xenopus laevis contains a fork head DNA-binding domain.	bind
50997	1	11500	5	NULL	NULL	NULL	NULL	erythroid cell-specific transcription factor	GP		bind									CACC element	NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_21_2778_s_608	11069894	A novel, erythroid cell-specific transcription factor that binds to the CACC element related to the kruppel family of nuclear proteins.	bind
50998	2	11500	5	NULL	NULL	NULL	NULL				is related to				CACC element	nuclear proteins	GP		kruppel family		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_21_2778_s_608	11069894	A novel, erythroid cell-specific transcription factor that binds to the CACC element related to the kruppel family of nuclear proteins.	bind
47803	1	11500	6	NULL	NULL	0	NULL	erythroid cell-specific transcription factor	NULL		bind	NULL					NULL			CACC element	NULL		0	NULL	NULL	NULL	gw60_genesdev_14_21_2778_s_608	11069894	A novel, erythroid cell-specific transcription factor that binds to the CACC element related to the kruppel family of nuclear proteins.	bind
47804	2	11500	6	10	NULL	0	NULL				is related to				CACC element	nuclear proteins			kruppel family		NULL		NULL	NULL	NULL	NULL	gw60_genesdev_14_21_2778_s_608	11069894	A novel, erythroid cell-specific transcription factor that binds to the CACC element related to the kruppel family of nuclear proteins.	bind
51000	1	11501	5	NULL	NULL	NULL	NULL	HF-1b	GP		is a type of					tissue restricted zinc finger protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_nature_407_6801_227_s_276	11001065	A novel, tissue restricted zinc finger protein (HF-1b) binds to the cardiac regulatory element (HF-1b/MEF-2) in the rat myosin light chain-2 gene.	bind
51001	2	11501	5	NULL	NULL	NULL	NULL	HF-1b	GP		bind					myosin light chain-2 gene	GP	rat		HF-1b/MEF-2	NULL		NULL	NULL	NULL	NULL	gw60_nature_407_6801_227_s_276	11001065	A novel, tissue restricted zinc finger protein (HF-1b) binds to the cardiac regulatory element (HF-1b/MEF-2) in the rat myosin light chain-2 gene.	bind
54151	3	11501	5	NULL	NULL	NULL	NULL	HF-1b/MEF-2	GP		is a type of					cardiac regulatory element	GP				NULL		NULL	NULL	NULL	NULL	gw60_nature_407_6801_227_s_276	11001065	A novel, tissue restricted zinc finger protein (HF-1b) binds to the cardiac regulatory element (HF-1b/MEF-2) in the rat myosin light chain-2 gene.	bind
50366	1	11501	6	10	NULL	0	NULL	HF-1b			bind					myosin light chain-2 gene		rat		HF-1b/MEF-2	NULL		NULL	NULL	NULL	NULL	gw60_nature_407_6801_227_s_276	11001065	A novel, tissue restricted zinc finger protein (HF-1b) binds to the cardiac regulatory element (HF-1b/MEF-2) in the rat myosin light chain-2 gene.	bind
50367	2	11501	6	10	NULL	0	NULL	HF-1b			is a type of					tissue restricted zinc finger protein					NULL		NULL	NULL	NULL	NULL	gw60_nature_407_6801_227_s_276	11001065	A novel, tissue restricted zinc finger protein (HF-1b) binds to the cardiac regulatory element (HF-1b/MEF-2) in the rat myosin light chain-2 gene.	bind
50368	3	11501	6	NULL	NULL	0	NULL	HF-1b/MEF-2	NULL		is a type of	NULL				cardiac regulatory element	NULL				NULL		0	NULL	NULL	NULL	gw60_nature_407_6801_227_s_276	11001065	A novel, tissue restricted zinc finger protein (HF-1b) binds to the cardiac regulatory element (HF-1b/MEF-2) in the rat myosin light chain-2 gene.	bind
51002	1	11506	5	NULL	NULL	NULL	NULL	glycerol phosphate dehydrogenase gene	GP	human;;mitochondrial	bind				NRF-2 site	NRF-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1576_1_1_s_163	12031478	A NRF-2 site in the human mitochondrial glycerol phosphate dehydrogenase gene binds NRF-2 and makes a major contribution to promoter activity [ 77].	bind
51003	2	11506	5	NULL	NULL	NULL	NULL	statement 1	Process		contribute to					promoter	NucleicAcid	activity of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1576_1_1_s_163	12031478	A NRF-2 site in the human mitochondrial glycerol phosphate dehydrogenase gene binds NRF-2 and makes a major contribution to promoter activity [ 77].	bind
50369	1	11506	6	NULL	NULL	0	NULL	glycerol phosphate dehydrogenase gene	NULL	human;; mitochondrial	bind	NULL			NRF-2 site	NRF-2	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1576_1_1_s_163	12031478	A NRF-2 site in the human mitochondrial glycerol phosphate dehydrogenase gene binds NRF-2 and makes a major contribution to promoter activity [ 77].	bind
50370	2	11506	6	NULL	NULL	0	NULL	statement 1	NULL		plays a role in	NULL				promoter	NULL	activity of 			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1576_1_1_s_163	12031478	A NRF-2 site in the human mitochondrial glycerol phosphate dehydrogenase gene binds NRF-2 and makes a major contribution to promoter activity [ 77].	bind
51004	1	11507	5	NULL	NULL	NULL	NULL	CRM1	GP		bind					STAT1	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_sci-stke_2003_195_12915721_s_8	12915721	A nuclear export signal of STAT1 appears  to be masked when dimers are bound to DNA, but it becomes accessible to  the CRM1 export carrier after dissociation from DNA. CRM1 binds STAT1  and transports the transcription factor back to the cytoplasm.	bind
51005	2	11507	5	NULL	NULL	NULL	NULL	STAT1	GP		is transported to					cytoplasm	CellComponent				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_sci-stke_2003_195_12915721_s_8	12915721	A nuclear export signal of STAT1 appears  to be masked when dimers are bound to DNA, but it becomes accessible to  the CRM1 export carrier after dissociation from DNA. CRM1 binds STAT1  and transports the transcription factor back to the cytoplasm.	bind
51006	3	11507	5	NULL	NULL	NULL	NULL	statement 1	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_sci-stke_2003_195_12915721_s_8	12915721	A nuclear export signal of STAT1 appears  to be masked when dimers are bound to DNA, but it becomes accessible to  the CRM1 export carrier after dissociation from DNA. CRM1 binds STAT1  and transports the transcription factor back to the cytoplasm.	bind
51007	4	11507	5	NULL	NULL	NULL	NULL	dimers	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_sci-stke_2003_195_12915721_s_8	12915721	A nuclear export signal of STAT1 appears  to be masked when dimers are bound to DNA, but it becomes accessible to  the CRM1 export carrier after dissociation from DNA. CRM1 binds STAT1  and transports the transcription factor back to the cytoplasm.	bind
51008	5	11507	5	NULL	NULL	NULL	NULL	statement 4	Process		masks					STAT1	GP		nuclear export signal		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_sci-stke_2003_195_12915721_s_8	12915721	A nuclear export signal of STAT1 appears  to be masked when dimers are bound to DNA, but it becomes accessible to  the CRM1 export carrier after dissociation from DNA. CRM1 binds STAT1  and transports the transcription factor back to the cytoplasm.	bind
51009	6	11507	5	NULL	NULL	NULL	NULL	STAT1	GP		is accessible to			nuclear export signal		CRM1 export carrier	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_sci-stke_2003_195_12915721_s_8	12915721	A nuclear export signal of STAT1 appears  to be masked when dimers are bound to DNA, but it becomes accessible to  the CRM1 export carrier after dissociation from DNA. CRM1 binds STAT1  and transports the transcription factor back to the cytoplasm.	bind
51010	7	11507	5	NULL	NULL	NULL	NULL	dimers	GP		dissociates from					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_sci-stke_2003_195_12915721_s_8	12915721	A nuclear export signal of STAT1 appears  to be masked when dimers are bound to DNA, but it becomes accessible to  the CRM1 export carrier after dissociation from DNA. CRM1 binds STAT1  and transports the transcription factor back to the cytoplasm.	bind
51011	8	11507	5	NULL	NULL	NULL	NULL	statement 6	Process		occurs after					statement 7	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_sci-stke_2003_195_12915721_s_8	12915721	A nuclear export signal of STAT1 appears  to be masked when dimers are bound to DNA, but it becomes accessible to  the CRM1 export carrier after dissociation from DNA. CRM1 binds STAT1  and transports the transcription factor back to the cytoplasm.	bind
50503	1	11507	6	NULL	NULL	0	NULL	CRM1	NULL		bind	NULL				STAT1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_sci-stke_2003_195_12915721_s_8	12915721	A nuclear export signal of STAT1 appears  to be masked when dimers are bound to DNA, but it becomes accessible to  the CRM1 export carrier after dissociation from DNA. CRM1 binds STAT1  and transports the transcription factor back to the cytoplasm.	bind
50504	2	11507	6	NULL	NULL	0	NULL	STAT1	NULL		is transported to	NULL				cytoplasm	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_sci-stke_2003_195_12915721_s_8	12915721	A nuclear export signal of STAT1 appears  to be masked when dimers are bound to DNA, but it becomes accessible to  the CRM1 export carrier after dissociation from DNA. CRM1 binds STAT1  and transports the transcription factor back to the cytoplasm.	bind
50505	3	11507	6	10	NULL	0	NULL	statement 1			leads to					statement 2					NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_sci-stke_2003_195_12915721_s_8	12915721	A nuclear export signal of STAT1 appears  to be masked when dimers are bound to DNA, but it becomes accessible to  the CRM1 export carrier after dissociation from DNA. CRM1 binds STAT1  and transports the transcription factor back to the cytoplasm.	bind
50506	4	11507	6	NULL	NULL	0	NULL	dimers	NULL		bind	NULL				DNA	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_sci-stke_2003_195_12915721_s_8	12915721	A nuclear export signal of STAT1 appears  to be masked when dimers are bound to DNA, but it becomes accessible to  the CRM1 export carrier after dissociation from DNA. CRM1 binds STAT1  and transports the transcription factor back to the cytoplasm.	bind
50507	5	11507	6	10	NULL	0	NULL	statement 4			masks					STAT1			nuclear export signal		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_sci-stke_2003_195_12915721_s_8	12915721	A nuclear export signal of STAT1 appears  to be masked when dimers are bound to DNA, but it becomes accessible to  the CRM1 export carrier after dissociation from DNA. CRM1 binds STAT1  and transports the transcription factor back to the cytoplasm.	bind
50508	7	11507	6	10	NULL	0	NULL	Dimers			dissociate from					DNA					NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_sci-stke_2003_195_12915721_s_8	12915721	A nuclear export signal of STAT1 appears  to be masked when dimers are bound to DNA, but it becomes accessible to  the CRM1 export carrier after dissociation from DNA. CRM1 binds STAT1  and transports the transcription factor back to the cytoplasm.	bind
50509	6	11507	6	10	NULL	0	NULL	STAT1			is accessible to			nuclear export signal		CRM1 export carrier					NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_sci-stke_2003_195_12915721_s_8	12915721	A nuclear export signal of STAT1 appears  to be masked when dimers are bound to DNA, but it becomes accessible to  the CRM1 export carrier after dissociation from DNA. CRM1 binds STAT1  and transports the transcription factor back to the cytoplasm.	bind
50510	8	11507	6	10	NULL	0	NULL	statement 6			occurs after					statement 7					NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_sci-stke_2003_195_12915721_s_8	12915721	A nuclear export signal of STAT1 appears  to be masked when dimers are bound to DNA, but it becomes accessible to  the CRM1 export carrier after dissociation from DNA. CRM1 binds STAT1  and transports the transcription factor back to the cytoplasm.	bind
51012	1	11508	5	NULL	NULL	NULL	NULL	nuclear factor	GP		is present in		exclusively			lens cells	Cell				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_development_113_2_1782865_s_5	1782865	A nuclear factor present exclusively in lens cells binds to  the 84 bp element in the region between positions -165 and -140.	bind
51013	2	11508	5	NULL	NULL	0	NULL		NULL		is present in between	NULL			84 bp element		NULL			positions -165 and -140	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_development_113_2_1782865_s_5	1782865	A nuclear factor present exclusively in lens cells binds to  the 84 bp element in the region between positions -165 and -140.	bind
51014	3	11508	5	NULL	NULL	NULL	NULL	statement 1	Process		bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_development_113_2_1782865_s_5	1782865	A nuclear factor present exclusively in lens cells binds to  the 84 bp element in the region between positions -165 and -140.	bind
50371	1	11508	6	NULL	NULL	0	NULL	nuclear factor	NULL		is present in	NULL	exclusively			lens cells	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_development_113_2_1782865_s_5	1782865	A nuclear factor present exclusively in lens cells binds to  the 84 bp element in the region between positions -165 and -140.	bind
50372	3	11508	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_development_113_2_1782865_s_5	1782865	A nuclear factor present exclusively in lens cells binds to  the 84 bp element in the region between positions -165 and -140.	bind
50373	2	11508	6	NULL	NULL	0	NULL		NULL		lies in the region between	NULL			84 bp element		NULL			positions -165 and -140	NULL		0	NULL	NULL	NULL	abs-batch0650-0679_development_113_2_1782865_s_5	1782865	A nuclear factor present exclusively in lens cells binds to  the 84 bp element in the region between positions -165 and -140.	bind
51015	1	11509	5	NULL	NULL	NULL	NULL	nuclear protein	GP		bind		selectively							dyad Gpal element	NULL		NULL	NULL	NULL	NULL	gw60_genetics_157_2_699_s_205	11156990	A nuclear protein binds selectively to the dyad Gpal element:   Nuclear extracts from Drosophila embryos or specific tissues were isolated and probed with a radiolabeled double-stranded 30-bp oligonucleotide (dPalGld) corresponding to the dyad Gpal (dGpal) and flanking sequences.	bind
51016	2	11509	5	NULL	NULL	NULL	NULL	dyad Gpal	GP		is					dGpal	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_157_2_699_s_205	11156990	A nuclear protein binds selectively to the dyad Gpal element:   Nuclear extracts from Drosophila embryos or specific tissues were isolated and probed with a radiolabeled double-stranded 30-bp oligonucleotide (dPalGld) corresponding to the dyad Gpal (dGpal) and flanking sequences.	bind
50382	1	11509	6	NULL	NULL	0	NULL	nuclear protein	NULL		bind	NULL	selectively				NULL			dyad Gpal element	NULL		NULL	NULL	NULL	NULL	gw60_genetics_157_2_699_s_205	11156990	A nuclear protein binds selectively to the dyad Gpal element:   Nuclear extracts from Drosophila embryos or specific tissues were isolated and probed with a radiolabeled double-stranded 30-bp oligonucleotide (dPalGld) corresponding to the dyad Gpal (dGpal) and flanking sequences.	bind
50383	2	11509	6	NULL	NULL	0	NULL	dyad Gpal	NULL		is	NULL				dGpal	NULL				NULL		0	NULL	NULL	NULL	gw60_genetics_157_2_699_s_205	11156990	A nuclear protein binds selectively to the dyad Gpal element:   Nuclear extracts from Drosophila embryos or specific tissues were isolated and probed with a radiolabeled double-stranded 30-bp oligonucleotide (dPalGld) corresponding to the dyad Gpal (dGpal) and flanking sequences.	bind
51017	1	11510	5	NULL	NULL	NULL	NULL	nuclear protein	GP		bind		specifically							A CGTG intrinsic DNA bending sequence	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_3_1282_s_102	7836392	A Nuclear Protein Binds Specifically to the  A CGTG Intrinsic DNA Bending Sequence In preliminary  experiments we demonstrated that a protein in nuclear extracts from  CHO, HeLa, and MCF7 cells, but absent in COS cell extracts, bound  specifically to A CGTG multimers (data not shown).	bind
51018	2	11510	5	NULL	NULL	NULL	NULL	nuclear protein	GP		is present in					CHO cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_3_1282_s_102	7836392	A Nuclear Protein Binds Specifically to the  A CGTG Intrinsic DNA Bending Sequence In preliminary  experiments we demonstrated that a protein in nuclear extracts from  CHO, HeLa, and MCF7 cells, but absent in COS cell extracts, bound  specifically to A CGTG multimers (data not shown).	bind
51019	3	11510	5	NULL	NULL	NULL	NULL	nuclear protein	GP		is present in					HeLa cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_3_1282_s_102	7836392	A Nuclear Protein Binds Specifically to the  A CGTG Intrinsic DNA Bending Sequence In preliminary  experiments we demonstrated that a protein in nuclear extracts from  CHO, HeLa, and MCF7 cells, but absent in COS cell extracts, bound  specifically to A CGTG multimers (data not shown).	bind
51020	4	11510	5	NULL	NULL	NULL	NULL	nuclear protein	GP		is present in					MCF7 cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_3_1282_s_102	7836392	A Nuclear Protein Binds Specifically to the  A CGTG Intrinsic DNA Bending Sequence In preliminary  experiments we demonstrated that a protein in nuclear extracts from  CHO, HeLa, and MCF7 cells, but absent in COS cell extracts, bound  specifically to A CGTG multimers (data not shown).	bind
51021	5	11510	5	NULL	NULL	NULL	NULL	nuclear protein	GP		is absent in					COS cell extracts	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_3_1282_s_102	7836392	A Nuclear Protein Binds Specifically to the  A CGTG Intrinsic DNA Bending Sequence In preliminary  experiments we demonstrated that a protein in nuclear extracts from  CHO, HeLa, and MCF7 cells, but absent in COS cell extracts, bound  specifically to A CGTG multimers (data not shown).	bind
51022	6	11510	5	NULL	NULL	NULL	NULL	statement 2	Process		bind		specifically							A CGTG multimers	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_3_1282_s_102	7836392	A Nuclear Protein Binds Specifically to the  A CGTG Intrinsic DNA Bending Sequence In preliminary  experiments we demonstrated that a protein in nuclear extracts from  CHO, HeLa, and MCF7 cells, but absent in COS cell extracts, bound  specifically to A CGTG multimers (data not shown).	bind
54152	7	11510	5	NULL	NULL	NULL	NULL	statement 3	Process		bind		specifically							A CGTG multimers 	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_3_1282_s_102	7836392	A Nuclear Protein Binds Specifically to the  A CGTG Intrinsic DNA Bending Sequence In preliminary  experiments we demonstrated that a protein in nuclear extracts from  CHO, HeLa, and MCF7 cells, but absent in COS cell extracts, bound  specifically to A CGTG multimers (data not shown).	bind
54153	8	11510	5	NULL	NULL	NULL	NULL	statement 4	Process		bind		specifically							A CGTG multimers 	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_3_1282_s_102	7836392	A Nuclear Protein Binds Specifically to the  A CGTG Intrinsic DNA Bending Sequence In preliminary  experiments we demonstrated that a protein in nuclear extracts from  CHO, HeLa, and MCF7 cells, but absent in COS cell extracts, bound  specifically to A CGTG multimers (data not shown).	bind
50384	1	11510	6	NULL	NULL	0	NULL	nuclear protein	NULL		bind	NULL					NULL			A CGTG Intrinsic DNA Bending Sequence	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_3_1282_s_102	7836392	A Nuclear Protein Binds Specifically to the  A CGTG Intrinsic DNA Bending Sequence In preliminary  experiments we demonstrated that a protein in nuclear extracts from  CHO, HeLa, and MCF7 cells, but absent in COS cell extracts, bound  specifically to A CGTG multimers (data not shown).	bind
50385	2	11510	6	NULL	NULL	0	NULL	nuclear protein	NULL		is present in	NULL				CHO cells extracts	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_3_1282_s_102	7836392	A Nuclear Protein Binds Specifically to the  A CGTG Intrinsic DNA Bending Sequence In preliminary  experiments we demonstrated that a protein in nuclear extracts from  CHO, HeLa, and MCF7 cells, but absent in COS cell extracts, bound  specifically to A CGTG multimers (data not shown).	bind
50511	3	11510	6	NULL	NULL	0	NULL	statement 2	NULL		bind	NULL	specifically				NULL			A CGTG multimers	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_3_1282_s_102	7836392	A Nuclear Protein Binds Specifically to the  A CGTG Intrinsic DNA Bending Sequence In preliminary  experiments we demonstrated that a protein in nuclear extracts from  CHO, HeLa, and MCF7 cells, but absent in COS cell extracts, bound  specifically to A CGTG multimers (data not shown).	bind
50512	4	11510	6	NULL	NULL	0	NULL	nuclear protein	NULL		is present in	NULL				HeLa cells extracts	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_3_1282_s_102	7836392	A Nuclear Protein Binds Specifically to the  A CGTG Intrinsic DNA Bending Sequence In preliminary  experiments we demonstrated that a protein in nuclear extracts from  CHO, HeLa, and MCF7 cells, but absent in COS cell extracts, bound  specifically to A CGTG multimers (data not shown).	bind
50513	5	11510	6	NULL	NULL	0	NULL	statement 4	NULL		bind	NULL	specifically				NULL			A CGTG multimers	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_3_1282_s_102	7836392	A Nuclear Protein Binds Specifically to the  A CGTG Intrinsic DNA Bending Sequence In preliminary  experiments we demonstrated that a protein in nuclear extracts from  CHO, HeLa, and MCF7 cells, but absent in COS cell extracts, bound  specifically to A CGTG multimers (data not shown).	bind
50514	6	11510	6	NULL	NULL	0	NULL	nuclear protein	NULL		is present in	NULL				MCF7 cells extract	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_3_1282_s_102	7836392	A Nuclear Protein Binds Specifically to the  A CGTG Intrinsic DNA Bending Sequence In preliminary  experiments we demonstrated that a protein in nuclear extracts from  CHO, HeLa, and MCF7 cells, but absent in COS cell extracts, bound  specifically to A CGTG multimers (data not shown).	bind
50515	7	11510	6	10	NULL	0	NULL	statement 6			bind		specifically							A CGTG multimers	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_3_1282_s_102	7836392	A Nuclear Protein Binds Specifically to the  A CGTG Intrinsic DNA Bending Sequence In preliminary  experiments we demonstrated that a protein in nuclear extracts from  CHO, HeLa, and MCF7 cells, but absent in COS cell extracts, bound  specifically to A CGTG multimers (data not shown).	bind
54154	8	11510	6	10	NULL	0	NULL	nuclear protein			is absent in					COS cell extracts					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_3_1282_s_102	7836392	A Nuclear Protein Binds Specifically to the  A CGTG Intrinsic DNA Bending Sequence In preliminary  experiments we demonstrated that a protein in nuclear extracts from  CHO, HeLa, and MCF7 cells, but absent in COS cell extracts, bound  specifically to A CGTG multimers (data not shown).	bind
51023	1	11511	5	NULL	NULL	NULL	NULL	ZBRK1	GP		complex with					BRCA1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_4_757_s_180	11090615	A Nuclear Protein Complex Including ZBRK1 and BRCA1 Binds to the ZBRK1 Recognition Sequence in  GADD45 Intron 3	bind
51024	2	11511	5	NULL	NULL	NULL	NULL				is present in				ZBRK1 Recognition Sequence	GADD45	GP			Intron 3	NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_4_757_s_180	11090615	A Nuclear Protein Complex Including ZBRK1 and BRCA1 Binds to the ZBRK1 Recognition Sequence in  GADD45 Intron 3	bind
51025	3	11511	5	NULL	NULL	NULL	NULL	statement 1	Process		bind					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_4_757_s_180	11090615	A Nuclear Protein Complex Including ZBRK1 and BRCA1 Binds to the ZBRK1 Recognition Sequence in  GADD45 Intron 3	bind
54156	4	11511	5	NULL	NULL	NULL	NULL	statement 1	GP		is a type of					Nuclear Protein Complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_4_757_s_180	11090615	A Nuclear Protein Complex Including ZBRK1 and BRCA1 Binds to the ZBRK1 Recognition Sequence in  GADD45 Intron 3	bind
50386	1	11511	6	NULL	NULL	0	NULL	ZBRK1	NULL		forms a complex with	NULL				BRCA1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcell_6_4_757_s_180	11090615	A Nuclear Protein Complex Including ZBRK1 and BRCA1 Binds to the ZBRK1 Recognition Sequence in  GADD45 Intron 3	bind
50387	2	11511	6	10	NULL	0	NULL				present in				ZBRK1 recognition sequence	GADD45				Intron 3	NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_4_757_s_180	11090615	A Nuclear Protein Complex Including ZBRK1 and BRCA1 Binds to the ZBRK1 Recognition Sequence in  GADD45 Intron 3	bind
54155	3	11511	6	10	NULL	0	NULL	statement 1			bind					statement 2					NULL		0	NULL	NULL	NULL	gw60_molcell_6_4_757_s_180	11090615	A Nuclear Protein Complex Including ZBRK1 and BRCA1 Binds to the ZBRK1 Recognition Sequence in  GADD45 Intron 3	bind
54157	4	11511	6	10	NULL	0	NULL	statement 1			is a type of					Nuclear Protein Complex					NULL		0	NULL	NULL	NULL	gw60_molcell_6_4_757_s_180	11090615	A Nuclear Protein Complex Including ZBRK1 and BRCA1 Binds to the ZBRK1 Recognition Sequence in  GADD45 Intron 3	bind
51026	1	11512	5	NULL	NULL	NULL	NULL	nuclear protein	GP	rat;;gastric corpus	bind		specifically					putative		AP2/SP1 site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7661_s_159	11113118	A nuclear protein isolated from rat gastric corpus also specifically bound to the putative AP2/SP1 site, as shown in Fig.  6 e.	bind
50388	1	11512	6	NULL	NULL	0	NULL	nuclear protein	NULL		is isolated from	NULL				gastric corpus	NULL	rat			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_10_7661_s_159	11113118	A nuclear protein isolated from rat gastric corpus also specifically bound to the putative AP2/SP1 site, as shown in Fig.  6 e.	bind
50389	2	11512	6	10	NULL	0	NULL	statement 1			bind		specifically					putative		AP2/SP1 site	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_10_7661_s_159	11113118	A nuclear protein isolated from rat gastric corpus also specifically bound to the putative AP2/SP1 site, as shown in Fig.  6 e.	bind
51027	1	11513	5	NULL	NULL	NULL	NULL	SRF	GP		is					serum response factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_407_1_7_s_5	9141471	A nuclear protein termed serum response factor (SRF) binds the CArG box motifs, the inner core of SRE, present in the promoter regions of many immediate early genes including  c-fos and several actins [ 1,   3].	bind
51028	2	11513	5	NULL	NULL	NULL	NULL	SRF	GP		is a type of					nuclear protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_407_1_7_s_5	9141471	A nuclear protein termed serum response factor (SRF) binds the CArG box motifs, the inner core of SRE, present in the promoter regions of many immediate early genes including  c-fos and several actins [ 1,   3].	bind
51029	3	11513	5	NULL	NULL	NULL	NULL	SRF	GP		bind									CArG box motifs	NULL		NULL	NULL	NULL	NULL	gw60_febslett_407_1_7_s_5	9141471	A nuclear protein termed serum response factor (SRF) binds the CArG box motifs, the inner core of SRE, present in the promoter regions of many immediate early genes including  c-fos and several actins [ 1,   3].	bind
51030	4	11513	5	NULL	NULL	NULL	NULL	SRF	GP		bind									inner core of SRE	NULL		NULL	NULL	NULL	NULL	gw60_febslett_407_1_7_s_5	9141471	A nuclear protein termed serum response factor (SRF) binds the CArG box motifs, the inner core of SRE, present in the promoter regions of many immediate early genes including  c-fos and several actins [ 1,   3].	bind
51031	5	11513	5	NULL	NULL	NULL	NULL	c-fos	GP		is a type of					immediate early genes	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_407_1_7_s_5	9141471	A nuclear protein termed serum response factor (SRF) binds the CArG box motifs, the inner core of SRE, present in the promoter regions of many immediate early genes including  c-fos and several actins [ 1,   3].	bind
51032	6	11513	5	NULL	NULL	NULL	NULL				is present in				CArG box motifs	c-fos	GP			promoter regions	NULL		NULL	NULL	NULL	NULL	gw60_febslett_407_1_7_s_5	9141471	A nuclear protein termed serum response factor (SRF) binds the CArG box motifs, the inner core of SRE, present in the promoter regions of many immediate early genes including  c-fos and several actins [ 1,   3].	bind
51033	7	11513	5	NULL	NULL	NULL	NULL				is present in				inner core of SRE	c-fos	GP			promoter region	NULL		NULL	NULL	NULL	NULL	gw60_febslett_407_1_7_s_5	9141471	A nuclear protein termed serum response factor (SRF) binds the CArG box motifs, the inner core of SRE, present in the promoter regions of many immediate early genes including  c-fos and several actins [ 1,   3].	bind
58809	8	11513	5	NULL	NULL	NULL	NULL				present in				CArG box motifs	actins	GP			promoter region	NULL		NULL	NULL	NULL	NULL	gw60_febslett_407_1_7_s_5	9141471	A nuclear protein termed serum response factor (SRF) binds the CArG box motifs, the inner core of SRE, present in the promoter regions of many immediate early genes including  c-fos and several actins [ 1,   3].	bind
58810	9	11513	5	NULL	NULL	NULL	NULL				present in				inner core of SRE	actins	GP			promoter region	NULL		NULL	NULL	NULL	NULL	gw60_febslett_407_1_7_s_5	9141471	A nuclear protein termed serum response factor (SRF) binds the CArG box motifs, the inner core of SRE, present in the promoter regions of many immediate early genes including  c-fos and several actins [ 1,   3].	bind
50516	1	11513	6	10	NULL	0	NULL	SRF			bind									CArG box motif 	NULL		NULL	NULL	NULL	NULL	gw60_febslett_407_1_7_s_5	9141471	A nuclear protein termed serum response factor (SRF) binds the CArG box motifs, the inner core of SRE, present in the promoter regions of many immediate early genes including  c-fos and several actins [ 1,   3].	bind
50517	2	11513	6	10	NULL	0	NULL	SRF			bind									inner core of SRE 	NULL		NULL	NULL	NULL	NULL	gw60_febslett_407_1_7_s_5	9141471	A nuclear protein termed serum response factor (SRF) binds the CArG box motifs, the inner core of SRE, present in the promoter regions of many immediate early genes including  c-fos and several actins [ 1,   3].	bind
50518	3	11513	6	NULL	NULL	0	NULL	SRF	NULL		is	NULL				serum response factor	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_407_1_7_s_5	9141471	A nuclear protein termed serum response factor (SRF) binds the CArG box motifs, the inner core of SRE, present in the promoter regions of many immediate early genes including  c-fos and several actins [ 1,   3].	bind
50519	4	11513	6	NULL	NULL	0	NULL	c-fos	NULL		is a type of	NULL				immediate early gene	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_407_1_7_s_5	9141471	A nuclear protein termed serum response factor (SRF) binds the CArG box motifs, the inner core of SRE, present in the promoter regions of many immediate early genes including  c-fos and several actins [ 1,   3].	bind
54158	5	11513	6	10	NULL	0	NULL	SRF			is a type of					nuclear protein					NULL		0	NULL	NULL	NULL	gw60_febslett_407_1_7_s_5	9141471	A nuclear protein termed serum response factor (SRF) binds the CArG box motifs, the inner core of SRE, present in the promoter regions of many immediate early genes including  c-fos and several actins [ 1,   3].	bind
58811	6	11513	6	10	NULL	0	NULL				present in				CArG box motifs	c-fos				promoter region	NULL		NULL	NULL	NULL	NULL	gw60_febslett_407_1_7_s_5	9141471	A nuclear protein termed serum response factor (SRF) binds the CArG box motifs, the inner core of SRE, present in the promoter regions of many immediate early genes including  c-fos and several actins [ 1,   3].	bind
58812	7	11513	6	10	NULL	0	NULL				present in				inner core of SRE	c-fos				promoter region	NULL		NULL	NULL	NULL	NULL	gw60_febslett_407_1_7_s_5	9141471	A nuclear protein termed serum response factor (SRF) binds the CArG box motifs, the inner core of SRE, present in the promoter regions of many immediate early genes including  c-fos and several actins [ 1,   3].	bind
58813	8	11513	6	10	NULL	0	NULL				present in				CArG box motifs	actins				promoter region	NULL		NULL	NULL	NULL	NULL	gw60_febslett_407_1_7_s_5	9141471	A nuclear protein termed serum response factor (SRF) binds the CArG box motifs, the inner core of SRE, present in the promoter regions of many immediate early genes including  c-fos and several actins [ 1,   3].	bind
58814	9	11513	6	10	NULL	0	NULL				present in				inner core of SRE	actins				promoter region	NULL		NULL	NULL	NULL	NULL	gw60_febslett_407_1_7_s_5	9141471	A nuclear protein termed serum response factor (SRF) binds the CArG box motifs, the inner core of SRE, present in the promoter regions of many immediate early genes including  c-fos and several actins [ 1,   3].	bind
51034	1	11514	5	NULL	NULL	NULL	NULL	nuclear protein	GP		bind		specifically			transposons	GP	maize			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_mol-gen-genet_263_3_10821183_s_1	10821183	A nuclear protein that binds specifically to several maize transposons is not essential for Ds1 excision..	bind
51035	2	11514	5	NULL	NULL	NULL	NULL	statement 1	Process		is not essential for					Ds1	GP	excision of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_mol-gen-genet_263_3_10821183_s_1	10821183	A nuclear protein that binds specifically to several maize transposons is not essential for Ds1 excision..	bind
50390	1	11514	6	NULL	NULL	0	NULL	nuclear protein	NULL		bind	NULL	specifically			transposons	NULL	Maize			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mol-gen-genet_263_3_10821183_s_1	10821183	A nuclear protein that binds specifically to several maize transposons is not essential for Ds1 excision..	bind
50391	2	11514	6	NULL	NULL	0	NULL	nuclear protein	NULL		is not essential for	NULL				Ds1	NULL	excision of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mol-gen-genet_263_3_10821183_s_1	10821183	A nuclear protein that binds specifically to several maize transposons is not essential for Ds1 excision..	bind
51036	1	11517	5	NULL	NULL	NULL	NULL	Sos1	GP		is a type of					Ras nucleotide exchange factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
51037	2	11517	5	NULL	NULL	NULL	NULL	Sos1	GP		bind					Grb-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
51038	3	11517	5	NULL	NULL	NULL	NULL	Grb-2	GP		is a type of					adaptor protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
51039	4	11517	5	NULL	NULL	NULL	NULL	3BP1 protein	GP		bind					c-Abl	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
51040	5	11517	5	NULL	NULL	NULL	NULL	c-Abl	GP		is a type of					tyrosine kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
51041	6	11517	5	NULL	NULL	NULL	NULL	3BP2 protein	GP		bind					c-Abl	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
51042	7	11517	5	NULL	NULL	NULL	NULL	dynamin	GP		bind								SH3 domains		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
51043	8	11517	5	NULL	NULL	NULL	NULL	CDC42	GP		is a type of					GTPase activating protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
51044	9	11517	5	NULL	NULL	NULL	NULL	CDC42	GP		bind					Src	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
51045	10	11517	5	NULL	NULL	NULL	NULL	CDC42	GP		bind					phosphatidylinositol 3-kinase	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
54159	11	11517	5	NULL	NULL	NULL	NULL	Grb2	GP		contains only								SH2 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
54160	12	11517	5	NULL	NULL	NULL	NULL	Grb2	GP		contains 								SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
50520	1	11517	6	10	NULL	0	NULL	Sos1			is a type of					Ras nucleotide exchange factor					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
50521	2	11517	6	NULL	NULL	0	NULL	Sos1	NULL		bind	NULL				Grb-2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
50522	3	11517	6	NULL	NULL	0	NULL	Grb-2	NULL		is a type of	NULL				adaptor protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
50523	4	11517	6	NULL	NULL	0	NULL	Grb-2	NULL		contains	NULL					NULL		SH2 domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
50525	5	11517	6	NULL	NULL	0	NULL	Grb-2	NULL		contains	NULL					NULL		SH3 domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
50527	6	11517	6	NULL	NULL	0	NULL	3BP1	NULL		bind	NULL				c-Abl	NULL		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
50528	7	11517	6	NULL	NULL	0	NULL	3BP2	NULL		bind	NULL				c-Abl	NULL		SH3 domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
50529	8	11517	6	NULL	NULL	0	NULL	c-Abl	NULL		is a type of	NULL				tyrosine kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
50530	9	11517	6	NULL	NULL	0	NULL	dynamin	NULL		bind	NULL					NULL		SH3 domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
50531	10	11517	6	NULL	NULL	0	NULL	CDC42	NULL		is a type of	NULL				GTPase activating protein	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
50532	11	11517	6	NULL	NULL	0	NULL	CDC42	NULL		bind	NULL				Src	NULL		SH3 domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
50533	12	11517	6	NULL	NULL	0	NULL	CDC42	NULL		bind	NULL				phosphatidylinositol 3-kinase	NULL		SH3 domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_35_20832_s_245	7657668	A number of  SH3-binding proteins have been identified, including the Ras nucleotide  exchange factor Sos1, which binds the SH2- and SH3-containing adaptor  protein Grb-2( 38,  39,  40) ; 3BP1 and 3BP2,  proteins of unknown function that bind the SH3 domain of the c-Abl  tyrosine kinase( 41,  42) ; dynamin, which binds a  variety of SH3 domains ( 43) ; and the GTPase activating protein  CDC42, which binds the SH3 domains of Src and phosphatidylinositol  3-kinase( 44) .	bind
51046	1	11518	5	NULL	NULL	NULL	NULL	Groucho/LEs	GP		bind					HES proteins	GP				NULL	Drosophila	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_42_26604_s_170	9334241	A number of  TLE and  HES family members are co-expressed in a variety of tissues and cell lines ( 18,  34,  42,  43), and Groucho/LEs bind to HES proteins in both  Drosophila and mammals ( 10,  12,  40), suggesting that they may be part of the high  Mr complexes that we have detected.	bind
51047	2	11518	5	NULL	NULL	NULL	NULL	Groucho/LEs	GP		bind					HES proteins	GP				NULL	Mammals	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_42_26604_s_170	9334241	A number of  TLE and  HES family members are co-expressed in a variety of tissues and cell lines ( 18,  34,  42,  43), and Groucho/LEs bind to HES proteins in both  Drosophila and mammals ( 10,  12,  40), suggesting that they may be part of the high  Mr complexes that we have detected.	bind
50392	1	11518	6	10	NULL	0	NULL	Groucho/LEs			bind					HES proteins					NULL	Drosophila	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_42_26604_s_170	9334241	A number of  TLE and  HES family members are co-expressed in a variety of tissues and cell lines ( 18,  34,  42,  43), and Groucho/LEs bind to HES proteins in both  Drosophila and mammals ( 10,  12,  40), suggesting that they may be part of the high  Mr complexes that we have detected.	bind
54162	2	11518	6	10	NULL	0	NULL	Groucho/LEs			bind					HES proteins					NULL	mammals	0	NULL	NULL	NULL	gw60_jbiolchem_272_42_26604_s_170	9334241	A number of  TLE and  HES family members are co-expressed in a variety of tissues and cell lines ( 18,  34,  42,  43), and Groucho/LEs bind to HES proteins in both  Drosophila and mammals ( 10,  12,  40), suggesting that they may be part of the high  Mr complexes that we have detected.	bind
51048	1	11521	5	NULL	NULL	NULL	NULL	(TORC) 1	GP		activates					PGC-1alpha	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_39_14379_s_4	16980408	A number of activators of PGC-1alpha transcription were found; the most potent activator was the transducer of regulated CREB (cAMP response element-binding protein) binding protein (TORC) 1, a coactivator of CREB.	bind
51049	2	11521	5	NULL	NULL	NULL	NULL	(TORC) 1	GP		is					transducer of regulated CREB binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_39_14379_s_4	16980408	A number of activators of PGC-1alpha transcription were found; the most potent activator was the transducer of regulated CREB (cAMP response element-binding protein) binding protein (TORC) 1, a coactivator of CREB.	bind
51050	3	11521	5	NULL	NULL	NULL	NULL	CREB	GP		is					cAMP response element-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_39_14379_s_4	16980408	A number of activators of PGC-1alpha transcription were found; the most potent activator was the transducer of regulated CREB (cAMP response element-binding protein) binding protein (TORC) 1, a coactivator of CREB.	bind
51051	4	11521	5	NULL	NULL	NULL	NULL	(TORC) 1	GP		is a coactivator of					CREB	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_39_14379_s_4	16980408	A number of activators of PGC-1alpha transcription were found; the most potent activator was the transducer of regulated CREB (cAMP response element-binding protein) binding protein (TORC) 1, a coactivator of CREB.	bind
50534	1	11521	6	10	NULL	0	NULL	(TORC)1			is a coactivator of					CREB					NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_39_14379_s_4	16980408	A number of activators of PGC-1alpha transcription were found; the most potent activator was the transducer of regulated CREB (cAMP response element-binding protein) binding protein (TORC) 1, a coactivator of CREB.	bind
50535	2	11521	6	10	NULL	0	NULL	(TORC)1			activates					PGC-1alpha		transcription of 			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_39_14379_s_4	16980408	A number of activators of PGC-1alpha transcription were found; the most potent activator was the transducer of regulated CREB (cAMP response element-binding protein) binding protein (TORC) 1, a coactivator of CREB.	bind
50536	3	11521	6	10	NULL	0	NULL	(TORC)1			is					transducer of regulated CREB					NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_39_14379_s_4	16980408	A number of activators of PGC-1alpha transcription were found; the most potent activator was the transducer of regulated CREB (cAMP response element-binding protein) binding protein (TORC) 1, a coactivator of CREB.	bind
50537	4	11521	6	NULL	NULL	0	NULL	CREB	NULL		is	NULL				cAMP response element-binding protein	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_39_14379_s_4	16980408	A number of activators of PGC-1alpha transcription were found; the most potent activator was the transducer of regulated CREB (cAMP response element-binding protein) binding protein (TORC) 1, a coactivator of CREB.	bind
51055	1	11522	5	NULL	NULL	NULL	NULL	PCBP2	GP		bind					IRES	GP	polio virus			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_2_639_s_23	12527772	A number of additional viral IRES binding/activating proteins have been identified, including the La autoantigen which is used by polio virus IRES ( 21), and poly r(C) binding protein 2 (PCBP2) which binds to polio virus IRES ( 22) and has been shown to activate entero/rhino virus IRESs  in vitro ( 23).	bind
51056	2	11522	5	NULL	NULL	NULL	NULL	PCBP2	GP		is					poly r(C) binding protein 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_2_639_s_23	12527772	A number of additional viral IRES binding/activating proteins have been identified, including the La autoantigen which is used by polio virus IRES ( 21), and poly r(C) binding protein 2 (PCBP2) which binds to polio virus IRES ( 22) and has been shown to activate entero/rhino virus IRESs  in vitro ( 23).	bind
51057	3	11522	5	NULL	NULL	NULL	NULL	PCBP2	GP		activates					IRES	GP	entero/rhino virus			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_2_639_s_23	12527772	A number of additional viral IRES binding/activating proteins have been identified, including the La autoantigen which is used by polio virus IRES ( 21), and poly r(C) binding protein 2 (PCBP2) which binds to polio virus IRES ( 22) and has been shown to activate entero/rhino virus IRESs  in vitro ( 23).	bind
50393	1	11522	6	NULL	NULL	0	NULL	PCBP2	NULL		bind	NULL				IRES	NULL	polio virus			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_2_639_s_23	12527772	A number of additional viral IRES binding/activating proteins have been identified, including the La autoantigen which is used by polio virus IRES ( 21), and poly r(C) binding protein 2 (PCBP2) which binds to polio virus IRES ( 22) and has been shown to activate entero/rhino virus IRESs  in vitro ( 23).	bind
50394	2	11522	6	NULL	NULL	0	NULL	PCBP2	NULL		is	NULL				poly r(C) binding protein 2	NULL				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_2_639_s_23	12527772	A number of additional viral IRES binding/activating proteins have been identified, including the La autoantigen which is used by polio virus IRES ( 21), and poly r(C) binding protein 2 (PCBP2) which binds to polio virus IRES ( 22) and has been shown to activate entero/rhino virus IRESs  in vitro ( 23).	bind
50395	3	11522	6	NULL	NULL	0	NULL	PCBP2	NULL		activates	NULL				IRES	NULL	entero/rhino virus			NULL	in vitro	0	NULL	NULL	NULL	gw60_nucleicacidsres_31_2_639_s_23	12527772	A number of additional viral IRES binding/activating proteins have been identified, including the La autoantigen which is used by polio virus IRES ( 21), and poly r(C) binding protein 2 (PCBP2) which binds to polio virus IRES ( 22) and has been shown to activate entero/rhino virus IRESs  in vitro ( 23).	bind
51058	1	11526	5	NULL	NULL	NULL	NULL	apoB sequences	AminoAcid		bind		noncovalently			apo(a)	GP				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_45_12_2227_s_26	15375179	A number of apoB sequences that noncovalently bind apo(a) have been reported.	bind
50396	1	11526	6	NULL	NULL	0	NULL	apoB sequences	NULL		bind	NULL	noncovalently			apo(a)	NULL				NULL		0	NULL	NULL	NULL	gw70_jlipidres_45_12_2227_s_26	15375179	A number of apoB sequences that noncovalently bind apo(a) have been reported.	bind
51059	1	11527	5	NULL	NULL	NULL	NULL	HSP47	GP		bind					collagen triple helix	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_38_35007_s_169	12114508	A number of approaches have been used recently to evaluate the binding of HSP47 to the collagen triple helix ( 12,  13).	bind
50397	1	11527	6	NULL	NULL	0	NULL	HSP47	NULL		bind	NULL				collagen triple helix	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_38_35007_s_169	12114508	A number of approaches have been used recently to evaluate the binding of HSP47 to the collagen triple helix ( 12,  13).	bind
51060	1	11528	5	NULL	NULL	NULL	NULL	PDZ45	GP		bind					GluR2 peptide	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_46_43216_s_131	11553623	A number of backbone amide resonances of PDZ45 experienced peptide-induced chemical shift changes in the overlay plot of the 1H-15N HSQC spectra of free PDZ45 ( black) and PDZ45 saturated with the 10-residue GluR2 peptide ( red), indicating that PDZ45 binds to the GluR2 peptide (Fig.  4 B).	bind
50398	1	11528	6	NULL	NULL	0	NULL	PDZ45	NULL		bind	NULL				GluR2 peptide	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_46_43216_s_131	11553623	A number of backbone amide resonances of PDZ45 experienced peptide-induced chemical shift changes in the overlay plot of the 1H-15N HSQC spectra of free PDZ45 ( black) and PDZ45 saturated with the 10-residue GluR2 peptide ( red), indicating that PDZ45 binds to the GluR2 peptide (Fig.  4 B).	bind
51061	1	11529	5	NULL	NULL	NULL	NULL	Bordetella pertussis	Organism		express					outer membrane proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
51062	2	11529	5	NULL	NULL	NULL	NULL	statement 1	Process		bind		specifically			lactoferrin	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
51063	3	11529	5	NULL	NULL	NULL	NULL	Helicobacter pylori	Organism		express					outer membrane proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
51064	4	11529	5	NULL	NULL	NULL	NULL	statement 3	Process		bind		specifically			lactoferrin	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
51065	5	11529	5	NULL	NULL	NULL	NULL	M. catarrhalis	Organism		express					outer membrane proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
51066	6	11529	5	NULL	NULL	NULL	NULL	statement 5	Process		bind		specifically			lactoferrin	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
51067	7	11529	5	NULL	NULL	NULL	NULL	Neisseria gonorrhoeae	Organism		express					outer membrane proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
51068	8	11529	5	NULL	NULL	NULL	NULL	statement 7	Process		bind		specifically			lactoferrin	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
51069	9	11529	5	NULL	NULL	NULL	NULL	Neisseria meningitidis	Organism		express					outer membrane proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
51070	10	11529	5	NULL	NULL	NULL	NULL	statement 9	Process		bind		specifically			lactoferrin	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
51071	11	11529	5	NULL	NULL	NULL	NULL	Prevotella nigrescens 	Organism		express					outer membrane proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
51072	12	11529	5	NULL	NULL	NULL	NULL	statement 11	Process		bind		specifically			lactoferrin	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
51073	13	11529	5	NULL	NULL	NULL	NULL	Treponema spp	Organism		express					outer membrane proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
51074	14	11529	5	NULL	NULL	NULL	NULL	statement 13	Process		bind		specifically			lactoferrin	GP	human			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
50399	1	11529	6	NULL	NULL	0	NULL	Bordetella pertussis	NULL		express	NULL				outer membrane proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
50400	2	11529	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL	specifically			lactoferrin	NULL	human			NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
50401	3	11529	6	NULL	NULL	0	NULL	Helicobacter pylori 	NULL		express	NULL				outer membrane proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
50402	4	11529	6	10	NULL	0	NULL	statement 3			bind		specifically			lactoferrin		human			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
50403	5	11529	6	NULL	NULL	0	NULL	M. catarrhalis	NULL		express	NULL				outer membrane proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
50404	6	11529	6	NULL	NULL	0	NULL	statement 5	NULL		bind	NULL	specifically			lactoferrin	NULL	human			NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
50405	7	11529	6	NULL	NULL	0	NULL	Neisseria gonorrhoeae	NULL		express	NULL				outer membrane proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
50406	8	11529	6	NULL	NULL	0	NULL	statement 7	NULL		bind	NULL	specifically			lactoferrin	NULL	human			NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
50407	9	11529	6	NULL	NULL	0	NULL	Neisseria meningitidis	NULL		express	NULL				outer membrane proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
50408	10	11529	6	NULL	NULL	0	NULL	statement 9	NULL		express	NULL	specifically			lactoferrin	NULL	human			NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
50409	11	11529	6	NULL	NULL	0	NULL	Prevotella nigrescens	NULL		express	NULL				outer membrane proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
50410	12	11529	6	NULL	NULL	0	NULL	statement 11	NULL		bind	NULL	specifically			lactoferrin	NULL	human			NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
50411	13	11529	6	NULL	NULL	0	NULL	Treponema spp.	NULL		express	NULL				outer membrane proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
50412	14	11529	6	NULL	NULL	0	NULL	statement 13	NULL		bind	NULL	specifically			lactoferrin	NULL	human			NULL		0	NULL	NULL	NULL	gw60_infectimmun_66_8_3656_s_22	9673246	A number of bacterial species, including  Bordetella pertussis ( 22),  Helicobacter pylori ( 9),  M. catarrhalis ( 33),  Neisseria gonorrhoeae ( 1),  Neisseria meningitidis ( 29,  33),  Prevotella nigrescens ( 8), and  Treponema spp. ( 34), have been shown to express outer membrane proteins which specifically bind human lactoferrin.	bind
51075	1	11530	5	NULL	NULL	NULL	NULL	GTP-binding proteins	GP	small	bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_3_904_s_138	12538863	A number of bacterial toxins specifically target the GTP-bound form of small GTP-binding proteins ( ,  ).	bind
51076	2	11530	5	NULL	NULL	NULL	NULL	bacterial toxins	GP		targets		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_3_904_s_138	12538863	A number of bacterial toxins specifically target the GTP-bound form of small GTP-binding proteins ( ,  ).	bind
50413	1	11530	6	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				GTP-binding proteins	NULL	small			NULL		0	NULL	NULL	NULL	gw70_pnas_100_3_904_s_138	12538863	A number of bacterial toxins specifically target the GTP-bound form of small GTP-binding proteins ( ,  ).	bind
50414	2	11530	6	NULL	NULL	0	NULL	bacterial toxins	NULL		target	NULL	specifically			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_100_3_904_s_138	12538863	A number of bacterial toxins specifically target the GTP-bound form of small GTP-binding proteins ( ,  ).	bind
51077	1	11533	5	NULL	NULL	NULL	NULL	catenins	GP		bind		directly			cadherin	GP		cytoplasmic tails		NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_275_39_10899158_s_3	10899158	A number of catenins directly bind cadherin cytoplasmic tails, contributing  to the modulation of cell-cell adhesion and motility processes.	bind
51078	2	11533	5	NULL	NULL	NULL	NULL	statement 1	Process		contribute to					cell-cell adhesion	Process	modulation of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_275_39_10899158_s_3	10899158	A number of catenins directly bind cadherin cytoplasmic tails, contributing  to the modulation of cell-cell adhesion and motility processes.	bind
51079	3	11533	5	NULL	NULL	NULL	NULL	statement 1	Process		contribute to					cell motility 	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_275_39_10899158_s_3	10899158	A number of catenins directly bind cadherin cytoplasmic tails, contributing  to the modulation of cell-cell adhesion and motility processes.	bind
50415	1	11533	6	NULL	NULL	0	NULL	catenins	NULL		bind	NULL	directly			cadherin	NULL		cytoplasmic tails		NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_275_39_10899158_s_3	10899158	A number of catenins directly bind cadherin cytoplasmic tails, contributing  to the modulation of cell-cell adhesion and motility processes.	bind
50416	2	11533	6	10	NULL	0	NULL	statement 1			contributes to					cell-cell adhesion		modulation of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_275_39_10899158_s_3	10899158	A number of catenins directly bind cadherin cytoplasmic tails, contributing  to the modulation of cell-cell adhesion and motility processes.	bind
50417	3	11533	6	NULL	NULL	0	NULL	statement 1	NULL		contributes to	NULL				cell motility	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_275_39_10899158_s_3	10899158	A number of catenins directly bind cadherin cytoplasmic tails, contributing  to the modulation of cell-cell adhesion and motility processes.	bind
51080	1	11535	5	NULL	NULL	NULL	NULL	LPL	GP		bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_24525_s_21	7592670	A number of conflicting reports show that binding  of LPL to heparin, a proteoglycan very similar to heparan sulfate, can  stabilize, stimulate, or inhibit catalytic efficiency of the lipase  depending on experimental conditions ( 13,  14,  15,  16) .	bind
51081	2	11535	5	NULL	NULL	NULL	NULL	heparin	Chemical		is a type of					proteoglycan	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_24525_s_21	7592670	A number of conflicting reports show that binding  of LPL to heparin, a proteoglycan very similar to heparan sulfate, can  stabilize, stimulate, or inhibit catalytic efficiency of the lipase  depending on experimental conditions ( 13,  14,  15,  16) .	bind
51082	3	11535	5	NULL	NULL	NULL	NULL	heparin	Chemical		is similar to					heparan sulfate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_41_24525_s_21	7592670	A number of conflicting reports show that binding  of LPL to heparin, a proteoglycan very similar to heparan sulfate, can  stabilize, stimulate, or inhibit catalytic efficiency of the lipase  depending on experimental conditions ( 13,  14,  15,  16) .	bind
50418	1	11535	6	NULL	NULL	0	NULL	LPL	NULL		bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_41_24525_s_21	7592670	A number of conflicting reports show that binding  of LPL to heparin, a proteoglycan very similar to heparan sulfate, can  stabilize, stimulate, or inhibit catalytic efficiency of the lipase  depending on experimental conditions ( 13,  14,  15,  16) .	bind
50419	2	11535	6	NULL	NULL	0	NULL	heparin	NULL		is a type of	NULL				proteoglycan	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_41_24525_s_21	7592670	A number of conflicting reports show that binding  of LPL to heparin, a proteoglycan very similar to heparan sulfate, can  stabilize, stimulate, or inhibit catalytic efficiency of the lipase  depending on experimental conditions ( 13,  14,  15,  16) .	bind
50420	3	11535	6	NULL	NULL	0	NULL	heparin	NULL		is similar to	NULL				heparan sulfate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_41_24525_s_21	7592670	A number of conflicting reports show that binding  of LPL to heparin, a proteoglycan very similar to heparan sulfate, can  stabilize, stimulate, or inhibit catalytic efficiency of the lipase  depending on experimental conditions ( 13,  14,  15,  16) .	bind
51083	1	11536	5	NULL	NULL	NULL	NULL	detoxification proteins	GP		bind					thioredoxin	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_11_3759_s_151	15004283	A number of detoxification proteins were found to bind thioredoxin.	bind
50421	1	11536	6	NULL	NULL	0	NULL	detoxification proteins	NULL		bind	NULL				thioredoxin	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_101_11_3759_s_151	15004283	A number of detoxification proteins were found to bind thioredoxin.	bind
51084	1	11537	5	NULL	NULL	NULL	NULL	PAKs	GP		bind		directly			Nck	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_8_6037_s_8	11096073	A number of different functions have been ascribed to PAKs; and PAKs can bind directly to growth factor signaling-adaptor molecule, Nck, and a guanine nucleotide exchanger, betaPIX.	bind
51085	2	11537	5	NULL	NULL	NULL	NULL	PAKs	GP		bind		directly			betaPIX	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_8_6037_s_8	11096073	A number of different functions have been ascribed to PAKs; and PAKs can bind directly to growth factor signaling-adaptor molecule, Nck, and a guanine nucleotide exchanger, betaPIX.	bind
51086	3	11537	5	NULL	NULL	NULL	NULL	Nck	GP		is a type of					growth factor signaling-adaptor molecule	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_8_6037_s_8	11096073	A number of different functions have been ascribed to PAKs; and PAKs can bind directly to growth factor signaling-adaptor molecule, Nck, and a guanine nucleotide exchanger, betaPIX.	bind
51087	4	11537	5	NULL	NULL	NULL	NULL	betaPIX	GP		is a type of					guanine nucleotide exchanger	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_8_6037_s_8	11096073	A number of different functions have been ascribed to PAKs; and PAKs can bind directly to growth factor signaling-adaptor molecule, Nck, and a guanine nucleotide exchanger, betaPIX.	bind
50422	1	11537	6	NULL	NULL	0	NULL	PAK	NULL		bind	NULL	directly			Nck	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_8_6037_s_8	11096073	A number of different functions have been ascribed to PAKs; and PAKs can bind directly to growth factor signaling-adaptor molecule, Nck, and a guanine nucleotide exchanger, betaPIX.	bind
50423	2	11537	6	NULL	NULL	0	NULL	Nck	NULL		is a type of	NULL				growth factor signaling-adaptor molecule	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_8_6037_s_8	11096073	A number of different functions have been ascribed to PAKs; and PAKs can bind directly to growth factor signaling-adaptor molecule, Nck, and a guanine nucleotide exchanger, betaPIX.	bind
50424	3	11537	6	NULL	NULL	0	NULL	PAK	NULL		bind	NULL	directly			betaPIX	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_8_6037_s_8	11096073	A number of different functions have been ascribed to PAKs; and PAKs can bind directly to growth factor signaling-adaptor molecule, Nck, and a guanine nucleotide exchanger, betaPIX.	bind
50425	4	11537	6	NULL	NULL	0	NULL	betaPIX	NULL		is a type of	NULL				guanine nucleotide exchanger	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_8_6037_s_8	11096073	A number of different functions have been ascribed to PAKs; and PAKs can bind directly to growth factor signaling-adaptor molecule, Nck, and a guanine nucleotide exchanger, betaPIX.	bind
51088	1	11539	5	NULL	NULL	NULL	NULL	PI lipids	Chemical		bind					AP-2	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_21_1383_s_85	11084340	A number of different PI lipids bind the adaptor protein complex AP-2, facilitating its self-assembly, and its interaction with clathrin and peptides that contain endocytic motifs  [8  .	bind
51089	2	11539	5	NULL	NULL	NULL	NULL	AP-2	GP		is a type of					adaptor protein complex	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_21_1383_s_85	11084340	A number of different PI lipids bind the adaptor protein complex AP-2, facilitating its self-assembly, and its interaction with clathrin and peptides that contain endocytic motifs  [8  .	bind
51090	3	11539	5	NULL	NULL	NULL	NULL	statement 1	Process		facilitates					AP-2	GP	self-assembly of			NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_21_1383_s_85	11084340	A number of different PI lipids bind the adaptor protein complex AP-2, facilitating its self-assembly, and its interaction with clathrin and peptides that contain endocytic motifs  [8  .	bind
51091	4	11539	5	NULL	NULL	NULL	NULL	AP-2	GP		interacts with					clathrin	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_21_1383_s_85	11084340	A number of different PI lipids bind the adaptor protein complex AP-2, facilitating its self-assembly, and its interaction with clathrin and peptides that contain endocytic motifs  [8  .	bind
51092	5	11539	5	NULL	NULL	NULL	NULL	peptides	AminoAcid		contains								endocytic motifs		NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_21_1383_s_85	11084340	A number of different PI lipids bind the adaptor protein complex AP-2, facilitating its self-assembly, and its interaction with clathrin and peptides that contain endocytic motifs  [8  .	bind
51093	6	11539	5	NULL	NULL	NULL	NULL	AP-2	GP		interacts with					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_21_1383_s_85	11084340	A number of different PI lipids bind the adaptor protein complex AP-2, facilitating its self-assembly, and its interaction with clathrin and peptides that contain endocytic motifs  [8  .	bind
51094	7	11539	5	NULL	NULL	NULL	NULL	statement 1	Process		facilitates					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_21_1383_s_85	11084340	A number of different PI lipids bind the adaptor protein complex AP-2, facilitating its self-assembly, and its interaction with clathrin and peptides that contain endocytic motifs  [8  .	bind
51095	8	11539	5	NULL	NULL	NULL	NULL	statement 1	Process		facilitates					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_21_1383_s_85	11084340	A number of different PI lipids bind the adaptor protein complex AP-2, facilitating its self-assembly, and its interaction with clathrin and peptides that contain endocytic motifs  [8  .	bind
50426	1	11539	6	NULL	NULL	0	NULL	PI lipids	NULL		bind	NULL				AP-2	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_21_1383_s_85	11084340	A number of different PI lipids bind the adaptor protein complex AP-2, facilitating its self-assembly, and its interaction with clathrin and peptides that contain endocytic motifs  [8  .	bind
50427	2	11539	6	NULL	NULL	0	NULL	AP-2	NULL		is a type of	NULL				adaptor protein complex	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_21_1383_s_85	11084340	A number of different PI lipids bind the adaptor protein complex AP-2, facilitating its self-assembly, and its interaction with clathrin and peptides that contain endocytic motifs  [8  .	bind
50428	3	11539	6	NULL	NULL	0	NULL	statement 1	NULL		facilitates	NULL				AP-2	NULL	self assembly of 			NULL		0	NULL	NULL	NULL	gw60_currbiol_10_21_1383_s_85	11084340	A number of different PI lipids bind the adaptor protein complex AP-2, facilitating its self-assembly, and its interaction with clathrin and peptides that contain endocytic motifs  [8  .	bind
50429	4	11539	6	NULL	NULL	0	NULL	AP-2	NULL		interacts with	NULL				clathrin	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_21_1383_s_85	11084340	A number of different PI lipids bind the adaptor protein complex AP-2, facilitating its self-assembly, and its interaction with clathrin and peptides that contain endocytic motifs  [8  .	bind
50430	5	11539	6	NULL	NULL	0	NULL	peptides	NULL		contain	NULL					NULL		endocytic motifs		NULL		0	NULL	NULL	NULL	gw60_currbiol_10_21_1383_s_85	11084340	A number of different PI lipids bind the adaptor protein complex AP-2, facilitating its self-assembly, and its interaction with clathrin and peptides that contain endocytic motifs  [8  .	bind
50431	6	11539	6	NULL	NULL	0	NULL	AP-2	NULL		interacts with	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_21_1383_s_85	11084340	A number of different PI lipids bind the adaptor protein complex AP-2, facilitating its self-assembly, and its interaction with clathrin and peptides that contain endocytic motifs  [8  .	bind
54163	7	11539	6	10	NULL	0	NULL	statement 1			facilitate					statement 4					NULL		0	NULL	NULL	NULL	gw60_currbiol_10_21_1383_s_85	11084340	A number of different PI lipids bind the adaptor protein complex AP-2, facilitating its self-assembly, and its interaction with clathrin and peptides that contain endocytic motifs  [8  .	bind
54164	8	11539	6	10	NULL	0	NULL	statement 1			facilitate					statement 6					NULL		0	NULL	NULL	NULL	gw60_currbiol_10_21_1383_s_85	11084340	A number of different PI lipids bind the adaptor protein complex AP-2, facilitating its self-assembly, and its interaction with clathrin and peptides that contain endocytic motifs  [8  .	bind
51096	1	11540	5	NULL	NULL	NULL	NULL	AP-1	GP		bind					 GADD45 gene	GP			binding site on promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_20061_s_248	10751396	A number of DNA-protein interactions, including binding of AP-1 and p53 on their respective binding sites, were required to maintain the poised chromatin structure of the  GADD45 gene promoter ( 47).	bind
51097	2	11540	5	NULL	NULL	NULL	NULL	p53	GP		bind					GADD45 gene 	GP			binding site on promoter	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_20061_s_248	10751396	A number of DNA-protein interactions, including binding of AP-1 and p53 on their respective binding sites, were required to maintain the poised chromatin structure of the  GADD45 gene promoter ( 47).	bind
56601	3	11540	5	NULL	NULL	NULL	NULL	statement 1	Process		required for					GADD45 gene 	GP	 poised chromatin structure of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_20061_s_248	10751396	A number of DNA-protein interactions, including binding of AP-1 and p53 on their respective binding sites, were required to maintain the poised chromatin structure of the  GADD45 gene promoter ( 47).	bind
56602	4	11540	5	NULL	NULL	NULL	NULL	statement 2	Process		required for					GADD45 gene 	GP	poised chromatin structure of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_20061_s_248	10751396	A number of DNA-protein interactions, including binding of AP-1 and p53 on their respective binding sites, were required to maintain the poised chromatin structure of the  GADD45 gene promoter ( 47).	bind
50432	1	11540	6	NULL	NULL	0	NULL	AP-1	NULL		bind	NULL				GADD45 gene	NULL			site on promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_26_20061_s_248	10751396	A number of DNA-protein interactions, including binding of AP-1 and p53 on their respective binding sites, were required to maintain the poised chromatin structure of the  GADD45 gene promoter ( 47).	bind
50433	2	11540	6	NULL	NULL	0	NULL	p53	NULL		bind	NULL				GADD45 gene	NULL			site on promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_26_20061_s_248	10751396	A number of DNA-protein interactions, including binding of AP-1 and p53 on their respective binding sites, were required to maintain the poised chromatin structure of the  GADD45 gene promoter ( 47).	bind
50434	3	11540	6	10	NULL	0	NULL	statement 1			is required for					GADD45 gene 		poised chromatin structure of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_20061_s_248	10751396	A number of DNA-protein interactions, including binding of AP-1 and p53 on their respective binding sites, were required to maintain the poised chromatin structure of the  GADD45 gene promoter ( 47).	bind
50435	4	11540	6	10	NULL	0	NULL	statement 2			is required for					GADD45 gene 		poised chromatin structure of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_26_20061_s_248	10751396	A number of DNA-protein interactions, including binding of AP-1 and p53 on their respective binding sites, were required to maintain the poised chromatin structure of the  GADD45 gene promoter ( 47).	bind
51098	1	11541	5	NULL	NULL	NULL	NULL	GTP	Chemical		bind					ARF proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_18_13465_s_275	10788460	A number of effector proteins were found to have the ability to increase the equilibrium level of GTP binding to ARF proteins.	bind
51099	2	11541	5	NULL	NULL	NULL	NULL	effector proteins	GP		increases					statement 1	Process	equilibrium level of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_18_13465_s_275	10788460	A number of effector proteins were found to have the ability to increase the equilibrium level of GTP binding to ARF proteins.	bind
50436	1	11541	6	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				ARF proteins	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13465_s_275	10788460	A number of effector proteins were found to have the ability to increase the equilibrium level of GTP binding to ARF proteins.	bind
54190	2	11541	6	10	NULL	0	NULL	effector proteins			increase					statement 1		equilibrium level of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13465_s_275	10788460	A number of effector proteins were found to have the ability to increase the equilibrium level of GTP binding to ARF proteins.	bind
51100	1	11542	5	NULL	NULL	NULL	NULL	Pumilio	GP		bind									NREs	NULL	embryo	NULL	NULL	NULL	NULL	gw60_genetics_153_4_1825_s_29	10581288	A number of experiments suggest that Pumilio is bound to the NREs throughout the embryo ( M URATA and WHARTON 1995   ;	bind
50437	1	11542	6	10	NULL	0	NULL	Pumilio			bind									NRE	NULL	 embryo	NULL	NULL	NULL	NULL	gw60_genetics_153_4_1825_s_29	10581288	A number of experiments suggest that Pumilio is bound to the NREs throughout the embryo ( M URATA and WHARTON 1995   ;	bind
51101	1	11543	5	NULL	NULL	NULL	NULL	TMR	GP		bind								Cys-374		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34172_s_169	12813032	A number of factors  could help explain this small difference, including the use of AMPPNP in place  of ATP, the binding of TMR to Cys-374, or the fact that this is the first  ATP-actin structure to have been determined without any other protein bound to  it.	bind
50438	1	11543	6	NULL	NULL	0	NULL	TMR	NULL		bind	NULL					NULL		Cys-374		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34172_s_169	12813032	A number of factors  could help explain this small difference, including the use of AMPPNP in place  of ATP, the binding of TMR to Cys-374, or the fact that this is the first  ATP-actin structure to have been determined without any other protein bound to  it.	bind
51102	1	11544	5	NULL	NULL	NULL	NULL	HNF-3	GP		is					hepatic nuclear factor 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3446_s_44	10652338	A number of factors bind to gAF2, although only binding of hepatic nuclear factor 3 (HNF-3) specifically correlates with the ability of the gAF2 element to induce the glucocorticoid response ( 28).	bind
51103	2	11544	5	NULL	NULL	NULL	NULL	HNF-3	GP		bind					gAF2	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3446_s_44	10652338	A number of factors bind to gAF2, although only binding of hepatic nuclear factor 3 (HNF-3) specifically correlates with the ability of the gAF2 element to induce the glucocorticoid response ( 28).	bind
51104	3	11544	5	NULL	NULL	NULL	NULL				induce				gAF2 element	glucocorticoid response	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3446_s_44	10652338	A number of factors bind to gAF2, although only binding of hepatic nuclear factor 3 (HNF-3) specifically correlates with the ability of the gAF2 element to induce the glucocorticoid response ( 28).	bind
51105	4	11544	5	NULL	NULL	NULL	NULL	statement 2	Process		corelates with		specifically			statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3446_s_44	10652338	A number of factors bind to gAF2, although only binding of hepatic nuclear factor 3 (HNF-3) specifically correlates with the ability of the gAF2 element to induce the glucocorticoid response ( 28).	bind
50439	1	11544	6	NULL	NULL	0	NULL		NULL		induce	NULL			gAF2 element	glucocorticoid response	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3446_s_44	10652338	A number of factors bind to gAF2, although only binding of hepatic nuclear factor 3 (HNF-3) specifically correlates with the ability of the gAF2 element to induce the glucocorticoid response ( 28).	bind
50440	2	11544	6	10	NULL	0	NULL	HNF-3			bind					gAF2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3446_s_44	10652338	A number of factors bind to gAF2, although only binding of hepatic nuclear factor 3 (HNF-3) specifically correlates with the ability of the gAF2 element to induce the glucocorticoid response ( 28).	bind
50441	3	11544	6	10	NULL	0	NULL	statement 2			correlates with		specifically			statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3446_s_44	10652338	A number of factors bind to gAF2, although only binding of hepatic nuclear factor 3 (HNF-3) specifically correlates with the ability of the gAF2 element to induce the glucocorticoid response ( 28).	bind
54191	4	11544	6	10	NULL	0	NULL	HNF-3			is					hepatic nuclear factor 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3446_s_44	10652338	A number of factors bind to gAF2, although only binding of hepatic nuclear factor 3 (HNF-3) specifically correlates with the ability of the gAF2 element to induce the glucocorticoid response ( 28).	bind
51106	1	11545	5	NULL	NULL	NULL	NULL	fibroblast growth factors	GP		bind					tyrosine kinase receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_22_11722_s_31	11050201	A number of fibroblast growth factors that bind and activate tyrosine kinase receptors are known to be present in inner ear organs ( 54,  55).	bind
51107	2	11545	5	NULL	NULL	NULL	NULL	statement 1	Process		activates					tyrosine kinase receptors	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_22_11722_s_31	11050201	A number of fibroblast growth factors that bind and activate tyrosine kinase receptors are known to be present in inner ear organs ( 54,  55).	bind
51108	3	11545	5	NULL	NULL	NULL	NULL	fibroblast growth factors	GP		is present in					inner ear organs	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_22_11722_s_31	11050201	A number of fibroblast growth factors that bind and activate tyrosine kinase receptors are known to be present in inner ear organs ( 54,  55).	bind
50442	1	11545	6	NULL	NULL	0	NULL	fibroblast growth factor	NULL		bind	NULL				tyrosine kinase receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_11722_s_31	11050201	A number of fibroblast growth factors that bind and activate tyrosine kinase receptors are known to be present in inner ear organs ( 54,  55).	bind
50443	2	11545	6	NULL	NULL	0	NULL	fibroblast growth factor	NULL		activates	NULL				tyrosine kinase receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_11722_s_31	11050201	A number of fibroblast growth factors that bind and activate tyrosine kinase receptors are known to be present in inner ear organs ( 54,  55).	bind
50444	3	11545	6	NULL	NULL	0	NULL	fibroblast growth factor	NULL		are present in	NULL				inner ear organs	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_11722_s_31	11050201	A number of fibroblast growth factors that bind and activate tyrosine kinase receptors are known to be present in inner ear organs ( 54,  55).	bind
51109	1	11546	5	NULL	NULL	NULL	NULL	GTP	Chemical		bind					ARF	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_11_3133_s_37	9802902	A number of GEFs, which promote binding of GTP to ARF by facilitating the release of GDP, have been identified (Chardin  et al., 1996  ; Peyroche  et al., 1996  ; Klarlund  et al., 1997  ; Meacci  et al., 1997  ; Morinaga  et al., 1997  ; Sata  et al., 1998  ).	bind
51110	2	11546	5	NULL	NULL	NULL	NULL	GEFs	GP		promotes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_11_3133_s_37	9802902	A number of GEFs, which promote binding of GTP to ARF by facilitating the release of GDP, have been identified (Chardin  et al., 1996  ; Peyroche  et al., 1996  ; Klarlund  et al., 1997  ; Meacci  et al., 1997  ; Morinaga  et al., 1997  ; Sata  et al., 1998  ).	bind
51111	3	11546	5	NULL	NULL	NULL	NULL	GEFs	GP		facilitates					GDP	Chemical	release of			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_11_3133_s_37	9802902	A number of GEFs, which promote binding of GTP to ARF by facilitating the release of GDP, have been identified (Chardin  et al., 1996  ; Peyroche  et al., 1996  ; Klarlund  et al., 1997  ; Meacci  et al., 1997  ; Morinaga  et al., 1997  ; Sata  et al., 1998  ).	bind
51112	4	11546	5	NULL	NULL	NULL	NULL	statement 3	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_9_11_3133_s_37	9802902	A number of GEFs, which promote binding of GTP to ARF by facilitating the release of GDP, have been identified (Chardin  et al., 1996  ; Peyroche  et al., 1996  ; Klarlund  et al., 1997  ; Meacci  et al., 1997  ; Morinaga  et al., 1997  ; Sata  et al., 1998  ).	bind
50445	1	11546	6	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				ARF	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_11_3133_s_37	9802902	A number of GEFs, which promote binding of GTP to ARF by facilitating the release of GDP, have been identified (Chardin  et al., 1996  ; Peyroche  et al., 1996  ; Klarlund  et al., 1997  ; Meacci  et al., 1997  ; Morinaga  et al., 1997  ; Sata  et al., 1998  ).	bind
50446	2	11546	6	NULL	NULL	0	NULL	GEF	NULL		promote	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_11_3133_s_37	9802902	A number of GEFs, which promote binding of GTP to ARF by facilitating the release of GDP, have been identified (Chardin  et al., 1996  ; Peyroche  et al., 1996  ; Klarlund  et al., 1997  ; Meacci  et al., 1997  ; Morinaga  et al., 1997  ; Sata  et al., 1998  ).	bind
50447	3	11546	6	NULL	NULL	0	NULL	GEF	NULL		facilitates	NULL				GDP	NULL	release of 			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_11_3133_s_37	9802902	A number of GEFs, which promote binding of GTP to ARF by facilitating the release of GDP, have been identified (Chardin  et al., 1996  ; Peyroche  et al., 1996  ; Klarlund  et al., 1997  ; Meacci  et al., 1997  ; Morinaga  et al., 1997  ; Sata  et al., 1998  ).	bind
50448	4	11546	6	NULL	NULL	0	NULL	statement 2	NULL		occurs via	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_11_3133_s_37	9802902	A number of GEFs, which promote binding of GTP to ARF by facilitating the release of GDP, have been identified (Chardin  et al., 1996  ; Peyroche  et al., 1996  ; Klarlund  et al., 1997  ; Meacci  et al., 1997  ; Morinaga  et al., 1997  ; Sata  et al., 1998  ).	bind
51113	1	11547	5	NULL	NULL	NULL	NULL	intimin	GP		bind		directly			host cells	Cell	uninfected			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_8_4637_s_189	10899867	A number of groups have reported that intimin can bind directly to uninfected host cells ( 2,  8) and to a receptor encoded by the bacteria, termed Tir, which is translocated into the host cell membrane via a type III secretion system ( 18).	bind
51114	2	11547	5	NULL	NULL	NULL	NULL	intimin	GP		bind		directly			Tir	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_8_4637_s_189	10899867	A number of groups have reported that intimin can bind directly to uninfected host cells ( 2,  8) and to a receptor encoded by the bacteria, termed Tir, which is translocated into the host cell membrane via a type III secretion system ( 18).	bind
51115	3	11547	5	NULL	NULL	NULL	NULL	Tir	GP		is a type of					receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_8_4637_s_189	10899867	A number of groups have reported that intimin can bind directly to uninfected host cells ( 2,  8) and to a receptor encoded by the bacteria, termed Tir, which is translocated into the host cell membrane via a type III secretion system ( 18).	bind
51116	4	11547	5	NULL	NULL	NULL	NULL	Tir	GP		is encoded by					bacteria	Organism				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_8_4637_s_189	10899867	A number of groups have reported that intimin can bind directly to uninfected host cells ( 2,  8) and to a receptor encoded by the bacteria, termed Tir, which is translocated into the host cell membrane via a type III secretion system ( 18).	bind
51117	5	11547	5	NULL	NULL	NULL	NULL	Tir	GP		is translocated to					host cell  membrane	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_8_4637_s_189	10899867	A number of groups have reported that intimin can bind directly to uninfected host cells ( 2,  8) and to a receptor encoded by the bacteria, termed Tir, which is translocated into the host cell membrane via a type III secretion system ( 18).	bind
51118	6	11547	5	NULL	NULL	NULL	NULL	statement 5	Process		via					type III secretion system	Process				NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_8_4637_s_189	10899867	A number of groups have reported that intimin can bind directly to uninfected host cells ( 2,  8) and to a receptor encoded by the bacteria, termed Tir, which is translocated into the host cell membrane via a type III secretion system ( 18).	bind
50449	1	11547	6	NULL	NULL	0	NULL	intimin	NULL		bind	NULL	directly			host cells	NULL	uninfected			NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_8_4637_s_189	10899867	A number of groups have reported that intimin can bind directly to uninfected host cells ( 2,  8) and to a receptor encoded by the bacteria, termed Tir, which is translocated into the host cell membrane via a type III secretion system ( 18).	bind
50450	2	11547	6	NULL	NULL	0	NULL	intimin	NULL		bind	NULL				Tir	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_8_4637_s_189	10899867	A number of groups have reported that intimin can bind directly to uninfected host cells ( 2,  8) and to a receptor encoded by the bacteria, termed Tir, which is translocated into the host cell membrane via a type III secretion system ( 18).	bind
50451	3	11547	6	10	NULL	0	NULL	Tir			is a type of					receptor  		bacteria			NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_8_4637_s_189	10899867	A number of groups have reported that intimin can bind directly to uninfected host cells ( 2,  8) and to a receptor encoded by the bacteria, termed Tir, which is translocated into the host cell membrane via a type III secretion system ( 18).	bind
50452	4	11547	6	NULL	NULL	0	NULL	Tir	NULL		is translocated into	NULL				host cell membrane	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_8_4637_s_189	10899867	A number of groups have reported that intimin can bind directly to uninfected host cells ( 2,  8) and to a receptor encoded by the bacteria, termed Tir, which is translocated into the host cell membrane via a type III secretion system ( 18).	bind
50453	5	11547	6	NULL	NULL	0	NULL	statement 4	NULL		occurs via	NULL				type III secretion system	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_8_4637_s_189	10899867	A number of groups have reported that intimin can bind directly to uninfected host cells ( 2,  8) and to a receptor encoded by the bacteria, termed Tir, which is translocated into the host cell membrane via a type III secretion system ( 18).	bind
51119	1	11548	5	NULL	NULL	NULL	NULL	GTP	Chemical		bind					Rho family members	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_33105_s_18	9407095	A number of guanine nucleotide exchange factors, which promote binding of GTP to Rho family members by facilitating the release of GDP, have been identified ( 16).	bind
51120	2	11548	5	NULL	NULL	NULL	NULL	guanine nucleotide exchange factors	GP		promotes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_33105_s_18	9407095	A number of guanine nucleotide exchange factors, which promote binding of GTP to Rho family members by facilitating the release of GDP, have been identified ( 16).	bind
51121	3	11548	5	NULL	NULL	NULL	NULL	guanine nucleotide exchange factors	GP		facilitates					GDP	Chemical	release of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_33105_s_18	9407095	A number of guanine nucleotide exchange factors, which promote binding of GTP to Rho family members by facilitating the release of GDP, have been identified ( 16).	bind
51122	4	11548	5	NULL	NULL	NULL	NULL	statement 3	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_33105_s_18	9407095	A number of guanine nucleotide exchange factors, which promote binding of GTP to Rho family members by facilitating the release of GDP, have been identified ( 16).	bind
50454	1	11548	6	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				Rho family members	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_33105_s_18	9407095	A number of guanine nucleotide exchange factors, which promote binding of GTP to Rho family members by facilitating the release of GDP, have been identified ( 16).	bind
50455	2	11548	6	NULL	NULL	0	NULL	guanine nucleotide exchange factors	NULL		promote	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_33105_s_18	9407095	A number of guanine nucleotide exchange factors, which promote binding of GTP to Rho family members by facilitating the release of GDP, have been identified ( 16).	bind
50456	3	11548	6	NULL	NULL	0	NULL	statement 2	NULL		occurs by facilitating	NULL				GDP	NULL	release of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_33105_s_18	9407095	A number of guanine nucleotide exchange factors, which promote binding of GTP to Rho family members by facilitating the release of GDP, have been identified ( 16).	bind
54192	4	11548	6	10	NULL	0	NULL	statement 3			leads to					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_33105_s_18	9407095	A number of guanine nucleotide exchange factors, which promote binding of GTP to Rho family members by facilitating the release of GDP, have been identified ( 16).	bind
51123	1	11549	5	NULL	NULL	NULL	NULL	HDAC	GP		is					histone deacetylases	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
51124	2	11549	5	NULL	NULL	NULL	NULL	HMT	GP		is					histone methyltransferases	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
51125	3	11549	5	NULL	NULL	NULL	NULL	HDAC	GP		is associated with					MeCP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
51126	4	11549	5	NULL	NULL	NULL	NULL	HDAC	GP		is associated with					MBD1	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
51127	5	11549	5	NULL	NULL	NULL	NULL	HDAC	GP		is associated with					MBD3	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
51128	6	11549	5	NULL	NULL	NULL	NULL	HDAC	GP		is associated with					DNA methyltransferases	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
51129	7	11549	5	NULL	NULL	NULL	NULL	HMT	GP		is associated with					MeCP2	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
51130	8	11549	5	NULL	NULL	NULL	NULL	HMT	GP		is associated with					MBD1	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
51131	9	11549	5	NULL	NULL	NULL	NULL	HMT	GP		is associated with					MBD3	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
51132	10	11549	5	NULL	NULL	NULL	NULL	HMT	GP		is associated with					DNA methyltransferases	GP				NULL		NULL	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
50469	1	11549	6	NULL	NULL	0	NULL	HDAC	NULL		is	NULL				histone deacetylase	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
50470	2	11549	6	NULL	NULL	0	NULL	HMT	NULL		is	NULL				histone methyltransferases	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
50471	3	11549	6	NULL	NULL	0	NULL	HDAC	NULL		associates with	NULL				MeCP2	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
50483	4	11549	6	NULL	NULL	0	NULL	HDAC	NULL		associates with	NULL				MBD1	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
50484	5	11549	6	NULL	NULL	0	NULL	HDAC	NULL		associates with	NULL				MBD3	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
50485	6	11549	6	NULL	NULL	0	NULL	HDAC	NULL		associates with	NULL				DNA methyltransferases	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
50486	7	11549	6	NULL	NULL	0	NULL	HMT	NULL		associates with	NULL				MeCP2	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
50487	8	11549	6	NULL	NULL	0	NULL	HMT	NULL		associates with	NULL				MBD1	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
50488	9	11549	6	NULL	NULL	0	NULL	HMT	NULL		associates with	NULL				MBD3	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
50489	10	11549	6	NULL	NULL	0	NULL	HMT	NULL		associates with	NULL				DNA methyltransferases	NULL				NULL		0	NULL	NULL	NULL	gw70_development_131_24_6185_s_29	15548582	A number of histone deacetylases (HDAC) and histone methyltransferases (HMT) are associated with MeCP2, MBD1, MBD3 and DNA methyltransferases.	bind
51133	1	11550	5	NULL	NULL	NULL	NULL	FK506	Chemical		is a type of					immunosuppressant	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_14_8351_s_187	9653190	A number of immunophilin ligands, including the immunosuppressant FK506, which also binds to FKBP12, are neurotrophic ( 22).	bind
51134	2	11550	5	NULL	NULL	NULL	NULL	FK506	Chemical		is a type of					immunophilin ligand	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_14_8351_s_187	9653190	A number of immunophilin ligands, including the immunosuppressant FK506, which also binds to FKBP12, are neurotrophic ( 22).	bind
51135	3	11550	5	NULL	NULL	NULL	NULL	FK506	Chemical		bind					FKBP12	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_14_8351_s_187	9653190	A number of immunophilin ligands, including the immunosuppressant FK506, which also binds to FKBP12, are neurotrophic ( 22).	bind
50490	1	11550	6	10	NULL	0	NULL	FK506			bind					FKBP12					NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_14_8351_s_187	9653190	A number of immunophilin ligands, including the immunosuppressant FK506, which also binds to FKBP12, are neurotrophic ( 22).	bind
50491	2	11550	6	NULL	NULL	0	NULL	FK506	NULL		is a type of	NULL				immunophilin ligand	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_14_8351_s_187	9653190	A number of immunophilin ligands, including the immunosuppressant FK506, which also binds to FKBP12, are neurotrophic ( 22).	bind
50492	3	11550	6	NULL	NULL	0	NULL	FKBP12	NULL		is	NULL				neurotrophic	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_95_14_8351_s_187	9653190	A number of immunophilin ligands, including the immunosuppressant FK506, which also binds to FKBP12, are neurotrophic ( 22).	bind
54193	4	11550	6	10	NULL	0	NULL	FK506			is a type of					immunosuppressant					NULL		0	NULL	NULL	NULL	gw60_pnas_95_14_8351_s_187	9653190	A number of immunophilin ligands, including the immunosuppressant FK506, which also binds to FKBP12, are neurotrophic ( 22).	bind
51136	1	11551	5	NULL	NULL	NULL	NULL	Tau	GP		bind					MTs	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_39_30335_s_20	10869348	A number of investigations on the binding of Tau to MTs have been reported ( 6-14).	bind
50493	1	11551	6	NULL	NULL	0	NULL	Tau	NULL		bind	NULL				MTs	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_39_30335_s_20	10869348	A number of investigations on the binding of Tau to MTs have been reported ( 6-14).	bind
51137	1	11552	5	NULL	NULL	NULL	NULL	KAP-1	GP		mediates							repression of	KRAB domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
51138	2	11552	5	NULL	NULL	NULL	NULL	KAP-1	GP		bind							multiple	KRAB repression domains		NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
51139	3	11552	5	NULL	NULL	NULL	NULL	KAP-1	GP		bind							multiple	KRAB repression domains		NULL	in vivo	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
51140	4	11552	5	NULL	NULL	NULL	NULL			mutant	abolishes			KRAB domain		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
51141	5	11552	5	NULL	NULL	NULL	NULL			mutant	abolishes			KRAB domain		repression	Process	decrease of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
51143	6	11552	5	NULL	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
51144	7	11552	5	NULL	NULL	NULL	NULL	KAP-1	GP	overexpression of	enhances					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
51145	8	11552	5	NULL	NULL	NULL	NULL	statement 7	Process		is dependent on							presence of	RBCC domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
51146	9	11552	5	NULL	NULL	NULL	NULL	KAP-1	GP		is fused to		heterologous						DNA binding domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
51147	10	11552	5	NULL	NULL	NULL	NULL	statement 9	Process		potentiate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
50494	1	11552	6	10	NULL	0	NULL	KAP-1			mediates							repression of	KRAB domain		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
50495	2	11552	6	NULL	NULL	0	NULL	KAP-1	NULL		bind	NULL					NULL		KRAB repression domain		NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
50496	3	11552	6	NULL	NULL	0	NULL	KAP-1	NULL		bind	NULL					NULL		KRAB repression domain		NULL	in vivo	0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
50538	4	11552	6	NULL	NULL	0	NULL		NULL	mutation of	eliminates	NULL		KRAB domain		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
50539	5	11552	6	10	NULL	0	NULL			mutant	abolishes			KRAB domain		repression		decrease of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
50540	6	11552	6	10	NULL	0	NULL	KAP-1		overexpression of	enhances					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
50541	7	11552	6	NULL	NULL	0	NULL	statement 6	NULL		is dependent on	NULL					NULL	presence of	RBCC domain		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
50542	8	11552	6	NULL	NULL	0	NULL	KAP-1	NULL		fuses with	NULL					NULL		DNA binding domain		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
50543	9	11552	6	NULL	NULL	0	NULL	statement 8	NULL		potentiate	NULL				repression	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
54195	10	11552	6	10	NULL	0	NULL	statement 4			is an alternative to					statement 5					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_6_4366_s_30	10330177	A number of lines of evidence have suggested that KAP-1 plays a key role in mediating KRAB domain repression: (i) KAP-1 binds to multiple KRAB repression domains both in vitro and in vivo, (ii) KRAB domain mutations which abolish repression decrease or eliminate the interaction with KAP-1, (iii) overexpression of KAP-1 enhances KRAB-mediated repression in a manner dependent on the presence of the RBCC domain, and (iv) heterologous fusions between KAP-1 and a DNA binding domain can potentiate repression ( 17,  36,  42).	bind
51148	1	11553	5	NULL	NULL	NULL	NULL	VnbP	GP		bind					vitronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclinmicrobiol_38_1_389_s_90	10618121	A number of matrix binding proteins have been described for GAS, including SfbI ( 25), SfbII ( 15), F1 ( 10) and FBBP ( 4) (which each bind to fibronectin), and VnbP, which binds to vitronectin ( 17).	bind
51149	2	11553	5	NULL	NULL	NULL	NULL	SfbI	GP		bind					fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclinmicrobiol_38_1_389_s_90	10618121	A number of matrix binding proteins have been described for GAS, including SfbI ( 25), SfbII ( 15), F1 ( 10) and FBBP ( 4) (which each bind to fibronectin), and VnbP, which binds to vitronectin ( 17).	bind
51150	3	11553	5	NULL	NULL	NULL	NULL	SfbII	GP		bind					fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclinmicrobiol_38_1_389_s_90	10618121	A number of matrix binding proteins have been described for GAS, including SfbI ( 25), SfbII ( 15), F1 ( 10) and FBBP ( 4) (which each bind to fibronectin), and VnbP, which binds to vitronectin ( 17).	bind
51151	4	11553	5	NULL	NULL	NULL	NULL	F1	GP		bind					fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclinmicrobiol_38_1_389_s_90	10618121	A number of matrix binding proteins have been described for GAS, including SfbI ( 25), SfbII ( 15), F1 ( 10) and FBBP ( 4) (which each bind to fibronectin), and VnbP, which binds to vitronectin ( 17).	bind
51152	5	11553	5	NULL	NULL	NULL	NULL	FBBP	GP		bind					fibronectin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jclinmicrobiol_38_1_389_s_90	10618121	A number of matrix binding proteins have been described for GAS, including SfbI ( 25), SfbII ( 15), F1 ( 10) and FBBP ( 4) (which each bind to fibronectin), and VnbP, which binds to vitronectin ( 17).	bind
50544	1	11553	6	NULL	NULL	0	NULL	SfbI	NULL		bind	NULL				fibronectin	NULL				NULL		0	NULL	NULL	NULL	gw60_jclinmicrobiol_38_1_389_s_90	10618121	A number of matrix binding proteins have been described for GAS, including SfbI ( 25), SfbII ( 15), F1 ( 10) and FBBP ( 4) (which each bind to fibronectin), and VnbP, which binds to vitronectin ( 17).	bind
50545	2	11553	6	NULL	NULL	0	NULL	SfbII	NULL		bind	NULL				fibronectin	NULL				NULL		0	NULL	NULL	NULL	gw60_jclinmicrobiol_38_1_389_s_90	10618121	A number of matrix binding proteins have been described for GAS, including SfbI ( 25), SfbII ( 15), F1 ( 10) and FBBP ( 4) (which each bind to fibronectin), and VnbP, which binds to vitronectin ( 17).	bind
50546	3	11553	6	NULL	NULL	0	NULL	F1	NULL		bind	NULL				fibronectin	NULL				NULL		0	NULL	NULL	NULL	gw60_jclinmicrobiol_38_1_389_s_90	10618121	A number of matrix binding proteins have been described for GAS, including SfbI ( 25), SfbII ( 15), F1 ( 10) and FBBP ( 4) (which each bind to fibronectin), and VnbP, which binds to vitronectin ( 17).	bind
50547	4	11553	6	NULL	NULL	0	NULL	FBBP	NULL		bind	NULL				fibronectin	NULL				NULL		0	NULL	NULL	NULL	gw60_jclinmicrobiol_38_1_389_s_90	10618121	A number of matrix binding proteins have been described for GAS, including SfbI ( 25), SfbII ( 15), F1 ( 10) and FBBP ( 4) (which each bind to fibronectin), and VnbP, which binds to vitronectin ( 17).	bind
50548	5	11553	6	NULL	NULL	0	NULL	VnbP	NULL		bind	NULL				vitronectin	NULL				NULL		0	NULL	NULL	NULL	gw60_jclinmicrobiol_38_1_389_s_90	10618121	A number of matrix binding proteins have been described for GAS, including SfbI ( 25), SfbII ( 15), F1 ( 10) and FBBP ( 4) (which each bind to fibronectin), and VnbP, which binds to vitronectin ( 17).	bind
51153	1	11554	5	NULL	NULL	NULL	NULL	ERK	GP		phosphorylates					SOS	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_9_2863_s_322	10982386	A number of mechanisms have been proposed to be involved in this down-regulation of the pathway, including ERK phosphorylation of SOS, which prevents SOS binding to Grb2 (Langlois  et al., 1995  ; Corbalan-Garcia  et al., 1996  ).	bind
51154	2	11554	5	NULL	NULL	NULL	NULL	SOS	GP		bind					Grb2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_9_2863_s_322	10982386	A number of mechanisms have been proposed to be involved in this down-regulation of the pathway, including ERK phosphorylation of SOS, which prevents SOS binding to Grb2 (Langlois  et al., 1995  ; Corbalan-Garcia  et al., 1996  ).	bind
51155	3	11554	5	NULL	NULL	NULL	NULL	statement 1	Process		prevents					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_9_2863_s_322	10982386	A number of mechanisms have been proposed to be involved in this down-regulation of the pathway, including ERK phosphorylation of SOS, which prevents SOS binding to Grb2 (Langlois  et al., 1995  ; Corbalan-Garcia  et al., 1996  ).	bind
50549	1	11554	6	NULL	NULL	0	NULL	SOS	NULL		bind	NULL				Grb2	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_9_2863_s_322	10982386	A number of mechanisms have been proposed to be involved in this down-regulation of the pathway, including ERK phosphorylation of SOS, which prevents SOS binding to Grb2 (Langlois  et al., 1995  ; Corbalan-Garcia  et al., 1996  ).	bind
50550	2	11554	6	NULL	NULL	0	NULL	ERK	NULL		phosphorylates	NULL				SOS	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_9_2863_s_322	10982386	A number of mechanisms have been proposed to be involved in this down-regulation of the pathway, including ERK phosphorylation of SOS, which prevents SOS binding to Grb2 (Langlois  et al., 1995  ; Corbalan-Garcia  et al., 1996  ).	bind
50551	3	11554	6	NULL	NULL	0	NULL	statement 2	NULL		prevents	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_9_2863_s_322	10982386	A number of mechanisms have been proposed to be involved in this down-regulation of the pathway, including ERK phosphorylation of SOS, which prevents SOS binding to Grb2 (Langlois  et al., 1995  ; Corbalan-Garcia  et al., 1996  ).	bind
51156	1	11555	5	NULL	NULL	NULL	NULL	SRF	GP		bind									CArG elements	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8398_s_24	9525950	A number of mechanisms have been shown to increase SRF binding to CArG elements including post-translational modification of SRF ( 17), increased SRF protein expression ( 34), and interaction of SRF with homeodomain factors that modulate SRF binding or kinetics ( 38).	bind
51157	2	11555	5	NULL	NULL	NULL	NULL	SRF	GP	post-translational modification of	increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8398_s_24	9525950	A number of mechanisms have been shown to increase SRF binding to CArG elements including post-translational modification of SRF ( 17), increased SRF protein expression ( 34), and interaction of SRF with homeodomain factors that modulate SRF binding or kinetics ( 38).	bind
51158	3	11555	5	NULL	NULL	NULL	NULL	SRF protein	GP	increased expression of	increases					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8398_s_24	9525950	A number of mechanisms have been shown to increase SRF binding to CArG elements including post-translational modification of SRF ( 17), increased SRF protein expression ( 34), and interaction of SRF with homeodomain factors that modulate SRF binding or kinetics ( 38).	bind
51159	4	11555	5	NULL	NULL	NULL	NULL	SRF	GP		interacts with					homeodomain factors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8398_s_24	9525950	A number of mechanisms have been shown to increase SRF binding to CArG elements including post-translational modification of SRF ( 17), increased SRF protein expression ( 34), and interaction of SRF with homeodomain factors that modulate SRF binding or kinetics ( 38).	bind
51160	5	11555	5	NULL	NULL	NULL	NULL	statement 4	Process		modulates					SRF	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8398_s_24	9525950	A number of mechanisms have been shown to increase SRF binding to CArG elements including post-translational modification of SRF ( 17), increased SRF protein expression ( 34), and interaction of SRF with homeodomain factors that modulate SRF binding or kinetics ( 38).	bind
50552	1	11555	6	NULL	NULL	0	NULL	SRF	NULL		bind	NULL					NULL			CArG element	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8398_s_24	9525950	A number of mechanisms have been shown to increase SRF binding to CArG elements including post-translational modification of SRF ( 17), increased SRF protein expression ( 34), and interaction of SRF with homeodomain factors that modulate SRF binding or kinetics ( 38).	bind
50553	2	11555	6	NULL	NULL	0	NULL	SRF	NULL	post-translational modification of	increase	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8398_s_24	9525950	A number of mechanisms have been shown to increase SRF binding to CArG elements including post-translational modification of SRF ( 17), increased SRF protein expression ( 34), and interaction of SRF with homeodomain factors that modulate SRF binding or kinetics ( 38).	bind
50555	3	11555	6	NULL	NULL	0	NULL	SRF	NULL		interacts with	NULL				homeodomain factors	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8398_s_24	9525950	A number of mechanisms have been shown to increase SRF binding to CArG elements including post-translational modification of SRF ( 17), increased SRF protein expression ( 34), and interaction of SRF with homeodomain factors that modulate SRF binding or kinetics ( 38).	bind
54196	4	11555	6	10	NULL	0	NULL	statement 3			modulate					SRF		binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8398_s_24	9525950	A number of mechanisms have been shown to increase SRF binding to CArG elements including post-translational modification of SRF ( 17), increased SRF protein expression ( 34), and interaction of SRF with homeodomain factors that modulate SRF binding or kinetics ( 38).	bind
54197	5	11555	6	10	NULL	0	NULL	SRF		increased expression of	increase					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8398_s_24	9525950	A number of mechanisms have been shown to increase SRF binding to CArG elements including post-translational modification of SRF ( 17), increased SRF protein expression ( 34), and interaction of SRF with homeodomain factors that modulate SRF binding or kinetics ( 38).	bind
51161	1	11556	5	NULL	NULL	NULL	NULL	cytochrome c	GP		bind					CcP	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1597_2_193_s_309	12044899	A number of models can be applied to the binding of cytochrome  c to CcP, ranging from a unique-independent sites model to a multiple-interacting sites model.	bind
50497	1	11556	6	NULL	NULL	0	NULL	cytochrome c	NULL		bind	NULL				CcP	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1597_2_193_s_309	12044899	A number of models can be applied to the binding of cytochrome  c to CcP, ranging from a unique-independent sites model to a multiple-interacting sites model.	bind
51162	1	11557	5	NULL	NULL	NULL	NULL	Munc18/n-Sec1/rbSec1	GP		bind					SNARE proteins	GP	individual			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
51163	2	11557	5	NULL	NULL	NULL	NULL	complexins	GP		bind					SNARE proteins	GP	individual			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
51164	3	11557	5	NULL	NULL	NULL	NULL	Munc-13	GP		bind					SNARE proteins	GP	individual			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
51165	4	11557	5	NULL	NULL	NULL	NULL	tomosyn	GP		bind					SNARE proteins	GP	individual			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
51166	5	11557	5	NULL	NULL	NULL	NULL	snapin	GP		bind					SNARE proteins	GP	individual			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
51167	6	11557	5	NULL	NULL	NULL	NULL	syntaphilin	GP		bind					SNARE proteins	GP	individual			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
51168	7	11557	5	NULL	NULL	NULL	NULL	SNARE proteins	GP	free	forms					functional release machinery	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
51169	8	11557	5	NULL	NULL	NULL	NULL	Munc18/n-Sec1/rbSec1	GP		regulates					statement 7	Process	availability;;propensity of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
51170	9	11557	5	NULL	NULL	NULL	NULL	complexins	GP		regulates					statement 7	Process	availability;;propensity of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
51171	10	11557	5	NULL	NULL	NULL	NULL	Munc-13	GP		regulates					statement 7	Process	availability;;propensity of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
51172	11	11557	5	NULL	NULL	NULL	NULL	tomosyn	GP		regulates					statement 7	Process	availability;;propensity of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
51173	12	11557	5	NULL	NULL	NULL	NULL	snapin	GP		regulates					statement 7	Process	availability;;propensity of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
51174	13	11557	5	NULL	NULL	NULL	NULL	syntaphilin	GP		regulates					statement 7	Process	availability;;propensity of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
50498	1	11557	6	NULL	NULL	0	NULL	Munc18/n-Sec1/rbSec1	NULL		bind	NULL				SNARE protein	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
50499	2	11557	6	NULL	NULL	0	NULL	complexins	NULL		bind	NULL				SNARE protein	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
50500	3	11557	6	NULL	NULL	0	NULL	Munc-13	NULL		bind	NULL				SNARE protein	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
50501	4	11557	6	NULL	NULL	0	NULL	tomosyn	NULL		bind	NULL				SNARE protein	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
50556	5	11557	6	NULL	NULL	0	NULL	snapin	NULL		bind	NULL				SNARE protein	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
50557	6	11557	6	NULL	NULL	0	NULL	syntaphilin	NULL		bind	NULL				SNARE protein	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
50558	7	11557	6	10	NULL	0	NULL	SNARE protein		free	forms					functional release machinery					NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
50559	8	11557	6	10	NULL	0	NULL	Munc18/n-Sec1/rbSec1			regulates					statement 7		availability of;;propensity of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
50560	9	11557	6	10	NULL	0	NULL	complexins			regulates					statement 7		availability of;;propensity of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
50561	10	11557	6	10	NULL	0	NULL	Munc-13			regulates					statement 7		availability of;;propensity of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
50562	11	11557	6	10	NULL	0	NULL	tomosyn			regulates					statement 7		availability of;;propensity of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
50563	12	11557	6	10	NULL	0	NULL	snapin			regulates					statement 7		availability of;;propensity of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
50564	13	11557	6	10	NULL	0	NULL	syntaphilin			regulates					statement 7		availability of;;propensity of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_24_14038_s_14	11707603	A number of molecules (including Munc18/n-Sec1/rbSec1, complexins, Munc-13, tomosyn, snapin, and syntaphilin that bind to individual SNARE proteins) have been suggested to regulate the availability and/or propensity of free SNARE proteins to form functional release machinery ( 19-25).	bind
51175	1	11558	5	NULL	NULL	NULL	NULL	CDK2 monomer	GP		bind					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1754_1_132_s_201	16271522	A number of monomeric CDK2 and T160-phosphorylated CDK2/cyclin A structures are available  bound to ATP or ATP-competitive CDK2-selective inhibitors which can be analysed to  determine which residues lie within 5  Ang  of any ligand atom.	bind
51176	2	11558	5	NULL	NULL	NULL	NULL	CDK2 monomer	GP		bind					CDK2-selective inhibitors	Chemical	ATP-competitive			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1754_1_132_s_201	16271522	A number of monomeric CDK2 and T160-phosphorylated CDK2/cyclin A structures are available  bound to ATP or ATP-competitive CDK2-selective inhibitors which can be analysed to  determine which residues lie within 5  Ang  of any ligand atom.	bind
51177	3	11558	5	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1754_1_132_s_201	16271522	A number of monomeric CDK2 and T160-phosphorylated CDK2/cyclin A structures are available  bound to ATP or ATP-competitive CDK2-selective inhibitors which can be analysed to  determine which residues lie within 5  Ang  of any ligand atom.	bind
51178	4	11558	5	NULL	NULL	NULL	NULL	CDK2/cyclin A	GP	phosphorylated	bind			T160		ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1754_1_132_s_201	16271522	A number of monomeric CDK2 and T160-phosphorylated CDK2/cyclin A structures are available  bound to ATP or ATP-competitive CDK2-selective inhibitors which can be analysed to  determine which residues lie within 5  Ang  of any ligand atom.	bind
51179	5	11558	5	NULL	NULL	NULL	NULL	CDK2/cyclin A	GP	phosphorylated	bind			T160		CDK2-selective inhibitors	Chemical	ATP-competitive			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1754_1_132_s_201	16271522	A number of monomeric CDK2 and T160-phosphorylated CDK2/cyclin A structures are available  bound to ATP or ATP-competitive CDK2-selective inhibitors which can be analysed to  determine which residues lie within 5  Ang  of any ligand atom.	bind
51180	6	11558	5	NULL	NULL	NULL	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1754_1_132_s_201	16271522	A number of monomeric CDK2 and T160-phosphorylated CDK2/cyclin A structures are available  bound to ATP or ATP-competitive CDK2-selective inhibitors which can be analysed to  determine which residues lie within 5  Ang  of any ligand atom.	bind
50566	1	11558	6	NULL	NULL	0	NULL	CDK2	NULL		bind	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1754_1_132_s_201	16271522	A number of monomeric CDK2 and T160-phosphorylated CDK2/cyclin A structures are available  bound to ATP or ATP-competitive CDK2-selective inhibitors which can be analysed to  determine which residues lie within 5  Ang  of any ligand atom.	bind
50567	2	11558	6	NULL	NULL	0	NULL	CDK2/cyclin A	NULL	phosphorylated	bind	NULL		T160		ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1754_1_132_s_201	16271522	A number of monomeric CDK2 and T160-phosphorylated CDK2/cyclin A structures are available  bound to ATP or ATP-competitive CDK2-selective inhibitors which can be analysed to  determine which residues lie within 5  Ang  of any ligand atom.	bind
50568	3	11558	6	NULL	NULL	0	NULL	CDK2	NULL		bind	NULL				CDK2-selective inhibitors	NULL	ATP-competitive			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1754_1_132_s_201	16271522	A number of monomeric CDK2 and T160-phosphorylated CDK2/cyclin A structures are available  bound to ATP or ATP-competitive CDK2-selective inhibitors which can be analysed to  determine which residues lie within 5  Ang  of any ligand atom.	bind
50569	4	11558	6	NULL	NULL	0	NULL	CDK2/cyclin A	NULL	phosphorylated	bind	NULL		T160		CDK2-selective inhibitors	NULL	ATP-competitive			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1754_1_132_s_201	16271522	A number of monomeric CDK2 and T160-phosphorylated CDK2/cyclin A structures are available  bound to ATP or ATP-competitive CDK2-selective inhibitors which can be analysed to  determine which residues lie within 5  Ang  of any ligand atom.	bind
50570	5	11558	6	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1754_1_132_s_201	16271522	A number of monomeric CDK2 and T160-phosphorylated CDK2/cyclin A structures are available  bound to ATP or ATP-competitive CDK2-selective inhibitors which can be analysed to  determine which residues lie within 5  Ang  of any ligand atom.	bind
50571	6	11558	6	NULL	NULL	0	NULL	statement 2	NULL		is an alternative to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1754_1_132_s_201	16271522	A number of monomeric CDK2 and T160-phosphorylated CDK2/cyclin A structures are available  bound to ATP or ATP-competitive CDK2-selective inhibitors which can be analysed to  determine which residues lie within 5  Ang  of any ligand atom.	bind
51181	1	11560	5	NULL	NULL	NULL	NULL			mutant	alter			beta2AR tail		receptors	GP	endocytic membrane trafficking of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_5_3305_s_26	15548537	A number of mutations of the beta2AR tail that alter the endocytic membrane trafficking of receptors also disrupt receptor interaction with NSF, and  in vitro studies indicate that NSF and PDZ proteins bind to the beta2AR tail competitively.	bind
51183	3	11560	5	NULL	NULL	NULL	NULL			mutant	disrupt			beta2AR tail		statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_5_3305_s_26	15548537	A number of mutations of the beta2AR tail that alter the endocytic membrane trafficking of receptors also disrupt receptor interaction with NSF, and  in vitro studies indicate that NSF and PDZ proteins bind to the beta2AR tail competitively.	bind
51184	2	11560	5	NULL	NULL	NULL	NULL	NSF proteins	GP		bind								beta2AR tail		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_5_3305_s_26	15548537	A number of mutations of the beta2AR tail that alter the endocytic membrane trafficking of receptors also disrupt receptor interaction with NSF, and  in vitro studies indicate that NSF and PDZ proteins bind to the beta2AR tail competitively.	bind
51185	4	11560	5	NULL	NULL	NULL	NULL	PDZ proteins	GP		bind								beta2AR tail		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_5_3305_s_26	15548537	A number of mutations of the beta2AR tail that alter the endocytic membrane trafficking of receptors also disrupt receptor interaction with NSF, and  in vitro studies indicate that NSF and PDZ proteins bind to the beta2AR tail competitively.	bind
51186	5	11560	5	NULL	NULL	NULL	NULL	statement 2	Process		competes with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_5_3305_s_26	15548537	A number of mutations of the beta2AR tail that alter the endocytic membrane trafficking of receptors also disrupt receptor interaction with NSF, and  in vitro studies indicate that NSF and PDZ proteins bind to the beta2AR tail competitively.	bind
50579	1	11560	6	NULL	NULL	0	NULL	NSF	NULL		bind	NULL					NULL		beta2AR tail		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_5_3305_s_26	15548537	A number of mutations of the beta2AR tail that alter the endocytic membrane trafficking of receptors also disrupt receptor interaction with NSF, and  in vitro studies indicate that NSF and PDZ proteins bind to the beta2AR tail competitively.	bind
50580	2	11560	6	NULL	NULL	0	NULL	PDZ protein	NULL		bind	NULL					NULL		beta2AR tail		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_5_3305_s_26	15548537	A number of mutations of the beta2AR tail that alter the endocytic membrane trafficking of receptors also disrupt receptor interaction with NSF, and  in vitro studies indicate that NSF and PDZ proteins bind to the beta2AR tail competitively.	bind
50581	3	11560	6	NULL	NULL	0	NULL	statement 1	NULL		competes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_5_3305_s_26	15548537	A number of mutations of the beta2AR tail that alter the endocytic membrane trafficking of receptors also disrupt receptor interaction with NSF, and  in vitro studies indicate that NSF and PDZ proteins bind to the beta2AR tail competitively.	bind
50582	4	11560	6	NULL	NULL	0	NULL		NULL	mutation of	alters	NULL		beta2AR tail		receptor	NULL	endocytic membrane trafficking of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_5_3305_s_26	15548537	A number of mutations of the beta2AR tail that alter the endocytic membrane trafficking of receptors also disrupt receptor interaction with NSF, and  in vitro studies indicate that NSF and PDZ proteins bind to the beta2AR tail competitively.	bind
50583	5	11560	6	NULL	NULL	0	NULL		NULL	mutation of	disrupts	NULL		beta2AR tail		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_5_3305_s_26	15548537	A number of mutations of the beta2AR tail that alter the endocytic membrane trafficking of receptors also disrupt receptor interaction with NSF, and  in vitro studies indicate that NSF and PDZ proteins bind to the beta2AR tail competitively.	bind
51187	1	11561	5	NULL	NULL	NULL	NULL	nAChR agonists	GP		bind					alpha4/beta2 receptor	GP				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jneurosci_20_17_6431_s_19	10964949	A number of nAChR agonists that bind to the alpha4/beta2 receptor configuration  in vitro are known to have an effect on anxiety (Pomerleau, 1986  ; Gilbert et al., 1989  ; Brioni et al., 1993  ), attention (Brioni et al., 1997  ), and antinociception (Tripathi et al., 1982  ; Damaj et al., 1998  ), implicating the alpha4/beta2 receptor in the mediation of a number of physiological processes.	bind
51188	2	11561	5	NULL	NULL	NULL	NULL	statement 1	Process		effects					anxiety	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_20_17_6431_s_19	10964949	A number of nAChR agonists that bind to the alpha4/beta2 receptor configuration  in vitro are known to have an effect on anxiety (Pomerleau, 1986  ; Gilbert et al., 1989  ; Brioni et al., 1993  ), attention (Brioni et al., 1997  ), and antinociception (Tripathi et al., 1982  ; Damaj et al., 1998  ), implicating the alpha4/beta2 receptor in the mediation of a number of physiological processes.	bind
51189	3	11561	5	NULL	NULL	NULL	NULL	statement 1	Process		effects					attention	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_20_17_6431_s_19	10964949	A number of nAChR agonists that bind to the alpha4/beta2 receptor configuration  in vitro are known to have an effect on anxiety (Pomerleau, 1986  ; Gilbert et al., 1989  ; Brioni et al., 1993  ), attention (Brioni et al., 1997  ), and antinociception (Tripathi et al., 1982  ; Damaj et al., 1998  ), implicating the alpha4/beta2 receptor in the mediation of a number of physiological processes.	bind
51190	4	11561	5	NULL	NULL	NULL	NULL	statement 1	Process		effects					antinociception	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_20_17_6431_s_19	10964949	A number of nAChR agonists that bind to the alpha4/beta2 receptor configuration  in vitro are known to have an effect on anxiety (Pomerleau, 1986  ; Gilbert et al., 1989  ; Brioni et al., 1993  ), attention (Brioni et al., 1997  ), and antinociception (Tripathi et al., 1982  ; Damaj et al., 1998  ), implicating the alpha4/beta2 receptor in the mediation of a number of physiological processes.	bind
50584	1	11561	6	NULL	NULL	0	NULL	nAChR agonists	NULL		bind	NULL				alpha4/beta2 receptor	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_jneurosci_20_17_6431_s_19	10964949	A number of nAChR agonists that bind to the alpha4/beta2 receptor configuration  in vitro are known to have an effect on anxiety (Pomerleau, 1986  ; Gilbert et al., 1989  ; Brioni et al., 1993  ), attention (Brioni et al., 1997  ), and antinociception (Tripathi et al., 1982  ; Damaj et al., 1998  ), implicating the alpha4/beta2 receptor in the mediation of a number of physiological processes.	bind
50585	2	11561	6	NULL	NULL	0	NULL	nAChR agonists	NULL		plays a role in	NULL				anxiety	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_17_6431_s_19	10964949	A number of nAChR agonists that bind to the alpha4/beta2 receptor configuration  in vitro are known to have an effect on anxiety (Pomerleau, 1986  ; Gilbert et al., 1989  ; Brioni et al., 1993  ), attention (Brioni et al., 1997  ), and antinociception (Tripathi et al., 1982  ; Damaj et al., 1998  ), implicating the alpha4/beta2 receptor in the mediation of a number of physiological processes.	bind
50586	3	11561	6	NULL	NULL	0	NULL	nAChR agonists	NULL		plays a role in	NULL				attention	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_17_6431_s_19	10964949	A number of nAChR agonists that bind to the alpha4/beta2 receptor configuration  in vitro are known to have an effect on anxiety (Pomerleau, 1986  ; Gilbert et al., 1989  ; Brioni et al., 1993  ), attention (Brioni et al., 1997  ), and antinociception (Tripathi et al., 1982  ; Damaj et al., 1998  ), implicating the alpha4/beta2 receptor in the mediation of a number of physiological processes.	bind
50587	4	11561	6	NULL	NULL	0	NULL	nAChR agonists	NULL		plays a role in	NULL				antinociception	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_17_6431_s_19	10964949	A number of nAChR agonists that bind to the alpha4/beta2 receptor configuration  in vitro are known to have an effect on anxiety (Pomerleau, 1986  ; Gilbert et al., 1989  ; Brioni et al., 1993  ), attention (Brioni et al., 1997  ), and antinociception (Tripathi et al., 1982  ; Damaj et al., 1998  ), implicating the alpha4/beta2 receptor in the mediation of a number of physiological processes.	bind
51191	1	11562	5	NULL	NULL	0	NULL		NULL		surround	NULL			negative elements		NULL			2L exon	NULL		0	NULL	NULL	NULL	gw60_neuron_25_2_359_s_291	10719891	A number of negative elements surrounding the  2L exon were found to bind PTB, and evidence was also found for positive acting splicing elements.	bind
51192	2	11562	5	NULL	NULL	NULL	NULL	statement 1	NucleicAcid		bind					PTB	GP				NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_2_359_s_291	10719891	A number of negative elements surrounding the  2L exon were found to bind PTB, and evidence was also found for positive acting splicing elements.	bind
50588	1	11562	6	10	NULL	0	NULL				surround				negative elements	2L exon					NULL		NULL	NULL	NULL	NULL	gw60_neuron_25_2_359_s_291	10719891	A number of negative elements surrounding the  2L exon were found to bind PTB, and evidence was also found for positive acting splicing elements.	bind
50589	2	11562	6	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				PTB	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_25_2_359_s_291	10719891	A number of negative elements surrounding the  2L exon were found to bind PTB, and evidence was also found for positive acting splicing elements.	bind
51193	1	11563	5	NULL	NULL	NULL	NULL	bZIP	GP		is a superfamily of 					transcription factors	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2500_s_35	8999965	A number of nuclear proteins specifically bind to the CRE and CRE-like sequences ( 25), and these are all members of the bZIP superfamily of transcription factors.	bind
51194	2	11563	5	NULL	NULL	NULL	NULL	bZIP	GP		bind		specifically							CRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2500_s_35	8999965	A number of nuclear proteins specifically bind to the CRE and CRE-like sequences ( 25), and these are all members of the bZIP superfamily of transcription factors.	bind
51195	3	11563	5	NULL	NULL	NULL	NULL	bZIP	GP		bind		specifically							CRE-like sequences	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2500_s_35	8999965	A number of nuclear proteins specifically bind to the CRE and CRE-like sequences ( 25), and these are all members of the bZIP superfamily of transcription factors.	bind
50590	1	11563	6	10	NULL	0	NULL	bZIP 			bind		specifically							CRE	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2500_s_35	8999965	A number of nuclear proteins specifically bind to the CRE and CRE-like sequences ( 25), and these are all members of the bZIP superfamily of transcription factors.	bind
50591	2	11563	6	10	NULL	0	NULL	bZIP			bind		specifically							CRE-like sequences	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_4_2500_s_35	8999965	A number of nuclear proteins specifically bind to the CRE and CRE-like sequences ( 25), and these are all members of the bZIP superfamily of transcription factors.	bind
54198	3	11563	6	10	NULL	0	NULL	bZIP			is a superfamily of					transcription factors					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_4_2500_s_35	8999965	A number of nuclear proteins specifically bind to the CRE and CRE-like sequences ( 25), and these are all members of the bZIP superfamily of transcription factors.	bind
51196	1	11564	5	NULL	NULL	NULL	NULL	TL	GP		bind					rifampin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1688_2_102_s_33	14990340	A number of observations led to the hypothesis that TL would bind rifampin with higher  affinity than albumin.	bind
51197	2	11564	5	NULL	NULL	NULL	NULL	TL	GP		bind					albumin	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1688_2_102_s_33	14990340	A number of observations led to the hypothesis that TL would bind rifampin with higher  affinity than albumin.	bind
51198	3	11564	5	NULL	NULL	NULL	NULL	statement 1	Process	affinity of	is higher than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1688_2_102_s_33	14990340	A number of observations led to the hypothesis that TL would bind rifampin with higher  affinity than albumin.	bind
50592	1	11564	6	NULL	NULL	0	NULL	TL	NULL		bind	NULL				rifampin	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1688_2_102_s_33	14990340	A number of observations led to the hypothesis that TL would bind rifampin with higher  affinity than albumin.	bind
50593	2	11564	6	NULL	NULL	0	NULL	TL	NULL		bind	NULL				albumin	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1688_2_102_s_33	14990340	A number of observations led to the hypothesis that TL would bind rifampin with higher  affinity than albumin.	bind
50594	3	11564	6	10	NULL	0	NULL	statement 1		affinity of	is higher than					statement 2		affinity of			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1688_2_102_s_33	14990340	A number of observations led to the hypothesis that TL would bind rifampin with higher  affinity than albumin.	bind
51203	1	11565	5	NULL	NULL	NULL	NULL	mAb 220	GP		reacts with					Equ c 1	GP	natural			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_28_21572_s_179	10787420	A number of observations provides further insight on candidate regions for the putative binding targets of human IgE and mouse mAb 220 in Equ c 1: (i) the epitopes are unlikely to include a protein-bound carbohydrate because mAb 220 and IgE serum display a similar reactivity for natural and recombinant Equ c 1	bind
51204	2	11565	5	NULL	NULL	NULL	NULL	mAb 220	GP		reacts with					Equ c 1	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_28_21572_s_179	10787420	A number of observations provides further insight on candidate regions for the putative binding targets of human IgE and mouse mAb 220 in Equ c 1: (i) the epitopes are unlikely to include a protein-bound carbohydrate because mAb 220 and IgE serum display a similar reactivity for natural and recombinant Equ c 1	bind
51205	3	11565	5	NULL	NULL	NULL	NULL	IgE serum	CellComponent		reacts with					Equ c 1	GP	natural			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_28_21572_s_179	10787420	A number of observations provides further insight on candidate regions for the putative binding targets of human IgE and mouse mAb 220 in Equ c 1: (i) the epitopes are unlikely to include a protein-bound carbohydrate because mAb 220 and IgE serum display a similar reactivity for natural and recombinant Equ c 1	bind
51206	4	11565	5	NULL	NULL	NULL	NULL	IgE serum	CellComponent		reacts with					Equ c 1	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_28_21572_s_179	10787420	A number of observations provides further insight on candidate regions for the putative binding targets of human IgE and mouse mAb 220 in Equ c 1: (i) the epitopes are unlikely to include a protein-bound carbohydrate because mAb 220 and IgE serum display a similar reactivity for natural and recombinant Equ c 1	bind
50595	1	11565	6	NULL	NULL	0	NULL	mAb 220	NULL		reacts with	NULL				Equ c 1	NULL	natural			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_28_21572_s_179	10787420	A number of observations provides further insight on candidate regions for the putative binding targets of human IgE and mouse mAb 220 in Equ c 1: (i) the epitopes are unlikely to include a protein-bound carbohydrate because mAb 220 and IgE serum display a similar reactivity for natural and recombinant Equ c 1	bind
50596	2	11565	6	NULL	NULL	0	NULL	mAb 220	NULL		reacts with	NULL				Equ c 1	NULL	recombinant			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_28_21572_s_179	10787420	A number of observations provides further insight on candidate regions for the putative binding targets of human IgE and mouse mAb 220 in Equ c 1: (i) the epitopes are unlikely to include a protein-bound carbohydrate because mAb 220 and IgE serum display a similar reactivity for natural and recombinant Equ c 1	bind
50597	3	11565	6	NULL	NULL	0	NULL	IgE serum	NULL		reacts with	NULL				Equ c 1	NULL	natural			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_28_21572_s_179	10787420	A number of observations provides further insight on candidate regions for the putative binding targets of human IgE and mouse mAb 220 in Equ c 1: (i) the epitopes are unlikely to include a protein-bound carbohydrate because mAb 220 and IgE serum display a similar reactivity for natural and recombinant Equ c 1	bind
50598	4	11565	6	NULL	NULL	0	NULL	IgE serum	NULL		reacts with	NULL				Equ c 1	NULL	recombinant			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_28_21572_s_179	10787420	A number of observations provides further insight on candidate regions for the putative binding targets of human IgE and mouse mAb 220 in Equ c 1: (i) the epitopes are unlikely to include a protein-bound carbohydrate because mAb 220 and IgE serum display a similar reactivity for natural and recombinant Equ c 1	bind
51199	1	11566	5	NULL	NULL	NULL	NULL	ADAMTS-1	GP		bind					ECM components	AbstractConcept				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_11_10109_s_310	14662755	A number of other ADAMTSs, including ADAMTS-1 ( ,  ), ADAMTS-5 ( ,  ), and ADAMTS-9 ( ) bind to ECM components, but not ADAMTS-13 ( ).	bind
51200	2	11566	5	NULL	NULL	NULL	NULL	ADAMTS-5	GP		bind					ECM components	AbstractConcept				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_11_10109_s_310	14662755	A number of other ADAMTSs, including ADAMTS-1 ( ,  ), ADAMTS-5 ( ,  ), and ADAMTS-9 ( ) bind to ECM components, but not ADAMTS-13 ( ).	bind
51201	3	11566	5	NULL	NULL	NULL	NULL	ADAMTS-9	GP		bind					ECM components	AbstractConcept				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_11_10109_s_310	14662755	A number of other ADAMTSs, including ADAMTS-1 ( ,  ), ADAMTS-5 ( ,  ), and ADAMTS-9 ( ) bind to ECM components, but not ADAMTS-13 ( ).	bind
51202	4	11566	5	NULL	NULL	NULL	NULL	ADAMTS-13	GP		does not bind					ECM components	AbstractConcept				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_11_10109_s_310	14662755	A number of other ADAMTSs, including ADAMTS-1 ( ,  ), ADAMTS-5 ( ,  ), and ADAMTS-9 ( ) bind to ECM components, but not ADAMTS-13 ( ).	bind
50599	1	11566	6	NULL	NULL	0	NULL	ADAMTS-1	NULL		bind	NULL				ECM components	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_11_10109_s_310	14662755	A number of other ADAMTSs, including ADAMTS-1 ( ,  ), ADAMTS-5 ( ,  ), and ADAMTS-9 ( ) bind to ECM components, but not ADAMTS-13 ( ).	bind
50600	2	11566	6	NULL	NULL	0	NULL	ADAMTS-5	NULL		bind	NULL				ECM components	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_11_10109_s_310	14662755	A number of other ADAMTSs, including ADAMTS-1 ( ,  ), ADAMTS-5 ( ,  ), and ADAMTS-9 ( ) bind to ECM components, but not ADAMTS-13 ( ).	bind
50601	3	11566	6	NULL	NULL	0	NULL	ADAMTS-9	NULL		bind	NULL				ECM components	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_11_10109_s_310	14662755	A number of other ADAMTSs, including ADAMTS-1 ( ,  ), ADAMTS-5 ( ,  ), and ADAMTS-9 ( ) bind to ECM components, but not ADAMTS-13 ( ).	bind
50602	4	11566	6	NULL	NULL	0	NULL	ADAMTS-13	NULL		does not bind	NULL				ECM components	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_11_10109_s_310	14662755	A number of other ADAMTSs, including ADAMTS-1 ( ,  ), ADAMTS-5 ( ,  ), and ADAMTS-9 ( ) bind to ECM components, but not ADAMTS-13 ( ).	bind
51210	1	11567	5	NULL	NULL	NULL	NULL	STAT2	GP		bind					p300/CBP-CH1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_13_1_64_s_295	9887100	A number of other factors, e.g., STAT2 (Bhattacharya et al. 1996  ), ets-1 (Yang et al. 1998  ), NFkappaB-p65 (Zhong et al. 1998  ), p53, and MDM2 (Grossman et al. 1998  ) bind to p300/CBP-CH1, and could occupy available binding sites.	bind
51211	2	11567	5	NULL	NULL	NULL	NULL	ets-1	GP		bind					p300/CBP-CH1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_13_1_64_s_295	9887100	A number of other factors, e.g., STAT2 (Bhattacharya et al. 1996  ), ets-1 (Yang et al. 1998  ), NFkappaB-p65 (Zhong et al. 1998  ), p53, and MDM2 (Grossman et al. 1998  ) bind to p300/CBP-CH1, and could occupy available binding sites.	bind
51212	3	11567	5	NULL	NULL	NULL	NULL	NFkappaB-p65	GP		bind					p300/CBP-CH1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_13_1_64_s_295	9887100	A number of other factors, e.g., STAT2 (Bhattacharya et al. 1996  ), ets-1 (Yang et al. 1998  ), NFkappaB-p65 (Zhong et al. 1998  ), p53, and MDM2 (Grossman et al. 1998  ) bind to p300/CBP-CH1, and could occupy available binding sites.	bind
51213	4	11567	5	NULL	NULL	NULL	NULL	p53	GP		bind					p300/CBP-CH1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_13_1_64_s_295	9887100	A number of other factors, e.g., STAT2 (Bhattacharya et al. 1996  ), ets-1 (Yang et al. 1998  ), NFkappaB-p65 (Zhong et al. 1998  ), p53, and MDM2 (Grossman et al. 1998  ) bind to p300/CBP-CH1, and could occupy available binding sites.	bind
51214	5	11567	5	NULL	NULL	NULL	NULL	MDM2	GP		bind					p300/CBP-CH1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_13_1_64_s_295	9887100	A number of other factors, e.g., STAT2 (Bhattacharya et al. 1996  ), ets-1 (Yang et al. 1998  ), NFkappaB-p65 (Zhong et al. 1998  ), p53, and MDM2 (Grossman et al. 1998  ) bind to p300/CBP-CH1, and could occupy available binding sites.	bind
50603	1	11567	6	NULL	NULL	0	NULL	STAT2	NULL		bind	NULL				p300/CBP-CH1	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_13_1_64_s_295	9887100	A number of other factors, e.g., STAT2 (Bhattacharya et al. 1996  ), ets-1 (Yang et al. 1998  ), NFkappaB-p65 (Zhong et al. 1998  ), p53, and MDM2 (Grossman et al. 1998  ) bind to p300/CBP-CH1, and could occupy available binding sites.	bind
50604	2	11567	6	NULL	NULL	0	NULL	ets-1	NULL		bind	NULL				p300/CBP-CH1	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_13_1_64_s_295	9887100	A number of other factors, e.g., STAT2 (Bhattacharya et al. 1996  ), ets-1 (Yang et al. 1998  ), NFkappaB-p65 (Zhong et al. 1998  ), p53, and MDM2 (Grossman et al. 1998  ) bind to p300/CBP-CH1, and could occupy available binding sites.	bind
50605	3	11567	6	NULL	NULL	0	NULL	NFkappaB-p65	NULL		bind	NULL				p300/CBP-CH1	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_13_1_64_s_295	9887100	A number of other factors, e.g., STAT2 (Bhattacharya et al. 1996  ), ets-1 (Yang et al. 1998  ), NFkappaB-p65 (Zhong et al. 1998  ), p53, and MDM2 (Grossman et al. 1998  ) bind to p300/CBP-CH1, and could occupy available binding sites.	bind
50606	4	11567	6	NULL	NULL	0	NULL	p53	NULL		bind	NULL				p300/CBP-CH1	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_13_1_64_s_295	9887100	A number of other factors, e.g., STAT2 (Bhattacharya et al. 1996  ), ets-1 (Yang et al. 1998  ), NFkappaB-p65 (Zhong et al. 1998  ), p53, and MDM2 (Grossman et al. 1998  ) bind to p300/CBP-CH1, and could occupy available binding sites.	bind
50607	5	11567	6	NULL	NULL	0	NULL	MDM2	NULL		bind	NULL				p300/CBP-CH1	NULL				NULL		0	NULL	NULL	NULL	gw60_genesdev_13_1_64_s_295	9887100	A number of other factors, e.g., STAT2 (Bhattacharya et al. 1996  ), ets-1 (Yang et al. 1998  ), NFkappaB-p65 (Zhong et al. 1998  ), p53, and MDM2 (Grossman et al. 1998  ) bind to p300/CBP-CH1, and could occupy available binding sites.	bind
51215	1	11569	5	NULL	NULL	NULL	NULL	IGF-I	GP		bind					insulin receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_443_3_271_s_16	10025946	A number of papers report the different activities of these seven binding proteins including regulating half-life in circulation, transporting IGF-I to specific tissues, preventing hypoglycemia by inhibiting the binding of IGF-I to the insulin receptor  [ 10,   11] and mediating p53-induced cell cycle arrest  [ 12,   13].	bind
51216	2	11569	5	NULL	NULL	NULL	NULL	p53	GP		induce					cell cycle arrest	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_443_3_271_s_16	10025946	A number of papers report the different activities of these seven binding proteins including regulating half-life in circulation, transporting IGF-I to specific tissues, preventing hypoglycemia by inhibiting the binding of IGF-I to the insulin receptor  [ 10,   11] and mediating p53-induced cell cycle arrest  [ 12,   13].	bind
51226	3	11569	5	NULL	NULL	NULL	NULL	statement 1	Process	inhibition of	prevents					hypoglycemia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	gw60_febslett_443_3_271_s_16	10025946	A number of papers report the different activities of these seven binding proteins including regulating half-life in circulation, transporting IGF-I to specific tissues, preventing hypoglycemia by inhibiting the binding of IGF-I to the insulin receptor  [ 10,   11] and mediating p53-induced cell cycle arrest  [ 12,   13].	bind
50608	1	11569	6	NULL	NULL	0	NULL	IGF-I	NULL		bind	NULL				insulin receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_443_3_271_s_16	10025946	A number of papers report the different activities of these seven binding proteins including regulating half-life in circulation, transporting IGF-I to specific tissues, preventing hypoglycemia by inhibiting the binding of IGF-I to the insulin receptor  [ 10,   11] and mediating p53-induced cell cycle arrest  [ 12,   13].	bind
50609	2	11569	6	NULL	NULL	0	NULL	p53	NULL		induces	NULL				cell cycle arrest	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_443_3_271_s_16	10025946	A number of papers report the different activities of these seven binding proteins including regulating half-life in circulation, transporting IGF-I to specific tissues, preventing hypoglycemia by inhibiting the binding of IGF-I to the insulin receptor  [ 10,   11] and mediating p53-induced cell cycle arrest  [ 12,   13].	bind
54199	3	11569	6	10	NULL	0	NULL	statement 1		inhibition of	prevents					hypoglycemia					NULL		0	NULL	NULL	NULL	gw60_febslett_443_3_271_s_16	10025946	A number of papers report the different activities of these seven binding proteins including regulating half-life in circulation, transporting IGF-I to specific tissues, preventing hypoglycemia by inhibiting the binding of IGF-I to the insulin receptor  [ 10,   11] and mediating p53-induced cell cycle arrest  [ 12,   13].	bind
51227	1	11570	5	NULL	NULL	NULL	NULL	pathogenic microbes	Organism		bind					fH	GP				NULL	in vivo	NULL	NULL	NULL	NULL	abs-batch0700-0719_j-immunol_176_12_16751403_s_4	16751403	A number of pathogenic microbes bind factor H (fH),  the negative regulator of the alternative pathway of complement activation,  to promote their survival in vivo.	bind
51228	2	11570	5	NULL	NULL	NULL	NULL	fH	GP		is					factor H	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_j-immunol_176_12_16751403_s_4	16751403	A number of pathogenic microbes bind factor H (fH),  the negative regulator of the alternative pathway of complement activation,  to promote their survival in vivo.	bind
51229	3	11570	5	NULL	NULL	NULL	NULL	fH	GP		regulates		negatively			complement 	GP	alternative pathway of ;;activation of			NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_j-immunol_176_12_16751403_s_4	16751403	A number of pathogenic microbes bind factor H (fH),  the negative regulator of the alternative pathway of complement activation,  to promote their survival in vivo.	bind
51230	4	11570	5	NULL	NULL	NULL	NULL	statement 1	Process		promotes					pathogenic microbes	Organism	survival of			NULL	in vivo	NULL	NULL	NULL	NULL	abs-batch0700-0719_j-immunol_176_12_16751403_s_4	16751403	A number of pathogenic microbes bind factor H (fH),  the negative regulator of the alternative pathway of complement activation,  to promote their survival in vivo.	bind
50610	1	11570	6	NULL	NULL	0	NULL	pathogenic microbes	NULL		bind	NULL				factor H	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_j-immunol_176_12_16751403_s_4	16751403	A number of pathogenic microbes bind factor H (fH),  the negative regulator of the alternative pathway of complement activation,  to promote their survival in vivo.	bind
50611	2	11570	6	NULL	NULL	0	NULL	fH	NULL		is	NULL				factor H	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_j-immunol_176_12_16751403_s_4	16751403	A number of pathogenic microbes bind factor H (fH),  the negative regulator of the alternative pathway of complement activation,  to promote their survival in vivo.	bind
50612	3	11570	6	10	NULL	0	NULL	fH			regulates		negatively 			complement		alternative pathway of ;;activation of			NULL		NULL	NULL	NULL	NULL	abs-batch0700-0719_j-immunol_176_12_16751403_s_4	16751403	A number of pathogenic microbes bind factor H (fH),  the negative regulator of the alternative pathway of complement activation,  to promote their survival in vivo.	bind
54200	4	11570	6	10	NULL	0	NULL	statement 1			promote					pathogenic microbes		survival of			NULL	in vivo	NULL	NULL	NULL	NULL	abs-batch0700-0719_j-immunol_176_12_16751403_s_4	16751403	A number of pathogenic microbes bind factor H (fH),  the negative regulator of the alternative pathway of complement activation,  to promote their survival in vivo.	bind
51231	1	11572	5	NULL	NULL	NULL	NULL	GPIa-IIa	GP		interacts with					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_52_0_161_s_37	11160773	A number of platelet proteins interact with collagen besides  2 1 (GPIa-IIa), including   IIb (GPIIb), GPIV, GPVI, and two other proteins: a 65,000-molecular-weight protein  that binds to type I collagen and an 85-90,000-molecular-weight protein ( 9).	bind
51232	2	11572	5	NULL	NULL	NULL	NULL	GPIIb	GP		interacts with					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_52_0_161_s_37	11160773	A number of platelet proteins interact with collagen besides  2 1 (GPIa-IIa), including   IIb (GPIIb), GPIV, GPVI, and two other proteins: a 65,000-molecular-weight protein  that binds to type I collagen and an 85-90,000-molecular-weight protein ( 9).	bind
51233	3	11572	5	NULL	NULL	NULL	NULL	GPIV	GP		interacts with					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_52_0_161_s_37	11160773	A number of platelet proteins interact with collagen besides  2 1 (GPIa-IIa), including   IIb (GPIIb), GPIV, GPVI, and two other proteins: a 65,000-molecular-weight protein  that binds to type I collagen and an 85-90,000-molecular-weight protein ( 9).	bind
51234	4	11572	5	NULL	NULL	NULL	NULL	GPVI	GP		interacts with					collagen	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_52_0_161_s_37	11160773	A number of platelet proteins interact with collagen besides  2 1 (GPIa-IIa), including   IIb (GPIIb), GPIV, GPVI, and two other proteins: a 65,000-molecular-weight protein  that binds to type I collagen and an 85-90,000-molecular-weight protein ( 9).	bind
51235	5	11572	5	NULL	NULL	NULL	NULL	GPIa-IIa	GP		is a type of					platelet protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_52_0_161_s_37	11160773	A number of platelet proteins interact with collagen besides  2 1 (GPIa-IIa), including   IIb (GPIIb), GPIV, GPVI, and two other proteins: a 65,000-molecular-weight protein  that binds to type I collagen and an 85-90,000-molecular-weight protein ( 9).	bind
51236	6	11572	5	NULL	NULL	NULL	NULL	GPIIb	GP		is a type of					platelet protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_52_0_161_s_37	11160773	A number of platelet proteins interact with collagen besides  2 1 (GPIa-IIa), including   IIb (GPIIb), GPIV, GPVI, and two other proteins: a 65,000-molecular-weight protein  that binds to type I collagen and an 85-90,000-molecular-weight protein ( 9).	bind
51237	7	11572	5	NULL	NULL	NULL	NULL	GPIV	GP		is a type of					platelet protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_52_0_161_s_37	11160773	A number of platelet proteins interact with collagen besides  2 1 (GPIa-IIa), including   IIb (GPIIb), GPIV, GPVI, and two other proteins: a 65,000-molecular-weight protein  that binds to type I collagen and an 85-90,000-molecular-weight protein ( 9).	bind
51238	8	11572	5	NULL	NULL	NULL	NULL	GPVI	GP		is a type of					platelet protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_52_0_161_s_37	11160773	A number of platelet proteins interact with collagen besides  2 1 (GPIa-IIa), including   IIb (GPIIb), GPIV, GPVI, and two other proteins: a 65,000-molecular-weight protein  that binds to type I collagen and an 85-90,000-molecular-weight protein ( 9).	bind
51240	9	11572	5	NULL	NULL	NULL	NULL	65,000 molecular-weight protein	GP		bind					type I collagen	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_52_0_161_s_37	11160773	A number of platelet proteins interact with collagen besides  2 1 (GPIa-IIa), including   IIb (GPIIb), GPIV, GPVI, and two other proteins: a 65,000-molecular-weight protein  that binds to type I collagen and an 85-90,000-molecular-weight protein ( 9).	bind
50749	1	11572	6	10	NULL	0	NULL	65,000 molecular-weight protein			bind					type I collagen					NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_52_0_161_s_37	11160773	A number of platelet proteins interact with collagen besides  2 1 (GPIa-IIa), including   IIb (GPIIb), GPIV, GPVI, and two other proteins: a 65,000-molecular-weight protein  that binds to type I collagen and an 85-90,000-molecular-weight protein ( 9).	bind
50750	2	11572	6	10	NULL	0	NULL	GPIa-IIa			interacts with					collagen					NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_52_0_161_s_37	11160773	A number of platelet proteins interact with collagen besides  2 1 (GPIa-IIa), including   IIb (GPIIb), GPIV, GPVI, and two other proteins: a 65,000-molecular-weight protein  that binds to type I collagen and an 85-90,000-molecular-weight protein ( 9).	bind
50751	3	11572	6	10	NULL	0	NULL	GPIIb			interacts with					collagen					NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_52_0_161_s_37	11160773	A number of platelet proteins interact with collagen besides  2 1 (GPIa-IIa), including   IIb (GPIIb), GPIV, GPVI, and two other proteins: a 65,000-molecular-weight protein  that binds to type I collagen and an 85-90,000-molecular-weight protein ( 9).	bind
50752	4	11572	6	10	NULL	0	NULL	GPIV			interacts with					collagen					NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_52_0_161_s_37	11160773	A number of platelet proteins interact with collagen besides  2 1 (GPIa-IIa), including   IIb (GPIIb), GPIV, GPVI, and two other proteins: a 65,000-molecular-weight protein  that binds to type I collagen and an 85-90,000-molecular-weight protein ( 9).	bind
50753	5	11572	6	10	NULL	0	NULL	GPVI			interacts with					collagen					NULL		NULL	NULL	NULL	NULL	gw70_annurevmed_52_0_161_s_37	11160773	A number of platelet proteins interact with collagen besides  2 1 (GPIa-IIa), including   IIb (GPIIb), GPIV, GPVI, and two other proteins: a 65,000-molecular-weight protein  that binds to type I collagen and an 85-90,000-molecular-weight protein ( 9).	bind
50754	6	11572	6	NULL	NULL	0	NULL	GPIa-IIa	NULL		is a type of	NULL				platelet protein	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevmed_52_0_161_s_37	11160773	A number of platelet proteins interact with collagen besides  2 1 (GPIa-IIa), including   IIb (GPIIb), GPIV, GPVI, and two other proteins: a 65,000-molecular-weight protein  that binds to type I collagen and an 85-90,000-molecular-weight protein ( 9).	bind
50755	7	11572	6	NULL	NULL	0	NULL	GPIIb	NULL		is a type of	NULL				platelet protein	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevmed_52_0_161_s_37	11160773	A number of platelet proteins interact with collagen besides  2 1 (GPIa-IIa), including   IIb (GPIIb), GPIV, GPVI, and two other proteins: a 65,000-molecular-weight protein  that binds to type I collagen and an 85-90,000-molecular-weight protein ( 9).	bind
50756	8	11572	6	NULL	NULL	0	NULL	GPIV	NULL		is a type of	NULL				platelet protein	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevmed_52_0_161_s_37	11160773	A number of platelet proteins interact with collagen besides  2 1 (GPIa-IIa), including   IIb (GPIIb), GPIV, GPVI, and two other proteins: a 65,000-molecular-weight protein  that binds to type I collagen and an 85-90,000-molecular-weight protein ( 9).	bind
50757	9	11572	6	NULL	NULL	0	NULL	GPVI	NULL		is a type of	NULL				platelet protein	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevmed_52_0_161_s_37	11160773	A number of platelet proteins interact with collagen besides  2 1 (GPIa-IIa), including   IIb (GPIIb), GPIV, GPVI, and two other proteins: a 65,000-molecular-weight protein  that binds to type I collagen and an 85-90,000-molecular-weight protein ( 9).	bind
51258	1	11573	5	NULL	NULL	NULL	NULL			positively charged	bind			arginine side chains		substrate	GP		pyrophosphate groups		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_21_20762_s_175	15788389	A number of positively charged arginine side chains bind to the substrate pyrophosphate groups, between which there is a Mg2+ ion coordinated to Asp26.	bind
51259	2	11573	5	NULL	NULL	NULL	NULL	Mg2+ ion	Chemical		is coordinated to								Asp26		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_21_20762_s_175	15788389	A number of positively charged arginine side chains bind to the substrate pyrophosphate groups, between which there is a Mg2+ ion coordinated to Asp26.	bind
50613	1	11573	6	10	NULL	0	NULL			positively charged	bind			arginine side chains		substrate			pyrophosphate groups		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_21_20762_s_175	15788389	A number of positively charged arginine side chains bind to the substrate pyrophosphate groups, between which there is a Mg2+ ion coordinated to Asp26.	bind
50614	2	11573	6	10	NULL	0	NULL	Mg2+ ion 			is coordinated to								Asp26		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_21_20762_s_175	15788389	A number of positively charged arginine side chains bind to the substrate pyrophosphate groups, between which there is a Mg2+ ion coordinated to Asp26.	bind
51260	1	11574	5	NULL	NULL	NULL	NULL	SHC	GP		bind					CBL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_24_14962_s_183	9614102	A number of previous reports have demonstrated GRB2-mediated SHC binding to CBL ( 20,  38,  45).	bind
51261	2	11574	5	NULL	NULL	NULL	NULL	GRB2	GP		mediates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_24_14962_s_183	9614102	A number of previous reports have demonstrated GRB2-mediated SHC binding to CBL ( 20,  38,  45).	bind
50615	1	11574	6	NULL	NULL	0	NULL	SHC	NULL		bind	NULL				CBL	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_24_14962_s_183	9614102	A number of previous reports have demonstrated GRB2-mediated SHC binding to CBL ( 20,  38,  45).	bind
50616	2	11574	6	10	NULL	0	NULL	GRB2			mediates					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_24_14962_s_183	9614102	A number of previous reports have demonstrated GRB2-mediated SHC binding to CBL ( 20,  38,  45).	bind
51262	1	11575	5	NULL	NULL	NULL	NULL	Mlp1	GP		is implicated in					mRNA	NucleicAcid	export of			NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1188_s_77	15905407	A number of previous studies have implicated Mlp1 in mRNA export; Mlp1 is known to bind to the hnRNP and mRNA export factor, Nab2 (Green et al. 2003 ).	bind
51263	2	11575	5	NULL	NULL	NULL	NULL	Mlp1	GP		bind					hnRNP	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1188_s_77	15905407	A number of previous studies have implicated Mlp1 in mRNA export; Mlp1 is known to bind to the hnRNP and mRNA export factor, Nab2 (Green et al. 2003 ).	bind
51264	3	11575	5	NULL	NULL	NULL	NULL	Mlp1	GP		bind					Nab2	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1188_s_77	15905407	A number of previous studies have implicated Mlp1 in mRNA export; Mlp1 is known to bind to the hnRNP and mRNA export factor, Nab2 (Green et al. 2003 ).	bind
51265	4	11575	5	NULL	NULL	NULL	NULL	Nab2	GP		is a type of					mRNA export factor	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_19_10_1188_s_77	15905407	A number of previous studies have implicated Mlp1 in mRNA export; Mlp1 is known to bind to the hnRNP and mRNA export factor, Nab2 (Green et al. 2003 ).	bind
50617	1	11575	6	NULL	NULL	0	NULL	Mlp1	NULL		bind	NULL				hnRNP	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_10_1188_s_77	15905407	A number of previous studies have implicated Mlp1 in mRNA export; Mlp1 is known to bind to the hnRNP and mRNA export factor, Nab2 (Green et al. 2003 ).	bind
50618	2	11575	6	NULL	NULL	0	NULL	Mlp1	NULL		bind	NULL				Nab2	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_10_1188_s_77	15905407	A number of previous studies have implicated Mlp1 in mRNA export; Mlp1 is known to bind to the hnRNP and mRNA export factor, Nab2 (Green et al. 2003 ).	bind
50619	3	11575	6	NULL	NULL	0	NULL	Nab2	NULL		is a type of	NULL				mRNA export factor	NULL				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_10_1188_s_77	15905407	A number of previous studies have implicated Mlp1 in mRNA export; Mlp1 is known to bind to the hnRNP and mRNA export factor, Nab2 (Green et al. 2003 ).	bind
58815	4	11575	6	10	NULL	0	NULL	Mlp1			is implicated in					mRNA		export of			NULL		0	NULL	NULL	NULL	gw70_genesdev_19_10_1188_s_77	15905407	A number of previous studies have implicated Mlp1 in mRNA export; Mlp1 is known to bind to the hnRNP and mRNA export factor, Nab2 (Green et al. 2003 ).	bind
51266	1	11576	5	NULL	NULL	NULL	NULL	MIBP1 homolog	GP	rat	bind		specifically						NF-kappaB-like motifs		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3736_s_211	10207097	A number of previous studies have shown that the rat MIBP1 homolog, the human MBP2 homolog, the partial MIBP1 clone AGIE-BP1, and the sequence-related transcription factor PRDII-BP1 bind specifically to NF-kappaB-like motifs with the consensus GGG N(4-5)CC ( 6,  11,  14,  17,  22).	bind
51267	2	11576	5	NULL	NULL	NULL	NULL	NF-kappaB-like motifs	GP		contains							consensus	GGG N(4-5)CC		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3736_s_211	10207097	A number of previous studies have shown that the rat MIBP1 homolog, the human MBP2 homolog, the partial MIBP1 clone AGIE-BP1, and the sequence-related transcription factor PRDII-BP1 bind specifically to NF-kappaB-like motifs with the consensus GGG N(4-5)CC ( 6,  11,  14,  17,  22).	bind
51268	3	11576	5	NULL	NULL	NULL	NULL	MBP2 homolog	GP	human	bind		specifically						NF-kappaB-like motifs		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3736_s_211	10207097	A number of previous studies have shown that the rat MIBP1 homolog, the human MBP2 homolog, the partial MIBP1 clone AGIE-BP1, and the sequence-related transcription factor PRDII-BP1 bind specifically to NF-kappaB-like motifs with the consensus GGG N(4-5)CC ( 6,  11,  14,  17,  22).	bind
51269	4	11576	5	NULL	NULL	NULL	NULL	AGIE-BP1	NucleicAcid		is a type of					partial MIBP1 clone	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3736_s_211	10207097	A number of previous studies have shown that the rat MIBP1 homolog, the human MBP2 homolog, the partial MIBP1 clone AGIE-BP1, and the sequence-related transcription factor PRDII-BP1 bind specifically to NF-kappaB-like motifs with the consensus GGG N(4-5)CC ( 6,  11,  14,  17,  22).	bind
51270	5	11576	5	NULL	NULL	NULL	NULL	AGIE-BP1	NucleicAcid		bind								NF-kappaB-like motifs		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3736_s_211	10207097	A number of previous studies have shown that the rat MIBP1 homolog, the human MBP2 homolog, the partial MIBP1 clone AGIE-BP1, and the sequence-related transcription factor PRDII-BP1 bind specifically to NF-kappaB-like motifs with the consensus GGG N(4-5)CC ( 6,  11,  14,  17,  22).	bind
51271	6	11576	5	NULL	NULL	NULL	NULL	PRDII-BP1	GP		is a type of					transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3736_s_211	10207097	A number of previous studies have shown that the rat MIBP1 homolog, the human MBP2 homolog, the partial MIBP1 clone AGIE-BP1, and the sequence-related transcription factor PRDII-BP1 bind specifically to NF-kappaB-like motifs with the consensus GGG N(4-5)CC ( 6,  11,  14,  17,  22).	bind
51272	7	11576	5	NULL	NULL	NULL	NULL	PRDII-BP1	GP		bind		specifically						NF-kappaB-like motifs		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3736_s_211	10207097	A number of previous studies have shown that the rat MIBP1 homolog, the human MBP2 homolog, the partial MIBP1 clone AGIE-BP1, and the sequence-related transcription factor PRDII-BP1 bind specifically to NF-kappaB-like motifs with the consensus GGG N(4-5)CC ( 6,  11,  14,  17,  22).	bind
50620	1	11576	6	NULL	NULL	0	NULL	MIBP1 homolog	NULL	rat	bind	NULL	specifically				NULL			NF-kappaB-like motifs	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3736_s_211	10207097	A number of previous studies have shown that the rat MIBP1 homolog, the human MBP2 homolog, the partial MIBP1 clone AGIE-BP1, and the sequence-related transcription factor PRDII-BP1 bind specifically to NF-kappaB-like motifs with the consensus GGG N(4-5)CC ( 6,  11,  14,  17,  22).	bind
50621	2	11576	6	10	NULL	0	NULL	NF-kappaB-like motifs			contains					GGG N(4-5)CC 		consensus			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3736_s_211	10207097	A number of previous studies have shown that the rat MIBP1 homolog, the human MBP2 homolog, the partial MIBP1 clone AGIE-BP1, and the sequence-related transcription factor PRDII-BP1 bind specifically to NF-kappaB-like motifs with the consensus GGG N(4-5)CC ( 6,  11,  14,  17,  22).	bind
50622	3	11576	6	10	NULL	0	NULL	MBP2 homolog		human	bind		specifically							NF-kappaB-like motifs	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3736_s_211	10207097	A number of previous studies have shown that the rat MIBP1 homolog, the human MBP2 homolog, the partial MIBP1 clone AGIE-BP1, and the sequence-related transcription factor PRDII-BP1 bind specifically to NF-kappaB-like motifs with the consensus GGG N(4-5)CC ( 6,  11,  14,  17,  22).	bind
50623	4	11576	6	NULL	NULL	0	NULL	PRDII-BP1	NULL		bind	NULL	specifically				NULL			NF-kappaB-like motifs	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3736_s_211	10207097	A number of previous studies have shown that the rat MIBP1 homolog, the human MBP2 homolog, the partial MIBP1 clone AGIE-BP1, and the sequence-related transcription factor PRDII-BP1 bind specifically to NF-kappaB-like motifs with the consensus GGG N(4-5)CC ( 6,  11,  14,  17,  22).	bind
50624	5	11576	6	NULL	NULL	0	NULL	PRDII-BP1	NULL		is a type of	NULL				transcription factor	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3736_s_211	10207097	A number of previous studies have shown that the rat MIBP1 homolog, the human MBP2 homolog, the partial MIBP1 clone AGIE-BP1, and the sequence-related transcription factor PRDII-BP1 bind specifically to NF-kappaB-like motifs with the consensus GGG N(4-5)CC ( 6,  11,  14,  17,  22).	bind
50625	6	11576	6	NULL	NULL	0	NULL	AGIE-BP1	NULL		bind	NULL					NULL			NF-kappaB-like motifs	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3736_s_211	10207097	A number of previous studies have shown that the rat MIBP1 homolog, the human MBP2 homolog, the partial MIBP1 clone AGIE-BP1, and the sequence-related transcription factor PRDII-BP1 bind specifically to NF-kappaB-like motifs with the consensus GGG N(4-5)CC ( 6,  11,  14,  17,  22).	bind
50626	7	11576	6	10	NULL	0	NULL	AGIE-BP1			is a type of					partial MIBP1 clone					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3736_s_211	10207097	A number of previous studies have shown that the rat MIBP1 homolog, the human MBP2 homolog, the partial MIBP1 clone AGIE-BP1, and the sequence-related transcription factor PRDII-BP1 bind specifically to NF-kappaB-like motifs with the consensus GGG N(4-5)CC ( 6,  11,  14,  17,  22).	bind
51281	1	11577	5	NULL	NULL	NULL	NULL	GM1	Chemical		is a type of					ganglioside	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_3204_s_11	12446685	A number of protein toxins utilize plasma membrane lipids as their receptors;  e.g. cholera toxin binds ganglioside GM1  ( 1), shiga toxin recognizes glycolipid Gb3  ( 2), and lysenin shows high affinity for sphingomyelin  ( 3).	bind
51282	2	11577	5	NULL	NULL	NULL	NULL	GM1	Chemical		is a type of					plasma membrane lipid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_3204_s_11	12446685	A number of protein toxins utilize plasma membrane lipids as their receptors;  e.g. cholera toxin binds ganglioside GM1  ( 1), shiga toxin recognizes glycolipid Gb3  ( 2), and lysenin shows high affinity for sphingomyelin  ( 3).	bind
51283	3	11577	5	NULL	NULL	NULL	NULL	cholera toxin	GP		bind					GM1	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_3204_s_11	12446685	A number of protein toxins utilize plasma membrane lipids as their receptors;  e.g. cholera toxin binds ganglioside GM1  ( 1), shiga toxin recognizes glycolipid Gb3  ( 2), and lysenin shows high affinity for sphingomyelin  ( 3).	bind
51284	4	11577	5	NULL	NULL	NULL	NULL	Gb3	Chemical		is a type of					glycolipid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_3204_s_11	12446685	A number of protein toxins utilize plasma membrane lipids as their receptors;  e.g. cholera toxin binds ganglioside GM1  ( 1), shiga toxin recognizes glycolipid Gb3  ( 2), and lysenin shows high affinity for sphingomyelin  ( 3).	bind
51285	5	11577	5	NULL	NULL	NULL	NULL	Gb3	Chemical		is a type of					plasma membrane lipid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_3204_s_11	12446685	A number of protein toxins utilize plasma membrane lipids as their receptors;  e.g. cholera toxin binds ganglioside GM1  ( 1), shiga toxin recognizes glycolipid Gb3  ( 2), and lysenin shows high affinity for sphingomyelin  ( 3).	bind
51286	6	11577	5	NULL	NULL	NULL	NULL	shiga toxin	GP		recognizes					Gb3	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_3204_s_11	12446685	A number of protein toxins utilize plasma membrane lipids as their receptors;  e.g. cholera toxin binds ganglioside GM1  ( 1), shiga toxin recognizes glycolipid Gb3  ( 2), and lysenin shows high affinity for sphingomyelin  ( 3).	bind
51287	7	11577	5	NULL	NULL	NULL	NULL	sphingomyelin	Chemical		is a type of					plasma membrane lipid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_3204_s_11	12446685	A number of protein toxins utilize plasma membrane lipids as their receptors;  e.g. cholera toxin binds ganglioside GM1  ( 1), shiga toxin recognizes glycolipid Gb3  ( 2), and lysenin shows high affinity for sphingomyelin  ( 3).	bind
51288	8	11577	5	NULL	NULL	NULL	NULL	lysenin	GP		affinity for		high			sphingomyelin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_3204_s_11	12446685	A number of protein toxins utilize plasma membrane lipids as their receptors;  e.g. cholera toxin binds ganglioside GM1  ( 1), shiga toxin recognizes glycolipid Gb3  ( 2), and lysenin shows high affinity for sphingomyelin  ( 3).	bind
50627	1	11577	6	NULL	NULL	0	NULL	cholera toxin	NULL		bind	NULL				GM1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_5_3204_s_11	12446685	A number of protein toxins utilize plasma membrane lipids as their receptors;  e.g. cholera toxin binds ganglioside GM1  ( 1), shiga toxin recognizes glycolipid Gb3  ( 2), and lysenin shows high affinity for sphingomyelin  ( 3).	bind
50628	2	11577	6	NULL	NULL	0	NULL	GM1	NULL		is a type of	NULL				ganglioside	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_3204_s_11	12446685	A number of protein toxins utilize plasma membrane lipids as their receptors;  e.g. cholera toxin binds ganglioside GM1  ( 1), shiga toxin recognizes glycolipid Gb3  ( 2), and lysenin shows high affinity for sphingomyelin  ( 3).	bind
50629	3	11577	6	10	NULL	0	NULL	shiga toxin			recognizes					Gb3					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_5_3204_s_11	12446685	A number of protein toxins utilize plasma membrane lipids as their receptors;  e.g. cholera toxin binds ganglioside GM1  ( 1), shiga toxin recognizes glycolipid Gb3  ( 2), and lysenin shows high affinity for sphingomyelin  ( 3).	bind
50630	4	11577	6	NULL	NULL	0	NULL	Gb3	NULL		is a type of	NULL				glycolipid	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_5_3204_s_11	12446685	A number of protein toxins utilize plasma membrane lipids as their receptors;  e.g. cholera toxin binds ganglioside GM1  ( 1), shiga toxin recognizes glycolipid Gb3  ( 2), and lysenin shows high affinity for sphingomyelin  ( 3).	bind
50631	5	11577	6	NULL	NULL	0	NULL	lysenin	NULL		has affinity for	NULL	high			sphingomyelin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_5_3204_s_11	12446685	A number of protein toxins utilize plasma membrane lipids as their receptors;  e.g. cholera toxin binds ganglioside GM1  ( 1), shiga toxin recognizes glycolipid Gb3  ( 2), and lysenin shows high affinity for sphingomyelin  ( 3).	bind
50632	6	11577	6	NULL	NULL	0	NULL	ganglioside	NULL		is a type of	NULL				plasma membrane lipids	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_5_3204_s_11	12446685	A number of protein toxins utilize plasma membrane lipids as their receptors;  e.g. cholera toxin binds ganglioside GM1  ( 1), shiga toxin recognizes glycolipid Gb3  ( 2), and lysenin shows high affinity for sphingomyelin  ( 3).	bind
50633	7	11577	6	NULL	NULL	0	NULL	glycolipid	NULL		is a type of	NULL				plasma membrane lipid	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_5_3204_s_11	12446685	A number of protein toxins utilize plasma membrane lipids as their receptors;  e.g. cholera toxin binds ganglioside GM1  ( 1), shiga toxin recognizes glycolipid Gb3  ( 2), and lysenin shows high affinity for sphingomyelin  ( 3).	bind
50634	8	11577	6	NULL	NULL	0	NULL	sphingomyelin	NULL		is a type of	NULL				plasma membrane lipid	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_5_3204_s_11	12446685	A number of protein toxins utilize plasma membrane lipids as their receptors;  e.g. cholera toxin binds ganglioside GM1  ( 1), shiga toxin recognizes glycolipid Gb3  ( 2), and lysenin shows high affinity for sphingomyelin  ( 3).	bind
51289	1	11579	5	NULL	NULL	NULL	NULL	Rho	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_7_1_12_s_264	8999996	A number of proteins have recently been identified that specifically interact with the GTP-bound form of Rho (reviewed in  [30]  ).	bind
50635	1	11579	6	NULL	NULL	0	NULL	GTP	NULL		bind	NULL				Rho	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_7_1_12_s_264	8999996	A number of proteins have recently been identified that specifically interact with the GTP-bound form of Rho (reviewed in  [30]  ).	bind
51290	1	11580	5	NULL	NULL	NULL	NULL	PRRs	GP		is present in					insects	Organism				NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
51291	2	11580	5	NULL	NULL	NULL	NULL	C-type lectins	Chemical		is a type of					PRR	GP				NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
51292	3	11580	5	NULL	NULL	NULL	NULL	C-type lectins	GP		bind					LPS	GP	bacterial			NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
51293	4	11580	5	NULL	NULL	NULL	NULL	LPS	GP		is a type of					peptidoglycan recognition protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
51294	5	11580	5	NULL	NULL	NULL	NULL	LPS	GP	bacterial	is expressed in					fat body	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
51295	6	11580	5	NULL	NULL	NULL	NULL	LPS	GP	bacterial	is expressed in					haemocytes	Cell				NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
51296	7	11580	5	NULL	NULL	NULL	NULL	LPS	GP	bacterial	is expressed in					epithelial cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
51297	8	11580	5	NULL	NULL	NULL	NULL	-1,3 glucan binding protein	GP		is a type of					PRR	GP				NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
51298	9	11580	5	NULL	NULL	NULL	NULL	-1,3 glucan binding protein	GP		recognizes					glucan	Chemical	fungal			NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
51299	10	11580	5	NULL	NULL	NULL	NULL	-1,3 glucan binding protein	GP		activates					ProPO-AS pathway	Process				NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
50636	1	11580	6	NULL	NULL	0	NULL	C-type lectins	NULL		bind	NULL				LPS	NULL	bacterial			NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
50637	2	11580	6	NULL	NULL	0	NULL	peptidoglycan recognition protein	NULL		is expressed in	NULL				fat body	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
50638	3	11580	6	NULL	NULL	0	NULL	peptidoglycan recognition protein	NULL		is expressed in	NULL				haemocytes	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
50639	4	11580	6	NULL	NULL	0	NULL	peptidoglycan recognition protein	NULL		is expressed in	NULL				epithelial cells	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
50640	5	11580	6	NULL	NULL	0	NULL	1,3 glucan binding protein	NULL		recognizes	NULL				fungal glucan	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
50641	6	11580	6	NULL	NULL	0	NULL	1,3 glucan binding protein	NULL		activates	NULL				ProPO-AS pathway	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
50642	7	11580	6	NULL	NULL	0	NULL	C-type lectins	NULL		is a type of	NULL				PRR	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
50643	8	11580	6	10	NULL	0	NULL	LPS			is a type of					peptidoglycan recognition protein					NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
50644	9	11580	6	NULL	NULL	0	NULL	1,3 glucan binding protein	NULL		is a type of	NULL				PRR	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
50645	10	11580	6	NULL	NULL	0	NULL	PRR	NULL		is present in	NULL				insects	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_28_1_101_s_147	14975532	A number of PRRs are present in insects  ( Table 2) and include: the C-type lectins which bind bacterial LPS, the peptidoglycan recognition  protein which is expressed in the fat body, haemocytes and epithelial cells and the   -1,3 glucan binding protein which recognises fungal glucan and activates the ProPO-AS  pathway.	bind
51300	1	11581	5	NULL	NULL	0	NULL		NULL		bind	NULL		PTB domains			NULL	phosphorylated	NP XY motifs		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_22_19119_s_262	11259429	A number of PTB domains have been identified, some of which bind phosphorylated NP XY motifs, whereas others bind unphosphorylated NP XY motifs ( 15).	bind
51301	2	11581	5	NULL	NULL	0	NULL		NULL		bind	NULL		PTB domains			NULL	unphosphorylated	NP XY motifs		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_22_19119_s_262	11259429	A number of PTB domains have been identified, some of which bind phosphorylated NP XY motifs, whereas others bind unphosphorylated NP XY motifs ( 15).	bind
50646	1	11581	6	NULL	NULL	0	NULL		NULL		bind	NULL		PTB domain			NULL	phosphorylated	NP XY motifs		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_22_19119_s_262	11259429	A number of PTB domains have been identified, some of which bind phosphorylated NP XY motifs, whereas others bind unphosphorylated NP XY motifs ( 15).	bind
50647	2	11581	6	NULL	NULL	0	NULL		NULL		bind	NULL		PTB domain			NULL	unphosphorylated	NP XY motifs		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_22_19119_s_262	11259429	A number of PTB domains have been identified, some of which bind phosphorylated NP XY motifs, whereas others bind unphosphorylated NP XY motifs ( 15).	bind
51302	1	11582	5	NULL	NULL	0	NULL		NULL	putative	is present in	NULL			GATA binding sites	CNS-1	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_116_5_1327_s_131	16628252	A number of putative GATA and Ikaros binding sites are present within both CNS-1 and VAE (Figure  5A).	bind
51303	2	11582	5	NULL	NULL	0	NULL		NULL	putative	is present in	NULL			GATA binding sites	VAE	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_116_5_1327_s_131	16628252	A number of putative GATA and Ikaros binding sites are present within both CNS-1 and VAE (Figure  5A).	bind
51304	3	11582	5	NULL	NULL	0	NULL		NULL	putative	is present in	NULL			Ikaros binding site	CNS-1	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_116_5_1327_s_131	16628252	A number of putative GATA and Ikaros binding sites are present within both CNS-1 and VAE (Figure  5A).	bind
51305	4	11582	5	NULL	NULL	0	NULL		NULL	putative	is present in	NULL			Ikaros binding site	VAE	NULL				NULL		0	NULL	NULL	NULL	gw70_jclininvest_116_5_1327_s_131	16628252	A number of putative GATA and Ikaros binding sites are present within both CNS-1 and VAE (Figure  5A).	bind
50648	1	11582	6	NULL	NULL	0	NULL	CNS-1	NULL		contains	NULL					NULL	putative		GATA binding sites	NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_5_1327_s_131	16628252	A number of putative GATA and Ikaros binding sites are present within both CNS-1 and VAE (Figure  5A).	bind
50649	2	11582	6	NULL	NULL	0	NULL	CNS-1	NULL		contains	NULL					NULL	putative		Ikaros binding site	NULL		0	NULL	NULL	NULL	gw70_jclininvest_116_5_1327_s_131	16628252	A number of putative GATA and Ikaros binding sites are present within both CNS-1 and VAE (Figure  5A).	bind
50650	3	11582	6	NULL	NULL	0	NULL	VAE	NULL		contains	NULL					NULL	putative		GATA binding site	NULL		0	NULL	NULL	NULL	gw70_jclininvest_116_5_1327_s_131	16628252	A number of putative GATA and Ikaros binding sites are present within both CNS-1 and VAE (Figure  5A).	bind
50651	4	11582	6	NULL	NULL	0	NULL	VAE	NULL		contains	NULL					NULL	putative		Ikaros binding site	NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_116_5_1327_s_131	16628252	A number of putative GATA and Ikaros binding sites are present within both CNS-1 and VAE (Figure  5A).	bind
51306	1	11583	5	NULL	NULL	NULL	NULL	Rac	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_29_17991_s_10	9660749	A number of Rac targets have been identified to date, based on their ability to interact preferentially with the GTP-bound form of Rac.	bind
50502	1	11583	6	NULL	NULL	0	NULL	Rac	NULL		bind	NULL				GTP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_29_17991_s_10	9660749	A number of Rac targets have been identified to date, based on their ability to interact preferentially with the GTP-bound form of Rac.	bind
51307	1	11585	5	NULL	NULL	NULL	NULL	c-Myc	GP	ectopic expression of	induce					hTERT	GP	expression of			NULL	human cells	NULL	NULL	NULL	NULL	gw60_pnas_98_7_3826_s_183	11274400	A number of recent observations support the identification of the  hTERT gene as a c-Myc target: ( i) ectopic expression of c-Myc induced  hTERT expression and activated telomerase activity in human cells ( 27); ( ii) the specific Myc binding motifs, E-boxes, are present in the  hTERT promoter, and the activity of the promoter is significantly increased by transient expression of c-Myc ( 7,  28,  29,  39); ( iii) ectopic expression of the Mad1 protein results in repression of  hTERT expression ( 30,  31); and ( iv)  in vivo interaction between N-Myc and the  hTERT promoter was recently observed in a neuroblastoma cell line transfected with N- myc ( 40).	bind
51308	2	11585	5	NULL	NULL	NULL	NULL	hTERT	GP		contains				promoter					Myc binding motifs	NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_7_3826_s_183	11274400	A number of recent observations support the identification of the  hTERT gene as a c-Myc target: ( i) ectopic expression of c-Myc induced  hTERT expression and activated telomerase activity in human cells ( 27); ( ii) the specific Myc binding motifs, E-boxes, are present in the  hTERT promoter, and the activity of the promoter is significantly increased by transient expression of c-Myc ( 7,  28,  29,  39); ( iii) ectopic expression of the Mad1 protein results in repression of  hTERT expression ( 30,  31); and ( iv)  in vivo interaction between N-Myc and the  hTERT promoter was recently observed in a neuroblastoma cell line transfected with N- myc ( 40).	bind
51309	3	11585	5	NULL	NULL	NULL	NULL	hTERT	GP		contains				promoter					E-boxes	NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_7_3826_s_183	11274400	A number of recent observations support the identification of the  hTERT gene as a c-Myc target: ( i) ectopic expression of c-Myc induced  hTERT expression and activated telomerase activity in human cells ( 27); ( ii) the specific Myc binding motifs, E-boxes, are present in the  hTERT promoter, and the activity of the promoter is significantly increased by transient expression of c-Myc ( 7,  28,  29,  39); ( iii) ectopic expression of the Mad1 protein results in repression of  hTERT expression ( 30,  31); and ( iv)  in vivo interaction between N-Myc and the  hTERT promoter was recently observed in a neuroblastoma cell line transfected with N- myc ( 40).	bind
51310	4	11585	5	NULL	NULL	NULL	NULL	c-Myc	GP	transient expression of	increase		significantly			hTERT	GP	activity of		promoter	NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_7_3826_s_183	11274400	A number of recent observations support the identification of the  hTERT gene as a c-Myc target: ( i) ectopic expression of c-Myc induced  hTERT expression and activated telomerase activity in human cells ( 27); ( ii) the specific Myc binding motifs, E-boxes, are present in the  hTERT promoter, and the activity of the promoter is significantly increased by transient expression of c-Myc ( 7,  28,  29,  39); ( iii) ectopic expression of the Mad1 protein results in repression of  hTERT expression ( 30,  31); and ( iv)  in vivo interaction between N-Myc and the  hTERT promoter was recently observed in a neuroblastoma cell line transfected with N- myc ( 40).	bind
51311	5	11585	5	NULL	NULL	NULL	NULL	Mad1 protein	GP	ectopic expression of	repress					hTERT	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_7_3826_s_183	11274400	A number of recent observations support the identification of the  hTERT gene as a c-Myc target: ( i) ectopic expression of c-Myc induced  hTERT expression and activated telomerase activity in human cells ( 27); ( ii) the specific Myc binding motifs, E-boxes, are present in the  hTERT promoter, and the activity of the promoter is significantly increased by transient expression of c-Myc ( 7,  28,  29,  39); ( iii) ectopic expression of the Mad1 protein results in repression of  hTERT expression ( 30,  31); and ( iv)  in vivo interaction between N-Myc and the  hTERT promoter was recently observed in a neuroblastoma cell line transfected with N- myc ( 40).	bind
51312	6	11585	5	NULL	NULL	NULL	NULL	N-Myc	GP		interacts with					hTERT	GP			promoter	NULL	in vivo in neuroblastoma cell line transfected with N- myc	NULL	NULL	NULL	NULL	gw60_pnas_98_7_3826_s_183	11274400	A number of recent observations support the identification of the  hTERT gene as a c-Myc target: ( i) ectopic expression of c-Myc induced  hTERT expression and activated telomerase activity in human cells ( 27); ( ii) the specific Myc binding motifs, E-boxes, are present in the  hTERT promoter, and the activity of the promoter is significantly increased by transient expression of c-Myc ( 7,  28,  29,  39); ( iii) ectopic expression of the Mad1 protein results in repression of  hTERT expression ( 30,  31); and ( iv)  in vivo interaction between N-Myc and the  hTERT promoter was recently observed in a neuroblastoma cell line transfected with N- myc ( 40).	bind
51313	7	11585	5	NULL	NULL	NULL	NULL	c-Myc	GP	ectopic expression of	activates					telomerase	GP	activity of			NULL	human cells	NULL	NULL	NULL	NULL	gw60_pnas_98_7_3826_s_183	11274400	A number of recent observations support the identification of the  hTERT gene as a c-Myc target: ( i) ectopic expression of c-Myc induced  hTERT expression and activated telomerase activity in human cells ( 27); ( ii) the specific Myc binding motifs, E-boxes, are present in the  hTERT promoter, and the activity of the promoter is significantly increased by transient expression of c-Myc ( 7,  28,  29,  39); ( iii) ectopic expression of the Mad1 protein results in repression of  hTERT expression ( 30,  31); and ( iv)  in vivo interaction between N-Myc and the  hTERT promoter was recently observed in a neuroblastoma cell line transfected with N- myc ( 40).	bind
50652	1	11585	6	10	NULL	0	NULL	N-Myc			interacts with					hTERT				promoter	NULL	in vivo in neuroblastoma cell line transfected with N- myc	NULL	NULL	NULL	NULL	gw60_pnas_98_7_3826_s_183	11274400	A number of recent observations support the identification of the  hTERT gene as a c-Myc target: ( i) ectopic expression of c-Myc induced  hTERT expression and activated telomerase activity in human cells ( 27); ( ii) the specific Myc binding motifs, E-boxes, are present in the  hTERT promoter, and the activity of the promoter is significantly increased by transient expression of c-Myc ( 7,  28,  29,  39); ( iii) ectopic expression of the Mad1 protein results in repression of  hTERT expression ( 30,  31); and ( iv)  in vivo interaction between N-Myc and the  hTERT promoter was recently observed in a neuroblastoma cell line transfected with N- myc ( 40).	bind
50653	2	11585	6	10	NULL	0	NULL	c-Myc		ectopic;; expression of	induces					hTERT		expression of 			NULL	human cells	NULL	NULL	NULL	NULL	gw60_pnas_98_7_3826_s_183	11274400	A number of recent observations support the identification of the  hTERT gene as a c-Myc target: ( i) ectopic expression of c-Myc induced  hTERT expression and activated telomerase activity in human cells ( 27); ( ii) the specific Myc binding motifs, E-boxes, are present in the  hTERT promoter, and the activity of the promoter is significantly increased by transient expression of c-Myc ( 7,  28,  29,  39); ( iii) ectopic expression of the Mad1 protein results in repression of  hTERT expression ( 30,  31); and ( iv)  in vivo interaction between N-Myc and the  hTERT promoter was recently observed in a neuroblastoma cell line transfected with N- myc ( 40).	bind
50654	3	11585	6	10	NULL	0	NULL	c-Myc		ectopic expression of	activates					telomerase 		activity of			NULL	human cells	NULL	NULL	NULL	NULL	gw60_pnas_98_7_3826_s_183	11274400	A number of recent observations support the identification of the  hTERT gene as a c-Myc target: ( i) ectopic expression of c-Myc induced  hTERT expression and activated telomerase activity in human cells ( 27); ( ii) the specific Myc binding motifs, E-boxes, are present in the  hTERT promoter, and the activity of the promoter is significantly increased by transient expression of c-Myc ( 7,  28,  29,  39); ( iii) ectopic expression of the Mad1 protein results in repression of  hTERT expression ( 30,  31); and ( iv)  in vivo interaction between N-Myc and the  hTERT promoter was recently observed in a neuroblastoma cell line transfected with N- myc ( 40).	bind
50655	4	11585	6	NULL	NULL	0	NULL	hTERT	NULL		contains	NULL					NULL	specific		Myc binding motif	NULL		0	NULL	NULL	NULL	gw60_pnas_98_7_3826_s_183	11274400	A number of recent observations support the identification of the  hTERT gene as a c-Myc target: ( i) ectopic expression of c-Myc induced  hTERT expression and activated telomerase activity in human cells ( 27); ( ii) the specific Myc binding motifs, E-boxes, are present in the  hTERT promoter, and the activity of the promoter is significantly increased by transient expression of c-Myc ( 7,  28,  29,  39); ( iii) ectopic expression of the Mad1 protein results in repression of  hTERT expression ( 30,  31); and ( iv)  in vivo interaction between N-Myc and the  hTERT promoter was recently observed in a neuroblastoma cell line transfected with N- myc ( 40).	bind
50656	5	11585	6	NULL	NULL	0	NULL	hTERT	NULL		contains	NULL					NULL			E-boxes	NULL		0	NULL	NULL	NULL	gw60_pnas_98_7_3826_s_183	11274400	A number of recent observations support the identification of the  hTERT gene as a c-Myc target: ( i) ectopic expression of c-Myc induced  hTERT expression and activated telomerase activity in human cells ( 27); ( ii) the specific Myc binding motifs, E-boxes, are present in the  hTERT promoter, and the activity of the promoter is significantly increased by transient expression of c-Myc ( 7,  28,  29,  39); ( iii) ectopic expression of the Mad1 protein results in repression of  hTERT expression ( 30,  31); and ( iv)  in vivo interaction between N-Myc and the  hTERT promoter was recently observed in a neuroblastoma cell line transfected with N- myc ( 40).	bind
50657	6	11585	6	NULL	NULL	0	NULL	hTERT	NULL	activity of	is increased 	NULL	significantly		promoter	c-Myc	NULL	transient expression of			NULL		0	NULL	NULL	NULL	gw60_pnas_98_7_3826_s_183	11274400	A number of recent observations support the identification of the  hTERT gene as a c-Myc target: ( i) ectopic expression of c-Myc induced  hTERT expression and activated telomerase activity in human cells ( 27); ( ii) the specific Myc binding motifs, E-boxes, are present in the  hTERT promoter, and the activity of the promoter is significantly increased by transient expression of c-Myc ( 7,  28,  29,  39); ( iii) ectopic expression of the Mad1 protein results in repression of  hTERT expression ( 30,  31); and ( iv)  in vivo interaction between N-Myc and the  hTERT promoter was recently observed in a neuroblastoma cell line transfected with N- myc ( 40).	bind
50658	7	11585	6	NULL	NULL	0	NULL	Mad1 protein	NULL	ectopic expression of	results in	NULL				hTERT	NULL	repression of			NULL		0	NULL	NULL	NULL	gw60_pnas_98_7_3826_s_183	11274400	A number of recent observations support the identification of the  hTERT gene as a c-Myc target: ( i) ectopic expression of c-Myc induced  hTERT expression and activated telomerase activity in human cells ( 27); ( ii) the specific Myc binding motifs, E-boxes, are present in the  hTERT promoter, and the activity of the promoter is significantly increased by transient expression of c-Myc ( 7,  28,  29,  39); ( iii) ectopic expression of the Mad1 protein results in repression of  hTERT expression ( 30,  31); and ( iv)  in vivo interaction between N-Myc and the  hTERT promoter was recently observed in a neuroblastoma cell line transfected with N- myc ( 40).	bind
51314	1	11586	5	NULL	NULL	NULL	NULL	Smad3	GP		bind		directly			DNA sequences	NucleicAcid	specific			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_19_3084_s_224	9765209	A number of recent reports show direct binding of Smad3 and Smad4 to specific DNA sequences, but these reports disagree on the consensus binding sequences (Yingling et al. 1997  ; Dennler et al. 1998  ; Vindevoghel et al. 1998  ; Zawel et al. 1998  ).	bind
51315	2	11586	5	NULL	NULL	NULL	NULL	Smad4	GP		bind		directly			DNA sequences	NucleicAcid	specific			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_19_3084_s_224	9765209	A number of recent reports show direct binding of Smad3 and Smad4 to specific DNA sequences, but these reports disagree on the consensus binding sequences (Yingling et al. 1997  ; Dennler et al. 1998  ; Vindevoghel et al. 1998  ; Zawel et al. 1998  ).	bind
50660	1	11586	6	NULL	NULL	0	NULL	Smad3	NULL		bind	NULL	directly			DNA sequencees	NULL	specific			NULL		0	NULL	NULL	NULL	gw60_genesdev_12_19_3084_s_224	9765209	A number of recent reports show direct binding of Smad3 and Smad4 to specific DNA sequences, but these reports disagree on the consensus binding sequences (Yingling et al. 1997  ; Dennler et al. 1998  ; Vindevoghel et al. 1998  ; Zawel et al. 1998  ).	bind
54218	2	11586	6	10	NULL	0	NULL	Smad4			bind		directly			DNA sequences		specific			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_19_3084_s_224	9765209	A number of recent reports show direct binding of Smad3 and Smad4 to specific DNA sequences, but these reports disagree on the consensus binding sequences (Yingling et al. 1997  ; Dennler et al. 1998  ; Vindevoghel et al. 1998  ; Zawel et al. 1998  ).	bind
51316	1	11587	5	NULL	NULL	NULL	NULL	importin	GP		is					cytosolic receptor	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_7_4197_s_336	9461616	A number of recent reports suggest that the nuclear targeting of most nuclear proteins is initiated by binding of cytosolic receptor (termed importin) to NLS.	bind
51317	2	11587	5	NULL	NULL	NULL	NULL	importin	GP		bind								NLS		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_7_4197_s_336	9461616	A number of recent reports suggest that the nuclear targeting of most nuclear proteins is initiated by binding of cytosolic receptor (termed importin) to NLS.	bind
51318	3	11587	5	NULL	NULL	NULL	NULL	statement 2	Process		initiates					nuclear proteins	GP	nuclear targeting of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_7_4197_s_336	9461616	A number of recent reports suggest that the nuclear targeting of most nuclear proteins is initiated by binding of cytosolic receptor (termed importin) to NLS.	bind
50661	1	11587	6	NULL	NULL	0	NULL	cytosolic receptor	NULL		bind	NULL				NLS	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_7_4197_s_336	9461616	A number of recent reports suggest that the nuclear targeting of most nuclear proteins is initiated by binding of cytosolic receptor (termed importin) to NLS.	bind
50662	2	11587	6	NULL	NULL	0	NULL	cytosolic receptor	NULL		is	NULL				importin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_7_4197_s_336	9461616	A number of recent reports suggest that the nuclear targeting of most nuclear proteins is initiated by binding of cytosolic receptor (termed importin) to NLS.	bind
58816	3	11587	6	10	NULL	0	NULL	statement 1			initiates					 nuclear proteins		nuclear targeting of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_7_4197_s_336	9461616	A number of recent reports suggest that the nuclear targeting of most nuclear proteins is initiated by binding of cytosolic receptor (termed importin) to NLS.	bind
51319	1	11588	5	NULL	NULL	NULL	NULL				is a type of				GATA binding site	regulatory site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_33_29856_s_27	15941713	A number of regulatory sites have been identified including a GATA binding site ( ), Sp1 and Sp3 binding sites ( ,  ), as well as a NF-kappaB site ( ) shown to be involved in basal transcriptional activity.	bind
51320	2	11588	5	NULL	NULL	NULL	NULL				is a type of				Sp1 binding site	regulatory site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_33_29856_s_27	15941713	A number of regulatory sites have been identified including a GATA binding site ( ), Sp1 and Sp3 binding sites ( ,  ), as well as a NF-kappaB site ( ) shown to be involved in basal transcriptional activity.	bind
51321	3	11588	5	NULL	NULL	NULL	NULL				is a type of				Sp3 binding site	regulatory site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_33_29856_s_27	15941713	A number of regulatory sites have been identified including a GATA binding site ( ), Sp1 and Sp3 binding sites ( ,  ), as well as a NF-kappaB site ( ) shown to be involved in basal transcriptional activity.	bind
51322	4	11588	5	NULL	NULL	NULL	NULL				is a type of				NF-kappaB site	regulatory site	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_33_29856_s_27	15941713	A number of regulatory sites have been identified including a GATA binding site ( ), Sp1 and Sp3 binding sites ( ,  ), as well as a NF-kappaB site ( ) shown to be involved in basal transcriptional activity.	bind
51323	5	11588	5	NULL	NULL	NULL	NULL				is involved in				GATA binding site	transcriptional activity	Process	basal			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_33_29856_s_27	15941713	A number of regulatory sites have been identified including a GATA binding site ( ), Sp1 and Sp3 binding sites ( ,  ), as well as a NF-kappaB site ( ) shown to be involved in basal transcriptional activity.	bind
51326	6	11588	5	NULL	NULL	NULL	NULL				is involved in				Sp1 binding sites	transcriptional activity	Process	basal			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_33_29856_s_27	15941713	A number of regulatory sites have been identified including a GATA binding site ( ), Sp1 and Sp3 binding sites ( ,  ), as well as a NF-kappaB site ( ) shown to be involved in basal transcriptional activity.	bind
51327	7	11588	5	NULL	NULL	NULL	NULL				is involved in				Sp3 binding sites	transcriptional activity	Process	basal			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_33_29856_s_27	15941713	A number of regulatory sites have been identified including a GATA binding site ( ), Sp1 and Sp3 binding sites ( ,  ), as well as a NF-kappaB site ( ) shown to be involved in basal transcriptional activity.	bind
51328	8	11588	5	NULL	NULL	NULL	NULL				is involved in				NF-kappaB site	transcriptional activity	Process	basal			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_33_29856_s_27	15941713	A number of regulatory sites have been identified including a GATA binding site ( ), Sp1 and Sp3 binding sites ( ,  ), as well as a NF-kappaB site ( ) shown to be involved in basal transcriptional activity.	bind
50663	1	11588	6	NULL	NULL	0	NULL		NULL		is involved in	NULL			GATA binding site	transcriptional activity	NULL	basal			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_33_29856_s_27	15941713	A number of regulatory sites have been identified including a GATA binding site ( ), Sp1 and Sp3 binding sites ( ,  ), as well as a NF-kappaB site ( ) shown to be involved in basal transcriptional activity.	bind
50664	2	11588	6	NULL	NULL	0	NULL		NULL		is involved in	NULL			Sp1 binding site	transcriptional activity	NULL	basal			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_33_29856_s_27	15941713	A number of regulatory sites have been identified including a GATA binding site ( ), Sp1 and Sp3 binding sites ( ,  ), as well as a NF-kappaB site ( ) shown to be involved in basal transcriptional activity.	bind
50665	3	11588	6	NULL	NULL	0	NULL		NULL		is involved in	NULL			Sp3 binding site	transcriptional activity	NULL	basal			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_33_29856_s_27	15941713	A number of regulatory sites have been identified including a GATA binding site ( ), Sp1 and Sp3 binding sites ( ,  ), as well as a NF-kappaB site ( ) shown to be involved in basal transcriptional activity.	bind
50666	4	11588	6	NULL	NULL	0	NULL		NULL		is involved in	NULL			NF-kappaB site	transcriptional activity	NULL	basal			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_33_29856_s_27	15941713	A number of regulatory sites have been identified including a GATA binding site ( ), Sp1 and Sp3 binding sites ( ,  ), as well as a NF-kappaB site ( ) shown to be involved in basal transcriptional activity.	bind
54219	5	11588	6	10	NULL	0	NULL				is a type of				GATA binding site	regulatory site					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_33_29856_s_27	15941713	A number of regulatory sites have been identified including a GATA binding site ( ), Sp1 and Sp3 binding sites ( ,  ), as well as a NF-kappaB site ( ) shown to be involved in basal transcriptional activity.	bind
54220	6	11588	6	10	NULL	0	NULL				is a type of				Sp1 binding site	regulatory site					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_33_29856_s_27	15941713	A number of regulatory sites have been identified including a GATA binding site ( ), Sp1 and Sp3 binding sites ( ,  ), as well as a NF-kappaB site ( ) shown to be involved in basal transcriptional activity.	bind
54221	7	11588	6	10	NULL	0	NULL				is a type of				Sp3 binding site	regulatory site					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_33_29856_s_27	15941713	A number of regulatory sites have been identified including a GATA binding site ( ), Sp1 and Sp3 binding sites ( ,  ), as well as a NF-kappaB site ( ) shown to be involved in basal transcriptional activity.	bind
54222	8	11588	6	10	NULL	0	NULL				is a type of				NF-kappaB site	regulatory site					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_33_29856_s_27	15941713	A number of regulatory sites have been identified including a GATA binding site ( ), Sp1 and Sp3 binding sites ( ,  ), as well as a NF-kappaB site ( ) shown to be involved in basal transcriptional activity.	bind
51329	1	11589	5	NULL	NULL	NULL	NULL	TAFI	GP		bind			Gly336;;Tyr341;;Glu363		plasminogen	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_6620_s_317	14660622	A number of residues in the His333-Val401 region have been reported to be involved in substrate binding (Gly336, Tyr341, and Glu363) ( ), but these three amino acids are conserved in both TAFI and pancreatic pro-CPB, suggesting that residues other than these are important for plasminogen and fibrinogen binding.	bind
51330	2	11589	5	NULL	NULL	NULL	NULL	TAFI	GP		bind			Gly336;;Tyr341;;Glu363		fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_6620_s_317	14660622	A number of residues in the His333-Val401 region have been reported to be involved in substrate binding (Gly336, Tyr341, and Glu363) ( ), but these three amino acids are conserved in both TAFI and pancreatic pro-CPB, suggesting that residues other than these are important for plasminogen and fibrinogen binding.	bind
51331	3	11589	5	NULL	NULL	NULL	NULL	pro-CPB	GP	pancreatic	bind			Gly336;;Tyr341;;Glu363		plasminogen	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_6620_s_317	14660622	A number of residues in the His333-Val401 region have been reported to be involved in substrate binding (Gly336, Tyr341, and Glu363) ( ), but these three amino acids are conserved in both TAFI and pancreatic pro-CPB, suggesting that residues other than these are important for plasminogen and fibrinogen binding.	bind
51332	4	11589	5	NULL	NULL	NULL	NULL	pro-CPB	GP	pancreatic	bind			Gly336;;Tyr341;;Glu363		fibrinogen	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_6620_s_317	14660622	A number of residues in the His333-Val401 region have been reported to be involved in substrate binding (Gly336, Tyr341, and Glu363) ( ), but these three amino acids are conserved in both TAFI and pancreatic pro-CPB, suggesting that residues other than these are important for plasminogen and fibrinogen binding.	bind
51333	5	11589	5	NULL	NULL	NULL	NULL				is conserved in			Gly336;;Tyr341;;Glu363		TAFI	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_6620_s_317	14660622	A number of residues in the His333-Val401 region have been reported to be involved in substrate binding (Gly336, Tyr341, and Glu363) ( ), but these three amino acids are conserved in both TAFI and pancreatic pro-CPB, suggesting that residues other than these are important for plasminogen and fibrinogen binding.	bind
51334	6	11589	5	NULL	NULL	NULL	NULL				is conserved in			Gly336;;Tyr341;;Glu363		pro-CPB	GP	pancreatic			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_8_6620_s_317	14660622	A number of residues in the His333-Val401 region have been reported to be involved in substrate binding (Gly336, Tyr341, and Glu363) ( ), but these three amino acids are conserved in both TAFI and pancreatic pro-CPB, suggesting that residues other than these are important for plasminogen and fibrinogen binding.	bind
51335	1	11590	5	NULL	NULL	NULL	NULL	Rho GTPases	GP		bind					GTP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51336	2	11590	5	NULL	NULL	NULL	NULL	Rho-kinase/ROKalpha/OCK-II	GP		is a type of					Rho effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51337	3	11590	5	NULL	NULL	NULL	NULL	Rho-kinase/ROKalpha/OCK-II	GP		associate with		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51338	4	11590	5	NULL	NULL	NULL	NULL	p160ROCK/ROKbeta/ROCK-I	GP		is an isoform of					Rho-kinase	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51339	5	11590	5	NULL	NULL	NULL	NULL	p160ROCK/ROKbeta/ROCK-I	GP		is a type of					Rho effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51340	6	11590	5	NULL	NULL	NULL	NULL	p160ROCK/ROKbeta/ROCK-I	GP		associate with		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51341	7	11590	5	NULL	NULL	NULL	NULL	PKN 1	GP		is					protein kinase N 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51342	8	11590	5	NULL	NULL	NULL	NULL	PKN 1	GP		is a type of					Rho effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51343	9	11590	5	NULL	NULL	NULL	NULL	PKN 1	GP		associate with		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51344	10	11590	5	NULL	NULL	NULL	NULL	rhophilin	GP		associate with		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51345	11	11590	5	NULL	NULL	NULL	NULL	rhotekin	GP		associate with		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51346	12	11590	5	NULL	NULL	NULL	NULL	citron	GP		associate with		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51347	13	11590	5	NULL	NULL	NULL	NULL	citron kinase	GP		associate with		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51348	14	11590	5	NULL	NULL	NULL	NULL	mDia	GP		associate with		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51349	15	11590	5	NULL	NULL	NULL	NULL	kinectin	GP		associate with		specifically			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51350	16	11590	5	NULL	NULL	NULL	NULL	rhophilin	GP		is a type of					Rho effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51351	17	11590	5	NULL	NULL	NULL	NULL	rhotekin	GP		is a type of					Rho effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51352	18	11590	5	NULL	NULL	NULL	NULL	citron	GP		is a type of					Rho effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51353	19	11590	5	NULL	NULL	NULL	NULL	citron kinase	GP		is a type of					Rho effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51354	20	11590	5	NULL	NULL	NULL	NULL	mDia	GP		is a type of					Rho effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51355	21	11590	5	NULL	NULL	NULL	NULL	kinectin	GP		is a type of					Rho effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50667	1	11590	6	NULL	NULL	0	NULL	Rho-kinase/ROKalpha/OCK-II	NULL		is a type of	NULL				Rho effector	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50668	2	11590	6	NULL	NULL	0	NULL	Rho GTPase	NULL		bind	NULL				GTP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50669	3	11590	6	NULL	NULL	0	NULL	Rho-kinase/ROKalpha/OCK-II	NULL		associates with	NULL	specifically			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50670	4	11590	6	NULL	NULL	0	NULL	p160ROCK/ROKbeta/ROCK-I	NULL		is a type of	NULL				Rho effector	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50671	5	11590	6	10	NULL	0	NULL	p160ROCK/ROKbeta/ROCK-I			is an isoform of					Rho-kinase					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50672	6	11590	6	NULL	NULL	0	NULL	p160ROCK/ROKbeta/ROCK-I	NULL		associates with	NULL	specifically			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50673	7	11590	6	10	NULL	0	NULL	PKN 1			associates with		specifically			statement 2					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50674	8	11590	6	10	NULL	0	NULL	PKN 1			is a type of					Rho effector					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50675	9	11590	6	10	NULL	0	NULL	PKN 1			is					protein kinase N					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50676	10	11590	6	NULL	NULL	0	NULL	rhophilin	NULL		is a type of	NULL				Rho effector	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50677	11	11590	6	NULL	NULL	0	NULL	rhophilin	NULL		associates with	NULL	specifically			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50678	12	11590	6	NULL	NULL	0	NULL	rhotekin	NULL		is a type of	NULL				Rho effector	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50679	13	11590	6	10	NULL	0	NULL	rhotekin			associates with		specifically			statement 2					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50680	14	11590	6	10	NULL	0	NULL	citron			associates with		specifically			statement 2					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50681	15	11590	6	NULL	NULL	0	NULL	citron	NULL		is a type of	NULL				Rho effector	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50682	16	11590	6	NULL	NULL	0	NULL	citron kinase	NULL		is a type of	NULL				Rho effector	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50683	17	11590	6	10	NULL	0	NULL	citron kinase			associates with		specifically			statement 2					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50684	18	11590	6	10	NULL	0	NULL	mDia			associates with		specifically			statement 2					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50685	19	11590	6	NULL	NULL	0	NULL	mDia	NULL		is a type of	NULL				Rho effector	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50686	20	11590	6	NULL	NULL	0	NULL	kinectin	NULL		is a type of	NULL				Rho effector	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
50687	21	11590	6	NULL	NULL	0	NULL	kinectin	NULL		associates with	NULL	specifically			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_46046_s_11	12954645	A number of Rho effectors have been identified which associate specifically with the GTP-bound forms of Rho GTPases, including Rho-kinase/ROKalpha/OCK-II, p160ROCK/ROKbeta/ROCK-I (an isoform of Rho-kinase) ( - ), protein kinase N (PKN)  1 ( ,  ), rhophilin ( ), rhotekin ( ), citron ( ), citron kinase ( ), mDia ( ), and kinectin ( ).	bind
51356	1	11591	5	NULL	NULL	NULL	NULL	p56 lck	GP		is involved in					TCR/CD3-dependent signal transduction pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_32_28714_s_9	12045189	A number of signal transducers known to be involved in the TCR/CD3-dependent signal transduction pathway, including p56 lck, p36 lat, and SLP-76, as well as capacitative entry of calcium, are crucial for the noticed CD43 co-stimulatory effect.	bind
51357	2	11591	5	NULL	NULL	NULL	NULL	p36 lat	GP		is involved in					TCR/CD3-dependent signal transduction pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_32_28714_s_9	12045189	A number of signal transducers known to be involved in the TCR/CD3-dependent signal transduction pathway, including p56 lck, p36 lat, and SLP-76, as well as capacitative entry of calcium, are crucial for the noticed CD43 co-stimulatory effect.	bind
51358	3	11591	5	NULL	NULL	NULL	NULL	SLP-76	GP		is involved in					TCR/CD3-dependent signal transduction pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_32_28714_s_9	12045189	A number of signal transducers known to be involved in the TCR/CD3-dependent signal transduction pathway, including p56 lck, p36 lat, and SLP-76, as well as capacitative entry of calcium, are crucial for the noticed CD43 co-stimulatory effect.	bind
51359	4	11591	5	NULL	NULL	NULL	NULL	p56 lck	GP		is a type of					signal transducer	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_32_28714_s_9	12045189	A number of signal transducers known to be involved in the TCR/CD3-dependent signal transduction pathway, including p56 lck, p36 lat, and SLP-76, as well as capacitative entry of calcium, are crucial for the noticed CD43 co-stimulatory effect.	bind
51360	5	11591	5	NULL	NULL	NULL	NULL	p36 lat	GP		is a type of					signal transducer	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_32_28714_s_9	12045189	A number of signal transducers known to be involved in the TCR/CD3-dependent signal transduction pathway, including p56 lck, p36 lat, and SLP-76, as well as capacitative entry of calcium, are crucial for the noticed CD43 co-stimulatory effect.	bind
51361	6	11591	5	NULL	NULL	NULL	NULL	SLP-76	GP		is a type of					signal transducer	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_32_28714_s_9	12045189	A number of signal transducers known to be involved in the TCR/CD3-dependent signal transduction pathway, including p56 lck, p36 lat, and SLP-76, as well as capacitative entry of calcium, are crucial for the noticed CD43 co-stimulatory effect.	bind
50688	1	11591	6	NULL	NULL	0	NULL	p56 lck	NULL		is involved in	NULL				TCR/CD3-dependent signal transduction pathway	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_32_28714_s_9	12045189	A number of signal transducers known to be involved in the TCR/CD3-dependent signal transduction pathway, including p56 lck, p36 lat, and SLP-76, as well as capacitative entry of calcium, are crucial for the noticed CD43 co-stimulatory effect.	bind
50689	2	11591	6	NULL	NULL	0	NULL	p36 lat	NULL		is involved in	NULL				TCR/CD3-dependent signal transduction pathway	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_32_28714_s_9	12045189	A number of signal transducers known to be involved in the TCR/CD3-dependent signal transduction pathway, including p56 lck, p36 lat, and SLP-76, as well as capacitative entry of calcium, are crucial for the noticed CD43 co-stimulatory effect.	bind
50690	3	11591	6	NULL	NULL	0	NULL	SLP-76	NULL		is involved in	NULL				TCR/CD3-dependent signal transduction pathway	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_32_28714_s_9	12045189	A number of signal transducers known to be involved in the TCR/CD3-dependent signal transduction pathway, including p56 lck, p36 lat, and SLP-76, as well as capacitative entry of calcium, are crucial for the noticed CD43 co-stimulatory effect.	bind
54223	4	11591	6	10	NULL	0	NULL	p56 lck			is a type of					signal transducer					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_32_28714_s_9	12045189	A number of signal transducers known to be involved in the TCR/CD3-dependent signal transduction pathway, including p56 lck, p36 lat, and SLP-76, as well as capacitative entry of calcium, are crucial for the noticed CD43 co-stimulatory effect.	bind
54224	5	11591	6	10	NULL	0	NULL	p36 lat			is a type of					signal transducer					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_32_28714_s_9	12045189	A number of signal transducers known to be involved in the TCR/CD3-dependent signal transduction pathway, including p56 lck, p36 lat, and SLP-76, as well as capacitative entry of calcium, are crucial for the noticed CD43 co-stimulatory effect.	bind
54225	6	11591	6	10	NULL	0	NULL	SLP-76			is a type of					signal transducer					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_32_28714_s_9	12045189	A number of signal transducers known to be involved in the TCR/CD3-dependent signal transduction pathway, including p56 lck, p36 lat, and SLP-76, as well as capacitative entry of calcium, are crucial for the noticed CD43 co-stimulatory effect.	bind
51363	1	11593	5	NULL	NULL	NULL	NULL	bFGF	GP		bind					heparin	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17711_s_191	8663454	A number of studies have pointed to the importance of 2- O-sulfated iduronic acid in binding of bFGF to heparin ( 45) and heparan sulfate ( 5,  46).	bind
51364	2	11593	5	NULL	NULL	NULL	NULL	bFGF	GP		bind					heparan sulfate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17711_s_191	8663454	A number of studies have pointed to the importance of 2- O-sulfated iduronic acid in binding of bFGF to heparin ( 45) and heparan sulfate ( 5,  46).	bind
51365	3	11593	5	NULL	NULL	NULL	NULL	2- O-sulfated iduronic acid	Chemical		is important for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17711_s_191	8663454	A number of studies have pointed to the importance of 2- O-sulfated iduronic acid in binding of bFGF to heparin ( 45) and heparan sulfate ( 5,  46).	bind
51366	4	11593	5	NULL	NULL	NULL	NULL	2- O-sulfated iduronic acid	Chemical		is important for					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17711_s_191	8663454	A number of studies have pointed to the importance of 2- O-sulfated iduronic acid in binding of bFGF to heparin ( 45) and heparan sulfate ( 5,  46).	bind
50691	1	11593	6	NULL	NULL	0	NULL	bFGF	NULL		bind	NULL				heparin	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17711_s_191	8663454	A number of studies have pointed to the importance of 2- O-sulfated iduronic acid in binding of bFGF to heparin ( 45) and heparan sulfate ( 5,  46).	bind
50692	2	11593	6	NULL	NULL	0	NULL	bFGF	NULL		bind	NULL				heparan sulfate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17711_s_191	8663454	A number of studies have pointed to the importance of 2- O-sulfated iduronic acid in binding of bFGF to heparin ( 45) and heparan sulfate ( 5,  46).	bind
50693	3	11593	6	NULL	NULL	0	NULL	2- O-sulfated iduronic acid	NULL		plays a role in	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17711_s_191	8663454	A number of studies have pointed to the importance of 2- O-sulfated iduronic acid in binding of bFGF to heparin ( 45) and heparan sulfate ( 5,  46).	bind
50694	4	11593	6	NULL	NULL	0	NULL	2- O-sulfated iduronic acid	NULL		plays a role in	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17711_s_191	8663454	A number of studies have pointed to the importance of 2- O-sulfated iduronic acid in binding of bFGF to heparin ( 45) and heparan sulfate ( 5,  46).	bind
51369	1	11594	5	NULL	NULL	NULL	NULL	CPT I	GP	rat;;liver	contains								malonyl-CoA binding sites		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_11_9058_s_23	12499375	A number of studies have shown that in rat liver CPT I there are two malonyl-CoA binding sites: one with greater capacity for binding and regulation of the inhibitor and not susceptible to competition from acyl-CoA, which behaves as an allosteric component ( 8-12); and a second acyl-CoA binding site, which is located near the catalytic  site ( 13).	bind
50695	1	11594	6	10	NULL	0	NULL	CPT I		rat;; liver	contains								malonyl-CoA binding sites		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_11_9058_s_23	12499375	A number of studies have shown that in rat liver CPT I there are two malonyl-CoA binding sites: one with greater capacity for binding and regulation of the inhibitor and not susceptible to competition from acyl-CoA, which behaves as an allosteric component ( 8-12); and a second acyl-CoA binding site, which is located near the catalytic  site ( 13).	bind
51367	1	11595	5	NULL	NULL	NULL	NULL	NGF	GP		bind					p75	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_61_4_710_s_282	11901208	A number of studies in other cell types have demonstrated the apoptosis-inducing effect of NGF binding to p75 (Kuner and Hertel, 1998  ; Sedel et al., 1999  ).	bind
51368	2	11595	5	NULL	NULL	NULL	NULL	apoptosis	Process		induce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_61_4_710_s_282	11901208	A number of studies in other cell types have demonstrated the apoptosis-inducing effect of NGF binding to p75 (Kuner and Hertel, 1998  ; Sedel et al., 1999  ).	bind
50696	1	11595	6	NULL	NULL	0	NULL	NGF	NULL		bind	NULL				p75	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_4_710_s_282	11901208	A number of studies in other cell types have demonstrated the apoptosis-inducing effect of NGF binding to p75 (Kuner and Hertel, 1998  ; Sedel et al., 1999  ).	bind
50697	2	11595	6	NULL	NULL	0	NULL	apoptosis	NULL		induces	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_4_710_s_282	11901208	A number of studies in other cell types have demonstrated the apoptosis-inducing effect of NGF binding to p75 (Kuner and Hertel, 1998  ; Sedel et al., 1999  ).	bind
51372	1	11596	5	NULL	NULL	NULL	NULL	collagen	GP		bind					GPVI	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
51373	2	11596	5	NULL	NULL	NULL	NULL	CRP	GP		bind					GPVI	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
51374	3	11596	5	NULL	NULL	NULL	NULL	Cvx	GP		bind					GPVI	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
51375	4	11596	5	NULL	NULL	NULL	NULL	statement 1	Process		induce					platelet	Cell	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
51376	5	11596	5	NULL	NULL	NULL	NULL	statement 2	Process		induce					platelet	Cell	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
51377	6	11596	5	NULL	NULL	NULL	NULL	statement 3	Process		induce					platelet	Cell	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
51378	7	11596	5	NULL	NULL	NULL	NULL	statement 4	Process		occurs through					Fc receptor gamma-chain	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
51379	8	11596	5	NULL	NULL	NULL	NULL	statement 4	Process		occurs through					Syk	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
51380	9	11596	5	NULL	NULL	NULL	NULL	statement 4	Process		occurs through					phospholipase C	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
51381	10	11596	5	NULL	NULL	NULL	NULL	statement 5	Process		occurs through					Fc receptor gamma-chain	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
51382	11	11596	5	NULL	NULL	NULL	NULL	statement 5	Process		occurs through					Syk	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
51383	12	11596	5	NULL	NULL	NULL	NULL	statement 5	Process		occurs through					phospholipase C	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
51384	13	11596	5	NULL	NULL	NULL	NULL	statement 6	Process		occurs through					Fc receptor gamma-chain	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
51385	14	11596	5	NULL	NULL	NULL	NULL	statement 6	Process		occurs through					Syk	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
51386	15	11596	5	NULL	NULL	NULL	NULL	statement 6	Process		occurs through					phospholipase C	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
51387	16	11596	5	NULL	NULL	NULL	NULL	collagen	GP		induce					platelet	Cell	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
51388	17	11596	5	NULL	NULL	NULL	NULL	GPVI	GP		is a key receptor for					statement 16	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
50698	1	11596	6	NULL	NULL	0	NULL	collagen	NULL		bind	NULL				GPVI	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
50699	2	11596	6	NULL	NULL	0	NULL	CRP	NULL		bind	NULL				GPVI	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
50700	3	11596	6	NULL	NULL	0	NULL	Cvx	NULL		bind	NULL				GPVI	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
50701	4	11596	6	NULL	NULL	0	NULL	statement 1	NULL		induces	NULL				platelet	NULL	activation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
50702	5	11596	6	NULL	NULL	0	NULL	statement 2	NULL		induces	NULL				platelet	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
50703	6	11596	6	NULL	NULL	0	NULL	statement 3	NULL		induces	NULL				platelet	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
50704	7	11596	6	NULL	NULL	0	NULL	statement 4	NULL		occurs via	NULL				Fc receptor gamma-chain	NULL	phosphorylation of 	Tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
50705	8	11596	6	NULL	NULL	0	NULL	statement 4	NULL		occurs via	NULL				Syk	NULL	phosphorylation of	Tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
50706	9	11596	6	NULL	NULL	0	NULL	statement 4	NULL		occurs via	NULL				phospholipase C	NULL	phosphorylation of	Tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
50707	10	11596	6	NULL	NULL	0	NULL	statement 5	NULL		occurs via	NULL				Fc receptor gamma-chain	NULL	phosphorylation of	Tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
50708	11	11596	6	NULL	NULL	0	NULL	statement 5	NULL		occurs via	NULL				Syk	NULL	phosphorylation of	Tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
50709	12	11596	6	NULL	NULL	0	NULL	statement 5	NULL		occurs via	NULL				phospholipase C	NULL	phosphorylation of	Tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
50710	13	11596	6	NULL	NULL	0	NULL	statement 6	NULL		occurs via	NULL				Fc receptor gamma-chain	NULL	phosphorylation of	Tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
50711	14	11596	6	NULL	NULL	0	NULL	statement 6	NULL		occurs via	NULL				Syk	NULL	phosphorylation of	Tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
50712	15	11596	6	NULL	NULL	0	NULL	statement 6	NULL		occurs via	NULL				phospholipase C	NULL	phosphorylation of	Tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
50713	16	11596	6	NULL	NULL	0	NULL	collagen	NULL		induces	NULL				platelet	NULL	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
50714	17	11596	6	NULL	NULL	0	NULL	GPVI	NULL		is a key receptor for	NULL				statement 16	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_48_46197_s_21	12356768	A number of studies showed that the binding of collagen, CRP, and Cvx to GPVI induced platelet activation through tyrosine phosphorylation of the Fc receptor gamma-chain, Syk, phospholipase C ,and many other proteins ( 10), thus indicating that GPVI is a key receptor for collagen-induced platelet activation.	bind
51389	1	11597	5	NULL	NULL	NULL	NULL	histone H1	GP		bind		weakly					consensus		NFI-binding sites	NULL		NULL	NULL	NULL	NULL	gw60_gene_249_1_31_s_185	10831836	A number of studies suggest that histone H1 can bind weakly to consensus NFI-binding sites, and that NFI may activate transcription by direct displacement of histone binding at such sites (   Gao and   Ristiniemi).	bind
51390	2	11597	5	NULL	NULL	NULL	NULL	NFI	GP		activate		may			transcription	Process				NULL		NULL	NULL	NULL	NULL	gw60_gene_249_1_31_s_185	10831836	A number of studies suggest that histone H1 can bind weakly to consensus NFI-binding sites, and that NFI may activate transcription by direct displacement of histone binding at such sites (   Gao and   Ristiniemi).	bind
51392	3	11597	5	NULL	NULL	NULL	NULL	NFI	GP		displaces		directly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_gene_249_1_31_s_185	10831836	A number of studies suggest that histone H1 can bind weakly to consensus NFI-binding sites, and that NFI may activate transcription by direct displacement of histone binding at such sites (   Gao and   Ristiniemi).	bind
51393	4	11597	5	NULL	NULL	NULL	NULL	statement 3	Process		leads to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_gene_249_1_31_s_185	10831836	A number of studies suggest that histone H1 can bind weakly to consensus NFI-binding sites, and that NFI may activate transcription by direct displacement of histone binding at such sites (   Gao and   Ristiniemi).	bind
50715	1	11597	6	NULL	NULL	0	NULL	histone H1	NULL		bind	NULL	weakly				NULL	consensus		NFI-binding sites	NULL		0	NULL	NULL	NULL	gw60_gene_249_1_31_s_185	10831836	A number of studies suggest that histone H1 can bind weakly to consensus NFI-binding sites, and that NFI may activate transcription by direct displacement of histone binding at such sites (   Gao and   Ristiniemi).	bind
50716	2	11597	6	NULL	NULL	0	NULL	NFI	NULL		displace	NULL	directly			histone H1	NULL				NULL	statement 1	NULL	NULL	NULL	NULL	gw60_gene_249_1_31_s_185	10831836	A number of studies suggest that histone H1 can bind weakly to consensus NFI-binding sites, and that NFI may activate transcription by direct displacement of histone binding at such sites (   Gao and   Ristiniemi).	bind
50717	3	11597	6	NULL	NULL	0	NULL	NFI	NULL		activate	NULL	may			transcription	NULL				NULL		0	NULL	NULL	NULL	gw60_gene_249_1_31_s_185	10831836	A number of studies suggest that histone H1 can bind weakly to consensus NFI-binding sites, and that NFI may activate transcription by direct displacement of histone binding at such sites (   Gao and   Ristiniemi).	bind
50718	4	11597	6	NULL	NULL	0	NULL	statement 3	NULL		occurs via	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_gene_249_1_31_s_185	10831836	A number of studies suggest that histone H1 can bind weakly to consensus NFI-binding sites, and that NFI may activate transcription by direct displacement of histone binding at such sites (   Gao and   Ristiniemi).	bind
51420	1	11598	5	NULL	NULL	NULL	NULL	TRX2 gene	GP		encodes					thioredoxin	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_7_1710_s_26	9130715	A number of such targets have now been identified, including the  TRX2 gene which encodes thioredoxin that confers increased resistance to oxidative stress (Kuge and Jones, 1994  ),  YCF1 which encodes an ATP-binding cassette transporter gene essential for cadmium tolerance (Wemmie  et al., 1994a  ),  GSH1 which encodes gamma-glutamylcysteine synthetase involved in glutathione biosynthesis (Wu and Moye-Rowley, 1994  ),  GLR1 which encodes glutathione reductase (Grant  et al., 1996  ), and the additional ABC transporter proteins  PDR5 and  SNQ2 (Miyahara  et al., 1996  ).	bind
51421	2	11598	5	NULL	NULL	NULL	NULL	TRX2 gene	GP		confers					oxidative stress	Process	increased resistance to			NULL		NULL	NULL	NULL	NULL	gw60_embo_16_7_1710_s_26	9130715	A number of such targets have now been identified, including the  TRX2 gene which encodes thioredoxin that confers increased resistance to oxidative stress (Kuge and Jones, 1994  ),  YCF1 which encodes an ATP-binding cassette transporter gene essential for cadmium tolerance (Wemmie  et al., 1994a  ),  GSH1 which encodes gamma-glutamylcysteine synthetase involved in glutathione biosynthesis (Wu and Moye-Rowley, 1994  ),  GLR1 which encodes glutathione reductase (Grant  et al., 1996  ), and the additional ABC transporter proteins  PDR5 and  SNQ2 (Miyahara  et al., 1996  ).	bind
51422	3	11598	5	NULL	NULL	NULL	NULL	YCF1	GP		encodes					ATP-binding cassette transporter gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_7_1710_s_26	9130715	A number of such targets have now been identified, including the  TRX2 gene which encodes thioredoxin that confers increased resistance to oxidative stress (Kuge and Jones, 1994  ),  YCF1 which encodes an ATP-binding cassette transporter gene essential for cadmium tolerance (Wemmie  et al., 1994a  ),  GSH1 which encodes gamma-glutamylcysteine synthetase involved in glutathione biosynthesis (Wu and Moye-Rowley, 1994  ),  GLR1 which encodes glutathione reductase (Grant  et al., 1996  ), and the additional ABC transporter proteins  PDR5 and  SNQ2 (Miyahara  et al., 1996  ).	bind
51423	4	11598	5	NULL	NULL	NULL	NULL	YCF1	GP		is essential for					cadmium 	Chemical	tolerance of			NULL		NULL	NULL	NULL	NULL	gw60_embo_16_7_1710_s_26	9130715	A number of such targets have now been identified, including the  TRX2 gene which encodes thioredoxin that confers increased resistance to oxidative stress (Kuge and Jones, 1994  ),  YCF1 which encodes an ATP-binding cassette transporter gene essential for cadmium tolerance (Wemmie  et al., 1994a  ),  GSH1 which encodes gamma-glutamylcysteine synthetase involved in glutathione biosynthesis (Wu and Moye-Rowley, 1994  ),  GLR1 which encodes glutathione reductase (Grant  et al., 1996  ), and the additional ABC transporter proteins  PDR5 and  SNQ2 (Miyahara  et al., 1996  ).	bind
51424	5	11598	5	NULL	NULL	NULL	NULL	GSH1	GP		encodes					gamma-glutamylcysteine synthetase	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_7_1710_s_26	9130715	A number of such targets have now been identified, including the  TRX2 gene which encodes thioredoxin that confers increased resistance to oxidative stress (Kuge and Jones, 1994  ),  YCF1 which encodes an ATP-binding cassette transporter gene essential for cadmium tolerance (Wemmie  et al., 1994a  ),  GSH1 which encodes gamma-glutamylcysteine synthetase involved in glutathione biosynthesis (Wu and Moye-Rowley, 1994  ),  GLR1 which encodes glutathione reductase (Grant  et al., 1996  ), and the additional ABC transporter proteins  PDR5 and  SNQ2 (Miyahara  et al., 1996  ).	bind
51425	6	11598	5	NULL	NULL	NULL	NULL	gamma-glutamylcysteine synthetase	GP		is involved in					glutathione	Chemical	biosynthesis of			NULL		NULL	NULL	NULL	NULL	gw60_embo_16_7_1710_s_26	9130715	A number of such targets have now been identified, including the  TRX2 gene which encodes thioredoxin that confers increased resistance to oxidative stress (Kuge and Jones, 1994  ),  YCF1 which encodes an ATP-binding cassette transporter gene essential for cadmium tolerance (Wemmie  et al., 1994a  ),  GSH1 which encodes gamma-glutamylcysteine synthetase involved in glutathione biosynthesis (Wu and Moye-Rowley, 1994  ),  GLR1 which encodes glutathione reductase (Grant  et al., 1996  ), and the additional ABC transporter proteins  PDR5 and  SNQ2 (Miyahara  et al., 1996  ).	bind
51426	7	11598	5	NULL	NULL	NULL	NULL	GLR1	GP		encodes					glutathione reductase	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_7_1710_s_26	9130715	A number of such targets have now been identified, including the  TRX2 gene which encodes thioredoxin that confers increased resistance to oxidative stress (Kuge and Jones, 1994  ),  YCF1 which encodes an ATP-binding cassette transporter gene essential for cadmium tolerance (Wemmie  et al., 1994a  ),  GSH1 which encodes gamma-glutamylcysteine synthetase involved in glutathione biosynthesis (Wu and Moye-Rowley, 1994  ),  GLR1 which encodes glutathione reductase (Grant  et al., 1996  ), and the additional ABC transporter proteins  PDR5 and  SNQ2 (Miyahara  et al., 1996  ).	bind
51427	8	11598	5	NULL	NULL	NULL	NULL	PDR5	GP		is a type of					ABC transporter protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_7_1710_s_26	9130715	A number of such targets have now been identified, including the  TRX2 gene which encodes thioredoxin that confers increased resistance to oxidative stress (Kuge and Jones, 1994  ),  YCF1 which encodes an ATP-binding cassette transporter gene essential for cadmium tolerance (Wemmie  et al., 1994a  ),  GSH1 which encodes gamma-glutamylcysteine synthetase involved in glutathione biosynthesis (Wu and Moye-Rowley, 1994  ),  GLR1 which encodes glutathione reductase (Grant  et al., 1996  ), and the additional ABC transporter proteins  PDR5 and  SNQ2 (Miyahara  et al., 1996  ).	bind
51428	9	11598	5	NULL	NULL	NULL	NULL	SNQ2 	GP		is a type of					ABC transporter protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_16_7_1710_s_26	9130715	A number of such targets have now been identified, including the  TRX2 gene which encodes thioredoxin that confers increased resistance to oxidative stress (Kuge and Jones, 1994  ),  YCF1 which encodes an ATP-binding cassette transporter gene essential for cadmium tolerance (Wemmie  et al., 1994a  ),  GSH1 which encodes gamma-glutamylcysteine synthetase involved in glutathione biosynthesis (Wu and Moye-Rowley, 1994  ),  GLR1 which encodes glutathione reductase (Grant  et al., 1996  ), and the additional ABC transporter proteins  PDR5 and  SNQ2 (Miyahara  et al., 1996  ).	bind
50719	1	11598	6	NULL	NULL	0	NULL	TRX2 gene	NULL		encodes	NULL				thioredoxin	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_7_1710_s_26	9130715	A number of such targets have now been identified, including the  TRX2 gene which encodes thioredoxin that confers increased resistance to oxidative stress (Kuge and Jones, 1994  ),  YCF1 which encodes an ATP-binding cassette transporter gene essential for cadmium tolerance (Wemmie  et al., 1994a  ),  GSH1 which encodes gamma-glutamylcysteine synthetase involved in glutathione biosynthesis (Wu and Moye-Rowley, 1994  ),  GLR1 which encodes glutathione reductase (Grant  et al., 1996  ), and the additional ABC transporter proteins  PDR5 and  SNQ2 (Miyahara  et al., 1996  ).	bind
50720	2	11598	6	10	NULL	0	NULL	TRX2 gene			confers					oxidative stress		increased resistance to			NULL		NULL	NULL	NULL	NULL	gw60_embo_16_7_1710_s_26	9130715	A number of such targets have now been identified, including the  TRX2 gene which encodes thioredoxin that confers increased resistance to oxidative stress (Kuge and Jones, 1994  ),  YCF1 which encodes an ATP-binding cassette transporter gene essential for cadmium tolerance (Wemmie  et al., 1994a  ),  GSH1 which encodes gamma-glutamylcysteine synthetase involved in glutathione biosynthesis (Wu and Moye-Rowley, 1994  ),  GLR1 which encodes glutathione reductase (Grant  et al., 1996  ), and the additional ABC transporter proteins  PDR5 and  SNQ2 (Miyahara  et al., 1996  ).	bind
50721	3	11598	6	NULL	NULL	0	NULL	YCF1	NULL		encodes	NULL				ATP-binding cassette transporter gene	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_7_1710_s_26	9130715	A number of such targets have now been identified, including the  TRX2 gene which encodes thioredoxin that confers increased resistance to oxidative stress (Kuge and Jones, 1994  ),  YCF1 which encodes an ATP-binding cassette transporter gene essential for cadmium tolerance (Wemmie  et al., 1994a  ),  GSH1 which encodes gamma-glutamylcysteine synthetase involved in glutathione biosynthesis (Wu and Moye-Rowley, 1994  ),  GLR1 which encodes glutathione reductase (Grant  et al., 1996  ), and the additional ABC transporter proteins  PDR5 and  SNQ2 (Miyahara  et al., 1996  ).	bind
50722	4	11598	6	10	NULL	0	NULL	statement 3			is essential for					cadmium		 tolerance of			NULL		NULL	NULL	NULL	NULL	gw60_embo_16_7_1710_s_26	9130715	A number of such targets have now been identified, including the  TRX2 gene which encodes thioredoxin that confers increased resistance to oxidative stress (Kuge and Jones, 1994  ),  YCF1 which encodes an ATP-binding cassette transporter gene essential for cadmium tolerance (Wemmie  et al., 1994a  ),  GSH1 which encodes gamma-glutamylcysteine synthetase involved in glutathione biosynthesis (Wu and Moye-Rowley, 1994  ),  GLR1 which encodes glutathione reductase (Grant  et al., 1996  ), and the additional ABC transporter proteins  PDR5 and  SNQ2 (Miyahara  et al., 1996  ).	bind
50723	5	11598	6	NULL	NULL	0	NULL	GSH1	NULL		encodes	NULL				gamma-glutamylcysteine synthetase	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_7_1710_s_26	9130715	A number of such targets have now been identified, including the  TRX2 gene which encodes thioredoxin that confers increased resistance to oxidative stress (Kuge and Jones, 1994  ),  YCF1 which encodes an ATP-binding cassette transporter gene essential for cadmium tolerance (Wemmie  et al., 1994a  ),  GSH1 which encodes gamma-glutamylcysteine synthetase involved in glutathione biosynthesis (Wu and Moye-Rowley, 1994  ),  GLR1 which encodes glutathione reductase (Grant  et al., 1996  ), and the additional ABC transporter proteins  PDR5 and  SNQ2 (Miyahara  et al., 1996  ).	bind
50724	6	11598	6	10	NULL	0	NULL	GSH1			is involved in					glutathione 		biosynthesis of			NULL		NULL	NULL	NULL	NULL	gw60_embo_16_7_1710_s_26	9130715	A number of such targets have now been identified, including the  TRX2 gene which encodes thioredoxin that confers increased resistance to oxidative stress (Kuge and Jones, 1994  ),  YCF1 which encodes an ATP-binding cassette transporter gene essential for cadmium tolerance (Wemmie  et al., 1994a  ),  GSH1 which encodes gamma-glutamylcysteine synthetase involved in glutathione biosynthesis (Wu and Moye-Rowley, 1994  ),  GLR1 which encodes glutathione reductase (Grant  et al., 1996  ), and the additional ABC transporter proteins  PDR5 and  SNQ2 (Miyahara  et al., 1996  ).	bind
50725	7	11598	6	NULL	NULL	0	NULL	GLR1	NULL		encodes	NULL				glutathione reductase	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_16_7_1710_s_26	9130715	A number of such targets have now been identified, including the  TRX2 gene which encodes thioredoxin that confers increased resistance to oxidative stress (Kuge and Jones, 1994  ),  YCF1 which encodes an ATP-binding cassette transporter gene essential for cadmium tolerance (Wemmie  et al., 1994a  ),  GSH1 which encodes gamma-glutamylcysteine synthetase involved in glutathione biosynthesis (Wu and Moye-Rowley, 1994  ),  GLR1 which encodes glutathione reductase (Grant  et al., 1996  ), and the additional ABC transporter proteins  PDR5 and  SNQ2 (Miyahara  et al., 1996  ).	bind
54226	8	11598	6	10	NULL	0	NULL	PDR5 			is a type of					ABC transporter protein					NULL		0	NULL	NULL	NULL	gw60_embo_16_7_1710_s_26	9130715	A number of such targets have now been identified, including the  TRX2 gene which encodes thioredoxin that confers increased resistance to oxidative stress (Kuge and Jones, 1994  ),  YCF1 which encodes an ATP-binding cassette transporter gene essential for cadmium tolerance (Wemmie  et al., 1994a  ),  GSH1 which encodes gamma-glutamylcysteine synthetase involved in glutathione biosynthesis (Wu and Moye-Rowley, 1994  ),  GLR1 which encodes glutathione reductase (Grant  et al., 1996  ), and the additional ABC transporter proteins  PDR5 and  SNQ2 (Miyahara  et al., 1996  ).	bind
54227	9	11598	6	10	NULL	0	NULL	SNQ2 			is a type of					ABC transporter protein					NULL		0	NULL	NULL	NULL	gw60_embo_16_7_1710_s_26	9130715	A number of such targets have now been identified, including the  TRX2 gene which encodes thioredoxin that confers increased resistance to oxidative stress (Kuge and Jones, 1994  ),  YCF1 which encodes an ATP-binding cassette transporter gene essential for cadmium tolerance (Wemmie  et al., 1994a  ),  GSH1 which encodes gamma-glutamylcysteine synthetase involved in glutathione biosynthesis (Wu and Moye-Rowley, 1994  ),  GLR1 which encodes glutathione reductase (Grant  et al., 1996  ), and the additional ABC transporter proteins  PDR5 and  SNQ2 (Miyahara  et al., 1996  ).	bind
51394	1	11599	5	NULL	NULL	NULL	NULL	PAI-1 promoter	NucleicAcid		is a type of					TGF-beta/SMAD-regulated promoters	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51395	2	11599	5	NULL	NULL	NULL	NULL	collagenase I promoter	NucleicAcid		is a type of					TGF-beta/SMAD-regulated promoters	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51396	3	11599	5	NULL	NULL	NULL	NULL	c-Jun promoter	NucleicAcid		is a type of					TGF-beta/SMAD-regulated promoters	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51397	4	11599	5	NULL	NULL	NULL	NULL	IgA promoter	NucleicAcid		is a type of					TGF-beta/SMAD-regulated promoters	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51398	5	11599	5	NULL	NULL	NULL	NULL	Jun B promoter	NucleicAcid		is a type of					TGF-beta/SMAD-regulated promoters	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51399	6	11599	5	NULL	NULL	NULL	NULL	PAI-1	GP		contains				promoter					GTCT	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51400	7	11599	5	NULL	NULL	NULL	NULL	PAI-1	GP		contains				promoter					AGAC	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51401	8	11599	5	NULL	NULL	NULL	NULL	collagenase I	GP		contains				promoter					GTCT	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51402	9	11599	5	NULL	NULL	NULL	NULL	collagenase I	GP		contains				promoter					AGAC	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51403	10	11599	5	NULL	NULL	NULL	NULL	c-Jun	GP		contains				promoter					GTCT	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51404	11	11599	5	NULL	NULL	NULL	NULL	c-Jun	GP		contains				promoter					AGAC	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51405	12	11599	5	NULL	NULL	NULL	NULL	IgA	GP		contains				promoter					GTCT	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51406	13	11599	5	NULL	NULL	NULL	NULL	IgA	GP		contains				promoter					AGAC	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51407	14	11599	5	NULL	NULL	NULL	NULL	Jun B	GP		contains				promoter					AGAC	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51408	15	11599	5	NULL	NULL	NULL	NULL	Smad3-Smad4 complex	GP		bind					statement 6	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51409	16	11599	5	NULL	NULL	NULL	NULL	Smad3-Smad4 complex	GP		bind					statement 7	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51410	17	11599	5	NULL	NULL	NULL	NULL	Smad3-Smad4 complex	GP		bind					statement 8	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51411	18	11599	5	NULL	NULL	NULL	NULL	Smad3-Smad4 complex	GP		bind					statement 9	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51412	19	11599	5	NULL	NULL	NULL	NULL	Smad3-Smad4 complex	GP		bind					statement 10	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51413	20	11599	5	NULL	NULL	NULL	NULL	Smad3-Smad4 complex	GP		bind					statement 11	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51414	21	11599	5	NULL	NULL	NULL	NULL	Smad3-Smad4 complex	GP		bind					statement 12	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51415	22	11599	5	NULL	NULL	NULL	NULL	Smad3-Smad4 complex	GP		bind					statement 13	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51416	23	11599	5	NULL	NULL	NULL	NULL	Smad3-Smad4 complex	GP		bind					statement 14	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
54228	24	11599	5	NULL	NULL	NULL	NULL	Jun B	GP		contains				promoter					GTCT	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
54229	25	11599	5	NULL	NULL	NULL	NULL	Smad3-Smad4 complex	GP		bind					statement 24	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50726	1	11599	6	NULL	NULL	0	NULL	PAI-1	NULL		contains	NULL			promoter		NULL			GTCT	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50727	2	11599	6	NULL	NULL	0	NULL	PAI-1	NULL		contains	NULL			promoter		NULL			AGAC	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50728	3	11599	6	NULL	NULL	0	NULL	collagenase I	NULL		contains	NULL			promoter		NULL			GTCT	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50729	4	11599	6	NULL	NULL	0	NULL	collagenase I	NULL		contains	NULL			promoter		NULL			AGAC	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50730	5	11599	6	NULL	NULL	0	NULL	c-Jun	NULL		contains	NULL			promoter		NULL			GTCT	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50731	6	11599	6	NULL	NULL	0	NULL	c-Jun	NULL		contains	NULL			promoter		NULL			AGAC	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50732	7	11599	6	NULL	NULL	0	NULL	IgA	NULL		contains	NULL			promoter		NULL			GTCT 	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50736	8	11599	6	NULL	NULL	0	NULL	IgA	NULL		contains	NULL			promoter		NULL			AGAC	NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50737	9	11599	6	NULL	NULL	0	NULL	Jun B	NULL		contains	NULL			promoter		NULL			GTCT	NULL		0	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50738	10	11599	6	NULL	NULL	0	NULL	Jun B	NULL		contains	NULL			promoter		NULL			AGAC	NULL		0	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50739	11	11599	6	NULL	NULL	0	NULL	Smad3-Smad4 complex	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50740	12	11599	6	NULL	NULL	0	NULL	Smad3-Smad4 complex	NULL		bind	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50741	13	11599	6	NULL	NULL	0	NULL	Smad3-Smad4 complex	NULL		bind	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50742	14	11599	6	NULL	NULL	0	NULL	Smad3-Smad4 complex	NULL		bind	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50743	15	11599	6	NULL	NULL	0	NULL	Smad3-Smad4 complex	NULL		bind	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50744	16	11599	6	NULL	NULL	0	NULL	Smad3-Smad4 complex	NULL		bind	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50745	17	11599	6	NULL	NULL	0	NULL	Smad3-Smad4 complex	NULL		bind	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50746	18	11599	6	NULL	NULL	0	NULL	Smad3-Smad4 complex	NULL		bind	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50747	19	11599	6	NULL	NULL	0	NULL	Smad3-Smad4 complex	NULL		bind	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
50748	20	11599	6	NULL	NULL	0	NULL	Smad3-Smad4 complex	NULL		bind	NULL				statement 10	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
54230	21	11599	6	10	NULL	0	NULL	PAI-1			is a type of					TGF-beta/SMAD-regulated promoter					NULL		0	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
54231	22	11599	6	10	NULL	0	NULL	collagenase I			is a type of					TGF-beta/SMAD-regulated promoter					NULL		0	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
54232	23	11599	6	10	NULL	0	NULL	c-Jun			is a type of					TGF-beta/SMAD-regulated promoter					NULL		0	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
54234	24	11599	6	10	NULL	0	NULL	IgA			is a type of					TGF-beta/SMAD-regulated promoter					NULL		0	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
54235	25	11599	6	10	NULL	0	NULL	Jun B			is a type of					TGF-beta/SMAD-regulated promoter					NULL		0	NULL	NULL	NULL	gw60_pnas_97_12_6397_s_17	10823886	A number of TGF-beta/SMAD-regulated promoters, such as the PAI-1, collagenase I, c-Jun, IgA, and Jun B promoters, contain one or multiple copies of the sequence GTCT or AGAC, which can be bound by the Smad3-Smad4 complex ( 15-24).	bind
51417	1	11600	5	NULL	NULL	NULL	NULL	SOS	GP		bind			proline-rich sequences		Grb2	GP		SH3 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_32_30552_s_283	11375989	A number of these are linked to intracellular signaling complexes found near the plasma membrane, for example, proline-rich sequences of SOS bind to the SH3 domains of Grb2, and this leads to the activation of ras and is therefore required for growth factor signaling ( 37).	bind
51418	2	11600	5	NULL	NULL	NULL	NULL	statement 1	Process		activates					ras	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_32_30552_s_283	11375989	A number of these are linked to intracellular signaling complexes found near the plasma membrane, for example, proline-rich sequences of SOS bind to the SH3 domains of Grb2, and this leads to the activation of ras and is therefore required for growth factor signaling ( 37).	bind
51419	3	11600	5	NULL	NULL	NULL	NULL	statement 1	Process		is required for					growth factor	GP	signaling of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_32_30552_s_283	11375989	A number of these are linked to intracellular signaling complexes found near the plasma membrane, for example, proline-rich sequences of SOS bind to the SH3 domains of Grb2, and this leads to the activation of ras and is therefore required for growth factor signaling ( 37).	bind
50733	1	11600	6	NULL	NULL	0	NULL	SOS	NULL		bind	NULL		proline rich sequences		Grb2	NULL		SH3 domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_32_30552_s_283	11375989	A number of these are linked to intracellular signaling complexes found near the plasma membrane, for example, proline-rich sequences of SOS bind to the SH3 domains of Grb2, and this leads to the activation of ras and is therefore required for growth factor signaling ( 37).	bind
50734	2	11600	6	10	NULL	0	NULL	statement 1			activates					ras					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_32_30552_s_283	11375989	A number of these are linked to intracellular signaling complexes found near the plasma membrane, for example, proline-rich sequences of SOS bind to the SH3 domains of Grb2, and this leads to the activation of ras and is therefore required for growth factor signaling ( 37).	bind
50735	3	11600	6	10	NULL	0	NULL	statement 2			is required for					growth factor 		signaling of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_32_30552_s_283	11375989	A number of these are linked to intracellular signaling complexes found near the plasma membrane, for example, proline-rich sequences of SOS bind to the SH3 domains of Grb2, and this leads to the activation of ras and is therefore required for growth factor signaling ( 37).	bind
67985	1	333026	5	NULL	NULL	NULL	NULL	CCZ1	GP		is a synonym of					YBR131w	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_biochem-biophys-res-commun_329_1_15721293_s_2	15721293	The CCZ1 (YBR131w) gene encodes a protein required for fusion of various  transport intermediates with the vacuole.	gene_phenotype
67986	2	333026	5	NULL	NULL	0	NULL	transport intermediates	AbstractConcept		fuse with					vacuole	CellComponent				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_biochem-biophys-res-commun_329_1_15721293_s_2	15721293	The CCZ1 (YBR131w) gene encodes a protein required for fusion of various  transport intermediates with the vacuole.	gene_phenotype
67987	1	333027	5	NULL	NULL	0	NULL	SEC4 gene	GP		encodes					Rab proteins	GP				NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
67988	2	333027	5	NULL	NULL	NULL	NULL	SEC4 gene	GP		plays a role in		important			vesicle	CellComponent	transport of			NULL	yeast	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
67989	3	333027	5	NULL	NULL	0	NULL	YPT1 gene	GP		encodes					Rab proteins	GP				NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
67990	4	333027	5	NULL	NULL	NULL	NULL	YPT1 gene	GP		plays a role in		important			vesicle	CellComponent	transport of			NULL	yeast	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
67991	5	333027	5	NULL	NULL	0	NULL	YPT31 gene	GP		encodes					Rab proteins	GP				NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
67992	6	333027	5	NULL	NULL	0	NULL	YPT31 gene	GP		plays a role in		important			vesicle	CellComponent	transport of			NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
67993	7	333027	5	NULL	NULL	0	NULL	YPT32 gene	GP		encodes					Rab proteins	GP				NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
67994	8	333027	5	NULL	NULL	0	NULL	YPT32 gene	GP		plays a role in		important			vesicle	CellComponent	transport of			NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
67995	9	333027	5	NULL	NULL	0	NULL	YPT51 gene	GP		encodes					Rab proteins	GP				NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
67996	10	333027	5	NULL	NULL	0	NULL	YPT51 gene	GP		plays a role in		important			vesicle	GP	transport of			NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
67997	11	333027	5	NULL	NULL	0	NULL	YPT52 gene	GP		encodes					Rab proteins	GP				NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
67998	12	333027	5	NULL	NULL	0	NULL	YPT52 gene	GP		plays a role in		important			vesicle	CellComponent	transport of			NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
67999	13	333027	5	NULL	NULL	0	NULL	YPT53 gene	GP		encodes					Rab proteins	GP				NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
68000	14	333027	5	NULL	NULL	0	NULL	YPT53 gene	GP		plays a role in		important			vesicle	CellComponent	transport of			NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
68001	15	333027	5	NULL	NULL	0	NULL	YPT6 gene	GP		encodes					Rab proteins	GP				NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
68002	16	333027	5	NULL	NULL	0	NULL	YPT6 gene	GP		plays a role in		important			vesicle	CellComponent	transport of			NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
68003	17	333027	5	NULL	NULL	0	NULL	YPT7 gene	GP		encodes					Rab proteins	GP				NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
68004	18	333027	5	NULL	NULL	0	NULL	YPT7 gene	GP		plays a role in		important			vesicle	CellComponent	transport of			NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
68005	19	333027	5	NULL	NULL	0	NULL	YBR264C gene	GP		encodes					Rab proteins	GP				NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
68006	20	333027	5	NULL	NULL	0	NULL	YBR264C gene	GP		plays a role in		important			vesicle	CellComponent	transport of			NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
68007	21	333027	5	NULL	NULL	0	NULL	YNL304W gene	GP		encodes					Rab proteins	GP				NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
68008	22	333027	5	NULL	NULL	0	NULL	YNL304W gene	GP		plays a role in		important			vesicle	CellComponent	transport of			NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3253_s_15	9452439	Eleven genes encoding Rab proteins ( SEC4,  YPT1,  YPT31,  YPT32,  YPT51,  YPT52,  YPT53,  YPT6,  YPT7,  YBR264C, and  YNL304W) are found in yeast where they play important roles in vesicle transport.	gene_phenotype
68009	1	333030	5	NULL	NULL	0	NULL	YDR330W	AminoAcid		is homologous to					ubiquitin regulatory protein domains	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_pnas_97_1_262_s_222	10618406	In the proteasome class, YDR330W has homology to ubiquitin regulatory protein domains, suggesting a role in ubiquitin-dependent proteasome activity.	gene_phenotype
68010	2	333030	5	NULL	NULL	0	NULL	proteasome	GP	activity of	is dependent on					ubiquitin	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_1_262_s_222	10618406	In the proteasome class, YDR330W has homology to ubiquitin regulatory protein domains, suggesting a role in ubiquitin-dependent proteasome activity.	gene_phenotype
68011	3	333030	5	NULL	NULL	0	NULL	statement 1	Process		plays a role in		may			statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_97_1_262_s_222	10618406	In the proteasome class, YDR330W has homology to ubiquitin regulatory protein domains, suggesting a role in ubiquitin-dependent proteasome activity.	gene_phenotype
68012	1	333031	5	NULL	NULL	0	NULL	Csm1	GP		interacts with		might			Lrs4 protein	GP				NULL		0	NULL	NULL	NULL	gw60_devcell_4_4_535_s_88	12689592	Genome-wide two-hybrid data  (Uetz et al., 2000  ) raised the possibility that Csm1 might interact with a protein called Lrs4 (loss of rDNA silencing; product of ORF YDR439W) that had been implicated in rDNA silencing  (Smith et al., 1999  ).	gene_phenotype
68013	2	333031	5	NULL	NULL	0	NULL	Lrs4	GP		is					loss of rDNA silencing	GP				NULL		0	NULL	NULL	NULL	gw60_devcell_4_4_535_s_88	12689592	Genome-wide two-hybrid data  (Uetz et al., 2000  ) raised the possibility that Csm1 might interact with a protein called Lrs4 (loss of rDNA silencing; product of ORF YDR439W) that had been implicated in rDNA silencing  (Smith et al., 1999  ).	gene_phenotype
68014	3	333031	5	NULL	NULL	0	NULL	Lrs4 protein	GP		is a product of					ORF	NucleicAcid		YDR439W		NULL		0	NULL	NULL	NULL	gw60_devcell_4_4_535_s_88	12689592	Genome-wide two-hybrid data  (Uetz et al., 2000  ) raised the possibility that Csm1 might interact with a protein called Lrs4 (loss of rDNA silencing; product of ORF YDR439W) that had been implicated in rDNA silencing  (Smith et al., 1999  ).	gene_phenotype
68015	4	333031	5	NULL	NULL	0	NULL	Lrs4 protein	GP		is implicated in					rDNA	NucleicAcid	silencing of			NULL		0	NULL	NULL	NULL	gw60_devcell_4_4_535_s_88	12689592	Genome-wide two-hybrid data  (Uetz et al., 2000  ) raised the possibility that Csm1 might interact with a protein called Lrs4 (loss of rDNA silencing; product of ORF YDR439W) that had been implicated in rDNA silencing  (Smith et al., 1999  ).	gene_phenotype
68016	1	333033	5	NULL	NULL	NULL	NULL	MAD2 gene	GP	budding yeast S. cerevisiae	is a type of					spindle checkpoint gene	GP	budding yeast S. cerevisiae			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_8_2607_s_79	10436016	The spindle checkpoint gene  MAD2 in the budding yeast  S. cerevisiae was originally identified (Li and Murray, 1991  ) as the ORF YJL031C, which encodes a subunit of an essential prenyltransferase (Li  et al., 1993  ) and has been renamed  BET4.	gene_phenotype
68017	2	333033	5	NULL	NULL	0	NULL	MAD2 gene	GP	budding yeast S. cerevisiae	is					ORF	NucleicAcid		YJL031C		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_8_2607_s_79	10436016	The spindle checkpoint gene  MAD2 in the budding yeast  S. cerevisiae was originally identified (Li and Murray, 1991  ) as the ORF YJL031C, which encodes a subunit of an essential prenyltransferase (Li  et al., 1993  ) and has been renamed  BET4.	gene_phenotype
68018	3	333033	5	NULL	NULL	0	NULL	MAD2 gene	GP	budding yeast S. cerevisiae	encodes					prenyltransferase	GP	subunit of;;essential			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_8_2607_s_79	10436016	The spindle checkpoint gene  MAD2 in the budding yeast  S. cerevisiae was originally identified (Li and Murray, 1991  ) as the ORF YJL031C, which encodes a subunit of an essential prenyltransferase (Li  et al., 1993  ) and has been renamed  BET4.	gene_phenotype
68019	4	333033	5	NULL	NULL	NULL	NULL	MAD2 gene	GP	budding yeast S. cerevisiae	is renamed as					BET4	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_10_8_2607_s_79	10436016	The spindle checkpoint gene  MAD2 in the budding yeast  S. cerevisiae was originally identified (Li and Murray, 1991  ) as the ORF YJL031C, which encodes a subunit of an essential prenyltransferase (Li  et al., 1993  ) and has been renamed  BET4.	gene_phenotype
68020	1	333034	5	NULL	NULL	0	NULL	Cnb1	GP		is a subunit of		regulatory	YKL190W		calcineurin	GP	S. cerevisiae			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_13_12231_s_79	15657058	A BLAST program search using the peptide sequence of Cnb1 (YKL190W), the regulatory subunit of calcineurin of  S. cerevisiae ( ,  ), against the  S. pombe protein data base at the Sanger Center revealed an open reading frame, SPCC830.06, which except for the N- and C-terminal domains, exhibits a significant similarity to the budding yeast Cnb1 (score = 680,  p = 8.7e - 69, identities = 142/174 (81%)).	gene_phenotype
68022	2	333034	5	NULL	NULL	0	NULL	Cnb1	GP	S. cerevisiae	is similar to		significantly			SPCC830.06	NucleicAcid	S. pombe			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_13_12231_s_79	15657058	A BLAST program search using the peptide sequence of Cnb1 (YKL190W), the regulatory subunit of calcineurin of  S. cerevisiae ( ,  ), against the  S. pombe protein data base at the Sanger Center revealed an open reading frame, SPCC830.06, which except for the N- and C-terminal domains, exhibits a significant similarity to the budding yeast Cnb1 (score = 680,  p = 8.7e - 69, identities = 142/174 (81%)).	gene_phenotype
68023	3	333034	5	NULL	NULL	0	NULL	SPCC830.06	NucleicAcid		is a type of					open reading frame	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_13_12231_s_79	15657058	A BLAST program search using the peptide sequence of Cnb1 (YKL190W), the regulatory subunit of calcineurin of  S. cerevisiae ( ,  ), against the  S. pombe protein data base at the Sanger Center revealed an open reading frame, SPCC830.06, which except for the N- and C-terminal domains, exhibits a significant similarity to the budding yeast Cnb1 (score = 680,  p = 8.7e - 69, identities = 142/174 (81%)).	gene_phenotype
68024	1	333036	5	NULL	NULL	0	NULL	CTR2	GP		encodes				orf19.4720	copper transporter	GP	putative			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4814_s_229	16030247	We also see prolonged induction of  CTR2 (orf19.4720), which encodes a putative copper transporter;  YOL075C (orf19.3120), which encodes a putative ferric cation transporter; and  YMR209C (orf19.4816), which encodes a protein of unknown function that contains a GMP kinase domain.	gene_phenotype
68028	2	333036	5	NULL	NULL	0	NULL				encodes			YOL075C	orf19.3120	ferric cation transporter	GP	putative			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4814_s_229	16030247	We also see prolonged induction of  CTR2 (orf19.4720), which encodes a putative copper transporter;  YOL075C (orf19.3120), which encodes a putative ferric cation transporter; and  YMR209C (orf19.4816), which encodes a protein of unknown function that contains a GMP kinase domain.	gene_phenotype
68029	3	333036	5	NULL	NULL	0	NULL				encodes			YMR209C	orf19.4816	protein	GP		GMP kinase domain		NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_10_4814_s_229	16030247	We also see prolonged induction of  CTR2 (orf19.4720), which encodes a putative copper transporter;  YOL075C (orf19.3120), which encodes a putative ferric cation transporter; and  YMR209C (orf19.4816), which encodes a protein of unknown function that contains a GMP kinase domain.	gene_phenotype
68030	1	333037	5	NULL	NULL	0	NULL	Abp140p	GP		is not homologous to					actin binding protein	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_99_2_751_s_27	11805329	Abp140p does not show homology to any known actin binding protein and is expressed in cells by fusion of two ORFs (YOR239W and YOR240W) by means of a +1 translational frameshift.	gene_phenotype
68031	2	333037	5	NULL	NULL	0	NULL	ORF	NucleicAcid		is fused to			YOR239W		ORF	NucleicAcid		YOR240W		NULL		0	NULL	NULL	NULL	gw60_pnas_99_2_751_s_27	11805329	Abp140p does not show homology to any known actin binding protein and is expressed in cells by fusion of two ORFs (YOR239W and YOR240W) by means of a +1 translational frameshift.	gene_phenotype
68032	3	333037	5	NULL	NULL	0	NULL	statement 2	Process		leads to					Abp140p	GP	expression of			NULL	cells	0	NULL	NULL	NULL	gw60_pnas_99_2_751_s_27	11805329	Abp140p does not show homology to any known actin binding protein and is expressed in cells by fusion of two ORFs (YOR239W and YOR240W) by means of a +1 translational frameshift.	gene_phenotype
68033	4	333037	5	NULL	NULL	0	NULL	+1 translational frameshift	Process		leads to					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_99_2_751_s_27	11805329	Abp140p does not show homology to any known actin binding protein and is expressed in cells by fusion of two ORFs (YOR239W and YOR240W) by means of a +1 translational frameshift.	gene_phenotype
68034	1	333038	5	NULL	NULL	NULL	NULL	sterol transport	Process	subcellular	is conserved in					yeast cells	Cell				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_164_4_547_s_41	14970192	Subcellular sterol transport may also be conserved between yeast and mammalian cells; Ncr1p (YPL006w) is an uncharacterized 1,170-residue transmembrane protein with a signal peptide, eight N-glycosylation sites, and 35% identity to the human Npc1 protein.	gene_phenotype
68035	2	333038	5	NULL	NULL	0	NULL	sterol transport	Process	subcellular	is conserved in					mammalian cells	Cell				NULL		0	NULL	NULL	NULL	gw70_cellbiol_164_4_547_s_41	14970192	Subcellular sterol transport may also be conserved between yeast and mammalian cells; Ncr1p (YPL006w) is an uncharacterized 1,170-residue transmembrane protein with a signal peptide, eight N-glycosylation sites, and 35% identity to the human Npc1 protein.	gene_phenotype
68036	3	333038	5	NULL	NULL	0	NULL	Ncr1p	GP		is a type of			YPL006w		1,170-residue transmembrane protein	GP	uncharacterized			NULL		0	NULL	NULL	NULL	gw70_cellbiol_164_4_547_s_41	14970192	Subcellular sterol transport may also be conserved between yeast and mammalian cells; Ncr1p (YPL006w) is an uncharacterized 1,170-residue transmembrane protein with a signal peptide, eight N-glycosylation sites, and 35% identity to the human Npc1 protein.	gene_phenotype
68037	4	333038	5	NULL	NULL	0	NULL	Ncr1p	GP		consists of			YPL006w					signal peptide;;N-glycosylation sites		NULL		0	NULL	NULL	NULL	gw70_cellbiol_164_4_547_s_41	14970192	Subcellular sterol transport may also be conserved between yeast and mammalian cells; Ncr1p (YPL006w) is an uncharacterized 1,170-residue transmembrane protein with a signal peptide, eight N-glycosylation sites, and 35% identity to the human Npc1 protein.	gene_phenotype
68038	5	333038	5	NULL	NULL	0	NULL	Ncr1p	GP		is similar to			YPL006w		Npc1 protein	GP	human			NULL		0	NULL	NULL	NULL	gw70_cellbiol_164_4_547_s_41	14970192	Subcellular sterol transport may also be conserved between yeast and mammalian cells; Ncr1p (YPL006w) is an uncharacterized 1,170-residue transmembrane protein with a signal peptide, eight N-glycosylation sites, and 35% identity to the human Npc1 protein.	gene_phenotype
68039	1	333040	5	NULL	NULL	0	NULL	YPR007C	AminoAcid		is a part of					sporulation cluster	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_18_0_829_s_223	10837077	Indeed, the essential  role in sporulation for one of the previously uncharacterized genes in the sporulation  cluster, YPR007C, which is predicted to encode a putative chromosome cohesion protein,  was established following its identification by this cluster analysis method ( 40).	gene_phenotype
68040	2	333040	5	NULL	NULL	0	NULL	YPR007C	AminoAcid		encodes		potentially			chromosome cohesion protein	GP	putative			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_18_0_829_s_223	10837077	Indeed, the essential  role in sporulation for one of the previously uncharacterized genes in the sporulation  cluster, YPR007C, which is predicted to encode a putative chromosome cohesion protein,  was established following its identification by this cluster analysis method ( 40).	gene_phenotype
68091	1	333042	5	NULL	NULL	0	NULL	Bcp1	GP		is a homolog of					BCCIP	GP	S. cerevisiae			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_5_1949_s_283	15713648	The  S. cerevisiae BCCIP homolog, Bcp1 (open reading frame number YDR361C), is essential for viability ( ) (Saccharomyces Genome Database at  http://www.yeastgenome.	gene_phenotype
68092	2	333042	5	NULL	NULL	0	NULL	Bcp1	GP		is essential for			YDR361C		viability	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_5_1949_s_283	15713648	The  S. cerevisiae BCCIP homolog, Bcp1 (open reading frame number YDR361C), is essential for viability ( ) (Saccharomyces Genome Database at  http://www.yeastgenome.	gene_phenotype
68093	1	333043	5	NULL	NULL	0	NULL	YDR374C	AminoAcid		is required for					sporulation	Process	efficient			NULL		0	NULL	NULL	NULL	gw60_pnas_99_21_13431_s_133	12370439	Indeed, two of these ( YDR374C and  SLZ1) have recently been shown in genome-wide deletion analysis to be required for efficient sporulation (A. Deutschbauer and R.W.D., unpublished data).	gene_phenotype
68094	2	333043	5	NULL	NULL	0	NULL	SLZ1	GP		is required for					sporulation	Process	efficient			NULL		0	NULL	NULL	NULL	gw60_pnas_99_21_13431_s_133	12370439	Indeed, two of these ( YDR374C and  SLZ1) have recently been shown in genome-wide deletion analysis to be required for efficient sporulation (A. Deutschbauer and R.W.D., unpublished data).	gene_phenotype
68095	1	333044	5	NULL	NULL	NULL	NULL	MAM1	GP		is					monopolar microtubule attachment during meiosis I	GP				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_7_1155_s_45	11163190	This paper concentrates on the role of just one  of these, a gene called  MAM1 ( monopolar microtubule  attachment during  meiosis I, ORF: YER106W), whose deletion  has no effect on vegetative growth but has extraordinary consequences during meiosis.	gene_phenotype
68096	2	333044	5	NULL	NULL	0	NULL	MAM1 gene	GP	deletion of	does not effect			YER106W	ORF	vegetative growth	Process				NULL		0	NULL	NULL	NULL	gw60_cell_103_7_1155_s_45	11163190	This paper concentrates on the role of just one  of these, a gene called  MAM1 ( monopolar microtubule  attachment during  meiosis I, ORF: YER106W), whose deletion  has no effect on vegetative growth but has extraordinary consequences during meiosis.	gene_phenotype
68097	3	333044	5	NULL	NULL	NULL	NULL	MAM1 gene	GP	deletion of	effects		extraordinary	YER106W	ORF	meiosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_103_7_1155_s_45	11163190	This paper concentrates on the role of just one  of these, a gene called  MAM1 ( monopolar microtubule  attachment during  meiosis I, ORF: YER106W), whose deletion  has no effect on vegetative growth but has extraordinary consequences during meiosis.	gene_phenotype
68098	1	333045	5	NULL	NULL	0	NULL	MAM1	GP		is necessary for			YER106W		sister kinetochores	Chromosome	monopolar attachment of			NULL		0	NULL	NULL	NULL	gw60_currbiol_11_13_1001_s_141	11470404	One of these ( YER106W, which we called  MAM1) has been analyzed in detail and been shown to be necessary for monopolar attachment of sister kinetochores during meiosis I  [4  .	gene_phenotype
68099	2	333045	5	NULL	NULL	0	NULL	statement 1	Process		occurs during					meiosis	Process				NULL		0	NULL	NULL	NULL	gw60_currbiol_11_13_1001_s_141	11470404	One of these ( YER106W, which we called  MAM1) has been analyzed in detail and been shown to be necessary for monopolar attachment of sister kinetochores during meiosis I  [4  .	gene_phenotype
68100	1	333046	5	NULL	NULL	0	NULL	HOP2 gene	GP	upregulated	is involved in					meiosis	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68101	2	333046	5	NULL	NULL	0	NULL	HOP2 gene	GP	upregulated	is involved in					sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68102	3	333046	5	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68103	4	333046	5	NULL	NULL	0	NULL	IME2 gene	GP	upregulated	is involved in					meiosis	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68104	5	333046	5	NULL	NULL	0	NULL	IME2 gene	GP	upregulated	is involved in					sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68105	6	333046	5	NULL	NULL	0	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68106	7	333046	5	NULL	NULL	0	NULL	REC102 gene	GP	upregulated	is involved in					meiosis	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68107	8	333046	5	NULL	NULL	0	NULL	REC102 gene	GP	upregulated	is involved in					sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68108	9	333046	5	NULL	NULL	0	NULL	statement 7	Process		is an alternative to					statement 8	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68109	10	333046	5	NULL	NULL	0	NULL	REC104 gene	GP	upregulated	is involved in					meiosis	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68110	11	333046	5	NULL	NULL	0	NULL	REC104 gene	GP	upregulated	is involved in					sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68111	12	333046	5	NULL	NULL	0	NULL	statement 10	Process		is an alternative to					statement 11	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68112	13	333046	5	NULL	NULL	0	NULL	RED1 gene	GP	upregulated	is involved in					meiosis	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68113	14	333046	5	NULL	NULL	0	NULL	RED1 gene	GP	upregulated	is involved in					sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68114	15	333046	5	NULL	NULL	0	NULL	statement 13	Process		is an alternative to					statement 12	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68115	16	333046	5	NULL	NULL	0	NULL	SLZ1 gene	GP	upregulated	is involved in					meiosis	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68116	17	333046	5	NULL	NULL	0	NULL	SLZ1 gene	GP	upregulated	is involved in					sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68117	18	333046	5	NULL	NULL	0	NULL	statement 16	Process		is an alternative to					statement 17	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68118	19	333046	5	NULL	NULL	0	NULL	SPO13 gene	GP	upregulated	is involved in					meiosis	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68119	20	333046	5	NULL	NULL	0	NULL	SPO13 gene	GP	upregulated	is involved in					sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68120	21	333046	5	NULL	NULL	0	NULL	statement 19	Process		is an alternative to					statement 20	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68121	22	333046	5	NULL	NULL	0	NULL	SPO16 gene	GP	upregulated	is involved in					meiosis	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68122	23	333046	5	NULL	NULL	0	NULL	SPO16 gene	GP	upregulated	is involved in					sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68123	24	333046	5	NULL	NULL	0	NULL	statement 22	Process		is an alternative to					statement 23	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68124	25	333046	5	NULL	NULL	0	NULL	SPR1 gene	GP	upregulated	is involved in					meiosis	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68125	26	333046	5	NULL	NULL	0	NULL	SPR1 gene	GP	upregulated	is involved in					sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68126	27	333046	5	NULL	NULL	0	NULL	statement 25	Process		is an alternative to					statement 26	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68127	28	333046	5	NULL	NULL	0	NULL	YER179W	AminoAcid	upregulated	is involved in					meiosis	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68128	29	333046	5	NULL	NULL	0	NULL	YER179W	AminoAcid	upregulated	is involved in					sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68129	30	333046	5	NULL	NULL	0	NULL	statement 28	Process		is an alternative to					statement 29	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68130	31	333046	5	NULL	NULL	0	NULL	ZIP1 gene	GP	upregulated	is involved in					meiosis	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68131	32	333046	5	NULL	NULL	0	NULL	ZIP1 gene	GP	upregulated	is involved in					sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68132	33	333046	5	NULL	NULL	0	NULL	statement 31	Process		is an alternative to					statement 32	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_1_159_s_112	14711638	These upregulated genes included 11 that were involved in meiosis or sporulation ( HOP2,  IME2,  REC102,  REC104,  RED1,  SLZ1,  SPO13,  SPO16,  SPR1,  YER179W, and  ZIP1).	gene_phenotype
68133	1	333048	5	NULL	NULL	0	NULL	YNL124W	AminoAcid		is involved in					RNA processing	Process				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_3_633_s_87	12565826	In  a similar example, we suggest that YNL124W and YIL104C are involved in RNA processing  and modification ( Fig. 4B).	gene_phenotype
68134	2	333048	5	NULL	NULL	0	NULL	YNL124W	AminoAcid		is involved in					RNA modification	Process				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_3_633_s_87	12565826	In  a similar example, we suggest that YNL124W and YIL104C are involved in RNA processing  and modification ( Fig. 4B).	gene_phenotype
68135	3	333048	5	NULL	NULL	0	NULL	YIL104C	AminoAcid		is involved in					RNA processing	Process				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_3_633_s_87	12565826	In  a similar example, we suggest that YNL124W and YIL104C are involved in RNA processing  and modification ( Fig. 4B).	gene_phenotype
68136	4	333048	5	NULL	NULL	0	NULL	YIL104C	AminoAcid		is involved in					RNA modification	Process				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_301_3_633_s_87	12565826	In  a similar example, we suggest that YNL124W and YIL104C are involved in RNA processing  and modification ( Fig. 4B).	gene_phenotype
68137	1	333049	5	NULL	NULL	NULL	NULL	taurocholate	Chemical		is translocated across					vacuolar membranes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_febslett_520_1_63_s_20	12044871	The Ybt1p/Bat1p ( YLL048c) transporter translocates taurocholate and other bile acids across vacuolar membranes [  29].	gene_phenotype
68138	2	333049	5	NULL	NULL	0	NULL	bile acids	Chemical		is translocated across					vacuolar membranes	CellComponent				NULL		0	NULL	NULL	NULL	gw60_febslett_520_1_63_s_20	12044871	The Ybt1p/Bat1p ( YLL048c) transporter translocates taurocholate and other bile acids across vacuolar membranes [  29].	gene_phenotype
68139	3	333049	5	NULL	NULL	0	NULL	Ybt1p/Bat1p transporter	GP		is required for			YLL048c		statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_520_1_63_s_20	12044871	The Ybt1p/Bat1p ( YLL048c) transporter translocates taurocholate and other bile acids across vacuolar membranes [  29].	gene_phenotype
68140	4	333049	5	NULL	NULL	0	NULL	Ybt1p/Bat1p transporter	GP		is required for			YLL048c		statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_520_1_63_s_20	12044871	The Ybt1p/Bat1p ( YLL048c) transporter translocates taurocholate and other bile acids across vacuolar membranes [  29].	gene_phenotype
68141	1	333050	5	NULL	NULL	NULL	NULL	PCH2	GP	splicing efficiency of	is similar to			YBR186W				splicing efficiency of	YDL115C		NULL	vegetative diploids	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_205	10734188	Five other new introns in meiotic genes we have tested (YBR186W/ PCH2, YDL115C, YLR093C/ NYV1 YLR211C and YNL012W/ SPO1; see Table  1) all appear to have similar splicing efficiencies in vegetative and sporulating diploids (data not shown), suggesting that their splicing is not selectively activated during meiosis.	gene_phenotype
68142	2	333050	5	NULL	NULL	0	NULL	PCH2	GP	splicing efficiency of	is similar to			YBR186W				splicing efficiency of	YDL115C		NULL	sporulating diploids	0	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_205	10734188	Five other new introns in meiotic genes we have tested (YBR186W/ PCH2, YDL115C, YLR093C/ NYV1 YLR211C and YNL012W/ SPO1; see Table  1) all appear to have similar splicing efficiencies in vegetative and sporulating diploids (data not shown), suggesting that their splicing is not selectively activated during meiosis.	gene_phenotype
68143	3	333050	5	NULL	NULL	0	NULL	NYV1	GP	splicing efficiency of	is similar to			YLR093C				splicing efficiency of	YLR211C		NULL	vegetative diploids	0	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_205	10734188	Five other new introns in meiotic genes we have tested (YBR186W/ PCH2, YDL115C, YLR093C/ NYV1 YLR211C and YNL012W/ SPO1; see Table  1) all appear to have similar splicing efficiencies in vegetative and sporulating diploids (data not shown), suggesting that their splicing is not selectively activated during meiosis.	gene_phenotype
68144	4	333050	5	NULL	NULL	NULL	NULL	NYV1	GP	splicing efficiency of	is similar to			YLR093C				splicing efficiency of	YLR211C		NULL	sporulating diploids	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_205	10734188	Five other new introns in meiotic genes we have tested (YBR186W/ PCH2, YDL115C, YLR093C/ NYV1 YLR211C and YNL012W/ SPO1; see Table  1) all appear to have similar splicing efficiencies in vegetative and sporulating diploids (data not shown), suggesting that their splicing is not selectively activated during meiosis.	gene_phenotype
68145	5	333050	5	NULL	NULL	0	NULL	PCH2	GP	splicing efficiency of	is similar to			YBR186W		NYV1	GP	splicing efficiency of	YLR093C		NULL	vegetative diploids	0	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_205	10734188	Five other new introns in meiotic genes we have tested (YBR186W/ PCH2, YDL115C, YLR093C/ NYV1 YLR211C and YNL012W/ SPO1; see Table  1) all appear to have similar splicing efficiencies in vegetative and sporulating diploids (data not shown), suggesting that their splicing is not selectively activated during meiosis.	gene_phenotype
68146	6	333050	5	NULL	NULL	0	NULL	PCH2	GP	splicing efficiency of	is similar to			YBR186W		NYV1	GP	splicing efficiency of	YLR093C		NULL	sporulating diploids	0	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_205	10734188	Five other new introns in meiotic genes we have tested (YBR186W/ PCH2, YDL115C, YLR093C/ NYV1 YLR211C and YNL012W/ SPO1; see Table  1) all appear to have similar splicing efficiencies in vegetative and sporulating diploids (data not shown), suggesting that their splicing is not selectively activated during meiosis.	gene_phenotype
68147	7	333050	5	NULL	NULL	NULL	NULL	PCH2	GP	splicing efficiency of	is similar to			YBR186W		SPO1	GP	splicing efficiency of	YNL012W		NULL	vegetative diploids	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_205	10734188	Five other new introns in meiotic genes we have tested (YBR186W/ PCH2, YDL115C, YLR093C/ NYV1 YLR211C and YNL012W/ SPO1; see Table  1) all appear to have similar splicing efficiencies in vegetative and sporulating diploids (data not shown), suggesting that their splicing is not selectively activated during meiosis.	gene_phenotype
68148	8	333050	5	NULL	NULL	NULL	NULL	PCH2	GP	splicing efficiency of	is similar to			YBR186W		SPO1	GP	splicing efficiency of	YNL012W		NULL	sporulating diploids	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_205	10734188	Five other new introns in meiotic genes we have tested (YBR186W/ PCH2, YDL115C, YLR093C/ NYV1 YLR211C and YNL012W/ SPO1; see Table  1) all appear to have similar splicing efficiencies in vegetative and sporulating diploids (data not shown), suggesting that their splicing is not selectively activated during meiosis.	gene_phenotype
68250	1	333051	5	NULL	NULL	0	NULL	YLR127c	NucleicAcid		is a type of					ORF	NucleicAcid				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_yeast_16_15_11054824_s_4	11054824	Two ORFs, YLR127c and YLR129w, are essential for viability,  whereas no growth phenotype could be detected following deletion of YLR124w,  YLR125w, YLR126c or YLR128w.	gene_phenotype
68251	2	333051	5	NULL	NULL	0	NULL	YLR129w	NucleicAcid		is a type of					ORF	NucleicAcid				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_yeast_16_15_11054824_s_4	11054824	Two ORFs, YLR127c and YLR129w, are essential for viability,  whereas no growth phenotype could be detected following deletion of YLR124w,  YLR125w, YLR126c or YLR128w.	gene_phenotype
68252	3	333051	5	NULL	NULL	0	NULL	YLR127c	NucleicAcid		is essential for					viability	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_yeast_16_15_11054824_s_4	11054824	Two ORFs, YLR127c and YLR129w, are essential for viability,  whereas no growth phenotype could be detected following deletion of YLR124w,  YLR125w, YLR126c or YLR128w.	gene_phenotype
68253	4	333051	5	NULL	NULL	0	NULL	YLR129w	NucleicAcid		is essential for					viability	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_yeast_16_15_11054824_s_4	11054824	Two ORFs, YLR127c and YLR129w, are essential for viability,  whereas no growth phenotype could be detected following deletion of YLR124w,  YLR125w, YLR126c or YLR128w.	gene_phenotype
68254	5	333051	5	NULL	NULL	0	NULL	YLR124w	NucleicAcid	deletion of	leads to					growth phenotype		absence of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_yeast_16_15_11054824_s_4	11054824	Two ORFs, YLR127c and YLR129w, are essential for viability,  whereas no growth phenotype could be detected following deletion of YLR124w,  YLR125w, YLR126c or YLR128w.	gene_phenotype
68255	6	333051	5	NULL	NULL	0	NULL	YLR125w	NucleicAcid	deletion of	leads to					growth phenotype		absence of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_yeast_16_15_11054824_s_4	11054824	Two ORFs, YLR127c and YLR129w, are essential for viability,  whereas no growth phenotype could be detected following deletion of YLR124w,  YLR125w, YLR126c or YLR128w.	gene_phenotype
68256	7	333051	5	NULL	NULL	0	NULL	YLR126c	NucleicAcid	deletion of	leads to					growth phenotype		absence of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_yeast_16_15_11054824_s_4	11054824	Two ORFs, YLR127c and YLR129w, are essential for viability,  whereas no growth phenotype could be detected following deletion of YLR124w,  YLR125w, YLR126c or YLR128w.	gene_phenotype
68257	8	333051	5	NULL	NULL	0	NULL	YLR128w	NucleicAcid	deletion of	leads to					growth phenotype		absence of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_yeast_16_15_11054824_s_4	11054824	Two ORFs, YLR127c and YLR129w, are essential for viability,  whereas no growth phenotype could be detected following deletion of YLR124w,  YLR125w, YLR126c or YLR128w.	gene_phenotype
68258	1	333053	5	NULL	NULL	0	NULL	YMR101c	NucleicAcid		is a type of					open reading frame	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_471_s_204	9858571	This DNA fragment contained a single open reading frame (YMR101c) encoding a protein of 343 amino acids and was able to complement the temperature-sensitive growth of the  rer2 mutant on a single-copy plasmid.	gene_phenotype
68259	2	333053	5	NULL	NULL	0	NULL	YMR101c	NucleicAcid		encodes					protein of 343 amino acids	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_471_s_204	9858571	This DNA fragment contained a single open reading frame (YMR101c) encoding a protein of 343 amino acids and was able to complement the temperature-sensitive growth of the  rer2 mutant on a single-copy plasmid.	gene_phenotype
68260	3	333053	5	NULL	NULL	NULL	NULL	rer2	GP	mutant;;growth of	is sensitive to					temperature					NULL	single-copy plasmid	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_471_s_204	9858571	This DNA fragment contained a single open reading frame (YMR101c) encoding a protein of 343 amino acids and was able to complement the temperature-sensitive growth of the  rer2 mutant on a single-copy plasmid.	gene_phenotype
68261	4	333053	5	NULL	NULL	0	NULL	YMR101c	NucleicAcid		complements					statement 3	Process				NULL	single-copy plasmid	0	NULL	NULL	NULL	gw60_molcellbiol_19_1_471_s_204	9858571	This DNA fragment contained a single open reading frame (YMR101c) encoding a protein of 343 amino acids and was able to complement the temperature-sensitive growth of the  rer2 mutant on a single-copy plasmid.	gene_phenotype
68262	1	333054	5	NULL	NULL	0	NULL	ADE17	GP		encodes					isozyme of 5-aminoimidazole-4-carboxamide ribonucleotide transformylase	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12369_s_114	11035792	The remaining four are  ADE17, which encodes an isozyme of 5-aminoimidazole-4-carboxamide ribonucleotide transformylase;  DLD3, encoding lactate dehydrogenase;  OAC1, encoding a mitochondrial oxaloacetate transport protein; and  YNL276C, an ORF with an unidentified function.	gene_phenotype
68263	2	333054	5	NULL	NULL	0	NULL	DLD3	GP		encodes					lactate dehydrogenase	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12369_s_114	11035792	The remaining four are  ADE17, which encodes an isozyme of 5-aminoimidazole-4-carboxamide ribonucleotide transformylase;  DLD3, encoding lactate dehydrogenase;  OAC1, encoding a mitochondrial oxaloacetate transport protein; and  YNL276C, an ORF with an unidentified function.	gene_phenotype
68264	3	333054	5	NULL	NULL	0	NULL	OAC1	GP		encodes					mitochondrial oxaloacetate transport protein	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12369_s_114	11035792	The remaining four are  ADE17, which encodes an isozyme of 5-aminoimidazole-4-carboxamide ribonucleotide transformylase;  DLD3, encoding lactate dehydrogenase;  OAC1, encoding a mitochondrial oxaloacetate transport protein; and  YNL276C, an ORF with an unidentified function.	gene_phenotype
68265	4	333054	5	NULL	NULL	0	NULL	YNL276C	NucleicAcid		is a type of					ORF	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12369_s_114	11035792	The remaining four are  ADE17, which encodes an isozyme of 5-aminoimidazole-4-carboxamide ribonucleotide transformylase;  DLD3, encoding lactate dehydrogenase;  OAC1, encoding a mitochondrial oxaloacetate transport protein; and  YNL276C, an ORF with an unidentified function.	gene_phenotype
68266	1	333055	5	NULL	NULL	0	NULL	Ume6-regulated genes	GP		is induced in		later			meiosis	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_99_21_13431_s_155	12370439	However, several Ume6-regulated genes (mostly of unknown function) appear to be induced later in meiosis (in expression clusters 5-7;  AUT7,  ECM8,  MPC54,  SMA1,  SLZ1,  SSA3,  YBR116C,  YKR005C,  YOL024W,  YOR338W,  YPR027C).	gene_phenotype
68267	1	333056	5	NULL	NULL	0	NULL	Letm1	GP		is transported across					inner mitochondrial membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_4_553_s_47	16476776	Letm1, Mdm38, and Ylh47 are transported across the inner mitochondrial membrane   The yeast proteins Mdm38 (Yol027c) and Ylh47 (Ypr125w) display significant sequence similarity to the human Letm1 protein ( Fig. 1 A), which has been implicated in WHS.	gene_phenotype
68268	2	333056	5	NULL	NULL	0	NULL	Mdm38	GP		is transported across					inner mitochondrial membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_4_553_s_47	16476776	Letm1, Mdm38, and Ylh47 are transported across the inner mitochondrial membrane   The yeast proteins Mdm38 (Yol027c) and Ylh47 (Ypr125w) display significant sequence similarity to the human Letm1 protein ( Fig. 1 A), which has been implicated in WHS.	gene_phenotype
68269	3	333056	5	NULL	NULL	0	NULL	Ylh47	GP		is transported across					inner mitochondrial membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_4_553_s_47	16476776	Letm1, Mdm38, and Ylh47 are transported across the inner mitochondrial membrane   The yeast proteins Mdm38 (Yol027c) and Ylh47 (Ypr125w) display significant sequence similarity to the human Letm1 protein ( Fig. 1 A), which has been implicated in WHS.	gene_phenotype
68273	4	333056	5	NULL	NULL	NULL	NULL	Mdm38 (Yol027c)	GP	sequence of	is similar to		significantly			Letm1 protein	GP	human;;sequence of			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_172_4_553_s_47	16476776	Letm1, Mdm38, and Ylh47 are transported across the inner mitochondrial membrane   The yeast proteins Mdm38 (Yol027c) and Ylh47 (Ypr125w) display significant sequence similarity to the human Letm1 protein ( Fig. 1 A), which has been implicated in WHS.	gene_phenotype
68276	5	333056	5	NULL	NULL	0	NULL	Ylh47 (Ypr125w)	GP	sequence of	is similar to		significantly			Letm1 protein	GP	human;;sequence of			NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_4_553_s_47	16476776	Letm1, Mdm38, and Ylh47 are transported across the inner mitochondrial membrane   The yeast proteins Mdm38 (Yol027c) and Ylh47 (Ypr125w) display significant sequence similarity to the human Letm1 protein ( Fig. 1 A), which has been implicated in WHS.	gene_phenotype
68277	6	333056	5	NULL	NULL	0	NULL	Letm1 protein	GP	human	is implicated in					WHS	MedicalFinding				NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_4_553_s_47	16476776	Letm1, Mdm38, and Ylh47 are transported across the inner mitochondrial membrane   The yeast proteins Mdm38 (Yol027c) and Ylh47 (Ypr125w) display significant sequence similarity to the human Letm1 protein ( Fig. 1 A), which has been implicated in WHS.	gene_phenotype
68278	1	333057	5	NULL	NULL	0	NULL	SGT1	GP		is required for					cell viability	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_4_1_21_s_33	10445024	SGT1 (YOR057w) encodes a 44.9 kDa protein with no obvious homology with other proteins in GenBank, and deletion analysis demonstrated that  SGT1 is required for cell viability (see Experimental Procedures).	gene_phenotype
68280	2	333057	5	NULL	NULL	0	NULL	YOR057w	NucleicAcid		is the locus name of					SGT1	GP				NULL		0	NULL	NULL	NULL	gw60_molcell_4_1_21_s_33	10445024	SGT1 (YOR057w) encodes a 44.9 kDa protein with no obvious homology with other proteins in GenBank, and deletion analysis demonstrated that  SGT1 is required for cell viability (see Experimental Procedures).	gene_phenotype
68281	3	333057	5	NULL	NULL	0	NULL	SGT1	GP		encodes					44.9 kDa protein	GP				NULL		0	NULL	NULL	NULL	gw60_molcell_4_1_21_s_33	10445024	SGT1 (YOR057w) encodes a 44.9 kDa protein with no obvious homology with other proteins in GenBank, and deletion analysis demonstrated that  SGT1 is required for cell viability (see Experimental Procedures).	gene_phenotype
68282	1	333058	5	NULL	NULL	0	NULL	YBT1	GP		is sensitive to		highly			methotrexate	Chemical				NULL		0	NULL	NULL	NULL	gw70_pnas_101_3_793_s_112	14718668	The  YBT1 and  YOR072w heterozygous deletion strains are highly sensitive to methotrexate, and both nonessential gene products may be involved in small molecule transport.	gene_phenotype
68283	2	333058	5	NULL	NULL	0	NULL	YBT1	GP		is involved in		may be			small molecule transport	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_3_793_s_112	14718668	The  YBT1 and  YOR072w heterozygous deletion strains are highly sensitive to methotrexate, and both nonessential gene products may be involved in small molecule transport.	gene_phenotype
68284	3	333058	5	NULL	NULL	0	NULL	YOR072w heterozygous deletion strains	NucleicAcid		is sensitive to		highly			methotrexate	Chemical				NULL		0	NULL	NULL	NULL	gw70_pnas_101_3_793_s_112	14718668	The  YBT1 and  YOR072w heterozygous deletion strains are highly sensitive to methotrexate, and both nonessential gene products may be involved in small molecule transport.	gene_phenotype
68285	4	333058	5	NULL	NULL	0	NULL	YOR072w heterozygous deletion strains	NucleicAcid		is involved in		may be			small molecule transport	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_3_793_s_112	14718668	The  YBT1 and  YOR072w heterozygous deletion strains are highly sensitive to methotrexate, and both nonessential gene products may be involved in small molecule transport.	gene_phenotype
68286	1	333059	5	NULL	NULL	0	NULL	YOR093C	NucleicAcid	S. cerevisiae 	is a paralog of					CPS1	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_100_10_5980_s_211	12730371	S. cerevisiae YOR093C (a paralog of  CPS1) expression was up-regulated by stress conditions such as heat shock or stationary growth ( ), but functional analysis showed that the yor093c null mutant is viable and did not show an altered phenotype ( ).	gene_phenotype
68287	2	333059	5	NULL	NULL	NULL	NULL	YOR093C	NucleicAcid	S. cerevisiae;;expression of	is up-regulated by					heat shock					NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_10_5980_s_211	12730371	S. cerevisiae YOR093C (a paralog of  CPS1) expression was up-regulated by stress conditions such as heat shock or stationary growth ( ), but functional analysis showed that the yor093c null mutant is viable and did not show an altered phenotype ( ).	gene_phenotype
68288	3	333059	5	NULL	NULL	0	NULL	YOR093C	NucleicAcid	S. cerevisiae;;expression of	is up-regulated by					stationary growth	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_100_10_5980_s_211	12730371	S. cerevisiae YOR093C (a paralog of  CPS1) expression was up-regulated by stress conditions such as heat shock or stationary growth ( ), but functional analysis showed that the yor093c null mutant is viable and did not show an altered phenotype ( ).	gene_phenotype
68289	4	333059	5	NULL	NULL	0	NULL	stationary growth	Process		is a type of					stress condition	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_100_10_5980_s_211	12730371	S. cerevisiae YOR093C (a paralog of  CPS1) expression was up-regulated by stress conditions such as heat shock or stationary growth ( ), but functional analysis showed that the yor093c null mutant is viable and did not show an altered phenotype ( ).	gene_phenotype
68290	5	333059	5	NULL	NULL	0	NULL	heat shock			is a type of					stress condition	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_100_10_5980_s_211	12730371	S. cerevisiae YOR093C (a paralog of  CPS1) expression was up-regulated by stress conditions such as heat shock or stationary growth ( ), but functional analysis showed that the yor093c null mutant is viable and did not show an altered phenotype ( ).	gene_phenotype
68291	6	333059	5	NULL	NULL	0	NULL	yor093c	NucleicAcid	null mutant	does not show					altered phenotype					NULL		0	NULL	NULL	NULL	gw70_pnas_100_10_5980_s_211	12730371	S. cerevisiae YOR093C (a paralog of  CPS1) expression was up-regulated by stress conditions such as heat shock or stationary growth ( ), but functional analysis showed that the yor093c null mutant is viable and did not show an altered phenotype ( ).	gene_phenotype
68292	1	333060	5	NULL	NULL	0	NULL	Leu9p protein	GP		is encoded by					YOR108w gene	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1089_s_135	11158296	However, to date this activity is attributed to a protein termed Leu9p (encoded by the gene  YOR108w), which exhibits high sequence similarity to Leu4p (W. Pelzer, unpublished data).	gene_phenotype
68293	2	333060	5	NULL	NULL	0	NULL	Leu9p protein	GP		is similar to		highly			Leu4p	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1089_s_135	11158296	However, to date this activity is attributed to a protein termed Leu9p (encoded by the gene  YOR108w), which exhibits high sequence similarity to Leu4p (W. Pelzer, unpublished data).	gene_phenotype
68294	1	333061	5	NULL	NULL	0	NULL	SSA4	GP		plays a role in					heat shock					NULL		0	NULL	NULL	NULL	gw60_nature_407_6802_395_s_179	11014197	Of the six transcripts that changed in wild-type cells after 30 min of 500 nM inhibitor treatment, three have no known function (YGR035C, YLR346C, YPL222W) and the others have roles in heat shock ( SSA4), osmotic stress response ( GRE2) and drug resistance ( YOR1).	gene_phenotype
68295	2	333061	5	NULL	NULL	0	NULL	GRE2	GP		plays a role in					osmotic stress response	Process				NULL		0	NULL	NULL	NULL	gw60_nature_407_6802_395_s_179	11014197	Of the six transcripts that changed in wild-type cells after 30 min of 500 nM inhibitor treatment, three have no known function (YGR035C, YLR346C, YPL222W) and the others have roles in heat shock ( SSA4), osmotic stress response ( GRE2) and drug resistance ( YOR1).	gene_phenotype
68296	3	333061	5	NULL	NULL	0	NULL	YOR1	GP		plays a role in					drug resistance	Process				NULL		0	NULL	NULL	NULL	gw60_nature_407_6802_395_s_179	11014197	Of the six transcripts that changed in wild-type cells after 30 min of 500 nM inhibitor treatment, three have no known function (YGR035C, YLR346C, YPL222W) and the others have roles in heat shock ( SSA4), osmotic stress response ( GRE2) and drug resistance ( YOR1).	gene_phenotype
68394	1	333062	5	NULL	NULL	NULL	NULL	YBL083C/ RHK1	GP		plays a role in		likely;;direct			germination	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_24_15530_s_243	12432101	Although a subset of our germination-defective strains derives from aneuploid spores or mutations in the parental diploid, we were successful in identifying genes,  YBL083C/ RHK1 and  PMA2, which likely play a direct role in germination.	gene_phenotype
68395	2	333062	5	NULL	NULL	0	NULL	PMA2	GP		plays a role in		likely;;direct			germination	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_99_24_15530_s_243	12432101	Although a subset of our germination-defective strains derives from aneuploid spores or mutations in the parental diploid, we were successful in identifying genes,  YBL083C/ RHK1 and  PMA2, which likely play a direct role in germination.	gene_phenotype
68403	1	333063	5	NULL	NULL	NULL	NULL	YSA1	GP		encodes					26-kDa ADP-sugar diphosphatase 2	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_16	10922370	YSA1 (ORF YBR111C) encodes a 26-kDa ADP-sugar diphosphatase 2 ( 1),  NPY1 (ORF YGL067W) encodes a 43.5- kDa NADH diphosphatase 3 ( 6),  PSU1 ( DCP2, ORF YNL118C) encodes a 109-kDa protein with an N-terminal nudix hydrolase domain whose enzymic activity is as yet undetermined but which may be involved in both transcriptional activation ( 7) and mRNA decapping ( 8), while  DDP1 (ORF YOR163W) encodes a 21.5-kDa enzyme that is a member of a unique subgroup of nudix hydrolases that can hydrolyze both diadenosine polyphosphates and non-nudix diphosphoinositol polyphosphate substrates ( 9,  10).	gene_phenotype
68569	2	333063	5	NULL	NULL	0	NULL	ORF YBR111C	NucleicAcid		is the locus name of					YSA1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_16	10922370	YSA1 (ORF YBR111C) encodes a 26-kDa ADP-sugar diphosphatase 2 ( 1),  NPY1 (ORF YGL067W) encodes a 43.5- kDa NADH diphosphatase 3 ( 6),  PSU1 ( DCP2, ORF YNL118C) encodes a 109-kDa protein with an N-terminal nudix hydrolase domain whose enzymic activity is as yet undetermined but which may be involved in both transcriptional activation ( 7) and mRNA decapping ( 8), while  DDP1 (ORF YOR163W) encodes a 21.5-kDa enzyme that is a member of a unique subgroup of nudix hydrolases that can hydrolyze both diadenosine polyphosphates and non-nudix diphosphoinositol polyphosphate substrates ( 9,  10).	gene_phenotype
68570	3	333063	5	NULL	NULL	0	NULL	ORF YGL067W	NucleicAcid		is the locus name of					NPY1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_16	10922370	YSA1 (ORF YBR111C) encodes a 26-kDa ADP-sugar diphosphatase 2 ( 1),  NPY1 (ORF YGL067W) encodes a 43.5- kDa NADH diphosphatase 3 ( 6),  PSU1 ( DCP2, ORF YNL118C) encodes a 109-kDa protein with an N-terminal nudix hydrolase domain whose enzymic activity is as yet undetermined but which may be involved in both transcriptional activation ( 7) and mRNA decapping ( 8), while  DDP1 (ORF YOR163W) encodes a 21.5-kDa enzyme that is a member of a unique subgroup of nudix hydrolases that can hydrolyze both diadenosine polyphosphates and non-nudix diphosphoinositol polyphosphate substrates ( 9,  10).	gene_phenotype
68571	4	333063	5	NULL	NULL	0	NULL	NPY1	GP		encodes					43.5- kDa NADH diphosphatase 3	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_16	10922370	YSA1 (ORF YBR111C) encodes a 26-kDa ADP-sugar diphosphatase 2 ( 1),  NPY1 (ORF YGL067W) encodes a 43.5- kDa NADH diphosphatase 3 ( 6),  PSU1 ( DCP2, ORF YNL118C) encodes a 109-kDa protein with an N-terminal nudix hydrolase domain whose enzymic activity is as yet undetermined but which may be involved in both transcriptional activation ( 7) and mRNA decapping ( 8), while  DDP1 (ORF YOR163W) encodes a 21.5-kDa enzyme that is a member of a unique subgroup of nudix hydrolases that can hydrolyze both diadenosine polyphosphates and non-nudix diphosphoinositol polyphosphate substrates ( 9,  10).	gene_phenotype
68572	5	333063	5	NULL	NULL	0	NULL	ORF YNL118C	NucleicAcid		is the locus name of					PSU1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_16	10922370	YSA1 (ORF YBR111C) encodes a 26-kDa ADP-sugar diphosphatase 2 ( 1),  NPY1 (ORF YGL067W) encodes a 43.5- kDa NADH diphosphatase 3 ( 6),  PSU1 ( DCP2, ORF YNL118C) encodes a 109-kDa protein with an N-terminal nudix hydrolase domain whose enzymic activity is as yet undetermined but which may be involved in both transcriptional activation ( 7) and mRNA decapping ( 8), while  DDP1 (ORF YOR163W) encodes a 21.5-kDa enzyme that is a member of a unique subgroup of nudix hydrolases that can hydrolyze both diadenosine polyphosphates and non-nudix diphosphoinositol polyphosphate substrates ( 9,  10).	gene_phenotype
68573	6	333063	5	NULL	NULL	0	NULL	PSU1	GP		is a synonym of					DCP2	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_16	10922370	YSA1 (ORF YBR111C) encodes a 26-kDa ADP-sugar diphosphatase 2 ( 1),  NPY1 (ORF YGL067W) encodes a 43.5- kDa NADH diphosphatase 3 ( 6),  PSU1 ( DCP2, ORF YNL118C) encodes a 109-kDa protein with an N-terminal nudix hydrolase domain whose enzymic activity is as yet undetermined but which may be involved in both transcriptional activation ( 7) and mRNA decapping ( 8), while  DDP1 (ORF YOR163W) encodes a 21.5-kDa enzyme that is a member of a unique subgroup of nudix hydrolases that can hydrolyze both diadenosine polyphosphates and non-nudix diphosphoinositol polyphosphate substrates ( 9,  10).	gene_phenotype
68574	7	333063	5	NULL	NULL	0	NULL	PSU1	GP		encodes					109-kDa protein	GP		N-terminal nudix hydrolase domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_16	10922370	YSA1 (ORF YBR111C) encodes a 26-kDa ADP-sugar diphosphatase 2 ( 1),  NPY1 (ORF YGL067W) encodes a 43.5- kDa NADH diphosphatase 3 ( 6),  PSU1 ( DCP2, ORF YNL118C) encodes a 109-kDa protein with an N-terminal nudix hydrolase domain whose enzymic activity is as yet undetermined but which may be involved in both transcriptional activation ( 7) and mRNA decapping ( 8), while  DDP1 (ORF YOR163W) encodes a 21.5-kDa enzyme that is a member of a unique subgroup of nudix hydrolases that can hydrolyze both diadenosine polyphosphates and non-nudix diphosphoinositol polyphosphate substrates ( 9,  10).	gene_phenotype
68575	8	333063	5	NULL	NULL	NULL	NULL	109-kDa protein	GP		is involved in		potentially	N-terminal nudix hydrolase domain		transcription	Process	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_16	10922370	YSA1 (ORF YBR111C) encodes a 26-kDa ADP-sugar diphosphatase 2 ( 1),  NPY1 (ORF YGL067W) encodes a 43.5- kDa NADH diphosphatase 3 ( 6),  PSU1 ( DCP2, ORF YNL118C) encodes a 109-kDa protein with an N-terminal nudix hydrolase domain whose enzymic activity is as yet undetermined but which may be involved in both transcriptional activation ( 7) and mRNA decapping ( 8), while  DDP1 (ORF YOR163W) encodes a 21.5-kDa enzyme that is a member of a unique subgroup of nudix hydrolases that can hydrolyze both diadenosine polyphosphates and non-nudix diphosphoinositol polyphosphate substrates ( 9,  10).	gene_phenotype
68576	9	333063	5	NULL	NULL	NULL	NULL	109-kDa protein	GP		is involved in		potentially	N-terminal nudix hydrolase domain		mRNA	NucleicAcid	decapping of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_16	10922370	YSA1 (ORF YBR111C) encodes a 26-kDa ADP-sugar diphosphatase 2 ( 1),  NPY1 (ORF YGL067W) encodes a 43.5- kDa NADH diphosphatase 3 ( 6),  PSU1 ( DCP2, ORF YNL118C) encodes a 109-kDa protein with an N-terminal nudix hydrolase domain whose enzymic activity is as yet undetermined but which may be involved in both transcriptional activation ( 7) and mRNA decapping ( 8), while  DDP1 (ORF YOR163W) encodes a 21.5-kDa enzyme that is a member of a unique subgroup of nudix hydrolases that can hydrolyze both diadenosine polyphosphates and non-nudix diphosphoinositol polyphosphate substrates ( 9,  10).	gene_phenotype
68577	10	333063	5	NULL	NULL	0	NULL	ORF YOR163W	NucleicAcid		is the locus name of					DDP1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_16	10922370	YSA1 (ORF YBR111C) encodes a 26-kDa ADP-sugar diphosphatase 2 ( 1),  NPY1 (ORF YGL067W) encodes a 43.5- kDa NADH diphosphatase 3 ( 6),  PSU1 ( DCP2, ORF YNL118C) encodes a 109-kDa protein with an N-terminal nudix hydrolase domain whose enzymic activity is as yet undetermined but which may be involved in both transcriptional activation ( 7) and mRNA decapping ( 8), while  DDP1 (ORF YOR163W) encodes a 21.5-kDa enzyme that is a member of a unique subgroup of nudix hydrolases that can hydrolyze both diadenosine polyphosphates and non-nudix diphosphoinositol polyphosphate substrates ( 9,  10).	gene_phenotype
68578	11	333063	5	NULL	NULL	0	NULL	DDP1	GP		encodes					21.5-kDa enzyme	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_16	10922370	YSA1 (ORF YBR111C) encodes a 26-kDa ADP-sugar diphosphatase 2 ( 1),  NPY1 (ORF YGL067W) encodes a 43.5- kDa NADH diphosphatase 3 ( 6),  PSU1 ( DCP2, ORF YNL118C) encodes a 109-kDa protein with an N-terminal nudix hydrolase domain whose enzymic activity is as yet undetermined but which may be involved in both transcriptional activation ( 7) and mRNA decapping ( 8), while  DDP1 (ORF YOR163W) encodes a 21.5-kDa enzyme that is a member of a unique subgroup of nudix hydrolases that can hydrolyze both diadenosine polyphosphates and non-nudix diphosphoinositol polyphosphate substrates ( 9,  10).	gene_phenotype
68580	12	333063	5	NULL	NULL	0	NULL	21.5-kDa enzyme	GP		is a member of					nudix hydrolases	GP	subgroup of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_16	10922370	YSA1 (ORF YBR111C) encodes a 26-kDa ADP-sugar diphosphatase 2 ( 1),  NPY1 (ORF YGL067W) encodes a 43.5- kDa NADH diphosphatase 3 ( 6),  PSU1 ( DCP2, ORF YNL118C) encodes a 109-kDa protein with an N-terminal nudix hydrolase domain whose enzymic activity is as yet undetermined but which may be involved in both transcriptional activation ( 7) and mRNA decapping ( 8), while  DDP1 (ORF YOR163W) encodes a 21.5-kDa enzyme that is a member of a unique subgroup of nudix hydrolases that can hydrolyze both diadenosine polyphosphates and non-nudix diphosphoinositol polyphosphate substrates ( 9,  10).	gene_phenotype
68581	13	333063	5	NULL	NULL	0	NULL	nudix hydrolases	GP		hydrolyzes					diadenosine polyphosphates	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_16	10922370	YSA1 (ORF YBR111C) encodes a 26-kDa ADP-sugar diphosphatase 2 ( 1),  NPY1 (ORF YGL067W) encodes a 43.5- kDa NADH diphosphatase 3 ( 6),  PSU1 ( DCP2, ORF YNL118C) encodes a 109-kDa protein with an N-terminal nudix hydrolase domain whose enzymic activity is as yet undetermined but which may be involved in both transcriptional activation ( 7) and mRNA decapping ( 8), while  DDP1 (ORF YOR163W) encodes a 21.5-kDa enzyme that is a member of a unique subgroup of nudix hydrolases that can hydrolyze both diadenosine polyphosphates and non-nudix diphosphoinositol polyphosphate substrates ( 9,  10).	gene_phenotype
68582	14	333063	5	NULL	NULL	0	NULL	nudix hydrolases	GP		hydrolyzes					non-nudix diphosphoinositol polyphosphate substrates	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_16	10922370	YSA1 (ORF YBR111C) encodes a 26-kDa ADP-sugar diphosphatase 2 ( 1),  NPY1 (ORF YGL067W) encodes a 43.5- kDa NADH diphosphatase 3 ( 6),  PSU1 ( DCP2, ORF YNL118C) encodes a 109-kDa protein with an N-terminal nudix hydrolase domain whose enzymic activity is as yet undetermined but which may be involved in both transcriptional activation ( 7) and mRNA decapping ( 8), while  DDP1 (ORF YOR163W) encodes a 21.5-kDa enzyme that is a member of a unique subgroup of nudix hydrolases that can hydrolyze both diadenosine polyphosphates and non-nudix diphosphoinositol polyphosphate substrates ( 9,  10).	gene_phenotype
68583	1	333068	5	NULL	NULL	NULL	NULL	GOD1	GP		is a synonym of					SWC4 gene	GP	budding yeast			NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_3_4_976_s_80	15302830	Within this group, 18 clones contained the  S. pombe homolog of the budding yeast gene  SWC4 (YGR002C; this gene has been also named  GOD1 and  EAF2 [ www.yeastgenome.	gene_phenotype
68584	2	333068	5	NULL	NULL	0	NULL	EAF2	GP		is a synonym of					SWC4 gene	GP	budding yeast			NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_3_4_976_s_80	15302830	Within this group, 18 clones contained the  S. pombe homolog of the budding yeast gene  SWC4 (YGR002C; this gene has been also named  GOD1 and  EAF2 [ www.yeastgenome.	gene_phenotype
68585	3	333068	5	NULL	NULL	0	NULL	YGR002C	NucleicAcid		is the locus name of					SWC4 gene	GP	budding yeast			NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_3_4_976_s_80	15302830	Within this group, 18 clones contained the  S. pombe homolog of the budding yeast gene  SWC4 (YGR002C; this gene has been also named  GOD1 and  EAF2 [ www.yeastgenome.	gene_phenotype
68586	1	333071	5	NULL	NULL	NULL	NULL	YIL073C	NucleicAcid		plays a role in		important			spore	Cell	viability of			NULL		NULL	NULL	NULL	NULL	gw60_nature_402_6760_413_s_132	10586881	In any case, our transposon-based approach is an effective means of identifying novel sporulation-induced genes; one gene identified in our screen is  YIL073C, which we found to be important for spore viability and synaptonemal complex formation.	gene_phenotype
68587	2	333071	5	NULL	NULL	0	NULL	YIL073C	NucleicAcid		plays a role in		important			synaptonemal complex	GP	fomation of			NULL		0	NULL	NULL	NULL	gw60_nature_402_6760_413_s_132	10586881	In any case, our transposon-based approach is an effective means of identifying novel sporulation-induced genes; one gene identified in our screen is  YIL073C, which we found to be important for spore viability and synaptonemal complex formation.	gene_phenotype
68588	1	333072	5	NULL	NULL	0	NULL	Afg3p	GP		plays a role in		may			mating	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_99_26_16893_s_172	12482955	YAL004W and  YJL107C are ORFs whose functions are not known; Afg3p, Bud14p, Dia2p, Erg28p, Hmg1p, Hmg2p, Rad6p, Sod1p, and Ste24p were not previously known to be associated with the pheromone-response pathway, but their annotations suggest they may play roles in mating (see SGD,  http://genome-www.	gene_phenotype
68589	2	333072	5	NULL	NULL	0	NULL	Bud14p	GP		plays a role in		may			mating	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_99_26_16893_s_172	12482955	YAL004W and  YJL107C are ORFs whose functions are not known; Afg3p, Bud14p, Dia2p, Erg28p, Hmg1p, Hmg2p, Rad6p, Sod1p, and Ste24p were not previously known to be associated with the pheromone-response pathway, but their annotations suggest they may play roles in mating (see SGD,  http://genome-www.	gene_phenotype
68590	3	333072	5	NULL	NULL	0	NULL	Dia2p	GP		plays a role in		may			mating	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_99_26_16893_s_172	12482955	YAL004W and  YJL107C are ORFs whose functions are not known; Afg3p, Bud14p, Dia2p, Erg28p, Hmg1p, Hmg2p, Rad6p, Sod1p, and Ste24p were not previously known to be associated with the pheromone-response pathway, but their annotations suggest they may play roles in mating (see SGD,  http://genome-www.	gene_phenotype
68591	4	333072	5	NULL	NULL	0	NULL	Erg28p	GP		plays a role in		may			mating	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_99_26_16893_s_172	12482955	YAL004W and  YJL107C are ORFs whose functions are not known; Afg3p, Bud14p, Dia2p, Erg28p, Hmg1p, Hmg2p, Rad6p, Sod1p, and Ste24p were not previously known to be associated with the pheromone-response pathway, but their annotations suggest they may play roles in mating (see SGD,  http://genome-www.	gene_phenotype
68592	5	333072	5	NULL	NULL	0	NULL	Hmg1p	GP		plays a role in		may			mating	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_99_26_16893_s_172	12482955	YAL004W and  YJL107C are ORFs whose functions are not known; Afg3p, Bud14p, Dia2p, Erg28p, Hmg1p, Hmg2p, Rad6p, Sod1p, and Ste24p were not previously known to be associated with the pheromone-response pathway, but their annotations suggest they may play roles in mating (see SGD,  http://genome-www.	gene_phenotype
68593	6	333072	5	NULL	NULL	0	NULL	Hmg2p	GP		plays a role in		may			mating	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_99_26_16893_s_172	12482955	YAL004W and  YJL107C are ORFs whose functions are not known; Afg3p, Bud14p, Dia2p, Erg28p, Hmg1p, Hmg2p, Rad6p, Sod1p, and Ste24p were not previously known to be associated with the pheromone-response pathway, but their annotations suggest they may play roles in mating (see SGD,  http://genome-www.	gene_phenotype
68594	7	333072	5	NULL	NULL	0	NULL	Rad6p	GP		plays a role in		may			mating	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_99_26_16893_s_172	12482955	YAL004W and  YJL107C are ORFs whose functions are not known; Afg3p, Bud14p, Dia2p, Erg28p, Hmg1p, Hmg2p, Rad6p, Sod1p, and Ste24p were not previously known to be associated with the pheromone-response pathway, but their annotations suggest they may play roles in mating (see SGD,  http://genome-www.	gene_phenotype
68595	8	333072	5	NULL	NULL	0	NULL	Sod1p	GP		plays a role in		may			mating	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_99_26_16893_s_172	12482955	YAL004W and  YJL107C are ORFs whose functions are not known; Afg3p, Bud14p, Dia2p, Erg28p, Hmg1p, Hmg2p, Rad6p, Sod1p, and Ste24p were not previously known to be associated with the pheromone-response pathway, but their annotations suggest they may play roles in mating (see SGD,  http://genome-www.	gene_phenotype
68596	9	333072	5	NULL	NULL	0	NULL	Ste24p	GP		plays a role in		may			mating	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_99_26_16893_s_172	12482955	YAL004W and  YJL107C are ORFs whose functions are not known; Afg3p, Bud14p, Dia2p, Erg28p, Hmg1p, Hmg2p, Rad6p, Sod1p, and Ste24p were not previously known to be associated with the pheromone-response pathway, but their annotations suggest they may play roles in mating (see SGD,  http://genome-www.	gene_phenotype
68597	1	333073	5	NULL	NULL	0	NULL	Rad26	GP		is purified from					chromatin	Chromosome				NULL		0	NULL	NULL	NULL	gw60_nature_415_6874_929_s_22	11859374	We found that the slower-migrating protein purified from chromatin was Rad26, whereas the faster-migrating protein was the product of the YKL054C ORF on budding yeast chromosome XI (predicted  Mr 83,900).	gene_phenotype
68598	2	333073	5	NULL	NULL	0	NULL	YKL054C ORF	NucleicAcid	budding yeast	is present in					chromosome XI	Chromosome				NULL		0	NULL	NULL	NULL	gw60_nature_415_6874_929_s_22	11859374	We found that the slower-migrating protein purified from chromatin was Rad26, whereas the faster-migrating protein was the product of the YKL054C ORF on budding yeast chromosome XI (predicted  Mr 83,900).	gene_phenotype
68599	1	333074	5	NULL	NULL	0	NULL	YLR135W	NucleicAcid		is the locus name of					SLX4	GP				NULL		0	NULL	NULL	NULL	gw60_genetics_154_3_1101_s_139	10757756	A strain that is null in both  SGS1 and  SLX4 (YLR135W) is inviable but can be maintained by a copy of  SGS1 on a  URA3-based plasmid.	gene_phenotype
68600	1	333075	5	NULL	NULL	0	NULL	YLR347c	NucleicAcid		is the locus name of					KAP95	GP				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_319_2_349_s_55	15178413	Another known gene  YLR347c ( KAP95) encodes a protein involved in nuclear transport [  28].	gene_phenotype
68601	2	333075	5	NULL	NULL	0	NULL	KAP95	GP		is involved in					nuclear transport	Process				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_319_2_349_s_55	15178413	Another known gene  YLR347c ( KAP95) encodes a protein involved in nuclear transport [  28].	gene_phenotype
68602	1	333076	5	NULL	NULL	0	NULL	Lem3p	GP		interacts with					KAP95	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_38_36041_s_272	12842877	The observation that Lem3p has been shown by high throughput mass spectrometric protein complex identification ( ) to interact with two proteins involved in nuclear import ( YLR347C/ KAP95 and  YJR132W/ NMD5) is consistent with a nuclear function.	gene_phenotype
68603	2	333076	5	NULL	NULL	0	NULL	Lem3p	GP		interacts with					NMD5	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_38_36041_s_272	12842877	The observation that Lem3p has been shown by high throughput mass spectrometric protein complex identification ( ) to interact with two proteins involved in nuclear import ( YLR347C/ KAP95 and  YJR132W/ NMD5) is consistent with a nuclear function.	gene_phenotype
68604	3	333076	5	NULL	NULL	0	NULL	YLR347C	NucleicAcid		is the locus name of					KAP95	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_38_36041_s_272	12842877	The observation that Lem3p has been shown by high throughput mass spectrometric protein complex identification ( ) to interact with two proteins involved in nuclear import ( YLR347C/ KAP95 and  YJR132W/ NMD5) is consistent with a nuclear function.	gene_phenotype
68605	4	333076	5	NULL	NULL	0	NULL	YJR132W	NucleicAcid		is the locus name of					NMD5	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_38_36041_s_272	12842877	The observation that Lem3p has been shown by high throughput mass spectrometric protein complex identification ( ) to interact with two proteins involved in nuclear import ( YLR347C/ KAP95 and  YJR132W/ NMD5) is consistent with a nuclear function.	gene_phenotype
68606	5	333076	5	NULL	NULL	0	NULL	KAP95	GP		is involved in					nuclear import	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_38_36041_s_272	12842877	The observation that Lem3p has been shown by high throughput mass spectrometric protein complex identification ( ) to interact with two proteins involved in nuclear import ( YLR347C/ KAP95 and  YJR132W/ NMD5) is consistent with a nuclear function.	gene_phenotype
68607	6	333076	5	NULL	NULL	0	NULL	NMD5	GP		is involved in					nuclear import	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_38_36041_s_272	12842877	The observation that Lem3p has been shown by high throughput mass spectrometric protein complex identification ( ) to interact with two proteins involved in nuclear import ( YLR347C/ KAP95 and  YJR132W/ NMD5) is consistent with a nuclear function.	gene_phenotype
68608	1	333078	5	NULL	NULL	0	NULL	dopamine transporter gene	GP	inactivation of	leads to					dopamine	Chemical	elevated;;extracellular			NULL	mice	0	NULL	NULL	NULL	gw70_pnas_100_19_11035_s_4	12958210	Here we document that mice with persistently elevated extracellular dopamine, resulting from inactivation of the dopamine transporter gene, sporadically develop severe symptoms of dyskinesia concomitant with apoptotic death of striatal dopamine-responsive gamma-aminobutyric acidergic neurons.	gene_phenotype
68609	2	333078	5	NULL	NULL	0	NULL	statement 1	Process		develops					dyskinesia	MedicalFinding	severe symptoms of			NULL		0	NULL	NULL	NULL	gw70_pnas_100_19_11035_s_4	12958210	Here we document that mice with persistently elevated extracellular dopamine, resulting from inactivation of the dopamine transporter gene, sporadically develop severe symptoms of dyskinesia concomitant with apoptotic death of striatal dopamine-responsive gamma-aminobutyric acidergic neurons.	gene_phenotype
68610	3	333078	5	NULL	NULL	0	NULL	statement 2	Process		is concomitant to					striatal dopamine-responsive gamma-aminobutyric acidergic neurons	Cell	apoptotic death of			NULL		0	NULL	NULL	NULL	gw70_pnas_100_19_11035_s_4	12958210	Here we document that mice with persistently elevated extracellular dopamine, resulting from inactivation of the dopamine transporter gene, sporadically develop severe symptoms of dyskinesia concomitant with apoptotic death of striatal dopamine-responsive gamma-aminobutyric acidergic neurons.	gene_phenotype
68611	1	333080	5	NULL	NULL	0	NULL	Rim15	GP		is a type of					yeast-specific kinase	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_24_13603_s_75	10570119	Rim15 is a yeast-specific kinase that is related to  Schizosaccharomyces pombe Cek1, and its similarity to budding yeast YNL161w places it as a distant member of the NDR family kinases.	gene_phenotype
68612	2	333080	5	NULL	NULL	0	NULL	Rim15	GP		is related to					Cek1	GP	Schizosaccharomyces pombe			NULL		0	NULL	NULL	NULL	gw60_pnas_96_24_13603_s_75	10570119	Rim15 is a yeast-specific kinase that is related to  Schizosaccharomyces pombe Cek1, and its similarity to budding yeast YNL161w places it as a distant member of the NDR family kinases.	gene_phenotype
68613	3	333080	5	NULL	NULL	0	NULL	Rim15	GP		is similar to					YNL161w	NucleicAcid	budding yeast			NULL		0	NULL	NULL	NULL	gw60_pnas_96_24_13603_s_75	10570119	Rim15 is a yeast-specific kinase that is related to  Schizosaccharomyces pombe Cek1, and its similarity to budding yeast YNL161w places it as a distant member of the NDR family kinases.	gene_phenotype
68614	4	333080	5	NULL	NULL	0	NULL	Rim15	GP		is a member of					NDR family kinases	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_24_13603_s_75	10570119	Rim15 is a yeast-specific kinase that is related to  Schizosaccharomyces pombe Cek1, and its similarity to budding yeast YNL161w places it as a distant member of the NDR family kinases.	gene_phenotype
69420	1	333082	5	NULL	NULL	0	NULL	gene product	GP	putative	is close to					l(3)S027714	NucleicAcid	insertion of			NULL		0	NULL	NULL	NULL	gw60_gene_246_1_157_s_208	10767537	BLASTX searches show that the putative gene product close to the  l(3)S027714 insertion is highly similar to  Xenopus XPMC2 (accession no. U10185), a cell cycle gene that can complement mitotic catastrophe mutations in yeast (  Su and Maller, 1995), and to a hypothetical exonuclease YOL080c of  Saccharomyces cerevisiae (accession no. Z74822).	gene_phenotype
69421	2	333082	5	NULL	NULL	0	NULL	statement 1	GP		is similar to		highly			XPMC2	GP	Xenopus			NULL		0	NULL	NULL	NULL	gw60_gene_246_1_157_s_208	10767537	BLASTX searches show that the putative gene product close to the  l(3)S027714 insertion is highly similar to  Xenopus XPMC2 (accession no. U10185), a cell cycle gene that can complement mitotic catastrophe mutations in yeast (  Su and Maller, 1995), and to a hypothetical exonuclease YOL080c of  Saccharomyces cerevisiae (accession no. Z74822).	gene_phenotype
69422	3	333082	5	NULL	NULL	0	NULL	XPMC2 gene	GP	Xenopus	is a type of					cell cycle gene	GP				NULL		0	NULL	NULL	NULL	gw60_gene_246_1_157_s_208	10767537	BLASTX searches show that the putative gene product close to the  l(3)S027714 insertion is highly similar to  Xenopus XPMC2 (accession no. U10185), a cell cycle gene that can complement mitotic catastrophe mutations in yeast (  Su and Maller, 1995), and to a hypothetical exonuclease YOL080c of  Saccharomyces cerevisiae (accession no. Z74822).	gene_phenotype
69423	4	333082	5	NULL	NULL	0	NULL	XPMC2	GP	Xenopus	complements					mitotic catastrophe mutations	Process				NULL	yeast	0	NULL	NULL	NULL	gw60_gene_246_1_157_s_208	10767537	BLASTX searches show that the putative gene product close to the  l(3)S027714 insertion is highly similar to  Xenopus XPMC2 (accession no. U10185), a cell cycle gene that can complement mitotic catastrophe mutations in yeast (  Su and Maller, 1995), and to a hypothetical exonuclease YOL080c of  Saccharomyces cerevisiae (accession no. Z74822).	gene_phenotype
69424	5	333082	5	NULL	NULL	0	NULL	statement 1	GP		is similar to					YOL080c	NucleicAcid	Saccharomyces cerevisiae			NULL		0	NULL	NULL	NULL	gw60_gene_246_1_157_s_208	10767537	BLASTX searches show that the putative gene product close to the  l(3)S027714 insertion is highly similar to  Xenopus XPMC2 (accession no. U10185), a cell cycle gene that can complement mitotic catastrophe mutations in yeast (  Su and Maller, 1995), and to a hypothetical exonuclease YOL080c of  Saccharomyces cerevisiae (accession no. Z74822).	gene_phenotype
69425	6	333082	5	NULL	NULL	0	NULL	YOL080c	NucleicAcid	Saccharomyces cerevisiae	is a type of					hypothetical exonuclease	GP				NULL		0	NULL	NULL	NULL	gw60_gene_246_1_157_s_208	10767537	BLASTX searches show that the putative gene product close to the  l(3)S027714 insertion is highly similar to  Xenopus XPMC2 (accession no. U10185), a cell cycle gene that can complement mitotic catastrophe mutations in yeast (  Su and Maller, 1995), and to a hypothetical exonuclease YOL080c of  Saccharomyces cerevisiae (accession no. Z74822).	gene_phenotype
68615	1	333083	5	NULL	NULL	NULL	NULL	RNAPII holoenzyme	GP	elongating 	is the product of					YPL086C ORF	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_1_123_s_26	10445034	Erdjument-Bromage et al. 1998  ) was used to identify the 60 kDa subunit of elongator and elongating RNAPII holoenzyme as the product of the YPL086C ORF on budding yeast chromosome XVI (predicted  Mr 63 kDa).	gene_phenotype
68616	2	333083	5	NULL	NULL	NULL	NULL	elongator	GP		is the product of			60 kDa subunit		YPL086C ORF	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcell_4_1_123_s_26	10445034	Erdjument-Bromage et al. 1998  ) was used to identify the 60 kDa subunit of elongator and elongating RNAPII holoenzyme as the product of the YPL086C ORF on budding yeast chromosome XVI (predicted  Mr 63 kDa).	gene_phenotype
68617	3	333083	5	NULL	NULL	0	NULL	YPL086C ORF	NucleicAcid		is present in					chromosome XVI	Chromosome	budding yeast			NULL		0	NULL	NULL	NULL	gw60_molcell_4_1_123_s_26	10445034	Erdjument-Bromage et al. 1998  ) was used to identify the 60 kDa subunit of elongator and elongating RNAPII holoenzyme as the product of the YPL086C ORF on budding yeast chromosome XVI (predicted  Mr 63 kDa).	gene_phenotype
68618	1	333084	5	NULL	NULL	0	NULL	YBR156C	NucleicAcid		is the locus name of					SLI15	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_7_1381_s_235	10385519	It has been reported previously that disruption of   YBR156C ( SLI15) leads to loss of cell viability ( 51).	gene_phenotype
68619	2	333084	5	NULL	NULL	0	NULL	SLI15	GP	disruption of	leads to					cell viability	Process	loss of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_145_7_1381_s_235	10385519	It has been reported previously that disruption of   YBR156C ( SLI15) leads to loss of cell viability ( 51).	gene_phenotype
68620	1	333086	5	NULL	NULL	0	NULL	YDR100W	NucleicAcid		plays a role in					vesicular transport	Process				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_5_1163_s_138	11861907	We found that cellular roles could be assigned to four other previously uncharacterized proteins in this way: YDR100W (vesicular transport/membrane fusion), YOR275C (vesicular transport), YIL151C (protein degradation) and SOH1 (Pol II transcription) (data not shown).	gene_phenotype
68621	2	333086	5	NULL	NULL	0	NULL	YDR100W 	NucleicAcid		plays a role in					membrane fusion	Process				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_5_1163_s_138	11861907	We found that cellular roles could be assigned to four other previously uncharacterized proteins in this way: YDR100W (vesicular transport/membrane fusion), YOR275C (vesicular transport), YIL151C (protein degradation) and SOH1 (Pol II transcription) (data not shown).	gene_phenotype
68623	3	333086	5	NULL	NULL	0	NULL	YOR275C	GP		plays a role in					vesicular transport	Process				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_5_1163_s_138	11861907	We found that cellular roles could be assigned to four other previously uncharacterized proteins in this way: YDR100W (vesicular transport/membrane fusion), YOR275C (vesicular transport), YIL151C (protein degradation) and SOH1 (Pol II transcription) (data not shown).	gene_phenotype
68625	4	333086	5	NULL	NULL	0	NULL	YIL151C	GP		plays a role in					protein degradation	Process				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_5_1163_s_138	11861907	We found that cellular roles could be assigned to four other previously uncharacterized proteins in this way: YDR100W (vesicular transport/membrane fusion), YOR275C (vesicular transport), YIL151C (protein degradation) and SOH1 (Pol II transcription) (data not shown).	gene_phenotype
68626	5	333086	5	NULL	NULL	0	NULL	SOH1	GP		plays a role in					Pol II transcription	Process				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_5_1163_s_138	11861907	We found that cellular roles could be assigned to four other previously uncharacterized proteins in this way: YDR100W (vesicular transport/membrane fusion), YOR275C (vesicular transport), YIL151C (protein degradation) and SOH1 (Pol II transcription) (data not shown).	gene_phenotype
68622	1	333087	5	NULL	NULL	0	NULL	Don1p	GP		is encoded by					ORF YDR273w	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_embo_19_14_3657_s_216	10899120	This protein, which we named Don1p (encoded by the ORF YDR273w), is expressed exclusively during meiosis.	gene_phenotype
68624	2	333087	5	NULL	NULL	0	NULL	Don1p	GP		is expressed during		exclusively			meiosis	Process				NULL		0	NULL	NULL	NULL	gw60_embo_19_14_3657_s_216	10899120	This protein, which we named Don1p (encoded by the ORF YDR273w), is expressed exclusively during meiosis.	gene_phenotype
68627	1	333088	5	NULL	NULL	0	NULL	YGR211w	NucleicAcid		is the locus name of					ZPR1 gene	GP	yeast			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_yeast_18_9_11427960_s_3	11427960	Sporulation and tetrad analysis showed that YGR211w,  recently identified as the yeast ZPR1 gene, is an essential gene.	gene_phenotype
68628	1	333089	5	NULL	NULL	0	NULL	YGR277C	NucleicAcid	yeast	is not essential for					viability	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_24_21431_s_168	11923312	The corresponding gene in yeast (YGR277C) is essential for viability, consistent with its expected functional role in the CoA biosynthetic pathway (Saccharomyces Genome Database).	gene_phenotype
68629	2	333089	5	NULL	NULL	0	NULL	YGR277C	NucleicAcid	yeast	plays a role in					CoA biosynthetic pathway	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_24_21431_s_168	11923312	The corresponding gene in yeast (YGR277C) is essential for viability, consistent with its expected functional role in the CoA biosynthetic pathway (Saccharomyces Genome Database).	gene_phenotype
68630	1	333090	5	NULL	NULL	0	NULL	Sl269	GP		complemented by					SPO7	GP				NULL		0	NULL	NULL	NULL	gw60_embo_17_22_6449_s_56	9822591	Sl269 was complemented by  SPO7 (DDBJ/EMBL/GenBank accession No. 349744; SGD accession No. YAL009w) and sl235 by a novel gene (DDBJ/EMBL/GenBank accession No. 500822; SGD accession No. YHR004c) designated  NEM1 (for  nuclear  envelope  morphology; see also below) (Figure  1A).	gene_phenotype
68631	2	333090	5	NULL	NULL	0	NULL	sl235	GP		complemented by					NEM1	GP				NULL		0	NULL	NULL	NULL	gw60_embo_17_22_6449_s_56	9822591	Sl269 was complemented by  SPO7 (DDBJ/EMBL/GenBank accession No. 349744; SGD accession No. YAL009w) and sl235 by a novel gene (DDBJ/EMBL/GenBank accession No. 500822; SGD accession No. YHR004c) designated  NEM1 (for  nuclear  envelope  morphology; see also below) (Figure  1A).	gene_phenotype
68632	3	333090	5	NULL	NULL	0	NULL	NEM1	GP		is					nuclear envelope morphology	GP				NULL		0	NULL	NULL	NULL	gw60_embo_17_22_6449_s_56	9822591	Sl269 was complemented by  SPO7 (DDBJ/EMBL/GenBank accession No. 349744; SGD accession No. YAL009w) and sl235 by a novel gene (DDBJ/EMBL/GenBank accession No. 500822; SGD accession No. YHR004c) designated  NEM1 (for  nuclear  envelope  morphology; see also below) (Figure  1A).	gene_phenotype
68633	1	333091	5	NULL	NULL	0	NULL	NES	AminoAcid		is					nuclear export signal	AminoAcid				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_12_4344_s_28	12773575	We and others have recently shown that the nuclear export signal (NES) for the large subunit is provided by the adapter protein Nmd3p (Yhr170wp).	gene_phenotype
68634	2	333091	5	NULL	NULL	0	NULL	large subunit	GP		is provided by			NES		Nmd3p	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_12_4344_s_28	12773575	We and others have recently shown that the nuclear export signal (NES) for the large subunit is provided by the adapter protein Nmd3p (Yhr170wp).	gene_phenotype
68635	3	333091	5	NULL	NULL	0	NULL	Nmd3p	GP		is a type of					adapter protein	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_12_4344_s_28	12773575	We and others have recently shown that the nuclear export signal (NES) for the large subunit is provided by the adapter protein Nmd3p (Yhr170wp).	gene_phenotype
68636	4	333091	5	NULL	NULL	0	NULL	Yhr170wp	NucleicAcid		is the locus name of					Nmd3p	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_12_4344_s_28	12773575	We and others have recently shown that the nuclear export signal (NES) for the large subunit is provided by the adapter protein Nmd3p (Yhr170wp).	gene_phenotype
68637	1	333093	5	NULL	NULL	NULL	NULL	HUL4 gene	GP	complete disruption of;;yeast	leads to					haploid yeast strains	Cell	viable			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_342_s_9	9858558	In addition, we show that haploid yeast strains bearing complete disruptions of either of two other hect E3 genes of yeast, designated  HUL4 (YJR036C) and  HUL5 (YGL141W), are viable.	gene_phenotype
68638	2	333093	5	NULL	NULL	NULL	NULL	HUL5 gene	GP	complete disruption of;;yeast	leads to					haploid yeast strains	Cell	viable			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_1_342_s_9	9858558	In addition, we show that haploid yeast strains bearing complete disruptions of either of two other hect E3 genes of yeast, designated  HUL4 (YJR036C) and  HUL5 (YGL141W), are viable.	gene_phenotype
68639	3	333093	5	NULL	NULL	0	NULL	HUL4 gene	GP	yeast	is a type of					hect E3 gene		yeast			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_342_s_9	9858558	In addition, we show that haploid yeast strains bearing complete disruptions of either of two other hect E3 genes of yeast, designated  HUL4 (YJR036C) and  HUL5 (YGL141W), are viable.	gene_phenotype
68640	4	333093	5	NULL	NULL	0	NULL	HUL5 gene	GP	yeast	is a type of					hect E3 gene	GP	yeast			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_342_s_9	9858558	In addition, we show that haploid yeast strains bearing complete disruptions of either of two other hect E3 genes of yeast, designated  HUL4 (YJR036C) and  HUL5 (YGL141W), are viable.	gene_phenotype
68641	5	333093	5	NULL	NULL	0	NULL	YJR036C	NucleicAcid		is the locus name of					HUL4	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_342_s_9	9858558	In addition, we show that haploid yeast strains bearing complete disruptions of either of two other hect E3 genes of yeast, designated  HUL4 (YJR036C) and  HUL5 (YGL141W), are viable.	gene_phenotype
68642	6	333093	5	NULL	NULL	0	NULL	YGL141W	NucleicAcid		is the locus name of					HUL5	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_342_s_9	9858558	In addition, we show that haploid yeast strains bearing complete disruptions of either of two other hect E3 genes of yeast, designated  HUL4 (YJR036C) and  HUL5 (YGL141W), are viable.	gene_phenotype
68645	1	333094	5	NULL	NULL	0	NULL	YCR023c	NucleicAcid		is a homolog of					multidrug resistance protein	GP				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_280	9348664	Proteins with transport related functions are given in  Table 18 and comprise the multidrug resistance protein homologues YCR023c and YJR124c, the  cation/Cl  symporter homologue YBR235w, the Na+/H+ antiporter homologues YDR456w, YJL094c, and YLR318w ( NHA1), the proline/betaine/ -ketoglutarate permease homologue YKL217w ( JEN1), and the anion permease homologue YNL275w.	gene_phenotype
68646	2	333094	5	NULL	NULL	0	NULL	YCR023c	NucleicAcid		plays a role in					transport	Process				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_280	9348664	Proteins with transport related functions are given in  Table 18 and comprise the multidrug resistance protein homologues YCR023c and YJR124c, the  cation/Cl  symporter homologue YBR235w, the Na+/H+ antiporter homologues YDR456w, YJL094c, and YLR318w ( NHA1), the proline/betaine/ -ketoglutarate permease homologue YKL217w ( JEN1), and the anion permease homologue YNL275w.	gene_phenotype
68647	3	333094	5	NULL	NULL	0	NULL	YJR124c	NucleicAcid		is a homolog of					multidrug resistance protein	GP				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_280	9348664	Proteins with transport related functions are given in  Table 18 and comprise the multidrug resistance protein homologues YCR023c and YJR124c, the  cation/Cl  symporter homologue YBR235w, the Na+/H+ antiporter homologues YDR456w, YJL094c, and YLR318w ( NHA1), the proline/betaine/ -ketoglutarate permease homologue YKL217w ( JEN1), and the anion permease homologue YNL275w.	gene_phenotype
68648	4	333094	5	NULL	NULL	NULL	NULL	YJR124c	NucleicAcid		plays a role in					transport	Process				NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_280	9348664	Proteins with transport related functions are given in  Table 18 and comprise the multidrug resistance protein homologues YCR023c and YJR124c, the  cation/Cl  symporter homologue YBR235w, the Na+/H+ antiporter homologues YDR456w, YJL094c, and YLR318w ( NHA1), the proline/betaine/ -ketoglutarate permease homologue YKL217w ( JEN1), and the anion permease homologue YNL275w.	gene_phenotype
68649	5	333094	5	NULL	NULL	NULL	NULL	YBR235w	NucleicAcid		is a homolog of					cation/Cl symporter	GP				NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_280	9348664	Proteins with transport related functions are given in  Table 18 and comprise the multidrug resistance protein homologues YCR023c and YJR124c, the  cation/Cl  symporter homologue YBR235w, the Na+/H+ antiporter homologues YDR456w, YJL094c, and YLR318w ( NHA1), the proline/betaine/ -ketoglutarate permease homologue YKL217w ( JEN1), and the anion permease homologue YNL275w.	gene_phenotype
68650	6	333094	5	NULL	NULL	0	NULL	YBR235w	NucleicAcid		plays a role in					transport	Process				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_280	9348664	Proteins with transport related functions are given in  Table 18 and comprise the multidrug resistance protein homologues YCR023c and YJR124c, the  cation/Cl  symporter homologue YBR235w, the Na+/H+ antiporter homologues YDR456w, YJL094c, and YLR318w ( NHA1), the proline/betaine/ -ketoglutarate permease homologue YKL217w ( JEN1), and the anion permease homologue YNL275w.	gene_phenotype
68651	7	333094	5	NULL	NULL	0	NULL	YDR456w	NucleicAcid		is a homolog of					Na+/H+ antiporter	GP				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_280	9348664	Proteins with transport related functions are given in  Table 18 and comprise the multidrug resistance protein homologues YCR023c and YJR124c, the  cation/Cl  symporter homologue YBR235w, the Na+/H+ antiporter homologues YDR456w, YJL094c, and YLR318w ( NHA1), the proline/betaine/ -ketoglutarate permease homologue YKL217w ( JEN1), and the anion permease homologue YNL275w.	gene_phenotype
68659	8	333094	5	NULL	NULL	0	NULL	YDR456w	NucleicAcid		plays a role in					transport	Process				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_280	9348664	Proteins with transport related functions are given in  Table 18 and comprise the multidrug resistance protein homologues YCR023c and YJR124c, the  cation/Cl  symporter homologue YBR235w, the Na+/H+ antiporter homologues YDR456w, YJL094c, and YLR318w ( NHA1), the proline/betaine/ -ketoglutarate permease homologue YKL217w ( JEN1), and the anion permease homologue YNL275w.	gene_phenotype
68660	9	333094	5	NULL	NULL	0	NULL	YJL094c	NucleicAcid		is a homolog of					Na+/H+ antiporter	GP				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_280	9348664	Proteins with transport related functions are given in  Table 18 and comprise the multidrug resistance protein homologues YCR023c and YJR124c, the  cation/Cl  symporter homologue YBR235w, the Na+/H+ antiporter homologues YDR456w, YJL094c, and YLR318w ( NHA1), the proline/betaine/ -ketoglutarate permease homologue YKL217w ( JEN1), and the anion permease homologue YNL275w.	gene_phenotype
68661	10	333094	5	NULL	NULL	0	NULL	YJL094c	NucleicAcid		plays a role in					transport	Process				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_280	9348664	Proteins with transport related functions are given in  Table 18 and comprise the multidrug resistance protein homologues YCR023c and YJR124c, the  cation/Cl  symporter homologue YBR235w, the Na+/H+ antiporter homologues YDR456w, YJL094c, and YLR318w ( NHA1), the proline/betaine/ -ketoglutarate permease homologue YKL217w ( JEN1), and the anion permease homologue YNL275w.	gene_phenotype
68664	11	333094	5	NULL	NULL	0	NULL	YLR318w	NucleicAcid		is a homolog of					Na+/H+ antiporter	GP				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_280	9348664	Proteins with transport related functions are given in  Table 18 and comprise the multidrug resistance protein homologues YCR023c and YJR124c, the  cation/Cl  symporter homologue YBR235w, the Na+/H+ antiporter homologues YDR456w, YJL094c, and YLR318w ( NHA1), the proline/betaine/ -ketoglutarate permease homologue YKL217w ( JEN1), and the anion permease homologue YNL275w.	gene_phenotype
68665	12	333094	5	NULL	NULL	0	NULL	YLR318w	NucleicAcid		plays a role in					transport	Process				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_280	9348664	Proteins with transport related functions are given in  Table 18 and comprise the multidrug resistance protein homologues YCR023c and YJR124c, the  cation/Cl  symporter homologue YBR235w, the Na+/H+ antiporter homologues YDR456w, YJL094c, and YLR318w ( NHA1), the proline/betaine/ -ketoglutarate permease homologue YKL217w ( JEN1), and the anion permease homologue YNL275w.	gene_phenotype
68666	13	333094	5	NULL	NULL	0	NULL	YLR318w	NucleicAcid		is the locus name of					NHA1	GP				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_280	9348664	Proteins with transport related functions are given in  Table 18 and comprise the multidrug resistance protein homologues YCR023c and YJR124c, the  cation/Cl  symporter homologue YBR235w, the Na+/H+ antiporter homologues YDR456w, YJL094c, and YLR318w ( NHA1), the proline/betaine/ -ketoglutarate permease homologue YKL217w ( JEN1), and the anion permease homologue YNL275w.	gene_phenotype
68667	14	333094	5	NULL	NULL	0	NULL	YKL217w	NucleicAcid		is the locus name of					JEN1	GP				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_280	9348664	Proteins with transport related functions are given in  Table 18 and comprise the multidrug resistance protein homologues YCR023c and YJR124c, the  cation/Cl  symporter homologue YBR235w, the Na+/H+ antiporter homologues YDR456w, YJL094c, and YLR318w ( NHA1), the proline/betaine/ -ketoglutarate permease homologue YKL217w ( JEN1), and the anion permease homologue YNL275w.	gene_phenotype
68669	15	333094	5	NULL	NULL	0	NULL	YKL217w	NucleicAcid		is a homolog of					proline/betaine/ -ketoglutarate permease	GP				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_280	9348664	Proteins with transport related functions are given in  Table 18 and comprise the multidrug resistance protein homologues YCR023c and YJR124c, the  cation/Cl  symporter homologue YBR235w, the Na+/H+ antiporter homologues YDR456w, YJL094c, and YLR318w ( NHA1), the proline/betaine/ -ketoglutarate permease homologue YKL217w ( JEN1), and the anion permease homologue YNL275w.	gene_phenotype
68670	16	333094	5	NULL	NULL	0	NULL	YKL217w	NucleicAcid		plays a role in					transport	Process				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_280	9348664	Proteins with transport related functions are given in  Table 18 and comprise the multidrug resistance protein homologues YCR023c and YJR124c, the  cation/Cl  symporter homologue YBR235w, the Na+/H+ antiporter homologues YDR456w, YJL094c, and YLR318w ( NHA1), the proline/betaine/ -ketoglutarate permease homologue YKL217w ( JEN1), and the anion permease homologue YNL275w.	gene_phenotype
68672	17	333094	5	NULL	NULL	0	NULL	YNL275w	NucleicAcid		is a homolog of					anion permease	GP				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_280	9348664	Proteins with transport related functions are given in  Table 18 and comprise the multidrug resistance protein homologues YCR023c and YJR124c, the  cation/Cl  symporter homologue YBR235w, the Na+/H+ antiporter homologues YDR456w, YJL094c, and YLR318w ( NHA1), the proline/betaine/ -ketoglutarate permease homologue YKL217w ( JEN1), and the anion permease homologue YNL275w.	gene_phenotype
68674	18	333094	5	NULL	NULL	0	NULL	YNL275w	NucleicAcid		plays a role in					transport	Process				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_280	9348664	Proteins with transport related functions are given in  Table 18 and comprise the multidrug resistance protein homologues YCR023c and YJR124c, the  cation/Cl  symporter homologue YBR235w, the Na+/H+ antiporter homologues YDR456w, YJL094c, and YLR318w ( NHA1), the proline/betaine/ -ketoglutarate permease homologue YKL217w ( JEN1), and the anion permease homologue YNL275w.	gene_phenotype
68679	1	333095	5	NULL	NULL	0	NULL	POX1	GP		encodes					acyl-CoA oxidase	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_487_1_91_s_113	11152891	In five cases, at least two different genes exist in  C. tropicalis because two different RSTs are similar to the same portion of a  S. cerevisiae gene:  POX1 (encoding acyl-CoA oxidase),  CAR1 (arginase)  JEN1 (carboxylic acid transporter protein)  SSU1 (sulfite sensitive protein) and  YMR155w (unknown function).	gene_phenotype
68680	2	333095	5	NULL	NULL	0	NULL	CAR1	GP		encodes					arginase	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_487_1_91_s_113	11152891	In five cases, at least two different genes exist in  C. tropicalis because two different RSTs are similar to the same portion of a  S. cerevisiae gene:  POX1 (encoding acyl-CoA oxidase),  CAR1 (arginase)  JEN1 (carboxylic acid transporter protein)  SSU1 (sulfite sensitive protein) and  YMR155w (unknown function).	gene_phenotype
68681	3	333095	5	NULL	NULL	0	NULL	JEN1 	GP		encodes					carboxylic acid transporter protein	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_487_1_91_s_113	11152891	In five cases, at least two different genes exist in  C. tropicalis because two different RSTs are similar to the same portion of a  S. cerevisiae gene:  POX1 (encoding acyl-CoA oxidase),  CAR1 (arginase)  JEN1 (carboxylic acid transporter protein)  SSU1 (sulfite sensitive protein) and  YMR155w (unknown function).	gene_phenotype
68682	4	333095	5	NULL	NULL	0	NULL	SSU1	GP		encodes					sulfite sensitive protein	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_487_1_91_s_113	11152891	In five cases, at least two different genes exist in  C. tropicalis because two different RSTs are similar to the same portion of a  S. cerevisiae gene:  POX1 (encoding acyl-CoA oxidase),  CAR1 (arginase)  JEN1 (carboxylic acid transporter protein)  SSU1 (sulfite sensitive protein) and  YMR155w (unknown function).	gene_phenotype
68692	1	333097	5	NULL	NULL	0	NULL	delta yol100w	NucleicAcid	disruption of	causes					vegetative growth	Process	very slow			NULL	CEN.PK2 strain	0	NULL	NULL	NULL	abs-batch0680-0699_yeast_14_7_9639312_s_5	9639312	In contrast to the lack of phenotypic consequences of delta yol100w disruptions  in the FY1679 background, in the CEN.PK2 strain even a heterozygous disruption  of the same gene caused striking effects, very slow vegetative growth  and highly impaired sporulation.	gene_phenotype
68693	2	333097	5	NULL	NULL	NULL	NULL	delta yol100w	NucleicAcid	disruption of	causes					sporulation	Process	highly impaired			NULL	CEN.PK2 strain	NULL	NULL	NULL	NULL	abs-batch0680-0699_yeast_14_7_9639312_s_5	9639312	In contrast to the lack of phenotypic consequences of delta yol100w disruptions  in the FY1679 background, in the CEN.PK2 strain even a heterozygous disruption  of the same gene caused striking effects, very slow vegetative growth  and highly impaired sporulation.	gene_phenotype
68695	1	333098	5	NULL	NULL	0	NULL	YOR177c	NucleicAcid		is a synonym of					MPC54	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_99_10_6895_s_78	12011448	YOR177c has since been named  MPC54 and is a meiosis-specific component of the spindle pole body ( 16).	gene_phenotype
68697	2	333098	5	NULL	NULL	0	NULL	MPC54	GP		is a component of		meiosis-specific			spindle pole body	CellComponent				NULL		0	NULL	NULL	NULL	gw60_pnas_99_10_6895_s_78	12011448	YOR177c has since been named  MPC54 and is a meiosis-specific component of the spindle pole body ( 16).	gene_phenotype
68698	1	333100	5	NULL	NULL	0	NULL	YPL120w	NucleicAcid		encodes					Vps30p/Atg6p	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_203_s_101	16267277	YPL120w encodes Vps30p/Atg6p, a protein known to be involved in both vesicle-mediated protein traffic to the vacuole and autophagy (Tsukada and Ohsumi, 1993 ; Seaman  et al., 1997 ; Kihara  et al., 2001 ).	gene_phenotype
68699	2	333100	5	NULL	NULL	0	NULL	protein	GP		trafficked to					vacuole	CellComponent				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_203_s_101	16267277	YPL120w encodes Vps30p/Atg6p, a protein known to be involved in both vesicle-mediated protein traffic to the vacuole and autophagy (Tsukada and Ohsumi, 1993 ; Seaman  et al., 1997 ; Kihara  et al., 2001 ).	gene_phenotype
68700	3	333100	5	NULL	NULL	0	NULL	vesicle	CellComponent		mediates					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_203_s_101	16267277	YPL120w encodes Vps30p/Atg6p, a protein known to be involved in both vesicle-mediated protein traffic to the vacuole and autophagy (Tsukada and Ohsumi, 1993 ; Seaman  et al., 1997 ; Kihara  et al., 2001 ).	gene_phenotype
68701	4	333100	5	NULL	NULL	0	NULL	Vps30p/Atg6p protein	GP		is involved in					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_203_s_101	16267277	YPL120w encodes Vps30p/Atg6p, a protein known to be involved in both vesicle-mediated protein traffic to the vacuole and autophagy (Tsukada and Ohsumi, 1993 ; Seaman  et al., 1997 ; Kihara  et al., 2001 ).	gene_phenotype
68702	5	333100	5	NULL	NULL	0	NULL	Vps30p/Atg6p protein	GP		is involved in					autophagy	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_203_s_101	16267277	YPL120w encodes Vps30p/Atg6p, a protein known to be involved in both vesicle-mediated protein traffic to the vacuole and autophagy (Tsukada and Ohsumi, 1993 ; Seaman  et al., 1997 ; Kihara  et al., 2001 ).	gene_phenotype
68705	1	333101	5	NULL	NULL	0	NULL	YPR082c	NucleicAcid		is the locus name of					Dib1p	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_16_4535_s_187	10449419	Dib1p (YPR082c) comprises 142 amino acids and is an orthologue of the  Schizosaccharomyces pombe Dim1p, which previously has been assigned a role in cell cycle progression (Berry and Gould, 1997  ; Berry  et al., 1999  ).	gene_phenotype
68706	2	333101	5	NULL	NULL	0	NULL	Dib1p	GP		is an orthologue of 					Dim1p	GP	Schizosaccharomyces pombe			NULL		0	NULL	NULL	NULL	gw60_embo_18_16_4535_s_187	10449419	Dib1p (YPR082c) comprises 142 amino acids and is an orthologue of the  Schizosaccharomyces pombe Dim1p, which previously has been assigned a role in cell cycle progression (Berry and Gould, 1997  ; Berry  et al., 1999  ).	gene_phenotype
68707	3	333101	5	NULL	NULL	0	NULL	Dim1p	GP		plays a role in					cell cycle	Process	progression of			NULL		0	NULL	NULL	NULL	gw60_embo_18_16_4535_s_187	10449419	Dib1p (YPR082c) comprises 142 amino acids and is an orthologue of the  Schizosaccharomyces pombe Dim1p, which previously has been assigned a role in cell cycle progression (Berry and Gould, 1997  ; Berry  et al., 1999  ).	gene_phenotype
68717	1	333103	5	NULL	NULL	0	NULL	Kap95p	GP	yeast	is similar to					Kap123p	GP	yeast			NULL		0	NULL	NULL	NULL	gw60_cell_89_5_715_s_24	9182759	Comparisons  of the yeast database reveal significant similarities between Kap95p, Kap123p, and two other yeast  ORFs: Pse1p (YMR308c), originally characterized as a gene affecting protein secretion (Chow et al.,  1992   ), and another recently characterized karyopherin beta homolog, Kap104p (YBR017c) (Aitchison et al., 1996   ).	gene_phenotype
68718	2	333103	5	NULL	NULL	0	NULL	Pse1p	GP	yeast	is similar to					Kap104p	GP	yeast			NULL		0	NULL	NULL	NULL	gw60_cell_89_5_715_s_24	9182759	Comparisons  of the yeast database reveal significant similarities between Kap95p, Kap123p, and two other yeast  ORFs: Pse1p (YMR308c), originally characterized as a gene affecting protein secretion (Chow et al.,  1992   ), and another recently characterized karyopherin beta homolog, Kap104p (YBR017c) (Aitchison et al., 1996   ).	gene_phenotype
68719	3	333103	5	NULL	NULL	0	NULL	YMR308c	NucleicAcid	yeast	is the locus name of					Pse1p	GP	yeast			NULL		0	NULL	NULL	NULL	gw60_cell_89_5_715_s_24	9182759	Comparisons  of the yeast database reveal significant similarities between Kap95p, Kap123p, and two other yeast  ORFs: Pse1p (YMR308c), originally characterized as a gene affecting protein secretion (Chow et al.,  1992   ), and another recently characterized karyopherin beta homolog, Kap104p (YBR017c) (Aitchison et al., 1996   ).	gene_phenotype
68720	4	333103	5	NULL	NULL	0	NULL	Pse1p	GP	yeast	affects					protein secretion	Process				NULL		0	NULL	NULL	NULL	gw60_cell_89_5_715_s_24	9182759	Comparisons  of the yeast database reveal significant similarities between Kap95p, Kap123p, and two other yeast  ORFs: Pse1p (YMR308c), originally characterized as a gene affecting protein secretion (Chow et al.,  1992   ), and another recently characterized karyopherin beta homolog, Kap104p (YBR017c) (Aitchison et al., 1996   ).	gene_phenotype
68721	5	333103	5	NULL	NULL	0	NULL	YBR017c	NucleicAcid	yeast	is the locus name of					Kap104p	GP	yeast			NULL		0	NULL	NULL	NULL	gw60_cell_89_5_715_s_24	9182759	Comparisons  of the yeast database reveal significant similarities between Kap95p, Kap123p, and two other yeast  ORFs: Pse1p (YMR308c), originally characterized as a gene affecting protein secretion (Chow et al.,  1992   ), and another recently characterized karyopherin beta homolog, Kap104p (YBR017c) (Aitchison et al., 1996   ).	gene_phenotype
68722	6	333103	5	NULL	NULL	0	NULL	Kap104p	GP	yeast	is a homolog of					karyopherin beta	GP				NULL		0	NULL	NULL	NULL	gw60_cell_89_5_715_s_24	9182759	Comparisons  of the yeast database reveal significant similarities between Kap95p, Kap123p, and two other yeast  ORFs: Pse1p (YMR308c), originally characterized as a gene affecting protein secretion (Chow et al.,  1992   ), and another recently characterized karyopherin beta homolog, Kap104p (YBR017c) (Aitchison et al., 1996   ).	gene_phenotype
68735	1	333104	5	NULL	NULL	0	NULL	Nab2p protein	GP	yeast	interacts with					yTRN	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_4141_s_196	9632798	In this study, we show that Nab2p, a yeast protein selected in an exhaustive genomic two-hybrid screen performed with yTRN (also known as YBR017c or Kap104p), specifically interacts with this protein, and we have identified an  S. cerevisiae M9-like nuclear import sequence, NAB35.	gene_phenotype
68736	2	333104	5	NULL	NULL	0	NULL	yTRN	GP		is a synonym of					Kap104p	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_4141_s_196	9632798	In this study, we show that Nab2p, a yeast protein selected in an exhaustive genomic two-hybrid screen performed with yTRN (also known as YBR017c or Kap104p), specifically interacts with this protein, and we have identified an  S. cerevisiae M9-like nuclear import sequence, NAB35.	gene_phenotype
68737	3	333104	5	NULL	NULL	0	NULL	YBR017c	NucleicAcid		is the locus name of					yTRN	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_4141_s_196	9632798	In this study, we show that Nab2p, a yeast protein selected in an exhaustive genomic two-hybrid screen performed with yTRN (also known as YBR017c or Kap104p), specifically interacts with this protein, and we have identified an  S. cerevisiae M9-like nuclear import sequence, NAB35.	gene_phenotype
68738	4	333104	5	NULL	NULL	NULL	NULL	NAB35	AminoAcid	S. cerevisiae	is a type of					M9-like nuclear import sequence	AminoAcid	S. cerevisiae			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4141_s_196	9632798	In this study, we show that Nab2p, a yeast protein selected in an exhaustive genomic two-hybrid screen performed with yTRN (also known as YBR017c or Kap104p), specifically interacts with this protein, and we have identified an  S. cerevisiae M9-like nuclear import sequence, NAB35.	gene_phenotype
68739	5	333104	5	NULL	NULL	0	NULL	NAB35	AminoAcid		interacts with					yTRN	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_4141_s_196	9632798	In this study, we show that Nab2p, a yeast protein selected in an exhaustive genomic two-hybrid screen performed with yTRN (also known as YBR017c or Kap104p), specifically interacts with this protein, and we have identified an  S. cerevisiae M9-like nuclear import sequence, NAB35.	gene_phenotype
68740	1	333105	5	NULL	NULL	0	NULL	Yhl035cp	NucleicAcid		is a member of					multidrug resistance family/ATP-binding cassette transporter family	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_6_4450_s_214	14534306	Yhl035cp is member of the multidrug resistance family/ATP-binding cassette transporter family and is 64% identical to the yeast bile acid transporter Ybt1p, while the predicted Ybr047wp shows no appreciable similarity with other proteins.	gene_phenotype
68741	2	333105	5	NULL	NULL	NULL	NULL	Yhl035cp	NucleicAcid		is similar to					Ybt1p	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_6_4450_s_214	14534306	Yhl035cp is member of the multidrug resistance family/ATP-binding cassette transporter family and is 64% identical to the yeast bile acid transporter Ybt1p, while the predicted Ybr047wp shows no appreciable similarity with other proteins.	gene_phenotype
68742	3	333105	5	NULL	NULL	0	NULL	Ybt1p	GP	yeast	is a type of					bile acid transporter	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_6_4450_s_214	14534306	Yhl035cp is member of the multidrug resistance family/ATP-binding cassette transporter family and is 64% identical to the yeast bile acid transporter Ybt1p, while the predicted Ybr047wp shows no appreciable similarity with other proteins.	gene_phenotype
68743	1	333106	5	NULL	NULL	0	NULL	YBR152w	NucleicAcid		activates					suppressor	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_1_577_s_122	9858581	The YEplac112-7A subclone efficiently suppressed the ts192 temperature-sensitive growth defect, confirming that YBR152w contained the suppressor activity (Fig.  1).	gene_phenotype
68744	1	333108	5	NULL	NULL	0	NULL	csm1Delta/csm1Delta	GP		causes					sporulation defect	Process				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_exp-cell-res_294_2_15023545_s_8	15023545	Genetic experiments showed that the two-hybrid isolates  MGS1, CLF1, MCM3, 5, 7 (CDC47), and YDL089w, when overexpressed, partially  suppress the csm1Delta/csm1Delta sporulation defect.	gene_phenotype
68745	2	333108	5	NULL	NULL	0	NULL	MGS1	GP	overexpression of	suppress		partially			statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_exp-cell-res_294_2_15023545_s_8	15023545	Genetic experiments showed that the two-hybrid isolates  MGS1, CLF1, MCM3, 5, 7 (CDC47), and YDL089w, when overexpressed, partially  suppress the csm1Delta/csm1Delta sporulation defect.	gene_phenotype
68747	3	333108	5	NULL	NULL	0	NULL	CLF1	GP	overexpression of	suppress		partially			statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_exp-cell-res_294_2_15023545_s_8	15023545	Genetic experiments showed that the two-hybrid isolates  MGS1, CLF1, MCM3, 5, 7 (CDC47), and YDL089w, when overexpressed, partially  suppress the csm1Delta/csm1Delta sporulation defect.	gene_phenotype
68748	4	333108	5	NULL	NULL	0	NULL	MCM3	GP	overexpression of	suppress		partially			statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_exp-cell-res_294_2_15023545_s_8	15023545	Genetic experiments showed that the two-hybrid isolates  MGS1, CLF1, MCM3, 5, 7 (CDC47), and YDL089w, when overexpressed, partially  suppress the csm1Delta/csm1Delta sporulation defect.	gene_phenotype
68749	5	333108	5	NULL	NULL	0	NULL	CDC47	GP	overexpression of	suppress		partially			statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_exp-cell-res_294_2_15023545_s_8	15023545	Genetic experiments showed that the two-hybrid isolates  MGS1, CLF1, MCM3, 5, 7 (CDC47), and YDL089w, when overexpressed, partially  suppress the csm1Delta/csm1Delta sporulation defect.	gene_phenotype
68750	6	333108	5	NULL	NULL	0	NULL	YDL089w	GP	overexpression of	suppress		partially			statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_exp-cell-res_294_2_15023545_s_8	15023545	Genetic experiments showed that the two-hybrid isolates  MGS1, CLF1, MCM3, 5, 7 (CDC47), and YDL089w, when overexpressed, partially  suppress the csm1Delta/csm1Delta sporulation defect.	gene_phenotype
68751	1	333109	5	NULL	NULL	0	NULL	MFB1	GP	yeast	is a type of					mitochondrial morphology gene	GP	yeast			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_9_3756_s_3	16790494	Here, we report the identification of a new yeast mitochondrial morphology gene called  MFB1 (YDR219C).	gene_phenotype
68752	2	333109	5	NULL	NULL	0	NULL	YDR219C	NucleicAcid		is the locus name of					MFB1	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_9_3756_s_3	16790494	Here, we report the identification of a new yeast mitochondrial morphology gene called  MFB1 (YDR219C).	gene_phenotype
68753	1	333110	5	NULL	NULL	0	NULL	Pal1p	GP	budding yeast	is the product of					YDR348c gene	NucleicAcid	budding yeast			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_9_4124_s_390	15975911	As with the budding yeast YDR348c gene product, Pal1p is also detected at the cell division site.	gene_phenotype
68754	2	333110	5	NULL	NULL	NULL	NULL	Pal1p	GP	budding yeast	plays a role in					cell division	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_9_4124_s_390	15975911	As with the budding yeast YDR348c gene product, Pal1p is also detected at the cell division site.	gene_phenotype
68755	1	333111	5	NULL	NULL	0	NULL	Pal1p	GP		interacts with		physically			Sla2p	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_9_4124_s_153	15975911	Pal1p Physically Interacts and Shows Overlapping Localization with Sla2p   The budding yeast Pal1p related protein YDR348c has been shown to copurify with Sla2p in genome-scale proteomic analyses in  S. cerevisiae (Gavin  et al., 2002 ).	gene_phenotype
68756	2	333111	5	NULL	NULL	0	NULL	Pal1p	GP		colocalize with					Sla2p	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_9_4124_s_153	15975911	Pal1p Physically Interacts and Shows Overlapping Localization with Sla2p   The budding yeast Pal1p related protein YDR348c has been shown to copurify with Sla2p in genome-scale proteomic analyses in  S. cerevisiae (Gavin  et al., 2002 ).	gene_phenotype
68757	3	333111	5	NULL	NULL	0	NULL	YDR348c	GP		is a type of					Pal1p related protein	GP	budding yeast			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_9_4124_s_153	15975911	Pal1p Physically Interacts and Shows Overlapping Localization with Sla2p   The budding yeast Pal1p related protein YDR348c has been shown to copurify with Sla2p in genome-scale proteomic analyses in  S. cerevisiae (Gavin  et al., 2002 ).	gene_phenotype
68758	4	333111	5	NULL	NULL	0	NULL	YDR348c	GP		copurify with					Sla2p	GP				NULL	S. cerevisiae	0	NULL	NULL	NULL	gw70_molbiolcell_16_9_4124_s_153	15975911	Pal1p Physically Interacts and Shows Overlapping Localization with Sla2p   The budding yeast Pal1p related protein YDR348c has been shown to copurify with Sla2p in genome-scale proteomic analyses in  S. cerevisiae (Gavin  et al., 2002 ).	gene_phenotype
68759	1	333112	5	NULL	NULL	0	NULL	Pal1p protein	GP	novel	localizes to					growing cell ends	CellComponent				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_9_4124_s_387	15975911	Pal1p, a Novel Protein that Localizes to the Growing Cell Ends and the Division Site   We identified Pal1p as a relative of the budding yeast uncharacterized ORF, YDR348c, which has been shown to localize to the bud neck	gene_phenotype
68760	2	333112	5	NULL	NULL	0	NULL	Pal1p protein	GP	novel	localizes to					division site	CellComponent				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_9_4124_s_387	15975911	Pal1p, a Novel Protein that Localizes to the Growing Cell Ends and the Division Site   We identified Pal1p as a relative of the budding yeast uncharacterized ORF, YDR348c, which has been shown to localize to the bud neck	gene_phenotype
68761	3	333112	5	NULL	NULL	0	NULL	Pal1p protein	GP		is related to					ORF, YDR348c	NucleicAcid	budding yeast;;uncharacterized			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_9_4124_s_387	15975911	Pal1p, a Novel Protein that Localizes to the Growing Cell Ends and the Division Site   We identified Pal1p as a relative of the budding yeast uncharacterized ORF, YDR348c, which has been shown to localize to the bud neck	gene_phenotype
68762	4	333112	5	NULL	NULL	0	NULL	ORF, YDR348c	NucleicAcid	budding yeast;;uncharacterized	localizes to					bud neck	CellComponent				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_9_4124_s_387	15975911	Pal1p, a Novel Protein that Localizes to the Growing Cell Ends and the Division Site   We identified Pal1p as a relative of the budding yeast uncharacterized ORF, YDR348c, which has been shown to localize to the bud neck	gene_phenotype
68763	1	333113	5	NULL	NULL	0	NULL	Pal1p	GP		is a type of					membrane-associated protein	GP	novel			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_9_4124_s_102	15975911	A Novel Membrane-associated Protein, Pal1p, Localizes to the Sites of Active Growth  and Cell Division   We identified a gene,  pal1 ( pears  and  lemons; encoded by SPCP1E11.04c), based on its homology to a novel uncharacterized ORF from budding yeast (YDR348c).	gene_phenotype
68764	2	333113	5	NULL	NULL	0	NULL	Pal1p	GP		localizes to					growth sites	CellComponent	active			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_9_4124_s_102	15975911	A Novel Membrane-associated Protein, Pal1p, Localizes to the Sites of Active Growth  and Cell Division   We identified a gene,  pal1 ( pears  and  lemons; encoded by SPCP1E11.04c), based on its homology to a novel uncharacterized ORF from budding yeast (YDR348c).	gene_phenotype
68765	3	333113	5	NULL	NULL	0	NULL	Pal1p	GP		localizes to					cell division site	CellComponent				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_9_4124_s_102	15975911	A Novel Membrane-associated Protein, Pal1p, Localizes to the Sites of Active Growth  and Cell Division   We identified a gene,  pal1 ( pears  and  lemons; encoded by SPCP1E11.04c), based on its homology to a novel uncharacterized ORF from budding yeast (YDR348c).	gene_phenotype
68766	4	333113	5	NULL	NULL	0	NULL	pal1	GP		is a synonym of					pears and lemons	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_9_4124_s_102	15975911	A Novel Membrane-associated Protein, Pal1p, Localizes to the Sites of Active Growth  and Cell Division   We identified a gene,  pal1 ( pears  and  lemons; encoded by SPCP1E11.04c), based on its homology to a novel uncharacterized ORF from budding yeast (YDR348c).	gene_phenotype
68767	5	333113	5	NULL	NULL	NULL	NULL	pal1	GP		is encoded by					SPCP1E11.04c	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_9_4124_s_102	15975911	A Novel Membrane-associated Protein, Pal1p, Localizes to the Sites of Active Growth  and Cell Division   We identified a gene,  pal1 ( pears  and  lemons; encoded by SPCP1E11.04c), based on its homology to a novel uncharacterized ORF from budding yeast (YDR348c).	gene_phenotype
68768	6	333113	5	NULL	NULL	0	NULL	pal1 gene	GP		is homologous to					ORF YDR348c	NucleicAcid	budding yeast;;uncharacterized			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_9_4124_s_102	15975911	A Novel Membrane-associated Protein, Pal1p, Localizes to the Sites of Active Growth  and Cell Division   We identified a gene,  pal1 ( pears  and  lemons; encoded by SPCP1E11.04c), based on its homology to a novel uncharacterized ORF from budding yeast (YDR348c).	gene_phenotype
68769	1	333115	5	NULL	NULL	0	NULL	Npl6p	GP		interacts with					Rsc8p	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_13_4723_s_291	12052880	As with the genes encoding most other RSC subunits,  NPL6 and  RSC58( YLR033W) are essential for yeast cell viability; moreover, Npl6p has been reported to interact with Rsc8p in yeast two-hybrid assays ( 11).	gene_phenotype
68770	2	333115	5	NULL	NULL	0	NULL	NPL6	GP		is essential for					yeast cells	Cell	viability of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_13_4723_s_291	12052880	As with the genes encoding most other RSC subunits,  NPL6 and  RSC58( YLR033W) are essential for yeast cell viability; moreover, Npl6p has been reported to interact with Rsc8p in yeast two-hybrid assays ( 11).	gene_phenotype
68771	3	333115	5	NULL	NULL	0	NULL	RSC58	GP		is essential for					yeast cells	Cell	viability of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_13_4723_s_291	12052880	As with the genes encoding most other RSC subunits,  NPL6 and  RSC58( YLR033W) are essential for yeast cell viability; moreover, Npl6p has been reported to interact with Rsc8p in yeast two-hybrid assays ( 11).	gene_phenotype
68772	4	333115	5	NULL	NULL	0	NULL	YLR033W	NucleicAcid		is the locus name of					RSC58	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_13_4723_s_291	12052880	As with the genes encoding most other RSC subunits,  NPL6 and  RSC58( YLR033W) are essential for yeast cell viability; moreover, Npl6p has been reported to interact with Rsc8p in yeast two-hybrid assays ( 11).	gene_phenotype
68773	1	333117	5	NULL	NULL	0	NULL	YNL129w protein	GP		does not activate					pyrimidine pathway	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_2_805_s_160	12570998	The inability of the delta urk1delta fur1 double mutant to grow on uracil, uridine, and cytosine shows that no other yeast gene products (e.g., YNL129w protein) have overlapping activity in the pyrimidine pathway.	gene_phenotype
68774	2	333117	5	NULL	NULL	0	NULL	delta urk1delta fur1	GP	double mutant	does not grow on					uracil	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_2_805_s_160	12570998	The inability of the delta urk1delta fur1 double mutant to grow on uracil, uridine, and cytosine shows that no other yeast gene products (e.g., YNL129w protein) have overlapping activity in the pyrimidine pathway.	gene_phenotype
68775	3	333117	5	NULL	NULL	0	NULL	delta urk1delta fur1	GP	double mutant	does not grow on					uridine	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_2_805_s_160	12570998	The inability of the delta urk1delta fur1 double mutant to grow on uracil, uridine, and cytosine shows that no other yeast gene products (e.g., YNL129w protein) have overlapping activity in the pyrimidine pathway.	gene_phenotype
68776	4	333117	5	NULL	NULL	0	NULL	delta urk1delta fur1	GP	double mutant	does not grow on					cytosine	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_2_805_s_160	12570998	The inability of the delta urk1delta fur1 double mutant to grow on uracil, uridine, and cytosine shows that no other yeast gene products (e.g., YNL129w protein) have overlapping activity in the pyrimidine pathway.	gene_phenotype
68777	1	333118	5	NULL	NULL	0	NULL	IMP2	GP		is important for					invasive growth	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_11_1882_s_99	16278455	IMP2,  NCE102,  PUT4,  XBP1, and  YOR161C are important for invasive or pseudohyphal growth ( ,  ).	gene_phenotype
68778	2	333118	5	NULL	NULL	0	NULL	IMP2	GP		is important for					pseudohyphal growth	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_11_1882_s_99	16278455	IMP2,  NCE102,  PUT4,  XBP1, and  YOR161C are important for invasive or pseudohyphal growth ( ,  ).	gene_phenotype
68779	3	333118	5	NULL	NULL	0	NULL	NCE102	GP		is important for					invasive growth	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_11_1882_s_99	16278455	IMP2,  NCE102,  PUT4,  XBP1, and  YOR161C are important for invasive or pseudohyphal growth ( ,  ).	gene_phenotype
68780	4	333118	5	NULL	NULL	0	NULL	NCE102	GP		is important for					pseudohyphal growth	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_11_1882_s_99	16278455	IMP2,  NCE102,  PUT4,  XBP1, and  YOR161C are important for invasive or pseudohyphal growth ( ,  ).	gene_phenotype
68781	5	333118	5	NULL	NULL	0	NULL	PUT4	GP		is important for					invasive growth	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_11_1882_s_99	16278455	IMP2,  NCE102,  PUT4,  XBP1, and  YOR161C are important for invasive or pseudohyphal growth ( ,  ).	gene_phenotype
68782	6	333118	5	NULL	NULL	0	NULL	PUT4	GP		is important for					pseudohyphal growth	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_11_1882_s_99	16278455	IMP2,  NCE102,  PUT4,  XBP1, and  YOR161C are important for invasive or pseudohyphal growth ( ,  ).	gene_phenotype
68783	7	333118	5	NULL	NULL	0	NULL	XBP1	GP		is important for					invasive growth	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_11_1882_s_99	16278455	IMP2,  NCE102,  PUT4,  XBP1, and  YOR161C are important for invasive or pseudohyphal growth ( ,  ).	gene_phenotype
68784	8	333118	5	NULL	NULL	0	NULL	XBP1	GP		is important for					pseudohyphal growth	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_11_1882_s_99	16278455	IMP2,  NCE102,  PUT4,  XBP1, and  YOR161C are important for invasive or pseudohyphal growth ( ,  ).	gene_phenotype
68785	9	333118	5	NULL	NULL	0	NULL	YOR161C	NucleicAcid		is important for					invasive growth	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_11_1882_s_99	16278455	IMP2,  NCE102,  PUT4,  XBP1, and  YOR161C are important for invasive or pseudohyphal growth ( ,  ).	gene_phenotype
68786	10	333118	5	NULL	NULL	0	NULL	YOR161C	NucleicAcid		is important for					pseudohyphal growth	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_11_1882_s_99	16278455	IMP2,  NCE102,  PUT4,  XBP1, and  YOR161C are important for invasive or pseudohyphal growth ( ,  ).	gene_phenotype
68787	11	333118	5	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_11_1882_s_99	16278455	IMP2,  NCE102,  PUT4,  XBP1, and  YOR161C are important for invasive or pseudohyphal growth ( ,  ).	gene_phenotype
68788	12	333118	5	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_11_1882_s_99	16278455	IMP2,  NCE102,  PUT4,  XBP1, and  YOR161C are important for invasive or pseudohyphal growth ( ,  ).	gene_phenotype
68789	13	333118	5	NULL	NULL	0	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_11_1882_s_99	16278455	IMP2,  NCE102,  PUT4,  XBP1, and  YOR161C are important for invasive or pseudohyphal growth ( ,  ).	gene_phenotype
68790	14	333118	5	NULL	NULL	0	NULL	statement 7	Process		is an alternative to					statement 8	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_11_1882_s_99	16278455	IMP2,  NCE102,  PUT4,  XBP1, and  YOR161C are important for invasive or pseudohyphal growth ( ,  ).	gene_phenotype
68791	15	333118	5	NULL	NULL	0	NULL	statement 9	Process		is an alternative to					statement 10	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_11_1882_s_99	16278455	IMP2,  NCE102,  PUT4,  XBP1, and  YOR161C are important for invasive or pseudohyphal growth ( ,  ).	gene_phenotype
68792	1	333119	5	NULL	NULL	NULL	NULL	apoptosis	Process		is induced by					THG	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_2_569_s_175	16382148	In contrast, coexpression of tTGase suppressed the enhanced sensitivity of GFP-IETD-Smac-transfected cells to THG-induced apoptosis.	gene_phenotype
68793	2	333119	5	NULL	NULL	0	NULL	cells	Cell		transfected with					GFP-IETD-Smac	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_2_569_s_175	16382148	In contrast, coexpression of tTGase suppressed the enhanced sensitivity of GFP-IETD-Smac-transfected cells to THG-induced apoptosis.	gene_phenotype
68794	3	333119	5	NULL	NULL	0	NULL	statement 2	Process		is sensitive to		enhanced			statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_2_569_s_175	16382148	In contrast, coexpression of tTGase suppressed the enhanced sensitivity of GFP-IETD-Smac-transfected cells to THG-induced apoptosis.	gene_phenotype
68795	4	333119	5	NULL	NULL	0	NULL	tTGase	GP	overexpression of	suppress					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_2_569_s_175	16382148	In contrast, coexpression of tTGase suppressed the enhanced sensitivity of GFP-IETD-Smac-transfected cells to THG-induced apoptosis.	gene_phenotype
68796	1	333121	5	NULL	NULL	0	NULL	Sko1 target genes	GP		encodes					Sed1	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1343_s_111	16087739	In particular, Sko1 target genes encode cell wall proteins (Sed1 and Cwp1), vacuolar or cytoplasmic transporters (Stl1, Hxt5, Put4, and Cot1), and confirmed or likely enzymatic activities (Faa1, Sor1, Ald6, and Yor246c).	gene_phenotype
68797	1	333121	5	NULL	NULL	0	NULL	Sko1 target genes	GP		encodes					Sed1	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1343_s_111	16087739	In particular, Sko1 target genes encode cell wall proteins (Sed1 and Cwp1), vacuolar or cytoplasmic transporters (Stl1, Hxt5, Put4, and Cot1), and confirmed or likely enzymatic activities (Faa1, Sor1, Ald6, and Yor246c).	gene_phenotype
68798	2	333121	5	NULL	NULL	0	NULL	Sko1 target genes	GP		encodes					Cwp1	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1343_s_111	16087739	In particular, Sko1 target genes encode cell wall proteins (Sed1 and Cwp1), vacuolar or cytoplasmic transporters (Stl1, Hxt5, Put4, and Cot1), and confirmed or likely enzymatic activities (Faa1, Sor1, Ald6, and Yor246c).	gene_phenotype
68799	3	333121	5	NULL	NULL	0	NULL	Sed1	GP		is a type of					cell wall protein	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1343_s_111	16087739	In particular, Sko1 target genes encode cell wall proteins (Sed1 and Cwp1), vacuolar or cytoplasmic transporters (Stl1, Hxt5, Put4, and Cot1), and confirmed or likely enzymatic activities (Faa1, Sor1, Ald6, and Yor246c).	gene_phenotype
68800	4	333121	5	NULL	NULL	0	NULL	Cwp1	GP		is a type of					cell wall protein	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1343_s_111	16087739	In particular, Sko1 target genes encode cell wall proteins (Sed1 and Cwp1), vacuolar or cytoplasmic transporters (Stl1, Hxt5, Put4, and Cot1), and confirmed or likely enzymatic activities (Faa1, Sor1, Ald6, and Yor246c).	gene_phenotype
68801	5	333121	5	NULL	NULL	0	NULL	Sko1 target genes	GP		encodes					Stl1	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1343_s_111	16087739	In particular, Sko1 target genes encode cell wall proteins (Sed1 and Cwp1), vacuolar or cytoplasmic transporters (Stl1, Hxt5, Put4, and Cot1), and confirmed or likely enzymatic activities (Faa1, Sor1, Ald6, and Yor246c).	gene_phenotype
68802	6	333121	5	NULL	NULL	0	NULL	Stl1	GP		is a type of					vacuolar or cytoplasmic transporter	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1343_s_111	16087739	In particular, Sko1 target genes encode cell wall proteins (Sed1 and Cwp1), vacuolar or cytoplasmic transporters (Stl1, Hxt5, Put4, and Cot1), and confirmed or likely enzymatic activities (Faa1, Sor1, Ald6, and Yor246c).	gene_phenotype
68803	7	333121	5	NULL	NULL	0	NULL	Sko1 target genes	GP		encodes					Hxt5	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1343_s_111	16087739	In particular, Sko1 target genes encode cell wall proteins (Sed1 and Cwp1), vacuolar or cytoplasmic transporters (Stl1, Hxt5, Put4, and Cot1), and confirmed or likely enzymatic activities (Faa1, Sor1, Ald6, and Yor246c).	gene_phenotype
68804	8	333121	5	NULL	NULL	0	NULL	Hxt5	GP		is a type of					vacuolar or cytoplasmic transporter	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1343_s_111	16087739	In particular, Sko1 target genes encode cell wall proteins (Sed1 and Cwp1), vacuolar or cytoplasmic transporters (Stl1, Hxt5, Put4, and Cot1), and confirmed or likely enzymatic activities (Faa1, Sor1, Ald6, and Yor246c).	gene_phenotype
68805	9	333121	5	NULL	NULL	0	NULL	Sko1 target genes	GP		encodes					Put4	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1343_s_111	16087739	In particular, Sko1 target genes encode cell wall proteins (Sed1 and Cwp1), vacuolar or cytoplasmic transporters (Stl1, Hxt5, Put4, and Cot1), and confirmed or likely enzymatic activities (Faa1, Sor1, Ald6, and Yor246c).	gene_phenotype
68806	10	333121	5	NULL	NULL	0	NULL	Put4	GP		is a type of					vacuolar or cytoplasmic transporter	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1343_s_111	16087739	In particular, Sko1 target genes encode cell wall proteins (Sed1 and Cwp1), vacuolar or cytoplasmic transporters (Stl1, Hxt5, Put4, and Cot1), and confirmed or likely enzymatic activities (Faa1, Sor1, Ald6, and Yor246c).	gene_phenotype
68807	11	333121	5	NULL	NULL	0	NULL	Sko1 target genes	GP		encodes					Cot1	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1343_s_111	16087739	In particular, Sko1 target genes encode cell wall proteins (Sed1 and Cwp1), vacuolar or cytoplasmic transporters (Stl1, Hxt5, Put4, and Cot1), and confirmed or likely enzymatic activities (Faa1, Sor1, Ald6, and Yor246c).	gene_phenotype
68808	12	333121	5	NULL	NULL	0	NULL	Cot1	GP		is a type of					vacuolar or cytoplasmic transporter	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1343_s_111	16087739	In particular, Sko1 target genes encode cell wall proteins (Sed1 and Cwp1), vacuolar or cytoplasmic transporters (Stl1, Hxt5, Put4, and Cot1), and confirmed or likely enzymatic activities (Faa1, Sor1, Ald6, and Yor246c).	gene_phenotype
68809	13	333121	5	NULL	NULL	0	NULL	Sko1 target genes	GP		encodes					Faa1	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1343_s_111	16087739	In particular, Sko1 target genes encode cell wall proteins (Sed1 and Cwp1), vacuolar or cytoplasmic transporters (Stl1, Hxt5, Put4, and Cot1), and confirmed or likely enzymatic activities (Faa1, Sor1, Ald6, and Yor246c).	gene_phenotype
68810	14	333121	5	NULL	NULL	0	NULL	Sko1 target genes	GP		encodes					Sor1	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1343_s_111	16087739	In particular, Sko1 target genes encode cell wall proteins (Sed1 and Cwp1), vacuolar or cytoplasmic transporters (Stl1, Hxt5, Put4, and Cot1), and confirmed or likely enzymatic activities (Faa1, Sor1, Ald6, and Yor246c).	gene_phenotype
68811	15	333121	5	NULL	NULL	0	NULL	Sko1 target genes	GP		encodes					Ald6	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1343_s_111	16087739	In particular, Sko1 target genes encode cell wall proteins (Sed1 and Cwp1), vacuolar or cytoplasmic transporters (Stl1, Hxt5, Put4, and Cot1), and confirmed or likely enzymatic activities (Faa1, Sor1, Ald6, and Yor246c).	gene_phenotype
68812	16	333121	5	NULL	NULL	0	NULL	Sko1 target genes	GP		encodes					Yor246c	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1343_s_111	16087739	In particular, Sko1 target genes encode cell wall proteins (Sed1 and Cwp1), vacuolar or cytoplasmic transporters (Stl1, Hxt5, Put4, and Cot1), and confirmed or likely enzymatic activities (Faa1, Sor1, Ald6, and Yor246c).	gene_phenotype
68813	16	333121	5	NULL	NULL	0	NULL	Sko1 target genes	GP		encodes					Yor246c	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_8_1343_s_111	16087739	In particular, Sko1 target genes encode cell wall proteins (Sed1 and Cwp1), vacuolar or cytoplasmic transporters (Stl1, Hxt5, Put4, and Cot1), and confirmed or likely enzymatic activities (Faa1, Sor1, Ald6, and Yor246c).	gene_phenotype
68815	1	333122	5	NULL	NULL	0	NULL	Zds2	GP		interacts with					Cdc11	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_202	11489916	Zds2 also interacts with the septin Cdc11, a sporulation-specific protein, Spr6 ( Kallal et al., 1990), and three proteins of unknown function, Yer124c, Yal004w, and Yel023c.	gene_phenotype
68816	2	333122	5	NULL	NULL	0	NULL	Cdc11	GP		is a type of					septin	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_202	11489916	Zds2 also interacts with the septin Cdc11, a sporulation-specific protein, Spr6 ( Kallal et al., 1990), and three proteins of unknown function, Yer124c, Yal004w, and Yel023c.	gene_phenotype
68817	3	333122	5	NULL	NULL	0	NULL	Zds2	GP		interacts with					Spr6	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_202	11489916	Zds2 also interacts with the septin Cdc11, a sporulation-specific protein, Spr6 ( Kallal et al., 1990), and three proteins of unknown function, Yer124c, Yal004w, and Yel023c.	gene_phenotype
68818	4	333122	5	NULL	NULL	0	NULL	Spr6	GP		is a type of					sporulation-specific protein	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_202	11489916	Zds2 also interacts with the septin Cdc11, a sporulation-specific protein, Spr6 ( Kallal et al., 1990), and three proteins of unknown function, Yer124c, Yal004w, and Yel023c.	gene_phenotype
68819	5	333122	5	NULL	NULL	0	NULL	Zds2	GP		interacts with					Yer124c	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_202	11489916	Zds2 also interacts with the septin Cdc11, a sporulation-specific protein, Spr6 ( Kallal et al., 1990), and three proteins of unknown function, Yer124c, Yal004w, and Yel023c.	gene_phenotype
68820	6	333122	5	NULL	NULL	0	NULL	Zds2	GP		interacts with					Yal004w	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_202	11489916	Zds2 also interacts with the septin Cdc11, a sporulation-specific protein, Spr6 ( Kallal et al., 1990), and three proteins of unknown function, Yer124c, Yal004w, and Yel023c.	gene_phenotype
68821	7	333122	5	NULL	NULL	0	NULL	Zds2	GP		interacts with					Yel023c	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_202	11489916	Zds2 also interacts with the septin Cdc11, a sporulation-specific protein, Spr6 ( Kallal et al., 1990), and three proteins of unknown function, Yer124c, Yal004w, and Yel023c.	gene_phenotype
68822	1	333123	5	NULL	NULL	0	NULL	YAL022c	NucleicAcid		is a type of					open reading frame	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_34_25931_s_84	10827169	FUN26, the protein of unknown function predicted from the YAL022c open reading frame, has limited (~18%) amino acid sequence identity with members of the ENT family of nucleoside transporters.	gene_phenotype
68823	2	333123	5	NULL	NULL	0	NULL	YAL022c	NucleicAcid		encodes		possibly			FUN26 protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_34_25931_s_84	10827169	FUN26, the protein of unknown function predicted from the YAL022c open reading frame, has limited (~18%) amino acid sequence identity with members of the ENT family of nucleoside transporters.	gene_phenotype
68824	3	333123	5	NULL	NULL	0	NULL	FUN26 protein	GP		is similar to					ENT family of nucleoside transporters	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_34_25931_s_84	10827169	FUN26, the protein of unknown function predicted from the YAL022c open reading frame, has limited (~18%) amino acid sequence identity with members of the ENT family of nucleoside transporters.	gene_phenotype
68825	1	333129	5	NULL	NULL	0	NULL	PBP2	GP	deletion of	leads to					growth	Process	decrease in;;rate of			NULL		0	NULL	NULL	NULL	gw60_currbiol_11_13_1001_s_144	11470404	Deletion of a third gene( YBR233W/ PBP2) also led to a decreased growth rate and caused a more modest meiotic chromosome missegregation, resulting in a spore viability of 5%.	gene_phenotype
68826	2	333129	5	NULL	NULL	0	NULL	PBP2	GP	deletion of	leads to					meiotic chromosome missegregation	Process				NULL		0	NULL	NULL	NULL	gw60_currbiol_11_13_1001_s_144	11470404	Deletion of a third gene( YBR233W/ PBP2) also led to a decreased growth rate and caused a more modest meiotic chromosome missegregation, resulting in a spore viability of 5%.	gene_phenotype
68827	3	333129	5	NULL	NULL	0	NULL	YBR233W	NucleicAcid		is the locus name of					PBP2	GP				NULL		0	NULL	NULL	NULL	gw60_currbiol_11_13_1001_s_144	11470404	Deletion of a third gene( YBR233W/ PBP2) also led to a decreased growth rate and caused a more modest meiotic chromosome missegregation, resulting in a spore viability of 5%.	gene_phenotype
68828	1	333130	5	NULL	NULL	NULL	NULL	YDL033c	NucleicAcid		is involved in		may be			tRNAs	NucleicAcid	2-thio modification of;;mt			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_2_1613_s_146	15509579	Thus, to examine the involvement of YDL033c in the 2-thio modification of the mt tRNAs for Lys, Glu, and Gln and the cytosolic tRNALys, total RNAs obtained from the YDL033c-deletion strain were subjected to polyacrylamide gel electrophoresis containing ( N-acryloylamino)phenylmercuric chloride (APM) combined with Northern blotting ( ,  ) (see "Experimental Procedures"`) ( Fig. 2).	gene_phenotype
68829	2	333130	5	NULL	NULL	0	NULL	YDL033c	NucleicAcid		is involved in		may be			tRNALys	NucleicAcid	2-thio modification of;;cytosolic			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_2_1613_s_146	15509579	Thus, to examine the involvement of YDL033c in the 2-thio modification of the mt tRNAs for Lys, Glu, and Gln and the cytosolic tRNALys, total RNAs obtained from the YDL033c-deletion strain were subjected to polyacrylamide gel electrophoresis containing ( N-acryloylamino)phenylmercuric chloride (APM) combined with Northern blotting ( ,  ) (see "Experimental Procedures"`) ( Fig. 2).	gene_phenotype
68830	1	333131	5	NULL	NULL	0	NULL	YLL034C	NucleicAcid		is a type of					mating pheromone	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_26_26830_s_237	15078868	Interestingly, most of the genes affected by  san1delta are affected transcriptionally by mating pheromone ( YLL034C, HSP12, YDL037C, and  YLL053C; see Ref.  ) or are involved in the pheromone response pathway ( PRM7).	gene_phenotype
68831	2	333131	5	NULL	NULL	0	NULL	HSP12	NucleicAcid		is a type of					mating pheromone	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_26_26830_s_237	15078868	Interestingly, most of the genes affected by  san1delta are affected transcriptionally by mating pheromone ( YLL034C, HSP12, YDL037C, and  YLL053C; see Ref.  ) or are involved in the pheromone response pathway ( PRM7).	gene_phenotype
68832	3	333131	5	NULL	NULL	0	NULL	YDL037C	NucleicAcid		is a type of					mating pheromone	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_26_26830_s_237	15078868	Interestingly, most of the genes affected by  san1delta are affected transcriptionally by mating pheromone ( YLL034C, HSP12, YDL037C, and  YLL053C; see Ref.  ) or are involved in the pheromone response pathway ( PRM7).	gene_phenotype
68833	4	333131	5	NULL	NULL	0	NULL	YLL053C	NucleicAcid		is a type of					mating pheromone	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_26_26830_s_237	15078868	Interestingly, most of the genes affected by  san1delta are affected transcriptionally by mating pheromone ( YLL034C, HSP12, YDL037C, and  YLL053C; see Ref.  ) or are involved in the pheromone response pathway ( PRM7).	gene_phenotype
68834	5	333131	5	NULL	NULL	0	NULL	PRM7	Process		is					pheromone response pathway	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_26_26830_s_237	15078868	Interestingly, most of the genes affected by  san1delta are affected transcriptionally by mating pheromone ( YLL034C, HSP12, YDL037C, and  YLL053C; see Ref.  ) or are involved in the pheromone response pathway ( PRM7).	gene_phenotype
68835	7	333131	5	NULL	NULL	NULL	NULL	statement 1	GP		affects		transcriptionaly			statement 6	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_26_26830_s_237	15078868	Interestingly, most of the genes affected by  san1delta are affected transcriptionally by mating pheromone ( YLL034C, HSP12, YDL037C, and  YLL053C; see Ref.  ) or are involved in the pheromone response pathway ( PRM7).	gene_phenotype
68836	6	333131	5	NULL	NULL	0	NULL	genes	GP		is affected by					san1delta	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_26_26830_s_237	15078868	Interestingly, most of the genes affected by  san1delta are affected transcriptionally by mating pheromone ( YLL034C, HSP12, YDL037C, and  YLL053C; see Ref.  ) or are involved in the pheromone response pathway ( PRM7).	gene_phenotype
68837	8	333131	5	NULL	NULL	0	NULL	statement 2	GP		affects		transcriptionaly			statement 6	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_26_26830_s_237	15078868	Interestingly, most of the genes affected by  san1delta are affected transcriptionally by mating pheromone ( YLL034C, HSP12, YDL037C, and  YLL053C; see Ref.  ) or are involved in the pheromone response pathway ( PRM7).	gene_phenotype
68838	9	333131	5	NULL	NULL	0	NULL	statement 3	GP		affects		transcriptionaly			statement 6	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_26_26830_s_237	15078868	Interestingly, most of the genes affected by  san1delta are affected transcriptionally by mating pheromone ( YLL034C, HSP12, YDL037C, and  YLL053C; see Ref.  ) or are involved in the pheromone response pathway ( PRM7).	gene_phenotype
68839	10	333131	5	NULL	NULL	0	NULL	statement 4	GP		affects		transcriptionaly			statement 6	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_26_26830_s_237	15078868	Interestingly, most of the genes affected by  san1delta are affected transcriptionally by mating pheromone ( YLL034C, HSP12, YDL037C, and  YLL053C; see Ref.  ) or are involved in the pheromone response pathway ( PRM7).	gene_phenotype
68840	11	333131	5	NULL	NULL	0	NULL	statement 6	GP		is involved in		tr			PRM7	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_26_26830_s_237	15078868	Interestingly, most of the genes affected by  san1delta are affected transcriptionally by mating pheromone ( YLL034C, HSP12, YDL037C, and  YLL053C; see Ref.  ) or are involved in the pheromone response pathway ( PRM7).	gene_phenotype
68841	1	333132	5	NULL	NULL	0	NULL	YDL105w	NucleicAcid	budding yeast	is a component of					SMC5+6 complex	GP	yeast			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_11_4866_s_143	15331764	Notably, budding yeast YDL105w was recently identified in a high throughput mass spectrometry and two-hybrid screen as a component of the yeast SMC5+6 complex (Hazbun  et al., 2003 ).	gene_phenotype
68842	1	333134	5	NULL	NULL	NULL	NULL	SEP7/SHS1	GP	deletion of	does not effect					sporulation	Process				NULL		NULL	NULL	NULL	NULL	gw60_genetics_163_1_47_s_200	12586695	Deletions of genes  SEP7/SHS1,  PHO91,  YDL121C, and  YJR003C had little or no effect on sporulation in our hands.	gene_phenotype
68843	2	333134	5	NULL	NULL	0	NULL	PHO91	GP	deletion of	does not effect					sporulation	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_163_1_47_s_200	12586695	Deletions of genes  SEP7/SHS1,  PHO91,  YDL121C, and  YJR003C had little or no effect on sporulation in our hands.	gene_phenotype
68844	3	333134	5	NULL	NULL	0	NULL	YDL121C	NucleicAcid	deletion of	does not effect					sporulation	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_163_1_47_s_200	12586695	Deletions of genes  SEP7/SHS1,  PHO91,  YDL121C, and  YJR003C had little or no effect on sporulation in our hands.	gene_phenotype
68845	4	333134	5	NULL	NULL	0	NULL	YJR003C	NucleicAcid	deletion of	does not effect					sporulation	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_163_1_47_s_200	12586695	Deletions of genes  SEP7/SHS1,  PHO91,  YDL121C, and  YJR003C had little or no effect on sporulation in our hands.	gene_phenotype
68846	1	333135	5	NULL	NULL	0	NULL	SWR1	GP		is a synonym of					YDR334W	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_47_44870_s_111	12244097	The name  SWR1 was proposed for  YDR334W after its identification in a genetic screen for suppressors of yeast impaired in nuclear transport.	gene_phenotype
68847	3	333135	5	NULL	NULL	0	NULL	SWR1	GP		suppress					statement 2	Cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_47_44870_s_111	12244097	The name  SWR1 was proposed for  YDR334W after its identification in a genetic screen for suppressors of yeast impaired in nuclear transport.	gene_phenotype
68848	2	333135	5	NULL	NULL	0	NULL	yeast	Cell		impaired in					nuclear transport	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_47_44870_s_111	12244097	The name  SWR1 was proposed for  YDR334W after its identification in a genetic screen for suppressors of yeast impaired in nuclear transport.	gene_phenotype
68849	1	333136	5	NULL	NULL	0	NULL	YER074W-A	NucleicAcid		suppress					yip1-4 Strain	Cell				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_4_1673_s_87	15659647	Identification of YER074W-A as a Novel Multicopy Suppressor of the yip1-4 Strain   Our recent biochemical, genetic, and morphological studies of Yip1p function in protein transport between the ER and the Golgi complex led to the finding that Yip1p plays a critical role in COPII vesicle biogenesis (Heidtman  et al., 2003 ).	gene_phenotype
68850	2	333136	5	NULL	NULL	0	NULL	Yip1p	GP		plays a role in		critical			COPII vesicle	CellComponent	biogenesis of			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_4_1673_s_87	15659647	Identification of YER074W-A as a Novel Multicopy Suppressor of the yip1-4 Strain   Our recent biochemical, genetic, and morphological studies of Yip1p function in protein transport between the ER and the Golgi complex led to the finding that Yip1p plays a critical role in COPII vesicle biogenesis (Heidtman  et al., 2003 ).	gene_phenotype
68851	1	333137	5	NULL	NULL	0	NULL	MEC1	GP	overexpression of	causes					silencing defect	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_158_1_145_s_100	11333225	We constructed a plasmid (pRC12) that had one of these ORFs (YER120W,  SCS2) and showed that this plasmid suppressed the silencing defect caused by  MEC1 overexpression ( Fig 1A).	gene_phenotype
68852	2	333137	5	NULL	NULL	0	NULL	plasmid (pRC12)	CellComponent		suppress					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_158_1_145_s_100	11333225	We constructed a plasmid (pRC12) that had one of these ORFs (YER120W,  SCS2) and showed that this plasmid suppressed the silencing defect caused by  MEC1 overexpression ( Fig 1A).	gene_phenotype
68853	3	333137	5	NULL	NULL	0	NULL	plasmid (pRC12)	CellComponent		contains					YER120W	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_genetics_158_1_145_s_100	11333225	We constructed a plasmid (pRC12) that had one of these ORFs (YER120W,  SCS2) and showed that this plasmid suppressed the silencing defect caused by  MEC1 overexpression ( Fig 1A).	gene_phenotype
68854	4	333137	5	NULL	NULL	0	NULL	plasmid (pRC12)	CellComponent		contains					SCS2	GP				NULL		0	NULL	NULL	NULL	gw60_genetics_158_1_145_s_100	11333225	We constructed a plasmid (pRC12) that had one of these ORFs (YER120W,  SCS2) and showed that this plasmid suppressed the silencing defect caused by  MEC1 overexpression ( Fig 1A).	gene_phenotype
68855	5	333137	5	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_158_1_145_s_100	11333225	We constructed a plasmid (pRC12) that had one of these ORFs (YER120W,  SCS2) and showed that this plasmid suppressed the silencing defect caused by  MEC1 overexpression ( Fig 1A).	gene_phenotype
68856	1	333139	5	NULL	NULL	NULL	NULL	YGL175C	NucleicAcid		is an ORF of					SAE2/ COM1	GP	full length			NULL		NULL	NULL	NULL	NULL	gw60_genetics_158_1_109_s_107	11333222	Further subcloning and complementation indicated that plasmids harboring the full-length  SAE2/ COM1 ORF alone (YGL175C) were sufficient for full complementation of the sporulation, MMS sensitivity, and mutator phenotypes (data not shown).	gene_phenotype
68857	2	333139	5	NULL	NULL	NULL	NULL	plasmids	CellComponent		harbor		alone			statement 1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genetics_158_1_109_s_107	11333222	Further subcloning and complementation indicated that plasmids harboring the full-length  SAE2/ COM1 ORF alone (YGL175C) were sufficient for full complementation of the sporulation, MMS sensitivity, and mutator phenotypes (data not shown).	gene_phenotype
68858	3	333139	5	NULL	NULL	NULL	NULL	statement 2	CellComponent		is sufficient for					sporulation	Process	full complementation of 			NULL		NULL	NULL	NULL	NULL	gw60_genetics_158_1_109_s_107	11333222	Further subcloning and complementation indicated that plasmids harboring the full-length  SAE2/ COM1 ORF alone (YGL175C) were sufficient for full complementation of the sporulation, MMS sensitivity, and mutator phenotypes (data not shown).	gene_phenotype
68859	4	333139	5	NULL	NULL	NULL	NULL	statement 3	CellComponent		is sufficient for					MMS sensitivity	Process				NULL		NULL	NULL	NULL	NULL	gw60_genetics_158_1_109_s_107	11333222	Further subcloning and complementation indicated that plasmids harboring the full-length  SAE2/ COM1 ORF alone (YGL175C) were sufficient for full complementation of the sporulation, MMS sensitivity, and mutator phenotypes (data not shown).	gene_phenotype
68860	5	333139	5	NULL	NULL	NULL	NULL	statement 3	CellComponent		is sufficient for					mutator phenotypes					NULL		NULL	NULL	NULL	NULL	gw60_genetics_158_1_109_s_107	11333222	Further subcloning and complementation indicated that plasmids harboring the full-length  SAE2/ COM1 ORF alone (YGL175C) were sufficient for full complementation of the sporulation, MMS sensitivity, and mutator phenotypes (data not shown).	gene_phenotype
68861	1	333140	5	NULL	NULL	0	NULL	YGL175C	NucleicAcid		is an ORF of					SAE2/ COM1 	GP	full length			NULL		0	NULL	NULL	NULL	gw60_genetics_158_1_109_s_190	11333222	We isolated a single complementing plasmid, and further subcloning and complementation indicated that a plasmid containing only the full-length  SAE2/ COM1 ORF (YGL175C) was sufficient for full complementation of the sporulation, MMS sensitivity, and DSB-induced mutator phenotypes (data not shown).	gene_phenotype
68862	2	333140	5	NULL	NULL	0	NULL	plasmid	CellComponent		contains		only			YGL175C	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_genetics_158_1_109_s_190	11333222	We isolated a single complementing plasmid, and further subcloning and complementation indicated that a plasmid containing only the full-length  SAE2/ COM1 ORF (YGL175C) was sufficient for full complementation of the sporulation, MMS sensitivity, and DSB-induced mutator phenotypes (data not shown).	gene_phenotype
68863	3	333140	5	NULL	NULL	0	NULL	statement 2	CellComponent		is sufficient for					sporulation	Process	full complement of			NULL		0	NULL	NULL	NULL	gw60_genetics_158_1_109_s_190	11333222	We isolated a single complementing plasmid, and further subcloning and complementation indicated that a plasmid containing only the full-length  SAE2/ COM1 ORF (YGL175C) was sufficient for full complementation of the sporulation, MMS sensitivity, and DSB-induced mutator phenotypes (data not shown).	gene_phenotype
68864	4	333140	5	NULL	NULL	0	NULL	statement 2	CellComponent		is sufficient for					MMS sensitivity	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_158_1_109_s_190	11333222	We isolated a single complementing plasmid, and further subcloning and complementation indicated that a plasmid containing only the full-length  SAE2/ COM1 ORF (YGL175C) was sufficient for full complementation of the sporulation, MMS sensitivity, and DSB-induced mutator phenotypes (data not shown).	gene_phenotype
68865	5	333140	5	NULL	NULL	NULL	NULL	mutator phenotypes			is induced by					DSB	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_genetics_158_1_109_s_190	11333222	We isolated a single complementing plasmid, and further subcloning and complementation indicated that a plasmid containing only the full-length  SAE2/ COM1 ORF (YGL175C) was sufficient for full complementation of the sporulation, MMS sensitivity, and DSB-induced mutator phenotypes (data not shown).	gene_phenotype
68866	6	333140	5	NULL	NULL	0	NULL	statement 2	CellComponent		is sufficient for					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_158_1_109_s_190	11333222	We isolated a single complementing plasmid, and further subcloning and complementation indicated that a plasmid containing only the full-length  SAE2/ COM1 ORF (YGL175C) was sufficient for full complementation of the sporulation, MMS sensitivity, and DSB-induced mutator phenotypes (data not shown).	gene_phenotype
68867	1	333141	5	NULL	NULL	0	NULL	suppressors of snf1 pcl8 pcl10	GP		affects		potentially			autophagy	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_17_5742_s_276	11486014	We also tested whether some of the other genes identified as high-copy-number suppressors of  snf1 pcl8 pcl10 affected autophagy by making deletions of  RCK2 and  YGR161C in the TN125 background.	gene_phenotype
68868	1	333142	5	NULL	NULL	0	NULL	RCK2 gene	GP	deletion of	does not affect					autophagy	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_17_5742_s_331	11486014	Note that  SNF1 may exert yet other controls over the maintenance of glycogen stores, since deletion of two of the genes identified in the genetic screen,  RCK2 and  YGR161C, does not affect autophagy.	gene_phenotype
68869	2	333142	5	NULL	NULL	0	NULL	YGR161C 	NucleicAcid		does not affect					autophagy	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_17_5742_s_331	11486014	Note that  SNF1 may exert yet other controls over the maintenance of glycogen stores, since deletion of two of the genes identified in the genetic screen,  RCK2 and  YGR161C, does not affect autophagy.	gene_phenotype
68870	3	333142	5	NULL	NULL	0	NULL	SNF1	GP		exerts		may			glycogen	Chemical	controls over;;maintenance of;;stores of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_17_5742_s_331	11486014	Note that  SNF1 may exert yet other controls over the maintenance of glycogen stores, since deletion of two of the genes identified in the genetic screen,  RCK2 and  YGR161C, does not affect autophagy.	gene_phenotype
68872	1	333143	5	NULL	NULL	0	NULL	polypeptides	GP		fold into					three-dimensional conformations	GP				NULL	within the ER	0	NULL	NULL	NULL	gw60_embo_17_12_3251_s_12	9628862	Commonly coupled with the translocation process, the polypeptides fold into their three-dimensional conformations within the ER where they may assemble with other proteins into oligomeric complexes.	gene_phenotype
68873	2	333143	5	NULL	NULL	NULL	NULL	statement 1	Process		leads to					oligomeric complexes	GP	formation of			NULL	within the ER	NULL	NULL	NULL	NULL	gw60_embo_17_12_3251_s_12	9628862	Commonly coupled with the translocation process, the polypeptides fold into their three-dimensional conformations within the ER where they may assemble with other proteins into oligomeric complexes.	gene_phenotype
68874	3	333143	5	NULL	NULL	0	NULL	statement 1	Process		is coupled with					translocation	Process				NULL		0	NULL	NULL	NULL	gw60_embo_17_12_3251_s_12	9628862	Commonly coupled with the translocation process, the polypeptides fold into their three-dimensional conformations within the ER where they may assemble with other proteins into oligomeric complexes.	gene_phenotype
68875	1	333145	5	NULL	NULL	0	NULL	YMR216C locus	NucleicAcid		corresponds to					SKY1 gene	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_659_s_88	11854447	The YMR216C locus corresponds to the  SKY1 (SR-protein-specific kinase from budding yeast) gene, which encodes a protein serine/threonine kinase with structural and functional homology to the human SR-protein-specific kinases (SRPKs).	gene_phenotype
68876	2	333145	5	NULL	NULL	0	NULL	SKY1	GP		is					SR-protein-specific kinase from budding yeast	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_659_s_88	11854447	The YMR216C locus corresponds to the  SKY1 (SR-protein-specific kinase from budding yeast) gene, which encodes a protein serine/threonine kinase with structural and functional homology to the human SR-protein-specific kinases (SRPKs).	gene_phenotype
68877	3	333145	5	NULL	NULL	0	NULL	SKY1 gene	GP		encodes					protein serine/threonine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_659_s_88	11854447	The YMR216C locus corresponds to the  SKY1 (SR-protein-specific kinase from budding yeast) gene, which encodes a protein serine/threonine kinase with structural and functional homology to the human SR-protein-specific kinases (SRPKs).	gene_phenotype
68878	4	333145	5	NULL	NULL	0	NULL	protein serine/threonine kinase	GP		is homologous to		structurally;;funtionally			SRPKs	GP	human			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_659_s_88	11854447	The YMR216C locus corresponds to the  SKY1 (SR-protein-specific kinase from budding yeast) gene, which encodes a protein serine/threonine kinase with structural and functional homology to the human SR-protein-specific kinases (SRPKs).	gene_phenotype
68879	5	333145	5	NULL	NULL	0	NULL	SRPKs	GP		is					SR-protein-specific kinases	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_659_s_88	11854447	The YMR216C locus corresponds to the  SKY1 (SR-protein-specific kinase from budding yeast) gene, which encodes a protein serine/threonine kinase with structural and functional homology to the human SR-protein-specific kinases (SRPKs).	gene_phenotype
68880	1	333148	5	NULL	NULL	0	NULL	Dus2	GP		is encoded by					ORF YNR015w	NucleicAcid				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_rna_8_3_12003496_s_6	12003496	We show that one of these proteins, Dus2,  encoded by ORF YNR015w, has activity with two other substrates: yeast  pre-tRNA(Tyr) and pre-tRNA(Leu).	gene_phenotype
68881	2	333148	5	NULL	NULL	0	NULL	Dus2	GP		has activity with					pre-tRNA(Tyr)	NucleicAcid	yeast			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_rna_8_3_12003496_s_6	12003496	We show that one of these proteins, Dus2,  encoded by ORF YNR015w, has activity with two other substrates: yeast  pre-tRNA(Tyr) and pre-tRNA(Leu).	gene_phenotype
68882	3	333148	5	NULL	NULL	0	NULL	Dus2	GP		has activity with					pre-tRNA(Leu)	NucleicAcid	yeast			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_rna_8_3_12003496_s_6	12003496	We show that one of these proteins, Dus2,  encoded by ORF YNR015w, has activity with two other substrates: yeast  pre-tRNA(Tyr) and pre-tRNA(Leu).	gene_phenotype
68883	1	333151	5	NULL	NULL	0	NULL	PRL1	GP		is similar to					family of WD proteins	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_19_3059_s_159	9765207	In the database, PRL1 identified a family of WD proteins with unknown function: PRL2 from  Arabidopsis shared 83%, PRL1 from fission yeast 69%, YPL151c from budding yeast 63% (Purnelle et al. 1996  ), and hypothetical gene product D1054.15 from  Caenorhabditis 62% sequence identity with PRL1.	gene_phenotype
68884	2	333151	5	NULL	NULL	0	NULL	PRL2	GP	Arabidopsis	is similar to					PRL1	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_19_3059_s_159	9765207	In the database, PRL1 identified a family of WD proteins with unknown function: PRL2 from  Arabidopsis shared 83%, PRL1 from fission yeast 69%, YPL151c from budding yeast 63% (Purnelle et al. 1996  ), and hypothetical gene product D1054.15 from  Caenorhabditis 62% sequence identity with PRL1.	gene_phenotype
68885	3	333151	5	NULL	NULL	0	NULL	PRL1	GP	fission yeast	is similar to					PRL1	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_19_3059_s_159	9765207	In the database, PRL1 identified a family of WD proteins with unknown function: PRL2 from  Arabidopsis shared 83%, PRL1 from fission yeast 69%, YPL151c from budding yeast 63% (Purnelle et al. 1996  ), and hypothetical gene product D1054.15 from  Caenorhabditis 62% sequence identity with PRL1.	gene_phenotype
68886	4	333151	5	NULL	NULL	0	NULL	YPL151c	NucleicAcid	budding yeast	is similar to					PRL1	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_19_3059_s_159	9765207	In the database, PRL1 identified a family of WD proteins with unknown function: PRL2 from  Arabidopsis shared 83%, PRL1 from fission yeast 69%, YPL151c from budding yeast 63% (Purnelle et al. 1996  ), and hypothetical gene product D1054.15 from  Caenorhabditis 62% sequence identity with PRL1.	gene_phenotype
68887	5	333151	5	NULL	NULL	0	NULL	D1054.15	GP	hypothetical gene product;;Caenorhabditis	is similar to					PRL1	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_19_3059_s_159	9765207	In the database, PRL1 identified a family of WD proteins with unknown function: PRL2 from  Arabidopsis shared 83%, PRL1 from fission yeast 69%, YPL151c from budding yeast 63% (Purnelle et al. 1996  ), and hypothetical gene product D1054.15 from  Caenorhabditis 62% sequence identity with PRL1.	gene_phenotype
68888	1	333152	5	NULL	NULL	0	NULL	YBL009W	NucleicAcid		is induced during		significantly			sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_4_472_s_365	15681610	The second homolog,  YBL009W, is significantly induced during sporulation (Chu et al. 1998 ).	gene_phenotype
68889	1	333153	5	NULL	NULL	0	NULL	Alk1p	GP		function during					mitosis	Process				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_4_472_s_366	15681610	The data suggest that Alk1p and Ybl009wp function during mitosis and meiosis, respectively (Higgins 2003 ).	gene_phenotype
68890	2	333153	5	NULL	NULL	0	NULL	Ybl009wp	NucleicAcid		function during					meiosis	Process				NULL		0	NULL	NULL	NULL	gw70_genesdev_19_4_472_s_366	15681610	The data suggest that Alk1p and Ybl009wp function during mitosis and meiosis, respectively (Higgins 2003 ).	gene_phenotype
68891	1	333154	5	NULL	NULL	0	NULL	KRR1T gene	GP		is essential for					Saccharomyces cerevisiae	Cell	viability of			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_5_1409_s_429	11359931	A novel cross-phylum family of proteins comprises a  KRR1T (YCL059c) gene which is essential for viability of  Saccharomyces cerevisiae cells.	gene_phenotype
68892	2	333154	5	NULL	NULL	0	NULL	YCL059c	NucleicAcid		is the locus name of					KRR1T	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_5_1409_s_429	11359931	A novel cross-phylum family of proteins comprises a  KRR1T (YCL059c) gene which is essential for viability of  Saccharomyces cerevisiae cells.	gene_phenotype
68893	1	333156	5	NULL	NULL	0	NULL	KRR1T	GP	Saccharomyces cerevisiae	is essential for					cell viability	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_acta-biochim-pol_47_4_11996121_s_2	11996121	The newly discovered Saccharomyces cerevisiae gene KRR1 (YCL059c) encodes  a protein essential for cell viability.	gene_phenotype
68894	2	333156	5	NULL	NULL	0	NULL	YCL059c	NucleicAcid		is the locus name of					KRR1	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_acta-biochim-pol_47_4_11996121_s_2	11996121	The newly discovered Saccharomyces cerevisiae gene KRR1 (YCL059c) encodes  a protein essential for cell viability.	gene_phenotype
68895	1	333159	5	NULL	NULL	0	NULL	YCR052w	NucleicAcid		is essential for					mitotic growth	Process				NULL		0	NULL	NULL	NULL	gw60_cell_87_7_1249_s_33	8980231	All  inviable spores germinated and divided three or four times, showing that  YCR052w is  essential for mitotic growth (  Figure 1).	gene_phenotype
68951	1	333161	5	NULL	NULL	NULL	NULL	YDL020C	NucleicAcid		is associated with		may be;;loosely			proteasome	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_1_262_s_194	10618406	Both YDL020C and YDR069C may be loosely associated with the proteasome ( 23-25), but the SVM does not classify them as belonging to the proteasome because they are regulated differently from the rest of the proteasome during sporulation.	gene_phenotype
68952	2	333161	5	NULL	NULL	NULL	NULL	YDR069C	NucleicAcid		is associated with		may be;;loosely			proteasome	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_1_262_s_194	10618406	Both YDL020C and YDR069C may be loosely associated with the proteasome ( 23-25), but the SVM does not classify them as belonging to the proteasome because they are regulated differently from the rest of the proteasome during sporulation.	gene_phenotype
68953	1	333163	5	NULL	NULL	0	NULL	YFL049W	NucleicAcid		is a type of					transcriptional regulator	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_34_3_955_s_9	16464826	Based on their transcriptional activity, localization and interaction patterns, at least six previously uncharacterized proteins are suggested to be bona fide transcriptional regulators (namely YFL049W, YJR070C, YDR520C, YGL066W/Sgf73, YKR064W and YCR082W/Ahc2).	gene_phenotype
68954	2	333163	5	NULL	NULL	0	NULL	YJR070C	NucleicAcid		is a type of					transcriptional regulator	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_34_3_955_s_9	16464826	Based on their transcriptional activity, localization and interaction patterns, at least six previously uncharacterized proteins are suggested to be bona fide transcriptional regulators (namely YFL049W, YJR070C, YDR520C, YGL066W/Sgf73, YKR064W and YCR082W/Ahc2).	gene_phenotype
68955	3	333163	5	NULL	NULL	0	NULL	YDR520C	NucleicAcid		is a type of					transcriptional regulator	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_34_3_955_s_9	16464826	Based on their transcriptional activity, localization and interaction patterns, at least six previously uncharacterized proteins are suggested to be bona fide transcriptional regulators (namely YFL049W, YJR070C, YDR520C, YGL066W/Sgf73, YKR064W and YCR082W/Ahc2).	gene_phenotype
68956	4	333163	5	NULL	NULL	0	NULL	Sgf73	GP		is a type of					transcriptional regulator	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_34_3_955_s_9	16464826	Based on their transcriptional activity, localization and interaction patterns, at least six previously uncharacterized proteins are suggested to be bona fide transcriptional regulators (namely YFL049W, YJR070C, YDR520C, YGL066W/Sgf73, YKR064W and YCR082W/Ahc2).	gene_phenotype
68957	5	333163	5	NULL	NULL	0	NULL	YKR064W	NucleicAcid		is a type of					transcriptional regulator	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_34_3_955_s_9	16464826	Based on their transcriptional activity, localization and interaction patterns, at least six previously uncharacterized proteins are suggested to be bona fide transcriptional regulators (namely YFL049W, YJR070C, YDR520C, YGL066W/Sgf73, YKR064W and YCR082W/Ahc2).	gene_phenotype
68958	6	333163	5	NULL	NULL	0	NULL	Ahc2	GP		is a type of					transcriptional regulator	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_34_3_955_s_9	16464826	Based on their transcriptional activity, localization and interaction patterns, at least six previously uncharacterized proteins are suggested to be bona fide transcriptional regulators (namely YFL049W, YJR070C, YDR520C, YGL066W/Sgf73, YKR064W and YCR082W/Ahc2).	gene_phenotype
68959	7	333163	5	NULL	NULL	0	NULL	YGL066W	NucleicAcid		is the locus name of					Sgf73	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_34_3_955_s_9	16464826	Based on their transcriptional activity, localization and interaction patterns, at least six previously uncharacterized proteins are suggested to be bona fide transcriptional regulators (namely YFL049W, YJR070C, YDR520C, YGL066W/Sgf73, YKR064W and YCR082W/Ahc2).	gene_phenotype
68960	8	333163	5	NULL	NULL	0	NULL	YCR082W	NucleicAcid		is the locus name of					Ahc2	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_34_3_955_s_9	16464826	Based on their transcriptional activity, localization and interaction patterns, at least six previously uncharacterized proteins are suggested to be bona fide transcriptional regulators (namely YFL049W, YJR070C, YDR520C, YGL066W/Sgf73, YKR064W and YCR082W/Ahc2).	gene_phenotype
68961	1	333168	5	NULL	NULL	0	NULL	YJL125c	NucleicAcid	Saccharomyces cerevisiae	is essential for					vegetative growth	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_20_7784_s_461	11003673	Disruption and basic functional analysis of five chromosome X novel ORFs of Saccharomyces cerevisiae reveals YJL125c as an essential gene for vegetative growth.	gene_phenotype
68962	1	333174	5	NULL	NULL	0	NULL	YLR126C	NucleicAcid		encodes					COG0518.1, GuaA			glutamine amidotransferase domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_6_4450_s_229	14534306	YLR126C encodes a protein with a glutamine amidotransferase domain (COG0518.1, GuaA), which is present in multiple proteins involved in nucleotide transport or metabolism as well as anthranilate synthases.	gene_phenotype
68963	2	333174	5	NULL	NULL	0	NULL	proteins	GP		is involved in			glutamine amidotransferase domain		nucleotide transport	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_6_4450_s_229	14534306	YLR126C encodes a protein with a glutamine amidotransferase domain (COG0518.1, GuaA), which is present in multiple proteins involved in nucleotide transport or metabolism as well as anthranilate synthases.	gene_phenotype
68964	3	333174	5	NULL	NULL	0	NULL	proteins	GP		is involved in			glutamine amidotransferase domain		metabolism	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_6_4450_s_229	14534306	YLR126C encodes a protein with a glutamine amidotransferase domain (COG0518.1, GuaA), which is present in multiple proteins involved in nucleotide transport or metabolism as well as anthranilate synthases.	gene_phenotype
68965	4	333174	5	NULL	NULL	0	NULL	YLR126C	NucleicAcid		encodes					anthranilate synthases	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_6_4450_s_229	14534306	YLR126C encodes a protein with a glutamine amidotransferase domain (COG0518.1, GuaA), which is present in multiple proteins involved in nucleotide transport or metabolism as well as anthranilate synthases.	gene_phenotype
68966	1	333175	5	NULL	NULL	0	NULL	YPR128C	NucleicAcid		is a member of					ATP/ADP carrier family of solute transporters	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_6_2937_s_108	10077615	The search for candidate PMPs was also successful, leading to the identification of YPR128C, an uncharacterized member of the ATP/ADP carrier family of solute transporters, and YOL044W, an orphan protein.	gene_phenotype
68967	2	333175	5	NULL	NULL	0	NULL	YOL044W	NucleicAcid		is a type of					orphan protein	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_6_2937_s_108	10077615	The search for candidate PMPs was also successful, leading to the identification of YPR128C, an uncharacterized member of the ATP/ADP carrier family of solute transporters, and YOL044W, an orphan protein.	gene_phenotype
68968	1	333178	5	NULL	NULL	0	NULL	YKR096w	NucleicAcid		is dispensable for					cell viability	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_103_25_9464_s_51	16769905	This effect is consistent with results from a large-scale deletion project that found YKR096w and YOR166c dispensable for cell viability ( ).	gene_phenotype
68969	2	333178	5	NULL	NULL	0	NULL	YOR166c	NucleicAcid		is dispensable for					cell viability	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_103_25_9464_s_51	16769905	This effect is consistent with results from a large-scale deletion project that found YKR096w and YOR166c dispensable for cell viability ( ).	gene_phenotype
68970	1	333181	5	NULL	NULL	NULL	NULL	aut4	Cell		is defective in					autophagic vesicles	CellComponent	lysis of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17621_s_102	8663607	Interestingly,  aut4 and  aut6 have different autophagy defects:  aut4, like  aut5, is defective in lysis of autophagic vesicles after delivery to the vacuole; vesicles accumulate in the vacuole in the absence of PMSF.  aut6, similar to  aut1,  2,  3, and  9, is defective in accumulation of vesicles	gene_phenotype
68971	2	333181	5	NULL	NULL	0	NULL	statement 1	Process		occurs after					vacuole	CellComponent	delivery to			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17621_s_102	8663607	Interestingly,  aut4 and  aut6 have different autophagy defects:  aut4, like  aut5, is defective in lysis of autophagic vesicles after delivery to the vacuole; vesicles accumulate in the vacuole in the absence of PMSF.  aut6, similar to  aut1,  2,  3, and  9, is defective in accumulation of vesicles	gene_phenotype
68972	3	333181	5	NULL	NULL	NULL	NULL	aut5	Cell		is defective in					autophagic vesicles	CellComponent	lysis of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_30_17621_s_102	8663607	Interestingly,  aut4 and  aut6 have different autophagy defects:  aut4, like  aut5, is defective in lysis of autophagic vesicles after delivery to the vacuole; vesicles accumulate in the vacuole in the absence of PMSF.  aut6, similar to  aut1,  2,  3, and  9, is defective in accumulation of vesicles	gene_phenotype
68973	4	333181	5	NULL	NULL	0	NULL	vesicles	CellComponent		accumulates in					vacuole	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17621_s_102	8663607	Interestingly,  aut4 and  aut6 have different autophagy defects:  aut4, like  aut5, is defective in lysis of autophagic vesicles after delivery to the vacuole; vesicles accumulate in the vacuole in the absence of PMSF.  aut6, similar to  aut1,  2,  3, and  9, is defective in accumulation of vesicles	gene_phenotype
68974	5	333181	5	NULL	NULL	0	NULL	statement 4	Process		in the absence of					PMSF	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17621_s_102	8663607	Interestingly,  aut4 and  aut6 have different autophagy defects:  aut4, like  aut5, is defective in lysis of autophagic vesicles after delivery to the vacuole; vesicles accumulate in the vacuole in the absence of PMSF.  aut6, similar to  aut1,  2,  3, and  9, is defective in accumulation of vesicles	gene_phenotype
68975	6	333181	5	NULL	NULL	0	NULL	aut6	Cell		is defective in					vesicle	CellComponent	accumulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17621_s_102	8663607	Interestingly,  aut4 and  aut6 have different autophagy defects:  aut4, like  aut5, is defective in lysis of autophagic vesicles after delivery to the vacuole; vesicles accumulate in the vacuole in the absence of PMSF.  aut6, similar to  aut1,  2,  3, and  9, is defective in accumulation of vesicles	gene_phenotype
68976	7	333181	5	NULL	NULL	0	NULL	aut1	Cell		is defective in					vesicle	CellComponent	accumulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17621_s_102	8663607	Interestingly,  aut4 and  aut6 have different autophagy defects:  aut4, like  aut5, is defective in lysis of autophagic vesicles after delivery to the vacuole; vesicles accumulate in the vacuole in the absence of PMSF.  aut6, similar to  aut1,  2,  3, and  9, is defective in accumulation of vesicles	gene_phenotype
68977	8	333181	5	NULL	NULL	0	NULL	aut2	Cell		is defective in					vesicle	CellComponent	accumulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17621_s_102	8663607	Interestingly,  aut4 and  aut6 have different autophagy defects:  aut4, like  aut5, is defective in lysis of autophagic vesicles after delivery to the vacuole; vesicles accumulate in the vacuole in the absence of PMSF.  aut6, similar to  aut1,  2,  3, and  9, is defective in accumulation of vesicles	gene_phenotype
68978	9	333181	5	NULL	NULL	0	NULL	aut3	Cell		is defective in					vesicle	CellComponent	accumulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17621_s_102	8663607	Interestingly,  aut4 and  aut6 have different autophagy defects:  aut4, like  aut5, is defective in lysis of autophagic vesicles after delivery to the vacuole; vesicles accumulate in the vacuole in the absence of PMSF.  aut6, similar to  aut1,  2,  3, and  9, is defective in accumulation of vesicles	gene_phenotype
68979	10	333181	5	NULL	NULL	0	NULL	aut9	Cell		is defective in					vesicle	CellComponent	accumulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17621_s_102	8663607	Interestingly,  aut4 and  aut6 have different autophagy defects:  aut4, like  aut5, is defective in lysis of autophagic vesicles after delivery to the vacuole; vesicles accumulate in the vacuole in the absence of PMSF.  aut6, similar to  aut1,  2,  3, and  9, is defective in accumulation of vesicles	gene_phenotype
68980	1	333182	5	NULL	NULL	NULL	NULL	cvt3	Process		is defective in					API	GP	maturation of			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_21_6005_s_252	10545112	This corroborates previous findings, in which the API maturation defects of  cvt3 and  cvt9 were found to be bypassed by the autophagy pathway, and two mutants defective in autophagy,  aut4 and  aut6, were found to process API normally (Harding  et al., 1996  ).	gene_phenotype
68981	2	333182	5	NULL	NULL	0	NULL	cvt9	Process		is defective in					API	GP	maturation of			NULL		0	NULL	NULL	NULL	gw60_embo_18_21_6005_s_252	10545112	This corroborates previous findings, in which the API maturation defects of  cvt3 and  cvt9 were found to be bypassed by the autophagy pathway, and two mutants defective in autophagy,  aut4 and  aut6, were found to process API normally (Harding  et al., 1996  ).	gene_phenotype
68982	3	333182	5	NULL	NULL	0	NULL	statement 1	Process		is bypassed by					autophagy pathway	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_6005_s_252	10545112	This corroborates previous findings, in which the API maturation defects of  cvt3 and  cvt9 were found to be bypassed by the autophagy pathway, and two mutants defective in autophagy,  aut4 and  aut6, were found to process API normally (Harding  et al., 1996  ).	gene_phenotype
68983	4	333182	5	NULL	NULL	0	NULL	statement 2	Process		is bypassed by					autophagy pathway	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_6005_s_252	10545112	This corroborates previous findings, in which the API maturation defects of  cvt3 and  cvt9 were found to be bypassed by the autophagy pathway, and two mutants defective in autophagy,  aut4 and  aut6, were found to process API normally (Harding  et al., 1996  ).	gene_phenotype
68984	5	333182	5	NULL	NULL	0	NULL	aut4	Cell		is defective in					autophagy	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_6005_s_252	10545112	This corroborates previous findings, in which the API maturation defects of  cvt3 and  cvt9 were found to be bypassed by the autophagy pathway, and two mutants defective in autophagy,  aut4 and  aut6, were found to process API normally (Harding  et al., 1996  ).	gene_phenotype
68985	6	333182	5	NULL	NULL	0	NULL	aut6	Cell		is defective in					autophagy	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_6005_s_252	10545112	This corroborates previous findings, in which the API maturation defects of  cvt3 and  cvt9 were found to be bypassed by the autophagy pathway, and two mutants defective in autophagy,  aut4 and  aut6, were found to process API normally (Harding  et al., 1996  ).	gene_phenotype
68986	7	333182	5	NULL	NULL	0	NULL	aut4	Cell		process		normally			API	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_6005_s_252	10545112	This corroborates previous findings, in which the API maturation defects of  cvt3 and  cvt9 were found to be bypassed by the autophagy pathway, and two mutants defective in autophagy,  aut4 and  aut6, were found to process API normally (Harding  et al., 1996  ).	gene_phenotype
68987	8	333182	5	NULL	NULL	0	NULL	aut6	Cell		process		normally			API	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_6005_s_252	10545112	This corroborates previous findings, in which the API maturation defects of  cvt3 and  cvt9 were found to be bypassed by the autophagy pathway, and two mutants defective in autophagy,  aut4 and  aut6, were found to process API normally (Harding  et al., 1996  ).	gene_phenotype
68988	1	333183	5	NULL	NULL	0	NULL	DAL5	GP		is a synonym of					allantoate permease	GP				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_157	9348664	The allantoate permease YJR152w ( DAL5) has given its name to the family, the other members of which might transport other  weak acids and include the proteins YAl067c ( GEO1) and YCR028c ( FEN2), which are both involved in some kind of resistance.	gene_phenotype
68989	2	333183	5	NULL	NULL	0	NULL	YJR152w	NucleicAcid		is the locus name of					DAL5	GP				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_157	9348664	The allantoate permease YJR152w ( DAL5) has given its name to the family, the other members of which might transport other  weak acids and include the proteins YAl067c ( GEO1) and YCR028c ( FEN2), which are both involved in some kind of resistance.	gene_phenotype
68990	3	333183	5	NULL	NULL	0	NULL	DAL5	GP		transport		might			acids	Chemical	weak			NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_157	9348664	The allantoate permease YJR152w ( DAL5) has given its name to the family, the other members of which might transport other  weak acids and include the proteins YAl067c ( GEO1) and YCR028c ( FEN2), which are both involved in some kind of resistance.	gene_phenotype
68991	4	333183	5	NULL	NULL	0	NULL	GEO1	GP		is involved in					resistance	Process				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_157	9348664	The allantoate permease YJR152w ( DAL5) has given its name to the family, the other members of which might transport other  weak acids and include the proteins YAl067c ( GEO1) and YCR028c ( FEN2), which are both involved in some kind of resistance.	gene_phenotype
68992	5	333183	5	NULL	NULL	0	NULL	FEN2	GP		is involved in					resistance	Process				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_157	9348664	The allantoate permease YJR152w ( DAL5) has given its name to the family, the other members of which might transport other  weak acids and include the proteins YAl067c ( GEO1) and YCR028c ( FEN2), which are both involved in some kind of resistance.	gene_phenotype
68993	6	333183	5	NULL	NULL	0	NULL	YAl067c	NucleicAcid		is the locus name of					GEO1	GP				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_157	9348664	The allantoate permease YJR152w ( DAL5) has given its name to the family, the other members of which might transport other  weak acids and include the proteins YAl067c ( GEO1) and YCR028c ( FEN2), which are both involved in some kind of resistance.	gene_phenotype
68994	7	333183	5	NULL	NULL	0	NULL	YCR028c	NucleicAcid		is the locus name of					FEN2	GP				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_2_113_s_157	9348664	The allantoate permease YJR152w ( DAL5) has given its name to the family, the other members of which might transport other  weak acids and include the proteins YAl067c ( GEO1) and YCR028c ( FEN2), which are both involved in some kind of resistance.	gene_phenotype
68995	1	333184	5	NULL	NULL	0	NULL	UGA2	GP		is a synonym of					SSADH	GP	yeast			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_42_41552_s_81	12882961	This mutant had only approximately 10% of the SSADH activity of the wild-type strain when grown on GABA as the sole nitrogen source (2.3 and 24.8 mumol/h/mg protein, respectively) and was found to overlap the YBR006W locus (data not shown), confirming that UGA2/YBR006w is the yeast SSADH ( ).	gene_phenotype
68996	2	333184	5	NULL	NULL	0	NULL	YBR006w	NucleicAcid		is the locus name of					UGA2	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_42_41552_s_81	12882961	This mutant had only approximately 10% of the SSADH activity of the wild-type strain when grown on GABA as the sole nitrogen source (2.3 and 24.8 mumol/h/mg protein, respectively) and was found to overlap the YBR006W locus (data not shown), confirming that UGA2/YBR006w is the yeast SSADH ( ).	gene_phenotype
68997	1	333185	5	NULL	NULL	0	NULL	YIH1	GP		is					yeast impact homolog 1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20243_s_52	10801780	As an approach to revealing the function of this protein family, we analyzed its budding yeast homolog YCR059C, or  yeast  impact  homolog 1 (YIH1), and identified GCN1 as its potential binding partner through a two-hybrid screening.	gene_phenotype
68998	2	333185	5	NULL	NULL	0	NULL	YIH1	GP		bind		potentially			GCN1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20243_s_52	10801780	As an approach to revealing the function of this protein family, we analyzed its budding yeast homolog YCR059C, or  yeast  impact  homolog 1 (YIH1), and identified GCN1 as its potential binding partner through a two-hybrid screening.	gene_phenotype
68999	3	333185	5	NULL	NULL	0	NULL	YCR059C	NucleicAcid	budding yeast	bind		potentially			GCN1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20243_s_52	10801780	As an approach to revealing the function of this protein family, we analyzed its budding yeast homolog YCR059C, or  yeast  impact  homolog 1 (YIH1), and identified GCN1 as its potential binding partner through a two-hybrid screening.	gene_phenotype
69000	1	333187	5	NULL	NULL	0	NULL	Ydr532c protein	GP		is a component of					SPB	CellComponent				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_12_5255_s_250	15371542	The 44-kDa Ydr532c protein has been identified as a component of the SPB and very recently as a new component of the budding yeast kinetochore (Giaever  et al., 2002 ;	gene_phenotype
69001	2	333187	5	NULL	NULL	0	NULL	Ydr532c protein	GP		is a component of					kinetochore	CellComponent	budding yeast			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_12_5255_s_250	15371542	The 44-kDa Ydr532c protein has been identified as a component of the SPB and very recently as a new component of the budding yeast kinetochore (Giaever  et al., 2002 ;	gene_phenotype
69002	1	333188	5	NULL	NULL	0	NULL	YER004W gene	GP		is a homolog of					Tip30 protein	GP	human			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_10_2987_s_304	11598186	Interestingly, the gene  YER004W has homology to the human protein Tip30, a tumor suppressor that mediates apoptosis (Shtivelman, 1997  ; Xiao  et al., 1998  , 2000  ), but its function in yeast remains to be discovered.	gene_phenotype
69003	2	333188	5	NULL	NULL	0	NULL	Tip30 protein	GP	human	is a type of					tumor suppressor	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_10_2987_s_304	11598186	Interestingly, the gene  YER004W has homology to the human protein Tip30, a tumor suppressor that mediates apoptosis (Shtivelman, 1997  ; Xiao  et al., 1998  , 2000  ), but its function in yeast remains to be discovered.	gene_phenotype
69004	3	333188	5	NULL	NULL	0	NULL	Tip30 protein	GP	human	mediates					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_10_2987_s_304	11598186	Interestingly, the gene  YER004W has homology to the human protein Tip30, a tumor suppressor that mediates apoptosis (Shtivelman, 1997  ; Xiao  et al., 1998  , 2000  ), but its function in yeast remains to be discovered.	gene_phenotype
69005	1	333189	5	NULL	NULL	0	NULL	Pth2	GP		is involved in					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_3_1436_s_266	16407407	We also identified homologues of mammalian proteins involved in apoptosis, such as Pth2 (a homologue of human Bit1; Jan  et al., 2004 ), Ndi1 (a homologue of AMID; Wu  et al., 2002 ), and Yer004w, which is homologous to mammalian HTATIP2, a protein acting in tumor suppression and apoptosis (Hodges  et al., 2002 ).	gene_phenotype
69006	2	333189	5	NULL	NULL	0	NULL	Pth2	GP		is a homolog of					Bit1	GP	human			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_3_1436_s_266	16407407	We also identified homologues of mammalian proteins involved in apoptosis, such as Pth2 (a homologue of human Bit1; Jan  et al., 2004 ), Ndi1 (a homologue of AMID; Wu  et al., 2002 ), and Yer004w, which is homologous to mammalian HTATIP2, a protein acting in tumor suppression and apoptosis (Hodges  et al., 2002 ).	gene_phenotype
69007	3	333189	5	NULL	NULL	0	NULL	Ndi1	GP		is involved in					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_3_1436_s_266	16407407	We also identified homologues of mammalian proteins involved in apoptosis, such as Pth2 (a homologue of human Bit1; Jan  et al., 2004 ), Ndi1 (a homologue of AMID; Wu  et al., 2002 ), and Yer004w, which is homologous to mammalian HTATIP2, a protein acting in tumor suppression and apoptosis (Hodges  et al., 2002 ).	gene_phenotype
69008	4	333189	5	NULL	NULL	0	NULL	Ndi1	GP		is a homolog of					AMID	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_3_1436_s_266	16407407	We also identified homologues of mammalian proteins involved in apoptosis, such as Pth2 (a homologue of human Bit1; Jan  et al., 2004 ), Ndi1 (a homologue of AMID; Wu  et al., 2002 ), and Yer004w, which is homologous to mammalian HTATIP2, a protein acting in tumor suppression and apoptosis (Hodges  et al., 2002 ).	gene_phenotype
69009	5	333189	5	NULL	NULL	0	NULL	Yer004w	GP		is a homolog of					HTATIP2	GP	mammalian			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_3_1436_s_266	16407407	We also identified homologues of mammalian proteins involved in apoptosis, such as Pth2 (a homologue of human Bit1; Jan  et al., 2004 ), Ndi1 (a homologue of AMID; Wu  et al., 2002 ), and Yer004w, which is homologous to mammalian HTATIP2, a protein acting in tumor suppression and apoptosis (Hodges  et al., 2002 ).	gene_phenotype
69010	6	333189	5	NULL	NULL	NULL	NULL	HTATIP2 protein	GP	mammalian	plays a role in					tuomr supression	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_17_3_1436_s_266	16407407	We also identified homologues of mammalian proteins involved in apoptosis, such as Pth2 (a homologue of human Bit1; Jan  et al., 2004 ), Ndi1 (a homologue of AMID; Wu  et al., 2002 ), and Yer004w, which is homologous to mammalian HTATIP2, a protein acting in tumor suppression and apoptosis (Hodges  et al., 2002 ).	gene_phenotype
69011	7	333189	5	NULL	NULL	0	NULL	HTATIP2 protein	GP	mammalian	plays a role in					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_3_1436_s_266	16407407	We also identified homologues of mammalian proteins involved in apoptosis, such as Pth2 (a homologue of human Bit1; Jan  et al., 2004 ), Ndi1 (a homologue of AMID; Wu  et al., 2002 ), and Yer004w, which is homologous to mammalian HTATIP2, a protein acting in tumor suppression and apoptosis (Hodges  et al., 2002 ).	gene_phenotype
69012	1	333191	5	NULL	NULL	0	NULL	Avt proteins	GP		is related to					synaptic vesicular transporters	CellComponent	Caenorhabditis elegans;;rat;;mouse			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_44_43051_s_240	12937179	Sequence analysis predicts that the three Avt proteins are related to the synaptic vesicular transporters found in  Caenorhabditis elegans, rat, and mouse; the protein encoded by  YER053C is a member of the mitochondrial carrier family.	gene_phenotype
69013	2	333191	5	NULL	NULL	0	NULL	protein encoded by YER053C	GP		is a member of					mitochondrial carrier family	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_44_43051_s_240	12937179	Sequence analysis predicts that the three Avt proteins are related to the synaptic vesicular transporters found in  Caenorhabditis elegans, rat, and mouse; the protein encoded by  YER053C is a member of the mitochondrial carrier family.	gene_phenotype
69014	1	333193	5	NULL	NULL	0	NULL	YFR022w	NucleicAcid	expression of	downregulated in					meiosis	Process				NULL		0	NULL	NULL	NULL	gw70_nature_430_6999_573_s_71	15229615	For example, YFR022w expression is downregulated in meiosis, and the locus now was  covered by cohesin extending from the neighbouring  PES4/YFR024c association site ( Supplementary Fig. S3).	gene_phenotype
69015	2	333193	5	NULL	NULL	0	NULL	YFR022w	NucleicAcid		is covered by					cohesin	GP				NULL		0	NULL	NULL	NULL	gw70_nature_430_6999_573_s_71	15229615	For example, YFR022w expression is downregulated in meiosis, and the locus now was  covered by cohesin extending from the neighbouring  PES4/YFR024c association site ( Supplementary Fig. S3).	gene_phenotype
69016	3	333193	5	NULL	NULL	0	NULL	cohesin	GP		extends from					PES4	GP	neighbouring association site of			NULL		0	NULL	NULL	NULL	gw70_nature_430_6999_573_s_71	15229615	For example, YFR022w expression is downregulated in meiosis, and the locus now was  covered by cohesin extending from the neighbouring  PES4/YFR024c association site ( Supplementary Fig. S3).	gene_phenotype
69017	4	333193	5	NULL	NULL	0	NULL	YFR024c	GP		is the locus name of					PES4	GP				NULL		0	NULL	NULL	NULL	gw70_nature_430_6999_573_s_71	15229615	For example, YFR022w expression is downregulated in meiosis, and the locus now was  covered by cohesin extending from the neighbouring  PES4/YFR024c association site ( Supplementary Fig. S3).	gene_phenotype
69018	1	333194	5	NULL	NULL	0	NULL	proteins encoded by YGL104c	NucleicAcid		is similar to					proteins encoded by YBR241c	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_1_85_s_356	9299703	The proteins  encoded by genes  YGL104c and  YBR241c display 47.4% identity to each other but less than 28% to the hexose transporters.	gene_phenotype
69019	2	333194	5	NULL	NULL	0	NULL	proteins encoded by YGL104c	NucleicAcid		is similar to					hexose transporters	GP				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_1_85_s_356	9299703	The proteins  encoded by genes  YGL104c and  YBR241c display 47.4% identity to each other but less than 28% to the hexose transporters.	gene_phenotype
69020	3	333194	5	NULL	NULL	0	NULL	statement 1	Process		lesser than					statement 2					NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_1_85_s_356	9299703	The proteins  encoded by genes  YGL104c and  YBR241c display 47.4% identity to each other but less than 28% to the hexose transporters.	gene_phenotype
69021	4	333194	5	NULL	NULL	0	NULL	proteins encoded by YBR241c	NucleicAcid		is similar to					hexose transporters	GP				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_1_85_s_356	9299703	The proteins  encoded by genes  YGL104c and  YBR241c display 47.4% identity to each other but less than 28% to the hexose transporters.	gene_phenotype
69022	5	333194	5	NULL	NULL	0	NULL	statement 1	Process		lesser than					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_21_1_85_s_356	9299703	The proteins  encoded by genes  YGL104c and  YBR241c display 47.4% identity to each other but less than 28% to the hexose transporters.	gene_phenotype
69023	1	333196	5	NULL	NULL	0	NULL	tetrads	Cell		is formed during					sporulation	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_9_2646_s_141	11553705	We therefore conclude that a novel gene  ADY1 at  YHR185C is required for the formation of tetrads in sporulation.	gene_phenotype
69024	2	333196	5	NULL	NULL	NULL	NULL	ADY1 gene	GP	novel	is required for					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_9_2646_s_141	11553705	We therefore conclude that a novel gene  ADY1 at  YHR185C is required for the formation of tetrads in sporulation.	gene_phenotype
69025	3	333196	5	NULL	NULL	0	NULL	ADY1	GP		is encoded by					YHR185C	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_9_2646_s_141	11553705	We therefore conclude that a novel gene  ADY1 at  YHR185C is required for the formation of tetrads in sporulation.	gene_phenotype
69026	1	333197	5	NULL	NULL	0	NULL	ADY1 gene	GP	novel	is required for					sporulation	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_9_2646_s_32	11553705	In a screen for genes required for sporulation, we identified a novel gene  ADY1 (accumulates dyads), corresponding to the open reading frame (ORF)  YHR185C.	gene_phenotype
69027	2	333197	5	NULL	NULL	0	NULL	ADY1 gene	GP		accumulates					dyads	Cell				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_9_2646_s_32	11553705	In a screen for genes required for sporulation, we identified a novel gene  ADY1 (accumulates dyads), corresponding to the open reading frame (ORF)  YHR185C.	gene_phenotype
69028	3	333197	5	NULL	NULL	0	NULL	ADY1 gene	GP		corresponds to					ORF YHR185C	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_9_2646_s_32	11553705	In a screen for genes required for sporulation, we identified a novel gene  ADY1 (accumulates dyads), corresponding to the open reading frame (ORF)  YHR185C.	gene_phenotype
69029	1	333198	5	NULL	NULL	0	NULL	ECM31	GP	deletion of	causes					pantothenic acid 	Chemical	auxotrophy of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_14_10794_s_149	11154694	Deletions in genes that have structural homology to the bacterial genes of the pantothenic acid pathway,  ECM31 and  YIL145c (see Fig.  1), caused pantothenic acid auxotrophy, but these strains did not grow on a beta-alanine supplement, indicating that these genes are downstream in the pathway (see Fig.  1).	gene_phenotype
69030	2	333198	5	NULL	NULL	0	NULL	YIL145c	GP	deletion of	causes					pantothenic acid	Chemical	auxotrophy of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_14_10794_s_149	11154694	Deletions in genes that have structural homology to the bacterial genes of the pantothenic acid pathway,  ECM31 and  YIL145c (see Fig.  1), caused pantothenic acid auxotrophy, but these strains did not grow on a beta-alanine supplement, indicating that these genes are downstream in the pathway (see Fig.  1).	gene_phenotype
69031	1	333199	5	NULL	NULL	0	NULL	ORF YKR031c	NucleicAcid	yeast	activates					PLD	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_5_2361_s_74	8576189	Thus, ORF  YKR031c seemed a likely candidate for a yeast protein having PLD  activity and was tentatively renamed  PLD1.	gene_phenotype
69032	2	333199	5	NULL	NULL	0	NULL	ORF YKR031c	NucleicAcid	yeast	is renamed as					PLD1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_5_2361_s_74	8576189	Thus, ORF  YKR031c seemed a likely candidate for a yeast protein having PLD  activity and was tentatively renamed  PLD1.	gene_phenotype
69033	1	333201	5	NULL	NULL	0	NULL	FOW1	GP	sequence of	is similar to		cloely			YMR241w protein	GP	yeast;;sequence of			NULL		0	NULL	NULL	NULL	gw70_nature_431_7008_582_s_93	15457264	FOW1 shares close sequence similarity with a yeast protein  (YMR241w) required for tricarboxylic acid transport 19.	gene_phenotype
69034	2	333201	5	NULL	NULL	0	NULL	YMR241w protein	GP	yeast	is required for					tricarboxylic acid	Chemical	transport of			NULL		0	NULL	NULL	NULL	gw70_nature_431_7008_582_s_93	15457264	FOW1 shares close sequence similarity with a yeast protein  (YMR241w) required for tricarboxylic acid transport 19.	gene_phenotype
69035	1	333202	5	NULL	NULL	0	NULL	Mss4	GP		is required for					actin cytoskeleton	CellComponent	polarization of			NULL		0	NULL	NULL	NULL	gw70_embo_23_19_3747_s_5	15372071	Like Mss4, Slm1 and its homolog Slm2 (Ynl047c) were required for  actin cytoskeleton polarization and viability.	gene_phenotype
69036	2	333202	5	NULL	NULL	0	NULL	Mss4	GP		is required for					actin cytoskeleton	CellComponent	viability of			NULL		0	NULL	NULL	NULL	gw70_embo_23_19_3747_s_5	15372071	Like Mss4, Slm1 and its homolog Slm2 (Ynl047c) were required for  actin cytoskeleton polarization and viability.	gene_phenotype
69037	3	333202	5	NULL	NULL	0	NULL	Slm1	GP		is required for					actin cytoskeleton	CellComponent	polarization of			NULL		0	NULL	NULL	NULL	gw70_embo_23_19_3747_s_5	15372071	Like Mss4, Slm1 and its homolog Slm2 (Ynl047c) were required for  actin cytoskeleton polarization and viability.	gene_phenotype
69038	4	333202	5	NULL	NULL	0	NULL	Slm1	GP		is required for					actin cytoskeleton	CellComponent	viability of			NULL		0	NULL	NULL	NULL	gw70_embo_23_19_3747_s_5	15372071	Like Mss4, Slm1 and its homolog Slm2 (Ynl047c) were required for  actin cytoskeleton polarization and viability.	gene_phenotype
69039	5	333202	5	NULL	NULL	0	NULL	Slm2	GP		is required for					actin cytoskeleton	CellComponent	polarization of			NULL		0	NULL	NULL	NULL	gw70_embo_23_19_3747_s_5	15372071	Like Mss4, Slm1 and its homolog Slm2 (Ynl047c) were required for  actin cytoskeleton polarization and viability.	gene_phenotype
69040	6	333202	5	NULL	NULL	0	NULL	Slm2	GP		is required for					actin cytoskeleton	CellComponent	viability of			NULL		0	NULL	NULL	NULL	gw70_embo_23_19_3747_s_5	15372071	Like Mss4, Slm1 and its homolog Slm2 (Ynl047c) were required for  actin cytoskeleton polarization and viability.	gene_phenotype
69041	7	333202	5	NULL	NULL	0	NULL	Slm2	GP		is a homolog of					Slm1	GP				NULL		0	NULL	NULL	NULL	gw70_embo_23_19_3747_s_5	15372071	Like Mss4, Slm1 and its homolog Slm2 (Ynl047c) were required for  actin cytoskeleton polarization and viability.	gene_phenotype
69042	8	333202	5	NULL	NULL	0	NULL	Ynl047c	NucleicAcid		encodes for					Slm2	GP				NULL		0	NULL	NULL	NULL	gw70_embo_23_19_3747_s_5	15372071	Like Mss4, Slm1 and its homolog Slm2 (Ynl047c) were required for  actin cytoskeleton polarization and viability.	gene_phenotype
69043	1	333203	5	NULL	NULL	0	NULL	YHR194W gene	GP		is a synonym of					MDM31	GP				NULL		0	NULL	NULL	NULL	gw70_genetics_171_2_517_s_107	16020778	Both  YHR194W and  YOR147W genes were identified previously in a genome-wide screen for mutants with an altered mitochondrial morphology and were designated as  MDM31 and  MDM32, respectively ( IMMER et al.).	gene_phenotype
69044	2	333203	5	NULL	NULL	0	NULL	YOR147W gene	GP		is a synonym of					MDM32	GP				NULL		0	NULL	NULL	NULL	gw70_genetics_171_2_517_s_107	16020778	Both  YHR194W and  YOR147W genes were identified previously in a genome-wide screen for mutants with an altered mitochondrial morphology and were designated as  MDM31 and  MDM32, respectively ( IMMER et al.).	gene_phenotype
69045	3	333203	5	NULL	NULL	0	NULL	MDM31	GP		plays a role in					mitochondria	CellComponent	morphology of			NULL		0	NULL	NULL	NULL	gw70_genetics_171_2_517_s_107	16020778	Both  YHR194W and  YOR147W genes were identified previously in a genome-wide screen for mutants with an altered mitochondrial morphology and were designated as  MDM31 and  MDM32, respectively ( IMMER et al.).	gene_phenotype
69046	4	333203	5	NULL	NULL	0	NULL	MDM32	GP		plays a role in					mitochondria	CellComponent	morphology of			NULL		0	NULL	NULL	NULL	gw70_genetics_171_2_517_s_107	16020778	Both  YHR194W and  YOR147W genes were identified previously in a genome-wide screen for mutants with an altered mitochondrial morphology and were designated as  MDM31 and  MDM32, respectively ( IMMER et al.).	gene_phenotype
69047	1	333204	5	NULL	NULL	0	NULL	YPL176c	NucleicAcid		is a synonym of					yeast transferrin receptor-like	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_99_22_14183_s_101	12374868	A GFP fusion of yeast transferrin receptor-like YPL176c (YPL176-GFP) localized in a punctate pattern along the surface of the body of the cell, mostly excluded from the shmoo tip (Fig.  3 c), and also was detergent-soluble (Fig.  3g).	gene_phenotype
69048	2	333204	5	NULL	NULL	0	NULL	YPL176-GFP	GP		is a type of					GFP fusion protein					NULL		0	NULL	NULL	NULL	gw60_pnas_99_22_14183_s_101	12374868	A GFP fusion of yeast transferrin receptor-like YPL176c (YPL176-GFP) localized in a punctate pattern along the surface of the body of the cell, mostly excluded from the shmoo tip (Fig.  3 c), and also was detergent-soluble (Fig.  3g).	gene_phenotype
69049	3	333204	5	NULL	NULL	0	NULL	YPL176-GFP	GP		is localized along					cell	Cell	surface of;;body of			NULL		0	NULL	NULL	NULL	gw60_pnas_99_22_14183_s_101	12374868	A GFP fusion of yeast transferrin receptor-like YPL176c (YPL176-GFP) localized in a punctate pattern along the surface of the body of the cell, mostly excluded from the shmoo tip (Fig.  3 c), and also was detergent-soluble (Fig.  3g).	gene_phenotype
69050	4	333204	5	NULL	NULL	0	NULL	statement 3	Process		occurs in					punctate pattern	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw60_pnas_99_22_14183_s_101	12374868	A GFP fusion of yeast transferrin receptor-like YPL176c (YPL176-GFP) localized in a punctate pattern along the surface of the body of the cell, mostly excluded from the shmoo tip (Fig.  3 c), and also was detergent-soluble (Fig.  3g).	gene_phenotype
69051	5	333204	5	NULL	NULL	0	NULL	YPL176-GFP	GP	localization of	excluded from		mostly			shmoo tip	CellComponent				NULL		0	NULL	NULL	NULL	gw60_pnas_99_22_14183_s_101	12374868	A GFP fusion of yeast transferrin receptor-like YPL176c (YPL176-GFP) localized in a punctate pattern along the surface of the body of the cell, mostly excluded from the shmoo tip (Fig.  3 c), and also was detergent-soluble (Fig.  3g).	gene_phenotype
69052	1	333207	5	NULL	NULL	0	NULL	Ydr527wp protein	GP	Saccharomyces cerevisiae	is required for					cell viability	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_16_7043_s_151	15282305	In addition, these proteins show significant similarities to the  Saccharomyces cerevisiae Ydr527wp protein (accession no.  NP 010816), which is required for cell viability and was shown to bind the Rpb10 subunit of RNAPII in a two-hybrid screen ( ,  ).	gene_phenotype
69053	2	333207	5	NULL	NULL	0	NULL	Ydr527wp protein	GP	Saccharomyces cerevisiae	bind					RNAPII	GP		Rpb10 subunit		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_16_7043_s_151	15282305	In addition, these proteins show significant similarities to the  Saccharomyces cerevisiae Ydr527wp protein (accession no.  NP 010816), which is required for cell viability and was shown to bind the Rpb10 subunit of RNAPII in a two-hybrid screen ( ,  ).	gene_phenotype
69054	1	333208	5	NULL	NULL	0	NULL	YGR156w	NucleicAcid		is the locus name of					PTI1	GP				NULL		0	NULL	NULL	NULL	gw60_molcell_10_6_1429_s_32	12504017	PTI1 (YGR156w) Is a Suppressor of  ctk1  Cold Sensitivity	gene_phenotype
69055	2	333208	5	NULL	NULL	0	NULL	ctk1	GP		is sensitive to					cold	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw60_molcell_10_6_1429_s_32	12504017	PTI1 (YGR156w) Is a Suppressor of  ctk1  Cold Sensitivity	gene_phenotype
69056	3	333208	5	NULL	NULL	0	NULL	PTI1	GP		is a suppressor of					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_10_6_1429_s_32	12504017	PTI1 (YGR156w) Is a Suppressor of  ctk1  Cold Sensitivity	gene_phenotype
69057	1	333210	5	NULL	NULL	0	NULL	yhl021c	NucleicAcid	mutant	does not show										NULL		0	NULL	NULL	NULL	gw60_genetics_155_4_1607_s_91	10924460	yhl021c mutants have no detectable phenotype in mitosis or meiosis.	gene_phenotype
69058	1	333211	5	NULL	NULL	NULL	NULL	haploid cells	Cell		contains					Ykl082c-YFP	GP	genomic			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_156	11489916	We found that haploid cells containing the genomic Ykl082c-YFP fusion were slow growing and temperature sensitive.	gene_phenotype
69059	2	333211	5	NULL	NULL	0	NULL	Ykl082c-YFP	GP		is a type of					fusion protein	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_156	11489916	We found that haploid cells containing the genomic Ykl082c-YFP fusion were slow growing and temperature sensitive.	gene_phenotype
69060	3	333211	5	NULL	NULL	0	NULL	statement 1	Process		shows					growth	Process	slow			NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_156	11489916	We found that haploid cells containing the genomic Ykl082c-YFP fusion were slow growing and temperature sensitive.	gene_phenotype
69061	4	333211	5	NULL	NULL	0	NULL	statement 1	Process		is sensitive to					temperature	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_156	11489916	We found that haploid cells containing the genomic Ykl082c-YFP fusion were slow growing and temperature sensitive.	gene_phenotype
69062	1	333217	5	NULL	NULL	0	NULL	YNR039c	NucleicAcid		encodes					zinc transporter proteins	GP	potential			NULL		0	NULL	NULL	NULL	gw60_pnas_97_14_7957_s_202	10884426	Several other genes in our list of Zap1p targets also encode potential zinc transporter proteins including YNR039c and YOL002c.	gene_phenotype
69063	2	333217	5	NULL	NULL	0	NULL	YOL002c	NucleicAcid		encodes					zinc transporter proteins	GP	potential			NULL		0	NULL	NULL	NULL	gw60_pnas_97_14_7957_s_202	10884426	Several other genes in our list of Zap1p targets also encode potential zinc transporter proteins including YNR039c and YOL002c.	gene_phenotype
69064	1	333219	5	NULL	NULL	0	NULL	Ypl244c protein	GP		is similar to		most			UDP-Gal transporter	GP	S. pombe			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4424_s_272	11067855	The function of Ypl244c is unknown, although this protein is most similar to the  S. pombe UDP-Gal transporter and appears to be localized in the Golgi ( 16).	gene_phenotype
69065	2	333219	5	NULL	NULL	0	NULL	Ypl244c protein	GP		is localized in		appears to be			Golgi	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4424_s_272	11067855	The function of Ypl244c is unknown, although this protein is most similar to the  S. pombe UDP-Gal transporter and appears to be localized in the Golgi ( 16).	gene_phenotype
69066	1	333220	5	NULL	NULL	0	NULL	UDP-sugar transporter family	GP		does not contain							conserved	GALNK motif		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4424_s_270	11067855	Two  S. cerevisiae proteins, Yel004p and Ypl244c, were identified as members of the UDP-sugar transporter family that do not contain the conserved GALNK motif.	gene_phenotype
69067	2	333220	5	NULL	NULL	0	NULL	Yel004p protein	GP		is a member of					statement 1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4424_s_270	11067855	Two  S. cerevisiae proteins, Yel004p and Ypl244c, were identified as members of the UDP-sugar transporter family that do not contain the conserved GALNK motif.	gene_phenotype
69068	3	333220	5	NULL	NULL	0	NULL	Ypl244c protein	GP		is a member of					statement 1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4424_s_270	11067855	Two  S. cerevisiae proteins, Yel004p and Ypl244c, were identified as members of the UDP-sugar transporter family that do not contain the conserved GALNK motif.	gene_phenotype
69069	1	333222	5	NULL	NULL	0	NULL	Ybr001c	NucleicAcid		encodes for					Nth2	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_132	16498703	Ybr001c  Nth2  2 Putative neutral trehalase, required for thermotolerance and may mediate resistance  to other cellular stresses  LIP  [ 16]	gene_phenotype
69070	1	333222	5	NULL	NULL	0	NULL	Ybr001c	NucleicAcid		encodes for					Nth2	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_132	16498703	Ybr001c  Nth2  2 Putative neutral trehalase, required for thermotolerance and may mediate resistance  to other cellular stresses  LIP  [ 16]	gene_phenotype
69071	1	333222	5	NULL	NULL	0	NULL	Ybr001c	NucleicAcid		encodes for					Nth2	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_132	16498703	Ybr001c  Nth2  2 Putative neutral trehalase, required for thermotolerance and may mediate resistance  to other cellular stresses  LIP  [ 16]	gene_phenotype
69072	2	333222	5	NULL	NULL	0	NULL	Nth2	GP		is a synonym of					Putative neutral trehalase	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_132	16498703	Ybr001c  Nth2  2 Putative neutral trehalase, required for thermotolerance and may mediate resistance  to other cellular stresses  LIP  [ 16]	gene_phenotype
69073	3	333222	5	NULL	NULL	0	NULL	Nth2	GP		is required for					thermotolerance	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_132	16498703	Ybr001c  Nth2  2 Putative neutral trehalase, required for thermotolerance and may mediate resistance  to other cellular stresses  LIP  [ 16]	gene_phenotype
69074	4	333222	5	NULL	NULL	0	NULL	Nth2	GP		mediates		may			cellular stresses	Process	resistance to			NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_132	16498703	Ybr001c  Nth2  2 Putative neutral trehalase, required for thermotolerance and may mediate resistance  to other cellular stresses  LIP  [ 16]	gene_phenotype
69076	1	333223	5	NULL	NULL	0	NULL	YBR201W	NucleicAcid		encodes for					DER1	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_363	15334557	DER1   YBR201W Endoplasmic reticulum membrane protein, required for the protein degradation process  associated with the ER, involved in the retrograde transport of misfolded or unassembled  proteins	gene_phenotype
69077	2	333223	5	NULL	NULL	0	NULL	DER1	GP		is a type of					Endoplasmic reticulum membrane protein	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_363	15334557	DER1   YBR201W Endoplasmic reticulum membrane protein, required for the protein degradation process  associated with the ER, involved in the retrograde transport of misfolded or unassembled  proteins	gene_phenotype
69078	3	333223	5	NULL	NULL	0	NULL	protein degradation	Process		is associated with					ER	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_363	15334557	DER1   YBR201W Endoplasmic reticulum membrane protein, required for the protein degradation process  associated with the ER, involved in the retrograde transport of misfolded or unassembled  proteins	gene_phenotype
69079	4	333223	5	NULL	NULL	0	NULL	DER1	GP		is required for					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_363	15334557	DER1   YBR201W Endoplasmic reticulum membrane protein, required for the protein degradation process  associated with the ER, involved in the retrograde transport of misfolded or unassembled  proteins	gene_phenotype
69080	5	333223	5	NULL	NULL	0	NULL	proteins	GP	misfolded	undergoes					transport	Process	retrograde			NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_363	15334557	DER1   YBR201W Endoplasmic reticulum membrane protein, required for the protein degradation process  associated with the ER, involved in the retrograde transport of misfolded or unassembled  proteins	gene_phenotype
69081	6	333223	5	NULL	NULL	0	NULL	DER1	GP		is involved in					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_363	15334557	DER1   YBR201W Endoplasmic reticulum membrane protein, required for the protein degradation process  associated with the ER, involved in the retrograde transport of misfolded or unassembled  proteins	gene_phenotype
69082	7	333223	5	NULL	NULL	0	NULL	proteins	GP	unassembled	undergoes					transport	Process	retrograde			NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_363	15334557	DER1   YBR201W Endoplasmic reticulum membrane protein, required for the protein degradation process  associated with the ER, involved in the retrograde transport of misfolded or unassembled  proteins	gene_phenotype
69083	8	333223	5	NULL	NULL	0	NULL	DER1	GP		is involved in					statement 7	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_363	15334557	DER1   YBR201W Endoplasmic reticulum membrane protein, required for the protein degradation process  associated with the ER, involved in the retrograde transport of misfolded or unassembled  proteins	gene_phenotype
69084	9	333223	5	NULL	NULL	0	NULL	statement 5	Process		is an alternative to					statement 7	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_363	15334557	DER1   YBR201W Endoplasmic reticulum membrane protein, required for the protein degradation process  associated with the ER, involved in the retrograde transport of misfolded or unassembled  proteins	gene_phenotype
69085	1	333224	5	NULL	NULL	0	NULL	yhr101c	NucleicAcid		is the locus name of					big1	GP				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_72	10436161	For example, the previously-constructed  yhr101c ( big1) and  ybr196c ( pgi1) null mutants show glucose sensitivity, and the  ybr256c ( rib5) deletion mutant requires a riboflavin supplement for viability ( 24).	gene_phenotype
69086	2	333224	5	NULL	NULL	0	NULL	ybr196c	NucleicAcid		is the locus name of					pgi1	GP				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_72	10436161	For example, the previously-constructed  yhr101c ( big1) and  ybr196c ( pgi1) null mutants show glucose sensitivity, and the  ybr256c ( rib5) deletion mutant requires a riboflavin supplement for viability ( 24).	gene_phenotype
69087	3	333224	5	NULL	NULL	0	NULL	ybr256c	NucleicAcid		is the locus name of					rib5	GP				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_72	10436161	For example, the previously-constructed  yhr101c ( big1) and  ybr196c ( pgi1) null mutants show glucose sensitivity, and the  ybr256c ( rib5) deletion mutant requires a riboflavin supplement for viability ( 24).	gene_phenotype
69088	4	333224	5	NULL	NULL	0	NULL	yhr101c	NucleicAcid	null mutant	is sensitive to					glucose	Chemical				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_72	10436161	For example, the previously-constructed  yhr101c ( big1) and  ybr196c ( pgi1) null mutants show glucose sensitivity, and the  ybr256c ( rib5) deletion mutant requires a riboflavin supplement for viability ( 24).	gene_phenotype
69089	5	333224	5	NULL	NULL	0	NULL	ybr196c	NucleicAcid	null mutant	is sensitive to					glucose	Chemical				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_72	10436161	For example, the previously-constructed  yhr101c ( big1) and  ybr196c ( pgi1) null mutants show glucose sensitivity, and the  ybr256c ( rib5) deletion mutant requires a riboflavin supplement for viability ( 24).	gene_phenotype
69090	6	333224	5	NULL	NULL	0	NULL	riboflavin supplement	Chemical		is required for					viability	Process				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_72	10436161	For example, the previously-constructed  yhr101c ( big1) and  ybr196c ( pgi1) null mutants show glucose sensitivity, and the  ybr256c ( rib5) deletion mutant requires a riboflavin supplement for viability ( 24).	gene_phenotype
69091	7	333224	5	NULL	NULL	0	NULL	ybr256c	NucleicAcid	deletion mutant	requires					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_72	10436161	For example, the previously-constructed  yhr101c ( big1) and  ybr196c ( pgi1) null mutants show glucose sensitivity, and the  ybr256c ( rib5) deletion mutant requires a riboflavin supplement for viability ( 24).	gene_phenotype
69092	1	333225	5	NULL	NULL	0	NULL	YCR002c	NucleicAcid		is the locus name of					CDC10	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_285	15334557	CDC10   YCR002c Component of septin ring of the mother-bud neck; required for cytokinesis	gene_phenotype
69093	2	333225	5	NULL	NULL	0	NULL	CDC10	GP		is a component of					mother-bud neck	CellComponent	septin ring of			NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_285	15334557	CDC10   YCR002c Component of septin ring of the mother-bud neck; required for cytokinesis	gene_phenotype
69094	3	333225	5	NULL	NULL	0	NULL	CDC10	GP		is required for					cytokinesis	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_285	15334557	CDC10   YCR002c Component of septin ring of the mother-bud neck; required for cytokinesis	gene_phenotype
67978	1	333228	7	NULL	NULL	0	NULL	Ycr072c	GP		is required for					cell	Cell	viability of			NULL		0	NULL	NULL	NULL	gw70_nature_435_7043_814_s_82	15944704	For the protein Ycr072c, which is required for the viability of the cell and appears  in the dark green community on the right, SGD provides no biological process (function).	gene_phenotype
68041	1	333231	7	NULL	NULL	NULL	NULL	Ydr001c Nth1 1, 2 Neutral trehalase	GP		degrades					trehalose	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_3_159_s_131	16498703	Ydr001c  Nth1 1, 2 Neutral trehalase, degrades trehalose; required for thermotolerance and may mediate  resistance to other cellular stresses; may be phosphorylated by Cdc28p  LIP  [ 16],[ 20]	gene_phenotype
68042	2	333231	7	NULL	NULL	0	NULL	trehalose	Chemical		required for					thermotolerance	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_131	16498703	Ydr001c  Nth1 1, 2 Neutral trehalase, degrades trehalose; required for thermotolerance and may mediate  resistance to other cellular stresses; may be phosphorylated by Cdc28p  LIP  [ 16],[ 20]	gene_phenotype
68043	3	333231	7	NULL	NULL	NULL	NULL	Ydr001c Nth1 1, 2 Neutral trehalase	GP		mediate		may			cellular stress	Process	resistance to			NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_3_159_s_131	16498703	Ydr001c  Nth1 1, 2 Neutral trehalase, degrades trehalose; required for thermotolerance and may mediate  resistance to other cellular stresses; may be phosphorylated by Cdc28p  LIP  [ 16],[ 20]	gene_phenotype
68044	4	333231	7	NULL	NULL	NULL	NULL	Cdc28p LIP	GP		phosphorylate					Ydr001c Nth1 1, 2 Neutral trehalase	GP				NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_3_159_s_131	16498703	Ydr001c  Nth1 1, 2 Neutral trehalase, degrades trehalose; required for thermotolerance and may mediate  resistance to other cellular stresses; may be phosphorylated by Cdc28p  LIP  [ 16],[ 20]	gene_phenotype
68045	1	333232	7	NULL	NULL	NULL	NULL	Ydr006c Sok1 1 Protein	GP	overexpression of	suppresses					growth defect	Process				NULL	mutants lacking protein kinase A activity	NULL	NULL	NULL	NULL	gw70_yeast_23_3_159_s_136	16498703	Ydr006c  Sok1  1 Protein whose overexpression suppresses the growth defect of mutants lacking protein  kinase A activity; involved in cAMP-mediated signalling; localized to the nucleus;  similar to the mouse testis-specific protein PBS13  LIP  [ 20]	gene_phenotype
68046	2	333232	7	NULL	NULL	0	NULL	cAMP	Chemical		mediates					signal	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_136	16498703	Ydr006c  Sok1  1 Protein whose overexpression suppresses the growth defect of mutants lacking protein  kinase A activity; involved in cAMP-mediated signalling; localized to the nucleus;  similar to the mouse testis-specific protein PBS13  LIP  [ 20]	gene_phenotype
68047	4	333232	7	NULL	NULL	NULL	NULL	Ydr006c Sok1 1 Protein	GP		localized to					nucleus	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_3_159_s_136	16498703	Ydr006c  Sok1  1 Protein whose overexpression suppresses the growth defect of mutants lacking protein  kinase A activity; involved in cAMP-mediated signalling; localized to the nucleus;  similar to the mouse testis-specific protein PBS13  LIP  [ 20]	gene_phenotype
68048	3	333232	7	NULL	NULL	0	NULL	Ydr006c Sok1 1 Protein	GP		involved in					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_136	16498703	Ydr006c  Sok1  1 Protein whose overexpression suppresses the growth defect of mutants lacking protein  kinase A activity; involved in cAMP-mediated signalling; localized to the nucleus;  similar to the mouse testis-specific protein PBS13  LIP  [ 20]	gene_phenotype
68049	5	333232	7	NULL	NULL	0	NULL	testis-specific protein PBS13 LIP	GP	mouse;;overexpression of	suppresses					growth defect	Process				NULL	mutants lacking protein kinase A activity	0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_136	16498703	Ydr006c  Sok1  1 Protein whose overexpression suppresses the growth defect of mutants lacking protein  kinase A activity; involved in cAMP-mediated signalling; localized to the nucleus;  similar to the mouse testis-specific protein PBS13  LIP  [ 20]	gene_phenotype
68050	6	333232	7	NULL	NULL	0	NULL	testis-specific protein PBS13 LIP	GP	mouse	involved in					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_136	16498703	Ydr006c  Sok1  1 Protein whose overexpression suppresses the growth defect of mutants lacking protein  kinase A activity; involved in cAMP-mediated signalling; localized to the nucleus;  similar to the mouse testis-specific protein PBS13  LIP  [ 20]	gene_phenotype
68051	7	333232	7	NULL	NULL	0	NULL	testis-specific protein PBS13 LIP	GP	mouse	localized to					nucleus	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_136	16498703	Ydr006c  Sok1  1 Protein whose overexpression suppresses the growth defect of mutants lacking protein  kinase A activity; involved in cAMP-mediated signalling; localized to the nucleus;  similar to the mouse testis-specific protein PBS13  LIP  [ 20]	gene_phenotype
68052	8	333232	7	NULL	NULL	0	NULL	statement 1	Process		is similar to					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_136	16498703	Ydr006c  Sok1  1 Protein whose overexpression suppresses the growth defect of mutants lacking protein  kinase A activity; involved in cAMP-mediated signalling; localized to the nucleus;  similar to the mouse testis-specific protein PBS13  LIP  [ 20]	gene_phenotype
68053	9	333232	7	NULL	NULL	0	NULL	statement 3	Process		is similar to					statement 6	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_136	16498703	Ydr006c  Sok1  1 Protein whose overexpression suppresses the growth defect of mutants lacking protein  kinase A activity; involved in cAMP-mediated signalling; localized to the nucleus;  similar to the mouse testis-specific protein PBS13  LIP  [ 20]	gene_phenotype
68054	10	333232	7	NULL	NULL	0	NULL	statement 4	Process		is similar to					statement 7	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_136	16498703	Ydr006c  Sok1  1 Protein whose overexpression suppresses the growth defect of mutants lacking protein  kinase A activity; involved in cAMP-mediated signalling; localized to the nucleus;  similar to the mouse testis-specific protein PBS13  LIP  [ 20]	gene_phenotype
68055	1	333233	7	NULL	NULL	0	NULL	Cdc7p-Dbf4p kinase complex	GP		required for			YDR052c DBF4 Regulatory subunit		Cdc7p kinase	GP	 activity of			NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_83	16498703	YDR052c   DBF4 Regulatory subunit of Cdc7p-Dbf4p kinase complex, required for Cdc7p kinase activity  and initiation of DNA replication; phosphorylates the Mcm2-7 family of proteins;  cell cycle-regulated  [ 49]	gene_phenotype
68056	2	333233	7	NULL	NULL	0	NULL	Cdc7p-Dbf4p kinase complex	GP		initiates			YDR052c DBF4 Regulatory subunit		DNA replication	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_83	16498703	YDR052c   DBF4 Regulatory subunit of Cdc7p-Dbf4p kinase complex, required for Cdc7p kinase activity  and initiation of DNA replication; phosphorylates the Mcm2-7 family of proteins;  cell cycle-regulated  [ 49]	gene_phenotype
68057	3	333233	7	NULL	NULL	0	NULL	Cdc7p-Dbf4p kinase complex	GP		phosphorylates			YDR052c DBF4 Regulatory subunit		Mcm2-7 family	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_83	16498703	YDR052c   DBF4 Regulatory subunit of Cdc7p-Dbf4p kinase complex, required for Cdc7p kinase activity  and initiation of DNA replication; phosphorylates the Mcm2-7 family of proteins;  cell cycle-regulated  [ 49]	gene_phenotype
68058	1	333234	7	NULL	NULL	0	NULL	NUM1 YDR150w Tubulin	GP		function		may			nuclear migration	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_218	15334557	NUM1   YDR150w Tubulin binding; may function in nuclear migration during mitosis and meiosis by affecting  astral microtubule functions, perhaps by being involved in polymerization and stabilization  of microtubules	gene_phenotype
68059	2	333234	7	NULL	NULL	0	NULL	statement 1	Process		occur during					mitosis	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_218	15334557	NUM1   YDR150w Tubulin binding; may function in nuclear migration during mitosis and meiosis by affecting  astral microtubule functions, perhaps by being involved in polymerization and stabilization  of microtubules	gene_phenotype
68060	3	333234	7	NULL	NULL	0	NULL	statement 1	Process		occur during					meiosis	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_218	15334557	NUM1   YDR150w Tubulin binding; may function in nuclear migration during mitosis and meiosis by affecting  astral microtubule functions, perhaps by being involved in polymerization and stabilization  of microtubules	gene_phenotype
68061	4	333234	7	NULL	NULL	NULL	NULL	statement 1	Process		occur by					astral microtubule functions	Process	affecting			NULL		NULL	NULL	NULL	NULL	gw70_yeast_21_11_927_s_218	15334557	NUM1   YDR150w Tubulin binding; may function in nuclear migration during mitosis and meiosis by affecting  astral microtubule functions, perhaps by being involved in polymerization and stabilization  of microtubules	gene_phenotype
68062	6	333234	7	NULL	NULL	NULL	NULL	statement 1	Process		affect					 microtubules	Chromosome	stabilization of			NULL		NULL	NULL	NULL	NULL	gw70_yeast_21_11_927_s_218	15334557	NUM1   YDR150w Tubulin binding; may function in nuclear migration during mitosis and meiosis by affecting  astral microtubule functions, perhaps by being involved in polymerization and stabilization  of microtubules	gene_phenotype
68063	5	333234	7	NULL	NULL	NULL	NULL	statement 1	Process		affect					microtubules	Chromosome	polymerization of			NULL		NULL	NULL	NULL	NULL	gw70_yeast_21_11_927_s_218	15334557	NUM1   YDR150w Tubulin binding; may function in nuclear migration during mitosis and meiosis by affecting  astral microtubule functions, perhaps by being involved in polymerization and stabilization  of microtubules	gene_phenotype
68064	7	333234	7	NULL	NULL	0	NULL	statement 4	Process		involves					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_218	15334557	NUM1   YDR150w Tubulin binding; may function in nuclear migration during mitosis and meiosis by affecting  astral microtubule functions, perhaps by being involved in polymerization and stabilization  of microtubules	gene_phenotype
68065	8	333234	7	NULL	NULL	0	NULL	statement 5	Process		involves					statement 6	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_218	15334557	NUM1   YDR150w Tubulin binding; may function in nuclear migration during mitosis and meiosis by affecting  astral microtubule functions, perhaps by being involved in polymerization and stabilization  of microtubules	gene_phenotype
68066	1	333235	7	NULL	NULL	0	NULL	SAC3 YDR159w Nuclear pore 	CellComponent	component of	involved in					mRNA	NucleicAcid	nuclear export of			NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_203	15334557	SAC3   YDR159w Nuclear pore component; involved in nuclear export of both mRNA and protein	gene_phenotype
68067	2	333235	7	NULL	NULL	NULL	NULL	SAC3 YDR159w Nuclear pore 	CellComponent	component of	involved in					protein	GP	nuclear export of			NULL		NULL	NULL	NULL	NULL	gw70_yeast_21_11_927_s_203	15334557	SAC3   YDR159w Nuclear pore component; involved in nuclear export of both mRNA and protein	gene_phenotype
68068	1	333236	7	NULL	NULL	0	NULL	YDR227W SIR4	GP		is a type of					silencing regulator	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_9_827_s_119	12845608	YDR227W   SIR4 Silencing regulator  2.0	gene_phenotype
68069	1	333239	7	NULL	NULL	0	NULL	YEL061c CIN8 Kinesin motor protein	GP		involved in					mitotic spindle assembly	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_84	16498703	YEL061c   CIN8 Kinesin motor protein involved in mitotic spindle assembly and chromosome segregation  [ 49]	gene_phenotype
68070	2	333239	7	NULL	NULL	0	NULL	YEL061c CIN8 Kinesin motor protein	GP		involved in					chromosome segregation	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_84	16498703	YEL061c   CIN8 Kinesin motor protein involved in mitotic spindle assembly and chromosome segregation  [ 49]	gene_phenotype
68071	1	333240	7	NULL	NULL	0	NULL	YER075c PTP3	GP		downregulate					Hog1p	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_19_7_587_s_67	11967829	YER075c   PTP3 Downregulate Hog1p and Fus3p MAPK, sporulation (Maeda  et al., [ 1994]; Wurgler-Murphy  et al., [ 1997]; Zhan  et al., [ 2000])	gene_phenotype
68072	2	333240	7	NULL	NULL	0	NULL	YER075c PTP3	GP		downregulates					Fus3p MAPK	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_19_7_587_s_67	11967829	YER075c   PTP3 Downregulate Hog1p and Fus3p MAPK, sporulation (Maeda  et al., [ 1994]; Wurgler-Murphy  et al., [ 1997]; Zhan  et al., [ 2000])	gene_phenotype
68073	1	333242	7	NULL	NULL	0	NULL	YGL001c 	GP	disruption of	viable in					hem 1delta strain	Organism				NULL		0	NULL	NULL	NULL	gw60_pnas_95_23_13794_s_8	9811880	The YGL001c (  ERG26) disruption also was viable in a   hem 1delta strain grown in the presence of ergosterol.	gene_phenotype
68074	2	333242	7	NULL	NULL	0	NULL	hem 1delta strain	Organism		grown					ergosterol	Chemical	in the presence of			NULL		0	NULL	NULL	NULL	gw60_pnas_95_23_13794_s_8	9811880	The YGL001c (  ERG26) disruption also was viable in a   hem 1delta strain grown in the presence of ergosterol.	gene_phenotype
68075	3	333242	7	NULL	NULL	0	NULL	YGL001c 	GP		is					ERG26	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_95_23_13794_s_8	9811880	The YGL001c (  ERG26) disruption also was viable in a   hem 1delta strain grown in the presence of ergosterol.	gene_phenotype
68076	1	333244	7	NULL	NULL	0	NULL	one segregant	Organism		derived from					SDG274	Organism				NULL		0	NULL	NULL	NULL	gw60_pnas_95_23_13794_s_104	9811880	However, one segregant derived from SDG274, SDG 274-6, was able to grow both aerobically and anaerobically on ergosterol media, suggesting that disruption of YGL001c gives rise to sterol auxotrophy and that a second mutation may have arisen in this strain.	gene_phenotype
68077	2	333244	7	NULL	NULL	0	NULL	one segregant	Organism		derived from					SDG 274-6	Organism				NULL		0	NULL	NULL	NULL	gw60_pnas_95_23_13794_s_104	9811880	However, one segregant derived from SDG274, SDG 274-6, was able to grow both aerobically and anaerobically on ergosterol media, suggesting that disruption of YGL001c gives rise to sterol auxotrophy and that a second mutation may have arisen in this strain.	gene_phenotype
68078	3	333244	7	NULL	NULL	NULL	NULL	statement 1	Organism		grow					aerobically	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_23_13794_s_104	9811880	However, one segregant derived from SDG274, SDG 274-6, was able to grow both aerobically and anaerobically on ergosterol media, suggesting that disruption of YGL001c gives rise to sterol auxotrophy and that a second mutation may have arisen in this strain.	gene_phenotype
68079	4	333244	7	NULL	NULL	NULL	NULL	statement 1	Organism		grow					anaerobically	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_23_13794_s_104	9811880	However, one segregant derived from SDG274, SDG 274-6, was able to grow both aerobically and anaerobically on ergosterol media, suggesting that disruption of YGL001c gives rise to sterol auxotrophy and that a second mutation may have arisen in this strain.	gene_phenotype
68080	5	333244	7	NULL	NULL	0	NULL	statement 2	Organism		grow					aerobically	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_95_23_13794_s_104	9811880	However, one segregant derived from SDG274, SDG 274-6, was able to grow both aerobically and anaerobically on ergosterol media, suggesting that disruption of YGL001c gives rise to sterol auxotrophy and that a second mutation may have arisen in this strain.	gene_phenotype
68081	6	333244	7	NULL	NULL	0	NULL	statement 2	Organism		grow					anaerobically	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_95_23_13794_s_104	9811880	However, one segregant derived from SDG274, SDG 274-6, was able to grow both aerobically and anaerobically on ergosterol media, suggesting that disruption of YGL001c gives rise to sterol auxotrophy and that a second mutation may have arisen in this strain.	gene_phenotype
68082	7	333244	7	NULL	NULL	NULL	NULL	statement 3	Process		grown on					ergosterol media	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_23_13794_s_104	9811880	However, one segregant derived from SDG274, SDG 274-6, was able to grow both aerobically and anaerobically on ergosterol media, suggesting that disruption of YGL001c gives rise to sterol auxotrophy and that a second mutation may have arisen in this strain.	gene_phenotype
68083	8	333244	7	NULL	NULL	0	NULL	statement 4	Process		grown on					ergosterol media	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_95_23_13794_s_104	9811880	However, one segregant derived from SDG274, SDG 274-6, was able to grow both aerobically and anaerobically on ergosterol media, suggesting that disruption of YGL001c gives rise to sterol auxotrophy and that a second mutation may have arisen in this strain.	gene_phenotype
68084	9	333244	7	NULL	NULL	0	NULL	statement 5	Process		grown on					ergosterol media	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_95_23_13794_s_104	9811880	However, one segregant derived from SDG274, SDG 274-6, was able to grow both aerobically and anaerobically on ergosterol media, suggesting that disruption of YGL001c gives rise to sterol auxotrophy and that a second mutation may have arisen in this strain.	gene_phenotype
68085	10	333244	7	NULL	NULL	0	NULL	statement 6	Process		grown on					ergosterol media	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_95_23_13794_s_104	9811880	However, one segregant derived from SDG274, SDG 274-6, was able to grow both aerobically and anaerobically on ergosterol media, suggesting that disruption of YGL001c gives rise to sterol auxotrophy and that a second mutation may have arisen in this strain.	gene_phenotype
68086	11	333244	7	NULL	NULL	0	NULL	YGL001c	GP	disruption of	gives rise to					sterol auxotrophy	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_95_23_13794_s_104	9811880	However, one segregant derived from SDG274, SDG 274-6, was able to grow both aerobically and anaerobically on ergosterol media, suggesting that disruption of YGL001c gives rise to sterol auxotrophy and that a second mutation may have arisen in this strain.	gene_phenotype
68087	12	333244	7	NULL	NULL	0	NULL	statement 3	Process		suggests					statement 11	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_95_23_13794_s_104	9811880	However, one segregant derived from SDG274, SDG 274-6, was able to grow both aerobically and anaerobically on ergosterol media, suggesting that disruption of YGL001c gives rise to sterol auxotrophy and that a second mutation may have arisen in this strain.	gene_phenotype
68088	13	333244	7	NULL	NULL	0	NULL	statement 4	Process		suggests					statement 11	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_95_23_13794_s_104	9811880	However, one segregant derived from SDG274, SDG 274-6, was able to grow both aerobically and anaerobically on ergosterol media, suggesting that disruption of YGL001c gives rise to sterol auxotrophy and that a second mutation may have arisen in this strain.	gene_phenotype
68089	14	333244	7	NULL	NULL	0	NULL	statement 5	Process		suggests					statement 11	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_95_23_13794_s_104	9811880	However, one segregant derived from SDG274, SDG 274-6, was able to grow both aerobically and anaerobically on ergosterol media, suggesting that disruption of YGL001c gives rise to sterol auxotrophy and that a second mutation may have arisen in this strain.	gene_phenotype
68090	15	333244	7	NULL	NULL	0	NULL	statement 6	Process		suggests					statement 11	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_95_23_13794_s_104	9811880	However, one segregant derived from SDG274, SDG 274-6, was able to grow both aerobically and anaerobically on ergosterol media, suggesting that disruption of YGL001c gives rise to sterol auxotrophy and that a second mutation may have arisen in this strain.	gene_phenotype
68176	4	333245	7	NULL	NULL	NULL	NULL	Ygl115w Snf4 1 Protein kinase activator	GP		involved in					glucose-repressed genes	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_3_159_s_126	16498703	Ygl115w  Snf4  1 Protein kinase activator found in a complex containing Snf1p and members of the Sip1p/Sip2p/Gal83p  family; activates the Snf1p protein kinase; involved in expression of glucose-repressed  genes, sporulation and peroxisome biogenesis  LIP  [ 16]	gene_phenotype
68177	3	333245	7	NULL	NULL	NULL	NULL	Ygl115w Snf4 1 Protein kinase activator	GP		activates					Snf1p protein kinase	GP				NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_3_159_s_126	16498703	Ygl115w  Snf4  1 Protein kinase activator found in a complex containing Snf1p and members of the Sip1p/Sip2p/Gal83p  family; activates the Snf1p protein kinase; involved in expression of glucose-repressed  genes, sporulation and peroxisome biogenesis  LIP  [ 16]	gene_phenotype
68178	5	333245	7	NULL	NULL	NULL	NULL	Ygl115w Snf4 1 Protein kinase activator	GP		involved in					sporulation	Process	expression of			NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_3_159_s_126	16498703	Ygl115w  Snf4  1 Protein kinase activator found in a complex containing Snf1p and members of the Sip1p/Sip2p/Gal83p  family; activates the Snf1p protein kinase; involved in expression of glucose-repressed  genes, sporulation and peroxisome biogenesis  LIP  [ 16]	gene_phenotype
68179	6	333245	7	NULL	NULL	NULL	NULL	Ygl115w Snf4 1 Protein kinase activator	GP		involved in					peroxisome	CellComponent	expression of;;biogenesis of			NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_3_159_s_126	16498703	Ygl115w  Snf4  1 Protein kinase activator found in a complex containing Snf1p and members of the Sip1p/Sip2p/Gal83p  family; activates the Snf1p protein kinase; involved in expression of glucose-repressed  genes, sporulation and peroxisome biogenesis  LIP  [ 16]	gene_phenotype
68181	1	333245	7	NULL	NULL	NULL	NULL	 Snf1p 	GP		in complex with					 Sip1p/Sip2p/Gal83p family	GP				NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_3_159_s_126	16498703	Ygl115w  Snf4  1 Protein kinase activator found in a complex containing Snf1p and members of the Sip1p/Sip2p/Gal83p  family; activates the Snf1p protein kinase; involved in expression of glucose-repressed  genes, sporulation and peroxisome biogenesis  LIP  [ 16]	gene_phenotype
68182	2	333245	7	NULL	NULL	0	NULL	Ygl115w Snf4 1 Protein kinase activator	GP		found in					statement 1	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_126	16498703	Ygl115w  Snf4  1 Protein kinase activator found in a complex containing Snf1p and members of the Sip1p/Sip2p/Gal83p  family; activates the Snf1p protein kinase; involved in expression of glucose-repressed  genes, sporulation and peroxisome biogenesis  LIP  [ 16]	gene_phenotype
68183	1	333246	7	NULL	NULL	0	NULL	ymr308c ( PSE1)	GP		is a type of					haploid null mutant	GP				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_73	10436161	In several cases, haploid null mutants were reported to have slow-growth phenotypes [ ymr308c ( PSE1),  yol022c,  ypl243c ( srp68),  ypl210c ( srp72), and  ydr353w ( trr1) ( 25)] or to be temperature sensitive [ ydr113c ( pds1) and  ygr216c ( gpi1) ( 26)].	gene_phenotype
68184	2	333246	7	NULL	NULL	0	NULL	yol022c	GP		is a type of					haploid null mutant	GP				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_73	10436161	In several cases, haploid null mutants were reported to have slow-growth phenotypes [ ymr308c ( PSE1),  yol022c,  ypl243c ( srp68),  ypl210c ( srp72), and  ydr353w ( trr1) ( 25)] or to be temperature sensitive [ ydr113c ( pds1) and  ygr216c ( gpi1) ( 26)].	gene_phenotype
68185	3	333246	7	NULL	NULL	0	NULL	 ypl243c ( srp68)	GP		is a type of					haploid null mutant	GP				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_73	10436161	In several cases, haploid null mutants were reported to have slow-growth phenotypes [ ymr308c ( PSE1),  yol022c,  ypl243c ( srp68),  ypl210c ( srp72), and  ydr353w ( trr1) ( 25)] or to be temperature sensitive [ ydr113c ( pds1) and  ygr216c ( gpi1) ( 26)].	gene_phenotype
68186	4	333246	7	NULL	NULL	0	NULL	ypl210c ( srp72)	GP		is a type of					haploid null mutant	GP				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_73	10436161	In several cases, haploid null mutants were reported to have slow-growth phenotypes [ ymr308c ( PSE1),  yol022c,  ypl243c ( srp68),  ypl210c ( srp72), and  ydr353w ( trr1) ( 25)] or to be temperature sensitive [ ydr113c ( pds1) and  ygr216c ( gpi1) ( 26)].	gene_phenotype
68187	5	333246	7	NULL	NULL	0	NULL	ydr353w ( trr1)	GP		is a type of					haploid null mutant	GP				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_73	10436161	In several cases, haploid null mutants were reported to have slow-growth phenotypes [ ymr308c ( PSE1),  yol022c,  ypl243c ( srp68),  ypl210c ( srp72), and  ydr353w ( trr1) ( 25)] or to be temperature sensitive [ ydr113c ( pds1) and  ygr216c ( gpi1) ( 26)].	gene_phenotype
68188	6	333246	7	NULL	NULL	0	NULL	statement 1	GP		possess					slow-growth phenotype	Process				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_73	10436161	In several cases, haploid null mutants were reported to have slow-growth phenotypes [ ymr308c ( PSE1),  yol022c,  ypl243c ( srp68),  ypl210c ( srp72), and  ydr353w ( trr1) ( 25)] or to be temperature sensitive [ ydr113c ( pds1) and  ygr216c ( gpi1) ( 26)].	gene_phenotype
68189	7	333246	7	NULL	NULL	0	NULL	statement 2	GP		possess					slow-growth phenotype	Process				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_73	10436161	In several cases, haploid null mutants were reported to have slow-growth phenotypes [ ymr308c ( PSE1),  yol022c,  ypl243c ( srp68),  ypl210c ( srp72), and  ydr353w ( trr1) ( 25)] or to be temperature sensitive [ ydr113c ( pds1) and  ygr216c ( gpi1) ( 26)].	gene_phenotype
68190	8	333246	7	NULL	NULL	0	NULL	statement 3	GP		possess					slow-growth phenotype	Process				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_73	10436161	In several cases, haploid null mutants were reported to have slow-growth phenotypes [ ymr308c ( PSE1),  yol022c,  ypl243c ( srp68),  ypl210c ( srp72), and  ydr353w ( trr1) ( 25)] or to be temperature sensitive [ ydr113c ( pds1) and  ygr216c ( gpi1) ( 26)].	gene_phenotype
68191	9	333246	7	NULL	NULL	NULL	NULL	statement 4	GP		possess					slow-growth phenotype	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_285_5429_901_s_73	10436161	In several cases, haploid null mutants were reported to have slow-growth phenotypes [ ymr308c ( PSE1),  yol022c,  ypl243c ( srp68),  ypl210c ( srp72), and  ydr353w ( trr1) ( 25)] or to be temperature sensitive [ ydr113c ( pds1) and  ygr216c ( gpi1) ( 26)].	gene_phenotype
68192	10	333246	7	NULL	NULL	0	NULL	statement 5	GP		possess					slow-growth phenotype	Process				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_73	10436161	In several cases, haploid null mutants were reported to have slow-growth phenotypes [ ymr308c ( PSE1),  yol022c,  ypl243c ( srp68),  ypl210c ( srp72), and  ydr353w ( trr1) ( 25)] or to be temperature sensitive [ ydr113c ( pds1) and  ygr216c ( gpi1) ( 26)].	gene_phenotype
68193	11	333246	7	NULL	NULL	0	NULL	ydr113c ( pds1)	GP		is a type of					haploid null mutant	GP				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_73	10436161	In several cases, haploid null mutants were reported to have slow-growth phenotypes [ ymr308c ( PSE1),  yol022c,  ypl243c ( srp68),  ypl210c ( srp72), and  ydr353w ( trr1) ( 25)] or to be temperature sensitive [ ydr113c ( pds1) and  ygr216c ( gpi1) ( 26)].	gene_phenotype
68194	12	333246	7	NULL	NULL	0	NULL	 ygr216c ( gpi1)	GP		is a type of					haploid null mutant	GP				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_73	10436161	In several cases, haploid null mutants were reported to have slow-growth phenotypes [ ymr308c ( PSE1),  yol022c,  ypl243c ( srp68),  ypl210c ( srp72), and  ydr353w ( trr1) ( 25)] or to be temperature sensitive [ ydr113c ( pds1) and  ygr216c ( gpi1) ( 26)].	gene_phenotype
68195	13	333246	7	NULL	NULL	0	NULL	statement 11	GP		is sensitive to					temperature	Process				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_73	10436161	In several cases, haploid null mutants were reported to have slow-growth phenotypes [ ymr308c ( PSE1),  yol022c,  ypl243c ( srp68),  ypl210c ( srp72), and  ydr353w ( trr1) ( 25)] or to be temperature sensitive [ ydr113c ( pds1) and  ygr216c ( gpi1) ( 26)].	gene_phenotype
68196	14	333246	7	NULL	NULL	0	NULL	statement 12	GP		is sensitive to					temperature	Process				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_73	10436161	In several cases, haploid null mutants were reported to have slow-growth phenotypes [ ymr308c ( PSE1),  yol022c,  ypl243c ( srp68),  ypl210c ( srp72), and  ydr353w ( trr1) ( 25)] or to be temperature sensitive [ ydr113c ( pds1) and  ygr216c ( gpi1) ( 26)].	gene_phenotype
68197	1	333247	7	NULL	NULL	NULL	NULL	ORF YHR105w 	GP	cells deleted for	shows					morphology		no defects in			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_140_3_577_s_150	9456318	A  null mutant of this gene was constructed, but cells deleted  for ORF YHR105w showed no defects in morphology,  vacuolar protein sorting, or Golgi membrane protein retention (data not shown).	gene_phenotype
68198	2	333247	7	NULL	NULL	NULL	NULL	ORF YHR105w 	GP	cells deleted for	shows					vacuolar protein	GP	no defects in sorting of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_140_3_577_s_150	9456318	A  null mutant of this gene was constructed, but cells deleted  for ORF YHR105w showed no defects in morphology,  vacuolar protein sorting, or Golgi membrane protein retention (data not shown).	gene_phenotype
68199	3	333247	7	NULL	NULL	NULL	NULL	ORF YHR105w 	GP	cells deleted for	shows					 Golgi membrane protein 	GP	no defects in retention of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_140_3_577_s_150	9456318	A  null mutant of this gene was constructed, but cells deleted  for ORF YHR105w showed no defects in morphology,  vacuolar protein sorting, or Golgi membrane protein retention (data not shown).	gene_phenotype
68200	1	333248	7	NULL	NULL	0	NULL	YHR171w	GP		is identified as					APG7	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_5_1353_s_228	10233149	YHR171w has recently been characterized and identified as  APG7, a gene required for nitrogen-starvation-induced autophagy in  S. cerevisiae (Tanida,  et al., 1999  ), as well as  CVT2, a gene necessary for constitutive delivery of pro-API from the cytosol to the vacuole by autophagy in  S. cerevisiae (Kim,  et al., 1999  ).	gene_phenotype
68201	2	333248	7	NULL	NULL	0	NULL	nitrogen-starvation	Process		induce					autophagy	Process				NULL	S. cerevisiae	0	NULL	NULL	NULL	gw60_molbiolcell_10_5_1353_s_228	10233149	YHR171w has recently been characterized and identified as  APG7, a gene required for nitrogen-starvation-induced autophagy in  S. cerevisiae (Tanida,  et al., 1999  ), as well as  CVT2, a gene necessary for constitutive delivery of pro-API from the cytosol to the vacuole by autophagy in  S. cerevisiae (Kim,  et al., 1999  ).	gene_phenotype
68202	3	333248	7	NULL	NULL	0	NULL	APG7	GP		is required for					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_5_1353_s_228	10233149	YHR171w has recently been characterized and identified as  APG7, a gene required for nitrogen-starvation-induced autophagy in  S. cerevisiae (Tanida,  et al., 1999  ), as well as  CVT2, a gene necessary for constitutive delivery of pro-API from the cytosol to the vacuole by autophagy in  S. cerevisiae (Kim,  et al., 1999  ).	gene_phenotype
68203	4	333248	7	NULL	NULL	NULL	NULL	pro-API	GP		 delivered from		constitutively			cytosol	CellComponent				NULL	S.cerevisiae	NULL	NULL	NULL	NULL	gw60_molbiolcell_10_5_1353_s_228	10233149	YHR171w has recently been characterized and identified as  APG7, a gene required for nitrogen-starvation-induced autophagy in  S. cerevisiae (Tanida,  et al., 1999  ), as well as  CVT2, a gene necessary for constitutive delivery of pro-API from the cytosol to the vacuole by autophagy in  S. cerevisiae (Kim,  et al., 1999  ).	gene_phenotype
68204	5	333248	7	NULL	NULL	NULL	NULL	pro-API	GP		 delivered to		constitutively			vacuole	CellComponent				NULL	S.cerevisiae	NULL	NULL	NULL	NULL	gw60_molbiolcell_10_5_1353_s_228	10233149	YHR171w has recently been characterized and identified as  APG7, a gene required for nitrogen-starvation-induced autophagy in  S. cerevisiae (Tanida,  et al., 1999  ), as well as  CVT2, a gene necessary for constitutive delivery of pro-API from the cytosol to the vacuole by autophagy in  S. cerevisiae (Kim,  et al., 1999  ).	gene_phenotype
68205	6	333248	7	NULL	NULL	0	NULL	statement 4	Process		occur along with					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_5_1353_s_228	10233149	YHR171w has recently been characterized and identified as  APG7, a gene required for nitrogen-starvation-induced autophagy in  S. cerevisiae (Tanida,  et al., 1999  ), as well as  CVT2, a gene necessary for constitutive delivery of pro-API from the cytosol to the vacuole by autophagy in  S. cerevisiae (Kim,  et al., 1999  ).	gene_phenotype
68206	7	333248	7	NULL	NULL	0	NULL	statement 6	Process		occur by					autophagy	Process				NULL	S.cerevisiae	0	NULL	NULL	NULL	gw60_molbiolcell_10_5_1353_s_228	10233149	YHR171w has recently been characterized and identified as  APG7, a gene required for nitrogen-starvation-induced autophagy in  S. cerevisiae (Tanida,  et al., 1999  ), as well as  CVT2, a gene necessary for constitutive delivery of pro-API from the cytosol to the vacuole by autophagy in  S. cerevisiae (Kim,  et al., 1999  ).	gene_phenotype
68207	8	333248	7	NULL	NULL	0	NULL	CVT2	GP		is necessary for					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_5_1353_s_228	10233149	YHR171w has recently been characterized and identified as  APG7, a gene required for nitrogen-starvation-induced autophagy in  S. cerevisiae (Tanida,  et al., 1999  ), as well as  CVT2, a gene necessary for constitutive delivery of pro-API from the cytosol to the vacuole by autophagy in  S. cerevisiae (Kim,  et al., 1999  ).	gene_phenotype
68208	1	333251	7	NULL	NULL	0	NULL	PDR15	GP		is a type of					major facilitator superfamily transporter	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_13_11427_s_6	12529331	These target genes code for ATP-binding cassette or major facilitator superfamily transporters such as  PDR15,  YOR1, or  AZR1 or for other proteins such as  SNG1,  YJL216c, or  YLL056c which are already known to be involved in the yeast pleiotropic drug resistance (PDR) phenomenon.	gene_phenotype
68209	2	333251	7	NULL	NULL	0	NULL	YOR1	GP		is a type of					major facilitator superfamily transporter	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_13_11427_s_6	12529331	These target genes code for ATP-binding cassette or major facilitator superfamily transporters such as  PDR15,  YOR1, or  AZR1 or for other proteins such as  SNG1,  YJL216c, or  YLL056c which are already known to be involved in the yeast pleiotropic drug resistance (PDR) phenomenon.	gene_phenotype
68210	3	333251	7	NULL	NULL	0	NULL	AZR1	GP		is a type of					major facilitator superfamily transporter	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_13_11427_s_6	12529331	These target genes code for ATP-binding cassette or major facilitator superfamily transporters such as  PDR15,  YOR1, or  AZR1 or for other proteins such as  SNG1,  YJL216c, or  YLL056c which are already known to be involved in the yeast pleiotropic drug resistance (PDR) phenomenon.	gene_phenotype
68211	4	333251	7	NULL	NULL	0	NULL	SNG1	GP		is involved in					PDR phenomenon	Process	yeast			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_13_11427_s_6	12529331	These target genes code for ATP-binding cassette or major facilitator superfamily transporters such as  PDR15,  YOR1, or  AZR1 or for other proteins such as  SNG1,  YJL216c, or  YLL056c which are already known to be involved in the yeast pleiotropic drug resistance (PDR) phenomenon.	gene_phenotype
68212	5	333251	7	NULL	NULL	0	NULL	YJL216c	GP		is involved in					PDR phenomenon	Process	yeast			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_13_11427_s_6	12529331	These target genes code for ATP-binding cassette or major facilitator superfamily transporters such as  PDR15,  YOR1, or  AZR1 or for other proteins such as  SNG1,  YJL216c, or  YLL056c which are already known to be involved in the yeast pleiotropic drug resistance (PDR) phenomenon.	gene_phenotype
68213	6	333251	7	NULL	NULL	0	NULL	YLL056c 	GP		is involved in					PDR phenomenon	Process	yeast			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_13_11427_s_6	12529331	These target genes code for ATP-binding cassette or major facilitator superfamily transporters such as  PDR15,  YOR1, or  AZR1 or for other proteins such as  SNG1,  YJL216c, or  YLL056c which are already known to be involved in the yeast pleiotropic drug resistance (PDR) phenomenon.	gene_phenotype
68214	7	333251	7	NULL	NULL	0	NULL	PDR	Process		is					pleiotropic drug resistance	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_13_11427_s_6	12529331	These target genes code for ATP-binding cassette or major facilitator superfamily transporters such as  PDR15,  YOR1, or  AZR1 or for other proteins such as  SNG1,  YJL216c, or  YLL056c which are already known to be involved in the yeast pleiotropic drug resistance (PDR) phenomenon.	gene_phenotype
68215	1	333252	7	NULL	NULL	NULL	NULL	TORC1	GP		controls			subunit of		growth	Process				NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_3_159_s_74	16498703	YJR066w, YKL203c  TOR1, TOR2 PIK-related protein kinase and rapamycin target; subunit of TORC1, a complex that  controls growth in response to nutrients by regulating translation, transcription,  ribosome biogenesis, nutrient transport and autophagy; involved in meiosis  [ 3	gene_phenotype
68216	2	333252	7	NULL	NULL	NULL	NULL	statement 1	Process		in response to					nutrients	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_3_159_s_74	16498703	YJR066w, YKL203c  TOR1, TOR2 PIK-related protein kinase and rapamycin target; subunit of TORC1, a complex that  controls growth in response to nutrients by regulating translation, transcription,  ribosome biogenesis, nutrient transport and autophagy; involved in meiosis  [ 3	gene_phenotype
68217	3	333252	7	NULL	NULL	0	NULL	statement 1	Process		occur by					translation	Process	regulating			NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_74	16498703	YJR066w, YKL203c  TOR1, TOR2 PIK-related protein kinase and rapamycin target; subunit of TORC1, a complex that  controls growth in response to nutrients by regulating translation, transcription,  ribosome biogenesis, nutrient transport and autophagy; involved in meiosis  [ 3	gene_phenotype
68218	4	333252	7	NULL	NULL	0	NULL	statement 1	Process		occur by					transcription	Process	regulating			NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_74	16498703	YJR066w, YKL203c  TOR1, TOR2 PIK-related protein kinase and rapamycin target; subunit of TORC1, a complex that  controls growth in response to nutrients by regulating translation, transcription,  ribosome biogenesis, nutrient transport and autophagy; involved in meiosis  [ 3	gene_phenotype
68219	5	333252	7	NULL	NULL	0	NULL	statement 1	Process		occur by					ribosome biogenesis	Process	regulating			NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_74	16498703	YJR066w, YKL203c  TOR1, TOR2 PIK-related protein kinase and rapamycin target; subunit of TORC1, a complex that  controls growth in response to nutrients by regulating translation, transcription,  ribosome biogenesis, nutrient transport and autophagy; involved in meiosis  [ 3	gene_phenotype
68220	6	333252	7	NULL	NULL	0	NULL	statement 1	Process		occur by					nutrient transport 	Process	regulating			NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_74	16498703	YJR066w, YKL203c  TOR1, TOR2 PIK-related protein kinase and rapamycin target; subunit of TORC1, a complex that  controls growth in response to nutrients by regulating translation, transcription,  ribosome biogenesis, nutrient transport and autophagy; involved in meiosis  [ 3	gene_phenotype
68221	7	333252	7	NULL	NULL	0	NULL	statement 1	Process		occur by					autophagy	Process	regulating			NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_74	16498703	YJR066w, YKL203c  TOR1, TOR2 PIK-related protein kinase and rapamycin target; subunit of TORC1, a complex that  controls growth in response to nutrients by regulating translation, transcription,  ribosome biogenesis, nutrient transport and autophagy; involved in meiosis  [ 3	gene_phenotype
68222	8	333252	7	NULL	NULL	0	NULL	TORC1	GP		is involved in			subunit of		meiosis	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_74	16498703	YJR066w, YKL203c  TOR1, TOR2 PIK-related protein kinase and rapamycin target; subunit of TORC1, a complex that  controls growth in response to nutrients by regulating translation, transcription,  ribosome biogenesis, nutrient transport and autophagy; involved in meiosis  [ 3	gene_phenotype
68223	1	333253	7	NULL	NULL	0	NULL	Srx1	GP	yeast	is present in					cytosol	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_49_50994_s_229	15448164	Although a global analysis of protein localization in budding yeast showed that yeast Srx (Srx1, YKL086W) was present in both cytosol and the nucleus ( ) ( yeastgfp.	gene_phenotype
68224	2	333253	7	NULL	NULL	0	NULL	Srx1	GP	yeast	is present in					nucleus	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_49_50994_s_229	15448164	Although a global analysis of protein localization in budding yeast showed that yeast Srx (Srx1, YKL086W) was present in both cytosol and the nucleus ( ) ( yeastgfp.	gene_phenotype
68225	3	333253	7	NULL	NULL	NULL	NULL	YKL086W	GP	yeast	is present in					cytosol	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_49_50994_s_229	15448164	Although a global analysis of protein localization in budding yeast showed that yeast Srx (Srx1, YKL086W) was present in both cytosol and the nucleus ( ) ( yeastgfp.	gene_phenotype
68226	4	333253	7	NULL	NULL	0	NULL	YKL086W	GP	yeast	is present in					nucleus	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_49_50994_s_229	15448164	Although a global analysis of protein localization in budding yeast showed that yeast Srx (Srx1, YKL086W) was present in both cytosol and the nucleus ( ) ( yeastgfp.	gene_phenotype
68227	1	333254	7	NULL	NULL	0	NULL	YPT52 YKR014C Rab5-like GTPase	GP		is involved in					vacuolar protein 	GP	sorting of			NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_359	15334557	YPT52   YKR014C Rab5-like GTPase involved in vacuolar protein sorting and endocytosis	gene_phenotype
68228	2	333254	7	NULL	NULL	0	NULL	YPT52 YKR014C Rab5-like GTPase	GP		is involved in					endocytosis	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_359	15334557	YPT52   YKR014C Rab5-like GTPase involved in vacuolar protein sorting and endocytosis	gene_phenotype
68229	1	333255	7	NULL	NULL	0	NULL	Gog5	GP	S. cerevisiae	is a type of					vanadate resistance protein	GP	S. cerevisiae			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1593_2_179_s_296	12581862	The sponge large subunit shares with the  S. cerevisiae vanadate resistance protein Gog5 (Z46659) an  E value of only 1.6; with respect to the small subunit, the  E value to the yeast cell viability protein Ylr409cp (U19729) is even only 2.4, as  estimated in the database [ 31].	gene_phenotype
68230	2	333255	7	NULL	NULL	0	NULL	Ylr409cp	GP		is a type of					yeast cell viability protein	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1593_2_179_s_296	12581862	The sponge large subunit shares with the  S. cerevisiae vanadate resistance protein Gog5 (Z46659) an  E value of only 1.6; with respect to the small subunit, the  E value to the yeast cell viability protein Ylr409cp (U19729) is even only 2.4, as  estimated in the database [ 31].	gene_phenotype
68231	1	333258	7	NULL	NULL	0	NULL	Ylr453c Rif2 2 Protein	GP		bind					Rap1p	GP		C-terminus		NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_150	16498703	Ylr453c  Rif2  2 Protein that binds to the Rap1p C-terminus and acts synergistically with Rif1p to  help control telomere length and establish telomeric silencing; deletion results  in telomere elongation  L2H  [ 24]	gene_phenotype
68232	2	333258	7	NULL	NULL	0	NULL	Ylr453c Rif2 2 Protein	GP		act synergistically with					Rif1p	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_150	16498703	Ylr453c  Rif2  2 Protein that binds to the Rap1p C-terminus and acts synergistically with Rif1p to  help control telomere length and establish telomeric silencing; deletion results  in telomere elongation  L2H  [ 24]	gene_phenotype
68233	3	333258	7	NULL	NULL	NULL	NULL	statement 2	Process		help to					telomere length	Chromosome	control			NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_3_159_s_150	16498703	Ylr453c  Rif2  2 Protein that binds to the Rap1p C-terminus and acts synergistically with Rif1p to  help control telomere length and establish telomeric silencing; deletion results  in telomere elongation  L2H  [ 24]	gene_phenotype
68234	4	333258	7	NULL	NULL	0	NULL	statement 2	Process		establish					telomeric silencing	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_150	16498703	Ylr453c  Rif2  2 Protein that binds to the Rap1p C-terminus and acts synergistically with Rif1p to  help control telomere length and establish telomeric silencing; deletion results  in telomere elongation  L2H  [ 24]	gene_phenotype
68235	5	333258	7	NULL	NULL	0	NULL	statement 2	Process	deletion of	results in					telomere elongation L2H	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_150	16498703	Ylr453c  Rif2  2 Protein that binds to the Rap1p C-terminus and acts synergistically with Rif1p to  help control telomere length and establish telomeric silencing; deletion results  in telomere elongation  L2H  [ 24]	gene_phenotype
68236	1	333262	7	NULL	NULL	0	NULL	Ypl032c Svl3 1 Protein	GP	mutant;;phenotype of	suggests					 vacuolar function	Process	potential role in			NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_137	16498703	Ypl032c  Svl3  1 Protein of unknown function, mutant phenotype suggests a potential role in vacuolar  function; green fluorescent protein fusion protein localizes to the cell periphery,  cytoplasm, bud and bud neck  LIP  [ 11],[ 20]	gene_phenotype
68237	1	333263	7	NULL	NULL	0	NULL	soluble vacuolar hydrolases	GP	precursors for	is transported from					late endosome	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_258	15334557	VPS28   YPL065w Protein involved in transport of precursors for soluble vacuolar hydrolases from the  late endosome to the vacuole	gene_phenotype
68238	2	333263	7	NULL	NULL	0	NULL	soluble vacuolar hydrolases	GP	precursors for	is transported to					vacuole	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_258	15334557	VPS28   YPL065w Protein involved in transport of precursors for soluble vacuolar hydrolases from the  late endosome to the vacuole	gene_phenotype
68239	3	333263	7	NULL	NULL	0	NULL	statement 1	Process		occur along with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_258	15334557	VPS28   YPL065w Protein involved in transport of precursors for soluble vacuolar hydrolases from the  late endosome to the vacuole	gene_phenotype
68240	4	333263	7	NULL	NULL	0	NULL	VPS28 YPL065w Protein	GP		is involved in					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_258	15334557	VPS28   YPL065w Protein involved in transport of precursors for soluble vacuolar hydrolases from the  late endosome to the vacuole	gene_phenotype
68241	1	333264	7	NULL	NULL	0	NULL	Cys4p	GP	activity of	requires					 pyridoxal phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_1_836_s_200	16391125	It is worth mentioning that Cys4p requires pyridoxal phosphate for its activity, and another protein identified in our studies, YPR127w, shows similarity to the  Schizosaccharomyces pombe pyridoxal reductase, thus establishing a possible link between these two proteins.	gene_phenotype
68242	1	333265	7	NULL	NULL	0	NULL	YPR141c KAR3	GP		directs			Minus-end		microtubule motor	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_85	16498703	YPR141c   KAR3 Minus-end-directed microtubule motor that functions in mitosis and meiosis, localizes  to the spindle pole body and localization is dependent on functional Cik1p, required  for nuclear fusion during mating; potential Cdc28p substrate  [ 49]	gene_phenotype
68243	2	333265	7	NULL	NULL	0	NULL	statement 1	Process		functions in					mitosis	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_85	16498703	YPR141c   KAR3 Minus-end-directed microtubule motor that functions in mitosis and meiosis, localizes  to the spindle pole body and localization is dependent on functional Cik1p, required  for nuclear fusion during mating; potential Cdc28p substrate  [ 49]	gene_phenotype
68244	3	333265	7	NULL	NULL	0	NULL	statement 1	Process		functions in					meiosis	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_85	16498703	YPR141c   KAR3 Minus-end-directed microtubule motor that functions in mitosis and meiosis, localizes  to the spindle pole body and localization is dependent on functional Cik1p, required  for nuclear fusion during mating; potential Cdc28p substrate  [ 49]	gene_phenotype
68245	4	333265	7	NULL	NULL	0	NULL	statement 1	Process		localizes to					spindle pole body	Chromosome				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_85	16498703	YPR141c   KAR3 Minus-end-directed microtubule motor that functions in mitosis and meiosis, localizes  to the spindle pole body and localization is dependent on functional Cik1p, required  for nuclear fusion during mating; potential Cdc28p substrate  [ 49]	gene_phenotype
68246	5	333265	7	NULL	NULL	0	NULL	statement 4	Process	localization of	depends on					Cik1p	GP	functional			NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_85	16498703	YPR141c   KAR3 Minus-end-directed microtubule motor that functions in mitosis and meiosis, localizes  to the spindle pole body and localization is dependent on functional Cik1p, required  for nuclear fusion during mating; potential Cdc28p substrate  [ 49]	gene_phenotype
68247	6	333265	7	NULL	NULL	0	NULL	statement 1	Process		required for					nuclear fusion	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_85	16498703	YPR141c   KAR3 Minus-end-directed microtubule motor that functions in mitosis and meiosis, localizes  to the spindle pole body and localization is dependent on functional Cik1p, required  for nuclear fusion during mating; potential Cdc28p substrate  [ 49]	gene_phenotype
68248	7	333265	7	NULL	NULL	0	NULL	statement 6	Process		occur during					mating	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_85	16498703	YPR141c   KAR3 Minus-end-directed microtubule motor that functions in mitosis and meiosis, localizes  to the spindle pole body and localization is dependent on functional Cik1p, required  for nuclear fusion during mating; potential Cdc28p substrate  [ 49]	gene_phenotype
68249	8	333265	7	NULL	NULL	0	NULL	statement 1	Process		is substrate for					Cdc28p	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_85	16498703	YPR141c   KAR3 Minus-end-directed microtubule motor that functions in mitosis and meiosis, localizes  to the spindle pole body and localization is dependent on functional Cik1p, required  for nuclear fusion during mating; potential Cdc28p substrate  [ 49]	gene_phenotype
68270	1	333267	7	NULL	NULL	0	NULL	S. cerevisiae	Organism		encode					Rri1p	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_37_34948_s_299	11457827	This activity appears to be conserved from budding yeast to humans, even though  S. cerevisiae encodes only one COP9 signalosome subunit ortholog termed Rri1p, a Mov34 family protein previously called D0888 ( 10) or YDL216c ( 14,  15).	gene_phenotype
68271	2	333267	7	NULL	NULL	0	NULL	Rri1p	GP		is orthologous to					COP9 signalosome subunit	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_37_34948_s_299	11457827	This activity appears to be conserved from budding yeast to humans, even though  S. cerevisiae encodes only one COP9 signalosome subunit ortholog termed Rri1p, a Mov34 family protein previously called D0888 ( 10) or YDL216c ( 14,  15).	gene_phenotype
68272	3	333267	7	NULL	NULL	0	NULL	Rri1p	GP		is a type of					Mov34 family protein 	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_37_34948_s_299	11457827	This activity appears to be conserved from budding yeast to humans, even though  S. cerevisiae encodes only one COP9 signalosome subunit ortholog termed Rri1p, a Mov34 family protein previously called D0888 ( 10) or YDL216c ( 14,  15).	gene_phenotype
68274	4	333267	7	NULL	NULL	NULL	NULL	Mov34 family protein 	GP		called as		previously			D0888	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_37_34948_s_299	11457827	This activity appears to be conserved from budding yeast to humans, even though  S. cerevisiae encodes only one COP9 signalosome subunit ortholog termed Rri1p, a Mov34 family protein previously called D0888 ( 10) or YDL216c ( 14,  15).	gene_phenotype
68275	5	333267	7	NULL	NULL	NULL	NULL	Mov34 family protein 	GP		 called as		previously			YDL216c	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_37_34948_s_299	11457827	This activity appears to be conserved from budding yeast to humans, even though  S. cerevisiae encodes only one COP9 signalosome subunit ortholog termed Rri1p, a Mov34 family protein previously called D0888 ( 10) or YDL216c ( 14,  15).	gene_phenotype
68279	1	333268	7	NULL	NULL	0	NULL	AKR1 YDR264c Protein	GP	palmitoylation of	required for					pheromone receptors	GP	endocytosis of			NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_267	15334557	AKR1   YDR264c Protein palmitoylation; required for endocytosis of pheromone receptors	gene_phenotype
68297	1	333271	7	NULL	NULL	0	NULL	FYV13 YGR160w	GP		required for					yeast viability	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_309	15334557	FYV13   YGR160w Required for yeast viability on toxin exposure	gene_phenotype
68298	2	333271	7	NULL	NULL	NULL	NULL	statement 1	Process		occur upon					toxin	GP	exposure to			NULL		NULL	NULL	NULL	NULL	gw70_yeast_21_11_927_s_309	15334557	FYV13   YGR160w Required for yeast viability on toxin exposure	gene_phenotype
68299	1	333272	7	NULL	NULL	0	NULL	YHR187W	GP		recovered from					 K. lactis toxin	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_32_29628_s_60	11390369	YHR187W was previously recovered from a genetic screen for resistance to killing by  K. lactis toxin ( 11) and named  IKI1.	gene_phenotype
68300	2	333272	7	NULL	NULL	0	NULL	 K. lactis toxin	GP		is					IKI1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_32_29628_s_60	11390369	YHR187W was previously recovered from a genetic screen for resistance to killing by  K. lactis toxin ( 11) and named  IKI1.	gene_phenotype
68301	1	333273	7	NULL	NULL	0	NULL	cAMP-dependent protein kinase	GP	cytoplasmic	contains			YJL164c TPK1 Subunit of					Tpk1p		NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_76	16498703	YJL164c   TPK1 Subunit of cytoplasmic cAMP-dependent protein kinase, which contains redundant catalytic  subunits Tpk1p, Tpk2p, and Tpk3p and regulatory subunit Bcy1p; promotes vegetative  growth in response to nutrients; inhibits filamentous growth  [ 18]	gene_phenotype
68302	2	333273	7	NULL	NULL	0	NULL	cAMP-dependent protein kinase	GP	cytoplasmic	contains			YJL164c TPK1 Subunit of					Tpk2p		NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_76	16498703	YJL164c   TPK1 Subunit of cytoplasmic cAMP-dependent protein kinase, which contains redundant catalytic  subunits Tpk1p, Tpk2p, and Tpk3p and regulatory subunit Bcy1p; promotes vegetative  growth in response to nutrients; inhibits filamentous growth  [ 18]	gene_phenotype
68303	3	333273	7	NULL	NULL	0	NULL	cAMP-dependent protein kinase	GP	cytoplasmic	contains			YJL164c TPK1 Subunit of					Tpk3p		NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_76	16498703	YJL164c   TPK1 Subunit of cytoplasmic cAMP-dependent protein kinase, which contains redundant catalytic  subunits Tpk1p, Tpk2p, and Tpk3p and regulatory subunit Bcy1p; promotes vegetative  growth in response to nutrients; inhibits filamentous growth  [ 18]	gene_phenotype
68304	4	333273	7	NULL	NULL	0	NULL	cAMP-dependent protein kinase	GP	cytoplasmic	contains			YJL164c TPK1 Subunit of					Bcy1p		NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_76	16498703	YJL164c   TPK1 Subunit of cytoplasmic cAMP-dependent protein kinase, which contains redundant catalytic  subunits Tpk1p, Tpk2p, and Tpk3p and regulatory subunit Bcy1p; promotes vegetative  growth in response to nutrients; inhibits filamentous growth  [ 18]	gene_phenotype
68305	5	333273	7	NULL	NULL	NULL	NULL	Tpk1p	GP		is a type of					catalytic subunit	GP				NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_3_159_s_76	16498703	YJL164c   TPK1 Subunit of cytoplasmic cAMP-dependent protein kinase, which contains redundant catalytic  subunits Tpk1p, Tpk2p, and Tpk3p and regulatory subunit Bcy1p; promotes vegetative  growth in response to nutrients; inhibits filamentous growth  [ 18]	gene_phenotype
68306	6	333273	7	NULL	NULL	0	NULL	Tpk2p	GP		is a type of					catalytic subunit	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_76	16498703	YJL164c   TPK1 Subunit of cytoplasmic cAMP-dependent protein kinase, which contains redundant catalytic  subunits Tpk1p, Tpk2p, and Tpk3p and regulatory subunit Bcy1p; promotes vegetative  growth in response to nutrients; inhibits filamentous growth  [ 18]	gene_phenotype
68307	7	333273	7	NULL	NULL	0	NULL	Tpk3p	GP		is a type of					catalytic subunit	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_76	16498703	YJL164c   TPK1 Subunit of cytoplasmic cAMP-dependent protein kinase, which contains redundant catalytic  subunits Tpk1p, Tpk2p, and Tpk3p and regulatory subunit Bcy1p; promotes vegetative  growth in response to nutrients; inhibits filamentous growth  [ 18]	gene_phenotype
68308	8	333273	7	NULL	NULL	0	NULL	Bcy1p	GP		is a type of					regulatory subunit	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_76	16498703	YJL164c   TPK1 Subunit of cytoplasmic cAMP-dependent protein kinase, which contains redundant catalytic  subunits Tpk1p, Tpk2p, and Tpk3p and regulatory subunit Bcy1p; promotes vegetative  growth in response to nutrients; inhibits filamentous growth  [ 18]	gene_phenotype
68309	9	333273	7	NULL	NULL	0	NULL	cAMP-dependent protein kinase	GP	cytoplasmic	promotes			YJL164c TPK1 Subunit of 		vegetative growth	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_76	16498703	YJL164c   TPK1 Subunit of cytoplasmic cAMP-dependent protein kinase, which contains redundant catalytic  subunits Tpk1p, Tpk2p, and Tpk3p and regulatory subunit Bcy1p; promotes vegetative  growth in response to nutrients; inhibits filamentous growth  [ 18]	gene_phenotype
68310	10	333273	7	NULL	NULL	0	NULL	statement 9	Process		in response to					nutrients	Chemical				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_76	16498703	YJL164c   TPK1 Subunit of cytoplasmic cAMP-dependent protein kinase, which contains redundant catalytic  subunits Tpk1p, Tpk2p, and Tpk3p and regulatory subunit Bcy1p; promotes vegetative  growth in response to nutrients; inhibits filamentous growth  [ 18]	gene_phenotype
68311	11	333273	7	NULL	NULL	0	NULL	cAMP-dependent protein kinase	GP	cytoplasmic	inhibits			YJL164c TPK1 Subunit of		filamentous growth	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_76	16498703	YJL164c   TPK1 Subunit of cytoplasmic cAMP-dependent protein kinase, which contains redundant catalytic  subunits Tpk1p, Tpk2p, and Tpk3p and regulatory subunit Bcy1p; promotes vegetative  growth in response to nutrients; inhibits filamentous growth  [ 18]	gene_phenotype
68312	1	333275	7	NULL	NULL	0	NULL	 VPS2	GP		allelic to					DID4	GP				NULL		0	NULL	NULL	NULL	gw60_devcell_3_2_271_s_41	12194857	These studies led to the identification and cloning of two additional class E  VPS genes,  VPS2 (allelic to  DID4,  GRD7, and  REN1; SGD ORF YKL002W, hereafter referred to as  VPS2) and  VPS20 (SGD ORF YMR077C), a gene found to be required for transport of the plasma membrane protein Ste6 to the vacuole  (Kranz et al., 2001  ).	gene_phenotype
68313	2	333275	7	NULL	NULL	0	NULL	VPS2	GP		allelic to					GRD7	GP				NULL		0	NULL	NULL	NULL	gw60_devcell_3_2_271_s_41	12194857	These studies led to the identification and cloning of two additional class E  VPS genes,  VPS2 (allelic to  DID4,  GRD7, and  REN1; SGD ORF YKL002W, hereafter referred to as  VPS2) and  VPS20 (SGD ORF YMR077C), a gene found to be required for transport of the plasma membrane protein Ste6 to the vacuole  (Kranz et al., 2001  ).	gene_phenotype
68314	3	333275	7	NULL	NULL	0	NULL	VPS2 	GP		allelic to					REN1	GP				NULL		0	NULL	NULL	NULL	gw60_devcell_3_2_271_s_41	12194857	These studies led to the identification and cloning of two additional class E  VPS genes,  VPS2 (allelic to  DID4,  GRD7, and  REN1; SGD ORF YKL002W, hereafter referred to as  VPS2) and  VPS20 (SGD ORF YMR077C), a gene found to be required for transport of the plasma membrane protein Ste6 to the vacuole  (Kranz et al., 2001  ).	gene_phenotype
68315	4	333275	7	NULL	NULL	0	NULL	SGD ORF YKL002W	GP		is					VPS2	GP				NULL		0	NULL	NULL	NULL	gw60_devcell_3_2_271_s_41	12194857	These studies led to the identification and cloning of two additional class E  VPS genes,  VPS2 (allelic to  DID4,  GRD7, and  REN1; SGD ORF YKL002W, hereafter referred to as  VPS2) and  VPS20 (SGD ORF YMR077C), a gene found to be required for transport of the plasma membrane protein Ste6 to the vacuole  (Kranz et al., 2001  ).	gene_phenotype
68316	5	333275	7	NULL	NULL	0	NULL	VPS20	GP		is					SGD ORF YMR077C	GP				NULL		0	NULL	NULL	NULL	gw60_devcell_3_2_271_s_41	12194857	These studies led to the identification and cloning of two additional class E  VPS genes,  VPS2 (allelic to  DID4,  GRD7, and  REN1; SGD ORF YKL002W, hereafter referred to as  VPS2) and  VPS20 (SGD ORF YMR077C), a gene found to be required for transport of the plasma membrane protein Ste6 to the vacuole  (Kranz et al., 2001  ).	gene_phenotype
68317	6	333275	7	NULL	NULL	0	NULL	Ste6	GP		transported to					vacuole	CellComponent				NULL		0	NULL	NULL	NULL	gw60_devcell_3_2_271_s_41	12194857	These studies led to the identification and cloning of two additional class E  VPS genes,  VPS2 (allelic to  DID4,  GRD7, and  REN1; SGD ORF YKL002W, hereafter referred to as  VPS2) and  VPS20 (SGD ORF YMR077C), a gene found to be required for transport of the plasma membrane protein Ste6 to the vacuole  (Kranz et al., 2001  ).	gene_phenotype
68318	7	333275	7	NULL	NULL	0	NULL	Ste6	GP		is a type of					plasma membrane protein	GP				NULL		0	NULL	NULL	NULL	gw60_devcell_3_2_271_s_41	12194857	These studies led to the identification and cloning of two additional class E  VPS genes,  VPS2 (allelic to  DID4,  GRD7, and  REN1; SGD ORF YKL002W, hereafter referred to as  VPS2) and  VPS20 (SGD ORF YMR077C), a gene found to be required for transport of the plasma membrane protein Ste6 to the vacuole  (Kranz et al., 2001  ).	gene_phenotype
68319	8	333275	7	NULL	NULL	0	NULL	VPS20	GP		is required for					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_devcell_3_2_271_s_41	12194857	These studies led to the identification and cloning of two additional class E  VPS genes,  VPS2 (allelic to  DID4,  GRD7, and  REN1; SGD ORF YKL002W, hereafter referred to as  VPS2) and  VPS20 (SGD ORF YMR077C), a gene found to be required for transport of the plasma membrane protein Ste6 to the vacuole  (Kranz et al., 2001  ).	gene_phenotype
68320	1	333276	7	NULL	NULL	0	NULL	Ylr435wp	GP		is					Tsr2	GP				NULL		0	NULL	NULL	NULL	gw60_cell_113_7_919_s_161	12837249	The second protein, Ylr435wp (referred to hereafter as Tsr2, for  Twenty  S RNA accumulation), is nonessential, but deletion resulted in slow growth (doubling time  2.5 hr) in addition to a prominent 20S accumulation and a corresponding 18S deficit   (Figure 4B).	gene_phenotype
68321	2	333276	7	NULL	NULL	0	NULL	Ylr435wp	GP	deletion of	results in					slow growth	Process				NULL		0	NULL	NULL	NULL	gw60_cell_113_7_919_s_161	12837249	The second protein, Ylr435wp (referred to hereafter as Tsr2, for  Twenty  S RNA accumulation), is nonessential, but deletion resulted in slow growth (doubling time  2.5 hr) in addition to a prominent 20S accumulation and a corresponding 18S deficit   (Figure 4B).	gene_phenotype
68322	1	333279	7	NULL	NULL	0	NULL	YNL310c	GP		encode					Zim17	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50243_s_121	15383543	Zim17 Is an Essential Component of the Import Machinery --  YNL310c, the gene encoding Zim17, is essential for viability (data not shown) ( ).	gene_phenotype
68323	2	333279	7	NULL	NULL	0	NULL	Zim17	GP		is essential for					viability	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50243_s_121	15383543	Zim17 Is an Essential Component of the Import Machinery --  YNL310c, the gene encoding Zim17, is essential for viability (data not shown) ( ).	gene_phenotype
68324	3	333279	7	NULL	NULL	0	NULL	Zim17	GP		is essential component of					Import Machinery	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50243_s_121	15383543	Zim17 Is an Essential Component of the Import Machinery --  YNL310c, the gene encoding Zim17, is essential for viability (data not shown) ( ).	gene_phenotype
68325	1	333280	7	NULL	NULL	0	NULL	YNL310c plasmid	NucleicAcid		maintains					cell viability	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50243_s_152	15383543	A plasmid with YNL310c under constitutive control maintains cell viability and the cells ( Zim17) remain viable and divide to form large colonies.	gene_phenotype
68326	2	333280	7	NULL	NULL	0	NULL	statement 1	Process		under					constitutive control	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50243_s_152	15383543	A plasmid with YNL310c under constitutive control maintains cell viability and the cells ( Zim17) remain viable and divide to form large colonies.	gene_phenotype
68327	1	333281	7	NULL	NULL	NULL	NULL	 yTRN	GP		interact with					M9-containing import substrates	GP	members of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4141_s_219	9632798	It seems that yTRN is more constrained than hTRN1 in its capacity to interact with various members of the M9-containing import substrates, although yTRN does apparently bind Nab4p (YOL123w or Hrp1p) ( 2), another nuclear mRNA-binding protein in  S. cerevisiae.	gene_phenotype
68328	2	333281	7	NULL	NULL	NULL	NULL	hTRN1 	GP		interact with					M9-containing import substrates	GP	members of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_7_4141_s_219	9632798	It seems that yTRN is more constrained than hTRN1 in its capacity to interact with various members of the M9-containing import substrates, although yTRN does apparently bind Nab4p (YOL123w or Hrp1p) ( 2), another nuclear mRNA-binding protein in  S. cerevisiae.	gene_phenotype
68329	3	333281	7	NULL	NULL	0	NULL	statement 1	Process		is more constrained than					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_4141_s_219	9632798	It seems that yTRN is more constrained than hTRN1 in its capacity to interact with various members of the M9-containing import substrates, although yTRN does apparently bind Nab4p (YOL123w or Hrp1p) ( 2), another nuclear mRNA-binding protein in  S. cerevisiae.	gene_phenotype
68330	4	333281	7	NULL	NULL	0	NULL	yTRN	GP		bind					Nab4p	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_4141_s_219	9632798	It seems that yTRN is more constrained than hTRN1 in its capacity to interact with various members of the M9-containing import substrates, although yTRN does apparently bind Nab4p (YOL123w or Hrp1p) ( 2), another nuclear mRNA-binding protein in  S. cerevisiae.	gene_phenotype
68331	5	333281	7	NULL	NULL	0	NULL	Nab4p 	GP		is a type of					nuclear mRNA-binding protein					NULL	S.cerevisiae	0	NULL	NULL	NULL	gw60_molcellbiol_18_7_4141_s_219	9632798	It seems that yTRN is more constrained than hTRN1 in its capacity to interact with various members of the M9-containing import substrates, although yTRN does apparently bind Nab4p (YOL123w or Hrp1p) ( 2), another nuclear mRNA-binding protein in  S. cerevisiae.	gene_phenotype
68332	1	333282	7	NULL	NULL	0	NULL	ODC1	GP		encode					mitochondrial transporter family	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1459_2_363_s_118	11004452	ODC1 and ODC2 (genome designation YPL134c and YOR222w, respectively) encode two closely related members of the mitochondrial transporter family (61% identity; 88% similarity).	gene_phenotype
68333	2	333282	7	NULL	NULL	0	NULL	ODC2	GP		encode					mitochondrial transporter family	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1459_2_363_s_118	11004452	ODC1 and ODC2 (genome designation YPL134c and YOR222w, respectively) encode two closely related members of the mitochondrial transporter family (61% identity; 88% similarity).	gene_phenotype
68334	1	333285	7	NULL	NULL	0	NULL	ALD5	GP		encode					NAD(P) ACDH	GP	minor form of mitochondrial			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_66_8_3151_s_53	10919763	ALD5 (YER073w) was shown to encode a minor form of the mitochondrial NAD(P) ACDH ( 49), which might play a role in regulation or biosynthesis of electron transport chain components ( 19).	gene_phenotype
68335	2	333285	7	NULL	NULL	0	NULL	NAD(P) ACDH	GP		play a role in					electron transport chain components	GP	regulation of			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_66_8_3151_s_53	10919763	ALD5 (YER073w) was shown to encode a minor form of the mitochondrial NAD(P) ACDH ( 49), which might play a role in regulation or biosynthesis of electron transport chain components ( 19).	gene_phenotype
68336	3	333285	7	NULL	NULL	0	NULL	NAD(P) ACDH	GP		play a role in					electron transport chain components	GP	biosynthesis of			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_66_8_3151_s_53	10919763	ALD5 (YER073w) was shown to encode a minor form of the mitochondrial NAD(P) ACDH ( 49), which might play a role in regulation or biosynthesis of electron transport chain components ( 19).	gene_phenotype
68337	1	333286	7	NULL	NULL	0	NULL	Pho87	GP		is a type of					putative phosphate transporter	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_12_4309_s_172	11102525	Furthermore, this similarity is shared among a total of nine  S. cerevisiae ORFs, including the putative phosphate transporter Pho87 (Bun-ya  et al., 1996  ), two proteins homologous to Pho87, Yjl198w and Ynr013, and Syg1 (Spain  et al., 1995  ), a multi-copy suppressor for a  GPA1 deletion.	gene_phenotype
68338	1	333287	7	NULL	NULL	0	NULL	ORF YJL204c	GP	strain disrupted for	shows					LY	Chemical	decreased levels of			NULL	vacuole	0	NULL	NULL	NULL	gw60_cellbiol_149_2_397_s_153	10769031	The strain, disrupted for the ORF  YJL204c, showed decreased levels of LY in the vacuole consistent with a defect in fluid-phase endocytosis (compare   Fig 1 A and   Fig 1 B).	gene_phenotype
68339	2	333287	7	NULL	NULL	0	NULL	statement 1	Process		consistent with					fluid-phase endocytosis	Process	defect in			NULL		0	NULL	NULL	NULL	gw60_cellbiol_149_2_397_s_153	10769031	The strain, disrupted for the ORF  YJL204c, showed decreased levels of LY in the vacuole consistent with a defect in fluid-phase endocytosis (compare   Fig 1 A and   Fig 1 B).	gene_phenotype
68340	1	333288	7	NULL	NULL	0	NULL	YKL146wp	GP		encode					AVT3 	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_25_22966_s_36	11959859	Recently it was shown that YKL146wp indeed codes for a protein that represents a vesicular amino acid transporter, designated as AVT3 ( 4).	gene_phenotype
68341	2	333288	7	NULL	NULL	NULL	NULL	AVT3	GP		is a type of					vesicular amino acid transporter	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_25_22966_s_36	11959859	Recently it was shown that YKL146wp indeed codes for a protein that represents a vesicular amino acid transporter, designated as AVT3 ( 4).	gene_phenotype
68342	1	333289	7	NULL	NULL	0	NULL	 YKL146wp	GP	S. cerevisiae	is a type of					putative amino acid transport protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_25_22966_s_35	11959859	We searched for mammalian AAAP family members based on the  S. cerevisiae protein sequence YKL146wp, which had been identified by genome-scanning analysis as a putative amino acid transport protein.	gene_phenotype
68343	1	333290	7	NULL	NULL	NULL	NULL	YKR082w	GP	double mutant	is not					viable	Process				NULL		NULL	NULL	NULL	NULL	gw60_gene_233_1_141_s_132	10375630	Alternatively, it could also be that double mutants in  YKR082w along with either  YKR081c or  YKR083c are not viable.	gene_phenotype
68344	2	333290	7	NULL	NULL	0	NULL	YKR081c	GP	double mutant	is not 					viable	Process				NULL		0	NULL	NULL	NULL	gw60_gene_233_1_141_s_132	10375630	Alternatively, it could also be that double mutants in  YKR082w along with either  YKR081c or  YKR083c are not viable.	gene_phenotype
68345	3	333290	7	NULL	NULL	0	NULL	YKR083c	GP	double mutant	is not					viable	Process				NULL		0	NULL	NULL	NULL	gw60_gene_233_1_141_s_132	10375630	Alternatively, it could also be that double mutants in  YKR082w along with either  YKR081c or  YKR083c are not viable.	gene_phenotype
68346	1	333293	7	NULL	NULL	0	NULL	ERG3	GP		is resistant to					fluconazole	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_163_4_1287_s_10	12702675	In a genome-wide screen of  4700 viable deletion strains, 13 were classified as resistant to fluconazole ( ERG3,  ERG6,  YMR102C,  YMR099C,  YPL056C,  ERG28,  OSH1,  SCS2,  CKA2,  SML1,  YBR147W,  YGR283C, and  YLR407W).	gene_phenotype
68347	2	333293	7	NULL	NULL	0	NULL	ERG6	GP		is resistant to					fluconazole	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_163_4_1287_s_10	12702675	In a genome-wide screen of  4700 viable deletion strains, 13 were classified as resistant to fluconazole ( ERG3,  ERG6,  YMR102C,  YMR099C,  YPL056C,  ERG28,  OSH1,  SCS2,  CKA2,  SML1,  YBR147W,  YGR283C, and  YLR407W).	gene_phenotype
68348	3	333293	7	NULL	NULL	0	NULL	YMR102C	GP		is resistant to					fluconazole	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_163_4_1287_s_10	12702675	In a genome-wide screen of  4700 viable deletion strains, 13 were classified as resistant to fluconazole ( ERG3,  ERG6,  YMR102C,  YMR099C,  YPL056C,  ERG28,  OSH1,  SCS2,  CKA2,  SML1,  YBR147W,  YGR283C, and  YLR407W).	gene_phenotype
68349	4	333293	7	NULL	NULL	0	NULL	YMR099C	GP		is resistant to					fluconazole	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_163_4_1287_s_10	12702675	In a genome-wide screen of  4700 viable deletion strains, 13 were classified as resistant to fluconazole ( ERG3,  ERG6,  YMR102C,  YMR099C,  YPL056C,  ERG28,  OSH1,  SCS2,  CKA2,  SML1,  YBR147W,  YGR283C, and  YLR407W).	gene_phenotype
68350	5	333293	7	NULL	NULL	0	NULL	YPL056C	GP		is resistant to					fluconazole	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_163_4_1287_s_10	12702675	In a genome-wide screen of  4700 viable deletion strains, 13 were classified as resistant to fluconazole ( ERG3,  ERG6,  YMR102C,  YMR099C,  YPL056C,  ERG28,  OSH1,  SCS2,  CKA2,  SML1,  YBR147W,  YGR283C, and  YLR407W).	gene_phenotype
68351	6	333293	7	NULL	NULL	0	NULL	ERG28	GP		is resistant to					fluconazole	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_163_4_1287_s_10	12702675	In a genome-wide screen of  4700 viable deletion strains, 13 were classified as resistant to fluconazole ( ERG3,  ERG6,  YMR102C,  YMR099C,  YPL056C,  ERG28,  OSH1,  SCS2,  CKA2,  SML1,  YBR147W,  YGR283C, and  YLR407W).	gene_phenotype
68352	7	333293	7	NULL	NULL	0	NULL	OSH1	GP		is resistant to					fluconazole	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_163_4_1287_s_10	12702675	In a genome-wide screen of  4700 viable deletion strains, 13 were classified as resistant to fluconazole ( ERG3,  ERG6,  YMR102C,  YMR099C,  YPL056C,  ERG28,  OSH1,  SCS2,  CKA2,  SML1,  YBR147W,  YGR283C, and  YLR407W).	gene_phenotype
68353	8	333293	7	NULL	NULL	0	NULL	SCS2	GP		is resistant to					fluconazole	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_163_4_1287_s_10	12702675	In a genome-wide screen of  4700 viable deletion strains, 13 were classified as resistant to fluconazole ( ERG3,  ERG6,  YMR102C,  YMR099C,  YPL056C,  ERG28,  OSH1,  SCS2,  CKA2,  SML1,  YBR147W,  YGR283C, and  YLR407W).	gene_phenotype
68354	9	333293	7	NULL	NULL	0	NULL	CKA2	GP		is resistant to					fluconazole	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_163_4_1287_s_10	12702675	In a genome-wide screen of  4700 viable deletion strains, 13 were classified as resistant to fluconazole ( ERG3,  ERG6,  YMR102C,  YMR099C,  YPL056C,  ERG28,  OSH1,  SCS2,  CKA2,  SML1,  YBR147W,  YGR283C, and  YLR407W).	gene_phenotype
68355	10	333293	7	NULL	NULL	0	NULL	SML1	GP		is resistant to					fluconazole	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_163_4_1287_s_10	12702675	In a genome-wide screen of  4700 viable deletion strains, 13 were classified as resistant to fluconazole ( ERG3,  ERG6,  YMR102C,  YMR099C,  YPL056C,  ERG28,  OSH1,  SCS2,  CKA2,  SML1,  YBR147W,  YGR283C, and  YLR407W).	gene_phenotype
68356	11	333293	7	NULL	NULL	0	NULL	YBR147W	GP		is resistant to					fluconazole	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_163_4_1287_s_10	12702675	In a genome-wide screen of  4700 viable deletion strains, 13 were classified as resistant to fluconazole ( ERG3,  ERG6,  YMR102C,  YMR099C,  YPL056C,  ERG28,  OSH1,  SCS2,  CKA2,  SML1,  YBR147W,  YGR283C, and  YLR407W).	gene_phenotype
68357	12	333293	7	NULL	NULL	0	NULL	YGR283C	GP		is resistant to					fluconazole	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_163_4_1287_s_10	12702675	In a genome-wide screen of  4700 viable deletion strains, 13 were classified as resistant to fluconazole ( ERG3,  ERG6,  YMR102C,  YMR099C,  YPL056C,  ERG28,  OSH1,  SCS2,  CKA2,  SML1,  YBR147W,  YGR283C, and  YLR407W).	gene_phenotype
68358	13	333293	7	NULL	NULL	0	NULL	YLR407W	GP		is resistant to					fluconazole	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_163_4_1287_s_10	12702675	In a genome-wide screen of  4700 viable deletion strains, 13 were classified as resistant to fluconazole ( ERG3,  ERG6,  YMR102C,  YMR099C,  YPL056C,  ERG28,  OSH1,  SCS2,  CKA2,  SML1,  YBR147W,  YGR283C, and  YLR407W).	gene_phenotype
68412	1	333297	7	NULL	NULL	0	NULL	methylglyoxal	Chemical	reducing activity of	depends on					NADPH	Chemical				NULL	Cells	0	NULL	NULL	NULL	gw70_yeast_20_6_545_s_221	12722185	NADPH-dependent methylglyoxal-reducing activity in cells containing GST fusions to  the indicated ORFs (strain 1, YOL151w; strain 2, YDR541c; strain 3, YGL039w; strain  4, YGL157w; strain 5, YNL241c).	gene_phenotype
68359	1	333298	7	NULL	NULL	0	NULL	Yol082p 	GP		is not required for					vegetative growth	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_31_29210_s_88	11382752	The null mutant of  YOL082w, which as described was viable ( 20), showed wild-type growth rate in SD medium with a doubling time of 150 min for both wild-type and  deltayol082 strains, indicating that Yol082p function is not required for vegetative growth.	gene_phenotype
68360	1	333300	7	NULL	NULL	0	NULL	PHO85 YPL031c Cyclin-dependent protein kinase	GP		is involved in					phosphate metabolism	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_317	15334557	PHO85   YPL031c Cyclin-dependent protein kinase; involved in phosphate and glycogen metabolism as  well as cell cycle progression	gene_phenotype
68361	2	333300	7	NULL	NULL	0	NULL	PHO85 YPL031c Cyclin-dependent protein kinase	GP		is involved in					glycogen metabolism	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_317	15334557	PHO85   YPL031c Cyclin-dependent protein kinase; involved in phosphate and glycogen metabolism as  well as cell cycle progression	gene_phenotype
68362	3	333300	7	NULL	NULL	0	NULL	PHO85 YPL031c Cyclin-dependent protein kinase	GP		is involved in					cell cycle progression	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_317	15334557	PHO85   YPL031c Cyclin-dependent protein kinase; involved in phosphate and glycogen metabolism as  well as cell cycle progression	gene_phenotype
68363	1	333301	7	NULL	NULL	NULL	NULL	Kap95	GP		imports					NLS protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68364	2	333301	7	NULL	NULL	NULL	NULL	Kap beta1	GP		imports					NLS protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68365	3	333301	7	NULL	NULL	0	NULL	Kap alpha	GP		helps					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68366	4	333301	7	NULL	NULL	0	NULL	Kap alpha	GP		helps					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68367	5	333301	7	NULL	NULL	0	NULL	Kap alpha	GP		complex with					Kap104	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68368	6	333301	7	NULL	NULL	0	NULL	statement 5	GP		complex with					Kap beta2	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68369	7	333301	7	NULL	NULL	0	NULL	statement 6	GP		imports					PSE1, Kap121	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68370	8	333301	7	NULL	NULL	0	NULL	statement 6	GP		imports					Kap beta3	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68371	9	333301	7	NULL	NULL	0	NULL	statement 6	GP		imports					Kap123	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68372	10	333301	7	NULL	NULL	0	NULL	statement 6	GP		imports					Kap108	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68373	11	333301	7	NULL	NULL	NULL	NULL	statement 6	GP		imports					Kap111	GP				NULL		NULL	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68374	12	333301	7	NULL	NULL	0	NULL	statement 6	GP		imports					mRNA-binding proteins	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68375	13	333301	7	NULL	NULL	0	NULL	statement 6	GP		exports		possibly			mRNA-binding proteins	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68376	14	333301	7	NULL	NULL	0	NULL	CSE1 CAS	GP		exports					 karyopherin alpha	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68377	15	333301	7	NULL	NULL	0	NULL	LOS1	GP		transports		possibly			tRNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68378	16	333301	7	NULL	NULL	0	NULL	XPO1 exportin	GP		exports					PDR6	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68379	17	333301	7	NULL	NULL	0	NULL	Kap alpha	GP		is					Karyopherin alpha Importin alpha	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68380	18	333301	7	NULL	NULL	0	NULL	Kap95	GP		is					Karyopherin beta1	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68381	19	333301	7	NULL	NULL	0	NULL	Kap beta1	GP		is					 Importin beta	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68382	20	333301	7	NULL	NULL	0	NULL	Kap95	GP		is a type of					import protein	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68383	21	333301	7	NULL	NULL	0	NULL	Kap beta1	GP		is a type of					import protein	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68384	22	333301	7	NULL	NULL	0	NULL	Kap104	GP		is					Karyopherin beta2	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68385	23	333301	7	NULL	NULL	0	NULL	Kap beta2	GP		is					transportin	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68386	24	333301	7	NULL	NULL	0	NULL	PSE1, Kap121	GP		is					hnRNPA1 Karyopherin beta3	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68387	25	333301	7	NULL	NULL	0	NULL	PSE1, Kap121	GP		is a type of					mRNA-binding proteins	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68388	26	333301	7	NULL	NULL	0	NULL	Kap123	GP		is					Karyopherin beta4	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68389	27	333301	7	NULL	NULL	0	NULL	Kap108	GP		is					SXM1	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68390	28	333301	7	NULL	NULL	0	NULL	Kap108	GP		is a type of					ribosomal protein	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68391	29	333301	7	NULL	NULL	0	NULL	Kap111	GP		is					MTR10	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68392	30	333301	7	NULL	NULL	0	NULL	PDR6	GP		contains					leucine-rich export sequences 	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68393	31	333301	7	NULL	NULL	0	NULL	PDR6 	GP		belongs to					karyopherin b4 family	GP				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68396	32	333301	7	NULL	NULL	0	NULL	KAP111	GP		is involved in					tRNA	NucleicAcid	processing			NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68397	33	333301	7	NULL	NULL	0	NULL	KAp111	GP		is involved in					mRNA	NucleicAcid	processing			NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1129_s_45	9508684	THE WORLD OF NUCLEAR TRANSPORTERS  Yeast Protein Homologs Function  Karyopherin alpha Importin  alpha (Kap  alpha) Helps import proteins with NLS sequences  Karyopherin beta1 (Kap95) Importin beta (Kap beta1) Imports NLS proteins, complexed with karyopherin  alpha (importin alpha)  Karyopherin beta2  (Kap104) transportin  (Kap beta2) Imports mRNA-binding proteins, such as hnRNPA1  Karyopherin beta3 (PSE1, Kap121) Kap beta3 Imports ribosomal proteins  Karyopherin beta4 (Kap123)   Imports ribosomal proteins  *SXM1  (Kap108)   Imports proteins involved in  processing tRNA and possibly mRNA  *MTR10  (Kap111)   Imports and possibly exports  mRNA-binding proteins  *CSE1 CAS Exports karyopherin  alpha  (importin  alpha)  *NMD5 Ran BP7,  [[ Ran BP8 Unknown  *LOS1   Possibly transports tRNA  *MSN5   Unknown  *CRM1 ]], XPO1  (Kap124) Exportin Exports proteins with leucine-rich export sequences  *PDR6   [[ Unknown  *YGL241W   Unknown  *YPL125W   Unknown  * Members ]] of the karyopherin b4 family	gene_phenotype
68398	1	333302	7	NULL	NULL	0	NULL	isw2delta	GP	mutation of	enhance		slightly			telomere-silencing defect					NULL	dpb4delta mutant cells	0	NULL	NULL	NULL	gw70_molcellbiol_24_1_217_s_180	14673157	On the other hand, the  isw2delta mutation slightly enhanced the telomere-silencing defect in  dpb4delta mutant cells, suggesting that the Isw2 protein solely, not as a complex, or a putative complex of Isw2 with the other WAC domain protein ( ), such as a product from YPL216w, plays a putative positive role in TPE.	gene_phenotype
68399	2	333302	7	NULL	NULL	NULL	NULL	Isw2 protein	GP		complex with		putatively			YPL216w	GP	product of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_1_217_s_180	14673157	On the other hand, the  isw2delta mutation slightly enhanced the telomere-silencing defect in  dpb4delta mutant cells, suggesting that the Isw2 protein solely, not as a complex, or a putative complex of Isw2 with the other WAC domain protein ( ), such as a product from YPL216w, plays a putative positive role in TPE.	gene_phenotype
68400	3	333302	7	NULL	NULL	0	NULL	YPL216w	GP	product of	is a type of					WAC domain protein	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_1_217_s_180	14673157	On the other hand, the  isw2delta mutation slightly enhanced the telomere-silencing defect in  dpb4delta mutant cells, suggesting that the Isw2 protein solely, not as a complex, or a putative complex of Isw2 with the other WAC domain protein ( ), such as a product from YPL216w, plays a putative positive role in TPE.	gene_phenotype
68401	4	333302	7	NULL	NULL	NULL	NULL	YPL216w	GP	product of	positive role in		putative			TPE	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_1_217_s_180	14673157	On the other hand, the  isw2delta mutation slightly enhanced the telomere-silencing defect in  dpb4delta mutant cells, suggesting that the Isw2 protein solely, not as a complex, or a putative complex of Isw2 with the other WAC domain protein ( ), such as a product from YPL216w, plays a putative positive role in TPE.	gene_phenotype
68402	5	333302	7	NULL	NULL	NULL	NULL	Isw2 protein	GP		positive role in		putative			TPE	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_1_217_s_180	14673157	On the other hand, the  isw2delta mutation slightly enhanced the telomere-silencing defect in  dpb4delta mutant cells, suggesting that the Isw2 protein solely, not as a complex, or a putative complex of Isw2 with the other WAC domain protein ( ), such as a product from YPL216w, plays a putative positive role in TPE.	gene_phenotype
68413	1	333303	7	NULL	NULL	0	NULL	 VMA11	GP		encode					 vacuolar ATPase	GP		proteolipid subunit of 		NULL		0	NULL	NULL	NULL	gw60_genetics_161_2_585_s_169	12072456	One is the unknown ORF YPL233w; two are known genes:  VMA11 encodes a proteolipid subunit of the vacuolar ATPase, an H[+]-translocating ATPase that hydrolyzes ATP to ADP and Pi, to drive protons across the vacuolar membrane into the lumen ( H IRATA et al. 1997   ), while  SSO1 encodes a syntaxin homolog (t-SNARE) involved in vesicle transport between the Golgi apparatus and the plasma membrane.	gene_phenotype
68414	2	333303	7	NULL	NULL	0	NULL	 vacuolar ATPase	GP		is a type of					H[+]-translocating ATPase	GP				NULL		0	NULL	NULL	NULL	gw60_genetics_161_2_585_s_169	12072456	One is the unknown ORF YPL233w; two are known genes:  VMA11 encodes a proteolipid subunit of the vacuolar ATPase, an H[+]-translocating ATPase that hydrolyzes ATP to ADP and Pi, to drive protons across the vacuolar membrane into the lumen ( H IRATA et al. 1997   ), while  SSO1 encodes a syntaxin homolog (t-SNARE) involved in vesicle transport between the Golgi apparatus and the plasma membrane.	gene_phenotype
68415	3	333303	7	NULL	NULL	0	NULL	ATP	Chemical		hydrolyzed to					ADP	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_161_2_585_s_169	12072456	One is the unknown ORF YPL233w; two are known genes:  VMA11 encodes a proteolipid subunit of the vacuolar ATPase, an H[+]-translocating ATPase that hydrolyzes ATP to ADP and Pi, to drive protons across the vacuolar membrane into the lumen ( H IRATA et al. 1997   ), while  SSO1 encodes a syntaxin homolog (t-SNARE) involved in vesicle transport between the Golgi apparatus and the plasma membrane.	gene_phenotype
68416	4	333303	7	NULL	NULL	0	NULL	ATP	Chemical		hydrolyzed to					Pi	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_161_2_585_s_169	12072456	One is the unknown ORF YPL233w; two are known genes:  VMA11 encodes a proteolipid subunit of the vacuolar ATPase, an H[+]-translocating ATPase that hydrolyzes ATP to ADP and Pi, to drive protons across the vacuolar membrane into the lumen ( H IRATA et al. 1997   ), while  SSO1 encodes a syntaxin homolog (t-SNARE) involved in vesicle transport between the Golgi apparatus and the plasma membrane.	gene_phenotype
68417	5	333303	7	NULL	NULL	0	NULL	statement 3	Process		occur along with					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_161_2_585_s_169	12072456	One is the unknown ORF YPL233w; two are known genes:  VMA11 encodes a proteolipid subunit of the vacuolar ATPase, an H[+]-translocating ATPase that hydrolyzes ATP to ADP and Pi, to drive protons across the vacuolar membrane into the lumen ( H IRATA et al. 1997   ), while  SSO1 encodes a syntaxin homolog (t-SNARE) involved in vesicle transport between the Golgi apparatus and the plasma membrane.	gene_phenotype
68418	6	333303	7	NULL	NULL	0	NULL	vacuolar ATPase	GP		catalyze					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_161_2_585_s_169	12072456	One is the unknown ORF YPL233w; two are known genes:  VMA11 encodes a proteolipid subunit of the vacuolar ATPase, an H[+]-translocating ATPase that hydrolyzes ATP to ADP and Pi, to drive protons across the vacuolar membrane into the lumen ( H IRATA et al. 1997   ), while  SSO1 encodes a syntaxin homolog (t-SNARE) involved in vesicle transport between the Golgi apparatus and the plasma membrane.	gene_phenotype
68419	7	333303	7	NULL	NULL	0	NULL	protons	Chemical		move from					vacuolar membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw60_genetics_161_2_585_s_169	12072456	One is the unknown ORF YPL233w; two are known genes:  VMA11 encodes a proteolipid subunit of the vacuolar ATPase, an H[+]-translocating ATPase that hydrolyzes ATP to ADP and Pi, to drive protons across the vacuolar membrane into the lumen ( H IRATA et al. 1997   ), while  SSO1 encodes a syntaxin homolog (t-SNARE) involved in vesicle transport between the Golgi apparatus and the plasma membrane.	gene_phenotype
68420	8	333303	7	NULL	NULL	0	NULL	protons	Chemical		move to					lumen	CellComponent				NULL		0	NULL	NULL	NULL	gw60_genetics_161_2_585_s_169	12072456	One is the unknown ORF YPL233w; two are known genes:  VMA11 encodes a proteolipid subunit of the vacuolar ATPase, an H[+]-translocating ATPase that hydrolyzes ATP to ADP and Pi, to drive protons across the vacuolar membrane into the lumen ( H IRATA et al. 1997   ), while  SSO1 encodes a syntaxin homolog (t-SNARE) involved in vesicle transport between the Golgi apparatus and the plasma membrane.	gene_phenotype
68421	9	333303	7	NULL	NULL	0	NULL	statement 7	Process		occur along with					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_161_2_585_s_169	12072456	One is the unknown ORF YPL233w; two are known genes:  VMA11 encodes a proteolipid subunit of the vacuolar ATPase, an H[+]-translocating ATPase that hydrolyzes ATP to ADP and Pi, to drive protons across the vacuolar membrane into the lumen ( H IRATA et al. 1997   ), while  SSO1 encodes a syntaxin homolog (t-SNARE) involved in vesicle transport between the Golgi apparatus and the plasma membrane.	gene_phenotype
68422	10	333303	7	NULL	NULL	0	NULL	statement 5	Process		drives					statement 9	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_161_2_585_s_169	12072456	One is the unknown ORF YPL233w; two are known genes:  VMA11 encodes a proteolipid subunit of the vacuolar ATPase, an H[+]-translocating ATPase that hydrolyzes ATP to ADP and Pi, to drive protons across the vacuolar membrane into the lumen ( H IRATA et al. 1997   ), while  SSO1 encodes a syntaxin homolog (t-SNARE) involved in vesicle transport between the Golgi apparatus and the plasma membrane.	gene_phenotype
68423	11	333303	7	NULL	NULL	0	NULL	 SSO1	GP		encode					 syntaxin homolog 	GP				NULL		0	NULL	NULL	NULL	gw60_genetics_161_2_585_s_169	12072456	One is the unknown ORF YPL233w; two are known genes:  VMA11 encodes a proteolipid subunit of the vacuolar ATPase, an H[+]-translocating ATPase that hydrolyzes ATP to ADP and Pi, to drive protons across the vacuolar membrane into the lumen ( H IRATA et al. 1997   ), while  SSO1 encodes a syntaxin homolog (t-SNARE) involved in vesicle transport between the Golgi apparatus and the plasma membrane.	gene_phenotype
68424	12	333303	7	NULL	NULL	0	NULL	 syntaxin homolog 	GP		is					t-SNARE	GP				NULL		0	NULL	NULL	NULL	gw60_genetics_161_2_585_s_169	12072456	One is the unknown ORF YPL233w; two are known genes:  VMA11 encodes a proteolipid subunit of the vacuolar ATPase, an H[+]-translocating ATPase that hydrolyzes ATP to ADP and Pi, to drive protons across the vacuolar membrane into the lumen ( H IRATA et al. 1997   ), while  SSO1 encodes a syntaxin homolog (t-SNARE) involved in vesicle transport between the Golgi apparatus and the plasma membrane.	gene_phenotype
68425	13	333303	7	NULL	NULL	0	NULL	vesicle	CellComponent		transported between					golgi apparatus	CellComponent				NULL		0	NULL	NULL	NULL	gw60_genetics_161_2_585_s_169	12072456	One is the unknown ORF YPL233w; two are known genes:  VMA11 encodes a proteolipid subunit of the vacuolar ATPase, an H[+]-translocating ATPase that hydrolyzes ATP to ADP and Pi, to drive protons across the vacuolar membrane into the lumen ( H IRATA et al. 1997   ), while  SSO1 encodes a syntaxin homolog (t-SNARE) involved in vesicle transport between the Golgi apparatus and the plasma membrane.	gene_phenotype
68426	14	333303	7	NULL	NULL	0	NULL	vesicle	CellComponent		transported between					plasma membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw60_genetics_161_2_585_s_169	12072456	One is the unknown ORF YPL233w; two are known genes:  VMA11 encodes a proteolipid subunit of the vacuolar ATPase, an H[+]-translocating ATPase that hydrolyzes ATP to ADP and Pi, to drive protons across the vacuolar membrane into the lumen ( H IRATA et al. 1997   ), while  SSO1 encodes a syntaxin homolog (t-SNARE) involved in vesicle transport between the Golgi apparatus and the plasma membrane.	gene_phenotype
68427	15	333303	7	NULL	NULL	0	NULL	statement 13	Process		occur along with					statement 14	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_161_2_585_s_169	12072456	One is the unknown ORF YPL233w; two are known genes:  VMA11 encodes a proteolipid subunit of the vacuolar ATPase, an H[+]-translocating ATPase that hydrolyzes ATP to ADP and Pi, to drive protons across the vacuolar membrane into the lumen ( H IRATA et al. 1997   ), while  SSO1 encodes a syntaxin homolog (t-SNARE) involved in vesicle transport between the Golgi apparatus and the plasma membrane.	gene_phenotype
68428	16	333303	7	NULL	NULL	0	NULL	t-SNARE	GP		is involved in					statement 15	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_161_2_585_s_169	12072456	One is the unknown ORF YPL233w; two are known genes:  VMA11 encodes a proteolipid subunit of the vacuolar ATPase, an H[+]-translocating ATPase that hydrolyzes ATP to ADP and Pi, to drive protons across the vacuolar membrane into the lumen ( H IRATA et al. 1997   ), while  SSO1 encodes a syntaxin homolog (t-SNARE) involved in vesicle transport between the Golgi apparatus and the plasma membrane.	gene_phenotype
68429	1	333304	7	NULL	NULL	0	NULL	 Sps2	GP		is homologous to					Ecm33	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_9_781_s_165	12845604	Finally, YPL261c and Sps2 (a protein with homology to GPI protein Ecm33), which  were also identified in their screen for GPI proteins, were excluded from our GPI  protein list because their N-terminal regions are unlikely to be signal peptides  for secretion.	gene_phenotype
68430	2	333304	7	NULL	NULL	0	NULL	Ecm33	GP		is a type of					GPI protein	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_9_781_s_165	12845604	Finally, YPL261c and Sps2 (a protein with homology to GPI protein Ecm33), which  were also identified in their screen for GPI proteins, were excluded from our GPI  protein list because their N-terminal regions are unlikely to be signal peptides  for secretion.	gene_phenotype
68431	4	333304	7	NULL	NULL	NULL	NULL	 YPL261c	GP		does not have					signal peptides	GP		N-terminal regions		NULL		NULL	NULL	NULL	NULL	gw70_yeast_20_9_781_s_165	12845604	Finally, YPL261c and Sps2 (a protein with homology to GPI protein Ecm33), which  were also identified in their screen for GPI proteins, were excluded from our GPI  protein list because their N-terminal regions are unlikely to be signal peptides  for secretion.	gene_phenotype
68432	4	333304	7	NULL	NULL	NULL	NULL	Sps2	GP		does not have					signal peptides	GP		N-terminal residues		NULL		NULL	NULL	NULL	NULL	gw70_yeast_20_9_781_s_165	12845604	Finally, YPL261c and Sps2 (a protein with homology to GPI protein Ecm33), which  were also identified in their screen for GPI proteins, were excluded from our GPI  protein list because their N-terminal regions are unlikely to be signal peptides  for secretion.	gene_phenotype
68433	3	333304	7	NULL	NULL	NULL	NULL	signal peptides	GP		required for					secretion	Process				NULL		NULL	NULL	NULL	NULL	gw70_yeast_20_9_781_s_165	12845604	Finally, YPL261c and Sps2 (a protein with homology to GPI protein Ecm33), which  were also identified in their screen for GPI proteins, were excluded from our GPI  protein list because their N-terminal regions are unlikely to be signal peptides  for secretion.	gene_phenotype
68434	1	333306	7	NULL	NULL	0	NULL	mde7 	GP		induced during					meiosis	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_157_4_1469_s_146	11290704	These include an  S. cerevisiae gene we have named  WHI4 (YDL224c, see below) and two genes from  S. pombe, named SPCC16C4.07 (about which nothing is known) and  mde7 (induced during meiosis in a  mei4-dependent fashion,   A BE and SHIMODA 2000   ; PombePD, Proteome;	gene_phenotype
68435	2	333306	7	NULL	NULL	0	NULL	statement 1	Process		depends on					mei4	GP				NULL		0	NULL	NULL	NULL	gw60_genetics_157_4_1469_s_146	11290704	These include an  S. cerevisiae gene we have named  WHI4 (YDL224c, see below) and two genes from  S. pombe, named SPCC16C4.07 (about which nothing is known) and  mde7 (induced during meiosis in a  mei4-dependent fashion,   A BE and SHIMODA 2000   ; PombePD, Proteome;	gene_phenotype
68436	1	333307	7	NULL	NULL	0	NULL	YDR260c	GP		encode					protein	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2118_s_99	10022899	These results thus suggested that the lack of the protein encoded by  YDR260c was responsible for the sporulation defect initially attributed by us to the  exg2 mutation.	gene_phenotype
68437	2	333307	7	NULL	NULL	NULL	NULL	statement 1	GP	lack of	is responsible for					sporulation defect	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2118_s_99	10022899	These results thus suggested that the lack of the protein encoded by  YDR260c was responsible for the sporulation defect initially attributed by us to the  exg2 mutation.	gene_phenotype
68438	1	333308	7	NULL	NULL	0	NULL	plasmid pJC5	NucleicAcid		carry					EXG2 gene	GP	full-length			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2118_s_98	10022899	Our results indicated that plasmid pJC5, carrying the full-length  EXG2 gene, was unable to complement the sporulation defect, while plasmids pRN30 (carrying  YDR260c and part of the 3' end of the  EXG2 coding sequence) and pPS47 (carrying only  YDR260c) restored the ability to form spores in the homozygous diploid mutant strain (Fig.  1).	gene_phenotype
68439	2	333308	7	NULL	NULL	0	NULL	statement 1	Process		unable to complement					sporulation defect	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2118_s_98	10022899	Our results indicated that plasmid pJC5, carrying the full-length  EXG2 gene, was unable to complement the sporulation defect, while plasmids pRN30 (carrying  YDR260c and part of the 3' end of the  EXG2 coding sequence) and pPS47 (carrying only  YDR260c) restored the ability to form spores in the homozygous diploid mutant strain (Fig.  1).	gene_phenotype
68440	3	333308	7	NULL	NULL	0	NULL	plasmids pRN30	NucleicAcid		carry					YDR260c	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2118_s_98	10022899	Our results indicated that plasmid pJC5, carrying the full-length  EXG2 gene, was unable to complement the sporulation defect, while plasmids pRN30 (carrying  YDR260c and part of the 3' end of the  EXG2 coding sequence) and pPS47 (carrying only  YDR260c) restored the ability to form spores in the homozygous diploid mutant strain (Fig.  1).	gene_phenotype
68441	4	333308	7	NULL	NULL	0	NULL	plasmids pRN30	NucleicAcid		carry					EXG2	GP		 part of the 3' end of coding sequence		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2118_s_98	10022899	Our results indicated that plasmid pJC5, carrying the full-length  EXG2 gene, was unable to complement the sporulation defect, while plasmids pRN30 (carrying  YDR260c and part of the 3' end of the  EXG2 coding sequence) and pPS47 (carrying only  YDR260c) restored the ability to form spores in the homozygous diploid mutant strain (Fig.  1).	gene_phenotype
68442	5	333308	7	NULL	NULL	0	NULL	statement 3	Process		occur along with					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2118_s_98	10022899	Our results indicated that plasmid pJC5, carrying the full-length  EXG2 gene, was unable to complement the sporulation defect, while plasmids pRN30 (carrying  YDR260c and part of the 3' end of the  EXG2 coding sequence) and pPS47 (carrying only  YDR260c) restored the ability to form spores in the homozygous diploid mutant strain (Fig.  1).	gene_phenotype
68443	6	333308	7	NULL	NULL	0	NULL	statement 5	Process		restore					spores	OrganismPart	ability to form			NULL	homozygous diploid mutant strain	0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2118_s_98	10022899	Our results indicated that plasmid pJC5, carrying the full-length  EXG2 gene, was unable to complement the sporulation defect, while plasmids pRN30 (carrying  YDR260c and part of the 3' end of the  EXG2 coding sequence) and pPS47 (carrying only  YDR260c) restored the ability to form spores in the homozygous diploid mutant strain (Fig.  1).	gene_phenotype
68444	7	333308	7	NULL	NULL	0	NULL	pPS47	NucleicAcid		carry					YDR260c	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_3_2118_s_98	10022899	Our results indicated that plasmid pJC5, carrying the full-length  EXG2 gene, was unable to complement the sporulation defect, while plasmids pRN30 (carrying  YDR260c and part of the 3' end of the  EXG2 coding sequence) and pPS47 (carrying only  YDR260c) restored the ability to form spores in the homozygous diploid mutant strain (Fig.  1).	gene_phenotype
68445	8	333308	7	NULL	NULL	NULL	NULL	statement 7	GP		restore					spores	OrganismPart	ability to form			NULL	homozygous diploid mutant strain	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_3_2118_s_98	10022899	Our results indicated that plasmid pJC5, carrying the full-length  EXG2 gene, was unable to complement the sporulation defect, while plasmids pRN30 (carrying  YDR260c and part of the 3' end of the  EXG2 coding sequence) and pPS47 (carrying only  YDR260c) restored the ability to form spores in the homozygous diploid mutant strain (Fig.  1).	gene_phenotype
68446	1	333310	7	NULL	NULL	0	NULL	 YER048w-a	GP	open reading frame	is					ISD11	GP				NULL		0	NULL	NULL	NULL	gw70_embo_25_1_184_s_32	16341089	The open reading frame YER048w-a, now termed  ISD11, was found to be essential for cell viability in a sporulation approach and code  for an 11 kDa protein with mitochondrial localization (  et al;   et al).	gene_phenotype
68447	2	333310	7	NULL	NULL	0	NULL	statement 1	Process		is essential for					cell viability	Process				NULL		0	NULL	NULL	NULL	gw70_embo_25_1_184_s_32	16341089	The open reading frame YER048w-a, now termed  ISD11, was found to be essential for cell viability in a sporulation approach and code  for an 11 kDa protein with mitochondrial localization (  et al;   et al).	gene_phenotype
68448	3	333310	7	NULL	NULL	0	NULL	statement 2	Process		occur in a					sporulation approach	Process				NULL		0	NULL	NULL	NULL	gw70_embo_25_1_184_s_32	16341089	The open reading frame YER048w-a, now termed  ISD11, was found to be essential for cell viability in a sporulation approach and code  for an 11 kDa protein with mitochondrial localization (  et al;   et al).	gene_phenotype
68449	1	333311	7	NULL	NULL	0	NULL	ORF YER048w-a	GP	S. cerevisiae	essential for					viability	Process				NULL		0	NULL	NULL	NULL	gw70_embo_25_1_174_s_32	16341090	The ORF YER048w-a of  S. cerevisiae was reported to be essential for viability and encodes a mitochondrial protein with  a molecular mass of 11 kDa, further onwards referred to as Isd11 (ISC biogenesis  desulfurase interacting protein).	gene_phenotype
68450	2	333311	7	NULL	NULL	0	NULL	ORF YER048w-a	GP	S. cerevisiae	encode					Isd11 	GP				NULL		0	NULL	NULL	NULL	gw70_embo_25_1_174_s_32	16341090	The ORF YER048w-a of  S. cerevisiae was reported to be essential for viability and encodes a mitochondrial protein with  a molecular mass of 11 kDa, further onwards referred to as Isd11 (ISC biogenesis  desulfurase interacting protein).	gene_phenotype
68451	3	333311	7	NULL	NULL	0	NULL	Isd11 	GP		is a type of					mitochondrial protein	GP				NULL		0	NULL	NULL	NULL	gw70_embo_25_1_174_s_32	16341090	The ORF YER048w-a of  S. cerevisiae was reported to be essential for viability and encodes a mitochondrial protein with  a molecular mass of 11 kDa, further onwards referred to as Isd11 (ISC biogenesis  desulfurase interacting protein).	gene_phenotype
68452	4	333311	7	NULL	NULL	0	NULL	Isd11 	GP		is 					ISC biogenesis desulfurase interacting protein	GP				NULL		0	NULL	NULL	NULL	gw70_embo_25_1_174_s_32	16341090	The ORF YER048w-a of  S. cerevisiae was reported to be essential for viability and encodes a mitochondrial protein with  a molecular mass of 11 kDa, further onwards referred to as Isd11 (ISC biogenesis  desulfurase interacting protein).	gene_phenotype
68453	1	333312	7	NULL	NULL	0	NULL	 isd11-deletion strain	GP		derived from					YPH499	Organism				NULL		0	NULL	NULL	NULL	gw70_embo_25_1_184_s_275	16341089	An  isd11-deletion strain (derived from YPH499) carrying a  URA3-plasmid with the  ISD11 (Yer048w-a FOMP6/EDI1) open reading frame was viable like yeast wild-type cells but was unable to grow  on 5-fluoroorotic acid, that is, the plasmid loss approach did not lead to a viable   isd11-deletion strain.	gene_phenotype
68454	2	333312	7	NULL	NULL	0	NULL	isd11-deletion strain	GP		carry					URA3-plasmid	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_embo_25_1_184_s_275	16341089	An  isd11-deletion strain (derived from YPH499) carrying a  URA3-plasmid with the  ISD11 (Yer048w-a FOMP6/EDI1) open reading frame was viable like yeast wild-type cells but was unable to grow  on 5-fluoroorotic acid, that is, the plasmid loss approach did not lead to a viable   isd11-deletion strain.	gene_phenotype
68455	3	333312	7	NULL	NULL	0	NULL	URA3-plasmid	NucleicAcid		carry					ISD11	GP	open reading frame			NULL		0	NULL	NULL	NULL	gw70_embo_25_1_184_s_275	16341089	An  isd11-deletion strain (derived from YPH499) carrying a  URA3-plasmid with the  ISD11 (Yer048w-a FOMP6/EDI1) open reading frame was viable like yeast wild-type cells but was unable to grow  on 5-fluoroorotic acid, that is, the plasmid loss approach did not lead to a viable   isd11-deletion strain.	gene_phenotype
68456	4	333312	7	NULL	NULL	NULL	NULL	statement 3	Process	viability of	is similar to					wild-type cells	Cell	yeast			NULL		NULL	NULL	NULL	NULL	gw70_embo_25_1_184_s_275	16341089	An  isd11-deletion strain (derived from YPH499) carrying a  URA3-plasmid with the  ISD11 (Yer048w-a FOMP6/EDI1) open reading frame was viable like yeast wild-type cells but was unable to grow  on 5-fluoroorotic acid, that is, the plasmid loss approach did not lead to a viable   isd11-deletion strain.	gene_phenotype
68458	5	333312	7	NULL	NULL	NULL	NULL	statement 4	Process		unable to grow on					5-fluoroorotic acid	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_embo_25_1_184_s_275	16341089	An  isd11-deletion strain (derived from YPH499) carrying a  URA3-plasmid with the  ISD11 (Yer048w-a FOMP6/EDI1) open reading frame was viable like yeast wild-type cells but was unable to grow  on 5-fluoroorotic acid, that is, the plasmid loss approach did not lead to a viable   isd11-deletion strain.	gene_phenotype
68459	1	333314	7	NULL	NULL	0	NULL	BUD27	GP		possess					random budding patterns	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_163_3_875_s_167	12663529	Two of these genes,  BUD27 (YFL023W) and  BUD30 (YDL151C), have random budding patterns when mutated ( N I and SNYDER 2001   ), and both are hypersensitive to killer toxin.	gene_phenotype
68460	2	333314	7	NULL	NULL	0	NULL	BUD30	GP		possess					random budding patterns	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_163_3_875_s_167	12663529	Two of these genes,  BUD27 (YFL023W) and  BUD30 (YDL151C), have random budding patterns when mutated ( N I and SNYDER 2001   ), and both are hypersensitive to killer toxin.	gene_phenotype
68461	3	333314	7	NULL	NULL	0	NULL	statement 1	Process		occur upon					mutation	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_163_3_875_s_167	12663529	Two of these genes,  BUD27 (YFL023W) and  BUD30 (YDL151C), have random budding patterns when mutated ( N I and SNYDER 2001   ), and both are hypersensitive to killer toxin.	gene_phenotype
68462	4	333314	7	NULL	NULL	0	NULL	statement 2	Process		occur upon					mutation	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_163_3_875_s_167	12663529	Two of these genes,  BUD27 (YFL023W) and  BUD30 (YDL151C), have random budding patterns when mutated ( N I and SNYDER 2001   ), and both are hypersensitive to killer toxin.	gene_phenotype
68463	5	333314	7	NULL	NULL	0	NULL	BUD27	GP		is hypersensitive to					killer toxin	GP				NULL		0	NULL	NULL	NULL	gw60_genetics_163_3_875_s_167	12663529	Two of these genes,  BUD27 (YFL023W) and  BUD30 (YDL151C), have random budding patterns when mutated ( N I and SNYDER 2001   ), and both are hypersensitive to killer toxin.	gene_phenotype
68464	6	333314	7	NULL	NULL	0	NULL	BUD30	GP		is hypersensitive to					killer toxin	GP				NULL		0	NULL	NULL	NULL	gw60_genetics_163_3_875_s_167	12663529	Two of these genes,  BUD27 (YFL023W) and  BUD30 (YDL151C), have random budding patterns when mutated ( N I and SNYDER 2001   ), and both are hypersensitive to killer toxin.	gene_phenotype
68465	2	333315	7	NULL	NULL	NULL	NULL	Brp1	GP		bind					statement 1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_24267_s_99	15855155	On the other hand, neither Brp1 ( i.e. YGL007W, an open reading frame of unknown function) or Fes1p, a protein that binds to a complex involved in the regulation of protein translation, has any documented role in transport function ( ,  ,  ,  ).	gene_phenotype
68466	1	333315	7	NULL	NULL	NULL	NULL	complex	GP		involved in					protein translation	Process	regulation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_24267_s_99	15855155	On the other hand, neither Brp1 ( i.e. YGL007W, an open reading frame of unknown function) or Fes1p, a protein that binds to a complex involved in the regulation of protein translation, has any documented role in transport function ( ,  ,  ,  ).	gene_phenotype
68467	3	333315	7	NULL	NULL	0	NULL	Fes1p	GP		bind					statement 1	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_25_24267_s_99	15855155	On the other hand, neither Brp1 ( i.e. YGL007W, an open reading frame of unknown function) or Fes1p, a protein that binds to a complex involved in the regulation of protein translation, has any documented role in transport function ( ,  ,  ,  ).	gene_phenotype
68468	1	333316	7	NULL	NULL	0	NULL	FYV4 YHR059w	GP		is required for					viability	Process	yeast			NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_306	15334557	FYV4   YHR059w Required for yeast viability on toxin exposure	gene_phenotype
68469	2	333316	7	NULL	NULL	0	NULL	statement 1	Process		occur upon					toxin	GP	exposure to			NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_306	15334557	FYV4   YHR059w Required for yeast viability on toxin exposure	gene_phenotype
68470	1	333317	7	NULL	NULL	0	NULL	YKL195w/ FMP15	GP		encode					MIA40	GP				NULL		0	NULL	NULL	NULL	gw70_embo_23_19_3735_s_277	15359280	Conditional mutants of  MIA40 (encoded by YKL195w/ FMP15) were generated by error-prone PCR and isolated by screening for a temperature-sensitive  growth phenotype according to the procedure described in   et al.	gene_phenotype
68471	1	333318	7	NULL	NULL	NULL	NULL	YGL068W	GP	deletion of	results in					cell cycle	Process	arrest of specific phase of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_7_3946_s_158	11274415	Of the 36 hypothetical ORFs identified in our screen, deletion of three of them ( YGL068W,  YPL063W,  YKL195W) resulted in arrest in a specific phase of the cell cycle, reflecting a role for these gene products in cell cycle progression.	gene_phenotype
68472	2	333318	7	NULL	NULL	NULL	NULL	 YPL063W	GP	deletion of	results in					cell cycle	Process	arrest of specific phase of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_7_3946_s_158	11274415	Of the 36 hypothetical ORFs identified in our screen, deletion of three of them ( YGL068W,  YPL063W,  YKL195W) resulted in arrest in a specific phase of the cell cycle, reflecting a role for these gene products in cell cycle progression.	gene_phenotype
68473	3	333318	7	NULL	NULL	0	NULL	YKL195W	GP	deletion of	results in					cell cycle	Process	arrest of specific phase of			NULL		0	NULL	NULL	NULL	gw60_pnas_98_7_3946_s_158	11274415	Of the 36 hypothetical ORFs identified in our screen, deletion of three of them ( YGL068W,  YPL063W,  YKL195W) resulted in arrest in a specific phase of the cell cycle, reflecting a role for these gene products in cell cycle progression.	gene_phenotype
68474	4	333318	7	NULL	NULL	NULL	NULL	YGL068W	GP		play a role in					cell cycle	Process	progression of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_7_3946_s_158	11274415	Of the 36 hypothetical ORFs identified in our screen, deletion of three of them ( YGL068W,  YPL063W,  YKL195W) resulted in arrest in a specific phase of the cell cycle, reflecting a role for these gene products in cell cycle progression.	gene_phenotype
68475	5	333318	7	NULL	NULL	0	NULL	YPL063W	GP		play a role in					cell cycle	Process	progression of			NULL		0	NULL	NULL	NULL	gw60_pnas_98_7_3946_s_158	11274415	Of the 36 hypothetical ORFs identified in our screen, deletion of three of them ( YGL068W,  YPL063W,  YKL195W) resulted in arrest in a specific phase of the cell cycle, reflecting a role for these gene products in cell cycle progression.	gene_phenotype
68476	6	333318	7	NULL	NULL	0	NULL	YKL195W	GP		play a role in					cell cycle	Process	progression of			NULL		0	NULL	NULL	NULL	gw60_pnas_98_7_3946_s_158	11274415	Of the 36 hypothetical ORFs identified in our screen, deletion of three of them ( YGL068W,  YPL063W,  YKL195W) resulted in arrest in a specific phase of the cell cycle, reflecting a role for these gene products in cell cycle progression.	gene_phenotype
68477	7	333318	7	NULL	NULL	0	NULL	statement 1	Process		reflect					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_98_7_3946_s_158	11274415	Of the 36 hypothetical ORFs identified in our screen, deletion of three of them ( YGL068W,  YPL063W,  YKL195W) resulted in arrest in a specific phase of the cell cycle, reflecting a role for these gene products in cell cycle progression.	gene_phenotype
68478	8	333318	7	NULL	NULL	0	NULL	statement 2	Process		reflect					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_98_7_3946_s_158	11274415	Of the 36 hypothetical ORFs identified in our screen, deletion of three of them ( YGL068W,  YPL063W,  YKL195W) resulted in arrest in a specific phase of the cell cycle, reflecting a role for these gene products in cell cycle progression.	gene_phenotype
68479	9	333318	7	NULL	NULL	0	NULL	statement 3	Process		reflect					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_98_7_3946_s_158	11274415	Of the 36 hypothetical ORFs identified in our screen, deletion of three of them ( YGL068W,  YPL063W,  YKL195W) resulted in arrest in a specific phase of the cell cycle, reflecting a role for these gene products in cell cycle progression.	gene_phenotype
68480	1	333319	7	NULL	NULL	0	NULL	YGL068W	GP	deletion of	result in					inviable microcolonies	Organism				NULL		0	NULL	NULL	NULL	gw60_pnas_98_7_3946_s_112	11274415	Indicative of a cdc phenotype, deletion of each of the three ORFs,  YGL068W,  YKL195W, and  YPL063W resulted in inviable microcolonies that were comprised of 90, 84, and 100% unbudded cells, respectively, whereas the population of unbudded cells in matched wild-type colonies was 52% (Table  3).	gene_phenotype
68481	2	333319	7	NULL	NULL	0	NULL	YKL195W	GP	deletion of	result in					inviable microcolonies	Organism				NULL		0	NULL	NULL	NULL	gw60_pnas_98_7_3946_s_112	11274415	Indicative of a cdc phenotype, deletion of each of the three ORFs,  YGL068W,  YKL195W, and  YPL063W resulted in inviable microcolonies that were comprised of 90, 84, and 100% unbudded cells, respectively, whereas the population of unbudded cells in matched wild-type colonies was 52% (Table  3).	gene_phenotype
68482	3	333319	7	NULL	NULL	0	NULL	YPL063W	GP	deletion of	result in					inviable microcolonies	Organism				NULL		0	NULL	NULL	NULL	gw60_pnas_98_7_3946_s_112	11274415	Indicative of a cdc phenotype, deletion of each of the three ORFs,  YGL068W,  YKL195W, and  YPL063W resulted in inviable microcolonies that were comprised of 90, 84, and 100% unbudded cells, respectively, whereas the population of unbudded cells in matched wild-type colonies was 52% (Table  3).	gene_phenotype
68483	4	333319	7	NULL	NULL	0	NULL	statement 1	Process		is indicative of					cdc phenotype	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_98_7_3946_s_112	11274415	Indicative of a cdc phenotype, deletion of each of the three ORFs,  YGL068W,  YKL195W, and  YPL063W resulted in inviable microcolonies that were comprised of 90, 84, and 100% unbudded cells, respectively, whereas the population of unbudded cells in matched wild-type colonies was 52% (Table  3).	gene_phenotype
68484	5	333319	7	NULL	NULL	0	NULL	statement 2	Process		is indicative of					cdc phenotype	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_98_7_3946_s_112	11274415	Indicative of a cdc phenotype, deletion of each of the three ORFs,  YGL068W,  YKL195W, and  YPL063W resulted in inviable microcolonies that were comprised of 90, 84, and 100% unbudded cells, respectively, whereas the population of unbudded cells in matched wild-type colonies was 52% (Table  3).	gene_phenotype
68485	6	333319	7	NULL	NULL	0	NULL	statement 3	Process		is indicative of					cdc phenotype	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_98_7_3946_s_112	11274415	Indicative of a cdc phenotype, deletion of each of the three ORFs,  YGL068W,  YKL195W, and  YPL063W resulted in inviable microcolonies that were comprised of 90, 84, and 100% unbudded cells, respectively, whereas the population of unbudded cells in matched wild-type colonies was 52% (Table  3).	gene_phenotype
68486	7	333319	7	NULL	NULL	0	NULL	inviable microcolonies	Organism		comprise of					unbudded cells	Cell				NULL		0	NULL	NULL	NULL	gw60_pnas_98_7_3946_s_112	11274415	Indicative of a cdc phenotype, deletion of each of the three ORFs,  YGL068W,  YKL195W, and  YPL063W resulted in inviable microcolonies that were comprised of 90, 84, and 100% unbudded cells, respectively, whereas the population of unbudded cells in matched wild-type colonies was 52% (Table  3).	gene_phenotype
68487	1	333320	7	NULL	NULL	0	NULL	EAP1	GP		is expressed					constitutively	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_13_4604_s_300	10848587	EAP1 (ORF YKL204w) is constitutively expressed at low levels (100 to 1,000 times less than actin mRNA [ 68]) and is not differentially regulated during batch growth, throughout the cell cycle, or during sporulation, based on yeast gene expression databases ( 21,  26,  68,  73,  78; SGD [see above]; P. O. Brown laboratory, Stanford University [ http://cmgm.stanford.	gene_phenotype
68488	2	333320	7	NULL	NULL	NULL	NULL	EAP1	GP		 not regulated during		differentially			batch growth	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4604_s_300	10848587	EAP1 (ORF YKL204w) is constitutively expressed at low levels (100 to 1,000 times less than actin mRNA [ 68]) and is not differentially regulated during batch growth, throughout the cell cycle, or during sporulation, based on yeast gene expression databases ( 21,  26,  68,  73,  78; SGD [see above]; P. O. Brown laboratory, Stanford University [ http://cmgm.stanford.	gene_phenotype
68489	3	333320	7	NULL	NULL	0	NULL	statement 2	Process		occur throughout					cell cycle	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_13_4604_s_300	10848587	EAP1 (ORF YKL204w) is constitutively expressed at low levels (100 to 1,000 times less than actin mRNA [ 68]) and is not differentially regulated during batch growth, throughout the cell cycle, or during sporulation, based on yeast gene expression databases ( 21,  26,  68,  73,  78; SGD [see above]; P. O. Brown laboratory, Stanford University [ http://cmgm.stanford.	gene_phenotype
68490	4	333320	7	NULL	NULL	NULL	NULL	statement 2	Process		occur during					sporulation	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4604_s_300	10848587	EAP1 (ORF YKL204w) is constitutively expressed at low levels (100 to 1,000 times less than actin mRNA [ 68]) and is not differentially regulated during batch growth, throughout the cell cycle, or during sporulation, based on yeast gene expression databases ( 21,  26,  68,  73,  78; SGD [see above]; P. O. Brown laboratory, Stanford University [ http://cmgm.stanford.	gene_phenotype
68491	5	333320	7	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_13_4604_s_300	10848587	EAP1 (ORF YKL204w) is constitutively expressed at low levels (100 to 1,000 times less than actin mRNA [ 68]) and is not differentially regulated during batch growth, throughout the cell cycle, or during sporulation, based on yeast gene expression databases ( 21,  26,  68,  73,  78; SGD [see above]; P. O. Brown laboratory, Stanford University [ http://cmgm.stanford.	gene_phenotype
68492	6	333320	7	NULL	NULL	NULL	NULL	EAP1	GP	constitutive expression of	is less than					actin mRNA	NucleicAcid	constitutive expression of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_13_4604_s_300	10848587	EAP1 (ORF YKL204w) is constitutively expressed at low levels (100 to 1,000 times less than actin mRNA [ 68]) and is not differentially regulated during batch growth, throughout the cell cycle, or during sporulation, based on yeast gene expression databases ( 21,  26,  68,  73,  78; SGD [see above]; P. O. Brown laboratory, Stanford University [ http://cmgm.stanford.	gene_phenotype
68541	1	333321	7	NULL	NULL	NULL	NULL	Gic2	GP		is a component of					vesicular transport machinery	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biochem-j_365_pt-1_11931638_s_4	11931638	We also identified  components of the vesicular transport machinery such as Gic2 and Msb3,  proteins involved in transcriptional regulation such as Mbf1, Gcr2 and  Reg2, and a variety of other different proteins (Ppt1, Lre1, Rps0A and  Ylr177w).	gene_phenotype
68542	2	333321	7	NULL	NULL	0	NULL	 Msb3	GP		is a component of					vesicular transport machinery	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biochem-j_365_pt-1_11931638_s_4	11931638	We also identified  components of the vesicular transport machinery such as Gic2 and Msb3,  proteins involved in transcriptional regulation such as Mbf1, Gcr2 and  Reg2, and a variety of other different proteins (Ppt1, Lre1, Rps0A and  Ylr177w).	gene_phenotype
68543	3	333321	7	NULL	NULL	0	NULL	Mbf1	GP		is involved in					transcriptional regulation	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biochem-j_365_pt-1_11931638_s_4	11931638	We also identified  components of the vesicular transport machinery such as Gic2 and Msb3,  proteins involved in transcriptional regulation such as Mbf1, Gcr2 and  Reg2, and a variety of other different proteins (Ppt1, Lre1, Rps0A and  Ylr177w).	gene_phenotype
68544	4	333321	7	NULL	NULL	0	NULL	Gcr2	GP		is involved in					transcriptional regulation	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biochem-j_365_pt-1_11931638_s_4	11931638	We also identified  components of the vesicular transport machinery such as Gic2 and Msb3,  proteins involved in transcriptional regulation such as Mbf1, Gcr2 and  Reg2, and a variety of other different proteins (Ppt1, Lre1, Rps0A and  Ylr177w).	gene_phenotype
68545	5	333321	7	NULL	NULL	0	NULL	Reg2	GP		is involved in					transcriptional regulation	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biochem-j_365_pt-1_11931638_s_4	11931638	We also identified  components of the vesicular transport machinery such as Gic2 and Msb3,  proteins involved in transcriptional regulation such as Mbf1, Gcr2 and  Reg2, and a variety of other different proteins (Ppt1, Lre1, Rps0A and  Ylr177w).	gene_phenotype
68546	1	333322	7	NULL	NULL	0	NULL	YOR049C	GP		is a type of					transporter gene family	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4020_s_122	11054416	It is quite possible, however, that increased expression of an as yet uncharacterized member of the transporter gene family, such as  YOR049C, could mediate the resistance of petite strains to 4-NQO.	gene_phenotype
68547	2	333322	7	NULL	NULL	0	NULL	petite strains	Organism		resistant to					4-NQO	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4020_s_122	11054416	It is quite possible, however, that increased expression of an as yet uncharacterized member of the transporter gene family, such as  YOR049C, could mediate the resistance of petite strains to 4-NQO.	gene_phenotype
68548	3	333322	7	NULL	NULL	0	NULL	YOR049C	GP		mediate		could			statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4020_s_122	11054416	It is quite possible, however, that increased expression of an as yet uncharacterized member of the transporter gene family, such as  YOR049C, could mediate the resistance of petite strains to 4-NQO.	gene_phenotype
68549	1	333323	7	NULL	NULL	0	NULL	 yeast cells 	Cell		lacks 					mitochondrial DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4020_s_181	11054416	Our studies support such a hypothesis; yeast cells lacking mitochondrial DNA acquire a multidrug-resistant phenotype perhaps as a result of increased expression of genes coding for membrane transporters ( e.g. PDR5 and  YOR049C) and show increased expression of genes coding for a number of cell surface proteins ( e.g. Hsp150, Sed1, and Cwp1) that may account for the changes in cell surface characteristics reported by Wilkie  et al. ( 70).	gene_phenotype
68550	2	333323	7	NULL	NULL	0	NULL	statement 1	Process		acquire					multidrug-resistance phenotype	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4020_s_181	11054416	Our studies support such a hypothesis; yeast cells lacking mitochondrial DNA acquire a multidrug-resistant phenotype perhaps as a result of increased expression of genes coding for membrane transporters ( e.g. PDR5 and  YOR049C) and show increased expression of genes coding for a number of cell surface proteins ( e.g. Hsp150, Sed1, and Cwp1) that may account for the changes in cell surface characteristics reported by Wilkie  et al. ( 70).	gene_phenotype
68551	3	333323	7	NULL	NULL	0	NULL	PDR5	GP		is a type of					membrane transporter	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4020_s_181	11054416	Our studies support such a hypothesis; yeast cells lacking mitochondrial DNA acquire a multidrug-resistant phenotype perhaps as a result of increased expression of genes coding for membrane transporters ( e.g. PDR5 and  YOR049C) and show increased expression of genes coding for a number of cell surface proteins ( e.g. Hsp150, Sed1, and Cwp1) that may account for the changes in cell surface characteristics reported by Wilkie  et al. ( 70).	gene_phenotype
68552	4	333323	7	NULL	NULL	0	NULL	YOR049C	GP		is a type of					membrane transporter	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4020_s_181	11054416	Our studies support such a hypothesis; yeast cells lacking mitochondrial DNA acquire a multidrug-resistant phenotype perhaps as a result of increased expression of genes coding for membrane transporters ( e.g. PDR5 and  YOR049C) and show increased expression of genes coding for a number of cell surface proteins ( e.g. Hsp150, Sed1, and Cwp1) that may account for the changes in cell surface characteristics reported by Wilkie  et al. ( 70).	gene_phenotype
68553	5	333323	7	NULL	NULL	0	NULL	statement 2	Process		because of					statement 3	Process	increased expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4020_s_181	11054416	Our studies support such a hypothesis; yeast cells lacking mitochondrial DNA acquire a multidrug-resistant phenotype perhaps as a result of increased expression of genes coding for membrane transporters ( e.g. PDR5 and  YOR049C) and show increased expression of genes coding for a number of cell surface proteins ( e.g. Hsp150, Sed1, and Cwp1) that may account for the changes in cell surface characteristics reported by Wilkie  et al. ( 70).	gene_phenotype
68554	6	333323	7	NULL	NULL	0	NULL	statement 2	Process		because of					statement 4	Process	increased expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4020_s_181	11054416	Our studies support such a hypothesis; yeast cells lacking mitochondrial DNA acquire a multidrug-resistant phenotype perhaps as a result of increased expression of genes coding for membrane transporters ( e.g. PDR5 and  YOR049C) and show increased expression of genes coding for a number of cell surface proteins ( e.g. Hsp150, Sed1, and Cwp1) that may account for the changes in cell surface characteristics reported by Wilkie  et al. ( 70).	gene_phenotype
68555	7	333323	7	NULL	NULL	0	NULL	Hsp150	GP		is a type of					cell surface proteins	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4020_s_181	11054416	Our studies support such a hypothesis; yeast cells lacking mitochondrial DNA acquire a multidrug-resistant phenotype perhaps as a result of increased expression of genes coding for membrane transporters ( e.g. PDR5 and  YOR049C) and show increased expression of genes coding for a number of cell surface proteins ( e.g. Hsp150, Sed1, and Cwp1) that may account for the changes in cell surface characteristics reported by Wilkie  et al. ( 70).	gene_phenotype
68556	8	333323	7	NULL	NULL	0	NULL	Sed1	GP		is a type of					cell surface protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4020_s_181	11054416	Our studies support such a hypothesis; yeast cells lacking mitochondrial DNA acquire a multidrug-resistant phenotype perhaps as a result of increased expression of genes coding for membrane transporters ( e.g. PDR5 and  YOR049C) and show increased expression of genes coding for a number of cell surface proteins ( e.g. Hsp150, Sed1, and Cwp1) that may account for the changes in cell surface characteristics reported by Wilkie  et al. ( 70).	gene_phenotype
68557	9	333323	7	NULL	NULL	0	NULL	Cwp1	GP		is a type of					cell surface protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4020_s_181	11054416	Our studies support such a hypothesis; yeast cells lacking mitochondrial DNA acquire a multidrug-resistant phenotype perhaps as a result of increased expression of genes coding for membrane transporters ( e.g. PDR5 and  YOR049C) and show increased expression of genes coding for a number of cell surface proteins ( e.g. Hsp150, Sed1, and Cwp1) that may account for the changes in cell surface characteristics reported by Wilkie  et al. ( 70).	gene_phenotype
68558	10	333323	7	NULL	NULL	0	NULL	Hsp150	GP		account for					cell surface	CellComponent	changes in characterisitics of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4020_s_181	11054416	Our studies support such a hypothesis; yeast cells lacking mitochondrial DNA acquire a multidrug-resistant phenotype perhaps as a result of increased expression of genes coding for membrane transporters ( e.g. PDR5 and  YOR049C) and show increased expression of genes coding for a number of cell surface proteins ( e.g. Hsp150, Sed1, and Cwp1) that may account for the changes in cell surface characteristics reported by Wilkie  et al. ( 70).	gene_phenotype
68559	11	333323	7	NULL	NULL	0	NULL	Sed1	GP		account for					cell surface	CellComponent	changes in characterisitics of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4020_s_181	11054416	Our studies support such a hypothesis; yeast cells lacking mitochondrial DNA acquire a multidrug-resistant phenotype perhaps as a result of increased expression of genes coding for membrane transporters ( e.g. PDR5 and  YOR049C) and show increased expression of genes coding for a number of cell surface proteins ( e.g. Hsp150, Sed1, and Cwp1) that may account for the changes in cell surface characteristics reported by Wilkie  et al. ( 70).	gene_phenotype
68560	12	333323	7	NULL	NULL	0	NULL	 Cwp1	GP		account for					cell surface	CellComponent	changes in characterisitics of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4020_s_181	11054416	Our studies support such a hypothesis; yeast cells lacking mitochondrial DNA acquire a multidrug-resistant phenotype perhaps as a result of increased expression of genes coding for membrane transporters ( e.g. PDR5 and  YOR049C) and show increased expression of genes coding for a number of cell surface proteins ( e.g. Hsp150, Sed1, and Cwp1) that may account for the changes in cell surface characteristics reported by Wilkie  et al. ( 70).	gene_phenotype
68561	13	333323	7	NULL	NULL	0	NULL	statement 2	Process		because of					Hsp150	GP	increased expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4020_s_181	11054416	Our studies support such a hypothesis; yeast cells lacking mitochondrial DNA acquire a multidrug-resistant phenotype perhaps as a result of increased expression of genes coding for membrane transporters ( e.g. PDR5 and  YOR049C) and show increased expression of genes coding for a number of cell surface proteins ( e.g. Hsp150, Sed1, and Cwp1) that may account for the changes in cell surface characteristics reported by Wilkie  et al. ( 70).	gene_phenotype
68562	14	333323	7	NULL	NULL	0	NULL	statement 2	Process		because of					Sed1	GP	increased expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4020_s_181	11054416	Our studies support such a hypothesis; yeast cells lacking mitochondrial DNA acquire a multidrug-resistant phenotype perhaps as a result of increased expression of genes coding for membrane transporters ( e.g. PDR5 and  YOR049C) and show increased expression of genes coding for a number of cell surface proteins ( e.g. Hsp150, Sed1, and Cwp1) that may account for the changes in cell surface characteristics reported by Wilkie  et al. ( 70).	gene_phenotype
68563	15	333323	7	NULL	NULL	0	NULL	statement 2	Process		because of					Cwp1	GP	increased expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4020_s_181	11054416	Our studies support such a hypothesis; yeast cells lacking mitochondrial DNA acquire a multidrug-resistant phenotype perhaps as a result of increased expression of genes coding for membrane transporters ( e.g. PDR5 and  YOR049C) and show increased expression of genes coding for a number of cell surface proteins ( e.g. Hsp150, Sed1, and Cwp1) that may account for the changes in cell surface characteristics reported by Wilkie  et al. ( 70).	gene_phenotype
68564	1	333324	7	NULL	NULL	0	NULL	haploid filamentous growth	Process		induce					ORF YOR225W	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12369_s_139	11035792	Also overexpressed 5.6-fold is the ORF  YOR225W, which has been shown to be induced in haploid filamentous growth, where its mRNA level is significantly increased in cells overproducing Tec1p compared with  tec1 null mutants ( 22).	gene_phenotype
68566	3	333324	7	NULL	NULL	0	NULL	YOR225W mRNA	NucleicAcid		increased in		significantly			statement 2	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12369_s_139	11035792	Also overexpressed 5.6-fold is the ORF  YOR225W, which has been shown to be induced in haploid filamentous growth, where its mRNA level is significantly increased in cells overproducing Tec1p compared with  tec1 null mutants ( 22).	gene_phenotype
68567	2	333324	7	NULL	NULL	0	NULL	cells	Cell		overproduce					Tec1p	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12369_s_139	11035792	Also overexpressed 5.6-fold is the ORF  YOR225W, which has been shown to be induced in haploid filamentous growth, where its mRNA level is significantly increased in cells overproducing Tec1p compared with  tec1 null mutants ( 22).	gene_phenotype
68568	4	333324	7	NULL	NULL	NULL	NULL	cells	Cell		produce					tec1 null mutant	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_22_12369_s_139	11035792	Also overexpressed 5.6-fold is the ORF  YOR225W, which has been shown to be induced in haploid filamentous growth, where its mRNA level is significantly increased in cells overproducing Tec1p compared with  tec1 null mutants ( 22).	gene_phenotype
68653	1	333325	7	NULL	NULL	0	NULL	peroxisomes	CellComponent	functional	required for					oleate	Chemical	metabolism of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_158_2_259_s_113	12135984	Viable yeast stains containing individual deletions of  YPL112c or  YOR084w constructed by an international consortium of laboratories ( Winzeler et al., 1999) (obtained from Resgen) were assayed for growth in the presence of oleate (requiring functional peroxisomes and mitochondria for metabolism) or acetate (requiring only mitochondria) as the sole carbon source.	gene_phenotype
68654	2	333325	7	NULL	NULL	0	NULL	mitochondria	CellComponent		required for					oleate	Chemical	metabolism of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_158_2_259_s_113	12135984	Viable yeast stains containing individual deletions of  YPL112c or  YOR084w constructed by an international consortium of laboratories ( Winzeler et al., 1999) (obtained from Resgen) were assayed for growth in the presence of oleate (requiring functional peroxisomes and mitochondria for metabolism) or acetate (requiring only mitochondria) as the sole carbon source.	gene_phenotype
68655	3	333325	7	NULL	NULL	0	NULL	mitochondria	CellComponent		required for					acetate	Chemical	metabolism of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_158_2_259_s_113	12135984	Viable yeast stains containing individual deletions of  YPL112c or  YOR084w constructed by an international consortium of laboratories ( Winzeler et al., 1999) (obtained from Resgen) were assayed for growth in the presence of oleate (requiring functional peroxisomes and mitochondria for metabolism) or acetate (requiring only mitochondria) as the sole carbon source.	gene_phenotype
68656	1	333326	7	NULL	NULL	0	NULL	IkappaB	GP		is a type of					inhibitor protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15494_s_25	9624136	The prototypical pathway involves its liberation from an inactive complex with the inhibitor protein, IkappaB, which resides in the cytosol ( 31,  32).	gene_phenotype
68657	2	333326	7	NULL	NULL	0	NULL	IkappaB	GP		resides in 					cytosol	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15494_s_25	9624136	The prototypical pathway involves its liberation from an inactive complex with the inhibitor protein, IkappaB, which resides in the cytosol ( 31,  32).	gene_phenotype
68658	1	333328	7	NULL	NULL	0	NULL	Sir2	GP		repress					HMR-proximal loci	Chromosome				NULL		0	NULL	NULL	NULL	gw60_cell_112_5_725_s_111	12628191	It is notable that several of the  HMR-proximal loci display repression by Sir2 in an  HTZ1+ genetic background (e.g.,  YCR106W in   Figure 3B), suggesting that a locus can be partially protected from silencing by Htz1; that is, in some cases, Htz1 may reduce but not eliminate heterochromatin formation.	gene_phenotype
68662	2	333328	7	NULL	NULL	0	NULL	statement 1	Process		occur in a					HTZ1+ 	GP	genetic background of			NULL		0	NULL	NULL	NULL	gw60_cell_112_5_725_s_111	12628191	It is notable that several of the  HMR-proximal loci display repression by Sir2 in an  HTZ1+ genetic background (e.g.,  YCR106W in   Figure 3B), suggesting that a locus can be partially protected from silencing by Htz1; that is, in some cases, Htz1 may reduce but not eliminate heterochromatin formation.	gene_phenotype
68663	3	333328	7	NULL	NULL	NULL	NULL	locus	Chromosome		protected from		partially			Htz1	GP	silencing by			NULL		NULL	NULL	NULL	NULL	gw60_cell_112_5_725_s_111	12628191	It is notable that several of the  HMR-proximal loci display repression by Sir2 in an  HTZ1+ genetic background (e.g.,  YCR106W in   Figure 3B), suggesting that a locus can be partially protected from silencing by Htz1; that is, in some cases, Htz1 may reduce but not eliminate heterochromatin formation.	gene_phenotype
68668	4	333328	7	NULL	NULL	0	NULL	statement 1	Process		suggests					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_cell_112_5_725_s_111	12628191	It is notable that several of the  HMR-proximal loci display repression by Sir2 in an  HTZ1+ genetic background (e.g.,  YCR106W in   Figure 3B), suggesting that a locus can be partially protected from silencing by Htz1; that is, in some cases, Htz1 may reduce but not eliminate heterochromatin formation.	gene_phenotype
68671	5	333328	7	NULL	NULL	0	NULL	Htz1	GP		eliminate		may			heterochromatin	Chromosome	formation of			NULL		0	NULL	NULL	NULL	gw60_cell_112_5_725_s_111	12628191	It is notable that several of the  HMR-proximal loci display repression by Sir2 in an  HTZ1+ genetic background (e.g.,  YCR106W in   Figure 3B), suggesting that a locus can be partially protected from silencing by Htz1; that is, in some cases, Htz1 may reduce but not eliminate heterochromatin formation.	gene_phenotype
68673	6	333328	7	NULL	NULL	0	NULL	 Htz1	GP		does not eliminate					heterochromatin	Chromosome	formation of			NULL		0	NULL	NULL	NULL	gw60_cell_112_5_725_s_111	12628191	It is notable that several of the  HMR-proximal loci display repression by Sir2 in an  HTZ1+ genetic background (e.g.,  YCR106W in   Figure 3B), suggesting that a locus can be partially protected from silencing by Htz1; that is, in some cases, Htz1 may reduce but not eliminate heterochromatin formation.	gene_phenotype
68675	1	333330	7	NULL	NULL	0	NULL	HPR1 YDR183w	GP		suppress					intrachromosomal recombination	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_312	15334557	HPR1   YDR183w Suppresses intrachromosomal recombination; possibly also involved in RNA elongation  from polymerase II promoters and mRNA nuclear export	gene_phenotype
68676	2	333330	7	NULL	NULL	NULL	NULL	polymerase II	GP		elongates			promoter		RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_yeast_21_11_927_s_312	15334557	HPR1   YDR183w Suppresses intrachromosomal recombination; possibly also involved in RNA elongation  from polymerase II promoters and mRNA nuclear export	gene_phenotype
68677	3	333330	7	NULL	NULL	0	NULL	HPR1 YDR183w 	GP		involved in		possibly			statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_312	15334557	HPR1   YDR183w Suppresses intrachromosomal recombination; possibly also involved in RNA elongation  from polymerase II promoters and mRNA nuclear export	gene_phenotype
68678	4	333330	7	NULL	NULL	0	NULL	HPR1 YDR183w 	GP		is involved in					mRNA 	NucleicAcid	nuclear export of			NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_312	15334557	HPR1   YDR183w Suppresses intrachromosomal recombination; possibly also involved in RNA elongation  from polymerase II promoters and mRNA nuclear export	gene_phenotype
68683	1	333331	7	NULL	NULL	0	NULL	YDR236c 	GP		is essential for					growth	Process				NULL	YPD medium	0	NULL	NULL	NULL	gw60_jbiolchem_275_37_28618_s_102	10887197	When  ydr236cdelta/ YDR236c diploids were sporulated and the resulting tetrads dissected, viability segregated 2+:2  and all viable spores were geneticin-sensitive, suggesting that  YDR236c is a single copy gene that is essential for growth on YPD medium.	gene_phenotype
68684	1	333334	7	NULL	NULL	0	NULL	ADH 	GP		contains			promoter		ORF YEL003w 	GP				NULL		0	NULL	NULL	NULL	gw60_embo_17_4_952_s_62	9463374	Only the  ADH promoter fusion with the intron-containing ORF YEL003w complemented  gim4 cells (data not shown) .	gene_phenotype
68685	2	333334	7	NULL	NULL	0	NULL	statement 1	Process		complement					gim4 cells	Cell				NULL		0	NULL	NULL	NULL	gw60_embo_17_4_952_s_62	9463374	Only the  ADH promoter fusion with the intron-containing ORF YEL003w complemented  gim4 cells (data not shown) .	gene_phenotype
68686	1	333335	7	NULL	NULL	NULL	NULL	Ndt1p	GP		is a gene product of					YIL006W	GP				NULL	S.cerevisiae	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_3_1524_s_26	16291748	In this study we provide evidence that the gene products of  YIL006W and  YEL006W, named Ndt1p and Ndt2p, respectively, are two isoforms of the mitochondrial NAD+ transporter in  S. cerevisiae.	gene_phenotype
68687	2	333335	7	NULL	NULL	NULL	NULL	Ndt2p	GP		is a gene product of					YEL006W	GP				NULL	S.cerevisiae	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_3_1524_s_26	16291748	In this study we provide evidence that the gene products of  YIL006W and  YEL006W, named Ndt1p and Ndt2p, respectively, are two isoforms of the mitochondrial NAD+ transporter in  S. cerevisiae.	gene_phenotype
68688	3	333335	7	NULL	NULL	NULL	NULL	Ndt1p	GP		is an isoform of					Ndt2p	GP				NULL	S. cerevisiae	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_3_1524_s_26	16291748	In this study we provide evidence that the gene products of  YIL006W and  YEL006W, named Ndt1p and Ndt2p, respectively, are two isoforms of the mitochondrial NAD+ transporter in  S. cerevisiae.	gene_phenotype
68690	4	333335	7	NULL	NULL	NULL	NULL	Ndt1p	GP		is a type of					mitochondrial NAD+ transporter	GP				NULL	S.cerevisiae	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_3_1524_s_26	16291748	In this study we provide evidence that the gene products of  YIL006W and  YEL006W, named Ndt1p and Ndt2p, respectively, are two isoforms of the mitochondrial NAD+ transporter in  S. cerevisiae.	gene_phenotype
68691	5	333335	7	NULL	NULL	0	NULL	Ndt2p	GP		is a type of					mitochondrial NAD+ transporter	GP				NULL	S.cerevisiae	0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1524_s_26	16291748	In this study we provide evidence that the gene products of  YIL006W and  YEL006W, named Ndt1p and Ndt2p, respectively, are two isoforms of the mitochondrial NAD+ transporter in  S. cerevisiae.	gene_phenotype
68694	1	333336	7	NULL	NULL	NULL	NULL	Rim2p	GP		transports					pyrimidine nucleotides	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_9_1249_s_284	16844075	The proteins encoded by YIL006w and YEL006w cluster in the phylogenetic tree of yeast  carriers with Rim2p and Flx1p, the transporters of pyrimidine nucleotides   [32] and FAD   [92], respectively, and so attempts to uncover their functions were predicated on the  assumption that they would transport nucleotide-type molecules also.	gene_phenotype
68696	2	333336	7	NULL	NULL	0	NULL	Flx1p	GP		transports					FAD	Chemical				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_9_1249_s_284	16844075	The proteins encoded by YIL006w and YEL006w cluster in the phylogenetic tree of yeast  carriers with Rim2p and Flx1p, the transporters of pyrimidine nucleotides   [32] and FAD   [92], respectively, and so attempts to uncover their functions were predicated on the  assumption that they would transport nucleotide-type molecules also.	gene_phenotype
68703	1	333338	7	NULL	NULL	0	NULL	YGL136c 	GP	deletion of	grew in		slowly			glycerol medium	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_yeast_16_7_10806424_s_7	10806424	Segregants bearing a deletion in YGL136c  grew slowly in complete glycerol medium at 37 degrees C. Cells deleted  in YGL133w showed abnormal morphology and reduced mating efficiency, but  these phenotypes were observed only when the YGL133w disruption was in  a MATalpha background.	gene_phenotype
68704	2	333338	7	NULL	NULL	NULL	NULL	YGL133w	GP	deletion of	shows					morphology		abnormal			NULL	cells	NULL	NULL	NULL	NULL	abs-batch0650-0679_yeast_16_7_10806424_s_7	10806424	Segregants bearing a deletion in YGL136c  grew slowly in complete glycerol medium at 37 degrees C. Cells deleted  in YGL133w showed abnormal morphology and reduced mating efficiency, but  these phenotypes were observed only when the YGL133w disruption was in  a MATalpha background.	gene_phenotype
68708	3	333338	7	NULL	NULL	0	NULL	YGL133w	GP	deletion of	reduced					mating 	Process	efficiency of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_yeast_16_7_10806424_s_7	10806424	Segregants bearing a deletion in YGL136c  grew slowly in complete glycerol medium at 37 degrees C. Cells deleted  in YGL133w showed abnormal morphology and reduced mating efficiency, but  these phenotypes were observed only when the YGL133w disruption was in  a MATalpha background.	gene_phenotype
68709	4	333338	7	NULL	NULL	0	NULL	statement 2	Process		occur in the					MATalpha	GP	background of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_yeast_16_7_10806424_s_7	10806424	Segregants bearing a deletion in YGL136c  grew slowly in complete glycerol medium at 37 degrees C. Cells deleted  in YGL133w showed abnormal morphology and reduced mating efficiency, but  these phenotypes were observed only when the YGL133w disruption was in  a MATalpha background.	gene_phenotype
68710	5	333338	7	NULL	NULL	0	NULL	statement 3	Process		occur in the 					MATalpha	GP	background of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_yeast_16_7_10806424_s_7	10806424	Segregants bearing a deletion in YGL136c  grew slowly in complete glycerol medium at 37 degrees C. Cells deleted  in YGL133w showed abnormal morphology and reduced mating efficiency, but  these phenotypes were observed only when the YGL133w disruption was in  a MATalpha background.	gene_phenotype
68711	1	333339	7	NULL	NULL	0	NULL	YGR203w	GP	deletion of	is					viable	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_36_13380_s_206	15329414	Deletion of YGR203w is viable but alters yeast fitness after 20 generations ( ).	gene_phenotype
68712	2	333339	7	NULL	NULL	0	NULL	YGR203w	GP	deletion of	alters					yeast	Organism	fitness of			NULL		0	NULL	NULL	NULL	gw70_pnas_101_36_13380_s_206	15329414	Deletion of YGR203w is viable but alters yeast fitness after 20 generations ( ).	gene_phenotype
68713	1	333340	7	NULL	NULL	NULL	NULL	CDC25 	GP		is homologous to					small CDC25-like protein	GP				NULL	yeast	NULL	NULL	NULL	NULL	gw70_pnas_101_36_13380_s_98	15329414	Arath;CDC25 is also homologous to small CDC25-like proteins found in yeast such as YGR203w from  S. cerevisiae or IBP1 from  Sch. pombe, where the latter was recently shown experimentally to display a tyrosine-phosphatase activity ( ).	gene_phenotype
68714	2	333340	7	NULL	NULL	NULL	NULL	YGR203w 	GP	S. cerevisiae	is a type of					small CDC25-like proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_36_13380_s_98	15329414	Arath;CDC25 is also homologous to small CDC25-like proteins found in yeast such as YGR203w from  S. cerevisiae or IBP1 from  Sch. pombe, where the latter was recently shown experimentally to display a tyrosine-phosphatase activity ( ).	gene_phenotype
68715	3	333340	7	NULL	NULL	0	NULL	IBP1	GP	Sch. pombe	is a type of					small CDC25-like protein	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_36_13380_s_98	15329414	Arath;CDC25 is also homologous to small CDC25-like proteins found in yeast such as YGR203w from  S. cerevisiae or IBP1 from  Sch. pombe, where the latter was recently shown experimentally to display a tyrosine-phosphatase activity ( ).	gene_phenotype
68716	4	333340	7	NULL	NULL	0	NULL	IBP1	GP		display					tyrosine-phosphatase activity	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_36_13380_s_98	15329414	Arath;CDC25 is also homologous to small CDC25-like proteins found in yeast such as YGR203w from  S. cerevisiae or IBP1 from  Sch. pombe, where the latter was recently shown experimentally to display a tyrosine-phosphatase activity ( ).	gene_phenotype
68723	1	333342	7	NULL	NULL	0	NULL	YIL083C gene	GP		essential for					viability	Process	yeast			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_24_21431_s_144	11923312	The YIL083C gene was found to be essential for yeast viability in a systematic gene knockout study (Saccharomyces Genome Database) (see Ref.  20), providing additional support for this functional prediction.	gene_phenotype
68724	1	333343	7	NULL	NULL	0	NULL	PRM1	GP		is linked to					membrane	CellComponent	biosynthesis of			NULL		0	NULL	NULL	NULL	gw70_genomeres_13_7_1706_s_133	12840046	The genes included  PRM1 (linked to  membrane biosynthesis),  FIG2, AGA1, FUS1 (cell fusion),  GIC2  (mating projection formation),  CIK1, KAR2 (nuclear fusion),  FUS3,  STE12, and  HYM1 (mating signaling) along with other genes of yet  unknown relevance ( YOR0343C, PEP1, SCH9, YIL036C, YIL083C, YOL155C).	gene_phenotype
68725	2	333343	7	NULL	NULL	0	NULL	FIG2	GP		is involved in					cell fusion	Process				NULL		0	NULL	NULL	NULL	gw70_genomeres_13_7_1706_s_133	12840046	The genes included  PRM1 (linked to  membrane biosynthesis),  FIG2, AGA1, FUS1 (cell fusion),  GIC2  (mating projection formation),  CIK1, KAR2 (nuclear fusion),  FUS3,  STE12, and  HYM1 (mating signaling) along with other genes of yet  unknown relevance ( YOR0343C, PEP1, SCH9, YIL036C, YIL083C, YOL155C).	gene_phenotype
68726	3	333343	7	NULL	NULL	0	NULL	AGA1	GP		is involved in					cell fusion	Process				NULL		0	NULL	NULL	NULL	gw70_genomeres_13_7_1706_s_133	12840046	The genes included  PRM1 (linked to  membrane biosynthesis),  FIG2, AGA1, FUS1 (cell fusion),  GIC2  (mating projection formation),  CIK1, KAR2 (nuclear fusion),  FUS3,  STE12, and  HYM1 (mating signaling) along with other genes of yet  unknown relevance ( YOR0343C, PEP1, SCH9, YIL036C, YIL083C, YOL155C).	gene_phenotype
68727	4	333343	7	NULL	NULL	0	NULL	FUS1	GP		is involved in					cell fusion	Process				NULL		0	NULL	NULL	NULL	gw70_genomeres_13_7_1706_s_133	12840046	The genes included  PRM1 (linked to  membrane biosynthesis),  FIG2, AGA1, FUS1 (cell fusion),  GIC2  (mating projection formation),  CIK1, KAR2 (nuclear fusion),  FUS3,  STE12, and  HYM1 (mating signaling) along with other genes of yet  unknown relevance ( YOR0343C, PEP1, SCH9, YIL036C, YIL083C, YOL155C).	gene_phenotype
68728	5	333343	7	NULL	NULL	0	NULL	GIC2	GP		is involved in					mating projection	Process	 formation of			NULL		0	NULL	NULL	NULL	gw70_genomeres_13_7_1706_s_133	12840046	The genes included  PRM1 (linked to  membrane biosynthesis),  FIG2, AGA1, FUS1 (cell fusion),  GIC2  (mating projection formation),  CIK1, KAR2 (nuclear fusion),  FUS3,  STE12, and  HYM1 (mating signaling) along with other genes of yet  unknown relevance ( YOR0343C, PEP1, SCH9, YIL036C, YIL083C, YOL155C).	gene_phenotype
68729	6	333343	7	NULL	NULL	0	NULL	CIK1	GP		is involved in					nuclear fusion	Process				NULL		0	NULL	NULL	NULL	gw70_genomeres_13_7_1706_s_133	12840046	The genes included  PRM1 (linked to  membrane biosynthesis),  FIG2, AGA1, FUS1 (cell fusion),  GIC2  (mating projection formation),  CIK1, KAR2 (nuclear fusion),  FUS3,  STE12, and  HYM1 (mating signaling) along with other genes of yet  unknown relevance ( YOR0343C, PEP1, SCH9, YIL036C, YIL083C, YOL155C).	gene_phenotype
68730	7	333343	7	NULL	NULL	0	NULL	KAR2	GP		is involved in					nuclear fusion	Process				NULL		0	NULL	NULL	NULL	gw70_genomeres_13_7_1706_s_133	12840046	The genes included  PRM1 (linked to  membrane biosynthesis),  FIG2, AGA1, FUS1 (cell fusion),  GIC2  (mating projection formation),  CIK1, KAR2 (nuclear fusion),  FUS3,  STE12, and  HYM1 (mating signaling) along with other genes of yet  unknown relevance ( YOR0343C, PEP1, SCH9, YIL036C, YIL083C, YOL155C).	gene_phenotype
68731	8	333343	7	NULL	NULL	0	NULL	FUS3	GP		is involved in					mating signaling	Process				NULL		0	NULL	NULL	NULL	gw70_genomeres_13_7_1706_s_133	12840046	The genes included  PRM1 (linked to  membrane biosynthesis),  FIG2, AGA1, FUS1 (cell fusion),  GIC2  (mating projection formation),  CIK1, KAR2 (nuclear fusion),  FUS3,  STE12, and  HYM1 (mating signaling) along with other genes of yet  unknown relevance ( YOR0343C, PEP1, SCH9, YIL036C, YIL083C, YOL155C).	gene_phenotype
68732	9	333343	7	NULL	NULL	0	NULL	STE12	GP		is involved in					mating signaling	Process				NULL		0	NULL	NULL	NULL	gw70_genomeres_13_7_1706_s_133	12840046	The genes included  PRM1 (linked to  membrane biosynthesis),  FIG2, AGA1, FUS1 (cell fusion),  GIC2  (mating projection formation),  CIK1, KAR2 (nuclear fusion),  FUS3,  STE12, and  HYM1 (mating signaling) along with other genes of yet  unknown relevance ( YOR0343C, PEP1, SCH9, YIL036C, YIL083C, YOL155C).	gene_phenotype
68733	10	333343	7	NULL	NULL	0	NULL	HYM1 	GP		is involved in					mating signaling	Process				NULL		0	NULL	NULL	NULL	gw70_genomeres_13_7_1706_s_133	12840046	The genes included  PRM1 (linked to  membrane biosynthesis),  FIG2, AGA1, FUS1 (cell fusion),  GIC2  (mating projection formation),  CIK1, KAR2 (nuclear fusion),  FUS3,  STE12, and  HYM1 (mating signaling) along with other genes of yet  unknown relevance ( YOR0343C, PEP1, SCH9, YIL036C, YIL083C, YOL155C).	gene_phenotype
68734	1	333344	7	NULL	NULL	0	NULL	14-3-3 protein	GP		mediate					anti-apoptotic signal	Process	essential			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_6_2201_s_269	12808022	14-3-3 proteins  mediate an essential anti-apoptotic signal.	gene_phenotype
68896	1	333345	7	NULL	NULL	0	NULL	HXT16	GP		is a type of					hexose transporter genes	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_1_437_s_235	15496405	The remaining 14 genes of the 35 genes of the discussed cluster were composed of two hexose transporter genes ( HXT16 and  HXT17), five genes encoding ribosomal proteins ( RSP10A, RPS25A, RPP1B, RPL4A, and  RPL9A), and seven genes belonging to different metabolic routes ( SUT1, OSH7, AGP1, IMD2, YLR089C, YAR075W, and  GPA1) ( Fig. 6,  middle panel).	gene_phenotype
68897	2	333345	7	NULL	NULL	0	NULL	HXT17	GP		is a type of					hexose transporter genes	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_1_437_s_235	15496405	The remaining 14 genes of the 35 genes of the discussed cluster were composed of two hexose transporter genes ( HXT16 and  HXT17), five genes encoding ribosomal proteins ( RSP10A, RPS25A, RPP1B, RPL4A, and  RPL9A), and seven genes belonging to different metabolic routes ( SUT1, OSH7, AGP1, IMD2, YLR089C, YAR075W, and  GPA1) ( Fig. 6,  middle panel).	gene_phenotype
68898	3	333345	7	NULL	NULL	NULL	NULL	RSP10A	GP		encode					ribosomal proteins 	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_1_437_s_235	15496405	The remaining 14 genes of the 35 genes of the discussed cluster were composed of two hexose transporter genes ( HXT16 and  HXT17), five genes encoding ribosomal proteins ( RSP10A, RPS25A, RPP1B, RPL4A, and  RPL9A), and seven genes belonging to different metabolic routes ( SUT1, OSH7, AGP1, IMD2, YLR089C, YAR075W, and  GPA1) ( Fig. 6,  middle panel).	gene_phenotype
68899	4	333345	7	NULL	NULL	0	NULL	RPS25A	GP		encode					ribosomal proteins	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_1_437_s_235	15496405	The remaining 14 genes of the 35 genes of the discussed cluster were composed of two hexose transporter genes ( HXT16 and  HXT17), five genes encoding ribosomal proteins ( RSP10A, RPS25A, RPP1B, RPL4A, and  RPL9A), and seven genes belonging to different metabolic routes ( SUT1, OSH7, AGP1, IMD2, YLR089C, YAR075W, and  GPA1) ( Fig. 6,  middle panel).	gene_phenotype
68900	5	333345	7	NULL	NULL	NULL	NULL	RPP1B	GP		encode					ribosomal proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_1_437_s_235	15496405	The remaining 14 genes of the 35 genes of the discussed cluster were composed of two hexose transporter genes ( HXT16 and  HXT17), five genes encoding ribosomal proteins ( RSP10A, RPS25A, RPP1B, RPL4A, and  RPL9A), and seven genes belonging to different metabolic routes ( SUT1, OSH7, AGP1, IMD2, YLR089C, YAR075W, and  GPA1) ( Fig. 6,  middle panel).	gene_phenotype
68901	6	333345	7	NULL	NULL	0	NULL	RPL4A	GP		encode					ribosomal proteins	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_1_437_s_235	15496405	The remaining 14 genes of the 35 genes of the discussed cluster were composed of two hexose transporter genes ( HXT16 and  HXT17), five genes encoding ribosomal proteins ( RSP10A, RPS25A, RPP1B, RPL4A, and  RPL9A), and seven genes belonging to different metabolic routes ( SUT1, OSH7, AGP1, IMD2, YLR089C, YAR075W, and  GPA1) ( Fig. 6,  middle panel).	gene_phenotype
68902	7	333345	7	NULL	NULL	0	NULL	RPL9A	GP		encode					ribosomal proteins	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_1_437_s_235	15496405	The remaining 14 genes of the 35 genes of the discussed cluster were composed of two hexose transporter genes ( HXT16 and  HXT17), five genes encoding ribosomal proteins ( RSP10A, RPS25A, RPP1B, RPL4A, and  RPL9A), and seven genes belonging to different metabolic routes ( SUT1, OSH7, AGP1, IMD2, YLR089C, YAR075W, and  GPA1) ( Fig. 6,  middle panel).	gene_phenotype
68903	1	333346	7	NULL	NULL	0	NULL	DH17	GP		is a type of					 C-terminal specific monoclonal antibody	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_30_27200_s_245	12004072	This was investigated by examining apoptotic HeLa-E cells with a C-terminal specific monoclonal antibody (DH17).	gene_phenotype
68904	1	333347	7	NULL	NULL	0	NULL	YNL026w	GP		is essential for					haploid progeny	Process	viability in			NULL		0	NULL	NULL	NULL	gw70_cellbiol_164_1_19_s_124	14699090	YNL026w is essential for viability in haploid progeny derived from IGY002.	gene_phenotype
68905	2	333347	7	NULL	NULL	0	NULL	YNL026w	GP		is derived from					IGY002	GP				NULL		0	NULL	NULL	NULL	gw70_cellbiol_164_1_19_s_124	14699090	YNL026w is essential for viability in haploid progeny derived from IGY002.	gene_phenotype
68906	1	333348	7	NULL	NULL	0	NULL	NAP-1	GP		is not essential for					S. cerevisiae	Organism	viability of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_40_25041_s_207	8798787	This NAP-1/SET-related ORF YNL246w protein may compensate for the absence of NAP-1 and thus be responsible, at least in part, for the observation that NAP-1 is not essential for viability of  S. cerevisiae ( 46).	gene_phenotype
68907	1	333349	7	NULL	NULL	0	NULL		Organism	yeast	harbor			patatin domain-containing proteins		lipolytic functions	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_491_s_271	16267052	Because three other patatin domain-containing proteins in yeast harbor lipolytic functions, including the phospholipase B activity of the neuropathy target esterase ortholog, Nte1 ( ,  ), a related enzymatic function for Yor081c appears likely.	gene_phenotype
68908	2	333349	7	NULL	NULL	0	NULL	Nte1	GP		activates					phospholipase B	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_491_s_271	16267052	Because three other patatin domain-containing proteins in yeast harbor lipolytic functions, including the phospholipase B activity of the neuropathy target esterase ortholog, Nte1 ( ,  ), a related enzymatic function for Yor081c appears likely.	gene_phenotype
68909	3	333349	7	NULL	NULL	NULL	NULL	 Nte1 	GP		is ortholog of					neuropathy target esterase	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_1_491_s_271	16267052	Because three other patatin domain-containing proteins in yeast harbor lipolytic functions, including the phospholipase B activity of the neuropathy target esterase ortholog, Nte1 ( ,  ), a related enzymatic function for Yor081c appears likely.	gene_phenotype
68910	1	333351	7	NULL	NULL	NULL	NULL	NKC6 cells	GP		produce					YOR071c	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_31_19165_s_123	9235906	As shown in Table  II, NKC6 cells producing YOR071c or YOR192c protein showed the thiamin transport activities of 13.7% and 41.0%, respectively, compared with the cells expressing THI10 protein.	gene_phenotype
68911	2	333351	7	NULL	NULL	0	NULL	NKC6 cells	GP		produce					YOR192c protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_31_19165_s_123	9235906	As shown in Table  II, NKC6 cells producing YOR071c or YOR192c protein showed the thiamin transport activities of 13.7% and 41.0%, respectively, compared with the cells expressing THI10 protein.	gene_phenotype
68912	3	333351	7	NULL	NULL	NULL	NULL	statement 1	Process		shows					 thiamin	Chemical	transport activities of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_31_19165_s_123	9235906	As shown in Table  II, NKC6 cells producing YOR071c or YOR192c protein showed the thiamin transport activities of 13.7% and 41.0%, respectively, compared with the cells expressing THI10 protein.	gene_phenotype
68913	4	333351	7	NULL	NULL	0	NULL	statement 2	Process		shows					thiamin	Chemical	transport activities of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_31_19165_s_123	9235906	As shown in Table  II, NKC6 cells producing YOR071c or YOR192c protein showed the thiamin transport activities of 13.7% and 41.0%, respectively, compared with the cells expressing THI10 protein.	gene_phenotype
68914	5	333351	7	NULL	NULL	0	NULL	Cells	Cell		express					THI10 protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_31_19165_s_123	9235906	As shown in Table  II, NKC6 cells producing YOR071c or YOR192c protein showed the thiamin transport activities of 13.7% and 41.0%, respectively, compared with the cells expressing THI10 protein.	gene_phenotype
68915	6	333351	7	NULL	NULL	0	NULL	statement 5	Process		shows					thiamin	Chemical	transport activities of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_31_19165_s_123	9235906	As shown in Table  II, NKC6 cells producing YOR071c or YOR192c protein showed the thiamin transport activities of 13.7% and 41.0%, respectively, compared with the cells expressing THI10 protein.	gene_phenotype
68916	1	333352	7	NULL	NULL	0	NULL	MEI5 YPL121c Meiotic protein	GP		required for					synapsis	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_314	15334557	MEI5   YPL121c Meiotic protein required for synapsis and meiotic recombination	gene_phenotype
68917	2	333352	7	NULL	NULL	0	NULL	MEI5 YPL121c Meiotic protein	GP		required for					meiotic recombination	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_314	15334557	MEI5   YPL121c Meiotic protein required for synapsis and meiotic recombination	gene_phenotype
68918	1	333353	7	NULL	NULL	0	NULL	Ppp4c-R2	GP		is essential for					microtubule-related processes 	GP	centrosomes			NULL	higher eukaryotes	0	NULL	NULL	NULL	abs-batch0740-0759_febs-j_273_14_16857015_s_6	16857015	Despite the essential function of Ppp4c-R2 in microtubule-related  processes at centrosomes in higher eukaryotes, S. cerevisiae diploid strains  with homozygous deletion of YBL046w and two or one functional copies of  the TUB2 gene were viable and no more sensitive to microtubule-depolymerizing  drugs than the control strain.	gene_phenotype
68919	2	333353	7	NULL	NULL	0	NULL	YBL046w	GP	S. cerevisiae;;diploid strains with homozygous deletion of	is					viable	Process				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_febs-j_273_14_16857015_s_6	16857015	Despite the essential function of Ppp4c-R2 in microtubule-related  processes at centrosomes in higher eukaryotes, S. cerevisiae diploid strains  with homozygous deletion of YBL046w and two or one functional copies of  the TUB2 gene were viable and no more sensitive to microtubule-depolymerizing  drugs than the control strain.	gene_phenotype
68920	3	333353	7	NULL	NULL	NULL	NULL	TUB2 gene	GP	S. cerevisiae;;diploid strains with homozygous deletion of 	is 					viable	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_febs-j_273_14_16857015_s_6	16857015	Despite the essential function of Ppp4c-R2 in microtubule-related  processes at centrosomes in higher eukaryotes, S. cerevisiae diploid strains  with homozygous deletion of YBL046w and two or one functional copies of  the TUB2 gene were viable and no more sensitive to microtubule-depolymerizing  drugs than the control strain.	gene_phenotype
68921	4	333353	7	NULL	NULL	NULL	NULL	statement 2	Process		is not sensitive to					microtubule-depolymerizing drugs	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_febs-j_273_14_16857015_s_6	16857015	Despite the essential function of Ppp4c-R2 in microtubule-related  processes at centrosomes in higher eukaryotes, S. cerevisiae diploid strains  with homozygous deletion of YBL046w and two or one functional copies of  the TUB2 gene were viable and no more sensitive to microtubule-depolymerizing  drugs than the control strain.	gene_phenotype
68922	5	333353	7	NULL	NULL	0	NULL	statement 3	Process		is not sensitive to					microtubule-depolymerizing drugs	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_febs-j_273_14_16857015_s_6	16857015	Despite the essential function of Ppp4c-R2 in microtubule-related  processes at centrosomes in higher eukaryotes, S. cerevisiae diploid strains  with homozygous deletion of YBL046w and two or one functional copies of  the TUB2 gene were viable and no more sensitive to microtubule-depolymerizing  drugs than the control strain.	gene_phenotype
68923	1	333355	7	NULL	NULL	0	NULL	Ybr296c protein	GP		is a type of					Na+-coupled phosphate transporter of the plasma membrane	GP	high-affinity			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1422_3_255_s_159	10548719	The strong sequence identity (45%) and similarity (67%) [ 15 and  73] between this gene product and the previously identified Pho-4 phosphate transporter of the related organism  Neurospora crassa [  83] suggested that the Ybr296c protein might be the previously proposed high-affinity Na+-coupled phosphate transporter of the plasma membrane [ 16].	gene_phenotype
68924	1	333356	7	NULL	NULL	NULL	NULL	YDL074C	GP	deletion of	increase					chromosome 	Chromosome	loss of			NULL	haploid strain	NULL	NULL	NULL	NULL	gw60_pnas_97_24_13203_s_108	11087867	Interestingly, however, deletion of the gene encoding one of these proteins (YDL074C), in a haploid strain, results in an approximately 10-fold increase in the rate of chromosome loss (J.R.S.N. and P.S.K., unpublished data), as measured by a colony sectoring assay ( 36).	gene_phenotype
68925	1	333357	7	NULL	NULL	0	NULL	YDR208w PTP2	GP		downregulate					Hog1p	GP	sporulation of			NULL		0	NULL	NULL	NULL	gw70_yeast_19_7_587_s_66	11967829	YDR208w   PTP2 Downregulate Hog1p and Fus3p MAPK, sporulation (James  et al., [ 1992]; Maeda  et al., [ 1994]; Wurgler-Murphy  et al., [ 1997]; Zhan  et al., [ 2000])	gene_phenotype
68926	2	333357	7	NULL	NULL	0	NULL	YDR208w PTP2	GP		downregulate					Fus3p MAPK	GP	sporulation of			NULL		0	NULL	NULL	NULL	gw70_yeast_19_7_587_s_66	11967829	YDR208w   PTP2 Downregulate Hog1p and Fus3p MAPK, sporulation (James  et al., [ 1992]; Maeda  et al., [ 1994]; Wurgler-Murphy  et al., [ 1997]; Zhan  et al., [ 2000])	gene_phenotype
68927	1	333358	7	NULL	NULL	0	NULL	YGR046w	GP	 Saccharomyces cerevisiae 	encode					Mmp37p	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_9_4051_s_27	16790493	We demonstrate that the  Saccharomyces cerevisiae open reading frame (ORF) YGR046w encoding Mmp37p is nonessential for yeast cell viability at 30 degrees C.	gene_phenotype
68928	2	333358	7	NULL	NULL	0	NULL	statement 1	Process		is nonessential for					 yeast cell	Cell	viability of			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_9_4051_s_27	16790493	We demonstrate that the  Saccharomyces cerevisiae open reading frame (ORF) YGR046w encoding Mmp37p is nonessential for yeast cell viability at 30 degrees C.	gene_phenotype
68929	3	333358	7	NULL	NULL	0	NULL	ORF	GP		is 					open reading frame	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_9_4051_s_27	16790493	We demonstrate that the  Saccharomyces cerevisiae open reading frame (ORF) YGR046w encoding Mmp37p is nonessential for yeast cell viability at 30 degrees C.	gene_phenotype
68930	1	333359	7	NULL	NULL	0	NULL	YJR059w	GP		corresponds to					PTK2/STK2	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_20_7654_s_137	11003661	YJR059w corresponds to  PTK2/STK2, the protein kinase gene previously described as being required for polyamine transport ( 26,  36).	gene_phenotype
68931	2	333359	7	NULL	NULL	0	NULL	PTK2/STK2	GP		is a type of					protein kinase gene	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_20_7654_s_137	11003661	YJR059w corresponds to  PTK2/STK2, the protein kinase gene previously described as being required for polyamine transport ( 26,  36).	gene_phenotype
68932	3	333359	7	NULL	NULL	0	NULL	PTK2/STK2	GP		is required for					polyamine transport	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_20_7654_s_137	11003661	YJR059w corresponds to  PTK2/STK2, the protein kinase gene previously described as being required for polyamine transport ( 26,  36).	gene_phenotype
68933	1	333360	7	NULL	NULL	NULL	NULL	Nse5	GP	budding yeast	does not have 					sequence homologues	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1617_s_120	16478984	Nse5 and Nse6, like KRE29 and YML023c in budding yeast, have no sequence homologues in other species.	gene_phenotype
68934	2	333360	7	NULL	NULL	0	NULL	Nse6	GP	budding yeast	does not have					sequence homologue	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1617_s_120	16478984	Nse5 and Nse6, like KRE29 and YML023c in budding yeast, have no sequence homologues in other species.	gene_phenotype
68935	3	333360	7	NULL	NULL	0	NULL	KRE29	GP	budding yeast	does not have					sequence homologues	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1617_s_120	16478984	Nse5 and Nse6, like KRE29 and YML023c in budding yeast, have no sequence homologues in other species.	gene_phenotype
68936	4	333360	7	NULL	NULL	0	NULL	YML023c	GP	budding yeast	does not have					sequence homologues	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1617_s_120	16478984	Nse5 and Nse6, like KRE29 and YML023c in budding yeast, have no sequence homologues in other species.	gene_phenotype
68937	1	333361	7	NULL	NULL	NULL	NULL	KRE29	GP		is homologous to		functionally			Nse5	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1617_s_386	16478984	It is possible that KRE29/YML023c and Nse5/6 are functionally homologous; however; KRE29 and YML023c are both essential for viability, whereas Nse5 and Nse6 are not.	gene_phenotype
68938	2	333361	7	NULL	NULL	NULL	NULL	YML023c	GP		is homologous to		functionally			Nse5	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1617_s_386	16478984	It is possible that KRE29/YML023c and Nse5/6 are functionally homologous; however; KRE29 and YML023c are both essential for viability, whereas Nse5 and Nse6 are not.	gene_phenotype
68939	3	333361	7	NULL	NULL	0	NULL	KRE29	GP		is essential for					viability	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1617_s_386	16478984	It is possible that KRE29/YML023c and Nse5/6 are functionally homologous; however; KRE29 and YML023c are both essential for viability, whereas Nse5 and Nse6 are not.	gene_phenotype
68940	4	333361	7	NULL	NULL	0	NULL	YML023c	GP		is essential for					viability	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1617_s_386	16478984	It is possible that KRE29/YML023c and Nse5/6 are functionally homologous; however; KRE29 and YML023c are both essential for viability, whereas Nse5 and Nse6 are not.	gene_phenotype
68941	5	333361	7	NULL	NULL	0	NULL	Nse5	GP		is not essential for					viability	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1617_s_386	16478984	It is possible that KRE29/YML023c and Nse5/6 are functionally homologous; however; KRE29 and YML023c are both essential for viability, whereas Nse5 and Nse6 are not.	gene_phenotype
68942	6	333361	7	NULL	NULL	0	NULL	Nse6 	GP		is not essential for					viability	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1617_s_386	16478984	It is possible that KRE29/YML023c and Nse5/6 are functionally homologous; however; KRE29 and YML023c are both essential for viability, whereas Nse5 and Nse6 are not.	gene_phenotype
68943	7	333361	7	NULL	NULL	0	NULL	KRE29	GP		is homologous to		functionally			Nse6	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1617_s_386	16478984	It is possible that KRE29/YML023c and Nse5/6 are functionally homologous; however; KRE29 and YML023c are both essential for viability, whereas Nse5 and Nse6 are not.	gene_phenotype
68944	8	333361	7	NULL	NULL	0	NULL	YML023c	GP		is homologous to		functionally			Nse6	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1617_s_386	16478984	It is possible that KRE29/YML023c and Nse5/6 are functionally homologous; however; KRE29 and YML023c are both essential for viability, whereas Nse5 and Nse6 are not.	gene_phenotype
68945	1	333362	7	NULL	NULL	NULL	NULL	SMC5/6 complex	GP	budding yeast	contains					Nse1	GP		well-conserved non-SMC subunits		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1617_s_36	16478984	In addition to the four well-conserved non-SMC subunits (Nse1 to -4), the budding yeast SMC5/6 complex contains two other essential subunits, YML023c and KRE29, which are not conserved at the primary sequence level in other species ( ,  ).	gene_phenotype
68946	2	333362	7	NULL	NULL	0	NULL	SMC5/6 complex	GP	budding yeast	contains					Nse2	GP		well-conserved non-SMC subunits		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1617_s_36	16478984	In addition to the four well-conserved non-SMC subunits (Nse1 to -4), the budding yeast SMC5/6 complex contains two other essential subunits, YML023c and KRE29, which are not conserved at the primary sequence level in other species ( ,  ).	gene_phenotype
68947	3	333362	7	NULL	NULL	NULL	NULL	SMC5/6 complex	GP	budding yeast	contains					Nse3	GP		well-conserved non-SMC subunits 		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1617_s_36	16478984	In addition to the four well-conserved non-SMC subunits (Nse1 to -4), the budding yeast SMC5/6 complex contains two other essential subunits, YML023c and KRE29, which are not conserved at the primary sequence level in other species ( ,  ).	gene_phenotype
68948	4	333362	7	NULL	NULL	NULL	NULL	SMC5/6 complex 	GP	budding yeast	contains					Nse4	GP		well-conserved non-SMC subunits		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_5_1617_s_36	16478984	In addition to the four well-conserved non-SMC subunits (Nse1 to -4), the budding yeast SMC5/6 complex contains two other essential subunits, YML023c and KRE29, which are not conserved at the primary sequence level in other species ( ,  ).	gene_phenotype
68949	5	333362	7	NULL	NULL	0	NULL	SMC5/6 complex 	GP	budding yeast	contains					YML023c subunits	GP	essential			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1617_s_36	16478984	In addition to the four well-conserved non-SMC subunits (Nse1 to -4), the budding yeast SMC5/6 complex contains two other essential subunits, YML023c and KRE29, which are not conserved at the primary sequence level in other species ( ,  ).	gene_phenotype
68950	6	333362	7	NULL	NULL	0	NULL	SMC5/6 complex	GP	budding yeast	contains					KRE29 subunits	GP	essential			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_5_1617_s_36	16478984	In addition to the four well-conserved non-SMC subunits (Nse1 to -4), the budding yeast SMC5/6 complex contains two other essential subunits, YML023c and KRE29, which are not conserved at the primary sequence level in other species ( ,  ).	gene_phenotype
69095	1	333363	7	NULL	NULL	0	NULL	SIL1 ORF	GP	deltasil1 null mutant	is non-essential for					viability	Process				NULL		0	NULL	NULL	NULL	gw60_embo_19_23_6440_s_136	11101517	Phenotypic analysis of a deltasil1 null mutant   The  SIL1 ORF (YOL031c) was disrupted as part of the Eurofan project and shown to be non-essential for viability.	gene_phenotype
69096	1	333364	7	NULL	NULL	0	NULL	GYP1	GP		is a type of					GTPase activating protein	GP				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_109	10436161	GYP1 ( YOR070C) is a GTPase activating protein for Sec4p, a protein in the secretion pathway ( 16).	gene_phenotype
69097	2	333364	7	NULL	NULL	0	NULL	GYP1	GP		is					YOR070C	GP				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_109	10436161	GYP1 ( YOR070C) is a GTPase activating protein for Sec4p, a protein in the secretion pathway ( 16).	gene_phenotype
69098	3	333364	7	NULL	NULL	0	NULL	statement 1	Process		is required for					Sec4p	GP				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_109	10436161	GYP1 ( YOR070C) is a GTPase activating protein for Sec4p, a protein in the secretion pathway ( 16).	gene_phenotype
69099	4	333364	7	NULL	NULL	0	NULL	Sec4p	GP		is a protein in					secretion pathway	Process				NULL		0	NULL	NULL	NULL	gw60_science_285_5429_901_s_109	10436161	GYP1 ( YOR070C) is a GTPase activating protein for Sec4p, a protein in the secretion pathway ( 16).	gene_phenotype
69100	1	333365	7	NULL	NULL	0	NULL	YPL157W gene 	GP	yeast strain;null mutation	is found to be					viable	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_98_18_10380_s_205	11517327	The yeast strain with null mutation of YPL157W gene has been generated by the  Saccharomyces Genome Deletion Project and has turned out to be viable.	gene_phenotype
69101	1	333366	7	NULL	NULL	0	NULL	YBL051C	GP		designated as					PIN4	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_7_2779_s_207	15024067	In another study,  YBL051C was designated  PIN4 because it is present on a plasmid that can induce prion formation in yeast cells when overexpressed at very high levels ( ).	gene_phenotype
69103	2	333366	7	NULL	NULL	0	NULL	statement 1	Process		induce					prion	GP	formation of			NULL	yeast cells	0	NULL	NULL	NULL	gw70_molcellbiol_24_7_2779_s_207	15024067	In another study,  YBL051C was designated  PIN4 because it is present on a plasmid that can induce prion formation in yeast cells when overexpressed at very high levels ( ).	gene_phenotype
69104	3	333366	7	NULL	NULL	0	NULL	statement 2	Process		occurs when					high levels	Process	overexpressed at			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_7_2779_s_207	15024067	In another study,  YBL051C was designated  PIN4 because it is present on a plasmid that can induce prion formation in yeast cells when overexpressed at very high levels ( ).	gene_phenotype
69105	1	333367	7	NULL	NULL	NULL	NULL	cells 	Cell	S. cerevisiae;;depleted of Ybr004cp	have					cell walls	Cell	weakened			NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_febs-j_272_5_15720390_s_4	15720390	S. cerevisiae cells depleted of Ybr004cp have weakened cell  walls and abnormal morphology, are unable to incorporate [3]inositol  into proteins, and accumulate a GPI intermediate having a single mannose  that is likely modified with ethanolamine phosphate.	gene_phenotype
69106	2	333367	7	NULL	NULL	NULL	NULL	cells	Cell	S. cerevisiae;;depleted of Ybr004cp	have					 morphology	Process	abnormal			NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_febs-j_272_5_15720390_s_4	15720390	S. cerevisiae cells depleted of Ybr004cp have weakened cell  walls and abnormal morphology, are unable to incorporate [3]inositol  into proteins, and accumulate a GPI intermediate having a single mannose  that is likely modified with ethanolamine phosphate.	gene_phenotype
69107	3	333367	7	NULL	NULL	0	NULL	inositol	Chemical		incorporated into					proteins	GP				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_febs-j_272_5_15720390_s_4	15720390	S. cerevisiae cells depleted of Ybr004cp have weakened cell  walls and abnormal morphology, are unable to incorporate [3]inositol  into proteins, and accumulate a GPI intermediate having a single mannose  that is likely modified with ethanolamine phosphate.	gene_phenotype
69108	4	333367	7	NULL	NULL	0	NULL	cells	Cell	S. cerevisiae;;depleted of Ybr004cp	are unable to incorporate					statement 3	Process				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_febs-j_272_5_15720390_s_4	15720390	S. cerevisiae cells depleted of Ybr004cp have weakened cell  walls and abnormal morphology, are unable to incorporate [3]inositol  into proteins, and accumulate a GPI intermediate having a single mannose  that is likely modified with ethanolamine phosphate.	gene_phenotype
69109	5	333367	7	NULL	NULL	0	NULL	GPI intermediate	Chemical	S. cerevisiae;;depleted of Ybr004cp	have					single mannose	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_febs-j_272_5_15720390_s_4	15720390	S. cerevisiae cells depleted of Ybr004cp have weakened cell  walls and abnormal morphology, are unable to incorporate [3]inositol  into proteins, and accumulate a GPI intermediate having a single mannose  that is likely modified with ethanolamine phosphate.	gene_phenotype
69110	6	333367	7	NULL	NULL	0	NULL	GPI intermediate	Chemical	single mannose	is modified with					ethanolamine phosphate	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_febs-j_272_5_15720390_s_4	15720390	S. cerevisiae cells depleted of Ybr004cp have weakened cell  walls and abnormal morphology, are unable to incorporate [3]inositol  into proteins, and accumulate a GPI intermediate having a single mannose  that is likely modified with ethanolamine phosphate.	gene_phenotype
69111	7	333367	7	NULL	NULL	0	NULL	Cells	Cell	S. cerevisiae;;depleted of Ybr004cp	accumulate					GPI intermediate	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_febs-j_272_5_15720390_s_4	15720390	S. cerevisiae cells depleted of Ybr004cp have weakened cell  walls and abnormal morphology, are unable to incorporate [3]inositol  into proteins, and accumulate a GPI intermediate having a single mannose  that is likely modified with ethanolamine phosphate.	gene_phenotype
69112	1	333369	7	NULL	NULL	0	NULL	CSM1	GP		is					chromosome segregation in meiosis	GP				NULL		0	NULL	NULL	NULL	gw60_devcell_4_4_535_s_81	12689592	CSM1 (chromosome segregation in meiosis; ORF YCR086W) has already been shown to have a role in meiotic chromosome segregation  (Rabitsch et al., 2001  ).	gene_phenotype
69113	2	333369	7	NULL	NULL	0	NULL	CSM1	GP		have a role in					meiotic chromosome segregation	Process				NULL		0	NULL	NULL	NULL	gw60_devcell_4_4_535_s_81	12689592	CSM1 (chromosome segregation in meiosis; ORF YCR086W) has already been shown to have a role in meiotic chromosome segregation  (Rabitsch et al., 2001  ).	gene_phenotype
69114	1	333370	7	NULL	NULL	NULL	NULL	Yer010c protein	GP		shares					RraA family	GP	a common fold with proteins of regulators of			NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_protein-sci_14_10_16195557_s_2	16195557	We present here the structure of Yer010c protein of unknown function, solved  by Multiple Anomalous Diffraction and revealing a common fold and oligomerization  state with proteins of the regulator of ribonuclease activity A (RraA)  family.	gene_phenotype
69115	2	333370	7	NULL	NULL	NULL	NULL	Yer010c protein	GP		shares					RraA family	GP	oligomerization state with proteins of regulators of			NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_protein-sci_14_10_16195557_s_2	16195557	We present here the structure of Yer010c protein of unknown function, solved  by Multiple Anomalous Diffraction and revealing a common fold and oligomerization  state with proteins of the regulator of ribonuclease activity A (RraA)  family.	gene_phenotype
69116	3	333370	7	NULL	NULL	0	NULL	RraA	GP		is					ribonuclease activity A 	GP				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_protein-sci_14_10_16195557_s_2	16195557	We present here the structure of Yer010c protein of unknown function, solved  by Multiple Anomalous Diffraction and revealing a common fold and oligomerization  state with proteins of the regulator of ribonuclease activity A (RraA)  family.	gene_phenotype
69117	1	333371	7	NULL	NULL	0	NULL	YHR158c	GP	overexpression of	suppresses		partially			mating defect	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_143_2_375_s_202	9786949	We conclude that overexpression of YHR158c partially suppresses the  mating defect exhibited by a subset of mutants defective in  cell fusion.	gene_phenotype
69118	2	333371	7	NULL	NULL	NULL	NULL	cell fusion	Process	subset of mutants defective in	shows					mating defect	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_143_2_375_s_202	9786949	We conclude that overexpression of YHR158c partially suppresses the  mating defect exhibited by a subset of mutants defective in  cell fusion.	gene_phenotype
69119	1	333372	7	NULL	NULL	0	NULL	ORF YIL019w	GP		is					FAF1	GP				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_319_2_349_s_62	15178413	ORF  YIL019w ( FAF1) encodes a protein of 346 amino acids essential for cell viability.	gene_phenotype
69120	2	333372	7	NULL	NULL	0	NULL	FAF1	GP		encode					 protein of 346 amino acids 	GP				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_319_2_349_s_62	15178413	ORF  YIL019w ( FAF1) encodes a protein of 346 amino acids essential for cell viability.	gene_phenotype
69121	3	333372	7	NULL	NULL	0	NULL	statement 1	GP		essential for					cell viability	Process				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_319_2_349_s_62	15178413	ORF  YIL019w ( FAF1) encodes a protein of 346 amino acids essential for cell viability.	gene_phenotype
69122	1	333373	7	NULL	NULL	0	NULL	YLL060C	GP	protein product of	activates					GST	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_45_29915_s_125	9792709	Again, after we had confirmed that the protein product of YLL060C exhibits GST activity (described below), we named it  GTT2 ( gluta thione  transferase  2).	gene_phenotype
69123	2	333373	7	NULL	NULL	0	NULL	YLL060C	GP	protein product of	is					GTT2	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_45_29915_s_125	9792709	Again, after we had confirmed that the protein product of YLL060C exhibits GST activity (described below), we named it  GTT2 ( gluta thione  transferase  2).	gene_phenotype
69124	3	333373	7	NULL	NULL	0	NULL	GTT2	GP		is					gluta thione transferase 2	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_45_29915_s_125	9792709	Again, after we had confirmed that the protein product of YLL060C exhibits GST activity (described below), we named it  GTT2 ( gluta thione  transferase  2).	gene_phenotype
69125	1	333375	7	NULL	NULL	0	NULL	YLR226w	GP		encode					BUR2	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7080_s_113	10982824	These results indicate that YLR226w encodes  BUR2, that  BUR2 is not essential for viability but is important for normal growth, and that loss of function causes the Bur  phenotype.	gene_phenotype
69126	2	333375	7	NULL	NULL	0	NULL	BUR2	GP		is not essential for					viability 	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7080_s_113	10982824	These results indicate that YLR226w encodes  BUR2, that  BUR2 is not essential for viability but is important for normal growth, and that loss of function causes the Bur  phenotype.	gene_phenotype
69127	3	333375	7	NULL	NULL	0	NULL	BUR2	GP		is important for					normal growth	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7080_s_113	10982824	These results indicate that YLR226w encodes  BUR2, that  BUR2 is not essential for viability but is important for normal growth, and that loss of function causes the Bur  phenotype.	gene_phenotype
69128	4	333375	7	NULL	NULL	0	NULL	function	Process	loss of	cause					Bur phenotype	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7080_s_113	10982824	These results indicate that YLR226w encodes  BUR2, that  BUR2 is not essential for viability but is important for normal growth, and that loss of function causes the Bur  phenotype.	gene_phenotype
69129	1	333376	7	NULL	NULL	0	NULL	YLR285W	GP	manipulation of	affects					lifespan	Process				NULL		0	NULL	NULL	NULL	gw70_nature_423_6936_181_s_107	12736687	e, Manipulation of YLR285W affects lifespan.	gene_phenotype
69130	1	333377	7	NULL	NULL	0	NULL	YLR285W	GP		increase					lifespan	Process	yeast			NULL		0	NULL	NULL	NULL	gw70_nature_423_6936_181_s_122	12736687	Additional copies of YLR285W increased yeast lifespan and this effect was not enhanced  by glucose restriction ( Fig. 4e).	gene_phenotype
69131	2	333377	7	NULL	NULL	0	NULL	glucose	Chemical	restriction of	does not enhance					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_nature_423_6936_181_s_122	12736687	Additional copies of YLR285W increased yeast lifespan and this effect was not enhanced  by glucose restriction ( Fig. 4e).	gene_phenotype
69132	1	333378	7	NULL	NULL	0	NULL	YLR285W	GP		increase					silencing	Process				NULL		0	NULL	NULL	NULL	gw70_nature_423_6936_181_s_121	12736687	Additional copies of YLR285W increased silencing, whereas deletion of this gene  led to a loss of silencing, similar to the effect of manipulating  PNC1 (ref.  16) ( Fig. 4d).	gene_phenotype
69133	2	333378	7	NULL	NULL	0	NULL	YLR285W gene	GP	deletion of	leads to					silencing	Process	loss of			NULL		0	NULL	NULL	NULL	gw70_nature_423_6936_181_s_121	12736687	Additional copies of YLR285W increased silencing, whereas deletion of this gene  led to a loss of silencing, similar to the effect of manipulating  PNC1 (ref.  16) ( Fig. 4d).	gene_phenotype
69134	3	333378	7	NULL	NULL	0	NULL	statement 2	Process		similar to					PNC1	GP	effect of manipulating			NULL		0	NULL	NULL	NULL	gw70_nature_423_6936_181_s_121	12736687	Additional copies of YLR285W increased silencing, whereas deletion of this gene  led to a loss of silencing, similar to the effect of manipulating  PNC1 (ref.  16) ( Fig. 4d).	gene_phenotype
69135	1	333379	7	NULL	NULL	0	NULL	YLR285W	GP		is not a true					longevity regulator	Process				NULL		0	NULL	NULL	NULL	gw70_nature_423_6936_181_s_123	12736687	Unlike  PNC1, YLR285W is not a true longevity regulator because its expression is not apparently  modulated by stimuli that extend lifespan 18, and its deletion does not abolish lifespan extension by glucose restriction ( Fig. 4e).	gene_phenotype
69136	2	333379	7	NULL	NULL	0	NULL	YLR285W	GP		is not like					PNC1	GP				NULL		0	NULL	NULL	NULL	gw70_nature_423_6936_181_s_123	12736687	Unlike  PNC1, YLR285W is not a true longevity regulator because its expression is not apparently  modulated by stimuli that extend lifespan 18, and its deletion does not abolish lifespan extension by glucose restriction ( Fig. 4e).	gene_phenotype
69137	3	333379	7	NULL	NULL	0	NULL	YLR285W	GP	expression of	 not modulated by		apparently			lifespan	Process	stimuli extending			NULL		0	NULL	NULL	NULL	gw70_nature_423_6936_181_s_123	12736687	Unlike  PNC1, YLR285W is not a true longevity regulator because its expression is not apparently  modulated by stimuli that extend lifespan 18, and its deletion does not abolish lifespan extension by glucose restriction ( Fig. 4e).	gene_phenotype
69138	4	333379	7	NULL	NULL	0	NULL	lifespan	Process		extend by					glucose	Chemical	restriction of			NULL		0	NULL	NULL	NULL	gw70_nature_423_6936_181_s_123	12736687	Unlike  PNC1, YLR285W is not a true longevity regulator because its expression is not apparently  modulated by stimuli that extend lifespan 18, and its deletion does not abolish lifespan extension by glucose restriction ( Fig. 4e).	gene_phenotype
69139	5	333379	7	NULL	NULL	0	NULL	YLR285W	GP	deletion of	does not abolish					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_nature_423_6936_181_s_123	12736687	Unlike  PNC1, YLR285W is not a true longevity regulator because its expression is not apparently  modulated by stimuli that extend lifespan 18, and its deletion does not abolish lifespan extension by glucose restriction ( Fig. 4e).	gene_phenotype
69140	1	333381	7	NULL	NULL	0	NULL	NPL6 YMR091c 	GP		is a type of					nuclear protein	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_202	15334557	NPL6   YMR091c Nuclear protein, possible role in nuclear protein import	gene_phenotype
69141	2	333381	7	NULL	NULL	0	NULL	statement 1	GP		role in		possible			nuclear protein	GP	import of			NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_202	15334557	NPL6   YMR091c Nuclear protein, possible role in nuclear protein import	gene_phenotype
69142	1	333383	7	NULL	NULL	NULL	NULL	IST2 mRNA	NucleicAcid		localize				RNA motifs from	bud tip	CellComponent	reporter mRNA to			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4752_s_311	15899876	As shown in Fig.  7D, the RNA motifs from the  IST2 and  YMR171c mRNAs were able to localize a reporter mRNA to the bud tip, suggesting that both act as functional localization elements.	gene_phenotype
69143	2	333383	7	NULL	NULL	NULL	NULL	YMR171c mRNA	NucleicAcid		localize				RNA motifs from	bud tip	CellComponent	reporter mRNA to			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4752_s_311	15899876	As shown in Fig.  7D, the RNA motifs from the  IST2 and  YMR171c mRNAs were able to localize a reporter mRNA to the bud tip, suggesting that both act as functional localization elements.	gene_phenotype
69144	3	333383	7	NULL	NULL	0	NULL	IST2 mRNA	NucleicAcid		act as					 functional localization elements	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_11_4752_s_311	15899876	As shown in Fig.  7D, the RNA motifs from the  IST2 and  YMR171c mRNAs were able to localize a reporter mRNA to the bud tip, suggesting that both act as functional localization elements.	gene_phenotype
69145	4	333383	7	NULL	NULL	NULL	NULL	YMR171c mRNA	NucleicAcid		act as 					 functional localization elements	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4752_s_311	15899876	As shown in Fig.  7D, the RNA motifs from the  IST2 and  YMR171c mRNAs were able to localize a reporter mRNA to the bud tip, suggesting that both act as functional localization elements.	gene_phenotype
69146	5	333383	7	NULL	NULL	0	NULL	statement 1	Process		suggest					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_11_4752_s_311	15899876	As shown in Fig.  7D, the RNA motifs from the  IST2 and  YMR171c mRNAs were able to localize a reporter mRNA to the bud tip, suggesting that both act as functional localization elements.	gene_phenotype
69147	6	333383	7	NULL	NULL	0	NULL	statement 2	Process		suggest					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_11_4752_s_311	15899876	As shown in Fig.  7D, the RNA motifs from the  IST2 and  YMR171c mRNAs were able to localize a reporter mRNA to the bud tip, suggesting that both act as functional localization elements.	gene_phenotype
69148	1	333384	7	NULL	NULL	NULL	NULL	She2p	GP		recognize					 ASH1 mRNA	NucleicAcid	bud-localized		RNA motif in the localization elements of	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_11_4752_s_340	15899876	The identification of the same RNA motif in the localization elements of the bud-localized  ASH1,  IST2, and  YMR171c mRNAs strongly supports our conclusion that this motif contains the main determinants required for their recognition by She2p.	gene_phenotype
69149	2	333384	7	NULL	NULL	0	NULL	She2p	GP		recognize					 IST2 mRNA	NucleicAcid	bud-localized		RNA motif in the localization elements of	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_11_4752_s_340	15899876	The identification of the same RNA motif in the localization elements of the bud-localized  ASH1,  IST2, and  YMR171c mRNAs strongly supports our conclusion that this motif contains the main determinants required for their recognition by She2p.	gene_phenotype
69150	3	333384	7	NULL	NULL	0	NULL	She2p	GP		recognize					YMR171c mRNA	NucleicAcid	bud-localized		RNA motif in the localization elements of	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_11_4752_s_340	15899876	The identification of the same RNA motif in the localization elements of the bud-localized  ASH1,  IST2, and  YMR171c mRNAs strongly supports our conclusion that this motif contains the main determinants required for their recognition by She2p.	gene_phenotype
69151	1	333385	7	NULL	NULL	0	NULL	YOR129c	GP	S.cerevisiae	is not required for					viability	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3658_s_283	15155805	In  S. cerevisiae, YOR129c is not required for viability (Winzeler  et al., 1999 ), but the observation that its expression is induced by mating pheromone in a Ste12p-dependent manner suggests that it may play a role in mating (Ren  et al., 2000 ).	gene_phenotype
69152	2	333385	7	NULL	NULL	0	NULL	YOR129c	GP	expression of	induced by					mating pheromone	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3658_s_283	15155805	In  S. cerevisiae, YOR129c is not required for viability (Winzeler  et al., 1999 ), but the observation that its expression is induced by mating pheromone in a Ste12p-dependent manner suggests that it may play a role in mating (Ren  et al., 2000 ).	gene_phenotype
69153	3	333385	7	NULL	NULL	0	NULL	statement 2	Process		depends on					Ste12p	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3658_s_283	15155805	In  S. cerevisiae, YOR129c is not required for viability (Winzeler  et al., 1999 ), but the observation that its expression is induced by mating pheromone in a Ste12p-dependent manner suggests that it may play a role in mating (Ren  et al., 2000 ).	gene_phenotype
69154	4	333385	7	NULL	NULL	0	NULL	YOR129c	GP		play a role in		may			mating	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3658_s_283	15155805	In  S. cerevisiae, YOR129c is not required for viability (Winzeler  et al., 1999 ), but the observation that its expression is induced by mating pheromone in a Ste12p-dependent manner suggests that it may play a role in mating (Ren  et al., 2000 ).	gene_phenotype
69155	1	333386	7	NULL	NULL	0	NULL	yor129c	GP	mutant	displays					mating projections	CellComponent	no defects in formation of			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3658_s_382	15155805	However, in both unilateral and bilateral mutant crosses,  yor129c mutants displayed no obvious defects in the formation of mating projections, in cell fusion, or in mating efficiency (our unpublished results).	gene_phenotype
69156	2	333386	7	NULL	NULL	0	NULL	yor129c	GP	mutant	displays					cell fusion	Process	no defects in			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3658_s_382	15155805	However, in both unilateral and bilateral mutant crosses,  yor129c mutants displayed no obvious defects in the formation of mating projections, in cell fusion, or in mating efficiency (our unpublished results).	gene_phenotype
69157	3	333386	7	NULL	NULL	0	NULL	yor129c	GP	mutant	displays					mating efficiency	Process	no defects in			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3658_s_382	15155805	However, in both unilateral and bilateral mutant crosses,  yor129c mutants displayed no obvious defects in the formation of mating projections, in cell fusion, or in mating efficiency (our unpublished results).	gene_phenotype
69158	1	333387	7	NULL	NULL	0	NULL	Yor284w-YFP fusion	GP		localized to					mobile punctate structures 	CellComponent				NULL	cell	0	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_317	11489916	The Yor284w-YFP fusion localized to a few distinct, mobile punctate structures in the cell (Figs. 4, M and  N and 6, A and  B).	gene_phenotype
69159	1	333388	7	NULL	NULL	0	NULL	Budding yeast	Organism		contains					Mpt5/Uth4	GP		conserved Puf motif		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_4	11157761	Budding yeast,  Saccharomyces cerevisiae, has five proteins with conserved Puf motifs: Mpt5/Uth4, Ygl014w, Yll013c, Jsn1 and Ypr042c.	gene_phenotype
69160	2	333388	7	NULL	NULL	0	NULL	Budding yeast	Organism		contains					Ygl014w	GP		conserved Puf motif		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_4	11157761	Budding yeast,  Saccharomyces cerevisiae, has five proteins with conserved Puf motifs: Mpt5/Uth4, Ygl014w, Yll013c, Jsn1 and Ypr042c.	gene_phenotype
69161	3	333388	7	NULL	NULL	0	NULL	Budding yeast	Organism		contains					Yll013c	GP		conserved Puf motif		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_4	11157761	Budding yeast,  Saccharomyces cerevisiae, has five proteins with conserved Puf motifs: Mpt5/Uth4, Ygl014w, Yll013c, Jsn1 and Ypr042c.	gene_phenotype
69162	4	333388	7	NULL	NULL	0	NULL	Budding yeast	Organism		contains					Jsn1	GP		conserved Puf motif		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_4	11157761	Budding yeast,  Saccharomyces cerevisiae, has five proteins with conserved Puf motifs: Mpt5/Uth4, Ygl014w, Yll013c, Jsn1 and Ypr042c.	gene_phenotype
69163	5	333388	7	NULL	NULL	NULL	NULL	Budding yeast	Organism		contains					Ypr042c	GP		conserved Puf motif		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_552_s_4	11157761	Budding yeast,  Saccharomyces cerevisiae, has five proteins with conserved Puf motifs: Mpt5/Uth4, Ygl014w, Yll013c, Jsn1 and Ypr042c.	gene_phenotype
69164	6	333388	7	NULL	NULL	0	NULL	Saccharomyces cerevisiae	Organism		contains					Mpt5/Uth4	GP		conserved Puf motif		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_4	11157761	Budding yeast,  Saccharomyces cerevisiae, has five proteins with conserved Puf motifs: Mpt5/Uth4, Ygl014w, Yll013c, Jsn1 and Ypr042c.	gene_phenotype
69165	7	333388	7	NULL	NULL	0	NULL	Saccharomyces cerevisiae	Organism		contains					Ygl014w	GP		conserved Puf motif		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_4	11157761	Budding yeast,  Saccharomyces cerevisiae, has five proteins with conserved Puf motifs: Mpt5/Uth4, Ygl014w, Yll013c, Jsn1 and Ypr042c.	gene_phenotype
69166	8	333388	7	NULL	NULL	0	NULL	Saccharomyces cerevisiae	Organism		contains					Yll013c	GP		conserved Puf motif		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_4	11157761	Budding yeast,  Saccharomyces cerevisiae, has five proteins with conserved Puf motifs: Mpt5/Uth4, Ygl014w, Yll013c, Jsn1 and Ypr042c.	gene_phenotype
69167	9	333388	7	NULL	NULL	0	NULL	 Saccharomyces cerevisiae	Organism		contains					Jsn1	GP		conserved Puf motif		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_4	11157761	Budding yeast,  Saccharomyces cerevisiae, has five proteins with conserved Puf motifs: Mpt5/Uth4, Ygl014w, Yll013c, Jsn1 and Ypr042c.	gene_phenotype
69168	10	333388	7	NULL	NULL	0	NULL	 Saccharomyces cerevisiae	Organism		contains					Ypr042c	GP		conserved Puf motif		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_4	11157761	Budding yeast,  Saccharomyces cerevisiae, has five proteins with conserved Puf motifs: Mpt5/Uth4, Ygl014w, Yll013c, Jsn1 and Ypr042c.	gene_phenotype
69248	1	333389	7	NULL	NULL	NULL	NULL	YPR042C	GP	null mutants	display					viability 	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_552_s_30	11157761	YPR042C null mutants are viable and display increased resistance to cycloheximide and paramomycin, both of which inhibit translation ( Waskiewicz   et al., 1998).	gene_phenotype
69249	2	333389	7	NULL	NULL	0	NULL	statement 1	Process		display					cycloheximide	Chemical	increased resistance to			NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_30	11157761	YPR042C null mutants are viable and display increased resistance to cycloheximide and paramomycin, both of which inhibit translation ( Waskiewicz   et al., 1998).	gene_phenotype
69250	3	333389	7	NULL	NULL	0	NULL	statement 1	Process		display					paramomycin	Chemical	increased resistance to			NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_30	11157761	YPR042C null mutants are viable and display increased resistance to cycloheximide and paramomycin, both of which inhibit translation ( Waskiewicz   et al., 1998).	gene_phenotype
69251	4	333389	7	NULL	NULL	0	NULL	cycloheximide	Chemical		inhibit					translation 	Process				NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_30	11157761	YPR042C null mutants are viable and display increased resistance to cycloheximide and paramomycin, both of which inhibit translation ( Waskiewicz   et al., 1998).	gene_phenotype
69252	5	333389	7	NULL	NULL	NULL	NULL	paramomycin	Chemical		inhibit					translation	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_552_s_30	11157761	YPR042C null mutants are viable and display increased resistance to cycloheximide and paramomycin, both of which inhibit translation ( Waskiewicz   et al., 1998).	gene_phenotype
69253	1	333390	7	NULL	NULL	NULL	NULL	 budding yeast	Organism		contains					Mpt5	GP		three to eight Puf repeats		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_552_s_24	11157761	The budding yeast,  Saccharomyces cerevisiae, has five proteins that contain three to eight Puf repeats: Mpt5, Ygl014w, Yll013c, Jsn1 and Ypr042c ( Zhang  et al., 1997).	gene_phenotype
69254	2	333390	7	NULL	NULL	0	NULL	 budding yeast	Organism		contains					Ygl014w	GP		three to eight Puf repeats		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_24	11157761	The budding yeast,  Saccharomyces cerevisiae, has five proteins that contain three to eight Puf repeats: Mpt5, Ygl014w, Yll013c, Jsn1 and Ypr042c ( Zhang  et al., 1997).	gene_phenotype
69255	3	333390	7	NULL	NULL	0	NULL	budding yeast	Organism		contains					Yll013c	GP		three to eight Puf repeats		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_24	11157761	The budding yeast,  Saccharomyces cerevisiae, has five proteins that contain three to eight Puf repeats: Mpt5, Ygl014w, Yll013c, Jsn1 and Ypr042c ( Zhang  et al., 1997).	gene_phenotype
69256	4	333390	7	NULL	NULL	0	NULL	budding yeast	Organism		contains					Jsn1	GP		three to eight Puf repeats		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_24	11157761	The budding yeast,  Saccharomyces cerevisiae, has five proteins that contain three to eight Puf repeats: Mpt5, Ygl014w, Yll013c, Jsn1 and Ypr042c ( Zhang  et al., 1997).	gene_phenotype
69257	5	333390	7	NULL	NULL	0	NULL	budding yeast	Organism		contains					Ypr042c	GP		three to eight Puf repeats		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_24	11157761	The budding yeast,  Saccharomyces cerevisiae, has five proteins that contain three to eight Puf repeats: Mpt5, Ygl014w, Yll013c, Jsn1 and Ypr042c ( Zhang  et al., 1997).	gene_phenotype
69258	6	333390	7	NULL	NULL	0	NULL	Saccharomyces cerevisiae	Organism		contains					Mpt5	GP		three to eight Puf repeats		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_24	11157761	The budding yeast,  Saccharomyces cerevisiae, has five proteins that contain three to eight Puf repeats: Mpt5, Ygl014w, Yll013c, Jsn1 and Ypr042c ( Zhang  et al., 1997).	gene_phenotype
69259	7	333390	7	NULL	NULL	0	NULL	Saccharomyces cerevisiae	Organism		contains					Ygl014w	GP		three to eight Puf repeats		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_24	11157761	The budding yeast,  Saccharomyces cerevisiae, has five proteins that contain three to eight Puf repeats: Mpt5, Ygl014w, Yll013c, Jsn1 and Ypr042c ( Zhang  et al., 1997).	gene_phenotype
69260	8	333390	7	NULL	NULL	0	NULL	Saccharomyces cerevisiae	Organism		contains					Yll013c	GP		three to eight Puf repeats		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_24	11157761	The budding yeast,  Saccharomyces cerevisiae, has five proteins that contain three to eight Puf repeats: Mpt5, Ygl014w, Yll013c, Jsn1 and Ypr042c ( Zhang  et al., 1997).	gene_phenotype
69261	9	333390	7	NULL	NULL	0	NULL	Saccharomyces cerevisiae	Organism		contains only					Jsn1	GP		three to eight Puf repeats		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_24	11157761	The budding yeast,  Saccharomyces cerevisiae, has five proteins that contain three to eight Puf repeats: Mpt5, Ygl014w, Yll013c, Jsn1 and Ypr042c ( Zhang  et al., 1997).	gene_phenotype
69262	10	333390	7	NULL	NULL	NULL	NULL	Saccharomyces cerevisiae	Organism		contains					Ypr042c	GP		three to eight Puf repeats		NULL		NULL	NULL	NULL	NULL	gw60_embo_20_3_552_s_24	11157761	The budding yeast,  Saccharomyces cerevisiae, has five proteins that contain three to eight Puf repeats: Mpt5, Ygl014w, Yll013c, Jsn1 and Ypr042c ( Zhang  et al., 1997).	gene_phenotype
69263	1	333391	7	NULL	NULL	0	NULL	YPR094w	GP		is required for					cell viability	Process				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_2_816_s_239	12054543	To date the molecular and biological functions of  YPR094w is unknown but the systematic deletion of  YPR094w is lethal [  23], pointing out that the protein is required for cell viability.	gene_phenotype
69264	2	333391	7	NULL	NULL	0	NULL	YPR094w	GP	systematic deletion of	is lethal to					cell	Cell				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_2_816_s_239	12054543	To date the molecular and biological functions of  YPR094w is unknown but the systematic deletion of  YPR094w is lethal [  23], pointing out that the protein is required for cell viability.	gene_phenotype
69266	1	333393	7	NULL	NULL	0	NULL	 Kar9 protein	GP		play a role in					mitotic spindle	Chromosome	orienting the			NULL	budding yeast	0	NULL	NULL	NULL	gw60_cellbiol_161_3_483_s_177	12743102	The role of the proteins Kar9 and Myo2 in orienting the mitotic spindle of budding yeast.	gene_phenotype
69267	2	333393	7	NULL	NULL	NULL	NULL	Myo2 protein	GP		play a role in					mitotic spindle	Chromosome	orienting the			NULL	budding yeast	NULL	NULL	NULL	NULL	gw60_cellbiol_161_3_483_s_177	12743102	The role of the proteins Kar9 and Myo2 in orienting the mitotic spindle of budding yeast.	gene_phenotype
69268	1	333394	7	NULL	NULL	0	NULL	 YKR087c	GP	yeast	encode					Oma1 	GP	yeast			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46414_s_191	12963738	For reasons outlined below, the yeast protein encoded by YKR087c was termed Oma1 (for overlapping activity with  m-AAA protease).	gene_phenotype
69269	2	333394	7	NULL	NULL	0	NULL	Oma1 	GP		is					overlapping activity with m-AAA protease	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46414_s_191	12963738	For reasons outlined below, the yeast protein encoded by YKR087c was termed Oma1 (for overlapping activity with  m-AAA protease).	gene_phenotype
69270	1	333395	7	NULL	NULL	0	NULL	ylr328w	GP	mutant	display					viability	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_160_3_877_s_360	11901108	Since  ylr328w mutants are viable ( W INZELER et al. 1999   ), the Ygr010w protein likely provides a redundant function.	gene_phenotype
69271	1	333396	7	NULL	NULL	0	NULL	KRI1 	GP	budding yeast	is					KRR1-interacting protein	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_21_7971_s_28	11027267	Here we report the characterization of  KRR1 and a novel  KRI1 (KRR1-interacting protein; YNL308c) gene of budding yeast cells.	gene_phenotype
69272	1	333399	7	NULL	NULL	0	NULL	Munc13 protein	GP		is involved in					vesicle	CellComponent	priming of			NULL		0	NULL	NULL	NULL	gw70_genetics_173_1_49_s_257	16489217	Interestingly, two proteins in this family,  S. pombe SPAC11E3.02c and  S. cerevisiae Yor296w, were previously cited in a study identifying a family of proteins related to the Munc13 protein, which is involved in vesicle priming for neurotransmitter secretion ( OCH et al.).	gene_phenotype
69273	2	333399	7	NULL	NULL	0	NULL	statement 1	Process		required for					neurotransmitter	GP	secretion of			NULL		0	NULL	NULL	NULL	gw70_genetics_173_1_49_s_257	16489217	Interestingly, two proteins in this family,  S. pombe SPAC11E3.02c and  S. cerevisiae Yor296w, were previously cited in a study identifying a family of proteins related to the Munc13 protein, which is involved in vesicle priming for neurotransmitter secretion ( OCH et al.).	gene_phenotype
69274	1	333400	7	NULL	NULL	NULL	NULL	Ypl113cp	GP		activates					hydroxyglutarate dehydrogenase	GP				NULL	S. cerevisiae	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_12_10264_s_35	12525494	Other proteins with homology to Ser3/33p may also be candidates for having hydroxyglutarate  dehydrogenase activity in  S. cerevisiae: (i) Ypl113cp (27% identity), (ii) Ygl185cp (21-23% identity), with similarities to hydroxyacid dehydrogenases, (iii) Fdh1p (26-27% identity), a formate dehydrogenase, and (iv) Ynl274cp (25-26% identity), which is a putative hydroxyisocaproate dehydrogenase ( ).	gene_phenotype
69275	2	333400	7	NULL	NULL	0	NULL	Ygl185cp	GP		is similar to					hydroxyacid dehydrogenases	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10264_s_35	12525494	Other proteins with homology to Ser3/33p may also be candidates for having hydroxyglutarate  dehydrogenase activity in  S. cerevisiae: (i) Ypl113cp (27% identity), (ii) Ygl185cp (21-23% identity), with similarities to hydroxyacid dehydrogenases, (iii) Fdh1p (26-27% identity), a formate dehydrogenase, and (iv) Ynl274cp (25-26% identity), which is a putative hydroxyisocaproate dehydrogenase ( ).	gene_phenotype
69276	3	333400	7	NULL	NULL	0	NULL	Fdh1p	GP		is a type of					formate dehydrogenase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10264_s_35	12525494	Other proteins with homology to Ser3/33p may also be candidates for having hydroxyglutarate  dehydrogenase activity in  S. cerevisiae: (i) Ypl113cp (27% identity), (ii) Ygl185cp (21-23% identity), with similarities to hydroxyacid dehydrogenases, (iii) Fdh1p (26-27% identity), a formate dehydrogenase, and (iv) Ynl274cp (25-26% identity), which is a putative hydroxyisocaproate dehydrogenase ( ).	gene_phenotype
69277	4	333400	7	NULL	NULL	0	NULL	Ynl274cp	GP		is a type of					putative hydroxyisocaproate dehydrogenase 	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10264_s_35	12525494	Other proteins with homology to Ser3/33p may also be candidates for having hydroxyglutarate  dehydrogenase activity in  S. cerevisiae: (i) Ypl113cp (27% identity), (ii) Ygl185cp (21-23% identity), with similarities to hydroxyacid dehydrogenases, (iii) Fdh1p (26-27% identity), a formate dehydrogenase, and (iv) Ynl274cp (25-26% identity), which is a putative hydroxyisocaproate dehydrogenase ( ).	gene_phenotype
69278	5	333400	7	NULL	NULL	0	NULL	Ser3/33p	GP		activates					hydroxyglutarate dehydrogenase 	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10264_s_35	12525494	Other proteins with homology to Ser3/33p may also be candidates for having hydroxyglutarate  dehydrogenase activity in  S. cerevisiae: (i) Ypl113cp (27% identity), (ii) Ygl185cp (21-23% identity), with similarities to hydroxyacid dehydrogenases, (iii) Fdh1p (26-27% identity), a formate dehydrogenase, and (iv) Ynl274cp (25-26% identity), which is a putative hydroxyisocaproate dehydrogenase ( ).	gene_phenotype
69279	1	333403	7	NULL	NULL	0	NULL	histidine	AminoAcid		transported into					vacuoles	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_6_4851_s_94	15572352	Uptake Activities of VBA2 (delta ybr293w) and VBA3 (delta ycl069w) Mutant Vacuolar Membrane Vesicles -- VBA2 ( YBR293w) and  VBA3 ( YCL069w) mutants ( Fig. 4) express candidate genes for histidine transport into vacuoles ( Fig. 1 B), so we measured uptake activities of vacuolar membrane vesicles from these cells.	gene_phenotype
69280	2	333403	7	NULL	NULL	NULL	NULL	VBA2	GP	mutant	express					candidate genes	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_6_4851_s_94	15572352	Uptake Activities of VBA2 (delta ybr293w) and VBA3 (delta ycl069w) Mutant Vacuolar Membrane Vesicles -- VBA2 ( YBR293w) and  VBA3 ( YCL069w) mutants ( Fig. 4) express candidate genes for histidine transport into vacuoles ( Fig. 1 B), so we measured uptake activities of vacuolar membrane vesicles from these cells.	gene_phenotype
69281	3	333403	7	NULL	NULL	0	NULL	VBA3	GP	mutant	express					candidate genes	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_6_4851_s_94	15572352	Uptake Activities of VBA2 (delta ybr293w) and VBA3 (delta ycl069w) Mutant Vacuolar Membrane Vesicles -- VBA2 ( YBR293w) and  VBA3 ( YCL069w) mutants ( Fig. 4) express candidate genes for histidine transport into vacuoles ( Fig. 1 B), so we measured uptake activities of vacuolar membrane vesicles from these cells.	gene_phenotype
69282	4	333403	7	NULL	NULL	0	NULL	statement 2	Process		required for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_6_4851_s_94	15572352	Uptake Activities of VBA2 (delta ybr293w) and VBA3 (delta ycl069w) Mutant Vacuolar Membrane Vesicles -- VBA2 ( YBR293w) and  VBA3 ( YCL069w) mutants ( Fig. 4) express candidate genes for histidine transport into vacuoles ( Fig. 1 B), so we measured uptake activities of vacuolar membrane vesicles from these cells.	gene_phenotype
69283	5	333403	7	NULL	NULL	0	NULL	statement 3	Process		required for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_6_4851_s_94	15572352	Uptake Activities of VBA2 (delta ybr293w) and VBA3 (delta ycl069w) Mutant Vacuolar Membrane Vesicles -- VBA2 ( YBR293w) and  VBA3 ( YCL069w) mutants ( Fig. 4) express candidate genes for histidine transport into vacuoles ( Fig. 1 B), so we measured uptake activities of vacuolar membrane vesicles from these cells.	gene_phenotype
69284	1	333404	7	NULL	NULL	0	NULL	fnx1	GP	substrate specificity of	is similar to					 ATR1/SNQ1	GP	budding yeast			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_9_5239_s_197	9710608	The substrate specificity of fnx1 is similar to that of ATR1/SNQ1 from budding yeast; however, the amino acid sequence of ATR1/SNQ1 is not as similar to that of fnx1 as the sequence of the yet uncharacterized  S. cerevisiae ORF ybr293w (Fig.  4A).	gene_phenotype
69285	2	333404	7	NULL	NULL	NULL	NULL	ATR1/SNQ1	GP	amino acid sequence of 	is not similar to					fnx1	GP	amino acid sequence of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5239_s_197	9710608	The substrate specificity of fnx1 is similar to that of ATR1/SNQ1 from budding yeast; however, the amino acid sequence of ATR1/SNQ1 is not as similar to that of fnx1 as the sequence of the yet uncharacterized  S. cerevisiae ORF ybr293w (Fig.  4A).	gene_phenotype
69286	1	333405	7	NULL	NULL	NULL	NULL	 tcrC gene product	GP	Streptomyces aureofaciens	required for					tetracycline	Chemical	resistance to			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_9_5239_s_172	9710608	Figure  4A shows a sequence alignment with (i) the ORF that had the highest BLAST score, ybr293w from  Saccharomyces cerevisiae, which has been classified in cluster II of the subgroup by computer analysis of the budding yeast genome ( 16), and (ii) the tcrC gene product of  Streptomyces aureofaciens, which has been shown to be required for tetracycline resistance ( 7).	gene_phenotype
69287	1	333406	7	NULL	NULL	NULL	NULL	H9438 protein	GP		is similar to					DLD	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_295_4_910_s_144	12127981	The H9438 and M2267 proteins share, on average, 28% identity and 48% similarity to three yeast proteins (DLD, AIP2, and YEL071W) that are known to exhibit  -lactate dehydrogenase activity [ 6.	gene_phenotype
69288	2	333406	7	NULL	NULL	NULL	NULL	H9438 protein	GP		is similar to					AIP2	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_295_4_910_s_144	12127981	The H9438 and M2267 proteins share, on average, 28% identity and 48% similarity to three yeast proteins (DLD, AIP2, and YEL071W) that are known to exhibit  -lactate dehydrogenase activity [ 6.	gene_phenotype
69289	3	333406	7	NULL	NULL	NULL	NULL	H9438 protein	GP		is similar to					YEL071W	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_295_4_910_s_144	12127981	The H9438 and M2267 proteins share, on average, 28% identity and 48% similarity to three yeast proteins (DLD, AIP2, and YEL071W) that are known to exhibit  -lactate dehydrogenase activity [ 6.	gene_phenotype
69290	4	333406	7	NULL	NULL	0	NULL	M2267 protein	GP		is similar to					DLD	GP	yeast			NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_295_4_910_s_144	12127981	The H9438 and M2267 proteins share, on average, 28% identity and 48% similarity to three yeast proteins (DLD, AIP2, and YEL071W) that are known to exhibit  -lactate dehydrogenase activity [ 6.	gene_phenotype
69291	5	333406	7	NULL	NULL	0	NULL	M2267 protein	GP		is similar to					AIP2	GP	yeast			NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_295_4_910_s_144	12127981	The H9438 and M2267 proteins share, on average, 28% identity and 48% similarity to three yeast proteins (DLD, AIP2, and YEL071W) that are known to exhibit  -lactate dehydrogenase activity [ 6.	gene_phenotype
69292	6	333406	7	NULL	NULL	NULL	NULL	M2267 protein	GP		is similar to					YEL071W	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_295_4_910_s_144	12127981	The H9438 and M2267 proteins share, on average, 28% identity and 48% similarity to three yeast proteins (DLD, AIP2, and YEL071W) that are known to exhibit  -lactate dehydrogenase activity [ 6.	gene_phenotype
69293	7	333406	7	NULL	NULL	0	NULL	DLD	GP	yeast	activates					lactate dehydrogenase 	GP				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_295_4_910_s_144	12127981	The H9438 and M2267 proteins share, on average, 28% identity and 48% similarity to three yeast proteins (DLD, AIP2, and YEL071W) that are known to exhibit  -lactate dehydrogenase activity [ 6.	gene_phenotype
69294	8	333406	7	NULL	NULL	0	NULL	AIP2	GP	yeast	activates					lactate dehydrogenase 	GP				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_295_4_910_s_144	12127981	The H9438 and M2267 proteins share, on average, 28% identity and 48% similarity to three yeast proteins (DLD, AIP2, and YEL071W) that are known to exhibit  -lactate dehydrogenase activity [ 6.	gene_phenotype
69295	9	333406	7	NULL	NULL	0	NULL	YEL071W	GP	yeast	activates					lactate dehydrogenase 	GP				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_295_4_910_s_144	12127981	The H9438 and M2267 proteins share, on average, 28% identity and 48% similarity to three yeast proteins (DLD, AIP2, and YEL071W) that are known to exhibit  -lactate dehydrogenase activity [ 6.	gene_phenotype
69296	1	333407	7	NULL	NULL	0	NULL	YIL006w	GP		characterized as		functionally			Ndt1p	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_8_2617_s_185	16469842	The previously proposed pyruvate carrier, YIL006w, has now been identified and functionally characterized as the mitochondrial NAD carrier protein (Ndt1p) by using transport assays with purified protein reconstituted into liposomes ( ).	gene_phenotype
69297	2	333407	7	NULL	NULL	0	NULL	Ndt1p	GP		is					mitochondrial NAD carrier protein	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_8_2617_s_185	16469842	The previously proposed pyruvate carrier, YIL006w, has now been identified and functionally characterized as the mitochondrial NAD carrier protein (Ndt1p) by using transport assays with purified protein reconstituted into liposomes ( ).	gene_phenotype
69298	1	333409	7	NULL	NULL	0	NULL	 Yil007c	GP		interacts with					Chs4	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_255	11489916	When used as bait in two-hybrid screens, Yil007c interacted with Chs4 and with Pfs1, a protein required for sporulation ( Deng and Saunders, 2001).	gene_phenotype
69299	2	333409	7	NULL	NULL	0	NULL	Yil007c	GP		interacts with					Pfs1	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_255	11489916	When used as bait in two-hybrid screens, Yil007c interacted with Chs4 and with Pfs1, a protein required for sporulation ( Deng and Saunders, 2001).	gene_phenotype
69300	3	333409	7	NULL	NULL	0	NULL	Pfs1 protein	GP		is required for					sporulation	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_255	11489916	When used as bait in two-hybrid screens, Yil007c interacted with Chs4 and with Pfs1, a protein required for sporulation ( Deng and Saunders, 2001).	gene_phenotype
69301	1	333410	7	NULL	NULL	0	NULL	Rho1	GP		interacts with					Yil007c	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_254	11489916	Rho1 also interacted with a novel protein, Yil007c, which may have a function in regulating cell wall synthesis and other processes during sporulation.	gene_phenotype
69302	2	333410	7	NULL	NULL	NULL	NULL	Yil007c	GP		function in		may			cell wall synthesis	Process	regulating			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_254	11489916	Rho1 also interacted with a novel protein, Yil007c, which may have a function in regulating cell wall synthesis and other processes during sporulation.	gene_phenotype
69303	3	333410	7	NULL	NULL	NULL	NULL	Yil007c	GP		function in		may			sporulation	Process	processes during			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_254	11489916	Rho1 also interacted with a novel protein, Yil007c, which may have a function in regulating cell wall synthesis and other processes during sporulation.	gene_phenotype
69304	4	333410	7	NULL	NULL	0	NULL	Yil007c	GP		is a type of					novel protein	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_254	11489916	Rho1 also interacted with a novel protein, Yil007c, which may have a function in regulating cell wall synthesis and other processes during sporulation.	gene_phenotype
69375	1	333412	7	NULL	NULL	NULL	NULL	 Pol32	GP	S. cerevisiae	interacts with					pol alpha	GP		catalytic subunits of		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_8_6285_s_292	15590683	S. cerevisiae protein YJR043C (Pol32) interacts with the catalytic subunits of pol alpha and it is required for the cell cycle progression in G2/M phase ( ).	gene_phenotype
69376	2	333412	7	NULL	NULL	0	NULL	statement 1	Process		is required for					cell cycle	Process	 progression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_6285_s_292	15590683	S. cerevisiae protein YJR043C (Pol32) interacts with the catalytic subunits of pol alpha and it is required for the cell cycle progression in G2/M phase ( ).	gene_phenotype
69377	3	333412	7	NULL	NULL	0	NULL	statement 2	Process		occur in					G2/M phase	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_6285_s_292	15590683	S. cerevisiae protein YJR043C (Pol32) interacts with the catalytic subunits of pol alpha and it is required for the cell cycle progression in G2/M phase ( ).	gene_phenotype
69378	4	333412	7	NULL	NULL	0	NULL	YJR043C	GP	S. cerevisiae	is					Pol32	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_6285_s_292	15590683	S. cerevisiae protein YJR043C (Pol32) interacts with the catalytic subunits of pol alpha and it is required for the cell cycle progression in G2/M phase ( ).	gene_phenotype
69379	1	333414	7	NULL	NULL	0	NULL	Pol32 protein	GP	Saccharomyces cerevisiae	interacts with					DNA polymerase alpha	GP		catalytic subunits of		NULL		0	NULL	NULL	NULL	abs-batch0680-0699_mol-gen-genet_260_6_9928933_s_1	9928933	The Saccharomyces cerevisiae protein YJR043C (Pol32) interacts with the catalytic subunit of DNA polymerase alpha and is required for cell cycle progression in G2/M..	gene_phenotype
69380	2	333414	7	NULL	NULL	0	NULL	statement 1	Process		is required for					cell cycle	Process	progression of			NULL		0	NULL	NULL	NULL	abs-batch0680-0699_mol-gen-genet_260_6_9928933_s_1	9928933	The Saccharomyces cerevisiae protein YJR043C (Pol32) interacts with the catalytic subunit of DNA polymerase alpha and is required for cell cycle progression in G2/M..	gene_phenotype
69381	3	333414	7	NULL	NULL	0	NULL	statement 2	Process		occur in					G2/M 	Process				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_mol-gen-genet_260_6_9928933_s_1	9928933	The Saccharomyces cerevisiae protein YJR043C (Pol32) interacts with the catalytic subunit of DNA polymerase alpha and is required for cell cycle progression in G2/M..	gene_phenotype
69382	4	333414	7	NULL	NULL	0	NULL	Pol32	GP		is					YJR043C	GP				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_mol-gen-genet_260_6_9928933_s_1	9928933	The Saccharomyces cerevisiae protein YJR043C (Pol32) interacts with the catalytic subunit of DNA polymerase alpha and is required for cell cycle progression in G2/M..	gene_phenotype
69383	1	333415	7	NULL	NULL	0	NULL	YJR043c ORF 	GP	sequence upstream of	reveals								MluI motif (ACGCGT)		NULL		0	NULL	NULL	NULL	abs-batch0680-0699_mol-gen-genet_260_6_9928933_s_10	9928933	Analysis  of the sequence upstream of the YJR043c ORF revealed the presence of an  MluI motif (ACGCGT), a sequence associated with many genes involved in  DNA replication in budding yeast.	gene_phenotype
69384	2	333415	7	NULL	NULL	0	NULL				associate with			MluI motif (ACGCGT)		DNA replication genes	GP	budding yeast			NULL		0	NULL	NULL	NULL	abs-batch0680-0699_mol-gen-genet_260_6_9928933_s_10	9928933	Analysis  of the sequence upstream of the YJR043c ORF revealed the presence of an  MluI motif (ACGCGT), a sequence associated with many genes involved in  DNA replication in budding yeast.	gene_phenotype
69385	1	333417	7	NULL	NULL	0	NULL	MPT5	GP		is a type of					RNA-binding proteins	GP		Puf family		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_42	11157761	We examined  HO expression and  ASH1 mRNA localization in yeast mutants lacking each of the five genes coding for members of the Puf family of RNA-binding proteins:  MPT5,  YGL014w,  YLL013c,  JSN1 and  YPR039c.	gene_phenotype
69386	2	333417	7	NULL	NULL	0	NULL	YGL014w	GP		is a type of					RNA-binding proteins	GP		Puf family		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_42	11157761	We examined  HO expression and  ASH1 mRNA localization in yeast mutants lacking each of the five genes coding for members of the Puf family of RNA-binding proteins:  MPT5,  YGL014w,  YLL013c,  JSN1 and  YPR039c.	gene_phenotype
69387	3	333417	7	NULL	NULL	0	NULL	YLL013c	GP		is a type of					RNA-binding proteins	GP		Puf family		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_42	11157761	We examined  HO expression and  ASH1 mRNA localization in yeast mutants lacking each of the five genes coding for members of the Puf family of RNA-binding proteins:  MPT5,  YGL014w,  YLL013c,  JSN1 and  YPR039c.	gene_phenotype
69388	4	333417	7	NULL	NULL	0	NULL	JSN1	GP		is a type of					RNA-binding proteins	GP		Puf family		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_42	11157761	We examined  HO expression and  ASH1 mRNA localization in yeast mutants lacking each of the five genes coding for members of the Puf family of RNA-binding proteins:  MPT5,  YGL014w,  YLL013c,  JSN1 and  YPR039c.	gene_phenotype
69389	5	333417	7	NULL	NULL	0	NULL	YPR039c	GP		is a type of					RNA-binding proteins	GP		Puf family		NULL		0	NULL	NULL	NULL	gw60_embo_20_3_552_s_42	11157761	We examined  HO expression and  ASH1 mRNA localization in yeast mutants lacking each of the five genes coding for members of the Puf family of RNA-binding proteins:  MPT5,  YGL014w,  YLL013c,  JSN1 and  YPR039c.	gene_phenotype
69390	1	333418	7	NULL	NULL	0	NULL	protein	GP		transported from					endoplasmic reticulum	CellComponent				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_10_6796_s_151	10490618	During the course of our study, Chen and coworkers ( 8) independently identified scSAP 130 as a protein, RSE1 (YML049c), in a screen of temperature-sensitive mutants defective in endoplasmic reticulum-to-golgi transport.	gene_phenotype
69391	2	333418	7	NULL	NULL	0	NULL	Protein	GP		transported to					golgi 	CellComponent				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_10_6796_s_151	10490618	During the course of our study, Chen and coworkers ( 8) independently identified scSAP 130 as a protein, RSE1 (YML049c), in a screen of temperature-sensitive mutants defective in endoplasmic reticulum-to-golgi transport.	gene_phenotype
69392	3	333418	7	NULL	NULL	0	NULL	statement 1			occur along with					statement 2					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_10_6796_s_151	10490618	During the course of our study, Chen and coworkers ( 8) independently identified scSAP 130 as a protein, RSE1 (YML049c), in a screen of temperature-sensitive mutants defective in endoplasmic reticulum-to-golgi transport.	gene_phenotype
69393	4	333418	7	NULL	NULL	0	NULL	scSAP130	GP		defective in					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_10_6796_s_151	10490618	During the course of our study, Chen and coworkers ( 8) independently identified scSAP 130 as a protein, RSE1 (YML049c), in a screen of temperature-sensitive mutants defective in endoplasmic reticulum-to-golgi transport.	gene_phenotype
69394	2	333419	7	NULL	NULL	NULL	NULL	ESA1	GP		is essential for					 cellular viability	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_4_2515_s_97	10082517	Thus, the YOR244w gene product is essential for cellular viability, and we have named it  ESA1, for essential  SAS family acetyltransferase.	gene_phenotype
69395	1	333419	7	NULL	NULL	0	NULL	YOR244w gene product	GP		is					ESA1	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_4_2515_s_97	10082517	Thus, the YOR244w gene product is essential for cellular viability, and we have named it  ESA1, for essential  SAS family acetyltransferase.	gene_phenotype
69396	3	333419	7	NULL	NULL	0	NULL	ESA1	GP		is					essential SAS family acetyltransferase	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_4_2515_s_97	10082517	Thus, the YOR244w gene product is essential for cellular viability, and we have named it  ESA1, for essential  SAS family acetyltransferase.	gene_phenotype
69397	1	333420	7	NULL	NULL	0	NULL	YOR244w ORF	GP		existed on					chromosome XV	Chromosome	yeast			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_4_2515_s_90	10082517	During analysis of the yeast  SAS2 and  SAS3 silencing genes ( 53), we discovered that another, very similar but previously uncharacterized open reading frame (ORF) (YOR244w) existed on yeast chromosome XV.	gene_phenotype
69398	2	333420	7	NULL	NULL	0	NULL	ORF	GP		is 					open reading frame	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_4_2515_s_90	10082517	During analysis of the yeast  SAS2 and  SAS3 silencing genes ( 53), we discovered that another, very similar but previously uncharacterized open reading frame (ORF) (YOR244w) existed on yeast chromosome XV.	gene_phenotype
69399	1	333421	7	NULL	NULL	0	NULL	YDR409W	GP	budding yeast	belongs to					PIAS family	GP				NULL		0	NULL	NULL	NULL	gw60_molcell_8_3_713_s_91	11583632	YDR409W of budding yeast,  Saccharomyces cerevisiae, also belongs to this PIAS family.	gene_phenotype
69400	2	333421	7	NULL	NULL	0	NULL	YDR409W	GP	Saccharomyces cerevisiae	belongs to					PIAS family	GP				NULL		0	NULL	NULL	NULL	gw60_molcell_8_3_713_s_91	11583632	YDR409W of budding yeast,  Saccharomyces cerevisiae, also belongs to this PIAS family.	gene_phenotype
69401	1	333422	7	NULL	NULL	0	NULL	YDR409w	GP	budding yeast	is					Siz1/Ull1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_52_48973_s_4	11577116	In our previous report (Takahashi, Y., Toh-e, A., and Kikuchi, Y. (2001)  Gene 275, 223-231), we showed that Siz1/Ull1 (YDR409w) of budding yeast, a member of the human PIAS family containing a RING-like domain, is a strong candidate for SUMO1/Smt3 ligase because the SUMO1/Smt3 modification of septin components was abolished in the  ull1 mutant and Ull1 associated with E2 (Ubc9) and the substrates (septin components) in immunoprecipitation experiments.	gene_phenotype
69402	2	333422	7	NULL	NULL	0	NULL	Siz1/Ull1	GP		is a member of					PIAS family 	GP	human			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_52_48973_s_4	11577116	In our previous report (Takahashi, Y., Toh-e, A., and Kikuchi, Y. (2001)  Gene 275, 223-231), we showed that Siz1/Ull1 (YDR409w) of budding yeast, a member of the human PIAS family containing a RING-like domain, is a strong candidate for SUMO1/Smt3 ligase because the SUMO1/Smt3 modification of septin components was abolished in the  ull1 mutant and Ull1 associated with E2 (Ubc9) and the substrates (septin components) in immunoprecipitation experiments.	gene_phenotype
69403	3	333422	7	NULL	NULL	0	NULL	PIAS family 	GP	human	contain					RING-like domain	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_52_48973_s_4	11577116	In our previous report (Takahashi, Y., Toh-e, A., and Kikuchi, Y. (2001)  Gene 275, 223-231), we showed that Siz1/Ull1 (YDR409w) of budding yeast, a member of the human PIAS family containing a RING-like domain, is a strong candidate for SUMO1/Smt3 ligase because the SUMO1/Smt3 modification of septin components was abolished in the  ull1 mutant and Ull1 associated with E2 (Ubc9) and the substrates (septin components) in immunoprecipitation experiments.	gene_phenotype
69404	4	333422	7	NULL	NULL	0	NULL	Siz1/Ull1	GP		is a candidate for		strong			SUMO1/Smt3 ligase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_52_48973_s_4	11577116	In our previous report (Takahashi, Y., Toh-e, A., and Kikuchi, Y. (2001)  Gene 275, 223-231), we showed that Siz1/Ull1 (YDR409w) of budding yeast, a member of the human PIAS family containing a RING-like domain, is a strong candidate for SUMO1/Smt3 ligase because the SUMO1/Smt3 modification of septin components was abolished in the  ull1 mutant and Ull1 associated with E2 (Ubc9) and the substrates (septin components) in immunoprecipitation experiments.	gene_phenotype
69405	5	333422	7	NULL	NULL	NULL	NULL	SUMO1/Smt3	GP	modification of 	is abolished in			septin components of		ull1	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_52_48973_s_4	11577116	In our previous report (Takahashi, Y., Toh-e, A., and Kikuchi, Y. (2001)  Gene 275, 223-231), we showed that Siz1/Ull1 (YDR409w) of budding yeast, a member of the human PIAS family containing a RING-like domain, is a strong candidate for SUMO1/Smt3 ligase because the SUMO1/Smt3 modification of septin components was abolished in the  ull1 mutant and Ull1 associated with E2 (Ubc9) and the substrates (septin components) in immunoprecipitation experiments.	gene_phenotype
69406	6	333422	7	NULL	NULL	0	NULL	Ull1 	GP		associate with					E2	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_52_48973_s_4	11577116	In our previous report (Takahashi, Y., Toh-e, A., and Kikuchi, Y. (2001)  Gene 275, 223-231), we showed that Siz1/Ull1 (YDR409w) of budding yeast, a member of the human PIAS family containing a RING-like domain, is a strong candidate for SUMO1/Smt3 ligase because the SUMO1/Smt3 modification of septin components was abolished in the  ull1 mutant and Ull1 associated with E2 (Ubc9) and the substrates (septin components) in immunoprecipitation experiments.	gene_phenotype
69407	7	333422	7	NULL	NULL	0	NULL	E2	GP		is					Ubc9	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_52_48973_s_4	11577116	In our previous report (Takahashi, Y., Toh-e, A., and Kikuchi, Y. (2001)  Gene 275, 223-231), we showed that Siz1/Ull1 (YDR409w) of budding yeast, a member of the human PIAS family containing a RING-like domain, is a strong candidate for SUMO1/Smt3 ligase because the SUMO1/Smt3 modification of septin components was abolished in the  ull1 mutant and Ull1 associated with E2 (Ubc9) and the substrates (septin components) in immunoprecipitation experiments.	gene_phenotype
69408	8	333422	7	NULL	NULL	0	NULL	Ull1 	GP		associate with					septin components	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_52_48973_s_4	11577116	In our previous report (Takahashi, Y., Toh-e, A., and Kikuchi, Y. (2001)  Gene 275, 223-231), we showed that Siz1/Ull1 (YDR409w) of budding yeast, a member of the human PIAS family containing a RING-like domain, is a strong candidate for SUMO1/Smt3 ligase because the SUMO1/Smt3 modification of septin components was abolished in the  ull1 mutant and Ull1 associated with E2 (Ubc9) and the substrates (septin components) in immunoprecipitation experiments.	gene_phenotype
69409	1	333423	7	NULL	NULL	0	NULL	PEA2 YER149c	GP		localized with					Spa2p	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_211	15334557	PEA2   YER149c Localized with Spa2p to sites of polarized growth and required for efficient mating,  bipolar budding and pheromone-induced shmoo formation	gene_phenotype
69410	2	333423	7	NULL	NULL	NULL	NULL	statement 1	Process		localized to					polarized growth	Process	sites of			NULL		NULL	NULL	NULL	NULL	gw70_yeast_21_11_927_s_211	15334557	PEA2   YER149c Localized with Spa2p to sites of polarized growth and required for efficient mating,  bipolar budding and pheromone-induced shmoo formation	gene_phenotype
69411	3	333423	7	NULL	NULL	0	NULL	statement 2	Process		required for					mating	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_211	15334557	PEA2   YER149c Localized with Spa2p to sites of polarized growth and required for efficient mating,  bipolar budding and pheromone-induced shmoo formation	gene_phenotype
69412	4	333423	7	NULL	NULL	NULL	NULL	statement 2	Process		required for					bipolar budding	Process				NULL		NULL	NULL	NULL	NULL	gw70_yeast_21_11_927_s_211	15334557	PEA2   YER149c Localized with Spa2p to sites of polarized growth and required for efficient mating,  bipolar budding and pheromone-induced shmoo formation	gene_phenotype
69413	5	333423	7	NULL	NULL	0	NULL	pheromone	GP		induce					shmoo formation	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_211	15334557	PEA2   YER149c Localized with Spa2p to sites of polarized growth and required for efficient mating,  bipolar budding and pheromone-induced shmoo formation	gene_phenotype
69414	6	333423	7	NULL	NULL	0	NULL	statement 2	Process		required for					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_211	15334557	PEA2   YER149c Localized with Spa2p to sites of polarized growth and required for efficient mating,  bipolar budding and pheromone-induced shmoo formation	gene_phenotype
69415	1	333424	7	NULL	NULL	0	NULL	PEA2 YER149C	GP		involved in					orientated growth	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_154	15645503	PEA2  YER149C Involved in orientated growth toward mating partner, required for stimulation of the  low-affinity Ca2+ in flux system that is activated in response to mating pheromone and is required  for cell-cell fusion (Sheu  et al., [ 2000])	gene_phenotype
69416	2	333424	7	NULL	NULL	0	NULL	statement 1	Process		toward					mating partner	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_154	15645503	PEA2  YER149C Involved in orientated growth toward mating partner, required for stimulation of the  low-affinity Ca2+ in flux system that is activated in response to mating pheromone and is required  for cell-cell fusion (Sheu  et al., [ 2000])	gene_phenotype
69417	3	333424	7	NULL	NULL	NULL	NULL	PEA2 YER149C	GP		required for					Ca2+ influx system	Process	stimulation of low-affinity			NULL		NULL	NULL	NULL	NULL	gw70_yeast_22_2_79_s_154	15645503	PEA2  YER149C Involved in orientated growth toward mating partner, required for stimulation of the  low-affinity Ca2+ in flux system that is activated in response to mating pheromone and is required  for cell-cell fusion (Sheu  et al., [ 2000])	gene_phenotype
69418	4	333424	7	NULL	NULL	0	NULL	 Ca2+ in flux system	Process		activated in					mating pheromone	GP	response to			NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_154	15645503	PEA2  YER149C Involved in orientated growth toward mating partner, required for stimulation of the  low-affinity Ca2+ in flux system that is activated in response to mating pheromone and is required  for cell-cell fusion (Sheu  et al., [ 2000])	gene_phenotype
69419	5	333424	7	NULL	NULL	0	NULL	 Ca2+ in flux system	Process		required for					cell-cell fusion	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_154	15645503	PEA2  YER149C Involved in orientated growth toward mating partner, required for stimulation of the  low-affinity Ca2+ in flux system that is activated in response to mating pheromone and is required  for cell-cell fusion (Sheu  et al., [ 2000])	gene_phenotype
69678	1	333426	6	NULL	NULL	0	NULL	YHL007c STE20	GP		is involved in					pheromone response	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_73	16498703	YHL007c   STE20 Signal transducing kinase of the PAK (p21-activated kinase) family, involved in pheromone  response and pseudohyphal/invasive growth pathways, activated by Cdc42p; binds Ste4p  at a GBB motif present in non-catalytic domains of PAK kinases  [ 44]	gene_phenotype
69679	2	333426	6	NULL	NULL	0	NULL	YHL007c STE20	GP		is a type of					PAK 	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_73	16498703	YHL007c   STE20 Signal transducing kinase of the PAK (p21-activated kinase) family, involved in pheromone  response and pseudohyphal/invasive growth pathways, activated by Cdc42p; binds Ste4p  at a GBB motif present in non-catalytic domains of PAK kinases  [ 44]	gene_phenotype
69680	3	333426	6	NULL	NULL	0	NULL	PAK	GP		is					p21-activated kinase	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_73	16498703	YHL007c   STE20 Signal transducing kinase of the PAK (p21-activated kinase) family, involved in pheromone  response and pseudohyphal/invasive growth pathways, activated by Cdc42p; binds Ste4p  at a GBB motif present in non-catalytic domains of PAK kinases  [ 44]	gene_phenotype
69681	4	333426	6	NULL	NULL	0	NULL	YHL007c STE20	GP		is involved in					pseudohyphal/invasive growth pathways	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_73	16498703	YHL007c   STE20 Signal transducing kinase of the PAK (p21-activated kinase) family, involved in pheromone  response and pseudohyphal/invasive growth pathways, activated by Cdc42p; binds Ste4p  at a GBB motif present in non-catalytic domains of PAK kinases  [ 44]	gene_phenotype
69682	5	333426	6	NULL	NULL	0	NULL	YHL007c STE20	GP		bind					Ste4p	GP			GBB motif	NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_73	16498703	YHL007c   STE20 Signal transducing kinase of the PAK (p21-activated kinase) family, involved in pheromone  response and pseudohyphal/invasive growth pathways, activated by Cdc42p; binds Ste4p  at a GBB motif present in non-catalytic domains of PAK kinases  [ 44]	gene_phenotype
69683	6	333426	6	NULL	NULL	NULL	NULL	YHL007c STE20	GP		is activated by					Cdc42p	GP				NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_3_159_s_73	16498703	YHL007c   STE20 Signal transducing kinase of the PAK (p21-activated kinase) family, involved in pheromone  response and pseudohyphal/invasive growth pathways, activated by Cdc42p; binds Ste4p  at a GBB motif present in non-catalytic domains of PAK kinases  [ 44]	gene_phenotype
69684	7	333426	6	NULL	NULL	0	NULL	GBB motif 			is present in					PAK kinase	GP		non-catalytic domain		NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_73	16498703	YHL007c   STE20 Signal transducing kinase of the PAK (p21-activated kinase) family, involved in pheromone  response and pseudohyphal/invasive growth pathways, activated by Cdc42p; binds Ste4p  at a GBB motif present in non-catalytic domains of PAK kinases  [ 44]	gene_phenotype
69685	1	333428	6	NULL	NULL	NULL	NULL	Yil159w Bnr1 1 Formin	GP		nucleates					linear actin filaments	CellComponent	formation of 			NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_3_159_s_140	16498703	Yil159w  Bnr1  1 Formin, nucleates the formation of linear actin filaments, involved in cell processes  such as budding and mitotic spindle orientation, which require the formation of polarized  actin cables; functionally redundant with  BNI1  LIP  [ 20]	gene_phenotype
69686	2	333428	6	NULL	NULL	0	NULL	Yil159w Bnr1 1 Formin	GP		is involved in					budding	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_140	16498703	Yil159w  Bnr1  1 Formin, nucleates the formation of linear actin filaments, involved in cell processes  such as budding and mitotic spindle orientation, which require the formation of polarized  actin cables; functionally redundant with  BNI1  LIP  [ 20]	gene_phenotype
69687	3	333428	6	NULL	NULL	0	NULL	Yil159w Bnr1 1 Formin	GP		is involved in					mitotic spindle	CellComponent	orientation of			NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_140	16498703	Yil159w  Bnr1  1 Formin, nucleates the formation of linear actin filaments, involved in cell processes  such as budding and mitotic spindle orientation, which require the formation of polarized  actin cables; functionally redundant with  BNI1  LIP  [ 20]	gene_phenotype
69688	4	333428	6	NULL	NULL	0	NULL	linear actin filaments	CellComponent		ia required for					actin cables	CellComponent	formation of;; polarized			NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_140	16498703	Yil159w  Bnr1  1 Formin, nucleates the formation of linear actin filaments, involved in cell processes  such as budding and mitotic spindle orientation, which require the formation of polarized  actin cables; functionally redundant with  BNI1  LIP  [ 20]	gene_phenotype
69689	5	333428	6	NULL	NULL	0	NULL	Yil159w Bnr1 1 Formin	GP		is functionally redundant with					BNI1 LIP	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_140	16498703	Yil159w  Bnr1  1 Formin, nucleates the formation of linear actin filaments, involved in cell processes  such as budding and mitotic spindle orientation, which require the formation of polarized  actin cables; functionally redundant with  BNI1  LIP  [ 20]	gene_phenotype
69690	1	333429	6	NULL	NULL	0	NULL	YJL094c	GP		shows closest homology to					KefC	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_12_6951_s_232	9507001	Of these, YJL094c also shows closest homology to a glutathione-regulated K+ efflux transporter (KefC) from  Escherichia coli ( 65), although it does not appear to contain a putative mitochondrial targeting signal at its N terminus.	gene_phenotype
69691	2	333429	6	NULL	NULL	NULL	NULL	KefC	GP		is					K+ efflux transporter	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_12_6951_s_232	9507001	Of these, YJL094c also shows closest homology to a glutathione-regulated K+ efflux transporter (KefC) from  Escherichia coli ( 65), although it does not appear to contain a putative mitochondrial targeting signal at its N terminus.	gene_phenotype
69704	3	333429	6	NULL	NULL	0	NULL	YJL094c	GP		does not contain					mitochondrial targeting signal	AminoAcid	putative	N terminus		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_12_6951_s_232	9507001	Of these, YJL094c also shows closest homology to a glutathione-regulated K+ efflux transporter (KefC) from  Escherichia coli ( 65), although it does not appear to contain a putative mitochondrial targeting signal at its N terminus.	gene_phenotype
69706	1	333430	6	NULL	NULL	0	NULL	YKR081c	GP		is necessary for					vegetative cell growth	Process				NULL		0	NULL	NULL	NULL	gw60_gene_233_1_141_s_152	10375630	This fact undoubtedly confirms that  YKR081c and  YKR083c are necessary for vegetative cell growth.	gene_phenotype
69708	2	333430	6	NULL	NULL	0	NULL	YKR083c	GP		is necessary for					vegetative cell growth	Process				NULL		0	NULL	NULL	NULL	gw60_gene_233_1_141_s_152	10375630	This fact undoubtedly confirms that  YKR081c and  YKR083c are necessary for vegetative cell growth.	gene_phenotype
69709	1	333431	6	NULL	NULL	0	NULL	YKR081c	GP		is necessary for					vegetative growth	Process				NULL		0	NULL	NULL	NULL	gw60_gene_233_1_141_s_124	10375630	Functional analysis of deletion FYBL3/Jz024:  YKR081c and  YKR083c are essential for vegetative growth;  YKR082c deletion renders heat-sensitive mutants	gene_phenotype
69712	2	333431	6	NULL	NULL	0	NULL	YKR083c	GP		is necessary for					vegetative growth	Process				NULL		0	NULL	NULL	NULL	gw60_gene_233_1_141_s_124	10375630	Functional analysis of deletion FYBL3/Jz024:  YKR081c and  YKR083c are essential for vegetative growth;  YKR082c deletion renders heat-sensitive mutants	gene_phenotype
69713	3	333431	6	NULL	NULL	0	NULL	YKR082c	GP	deletion of	renders					heat-sensitive mutant					NULL		0	NULL	NULL	NULL	gw60_gene_233_1_141_s_124	10375630	Functional analysis of deletion FYBL3/Jz024:  YKR081c and  YKR083c are essential for vegetative growth;  YKR082c deletion renders heat-sensitive mutants	gene_phenotype
69715	1	333432	6	NULL	NULL	NULL	NULL	bilirubin	GP	Saccharomyces cerevisiae;; unconjugated	is transported to					vacuoles	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_16_4761_s_481	11466279	The products of YCF1 and YLL015w (BPT1) cooperate for the ATP-dependent vacuolar transport of unconjugated bilirubin in  Saccharomyces cerevisiae.	gene_phenotype
69718	2	333432	6	NULL	NULL	0	NULL	YCF1 product	GP		cooperates for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_16_4761_s_481	11466279	The products of YCF1 and YLL015w (BPT1) cooperate for the ATP-dependent vacuolar transport of unconjugated bilirubin in  Saccharomyces cerevisiae.	gene_phenotype
69719	3	333432	6	NULL	NULL	0	NULL	YLL015w product	GP		cooperates for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_16_4761_s_481	11466279	The products of YCF1 and YLL015w (BPT1) cooperate for the ATP-dependent vacuolar transport of unconjugated bilirubin in  Saccharomyces cerevisiae.	gene_phenotype
69720	4	333432	6	NULL	NULL	0	NULL	statement 1	Process		is dependent on					ATP	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_16_4761_s_481	11466279	The products of YCF1 and YLL015w (BPT1) cooperate for the ATP-dependent vacuolar transport of unconjugated bilirubin in  Saccharomyces cerevisiae.	gene_phenotype
69721	1	333433	6	NULL	NULL	0	NULL	Bpt1p	GP		localizes to					vacuoles	CellComponent				NULL		0	NULL	NULL	NULL	gw60_febslett_520_1_63_s_68	12044871	A previous study characterized Bpt1p ( YLL015w) as a transporter mediating uptake of unconjugated bilirubins into vacuolar vesicles [ 30], implying vacuolar localization of Bpt1p.	gene_phenotype
69722	2	333433	6	NULL	NULL	0	NULL	bilirubins	GP	unconjugated	are tranported to					vacuolar vesicles	CellComponent				NULL		0	NULL	NULL	NULL	gw60_febslett_520_1_63_s_68	12044871	A previous study characterized Bpt1p ( YLL015w) as a transporter mediating uptake of unconjugated bilirubins into vacuolar vesicles [ 30], implying vacuolar localization of Bpt1p.	gene_phenotype
69724	3	333433	6	NULL	NULL	NULL	NULL	Bpt1p ( YLL015w)	GP		mediates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_520_1_63_s_68	12044871	A previous study characterized Bpt1p ( YLL015w) as a transporter mediating uptake of unconjugated bilirubins into vacuolar vesicles [ 30], implying vacuolar localization of Bpt1p.	gene_phenotype
69732	1	333435	6	NULL	NULL	0	NULL	Bpt1p	GP		is					bile pigment transporter-1	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_520_1_63_s_21	12044871	Furthermore, Bpt1p (bile pigment transporter-1/ YLL015w), the closest yeast homologue of Ycf1p, was originally discovered as a pump mediating vacuolar uptake of unconjugated bile pigments and magnetic resonance contrast agents [  30 and   31].	gene_phenotype
69733	2	333435	6	NULL	NULL	0	NULL	Bpt1p	GP		is homologue of 					Ycf1	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_520_1_63_s_21	12044871	Furthermore, Bpt1p (bile pigment transporter-1/ YLL015w), the closest yeast homologue of Ycf1p, was originally discovered as a pump mediating vacuolar uptake of unconjugated bile pigments and magnetic resonance contrast agents [  30 and   31].	gene_phenotype
69736	3	333435	6	NULL	NULL	0	NULL	vacuoles	CellComponent		uptake					bile pigments	unconjugated				NULL		0	NULL	NULL	NULL	gw60_febslett_520_1_63_s_21	12044871	Furthermore, Bpt1p (bile pigment transporter-1/ YLL015w), the closest yeast homologue of Ycf1p, was originally discovered as a pump mediating vacuolar uptake of unconjugated bile pigments and magnetic resonance contrast agents [  30 and   31].	gene_phenotype
69738	4	333435	6	NULL	NULL	0	NULL	Bpt1p	GP		mediates					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_520_1_63_s_21	12044871	Furthermore, Bpt1p (bile pigment transporter-1/ YLL015w), the closest yeast homologue of Ycf1p, was originally discovered as a pump mediating vacuolar uptake of unconjugated bile pigments and magnetic resonance contrast agents [  30 and   31].	gene_phenotype
69743	1	333437	6	NULL	NULL	0	NULL	LIF1 		transcriptional repression of	causes					NHEJ 		regulation of;; mating-type-dependent			NULL		0	NULL	NULL	NULL	gw60_nature_414_6864_666_s_14	11740566	Here we report that mating-type-dependent regulation of NHEJ in budding yeast is caused in part by transcriptional repression of both  LIF1 and the gene  NEJ1 (YLR265C) -- identified from microarray screening of messenger RNAs.	gene_phenotype
69746	2	333437	6	NULL	NULL	0	NULL	NEJ1 (YLR265C)	GP		causes					NHEJ	GP	regulation of;; mating-type-dependent			NULL		0	NULL	NULL	NULL	gw60_nature_414_6864_666_s_14	11740566	Here we report that mating-type-dependent regulation of NHEJ in budding yeast is caused in part by transcriptional repression of both  LIF1 and the gene  NEJ1 (YLR265C) -- identified from microarray screening of messenger RNAs.	gene_phenotype
69783	1	333439	6	NULL	NULL	0	NULL	neural crest cell	Cell		are present 					otic vesicle	CellComponent	anterior to			NULL		0	NULL	NULL	NULL	gw60_genesdev_17_1_141_s_124	12514106	Interestingly, more neural crest cells were observed anterior to the otic vesicle in a region next to the second branchial arch in the  Fgfr1n7/n7 mutants compared with the wild-type embryos.	gene_phenotype
69784	2	333439	6	NULL	NULL	0	NULL	otic vesicle	OrganismPart		is present 					second branchial arch	OrganismPart				NULL	Fgfr1n7/n7 mutants 	0	NULL	NULL	NULL	gw60_genesdev_17_1_141_s_124	12514106	Interestingly, more neural crest cells were observed anterior to the otic vesicle in a region next to the second branchial arch in the  Fgfr1n7/n7 mutants compared with the wild-type embryos.	gene_phenotype
69785	1	333440	6	NULL	NULL	0	NULL	cdc15p			is involved in					cytokinesis					NULL	Schizosaccharomyces pombe	0	NULL	NULL	NULL	gw60_jbiolchem_273_43_28341_s_73	9774458	Ymr032wp is homologous to cdc15p, which is involved in cytokinesis in  Schizosaccharomyces pombe ( 29).	gene_phenotype
69786	2	333440	6	NULL	NULL	0	NULL	Ymr032wp			is homologous to					cdc15p					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_43_28341_s_73	9774458	Ymr032wp is homologous to cdc15p, which is involved in cytokinesis in  Schizosaccharomyces pombe ( 29).	gene_phenotype
69787	1	333441	6	NULL	NULL	0	NULL	Ymr032wp			is homologous to					cdc15p					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_43_28341_s_7	9774458	Ymr032wp was homologous to cdc15p, which is involved in cytokinesis in  Schizosaccharomyces pombe, and we named this gene  HOF1 (homolog of cdc 15).	gene_phenotype
69788	2	333441	6	NULL	NULL	0	NULL	Ymr032wp			is 					HOF1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_43_28341_s_7	9774458	Ymr032wp was homologous to cdc15p, which is involved in cytokinesis in  Schizosaccharomyces pombe, and we named this gene  HOF1 (homolog of cdc 15).	gene_phenotype
69789	3	333441	6	NULL	NULL	0	NULL	HOF1			is					homolog of cdc 15					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_43_28341_s_7	9774458	Ymr032wp was homologous to cdc15p, which is involved in cytokinesis in  Schizosaccharomyces pombe, and we named this gene  HOF1 (homolog of cdc 15).	gene_phenotype
69790	3	333441	6	NULL	NULL	0	NULL	HOF1			is					homolog of cdc 15					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_43_28341_s_7	9774458	Ymr032wp was homologous to cdc15p, which is involved in cytokinesis in  Schizosaccharomyces pombe, and we named this gene  HOF1 (homolog of cdc 15).	gene_phenotype
69791	4	333441	6	NULL	NULL	0	NULL	cdc15p			is involved in					cytokinesis					NULL	Schizosaccharomyces pombe	0	NULL	NULL	NULL	gw60_jbiolchem_273_43_28341_s_7	9774458	Ymr032wp was homologous to cdc15p, which is involved in cytokinesis in  Schizosaccharomyces pombe, and we named this gene  HOF1 (homolog of cdc 15).	gene_phenotype
69792	1	333444	6	NULL	NULL	0	NULL	Ydl119c	GP		is a member of					mitochondrial carrier family of membrane transporters	GP				NULL		0	NULL	NULL	NULL	gw60_chembiol_10_6_521_s_159	12837385	A strain deleted for Ydl119c, a member of the mitochondrial carrier family of membrane transporters, which are involved in the transport of a number of different metabolites across the inner mitochondrial membrane   [25, 26]  , is sensitive to SFK1.	gene_phenotype
69793	2	333444	6	NULL	NULL	0	NULL	Ydl119c	GP	deletion mutant	is sensitive to					SFK1	Chemical				NULL		0	NULL	NULL	NULL	gw60_chembiol_10_6_521_s_159	12837385	A strain deleted for Ydl119c, a member of the mitochondrial carrier family of membrane transporters, which are involved in the transport of a number of different metabolites across the inner mitochondrial membrane   [25, 26]  , is sensitive to SFK1.	gene_phenotype
69794	3	333444	6	NULL	NULL	0	NULL	metabolites	Chemical		transported across					mitochondrial membrane 	CellComponent	inner 			NULL		0	NULL	NULL	NULL	gw60_chembiol_10_6_521_s_159	12837385	A strain deleted for Ydl119c, a member of the mitochondrial carrier family of membrane transporters, which are involved in the transport of a number of different metabolites across the inner mitochondrial membrane   [25, 26]  , is sensitive to SFK1.	gene_phenotype
69805	1	333445	6	NULL	NULL	NULL	NULL	Ggc1p			clusters together with					transporters for nucleotides					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_20_20850_s_224	14998997	In a phylogenetic tree of the  S. cerevisiae members of the mitochondrial carrier family ( ,  ), Ggc1p clusters together with transporters for nucleotides or nucleotide analogs (the three isoforms of the ADP/ATP carrier (  -  ) and the carriers for coenzyme A ( ) and for thiamine pyrophosphate ( ) and with YDL119c (20% identity), which has not yet been identified).	gene_phenotype
69807	2	333445	6	NULL	NULL	0	NULL	Ggc1p			clusters together with					nucleotide analogs					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_20_20850_s_224	14998997	In a phylogenetic tree of the  S. cerevisiae members of the mitochondrial carrier family ( ,  ), Ggc1p clusters together with transporters for nucleotides or nucleotide analogs (the three isoforms of the ADP/ATP carrier (  -  ) and the carriers for coenzyme A ( ) and for thiamine pyrophosphate ( ) and with YDL119c (20% identity), which has not yet been identified).	gene_phenotype
69812	1	333446	6	NULL	NULL	0	NULL	FOB1	GP	wild type	interacts with					FOB1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_3_1932_s_214	14576157	Two-hybrid analyses of protein-protein interactions between wild type  FOB1 or  YDR026C and  FOB1 or its mutant forms and lack of replication fork arrest activity of  YDR026C.	gene_phenotype
69813	2	333446	6	NULL	NULL	0	NULL	YDR026C 	GP	wild type	bind					FOB1	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_3_1932_s_214	14576157	Two-hybrid analyses of protein-protein interactions between wild type  FOB1 or  YDR026C and  FOB1 or its mutant forms and lack of replication fork arrest activity of  YDR026C.	gene_phenotype
69845	1	333447	6	NULL	NULL	0	NULL	Fob1p	GP	mutant	bind					protein encoded in the locus YDR026C	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_3_1932_s_8	14576157	The mutant did not diminish nucleolar transport, and interaction of the mutant form of Fob1p with itself and with another protein encoded in the locus  YDR026C suggested that the mutation did not cause global misfolding of the protein.	gene_phenotype
69846	1	333448	6	NULL	NULL	0	NULL	Nmd3	GP		is a type of					export adapter					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_10_3718_s_29	16648468	For the large subunit, these include the export adapter Nmd3 that provides the nuclear export signal ( ), Tif6 ( ), the uncharacterized protein Arx1 (encoded by YDR101c) ( ), and Rlp24, related to Rpl24 found in mature subunits ( ).	gene_phenotype
69847	2	333448	6	NULL	NULL	NULL	NULL	Nmd3	GP		provides					nuclear export signal	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_10_3718_s_29	16648468	For the large subunit, these include the export adapter Nmd3 that provides the nuclear export signal ( ), Tif6 ( ), the uncharacterized protein Arx1 (encoded by YDR101c) ( ), and Rlp24, related to Rpl24 found in mature subunits ( ).	gene_phenotype
69848	1	333449	6	NULL	NULL	NULL	NULL	Nmd3	GP		is a type of					nuclear export factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_20_5539_s_180	12374754	The nuclear export factor Nmd3 joins the 60S pre-ribosome at the level of Arx1 (Ydr101c, termed Arx1 for  associated with  ribosomal e xport complex), which could be the trigger for the acquisition of export competence.	gene_phenotype
69849	2	333449	6	NULL	NULL	0	NULL	Nmd3	GP		bind					60S pre-ribosome	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_embo_21_20_5539_s_180	12374754	The nuclear export factor Nmd3 joins the 60S pre-ribosome at the level of Arx1 (Ydr101c, termed Arx1 for  associated with  ribosomal e xport complex), which could be the trigger for the acquisition of export competence.	gene_phenotype
69850	3	333449	6	NULL	NULL	NULL	NULL	statement 2	Process		occurs at the 					Arx1	GP	level of 			NULL		NULL	NULL	NULL	NULL	gw60_embo_21_20_5539_s_180	12374754	The nuclear export factor Nmd3 joins the 60S pre-ribosome at the level of Arx1 (Ydr101c, termed Arx1 for  associated with  ribosomal e xport complex), which could be the trigger for the acquisition of export competence.	gene_phenotype
69851	1	333452	6	NULL	NULL	NULL	NULL	ERV14	GP		encode			YGL054C		COPII vesicle coat protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_163_3_875_s_165	12663529	ERV14 (YGL054C) and  ERV41 (YNL067C) encode COPII vesicle coat proteins involved in endoplasmic reticulum (ER)-to-Golgi trafficking ( O TTE et al. 2001   ), and both show toxin resistance.	gene_phenotype
69852	2	333452	6	NULL	NULL	NULL	NULL	ERV41	GP		encodes			YNL067C		COPII vesicle coat protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_163_3_875_s_165	12663529	ERV14 (YGL054C) and  ERV41 (YNL067C) encode COPII vesicle coat proteins involved in endoplasmic reticulum (ER)-to-Golgi trafficking ( O TTE et al. 2001   ), and both show toxin resistance.	gene_phenotype
69853	3	333452	6	NULL	NULL	NULL	NULL	COPII vesicle coat proteins	GP		is involved in					ER to Golgi trafficking	Process				NULL		NULL	NULL	NULL	NULL	gw60_genetics_163_3_875_s_165	12663529	ERV14 (YGL054C) and  ERV41 (YNL067C) encode COPII vesicle coat proteins involved in endoplasmic reticulum (ER)-to-Golgi trafficking ( O TTE et al. 2001   ), and both show toxin resistance.	gene_phenotype
69854	4	333452	6	NULL	NULL	0	NULL	ERV14	GP		show			YGL054C		toxin	Chemical	resistance to			NULL		0	NULL	NULL	NULL	gw60_genetics_163_3_875_s_165	12663529	ERV14 (YGL054C) and  ERV41 (YNL067C) encode COPII vesicle coat proteins involved in endoplasmic reticulum (ER)-to-Golgi trafficking ( O TTE et al. 2001   ), and both show toxin resistance.	gene_phenotype
69855	1	333454	6	NULL	NULL	0	NULL	Ygl129c	GP		is a type of					ribosomal protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_19_15861_s_10	11278769	Another newly identified ribosomal protein, Ygl129c, was previously shown to be a member of the DAP-3 family of mitochondrial apoptosis mediators.	gene_phenotype
69856	2	333454	6	NULL	NULL	0	NULL	Ygl129c	GP		is a member of					DAP-3 family of mitochondrial apoptosis mediators	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_19_15861_s_10	11278769	Another newly identified ribosomal protein, Ygl129c, was previously shown to be a member of the DAP-3 family of mitochondrial apoptosis mediators.	gene_phenotype
69857	1	333456	6	NULL	NULL	0	NULL	CRH1	GP		is regulated by					cell cycle	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_9_3245_s_9	10757808	CRH1 and  YLR213c (renamed  CRR1, for  CRH related) were found to be cell cycle regulated and also expressed under sporulation conditions, whereas  CRH2 expression did not vary during the mitotic cycle.	gene_phenotype
69858	2	333456	6	NULL	NULL	0	NULL	YLR213c	GP		is					CRR1	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_9_3245_s_9	10757808	CRH1 and  YLR213c (renamed  CRR1, for  CRH related) were found to be cell cycle regulated and also expressed under sporulation conditions, whereas  CRH2 expression did not vary during the mitotic cycle.	gene_phenotype
69859	3	333456	6	NULL	NULL	0	NULL	YLR213c	GP		is regulated by					cell cycle	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_9_3245_s_9	10757808	CRH1 and  YLR213c (renamed  CRR1, for  CRH related) were found to be cell cycle regulated and also expressed under sporulation conditions, whereas  CRH2 expression did not vary during the mitotic cycle.	gene_phenotype
69860	4	333456	6	NULL	NULL	NULL	NULL	CRH2	GP	expression of	does not vary					mitotic cycle	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_9_3245_s_9	10757808	CRH1 and  YLR213c (renamed  CRR1, for  CRH related) were found to be cell cycle regulated and also expressed under sporulation conditions, whereas  CRH2 expression did not vary during the mitotic cycle.	gene_phenotype
70068	1	333458	6	NULL	NULL	0	NULL	YOL091w product	GP		plays a role in					sporulation	Process				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_yeast_14_4_9559547_s_11	9559547	Disruption of YOR322c causes osmotically  sensitive growth on YEPD at 37 degrees C and the product of YOL091w appears  to play a role in sporulation since the homozygous diploid disruptant  has lost the ability to sporulate.	gene_phenotype
70070	2	333458	6	NULL	NULL	0	NULL	YOR322c	GP	homozygous mutant	does not					sporulate	Process				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_yeast_14_4_9559547_s_11	9559547	Disruption of YOR322c causes osmotically  sensitive growth on YEPD at 37 degrees C and the product of YOL091w appears  to play a role in sporulation since the homozygous diploid disruptant  has lost the ability to sporulate.	gene_phenotype
69893	1	333464	6	NULL	NULL	0	NULL	YBL091C-A ORF	GP	deletion of	silences					telomere	Chromosome				NULL		0	NULL	NULL	NULL	gw60_genetics_158_1_145_s_152	11333225	Furthermore, a strain with a deletion of the YBL091C-A ORF and an  scs2 mutation has approximately the same telomeric silencing defect as the single  scs2delta mutant ( Fig 3).	gene_phenotype
69894	2	333464	6	NULL	NULL	0	NULL	scs2	GP	deletion of	silences					telomere	Chromosome				NULL		0	NULL	NULL	NULL	gw60_genetics_158_1_145_s_152	11333225	Furthermore, a strain with a deletion of the YBL091C-A ORF and an  scs2 mutation has approximately the same telomeric silencing defect as the single  scs2delta mutant ( Fig 3).	gene_phenotype
69895	3	333464	6	NULL	NULL	0	NULL	scs2delta	GP	mutation of	silences					telomere	Chromosome				NULL		0	NULL	NULL	NULL	gw60_genetics_158_1_145_s_152	11333225	Furthermore, a strain with a deletion of the YBL091C-A ORF and an  scs2 mutation has approximately the same telomeric silencing defect as the single  scs2delta mutant ( Fig 3).	gene_phenotype
69896	1	333465	6	NULL	NULL	NULL	NULL	STE11	GP		is required for					pheromone response	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_13_7508_s_176	9636180	The observation that disruption of the YBR059C and YGR179C genes increased alpha factor sensitivity, combined with previous results ( 30-32) demonstrating that the  STE11 and  STE50 genes are required for pheromone response, indicate that four of the ORF-derived perturbagens originate from genes that play a role in pheromone response.	gene_phenotype
69897	2	333465	6	NULL	NULL	0	NULL	STE50	GP		is required for					pheromone response	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_95_13_7508_s_176	9636180	The observation that disruption of the YBR059C and YGR179C genes increased alpha factor sensitivity, combined with previous results ( 30-32) demonstrating that the  STE11 and  STE50 genes are required for pheromone response, indicate that four of the ORF-derived perturbagens originate from genes that play a role in pheromone response.	gene_phenotype
69898	3	333465	6	NULL	NULL	0	NULL	YBR059C	GP	disruption of	increases					alpha factor	GP	sensitivity of 			NULL		0	NULL	NULL	NULL	gw60_pnas_95_13_7508_s_176	9636180	The observation that disruption of the YBR059C and YGR179C genes increased alpha factor sensitivity, combined with previous results ( 30-32) demonstrating that the  STE11 and  STE50 genes are required for pheromone response, indicate that four of the ORF-derived perturbagens originate from genes that play a role in pheromone response.	gene_phenotype
69899	4	333465	6	NULL	NULL	0	NULL	YGR179C gene	GP	disruption of	increases					alpha factor	GP	sensitivity of			NULL		0	NULL	NULL	NULL	gw60_pnas_95_13_7508_s_176	9636180	The observation that disruption of the YBR059C and YGR179C genes increased alpha factor sensitivity, combined with previous results ( 30-32) demonstrating that the  STE11 and  STE50 genes are required for pheromone response, indicate that four of the ORF-derived perturbagens originate from genes that play a role in pheromone response.	gene_phenotype
69900	1	333466	6	NULL	NULL	0	NULL	YBR265w	GP		is 					TSC10 gene	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_46_30688_s_122	9804843	When this transformant was crossed to a wild-type ( TSC10) haploid and the diploids were sporulated and dissected, all products of meiosis were temperature-resistant, indicating that YBR265w is the wild-type  TSC10 gene.	gene_phenotype
69901	1	333467	6	NULL	NULL	NULL	NULL	FY1679-derived delta ygl194c/delta ygl194c	GP		reduces					sporulation	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_yeast_14_7_9639312_s_4	9639312	A diploid FY1679-derived delta  ygl194c/delta ygl194c homozygous disruptant displayed reduced sporulation.	gene_phenotype
69906	1	333468	6	NULL	NULL	NULL	NULL	YGL194c 3	GP		is sensitive to					brefeldin A	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_306	14587103	YGL194c  3  3  C  Hos2 Histone deacetylase Repression of early sporulation genes Sensitivity to brefeldin A	gene_phenotype
69907	2	333468	6	NULL	NULL	0	NULL	Hos2 	GP		is sensitive to					brefeldin A	Chemical				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_306	14587103	YGL194c  3  3  C  Hos2 Histone deacetylase Repression of early sporulation genes Sensitivity to brefeldin A	gene_phenotype
69914	1	333471	6	NULL	NULL	NULL	NULL	YJL112w	GP	mutant	displays					mitochondria morphology	CellComponent	defects in			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_151_2_333_s_113	11038180	Cells bearing a null-mutation in YJL112w displayed mitochondrial morphology and distribution defects identical to those found in  gag mutant cells (data not shown).	gene_phenotype
69917	2	333471	6	NULL	NULL	0	NULL	gag	GP	mutant	displays					mitochondria distribution	CellComponent	defects in			NULL		0	NULL	NULL	NULL	gw60_cellbiol_151_2_333_s_113	11038180	Cells bearing a null-mutation in YJL112w displayed mitochondrial morphology and distribution defects identical to those found in  gag mutant cells (data not shown).	gene_phenotype
69919	3	333471	6	NULL	NULL	0	NULL	YJL112w	GP	mutant	displays					mitochondria morphology	CellComponent	defects in			NULL		0	NULL	NULL	NULL	gw60_cellbiol_151_2_333_s_113	11038180	Cells bearing a null-mutation in YJL112w displayed mitochondrial morphology and distribution defects identical to those found in  gag mutant cells (data not shown).	gene_phenotype
69921	4	333471	6	NULL	NULL	NULL	NULL	gag	GP	mutant	displays					mitochondria distribution	CellComponent	defects in			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_151_2_333_s_113	11038180	Cells bearing a null-mutation in YJL112w displayed mitochondrial morphology and distribution defects identical to those found in  gag mutant cells (data not shown).	gene_phenotype
69925	1	333472	6	NULL	NULL	NULL	NULL	YLR118c	GP		activates					lysophospholipase	GP				NULL	S. cerevisiae	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_31740_s_30	12080046	We now have demonstrated that YLR118c, a  S. cerevisiae open reading frame, encodes an enzyme with both lysophospholipase and acyl-protein thioesterase activity  in vitro.	gene_phenotype
69928	2	333472	6	NULL	NULL	NULL	NULL	YLR118c	GP		activates					acyl-protein thioesterase	GP				NULL	S. cerevisiae	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_31740_s_30	12080046	We now have demonstrated that YLR118c, a  S. cerevisiae open reading frame, encodes an enzyme with both lysophospholipase and acyl-protein thioesterase activity  in vitro.	gene_phenotype
69932	1	333473	6	NULL	NULL	NULL	NULL	YLR118C	GP		activates					acyl-protein thioesterase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_31740_s_178	12080046	Yeast Strains Bearing a Deletion of the APT1 Gene--  Having established that the protein encoded by YLR118C did indeed have acyl-protein thioesterase activity, we proceeded to create a yeast strain that lacked the APT1 gene to assess further the  in vivo function of Apt1p.	gene_phenotype
69982	1	333477	6	NULL	NULL	NULL	NULL	ynl242w	GP		is defective in					sporulation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_32_30442_s_196	11382760	The  ynl242w homozygous null strain was found to be defective in sporulation and the gene was named  SPO72.	gene_phenotype
69983	2	333477	6	NULL	NULL	0	NULL	ynl242w	GP		is					SPO72	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_32_30442_s_196	11382760	The  ynl242w homozygous null strain was found to be defective in sporulation and the gene was named  SPO72.	gene_phenotype
69984	1	333478	6	NULL	NULL	0	NULL	ynl242w mutant	GP		is defective in					sporulation	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_32_30442_s_209	11382760	The defect in autophagy seen in the  apg2delta strain explains the previously observed sporulation defect of the  ynl242w mutant ( 29).	gene_phenotype
70073	1	333479	6	NULL	NULL	0	NULL	starvation	Process		induces					autophagy	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_42422_s_232	11533052	We have shown recently that YNL242w complemented  apg2, a mutant defective in starvation-induced autophagy ( 42).	gene_phenotype
70074	2	333479	6	NULL	NULL	0	NULL	YNL242w	GP		is defective in					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_42422_s_232	11533052	We have shown recently that YNL242w complemented  apg2, a mutant defective in starvation-induced autophagy ( 42).	gene_phenotype
70077	1	333480	6	NULL	NULL	0	NULL	proteins	GP		moved from					cytoplasm	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_32_30442_s_198	11382760	Because our studies suggest a more specific role for the  YNL242w gene product in transport of proteins from the cytoplasm to the vacuole, we will refer to this ORF as  APG2 hereafter in this study.	gene_phenotype
70078	2	333480	6	NULL	NULL	0	NULL	proteins	GP		moved to					vacuoles	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_32_30442_s_198	11382760	Because our studies suggest a more specific role for the  YNL242w gene product in transport of proteins from the cytoplasm to the vacuole, we will refer to this ORF as  APG2 hereafter in this study.	gene_phenotype
70079	3	333480	6	NULL	NULL	0	NULL	statement 2	Process		occurs after					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_32_30442_s_198	11382760	Because our studies suggest a more specific role for the  YNL242w gene product in transport of proteins from the cytoplasm to the vacuole, we will refer to this ORF as  APG2 hereafter in this study.	gene_phenotype
70080	4	333480	6	NULL	NULL	0	NULL	YNL242w	GP		is					APG2	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_32_30442_s_198	11382760	Because our studies suggest a more specific role for the  YNL242w gene product in transport of proteins from the cytoplasm to the vacuole, we will refer to this ORF as  APG2 hereafter in this study.	gene_phenotype
70081	5	333480	6	NULL	NULL	0	NULL	YNL242w	GP		plays a role in					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_32_30442_s_198	11382760	Because our studies suggest a more specific role for the  YNL242w gene product in transport of proteins from the cytoplasm to the vacuole, we will refer to this ORF as  APG2 hereafter in this study.	gene_phenotype
71732	1	333483	6	NULL	NULL	0	NULL	omega -Minus region	CellComponent		determines					fusion protein	GP	localization of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_41_26946_s_88	9756943	Identification of omega -Minus Regions Determining Cellular Localization of the Fusion Proteins-- Our previous study ( 24) has shown that the addition of the most C-terminal 40 amino acids of Yjr151c or Ydr077w to a reporter protein directs the resulting fusion proteins into the cell wall and that the addition of the C-terminal amino acids of Yir039c or Ylr120c directs their fusion proteins to the plasma membrane.	gene_phenotype
71733	2	333483	6	NULL	NULL	0	NULL	fusion protein	GP		is directed to					cell wall	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_41_26946_s_88	9756943	Identification of omega -Minus Regions Determining Cellular Localization of the Fusion Proteins-- Our previous study ( 24) has shown that the addition of the most C-terminal 40 amino acids of Yjr151c or Ydr077w to a reporter protein directs the resulting fusion proteins into the cell wall and that the addition of the C-terminal amino acids of Yir039c or Ylr120c directs their fusion proteins to the plasma membrane.	gene_phenotype
71734	3	333483	6	NULL	NULL	0	NULL				directs			C-terminal 40 amino acids of Yjr151c		statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_41_26946_s_88	9756943	Identification of omega -Minus Regions Determining Cellular Localization of the Fusion Proteins-- Our previous study ( 24) has shown that the addition of the most C-terminal 40 amino acids of Yjr151c or Ydr077w to a reporter protein directs the resulting fusion proteins into the cell wall and that the addition of the C-terminal amino acids of Yir039c or Ylr120c directs their fusion proteins to the plasma membrane.	gene_phenotype
71735	4	333483	6	NULL	NULL	0	NULL				directs			C-terminal 40 amino acids of Ydr077w		statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_41_26946_s_88	9756943	Identification of omega -Minus Regions Determining Cellular Localization of the Fusion Proteins-- Our previous study ( 24) has shown that the addition of the most C-terminal 40 amino acids of Yjr151c or Ydr077w to a reporter protein directs the resulting fusion proteins into the cell wall and that the addition of the C-terminal amino acids of Yir039c or Ylr120c directs their fusion proteins to the plasma membrane.	gene_phenotype
71736	5	333483	6	NULL	NULL	0	NULL	fusion protein	GP		is directed to					plasma membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_41_26946_s_88	9756943	Identification of omega -Minus Regions Determining Cellular Localization of the Fusion Proteins-- Our previous study ( 24) has shown that the addition of the most C-terminal 40 amino acids of Yjr151c or Ydr077w to a reporter protein directs the resulting fusion proteins into the cell wall and that the addition of the C-terminal amino acids of Yir039c or Ylr120c directs their fusion proteins to the plasma membrane.	gene_phenotype
71737	6	333483	6	NULL	NULL	0	NULL				directs			C-terminal amino acids of Yir039c		statement 5					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_41_26946_s_88	9756943	Identification of omega -Minus Regions Determining Cellular Localization of the Fusion Proteins-- Our previous study ( 24) has shown that the addition of the most C-terminal 40 amino acids of Yjr151c or Ydr077w to a reporter protein directs the resulting fusion proteins into the cell wall and that the addition of the C-terminal amino acids of Yir039c or Ylr120c directs their fusion proteins to the plasma membrane.	gene_phenotype
71738	7	333483	6	NULL	NULL	0	NULL				directs			C-terminal amino acids of  Ylr120c		statement 5					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_41_26946_s_88	9756943	Identification of omega -Minus Regions Determining Cellular Localization of the Fusion Proteins-- Our previous study ( 24) has shown that the addition of the most C-terminal 40 amino acids of Yjr151c or Ydr077w to a reporter protein directs the resulting fusion proteins into the cell wall and that the addition of the C-terminal amino acids of Yir039c or Ylr120c directs their fusion proteins to the plasma membrane.	gene_phenotype
71739	1	333485	6	NULL	NULL	0	NULL	YNL072w gene			encodes					RNase H					NULL		0	NULL	NULL	NULL	gw60_febslett_421_1_23_s_108	9462832	The following criteria convinced us that gene YNL072w does indeed encode a RNase H: (i) expression in and purification from  E. coli resulted in a protein which is strongly recognized by an antibody, raised against purified calf thymus RNase HI, and (ii) a yeast strain from whose genome gene YNL072w was deleted showed a significant decrease in total RNase H activity ( Fig. 3).	gene_phenotype
71740	2	333485	6	NULL	NULL	0	NULL	YNL072w gene		deletion of	decreases					RNase H		activity of			NULL		0	NULL	NULL	NULL	gw60_febslett_421_1_23_s_108	9462832	The following criteria convinced us that gene YNL072w does indeed encode a RNase H: (i) expression in and purification from  E. coli resulted in a protein which is strongly recognized by an antibody, raised against purified calf thymus RNase HI, and (ii) a yeast strain from whose genome gene YNL072w was deleted showed a significant decrease in total RNase H activity ( Fig. 3).	gene_phenotype
71741	1	333486	6	NULL	NULL	0	NULL	ORF YNL072w	GP		is located on					chromosome XIV	Chromosome				NULL		0	NULL	NULL	NULL	gw60_febslett_421_1_23_s_63	9462832	When searching the budding yeast genome for homologies with the sequence of the enzymatically active subunit of human RNase HI (Frank et al., in preparation) we found ORF YNL072w on chromosome XIV, which encodes a hypothetical protein of 34.9 kDa.	gene_phenotype
71742	2	333486	6	NULL	NULL	NULL	NULL	statement 1	Process		encodes					hypothetical protein of 34.9 kDa	GP				NULL		NULL	NULL	NULL	NULL	gw60_febslett_421_1_23_s_63	9462832	When searching the budding yeast genome for homologies with the sequence of the enzymatically active subunit of human RNase HI (Frank et al., in preparation) we found ORF YNL072w on chromosome XIV, which encodes a hypothetical protein of 34.9 kDa.	gene_phenotype
71743	1	333488	6	NULL	NULL	0	NULL	AUT7 (YBL078c)	GP		is essential for					autophagy					NULL		0	NULL	NULL	NULL	gw60_embo_17_13_3597_s_101	9649430	AUT7 (YBL078c) is essential for autophagy	gene_phenotype
71744	1	333489	6	NULL	NULL	0	NULL	ORF YBL078c (AUT7)	GP		acts as a 					aut2-1 suppressor	GP	mutant			NULL		0	NULL	NULL	NULL	gw60_embo_17_13_3597_s_83	9649430	Isolation of ORF YBL078c (AUT7), an extragenic suppressor of aut2-1 mutant phenotypes: another gene essential for autophagy	gene_phenotype
71765	1	333491	6	NULL	NULL	0	NULL	 GPI-CWPs Ccw12	GP		contains					133 amino acids	amino acid				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_3_239_s_146	12165426	Some proteins, like the very small  but presumably abundant GPI-CWPs Ccw12 and Ydr134c with a predicted unprocessed size  of 133 and 66 amino acids, respectively, and a codon adaptation index of 0.870 and  0.646, respectively, may be used as a means to present mannan to the cell surface  ( Fig. 1).	gene_phenotype
71766	2	333491	6	NULL	NULL	0	NULL	GPI-CWPs Ydr134c	GP		contains					66 amino acids	amino acid				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_3_239_s_146	12165426	Some proteins, like the very small  but presumably abundant GPI-CWPs Ccw12 and Ydr134c with a predicted unprocessed size  of 133 and 66 amino acids, respectively, and a codon adaptation index of 0.870 and  0.646, respectively, may be used as a means to present mannan to the cell surface  ( Fig. 1).	gene_phenotype
71767	3	333491	6	NULL	NULL	0	NULL	mannan	chemical		is presented to					cell surface	cell component				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_3_239_s_146	12165426	Some proteins, like the very small  but presumably abundant GPI-CWPs Ccw12 and Ydr134c with a predicted unprocessed size  of 133 and 66 amino acids, respectively, and a codon adaptation index of 0.870 and  0.646, respectively, may be used as a means to present mannan to the cell surface  ( Fig. 1).	gene_phenotype
71768	1	333492	6	NULL	NULL	0	NULL	YER130c gene	GP		is activated by					Haa1p	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_36_37973_s_188	15229222	The  YER130c gene was shown to be activated by Haa1p, a transcription factor that also activates the  TPO2 gene encoding the polyamine transport protein (see below) ( ).	gene_phenotype
71769	2	333492	6	NULL	NULL	0	NULL	Haa1p	GP		is a type of					Transcription factor	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_36_37973_s_188	15229222	The  YER130c gene was shown to be activated by Haa1p, a transcription factor that also activates the  TPO2 gene encoding the polyamine transport protein (see below) ( ).	gene_phenotype
71770	3	333492	6	NULL	NULL	0	NULL	TPO2 gene	GP		encodes					polyamine transport protein	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_36_37973_s_188	15229222	The  YER130c gene was shown to be activated by Haa1p, a transcription factor that also activates the  TPO2 gene encoding the polyamine transport protein (see below) ( ).	gene_phenotype
71771	4	333492	6	NULL	NULL	0	NULL	Haa1p	GP		activates					TPO2 gene	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_36_37973_s_188	15229222	The  YER130c gene was shown to be activated by Haa1p, a transcription factor that also activates the  TPO2 gene encoding the polyamine transport protein (see below) ( ).	gene_phenotype
71772	1	333494	6	NULL	NULL	0	NULL	YGL183	GP		is a type of					multicopy plasmid	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_9_3078_s_145	11940665	A multicopy plasmid carrying YGL183c suppresses the  hop2-ts defects in spore formation and viable spore production (Fig.  1B); sporulation efficiency is 5%, and spore viability is 82%.	gene_phenotype
71773	2	333494	6	NULL	NULL	0	NULL	hop2-ts	GP		defects in					spore	organism part	formation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_9_3078_s_145	11940665	A multicopy plasmid carrying YGL183c suppresses the  hop2-ts defects in spore formation and viable spore production (Fig.  1B); sporulation efficiency is 5%, and spore viability is 82%.	gene_phenotype
71774	3	333494	6	NULL	NULL	0	NULL	hop2-ts	GP		defects in					spore	organism part	viable;; production of 			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_9_3078_s_145	11940665	A multicopy plasmid carrying YGL183c suppresses the  hop2-ts defects in spore formation and viable spore production (Fig.  1B); sporulation efficiency is 5%, and spore viability is 82%.	gene_phenotype
71775	1	333496	6	NULL	NULL	NULL	NULL	SPA2 YLL021W Protein	GP		is involved in					cell polarity	process				NULL		NULL	NULL	NULL	NULL	gw70_yeast_22_2_79_s_155	15645503	SPA2  YLL021W Protein involved in cell polarity and cell fusion during mating.	gene_phenotype
71776	2	333496	6	NULL	NULL	0	NULL	SPA2 YLL021W Protein	GP		is involved in					cell fusion	process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_155	15645503	SPA2  YLL021W Protein involved in cell polarity and cell fusion during mating.	gene_phenotype
71777	1	333497	6	NULL	NULL	0	NULL	FUS1	GP		is induced by					pheromone	chemical				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_70	10657304	Genes labeled in the plots include previously identified ( FUS1,  FIG1) and novel ( YML047C,  YPL192C) pheromone-induced genes and mitotic cell cycle S phase-induced genes ( HHF1, histone H4, and  RNR1, ribonucleotide reductase large subunit).	gene_phenotype
71778	2	333497	6	NULL	NULL	0	NULL	FIG1	GP		is induced by					pheromone	chemical				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_70	10657304	Genes labeled in the plots include previously identified ( FUS1,  FIG1) and novel ( YML047C,  YPL192C) pheromone-induced genes and mitotic cell cycle S phase-induced genes ( HHF1, histone H4, and  RNR1, ribonucleotide reductase large subunit).	gene_phenotype
71779	3	333497	6	NULL	NULL	0	NULL	YML047C	GP		is induced by					pheromone	chemical				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_70	10657304	Genes labeled in the plots include previously identified ( FUS1,  FIG1) and novel ( YML047C,  YPL192C) pheromone-induced genes and mitotic cell cycle S phase-induced genes ( HHF1, histone H4, and  RNR1, ribonucleotide reductase large subunit).	gene_phenotype
71780	4	333497	6	NULL	NULL	0	NULL	YPL192C	GP		is induced by					pheromone	chemical				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_70	10657304	Genes labeled in the plots include previously identified ( FUS1,  FIG1) and novel ( YML047C,  YPL192C) pheromone-induced genes and mitotic cell cycle S phase-induced genes ( HHF1, histone H4, and  RNR1, ribonucleotide reductase large subunit).	gene_phenotype
71781	5	333497	6	NULL	NULL	NULL	NULL	HHF1	GP		is induced by					 mitotic cell cycle S phase	process				NULL		NULL	NULL	NULL	NULL	gw60_science_287_5454_873_s_70	10657304	Genes labeled in the plots include previously identified ( FUS1,  FIG1) and novel ( YML047C,  YPL192C) pheromone-induced genes and mitotic cell cycle S phase-induced genes ( HHF1, histone H4, and  RNR1, ribonucleotide reductase large subunit).	gene_phenotype
71782	6	333497	6	NULL	NULL	NULL	NULL	histone H4	GP		is induced by					mitotic cell cycle S phase	process				NULL		NULL	NULL	NULL	NULL	gw60_science_287_5454_873_s_70	10657304	Genes labeled in the plots include previously identified ( FUS1,  FIG1) and novel ( YML047C,  YPL192C) pheromone-induced genes and mitotic cell cycle S phase-induced genes ( HHF1, histone H4, and  RNR1, ribonucleotide reductase large subunit).	gene_phenotype
71783	7	333497	6	NULL	NULL	0	NULL	RNR1	GP		is induced by					mitotic cell cycle S phase	process				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_70	10657304	Genes labeled in the plots include previously identified ( FUS1,  FIG1) and novel ( YML047C,  YPL192C) pheromone-induced genes and mitotic cell cycle S phase-induced genes ( HHF1, histone H4, and  RNR1, ribonucleotide reductase large subunit).	gene_phenotype
71784	8	333497	6	NULL	NULL	0	NULL	ribonucleotide reductase large subunit	GP		is induced by					mitotic cell cycle S phase	process				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_70	10657304	Genes labeled in the plots include previously identified ( FUS1,  FIG1) and novel ( YML047C,  YPL192C) pheromone-induced genes and mitotic cell cycle S phase-induced genes ( HHF1, histone H4, and  RNR1, ribonucleotide reductase large subunit).	gene_phenotype
71785	1	333498	6	NULL	NULL	0	NULL	YML070W/ DAK1	GP		results in					DAK activity	process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1415_s_131	12401799	Overexpression of the  YML070W/ DAK1 gene product in a DAK double deletion strain resulted in a roughly 250-fold enhanced specific DAK activity compared with the wild type to 1040 units/mg protein during growth in basal medium	gene_phenotype
71786	1	333499	6	NULL	NULL	0	NULL	YNL278W	GP	mutant	shows					cell shape	PhysicalPhenomenon	abnormal			NULL		0	NULL	NULL	NULL	gw70_yeast_20_5_407_s_135	12673624	The disruptant of  YNL278W showed abnormal cell shape and abnormal deposition of chitin (Figure  2B).	gene_phenotype
71787	2	333499	6	NULL	NULL	0	NULL	YNL278W	GP	mutant	shows					chitin 	cell component	abnormal;; deposition of 			NULL		0	NULL	NULL	NULL	gw70_yeast_20_5_407_s_135	12673624	The disruptant of  YNL278W showed abnormal cell shape and abnormal deposition of chitin (Figure  2B).	gene_phenotype
71788	1	333500	6	NULL	NULL	0	NULL	Nug1	GP	yeast	is essential for					viability	process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_460_s_138	16251348	In contrast, genes encoding similar putative GTPases from yeast,  Nug1 ( YER006W) and  Nug2/Nog2 ( YNR053C; Bassler  et al., 2001 ; Saveanu  et al., 2001 ) were essential for viability.	gene_phenotype
71789	2	333500	6	NULL	NULL	0	NULL	Nug2/Nog2	GP		is essential for					viability	process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_1_460_s_138	16251348	In contrast, genes encoding similar putative GTPases from yeast,  Nug1 ( YER006W) and  Nug2/Nog2 ( YNR053C; Bassler  et al., 2001 ; Saveanu  et al., 2001 ) were essential for viability.	gene_phenotype
71790	1	333501	6	NULL	NULL	0	NULL	Ynr074cp	GP	purified	degrades					nuclei	cell component	yeast			NULL		0	NULL	NULL	NULL	gw70_cellbiol_166_7_969_s_6	15381687	Purified Ynr074cp degrades yeast nuclei and plasmid DNA.  YNR074C disruption rescues yeast cells from oxygen stress and delays age-induced apoptosis.	gene_phenotype
71791	2	333501	6	NULL	NULL	0	NULL	Ynr074cp	GP		degrades					plasmid DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_cellbiol_166_7_969_s_6	15381687	Purified Ynr074cp degrades yeast nuclei and plasmid DNA.  YNR074C disruption rescues yeast cells from oxygen stress and delays age-induced apoptosis.	gene_phenotype
71792	3	333501	6	NULL	NULL	0	NULL	age	PhysicalPhenomenon		induces					apoptosis	process				NULL		0	NULL	NULL	NULL	gw70_cellbiol_166_7_969_s_6	15381687	Purified Ynr074cp degrades yeast nuclei and plasmid DNA.  YNR074C disruption rescues yeast cells from oxygen stress and delays age-induced apoptosis.	gene_phenotype
71793	4	333501	6	NULL	NULL	NULL	NULL	Ynr074cp	GP	disruption of	delays					statement 3	process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_7_969_s_6	15381687	Purified Ynr074cp degrades yeast nuclei and plasmid DNA.  YNR074C disruption rescues yeast cells from oxygen stress and delays age-induced apoptosis.	gene_phenotype
71794	5	333501	6	NULL	NULL	0	NULL	oxygen stress	PhysicalPhenomenon		disrupts					yeast cells	Cell				NULL		0	NULL	NULL	NULL	gw70_cellbiol_166_7_969_s_6	15381687	Purified Ynr074cp degrades yeast nuclei and plasmid DNA.  YNR074C disruption rescues yeast cells from oxygen stress and delays age-induced apoptosis.	gene_phenotype
71795	6	333501	6	NULL	NULL	NULL	NULL	Ynr074cp	GP	disruption of	rescues					statement 5	process				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_7_969_s_6	15381687	Purified Ynr074cp degrades yeast nuclei and plasmid DNA.  YNR074C disruption rescues yeast cells from oxygen stress and delays age-induced apoptosis.	gene_phenotype
71796	1	333503	6	NULL	NULL	0	NULL	Ynr074cp	GP		is homologous to					AIF	GP				NULL		0	NULL	NULL	NULL	gw70_cellbiol_166_7_969_s_4	15381687	Here, we show that the yeast AIF homologue Ynr074cp controls yeast apoptosis.	gene_phenotype
71797	2	333503	6	NULL	NULL	0	NULL	Ynr074cp	GP	yeast	controls					apoptosis	process				NULL		0	NULL	NULL	NULL	gw70_cellbiol_166_7_969_s_4	15381687	Here, we show that the yeast AIF homologue Ynr074cp controls yeast apoptosis.	gene_phenotype
71798	1	333504	6	NULL	NULL	0	NULL	AIF	GP		migrate to					nucleus	cell component				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_4_1802_s_257	16436509	We also tried to investigate whether Ndi1p migrate to nucleus, because AIF (possibly its yeast homologue YNR074C, too) does during apoptosis (Susin  et al., 1999 ;	gene_phenotype
71799	2	333504	6	NULL	NULL	0	NULL	statement 1	process		occurs during					apoptosis	process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_4_1802_s_257	16436509	We also tried to investigate whether Ndi1p migrate to nucleus, because AIF (possibly its yeast homologue YNR074C, too) does during apoptosis (Susin  et al., 1999 ;	gene_phenotype
71800	1	333505	6	NULL	NULL	NULL	NULL	Aif1p	GP		translocates from					mitochondria	cell component				NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_166_7_969_s_56	15381687	Aif1p translocates from mitochondria to the nucleus upon apoptosis induction   To determine the cellular localization of Aif1p in yeast cells, we expressed GFP-tagged Ynr074cp (Aif1pyEGFP).	gene_phenotype
71801	2	333505	6	NULL	NULL	0	NULL	Aif1p	GP		translocates to					nucleus	cell component				NULL		0	NULL	NULL	NULL	gw70_cellbiol_166_7_969_s_56	15381687	Aif1p translocates from mitochondria to the nucleus upon apoptosis induction   To determine the cellular localization of Aif1p in yeast cells, we expressed GFP-tagged Ynr074cp (Aif1pyEGFP).	gene_phenotype
71802	3	333505	6	NULL	NULL	0	NULL	statement 1	process		occurs upon					apoptosis	process	induction of 			NULL		0	NULL	NULL	NULL	gw70_cellbiol_166_7_969_s_56	15381687	Aif1p translocates from mitochondria to the nucleus upon apoptosis induction   To determine the cellular localization of Aif1p in yeast cells, we expressed GFP-tagged Ynr074cp (Aif1pyEGFP).	gene_phenotype
71803	4	333505	6	NULL	NULL	0	NULL	statement 2	process		occurs upon					apoptosis	process	induction of 			NULL		0	NULL	NULL	NULL	gw70_cellbiol_166_7_969_s_56	15381687	Aif1p translocates from mitochondria to the nucleus upon apoptosis induction   To determine the cellular localization of Aif1p in yeast cells, we expressed GFP-tagged Ynr074cp (Aif1pyEGFP).	gene_phenotype
71808	1	333507	6	NULL	NULL	NULL	NULL	Nse1p	GP		bind					Rhc18p	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_24_21585_s_114	11927594	Nse1p Forms a Large Complex with Rhc18p and Yol034wp-- To identify proteins associating with Nse1p in budding yeast cells, we attempted to immunopurify complexes containing Nse1p.	gene_phenotype
71809	2	333507	6	NULL	NULL	0	NULL	Nse1p	GP		bind					Yo1034wp	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_24_21585_s_114	11927594	Nse1p Forms a Large Complex with Rhc18p and Yol034wp-- To identify proteins associating with Nse1p in budding yeast cells, we attempted to immunopurify complexes containing Nse1p.	gene_phenotype
71810	3	333507	6	NULL	NULL	NULL	NULL	statement 1	process		occurs simultaneously with					statement 2	process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_24_21585_s_114	11927594	Nse1p Forms a Large Complex with Rhc18p and Yol034wp-- To identify proteins associating with Nse1p in budding yeast cells, we attempted to immunopurify complexes containing Nse1p.	gene_phenotype
71811	1	333509	6	NULL	NULL	0	NULL	CDC53			has sequence homology with					cullins					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_25_22828_s_129	12676951	The Budding Yeast S. cerevisiae Genome Contains Four Cullin  Genes -- CDC53, CUL3 (ORF YGR003w),  CUL8 (ORF YJL047c), and a  more distant relative,  APC2, which shares only limited sequence  homology with cullins ( Fig.  1 A).	gene_phenotype
71812	2	333509	6	NULL	NULL	0	NULL	CUL3 (ORF YGR003w)			has sequence homology with					cullins					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_25_22828_s_129	12676951	The Budding Yeast S. cerevisiae Genome Contains Four Cullin  Genes -- CDC53, CUL3 (ORF YGR003w),  CUL8 (ORF YJL047c), and a  more distant relative,  APC2, which shares only limited sequence  homology with cullins ( Fig.  1 A).	gene_phenotype
71813	3	333509	6	NULL	NULL	0	NULL	CUL8 (ORF YJL047c)			has sequence homology with					cullins					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_25_22828_s_129	12676951	The Budding Yeast S. cerevisiae Genome Contains Four Cullin  Genes -- CDC53, CUL3 (ORF YGR003w),  CUL8 (ORF YJL047c), and a  more distant relative,  APC2, which shares only limited sequence  homology with cullins ( Fig.  1 A).	gene_phenotype
71814	4	333509	6	NULL	NULL	0	NULL	APC2			has sequence homology with					cullins					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_25_22828_s_129	12676951	The Budding Yeast S. cerevisiae Genome Contains Four Cullin  Genes -- CDC53, CUL3 (ORF YGR003w),  CUL8 (ORF YJL047c), and a  more distant relative,  APC2, which shares only limited sequence  homology with cullins ( Fig.  1 A).	gene_phenotype
71815	1	333511	6	NULL	NULL	0	NULL	YBR016w	GP	polarized distribution of	involves					endocytosis					NULL		0	NULL	NULL	NULL	gw60_currbiol_13_18_1636_s_80	13678596	(B) The polarized distribution of YBR016w involves endocytosis.	gene_phenotype
71816	1	333512	6	NULL	NULL	0	NULL	Fth1	GP		is required for					endocytosis	process	normal;; liquid phase			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_11_4676_s_191	14593073	These Fks1-interacting proteins include Fth1, a protein required for normal fluid phase endocytosis (Wiederkehr  et al., 2001 ); Srv2, a protein involved in actin organization and internalization (Wesp  et al., 1997 ); Ygl051w, a protein that interacts with the endocytic protein Pan1 (Wendland  et al., 1996 ; Poirey  et al., 2002 ); Lcb2, a protein required for receptor internalization that is in involved in the production of sphingoid bases and in activation of the Pkh kinases (Zanolari  et al., 2000 ; Friant  et al., 2001 ); and Stt4, a PI-4 kinase that contributes to localization of Rom2 (Audhya  et al., 2000 ; Audhya and Emr, 2002 ).	gene_phenotype
71817	2	333512	6	NULL	NULL	0	NULL	Srv2	GP		is involved in					actin	cell component	organization of 			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_11_4676_s_191	14593073	These Fks1-interacting proteins include Fth1, a protein required for normal fluid phase endocytosis (Wiederkehr  et al., 2001 ); Srv2, a protein involved in actin organization and internalization (Wesp  et al., 1997 ); Ygl051w, a protein that interacts with the endocytic protein Pan1 (Wendland  et al., 1996 ; Poirey  et al., 2002 ); Lcb2, a protein required for receptor internalization that is in involved in the production of sphingoid bases and in activation of the Pkh kinases (Zanolari  et al., 2000 ; Friant  et al., 2001 ); and Stt4, a PI-4 kinase that contributes to localization of Rom2 (Audhya  et al., 2000 ; Audhya and Emr, 2002 ).	gene_phenotype
71818	3	333512	6	NULL	NULL	0	NULL	Srv2	GP		is involved in					actin	cell component	internalization of 			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_11_4676_s_191	14593073	These Fks1-interacting proteins include Fth1, a protein required for normal fluid phase endocytosis (Wiederkehr  et al., 2001 ); Srv2, a protein involved in actin organization and internalization (Wesp  et al., 1997 ); Ygl051w, a protein that interacts with the endocytic protein Pan1 (Wendland  et al., 1996 ; Poirey  et al., 2002 ); Lcb2, a protein required for receptor internalization that is in involved in the production of sphingoid bases and in activation of the Pkh kinases (Zanolari  et al., 2000 ; Friant  et al., 2001 ); and Stt4, a PI-4 kinase that contributes to localization of Rom2 (Audhya  et al., 2000 ; Audhya and Emr, 2002 ).	gene_phenotype
71819	4	333512	6	NULL	NULL	0	NULL	Srv2	GP		bind					Pan1	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_11_4676_s_191	14593073	These Fks1-interacting proteins include Fth1, a protein required for normal fluid phase endocytosis (Wiederkehr  et al., 2001 ); Srv2, a protein involved in actin organization and internalization (Wesp  et al., 1997 ); Ygl051w, a protein that interacts with the endocytic protein Pan1 (Wendland  et al., 1996 ; Poirey  et al., 2002 ); Lcb2, a protein required for receptor internalization that is in involved in the production of sphingoid bases and in activation of the Pkh kinases (Zanolari  et al., 2000 ; Friant  et al., 2001 ); and Stt4, a PI-4 kinase that contributes to localization of Rom2 (Audhya  et al., 2000 ; Audhya and Emr, 2002 ).	gene_phenotype
71820	5	333512	6	NULL	NULL	0	NULL	Lcb2	GP		is required for					receptor	GP	internalization of 			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_11_4676_s_191	14593073	These Fks1-interacting proteins include Fth1, a protein required for normal fluid phase endocytosis (Wiederkehr  et al., 2001 ); Srv2, a protein involved in actin organization and internalization (Wesp  et al., 1997 ); Ygl051w, a protein that interacts with the endocytic protein Pan1 (Wendland  et al., 1996 ; Poirey  et al., 2002 ); Lcb2, a protein required for receptor internalization that is in involved in the production of sphingoid bases and in activation of the Pkh kinases (Zanolari  et al., 2000 ; Friant  et al., 2001 ); and Stt4, a PI-4 kinase that contributes to localization of Rom2 (Audhya  et al., 2000 ; Audhya and Emr, 2002 ).	gene_phenotype
71821	6	333512	6	NULL	NULL	0	NULL	Lcb2	GP		is involved in					sphingoid bases	chemical	production of 			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_11_4676_s_191	14593073	These Fks1-interacting proteins include Fth1, a protein required for normal fluid phase endocytosis (Wiederkehr  et al., 2001 ); Srv2, a protein involved in actin organization and internalization (Wesp  et al., 1997 ); Ygl051w, a protein that interacts with the endocytic protein Pan1 (Wendland  et al., 1996 ; Poirey  et al., 2002 ); Lcb2, a protein required for receptor internalization that is in involved in the production of sphingoid bases and in activation of the Pkh kinases (Zanolari  et al., 2000 ; Friant  et al., 2001 ); and Stt4, a PI-4 kinase that contributes to localization of Rom2 (Audhya  et al., 2000 ; Audhya and Emr, 2002 ).	gene_phenotype
71822	7	333512	6	NULL	NULL	0	NULL	Lcb2	GP		is required for					Pkh kinase	GP	activation of 			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_11_4676_s_191	14593073	These Fks1-interacting proteins include Fth1, a protein required for normal fluid phase endocytosis (Wiederkehr  et al., 2001 ); Srv2, a protein involved in actin organization and internalization (Wesp  et al., 1997 ); Ygl051w, a protein that interacts with the endocytic protein Pan1 (Wendland  et al., 1996 ; Poirey  et al., 2002 ); Lcb2, a protein required for receptor internalization that is in involved in the production of sphingoid bases and in activation of the Pkh kinases (Zanolari  et al., 2000 ; Friant  et al., 2001 ); and Stt4, a PI-4 kinase that contributes to localization of Rom2 (Audhya  et al., 2000 ; Audhya and Emr, 2002 ).	gene_phenotype
71823	8	333512	6	NULL	NULL	0	NULL	Stt4	GP		is a type of					PI-4 kinase	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_11_4676_s_191	14593073	These Fks1-interacting proteins include Fth1, a protein required for normal fluid phase endocytosis (Wiederkehr  et al., 2001 ); Srv2, a protein involved in actin organization and internalization (Wesp  et al., 1997 ); Ygl051w, a protein that interacts with the endocytic protein Pan1 (Wendland  et al., 1996 ; Poirey  et al., 2002 ); Lcb2, a protein required for receptor internalization that is in involved in the production of sphingoid bases and in activation of the Pkh kinases (Zanolari  et al., 2000 ; Friant  et al., 2001 ); and Stt4, a PI-4 kinase that contributes to localization of Rom2 (Audhya  et al., 2000 ; Audhya and Emr, 2002 ).	gene_phenotype
71824	9	333512	6	NULL	NULL	0	NULL	Stt4	GP		contributes to					Rom2	GP	localization of 			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_11_4676_s_191	14593073	These Fks1-interacting proteins include Fth1, a protein required for normal fluid phase endocytosis (Wiederkehr  et al., 2001 ); Srv2, a protein involved in actin organization and internalization (Wesp  et al., 1997 ); Ygl051w, a protein that interacts with the endocytic protein Pan1 (Wendland  et al., 1996 ; Poirey  et al., 2002 ); Lcb2, a protein required for receptor internalization that is in involved in the production of sphingoid bases and in activation of the Pkh kinases (Zanolari  et al., 2000 ; Friant  et al., 2001 ); and Stt4, a PI-4 kinase that contributes to localization of Rom2 (Audhya  et al., 2000 ; Audhya and Emr, 2002 ).	gene_phenotype
71825	1	333513	6	NULL	NULL	NULL	NULL	YJR110w	GP	yeast	encodes					myotubularin-like protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_16_8910_s_142	10900271	Budding yeast contain a single ORF (YJR110w) that encodes a myotubularin-like protein ( 5,  8).	gene_phenotype
71826	1	333514	6	NULL	NULL	0	NULL	YJR110w	GP	recombinant	possesses					PI(3)P phosphatase activity	process				NULL		0	NULL	NULL	NULL	gw60_pnas_97_16_8910_s_144	10900271	In addition, we have found that a recombinant YJR110w fusion protein possesses  in vitro PI(3)P phosphatase activity comparable to that of myotubularin (data not shown).	gene_phenotype
71827	1	333515	6	NULL	NULL	0	NULL	YMR1	GP		is					myotubularin-related gene	GP				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_70_0_247_s_421	11395408	Consistent with these observations, a null mutant strain of budding yeast in which  the myotubularin-related gene  YMR1 (YJR110w) is deleted exhibits increased PI(3)P levels compared to wild-type yeast  ( 138).	gene_phenotype
71828	2	333515	6	NULL	NULL	0	NULL	YJR110w	GP		increases					PI(3)P 	GP	levels of 			NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_70_0_247_s_421	11395408	Consistent with these observations, a null mutant strain of budding yeast in which  the myotubularin-related gene  YMR1 (YJR110w) is deleted exhibits increased PI(3)P levels compared to wild-type yeast  ( 138).	gene_phenotype
71829	1	333517	6	NULL	NULL	0	NULL	calcineurin	GP		is required for					cell wall	organism part				NULL		0	NULL	NULL	NULL	gw60_embo_19_14_3618_s_185	10899116	Calcineurin mutations are synthetically lethal with  vph6 or  fks1 mutations (because calcineurin is required for cell wall biosynthesis or cation homeostasis in such mutants), whereas  ykl159c vph6 and  ykl159c fks1 double mutants were viable (not shown).	gene_phenotype
71830	2	333517	6	NULL	NULL	0	NULL	calcineurin	GP		is required for					cation homeostasis	process				NULL		0	NULL	NULL	NULL	gw60_embo_19_14_3618_s_185	10899116	Calcineurin mutations are synthetically lethal with  vph6 or  fks1 mutations (because calcineurin is required for cell wall biosynthesis or cation homeostasis in such mutants), whereas  ykl159c vph6 and  ykl159c fks1 double mutants were viable (not shown).	gene_phenotype
71831	1	333518	6	NULL	NULL	NULL	NULL	YKL159c	GP		is a homolog of					CBP1	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_19_14_3618_s_39	10899116	Saccharomyces cerevisiae mutants lacking the CBP1 homolog YKL159c were viable and sensitive to cation stress, similar to calcineurin mutants.	gene_phenotype
71832	1	333520	6	NULL	NULL	0	NULL	APG17 YLR423c	GP		is required for					Apg1 protein kinase	GP	activation of 			NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_268	15334557	APG17   YLR423c Required for activation of Apg1 protein kinase; autophagy pathway	gene_phenotype
71835	1	333522	6	NULL	NULL	0	NULL	Ykt6p	GP		is involved in					 endoplasmic reticulum-Golgi transport	process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24323_s_188	15044472	In addition, two other proteins were identified: Ykt6p, a protein involved in endoplasmic reticulum-Golgi transport, and YOR051C, an uncharacterized protein associated with the nuclear pore complex ( ).	gene_phenotype
71836	2	333522	6	NULL	NULL	0	NULL	YOR051C	GP		is associated with					nuclear pore complex	cell component				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24323_s_188	15044472	In addition, two other proteins were identified: Ykt6p, a protein involved in endoplasmic reticulum-Golgi transport, and YOR051C, an uncharacterized protein associated with the nuclear pore complex ( ).	gene_phenotype
71840	1	333524	6	NULL	NULL	0	NULL	SPS2	GP		is not essential for					sporulation	process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_5_3259_s_205	16672465	Homozygous haploid null  SPS2 and  YCL048w mutants of  S. cerevisiae sporulate as efficiently as wild-type strains with normal spore viability, suggesting that these genes are not essential for sporulation ( ,  ).	gene_phenotype
71841	2	333524	6	NULL	NULL	NULL	NULL	YCL048w	GP		is not essential for					sporulation	process				NULL		NULL	NULL	NULL	NULL	gw70_applenvironmicrob_72_5_3259_s_205	16672465	Homozygous haploid null  SPS2 and  YCL048w mutants of  S. cerevisiae sporulate as efficiently as wild-type strains with normal spore viability, suggesting that these genes are not essential for sporulation ( ,  ).	gene_phenotype
71837	1	333525	6	NULL	NULL	0	NULL	YCL048w/ SPS2	GP	homozygous;; mutant	produces					spores	organism part	blebbed			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_5_3259_s_206	16672465	However, the  YCL048w/ SPS2 homozygous diploid null mutant produced aberrant, blebbed spores surrounded by abnormal cell walls ( ), showing that these two  ECM33 homologs indeed play essential roles in ascospore formation.	gene_phenotype
71838	2	333525	6	NULL	NULL	0	NULL	YCL048w/ SPS2	GP	homozygous;; mutant	is surrounded by					cell wall	cell component	abnormal			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_5_3259_s_206	16672465	However, the  YCL048w/ SPS2 homozygous diploid null mutant produced aberrant, blebbed spores surrounded by abnormal cell walls ( ), showing that these two  ECM33 homologs indeed play essential roles in ascospore formation.	gene_phenotype
71839	3	333525	6	NULL	NULL	0	NULL	YCL048w/ SPS2	GP		plays a role in					ascospore	cell component	formation of			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_5_3259_s_206	16672465	However, the  YCL048w/ SPS2 homozygous diploid null mutant produced aberrant, blebbed spores surrounded by abnormal cell walls ( ), showing that these two  ECM33 homologs indeed play essential roles in ascospore formation.	gene_phenotype
68151	1	333526	11	NULL	NULL	0	NULL	Ecm33p	GP		is associate with					sporulation	Process				NULL	S. cerevisiae	0	NULL	NULL	NULL	gw70_applenvironmicrob_72_5_3259_s_139	16672465	In  S. cerevisiae, Ecm33p belongs to a family which contains four members that are separated into two clusters (Sps2p and YCL048wp; Pst1p and Ecm33p) and that are associated with a sporulation function, at least for the first cluster (A. M. Neiman, personal communication;  ).	gene_phenotype
68152	2	333526	11	NULL	NULL	0	NULL	Pst1p	GP		is associate with					sporulation	Process				NULL	S. cerevisiae	0	NULL	NULL	NULL	gw70_applenvironmicrob_72_5_3259_s_139	16672465	In  S. cerevisiae, Ecm33p belongs to a family which contains four members that are separated into two clusters (Sps2p and YCL048wp; Pst1p and Ecm33p) and that are associated with a sporulation function, at least for the first cluster (A. M. Neiman, personal communication;  ).	gene_phenotype
68153	3	333526	11	NULL	NULL	0	NULL	YCL048wp	GP		is associate with					sporulation	Process				NULL	S. cerevisiae	0	NULL	NULL	NULL	gw70_applenvironmicrob_72_5_3259_s_139	16672465	In  S. cerevisiae, Ecm33p belongs to a family which contains four members that are separated into two clusters (Sps2p and YCL048wp; Pst1p and Ecm33p) and that are associated with a sporulation function, at least for the first cluster (A. M. Neiman, personal communication;  ).	gene_phenotype
68154	4	333526	11	NULL	NULL	0	NULL	Sps2p	GP		is associate with					sporulation	Process				NULL	S. cerevisiae	0	NULL	NULL	NULL	gw70_applenvironmicrob_72_5_3259_s_139	16672465	In  S. cerevisiae, Ecm33p belongs to a family which contains four members that are separated into two clusters (Sps2p and YCL048wp; Pst1p and Ecm33p) and that are associated with a sporulation function, at least for the first cluster (A. M. Neiman, personal communication;  ).	gene_phenotype
68155	1	333527	11	NULL	NULL	0	NULL	FEN2	GP	mutant	is					YCR028c	GP				NULL	mitochondrial	0	NULL	NULL	NULL	gw70_genetics_166_2_707_s_314	15020461	However,  FEN2 (YCR028c) was listed in a table of mitochondrial mutants that showed a reduction in cell size.	gene_phenotype
68156	2	333527	11	NULL	NULL	0	NULL	FEN2	GP		shows					reduction in cell size	Process				NULL	mitochondrial	0	NULL	NULL	NULL	gw70_genetics_166_2_707_s_314	15020461	However,  FEN2 (YCR028c) was listed in a table of mitochondrial mutants that showed a reduction in cell size.	gene_phenotype
68157	1	333528	11	NULL	NULL	0	NULL	YCR028c	GP		binds					Single-stranded DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_147	15334557	RIM1   YCR028c Single-stranded DNA-binding protein; essential for mitochondrial genome maintenance	gene_phenotype
68158	2	333528	11	NULL	NULL	0	NULL	YCR028c	GP		is essential for					genome maintenance	Process	mitochondrial			NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_147	15334557	RIM1   YCR028c Single-stranded DNA-binding protein; essential for mitochondrial genome maintenance	gene_phenotype
68159	1	333530	11	NULL	NULL	NULL	NULL	YDR205W	NucleicAcid	S. cerevisiae	is the locus name of					MSC2 protein	GP	S. cerevisiae			NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_27_2_313_s_390	12829273	A third  S. cerevisiae protein, MSC2 (YDR205W), is also involved in zinc transport [  ].	gene_phenotype
68160	2	333530	11	NULL	NULL	NULL	NULL	statement 1	GP		is involved in 					zinc transport	Process				NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_27_2_313_s_390	12829273	A third  S. cerevisiae protein, MSC2 (YDR205W), is also involved in zinc transport [  ].	gene_phenotype
68161	1	333531	11	NULL	NULL	NULL	NULL	YDR205W	NucleicAcid	 yeast 	is a type of 					membrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_7_5036_s_2	11058603	The sequence of the yeast gene YDR205W places it within the family of cation diffusion facilitators: membrane proteins that transport transition metals.	gene_phenotype
68162	2	333531	11	NULL	NULL	NULL	NULL	YDR205W	NucleicAcid	 yeast 	is a type of 					cation diffusion facilitator	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_7_5036_s_2	11058603	The sequence of the yeast gene YDR205W places it within the family of cation diffusion facilitators: membrane proteins that transport transition metals.	gene_phenotype
68163	3	333531	11	NULL	NULL	NULL	NULL	YDR205W	NucleicAcid	 yeast 	transports					transition metals	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_7_5036_s_2	11058603	The sequence of the yeast gene YDR205W places it within the family of cation diffusion facilitators: membrane proteins that transport transition metals.	gene_phenotype
68164	1	333532	11	NULL	NULL	0	NULL	YDR205W	GP	Deletion	 increases					unequal sister chromatid recombination	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_7_5036_s_3	11058603	Deletion of YDR205W was reported to result in an increase in unequal sister chromatid recombination and was named meiotic sister chromatid recombination 2 ( MSC2; Thompson, D.	gene_phenotype
68165	2	333532	11	NULL	NULL	0	NULL	statement 1	Process		is					meiotic sister chromatid recombination 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_7_5036_s_3	11058603	Deletion of YDR205W was reported to result in an increase in unequal sister chromatid recombination and was named meiotic sister chromatid recombination 2 ( MSC2; Thompson, D.	gene_phenotype
68166	3	333532	11	NULL	NULL	NULL	NULL	meiotic sister chromatid recombination 2	Process		is					MSC2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_7_5036_s_3	11058603	Deletion of YDR205W was reported to result in an increase in unequal sister chromatid recombination and was named meiotic sister chromatid recombination 2 ( MSC2; Thompson, D.	gene_phenotype
68167	1	333533	11	10	NULL	NULL	NULL	nhx1delta cells	Cell		secretes					CPY	GP				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_12_4277_s_149	11102523	The secretion of CPY by  nhx1delta cells was therefore due to the loss of Nhx1p rather than the loss of a protein encoded by the YDR455C ORF.	gene_phenotype
68168	2	333533	11	NULL	NULL	0	NULL	Nhx1p	GP	 loss of	leads to					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_12_4277_s_149	11102523	The secretion of CPY by  nhx1delta cells was therefore due to the loss of Nhx1p rather than the loss of a protein encoded by the YDR455C ORF.	gene_phenotype
68644	3	333533	11	NULL	NULL	0	NULL	YDR455C ORF	NucleicAcid	loss of;;protein encoded by	does not lead to					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_12_4277_s_149	11102523	The secretion of CPY by  nhx1delta cells was therefore due to the loss of Nhx1p rather than the loss of a protein encoded by the YDR455C ORF.	gene_phenotype
68169	1	333534	11	NULL	NULL	NULL	NULL	statement 4	NucleicAcid		is required for 					 growth	Process				NULL		NULL	NULL	NULL	NULL	gw70_genomeres_16_3_365_s_194	16510898	YGR271C-A and  YGR272C constitute a contiguous ORF required for growth at 37 degrees C, growth on HU-containing  media and cell cycle progression.	gene_phenotype
68170	2	333534	11	NULL	NULL	NULL	NULL	statement 4	NucleicAcid		is required for 					 growth	Process				NULL	on HU-containing media	NULL	NULL	NULL	NULL	gw70_genomeres_16_3_365_s_194	16510898	YGR271C-A and  YGR272C constitute a contiguous ORF required for growth at 37 degrees C, growth on HU-containing  media and cell cycle progression.	gene_phenotype
68171	3	333534	11	NULL	NULL	NULL	NULL	statement 4	NucleicAcid		is required for 					cell cycle progression	Process				NULL		NULL	NULL	NULL	NULL	gw70_genomeres_16_3_365_s_194	16510898	YGR271C-A and  YGR272C constitute a contiguous ORF required for growth at 37 degrees C, growth on HU-containing  media and cell cycle progression.	gene_phenotype
68643	4	333534	11	NULL	NULL	0	NULL	YGR271C-A ORF	NucleicAcid		is contiguous to					YGR272C ORF	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_genomeres_16_3_365_s_194	16510898	YGR271C-A and  YGR272C constitute a contiguous ORF required for growth at 37 degrees C, growth on HU-containing  media and cell cycle progression.	gene_phenotype
68175	1	333535	11	NULL	NULL	NULL	NULL	YGR272c ORF	NucleicAcid	inactivation 	 result in					slower growth rate	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_yeast_16_4_10669875_s_5	10669875	The same analysis also revealed that sporulation  of the ygr272cDelta heterozygous diploid produced two small colonies per  ascus that were also G418-resistant, indicating that the inactivation  of ORF YGR272c could result in a slower growth rate.	gene_phenotype
68404	1	333536	11	NULL	NULL	NULL	NULL	Ynl189w	NucleicAcid		is the locus name of					Srp1	GP				NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_3_159_s_144	16498703	Ynl189w  Srp1  1 Karyopherin   homologue, forms a dimer with karyopherin   Kap95p to mediate import of nuclear proteins; binds the nuclear localization signal  of the substrate during import; may also play a role in regulation of protein degradation  L2H  [ 24]	gene_phenotype
68405	2	333536	11	NULL	NULL	0	NULL	Srp1	GP		is  homologue of					Karyopherin	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_144	16498703	Ynl189w  Srp1  1 Karyopherin   homologue, forms a dimer with karyopherin   Kap95p to mediate import of nuclear proteins; binds the nuclear localization signal  of the substrate during import; may also play a role in regulation of protein degradation  L2H  [ 24]	gene_phenotype
68406	3	333536	11	NULL	NULL	0	NULL	Srp1	GP		dimerise with					Kap95p	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_144	16498703	Ynl189w  Srp1  1 Karyopherin   homologue, forms a dimer with karyopherin   Kap95p to mediate import of nuclear proteins; binds the nuclear localization signal  of the substrate during import; may also play a role in regulation of protein degradation  L2H  [ 24]	gene_phenotype
68407	4	333536	11	NULL	NULL	NULL	NULL	statement 3	GP		import					 nuclear proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_3_159_s_144	16498703	Ynl189w  Srp1  1 Karyopherin   homologue, forms a dimer with karyopherin   Kap95p to mediate import of nuclear proteins; binds the nuclear localization signal  of the substrate during import; may also play a role in regulation of protein degradation  L2H  [ 24]	gene_phenotype
68408	5	333536	11	NULL	NULL	NULL	NULL	Srp1	GP		regulate		may			protein degradation	Process				NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_3_159_s_144	16498703	Ynl189w  Srp1  1 Karyopherin   homologue, forms a dimer with karyopherin   Kap95p to mediate import of nuclear proteins; binds the nuclear localization signal  of the substrate during import; may also play a role in regulation of protein degradation  L2H  [ 24]	gene_phenotype
69243	6	333536	11	NULL	NULL	0	NULL	Kap95p	GP		is a type of 					karyopherin	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_144	16498703	Ynl189w  Srp1  1 Karyopherin   homologue, forms a dimer with karyopherin   Kap95p to mediate import of nuclear proteins; binds the nuclear localization signal  of the substrate during import; may also play a role in regulation of protein degradation  L2H  [ 24]	gene_phenotype
68409	1	333537	11	NULL	NULL	0	NULL	M1 RNA	NucleicAcid		mediate					cleavage	Process				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_21_6920_s_130	16332695	However, in the presence of 40 mM Sr2+ and 0.1 mM Mg2+ we did not observe M1 RNA mediated cleavage (data not shown).	gene_phenotype
68495	1	333539	11	NULL	NULL	0	NULL	Sct1p	GP		is a type of 					choline transporter suppressor	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_41710_s_37	11544256	In the present study, we demonstrate that the choline transporter suppressor, Sct1p, encoded by  YBL011w, and a closely related protein encoded by  YKR067w, are two yeast  sn-1 acyltransferases catalyzing both G-3-P and DHAP acylation.	gene_phenotype
68496	2	333539	11	NULL	NULL	NULL	NULL	statement 1	GP		is encoded by					YBL011w	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_41710_s_37	11544256	In the present study, we demonstrate that the choline transporter suppressor, Sct1p, encoded by  YBL011w, and a closely related protein encoded by  YKR067w, are two yeast  sn-1 acyltransferases catalyzing both G-3-P and DHAP acylation.	gene_phenotype
68497	3	333539	11	NULL	NULL	NULL	NULL	statement 1	GP		is a type of 					sn-1 acyltransferases	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_45_41710_s_37	11544256	In the present study, we demonstrate that the choline transporter suppressor, Sct1p, encoded by  YBL011w, and a closely related protein encoded by  YKR067w, are two yeast  sn-1 acyltransferases catalyzing both G-3-P and DHAP acylation.	gene_phenotype
68498	4	333539	11	NULL	NULL	0	NULL	statement 3	GP		 acylate					G-3-P	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_41710_s_37	11544256	In the present study, we demonstrate that the choline transporter suppressor, Sct1p, encoded by  YBL011w, and a closely related protein encoded by  YKR067w, are two yeast  sn-1 acyltransferases catalyzing both G-3-P and DHAP acylation.	gene_phenotype
68499	5	333539	11	NULL	NULL	0	NULL	statement 3	GP		acylate					DHAP	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_41710_s_37	11544256	In the present study, we demonstrate that the choline transporter suppressor, Sct1p, encoded by  YBL011w, and a closely related protein encoded by  YKR067w, are two yeast  sn-1 acyltransferases catalyzing both G-3-P and DHAP acylation.	gene_phenotype
68500	1	333540	11	NULL	NULL	NULL	NULL	YBR026c	NucleicAcid		restore					respiratory growth	Process				NULL	ybr026cdelta strain	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_18_6243_s_267	11509667	The complementation experiments with either  YBR026c or  ETR1 showed that either of these genes was sufficient for restoring respiratory growth to the  ybr026cdelta strain (Fig.  4).	gene_phenotype
68501	2	333540	11	NULL	NULL	NULL	NULL	ETR1 gene	GP		restore					respiratory growth	Process	ybr026cdelta strain			NULL	ybr026cdelta strain	NULL	NULL	NULL	NULL	gw60_molcellbiol_21_18_6243_s_267	11509667	The complementation experiments with either  YBR026c or  ETR1 showed that either of these genes was sufficient for restoring respiratory growth to the  ybr026cdelta strain (Fig.  4).	gene_phenotype
68502	1	333541	11	NULL	NULL	NULL	NULL	YOR267c	NucleicAcid		is a type of 					 protein kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_20_7654_s_177	11003661	As indicated above, the protein kinase YOR267c also affected Pma1 activity, although to a lesser extent than Ptk2.	gene_phenotype
68503	2	333541	11	NULL	NULL	NULL	NULL	statement 1	GP		affects					 Pma1	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_20_7654_s_177	11003661	As indicated above, the protein kinase YOR267c also affected Pma1 activity, although to a lesser extent than Ptk2.	gene_phenotype
68504	3	333541	11	NULL	NULL	NULL	NULL	Ptk2	GP		affects					Pma1	GP	activity of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_20_7654_s_177	11003661	As indicated above, the protein kinase YOR267c also affected Pma1 activity, although to a lesser extent than Ptk2.	gene_phenotype
68505	4	333541	11	NULL	NULL	0	NULL	statement 2	Process		is lesser than					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_20_7654_s_177	11003661	As indicated above, the protein kinase YOR267c also affected Pma1 activity, although to a lesser extent than Ptk2.	gene_phenotype
69245	1	333543	11	NULL	NULL	0	NULL	LB	AminoAcid		function as					scilencer-barrier	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw60_genetics_160_4_1401_s_209	11973296	Our preliminary deletion analysis indicates that sequences from both the UAS and the ORF of  YCL069W contribute to the silencing-barrier function of LB (X. BI, unpublished results).	gene_phenotype
69246	2	333543	11	NULL	NULL	0	NULL	UAS	NucleicAcid		contribute to					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_160_4_1401_s_209	11973296	Our preliminary deletion analysis indicates that sequences from both the UAS and the ORF of  YCL069W contribute to the silencing-barrier function of LB (X. BI, unpublished results).	gene_phenotype
69247	3	333543	11	NULL	NULL	0	NULL	YCL069W ORF	NucleicAcid		contribute to					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_160_4_1401_s_209	11973296	Our preliminary deletion analysis indicates that sequences from both the UAS and the ORF of  YCL069W contribute to the silencing-barrier function of LB (X. BI, unpublished results).	gene_phenotype
68508	1	333547	11	NULL	NULL	0	NULL	Fcy2p	GP		is a transporter for					 adenine	NucleicAcid				NULL	S. cerevisiae	0	NULL	NULL	NULL	gw70_jbiolchem_278_21_18990_s_121	12649274	The identified ORF, YGL186C, codes for a protein  with homology to Fcy2p, the  S. cerevisiae transporter for adenine,  guanine, and cytosine ( ,  ).	gene_phenotype
68509	2	333547	11	NULL	NULL	0	NULL	Fcy2p	GP		is a transporter for					guanine	NucleicAcid				NULL	S. cerevisiae	0	NULL	NULL	NULL	gw70_jbiolchem_278_21_18990_s_121	12649274	The identified ORF, YGL186C, codes for a protein  with homology to Fcy2p, the  S. cerevisiae transporter for adenine,  guanine, and cytosine ( ,  ).	gene_phenotype
68510	3	333547	11	NULL	NULL	0	NULL	Fcy2p	GP		is a transporter for					 cytosine	NucleicAcid				NULL	S. cerevisiae	0	NULL	NULL	NULL	gw70_jbiolchem_278_21_18990_s_121	12649274	The identified ORF, YGL186C, codes for a protein  with homology to Fcy2p, the  S. cerevisiae transporter for adenine,  guanine, and cytosine ( ,  ).	gene_phenotype
70491	4	333547	11	NULL	NULL	0	NULL	YGL186C	NucleicAcid		is a type of 					ORF	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_21_18990_s_121	12649274	The identified ORF, YGL186C, codes for a protein  with homology to Fcy2p, the  S. cerevisiae transporter for adenine,  guanine, and cytosine ( ,  ).	gene_phenotype
70492	5	333547	11	NULL	NULL	0	NULL	YGL186C protein	GP		is homologous to					Fcy2p	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_21_18990_s_121	12649274	The identified ORF, YGL186C, codes for a protein  with homology to Fcy2p, the  S. cerevisiae transporter for adenine,  guanine, and cytosine ( ,  ).	gene_phenotype
68512	2	333549	11	NULL	NULL	NULL	NULL	 lyso-PC 	Chemical		is					lysophosphatidylcholine	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biochem-j_387_pt-3_15588229_s_2	15588229	When the yeast protein Ypr140w was expressed in Escherichia coli, a lyso-PC  [lysophosphatidylcholine (1-acylglycerophosphorylcholine)] acyltransferase  activity was found associated with the membranes of the bacteria.	gene_phenotype
69169	3	333549	11	NULL	NULL	NULL	NULL	Ypr140w protein	GP	yeast	is expressed in					Escherichia coli	Organism				NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_biochem-j_387_pt-3_15588229_s_2	15588229	When the yeast protein Ypr140w was expressed in Escherichia coli, a lyso-PC  [lysophosphatidylcholine (1-acylglycerophosphorylcholine)] acyltransferase  activity was found associated with the membranes of the bacteria.	gene_phenotype
70493	4	333549	11	NULL	NULL	0	NULL	1-acylglycerophosphorylcholine	Chemical		is a synonym of					lyso-PC	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_biochem-j_387_pt-3_15588229_s_2	15588229	When the yeast protein Ypr140w was expressed in Escherichia coli, a lyso-PC  [lysophosphatidylcholine (1-acylglycerophosphorylcholine)] acyltransferase  activity was found associated with the membranes of the bacteria.	gene_phenotype
70494	5	333549	11	NULL	NULL	0	NULL	statement 3	GP		activates					lyso- PC acyltransferase	GP				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_biochem-j_387_pt-3_15588229_s_2	15588229	When the yeast protein Ypr140w was expressed in Escherichia coli, a lyso-PC  [lysophosphatidylcholine (1-acylglycerophosphorylcholine)] acyltransferase  activity was found associated with the membranes of the bacteria.	gene_phenotype
70495	6	333549	11	NULL	NULL	0	NULL	statement 5	Process		is associated with					Escherichia coli	Organism	membranes of			NULL		0	NULL	NULL	NULL	abs-batch0517-0529_biochem-j_387_pt-3_15588229_s_2	15588229	When the yeast protein Ypr140w was expressed in Escherichia coli, a lyso-PC  [lysophosphatidylcholine (1-acylglycerophosphorylcholine)] acyltransferase  activity was found associated with the membranes of the bacteria.	gene_phenotype
68513	1	333550	11	NULL	NULL	NULL	NULL	Ycl045cp	NucleicAcid		is a type of 					class I membrane proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_30_11148_s_98	16847257	Ycl045cp has the same predicted topology as Erp1p (they are both class I membrane proteins with a large luminal domain and a short C-terminal cytoplasmic tail), and we suggest that Ycl045cp is also part of the ER-Golgi transport machinery.	gene_phenotype
68514	2	333550	11	NULL	NULL	NULL	NULL	statement 1	GP		contains								large luminal domain;; short C-terminal cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_30_11148_s_98	16847257	Ycl045cp has the same predicted topology as Erp1p (they are both class I membrane proteins with a large luminal domain and a short C-terminal cytoplasmic tail), and we suggest that Ycl045cp is also part of the ER-Golgi transport machinery.	gene_phenotype
68516	4	333550	11	NULL	NULL	0	NULL	Erp1p	GP		is a type of 					class I membrane protein	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_30_11148_s_98	16847257	Ycl045cp has the same predicted topology as Erp1p (they are both class I membrane proteins with a large luminal domain and a short C-terminal cytoplasmic tail), and we suggest that Ycl045cp is also part of the ER-Golgi transport machinery.	gene_phenotype
68517	5	333550	11	NULL	NULL	NULL	NULL	statement 4			has a								large luminal domain;; short C-terminal cytoplasmic tail		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_30_11148_s_98	16847257	Ycl045cp has the same predicted topology as Erp1p (they are both class I membrane proteins with a large luminal domain and a short C-terminal cytoplasmic tail), and we suggest that Ycl045cp is also part of the ER-Golgi transport machinery.	gene_phenotype
68519	7	333550	11	NULL	NULL	NULL	NULL	statement 1	GP		is a part of 					transport machinery	Process	ER-Golgi 			NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_30_11148_s_98	16847257	Ycl045cp has the same predicted topology as Erp1p (they are both class I membrane proteins with a large luminal domain and a short C-terminal cytoplasmic tail), and we suggest that Ycl045cp is also part of the ER-Golgi transport machinery.	gene_phenotype
68520	1	333551	11	NULL	NULL	NULL	NULL	Sge1p	GP		is a type of 					multidrug transporter	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_30_11148_s_83	16847257	In particular, overexpression of the multidrug transporter Sge1p ( ), the COPII vesicle transport protein Erp1p ( ), and the functionally unclassified protein Ycl045cp induces hypertolerance to paraquat.	gene_phenotype
68521	2	333551	11	NULL	NULL	0	NULL	Erp1p	GP		is a type of 					COPII vesicle transport protein	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_30_11148_s_83	16847257	In particular, overexpression of the multidrug transporter Sge1p ( ), the COPII vesicle transport protein Erp1p ( ), and the functionally unclassified protein Ycl045cp induces hypertolerance to paraquat.	gene_phenotype
68522	3	333551	11	NULL	NULL	NULL	NULL	statement 1	GP	overexpression of	is hypertolerant to 					paraquat	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_30_11148_s_83	16847257	In particular, overexpression of the multidrug transporter Sge1p ( ), the COPII vesicle transport protein Erp1p ( ), and the functionally unclassified protein Ycl045cp induces hypertolerance to paraquat.	gene_phenotype
68523	4	333551	11	NULL	NULL	NULL	NULL	statement 2	GP	overexpression of	is hypertolerant to 					paraquat	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_30_11148_s_83	16847257	In particular, overexpression of the multidrug transporter Sge1p ( ), the COPII vesicle transport protein Erp1p ( ), and the functionally unclassified protein Ycl045cp induces hypertolerance to paraquat.	gene_phenotype
68524	5	333551	11	NULL	NULL	NULL	NULL	Ycl045cp protein		overexpression of	is hypertolerant to 					paraquat	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_30_11148_s_83	16847257	In particular, overexpression of the multidrug transporter Sge1p ( ), the COPII vesicle transport protein Erp1p ( ), and the functionally unclassified protein Ycl045cp induces hypertolerance to paraquat.	gene_phenotype
68525	1	333552	11	NULL	NULL	NULL	NULL	GET1	GP		involved in					Golgi-ER trafficking	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_30_11148_s_99	16847257	Consistent with this proposal, a recent genomewide epistatic miniarray analysis ( ) has identified genetic interactions between  YCL045C and  GET1 (involved in Golgi-ER trafficking),  PMR1 (Ca2+ transport into the Golgi), and  SSH1 (protein translocation into the ER).	gene_phenotype
68526	2	333552	11	NULL	NULL	NULL	NULL	GET1	GP		interacts with 		Genetic			YCL045C	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_30_11148_s_99	16847257	Consistent with this proposal, a recent genomewide epistatic miniarray analysis ( ) has identified genetic interactions between  YCL045C and  GET1 (involved in Golgi-ER trafficking),  PMR1 (Ca2+ transport into the Golgi), and  SSH1 (protein translocation into the ER).	gene_phenotype
68527	3	333552	11	NULL	NULL	NULL	NULL	Ca2+	Chemical		is transported into					golgi	Cell Component				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_30_11148_s_99	16847257	Consistent with this proposal, a recent genomewide epistatic miniarray analysis ( ) has identified genetic interactions between  YCL045C and  GET1 (involved in Golgi-ER trafficking),  PMR1 (Ca2+ transport into the Golgi), and  SSH1 (protein translocation into the ER).	gene_phenotype
68528	4	333552	11	NULL	NULL	NULL	NULL	protein	GP		translocate to					ER	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_30_11148_s_99	16847257	Consistent with this proposal, a recent genomewide epistatic miniarray analysis ( ) has identified genetic interactions between  YCL045C and  GET1 (involved in Golgi-ER trafficking),  PMR1 (Ca2+ transport into the Golgi), and  SSH1 (protein translocation into the ER).	gene_phenotype
70498	6	333552	11	NULL	NULL	0	NULL	PMR1	GP		plays a role in					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_103_30_11148_s_99	16847257	Consistent with this proposal, a recent genomewide epistatic miniarray analysis ( ) has identified genetic interactions between  YCL045C and  GET1 (involved in Golgi-ER trafficking),  PMR1 (Ca2+ transport into the Golgi), and  SSH1 (protein translocation into the ER).	gene_phenotype
70499	7	333552	11	NULL	NULL	0	NULL	SSH1	GP		plays a role in					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_103_30_11148_s_99	16847257	Consistent with this proposal, a recent genomewide epistatic miniarray analysis ( ) has identified genetic interactions between  YCL045C and  GET1 (involved in Golgi-ER trafficking),  PMR1 (Ca2+ transport into the Golgi), and  SSH1 (protein translocation into the ER).	gene_phenotype
70500	8	333552	11	NULL	NULL	0	NULL	PMR1	GP		interacts with 		genetic			SSH1	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_30_11148_s_99	16847257	Consistent with this proposal, a recent genomewide epistatic miniarray analysis ( ) has identified genetic interactions between  YCL045C and  GET1 (involved in Golgi-ER trafficking),  PMR1 (Ca2+ transport into the Golgi), and  SSH1 (protein translocation into the ER).	gene_phenotype
68530	1	333555	11	NULL	NULL	NULL	NULL	YGR024c	NucleicAcid		activates		possibly		 	tRNAHis guanylyltransferase	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_23_2889_s_86	14633974	To determine whether ORFs YGR024c and/or YDL076c are required for tRNAHis guanylyltransferase activity, we analyzed the tRNA of strains that lacked each protein.	gene_phenotype
68531	2	333555	11	NULL	NULL	NULL	NULL	YDL076c 	NucleicAcid		activates		possibly			tRNAHis guanylyltransferase 	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_23_2889_s_86	14633974	To determine whether ORFs YGR024c and/or YDL076c are required for tRNAHis guanylyltransferase activity, we analyzed the tRNA of strains that lacked each protein.	gene_phenotype
70496	3	333555	11	NULL	NULL	0	NULL	YGR024c 	NucleicAcid		is a type of 					ORF	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_23_2889_s_86	14633974	To determine whether ORFs YGR024c and/or YDL076c are required for tRNAHis guanylyltransferase activity, we analyzed the tRNA of strains that lacked each protein.	gene_phenotype
70497	4	333555	11	NULL	NULL	0	NULL	YDL076c 	NucleicAcid		is a type of 					ORF	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_23_2889_s_86	14633974	To determine whether ORFs YGR024c and/or YDL076c are required for tRNAHis guanylyltransferase activity, we analyzed the tRNA of strains that lacked each protein.	gene_phenotype
68532	1	333556	11	NULL	NULL	NULL	NULL	YDL076c protein	GP		copurifies with								tRNAHis		NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_23_2889_s_214	14633974	One or more of these activities could be stimulated by the protein encoded by ORF YDL076c, which also copurifies with tRNAHis guanylyltransferase activity (see above).	gene_phenotype
70490	2	333556	11	NULL	NULL	0	NULL	YDL076c	NucleicAcid		is a type of 					ORF	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_23_2889_s_214	14633974	One or more of these activities could be stimulated by the protein encoded by ORF YDL076c, which also copurifies with tRNAHis guanylyltransferase activity (see above).	gene_phenotype
69170	1	333558	11	NULL	NULL	NULL	NULL	Ygr189c	NucleicAcid		is the locus name of					Crh1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_9_3245_s_289	10757808	By means of fusion of the C-terminal domain of each protein to a reporter protein including a secretion signal, alpha-galactosidase, and a hemagglutinin (HA) epitope, these authors showed that Ygr189c (Crh1) and Yel040w (Crh2) fusion proteins were incorporated into the cell wall and released after treatment with laminarinase ( 14).	gene_phenotype
69171	2	333558	11	NULL	NULL	0	NULL	Yel040w	NucleicAcid		is the locus name of					Crh2	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_9_3245_s_289	10757808	By means of fusion of the C-terminal domain of each protein to a reporter protein including a secretion signal, alpha-galactosidase, and a hemagglutinin (HA) epitope, these authors showed that Ygr189c (Crh1) and Yel040w (Crh2) fusion proteins were incorporated into the cell wall and released after treatment with laminarinase ( 14).	gene_phenotype
69172	3	333558	11	NULL	NULL	NULL	NULL	Crh1	GP		is a type of 					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_9_3245_s_289	10757808	By means of fusion of the C-terminal domain of each protein to a reporter protein including a secretion signal, alpha-galactosidase, and a hemagglutinin (HA) epitope, these authors showed that Ygr189c (Crh1) and Yel040w (Crh2) fusion proteins were incorporated into the cell wall and released after treatment with laminarinase ( 14).	gene_phenotype
69173	4	333558	11	NULL	NULL	NULL	NULL	Crh2	GP		is a type of 					fusion protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_9_3245_s_289	10757808	By means of fusion of the C-terminal domain of each protein to a reporter protein including a secretion signal, alpha-galactosidase, and a hemagglutinin (HA) epitope, these authors showed that Ygr189c (Crh1) and Yel040w (Crh2) fusion proteins were incorporated into the cell wall and released after treatment with laminarinase ( 14).	gene_phenotype
69174	5	333558	11	NULL	NULL	NULL	NULL	Crh1	GP		is incorporated into					cell wall	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_9_3245_s_289	10757808	By means of fusion of the C-terminal domain of each protein to a reporter protein including a secretion signal, alpha-galactosidase, and a hemagglutinin (HA) epitope, these authors showed that Ygr189c (Crh1) and Yel040w (Crh2) fusion proteins were incorporated into the cell wall and released after treatment with laminarinase ( 14).	gene_phenotype
69175	6	333558	11	NULL	NULL	NULL	NULL	Crh2	GP		is incorporated into					cell wall	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_9_3245_s_289	10757808	By means of fusion of the C-terminal domain of each protein to a reporter protein including a secretion signal, alpha-galactosidase, and a hemagglutinin (HA) epitope, these authors showed that Ygr189c (Crh1) and Yel040w (Crh2) fusion proteins were incorporated into the cell wall and released after treatment with laminarinase ( 14).	gene_phenotype
69176	7	333558	11	NULL	NULL	NULL	NULL	laminarinase	GP	treatment	releases					Crh1	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_9_3245_s_289	10757808	By means of fusion of the C-terminal domain of each protein to a reporter protein including a secretion signal, alpha-galactosidase, and a hemagglutinin (HA) epitope, these authors showed that Ygr189c (Crh1) and Yel040w (Crh2) fusion proteins were incorporated into the cell wall and released after treatment with laminarinase ( 14).	gene_phenotype
69177	8	333558	11	NULL	NULL	NULL	NULL	laminarinase	GP	treatment	releases					Crh2	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_9_3245_s_289	10757808	By means of fusion of the C-terminal domain of each protein to a reporter protein including a secretion signal, alpha-galactosidase, and a hemagglutinin (HA) epitope, these authors showed that Ygr189c (Crh1) and Yel040w (Crh2) fusion proteins were incorporated into the cell wall and released after treatment with laminarinase ( 14).	gene_phenotype
70843	9	333558	11	NULL	NULL	0	NULL	statement 5	Process		occurs along with					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_9_3245_s_289	10757808	By means of fusion of the C-terminal domain of each protein to a reporter protein including a secretion signal, alpha-galactosidase, and a hemagglutinin (HA) epitope, these authors showed that Ygr189c (Crh1) and Yel040w (Crh2) fusion proteins were incorporated into the cell wall and released after treatment with laminarinase ( 14).	gene_phenotype
70844	10	333558	11	NULL	NULL	0	NULL	statement 6	Process		occurs along with					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_9_3245_s_289	10757808	By means of fusion of the C-terminal domain of each protein to a reporter protein including a secretion signal, alpha-galactosidase, and a hemagglutinin (HA) epitope, these authors showed that Ygr189c (Crh1) and Yel040w (Crh2) fusion proteins were incorporated into the cell wall and released after treatment with laminarinase ( 14).	gene_phenotype
69178	1	333559	11	NULL	NULL	0	NULL	YER062C	NucleicAcid		is the locus name of					Gpp2p	GP				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_182_1_1_s_39	10612722	Biochemical characterisation of the glycerol-3-phosphate phosphatase in  S. cerevisiae clearly linked the salt-induced  YER062C encoded protein (named Gpp2p) to this enzymatic activity and revealed a totally new protein class of small phosphatases [  19].	gene_phenotype
69179	2	333559	11	NULL	NULL	0	NULL	salt	Chemical		induced					statement 1	GP				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_182_1_1_s_39	10612722	Biochemical characterisation of the glycerol-3-phosphate phosphatase in  S. cerevisiae clearly linked the salt-induced  YER062C encoded protein (named Gpp2p) to this enzymatic activity and revealed a totally new protein class of small phosphatases [  19].	gene_phenotype
69180	3	333559	11	NULL	NULL	0	NULL	glycerol-3-phosphate phosphatase	GP	S. cerevisiae	linked to					statement 2	GP				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_182_1_1_s_39	10612722	Biochemical characterisation of the glycerol-3-phosphate phosphatase in  S. cerevisiae clearly linked the salt-induced  YER062C encoded protein (named Gpp2p) to this enzymatic activity and revealed a totally new protein class of small phosphatases [  19].	gene_phenotype
69181	1	333560	11	NULL	NULL	NULL	NULL	Uso1p protein	GP		 involved in					ER-vesicle transport	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_10_4595_s_249	16030260	The protein encoded by YFR016c has 22% similarity over a segment of 108 amino acids residues to Uso1p, a protein involved in ER-vesicle transport.	gene_phenotype
69185	1	333563	11	NULL	NULL	0	NULL	 TPO1	GP		is encoded by					YLL028w	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_8	9920864	The results indicate that a membrane protein encoded by  YLL028w ( TPO1) is a polyamine transport protein on the vacuolar membrane.	gene_phenotype
69186	2	333563	11	NULL	NULL	NULL	NULL	TPO1	GP		is a type of 					membrane protein 	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_8	9920864	The results indicate that a membrane protein encoded by  YLL028w ( TPO1) is a polyamine transport protein on the vacuolar membrane.	gene_phenotype
69187	3	333563	11	NULL	NULL	NULL	NULL	TPO1	GP		is a type of 					polyamine transport protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_8	9920864	The results indicate that a membrane protein encoded by  YLL028w ( TPO1) is a polyamine transport protein on the vacuolar membrane.	gene_phenotype
70845	4	333563	11	NULL	NULL	0	NULL	 TPO1	GP		is present on					vacuolar membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_8	9920864	The results indicate that a membrane protein encoded by  YLL028w ( TPO1) is a polyamine transport protein on the vacuolar membrane.	gene_phenotype
69191	1	333565	11	NULL	NULL	0	NULL	 transformed cells	Cell		are resistant to 					MGBG	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_5	9920864	The transformed cells became resistant to MGBG (methylglyoxal bis(guanylhydrazone)) and paraquat, but not Ni2+ and Co2+, suggesting that the protein encoded by  YLL028w is a transport protein specific for polyamines.	gene_phenotype
69192	2	333565	11	NULL	NULL	0	NULL	MGBG	Chemical		is					methylglyoxal bis guanylhydrazone	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_5	9920864	The transformed cells became resistant to MGBG (methylglyoxal bis(guanylhydrazone)) and paraquat, but not Ni2+ and Co2+, suggesting that the protein encoded by  YLL028w is a transport protein specific for polyamines.	gene_phenotype
69193	3	333565	11	NULL	NULL	0	NULL	transformed cells	Cell		are resistant to 					 paraquat	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_5	9920864	The transformed cells became resistant to MGBG (methylglyoxal bis(guanylhydrazone)) and paraquat, but not Ni2+ and Co2+, suggesting that the protein encoded by  YLL028w is a transport protein specific for polyamines.	gene_phenotype
69194	4	333565	11	NULL	NULL	0	NULL	transformed cells	Cell		are not resistant to 					Ni2+	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_5	9920864	The transformed cells became resistant to MGBG (methylglyoxal bis(guanylhydrazone)) and paraquat, but not Ni2+ and Co2+, suggesting that the protein encoded by  YLL028w is a transport protein specific for polyamines.	gene_phenotype
69195	5	333565	11	NULL	NULL	0	NULL	transformed cells	Cell		are not resistant to 					Co2+	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_5	9920864	The transformed cells became resistant to MGBG (methylglyoxal bis(guanylhydrazone)) and paraquat, but not Ni2+ and Co2+, suggesting that the protein encoded by  YLL028w is a transport protein specific for polyamines.	gene_phenotype
69196	6	333565	11	NULL	NULL	0	NULL	YLL028w	NucleicAcid		encodes for a 					transport protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_5	9920864	The transformed cells became resistant to MGBG (methylglyoxal bis(guanylhydrazone)) and paraquat, but not Ni2+ and Co2+, suggesting that the protein encoded by  YLL028w is a transport protein specific for polyamines.	gene_phenotype
69197	7	333565	11	NULL	NULL	0	NULL	statement 6	GP		is specific for					polyamines	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_5	9920864	The transformed cells became resistant to MGBG (methylglyoxal bis(guanylhydrazone)) and paraquat, but not Ni2+ and Co2+, suggesting that the protein encoded by  YLL028w is a transport protein specific for polyamines.	gene_phenotype
69198	1	333566	11	NULL	NULL	NULL	NULL	YLL028w	NucleicAcid		is a type of					 membrane protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_19	9920864	A membrane protein on vacuoles, which catalyzes proton gradient-dependent polyamine (putrescine, spermidine, and spermine) transport ( 18), was encoded by one of the genes ( YLL028w).	gene_phenotype
69199	2	333566	11	NULL	NULL	0	NULL	putrescine	Chemical		is a type of 					polyamine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_19	9920864	A membrane protein on vacuoles, which catalyzes proton gradient-dependent polyamine (putrescine, spermidine, and spermine) transport ( 18), was encoded by one of the genes ( YLL028w).	gene_phenotype
69200	3	333566	11	NULL	NULL	0	NULL	spermidine	Chemical		is a type of 					polyamine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_19	9920864	A membrane protein on vacuoles, which catalyzes proton gradient-dependent polyamine (putrescine, spermidine, and spermine) transport ( 18), was encoded by one of the genes ( YLL028w).	gene_phenotype
69201	4	333566	11	NULL	NULL	0	NULL	spermine	Chemical		is a type of 					polyamine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_19	9920864	A membrane protein on vacuoles, which catalyzes proton gradient-dependent polyamine (putrescine, spermidine, and spermine) transport ( 18), was encoded by one of the genes ( YLL028w).	gene_phenotype
69202	5	333566	11	NULL	NULL	NULL	NULL	putrescine	Chemical	 transport of	is dependent on					proton	Chemical	gradient of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_19	9920864	A membrane protein on vacuoles, which catalyzes proton gradient-dependent polyamine (putrescine, spermidine, and spermine) transport ( 18), was encoded by one of the genes ( YLL028w).	gene_phenotype
69203	6	333566	11	NULL	NULL	NULL	NULL	spermidine	Chemical	transport of	is dependent on					proton	Chemical	gradient of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_19	9920864	A membrane protein on vacuoles, which catalyzes proton gradient-dependent polyamine (putrescine, spermidine, and spermine) transport ( 18), was encoded by one of the genes ( YLL028w).	gene_phenotype
69204	7	333566	11	NULL	NULL	NULL	NULL	 spermine	Chemical	transport of	is dependent on					proton	Chemical	gradient of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_19	9920864	A membrane protein on vacuoles, which catalyzes proton gradient-dependent polyamine (putrescine, spermidine, and spermine) transport ( 18), was encoded by one of the genes ( YLL028w).	gene_phenotype
70846	8	333566	11	NULL	NULL	NULL	NULL	YLL028w	NucleicAcid		catalyzes					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_19	9920864	A membrane protein on vacuoles, which catalyzes proton gradient-dependent polyamine (putrescine, spermidine, and spermine) transport ( 18), was encoded by one of the genes ( YLL028w).	gene_phenotype
70847	9	333566	11	NULL	NULL	0	NULL	YLL028w	NucleicAcid		catalyzes					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_19	9920864	A membrane protein on vacuoles, which catalyzes proton gradient-dependent polyamine (putrescine, spermidine, and spermine) transport ( 18), was encoded by one of the genes ( YLL028w).	gene_phenotype
70848	10	333566	11	NULL	NULL	0	NULL	YLL028w	NucleicAcid		catalyzes					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3265_s_19	9920864	A membrane protein on vacuoles, which catalyzes proton gradient-dependent polyamine (putrescine, spermidine, and spermine) transport ( 18), was encoded by one of the genes ( YLL028w).	gene_phenotype
69205	1	333567	11	NULL	NULL	0	NULL	Ino4p	GP		 interacts with					yeast proteins	GP				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_22_4460_s_195	11071933	beta-Galactosidase activity resulting from two-hybrid interactions between Ino4p and Bck2p, YLR422W and YNR064C     CHO1 expression is regulated by growth phase   The above results indicate that Ino4p interacts with several yeast proteins.	gene_phenotype
69206	2	333567	11	NULL	NULL	0	NULL	Ino4p	GP		interacts with 					Bck2p	GP				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_22_4460_s_195	11071933	beta-Galactosidase activity resulting from two-hybrid interactions between Ino4p and Bck2p, YLR422W and YNR064C     CHO1 expression is regulated by growth phase   The above results indicate that Ino4p interacts with several yeast proteins.	gene_phenotype
69207	3	333567	11	NULL	NULL	0	NULL	YLR422W	GP		interacts with 					YNR064C	GP				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_22_4460_s_195	11071933	beta-Galactosidase activity resulting from two-hybrid interactions between Ino4p and Bck2p, YLR422W and YNR064C     CHO1 expression is regulated by growth phase   The above results indicate that Ino4p interacts with several yeast proteins.	gene_phenotype
69208	4	333567	11	NULL	NULL	NULL	NULL	growth phase	Process		regulates					CHO1	GP	 the expression of 			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_22_4460_s_195	11071933	beta-Galactosidase activity resulting from two-hybrid interactions between Ino4p and Bck2p, YLR422W and YNR064C     CHO1 expression is regulated by growth phase   The above results indicate that Ino4p interacts with several yeast proteins.	gene_phenotype
69209	5	333567	11	NULL	NULL	NULL	NULL	statement 2	Process		activates					beta-Galactosidase	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_22_4460_s_195	11071933	beta-Galactosidase activity resulting from two-hybrid interactions between Ino4p and Bck2p, YLR422W and YNR064C     CHO1 expression is regulated by growth phase   The above results indicate that Ino4p interacts with several yeast proteins.	gene_phenotype
69210	6	333567	11	NULL	NULL	NULL	NULL	statement 3	Process		activates					beta-Galactosidase	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_22_4460_s_195	11071933	beta-Galactosidase activity resulting from two-hybrid interactions between Ino4p and Bck2p, YLR422W and YNR064C     CHO1 expression is regulated by growth phase   The above results indicate that Ino4p interacts with several yeast proteins.	gene_phenotype
69211	1	333568	11	NULL	NULL	0	NULL	YMR159c	NucleicAcid		is essential for					autophagy	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_14_3888_s_70	10406794	Thus, YMR159c turned out to be essential for autophagy.	gene_phenotype
69212	1	333569	11	NULL	NULL	0	NULL	YNR051c	NucleicAcid		encodes for					BRE5	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_406	14587103	YNR051c/BRE5 encodes for a protein with no similarity to other proteins in the data bases;   ynr051c has been recently identified in the Secretion Node by Muren  et al. ([ 2001]) as a Brefeldin-sensitive strain.	gene_phenotype
69213	2	333569	11	NULL	NULL	NULL	NULL	YNR051c	NucleicAcid		is present in					Secretion Node	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_406	14587103	YNR051c/BRE5 encodes for a protein with no similarity to other proteins in the data bases;   ynr051c has been recently identified in the Secretion Node by Muren  et al. ([ 2001]) as a Brefeldin-sensitive strain.	gene_phenotype
70849	3	333569	11	NULL	NULL	0	NULL	YNR051c	NucleicAcid		is a type of 					Brefeldin-sensitive strain	Organism				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_406	14587103	YNR051c/BRE5 encodes for a protein with no similarity to other proteins in the data bases;   ynr051c has been recently identified in the Secretion Node by Muren  et al. ([ 2001]) as a Brefeldin-sensitive strain.	gene_phenotype
69214	1	333570	11	NULL	NULL	0	NULL	 yfr021w	NucleicAcid		is the locus name of					aut10	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_508_1_23_s_75	11707261	aut10  ( yfr021w ) cells are defective in the cvt pathway and autophagy	gene_phenotype
69215	2	333570	11	NULL	NULL	0	NULL	aut10 cells	Cell		are defective in					cvt pathway	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_508_1_23_s_75	11707261	aut10  ( yfr021w ) cells are defective in the cvt pathway and autophagy	gene_phenotype
69216	3	333570	11	NULL	NULL	0	NULL	aut10 cells	Cell		are defective in					 autophagy	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_508_1_23_s_75	11707261	aut10  ( yfr021w ) cells are defective in the cvt pathway and autophagy	gene_phenotype
69217	1	333571	11	NULL	NULL	NULL	NULL	YFR021w 	NucleicAcid		is a type of 					ORF	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_febslett_508_1_23_s_71	11707261	As shown below,  YFR021w is essential for autophagy, we therefore term this open reading frame  AUT10.	gene_phenotype
69218	2	333571	11	NULL	NULL	NULL	NULL	YFR021w ORF	NucleicAcid		is essential for					autophagy	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_508_1_23_s_71	11707261	As shown below,  YFR021w is essential for autophagy, we therefore term this open reading frame  AUT10.	gene_phenotype
70850	3	333571	11	NULL	NULL	0	NULL	YFR021w	NucleicAcid		is a synonym of					AUT10	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_508_1_23_s_71	11707261	As shown below,  YFR021w is essential for autophagy, we therefore term this open reading frame  AUT10.	gene_phenotype
69219	1	333572	11	NULL	NULL	NULL	NULL	YFR021w 	NucleicAcid		is a type of 					ORF	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_12_3821_s_248	11739783	Based on the above-mentioned phenomenon, we decided to examine whether the  S. cerevisiae homolog of  GSA12, the open reading frame  YFR021w, could also be a component in the Cvt/autophagic pathway and pexophagy in this yeast.	gene_phenotype
70851	2	333572	11	NULL	NULL	0	NULL	YFR021w	NucleicAcid	 S. cerevisiae	is a homolog of					GSA12	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_12_3821_s_248	11739783	Based on the above-mentioned phenomenon, we decided to examine whether the  S. cerevisiae homolog of  GSA12, the open reading frame  YFR021w, could also be a component in the Cvt/autophagic pathway and pexophagy in this yeast.	gene_phenotype
70852	3	333572	11	NULL	NULL	0	NULL	YFR021w	NucleicAcid	S. cerevisiae	is a component in		possibly			Cvt/autophagic pathway	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_12_3821_s_248	11739783	Based on the above-mentioned phenomenon, we decided to examine whether the  S. cerevisiae homolog of  GSA12, the open reading frame  YFR021w, could also be a component in the Cvt/autophagic pathway and pexophagy in this yeast.	gene_phenotype
70853	4	333572	11	NULL	NULL	0	NULL	YFR021w	NucleicAcid	S. cerevisiae	is a component in		possibly			pexophagy	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_12_3821_s_248	11739783	Based on the above-mentioned phenomenon, we decided to examine whether the  S. cerevisiae homolog of  GSA12, the open reading frame  YFR021w, could also be a component in the Cvt/autophagic pathway and pexophagy in this yeast.	gene_phenotype
69220	1	333573	11	NULL	NULL	0	NULL	YLR018c	NucleicAcid		is the locus name of					Pom34	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_397	14587103	YLR018c  2  0.5  C  Pom34 Component of the nuclear pore Nuclear-cytoplasmic transport	gene_phenotype
69221	2	333573	11	NULL	NULL	NULL	NULL	Pom34	GP		is a component of					 nuclear pore	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_397	14587103	YLR018c  2  0.5  C  Pom34 Component of the nuclear pore Nuclear-cytoplasmic transport	gene_phenotype
69222	3	333573	11	NULL	NULL	NULL	NULL	statement 2	GP		is essential for					Nuclear-cytoplasmic transport	Process				NULL		NULL	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_397	14587103	YLR018c  2  0.5  C  Pom34 Component of the nuclear pore Nuclear-cytoplasmic transport	gene_phenotype
69223	1	333574	11	NULL	NULL	0	NULL	YLR018c	NucleicAcid		encodes for					Pom34p	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_407	14587103	Finally,  YLR018c encodes Pom34p, a integral membrane protein that forms part of the nuclear pore complex  and is involved in the nuclear cytoplasmic transport (Rout  et al., [ 2000]).	gene_phenotype
69224	2	333574	11	NULL	NULL	0	NULL	Pom34p	GP		is a type of 					integral membrane protein	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_407	14587103	Finally,  YLR018c encodes Pom34p, a integral membrane protein that forms part of the nuclear pore complex  and is involved in the nuclear cytoplasmic transport (Rout  et al., [ 2000]).	gene_phenotype
69225	3	333574	11	NULL	NULL	NULL	NULL	Pom34p	GP		 forms a part of					nuclear pore complex	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_407	14587103	Finally,  YLR018c encodes Pom34p, a integral membrane protein that forms part of the nuclear pore complex  and is involved in the nuclear cytoplasmic transport (Rout  et al., [ 2000]).	gene_phenotype
69226	4	333574	11	NULL	NULL	NULL	NULL	statement 3	GP		 is involved in					nuclear cytoplasmic transport	Process				NULL		NULL	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_407	14587103	Finally,  YLR018c encodes Pom34p, a integral membrane protein that forms part of the nuclear pore complex  and is involved in the nuclear cytoplasmic transport (Rout  et al., [ 2000]).	gene_phenotype
69227	1	333575	11	NULL	NULL	0	NULL	Ylr145w	NucleicAcid		is a component of					RNase MRP	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_12_11352_s_32	15637077	We demonstrate that the Ylr145w protein is indeed a protein component of RNase MRP essential for its activity but is not a component of RNase P.	gene_phenotype
69228	2	333575	11	NULL	NULL	NULL	NULL	statement 1	NucleicAcid		activates					RNase MRP	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_12_11352_s_32	15637077	We demonstrate that the Ylr145w protein is indeed a protein component of RNase MRP essential for its activity but is not a component of RNase P.	gene_phenotype
69229	3	333575	11	NULL	NULL	0	NULL	Ylr145w	NucleicAcid		 is not a component of					RNase P	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_12_11352_s_32	15637077	We demonstrate that the Ylr145w protein is indeed a protein component of RNase MRP essential for its activity but is not a component of RNase P.	gene_phenotype
69322	1	333577	11	NULL	NULL	0	NULL	Epidermal growth factor receptor	GP		undergoes					 internalization	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_6_2_225_s_263	10983971	Epidermal growth factor receptor internalization rate is regulated by negative charges near the SH2 binding site Tyr992.	gene_phenotype
69323	2	333577	11	NULL	NULL	NULL	NULL	statement 1	Process	rate of	 is regulated by					Epidermal growth factor receptor	GP	negative charges near	SH2 binding site Tyr992		NULL		NULL	NULL	NULL	NULL	gw60_molcell_6_2_225_s_263	10983971	Epidermal growth factor receptor internalization rate is regulated by negative charges near the SH2 binding site Tyr992.	gene_phenotype
69230	1	333580	11	NULL	NULL	0	NULL	Vma9p	GP		encoded by					YCL005W-A	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_17_17361_s_6	14970230	The functional significance of these proteins for V-ATPase activity had not been tested, but we show that the protein encoded by  YCL005W-A, which we call Vma9p, is essential for V-ATPase activity in yeast.	gene_phenotype
69231	2	333580	11	NULL	NULL	NULL	NULL	Vma9p	GP		activates					 V-ATPase 	GP				NULL	Yeast	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_17_17361_s_6	14970230	The functional significance of these proteins for V-ATPase activity had not been tested, but we show that the protein encoded by  YCL005W-A, which we call Vma9p, is essential for V-ATPase activity in yeast.	gene_phenotype
69232	1	333581	11	NULL	NULL	0	NULL	 Vma9p	GP		encoded by					YCL005W-A	NucleicAcid				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_17_14970230_s_6	14970230	The functional significance of these proteins for V-ATPase  activity had not been tested, but we show that the protein encoded by  YCL005W-A, which we call Vma9p, is essential for V-ATPase activity in  yeast.	gene_phenotype
69234	2	333581	11	NULL	NULL	NULL	NULL	Vma9p	GP		activates					V-ATPase 	GP				NULL	yeast	NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_17_14970230_s_6	14970230	The functional significance of these proteins for V-ATPase  activity had not been tested, but we show that the protein encoded by  YCL005W-A, which we call Vma9p, is essential for V-ATPase activity in  yeast.	gene_phenotype
69236	1	333583	11	NULL	NULL	0	NULL	YCR098C ORF	NucleicAcid		is the locus name of					GIT1 gene	GP				NULL		0	NULL	NULL	NULL	gw60_genetics_149_4_1707_s_190	9691030	The  GIT1 gene was originally sequenced as part of the  S. cerevisiae genome sequencing project (this ORF was first labeled as YCR137 but is now YCR098C), but no function was assigned to it other than homology to carbohydrate transport proteins ( S OR et al. 1992   ).	gene_phenotype
69237	2	333583	11	NULL	NULL	NULL	NULL	GIT1 gene	GP		is homologus to					carbohydrate transport protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_149_4_1707_s_190	9691030	The  GIT1 gene was originally sequenced as part of the  S. cerevisiae genome sequencing project (this ORF was first labeled as YCR137 but is now YCR098C), but no function was assigned to it other than homology to carbohydrate transport proteins ( S OR et al. 1992   ).	gene_phenotype
69238	1	333585	11	NULL	NULL	0	NULL	YER089c	NucleicAcid		is the locus name of					PTC2	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_2_157_s_148	12518319	PTC2 (YER089c) encodes one of the five members of the type 2C Ser-Thr phosphatase (PP2C)  family in budding yeast (Stark, [ 1996]).	gene_phenotype
71540	2	333585	11	NULL	NULL	0	NULL	PTC2	GP		is a member of					PP2C family	GP				NULL	budding yeast	0	NULL	NULL	NULL	gw70_yeast_20_2_157_s_148	12518319	PTC2 (YER089c) encodes one of the five members of the type 2C Ser-Thr phosphatase (PP2C)  family in budding yeast (Stark, [ 1996]).	gene_phenotype
71541	3	333585	11	NULL	NULL	0	NULL	PP2C	GP		is					type 2C Ser-Thr phosphatase	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_2_157_s_148	12518319	PTC2 (YER089c) encodes one of the five members of the type 2C Ser-Thr phosphatase (PP2C)  family in budding yeast (Stark, [ 1996]).	gene_phenotype
71542	1	333588	11	NULL	NULL	0	NULL	Ykl155c	NucleicAcid		is associated with					Small Ribosomal Subunit of Mitochondria	CellComponent	components of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_19_15861_s_53	11278769	Ykl155c Is Associated with Components of the Small Ribosomal Subunit of Mitochondria-- A yeast strain deleted for  YKL155C was viable but unable to grow on glycerol as the sole carbon source (respiration-deficient; data not shown).	gene_phenotype
69239	1	333589	11	NULL	NULL	0	NULL	VBA1	GP		is					vacuolar basic amino acid transporter	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_6_4851_s_79	15572352	These results suggest that the product of the  YMR088c gene ( VBA1,  vacuolar  basic  amino acid transporter) is required for vacuolar uptake of at least histidine and lysine.	gene_phenotype
69240	2	333589	11	NULL	NULL	NULL	NULL	YMR088c	NucleicAcid		is the locus name of					VBA1	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_6_4851_s_79	15572352	These results suggest that the product of the  YMR088c gene ( VBA1,  vacuolar  basic  amino acid transporter) is required for vacuolar uptake of at least histidine and lysine.	gene_phenotype
69241	3	333589	11	NULL	NULL	NULL	NULL	VBA1	GP		is required for					histidine	amino acid	 vacuolar uptake of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_6_4851_s_79	15572352	These results suggest that the product of the  YMR088c gene ( VBA1,  vacuolar  basic  amino acid transporter) is required for vacuolar uptake of at least histidine and lysine.	gene_phenotype
69242	4	333589	11	NULL	NULL	NULL	NULL	VBA1	GP		is required for 					 lysine	amino acid	vacuolar uptake of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_6_4851_s_79	15572352	These results suggest that the product of the  YMR088c gene ( VBA1,  vacuolar  basic  amino acid transporter) is required for vacuolar uptake of at least histidine and lysine.	gene_phenotype
69305	1	333590	11	NULL	NULL	0	NULL	VBA1	GP		is					vacuolar basic amino acid transporter 1	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_6_4851_s_3	15572352	ATP-dependent uptake of histidine and lysine by isolated vacuolar membrane vesicles was impaired in  YMR088c, a vacuolar basic amino acid transporter 1 ( VBA1)-deleted strain, whereas uptake of tyrosine or calcium was little affected.	gene_phenotype
69306	2	333590	11	NULL	NULL	0	NULL	 YMR088c	NucleicAcid		is a type of 					a vacuolar basic amino acid transporter 1 deleted strain					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_6_4851_s_3	15572352	ATP-dependent uptake of histidine and lysine by isolated vacuolar membrane vesicles was impaired in  YMR088c, a vacuolar basic amino acid transporter 1 ( VBA1)-deleted strain, whereas uptake of tyrosine or calcium was little affected.	gene_phenotype
69307	3	333590	11	NULL	NULL	NULL	NULL	histidine	AminoAcid		is uptaken by					vacuolar membrane vesicles	Cell Component	isolated			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_6_4851_s_3	15572352	ATP-dependent uptake of histidine and lysine by isolated vacuolar membrane vesicles was impaired in  YMR088c, a vacuolar basic amino acid transporter 1 ( VBA1)-deleted strain, whereas uptake of tyrosine or calcium was little affected.	gene_phenotype
71543	4	333590	11	NULL	NULL	0	NULL	statement 3	Process		is dependent on					ATP	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_6_4851_s_3	15572352	ATP-dependent uptake of histidine and lysine by isolated vacuolar membrane vesicles was impaired in  YMR088c, a vacuolar basic amino acid transporter 1 ( VBA1)-deleted strain, whereas uptake of tyrosine or calcium was little affected.	gene_phenotype
71544	5	333590	11	NULL	NULL	0	NULL	statement 4	Process		is impaired in					YMR088c	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_6_4851_s_3	15572352	ATP-dependent uptake of histidine and lysine by isolated vacuolar membrane vesicles was impaired in  YMR088c, a vacuolar basic amino acid transporter 1 ( VBA1)-deleted strain, whereas uptake of tyrosine or calcium was little affected.	gene_phenotype
71545	6	333590	11	NULL	NULL	0	NULL	 lysine	AminoAcid		is uptaken by					vacuolar membrane vesicles	Cell Component	isolated			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_6_4851_s_3	15572352	ATP-dependent uptake of histidine and lysine by isolated vacuolar membrane vesicles was impaired in  YMR088c, a vacuolar basic amino acid transporter 1 ( VBA1)-deleted strain, whereas uptake of tyrosine or calcium was little affected.	gene_phenotype
71546	7	333590	11	NULL	NULL	NULL	NULL	statement 6	Process		is dependent on					ATP	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_6_4851_s_3	15572352	ATP-dependent uptake of histidine and lysine by isolated vacuolar membrane vesicles was impaired in  YMR088c, a vacuolar basic amino acid transporter 1 ( VBA1)-deleted strain, whereas uptake of tyrosine or calcium was little affected.	gene_phenotype
71547	8	333590	11	NULL	NULL	0	NULL	statement 7	Process		is impaired in					YMR088c	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_6_4851_s_3	15572352	ATP-dependent uptake of histidine and lysine by isolated vacuolar membrane vesicles was impaired in  YMR088c, a vacuolar basic amino acid transporter 1 ( VBA1)-deleted strain, whereas uptake of tyrosine or calcium was little affected.	gene_phenotype
69328	1	333598	11	NULL	NULL	0	NULL	ATG4 gene	GP		participate in					 autophagy	Process				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-yeast-res_5_9_15925308_s_9	15925308	Notably, the genes participating in autophagy (ATG4 and  ATG8), the genes encoding a vacuolar protease (PRB1), vacuolar protease  inhibitors (PAI3, PBI2 and TFS1) and YHR138c (a PBI2 homolog) were up-regulated  in the rns4 mutant.	gene_phenotype
69329	2	333598	11	NULL	NULL	0	NULL	ATG8 gene	GP		participate in					autophagy	Process				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-yeast-res_5_9_15925308_s_9	15925308	Notably, the genes participating in autophagy (ATG4 and  ATG8), the genes encoding a vacuolar protease (PRB1), vacuolar protease  inhibitors (PAI3, PBI2 and TFS1) and YHR138c (a PBI2 homolog) were up-regulated  in the rns4 mutant.	gene_phenotype
69330	3	333598	11	NULL	NULL	0	NULL	PRB1 gene	GP		is a type of 					 vacuolar protease	GP				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-yeast-res_5_9_15925308_s_9	15925308	Notably, the genes participating in autophagy (ATG4 and  ATG8), the genes encoding a vacuolar protease (PRB1), vacuolar protease  inhibitors (PAI3, PBI2 and TFS1) and YHR138c (a PBI2 homolog) were up-regulated  in the rns4 mutant.	gene_phenotype
69331	4	333598	11	NULL	NULL	0	NULL	PAI3	GP		is a type of 					vacuolar protease inhibitor	GP				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-yeast-res_5_9_15925308_s_9	15925308	Notably, the genes participating in autophagy (ATG4 and  ATG8), the genes encoding a vacuolar protease (PRB1), vacuolar protease  inhibitors (PAI3, PBI2 and TFS1) and YHR138c (a PBI2 homolog) were up-regulated  in the rns4 mutant.	gene_phenotype
69332	5	333598	11	NULL	NULL	0	NULL	PBI2	GP		is a type of 					vacuolar protease inhibitor	GP				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-yeast-res_5_9_15925308_s_9	15925308	Notably, the genes participating in autophagy (ATG4 and  ATG8), the genes encoding a vacuolar protease (PRB1), vacuolar protease  inhibitors (PAI3, PBI2 and TFS1) and YHR138c (a PBI2 homolog) were up-regulated  in the rns4 mutant.	gene_phenotype
69333	6	333598	11	NULL	NULL	0	NULL	TFS1	GP		is a type of 					vacuolar protease inhibitor	GP				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-yeast-res_5_9_15925308_s_9	15925308	Notably, the genes participating in autophagy (ATG4 and  ATG8), the genes encoding a vacuolar protease (PRB1), vacuolar protease  inhibitors (PAI3, PBI2 and TFS1) and YHR138c (a PBI2 homolog) were up-regulated  in the rns4 mutant.	gene_phenotype
69334	7	333598	11	NULL	NULL	0	NULL	YHR138c	GP		is homologous to					 PBI2 	GP				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-yeast-res_5_9_15925308_s_9	15925308	Notably, the genes participating in autophagy (ATG4 and  ATG8), the genes encoding a vacuolar protease (PRB1), vacuolar protease  inhibitors (PAI3, PBI2 and TFS1) and YHR138c (a PBI2 homolog) were up-regulated  in the rns4 mutant.	gene_phenotype
69335	8	333598	11	NULL	NULL	0	NULL	rns4	GP	mutant	 up-regulate					ATG4	GP				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-yeast-res_5_9_15925308_s_9	15925308	Notably, the genes participating in autophagy (ATG4 and  ATG8), the genes encoding a vacuolar protease (PRB1), vacuolar protease  inhibitors (PAI3, PBI2 and TFS1) and YHR138c (a PBI2 homolog) were up-regulated  in the rns4 mutant.	gene_phenotype
69336	9	333598	11	NULL	NULL	0	NULL	rns4	GP	mutant	up-regulate					ATG8	GP				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-yeast-res_5_9_15925308_s_9	15925308	Notably, the genes participating in autophagy (ATG4 and  ATG8), the genes encoding a vacuolar protease (PRB1), vacuolar protease  inhibitors (PAI3, PBI2 and TFS1) and YHR138c (a PBI2 homolog) were up-regulated  in the rns4 mutant.	gene_phenotype
69337	10	333598	11	NULL	NULL	0	NULL	rns4 	GP	mutant	 up-regulate					PRB1	GP				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-yeast-res_5_9_15925308_s_9	15925308	Notably, the genes participating in autophagy (ATG4 and  ATG8), the genes encoding a vacuolar protease (PRB1), vacuolar protease  inhibitors (PAI3, PBI2 and TFS1) and YHR138c (a PBI2 homolog) were up-regulated  in the rns4 mutant.	gene_phenotype
69338	11	333598	11	NULL	NULL	0	NULL	rns4	GP	mutant	up-regulate					PAI3	GP				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-yeast-res_5_9_15925308_s_9	15925308	Notably, the genes participating in autophagy (ATG4 and  ATG8), the genes encoding a vacuolar protease (PRB1), vacuolar protease  inhibitors (PAI3, PBI2 and TFS1) and YHR138c (a PBI2 homolog) were up-regulated  in the rns4 mutant.	gene_phenotype
69339	12	333598	11	NULL	NULL	0	NULL	rns4	GP	mutant	up-regulate					PBI2	GP				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-yeast-res_5_9_15925308_s_9	15925308	Notably, the genes participating in autophagy (ATG4 and  ATG8), the genes encoding a vacuolar protease (PRB1), vacuolar protease  inhibitors (PAI3, PBI2 and TFS1) and YHR138c (a PBI2 homolog) were up-regulated  in the rns4 mutant.	gene_phenotype
69340	13	333598	11	NULL	NULL	0	NULL	rns4	GP	mutant	up-regulate					TFS1	GP				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-yeast-res_5_9_15925308_s_9	15925308	Notably, the genes participating in autophagy (ATG4 and  ATG8), the genes encoding a vacuolar protease (PRB1), vacuolar protease  inhibitors (PAI3, PBI2 and TFS1) and YHR138c (a PBI2 homolog) were up-regulated  in the rns4 mutant.	gene_phenotype
69341	14	333598	11	NULL	NULL	0	NULL	rns4	GP	mutant	up-regulate					YHR138c	GP				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-yeast-res_5_9_15925308_s_9	15925308	Notably, the genes participating in autophagy (ATG4 and  ATG8), the genes encoding a vacuolar protease (PRB1), vacuolar protease  inhibitors (PAI3, PBI2 and TFS1) and YHR138c (a PBI2 homolog) were up-regulated  in the rns4 mutant.	gene_phenotype
71745	1	333599	11	NULL	NULL	0	NULL	Bar1p	GP		is a type of					protease	GP				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_16_4741_s_4	10438739	Analysis of the amino-terminal sequences revealed that the 120-kDa mannoprotein is Bar1p, the protease involved in the so-called barrier activity in yeast cells, and that the 45- and 40-kDa mannoproteins are the Kex2-unprocessed and Kex2-processed forms of the gene product of open reading frame (ORF)  YJL158c, an ORF that belongs to the  PIR (protein with internal repeats) family of genes, composed thus far of  PIR1,  PIR2/HSP150, and  PIR3.	gene_phenotype
71746	2	333599	11	NULL	NULL	0	NULL	Bar1p	GP		is involved in					barrier activity	Process				NULL	yeast cells	0	NULL	NULL	NULL	gw60_jbacteriol_181_16_4741_s_4	10438739	Analysis of the amino-terminal sequences revealed that the 120-kDa mannoprotein is Bar1p, the protease involved in the so-called barrier activity in yeast cells, and that the 45- and 40-kDa mannoproteins are the Kex2-unprocessed and Kex2-processed forms of the gene product of open reading frame (ORF)  YJL158c, an ORF that belongs to the  PIR (protein with internal repeats) family of genes, composed thus far of  PIR1,  PIR2/HSP150, and  PIR3.	gene_phenotype
71747	3	333599	11	NULL	NULL	0	NULL	YJL158c	NucleicAcid		is a type of					ORF	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_16_4741_s_4	10438739	Analysis of the amino-terminal sequences revealed that the 120-kDa mannoprotein is Bar1p, the protease involved in the so-called barrier activity in yeast cells, and that the 45- and 40-kDa mannoproteins are the Kex2-unprocessed and Kex2-processed forms of the gene product of open reading frame (ORF)  YJL158c, an ORF that belongs to the  PIR (protein with internal repeats) family of genes, composed thus far of  PIR1,  PIR2/HSP150, and  PIR3.	gene_phenotype
71748	4	333599	11	NULL	NULL	0	NULL	YJL158c	NucleicAcid		is a member of					PIR gene family	GP				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_16_4741_s_4	10438739	Analysis of the amino-terminal sequences revealed that the 120-kDa mannoprotein is Bar1p, the protease involved in the so-called barrier activity in yeast cells, and that the 45- and 40-kDa mannoproteins are the Kex2-unprocessed and Kex2-processed forms of the gene product of open reading frame (ORF)  YJL158c, an ORF that belongs to the  PIR (protein with internal repeats) family of genes, composed thus far of  PIR1,  PIR2/HSP150, and  PIR3.	gene_phenotype
71749	5	333599	11	NULL	NULL	0	NULL	PIR	GP		is					protein with internal repeats	GP				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_16_4741_s_4	10438739	Analysis of the amino-terminal sequences revealed that the 120-kDa mannoprotein is Bar1p, the protease involved in the so-called barrier activity in yeast cells, and that the 45- and 40-kDa mannoproteins are the Kex2-unprocessed and Kex2-processed forms of the gene product of open reading frame (ORF)  YJL158c, an ORF that belongs to the  PIR (protein with internal repeats) family of genes, composed thus far of  PIR1,  PIR2/HSP150, and  PIR3.	gene_phenotype
71750	1	333600	11	NULL	NULL	0	NULL	HGT1	GP		is encoded by					YJL212c	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13259_s_112	10788431	Altogether, the data strongly suggest that the protein encoded by YJL212c (from now on referred to as HGT1, high affinity glutathione transporter 1) is probably the glutathione transporter in the plasma membrane of these cells.	gene_phenotype
71751	2	333600	11	NULL	NULL	0	NULL	YJL212c	NucleicAcid	probably	is a type of					glutathione transporter	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13259_s_112	10788431	Altogether, the data strongly suggest that the protein encoded by YJL212c (from now on referred to as HGT1, high affinity glutathione transporter 1) is probably the glutathione transporter in the plasma membrane of these cells.	gene_phenotype
71752	3	333600	11	NULL	NULL	0	NULL	YJL212c	NucleicAcid		is present on					plasma membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13259_s_112	10788431	Altogether, the data strongly suggest that the protein encoded by YJL212c (from now on referred to as HGT1, high affinity glutathione transporter 1) is probably the glutathione transporter in the plasma membrane of these cells.	gene_phenotype
71753	4	333600	11	NULL	NULL	0	NULL	HGT1	GP		is					high affinity glutathione transporter 1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13259_s_112	10788431	Altogether, the data strongly suggest that the protein encoded by YJL212c (from now on referred to as HGT1, high affinity glutathione transporter 1) is probably the glutathione transporter in the plasma membrane of these cells.	gene_phenotype
69343	2	333604	11	NULL	NULL	0	NULL	GSH1 	GP	locus	undergoes					disruption	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13259_s_48	10788431	The disruption at the  GSH1 locus was followed by glutathione auxotrophy, while disruption at either the  YPR194c locus or the  PTR2 locus was followed either by uracile prototrophy or resistance to G418, respectively.	gene_phenotype
69344	3	333604	11	NULL	NULL	NULL	NULL	statement 2	Process		followed by					auxotrophy	Process	 glutathione			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_18_13259_s_48	10788431	The disruption at the  GSH1 locus was followed by glutathione auxotrophy, while disruption at either the  YPR194c locus or the  PTR2 locus was followed either by uracile prototrophy or resistance to G418, respectively.	gene_phenotype
69345	4	333604	11	NULL	NULL	0	NULL	YPR194c	NucleicAcid	locus	undergoes					disruption	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13259_s_48	10788431	The disruption at the  GSH1 locus was followed by glutathione auxotrophy, while disruption at either the  YPR194c locus or the  PTR2 locus was followed either by uracile prototrophy or resistance to G418, respectively.	gene_phenotype
69346	5	333604	11	NULL	NULL	0	NULL	PTR2	GP	locus	undergoes					disruption	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13259_s_48	10788431	The disruption at the  GSH1 locus was followed by glutathione auxotrophy, while disruption at either the  YPR194c locus or the  PTR2 locus was followed either by uracile prototrophy or resistance to G418, respectively.	gene_phenotype
69348	6	333604	11	NULL	NULL	0	NULL	statement 4	Process		followed by					prototrophy	Process	uracile			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13259_s_48	10788431	The disruption at the  GSH1 locus was followed by glutathione auxotrophy, while disruption at either the  YPR194c locus or the  PTR2 locus was followed either by uracile prototrophy or resistance to G418, respectively.	gene_phenotype
69349	7	333604	11	NULL	NULL	0	NULL	statement 4	Process		followed by					resistance	Process	 to G418			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13259_s_48	10788431	The disruption at the  GSH1 locus was followed by glutathione auxotrophy, while disruption at either the  YPR194c locus or the  PTR2 locus was followed either by uracile prototrophy or resistance to G418, respectively.	gene_phenotype
69350	8	333604	11	NULL	NULL	0	NULL	statement 5	Process		followed by					prototrophy	Process	uracile			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13259_s_48	10788431	The disruption at the  GSH1 locus was followed by glutathione auxotrophy, while disruption at either the  YPR194c locus or the  PTR2 locus was followed either by uracile prototrophy or resistance to G418, respectively.	gene_phenotype
69351	9	333604	11	NULL	NULL	0	NULL	statement 5	Process		followed by					 resistance	Process	to G418			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13259_s_48	10788431	The disruption at the  GSH1 locus was followed by glutathione auxotrophy, while disruption at either the  YPR194c locus or the  PTR2 locus was followed either by uracile prototrophy or resistance to G418, respectively.	gene_phenotype
71754	1	333605	11	NULL	NULL	0	NULL	YPR194c	NucleicAcid		encodes					oligopeptide transporter protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13259_s_237	10788431	Therefore, either  YPR194c indeed encodes an oligopeptide transporter protein that is very closely related to  HGT1, or, more likely, it encodes a glutathione transporter localized into a different organelle.	gene_phenotype
71755	2	333605	11	NULL	NULL	0	NULL	YPR194c	NucleicAcid	closely	is related to					HGT1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13259_s_237	10788431	Therefore, either  YPR194c indeed encodes an oligopeptide transporter protein that is very closely related to  HGT1, or, more likely, it encodes a glutathione transporter localized into a different organelle.	gene_phenotype
71756	3	333605	11	NULL	NULL	0	NULL	YPR194c	NucleicAcid		encodes					glutathione transporter	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13259_s_237	10788431	Therefore, either  YPR194c indeed encodes an oligopeptide transporter protein that is very closely related to  HGT1, or, more likely, it encodes a glutathione transporter localized into a different organelle.	gene_phenotype
71757	4	333605	11	NULL	NULL	0	NULL	statement 1	Process		is an alternative to 					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13259_s_237	10788431	Therefore, either  YPR194c indeed encodes an oligopeptide transporter protein that is very closely related to  HGT1, or, more likely, it encodes a glutathione transporter localized into a different organelle.	gene_phenotype
69352	1	333606	11	NULL	NULL	0	NULL	YDR384c	NucleicAcid		is the locus name of					ATO3	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_45882_s_30	12966084	Here we characterize a retrograde responsive gene,  ATO3 ( YDR384c), whose elevated expression in rhoo petite cells is largely independent of the  RTG genes.	gene_phenotype
69353	2	333606	11	NULL	NULL	NULL	NULL	ATO3	GP	elevated expression of	is independent of		largely			RTG genes	GP				NULL	rhoo petite cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_45882_s_30	12966084	Here we characterize a retrograde responsive gene,  ATO3 ( YDR384c), whose elevated expression in rhoo petite cells is largely independent of the  RTG genes.	gene_phenotype
69355	1	333607	11	NULL	NULL	NULL	NULL	 RPA	GP		is imported to 					nucleus	Cell Component				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_4_729_s_278	11266464	To examine the effect of Ybr137wp on nuclear import of RPA, the localization of Rpa2p-PrA was examined in wild-type and  YBR137W deletion ( YBR137Wdelta) strains.	gene_phenotype
69356	2	333607	11	NULL	NULL	NULL	NULL	Ybr137wp	NucleicAcid		plays a role in		possibly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_152_4_729_s_278	11266464	To examine the effect of Ybr137wp on nuclear import of RPA, the localization of Rpa2p-PrA was examined in wild-type and  YBR137W deletion ( YBR137Wdelta) strains.	gene_phenotype
69358	1	333610	11	NULL	NULL	0	NULL	YMR110c	NucleicAcid		is a type of 					hypothetical open reading frame	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_genetics_163_1_69_s_21	12586697	MSC7/YHR039c encodes a protein with homology to aldehyde deydrogenases that affects meiotic sister-chromatid recombination ( T HOMPSON and STAHL 1999   ), and  YMR110c is a hypothetical open reading frame that could code for an aldehyde-dehydrogenase-related protein.	gene_phenotype
69359	2	333610	11	10	NULL	NULL	NULL	statement 1	NucleicAcid		code for					aldehyde-dehydrogenase-related protein	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_163_1_69_s_21	12586697	MSC7/YHR039c encodes a protein with homology to aldehyde deydrogenases that affects meiotic sister-chromatid recombination ( T HOMPSON and STAHL 1999   ), and  YMR110c is a hypothetical open reading frame that could code for an aldehyde-dehydrogenase-related protein.	gene_phenotype
69360	3	333610	11	NULL	NULL	0	NULL	MSC7/YHR039c	GP		is homologous to					aldehyde deydrogenases	GP				NULL		0	NULL	NULL	NULL	gw60_genetics_163_1_69_s_21	12586697	MSC7/YHR039c encodes a protein with homology to aldehyde deydrogenases that affects meiotic sister-chromatid recombination ( T HOMPSON and STAHL 1999   ), and  YMR110c is a hypothetical open reading frame that could code for an aldehyde-dehydrogenase-related protein.	gene_phenotype
69361	4	333610	11	NULL	NULL	0	NULL	MSC7/YHR039c	GP		affects					meiotic sister-chromatid recombination	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_163_1_69_s_21	12586697	MSC7/YHR039c encodes a protein with homology to aldehyde deydrogenases that affects meiotic sister-chromatid recombination ( T HOMPSON and STAHL 1999   ), and  YMR110c is a hypothetical open reading frame that could code for an aldehyde-dehydrogenase-related protein.	gene_phenotype
69362	1	333614	11	NULL	NULL	0	NULL	YSW1 gene	GP		is a type of 					spore-specific protein	GP				NULL		0	NULL	NULL	NULL	gw70_nature_423_6937_241_s_322	12748633	The protein encoded by YBR184W has not been studied extensively, but expression studies  show that the gene is induced during sporulation 33, and sequence analysis shows that it is similar to the gene  YSW1, which encodes a spore-specific protein.	gene_phenotype
69363	2	333614	11	NULL	NULL	NULL	NULL	YBR184W gene	GP		is induced during					sporulation	Process				NULL		NULL	NULL	NULL	NULL	gw70_nature_423_6937_241_s_322	12748633	The protein encoded by YBR184W has not been studied extensively, but expression studies  show that the gene is induced during sporulation 33, and sequence analysis shows that it is similar to the gene  YSW1, which encodes a spore-specific protein.	gene_phenotype
69364	3	333614	11	NULL	NULL	NULL	NULL	YBR184W gene	GP		is similar to					YSW1 gene	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_423_6937_241_s_322	12748633	The protein encoded by YBR184W has not been studied extensively, but expression studies  show that the gene is induced during sporulation 33, and sequence analysis shows that it is similar to the gene  YSW1, which encodes a spore-specific protein.	gene_phenotype
69365	1	333615	11	NULL	NULL	NULL	NULL	YGR194c gene	GP		 encodes 					xylulokinase	GP				NULL	Saccharomyces cerevisiae	NULL	NULL	NULL	NULL	gw60_applenvironmicrob_69_1_495_s_426	12514033	The YGR194c ( XKS1) gene encodes the xylulokinase from the budding yeast  Saccharomyces cerevisiae.	gene_phenotype
69366	2	333615	11	NULL	NULL	NULL	NULL	YGR194c gene	GP		 is a synonym of 					 XKS1 gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_69_1_495_s_426	12514033	The YGR194c ( XKS1) gene encodes the xylulokinase from the budding yeast  Saccharomyces cerevisiae.	gene_phenotype
69367	1	333618	11	NULL	NULL	NULL	NULL	YGR194c gene	GP		encodes for					xylulokinase	GP				NULL	Saccharomyces cerevisiae	NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_190_1_39_s_207	10981687	J.M. Rodrigez-Pena, V.J. Cid, J. Arroyo and C. Nombela, The YGR194c (XKS1) gene encodes the xylulokinase from the budding yeast  Saccharomyces cerevisiae.	gene_phenotype
69368	2	333618	11	NULL	NULL	NULL	NULL	YGR194c gene	GP		 is a synonym of 					 XKS1 gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_190_1_39_s_207	10981687	J.M. Rodrigez-Pena, V.J. Cid, J. Arroyo and C. Nombela, The YGR194c (XKS1) gene encodes the xylulokinase from the budding yeast  Saccharomyces cerevisiae.	gene_phenotype
71758	1	333621	11	NULL	NULL	0	NULL	YJR070C protein	GP		activates					DOHH	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_51_s_83	16371467	We isolated the pYEX-4T-1/yDOHH plasmid from a single A7 clone expressing DOHH activity in the form of a 62-kDa GST fusion protein (data not shown) and confirmed the nucleotide sequence of the complete ORF.  YJR070C encodes a protein of 325 aa (36 kDa) with DOHH activity.	gene_phenotype
69373	1	333624	11	NULL	NULL	0	NULL	AUT7  gene	GP		is essential for					 autophagy	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_99_26_16875_s_257	12486219	From the list of LAPs for  YNL101W (Table 8, which is published as supporting information on the PNAS web site), we find several genes involved in autophagy, protein degradation, and transport:  AUT7 (essential for autophagy, appearing six times),  PRE6 and  PUP1 (20S proteasome subunits),  RPT6 (26S proteasome-regulatory subunit),  CLC1 (clathrin light chain),  YPT52	gene_phenotype
69374	2	333624	11	NULL	NULL	0	NULL	CLC1 gene	GP		is a type of 					clathrin light chain	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_99_26_16875_s_257	12486219	From the list of LAPs for  YNL101W (Table 8, which is published as supporting information on the PNAS web site), we find several genes involved in autophagy, protein degradation, and transport:  AUT7 (essential for autophagy, appearing six times),  PRE6 and  PUP1 (20S proteasome subunits),  RPT6 (26S proteasome-regulatory subunit),  CLC1 (clathrin light chain),  YPT52	gene_phenotype
71763	3	333624	11	NULL	NULL	0	NULL	PUP1	GP		is a type of 					20S proteasome subunits	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_99_26_16875_s_257	12486219	From the list of LAPs for  YNL101W (Table 8, which is published as supporting information on the PNAS web site), we find several genes involved in autophagy, protein degradation, and transport:  AUT7 (essential for autophagy, appearing six times),  PRE6 and  PUP1 (20S proteasome subunits),  RPT6 (26S proteasome-regulatory subunit),  CLC1 (clathrin light chain),  YPT52	gene_phenotype
71764	4	333624	11	NULL	NULL	0	NULL	RPT6	GP		is a type of 					26S proteasome-regulatory subunit	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_99_26_16875_s_257	12486219	From the list of LAPs for  YNL101W (Table 8, which is published as supporting information on the PNAS web site), we find several genes involved in autophagy, protein degradation, and transport:  AUT7 (essential for autophagy, appearing six times),  PRE6 and  PUP1 (20S proteasome subunits),  RPT6 (26S proteasome-regulatory subunit),  CLC1 (clathrin light chain),  YPT52	gene_phenotype
69698	1	333627	11	NULL	NULL	0	NULL	SPO70 gene	GP	 intron removal	is activated in					 meiosis	Process				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_7	10734188	One gene (YGR225W/ SPO70) has an intron whose removal is activated during meiosis under control of the  MER1 gene.	gene_phenotype
69699	2	333627	11	NULL	NULL	0	NULL	statement 1	Process		is controlled by 					MER1 gene	GP				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_7	10734188	One gene (YGR225W/ SPO70) has an intron whose removal is activated during meiosis under control of the  MER1 gene.	gene_phenotype
69700	3	333627	11	NULL	NULL	0	NULL	YGR225W	NucleicAcid		is the locus name of					SPO70	GP				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_7	10734188	One gene (YGR225W/ SPO70) has an intron whose removal is activated during meiosis under control of the  MER1 gene.	gene_phenotype
69994	1	333629	11	NULL	NULL	0	NULL	YGR225W	NucleicAcid		undergoes					splicing	Process	meiotic time			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_186	10734188	We measured splicing of YGR225W/ SPO70 during a meiotic time course using a strain capable of synchronous and efficient meiosis ( 19, 22).	gene_phenotype
70052	2	333630	11	NULL	NULL	0	NULL	 YGR225W	NucleicAcid		is the locus name of					SPO70	GP				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_187	10734188	During meiosis and sporulation, efficiency of YGR225W/ SPO70 splicing is low but increases, as shown by the increase in the ratio of spliced to unspliced RT - PCR product (Fig.  4A).	gene_phenotype
70053	3	333630	11	NULL	NULL	NULL	NULL	YGR225W	Process	splicing of	is less efficient during 					meiosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_187	10734188	During meiosis and sporulation, efficiency of YGR225W/ SPO70 splicing is low but increases, as shown by the increase in the ratio of spliced to unspliced RT - PCR product (Fig.  4A).	gene_phenotype
70054	4	333630	11	NULL	NULL	NULL	NULL	YGR225W	Process	splicing of	is less efficient during 					sporulation	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_187	10734188	During meiosis and sporulation, efficiency of YGR225W/ SPO70 splicing is low but increases, as shown by the increase in the ratio of spliced to unspliced RT - PCR product (Fig.  4A).	gene_phenotype
70055	1	333632	11	NULL	NULL	0	NULL	YGR225W	NucleicAcid		undergoes					Splicing	Process				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_184	10734188	Splicing of YGR225W/ SPO70 is activated during meiosis by  MER1   or the vast majority of introns tested, splicing took place with approximately equivalent efficiencies under the expression conditions we tested.	gene_phenotype
70056	2	333632	11	NULL	NULL	0	NULL	YGR225W	NucleicAcid		is the locus name of					SPO70	GP				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_184	10734188	Splicing of YGR225W/ SPO70 is activated during meiosis by  MER1   or the vast majority of introns tested, splicing took place with approximately equivalent efficiencies under the expression conditions we tested.	gene_phenotype
70057	3	333632	11	NULL	NULL	0	NULL	MER1	GP		activates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_184	10734188	Splicing of YGR225W/ SPO70 is activated during meiosis by  MER1   or the vast majority of introns tested, splicing took place with approximately equivalent efficiencies under the expression conditions we tested.	gene_phenotype
70058	4	333632	11	NULL	NULL	0	NULL	intron	NucleicAcid		activates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_184	10734188	Splicing of YGR225W/ SPO70 is activated during meiosis by  MER1   or the vast majority of introns tested, splicing took place with approximately equivalent efficiencies under the expression conditions we tested.	gene_phenotype
70059	5	333632	11	NULL	NULL	0	NULL	statement 3	Process		happens during					meiosis	Process				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_8_1700_s_184	10734188	Splicing of YGR225W/ SPO70 is activated during meiosis by  MER1   or the vast majority of introns tested, splicing took place with approximately equivalent efficiencies under the expression conditions we tested.	gene_phenotype
70060	1	333633	11	NULL	NULL	0	NULL	Imp2p	GP		is a type of 					transcriptional activator	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_13_1085_s_2	14558142	Imp2p (Yil154c) is a transcriptional activator involved in glucose derepression of  the maltose, galactose and raffinose utilization pathways and in resistance to thermal,  oxidative or osmotic stress.	gene_phenotype
70061	2	333633	11	NULL	NULL	0	NULL	Yil154c	NucleicAcid		is the locus name of					Imp2p	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_13_1085_s_2	14558142	Imp2p (Yil154c) is a transcriptional activator involved in glucose derepression of  the maltose, galactose and raffinose utilization pathways and in resistance to thermal,  oxidative or osmotic stress.	gene_phenotype
70062	3	333633	11	NULL	NULL	0	NULL	glucose	Chemical		undergoes					derepression	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_13_1085_s_2	14558142	Imp2p (Yil154c) is a transcriptional activator involved in glucose derepression of  the maltose, galactose and raffinose utilization pathways and in resistance to thermal,  oxidative or osmotic stress.	gene_phenotype
70063	4	333633	11	NULL	NULL	0	NULL	statement 3	Process		occurs in 					raffinose utilization pathway	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_13_1085_s_2	14558142	Imp2p (Yil154c) is a transcriptional activator involved in glucose derepression of  the maltose, galactose and raffinose utilization pathways and in resistance to thermal,  oxidative or osmotic stress.	gene_phenotype
70064	5	333633	11	NULL	NULL	0	NULL	statement 3	Process		occurs in 					maltose utilization pathway	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_13_1085_s_2	14558142	Imp2p (Yil154c) is a transcriptional activator involved in glucose derepression of  the maltose, galactose and raffinose utilization pathways and in resistance to thermal,  oxidative or osmotic stress.	gene_phenotype
70065	6	333633	11	NULL	NULL	0	NULL	statement 3	Process		occurs in 					galactose utilization pathway	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_13_1085_s_2	14558142	Imp2p (Yil154c) is a transcriptional activator involved in glucose derepression of  the maltose, galactose and raffinose utilization pathways and in resistance to thermal,  oxidative or osmotic stress.	gene_phenotype
70066	7	333633	11	NULL	NULL	0	NULL	Imp2p	GP		 involved in 					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_13_1085_s_2	14558142	Imp2p (Yil154c) is a transcriptional activator involved in glucose derepression of  the maltose, galactose and raffinose utilization pathways and in resistance to thermal,  oxidative or osmotic stress.	gene_phenotype
70067	1	333637	11	NULL	NULL	0	NULL	ygr231c	NucleicAcid		shows					mannosyl phosphorylation	Process	decrease in			NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_379	14587103	It is likely that the drop in mannosyl phosphorylation seen in   ygr231c is, as the shorter lifespan, an indirect effect of an increased oxidative stress  or a decrease in the metabolic efficiency.	gene_phenotype
70069	2	333637	11	NULL	NULL	0	NULL	statement 1	Process		is an indirect effect of					oxidative stress 	Process	 increased			NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_379	14587103	It is likely that the drop in mannosyl phosphorylation seen in   ygr231c is, as the shorter lifespan, an indirect effect of an increased oxidative stress  or a decrease in the metabolic efficiency.	gene_phenotype
70071	3	333637	11	NULL	NULL	0	NULL	statement 1	Process		is an indirect effect of					metabolic efficiency	Process	decrease in			NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_379	14587103	It is likely that the drop in mannosyl phosphorylation seen in   ygr231c is, as the shorter lifespan, an indirect effect of an increased oxidative stress  or a decrease in the metabolic efficiency.	gene_phenotype
70072	4	333637	11	NULL	NULL	0	NULL	statement 2	Process		is an alternative to 					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_379	14587103	It is likely that the drop in mannosyl phosphorylation seen in   ygr231c is, as the shorter lifespan, an indirect effect of an increased oxidative stress  or a decrease in the metabolic efficiency.	gene_phenotype
70075	1	333638	11	NULL	NULL	NULL	NULL	YJR075w	NucleicAcid		corresponds to					HOC1	GP				NULL		NULL	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_223	14587103	YJR075w corresponds to  HOC1, which encodes a type II membrane protein that associates with several other components  (Mnn9p, Anp1p, Mnn10p, Mnn11p) in the  cis-Golgi to form a complex endowed with  1,6-mannosyltransferase activity (complex II).	gene_phenotype
70076	2	333638	11	NULL	NULL	0	NULL	HOC1	GP		is a type of 					type II membrane protein	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_223	14587103	YJR075w corresponds to  HOC1, which encodes a type II membrane protein that associates with several other components  (Mnn9p, Anp1p, Mnn10p, Mnn11p) in the  cis-Golgi to form a complex endowed with  1,6-mannosyltransferase activity (complex II).	gene_phenotype
70091	3	333638	11	NULL	NULL	0	NULL	HOC1	GP		associates with					Mnn9p	GP				NULL	 cis-Golgi	0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_223	14587103	YJR075w corresponds to  HOC1, which encodes a type II membrane protein that associates with several other components  (Mnn9p, Anp1p, Mnn10p, Mnn11p) in the  cis-Golgi to form a complex endowed with  1,6-mannosyltransferase activity (complex II).	gene_phenotype
70112	4	333638	11	NULL	NULL	0	NULL	HOC1	GP		associates with					Anp1p	GP				NULL	 cis-Golgi	0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_223	14587103	YJR075w corresponds to  HOC1, which encodes a type II membrane protein that associates with several other components  (Mnn9p, Anp1p, Mnn10p, Mnn11p) in the  cis-Golgi to form a complex endowed with  1,6-mannosyltransferase activity (complex II).	gene_phenotype
70113	5	333638	11	NULL	NULL	0	NULL	 HOC1	GP		associates with					Mnn10p	GP				NULL	 cis-Golgi	0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_223	14587103	YJR075w corresponds to  HOC1, which encodes a type II membrane protein that associates with several other components  (Mnn9p, Anp1p, Mnn10p, Mnn11p) in the  cis-Golgi to form a complex endowed with  1,6-mannosyltransferase activity (complex II).	gene_phenotype
70114	6	333638	11	NULL	NULL	0	NULL	HOC1	GP		associates with					Mnn11p	GP				NULL	cis-Golgi	0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_223	14587103	YJR075w corresponds to  HOC1, which encodes a type II membrane protein that associates with several other components  (Mnn9p, Anp1p, Mnn10p, Mnn11p) in the  cis-Golgi to form a complex endowed with  1,6-mannosyltransferase activity (complex II).	gene_phenotype
70115	7	333638	11	NULL	NULL	0	NULL	statement 3	GP		complex with 					statement 4	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_223	14587103	YJR075w corresponds to  HOC1, which encodes a type II membrane protein that associates with several other components  (Mnn9p, Anp1p, Mnn10p, Mnn11p) in the  cis-Golgi to form a complex endowed with  1,6-mannosyltransferase activity (complex II).	gene_phenotype
70116	8	333638	11	NULL	NULL	0	NULL	statement 5	GP		complex with 					statement 6	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_223	14587103	YJR075w corresponds to  HOC1, which encodes a type II membrane protein that associates with several other components  (Mnn9p, Anp1p, Mnn10p, Mnn11p) in the  cis-Golgi to form a complex endowed with  1,6-mannosyltransferase activity (complex II).	gene_phenotype
70117	9	333638	11	NULL	NULL	0	NULL	statement 7	GP		complex with 					statement 8	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_223	14587103	YJR075w corresponds to  HOC1, which encodes a type II membrane protein that associates with several other components  (Mnn9p, Anp1p, Mnn10p, Mnn11p) in the  cis-Golgi to form a complex endowed with  1,6-mannosyltransferase activity (complex II).	gene_phenotype
70118	10	333638	11	NULL	NULL	0	NULL	statement 7	GP		activates					1,6-mannosyltransferase	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_223	14587103	YJR075w corresponds to  HOC1, which encodes a type II membrane protein that associates with several other components  (Mnn9p, Anp1p, Mnn10p, Mnn11p) in the  cis-Golgi to form a complex endowed with  1,6-mannosyltransferase activity (complex II).	gene_phenotype
70119	11	333638	11	NULL	NULL	0	NULL	statement 8	GP		activates					1,6-mannosyltransferase	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_223	14587103	YJR075w corresponds to  HOC1, which encodes a type II membrane protein that associates with several other components  (Mnn9p, Anp1p, Mnn10p, Mnn11p) in the  cis-Golgi to form a complex endowed with  1,6-mannosyltransferase activity (complex II).	gene_phenotype
70120	12	333638	11	NULL	NULL	0	NULL	statement 9	GP		activates					1,6-mannosyltransferase	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_223	14587103	YJR075w corresponds to  HOC1, which encodes a type II membrane protein that associates with several other components  (Mnn9p, Anp1p, Mnn10p, Mnn11p) in the  cis-Golgi to form a complex endowed with  1,6-mannosyltransferase activity (complex II).	gene_phenotype
71843	1	333639	11	NULL	NULL	0	NULL	YMR233W	NucleicAcid		is deleted from					NOY556	Organism	wild type strain			NULL		0	NULL	NULL	NULL	gw60_embo_20_16_4512_s_151	11500378	We found that deletion of  YMR233W from a standard wild-type strain (NOY556) or from a  uaf30 delta strain did not cause any alteration in growth phenotypes, as judged either by colony size (Figure  3A) or by measuring doubling time in YEPD liquid medium (Figure  3B).	gene_phenotype
71844	2	333639	11	NULL	NULL	0	NULL	statement 1	Process		does not alter					growth phenotype	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw60_embo_20_16_4512_s_151	11500378	We found that deletion of  YMR233W from a standard wild-type strain (NOY556) or from a  uaf30 delta strain did not cause any alteration in growth phenotypes, as judged either by colony size (Figure  3A) or by measuring doubling time in YEPD liquid medium (Figure  3B).	gene_phenotype
71845	3	333639	11	NULL	NULL	0	NULL	YMR233W	NucleicAcid		is deleted from					uaf30 delta strain	Organism				NULL		0	NULL	NULL	NULL	gw60_embo_20_16_4512_s_151	11500378	We found that deletion of  YMR233W from a standard wild-type strain (NOY556) or from a  uaf30 delta strain did not cause any alteration in growth phenotypes, as judged either by colony size (Figure  3A) or by measuring doubling time in YEPD liquid medium (Figure  3B).	gene_phenotype
71846	4	333639	11	NULL	NULL	0	NULL	statement 3	Process		does not alter					growth phenotype	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw60_embo_20_16_4512_s_151	11500378	We found that deletion of  YMR233W from a standard wild-type strain (NOY556) or from a  uaf30 delta strain did not cause any alteration in growth phenotypes, as judged either by colony size (Figure  3A) or by measuring doubling time in YEPD liquid medium (Figure  3B).	gene_phenotype
70124	1	333642	11	NULL	NULL	0	NULL	Cap1 protein	GP	full-length	 less active than					Cap1 protein	GP	truncated			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_31_19304_s_182	9235926	Interestingly, the full-length Cap1 protein was approximately 3 times less active than the truncated Cap1 protein in this assay, indicating that the C-terminal domain of Cap1 behaves as an inhibitor of Cap1 activity with respect to the transcriptional regulation of  YBR008c in  S. cerevisiae (Fig.  6 A).	gene_phenotype
71847	2	333642	11	NULL	NULL	0	NULL	Cap1	GP	C terminal domain of	is an inhibitor of					Cap1 activity	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_31_19304_s_182	9235926	Interestingly, the full-length Cap1 protein was approximately 3 times less active than the truncated Cap1 protein in this assay, indicating that the C-terminal domain of Cap1 behaves as an inhibitor of Cap1 activity with respect to the transcriptional regulation of  YBR008c in  S. cerevisiae (Fig.  6 A).	gene_phenotype
71848	3	333642	11	NULL	NULL	0	NULL	statement 2	Process		with respect to					YBR008c	NucleicAcid	transcriptional regulation of			NULL	S.cerevisiae	0	NULL	NULL	NULL	gw60_jbiolchem_272_31_19304_s_182	9235926	Interestingly, the full-length Cap1 protein was approximately 3 times less active than the truncated Cap1 protein in this assay, indicating that the C-terminal domain of Cap1 behaves as an inhibitor of Cap1 activity with respect to the transcriptional regulation of  YBR008c in  S. cerevisiae (Fig.  6 A).	gene_phenotype
70136	1	333644	11	NULL	NULL	0	NULL	YGL087c ORF	NucleicAcid		 is located on					chromosome VII	Chromosome				NULL	 Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_febslett_423_1_49_s_8	9580084	The YGL087c open reading frame of the budding yeast  Saccharomyces cerevisiae is located on chromosome VII  [ 9], encodes a protein with 38% identity to human UEV-1A [ 1, and maintains the same structural features of this class of proteins.	gene_phenotype
70137	1	333645	11	NULL	NULL	0	NULL	Ynr002cp	NucleicAcid		is a type of 					ATO protein	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_30_11142_s_57	16847258	Ynr002cp belongs to a family of ATO (ammonia/ammonium transport outward) proteins ( ) of which only three were represented in our data set and was not studied further.	gene_phenotype
70138	2	333645	11	NULL	NULL	0	NULL	ATO	GP		is					ammonia/ammonium transport outward	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_30_11142_s_57	16847258	Ynr002cp belongs to a family of ATO (ammonia/ammonium transport outward) proteins ( ) of which only three were represented in our data set and was not studied further.	gene_phenotype
70139	1	333646	11	NULL	NULL	NULL	NULL	 ATO3	GP		is a type of 					putative ammonia exporter	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_46_45882_s_191	12966084	What is the relationship between the elevated expression of  ATO3 (and other putative ammonia exporters,  YCR010c and  YNR002c; see Epstein  et al., Ref.  ) in respiratory deficient rhoo petite cells and ammonia production in respiratory competent cells in colonies that are in late stages of growth?	gene_phenotype
70140	2	333646	11	NULL	NULL	0	NULL	YCR010c	NucleicAcid		is a type of 					putative ammonia exporter	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_45882_s_191	12966084	What is the relationship between the elevated expression of  ATO3 (and other putative ammonia exporters,  YCR010c and  YNR002c; see Epstein  et al., Ref.  ) in respiratory deficient rhoo petite cells and ammonia production in respiratory competent cells in colonies that are in late stages of growth?	gene_phenotype
70141	3	333646	11	NULL	NULL	0	NULL	 YNR002c	NucleicAcid		is a type of 					putative ammonia exporter	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_46_45882_s_191	12966084	What is the relationship between the elevated expression of  ATO3 (and other putative ammonia exporters,  YCR010c and  YNR002c; see Epstein  et al., Ref.  ) in respiratory deficient rhoo petite cells and ammonia production in respiratory competent cells in colonies that are in late stages of growth?	gene_phenotype
71853	1	333647	11	NULL	NULL	0	NULL	Ddi1	GP		is a type of					ubiquitin like protein	GP				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_3_986_s_83	12051757	Since the search for a budding yeast database revealed the presence of two ubiquitin-like proteins, Ddi1 and Yol111c, we examined whether the two ubiquitin-like proteins Ddi1 and Yol111c, as well as Rad23 [ 11,  12,  13 and  14] and Dsk2 [ 12 and  15], can interact with polyubiquitinated proteins and also with the 26S proteasome.	gene_phenotype
71854	2	333647	11	NULL	NULL	0	NULL	Yol111c	NucleicAcid		is a type of 					ubiquitin like protein	GP				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_3_986_s_83	12051757	Since the search for a budding yeast database revealed the presence of two ubiquitin-like proteins, Ddi1 and Yol111c, we examined whether the two ubiquitin-like proteins Ddi1 and Yol111c, as well as Rad23 [ 11,  12,  13 and  14] and Dsk2 [ 12 and  15], can interact with polyubiquitinated proteins and also with the 26S proteasome.	gene_phenotype
71855	3	333647	11	NULL	NULL	0	NULL	Ddi1	GP		interacts with		possibly			polyubiquitinated proteins	GP				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_3_986_s_83	12051757	Since the search for a budding yeast database revealed the presence of two ubiquitin-like proteins, Ddi1 and Yol111c, we examined whether the two ubiquitin-like proteins Ddi1 and Yol111c, as well as Rad23 [ 11,  12,  13 and  14] and Dsk2 [ 12 and  15], can interact with polyubiquitinated proteins and also with the 26S proteasome.	gene_phenotype
71856	4	333647	11	NULL	NULL	0	NULL	Ddi1	GP		interacts with 		possibly			26S proteasome	Cell Component				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_3_986_s_83	12051757	Since the search for a budding yeast database revealed the presence of two ubiquitin-like proteins, Ddi1 and Yol111c, we examined whether the two ubiquitin-like proteins Ddi1 and Yol111c, as well as Rad23 [ 11,  12,  13 and  14] and Dsk2 [ 12 and  15], can interact with polyubiquitinated proteins and also with the 26S proteasome.	gene_phenotype
71857	5	333647	11	NULL	NULL	0	NULL	Yol111c	NucleicAcid		interacts with		possibly			polyubiquitinated proteins	GP				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_3_986_s_83	12051757	Since the search for a budding yeast database revealed the presence of two ubiquitin-like proteins, Ddi1 and Yol111c, we examined whether the two ubiquitin-like proteins Ddi1 and Yol111c, as well as Rad23 [ 11,  12,  13 and  14] and Dsk2 [ 12 and  15], can interact with polyubiquitinated proteins and also with the 26S proteasome.	gene_phenotype
71858	6	333647	11	NULL	NULL	0	NULL	Yol111c	NucleicAcid		interacts with 		possibly			26S proteasome	Cell Component				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_3_986_s_83	12051757	Since the search for a budding yeast database revealed the presence of two ubiquitin-like proteins, Ddi1 and Yol111c, we examined whether the two ubiquitin-like proteins Ddi1 and Yol111c, as well as Rad23 [ 11,  12,  13 and  14] and Dsk2 [ 12 and  15], can interact with polyubiquitinated proteins and also with the 26S proteasome.	gene_phenotype
71859	7	333647	11	NULL	NULL	0	NULL	 Rad 23	GP		interacts with		possibly			polyubiquitinated proteins	GP				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_3_986_s_83	12051757	Since the search for a budding yeast database revealed the presence of two ubiquitin-like proteins, Ddi1 and Yol111c, we examined whether the two ubiquitin-like proteins Ddi1 and Yol111c, as well as Rad23 [ 11,  12,  13 and  14] and Dsk2 [ 12 and  15], can interact with polyubiquitinated proteins and also with the 26S proteasome.	gene_phenotype
71860	8	333647	11	NULL	NULL	NULL	NULL	Rad 23	GP		interacts with		possibly			26S proteasome	Cell Component				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_3_986_s_83	12051757	Since the search for a budding yeast database revealed the presence of two ubiquitin-like proteins, Ddi1 and Yol111c, we examined whether the two ubiquitin-like proteins Ddi1 and Yol111c, as well as Rad23 [ 11,  12,  13 and  14] and Dsk2 [ 12 and  15], can interact with polyubiquitinated proteins and also with the 26S proteasome.	gene_phenotype
71861	9	333647	11	NULL	NULL	0	NULL	Dsk2	GP		interacts with 		possibly			polyubiquitinated proteins	GP				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_3_986_s_83	12051757	Since the search for a budding yeast database revealed the presence of two ubiquitin-like proteins, Ddi1 and Yol111c, we examined whether the two ubiquitin-like proteins Ddi1 and Yol111c, as well as Rad23 [ 11,  12,  13 and  14] and Dsk2 [ 12 and  15], can interact with polyubiquitinated proteins and also with the 26S proteasome.	gene_phenotype
71862	10	333647	11	NULL	NULL	0	NULL	Dsk2	GP		interacts with 		possibly			26S proteasome	Cell Component				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_293_3_986_s_83	12051757	Since the search for a budding yeast database revealed the presence of two ubiquitin-like proteins, Ddi1 and Yol111c, we examined whether the two ubiquitin-like proteins Ddi1 and Yol111c, as well as Rad23 [ 11,  12,  13 and  14] and Dsk2 [ 12 and  15], can interact with polyubiquitinated proteins and also with the 26S proteasome.	gene_phenotype
70142	1	333650	11	NULL	NULL	0	NULL	 YAL048c protein	NucleicAcid		 is involved in					vesicle transport	Process	 in the secretory pathway			NULL		0	NULL	NULL	NULL	abs-batch0680-0699_yeast_15_5_10220001_s_10	10220001	We suggest that the YAL048c protein is involved in vesicle transport  in the secretory pathway.	gene_phenotype
70143	1	333651	11	NULL	NULL	0	NULL	 Sso1 	GP		is a type of 					syntaxin	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_1_s_224	12489121	Overexpression of syntaxins Sso1 and Sso2, functioning  at the targeting/fusion of the Golgi-derived secretory vesicles to the plasma membrane,  polyubiquitin,  PSE1 and YAL048c ORF or the disruption of protease Yps1p, Yap3p encoding genes also enhance  heterologous protein secretion (Knittler and Haas, [ 1992]; Chow  et al., [ 1992]; Chen  et al., [ 1994]; Robinson  et al., [ 1994]; Ruohonen  et al., [ 1997];	gene_phenotype
70144	2	333651	11	NULL	NULL	0	NULL	Sso2	GP		is a type of 					syntaxin	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_1_s_224	12489121	Overexpression of syntaxins Sso1 and Sso2, functioning  at the targeting/fusion of the Golgi-derived secretory vesicles to the plasma membrane,  polyubiquitin,  PSE1 and YAL048c ORF or the disruption of protease Yps1p, Yap3p encoding genes also enhance  heterologous protein secretion (Knittler and Haas, [ 1992]; Chow  et al., [ 1992]; Chen  et al., [ 1994]; Robinson  et al., [ 1994]; Ruohonen  et al., [ 1997];	gene_phenotype
70483	3	333651	11	NULL	NULL	0	NULL	secretory vesicles	cell component		is derived from					Golgi	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_1_s_224	12489121	Overexpression of syntaxins Sso1 and Sso2, functioning  at the targeting/fusion of the Golgi-derived secretory vesicles to the plasma membrane,  polyubiquitin,  PSE1 and YAL048c ORF or the disruption of protease Yps1p, Yap3p encoding genes also enhance  heterologous protein secretion (Knittler and Haas, [ 1992]; Chow  et al., [ 1992]; Chen  et al., [ 1994]; Robinson  et al., [ 1994]; Ruohonen  et al., [ 1997];	gene_phenotype
70484	4	333651	11	NULL	NULL	0	NULL	statement 3	cell component		is targeted to					 plasma membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_1_s_224	12489121	Overexpression of syntaxins Sso1 and Sso2, functioning  at the targeting/fusion of the Golgi-derived secretory vesicles to the plasma membrane,  polyubiquitin,  PSE1 and YAL048c ORF or the disruption of protease Yps1p, Yap3p encoding genes also enhance  heterologous protein secretion (Knittler and Haas, [ 1992]; Chow  et al., [ 1992]; Chen  et al., [ 1994]; Robinson  et al., [ 1994]; Ruohonen  et al., [ 1997];	gene_phenotype
70485	5	333651	11	NULL	NULL	0	NULL	statement 3	cell component		is fused to 					 plasma membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_1_s_224	12489121	Overexpression of syntaxins Sso1 and Sso2, functioning  at the targeting/fusion of the Golgi-derived secretory vesicles to the plasma membrane,  polyubiquitin,  PSE1 and YAL048c ORF or the disruption of protease Yps1p, Yap3p encoding genes also enhance  heterologous protein secretion (Knittler and Haas, [ 1992]; Chow  et al., [ 1992]; Chen  et al., [ 1994]; Robinson  et al., [ 1994]; Ruohonen  et al., [ 1997];	gene_phenotype
70486	6	333651	11	NULL	NULL	0	NULL	statement 4	Process		ia alternative to 					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_1_s_224	12489121	Overexpression of syntaxins Sso1 and Sso2, functioning  at the targeting/fusion of the Golgi-derived secretory vesicles to the plasma membrane,  polyubiquitin,  PSE1 and YAL048c ORF or the disruption of protease Yps1p, Yap3p encoding genes also enhance  heterologous protein secretion (Knittler and Haas, [ 1992]; Chow  et al., [ 1992]; Chen  et al., [ 1994]; Robinson  et al., [ 1994]; Ruohonen  et al., [ 1997];	gene_phenotype
70487	7	333651	11	NULL	NULL	0	NULL	Sso1	GP		plays a role in					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_1_s_224	12489121	Overexpression of syntaxins Sso1 and Sso2, functioning  at the targeting/fusion of the Golgi-derived secretory vesicles to the plasma membrane,  polyubiquitin,  PSE1 and YAL048c ORF or the disruption of protease Yps1p, Yap3p encoding genes also enhance  heterologous protein secretion (Knittler and Haas, [ 1992]; Chow  et al., [ 1992]; Chen  et al., [ 1994]; Robinson  et al., [ 1994]; Ruohonen  et al., [ 1997];	gene_phenotype
70488	8	333651	11	NULL	NULL	0	NULL	Sso1	GP		plays a role in					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_1_s_224	12489121	Overexpression of syntaxins Sso1 and Sso2, functioning  at the targeting/fusion of the Golgi-derived secretory vesicles to the plasma membrane,  polyubiquitin,  PSE1 and YAL048c ORF or the disruption of protease Yps1p, Yap3p encoding genes also enhance  heterologous protein secretion (Knittler and Haas, [ 1992]; Chow  et al., [ 1992]; Chen  et al., [ 1994]; Robinson  et al., [ 1994]; Ruohonen  et al., [ 1997];	gene_phenotype
70489	9	333651	11	NULL	NULL	0	NULL	Sso1	GP	Overexpression of	enhance					protein	GP	secretion of;;heterologous			NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_1_s_224	12489121	Overexpression of syntaxins Sso1 and Sso2, functioning  at the targeting/fusion of the Golgi-derived secretory vesicles to the plasma membrane,  polyubiquitin,  PSE1 and YAL048c ORF or the disruption of protease Yps1p, Yap3p encoding genes also enhance  heterologous protein secretion (Knittler and Haas, [ 1992]; Chow  et al., [ 1992]; Chen  et al., [ 1994]; Robinson  et al., [ 1994]; Ruohonen  et al., [ 1997];	gene_phenotype
70501	10	333651	11	NULL	NULL	0	NULL	Sso2	GP		plays a role in					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_1_s_224	12489121	Overexpression of syntaxins Sso1 and Sso2, functioning  at the targeting/fusion of the Golgi-derived secretory vesicles to the plasma membrane,  polyubiquitin,  PSE1 and YAL048c ORF or the disruption of protease Yps1p, Yap3p encoding genes also enhance  heterologous protein secretion (Knittler and Haas, [ 1992]; Chow  et al., [ 1992]; Chen  et al., [ 1994]; Robinson  et al., [ 1994]; Ruohonen  et al., [ 1997];	gene_phenotype
70502	11	333651	11	NULL	NULL	0	NULL	Sso2	GP		plays a role in					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_1_s_224	12489121	Overexpression of syntaxins Sso1 and Sso2, functioning  at the targeting/fusion of the Golgi-derived secretory vesicles to the plasma membrane,  polyubiquitin,  PSE1 and YAL048c ORF or the disruption of protease Yps1p, Yap3p encoding genes also enhance  heterologous protein secretion (Knittler and Haas, [ 1992]; Chow  et al., [ 1992]; Chen  et al., [ 1994]; Robinson  et al., [ 1994]; Ruohonen  et al., [ 1997];	gene_phenotype
70503	12	333651	11	10	NULL	NULL	NULL	Sso2	GP	overexpression of	enhance					protein	GP	secretion of;;heterologous			NULL		NULL	NULL	NULL	NULL	gw70_yeast_20_1_1_s_224	12489121	Overexpression of syntaxins Sso1 and Sso2, functioning  at the targeting/fusion of the Golgi-derived secretory vesicles to the plasma membrane,  polyubiquitin,  PSE1 and YAL048c ORF or the disruption of protease Yps1p, Yap3p encoding genes also enhance  heterologous protein secretion (Knittler and Haas, [ 1992]; Chow  et al., [ 1992]; Chen  et al., [ 1994]; Robinson  et al., [ 1994]; Ruohonen  et al., [ 1997];	gene_phenotype
70504	13	333651	11	NULL	NULL	0	NULL	polyubiquitin	GP		enhance					protein	GP	secretion of;;heterologous			NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_1_s_224	12489121	Overexpression of syntaxins Sso1 and Sso2, functioning  at the targeting/fusion of the Golgi-derived secretory vesicles to the plasma membrane,  polyubiquitin,  PSE1 and YAL048c ORF or the disruption of protease Yps1p, Yap3p encoding genes also enhance  heterologous protein secretion (Knittler and Haas, [ 1992]; Chow  et al., [ 1992]; Chen  et al., [ 1994]; Robinson  et al., [ 1994]; Ruohonen  et al., [ 1997];	gene_phenotype
70505	14	333651	11	NULL	NULL	0	NULL	PSE1	GP		enhance					protein	GP	secretion of;;heterologous			NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_1_s_224	12489121	Overexpression of syntaxins Sso1 and Sso2, functioning  at the targeting/fusion of the Golgi-derived secretory vesicles to the plasma membrane,  polyubiquitin,  PSE1 and YAL048c ORF or the disruption of protease Yps1p, Yap3p encoding genes also enhance  heterologous protein secretion (Knittler and Haas, [ 1992]; Chow  et al., [ 1992]; Chen  et al., [ 1994]; Robinson  et al., [ 1994]; Ruohonen  et al., [ 1997];	gene_phenotype
70506	15	333651	11	NULL	NULL	0	NULL	YAL048c ORF	NucleicAcid		enhance					protein	GP	secretion of;;heterologous			NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_1_s_224	12489121	Overexpression of syntaxins Sso1 and Sso2, functioning  at the targeting/fusion of the Golgi-derived secretory vesicles to the plasma membrane,  polyubiquitin,  PSE1 and YAL048c ORF or the disruption of protease Yps1p, Yap3p encoding genes also enhance  heterologous protein secretion (Knittler and Haas, [ 1992]; Chow  et al., [ 1992]; Chen  et al., [ 1994]; Robinson  et al., [ 1994]; Ruohonen  et al., [ 1997];	gene_phenotype
70507	16	333651	11	NULL	NULL	0	NULL	Yps1p gene	GP	disruption of	enhance					protein	GP	secretion of;;heterologous			NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_1_s_224	12489121	Overexpression of syntaxins Sso1 and Sso2, functioning  at the targeting/fusion of the Golgi-derived secretory vesicles to the plasma membrane,  polyubiquitin,  PSE1 and YAL048c ORF or the disruption of protease Yps1p, Yap3p encoding genes also enhance  heterologous protein secretion (Knittler and Haas, [ 1992]; Chow  et al., [ 1992]; Chen  et al., [ 1994]; Robinson  et al., [ 1994]; Ruohonen  et al., [ 1997];	gene_phenotype
70508	17	333651	11	NULL	NULL	0	NULL	Yap3p gene	GP	disruption of	enhance					protein	GP	secretion of;;heterologous			NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_1_s_224	12489121	Overexpression of syntaxins Sso1 and Sso2, functioning  at the targeting/fusion of the Golgi-derived secretory vesicles to the plasma membrane,  polyubiquitin,  PSE1 and YAL048c ORF or the disruption of protease Yps1p, Yap3p encoding genes also enhance  heterologous protein secretion (Knittler and Haas, [ 1992]; Chow  et al., [ 1992]; Chen  et al., [ 1994]; Robinson  et al., [ 1994]; Ruohonen  et al., [ 1997];	gene_phenotype
71863	18	333651	11	NULL	NULL	0	NULL	Yps1p	GP		is a type of 					protease	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_1_s_224	12489121	Overexpression of syntaxins Sso1 and Sso2, functioning  at the targeting/fusion of the Golgi-derived secretory vesicles to the plasma membrane,  polyubiquitin,  PSE1 and YAL048c ORF or the disruption of protease Yps1p, Yap3p encoding genes also enhance  heterologous protein secretion (Knittler and Haas, [ 1992]; Chow  et al., [ 1992]; Chen  et al., [ 1994]; Robinson  et al., [ 1994]; Ruohonen  et al., [ 1997];	gene_phenotype
71864	19	333651	11	NULL	NULL	0	NULL	Yps3p	GP		is a type of 					protease	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_1_s_224	12489121	Overexpression of syntaxins Sso1 and Sso2, functioning  at the targeting/fusion of the Golgi-derived secretory vesicles to the plasma membrane,  polyubiquitin,  PSE1 and YAL048c ORF or the disruption of protease Yps1p, Yap3p encoding genes also enhance  heterologous protein secretion (Knittler and Haas, [ 1992]; Chow  et al., [ 1992]; Chen  et al., [ 1994]; Robinson  et al., [ 1994]; Ruohonen  et al., [ 1997];	gene_phenotype
70145	1	333654	11	NULL	NULL	0	NULL	YDL193w	NucleicAcid	Null mutations	is					 lethal	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_485_1_29_s_112	11086160	Null mutations of YDL193w are lethal, thus, the gene was a suitable test system for the N-terminal tagging method since malfunction of the Cre/lox system or frame-shift mutations caused by mis-integration of yEGFP would result in loss of function and therefore loss of viability.	gene_phenotype
70152	1	333658	11	NULL	NULL	NULL	NULL	YOR1 gene	GP	S. cerevisiae homolog	transports					 small molecule 	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70154	2	333658	11	NULL	NULL	NULL	NULL	RTA1 gene	GP	S. cerevisiae homolog	transports					 small molecule 	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70155	3	333658	11	NULL	NULL	NULL	NULL	RSB1 gene	GP	S. cerevisiae homolog	transports					 small molecule 	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70509	4	333658	11	NULL	NULL	NULL	NULL	RPN4 gene	GP	S. cerevisiae homolog	transports					small molecule	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70510	5	333658	11	NULL	NULL	0	NULL	YLR346c gene	GP	S. cerevisiae homolog	transports					small molecule	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70511	6	333658	11	NULL	NULL	0	NULL	YMR102c gene	GP	S. cerevisiae homolog	transports					small molecule	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70512	7	333658	11	NULL	NULL	0	NULL	CDR1 gene	GP	S. cerevisiae homolog	transports					small molecule	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70513	8	333658	11	NULL	NULL	0	NULL	PDH1 gene	GP	S. cerevisiae homolog	transports					small molecule	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70514	9	333658	11	NULL	NULL	0	NULL	PDR1  gene	GP	S. cerevisiae homolog	transports					small molecule	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70515	10	333658	11	NULL	NULL	0	NULL	PDR12 gene	GP	S. cerevisiae homolog	transports					small molecule	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70516	11	333658	11	NULL	NULL	0	NULL	YOR1 gene	GP	S. cerevisiae homolog	regulate					transcription 	Process				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70517	12	333658	11	NULL	NULL	0	NULL	RTA1 gene	GP	S. cerevisiae homolog	regulate					transcription	Process				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70518	13	333658	11	NULL	NULL	0	NULL	RSB1 gene	GP	S. cerevisiae homolog	regulate					transcription	Process				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70519	14	333658	11	NULL	NULL	0	NULL	RPN4 gene	GP	S. cerevisiae homolog	regulate					transcription	Process				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70520	15	333658	11	NULL	NULL	0	NULL	YLR346c gene	GP	S. cerevisiae homolog	regulate					transcription	Process				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70521	16	333658	11	NULL	NULL	0	NULL	YMR102c gene	GP	S. cerevisiae homolog	regulate					transcription	Process				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70522	17	333658	11	NULL	NULL	0	NULL	CDR1 gene	GP	S. cerevisiae homolog	regulate					transcription	Process				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70523	18	333658	11	NULL	NULL	0	NULL	PDH1 gene	GP	S. cerevisiae homolog	regulate					transcription	Process				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70524	19	333658	11	NULL	NULL	0	NULL	PDR1  gene	GP	S. cerevisiae homolog	regulate					transcription	Process				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70525	20	333658	11	NULL	NULL	0	NULL	PDR12 gene	GP	S. cerevisiae homolog	regulate					transcription	Process				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_mol-microbiol_61_3_16803598_s_10	16803598	Homologues of 10 S. cerevisiae  genes previously shown to be Pdr1-Pdr3 targets were upregulated (YOR1,  RTA1, RSB1, RPN4, YLR346c and YMR102c along with CDR1, PDH1 and PDR1 itself)  or downregulated (PDR12); roles for these genes include small molecule  transport and transcriptional regulation.	gene_phenotype
70291	1	333660	11	NULL	NULL	0	NULL	 gamma-ray	Chemical		induced					mitotic interchromosomal recombination	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mutat-res_486_1_11356335_s_6	11356335	REC41 is required for normal  levels of interplasmid recombination and gamma-ray induced mitotic interchromosomal  recombination.	gene_phenotype
70292	2	333660	11	NULL	NULL	0	NULL	REC41	GP		is required for 					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mutat-res_486_1_11356335_s_6	11356335	REC41 is required for normal  levels of interplasmid recombination and gamma-ray induced mitotic interchromosomal  recombination.	gene_phenotype
70293	3	333660	11	NULL	NULL	0	NULL	REC41	GP		is required for 					 interplasmid recombination	Process	normal level			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mutat-res_486_1_11356335_s_6	11356335	REC41 is required for normal  levels of interplasmid recombination and gamma-ray induced mitotic interchromosomal  recombination.	gene_phenotype
70294	1	333661	11	NULL	NULL	0	NULL	rec41	GP		undergoes					mutation	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mutat-res_486_1_11356335_s_13	11356335	The rec41 mutation has an effect  on meiosis, likely meiotic recombination, even in the heterozygous state.	gene_phenotype
70295	2	333661	11	NULL	NULL	0	NULL	statement 1	Process		has an effect on					meiosis	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mutat-res_486_1_11356335_s_13	11356335	The rec41 mutation has an effect  on meiosis, likely meiotic recombination, even in the heterozygous state.	gene_phenotype
70296	3	333661	11	NULL	NULL	0	NULL	statement 1	Process		has an effect on					meiotic recombination	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mutat-res_486_1_11356335_s_13	11356335	The rec41 mutation has an effect  on meiosis, likely meiotic recombination, even in the heterozygous state.	gene_phenotype
70297	4	333661	11	NULL	NULL	0	NULL	statement 1	Process		has an effect on					heterozygous state	Chromosome				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mutat-res_486_1_11356335_s_13	11356335	The rec41 mutation has an effect  on meiosis, likely meiotic recombination, even in the heterozygous state.	gene_phenotype
70298	1	333662	11	NULL	NULL	0	NULL	REC46 gene	GP	Saccharomyes cerevisiae	controls					mitotic chromosomal stablity	Chromosome				NULL		0	NULL	NULL	NULL	gw70_yeast_19_6_553_s_370	11921104	The  REC46 gene of  Saccharomyes cerevisiae controls mitotic chromosomal stablity, recombination and sporulation: cell-type and  life cycle stage-specific expression of  rec46-1 mutation.	gene_phenotype
70299	2	333662	11	NULL	NULL	0	NULL	REC46 gene	GP	Saccharomyes cerevisiae	controls					recombination	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_19_6_553_s_370	11921104	The  REC46 gene of  Saccharomyes cerevisiae controls mitotic chromosomal stablity, recombination and sporulation: cell-type and  life cycle stage-specific expression of  rec46-1 mutation.	gene_phenotype
70300	3	333662	11	NULL	NULL	0	NULL	REC46 gene	GP	Saccharomyes cerevisiae	controls					sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_19_6_553_s_370	11921104	The  REC46 gene of  Saccharomyes cerevisiae controls mitotic chromosomal stablity, recombination and sporulation: cell-type and  life cycle stage-specific expression of  rec46-1 mutation.	gene_phenotype
70301	1	333664	11	NULL	NULL	0	NULL	YLR324w gene	GP	deletion	alter					peroxisome	CellComponent	number;;size			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_2_665_s_178	14617799	Cells harboring deletions in one or more of the  YLR324w, YGR004w and  YBR168w genes exhibit peroxisomes that are altered in number and/or size.	gene_phenotype
70302	2	333664	11	NULL	NULL	0	NULL	YGR004w  gene	GP	deletion	alter					peroxisome	CellComponent	number;;size			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_2_665_s_178	14617799	Cells harboring deletions in one or more of the  YLR324w, YGR004w and  YBR168w genes exhibit peroxisomes that are altered in number and/or size.	gene_phenotype
70303	3	333664	11	NULL	NULL	0	NULL	YBR168w gene	GP	deletion	alter					peroxisome	CellComponent	number;;size			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_2_665_s_178	14617799	Cells harboring deletions in one or more of the  YLR324w, YGR004w and  YBR168w genes exhibit peroxisomes that are altered in number and/or size.	gene_phenotype
70304	1	333666	11	NULL	NULL	0	NULL	YLR324w gene	GP	S. cerevisiae	controls					peroxisome	CellComponent	number;;size			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_2_665_s_281	14617799	Many proteins, including those encoded by the genes  YLR324w, YGR004w, and  YBR168w of  S. cerevisiae, are involved in controlling peroxisome number and size in the cell.	gene_phenotype
70305	2	333666	11	NULL	NULL	0	NULL	YGR004w  gene	GP	S. cerevisiae	controls					peroxisome	CellComponent	number;;size			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_2_665_s_281	14617799	Many proteins, including those encoded by the genes  YLR324w, YGR004w, and  YBR168w of  S. cerevisiae, are involved in controlling peroxisome number and size in the cell.	gene_phenotype
70306	3	333666	11	NULL	NULL	0	NULL	YBR168w gene	GP	S. cerevisiae	controls					peroxisome	CellComponent	number;;size			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_2_665_s_281	14617799	Many proteins, including those encoded by the genes  YLR324w, YGR004w, and  YBR168w of  S. cerevisiae, are involved in controlling peroxisome number and size in the cell.	gene_phenotype
70307	1	333667	11	NULL	NULL	NULL	NULL	YLR324w gene	GP	deletion	increased					peroxisome	CellComponent	number;;size;;clustering			NULL	 strain DK2 	NULL	NULL	NULL	NULL	gw70_molbiolcell_15_2_665_s_174	14617799	Cells of strain  DK2 ( Figure 5F) carrying deletions in the  YLR324w and  YBR168w genes showed increased numbers of peroxisomes ( Table 3) of normal to enlarged size ( Figure 5I), some of which exhibited clustering, whereas cells of strain  DK3 ( Figure 5G) deleted for the  YGR004w and  YBR168w genes also contained greatly enlarged peroxisomes ( Figure 5I;  Table 3).	gene_phenotype
70308	2	333667	11	NULL	NULL	NULL	NULL	YBR168w gene	GP	deletion	increased					peroxisome	CellComponent	number;;size;;clustering			NULL	 strain DK2 	NULL	NULL	NULL	NULL	gw70_molbiolcell_15_2_665_s_174	14617799	Cells of strain  DK2 ( Figure 5F) carrying deletions in the  YLR324w and  YBR168w genes showed increased numbers of peroxisomes ( Table 3) of normal to enlarged size ( Figure 5I), some of which exhibited clustering, whereas cells of strain  DK3 ( Figure 5G) deleted for the  YGR004w and  YBR168w genes also contained greatly enlarged peroxisomes ( Figure 5I;  Table 3).	gene_phenotype
70309	3	333667	11	NULL	NULL	0	NULL	YGR004w  gene	GP	deletion	enlarged					peroxisomes	CellComponent				NULL	 strain DK3	0	NULL	NULL	NULL	gw70_molbiolcell_15_2_665_s_174	14617799	Cells of strain  DK2 ( Figure 5F) carrying deletions in the  YLR324w and  YBR168w genes showed increased numbers of peroxisomes ( Table 3) of normal to enlarged size ( Figure 5I), some of which exhibited clustering, whereas cells of strain  DK3 ( Figure 5G) deleted for the  YGR004w and  YBR168w genes also contained greatly enlarged peroxisomes ( Figure 5I;  Table 3).	gene_phenotype
70310	4	333667	11	NULL	NULL	0	NULL	YBR168w gene	GP	deletion	enlarged					peroxisome	CellComponent				NULL	 strain DK3	0	NULL	NULL	NULL	gw70_molbiolcell_15_2_665_s_174	14617799	Cells of strain  DK2 ( Figure 5F) carrying deletions in the  YLR324w and  YBR168w genes showed increased numbers of peroxisomes ( Table 3) of normal to enlarged size ( Figure 5I), some of which exhibited clustering, whereas cells of strain  DK3 ( Figure 5G) deleted for the  YGR004w and  YBR168w genes also contained greatly enlarged peroxisomes ( Figure 5I;  Table 3).	gene_phenotype
71865	1	333668	11	NULL	NULL	0	NULL	YGR004w	NucleicAcid	over expression of	complement		partially			peroxisomal morphology	physical phenomenon	abnormal			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_2_665_s_192	14617799	Overexpression of YGR004w Can Partially Complement the Abnormal Peroxisomal Morphology  Observed in Cells Deleted for One or Both of YLR324w and YBR168w   ecause cells deleted for one or more of the  YLR324w, YGR004w, and  YBR168w genes are compromised in their regulation of peroxisome size and number, we investigated the effects of overexpression of these genes on the overall peroxisome phenotype in cells harboring various combinations of deletions of these genes.	gene_phenotype
71866	2	333668	11	NULL	NULL	0	NULL	cells	Cell		deleted with					YLR324w	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_2_665_s_192	14617799	Overexpression of YGR004w Can Partially Complement the Abnormal Peroxisomal Morphology  Observed in Cells Deleted for One or Both of YLR324w and YBR168w   ecause cells deleted for one or more of the  YLR324w, YGR004w, and  YBR168w genes are compromised in their regulation of peroxisome size and number, we investigated the effects of overexpression of these genes on the overall peroxisome phenotype in cells harboring various combinations of deletions of these genes.	gene_phenotype
71867	3	333668	11	NULL	NULL	0	NULL	cells	Cell		deleted with					YBR168w	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_2_665_s_192	14617799	Overexpression of YGR004w Can Partially Complement the Abnormal Peroxisomal Morphology  Observed in Cells Deleted for One or Both of YLR324w and YBR168w   ecause cells deleted for one or more of the  YLR324w, YGR004w, and  YBR168w genes are compromised in their regulation of peroxisome size and number, we investigated the effects of overexpression of these genes on the overall peroxisome phenotype in cells harboring various combinations of deletions of these genes.	gene_phenotype
71868	4	333668	11	NULL	NULL	0	NULL	statement 1	Process		is observed in					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_2_665_s_192	14617799	Overexpression of YGR004w Can Partially Complement the Abnormal Peroxisomal Morphology  Observed in Cells Deleted for One or Both of YLR324w and YBR168w   ecause cells deleted for one or more of the  YLR324w, YGR004w, and  YBR168w genes are compromised in their regulation of peroxisome size and number, we investigated the effects of overexpression of these genes on the overall peroxisome phenotype in cells harboring various combinations of deletions of these genes.	gene_phenotype
71869	5	333668	11	NULL	NULL	0	NULL	statement 1	Process		is observed in					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_2_665_s_192	14617799	Overexpression of YGR004w Can Partially Complement the Abnormal Peroxisomal Morphology  Observed in Cells Deleted for One or Both of YLR324w and YBR168w   ecause cells deleted for one or more of the  YLR324w, YGR004w, and  YBR168w genes are compromised in their regulation of peroxisome size and number, we investigated the effects of overexpression of these genes on the overall peroxisome phenotype in cells harboring various combinations of deletions of these genes.	gene_phenotype
70481	1	333670	11	NULL	NULL	0	NULL	YER064C gene	GP		is a type of 		potential			small molecule transporter	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1517_2_177_s_204	11342098	YER064C is a gene of unknown function but is predicted to be a small molecule transporter localized to an integral membrane [  38].	gene_phenotype
70482	2	333670	11	NULL	NULL	0	NULL	YER064C gene	NucleicAcid		is localized to		potentially			 integral membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1517_2_177_s_204	11342098	YER064C is a gene of unknown function but is predicted to be a small molecule transporter localized to an integral membrane [  38].	gene_phenotype
70318	1	333671	11	NULL	NULL	0	NULL	Yer064Cp	GP		is a type of 					 nuclear protein	GP				NULL		0	NULL	NULL	NULL	gw70_genetics_174_1_191_s_30	16783004	Yer064Cp, a nuclear protein of unknown function, is important for the activation of some  ERG genes ( ENNEDY et al;  ERMANN et al).	gene_phenotype
70319	2	333671	11	NULL	NULL	0	NULL	Yer064Cp	GP		activates					ERG genes	GP				NULL		0	NULL	NULL	NULL	gw70_genetics_174_1_191_s_30	16783004	Yer064Cp, a nuclear protein of unknown function, is important for the activation of some  ERG genes ( ENNEDY et al;  ERMANN et al).	gene_phenotype
70320	1	333672	11	NULL	NULL	0	NULL	 sst2	GP	mutant	 increases					pheromone sensitivity	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_2_330_s_8	16467474	A number of mutants produced an increase ( sst2,  bar1,  asc1, and  ygl024w) or decrease ( cla4) in pheromone sensitivity or resulted in pheromone-independent signaling ( sst2,  pbs2,  gas1, and  ygl024w).	gene_phenotype
70321	2	333672	11	NULL	NULL	0	NULL	bar1	GP	mutant	increases					pheromone sensitivity	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_2_330_s_8	16467474	A number of mutants produced an increase ( sst2,  bar1,  asc1, and  ygl024w) or decrease ( cla4) in pheromone sensitivity or resulted in pheromone-independent signaling ( sst2,  pbs2,  gas1, and  ygl024w).	gene_phenotype
70322	3	333672	11	NULL	NULL	0	NULL	asc1	GP	mutant	increases					pheromone sensitivity	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_2_330_s_8	16467474	A number of mutants produced an increase ( sst2,  bar1,  asc1, and  ygl024w) or decrease ( cla4) in pheromone sensitivity or resulted in pheromone-independent signaling ( sst2,  pbs2,  gas1, and  ygl024w).	gene_phenotype
70323	4	333672	11	NULL	NULL	0	NULL	ygl024w	GP	mutant	increases					pheromone sensitivity	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_2_330_s_8	16467474	A number of mutants produced an increase ( sst2,  bar1,  asc1, and  ygl024w) or decrease ( cla4) in pheromone sensitivity or resulted in pheromone-independent signaling ( sst2,  pbs2,  gas1, and  ygl024w).	gene_phenotype
70324	5	333672	11	NULL	NULL	0	NULL	cla4	GP	mutant	decreases					pheromone sensitivity	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_2_330_s_8	16467474	A number of mutants produced an increase ( sst2,  bar1,  asc1, and  ygl024w) or decrease ( cla4) in pheromone sensitivity or resulted in pheromone-independent signaling ( sst2,  pbs2,  gas1, and  ygl024w).	gene_phenotype
70325	6	333672	11	NULL	NULL	0	NULL	sst2	GP	mutant	resulted in 					pheromone-independent signaling 	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_2_330_s_8	16467474	A number of mutants produced an increase ( sst2,  bar1,  asc1, and  ygl024w) or decrease ( cla4) in pheromone sensitivity or resulted in pheromone-independent signaling ( sst2,  pbs2,  gas1, and  ygl024w).	gene_phenotype
70326	7	333672	11	NULL	NULL	0	NULL	 pbs2	GP	mutant	resulted in 					pheromone-independent signaling 	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_2_330_s_8	16467474	A number of mutants produced an increase ( sst2,  bar1,  asc1, and  ygl024w) or decrease ( cla4) in pheromone sensitivity or resulted in pheromone-independent signaling ( sst2,  pbs2,  gas1, and  ygl024w).	gene_phenotype
70329	8	333672	11	NULL	NULL	0	NULL	gas1	GP	mutant	resulted in 					pheromone-independent signaling	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_2_330_s_8	16467474	A number of mutants produced an increase ( sst2,  bar1,  asc1, and  ygl024w) or decrease ( cla4) in pheromone sensitivity or resulted in pheromone-independent signaling ( sst2,  pbs2,  gas1, and  ygl024w).	gene_phenotype
70330	9	333672	11	NULL	NULL	0	NULL	ygl024w	GP	mutant	resulted in 					pheromone-independent signaling	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_2_330_s_8	16467474	A number of mutants produced an increase ( sst2,  bar1,  asc1, and  ygl024w) or decrease ( cla4) in pheromone sensitivity or resulted in pheromone-independent signaling ( sst2,  pbs2,  gas1, and  ygl024w).	gene_phenotype
70334	1	333674	11	NULL	NULL	0	NULL	YGL024W	NucleicAcid	Deletion	removes					Pgd1 protein	GP		N-terminal		NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_2_330_s_432	16467474	Deletion of  YGL024W removes the N-terminal portion of the Pgd1 protein and enhances signaling activity, while deletion of the entire  PGD1 gene removes both the N-terminal and C-terminal portions, and signaling is unaffected.	gene_phenotype
70336	2	333674	11	NULL	NULL	0	NULL	statement 1	Process		activates					signaling	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_2_330_s_432	16467474	Deletion of  YGL024W removes the N-terminal portion of the Pgd1 protein and enhances signaling activity, while deletion of the entire  PGD1 gene removes both the N-terminal and C-terminal portions, and signaling is unaffected.	gene_phenotype
70356	1	333677	11	NULL	NULL	0	NULL	 SRO77 gene	GP		involved in					endocytosis	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_10_4075_s_365	15870279	Finally, genes involved in endocytosis ( SRO77 and  AKR2) were also up-regulated, including several (e.g.,  IZH4,  CLC1,  AKR1,  RVS161,  AFR1, and YBR108W) that were induced much earlier in the time course.	gene_phenotype
70357	2	333677	11	NULL	NULL	0	NULL	AKR2 gene	GP		involved in					endocytosis	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_10_4075_s_365	15870279	Finally, genes involved in endocytosis ( SRO77 and  AKR2) were also up-regulated, including several (e.g.,  IZH4,  CLC1,  AKR1,  RVS161,  AFR1, and YBR108W) that were induced much earlier in the time course.	gene_phenotype
70359	1	333679	11	NULL	NULL	0	NULL	YLR424W gene	NucleicAcid	 S. cerevisiae	required for					viability	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_12_1_5_s_192	12887888	For example, YLR424W, a  S. cerevisiae gene of unknown function required for viability and containing a G-patch putative RNA binding motif, is a component of T1 and T3-6.	gene_phenotype
70360	2	333679	11	NULL	NULL	0	NULL	YLR424W gene	NucleicAcid	S. cerevisiae	containing					G-patch putative RNA binding motif	GP				NULL		0	NULL	NULL	NULL	gw60_molcell_12_1_5_s_192	12887888	For example, YLR424W, a  S. cerevisiae gene of unknown function required for viability and containing a G-patch putative RNA binding motif, is a component of T1 and T3-6.	gene_phenotype
70361	3	333679	11	NULL	NULL	0	NULL	YLR424W gene	NucleicAcid	S. cerevisiae	 is a component of					 T1	GP				NULL		0	NULL	NULL	NULL	gw60_molcell_12_1_5_s_192	12887888	For example, YLR424W, a  S. cerevisiae gene of unknown function required for viability and containing a G-patch putative RNA binding motif, is a component of T1 and T3-6.	gene_phenotype
70363	4	333679	11	NULL	NULL	0	NULL	YLR424W gene	NucleicAcid	S. cerevisiae	is a component of					T3-6	GP				NULL		0	NULL	NULL	NULL	gw60_molcell_12_1_5_s_192	12887888	For example, YLR424W, a  S. cerevisiae gene of unknown function required for viability and containing a G-patch putative RNA binding motif, is a component of T1 and T3-6.	gene_phenotype
70366	1	333680	11	NULL	NULL	NULL	NULL	 YLR324w gene	NucleicAcid	deletion	increases					 peroxisome	CellComponent	number;;size			NULL	strain DK1	NULL	NULL	NULL	NULL	gw70_molbiolcell_15_2_665_s_173	14617799	Cells of strain  DK1 ( Figure 5E) carrying deletions in the  YLR324w and  YGR004w genes exhibited a mixed phenotype of increased numbers of peroxisomes ( Table 3) of normal to enlarged size ( Figure 5I;  Table 3).	gene_phenotype
70367	2	333680	11	NULL	NULL	0	NULL	YGR004w gene	NucleicAcid	deletion	increases					peroxisomes	CellComponent	number;;size			NULL	strain DK1	0	NULL	NULL	NULL	gw70_molbiolcell_15_2_665_s_173	14617799	Cells of strain  DK1 ( Figure 5E) carrying deletions in the  YLR324w and  YGR004w genes exhibited a mixed phenotype of increased numbers of peroxisomes ( Table 3) of normal to enlarged size ( Figure 5I;  Table 3).	gene_phenotype
70395	1	333682	11	NULL	NULL	0	NULL	SMK1	GP		encodes for					MAP kinase	GP	 sporulation pathway			NULL		0	NULL	NULL	NULL	gw60_genetics_163_3_875_s_286	12663529	Mutants in  SMK1,  MPK1, and  YKL161c, which encode, respectively, the MAP kinase of the sporulation pathway, the cell integrity pathway, and a putative uncharacterized pathway, are not toxin hypersensitive.	gene_phenotype
70396	2	333682	11	NULL	NULL	0	NULL	MPK1	GP		encodes for					MAP kinase	GP	cell integrity pathway			NULL		0	NULL	NULL	NULL	gw60_genetics_163_3_875_s_286	12663529	Mutants in  SMK1,  MPK1, and  YKL161c, which encode, respectively, the MAP kinase of the sporulation pathway, the cell integrity pathway, and a putative uncharacterized pathway, are not toxin hypersensitive.	gene_phenotype
70397	3	333682	11	NULL	NULL	0	NULL	YKL161c	GP		encodes for					MAP kinase	GP	 putative uncharacterized pathway			NULL		0	NULL	NULL	NULL	gw60_genetics_163_3_875_s_286	12663529	Mutants in  SMK1,  MPK1, and  YKL161c, which encode, respectively, the MAP kinase of the sporulation pathway, the cell integrity pathway, and a putative uncharacterized pathway, are not toxin hypersensitive.	gene_phenotype
70398	4	333682	11	NULL	NULL	0	NULL	statement 1	Process		is not hypersensitive to					toxin	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_163_3_875_s_286	12663529	Mutants in  SMK1,  MPK1, and  YKL161c, which encode, respectively, the MAP kinase of the sporulation pathway, the cell integrity pathway, and a putative uncharacterized pathway, are not toxin hypersensitive.	gene_phenotype
70399	5	333682	11	NULL	NULL	0	NULL	statement 2	Process		is not hypersensitive to					toxin	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_163_3_875_s_286	12663529	Mutants in  SMK1,  MPK1, and  YKL161c, which encode, respectively, the MAP kinase of the sporulation pathway, the cell integrity pathway, and a putative uncharacterized pathway, are not toxin hypersensitive.	gene_phenotype
70400	6	333682	11	NULL	NULL	0	NULL	statement 3	Process		is not hypersensitive to					toxin	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_163_3_875_s_286	12663529	Mutants in  SMK1,  MPK1, and  YKL161c, which encode, respectively, the MAP kinase of the sporulation pathway, the cell integrity pathway, and a putative uncharacterized pathway, are not toxin hypersensitive.	gene_phenotype
70401	1	333683	11	NULL	NULL	0	NULL	YLR205c	NucleicAcid		is a type of 					 heme oxygenase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_11_7762_s_216	11112771	In a frataxin-deficient strain mitochondrial free iron accumulates and cannot be extruded from mitochondria, so that Aft1p encounters a low iron signal and stimulates the transcription of genes encoding the plasma membrane iron and siderophore transporters, the heme oxygenase (YLR205c) and the vacuolar iron transporter ( FET5/ FTH1).	gene_phenotype
70402	2	333683	11	NULL	NULL	0	NULL	FET5/ FTH1	GP		is a type of 					vacuolar iron transporter	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_11_7762_s_216	11112771	In a frataxin-deficient strain mitochondrial free iron accumulates and cannot be extruded from mitochondria, so that Aft1p encounters a low iron signal and stimulates the transcription of genes encoding the plasma membrane iron and siderophore transporters, the heme oxygenase (YLR205c) and the vacuolar iron transporter ( FET5/ FTH1).	gene_phenotype
70403	3	333683	11	NULL	NULL	NULL	NULL	 Aft1p	GP		stimulates					 YLR205c	GP	transcription of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_11_7762_s_216	11112771	In a frataxin-deficient strain mitochondrial free iron accumulates and cannot be extruded from mitochondria, so that Aft1p encounters a low iron signal and stimulates the transcription of genes encoding the plasma membrane iron and siderophore transporters, the heme oxygenase (YLR205c) and the vacuolar iron transporter ( FET5/ FTH1).	gene_phenotype
70404	4	333683	11	NULL	NULL	NULL	NULL	 Aft1p	GP		stimulates					FET5/ FTH1	GP	transcription of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_11_7762_s_216	11112771	In a frataxin-deficient strain mitochondrial free iron accumulates and cannot be extruded from mitochondria, so that Aft1p encounters a low iron signal and stimulates the transcription of genes encoding the plasma membrane iron and siderophore transporters, the heme oxygenase (YLR205c) and the vacuolar iron transporter ( FET5/ FTH1).	gene_phenotype
71870	5	333683	11	NULL	NULL	0	NULL	free iron	Chemical	mitochondrial	accumulates in					frataxin-deficient strain	Organism				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_11_7762_s_216	11112771	In a frataxin-deficient strain mitochondrial free iron accumulates and cannot be extruded from mitochondria, so that Aft1p encounters a low iron signal and stimulates the transcription of genes encoding the plasma membrane iron and siderophore transporters, the heme oxygenase (YLR205c) and the vacuolar iron transporter ( FET5/ FTH1).	gene_phenotype
71871	6	333683	11	NULL	NULL	0	NULL	free iron	Chemical	mitochondrial	is not extruded from					mitochondria	Cell Component				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_11_7762_s_216	11112771	In a frataxin-deficient strain mitochondrial free iron accumulates and cannot be extruded from mitochondria, so that Aft1p encounters a low iron signal and stimulates the transcription of genes encoding the plasma membrane iron and siderophore transporters, the heme oxygenase (YLR205c) and the vacuolar iron transporter ( FET5/ FTH1).	gene_phenotype
71872	7	333683	11	NULL	NULL	0	NULL	statement 1	Process		occurs along with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_11_7762_s_216	11112771	In a frataxin-deficient strain mitochondrial free iron accumulates and cannot be extruded from mitochondria, so that Aft1p encounters a low iron signal and stimulates the transcription of genes encoding the plasma membrane iron and siderophore transporters, the heme oxygenase (YLR205c) and the vacuolar iron transporter ( FET5/ FTH1).	gene_phenotype
71873	8	333683	11	NULL	NULL	0	NULL	Aft1p	GP		encounters					low iron signal	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_11_7762_s_216	11112771	In a frataxin-deficient strain mitochondrial free iron accumulates and cannot be extruded from mitochondria, so that Aft1p encounters a low iron signal and stimulates the transcription of genes encoding the plasma membrane iron and siderophore transporters, the heme oxygenase (YLR205c) and the vacuolar iron transporter ( FET5/ FTH1).	gene_phenotype
71877	9	333683	11	NULL	NULL	0	NULL	statement 2	Process		leads to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_11_7762_s_216	11112771	In a frataxin-deficient strain mitochondrial free iron accumulates and cannot be extruded from mitochondria, so that Aft1p encounters a low iron signal and stimulates the transcription of genes encoding the plasma membrane iron and siderophore transporters, the heme oxygenase (YLR205c) and the vacuolar iron transporter ( FET5/ FTH1).	gene_phenotype
71880	10	333683	11	NULL	NULL	0	NULL	statement 4	Process		stimulates					plasma membrane iron transporter gene	GP	transcription of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_11_7762_s_216	11112771	In a frataxin-deficient strain mitochondrial free iron accumulates and cannot be extruded from mitochondria, so that Aft1p encounters a low iron signal and stimulates the transcription of genes encoding the plasma membrane iron and siderophore transporters, the heme oxygenase (YLR205c) and the vacuolar iron transporter ( FET5/ FTH1).	gene_phenotype
71882	11	333683	11	NULL	NULL	0	NULL	statement 4	Process		stimulates					siderophore transporter gene	transcription of				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_11_7762_s_216	11112771	In a frataxin-deficient strain mitochondrial free iron accumulates and cannot be extruded from mitochondria, so that Aft1p encounters a low iron signal and stimulates the transcription of genes encoding the plasma membrane iron and siderophore transporters, the heme oxygenase (YLR205c) and the vacuolar iron transporter ( FET5/ FTH1).	gene_phenotype
70405	1	333687	11	NULL	NULL	0	NULL	Cin5	GP		undergoes					cellular localization	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_59_3_470_s_100	11179441	We examined the cellular localization of Cin5 and Ydr259c by inducing the expression of fusion proteins of Cin5 or Ydr259c with GFP in W303B cells (Fig.  5A).	gene_phenotype
70406	2	333687	11	NULL	NULL	0	NULL	Ydr259c	NucleicAcid		undergoes					cellular localization	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_59_3_470_s_100	11179441	We examined the cellular localization of Cin5 and Ydr259c by inducing the expression of fusion proteins of Cin5 or Ydr259c with GFP in W303B cells (Fig.  5A).	gene_phenotype
70407	3	333687	11	NULL	NULL	0	NULL	Cin5	GP		is a type of 					fusion protein	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_59_3_470_s_100	11179441	We examined the cellular localization of Cin5 and Ydr259c by inducing the expression of fusion proteins of Cin5 or Ydr259c with GFP in W303B cells (Fig.  5A).	gene_phenotype
70408	4	333687	11	NULL	NULL	0	NULL	Ydr259c	GP		is a type of 					fusion protein	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_59_3_470_s_100	11179441	We examined the cellular localization of Cin5 and Ydr259c by inducing the expression of fusion proteins of Cin5 or Ydr259c with GFP in W303B cells (Fig.  5A).	gene_phenotype
70409	5	333687	11	NULL	NULL	0	NULL	Cin5	GP		binds					GFP	GP				NULL	W303B cells	0	NULL	NULL	NULL	gw60_molpharmacol_59_3_470_s_100	11179441	We examined the cellular localization of Cin5 and Ydr259c by inducing the expression of fusion proteins of Cin5 or Ydr259c with GFP in W303B cells (Fig.  5A).	gene_phenotype
70410	6	333687	11	NULL	NULL	0	NULL	statement 5	Process		 induce the expression of					Cin5	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_59_3_470_s_100	11179441	We examined the cellular localization of Cin5 and Ydr259c by inducing the expression of fusion proteins of Cin5 or Ydr259c with GFP in W303B cells (Fig.  5A).	gene_phenotype
70411	7	333687	11	NULL	NULL	0	NULL	Ydr259c	NucleicAcid		binds					GFP	GP				NULL	 W303B cells	0	NULL	NULL	NULL	gw60_molpharmacol_59_3_470_s_100	11179441	We examined the cellular localization of Cin5 and Ydr259c by inducing the expression of fusion proteins of Cin5 or Ydr259c with GFP in W303B cells (Fig.  5A).	gene_phenotype
70412	8	333687	11	NULL	NULL	0	NULL	statement 7	Process		induce the expression of					Ydr259c	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_59_3_470_s_100	11179441	We examined the cellular localization of Cin5 and Ydr259c by inducing the expression of fusion proteins of Cin5 or Ydr259c with GFP in W303B cells (Fig.  5A).	gene_phenotype
70413	9	333687	11	NULL	NULL	0	NULL	statement 6	Process		induces					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_59_3_470_s_100	11179441	We examined the cellular localization of Cin5 and Ydr259c by inducing the expression of fusion proteins of Cin5 or Ydr259c with GFP in W303B cells (Fig.  5A).	gene_phenotype
70414	10	333687	11	NULL	NULL	0	NULL	statement 8	Process		induces					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_59_3_470_s_100	11179441	We examined the cellular localization of Cin5 and Ydr259c by inducing the expression of fusion proteins of Cin5 or Ydr259c with GFP in W303B cells (Fig.  5A).	gene_phenotype
70415	1	333688	11	NULL	NULL	0	NULL	 Cin5	GP		localized in the					nuclei	CellComponent	 yeast cell			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_59_3_470_s_8	11179441	An experiment with fusion proteins with green fluorescent protein revealed that Cin5 and Ydr259c were localized constitutively in the nuclei of yeast cells.	gene_phenotype
70416	2	333688	11	NULL	NULL	0	NULL	Ydr259c	GP		localized in the					 nuclei	CellComponent	yeast cell			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_59_3_470_s_8	11179441	An experiment with fusion proteins with green fluorescent protein revealed that Cin5 and Ydr259c were localized constitutively in the nuclei of yeast cells.	gene_phenotype
71892	1	333693	11	NULL	NULL	0	NULL	YOR193w	NucleicAcid		controls					peroxisome size	Cell Component				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_10_4089_s_261	14517321	These abnormally large peroxisomes could result from a disruption of components of the peroxisome division machinery in cells of the gene deletion strains, which is consistent with a role for  YOR193w in the control of peroxisome size, as has been proposed for  PEX25 and  PEX11 (Marshall  et al., 1995 ; Erdmann and Blobel, 1995 ; Smith  et al., 2002 ).	gene_phenotype
71894	2	333693	11	NULL	NULL	0	NULL	PEX25	GP		controls		possibly			peroxisome size	Cell Component				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_10_4089_s_261	14517321	These abnormally large peroxisomes could result from a disruption of components of the peroxisome division machinery in cells of the gene deletion strains, which is consistent with a role for  YOR193w in the control of peroxisome size, as has been proposed for  PEX25 and  PEX11 (Marshall  et al., 1995 ; Erdmann and Blobel, 1995 ; Smith  et al., 2002 ).	gene_phenotype
71896	3	333693	11	NULL	NULL	0	NULL	PEX11	GP		controls		possibly			peroxisome size	Cell Component				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_10_4089_s_261	14517321	These abnormally large peroxisomes could result from a disruption of components of the peroxisome division machinery in cells of the gene deletion strains, which is consistent with a role for  YOR193w in the control of peroxisome size, as has been proposed for  PEX25 and  PEX11 (Marshall  et al., 1995 ; Erdmann and Blobel, 1995 ; Smith  et al., 2002 ).	gene_phenotype
70417	1	333696	11	NULL	NULL	0	NULL	YGL133w	NucleicAcid	deletion	showed					abnormal morphology	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_336	14587103	In addition,   cells deleted in  YGL133w showed abnormal morphology (resembling the schmoo) and reduced mating efficiency  but, unlike the cell wall defects, these phenotypes were not observed when the  YGL133w disruption was in a  MAT a background (Escribano and Mazon, [ 2000]).	gene_phenotype
70418	2	333696	11	NULL	NULL	0	NULL	YGL133w	NucleicAcid	deletion	reduced					mating efficiency	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_336	14587103	In addition,   cells deleted in  YGL133w showed abnormal morphology (resembling the schmoo) and reduced mating efficiency  but, unlike the cell wall defects, these phenotypes were not observed when the  YGL133w disruption was in a  MAT a background (Escribano and Mazon, [ 2000]).	gene_phenotype
70419	1	333698	11	NULL	NULL	0	NULL	 YKR020w	NucleicAcid		 is essential for					Cvt vesicle formation	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_5009_s_4	12446664	We found that the  YKR020w gene product is essential for Cvt vesicle formation but not for pexophagy or induction of autophagy.	gene_phenotype
70420	2	333698	11	NULL	NULL	0	NULL	 YKR020w	NucleicAcid		is not essential for 					pexophagy	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_5009_s_4	12446664	We found that the  YKR020w gene product is essential for Cvt vesicle formation but not for pexophagy or induction of autophagy.	gene_phenotype
70421	3	333698	11	NULL	NULL	0	NULL	YKR020w	NucleicAcid		is not essential for 					autophagy	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_5009_s_4	12446664	We found that the  YKR020w gene product is essential for Cvt vesicle formation but not for pexophagy or induction of autophagy.	gene_phenotype
70422	1	333700	11	10	NULL	NULL	NULL	SIN3 gene	GP		 involved in					heterochromatin formation	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_4_1610_s_122	12686613	Mutation of  SIN3 or  SET2, genes involved in heterochromatin formation and gene silencing, completely suppressed the CPY secretion defect of the  vps51-1 strain but not that of  ykr020wdelta, suggesting that the upstream transposon insertion leads to transcriptional repression of  YKR020w (unpublished data).	gene_phenotype
70423	2	333700	11	10	NULL	NULL	NULL	SET2 gene	GP		 involved in					heterochromatin formation	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_4_1610_s_122	12686613	Mutation of  SIN3 or  SET2, genes involved in heterochromatin formation and gene silencing, completely suppressed the CPY secretion defect of the  vps51-1 strain but not that of  ykr020wdelta, suggesting that the upstream transposon insertion leads to transcriptional repression of  YKR020w (unpublished data).	gene_phenotype
70424	3	333700	11	10	NULL	NULL	NULL	SIN3 gene	GP		 involved in					gene silencing	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_4_1610_s_122	12686613	Mutation of  SIN3 or  SET2, genes involved in heterochromatin formation and gene silencing, completely suppressed the CPY secretion defect of the  vps51-1 strain but not that of  ykr020wdelta, suggesting that the upstream transposon insertion leads to transcriptional repression of  YKR020w (unpublished data).	gene_phenotype
70425	4	333700	11	10	NULL	NULL	NULL	SET2 gene	GP		involved in					gene silencing	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_4_1610_s_122	12686613	Mutation of  SIN3 or  SET2, genes involved in heterochromatin formation and gene silencing, completely suppressed the CPY secretion defect of the  vps51-1 strain but not that of  ykr020wdelta, suggesting that the upstream transposon insertion leads to transcriptional repression of  YKR020w (unpublished data).	gene_phenotype
70426	1	333701	11	NULL	NULL	NULL	NULL	YKR020w ORF	NucleicAcid	Deletion	secrets		increase			CPY 	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_14_4_1610_s_106	12686613	Deletion of the  YKR020w ORF gave rise to levels of CPY secretion and vacuolar morphology defects indistinguishable from those of the  vps51-1 mutant (compare Figures  1C and  2A), consistent with the results of a recent genome-wide screen for  vps mutants (Bonangelino  et al., 2002 ).	gene_phenotype
70427	2	333701	11	NULL	NULL	0	NULL	YKR020w ORF	NucleicAcid	deletion	defects					vacuolar morphology	CellComponent				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_14_4_1610_s_106	12686613	Deletion of the  YKR020w ORF gave rise to levels of CPY secretion and vacuolar morphology defects indistinguishable from those of the  vps51-1 mutant (compare Figures  1C and  2A), consistent with the results of a recent genome-wide screen for  vps mutants (Bonangelino  et al., 2002 ).	gene_phenotype
70428	1	333702	11	NULL	NULL	0	NULL	PDR16 gene	GP		involved in 					phospholipid synthesis	Process				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_gene_272_1-2_11470516_s_3	11470516	Among 20 genes containing binding consensus  sequences for the transcription factor Pdr1p in their promoter, we studied  more particularly the regulation and function of PDR16 (involved in phospholipid  synthesis), TPO1 (involved in vacuolar transport of polyamines), YAL061W  (homologous to polyol dehydrogenases) and YLR346C (unknown function).	gene_phenotype
70429	2	333702	11	NULL	NULL	0	NULL	TPO1 gene	GP		involved in					vacuolar transport	Process	of polyamines			NULL		0	NULL	NULL	NULL	abs-batch0517-0529_gene_272_1-2_11470516_s_3	11470516	Among 20 genes containing binding consensus  sequences for the transcription factor Pdr1p in their promoter, we studied  more particularly the regulation and function of PDR16 (involved in phospholipid  synthesis), TPO1 (involved in vacuolar transport of polyamines), YAL061W  (homologous to polyol dehydrogenases) and YLR346C (unknown function).	gene_phenotype
70430	3	333702	11	NULL	NULL	0	NULL	YAL061W gene	NucleicAcid		homologous to					polyol dehydrogenase	GP				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_gene_272_1-2_11470516_s_3	11470516	Among 20 genes containing binding consensus  sequences for the transcription factor Pdr1p in their promoter, we studied  more particularly the regulation and function of PDR16 (involved in phospholipid  synthesis), TPO1 (involved in vacuolar transport of polyamines), YAL061W  (homologous to polyol dehydrogenases) and YLR346C (unknown function).	gene_phenotype
70431	1	333703	11	NULL	NULL	0	NULL	YOR249c ORF	NucleicAcid	Deletion	reduces					viability	Process				NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1219_s_50	9469815	Deletion of this ORF from the  S. cerevisiae genome indicates that YOR249c is essential for viability, and the null mutants exhibit a terminal G2-M arrest phenotype as would be expected for APC genes ( 23).	gene_phenotype
70432	2	333703	11	NULL	NULL	0	NULL	 YOR249c ORF 	NucleicAcid	null mutant	exhibit					G2-M arrest	Process	terminal			NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1219_s_50	9469815	Deletion of this ORF from the  S. cerevisiae genome indicates that YOR249c is essential for viability, and the null mutants exhibit a terminal G2-M arrest phenotype as would be expected for APC genes ( 23).	gene_phenotype
70433	3	333703	11	NULL	NULL	0	NULL	APC gene	GP		exhibit					G2-M arrest	Process	terminal			NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1219_s_50	9469815	Deletion of this ORF from the  S. cerevisiae genome indicates that YOR249c is essential for viability, and the null mutants exhibit a terminal G2-M arrest phenotype as would be expected for APC genes ( 23).	gene_phenotype
70434	1	333705	11	NULL	NULL	0	NULL	 Crn1	GP		is a type of 					actin-bundling protein	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_328	11489916	Ynl094w also interacted with the actin-bundling protein Crn1 ( Goode et al., 1999) and with Sro77, a protein which functions in polarized secretion ( Kagami et al., 1998;  Lehman et al., 1999).	gene_phenotype
70435	2	333705	11	NULL	NULL	0	NULL	Sro77	GP		 functions in					polarized secretion	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_328	11489916	Ynl094w also interacted with the actin-bundling protein Crn1 ( Goode et al., 1999) and with Sro77, a protein which functions in polarized secretion ( Kagami et al., 1998;  Lehman et al., 1999).	gene_phenotype
70436	3	333705	11	NULL	NULL	NULL	NULL	Ynl094w	NucleicAcid		interacts with 					Crn1	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_328	11489916	Ynl094w also interacted with the actin-bundling protein Crn1 ( Goode et al., 1999) and with Sro77, a protein which functions in polarized secretion ( Kagami et al., 1998;  Lehman et al., 1999).	gene_phenotype
70437	4	333705	11	NULL	NULL	0	NULL	Ynl094w	GP		interacts with 					Sro77	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_154_3_549_s_328	11489916	Ynl094w also interacted with the actin-bundling protein Crn1 ( Goode et al., 1999) and with Sro77, a protein which functions in polarized secretion ( Kagami et al., 1998;  Lehman et al., 1999).	gene_phenotype
70438	1	333707	11	NULL	NULL	0	NULL	COS12 gene	GP		derepress					 telomeric silencing	Process				NULL		0	NULL	NULL	NULL	gw60_science_285_5427_591_s_100	10417390	Furthermore, transcription of a number of genes located very near telomeres, including  COS12,  YER188W, and  YAL069W, increased 1.6- to 2.5-fold, consistent with derepression of telomeric silencing.	gene_phenotype
70439	2	333707	11	NULL	NULL	0	NULL	YER188W gene	NucleicAcid		derepress					telomeric silencing	Process				NULL		0	NULL	NULL	NULL	gw60_science_285_5427_591_s_100	10417390	Furthermore, transcription of a number of genes located very near telomeres, including  COS12,  YER188W, and  YAL069W, increased 1.6- to 2.5-fold, consistent with derepression of telomeric silencing.	gene_phenotype
70440	3	333707	11	NULL	NULL	0	NULL	YAL069W gene	NucleicAcid		derepress					telomeric silencing	Process				NULL		0	NULL	NULL	NULL	gw60_science_285_5427_591_s_100	10417390	Furthermore, transcription of a number of genes located very near telomeres, including  COS12,  YER188W, and  YAL069W, increased 1.6- to 2.5-fold, consistent with derepression of telomeric silencing.	gene_phenotype
70441	1	333708	11	NULL	NULL	0	NULL	 YHR076w gene	NucleicAcid		encodes					 type 2C protein phosphatase	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_2_185_s_576	12568102	The  YHR076w gene encodes a type 2C protein phosphatase and represents the seventh PP2C gene in  budding yeast (Letter).	gene_phenotype
70442	2	333708	11	NULL	NULL	0	NULL	YHR076w gene	NucleicAcid		 represents					seventh PP2C gene	GP	budding yeast			NULL		0	NULL	NULL	NULL	gw70_yeast_20_2_185_s_576	12568102	The  YHR076w gene encodes a type 2C protein phosphatase and represents the seventh PP2C gene in  budding yeast (Letter).	gene_phenotype
70443	1	333710	11	NULL	NULL	0	NULL	PGU1	GP		is a type of 					secreted protein	GP				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_306	10657304	Genes encoding secreted proteins ( PGU1 and  PRY2), potential cell-surface proteins ( YLR042c,  YIL117c), proteins involved in glycosylation and chitin biosynthesis ( KTR2,  CHS7, and  GFA1), and a regulatory protein implicated in invasive and filamentous growth ( PHD1) were all induced by Kss1p signaling.	gene_phenotype
70444	2	333710	11	NULL	NULL	0	NULL	 PRY2	GP		is a type of 					secreted proteins	GP				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_306	10657304	Genes encoding secreted proteins ( PGU1 and  PRY2), potential cell-surface proteins ( YLR042c,  YIL117c), proteins involved in glycosylation and chitin biosynthesis ( KTR2,  CHS7, and  GFA1), and a regulatory protein implicated in invasive and filamentous growth ( PHD1) were all induced by Kss1p signaling.	gene_phenotype
70445	3	333710	11	NULL	NULL	0	NULL	YLR042c	NucleicAcid		is a type of 					cell-surface protein	GP				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_306	10657304	Genes encoding secreted proteins ( PGU1 and  PRY2), potential cell-surface proteins ( YLR042c,  YIL117c), proteins involved in glycosylation and chitin biosynthesis ( KTR2,  CHS7, and  GFA1), and a regulatory protein implicated in invasive and filamentous growth ( PHD1) were all induced by Kss1p signaling.	gene_phenotype
70446	4	333710	11	NULL	NULL	0	NULL	YIL117c	NucleicAcid		is a type of 					cell-surface protein	GP				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_306	10657304	Genes encoding secreted proteins ( PGU1 and  PRY2), potential cell-surface proteins ( YLR042c,  YIL117c), proteins involved in glycosylation and chitin biosynthesis ( KTR2,  CHS7, and  GFA1), and a regulatory protein implicated in invasive and filamentous growth ( PHD1) were all induced by Kss1p signaling.	gene_phenotype
70447	5	333710	11	NULL	NULL	0	NULL	chitin	Chemical		undergoes					biosynthesis	Process				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_306	10657304	Genes encoding secreted proteins ( PGU1 and  PRY2), potential cell-surface proteins ( YLR042c,  YIL117c), proteins involved in glycosylation and chitin biosynthesis ( KTR2,  CHS7, and  GFA1), and a regulatory protein implicated in invasive and filamentous growth ( PHD1) were all induced by Kss1p signaling.	gene_phenotype
70448	6	333710	11	NULL	NULL	0	NULL	 KTR2	GP		involved in					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_306	10657304	Genes encoding secreted proteins ( PGU1 and  PRY2), potential cell-surface proteins ( YLR042c,  YIL117c), proteins involved in glycosylation and chitin biosynthesis ( KTR2,  CHS7, and  GFA1), and a regulatory protein implicated in invasive and filamentous growth ( PHD1) were all induced by Kss1p signaling.	gene_phenotype
70449	7	333710	11	NULL	NULL	0	NULL	CHS7	GP		involved in					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_306	10657304	Genes encoding secreted proteins ( PGU1 and  PRY2), potential cell-surface proteins ( YLR042c,  YIL117c), proteins involved in glycosylation and chitin biosynthesis ( KTR2,  CHS7, and  GFA1), and a regulatory protein implicated in invasive and filamentous growth ( PHD1) were all induced by Kss1p signaling.	gene_phenotype
70450	8	333710	11	NULL	NULL	0	NULL	GFA1	GP		involved in					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_306	10657304	Genes encoding secreted proteins ( PGU1 and  PRY2), potential cell-surface proteins ( YLR042c,  YIL117c), proteins involved in glycosylation and chitin biosynthesis ( KTR2,  CHS7, and  GFA1), and a regulatory protein implicated in invasive and filamentous growth ( PHD1) were all induced by Kss1p signaling.	gene_phenotype
70451	9	333710	11	NULL	NULL	0	NULL	PHD1	GP		is a type of 					filamentous growth protien	GP				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_306	10657304	Genes encoding secreted proteins ( PGU1 and  PRY2), potential cell-surface proteins ( YLR042c,  YIL117c), proteins involved in glycosylation and chitin biosynthesis ( KTR2,  CHS7, and  GFA1), and a regulatory protein implicated in invasive and filamentous growth ( PHD1) were all induced by Kss1p signaling.	gene_phenotype
70452	10	333710	11	NULL	NULL	0	NULL	Kss1p	GP	signaling	induced					PGU1	GP				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_306	10657304	Genes encoding secreted proteins ( PGU1 and  PRY2), potential cell-surface proteins ( YLR042c,  YIL117c), proteins involved in glycosylation and chitin biosynthesis ( KTR2,  CHS7, and  GFA1), and a regulatory protein implicated in invasive and filamentous growth ( PHD1) were all induced by Kss1p signaling.	gene_phenotype
70453	11	333710	11	NULL	NULL	0	NULL	Kss1p	GP	signaling	induced					PRY2	GP				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_306	10657304	Genes encoding secreted proteins ( PGU1 and  PRY2), potential cell-surface proteins ( YLR042c,  YIL117c), proteins involved in glycosylation and chitin biosynthesis ( KTR2,  CHS7, and  GFA1), and a regulatory protein implicated in invasive and filamentous growth ( PHD1) were all induced by Kss1p signaling.	gene_phenotype
70454	12	333710	11	NULL	NULL	0	NULL	 Kss1p	GP	signaling	induced					YLR042c	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_306	10657304	Genes encoding secreted proteins ( PGU1 and  PRY2), potential cell-surface proteins ( YLR042c,  YIL117c), proteins involved in glycosylation and chitin biosynthesis ( KTR2,  CHS7, and  GFA1), and a regulatory protein implicated in invasive and filamentous growth ( PHD1) were all induced by Kss1p signaling.	gene_phenotype
70455	13	333710	11	NULL	NULL	0	NULL	Kss1p	GP	signaling	induced					YIL117c	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_306	10657304	Genes encoding secreted proteins ( PGU1 and  PRY2), potential cell-surface proteins ( YLR042c,  YIL117c), proteins involved in glycosylation and chitin biosynthesis ( KTR2,  CHS7, and  GFA1), and a regulatory protein implicated in invasive and filamentous growth ( PHD1) were all induced by Kss1p signaling.	gene_phenotype
70456	14	333710	11	NULL	NULL	0	NULL	Kss1p	GP	signaling	induced					 KTR2	GP				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_306	10657304	Genes encoding secreted proteins ( PGU1 and  PRY2), potential cell-surface proteins ( YLR042c,  YIL117c), proteins involved in glycosylation and chitin biosynthesis ( KTR2,  CHS7, and  GFA1), and a regulatory protein implicated in invasive and filamentous growth ( PHD1) were all induced by Kss1p signaling.	gene_phenotype
70457	15	333710	11	NULL	NULL	0	NULL	Kss1p	GP	signaling	induced					CHS7	GP				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_306	10657304	Genes encoding secreted proteins ( PGU1 and  PRY2), potential cell-surface proteins ( YLR042c,  YIL117c), proteins involved in glycosylation and chitin biosynthesis ( KTR2,  CHS7, and  GFA1), and a regulatory protein implicated in invasive and filamentous growth ( PHD1) were all induced by Kss1p signaling.	gene_phenotype
70458	16	333710	11	NULL	NULL	0	NULL	Kss1p	GP	signaling	induced					GFA1	GP				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_306	10657304	Genes encoding secreted proteins ( PGU1 and  PRY2), potential cell-surface proteins ( YLR042c,  YIL117c), proteins involved in glycosylation and chitin biosynthesis ( KTR2,  CHS7, and  GFA1), and a regulatory protein implicated in invasive and filamentous growth ( PHD1) were all induced by Kss1p signaling.	gene_phenotype
70459	17	333710	11	NULL	NULL	0	NULL	Kss1p	GP	signaling	induced					PHD1	GP				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_306	10657304	Genes encoding secreted proteins ( PGU1 and  PRY2), potential cell-surface proteins ( YLR042c,  YIL117c), proteins involved in glycosylation and chitin biosynthesis ( KTR2,  CHS7, and  GFA1), and a regulatory protein implicated in invasive and filamentous growth ( PHD1) were all induced by Kss1p signaling.	gene_phenotype
70460	1	333713	11	NULL	NULL	0	NULL	YML059c	NucleicAcid		activates					Serine Esterase	GP	OP-sensitive			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_100	15044461	YML059c Has OP-sensitive Serine Esterase Activity and Can Deacylate Exogenous Lysophospholipid -- Sequence similarity between YML059c and NTE (39% identity in the catalytic domain; see  Fig. 2 a and alignments in Ref.  ) strongly suggest that the yeast protein may have serine esterase activity.	gene_phenotype
70461	2	333713	11	NULL	NULL	0	NULL	YML059c	NucleicAcid		Deacylate					Lysophospholipid	Chemical	Exogenous			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_100	15044461	YML059c Has OP-sensitive Serine Esterase Activity and Can Deacylate Exogenous Lysophospholipid -- Sequence similarity between YML059c and NTE (39% identity in the catalytic domain; see  Fig. 2 a and alignments in Ref.  ) strongly suggest that the yeast protein may have serine esterase activity.	gene_phenotype
70462	1	333718	11	NULL	NULL	0	NULL	 transporter protein 	GP		intake					Cho	Chemical	Extracellular			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_17	15044461	Extracellular Cho is taken up into the cell by a transporter protein ( 1) and phosphorylated via choline kinase ( 2);  3, phosphocholine ( PCho) is condenses with CTP in the rate-limiting step for PtdCho synthesis mediated by  CTP-phosphocholine cytidylyltransferase ( CCT);  4, CDP-choline reacts with diacylglycerol catalyzed by choline phosphotransferase;   5, PtdCho can be hydrolyzed by phospholipase D, forming phosphatidic acid and Cho;  the latter can be phosphorylated ( step 2) or secreted ( step 6) from the cell;  7, PtdCho is deacylated at both sn-2 and sn-1 positions to yield GroPCho and two molecules  of free fatty acid; we show here that this deacylation is mediated by NTE in mammalian  cells and by its homologue, YML059c, in yeast.	gene_phenotype
70463	2	333718	11	NULL	NULL	0	NULL	choline kinase	GP		phosphorylates					Cho	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_17	15044461	Extracellular Cho is taken up into the cell by a transporter protein ( 1) and phosphorylated via choline kinase ( 2);  3, phosphocholine ( PCho) is condenses with CTP in the rate-limiting step for PtdCho synthesis mediated by  CTP-phosphocholine cytidylyltransferase ( CCT);  4, CDP-choline reacts with diacylglycerol catalyzed by choline phosphotransferase;   5, PtdCho can be hydrolyzed by phospholipase D, forming phosphatidic acid and Cho;  the latter can be phosphorylated ( step 2) or secreted ( step 6) from the cell;  7, PtdCho is deacylated at both sn-2 and sn-1 positions to yield GroPCho and two molecules  of free fatty acid; we show here that this deacylation is mediated by NTE in mammalian  cells and by its homologue, YML059c, in yeast.	gene_phenotype
70464	3	333718	11	NULL	NULL	0	NULL	CCT	GP		is					CTP-phosphocholine cytidylyltransferase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_17	15044461	Extracellular Cho is taken up into the cell by a transporter protein ( 1) and phosphorylated via choline kinase ( 2);  3, phosphocholine ( PCho) is condenses with CTP in the rate-limiting step for PtdCho synthesis mediated by  CTP-phosphocholine cytidylyltransferase ( CCT);  4, CDP-choline reacts with diacylglycerol catalyzed by choline phosphotransferase;   5, PtdCho can be hydrolyzed by phospholipase D, forming phosphatidic acid and Cho;  the latter can be phosphorylated ( step 2) or secreted ( step 6) from the cell;  7, PtdCho is deacylated at both sn-2 and sn-1 positions to yield GroPCho and two molecules  of free fatty acid; we show here that this deacylation is mediated by NTE in mammalian  cells and by its homologue, YML059c, in yeast.	gene_phenotype
70465	4	333718	11	NULL	NULL	0	NULL	CTP-phosphocholine cytidylyltransferase	GP		synthesises					PtdCho	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_17	15044461	Extracellular Cho is taken up into the cell by a transporter protein ( 1) and phosphorylated via choline kinase ( 2);  3, phosphocholine ( PCho) is condenses with CTP in the rate-limiting step for PtdCho synthesis mediated by  CTP-phosphocholine cytidylyltransferase ( CCT);  4, CDP-choline reacts with diacylglycerol catalyzed by choline phosphotransferase;   5, PtdCho can be hydrolyzed by phospholipase D, forming phosphatidic acid and Cho;  the latter can be phosphorylated ( step 2) or secreted ( step 6) from the cell;  7, PtdCho is deacylated at both sn-2 and sn-1 positions to yield GroPCho and two molecules  of free fatty acid; we show here that this deacylation is mediated by NTE in mammalian  cells and by its homologue, YML059c, in yeast.	gene_phenotype
70466	5	333718	11	NULL	NULL	0	NULL	CDP-choline	Chemical		 reacts with					diacylglycerol	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_17	15044461	Extracellular Cho is taken up into the cell by a transporter protein ( 1) and phosphorylated via choline kinase ( 2);  3, phosphocholine ( PCho) is condenses with CTP in the rate-limiting step for PtdCho synthesis mediated by  CTP-phosphocholine cytidylyltransferase ( CCT);  4, CDP-choline reacts with diacylglycerol catalyzed by choline phosphotransferase;   5, PtdCho can be hydrolyzed by phospholipase D, forming phosphatidic acid and Cho;  the latter can be phosphorylated ( step 2) or secreted ( step 6) from the cell;  7, PtdCho is deacylated at both sn-2 and sn-1 positions to yield GroPCho and two molecules  of free fatty acid; we show here that this deacylation is mediated by NTE in mammalian  cells and by its homologue, YML059c, in yeast.	gene_phenotype
70467	6	333718	11	NULL	NULL	0	NULL	statement 5	Process		catalyzed by					choline phosphotransferase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_17	15044461	Extracellular Cho is taken up into the cell by a transporter protein ( 1) and phosphorylated via choline kinase ( 2);  3, phosphocholine ( PCho) is condenses with CTP in the rate-limiting step for PtdCho synthesis mediated by  CTP-phosphocholine cytidylyltransferase ( CCT);  4, CDP-choline reacts with diacylglycerol catalyzed by choline phosphotransferase;   5, PtdCho can be hydrolyzed by phospholipase D, forming phosphatidic acid and Cho;  the latter can be phosphorylated ( step 2) or secreted ( step 6) from the cell;  7, PtdCho is deacylated at both sn-2 and sn-1 positions to yield GroPCho and two molecules  of free fatty acid; we show here that this deacylation is mediated by NTE in mammalian  cells and by its homologue, YML059c, in yeast.	gene_phenotype
70468	7	333718	11	NULL	NULL	0	NULL	 phospholipase D	GP		hydrolyzes 					PtdCho	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_17	15044461	Extracellular Cho is taken up into the cell by a transporter protein ( 1) and phosphorylated via choline kinase ( 2);  3, phosphocholine ( PCho) is condenses with CTP in the rate-limiting step for PtdCho synthesis mediated by  CTP-phosphocholine cytidylyltransferase ( CCT);  4, CDP-choline reacts with diacylglycerol catalyzed by choline phosphotransferase;   5, PtdCho can be hydrolyzed by phospholipase D, forming phosphatidic acid and Cho;  the latter can be phosphorylated ( step 2) or secreted ( step 6) from the cell;  7, PtdCho is deacylated at both sn-2 and sn-1 positions to yield GroPCho and two molecules  of free fatty acid; we show here that this deacylation is mediated by NTE in mammalian  cells and by its homologue, YML059c, in yeast.	gene_phenotype
70469	8	333718	11	NULL	NULL	0	NULL	statement 7	Process		forms					phosphatidic acid	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_17	15044461	Extracellular Cho is taken up into the cell by a transporter protein ( 1) and phosphorylated via choline kinase ( 2);  3, phosphocholine ( PCho) is condenses with CTP in the rate-limiting step for PtdCho synthesis mediated by  CTP-phosphocholine cytidylyltransferase ( CCT);  4, CDP-choline reacts with diacylglycerol catalyzed by choline phosphotransferase;   5, PtdCho can be hydrolyzed by phospholipase D, forming phosphatidic acid and Cho;  the latter can be phosphorylated ( step 2) or secreted ( step 6) from the cell;  7, PtdCho is deacylated at both sn-2 and sn-1 positions to yield GroPCho and two molecules  of free fatty acid; we show here that this deacylation is mediated by NTE in mammalian  cells and by its homologue, YML059c, in yeast.	gene_phenotype
70470	9	333718	11	NULL	NULL	0	NULL	statement 7	Process		forms					Cho	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_17	15044461	Extracellular Cho is taken up into the cell by a transporter protein ( 1) and phosphorylated via choline kinase ( 2);  3, phosphocholine ( PCho) is condenses with CTP in the rate-limiting step for PtdCho synthesis mediated by  CTP-phosphocholine cytidylyltransferase ( CCT);  4, CDP-choline reacts with diacylglycerol catalyzed by choline phosphotransferase;   5, PtdCho can be hydrolyzed by phospholipase D, forming phosphatidic acid and Cho;  the latter can be phosphorylated ( step 2) or secreted ( step 6) from the cell;  7, PtdCho is deacylated at both sn-2 and sn-1 positions to yield GroPCho and two molecules  of free fatty acid; we show here that this deacylation is mediated by NTE in mammalian  cells and by its homologue, YML059c, in yeast.	gene_phenotype
70471	10	333718	11	NULL	NULL	0	NULL	statement 8	Process		occurs along with					statement 9	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_17	15044461	Extracellular Cho is taken up into the cell by a transporter protein ( 1) and phosphorylated via choline kinase ( 2);  3, phosphocholine ( PCho) is condenses with CTP in the rate-limiting step for PtdCho synthesis mediated by  CTP-phosphocholine cytidylyltransferase ( CCT);  4, CDP-choline reacts with diacylglycerol catalyzed by choline phosphotransferase;   5, PtdCho can be hydrolyzed by phospholipase D, forming phosphatidic acid and Cho;  the latter can be phosphorylated ( step 2) or secreted ( step 6) from the cell;  7, PtdCho is deacylated at both sn-2 and sn-1 positions to yield GroPCho and two molecules  of free fatty acid; we show here that this deacylation is mediated by NTE in mammalian  cells and by its homologue, YML059c, in yeast.	gene_phenotype
70472	11	333718	11	NULL	NULL	0	NULL	Cho	Chemical		undergoes					phosphorylation	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_17	15044461	Extracellular Cho is taken up into the cell by a transporter protein ( 1) and phosphorylated via choline kinase ( 2);  3, phosphocholine ( PCho) is condenses with CTP in the rate-limiting step for PtdCho synthesis mediated by  CTP-phosphocholine cytidylyltransferase ( CCT);  4, CDP-choline reacts with diacylglycerol catalyzed by choline phosphotransferase;   5, PtdCho can be hydrolyzed by phospholipase D, forming phosphatidic acid and Cho;  the latter can be phosphorylated ( step 2) or secreted ( step 6) from the cell;  7, PtdCho is deacylated at both sn-2 and sn-1 positions to yield GroPCho and two molecules  of free fatty acid; we show here that this deacylation is mediated by NTE in mammalian  cells and by its homologue, YML059c, in yeast.	gene_phenotype
70473	12	333718	11	NULL	NULL	0	NULL	Cho	Chemical		undergoes					Secretion 	Process	 from the cell			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_17	15044461	Extracellular Cho is taken up into the cell by a transporter protein ( 1) and phosphorylated via choline kinase ( 2);  3, phosphocholine ( PCho) is condenses with CTP in the rate-limiting step for PtdCho synthesis mediated by  CTP-phosphocholine cytidylyltransferase ( CCT);  4, CDP-choline reacts with diacylglycerol catalyzed by choline phosphotransferase;   5, PtdCho can be hydrolyzed by phospholipase D, forming phosphatidic acid and Cho;  the latter can be phosphorylated ( step 2) or secreted ( step 6) from the cell;  7, PtdCho is deacylated at both sn-2 and sn-1 positions to yield GroPCho and two molecules  of free fatty acid; we show here that this deacylation is mediated by NTE in mammalian  cells and by its homologue, YML059c, in yeast.	gene_phenotype
70474	13	333718	11	NULL	NULL	0	NULL	PtdCho	Chemical		undergoes					deacylation	Process	at sn-2 and sn-1 positions			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_17	15044461	Extracellular Cho is taken up into the cell by a transporter protein ( 1) and phosphorylated via choline kinase ( 2);  3, phosphocholine ( PCho) is condenses with CTP in the rate-limiting step for PtdCho synthesis mediated by  CTP-phosphocholine cytidylyltransferase ( CCT);  4, CDP-choline reacts with diacylglycerol catalyzed by choline phosphotransferase;   5, PtdCho can be hydrolyzed by phospholipase D, forming phosphatidic acid and Cho;  the latter can be phosphorylated ( step 2) or secreted ( step 6) from the cell;  7, PtdCho is deacylated at both sn-2 and sn-1 positions to yield GroPCho and two molecules  of free fatty acid; we show here that this deacylation is mediated by NTE in mammalian  cells and by its homologue, YML059c, in yeast.	gene_phenotype
70475	14	333718	11	NULL	NULL	0	NULL	statement 13	Process		 yield					GroPCho	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_17	15044461	Extracellular Cho is taken up into the cell by a transporter protein ( 1) and phosphorylated via choline kinase ( 2);  3, phosphocholine ( PCho) is condenses with CTP in the rate-limiting step for PtdCho synthesis mediated by  CTP-phosphocholine cytidylyltransferase ( CCT);  4, CDP-choline reacts with diacylglycerol catalyzed by choline phosphotransferase;   5, PtdCho can be hydrolyzed by phospholipase D, forming phosphatidic acid and Cho;  the latter can be phosphorylated ( step 2) or secreted ( step 6) from the cell;  7, PtdCho is deacylated at both sn-2 and sn-1 positions to yield GroPCho and two molecules  of free fatty acid; we show here that this deacylation is mediated by NTE in mammalian  cells and by its homologue, YML059c, in yeast.	gene_phenotype
70476	15	333718	11	NULL	NULL	0	NULL	statement 13	Process		 yield					free fatty acid	Chemical	two molecules			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_17	15044461	Extracellular Cho is taken up into the cell by a transporter protein ( 1) and phosphorylated via choline kinase ( 2);  3, phosphocholine ( PCho) is condenses with CTP in the rate-limiting step for PtdCho synthesis mediated by  CTP-phosphocholine cytidylyltransferase ( CCT);  4, CDP-choline reacts with diacylglycerol catalyzed by choline phosphotransferase;   5, PtdCho can be hydrolyzed by phospholipase D, forming phosphatidic acid and Cho;  the latter can be phosphorylated ( step 2) or secreted ( step 6) from the cell;  7, PtdCho is deacylated at both sn-2 and sn-1 positions to yield GroPCho and two molecules  of free fatty acid; we show here that this deacylation is mediated by NTE in mammalian  cells and by its homologue, YML059c, in yeast.	gene_phenotype
70477	16	333718	11	NULL	NULL	0	NULL	statement 14	Process		occurs along with					statement 15	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_17	15044461	Extracellular Cho is taken up into the cell by a transporter protein ( 1) and phosphorylated via choline kinase ( 2);  3, phosphocholine ( PCho) is condenses with CTP in the rate-limiting step for PtdCho synthesis mediated by  CTP-phosphocholine cytidylyltransferase ( CCT);  4, CDP-choline reacts with diacylglycerol catalyzed by choline phosphotransferase;   5, PtdCho can be hydrolyzed by phospholipase D, forming phosphatidic acid and Cho;  the latter can be phosphorylated ( step 2) or secreted ( step 6) from the cell;  7, PtdCho is deacylated at both sn-2 and sn-1 positions to yield GroPCho and two molecules  of free fatty acid; we show here that this deacylation is mediated by NTE in mammalian  cells and by its homologue, YML059c, in yeast.	gene_phenotype
70478	17	333718	11	NULL	NULL	0	NULL	NTE	GP	mammalian cells	mediate					statement 13	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_17	15044461	Extracellular Cho is taken up into the cell by a transporter protein ( 1) and phosphorylated via choline kinase ( 2);  3, phosphocholine ( PCho) is condenses with CTP in the rate-limiting step for PtdCho synthesis mediated by  CTP-phosphocholine cytidylyltransferase ( CCT);  4, CDP-choline reacts with diacylglycerol catalyzed by choline phosphotransferase;   5, PtdCho can be hydrolyzed by phospholipase D, forming phosphatidic acid and Cho;  the latter can be phosphorylated ( step 2) or secreted ( step 6) from the cell;  7, PtdCho is deacylated at both sn-2 and sn-1 positions to yield GroPCho and two molecules  of free fatty acid; we show here that this deacylation is mediated by NTE in mammalian  cells and by its homologue, YML059c, in yeast.	gene_phenotype
70479	18	333718	11	NULL	NULL	0	NULL	YML059c	NucleicAcid	yeast	mediate					statement 13	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_17	15044461	Extracellular Cho is taken up into the cell by a transporter protein ( 1) and phosphorylated via choline kinase ( 2);  3, phosphocholine ( PCho) is condenses with CTP in the rate-limiting step for PtdCho synthesis mediated by  CTP-phosphocholine cytidylyltransferase ( CCT);  4, CDP-choline reacts with diacylglycerol catalyzed by choline phosphotransferase;   5, PtdCho can be hydrolyzed by phospholipase D, forming phosphatidic acid and Cho;  the latter can be phosphorylated ( step 2) or secreted ( step 6) from the cell;  7, PtdCho is deacylated at both sn-2 and sn-1 positions to yield GroPCho and two molecules  of free fatty acid; we show here that this deacylation is mediated by NTE in mammalian  cells and by its homologue, YML059c, in yeast.	gene_phenotype
70480	19	333718	11	NULL	NULL	0	NULL	YML059c	NucleicAcid	yeast	is a  homologue of					NTE	GP	mammalian cell			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_23_24024_s_17	15044461	Extracellular Cho is taken up into the cell by a transporter protein ( 1) and phosphorylated via choline kinase ( 2);  3, phosphocholine ( PCho) is condenses with CTP in the rate-limiting step for PtdCho synthesis mediated by  CTP-phosphocholine cytidylyltransferase ( CCT);  4, CDP-choline reacts with diacylglycerol catalyzed by choline phosphotransferase;   5, PtdCho can be hydrolyzed by phospholipase D, forming phosphatidic acid and Cho;  the latter can be phosphorylated ( step 2) or secreted ( step 6) from the cell;  7, PtdCho is deacylated at both sn-2 and sn-1 positions to yield GroPCho and two molecules  of free fatty acid; we show here that this deacylation is mediated by NTE in mammalian  cells and by its homologue, YML059c, in yeast.	gene_phenotype
71874	1	333725	11	NULL	NULL	NULL	NULL	Sac1p-like protein	GP	Budding yeast	 regulate		possibly			PI(3)P levels	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_16_8910_s_150	10900271	Budding yeast express several Sac1p-like proteins, as well as a PTEN-like phosphatase (YNL128w), which are also thought to play a role in regulating PI(3)P levels ( 36,  37).	gene_phenotype
71875	2	333725	11	NULL	NULL	0	NULL	PTEN-like phosphatase	GP	Budding yeast	regulate		possibly			PI(3)P levels	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_97_16_8910_s_150	10900271	Budding yeast express several Sac1p-like proteins, as well as a PTEN-like phosphatase (YNL128w), which are also thought to play a role in regulating PI(3)P levels ( 36,  37).	gene_phenotype
71876	3	333725	11	NULL	NULL	0	NULL	YNL128w	NucleicAcid		is a synonym of					PTEN-like phosphatase	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_16_8910_s_150	10900271	Budding yeast express several Sac1p-like proteins, as well as a PTEN-like phosphatase (YNL128w), which are also thought to play a role in regulating PI(3)P levels ( 36,  37).	gene_phenotype
69705	1	333726	5	NULL	NULL	0	NULL	YNL128w	NucleicAcid		plays a role in		may			sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_70_0_247_s_329	11395408	A single report has demonstrated that YNL128w is one of  158 genes whose expression is induced from 2 to 5 hours after transfer to sporulation  medium during the completion of meiotic prophase, which suggests it may play a role  in sporulation ( 107).	gene_phenotype
69710	1	333728	5	NULL	NULL	0	NULL	YLR109W	NucleicAcid		activates					tert-butyl hydroperoxide 2	Chemical	defense against			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22480_s_220	9712873	YLR109W displays defense activity against  tert-butyl hydroperoxide 2 and represents a subclass of the AhpC/TSA protein family localized in the peroxisome.	gene_phenotype
69711	2	333728	5	NULL	NULL	0	NULL	AhpC/TSA protein family	GP		is localized in					peroxisome	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22480_s_220	9712873	YLR109W displays defense activity against  tert-butyl hydroperoxide 2 and represents a subclass of the AhpC/TSA protein family localized in the peroxisome.	gene_phenotype
69714	3	333728	5	NULL	NULL	0	NULL	YLR109W	NucleicAcid		represent					AhpC/TSA protein family	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_35_22480_s_220	9712873	YLR109W displays defense activity against  tert-butyl hydroperoxide 2 and represents a subclass of the AhpC/TSA protein family localized in the peroxisome.	gene_phenotype
69716	1	333730	5	NULL	NULL	0	NULL	YOL095c protein	GP		is located in					mitochondria	CellComponent	yeast			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_5_1816_s_23	10669756	The YOL095c protein is located in yeast mitochondria, and is required for wild-type (wt) [ rho+] mitochondrial genome maintenance.	gene_phenotype
69717	2	333730	5	NULL	NULL	0	NULL	YOL095c protein	GP		is required for					genome maintenance	Process	wild-type;;[ rho+] mitochondria			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_5_1816_s_23	10669756	The YOL095c protein is located in yeast mitochondria, and is required for wild-type (wt) [ rho+] mitochondrial genome maintenance.	gene_phenotype
69725	1	333733	5	NULL	NULL	0	NULL	YIL113w disruptant strain	Organism		responds to		normally			mating pheromone	Chemical				NULL		0	NULL	NULL	NULL	gw60_febslett_527_1_186_s_190	12220658	This conclusion is supported by our own findings in which a  YIL113w disruptant strain exhibited a normal response to mating pheromone, indicating that Yil113p is not involved in regulating the Fus3p MAPK (M.C., unpublished observations) and by the results of a study in which disruption of  YIL113w alone or in combination with  PTP2 and/or  MSG5 was found to have no effect on phosphorylation of the Hog1p MAPK, indicating that Yil113p is not involved in regulating the response to osmotic stress in  S. cerevisiae [ 7.	gene_phenotype
69726	2	333733	5	NULL	NULL	0	NULL	Yil113p	NucleicAcid		does not regulate					Fus3p	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_527_1_186_s_190	12220658	This conclusion is supported by our own findings in which a  YIL113w disruptant strain exhibited a normal response to mating pheromone, indicating that Yil113p is not involved in regulating the Fus3p MAPK (M.C., unpublished observations) and by the results of a study in which disruption of  YIL113w alone or in combination with  PTP2 and/or  MSG5 was found to have no effect on phosphorylation of the Hog1p MAPK, indicating that Yil113p is not involved in regulating the response to osmotic stress in  S. cerevisiae [ 7.	gene_phenotype
69727	3	333733	5	NULL	NULL	0	NULL	Fus3p	GP		is a type of					MAPK	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_527_1_186_s_190	12220658	This conclusion is supported by our own findings in which a  YIL113w disruptant strain exhibited a normal response to mating pheromone, indicating that Yil113p is not involved in regulating the Fus3p MAPK (M.C., unpublished observations) and by the results of a study in which disruption of  YIL113w alone or in combination with  PTP2 and/or  MSG5 was found to have no effect on phosphorylation of the Hog1p MAPK, indicating that Yil113p is not involved in regulating the response to osmotic stress in  S. cerevisiae [ 7.	gene_phenotype
69729	4	333733	5	NULL	NULL	0	NULL	YIL113w	NucleicAcid	disruption of	does not effect					Hog1p	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_febslett_527_1_186_s_190	12220658	This conclusion is supported by our own findings in which a  YIL113w disruptant strain exhibited a normal response to mating pheromone, indicating that Yil113p is not involved in regulating the Fus3p MAPK (M.C., unpublished observations) and by the results of a study in which disruption of  YIL113w alone or in combination with  PTP2 and/or  MSG5 was found to have no effect on phosphorylation of the Hog1p MAPK, indicating that Yil113p is not involved in regulating the response to osmotic stress in  S. cerevisiae [ 7.	gene_phenotype
69730	5	333733	5	NULL	NULL	0	NULL	Hog1p	GP		is a type of					MAPK	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_527_1_186_s_190	12220658	This conclusion is supported by our own findings in which a  YIL113w disruptant strain exhibited a normal response to mating pheromone, indicating that Yil113p is not involved in regulating the Fus3p MAPK (M.C., unpublished observations) and by the results of a study in which disruption of  YIL113w alone or in combination with  PTP2 and/or  MSG5 was found to have no effect on phosphorylation of the Hog1p MAPK, indicating that Yil113p is not involved in regulating the response to osmotic stress in  S. cerevisiae [ 7.	gene_phenotype
69731	6	333733	5	NULL	NULL	NULL	NULL	Yil113p	NucleicAcid		does not regulate					osmotic stress	PhysicalPhenomenon	response to			NULL	S. cerevisiae	NULL	NULL	NULL	NULL	gw60_febslett_527_1_186_s_190	12220658	This conclusion is supported by our own findings in which a  YIL113w disruptant strain exhibited a normal response to mating pheromone, indicating that Yil113p is not involved in regulating the Fus3p MAPK (M.C., unpublished observations) and by the results of a study in which disruption of  YIL113w alone or in combination with  PTP2 and/or  MSG5 was found to have no effect on phosphorylation of the Hog1p MAPK, indicating that Yil113p is not involved in regulating the response to osmotic stress in  S. cerevisiae [ 7.	gene_phenotype
69734	1	333734	5	NULL	NULL	0	NULL	YKL174c	NucleicAcid		encodes					TPO5 protein	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_13_12637_s_96	15668236	Inhibition of putrescine and spermidine uptake activity by TPO5 protein encoded by  YKL174c.	gene_phenotype
69735	2	333734	5	NULL	NULL	0	NULL	TPO5 protein	GP		inhibits					putrescine	Chemical	uptake of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_13_12637_s_96	15668236	Inhibition of putrescine and spermidine uptake activity by TPO5 protein encoded by  YKL174c.	gene_phenotype
69737	3	333734	5	NULL	NULL	0	NULL	TPO5 protein	GP		inhibits					spermidine	Chemical	uptake of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_13_12637_s_96	15668236	Inhibition of putrescine and spermidine uptake activity by TPO5 protein encoded by  YKL174c.	gene_phenotype
69739	1	333735	5	NULL	NULL	0	NULL	YKL174c	NucleicAcid		encodes					TPO5 protein	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_13_12637_s_111	15668236	Effect of amino acids on putrescine excretion activity by TPO5 protein encoded by  YKL174c.	gene_phenotype
69740	2	333735	5	NULL	NULL	0	NULL	TPO5 protein	GP		activates					putrescine	Chemical	excretion of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_13_12637_s_111	15668236	Effect of amino acids on putrescine excretion activity by TPO5 protein encoded by  YKL174c.	gene_phenotype
69741	3	333735	5	NULL	NULL	0	NULL	amino acids	AminoAcid		effects		possibly			statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_13_12637_s_111	15668236	Effect of amino acids on putrescine excretion activity by TPO5 protein encoded by  YKL174c.	gene_phenotype
69742	1	333736	5	NULL	NULL	0	NULL	YKL174c protein	GP		is homologous to		highly			UGA4	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_13_12637_s_76	15668236	Among these proteins, there is one, termed YKL174c, whose function is unknown but which is highly homologous with UGA4, a gamma-aminobutyric acid and putrescine transport protein on the vacuolar membrane ( ).	gene_phenotype
69744	2	333736	5	NULL	NULL	0	NULL	UGA4	GP		is present in					vacuolar membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_13_12637_s_76	15668236	Among these proteins, there is one, termed YKL174c, whose function is unknown but which is highly homologous with UGA4, a gamma-aminobutyric acid and putrescine transport protein on the vacuolar membrane ( ).	gene_phenotype
69745	3	333736	5	NULL	NULL	0	NULL	UGA4	GP		is a type of					gamma-aminobutyric acid and putrescine transport protein	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_13_12637_s_76	15668236	Among these proteins, there is one, termed YKL174c, whose function is unknown but which is highly homologous with UGA4, a gamma-aminobutyric acid and putrescine transport protein on the vacuolar membrane ( ).	gene_phenotype
69747	1	333737	5	NULL	NULL	0	NULL	YKL174c gene	GP		is homologous to		highly			UGA4	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_13_12637_s_203	15668236	We studied the function of a protein encoded by an unidentified gene  YKL174c, which has high homology with UGA4, a member of the family of amino acid-polyamine-organocation transporters in  S. cerevisiae.	gene_phenotype
69748	2	333737	5	NULL	NULL	NULL	NULL	UGA4	GP		is a member of					amino acid-polyamine-organocation transporters family	GP				NULL	S. cerevisiae	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_13_12637_s_203	15668236	We studied the function of a protein encoded by an unidentified gene  YKL174c, which has high homology with UGA4, a member of the family of amino acid-polyamine-organocation transporters in  S. cerevisiae.	gene_phenotype
69749	1	333739	5	NULL	NULL	0	NULL	ydl117w cells	Cell		is defective in					cytokinesis	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_361	14587103	However,   ydl117w cells not only show defects in cytokinesis but also exhibit an aberrant mother-bud  neck phenotype, which often appears as a large, bent or misshapen cell (Korinek  et al., [ 2000]).	gene_phenotype
69750	2	333739	5	NULL	NULL	0	NULL	ydl117w cells	Cell		exhibit					mother-bud neck phenotype	PhysicalPhenomenon	aberrant			NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_361	14587103	However,   ydl117w cells not only show defects in cytokinesis but also exhibit an aberrant mother-bud  neck phenotype, which often appears as a large, bent or misshapen cell (Korinek  et al., [ 2000]).	gene_phenotype
69751	3	333739	5	NULL	NULL	0	NULL	mother-bud neck phenotype	PhysicalPhenomenon	aberrant	appears as					large cell	Cell				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_361	14587103	However,   ydl117w cells not only show defects in cytokinesis but also exhibit an aberrant mother-bud  neck phenotype, which often appears as a large, bent or misshapen cell (Korinek  et al., [ 2000]).	gene_phenotype
69752	4	333739	5	NULL	NULL	0	NULL	mother-bud neck phenotype	PhysicalPhenomenon	aberrant	appears as					bent cell	Cell				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_361	14587103	However,   ydl117w cells not only show defects in cytokinesis but also exhibit an aberrant mother-bud  neck phenotype, which often appears as a large, bent or misshapen cell (Korinek  et al., [ 2000]).	gene_phenotype
69753	5	333739	5	NULL	NULL	0	NULL	mother-bud neck phenotype	PhysicalPhenomenon	aberrant	appears as					misshapen cell	Cell				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_361	14587103	However,   ydl117w cells not only show defects in cytokinesis but also exhibit an aberrant mother-bud  neck phenotype, which often appears as a large, bent or misshapen cell (Korinek  et al., [ 2000]).	gene_phenotype
69754	6	333739	5	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_361	14587103	However,   ydl117w cells not only show defects in cytokinesis but also exhibit an aberrant mother-bud  neck phenotype, which often appears as a large, bent or misshapen cell (Korinek  et al., [ 2000]).	gene_phenotype
69755	7	333739	5	NULL	NULL	0	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_14_1189_s_361	14587103	However,   ydl117w cells not only show defects in cytokinesis but also exhibit an aberrant mother-bud  neck phenotype, which often appears as a large, bent or misshapen cell (Korinek  et al., [ 2000]).	gene_phenotype
69756	1	333740	5	NULL	NULL	0	NULL	Ydl117w	NucleicAcid		is the locus name of					Cyk3	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_139	16498703	Ydl117w  Cyk3  1 SH3-domain protein located in the mother-bud neck and the cytokinetic actin ring;  mutant phenotype and genetic interactions suggest a role in cytokinesis  LIP  [ 20]	gene_phenotype
69757	2	333740	5	NULL	NULL	0	NULL	Cyk3	GP		is a type of					SH3-domain protein	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_139	16498703	Ydl117w  Cyk3  1 SH3-domain protein located in the mother-bud neck and the cytokinetic actin ring;  mutant phenotype and genetic interactions suggest a role in cytokinesis  LIP  [ 20]	gene_phenotype
69758	3	333740	5	NULL	NULL	0	NULL	Cyk3	GP		is located in					mother-bud neck	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_139	16498703	Ydl117w  Cyk3  1 SH3-domain protein located in the mother-bud neck and the cytokinetic actin ring;  mutant phenotype and genetic interactions suggest a role in cytokinesis  LIP  [ 20]	gene_phenotype
69759	4	333740	5	NULL	NULL	0	NULL	Cyk3	GP		is located in					cytokinetic actin ring	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_139	16498703	Ydl117w  Cyk3  1 SH3-domain protein located in the mother-bud neck and the cytokinetic actin ring;  mutant phenotype and genetic interactions suggest a role in cytokinesis  LIP  [ 20]	gene_phenotype
69760	5	333740	5	NULL	NULL	0	NULL	Cyk3	GP		plays a role in					cytokinesis	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_3_159_s_139	16498703	Ydl117w  Cyk3  1 SH3-domain protein located in the mother-bud neck and the cytokinetic actin ring;  mutant phenotype and genetic interactions suggest a role in cytokinesis  LIP  [ 20]	gene_phenotype
69761	1	333744	5	NULL	NULL	0	NULL	GST - Pus7	GP		is a type of					fusion protein	GP				NULL		0	NULL	NULL	NULL	gw60_embo_22_8_1889_s_76	12682021	Pseudouridylase activity of the GST - Pus7 (YOR243c) fusion protein expressed in either  S.cerevisiae (lanes 1 - 4) or  E.coli (lanes 5 - 8) was assayed  in vitro and compared.	gene_phenotype
69764	2	333744	5	NULL	NULL	0	NULL	YOR243c	NucleicAcid		is the locus name of					Pus7	GP				NULL		0	NULL	NULL	NULL	gw60_embo_22_8_1889_s_76	12682021	Pseudouridylase activity of the GST - Pus7 (YOR243c) fusion protein expressed in either  S.cerevisiae (lanes 1 - 4) or  E.coli (lanes 5 - 8) was assayed  in vitro and compared.	gene_phenotype
69765	3	333744	5	NULL	NULL	NULL	NULL	GST - Pus7	GP		activates					pseudouridylase	GP				NULL	S.cerevisiae, in vitro	NULL	NULL	NULL	NULL	gw60_embo_22_8_1889_s_76	12682021	Pseudouridylase activity of the GST - Pus7 (YOR243c) fusion protein expressed in either  S.cerevisiae (lanes 1 - 4) or  E.coli (lanes 5 - 8) was assayed  in vitro and compared.	gene_phenotype
69766	4	333744	5	NULL	NULL	NULL	NULL	GST - Pus7	GP		activates					pseudouridylase	GP				NULL	E.coli, in vitro	NULL	NULL	NULL	NULL	gw60_embo_22_8_1889_s_76	12682021	Pseudouridylase activity of the GST - Pus7 (YOR243c) fusion protein expressed in either  S.cerevisiae (lanes 1 - 4) or  E.coli (lanes 5 - 8) was assayed  in vitro and compared.	gene_phenotype
69769	1	333745	5	NULL	NULL	0	NULL	psi35	GP		is formed in					U2	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_embo_22_8_1889_s_7	12682021	When the GST YOR243c protein is expressed  in  Escherichia coli, pseudouridylation activity is comparable to that expressed in  S.cerevisiae, demonstrating that this protein (designated Pus7) alone can catalyze psi35 formation in U2.	gene_phenotype
69770	2	333745	5	NULL	NULL	0	NULL	Pus7 protein	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_embo_22_8_1889_s_7	12682021	When the GST YOR243c protein is expressed  in  Escherichia coli, pseudouridylation activity is comparable to that expressed in  S.cerevisiae, demonstrating that this protein (designated Pus7) alone can catalyze psi35 formation in U2.	gene_phenotype
69771	1	333746	5	NULL	NULL	0	NULL	YOR243c protein	GP		catalyzes					U2 snRNA	NucleicAcid	yeast;;pseudouridylation		position 35	NULL		0	NULL	NULL	NULL	gw70_embo_22_8_1889_s_72	12682021	These results clearly demonstrate that YOR243c encodes a protein that catalyzes  yeast U2 snRNA pseudouridylation at position 35, and demonstrate further that the  activity occurs in a guide RNA-independent manner.	gene_phenotype
69772	2	333746	5	NULL	NULL	0	NULL	statement 1	Process		is dependent on					guide RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_embo_22_8_1889_s_72	12682021	These results clearly demonstrate that YOR243c encodes a protein that catalyzes  yeast U2 snRNA pseudouridylation at position 35, and demonstrate further that the  activity occurs in a guide RNA-independent manner.	gene_phenotype
69773	1	333747	5	NULL	NULL	0	NULL	YOR243c	NucleicAcid		is the locus name of					Pus7	GP				NULL		0	NULL	NULL	NULL	gw70_embo_22_8_1889_s_74	12682021	Figure 3  seudouridylase activity of the GST Pus7 (YOR243c) fusion protein expressed in either   S.cerevisiae (lanes 1 4) or  E.coli (lanes 5 8) was assayed  in vitro and compared.	gene_phenotype
69774	2	333747	5	NULL	NULL	NULL	NULL	GST - Pus7	GP		activates					pseudouridylase	GP				NULL	S.cerevisiae, in vitro	NULL	NULL	NULL	NULL	gw70_embo_22_8_1889_s_74	12682021	Figure 3  seudouridylase activity of the GST Pus7 (YOR243c) fusion protein expressed in either   S.cerevisiae (lanes 1 4) or  E.coli (lanes 5 8) was assayed  in vitro and compared.	gene_phenotype
69775	3	333747	5	NULL	NULL	0	NULL	GST - Pus7	GP		activates					pseudouridylase	GP				NULL	E.coli, in vitro	0	NULL	NULL	NULL	gw70_embo_22_8_1889_s_74	12682021	Figure 3  seudouridylase activity of the GST Pus7 (YOR243c) fusion protein expressed in either   S.cerevisiae (lanes 1 4) or  E.coli (lanes 5 8) was assayed  in vitro and compared.	gene_phenotype
69776	4	333747	5	NULL	NULL	0	NULL	GST Pus7	GP		is a type of					fusion protein	GP				NULL		0	NULL	NULL	NULL	gw70_embo_22_8_1889_s_74	12682021	Figure 3  seudouridylase activity of the GST Pus7 (YOR243c) fusion protein expressed in either   S.cerevisiae (lanes 1 4) or  E.coli (lanes 5 8) was assayed  in vitro and compared.	gene_phenotype
69861	1	333748	5	NULL	NULL	0	NULL	YOR243c protein	GP		catalyzes					U2 snRNA	NucleicAcid	yeast;;pseudouridylation of		position 35	NULL		0	NULL	NULL	NULL	gw60_embo_22_8_1889_s_73	12682021	These results clearly demonstrate that YOR243c encodes a protein that catalyzes yeast U2 snRNA pseudouridylation at position 35, and demonstrate further that the activity occurs in a guide RNA-independent manner.	gene_phenotype
69862	2	333748	5	NULL	NULL	0	NULL	statement 1	Process		is dependent on					guide RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_embo_22_8_1889_s_73	12682021	These results clearly demonstrate that YOR243c encodes a protein that catalyzes yeast U2 snRNA pseudouridylation at position 35, and demonstrate further that the activity occurs in a guide RNA-independent manner.	gene_phenotype
69863	1	333750	5	NULL	NULL	0	NULL	Ygr223c	NucleicAcid		has no function in		obvious			Cvt pathway	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_36_37741_s_127	15194695	Ygr223c has no obvious function in the Cvt pathway and autophagy.	gene_phenotype
69864	2	333750	5	NULL	NULL	0	NULL	Ygr223c	NucleicAcid		has no function in		obvious			autophagy	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_36_37741_s_127	15194695	Ygr223c has no obvious function in the Cvt pathway and autophagy.	gene_phenotype
69865	1	333752	5	NULL	NULL	0	NULL	Atg18	GP		is required for					autophagy	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3553_s_314	15155809	Atg18 is required for all types of autophagy, whereas a strong phenotype has not yet been found for Ygr223c.	gene_phenotype
69866	2	333752	5	NULL	NULL	0	NULL	Ygr223c	NucleicAcid		does not show					phenotype	PhysicalPhenomenon	strong			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3553_s_314	15155809	Atg18 is required for all types of autophagy, whereas a strong phenotype has not yet been found for Ygr223c.	gene_phenotype
69867	1	333753	5	NULL	NULL	NULL	NULL	Atg18 protein	GP	yeast	is homologous to					Atg21 protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_36_37741_s_122	15194695	The Homologous Proteins Atg18 and Atg21 Play Distinct Roles in Autophagy and the Cvt Pathway -- Atg21 has two yeast homologues, Atg18 ( 20% identity) and the protein of so far unknown function, Ygr223c ( 14% identity).	gene_phenotype
69868	2	333753	5	NULL	NULL	0	NULL	Atg18 protein	GP		plays a role in		distinct			autophagy	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_36_37741_s_122	15194695	The Homologous Proteins Atg18 and Atg21 Play Distinct Roles in Autophagy and the Cvt Pathway -- Atg21 has two yeast homologues, Atg18 ( 20% identity) and the protein of so far unknown function, Ygr223c ( 14% identity).	gene_phenotype
69869	3	333753	5	NULL	NULL	0	NULL	Atg18 protein	GP		plays a role in		distinct			Cvt Pathway	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_36_37741_s_122	15194695	The Homologous Proteins Atg18 and Atg21 Play Distinct Roles in Autophagy and the Cvt Pathway -- Atg21 has two yeast homologues, Atg18 ( 20% identity) and the protein of so far unknown function, Ygr223c ( 14% identity).	gene_phenotype
69870	4	333753	5	NULL	NULL	0	NULL	Atg21 protein	GP		plays a role in		distinct			autophagy	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_36_37741_s_122	15194695	The Homologous Proteins Atg18 and Atg21 Play Distinct Roles in Autophagy and the Cvt Pathway -- Atg21 has two yeast homologues, Atg18 ( 20% identity) and the protein of so far unknown function, Ygr223c ( 14% identity).	gene_phenotype
69871	5	333753	5	NULL	NULL	0	NULL	Atg21 protein	GP		plays a role in		distinct			Cvt Pathway	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_36_37741_s_122	15194695	The Homologous Proteins Atg18 and Atg21 Play Distinct Roles in Autophagy and the Cvt Pathway -- Atg21 has two yeast homologues, Atg18 ( 20% identity) and the protein of so far unknown function, Ygr223c ( 14% identity).	gene_phenotype
69872	6	333753	5	NULL	NULL	0	NULL	Atg21 protein	GP		is homologous to					Ygr223c protein	GP	yeast			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_36_37741_s_122	15194695	The Homologous Proteins Atg18 and Atg21 Play Distinct Roles in Autophagy and the Cvt Pathway -- Atg21 has two yeast homologues, Atg18 ( 20% identity) and the protein of so far unknown function, Ygr223c ( 14% identity).	gene_phenotype
69873	1	333754	5	NULL	NULL	0	NULL	Atg21	GP		is homologous to					Atg21 protein	GP	yeast			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_36_37741_s_345	15194695	Atg21 is a very promising candidate for studies aiming to learn more about the mechanistic features and differences of autophagy and the Cvt pathway, since it shares homologies with two further yeast proteins, Atg18 and Ygr223c.	gene_phenotype
69874	2	333754	5	NULL	NULL	0	NULL	Atg21	GP		is homologous to					Ygr223c protein	GP	yeast			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_36_37741_s_345	15194695	Atg21 is a very promising candidate for studies aiming to learn more about the mechanistic features and differences of autophagy and the Cvt pathway, since it shares homologies with two further yeast proteins, Atg18 and Ygr223c.	gene_phenotype
69875	3	333754	5	NULL	NULL	0	NULL	Atg21	GP		plays a role in		possibly			autophagy	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_36_37741_s_345	15194695	Atg21 is a very promising candidate for studies aiming to learn more about the mechanistic features and differences of autophagy and the Cvt pathway, since it shares homologies with two further yeast proteins, Atg18 and Ygr223c.	gene_phenotype
69876	4	333754	5	NULL	NULL	0	NULL	Atg21	GP		plays a role in		possibly			Cvt pathway	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_36_37741_s_345	15194695	Atg21 is a very promising candidate for studies aiming to learn more about the mechanistic features and differences of autophagy and the Cvt pathway, since it shares homologies with two further yeast proteins, Atg18 and Ygr223c.	gene_phenotype
69877	1	333755	5	NULL	NULL	0	NULL	Ygr223c	NucleicAcid		has no function in		obvious			Cvt pathway	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_36_37741_s_346	15194695	As shown here, Ygr223c has no obvious function in the Cvt pathway or autophagy ( Fig. 1 A), whereas Atg18 has been shown to function in both biogenesis of autophagosomes and Cvt vesicles ( ,  ).	gene_phenotype
69878	2	333755	5	NULL	NULL	0	NULL	Ygr223c	NucleicAcid		has no function in		obvious			autophagy	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_36_37741_s_346	15194695	As shown here, Ygr223c has no obvious function in the Cvt pathway or autophagy ( Fig. 1 A), whereas Atg18 has been shown to function in both biogenesis of autophagosomes and Cvt vesicles ( ,  ).	gene_phenotype
69879	3	333755	5	NULL	NULL	0	NULL	Atg18	GP		functions in					autophagosomes	CellComponent	biogenesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_36_37741_s_346	15194695	As shown here, Ygr223c has no obvious function in the Cvt pathway or autophagy ( Fig. 1 A), whereas Atg18 has been shown to function in both biogenesis of autophagosomes and Cvt vesicles ( ,  ).	gene_phenotype
69880	4	333755	5	NULL	NULL	0	NULL	Atg18	GP		functions in					Cvt vesicles	CellComponent	biogenesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_36_37741_s_346	15194695	As shown here, Ygr223c has no obvious function in the Cvt pathway or autophagy ( Fig. 1 A), whereas Atg18 has been shown to function in both biogenesis of autophagosomes and Cvt vesicles ( ,  ).	gene_phenotype
69881	1	333756	5	NULL	NULL	NULL	NULL	Atg8	GP		is localized to		efficiently			PAS	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_8_3553_s_196	15155809	Atg21 Is Required for Efficient Localization of Atg8 to the PAS   As mentioned above, no Cvt pathway- or autophagy-specific proteins were found to be required for the localization of Atg21, and the Atg18, Atg21, and Ygr223c proteins were not dependent on each other for localization (our unpublished data).	gene_phenotype
69882	2	333756	5	NULL	NULL	0	NULL	Atg21	GP		is required for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3553_s_196	15155809	Atg21 Is Required for Efficient Localization of Atg8 to the PAS   As mentioned above, no Cvt pathway- or autophagy-specific proteins were found to be required for the localization of Atg21, and the Atg18, Atg21, and Ygr223c proteins were not dependent on each other for localization (our unpublished data).	gene_phenotype
69883	3	333756	5	NULL	NULL	0	NULL	Cvt pathway proteins	GP		is not required for					Atg21	GP	localization of			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3553_s_196	15155809	Atg21 Is Required for Efficient Localization of Atg8 to the PAS   As mentioned above, no Cvt pathway- or autophagy-specific proteins were found to be required for the localization of Atg21, and the Atg18, Atg21, and Ygr223c proteins were not dependent on each other for localization (our unpublished data).	gene_phenotype
69884	4	333756	5	NULL	NULL	0	NULL	autophagy-specific proteins	GP		is not required for					Atg21	GP	localization of			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3553_s_196	15155809	Atg21 Is Required for Efficient Localization of Atg8 to the PAS   As mentioned above, no Cvt pathway- or autophagy-specific proteins were found to be required for the localization of Atg21, and the Atg18, Atg21, and Ygr223c proteins were not dependent on each other for localization (our unpublished data).	gene_phenotype
69885	5	333756	5	NULL	NULL	0	NULL	Atg18 protein	GP	localization of	is not dependent on					Atg21 protein	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3553_s_196	15155809	Atg21 Is Required for Efficient Localization of Atg8 to the PAS   As mentioned above, no Cvt pathway- or autophagy-specific proteins were found to be required for the localization of Atg21, and the Atg18, Atg21, and Ygr223c proteins were not dependent on each other for localization (our unpublished data).	gene_phenotype
69886	6	333756	5	NULL	NULL	0	NULL	Atg21 protein	GP	localization of	is not dependent on					Ygr223c protein	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3553_s_196	15155809	Atg21 Is Required for Efficient Localization of Atg8 to the PAS   As mentioned above, no Cvt pathway- or autophagy-specific proteins were found to be required for the localization of Atg21, and the Atg18, Atg21, and Ygr223c proteins were not dependent on each other for localization (our unpublished data).	gene_phenotype
69887	7	333756	5	NULL	NULL	0	NULL	Atg21 protein	GP	localization of	is not dependent on					Ygr223c protein	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3553_s_196	15155809	Atg21 Is Required for Efficient Localization of Atg8 to the PAS   As mentioned above, no Cvt pathway- or autophagy-specific proteins were found to be required for the localization of Atg21, and the Atg18, Atg21, and Ygr223c proteins were not dependent on each other for localization (our unpublished data).	gene_phenotype
69888	8	333756	5	NULL	NULL	0	NULL	Atg21 protein	GP	localization of	is not dependent on					Atg18 protein	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3553_s_196	15155809	Atg21 Is Required for Efficient Localization of Atg8 to the PAS   As mentioned above, no Cvt pathway- or autophagy-specific proteins were found to be required for the localization of Atg21, and the Atg18, Atg21, and Ygr223c proteins were not dependent on each other for localization (our unpublished data).	gene_phenotype
69889	9	333756	5	NULL	NULL	0	NULL	Ygr223c protein	GP	localization of	is not dependent on					Atg21 protein	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3553_s_196	15155809	Atg21 Is Required for Efficient Localization of Atg8 to the PAS   As mentioned above, no Cvt pathway- or autophagy-specific proteins were found to be required for the localization of Atg21, and the Atg18, Atg21, and Ygr223c proteins were not dependent on each other for localization (our unpublished data).	gene_phenotype
69890	10	333756	5	NULL	NULL	0	NULL	Ygr223c protein	GP	localization of	is not dependent on					Atg18 protein	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_8_3553_s_196	15155809	Atg21 Is Required for Efficient Localization of Atg8 to the PAS   As mentioned above, no Cvt pathway- or autophagy-specific proteins were found to be required for the localization of Atg21, and the Atg18, Atg21, and Ygr223c proteins were not dependent on each other for localization (our unpublished data).	gene_phenotype
69891	1	333759	5	NULL	NULL	0	NULL	Af1521	GP		is homologous to			macro domain		YBR022W gene product	GP	yeast			NULL		0	NULL	NULL	NULL	gw70_embo_24_11_1911_s_48	15902274	A screen in the yeast  Saccharomyces cerevisiae identified a protein with homology to the  macro domain of Af1521, the YBR022W gene product, as exhibiting ADP-ribose-1"`-phosphate  (Appr-1"`-P) processing activity (  et al).	gene_phenotype
69892	2	333759	5	NULL	NULL	0	NULL	YBR022W gene product	GP		activates					ADP-ribose-1"`-phosphate (Appr-1"`-P)	Chemical	processing of			NULL		0	NULL	NULL	NULL	gw70_embo_24_11_1911_s_48	15902274	A screen in the yeast  Saccharomyces cerevisiae identified a protein with homology to the  macro domain of Af1521, the YBR022W gene product, as exhibiting ADP-ribose-1"`-phosphate  (Appr-1"`-P) processing activity (  et al).	gene_phenotype
69903	1	333762	5	NULL	NULL	0	NULL	YGR173w	NucleicAcid		plays a role in		potentially			purine salvage	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_7_553_s_408	16710832	For YGR173w, weak evidence was found for the present annotation  purine salvage, tRNA modification and ribonucleoside monophosphate biosynthesis pathways  and GeneFAS annotated similar terms (cell growth and/or maintenance, metabolism,  cell organization and biogenesis nucleobase, nucleoside, nucleotide and nucleic acid  metabolism, cytoplasm organization and biogenesis, transport, ribosome biogenesis  and assembly, transcription, RNA metabolism biosynthesis transcription, DNA-dependent  ribosome biogenesis, RNA processing, organic acid metabolism, carbohydrate metabolism,  aromatic compound metabolism, heterocycle metabolism, ion transport, catabolism).	gene_phenotype
69904	2	333762	5	NULL	NULL	0	NULL	YGR173w	NucleicAcid		plays a role in		potentially			tRNA	NucleicAcid	modification of			NULL		0	NULL	NULL	NULL	gw70_yeast_23_7_553_s_408	16710832	For YGR173w, weak evidence was found for the present annotation  purine salvage, tRNA modification and ribonucleoside monophosphate biosynthesis pathways  and GeneFAS annotated similar terms (cell growth and/or maintenance, metabolism,  cell organization and biogenesis nucleobase, nucleoside, nucleotide and nucleic acid  metabolism, cytoplasm organization and biogenesis, transport, ribosome biogenesis  and assembly, transcription, RNA metabolism biosynthesis transcription, DNA-dependent  ribosome biogenesis, RNA processing, organic acid metabolism, carbohydrate metabolism,  aromatic compound metabolism, heterocycle metabolism, ion transport, catabolism).	gene_phenotype
69905	3	333762	5	NULL	NULL	0	NULL	YGR173w	NucleicAcid		plays a role in		potentially			ribonucleoside monophosphate biosynthesis pathways	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_7_553_s_408	16710832	For YGR173w, weak evidence was found for the present annotation  purine salvage, tRNA modification and ribonucleoside monophosphate biosynthesis pathways  and GeneFAS annotated similar terms (cell growth and/or maintenance, metabolism,  cell organization and biogenesis nucleobase, nucleoside, nucleotide and nucleic acid  metabolism, cytoplasm organization and biogenesis, transport, ribosome biogenesis  and assembly, transcription, RNA metabolism biosynthesis transcription, DNA-dependent  ribosome biogenesis, RNA processing, organic acid metabolism, carbohydrate metabolism,  aromatic compound metabolism, heterocycle metabolism, ion transport, catabolism).	gene_phenotype
69908	1	333763	5	NULL	NULL	0	NULL	YPR016c	NucleicAcid		is required for					viability	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11653_s_136	10206977	None of the viable segregants were TRP+, indicating that  YPR016c is required for viability.	gene_phenotype
69909	1	333764	5	NULL	NULL	NULL	NULL	YPR016c gene product 	GP	yeast	is a synonym of					eIF6	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_17_11653_s_25	10206977	Furthermore, expression of either  YPR016c-GFP or murine eIF6-GFP fusion proteins restored viability, suggesting that the  YPR016c gene product is indeed yeast eIF6.	gene_phenotype
69910	2	333764	5	NULL	NULL	0	NULL	YPR016c-GFP	GP	expression of	restores					viability	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11653_s_25	10206977	Furthermore, expression of either  YPR016c-GFP or murine eIF6-GFP fusion proteins restored viability, suggesting that the  YPR016c gene product is indeed yeast eIF6.	gene_phenotype
69911	3	333764	5	NULL	NULL	0	NULL	eIF6-GFP	GP	murine;;expression of	restores					viability	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11653_s_25	10206977	Furthermore, expression of either  YPR016c-GFP or murine eIF6-GFP fusion proteins restored viability, suggesting that the  YPR016c gene product is indeed yeast eIF6.	gene_phenotype
69912	4	333764	5	NULL	NULL	0	NULL	eIF6-GFP	GP		is a type of					fusion protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11653_s_25	10206977	Furthermore, expression of either  YPR016c-GFP or murine eIF6-GFP fusion proteins restored viability, suggesting that the  YPR016c gene product is indeed yeast eIF6.	gene_phenotype
69913	5	333764	5	NULL	NULL	0	NULL	YPR016c-GFP	GP		is a type of					fusion protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11653_s_25	10206977	Furthermore, expression of either  YPR016c-GFP or murine eIF6-GFP fusion proteins restored viability, suggesting that the  YPR016c gene product is indeed yeast eIF6.	gene_phenotype
69915	1	333766	5	NULL	NULL	0	NULL	YPR016c-GFP	GP		substitute for					YPR016c protein product	GP	endogenous			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11653_s_140	10206977	Tetrad analysis of LWY1 harboring pLW-2 produced four viable segregants (two TRP+ segregants and two TRP  segregants), indicating that the  YPR016c-GFP fusion protein was functional and could substitute for the endogenous  YPR016c protein product.	gene_phenotype
69916	2	333766	5	NULL	NULL	0	NULL	YPR016c-GFP	GP		is a type of					fusion protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11653_s_140	10206977	Tetrad analysis of LWY1 harboring pLW-2 produced four viable segregants (two TRP+ segregants and two TRP  segregants), indicating that the  YPR016c-GFP fusion protein was functional and could substitute for the endogenous  YPR016c protein product.	gene_phenotype
69918	1	333767	5	NULL	NULL	0	NULL	YPR016c	GP	presence of	restores					viability	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11653_s_7	10206977	Viability was restored in the presence of either  YPR016c or murine eIF6, when either was expressed as amino-terminal green fluorescent protein fusion protein.	gene_phenotype
69920	2	333767	5	NULL	NULL	0	NULL	eIF6	GP	presence of;;murine	restores					viability	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11653_s_7	10206977	Viability was restored in the presence of either  YPR016c or murine eIF6, when either was expressed as amino-terminal green fluorescent protein fusion protein.	gene_phenotype
69922	3	333767	5	NULL	NULL	0	NULL	eIF6	GP	murine	is expressed as			amino-terminal		green fluorescent protein fusion protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11653_s_7	10206977	Viability was restored in the presence of either  YPR016c or murine eIF6, when either was expressed as amino-terminal green fluorescent protein fusion protein.	gene_phenotype
69923	4	333767	5	NULL	NULL	0	NULL	YPR016c	GP		is expressed as			amino-terminal		green fluorescent protein fusion protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11653_s_7	10206977	Viability was restored in the presence of either  YPR016c or murine eIF6, when either was expressed as amino-terminal green fluorescent protein fusion protein.	gene_phenotype
69924	1	333768	5	NULL	NULL	NULL	NULL	eIF6	GP		is homologous to					TIF6	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_5_1453_s_15	11238882	Detailed characterization of the yeast gene encoding eIF6, designated  TIF6, showed that  TIF6 is a single-copy gene that maps on chromosome XVI (as YPR016C) and is essential for cell growth and viability.	gene_phenotype
69926	2	333768	5	NULL	NULL	NULL	NULL	TIF6	GP	yeast	is a type of					single-copy gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_5_1453_s_15	11238882	Detailed characterization of the yeast gene encoding eIF6, designated  TIF6, showed that  TIF6 is a single-copy gene that maps on chromosome XVI (as YPR016C) and is essential for cell growth and viability.	gene_phenotype
69927	3	333768	5	NULL	NULL	NULL	NULL	TIF6 gene	GP	yeast	maps to					chromosome XVI	Chromosome				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_5_1453_s_15	11238882	Detailed characterization of the yeast gene encoding eIF6, designated  TIF6, showed that  TIF6 is a single-copy gene that maps on chromosome XVI (as YPR016C) and is essential for cell growth and viability.	gene_phenotype
69929	4	333768	5	NULL	NULL	NULL	NULL	YPR016C	NucleicAcid		is the locus name of					TIF6	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_5_1453_s_15	11238882	Detailed characterization of the yeast gene encoding eIF6, designated  TIF6, showed that  TIF6 is a single-copy gene that maps on chromosome XVI (as YPR016C) and is essential for cell growth and viability.	gene_phenotype
69930	5	333768	5	NULL	NULL	NULL	NULL	TIF6	GP	yeast	is essential for					cell growth	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_5_1453_s_15	11238882	Detailed characterization of the yeast gene encoding eIF6, designated  TIF6, showed that  TIF6 is a single-copy gene that maps on chromosome XVI (as YPR016C) and is essential for cell growth and viability.	gene_phenotype
69931	6	333768	5	NULL	NULL	0	NULL	TIF6	GP	yeast	is essential for					cell viability	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_5_1453_s_15	11238882	Detailed characterization of the yeast gene encoding eIF6, designated  TIF6, showed that  TIF6 is a single-copy gene that maps on chromosome XVI (as YPR016C) and is essential for cell growth and viability.	gene_phenotype
69933	1	333769	5	NULL	NULL	0	NULL	YPR016c-GFP	GP		is a type of					fusion protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11653_s_147	10206977	This result demonstrated that the cells were dependent upon  GAL1-regulated expression of either the  YPR016c-GFP (in LWY4) or the murine eIF6-GFP (in LWY6) fusion proteins for viability.	gene_phenotype
69934	2	333769	5	NULL	NULL	0	NULL	eIF6-GFP	GP	murine	is a type of					fusion protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11653_s_147	10206977	This result demonstrated that the cells were dependent upon  GAL1-regulated expression of either the  YPR016c-GFP (in LWY4) or the murine eIF6-GFP (in LWY6) fusion proteins for viability.	gene_phenotype
69935	3	333769	5	NULL	NULL	0	NULL	YPR016c-GFP	GP		plays a role in					cell viability	Process				NULL	LWY4	0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11653_s_147	10206977	This result demonstrated that the cells were dependent upon  GAL1-regulated expression of either the  YPR016c-GFP (in LWY4) or the murine eIF6-GFP (in LWY6) fusion proteins for viability.	gene_phenotype
69936	4	333769	5	NULL	NULL	NULL	NULL	eIF6-GFP	GP	murine	plays a role in					cell viability	Process				NULL	LWY6	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_17_11653_s_147	10206977	This result demonstrated that the cells were dependent upon  GAL1-regulated expression of either the  YPR016c-GFP (in LWY4) or the murine eIF6-GFP (in LWY6) fusion proteins for viability.	gene_phenotype
69937	1	333771	5	NULL	NULL	0	NULL	eIF6-GFP	GP	overexpression of	does not effect		major			cell growth	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11653_s_143	10206977	As shown in Fig.  3 ( left side), the growth rates of LWY4 (harboring  GAL1- YPR016c-GFP) and LWY6 (harboring  GAL1-murine eIF6-GFP)  versus control appeared somewhat slower on SGal, indicating that overexpression of the eIF6-GFP fusion proteins had no major effects on cell growth.	gene_phenotype
69938	2	333771	5	NULL	NULL	0	NULL	eIF6-GFP	GP		is a type of					fusion protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11653_s_143	10206977	As shown in Fig.  3 ( left side), the growth rates of LWY4 (harboring  GAL1- YPR016c-GFP) and LWY6 (harboring  GAL1-murine eIF6-GFP)  versus control appeared somewhat slower on SGal, indicating that overexpression of the eIF6-GFP fusion proteins had no major effects on cell growth.	gene_phenotype
69939	1	333773	5	NULL	NULL	0	NULL	autophagy mutants	GP		is sensitive to					nitrogen	Chemical				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_69_0_303_s_259	10966461	In addition,  cvt3 does not display the degree of nitrogen sensitivity typical of autophagy mutants  ( 16).	gene_phenotype
69940	2	333773	5	NULL	NULL	NULL	NULL	cvt3	GP		is sensitive to					nitrogen	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_69_0_303_s_259	10966461	In addition,  cvt3 does not display the degree of nitrogen sensitivity typical of autophagy mutants  ( 16).	gene_phenotype
69941	3	333773	5	NULL	NULL	0	NULL	statement 2	Process	degree of	lesser than					statement 1	Process	degree of			NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_69_0_303_s_259	10966461	In addition,  cvt3 does not display the degree of nitrogen sensitivity typical of autophagy mutants  ( 16).	gene_phenotype
69942	1	333774	5	NULL	NULL	0	NULL	cvt9	GP	mutant	is required for					Cvt	GP	trafficking of			NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_3_463_s_235	11528006	The  cvt9 mutant and the as yet uncharacterized  cvt3 mutant are the two original mutations that were identified as being required for Cvt trafficking but not for autophagy ( ).	gene_phenotype
69943	2	333774	5	NULL	NULL	0	NULL	cvt3	GP	mutant	is required for					Cvt	GP	trafficking of			NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_3_463_s_235	11528006	The  cvt9 mutant and the as yet uncharacterized  cvt3 mutant are the two original mutations that were identified as being required for Cvt trafficking but not for autophagy ( ).	gene_phenotype
69944	3	333774	5	NULL	NULL	0	NULL	cvt9	GP	mutant	is not required for					autophagy	Process				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_3_463_s_235	11528006	The  cvt9 mutant and the as yet uncharacterized  cvt3 mutant are the two original mutations that were identified as being required for Cvt trafficking but not for autophagy ( ).	gene_phenotype
69945	4	333774	5	NULL	NULL	0	NULL	cvt3	GP	mutant	is not required for					autophagy	Process				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_65_3_463_s_235	11528006	The  cvt9 mutant and the as yet uncharacterized  cvt3 mutant are the two original mutations that were identified as being required for Cvt trafficking but not for autophagy ( ).	gene_phenotype
69946	1	333775	5	NULL	NULL	0	NULL	cvt3	GP	mutant	induce					autophagy	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_7_1687_s_177	9412464	Induction of autophagy may be  slower in the  cvt3 mutant compared to wild-type, and the  resulting autophagosomes appear to be slightly aberrant.	gene_phenotype
69947	2	333775	5	NULL	NULL	0	NULL	Cvt	GP	wild-type	induce					autophagy	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_7_1687_s_177	9412464	Induction of autophagy may be  slower in the  cvt3 mutant compared to wild-type, and the  resulting autophagosomes appear to be slightly aberrant.	gene_phenotype
69948	3	333775	5	NULL	NULL	0	NULL	statement 1	Process		slower than					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_7_1687_s_177	9412464	Induction of autophagy may be  slower in the  cvt3 mutant compared to wild-type, and the  resulting autophagosomes appear to be slightly aberrant.	gene_phenotype
69949	4	333775	5	NULL	NULL	0	NULL	statement 1	Process		leads to					autophagosomes	CellComponent	formation of;;aberrent			NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_7_1687_s_177	9412464	Induction of autophagy may be  slower in the  cvt3 mutant compared to wild-type, and the  resulting autophagosomes appear to be slightly aberrant.	gene_phenotype
70031	1	333776	5	NULL	NULL	0	NULL	cvt3	GP		is sensitive to					nitrogen	Chemical				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_69_0_303_s_212	10966461	In addition,   cvt3  does not display the degree of nitrogen sensitivity typical of  autophagy mutants ( 16).	gene_phenotype
70032	1	333777	5	NULL	NULL	0	NULL	Aut7p	GP		is stabilized in					cvt3 strain	Cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_8_5845_s_209	10681575	Further, Aut7p was also observed to be stabilized in the  cvt3 strain under vegetative growth conditions (data not shown).	gene_phenotype
70033	2	333777	5	NULL	NULL	0	NULL	statement 1	Process		under condition of					vegetative growth	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_8_5845_s_209	10681575	Further, Aut7p was also observed to be stabilized in the  cvt3 strain under vegetative growth conditions (data not shown).	gene_phenotype
70034	1	333778	5	NULL	NULL	0	NULL	cvt3	GP	mutant	is defective in					Cvt pathway	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_8_5845_s_220	10681575	The  cvt3 mutant is defective in the Cvt pathway but displays an essentially normal phenotype for autophagy ( 9,  10).	gene_phenotype
70035	2	333778	5	NULL	NULL	0	NULL	cvt3	GP	mutant	displays					autophagy	Process	normal phenotype for			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_8_5845_s_220	10681575	The  cvt3 mutant is defective in the Cvt pathway but displays an essentially normal phenotype for autophagy ( 9,  10).	gene_phenotype
70036	1	333779	5	NULL	NULL	0	NULL	cvt3	GP		is defective in					autophagy	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17621_s_93	8663607	Three groups,  cvt3,  6, and  9, appeared less defective in autophagy than the  aut mutants using this test.	gene_phenotype
70037	2	333779	5	NULL	NULL	0	NULL	cvt6	GP		is defective in					autophagy	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17621_s_93	8663607	Three groups,  cvt3,  6, and  9, appeared less defective in autophagy than the  aut mutants using this test.	gene_phenotype
70038	3	333779	5	NULL	NULL	0	NULL	cvt9	GP		is defective in					autophagy	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17621_s_93	8663607	Three groups,  cvt3,  6, and  9, appeared less defective in autophagy than the  aut mutants using this test.	gene_phenotype
70039	4	333779	5	NULL	NULL	0	NULL	aut	GP	mutant	is defective in					autophagy	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17621_s_93	8663607	Three groups,  cvt3,  6, and  9, appeared less defective in autophagy than the  aut mutants using this test.	gene_phenotype
70040	5	333779	5	NULL	NULL	0	NULL	statement 1	Process		lesser than					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17621_s_93	8663607	Three groups,  cvt3,  6, and  9, appeared less defective in autophagy than the  aut mutants using this test.	gene_phenotype
70041	6	333779	5	NULL	NULL	0	NULL	statement 2	Process		lesser than					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17621_s_93	8663607	Three groups,  cvt3,  6, and  9, appeared less defective in autophagy than the  aut mutants using this test.	gene_phenotype
70042	7	333779	5	NULL	NULL	0	NULL	statement 3	Process		lesser than					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_30_17621_s_93	8663607	Three groups,  cvt3,  6, and  9, appeared less defective in autophagy than the  aut mutants using this test.	gene_phenotype
70043	1	333782	5	NULL	NULL	0	NULL	cvt3	GP	mutant	is defective in					Cvt pathway	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_7_1687_s_182	9412464	The finding that  the  cvt3 mutant is defective for the Cvt pathway but not  autophagy provides independent support for the idea that  two separate but related pathways are responsible for targeting API to the vacuole.	gene_phenotype
70044	2	333782	5	NULL	NULL	0	NULL	cvt3	GP	mutant	is not defective in					autophagy	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_7_1687_s_182	9412464	The finding that  the  cvt3 mutant is defective for the Cvt pathway but not  autophagy provides independent support for the idea that  two separate but related pathways are responsible for targeting API to the vacuole.	gene_phenotype
70045	3	333782	5	NULL	NULL	0	NULL	API	GP		targeted to					vacuole	CellComponent				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_7_1687_s_182	9412464	The finding that  the  cvt3 mutant is defective for the Cvt pathway but not  autophagy provides independent support for the idea that  two separate but related pathways are responsible for targeting API to the vacuole.	gene_phenotype
70046	1	333784	5	NULL	NULL	0	NULL	CVT3 gene product	GP		is essential for					Cvt pathway	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_7_1687_s_178	9412464	These results support our biochemical analysis and suggest  that the  CVT3 gene encodes a molecule that is essential  for the Cvt pathway but not for autophagy; under starvation conditions, API can be transported by autophagy,  even though the Cvt pathway is defective.	gene_phenotype
70047	2	333784	5	NULL	NULL	0	NULL	CVT3 gene product	GP		is not essential for					autophagy	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_7_1687_s_178	9412464	These results support our biochemical analysis and suggest  that the  CVT3 gene encodes a molecule that is essential  for the Cvt pathway but not for autophagy; under starvation conditions, API can be transported by autophagy,  even though the Cvt pathway is defective.	gene_phenotype
70048	3	333784	5	NULL	NULL	0	NULL	API	GP		is transfered by					autophagy	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_7_1687_s_178	9412464	These results support our biochemical analysis and suggest  that the  CVT3 gene encodes a molecule that is essential  for the Cvt pathway but not for autophagy; under starvation conditions, API can be transported by autophagy,  even though the Cvt pathway is defective.	gene_phenotype
70049	4	333784	5	NULL	NULL	NULL	NULL	statement 3	Process		under condition of					starvation	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_139_7_1687_s_178	9412464	These results support our biochemical analysis and suggest  that the  CVT3 gene encodes a molecule that is essential  for the Cvt pathway but not for autophagy; under starvation conditions, API can be transported by autophagy,  even though the Cvt pathway is defective.	gene_phenotype
70050	5	333784	5	NULL	NULL	0	NULL	statement 3	Process		in the presence of					Cvt pathway	Process	defective			NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_7_1687_s_178	9412464	These results support our biochemical analysis and suggest  that the  CVT3 gene encodes a molecule that is essential  for the Cvt pathway but not for autophagy; under starvation conditions, API can be transported by autophagy,  even though the Cvt pathway is defective.	gene_phenotype
70082	1	333785	5	NULL	NULL	0	NULL	API	GP		is transported		completely			cvt3	Cell				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_7_1687_s_180	9412464	In addition, the observation that the transport of API approaches completion  in  cvt3 under starvation conditions suggests that a selective  autophagic mechanism is used; nonselective transport of  cytosolic protein such as Pho8delta60p by autophagy appears  to plateau at ~30% import (Scott et al., 1996  ).	gene_phenotype
70083	2	333785	5	NULL	NULL	0	NULL	statement 1	Process		under condition of					starvation	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_7_1687_s_180	9412464	In addition, the observation that the transport of API approaches completion  in  cvt3 under starvation conditions suggests that a selective  autophagic mechanism is used; nonselective transport of  cytosolic protein such as Pho8delta60p by autophagy appears  to plateau at ~30% import (Scott et al., 1996  ).	gene_phenotype
70084	3	333785	5	NULL	NULL	0	NULL	statement 1	Process		involves					autophagic mechanism	Process	selective			NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_7_1687_s_180	9412464	In addition, the observation that the transport of API approaches completion  in  cvt3 under starvation conditions suggests that a selective  autophagic mechanism is used; nonselective transport of  cytosolic protein such as Pho8delta60p by autophagy appears  to plateau at ~30% import (Scott et al., 1996  ).	gene_phenotype
70085	4	333785	5	NULL	NULL	0	NULL	Pho8delta60p	GP	nonselective;;transport of	occurs by					autophagy	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_7_1687_s_180	9412464	In addition, the observation that the transport of API approaches completion  in  cvt3 under starvation conditions suggests that a selective  autophagic mechanism is used; nonselective transport of  cytosolic protein such as Pho8delta60p by autophagy appears  to plateau at ~30% import (Scott et al., 1996  ).	gene_phenotype
70086	5	333785	5	NULL	NULL	0	NULL	Pho8delta60p	GP		is a type of					cytosolic protein	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_139_7_1687_s_180	9412464	In addition, the observation that the transport of API approaches completion  in  cvt3 under starvation conditions suggests that a selective  autophagic mechanism is used; nonselective transport of  cytosolic protein such as Pho8delta60p by autophagy appears  to plateau at ~30% import (Scott et al., 1996  ).	gene_phenotype
70087	1	333787	5	NULL	NULL	0	NULL	galactolipid	Chemical	defeciency	impede					node of Ranvier	CellComponent	maintenance of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_156_3_567_s_135	11827985	Galactolipid and MAG deficiencies impede node of Ranvier maintanence, not formation   The dramatic consequences of galactolipid and MAG elimination on nodal regions were observed around the life expectancy endpoint for this mutant line.	gene_phenotype
70088	2	333787	5	NULL	NULL	0	NULL	MAG	Chemical	defeciency	impede					node of Ranvier	CellComponent	maintenance of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_156_3_567_s_135	11827985	Galactolipid and MAG deficiencies impede node of Ranvier maintanence, not formation   The dramatic consequences of galactolipid and MAG elimination on nodal regions were observed around the life expectancy endpoint for this mutant line.	gene_phenotype
70089	3	333787	5	NULL	NULL	0	NULL	galactolipid	Chemical	defeciency	does not impede					node of Ranvier	CellComponent	formation of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_156_3_567_s_135	11827985	Galactolipid and MAG deficiencies impede node of Ranvier maintanence, not formation   The dramatic consequences of galactolipid and MAG elimination on nodal regions were observed around the life expectancy endpoint for this mutant line.	gene_phenotype
70090	4	333787	5	NULL	NULL	0	NULL	MAG	Chemical	defeciency	does not impede					node of Ranvier	CellComponent	formation of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_156_3_567_s_135	11827985	Galactolipid and MAG deficiencies impede node of Ranvier maintanence, not formation   The dramatic consequences of galactolipid and MAG elimination on nodal regions were observed around the life expectancy endpoint for this mutant line.	gene_phenotype
70092	1	333788	5	NULL	NULL	0	NULL	Ylr022cp	NucleicAcid		is required for					G1 cell cycle	Process	progression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_19_19221_s_174	15701631	Ylr022cp is required for G1 cell cycle progression.	gene_phenotype
70093	1	333790	5	NULL	NULL	0	NULL	Ylr022cp	NucleicAcid		is required for					G1 Cell Cycle	Process	progression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_19_19221_s_194	15701631	Ylr022cp Is Required for G1 Cell Cycle Progression --	gene_phenotype
70094	1	333791	5	NULL	NULL	0	NULL	YLR022C gene	GP		is essential for					cell viability	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_19_19213_s_154	15701634	Strains lacking the  YLR022C gene are not viable, indicating it is an essential gene, whereas strains lacking  YHR087W are viable ( ).	gene_phenotype
70095	2	333791	5	NULL	NULL	0	NULL	YHR087W gene	NucleicAcid		is not essential for					cell viability	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_19_19213_s_154	15701634	Strains lacking the  YLR022C gene are not viable, indicating it is an essential gene, whereas strains lacking  YHR087W are viable ( ).	gene_phenotype
70096	1	333792	5	NULL	NULL	0	NULL	YLR022C	NucleicAcid		is an orthologue of					SBDS	GP	Saccharomyces cerevisiae			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_19_19221_s_19	15701631	Haploid spores deleted for the  Saccharomyces cerevisiae SBDS orthologue  YLR022C were reported to be inviable ( ).	gene_phenotype
70097	2	333792	5	NULL	NULL	0	NULL	YLR022C	NucleicAcid		is required for					haploid spores	Cell	viability of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_19_19221_s_19	15701631	Haploid spores deleted for the  Saccharomyces cerevisiae SBDS orthologue  YLR022C were reported to be inviable ( ).	gene_phenotype
70098	1	333795	5	NULL	NULL	0	NULL	AGP2	GP		is a type of					transport protein	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_9	10545096	In addition to the previously reported carnitine acetyl-CoA transferase ( CAT2), we identified the genes for the yeast orthologue of the human mitochondrial carnitine acylcarnitine translocase ( YOR100C or  CAC) and for a transport protein ( AGP2) required for carnitine transport across the plasma membrane.	gene_phenotype
70099	2	333795	5	NULL	NULL	0	NULL	carnitine	Chemical		is transported across					plasma membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_9	10545096	In addition to the previously reported carnitine acetyl-CoA transferase ( CAT2), we identified the genes for the yeast orthologue of the human mitochondrial carnitine acylcarnitine translocase ( YOR100C or  CAC) and for a transport protein ( AGP2) required for carnitine transport across the plasma membrane.	gene_phenotype
70100	3	333795	5	NULL	NULL	0	NULL	AGP2	GP		is required for					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_9	10545096	In addition to the previously reported carnitine acetyl-CoA transferase ( CAT2), we identified the genes for the yeast orthologue of the human mitochondrial carnitine acylcarnitine translocase ( YOR100C or  CAC) and for a transport protein ( AGP2) required for carnitine transport across the plasma membrane.	gene_phenotype
70101	4	333795	5	NULL	NULL	0	NULL	CAC	GP	yeast	is an orthologue of					mitochondrial carnitine acylcarnitine translocase	GP	human			NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_9	10545096	In addition to the previously reported carnitine acetyl-CoA transferase ( CAT2), we identified the genes for the yeast orthologue of the human mitochondrial carnitine acylcarnitine translocase ( YOR100C or  CAC) and for a transport protein ( AGP2) required for carnitine transport across the plasma membrane.	gene_phenotype
70102	5	333795	5	NULL	NULL	0	NULL	CAT2	GP		is					carnitine acetyl-CoA transferase	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_9	10545096	In addition to the previously reported carnitine acetyl-CoA transferase ( CAT2), we identified the genes for the yeast orthologue of the human mitochondrial carnitine acylcarnitine translocase ( YOR100C or  CAC) and for a transport protein ( AGP2) required for carnitine transport across the plasma membrane.	gene_phenotype
70103	6	333795	5	NULL	NULL	0	NULL	YOR100C	NucleicAcid		is the locus name of					CAC	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_9	10545096	In addition to the previously reported carnitine acetyl-CoA transferase ( CAT2), we identified the genes for the yeast orthologue of the human mitochondrial carnitine acylcarnitine translocase ( YOR100C or  CAC) and for a transport protein ( AGP2) required for carnitine transport across the plasma membrane.	gene_phenotype
70104	1	333796	5	NULL	NULL	0	NULL	YOR100C gene product	GP		is a member of					mitochondrial carrier family	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_111	10545096	Taken together, our experiments show that the gene product of  YOR100C is a member of the mitochondrial carrier family, which is induced on oleate, involved in the transport of acetyl-CoA from peroxisomes to mitochondria and functions as a carnitine acylcarnitine translocase in the mitochondrial inner membrane of  S.cerevisiae.	gene_phenotype
70105	2	333796	5	NULL	NULL	0	NULL	oleate	Chemical		induce					YOR100C gene product	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_111	10545096	Taken together, our experiments show that the gene product of  YOR100C is a member of the mitochondrial carrier family, which is induced on oleate, involved in the transport of acetyl-CoA from peroxisomes to mitochondria and functions as a carnitine acylcarnitine translocase in the mitochondrial inner membrane of  S.cerevisiae.	gene_phenotype
70106	3	333796	5	NULL	NULL	0	NULL	acetyl-CoA	GP		is transported from					peroxisomes	CellComponent				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_111	10545096	Taken together, our experiments show that the gene product of  YOR100C is a member of the mitochondrial carrier family, which is induced on oleate, involved in the transport of acetyl-CoA from peroxisomes to mitochondria and functions as a carnitine acylcarnitine translocase in the mitochondrial inner membrane of  S.cerevisiae.	gene_phenotype
70107	4	333796	5	NULL	NULL	0	NULL	acetyl-CoA	GP		is transported to					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_111	10545096	Taken together, our experiments show that the gene product of  YOR100C is a member of the mitochondrial carrier family, which is induced on oleate, involved in the transport of acetyl-CoA from peroxisomes to mitochondria and functions as a carnitine acylcarnitine translocase in the mitochondrial inner membrane of  S.cerevisiae.	gene_phenotype
70108	5	333796	5	NULL	NULL	0	NULL	statement 3	Process		occurs along with					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_111	10545096	Taken together, our experiments show that the gene product of  YOR100C is a member of the mitochondrial carrier family, which is induced on oleate, involved in the transport of acetyl-CoA from peroxisomes to mitochondria and functions as a carnitine acylcarnitine translocase in the mitochondrial inner membrane of  S.cerevisiae.	gene_phenotype
70109	6	333796	5	NULL	NULL	0	NULL	YOR100C gene product	GP		is involved in					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_111	10545096	Taken together, our experiments show that the gene product of  YOR100C is a member of the mitochondrial carrier family, which is induced on oleate, involved in the transport of acetyl-CoA from peroxisomes to mitochondria and functions as a carnitine acylcarnitine translocase in the mitochondrial inner membrane of  S.cerevisiae.	gene_phenotype
70110	7	333796	5	NULL	NULL	0	NULL	YOR100C gene product	GP		is involved in					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_111	10545096	Taken together, our experiments show that the gene product of  YOR100C is a member of the mitochondrial carrier family, which is induced on oleate, involved in the transport of acetyl-CoA from peroxisomes to mitochondria and functions as a carnitine acylcarnitine translocase in the mitochondrial inner membrane of  S.cerevisiae.	gene_phenotype
70111	8	333796	5	NULL	NULL	0	NULL	YOR100C gene product	GP		functions as					carnitine acylcarnitine translocase	GP				NULL	mitochondrial inner membrane of S.cerevisiae.	0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_111	10545096	Taken together, our experiments show that the gene product of  YOR100C is a member of the mitochondrial carrier family, which is induced on oleate, involved in the transport of acetyl-CoA from peroxisomes to mitochondria and functions as a carnitine acylcarnitine translocase in the mitochondrial inner membrane of  S.cerevisiae.	gene_phenotype
70121	1	333797	5	NULL	NULL	0	NULL	ORF YBL064C protein	GP		is homologous to					peroxiredoxins	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_16296_s_216	10821871	The protein coded by the ORF YBL064C showed homology to peroxiredoxins and had a potential mitochondrial targeting signal, and although the product of ORF YBL064C belongs to the 1-Cys Prx group, we decided to test whether it had specific TPx activity with the mitochondrial thioredoxin system.	gene_phenotype
70122	2	333797	5	NULL	NULL	0	NULL	ORF YBL064C protein	GP		contains					mitochondrial targeting signal	AminoAcid	potential			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_16296_s_216	10821871	The protein coded by the ORF YBL064C showed homology to peroxiredoxins and had a potential mitochondrial targeting signal, and although the product of ORF YBL064C belongs to the 1-Cys Prx group, we decided to test whether it had specific TPx activity with the mitochondrial thioredoxin system.	gene_phenotype
70123	3	333797	5	NULL	NULL	0	NULL	ORF YBL064C protein	GP		belongs tp					1-Cys Prx group	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_16296_s_216	10821871	The protein coded by the ORF YBL064C showed homology to peroxiredoxins and had a potential mitochondrial targeting signal, and although the product of ORF YBL064C belongs to the 1-Cys Prx group, we decided to test whether it had specific TPx activity with the mitochondrial thioredoxin system.	gene_phenotype
70125	4	333797	5	NULL	NULL	NULL	NULL	ORF YBL064C protein	GP		activates		potentially			TPx	GP				NULL	mitochondrial thioredoxin system	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_16296_s_216	10821871	The protein coded by the ORF YBL064C showed homology to peroxiredoxins and had a potential mitochondrial targeting signal, and although the product of ORF YBL064C belongs to the 1-Cys Prx group, we decided to test whether it had specific TPx activity with the mitochondrial thioredoxin system.	gene_phenotype
70126	1	333799	5	NULL	NULL	0	NULL	YGR024c	NucleicAcid		is a type of					ORF	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_23_2889_s_118	14633974	THG1 (ORF YGR024c) encodes a protein with tRNAHis guanylyltransferase activity	gene_phenotype
70127	2	333799	5	NULL	NULL	0	NULL	YGR024c	NucleicAcid		is the locus name of					THG1	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_23_2889_s_118	14633974	THG1 (ORF YGR024c) encodes a protein with tRNAHis guanylyltransferase activity	gene_phenotype
70128	3	333799	5	NULL	NULL	0	NULL	THG1	GP		activates					tRNAHis guanylyltransferase	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_23_2889_s_118	14633974	THG1 (ORF YGR024c) encodes a protein with tRNAHis guanylyltransferase activity	gene_phenotype
70129	1	333800	5	NULL	NULL	0	NULL	YGR024c	NucleicAcid		is a type of					ORF	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_23_2889_s_41	14633974	Using a previously described biochemical genomics approach (Martzen et al. 1999 ), and an assay based on incorporation of [alpha-32]GTP into a tRNAHis substrate, we identified a 28-kD protein, encoded by the essential ORF YGR024c, that copurifies with tRNAHis guanylyltransferase activity.	gene_phenotype
70130	2	333800	5	NULL	NULL	0	NULL	YGR024c protein	GP		activates					tRNAHis guanylyltransferase	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_23_2889_s_41	14633974	Using a previously described biochemical genomics approach (Martzen et al. 1999 ), and an assay based on incorporation of [alpha-32]GTP into a tRNAHis substrate, we identified a 28-kD protein, encoded by the essential ORF YGR024c, that copurifies with tRNAHis guanylyltransferase activity.	gene_phenotype
70131	1	333801	5	NULL	NULL	0	NULL	YJR019C	NucleicAcid		is renamed as					PTE1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_14_9216_s_247	10092594	We propose that  YJR019C and human  hTE both be renamed  PTE1 to reflect the peroxisomal distribution and acyl-CoA thioesterase activity of their gene products.	gene_phenotype
70132	2	333801	5	NULL	NULL	0	NULL	hTE	GP	human	is renamed as					PTE1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_14_9216_s_247	10092594	We propose that  YJR019C and human  hTE both be renamed  PTE1 to reflect the peroxisomal distribution and acyl-CoA thioesterase activity of their gene products.	gene_phenotype
70133	3	333801	5	NULL	NULL	0	NULL	PTE1	GP		distributed in					peroxisome	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_14_9216_s_247	10092594	We propose that  YJR019C and human  hTE both be renamed  PTE1 to reflect the peroxisomal distribution and acyl-CoA thioesterase activity of their gene products.	gene_phenotype
70134	4	333801	5	NULL	NULL	0	NULL	PTE1	GP		activates					acyl-CoA thioesterase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_14_9216_s_247	10092594	We propose that  YJR019C and human  hTE both be renamed  PTE1 to reflect the peroxisomal distribution and acyl-CoA thioesterase activity of their gene products.	gene_phenotype
70135	1	333803	5	NULL	NULL	0	NULL	YKL187c	NucleicAcid		is linked to		probably			succinate dehydrogenase	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_7_553_s_386	16710832	YKL187c is linked to a probable succinate dehydrogenase by STRING and annotated to  15 terms ( p > 0.25) by GeneFAS (cell growth and/or maintenance, metabolism, organic acid metabolism,  energy pathways, transport, electron transport, phosphorus metabolism, cell communication,  carboxylic acid metabolism, carbohydrate metabolism, energy derivation by oxidation  of organic compounds, coenzymes and prosthetic group metabolism, signal transduction,  oxidative phosphorylation, phosphate metabolism, response to stress, main pathways  of carbohydrate metabolism, phosphorylation biosynthesis, TCA intermediate metabolism,  main pathways of carbohydrate metabolism, amine metabolism, amino acid and derivative  metabolism, tricarboxylic acid cycle, and lipid metabolism), most of which are related  to the un-supported  carbohydrate and alcohol metabolism  annotation made in this study.	gene_phenotype
70146	1	333805	5	NULL	NULL	0	NULL	YLR011wp protein	GP		activates					reductase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34890_s_238	15184374	The biochemical studies aimed to identify YLR011wp  in vivo activity showed that the protein bears several reductase activities that are NAD(P)H-dependent and involve FMN as a cofactor.	gene_phenotype
70147	2	333805	5	NULL	NULL	0	NULL	statement 1	Process		is dependent on					NAD(P)H	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34890_s_238	15184374	The biochemical studies aimed to identify YLR011wp  in vivo activity showed that the protein bears several reductase activities that are NAD(P)H-dependent and involve FMN as a cofactor.	gene_phenotype
70148	3	333805	5	NULL	NULL	0	NULL	statement 1	Process		involves					FMN	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34890_s_238	15184374	The biochemical studies aimed to identify YLR011wp  in vivo activity showed that the protein bears several reductase activities that are NAD(P)H-dependent and involve FMN as a cofactor.	gene_phenotype
70149	4	333805	5	NULL	NULL	0	NULL	FMN	Chemical		acts as					cofactor	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34890_s_238	15184374	The biochemical studies aimed to identify YLR011wp  in vivo activity showed that the protein bears several reductase activities that are NAD(P)H-dependent and involve FMN as a cofactor.	gene_phenotype
70150	1	333806	5	NULL	NULL	NULL	NULL	YLR011wp	NucleicAcid		is an acceptor of		natural			electron transfer	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_33_34890_s_183	15184374	Therefore, if YLR011wp has a natural acceptor for electron transfer via FMN, the FMN reductase activity detected reflects either the reduction of free oxidized FMN via enzyme-bound FMN ( Fig. 5 b) or the rapid exchange reaction between the reduced and oxidized forms of FMN at the protein FMN binding site ( Fig. 5 c).	gene_phenotype
70151	2	333806	5	NULL	NULL	0	NULL	statement 1	Process		via					FMN	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34890_s_183	15184374	Therefore, if YLR011wp has a natural acceptor for electron transfer via FMN, the FMN reductase activity detected reflects either the reduction of free oxidized FMN via enzyme-bound FMN ( Fig. 5 b) or the rapid exchange reaction between the reduced and oxidized forms of FMN at the protein FMN binding site ( Fig. 5 c).	gene_phenotype
70153	3	333806	5	NULL	NULL	0	NULL	YLR011wp	NucleicAcid		activates					FMN reductase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34890_s_183	15184374	Therefore, if YLR011wp has a natural acceptor for electron transfer via FMN, the FMN reductase activity detected reflects either the reduction of free oxidized FMN via enzyme-bound FMN ( Fig. 5 b) or the rapid exchange reaction between the reduced and oxidized forms of FMN at the protein FMN binding site ( Fig. 5 c).	gene_phenotype
70156	4	333806	5	NULL	NULL	NULL	NULL	FMN	Chemical	free;;oxidized	undergoes					reduction	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_33_34890_s_183	15184374	Therefore, if YLR011wp has a natural acceptor for electron transfer via FMN, the FMN reductase activity detected reflects either the reduction of free oxidized FMN via enzyme-bound FMN ( Fig. 5 b) or the rapid exchange reaction between the reduced and oxidized forms of FMN at the protein FMN binding site ( Fig. 5 c).	gene_phenotype
70157	5	333806	5	NULL	NULL	0	NULL	statement 4	Process		via					enzyme-bound FMN	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34890_s_183	15184374	Therefore, if YLR011wp has a natural acceptor for electron transfer via FMN, the FMN reductase activity detected reflects either the reduction of free oxidized FMN via enzyme-bound FMN ( Fig. 5 b) or the rapid exchange reaction between the reduced and oxidized forms of FMN at the protein FMN binding site ( Fig. 5 c).	gene_phenotype
70158	6	333806	5	NULL	NULL	0	NULL	FMN	Chemical	reduced	is exchanged with					FMN	Chemical	oxidized			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34890_s_183	15184374	Therefore, if YLR011wp has a natural acceptor for electron transfer via FMN, the FMN reductase activity detected reflects either the reduction of free oxidized FMN via enzyme-bound FMN ( Fig. 5 b) or the rapid exchange reaction between the reduced and oxidized forms of FMN at the protein FMN binding site ( Fig. 5 c).	gene_phenotype
70159	7	333806	5	NULL	NULL	0	NULL	statement 6	Process		occurs at					protein FMN binding site	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34890_s_183	15184374	Therefore, if YLR011wp has a natural acceptor for electron transfer via FMN, the FMN reductase activity detected reflects either the reduction of free oxidized FMN via enzyme-bound FMN ( Fig. 5 b) or the rapid exchange reaction between the reduced and oxidized forms of FMN at the protein FMN binding site ( Fig. 5 c).	gene_phenotype
70160	8	333806	5	NULL	NULL	0	NULL	statement 6	Process		is a type of					rapid exchange reaction	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34890_s_183	15184374	Therefore, if YLR011wp has a natural acceptor for electron transfer via FMN, the FMN reductase activity detected reflects either the reduction of free oxidized FMN via enzyme-bound FMN ( Fig. 5 b) or the rapid exchange reaction between the reduced and oxidized forms of FMN at the protein FMN binding site ( Fig. 5 c).	gene_phenotype
70161	9	333806	5	NULL	NULL	0	NULL	statement 3	Process		reflects					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34890_s_183	15184374	Therefore, if YLR011wp has a natural acceptor for electron transfer via FMN, the FMN reductase activity detected reflects either the reduction of free oxidized FMN via enzyme-bound FMN ( Fig. 5 b) or the rapid exchange reaction between the reduced and oxidized forms of FMN at the protein FMN binding site ( Fig. 5 c).	gene_phenotype
70162	10	333806	5	NULL	NULL	0	NULL	statement 3	Process		reflects					statement 6	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34890_s_183	15184374	Therefore, if YLR011wp has a natural acceptor for electron transfer via FMN, the FMN reductase activity detected reflects either the reduction of free oxidized FMN via enzyme-bound FMN ( Fig. 5 b) or the rapid exchange reaction between the reduced and oxidized forms of FMN at the protein FMN binding site ( Fig. 5 c).	gene_phenotype
70163	11	333806	5	NULL	NULL	0	NULL	statement 9	Process		is an alternative to					statement 10	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34890_s_183	15184374	Therefore, if YLR011wp has a natural acceptor for electron transfer via FMN, the FMN reductase activity detected reflects either the reduction of free oxidized FMN via enzyme-bound FMN ( Fig. 5 b) or the rapid exchange reaction between the reduced and oxidized forms of FMN at the protein FMN binding site ( Fig. 5 c).	gene_phenotype
70164	1	333811	5	NULL	NULL	0	NULL	Ypr128cp	NucleicAcid		is the locus name of					Ant1p	GP				NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_3	11566870	Here we report the identification and functional reconstitution of Ant1p (Ypr128cp), a peroxisomal transporter in the yeast  Saccharomyces cerevisiae, which has the characteristic sequence features of the mitochondrial carrier family.	gene_phenotype
70165	2	333811	5	NULL	NULL	0	NULL	Ant1p	GP		is a type of					peroxisomal transporter	GP				NULL	yeast Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_3	11566870	Here we report the identification and functional reconstitution of Ant1p (Ypr128cp), a peroxisomal transporter in the yeast  Saccharomyces cerevisiae, which has the characteristic sequence features of the mitochondrial carrier family.	gene_phenotype
70166	3	333811	5	NULL	NULL	0	NULL	Ant1p 	GP	sequence features of	is characteristic to					mitochondrial carrier family	GP				NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_3	11566870	Here we report the identification and functional reconstitution of Ant1p (Ypr128cp), a peroxisomal transporter in the yeast  Saccharomyces cerevisiae, which has the characteristic sequence features of the mitochondrial carrier family.	gene_phenotype
70167	2	333815	5	NULL	NULL	NULL	NULL	QAOS	MedicalProcedure		measures					statement 1	Process				NULL	in vivo in budding yeast cdc13 mutants	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4414_s_119	11691929	The data in the right lanes of Figure  1B are in complete agreement with our previous findings and show that QAOS is capable of measuring ssDNA produced at  YER186C in vivo, in budding yeast  cdc13 mutants.	gene_phenotype
70168	1	333815	5	NULL	NULL	NULL	NULL	ssDNA	NucleicAcid		is produced at					YER186C	NucleicAcid				NULL	in vivo in budding yeast cdc13 mutants	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_21_4414_s_119	11691929	The data in the right lanes of Figure  1B are in complete agreement with our previous findings and show that QAOS is capable of measuring ssDNA produced at  YER186C in vivo, in budding yeast  cdc13 mutants.	gene_phenotype
70169	1	333817	5	NULL	NULL	0	NULL	YAL061W	NucleicAcid		is a type of					sporulation gene	GP				NULL		0	NULL	NULL	NULL	gw60_genetics_163_1_47_s_114	12586695	YAL061W is a representative essential sporulation gene and the deletion mutant shows an  IME1 expression phenotype consistent with an arrest after  IME1 induction.	gene_phenotype
70170	2	333817	5	NULL	NULL	0	NULL	YAL061W	NucleicAcid	deletion mutant	shows					IME1 expression phenotype	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw60_genetics_163_1_47_s_114	12586695	YAL061W is a representative essential sporulation gene and the deletion mutant shows an  IME1 expression phenotype consistent with an arrest after  IME1 induction.	gene_phenotype
70171	3	333817	5	NULL	NULL	0	NULL	arrest	Process		occurs after					IME1	GP	induction of			NULL		0	NULL	NULL	NULL	gw60_genetics_163_1_47_s_114	12586695	YAL061W is a representative essential sporulation gene and the deletion mutant shows an  IME1 expression phenotype consistent with an arrest after  IME1 induction.	gene_phenotype
70172	4	333817	5	NULL	NULL	0	NULL	statement 2	Process		consistent with					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_163_1_47_s_114	12586695	YAL061W is a representative essential sporulation gene and the deletion mutant shows an  IME1 expression phenotype consistent with an arrest after  IME1 induction.	gene_phenotype
70173	1	333818	5	NULL	NULL	0	NULL	YHR087W orthologue	GP	S. pombe	is expressed during					sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_19_19213_s_112	15701634	This protein did not have a previously known structure or function; however, the YHR087W orthologue in  S. pombe is expressed during sporulation and environmental stress ( ,  ).	gene_phenotype
70174	2	333818	5	NULL	NULL	0	NULL	YHR087W orthologue	GP	S. pombe	is expressed during					environmental stress	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_19_19213_s_112	15701634	This protein did not have a previously known structure or function; however, the YHR087W orthologue in  S. pombe is expressed during sporulation and environmental stress ( ,  ).	gene_phenotype
70175	1	333819	5	NULL	NULL	0	NULL	YER158c	NucleicAcid		regulates		possibly			pheromone signaling	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_155_1_43_s_256	10790383	To determine whether  YER158c can regulate pheromone signaling, cells carrying the  YER158c sequences cloned into a 2mu multicopy vector were assayed for their sensitivity to alpha-factor in a halo assay ( Fig 8).	gene_phenotype
70176	1	333820	5	NULL	NULL	0	NULL	Kss1	GP		is a type of					MAP kinase	GP				NULL		0	NULL	NULL	NULL	gw70_genomeres_15_4_560_s_90	15805496	Sequencing revealed six proteins: Kss1, the MAP kinase for the filamentous growth pathway; Tpk2, a cAMP-dependent kinase subunit; Gis2, an uncharacterized protein involved in glucose sensing; Ypc1, a ceramidase enzyme; and two uncharacterized proteins, Yer158c and Ybr062c.	gene_phenotype
70177	2	333820	5	NULL	NULL	0	NULL	Kss1	GP		is involved in					filamentous growth pathway	Process				NULL		0	NULL	NULL	NULL	gw70_genomeres_15_4_560_s_90	15805496	Sequencing revealed six proteins: Kss1, the MAP kinase for the filamentous growth pathway; Tpk2, a cAMP-dependent kinase subunit; Gis2, an uncharacterized protein involved in glucose sensing; Ypc1, a ceramidase enzyme; and two uncharacterized proteins, Yer158c and Ybr062c.	gene_phenotype
70178	3	333820	5	NULL	NULL	0	NULL	Tpk2	GP		is a type of					cAMP-dependent kinase subunit	GP				NULL		0	NULL	NULL	NULL	gw70_genomeres_15_4_560_s_90	15805496	Sequencing revealed six proteins: Kss1, the MAP kinase for the filamentous growth pathway; Tpk2, a cAMP-dependent kinase subunit; Gis2, an uncharacterized protein involved in glucose sensing; Ypc1, a ceramidase enzyme; and two uncharacterized proteins, Yer158c and Ybr062c.	gene_phenotype
70179	4	333820	5	NULL	NULL	0	NULL	Gis2	GP		is involved in					glucose	Chemical	sensing of			NULL		0	NULL	NULL	NULL	gw70_genomeres_15_4_560_s_90	15805496	Sequencing revealed six proteins: Kss1, the MAP kinase for the filamentous growth pathway; Tpk2, a cAMP-dependent kinase subunit; Gis2, an uncharacterized protein involved in glucose sensing; Ypc1, a ceramidase enzyme; and two uncharacterized proteins, Yer158c and Ybr062c.	gene_phenotype
70180	5	333820	5	NULL	NULL	0	NULL	Ypc1	GP		is a type of					ceramidase enzyme	GP				NULL		0	NULL	NULL	NULL	gw70_genomeres_15_4_560_s_90	15805496	Sequencing revealed six proteins: Kss1, the MAP kinase for the filamentous growth pathway; Tpk2, a cAMP-dependent kinase subunit; Gis2, an uncharacterized protein involved in glucose sensing; Ypc1, a ceramidase enzyme; and two uncharacterized proteins, Yer158c and Ybr062c.	gene_phenotype
70181	1	333821	5	NULL	NULL	0	NULL	YER158c	NucleicAcid	expression of	is not regulated by					cell cycle	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_155_1_43_s_252	10790383	DNA microarray analysis indicates that  YER158c expression is not cell cycle regulated ( S MITH et al. 1996   ;   S PELLMAN et al. 1998   ), is induced during diauxic growth ( D ERISI et al. 1997   ), and is repressed during sporulation ( C HU et al. 1998   ).	gene_phenotype
70182	2	333821	5	NULL	NULL	0	NULL	YER158c	NucleicAcid	expression of	is induced during					diauxic growth	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_155_1_43_s_252	10790383	DNA microarray analysis indicates that  YER158c expression is not cell cycle regulated ( S MITH et al. 1996   ;   S PELLMAN et al. 1998   ), is induced during diauxic growth ( D ERISI et al. 1997   ), and is repressed during sporulation ( C HU et al. 1998   ).	gene_phenotype
70183	3	333821	5	NULL	NULL	0	NULL	YER158c	NucleicAcid	expression of	is repressed during					sporulation	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_155_1_43_s_252	10790383	DNA microarray analysis indicates that  YER158c expression is not cell cycle regulated ( S MITH et al. 1996   ;   S PELLMAN et al. 1998   ), is induced during diauxic growth ( D ERISI et al. 1997   ), and is repressed during sporulation ( C HU et al. 1998   ).	gene_phenotype
70184	2	333824	5	NULL	NULL	NULL	NULL	peroxisomes	CellComponent	yeast	activates					delta3,delta2-enoyl-CoA isomerase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33184_s_225	9837886	Although a prior report suggested that the delta3,delta2-enoyl-CoA isomerase activity of yeast peroxisomes is an intrinsic feature of acyl-CoA oxidase (Pox1) ( 35), our findings demonstrate that this activity is dependent on the protein encoded by  YLR284C.	gene_phenotype
70185	1	333824	5	NULL	NULL	NULL	NULL	acyl-CoA oxidase	GP		is a synonym of					Pox1	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_50_33184_s_225	9837886	Although a prior report suggested that the delta3,delta2-enoyl-CoA isomerase activity of yeast peroxisomes is an intrinsic feature of acyl-CoA oxidase (Pox1) ( 35), our findings demonstrate that this activity is dependent on the protein encoded by  YLR284C.	gene_phenotype
70186	3	333824	5	NULL	NULL	0	NULL	statement 2	Process		is an intrinsic feature of					acyl-CoA oxidase 	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_50_33184_s_225	9837886	Although a prior report suggested that the delta3,delta2-enoyl-CoA isomerase activity of yeast peroxisomes is an intrinsic feature of acyl-CoA oxidase (Pox1) ( 35), our findings demonstrate that this activity is dependent on the protein encoded by  YLR284C.	gene_phenotype
70187	4	333824	5	NULL	NULL	0	NULL	statement 2	Process		is dependent on					YLR284C protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_50_33184_s_225	9837886	Although a prior report suggested that the delta3,delta2-enoyl-CoA isomerase activity of yeast peroxisomes is an intrinsic feature of acyl-CoA oxidase (Pox1) ( 35), our findings demonstrate that this activity is dependent on the protein encoded by  YLR284C.	gene_phenotype
70188	1	333825	5	NULL	NULL	0	NULL	YOL151w	NucleicAcid		is the locus name of					GRE2	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_6_545_s_231	12722185	We conclude that GRE2/YOL151w, but not YDR541c, YGL039w or YGL157w, encodes a  protein with methylglyoxal-reducing activity.	gene_phenotype
70189	2	333825	5	NULL	NULL	0	NULL	GRE2	GP		activates					methylglyoxal	Chemical	reduction of			NULL		0	NULL	NULL	NULL	gw70_yeast_20_6_545_s_231	12722185	We conclude that GRE2/YOL151w, but not YDR541c, YGL039w or YGL157w, encodes a  protein with methylglyoxal-reducing activity.	gene_phenotype
70190	3	333825	5	NULL	NULL	0	NULL	YDR541c protein	GP		does not activate					methylglyoxal	Chemical	reduction of			NULL		0	NULL	NULL	NULL	gw70_yeast_20_6_545_s_231	12722185	We conclude that GRE2/YOL151w, but not YDR541c, YGL039w or YGL157w, encodes a  protein with methylglyoxal-reducing activity.	gene_phenotype
70191	4	333825	5	NULL	NULL	0	NULL	YGL039w protein	GP		does not activate					methylglyoxal	Chemical	reduction of			NULL		0	NULL	NULL	NULL	gw70_yeast_20_6_545_s_231	12722185	We conclude that GRE2/YOL151w, but not YDR541c, YGL039w or YGL157w, encodes a  protein with methylglyoxal-reducing activity.	gene_phenotype
70192	5	333825	5	NULL	NULL	0	NULL	YGL157w protein	GP		activates					methylglyoxal	Chemical	reduction of			NULL		0	NULL	NULL	NULL	gw70_yeast_20_6_545_s_231	12722185	We conclude that GRE2/YOL151w, but not YDR541c, YGL039w or YGL157w, encodes a  protein with methylglyoxal-reducing activity.	gene_phenotype
70193	1	333827	5	NULL	NULL	0	NULL	YHR150w	NucleicAcid		encodes					peroxisomal integral membrane proteins	GP				NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw70_cellbiol_161_2_321_s_1	12707309	YHR150w and YDR479c encode peroxisomal integral membrane proteins involved in the regulation of peroxisome number, size, and distribution in Saccharomyces cerevisiae.	gene_phenotype
70194	2	333827	5	NULL	NULL	0	NULL	YDR479c	NucleicAcid		encodes					peroxisomal integral membrane proteins	GP				NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw70_cellbiol_161_2_321_s_1	12707309	YHR150w and YDR479c encode peroxisomal integral membrane proteins involved in the regulation of peroxisome number, size, and distribution in Saccharomyces cerevisiae.	gene_phenotype
70195	3	333827	5	NULL	NULL	0	NULL	peroxisomal integral membrane proteins	GP		regulates					peroxisome	CellComponent	number of			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw70_cellbiol_161_2_321_s_1	12707309	YHR150w and YDR479c encode peroxisomal integral membrane proteins involved in the regulation of peroxisome number, size, and distribution in Saccharomyces cerevisiae.	gene_phenotype
70196	4	333827	5	NULL	NULL	0	NULL	peroxisomal integral membrane proteins	GP		regulates					peroxisome	CellComponent	size of			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw70_cellbiol_161_2_321_s_1	12707309	YHR150w and YDR479c encode peroxisomal integral membrane proteins involved in the regulation of peroxisome number, size, and distribution in Saccharomyces cerevisiae.	gene_phenotype
70197	5	333827	5	NULL	NULL	0	NULL	peroxisomal integral membrane proteins	GP		regulates					peroxisome	CellComponent	distribution of			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw70_cellbiol_161_2_321_s_1	12707309	YHR150w and YDR479c encode peroxisomal integral membrane proteins involved in the regulation of peroxisome number, size, and distribution in Saccharomyces cerevisiae.	gene_phenotype
70198	1	333828	5	NULL	NULL	0	NULL	YHR150w	NucleicAcid		controls					peroxisome	CellComponent	size of			NULL		0	NULL	NULL	NULL	gw70_cellbiol_161_2_321_s_183	12707309	These characteristics of peroxisomes of the deletion strains are consistent with a role for  YHR150w and  YDR479c in the control of peroxisome size, number, and distribution within cells.	gene_phenotype
70199	2	333828	5	NULL	NULL	0	NULL	YHR150w	NucleicAcid		controls					peroxisome	CellComponent	number of			NULL		0	NULL	NULL	NULL	gw70_cellbiol_161_2_321_s_183	12707309	These characteristics of peroxisomes of the deletion strains are consistent with a role for  YHR150w and  YDR479c in the control of peroxisome size, number, and distribution within cells.	gene_phenotype
70200	3	333828	5	NULL	NULL	0	NULL	YHR150w	NucleicAcid		controls					peroxisome	CellComponent	distribution of			NULL		0	NULL	NULL	NULL	gw70_cellbiol_161_2_321_s_183	12707309	These characteristics of peroxisomes of the deletion strains are consistent with a role for  YHR150w and  YDR479c in the control of peroxisome size, number, and distribution within cells.	gene_phenotype
70201	4	333828	5	NULL	NULL	0	NULL	YDR479c	NucleicAcid		controls					peroxisome	CellComponent	size of			NULL		0	NULL	NULL	NULL	gw70_cellbiol_161_2_321_s_183	12707309	These characteristics of peroxisomes of the deletion strains are consistent with a role for  YHR150w and  YDR479c in the control of peroxisome size, number, and distribution within cells.	gene_phenotype
70202	5	333828	5	NULL	NULL	0	NULL	YDR479c	NucleicAcid		controls					peroxisome	CellComponent	number of			NULL		0	NULL	NULL	NULL	gw70_cellbiol_161_2_321_s_183	12707309	These characteristics of peroxisomes of the deletion strains are consistent with a role for  YHR150w and  YDR479c in the control of peroxisome size, number, and distribution within cells.	gene_phenotype
70203	6	333828	5	NULL	NULL	0	NULL	YDR479c	NucleicAcid		controls					peroxisome	CellComponent	distribution of			NULL		0	NULL	NULL	NULL	gw70_cellbiol_161_2_321_s_183	12707309	These characteristics of peroxisomes of the deletion strains are consistent with a role for  YHR150w and  YDR479c in the control of peroxisome size, number, and distribution within cells.	gene_phenotype
70213	1	333834	5	NULL	NULL	0	NULL	YNL063w protein	GP		does not activate					protoporphyrinogen	GP				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_173_1_175_s_150	10220893	Biochemical analysis and complementation assays provide evidence that the protein encoded by YNL063w is not involved in protoporphyrinogen activity.	gene_phenotype
70214	1	333835	5	NULL	NULL	0	NULL	YNL063w protein	GP	S. cerevisiae	does not activate					protoporphyrinogen	GP				NULL		0	NULL	NULL	NULL	gw60_embo_21_4_769_s_183	11847124	A functional analysis of the  S. cerevisiaeprotein, called YNL063w, concluded that it did not possess protoporphyrinogen activity ( Le Guen  et al., 1999), thought to be the role of the  E.coli HemK protein ( Nakayashiki  et al., 1995).	gene_phenotype
70215	2	333835	5	NULL	NULL	0	NULL	YNL063w protein	GP	S. cerevisiae	plays a role as		possibly			HemK protein	GP	E.coli			NULL		0	NULL	NULL	NULL	gw60_embo_21_4_769_s_183	11847124	A functional analysis of the  S. cerevisiaeprotein, called YNL063w, concluded that it did not possess protoporphyrinogen activity ( Le Guen  et al., 1999), thought to be the role of the  E.coli HemK protein ( Nakayashiki  et al., 1995).	gene_phenotype
70216	1	333836	5	NULL	NULL	0	NULL	ORF YNL063w product	GP		is similar to					hemK gene	GP	E.coli			NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_173_1_175_s_25	10220893	In order to find out whether the product of the ORF YNL063w, which is similar to the  hemK gene of  E. coli, is also involved in the protoporphyrinogen oxidase activity, we investigated the possible role in heme synthesis of this protein in yeast.	gene_phenotype
70218	2	333836	5	NULL	NULL	0	NULL	ORF YNL063w product	GP		activates		potentially			protoporphyrinogen oxidase	GP				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_173_1_175_s_25	10220893	In order to find out whether the product of the ORF YNL063w, which is similar to the  hemK gene of  E. coli, is also involved in the protoporphyrinogen oxidase activity, we investigated the possible role in heme synthesis of this protein in yeast.	gene_phenotype
70219	1	333837	5	NULL	NULL	0	NULL	YLR127c	NucleicAcid		encodes		possibly			APC subunit	GP	budding yeast			NULL		0	NULL	NULL	NULL	gw60_science_279_5354_1219_s_61	9469815	To determine whether YLR127c encodes an APC subunit in budding yeast, we cloned the gene encoding YLR127c and inserted a triple hemagglutinin (HA) epitope tag at the NH2-terminus ( 26).	gene_phenotype
70230	1	333839	5	NULL	NULL	0	NULL	IPTG	Chemical	application of	leads to					ATP/ADP transporter		presence of;;functional			NULL	cytoplasmic membrane of E. coli harboring plasmid pET6 	0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9630_s_187	9545295	As the data above clearly show that IPTG application to  E. coli harboring plasmid pET6 leads to the presence of a functional ATP/ADP transporter in the cytoplasmic bacterial membrane it was tempting to analyze IPTG-induced protein synthesis in more detail.	gene_phenotype
70311	1	333840	5	NULL	NULL	0	NULL	Yor145c protein	GP		is a type of					nucleolar protein	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_10_2524_s_2	12736301	A strain of  Saccharomyces cerevisiae, defective in small subunit ribosomal RNA processing, has a mutation in  YOR145c ORF that converts Gly235 to Asp. Yor145c is a nucleolar protein required for cell viability and has been reported recently to be present in 90S pre-ribosomal particles.	gene_phenotype
70312	2	333840	5	NULL	NULL	0	NULL	Yor145c protein	GP		is required for					cell viability	Process				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_10_2524_s_2	12736301	A strain of  Saccharomyces cerevisiae, defective in small subunit ribosomal RNA processing, has a mutation in  YOR145c ORF that converts Gly235 to Asp. Yor145c is a nucleolar protein required for cell viability and has been reported recently to be present in 90S pre-ribosomal particles.	gene_phenotype
70313	3	333840	5	NULL	NULL	0	NULL	Yor145c protein	GP		is present in					90S pre-ribosomal particles	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_10_2524_s_2	12736301	A strain of  Saccharomyces cerevisiae, defective in small subunit ribosomal RNA processing, has a mutation in  YOR145c ORF that converts Gly235 to Asp. Yor145c is a nucleolar protein required for cell viability and has been reported recently to be present in 90S pre-ribosomal particles.	gene_phenotype
70314	4	333840	5	NULL	NULL	0	NULL	Gly235	AminoAcid		is converted to					Asp	AminoAcid				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_10_2524_s_2	12736301	A strain of  Saccharomyces cerevisiae, defective in small subunit ribosomal RNA processing, has a mutation in  YOR145c ORF that converts Gly235 to Asp. Yor145c is a nucleolar protein required for cell viability and has been reported recently to be present in 90S pre-ribosomal particles.	gene_phenotype
70315	5	333840	5	NULL	NULL	0	NULL	YOR145c ORF	NucleicAcid	mutant	is required for					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_10_2524_s_2	12736301	A strain of  Saccharomyces cerevisiae, defective in small subunit ribosomal RNA processing, has a mutation in  YOR145c ORF that converts Gly235 to Asp. Yor145c is a nucleolar protein required for cell viability and has been reported recently to be present in 90S pre-ribosomal particles.	gene_phenotype
70316	6	333840	5	NULL	NULL	0	NULL	Saccharomyces cerevisiae strain	Organism		is defective in					small subunit ribosomal RNA	NucleicAcid	processing of			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_10_2524_s_2	12736301	A strain of  Saccharomyces cerevisiae, defective in small subunit ribosomal RNA processing, has a mutation in  YOR145c ORF that converts Gly235 to Asp. Yor145c is a nucleolar protein required for cell viability and has been reported recently to be present in 90S pre-ribosomal particles.	gene_phenotype
70317	7	333840	5	NULL	NULL	0	NULL	statement 6	Process		contains					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_10_2524_s_2	12736301	A strain of  Saccharomyces cerevisiae, defective in small subunit ribosomal RNA processing, has a mutation in  YOR145c ORF that converts Gly235 to Asp. Yor145c is a nucleolar protein required for cell viability and has been reported recently to be present in 90S pre-ribosomal particles.	gene_phenotype
70327	1	333842	5	NULL	NULL	0	NULL	telomere	Chromosome	proximity of	is involved in		potentially			IMD1	GP	silencing of			NULL		0	NULL	NULL	NULL	gw70_genetics_173_2_1169_s_66	16582424	Thus, telomere proximity appears to be involved in the silencing of YAR073W/ IMD1.	gene_phenotype
70328	2	333842	5	NULL	NULL	0	NULL	YAR073W	NucleicAcid		is the locus name of					IMD1	GP				NULL		0	NULL	NULL	NULL	gw70_genetics_173_2_1169_s_66	16582424	Thus, telomere proximity appears to be involved in the silencing of YAR073W/ IMD1.	gene_phenotype
70331	1	333843	5	NULL	NULL	NULL	NULL	MD1	GP		is controlled by		potentially			TPE	Process	bona fide			NULL		NULL	NULL	NULL	NULL	gw70_genetics_173_2_1169_s_60	16582424	To examine whether YAR073W /MD1 was controlled by a  bona fide TPE, two different homeologous fragments from the middle of  Saccharomyces carlsbergensis chromosome  III, 7.0 and 8.4 kb in length, were inserted between YAR073W/ IMD1 and its proximal telomere and transcript levels were determined by quantitative RT - PCR as above.	gene_phenotype
70332	2	333843	5	NULL	NULL	0	NULL	YAR073W	NucleicAcid		is the locus name of					MD1	GP				NULL		0	NULL	NULL	NULL	gw70_genetics_173_2_1169_s_60	16582424	To examine whether YAR073W /MD1 was controlled by a  bona fide TPE, two different homeologous fragments from the middle of  Saccharomyces carlsbergensis chromosome  III, 7.0 and 8.4 kb in length, were inserted between YAR073W/ IMD1 and its proximal telomere and transcript levels were determined by quantitative RT - PCR as above.	gene_phenotype
70333	1	333844	5	NULL	NULL	0	NULL	YAR073W	NucleicAcid		is the locus name of					IMD1	GP				NULL		0	NULL	NULL	NULL	gw70_genetics_173_2_1169_s_23	16582424	In this report we demonstrate that the endmost chromosome  I ORF, YAR073W/ IMD1, is indeed silenced by its telomere, suggesting that telomeres play a role in silencing actual genes.	gene_phenotype
70335	2	333844	5	NULL	NULL	0	NULL	YAR073W	NucleicAcid		is a type of					chromosome I ORF	NucleicAcid	endmost			NULL		0	NULL	NULL	NULL	gw70_genetics_173_2_1169_s_23	16582424	In this report we demonstrate that the endmost chromosome  I ORF, YAR073W/ IMD1, is indeed silenced by its telomere, suggesting that telomeres play a role in silencing actual genes.	gene_phenotype
70337	3	333844	5	NULL	NULL	0	NULL	IMD1	GP		is silenced by					telomere	Chromosome				NULL		0	NULL	NULL	NULL	gw70_genetics_173_2_1169_s_23	16582424	In this report we demonstrate that the endmost chromosome  I ORF, YAR073W/ IMD1, is indeed silenced by its telomere, suggesting that telomeres play a role in silencing actual genes.	gene_phenotype
70338	4	333844	5	NULL	NULL	0	NULL	telomeres	Chromosome		plays a role in					genes	GP	silencing of;;actual			NULL		0	NULL	NULL	NULL	gw70_genetics_173_2_1169_s_23	16582424	In this report we demonstrate that the endmost chromosome  I ORF, YAR073W/ IMD1, is indeed silenced by its telomere, suggesting that telomeres play a role in silencing actual genes.	gene_phenotype
70339	1	333847	5	NULL	NULL	0	NULL	MJ0051 protein	GP	archaeal	activates					peptidyl-tRNA hydrolase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_35_37142_s_24	15210688	The SSO0175 and MJ0051 archaeal proteins, as well as the Ybl057c protein from  Saccharomyces cerevisiae (all from the PACE07 group), have been shown to have peptidyl-tRNA hydrolase activity and are thus involved in recycling peptidyl-tRNA molecules prematurely dissociated from the mRNA template ( ,  ).	gene_phenotype
70340	2	333847	5	NULL	NULL	0	NULL	SSO0175 protein	GP	archaeal	activates					peptidyl-tRNA hydrolase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_35_37142_s_24	15210688	The SSO0175 and MJ0051 archaeal proteins, as well as the Ybl057c protein from  Saccharomyces cerevisiae (all from the PACE07 group), have been shown to have peptidyl-tRNA hydrolase activity and are thus involved in recycling peptidyl-tRNA molecules prematurely dissociated from the mRNA template ( ,  ).	gene_phenotype
70341	3	333847	5	NULL	NULL	0	NULL	Ybl057c protein	GP	Saccharomyces cerevisiae	activates					peptidyl-tRNA hydrolase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_35_37142_s_24	15210688	The SSO0175 and MJ0051 archaeal proteins, as well as the Ybl057c protein from  Saccharomyces cerevisiae (all from the PACE07 group), have been shown to have peptidyl-tRNA hydrolase activity and are thus involved in recycling peptidyl-tRNA molecules prematurely dissociated from the mRNA template ( ,  ).	gene_phenotype
70342	4	333847	5	NULL	NULL	0	NULL	peptidyl-tRNA molecules	NucleicAcid		is dissociated from		prematurely			mRNA template	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_35_37142_s_24	15210688	The SSO0175 and MJ0051 archaeal proteins, as well as the Ybl057c protein from  Saccharomyces cerevisiae (all from the PACE07 group), have been shown to have peptidyl-tRNA hydrolase activity and are thus involved in recycling peptidyl-tRNA molecules prematurely dissociated from the mRNA template ( ,  ).	gene_phenotype
70343	5	333847	5	NULL	NULL	0	NULL	SSO0175 protein	GP	archaeal	recycles					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_35_37142_s_24	15210688	The SSO0175 and MJ0051 archaeal proteins, as well as the Ybl057c protein from  Saccharomyces cerevisiae (all from the PACE07 group), have been shown to have peptidyl-tRNA hydrolase activity and are thus involved in recycling peptidyl-tRNA molecules prematurely dissociated from the mRNA template ( ,  ).	gene_phenotype
70344	6	333847	5	NULL	NULL	0	NULL	MJ0051 protein	GP	archaeal	recycles					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_35_37142_s_24	15210688	The SSO0175 and MJ0051 archaeal proteins, as well as the Ybl057c protein from  Saccharomyces cerevisiae (all from the PACE07 group), have been shown to have peptidyl-tRNA hydrolase activity and are thus involved in recycling peptidyl-tRNA molecules prematurely dissociated from the mRNA template ( ,  ).	gene_phenotype
70345	7	333847	5	NULL	NULL	0	NULL	Ybl057c protein	GP	Saccharomyces cerevisiae	recycles					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_35_37142_s_24	15210688	The SSO0175 and MJ0051 archaeal proteins, as well as the Ybl057c protein from  Saccharomyces cerevisiae (all from the PACE07 group), have been shown to have peptidyl-tRNA hydrolase activity and are thus involved in recycling peptidyl-tRNA molecules prematurely dissociated from the mRNA template ( ,  ).	gene_phenotype
70346	1	333848	5	NULL	NULL	0	NULL	Msb2	GP		associate with		forced			Ybr062c	GP				NULL		0	NULL	NULL	NULL	gw70_genomeres_15_4_560_s_75	15805496	( B) Induction of the filamentous growth pathway occurs when Msb2 and Ybr062c are forced  to associate as leucine zipper fusions.	gene_phenotype
70347	2	333848	5	NULL	NULL	0	NULL	statement 1	Process		forms					leucine zipper fusions	GP				NULL		0	NULL	NULL	NULL	gw70_genomeres_15_4_560_s_75	15805496	( B) Induction of the filamentous growth pathway occurs when Msb2 and Ybr062c are forced  to associate as leucine zipper fusions.	gene_phenotype
70348	3	333848	5	NULL	NULL	0	NULL	statement 2	Process		induce					filamentous growth pathway	Process				NULL		0	NULL	NULL	NULL	gw70_genomeres_15_4_560_s_75	15805496	( B) Induction of the filamentous growth pathway occurs when Msb2 and Ybr062c are forced  to associate as leucine zipper fusions.	gene_phenotype
70349	1	333849	5	NULL	NULL	NULL	NULL	Ybr062c	NucleicAcid		interacts with		forced			Msb2	GP				NULL		NULL	NULL	NULL	NULL	gw70_genomeres_15_4_560_s_79	15805496	( C) Forced interaction between Ybr062c and Msb2 results in morphologies associated with  filamentous growth pathway hyperactivation.	gene_phenotype
70350	2	333849	5	NULL	NULL	0	NULL	statement 1	Process		is associated with					filamentous growth pathway	Process	hyperactivation of			NULL		0	NULL	NULL	NULL	gw70_genomeres_15_4_560_s_79	15805496	( C) Forced interaction between Ybr062c and Msb2 results in morphologies associated with  filamentous growth pathway hyperactivation.	gene_phenotype
70351	1	333850	5	NULL	NULL	0	NULL	Ybr062c	NucleicAcid		is not fused to					Fos	GP				NULL		0	NULL	NULL	NULL	gw70_genomeres_15_4_560_s_98	15805496	Overexpression of Ybr062c did not activate the filamentous growth pathway when not fused to Fos ( Fig. 3B); thus, it would not have been obtained in a high copy screen.	gene_phenotype
70352	2	333850	5	NULL	NULL	0	NULL	statement 1	Process	overexpression of	does not activate					filamentous growth pathway	Process				NULL		0	NULL	NULL	NULL	gw70_genomeres_15_4_560_s_98	15805496	Overexpression of Ybr062c did not activate the filamentous growth pathway when not fused to Fos ( Fig. 3B); thus, it would not have been obtained in a high copy screen.	gene_phenotype
70353	1	333851	5	NULL	NULL	0	NULL	YBR062c gene	GP	deletion of	does not disrupt					filamentous growth pathway	Process				NULL		0	NULL	NULL	NULL	gw70_genomeres_15_4_560_s_102	15805496	Deletion of the  YBR062c gene did not disrupt the filamentous growth pathway (data not shown), and as such, it would not have been recovered in a screen for loss-of-function mutations.	gene_phenotype
70354	1	333852	5	NULL	NULL	0	NULL	Ybr062c	NucleicAcid		does not play a role in		may;;primary			filamentous growth pathway	Process	activation of			NULL		0	NULL	NULL	NULL	gw70_genomeres_15_4_560_s_104	15805496	However, given the artificial nature of our screen, Ybr062c may not play a primary role in filamentous growth pathway activation but may influence another aspect of Msb2 function.	gene_phenotype
70355	2	333852	5	NULL	NULL	0	NULL	Ybr062c	NucleicAcid		influences					Msb2	GP	function of			NULL		0	NULL	NULL	NULL	gw70_genomeres_15_4_560_s_104	15805496	However, given the artificial nature of our screen, Ybr062c may not play a primary role in filamentous growth pathway activation but may influence another aspect of Msb2 function.	gene_phenotype
70358	1	333856	5	NULL	NULL	0	NULL	YFL030w protein	GP	yeast	activates					alanine:glyoxylate aminotransferase	GP				NULL		0	NULL	NULL	NULL	abs-batch0550-0559_biochimie_87_12_16226833_s_1	16226833	Crystal structure and confirmation of the alanine:glyoxylate aminotransferase activity of the YFL030w yeast protein..	gene_phenotype
70362	1	333862	5	NULL	NULL	0	NULL	YNR064c protein	GP		activates		low			epoxide hydrolase	GP				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_biochim-biophys-acta_1748_2_15769598_s_5	15769598	The YNR064c protein displayed low but reproducible epoxide hydrolase activity  with racemic phenanthrene 9,10-oxide and trans- or cis-stilbene oxide.	gene_phenotype
70364	2	333862	5	NULL	NULL	0	NULL	statement 1	Process		occurs with					phenanthrene 9,10-oxide	Chemical	racemic			NULL		0	NULL	NULL	NULL	abs-batch0680-0699_biochim-biophys-acta_1748_2_15769598_s_5	15769598	The YNR064c protein displayed low but reproducible epoxide hydrolase activity  with racemic phenanthrene 9,10-oxide and trans- or cis-stilbene oxide.	gene_phenotype
70365	3	333862	5	NULL	NULL	0	NULL	statement 1	Process		occurs with					trans- or cis-stilbene oxide	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_biochim-biophys-acta_1748_2_15769598_s_5	15769598	The YNR064c protein displayed low but reproducible epoxide hydrolase activity  with racemic phenanthrene 9,10-oxide and trans- or cis-stilbene oxide.	gene_phenotype
70368	1	333863	5	NULL	NULL	0	NULL	YA9E protein	GP		activates					Ap nA hydrolase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_13_8604_s_208	10085096	The gene encoding YA9E has recently been cloned and expressed, 4 and the protein has Ap nA hydrolase activity with Ap6A and Ap5A as the preferred substrates, but with some activity toward Ap4A, in contrast to YOR163w, which has no activity with this substrate.	gene_phenotype
70369	2	333863	5	NULL	NULL	0	NULL	Ap6A	GP		is a substrate of		preferred			Ap nA hydrolase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_13_8604_s_208	10085096	The gene encoding YA9E has recently been cloned and expressed, 4 and the protein has Ap nA hydrolase activity with Ap6A and Ap5A as the preferred substrates, but with some activity toward Ap4A, in contrast to YOR163w, which has no activity with this substrate.	gene_phenotype
70370	3	333863	5	NULL	NULL	0	NULL	Ap5A	GP		is a substrate of		preferred			Ap nA hydrolase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_13_8604_s_208	10085096	The gene encoding YA9E has recently been cloned and expressed, 4 and the protein has Ap nA hydrolase activity with Ap6A and Ap5A as the preferred substrates, but with some activity toward Ap4A, in contrast to YOR163w, which has no activity with this substrate.	gene_phenotype
70371	4	333863	5	NULL	NULL	0	NULL	Ap4A	GP		is a substrate of					Ap nA hydrolase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_13_8604_s_208	10085096	The gene encoding YA9E has recently been cloned and expressed, 4 and the protein has Ap nA hydrolase activity with Ap6A and Ap5A as the preferred substrates, but with some activity toward Ap4A, in contrast to YOR163w, which has no activity with this substrate.	gene_phenotype
70372	5	333863	5	NULL	NULL	0	NULL	YOR163w	NucleicAcid		has no activity with					Ap4A	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_13_8604_s_208	10085096	The gene encoding YA9E has recently been cloned and expressed, 4 and the protein has Ap nA hydrolase activity with Ap6A and Ap5A as the preferred substrates, but with some activity toward Ap4A, in contrast to YOR163w, which has no activity with this substrate.	gene_phenotype
70373	1	333864	5	NULL	NULL	0	NULL	YGL098w	NucleicAcid		codes for					SNARE-like protein	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_21_6_463_s_149	15116429	While this manuscript was in preparation, it was reported  that the  YGL098w codes for a product that is an ER-located SNARE-like protein involved in retrograde  transport of the vesicles (Dilcher  et al., [ 2003];	gene_phenotype
70374	2	333864	5	NULL	NULL	0	NULL	SNARE-like protein	GP		is located in					ER	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_21_6_463_s_149	15116429	While this manuscript was in preparation, it was reported  that the  YGL098w codes for a product that is an ER-located SNARE-like protein involved in retrograde  transport of the vesicles (Dilcher  et al., [ 2003];	gene_phenotype
70375	3	333864	5	NULL	NULL	0	NULL	SNARE-like protein	GP		is involved in					vesicle	CellComponent	retrograde transport of 			NULL		0	NULL	NULL	NULL	gw70_yeast_21_6_463_s_149	15116429	While this manuscript was in preparation, it was reported  that the  YGL098w codes for a product that is an ER-located SNARE-like protein involved in retrograde  transport of the vesicles (Dilcher  et al., [ 2003];	gene_phenotype
70376	1	333865	5	NULL	NULL	0	NULL	YGL098w gene	GP		is essential for					vegetative growth	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_yeast_16_4_10669874_s_7	10669874	Tetrad analysis of  heterozygous deletant strains revealed that YGL098w is an essential gene  for vegetative growth in three backgrounds, whereas the other five genes  are non-essential, although we have found some phenotypes in one of them.	gene_phenotype
70377	1	333866	5	NULL	NULL	0	NULL	YMR099cp	NucleicAcid		bind					hexose-6-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_40_30175_s_131	16857670	The fact that sulfate ions often substitute for phosphate groups in protein structures ( ,  ) suggests that YMR099cp binds a hexose-6-phosphate and that it hence may have hexose-6-phosphate mutarotase (or 1-epimerase) activity.	gene_phenotype
70378	2	333866	5	NULL	NULL	0	NULL	YMR099cp	GP		activates					hexose-6-phosphate mutarotase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_40_30175_s_131	16857670	The fact that sulfate ions often substitute for phosphate groups in protein structures ( ,  ) suggests that YMR099cp binds a hexose-6-phosphate and that it hence may have hexose-6-phosphate mutarotase (or 1-epimerase) activity.	gene_phenotype
70379	3	333866	5	NULL	NULL	0	NULL	YMR099cp	NucleicAcid		activates					1-epimerase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_40_30175_s_131	16857670	The fact that sulfate ions often substitute for phosphate groups in protein structures ( ,  ) suggests that YMR099cp binds a hexose-6-phosphate and that it hence may have hexose-6-phosphate mutarotase (or 1-epimerase) activity.	gene_phenotype
70380	4	333866	5	NULL	NULL	0	NULL	sulfate ions	Chemical		substitute for					phosphate groups	Chemical				NULL	protein structures	0	NULL	NULL	NULL	gw70_jbiolchem_281_40_30175_s_131	16857670	The fact that sulfate ions often substitute for phosphate groups in protein structures ( ,  ) suggests that YMR099cp binds a hexose-6-phosphate and that it hence may have hexose-6-phosphate mutarotase (or 1-epimerase) activity.	gene_phenotype
70381	1	333867	5	NULL	NULL	0	NULL	YMR099cp protein	GP		activates					glucose-6-phosphate epimerase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_40_30175_s_142	16857670	In the second phase, faster generation of NAD(P)H reflecting higher velocity constant ( k+1) for the interconversion between glucose 6-phosphate anomers is obtained with increasing concentration of YMR099cp, demonstrating the glucose-6-phosphate epimerase activity of the protein ( Fig. 3 B,  inset).	gene_phenotype
70382	1	333869	5	NULL	NULL	0	NULL	YOR300W	NucleicAcid		is the locus name of					HUF1	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_162	15645503	HUF1  YOR300W May be involved in bipolar budding and bud site selection This study	gene_phenotype
70383	2	333869	5	NULL	NULL	0	NULL	HUF1	GP		is involved in					bipolar budding	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_162	15645503	HUF1  YOR300W May be involved in bipolar budding and bud site selection This study	gene_phenotype
70384	3	333869	5	NULL	NULL	0	NULL	HUF1	GP		is involved in					bud site selection 	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_162	15645503	HUF1  YOR300W May be involved in bipolar budding and bud site selection This study	gene_phenotype
70385	1	333870	5	NULL	NULL	0	NULL	bni1	GP	homozygous;;mutant	does not undergo					filamentous growth	Process				NULL	SLAD	0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_192	15645503	Homozygous  bni1 ,  bud2 ,  cap2 ,  ecm25 ,  gas1 ,  ilm1 ,  pea2 ,  sce66 ,  tpm1  and  YOR300W  1278 b mutants did not undergo filamentous growth on SLAD (Figure  3).	gene_phenotype
70386	2	333870	5	NULL	NULL	0	NULL	bud2	GP	homozygous;;mutant	does not undergo					filamentous growth	Process				NULL	SLAD	0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_192	15645503	Homozygous  bni1 ,  bud2 ,  cap2 ,  ecm25 ,  gas1 ,  ilm1 ,  pea2 ,  sce66 ,  tpm1  and  YOR300W  1278 b mutants did not undergo filamentous growth on SLAD (Figure  3).	gene_phenotype
70387	3	333870	5	NULL	NULL	0	NULL	cap2 	GP	homozygous;;mutant	does not undergo					filamentous growth	Process				NULL	SLAD	0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_192	15645503	Homozygous  bni1 ,  bud2 ,  cap2 ,  ecm25 ,  gas1 ,  ilm1 ,  pea2 ,  sce66 ,  tpm1  and  YOR300W  1278 b mutants did not undergo filamentous growth on SLAD (Figure  3).	gene_phenotype
70388	4	333870	5	NULL	NULL	0	NULL	ecm25	GP	homozygous;;mutant	does not undergo					filamentous growth	Process				NULL	SLAD	0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_192	15645503	Homozygous  bni1 ,  bud2 ,  cap2 ,  ecm25 ,  gas1 ,  ilm1 ,  pea2 ,  sce66 ,  tpm1  and  YOR300W  1278 b mutants did not undergo filamentous growth on SLAD (Figure  3).	gene_phenotype
70389	5	333870	5	NULL	NULL	0	NULL	gas1	GP	homozygous;;mutant	does not undergo					filamentous growth	Process				NULL	SLAD	0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_192	15645503	Homozygous  bni1 ,  bud2 ,  cap2 ,  ecm25 ,  gas1 ,  ilm1 ,  pea2 ,  sce66 ,  tpm1  and  YOR300W  1278 b mutants did not undergo filamentous growth on SLAD (Figure  3).	gene_phenotype
70390	6	333870	5	NULL	NULL	0	NULL	ilm1	GP	homozygous;;mutant	does not undergo					filamentous growth	Process				NULL	SLAD	0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_192	15645503	Homozygous  bni1 ,  bud2 ,  cap2 ,  ecm25 ,  gas1 ,  ilm1 ,  pea2 ,  sce66 ,  tpm1  and  YOR300W  1278 b mutants did not undergo filamentous growth on SLAD (Figure  3).	gene_phenotype
70391	7	333870	5	NULL	NULL	0	NULL	pea2	GP	homozygous;;mutant	does not undergo					filamentous growth	Process				NULL	SLAD	0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_192	15645503	Homozygous  bni1 ,  bud2 ,  cap2 ,  ecm25 ,  gas1 ,  ilm1 ,  pea2 ,  sce66 ,  tpm1  and  YOR300W  1278 b mutants did not undergo filamentous growth on SLAD (Figure  3).	gene_phenotype
70392	8	333870	5	NULL	NULL	0	NULL	sce66	GP	homozygous;;mutant	does not undergo					filamentous growth	Process				NULL	SLAD	0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_192	15645503	Homozygous  bni1 ,  bud2 ,  cap2 ,  ecm25 ,  gas1 ,  ilm1 ,  pea2 ,  sce66 ,  tpm1  and  YOR300W  1278 b mutants did not undergo filamentous growth on SLAD (Figure  3).	gene_phenotype
70393	9	333870	5	NULL	NULL	0	NULL	tpm1	GP	homozygous;;mutant	does not undergo					filamentous growth	Process				NULL	SLAD	0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_192	15645503	Homozygous  bni1 ,  bud2 ,  cap2 ,  ecm25 ,  gas1 ,  ilm1 ,  pea2 ,  sce66 ,  tpm1  and  YOR300W  1278 b mutants did not undergo filamentous growth on SLAD (Figure  3).	gene_phenotype
70394	10	333870	5	NULL	NULL	0	NULL	YOR300W	NucleicAcid	homozygous;;mutant	does not undergo					filamentous growth	Process				NULL	SLAD	0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_192	15645503	Homozygous  bni1 ,  bud2 ,  cap2 ,  ecm25 ,  gas1 ,  ilm1 ,  pea2 ,  sce66 ,  tpm1  and  YOR300W  1278 b mutants did not undergo filamentous growth on SLAD (Figure  3).	gene_phenotype
70527	1	333871	5	NULL	NULL	0	NULL	ABP1	GP		regulates					actin cytoskeleton	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70528	2	333871	5	NULL	NULL	0	NULL	ABP1	GP		regulates					cell polarity	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70529	3	333871	5	NULL	NULL	0	NULL	BNI1	GP		regulates					actin cytoskeleton	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70530	4	333871	5	NULL	NULL	0	NULL	BNI1	GP		regulates					cell polarity	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70531	5	333871	5	NULL	NULL	0	NULL	BUD2	GP		regulates					actin cytoskeleton	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70532	6	333871	5	NULL	NULL	0	NULL	BUD2	GP		regulates					cell polarity	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70533	7	333871	5	NULL	NULL	0	NULL	CAP2	GP		regulates					actin cytoskeleton	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70534	8	333871	5	NULL	NULL	0	NULL	CAP2	GP		regulates					cell polarity	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70535	9	333871	5	NULL	NULL	0	NULL	PEA2	GP		regulates					actin cytoskeleton	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70536	10	333871	5	NULL	NULL	0	NULL	PEA2	GP		regulates					cell polarity	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70537	11	333871	5	NULL	NULL	NULL	NULL	SPA2	GP		regulates					actin cytoskeleton	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70538	12	333871	5	NULL	NULL	0	NULL	SPA2	GP		regulates					cell polarity	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70539	13	333871	5	NULL	NULL	0	NULL	TPM1	GP		regulates					actin cytoskeleton	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70540	14	333871	5	NULL	NULL	0	NULL	TPM1	GP		regulates					cell polarity	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70541	15	333871	5	NULL	NULL	0	NULL	YOR300W	NucleicAcid		regulates					actin cytoskeleton	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70542	16	333871	5	NULL	NULL	0	NULL	YOR300W	NucleicAcid		regulates					cell polarity	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70543	17	333871	5	NULL	NULL	0	NULL	ECM25	GP		regulates					cell wall	CellComponent	structure of			NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70544	18	333871	5	NULL	NULL	0	NULL	GAS1	GP		regulates					cell wall	CellComponent	structure of			NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70545	19	333871	5	NULL	NULL	0	NULL	PRS3	GP		regulates					cell wall	CellComponent	structure of			NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70546	20	333871	5	NULL	NULL	0	NULL	SEC66	GP		regulates					protein secretion	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70547	21	333871	5	NULL	NULL	0	NULL	RPL21A	GP		regulates					protein secretion	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70548	22	333871	5	NULL	NULL	0	NULL	RPL34B	GP		regulates					protein secretion	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70549	23	333871	5	NULL	NULL	0	NULL	ILM1	GP		regulates					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70550	24	333871	5	NULL	NULL	0	NULL	UGO1	GP		regulates					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_22_14_1143_s_31	16240455	The genes encode factors that regulate actin cytoskeleton/cell polarity ( ABP1, BNI1, BUD2, CAP2, PEA2, SPA2, TPM1 and YOR300W), cell wall structure and biosynthesis ( ECM25, GAS1 and  PRS3), protein secretion ( SEC66, RPL21A and  RPL34B) and mitochondria ( ILM1 and  UGO1).	gene_phenotype
70551	1	333872	5	NULL	NULL	0	NULL	ABP1	GP		regulates					actin cytoskeleton	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70552	2	333872	5	NULL	NULL	0	NULL	ABP1	GP		regulates					cell polarity	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70553	3	333872	5	NULL	NULL	0	NULL	CAP2	GP		regulates					actin cytoskeleton	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70554	4	333872	5	NULL	NULL	0	NULL	CAP2	GP		regulates					cell polarity	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70555	5	333872	5	NULL	NULL	0	NULL	HUF1	GP		regulates					actin cytoskeleton	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70556	6	333872	5	NULL	NULL	0	NULL	HUF1	GP		regulates					cell polarity	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70557	7	333872	5	NULL	NULL	0	NULL	YOR300W	NucleicAcid		is the locus name of					HUF1	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70558	8	333872	5	NULL	NULL	0	NULL	BNI1	GP		regulates					actin cytoskeleton	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70559	9	333872	5	NULL	NULL	0	NULL	BNI1	GP		regulates					cell polarity	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70560	10	333872	5	NULL	NULL	0	NULL	BUD2	GP		regulates					actin cytoskeleton	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70561	11	333872	5	NULL	NULL	0	NULL	BUD2	GP		regulates					cell polarity	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70562	12	333872	5	NULL	NULL	0	NULL	PEA2	GP		regulates					actin cytoskeleton	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70563	13	333872	5	NULL	NULL	0	NULL	PEA2	GP		regulates					cell polarity	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70564	14	333872	5	NULL	NULL	0	NULL	SPA2	GP		regulates					actin cytoskeleton	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70565	15	333872	5	NULL	NULL	0	NULL	SPA2	GP		regulates					cell polarity	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70566	16	333872	5	NULL	NULL	0	NULL	TPM1	GP		regulates					actin cytoskeleton	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70567	17	333872	5	NULL	NULL	0	NULL	TPM1	GP		regulates					cell polarity	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70568	18	333872	5	NULL	NULL	NULL	NULL	ECM25 gene	GP		is involved in		likely			cell wall	CellComponent	biosynthesis of			NULL		NULL	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70569	19	333872	5	NULL	NULL	0	NULL	GAS1 gene	GP		is involved in		likely			cell wall	CellComponent	biosynthesis of			NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70570	20	333872	5	NULL	NULL	NULL	NULL	PRS3 gene	GP		is involved in		likely			cell wall	CellComponent	biosynthesis of			NULL		NULL	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70571	21	333872	5	NULL	NULL	0	NULL	SEC66	GP		regulates		possibly			protein secretion	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70572	22	333872	5	NULL	NULL	0	NULL	RPL21A	GP		regulates		possibly			protein secretion	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70573	23	333872	5	NULL	NULL	0	NULL	RPL34B	GP		regulates		possibly			protein secretion	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70574	24	333872	5	NULL	NULL	0	NULL	IML1	GP		is involved in					mitochondria	CellComponent	normal function of			NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70575	25	333872	5	NULL	NULL	0	NULL	UGO1	GP		is involved in					mitochondria	CellComponent	normal function of			NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70576	26	333872	5	NULL	NULL	NULL	NULL	filamentous growth	Process	slow	is induced by					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70577	27	333872	5	NULL	NULL	NULL	NULL	ABP1 gene	GP		is required for					statement 26	Process				NULL		NULL	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70578	28	333872	5	NULL	NULL	NULL	NULL	ABP1 gene	GP		is required for					filamentous growth	Process	classic form of			NULL		NULL	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70579	29	333872	5	NULL	NULL	NULL	NULL	CAP2 gene	GP		is required for					statement 26	Process				NULL		NULL	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70580	30	333872	5	NULL	NULL	NULL	NULL	CAP2 gene	GP		is required for					filamentous growth	Process	classic form of			NULL		NULL	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70581	31	333872	5	NULL	NULL	NULL	NULL	HUF1 gene	GP		is required for					statement 26	Process				NULL		NULL	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70582	32	333872	5	NULL	NULL	NULL	NULL	HUF1 gene	GP		is required for					filamentous growth	Process	classic form of			NULL		NULL	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70583	33	333872	5	NULL	NULL	NULL	NULL	BNI1 gene	GP		is required for					statement 26	Process				NULL		NULL	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70584	34	333872	5	NULL	NULL	NULL	NULL	BNI1 gene	GP		is required for					filamentous growth	Process	classic form of			NULL		NULL	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70585	35	333872	5	NULL	NULL	NULL	NULL	BUD2 gene	GP		is required for					statement 26	Process				NULL		NULL	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70586	36	333872	5	NULL	NULL	NULL	NULL	BUD2 gene	GP		is required for					filamentous growth	Process	classic form of			NULL		NULL	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70587	37	333872	5	NULL	NULL	0	NULL	PEA2 gene	GP		is required for					statement 26	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70588	38	333872	5	NULL	NULL	0	NULL	PEA2 gene	GP		is required for					filamentous growth	Process	classic form of			NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70589	39	333872	5	NULL	NULL	0	NULL	SPA2 gene	GP		is required for					statement 26	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70590	40	333872	5	NULL	NULL	0	NULL	SPA2 gene	GP		is required for					filamentous growth	Process	classic form of			NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70591	41	333872	5	NULL	NULL	0	NULL	TPM1 gene	GP		is required for					statement 26	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70592	42	333872	5	NULL	NULL	0	NULL	TPM1 gene	GP		is required for					filamentous growth	Process	classic form of			NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70593	43	333872	5	NULL	NULL	0	NULL	ECM25 gene	GP		is required for					statement 26	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70594	44	333872	5	NULL	NULL	0	NULL	ECM25 gene	GP		is required for					filamentous growth	Process	classic form of			NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70595	45	333872	5	NULL	NULL	0	NULL	GAS1 gene	GP		is required for					statement 26	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70596	46	333872	5	NULL	NULL	0	NULL	GAS1 gene	GP		is required for					filamentous growth	Process	classic form of			NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70597	47	333872	5	NULL	NULL	0	NULL	PRS3 gene	GP		is required for					statement 26	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70598	48	333872	5	NULL	NULL	0	NULL	PRS3 gene	GP		is required for					filamentous growth	Process	classic form of			NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70599	49	333872	5	NULL	NULL	0	NULL	SEC66 gene	GP		is required for					statement 26	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70600	50	333872	5	NULL	NULL	0	NULL	SEC66 gene	GP		is required for					filamentous growth	Process	classic form of			NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70601	51	333872	5	NULL	NULL	0	NULL	RPL21A gene	GP		is required for					statement 26	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70602	52	333872	5	NULL	NULL	0	NULL	RPL21A gene	GP		is required for					filamentous growth	Process	classic form of			NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70603	53	333872	5	NULL	NULL	0	NULL	RPL34B gene	GP		is required for					statement 26	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70604	54	333872	5	NULL	NULL	0	NULL	RPL34B gene	GP		is required for					filamentous growth	Process	classic form of			NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70605	55	333872	5	NULL	NULL	0	NULL	IML1 gene	GP		is required for					statement 26	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70606	56	333872	5	NULL	NULL	0	NULL	IML1 gene	GP		is required for					filamentous growth	Process	classic form of			NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70607	57	333872	5	NULL	NULL	0	NULL	UGO1 gene	GP		is required for					statement 26	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70608	58	333872	5	NULL	NULL	0	NULL	UGO1 gene	GP		is required for					filamentous growth	Process	classic form of			NULL		0	NULL	NULL	NULL	gw70_yeast_22_2_79_s_3	15645503	We screened the BY yeast deletion strains and identified four classes of non-essential  genes that are required for both slowed DNA-induced filamentous growth and classic  forms of filamentous growth: (a) genes encoding regulators of the actin cytoskeleton  and cell polarity,  ABP1, CAP2 and  HUF1 (= YOR300W), in addition to the previously known  BNI1, BUD2, PEA2, SPA2 and  TPM1; (b) genes that are likely involved in cell wall biosynthesis,  ECM25, GAS1 and  PRS3; (c) genes encoding possible regulators of protein secretion,  SEC66, RPL21A and  RPL34B; (d) genes encoding factors for normal mitochondrial function,  IML1 and  UGO1.	gene_phenotype
70609	1	333873	5	NULL	NULL	NULL	NULL	sporulation	Process	defect in	is conferred by					cpr1delta/ cpr1delta	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_300	15643056	Thus, the sporulation defect conferred by a  cpr1delta/ cpr1delta mutation is suppressed by deletion of  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2.	gene_phenotype
70610	2	333873	5	NULL	NULL	0	NULL	SNT1	GP	deletion of	suppress					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_300	15643056	Thus, the sporulation defect conferred by a  cpr1delta/ cpr1delta mutation is suppressed by deletion of  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2.	gene_phenotype
70611	3	333873	5	NULL	NULL	0	NULL	SIF2	GP	deletion of	suppress					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_300	15643056	Thus, the sporulation defect conferred by a  cpr1delta/ cpr1delta mutation is suppressed by deletion of  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2.	gene_phenotype
70612	4	333873	5	NULL	NULL	0	NULL	YIL112W	NucleicAcid	deletion of	suppress					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_300	15643056	Thus, the sporulation defect conferred by a  cpr1delta/ cpr1delta mutation is suppressed by deletion of  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2.	gene_phenotype
70613	5	333873	5	NULL	NULL	0	NULL	SET3	GP	deletion of	suppress					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_300	15643056	Thus, the sporulation defect conferred by a  cpr1delta/ cpr1delta mutation is suppressed by deletion of  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2.	gene_phenotype
70614	6	333873	5	NULL	NULL	0	NULL	HOS2	GP	deletion of	suppress					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_300	15643056	Thus, the sporulation defect conferred by a  cpr1delta/ cpr1delta mutation is suppressed by deletion of  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2.	gene_phenotype
70615	1	333874	5	NULL	NULL	0	NULL	cpr1	GP	mutation of	effects		negatively			sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_303	15643056	Our data show that mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2 counteract the negative effects of the  cpr1 mutation on sporulation, providing genetic evidence that the physical interactions observed between Cpr1 and the Set3 complex are functional.	gene_phenotype
70616	2	333874	5	NULL	NULL	0	NULL	SNT1	GP	mutant	counteract					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_303	15643056	Our data show that mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2 counteract the negative effects of the  cpr1 mutation on sporulation, providing genetic evidence that the physical interactions observed between Cpr1 and the Set3 complex are functional.	gene_phenotype
70617	3	333874	5	NULL	NULL	0	NULL	SIF2	GP	mutant	counteract					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_303	15643056	Our data show that mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2 counteract the negative effects of the  cpr1 mutation on sporulation, providing genetic evidence that the physical interactions observed between Cpr1 and the Set3 complex are functional.	gene_phenotype
70618	4	333874	5	NULL	NULL	0	NULL	YIL112W	NucleicAcid	mutant	counteract					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_303	15643056	Our data show that mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2 counteract the negative effects of the  cpr1 mutation on sporulation, providing genetic evidence that the physical interactions observed between Cpr1 and the Set3 complex are functional.	gene_phenotype
70619	5	333874	5	NULL	NULL	0	NULL	SET3	GP	mutant	counteract					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_303	15643056	Our data show that mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2 counteract the negative effects of the  cpr1 mutation on sporulation, providing genetic evidence that the physical interactions observed between Cpr1 and the Set3 complex are functional.	gene_phenotype
70620	6	333874	5	NULL	NULL	0	NULL	HOS2	GP	mutant	counteract					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_303	15643056	Our data show that mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2 counteract the negative effects of the  cpr1 mutation on sporulation, providing genetic evidence that the physical interactions observed between Cpr1 and the Set3 complex are functional.	gene_phenotype
70621	7	333874	5	NULL	NULL	NULL	NULL	Cpr1	GP		interacts with		physically;;functionally			Set3 complex	GP				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_303	15643056	Our data show that mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2 counteract the negative effects of the  cpr1 mutation on sporulation, providing genetic evidence that the physical interactions observed between Cpr1 and the Set3 complex are functional.	gene_phenotype
70622	1	333875	5	NULL	NULL	0	NULL	SNT1	GP	mutant	enhances					sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_343	15643056	Another way to view this result is that deletion of  CPR1 partially counteracts the enhanced sporulation phenotype conferred by mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2, indicating that cyclophilin A is required for full expression of this phenotype and therefore plays a positive role in meiosis regulation outside of its physical interactions with the Set3 complex.	gene_phenotype
70623	2	333875	5	NULL	NULL	0	NULL	SIF2	GP	mutant	enhances					sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_343	15643056	Another way to view this result is that deletion of  CPR1 partially counteracts the enhanced sporulation phenotype conferred by mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2, indicating that cyclophilin A is required for full expression of this phenotype and therefore plays a positive role in meiosis regulation outside of its physical interactions with the Set3 complex.	gene_phenotype
70624	3	333875	5	NULL	NULL	0	NULL	YIL112W	NucleicAcid	mutant	enhances					sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_343	15643056	Another way to view this result is that deletion of  CPR1 partially counteracts the enhanced sporulation phenotype conferred by mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2, indicating that cyclophilin A is required for full expression of this phenotype and therefore plays a positive role in meiosis regulation outside of its physical interactions with the Set3 complex.	gene_phenotype
70625	4	333875	5	NULL	NULL	0	NULL	SET3	GP	mutant	enhances					sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_343	15643056	Another way to view this result is that deletion of  CPR1 partially counteracts the enhanced sporulation phenotype conferred by mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2, indicating that cyclophilin A is required for full expression of this phenotype and therefore plays a positive role in meiosis regulation outside of its physical interactions with the Set3 complex.	gene_phenotype
70626	5	333875	5	NULL	NULL	0	NULL	HOS2	GP	mutant	enhances					sporulation	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_343	15643056	Another way to view this result is that deletion of  CPR1 partially counteracts the enhanced sporulation phenotype conferred by mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2, indicating that cyclophilin A is required for full expression of this phenotype and therefore plays a positive role in meiosis regulation outside of its physical interactions with the Set3 complex.	gene_phenotype
70627	6	333875	5	NULL	NULL	0	NULL	CPR1	GP	deletion of	counteract		partially			statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_343	15643056	Another way to view this result is that deletion of  CPR1 partially counteracts the enhanced sporulation phenotype conferred by mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2, indicating that cyclophilin A is required for full expression of this phenotype and therefore plays a positive role in meiosis regulation outside of its physical interactions with the Set3 complex.	gene_phenotype
70628	7	333875	5	NULL	NULL	0	NULL	CPR1	GP	deletion of	counteract		partially			statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_343	15643056	Another way to view this result is that deletion of  CPR1 partially counteracts the enhanced sporulation phenotype conferred by mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2, indicating that cyclophilin A is required for full expression of this phenotype and therefore plays a positive role in meiosis regulation outside of its physical interactions with the Set3 complex.	gene_phenotype
70629	8	333875	5	NULL	NULL	0	NULL	CPR1	GP	deletion of	counteract		partially			statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_343	15643056	Another way to view this result is that deletion of  CPR1 partially counteracts the enhanced sporulation phenotype conferred by mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2, indicating that cyclophilin A is required for full expression of this phenotype and therefore plays a positive role in meiosis regulation outside of its physical interactions with the Set3 complex.	gene_phenotype
70630	9	333875	5	NULL	NULL	0	NULL	CPR1	GP	deletion of	counteract		partially			statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_343	15643056	Another way to view this result is that deletion of  CPR1 partially counteracts the enhanced sporulation phenotype conferred by mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2, indicating that cyclophilin A is required for full expression of this phenotype and therefore plays a positive role in meiosis regulation outside of its physical interactions with the Set3 complex.	gene_phenotype
70631	10	333875	5	NULL	NULL	0	NULL	CPR1	GP	deletion of	counteract		partially			statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_343	15643056	Another way to view this result is that deletion of  CPR1 partially counteracts the enhanced sporulation phenotype conferred by mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2, indicating that cyclophilin A is required for full expression of this phenotype and therefore plays a positive role in meiosis regulation outside of its physical interactions with the Set3 complex.	gene_phenotype
70632	11	333875	5	NULL	NULL	0	NULL	cyclophilin A	GP		is required for					sporulation	Process	full expression of			NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_343	15643056	Another way to view this result is that deletion of  CPR1 partially counteracts the enhanced sporulation phenotype conferred by mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2, indicating that cyclophilin A is required for full expression of this phenotype and therefore plays a positive role in meiosis regulation outside of its physical interactions with the Set3 complex.	gene_phenotype
70633	12	333875	5	NULL	NULL	NULL	NULL	CPR1	GP		regulates		positive			meiosis	Process				NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_343	15643056	Another way to view this result is that deletion of  CPR1 partially counteracts the enhanced sporulation phenotype conferred by mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2, indicating that cyclophilin A is required for full expression of this phenotype and therefore plays a positive role in meiosis regulation outside of its physical interactions with the Set3 complex.	gene_phenotype
70634	13	333875	5	NULL	NULL	0	NULL	CPR1	GP		interacts with		physically			Set3 complex	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_1_17_s_343	15643056	Another way to view this result is that deletion of  CPR1 partially counteracts the enhanced sporulation phenotype conferred by mutations in  SNT1,  SIF2,  YIL112W,  SET3, or  HOS2, indicating that cyclophilin A is required for full expression of this phenotype and therefore plays a positive role in meiosis regulation outside of its physical interactions with the Set3 complex.	gene_phenotype
70635	1	333877	5	NULL	NULL	0	NULL	YBR159w protein	GP		activates					3-ketoacyl-CoA reductase					NULL	yeast microsomes	0	NULL	NULL	NULL	gw70_jbiolchem_278_9_7335_s_43	12482854	The  YBR159w gene encoded the protein that was responsible for the majority of the 3-ketoacyl-CoA reductase activity in yeast microsomes ( ).	gene_phenotype
70636	1	333879	5	NULL	NULL	0	NULL	Ayr1p	GP		activates					3-ketoreductase	GP	residual			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_38_35440_s_10	12087109	By disrupting the orthologs of  Ybr159w in the  ybr159delta mutant we found that the  ybr159deltaayr1delta double mutant was inviable, suggesting that Ayr1p is responsible for the residual 3-ketoreductase activity.	gene_phenotype
70637	1	333883	5	NULL	NULL	0	NULL	YBR159w gene	GP	deletion of	slows					growth	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_38_35440_s_123	12087109	Deletion of the YBR159w Gene Causes Slow Growth, Suppression of the Ca2+-sensitive Phenotype Associated with the csg2delta Mutation, and Synthetic Lethality with the elo2delta Mutation-- The Ybr159p protein was previously shown to be required for C2 elongation of polyunsaturated fatty acids mediated by heterologous expression of a  C. elegans polyunsaturated fatty acid-elongating activity F56H11.4 activity in  S. cerevisiae ( 11).	gene_phenotype
70638	2	333883	5	NULL	NULL	0	NULL	Ca2+-sensitive phenotype	PhysicalPhenomenon	suppression of	is associated with					csg2delta	GP	mutant			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_38_35440_s_123	12087109	Deletion of the YBR159w Gene Causes Slow Growth, Suppression of the Ca2+-sensitive Phenotype Associated with the csg2delta Mutation, and Synthetic Lethality with the elo2delta Mutation-- The Ybr159p protein was previously shown to be required for C2 elongation of polyunsaturated fatty acids mediated by heterologous expression of a  C. elegans polyunsaturated fatty acid-elongating activity F56H11.4 activity in  S. cerevisiae ( 11).	gene_phenotype
70639	3	333883	5	NULL	NULL	0	NULL	lethality	Process	synthetic	is associated with					elo2delta	GP	mutant			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_38_35440_s_123	12087109	Deletion of the YBR159w Gene Causes Slow Growth, Suppression of the Ca2+-sensitive Phenotype Associated with the csg2delta Mutation, and Synthetic Lethality with the elo2delta Mutation-- The Ybr159p protein was previously shown to be required for C2 elongation of polyunsaturated fatty acids mediated by heterologous expression of a  C. elegans polyunsaturated fatty acid-elongating activity F56H11.4 activity in  S. cerevisiae ( 11).	gene_phenotype
70640	4	333883	5	NULL	NULL	0	NULL	polyunsaturated fatty acids	Chemical	C2 elongation of 	is mediated by					F56H11.4 activity	GP	C. elegans			NULL	S. cerevisiae	0	NULL	NULL	NULL	gw60_jbiolchem_277_38_35440_s_123	12087109	Deletion of the YBR159w Gene Causes Slow Growth, Suppression of the Ca2+-sensitive Phenotype Associated with the csg2delta Mutation, and Synthetic Lethality with the elo2delta Mutation-- The Ybr159p protein was previously shown to be required for C2 elongation of polyunsaturated fatty acids mediated by heterologous expression of a  C. elegans polyunsaturated fatty acid-elongating activity F56H11.4 activity in  S. cerevisiae ( 11).	gene_phenotype
70641	5	333883	5	NULL	NULL	0	NULL	Ybr159p protein	GP		is required for					statement 1	Process				NULL	S.cerevisiae	0	NULL	NULL	NULL	gw60_jbiolchem_277_38_35440_s_123	12087109	Deletion of the YBR159w Gene Causes Slow Growth, Suppression of the Ca2+-sensitive Phenotype Associated with the csg2delta Mutation, and Synthetic Lethality with the elo2delta Mutation-- The Ybr159p protein was previously shown to be required for C2 elongation of polyunsaturated fatty acids mediated by heterologous expression of a  C. elegans polyunsaturated fatty acid-elongating activity F56H11.4 activity in  S. cerevisiae ( 11).	gene_phenotype
70642	6	333883	5	NULL	NULL	0	NULL	F56H11.4	GP		is a synonym of					polyunsaturated fatty acid-elongating	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_38_35440_s_123	12087109	Deletion of the YBR159w Gene Causes Slow Growth, Suppression of the Ca2+-sensitive Phenotype Associated with the csg2delta Mutation, and Synthetic Lethality with the elo2delta Mutation-- The Ybr159p protein was previously shown to be required for C2 elongation of polyunsaturated fatty acids mediated by heterologous expression of a  C. elegans polyunsaturated fatty acid-elongating activity F56H11.4 activity in  S. cerevisiae ( 11).	gene_phenotype
70647	1	333884	5	NULL	NULL	0	NULL	snoRNAs	NucleicAcid		is					small nucleolar RNAs	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_pnas_103_32_11898_s_18	16882719	Similarly, many small nucleolar RNAs (snoRNAs) depend on the exosome during their maturation ( ,  ), and deletion of Rrp6p in yeast also leads to accumulation of extended forms of both polycistronic snoRNAs ( ) and the independently transcribed snoRNAs, such as snR33 and snR40 ( ).	gene_phenotype
70648	2	333884	5	NULL	NULL	NULL	NULL	snoRNAs	NucleicAcid		depends on					snoRNAs	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_32_11898_s_18	16882719	Similarly, many small nucleolar RNAs (snoRNAs) depend on the exosome during their maturation ( ,  ), and deletion of Rrp6p in yeast also leads to accumulation of extended forms of both polycistronic snoRNAs ( ) and the independently transcribed snoRNAs, such as snR33 and snR40 ( ).	gene_phenotype
70755	3	333884	5	NULL	NULL	0	NULL	statement 2	Process		occurs during					snoRNAs	NucleicAcid	maturation of			NULL		0	NULL	NULL	NULL	gw70_pnas_103_32_11898_s_18	16882719	Similarly, many small nucleolar RNAs (snoRNAs) depend on the exosome during their maturation ( ,  ), and deletion of Rrp6p in yeast also leads to accumulation of extended forms of both polycistronic snoRNAs ( ) and the independently transcribed snoRNAs, such as snR33 and snR40 ( ).	gene_phenotype
70756	4	333884	5	NULL	NULL	NULL	NULL	Rrp6p	GP	deletion of	accumulates					snoRNAs	NucleicAcid	extended forms of;;polycistronic			NULL	yeast	NULL	NULL	NULL	NULL	gw70_pnas_103_32_11898_s_18	16882719	Similarly, many small nucleolar RNAs (snoRNAs) depend on the exosome during their maturation ( ,  ), and deletion of Rrp6p in yeast also leads to accumulation of extended forms of both polycistronic snoRNAs ( ) and the independently transcribed snoRNAs, such as snR33 and snR40 ( ).	gene_phenotype
70757	5	333884	5	NULL	NULL	0	NULL	Rrp6p	GP	deletion of	accumulates					snR33As	NucleicAcid				NULL	yeast	0	NULL	NULL	NULL	gw70_pnas_103_32_11898_s_18	16882719	Similarly, many small nucleolar RNAs (snoRNAs) depend on the exosome during their maturation ( ,  ), and deletion of Rrp6p in yeast also leads to accumulation of extended forms of both polycistronic snoRNAs ( ) and the independently transcribed snoRNAs, such as snR33 and snR40 ( ).	gene_phenotype
70758	6	333884	5	NULL	NULL	0	NULL	Rrp6p	GP	deletion of	accumulates					snR40	NucleicAcid				NULL	yeast	0	NULL	NULL	NULL	gw70_pnas_103_32_11898_s_18	16882719	Similarly, many small nucleolar RNAs (snoRNAs) depend on the exosome during their maturation ( ,  ), and deletion of Rrp6p in yeast also leads to accumulation of extended forms of both polycistronic snoRNAs ( ) and the independently transcribed snoRNAs, such as snR33 and snR40 ( ).	gene_phenotype
70759	7	333884	5	NULL	NULL	0	NULL	snR33	NucleicAcid		is a type of					independently transcribed snoRNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_pnas_103_32_11898_s_18	16882719	Similarly, many small nucleolar RNAs (snoRNAs) depend on the exosome during their maturation ( ,  ), and deletion of Rrp6p in yeast also leads to accumulation of extended forms of both polycistronic snoRNAs ( ) and the independently transcribed snoRNAs, such as snR33 and snR40 ( ).	gene_phenotype
70760	8	333884	5	NULL	NULL	0	NULL	snR40	NucleicAcid		is a type of					independently transcribed snoRNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_pnas_103_32_11898_s_18	16882719	Similarly, many small nucleolar RNAs (snoRNAs) depend on the exosome during their maturation ( ,  ), and deletion of Rrp6p in yeast also leads to accumulation of extended forms of both polycistronic snoRNAs ( ) and the independently transcribed snoRNAs, such as snR33 and snR40 ( ).	gene_phenotype
70761	1	333885	5	NULL	NULL	0	NULL	YKR079C gene	GP		is indispensable for					yeast	Cell	viability of			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_9_2272_s_177	12711671	The  YKR079C gene has been shown to be indispensable for yeast viability ( 1), suggesting that the yeast genome may have only one gene that encodes an enzyme responsible for correctly removing 3' trailers from pre-tRNAs.	gene_phenotype
70762	1	333886	5	NULL	NULL	0	NULL	ELAC1	GP	human	activates		possibly			tRNA 3'	NucleicAcid	processing of			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_9_2272_s_136	12711671	To examine whether ELAC1 has also the tRNA 3' processing activity as ELAC2-deltaN, we cloned a human cDNA encoding ELAC1 into the plasmid pGEX-4T-3, and expressed and purified the GST - ELAC1 fusion protein as described for GST - YKR079C (Fig.  2).	gene_phenotype
70763	2	333886	5	NULL	NULL	0	NULL	ELAC2-deltaN	GP		activates					tRNA 3'	NucleicAcid	processing of			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_31_9_2272_s_136	12711671	To examine whether ELAC1 has also the tRNA 3' processing activity as ELAC2-deltaN, we cloned a human cDNA encoding ELAC1 into the plasmid pGEX-4T-3, and expressed and purified the GST - ELAC1 fusion protein as described for GST - YKR079C (Fig.  2).	gene_phenotype
70764	1	333888	5	NULL	NULL	0	NULL	MAPK pathway	Process		is regulated by					PKC	GP				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_49	10657304	MPK1,  MLP1,  RLM1, and  YLR194C were induced under conditions that activate the PKC-regulated MAPK pathway;  KSS1,  YLRO42C,  PGU1, and  SVS1 are potential filamentous growth genes induced preferentially by Kss1p signaling.	gene_phenotype
70765	2	333888	5	NULL	NULL	0	NULL	KSS1	GP		is induced by		preferentially			Kss1p signaling	Process				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_49	10657304	MPK1,  MLP1,  RLM1, and  YLR194C were induced under conditions that activate the PKC-regulated MAPK pathway;  KSS1,  YLRO42C,  PGU1, and  SVS1 are potential filamentous growth genes induced preferentially by Kss1p signaling.	gene_phenotype
70768	3	333888	5	NULL	NULL	0	NULL	YLRO42C	NucleicAcid		is induced by		preferentially			Kss1p signaling	Process				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_49	10657304	MPK1,  MLP1,  RLM1, and  YLR194C were induced under conditions that activate the PKC-regulated MAPK pathway;  KSS1,  YLRO42C,  PGU1, and  SVS1 are potential filamentous growth genes induced preferentially by Kss1p signaling.	gene_phenotype
70769	4	333888	5	NULL	NULL	0	NULL	PGU1	GP		is induced by		preferentially			Kss1p signaling	Process				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_49	10657304	MPK1,  MLP1,  RLM1, and  YLR194C were induced under conditions that activate the PKC-regulated MAPK pathway;  KSS1,  YLRO42C,  PGU1, and  SVS1 are potential filamentous growth genes induced preferentially by Kss1p signaling.	gene_phenotype
70770	5	333888	5	NULL	NULL	0	NULL	SVS1	GP		is induced by		preferentially			Kss1p signaling	Process				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_49	10657304	MPK1,  MLP1,  RLM1, and  YLR194C were induced under conditions that activate the PKC-regulated MAPK pathway;  KSS1,  YLRO42C,  PGU1, and  SVS1 are potential filamentous growth genes induced preferentially by Kss1p signaling.	gene_phenotype
70773	6	333888	5	NULL	NULL	0	NULL	KSS1	GP		is a type of					filamentous growth gene	GP	potential			NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_49	10657304	MPK1,  MLP1,  RLM1, and  YLR194C were induced under conditions that activate the PKC-regulated MAPK pathway;  KSS1,  YLRO42C,  PGU1, and  SVS1 are potential filamentous growth genes induced preferentially by Kss1p signaling.	gene_phenotype
70774	7	333888	5	NULL	NULL	0	NULL	YLRO42C	GP		is a type of					filamentous growth gene	GP	potential			NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_49	10657304	MPK1,  MLP1,  RLM1, and  YLR194C were induced under conditions that activate the PKC-regulated MAPK pathway;  KSS1,  YLRO42C,  PGU1, and  SVS1 are potential filamentous growth genes induced preferentially by Kss1p signaling.	gene_phenotype
70775	8	333888	5	NULL	NULL	0	NULL	PGU1	GP		is a type of					filamentous growth gene	GP	potential			NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_49	10657304	MPK1,  MLP1,  RLM1, and  YLR194C were induced under conditions that activate the PKC-regulated MAPK pathway;  KSS1,  YLRO42C,  PGU1, and  SVS1 are potential filamentous growth genes induced preferentially by Kss1p signaling.	gene_phenotype
70776	9	333888	5	NULL	NULL	0	NULL	SVS1	GP		is a type of					filamentous growth gene	GP	potential			NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_49	10657304	MPK1,  MLP1,  RLM1, and  YLR194C were induced under conditions that activate the PKC-regulated MAPK pathway;  KSS1,  YLRO42C,  PGU1, and  SVS1 are potential filamentous growth genes induced preferentially by Kss1p signaling.	gene_phenotype
70777	1	333890	5	NULL	NULL	0	NULL	Prp40p	GP		contains					NESs	AminoAcid	redundant			NULL		0	NULL	NULL	NULL	gw70_genetics_166_1_53_s_11	15020406	Although we do not expect that yeast snRNPs undergo compartmentalized biogenesis like their metazoan counterparts, our results suggest that Prp40p and Ynl187wp contain redundant NESs that aid in an important, Crm1p-mediated nuclear export event.	gene_phenotype
70778	2	333890	5	NULL	NULL	0	NULL	Ynl187wp	NucleicAcid		contains					NESs	AminoAcid	redundant			NULL		0	NULL	NULL	NULL	gw70_genetics_166_1_53_s_11	15020406	Although we do not expect that yeast snRNPs undergo compartmentalized biogenesis like their metazoan counterparts, our results suggest that Prp40p and Ynl187wp contain redundant NESs that aid in an important, Crm1p-mediated nuclear export event.	gene_phenotype
70779	3	333890	5	NULL	NULL	0	NULL	nuclear export	Process		is mediated by					Crm1p	GP				NULL		0	NULL	NULL	NULL	gw70_genetics_166_1_53_s_11	15020406	Although we do not expect that yeast snRNPs undergo compartmentalized biogenesis like their metazoan counterparts, our results suggest that Prp40p and Ynl187wp contain redundant NESs that aid in an important, Crm1p-mediated nuclear export event.	gene_phenotype
70780	4	333890	5	NULL	NULL	0	NULL	NESs	AminoAcid	redundant	aid in					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_genetics_166_1_53_s_11	15020406	Although we do not expect that yeast snRNPs undergo compartmentalized biogenesis like their metazoan counterparts, our results suggest that Prp40p and Ynl187wp contain redundant NESs that aid in an important, Crm1p-mediated nuclear export event.	gene_phenotype
70781	1	333891	5	NULL	NULL	0	NULL	nuclear export	Process		is mediated by					Crm1p	GP				NULL		0	NULL	NULL	NULL	gw70_genetics_166_1_53_s_408	15020406	Together our results suggest a model in which Prp40p and Ynl187wp contain redundant, functional leucine-rich nuclear export signals that aid in a Crm1p-mediated nuclear export event.	gene_phenotype
70782	2	333891	5	NULL	NULL	0	NULL	Prp40p	GP		contains					leucine-rich nuclear export signals	AminoAcid	redundant;;functional			NULL		0	NULL	NULL	NULL	gw70_genetics_166_1_53_s_408	15020406	Together our results suggest a model in which Prp40p and Ynl187wp contain redundant, functional leucine-rich nuclear export signals that aid in a Crm1p-mediated nuclear export event.	gene_phenotype
70783	3	333891	5	NULL	NULL	0	NULL	Ynl187wp	NucleicAcid		contains					leucine-rich nuclear export signals	AminoAcid	redundant;;functional			NULL		0	NULL	NULL	NULL	gw70_genetics_166_1_53_s_408	15020406	Together our results suggest a model in which Prp40p and Ynl187wp contain redundant, functional leucine-rich nuclear export signals that aid in a Crm1p-mediated nuclear export event.	gene_phenotype
70784	4	333891	5	NULL	NULL	0	NULL	leucine-rich nuclear export signals	AminoAcid	redundant;;functional	aid in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_genetics_166_1_53_s_408	15020406	Together our results suggest a model in which Prp40p and Ynl187wp contain redundant, functional leucine-rich nuclear export signals that aid in a Crm1p-mediated nuclear export event.	gene_phenotype
70785	1	333892	5	NULL	NULL	NULL	NULL	NESs	AminoAcid		is mutated in					prp40delta	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_genetics_166_1_53_s_357	15020406	Mutation of both NESs ( prp40delta 2 ynl187w-slf) would thus result in the loss of nuclear export of a complex.	gene_phenotype
70786	2	333892	5	NULL	NULL	NULL	NULL	NESs	AminoAcid		is mutated in					ynl187w-slf	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_genetics_166_1_53_s_357	15020406	Mutation of both NESs ( prp40delta 2 ynl187w-slf) would thus result in the loss of nuclear export of a complex.	gene_phenotype
70787	3	333892	5	NULL	NULL	NULL	NULL	statement 1	Process		results in					nuclear export	Process	loss of			NULL		NULL	NULL	NULL	NULL	gw70_genetics_166_1_53_s_357	15020406	Mutation of both NESs ( prp40delta 2 ynl187w-slf) would thus result in the loss of nuclear export of a complex.	gene_phenotype
70788	4	333892	5	NULL	NULL	NULL	NULL	statement 2	Process		results in					nuclear export	Process	loss of			NULL		NULL	NULL	NULL	NULL	gw70_genetics_166_1_53_s_357	15020406	Mutation of both NESs ( prp40delta 2 ynl187w-slf) would thus result in the loss of nuclear export of a complex.	gene_phenotype
70789	1	333893	5	NULL	NULL	0	NULL	SUL1 gene	GP		is involved in					sulphate	Chemical	uptake of			NULL		0	NULL	NULL	NULL	gw70_yeast_19_6_475_s_42	11921096	Three genes are involved in sulphate uptake:  SUL1 and  SUL2 encoding high-affinity sulphate transport proteins, and  SUL3 encoding a factor involved in the transcriptional regulation of  SUL2 (Cherest  et al., [ 1997]).	gene_phenotype
70790	2	333893	5	NULL	NULL	0	NULL	SUL2 gene	GP		is involved in					sulphate	Chemical	uptake of			NULL		0	NULL	NULL	NULL	gw70_yeast_19_6_475_s_42	11921096	Three genes are involved in sulphate uptake:  SUL1 and  SUL2 encoding high-affinity sulphate transport proteins, and  SUL3 encoding a factor involved in the transcriptional regulation of  SUL2 (Cherest  et al., [ 1997]).	gene_phenotype
70791	3	333893	5	NULL	NULL	0	NULL	SUL3 gene	GP		is involved in					sulphate	Chemical	uptake of			NULL		0	NULL	NULL	NULL	gw70_yeast_19_6_475_s_42	11921096	Three genes are involved in sulphate uptake:  SUL1 and  SUL2 encoding high-affinity sulphate transport proteins, and  SUL3 encoding a factor involved in the transcriptional regulation of  SUL2 (Cherest  et al., [ 1997]).	gene_phenotype
70792	4	333893	5	NULL	NULL	0	NULL	SUL1 gene	GP		encodes for					sulphate transport proteins	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_19_6_475_s_42	11921096	Three genes are involved in sulphate uptake:  SUL1 and  SUL2 encoding high-affinity sulphate transport proteins, and  SUL3 encoding a factor involved in the transcriptional regulation of  SUL2 (Cherest  et al., [ 1997]).	gene_phenotype
70793	5	333893	5	NULL	NULL	NULL	NULL	SUL2 gene	GP		encodes for					sulphate transport proteins	GP				NULL		NULL	NULL	NULL	NULL	gw70_yeast_19_6_475_s_42	11921096	Three genes are involved in sulphate uptake:  SUL1 and  SUL2 encoding high-affinity sulphate transport proteins, and  SUL3 encoding a factor involved in the transcriptional regulation of  SUL2 (Cherest  et al., [ 1997]).	gene_phenotype
70794	6	333893	5	NULL	NULL	0	NULL	SUL3 gene	GP		is involved in					SUL2	GP	transcriptional regulation of			NULL		0	NULL	NULL	NULL	gw70_yeast_19_6_475_s_42	11921096	Three genes are involved in sulphate uptake:  SUL1 and  SUL2 encoding high-affinity sulphate transport proteins, and  SUL3 encoding a factor involved in the transcriptional regulation of  SUL2 (Cherest  et al., [ 1997]).	gene_phenotype
70795	1	333894	5	NULL	NULL	0	NULL	YOL002c protein	GP		accumulates					polyphosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_22_19609_s_231	11916977	The YOL002c Protein Is Involved in Polyphosphate Accumulation and in Regulation of Acid Phosphatase Activity-- Polyphosphate is a linear polymer of up to hundreds of Pi residues linked by phosphoanhydride bonds.	gene_phenotype
70796	2	333894	5	NULL	NULL	0	NULL	YOL002c protein	GP		regulates					acid phosphatase activity	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_22_19609_s_231	11916977	The YOL002c Protein Is Involved in Polyphosphate Accumulation and in Regulation of Acid Phosphatase Activity-- Polyphosphate is a linear polymer of up to hundreds of Pi residues linked by phosphoanhydride bonds.	gene_phenotype
70797	3	333894	5	NULL	NULL	0	NULL	Pi residues	Chemical	hundreds of	is linked by					phosphoanhydride bonds	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_22_19609_s_231	11916977	The YOL002c Protein Is Involved in Polyphosphate Accumulation and in Regulation of Acid Phosphatase Activity-- Polyphosphate is a linear polymer of up to hundreds of Pi residues linked by phosphoanhydride bonds.	gene_phenotype
70798	4	333894	5	NULL	NULL	0	NULL	polyphosphate	Chemical		is a polymer of		linear			statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_22_19609_s_231	11916977	The YOL002c Protein Is Involved in Polyphosphate Accumulation and in Regulation of Acid Phosphatase Activity-- Polyphosphate is a linear polymer of up to hundreds of Pi residues linked by phosphoanhydride bonds.	gene_phenotype
70799	1	333895	5	NULL	NULL	0	NULL	YOL002c	NucleicAcid	deletion of	derepress					acid phosphatase activity	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_22_19609_s_284	11916977	Because deletion of  YOL002c results in a strain that is incapable of derepressing acid phosphatase activity ( i.e. constitutive  PHO5 expression), it is possible that this protein plays a similar role to that of Pho23p.	gene_phenotype
70800	2	333895	5	NULL	NULL	0	NULL	YOL002c protein	GP	role of	is similar to					Pho23p	GP	role of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_22_19609_s_284	11916977	Because deletion of  YOL002c results in a strain that is incapable of derepressing acid phosphatase activity ( i.e. constitutive  PHO5 expression), it is possible that this protein plays a similar role to that of Pho23p.	gene_phenotype
70801	2	333896	5	NULL	NULL	0	NULL	Yjl103c protein	GP		interacts with					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_7_553_s_261	16710832	The Yjl103c protein interacts (Hazbun  et al., [ 2003]) with the products of genes involved in nuclear positioning ( p < 5.0 x 10-3).	gene_phenotype
70802	1	333896	5	NULL	NULL	0	NULL	gene products	GP		is involved in					nucleus	CellComponent	positioning of			NULL		0	NULL	NULL	NULL	gw70_yeast_23_7_553_s_261	16710832	The Yjl103c protein interacts (Hazbun  et al., [ 2003]) with the products of genes involved in nuclear positioning ( p < 5.0 x 10-3).	gene_phenotype
70803	1	333897	5	NULL	NULL	NULL	NULL	YJL103c	NucleicAcid		is involved in		possibly			oxidative phosphorylation	Process				NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_7_553_s_129	16710832	Only one unknown ORF was detected to be downregulated due to the  hap4 deletion (YJL103c); this already has a biological term annotation (oxidative phosphorylation)  which rests on indirect evidence.	gene_phenotype
70804	1	333898	5	NULL	NULL	0	NULL	YJL103c product	GP		is involved in		possibly			oxidative phosphorylation	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_7_553_s_262	16710832	The product of YJL103c was recently annotated to be involved in oxidative phosphorylation,  as inferred by sequence and structure similarity (Deng  et al., [ 2005]), and was defined as a zinc cluster protein by phenotype screening (Akache  et al., [ 2001]).	gene_phenotype
70805	2	333898	5	NULL	NULL	0	NULL	YJL103c product	GP		is a type of					zinc cluster protein	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_7_553_s_262	16710832	The product of YJL103c was recently annotated to be involved in oxidative phosphorylation,  as inferred by sequence and structure similarity (Deng  et al., [ 2005]), and was defined as a zinc cluster protein by phenotype screening (Akache  et al., [ 2001]).	gene_phenotype
70806	1	333901	5	NULL	NULL	NULL	NULL	Sen1p	GP	inactivation of	leads to					RNA	NucleicAcid	altered accumulation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_443	9819377	In addition, other RNAs have recently been shown to exhibit altered accumulation upon inactivation of Sen1p, including RNAs of unexpected size containing U5, snR40, and snR45 sequences ( 39).	gene_phenotype
70807	1	333903	5	NULL	NULL	0	NULL	YDR533Cp	NucleicAcid		is related to					Hsp31	GP	Escherichia coli			NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1531_s_6	14745011	The structure indicates that the closest relative to YDR533Cp is the  Escherichia coli heat shock protein Hsp31 (YedU), which has both chaperone and protease activity.	gene_phenotype
70808	2	333903	5	NULL	NULL	0	NULL	Hsp31	GP		is a type of					heat shock protein	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1531_s_6	14745011	The structure indicates that the closest relative to YDR533Cp is the  Escherichia coli heat shock protein Hsp31 (YedU), which has both chaperone and protease activity.	gene_phenotype
70809	3	333903	5	NULL	NULL	0	NULL	YedU	GP		is a synonym of					Hsp31	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1531_s_6	14745011	The structure indicates that the closest relative to YDR533Cp is the  Escherichia coli heat shock protein Hsp31 (YedU), which has both chaperone and protease activity.	gene_phenotype
70810	4	333903	5	NULL	NULL	0	NULL	Hsp31	GP		activates					chaperone	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1531_s_6	14745011	The structure indicates that the closest relative to YDR533Cp is the  Escherichia coli heat shock protein Hsp31 (YedU), which has both chaperone and protease activity.	gene_phenotype
70811	5	333903	5	NULL	NULL	0	NULL	Hsp31	GP		activates					protease	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1531_s_6	14745011	The structure indicates that the closest relative to YDR533Cp is the  Escherichia coli heat shock protein Hsp31 (YedU), which has both chaperone and protease activity.	gene_phenotype
70812	1	333908	5	NULL	NULL	NULL	NULL	YNR022c gene	GP		plays a role in					growth	Process				NULL		NULL	NULL	NULL	NULL	gw70_yeast_19_7_587_s_191	11967829	To our knowledge, this is the first report that  the  YNR022c and  YCR079w genes play some role in the growth at low and high temperatures, although the temperature-sensitive  growth of the  ptc1 disruptant has been reported previously (Maeda  et al., [ 1993]).	gene_phenotype
70813	2	333908	5	NULL	NULL	0	NULL	YCR079w gene	GP		plays a role in					growth	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_19_7_587_s_191	11967829	To our knowledge, this is the first report that  the  YNR022c and  YCR079w genes play some role in the growth at low and high temperatures, although the temperature-sensitive  growth of the  ptc1 disruptant has been reported previously (Maeda  et al., [ 1993]).	gene_phenotype
70814	1	333910	5	NULL	NULL	NULL	NULL	Yjl200c protein	GP		activates		probably			aconitate hydratase	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_3_762_s_203	16428434	For the protein Yjl200c, an uncharacterized open reading frame with postulated aconitate hydratase activity, an involvement in TCA cycle reactions seems plausible.	gene_phenotype
70815	2	333910	5	NULL	NULL	0	NULL	Yjl200c protein	GP		is involved in		probably			TCA cycle reactions	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_3_762_s_203	16428434	For the protein Yjl200c, an uncharacterized open reading frame with postulated aconitate hydratase activity, an involvement in TCA cycle reactions seems plausible.	gene_phenotype
70816	1	333911	5	NULL	NULL	0	NULL	YJL200c 	NucleicAcid		activates		possibly			aconitate hydratase	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_7_553_s_272	16710832	YJL200c was annotated with the term  aconitate hydratase activity  by sequence homology (Tatusov  et al., [ 2000]) and the location of its protein in the mitochondrion has been determined by direct  assay	gene_phenotype
70817	2	333911	5	NULL	NULL	0	NULL	Yjl200c protein	GP		is located in					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_23_7_553_s_272	16710832	YJL200c was annotated with the term  aconitate hydratase activity  by sequence homology (Tatusov  et al., [ 2000]) and the location of its protein in the mitochondrion has been determined by direct  assay	gene_phenotype
70818	1	333912	5	NULL	NULL	0	NULL	YGR284c	NucleicAcid		is the locus name of					ERV29	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_246	15334557	ERV29   YGR284c ER-Golgi transport vesicle protein	gene_phenotype
70819	2	333912	5	NULL	NULL	0	NULL	ERV29	GP		is a type of					ER-Golgi transport vesicle protein	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_21_11_927_s_246	15334557	ERV29   YGR284c ER-Golgi transport vesicle protein	gene_phenotype
70820	1	333915	5	NULL	NULL	0	NULL	YLR151c protein	GP		is a homolog of		functional			MutT	GP	S.cerevisiae			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_18_5339_s_136	15475388	Purification of recombinant YLR151c protein and pyrophosphatase activity for the oxidized  deoxyribonucleotide triphosphates   Our observations from genetic approach strongly suggest that YLR151c is one of the important candidates for a functional homologue of MutT in  S.cerevisiae.	gene_phenotype
70821	1	333923	5	NULL	NULL	0	NULL	YLR151c	NucleicAcid		activates					pyrophosphatase	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_18_5339_s_179	15475388	Effects of pH (left) and salt concentration (right) in the reaction mixture on pyrophosphatase  activity of YLR151c against 8-oxo-dGTP: 20 muM 8-oxo-dGTP was treated with 75 nM  GST-YLR151c fusion protein at 30 degrees C for 60 min at various pH and various salt  concentrations.	gene_phenotype
70822	1	333924	5	NULL	NULL	NULL	NULL	PCD1	GP	S. cerevisiae	is a type of					nudix hydrolase gene	GP	S. cerevisiae			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_17	10922370	Here we show that the fifth  S. cerevisiae nudix hydrolase gene,  PCD1 (ORF YLR151C) on chromosome XII, encodes a protein with an entirely new enzyme activity: a  peroxisomal  coenzyme A  diphosphatase, Pcd1p, that cleaves 3''-phosphoadenosine 5''-monophosphate (3'',5''-ADP) from coenzyme A and CoA derivatives.	gene_phenotype
70823	2	333924	5	NULL	NULL	NULL	NULL	YLR151C	NucleicAcid	S. cerevisiae	is a type of					ORF	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_17	10922370	Here we show that the fifth  S. cerevisiae nudix hydrolase gene,  PCD1 (ORF YLR151C) on chromosome XII, encodes a protein with an entirely new enzyme activity: a  peroxisomal  coenzyme A  diphosphatase, Pcd1p, that cleaves 3''-phosphoadenosine 5''-monophosphate (3'',5''-ADP) from coenzyme A and CoA derivatives.	gene_phenotype
70824	3	333924	5	NULL	NULL	NULL	NULL	YLR151C	NucleicAcid	S. cerevisiae	is the locus name of					PCD1	GP	S.cerevisiae			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_17	10922370	Here we show that the fifth  S. cerevisiae nudix hydrolase gene,  PCD1 (ORF YLR151C) on chromosome XII, encodes a protein with an entirely new enzyme activity: a  peroxisomal  coenzyme A  diphosphatase, Pcd1p, that cleaves 3''-phosphoadenosine 5''-monophosphate (3'',5''-ADP) from coenzyme A and CoA derivatives.	gene_phenotype
70825	4	333924	5	NULL	NULL	NULL	NULL	YLR151C	NucleicAcid	S. cerevisiae	is located in					chromosome XII	Chromosome	S.cerevisiae			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_17	10922370	Here we show that the fifth  S. cerevisiae nudix hydrolase gene,  PCD1 (ORF YLR151C) on chromosome XII, encodes a protein with an entirely new enzyme activity: a  peroxisomal  coenzyme A  diphosphatase, Pcd1p, that cleaves 3''-phosphoadenosine 5''-monophosphate (3'',5''-ADP) from coenzyme A and CoA derivatives.	gene_phenotype
70826	5	333924	5	NULL	NULL	NULL	NULL	YLR151C	NucleicAcid	S. cerevisiae	encodes for					peroxisomal coenzyme A diphosphatase	GP	S.cerevisiae			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_17	10922370	Here we show that the fifth  S. cerevisiae nudix hydrolase gene,  PCD1 (ORF YLR151C) on chromosome XII, encodes a protein with an entirely new enzyme activity: a  peroxisomal  coenzyme A  diphosphatase, Pcd1p, that cleaves 3''-phosphoadenosine 5''-monophosphate (3'',5''-ADP) from coenzyme A and CoA derivatives.	gene_phenotype
70827	6	333924	5	NULL	NULL	0	NULL	peroxisomal coenzyme A diphosphatase	GP	S. cerevisiae	is a synonym of					Pcd1p	GP	S.cerevisiae			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_17	10922370	Here we show that the fifth  S. cerevisiae nudix hydrolase gene,  PCD1 (ORF YLR151C) on chromosome XII, encodes a protein with an entirely new enzyme activity: a  peroxisomal  coenzyme A  diphosphatase, Pcd1p, that cleaves 3''-phosphoadenosine 5''-monophosphate (3'',5''-ADP) from coenzyme A and CoA derivatives.	gene_phenotype
70828	7	333924	5	NULL	NULL	0	NULL	3'',5''-ADP	Chemical		is					3''-phosphoadenosine 5''-monophosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_17	10922370	Here we show that the fifth  S. cerevisiae nudix hydrolase gene,  PCD1 (ORF YLR151C) on chromosome XII, encodes a protein with an entirely new enzyme activity: a  peroxisomal  coenzyme A  diphosphatase, Pcd1p, that cleaves 3''-phosphoadenosine 5''-monophosphate (3'',5''-ADP) from coenzyme A and CoA derivatives.	gene_phenotype
70829	8	333924	5	NULL	NULL	0	NULL	3'',5''-ADP	Chemical		is cleaved from					coenzyme A 	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_17	10922370	Here we show that the fifth  S. cerevisiae nudix hydrolase gene,  PCD1 (ORF YLR151C) on chromosome XII, encodes a protein with an entirely new enzyme activity: a  peroxisomal  coenzyme A  diphosphatase, Pcd1p, that cleaves 3''-phosphoadenosine 5''-monophosphate (3'',5''-ADP) from coenzyme A and CoA derivatives.	gene_phenotype
70830	9	333924	5	NULL	NULL	0	NULL	3'',5''-ADP	Chemical		is cleaved from					CoA derivatives	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_17	10922370	Here we show that the fifth  S. cerevisiae nudix hydrolase gene,  PCD1 (ORF YLR151C) on chromosome XII, encodes a protein with an entirely new enzyme activity: a  peroxisomal  coenzyme A  diphosphatase, Pcd1p, that cleaves 3''-phosphoadenosine 5''-monophosphate (3'',5''-ADP) from coenzyme A and CoA derivatives.	gene_phenotype
70831	10	333924	5	NULL	NULL	NULL	NULL	Pcd1p	GP	S. cerevisiae	catalyzes					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_17	10922370	Here we show that the fifth  S. cerevisiae nudix hydrolase gene,  PCD1 (ORF YLR151C) on chromosome XII, encodes a protein with an entirely new enzyme activity: a  peroxisomal  coenzyme A  diphosphatase, Pcd1p, that cleaves 3''-phosphoadenosine 5''-monophosphate (3'',5''-ADP) from coenzyme A and CoA derivatives.	gene_phenotype
70832	11	333924	5	NULL	NULL	0	NULL	Pcd1p	GP	S. cerevisiae	catalyzes					statement 9	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_42_32925_s_17	10922370	Here we show that the fifth  S. cerevisiae nudix hydrolase gene,  PCD1 (ORF YLR151C) on chromosome XII, encodes a protein with an entirely new enzyme activity: a  peroxisomal  coenzyme A  diphosphatase, Pcd1p, that cleaves 3''-phosphoadenosine 5''-monophosphate (3'',5''-ADP) from coenzyme A and CoA derivatives.	gene_phenotype
70833	1	333925	5	NULL	NULL	0	NULL	pheromone	GP	treatment of wt cells	increases					PGU1	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_115	10657304	PGU1 and  YLR042c also showed increased expression after pheromone treatment of wt cells ( Fig. 2B), which suggests overlap between the mating and filamentation responses.	gene_phenotype
70834	2	333925	5	NULL	NULL	0	NULL	pheromone	GP	treatment of wt cells	increases					YLR042c	NucleicAcid	expression of			NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_115	10657304	PGU1 and  YLR042c also showed increased expression after pheromone treatment of wt cells ( Fig. 2B), which suggests overlap between the mating and filamentation responses.	gene_phenotype
70835	3	333925	5	NULL	NULL	0	NULL	mating response	Process		overlaps with					filamentation response	Process				NULL		0	NULL	NULL	NULL	gw60_science_287_5454_873_s_115	10657304	PGU1 and  YLR042c also showed increased expression after pheromone treatment of wt cells ( Fig. 2B), which suggests overlap between the mating and filamentation responses.	gene_phenotype
70836	1	333927	5	NULL	NULL	0	NULL	FLO11	GP		doet not corelate with					invasive growth 	Process				NULL		0	NULL	NULL	NULL	gw70_genetics_165_3_997_s_301	14668360	For example, a genome-wide analysis of  TEC1-regulated genes in haploids  vs. diploids revealed just two common genes,  FLO11 and  YLR042C, both of which fail to correlate with invasive growth in other circumstances ( MADHANI et al. 1999  ;   PALECEK  et al. 2000  ).	gene_phenotype
70837	2	333927	5	NULL	NULL	0	NULL	YLR042C	NucleicAcid		doet not corelate with					invasive growth	Process				NULL		0	NULL	NULL	NULL	gw70_genetics_165_3_997_s_301	14668360	For example, a genome-wide analysis of  TEC1-regulated genes in haploids  vs. diploids revealed just two common genes,  FLO11 and  YLR042C, both of which fail to correlate with invasive growth in other circumstances ( MADHANI et al. 1999  ;   PALECEK  et al. 2000  ).	gene_phenotype
70838	1	333930	5	NULL	NULL	0	NULL	Campylobacter	Organism		infects					human	Organism				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_19_20327_s_10	14985343	Campylobacter infection in humans occurs primarily through the consumption of contaminated poultry products ( ).	gene_phenotype
70839	2	333930	5	NULL	NULL	0	NULL	statement 1	Process		through		primarily			poultry products	OrganismPart	consumption of;;contaminated			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_19_20327_s_10	14985343	Campylobacter infection in humans occurs primarily through the consumption of contaminated poultry products ( ).	gene_phenotype
70840	1	333932	5	NULL	NULL	0	NULL	YLL031c	NucleicAcid	depletion of	accumulates					GPI proteins	GP	immature 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24458_s_108	10823837	Depletion of YLL031c Leads to the Accumulation of Immature GPI Proteins-- If Gas1p does not receive a GPI anchor in the ER, it fails to be transported to the Golgi ( 25), because, as shown by  in vitro experiments using a vesicle budding assay, nonanchored Gas1p is not packaged into COPII-coated transport vesicles budding off the ER ( 26).	gene_phenotype
70841	2	333932	5	NULL	NULL	NULL	NULL	transport vesicles	CellComponent	COPII-coated	buds off from					ER	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24458_s_108	10823837	Depletion of YLL031c Leads to the Accumulation of Immature GPI Proteins-- If Gas1p does not receive a GPI anchor in the ER, it fails to be transported to the Golgi ( 25), because, as shown by  in vitro experiments using a vesicle budding assay, nonanchored Gas1p is not packaged into COPII-coated transport vesicles budding off the ER ( 26).	gene_phenotype
70842	3	333932	5	NULL	NULL	0	NULL	Gas1p	GP	nonanchored	is not packaged into					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24458_s_108	10823837	Depletion of YLL031c Leads to the Accumulation of Immature GPI Proteins-- If Gas1p does not receive a GPI anchor in the ER, it fails to be transported to the Golgi ( 25), because, as shown by  in vitro experiments using a vesicle budding assay, nonanchored Gas1p is not packaged into COPII-coated transport vesicles budding off the ER ( 26).	gene_phenotype
70855	4	333932	5	NULL	NULL	NULL	NULL	Gas1p	GP		is not transported to					Golgi	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_32_24458_s_108	10823837	Depletion of YLL031c Leads to the Accumulation of Immature GPI Proteins-- If Gas1p does not receive a GPI anchor in the ER, it fails to be transported to the Golgi ( 25), because, as shown by  in vitro experiments using a vesicle budding assay, nonanchored Gas1p is not packaged into COPII-coated transport vesicles budding off the ER ( 26).	gene_phenotype
70856	5	333932	5	NULL	NULL	0	NULL	Gas1p	GP		does not receive					GPI anchor	GP				NULL	ER	0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24458_s_108	10823837	Depletion of YLL031c Leads to the Accumulation of Immature GPI Proteins-- If Gas1p does not receive a GPI anchor in the ER, it fails to be transported to the Golgi ( 25), because, as shown by  in vitro experiments using a vesicle budding assay, nonanchored Gas1p is not packaged into COPII-coated transport vesicles budding off the ER ( 26).	gene_phenotype
70857	6	333932	5	NULL	NULL	0	NULL	statement 5	Process		leads to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_32_24458_s_108	10823837	Depletion of YLL031c Leads to the Accumulation of Immature GPI Proteins-- If Gas1p does not receive a GPI anchor in the ER, it fails to be transported to the Golgi ( 25), because, as shown by  in vitro experiments using a vesicle budding assay, nonanchored Gas1p is not packaged into COPII-coated transport vesicles budding off the ER ( 26).	gene_phenotype
70858	1	333933	5	NULL	NULL	0	NULL	YAR031W	NucleicAcid	lack of	is not a consequence of					truncation	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_2_171_s_158	12518320	We concluded that the lack of YAR031W and of the rest of telomere-proximal ORFs  was not a consequence of a truncation, but rather of a recombination event that did  not implicate a gross change on the total length of the chromosome I left arm.	gene_phenotype
70859	2	333933	5	NULL	NULL	0	NULL	YAR031W	NucleicAcid	lack of	is consequence of					recombination event	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_2_171_s_158	12518320	We concluded that the lack of YAR031W and of the rest of telomere-proximal ORFs  was not a consequence of a truncation, but rather of a recombination event that did  not implicate a gross change on the total length of the chromosome I left arm.	gene_phenotype
70860	3	333933	5	NULL	NULL	0	NULL	statement 2	Process		does not change					chromosome I	Chromosome	total length of;;left arm of			NULL		0	NULL	NULL	NULL	gw70_yeast_20_2_171_s_158	12518320	We concluded that the lack of YAR031W and of the rest of telomere-proximal ORFs  was not a consequence of a truncation, but rather of a recombination event that did  not implicate a gross change on the total length of the chromosome I left arm.	gene_phenotype
70861	1	333934	5	NULL	NULL	0	NULL	Blm1	GP		is a synonym of					Bloom's Syndrome helicase	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_4_1724_s_377	14742710	Blm1 is the Bloom's Syndrome helicase homologous to budding yeast Sgs1, a ctf4delta interacting gene that also contributes to cohesion.	gene_phenotype
70862	2	333934	5	NULL	NULL	0	NULL	Bloom's Syndrome helicase	Process		is homologous to					Sgs1	GP	budding yeast			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_4_1724_s_377	14742710	Blm1 is the Bloom's Syndrome helicase homologous to budding yeast Sgs1, a ctf4delta interacting gene that also contributes to cohesion.	gene_phenotype
70863	3	333934	5	NULL	NULL	0	NULL	Sgs1	GP	budding yeast	interacts with					ctf4delta gene	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_4_1724_s_377	14742710	Blm1 is the Bloom's Syndrome helicase homologous to budding yeast Sgs1, a ctf4delta interacting gene that also contributes to cohesion.	gene_phenotype
70864	4	333934	5	NULL	NULL	0	NULL	ctf4delta gene	GP		contribute to					cohesion	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_4_1724_s_377	14742710	Blm1 is the Bloom's Syndrome helicase homologous to budding yeast Sgs1, a ctf4delta interacting gene that also contributes to cohesion.	gene_phenotype
70865	1	333935	5	NULL	NULL	0	NULL	Blm3p	GP		is a homolog of					PA200	GP				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_methods-enzymol_398_1_16275339_s_3	16275339	Homologs of PA200  have been found in rat, frog, birds, worms, and budding yeast, where it  is called Blm3p (now known as Blm10p), but not in Drosophila or fission  yeast.	gene_phenotype
70866	2	333935	5	NULL	NULL	0	NULL	Blm3p	GP		is a synonym of					Blm10p	GP				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_methods-enzymol_398_1_16275339_s_3	16275339	Homologs of PA200  have been found in rat, frog, birds, worms, and budding yeast, where it  is called Blm3p (now known as Blm10p), but not in Drosophila or fission  yeast.	gene_phenotype
70867	3	333935	5	NULL	NULL	0	NULL	Blm10p	GP		is present in					rat	Organism				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_methods-enzymol_398_1_16275339_s_3	16275339	Homologs of PA200  have been found in rat, frog, birds, worms, and budding yeast, where it  is called Blm3p (now known as Blm10p), but not in Drosophila or fission  yeast.	gene_phenotype
70868	4	333935	5	NULL	NULL	0	NULL	Blm10p	GP		is present in					frog	Organism				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_methods-enzymol_398_1_16275339_s_3	16275339	Homologs of PA200  have been found in rat, frog, birds, worms, and budding yeast, where it  is called Blm3p (now known as Blm10p), but not in Drosophila or fission  yeast.	gene_phenotype
70869	5	333935	5	NULL	NULL	0	NULL	Blm10p	GP		is present in					birds	Organism				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_methods-enzymol_398_1_16275339_s_3	16275339	Homologs of PA200  have been found in rat, frog, birds, worms, and budding yeast, where it  is called Blm3p (now known as Blm10p), but not in Drosophila or fission  yeast.	gene_phenotype
70870	6	333935	5	NULL	NULL	0	NULL	Blm10p	GP		is present in					worms	Organism				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_methods-enzymol_398_1_16275339_s_3	16275339	Homologs of PA200  have been found in rat, frog, birds, worms, and budding yeast, where it  is called Blm3p (now known as Blm10p), but not in Drosophila or fission  yeast.	gene_phenotype
70871	7	333935	5	NULL	NULL	0	NULL	Blm10p	GP		is present in					budding yeast	Organism				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_methods-enzymol_398_1_16275339_s_3	16275339	Homologs of PA200  have been found in rat, frog, birds, worms, and budding yeast, where it  is called Blm3p (now known as Blm10p), but not in Drosophila or fission  yeast.	gene_phenotype
70872	8	333935	5	NULL	NULL	0	NULL	Blm10p	GP		is not present in					Drosophila	Organism				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_methods-enzymol_398_1_16275339_s_3	16275339	Homologs of PA200  have been found in rat, frog, birds, worms, and budding yeast, where it  is called Blm3p (now known as Blm10p), but not in Drosophila or fission  yeast.	gene_phenotype
70873	9	333935	5	NULL	NULL	0	NULL	Blm10p	GP		is not present in					fission yeast	Organism				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_methods-enzymol_398_1_16275339_s_3	16275339	Homologs of PA200  have been found in rat, frog, birds, worms, and budding yeast, where it  is called Blm3p (now known as Blm10p), but not in Drosophila or fission  yeast.	gene_phenotype
70874	1	333936	5	NULL	NULL	0	NULL	YNR007c	NucleicAcid		is the locus name of					AUT1	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_79_s_288	12489128	YNR007c ( AUT1) is essential for autophagocytosis or transport of proteins from cytoplasm to vacuole  (Schlumpberger  et al., [ 1997]).	gene_phenotype
70875	2	333936	5	NULL	NULL	0	NULL	AUT1	GP		is essential for					autophagocytosis	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_79_s_288	12489128	YNR007c ( AUT1) is essential for autophagocytosis or transport of proteins from cytoplasm to vacuole  (Schlumpberger  et al., [ 1997]).	gene_phenotype
70876	3	333936	5	NULL	NULL	0	NULL	protein	GP		is transported from					cytoplasm	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_79_s_288	12489128	YNR007c ( AUT1) is essential for autophagocytosis or transport of proteins from cytoplasm to vacuole  (Schlumpberger  et al., [ 1997]).	gene_phenotype
70877	4	333936	5	NULL	NULL	0	NULL	protein	GP		is transported to					vacuole	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_79_s_288	12489128	YNR007c ( AUT1) is essential for autophagocytosis or transport of proteins from cytoplasm to vacuole  (Schlumpberger  et al., [ 1997]).	gene_phenotype
70878	5	333936	5	NULL	NULL	0	NULL	statement 3	Process		occurs along with					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_79_s_288	12489128	YNR007c ( AUT1) is essential for autophagocytosis or transport of proteins from cytoplasm to vacuole  (Schlumpberger  et al., [ 1997]).	gene_phenotype
70879	6	333936	5	NULL	NULL	0	NULL	AUT1	GP		is essential for					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_79_s_288	12489128	YNR007c ( AUT1) is essential for autophagocytosis or transport of proteins from cytoplasm to vacuole  (Schlumpberger  et al., [ 1997]).	gene_phenotype
70880	7	333936	5	NULL	NULL	0	NULL	AUT1	GP		is essential for					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_79_s_288	12489128	YNR007c ( AUT1) is essential for autophagocytosis or transport of proteins from cytoplasm to vacuole  (Schlumpberger  et al., [ 1997]).	gene_phenotype
70881	1	333942	5	NULL	NULL	0	NULL	piD261	GP	Saccharomyces cerevisiae	activates					Ser/Thr-specific protein kinase 	GP				NULL		0	NULL	NULL	NULL	gw60_genomeres_8_10_1038_s_33	9799791	This hypothesis is supported by biochemical data in the case of  Saccharomyces cerevisiae piD261 (YGR262C), which is a member of one of the identified protein families (see below) and has been shown to possess Ser/Thr-specific protein kinase activity (Stocchetto et al. 1997  ).	gene_phenotype
70882	2	333942	5	NULL	NULL	0	NULL	YGR262C	NucleicAcid	Saccharomyces cerevisiae	is the locus name of					piD261	GP	Saccharomyces cerevisiae			NULL		0	NULL	NULL	NULL	gw60_genomeres_8_10_1038_s_33	9799791	This hypothesis is supported by biochemical data in the case of  Saccharomyces cerevisiae piD261 (YGR262C), which is a member of one of the identified protein families (see below) and has been shown to possess Ser/Thr-specific protein kinase activity (Stocchetto et al. 1997  ).	gene_phenotype
70883	1	333943	5	NULL	NULL	0	NULL	YGR262C	NucleicAcid	Saccharomyces cerevisiae	is the locus name of					piD261 protein	GP	Saccharomyces cerevisiae			NULL		0	NULL	NULL	NULL	gw60_genomeres_8_10_1038_s_71	9799791	However, in light of the fact that the  S. cerevisiae piD261 (YGR262C) protein (which does not contain the APE motif) has been shown to possess Ser/Thr-specific protein kinase activity (Stocchetto et al. 1997  ), this element is apparently not strictly essential for protein kinase catalytic activity.	gene_phenotype
70884	2	333943	5	NULL	NULL	0	NULL	piD261 protein	GP	Saccharomyces cerevisiae	does not contain					APE motif	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_genomeres_8_10_1038_s_71	9799791	However, in light of the fact that the  S. cerevisiae piD261 (YGR262C) protein (which does not contain the APE motif) has been shown to possess Ser/Thr-specific protein kinase activity (Stocchetto et al. 1997  ), this element is apparently not strictly essential for protein kinase catalytic activity.	gene_phenotype
70885	3	333943	5	NULL	NULL	0	NULL	piD261 protein	GP	Saccharomyces cerevisiae	activates					Ser/Thr-specific protein kinase	GP				NULL		0	NULL	NULL	NULL	gw60_genomeres_8_10_1038_s_71	9799791	However, in light of the fact that the  S. cerevisiae piD261 (YGR262C) protein (which does not contain the APE motif) has been shown to possess Ser/Thr-specific protein kinase activity (Stocchetto et al. 1997  ), this element is apparently not strictly essential for protein kinase catalytic activity.	gene_phenotype
70886	1	333948	5	NULL	NULL	0	NULL	ybr078w/ ecm33 cells	Cell	growth of	is sensitive to					temperature	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_218_1_175_s_63	12583915	Temperature-sensitive growth of  ybr078w/ ecm33  cells	gene_phenotype
70887	1	333949	5	NULL	NULL	0	NULL	YBR078W	NucleicAcid		is the locus name of					ECM33	GP				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_218_1_175_s_20	12583915	A disruptant strain of  YBR078W/ ECM33 exhibited a temperature-sensitive (ts) growth phenotype [  13] and the hypersensitivity to oxidative stress [  14].	gene_phenotype
70888	2	333949	5	NULL	NULL	0	NULL	ECM33	GP	growth of;;disruptant strain of	is sensitive to					temperature	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_218_1_175_s_20	12583915	A disruptant strain of  YBR078W/ ECM33 exhibited a temperature-sensitive (ts) growth phenotype [  13] and the hypersensitivity to oxidative stress [  14].	gene_phenotype
70889	3	333949	5	NULL	NULL	0	NULL	ECM33	GP	growth of;;disruptant strain of	is hypersensitive to					oxidative stress	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_218_1_175_s_20	12583915	A disruptant strain of  YBR078W/ ECM33 exhibited a temperature-sensitive (ts) growth phenotype [  13] and the hypersensitivity to oxidative stress [  14].	gene_phenotype
70890	1	333950	5	NULL	NULL	0	NULL	YBR078W	NucleicAcid		is the locus name of					ECM33	GP				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_218_1_175_s_64	12583915	A deleted strain of  YBR078W/ ECM33 has shown a temperature-sensitive (ts) growth phenotype in a previous report [ 13].	gene_phenotype
70891	2	333950	5	NULL	NULL	0	NULL	ECM33 	GP	growth of;;deleted strain of	is sensitive to					temperature	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_218_1_175_s_64	12583915	A deleted strain of  YBR078W/ ECM33 has shown a temperature-sensitive (ts) growth phenotype in a previous report [ 13].	gene_phenotype
70892	1	333952	5	NULL	NULL	0	NULL	YDL247w product	GP		is homologous to		highly			MAL61	GP				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_450_s_154	0009925567	The high levels of homology exhibited by the products of YDL247w and YJR160c to MAL61 and AGT1 suggest that these proteins play a role in alpha-glucoside transport.	gene_phenotype
70893	2	333952	5	NULL	NULL	0	NULL	YJR160c product	GP		is homologous to		highly			AGT1	GP				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_450_s_154	0009925567	The high levels of homology exhibited by the products of YDL247w and YJR160c to MAL61 and AGT1 suggest that these proteins play a role in alpha-glucoside transport.	gene_phenotype
70894	3	333952	5	NULL	NULL	0	NULL	YDL247w product	GP		plays a role in					alpha-glucoside	Chemical	transport of			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_450_s_154	0009925567	The high levels of homology exhibited by the products of YDL247w and YJR160c to MAL61 and AGT1 suggest that these proteins play a role in alpha-glucoside transport.	gene_phenotype
70895	4	333952	5	NULL	NULL	0	NULL	YJR160c product	GP		plays a role in					alpha-glucoside	Chemical	transport of			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_450_s_154	0009925567	The high levels of homology exhibited by the products of YDL247w and YJR160c to MAL61 and AGT1 suggest that these proteins play a role in alpha-glucoside transport.	gene_phenotype
70896	1	333953	5	NULL	NULL	0	NULL	YDL247w protein	GP		transports		low affinity;;possibly			maltose	Chemical				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_450_s_229	0009925567	One possible function of the proteins encoded by YDL247w and YJR160c might be in low-affinity transport of maltose, although this phenomenon has been ruled out in one study as an artifact ( 1).	gene_phenotype
70897	2	333953	5	NULL	NULL	0	NULL	YJR160c protein	GP		transports		low affinity;;possibly			maltose	Chemical				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_450_s_229	0009925567	One possible function of the proteins encoded by YDL247w and YJR160c might be in low-affinity transport of maltose, although this phenomenon has been ruled out in one study as an artifact ( 1).	gene_phenotype
70898	1	333954	5	NULL	NULL	0	NULL	YGL157W protein	GP		is similar to					oxidoreductases	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_3_1_221_s_211	14871952	The protein encoded by  YGL157W is similar to oxidoreductases with dihydroflavanol 4-reductase activity (Gene Ontology Consortium, SGD;  http://www.geneontology.	gene_phenotype
70899	2	333954	5	NULL	NULL	0	NULL	YGL157W protein	GP		activates					dihydroflavanol 4-reductase	GP				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_3_1_221_s_211	14871952	The protein encoded by  YGL157W is similar to oxidoreductases with dihydroflavanol 4-reductase activity (Gene Ontology Consortium, SGD;  http://www.geneontology.	gene_phenotype
70900	1	333955	5	NULL	NULL	0	NULL	YdfG protein	GP	hypothetical;;E. coli	activates					serine dehydrogenase	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1645_1_89_s_161	12535615	Two hypothetical proteins of  E. coli and  S. cerevisiae, YdfG and YMR226C, showed NADP+-dependent  -serine dehydrogenase activity.	gene_phenotype
70901	2	333955	5	NULL	NULL	0	NULL	statement 1	Process		is dependent on					NADP+	Chemical				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1645_1_89_s_161	12535615	Two hypothetical proteins of  E. coli and  S. cerevisiae, YdfG and YMR226C, showed NADP+-dependent  -serine dehydrogenase activity.	gene_phenotype
70902	3	333955	5	NULL	NULL	0	NULL	YMR226C protein	GP	hypothetical;;S. cerevisiae	activates					serine dehydrogenase	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1645_1_89_s_161	12535615	Two hypothetical proteins of  E. coli and  S. cerevisiae, YdfG and YMR226C, showed NADP+-dependent  -serine dehydrogenase activity.	gene_phenotype
70903	4	333955	5	NULL	NULL	0	NULL	statement 3	Process		is dependent on					NADP+	Chemical				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1645_1_89_s_161	12535615	Two hypothetical proteins of  E. coli and  S. cerevisiae, YdfG and YMR226C, showed NADP+-dependent  -serine dehydrogenase activity.	gene_phenotype
70904	1	333958	5	NULL	NULL	0	NULL	RTM1	GP		mediates					TEV-specific resistance	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_97_1_489_s_215	10618445	Two hypotheses for how RTM1 mediates TEV-specific resistance are viable.	gene_phenotype
70905	1	333959	5	NULL	NULL	0	NULL	RTM1	GP		mediates					TEV	Organism	specific recognition of			NULL		0	NULL	NULL	NULL	gw60_pnas_96_2_772_s_221	9892709	The hypothesis that RTM1 and/or RTM2 mediate specific recognition of TEV and elicitation of silencing is worth testing.	gene_phenotype
70906	2	333959	5	NULL	NULL	0	NULL	RTM2	GP		mediates					TEV	Organism	specific recognition of			NULL		0	NULL	NULL	NULL	gw60_pnas_96_2_772_s_221	9892709	The hypothesis that RTM1 and/or RTM2 mediate specific recognition of TEV and elicitation of silencing is worth testing.	gene_phenotype
70907	1	333960	5	NULL	NULL	0	NULL	TEV	Organism		prevents					silencing signal	AminoAcid	systemic spread of;;sequence-specific			NULL		0	NULL	NULL	NULL	gw60_cell_103_1_157_s_262	11051555	Conceivably, the products of RTM1 and RTM2 could  affect the ability of TEV to prevent systemic spread of the sequence-specific  silencing signal (Chisholm et al., 2000   ).	gene_phenotype
70908	2	333960	5	NULL	NULL	0	NULL	RTM1	GP		affects					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cell_103_1_157_s_262	11051555	Conceivably, the products of RTM1 and RTM2 could  affect the ability of TEV to prevent systemic spread of the sequence-specific  silencing signal (Chisholm et al., 2000   ).	gene_phenotype
70910	3	333960	5	NULL	NULL	0	NULL	RTM2 	GP		affects					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cell_103_1_157_s_262	11051555	Conceivably, the products of RTM1 and RTM2 could  affect the ability of TEV to prevent systemic spread of the sequence-specific  silencing signal (Chisholm et al., 2000   ).	gene_phenotype
70911	1	333961	5	NULL	NULL	0	NULL	YFL007w	NucleicAcid	deletion of	does not affect					viability	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_19_8_699_s_79	12185839	Deletion of neither  YFL007w nor  YFL006w affects viability (Winzeler  et al., [ 1999]), indicating that thegene is not essential.	gene_phenotype
70912	2	333961	5	NULL	NULL	0	NULL	YFL006w	NucleicAcid	deletion of	does not affect					viability	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_19_8_699_s_79	12185839	Deletion of neither  YFL007w nor  YFL006w affects viability (Winzeler  et al., [ 1999]), indicating that thegene is not essential.	gene_phenotype
70913	1	333962	5	NULL	NULL	0	NULL	YFL007w protein	GP	purified	co-associates with					Sir4 protein	Process	purified			NULL		0	NULL	NULL	NULL	gw70_yeast_19_8_699_s_90	12185839	Systematic mass spectrometric analysis of purified protein  complexes have identified YFL007w and YFL006w in co-association with the chromatin  silencing regulator Sir4 (Ho  et al.  Nature 2002;  415: 180) and with the 26S proteasome subunit Scl1 (Gavin  et al.  Nature 2002;  415: 141).	gene_phenotype
70914	2	333962	5	NULL	NULL	0	NULL	YFL006w protein	GP	purified	co-associates with					Sir4 protein	GP	purified			NULL		0	NULL	NULL	NULL	gw70_yeast_19_8_699_s_90	12185839	Systematic mass spectrometric analysis of purified protein  complexes have identified YFL007w and YFL006w in co-association with the chromatin  silencing regulator Sir4 (Ho  et al.  Nature 2002;  415: 180) and with the 26S proteasome subunit Scl1 (Gavin  et al.  Nature 2002;  415: 141).	gene_phenotype
70915	3	333962	5	NULL	NULL	0	NULL	Sir4 	GP		is a type of					chromatin silencing regulator	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_19_8_699_s_90	12185839	Systematic mass spectrometric analysis of purified protein  complexes have identified YFL007w and YFL006w in co-association with the chromatin  silencing regulator Sir4 (Ho  et al.  Nature 2002;  415: 180) and with the 26S proteasome subunit Scl1 (Gavin  et al.  Nature 2002;  415: 141).	gene_phenotype
70916	4	333962	5	NULL	NULL	0	NULL	Scl1	GP		is a subunit of					26S proteasome	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_19_8_699_s_90	12185839	Systematic mass spectrometric analysis of purified protein  complexes have identified YFL007w and YFL006w in co-association with the chromatin  silencing regulator Sir4 (Ho  et al.  Nature 2002;  415: 180) and with the 26S proteasome subunit Scl1 (Gavin  et al.  Nature 2002;  415: 141).	gene_phenotype
70917	5	333962	5	NULL	NULL	0	NULL	YFL007w protein \t	GP	purified	co-associates with					Scl1 protein	GP	purified			NULL		0	NULL	NULL	NULL	gw70_yeast_19_8_699_s_90	12185839	Systematic mass spectrometric analysis of purified protein  complexes have identified YFL007w and YFL006w in co-association with the chromatin  silencing regulator Sir4 (Ho  et al.  Nature 2002;  415: 180) and with the 26S proteasome subunit Scl1 (Gavin  et al.  Nature 2002;  415: 141).	gene_phenotype
70918	6	333962	5	NULL	NULL	0	NULL	YFL006w protein	GP	purified	co-associates with					Scl1 protein	GP	purified			NULL		0	NULL	NULL	NULL	gw70_yeast_19_8_699_s_90	12185839	Systematic mass spectrometric analysis of purified protein  complexes have identified YFL007w and YFL006w in co-association with the chromatin  silencing regulator Sir4 (Ho  et al.  Nature 2002;  415: 180) and with the 26S proteasome subunit Scl1 (Gavin  et al.  Nature 2002;  415: 141).	gene_phenotype
70919	1	333964	5	NULL	NULL	0	NULL	snR85	NucleicAcid		is required for		potentially			psi modification	Process	guiding			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_14_4281_s_225	15306656	Unfortunately, we were unable to determine whether the sixth verified RNA (snR85) is required for guiding its predicted psi modification.	gene_phenotype
71912	1	333965	5	NULL	NULL	0	NULL	184-nt 6 S	NucleicAcid	E. coli	modulates					promoter use	Process				NULL		0	NULL	NULL	NULL	gw60_science_296_5571_1260_s_21	12016301	[[ Process Example Function Reference     Transcription 184-nt  E. coli 6 S Modulates promoter use ]] ( 9,  14)   331-nt human 7SK  Inhibits transcription elongation factor P-TEFb ( 15,  16,  46)   875-nt human SRA Steroid receptor coactivator ( 12,  17)  Gene silencing  16,500-nt human  Xist Required for X-chromosome inactivation ( 12,  13)   ~100,000-nt human  Air Required for autosomal gene imprinting ( 11)  Replication 451-nt human telomerase RNA Core of telomerase and telomere template ( 18,  46)  RNA processing 377-nt  E. coli RNase P Catalytic core of RNase P ( 9,  19)   186-nt human U2 snRNA Core of spliceosome ( 20,  46)  RNA modification 102-nt  S. cerevisiae U18 C/D snoRNA Directs 2''- O-ribose methylation of target rRNA  ( 21,  47)   189-nt  S. cerevisiae snR8 H/ACA snoRNA Directs pseudouridylation of target rRNA ( 21,  47)   68-nt  T. brucei gCYb gRNA Directs the insertion and excision of uridines ( 23,  24,  48)  RNA stability 80-nt  E. coli RyhB sRNA Targets mRNAs for degradation?	gene_phenotype
71913	2	333965	5	NULL	NULL	0	NULL	331-nt 7SK	NucleicAcid	human	inhibits					P-TEFb	GP				NULL		0	NULL	NULL	NULL	gw60_science_296_5571_1260_s_21	12016301	[[ Process Example Function Reference     Transcription 184-nt  E. coli 6 S Modulates promoter use ]] ( 9,  14)   331-nt human 7SK  Inhibits transcription elongation factor P-TEFb ( 15,  16,  46)   875-nt human SRA Steroid receptor coactivator ( 12,  17)  Gene silencing  16,500-nt human  Xist Required for X-chromosome inactivation ( 12,  13)   ~100,000-nt human  Air Required for autosomal gene imprinting ( 11)  Replication 451-nt human telomerase RNA Core of telomerase and telomere template ( 18,  46)  RNA processing 377-nt  E. coli RNase P Catalytic core of RNase P ( 9,  19)   186-nt human U2 snRNA Core of spliceosome ( 20,  46)  RNA modification 102-nt  S. cerevisiae U18 C/D snoRNA Directs 2''- O-ribose methylation of target rRNA  ( 21,  47)   189-nt  S. cerevisiae snR8 H/ACA snoRNA Directs pseudouridylation of target rRNA ( 21,  47)   68-nt  T. brucei gCYb gRNA Directs the insertion and excision of uridines ( 23,  24,  48)  RNA stability 80-nt  E. coli RyhB sRNA Targets mRNAs for degradation?	gene_phenotype
71914	3	333965	5	NULL	NULL	0	NULL	P-TEFb	GP		is a type of					transcription elongation factor	GP				NULL		0	NULL	NULL	NULL	gw60_science_296_5571_1260_s_21	12016301	[[ Process Example Function Reference     Transcription 184-nt  E. coli 6 S Modulates promoter use ]] ( 9,  14)   331-nt human 7SK  Inhibits transcription elongation factor P-TEFb ( 15,  16,  46)   875-nt human SRA Steroid receptor coactivator ( 12,  17)  Gene silencing  16,500-nt human  Xist Required for X-chromosome inactivation ( 12,  13)   ~100,000-nt human  Air Required for autosomal gene imprinting ( 11)  Replication 451-nt human telomerase RNA Core of telomerase and telomere template ( 18,  46)  RNA processing 377-nt  E. coli RNase P Catalytic core of RNase P ( 9,  19)   186-nt human U2 snRNA Core of spliceosome ( 20,  46)  RNA modification 102-nt  S. cerevisiae U18 C/D snoRNA Directs 2''- O-ribose methylation of target rRNA  ( 21,  47)   189-nt  S. cerevisiae snR8 H/ACA snoRNA Directs pseudouridylation of target rRNA ( 21,  47)   68-nt  T. brucei gCYb gRNA Directs the insertion and excision of uridines ( 23,  24,  48)  RNA stability 80-nt  E. coli RyhB sRNA Targets mRNAs for degradation?	gene_phenotype
71915	4	333965	5	NULL	NULL	0	NULL	875-nt SRA	NucleicAcid	human	is a type of					Steroid receptor coactivator	GP				NULL		0	NULL	NULL	NULL	gw60_science_296_5571_1260_s_21	12016301	[[ Process Example Function Reference     Transcription 184-nt  E. coli 6 S Modulates promoter use ]] ( 9,  14)   331-nt human 7SK  Inhibits transcription elongation factor P-TEFb ( 15,  16,  46)   875-nt human SRA Steroid receptor coactivator ( 12,  17)  Gene silencing  16,500-nt human  Xist Required for X-chromosome inactivation ( 12,  13)   ~100,000-nt human  Air Required for autosomal gene imprinting ( 11)  Replication 451-nt human telomerase RNA Core of telomerase and telomere template ( 18,  46)  RNA processing 377-nt  E. coli RNase P Catalytic core of RNase P ( 9,  19)   186-nt human U2 snRNA Core of spliceosome ( 20,  46)  RNA modification 102-nt  S. cerevisiae U18 C/D snoRNA Directs 2''- O-ribose methylation of target rRNA  ( 21,  47)   189-nt  S. cerevisiae snR8 H/ACA snoRNA Directs pseudouridylation of target rRNA ( 21,  47)   68-nt  T. brucei gCYb gRNA Directs the insertion and excision of uridines ( 23,  24,  48)  RNA stability 80-nt  E. coli RyhB sRNA Targets mRNAs for degradation?	gene_phenotype
71916	5	333965	5	NULL	NULL	0	NULL	16,500-nt Xist	NucleicAcid	human	is required for					X-chromosome	Chromosome	inactivation of			NULL		0	NULL	NULL	NULL	gw60_science_296_5571_1260_s_21	12016301	[[ Process Example Function Reference     Transcription 184-nt  E. coli 6 S Modulates promoter use ]] ( 9,  14)   331-nt human 7SK  Inhibits transcription elongation factor P-TEFb ( 15,  16,  46)   875-nt human SRA Steroid receptor coactivator ( 12,  17)  Gene silencing  16,500-nt human  Xist Required for X-chromosome inactivation ( 12,  13)   ~100,000-nt human  Air Required for autosomal gene imprinting ( 11)  Replication 451-nt human telomerase RNA Core of telomerase and telomere template ( 18,  46)  RNA processing 377-nt  E. coli RNase P Catalytic core of RNase P ( 9,  19)   186-nt human U2 snRNA Core of spliceosome ( 20,  46)  RNA modification 102-nt  S. cerevisiae U18 C/D snoRNA Directs 2''- O-ribose methylation of target rRNA  ( 21,  47)   189-nt  S. cerevisiae snR8 H/ACA snoRNA Directs pseudouridylation of target rRNA ( 21,  47)   68-nt  T. brucei gCYb gRNA Directs the insertion and excision of uridines ( 23,  24,  48)  RNA stability 80-nt  E. coli RyhB sRNA Targets mRNAs for degradation?	gene_phenotype
71917	6	333965	5	NULL	NULL	0	NULL	100,000-nt Air	NucleicAcid	human	is required for					autosomal gene imprinting	Process				NULL		0	NULL	NULL	NULL	gw60_science_296_5571_1260_s_21	12016301	[[ Process Example Function Reference     Transcription 184-nt  E. coli 6 S Modulates promoter use ]] ( 9,  14)   331-nt human 7SK  Inhibits transcription elongation factor P-TEFb ( 15,  16,  46)   875-nt human SRA Steroid receptor coactivator ( 12,  17)  Gene silencing  16,500-nt human  Xist Required for X-chromosome inactivation ( 12,  13)   ~100,000-nt human  Air Required for autosomal gene imprinting ( 11)  Replication 451-nt human telomerase RNA Core of telomerase and telomere template ( 18,  46)  RNA processing 377-nt  E. coli RNase P Catalytic core of RNase P ( 9,  19)   186-nt human U2 snRNA Core of spliceosome ( 20,  46)  RNA modification 102-nt  S. cerevisiae U18 C/D snoRNA Directs 2''- O-ribose methylation of target rRNA  ( 21,  47)   189-nt  S. cerevisiae snR8 H/ACA snoRNA Directs pseudouridylation of target rRNA ( 21,  47)   68-nt  T. brucei gCYb gRNA Directs the insertion and excision of uridines ( 23,  24,  48)  RNA stability 80-nt  E. coli RyhB sRNA Targets mRNAs for degradation?	gene_phenotype
71918	7	333965	5	NULL	NULL	0	NULL	451-nt telomerase RNA	NucleicAcid	human	is the core of					telomerase	GP				NULL		0	NULL	NULL	NULL	gw60_science_296_5571_1260_s_21	12016301	[[ Process Example Function Reference     Transcription 184-nt  E. coli 6 S Modulates promoter use ]] ( 9,  14)   331-nt human 7SK  Inhibits transcription elongation factor P-TEFb ( 15,  16,  46)   875-nt human SRA Steroid receptor coactivator ( 12,  17)  Gene silencing  16,500-nt human  Xist Required for X-chromosome inactivation ( 12,  13)   ~100,000-nt human  Air Required for autosomal gene imprinting ( 11)  Replication 451-nt human telomerase RNA Core of telomerase and telomere template ( 18,  46)  RNA processing 377-nt  E. coli RNase P Catalytic core of RNase P ( 9,  19)   186-nt human U2 snRNA Core of spliceosome ( 20,  46)  RNA modification 102-nt  S. cerevisiae U18 C/D snoRNA Directs 2''- O-ribose methylation of target rRNA  ( 21,  47)   189-nt  S. cerevisiae snR8 H/ACA snoRNA Directs pseudouridylation of target rRNA ( 21,  47)   68-nt  T. brucei gCYb gRNA Directs the insertion and excision of uridines ( 23,  24,  48)  RNA stability 80-nt  E. coli RyhB sRNA Targets mRNAs for degradation?	gene_phenotype
71919	8	333965	5	NULL	NULL	0	NULL	451-nt telomerase RNA	NucleicAcid	human	is the core of					telomere template	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_science_296_5571_1260_s_21	12016301	[[ Process Example Function Reference     Transcription 184-nt  E. coli 6 S Modulates promoter use ]] ( 9,  14)   331-nt human 7SK  Inhibits transcription elongation factor P-TEFb ( 15,  16,  46)   875-nt human SRA Steroid receptor coactivator ( 12,  17)  Gene silencing  16,500-nt human  Xist Required for X-chromosome inactivation ( 12,  13)   ~100,000-nt human  Air Required for autosomal gene imprinting ( 11)  Replication 451-nt human telomerase RNA Core of telomerase and telomere template ( 18,  46)  RNA processing 377-nt  E. coli RNase P Catalytic core of RNase P ( 9,  19)   186-nt human U2 snRNA Core of spliceosome ( 20,  46)  RNA modification 102-nt  S. cerevisiae U18 C/D snoRNA Directs 2''- O-ribose methylation of target rRNA  ( 21,  47)   189-nt  S. cerevisiae snR8 H/ACA snoRNA Directs pseudouridylation of target rRNA ( 21,  47)   68-nt  T. brucei gCYb gRNA Directs the insertion and excision of uridines ( 23,  24,  48)  RNA stability 80-nt  E. coli RyhB sRNA Targets mRNAs for degradation?	gene_phenotype
71920	9	333965	5	NULL	NULL	0	NULL	377-nt RNase P	NucleicAcid	E. coli	is the catalytic core of					RNase P	GP				NULL		0	NULL	NULL	NULL	gw60_science_296_5571_1260_s_21	12016301	[[ Process Example Function Reference     Transcription 184-nt  E. coli 6 S Modulates promoter use ]] ( 9,  14)   331-nt human 7SK  Inhibits transcription elongation factor P-TEFb ( 15,  16,  46)   875-nt human SRA Steroid receptor coactivator ( 12,  17)  Gene silencing  16,500-nt human  Xist Required for X-chromosome inactivation ( 12,  13)   ~100,000-nt human  Air Required for autosomal gene imprinting ( 11)  Replication 451-nt human telomerase RNA Core of telomerase and telomere template ( 18,  46)  RNA processing 377-nt  E. coli RNase P Catalytic core of RNase P ( 9,  19)   186-nt human U2 snRNA Core of spliceosome ( 20,  46)  RNA modification 102-nt  S. cerevisiae U18 C/D snoRNA Directs 2''- O-ribose methylation of target rRNA  ( 21,  47)   189-nt  S. cerevisiae snR8 H/ACA snoRNA Directs pseudouridylation of target rRNA ( 21,  47)   68-nt  T. brucei gCYb gRNA Directs the insertion and excision of uridines ( 23,  24,  48)  RNA stability 80-nt  E. coli RyhB sRNA Targets mRNAs for degradation?	gene_phenotype
71921	10	333965	5	NULL	NULL	0	NULL	186-nt U2snRNA	NucleicAcid	human	is the core of					spliceosome	CellComponent				NULL		0	NULL	NULL	NULL	gw60_science_296_5571_1260_s_21	12016301	[[ Process Example Function Reference     Transcription 184-nt  E. coli 6 S Modulates promoter use ]] ( 9,  14)   331-nt human 7SK  Inhibits transcription elongation factor P-TEFb ( 15,  16,  46)   875-nt human SRA Steroid receptor coactivator ( 12,  17)  Gene silencing  16,500-nt human  Xist Required for X-chromosome inactivation ( 12,  13)   ~100,000-nt human  Air Required for autosomal gene imprinting ( 11)  Replication 451-nt human telomerase RNA Core of telomerase and telomere template ( 18,  46)  RNA processing 377-nt  E. coli RNase P Catalytic core of RNase P ( 9,  19)   186-nt human U2 snRNA Core of spliceosome ( 20,  46)  RNA modification 102-nt  S. cerevisiae U18 C/D snoRNA Directs 2''- O-ribose methylation of target rRNA  ( 21,  47)   189-nt  S. cerevisiae snR8 H/ACA snoRNA Directs pseudouridylation of target rRNA ( 21,  47)   68-nt  T. brucei gCYb gRNA Directs the insertion and excision of uridines ( 23,  24,  48)  RNA stability 80-nt  E. coli RyhB sRNA Targets mRNAs for degradation?	gene_phenotype
71922	11	333965	5	NULL	NULL	0	NULL	102-nt U18 C/D snoRNA	NucleicAcid	S. cerevisiae	directs					target rRNA	NucleicAcid	2''- O-ribose methylation of			NULL		0	NULL	NULL	NULL	gw60_science_296_5571_1260_s_21	12016301	[[ Process Example Function Reference     Transcription 184-nt  E. coli 6 S Modulates promoter use ]] ( 9,  14)   331-nt human 7SK  Inhibits transcription elongation factor P-TEFb ( 15,  16,  46)   875-nt human SRA Steroid receptor coactivator ( 12,  17)  Gene silencing  16,500-nt human  Xist Required for X-chromosome inactivation ( 12,  13)   ~100,000-nt human  Air Required for autosomal gene imprinting ( 11)  Replication 451-nt human telomerase RNA Core of telomerase and telomere template ( 18,  46)  RNA processing 377-nt  E. coli RNase P Catalytic core of RNase P ( 9,  19)   186-nt human U2 snRNA Core of spliceosome ( 20,  46)  RNA modification 102-nt  S. cerevisiae U18 C/D snoRNA Directs 2''- O-ribose methylation of target rRNA  ( 21,  47)   189-nt  S. cerevisiae snR8 H/ACA snoRNA Directs pseudouridylation of target rRNA ( 21,  47)   68-nt  T. brucei gCYb gRNA Directs the insertion and excision of uridines ( 23,  24,  48)  RNA stability 80-nt  E. coli RyhB sRNA Targets mRNAs for degradation?	gene_phenotype
71923	12	333965	5	NULL	NULL	0	NULL	189-nt snR8 H/ACA snoRNA	NucleicAcid	S. cerevisiae	directs					target rRNA	NucleicAcid	pseudouridylation of			NULL		0	NULL	NULL	NULL	gw60_science_296_5571_1260_s_21	12016301	[[ Process Example Function Reference     Transcription 184-nt  E. coli 6 S Modulates promoter use ]] ( 9,  14)   331-nt human 7SK  Inhibits transcription elongation factor P-TEFb ( 15,  16,  46)   875-nt human SRA Steroid receptor coactivator ( 12,  17)  Gene silencing  16,500-nt human  Xist Required for X-chromosome inactivation ( 12,  13)   ~100,000-nt human  Air Required for autosomal gene imprinting ( 11)  Replication 451-nt human telomerase RNA Core of telomerase and telomere template ( 18,  46)  RNA processing 377-nt  E. coli RNase P Catalytic core of RNase P ( 9,  19)   186-nt human U2 snRNA Core of spliceosome ( 20,  46)  RNA modification 102-nt  S. cerevisiae U18 C/D snoRNA Directs 2''- O-ribose methylation of target rRNA  ( 21,  47)   189-nt  S. cerevisiae snR8 H/ACA snoRNA Directs pseudouridylation of target rRNA ( 21,  47)   68-nt  T. brucei gCYb gRNA Directs the insertion and excision of uridines ( 23,  24,  48)  RNA stability 80-nt  E. coli RyhB sRNA Targets mRNAs for degradation?	gene_phenotype
71924	13	333965	5	NULL	NULL	0	NULL	68-nt gCYb gRNA	NucleicAcid	T. brucei	directs					uridine	NucleicAcid	insertion of;;excision of			NULL		0	NULL	NULL	NULL	gw60_science_296_5571_1260_s_21	12016301	[[ Process Example Function Reference     Transcription 184-nt  E. coli 6 S Modulates promoter use ]] ( 9,  14)   331-nt human 7SK  Inhibits transcription elongation factor P-TEFb ( 15,  16,  46)   875-nt human SRA Steroid receptor coactivator ( 12,  17)  Gene silencing  16,500-nt human  Xist Required for X-chromosome inactivation ( 12,  13)   ~100,000-nt human  Air Required for autosomal gene imprinting ( 11)  Replication 451-nt human telomerase RNA Core of telomerase and telomere template ( 18,  46)  RNA processing 377-nt  E. coli RNase P Catalytic core of RNase P ( 9,  19)   186-nt human U2 snRNA Core of spliceosome ( 20,  46)  RNA modification 102-nt  S. cerevisiae U18 C/D snoRNA Directs 2''- O-ribose methylation of target rRNA  ( 21,  47)   189-nt  S. cerevisiae snR8 H/ACA snoRNA Directs pseudouridylation of target rRNA ( 21,  47)   68-nt  T. brucei gCYb gRNA Directs the insertion and excision of uridines ( 23,  24,  48)  RNA stability 80-nt  E. coli RyhB sRNA Targets mRNAs for degradation?	gene_phenotype
71925	15	333965	5	NULL	NULL	0	NULL	80-nt RyhB sRNA	NucleicAcid	E. coli	is required for					statement 14	Process				NULL		0	NULL	NULL	NULL	gw60_science_296_5571_1260_s_21	12016301	[[ Process Example Function Reference     Transcription 184-nt  E. coli 6 S Modulates promoter use ]] ( 9,  14)   331-nt human 7SK  Inhibits transcription elongation factor P-TEFb ( 15,  16,  46)   875-nt human SRA Steroid receptor coactivator ( 12,  17)  Gene silencing  16,500-nt human  Xist Required for X-chromosome inactivation ( 12,  13)   ~100,000-nt human  Air Required for autosomal gene imprinting ( 11)  Replication 451-nt human telomerase RNA Core of telomerase and telomere template ( 18,  46)  RNA processing 377-nt  E. coli RNase P Catalytic core of RNase P ( 9,  19)   186-nt human U2 snRNA Core of spliceosome ( 20,  46)  RNA modification 102-nt  S. cerevisiae U18 C/D snoRNA Directs 2''- O-ribose methylation of target rRNA  ( 21,  47)   189-nt  S. cerevisiae snR8 H/ACA snoRNA Directs pseudouridylation of target rRNA ( 21,  47)   68-nt  T. brucei gCYb gRNA Directs the insertion and excision of uridines ( 23,  24,  48)  RNA stability 80-nt  E. coli RyhB sRNA Targets mRNAs for degradation?	gene_phenotype
71926	14	333965	5	NULL	NULL	0	NULL	mRNA	NucleicAcid		is targeted for					degradation	Process				NULL		0	NULL	NULL	NULL	gw60_science_296_5571_1260_s_21	12016301	[[ Process Example Function Reference     Transcription 184-nt  E. coli 6 S Modulates promoter use ]] ( 9,  14)   331-nt human 7SK  Inhibits transcription elongation factor P-TEFb ( 15,  16,  46)   875-nt human SRA Steroid receptor coactivator ( 12,  17)  Gene silencing  16,500-nt human  Xist Required for X-chromosome inactivation ( 12,  13)   ~100,000-nt human  Air Required for autosomal gene imprinting ( 11)  Replication 451-nt human telomerase RNA Core of telomerase and telomere template ( 18,  46)  RNA processing 377-nt  E. coli RNase P Catalytic core of RNase P ( 9,  19)   186-nt human U2 snRNA Core of spliceosome ( 20,  46)  RNA modification 102-nt  S. cerevisiae U18 C/D snoRNA Directs 2''- O-ribose methylation of target rRNA  ( 21,  47)   189-nt  S. cerevisiae snR8 H/ACA snoRNA Directs pseudouridylation of target rRNA ( 21,  47)   68-nt  T. brucei gCYb gRNA Directs the insertion and excision of uridines ( 23,  24,  48)  RNA stability 80-nt  E. coli RyhB sRNA Targets mRNAs for degradation?	gene_phenotype
70920	1	333966	5	NULL	NULL	0	NULL	YGR280c gene	GP		is essential for					yeast	Organism	vegetative growth of			NULL	rich medium	0	NULL	NULL	NULL	gw70_yeast_20_1_79_s_5	12489128	Tetrad analysis, following  sporulation of the heterozygous disruptants, revealed that YGR280c and YNL006w are  essential genes for vegetative yeast growth in rich medium.	gene_phenotype
70921	2	333966	5	NULL	NULL	0	NULL	YNL006w gene	GP		is essential for					yeast	Organism	vegetative growth of			NULL	rich medium	0	NULL	NULL	NULL	gw70_yeast_20_1_79_s_5	12489128	Tetrad analysis, following  sporulation of the heterozygous disruptants, revealed that YGR280c and YNL006w are  essential genes for vegetative yeast growth in rich medium.	gene_phenotype
70925	4	333969	5	NULL	NULL	0	NULL	YGR280c	NucleicAcid		is a type of					ORF	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_79_s_293	12489128	The conclusion of the present study is that two of the 12 ORFs analysed are essential  for yeast viability (YGR280c and YNL006w).	gene_phenotype
70927	3	333969	5	NULL	NULL	0	NULL	YGR280c	NucleicAcid		is a type of					ORF	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_79_s_293	12489128	The conclusion of the present study is that two of the 12 ORFs analysed are essential  for yeast viability (YGR280c and YNL006w).	gene_phenotype
70929	2	333969	5	NULL	NULL	NULL	NULL	YNL006w	NucleicAcid		is essential for					yeast	Organism	viability of			NULL		NULL	NULL	NULL	NULL	gw70_yeast_20_1_79_s_293	12489128	The conclusion of the present study is that two of the 12 ORFs analysed are essential  for yeast viability (YGR280c and YNL006w).	gene_phenotype
70930	1	333969	5	NULL	NULL	0	NULL	YGR280c	NucleicAcid		is essential for					yeast	Organism	viability of			NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_79_s_293	12489128	The conclusion of the present study is that two of the 12 ORFs analysed are essential  for yeast viability (YGR280c and YNL006w).	gene_phenotype
71040	1	333971	5	NULL	NULL	0	NULL	permeases	GP		is transported from					Golgi	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_79_s_7	12489128	The protein encoded by  YNL006w ( LST8) is now known to be involved in transport of permeases from the Golgi to the plasma  membrane.	gene_phenotype
71043	2	333971	5	NULL	NULL	0	NULL	permeases	GP		is transported to					plasma membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_79_s_7	12489128	The protein encoded by  YNL006w ( LST8) is now known to be involved in transport of permeases from the Golgi to the plasma  membrane.	gene_phenotype
71045	3	333971	5	NULL	NULL	0	NULL	statement 1	Process		occurs along with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_79_s_7	12489128	The protein encoded by  YNL006w ( LST8) is now known to be involved in transport of permeases from the Golgi to the plasma  membrane.	gene_phenotype
71047	4	333971	5	NULL	NULL	0	NULL	LST8 protein	GP		is encoded by					YNL006w	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_79_s_7	12489128	The protein encoded by  YNL006w ( LST8) is now known to be involved in transport of permeases from the Golgi to the plasma  membrane.	gene_phenotype
71048	5	333971	5	NULL	NULL	0	NULL	LST8 protein	GP		is involved in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_79_s_7	12489128	The protein encoded by  YNL006w ( LST8) is now known to be involved in transport of permeases from the Golgi to the plasma  membrane.	gene_phenotype
71050	6	333971	5	NULL	NULL	0	NULL	LST8 protein	GP		is involved in					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_79_s_7	12489128	The protein encoded by  YNL006w ( LST8) is now known to be involved in transport of permeases from the Golgi to the plasma  membrane.	gene_phenotype
71052	1	333972	5	NULL	NULL	0	NULL	haploid YNL006w	NucleicAcid	disruptants 	is not impaired in					spore	Cell	germination of			NULL		0	NULL	NULL	NULL	gw70_yeast_20_1_79_s_248	12489128	Microscopic analysis revealed that haploid YNL006w disruptants were not impaired  in spore germination, but stopped growth after the formation of microcolonies.	gene_phenotype
71053	1	333975	5	NULL	NULL	0	NULL	cap structure	NucleicAcid		protects					RNA	NucleicAcid	5' end of			NULL		0	NULL	NULL	NULL	gw60_embo_18_2_457_s_78	9889201	Collectively, our results demonstrate that the cap structure, most likely by protecting the 5' end of the RNA, plays an important role in the accumulation of the wild-type snR5 and the mutant snR36- S1 and snR36- S2 box H/ACA snoRNAs.	gene_phenotype
71054	2	333975	5	NULL	NULL	0	NULL	cap structure	NucleicAcid		plays a role in		important			snR5	NucleicAcid	accumulation of;;wild-type			NULL		0	NULL	NULL	NULL	gw60_embo_18_2_457_s_78	9889201	Collectively, our results demonstrate that the cap structure, most likely by protecting the 5' end of the RNA, plays an important role in the accumulation of the wild-type snR5 and the mutant snR36- S1 and snR36- S2 box H/ACA snoRNAs.	gene_phenotype
71055	3	333975	5	NULL	NULL	NULL	NULL	statement 2	Process		via		most likely			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_2_457_s_78	9889201	Collectively, our results demonstrate that the cap structure, most likely by protecting the 5' end of the RNA, plays an important role in the accumulation of the wild-type snR5 and the mutant snR36- S1 and snR36- S2 box H/ACA snoRNAs.	gene_phenotype
71056	4	333975	5	NULL	NULL	0	NULL	cap structure	NucleicAcid		plays a role in		important			snR36- S1	NucleicAcid	accumulation of;;mutant			NULL		0	NULL	NULL	NULL	gw60_embo_18_2_457_s_78	9889201	Collectively, our results demonstrate that the cap structure, most likely by protecting the 5' end of the RNA, plays an important role in the accumulation of the wild-type snR5 and the mutant snR36- S1 and snR36- S2 box H/ACA snoRNAs.	gene_phenotype
71057	5	333975	5	NULL	NULL	0	NULL	statement 4	Process		via					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_2_457_s_78	9889201	Collectively, our results demonstrate that the cap structure, most likely by protecting the 5' end of the RNA, plays an important role in the accumulation of the wild-type snR5 and the mutant snR36- S1 and snR36- S2 box H/ACA snoRNAs.	gene_phenotype
71058	6	333975	5	NULL	NULL	0	NULL	cap structure	NucleicAcid		plays a role in		important			snR36- S2	NucleicAcid	accumulation of;;mutant		box H/ACA	NULL		0	NULL	NULL	NULL	gw60_embo_18_2_457_s_78	9889201	Collectively, our results demonstrate that the cap structure, most likely by protecting the 5' end of the RNA, plays an important role in the accumulation of the wild-type snR5 and the mutant snR36- S1 and snR36- S2 box H/ACA snoRNAs.	gene_phenotype
71059	7	333975	5	NULL	NULL	0	NULL	statement 6	Process		via					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_2_457_s_78	9889201	Collectively, our results demonstrate that the cap structure, most likely by protecting the 5' end of the RNA, plays an important role in the accumulation of the wild-type snR5 and the mutant snR36- S1 and snR36- S2 box H/ACA snoRNAs.	gene_phenotype
71060	8	333975	5	NULL	NULL	0	NULL	snR36- S2	NucleicAcid		is a type of					snoRNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_embo_18_2_457_s_78	9889201	Collectively, our results demonstrate that the cap structure, most likely by protecting the 5' end of the RNA, plays an important role in the accumulation of the wild-type snR5 and the mutant snR36- S1 and snR36- S2 box H/ACA snoRNAs.	gene_phenotype
71061	9	333975	5	NULL	NULL	0	NULL	snR36- S1	NucleicAcid		is a type of					snoRNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_embo_18_2_457_s_78	9889201	Collectively, our results demonstrate that the cap structure, most likely by protecting the 5' end of the RNA, plays an important role in the accumulation of the wild-type snR5 and the mutant snR36- S1 and snR36- S2 box H/ACA snoRNAs.	gene_phenotype
71062	1	333977	5	NULL	NULL	0	NULL	ycl012c ::G418	NucleicAcid	mutant	does not show					vegetative growth	Process	phenotypic change;;normal			NULL		0	NULL	NULL	NULL	gw70_yeast_20_8_731_s_209	12794934	The  ycl012c ::G418 mutant does not show any phenotypic change in normal vegetative growth, mating, or  sporulation.	gene_phenotype
71063	2	333977	5	NULL	NULL	0	NULL	ycl012c ::G418	NucleicAcid	mutant	does not show					mating	Process	phenotypic change;;normal			NULL		0	NULL	NULL	NULL	gw70_yeast_20_8_731_s_209	12794934	The  ycl012c ::G418 mutant does not show any phenotypic change in normal vegetative growth, mating, or  sporulation.	gene_phenotype
71064	3	333977	5	NULL	NULL	0	NULL	ycl012c ::G418	NucleicAcid	mutant	does not show					sporulation	Process	phenotypic change;;normal			NULL		0	NULL	NULL	NULL	gw70_yeast_20_8_731_s_209	12794934	The  ycl012c ::G418 mutant does not show any phenotypic change in normal vegetative growth, mating, or  sporulation.	gene_phenotype
71065	1	333979	5	NULL	NULL	0	NULL	silencing	Process		is mediated by					Sir protein	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_17_5206_s_143	15459290	When tested alongside the  HMR-tRNA in the  MATa1 reporter gene assay,  TRT2 showed a partial barrier activity to Sir protein-mediated silencing ( ), while it appears to completely prevent the spread of alpha2 operator repression in this study.	gene_phenotype
71066	2	333979	5	NULL	NULL	0	NULL	partial barrier activity	Process		is shown to					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_17_5206_s_143	15459290	When tested alongside the  HMR-tRNA in the  MATa1 reporter gene assay,  TRT2 showed a partial barrier activity to Sir protein-mediated silencing ( ), while it appears to completely prevent the spread of alpha2 operator repression in this study.	gene_phenotype
71067	3	333979	5	NULL	NULL	0	NULL	TRT2	GP		plays a role in					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_17_5206_s_143	15459290	When tested alongside the  HMR-tRNA in the  MATa1 reporter gene assay,  TRT2 showed a partial barrier activity to Sir protein-mediated silencing ( ), while it appears to completely prevent the spread of alpha2 operator repression in this study.	gene_phenotype
71068	4	333979	5	NULL	NULL	0	NULL	TRT2	GP		prevents		completely			alpha2	GP	spread of;;repression of		operator	NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_17_5206_s_143	15459290	When tested alongside the  HMR-tRNA in the  MATa1 reporter gene assay,  TRT2 showed a partial barrier activity to Sir protein-mediated silencing ( ), while it appears to completely prevent the spread of alpha2 operator repression in this study.	gene_phenotype
71069	1	333980	5	NULL	NULL	0	NULL	MATa1	GP		is derepressed in					sir1	GP	mutant			NULL		0	NULL	NULL	NULL	gw60_molcell_6_4_769_s_54	11090616	[In new window] We also examined silencing of a  URA3 gene at  HMR by monitoring the growth of cells on medium lacking uracil or containing 5-FOA. As seen for  MATa1, the  URA3 gene at  HMR was derepressed in the  sir1 mutants (see   Figure 1).	gene_phenotype
71070	2	333980	5	NULL	NULL	0	NULL	URA3 gene	GP		is present in					HMR	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molcell_6_4_769_s_54	11090616	[In new window] We also examined silencing of a  URA3 gene at  HMR by monitoring the growth of cells on medium lacking uracil or containing 5-FOA. As seen for  MATa1, the  URA3 gene at  HMR was derepressed in the  sir1 mutants (see   Figure 1).	gene_phenotype
71071	3	333980	5	NULL	NULL	0	NULL	URA3 gene	GP		is derepressed in					sir1	GP	mutant			NULL		0	NULL	NULL	NULL	gw60_molcell_6_4_769_s_54	11090616	[In new window] We also examined silencing of a  URA3 gene at  HMR by monitoring the growth of cells on medium lacking uracil or containing 5-FOA. As seen for  MATa1, the  URA3 gene at  HMR was derepressed in the  sir1 mutants (see   Figure 1).	gene_phenotype
71902	1	333982	5	NULL	NULL	0	NULL	HMR-tRNA	NucleicAcid		blocks					MATa1	GP	repression of			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_17_5206_s_142	15459290	We have previously shown that the  HMR-tRNA ( tRNA Thr [AGU] CR1) acts as a barrier to the spread of silencing at the  HMR locus, as it blocks repression of a  MATa1 reporter gene when juxtaposed between the gene and the silencer, and its deletion from the natural chromosome leads to a 60% reduction of expression of the downstream  GIT1 gene ( ).	gene_phenotype
71903	2	333982	5	NULL	NULL	0	NULL	MATa1	GP		is a type of					repressor gene	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_17_5206_s_142	15459290	We have previously shown that the  HMR-tRNA ( tRNA Thr [AGU] CR1) acts as a barrier to the spread of silencing at the  HMR locus, as it blocks repression of a  MATa1 reporter gene when juxtaposed between the gene and the silencer, and its deletion from the natural chromosome leads to a 60% reduction of expression of the downstream  GIT1 gene ( ).	gene_phenotype
71904	3	333982	5	NULL	NULL	0	NULL	HMR-tRNA	NucleicAcid		is juxtaposed between					gene	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_17_5206_s_142	15459290	We have previously shown that the  HMR-tRNA ( tRNA Thr [AGU] CR1) acts as a barrier to the spread of silencing at the  HMR locus, as it blocks repression of a  MATa1 reporter gene when juxtaposed between the gene and the silencer, and its deletion from the natural chromosome leads to a 60% reduction of expression of the downstream  GIT1 gene ( ).	gene_phenotype
71905	4	333982	5	NULL	NULL	0	NULL	HMR-tRNA	NucleicAcid		is juxtaposed between					silencer	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_17_5206_s_142	15459290	We have previously shown that the  HMR-tRNA ( tRNA Thr [AGU] CR1) acts as a barrier to the spread of silencing at the  HMR locus, as it blocks repression of a  MATa1 reporter gene when juxtaposed between the gene and the silencer, and its deletion from the natural chromosome leads to a 60% reduction of expression of the downstream  GIT1 gene ( ).	gene_phenotype
71906	5	333982	5	NULL	NULL	0	NULL	statement 3	Process		occurs along with					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_17_5206_s_142	15459290	We have previously shown that the  HMR-tRNA ( tRNA Thr [AGU] CR1) acts as a barrier to the spread of silencing at the  HMR locus, as it blocks repression of a  MATa1 reporter gene when juxtaposed between the gene and the silencer, and its deletion from the natural chromosome leads to a 60% reduction of expression of the downstream  GIT1 gene ( ).	gene_phenotype
71907	6	333982	5	NULL	NULL	0	NULL	statement 5	Process		leads to					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_17_5206_s_142	15459290	We have previously shown that the  HMR-tRNA ( tRNA Thr [AGU] CR1) acts as a barrier to the spread of silencing at the  HMR locus, as it blocks repression of a  MATa1 reporter gene when juxtaposed between the gene and the silencer, and its deletion from the natural chromosome leads to a 60% reduction of expression of the downstream  GIT1 gene ( ).	gene_phenotype
71908	7	333982	5	NULL	NULL	0	NULL	silencing	Process		occurs at					HMR locus	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_17_5206_s_142	15459290	We have previously shown that the  HMR-tRNA ( tRNA Thr [AGU] CR1) acts as a barrier to the spread of silencing at the  HMR locus, as it blocks repression of a  MATa1 reporter gene when juxtaposed between the gene and the silencer, and its deletion from the natural chromosome leads to a 60% reduction of expression of the downstream  GIT1 gene ( ).	gene_phenotype
71909	8	333982	5	NULL	NULL	0	NULL	HMR-tRNA	NucleicAcid		is a barrier to					statement 7	Process	spread of			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_17_5206_s_142	15459290	We have previously shown that the  HMR-tRNA ( tRNA Thr [AGU] CR1) acts as a barrier to the spread of silencing at the  HMR locus, as it blocks repression of a  MATa1 reporter gene when juxtaposed between the gene and the silencer, and its deletion from the natural chromosome leads to a 60% reduction of expression of the downstream  GIT1 gene ( ).	gene_phenotype
71910	9	333982	5	NULL	NULL	0	NULL	HMR-tRNA	NucleicAcid	deletion of	reduce					GIT1 gene	GP	expression of;;downstream			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_17_5206_s_142	15459290	We have previously shown that the  HMR-tRNA ( tRNA Thr [AGU] CR1) acts as a barrier to the spread of silencing at the  HMR locus, as it blocks repression of a  MATa1 reporter gene when juxtaposed between the gene and the silencer, and its deletion from the natural chromosome leads to a 60% reduction of expression of the downstream  GIT1 gene ( ).	gene_phenotype
71911	10	333982	5	NULL	NULL	0	NULL	HMR-tRNA	NucleicAcid		is					tRNA Thr [AGU] CR1	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_17_5206_s_142	15459290	We have previously shown that the  HMR-tRNA ( tRNA Thr [AGU] CR1) acts as a barrier to the spread of silencing at the  HMR locus, as it blocks repression of a  MATa1 reporter gene when juxtaposed between the gene and the silencer, and its deletion from the natural chromosome leads to a 60% reduction of expression of the downstream  GIT1 gene ( ).	gene_phenotype
71079	1	333984	5	NULL	NULL	NULL	NULL	snR190	NucleicAcid		is a type of					snoRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3726_s_3	9649442	We show that the snR190 and U14 snoRNAs from the yeast  Saccharomyces cerevisiae are co-transcribed as a dicistronic precursor which is processed by the RNA endonuclease Rnt1, the yeast ortholog of bacterial RNase III.  RNT1 disruption results in a dramatic decrease in the levels of mature U14 and snR190 and in accumulation of dicistronic snR190-U14 RNAs.	gene_phenotype
71080	2	333984	5	NULL	NULL	NULL	NULL	U14	NucleicAcid		is a type of					snoRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3726_s_3	9649442	We show that the snR190 and U14 snoRNAs from the yeast  Saccharomyces cerevisiae are co-transcribed as a dicistronic precursor which is processed by the RNA endonuclease Rnt1, the yeast ortholog of bacterial RNase III.  RNT1 disruption results in a dramatic decrease in the levels of mature U14 and snR190 and in accumulation of dicistronic snR190-U14 RNAs.	gene_phenotype
71081	3	333984	5	NULL	NULL	0	NULL	snR190	NucleicAcid	Saccharomyces cerevisiae	is co-transcribed with					U14	NucleicAcid	Saccharomyces cerevisiae			NULL		0	NULL	NULL	NULL	gw60_embo_17_13_3726_s_3	9649442	We show that the snR190 and U14 snoRNAs from the yeast  Saccharomyces cerevisiae are co-transcribed as a dicistronic precursor which is processed by the RNA endonuclease Rnt1, the yeast ortholog of bacterial RNase III.  RNT1 disruption results in a dramatic decrease in the levels of mature U14 and snR190 and in accumulation of dicistronic snR190-U14 RNAs.	gene_phenotype
71082	4	333984	5	NULL	NULL	0	NULL	statement 3	Process		occurs as					dicistronic precursor	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_embo_17_13_3726_s_3	9649442	We show that the snR190 and U14 snoRNAs from the yeast  Saccharomyces cerevisiae are co-transcribed as a dicistronic precursor which is processed by the RNA endonuclease Rnt1, the yeast ortholog of bacterial RNase III.  RNT1 disruption results in a dramatic decrease in the levels of mature U14 and snR190 and in accumulation of dicistronic snR190-U14 RNAs.	gene_phenotype
71083	5	333984	5	NULL	NULL	0	NULL	Rnt1	GP		is a type of					RNA endonuclease	GP				NULL		0	NULL	NULL	NULL	gw60_embo_17_13_3726_s_3	9649442	We show that the snR190 and U14 snoRNAs from the yeast  Saccharomyces cerevisiae are co-transcribed as a dicistronic precursor which is processed by the RNA endonuclease Rnt1, the yeast ortholog of bacterial RNase III.  RNT1 disruption results in a dramatic decrease in the levels of mature U14 and snR190 and in accumulation of dicistronic snR190-U14 RNAs.	gene_phenotype
71084	6	333984	5	NULL	NULL	NULL	NULL	dicistronic precursor	NucleicAcid		is processed by					Rnt1	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw60_embo_17_13_3726_s_3	9649442	We show that the snR190 and U14 snoRNAs from the yeast  Saccharomyces cerevisiae are co-transcribed as a dicistronic precursor which is processed by the RNA endonuclease Rnt1, the yeast ortholog of bacterial RNase III.  RNT1 disruption results in a dramatic decrease in the levels of mature U14 and snR190 and in accumulation of dicistronic snR190-U14 RNAs.	gene_phenotype
71085	7	333984	5	NULL	NULL	0	NULL	Rnt1	GP	yeast	is an orthologue of					RNase III	GP	bacteria			NULL		0	NULL	NULL	NULL	gw60_embo_17_13_3726_s_3	9649442	We show that the snR190 and U14 snoRNAs from the yeast  Saccharomyces cerevisiae are co-transcribed as a dicistronic precursor which is processed by the RNA endonuclease Rnt1, the yeast ortholog of bacterial RNase III.  RNT1 disruption results in a dramatic decrease in the levels of mature U14 and snR190 and in accumulation of dicistronic snR190-U14 RNAs.	gene_phenotype
71087	8	333984	5	NULL	NULL	0	NULL	RNT1	GP	disruption of	decreases		dramatically			U14	NucleicAcid	levels of;;mature			NULL		0	NULL	NULL	NULL	gw60_embo_17_13_3726_s_3	9649442	We show that the snR190 and U14 snoRNAs from the yeast  Saccharomyces cerevisiae are co-transcribed as a dicistronic precursor which is processed by the RNA endonuclease Rnt1, the yeast ortholog of bacterial RNase III.  RNT1 disruption results in a dramatic decrease in the levels of mature U14 and snR190 and in accumulation of dicistronic snR190-U14 RNAs.	gene_phenotype
71088	9	333984	5	NULL	NULL	0	NULL	RNT1	GP	disruption of	decreases		dramatically			snR190	NucleicAcid	levels of;;mature			NULL		0	NULL	NULL	NULL	gw60_embo_17_13_3726_s_3	9649442	We show that the snR190 and U14 snoRNAs from the yeast  Saccharomyces cerevisiae are co-transcribed as a dicistronic precursor which is processed by the RNA endonuclease Rnt1, the yeast ortholog of bacterial RNase III.  RNT1 disruption results in a dramatic decrease in the levels of mature U14 and snR190 and in accumulation of dicistronic snR190-U14 RNAs.	gene_phenotype
71089	10	333984	5	NULL	NULL	0	NULL	RNT1	GP	disruption of	decreases		dramatically			snR190-U14 RNAs	NucleicAcid	accumulation of;;dicistronic			NULL		0	NULL	NULL	NULL	gw60_embo_17_13_3726_s_3	9649442	We show that the snR190 and U14 snoRNAs from the yeast  Saccharomyces cerevisiae are co-transcribed as a dicistronic precursor which is processed by the RNA endonuclease Rnt1, the yeast ortholog of bacterial RNase III.  RNT1 disruption results in a dramatic decrease in the levels of mature U14 and snR190 and in accumulation of dicistronic snR190-U14 RNAs.	gene_phenotype
71107	1	333987	5	NULL	NULL	0	NULL	Rnt1	GP		cleaves					dicistronic RNAs	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_embo_17_13_3726_s_159	9649442	The ability of recombinant Rnt1 to chase the endogenous dicistronic RNAs into mature U14 and snR190 in  rnt1delta extracts, and the accumulation of 5''-extended forms of U14 and snR190 in the  rat1 and  xrn1 exonuclease mutants (Petfalski  et al., 1998  ) suggest a pathway in which the dicistronic RNAs are first cleaved by Rnt1 and then processed to the mature ends by exonucleases which are present in the extract.	gene_phenotype
71108	2	333987	5	NULL	NULL	0	NULL	exonucleases	GP		process					dicistronic RNAs	NucleicAcid	cleaved			NULL		0	NULL	NULL	NULL	gw60_embo_17_13_3726_s_159	9649442	The ability of recombinant Rnt1 to chase the endogenous dicistronic RNAs into mature U14 and snR190 in  rnt1delta extracts, and the accumulation of 5''-extended forms of U14 and snR190 in the  rat1 and  xrn1 exonuclease mutants (Petfalski  et al., 1998  ) suggest a pathway in which the dicistronic RNAs are first cleaved by Rnt1 and then processed to the mature ends by exonucleases which are present in the extract.	gene_phenotype
71109	3	333987	5	NULL	NULL	0	NULL	statement 1	Process		is followed by					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_embo_17_13_3726_s_159	9649442	The ability of recombinant Rnt1 to chase the endogenous dicistronic RNAs into mature U14 and snR190 in  rnt1delta extracts, and the accumulation of 5''-extended forms of U14 and snR190 in the  rat1 and  xrn1 exonuclease mutants (Petfalski  et al., 1998  ) suggest a pathway in which the dicistronic RNAs are first cleaved by Rnt1 and then processed to the mature ends by exonucleases which are present in the extract.	gene_phenotype
71110	1	333988	5	NULL	NULL	0	NULL	Rcl1p	GP	depletion of	affects		possibly			snoRNAs	NucleicAcid	accumulation of			NULL		0	NULL	NULL	NULL	gw60_embo_19_9_2115_s_172	10790377	We therefore investigated whether depletion of Rcl1p affects the accumulation of these or other snoRNAs; the snoRNAs investigated included some transcribed from independent genes as monomeric (U3, snR10 and snR30) or dimeric (U14 and snR190) RNAs, or processed from introns (U24) (reviewed by  Maxwell and Fournier, 1995;  Tollervey and Kiss, 1997).	gene_phenotype
71111	1	333989	5	NULL	NULL	0	NULL	UMOs	NucleicAcid		is a type of					co-linear DNA sequence	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_embo_17_13_3726_s_99	9649442	These probes gave rise to protected bands of the same size as snR190 and U14 snoRNAs in RNAs from the wild-type cells, and of the same size as the UMOs species from the  rnt1delta cells (data not shown), indicating that the UMOs are co-linear with the DNA sequence and that they do not arise from a splicing or a genomic rearrangement event.	gene_phenotype
71112	2	333989	5	NULL	NULL	0	NULL	UMOs	NucleicAcid		does not arise from					splicing	Process				NULL		0	NULL	NULL	NULL	gw60_embo_17_13_3726_s_99	9649442	These probes gave rise to protected bands of the same size as snR190 and U14 snoRNAs in RNAs from the wild-type cells, and of the same size as the UMOs species from the  rnt1delta cells (data not shown), indicating that the UMOs are co-linear with the DNA sequence and that they do not arise from a splicing or a genomic rearrangement event.	gene_phenotype
71113	3	333989	5	NULL	NULL	0	NULL	UMOs	NucleicAcid		does not arise from					genomic rearrangement event	Process				NULL		0	NULL	NULL	NULL	gw60_embo_17_13_3726_s_99	9649442	These probes gave rise to protected bands of the same size as snR190 and U14 snoRNAs in RNAs from the wild-type cells, and of the same size as the UMOs species from the  rnt1delta cells (data not shown), indicating that the UMOs are co-linear with the DNA sequence and that they do not arise from a splicing or a genomic rearrangement event.	gene_phenotype
71114	4	333989	5	NULL	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_embo_17_13_3726_s_99	9649442	These probes gave rise to protected bands of the same size as snR190 and U14 snoRNAs in RNAs from the wild-type cells, and of the same size as the UMOs species from the  rnt1delta cells (data not shown), indicating that the UMOs are co-linear with the DNA sequence and that they do not arise from a splicing or a genomic rearrangement event.	gene_phenotype
71115	1	333990	5	NULL	NULL	0	NULL	U14	NucleicAcid		is essential for					cell viability	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_12_7897_s_238	10567516	However, the snR190-U14 precursor probably retains at least some functionality, since U14 is essential for cell viability and depletion of U14 does block pre-rRNA processing at sites A1 and A2 ( 113).	gene_phenotype
71116	2	333990	5	NULL	NULL	0	NULL	U14	NucleicAcid	depletion of	block					pre-rRNA	NucleicAcid	processing of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_12_7897_s_238	10567516	However, the snR190-U14 precursor probably retains at least some functionality, since U14 is essential for cell viability and depletion of U14 does block pre-rRNA processing at sites A1 and A2 ( 113).	gene_phenotype
71117	1	333992	5	NULL	NULL	0	NULL	NME1	GP	S. cerevisiae	is necessary for					viability	Process				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_66_0_409_s_136	9242913	Cloning of the  S. cerevisiae gene encoding the RNA component of RNase MRP ( NME1) revealed that it is necessary for viability, consistent with an essential nuclear  function ( 50).	gene_phenotype
71118	2	333992	5	NULL	NULL	0	NULL	NME1	GP	S. cerevisiae	is essential for					nuclear function	Process				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_66_0_409_s_136	9242913	Cloning of the  S. cerevisiae gene encoding the RNA component of RNase MRP ( NME1) revealed that it is necessary for viability, consistent with an essential nuclear  function ( 50).	gene_phenotype
71119	3	333992	5	NULL	NULL	NULL	NULL	NME1	GP	S. cerevisiae	is RNA component of					MRP	GP	S.cerevisiae			NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_66_0_409_s_136	9242913	Cloning of the  S. cerevisiae gene encoding the RNA component of RNase MRP ( NME1) revealed that it is necessary for viability, consistent with an essential nuclear  function ( 50).	gene_phenotype
71120	4	333992	5	NULL	NULL	0	NULL	MRP	GP		is a type of					RNase	GP				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_66_0_409_s_136	9242913	Cloning of the  S. cerevisiae gene encoding the RNA component of RNase MRP ( NME1) revealed that it is necessary for viability, consistent with an essential nuclear  function ( 50).	gene_phenotype
71121	1	333994	5	NULL	NULL	0	NULL	hc PUS4	GP	presence of	accumulates					tRNA precursors	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_7_2505_s_6	10713174	The presence of hc PUS4 or hc NME1 led to the accumulation of certain tRNA precursors, and their Gcd  phenotypes were reversed by overexpressing the RNA component of RNase P ( RPR1), responsible for 5''-end processing of all tRNAs.	gene_phenotype
71122	2	333994	5	NULL	NULL	0	NULL	hc NME1	GP	presence of	accumulates					tRNA precursors	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_7_2505_s_6	10713174	The presence of hc PUS4 or hc NME1 led to the accumulation of certain tRNA precursors, and their Gcd  phenotypes were reversed by overexpressing the RNA component of RNase P ( RPR1), responsible for 5''-end processing of all tRNAs.	gene_phenotype
71123	3	333994	5	NULL	NULL	0	NULL	RPR1	GP		is responsible for					tRNAs	NucleicAcid	5''-end processing of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_7_2505_s_6	10713174	The presence of hc PUS4 or hc NME1 led to the accumulation of certain tRNA precursors, and their Gcd  phenotypes were reversed by overexpressing the RNA component of RNase P ( RPR1), responsible for 5''-end processing of all tRNAs.	gene_phenotype
71124	4	333994	5	NULL	NULL	NULL	NULL	RPR1	GP	overexpression of	reverse					Gcd phenotypes	PhysicalPhenomenon				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_7_2505_s_6	10713174	The presence of hc PUS4 or hc NME1 led to the accumulation of certain tRNA precursors, and their Gcd  phenotypes were reversed by overexpressing the RNA component of RNase P ( RPR1), responsible for 5''-end processing of all tRNAs.	gene_phenotype
71125	5	333994	5	NULL	NULL	0	NULL	RPR1	GP		is RNA component of					RNase P	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_7_2505_s_6	10713174	The presence of hc PUS4 or hc NME1 led to the accumulation of certain tRNA precursors, and their Gcd  phenotypes were reversed by overexpressing the RNA component of RNase P ( RPR1), responsible for 5''-end processing of all tRNAs.	gene_phenotype
71182	1	333995	5	NULL	NULL	0	NULL	RMRP	GP	mutation	is introduced into					NME1	GP	yeast			NULL		0	NULL	NULL	NULL	abs-batch0540-0549_hum-mol-genet_14_23_16254002_s_7	16254002	RMRP mutations introduced into  the yeast ortholog, NME1, exhibited normal mitochondrial function, chromosomal  segregation and cell cycle progression, while a CHH fibroblast cell line  exhibited normal mitochondrial content.	gene_phenotype
71183	2	333995	5	NULL	NULL	0	NULL	statement 1	Process		exhibit					mitochondria	CellComponent	normal function of			NULL		0	NULL	NULL	NULL	abs-batch0540-0549_hum-mol-genet_14_23_16254002_s_7	16254002	RMRP mutations introduced into  the yeast ortholog, NME1, exhibited normal mitochondrial function, chromosomal  segregation and cell cycle progression, while a CHH fibroblast cell line  exhibited normal mitochondrial content.	gene_phenotype
71186	3	333995	5	NULL	NULL	0	NULL	statement 1	Process		exhibit					chromosome	Chromosome	normal segregation of			NULL		0	NULL	NULL	NULL	abs-batch0540-0549_hum-mol-genet_14_23_16254002_s_7	16254002	RMRP mutations introduced into  the yeast ortholog, NME1, exhibited normal mitochondrial function, chromosomal  segregation and cell cycle progression, while a CHH fibroblast cell line  exhibited normal mitochondrial content.	gene_phenotype
71188	4	333995	5	NULL	NULL	0	NULL	statement 1	Process		exhibit					cell cycle	Process	normal progression of			NULL		0	NULL	NULL	NULL	abs-batch0540-0549_hum-mol-genet_14_23_16254002_s_7	16254002	RMRP mutations introduced into  the yeast ortholog, NME1, exhibited normal mitochondrial function, chromosomal  segregation and cell cycle progression, while a CHH fibroblast cell line  exhibited normal mitochondrial content.	gene_phenotype
71189	5	333995	5	NULL	NULL	0	NULL	CHH	Cell		is a type of					fibroblast cell line	Cell				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_hum-mol-genet_14_23_16254002_s_7	16254002	RMRP mutations introduced into  the yeast ortholog, NME1, exhibited normal mitochondrial function, chromosomal  segregation and cell cycle progression, while a CHH fibroblast cell line  exhibited normal mitochondrial content.	gene_phenotype
71190	6	333995	5	NULL	NULL	0	NULL	CHH	Cell		exhibit					mitochondria	CellComponent	normal content of			NULL		0	NULL	NULL	NULL	abs-batch0540-0549_hum-mol-genet_14_23_16254002_s_7	16254002	RMRP mutations introduced into  the yeast ortholog, NME1, exhibited normal mitochondrial function, chromosomal  segregation and cell cycle progression, while a CHH fibroblast cell line  exhibited normal mitochondrial content.	gene_phenotype
71192	1	333996	5	NULL	NULL	0	NULL	GCN4 mRNA	NucleicAcid	translation of	is induced by					NME1	GP	overexpression of			NULL		0	NULL	NULL	NULL	gw70_genesdev_17_2_162_s_103	12533506	Thus,  GCN4 mRNA translation can be induced by overexpression of either  NME1, encoding the RNA subunit of RNase MRP (Tavernarakis et al. 1996 ), or of  PUS4, encoding psi55 pseudouridylase (Qiu et al. 2000 ), and both phenotypes are correlated with increased accumulation of pre-tRNAs.	gene_phenotype
71194	2	333996	5	NULL	NULL	NULL	NULL	NME1	GP		encodes for					RNA subunit of MRP	GP				NULL		NULL	NULL	NULL	NULL	gw70_genesdev_17_2_162_s_103	12533506	Thus,  GCN4 mRNA translation can be induced by overexpression of either  NME1, encoding the RNA subunit of RNase MRP (Tavernarakis et al. 1996 ), or of  PUS4, encoding psi55 pseudouridylase (Qiu et al. 2000 ), and both phenotypes are correlated with increased accumulation of pre-tRNAs.	gene_phenotype
71195	3	333996	5	NULL	NULL	0	NULL	MRP	GP		is a type of					RNase	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_2_162_s_103	12533506	Thus,  GCN4 mRNA translation can be induced by overexpression of either  NME1, encoding the RNA subunit of RNase MRP (Tavernarakis et al. 1996 ), or of  PUS4, encoding psi55 pseudouridylase (Qiu et al. 2000 ), and both phenotypes are correlated with increased accumulation of pre-tRNAs.	gene_phenotype
71196	4	333996	5	NULL	NULL	0	NULL	GCN4 mRNA	NucleicAcid	translation of	is induced by					PUS4	GP	overexpression of			NULL		0	NULL	NULL	NULL	gw70_genesdev_17_2_162_s_103	12533506	Thus,  GCN4 mRNA translation can be induced by overexpression of either  NME1, encoding the RNA subunit of RNase MRP (Tavernarakis et al. 1996 ), or of  PUS4, encoding psi55 pseudouridylase (Qiu et al. 2000 ), and both phenotypes are correlated with increased accumulation of pre-tRNAs.	gene_phenotype
71197	5	333996	5	NULL	NULL	0	NULL	PUS4	GP		encodes for					psi55 pseudouridylase 	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_2_162_s_103	12533506	Thus,  GCN4 mRNA translation can be induced by overexpression of either  NME1, encoding the RNA subunit of RNase MRP (Tavernarakis et al. 1996 ), or of  PUS4, encoding psi55 pseudouridylase (Qiu et al. 2000 ), and both phenotypes are correlated with increased accumulation of pre-tRNAs.	gene_phenotype
71198	1	333997	5	NULL	NULL	0	NULL	PCNA	GP		plays a role in		putative			metastasis	Process				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71199	2	333997	5	NULL	NULL	0	NULL	p53	GP		plays a role in		putative			metastasis	Process				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71200	3	333997	5	NULL	NULL	0	NULL	Rb	GP		plays a role in		putative			metastasis	Process				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71201	4	333997	5	NULL	NULL	0	NULL	myc	GP		plays a role in		putative			metastasis	Process				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71202	5	333997	5	NULL	NULL	0	NULL	bcl-2	GP		plays a role in		putative			metastasis	Process				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71203	6	333997	5	NULL	NULL	0	NULL	EGF	GP		plays a role in		putative			metastasis	Process				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71204	7	333997	5	NULL	NULL	0	NULL	EGFR	GP		plays a role in		putative			metastasis	Process				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71205	8	333997	5	NULL	NULL	0	NULL	neu	GP		plays a role in		putative			metastasis	Process				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71206	9	333997	5	NULL	NULL	0	NULL	nm23	GP		plays a role in		putative			metastasis	Process				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71207	10	333997	5	NULL	NULL	0	NULL	desmoplakin	GP		plays a role in		putative			metastasis	Process				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71208	11	333997	5	NULL	NULL	0	NULL	N-CAM	GP		plays a role in		putative			metastasis	Process				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71209	12	333997	5	NULL	NULL	0	NULL	Ep-CAM	GP		plays a role in		putative			metastasis	Process				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71210	13	333997	5	NULL	NULL	0	NULL	E-cadherin	GP		plays a role in		putative			metastasis	Process				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71211	14	333997	5	NULL	NULL	NULL	NULL	CCND1	GP		plays a role in		putative			metastasis	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71212	15	333997	5	NULL	NULL	0	NULL	EMS1	GP		plays a role in		putative			metastasis	Process				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71213	16	333997	5	NULL	NULL	0	NULL	PCNA	GP		is					proliferating cell nuclear antigen	GP				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71214	17	333997	5	NULL	NULL	0	NULL	Rb	GP		is					retinoblastoma tumor-suppressor gene	GP				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71215	18	333997	5	NULL	NULL	0	NULL	bcl-2	GP		is an inhibitor of					apoptosis	Process				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71216	19	333997	5	NULL	NULL	0	NULL	EGF	GP		is					epidermal growth factor	GP				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71217	20	333997	5	NULL	NULL	0	NULL	EGFR	GP		is					EGF-receptor	GP				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71224	21	333997	5	NULL	NULL	0	NULL	NME1	GP		is a synonym of					nm23	GP				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71225	22	333997	5	NULL	NULL	0	NULL	NME1	GP		is a suppressor of		putative			metastasis	Process				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71226	23	333997	5	NULL	NULL	0	NULL	N-CAM	GP		is					neuron cell-adhesion molecule	GP				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71227	24	333997	5	NULL	NULL	0	NULL	Ep-CAM	GP		is					epithelial cell-adhesion molecule	GP				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71228	25	333997	5	NULL	NULL	0	NULL	CCND1	GP		is					cyclin D1	GP				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_arch-otolaryngol-head-neck-surg_123_4_9109790_s_11	9109790	The following markers were selected on their  putative role in the process of metastasis and were studied using immunohistochemical  and/or Southern blot techniques: proliferating cell nuclear antigen (PCNA),  p53, retinoblastoma tumor-suppressor gene (Rb), myc, bcl-2 (inhibitor  of apoptosis), epidermal growth factor (EGF), EGF-receptor (EGFR), neu,  nm23 (also known as NME1, putative metastasis suppressor), desmoplakin,  neuron cell-adhesion molecule (N-CAM), epithelial cell-adhesion molecule  (Ep-CAM), E-cadherin, cyclin D1 (CCND1), and EMS1.	gene_phenotype
71229	1	333999	5	NULL	NULL	0	NULL	snR10	GP	loss of	impairs					protein synthesis	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_11_2_425_s_237	12620230	Loss of snR10 itself impairs protein synthesis activity, and this defect is not rescued by expression of the snR10 C gene   (Figure 6C).	gene_phenotype
71230	2	333999	5	NULL	NULL	0	NULL	snR10 C gene	GP	expression of	does not rescue					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_11_2_425_s_237	12620230	Loss of snR10 itself impairs protein synthesis activity, and this defect is not rescued by expression of the snR10 C gene   (Figure 6C).	gene_phenotype
71231	1	334000	5	NULL	NULL	0	NULL	U14	NucleicAcid		plays a role in		possibly			rRNA	NucleicAcid	modifying the folding of			NULL		0	NULL	NULL	NULL	gw70_annurevgenet_33_0_261_s_221	10690410	It may be that U14, snR10, and snR30/U17 are derived from conventional modification  guide RNAs but have assumed roles in modifying the folding of the rRNA.	gene_phenotype
71232	2	334000	5	NULL	NULL	0	NULL	snR10	GP		plays a role in		possibly			rRNA	NucleicAcid	modifying the folding of			NULL		0	NULL	NULL	NULL	gw70_annurevgenet_33_0_261_s_221	10690410	It may be that U14, snR10, and snR30/U17 are derived from conventional modification  guide RNAs but have assumed roles in modifying the folding of the rRNA.	gene_phenotype
71233	3	334000	5	NULL	NULL	0	NULL	snR30/U17	NucleicAcid		plays a role in		possibly			rRNA	NucleicAcid	modifying the folding of			NULL		0	NULL	NULL	NULL	gw70_annurevgenet_33_0_261_s_221	10690410	It may be that U14, snR10, and snR30/U17 are derived from conventional modification  guide RNAs but have assumed roles in modifying the folding of the rRNA.	gene_phenotype
71246	1	334001	5	NULL	NULL	0	NULL	SNR10	NucleicAcid		is a type of					H/ACA small RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_pnas_103_11_4192_s_60	16537507	( a)  SNR10 is a 245-bases-long essential H/ACA small RNA required for modification of rRNA precursor  sequence.	gene_phenotype
71247	2	334001	5	NULL	NULL	0	NULL	SNR10	GP		is required for					rRNA precursor sequence	NucleicAcid	modification of			NULL		0	NULL	NULL	NULL	gw70_pnas_103_11_4192_s_60	16537507	( a)  SNR10 is a 245-bases-long essential H/ACA small RNA required for modification of rRNA precursor  sequence.	gene_phenotype
71248	1	334002	5	NULL	NULL	0	NULL	snR30	NucleicAcid		is required for					cell viability	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_38	14749391	While yeast cells lacking snR10 are only slightly impaired in cell growth and in processing of 35S pre-rRNA, snR30 is essential for cell viability ( ,  ).	gene_phenotype
71249	2	334002	5	NULL	NULL	0	NULL	yeast cells	Cell		lacks					snR10	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_38	14749391	While yeast cells lacking snR10 are only slightly impaired in cell growth and in processing of 35S pre-rRNA, snR30 is essential for cell viability ( ,  ).	gene_phenotype
71250	3	334002	5	NULL	NULL	0	NULL	statement 2	Cell		impaired in		slightly			cell growth	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_38	14749391	While yeast cells lacking snR10 are only slightly impaired in cell growth and in processing of 35S pre-rRNA, snR30 is essential for cell viability ( ,  ).	gene_phenotype
71251	4	334002	5	NULL	NULL	0	NULL	statement 2	Cell		impaired in		slightly			35S pre-rRNA	NucleicAcid	processing of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_38	14749391	While yeast cells lacking snR10 are only slightly impaired in cell growth and in processing of 35S pre-rRNA, snR30 is essential for cell viability ( ,  ).	gene_phenotype
71252	1	334003	5	NULL	NULL	0	NULL	snoRNAs	NucleicAcid		is required for					rRNA	NucleicAcid	modification of			NULL		0	NULL	NULL	NULL	gw60_genesdev_12_4_527_s_30	9472021	In contrast, none of the snoRNAs that direct rRNA modification is essential for cell viability, although the absence of the   guide snoRNA, snR10, leads to some cold sensitivity (Tollervey 1987  ; Ni et al. 1997  ).	gene_phenotype
71253	2	334003	5	NULL	NULL	0	NULL	statement 1	Process		is not essential for					cell viability	Process				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_4_527_s_30	9472021	In contrast, none of the snoRNAs that direct rRNA modification is essential for cell viability, although the absence of the   guide snoRNA, snR10, leads to some cold sensitivity (Tollervey 1987  ; Ni et al. 1997  ).	gene_phenotype
71254	3	334003	5	NULL	NULL	0	NULL	snR10	NucleicAcid	absence of	leads to					cold sensitivity	Process				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_4_527_s_30	9472021	In contrast, none of the snoRNAs that direct rRNA modification is essential for cell viability, although the absence of the   guide snoRNA, snR10, leads to some cold sensitivity (Tollervey 1987  ; Ni et al. 1997  ).	gene_phenotype
71255	4	334003	5	NULL	NULL	0	NULL	snR10	NucleicAcid		is a type of					guide snoRNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_4_527_s_30	9472021	In contrast, none of the snoRNAs that direct rRNA modification is essential for cell viability, although the absence of the   guide snoRNA, snR10, leads to some cold sensitivity (Tollervey 1987  ; Ni et al. 1997  ).	gene_phenotype
71256	1	334004	5	NULL	NULL	0	NULL	snR30	NucleicAcid		is a type of					box H/ACA snoRNAs	NucleicAcid				NULL	yeast	0	NULL	NULL	NULL	gw60_cellbiol_144_6_1123_s_322	10087258	This is not surprising, given that all  box H/ACA snoRNAs found in yeast, with the exception of snR30 (Morrissey and Tollervey, 1993  ) and snR10 (Tollervey, 1987  ; Tollervey and Guthrie, 1985  ), are dispensable for viability.	gene_phenotype
71257	2	334004	5	NULL	NULL	0	NULL	snR10	NucleicAcid		is a type of					box H/ACA snoRNAs	NucleicAcid				NULL	yeast	0	NULL	NULL	NULL	gw60_cellbiol_144_6_1123_s_322	10087258	This is not surprising, given that all  box H/ACA snoRNAs found in yeast, with the exception of snR30 (Morrissey and Tollervey, 1993  ) and snR10 (Tollervey, 1987  ; Tollervey and Guthrie, 1985  ), are dispensable for viability.	gene_phenotype
71258	3	334004	5	NULL	NULL	0	NULL	box H/ACA snoRNAs	NucleicAcid		is dispensable for					viability	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_144_6_1123_s_322	10087258	This is not surprising, given that all  box H/ACA snoRNAs found in yeast, with the exception of snR30 (Morrissey and Tollervey, 1993  ) and snR10 (Tollervey, 1987  ; Tollervey and Guthrie, 1985  ), are dispensable for viability.	gene_phenotype
71259	4	334004	5	NULL	NULL	0	NULL	snR10	NucleicAcid		is not dispensable for					viability					NULL		0	NULL	NULL	NULL	gw60_cellbiol_144_6_1123_s_322	10087258	This is not surprising, given that all  box H/ACA snoRNAs found in yeast, with the exception of snR30 (Morrissey and Tollervey, 1993  ) and snR10 (Tollervey, 1987  ; Tollervey and Guthrie, 1985  ), are dispensable for viability.	gene_phenotype
71260	5	334004	5	NULL	NULL	0	NULL	snR30	NucleicAcid		is not dispensable for					viability	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_144_6_1123_s_322	10087258	This is not surprising, given that all  box H/ACA snoRNAs found in yeast, with the exception of snR30 (Morrissey and Tollervey, 1993  ) and snR10 (Tollervey, 1987  ; Tollervey and Guthrie, 1985  ), are dispensable for viability.	gene_phenotype
71261	1	334005	5	NULL	NULL	0	NULL	snR10	GP		influences					18S RNA	NucleicAcid	production of			NULL		0	NULL	NULL	NULL	gw60_molcell_11_2_425_s_192	12620230	Because snR10 also influences production of 18S RNA and accumulation of 40S subunits, it is important to determine if the defects observed in growth and ribosome activity are due to loss of the  2919 modification or impaired processing of 18S rRNA.	gene_phenotype
71262	2	334005	5	NULL	NULL	0	NULL	snR10	NucleicAcid		influences					40S subunits	NucleicAcid	accumulation of			NULL		0	NULL	NULL	NULL	gw60_molcell_11_2_425_s_192	12620230	Because snR10 also influences production of 18S RNA and accumulation of 40S subunits, it is important to determine if the defects observed in growth and ribosome activity are due to loss of the  2919 modification or impaired processing of 18S rRNA.	gene_phenotype
71900	2	334007	5	NULL	NULL	0	NULL	RXR-TR heterodimer	GP	obligate	mediates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_6_3375_s_77	9452457	Thus T-CoR repressed gene activation mediated by an obligate RXR-TR heterodimer from the sub-optimal TRE 6DR4.	gene_phenotype
71901	1	334007	5	NULL	NULL	NULL	NULL	gene activation	Process		is repressed by					T-CoR	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_6_3375_s_77	9452457	Thus T-CoR repressed gene activation mediated by an obligate RXR-TR heterodimer from the sub-optimal TRE 6DR4.	gene_phenotype
71263	1	334008	5	NULL	NULL	0	NULL	snR10	NucleicAcid		is essential for					rRNA	NucleicAcid	processing of			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_11_3877_s_24	10564278	Some snoRNAs of the box H/ACA family are essential for rRNA processing (snR10 [Tollervey, 1987  ], snR30 [Morrissey and Tollervey, 1993  ], and E1 = U17, E2, and E3 [Mishra and Elicieri, 1997  ]), but the majority function as guide RNAs for pseudouridine modifications in rRNA (Ganot  et al., 1997a  ; Ni  et al., 1997  ; Smith and Steitz, 1997  ).	gene_phenotype
71264	2	334008	5	NULL	NULL	0	NULL	snR30	NucleicAcid		is essential for					rRNA	NucleicAcid	processing of			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_11_3877_s_24	10564278	Some snoRNAs of the box H/ACA family are essential for rRNA processing (snR10 [Tollervey, 1987  ], snR30 [Morrissey and Tollervey, 1993  ], and E1 = U17, E2, and E3 [Mishra and Elicieri, 1997  ]), but the majority function as guide RNAs for pseudouridine modifications in rRNA (Ganot  et al., 1997a  ; Ni  et al., 1997  ; Smith and Steitz, 1997  ).	gene_phenotype
71265	3	334008	5	NULL	NULL	0	NULL	E1	NucleicAcid		is essential for					rRNA	NucleicAcid	processing of			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_11_3877_s_24	10564278	Some snoRNAs of the box H/ACA family are essential for rRNA processing (snR10 [Tollervey, 1987  ], snR30 [Morrissey and Tollervey, 1993  ], and E1 = U17, E2, and E3 [Mishra and Elicieri, 1997  ]), but the majority function as guide RNAs for pseudouridine modifications in rRNA (Ganot  et al., 1997a  ; Ni  et al., 1997  ; Smith and Steitz, 1997  ).	gene_phenotype
71266	4	334008	5	NULL	NULL	0	NULL	snR10	NucleicAcid		is a member of					box H/ACA family of snoRNAs 	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_11_3877_s_24	10564278	Some snoRNAs of the box H/ACA family are essential for rRNA processing (snR10 [Tollervey, 1987  ], snR30 [Morrissey and Tollervey, 1993  ], and E1 = U17, E2, and E3 [Mishra and Elicieri, 1997  ]), but the majority function as guide RNAs for pseudouridine modifications in rRNA (Ganot  et al., 1997a  ; Ni  et al., 1997  ; Smith and Steitz, 1997  ).	gene_phenotype
71267	5	334008	5	NULL	NULL	0	NULL	snR30	NucleicAcid		is a member of					box H/ACA family of snoRNAs	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_11_3877_s_24	10564278	Some snoRNAs of the box H/ACA family are essential for rRNA processing (snR10 [Tollervey, 1987  ], snR30 [Morrissey and Tollervey, 1993  ], and E1 = U17, E2, and E3 [Mishra and Elicieri, 1997  ]), but the majority function as guide RNAs for pseudouridine modifications in rRNA (Ganot  et al., 1997a  ; Ni  et al., 1997  ; Smith and Steitz, 1997  ).	gene_phenotype
71268	6	334008	5	NULL	NULL	0	NULL	E1 	NucleicAcid		is a member of					box H/ACA family of snoRNAs	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_11_3877_s_24	10564278	Some snoRNAs of the box H/ACA family are essential for rRNA processing (snR10 [Tollervey, 1987  ], snR30 [Morrissey and Tollervey, 1993  ], and E1 = U17, E2, and E3 [Mishra and Elicieri, 1997  ]), but the majority function as guide RNAs for pseudouridine modifications in rRNA (Ganot  et al., 1997a  ; Ni  et al., 1997  ; Smith and Steitz, 1997  ).	gene_phenotype
71269	7	334008	5	NULL	NULL	0	NULL	box H/ACA family of snoRNAs	NucleicAcid	majority of	functions as					guide RNAs	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_11_3877_s_24	10564278	Some snoRNAs of the box H/ACA family are essential for rRNA processing (snR10 [Tollervey, 1987  ], snR30 [Morrissey and Tollervey, 1993  ], and E1 = U17, E2, and E3 [Mishra and Elicieri, 1997  ]), but the majority function as guide RNAs for pseudouridine modifications in rRNA (Ganot  et al., 1997a  ; Ni  et al., 1997  ; Smith and Steitz, 1997  ).	gene_phenotype
71270	8	334008	5	NULL	NULL	0	NULL	guide RNAs	NucleicAcid		is required for					rRNA	NucleicAcid	pseudouridine modifications of			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_10_11_3877_s_24	10564278	Some snoRNAs of the box H/ACA family are essential for rRNA processing (snR10 [Tollervey, 1987  ], snR30 [Morrissey and Tollervey, 1993  ], and E1 = U17, E2, and E3 [Mishra and Elicieri, 1997  ]), but the majority function as guide RNAs for pseudouridine modifications in rRNA (Ganot  et al., 1997a  ; Ni  et al., 1997  ; Smith and Steitz, 1997  ).	gene_phenotype
71271	1	334014	5	NULL	NULL	0	NULL	cold sensitivity	Process	suppression of	involves		may			PET494	GP	stimulation of;;transcription of			NULL		0	NULL	NULL	NULL	gw70_yeast_20_11_955_s_418	12898711	As no sequence changes distinguishing  PET494 from the wild-type allele were found, the suppression of the cold sensitivity seemed  to involve stimulation of the  PET494 transcription.	gene_phenotype
71878	1	334022	5	NULL	NULL	0	NULL	PET54	GP		is an activator of					translation	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1826_s_104	9528754	The wild-type function of the  COX3-specific translational activators  PET54,  PET122, and  PET494 was required for respiratory growth of the  cox3-15 strains carrying  MRP21 or  MRP51 suppressor alleles.	gene_phenotype
71879	2	334022	5	NULL	NULL	0	NULL	statement 1	Process		is specific to					COX3	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1826_s_104	9528754	The wild-type function of the  COX3-specific translational activators  PET54,  PET122, and  PET494 was required for respiratory growth of the  cox3-15 strains carrying  MRP21 or  MRP51 suppressor alleles.	gene_phenotype
71881	3	334022	5	NULL	NULL	0	NULL	PET122	GP		is an activator of					translation	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1826_s_104	9528754	The wild-type function of the  COX3-specific translational activators  PET54,  PET122, and  PET494 was required for respiratory growth of the  cox3-15 strains carrying  MRP21 or  MRP51 suppressor alleles.	gene_phenotype
71883	4	334022	5	NULL	NULL	0	NULL	statement 1	Process		is specific to					COX3	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1826_s_104	9528754	The wild-type function of the  COX3-specific translational activators  PET54,  PET122, and  PET494 was required for respiratory growth of the  cox3-15 strains carrying  MRP21 or  MRP51 suppressor alleles.	gene_phenotype
71884	5	334022	5	NULL	NULL	0	NULL	PET494	GP		is an activator of					translation	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1826_s_104	9528754	The wild-type function of the  COX3-specific translational activators  PET54,  PET122, and  PET494 was required for respiratory growth of the  cox3-15 strains carrying  MRP21 or  MRP51 suppressor alleles.	gene_phenotype
71885	6	334022	5	NULL	NULL	0	NULL	statement 1	Process		is specific to					COX3	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1826_s_104	9528754	The wild-type function of the  COX3-specific translational activators  PET54,  PET122, and  PET494 was required for respiratory growth of the  cox3-15 strains carrying  MRP21 or  MRP51 suppressor alleles.	gene_phenotype
71886	7	334022	5	NULL	NULL	0	NULL	cox3-15 strain	Organism		carry					MRP21	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1826_s_104	9528754	The wild-type function of the  COX3-specific translational activators  PET54,  PET122, and  PET494 was required for respiratory growth of the  cox3-15 strains carrying  MRP21 or  MRP51 suppressor alleles.	gene_phenotype
71887	8	334022	5	NULL	NULL	0	NULL	cox3-15 strain	Organism		carry					MRP51	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1826_s_104	9528754	The wild-type function of the  COX3-specific translational activators  PET54,  PET122, and  PET494 was required for respiratory growth of the  cox3-15 strains carrying  MRP21 or  MRP51 suppressor alleles.	gene_phenotype
71888	9	334022	5	NULL	NULL	0	NULL	statement 7	Process		is an alternative to					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1826_s_104	9528754	The wild-type function of the  COX3-specific translational activators  PET54,  PET122, and  PET494 was required for respiratory growth of the  cox3-15 strains carrying  MRP21 or  MRP51 suppressor alleles.	gene_phenotype
71889	10	334022	5	NULL	NULL	0	NULL	MRP21	GP		is a type of					suppressor allele	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1826_s_104	9528754	The wild-type function of the  COX3-specific translational activators  PET54,  PET122, and  PET494 was required for respiratory growth of the  cox3-15 strains carrying  MRP21 or  MRP51 suppressor alleles.	gene_phenotype
71890	11	334022	5	NULL	NULL	0	NULL	MRP51	GP		is a type of					suppressor allele	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1826_s_104	9528754	The wild-type function of the  COX3-specific translational activators  PET54,  PET122, and  PET494 was required for respiratory growth of the  cox3-15 strains carrying  MRP21 or  MRP51 suppressor alleles.	gene_phenotype
71891	12	334022	5	NULL	NULL	0	NULL	PET54	GP	wild-type function of	is required for					statement 7	Process	respiratory growth of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1826_s_104	9528754	The wild-type function of the  COX3-specific translational activators  PET54,  PET122, and  PET494 was required for respiratory growth of the  cox3-15 strains carrying  MRP21 or  MRP51 suppressor alleles.	gene_phenotype
71893	13	334022	5	NULL	NULL	NULL	NULL	PET54	GP	wild-type function of	is required for					statement 8	Process	respiratory growth of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_4_1826_s_104	9528754	The wild-type function of the  COX3-specific translational activators  PET54,  PET122, and  PET494 was required for respiratory growth of the  cox3-15 strains carrying  MRP21 or  MRP51 suppressor alleles.	gene_phenotype
71895	14	334022	5	NULL	NULL	0	NULL	PET122	GP	wild-type function of	is required for					statement 7	Process	respiratory growth of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1826_s_104	9528754	The wild-type function of the  COX3-specific translational activators  PET54,  PET122, and  PET494 was required for respiratory growth of the  cox3-15 strains carrying  MRP21 or  MRP51 suppressor alleles.	gene_phenotype
71897	15	334022	5	NULL	NULL	0	NULL	PET122	GP	wild-type function of	is required for					statement 8	Process	respiratory growth of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1826_s_104	9528754	The wild-type function of the  COX3-specific translational activators  PET54,  PET122, and  PET494 was required for respiratory growth of the  cox3-15 strains carrying  MRP21 or  MRP51 suppressor alleles.	gene_phenotype
71898	16	334022	5	NULL	NULL	0	NULL	PET494	GP	wild-type function of	is required for					statement 7	Process	respiratory growth of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1826_s_104	9528754	The wild-type function of the  COX3-specific translational activators  PET54,  PET122, and  PET494 was required for respiratory growth of the  cox3-15 strains carrying  MRP21 or  MRP51 suppressor alleles.	gene_phenotype
71899	17	334022	5	NULL	NULL	0	NULL	PET494	GP	wild-type function of	is required for					statement 8	Process	respiratory growth of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1826_s_104	9528754	The wild-type function of the  COX3-specific translational activators  PET54,  PET122, and  PET494 was required for respiratory growth of the  cox3-15 strains carrying  MRP21 or  MRP51 suppressor alleles.	gene_phenotype
69692	1	334026	7	NULL	NULL	0	NULL	R30m1 cells	Cell		does not grow on					glucose-containing medium	Chemical				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_187	14749391	In contrast to the efficient expression of snR30m1 and snR30m2, neither the  R30m1 nor the  R30m2 cells could grow on glucose-containing medium (Fig.  6C), demonstrating that the m1 and m2 motifs of snR30, although not required for RNA accumulation, are essential for cell viability.	gene_phenotype
69693	2	334026	7	NULL	NULL	0	NULL	R30m2 cells	Cell		does not grow on					glucose-containing medium	Chemical				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_187	14749391	In contrast to the efficient expression of snR30m1 and snR30m2, neither the  R30m1 nor the  R30m2 cells could grow on glucose-containing medium (Fig.  6C), demonstrating that the m1 and m2 motifs of snR30, although not required for RNA accumulation, are essential for cell viability.	gene_phenotype
69694	3	334026	7	NULL	NULL	0	NULL	snR30	NucleicAcid		not required for			m1 motif		RNA	NucleicAcid	accumulation of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_187	14749391	In contrast to the efficient expression of snR30m1 and snR30m2, neither the  R30m1 nor the  R30m2 cells could grow on glucose-containing medium (Fig.  6C), demonstrating that the m1 and m2 motifs of snR30, although not required for RNA accumulation, are essential for cell viability.	gene_phenotype
69695	4	334026	7	NULL	NULL	0	NULL	snR30	NucleicAcid		not required for			m2 motif		RNA	NucleicAcid	accumulation of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_187	14749391	In contrast to the efficient expression of snR30m1 and snR30m2, neither the  R30m1 nor the  R30m2 cells could grow on glucose-containing medium (Fig.  6C), demonstrating that the m1 and m2 motifs of snR30, although not required for RNA accumulation, are essential for cell viability.	gene_phenotype
69696	5	334026	7	NULL	NULL	0	NULL	snR30	NucleicAcid		is essential for			m1 motif		cell viability	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_187	14749391	In contrast to the efficient expression of snR30m1 and snR30m2, neither the  R30m1 nor the  R30m2 cells could grow on glucose-containing medium (Fig.  6C), demonstrating that the m1 and m2 motifs of snR30, although not required for RNA accumulation, are essential for cell viability.	gene_phenotype
69697	6	334026	7	NULL	NULL	0	NULL	snR30	NucleicAcid		is essential for			m2 motif		cell viability	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_187	14749391	In contrast to the efficient expression of snR30m1 and snR30m2, neither the  R30m1 nor the  R30m2 cells could grow on glucose-containing medium (Fig.  6C), demonstrating that the m1 and m2 motifs of snR30, although not required for RNA accumulation, are essential for cell viability.	gene_phenotype
69762	1	334027	7	NULL	NULL	0	NULL	yeast cells	Cell		express					snR30m2	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_253	14749391	Moreover, we have recently found that the viability of yeast cells expressing snR30m2, but not snR30m1, could be restored by coexpression of the human U17a snoRNA (our unpublished data).	gene_phenotype
69763	2	334027	7	NULL	NULL	0	NULL	statement 1	Process	viability of	restored by					U17a snoRNA	NucleicAcid	coexpression of;;human			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_253	14749391	Moreover, we have recently found that the viability of yeast cells expressing snR30m2, but not snR30m1, could be restored by coexpression of the human U17a snoRNA (our unpublished data).	gene_phenotype
69767	1	334028	7	NULL	NULL	0	NULL	cell viability elements	Chemical		located in the					snR30	NucleicAcid			3' hairpin	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_104	14749391	Elements essential for cell viability are located in the 3' hairpin of snR30.	gene_phenotype
69768	1	334029	7	NULL	NULL	0	NULL	snR30	NucleicAcid		essential for			 conserved m1 element		cell viability	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_189	14749391	The conserved m1 and m2 elements of snR30 are essential for cell viability.	gene_phenotype
69777	2	334029	7	NULL	NULL	NULL	NULL	snR30	NucleicAcid		essential for			conserved m2 element		cell viability	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_189	14749391	The conserved m1 and m2 elements of snR30 are essential for cell viability.	gene_phenotype
69778	1	334030	7	NULL	NULL	0	NULL	R5-R30S chimeric RNA 	NucleicAcid		support					cell growth	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_143	14749391	In conclusion, the results of the deletion analysis of snR30, taken together with the finding that R5-R30S chimeric RNA can support cell growth, indicate that all the elements essential for cell viability are contained within the 3''-terminal hairpin of snR30.	gene_phenotype
69779	2	334030	7	NULL	NULL	0	NULL	cell viability elements	Chemical		contained within					snR30	NucleicAcid		3''-terminal hairpin		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_143	14749391	In conclusion, the results of the deletion analysis of snR30, taken together with the finding that R5-R30S chimeric RNA can support cell growth, indicate that all the elements essential for cell viability are contained within the 3''-terminal hairpin of snR30.	gene_phenotype
69780	3	334030	7	NULL	NULL	0	NULL	statement 1	Process		indicate					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_143	14749391	In conclusion, the results of the deletion analysis of snR30, taken together with the finding that R5-R30S chimeric RNA can support cell growth, indicate that all the elements essential for cell viability are contained within the 3''-terminal hairpin of snR30.	gene_phenotype
69781	1	334031	7	NULL	NULL	0	NULL	 snR30	NucleicAcid	yeast	required for					18S rRNA	NucleicAcid	production of			NULL		0	NULL	NULL	NULL	gw60_cell_89_5_799_s_31	9182768	Yeast snR30 is required for production of 18S rRNA and, therefore, for cell  viability (Bally et al., 1988   ;  Morrissey and Tollervey, 1993   ).	gene_phenotype
69782	2	334031	7	NULL	NULL	0	NULL	statement 1	Process		required for					cell viability	Process				NULL		0	NULL	NULL	NULL	gw60_cell_89_5_799_s_31	9182768	Yeast snR30 is required for production of 18S rRNA and, therefore, for cell  viability (Bally et al., 1988   ;  Morrissey and Tollervey, 1993   ).	gene_phenotype
69795	1	334032	7	NULL	NULL	0	NULL	snR30 RNA	NucleicAcid	depletion of essential	leads to					 27SA3 pre-rRNA	NucleicAcid	accumulation of			NULL		0	NULL	NULL	NULL	gw60_pnas_97_24_13027_s_229	11087857	Depletion of the essential snR30 RNA, a member of the box H/ACA class of snoRNAs, leads to accumulation of the 27SA3 pre-rRNA ( 6).	gene_phenotype
69796	2	334032	7	NULL	NULL	0	NULL	snR30 RNA	NucleicAcid		is a member of					snoRNA	NucleicAcid			box H/ACA class 	NULL		0	NULL	NULL	NULL	gw60_pnas_97_24_13027_s_229	11087857	Depletion of the essential snR30 RNA, a member of the box H/ACA class of snoRNAs, leads to accumulation of the 27SA3 pre-rRNA ( 6).	gene_phenotype
69797	1	334033	7	NULL	NULL	NULL	NULL	snR30	NucleicAcid	removal of	does not influence				internal hairpin of from U398 to A529	R30-dIH RNA	NucleicAcid	accumulation of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_115	14749391	Likewise, removal of the internal hairpin of snR30 (from U398 to A529) had no influence on the accumulation of the resulting R30-dIH RNA (Fig.  3D, lane 5).	gene_phenotype
69798	1	334034	7	NULL	NULL	0	NULL	snR30	NucleicAcid		carries				3''-terminal hairpin	cell viability	Process	critical for		elements	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_230	14749391	Expression of an snR5-snR30 chimeric RNA (R5-R30S) demonstrated that the 3''-terminal hairpin of snR30 carries all the elements that are critical for cell viability (Fig.  3).	gene_phenotype
69799	1	334036	7	NULL	NULL	0	NULL	snR30	NucleicAcid		play critical role in			 m1 motif		cell viability	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_201	14749391	To test whether the critical role played by the m1 and m2 motifs of snR30 in cell viability is connected to 18S production, the processing of pre-rRNA in the  R30m1 and  R30m2 strains was investigated.	gene_phenotype
69800	2	334036	7	NULL	NULL	0	NULL	snR30	NucleicAcid		play critical role in			m2 motif		cell viability	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_4_1769_s_201	14749391	To test whether the critical role played by the m1 and m2 motifs of snR30 in cell viability is connected to 18S production, the processing of pre-rRNA in the  R30m1 and  R30m2 strains was investigated.	gene_phenotype
69801	1	334037	7	NULL	NULL	0	NULL	H/ACA RNA 	NucleicAcid	trypanosome	involved in					rRNA	NucleicAcid	maturation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_41_34558_s_55	16107339	The first trypanosome H/ACA RNA involved in rRNA maturation, the snR30 homologue, was identified in this study, and the defects in rRNA maturation during CBF5 silencing can be attributed in part to its absence.	gene_phenotype
69802	2	334037	7	NULL	NULL	0	NULL	H/ACA RNA 	NucleicAcid	trypanosome	is a homologue of					snR30	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_41_34558_s_55	16107339	The first trypanosome H/ACA RNA involved in rRNA maturation, the snR30 homologue, was identified in this study, and the defects in rRNA maturation during CBF5 silencing can be attributed in part to its absence.	gene_phenotype
69803	3	334037	7	NULL	NULL	NULL	NULL	rRNA	NucleicAcid	defects in maturation of	is attributed to		partly			H/ACA RNA	NucleicAcid	absence of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_41_34558_s_55	16107339	The first trypanosome H/ACA RNA involved in rRNA maturation, the snR30 homologue, was identified in this study, and the defects in rRNA maturation during CBF5 silencing can be attributed in part to its absence.	gene_phenotype
69804	4	334037	7	NULL	NULL	0	NULL	rRNA	NucleicAcid	defects in maturation of	occur during					CBF5	GP	silencing of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_41_34558_s_55	16107339	The first trypanosome H/ACA RNA involved in rRNA maturation, the snR30 homologue, was identified in this study, and the defects in rRNA maturation during CBF5 silencing can be attributed in part to its absence.	gene_phenotype
69806	1	334038	7	NULL	NULL	NULL	NULL	 snoRNA snR30	NucleicAcid		essential for				box H/ACA	rRNA	NucleicAcid	processing of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_26_23553_s_281	12700234	Because box H/ACA snoRNA snR30 is essential for rRNA  processing and consequently viability of yeast  ( ), its depletion is the  likely cause for growth arrest after Srp40p depletion.	gene_phenotype
69808	2	334038	7	NULL	NULL	NULL	NULL	snoRNA snR30 	NucleicAcid		essential for			 	box H/ACA	viability	Process	yeast			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_26_23553_s_281	12700234	Because box H/ACA snoRNA snR30 is essential for rRNA  processing and consequently viability of yeast  ( ), its depletion is the  likely cause for growth arrest after Srp40p depletion.	gene_phenotype
69809	3	334038	7	NULL	NULL	0	NULL	snoRNA snR30	NucleicAcid	depletion of	cause for				box H/ACA	growth arrest	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_26_23553_s_281	12700234	Because box H/ACA snoRNA snR30 is essential for rRNA  processing and consequently viability of yeast  ( ), its depletion is the  likely cause for growth arrest after Srp40p depletion.	gene_phenotype
69810	4	334038	7	NULL	NULL	0	NULL	statement 3	Process		occur after					Srp40p	GP	depletion of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_26_23553_s_281	12700234	Because box H/ACA snoRNA snR30 is essential for rRNA  processing and consequently viability of yeast  ( ), its depletion is the  likely cause for growth arrest after Srp40p depletion.	gene_phenotype
69811	1	334039	7	NULL	NULL	0	NULL	snoRNA	NucleicAcid	yeast	is required for				box H/ACA	18S rRNA	NucleicAcid	processing of			NULL		0	NULL	NULL	NULL	gw60_embo_16_15_4770_s_27	9303321	All yeast box H/ACA snoRNAs tested, with the exception of snR30 which is required for 18S rRNA processing (Morrissey and Tollervey, 1993  ), are dispensable for viability (Maxwell and Fournier, 1995  ; Balakin  et al., 1996  , and references therein).	gene_phenotype
69814	2	334039	7	NULL	NULL	0	NULL	snR30	NucleicAcid		is not required for					18S rRNA	NucleicAcid	processing of			NULL		0	NULL	NULL	NULL	gw60_embo_16_15_4770_s_27	9303321	All yeast box H/ACA snoRNAs tested, with the exception of snR30 which is required for 18S rRNA processing (Morrissey and Tollervey, 1993  ), are dispensable for viability (Maxwell and Fournier, 1995  ; Balakin  et al., 1996  , and references therein).	gene_phenotype
69815	3	334039	7	NULL	NULL	0	NULL	snoRNA	NucleicAcid	yeast	is dispensable for				box H/ACA	viability	Process				NULL		0	NULL	NULL	NULL	gw60_embo_16_15_4770_s_27	9303321	All yeast box H/ACA snoRNAs tested, with the exception of snR30 which is required for 18S rRNA processing (Morrissey and Tollervey, 1993  ), are dispensable for viability (Maxwell and Fournier, 1995  ; Balakin  et al., 1996  , and references therein).	gene_phenotype
69816	1	334045	7	NULL	NULL	0	NULL	crd1delta	GP	Uncoupled Oxidative Phosphorylation of	is independent of					PET56	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_134	15169766	Uncoupled Oxidative Phosphorylation in crd1delta Is Independent of PET56  -- Mitochondrial function was assayed in  crd1delta mutant cells in the  PET56 genetic background.	gene_phenotype
69817	1	334046	7	NULL	NULL	0	NULL	crd1delta	GP	Coupling in;;mutant	is defective in					PET56 background	GP				NULL	mitochondria	0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_171	15169766	(ii) Coupling and oxidative phosphorylation are defective in  crd1delta mutant mitochondria in  PET56 and  pet56 genetic backgrounds.	gene_phenotype
69818	2	334046	7	NULL	NULL	NULL	NULL	crd1delta	GP	oxidative phosphorylation of;;mutant	is defective in					PET56 background	GP				NULL	mitochondria	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_171	15169766	(ii) Coupling and oxidative phosphorylation are defective in  crd1delta mutant mitochondria in  PET56 and  pet56 genetic backgrounds.	gene_phenotype
69819	3	334046	7	NULL	NULL	NULL	NULL	crd1delta	GP	Coupling in;;mutant	is defective in					pet56 genetic background	GP				NULL	mitochondria	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_171	15169766	(ii) Coupling and oxidative phosphorylation are defective in  crd1delta mutant mitochondria in  PET56 and  pet56 genetic backgrounds.	gene_phenotype
69820	4	334046	7	NULL	NULL	0	NULL	crd1delta	GP	oxidative phosphorylation of;;mutant	is defective in					pet56 genetic background	GP				NULL	mitochondria	0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_171	15169766	(ii) Coupling and oxidative phosphorylation are defective in  crd1delta mutant mitochondria in  PET56 and  pet56 genetic backgrounds.	gene_phenotype
69821	1	334048	7	NULL	NULL	0	NULL	PET56 gene	GP	wild type;;expression of	does not affect					viability	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_107	15169766	Expression of the wild type  PET56 gene did not affect viability.	gene_phenotype
69822	1	334049	7	NULL	NULL	0	NULL	crd1delta	GP	mutant	forms					Petite	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_121	15169766	Increased Petite Formation in crd1delta Mutants at Elevated Temperatures Is Independent of pet56  --	gene_phenotype
69823	2	334049	7	NULL	NULL	0	NULL	temperature		elevated	increase					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_121	15169766	Increased Petite Formation in crd1delta Mutants at Elevated Temperatures Is Independent of pet56  --	gene_phenotype
69824	3	334049	7	NULL	NULL	0	NULL	statement 2	Process		is independent of					pet56	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_121	15169766	Increased Petite Formation in crd1delta Mutants at Elevated Temperatures Is Independent of pet56  --	gene_phenotype
69825	1	334050	7	NULL	NULL	0	NULL	crd1delta	GP	mutant	shows					oxidative phosphorylation	Process	defective			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_142	15169766	The  crd1delta mutant in the  PET56 background exhibits defective oxidative phosphorylation.	gene_phenotype
69826	2	334050	7	NULL	NULL	0	NULL	statement 1	Process		occur in					PET56 background	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_142	15169766	The  crd1delta mutant in the  PET56 background exhibits defective oxidative phosphorylation.	gene_phenotype
69827	1	334051	7	NULL	NULL	NULL	NULL	DNA	NucleicAcid	Decreased viability of;;mitochondrial	occurs at					 temperature		elevated			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_169	15169766	(i) Decreased viability and loss of mitochondrial DNA at elevated temperature are independent of  pet56.	gene_phenotype
69828	2	334051	7	NULL	NULL	0	NULL	DNA	NucleicAcid	loss of;;mitochondrial	occur at					temperature		elevated			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_169	15169766	(i) Decreased viability and loss of mitochondrial DNA at elevated temperature are independent of  pet56.	gene_phenotype
69829	3	334051	7	NULL	NULL	0	NULL	statement 1	Process		is independent of					pet56	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_169	15169766	(i) Decreased viability and loss of mitochondrial DNA at elevated temperature are independent of  pet56.	gene_phenotype
69830	4	334051	7	NULL	NULL	0	NULL	statement 2	Process		is independent of					pet56	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_169	15169766	(i) Decreased viability and loss of mitochondrial DNA at elevated temperature are independent of  pet56.	gene_phenotype
69831	1	334052	7	NULL	NULL	NULL	NULL	crd1delta	GP	viability of;;mutant	is lost upon					pet56 background	GP	growth in			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_105	15169766	The  crd1delta mutant lost viability after prolonged growth in liquid culture (24 and 72 h in  pet56 and  PET56 backgrounds, respectively ( Fig. 3).	gene_phenotype
69832	2	334052	7	NULL	NULL	0	NULL	crd1delta	GP	viability of;;mutant	is lost upon					PET56 background	GP	growth in			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_105	15169766	The  crd1delta mutant lost viability after prolonged growth in liquid culture (24 and 72 h in  pet56 and  PET56 backgrounds, respectively ( Fig. 3).	gene_phenotype
69833	1	334054	7	NULL	NULL	0	NULL	 DL1	GP		shows					mitochondrial function	Process	little			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_102	12840009	Even YPH500 ( pet56) maintained only 40% viability  under these conditions as compared with DL1 and YZD5 ( PET56), which  showed little or no loss of mitochondrial function.	gene_phenotype
69834	2	334054	7	NULL	NULL	0	NULL	YZD5	GP		shows					mitochondrial function	Process	little			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_102	12840009	Even YPH500 ( pet56) maintained only 40% viability  under these conditions as compared with DL1 and YZD5 ( PET56), which  showed little or no loss of mitochondrial function.	gene_phenotype
69835	3	334054	7	NULL	NULL	0	NULL	DL1	GP		shows					mitochondrial function	Process	no loss of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_102	12840009	Even YPH500 ( pet56) maintained only 40% viability  under these conditions as compared with DL1 and YZD5 ( PET56), which  showed little or no loss of mitochondrial function.	gene_phenotype
69836	4	334054	7	NULL	NULL	0	NULL	YZD5	GP		shows					mitochondrial function	Process	no loss of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_102	12840009	Even YPH500 ( pet56) maintained only 40% viability  under these conditions as compared with DL1 and YZD5 ( PET56), which  showed little or no loss of mitochondrial function.	gene_phenotype
69837	5	334054	7	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_102	12840009	Even YPH500 ( pet56) maintained only 40% viability  under these conditions as compared with DL1 and YZD5 ( PET56), which  showed little or no loss of mitochondrial function.	gene_phenotype
69838	6	334054	7	NULL	NULL	0	NULL	statement 2	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_102	12840009	Even YPH500 ( pet56) maintained only 40% viability  under these conditions as compared with DL1 and YZD5 ( PET56), which  showed little or no loss of mitochondrial function.	gene_phenotype
69839	1	334055	7	NULL	NULL	0	NULL	PET56	GP	reduced expression of	slows					growth	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_25	15169766	Reduced expression of  PET56 was found to slow growth, decrease mitochondrial DNA stability, and decrease cell viability at elevated temperatures ( ,  ).	gene_phenotype
69840	2	334055	7	NULL	NULL	0	NULL	statement 1	Process		occur at					temperature		elevated			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_25	15169766	Reduced expression of  PET56 was found to slow growth, decrease mitochondrial DNA stability, and decrease cell viability at elevated temperatures ( ,  ).	gene_phenotype
69841	3	334055	7	NULL	NULL	0	NULL	PET56	GP	reduced expression of	decrease					DNA	NucleicAcid	stability of;;mitochondrial			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_25	15169766	Reduced expression of  PET56 was found to slow growth, decrease mitochondrial DNA stability, and decrease cell viability at elevated temperatures ( ,  ).	gene_phenotype
69842	4	334055	7	NULL	NULL	0	NULL	statement 3	Process		occur at					temperature		elevated			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_25	15169766	Reduced expression of  PET56 was found to slow growth, decrease mitochondrial DNA stability, and decrease cell viability at elevated temperatures ( ,  ).	gene_phenotype
69843	5	334055	7	NULL	NULL	0	NULL	PET56	GP	reduced expression of	decrease					cell viability	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_25	15169766	Reduced expression of  PET56 was found to slow growth, decrease mitochondrial DNA stability, and decrease cell viability at elevated temperatures ( ,  ).	gene_phenotype
69844	6	334055	7	NULL	NULL	0	NULL	statement 5	Process		occur at					temperature		elevated			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_25	15169766	Reduced expression of  PET56 was found to slow growth, decrease mitochondrial DNA stability, and decrease cell viability at elevated temperatures ( ,  ).	gene_phenotype
69950	1	334056	7	NULL	NULL	0	NULL	 crd1delta	GP		loses					viability	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_115	15169766	Expression of  CRD1 but not  PET56 protects  crd1delta from loss of viability following prolonged culture at elevated temperatures.	gene_phenotype
69951	2	334056	7	NULL	NULL	0	NULL	statement 1	Process		occur at					temperature		elevated			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_115	15169766	Expression of  CRD1 but not  PET56 protects  crd1delta from loss of viability following prolonged culture at elevated temperatures.	gene_phenotype
69952	3	334056	7	NULL	NULL	0	NULL	CRD1	GP	expression of	protects					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_115	15169766	Expression of  CRD1 but not  PET56 protects  crd1delta from loss of viability following prolonged culture at elevated temperatures.	gene_phenotype
69953	4	334056	7	NULL	NULL	0	NULL	PET56	GP	expression of	protects					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_115	15169766	Expression of  CRD1 but not  PET56 protects  crd1delta from loss of viability following prolonged culture at elevated temperatures.	gene_phenotype
69954	1	334057	7	NULL	NULL	NULL	NULL	petite cells 	Cell		present in					crd1delta	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_123	15169766	As seen in  Fig. 4, the percentage of petite cells in the  crd1delta mutant in the  pet56 background was greater than among wild type cells.	gene_phenotype
69955	2	334057	7	NULL	NULL	0	NULL	statement 1	Process		occur in the					pet56 background	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_123	15169766	As seen in  Fig. 4, the percentage of petite cells in the  crd1delta mutant in the  pet56 background was greater than among wild type cells.	gene_phenotype
69956	3	334057	7	NULL	NULL	NULL	NULL	petite cells	Cell		present in					crd1delta 	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_123	15169766	As seen in  Fig. 4, the percentage of petite cells in the  crd1delta mutant in the  pet56 background was greater than among wild type cells.	gene_phenotype
69957	4	334057	7	NULL	NULL	0	NULL	statement 1	Process		is greater than					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_123	15169766	As seen in  Fig. 4, the percentage of petite cells in the  crd1delta mutant in the  pet56 background was greater than among wild type cells.	gene_phenotype
69958	1	334058	7	NULL	NULL	0	NULL	PET56	GP	null mutants	is defective in					mitochondrial large ribosomal subunit	CellComponent	assembly of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_26	12840009	Null mutants in   PET56 are defective in assembly of the mitochondrial large ribosomal  subunit and do not grow on nonfermentable carbon sources, but partial loss of   PET56 expression results in slowed growth, mtDNA instability, and  loss of cell viability at elevated temperatures  ( ,   ) similar to the properties  of  crd1delta strains containing the   his3delta 200 allele  ( ).	gene_phenotype
69959	2	334058	7	NULL	NULL	0	NULL	statement 1	Process		does not grow on					nonfermentable carbon sources	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_26	12840009	Null mutants in   PET56 are defective in assembly of the mitochondrial large ribosomal  subunit and do not grow on nonfermentable carbon sources, but partial loss of   PET56 expression results in slowed growth, mtDNA instability, and  loss of cell viability at elevated temperatures  ( ,   ) similar to the properties  of  crd1delta strains containing the   his3delta 200 allele  ( ).	gene_phenotype
69960	3	334058	7	NULL	NULL	0	NULL	PET56	GP	partial loss of expression of	results in					slowed growth	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_26	12840009	Null mutants in   PET56 are defective in assembly of the mitochondrial large ribosomal  subunit and do not grow on nonfermentable carbon sources, but partial loss of   PET56 expression results in slowed growth, mtDNA instability, and  loss of cell viability at elevated temperatures  ( ,   ) similar to the properties  of  crd1delta strains containing the   his3delta 200 allele  ( ).	gene_phenotype
69961	4	334058	7	NULL	NULL	0	NULL	PET56	GP	partial loss of expression of	results in					 mtDNA	NucleicAcid	instability of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_26	12840009	Null mutants in   PET56 are defective in assembly of the mitochondrial large ribosomal  subunit and do not grow on nonfermentable carbon sources, but partial loss of   PET56 expression results in slowed growth, mtDNA instability, and  loss of cell viability at elevated temperatures  ( ,   ) similar to the properties  of  crd1delta strains containing the   his3delta 200 allele  ( ).	gene_phenotype
69962	5	334058	7	NULL	NULL	0	NULL	PET56	GP	partial loss of expression of	results in					cell viability	Process	loss of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_26	12840009	Null mutants in   PET56 are defective in assembly of the mitochondrial large ribosomal  subunit and do not grow on nonfermentable carbon sources, but partial loss of   PET56 expression results in slowed growth, mtDNA instability, and  loss of cell viability at elevated temperatures  ( ,   ) similar to the properties  of  crd1delta strains containing the   his3delta 200 allele  ( ).	gene_phenotype
69963	6	334058	7	NULL	NULL	0	NULL	statement 3	Process		occur at					temperature		elevated			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_26	12840009	Null mutants in   PET56 are defective in assembly of the mitochondrial large ribosomal  subunit and do not grow on nonfermentable carbon sources, but partial loss of   PET56 expression results in slowed growth, mtDNA instability, and  loss of cell viability at elevated temperatures  ( ,   ) similar to the properties  of  crd1delta strains containing the   his3delta 200 allele  ( ).	gene_phenotype
69964	7	334058	7	NULL	NULL	0	NULL	statement 4	Process		occur at					temperature		elevated			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_26	12840009	Null mutants in   PET56 are defective in assembly of the mitochondrial large ribosomal  subunit and do not grow on nonfermentable carbon sources, but partial loss of   PET56 expression results in slowed growth, mtDNA instability, and  loss of cell viability at elevated temperatures  ( ,   ) similar to the properties  of  crd1delta strains containing the   his3delta 200 allele  ( ).	gene_phenotype
69965	8	334058	7	NULL	NULL	0	NULL	statement 5	Process		occur at					temperature		elevated			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_26	12840009	Null mutants in   PET56 are defective in assembly of the mitochondrial large ribosomal  subunit and do not grow on nonfermentable carbon sources, but partial loss of   PET56 expression results in slowed growth, mtDNA instability, and  loss of cell viability at elevated temperatures  ( ,   ) similar to the properties  of  crd1delta strains containing the   his3delta 200 allele  ( ).	gene_phenotype
69966	9	334058	7	NULL	NULL	0	NULL	crd1delta strains	GP		contain					 his3delta 200 allele	Chromosome				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_26	12840009	Null mutants in   PET56 are defective in assembly of the mitochondrial large ribosomal  subunit and do not grow on nonfermentable carbon sources, but partial loss of   PET56 expression results in slowed growth, mtDNA instability, and  loss of cell viability at elevated temperatures  ( ,   ) similar to the properties  of  crd1delta strains containing the   his3delta 200 allele  ( ).	gene_phenotype
69967	10	334058	7	NULL	NULL	NULL	NULL	statement 9	GP	properties of	similar to					PET56	GP	properties of;; partial loss of expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_26	12840009	Null mutants in   PET56 are defective in assembly of the mitochondrial large ribosomal  subunit and do not grow on nonfermentable carbon sources, but partial loss of   PET56 expression results in slowed growth, mtDNA instability, and  loss of cell viability at elevated temperatures  ( ,   ) similar to the properties  of  crd1delta strains containing the   his3delta 200 allele  ( ).	gene_phenotype
69968	1	334059	7	NULL	NULL	NULL	NULL	his3delta 200 allele 	Chromosome	strains containing	shows					 growth	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_89	12840009	Because strains carrying the  his3delta 200 allele (and thus  also the  pet56 defective) grew much poorer than cells that were wild  type for  PET56 ( his3 - 11,15 allele), we investigated  whether the difference was because of reduced cell viability and/or mtDNA  instability for the  his3delta 200-containing strains.	gene_phenotype
69969	2	334059	7	NULL	NULL	0	NULL	PET56	GP	wild type	shows					growth	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_89	12840009	Because strains carrying the  his3delta 200 allele (and thus  also the  pet56 defective) grew much poorer than cells that were wild  type for  PET56 ( his3 - 11,15 allele), we investigated  whether the difference was because of reduced cell viability and/or mtDNA  instability for the  his3delta 200-containing strains.	gene_phenotype
69970	3	334059	7	NULL	NULL	0	NULL	statement 1	Process		is poorer than					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_89	12840009	Because strains carrying the  his3delta 200 allele (and thus  also the  pet56 defective) grew much poorer than cells that were wild  type for  PET56 ( his3 - 11,15 allele), we investigated  whether the difference was because of reduced cell viability and/or mtDNA  instability for the  his3delta 200-containing strains.	gene_phenotype
69971	4	334059	7	NULL	NULL	NULL	NULL	PET56	GP		contains					his3 - 11,15 allele	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_89	12840009	Because strains carrying the  his3delta 200 allele (and thus  also the  pet56 defective) grew much poorer than cells that were wild  type for  PET56 ( his3 - 11,15 allele), we investigated  whether the difference was because of reduced cell viability and/or mtDNA  instability for the  his3delta 200-containing strains.	gene_phenotype
69974	1	334060	7	NULL	NULL	NULL	NULL	PET56	GP		increase					CRD1	GP	cell viability of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_103	12840009	When YPH500 and YZD2,  carrying the  his3delta 200 allele with its associated  defective  pet56, were supplied with a plasmid-borne copy of   PET56, cell viability for both the  CRD1 and   crd1delta strains was significantly increased particularly when  they were plated on YPEG for which mitochondrial function is required.	gene_phenotype
69975	2	334060	7	NULL	NULL	0	NULL	PET56	GP		increase					crd1delta strains	GP	cell viability of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_103	12840009	When YPH500 and YZD2,  carrying the  his3delta 200 allele with its associated  defective  pet56, were supplied with a plasmid-borne copy of   PET56, cell viability for both the  CRD1 and   crd1delta strains was significantly increased particularly when  they were plated on YPEG for which mitochondrial function is required.	gene_phenotype
69976	1	334061	7	NULL	NULL	0	NULL	crd1delta	GP	mutant	shows					poor growth	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_192	12840009	The poor viability  properties of YPH500 and YZD2 were largely corrected by introducing a  plasmid-borne copy of  PET56 confirming that the synergistic effects  of the  crd1delta and  pet56 mutations were the primary  reason for the poor growth properties rather than the lack of CL.	gene_phenotype
69977	2	334061	7	NULL	NULL	NULL	NULL	pet56 	GP	mutant	shows					poor growth	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_192	12840009	The poor viability  properties of YPH500 and YZD2 were largely corrected by introducing a  plasmid-borne copy of  PET56 confirming that the synergistic effects  of the  crd1delta and  pet56 mutations were the primary  reason for the poor growth properties rather than the lack of CL.	gene_phenotype
69978	3	334061	7	NULL	NULL	0	NULL	CL	Chemical	lack of	does not contribute to					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_192	12840009	The poor viability  properties of YPH500 and YZD2 were largely corrected by introducing a  plasmid-borne copy of  PET56 confirming that the synergistic effects  of the  crd1delta and  pet56 mutations were the primary  reason for the poor growth properties rather than the lack of CL.	gene_phenotype
69979	4	334061	7	NULL	NULL	0	NULL	CL	Chemical	lack of	does not contribute to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_192	12840009	The poor viability  properties of YPH500 and YZD2 were largely corrected by introducing a  plasmid-borne copy of  PET56 confirming that the synergistic effects  of the  crd1delta and  pet56 mutations were the primary  reason for the poor growth properties rather than the lack of CL.	gene_phenotype
69980	1	334062	7	NULL	NULL	0	NULL	crd1delta	GP	mutant	forms					petite	cell				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_125	15169766	In the  PET56 background as well,  crd1delta mutant cells exhibited a higher frequency of petite formation than did the wild type when grown at 39  degrees C.	gene_phenotype
69981	2	334062	7	NULL	NULL	0	NULL	statement 1	Process		occur at					PET56 background	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_125	15169766	In the  PET56 background as well,  crd1delta mutant cells exhibited a higher frequency of petite formation than did the wild type when grown at 39  degrees C.	gene_phenotype
69985	3	334062	7	NULL	NULL	0	NULL	crd1delta	GP	wild type	forms					petite	Cell				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_125	15169766	In the  PET56 background as well,  crd1delta mutant cells exhibited a higher frequency of petite formation than did the wild type when grown at 39  degrees C.	gene_phenotype
69986	4	334062	7	NULL	NULL	0	NULL	statement 1	Process		higher frequecy than					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_125	15169766	In the  PET56 background as well,  crd1delta mutant cells exhibited a higher frequency of petite formation than did the wild type when grown at 39  degrees C.	gene_phenotype
69987	1	334063	7	NULL	NULL	0	NULL	CRD1	GP	expression of	reduces					petite cells	cell				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_126	15169766	In both strain backgrounds, expression of  CRD1 led to a reduction in the number of petite cells in the  crd1delta mutant to wild type levels, whereas the expression of  PET56 had no effect.	gene_phenotype
69988	2	334063	7	NULL	NULL	0	NULL	statement 1	Process		occur in					crd1delta	GP	mutant			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_126	15169766	In both strain backgrounds, expression of  CRD1 led to a reduction in the number of petite cells in the  crd1delta mutant to wild type levels, whereas the expression of  PET56 had no effect.	gene_phenotype
69989	3	334063	7	NULL	NULL	NULL	NULL	statement 1	Process		is reduced to					crd1delta	GP	wild type			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_126	15169766	In both strain backgrounds, expression of  CRD1 led to a reduction in the number of petite cells in the  crd1delta mutant to wild type levels, whereas the expression of  PET56 had no effect.	gene_phenotype
69990	4	334063	7	NULL	NULL	0	NULL	PET56	GP	expression of	does not effect					petite cells	Cell				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_31_32294_s_126	15169766	In both strain backgrounds, expression of  CRD1 led to a reduction in the number of petite cells in the  crd1delta mutant to wild type levels, whereas the expression of  PET56 had no effect.	gene_phenotype
69991	1	334065	7	NULL	NULL	NULL	NULL	mitochondrial DNA	NucleicAcid	instability of	is due to					PET56 gene	GP	reduced expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_7	12840009	We present evidence that  mitochondrial DNA instability, loss of viability, and defects in the ETS  exhibited at elevated temperatures by some mutants are caused by the reduced  expression of the  PET56 gene in the presence of the   his3delta 200 allele and not the lack of CL alone.	gene_phenotype
69992	2	334065	7	NULL	NULL	0	NULL	viability	Process	loss of	is due to					PET56 gene	GP	reduced expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_7	12840009	We present evidence that  mitochondrial DNA instability, loss of viability, and defects in the ETS  exhibited at elevated temperatures by some mutants are caused by the reduced  expression of the  PET56 gene in the presence of the   his3delta 200 allele and not the lack of CL alone.	gene_phenotype
69993	3	334065	7	NULL	NULL	NULL	NULL	ETS	Process	defects in	is due to					PET56 gene	GP	reduced expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_7	12840009	We present evidence that  mitochondrial DNA instability, loss of viability, and defects in the ETS  exhibited at elevated temperatures by some mutants are caused by the reduced  expression of the  PET56 gene in the presence of the   his3delta 200 allele and not the lack of CL alone.	gene_phenotype
69995	4	334065	7	NULL	NULL	0	NULL	statement 1	Process		in the presence of					his3delta 200 allele	Chromosome				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_7	12840009	We present evidence that  mitochondrial DNA instability, loss of viability, and defects in the ETS  exhibited at elevated temperatures by some mutants are caused by the reduced  expression of the  PET56 gene in the presence of the   his3delta 200 allele and not the lack of CL alone.	gene_phenotype
69996	5	334065	7	NULL	NULL	0	NULL	statement 2	Process		in the presence of					his3delta 200 allele	Chromosome				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_7	12840009	We present evidence that  mitochondrial DNA instability, loss of viability, and defects in the ETS  exhibited at elevated temperatures by some mutants are caused by the reduced  expression of the  PET56 gene in the presence of the   his3delta 200 allele and not the lack of CL alone.	gene_phenotype
69997	6	334065	7	NULL	NULL	0	NULL	statement 3	Process		in the presence of					his3delta 200 allele	Chromosome				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_7	12840009	We present evidence that  mitochondrial DNA instability, loss of viability, and defects in the ETS  exhibited at elevated temperatures by some mutants are caused by the reduced  expression of the  PET56 gene in the presence of the   his3delta 200 allele and not the lack of CL alone.	gene_phenotype
69998	7	334065	7	NULL	NULL	0	NULL	statement 1	Process		not the lack of					CL	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_7	12840009	We present evidence that  mitochondrial DNA instability, loss of viability, and defects in the ETS  exhibited at elevated temperatures by some mutants are caused by the reduced  expression of the  PET56 gene in the presence of the   his3delta 200 allele and not the lack of CL alone.	gene_phenotype
69999	8	334065	7	NULL	NULL	0	NULL	statement 2	Process		not the lack of					CL	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_7	12840009	We present evidence that  mitochondrial DNA instability, loss of viability, and defects in the ETS  exhibited at elevated temperatures by some mutants are caused by the reduced  expression of the  PET56 gene in the presence of the   his3delta 200 allele and not the lack of CL alone.	gene_phenotype
70000	9	334065	7	NULL	NULL	0	NULL	statement 3	Process		not the lack of					CL	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_7	12840009	We present evidence that  mitochondrial DNA instability, loss of viability, and defects in the ETS  exhibited at elevated temperatures by some mutants are caused by the reduced  expression of the  PET56 gene in the presence of the   his3delta 200 allele and not the lack of CL alone.	gene_phenotype
70001	1	334066	7	NULL	NULL	NULL	NULL	small colonies	Cell		obtained with					mrm2delta strain	Organism	high frequency of			NULL		NULL	NULL	NULL	NULL	gw60_embo_21_5_1139_s_66	11867542	After passing several generations on glucose medium, small colonies were obtained with high frequency for the  mrm2delta strain (Figure  2B), reminiscent of the cytoplasmic petite colonies obtained with a strain disrupted for  PET56 ( Sirum-Connolly and Mason, 1993).	gene_phenotype
70002	2	334066	7	NULL	NULL	0	NULL	statement 1	Process		occur in					glucose medium	Chemical				NULL		0	NULL	NULL	NULL	gw60_embo_21_5_1139_s_66	11867542	After passing several generations on glucose medium, small colonies were obtained with high frequency for the  mrm2delta strain (Figure  2B), reminiscent of the cytoplasmic petite colonies obtained with a strain disrupted for  PET56 ( Sirum-Connolly and Mason, 1993).	gene_phenotype
70003	3	334066	7	NULL	NULL	0	NULL	cytoplasmic petite colonies 	Cell	reminiscent of 	obtained upon					strain disrupted for PET56	Organism				NULL		0	NULL	NULL	NULL	gw60_embo_21_5_1139_s_66	11867542	After passing several generations on glucose medium, small colonies were obtained with high frequency for the  mrm2delta strain (Figure  2B), reminiscent of the cytoplasmic petite colonies obtained with a strain disrupted for  PET56 ( Sirum-Connolly and Mason, 1993).	gene_phenotype
70004	1	334067	7	NULL	NULL	0	NULL	CRD1 cells	Cell		transcription level of		high			PET56	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_98	12840009	There was little statistical difference in viability between   crd1delta and  CRD1 cells with a high transcription level  of  PET56 (YZD5 and DL1, respectively) when grown in YPD and plated on  YPD plates ( Fig. 2,  first  bar in each strain set), whereas  crd1delta cells (YZD2) with a  low transcription level of  PET56 showed a 40% reduction in cell  viability compared with its  CRD1 parental strain (YPH500).	gene_phenotype
70005	2	334067	7	NULL	NULL	0	NULL	crd1delta	GP	viability of	is different from					statement 1	Process	viability of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_98	12840009	There was little statistical difference in viability between   crd1delta and  CRD1 cells with a high transcription level  of  PET56 (YZD5 and DL1, respectively) when grown in YPD and plated on  YPD plates ( Fig. 2,  first  bar in each strain set), whereas  crd1delta cells (YZD2) with a  low transcription level of  PET56 showed a 40% reduction in cell  viability compared with its  CRD1 parental strain (YPH500).	gene_phenotype
70006	3	334067	7	NULL	NULL	0	NULL	crd1delta cells	Cell		transcription level of		low			PET56	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_98	12840009	There was little statistical difference in viability between   crd1delta and  CRD1 cells with a high transcription level  of  PET56 (YZD5 and DL1, respectively) when grown in YPD and plated on  YPD plates ( Fig. 2,  first  bar in each strain set), whereas  crd1delta cells (YZD2) with a  low transcription level of  PET56 showed a 40% reduction in cell  viability compared with its  CRD1 parental strain (YPH500).	gene_phenotype
70007	4	334067	7	NULL	NULL	0	NULL	statement 3	Process	viability of	is less than					statement 1	Process	viability of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35204_s_98	12840009	There was little statistical difference in viability between   crd1delta and  CRD1 cells with a high transcription level  of  PET56 (YZD5 and DL1, respectively) when grown in YPD and plated on  YPD plates ( Fig. 2,  first  bar in each strain set), whereas  crd1delta cells (YZD2) with a  low transcription level of  PET56 showed a 40% reduction in cell  viability compared with its  CRD1 parental strain (YPH500).	gene_phenotype
70008	1	334069	7	NULL	NULL	0	NULL	E.coli cell extracts	Cell		carry					nagK	GP				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_2_700_s_188	11133965	Cell extracts of  E. coli(pWWF52) carrying  nagK inserted in pET5a (Table  1) showed no activity against fumarylpyruvate, formed from gentisate by the joint action of NagI and NagK, even though SDS-PAGE of induced cells showed a polypeptide of the right size (~21 kDa) expressed from this construct (data not shown); we assume that the high levels of expression produced an insoluble product in inclusion bodies.	gene_phenotype
70009	2	334069	7	NULL	NULL	NULL	NULL	statement 1	Process		 no activity against					fumarylpyruvate	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_2_700_s_188	11133965	Cell extracts of  E. coli(pWWF52) carrying  nagK inserted in pET5a (Table  1) showed no activity against fumarylpyruvate, formed from gentisate by the joint action of NagI and NagK, even though SDS-PAGE of induced cells showed a polypeptide of the right size (~21 kDa) expressed from this construct (data not shown); we assume that the high levels of expression produced an insoluble product in inclusion bodies.	gene_phenotype
70010	1	334070	7	NULL	NULL	0	NULL	S. cerevisiae 	Organism		is orthologous to					S. bayanus 	Organism				NULL		0	NULL	NULL	NULL	gw60_genetics_154_3_999_s_177	10757749	Sequence comparisons among specific translational activators from budding yeasts:   Comparison of the proteins coded by orthologous genes of the sister species  S. cerevisiae and  S. bayanus reveals that they are all similar in sequence: 73% identity for Pet111p, 72% for Pet54p and Pet122p, and 76% for Pet494p.	gene_phenotype
70011	2	334070	7	NULL	NULL	0	NULL	S. cerevisiae	Organism	sequence of	is similar to					S. bayanus 	Organism	sequence of			NULL		0	NULL	NULL	NULL	gw60_genetics_154_3_999_s_177	10757749	Sequence comparisons among specific translational activators from budding yeasts:   Comparison of the proteins coded by orthologous genes of the sister species  S. cerevisiae and  S. bayanus reveals that they are all similar in sequence: 73% identity for Pet111p, 72% for Pet54p and Pet122p, and 76% for Pet494p.	gene_phenotype
70012	1	334071	7	NULL	NULL	NULL	NULL	pre- RPR1 complex 	GP		shows					catalytic activity	Process				NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_71_0_165_s_156	12045094	Consistent  with this, recent studies have shown that the pre- RPR1 complex has catalytic activity (C. Srisawat, personal communication), which is not  surprising considering that each of the protein subunits in the mature holoenzyme  can immunoprecipitate the pre- RPR1 RNA.	gene_phenotype
70013	2	334071	7	NULL	NULL	0	NULL	mature holoenzyme	GP		bind			protein subunit		pre- RPR1 RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_71_0_165_s_156	12045094	Consistent  with this, recent studies have shown that the pre- RPR1 complex has catalytic activity (C. Srisawat, personal communication), which is not  surprising considering that each of the protein subunits in the mature holoenzyme  can immunoprecipitate the pre- RPR1 RNA.	gene_phenotype
70014	1	334074	7	NULL	NULL	0	NULL	RPR1 RNA	NucleicAcid	accumulation of	is defecient in					mutant cells	Cell				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_10_3264_s_196	11971960	The accumulation of RPR1 RNA was also deficient in mutant cells and the proportion of mature to pre-RPR1 RNA was very different (Fig.  5D).	gene_phenotype
70015	1	334075	7	NULL	NULL	0	NULL	 RNase P	GP	nuclear	is a type of					RNA-based enzyme	GP				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_71_0_165_s_218	12045094	The importance of the critical regions in the  yeast  RPR1 RNA for RNase P activity supports the hypothesis that nuclear RNase P is an RNA-based  enzyme.	gene_phenotype
70016	2	334075	7	NULL	NULL	0	NULL	RPR1 RNA	NucleicAcid	critical regions in;;yeast	shows					RNase P activity	Process				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_71_0_165_s_218	12045094	The importance of the critical regions in the  yeast  RPR1 RNA for RNase P activity supports the hypothesis that nuclear RNase P is an RNA-based  enzyme.	gene_phenotype
70017	3	334075	7	NULL	NULL	0	NULL	statement 2	Process		support					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_71_0_165_s_218	12045094	The importance of the critical regions in the  yeast  RPR1 RNA for RNase P activity supports the hypothesis that nuclear RNase P is an RNA-based  enzyme.	gene_phenotype
70018	1	334076	7	NULL	NULL	0	NULL	RNase P	GP	wild-type	localizes to			RNA subunit of		nucleolus	CellComponent				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_16_2463_s_80	9716399	The fluorescent probe to the wild-type RNA subunit of RNase P,  RPR1 RNA, showed clear localization of most of the signal to the nucleolus (Fig.  4a-c).	gene_phenotype
70019	2	334076	7	NULL	NULL	0	NULL	RPR1 RNA	NucleicAcid		localizes to					nucleolus	CellComponent				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_16_2463_s_80	9716399	The fluorescent probe to the wild-type RNA subunit of RNase P,  RPR1 RNA, showed clear localization of most of the signal to the nucleolus (Fig.  4a-c).	gene_phenotype
70020	1	334078	7	NULL	NULL	0	NULL	RNase P	GP	mutation in	leads to			RNA subunit		 5.8 rRNA	NucleicAcid	accumulation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_12_7897_s_251	10567516	Interestingly, a mutation in the RNase P RNA subunit ( rpr1) leads to the accumulation of an aberrant form of 5.8 rRNA that is 3' extended for about 30 nucleotides ( 28).	gene_phenotype
70021	2	334078	7	NULL	NULL	0	NULL	 5.8 rRNA	NucleicAcid		is extended for					30 nucleotides	Chemical				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_12_7897_s_251	10567516	Interestingly, a mutation in the RNase P RNA subunit ( rpr1) leads to the accumulation of an aberrant form of 5.8 rRNA that is 3' extended for about 30 nucleotides ( 28).	gene_phenotype
70022	3	334078	7	NULL	NULL	0	NULL	RNase P	GP		is			RNA subunit		rpr1	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_12_7897_s_251	10567516	Interestingly, a mutation in the RNase P RNA subunit ( rpr1) leads to the accumulation of an aberrant form of 5.8 rRNA that is 3' extended for about 30 nucleotides ( 28).	gene_phenotype
70023	1	334079	7	NULL	NULL	0	NULL	RNase P	GP	yeast;;nuclear	important role in			P4		pre-tRNA	NucleicAcid	binding of			NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_71_0_165_s_180	12045094	For yeast nuclear  RNase P, mutagenesis studies of the conserved nucleotides within and near P4 have  suggested an important role in pre-tRNA binding, catalysis, and  RPR1 RNA maturation ( 103).	gene_phenotype
70024	2	334079	7	NULL	NULL	0	NULL	RNase P	GP	yeast;;nuclear	important role in			P4		catalysis	Process				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_71_0_165_s_180	12045094	For yeast nuclear  RNase P, mutagenesis studies of the conserved nucleotides within and near P4 have  suggested an important role in pre-tRNA binding, catalysis, and  RPR1 RNA maturation ( 103).	gene_phenotype
70025	3	334079	7	NULL	NULL	0	NULL	RNase P	GP	yeast;;nuclear	important role in			P4		RPR1 RNA	NucleicAcid	maturation of			NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_71_0_165_s_180	12045094	For yeast nuclear  RNase P, mutagenesis studies of the conserved nucleotides within and near P4 have  suggested an important role in pre-tRNA binding, catalysis, and  RPR1 RNA maturation ( 103).	gene_phenotype
70026	1	334080	7	NULL	NULL	0	NULL	tRNA methyltransferase 	GP	activity of	contributes to					RPR1 RNA	NucleicAcid	stability of			NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_71_0_165_s_256	12045094	Previous work has  linked a tRNA methyltransferase activity to the stability of  RPR1 RNA ( 136), although none of the identified subunits have any detectable sequence homology  to known tRNA processing or modification enzymes.	gene_phenotype
70027	1	334083	7	NULL	NULL	0	NULL	RNase P	GP	yeast	composed of					RPR1 RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_10_3264_s_285	11971960	Yeast RNase P is also composed of one RNA subunit (RPR1 RNA) and nine protein subunits that are all essential for cell viability ( 8,  11,  16,  38,  41,  59).	gene_phenotype
70028	2	334083	7	NULL	NULL	NULL	NULL	RNA subunit	NucleicAcid		is a type of					RPR1 RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_10_3264_s_285	11971960	Yeast RNase P is also composed of one RNA subunit (RPR1 RNA) and nine protein subunits that are all essential for cell viability ( 8,  11,  16,  38,  41,  59).	gene_phenotype
70029	3	334083	7	NULL	NULL	0	NULL	RNase P	GP	yeast	composed of					protein subunits	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_10_3264_s_285	11971960	Yeast RNase P is also composed of one RNA subunit (RPR1 RNA) and nine protein subunits that are all essential for cell viability ( 8,  11,  16,  38,  41,  59).	gene_phenotype
70030	4	334083	7	NULL	NULL	0	NULL	statement 3	GP		is essential for					cell viability	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_10_3264_s_285	11971960	Yeast RNase P is also composed of one RNA subunit (RPR1 RNA) and nine protein subunits that are all essential for cell viability ( 8,  11,  16,  38,  41,  59).	gene_phenotype
70204	1	334085	7	NULL	NULL	NULL	NULL	hcPUS4	GP	presence of	leads to					tRNA precursor	NucleicAcid	accumulation of			NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_mol-cell-biol_20_7_10713174_s_6	10713174	The presence of hcPUS4 or hcNME1 led to the accumulation of certain  tRNA precursors, and their Gcd(-) phenotypes were reversed by overexpressing  the RNA component of RNase P (RPR1), responsible for 5''-end processing  of all tRNAs.	gene_phenotype
70205	2	334085	7	NULL	NULL	0	NULL	hcNME1	GP	presence of	leads to					tRNA precursor	NucleicAcid	accumulation of			NULL		0	NULL	NULL	NULL	abs-batch0517-0529_mol-cell-biol_20_7_10713174_s_6	10713174	The presence of hcPUS4 or hcNME1 led to the accumulation of certain  tRNA precursors, and their Gcd(-) phenotypes were reversed by overexpressing  the RNA component of RNase P (RPR1), responsible for 5''-end processing  of all tRNAs.	gene_phenotype
70206	3	334085	7	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_mol-cell-biol_20_7_10713174_s_6	10713174	The presence of hcPUS4 or hcNME1 led to the accumulation of certain  tRNA precursors, and their Gcd(-) phenotypes were reversed by overexpressing  the RNA component of RNase P (RPR1), responsible for 5''-end processing  of all tRNAs.	gene_phenotype
70207	4	334085	7	NULL	NULL	NULL	NULL	Gcd(-) phenotype	Process		reversed by					RNase P	GP	overexpressing	RNA component of		NULL		NULL	NULL	NULL	NULL	abs-batch0517-0529_mol-cell-biol_20_7_10713174_s_6	10713174	The presence of hcPUS4 or hcNME1 led to the accumulation of certain  tRNA precursors, and their Gcd(-) phenotypes were reversed by overexpressing  the RNA component of RNase P (RPR1), responsible for 5''-end processing  of all tRNAs.	gene_phenotype
70208	5	334085	7	NULL	NULL	0	NULL	RNase P	GP		is			RNA component		RPR1	NucleicAcid				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_mol-cell-biol_20_7_10713174_s_6	10713174	The presence of hcPUS4 or hcNME1 led to the accumulation of certain  tRNA precursors, and their Gcd(-) phenotypes were reversed by overexpressing  the RNA component of RNase P (RPR1), responsible for 5''-end processing  of all tRNAs.	gene_phenotype
70209	6	334085	7	NULL	NULL	0	NULL	RNase P	GP		responsible for					tRNA	NucleicAcid			 5''-end processing of	NULL		0	NULL	NULL	NULL	abs-batch0517-0529_mol-cell-biol_20_7_10713174_s_6	10713174	The presence of hcPUS4 or hcNME1 led to the accumulation of certain  tRNA precursors, and their Gcd(-) phenotypes were reversed by overexpressing  the RNA component of RNase P (RPR1), responsible for 5''-end processing  of all tRNAs.	gene_phenotype
70210	1	334089	7	NULL	NULL	0	NULL	Lsm2 - Lsm7 complex 	GP		is not required for					snR5 RNA	NucleicAcid	accumulation of			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_6_2842_s_288	15075370	Thus, the Lsm2 - Lsm7 complex does not appear to be required for the accumulation of snR5 RNA or for its role in pseudouridylation.	gene_phenotype
70211	2	334089	7	NULL	NULL	0	NULL	Lsm2 - Lsm7 complex	GP		is not required for					pseudouridylation	Process	role in			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_6_2842_s_288	15075370	Thus, the Lsm2 - Lsm7 complex does not appear to be required for the accumulation of snR5 RNA or for its role in pseudouridylation.	gene_phenotype
70212	1	334090	7	NULL	NULL	NULL	NULL	elements	NucleicAcid		essential for					RNA	NucleicAcid	accumulation of			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_2_457_s_48	9889201	Since the actin mRNA was expressed correctly (data not shown), we concluded that the snR5 RNA lacks elements that are essential for RNA accumulation.	gene_phenotype
70217	2	334090	7	NULL	NULL	0	NULL	snR5 RNA	NucleicAcid		lacks					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_2_457_s_48	9889201	Since the actin mRNA was expressed correctly (data not shown), we concluded that the snR5 RNA lacks elements that are essential for RNA accumulation.	gene_phenotype
70220	1	334091	7	NULL	NULL	0	NULL	Lsm Proteins	GP		is not required for					snR5 RNA	NucleicAcid	accumulation of			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_6_2842_s_246	15075370	Lsm Proteins Are Not Required for snR5 RNA Accumulation or Its Function in Pseudouridylation   To examine the role of Lsm proteins in snR5 function, we used strains in which  LSM2, LSM3, and  LSM8 were under control of the glucose-repressible  GAL promoter (Mayes  et al., 1999 ) to deplete the proteins.	gene_phenotype
70221	2	334091	7	NULL	NULL	0	NULL	Lsm Proteins	GP		is not required for					Pseudouridylation	Process	function in			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_6_2842_s_246	15075370	Lsm Proteins Are Not Required for snR5 RNA Accumulation or Its Function in Pseudouridylation   To examine the role of Lsm proteins in snR5 function, we used strains in which  LSM2, LSM3, and  LSM8 were under control of the glucose-repressible  GAL promoter (Mayes  et al., 1999 ) to deplete the proteins.	gene_phenotype
70222	3	334091	7	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_6_2842_s_246	15075370	Lsm Proteins Are Not Required for snR5 RNA Accumulation or Its Function in Pseudouridylation   To examine the role of Lsm proteins in snR5 function, we used strains in which  LSM2, LSM3, and  LSM8 were under control of the glucose-repressible  GAL promoter (Mayes  et al., 1999 ) to deplete the proteins.	gene_phenotype
70223	1	334092	7	NULL	NULL	0	NULL	SNR5	NucleicAcid		supports				promoter	transcription	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_2_457_s_71	9889201	The differences in the levels of RNA accumulation probably reflect the fact that the  SNR5 promoter supports transcription more efficiently than does the  ADH promoter.	gene_phenotype
70224	2	334092	7	NULL	NULL	0	NULL	ADH	GP		supports				promoter	transcription	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_2_457_s_71	9889201	The differences in the levels of RNA accumulation probably reflect the fact that the  SNR5 promoter supports transcription more efficiently than does the  ADH promoter.	gene_phenotype
70225	3	334092	7	NULL	NULL	0	NULL	statement 1	Process		is more efficient than					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_2_457_s_71	9889201	The differences in the levels of RNA accumulation probably reflect the fact that the  SNR5 promoter supports transcription more efficiently than does the  ADH promoter.	gene_phenotype
70226	1	334093	7	NULL	NULL	NULL	NULL	U1003 residue	Chemical		converted to		site-specifically			pseudouridine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_5_799_s_190	9182768	Mapping the pseudouridylation sites in 25S rRNA isolated from the deltasnR5/RES strain  demonstrated that restoration of the accumulation of snR5 RNA reestablished the site-specific  conversion of U1003 and U1123 residues into pseudouridine (  Figure 6, lanes 3 and 6).	gene_phenotype
70227	2	334093	7	NULL	NULL	NULL	NULL	U1123 residue	Chemical		converted to		site-specifically			pseudouridine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_5_799_s_190	9182768	Mapping the pseudouridylation sites in 25S rRNA isolated from the deltasnR5/RES strain  demonstrated that restoration of the accumulation of snR5 RNA reestablished the site-specific  conversion of U1003 and U1123 residues into pseudouridine (  Figure 6, lanes 3 and 6).	gene_phenotype
70228	3	334093	7	NULL	NULL	NULL	NULL	snR5 RNA	NucleicAcid		reestablishes					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_5_799_s_190	9182768	Mapping the pseudouridylation sites in 25S rRNA isolated from the deltasnR5/RES strain  demonstrated that restoration of the accumulation of snR5 RNA reestablished the site-specific  conversion of U1003 and U1123 residues into pseudouridine (  Figure 6, lanes 3 and 6).	gene_phenotype
70229	4	334093	7	NULL	NULL	NULL	NULL	snR5 RNA	NucleicAcid		reestablishes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_cell_89_5_799_s_190	9182768	Mapping the pseudouridylation sites in 25S rRNA isolated from the deltasnR5/RES strain  demonstrated that restoration of the accumulation of snR5 RNA reestablished the site-specific  conversion of U1003 and U1123 residues into pseudouridine (  Figure 6, lanes 3 and 6).	gene_phenotype
70231	1	334094	7	NULL	NULL	0	NULL	RPL7A	GP		harbors					snR39	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_2981_s_336	15798187	Deletion of RPL7A that harbors snR39 within its introns moderately impairs growth and affects budding ( ); however, deletion of RPL7B that harbors snR59 in its intron has no effect on growth ( ).	gene_phenotype
70232	2	334094	7	NULL	NULL	0	NULL	 RPL7A	GP	deletion of	impairs		moderately			growth	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_2981_s_336	15798187	Deletion of RPL7A that harbors snR39 within its introns moderately impairs growth and affects budding ( ); however, deletion of RPL7B that harbors snR59 in its intron has no effect on growth ( ).	gene_phenotype
70233	3	334094	7	NULL	NULL	NULL	NULL	 RPL7A	GP	deletion of	affects		moderately			budding	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_2981_s_336	15798187	Deletion of RPL7A that harbors snR39 within its introns moderately impairs growth and affects budding ( ); however, deletion of RPL7B that harbors snR59 in its intron has no effect on growth ( ).	gene_phenotype
70234	4	334094	7	NULL	NULL	0	NULL	RPL7B	GP		harbors					snR59	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_2981_s_336	15798187	Deletion of RPL7A that harbors snR39 within its introns moderately impairs growth and affects budding ( ); however, deletion of RPL7B that harbors snR59 in its intron has no effect on growth ( ).	gene_phenotype
70235	5	334094	7	NULL	NULL	NULL	NULL	RPL7B	Process	deletion of	has no effect on					growth	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_8_2981_s_336	15798187	Deletion of RPL7A that harbors snR39 within its introns moderately impairs growth and affects budding ( ); however, deletion of RPL7B that harbors snR59 in its intron has no effect on growth ( ).	gene_phenotype
70236	1	334095	7	NULL	NULL	0	NULL	U65/U24 transcript	NucleicAcid		carries					U65 sequence	GP	mutant			NULL		0	NULL	NULL	NULL	gw60_embo_18_2_457_s_128	9889201	Therefore, a U65/U24 fusion snoRNA was constructed and placed under the control of the  SNR5 promoter (Figure  4A), anticipating that the U65/U24 transcript, even if carrying mutant U65 sequences, would be stable in yeast cells due to the presence of the 5''-terminal cap structure and the 3''-terminal U24 snoRNP particle.	gene_phenotype
70237	2	334095	7	NULL	NULL	0	NULL	statement 1	Process		stable in					yeast cells	Cell				NULL		0	NULL	NULL	NULL	gw60_embo_18_2_457_s_128	9889201	Therefore, a U65/U24 fusion snoRNA was constructed and placed under the control of the  SNR5 promoter (Figure  4A), anticipating that the U65/U24 transcript, even if carrying mutant U65 sequences, would be stable in yeast cells due to the presence of the 5''-terminal cap structure and the 3''-terminal U24 snoRNP particle.	gene_phenotype
70238	3	334095	7	NULL	NULL	NULL	NULL	statement 2	Process		due to					 cap structure	Process	presence of		5''-terminal	NULL		NULL	NULL	NULL	NULL	gw60_embo_18_2_457_s_128	9889201	Therefore, a U65/U24 fusion snoRNA was constructed and placed under the control of the  SNR5 promoter (Figure  4A), anticipating that the U65/U24 transcript, even if carrying mutant U65 sequences, would be stable in yeast cells due to the presence of the 5''-terminal cap structure and the 3''-terminal U24 snoRNP particle.	gene_phenotype
70239	4	334095	7	NULL	NULL	NULL	NULL	statement 2	Process		due to					U24 snoRNP particle	NucleicAcid	presence of		3''-terminal	NULL		NULL	NULL	NULL	NULL	gw60_embo_18_2_457_s_128	9889201	Therefore, a U65/U24 fusion snoRNA was constructed and placed under the control of the  SNR5 promoter (Figure  4A), anticipating that the U65/U24 transcript, even if carrying mutant U65 sequences, would be stable in yeast cells due to the presence of the 5''-terminal cap structure and the 3''-terminal U24 snoRNP particle.	gene_phenotype
70240	1	334096	7	NULL	NULL	NULL	NULL			mutation in	cause				repeat 1	snR13F RNA	NucleicAcid	decreased accumulation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_401	9819377	The mutation in repeat 1 caused decreased accumulation of snR13F RNA without a concomitant increase in 5''-truncated snR13T and 3''-extended snR13RR.	gene_phenotype
70241	2	334096	7	NULL	NULL	NULL	NULL	statement 1	Process		does not increase					snR13T	NucleicAcid			5''-truncated	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_401	9819377	The mutation in repeat 1 caused decreased accumulation of snR13F RNA without a concomitant increase in 5''-truncated snR13T and 3''-extended snR13RR.	gene_phenotype
70242	3	334096	7	NULL	NULL	0	NULL	statement 1	Process		does not increase					snR13RR	NucleicAcid			3''-extended	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_401	9819377	The mutation in repeat 1 caused decreased accumulation of snR13F RNA without a concomitant increase in 5''-truncated snR13T and 3''-extended snR13RR.	gene_phenotype
70243	1	334097	7	NULL	NULL	NULL	NULL			mutation in	failed to cause				repeat 3	snR13T RNA	NucleicAcid	increase in accumulation			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_402	9819377	Both of the mutations in repeat 3 failed to cause detectable increases in the accumulation of snR13T and snR13R RNAs.	gene_phenotype
70244	2	334097	7	NULL	NULL	NULL	NULL			mutations in	failed to cause				repeat 3	snR13R RNA	NucleicAcid	increase in accumulation			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_402	9819377	Both of the mutations in repeat 3 failed to cause detectable increases in the accumulation of snR13T and snR13R RNAs.	gene_phenotype
70245	1	334099	7	NULL	NULL	0	NULL	 Sen1p	GP	inactivation of	accumulate					snR13 RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_169	9819377	Kinetics of accumulation of snR13 RNAs following inactivation of Sen1p.	gene_phenotype
70246	1	334102	7	NULL	NULL	0	NULL	snR13F RNA	NucleicAcid		is not essential for					growth	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_178	9819377	This strain was found to be viable and failed to produce any detectable snR13F RNA as judged by Northern blotting, indicating that the RNA is not essential for growth.	gene_phenotype
70247	1	334103	7	NULL	NULL	0	NULL	nrd1	GP	mutant allele of	reduce					snR13 	NucleicAcid	accumulation of mature			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_8_2441_s_290	15121901	Mutant alleles of  nrd1 and  sen1 exhibit reduced accumulation of mature snR13 and increased accumulation of RNAs that extend through the snR13 transcription termination site and extend to the site of transcription termination of the next downstream gene on the chromosome ( 7, 8, 16).	gene_phenotype
70248	2	334103	7	NULL	NULL	0	NULL	sen1	GP	mutant allele of	reduce					snR13	NucleicAcid	accumulation of mature			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_8_2441_s_290	15121901	Mutant alleles of  nrd1 and  sen1 exhibit reduced accumulation of mature snR13 and increased accumulation of RNAs that extend through the snR13 transcription termination site and extend to the site of transcription termination of the next downstream gene on the chromosome ( 7, 8, 16).	gene_phenotype
70249	3	334103	7	NULL	NULL	0	NULL	RNAs	NucleicAcid		extend through					snR13	NucleicAcid			transcription termination site	NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_8_2441_s_290	15121901	Mutant alleles of  nrd1 and  sen1 exhibit reduced accumulation of mature snR13 and increased accumulation of RNAs that extend through the snR13 transcription termination site and extend to the site of transcription termination of the next downstream gene on the chromosome ( 7, 8, 16).	gene_phenotype
70250	4	334103	7	NULL	NULL	NULL	NULL	RNAs	NucleicAcid		extend to					transcription	Process			 termination site of	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_8_2441_s_290	15121901	Mutant alleles of  nrd1 and  sen1 exhibit reduced accumulation of mature snR13 and increased accumulation of RNAs that extend through the snR13 transcription termination site and extend to the site of transcription termination of the next downstream gene on the chromosome ( 7, 8, 16).	gene_phenotype
70251	5	334103	7	NULL	NULL	0	NULL	transcription 	Process		present on				termination site	chromosome	Chromosome			next downstream gene 	NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_8_2441_s_290	15121901	Mutant alleles of  nrd1 and  sen1 exhibit reduced accumulation of mature snR13 and increased accumulation of RNAs that extend through the snR13 transcription termination site and extend to the site of transcription termination of the next downstream gene on the chromosome ( 7, 8, 16).	gene_phenotype
70252	6	334103	7	NULL	NULL	0	NULL	statement 3	Process		occur along with					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_8_2441_s_290	15121901	Mutant alleles of  nrd1 and  sen1 exhibit reduced accumulation of mature snR13 and increased accumulation of RNAs that extend through the snR13 transcription termination site and extend to the site of transcription termination of the next downstream gene on the chromosome ( 7, 8, 16).	gene_phenotype
70253	7	334103	7	NULL	NULL	0	NULL	nrd1 	GP	mutant allele of	increase					statement 6	Process				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_8_2441_s_290	15121901	Mutant alleles of  nrd1 and  sen1 exhibit reduced accumulation of mature snR13 and increased accumulation of RNAs that extend through the snR13 transcription termination site and extend to the site of transcription termination of the next downstream gene on the chromosome ( 7, 8, 16).	gene_phenotype
70254	8	334103	7	NULL	NULL	0	NULL	sen1	GP	mutant allele of	increase					statement 6	Process				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_8_2441_s_290	15121901	Mutant alleles of  nrd1 and  sen1 exhibit reduced accumulation of mature snR13 and increased accumulation of RNAs that extend through the snR13 transcription termination site and extend to the site of transcription termination of the next downstream gene on the chromosome ( 7, 8, 16).	gene_phenotype
70255	1	334104	7	NULL	NULL	0	NULL	snR13 transcripts	GP	wild-type	shows					new RNA	NucleicAcid	accumulation in the mutant strain of 			NULL		0	NULL	NULL	NULL	gw60_nature_413_6853_327_s_28	11565036	Northern blot analysis of snR13 and Trs31 transcripts from wild-type and  nrd1 mutant strains shows the accumulation in the mutant strain of a new RNA species, which is larger than the normal Trs31 mRNA, that is detected by probes complementary to either mature snR13 RNA or Trs31 mRNA ( Fig. 1b).	gene_phenotype
70256	2	334104	7	NULL	NULL	0	NULL	Trs31 transcript	GP	wild-type	shows					new RNA	NucleicAcid	accumulation in the mutant strain of 			NULL		0	NULL	NULL	NULL	gw60_nature_413_6853_327_s_28	11565036	Northern blot analysis of snR13 and Trs31 transcripts from wild-type and  nrd1 mutant strains shows the accumulation in the mutant strain of a new RNA species, which is larger than the normal Trs31 mRNA, that is detected by probes complementary to either mature snR13 RNA or Trs31 mRNA ( Fig. 1b).	gene_phenotype
70257	3	334104	7	NULL	NULL	0	NULL	new RNA	NucleicAcid		is larger than					Trs31 mRNA	NucleicAcid	normal			NULL		0	NULL	NULL	NULL	gw60_nature_413_6853_327_s_28	11565036	Northern blot analysis of snR13 and Trs31 transcripts from wild-type and  nrd1 mutant strains shows the accumulation in the mutant strain of a new RNA species, which is larger than the normal Trs31 mRNA, that is detected by probes complementary to either mature snR13 RNA or Trs31 mRNA ( Fig. 1b).	gene_phenotype
70258	1	334105	7	NULL	NULL	0	NULL	 swd2- 3	GP	mutant;;viability of	occur upon					Ref2	GP	overexpression of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_7_2932_s_333	15024081	The viability of the  swd2- 3 and  swd2- 5 mutants at 37 degrees C when Ref2 is overexpressed, together with the recovery of  SNR13 termination, is consistent with this interpretation.	gene_phenotype
70259	2	334105	7	NULL	NULL	0	NULL	swd2- 5	GP	mutant;;viability of	occur upon					Ref2	GP	overexpression of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_7_2932_s_333	15024081	The viability of the  swd2- 3 and  swd2- 5 mutants at 37 degrees C when Ref2 is overexpressed, together with the recovery of  SNR13 termination, is consistent with this interpretation.	gene_phenotype
70260	1	334107	7	NULL	NULL	0	NULL	 snR13	NucleicAcid		is dispensable for					viability	Process				NULL		0	NULL	NULL	NULL	gw60_nature_413_6853_327_s_94	11565036	This function may be more vital to the cell than Nrd1-dependent 3''-end maturation of snoRNAs because most snoRNAs, including snR13, are dispensable for viability.	gene_phenotype
70261	2	334107	7	NULL	NULL	0	NULL	 snR13	NucleicAcid		is a type of					snoRNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_nature_413_6853_327_s_94	11565036	This function may be more vital to the cell than Nrd1-dependent 3''-end maturation of snoRNAs because most snoRNAs, including snR13, are dispensable for viability.	gene_phenotype
70262	3	334107	7	NULL	NULL	0	NULL	snoRNAs	NucleicAcid	maturation of	depends on					Nrd1	GP				NULL		0	NULL	NULL	NULL	gw60_nature_413_6853_327_s_94	11565036	This function may be more vital to the cell than Nrd1-dependent 3''-end maturation of snoRNAs because most snoRNAs, including snR13, are dispensable for viability.	gene_phenotype
70263	1	334108	7	NULL	NULL	0	NULL			mutant	cause				5' C2U4 repeat	snR13F	NucleicAcid	underaccumulation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_11	9819377	A mutation in the 5' C2U4 repeat causes underaccumulation of snR13F, whereas mutations in the 3' C2U4 repeat cause the accumulation of two novel RNAs that migrate in the 500-nt range.	gene_phenotype
70264	2	334108	7	NULL	NULL	0	NULL			mutant	cause				 3' C2U4 repeat	snR13F	NucleicAcid	underaccumulation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_11	9819377	A mutation in the 5' C2U4 repeat causes underaccumulation of snR13F, whereas mutations in the 3' C2U4 repeat cause the accumulation of two novel RNAs that migrate in the 500-nt range.	gene_phenotype
70265	1	334109	7	NULL	NULL	0	NULL	snR13-RNEW 	NucleicAcid		failed to cause					snR13 RNA	NucleicAcid	accumulation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_325	9819377	snR13-RNEW failed to cause any changes in snR13 RNA accumulation (Fig.  9B, lane 5), showing that C2U4 is insufficient by itself to specify a site for 3' end formation in the absence of a proper context.	gene_phenotype
70266	2	334109	7	NULL	NULL	0	NULL				is insufficient 				C2U4	formation	Process	to specify site for		3' end	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_325	9819377	snR13-RNEW failed to cause any changes in snR13 RNA accumulation (Fig.  9B, lane 5), showing that C2U4 is insufficient by itself to specify a site for 3' end formation in the absence of a proper context.	gene_phenotype
70267	1	334110	7	NULL	NULL	NULL	NULL	snR13 RNA	NucleicAcid	changes in;;accumulation of	result from					Sen1p	GP	requirement of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_385	9819377	The changes in synthetic rates and levels of accumulation of the snR13 RNAs result from a requirement of Sen1p to both stabilize the 5' terminus and to promote formation of the 3' terminus from a 3''-extended RNA.	gene_phenotype
70268	2	334110	7	NULL	NULL	0	NULL	statement 1	Process		stabilize									5' terminus	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_385	9819377	The changes in synthetic rates and levels of accumulation of the snR13 RNAs result from a requirement of Sen1p to both stabilize the 5' terminus and to promote formation of the 3' terminus from a 3''-extended RNA.	gene_phenotype
70269	3	334110	7	NULL	NULL	0	NULL				formed from				3' terminus 	3''-extended RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_385	9819377	The changes in synthetic rates and levels of accumulation of the snR13 RNAs result from a requirement of Sen1p to both stabilize the 5' terminus and to promote formation of the 3' terminus from a 3''-extended RNA.	gene_phenotype
70270	4	334110	7	NULL	NULL	0	NULL	statement 1	Process		promote					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_385	9819377	The changes in synthetic rates and levels of accumulation of the snR13 RNAs result from a requirement of Sen1p to both stabilize the 5' terminus and to promote formation of the 3' terminus from a 3''-extended RNA.	gene_phenotype
70271	1	334111	7	NULL	NULL	0	NULL	altered RNA	NucleicAcid	accumulation of	precedes					cell viability	Process	loss of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_156	9819377	This probe detects [[ only snR13R RNA.                    Because ]]  SEN1 is an essential gene ( 10), we assessed whether the onset of altered RNA accumulation precedes loss of cell viability following a shift to the restrictive temperature.	gene_phenotype
70272	2	334111	7	NULL	NULL	0	NULL	statement 1	Process		followed by					 restrictive temperature		shift to			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_156	9819377	This probe detects [[ only snR13R RNA.                    Because ]]  SEN1 is an essential gene ( 10), we assessed whether the onset of altered RNA accumulation precedes loss of cell viability following a shift to the restrictive temperature.	gene_phenotype
70273	1	334113	7	NULL	NULL	NULL	NULL	CF IA 	GP		is involved in					chromosomal snoRNA transcripts	NucleicAcid			3"`-end formation of	NULL	rna15- 2 strain	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_5_1379_s_266	11839805	Analysis of the endogenous transcripts produced in a  rna15- 2 strain at the nonpermissive temperature showed the accumulation of a read-through RNA extending inside the gene downstream to the snR13 coding region, showing that CF IA is indeed involved in the 3"`-end formation of chromosomal snoRNA transcripts.	gene_phenotype
70274	1	334114	7	NULL	NULL	NULL	NULL	sen1-1	GP	double mutant	accumulation of		reduce			novel RNAs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_12	9819377	At the restrictive temperature, double mutants carrying  sen1-1 and mutations in the 3' C2U4 repeat show reduced accumulation of the novel RNAs and increased accumulation of snR13R RNA, indicating that Sen1p and the 3' C2U4 sequence act in a common pathway to facilitate 3' end formation.	gene_phenotype
70275	2	334114	7	NULL	NULL	NULL	NULL			mutations in	accumulation of		reduce		3' C2U4 repeat 	novel RNAs	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_12	9819377	At the restrictive temperature, double mutants carrying  sen1-1 and mutations in the 3' C2U4 repeat show reduced accumulation of the novel RNAs and increased accumulation of snR13R RNA, indicating that Sen1p and the 3' C2U4 sequence act in a common pathway to facilitate 3' end formation.	gene_phenotype
70276	3	334114	7	NULL	NULL	0	NULL	sen1-1	GP	double mutant	increase					snR13R RNA	NucleicAcid	accumulation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_12	9819377	At the restrictive temperature, double mutants carrying  sen1-1 and mutations in the 3' C2U4 repeat show reduced accumulation of the novel RNAs and increased accumulation of snR13R RNA, indicating that Sen1p and the 3' C2U4 sequence act in a common pathway to facilitate 3' end formation.	gene_phenotype
70277	4	334114	7	NULL	NULL	NULL	NULL			mutations in	increase				 3' C2U4 repeat 	snR13R RNA	NucleicAcid	accumulation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_12	9819377	At the restrictive temperature, double mutants carrying  sen1-1 and mutations in the 3' C2U4 repeat show reduced accumulation of the novel RNAs and increased accumulation of snR13R RNA, indicating that Sen1p and the 3' C2U4 sequence act in a common pathway to facilitate 3' end formation.	gene_phenotype
70278	5	334114	7	NULL	NULL	NULL	NULL	Sen1p	GP		facilitate					RNA	NucleicAcid			3' end formation 	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_12	9819377	At the restrictive temperature, double mutants carrying  sen1-1 and mutations in the 3' C2U4 repeat show reduced accumulation of the novel RNAs and increased accumulation of snR13R RNA, indicating that Sen1p and the 3' C2U4 sequence act in a common pathway to facilitate 3' end formation.	gene_phenotype
70279	6	334114	7	NULL	NULL	NULL	NULL				facilitate				 3' C2U4 sequence	RNA	NucleicAcid			 3' end formation	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_12_6885_s_12	9819377	At the restrictive temperature, double mutants carrying  sen1-1 and mutations in the 3' C2U4 repeat show reduced accumulation of the novel RNAs and increased accumulation of snR13R RNA, indicating that Sen1p and the 3' C2U4 sequence act in a common pathway to facilitate 3' end formation.	gene_phenotype
70280	1	334116	7	NULL	NULL	0	NULL	polalphats13 cdc22	GP	Double mutant 	arrested with					cdc22-like phenotype	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_8_2107_s_216	9693370	Double mutant  polalphats13 cdc22 ( cdc22 encodes the large subunit of ribonucleotide reductase) arrested with a  cdc22-like phenotype with a very low percent of abnormal nuclear morphology.	gene_phenotype
70281	2	334116	7	NULL	NULL	0	NULL	cdc22	GP		encode					ribonucleotide reductase	GP		large subunit of		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_8_2107_s_216	9693370	Double mutant  polalphats13 cdc22 ( cdc22 encodes the large subunit of ribonucleotide reductase) arrested with a  cdc22-like phenotype with a very low percent of abnormal nuclear morphology.	gene_phenotype
70283	1	334118	7	NULL	NULL	0	NULL	cdc22+	GP	overexpression of	did not complement					sporulation deficiency	Process				NULL	cdt2-M1 cells	0	NULL	NULL	NULL	gw70_genetics_164_3_881_s_295	12871901	We found that overexpression of  cdc22+ did not complement the sporulation deficiency of  cdt2-M1 cells (data not shown).	gene_phenotype
70284	1	334119	7	NULL	NULL	0	NULL	checkpoint signal	Process		activates					Cds1p	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_102_16_5797_s_159	15805194	The checkpoint signal that activates Cds1p is generated in the  cdc22 or HU treated cells but not in  orp1 cdc18 cells during the mitotic cell cycle ( ).	gene_phenotype
70285	2	334119	7	NULL	NULL	0	NULL	statement 1	Process		is generated in					cdc22 cells	Cell				NULL		0	NULL	NULL	NULL	gw70_pnas_102_16_5797_s_159	15805194	The checkpoint signal that activates Cds1p is generated in the  cdc22 or HU treated cells but not in  orp1 cdc18 cells during the mitotic cell cycle ( ).	gene_phenotype
70286	3	334119	7	NULL	NULL	0	NULL	statement 1	Process		is generated in					HU treated cells	Cell				NULL		0	NULL	NULL	NULL	gw70_pnas_102_16_5797_s_159	15805194	The checkpoint signal that activates Cds1p is generated in the  cdc22 or HU treated cells but not in  orp1 cdc18 cells during the mitotic cell cycle ( ).	gene_phenotype
70287	4	334119	7	NULL	NULL	0	NULL	statement 1	Process		is not generated in					orp1 cdc18 cells 	Cell				NULL		0	NULL	NULL	NULL	gw70_pnas_102_16_5797_s_159	15805194	The checkpoint signal that activates Cds1p is generated in the  cdc22 or HU treated cells but not in  orp1 cdc18 cells during the mitotic cell cycle ( ).	gene_phenotype
70288	5	334119	7	NULL	NULL	0	NULL	statement 2	Process		occur during					mitotic cell cycle	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_102_16_5797_s_159	15805194	The checkpoint signal that activates Cds1p is generated in the  cdc22 or HU treated cells but not in  orp1 cdc18 cells during the mitotic cell cycle ( ).	gene_phenotype
70289	6	334119	7	NULL	NULL	0	NULL	statement 3	Process		occur during					mitotic cell cycle	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_102_16_5797_s_159	15805194	The checkpoint signal that activates Cds1p is generated in the  cdc22 or HU treated cells but not in  orp1 cdc18 cells during the mitotic cell cycle ( ).	gene_phenotype
70290	7	334119	7	NULL	NULL	0	NULL	statement 4	Process		occur during					mitotic cell cycle	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_102_16_5797_s_159	15805194	The checkpoint signal that activates Cds1p is generated in the  cdc22 or HU treated cells but not in  orp1 cdc18 cells during the mitotic cell cycle ( ).	gene_phenotype
70526	1	334123	7	NULL	NULL	NULL	NULL	rad1- 1 cdc22- M45	Cell	mutant	proceed through					cell division	Process				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_14_3030_s_160	11452028	Some of the quantitative effects reflect the smaller average size of the  rad1- 1 cdc22- M45 mutant cells that proceed through cell division.	gene_phenotype
70643	1	334126	7	NULL	NULL	0	NULL	Spd1p	GP		inhibit					Suc22p activity	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_90	16317005	To differentiate between inhibition of Suc22p and Cdc22p activity by Spd1p, we took advantage of the observation that budding yeast Rnr1p forms an active RNR complex with fission yeast Suc22p, although the amino acid sequence identity is only 66% between Rnr1p and Cdc22p.	gene_phenotype
70644	2	334126	7	NULL	NULL	0	NULL	Spd1p	GP		inhibit					Cdc22p activity	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_90	16317005	To differentiate between inhibition of Suc22p and Cdc22p activity by Spd1p, we took advantage of the observation that budding yeast Rnr1p forms an active RNR complex with fission yeast Suc22p, although the amino acid sequence identity is only 66% between Rnr1p and Cdc22p.	gene_phenotype
70645	3	334126	7	NULL	NULL	0	NULL	Rnr1p	GP	budding yeast	forms complex with					Suc22p	GP	fission yeast 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_90	16317005	To differentiate between inhibition of Suc22p and Cdc22p activity by Spd1p, we took advantage of the observation that budding yeast Rnr1p forms an active RNR complex with fission yeast Suc22p, although the amino acid sequence identity is only 66% between Rnr1p and Cdc22p.	gene_phenotype
70646	4	334126	7	NULL	NULL	0	NULL	statement 3	Process		is a type of					RNR complex	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_90	16317005	To differentiate between inhibition of Suc22p and Cdc22p activity by Spd1p, we took advantage of the observation that budding yeast Rnr1p forms an active RNR complex with fission yeast Suc22p, although the amino acid sequence identity is only 66% between Rnr1p and Cdc22p.	gene_phenotype
70649	1	334127	7	NULL	NULL	0	NULL	Spd1	GP		inhibitor of		very weak			RNR	GP	budding yeast			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_92	16317005	Because Spd1 is a very weak inhibitor of the budding yeast RNR, these results strongly indicate that Spd1 inhibits the fission yeast RNR by specifically interacting with Cdc22p.	gene_phenotype
70650	2	334127	7	NULL	NULL	0	NULL	 Spd1	GP		interact with		specifically			Cdc22p	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_92	16317005	Because Spd1 is a very weak inhibitor of the budding yeast RNR, these results strongly indicate that Spd1 inhibits the fission yeast RNR by specifically interacting with Cdc22p.	gene_phenotype
70651	3	334127	7	NULL	NULL	0	NULL	Spd1	GP		inhibit					RNR	GP	fission yeast			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_92	16317005	Because Spd1 is a very weak inhibitor of the budding yeast RNR, these results strongly indicate that Spd1 inhibits the fission yeast RNR by specifically interacting with Cdc22p.	gene_phenotype
70652	4	334127	7	NULL	NULL	0	NULL	statement 3	Process		occur by					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_92	16317005	Because Spd1 is a very weak inhibitor of the budding yeast RNR, these results strongly indicate that Spd1 inhibits the fission yeast RNR by specifically interacting with Cdc22p.	gene_phenotype
70653	1	334130	7	NULL	NULL	0	NULL	cdt2+	GP	transcription of	fluctuates through					mitotic cell cycle	Process				NULL		0	NULL	NULL	NULL	gw70_genetics_164_3_881_s_128	12871901	As previously reported, transcription of  cdt2+ fluctuates through the mitotic cell cycle with a peak at G1-S phase, similar to the expression pattern of  cdc22+, another target of DSC1 ( Fig 2A).	gene_phenotype
70654	2	334130	7	NULL	NULL	0	NULL	statement 1	Process		peak at					G1-S phase	Process				NULL		0	NULL	NULL	NULL	gw70_genetics_164_3_881_s_128	12871901	As previously reported, transcription of  cdt2+ fluctuates through the mitotic cell cycle with a peak at G1-S phase, similar to the expression pattern of  cdc22+, another target of DSC1 ( Fig 2A).	gene_phenotype
70655	3	334130	7	NULL	NULL	0	NULL	cdt2+	GP	transcription of	is similar to					cdc22+	GP	expression pattern of			NULL		0	NULL	NULL	NULL	gw70_genetics_164_3_881_s_128	12871901	As previously reported, transcription of  cdt2+ fluctuates through the mitotic cell cycle with a peak at G1-S phase, similar to the expression pattern of  cdc22+, another target of DSC1 ( Fig 2A).	gene_phenotype
70656	4	334130	7	NULL	NULL	0	NULL	cdc22+	GP		is target of					DSC1	GP				NULL		0	NULL	NULL	NULL	gw70_genetics_164_3_881_s_128	12871901	As previously reported, transcription of  cdt2+ fluctuates through the mitotic cell cycle with a peak at G1-S phase, similar to the expression pattern of  cdc22+, another target of DSC1 ( Fig 2A).	gene_phenotype
70657	1	334131	7	NULL	NULL	0	NULL	cdc18	GP 	transcription of	is accompanied by					cdc22	GP	mitotic transcription of			NULL		0	NULL	NULL	NULL	gw60_embo_17_19_5689_s_193	9755169	(iii) This  cdc18 transcription is accompanied by the mitotic transcription of other  cdc10-dependent genes, such as  cdc22 and  cdt1, and requires the continued activity of the cdc10p `start'' transcription factor (homologous to the budding yeast Swi6p `start'' transcription factor).	gene_phenotype
70658	2	334131	7	NULL	NULL	0	NULL	cdc18	GP	transcription of	is accompanied by					cdt1	GP	mitotic transcription of			NULL		0	NULL	NULL	NULL	gw60_embo_17_19_5689_s_193	9755169	(iii) This  cdc18 transcription is accompanied by the mitotic transcription of other  cdc10-dependent genes, such as  cdc22 and  cdt1, and requires the continued activity of the cdc10p `start'' transcription factor (homologous to the budding yeast Swi6p `start'' transcription factor).	gene_phenotype
70659	3	334131	7	NULL	NULL	0	NULL	cdc22	GP		is a type of					 cdc10-dependent gene	GP				NULL		0	NULL	NULL	NULL	gw60_embo_17_19_5689_s_193	9755169	(iii) This  cdc18 transcription is accompanied by the mitotic transcription of other  cdc10-dependent genes, such as  cdc22 and  cdt1, and requires the continued activity of the cdc10p `start'' transcription factor (homologous to the budding yeast Swi6p `start'' transcription factor).	gene_phenotype
70660	4	334131	7	NULL	NULL	0	NULL	cdt1	GP		is a type of					cdc10-dependent gene	GP				NULL		0	NULL	NULL	NULL	gw60_embo_17_19_5689_s_193	9755169	(iii) This  cdc18 transcription is accompanied by the mitotic transcription of other  cdc10-dependent genes, such as  cdc22 and  cdt1, and requires the continued activity of the cdc10p `start'' transcription factor (homologous to the budding yeast Swi6p `start'' transcription factor).	gene_phenotype
70661	5	334131	7	NULL	NULL	0	NULL	 cdc18	GP	transcription of	requires					cdc10p `start'' transcription factor	GP	continued activity of			NULL		0	NULL	NULL	NULL	gw60_embo_17_19_5689_s_193	9755169	(iii) This  cdc18 transcription is accompanied by the mitotic transcription of other  cdc10-dependent genes, such as  cdc22 and  cdt1, and requires the continued activity of the cdc10p `start'' transcription factor (homologous to the budding yeast Swi6p `start'' transcription factor).	gene_phenotype
70662	6	334131	7	NULL	NULL	0	NULL	cdc10p `start'' transcription factor	GP		is homologous to					Swi6p `start'' transcription factor	GP	budding yeast			NULL		0	NULL	NULL	NULL	gw60_embo_17_19_5689_s_193	9755169	(iii) This  cdc18 transcription is accompanied by the mitotic transcription of other  cdc10-dependent genes, such as  cdc22 and  cdt1, and requires the continued activity of the cdc10p `start'' transcription factor (homologous to the budding yeast Swi6p `start'' transcription factor).	gene_phenotype
70663	1	334132	7	NULL	NULL	NULL	NULL	DSC1	GP		bind									MCB sequences	NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5745_s_19	12411492	DSC1 binds to MCB sequences (  M luI cell  cycle  box; ACGCGT) that are present in the promoters of  cdc22+,  cdc18+,  cdt1+ and  cig2+, all of which are expressed maximally at the G1 - S boundary during the mitotic cell cycle.	gene_phenotype
70664	2	334132	7	NULL	NULL	0	NULL	MCB sequences	GP		present in					cdc22+	GP	promoters of 			NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5745_s_19	12411492	DSC1 binds to MCB sequences (  M luI cell  cycle  box; ACGCGT) that are present in the promoters of  cdc22+,  cdc18+,  cdt1+ and  cig2+, all of which are expressed maximally at the G1 - S boundary during the mitotic cell cycle.	gene_phenotype
70665	3	334132	7	NULL	NULL	0	NULL	MCB sequences	GP		present in					cdc18+	GP	promoters of			NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5745_s_19	12411492	DSC1 binds to MCB sequences (  M luI cell  cycle  box; ACGCGT) that are present in the promoters of  cdc22+,  cdc18+,  cdt1+ and  cig2+, all of which are expressed maximally at the G1 - S boundary during the mitotic cell cycle.	gene_phenotype
70666	4	334132	7	NULL	NULL	0	NULL	MCB sequences 	GP		present in					 cdt1+	GP	promoters of			NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5745_s_19	12411492	DSC1 binds to MCB sequences (  M luI cell  cycle  box; ACGCGT) that are present in the promoters of  cdc22+,  cdc18+,  cdt1+ and  cig2+, all of which are expressed maximally at the G1 - S boundary during the mitotic cell cycle.	gene_phenotype
70667	5	334132	7	NULL	NULL	0	NULL	MCB sequences	GP		present in					cig2+	GP	promoters of			NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5745_s_19	12411492	DSC1 binds to MCB sequences (  M luI cell  cycle  box; ACGCGT) that are present in the promoters of  cdc22+,  cdc18+,  cdt1+ and  cig2+, all of which are expressed maximally at the G1 - S boundary during the mitotic cell cycle.	gene_phenotype
70668	6	334132	7	NULL	NULL	0	NULL	cdc22+	GP		expressed maximally at					G1 - S boundary 	Process				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5745_s_19	12411492	DSC1 binds to MCB sequences (  M luI cell  cycle  box; ACGCGT) that are present in the promoters of  cdc22+,  cdc18+,  cdt1+ and  cig2+, all of which are expressed maximally at the G1 - S boundary during the mitotic cell cycle.	gene_phenotype
70669	7	334132	7	NULL	NULL	0	NULL	cdc18+	GP		expressed maximally at					G1-S boundary	Process				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5745_s_19	12411492	DSC1 binds to MCB sequences (  M luI cell  cycle  box; ACGCGT) that are present in the promoters of  cdc22+,  cdc18+,  cdt1+ and  cig2+, all of which are expressed maximally at the G1 - S boundary during the mitotic cell cycle.	gene_phenotype
70670	8	334132	7	NULL	NULL	0	NULL	cdt1+	GP		expressed maximally at					G1-S boundary	Process				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5745_s_19	12411492	DSC1 binds to MCB sequences (  M luI cell  cycle  box; ACGCGT) that are present in the promoters of  cdc22+,  cdc18+,  cdt1+ and  cig2+, all of which are expressed maximally at the G1 - S boundary during the mitotic cell cycle.	gene_phenotype
70671	9	334132	7	NULL	NULL	0	NULL	cig2+	GP		expressed maximally at					G1-S boundary	Process				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5745_s_19	12411492	DSC1 binds to MCB sequences (  M luI cell  cycle  box; ACGCGT) that are present in the promoters of  cdc22+,  cdc18+,  cdt1+ and  cig2+, all of which are expressed maximally at the G1 - S boundary during the mitotic cell cycle.	gene_phenotype
70672	10	334132	7	NULL	NULL	0	NULL	statement 6	Process		occur during					mitotic cell cycle	Process				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5745_s_19	12411492	DSC1 binds to MCB sequences (  M luI cell  cycle  box; ACGCGT) that are present in the promoters of  cdc22+,  cdc18+,  cdt1+ and  cig2+, all of which are expressed maximally at the G1 - S boundary during the mitotic cell cycle.	gene_phenotype
70673	11	334132	7	NULL	NULL	0	NULL	statement 7	Process		occur during					mitotic cell cycle	Process				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5745_s_19	12411492	DSC1 binds to MCB sequences (  M luI cell  cycle  box; ACGCGT) that are present in the promoters of  cdc22+,  cdc18+,  cdt1+ and  cig2+, all of which are expressed maximally at the G1 - S boundary during the mitotic cell cycle.	gene_phenotype
70674	12	334132	7	NULL	NULL	0	NULL	statement 8	Process		occur during					mitotic cell cycle	Process				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5745_s_19	12411492	DSC1 binds to MCB sequences (  M luI cell  cycle  box; ACGCGT) that are present in the promoters of  cdc22+,  cdc18+,  cdt1+ and  cig2+, all of which are expressed maximally at the G1 - S boundary during the mitotic cell cycle.	gene_phenotype
70675	13	334132	7	NULL	NULL	0	NULL	statement 9	Process		occur during					mitotic cell cycle	Process				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5745_s_19	12411492	DSC1 binds to MCB sequences (  M luI cell  cycle  box; ACGCGT) that are present in the promoters of  cdc22+,  cdc18+,  cdt1+ and  cig2+, all of which are expressed maximally at the G1 - S boundary during the mitotic cell cycle.	gene_phenotype
70676	14	334132	7	NULL	NULL	0	NULL	MCB sequences 	GP		is					M luI cell cycle box; ACGCGT	GP				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5745_s_19	12411492	DSC1 binds to MCB sequences (  M luI cell  cycle  box; ACGCGT) that are present in the promoters of  cdc22+,  cdc18+,  cdt1+ and  cig2+, all of which are expressed maximally at the G1 - S boundary during the mitotic cell cycle.	gene_phenotype
70677	1	334133	7	NULL	NULL	NULL	NULL	mik1+ transcript	GP	abundance of	coincides with					cdc22+ transcript	GP	abundance of			NULL	wild-type cells	NULL	NULL	NULL	NULL	gw60_febslett_503_2_131_s_67	11513869	In a synchronous population of wild-type cells, size selected by elutriation,  mik1+ transcript was found to vary in abundance ( Fig. 1B) coincident with  cdc22+ transcript, thus peaking at the G1-S boundary.	gene_phenotype
70678	2	334133	7	NULL	NULL	0	NULL	statement 1	Process		peaks at					G1-S boundary	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_503_2_131_s_67	11513869	In a synchronous population of wild-type cells, size selected by elutriation,  mik1+ transcript was found to vary in abundance ( Fig. 1B) coincident with  cdc22+ transcript, thus peaking at the G1-S boundary.	gene_phenotype
70679	1	334135	7	NULL	NULL	0	NULL	cdc18	GP		required for					DNA replication	Process				NULL		0	NULL	NULL	NULL	gw60_nature_409_6818_359_s_30	11201746	Two genes required for DNA replication,  cdc18 and  cdc22, were induced only during G1-exit meiosis ( Fig. 1c), which was consistent with the fact that G2-exit meiotic cells do not undergo a pre-meiotic S phase.	gene_phenotype
70680	2	334135	7	NULL	NULL	0	NULL	cdc22	GP		required for					DNA replication	Process				NULL		0	NULL	NULL	NULL	gw60_nature_409_6818_359_s_30	11201746	Two genes required for DNA replication,  cdc18 and  cdc22, were induced only during G1-exit meiosis ( Fig. 1c), which was consistent with the fact that G2-exit meiotic cells do not undergo a pre-meiotic S phase.	gene_phenotype
70681	3	334135	7	NULL	NULL	0	NULL	statement 1	Process		induced at					G1-exit meiosis	Process				NULL		0	NULL	NULL	NULL	gw60_nature_409_6818_359_s_30	11201746	Two genes required for DNA replication,  cdc18 and  cdc22, were induced only during G1-exit meiosis ( Fig. 1c), which was consistent with the fact that G2-exit meiotic cells do not undergo a pre-meiotic S phase.	gene_phenotype
70682	4	334135	7	NULL	NULL	NULL	NULL	statement 2	Process		induced at					G1-exit meiosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_nature_409_6818_359_s_30	11201746	Two genes required for DNA replication,  cdc18 and  cdc22, were induced only during G1-exit meiosis ( Fig. 1c), which was consistent with the fact that G2-exit meiotic cells do not undergo a pre-meiotic S phase.	gene_phenotype
70683	5	334135	7	NULL	NULL	0	NULL	G2-exit meiotic cells	Cell		does not undergo					pre-meiotic S phase	Process				NULL		0	NULL	NULL	NULL	gw60_nature_409_6818_359_s_30	11201746	Two genes required for DNA replication,  cdc18 and  cdc22, were induced only during G1-exit meiosis ( Fig. 1c), which was consistent with the fact that G2-exit meiotic cells do not undergo a pre-meiotic S phase.	gene_phenotype
70684	1	334136	7	NULL	NULL	0	NULL	cdc22+ gene	GP	Schizosaccharomyces pombe	encode					ribonucleotide reductase	GP		large subunit of		NULL		0	NULL	NULL	NULL	abs-batch0517-0529_mol-genet-genomics_269_6_12898217_s_2	12898217	The cdc22+ gene of the fission yeast, Schizosaccharomyces pombe, encodes  the large subunit of ribonucleotide reductase, and is periodically expressed  during the mitotic cell cycle, transcript abundance reaching a maximum  at the G1-S boundary.	gene_phenotype
70685	2	334136	7	NULL	NULL	0	NULL	statement 1	Process		expressed during		periodically			mitotic cell cycle	Process				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_mol-genet-genomics_269_6_12898217_s_2	12898217	The cdc22+ gene of the fission yeast, Schizosaccharomyces pombe, encodes  the large subunit of ribonucleotide reductase, and is periodically expressed  during the mitotic cell cycle, transcript abundance reaching a maximum  at the G1-S boundary.	gene_phenotype
70686	3	334136	7	NULL	NULL	0	NULL	cdc22+ transcript	GP	abundance of	reaches 					G1-S boundary	Process	maximum at			NULL		0	NULL	NULL	NULL	abs-batch0517-0529_mol-genet-genomics_269_6_12898217_s_2	12898217	The cdc22+ gene of the fission yeast, Schizosaccharomyces pombe, encodes  the large subunit of ribonucleotide reductase, and is periodically expressed  during the mitotic cell cycle, transcript abundance reaching a maximum  at the G1-S boundary.	gene_phenotype
70687	4	334136	7	NULL	NULL	0	NULL	Schizosaccharomyces pombe	Organism		is a type of					fission yeast	Organism				NULL		0	NULL	NULL	NULL	abs-batch0517-0529_mol-genet-genomics_269_6_12898217_s_2	12898217	The cdc22+ gene of the fission yeast, Schizosaccharomyces pombe, encodes  the large subunit of ribonucleotide reductase, and is periodically expressed  during the mitotic cell cycle, transcript abundance reaching a maximum  at the G1-S boundary.	gene_phenotype
70688	1	334137	7	NULL	NULL	0	NULL	Sml1	GP		bind					Rnr1p	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_28	16317005	This mode of regulation is similar to the regulation of RNR activity in budding yeast, where binding of the low molecular weight inhibitor Sml1 to the Cdc22p homologue, the Rnr1p, controls RNR activity.	gene_phenotype
70689	2	334137	7	NULL	NULL	NULL	NULL	statement 1	Process		controls					RNR activity	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_28	16317005	This mode of regulation is similar to the regulation of RNR activity in budding yeast, where binding of the low molecular weight inhibitor Sml1 to the Cdc22p homologue, the Rnr1p, controls RNR activity.	gene_phenotype
70690	3	334137	7	NULL	NULL	0	NULL	Rnr1p	GP		is homologous to					Cdc22p	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_28	16317005	This mode of regulation is similar to the regulation of RNR activity in budding yeast, where binding of the low molecular weight inhibitor Sml1 to the Cdc22p homologue, the Rnr1p, controls RNR activity.	gene_phenotype
70691	4	334137	7	NULL	NULL	0	NULL	Sml1	GP		is a type of					low molecular weight inhibitor	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_28	16317005	This mode of regulation is similar to the regulation of RNR activity in budding yeast, where binding of the low molecular weight inhibitor Sml1 to the Cdc22p homologue, the Rnr1p, controls RNR activity.	gene_phenotype
70692	5	334137	7	NULL	NULL	0	NULL	statement 1	Process		occur in					budding yeast	Organism				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_28	16317005	This mode of regulation is similar to the regulation of RNR activity in budding yeast, where binding of the low molecular weight inhibitor Sml1 to the Cdc22p homologue, the Rnr1p, controls RNR activity.	gene_phenotype
70693	1	334138	7	NULL	NULL	0	NULL	Spd1p	GP		interacts with					Cdc22p	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_56	16317005	The interaction between Spd1p and Cdc22p, Suc22p, budding yeast Rnr1p, Sml1p, and mouse R1 protein was studied by biosensor analysis using a BIAcore 2000 (Biacore International AB).	gene_phenotype
70694	2	334138	7	NULL	NULL	0	NULL	Spd1p	GP		interacts with					Suc22p	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_56	16317005	The interaction between Spd1p and Cdc22p, Suc22p, budding yeast Rnr1p, Sml1p, and mouse R1 protein was studied by biosensor analysis using a BIAcore 2000 (Biacore International AB).	gene_phenotype
70695	3	334138	7	NULL	NULL	0	NULL	Spd1p	GP		interacts with					 Rnr1p	GP	budding yeast			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_56	16317005	The interaction between Spd1p and Cdc22p, Suc22p, budding yeast Rnr1p, Sml1p, and mouse R1 protein was studied by biosensor analysis using a BIAcore 2000 (Biacore International AB).	gene_phenotype
70696	4	334138	7	NULL	NULL	0	NULL	Spd1p	GP		interacts with					Sml1p	GP	budding yeast			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_56	16317005	The interaction between Spd1p and Cdc22p, Suc22p, budding yeast Rnr1p, Sml1p, and mouse R1 protein was studied by biosensor analysis using a BIAcore 2000 (Biacore International AB).	gene_phenotype
70697	5	334138	7	NULL	NULL	0	NULL	Spd1p	GP		interacts with					R1 protein	GP	mouse			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_56	16317005	The interaction between Spd1p and Cdc22p, Suc22p, budding yeast Rnr1p, Sml1p, and mouse R1 protein was studied by biosensor analysis using a BIAcore 2000 (Biacore International AB).	gene_phenotype
70698	1	334139	7	NULL	NULL	NULL	NULL	Spd1p	GP		inhibit					Cdc22p plus Suc22p	GP	recombinant			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_87	16317005	Inhibition by Spd1p -- Recombinant Cdc22p plus Suc22p was assayed for activity using the CDP reduction assay, with ATP as a positive effector in the presence of increasing amounts of Spd1 protein ( Fig. 2).	gene_phenotype
70700	1	334140	7	NULL	NULL	0	NULL	Spd1 protein	GP		inhibit		very little			Rnr1p plus Suc22p	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1778_s_91	16317005	Assaying recombinant budding yeast Rnr1p plus Suc22p for activity using the CDP reduction assay in the presence of increasing amounts of Spd1 protein showed very little inhibition compared with the results with Cdc22p and Suc22p ( Fig. 2).	gene_phenotype
70701	1	334141	7	NULL	NULL	0	NULL	DSC1	GP		control					cdc22+ genes	GP				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5745_s_278	12411492	There is precedence in fission yeast for groups of genes being regulated by a similar transcription factor complex in both mitosis and meiosis: DSC1 and MCB sequences control  cdc22+ and the  rec+ genes during the two life cycles (L.Cunliffe, S.White and C.J.McInerny, unpublished data).	gene_phenotype
70702	2	334141	7	NULL	NULL	0	NULL	DSC1	GP		control					 rec+ genes	GP				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5745_s_278	12411492	There is precedence in fission yeast for groups of genes being regulated by a similar transcription factor complex in both mitosis and meiosis: DSC1 and MCB sequences control  cdc22+ and the  rec+ genes during the two life cycles (L.Cunliffe, S.White and C.J.McInerny, unpublished data).	gene_phenotype
70703	3	334141	7	NULL	NULL	NULL	NULL				control				MCB sequences	cdc22+ genes	GP				NULL		NULL	NULL	NULL	NULL	gw60_embo_21_21_5745_s_278	12411492	There is precedence in fission yeast for groups of genes being regulated by a similar transcription factor complex in both mitosis and meiosis: DSC1 and MCB sequences control  cdc22+ and the  rec+ genes during the two life cycles (L.Cunliffe, S.White and C.J.McInerny, unpublished data).	gene_phenotype
70704	4	334141	7	NULL	NULL	0	NULL				control				MCB sequences	rec+ genes	GP				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5745_s_278	12411492	There is precedence in fission yeast for groups of genes being regulated by a similar transcription factor complex in both mitosis and meiosis: DSC1 and MCB sequences control  cdc22+ and the  rec+ genes during the two life cycles (L.Cunliffe, S.White and C.J.McInerny, unpublished data).	gene_phenotype
70705	5	334141	7	NULL	NULL	0	NULL	statement 3	Process		occur during					lifecycle	Process				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5745_s_278	12411492	There is precedence in fission yeast for groups of genes being regulated by a similar transcription factor complex in both mitosis and meiosis: DSC1 and MCB sequences control  cdc22+ and the  rec+ genes during the two life cycles (L.Cunliffe, S.White and C.J.McInerny, unpublished data).	gene_phenotype
70706	6	334141	7	NULL	NULL	0	NULL	statement 4	Process		occur during					lifecycle	Process				NULL		0	NULL	NULL	NULL	gw60_embo_21_21_5745_s_278	12411492	There is precedence in fission yeast for groups of genes being regulated by a similar transcription factor complex in both mitosis and meiosis: DSC1 and MCB sequences control  cdc22+ and the  rec+ genes during the two life cycles (L.Cunliffe, S.White and C.J.McInerny, unpublished data).	gene_phenotype
70707	1	334143	7	NULL	NULL	0	NULL	YML083c	GP		shows					higher transcript levels 	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_5_439_s_57	12673627	YML083c and  DAN1 exhibited 29- and 40-fold higher transcript levels during anaerobic growth respectively  (Ter Linde  et al., [ 1999]).	gene_phenotype
70708	2	334143	7	NULL	NULL	0	NULL	DAN1 	GP		shows					higher transcript levels 	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_5_439_s_57	12673627	YML083c and  DAN1 exhibited 29- and 40-fold higher transcript levels during anaerobic growth respectively  (Ter Linde  et al., [ 1999]).	gene_phenotype
70709	3	334143	7	NULL	NULL	0	NULL	statement 1	Process		during					anaerobic growth	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_5_439_s_57	12673627	YML083c and  DAN1 exhibited 29- and 40-fold higher transcript levels during anaerobic growth respectively  (Ter Linde  et al., [ 1999]).	gene_phenotype
70710	4	334143	7	NULL	NULL	0	NULL	statement 2	Process		during					anaerobic growth	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_5_439_s_57	12673627	YML083c and  DAN1 exhibited 29- and 40-fold higher transcript levels during anaerobic growth respectively  (Ter Linde  et al., [ 1999]).	gene_phenotype
70711	1	334144	7	NULL	NULL	0	NULL	YML083c protein	GP		plays					sterols	Chemical	non-essential role in transport of			NULL		0	NULL	NULL	NULL	gw70_yeast_20_5_439_s_421	12673627	It is possible that the YML083c protein plays a non-essential role in the transport  of sterols, as suggested by the fact that regulation by Upc2 affects control of this  process (Crowley  et al., [ 1998]).	gene_phenotype
70712	2	334144	7	NULL	NULL	0	NULL	Upc2	GP	regulation by	controls					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_5_439_s_421	12673627	It is possible that the YML083c protein plays a non-essential role in the transport  of sterols, as suggested by the fact that regulation by Upc2 affects control of this  process (Crowley  et al., [ 1998]).	gene_phenotype
70713	3	334144	7	NULL	NULL	0	NULL	statement 2	Process		suggests					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_5_439_s_421	12673627	It is possible that the YML083c protein plays a non-essential role in the transport  of sterols, as suggested by the fact that regulation by Upc2 affects control of this  process (Crowley  et al., [ 1998]).	gene_phenotype
70714	1	334145	7	NULL	NULL	0	NULL	YML083c	GP		is a type of					ORFs	GP	Saccharomyces cerevisiae			NULL		0	NULL	NULL	NULL	gw70_yeast_20_5_439_s_2	12673627	YML083c and  DAN1 were among the  Saccharomyces cerevisiae ORFs that displayed the strongest increase in transcript abundance during anaerobic  growth compared to aerobic growth, as determined by oligonucleotide microarrays.	gene_phenotype
70715	2	334145	7	NULL	NULL	0	NULL	DAN1	GP		is a type of					ORFs	GP	Saccharomyces cerevisiae			NULL		0	NULL	NULL	NULL	gw70_yeast_20_5_439_s_2	12673627	YML083c and  DAN1 were among the  Saccharomyces cerevisiae ORFs that displayed the strongest increase in transcript abundance during anaerobic  growth compared to aerobic growth, as determined by oligonucleotide microarrays.	gene_phenotype
70716	3	334145	7	NULL	NULL	NULL	NULL	statement 1	Process		displays					transcript	NucleicAcid	 increase in abundance of			NULL		NULL	NULL	NULL	NULL	gw70_yeast_20_5_439_s_2	12673627	YML083c and  DAN1 were among the  Saccharomyces cerevisiae ORFs that displayed the strongest increase in transcript abundance during anaerobic  growth compared to aerobic growth, as determined by oligonucleotide microarrays.	gene_phenotype
70717	4	334145	7	NULL	NULL	NULL	NULL	statement 2	Process		displays					transcript	NucleicAcid	increase in abundance of			NULL		NULL	NULL	NULL	NULL	gw70_yeast_20_5_439_s_2	12673627	YML083c and  DAN1 were among the  Saccharomyces cerevisiae ORFs that displayed the strongest increase in transcript abundance during anaerobic  growth compared to aerobic growth, as determined by oligonucleotide microarrays.	gene_phenotype
70718	5	334145	7	NULL	NULL	0	NULL	statement 3	Process		occur during					aerobic growth	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_5_439_s_2	12673627	YML083c and  DAN1 were among the  Saccharomyces cerevisiae ORFs that displayed the strongest increase in transcript abundance during anaerobic  growth compared to aerobic growth, as determined by oligonucleotide microarrays.	gene_phenotype
70719	6	334145	7	NULL	NULL	0	NULL	statement 3	Process		occur during					anaerobic growth	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_5_439_s_2	12673627	YML083c and  DAN1 were among the  Saccharomyces cerevisiae ORFs that displayed the strongest increase in transcript abundance during anaerobic  growth compared to aerobic growth, as determined by oligonucleotide microarrays.	gene_phenotype
70720	7	334145	7	NULL	NULL	0	NULL	statement 4	Process		occur during					aerobic growth	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_5_439_s_2	12673627	YML083c and  DAN1 were among the  Saccharomyces cerevisiae ORFs that displayed the strongest increase in transcript abundance during anaerobic  growth compared to aerobic growth, as determined by oligonucleotide microarrays.	gene_phenotype
70721	8	334145	7	NULL	NULL	0	NULL	statement 4	Process		occur during					anaerobic growth	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_5_439_s_2	12673627	YML083c and  DAN1 were among the  Saccharomyces cerevisiae ORFs that displayed the strongest increase in transcript abundance during anaerobic  growth compared to aerobic growth, as determined by oligonucleotide microarrays.	gene_phenotype
70722	9	334145	7	NULL	NULL	0	NULL	statement 6	Process		is stronger than					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_5_439_s_2	12673627	YML083c and  DAN1 were among the  Saccharomyces cerevisiae ORFs that displayed the strongest increase in transcript abundance during anaerobic  growth compared to aerobic growth, as determined by oligonucleotide microarrays.	gene_phenotype
70723	10	334145	7	NULL	NULL	0	NULL	statement 8	Process		is stronger than					statement 7	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_20_5_439_s_2	12673627	YML083c and  DAN1 were among the  Saccharomyces cerevisiae ORFs that displayed the strongest increase in transcript abundance during anaerobic  growth compared to aerobic growth, as determined by oligonucleotide microarrays.	gene_phenotype
70724	1	334146	7	NULL	NULL	0	NULL	mRNA 	NucleicAcid		shows					anaerobic growth	Process	higher level during			NULL		0	NULL	NULL	NULL	gw70_yeast_20_5_439_s_200	12673627	The behaviour of the full-length YML083c promoter- lacZ fusion borne on a single-copy plasmid was consistent with the microarray data, which  indicated a much higher mRNA level during anaerobic growth.	gene_phenotype
70725	2	334146	7	NULL	NULL	NULL	NULL	YML083c	GP	behaviour of;;full-length	indicates				promoter	statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_yeast_20_5_439_s_200	12673627	The behaviour of the full-length YML083c promoter- lacZ fusion borne on a single-copy plasmid was consistent with the microarray data, which  indicated a much higher mRNA level during anaerobic growth.	gene_phenotype
70726	1	334147	7	NULL	NULL	0	NULL	Mpr1p	GP	purified;;recombinant E. coli cells	acetylates					AZC	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_41998_s_166	11555637	AZC Acetylation by Mpr1p-- The His-tagged fusion Mpr1p was purified from the recombinant  E. coli cells expressing the  MPR1 gene as described under	gene_phenotype
70727	1	334148	7	NULL	NULL	NULL	NULL	Sporulation	Process		generates					mpr1::his7+ spc1::ura4+	Chromosome	viable  haploid segregants of			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_66	10749922	Sporulation and tetrad dissection generated viable haploid segregants of  mpr1::his7+ spc1::ura4+ and  mpr1::his7+ spc1+, which indicated that  mpr1+ is not essential for cellular viability.	gene_phenotype
70728	2	334148	7	NULL	NULL	NULL	NULL	tetrad dissection	Process		generates					mpr1::his7+ spc1+	Chromosome	viable haploid segregants of			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_66	10749922	Sporulation and tetrad dissection generated viable haploid segregants of  mpr1::his7+ spc1::ura4+ and  mpr1::his7+ spc1+, which indicated that  mpr1+ is not essential for cellular viability.	gene_phenotype
70729	3	334148	7	NULL	NULL	0	NULL	mpr1+	GP		is not essential for					cellular viability	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_66	10749922	Sporulation and tetrad dissection generated viable haploid segregants of  mpr1::his7+ spc1::ura4+ and  mpr1::his7+ spc1+, which indicated that  mpr1+ is not essential for cellular viability.	gene_phenotype
70730	1	334150	7	NULL	NULL	NULL	NULL				is essential for			 conserved phosphorylation site His-221		Mpr1 function	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_48	10749922	In addition, the conserved phosphorylation site, His-221, is essential for Mpr1 function, and Mpr1 binds to the Mcs4 response regulator in response to oxidative stress.	gene_phenotype
70731	2	334150	7	NULL	NULL	0	NULL	Mpr1	GP		bind					Mcs4 response regulator	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_48	10749922	In addition, the conserved phosphorylation site, His-221, is essential for Mpr1 function, and Mpr1 binds to the Mcs4 response regulator in response to oxidative stress.	gene_phenotype
70732	3	334150	7	NULL	NULL	0	NULL	statement 2	Process		in response to					oxidative stress	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_48	10749922	In addition, the conserved phosphorylation site, His-221, is essential for Mpr1 function, and Mpr1 binds to the Mcs4 response regulator in response to oxidative stress.	gene_phenotype
70733	1	334151	7	NULL	NULL	0	NULL	Mpr1 	GP		is homologous to					Ypd1	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_94	10749922	Mpr1 Is Homologous to Ypd1, a Response Regulator Phosphotransferase in Budding Yeast	gene_phenotype
70734	2	334151	7	NULL	NULL	0	NULL	Ypd1	GP		is a type of					Response Regulator Phosphotransferase					NULL	budding yeast	0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_94	10749922	Mpr1 Is Homologous to Ypd1, a Response Regulator Phosphotransferase in Budding Yeast	gene_phenotype
70735	1	334152	7	NULL	NULL	0	NULL	Mpr1	GP		is crucial for			Putative Histidine Phosphorylation Site		Oxidative Stress Signaling	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_136	10749922	The Putative Histidine Phosphorylation Site of Mpr1 Is Crucial for Oxidative Stress Signaling	gene_phenotype
70736	1	334153	7	NULL	NULL	0	NULL	Mpr1	GP	fission yeast	is homologous to					Ypd1 response regulator phosphotransferase	GP	budding yeast			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_20_17722_s_17	11886858	Fission yeast Mpr1 is homologous to the Ypd1 response regulator phosphotransferase in budding yeast.	gene_phenotype
70737	1	334154	7	NULL	NULL	0	NULL	Mpr1 	GP		combines with					l-proline	AminoAcid				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_j-biochem-(tokyo)_138_4_16272133_s_5	16272133	The combination of  Mpr1 and l-proline could further enhance the resistance to freezing stress.	gene_phenotype
70738	2	334154	7	NULL	NULL	0	NULL	statement 1	Process		enhance					freezing stress	Process	resistance to			NULL		0	NULL	NULL	NULL	abs-batch0540-0549_j-biochem-(tokyo)_138_4_16272133_s_5	16272133	The combination of  Mpr1 and l-proline could further enhance the resistance to freezing stress.	gene_phenotype
70740	1	334156	7	NULL	NULL	NULL	NULL	Mpr1	GP		is conserved between			His-221 phosphorylation site		 Ypd1	GP		His-221 phosphorylation site		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_137	10749922	Sequence conservation of the histidine phosphorylation site between Mpr1 and Ypd1 (Figure  1A) prompted us to test whether phosphorylation of His-221 in Mpr1 is required for oxidative stress signaling.	gene_phenotype
70741	1	334157	7	NULL	NULL	0	NULL	MPR1	GP	overexpression of	leads to					cell viability	Process	increase in			NULL		0	NULL	NULL	NULL	gw70_pnas_101_34_12616_s_5	15308773	In contrast, overexpression of  MPR1 leads to an increase in cell viability and a decrease in ROS level after oxidative treatments.	gene_phenotype
70742	2	334157	7	NULL	NULL	0	NULL	MPR1	GP	overexpression of	decrease					ROS level	Chemical				NULL		0	NULL	NULL	NULL	gw70_pnas_101_34_12616_s_5	15308773	In contrast, overexpression of  MPR1 leads to an increase in cell viability and a decrease in ROS level after oxidative treatments.	gene_phenotype
70743	3	334157	7	NULL	NULL	0	NULL	statement 1	Process		occur after					oxidative treatment	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_34_12616_s_5	15308773	In contrast, overexpression of  MPR1 leads to an increase in cell viability and a decrease in ROS level after oxidative treatments.	gene_phenotype
70744	4	334157	7	NULL	NULL	0	NULL	statement 2	Process		occur after					oxidative treatment	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_34_12616_s_5	15308773	In contrast, overexpression of  MPR1 leads to an increase in cell viability and a decrease in ROS level after oxidative treatments.	gene_phenotype
70745	1	334158	7	NULL	NULL	0	NULL	 MPR genes	GP	null mutant	displays					hypersensitivity	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_34_12616_s_254	15308773	In summary, the null mutant of the  MPR genes displayed hypersensitivity to oxidative stress, and the expression of the  MPR1 gene conferred stress resistance.	gene_phenotype
70746	2	334158	7	NULL	NULL	0	NULL	statement 1	Process		in response to					oxidative stress	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_34_12616_s_254	15308773	In summary, the null mutant of the  MPR genes displayed hypersensitivity to oxidative stress, and the expression of the  MPR1 gene conferred stress resistance.	gene_phenotype
70747	3	334158	7	NULL	NULL	0	NULL	MPR1 gene 	GP	expression of	confers					stress	Process	resistance to			NULL		0	NULL	NULL	NULL	gw70_pnas_101_34_12616_s_254	15308773	In summary, the null mutant of the  MPR genes displayed hypersensitivity to oxidative stress, and the expression of the  MPR1 gene conferred stress resistance.	gene_phenotype
70748	1	334159	7	NULL	NULL	0	NULL	mpr1+ gene	GP	fission yeast	encode					novel protein	GP		histidine-containing phosphotransfer domain 		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_4	10749922	The fission yeast  mpr1+ gene encodes a novel protein with a histidine-containing phosphotransfer domain homologous to the budding yeast Ypd1.	gene_phenotype
70749	2	334159	7	NULL	NULL	0	NULL	novel protein	GP		is homologous to			histidine-containing phosphotransfer domain 		Ypd1	GP	budding yeast			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_4	10749922	The fission yeast  mpr1+ gene encodes a novel protein with a histidine-containing phosphotransfer domain homologous to the budding yeast Ypd1.	gene_phenotype
70750	1	334160	7	NULL	NULL	0	NULL	Mpr1	GP	fission yeast	homologous to		highly			Ypd1 response regulator phosphotransferase	GP	budding yeast			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_46	10749922	In this report, we have characterized the fission yeast Mpr1, which is highly homologous to the Ypd1 response regulator phosphotransferase in budding yeast.	gene_phenotype
70751	1	334161	7	NULL	NULL	0	NULL	Mpr1 	GP	fission yeast	is homologous to					Ypd1 protein	GP	budding yeast			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_103	10749922	Mpr1 is a fission yeast homologue of the budding yeast Ypd1 protein, a response regulator phosphotransferase.	gene_phenotype
70752	2	334161	7	NULL	NULL	0	NULL	Ypd1 protein	GP		is a type of					response regulator phosphotransferase	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_103	10749922	Mpr1 is a fission yeast homologue of the budding yeast Ypd1 protein, a response regulator phosphotransferase.	gene_phenotype
70754	1	334162	7	NULL	NULL	NULL	NULL	Mpr1	GP		is required for			putative phosphorylation site His-221		oxidative stress signaling 	Process	function in			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_143	10749922	These results indicate that the putative phosphorylation site, His-221, is required for the Mpr1 function in oxidative stress signaling to Spc1.	gene_phenotype
70766	1	334165	7	NULL	NULL	0	NULL	AZC resistance strain	Organism		produce					Mpr1 proteins	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_41998_s_143	11555637	AZC resistance and acetylation activity in the strains producing the various Mpr1 proteins correlated with each other.	gene_phenotype
70767	2	334165	7	NULL	NULL	0	NULL	acetylation activity in the strains	Process		produce					Mpr1 proteins	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_45_41998_s_143	11555637	AZC resistance and acetylation activity in the strains producing the various Mpr1 proteins correlated with each other.	gene_phenotype
70771	1	334166	7	NULL	NULL	0	NULL	ASA	Chemical		converted to					 L-azetidine-2-carboxylic acid	Chemical				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_3_5_1287_s_229	15470257	A plasmid expressing  MPR1 did not rescue viability of  fpr1delta hom6delta double mutants, suggesting that ASA conversion into L-azetidine-2-carboxylic acid is not the basis for ASA toxicity.	gene_phenotype
70772	2	334166	7	NULL	NULL	0	NULL	statement 1	Process		is not the basis for					ASA toxicity	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_3_5_1287_s_229	15470257	A plasmid expressing  MPR1 did not rescue viability of  fpr1delta hom6delta double mutants, suggesting that ASA conversion into L-azetidine-2-carboxylic acid is not the basis for ASA toxicity.	gene_phenotype
70926	1	334167	7	NULL	NULL	NULL	NULL	 CKY8	Organism		carries					MPR1	GP				NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_34_12616_s_121	15308773	In contrast, overexpression of  MPR1 in strain CKY8 showed a 3-fold higher cell viability compared with that of strain CKY8 carrying only the vector against heat shock.	gene_phenotype
70928	2	334167	7	NULL	NULL	0	NULL	CKY8	Organism		carries					heat shock	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_34_12616_s_121	15308773	In contrast, overexpression of  MPR1 in strain CKY8 showed a 3-fold higher cell viability compared with that of strain CKY8 carrying only the vector against heat shock.	gene_phenotype
70931	3	334167	7	NULL	NULL	0	NULL	statement 1	Process	cell viability of	is higher  than					statement 2	Process	cell viability of			NULL		0	NULL	NULL	NULL	gw70_pnas_101_34_12616_s_121	15308773	In contrast, overexpression of  MPR1 in strain CKY8 showed a 3-fold higher cell viability compared with that of strain CKY8 carrying only the vector against heat shock.	gene_phenotype
70932	1	334168	7	NULL	NULL	0	NULL	Saccharomyces cerevisiae	Organism	budding yeast	encode					uncharacterized N-acetyltransferase	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_34_12616_s_2	15308773	he  MPR1 gene, which is found in the sigma1278b strain but is not present in the sequenced laboratory strain S288C, of the budding yeast  Saccharomyces cerevisiae encodes a previously uncharacterized  N-acetyltransferase that detoxifies the proline analogue azetidine-2-carboxylate (AZC).	gene_phenotype
70933	2	334168	7	NULL	NULL	0	NULL	statement 1	GP		detoxifies					AZC	Chemical				NULL		0	NULL	NULL	NULL	gw70_pnas_101_34_12616_s_2	15308773	he  MPR1 gene, which is found in the sigma1278b strain but is not present in the sequenced laboratory strain S288C, of the budding yeast  Saccharomyces cerevisiae encodes a previously uncharacterized  N-acetyltransferase that detoxifies the proline analogue azetidine-2-carboxylate (AZC).	gene_phenotype
70934	3	334168	7	NULL	NULL	0	NULL	AZC	Chemical		is					azetidine-2-carboxylate	Chemical				NULL		0	NULL	NULL	NULL	gw70_pnas_101_34_12616_s_2	15308773	he  MPR1 gene, which is found in the sigma1278b strain but is not present in the sequenced laboratory strain S288C, of the budding yeast  Saccharomyces cerevisiae encodes a previously uncharacterized  N-acetyltransferase that detoxifies the proline analogue azetidine-2-carboxylate (AZC).	gene_phenotype
70935	4	334168	7	NULL	NULL	0	NULL	AZC	Chemical		is a type of					proline analogue	Chemical				NULL		0	NULL	NULL	NULL	gw70_pnas_101_34_12616_s_2	15308773	he  MPR1 gene, which is found in the sigma1278b strain but is not present in the sequenced laboratory strain S288C, of the budding yeast  Saccharomyces cerevisiae encodes a previously uncharacterized  N-acetyltransferase that detoxifies the proline analogue azetidine-2-carboxylate (AZC).	gene_phenotype
70936	1	334169	7	NULL	NULL	0	NULL	mpr1+	GP		is not essential for					viability	Process				NULL	spc1+ background	0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_118	10749922	All of the dissected tetrads gave rise to four viable spores with 2:2 segregation of His+ and His  phenotypes regardless of the uracil auxotrophy, indicating that  mpr1+ is not essential for viability in both  spc1+ and  spc1  backgrounds.	gene_phenotype
70937	2	334169	7	NULL	NULL	NULL	NULL	mpr1+	GP		is not essential for					viability	Process				NULL	spc1 background	NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_118	10749922	All of the dissected tetrads gave rise to four viable spores with 2:2 segregation of His+ and His  phenotypes regardless of the uracil auxotrophy, indicating that  mpr1+ is not essential for viability in both  spc1+ and  spc1  backgrounds.	gene_phenotype
70938	1	334170	7	NULL	NULL	NULL	NULL	oxidative stress signaling 	Process		in response to					Spc1 SAPK cascade	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_129	10749922	These results implicate Mpr1 in oxidative stress signaling to the Spc1 SAPK cascade, which contrasts with the function of Ypd1 in osmostress signaling of budding yeast (Posas  et al., 1996  ).	gene_phenotype
70939	2	334170	7	NULL	NULL	0	NULL	Ypd1	GP	function of	in response to					osmostress signaling	Process	budding yeast			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_129	10749922	These results implicate Mpr1 in oxidative stress signaling to the Spc1 SAPK cascade, which contrasts with the function of Ypd1 in osmostress signaling of budding yeast (Posas  et al., 1996  ).	gene_phenotype
70940	4	334170	7	NULL	NULL	NULL	NULL	statement 3	Process		in contrast to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_129	10749922	These results implicate Mpr1 in oxidative stress signaling to the Spc1 SAPK cascade, which contrasts with the function of Ypd1 in osmostress signaling of budding yeast (Posas  et al., 1996  ).	gene_phenotype
70941	3	334170	7	NULL	NULL	0	NULL	 Mpr1	GP		implicated in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_129	10749922	These results implicate Mpr1 in oxidative stress signaling to the Spc1 SAPK cascade, which contrasts with the function of Ypd1 in osmostress signaling of budding yeast (Posas  et al., 1996  ).	gene_phenotype
70942	1	334171	7	NULL	NULL	0	NULL	Mpr1	GP		is most homologous to					Ypd1 protein	GP	budding yeast			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_273	10749922	Mpr1 is most homologous to the budding yeast Ypd1 protein, which transfers a phosphoryl group from the receiver domain of Sln1 to the Ssk1 response regulator in osmostress signaling to the Hog1 MAPK cascade.	gene_phenotype
70943	2	334171	7	NULL	NULL	0	NULL	Sln1	GP		transferred to			phosphoryl group from the receiver domain		Ssk1 response regulator	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_273	10749922	Mpr1 is most homologous to the budding yeast Ypd1 protein, which transfers a phosphoryl group from the receiver domain of Sln1 to the Ssk1 response regulator in osmostress signaling to the Hog1 MAPK cascade.	gene_phenotype
70944	3	334171	7	NULL	NULL	0	NULL	statement 2	Process		occur in					Hog1 MAPK cascade	Process	osmostress signaling to 			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_273	10749922	Mpr1 is most homologous to the budding yeast Ypd1 protein, which transfers a phosphoryl group from the receiver domain of Sln1 to the Ssk1 response regulator in osmostress signaling to the Hog1 MAPK cascade.	gene_phenotype
70945	4	334171	7	NULL	NULL	0	NULL	Ypd1 protein	GP		carries out					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_273	10749922	Mpr1 is most homologous to the budding yeast Ypd1 protein, which transfers a phosphoryl group from the receiver domain of Sln1 to the Ssk1 response regulator in osmostress signaling to the Hog1 MAPK cascade.	gene_phenotype
70946	1	334172	7	NULL	NULL	0	NULL	Mpr1-Mcs4 pathway	Process		is highly					conserved	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_278	10749922	Considering the highly conserved architecture of the Mpr1-Mcs4 pathway and the budding yeast Ypd1-Ssk1 pathway, it is surprising that Mpr1 and Mcs4 are involved in transmitting oxidative stress rather than osmostress signals to a SAPK cascade.	gene_phenotype
70947	2	334172	7	NULL	NULL	NULL	NULL	Ypd1-Ssk1 pathway	Process		is highly					conserved	Process				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_278	10749922	Considering the highly conserved architecture of the Mpr1-Mcs4 pathway and the budding yeast Ypd1-Ssk1 pathway, it is surprising that Mpr1 and Mcs4 are involved in transmitting oxidative stress rather than osmostress signals to a SAPK cascade.	gene_phenotype
70948	3	334172	7	NULL	NULL	0	NULL	Mpr1	GP		is involved in					oxidative stress	Process	transmitting 			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_278	10749922	Considering the highly conserved architecture of the Mpr1-Mcs4 pathway and the budding yeast Ypd1-Ssk1 pathway, it is surprising that Mpr1 and Mcs4 are involved in transmitting oxidative stress rather than osmostress signals to a SAPK cascade.	gene_phenotype
70949	4	334172	7	NULL	NULL	0	NULL	Mcs4	GP		is involved in					oxidative stress	Process	transmitting 			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_278	10749922	Considering the highly conserved architecture of the Mpr1-Mcs4 pathway and the budding yeast Ypd1-Ssk1 pathway, it is surprising that Mpr1 and Mcs4 are involved in transmitting oxidative stress rather than osmostress signals to a SAPK cascade.	gene_phenotype
70950	5	334172	7	NULL	NULL	0	NULL	Mpr1	GP		is not involved in					 osmostress signals 	Process	transmitting 			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_278	10749922	Considering the highly conserved architecture of the Mpr1-Mcs4 pathway and the budding yeast Ypd1-Ssk1 pathway, it is surprising that Mpr1 and Mcs4 are involved in transmitting oxidative stress rather than osmostress signals to a SAPK cascade.	gene_phenotype
70951	6	334172	7	NULL	NULL	0	NULL	Mcs4	GP		is not involved in					osmostress signaling	Process	transmitting 			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_278	10749922	Considering the highly conserved architecture of the Mpr1-Mcs4 pathway and the budding yeast Ypd1-Ssk1 pathway, it is surprising that Mpr1 and Mcs4 are involved in transmitting oxidative stress rather than osmostress signals to a SAPK cascade.	gene_phenotype
70952	7	334172	7	NULL	NULL	0	NULL	osmostress signals	Process		in response to					SAPK cascade	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_278	10749922	Considering the highly conserved architecture of the Mpr1-Mcs4 pathway and the budding yeast Ypd1-Ssk1 pathway, it is surprising that Mpr1 and Mcs4 are involved in transmitting oxidative stress rather than osmostress signals to a SAPK cascade.	gene_phenotype
70953	1	334173	7	NULL	NULL	0	NULL	MPR1 gene	GP	expression of;;strain FH506	confers					AZC resistance	Process	S. cerevisiae strain			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_15_4249_s_206	10894734	Expression of the  MPR1 and  MPR2 genes isolated from strain FH506 conferred AZC resistance to other  S. cerevisiae strains but did not cause increases in proline content and cell viability after freezing of the host cells (data not shown).	gene_phenotype
70954	2	334173	7	NULL	NULL	0	NULL	MPR2 gene	GP	expression of;;strain FH506	confers					AZC resistance	Process	S. cerevisiae strain			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_15_4249_s_206	10894734	Expression of the  MPR1 and  MPR2 genes isolated from strain FH506 conferred AZC resistance to other  S. cerevisiae strains but did not cause increases in proline content and cell viability after freezing of the host cells (data not shown).	gene_phenotype
70955	3	334173	7	NULL	NULL	NULL	NULL	MPR1 gene	GP	expression of;;strain FH506	does not increase					proline content	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_15_4249_s_206	10894734	Expression of the  MPR1 and  MPR2 genes isolated from strain FH506 conferred AZC resistance to other  S. cerevisiae strains but did not cause increases in proline content and cell viability after freezing of the host cells (data not shown).	gene_phenotype
70956	4	334173	7	NULL	NULL	0	NULL	MPR2 gene	GP	expression of;;strain FH506	does not increase					proline content	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_15_4249_s_206	10894734	Expression of the  MPR1 and  MPR2 genes isolated from strain FH506 conferred AZC resistance to other  S. cerevisiae strains but did not cause increases in proline content and cell viability after freezing of the host cells (data not shown).	gene_phenotype
70957	5	334173	7	NULL	NULL	0	NULL	MPR1 gene	GP	expression of;;strain FH506	does not increase					cell viability	Process				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_15_4249_s_206	10894734	Expression of the  MPR1 and  MPR2 genes isolated from strain FH506 conferred AZC resistance to other  S. cerevisiae strains but did not cause increases in proline content and cell viability after freezing of the host cells (data not shown).	gene_phenotype
70958	6	334173	7	NULL	NULL	0	NULL	MPR2 gene	GP	expression of;;strain FH506	does not increase					cell viability	Process				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_15_4249_s_206	10894734	Expression of the  MPR1 and  MPR2 genes isolated from strain FH506 conferred AZC resistance to other  S. cerevisiae strains but did not cause increases in proline content and cell viability after freezing of the host cells (data not shown).	gene_phenotype
70959	1	334176	7	NULL	NULL	0	NULL	oxidative stress	Process		activates					Spc1	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_5	10749922	Spc1 activation upon oxidative stress is severely impaired in the  deltampr1 mutant as well as in the  mpr1HQ strain, in which the putative phosphorylation site Mpr1-His221 is substituted with glutamine.	gene_phenotype
70960	2	334176	7	NULL	NULL	NULL	NULL	statement 1	Process		is  impaired in		severely			deltampr1	GP	mutant			NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_5	10749922	Spc1 activation upon oxidative stress is severely impaired in the  deltampr1 mutant as well as in the  mpr1HQ strain, in which the putative phosphorylation site Mpr1-His221 is substituted with glutamine.	gene_phenotype
70961	3	334176	7	NULL	NULL	NULL	NULL	statement 1	Process		is impaired in		severely			mpr1HQ strain	Organism				NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_5	10749922	Spc1 activation upon oxidative stress is severely impaired in the  deltampr1 mutant as well as in the  mpr1HQ strain, in which the putative phosphorylation site Mpr1-His221 is substituted with glutamine.	gene_phenotype
70962	4	334176	7	NULL	NULL	0	NULL	mpr1HQ strain	Organism		is substituted with			putative phosphorylation site Mpr1-His221		mpr1HQ strain	Organism		putative phosphorylation site Mpr1-Gln221		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_11_4_1169_s_5	10749922	Spc1 activation upon oxidative stress is severely impaired in the  deltampr1 mutant as well as in the  mpr1HQ strain, in which the putative phosphorylation site Mpr1-His221 is substituted with glutamine.	gene_phenotype
70963	1	334178	7	NULL	NULL	0	NULL	RPN11	GP		complements					mpr1-1 	GP	temperature-sensitive growth of			NULL		0	NULL	NULL	NULL	gw60_science_298_5593_611_s_81	12183636	Plasmid-borne  RPN11 but not  rpn11AXA complemented the temperature-sensitive growth of  mpr1-1 ( Fig. 2C).	gene_phenotype
70964	2	334178	7	NULL	NULL	0	NULL	rpn11AXA	GP		does not complement					mpr1-1 	GP	temperature-sensitive growth of			NULL		0	NULL	NULL	NULL	gw60_science_298_5593_611_s_81	12183636	Plasmid-borne  RPN11 but not  rpn11AXA complemented the temperature-sensitive growth of  mpr1-1 ( Fig. 2C).	gene_phenotype
70965	1	334179	7	NULL	NULL	0	NULL	ry 	GP	mutation of	restores					mpr1-1	GP	defect of;;mutant			NULL		0	NULL	NULL	NULL	gw60_gene_286_1_43_s_138	11943459	The  ry mutation which restores a defect of the  mpr1-1 mutant indicates the existence of an additional factor interacting with Rpn11 and involved in the maintenance of the mitochondrial morphology.	gene_phenotype
70966	1	334180	7	NULL	NULL	0	NULL	mpr1-1	GP	effects of mutation on	is restored in					 Wm-ru-ry	GP	triple mutant			NULL		0	NULL	NULL	NULL	gw60_gene_286_1_43_s_136	11943459	The effects of  mpr1-1 mutation on mitochondrial morphology are only restored in the Wm-ru-ry triple mutant which was isolated from Wm-ru as a spontaneous revertant which grows on non-fermentable carbon source at 36 degrees C.	gene_phenotype
70967	1	334181	7	NULL	NULL	0	NULL	mpr1-1 cells	Cell		displays					aberrant morphology	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_10_2917_s_170	9763452	In this condition,  mpr1-1 cells exhibited an aberrant morphology characterized by elongated daughter cells unable to perform a further division, whereas the nucleus was mislocalized and often only present in the first bud (Figure  4E).	gene_phenotype
70968	2	334181	7	NULL	NULL	0	NULL	aberrant morphology	Process		characterized by					elongated daughter cells	Cell				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_10_2917_s_170	9763452	In this condition,  mpr1-1 cells exhibited an aberrant morphology characterized by elongated daughter cells unable to perform a further division, whereas the nucleus was mislocalized and often only present in the first bud (Figure  4E).	gene_phenotype
70969	3	334181	7	NULL	NULL	0	NULL	elongated daughter cells	Cell		does not undergo					division	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_10_2917_s_170	9763452	In this condition,  mpr1-1 cells exhibited an aberrant morphology characterized by elongated daughter cells unable to perform a further division, whereas the nucleus was mislocalized and often only present in the first bud (Figure  4E).	gene_phenotype
70970	4	334181	7	NULL	NULL	0	NULL	elongated daughter cells	cell		shows					mislocalized nucleus	CellComponent				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_10_2917_s_170	9763452	In this condition,  mpr1-1 cells exhibited an aberrant morphology characterized by elongated daughter cells unable to perform a further division, whereas the nucleus was mislocalized and often only present in the first bud (Figure  4E).	gene_phenotype
70971	1	334182	7	NULL	NULL	0	NULL	 punctate mitochondrial morphology 	GP		is observed in					 mpr1-1	GP	mutant			NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_10_2917_s_276	9763452	The punctate mitochondrial morphology we observe in the  mpr1-1 mutant growing on rich medium containing glucose has also been observed in the  yme1 mutant altered in a mitochondrial protease.	gene_phenotype
70972	2	334182	7	NULL	NULL	0	NULL	yme1	GP	mutant	altered in					mitochondrial protease	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_10_2917_s_276	9763452	The punctate mitochondrial morphology we observe in the  mpr1-1 mutant growing on rich medium containing glucose has also been observed in the  yme1 mutant altered in a mitochondrial protease.	gene_phenotype
70973	3	334182	7	NULL	NULL	0	NULL	punctate mitochondrial morphology	Process		is observed in					statement 2	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_9_10_2917_s_276	9763452	The punctate mitochondrial morphology we observe in the  mpr1-1 mutant growing on rich medium containing glucose has also been observed in the  yme1 mutant altered in a mitochondrial protease.	gene_phenotype
70974	1	334183	7	NULL	NULL	0	NULL	mpr1-1	GP	mutant	reveals					mitosis	Process	defect in exit from			NULL		0	NULL	NULL	NULL	gw60_gene_286_1_43_s_81	11943459	Microscopic observation of the  mpr1-1 mutant strain after DAPI staining had previously revealed a defect in the exit from mitosis, with large buds during growth at 24 degrees C and aberrant bud morphology when cells were shifted at the non-permissive temperature.	gene_phenotype
70975	1	334184	7	NULL	NULL	NULL	NULL	DNA	NucleicAcid	increase in	is not restricted to					nuclear DNA	NucleicAcid	increase of			NULL	 [ rho+] mpr1-1 strain	NULL	NULL	NULL	NULL	gw60_molbiolcell_9_10_2917_s_199	9763452	In other words, the increase in DNA content per cell is not restricted to an increase of nuclear DNA but reaches higher values in the [ rho+]  mpr1-1 strain than in the [ rho degrees ] derivative, suggesting an important contribution of mitochondrial DNA to the aberrant flow cytometry profile.	gene_phenotype
70977	1	334185	7	NULL	NULL	NULL	NULL	mpr1-1	GP	frameshift in 	leads to			RPN11		temperature-sensitive growth	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_298_5593_611_s_80	12183636	To facilitate further phenotypic characterization of the  AXA mutant, we used  mpr1-1, which contains a frameshift in  RPN11 that leads to temperature-sensitive growth and expression of a prematurely terminated Rpn11mpr1-1 protein (285 versus 306 amino acids for wild type) ( 16).	gene_phenotype
70978	2	334185	7	NULL	NULL	0	NULL	mpr1-1	GP	frameshift in 	leads to			RPN11		Rpn11mpr1-1 protein	GP	expression of;;prematurely terminated 			NULL		0	NULL	NULL	NULL	gw60_science_298_5593_611_s_80	12183636	To facilitate further phenotypic characterization of the  AXA mutant, we used  mpr1-1, which contains a frameshift in  RPN11 that leads to temperature-sensitive growth and expression of a prematurely terminated Rpn11mpr1-1 protein (285 versus 306 amino acids for wild type) ( 16).	gene_phenotype
70979	1	334187	7	NULL	NULL	0	NULL	scR1 	GP	Nuclear export of	is mediated by					Xpo1p	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_8	11352936	Nuclear export of scR1 is mediated by the nuclear export signal receptor Xpo1p, is distinct from mRNA transport, and requires, as evidenced by the nucleolar accumulation of scR1 in a  dis3/rrp44 exosome component mutant, an intact scR1 3' end.	gene_phenotype
70980	2	334187	7	NULL	NULL	0	NULL	Xpo1p	GP		is a type of					nuclear export signal receptor	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_8	11352936	Nuclear export of scR1 is mediated by the nuclear export signal receptor Xpo1p, is distinct from mRNA transport, and requires, as evidenced by the nucleolar accumulation of scR1 in a  dis3/rrp44 exosome component mutant, an intact scR1 3' end.	gene_phenotype
70981	3	334187	7	NULL	NULL	0	NULL	statement 1	Process		is distinct from					mRNA 	NucleicAcid	transport of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_8	11352936	Nuclear export of scR1 is mediated by the nuclear export signal receptor Xpo1p, is distinct from mRNA transport, and requires, as evidenced by the nucleolar accumulation of scR1 in a  dis3/rrp44 exosome component mutant, an intact scR1 3' end.	gene_phenotype
70982	4	334187	7	NULL	NULL	0	NULL	statement 1	Process		requires					scR1	GP	nucleolar accumulation of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_8	11352936	Nuclear export of scR1 is mediated by the nuclear export signal receptor Xpo1p, is distinct from mRNA transport, and requires, as evidenced by the nucleolar accumulation of scR1 in a  dis3/rrp44 exosome component mutant, an intact scR1 3' end.	gene_phenotype
70983	5	334187	7	NULL	NULL	0	NULL	statement 4	Process		occur in a					dis3/rrp44 exosome component mutant	CellComponent				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_8	11352936	Nuclear export of scR1 is mediated by the nuclear export signal receptor Xpo1p, is distinct from mRNA transport, and requires, as evidenced by the nucleolar accumulation of scR1 in a  dis3/rrp44 exosome component mutant, an intact scR1 3' end.	gene_phenotype
70984	6	334187	7	NULL	NULL	0	NULL	statement 1	Process		requires					scR1	GP		intact 3' end		NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_8	11352936	Nuclear export of scR1 is mediated by the nuclear export signal receptor Xpo1p, is distinct from mRNA transport, and requires, as evidenced by the nucleolar accumulation of scR1 in a  dis3/rrp44 exosome component mutant, an intact scR1 3' end.	gene_phenotype
70985	1	334189	7	NULL	NULL	0	NULL	Ran cycle	Process	intact	is required for					scR1	GP	nuclear export of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_170	11352936	These data show that an intact Ran cycle is required for scR1 nuclear export.	gene_phenotype
70986	1	334190	7	NULL	NULL	NULL	NULL	exportin	GP		be involved in		might			scR1	GP	nuclear export of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_172	11352936	Alternatively, (an) exportin(s) might be involved in scR1 nuclear export.	gene_phenotype
70987	1	334191	7	NULL	NULL	0	NULL	scR1	GP		exported to					nucleus	CellComponent				NULL	LMB-sensitive strain	0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_201	11352936	Therefore, we analyzed nuclear export of scR1 in the LMB-sensitive strain.	gene_phenotype
70988	1	334192	7	NULL	NULL	0	NULL	Nucleoporins	CellComponent	subset of	is involved in					scR1	GP	nuclear export of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_266	11352936	A Subset of Nucleoporins Is Involved in scR1 Nuclear Export   The finding that Nsp1p is required for scR1 nuclear export prompted us to investigate the requirement of NPC components in this process.	gene_phenotype
70989	2	334192	7	NULL	NULL	0	NULL	Nsp1p	GP		is required for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_266	11352936	A Subset of Nucleoporins Is Involved in scR1 Nuclear Export   The finding that Nsp1p is required for scR1 nuclear export prompted us to investigate the requirement of NPC components in this process.	gene_phenotype
70990	1	334193	7	NULL	NULL	NULL	NULL	scR1	GP		is required for			intact 3' end		scR1	GP	nuclear export of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_328	11352936	The correlation between this 3' end shortening and nucleolar accumulation of scR1 in the  rrp44-1 mutant cells suggests that an intact 3' end is required for scR1 nuclear export.	gene_phenotype
70991	2	334193	7	NULL	NULL	0	NULL	scR1	GP		accumulates in					nucleolus	Cell				NULL	 rrp44-1 mutant cells	0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_328	11352936	The correlation between this 3' end shortening and nucleolar accumulation of scR1 in the  rrp44-1 mutant cells suggests that an intact 3' end is required for scR1 nuclear export.	gene_phenotype
70992	3	334193	7	NULL	NULL	0	NULL	statement 2	Process		suggests					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_328	11352936	The correlation between this 3' end shortening and nucleolar accumulation of scR1 in the  rrp44-1 mutant cells suggests that an intact 3' end is required for scR1 nuclear export.	gene_phenotype
70993	1	334194	7	NULL	NULL	NULL	NULL	flies 	Organism	heterozygous deletions	viable with					Scr1	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_161_2_733_s_115	12072469	We observed similar results with the hypomorphic mutation  Scr1, but because the viability of flies heterozygous for the deletions was much greater with  Scr1 than with  Scr4, we were able to examine more males.	gene_phenotype
70994	2	334194	7	NULL	NULL	NULL	NULL	flies	Organism	 heterozygous deletions	viable with					Scr4	GP				NULL		NULL	NULL	NULL	NULL	gw60_genetics_161_2_733_s_115	12072469	We observed similar results with the hypomorphic mutation  Scr1, but because the viability of flies heterozygous for the deletions was much greater with  Scr1 than with  Scr4, we were able to examine more males.	gene_phenotype
70995	3	334194	7	NULL	NULL	0	NULL	statement 1	Process	viability of	is greater than					statement 2	Process	viability of			NULL		0	NULL	NULL	NULL	gw60_genetics_161_2_733_s_115	12072469	We observed similar results with the hypomorphic mutation  Scr1, but because the viability of flies heterozygous for the deletions was much greater with  Scr1 than with  Scr4, we were able to examine more males.	gene_phenotype
70996	1	334195	7	NULL	NULL	0	NULL	Core SRP Proteins 	GP		concentrate in					Nucleolus	CellComponent				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_134	11352936	The Core SRP Proteins Concentrate in the Nucleolus   The requirement of the four SRP core proteins for the export of scR1 into the cytoplasm suggests that these proteins assemble with scR1 inside the nucleus to form a transport-competent particle.	gene_phenotype
70997	2	334195	7	NULL	NULL	0	NULL	 scR1	GP		exported to					cytoplasm	CellComponent				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_134	11352936	The Core SRP Proteins Concentrate in the Nucleolus   The requirement of the four SRP core proteins for the export of scR1 into the cytoplasm suggests that these proteins assemble with scR1 inside the nucleus to form a transport-competent particle.	gene_phenotype
70998	3	334195	7	NULL	NULL	0	NULL	four SRP core proteins	GP		required for					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_134	11352936	The Core SRP Proteins Concentrate in the Nucleolus   The requirement of the four SRP core proteins for the export of scR1 into the cytoplasm suggests that these proteins assemble with scR1 inside the nucleus to form a transport-competent particle.	gene_phenotype
70999	4	334195	7	NULL	NULL	0	NULL	four SRP core proteins	GP		assemble with					scR1	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_134	11352936	The Core SRP Proteins Concentrate in the Nucleolus   The requirement of the four SRP core proteins for the export of scR1 into the cytoplasm suggests that these proteins assemble with scR1 inside the nucleus to form a transport-competent particle.	gene_phenotype
71000	5	334195	7	NULL	NULL	0	NULL	statement 4	Process		occur in					nucleus	CellComponent				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_134	11352936	The Core SRP Proteins Concentrate in the Nucleolus   The requirement of the four SRP core proteins for the export of scR1 into the cytoplasm suggests that these proteins assemble with scR1 inside the nucleus to form a transport-competent particle.	gene_phenotype
71001	6	334195	7	NULL	NULL	0	NULL	statement 5	Process		form					 transport-competent particle	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_134	11352936	The Core SRP Proteins Concentrate in the Nucleolus   The requirement of the four SRP core proteins for the export of scR1 into the cytoplasm suggests that these proteins assemble with scR1 inside the nucleus to form a transport-competent particle.	gene_phenotype
71002	7	334195	7	NULL	NULL	0	NULL	statement 3	Process		suggests					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_134	11352936	The Core SRP Proteins Concentrate in the Nucleolus   The requirement of the four SRP core proteins for the export of scR1 into the cytoplasm suggests that these proteins assemble with scR1 inside the nucleus to form a transport-competent particle.	gene_phenotype
71003	1	334196	7	NULL	NULL	0	NULL	scR1	GP		localizes in		normally			los1- mutant cells	Cell				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_174	11352936	In the  los1-,  cse1-1, and  msn5- mutant cells, the localization of scR1 was normal and indistinguishable from that in wild-type cells, suggesting that the corresponding proteins are not involved in the nuclear export of scR1 (data not shown).	gene_phenotype
71004	2	334196	7	NULL	NULL	0	NULL	scR1	GP		localizes in		normally			cse1-1 mutant cells	Cell				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_174	11352936	In the  los1-,  cse1-1, and  msn5- mutant cells, the localization of scR1 was normal and indistinguishable from that in wild-type cells, suggesting that the corresponding proteins are not involved in the nuclear export of scR1 (data not shown).	gene_phenotype
71005	3	334196	7	NULL	NULL	NULL	NULL	scR1	GP		localizes in		normally			msn5- mutant cells	Cell				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_174	11352936	In the  los1-,  cse1-1, and  msn5- mutant cells, the localization of scR1 was normal and indistinguishable from that in wild-type cells, suggesting that the corresponding proteins are not involved in the nuclear export of scR1 (data not shown).	gene_phenotype
71006	4	334196	7	NULL	NULL	0	NULL	 los1	GP		is not involved in					scR1	GP	nuclear export of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_174	11352936	In the  los1-,  cse1-1, and  msn5- mutant cells, the localization of scR1 was normal and indistinguishable from that in wild-type cells, suggesting that the corresponding proteins are not involved in the nuclear export of scR1 (data not shown).	gene_phenotype
71007	5	334196	7	NULL	NULL	0	NULL	cse1-1	GP		is not involved in					scR1	GP	nuclear export of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_174	11352936	In the  los1-,  cse1-1, and  msn5- mutant cells, the localization of scR1 was normal and indistinguishable from that in wild-type cells, suggesting that the corresponding proteins are not involved in the nuclear export of scR1 (data not shown).	gene_phenotype
71008	6	334196	7	NULL	NULL	0	NULL	msn5	GP		is not involved in					scR1	GP	nuclear export of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_174	11352936	In the  los1-,  cse1-1, and  msn5- mutant cells, the localization of scR1 was normal and indistinguishable from that in wild-type cells, suggesting that the corresponding proteins are not involved in the nuclear export of scR1 (data not shown).	gene_phenotype
71009	7	334196	7	NULL	NULL	0	NULL	statement 1	Process		is indistinguishable from					wild-type cells	Cell				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_174	11352936	In the  los1-,  cse1-1, and  msn5- mutant cells, the localization of scR1 was normal and indistinguishable from that in wild-type cells, suggesting that the corresponding proteins are not involved in the nuclear export of scR1 (data not shown).	gene_phenotype
71010	8	334196	7	NULL	NULL	0	NULL	statement 2	Process		is indistinguishable from					wild-type cells	Cell				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_174	11352936	In the  los1-,  cse1-1, and  msn5- mutant cells, the localization of scR1 was normal and indistinguishable from that in wild-type cells, suggesting that the corresponding proteins are not involved in the nuclear export of scR1 (data not shown).	gene_phenotype
71011	9	334196	7	NULL	NULL	0	NULL	statement 3	Process		is indistinguishable from					wild-type cells	Cell				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_174	11352936	In the  los1-,  cse1-1, and  msn5- mutant cells, the localization of scR1 was normal and indistinguishable from that in wild-type cells, suggesting that the corresponding proteins are not involved in the nuclear export of scR1 (data not shown).	gene_phenotype
71012	10	334196	7	NULL	NULL	0	NULL	statement 1	Process		suggest					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_174	11352936	In the  los1-,  cse1-1, and  msn5- mutant cells, the localization of scR1 was normal and indistinguishable from that in wild-type cells, suggesting that the corresponding proteins are not involved in the nuclear export of scR1 (data not shown).	gene_phenotype
71013	11	334196	7	NULL	NULL	0	NULL	statement 2	Process		suggest					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_174	11352936	In the  los1-,  cse1-1, and  msn5- mutant cells, the localization of scR1 was normal and indistinguishable from that in wild-type cells, suggesting that the corresponding proteins are not involved in the nuclear export of scR1 (data not shown).	gene_phenotype
71014	12	334196	7	NULL	NULL	0	NULL	statement 3	Process		suggest					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_174	11352936	In the  los1-,  cse1-1, and  msn5- mutant cells, the localization of scR1 was normal and indistinguishable from that in wild-type cells, suggesting that the corresponding proteins are not involved in the nuclear export of scR1 (data not shown).	gene_phenotype
71015	1	334197	7	NULL	NULL	0	NULL	rrp44-1 cells	Cell	mutation in	does not affect					scR1	GP	overall stability of 			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_241	11352936	Taken together, these data suggest that the mutation in the  rrp44-1 cells does not affect the overall stability of scR1, but leads to aberrant processing of scR1 3' ends, thus possibly rendering the RNA incompetent for nuclear export.	gene_phenotype
71016	2	334197	7	NULL	NULL	0	NULL	rrp44-1 cells	Cell	mutation in	leads to					scR1	GP	aberrant processing of	3' end		NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_241	11352936	Taken together, these data suggest that the mutation in the  rrp44-1 cells does not affect the overall stability of scR1, but leads to aberrant processing of scR1 3' ends, thus possibly rendering the RNA incompetent for nuclear export.	gene_phenotype
71017	3	334197	7	NULL	NULL	NULL	NULL	statement 2	Process		renders		possibly			RNA	NucleicAcid	incompetent 			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_241	11352936	Taken together, these data suggest that the mutation in the  rrp44-1 cells does not affect the overall stability of scR1, but leads to aberrant processing of scR1 3' ends, thus possibly rendering the RNA incompetent for nuclear export.	gene_phenotype
71018	4	334197	7	NULL	NULL	NULL	NULL	RNA	NucleicAcid		required for					scR1	Process	nuclear export of			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_241	11352936	Taken together, these data suggest that the mutation in the  rrp44-1 cells does not affect the overall stability of scR1, but leads to aberrant processing of scR1 3' ends, thus possibly rendering the RNA incompetent for nuclear export.	gene_phenotype
71019	1	334198	7	NULL	NULL	0	NULL	Nsp1p 	GP		is required for					SRP-RNA	GP	nuclear export of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_242	11352936	The Essential Nucleoporin Nsp1p Is Required for SRP-RNA Nuclear Export   o find other factors involved in scR1 nuclear export, we started screening a collection of random yeast  ts mutants using the scR1 FISH assay.	gene_phenotype
71020	2	334198	7	NULL	NULL	0	NULL	Nsp1p	GP		is a type of					Nucleoporin	CellComponent	essential			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_242	11352936	The Essential Nucleoporin Nsp1p Is Required for SRP-RNA Nuclear Export   o find other factors involved in scR1 nuclear export, we started screening a collection of random yeast  ts mutants using the scR1 FISH assay.	gene_phenotype
71021	1	334199	7	NULL	NULL	0	NULL	sCCPH	GP		acts as					Factor I cofactor	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_184	16760474	Factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement proteins C3b and C4b.	gene_phenotype
71022	2	334199	7	NULL	NULL	0	NULL	VCP	GP		acts as					Factor I cofactor	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_184	16760474	Factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement proteins C3b and C4b.	gene_phenotype
71023	3	334199	7	NULL	NULL	0	NULL	factor H 	GP		acts as					Factor I cofactor	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_184	16760474	Factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement proteins C3b and C4b.	gene_phenotype
71024	4	334199	7	NULL	NULL	NULL	NULL	sCR1	GP		acts as					Factor I cofactor	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_184	16760474	Factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement proteins C3b and C4b.	gene_phenotype
71025	5	334199	7	NULL	NULL	0	NULL	fH	GP		is					factor H	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_184	16760474	Factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement proteins C3b and C4b.	gene_phenotype
71026	6	334199	7	NULL	NULL	NULL	NULL	statement 1	GP		cofactor for					C3b	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_184	16760474	Factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement proteins C3b and C4b.	gene_phenotype
71027	7	334199	7	NULL	NULL	NULL	NULL	statement 1	GP		cofactor for					C4b	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_184	16760474	Factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement proteins C3b and C4b.	gene_phenotype
71028	8	334199	7	NULL	NULL	0	NULL	statement 2	GP		cofactor for					C3b	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_184	16760474	Factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement proteins C3b and C4b.	gene_phenotype
71029	9	334199	7	NULL	NULL	0	NULL	statement 2	GP		cofactor for					C4b	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_184	16760474	Factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement proteins C3b and C4b.	gene_phenotype
71030	10	334199	7	NULL	NULL	0	NULL	statement 3	GP		cofactor for					C3b	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_184	16760474	Factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement proteins C3b and C4b.	gene_phenotype
71031	11	334199	7	NULL	NULL	0	NULL	statement 3	GP		cofactor for					C4b	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_184	16760474	Factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement proteins C3b and C4b.	gene_phenotype
71032	12	334199	7	NULL	NULL	0	NULL	statement 4	GP		cofactor for					C3b	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_184	16760474	Factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement proteins C3b and C4b.	gene_phenotype
71033	13	334199	7	NULL	NULL	0	NULL	statement 4	GP		cofactor for					C4b	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_184	16760474	Factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement proteins C3b and C4b.	gene_phenotype
71034	14	334199	7	NULL	NULL	0	NULL	C3b	GP		is a type of					complement protein	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_184	16760474	Factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement proteins C3b and C4b.	gene_phenotype
71035	15	334199	7	NULL	NULL	0	NULL	C4b	GP		is a type of					complement protein	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_184	16760474	Factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement proteins C3b and C4b.	gene_phenotype
71036	1	334200	7	NULL	NULL	0	NULL	 sCCPH	GP		acts as					Factor I cofactor	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_193	16760474	Time course of factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement protein C3b.	gene_phenotype
71037	2	334200	7	NULL	NULL	0	NULL	VCP	GP		acts as					Factor I cofactor	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_193	16760474	Time course of factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement protein C3b.	gene_phenotype
71038	3	334200	7	NULL	NULL	0	NULL	fH	GP		acts as					Factor I cofactor	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_193	16760474	Time course of factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement protein C3b.	gene_phenotype
71039	4	334200	7	NULL	NULL	0	NULL	sCR1	GP		acts as					Factor I cofactor	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_193	16760474	Time course of factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement protein C3b.	gene_phenotype
71041	5	334200	7	NULL	NULL	0	NULL	statement 1	GP		cofactor for					C3b	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_193	16760474	Time course of factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement protein C3b.	gene_phenotype
71042	6	334200	7	NULL	NULL	0	NULL	statement 2	GP		cofactor for					C3b	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_193	16760474	Time course of factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement protein C3b.	gene_phenotype
71044	7	334200	7	NULL	NULL	0	NULL	statement 3	GP		cofactor for					C3b	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_193	16760474	Time course of factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement protein C3b.	gene_phenotype
71046	8	334200	7	NULL	NULL	0	NULL	statement 4	GP		cofactor for					C3b	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_193	16760474	Time course of factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement protein C3b.	gene_phenotype
71049	9	334200	7	NULL	NULL	0	NULL	C3b	GP		is a type of					complement protein	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_193	16760474	Time course of factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement protein C3b.	gene_phenotype
71051	10	334200	7	NULL	NULL	0	NULL	fH	GP		is					factor H	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_193	16760474	Time course of factor I cofactor activity of sCCPH, VCP, factor H ( fH), and sCR1 for complement protein C3b.	gene_phenotype
71072	1	334201	7	NULL	NULL	0	NULL	sCCPH	GP		acts as					Factor I cofactor	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_227	16760474	Time course of factor I cofactor activity of sCCPH, VCP, and sCR1 for complement protein  C4b.	gene_phenotype
71073	2	334201	7	NULL	NULL	0	NULL	VCP	GP		acts as					Factor I cofactor	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_227	16760474	Time course of factor I cofactor activity of sCCPH, VCP, and sCR1 for complement protein  C4b.	gene_phenotype
71074	3	334201	7	NULL	NULL	0	NULL	sCR1	GP		acts as					Factor I cofactor	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_227	16760474	Time course of factor I cofactor activity of sCCPH, VCP, and sCR1 for complement protein  C4b.	gene_phenotype
71075	4	334201	7	NULL	NULL	0	NULL	statement 1	GP		cofactor for					C4b	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_227	16760474	Time course of factor I cofactor activity of sCCPH, VCP, and sCR1 for complement protein  C4b.	gene_phenotype
71076	5	334201	7	NULL	NULL	0	NULL	statement 2	GP		cofactor for					C4b	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_227	16760474	Time course of factor I cofactor activity of sCCPH, VCP, and sCR1 for complement protein  C4b.	gene_phenotype
71077	6	334201	7	NULL	NULL	0	NULL	statement 3	GP		cofactor for					C4b	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_227	16760474	Time course of factor I cofactor activity of sCCPH, VCP, and sCR1 for complement protein  C4b.	gene_phenotype
71078	7	334201	7	NULL	NULL	0	NULL	C4b	GP		is a type of					complement protein	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_227	16760474	Time course of factor I cofactor activity of sCCPH, VCP, and sCR1 for complement protein  C4b.	gene_phenotype
71086	1	334203	7	NULL	NULL	0	NULL	scR1	GP	export pathway of	is identical to					mRNA	NucleicAcid	export pathway of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_188	11352936	(A)+ RNA nuclear accumulation, or even reflects the use of identical export pathways for both scR1 and mRNA.	gene_phenotype
71090	1	334204	7	NULL	NULL	0	NULL	scR1		nuclear accumulation	is not consequence of					mRNA	NucleicAcid	export defect of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_192	11352936	(A)+ RNA, suggesting that the scR1 nuclear accumulation was not simply a consequence of the export defect for mRNA (data not shown).	gene_phenotype
71091	1	334205	7	NULL	NULL	0	NULL	mRNA	NucleicAcid	nuclear export mechanism of	is distinct from					scR1	GP	nuclear export mechanism of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_195	11352936	This, and the data presented below, strongly argue for distinct nuclear export mechanisms for mRNA and scR1.	gene_phenotype
71092	1	334206	7	NULL	NULL	0	NULL	scR1	GP	nuclear export of	involves		directly			Xpo1p	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_205	11352936	We conclude that nuclear export of scR1 directly involves the NES-export receptor Xpo1p and does not overlap with the mRNA export pathway.	gene_phenotype
71093	2	334206	7	NULL	NULL	0	NULL	Xpo1p	GP		is a type of					NES-export receptor	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_205	11352936	We conclude that nuclear export of scR1 directly involves the NES-export receptor Xpo1p and does not overlap with the mRNA export pathway.	gene_phenotype
71094	3	334206	7	NULL	NULL	0	NULL	statement 1	Process		does not overlap with					mRNA	NucleicAcid	export pathway of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_205	11352936	We conclude that nuclear export of scR1 directly involves the NES-export receptor Xpo1p and does not overlap with the mRNA export pathway.	gene_phenotype
71095	1	334208	7	NULL	NULL	0	NULL	 scR1	GP	strong nuclear export defect	present in					nup159 cells	Cell	mutant;;rat			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_357	11352936	(A)+ RNA in the  srx1-1 cells at the restrictive temperature, as well as the strong scR1 nuclear export defect present in  nup159 ( rat7) mutant cells.	gene_phenotype
71096	1	334210	7	NULL	NULL	0	NULL	 sCCPH	GP		cofactor for					C4b	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_177	16760474	The cofactor activity of sCCPH for C4b was similar to VCP and sCR1, and like these proteins it also supported the cleavages at both the sites and led to generation of C4c and C4d.	gene_phenotype
71097	2	334210	7	NULL	NULL	0	NULL	VCP	GP		cofactor for					C4b	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_177	16760474	The cofactor activity of sCCPH for C4b was similar to VCP and sCR1, and like these proteins it also supported the cleavages at both the sites and led to generation of C4c and C4d.	gene_phenotype
71098	3	334210	7	NULL	NULL	0	NULL	sCR1	GP		cofactor for					C4b	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_177	16760474	The cofactor activity of sCCPH for C4b was similar to VCP and sCR1, and like these proteins it also supported the cleavages at both the sites and led to generation of C4c and C4d.	gene_phenotype
71099	4	334210	7	NULL	NULL	0	NULL	statement 1	Process		is similar to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_177	16760474	The cofactor activity of sCCPH for C4b was similar to VCP and sCR1, and like these proteins it also supported the cleavages at both the sites and led to generation of C4c and C4d.	gene_phenotype
71100	5	334210	7	NULL	NULL	0	NULL	statement 1	Process		is similar to					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_177	16760474	The cofactor activity of sCCPH for C4b was similar to VCP and sCR1, and like these proteins it also supported the cleavages at both the sites and led to generation of C4c and C4d.	gene_phenotype
71101	6	334210	7	NULL	NULL	0	NULL	C4b	GP		cleaves to					C4c	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_177	16760474	The cofactor activity of sCCPH for C4b was similar to VCP and sCR1, and like these proteins it also supported the cleavages at both the sites and led to generation of C4c and C4d.	gene_phenotype
71102	7	334210	7	NULL	NULL	0	NULL	C4b	GP		cleaves to					C4d	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_177	16760474	The cofactor activity of sCCPH for C4b was similar to VCP and sCR1, and like these proteins it also supported the cleavages at both the sites and led to generation of C4c and C4d.	gene_phenotype
71103	8	334210	7	NULL	NULL	0	NULL	statement 6	Process		occur along with					statement 7	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_177	16760474	The cofactor activity of sCCPH for C4b was similar to VCP and sCR1, and like these proteins it also supported the cleavages at both the sites and led to generation of C4c and C4d.	gene_phenotype
71104	9	334210	7	NULL	NULL	0	NULL	sCCPH 	GP		supports 					statement 8	Process	cleavage of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_32_23119_s_177	16760474	The cofactor activity of sCCPH for C4b was similar to VCP and sCR1, and like these proteins it also supported the cleavages at both the sites and led to generation of C4c and C4d.	gene_phenotype
71105	1	334211	7	NULL	NULL	0	NULL	 anti-human CD46 mAb	GP		is specific for								SCR1 domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_28_25964_s_89	12724329	The cell mixture was lysed and subjected to  immunoprecipitation with an anti-human CD46 mAb (J4 - 48); this mAb is  specific for the SCR1 domain, which is dispensable for HHV-6 fusion  ( ,   ).	gene_phenotype
71106	2	334211	7	NULL	NULL	0	NULL				dispensable for			SCR1 domain		HHV-6 fusion	Organism				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_28_25964_s_89	12724329	The cell mixture was lysed and subjected to  immunoprecipitation with an anti-human CD46 mAb (J4 - 48); this mAb is  specific for the SCR1 domain, which is dispensable for HHV-6 fusion  ( ,   ).	gene_phenotype
71126	1	334213	7	NULL	NULL	0	NULL	 Xpo1p 	GP		is involved in					scR1 	GP	nuclear export of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_345	11352936	The involvement of Xpo1p in scR1 nuclear export was also suggested in another report that appeared shortly before this manuscript was submitted ( Ciufo and Brown 2000   ).	gene_phenotype
71127	1	334214	7	NULL	NULL	0	NULL	SRP	GP	yeast	is assembled into					core particle	GP				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_20_1256_s_42	11069106	Here, we report that yeast SRP is assembled in the nucleus into a core particle containing Srp14p, 21p, 68 and 72p, and scR1, which is a nuclear-export substrate.	gene_phenotype
71128	2	334214	7	NULL	NULL	0	NULL	core particle	GP		contains					Srp14p	GP				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_20_1256_s_42	11069106	Here, we report that yeast SRP is assembled in the nucleus into a core particle containing Srp14p, 21p, 68 and 72p, and scR1, which is a nuclear-export substrate.	gene_phenotype
71129	3	334214	7	NULL	NULL	0	NULL	core particle	GP		contains					Srp21p	GP				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_20_1256_s_42	11069106	Here, we report that yeast SRP is assembled in the nucleus into a core particle containing Srp14p, 21p, 68 and 72p, and scR1, which is a nuclear-export substrate.	gene_phenotype
71130	4	334214	7	NULL	NULL	0	NULL	core particle	GP		contains					Srp68p	GP				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_20_1256_s_42	11069106	Here, we report that yeast SRP is assembled in the nucleus into a core particle containing Srp14p, 21p, 68 and 72p, and scR1, which is a nuclear-export substrate.	gene_phenotype
71131	5	334214	7	NULL	NULL	0	NULL	core particle	GP		contains					Srp72p	GP				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_20_1256_s_42	11069106	Here, we report that yeast SRP is assembled in the nucleus into a core particle containing Srp14p, 21p, 68 and 72p, and scR1, which is a nuclear-export substrate.	gene_phenotype
71132	6	334214	7	NULL	NULL	0	NULL	core particle	GP		contains					 scR1	GP				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_20_1256_s_42	11069106	Here, we report that yeast SRP is assembled in the nucleus into a core particle containing Srp14p, 21p, 68 and 72p, and scR1, which is a nuclear-export substrate.	gene_phenotype
71133	7	334214	7	NULL	NULL	0	NULL	scR1	GP		is a type of					nuclear-export substrate	GP				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_20_1256_s_42	11069106	Here, we report that yeast SRP is assembled in the nucleus into a core particle containing Srp14p, 21p, 68 and 72p, and scR1, which is a nuclear-export substrate.	gene_phenotype
71134	8	334214	7	NULL	NULL	0	NULL	statement 1	Process		is assembled in					nucleus	CellComponent				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_20_1256_s_42	11069106	Here, we report that yeast SRP is assembled in the nucleus into a core particle containing Srp14p, 21p, 68 and 72p, and scR1, which is a nuclear-export substrate.	gene_phenotype
71135	9	334214	7	NULL	NULL	NULL	NULL	statement 2	GP		occur along with					statement 3	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_20_1256_s_42	11069106	Here, we report that yeast SRP is assembled in the nucleus into a core particle containing Srp14p, 21p, 68 and 72p, and scR1, which is a nuclear-export substrate.	gene_phenotype
71136	10	334214	7	NULL	NULL	NULL	NULL	statement 2	GP		occur along with					statement 4	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_20_1256_s_42	11069106	Here, we report that yeast SRP is assembled in the nucleus into a core particle containing Srp14p, 21p, 68 and 72p, and scR1, which is a nuclear-export substrate.	gene_phenotype
71137	11	334214	7	NULL	NULL	0	NULL	statement 2	GP		occur along with					statement 5	GP				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_20_1256_s_42	11069106	Here, we report that yeast SRP is assembled in the nucleus into a core particle containing Srp14p, 21p, 68 and 72p, and scR1, which is a nuclear-export substrate.	gene_phenotype
71138	12	334214	7	NULL	NULL	0	NULL	statement 2	GP		occur along with					statement 6	GP				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_20_1256_s_42	11069106	Here, we report that yeast SRP is assembled in the nucleus into a core particle containing Srp14p, 21p, 68 and 72p, and scR1, which is a nuclear-export substrate.	gene_phenotype
71139	1	334215	7	NULL	NULL	0	NULL	SRP components	GP		localizes in					nucleus	CellComponent				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_20_1256_s_135	11069106	A final issue raised by nuclear localisation of SRP components was which, if any, of the known pathways of export are responsible for transporting scR1 and the imported proteins to the cytoplasm.	gene_phenotype
71140	1	334216	7	NULL	NULL	NULL	NULL	scR1	GP		is present throughout					sporulation	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_43_40505_s_236	12181322	It is noteworthy that scR1, which was known to undergo very little variation in various physiological situations, is also present at a constant level throughout sporulation and spore germination.	gene_phenotype
71141	2	334216	7	NULL	NULL	0	NULL	scR1	GP		is present throughout					spore germination	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_43_40505_s_236	12181322	It is noteworthy that scR1, which was known to undergo very little variation in various physiological situations, is also present at a constant level throughout sporulation and spore germination.	gene_phenotype
71142	1	334218	7	NULL	NULL	0	NULL	 SCR1 gene 	GP		is unaffected by					silencing	Process	changes in 			NULL		0	NULL	NULL	NULL	gw60_science_276_5318_1547_s_109	9171055	To examine this  possibility, we quantitated mRNA levels of  GAL4-SIR1 and  normalized them to those of the  SCR1 gene ( 19),  whose expression is unaffected by changes in silencing or the cell  cycle.	gene_phenotype
71143	2	334218	7	NULL	NULL	0	NULL	SCR1 gene	GP		is unaffected by					cell cycle	Process	changes in			NULL		0	NULL	NULL	NULL	gw60_science_276_5318_1547_s_109	9171055	To examine this  possibility, we quantitated mRNA levels of  GAL4-SIR1 and  normalized them to those of the  SCR1 gene ( 19),  whose expression is unaffected by changes in silencing or the cell  cycle.	gene_phenotype
71144	1	334219	7	NULL	NULL	0	NULL	SCR1	GP		encode					natural cycloheximide resistance	Process	Schwanniomyces occidentalis			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_eur-j-biochem_213_2_8477754_s_2	8477754	Two genes (SCR1 and SCR2) encoding natural cycloheximide resistance in  the budding yeast Schwanniomyces occidentalis have been cloned by expression  in Saccharomyces cerevisiae.	gene_phenotype
71145	2	334219	7	NULL	NULL	0	NULL	 SCR2	GP		encode					natural cycloheximide resistance	Process	Schwanniomyces occidentalis			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_eur-j-biochem_213_2_8477754_s_2	8477754	Two genes (SCR1 and SCR2) encoding natural cycloheximide resistance in  the budding yeast Schwanniomyces occidentalis have been cloned by expression  in Saccharomyces cerevisiae.	gene_phenotype
71146	3	334219	7	NULL	NULL	0	NULL	Schwanniomyces occidentalis	Organism		is a type of					budding yeast	Organism				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_eur-j-biochem_213_2_8477754_s_2	8477754	Two genes (SCR1 and SCR2) encoding natural cycloheximide resistance in  the budding yeast Schwanniomyces occidentalis have been cloned by expression  in Saccharomyces cerevisiae.	gene_phenotype
71147	1	334221	7	NULL	NULL	0	NULL	SCR1	GP		is present in					Sw. occidentalis	Organism				NULL		0	NULL	NULL	NULL	gw70_yeast_19_9_735_s_34	12112229	Previously, we reported that two genes ( SCR1 and  SCR2) from the budding yeast  Sw. occidentalis were cloned and expressed in  S. cerevisiae (del Pozo  et al., [ 1993]).	gene_phenotype
71148	2	334221	7	NULL	NULL	0	NULL	SCR2	GP		is present in					Sw. occidentalis	Organism				NULL		0	NULL	NULL	NULL	gw70_yeast_19_9_735_s_34	12112229	Previously, we reported that two genes ( SCR1 and  SCR2) from the budding yeast  Sw. occidentalis were cloned and expressed in  S. cerevisiae (del Pozo  et al., [ 1993]).	gene_phenotype
71149	3	334221	7	NULL	NULL	0	NULL	Sw. occidentalis	Organism		is a type of					budding yeast	Organism				NULL		0	NULL	NULL	NULL	gw70_yeast_19_9_735_s_34	12112229	Previously, we reported that two genes ( SCR1 and  SCR2) from the budding yeast  Sw. occidentalis were cloned and expressed in  S. cerevisiae (del Pozo  et al., [ 1993]).	gene_phenotype
71150	1	334222	7	NULL	NULL	0	NULL	competent SRP	GP		assemble with					nuclear export	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_48	11352936	Our results suggest that assembly of a nuclear export - competent SRP takes place in the nucleolus and requires the four "`core"' SRP proteins, which are actively imported into the nucleus by the ribosomal import pathway, as well as an intact scR1 3' end.	gene_phenotype
71151	2	334222	7	NULL	NULL	0	NULL	statement 1	Process		takes place in					nucleolus	CellComponent				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_48	11352936	Our results suggest that assembly of a nuclear export - competent SRP takes place in the nucleolus and requires the four "`core"' SRP proteins, which are actively imported into the nucleus by the ribosomal import pathway, as well as an intact scR1 3' end.	gene_phenotype
71152	3	334222	7	NULL	NULL	0	NULL	statement 1	Process		requires					four "`core"' SRP proteins	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_48	11352936	Our results suggest that assembly of a nuclear export - competent SRP takes place in the nucleolus and requires the four "`core"' SRP proteins, which are actively imported into the nucleus by the ribosomal import pathway, as well as an intact scR1 3' end.	gene_phenotype
71153	4	334222	7	NULL	NULL	0	NULL	four "`core"' SRP proteins	GP		imported into		actively			nucleus	CellComponent				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_48	11352936	Our results suggest that assembly of a nuclear export - competent SRP takes place in the nucleolus and requires the four "`core"' SRP proteins, which are actively imported into the nucleus by the ribosomal import pathway, as well as an intact scR1 3' end.	gene_phenotype
71154	5	334222	7	NULL	NULL	0	NULL	statement 4	Process		occur by					ribosomal import pathway	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_48	11352936	Our results suggest that assembly of a nuclear export - competent SRP takes place in the nucleolus and requires the four "`core"' SRP proteins, which are actively imported into the nucleus by the ribosomal import pathway, as well as an intact scR1 3' end.	gene_phenotype
71155	6	334222	7	NULL	NULL	0	NULL	statement 1	Process		requires					scR1	GP	intact	3' end		NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_48	11352936	Our results suggest that assembly of a nuclear export - competent SRP takes place in the nucleolus and requires the four "`core"' SRP proteins, which are actively imported into the nucleus by the ribosomal import pathway, as well as an intact scR1 3' end.	gene_phenotype
71156	1	334223	7	NULL	NULL	0	NULL	ts strain	Organism	mutated	cause					scR1	GP	inhibition of nuclear export of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_244	11352936	The mutated gene in this  ts strain which causes inhibiton of scR1 nuclear export was cloned by complementation and found to correspond to the essential nucleoporin Nsp1p ( Fig 8 A and data not shown).	gene_phenotype
71157	2	334223	7	NULL	NULL	0	NULL	Nsp1p	GP		is a type of					nucleoporin	CellComponent	essential			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_244	11352936	The mutated gene in this  ts strain which causes inhibiton of scR1 nuclear export was cloned by complementation and found to correspond to the essential nucleoporin Nsp1p ( Fig 8 A and data not shown).	gene_phenotype
71158	3	334223	7	NULL	NULL	0	NULL	statement 1	Process		is because of					Nsp1p	GP	mutated			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_244	11352936	The mutated gene in this  ts strain which causes inhibiton of scR1 nuclear export was cloned by complementation and found to correspond to the essential nucleoporin Nsp1p ( Fig 8 A and data not shown).	gene_phenotype
71159	1	334224	7	NULL	NULL	NULL	NULL	scR1	GP		does not accumulate at					permissive temperature					NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_283	11352936	No accumulation of scR1 was observed in these cells at the permissive, semi-, or nonpermissive temperatures, although polyadenylated RNA was found to accumulate under the latter two conditions ( Fig 9 B and data not shown).	gene_phenotype
71160	2	334224	7	NULL	NULL	0	NULL	scR1	GP		does not accumulate at					semi-permissive temperature					NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_283	11352936	No accumulation of scR1 was observed in these cells at the permissive, semi-, or nonpermissive temperatures, although polyadenylated RNA was found to accumulate under the latter two conditions ( Fig 9 B and data not shown).	gene_phenotype
71161	3	334224	7	NULL	NULL	0	NULL	scR1	GP		does not accumulate at					nonpermissive temperature					NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_283	11352936	No accumulation of scR1 was observed in these cells at the permissive, semi-, or nonpermissive temperatures, although polyadenylated RNA was found to accumulate under the latter two conditions ( Fig 9 B and data not shown).	gene_phenotype
71162	4	334224	7	NULL	NULL	0	NULL	polyadenylated RNA	NucleicAcid		accumulate at					semi-permissive temperature					NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_283	11352936	No accumulation of scR1 was observed in these cells at the permissive, semi-, or nonpermissive temperatures, although polyadenylated RNA was found to accumulate under the latter two conditions ( Fig 9 B and data not shown).	gene_phenotype
71163	5	334224	7	NULL	NULL	NULL	NULL	polyadenylated RNA	NucleicAcid		accumulate at					nonpermissive temperature					NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_283	11352936	No accumulation of scR1 was observed in these cells at the permissive, semi-, or nonpermissive temperatures, although polyadenylated RNA was found to accumulate under the latter two conditions ( Fig 9 B and data not shown).	gene_phenotype
71164	1	334225	7	NULL	NULL	0	NULL	Nsp1p	GP		is a subset of					nucleoporins	CellComponent				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_284	11352936	Taken together, these data provide evidence that a subset of nucleoporins, consisting of Nsp1p and Nup159p, is important for scR1 nuclear export, whereas other nucleoporins, such as Nup85p, seem to be less important.	gene_phenotype
71165	2	334225	7	NULL	NULL	NULL	NULL	Nup159p	GP		is a subset of					nucleoporins	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_284	11352936	Taken together, these data provide evidence that a subset of nucleoporins, consisting of Nsp1p and Nup159p, is important for scR1 nuclear export, whereas other nucleoporins, such as Nup85p, seem to be less important.	gene_phenotype
71166	3	334225	7	NULL	NULL	0	NULL	statement 1	Process		is required for					scR1	GP	nuclear export of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_284	11352936	Taken together, these data provide evidence that a subset of nucleoporins, consisting of Nsp1p and Nup159p, is important for scR1 nuclear export, whereas other nucleoporins, such as Nup85p, seem to be less important.	gene_phenotype
71167	4	334225	7	NULL	NULL	0	NULL	statement 2	Process		is required for					scR1	GP	nuclear export of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_284	11352936	Taken together, these data provide evidence that a subset of nucleoporins, consisting of Nsp1p and Nup159p, is important for scR1 nuclear export, whereas other nucleoporins, such as Nup85p, seem to be less important.	gene_phenotype
71168	5	334225	7	NULL	NULL	0	NULL	Nup85p	GP		is a subset of					nucleoporins	CellComponent				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_284	11352936	Taken together, these data provide evidence that a subset of nucleoporins, consisting of Nsp1p and Nup159p, is important for scR1 nuclear export, whereas other nucleoporins, such as Nup85p, seem to be less important.	gene_phenotype
71169	6	334225	7	NULL	NULL	0	NULL	Nup85p	GP		important for		less			scR1	GP	nuclear export of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_284	11352936	Taken together, these data provide evidence that a subset of nucleoporins, consisting of Nsp1p and Nup159p, is important for scR1 nuclear export, whereas other nucleoporins, such as Nup85p, seem to be less important.	gene_phenotype
71956	1	334227	11	NULL	NULL	0	NULL	 pre-SRP proteins	GP	absence of 	accumulate					scR1	GP	nuclear			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_341	11352936	However, the fact that absence of any one of the pre-SRP proteins leads to nuclear accumulation of scR1 suggests that SRP export is more complex than simple NES export.	gene_phenotype
71957	2	334227	11	NULL	NULL	0	NULL	SRP export	Process		is complex than		possibly			NES export	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_341	11352936	However, the fact that absence of any one of the pre-SRP proteins leads to nuclear accumulation of scR1 suggests that SRP export is more complex than simple NES export.	gene_phenotype
71958	1	334228	11	NULL	NULL	0	NULL	CRM1	GP		mediate					U snRNA	NucleicAcid	nuclear export			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_344	11352936	Alternatively, an adapter protein, similar to the recently identified PHAX, which is required for CRM1-mediated U snRNA nuclear export ( Ohno et al. 2000   ), might be necessary for scR1 nuclear export.	gene_phenotype
71959	2	334228	11	NULL	NULL	0	NULL	adapter protein	GP		required for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_344	11352936	Alternatively, an adapter protein, similar to the recently identified PHAX, which is required for CRM1-mediated U snRNA nuclear export ( Ohno et al. 2000   ), might be necessary for scR1 nuclear export.	gene_phenotype
71960	3	334228	11	NULL	NULL	0	NULL	adapter protein	GP		necessary for		possibly			scR1 	GP	nuclear export			NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_344	11352936	Alternatively, an adapter protein, similar to the recently identified PHAX, which is required for CRM1-mediated U snRNA nuclear export ( Ohno et al. 2000   ), might be necessary for scR1 nuclear export.	gene_phenotype
71961	1	334229	11	NULL	NULL	0	NULL	scR1	GP	Newly transcribed	assemble with					Srp14p	GP				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_20_1256_s_183	11069106	Newly transcribed scR1 is assembled with Srp14p, Srp21p, Srp68p and Srp72p to form a core SRP that is a substrate for export to the cytoplasm through a route sensitive to inactivation of the NES-binding protein Xpo1p/Crm1p or lack of Yrb2p activity at low temperature.	gene_phenotype
71962	2	334229	11	NULL	NULL	0	NULL	statement 1	GP		assemble with					Srp21p	GP				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_20_1256_s_183	11069106	Newly transcribed scR1 is assembled with Srp14p, Srp21p, Srp68p and Srp72p to form a core SRP that is a substrate for export to the cytoplasm through a route sensitive to inactivation of the NES-binding protein Xpo1p/Crm1p or lack of Yrb2p activity at low temperature.	gene_phenotype
71963	3	334229	11	NULL	NULL	0	NULL	statement 2	GP		assemble with					Srp68p	GP				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_20_1256_s_183	11069106	Newly transcribed scR1 is assembled with Srp14p, Srp21p, Srp68p and Srp72p to form a core SRP that is a substrate for export to the cytoplasm through a route sensitive to inactivation of the NES-binding protein Xpo1p/Crm1p or lack of Yrb2p activity at low temperature.	gene_phenotype
71964	4	334229	11	NULL	NULL	0	NULL	statement 3	GP		assemble with					Srp72p	GP				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_20_1256_s_183	11069106	Newly transcribed scR1 is assembled with Srp14p, Srp21p, Srp68p and Srp72p to form a core SRP that is a substrate for export to the cytoplasm through a route sensitive to inactivation of the NES-binding protein Xpo1p/Crm1p or lack of Yrb2p activity at low temperature.	gene_phenotype
71965	5	334229	11	NULL	NULL	0	NULL	statement 4	GP		forms					core SRP	GP				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_20_1256_s_183	11069106	Newly transcribed scR1 is assembled with Srp14p, Srp21p, Srp68p and Srp72p to form a core SRP that is a substrate for export to the cytoplasm through a route sensitive to inactivation of the NES-binding protein Xpo1p/Crm1p or lack of Yrb2p activity at low temperature.	gene_phenotype
71966	6	334229	11	NULL	NULL	0	NULL	core SRP	GP		export to					cytoplasm	Cell Component				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_20_1256_s_183	11069106	Newly transcribed scR1 is assembled with Srp14p, Srp21p, Srp68p and Srp72p to form a core SRP that is a substrate for export to the cytoplasm through a route sensitive to inactivation of the NES-binding protein Xpo1p/Crm1p or lack of Yrb2p activity at low temperature.	gene_phenotype
71971	1	334233	11	NULL	NULL	0	NULL	Prp43p	GP	depletion	accumulate		transient			23S pre-rRNAs	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_21_9269_s_167	16227579	Prp43p depletion is accompanied by a transient accumulation of the 35S and 23S pre-rRNAs and a strong decrease in the steady-state levels of the 27SA2, 27SB, 20S, and 7S pre-rRNAs and of all mature rRNAs, while levels of Scr1 RNA or tRNA-trp were little affected (Fig.  1B and  1C).	gene_phenotype
71974	2	334233	11	NULL	NULL	0	NULL	Prp43p	GP	depletion	accumulate		transient			 35S	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_21_9269_s_167	16227579	Prp43p depletion is accompanied by a transient accumulation of the 35S and 23S pre-rRNAs and a strong decrease in the steady-state levels of the 27SA2, 27SB, 20S, and 7S pre-rRNAs and of all mature rRNAs, while levels of Scr1 RNA or tRNA-trp were little affected (Fig.  1B and  1C).	gene_phenotype
71976	3	334233	11	NULL	NULL	0	NULL	Prp43p	GP	depletion	decreases		strongly			27SA2	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_21_9269_s_167	16227579	Prp43p depletion is accompanied by a transient accumulation of the 35S and 23S pre-rRNAs and a strong decrease in the steady-state levels of the 27SA2, 27SB, 20S, and 7S pre-rRNAs and of all mature rRNAs, while levels of Scr1 RNA or tRNA-trp were little affected (Fig.  1B and  1C).	gene_phenotype
71977	4	334233	11	NULL	NULL	0	NULL	Prp43p	GP	depletion	decreases		strongly			 27SB	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_21_9269_s_167	16227579	Prp43p depletion is accompanied by a transient accumulation of the 35S and 23S pre-rRNAs and a strong decrease in the steady-state levels of the 27SA2, 27SB, 20S, and 7S pre-rRNAs and of all mature rRNAs, while levels of Scr1 RNA or tRNA-trp were little affected (Fig.  1B and  1C).	gene_phenotype
71978	5	334233	11	NULL	NULL	0	NULL	Prp43p	GP	depletion	decreases		strongly			20S	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_21_9269_s_167	16227579	Prp43p depletion is accompanied by a transient accumulation of the 35S and 23S pre-rRNAs and a strong decrease in the steady-state levels of the 27SA2, 27SB, 20S, and 7S pre-rRNAs and of all mature rRNAs, while levels of Scr1 RNA or tRNA-trp were little affected (Fig.  1B and  1C).	gene_phenotype
71980	6	334233	11	NULL	NULL	0	NULL	Prp43p	GP	depletion	decreases		strongly			7S pre-rRNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_21_9269_s_167	16227579	Prp43p depletion is accompanied by a transient accumulation of the 35S and 23S pre-rRNAs and a strong decrease in the steady-state levels of the 27SA2, 27SB, 20S, and 7S pre-rRNAs and of all mature rRNAs, while levels of Scr1 RNA or tRNA-trp were little affected (Fig.  1B and  1C).	gene_phenotype
71981	7	334233	11	NULL	NULL	0	NULL	Prp43p	GP	depletion	decreases		strongly			mature rRNAs	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_21_9269_s_167	16227579	Prp43p depletion is accompanied by a transient accumulation of the 35S and 23S pre-rRNAs and a strong decrease in the steady-state levels of the 27SA2, 27SB, 20S, and 7S pre-rRNAs and of all mature rRNAs, while levels of Scr1 RNA or tRNA-trp were little affected (Fig.  1B and  1C).	gene_phenotype
71982	8	334233	11	NULL	NULL	NULL	NULL	Prp43p	GP	depletion	not affected					Scr1 RNA	NucleicAcid	levels			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_21_9269_s_167	16227579	Prp43p depletion is accompanied by a transient accumulation of the 35S and 23S pre-rRNAs and a strong decrease in the steady-state levels of the 27SA2, 27SB, 20S, and 7S pre-rRNAs and of all mature rRNAs, while levels of Scr1 RNA or tRNA-trp were little affected (Fig.  1B and  1C).	gene_phenotype
71983	9	334233	11	NULL	NULL	0	NULL	Prp43p	GP	depletion	not affected					tRNA-trp	NucleicAcid	levels			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_21_9269_s_167	16227579	Prp43p depletion is accompanied by a transient accumulation of the 35S and 23S pre-rRNAs and a strong decrease in the steady-state levels of the 27SA2, 27SB, 20S, and 7S pre-rRNAs and of all mature rRNAs, while levels of Scr1 RNA or tRNA-trp were little affected (Fig.  1B and  1C).	gene_phenotype
72025	1	334235	11	NULL	NULL	NULL	NULL	soluble Crry	GP	mouse 	is					sCrry	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_115_9_2444_s_27	16127466	Because of the species-selective activity of complement-inhibitory proteins, we decided to construct a novel recombinant protein consisting of a mouse CR2-targeting moiety linked to mouse soluble Crry (sCrry), an inhibitor of C3 activation which is a structural and functional analog of human soluble CR1 (sCR1).	gene_phenotype
72026	2	334235	11	NULL	NULL	NULL	NULL	soluble Crry	GP	mouse 	is an inhibitor of					C3	GP				NULL		NULL	NULL	NULL	NULL	gw70_jclininvest_115_9_2444_s_27	16127466	Because of the species-selective activity of complement-inhibitory proteins, we decided to construct a novel recombinant protein consisting of a mouse CR2-targeting moiety linked to mouse soluble Crry (sCrry), an inhibitor of C3 activation which is a structural and functional analog of human soluble CR1 (sCR1).	gene_phenotype
72029	3	334235	11	NULL	NULL	0	NULL	soluble Crry	GP		 is an analog of		 structural;;functional 			soluble CR1	GP	human			NULL		0	NULL	NULL	NULL	gw70_jclininvest_115_9_2444_s_27	16127466	Because of the species-selective activity of complement-inhibitory proteins, we decided to construct a novel recombinant protein consisting of a mouse CR2-targeting moiety linked to mouse soluble Crry (sCrry), an inhibitor of C3 activation which is a structural and functional analog of human soluble CR1 (sCR1).	gene_phenotype
72031	4	334235	11	NULL	NULL	0	NULL	soluble CR1	GP		is					sCR1	GP				NULL		0	NULL	NULL	NULL	gw70_jclininvest_115_9_2444_s_27	16127466	Because of the species-selective activity of complement-inhibitory proteins, we decided to construct a novel recombinant protein consisting of a mouse CR2-targeting moiety linked to mouse soluble Crry (sCrry), an inhibitor of C3 activation which is a structural and functional analog of human soluble CR1 (sCR1).	gene_phenotype
72037	1	334237	11	NULL	NULL	0	NULL	Xpo1p	GP		Exports		 Nuclear			SRP-RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_167	11352936	The Nuclear Export of the SRP-RNA Is Distinct from mRNA Export and Mediated by Xpo1p   o identify the nuclear export route of scR1, we localized SRP-RNA in strains with an impaired Ran cycle, i.e., the above mentioned  rna1-1 and  prp20-1 mutant cells ( Aebi et al. 1990   ;   Corbett et al. 1995   ).	gene_phenotype
72038	2	334237	11	NULL	NULL	0	NULL	SRP-RNA export	Process	Nuclear	 Is Distinct from					mRNA Export	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_167	11352936	The Nuclear Export of the SRP-RNA Is Distinct from mRNA Export and Mediated by Xpo1p   o identify the nuclear export route of scR1, we localized SRP-RNA in strains with an impaired Ran cycle, i.e., the above mentioned  rna1-1 and  prp20-1 mutant cells ( Aebi et al. 1990   ;   Corbett et al. 1995   ).	gene_phenotype
72044	1	334239	11	NULL	NULL	NULL	NULL	Nucleolar factors	GP		stimulates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_309	11352936	Nucleolar factors, or even scR1 or the rRNA nascent transcripts themselves, respectively, may facilitate the release of cargo destined for this compartment, similar to the stimulated release of the yeast protein Npl3p from its nuclear import receptor Mtr10p through RNA binding ( Senger et al. 1998   ).	gene_phenotype
72045	2	334239	11	NULL	NULL	0	NULL	Mtr10p	GP		is a type of 					nuclear import receptor	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_309	11352936	Nucleolar factors, or even scR1 or the rRNA nascent transcripts themselves, respectively, may facilitate the release of cargo destined for this compartment, similar to the stimulated release of the yeast protein Npl3p from its nuclear import receptor Mtr10p through RNA binding ( Senger et al. 1998   ).	gene_phenotype
72046	3	334239	11	NULL	NULL	NULL	NULL	Npl3p protein	GP	yeast	released from					Mtr10p	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_309	11352936	Nucleolar factors, or even scR1 or the rRNA nascent transcripts themselves, respectively, may facilitate the release of cargo destined for this compartment, similar to the stimulated release of the yeast protein Npl3p from its nuclear import receptor Mtr10p through RNA binding ( Senger et al. 1998   ).	gene_phenotype
72047	4	334239	11	NULL	NULL	0	NULL	statement 3	Process		occurs through					RNA binding	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_309	11352936	Nucleolar factors, or even scR1 or the rRNA nascent transcripts themselves, respectively, may facilitate the release of cargo destined for this compartment, similar to the stimulated release of the yeast protein Npl3p from its nuclear import receptor Mtr10p through RNA binding ( Senger et al. 1998   ).	gene_phenotype
72048	5	334239	11	NULL	NULL	0	NULL	scR1	GP		stimulates					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_309	11352936	Nucleolar factors, or even scR1 or the rRNA nascent transcripts themselves, respectively, may facilitate the release of cargo destined for this compartment, similar to the stimulated release of the yeast protein Npl3p from its nuclear import receptor Mtr10p through RNA binding ( Senger et al. 1998   ).	gene_phenotype
72049	6	334239	11	NULL	NULL	0	NULL	rRNA	NucleicAcid	nascent transcripts	stimulates					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_309	11352936	Nucleolar factors, or even scR1 or the rRNA nascent transcripts themselves, respectively, may facilitate the release of cargo destined for this compartment, similar to the stimulated release of the yeast protein Npl3p from its nuclear import receptor Mtr10p through RNA binding ( Senger et al. 1998   ).	gene_phenotype
72050	7	334239	11	NULL	NULL	0	NULL	Nucleolar factors	GP		release		may			cargo	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_309	11352936	Nucleolar factors, or even scR1 or the rRNA nascent transcripts themselves, respectively, may facilitate the release of cargo destined for this compartment, similar to the stimulated release of the yeast protein Npl3p from its nuclear import receptor Mtr10p through RNA binding ( Senger et al. 1998   ).	gene_phenotype
72051	8	334239	11	NULL	NULL	0	NULL	scR1	GP		releases		may			cargo	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_309	11352936	Nucleolar factors, or even scR1 or the rRNA nascent transcripts themselves, respectively, may facilitate the release of cargo destined for this compartment, similar to the stimulated release of the yeast protein Npl3p from its nuclear import receptor Mtr10p through RNA binding ( Senger et al. 1998   ).	gene_phenotype
72053	9	334239	11	NULL	NULL	0	NULL	rRNA	NucleicAcid	nascent transcripts	release		may			cargo	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_153_4_745_s_309	11352936	Nucleolar factors, or even scR1 or the rRNA nascent transcripts themselves, respectively, may facilitate the release of cargo destined for this compartment, similar to the stimulated release of the yeast protein Npl3p from its nuclear import receptor Mtr10p through RNA binding ( Senger et al. 1998   ).	gene_phenotype
72091	1	334252	11	NULL	NULL	NULL	NULL	GLFs	GP	L. major;;C. neoformans	encoded					UGM	GP	 activity			NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_6_1147_s_142	15947206	UGM activity of  L. major and  C. neoformans GLFs.  To confirm directly that candidate  GLFs encoded UGM activity, we first expressed high levels of protein in  E. coli using the pET3a system.	gene_phenotype
72092	1	334253	11	NULL	NULL	0	NULL	mutS	GP	T. aquaticus	increases					spontaneous mutation	Process	frequency			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_9_5040_s_124	8617781	Whereas the pET3a vector alone yielded a mutation  frequency similar to that of the host  E. coli  BL21, the  presence of  T. aquaticus mutS  resulted in a 14.3-fold increase  in the frequency of spontaneous mutation.	gene_phenotype
72093	1	334266	11	NULL	NULL	0	NULL	thioredoxin	GP		is					trx	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_24_14061_s_123	10570198	rPfCHT1 was expressed as a thioredoxin (trx) fusion protein in the expression plasmid pET32b by using as host cells the  E. coli mutant nonreducing strain AD494, which allows for intracytoplasmic formation of disulfide bonds.	gene_phenotype
72094	2	334266	11	NULL	NULL	0	NULL	thioredoxin	GP		is a type of 					 fusion protein	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_24_14061_s_123	10570198	rPfCHT1 was expressed as a thioredoxin (trx) fusion protein in the expression plasmid pET32b by using as host cells the  E. coli mutant nonreducing strain AD494, which allows for intracytoplasmic formation of disulfide bonds.	gene_phenotype
72095	3	334266	11	NULL	NULL	0	NULL	rPfCHT1	GP		expressed as					thioredoxin	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_24_14061_s_123	10570198	rPfCHT1 was expressed as a thioredoxin (trx) fusion protein in the expression plasmid pET32b by using as host cells the  E. coli mutant nonreducing strain AD494, which allows for intracytoplasmic formation of disulfide bonds.	gene_phenotype
72096	1	334270	11	NULL	NULL	NULL	NULL	paraxanthine	Chemical		convert to					caffeine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_febslett_534_1_75_s_170	12527364	Although recombinant CtCS7 was produced in  E. coli soluble extract, only the thioredoxin (Trx) fusion protein from the pET32a system had weak activity to convert paraxanthine to caffeine in this assay system.	gene_phenotype
72097	2	334270	11	NULL	NULL	0	NULL	 thioredoxin	GP		has activity to 					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_534_1_75_s_170	12527364	Although recombinant CtCS7 was produced in  E. coli soluble extract, only the thioredoxin (Trx) fusion protein from the pET32a system had weak activity to convert paraxanthine to caffeine in this assay system.	gene_phenotype
72098	3	334270	11	NULL	NULL	0	NULL	 thioredoxin	GP		is					Trx	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_534_1_75_s_170	12527364	Although recombinant CtCS7 was produced in  E. coli soluble extract, only the thioredoxin (Trx) fusion protein from the pET32a system had weak activity to convert paraxanthine to caffeine in this assay system.	gene_phenotype
72099	4	334270	11	NULL	NULL	0	NULL	thioredoxin	GP		is a type of 					fusion protein	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_534_1_75_s_170	12527364	Although recombinant CtCS7 was produced in  E. coli soluble extract, only the thioredoxin (Trx) fusion protein from the pET32a system had weak activity to convert paraxanthine to caffeine in this assay system.	gene_phenotype
72100	1	334273	11	NULL	NULL	0	NULL	RepA protein	GP		binds to		specifically			oriV DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_15_5003_s_260	15262938	A protein preparation generated in the same way as for His-tagged RepA but with  E. coli BL21 cells containing an empty expression vector (pET30a) showed no binding activity (not shown), implying that the RepA protein specifically binds to  oriV DNA.	gene_phenotype
72101	1	334275	11	NULL	NULL	0	NULL	ApaH protein	GP	S. Typhimurium	had the					enzymic activity	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32602_s_92	12824172	To confirm that the   S. Typhimurium ApaH and YgdP proteins had the enzymic activities  predicted from their sequences, they were cloned and expressed in  E.  coli BL21(DE3) cells: ApaH in pET15b as a His-tagged 33.6-kDa protein and  YgdP in pET32b as a His-tagged thioredoxin fusion protein of total mass 39.2  kDa.	gene_phenotype
72102	2	334275	11	NULL	NULL	NULL	NULL	YgdP protein	GP	S. Typhimurium	had the					enzymic activity	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32602_s_92	12824172	To confirm that the   S. Typhimurium ApaH and YgdP proteins had the enzymic activities  predicted from their sequences, they were cloned and expressed in  E.  coli BL21(DE3) cells: ApaH in pET15b as a His-tagged 33.6-kDa protein and  YgdP in pET32b as a His-tagged thioredoxin fusion protein of total mass 39.2  kDa.	gene_phenotype
72103	1	334277	11	NULL	NULL	0	NULL	CRP1	GP	maize chloroplast	processing					petD RNA	NucleicAcid	chloroplast			NULL		0	NULL	NULL	NULL	gw60_pnas_99_16_10887_s_197	12136123	This hypothesis is supported by the involvement in RNA metabolism and/or translation of the very few PPR motif-containing proteins characterized so far: maize chloroplast CRP1, involved in chloroplast  petD RNA processing and  petD and  petA translation ( 37),  Chlamydomonas MCA1, required for the accumulation of the chloroplast  petA transcript ( 38), yeast PET309, required for the stability and translation of the  coxI mitochondrial mRNA ( 39), and  Drosophila BSF, which binds to and stabilizes the bicoid mRNA ( 40).	gene_phenotype
72104	2	334277	11	NULL	NULL	0	NULL	CRP1	GP	maize chloroplast	translate					petD	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_99_16_10887_s_197	12136123	This hypothesis is supported by the involvement in RNA metabolism and/or translation of the very few PPR motif-containing proteins characterized so far: maize chloroplast CRP1, involved in chloroplast  petD RNA processing and  petD and  petA translation ( 37),  Chlamydomonas MCA1, required for the accumulation of the chloroplast  petA transcript ( 38), yeast PET309, required for the stability and translation of the  coxI mitochondrial mRNA ( 39), and  Drosophila BSF, which binds to and stabilizes the bicoid mRNA ( 40).	gene_phenotype
72105	3	334277	11	NULL	NULL	0	NULL	CRP1	GP	maize chloroplast	translate					petA	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_99_16_10887_s_197	12136123	This hypothesis is supported by the involvement in RNA metabolism and/or translation of the very few PPR motif-containing proteins characterized so far: maize chloroplast CRP1, involved in chloroplast  petD RNA processing and  petD and  petA translation ( 37),  Chlamydomonas MCA1, required for the accumulation of the chloroplast  petA transcript ( 38), yeast PET309, required for the stability and translation of the  coxI mitochondrial mRNA ( 39), and  Drosophila BSF, which binds to and stabilizes the bicoid mRNA ( 40).	gene_phenotype
72106	4	334277	11	NULL	NULL	0	NULL	MCA1	GP	Chlamydomonas	accumulate					petA transcript	GP	chloroplast			NULL		0	NULL	NULL	NULL	gw60_pnas_99_16_10887_s_197	12136123	This hypothesis is supported by the involvement in RNA metabolism and/or translation of the very few PPR motif-containing proteins characterized so far: maize chloroplast CRP1, involved in chloroplast  petD RNA processing and  petD and  petA translation ( 37),  Chlamydomonas MCA1, required for the accumulation of the chloroplast  petA transcript ( 38), yeast PET309, required for the stability and translation of the  coxI mitochondrial mRNA ( 39), and  Drosophila BSF, which binds to and stabilizes the bicoid mRNA ( 40).	gene_phenotype
72107	5	334277	11	NULL	NULL	0	NULL	PET309	GP	yeast	stabilize 					coxI mRNA	NucleicAcid	mitochondrial 			NULL		0	NULL	NULL	NULL	gw60_pnas_99_16_10887_s_197	12136123	This hypothesis is supported by the involvement in RNA metabolism and/or translation of the very few PPR motif-containing proteins characterized so far: maize chloroplast CRP1, involved in chloroplast  petD RNA processing and  petD and  petA translation ( 37),  Chlamydomonas MCA1, required for the accumulation of the chloroplast  petA transcript ( 38), yeast PET309, required for the stability and translation of the  coxI mitochondrial mRNA ( 39), and  Drosophila BSF, which binds to and stabilizes the bicoid mRNA ( 40).	gene_phenotype
72108	6	334277	11	NULL	NULL	0	NULL	PET309	GP	yeast	translate					coxI mRNA	NucleicAcid	mitochondrial 			NULL		0	NULL	NULL	NULL	gw60_pnas_99_16_10887_s_197	12136123	This hypothesis is supported by the involvement in RNA metabolism and/or translation of the very few PPR motif-containing proteins characterized so far: maize chloroplast CRP1, involved in chloroplast  petD RNA processing and  petD and  petA translation ( 37),  Chlamydomonas MCA1, required for the accumulation of the chloroplast  petA transcript ( 38), yeast PET309, required for the stability and translation of the  coxI mitochondrial mRNA ( 39), and  Drosophila BSF, which binds to and stabilizes the bicoid mRNA ( 40).	gene_phenotype
72109	7	334277	11	NULL	NULL	0	NULL	BSF	GP	Drosophila 	binds to					bicoid mRNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_pnas_99_16_10887_s_197	12136123	This hypothesis is supported by the involvement in RNA metabolism and/or translation of the very few PPR motif-containing proteins characterized so far: maize chloroplast CRP1, involved in chloroplast  petD RNA processing and  petD and  petA translation ( 37),  Chlamydomonas MCA1, required for the accumulation of the chloroplast  petA transcript ( 38), yeast PET309, required for the stability and translation of the  coxI mitochondrial mRNA ( 39), and  Drosophila BSF, which binds to and stabilizes the bicoid mRNA ( 40).	gene_phenotype
72110	8	334277	11	NULL	NULL	0	NULL	BSF	GP	Drosophila	stabilizes					bicoid mRNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_pnas_99_16_10887_s_197	12136123	This hypothesis is supported by the involvement in RNA metabolism and/or translation of the very few PPR motif-containing proteins characterized so far: maize chloroplast CRP1, involved in chloroplast  petD RNA processing and  petD and  petA translation ( 37),  Chlamydomonas MCA1, required for the accumulation of the chloroplast  petA transcript ( 38), yeast PET309, required for the stability and translation of the  coxI mitochondrial mRNA ( 39), and  Drosophila BSF, which binds to and stabilizes the bicoid mRNA ( 40).	gene_phenotype
72111	1	334280	11	NULL	NULL	0	NULL	tlc1h strain	Cell		has					meiosis	Process	altered			NULL		0	NULL	NULL	NULL	gw60_embo_22_7_1688_s_138	12660174	The  tlc1h strain has altered meiosis.	gene_phenotype
72113	1	334289	11	NULL	NULL	0	NULL	TLC1	GP		is not required for		directly			telomeric silencing	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_355	9755194	Thus,  TLC1 is not directly required for telomeric silencing.	gene_phenotype
72114	1	334294	11	NULL	NULL	0	NULL	TLC1	GP		is not required for		normally 			telomeric silencing	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_538	9755194	Furthermore,  TLC1 interferes with the telomeric silencing factor when overexpressed, but  TLC1 is not normally required for its telomeric silencing function.	gene_phenotype
72115	1	334309	11	NULL	NULL	0	NULL	yku80	GP		suppresses					TLC1 overexpression	GP	on telomeric silencing			NULL		0	NULL	NULL	NULL	gw70_genesdev_17_19_2384_s_79	12975323	Isolation of a new  yku80 allele that suppresses the effect of  TLC1 overexpression on telomeric silencing.	gene_phenotype
72140	1	334311	11	NULL	NULL	0	NULL	slx8	GP	mutation	did not affect					telomere length	Chromosome	steady-state			NULL	TLC1+ cells	0	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_506_s_167	16428246	slx8 mutation did not affect steady-state telomere length in  TLC1+ cells.	gene_phenotype
72141	1	334312	11	NULL	NULL	0	NULL	 yKu70/80	GP		interacts with 		possibly			TLC1	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2090_s_28	15824061	These observations suggest that the interaction of yKu70/80 with TLC1 is important for maintaining the telomere length.	gene_phenotype
72142	2	334312	11	NULL	NULL	0	NULL	statement 1	Process		maintain					telomere length	Chromosome				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2090_s_28	15824061	These observations suggest that the interaction of yKu70/80 with TLC1 is important for maintaining the telomere length.	gene_phenotype
72143	1	334318	11	NULL	NULL	0	NULL	TLC1	GP		does not affect		directly			 telomeric silencing	Chromosome				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_360	9755194	TLC1 does not appear to play a direct role in telomeric silencing.	gene_phenotype
72144	1	334319	11	NULL	NULL	0	NULL	EST2	GP		affect 					telomere length	Chromosome				NULL		0	NULL	NULL	NULL	gw60_cell_99_7_723_s_25	10619426	In this  organism, over 25 genes affect telomere length in addition to  EST2 and  TLC1.	gene_phenotype
72145	2	334319	11	NULL	NULL	0	NULL	TLC1	GP		affects					telomere length	Chromosome				NULL		0	NULL	NULL	NULL	gw60_cell_99_7_723_s_25	10619426	In this  organism, over 25 genes affect telomere length in addition to  EST2 and  TLC1.	gene_phenotype
72146	1	334326	11	NULL	NULL	0	NULL	TLC1	GP	overexpression of	 restores					telomere length	Chromosome	wild-type			NULL	 mtr10delta mutant	0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_91	12167699	(B) Overexpression of  TLC1 restored wild-type telomere length in the  mtr10delta mutant.	gene_phenotype
72166	1	334332	11	NULL	NULL	0	NULL	TLC1	GP	overexpression 	shortens					telomere length	Chromosome				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_304	9755194	Only  TLC1 and  SIR4 overexpression had significant and reproducible effects of shortening telomere length, consistent with earlier reports for  TLC1 ( S INGER and GOTTSCHLING 1994   ).	gene_phenotype
72167	2	334332	11	NULL	NULL	0	NULL	SIR4	GP	overexpression of	shortens					telomere length	Chromosome				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_304	9755194	Only  TLC1 and  SIR4 overexpression had significant and reproducible effects of shortening telomere length, consistent with earlier reports for  TLC1 ( S INGER and GOTTSCHLING 1994   ).	gene_phenotype
72168	1	334334	11	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid		accumulates					TLC1	GP	mature form			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_172	11160879	Both the integrity of the Sm site on the TLC1 RNA and the presence of at least two of the Sm proteins are needed for accumulation of the mature form of TLC1 ( 16).	gene_phenotype
72169	2	334334	11	NULL	NULL	0	NULL	Sm proteins	GP		accumulates					 TLC1	GP	mature form			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_172	11160879	Both the integrity of the Sm site on the TLC1 RNA and the presence of at least two of the Sm proteins are needed for accumulation of the mature form of TLC1 ( 16).	gene_phenotype
72170	1	334335	11	NULL	NULL	0	NULL	tel1	GP	mutation	has synergistic effect on					telomere-DSB fusions	Process				NULL	tel1 tlc1 cells	0	NULL	NULL	NULL	gw60_molcell_11_5_1379_s_92	12769860	The  tel1 and  tlc1 mutations had a synergistic effect on telomere-DSB fusions, which occurred in greater than 1 in 103 genomes in  tel1 tlc1 cells.	gene_phenotype
72171	2	334335	11	NULL	NULL	0	NULL	tlc1	GP	mutation	has synergistic effect on					telomere-DSB fusion	Process				NULL	tel1 tlc1 cells	0	NULL	NULL	NULL	gw60_molcell_11_5_1379_s_92	12769860	The  tel1 and  tlc1 mutations had a synergistic effect on telomere-DSB fusions, which occurred in greater than 1 in 103 genomes in  tel1 tlc1 cells.	gene_phenotype
72172	1	334344	11	NULL	NULL	0	NULL	RAD52	GP	loss of	does not affect					telomere length	Chromosome				NULL	S. cerevisiae	0	NULL	NULL	NULL	gw70_genesdev_18_15_1781_s_199	15289453	Thus, while loss of  RAD52 or  RAD51 does not affect telomere length in  S. cerevisiae, rad52 tlc1, rad51 tlc1, or rad52 est1 double mutant cells senesce at a faster rate than  tlc1 or  est1 single mutants (Lundblad and Blackburn 1993 ;	gene_phenotype
72173	2	334344	11	NULL	NULL	0	NULL	RAD51	GP	loss of	does not affect					telomere length	Chromosome				NULL	S. cerevisiae	0	NULL	NULL	NULL	gw70_genesdev_18_15_1781_s_199	15289453	Thus, while loss of  RAD52 or  RAD51 does not affect telomere length in  S. cerevisiae, rad52 tlc1, rad51 tlc1, or rad52 est1 double mutant cells senesce at a faster rate than  tlc1 or  est1 single mutants (Lundblad and Blackburn 1993 ;	gene_phenotype
72192	1	334351	11	NULL	NULL	0	NULL	Ku	GP		binds					TLC1 RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_19_2384_s_101	12975323	The mutation might reduce Ku's ability to bind TLC1 RNA, or the mutation might enhance Ku's interactions with other silencing factors, leaving its ability to bind TLC1 RNA unchanged.	gene_phenotype
72193	2	334351	11	NULL	NULL	0	NULL	Ku	GP	mutation	reduces					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_19_2384_s_101	12975323	The mutation might reduce Ku's ability to bind TLC1 RNA, or the mutation might enhance Ku's interactions with other silencing factors, leaving its ability to bind TLC1 RNA unchanged.	gene_phenotype
72194	1	334352	11	NULL	NULL	0	NULL	Ku70/80	GP	budding yeast	interacts with					TLC1	GP			stem - loop region	NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2090_s_26	15824061	It has been shown in budding yeast that Ku70/80 (yKu70/80) interacts with a stem - loop region of TLC1, and yeast harboring a  yKu80 allele that is defective for TLC1 binding possesses shortened telomeres ( ).	gene_phenotype
72195	1	334357	11	NULL	NULL	0	NULL	TLC1	GP		is a type of 					telomerase RNA gene	GP				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_535	9755194	TLC1:   s described in our earlier work, overexpression of the telomerase RNA gene  TLC1 disrupts telomeric silencing specifically and causes shortening of the telomeric DNA tract ( S INGER and GOTTSCHLING 1994   ).	gene_phenotype
72196	2	334357	11	NULL	NULL	0	NULL	TLC1	GP	overexpression of	disrupts		specifically			telomeric silencing	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_535	9755194	TLC1:   s described in our earlier work, overexpression of the telomerase RNA gene  TLC1 disrupts telomeric silencing specifically and causes shortening of the telomeric DNA tract ( S INGER and GOTTSCHLING 1994   ).	gene_phenotype
72197	3	334357	11	NULL	NULL	0	NULL	TLC1	GP	overexpression of	shortens					telomeric DNA tract	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_535	9755194	TLC1:   s described in our earlier work, overexpression of the telomerase RNA gene  TLC1 disrupts telomeric silencing specifically and causes shortening of the telomeric DNA tract ( S INGER and GOTTSCHLING 1994   ).	gene_phenotype
72198	1	334358	11	NULL	NULL	0	NULL	TLC1	GP		 was not required for		directly 			silencing	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_536	9755194	In the present study, we found that  TLC1 was not directly required for silencing; strains without  TLC1 and with only half the normal length of telomeric DNA at the end of the chromosome were still silenced ( Table 3).	gene_phenotype
72199	1	334359	11	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid		interacting with					silencing factor	GP	telomere-specific			NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_537	9755194	From these results, we suggest that the loss of telomeric silencing when  TLC1 is overexpressed is not the consequence of telomere DNA shortening, but rather, that  TLC1 RNA is interacting with a telomere-specific silencing factor.	gene_phenotype
72200	2	334359	11	NULL	NULL	0	NULL	 TLC1	GP	overexpression of	leads to		possibly			telomeric silencing	Process	loss of			NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_537	9755194	From these results, we suggest that the loss of telomeric silencing when  TLC1 is overexpressed is not the consequence of telomere DNA shortening, but rather, that  TLC1 RNA is interacting with a telomere-specific silencing factor.	gene_phenotype
73131	3	334359	11	NULL	NULL	0	NULL	telomere DNA	NucleicAcid	shortening of	does not lead to					telomeric silencing	Process	loss of			NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_537	9755194	From these results, we suggest that the loss of telomeric silencing when  TLC1 is overexpressed is not the consequence of telomere DNA shortening, but rather, that  TLC1 RNA is interacting with a telomere-specific silencing factor.	gene_phenotype
73132	4	334359	11	NULL	NULL	0	NULL	statement 2	Process		is a consequence of					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_537	9755194	From these results, we suggest that the loss of telomeric silencing when  TLC1 is overexpressed is not the consequence of telomere DNA shortening, but rather, that  TLC1 RNA is interacting with a telomere-specific silencing factor.	gene_phenotype
72201	1	334361	11	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid		is a type of 					telomerase RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_currbiol_8_3_177_s_86	9443919	In yeast, the telomerase RNA  TLC1 and the Est1, Est2, Est3, and Est4/Cdc13 proteins are each essential for maintenance of telomere length  in vivo   [17-19]  , but only Est2 and  TLC1 are essential for telomerase activity in cell lysates    [8,20,21]  .	gene_phenotype
72202	2	334361	11	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid		maintain					telomere length	Chromosome				NULL	In yeast;;in vivo	0	NULL	NULL	NULL	gw60_currbiol_8_3_177_s_86	9443919	In yeast, the telomerase RNA  TLC1 and the Est1, Est2, Est3, and Est4/Cdc13 proteins are each essential for maintenance of telomere length  in vivo   [17-19]  , but only Est2 and  TLC1 are essential for telomerase activity in cell lysates    [8,20,21]  .	gene_phenotype
72203	3	334361	11	NULL	NULL	0	NULL	Est1 protein	GP		maintain					telomere length	Chromosome				NULL	In yeast;;in vivo	0	NULL	NULL	NULL	gw60_currbiol_8_3_177_s_86	9443919	In yeast, the telomerase RNA  TLC1 and the Est1, Est2, Est3, and Est4/Cdc13 proteins are each essential for maintenance of telomere length  in vivo   [17-19]  , but only Est2 and  TLC1 are essential for telomerase activity in cell lysates    [8,20,21]  .	gene_phenotype
72204	4	334361	11	NULL	NULL	0	NULL	Est2 protein	GP		maintain					telomere length	Chromosome				NULL	In yeast;;in vivo	0	NULL	NULL	NULL	gw60_currbiol_8_3_177_s_86	9443919	In yeast, the telomerase RNA  TLC1 and the Est1, Est2, Est3, and Est4/Cdc13 proteins are each essential for maintenance of telomere length  in vivo   [17-19]  , but only Est2 and  TLC1 are essential for telomerase activity in cell lysates    [8,20,21]  .	gene_phenotype
72205	5	334361	11	NULL	NULL	0	NULL	Est3 protein	GP		maintain					telomere length	Chromosome				NULL	In yeast;;in vivo	0	NULL	NULL	NULL	gw60_currbiol_8_3_177_s_86	9443919	In yeast, the telomerase RNA  TLC1 and the Est1, Est2, Est3, and Est4/Cdc13 proteins are each essential for maintenance of telomere length  in vivo   [17-19]  , but only Est2 and  TLC1 are essential for telomerase activity in cell lysates    [8,20,21]  .	gene_phenotype
72206	6	334361	11	NULL	NULL	0	NULL	Est4/Cdc13 protein	GP		maintain					telomere length	Chromosome				NULL	In yeast;;in vivo	0	NULL	NULL	NULL	gw60_currbiol_8_3_177_s_86	9443919	In yeast, the telomerase RNA  TLC1 and the Est1, Est2, Est3, and Est4/Cdc13 proteins are each essential for maintenance of telomere length  in vivo   [17-19]  , but only Est2 and  TLC1 are essential for telomerase activity in cell lysates    [8,20,21]  .	gene_phenotype
72207	7	334361	11	NULL	NULL	0	NULL	Est2	GP		activates					 telomerase	GP				NULL	 in cell lysates	0	NULL	NULL	NULL	gw60_currbiol_8_3_177_s_86	9443919	In yeast, the telomerase RNA  TLC1 and the Est1, Est2, Est3, and Est4/Cdc13 proteins are each essential for maintenance of telomere length  in vivo   [17-19]  , but only Est2 and  TLC1 are essential for telomerase activity in cell lysates    [8,20,21]  .	gene_phenotype
72208	8	334361	11	NULL	NULL	0	NULL	TLC1 	GP		activates					telomerase	GP				NULL	 in cell lysates	0	NULL	NULL	NULL	gw60_currbiol_8_3_177_s_86	9443919	In yeast, the telomerase RNA  TLC1 and the Est1, Est2, Est3, and Est4/Cdc13 proteins are each essential for maintenance of telomere length  in vivo   [17-19]  , but only Est2 and  TLC1 are essential for telomerase activity in cell lysates    [8,20,21]  .	gene_phenotype
72209	1	334364	11	NULL	NULL	0	NULL	dnl4	GP	mutation	suppress		completely			telomere-DSB fusions	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1379_s_142	12769860	Unlike the  dnl4 mutation,  exo1 did not completely suppress telomere-DSB fusions, whose frequency was significantly greater in  exo1 tlc1 and  exo1 tel1 tlc1 than in completely wild-type cells   (Figure 2E).	gene_phenotype
72210	2	334364	11	NULL	NULL	0	NULL	exo1	GP		did not suppress		completely 			telomere-DSB fusions	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1379_s_142	12769860	Unlike the  dnl4 mutation,  exo1 did not completely suppress telomere-DSB fusions, whose frequency was significantly greater in  exo1 tlc1 and  exo1 tel1 tlc1 than in completely wild-type cells   (Figure 2E).	gene_phenotype
72211	1	334372	11	NULL	NULL	0	NULL	TLC1	GP		encodes					telomerase	NucleicAcid	RNA subunit			NULL		0	NULL	NULL	NULL	gw70_annurevgenet_34_0_331_s_1049	11092831	Interactions of TLC1 (which encodes  the RNA subunit of telomerase), TEL1, and MEC1 in regulating telomere length in the  yeast  Saccharomyces cerevisiae.	gene_phenotype
73133	2	334372	11	NULL	NULL	0	NULL	TLC1	GP	interaction of	regulates					telomere	Chromosome	length of			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw70_annurevgenet_34_0_331_s_1049	11092831	Interactions of TLC1 (which encodes  the RNA subunit of telomerase), TEL1, and MEC1 in regulating telomere length in the  yeast  Saccharomyces cerevisiae.	gene_phenotype
73134	3	334372	11	NULL	NULL	0	NULL	TEL1	GP	interaction of	regulates					telomere	Chromosome	length of			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw70_annurevgenet_34_0_331_s_1049	11092831	Interactions of TLC1 (which encodes  the RNA subunit of telomerase), TEL1, and MEC1 in regulating telomere length in the  yeast  Saccharomyces cerevisiae.	gene_phenotype
73135	4	334372	11	NULL	NULL	0	NULL	MEC1	GP	interaction of	regulates					telomere	Chromosome	length of			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw70_annurevgenet_34_0_331_s_1049	11092831	Interactions of TLC1 (which encodes  the RNA subunit of telomerase), TEL1, and MEC1 in regulating telomere length in the  yeast  Saccharomyces cerevisiae.	gene_phenotype
72212	1	334374	11	NULL	NULL	0	NULL	EST2 gene	GP	S.cerevisiae	activates					telomerase	GP				NULL	in vivo	0	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_407_s_15	16418502	In budding yeast  S.cerevisiae, at least five genes,  EST2,  TLC1,  EST1,  EST3 and  CDC13, are required for telomerase activity  in vivo.	gene_phenotype
72213	2	334374	11	NULL	NULL	0	NULL	TLC1 gene	GP	S.cerevisiae	activates					telomerase	GP				NULL	in vivo	0	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_407_s_15	16418502	In budding yeast  S.cerevisiae, at least five genes,  EST2,  TLC1,  EST1,  EST3 and  CDC13, are required for telomerase activity  in vivo.	gene_phenotype
72214	3	334374	11	NULL	NULL	0	NULL	EST1 gene	GP	S. cerevisiae	activates					telomerase	GP				NULL	in vivo	0	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_407_s_15	16418502	In budding yeast  S.cerevisiae, at least five genes,  EST2,  TLC1,  EST1,  EST3 and  CDC13, are required for telomerase activity  in vivo.	gene_phenotype
72215	4	334374	11	NULL	NULL	0	NULL	EST3 gene	GP	S. cerevisiae	activates					telomerase	GP				NULL	in vivo	0	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_407_s_15	16418502	In budding yeast  S.cerevisiae, at least five genes,  EST2,  TLC1,  EST1,  EST3 and  CDC13, are required for telomerase activity  in vivo.	gene_phenotype
72216	5	334374	11	NULL	NULL	0	NULL	CDC13 gene	GP	S. cerevisiae	activates					telomerase	GP				NULL	in vivo	0	NULL	NULL	NULL	gw70_nucleicacidsres_34_2_407_s_15	16418502	In budding yeast  S.cerevisiae, at least five genes,  EST2,  TLC1,  EST1,  EST3 and  CDC13, are required for telomerase activity  in vivo.	gene_phenotype
72217	1	334381	11	NULL	NULL	0	NULL	Cdc13p	GP		is a type of 					telomeric component	Chromosome				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_4_1623_s_254	14742705	Hence, mutations of a telomeric component, Cdc13p, other than in the  TLC1 template also lead to a chromosome segregation defect.	gene_phenotype
72218	2	334381	11	NULL	NULL	NULL	NULL	Cdc13p	GP	mutations	leads to					chromosome segregation	Process	defective			NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_4_1623_s_254	14742705	Hence, mutations of a telomeric component, Cdc13p, other than in the  TLC1 template also lead to a chromosome segregation defect.	gene_phenotype
72219	1	334384	11	NULL	NULL	0	NULL	Ku	GP		regulates					telomere length	Chromosome				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_22_8202_s_270	14585978	Ku regulates telomere length, in part, via an interaction with a stem-loop structure present in TLC1, the telomerase RNA subunit ( ,  ).	gene_phenotype
72220	2	334384	11	NULL	NULL	0	NULL	Ku	GP		interacts with 					TLC1	GP			stem-loop	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_22_8202_s_270	14585978	Ku regulates telomere length, in part, via an interaction with a stem-loop structure present in TLC1, the telomerase RNA subunit ( ,  ).	gene_phenotype
72221	3	334384	11	NULL	NULL	0	NULL	statement 2	Process		leads to		partially			statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_22_8202_s_270	14585978	Ku regulates telomere length, in part, via an interaction with a stem-loop structure present in TLC1, the telomerase RNA subunit ( ,  ).	gene_phenotype
72222	1	334386	11	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid	Saccharomyces	binds to					Sm protein	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_272	12458198	In contrast, the  Saccharomyces TLC1 RNA is bound by Sm proteins and requires the same proteins for accumulation ( ).	gene_phenotype
72223	2	334386	11	NULL	NULL	0	NULL	statement 1	Process		is required for 					accumulation	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_272	12458198	In contrast, the  Saccharomyces TLC1 RNA is bound by Sm proteins and requires the same proteins for accumulation ( ).	gene_phenotype
72224	1	334387	11	NULL	NULL	0	NULL	Tlc1	GP	yeast	is a type of 					telomerase	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_102_32_11290_s_202	16040803	More relevant to our studies, Mtr10 was implicated in nuclear import of the RNA component of yeast telomerase, Tlc1 ( ).	gene_phenotype
72225	2	334387	11	NULL	NULL	0	NULL	Mtr10	GP		import		nuclear			Tlc1	GP	RNA component			NULL		0	NULL	NULL	NULL	gw70_pnas_102_32_11290_s_202	16040803	More relevant to our studies, Mtr10 was implicated in nuclear import of the RNA component of yeast telomerase, Tlc1 ( ).	gene_phenotype
72226	1	334388	11	NULL	NULL	0	NULL	 TLC1	GP		encodes					telomerase	GP	RNA subunit of			NULL		0	NULL	NULL	NULL	gw60_genesdev_15_14_1845_s_528	11459833	Interactions of  TLC1 (which encodes the RNA subunit of telomerase),  TEL1, and  MEC1 in regulating telomere length in the yeast  Saccharomyces cerevisiae.	gene_phenotype
72227	2	334388	11	NULL	NULL	NULL	NULL	TLC1	GP	Interactions of 	 regulate					telomere	Chromosome	length of			NULL	Saccharomyces cerevisiae	NULL	NULL	NULL	NULL	gw60_genesdev_15_14_1845_s_528	11459833	Interactions of  TLC1 (which encodes the RNA subunit of telomerase),  TEL1, and  MEC1 in regulating telomere length in the yeast  Saccharomyces cerevisiae.	gene_phenotype
72228	3	334388	11	NULL	NULL	NULL	NULL	TEL1	GP	interaction of	regulate					telomere	Chromosome	length of			NULL	Saccharomyces cerevisiae	NULL	NULL	NULL	NULL	gw60_genesdev_15_14_1845_s_528	11459833	Interactions of  TLC1 (which encodes the RNA subunit of telomerase),  TEL1, and  MEC1 in regulating telomere length in the yeast  Saccharomyces cerevisiae.	gene_phenotype
72229	4	334388	11	NULL	NULL	NULL	NULL	MEC1	GP	interaction of	regulate					telomere	Chromosome	length of			NULL	Saccharomyces cerevisiae	NULL	NULL	NULL	NULL	gw60_genesdev_15_14_1845_s_528	11459833	Interactions of  TLC1 (which encodes the RNA subunit of telomerase),  TEL1, and  MEC1 in regulating telomere length in the yeast  Saccharomyces cerevisiae.	gene_phenotype
72230	1	334389	11	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid		influence		possibly			telomere clustering	Process	at the nuclear periphery			NULL		0	NULL	NULL	NULL	gw60_genetics_160_1_49_s_373	11805044	The possibility that  TLC1 RNA might also influence telomere clustering and/or localization at the nuclear periphery remains to be investigated.	gene_phenotype
72231	2	334389	11	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid		influence					localization	Process	at the nuclear periphery			NULL		0	NULL	NULL	NULL	gw60_genetics_160_1_49_s_373	11805044	The possibility that  TLC1 RNA might also influence telomere clustering and/or localization at the nuclear periphery remains to be investigated.	gene_phenotype
72232	1	334393	11	10	NULL	NULL	NULL	SIR4	GP	overexpression of	disrupts					telomeric silencing	Process				NULL		NULL	NULL	NULL	NULL	gw60_genetics_150_2_613_s_239	9755194	Overexpression of clones containing  SIR4,  DOT1,  TLC1,  ASF1,  DNA2, and  DOT4 each had a strong effect of disrupting telomeric silencing.	gene_phenotype
72233	2	334393	11	NULL	NULL	NULL	NULL	DOT1	GP	overexpression of	disrupts					telomeric silencing	Process				NULL		NULL	NULL	NULL	NULL	gw60_genetics_150_2_613_s_239	9755194	Overexpression of clones containing  SIR4,  DOT1,  TLC1,  ASF1,  DNA2, and  DOT4 each had a strong effect of disrupting telomeric silencing.	gene_phenotype
72234	3	334393	11	NULL	NULL	0	NULL	TLC1	GP	overexpression of	disrupts					telomeric silencing	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_239	9755194	Overexpression of clones containing  SIR4,  DOT1,  TLC1,  ASF1,  DNA2, and  DOT4 each had a strong effect of disrupting telomeric silencing.	gene_phenotype
72235	4	334393	11	NULL	NULL	0	NULL	ASF1	GP	Overexpression of	disrupts					telomeric silencing	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_239	9755194	Overexpression of clones containing  SIR4,  DOT1,  TLC1,  ASF1,  DNA2, and  DOT4 each had a strong effect of disrupting telomeric silencing.	gene_phenotype
72236	5	334393	11	NULL	NULL	0	NULL	DNA2	GP	overexpression of	disrupts					telomeric silencing	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_239	9755194	Overexpression of clones containing  SIR4,  DOT1,  TLC1,  ASF1,  DNA2, and  DOT4 each had a strong effect of disrupting telomeric silencing.	gene_phenotype
72237	6	334393	11	NULL	NULL	0	NULL	DOT4	GP	overexpression of	disrupts					telomeric silencing	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_239	9755194	Overexpression of clones containing  SIR4,  DOT1,  TLC1,  ASF1,  DNA2, and  DOT4 each had a strong effect of disrupting telomeric silencing.	gene_phenotype
72238	1	334394	11	NULL	NULL	0	NULL	TLC1 gene	GP	overexpression of	regulate					telomere length	Chromosome				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_306	9755194	Thus, overexpression of only three  DOT genes,  TLC1,  SIR4, and  DOT5, affected telomere length regulation and telomeric silencing.	gene_phenotype
72239	2	334394	11	NULL	NULL	0	NULL	TLC1 gene	GP	overexpression of	affects					telomeric silencing	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_306	9755194	Thus, overexpression of only three  DOT genes,  TLC1,  SIR4, and  DOT5, affected telomere length regulation and telomeric silencing.	gene_phenotype
72240	3	334394	11	NULL	NULL	0	NULL	SIR4 gene	GP	overexpression of	regulate					telomere length	Chromosome				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_306	9755194	Thus, overexpression of only three  DOT genes,  TLC1,  SIR4, and  DOT5, affected telomere length regulation and telomeric silencing.	gene_phenotype
72241	4	334394	11	NULL	NULL	0	NULL	SIR4 gene	GP	overexpression of	affects					telomeric silencing	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_306	9755194	Thus, overexpression of only three  DOT genes,  TLC1,  SIR4, and  DOT5, affected telomere length regulation and telomeric silencing.	gene_phenotype
72242	5	334394	11	NULL	NULL	0	NULL	DOT5 gene	GP	overexpression of	regulate					telomere length	Chromosome				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_306	9755194	Thus, overexpression of only three  DOT genes,  TLC1,  SIR4, and  DOT5, affected telomere length regulation and telomeric silencing.	gene_phenotype
72243	6	334394	11	NULL	NULL	0	NULL	DOT5 gene	GP	overexpression of	affects					telomeric silencing	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_306	9755194	Thus, overexpression of only three  DOT genes,  TLC1,  SIR4, and  DOT5, affected telomere length regulation and telomeric silencing.	gene_phenotype
72244	7	334394	11	NULL	NULL	0	NULL	TLC1	GP		is a type of 					DOT gene	GP				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_306	9755194	Thus, overexpression of only three  DOT genes,  TLC1,  SIR4, and  DOT5, affected telomere length regulation and telomeric silencing.	gene_phenotype
72245	8	334394	11	NULL	NULL	0	NULL	SIR4	GP		is a type of 					DOT gene	GP				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_306	9755194	Thus, overexpression of only three  DOT genes,  TLC1,  SIR4, and  DOT5, affected telomere length regulation and telomeric silencing.	gene_phenotype
72246	9	334394	11	NULL	NULL	0	NULL	DOT5	GP		is a type of 					DOT genes	GP				NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_306	9755194	Thus, overexpression of only three  DOT genes,  TLC1,  SIR4, and  DOT5, affected telomere length regulation and telomeric silencing.	gene_phenotype
72247	1	334395	11	NULL	NULL	NULL	NULL	TLC1 	GP		encodes					template RNA	NucleicAcid				NULL	Saccharomyces cerevisiae	NULL	NULL	NULL	NULL	gw60_genetics_162_3_1101_s_19	12454059	In the budding yeast  Saccharomyces cerevisiae, the template RNA and the catalytic subunit are encoded by  TLC1 and  EST2, respectively ( S INGER and GOTTSCHLING 1994   ;	gene_phenotype
72248	2	334395	11	NULL	NULL	0	NULL	EST2	GP		encodes					catalytic subunit	GP				NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_genetics_162_3_1101_s_19	12454059	In the budding yeast  Saccharomyces cerevisiae, the template RNA and the catalytic subunit are encoded by  TLC1 and  EST2, respectively ( S INGER and GOTTSCHLING 1994   ;	gene_phenotype
73136	1	334401	11	NULL	NULL	0	NULL	Smd1 protein	GP		co-immunoprecipitates with					TLC1 RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_nature_401_6749_177_s_55	10490028	Figure 3  HA-tagged Smd1 protein co-immunoprecipitates  TLC1 RNA and  in vitro telomerase activity.	gene_phenotype
72249	1	334409	11	NULL	NULL	0	NULL	GGA	GP		co localize with					TGN46	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_6_2385_s_388	12808037	We find that GGAs and p56 show good  colocalization with the TGN marker TGN46, as well as with other proteins  associated with the Golgi stack ( Figure 4,  g - i; our unpublished observations).	gene_phenotype
72250	2	334409	11	NULL	NULL	0	NULL	p56 	GP		co localize with					TGN46	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_6_2385_s_388	12808037	We find that GGAs and p56 show good  colocalization with the TGN marker TGN46, as well as with other proteins  associated with the Golgi stack ( Figure 4,  g - i; our unpublished observations).	gene_phenotype
72251	3	334409	11	NULL	NULL	0	NULL	TGN46	GP		is a type of 					TGN marker	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_6_2385_s_388	12808037	We find that GGAs and p56 show good  colocalization with the TGN marker TGN46, as well as with other proteins  associated with the Golgi stack ( Figure 4,  g - i; our unpublished observations).	gene_phenotype
72252	1	334415	11	NULL	NULL	0	NULL	TLC1	GP		encodes					telomerase	GP	RNA component			NULL	yeast	0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_16	10454554	In yeast, the RNA component of telomerase is encoded by  TLC1 ( 33), and the protein component with reverse transcriptase activity is encoded by  EST2 ( 16).	gene_phenotype
72253	2	334415	11	NULL	NULL	0	NULL	EST2	GP		encodes					telomerase	GP	protein component			NULL	yeast	0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_16	10454554	In yeast, the RNA component of telomerase is encoded by  TLC1 ( 33), and the protein component with reverse transcriptase activity is encoded by  EST2 ( 16).	gene_phenotype
72254	1	334417	11	NULL	NULL	0	NULL	Est1 protein	GP		coimmunoprecipitates with					Tlc1	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_6_1947_s_4	10688642	We previously showed that Est1 protein coimmunoprecipitates with Tlc1 (the telomerase RNA) as well as with telomerase activity.	gene_phenotype
72255	1	334425	11	NULL	NULL	0	NULL	Mtr10p	GP		functions in					nucleocytoplasmic transport	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_282	12167699	Because Mtr10p functions in nucleocytoplasmic transport, we used RNA FISH to ask whether Tlc1 localization was abnormal in  mtr10 mutants.	gene_phenotype
72256	1	334427	11	NULL	NULL	0	NULL	TLC1 gene	GP		encodes					telomerase RNA subunit	NucleicAcid				NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_molcellbiol_22_7_2366_s_11	11884619	In the budding yeast  Saccharomyces cerevisiae, the telomerase RNA subunit is approximately 1.3 kb and is encoded by the  TLC1 gene ( 38).	gene_phenotype
72258	1	334440	11	NULL	NULL	0	NULL	C3TA2 telomere	Chromosome		did not impair					chromosome stability	Process				NULL		0	NULL	NULL	NULL	gw70_embo_22_7_1688_s_216	12660174	Although the C3TA2 telomere did not impair chromosome stability, meiosis was compromised in the  tlc1h strain, as demonstrated by a paucity of four spore tetrads ( Figure 4B).	gene_phenotype
72260	2	334440	11	NULL	NULL	0	NULL	C3TA2 telomere	Chromosome		compromised					meiosis	Process				NULL	tlc1h strain	0	NULL	NULL	NULL	gw70_embo_22_7_1688_s_216	12660174	Although the C3TA2 telomere did not impair chromosome stability, meiosis was compromised in the  tlc1h strain, as demonstrated by a paucity of four spore tetrads ( Figure 4B).	gene_phenotype
72262	1	334441	11	NULL	NULL	0	NULL	Rap1	GP		is required for					meiosis	Process	efficient			NULL	S.pombe	0	NULL	NULL	NULL	gw70_embo_22_7_1688_s_217	12660174	Because Rap1 is required for efficient meiosis in  S.pombe ( ;  ), it is tempting to speculate that the meiotic defect of the  tlc1h strain is due to the lack of Rap1p at the C3TA2 telomere.	gene_phenotype
75851	1	334443	11	NULL	NULL	0	NULL	 C3TA2 telomere	GP		did not impair					chromosome stability	Process				NULL		0	NULL	NULL	NULL	gw60_embo_22_7_1688_s_213	12660174	Although the C3TA2 telomere did not impair chromosome stability, meiosis was compromised in the  tlc1h strain, as demonstrated by a paucity of four spore tetrads (Figure  4B).	gene_phenotype
75852	2	334443	11	NULL	NULL	0	NULL	tlc1h strain	Organism		compromised					meiosis	Process				NULL		0	NULL	NULL	NULL	gw60_embo_22_7_1688_s_213	12660174	Although the C3TA2 telomere did not impair chromosome stability, meiosis was compromised in the  tlc1h strain, as demonstrated by a paucity of four spore tetrads (Figure  4B).	gene_phenotype
72289	1	334444	11	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid	high levels of 	negatively affect		may			 Ku	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_19_2384_s_77	12975323	We reasoned that if high levels of TLC1 RNA negatively affect Ku, then it might be possible to identify alleles of Ku that would suppress the effects of  TLC1 overexpression and give rise to colonies that maintain telomeric silencing (i.e., remain pink and Ura-).	gene_phenotype
72294	1	334446	11	NULL	NULL	NULL	NULL	TLC1	GP		is a synonym of					telomerase RNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8729_s_250	14612413	In  S. cerevisiae, a mutation in the template domain of telomerase RNA,  TLC1, termed  tlc1- C476G, which reduces Rap1p in vitro binding affinity to the telomeric repeats by 300-fold, results in an increase in telomere length in a manner similar to that observed in  K. lactis ter1- Acc ( ) (Fig.  5, compare lanes 2 and 3 to lane 1).	gene_phenotype
72297	2	334446	11	NULL	NULL	0	NULL	Rap1p	GP	in vitro	binds to					 telomeric repeats	Chromosome				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8729_s_250	14612413	In  S. cerevisiae, a mutation in the template domain of telomerase RNA,  TLC1, termed  tlc1- C476G, which reduces Rap1p in vitro binding affinity to the telomeric repeats by 300-fold, results in an increase in telomere length in a manner similar to that observed in  K. lactis ter1- Acc ( ) (Fig.  5, compare lanes 2 and 3 to lane 1).	gene_phenotype
73137	3	334446	11	NULL	NULL	NULL	NULL	TLC1	GP	mutation of	is termed as				template domain	tlc1- C476G	GP				NULL	S. cerevisiae	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8729_s_250	14612413	In  S. cerevisiae, a mutation in the template domain of telomerase RNA,  TLC1, termed  tlc1- C476G, which reduces Rap1p in vitro binding affinity to the telomeric repeats by 300-fold, results in an increase in telomere length in a manner similar to that observed in  K. lactis ter1- Acc ( ) (Fig.  5, compare lanes 2 and 3 to lane 1).	gene_phenotype
73138	4	334446	11	NULL	NULL	NULL	NULL	Rap1p	GP		bind					telomeric repeats	GP				NULL	S. cerevisiae;;in vitro	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8729_s_250	14612413	In  S. cerevisiae, a mutation in the template domain of telomerase RNA,  TLC1, termed  tlc1- C476G, which reduces Rap1p in vitro binding affinity to the telomeric repeats by 300-fold, results in an increase in telomere length in a manner similar to that observed in  K. lactis ter1- Acc ( ) (Fig.  5, compare lanes 2 and 3 to lane 1).	gene_phenotype
73139	5	334446	11	NULL	NULL	0	NULL	tlc1- C476G	GP		reduces					statement 3	GP	affinity of			NULL	S. cerevisiae	0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8729_s_250	14612413	In  S. cerevisiae, a mutation in the template domain of telomerase RNA,  TLC1, termed  tlc1- C476G, which reduces Rap1p in vitro binding affinity to the telomeric repeats by 300-fold, results in an increase in telomere length in a manner similar to that observed in  K. lactis ter1- Acc ( ) (Fig.  5, compare lanes 2 and 3 to lane 1).	gene_phenotype
73140	6	334446	11	NULL	NULL	0	NULL	statement 4	GP		increases					telomere	Chromosome	length of			NULL	S. cerevisiae	0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8729_s_250	14612413	In  S. cerevisiae, a mutation in the template domain of telomerase RNA,  TLC1, termed  tlc1- C476G, which reduces Rap1p in vitro binding affinity to the telomeric repeats by 300-fold, results in an increase in telomere length in a manner similar to that observed in  K. lactis ter1- Acc ( ) (Fig.  5, compare lanes 2 and 3 to lane 1).	gene_phenotype
72304	1	334453	11	NULL	NULL	0	NULL	TR subunit TLC1	GP	overexpression of 	increases					telomerase activity	Process				NULL	budding yeast;;in cell extracts	0	NULL	NULL	NULL	gw70_embo_25_3_565_s_56	16424902	In budding yeast, overexpression of the TR subunit TLC1 together with the TERT subunit  Est2p also results in higher telomerase activity levels in cell extracts (  et al).	gene_phenotype
72305	2	334453	11	NULL	NULL	0	NULL	TERT subunit Est2p	GP	overexpression of	increases					telomerase activity	Process				NULL	budding yeast;;in cell extracts	0	NULL	NULL	NULL	gw70_embo_25_3_565_s_56	16424902	In budding yeast, overexpression of the TR subunit TLC1 together with the TERT subunit  Est2p also results in higher telomerase activity levels in cell extracts (  et al).	gene_phenotype
72309	3	334453	11	NULL	NULL	0	NULL	statement 1	GP		acts together with					statement 1	GP				NULL		0	NULL	NULL	NULL	gw70_embo_25_3_565_s_56	16424902	In budding yeast, overexpression of the TR subunit TLC1 together with the TERT subunit  Est2p also results in higher telomerase activity levels in cell extracts (  et al).	gene_phenotype
72315	1	334461	11	NULL	NULL	0	NULL	 Ku	GP		is a type of 					DNA repair protein	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2090_s_4	15824061	The interaction between the DNA repair protein Ku and the RNA component of telomerase (TLC1) in  Saccharomyces cerevisiae has been shown to be important for maintaining telomere length.	gene_phenotype
72316	2	334461	11	NULL	NULL	0	NULL	TLC1	GP		is a type of 					RNA component of telomerase	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2090_s_4	15824061	The interaction between the DNA repair protein Ku and the RNA component of telomerase (TLC1) in  Saccharomyces cerevisiae has been shown to be important for maintaining telomere length.	gene_phenotype
72317	3	334461	11	NULL	NULL	0	NULL	Ku	GP		interacts with 					TLC1	GP				NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2090_s_4	15824061	The interaction between the DNA repair protein Ku and the RNA component of telomerase (TLC1) in  Saccharomyces cerevisiae has been shown to be important for maintaining telomere length.	gene_phenotype
72318	4	334461	11	NULL	NULL	0	NULL	statement 3	Process		maintains					telomere length	Chromosome				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2090_s_4	15824061	The interaction between the DNA repair protein Ku and the RNA component of telomerase (TLC1) in  Saccharomyces cerevisiae has been shown to be important for maintaining telomere length.	gene_phenotype
72321	1	334471	11	NULL	NULL	0	NULL	EST2	GP	Deletion	 shortens					 telomeres	Chromosome				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_2_837_s_22	14701754	Deletion of either  EST2 or  TLC1 causes a progressive shortening of telomeres and eventual loss of culture viability ( ) that is analogous to the replicative senescence of cultured human fibroblasts.	gene_phenotype
72322	2	334471	11	NULL	NULL	0	NULL	TLC1	GP	Deletion	shortens					telomere	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_2_837_s_22	14701754	Deletion of either  EST2 or  TLC1 causes a progressive shortening of telomeres and eventual loss of culture viability ( ) that is analogous to the replicative senescence of cultured human fibroblasts.	gene_phenotype
72323	3	334471	11	NULL	NULL	0	NULL	statement 1	Process		is an alternative to 					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_2_837_s_22	14701754	Deletion of either  EST2 or  TLC1 causes a progressive shortening of telomeres and eventual loss of culture viability ( ) that is analogous to the replicative senescence of cultured human fibroblasts.	gene_phenotype
72324	4	334471	11	NULL	NULL	0	NULL	statement 1	Process		leads to					loss of culture viability	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_2_837_s_22	14701754	Deletion of either  EST2 or  TLC1 causes a progressive shortening of telomeres and eventual loss of culture viability ( ) that is analogous to the replicative senescence of cultured human fibroblasts.	gene_phenotype
72325	5	334471	11	NULL	NULL	0	NULL	statement 2	Process		leads to					loss of culture viability	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_2_837_s_22	14701754	Deletion of either  EST2 or  TLC1 causes a progressive shortening of telomeres and eventual loss of culture viability ( ) that is analogous to the replicative senescence of cultured human fibroblasts.	gene_phenotype
72326	1	334472	11	NULL	NULL	0	NULL	Ku	GP		regulate					telomere length	Chromosome				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_22_8202_s_23	14585978	First, Ku is required for telomere length regulation ( ), an activity that is mediated through a 48-nucleotide stem-loop structure of TLC1, the RNA subunit of yeast telomerase ( ,  ).	gene_phenotype
72328	2	334472	11	NULL	NULL	0	NULL	statement 1	Process		mediated through					 TLC1	GP	 stem-loop structure			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_22_8202_s_23	14585978	First, Ku is required for telomere length regulation ( ), an activity that is mediated through a 48-nucleotide stem-loop structure of TLC1, the RNA subunit of yeast telomerase ( ,  ).	gene_phenotype
73121	1	334475	11	NULL	NULL	0	NULL	telomerase activity	Process	loss of	correlates with					TERT protein	GP	reduced amount of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_39	12458198	In addition, for mutations in these motifs, the extent of telomerase activity loss correlates with the extent of reduction in the amount of TERT protein and TERT-associated TLC1 RNA.	gene_phenotype
73122	2	334475	11	NULL	NULL	NULL	NULL	telomerase activity	Process	loss of	correlates with					statement 3	Process	reduced amount of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_39	12458198	In addition, for mutations in these motifs, the extent of telomerase activity loss correlates with the extent of reduction in the amount of TERT protein and TERT-associated TLC1 RNA.	gene_phenotype
73123	3	334475	11	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid		associates with					TERT	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_39	12458198	In addition, for mutations in these motifs, the extent of telomerase activity loss correlates with the extent of reduction in the amount of TERT protein and TERT-associated TLC1 RNA.	gene_phenotype
72353	1	334480	11	NULL	NULL	NULL	NULL	TLC1 RNA	NucleicAcid	 overexpression 	 reduce					telomere	Chromosome	length of			NULL	 yeast cell	NULL	NULL	NULL	NULL	gw60_genetics_160_1_49_s_361	11805044	Third, overexpression of  TLC1 RNA has been shown to cause a modest  reduction in average telomere lengths in yeast cells ( S INGER and GOTTSCHLING 1994   ).	gene_phenotype
75853	1	334484	11	NULL	NULL	0	NULL	DOT1 gene	GP		 reduced					silencing	Process	when overexpressed			NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_7	9755194	With the exception of  TLC1, all these genes, particularly  DOT1 and  DOT4, also reduced silencing at other repressed loci ( HM loci and rDNA) when overexpressed.	gene_phenotype
75854	2	334484	11	NULL	NULL	0	NULL	DOT4 gene	GP		reduced					silencing	Process	when overexpressed			NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_7	9755194	With the exception of  TLC1, all these genes, particularly  DOT1 and  DOT4, also reduced silencing at other repressed loci ( HM loci and rDNA) when overexpressed.	gene_phenotype
75855	3	334484	11	NULL	NULL	0	NULL	TLC1 gene	GP		not reduced					silencing	Process	when overexpressed			NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_7	9755194	With the exception of  TLC1, all these genes, particularly  DOT1 and  DOT4, also reduced silencing at other repressed loci ( HM loci and rDNA) when overexpressed.	gene_phenotype
73124	1	334486	11	NULL	NULL	0	NULL	TLC1	GP		regulates					telomere	Chromosome	length of			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2382_s_572	11376157	56       Ritchie,K., Mallory,J. and Petes,T.D. (1999) Interactions of  TLC1,  TEL1 and  MEC1 in regulating telomere length in the yeast  Saccharomyces cerevisiae.	gene_phenotype
73125	2	334486	11	NULL	NULL	0	NULL	TEL1	GP		regulates					telomere	Chromosome	length of			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2382_s_572	11376157	56       Ritchie,K., Mallory,J. and Petes,T.D. (1999) Interactions of  TLC1,  TEL1 and  MEC1 in regulating telomere length in the yeast  Saccharomyces cerevisiae.	gene_phenotype
73126	3	334486	11	NULL	NULL	0	NULL	MEC1	GP		regulates					telomere	Chromosome	length of			NULL	 Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_nucleicacidsres_29_11_2382_s_572	11376157	56       Ritchie,K., Mallory,J. and Petes,T.D. (1999) Interactions of  TLC1,  TEL1 and  MEC1 in regulating telomere length in the yeast  Saccharomyces cerevisiae.	gene_phenotype
75856	1	334490	11	NULL	NULL	0	NULL	telomeres	Chromosome	a small fraction	undergoes		possibly			catastrophic shortening	Process				NULL	in tel1 tlc1 cells	0	NULL	NULL	NULL	gw60_molcell_11_5_1379_s_134	12769860	[In new window] This finding suggests that in  tel1 tlc1 cells, a small fraction of telomeres undergoes catastrophic shortening, causing loss of chromosome end protection and fusion to a DSB.	gene_phenotype
75857	2	334490	11	NULL	NULL	0	NULL	statement 1	Process		losses					end protection	Process	chromosome			NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1379_s_134	12769860	[In new window] This finding suggests that in  tel1 tlc1 cells, a small fraction of telomeres undergoes catastrophic shortening, causing loss of chromosome end protection and fusion to a DSB.	gene_phenotype
75858	3	334490	11	NULL	NULL	0	NULL	statement 1	Process		causes					DSB fusion	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1379_s_134	12769860	[In new window] This finding suggests that in  tel1 tlc1 cells, a small fraction of telomeres undergoes catastrophic shortening, causing loss of chromosome end protection and fusion to a DSB.	gene_phenotype
75859	1	334493	11	NULL	NULL	0	NULL	Telomere length	Chromosome	tlc1 rad50 double mutant	shortened					progressively	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_5_1819_s_159	11238918	Telomere length in the  tlc1 rad50 double mutant shortened progressively, and in two of three independent experiments only type I survivors were found.	gene_phenotype
72354	1	334497	11	NULL	NULL	0	NULL	TLC1	GP	Overexpression of	restore					telomere length	Chromosome	wild-type			NULL	mtr10delta cells	0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_206	12167699	Overexpression of  TLC1 restored wild-type telomere length in  mtr10delta cells, whereas no significant changes were observed with the other genes assayed (Fig.  2B).	gene_phenotype
75860	1	334498	11	NULL	NULL	0	NULL	 Tlc1 tail	GP		occurs in the 					nucleus	CellComponent				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_362	12167699	(A) tail of Tlc1 occurs in the nucleus, which supports the hypothesis that in yeast the Sm proteins follow an RNA-independent nuclear import pathway ( 2).	gene_phenotype
75861	1	334502	11	NULL	NULL	0	NULL	 meiosis	Process		produces					four viable spores	Cell Component	from YMY2			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_50_33360_s_147	9837911	After meiosis, four viable spores were produced from YMY2, indicating that spores bearing a  TLC1 gene disruption are viable, as previously reported ( 25).	gene_phenotype
73127	1	334503	11	NULL	NULL	0	NULL	SLX5	GP		is in complex with					SLX8	GP				NULL		0	NULL	NULL	NULL	abs-batch0580-0599_nucleic-acids-res_34_2_16428246_s_7	16428246	However, mutations in SLX5 or  SLX8, which encode proteins that function together in a complex that is  required for viability in sgs1 mutants, do speed the senescence of tlc1  mutants.	gene_phenotype
73128	2	334503	11	NULL	NULL	0	NULL	stat1	GP		is required for					sgs1	GP	viability of;;mutant			NULL		0	NULL	NULL	NULL	abs-batch0580-0599_nucleic-acids-res_34_2_16428246_s_7	16428246	However, mutations in SLX5 or  SLX8, which encode proteins that function together in a complex that is  required for viability in sgs1 mutants, do speed the senescence of tlc1  mutants.	gene_phenotype
73129	3	334503	11	NULL	NULL	0	NULL	stat1	GP		speed					tlc1	GP	senescence of;;mutant			NULL		0	NULL	NULL	NULL	abs-batch0580-0599_nucleic-acids-res_34_2_16428246_s_7	16428246	However, mutations in SLX5 or  SLX8, which encode proteins that function together in a complex that is  required for viability in sgs1 mutants, do speed the senescence of tlc1  mutants.	gene_phenotype
72355	1	334505	11	NULL	NULL	NULL	NULL	TLC1	GP	wild-type	maintains					telomere	Chromosome	length of			NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_31_6_1646_s_162	12626706	While the presence of wild-type  TLC1 allowed normal telomere length maintenance (266  plus-or-minus  18 nt,  n = 20), cells that had received an empty vector lacked telomerase activity and consequently had significantly shorter telomeres (179  plus-or-minus  34 nt,  n = 20, shorter than wild-type  TLC1 P < 0.001,  t-test) 25 generations after a plasmid containing wild-type  TLC1 had been shuffled out.	gene_phenotype
72356	1	334509	11	NULL	NULL	0	NULL	Rap1	GP		is required for					meiosis	Process	efficient			NULL	S.pombe	0	NULL	NULL	NULL	gw60_embo_22_7_1688_s_214	12660174	Because Rap1 is required for efficient meiosis in  S.pombe ( Chikashige and Hiraoka, 2001;  Kanoh and Ishikawa, 2001), it is tempting to speculate that the meiotic defect of the  tlc1h strain is due to the lack of Rap1p at the C3TA2 telomere.	gene_phenotype
73130	2	334509	11	NULL	NULL	0	NULL	tlc1h strain	GP	meiotic defect of	is due to		potentially			Rap1p	GP	lack of			NULL	C3TA2 telomere	0	NULL	NULL	NULL	gw60_embo_22_7_1688_s_214	12660174	Because Rap1 is required for efficient meiosis in  S.pombe ( Chikashige and Hiraoka, 2001;  Kanoh and Ishikawa, 2001), it is tempting to speculate that the meiotic defect of the  tlc1h strain is due to the lack of Rap1p at the C3TA2 telomere.	gene_phenotype
72357	1	334514	11	NULL	NULL	0	NULL	Ku protein	GP	mutant	does not bind					 TLC1 RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_19_2384_s_103	12975323	Unlike the wild-type protein, the mutant Ku protein had no detectable TLC1 RNA-binding activity; no shifted species were seen, even in the presence of high levels of mutant Ku protein ( Fig. 3A).	gene_phenotype
72358	2	334514	11	NULL	NULL	0	NULL	Ku protein	GP	wild-type	binds					TLC1 RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_19_2384_s_103	12975323	Unlike the wild-type protein, the mutant Ku protein had no detectable TLC1 RNA-binding activity; no shifted species were seen, even in the presence of high levels of mutant Ku protein ( Fig. 3A).	gene_phenotype
72359	1	334515	11	NULL	NULL	0	NULL	Ku protein	GP		interacts with 					TLC1 RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_19_2384_s_247	12975323	In addition to the protein-RNA interaction between Ku and TLC1, there is also a protein-protein interaction between Cdc13p and Est1p that is essential for telomerase activity in vivo (Evans and Lundblad 1999 ; Pennock et al. 2001 ).	gene_phenotype
72360	2	334515	11	NULL	NULL	0	NULL	Cdc13p protein	GP		interacts with 					Est1p protein	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_19_2384_s_247	12975323	In addition to the protein-RNA interaction between Ku and TLC1, there is also a protein-protein interaction between Cdc13p and Est1p that is essential for telomerase activity in vivo (Evans and Lundblad 1999 ; Pennock et al. 2001 ).	gene_phenotype
72361	3	334515	11	NULL	NULL	0	NULL	statement 2	Process		is essential for					telomerase activity	Process				NULL	in vivo	0	NULL	NULL	NULL	gw70_genesdev_17_19_2384_s_247	12975323	In addition to the protein-RNA interaction between Ku and TLC1, there is also a protein-protein interaction between Cdc13p and Est1p that is essential for telomerase activity in vivo (Evans and Lundblad 1999 ; Pennock et al. 2001 ).	gene_phenotype
72362	1	334516	11	NULL	NULL	0	NULL	Ku	GP	S. cerevisiae	 interacting with		directly 			TLC1	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_18_15_1781_s_168	15289453	One mechanism by which Ku functions at the telomere has been revealed by work showing that  S. cerevisiae Ku regulates telomere length by interacting directly with TLC1 (Peterson et al. 2001 ; Stellwagen et al. 2003 ).	gene_phenotype
72363	2	334516	11	NULL	NULL	0	NULL	statement 1	Process		regulate					telomere length	Chromosome				NULL		0	NULL	NULL	NULL	gw70_genesdev_18_15_1781_s_168	15289453	One mechanism by which Ku functions at the telomere has been revealed by work showing that  S. cerevisiae Ku regulates telomere length by interacting directly with TLC1 (Peterson et al. 2001 ; Stellwagen et al. 2003 ).	gene_phenotype
72364	1	334523	11	NULL	NULL	0	NULL	Ku70/80	GP		interacts with 					hTR	GP				NULL	budding yeast	0	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2090_s_80	15824061	Interaction of Ku70/80 with hTR   In budding yeast, genetic studies show that yKu70/80 interacts with a 48 nt (nucleotides 288 - 335) stem - loop region of the RNA template (TLC1) of yeast telomerase ( ).	gene_phenotype
72365	2	334523	11	NULL	NULL	0	NULL	 yKu70/80	GP		interacts with					TLC1 RNA	NucleicAcid	 stem - loop region			NULL	 yeast 	0	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2090_s_80	15824061	Interaction of Ku70/80 with hTR   In budding yeast, genetic studies show that yKu70/80 interacts with a 48 nt (nucleotides 288 - 335) stem - loop region of the RNA template (TLC1) of yeast telomerase ( ).	gene_phenotype
71967	1	334527	5	NULL	NULL	0	NULL	TLC1 template sequence	NucleicAcid		directs		normally			telomeric TG1 - 3 repeats	NucleicAcid	synthesis of			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_4_1623_s_20	14742705	The  TLC1 template sequence normally directs the synthesis of telomeric TG1 - 3 repeats, which contain specific DNA binding sites for proteins involved in telomere length regulation and protection.	gene_phenotype
71968	2	334527	5	NULL	NULL	0	NULL	telomeric TG1 - 3 repeats	NucleicAcid		is involved in					telomere length	PhysicalPhenomenon	regulation of			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_4_1623_s_20	14742705	The  TLC1 template sequence normally directs the synthesis of telomeric TG1 - 3 repeats, which contain specific DNA binding sites for proteins involved in telomere length regulation and protection.	gene_phenotype
71969	3	334527	5	NULL	NULL	0	NULL	telomeric TG1 - 3 repeats	NucleicAcid		is involved in					telomere length	PhysicalPhenomenon	protection of			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_4_1623_s_20	14742705	The  TLC1 template sequence normally directs the synthesis of telomeric TG1 - 3 repeats, which contain specific DNA binding sites for proteins involved in telomere length regulation and protection.	gene_phenotype
71970	1	334530	5	NULL	NULL	NULL	NULL	TLC1	NucleicAcid	complete deletion of	causes					cell cycle arrest	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_15_4_1623_s_256	14742705	Complete deletion of  TLC1 causes cell cycle arrest, activates a checkpoint (Enomoto  et al., 2002 ; IJpma and Greider, 2003 ), and causes chromosomal fusions when telomeres become short (Hackett  et al., 2001 ).	gene_phenotype
71972	2	334530	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	complete deletion of	activates					checkpoint	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_4_1623_s_256	14742705	Complete deletion of  TLC1 causes cell cycle arrest, activates a checkpoint (Enomoto  et al., 2002 ; IJpma and Greider, 2003 ), and causes chromosomal fusions when telomeres become short (Hackett  et al., 2001 ).	gene_phenotype
71973	3	334530	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	complete deletion of	causes					chromosomal fusions	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_4_1623_s_256	14742705	Complete deletion of  TLC1 causes cell cycle arrest, activates a checkpoint (Enomoto  et al., 2002 ; IJpma and Greider, 2003 ), and causes chromosomal fusions when telomeres become short (Hackett  et al., 2001 ).	gene_phenotype
71975	4	334530	5	NULL	NULL	0	NULL	telomere	Chromosome	short	leads to					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_4_1623_s_256	14742705	Complete deletion of  TLC1 causes cell cycle arrest, activates a checkpoint (Enomoto  et al., 2002 ; IJpma and Greider, 2003 ), and causes chromosomal fusions when telomeres become short (Hackett  et al., 2001 ).	gene_phenotype
71979	1	334536	5	NULL	NULL	0	NULL	Est2	GP		associate with					tlc1-62 RNA	NucleicAcid	mutant			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_17_7720_s_252	15314178	The telomere length of the  tlc1-62 strain was indistinguishable from that of a  TLC1 strain (Fig.  8B), and Est2 association with the  tlc1-62 mutant RNA was reduced by less than twofold (Fig.  8C).	gene_phenotype
71984	1	334541	5	NULL	NULL	0	NULL	Ku	GP		plays a role in					telomere length	PhysicalPhenomenon	regulation of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_22_8202_s_375	14585978	In contrast, Ku's role in telomere length regulation is mediated through an interaction with a stem-loop structure of the TLC1 RNA subunit of telomerase ( ,  ) and may additionally require a function provided by the Est1 telomerase subunit ( ).	gene_phenotype
71985	2	334541	5	NULL	NULL	0	NULL	Ku	GP		interacts with					telomerase	GP	stem-loop structure of	TLC1 RNA subunit		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_22_8202_s_375	14585978	In contrast, Ku's role in telomere length regulation is mediated through an interaction with a stem-loop structure of the TLC1 RNA subunit of telomerase ( ,  ) and may additionally require a function provided by the Est1 telomerase subunit ( ).	gene_phenotype
71986	3	334541	5	NULL	NULL	0	NULL	statement 2	Process		mediates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_22_8202_s_375	14585978	In contrast, Ku's role in telomere length regulation is mediated through an interaction with a stem-loop structure of the TLC1 RNA subunit of telomerase ( ,  ) and may additionally require a function provided by the Est1 telomerase subunit ( ).	gene_phenotype
71987	4	334541	5	NULL	NULL	NULL	NULL	statement 1	Process		requires		additionally			telomerase 	GP	function of	Est1 subunit		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_22_8202_s_375	14585978	In contrast, Ku's role in telomere length regulation is mediated through an interaction with a stem-loop structure of the TLC1 RNA subunit of telomerase ( ,  ) and may additionally require a function provided by the Est1 telomerase subunit ( ).	gene_phenotype
71988	1	334542	5	NULL	NULL	0	NULL	Tlc1	GP		is not ubiquitous within					obligate intracellular organisms	Organism				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_17_6261_s_24	16923893	However, the Tlc1 family of transporters is not ubiquitous within obligate intracellular organisms; it is absent from the genomes of  Coxiella,  Anaplasma, and  Ehrlichia spp., which grow inside host-derived vesicles.	gene_phenotype
71989	2	334542	5	NULL	NULL	0	NULL	Tlc1	GP		is a family of					transporters	GP				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_17_6261_s_24	16923893	However, the Tlc1 family of transporters is not ubiquitous within obligate intracellular organisms; it is absent from the genomes of  Coxiella,  Anaplasma, and  Ehrlichia spp., which grow inside host-derived vesicles.	gene_phenotype
71990	3	334542	5	NULL	NULL	0	NULL	Tlc1	GP		is absent from					Coxiella	Organism	genome of			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_17_6261_s_24	16923893	However, the Tlc1 family of transporters is not ubiquitous within obligate intracellular organisms; it is absent from the genomes of  Coxiella,  Anaplasma, and  Ehrlichia spp., which grow inside host-derived vesicles.	gene_phenotype
71991	4	334542	5	NULL	NULL	0	NULL	Tlc1	GP		is absent from					Anaplasma	Organism	genome of			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_17_6261_s_24	16923893	However, the Tlc1 family of transporters is not ubiquitous within obligate intracellular organisms; it is absent from the genomes of  Coxiella,  Anaplasma, and  Ehrlichia spp., which grow inside host-derived vesicles.	gene_phenotype
71992	5	334542	5	NULL	NULL	0	NULL	Tlc1	GP		is absent from					Ehrlichia spp.	Organism	genome of			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_17_6261_s_24	16923893	However, the Tlc1 family of transporters is not ubiquitous within obligate intracellular organisms; it is absent from the genomes of  Coxiella,  Anaplasma, and  Ehrlichia spp., which grow inside host-derived vesicles.	gene_phenotype
71993	6	334542	5	NULL	NULL	0	NULL	Ehrlichia spp.	Organism		grow inside					host-derived vesicles	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_17_6261_s_24	16923893	However, the Tlc1 family of transporters is not ubiquitous within obligate intracellular organisms; it is absent from the genomes of  Coxiella,  Anaplasma, and  Ehrlichia spp., which grow inside host-derived vesicles.	gene_phenotype
71994	7	334542	5	NULL	NULL	0	NULL	Anaplasma	Organism		grow inside					host-derived vesicles	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_17_6261_s_24	16923893	However, the Tlc1 family of transporters is not ubiquitous within obligate intracellular organisms; it is absent from the genomes of  Coxiella,  Anaplasma, and  Ehrlichia spp., which grow inside host-derived vesicles.	gene_phenotype
71995	8	334542	5	NULL	NULL	0	NULL	Coxiella	Organism		grow inside					host-derived vesicles	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_17_6261_s_24	16923893	However, the Tlc1 family of transporters is not ubiquitous within obligate intracellular organisms; it is absent from the genomes of  Coxiella,  Anaplasma, and  Ehrlichia spp., which grow inside host-derived vesicles.	gene_phenotype
71996	1	334543	5	NULL	NULL	NULL	NULL	telomerase RNAs	NucleicAcid	Kluyveromyces budding yeast;;sequence of	is different from					TLC1	NucleicAcid	Saccharomyces;;sequence of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_27_10024_s_81	15226497	Kluyveromyces budding yeast telomerase RNAs are significantly different in sequence from  Saccharomyces TLC1, making them useful for studying some conserved elements ( ,  ) but essentially useless for beginning to deduce overall RNA secondary structure.	gene_phenotype
71997	1	334544	5	NULL	NULL	0	NULL	TLC1	NucleicAcid		associate with					Est1p	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_41_14713_s_81	15371596	A conserved bulged-stem structure previously identified in seven budding yeast TERs is necessary for association of TLC1 with Est1p, a TER holoenzyme component, and various mutations within this bulged-stem structure cause senescence ( ).	gene_phenotype
71998	2	334544	5	NULL	NULL	0	NULL	bulged-stem structure	PhysicalPhenomenon	conserved	is present in					TERs	GP	budding yeast			NULL		0	NULL	NULL	NULL	gw70_pnas_101_41_14713_s_81	15371596	A conserved bulged-stem structure previously identified in seven budding yeast TERs is necessary for association of TLC1 with Est1p, a TER holoenzyme component, and various mutations within this bulged-stem structure cause senescence ( ).	gene_phenotype
71999	3	334544	5	NULL	NULL	0	NULL	statement 2	Process		is necessary for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_41_14713_s_81	15371596	A conserved bulged-stem structure previously identified in seven budding yeast TERs is necessary for association of TLC1 with Est1p, a TER holoenzyme component, and various mutations within this bulged-stem structure cause senescence ( ).	gene_phenotype
72000	4	334544	5	NULL	NULL	0	NULL	Est1p	GP		is a component of					TER holoenzyme	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_41_14713_s_81	15371596	A conserved bulged-stem structure previously identified in seven budding yeast TERs is necessary for association of TLC1 with Est1p, a TER holoenzyme component, and various mutations within this bulged-stem structure cause senescence ( ).	gene_phenotype
72001	5	334544	5	NULL	NULL	0	NULL	bulged-stem structure	PhysicalPhenomenon	mutation in	causes					senescence	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_41_14713_s_81	15371596	A conserved bulged-stem structure previously identified in seven budding yeast TERs is necessary for association of TLC1 with Est1p, a TER holoenzyme component, and various mutations within this bulged-stem structure cause senescence ( ).	gene_phenotype
72002	1	334545	5	NULL	NULL	NULL	NULL	telomerase	GP		maintains					telomere	Chromosome	length of			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_21_6127_s_12	11689452	Maintenance of telomere length and structure usually requires telomerase, which is comprised of a reverse transcriptase (TERT in mammals, Est2 in the yeast  Saccharomyces cerevisiae) and an RNA template (TR in mammals,  TLC1 in  S.cerevisiae).	gene_phenotype
72003	2	334545	5	NULL	NULL	0	NULL	telomerase	GP		maintains					telomere	Chromosome	structure of			NULL		0	NULL	NULL	NULL	gw60_embo_20_21_6127_s_12	11689452	Maintenance of telomere length and structure usually requires telomerase, which is comprised of a reverse transcriptase (TERT in mammals, Est2 in the yeast  Saccharomyces cerevisiae) and an RNA template (TR in mammals,  TLC1 in  S.cerevisiae).	gene_phenotype
72004	3	334545	5	NULL	NULL	0	NULL	telomerase	GP		comprise of					reverse transcriptase	GP				NULL		0	NULL	NULL	NULL	gw60_embo_20_21_6127_s_12	11689452	Maintenance of telomere length and structure usually requires telomerase, which is comprised of a reverse transcriptase (TERT in mammals, Est2 in the yeast  Saccharomyces cerevisiae) and an RNA template (TR in mammals,  TLC1 in  S.cerevisiae).	gene_phenotype
72005	4	334545	5	NULL	NULL	0	NULL	telomerase	GP		comprise of					RNA template	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_embo_20_21_6127_s_12	11689452	Maintenance of telomere length and structure usually requires telomerase, which is comprised of a reverse transcriptase (TERT in mammals, Est2 in the yeast  Saccharomyces cerevisiae) and an RNA template (TR in mammals,  TLC1 in  S.cerevisiae).	gene_phenotype
72006	5	334545	5	NULL	NULL	0	NULL	statement 3	Process		occurs along with					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_embo_20_21_6127_s_12	11689452	Maintenance of telomere length and structure usually requires telomerase, which is comprised of a reverse transcriptase (TERT in mammals, Est2 in the yeast  Saccharomyces cerevisiae) and an RNA template (TR in mammals,  TLC1 in  S.cerevisiae).	gene_phenotype
72007	6	334545	5	NULL	NULL	0	NULL	TERT	GP	mammals	is a type of					reverse transcriptase	GP				NULL		0	NULL	NULL	NULL	gw60_embo_20_21_6127_s_12	11689452	Maintenance of telomere length and structure usually requires telomerase, which is comprised of a reverse transcriptase (TERT in mammals, Est2 in the yeast  Saccharomyces cerevisiae) and an RNA template (TR in mammals,  TLC1 in  S.cerevisiae).	gene_phenotype
72008	7	334545	5	NULL	NULL	0	NULL	Est2	GP	Saccharomyces cerevisiae	is a type of					reverse transcriptase	GP				NULL		0	NULL	NULL	NULL	gw60_embo_20_21_6127_s_12	11689452	Maintenance of telomere length and structure usually requires telomerase, which is comprised of a reverse transcriptase (TERT in mammals, Est2 in the yeast  Saccharomyces cerevisiae) and an RNA template (TR in mammals,  TLC1 in  S.cerevisiae).	gene_phenotype
72009	8	334545	5	NULL	NULL	0	NULL	TR	NucleicAcid	mammals	is a type of					RNA template	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_embo_20_21_6127_s_12	11689452	Maintenance of telomere length and structure usually requires telomerase, which is comprised of a reverse transcriptase (TERT in mammals, Est2 in the yeast  Saccharomyces cerevisiae) and an RNA template (TR in mammals,  TLC1 in  S.cerevisiae).	gene_phenotype
72010	9	334545	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	S. cerevisiae	is a type of					RNA template	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_embo_20_21_6127_s_12	11689452	Maintenance of telomere length and structure usually requires telomerase, which is comprised of a reverse transcriptase (TERT in mammals, Est2 in the yeast  Saccharomyces cerevisiae) and an RNA template (TR in mammals,  TLC1 in  S.cerevisiae).	gene_phenotype
72011	1	334546	5	NULL	NULL	0	NULL	TLC1	NucleicAcid		encodes					telomerase	GP			RNA subunit	NULL		0	NULL	NULL	NULL	gw60_embo_20_21_6127_s_406	11689452	Ritchie,K.B., Mallory,J.C. and Petes,T.D. (1999) Interactions of  TLC1 (which encodes the RNA subunit of telomerase),  TEL1, and  MEC1 in regulating telomere length in the yeast  Saccharomyces cerevisiae.	gene_phenotype
72012	2	334546	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	intractions of	regulates					telomere	Chromosome	length of			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_embo_20_21_6127_s_406	11689452	Ritchie,K.B., Mallory,J.C. and Petes,T.D. (1999) Interactions of  TLC1 (which encodes the RNA subunit of telomerase),  TEL1, and  MEC1 in regulating telomere length in the yeast  Saccharomyces cerevisiae.	gene_phenotype
72013	3	334546	5	NULL	NULL	0	NULL	TEL1	GP	intractions of	regulates					telomere	Chromosome	length of			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_embo_20_21_6127_s_406	11689452	Ritchie,K.B., Mallory,J.C. and Petes,T.D. (1999) Interactions of  TLC1 (which encodes the RNA subunit of telomerase),  TEL1, and  MEC1 in regulating telomere length in the yeast  Saccharomyces cerevisiae.	gene_phenotype
72014	4	334546	5	NULL	NULL	NULL	NULL	MEC1	GP	intractions of	regulates					telomere	Chromosome	length of			NULL	Saccharomyces cerevisiae	NULL	NULL	NULL	NULL	gw60_embo_20_21_6127_s_406	11689452	Ritchie,K.B., Mallory,J.C. and Petes,T.D. (1999) Interactions of  TLC1 (which encodes the RNA subunit of telomerase),  TEL1, and  MEC1 in regulating telomere length in the yeast  Saccharomyces cerevisiae.	gene_phenotype
72015	1	334551	5	NULL	NULL	0	NULL	genome	NucleicAcid		is instable in					tel1 mec1 cells	Cell				NULL		0	NULL	NULL	NULL	gw60_genetics_161_2_493_s_126	12072449	The  tlc1 mutation had only modest (threefold) effects, indicating that the elevated rates of genome instability in the  tel1 mec1 cells are not solely attributable to a deficiency in telomere length regulation.	gene_phenotype
72016	2	334551	5	NULL	NULL	0	NULL	statement 1	Process	elevated rates of 	is not attributable to		solely 			telomere	Chromosome	deficiency of;;regulation of;;length of			NULL		0	NULL	NULL	NULL	gw60_genetics_161_2_493_s_126	12072449	The  tlc1 mutation had only modest (threefold) effects, indicating that the elevated rates of genome instability in the  tel1 mec1 cells are not solely attributable to a deficiency in telomere length regulation.	gene_phenotype
72017	1	334553	5	NULL	NULL	0	NULL	tlc1	NucleicAcid		is a synonym of					telomerase RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_genetics_161_4_1437_s_411	12196391	In  S. cerevisiae, it was observed that telomerase RNA ( tlc1) deletion hastened the loss of viability of  tel1delta mec1delta cells, suggesting that telomerase activity allows cells to partially counteract telomere loss ( C HAN et al. 2001   ).	gene_phenotype
72018	2	334553	5	NULL	NULL	0	NULL	tlc1	NucleicAcid	deletion of	hasten					tel1delta mec1delta cells	Cell	loss of;;viability of			NULL		0	NULL	NULL	NULL	gw60_genetics_161_4_1437_s_411	12196391	In  S. cerevisiae, it was observed that telomerase RNA ( tlc1) deletion hastened the loss of viability of  tel1delta mec1delta cells, suggesting that telomerase activity allows cells to partially counteract telomere loss ( C HAN et al. 2001   ).	gene_phenotype
72019	3	334553	5	NULL	NULL	0	NULL	cells	Cell		counteract		partially			telomere	Chromosome	loss of			NULL		0	NULL	NULL	NULL	gw60_genetics_161_4_1437_s_411	12196391	In  S. cerevisiae, it was observed that telomerase RNA ( tlc1) deletion hastened the loss of viability of  tel1delta mec1delta cells, suggesting that telomerase activity allows cells to partially counteract telomere loss ( C HAN et al. 2001   ).	gene_phenotype
72020	4	334553	5	NULL	NULL	0	NULL	telomerase activity	Process		allows					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_161_4_1437_s_411	12196391	In  S. cerevisiae, it was observed that telomerase RNA ( tlc1) deletion hastened the loss of viability of  tel1delta mec1delta cells, suggesting that telomerase activity allows cells to partially counteract telomere loss ( C HAN et al. 2001   ).	gene_phenotype
72021	1	334559	5	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid	overexpression of	increases					ionizing radiation	PhysicalPhenomenon	resistance to			NULL		0	NULL	NULL	NULL	gw60_genetics_160_1_49_s_339	11805044	Overexpression of  TLC1 RNA increased resistance to ionizing radiation (thought to be primarily dependent on recombinational repair processes) to a lesser extent than to MMS, which produces lesions that are repaired by several pathways ( X IAO et al. 1996   ).	gene_phenotype
72022	2	334559	5	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid	overexpression of	increases					MMS	Chemical	resistance to			NULL		0	NULL	NULL	NULL	gw60_genetics_160_1_49_s_339	11805044	Overexpression of  TLC1 RNA increased resistance to ionizing radiation (thought to be primarily dependent on recombinational repair processes) to a lesser extent than to MMS, which produces lesions that are repaired by several pathways ( X IAO et al. 1996   ).	gene_phenotype
72023	3	334559	5	NULL	NULL	0	NULL	statement 1	Process		lesser than					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_160_1_49_s_339	11805044	Overexpression of  TLC1 RNA increased resistance to ionizing radiation (thought to be primarily dependent on recombinational repair processes) to a lesser extent than to MMS, which produces lesions that are repaired by several pathways ( X IAO et al. 1996   ).	gene_phenotype
72024	1	334560	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	overexpression of	reduce					telomere	Chromosome	silencing of			NULL		0	NULL	NULL	NULL	gw60_genetics_160_1_49_s_370	11805044	TLC1 was originally identified as one of several genes that reduced silencing at telomeres (but not at internal mating type loci) when overexpressed ( S INGER and GOTTSCHLING 1994   ;   S INGER  et al. 1998   ).	gene_phenotype
72027	1	334562	5	NULL	NULL	0	NULL	DNA	NucleicAcid	recombination of	plays a role in		possibly			telomere	Chromosome	maintenance of			NULL		0	NULL	NULL	NULL	gw60_genetics_152_1_143_s_49	10224249	To understand the role of DNA recombination in telomere maintenance more completely, we examined telomere length in a set of isogenic yeast mutants of the  RAD52 epistasis group in both the absence and presence of the telomerase RNA component  TLC1.	gene_phenotype
72028	1	334568	5	NULL	NULL	0	NULL	DOT1	NucleicAcid		plays a role in		potentially			telomere	Chromosome	silencing of			NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_320	9755194	To ascertain whether any of the other  DOT genes are important for telomeric silencing, the genomic copy of  DOT1,  DOT4,  DOT5,  DOT6,  TLC1, or  ASF1 was deleted and the effect on silencing was examined.	gene_phenotype
72030	2	334568	5	NULL	NULL	0	NULL	DOT4	NucleicAcid		plays a role in		potentially			telomere	Chromosome	silencing of			NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_320	9755194	To ascertain whether any of the other  DOT genes are important for telomeric silencing, the genomic copy of  DOT1,  DOT4,  DOT5,  DOT6,  TLC1, or  ASF1 was deleted and the effect on silencing was examined.	gene_phenotype
72032	3	334568	5	NULL	NULL	0	NULL	DOT5	NucleicAcid		plays a role in		potentially			telomere	Chromosome	silencing of			NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_320	9755194	To ascertain whether any of the other  DOT genes are important for telomeric silencing, the genomic copy of  DOT1,  DOT4,  DOT5,  DOT6,  TLC1, or  ASF1 was deleted and the effect on silencing was examined.	gene_phenotype
72033	4	334568	5	NULL	NULL	0	NULL	DOT6	NucleicAcid		plays a role in		potentially			telomere	Chromosome	silencing of			NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_320	9755194	To ascertain whether any of the other  DOT genes are important for telomeric silencing, the genomic copy of  DOT1,  DOT4,  DOT5,  DOT6,  TLC1, or  ASF1 was deleted and the effect on silencing was examined.	gene_phenotype
72034	5	334568	5	NULL	NULL	0	NULL	TLC1	NucleicAcid		plays a role in		potentially			telomere	Chromosome	silencing of			NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_320	9755194	To ascertain whether any of the other  DOT genes are important for telomeric silencing, the genomic copy of  DOT1,  DOT4,  DOT5,  DOT6,  TLC1, or  ASF1 was deleted and the effect on silencing was examined.	gene_phenotype
72035	6	334568	5	NULL	NULL	0	NULL	ASF1	NucleicAcid		plays a role in		potentially			telomere	Chromosome	silencing of			NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_320	9755194	To ascertain whether any of the other  DOT genes are important for telomeric silencing, the genomic copy of  DOT1,  DOT4,  DOT5,  DOT6,  TLC1, or  ASF1 was deleted and the effect on silencing was examined.	gene_phenotype
72036	1	334569	5	NULL	NULL	NULL	NULL	dot4	GP		plays a role in					rDNA	NucleicAcid	silencing of			NULL		NULL	NULL	NULL	NULL	gw60_genetics_150_2_613_s_386	9755194	While  dot4 cells had slightly less rDNA silencing than wild-type cells, as judged by sensitivity to 5-FOA, deletion of  DOT1,  DOT5,  DOT6, and  TLC1 had no effect.	gene_phenotype
72039	2	334569	5	NULL	NULL	0	NULL	DOT1	GP	deletion of	does not effect					rDNA	NucleicAcid	silencing of			NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_386	9755194	While  dot4 cells had slightly less rDNA silencing than wild-type cells, as judged by sensitivity to 5-FOA, deletion of  DOT1,  DOT5,  DOT6, and  TLC1 had no effect.	gene_phenotype
72040	3	334569	5	NULL	NULL	0	NULL	DOT5	GP	deletion of	does not effect					rDNA	NucleicAcid	silencing of			NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_386	9755194	While  dot4 cells had slightly less rDNA silencing than wild-type cells, as judged by sensitivity to 5-FOA, deletion of  DOT1,  DOT5,  DOT6, and  TLC1 had no effect.	gene_phenotype
72041	4	334569	5	NULL	NULL	0	NULL	DOT6	GP	deletion of	does not effect					rDNA	NucleicAcid	silencing of			NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_386	9755194	While  dot4 cells had slightly less rDNA silencing than wild-type cells, as judged by sensitivity to 5-FOA, deletion of  DOT1,  DOT5,  DOT6, and  TLC1 had no effect.	gene_phenotype
72042	5	334569	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	deletion of	does not effect					rDNA	NucleicAcid	silencing of			NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_386	9755194	While  dot4 cells had slightly less rDNA silencing than wild-type cells, as judged by sensitivity to 5-FOA, deletion of  DOT1,  DOT5,  DOT6, and  TLC1 had no effect.	gene_phenotype
72043	1	334570	5	NULL	NULL	0	NULL	Est1 protein	GP		co-immunoprecipitate with		potentially			telomerase 	GP			TLC1 RNA subunit	NULL		0	NULL	NULL	NULL	gw60_genetics_162_3_1101_s_211	12454059	To test this, each mutant Est1 protein was examined for the ability to co-immunoprecipitate the TLC1 telomerase RNA subunit ( Fig 5A and data not shown); a subset was also tested for association with enzyme activity ( Fig 5B).	gene_phenotype
72052	1	334571	5	NULL	NULL	0	NULL	stem-loop structure	NucleicAcid		is present in					telomerase	GP			TLC1 component	NULL		0	NULL	NULL	NULL	gw60_genetics_162_3_1101_s_362	12454059	Recent work from the Gottschling laboratory has shown that a 48-nt stem-loop structure in the TLC1 component of telomerase influences telomere length through the same pathway as Ku ( P ETERSON  et al. 2001   ).	gene_phenotype
72054	2	334571	5	NULL	NULL	0	NULL	statement 1	Process		influences					telomere	Chromosome	length of			NULL		0	NULL	NULL	NULL	gw60_genetics_162_3_1101_s_362	12454059	Recent work from the Gottschling laboratory has shown that a 48-nt stem-loop structure in the TLC1 component of telomerase influences telomere length through the same pathway as Ku ( P ETERSON  et al. 2001   ).	gene_phenotype
72055	1	334574	5	NULL	NULL	0	NULL	Est protein	GP		interacts with					TLC1	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_13_809_s_30	10898986	[In new window] This interaction between the Est proteins and TLC1 reflected an association with an active telomerase complex, since enzyme activity was identified in each of the Est protein IPs (  Figure 1b).	gene_phenotype
72056	2	334574	5	NULL	NULL	0	NULL	statement 1	Process		associate with					telomerase complex	GP	active			NULL		0	NULL	NULL	NULL	gw60_currbiol_10_13_809_s_30	10898986	[In new window] This interaction between the Est proteins and TLC1 reflected an association with an active telomerase complex, since enzyme activity was identified in each of the Est protein IPs (  Figure 1b).	gene_phenotype
72057	3	334574	5	NULL	NULL	0	NULL	Est protein	GP		activates					enzyme	GP				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_13_809_s_30	10898986	[In new window] This interaction between the Est proteins and TLC1 reflected an association with an active telomerase complex, since enzyme activity was identified in each of the Est protein IPs (  Figure 1b).	gene_phenotype
73594	1	334575	5	NULL	NULL	0	NULL	est1	GP	mutant	inactivates		catalytically			telomerase	GP				NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73595	2	334575	5	NULL	NULL	0	NULL	est2	GP	mutant	inactivates		catalytically			telomerase	GP				NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73596	3	334575	5	NULL	NULL	0	NULL	est3	GP	mutant	inactivates		catalytically			telomerase	GP				NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73597	4	334575	5	NULL	NULL	0	NULL	cdc13-2	GP	mutant	inactivates		catalytically			telomerase	GP				NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73598	5	334575	5	NULL	NULL	0	NULL	tlc1	GP	mutant	inactivates		catalytically			telomerase	GP				NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73599	6	334575	5	NULL	NULL	0	NULL	tel1	GP	inactive	affects					telomerase	GP				NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73600	7	334575	5	NULL	NULL	0	NULL	sir1-4	GP	inactive	affects					telomerase	GP				NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73601	8	334575	5	NULL	NULL	0	NULL	yku70	GP	inactive	affects					telomerase	GP				NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73602	9	334575	5	NULL	NULL	0	NULL	yku80	GP	inactive	affects					telomerase	GP				NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73603	10	334575	5	NULL	NULL	0	NULL	rif1	GP	inactive	affects					telomerase	GP				NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73604	11	334575	5	NULL	NULL	0	NULL	rif2	GP	inactive	affects					telomerase	GP				NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73605	12	334575	5	NULL	NULL	0	NULL	statement 1	Process		does not effect		significantly			GCR	PhysicalPhenomenon	rate of			NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73606	13	334575	5	NULL	NULL	0	NULL	statement 2	Process		does not effect		significantly			GCR	PhysicalPhenomenon	rate of			NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73607	14	334575	5	NULL	NULL	0	NULL	statement 3	Process		does not effect		significantly			GCR	PhysicalPhenomenon	rate of			NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73608	15	334575	5	NULL	NULL	0	NULL	statement 4	Process		does not effect		significantly			GCR	PhysicalPhenomenon	rate of			NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73609	16	334575	5	NULL	NULL	0	NULL	statement 5	Process		does not effect		significantly			GCR	PhysicalPhenomenon	rate of			NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73610	17	334575	5	NULL	NULL	0	NULL	statement 6	Process		does not effect		significantly			GCR	PhysicalPhenomenon	rate of			NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73611	18	334575	5	NULL	NULL	0	NULL	statement 7	Process		does not effect		significantly			GCR	PhysicalPhenomenon	rate of			NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73612	19	334575	5	NULL	NULL	0	NULL	statement 8	Process		does not effect		significantly			GCR	PhysicalPhenomenon	rate of			NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73613	20	334575	5	NULL	NULL	0	NULL	statement 9	Process		does not effect		significantly			GCR	PhysicalPhenomenon	rate of			NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73614	21	334575	5	NULL	NULL	0	NULL	statement 10	Process		does not effect		significantly			GCR	PhysicalPhenomenon	rate of			NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
73615	22	334575	5	NULL	NULL	0	NULL	statement 11	Process		does not effect		significantly			GCR	PhysicalPhenomenon	rate of			NULL		0	NULL	NULL	NULL	gw60_nature_411_6841_1073_s_18	11429610	Mutations that inactivated the catalytic activity of telomerase ( est1, est2, est3, cdc13-2, tlc1) or inactivated proteins that affect telomeres ( tel1, sir1-4, yku70, yku80, rif1, rif2) 6,  7 had no significant effect on the GCR rate.	gene_phenotype
72058	1	334577	5	NULL	NULL	NULL	NULL	Tlc1	GP	Chlamydia	transports					nucleotide triphosphates	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_6_1397_s_270	10684935	All four  Chlamydia genomes also encode two proteins known to be dedicated to the transport of nucleotide triphosphates, Tlc1 and Tlc2, both homologs of Tlc, an ATP/ADP translocase from the obligate intracellular parasite  Rickettsia prowazakii ( 38).	gene_phenotype
72059	2	334577	5	NULL	NULL	NULL	NULL	Tlc2	GP	Chlamydia	transports					nucleotide triphosphates	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_6_1397_s_270	10684935	All four  Chlamydia genomes also encode two proteins known to be dedicated to the transport of nucleotide triphosphates, Tlc1 and Tlc2, both homologs of Tlc, an ATP/ADP translocase from the obligate intracellular parasite  Rickettsia prowazakii ( 38).	gene_phenotype
72060	3	334577	5	NULL	NULL	NULL	NULL	Tlc1	GP	Chlamydia	is homologous to					Tlc	GP	Rickettsia prowazakii 			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_6_1397_s_270	10684935	All four  Chlamydia genomes also encode two proteins known to be dedicated to the transport of nucleotide triphosphates, Tlc1 and Tlc2, both homologs of Tlc, an ATP/ADP translocase from the obligate intracellular parasite  Rickettsia prowazakii ( 38).	gene_phenotype
72061	4	334577	5	NULL	NULL	0	NULL	Tlc2	GP	Chlamydia	is homologous to					ATP/ADP translocase	GP	Rickettsia prowazakii			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_6_1397_s_270	10684935	All four  Chlamydia genomes also encode two proteins known to be dedicated to the transport of nucleotide triphosphates, Tlc1 and Tlc2, both homologs of Tlc, an ATP/ADP translocase from the obligate intracellular parasite  Rickettsia prowazakii ( 38).	gene_phenotype
72062	5	334577	5	NULL	NULL	0	NULL	Rickettsia prowazakii	Organism		is a type of					obligate intracellular parasite	Organism				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_6_1397_s_270	10684935	All four  Chlamydia genomes also encode two proteins known to be dedicated to the transport of nucleotide triphosphates, Tlc1 and Tlc2, both homologs of Tlc, an ATP/ADP translocase from the obligate intracellular parasite  Rickettsia prowazakii ( 38).	gene_phenotype
72063	1	334578	5	NULL	NULL	0	NULL	Tlc1 protein	GP	C.trachomatis serovar L2	is homologous to					ATP/ADP tranlocase	GP				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_6_1397_s_271	10684935	The Tlc1 protein of  C.trachomatis serovar L2 is an ATP/ADP tranlocase, whereas the Tlc2 protein, although sharing a high degree of sequence similarity, is a more general NTP transporter, apparently utilizing an H+ pump to energize the process ( 39).	gene_phenotype
72064	2	334578	5	NULL	NULL	0	NULL	Tlc2 protein	GP	C.trachomatis serovar L2	is homologous to					NTP transporter	GP				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_6_1397_s_271	10684935	The Tlc1 protein of  C.trachomatis serovar L2 is an ATP/ADP tranlocase, whereas the Tlc2 protein, although sharing a high degree of sequence similarity, is a more general NTP transporter, apparently utilizing an H+ pump to energize the process ( 39).	gene_phenotype
72065	1	334579	5	NULL	NULL	0	NULL	Cbf5p	GP		is a type of					H/ACA snoRNP protein	GP				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_8	11160879	We show that the presence of the H/ACA snoRNP proteins Cbf5p, Nhp2p and Nop10p, but not Gar1p, is required for the accumulation of mature non-polyadenylated hTR in yeast, while accumulation of TLC1 RNA is not affected by the absence of any of these proteins.	gene_phenotype
72066	2	334579	5	NULL	NULL	0	NULL	Nhp2p 	GP		is a type of					H/ACA snoRNP protein	GP				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_8	11160879	We show that the presence of the H/ACA snoRNP proteins Cbf5p, Nhp2p and Nop10p, but not Gar1p, is required for the accumulation of mature non-polyadenylated hTR in yeast, while accumulation of TLC1 RNA is not affected by the absence of any of these proteins.	gene_phenotype
72067	3	334579	5	NULL	NULL	0	NULL	Nop10p	GP		is a type of					H/ACA snoRNP protein	GP				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_8	11160879	We show that the presence of the H/ACA snoRNP proteins Cbf5p, Nhp2p and Nop10p, but not Gar1p, is required for the accumulation of mature non-polyadenylated hTR in yeast, while accumulation of TLC1 RNA is not affected by the absence of any of these proteins.	gene_phenotype
72068	4	334579	5	NULL	NULL	0	NULL	Gar1p	GP		is a type of					H/ACA snoRNP protein	GP				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_8	11160879	We show that the presence of the H/ACA snoRNP proteins Cbf5p, Nhp2p and Nop10p, but not Gar1p, is required for the accumulation of mature non-polyadenylated hTR in yeast, while accumulation of TLC1 RNA is not affected by the absence of any of these proteins.	gene_phenotype
72069	5	334579	5	NULL	NULL	0	NULL	Cbf5p	GP	presence of	is required for					hTR	GP	accumulation of;;mature;;non-polyadenylated			NULL	yeast	0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_8	11160879	We show that the presence of the H/ACA snoRNP proteins Cbf5p, Nhp2p and Nop10p, but not Gar1p, is required for the accumulation of mature non-polyadenylated hTR in yeast, while accumulation of TLC1 RNA is not affected by the absence of any of these proteins.	gene_phenotype
72070	6	334579	5	NULL	NULL	NULL	NULL	Nhp2p	GP	presence of	is required for					hTR	GP	accumulation of;;mature;;non-polyadenylated			NULL	yeast	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_8	11160879	We show that the presence of the H/ACA snoRNP proteins Cbf5p, Nhp2p and Nop10p, but not Gar1p, is required for the accumulation of mature non-polyadenylated hTR in yeast, while accumulation of TLC1 RNA is not affected by the absence of any of these proteins.	gene_phenotype
72071	7	334579	5	NULL	NULL	0	NULL	Nop10p	GP	presence of	is required for					hTR	GP	accumulation of;;mature;;non-polyadenylated			NULL	yeast	0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_8	11160879	We show that the presence of the H/ACA snoRNP proteins Cbf5p, Nhp2p and Nop10p, but not Gar1p, is required for the accumulation of mature non-polyadenylated hTR in yeast, while accumulation of TLC1 RNA is not affected by the absence of any of these proteins.	gene_phenotype
72072	8	334579	5	NULL	NULL	0	NULL	Gar1p	GP	presence of	is not required for					hTR	GP	accumulation of;;mature;;non-polyadenylated			NULL	yeast	0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_8	11160879	We show that the presence of the H/ACA snoRNP proteins Cbf5p, Nhp2p and Nop10p, but not Gar1p, is required for the accumulation of mature non-polyadenylated hTR in yeast, while accumulation of TLC1 RNA is not affected by the absence of any of these proteins.	gene_phenotype
72073	9	334579	5	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid	accumulation of	is not affected by					Cbf5p	GP	absence of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_8	11160879	We show that the presence of the H/ACA snoRNP proteins Cbf5p, Nhp2p and Nop10p, but not Gar1p, is required for the accumulation of mature non-polyadenylated hTR in yeast, while accumulation of TLC1 RNA is not affected by the absence of any of these proteins.	gene_phenotype
72074	10	334579	5	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid	accumulation of	is not affected by					Nhp2p	GP	absence of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_8	11160879	We show that the presence of the H/ACA snoRNP proteins Cbf5p, Nhp2p and Nop10p, but not Gar1p, is required for the accumulation of mature non-polyadenylated hTR in yeast, while accumulation of TLC1 RNA is not affected by the absence of any of these proteins.	gene_phenotype
72075	11	334579	5	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid	accumulation of	is not affected by					Nop10p	GP	absence of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_8	11160879	We show that the presence of the H/ACA snoRNP proteins Cbf5p, Nhp2p and Nop10p, but not Gar1p, is required for the accumulation of mature non-polyadenylated hTR in yeast, while accumulation of TLC1 RNA is not affected by the absence of any of these proteins.	gene_phenotype
72076	12	334579	5	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid	accumulation of	is not affected by					Gar1p	GP	absence of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_8	11160879	We show that the presence of the H/ACA snoRNP proteins Cbf5p, Nhp2p and Nop10p, but not Gar1p, is required for the accumulation of mature non-polyadenylated hTR in yeast, while accumulation of TLC1 RNA is not affected by the absence of any of these proteins.	gene_phenotype
72077	1	334580	5	NULL	NULL	0	NULL	Sm protein	GP		bind					TLC1 RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_173	11160879	Thus it seems that Sm protein binding to TLC1 RNA is required for its accumulation, just as assembly of H/ACA snoRNP proteins on the H/ACA domain of hTR is required for the accumulation of this RNA.	gene_phenotype
72078	2	334580	5	NULL	NULL	0	NULL	H/ACA snoRNP proteins	GP		assemble on					hTR	GP		H/ACA domain		NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_173	11160879	Thus it seems that Sm protein binding to TLC1 RNA is required for its accumulation, just as assembly of H/ACA snoRNP proteins on the H/ACA domain of hTR is required for the accumulation of this RNA.	gene_phenotype
72079	3	334580	5	NULL	NULL	0	NULL	statement 1	Process		is required for					TLC1 RNA	NucleicAcid	accumulation of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_173	11160879	Thus it seems that Sm protein binding to TLC1 RNA is required for its accumulation, just as assembly of H/ACA snoRNP proteins on the H/ACA domain of hTR is required for the accumulation of this RNA.	gene_phenotype
72080	4	334580	5	NULL	NULL	0	NULL	statement 2	Process		is required for					TLC1 RNA	NucleicAcid	accumulation of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_29_3_598_s_173	11160879	Thus it seems that Sm protein binding to TLC1 RNA is required for its accumulation, just as assembly of H/ACA snoRNP proteins on the H/ACA domain of hTR is required for the accumulation of this RNA.	gene_phenotype
72081	1	334587	5	NULL	NULL	0	NULL	TLC1	NucleicAcid		encodes					telomerase	GP			RNA subunit	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_4	10454554	Mutations of  TLC1 (encoding the RNA subunit of telomerase) result in strains that have continually shortening telomeres and a gradual loss of cell viability; survivors of senescence arise as a consequence of a Rad52p-dependent recombination events that amplify telomeric and subtelomeric repeats.	gene_phenotype
72082	2	334587	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	mutant	results in					telomere	Chromosome	short			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_4	10454554	Mutations of  TLC1 (encoding the RNA subunit of telomerase) result in strains that have continually shortening telomeres and a gradual loss of cell viability; survivors of senescence arise as a consequence of a Rad52p-dependent recombination events that amplify telomeric and subtelomeric repeats.	gene_phenotype
72083	3	334587	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	mutant	results in					cell viability	Process	gradual loss of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_4	10454554	Mutations of  TLC1 (encoding the RNA subunit of telomerase) result in strains that have continually shortening telomeres and a gradual loss of cell viability; survivors of senescence arise as a consequence of a Rad52p-dependent recombination events that amplify telomeric and subtelomeric repeats.	gene_phenotype
72084	4	334587	5	NULL	NULL	0	NULL	Rad52p-dependent recombination	Process		amplify					telomeric repeats	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_4	10454554	Mutations of  TLC1 (encoding the RNA subunit of telomerase) result in strains that have continually shortening telomeres and a gradual loss of cell viability; survivors of senescence arise as a consequence of a Rad52p-dependent recombination events that amplify telomeric and subtelomeric repeats.	gene_phenotype
72085	5	334587	5	NULL	NULL	0	NULL	Rad52p-dependent recombination	Process		amplify					ubtelomeric repeats	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_4	10454554	Mutations of  TLC1 (encoding the RNA subunit of telomerase) result in strains that have continually shortening telomeres and a gradual loss of cell viability; survivors of senescence arise as a consequence of a Rad52p-dependent recombination events that amplify telomeric and subtelomeric repeats.	gene_phenotype
72086	1	334588	5	NULL	NULL	0	NULL	MEC1	GP	mutation of	reduce					telomere	Chromosome	length of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_5	10454554	We show that a mutation in  MEC1 (a gene related in sequence to  TEL1 and  ATM) reduces telomere length and that  tel1 mec1 double mutant strains have a senescent phenotype similar to that found in  tlc1 strains.	gene_phenotype
72087	2	334588	5	NULL	NULL	0	NULL	MEC1 gene	GP		is related to					TEL1	GP	sequence of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_5	10454554	We show that a mutation in  MEC1 (a gene related in sequence to  TEL1 and  ATM) reduces telomere length and that  tel1 mec1 double mutant strains have a senescent phenotype similar to that found in  tlc1 strains.	gene_phenotype
72088	3	334588	5	NULL	NULL	0	NULL	MEC1 gene	GP		is related to					ATM	GP	sequence of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_5	10454554	We show that a mutation in  MEC1 (a gene related in sequence to  TEL1 and  ATM) reduces telomere length and that  tel1 mec1 double mutant strains have a senescent phenotype similar to that found in  tlc1 strains.	gene_phenotype
72089	4	334588	5	NULL	NULL	0	NULL	tel1 mec1 strain	Cell	double mutant	contains					senescent phenotype	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_5	10454554	We show that a mutation in  MEC1 (a gene related in sequence to  TEL1 and  ATM) reduces telomere length and that  tel1 mec1 double mutant strains have a senescent phenotype similar to that found in  tlc1 strains.	gene_phenotype
72090	5	334588	5	NULL	NULL	0	NULL	statement 4	Process		is similar to					tlc1 strains	Cell				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_5	10454554	We show that a mutation in  MEC1 (a gene related in sequence to  TEL1 and  ATM) reduces telomere length and that  tel1 mec1 double mutant strains have a senescent phenotype similar to that found in  tlc1 strains.	gene_phenotype
72174	1	334589	5	NULL	NULL	0	NULL	cell viability	Process		is associated with					telomeric repeats	NucleicAcid	loss of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_20	10454554	Although yeast strains with a mutation in  EST or  TLC1 genes undergo dramatic loss of cell viability associated with loss of telomeric repeats, fast-growing survivors arise within the mutant cultures ( 18,  19).	gene_phenotype
72175	3	334589	5	NULL	NULL	NULL	NULL	statement 2	Cell		undergoes					statement 1	Process	dramatic loss of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_20	10454554	Although yeast strains with a mutation in  EST or  TLC1 genes undergo dramatic loss of cell viability associated with loss of telomeric repeats, fast-growing survivors arise within the mutant cultures ( 18,  19).	gene_phenotype
72176	2	334589	5	NULL	NULL	0	NULL	yeast strain	Cell		contains					EST gene	GP	mutant			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_20	10454554	Although yeast strains with a mutation in  EST or  TLC1 genes undergo dramatic loss of cell viability associated with loss of telomeric repeats, fast-growing survivors arise within the mutant cultures ( 18,  19).	gene_phenotype
72177	4	334589	5	NULL	NULL	0	NULL	yeast strain	Cell		contains					TLC1 gene	GP	mutant			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_20	10454554	Although yeast strains with a mutation in  EST or  TLC1 genes undergo dramatic loss of cell viability associated with loss of telomeric repeats, fast-growing survivors arise within the mutant cultures ( 18,  19).	gene_phenotype
72178	5	334589	5	NULL	NULL	0	NULL	statement 4	Cell		undergoes					statement 1	Process	dramatic loss of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_20	10454554	Although yeast strains with a mutation in  EST or  TLC1 genes undergo dramatic loss of cell viability associated with loss of telomeric repeats, fast-growing survivors arise within the mutant cultures ( 18,  19).	gene_phenotype
73584	1	334590	5	NULL	NULL	NULL	NULL	est1 gene	GP	mutation of;;yeast	shortens		continually			telomere	Chromosome				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_108	10454554	[[            Mutations ]] in five yeast genes ( est1 to - 4 and  tlc1), including the RNA and protein subunits of telomerase, result in continually shortening telomeres and a senescent phenotype, a gradual loss of cell viability during vegetative subculturing ( 13,  19,  33).	gene_phenotype
73585	2	334590	5	NULL	NULL	0	NULL	est1 gene	GP	mutation of;;yeast	results in					senescent phenotype	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_108	10454554	[[            Mutations ]] in five yeast genes ( est1 to - 4 and  tlc1), including the RNA and protein subunits of telomerase, result in continually shortening telomeres and a senescent phenotype, a gradual loss of cell viability during vegetative subculturing ( 13,  19,  33).	gene_phenotype
73586	3	334590	5	NULL	NULL	0	NULL	est2 gene	GP	mutation of;;yeast	shortens		continually			telomere	Chromosome				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_108	10454554	[[            Mutations ]] in five yeast genes ( est1 to - 4 and  tlc1), including the RNA and protein subunits of telomerase, result in continually shortening telomeres and a senescent phenotype, a gradual loss of cell viability during vegetative subculturing ( 13,  19,  33).	gene_phenotype
73587	4	334590	5	NULL	NULL	0	NULL	est2 gene	GP	mutation of;;yeast	results in					senescent phenotype	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_108	10454554	[[            Mutations ]] in five yeast genes ( est1 to - 4 and  tlc1), including the RNA and protein subunits of telomerase, result in continually shortening telomeres and a senescent phenotype, a gradual loss of cell viability during vegetative subculturing ( 13,  19,  33).	gene_phenotype
73588	5	334590	5	NULL	NULL	0	NULL	est3 gene	GP	mutation of;;yeast	shortens		continually			telomere	Chromosome				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_108	10454554	[[            Mutations ]] in five yeast genes ( est1 to - 4 and  tlc1), including the RNA and protein subunits of telomerase, result in continually shortening telomeres and a senescent phenotype, a gradual loss of cell viability during vegetative subculturing ( 13,  19,  33).	gene_phenotype
73589	6	334590	5	NULL	NULL	0	NULL	est3 gene	GP	mutation of;;yeast	results in					senescent phenotype	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_108	10454554	[[            Mutations ]] in five yeast genes ( est1 to - 4 and  tlc1), including the RNA and protein subunits of telomerase, result in continually shortening telomeres and a senescent phenotype, a gradual loss of cell viability during vegetative subculturing ( 13,  19,  33).	gene_phenotype
73590	7	334590	5	NULL	NULL	0	NULL	est4 gene	GP	mutation of;;yeast	results in					senescent phenotype	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_108	10454554	[[            Mutations ]] in five yeast genes ( est1 to - 4 and  tlc1), including the RNA and protein subunits of telomerase, result in continually shortening telomeres and a senescent phenotype, a gradual loss of cell viability during vegetative subculturing ( 13,  19,  33).	gene_phenotype
73591	8	334590	5	NULL	NULL	0	NULL	senescent phenotype	PhysicalPhenomenon		loses		gradually			cell viability	Process				NULL	during vegetative subculturing	0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_108	10454554	[[            Mutations ]] in five yeast genes ( est1 to - 4 and  tlc1), including the RNA and protein subunits of telomerase, result in continually shortening telomeres and a senescent phenotype, a gradual loss of cell viability during vegetative subculturing ( 13,  19,  33).	gene_phenotype
73592	9	334590	5	NULL	NULL	0	NULL	tlc1 gene	GP	mutation of;;yeast	shortens		continually			telomere	Chromosome				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_108	10454554	[[            Mutations ]] in five yeast genes ( est1 to - 4 and  tlc1), including the RNA and protein subunits of telomerase, result in continually shortening telomeres and a senescent phenotype, a gradual loss of cell viability during vegetative subculturing ( 13,  19,  33).	gene_phenotype
73593	10	334590	5	NULL	NULL	0	NULL	tlc1 gene	GP	mutation of;;yeast	results in					senescent phenotype	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6065_s_108	10454554	[[            Mutations ]] in five yeast genes ( est1 to - 4 and  tlc1), including the RNA and protein subunits of telomerase, result in continually shortening telomeres and a senescent phenotype, a gradual loss of cell viability during vegetative subculturing ( 13,  19,  33).	gene_phenotype
72179	1	334592	5	NULL	NULL	NULL	NULL	EST1 gene	GP	mutation of	leads to					telomere	Chromosome	progressive shortening of			NULL	Saccharomyces cerevisiae	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_1947_s_19	10688642	For the yeast  Saccharomyces cerevisiae, genetic screens have identified five genes ( EST1,  EST2,  EST3,  EST4/CDC13, and  TLC1) ( 20,  27,  39) whose mutations lead to progressive telomere shortening and eventual loss of viability (i.e., senescence).	gene_phenotype
72180	2	334592	5	NULL	NULL	0	NULL	statement 1	Process		leads to		eventualy			senescence	Process				NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_molcellbiol_20_6_1947_s_19	10688642	For the yeast  Saccharomyces cerevisiae, genetic screens have identified five genes ( EST1,  EST2,  EST3,  EST4/CDC13, and  TLC1) ( 20,  27,  39) whose mutations lead to progressive telomere shortening and eventual loss of viability (i.e., senescence).	gene_phenotype
72181	3	334592	5	NULL	NULL	0	NULL	EST2 gene	GP	mutation of	leads to					telomere	Chromosome	progressive shortening of			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_molcellbiol_20_6_1947_s_19	10688642	For the yeast  Saccharomyces cerevisiae, genetic screens have identified five genes ( EST1,  EST2,  EST3,  EST4/CDC13, and  TLC1) ( 20,  27,  39) whose mutations lead to progressive telomere shortening and eventual loss of viability (i.e., senescence).	gene_phenotype
72182	4	334592	5	NULL	NULL	0	NULL	statement 3	Process		leads to		eventualy			senescence	Process				NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_molcellbiol_20_6_1947_s_19	10688642	For the yeast  Saccharomyces cerevisiae, genetic screens have identified five genes ( EST1,  EST2,  EST3,  EST4/CDC13, and  TLC1) ( 20,  27,  39) whose mutations lead to progressive telomere shortening and eventual loss of viability (i.e., senescence).	gene_phenotype
72183	5	334592	5	NULL	NULL	0	NULL	EST3 gene	GP	mutation of	leads to					telomere	Chromosome	progressive shortening of			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_molcellbiol_20_6_1947_s_19	10688642	For the yeast  Saccharomyces cerevisiae, genetic screens have identified five genes ( EST1,  EST2,  EST3,  EST4/CDC13, and  TLC1) ( 20,  27,  39) whose mutations lead to progressive telomere shortening and eventual loss of viability (i.e., senescence).	gene_phenotype
72184	6	334592	5	NULL	NULL	0	NULL	statement 5	Process		leads to		eventualy			senescence	Process				NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_molcellbiol_20_6_1947_s_19	10688642	For the yeast  Saccharomyces cerevisiae, genetic screens have identified five genes ( EST1,  EST2,  EST3,  EST4/CDC13, and  TLC1) ( 20,  27,  39) whose mutations lead to progressive telomere shortening and eventual loss of viability (i.e., senescence).	gene_phenotype
72185	7	334592	5	NULL	NULL	0	NULL	EST4/CDC13 gene	GP	mutation of	leads to					telomere	Chromosome	progressive shortening of			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_molcellbiol_20_6_1947_s_19	10688642	For the yeast  Saccharomyces cerevisiae, genetic screens have identified five genes ( EST1,  EST2,  EST3,  EST4/CDC13, and  TLC1) ( 20,  27,  39) whose mutations lead to progressive telomere shortening and eventual loss of viability (i.e., senescence).	gene_phenotype
72186	8	334592	5	NULL	NULL	NULL	NULL	statement 7	Process		leads to		eventualy			senescence	Process				NULL	Saccharomyces cerevisiae	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_6_1947_s_19	10688642	For the yeast  Saccharomyces cerevisiae, genetic screens have identified five genes ( EST1,  EST2,  EST3,  EST4/CDC13, and  TLC1) ( 20,  27,  39) whose mutations lead to progressive telomere shortening and eventual loss of viability (i.e., senescence).	gene_phenotype
72187	9	334592	5	NULL	NULL	0	NULL	TLC1 gene	GP	mutation of	leads to					telomere	Chromosome	progressive shortening of			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_molcellbiol_20_6_1947_s_19	10688642	For the yeast  Saccharomyces cerevisiae, genetic screens have identified five genes ( EST1,  EST2,  EST3,  EST4/CDC13, and  TLC1) ( 20,  27,  39) whose mutations lead to progressive telomere shortening and eventual loss of viability (i.e., senescence).	gene_phenotype
72188	10	334592	5	NULL	NULL	0	NULL	statement 9	Process		leads to		eventualy			senescence	Process				NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_molcellbiol_20_6_1947_s_19	10688642	For the yeast  Saccharomyces cerevisiae, genetic screens have identified five genes ( EST1,  EST2,  EST3,  EST4/CDC13, and  TLC1) ( 20,  27,  39) whose mutations lead to progressive telomere shortening and eventual loss of viability (i.e., senescence).	gene_phenotype
72189	1	334594	5	NULL	NULL	0	NULL	TLC1 gene	GP		encodes					telomerase	GP			RNA component	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_3_786_s_21	10629035	Yeast strains carrying a deletion of the  TLC1 gene, which encodes the RNA component of telomerase, show progressive telomere shortening, which ultimately leads to a loss of cell viability ( 53).	gene_phenotype
72190	2	334594	5	NULL	NULL	NULL	NULL	TLC1 gene	GP	deletion of	leads to					telomere	Chromosome	progressive shortening of			NULL	yeast strains	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_3_786_s_21	10629035	Yeast strains carrying a deletion of the  TLC1 gene, which encodes the RNA component of telomerase, show progressive telomere shortening, which ultimately leads to a loss of cell viability ( 53).	gene_phenotype
72191	3	334594	5	NULL	NULL	0	NULL	statement 2	Process		leads to		ultimately			cell viability	Process	loss of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_3_786_s_21	10629035	Yeast strains carrying a deletion of the  TLC1 gene, which encodes the RNA component of telomerase, show progressive telomere shortening, which ultimately leads to a loss of cell viability ( 53).	gene_phenotype
73579	1	334595	5	NULL	NULL	0	NULL	 yku80delta	GP	growth defect of;;mutant	is sensitive to					temperature	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_11_3721_s_15	12748277	Some of these components are interconnected; for instance, overexpression of the catalytic subunit of telomerase,  EST2, or of the telomerase RNA gene,  TLC1, suppressed the temperature-sensitive growth defect of a  yku80delta mutant at 37 degrees C ( 38,  49).	gene_phenotype
73580	2	334595	5	NULL	NULL	0	NULL	EST2	GP	overexpression of	suppress					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_11_3721_s_15	12748277	Some of these components are interconnected; for instance, overexpression of the catalytic subunit of telomerase,  EST2, or of the telomerase RNA gene,  TLC1, suppressed the temperature-sensitive growth defect of a  yku80delta mutant at 37 degrees C ( 38,  49).	gene_phenotype
73581	3	334595	5	NULL	NULL	NULL	NULL	TLC1 gene	GP	overexpression of	suppress					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_11_3721_s_15	12748277	Some of these components are interconnected; for instance, overexpression of the catalytic subunit of telomerase,  EST2, or of the telomerase RNA gene,  TLC1, suppressed the temperature-sensitive growth defect of a  yku80delta mutant at 37 degrees C ( 38,  49).	gene_phenotype
73582	4	334595	5	NULL	NULL	0	NULL	TLC1 gene	GP		is a type of					telomerase RNA gene	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_11_3721_s_15	12748277	Some of these components are interconnected; for instance, overexpression of the catalytic subunit of telomerase,  EST2, or of the telomerase RNA gene,  TLC1, suppressed the temperature-sensitive growth defect of a  yku80delta mutant at 37 degrees C ( 38,  49).	gene_phenotype
73583	5	334595	5	NULL	NULL	0	NULL	EST2	GP		is a subunit of		catalytic			telomerase	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_11_3721_s_15	12748277	Some of these components are interconnected; for instance, overexpression of the catalytic subunit of telomerase,  EST2, or of the telomerase RNA gene,  TLC1, suppressed the temperature-sensitive growth defect of a  yku80delta mutant at 37 degrees C ( 38,  49).	gene_phenotype
72257	1	334597	5	NULL	NULL	NULL	NULL	mtr10	GP		effects		specifically			Tlc1	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_301	12167699	The dispersed localization was not due to nuclear envelope leakiness, because the nucleolar RNA U3 had normal localization in  mtr10 cells (Fig.  6A), further suggesting a rather specific effect of  mtr10 on Tlc1.	gene_phenotype
72259	2	334597	5	NULL	NULL	0	NULL	RNA U3	NucleicAcid	nucleolar	is localized in		normal			mtr10 cells	Cell				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_301	12167699	The dispersed localization was not due to nuclear envelope leakiness, because the nucleolar RNA U3 had normal localization in  mtr10 cells (Fig.  6A), further suggesting a rather specific effect of  mtr10 on Tlc1.	gene_phenotype
72261	1	334598	5	NULL	NULL	0	NULL	telomere	Chromosome		is shortened in					mtr10 cells	Cell				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_308	12167699	This is the most likely cause of the telomere shortening observed in  mtr10 cells, because overexpression of  TLC1 in the mutant restored both telomere length and levels of mTlc1 without suppressing other aspects of the  mtr10 phenotype.	gene_phenotype
72263	2	334598	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	overexpression of	restores					telomere	Chromosome	length of			NULL	mutant mtr10 cells	0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_308	12167699	This is the most likely cause of the telomere shortening observed in  mtr10 cells, because overexpression of  TLC1 in the mutant restored both telomere length and levels of mTlc1 without suppressing other aspects of the  mtr10 phenotype.	gene_phenotype
72264	3	334598	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	overexpression of	restores					mTlc1	NucleicAcid	level of			NULL	mutant mtr10 cells	0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_308	12167699	This is the most likely cause of the telomere shortening observed in  mtr10 cells, because overexpression of  TLC1 in the mutant restored both telomere length and levels of mTlc1 without suppressing other aspects of the  mtr10 phenotype.	gene_phenotype
72265	1	334599	5	NULL	NULL	0	NULL	Est2p	GP		is a subunit of					telomerase	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_7_2182_s_254	11884605	It has been shown that overexpression of telomerase subunit Est2p or TLC1 suppresses checkpoint activation and restores viability at high temperature in Yku- cells without apparently modifying telomere length ( 75).	gene_phenotype
72266	2	334599	5	NULL	NULL	NULL	NULL	Est2p	GP	overexpression of	suppress					checkpoint	Process	activation of			NULL	Yku- cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_7_2182_s_254	11884605	It has been shown that overexpression of telomerase subunit Est2p or TLC1 suppresses checkpoint activation and restores viability at high temperature in Yku- cells without apparently modifying telomere length ( 75).	gene_phenotype
72267	3	334599	5	NULL	NULL	NULL	NULL	TLC1	NucleicAcid	overexpression of	suppress					checkpoint	Process	activation of			NULL	Yku- cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_7_2182_s_254	11884605	It has been shown that overexpression of telomerase subunit Est2p or TLC1 suppresses checkpoint activation and restores viability at high temperature in Yku- cells without apparently modifying telomere length ( 75).	gene_phenotype
72268	4	334599	5	NULL	NULL	0	NULL	statement 2	Process		restores					viability	Process				NULL	Yku- cells	0	NULL	NULL	NULL	gw60_molcellbiol_22_7_2182_s_254	11884605	It has been shown that overexpression of telomerase subunit Est2p or TLC1 suppresses checkpoint activation and restores viability at high temperature in Yku- cells without apparently modifying telomere length ( 75).	gene_phenotype
72269	5	334599	5	NULL	NULL	NULL	NULL	statement 4	Process		occurs without modifying					telomere	Chromosome	length of			NULL	Yku- cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_7_2182_s_254	11884605	It has been shown that overexpression of telomerase subunit Est2p or TLC1 suppresses checkpoint activation and restores viability at high temperature in Yku- cells without apparently modifying telomere length ( 75).	gene_phenotype
72270	6	334599	5	NULL	NULL	0	NULL	statement 3	Process		restores					viability	Process				NULL	Yku- cells	0	NULL	NULL	NULL	gw60_molcellbiol_22_7_2182_s_254	11884605	It has been shown that overexpression of telomerase subunit Est2p or TLC1 suppresses checkpoint activation and restores viability at high temperature in Yku- cells without apparently modifying telomere length ( 75).	gene_phenotype
72271	7	334599	5	NULL	NULL	NULL	NULL	statement 6	Process		occurs without modifying					telomere	Chromosome	length of			NULL	Yku- cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_22_7_2182_s_254	11884605	It has been shown that overexpression of telomerase subunit Est2p or TLC1 suppresses checkpoint activation and restores viability at high temperature in Yku- cells without apparently modifying telomere length ( 75).	gene_phenotype
72272	1	334600	5	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid	viable alleles of	is required for					telomere	Chromosome	function of			NULL	in vivo	0	NULL	NULL	NULL	gw60_molcellbiol_22_7_2366_s_3	11884619	A selection for viable alleles of  TLC1 RNA from a large library of random deletion alleles revealed that less than half ( 0.5 kb of the  1.3-kb RNA) is required for telomerase function in vivo.	gene_phenotype
72273	1	334601	5	NULL	NULL	NULL	NULL	telomerase	GP	yeast	is encoded by				RNA subunit	TLC1 gene	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_17_9202_s_23	9256460	Although the RNA subunit of yeast telomerase is known to be encoded by the gene  TLC1 ( 20) and is essential for telomerase catalysis ( 19), no yeast protein has heretofore been found to be essential for telomerase enzyme activity.	gene_phenotype
72274	2	334601	5	NULL	NULL	0	NULL	TLC1 gene	GP	yeast	is essential for					telomerase	GP	catalysis of			NULL		0	NULL	NULL	NULL	gw60_pnas_94_17_9202_s_23	9256460	Although the RNA subunit of yeast telomerase is known to be encoded by the gene  TLC1 ( 20) and is essential for telomerase catalysis ( 19), no yeast protein has heretofore been found to be essential for telomerase enzyme activity.	gene_phenotype
72275	1	334602	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	mutant	decreases		gradually			telomere	Chromosome	length of			NULL		0	NULL	NULL	NULL	gw60_pnas_94_17_9202_s_24	9256460	TLC1 mutants ( 20) exhibit two phenotypes that are shared by mutants of the genes  EST1 ( 21) and  CDC13 ( 22-24): a gradual decrease in telomere length and a consequent decline in cell viability.	gene_phenotype
72276	2	334602	5	NULL	NULL	0	NULL	statement 1	Process		decline		consequently			cell viability	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_17_9202_s_24	9256460	TLC1 mutants ( 20) exhibit two phenotypes that are shared by mutants of the genes  EST1 ( 21) and  CDC13 ( 22-24): a gradual decrease in telomere length and a consequent decline in cell viability.	gene_phenotype
72277	3	334602	5	NULL	NULL	0	NULL	EST1 gene	GP	mutant	decreases		gradually			telomere	Chromosome	length of			NULL		0	NULL	NULL	NULL	gw60_pnas_94_17_9202_s_24	9256460	TLC1 mutants ( 20) exhibit two phenotypes that are shared by mutants of the genes  EST1 ( 21) and  CDC13 ( 22-24): a gradual decrease in telomere length and a consequent decline in cell viability.	gene_phenotype
72278	4	334602	5	NULL	NULL	NULL	NULL	statement 3	Process		decline		consequently			cell viability	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_17_9202_s_24	9256460	TLC1 mutants ( 20) exhibit two phenotypes that are shared by mutants of the genes  EST1 ( 21) and  CDC13 ( 22-24): a gradual decrease in telomere length and a consequent decline in cell viability.	gene_phenotype
72279	5	334602	5	NULL	NULL	0	NULL	CDC13 gene	GP	mutant	decreases		gradually			telomere	Chromosome	length of			NULL		0	NULL	NULL	NULL	gw60_pnas_94_17_9202_s_24	9256460	TLC1 mutants ( 20) exhibit two phenotypes that are shared by mutants of the genes  EST1 ( 21) and  CDC13 ( 22-24): a gradual decrease in telomere length and a consequent decline in cell viability.	gene_phenotype
72280	6	334602	5	NULL	NULL	0	NULL	statement 5	Process		decreases		consequently			cell viability	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_17_9202_s_24	9256460	TLC1 mutants ( 20) exhibit two phenotypes that are shared by mutants of the genes  EST1 ( 21) and  CDC13 ( 22-24): a gradual decrease in telomere length and a consequent decline in cell viability.	gene_phenotype
72281	1	334603	5	NULL	NULL	0	NULL	tTLC1	NucleicAcid		is					dominant truncated allele of TLC1	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_pnas_94_18_9768_s_57	9275199	Thus, we overexpressed the dominant truncated allele of  TLC1 ( tTLC1), which was shown to result in telomeres adopting a shorter steady-state length (ref.  9; Fig.  1 A, lane 3).	gene_phenotype
72282	3	334603	5	NULL	NULL	0	NULL	tTLC1	NucleicAcid		results in					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_18_9768_s_57	9275199	Thus, we overexpressed the dominant truncated allele of  TLC1 ( tTLC1), which was shown to result in telomeres adopting a shorter steady-state length (ref.  9; Fig.  1 A, lane 3).	gene_phenotype
72283	2	334603	5	NULL	NULL	0	NULL	telomere	Chromosome		adopt					steady-state length	PhysicalPhenomenon	short			NULL		0	NULL	NULL	NULL	gw60_pnas_94_18_9768_s_57	9275199	Thus, we overexpressed the dominant truncated allele of  TLC1 ( tTLC1), which was shown to result in telomeres adopting a shorter steady-state length (ref.  9; Fig.  1 A, lane 3).	gene_phenotype
72284	1	334604	5	NULL	NULL	0	NULL	telomere 	Chromosome	length of	is inversly related to					lifespan	Time				NULL		0	NULL	NULL	NULL	gw60_pnas_94_18_9768_s_87	9275199	While the above experiments suggested that telomere length was inversely related to lifespan, it was possible that the mutations in  TLC1 or  RAP1 used to alter telomere length affected lifespan in some other way.	gene_phenotype
72285	2	334604	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	mutation of	alter					telomere	Chromosome	length of			NULL		0	NULL	NULL	NULL	gw60_pnas_94_18_9768_s_87	9275199	While the above experiments suggested that telomere length was inversely related to lifespan, it was possible that the mutations in  TLC1 or  RAP1 used to alter telomere length affected lifespan in some other way.	gene_phenotype
72286	3	334604	5	NULL	NULL	0	NULL	statement 2	Process		affects		possibly			lifespan	Time				NULL		0	NULL	NULL	NULL	gw60_pnas_94_18_9768_s_87	9275199	While the above experiments suggested that telomere length was inversely related to lifespan, it was possible that the mutations in  TLC1 or  RAP1 used to alter telomere length affected lifespan in some other way.	gene_phenotype
72287	4	334604	5	NULL	NULL	0	NULL	RAP1	GP	mutation of	alter					telomere	Chromosome	length of			NULL		0	NULL	NULL	NULL	gw60_pnas_94_18_9768_s_87	9275199	While the above experiments suggested that telomere length was inversely related to lifespan, it was possible that the mutations in  TLC1 or  RAP1 used to alter telomere length affected lifespan in some other way.	gene_phenotype
72288	5	334604	5	NULL	NULL	0	NULL	statement 4	Process		affects		possibly			lifespan	Time				NULL		0	NULL	NULL	NULL	gw60_pnas_94_18_9768_s_87	9275199	While the above experiments suggested that telomere length was inversely related to lifespan, it was possible that the mutations in  TLC1 or  RAP1 used to alter telomere length affected lifespan in some other way.	gene_phenotype
72290	1	334605	5	NULL	NULL	0	NULL	rad50	GP	mutant	resistant to					ionizing radiation	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	abs-batch0550-0559_genetics_160_1_11805044_s_4	11805044	Overexpression of EXO1 or TLC1 increased the resistance of rad50,  mre11, and xrs2 mutants to ionizing radiation and MMS, but did not increase  resistance in strains defective in recombination (rad51, rad52, rad54,  rad59) or NHEJ only (yku70, sir4).	gene_phenotype
72291	2	334605	5	NULL	NULL	0	NULL	mre11	GP	mutant	resistant to					ionizing radiation	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	abs-batch0550-0559_genetics_160_1_11805044_s_4	11805044	Overexpression of EXO1 or TLC1 increased the resistance of rad50,  mre11, and xrs2 mutants to ionizing radiation and MMS, but did not increase  resistance in strains defective in recombination (rad51, rad52, rad54,  rad59) or NHEJ only (yku70, sir4).	gene_phenotype
72292	3	334605	5	NULL	NULL	0	NULL	xrs2	GP	mutant	resistant to					ionizing radiation	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	abs-batch0550-0559_genetics_160_1_11805044_s_4	11805044	Overexpression of EXO1 or TLC1 increased the resistance of rad50,  mre11, and xrs2 mutants to ionizing radiation and MMS, but did not increase  resistance in strains defective in recombination (rad51, rad52, rad54,  rad59) or NHEJ only (yku70, sir4).	gene_phenotype
72293	4	334605	5	NULL	NULL	0	NULL	rad50	GP	mutant	resistant to					MMS	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0550-0559_genetics_160_1_11805044_s_4	11805044	Overexpression of EXO1 or TLC1 increased the resistance of rad50,  mre11, and xrs2 mutants to ionizing radiation and MMS, but did not increase  resistance in strains defective in recombination (rad51, rad52, rad54,  rad59) or NHEJ only (yku70, sir4).	gene_phenotype
72295	5	334605	5	NULL	NULL	0	NULL	mre11	GP	mutant	resistant to					MMS	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0550-0559_genetics_160_1_11805044_s_4	11805044	Overexpression of EXO1 or TLC1 increased the resistance of rad50,  mre11, and xrs2 mutants to ionizing radiation and MMS, but did not increase  resistance in strains defective in recombination (rad51, rad52, rad54,  rad59) or NHEJ only (yku70, sir4).	gene_phenotype
72296	6	334605	5	NULL	NULL	0	NULL	xrs2	GP	mutant	resistant to					MMS	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0550-0559_genetics_160_1_11805044_s_4	11805044	Overexpression of EXO1 or TLC1 increased the resistance of rad50,  mre11, and xrs2 mutants to ionizing radiation and MMS, but did not increase  resistance in strains defective in recombination (rad51, rad52, rad54,  rad59) or NHEJ only (yku70, sir4).	gene_phenotype
72298	7	334605	5	NULL	NULL	0	NULL	EXO1	GP	overexpression of	increases					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0550-0559_genetics_160_1_11805044_s_4	11805044	Overexpression of EXO1 or TLC1 increased the resistance of rad50,  mre11, and xrs2 mutants to ionizing radiation and MMS, but did not increase  resistance in strains defective in recombination (rad51, rad52, rad54,  rad59) or NHEJ only (yku70, sir4).	gene_phenotype
72299	8	334605	5	NULL	NULL	0	NULL	EXO1	GP	overexpression of	increases					statement 2	Process				NULL		0	NULL	NULL	NULL	abs-batch0550-0559_genetics_160_1_11805044_s_4	11805044	Overexpression of EXO1 or TLC1 increased the resistance of rad50,  mre11, and xrs2 mutants to ionizing radiation and MMS, but did not increase  resistance in strains defective in recombination (rad51, rad52, rad54,  rad59) or NHEJ only (yku70, sir4).	gene_phenotype
72300	1	334607	5	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid	viable alleles of	is required for					telomerase	GP	function of			NULL	in vivo	0	NULL	NULL	NULL	abs-batch0650-0679_mol-cell-biol_22_7_11884619_s_3	11884619	A selection for viable alleles of TLC1 RNA from a large library  of random deletion alleles revealed that less than half (approximately  0.5 kb of the approximately 1.3-kb RNA) is required for telomerase function  in vivo.	gene_phenotype
72301	1	334608	5	NULL	NULL	0	NULL	EST2	GP	overexpression of	does not restore					DNA repair	Process	efficient			NULL	yku80 mutants	0	NULL	NULL	NULL	abs-batch0650-0679_embo-rep_2_3_11266360_s_5	11266360	We show that overexpression of EST2 or TLC1 in  yku80 mutants does not restore efficient DNA repair, or restore normal  telomere function, as measured by telomere length, single-stranded G-rich  strand or transcriptional silencing.	gene_phenotype
72302	2	334608	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	overexpression of	does not restore					DNA repair	Process	efficient			NULL	yku80 mutants	0	NULL	NULL	NULL	abs-batch0650-0679_embo-rep_2_3_11266360_s_5	11266360	We show that overexpression of EST2 or TLC1 in  yku80 mutants does not restore efficient DNA repair, or restore normal  telomere function, as measured by telomere length, single-stranded G-rich  strand or transcriptional silencing.	gene_phenotype
72303	3	334608	5	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_embo-rep_2_3_11266360_s_5	11266360	We show that overexpression of EST2 or TLC1 in  yku80 mutants does not restore efficient DNA repair, or restore normal  telomere function, as measured by telomere length, single-stranded G-rich  strand or transcriptional silencing.	gene_phenotype
72306	4	334608	5	NULL	NULL	0	NULL	EST2	GP	overexpression of	does not restore					telomere	Chromosome	normal function of			NULL	yku80 mutants	0	NULL	NULL	NULL	abs-batch0650-0679_embo-rep_2_3_11266360_s_5	11266360	We show that overexpression of EST2 or TLC1 in  yku80 mutants does not restore efficient DNA repair, or restore normal  telomere function, as measured by telomere length, single-stranded G-rich  strand or transcriptional silencing.	gene_phenotype
72307	5	334608	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	overexpression of	does not restore					telomere	Chromosome	normal function of			NULL	yku80 mutants	0	NULL	NULL	NULL	abs-batch0650-0679_embo-rep_2_3_11266360_s_5	11266360	We show that overexpression of EST2 or TLC1 in  yku80 mutants does not restore efficient DNA repair, or restore normal  telomere function, as measured by telomere length, single-stranded G-rich  strand or transcriptional silencing.	gene_phenotype
72308	6	334608	5	NULL	NULL	0	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_embo-rep_2_3_11266360_s_5	11266360	We show that overexpression of EST2 or TLC1 in  yku80 mutants does not restore efficient DNA repair, or restore normal  telomere function, as measured by telomere length, single-stranded G-rich  strand or transcriptional silencing.	gene_phenotype
72319	1	334610	5	NULL	NULL	0	NULL	telomeric circle-mediated targeting	Process		occurs in		frequently			type I tlc1 survivors	Cell	established			NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_4_2_327_s_215	15701795	In addition, established type I and type II  tlc1 survivors both displayed a 20% higher frequency in telomeric circle-mediated targeting than the  tlc1 cells right from sporulation and prior to the survivor formation (Table  1), suggesting that telomeric circle-mediated targeting occurs more frequently in established type I and type II survivors.	gene_phenotype
72320	2	334610	5	NULL	NULL	NULL	NULL	telomeric circle-mediated targeting	Process		occurs in		frequently			type II tlc1 survivors	Cell	established			NULL		NULL	NULL	NULL	NULL	gw70_eukaryotcell_4_2_327_s_215	15701795	In addition, established type I and type II  tlc1 survivors both displayed a 20% higher frequency in telomeric circle-mediated targeting than the  tlc1 cells right from sporulation and prior to the survivor formation (Table  1), suggesting that telomeric circle-mediated targeting occurs more frequently in established type I and type II survivors.	gene_phenotype
72327	2	334611	5	NULL	NULL	NULL	NULL	telomere	Chromosome	defect in	leads to		probably			tlc1-h tlc1-h homozygote 	Cell	poor sporulation efficiency of 			NULL		NULL	NULL	NULL	NULL	gw70_embo_22_7_1697_s_120	12660175	Since the sporulation efficiency of  tlc1-h tlc1-h homozygote was very poor, probably due to their telomeric defects, the production  of mutated haploid cells from the diploids was very inefficient.	gene_phenotype
72329	1	334611	5	NULL	NULL	0	NULL	haploid cells	Cell		is produced from					diploids	Cell				NULL		0	NULL	NULL	NULL	gw70_embo_22_7_1697_s_120	12660175	Since the sporulation efficiency of  tlc1-h tlc1-h homozygote was very poor, probably due to their telomeric defects, the production  of mutated haploid cells from the diploids was very inefficient.	gene_phenotype
72330	3	334611	5	NULL	NULL	0	NULL	statement 2	Process		leads to					statement 1	Process	inefficient;;mutant			NULL		0	NULL	NULL	NULL	gw70_embo_22_7_1697_s_120	12660175	Since the sporulation efficiency of  tlc1-h tlc1-h homozygote was very poor, probably due to their telomeric defects, the production  of mutated haploid cells from the diploids was very inefficient.	gene_phenotype
72331	1	334613	5	NULL	NULL	NULL	NULL	Rap1p	GP		is absent in					VII-L telomere	Chromosome				NULL		NULL	NULL	NULL	NULL	gw70_embo_22_7_1688_s_219	12660174	Since the YH/YH diploid, with its mixture of yeast and vertebrate telomeric DNA  at all telomeres, was as defective in meiosis as the H/H strain that was homozygous  for the C3TA2 telomere ( Figure 4B), the meiotic defect of the  tlc1h strain can not be attributed solely to the absence of Rap1p at the VII-L telomere.	gene_phenotype
72332	2	334613	5	NULL	NULL	0	NULL	tlc1h strain	Cell	meiotic defect of 	is not attributed to		solely			statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_embo_22_7_1688_s_219	12660174	Since the YH/YH diploid, with its mixture of yeast and vertebrate telomeric DNA  at all telomeres, was as defective in meiosis as the H/H strain that was homozygous  for the C3TA2 telomere ( Figure 4B), the meiotic defect of the  tlc1h strain can not be attributed solely to the absence of Rap1p at the VII-L telomere.	gene_phenotype
72333	3	334613	5	NULL	NULL	0	NULL	YH/YH diploid	Cell		contains					telomeric DNA	NucleicAcid	mixture of;;yeast and vertebrate			NULL	telomeres	0	NULL	NULL	NULL	gw70_embo_22_7_1688_s_219	12660174	Since the YH/YH diploid, with its mixture of yeast and vertebrate telomeric DNA  at all telomeres, was as defective in meiosis as the H/H strain that was homozygous  for the C3TA2 telomere ( Figure 4B), the meiotic defect of the  tlc1h strain can not be attributed solely to the absence of Rap1p at the VII-L telomere.	gene_phenotype
72334	4	334613	5	NULL	NULL	0	NULL	statement 3	Cell		is defective in					meiosis	Process				NULL		0	NULL	NULL	NULL	gw70_embo_22_7_1688_s_219	12660174	Since the YH/YH diploid, with its mixture of yeast and vertebrate telomeric DNA  at all telomeres, was as defective in meiosis as the H/H strain that was homozygous  for the C3TA2 telomere ( Figure 4B), the meiotic defect of the  tlc1h strain can not be attributed solely to the absence of Rap1p at the VII-L telomere.	gene_phenotype
72335	5	334613	5	NULL	NULL	0	NULL	H/H strain	Cell		is homozygous for					C3TA2 telomere	Chromosome				NULL		0	NULL	NULL	NULL	gw70_embo_22_7_1688_s_219	12660174	Since the YH/YH diploid, with its mixture of yeast and vertebrate telomeric DNA  at all telomeres, was as defective in meiosis as the H/H strain that was homozygous  for the C3TA2 telomere ( Figure 4B), the meiotic defect of the  tlc1h strain can not be attributed solely to the absence of Rap1p at the VII-L telomere.	gene_phenotype
72336	6	334613	5	NULL	NULL	0	NULL	statement 5	Cell		is defective in					meiosis	Process				NULL		0	NULL	NULL	NULL	gw70_embo_22_7_1688_s_219	12660174	Since the YH/YH diploid, with its mixture of yeast and vertebrate telomeric DNA  at all telomeres, was as defective in meiosis as the H/H strain that was homozygous  for the C3TA2 telomere ( Figure 4B), the meiotic defect of the  tlc1h strain can not be attributed solely to the absence of Rap1p at the VII-L telomere.	gene_phenotype
72337	1	334614	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	full-length	disrupts					telomeric silencing	Process				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_19_2384_s_47	12975323	The triple stem-loop had been found previously to most closely match the activity of full-length TLC1 in disrupting telomeric silencing (Peterson et al. 2001 ), perhaps because the stem-loop can fold most stably in this construct.	gene_phenotype
72338	2	334614	5	NULL	NULL	0	NULL	triple stem-loop	NucleicAcid		disrupts					telomeric silencing	Process				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_19_2384_s_47	12975323	The triple stem-loop had been found previously to most closely match the activity of full-length TLC1 in disrupting telomeric silencing (Peterson et al. 2001 ), perhaps because the stem-loop can fold most stably in this construct.	gene_phenotype
72339	1	334615	5	NULL	NULL	0	NULL	Ku	GP		bind					TLC1 RNA	NucleicAcid			stem-loop	NULL		0	NULL	NULL	NULL	gw70_genesdev_17_19_2384_s_156	12975323	It disrupts Ku's ability to bind the 48-nucleotide stem-loop of TLC1 RNA, but retains Ku's ability to bind DNA, as well as many of Ku's DNA-based activities, namely telomeric silencing, chromosome end protection, and DNA repair via NHEJ.	gene_phenotype
72340	2	334615	5	NULL	NULL	0	NULL	Ku	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_19_2384_s_156	12975323	It disrupts Ku's ability to bind the 48-nucleotide stem-loop of TLC1 RNA, but retains Ku's ability to bind DNA, as well as many of Ku's DNA-based activities, namely telomeric silencing, chromosome end protection, and DNA repair via NHEJ.	gene_phenotype
72341	3	334615	5	NULL	NULL	0	NULL	Ku	GP		activates					telomeric silencing	Process				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_19_2384_s_156	12975323	It disrupts Ku's ability to bind the 48-nucleotide stem-loop of TLC1 RNA, but retains Ku's ability to bind DNA, as well as many of Ku's DNA-based activities, namely telomeric silencing, chromosome end protection, and DNA repair via NHEJ.	gene_phenotype
72342	4	334615	5	NULL	NULL	0	NULL	Ku	GP		activates					chromosome end 	Chromosome	protection of			NULL		0	NULL	NULL	NULL	gw70_genesdev_17_19_2384_s_156	12975323	It disrupts Ku's ability to bind the 48-nucleotide stem-loop of TLC1 RNA, but retains Ku's ability to bind DNA, as well as many of Ku's DNA-based activities, namely telomeric silencing, chromosome end protection, and DNA repair via NHEJ.	gene_phenotype
72343	5	334615	5	NULL	NULL	0	NULL	Ku	GP		activates					DNA	NucleicAcid	repair of			NULL		0	NULL	NULL	NULL	gw70_genesdev_17_19_2384_s_156	12975323	It disrupts Ku's ability to bind the 48-nucleotide stem-loop of TLC1 RNA, but retains Ku's ability to bind DNA, as well as many of Ku's DNA-based activities, namely telomeric silencing, chromosome end protection, and DNA repair via NHEJ.	gene_phenotype
72344	6	334615	5	NULL	NULL	0	NULL	statement 5	Process		via					NHEJ	Process				NULL		0	NULL	NULL	NULL	gw70_genesdev_17_19_2384_s_156	12975323	It disrupts Ku's ability to bind the 48-nucleotide stem-loop of TLC1 RNA, but retains Ku's ability to bind DNA, as well as many of Ku's DNA-based activities, namely telomeric silencing, chromosome end protection, and DNA repair via NHEJ.	gene_phenotype
72345	1	334616	5	NULL	NULL	0	NULL	telomerase activity	Process		is dependent on					Est2p activity	Process	Saccharomyces cerevisiae			NULL	in vitro	0	NULL	NULL	NULL	gw70_genesdev_18_15_1781_s_21	15289453	Although in vitro telomerase activity is dependent on the activity of the reverse transcriptase catalytic subunit (Est2p in the budding yeast  Saccharomyces cerevisiae; TERT in mammals) and the telomerase RNA template (Tlc1 in  S. cerevisiae and hTR in humans), other factors are clearly needed for telomerase action in vivo (see  Table 1).	gene_phenotype
72346	2	334616	5	NULL	NULL	0	NULL	telomerase activity	Process		is dependent on					TERT activity	Process	mammals			NULL	in vitro	0	NULL	NULL	NULL	gw70_genesdev_18_15_1781_s_21	15289453	Although in vitro telomerase activity is dependent on the activity of the reverse transcriptase catalytic subunit (Est2p in the budding yeast  Saccharomyces cerevisiae; TERT in mammals) and the telomerase RNA template (Tlc1 in  S. cerevisiae and hTR in humans), other factors are clearly needed for telomerase action in vivo (see  Table 1).	gene_phenotype
72347	3	334616	5	NULL	NULL	0	NULL	telomerase activity	Process		is dependent on					Tlc1	NucleicAcid	S.cerevisiae			NULL	in vitro	0	NULL	NULL	NULL	gw70_genesdev_18_15_1781_s_21	15289453	Although in vitro telomerase activity is dependent on the activity of the reverse transcriptase catalytic subunit (Est2p in the budding yeast  Saccharomyces cerevisiae; TERT in mammals) and the telomerase RNA template (Tlc1 in  S. cerevisiae and hTR in humans), other factors are clearly needed for telomerase action in vivo (see  Table 1).	gene_phenotype
72348	4	334616	5	NULL	NULL	NULL	NULL	telomerase activity	Process		is dependent on					hTR	NucleicAcid	human			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_genesdev_18_15_1781_s_21	15289453	Although in vitro telomerase activity is dependent on the activity of the reverse transcriptase catalytic subunit (Est2p in the budding yeast  Saccharomyces cerevisiae; TERT in mammals) and the telomerase RNA template (Tlc1 in  S. cerevisiae and hTR in humans), other factors are clearly needed for telomerase action in vivo (see  Table 1).	gene_phenotype
72349	5	334616	5	NULL	NULL	0	NULL	Est2p	GP	Saccharomyces cerevisiae	is a subunit of		catalytic			reverse transcriptase	GP	Saccharomyces cerevisiae			NULL		0	NULL	NULL	NULL	gw70_genesdev_18_15_1781_s_21	15289453	Although in vitro telomerase activity is dependent on the activity of the reverse transcriptase catalytic subunit (Est2p in the budding yeast  Saccharomyces cerevisiae; TERT in mammals) and the telomerase RNA template (Tlc1 in  S. cerevisiae and hTR in humans), other factors are clearly needed for telomerase action in vivo (see  Table 1).	gene_phenotype
72350	6	334616	5	NULL	NULL	0	NULL	TERT	GP	mammals	is a subunit of		catalytic			reverse transcriptase	GP	mammals			NULL		0	NULL	NULL	NULL	gw70_genesdev_18_15_1781_s_21	15289453	Although in vitro telomerase activity is dependent on the activity of the reverse transcriptase catalytic subunit (Est2p in the budding yeast  Saccharomyces cerevisiae; TERT in mammals) and the telomerase RNA template (Tlc1 in  S. cerevisiae and hTR in humans), other factors are clearly needed for telomerase action in vivo (see  Table 1).	gene_phenotype
72351	7	334616	5	NULL	NULL	0	NULL	Tlc1	NucleicAcid	S. cerevisiae	is a type of					telomerase RNA template	NucleicAcid	S.cerevisiae			NULL		0	NULL	NULL	NULL	gw70_genesdev_18_15_1781_s_21	15289453	Although in vitro telomerase activity is dependent on the activity of the reverse transcriptase catalytic subunit (Est2p in the budding yeast  Saccharomyces cerevisiae; TERT in mammals) and the telomerase RNA template (Tlc1 in  S. cerevisiae and hTR in humans), other factors are clearly needed for telomerase action in vivo (see  Table 1).	gene_phenotype
72352	8	334616	5	NULL	NULL	0	NULL	hTR	NucleicAcid	human	is a type of					telomerase RNA template	NucleicAcid	human			NULL		0	NULL	NULL	NULL	gw70_genesdev_18_15_1781_s_21	15289453	Although in vitro telomerase activity is dependent on the activity of the reverse transcriptase catalytic subunit (Est2p in the budding yeast  Saccharomyces cerevisiae; TERT in mammals) and the telomerase RNA template (Tlc1 in  S. cerevisiae and hTR in humans), other factors are clearly needed for telomerase action in vivo (see  Table 1).	gene_phenotype
72381	1	334619	5	NULL	NULL	0	NULL	repetitive sequences	NucleicAcid		is maintained by					telomerase	GP				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72382	2	334619	5	NULL	NULL	0	NULL	telomeres	Chromosome		is composed of					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72383	3	334619	5	NULL	NULL	NULL	NULL	telomerase	GP		is a complex of					hTERT	GP				NULL	human	NULL	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72384	4	334619	5	NULL	NULL	0	NULL	telomerase	GP		is a complex of					hTERC	NucleicAcid				NULL	human	0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72385	5	334619	5	NULL	NULL	0	NULL	telomerase	GP		is a complex of					Est1 protein	GP				NULL	human	0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72386	6	334619	5	NULL	NULL	0	NULL	telomerase	GP		is a complex of					dyskerin	GP				NULL	human	0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72387	7	334619	5	NULL	NULL	0	NULL	statement 3	Process		occurs along with					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72388	8	334619	5	NULL	NULL	0	NULL	statement 5	Process		occurs along with					statement 6	Process				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72389	9	334619	5	NULL	NULL	0	NULL	statement 7	Process		occurs along with					statement 8	Process				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72390	10	334619	5	NULL	NULL	0	NULL	telomerase	GP		is a complex of					Est2	GP				NULL	budding yeast	0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72391	11	334619	5	NULL	NULL	0	NULL	telomerase	GP		is a complex of					Tlc1	NucleicAcid				NULL	budding yeast	0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72392	12	334619	5	NULL	NULL	0	NULL	telomerase	GP		is a complex of					Est1 protein	GP				NULL	budding yeast	0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72393	13	334619	5	NULL	NULL	0	NULL	telomerase	GP		is a complex of					Est3 protein	GP				NULL	budding yeast	0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72394	14	334619	5	NULL	NULL	0	NULL	telomerase	GP		is a complex of					Sm protein	GP				NULL	budding yeast	0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72395	15	334619	5	NULL	NULL	0	NULL	statement 10	Process		occurs along with					statement 11	Process				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72396	16	334619	5	NULL	NULL	0	NULL	statement 12	Process		occurs along with					statement 13	Process				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72397	17	334619	5	NULL	NULL	0	NULL	statement 15	Process		occurs along with					statement 16	Process				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72398	18	334619	5	NULL	NULL	0	NULL	statement 17	Process		occurs along with					statement 14	Process				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72399	19	334619	5	NULL	NULL	0	NULL	hTERT	GP		is a type of					reverse transcriptase	GP				NULL	human	0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72400	20	334619	5	NULL	NULL	0	NULL	Est2	GP		is a type of					reverse transcriptase	GP				NULL	budding yeast	0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72401	21	334619	5	NULL	NULL	0	NULL	hTERC	NucleicAcid		is a type of					template RNA	NucleicAcid				NULL	human	0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72402	22	334619	5	NULL	NULL	0	NULL	Tlc1	NucleicAcid		is a type of					template RNA	NucleicAcid				NULL	budding yeast	0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72403	23	334619	5	NULL	NULL	0	NULL	Est1 protein	GP		is a type of					accessory factor	GP				NULL	human	0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72404	24	334619	5	NULL	NULL	0	NULL	dyskerin	GP		is a type of					accessory factor	GP				NULL	human	0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72405	25	334619	5	NULL	NULL	0	NULL	Est1 protein	GP		is a type of					accessory factor	GP				NULL	budding yeast	0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72406	26	334619	5	NULL	NULL	0	NULL	Est3 protein	GP		is a type of					accessory factor	GP				NULL	budding yeast	0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72407	27	334619	5	NULL	NULL	0	NULL	Sm protein	GP		is a type of					accessory factor	GP				NULL	budding yeast	0	NULL	NULL	NULL	gw70_annurevbiochem_73_0_177_s_14	15189140	Telomeres are composed of repetitive sequences that can be maintained  by telomerase, a complex containing a reverse transcriptase (hTERT in humans and  Est2 in budding yeast), a template RNA (hTERC in humans and Tlc1 in yeast), and accessory  factors (the Est1 proteins and dyskerin in humans and Est1, Est3, and Sm proteins  in budding yeast).	gene_phenotype
72408	1	334620	5	NULL	NULL	0	NULL	yKu80-135i 	GP	mutation of	leads to					telomere	Chromosome	accelerated loss of;; length			NULL	budding yeast strains	0	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2090_s_205	15824061	Budding yeast strains harboring the  yKu80-135i mutation or  tlc1delta 48 (TLC1 lacking 48 nt Ku binding stem - loop) show accelerated loss of telomere length, which is not attributed to loss of telomerase activity but to reduced kinetics of telomere addition ( ).	gene_phenotype
72409	2	334620	5	NULL	NULL	0	NULL	tlc1delta 48	NucleicAcid	mutation of	leads to					telomere	Chromosome	accelerated loss of;; length			NULL	budding yeast strains	0	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2090_s_205	15824061	Budding yeast strains harboring the  yKu80-135i mutation or  tlc1delta 48 (TLC1 lacking 48 nt Ku binding stem - loop) show accelerated loss of telomere length, which is not attributed to loss of telomerase activity but to reduced kinetics of telomere addition ( ).	gene_phenotype
72410	3	334620	5	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL	budding yeast strains	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2090_s_205	15824061	Budding yeast strains harboring the  yKu80-135i mutation or  tlc1delta 48 (TLC1 lacking 48 nt Ku binding stem - loop) show accelerated loss of telomere length, which is not attributed to loss of telomerase activity but to reduced kinetics of telomere addition ( ).	gene_phenotype
72411	4	334620	5	NULL	NULL	0	NULL	tlc1delta 48	NucleicAcid		is					TLC1 lacking 48 nt Ku binding stem - loop	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2090_s_205	15824061	Budding yeast strains harboring the  yKu80-135i mutation or  tlc1delta 48 (TLC1 lacking 48 nt Ku binding stem - loop) show accelerated loss of telomere length, which is not attributed to loss of telomerase activity but to reduced kinetics of telomere addition ( ).	gene_phenotype
72412	5	334620	5	NULL	NULL	NULL	NULL	statement 1	Process		is not attributed to					telomere activity	Process	loss of			NULL	budding yeast strains	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2090_s_205	15824061	Budding yeast strains harboring the  yKu80-135i mutation or  tlc1delta 48 (TLC1 lacking 48 nt Ku binding stem - loop) show accelerated loss of telomere length, which is not attributed to loss of telomerase activity but to reduced kinetics of telomere addition ( ).	gene_phenotype
72413	6	334620	5	NULL	NULL	NULL	NULL	statement 1	Process		is attributed to					telomere	Chromosome	reduced kinetics of;;addition of			NULL	budding yeast strains	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2090_s_205	15824061	Budding yeast strains harboring the  yKu80-135i mutation or  tlc1delta 48 (TLC1 lacking 48 nt Ku binding stem - loop) show accelerated loss of telomere length, which is not attributed to loss of telomerase activity but to reduced kinetics of telomere addition ( ).	gene_phenotype
72414	7	334620	5	NULL	NULL	NULL	NULL	statement 2	Process		is not attributed to					telomere activity	Process	loss of			NULL	budding yeast strains	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2090_s_205	15824061	Budding yeast strains harboring the  yKu80-135i mutation or  tlc1delta 48 (TLC1 lacking 48 nt Ku binding stem - loop) show accelerated loss of telomere length, which is not attributed to loss of telomerase activity but to reduced kinetics of telomere addition ( ).	gene_phenotype
72415	8	334620	5	NULL	NULL	NULL	NULL	statement 2	Process		is attributed to					telomere	Chromosome	reduced kinetics of;;addition of			NULL	budding yeast strains	NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_7_2090_s_205	15824061	Budding yeast strains harboring the  yKu80-135i mutation or  tlc1delta 48 (TLC1 lacking 48 nt Ku binding stem - loop) show accelerated loss of telomere length, which is not attributed to loss of telomerase activity but to reduced kinetics of telomere addition ( ).	gene_phenotype
72416	1	334623	5	NULL	NULL	0	NULL	telomere	Chromosome	progressive shortening of	is accompanied by					cell viability	Process	gradual loss of			NULL	delta tlc1	0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8729_s_30	14612413	Yeast cells defective in the telomerase pathway, as the  Saccharomyces cerevisiae mutants delta tlc1 and  deltaest1- 4 or the  Kluyveromyces lactis telomerase mutant delta ter1 show a phenotype very similar to that seen in mammalian cells: progressive telomere shortening accompanied by gradual loss of cell viability through a senescence-like mechanism ( ,  ,  ,  ).	gene_phenotype
72417	2	334623	5	NULL	NULL	0	NULL	statement 1	Process		occurs through					senescence-like mechanism	Process				NULL	delta tlc1	0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8729_s_30	14612413	Yeast cells defective in the telomerase pathway, as the  Saccharomyces cerevisiae mutants delta tlc1 and  deltaest1- 4 or the  Kluyveromyces lactis telomerase mutant delta ter1 show a phenotype very similar to that seen in mammalian cells: progressive telomere shortening accompanied by gradual loss of cell viability through a senescence-like mechanism ( ,  ,  ,  ).	gene_phenotype
72418	3	334623	5	NULL	NULL	NULL	NULL	telomere	Chromosome	progressive shortening of	is accompanied by					cell viability	Process	gradual loss of			NULL	deltaest1- 4	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8729_s_30	14612413	Yeast cells defective in the telomerase pathway, as the  Saccharomyces cerevisiae mutants delta tlc1 and  deltaest1- 4 or the  Kluyveromyces lactis telomerase mutant delta ter1 show a phenotype very similar to that seen in mammalian cells: progressive telomere shortening accompanied by gradual loss of cell viability through a senescence-like mechanism ( ,  ,  ,  ).	gene_phenotype
72419	4	334623	5	NULL	NULL	0	NULL	statement 3	Process		occurs through					senescence-like mechanism	Process				NULL	deltaest1- 4	0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8729_s_30	14612413	Yeast cells defective in the telomerase pathway, as the  Saccharomyces cerevisiae mutants delta tlc1 and  deltaest1- 4 or the  Kluyveromyces lactis telomerase mutant delta ter1 show a phenotype very similar to that seen in mammalian cells: progressive telomere shortening accompanied by gradual loss of cell viability through a senescence-like mechanism ( ,  ,  ,  ).	gene_phenotype
72420	5	334623	5	NULL	NULL	NULL	NULL	telomere	Chromosome	progressive shortening of	is accompanied by					cell viability	Process	gradual loss of			NULL	delta ter1	NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8729_s_30	14612413	Yeast cells defective in the telomerase pathway, as the  Saccharomyces cerevisiae mutants delta tlc1 and  deltaest1- 4 or the  Kluyveromyces lactis telomerase mutant delta ter1 show a phenotype very similar to that seen in mammalian cells: progressive telomere shortening accompanied by gradual loss of cell viability through a senescence-like mechanism ( ,  ,  ,  ).	gene_phenotype
72421	6	334623	5	NULL	NULL	0	NULL	statement 5	Process		occurs through					senescence-like mechanism	Process				NULL	delta ter1	0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8729_s_30	14612413	Yeast cells defective in the telomerase pathway, as the  Saccharomyces cerevisiae mutants delta tlc1 and  deltaest1- 4 or the  Kluyveromyces lactis telomerase mutant delta ter1 show a phenotype very similar to that seen in mammalian cells: progressive telomere shortening accompanied by gradual loss of cell viability through a senescence-like mechanism ( ,  ,  ,  ).	gene_phenotype
72422	7	334623	5	NULL	NULL	0	NULL	delta tlc1	Organism		is a mutant of					Saccharomyces cerevisiae	Organism				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8729_s_30	14612413	Yeast cells defective in the telomerase pathway, as the  Saccharomyces cerevisiae mutants delta tlc1 and  deltaest1- 4 or the  Kluyveromyces lactis telomerase mutant delta ter1 show a phenotype very similar to that seen in mammalian cells: progressive telomere shortening accompanied by gradual loss of cell viability through a senescence-like mechanism ( ,  ,  ,  ).	gene_phenotype
72423	8	334623	5	NULL	NULL	0	NULL	statement 7	Organism		is defective in					telomerase pathway	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8729_s_30	14612413	Yeast cells defective in the telomerase pathway, as the  Saccharomyces cerevisiae mutants delta tlc1 and  deltaest1- 4 or the  Kluyveromyces lactis telomerase mutant delta ter1 show a phenotype very similar to that seen in mammalian cells: progressive telomere shortening accompanied by gradual loss of cell viability through a senescence-like mechanism ( ,  ,  ,  ).	gene_phenotype
72424	9	334623	5	NULL	NULL	0	NULL	deltaest1- 4	Organism		is a mutant of					Saccharomyces cerevisiae	Organism				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8729_s_30	14612413	Yeast cells defective in the telomerase pathway, as the  Saccharomyces cerevisiae mutants delta tlc1 and  deltaest1- 4 or the  Kluyveromyces lactis telomerase mutant delta ter1 show a phenotype very similar to that seen in mammalian cells: progressive telomere shortening accompanied by gradual loss of cell viability through a senescence-like mechanism ( ,  ,  ,  ).	gene_phenotype
72425	10	334623	5	NULL	NULL	0	NULL	statement 9	Process		is defective in					telomerase pathway	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8729_s_30	14612413	Yeast cells defective in the telomerase pathway, as the  Saccharomyces cerevisiae mutants delta tlc1 and  deltaest1- 4 or the  Kluyveromyces lactis telomerase mutant delta ter1 show a phenotype very similar to that seen in mammalian cells: progressive telomere shortening accompanied by gradual loss of cell viability through a senescence-like mechanism ( ,  ,  ,  ).	gene_phenotype
72426	11	334623	5	NULL	NULL	0	NULL	delta ter1	Organism		is a mutant of					Kluyveromyces lactis	Organism				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8729_s_30	14612413	Yeast cells defective in the telomerase pathway, as the  Saccharomyces cerevisiae mutants delta tlc1 and  deltaest1- 4 or the  Kluyveromyces lactis telomerase mutant delta ter1 show a phenotype very similar to that seen in mammalian cells: progressive telomere shortening accompanied by gradual loss of cell viability through a senescence-like mechanism ( ,  ,  ,  ).	gene_phenotype
72427	12	334623	5	NULL	NULL	0	NULL	statement 11	Organism		is defective in					telomerase pathway	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8729_s_30	14612413	Yeast cells defective in the telomerase pathway, as the  Saccharomyces cerevisiae mutants delta tlc1 and  deltaest1- 4 or the  Kluyveromyces lactis telomerase mutant delta ter1 show a phenotype very similar to that seen in mammalian cells: progressive telomere shortening accompanied by gradual loss of cell viability through a senescence-like mechanism ( ,  ,  ,  ).	gene_phenotype
72428	1	334625	5	NULL	NULL	0	NULL	Gnop1	GP		is an ortholog of					PinX1	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_50_51745_s_131	15381700	In the budding yeast, the PinX1 orthologue Gnop1 appears to inhibit telomerase biogenesis by sequestering the uncomplexed TERT protein (Est2p) and preventing its association with the telomerase template RNA (TLC1) ( ), consistent with the localization of this protein to the nucleolus ( ) where telomerase assembly is believed to occur.	gene_phenotype
72429	2	334625	5	NULL	NULL	0	NULL	Gnop1	GP		inhibits		appear to			telomerase	GP	biogenesis of			NULL	budding yeast	0	NULL	NULL	NULL	gw70_jbiolchem_279_50_51745_s_131	15381700	In the budding yeast, the PinX1 orthologue Gnop1 appears to inhibit telomerase biogenesis by sequestering the uncomplexed TERT protein (Est2p) and preventing its association with the telomerase template RNA (TLC1) ( ), consistent with the localization of this protein to the nucleolus ( ) where telomerase assembly is believed to occur.	gene_phenotype
72430	3	334625	5	NULL	NULL	0	NULL	Gnop1	GP		sequester					TERT protein	GP	uncomplexed			NULL	budding yeast	0	NULL	NULL	NULL	gw70_jbiolchem_279_50_51745_s_131	15381700	In the budding yeast, the PinX1 orthologue Gnop1 appears to inhibit telomerase biogenesis by sequestering the uncomplexed TERT protein (Est2p) and preventing its association with the telomerase template RNA (TLC1) ( ), consistent with the localization of this protein to the nucleolus ( ) where telomerase assembly is believed to occur.	gene_phenotype
72434	4	334625	5	NULL	NULL	0	NULL	TERT protein	GP		associates with					TLC1	NucleicAcid				NULL	budding yeast	0	NULL	NULL	NULL	gw70_jbiolchem_279_50_51745_s_131	15381700	In the budding yeast, the PinX1 orthologue Gnop1 appears to inhibit telomerase biogenesis by sequestering the uncomplexed TERT protein (Est2p) and preventing its association with the telomerase template RNA (TLC1) ( ), consistent with the localization of this protein to the nucleolus ( ) where telomerase assembly is believed to occur.	gene_phenotype
72435	5	334625	5	NULL	NULL	0	NULL	statement 3	Process		prevent					statement 4	Process				NULL	budding yeast	0	NULL	NULL	NULL	gw70_jbiolchem_279_50_51745_s_131	15381700	In the budding yeast, the PinX1 orthologue Gnop1 appears to inhibit telomerase biogenesis by sequestering the uncomplexed TERT protein (Est2p) and preventing its association with the telomerase template RNA (TLC1) ( ), consistent with the localization of this protein to the nucleolus ( ) where telomerase assembly is believed to occur.	gene_phenotype
72436	6	334625	5	NULL	NULL	0	NULL	statement 5	Process		leads to					statement 2	Process				NULL	budding yeast	0	NULL	NULL	NULL	gw70_jbiolchem_279_50_51745_s_131	15381700	In the budding yeast, the PinX1 orthologue Gnop1 appears to inhibit telomerase biogenesis by sequestering the uncomplexed TERT protein (Est2p) and preventing its association with the telomerase template RNA (TLC1) ( ), consistent with the localization of this protein to the nucleolus ( ) where telomerase assembly is believed to occur.	gene_phenotype
72437	7	334625	5	NULL	NULL	0	NULL	Gnop1	GP		is localized to					nucleolus	CellComponent				NULL	budding yeast	0	NULL	NULL	NULL	gw70_jbiolchem_279_50_51745_s_131	15381700	In the budding yeast, the PinX1 orthologue Gnop1 appears to inhibit telomerase biogenesis by sequestering the uncomplexed TERT protein (Est2p) and preventing its association with the telomerase template RNA (TLC1) ( ), consistent with the localization of this protein to the nucleolus ( ) where telomerase assembly is believed to occur.	gene_phenotype
72438	8	334625	5	NULL	NULL	0	NULL	telomerase	GP	assembly of	occurs in		possibly			nucleolus	CellComponent				NULL	budding yeast	0	NULL	NULL	NULL	gw70_jbiolchem_279_50_51745_s_131	15381700	In the budding yeast, the PinX1 orthologue Gnop1 appears to inhibit telomerase biogenesis by sequestering the uncomplexed TERT protein (Est2p) and preventing its association with the telomerase template RNA (TLC1) ( ), consistent with the localization of this protein to the nucleolus ( ) where telomerase assembly is believed to occur.	gene_phenotype
72439	9	334625	5	NULL	NULL	0	NULL	Est2p	GP		is a synonym of					TERT protein	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_50_51745_s_131	15381700	In the budding yeast, the PinX1 orthologue Gnop1 appears to inhibit telomerase biogenesis by sequestering the uncomplexed TERT protein (Est2p) and preventing its association with the telomerase template RNA (TLC1) ( ), consistent with the localization of this protein to the nucleolus ( ) where telomerase assembly is believed to occur.	gene_phenotype
72440	10	334625	5	NULL	NULL	0	NULL	TLC1	NucleicAcid		is a type of					telomere template	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_50_51745_s_131	15381700	In the budding yeast, the PinX1 orthologue Gnop1 appears to inhibit telomerase biogenesis by sequestering the uncomplexed TERT protein (Est2p) and preventing its association with the telomerase template RNA (TLC1) ( ), consistent with the localization of this protein to the nucleolus ( ) where telomerase assembly is believed to occur.	gene_phenotype
72441	1	334626	5	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid		is associated with					TERT	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_142	12458198	Mutations in the CP, QFP, and T Motifs Caused a Reduction in the Amount of TERT Protein  and TERT-associated TLC1 RNA-- To determine the basis for the activity loss manifested by the SCR mutants, we estimated  the levels of TERT protein in wild type and mutant strains using antibodies directed against the protein A tag.	gene_phenotype
72442	2	334626	5	NULL	NULL	NULL	NULL	CP motif	AminoAcid	mutation of	reduce					TERT protein	GP	amount of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_142	12458198	Mutations in the CP, QFP, and T Motifs Caused a Reduction in the Amount of TERT Protein  and TERT-associated TLC1 RNA-- To determine the basis for the activity loss manifested by the SCR mutants, we estimated  the levels of TERT protein in wild type and mutant strains using antibodies directed against the protein A tag.	gene_phenotype
72443	3	334626	5	NULL	NULL	NULL	NULL	CP motif	AminoAcid	mutation of	reduce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_142	12458198	Mutations in the CP, QFP, and T Motifs Caused a Reduction in the Amount of TERT Protein  and TERT-associated TLC1 RNA-- To determine the basis for the activity loss manifested by the SCR mutants, we estimated  the levels of TERT protein in wild type and mutant strains using antibodies directed against the protein A tag.	gene_phenotype
72444	4	334626	5	NULL	NULL	NULL	NULL	QFP motif	AminoAcid	mutation of	reduce					TERT protein	GP	amount of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_142	12458198	Mutations in the CP, QFP, and T Motifs Caused a Reduction in the Amount of TERT Protein  and TERT-associated TLC1 RNA-- To determine the basis for the activity loss manifested by the SCR mutants, we estimated  the levels of TERT protein in wild type and mutant strains using antibodies directed against the protein A tag.	gene_phenotype
72445	5	334626	5	NULL	NULL	NULL	NULL	QFP motif	AminoAcid	mutation of	reduce					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_142	12458198	Mutations in the CP, QFP, and T Motifs Caused a Reduction in the Amount of TERT Protein  and TERT-associated TLC1 RNA-- To determine the basis for the activity loss manifested by the SCR mutants, we estimated  the levels of TERT protein in wild type and mutant strains using antibodies directed against the protein A tag.	gene_phenotype
72446	6	334626	5	NULL	NULL	0	NULL	T Motif	AminoAcid	mutation of	reduce					TERT protein	GP	amount of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_142	12458198	Mutations in the CP, QFP, and T Motifs Caused a Reduction in the Amount of TERT Protein  and TERT-associated TLC1 RNA-- To determine the basis for the activity loss manifested by the SCR mutants, we estimated  the levels of TERT protein in wild type and mutant strains using antibodies directed against the protein A tag.	gene_phenotype
72447	7	334626	5	NULL	NULL	0	NULL	T Motif	AminoAcid	mutation of	reduce					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_142	12458198	Mutations in the CP, QFP, and T Motifs Caused a Reduction in the Amount of TERT Protein  and TERT-associated TLC1 RNA-- To determine the basis for the activity loss manifested by the SCR mutants, we estimated  the levels of TERT protein in wild type and mutant strains using antibodies directed against the protein A tag.	gene_phenotype
72448	1	334627	5	NULL	NULL	NULL	NULL	CP motif	AminoAcid	mutation of	affects					RNP	GP	assembly of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_176	12458198	Overexpression of the Mutant Proteins Does Not Result in Telomere Shortening-- The concomitant reduction in the level of telomerase activity, TERT protein, and  TERT-associated TLC1 RNA suggests that mutations in the CP, QFP, and T motifs affected RNP assembly rather than the  in vivo and  in vitro activity of telomerase.	gene_phenotype
72449	2	334627	5	NULL	NULL	0	NULL	QFP motif	AminoAcid	mutation of	affects					RNP	GP	assembly of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_176	12458198	Overexpression of the Mutant Proteins Does Not Result in Telomere Shortening-- The concomitant reduction in the level of telomerase activity, TERT protein, and  TERT-associated TLC1 RNA suggests that mutations in the CP, QFP, and T motifs affected RNP assembly rather than the  in vivo and  in vitro activity of telomerase.	gene_phenotype
72450	3	334627	5	NULL	NULL	0	NULL	T motif	AminoAcid	mutation of	affects					RNP	GP	assembly of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_176	12458198	Overexpression of the Mutant Proteins Does Not Result in Telomere Shortening-- The concomitant reduction in the level of telomerase activity, TERT protein, and  TERT-associated TLC1 RNA suggests that mutations in the CP, QFP, and T motifs affected RNP assembly rather than the  in vivo and  in vitro activity of telomerase.	gene_phenotype
72451	4	334627	5	NULL	NULL	0	NULL	CP motif	AminoAcid	mutation of	does not affect					telomere activity	Process				NULL	in vitro	0	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_176	12458198	Overexpression of the Mutant Proteins Does Not Result in Telomere Shortening-- The concomitant reduction in the level of telomerase activity, TERT protein, and  TERT-associated TLC1 RNA suggests that mutations in the CP, QFP, and T motifs affected RNP assembly rather than the  in vivo and  in vitro activity of telomerase.	gene_phenotype
72452	5	334627	5	NULL	NULL	0	NULL	CP motif	AminoAcid	mutation of	does not affect					telomere activity	Process				NULL	in vivo	0	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_176	12458198	Overexpression of the Mutant Proteins Does Not Result in Telomere Shortening-- The concomitant reduction in the level of telomerase activity, TERT protein, and  TERT-associated TLC1 RNA suggests that mutations in the CP, QFP, and T motifs affected RNP assembly rather than the  in vivo and  in vitro activity of telomerase.	gene_phenotype
72453	6	334627	5	NULL	NULL	0	NULL	QFP motif	AminoAcid	mutation of	does not affect					telomere activity	Process				NULL	in vitro	0	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_176	12458198	Overexpression of the Mutant Proteins Does Not Result in Telomere Shortening-- The concomitant reduction in the level of telomerase activity, TERT protein, and  TERT-associated TLC1 RNA suggests that mutations in the CP, QFP, and T motifs affected RNP assembly rather than the  in vivo and  in vitro activity of telomerase.	gene_phenotype
72454	7	334627	5	NULL	NULL	0	NULL	QFP motif	AminoAcid	mutation of	does not affect					telomere activity	Process				NULL	in vivo	0	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_176	12458198	Overexpression of the Mutant Proteins Does Not Result in Telomere Shortening-- The concomitant reduction in the level of telomerase activity, TERT protein, and  TERT-associated TLC1 RNA suggests that mutations in the CP, QFP, and T motifs affected RNP assembly rather than the  in vivo and  in vitro activity of telomerase.	gene_phenotype
72455	8	334627	5	NULL	NULL	0	NULL	T Motif	AminoAcid	mutation of	does not affect					telomere activity	Process				NULL	in vitro	0	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_176	12458198	Overexpression of the Mutant Proteins Does Not Result in Telomere Shortening-- The concomitant reduction in the level of telomerase activity, TERT protein, and  TERT-associated TLC1 RNA suggests that mutations in the CP, QFP, and T motifs affected RNP assembly rather than the  in vivo and  in vitro activity of telomerase.	gene_phenotype
72456	9	334627	5	NULL	NULL	0	NULL	T Motif	AminoAcid	mutation of	does not affect					telomere activity	Process				NULL	in vivo	0	NULL	NULL	NULL	gw70_jbiolchem_278_6_3882_s_176	12458198	Overexpression of the Mutant Proteins Does Not Result in Telomere Shortening-- The concomitant reduction in the level of telomerase activity, TERT protein, and  TERT-associated TLC1 RNA suggests that mutations in the CP, QFP, and T motifs affected RNP assembly rather than the  in vivo and  in vitro activity of telomerase.	gene_phenotype
72457	1	334629	5	NULL	NULL	0	NULL	telomerase	GP		consists of			catalytic core		TLC1	NucleicAcid	Saccharomyces cerevisiae			NULL		0	NULL	NULL	NULL	gw70_pnas_102_28_9778_s_9	15994230	The catalytic core of telomerase consists minimally of two components: an RNA in which the template is embedded (named TLC1 in the budding yeast  Saccharomyces cerevisiae), and a reverse transcriptase (RT)-like protein that mediates catalysis (named TERT in general and Est2p in yeast) (  -  ).	gene_phenotype
72458	2	334629	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	Saccharomyces cerevisiae	is a type of					RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_pnas_102_28_9778_s_9	15994230	The catalytic core of telomerase consists minimally of two components: an RNA in which the template is embedded (named TLC1 in the budding yeast  Saccharomyces cerevisiae), and a reverse transcriptase (RT)-like protein that mediates catalysis (named TERT in general and Est2p in yeast) (  -  ).	gene_phenotype
72459	3	334629	5	NULL	NULL	0	NULL	telomerase	GP		consists of			catalytic core		TERT	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_102_28_9778_s_9	15994230	The catalytic core of telomerase consists minimally of two components: an RNA in which the template is embedded (named TLC1 in the budding yeast  Saccharomyces cerevisiae), and a reverse transcriptase (RT)-like protein that mediates catalysis (named TERT in general and Est2p in yeast) (  -  ).	gene_phenotype
72460	4	334629	5	NULL	NULL	0	NULL	telomerase	GP		consists of			catalytic core		Est2p	GP	yeast			NULL		0	NULL	NULL	NULL	gw70_pnas_102_28_9778_s_9	15994230	The catalytic core of telomerase consists minimally of two components: an RNA in which the template is embedded (named TLC1 in the budding yeast  Saccharomyces cerevisiae), and a reverse transcriptase (RT)-like protein that mediates catalysis (named TERT in general and Est2p in yeast) (  -  ).	gene_phenotype
72461	5	334629	5	NULL	NULL	0	NULL	TERT	GP		is a type of					reverse transcriptase like protein	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_102_28_9778_s_9	15994230	The catalytic core of telomerase consists minimally of two components: an RNA in which the template is embedded (named TLC1 in the budding yeast  Saccharomyces cerevisiae), and a reverse transcriptase (RT)-like protein that mediates catalysis (named TERT in general and Est2p in yeast) (  -  ).	gene_phenotype
72462	6	334629	5	NULL	NULL	0	NULL	Est2p	GP	yeast	is a type of					reverse transcriptase like protein	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_102_28_9778_s_9	15994230	The catalytic core of telomerase consists minimally of two components: an RNA in which the template is embedded (named TLC1 in the budding yeast  Saccharomyces cerevisiae), and a reverse transcriptase (RT)-like protein that mediates catalysis (named TERT in general and Est2p in yeast) (  -  ).	gene_phenotype
72463	7	334629	5	NULL	NULL	0	NULL	statement 5	Process		mediates					catalysis	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_102_28_9778_s_9	15994230	The catalytic core of telomerase consists minimally of two components: an RNA in which the template is embedded (named TLC1 in the budding yeast  Saccharomyces cerevisiae), and a reverse transcriptase (RT)-like protein that mediates catalysis (named TERT in general and Est2p in yeast) (  -  ).	gene_phenotype
72464	8	334629	5	NULL	NULL	0	NULL	statement 6	Process		mediates					catalysis	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_102_28_9778_s_9	15994230	The catalytic core of telomerase consists minimally of two components: an RNA in which the template is embedded (named TLC1 in the budding yeast  Saccharomyces cerevisiae), and a reverse transcriptase (RT)-like protein that mediates catalysis (named TERT in general and Est2p in yeast) (  -  ).	gene_phenotype
72465	1	334630	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	deletion of;;either side of;;predicted;;S. cerevisiae	decrease		modestly		 helix 4	telomere	Chromosome	length of			NULL		0	NULL	NULL	NULL	gw70_pnas_101_41_14713_s_128	15371596	Deletion of either side of predicted helix 4 in  S. cerevisiae TLC1 (mutants 12, 13, and 170) or changing the sequences surrounding helix 4 (mutants 14, 15, and 16) only modestly decreased telomere length or cell growth ( Fig. 2 and Tables 1 and 2).	gene_phenotype
72466	2	334630	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	deletion of;;either side of;;predicted;;S. cerevisiae	decrease		modestly		helix 4	cell growth	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_41_14713_s_128	15371596	Deletion of either side of predicted helix 4 in  S. cerevisiae TLC1 (mutants 12, 13, and 170) or changing the sequences surrounding helix 4 (mutants 14, 15, and 16) only modestly decreased telomere length or cell growth ( Fig. 2 and Tables 1 and 2).	gene_phenotype
72467	3	334630	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	changing sequence surrounding	decrease		modestly		helix 4	telomere	Chromosome	length of			NULL		0	NULL	NULL	NULL	gw70_pnas_101_41_14713_s_128	15371596	Deletion of either side of predicted helix 4 in  S. cerevisiae TLC1 (mutants 12, 13, and 170) or changing the sequences surrounding helix 4 (mutants 14, 15, and 16) only modestly decreased telomere length or cell growth ( Fig. 2 and Tables 1 and 2).	gene_phenotype
72468	4	334630	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	changing sequence surrounding	decrease		modestly		helix 4	cell growth	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_41_14713_s_128	15371596	Deletion of either side of predicted helix 4 in  S. cerevisiae TLC1 (mutants 12, 13, and 170) or changing the sequences surrounding helix 4 (mutants 14, 15, and 16) only modestly decreased telomere length or cell growth ( Fig. 2 and Tables 1 and 2).	gene_phenotype
72469	5	334630	5	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_41_14713_s_128	15371596	Deletion of either side of predicted helix 4 in  S. cerevisiae TLC1 (mutants 12, 13, and 170) or changing the sequences surrounding helix 4 (mutants 14, 15, and 16) only modestly decreased telomere length or cell growth ( Fig. 2 and Tables 1 and 2).	gene_phenotype
72470	6	334630	5	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_41_14713_s_128	15371596	Deletion of either side of predicted helix 4 in  S. cerevisiae TLC1 (mutants 12, 13, and 170) or changing the sequences surrounding helix 4 (mutants 14, 15, and 16) only modestly decreased telomere length or cell growth ( Fig. 2 and Tables 1 and 2).	gene_phenotype
72471	1	334632	5	NULL	NULL	0	NULL	Est1p	GP		activates		nonspecific			RNA	NucleicAcid	binding of			NULL	in vitro	0	NULL	NULL	NULL	gw60_genesdev_12_8_1073_s_147	9553037	Est1p also exhibits a nonspecific RNA binding activity in vitro, with no enhanced binding to the  TLC1 telomerase RNA (Virta-Pearlman et al. 1996  ), although this lack of specificity could be the result of incorrect folding of the 1.3-kb yeast telomerase RNA or the lack of another protein binding partner.	gene_phenotype
72472	2	334632	5	NULL	NULL	0	NULL	Est1p	GP		does not bind					TLC1	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_8_1073_s_147	9553037	Est1p also exhibits a nonspecific RNA binding activity in vitro, with no enhanced binding to the  TLC1 telomerase RNA (Virta-Pearlman et al. 1996  ), although this lack of specificity could be the result of incorrect folding of the 1.3-kb yeast telomerase RNA or the lack of another protein binding partner.	gene_phenotype
72473	3	334632	5	NULL	NULL	0	NULL	TLC1	NucleicAcid		is a type of					telomerase RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_8_1073_s_147	9553037	Est1p also exhibits a nonspecific RNA binding activity in vitro, with no enhanced binding to the  TLC1 telomerase RNA (Virta-Pearlman et al. 1996  ), although this lack of specificity could be the result of incorrect folding of the 1.3-kb yeast telomerase RNA or the lack of another protein binding partner.	gene_phenotype
72474	4	334632	5	NULL	NULL	0	NULL	telomerase RNA	NucleicAcid	incorrect folding of;;yeast	leads to		may			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_8_1073_s_147	9553037	Est1p also exhibits a nonspecific RNA binding activity in vitro, with no enhanced binding to the  TLC1 telomerase RNA (Virta-Pearlman et al. 1996  ), although this lack of specificity could be the result of incorrect folding of the 1.3-kb yeast telomerase RNA or the lack of another protein binding partner.	gene_phenotype
72475	5	334632	5	NULL	NULL	0	NULL	protein binding partner	GP	lack of	leads to		may			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_8_1073_s_147	9553037	Est1p also exhibits a nonspecific RNA binding activity in vitro, with no enhanced binding to the  TLC1 telomerase RNA (Virta-Pearlman et al. 1996  ), although this lack of specificity could be the result of incorrect folding of the 1.3-kb yeast telomerase RNA or the lack of another protein binding partner.	gene_phenotype
72476	1	334633	5	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid		serve as					template	NucleicAcid				NULL	at the ends of yeast chromosomes	0	NULL	NULL	NULL	gw60_genetics_160_1_49_s_149	11805044	TLC1 RNA serves as template for DNA synthesis at the ends of yeast chromosomes during S phase and may have additional functions in telomere silencing and length maintenance ( P RESCOTT and BLACKBURN 1997   ;   S INGER et al. 1998   ;	gene_phenotype
72477	2	334633	5	NULL	NULL	0	NULL	statement 1	Process		is required for					DNA	NucleicAcid	synthesis of			NULL	at the ends of yeast chromosomes	0	NULL	NULL	NULL	gw60_genetics_160_1_49_s_149	11805044	TLC1 RNA serves as template for DNA synthesis at the ends of yeast chromosomes during S phase and may have additional functions in telomere silencing and length maintenance ( P RESCOTT and BLACKBURN 1997   ;   S INGER et al. 1998   ;	gene_phenotype
72478	3	334633	5	NULL	NULL	NULL	NULL	statement 2	Process		occurs during					S phase	Time				NULL	at the ends of yeast chromosomes	NULL	NULL	NULL	NULL	gw60_genetics_160_1_49_s_149	11805044	TLC1 RNA serves as template for DNA synthesis at the ends of yeast chromosomes during S phase and may have additional functions in telomere silencing and length maintenance ( P RESCOTT and BLACKBURN 1997   ;   S INGER et al. 1998   ;	gene_phenotype
72479	4	334633	5	NULL	NULL	0	NULL	statement 2	Process		silence		may			telomere	Chromosome				NULL		0	NULL	NULL	NULL	gw60_genetics_160_1_49_s_149	11805044	TLC1 RNA serves as template for DNA synthesis at the ends of yeast chromosomes during S phase and may have additional functions in telomere silencing and length maintenance ( P RESCOTT and BLACKBURN 1997   ;   S INGER et al. 1998   ;	gene_phenotype
72480	5	334633	5	NULL	NULL	0	NULL	statement 2	Process		maintains		may			telomere	Chromosome	length of			NULL		0	NULL	NULL	NULL	gw60_genetics_160_1_49_s_149	11805044	TLC1 RNA serves as template for DNA synthesis at the ends of yeast chromosomes during S phase and may have additional functions in telomere silencing and length maintenance ( P RESCOTT and BLACKBURN 1997   ;   S INGER et al. 1998   ;	gene_phenotype
72481	1	334637	5	NULL	NULL	0	NULL	tlc1-48 allele	NucleicAcid		impairs					TLC1 activity	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_162_3_1101_s_247	12454059	This epistasis behavior is reminiscent of that of a mutation in another subunit in telomerase: the  tlc1-48 allele impairs an activity of  TLC1 that has been proposed to interact, either directly or indirectly, with the Ku heterodimer to facilitate telomere length maintenance ( P ETERSON et al. 2001   ).	gene_phenotype
72482	2	334637	5	NULL	NULL	0	NULL	TLC1	NucleicAcid		interacts with					Ku heterodimer	GP				NULL		0	NULL	NULL	NULL	gw60_genetics_162_3_1101_s_247	12454059	This epistasis behavior is reminiscent of that of a mutation in another subunit in telomerase: the  tlc1-48 allele impairs an activity of  TLC1 that has been proposed to interact, either directly or indirectly, with the Ku heterodimer to facilitate telomere length maintenance ( P ETERSON et al. 2001   ).	gene_phenotype
72483	3	334637	5	NULL	NULL	0	NULL	statement 2	Process		maintains					telomere	Chromosome	length of			NULL		0	NULL	NULL	NULL	gw60_genetics_162_3_1101_s_247	12454059	This epistasis behavior is reminiscent of that of a mutation in another subunit in telomerase: the  tlc1-48 allele impairs an activity of  TLC1 that has been proposed to interact, either directly or indirectly, with the Ku heterodimer to facilitate telomere length maintenance ( P ETERSON et al. 2001   ).	gene_phenotype
72484	1	334641	5	NULL	NULL	0	NULL	TLC1	NucleicAcid	mutant	causes					lethal phenotype	PhysicalPhenomenon	delayed			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_nucleicacidsres_28_14_2690_s_17	10908324	In the budding yeast  Saccharomyces cerevisiae mutations in the genes coding for the RNA or the protein subunits of telomerase ( TLC1 and  EST1-3, respectively) cause a delayed lethal phenotype after about 75 generations, which is accompanied by progressive telomere shortening ( 8 -  10).	gene_phenotype
72485	2	334641	5	NULL	NULL	0	NULL	statement 1	Process		is accompanied by					telomere	Chromosome	progressive shortening of			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_nucleicacidsres_28_14_2690_s_17	10908324	In the budding yeast  Saccharomyces cerevisiae mutations in the genes coding for the RNA or the protein subunits of telomerase ( TLC1 and  EST1-3, respectively) cause a delayed lethal phenotype after about 75 generations, which is accompanied by progressive telomere shortening ( 8 -  10).	gene_phenotype
72486	3	334641	5	NULL	NULL	0	NULL	EST1	GP	mutant	causes					lethal phenotype	PhysicalPhenomenon	delayed			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_nucleicacidsres_28_14_2690_s_17	10908324	In the budding yeast  Saccharomyces cerevisiae mutations in the genes coding for the RNA or the protein subunits of telomerase ( TLC1 and  EST1-3, respectively) cause a delayed lethal phenotype after about 75 generations, which is accompanied by progressive telomere shortening ( 8 -  10).	gene_phenotype
72487	4	334641	5	NULL	NULL	0	NULL	statement 3	Process		is accompanied by					telomere	Chromosome	progressive shortening of			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_nucleicacidsres_28_14_2690_s_17	10908324	In the budding yeast  Saccharomyces cerevisiae mutations in the genes coding for the RNA or the protein subunits of telomerase ( TLC1 and  EST1-3, respectively) cause a delayed lethal phenotype after about 75 generations, which is accompanied by progressive telomere shortening ( 8 -  10).	gene_phenotype
72488	5	334641	5	NULL	NULL	NULL	NULL	EST2	GP	mutant	causes					lethal phenotype	PhysicalPhenomenon	delayed			NULL	Saccharomyces cerevisiae	NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_14_2690_s_17	10908324	In the budding yeast  Saccharomyces cerevisiae mutations in the genes coding for the RNA or the protein subunits of telomerase ( TLC1 and  EST1-3, respectively) cause a delayed lethal phenotype after about 75 generations, which is accompanied by progressive telomere shortening ( 8 -  10).	gene_phenotype
72489	6	334641	5	NULL	NULL	0	NULL	statement 5	Process		is accompanied by					telomere	Chromosome	progressive shortening of			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_nucleicacidsres_28_14_2690_s_17	10908324	In the budding yeast  Saccharomyces cerevisiae mutations in the genes coding for the RNA or the protein subunits of telomerase ( TLC1 and  EST1-3, respectively) cause a delayed lethal phenotype after about 75 generations, which is accompanied by progressive telomere shortening ( 8 -  10).	gene_phenotype
72490	7	334641	5	NULL	NULL	0	NULL	EST3	GP	mutant	causes					lethal phenotype	PhysicalPhenomenon	delayed			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_nucleicacidsres_28_14_2690_s_17	10908324	In the budding yeast  Saccharomyces cerevisiae mutations in the genes coding for the RNA or the protein subunits of telomerase ( TLC1 and  EST1-3, respectively) cause a delayed lethal phenotype after about 75 generations, which is accompanied by progressive telomere shortening ( 8 -  10).	gene_phenotype
72491	8	334641	5	NULL	NULL	0	NULL	statement 7	Process		is accompanied by					telomere	Chromosome	progressive shortening of			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	gw60_nucleicacidsres_28_14_2690_s_17	10908324	In the budding yeast  Saccharomyces cerevisiae mutations in the genes coding for the RNA or the protein subunits of telomerase ( TLC1 and  EST1-3, respectively) cause a delayed lethal phenotype after about 75 generations, which is accompanied by progressive telomere shortening ( 8 -  10).	gene_phenotype
72494	1	334642	5	NULL	NULL	0	NULL	mec1 cells	Cell		contains					telomere	Chromosome	wild type;;length of			NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1379_s_25	12769860	Telomere length is wild-type in  mec1 cells, but deleting both Tel1p and Mec1p results in the same initial overall rate of telomere shortening and eventual cellular senescence as deleting telomerase (although  tel1 mec1 cells divide for somewhat longer than  tlc1 cells)   (Chan et al., 2001  ; Ritchie et al., 1999  ).	gene_phenotype
72495	2	334642	5	NULL	NULL	0	NULL	Tel1p	GP	deletion of	shortens					telomere	Chromosome	length of			NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1379_s_25	12769860	Telomere length is wild-type in  mec1 cells, but deleting both Tel1p and Mec1p results in the same initial overall rate of telomere shortening and eventual cellular senescence as deleting telomerase (although  tel1 mec1 cells divide for somewhat longer than  tlc1 cells)   (Chan et al., 2001  ; Ritchie et al., 1999  ).	gene_phenotype
72496	3	334642	5	NULL	NULL	0	NULL	Mec1p	GP	deletion of	shortens					telomere	Chromosome	length of			NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1379_s_25	12769860	Telomere length is wild-type in  mec1 cells, but deleting both Tel1p and Mec1p results in the same initial overall rate of telomere shortening and eventual cellular senescence as deleting telomerase (although  tel1 mec1 cells divide for somewhat longer than  tlc1 cells)   (Chan et al., 2001  ; Ritchie et al., 1999  ).	gene_phenotype
72497	4	334642	5	NULL	NULL	0	NULL	statement 2	Process		leads to		eventualy			cellular senescence	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1379_s_25	12769860	Telomere length is wild-type in  mec1 cells, but deleting both Tel1p and Mec1p results in the same initial overall rate of telomere shortening and eventual cellular senescence as deleting telomerase (although  tel1 mec1 cells divide for somewhat longer than  tlc1 cells)   (Chan et al., 2001  ; Ritchie et al., 1999  ).	gene_phenotype
72498	5	334642	5	NULL	NULL	0	NULL	statement 3	Process		leads to		eventualy			cellular senescence	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1379_s_25	12769860	Telomere length is wild-type in  mec1 cells, but deleting both Tel1p and Mec1p results in the same initial overall rate of telomere shortening and eventual cellular senescence as deleting telomerase (although  tel1 mec1 cells divide for somewhat longer than  tlc1 cells)   (Chan et al., 2001  ; Ritchie et al., 1999  ).	gene_phenotype
72501	6	334642	5	NULL	NULL	NULL	NULL	telomerase	GP	deletion of	shortens					telomere	Chromosome	length of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1379_s_25	12769860	Telomere length is wild-type in  mec1 cells, but deleting both Tel1p and Mec1p results in the same initial overall rate of telomere shortening and eventual cellular senescence as deleting telomerase (although  tel1 mec1 cells divide for somewhat longer than  tlc1 cells)   (Chan et al., 2001  ; Ritchie et al., 1999  ).	gene_phenotype
72502	7	334642	5	NULL	NULL	NULL	NULL	statement 6	Process		leads to		eventualy			cellular senescence	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1379_s_25	12769860	Telomere length is wild-type in  mec1 cells, but deleting both Tel1p and Mec1p results in the same initial overall rate of telomere shortening and eventual cellular senescence as deleting telomerase (although  tel1 mec1 cells divide for somewhat longer than  tlc1 cells)   (Chan et al., 2001  ; Ritchie et al., 1999  ).	gene_phenotype
72866	1	334644	5	NULL	NULL	NULL	NULL	telomeric DNA	NucleicAcid	gradual loss of	occurs during					spore	Cell	growth of			NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_5_1379_s_151	12769860	Gradual loss of telomeric DNA during spore growth produced  tlc1 tel1 cells with an average telomere length of about 480 bp at the time they were assayed (compared to a mean length of 350 bp in wild-type cells;   Figure 3A).	gene_phenotype
72867	2	334644	5	NULL	NULL	0	NULL	tlc1 tel1 cells	Cell		contains					telomere	Chromosome	average length of			NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1379_s_151	12769860	Gradual loss of telomeric DNA during spore growth produced  tlc1 tel1 cells with an average telomere length of about 480 bp at the time they were assayed (compared to a mean length of 350 bp in wild-type cells;   Figure 3A).	gene_phenotype
72868	3	334644	5	NULL	NULL	0	NULL	statement 1	Process		produce					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_11_5_1379_s_151	12769860	Gradual loss of telomeric DNA during spore growth produced  tlc1 tel1 cells with an average telomere length of about 480 bp at the time they were assayed (compared to a mean length of 350 bp in wild-type cells;   Figure 3A).	gene_phenotype
72875	1	334646	5	NULL	NULL	0	NULL	snRNAs	NucleicAcid		is a type of					RNA polymerase II transcripts	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_23	12167699	In addition to their high uridine content, snRNAs and Tlc1 are RNA polymerase II transcripts; they have a 5''-2,2,7-trimethylguanosine (TMG) cap; and they bind the Sm proteins through a specific sequence termed the Sm site, which is essential for their accumulation ( 4,  45; snRNP biogenesis has been reviewed in reference  55).	gene_phenotype
72876	2	334646	5	NULL	NULL	0	NULL	Tlc1	NucleicAcid		is a type of					RNA polymerase II transcripts	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_23	12167699	In addition to their high uridine content, snRNAs and Tlc1 are RNA polymerase II transcripts; they have a 5''-2,2,7-trimethylguanosine (TMG) cap; and they bind the Sm proteins through a specific sequence termed the Sm site, which is essential for their accumulation ( 4,  45; snRNP biogenesis has been reviewed in reference  55).	gene_phenotype
72878	3	334646	5	NULL	NULL	0	NULL	snRNAs	NucleicAcid		contains					uridine	NucleicAcid	high			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_23	12167699	In addition to their high uridine content, snRNAs and Tlc1 are RNA polymerase II transcripts; they have a 5''-2,2,7-trimethylguanosine (TMG) cap; and they bind the Sm proteins through a specific sequence termed the Sm site, which is essential for their accumulation ( 4,  45; snRNP biogenesis has been reviewed in reference  55).	gene_phenotype
72879	4	334646	5	NULL	NULL	0	NULL	Tlc1	NucleicAcid		contains					uridine	NucleicAcid	high			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_23	12167699	In addition to their high uridine content, snRNAs and Tlc1 are RNA polymerase II transcripts; they have a 5''-2,2,7-trimethylguanosine (TMG) cap; and they bind the Sm proteins through a specific sequence termed the Sm site, which is essential for their accumulation ( 4,  45; snRNP biogenesis has been reviewed in reference  55).	gene_phenotype
72880	5	334646	5	NULL	NULL	0	NULL	TMG	NucleicAcid		is					2,2,7-trimethylguanosine	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_23	12167699	In addition to their high uridine content, snRNAs and Tlc1 are RNA polymerase II transcripts; they have a 5''-2,2,7-trimethylguanosine (TMG) cap; and they bind the Sm proteins through a specific sequence termed the Sm site, which is essential for their accumulation ( 4,  45; snRNP biogenesis has been reviewed in reference  55).	gene_phenotype
72881	6	334646	5	NULL	NULL	0	NULL	snRNAs	NucleicAcid		contains					TMG cap	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_23	12167699	In addition to their high uridine content, snRNAs and Tlc1 are RNA polymerase II transcripts; they have a 5''-2,2,7-trimethylguanosine (TMG) cap; and they bind the Sm proteins through a specific sequence termed the Sm site, which is essential for their accumulation ( 4,  45; snRNP biogenesis has been reviewed in reference  55).	gene_phenotype
72882	7	334646	5	NULL	NULL	0	NULL	Tlc1	NucleicAcid		contains					TMG cap	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_23	12167699	In addition to their high uridine content, snRNAs and Tlc1 are RNA polymerase II transcripts; they have a 5''-2,2,7-trimethylguanosine (TMG) cap; and they bind the Sm proteins through a specific sequence termed the Sm site, which is essential for their accumulation ( 4,  45; snRNP biogenesis has been reviewed in reference  55).	gene_phenotype
72883	8	334646	5	NULL	NULL	NULL	NULL	snRNAs	NucleicAcid		bind				Sm site	Sm proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_23	12167699	In addition to their high uridine content, snRNAs and Tlc1 are RNA polymerase II transcripts; they have a 5''-2,2,7-trimethylguanosine (TMG) cap; and they bind the Sm proteins through a specific sequence termed the Sm site, which is essential for their accumulation ( 4,  45; snRNP biogenesis has been reviewed in reference  55).	gene_phenotype
72884	9	334646	5	NULL	NULL	NULL	NULL	Tlc1	NucleicAcid		bind				Sm site	Sm proteins	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_23	12167699	In addition to their high uridine content, snRNAs and Tlc1 are RNA polymerase II transcripts; they have a 5''-2,2,7-trimethylguanosine (TMG) cap; and they bind the Sm proteins through a specific sequence termed the Sm site, which is essential for their accumulation ( 4,  45; snRNP biogenesis has been reviewed in reference  55).	gene_phenotype
72888	10	334646	5	NULL	NULL	NULL	NULL	snRNAs	NucleicAcid		is essential for				Sm site	snRNAs	NucleicAcid	accumulation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_23	12167699	In addition to their high uridine content, snRNAs and Tlc1 are RNA polymerase II transcripts; they have a 5''-2,2,7-trimethylguanosine (TMG) cap; and they bind the Sm proteins through a specific sequence termed the Sm site, which is essential for their accumulation ( 4,  45; snRNP biogenesis has been reviewed in reference  55).	gene_phenotype
72889	11	334646	5	NULL	NULL	0	NULL	Tlc1	NucleicAcid		is essential for					Tlc1	NucleicAcid	accumulation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6046_s_23	12167699	In addition to their high uridine content, snRNAs and Tlc1 are RNA polymerase II transcripts; they have a 5''-2,2,7-trimethylguanosine (TMG) cap; and they bind the Sm proteins through a specific sequence termed the Sm site, which is essential for their accumulation ( 4,  45; snRNP biogenesis has been reviewed in reference  55).	gene_phenotype
72890	1	334647	5	NULL	NULL	0	NULL	snRNP	GP		is a type of					small nuclear ribonucleoprotein particle	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_7_2366_s_22	11884619	In addition,  TLC1 RNA contains an Sm binding site near its 3' end that is important for the stability of the RNA and is bound by Sm proteins, therefore leading to the classification of  S. cerevisiae telomerase as an Sm snRNP (small nuclear ribonucleoprotein particle) ( 35).	gene_phenotype
72891	2	334647	5	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid		is present near				Sm binding site	TLC1 RNA	NucleicAcid			3' end	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_7_2366_s_22	11884619	In addition,  TLC1 RNA contains an Sm binding site near its 3' end that is important for the stability of the RNA and is bound by Sm proteins, therefore leading to the classification of  S. cerevisiae telomerase as an Sm snRNP (small nuclear ribonucleoprotein particle) ( 35).	gene_phenotype
72892	3	334647	5	NULL	NULL	0	NULL	statement 2	NucleicAcid		is important for					RNA	NucleicAcid	stability of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_7_2366_s_22	11884619	In addition,  TLC1 RNA contains an Sm binding site near its 3' end that is important for the stability of the RNA and is bound by Sm proteins, therefore leading to the classification of  S. cerevisiae telomerase as an Sm snRNP (small nuclear ribonucleoprotein particle) ( 35).	gene_phenotype
72893	4	334647	5	NULL	NULL	0	NULL	Sm proteins	GP		bind					TLC1 RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_7_2366_s_22	11884619	In addition,  TLC1 RNA contains an Sm binding site near its 3' end that is important for the stability of the RNA and is bound by Sm proteins, therefore leading to the classification of  S. cerevisiae telomerase as an Sm snRNP (small nuclear ribonucleoprotein particle) ( 35).	gene_phenotype
72894	5	334647	5	NULL	NULL	0	NULL	telomerase	GP	S. cerevisiae	is classified as					snRNP	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_7_2366_s_22	11884619	In addition,  TLC1 RNA contains an Sm binding site near its 3' end that is important for the stability of the RNA and is bound by Sm proteins, therefore leading to the classification of  S. cerevisiae telomerase as an Sm snRNP (small nuclear ribonucleoprotein particle) ( 35).	gene_phenotype
72895	1	334648	5	NULL	NULL	0	NULL	CP motif	AminoAcid	mutation of	reduce					TERT protein	GP	amount of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_6_3882_s_143	12458198	Mutations in the CP, QFP, and T Motifs Caused a Reduction in the Amount of TERT Protein and TERT-associated TLC1 RNA-- To determine the basis for the activity loss manifested by the SCR mutants, we estimated the levels of TERT protein in wild type and mutant strains using antibodies directed against the protein A tag.	gene_phenotype
72896	2	334648	5	NULL	NULL	0	NULL	QFP motif	AminoAcid	mutation of	reduce					TERT protein	GP	amount of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_6_3882_s_143	12458198	Mutations in the CP, QFP, and T Motifs Caused a Reduction in the Amount of TERT Protein and TERT-associated TLC1 RNA-- To determine the basis for the activity loss manifested by the SCR mutants, we estimated the levels of TERT protein in wild type and mutant strains using antibodies directed against the protein A tag.	gene_phenotype
72897	3	334648	5	NULL	NULL	0	NULL	T Motif	AminoAcid	mutation of	reduce					TERT protein	GP	amount of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_6_3882_s_143	12458198	Mutations in the CP, QFP, and T Motifs Caused a Reduction in the Amount of TERT Protein and TERT-associated TLC1 RNA-- To determine the basis for the activity loss manifested by the SCR mutants, we estimated the levels of TERT protein in wild type and mutant strains using antibodies directed against the protein A tag.	gene_phenotype
72898	4	334648	5	NULL	NULL	0	NULL	TLC1 RNA	NucleicAcid		associates with					TERT	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_6_3882_s_143	12458198	Mutations in the CP, QFP, and T Motifs Caused a Reduction in the Amount of TERT Protein and TERT-associated TLC1 RNA-- To determine the basis for the activity loss manifested by the SCR mutants, we estimated the levels of TERT protein in wild type and mutant strains using antibodies directed against the protein A tag.	gene_phenotype
72899	5	334648	5	NULL	NULL	0	NULL	CP motif	AminoAcid	mutation of	reduce					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_6_3882_s_143	12458198	Mutations in the CP, QFP, and T Motifs Caused a Reduction in the Amount of TERT Protein and TERT-associated TLC1 RNA-- To determine the basis for the activity loss manifested by the SCR mutants, we estimated the levels of TERT protein in wild type and mutant strains using antibodies directed against the protein A tag.	gene_phenotype
72900	6	334648	5	NULL	NULL	0	NULL	QFP motif	AminoAcid	mutation of	reduce					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_6_3882_s_143	12458198	Mutations in the CP, QFP, and T Motifs Caused a Reduction in the Amount of TERT Protein and TERT-associated TLC1 RNA-- To determine the basis for the activity loss manifested by the SCR mutants, we estimated the levels of TERT protein in wild type and mutant strains using antibodies directed against the protein A tag.	gene_phenotype
72901	7	334648	5	NULL	NULL	0	NULL	T Motif	AminoAcid	mutation of	reduce					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_6_3882_s_143	12458198	Mutations in the CP, QFP, and T Motifs Caused a Reduction in the Amount of TERT Protein and TERT-associated TLC1 RNA-- To determine the basis for the activity loss manifested by the SCR mutants, we estimated the levels of TERT protein in wild type and mutant strains using antibodies directed against the protein A tag.	gene_phenotype
72902	1	334651	5	NULL	NULL	0	NULL	telomerase	GP		adds					repeats	NucleicAcid	new			NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11409_s_256	11016977	Concurrent disruption of both the ability of telomerase to add new repeats and the ability of those repeats to negatively regulate telomere length might explain the simultaneously existing populations of elongated and shortened telomeres exhibited initially by certain  ter1 and  tlc1 template mutants (this work and ref.  14).	gene_phenotype
73060	2	334651	5	NULL	NULL	0	NULL	repeats	NucleicAcid	newly added	regulate		negatively			telomere	Chromosome	length of			NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11409_s_256	11016977	Concurrent disruption of both the ability of telomerase to add new repeats and the ability of those repeats to negatively regulate telomere length might explain the simultaneously existing populations of elongated and shortened telomeres exhibited initially by certain  ter1 and  tlc1 template mutants (this work and ref.  14).	gene_phenotype
73061	3	334651	5	NULL	NULL	0	NULL	telomere	Chromosome	elongated	exists with		simultaneously			telomere	Chromosome	shortened			NULL	ter1 template mutants	0	NULL	NULL	NULL	gw60_pnas_97_21_11409_s_256	11016977	Concurrent disruption of both the ability of telomerase to add new repeats and the ability of those repeats to negatively regulate telomere length might explain the simultaneously existing populations of elongated and shortened telomeres exhibited initially by certain  ter1 and  tlc1 template mutants (this work and ref.  14).	gene_phenotype
73062	4	334651	5	NULL	NULL	0	NULL	telomere	Chromosome	elongated	exists with		simultaneously			telomere	Chromosome	shortened			NULL	tlc1 template mutants	0	NULL	NULL	NULL	gw60_pnas_97_21_11409_s_256	11016977	Concurrent disruption of both the ability of telomerase to add new repeats and the ability of those repeats to negatively regulate telomere length might explain the simultaneously existing populations of elongated and shortened telomeres exhibited initially by certain  ter1 and  tlc1 template mutants (this work and ref.  14).	gene_phenotype
73063	5	334651	5	NULL	NULL	NULL	NULL	statement 1	Process		is disrupted with		concurrently			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11409_s_256	11016977	Concurrent disruption of both the ability of telomerase to add new repeats and the ability of those repeats to negatively regulate telomere length might explain the simultaneously existing populations of elongated and shortened telomeres exhibited initially by certain  ter1 and  tlc1 template mutants (this work and ref.  14).	gene_phenotype
73064	6	334651	5	NULL	NULL	NULL	NULL	statement 5	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11409_s_256	11016977	Concurrent disruption of both the ability of telomerase to add new repeats and the ability of those repeats to negatively regulate telomere length might explain the simultaneously existing populations of elongated and shortened telomeres exhibited initially by certain  ter1 and  tlc1 template mutants (this work and ref.  14).	gene_phenotype
73065	7	334651	5	NULL	NULL	NULL	NULL	statement 5	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11409_s_256	11016977	Concurrent disruption of both the ability of telomerase to add new repeats and the ability of those repeats to negatively regulate telomere length might explain the simultaneously existing populations of elongated and shortened telomeres exhibited initially by certain  ter1 and  tlc1 template mutants (this work and ref.  14).	gene_phenotype
73066	1	334655	5	NULL	NULL	0	NULL	telomere	Chromosome	shortening of	is followed by					viability	Process	progressive loss of			NULL		0	NULL	NULL	NULL	gw60_genesdev_12_8_1073_s_136	9553037	Strains carrying deletions of  EST1, EST2, EST3, or  TLC1 exhibit the in vivo phenotypes predicted for a telomerase defect (telomere shortening and progressive loss of viability, termed yeast cellular senescence), and epistasis tests have shown that these four genes act in a single pathway for telomere replication (Lundblad and Szostak 1989  ; Lendvay et al. 1996  ; Lingner et al. 1997b  ).	gene_phenotype
73067	2	334655	5	NULL	NULL	0	NULL	statement 1	Process		is termed as					yeast cellular senescence	Process				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_8_1073_s_136	9553037	Strains carrying deletions of  EST1, EST2, EST3, or  TLC1 exhibit the in vivo phenotypes predicted for a telomerase defect (telomere shortening and progressive loss of viability, termed yeast cellular senescence), and epistasis tests have shown that these four genes act in a single pathway for telomere replication (Lundblad and Szostak 1989  ; Lendvay et al. 1996  ; Lingner et al. 1997b  ).	gene_phenotype
73068	3	334655	5	NULL	NULL	0	NULL	yeast cellular senescence	Process		is a type of					telomerase defect	Process				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_8_1073_s_136	9553037	Strains carrying deletions of  EST1, EST2, EST3, or  TLC1 exhibit the in vivo phenotypes predicted for a telomerase defect (telomere shortening and progressive loss of viability, termed yeast cellular senescence), and epistasis tests have shown that these four genes act in a single pathway for telomere replication (Lundblad and Szostak 1989  ; Lendvay et al. 1996  ; Lingner et al. 1997b  ).	gene_phenotype
73069	4	334655	5	NULL	NULL	0	NULL	EST1	GP	deletion of	leads to					yeast cellular senescence	Process				NULL	in vivo	0	NULL	NULL	NULL	gw60_genesdev_12_8_1073_s_136	9553037	Strains carrying deletions of  EST1, EST2, EST3, or  TLC1 exhibit the in vivo phenotypes predicted for a telomerase defect (telomere shortening and progressive loss of viability, termed yeast cellular senescence), and epistasis tests have shown that these four genes act in a single pathway for telomere replication (Lundblad and Szostak 1989  ; Lendvay et al. 1996  ; Lingner et al. 1997b  ).	gene_phenotype
73070	5	334655	5	NULL	NULL	0	NULL	EST2	GP	deletion of	leads to					yeast cellular senescence	Process				NULL	in vivo	0	NULL	NULL	NULL	gw60_genesdev_12_8_1073_s_136	9553037	Strains carrying deletions of  EST1, EST2, EST3, or  TLC1 exhibit the in vivo phenotypes predicted for a telomerase defect (telomere shortening and progressive loss of viability, termed yeast cellular senescence), and epistasis tests have shown that these four genes act in a single pathway for telomere replication (Lundblad and Szostak 1989  ; Lendvay et al. 1996  ; Lingner et al. 1997b  ).	gene_phenotype
73071	6	334655	5	NULL	NULL	0	NULL	EST3	GP	deletion of	leads to					yeast cellular senescence	Process				NULL	in vivo	0	NULL	NULL	NULL	gw60_genesdev_12_8_1073_s_136	9553037	Strains carrying deletions of  EST1, EST2, EST3, or  TLC1 exhibit the in vivo phenotypes predicted for a telomerase defect (telomere shortening and progressive loss of viability, termed yeast cellular senescence), and epistasis tests have shown that these four genes act in a single pathway for telomere replication (Lundblad and Szostak 1989  ; Lendvay et al. 1996  ; Lingner et al. 1997b  ).	gene_phenotype
73072	7	334655	5	NULL	NULL	0	NULL	TLC1	GP	deletion of	leads to					yeast cellular senescence	Process				NULL	in vivo	0	NULL	NULL	NULL	gw60_genesdev_12_8_1073_s_136	9553037	Strains carrying deletions of  EST1, EST2, EST3, or  TLC1 exhibit the in vivo phenotypes predicted for a telomerase defect (telomere shortening and progressive loss of viability, termed yeast cellular senescence), and epistasis tests have shown that these four genes act in a single pathway for telomere replication (Lundblad and Szostak 1989  ; Lendvay et al. 1996  ; Lingner et al. 1997b  ).	gene_phenotype
73073	8	334655	5	NULL	NULL	0	NULL	EST1 gene	GP		plays a role in					telomere	Chromosome	replication of			NULL		0	NULL	NULL	NULL	gw60_genesdev_12_8_1073_s_136	9553037	Strains carrying deletions of  EST1, EST2, EST3, or  TLC1 exhibit the in vivo phenotypes predicted for a telomerase defect (telomere shortening and progressive loss of viability, termed yeast cellular senescence), and epistasis tests have shown that these four genes act in a single pathway for telomere replication (Lundblad and Szostak 1989  ; Lendvay et al. 1996  ; Lingner et al. 1997b  ).	gene_phenotype
73074	9	334655	5	NULL	NULL	0	NULL	EST2 gene	GP		plays a role in					telomere	Chromosome	replication of			NULL		0	NULL	NULL	NULL	gw60_genesdev_12_8_1073_s_136	9553037	Strains carrying deletions of  EST1, EST2, EST3, or  TLC1 exhibit the in vivo phenotypes predicted for a telomerase defect (telomere shortening and progressive loss of viability, termed yeast cellular senescence), and epistasis tests have shown that these four genes act in a single pathway for telomere replication (Lundblad and Szostak 1989  ; Lendvay et al. 1996  ; Lingner et al. 1997b  ).	gene_phenotype
73075	10	334655	5	NULL	NULL	0	NULL	EST3 gene	GP		plays a role in					telomere	Chromosome	replication of			NULL		0	NULL	NULL	NULL	gw60_genesdev_12_8_1073_s_136	9553037	Strains carrying deletions of  EST1, EST2, EST3, or  TLC1 exhibit the in vivo phenotypes predicted for a telomerase defect (telomere shortening and progressive loss of viability, termed yeast cellular senescence), and epistasis tests have shown that these four genes act in a single pathway for telomere replication (Lundblad and Szostak 1989  ; Lendvay et al. 1996  ; Lingner et al. 1997b  ).	gene_phenotype
73076	11	334655	5	NULL	NULL	0	NULL	TLC1 gene	GP		plays a role in					telomere	Chromosome	replication of			NULL		0	NULL	NULL	NULL	gw60_genesdev_12_8_1073_s_136	9553037	Strains carrying deletions of  EST1, EST2, EST3, or  TLC1 exhibit the in vivo phenotypes predicted for a telomerase defect (telomere shortening and progressive loss of viability, termed yeast cellular senescence), and epistasis tests have shown that these four genes act in a single pathway for telomere replication (Lundblad and Szostak 1989  ; Lendvay et al. 1996  ; Lingner et al. 1997b  ).	gene_phenotype
73077	1	334656	5	NULL	NULL	0	NULL	DOT genes	GP		maintain		may			telomeric DNA	NucleicAcid	normal structure of			NULL		0	NULL	NULL	NULL	gw60_genetics_150_2_613_s_406	9755194	Effects of deleting the  DOT genes on telomeric DNA tract length:   Finally, to assess whether the  DOT genes have a role in maintaining normal telomeric DNA structure, telomere length was measured using a TG1-3 probe that detected all telomeres in the cell in strains deleted for one of the nonessential genes isolated in the screen [ DOT1,  DOT4,  DOT5,  DOT6,  ASF1, and  SIR4 ( TLC1 results were published earlier in   S INGER and GOTTSCHLING 1994   )].	gene_phenotype
73078	1	334657	5	NULL	NULL	0	NULL	tlc1-h cells	Cell		is a synonym of					humanized yeast	Cell				NULL		0	NULL	NULL	NULL	gw70_embo_25_4_846_s_38	16467854	In  tlc1-h cells, also known as humanized yeast (  et al), a telomere formed only by vertebrate repeats can be maintained at a regulated mean  length ( ;   et al).	gene_phenotype
73079	2	334657	5	NULL	NULL	NULL	NULL	telomere	Chromosome		is formed by		only			repeats	NucleicAcid	vertebrate			NULL	humanized yeast	NULL	NULL	NULL	NULL	gw70_embo_25_4_846_s_38	16467854	In  tlc1-h cells, also known as humanized yeast (  et al), a telomere formed only by vertebrate repeats can be maintained at a regulated mean  length ( ;   et al).	gene_phenotype
73080	1	334658	5	NULL	NULL	0	NULL	repeats	NucleicAcid	vertebrate	regulates					telomere	Chromosome	length of			NULL		0	NULL	NULL	NULL	gw70_embo_25_4_846_s_39	16467854	It is noteworthy that, in  tlc1-h cells containing a functional  TEL1 gene, the number of vertebrate repeats at a chromosome end is determined in a Rap1-independent  manner, indicating that  TEL1 does not completely abolish the ability of vertebrate repeats to regulate telomere  length.	gene_phenotype
73081	2	334658	5	NULL	NULL	0	NULL	TEL1	GP		does not abolish		completely			statement 1	Process				NULL	tlc1-h cells	0	NULL	NULL	NULL	gw70_embo_25_4_846_s_39	16467854	It is noteworthy that, in  tlc1-h cells containing a functional  TEL1 gene, the number of vertebrate repeats at a chromosome end is determined in a Rap1-independent  manner, indicating that  TEL1 does not completely abolish the ability of vertebrate repeats to regulate telomere  length.	gene_phenotype
73082	3	334658	5	NULL	NULL	0	NULL	tlc1-h cells	Cell		contains					TEL1 gene	GP	functional			NULL		0	NULL	NULL	NULL	gw70_embo_25_4_846_s_39	16467854	It is noteworthy that, in  tlc1-h cells containing a functional  TEL1 gene, the number of vertebrate repeats at a chromosome end is determined in a Rap1-independent  manner, indicating that  TEL1 does not completely abolish the ability of vertebrate repeats to regulate telomere  length.	gene_phenotype
73083	1	334659	5	NULL	NULL	0	NULL	tlc1-h cells	Cell		is a synonym of					humanized yeast	Cell				NULL		0	NULL	NULL	NULL	gw70_embo_22_7_1697_s_184	12660175	In  tlc1-h cells, also known as humanized yeast (  et al), a T2AG3-only telomere formed only by vertebrate repeats can be maintained at a regulated  mean length ( Figure 5B).	gene_phenotype
73084	2	334659	5	NULL	NULL	0	NULL	T2AG3-only telomere	Chromosome		is formed by		only			repeats	NucleicAcid	vertebrate			NULL	humanized yeast\t\t	0	NULL	NULL	NULL	gw70_embo_22_7_1697_s_184	12660175	In  tlc1-h cells, also known as humanized yeast (  et al), a T2AG3-only telomere formed only by vertebrate repeats can be maintained at a regulated  mean length ( Figure 5B).	gene_phenotype
73085	1	334663	5	NULL	NULL	0	NULL	Campylobacter pyloridis	OrganismPart		is associated with					intercellular spaces	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_18_5274_s_172	10960117	Campylobacter pyloridis and gastritis: association with intercellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium.	gene_phenotype
73086	2	334663	5	NULL	NULL	0	NULL	statement 1	Process		plays a role in		important			gastric epithelium	Cell	colonization of			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_18_5274_s_172	10960117	Campylobacter pyloridis and gastritis: association with intercellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium.	gene_phenotype
73087	3	334663	5	NULL	NULL	NULL	NULL	Campylobacter pyloridis	Organism		is adapted to					mucus 	Chemical	environment of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_18_5274_s_172	10960117	Campylobacter pyloridis and gastritis: association with intercellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium.	gene_phenotype
73088	4	334663	5	NULL	NULL	0	NULL	statement 3	Process		plays a role in		important			gastric epithelium	Cell	colonization of			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_18_5274_s_172	10960117	Campylobacter pyloridis and gastritis: association with intercellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium.	gene_phenotype
73089	5	334663	5	NULL	NULL	0	NULL	gastritis	MedicalFinding		is associated with					intercellular spaces	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_18_5274_s_172	10960117	Campylobacter pyloridis and gastritis: association with intercellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium.	gene_phenotype
73090	6	334663	5	NULL	NULL	0	NULL	statement 5	Process		plays a role in		important			gastric epithelium	Cell	colonization of			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_18_5274_s_172	10960117	Campylobacter pyloridis and gastritis: association with intercellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium.	gene_phenotype
73091	7	334663	5	NULL	NULL	NULL	NULL	gastritis	MedicalFinding		is adapted to					mucus	Chemical	environment of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_182_18_5274_s_172	10960117	Campylobacter pyloridis and gastritis: association with intercellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium.	gene_phenotype
73092	8	334663	5	NULL	NULL	0	NULL	statement 7	Process		plays a role in		important			gastric epithelium	Cell	colonization of			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_18_5274_s_172	10960117	Campylobacter pyloridis and gastritis: association with intercellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium.	gene_phenotype
73093	1	334665	5	NULL	NULL	0	NULL	LPS	Chemical		induce					IkappaB	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_11_10776_s_219	14679201	D, NO inhibits LPS-induced IkappaB phosphorylation.	gene_phenotype
73094	2	334665	5	NULL	NULL	0	NULL	NO	Chemical		inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_11_10776_s_219	14679201	D, NO inhibits LPS-induced IkappaB phosphorylation.	gene_phenotype
73095	1	334667	5	NULL	NULL	0	NULL	suppressive petites	NucleicAcid		is a dominant deletion mutant of					mtDNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_pnas_94_23_12503_s_73	9356479	Suppressive petites, for example, are dominant deletion mutants of mtDNA, which depend, like mtDNA itself, on chromosomal genes (e.g.,  PET18), for their replication.	gene_phenotype
73096	2	334667	5	NULL	NULL	0	NULL	statement 1	Process	replication of	is dependent on					 PET18	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_94_23_12503_s_73	9356479	Suppressive petites, for example, are dominant deletion mutants of mtDNA, which depend, like mtDNA itself, on chromosomal genes (e.g.,  PET18), for their replication.	gene_phenotype
73097	3	334667	5	NULL	NULL	0	NULL	 PET18	GP		is a type of					chromosomal gene	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_94_23_12503_s_73	9356479	Suppressive petites, for example, are dominant deletion mutants of mtDNA, which depend, like mtDNA itself, on chromosomal genes (e.g.,  PET18), for their replication.	gene_phenotype
73098	4	334667	5	NULL	NULL	0	NULL	mtDNA	NucleicAcid	replication of	is dependent on					PET18	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_94_23_12503_s_73	9356479	Suppressive petites, for example, are dominant deletion mutants of mtDNA, which depend, like mtDNA itself, on chromosomal genes (e.g.,  PET18), for their replication.	gene_phenotype
73099	1	334668	5	NULL	NULL	0	NULL	PET111	GP	null mutation;;S. kluyveri	prevents					respiratory growth	Process				NULL	nonfermentable carbon source	0	NULL	NULL	NULL	gw60_genetics_154_3_999_s_238	10757749	These null mutations in  S. kluyveri PET111,  K. lactis PET111, or  S. kluyveri PET122 all prevented respiratory growth on nonfermentable carbon sources.	gene_phenotype
73100	2	334668	5	NULL	NULL	0	NULL	PET111	GP	null mutant;;K. lactis	prevents					respiratory growth	Process				NULL	nonfermentable carbon source	0	NULL	NULL	NULL	gw60_genetics_154_3_999_s_238	10757749	These null mutations in  S. kluyveri PET111,  K. lactis PET111, or  S. kluyveri PET122 all prevented respiratory growth on nonfermentable carbon sources.	gene_phenotype
73101	3	334668	5	NULL	NULL	0	NULL	PET122	GP	null mutant;;S. kluyveri	prevents					respiratory growth	Process				NULL	nonfermentable carbon source	0	NULL	NULL	NULL	gw60_genetics_154_3_999_s_238	10757749	These null mutations in  S. kluyveri PET111,  K. lactis PET111, or  S. kluyveri PET122 all prevented respiratory growth on nonfermentable carbon sources.	gene_phenotype
73102	1	334672	5	NULL	NULL	0	NULL	pet18 gene	GP	mutant	confer					respire	Process	inability to			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	abs-batch0650-0679_mol-gen-genet_165_2_366371_s_2	366371	Mutations in the pet18 gene of Saccharomyces cerevisiae (formerly denoted  pets) confer three phenotypes on mutant strains: (i) inability to respire  (petite), (ii) inability to maintain the double-stranded RNA killer plasmid  (sensitive), and (iii) temperature sensitivity for growth.	gene_phenotype
73103	2	334672	5	NULL	NULL	NULL	NULL	pet18 gene	GP	mutant	confer					double-stranded RNA killer plasmid	CellComponent	inability to maintain			NULL	Saccharomyces cerevisiae	NULL	NULL	NULL	NULL	abs-batch0650-0679_mol-gen-genet_165_2_366371_s_2	366371	Mutations in the pet18 gene of Saccharomyces cerevisiae (formerly denoted  pets) confer three phenotypes on mutant strains: (i) inability to respire  (petite), (ii) inability to maintain the double-stranded RNA killer plasmid  (sensitive), and (iii) temperature sensitivity for growth.	gene_phenotype
73104	3	334672	5	NULL	NULL	0	NULL	pet18 gene	GP	mutant	confer					growth	Process	temperature sensitivity of			NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	abs-batch0650-0679_mol-gen-genet_165_2_366371_s_2	366371	Mutations in the pet18 gene of Saccharomyces cerevisiae (formerly denoted  pets) confer three phenotypes on mutant strains: (i) inability to respire  (petite), (ii) inability to maintain the double-stranded RNA killer plasmid  (sensitive), and (iii) temperature sensitivity for growth.	gene_phenotype
73105	1	334674	5	NULL	NULL	0	NULL	axoplasmic transport	Process		is required for					AR	GP	 normal expression of			NULL		0	NULL	NULL	NULL	gw60_pnas_94_4_1521_s_136	9037086	Thus, axoplasmic transport is required for normal expression of AR.	gene_phenotype
73141	1	334680	5	NULL	NULL	0	NULL	ascii	Cell		contains					respiratory growth-deficient spore	Cell				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_24_16305_s_98	16608846	As expected, the ascii usually contained two spores, both respiratory growth-deficient and leucine-prototrophic, as a result of the  pet111 deletion (not shown).	gene_phenotype
73142	2	334680	5	NULL	NULL	0	NULL	ascii	Cell		contains					leucine-prototrophic spore	Cell				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_24_16305_s_98	16608846	As expected, the ascii usually contained two spores, both respiratory growth-deficient and leucine-prototrophic, as a result of the  pet111 deletion (not shown).	gene_phenotype
73143	3	334680	5	NULL	NULL	0	NULL	pet111	GP	deletion of	leads to					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_24_16305_s_98	16608846	As expected, the ascii usually contained two spores, both respiratory growth-deficient and leucine-prototrophic, as a result of the  pet111 deletion (not shown).	gene_phenotype
73144	4	334680	5	NULL	NULL	0	NULL	pet111	GP	deletion of	leads to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_24_16305_s_98	16608846	As expected, the ascii usually contained two spores, both respiratory growth-deficient and leucine-prototrophic, as a result of the  pet111 deletion (not shown).	gene_phenotype
73145	1	334682	5	NULL	NULL	0	NULL	cox2-11 strain	Cell		contains					suppressor	AbstractConcept				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1826_s_96	9528754	Respiratory growth of the  cox2-11 strains containing these suppressors remained dependent upon the function of the  PET111 gene.	gene_phenotype
73146	2	334682	5	NULL	NULL	0	NULL	statement 1	Cell	respiratory growth of	is dependent on					 PET111 gene	GP	function of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_4_1826_s_96	9528754	Respiratory growth of the  cox2-11 strains containing these suppressors remained dependent upon the function of the  PET111 gene.	gene_phenotype
73147	1	334683	5	NULL	NULL	0	NULL	JM109(DE3)(pLysS) cells	Cell		harbor					pET11d- uxuR vector	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_12_3695_s_204	10368143	Indeed, JM109(DE3)(pLysS) cells harboring the pET11d- uxuR vector were viable and permitted low-level expression of UxuR.	gene_phenotype
73148	2	334683	5	NULL	NULL	0	NULL	UxuR	GP		is expressed in		low			statement 1	Cell				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_12_3695_s_204	10368143	Indeed, JM109(DE3)(pLysS) cells harboring the pET11d- uxuR vector were viable and permitted low-level expression of UxuR.	gene_phenotype
73149	1	334695	5	NULL	NULL	0	NULL	 CBT1	GP	deletion of	accumulates					15S RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_genetics_171_3_949_s_140	16118200	Deletion of  CBT1 results in accumulation of 15S and  RPM1 RNAs with unprocessed 5' ends:   The defect in 5' processing of  COB in the  cbt1 deletion strains is similar to that previously shown for  pet127 mutants ( IESENBERGERand F 1997), although it is not as pronounced.	gene_phenotype
73150	2	334695	5	NULL	NULL	0	NULL	15S RNA	NucleicAcid		contains					5' ends	NucleicAcid	unprocessed			NULL		0	NULL	NULL	NULL	gw70_genetics_171_3_949_s_140	16118200	Deletion of  CBT1 results in accumulation of 15S and  RPM1 RNAs with unprocessed 5' ends:   The defect in 5' processing of  COB in the  cbt1 deletion strains is similar to that previously shown for  pet127 mutants ( IESENBERGERand F 1997), although it is not as pronounced.	gene_phenotype
73151	3	334695	5	NULL	NULL	0	NULL	 CBT1	GP	deletion of	accumulates					RPM1 RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_genetics_171_3_949_s_140	16118200	Deletion of  CBT1 results in accumulation of 15S and  RPM1 RNAs with unprocessed 5' ends:   The defect in 5' processing of  COB in the  cbt1 deletion strains is similar to that previously shown for  pet127 mutants ( IESENBERGERand F 1997), although it is not as pronounced.	gene_phenotype
73152	4	334695	5	NULL	NULL	0	NULL	RPM1 RNA	NucleicAcid		contains					5' ends	NucleicAcid	unprocessed			NULL		0	NULL	NULL	NULL	gw70_genetics_171_3_949_s_140	16118200	Deletion of  CBT1 results in accumulation of 15S and  RPM1 RNAs with unprocessed 5' ends:   The defect in 5' processing of  COB in the  cbt1 deletion strains is similar to that previously shown for  pet127 mutants ( IESENBERGERand F 1997), although it is not as pronounced.	gene_phenotype
73153	1	334696	5	NULL	NULL	0	NULL	pet127	GP	mutation of	supress					ACG	NucleicAcid	respiratory deficiency of;;mutant			NULL		0	NULL	NULL	NULL	gw60_genetics_151_4_1315_s_219	10101159	The  pet127 mutation did suppress the respiratory deficiency of the ACG and CCU mutants and allowed very slow growth of the CAG mutant at 30 degrees  (observed after 7 days of incubation).	gene_phenotype
73154	2	334696	5	NULL	NULL	NULL	NULL	pet127	GP	mutation of	supress					CCU	NucleicAcid	respiratory deficiency of;;mutant			NULL		NULL	NULL	NULL	NULL	gw60_genetics_151_4_1315_s_219	10101159	The  pet127 mutation did suppress the respiratory deficiency of the ACG and CCU mutants and allowed very slow growth of the CAG mutant at 30 degrees  (observed after 7 days of incubation).	gene_phenotype
73155	3	334696	5	NULL	NULL	0	NULL	pet127	GP	mutation of	allows					CAG	NucleicAcid	very slow growth of;;mutant			NULL		0	NULL	NULL	NULL	gw60_genetics_151_4_1315_s_219	10101159	The  pet127 mutation did suppress the respiratory deficiency of the ACG and CCU mutants and allowed very slow growth of the CAG mutant at 30 degrees  (observed after 7 days of incubation).	gene_phenotype
73156	1	334714	5	NULL	NULL	0	NULL	 PET127 gene product	GP		is involved in					RNA	NucleicAcid	metabolism of;;mitochondrial			NULL		0	NULL	NULL	NULL	gw70_genetics_171_3_949_s_70	16118200	Suppressors of the temperature-sensitive respiratory growth phenotype of strains with the CCG triplet mutated to CC U or  ACG have been linked ( HEN et al) to the  PET127 and  DSS1 genes, which encode products involved in mitochondrial RNA metabolism ( IESENBERGEROX;  ZIEMBOWSKI et al ).	gene_phenotype
73157	2	334714	5	NULL	NULL	0	NULL	DSS1 gene product	GP		is involved in					RNA	NucleicAcid	metabolism of;;mitochondrial			NULL		0	NULL	NULL	NULL	gw70_genetics_171_3_949_s_70	16118200	Suppressors of the temperature-sensitive respiratory growth phenotype of strains with the CCG triplet mutated to CC U or  ACG have been linked ( HEN et al) to the  PET127 and  DSS1 genes, which encode products involved in mitochondrial RNA metabolism ( IESENBERGEROX;  ZIEMBOWSKI et al ).	gene_phenotype
73158	1	334730	5	NULL	NULL	0	NULL	AFP1	GP	 E. coli BL21(DE3) cell extracts	causes					antifungal activity	Process				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_24_7421_s_260	10601197	As antifungal activity has also been demonstrated for AFP1 isolated to homogeneity from  E. coli BL21(DE3) cell extracts carrying the portion of the  afp1 gene for the mature AFP1 protein in the T7 RNA polymerase-based pET11a (data not shown), there is no doubt that antifungal activity is caused by AFP1 alone.	gene_phenotype
73228	1	334764	5	NULL	NULL	0	NULL	pet20- strain	Cell		is sensitive to					calcium chloride	Chemical				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_282	16491469	In addition to the lower cytochrome  c level and diminished growth on YPG, the  pet20-  strain was sensitive to a number of mitochondria-specific drugs, such as: calcium  chloride, which regulates mitochondrial function; oligomycin, an inhibitor of ATP  synthase and oxidative phosphorylation; potassium ferricyanide, an inhibitor of oxidative  phosphorylation; and hydrogen peroxide, a strong oxidant and stress agent that affects  proton/electron balance in the cell (Figure  2B).	gene_phenotype
73229	2	334764	5	NULL	NULL	0	NULL	calcium chloride	Chemical		is a type of					mitochondria-specific drug	Chemical				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_282	16491469	In addition to the lower cytochrome  c level and diminished growth on YPG, the  pet20-  strain was sensitive to a number of mitochondria-specific drugs, such as: calcium  chloride, which regulates mitochondrial function; oligomycin, an inhibitor of ATP  synthase and oxidative phosphorylation; potassium ferricyanide, an inhibitor of oxidative  phosphorylation; and hydrogen peroxide, a strong oxidant and stress agent that affects  proton/electron balance in the cell (Figure  2B).	gene_phenotype
73230	3	334764	5	NULL	NULL	0	NULL	calcium chloride	Chemical		regulates					mitochondria	CellComponent	function of			NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_282	16491469	In addition to the lower cytochrome  c level and diminished growth on YPG, the  pet20-  strain was sensitive to a number of mitochondria-specific drugs, such as: calcium  chloride, which regulates mitochondrial function; oligomycin, an inhibitor of ATP  synthase and oxidative phosphorylation; potassium ferricyanide, an inhibitor of oxidative  phosphorylation; and hydrogen peroxide, a strong oxidant and stress agent that affects  proton/electron balance in the cell (Figure  2B).	gene_phenotype
73231	4	334764	5	NULL	NULL	0	NULL	pet20- strain	Cell		is sensitive to					oligomycin	Chemical				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_282	16491469	In addition to the lower cytochrome  c level and diminished growth on YPG, the  pet20-  strain was sensitive to a number of mitochondria-specific drugs, such as: calcium  chloride, which regulates mitochondrial function; oligomycin, an inhibitor of ATP  synthase and oxidative phosphorylation; potassium ferricyanide, an inhibitor of oxidative  phosphorylation; and hydrogen peroxide, a strong oxidant and stress agent that affects  proton/electron balance in the cell (Figure  2B).	gene_phenotype
73232	5	334764	5	NULL	NULL	0	NULL	oligomycin	Chemical		is a type of					mitochondria-specific drug	Chemical				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_282	16491469	In addition to the lower cytochrome  c level and diminished growth on YPG, the  pet20-  strain was sensitive to a number of mitochondria-specific drugs, such as: calcium  chloride, which regulates mitochondrial function; oligomycin, an inhibitor of ATP  synthase and oxidative phosphorylation; potassium ferricyanide, an inhibitor of oxidative  phosphorylation; and hydrogen peroxide, a strong oxidant and stress agent that affects  proton/electron balance in the cell (Figure  2B).	gene_phenotype
73233	6	334764	5	NULL	NULL	0	NULL	oligomycin	Chemical		is an inhibitor of					ATP synthase	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_282	16491469	In addition to the lower cytochrome  c level and diminished growth on YPG, the  pet20-  strain was sensitive to a number of mitochondria-specific drugs, such as: calcium  chloride, which regulates mitochondrial function; oligomycin, an inhibitor of ATP  synthase and oxidative phosphorylation; potassium ferricyanide, an inhibitor of oxidative  phosphorylation; and hydrogen peroxide, a strong oxidant and stress agent that affects  proton/electron balance in the cell (Figure  2B).	gene_phenotype
73235	7	334764	5	NULL	NULL	0	NULL	oligomycin	Chemical		is an inhibitor of					oxidative phosphorylation	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_282	16491469	In addition to the lower cytochrome  c level and diminished growth on YPG, the  pet20-  strain was sensitive to a number of mitochondria-specific drugs, such as: calcium  chloride, which regulates mitochondrial function; oligomycin, an inhibitor of ATP  synthase and oxidative phosphorylation; potassium ferricyanide, an inhibitor of oxidative  phosphorylation; and hydrogen peroxide, a strong oxidant and stress agent that affects  proton/electron balance in the cell (Figure  2B).	gene_phenotype
73237	8	334764	5	NULL	NULL	0	NULL	pet20- strain	Cell		is sensitive to					potassium ferricyanide	Chemical				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_282	16491469	In addition to the lower cytochrome  c level and diminished growth on YPG, the  pet20-  strain was sensitive to a number of mitochondria-specific drugs, such as: calcium  chloride, which regulates mitochondrial function; oligomycin, an inhibitor of ATP  synthase and oxidative phosphorylation; potassium ferricyanide, an inhibitor of oxidative  phosphorylation; and hydrogen peroxide, a strong oxidant and stress agent that affects  proton/electron balance in the cell (Figure  2B).	gene_phenotype
73238	9	334764	5	NULL	NULL	0	NULL	potassium ferricyanide	Chemical		is a type of					mitochondria-specific drug	Chemical				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_282	16491469	In addition to the lower cytochrome  c level and diminished growth on YPG, the  pet20-  strain was sensitive to a number of mitochondria-specific drugs, such as: calcium  chloride, which regulates mitochondrial function; oligomycin, an inhibitor of ATP  synthase and oxidative phosphorylation; potassium ferricyanide, an inhibitor of oxidative  phosphorylation; and hydrogen peroxide, a strong oxidant and stress agent that affects  proton/electron balance in the cell (Figure  2B).	gene_phenotype
73239	10	334764	5	NULL	NULL	0	NULL	potassium ferricyanide	Chemical		is an inhibitor of					oxidative phosphorylation	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_282	16491469	In addition to the lower cytochrome  c level and diminished growth on YPG, the  pet20-  strain was sensitive to a number of mitochondria-specific drugs, such as: calcium  chloride, which regulates mitochondrial function; oligomycin, an inhibitor of ATP  synthase and oxidative phosphorylation; potassium ferricyanide, an inhibitor of oxidative  phosphorylation; and hydrogen peroxide, a strong oxidant and stress agent that affects  proton/electron balance in the cell (Figure  2B).	gene_phenotype
73240	11	334764	5	NULL	NULL	0	NULL	pet20- strain	Cell		is sensitive to					hydrogen peroxide	Chemical				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_282	16491469	In addition to the lower cytochrome  c level and diminished growth on YPG, the  pet20-  strain was sensitive to a number of mitochondria-specific drugs, such as: calcium  chloride, which regulates mitochondrial function; oligomycin, an inhibitor of ATP  synthase and oxidative phosphorylation; potassium ferricyanide, an inhibitor of oxidative  phosphorylation; and hydrogen peroxide, a strong oxidant and stress agent that affects  proton/electron balance in the cell (Figure  2B).	gene_phenotype
73241	12	334764	5	NULL	NULL	0	NULL	hydrogen peroxide	Chemical		is a type of					mitochondria-specific drug	Chemical				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_282	16491469	In addition to the lower cytochrome  c level and diminished growth on YPG, the  pet20-  strain was sensitive to a number of mitochondria-specific drugs, such as: calcium  chloride, which regulates mitochondrial function; oligomycin, an inhibitor of ATP  synthase and oxidative phosphorylation; potassium ferricyanide, an inhibitor of oxidative  phosphorylation; and hydrogen peroxide, a strong oxidant and stress agent that affects  proton/electron balance in the cell (Figure  2B).	gene_phenotype
73242	13	334764	5	NULL	NULL	NULL	NULL	hydrogen peroxide	Chemical		is a type of					strong oxidant	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_2_127_s_282	16491469	In addition to the lower cytochrome  c level and diminished growth on YPG, the  pet20-  strain was sensitive to a number of mitochondria-specific drugs, such as: calcium  chloride, which regulates mitochondrial function; oligomycin, an inhibitor of ATP  synthase and oxidative phosphorylation; potassium ferricyanide, an inhibitor of oxidative  phosphorylation; and hydrogen peroxide, a strong oxidant and stress agent that affects  proton/electron balance in the cell (Figure  2B).	gene_phenotype
73243	14	334764	5	NULL	NULL	0	NULL	hydrogen peroxide	Chemical		is a type of					stress agent	Chemical				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_282	16491469	In addition to the lower cytochrome  c level and diminished growth on YPG, the  pet20-  strain was sensitive to a number of mitochondria-specific drugs, such as: calcium  chloride, which regulates mitochondrial function; oligomycin, an inhibitor of ATP  synthase and oxidative phosphorylation; potassium ferricyanide, an inhibitor of oxidative  phosphorylation; and hydrogen peroxide, a strong oxidant and stress agent that affects  proton/electron balance in the cell (Figure  2B).	gene_phenotype
73244	15	334764	5	NULL	NULL	0	NULL	hydrogen peroxide	Chemical		balance					 proton/electron	Chemical				NULL	cell	0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_282	16491469	In addition to the lower cytochrome  c level and diminished growth on YPG, the  pet20-  strain was sensitive to a number of mitochondria-specific drugs, such as: calcium  chloride, which regulates mitochondrial function; oligomycin, an inhibitor of ATP  synthase and oxidative phosphorylation; potassium ferricyanide, an inhibitor of oxidative  phosphorylation; and hydrogen peroxide, a strong oxidant and stress agent that affects  proton/electron balance in the cell (Figure  2B).	gene_phenotype
73245	1	334766	5	NULL	NULL	NULL	NULL	Pet20p	GP		constitutes		may			mitochondrial complex	GP	uncharacterized	non-catalytic subunit		NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_2_127_s_8	16491469	It is also possible that Pet20p may constitute  a non-catalytic subunit of an uncharacterized mitochondrial complex or serve as a  transporter or a coupling factor.	gene_phenotype
73246	2	334766	5	NULL	NULL	0	NULL	Pet20p	GP		serve as		may			transporter	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_8	16491469	It is also possible that Pet20p may constitute  a non-catalytic subunit of an uncharacterized mitochondrial complex or serve as a  transporter or a coupling factor.	gene_phenotype
73247	3	334766	5	NULL	NULL	0	NULL	Pet20p	GP		serve as		may			coupling factor	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_8	16491469	It is also possible that Pet20p may constitute  a non-catalytic subunit of an uncharacterized mitochondrial complex or serve as a  transporter or a coupling factor.	gene_phenotype
73248	1	334792	5	NULL	NULL	0	NULL	Pet20p	GP		is involved in		might be			mitochondrial constituent	CellComponent	correct folding of			NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_279	16491469	Based on the cytochrome content,  phenotypic analysis, protein localization and mitochondrial potential analysis, we  suggest that Pet20p might be involved in correct folding, positioning or compartmentalization  of some mitochondrial constituent which functions to couple electron chain transport  and/or molecular transport across membranes, but does not intrinsically serve an  enzymatic or structural function.	gene_phenotype
73249	2	334792	5	NULL	NULL	0	NULL	Pet20p	GP		is involved in		might be			mitochondrial constituent	CellComponent	positioning of			NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_279	16491469	Based on the cytochrome content,  phenotypic analysis, protein localization and mitochondrial potential analysis, we  suggest that Pet20p might be involved in correct folding, positioning or compartmentalization  of some mitochondrial constituent which functions to couple electron chain transport  and/or molecular transport across membranes, but does not intrinsically serve an  enzymatic or structural function.	gene_phenotype
73250	3	334792	5	NULL	NULL	0	NULL	Pet20p	GP		is involved in		might be			mitochondrial constituent	CellComponent	compartmentalization of 			NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_279	16491469	Based on the cytochrome content,  phenotypic analysis, protein localization and mitochondrial potential analysis, we  suggest that Pet20p might be involved in correct folding, positioning or compartmentalization  of some mitochondrial constituent which functions to couple electron chain transport  and/or molecular transport across membranes, but does not intrinsically serve an  enzymatic or structural function.	gene_phenotype
73251	4	334792	5	NULL	NULL	0	NULL	electron chain 	Chemical	transport of	is coupled to					molecules	AbstractConcept	transport of			NULL	across membranes	0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_279	16491469	Based on the cytochrome content,  phenotypic analysis, protein localization and mitochondrial potential analysis, we  suggest that Pet20p might be involved in correct folding, positioning or compartmentalization  of some mitochondrial constituent which functions to couple electron chain transport  and/or molecular transport across membranes, but does not intrinsically serve an  enzymatic or structural function.	gene_phenotype
73252	5	334792	5	NULL	NULL	0	NULL	mitochondrial constituent	CellComponent		functions in					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_279	16491469	Based on the cytochrome content,  phenotypic analysis, protein localization and mitochondrial potential analysis, we  suggest that Pet20p might be involved in correct folding, positioning or compartmentalization  of some mitochondrial constituent which functions to couple electron chain transport  and/or molecular transport across membranes, but does not intrinsically serve an  enzymatic or structural function.	gene_phenotype
73253	6	334792	5	NULL	NULL	0	NULL	mitochondrial constituent	CellComponent		does not serve					 enzymatic function	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_279	16491469	Based on the cytochrome content,  phenotypic analysis, protein localization and mitochondrial potential analysis, we  suggest that Pet20p might be involved in correct folding, positioning or compartmentalization  of some mitochondrial constituent which functions to couple electron chain transport  and/or molecular transport across membranes, but does not intrinsically serve an  enzymatic or structural function.	gene_phenotype
73263	7	334792	5	NULL	NULL	0	NULL	mitochondrial constituent	CellComponent		does not serve					structural function	Process				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_279	16491469	Based on the cytochrome content,  phenotypic analysis, protein localization and mitochondrial potential analysis, we  suggest that Pet20p might be involved in correct folding, positioning or compartmentalization  of some mitochondrial constituent which functions to couple electron chain transport  and/or molecular transport across membranes, but does not intrinsically serve an  enzymatic or structural function.	gene_phenotype
73266	1	334793	5	NULL	NULL	0	NULL	Pet20p	GP	sequence of	is similar to					Ndufa6	GP	sequence of			NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_281	16491469	The sequence similarities  of Pet20p to the following proteins (Figure  1A) strongly support such suggestion: Ndufa6, NADH dehydrogenase (ubiquinone) 1  subcomplex subunit 6, a mitochondrial inner membrane protein; yeast Cox14p, a mitochondrial  protein that is required for assembly of cytochrome  c oxidase; and ABCA2, a member of the superfamily of ATP-binding cassette (ABC) transporters.	gene_phenotype
73267	2	334793	5	NULL	NULL	0	NULL	Ndufa6	GP		is					NADH dehydrogenase (ubiquinone) 1 subcomplex subunit 6	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_281	16491469	The sequence similarities  of Pet20p to the following proteins (Figure  1A) strongly support such suggestion: Ndufa6, NADH dehydrogenase (ubiquinone) 1  subcomplex subunit 6, a mitochondrial inner membrane protein; yeast Cox14p, a mitochondrial  protein that is required for assembly of cytochrome  c oxidase; and ABCA2, a member of the superfamily of ATP-binding cassette (ABC) transporters.	gene_phenotype
73269	3	334793	5	NULL	NULL	0	NULL	Ndufa6	GP		is a type of					mitochondrial inner membrane protein	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_281	16491469	The sequence similarities  of Pet20p to the following proteins (Figure  1A) strongly support such suggestion: Ndufa6, NADH dehydrogenase (ubiquinone) 1  subcomplex subunit 6, a mitochondrial inner membrane protein; yeast Cox14p, a mitochondrial  protein that is required for assembly of cytochrome  c oxidase; and ABCA2, a member of the superfamily of ATP-binding cassette (ABC) transporters.	gene_phenotype
73270	4	334793	5	NULL	NULL	0	NULL	Pet20p	GP	sequence of	is similar to					Cox14p	GP	sequence of;;yeast			NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_281	16491469	The sequence similarities  of Pet20p to the following proteins (Figure  1A) strongly support such suggestion: Ndufa6, NADH dehydrogenase (ubiquinone) 1  subcomplex subunit 6, a mitochondrial inner membrane protein; yeast Cox14p, a mitochondrial  protein that is required for assembly of cytochrome  c oxidase; and ABCA2, a member of the superfamily of ATP-binding cassette (ABC) transporters.	gene_phenotype
73272	5	334793	5	NULL	NULL	0	NULL	Cox14p	GP	yeast	is a type of					mitochondrial protein	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_281	16491469	The sequence similarities  of Pet20p to the following proteins (Figure  1A) strongly support such suggestion: Ndufa6, NADH dehydrogenase (ubiquinone) 1  subcomplex subunit 6, a mitochondrial inner membrane protein; yeast Cox14p, a mitochondrial  protein that is required for assembly of cytochrome  c oxidase; and ABCA2, a member of the superfamily of ATP-binding cassette (ABC) transporters.	gene_phenotype
73273	6	334793	5	NULL	NULL	0	NULL	Cox14p	GP	yeast	is required for					cytochrome c oxidase	GP	assembly of			NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_281	16491469	The sequence similarities  of Pet20p to the following proteins (Figure  1A) strongly support such suggestion: Ndufa6, NADH dehydrogenase (ubiquinone) 1  subcomplex subunit 6, a mitochondrial inner membrane protein; yeast Cox14p, a mitochondrial  protein that is required for assembly of cytochrome  c oxidase; and ABCA2, a member of the superfamily of ATP-binding cassette (ABC) transporters.	gene_phenotype
73275	7	334793	5	NULL	NULL	0	NULL	Pet20p	GP	sequence of	is similar to					ABCA2	GP	sequence of			NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_281	16491469	The sequence similarities  of Pet20p to the following proteins (Figure  1A) strongly support such suggestion: Ndufa6, NADH dehydrogenase (ubiquinone) 1  subcomplex subunit 6, a mitochondrial inner membrane protein; yeast Cox14p, a mitochondrial  protein that is required for assembly of cytochrome  c oxidase; and ABCA2, a member of the superfamily of ATP-binding cassette (ABC) transporters.	gene_phenotype
73279	8	334793	5	NULL	NULL	0	NULL	ABCA2	GP		is a member of					ABC transporters superfamilty	GP				NULL		0	NULL	NULL	NULL	gw70_yeast_23_2_127_s_281	16491469	The sequence similarities  of Pet20p to the following proteins (Figure  1A) strongly support such suggestion: Ndufa6, NADH dehydrogenase (ubiquinone) 1  subcomplex subunit 6, a mitochondrial inner membrane protein; yeast Cox14p, a mitochondrial  protein that is required for assembly of cytochrome  c oxidase; and ABCA2, a member of the superfamily of ATP-binding cassette (ABC) transporters.	gene_phenotype
73281	9	334793	5	NULL	NULL	NULL	NULL	ABC transporters	GP		is					ATP-binding cassette transporters	GP				NULL		NULL	NULL	NULL	NULL	gw70_yeast_23_2_127_s_281	16491469	The sequence similarities  of Pet20p to the following proteins (Figure  1A) strongly support such suggestion: Ndufa6, NADH dehydrogenase (ubiquinone) 1  subcomplex subunit 6, a mitochondrial inner membrane protein; yeast Cox14p, a mitochondrial  protein that is required for assembly of cytochrome  c oxidase; and ABCA2, a member of the superfamily of ATP-binding cassette (ABC) transporters.	gene_phenotype
73296	1	334801	5	NULL	NULL	0	NULL	LpxP protein	GP	controlled overproduction of	increases					palmitoleoyltransferase activity	Process				NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_277_16_14186_s_202	11830594	Massive Overproduction of Palmitoleoyltransferase in Cells Expressing lpxP Behind a T7lac Promoter-- The  lpxP gene was cloned into a T7 polymerase expression vector, pET21a+, to confirm that controlled overproduction of the LpxP protein from a non-native promoter results in increased  in vitro palmitoleoyltransferase activity.	gene_phenotype
51560	1	334823	5	NULL	NULL	0	NULL	Cyp 7a	NULL		is	NULL				cholesterol 7alpha-hydroxylase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_35_31441_s_30	12052824	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase (Cyp 7a) ( 14-17), the enzyme catalyzing the first and rate-limiting step of bile acid synthesis ( 18), and activates expression of intestinal bile acid-binding protein ( 11), phospholipid transfer protein ( 19), BSEP ( 20), and dehydroepiandrosterone sulfotransferase ( 21).	transcription
51561	2	334823	5	NULL	NULL	NULL	NULL	FXR			inhibit					Cyp 7a		expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_31441_s_30	12052824	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase (Cyp 7a) ( 14-17), the enzyme catalyzing the first and rate-limiting step of bile acid synthesis ( 18), and activates expression of intestinal bile acid-binding protein ( 11), phospholipid transfer protein ( 19), BSEP ( 20), and dehydroepiandrosterone sulfotransferase ( 21).	transcription
51562	3	334823	5	NULL	NULL	NULL	NULL	Cyp 7a			catalyzes					bile acid		synthesis of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_31441_s_30	12052824	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase (Cyp 7a) ( 14-17), the enzyme catalyzing the first and rate-limiting step of bile acid synthesis ( 18), and activates expression of intestinal bile acid-binding protein ( 11), phospholipid transfer protein ( 19), BSEP ( 20), and dehydroepiandrosterone sulfotransferase ( 21).	transcription
51563	4	334823	5	NULL	NULL	NULL	NULL	FXR			activates					intestinal bile acid-binding protein		expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_31441_s_30	12052824	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase (Cyp 7a) ( 14-17), the enzyme catalyzing the first and rate-limiting step of bile acid synthesis ( 18), and activates expression of intestinal bile acid-binding protein ( 11), phospholipid transfer protein ( 19), BSEP ( 20), and dehydroepiandrosterone sulfotransferase ( 21).	transcription
51564	5	334823	5	NULL	NULL	NULL	NULL	FXR			activates					phospholipid transfer protein		expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_31441_s_30	12052824	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase (Cyp 7a) ( 14-17), the enzyme catalyzing the first and rate-limiting step of bile acid synthesis ( 18), and activates expression of intestinal bile acid-binding protein ( 11), phospholipid transfer protein ( 19), BSEP ( 20), and dehydroepiandrosterone sulfotransferase ( 21).	transcription
51565	6	334823	5	NULL	NULL	NULL	NULL	FXR			activates					BSEP		expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_31441_s_30	12052824	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase (Cyp 7a) ( 14-17), the enzyme catalyzing the first and rate-limiting step of bile acid synthesis ( 18), and activates expression of intestinal bile acid-binding protein ( 11), phospholipid transfer protein ( 19), BSEP ( 20), and dehydroepiandrosterone sulfotransferase ( 21).	transcription
51566	7	334823	5	NULL	NULL	NULL	NULL	FXR			activates					dehydroepiandrosterone sulfotransferase		expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_31441_s_30	12052824	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase (Cyp 7a) ( 14-17), the enzyme catalyzing the first and rate-limiting step of bile acid synthesis ( 18), and activates expression of intestinal bile acid-binding protein ( 11), phospholipid transfer protein ( 19), BSEP ( 20), and dehydroepiandrosterone sulfotransferase ( 21).	transcription
54318	8	334823	5	NULL	NULL	NULL	NULL	Cyp 7a			is a type of					enzyme					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_35_31441_s_30	12052824	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase (Cyp 7a) ( 14-17), the enzyme catalyzing the first and rate-limiting step of bile acid synthesis ( 18), and activates expression of intestinal bile acid-binding protein ( 11), phospholipid transfer protein ( 19), BSEP ( 20), and dehydroepiandrosterone sulfotransferase ( 21).	transcription
51939	1	334823	6	NULL	NULL	0	NULL	Cyp 7a	NULL		is	NULL				cholesterol 7alpha-hydroxylase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_35_31441_s_30	12052824	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase (Cyp 7a) ( 14-17), the enzyme catalyzing the first and rate-limiting step of bile acid synthesis ( 18), and activates expression of intestinal bile acid-binding protein ( 11), phospholipid transfer protein ( 19), BSEP ( 20), and dehydroepiandrosterone sulfotransferase ( 21).	transcription
51940	2	334823	6	NULL	NULL	0	NULL	Cyp 7a	NULL		is a type of	NULL				enzyme	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_35_31441_s_30	12052824	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase (Cyp 7a) ( 14-17), the enzyme catalyzing the first and rate-limiting step of bile acid synthesis ( 18), and activates expression of intestinal bile acid-binding protein ( 11), phospholipid transfer protein ( 19), BSEP ( 20), and dehydroepiandrosterone sulfotransferase ( 21).	transcription
51941	3	334823	6	NULL	NULL	0	NULL	Cyp 7a	NULL		catalyzes	NULL				bile acid 	NULL	synthesis of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_35_31441_s_30	12052824	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase (Cyp 7a) ( 14-17), the enzyme catalyzing the first and rate-limiting step of bile acid synthesis ( 18), and activates expression of intestinal bile acid-binding protein ( 11), phospholipid transfer protein ( 19), BSEP ( 20), and dehydroepiandrosterone sulfotransferase ( 21).	transcription
51942	4	334823	6	NULL	NULL	0	NULL	FXR	NULL		inhibits	NULL				Cyp 7a	NULL	expression of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_35_31441_s_30	12052824	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase (Cyp 7a) ( 14-17), the enzyme catalyzing the first and rate-limiting step of bile acid synthesis ( 18), and activates expression of intestinal bile acid-binding protein ( 11), phospholipid transfer protein ( 19), BSEP ( 20), and dehydroepiandrosterone sulfotransferase ( 21).	transcription
51943	5	334823	6	NULL	NULL	0	NULL	FXR	NULL		activates	NULL				bile acid-binding protein	NULL	expression of;; intestinal			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_35_31441_s_30	12052824	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase (Cyp 7a) ( 14-17), the enzyme catalyzing the first and rate-limiting step of bile acid synthesis ( 18), and activates expression of intestinal bile acid-binding protein ( 11), phospholipid transfer protein ( 19), BSEP ( 20), and dehydroepiandrosterone sulfotransferase ( 21).	transcription
51944	6	334823	6	NULL	NULL	0	NULL	FXR	NULL		activates	NULL				phospholipid transfer protein	NULL	expression of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_35_31441_s_30	12052824	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase (Cyp 7a) ( 14-17), the enzyme catalyzing the first and rate-limiting step of bile acid synthesis ( 18), and activates expression of intestinal bile acid-binding protein ( 11), phospholipid transfer protein ( 19), BSEP ( 20), and dehydroepiandrosterone sulfotransferase ( 21).	transcription
51945	7	334823	6	NULL	NULL	0	NULL	FXR	NULL		activates	NULL				BSEP	NULL	expression of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_35_31441_s_30	12052824	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase (Cyp 7a) ( 14-17), the enzyme catalyzing the first and rate-limiting step of bile acid synthesis ( 18), and activates expression of intestinal bile acid-binding protein ( 11), phospholipid transfer protein ( 19), BSEP ( 20), and dehydroepiandrosterone sulfotransferase ( 21).	transcription
51946	8	334823	6	NULL	NULL	0	NULL	FXR	NULL		activates	NULL				dehydroepiandrosterone sulfotransferase	NULL	expression of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_35_31441_s_30	12052824	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase (Cyp 7a) ( 14-17), the enzyme catalyzing the first and rate-limiting step of bile acid synthesis ( 18), and activates expression of intestinal bile acid-binding protein ( 11), phospholipid transfer protein ( 19), BSEP ( 20), and dehydroepiandrosterone sulfotransferase ( 21).	transcription
51567	1	334824	5	NULL	NULL	0	NULL	campesterol	NULL		is a substrate of	NULL	hypothesized			DET2	NULL	Arabidopsis			NULL		0	NULL	NULL	NULL	gw60_pnas_94_8_3554_s_70	9108014	Because the hypothesized substrates of  Arabidopsis DET2 in BR biosynthesis is campesterol or its analogs (sitosterol or stigmasterol), which contain a 3beta-hydroxyl,delta5,6 structure, we measured the steroid 5alpha-reductase activity of DET2 toward several radiolabeled steroids with this structure including cholesterol, pregnenolone, and dehydroepiandrosterone.	transcription
51568	2	334824	5	NULL	NULL	0	NULL	statement 1	NULL		plays a role in	NULL				BR	NULL	biosynthesis of			NULL		0	NULL	NULL	NULL	gw60_pnas_94_8_3554_s_70	9108014	Because the hypothesized substrates of  Arabidopsis DET2 in BR biosynthesis is campesterol or its analogs (sitosterol or stigmasterol), which contain a 3beta-hydroxyl,delta5,6 structure, we measured the steroid 5alpha-reductase activity of DET2 toward several radiolabeled steroids with this structure including cholesterol, pregnenolone, and dehydroepiandrosterone.	transcription
51569	3	334824	5	NULL	NULL	0	NULL	sitosterol	NULL		is an analog of	NULL				campesterol	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_94_8_3554_s_70	9108014	Because the hypothesized substrates of  Arabidopsis DET2 in BR biosynthesis is campesterol or its analogs (sitosterol or stigmasterol), which contain a 3beta-hydroxyl,delta5,6 structure, we measured the steroid 5alpha-reductase activity of DET2 toward several radiolabeled steroids with this structure including cholesterol, pregnenolone, and dehydroepiandrosterone.	transcription
51570	4	334824	5	NULL	NULL	0	NULL	stigmasterol	NULL		is an analog of	NULL				campesterol	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_94_8_3554_s_70	9108014	Because the hypothesized substrates of  Arabidopsis DET2 in BR biosynthesis is campesterol or its analogs (sitosterol or stigmasterol), which contain a 3beta-hydroxyl,delta5,6 structure, we measured the steroid 5alpha-reductase activity of DET2 toward several radiolabeled steroids with this structure including cholesterol, pregnenolone, and dehydroepiandrosterone.	transcription
51571	5	334824	5	NULL	NULL	0	NULL	sitosterol	NULL		is a substrate of	NULL	hypothesized			DET2	NULL	Arabidopsis			NULL		0	NULL	NULL	NULL	gw60_pnas_94_8_3554_s_70	9108014	Because the hypothesized substrates of  Arabidopsis DET2 in BR biosynthesis is campesterol or its analogs (sitosterol or stigmasterol), which contain a 3beta-hydroxyl,delta5,6 structure, we measured the steroid 5alpha-reductase activity of DET2 toward several radiolabeled steroids with this structure including cholesterol, pregnenolone, and dehydroepiandrosterone.	transcription
51572	6	334824	5	NULL	NULL	0	NULL	statement 5	NULL		plays a role in	NULL				BR	NULL	biosynthesis of			NULL		0	NULL	NULL	NULL	gw60_pnas_94_8_3554_s_70	9108014	Because the hypothesized substrates of  Arabidopsis DET2 in BR biosynthesis is campesterol or its analogs (sitosterol or stigmasterol), which contain a 3beta-hydroxyl,delta5,6 structure, we measured the steroid 5alpha-reductase activity of DET2 toward several radiolabeled steroids with this structure including cholesterol, pregnenolone, and dehydroepiandrosterone.	transcription
51573	7	334824	5	NULL	NULL	0	NULL	stigmasterol	NULL		is a substrate of	NULL	hypothesized			DET2	NULL	Arabidopsis			NULL		0	NULL	NULL	NULL	gw60_pnas_94_8_3554_s_70	9108014	Because the hypothesized substrates of  Arabidopsis DET2 in BR biosynthesis is campesterol or its analogs (sitosterol or stigmasterol), which contain a 3beta-hydroxyl,delta5,6 structure, we measured the steroid 5alpha-reductase activity of DET2 toward several radiolabeled steroids with this structure including cholesterol, pregnenolone, and dehydroepiandrosterone.	transcription
51574	8	334824	5	NULL	NULL	0	NULL	statement 7	NULL		plays a role in	NULL				BR	NULL	biosynthesis of			NULL		0	NULL	NULL	NULL	gw60_pnas_94_8_3554_s_70	9108014	Because the hypothesized substrates of  Arabidopsis DET2 in BR biosynthesis is campesterol or its analogs (sitosterol or stigmasterol), which contain a 3beta-hydroxyl,delta5,6 structure, we measured the steroid 5alpha-reductase activity of DET2 toward several radiolabeled steroids with this structure including cholesterol, pregnenolone, and dehydroepiandrosterone.	transcription
51947	1	334824	6	NULL	NULL	0	NULL	DET2	NULL	arabidopsis	exhibits	NULL				steroid 5alpha-reductase activity	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_8_3554_s_70	9108014	Because the hypothesized substrates of  Arabidopsis DET2 in BR biosynthesis is campesterol or its analogs (sitosterol or stigmasterol), which contain a 3beta-hydroxyl,delta5,6 structure, we measured the steroid 5alpha-reductase activity of DET2 toward several radiolabeled steroids with this structure including cholesterol, pregnenolone, and dehydroepiandrosterone.	transcription
51948	2	334824	6	NULL	NULL	0	NULL	campesterol	NULL		contains	NULL				3beta-hydroxyl,delta5,6 structure	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_8_3554_s_70	9108014	Because the hypothesized substrates of  Arabidopsis DET2 in BR biosynthesis is campesterol or its analogs (sitosterol or stigmasterol), which contain a 3beta-hydroxyl,delta5,6 structure, we measured the steroid 5alpha-reductase activity of DET2 toward several radiolabeled steroids with this structure including cholesterol, pregnenolone, and dehydroepiandrosterone.	transcription
51949	3	334824	6	NULL	NULL	0	NULL	sitosterol	NULL		contains	NULL				3beta-hydroxyl,delta5,6 structure	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_94_8_3554_s_70	9108014	Because the hypothesized substrates of  Arabidopsis DET2 in BR biosynthesis is campesterol or its analogs (sitosterol or stigmasterol), which contain a 3beta-hydroxyl,delta5,6 structure, we measured the steroid 5alpha-reductase activity of DET2 toward several radiolabeled steroids with this structure including cholesterol, pregnenolone, and dehydroepiandrosterone.	transcription
51950	4	334824	6	NULL	NULL	0	NULL	stigmasterol	NULL		contains	NULL				3beta-hydroxyl,delta5,6 structure	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_94_8_3554_s_70	9108014	Because the hypothesized substrates of  Arabidopsis DET2 in BR biosynthesis is campesterol or its analogs (sitosterol or stigmasterol), which contain a 3beta-hydroxyl,delta5,6 structure, we measured the steroid 5alpha-reductase activity of DET2 toward several radiolabeled steroids with this structure including cholesterol, pregnenolone, and dehydroepiandrosterone.	transcription
51575	1	334825	5	NULL	NULL	0	NULL	Cyp 7a1	NULL		is	NULL				cholesterol 7alpha-hydroxylase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51576	2	334825	5	NULL	NULL	0	NULL	FXR	NULL		inhibit	NULL				Cyp 7a1	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51577	3	334825	5	NULL	NULL	0	NULL	FXR	NULL		inhibit	NULL				sterol 12alpha-hydroxylase	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51578	4	334825	5	NULL	NULL	0	NULL	FXR	NULL		inhibit	NULL				Na+/taurocholate co-transporting polypeptide	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51579	5	334825	5	NULL	NULL	0	NULL	FXR	NULL		inhibit	NULL				apolipoprotein A-I	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51580	6	334825	5	NULL	NULL	0	NULL	I-BABP	NULL		is	NULL				intestinal bile acid-binding protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51581	7	334825	5	NULL	NULL	0	NULL	FXR	NULL		activates	NULL				I-BABP	NULL	expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51582	8	334825	5	NULL	NULL	0	NULL	FXR	NULL		activates	NULL				phospholipid transfer protein	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51583	9	334825	5	NULL	NULL	0	NULL	BSEP	NULL		is	NULL				bile salt export pump	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51584	10	334825	5	NULL	NULL	0	NULL	FXR	NULL		activates	NULL				BSEP	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51585	11	334825	5	NULL	NULL	0	NULL	FXR	NULL		activates	NULL				dehydroepiandrosterone sulfotransferase	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51586	12	334825	5	NULL	NULL	0	NULL	FXR	NULL		activates	NULL				apolipoprotein C-II	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51951	1	334825	6	NULL	NULL	0	NULL	FXR	NULL		inhibits	NULL				Cyp 7a1	NULL	expression of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51952	2	334825	6	NULL	NULL	0	NULL	Cyp 7a	NULL		is	NULL				cholesterol 7alpha-hydroxylase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51953	3	334825	6	NULL	NULL	0	NULL	FXR	NULL		inhibits	NULL				sterol 12alpha-hydroxylase	NULL	expression of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51954	4	334825	6	NULL	NULL	0	NULL	FXR	NULL		inhibits	NULL				Na+/taurocholate co-transporting polypeptide	NULL	expression of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51955	5	334825	6	NULL	NULL	0	NULL	FXR	NULL		inhibits	NULL				apolipoprotein A-I	NULL	expression of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51956	6	334825	6	NULL	NULL	0	NULL	I-BABP	NULL		is	NULL				intestinal bile acid-binding protein	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51957	7	334825	6	NULL	NULL	0	NULL	FXR	NULL		activates	NULL				I-BABP	NULL	expression of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51958	8	334825	6	NULL	NULL	0	NULL	FXR	NULL		activates	NULL				phospholipid transfer protein	NULL	expression of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51959	9	334825	6	NULL	NULL	0	NULL	BSEP	NULL		is	NULL				bile salt export pump	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51960	10	334825	6	NULL	NULL	0	NULL	FXR	NULL		activates	NULL				BSEP	NULL	expression of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51961	11	334825	6	NULL	NULL	0	NULL	FXR	NULL		activates	NULL				dehydroepiandrosterone sulfotransferase	NULL	expression of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51962	12	334825	6	NULL	NULL	0	NULL	FXR	NULL		activates	NULL				apolipoprotein C-II	NULL	expression of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10214_s_20	12525500	It has been shown that FXR inhibits expression of cholesterol 7alpha-hydroxylase ( Cyp 7a1) ( ), sterol 12alpha-hydroxylase ( ), the Na+/taurocholate co-transporting polypeptide ( ) and apolipoprotein A-I ( ), and activates expression of intestinal bile acid-binding protein ( I-BABP) ( ), phospholipid transfer protein ( ), bile salt export pump ( BSEP) ( ,  ), dehydroepiandrosterone sulfotransferase ( ), and apolipoprotein C-II ( ).	transcription
51587	1	334826	5	NULL	NULL	0	NULL	SF1	NULL		is a type of	NULL				steroidogenic factor	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
51588	2	334826	5	NULL	NULL	0	NULL	SF1	NULL		regulates	NULL				cytochrome P450s	NULL	transcription of			NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
51590	3	334826	5	NULL	NULL	0	NULL	cholesterol	NULL		is converted to	NULL				pregnenolone	NULL				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
51591	4	334826	5	NULL	NULL	0	NULL	P450ssc/Cyp11A1	NULL		catalyzes	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
51592	5	334826	5	NULL	NULL	0	NULL	StAR	NULL		is a type of	NULL				steroidogenic acute regulatory protein	NULL				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
51593	6	334826	5	NULL	NULL	0	NULL	cholesterol	NULL		is accessible to	NULL				P450ssc	NULL				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
51594	7	334826	5	NULL	NULL	0	NULL	StAR	NULL		regulates	NULL				statement 6	NULL				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
51596	8	334826	5	NULL	NULL	0	NULL	P450c17/Cyp17	NULL		is a type of	NULL				theca cell marker	NULL				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
51597	9	334826	5	NULL	NULL	0	NULL	P450c17/Cyp17	NULL		catalyzes	NULL				DHEA	NULL	formation of			NULL		NULL	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
51598	10	334826	5	NULL	NULL	0	NULL	DHEA	NULL		is	NULL				dehydroepiandrosterone	NULL				NULL		NULL	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
51599	11	334826	5	NULL	NULL	0	NULL	P450c17/Cyp17	NULL		is upregulated by	NULL				Gdf9	NULL				NULL	preantral follicles	NULL	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
52906	1	334826	6	NULL	NULL	0	NULL	SF1	NULL		is expressed in	NULL				luteal cells	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
52907	2	334826	6	NULL	NULL	0	NULL	SF1	NULL		is expressed in	NULL				stroma	NULL	adult			NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
52908	3	334826	6	NULL	NULL	0	NULL	SF1	NULL		is	NULL				steroidogenic factor 1	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
52909	4	334826	6	NULL	NULL	0	NULL	SF1	NULL		regulates	NULL				cytochrome P450	NULL	transcription of 			NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
52910	5	334826	6	NULL	NULL	0	NULL	SF1	NULL		is	NULL				H3053B11	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
52911	6	334826	6	NULL	NULL	0	NULL	cholesterol	NULL		is converted to	NULL				pregnenolone	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
52912	7	334826	6	NULL	NULL	0	NULL	P450ssc	NULL		catalyzes	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
52913	8	334826	6	NULL	NULL	0	NULL	P450ssc	NULL		is	NULL				Cyp11A1 	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
52914	9	334826	6	NULL	NULL	0	NULL	P450ssc	NULL		is	NULL				H3094D01	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
52915	10	334826	6	NULL	NULL	0	NULL	StAR	NULL		is	NULL				steroidogenic acute regulatory protein	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
52916	11	334826	6	NULL	NULL	0	NULL	StAR	NULL		is	NULL				H3097G04	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
52917	12	334826	6	NULL	NULL	0	NULL	cholesterol	NULL		is accessible to	NULL				P450ssc	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
52918	13	334826	6	NULL	NULL	0	NULL	StAR	NULL		catalyzes	NULL				statement 12	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
52919	14	334826	6	NULL	NULL	0	NULL	P450c17	NULL		is	NULL				Cyp17	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
52921	15	334826	6	NULL	NULL	0	NULL	DHEA	NULL		is	NULL				dehydroepiandrosterone 	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
52922	16	334826	6	NULL	NULL	0	NULL	P450c17	NULL		is a type of	NULL				theca cell marker	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
52923	17	334826	6	NULL	NULL	0	NULL	P450c17	NULL		catalyzes	NULL				DHEA	NULL	formation of			NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
52924	18	334826	6	NULL	NULL	0	NULL	P450c17	NULL		is	NULL				H3018A11	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
52925	19	334826	6	NULL	NULL	0	NULL	Gdf9	NULL		upregulates	NULL				p450c17	NULL				NULL	preantral follicles	0	NULL	NULL	NULL	gw70_devbiol_279_2_271_s_287	15733658	In addition, the adult ovary gene set included all relevant steroidogenic regulators  and enzymes that are expressed in luteal cells and adult stroma (including steroidogenic  factor  SF1 (H3053B11, confirmatory data in  Fig. 4), which regulates transcription of all cytochrome  P450s; P450ssc/Cyp11A1 (H3094D01), catalyzing the conversion of cholesterol to pregnenolone;  steroidogenic acute regulatory protein StAR (H3097G04), which regulates accessibility  of cholesterol to P450ssc; P450c17/Cyp17 (H3018A11), a theca cell marker that catalyzes  the formation of dehydroepiandrosterone (DHEA) and is upregulated by Gdf9 in preantral  follicles (  Vitt et al., 2000); and two clones (H3059B01, H3070C08) for placental 3- -hydroxysteroid dehydrogenase  Hsd3b1 (see OMIM109715)).	transcription
51600	1	334827	5	NULL	NULL	0	NULL	L-glutamine	NULL	hydrolysis of	produce	NULL				ammonia	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24579_s_145	11967268	Interdomain Channeling and Synchronization--  During catalysis of Fd-GltS, ammonia produced by L-glutamine hydrolysis is channeled to the 2-oxoglutarate-binding site, in which 2-iminoglutarate is formed.	transcription
51601	2	334827	5	NULL	NULL	0	NULL	statement 1	NULL		occurs during	NULL				Fd-GltS	NULL	catalysis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24579_s_145	11967268	Interdomain Channeling and Synchronization--  During catalysis of Fd-GltS, ammonia produced by L-glutamine hydrolysis is channeled to the 2-oxoglutarate-binding site, in which 2-iminoglutarate is formed.	transcription
51602	3	334827	5	NULL	NULL	0	NULL	ammonia	NULL		is channeled to	NULL					NULL		2-oxoglutarate-binding site		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24579_s_145	11967268	Interdomain Channeling and Synchronization--  During catalysis of Fd-GltS, ammonia produced by L-glutamine hydrolysis is channeled to the 2-oxoglutarate-binding site, in which 2-iminoglutarate is formed.	transcription
51603	4	334827	5	NULL	NULL	0	NULL	2-iminoglutarate	NULL		is formed in	NULL					NULL		2-oxoglutarate-binding site		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24579_s_145	11967268	Interdomain Channeling and Synchronization--  During catalysis of Fd-GltS, ammonia produced by L-glutamine hydrolysis is channeled to the 2-oxoglutarate-binding site, in which 2-iminoglutarate is formed.	transcription
51963	1	334827	6	NULL	NULL	0	NULL	L-glutamine	NULL	hydrolysis of	produces	NULL				ammonia	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24579_s_145	11967268	Interdomain Channeling and Synchronization--  During catalysis of Fd-GltS, ammonia produced by L-glutamine hydrolysis is channeled to the 2-oxoglutarate-binding site, in which 2-iminoglutarate is formed.	transcription
51964	2	334827	6	NULL	NULL	0	NULL	statement 1	NULL		occurs during	NULL				Fd-GltS	NULL	catalysis of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24579_s_145	11967268	Interdomain Channeling and Synchronization--  During catalysis of Fd-GltS, ammonia produced by L-glutamine hydrolysis is channeled to the 2-oxoglutarate-binding site, in which 2-iminoglutarate is formed.	transcription
51965	3	334827	6	NULL	NULL	0	NULL	ammonia	NULL		is channeled to	NULL					NULL		2-oxoglutarate-binding site		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24579_s_145	11967268	Interdomain Channeling and Synchronization--  During catalysis of Fd-GltS, ammonia produced by L-glutamine hydrolysis is channeled to the 2-oxoglutarate-binding site, in which 2-iminoglutarate is formed.	transcription
51966	4	334827	6	NULL	NULL	0	NULL	2-iminoglutarate	NULL		is formed in	NULL					NULL		2-oxoglutarate-binding site		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24579_s_145	11967268	Interdomain Channeling and Synchronization--  During catalysis of Fd-GltS, ammonia produced by L-glutamine hydrolysis is channeled to the 2-oxoglutarate-binding site, in which 2-iminoglutarate is formed.	transcription
52026	1	334828	5	NULL	NULL	0	NULL	ammonia	NULL		is added to	NULL				2-oxoglutarate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24579_s_76	11967268	In the FMN-binding domain the 2-iminoglutarate intermediate, formed upon the addition of ammonia onto 2-oxoglutarate, is reduced by the FMN cofactor producing the second molecule of L-glutamate (Scheme 1).	transcription
52027	2	334828	5	NULL	NULL	0	NULL	statement 1	NULL		forms	NULL				2-iminoglutarate intermediate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24579_s_76	11967268	In the FMN-binding domain the 2-iminoglutarate intermediate, formed upon the addition of ammonia onto 2-oxoglutarate, is reduced by the FMN cofactor producing the second molecule of L-glutamate (Scheme 1).	transcription
52028	3	334828	5	NULL	NULL	0	NULL	2-iminoglutarate intermediate	NULL		is reduced by	NULL				FMN cofactor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24579_s_76	11967268	In the FMN-binding domain the 2-iminoglutarate intermediate, formed upon the addition of ammonia onto 2-oxoglutarate, is reduced by the FMN cofactor producing the second molecule of L-glutamate (Scheme 1).	transcription
52029	4	334828	5	NULL	NULL	0	NULL	statement 3	NULL		produce	NULL				L-glutamate	NULL	second molecule of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24579_s_76	11967268	In the FMN-binding domain the 2-iminoglutarate intermediate, formed upon the addition of ammonia onto 2-oxoglutarate, is reduced by the FMN cofactor producing the second molecule of L-glutamate (Scheme 1).	transcription
51997	1	334828	6	NULL	NULL	0	NULL	ammonia	NULL		is added onto	NULL				2-oxoglutarate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24579_s_76	11967268	In the FMN-binding domain the 2-iminoglutarate intermediate, formed upon the addition of ammonia onto 2-oxoglutarate, is reduced by the FMN cofactor producing the second molecule of L-glutamate (Scheme 1).	transcription
51998	2	334828	6	NULL	NULL	0	NULL	statement 1	NULL		forms	NULL				2-iminoglutarate intermediate	NULL		FMN-binding domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24579_s_76	11967268	In the FMN-binding domain the 2-iminoglutarate intermediate, formed upon the addition of ammonia onto 2-oxoglutarate, is reduced by the FMN cofactor producing the second molecule of L-glutamate (Scheme 1).	transcription
51999	3	334828	6	NULL	NULL	0	NULL	FMN cofactor	NULL		produces	NULL				L-glutamate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24579_s_76	11967268	In the FMN-binding domain the 2-iminoglutarate intermediate, formed upon the addition of ammonia onto 2-oxoglutarate, is reduced by the FMN cofactor producing the second molecule of L-glutamate (Scheme 1).	transcription
52000	4	334828	6	NULL	NULL	0	NULL	statement 2	NULL		is reduced by	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24579_s_76	11967268	In the FMN-binding domain the 2-iminoglutarate intermediate, formed upon the addition of ammonia onto 2-oxoglutarate, is reduced by the FMN cofactor producing the second molecule of L-glutamate (Scheme 1).	transcription
51604	1	334830	5	NULL	NULL	0	NULL	oxoglutarate/fumarate exchange reaction	NULL		is catalyzed by	NULL				ACR1	NULL	reconstituted			NULL		0	NULL	NULL	NULL	gw60_febslett_417_1_114_s_86	9395087	The [14]oxoglutarate/fumarate exchange reaction catalysed by reconstituted ACR1 was inhibited by sulphydryl reagents (mersalyl,  p-chloromercuribenzene sulphonate and mercuric chloride), by pyridoxal 5-phosphate and by bathophenanthroline (see  Table 2).	transcription
51605	2	334830	5	NULL	NULL	0	NULL	mersalyl	NULL		is a type of	NULL				sulphydryl reagents	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_417_1_114_s_86	9395087	The [14]oxoglutarate/fumarate exchange reaction catalysed by reconstituted ACR1 was inhibited by sulphydryl reagents (mersalyl,  p-chloromercuribenzene sulphonate and mercuric chloride), by pyridoxal 5-phosphate and by bathophenanthroline (see  Table 2).	transcription
51606	3	334830	5	NULL	NULL	0	NULL	mersalyl	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_417_1_114_s_86	9395087	The [14]oxoglutarate/fumarate exchange reaction catalysed by reconstituted ACR1 was inhibited by sulphydryl reagents (mersalyl,  p-chloromercuribenzene sulphonate and mercuric chloride), by pyridoxal 5-phosphate and by bathophenanthroline (see  Table 2).	transcription
51607	4	334830	5	NULL	NULL	0	NULL	p-chloromercuribenzene sulphonate	NULL		is a type of	NULL				sulphydryl reagents	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_417_1_114_s_86	9395087	The [14]oxoglutarate/fumarate exchange reaction catalysed by reconstituted ACR1 was inhibited by sulphydryl reagents (mersalyl,  p-chloromercuribenzene sulphonate and mercuric chloride), by pyridoxal 5-phosphate and by bathophenanthroline (see  Table 2).	transcription
51608	5	334830	5	NULL	NULL	0	NULL	p-chloromercuribenzene sulphonate	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_417_1_114_s_86	9395087	The [14]oxoglutarate/fumarate exchange reaction catalysed by reconstituted ACR1 was inhibited by sulphydryl reagents (mersalyl,  p-chloromercuribenzene sulphonate and mercuric chloride), by pyridoxal 5-phosphate and by bathophenanthroline (see  Table 2).	transcription
51609	6	334830	5	NULL	NULL	0	NULL	mercuric chloride	NULL		is a type of	NULL				sulphydryl reagents	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_417_1_114_s_86	9395087	The [14]oxoglutarate/fumarate exchange reaction catalysed by reconstituted ACR1 was inhibited by sulphydryl reagents (mersalyl,  p-chloromercuribenzene sulphonate and mercuric chloride), by pyridoxal 5-phosphate and by bathophenanthroline (see  Table 2).	transcription
51610	7	334830	5	NULL	NULL	0	NULL	mercuric chloride	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_417_1_114_s_86	9395087	The [14]oxoglutarate/fumarate exchange reaction catalysed by reconstituted ACR1 was inhibited by sulphydryl reagents (mersalyl,  p-chloromercuribenzene sulphonate and mercuric chloride), by pyridoxal 5-phosphate and by bathophenanthroline (see  Table 2).	transcription
51611	8	334830	5	NULL	NULL	0	NULL	pyridoxal 5-phosphate	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_417_1_114_s_86	9395087	The [14]oxoglutarate/fumarate exchange reaction catalysed by reconstituted ACR1 was inhibited by sulphydryl reagents (mersalyl,  p-chloromercuribenzene sulphonate and mercuric chloride), by pyridoxal 5-phosphate and by bathophenanthroline (see  Table 2).	transcription
51612	9	334830	5	NULL	NULL	0	NULL	bathophenanthroline	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_417_1_114_s_86	9395087	The [14]oxoglutarate/fumarate exchange reaction catalysed by reconstituted ACR1 was inhibited by sulphydryl reagents (mersalyl,  p-chloromercuribenzene sulphonate and mercuric chloride), by pyridoxal 5-phosphate and by bathophenanthroline (see  Table 2).	transcription
52001	1	334830	6	NULL	NULL	0	NULL	ACR1	NULL	reconstituted	catalyzes	NULL				oxoglutarate/fumarate exchange reaction	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_417_1_114_s_86	9395087	The [14]oxoglutarate/fumarate exchange reaction catalysed by reconstituted ACR1 was inhibited by sulphydryl reagents (mersalyl,  p-chloromercuribenzene sulphonate and mercuric chloride), by pyridoxal 5-phosphate and by bathophenanthroline (see  Table 2).	transcription
52002	2	334830	6	NULL	NULL	0	NULL	mersalyl	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_417_1_114_s_86	9395087	The [14]oxoglutarate/fumarate exchange reaction catalysed by reconstituted ACR1 was inhibited by sulphydryl reagents (mersalyl,  p-chloromercuribenzene sulphonate and mercuric chloride), by pyridoxal 5-phosphate and by bathophenanthroline (see  Table 2).	transcription
52003	3	334830	6	NULL	NULL	0	NULL	p-chloromercuribenzene sulphonate	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_417_1_114_s_86	9395087	The [14]oxoglutarate/fumarate exchange reaction catalysed by reconstituted ACR1 was inhibited by sulphydryl reagents (mersalyl,  p-chloromercuribenzene sulphonate and mercuric chloride), by pyridoxal 5-phosphate and by bathophenanthroline (see  Table 2).	transcription
52004	4	334830	6	NULL	NULL	0	NULL	mercuric chloride	NULL		inhibits	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_417_1_114_s_86	9395087	The [14]oxoglutarate/fumarate exchange reaction catalysed by reconstituted ACR1 was inhibited by sulphydryl reagents (mersalyl,  p-chloromercuribenzene sulphonate and mercuric chloride), by pyridoxal 5-phosphate and by bathophenanthroline (see  Table 2).	transcription
52005	5	334830	6	NULL	NULL	0	NULL	mersalyl	NULL		is a type of	NULL				sulphydryl reagents	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_417_1_114_s_86	9395087	The [14]oxoglutarate/fumarate exchange reaction catalysed by reconstituted ACR1 was inhibited by sulphydryl reagents (mersalyl,  p-chloromercuribenzene sulphonate and mercuric chloride), by pyridoxal 5-phosphate and by bathophenanthroline (see  Table 2).	transcription
52006	6	334830	6	NULL	NULL	0	NULL	p-chloromercuribenzene sulphonate	NULL		is a type of	NULL				sulphydryl reagents	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_417_1_114_s_86	9395087	The [14]oxoglutarate/fumarate exchange reaction catalysed by reconstituted ACR1 was inhibited by sulphydryl reagents (mersalyl,  p-chloromercuribenzene sulphonate and mercuric chloride), by pyridoxal 5-phosphate and by bathophenanthroline (see  Table 2).	transcription
52007	7	334830	6	NULL	NULL	0	NULL	mercuric chloride	NULL		is a type of	NULL				sulphydryl reagents	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_417_1_114_s_86	9395087	The [14]oxoglutarate/fumarate exchange reaction catalysed by reconstituted ACR1 was inhibited by sulphydryl reagents (mersalyl,  p-chloromercuribenzene sulphonate and mercuric chloride), by pyridoxal 5-phosphate and by bathophenanthroline (see  Table 2).	transcription
51613	1	334831	5	NULL	NULL	0	NULL	fructose-6-phosphate specific enzyme	NULL		is a type of	NULL				phosphoketolases	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_235_1_35_s_139	15158259	To date, two types of phosphoketolases have been described in  Bifidobacterium: a fructose-6-phosphate specific enzyme, which catalyzes the conversion of fructose-6-phosphate  to eritrose-4-phosphate and acetyl-phosphate, and a dual substrate xylulose-5-phosphate/fructose-6-phosphate  phosphoketolase, which can also act on xylulose-5-phosphate rendering acetyl-phosphate  and glyceraldehyde-3-phosphate [ 20 and   21].	transcription
51614	2	334831	5	NULL	NULL	0	NULL	fructose-6-phosphate	NULL		is converted to	NULL				eritrose-4-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_235_1_35_s_139	15158259	To date, two types of phosphoketolases have been described in  Bifidobacterium: a fructose-6-phosphate specific enzyme, which catalyzes the conversion of fructose-6-phosphate  to eritrose-4-phosphate and acetyl-phosphate, and a dual substrate xylulose-5-phosphate/fructose-6-phosphate  phosphoketolase, which can also act on xylulose-5-phosphate rendering acetyl-phosphate  and glyceraldehyde-3-phosphate [ 20 and   21].	transcription
51615	3	334831	5	NULL	NULL	0	NULL	fructose-6-phosphate	NULL		is converted to	NULL				acetyl-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_235_1_35_s_139	15158259	To date, two types of phosphoketolases have been described in  Bifidobacterium: a fructose-6-phosphate specific enzyme, which catalyzes the conversion of fructose-6-phosphate  to eritrose-4-phosphate and acetyl-phosphate, and a dual substrate xylulose-5-phosphate/fructose-6-phosphate  phosphoketolase, which can also act on xylulose-5-phosphate rendering acetyl-phosphate  and glyceraldehyde-3-phosphate [ 20 and   21].	transcription
51616	4	334831	5	NULL	NULL	0	NULL	fructose-6-phosphate specific enzyme	NULL	Bifidobacterium	catalyzes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_235_1_35_s_139	15158259	To date, two types of phosphoketolases have been described in  Bifidobacterium: a fructose-6-phosphate specific enzyme, which catalyzes the conversion of fructose-6-phosphate  to eritrose-4-phosphate and acetyl-phosphate, and a dual substrate xylulose-5-phosphate/fructose-6-phosphate  phosphoketolase, which can also act on xylulose-5-phosphate rendering acetyl-phosphate  and glyceraldehyde-3-phosphate [ 20 and   21].	transcription
51617	5	334831	5	NULL	NULL	0	NULL	fructose-6-phosphate specific enzyme	NULL	Bifidobacterium	catalyzes	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_235_1_35_s_139	15158259	To date, two types of phosphoketolases have been described in  Bifidobacterium: a fructose-6-phosphate specific enzyme, which catalyzes the conversion of fructose-6-phosphate  to eritrose-4-phosphate and acetyl-phosphate, and a dual substrate xylulose-5-phosphate/fructose-6-phosphate  phosphoketolase, which can also act on xylulose-5-phosphate rendering acetyl-phosphate  and glyceraldehyde-3-phosphate [ 20 and   21].	transcription
51618	6	334831	5	NULL	NULL	0	NULL	xylulose-5-phosphate/fructose-6-phosphate phosphoketolase	NULL		is a type of	NULL				dual substrate	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_235_1_35_s_139	15158259	To date, two types of phosphoketolases have been described in  Bifidobacterium: a fructose-6-phosphate specific enzyme, which catalyzes the conversion of fructose-6-phosphate  to eritrose-4-phosphate and acetyl-phosphate, and a dual substrate xylulose-5-phosphate/fructose-6-phosphate  phosphoketolase, which can also act on xylulose-5-phosphate rendering acetyl-phosphate  and glyceraldehyde-3-phosphate [ 20 and   21].	transcription
51619	7	334831	5	NULL	NULL	0	NULL	xylulose-5-phosphate/fructose-6-phosphate phosphoketolase	NULL	Bifidobacterium	acts on	NULL				xylulose-5-phosphate	NULL				NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiollett_235_1_35_s_139	15158259	To date, two types of phosphoketolases have been described in  Bifidobacterium: a fructose-6-phosphate specific enzyme, which catalyzes the conversion of fructose-6-phosphate  to eritrose-4-phosphate and acetyl-phosphate, and a dual substrate xylulose-5-phosphate/fructose-6-phosphate  phosphoketolase, which can also act on xylulose-5-phosphate rendering acetyl-phosphate  and glyceraldehyde-3-phosphate [ 20 and   21].	transcription
51620	8	334831	5	NULL	NULL	0	NULL	statement 7	NULL		renders	NULL				acetyl-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_235_1_35_s_139	15158259	To date, two types of phosphoketolases have been described in  Bifidobacterium: a fructose-6-phosphate specific enzyme, which catalyzes the conversion of fructose-6-phosphate  to eritrose-4-phosphate and acetyl-phosphate, and a dual substrate xylulose-5-phosphate/fructose-6-phosphate  phosphoketolase, which can also act on xylulose-5-phosphate rendering acetyl-phosphate  and glyceraldehyde-3-phosphate [ 20 and   21].	transcription
51621	9	334831	5	NULL	NULL	0	NULL	statement 7	NULL		renders	NULL				glyceraldehyde-3-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_235_1_35_s_139	15158259	To date, two types of phosphoketolases have been described in  Bifidobacterium: a fructose-6-phosphate specific enzyme, which catalyzes the conversion of fructose-6-phosphate  to eritrose-4-phosphate and acetyl-phosphate, and a dual substrate xylulose-5-phosphate/fructose-6-phosphate  phosphoketolase, which can also act on xylulose-5-phosphate rendering acetyl-phosphate  and glyceraldehyde-3-phosphate [ 20 and   21].	transcription
52926	1	334831	6	NULL	NULL	0	NULL	fructose-6-phosphate	NULL		is converted to	NULL				eritrose-4-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_235_1_35_s_139	15158259	To date, two types of phosphoketolases have been described in  Bifidobacterium: a fructose-6-phosphate specific enzyme, which catalyzes the conversion of fructose-6-phosphate  to eritrose-4-phosphate and acetyl-phosphate, and a dual substrate xylulose-5-phosphate/fructose-6-phosphate  phosphoketolase, which can also act on xylulose-5-phosphate rendering acetyl-phosphate  and glyceraldehyde-3-phosphate [ 20 and   21].	transcription
52927	2	334831	6	NULL	NULL	0	NULL	fructose-6-phosphate	NULL		is converted to	NULL				acetyl-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_235_1_35_s_139	15158259	To date, two types of phosphoketolases have been described in  Bifidobacterium: a fructose-6-phosphate specific enzyme, which catalyzes the conversion of fructose-6-phosphate  to eritrose-4-phosphate and acetyl-phosphate, and a dual substrate xylulose-5-phosphate/fructose-6-phosphate  phosphoketolase, which can also act on xylulose-5-phosphate rendering acetyl-phosphate  and glyceraldehyde-3-phosphate [ 20 and   21].	transcription
52928	3	334831	6	NULL	NULL	0	NULL	statement 1	NULL		occurs simultaneously with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_235_1_35_s_139	15158259	To date, two types of phosphoketolases have been described in  Bifidobacterium: a fructose-6-phosphate specific enzyme, which catalyzes the conversion of fructose-6-phosphate  to eritrose-4-phosphate and acetyl-phosphate, and a dual substrate xylulose-5-phosphate/fructose-6-phosphate  phosphoketolase, which can also act on xylulose-5-phosphate rendering acetyl-phosphate  and glyceraldehyde-3-phosphate [ 20 and   21].	transcription
52929	4	334831	6	NULL	NULL	0	NULL	fructose-6-phosphate	NULL		catalyzes	NULL				statement 1	NULL				NULL	Bifidobacterium	NULL	NULL	NULL	NULL	gw70_femsmicrobiollett_235_1_35_s_139	15158259	To date, two types of phosphoketolases have been described in  Bifidobacterium: a fructose-6-phosphate specific enzyme, which catalyzes the conversion of fructose-6-phosphate  to eritrose-4-phosphate and acetyl-phosphate, and a dual substrate xylulose-5-phosphate/fructose-6-phosphate  phosphoketolase, which can also act on xylulose-5-phosphate rendering acetyl-phosphate  and glyceraldehyde-3-phosphate [ 20 and   21].	transcription
52930	5	334831	6	NULL	NULL	0	NULL	fructose-6-phosphate	NULL		catalyzes	NULL				statement 2	NULL				NULL	Bifidobacterium	0	NULL	NULL	NULL	gw70_femsmicrobiollett_235_1_35_s_139	15158259	To date, two types of phosphoketolases have been described in  Bifidobacterium: a fructose-6-phosphate specific enzyme, which catalyzes the conversion of fructose-6-phosphate  to eritrose-4-phosphate and acetyl-phosphate, and a dual substrate xylulose-5-phosphate/fructose-6-phosphate  phosphoketolase, which can also act on xylulose-5-phosphate rendering acetyl-phosphate  and glyceraldehyde-3-phosphate [ 20 and   21].	transcription
52931	6	334831	6	NULL	NULL	0	NULL	xylulose-5-phosphate	NULL		is converted to	NULL				acetyl-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_235_1_35_s_139	15158259	To date, two types of phosphoketolases have been described in  Bifidobacterium: a fructose-6-phosphate specific enzyme, which catalyzes the conversion of fructose-6-phosphate  to eritrose-4-phosphate and acetyl-phosphate, and a dual substrate xylulose-5-phosphate/fructose-6-phosphate  phosphoketolase, which can also act on xylulose-5-phosphate rendering acetyl-phosphate  and glyceraldehyde-3-phosphate [ 20 and   21].	transcription
52932	7	334831	6	NULL	NULL	0	NULL	xylulose-5-phosphate	NULL		is converted to	NULL				glyceraldehyde-3-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_235_1_35_s_139	15158259	To date, two types of phosphoketolases have been described in  Bifidobacterium: a fructose-6-phosphate specific enzyme, which catalyzes the conversion of fructose-6-phosphate  to eritrose-4-phosphate and acetyl-phosphate, and a dual substrate xylulose-5-phosphate/fructose-6-phosphate  phosphoketolase, which can also act on xylulose-5-phosphate rendering acetyl-phosphate  and glyceraldehyde-3-phosphate [ 20 and   21].	transcription
52933	8	334831	6	NULL	NULL	0	NULL	statement 6	NULL		occurs simultaneously with	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_235_1_35_s_139	15158259	To date, two types of phosphoketolases have been described in  Bifidobacterium: a fructose-6-phosphate specific enzyme, which catalyzes the conversion of fructose-6-phosphate  to eritrose-4-phosphate and acetyl-phosphate, and a dual substrate xylulose-5-phosphate/fructose-6-phosphate  phosphoketolase, which can also act on xylulose-5-phosphate rendering acetyl-phosphate  and glyceraldehyde-3-phosphate [ 20 and   21].	transcription
52934	9	334831	6	NULL	NULL	0	NULL	xylulose-5-phosphate/fructose-6-phosphate phosphoketolase	NULL		catalyzes	NULL				statement 6	NULL				NULL	Bifidobacterium	NULL	NULL	NULL	NULL	gw70_femsmicrobiollett_235_1_35_s_139	15158259	To date, two types of phosphoketolases have been described in  Bifidobacterium: a fructose-6-phosphate specific enzyme, which catalyzes the conversion of fructose-6-phosphate  to eritrose-4-phosphate and acetyl-phosphate, and a dual substrate xylulose-5-phosphate/fructose-6-phosphate  phosphoketolase, which can also act on xylulose-5-phosphate rendering acetyl-phosphate  and glyceraldehyde-3-phosphate [ 20 and   21].	transcription
52935	10	334831	6	NULL	NULL	0	NULL	xylulose-5-phosphate/fructose-6-phosphate phosphoketolase	NULL		catalyzes	NULL				statement 7	NULL				NULL	Bifidobacterium	NULL	NULL	NULL	NULL	gw70_femsmicrobiollett_235_1_35_s_139	15158259	To date, two types of phosphoketolases have been described in  Bifidobacterium: a fructose-6-phosphate specific enzyme, which catalyzes the conversion of fructose-6-phosphate  to eritrose-4-phosphate and acetyl-phosphate, and a dual substrate xylulose-5-phosphate/fructose-6-phosphate  phosphoketolase, which can also act on xylulose-5-phosphate rendering acetyl-phosphate  and glyceraldehyde-3-phosphate [ 20 and   21].	transcription
51622	1	334832	5	NULL	NULL	0	NULL	fructose-1-phosphate	NULL	presence of	activates	NULL				glyceraldehyde-3-phosphate dehydrogenase	NULL	T. tenax			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_8_2836_s_185	16585745	T. tenax glyceraldehyde-3-phosphate dehydrogenase was found to be activated by the presence of fructose-1-phosphate and fructose-6-phosphate ( ); however, activation of  M. jannaschii lactaldehyde dehydrogenase by these sugar-phosphates was not observed.	transcription
51623	2	334832	5	NULL	NULL	0	NULL	fructose-6-phosphate	NULL	presence of	activates	NULL				glyceraldehyde-3-phosphate dehydrogenase	NULL	T. tenax			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_8_2836_s_185	16585745	T. tenax glyceraldehyde-3-phosphate dehydrogenase was found to be activated by the presence of fructose-1-phosphate and fructose-6-phosphate ( ); however, activation of  M. jannaschii lactaldehyde dehydrogenase by these sugar-phosphates was not observed.	transcription
51624	3	334832	5	NULL	NULL	0	NULL	fructose-1-phosphate	NULL	presence of	does not activate	NULL				lactaldehyde dehydrogenase	NULL	M. jannaschii 			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_8_2836_s_185	16585745	T. tenax glyceraldehyde-3-phosphate dehydrogenase was found to be activated by the presence of fructose-1-phosphate and fructose-6-phosphate ( ); however, activation of  M. jannaschii lactaldehyde dehydrogenase by these sugar-phosphates was not observed.	transcription
51625	4	334832	5	NULL	NULL	0	NULL	fructose-6-phosphate	NULL	presence of	does not activate	NULL				lactaldehyde dehydrogenase	NULL	M. jannaschii			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_8_2836_s_185	16585745	T. tenax glyceraldehyde-3-phosphate dehydrogenase was found to be activated by the presence of fructose-1-phosphate and fructose-6-phosphate ( ); however, activation of  M. jannaschii lactaldehyde dehydrogenase by these sugar-phosphates was not observed.	transcription
52008	1	334832	6	NULL	NULL	0	NULL	glyceraldehyde-3-phosphate dehydrogenase	NULL	T. tenax	is activated by	NULL				fructose-1-phosphate	NULL	presence of 			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_8_2836_s_185	16585745	T. tenax glyceraldehyde-3-phosphate dehydrogenase was found to be activated by the presence of fructose-1-phosphate and fructose-6-phosphate ( ); however, activation of  M. jannaschii lactaldehyde dehydrogenase by these sugar-phosphates was not observed.	transcription
52009	2	334832	6	NULL	NULL	0	NULL	glyceraldehyde-3-phosphate dehydrogenase	NULL	T. tenax	is activated by	NULL				fructose-6-phosphate	NULL	presence of 			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_8_2836_s_185	16585745	T. tenax glyceraldehyde-3-phosphate dehydrogenase was found to be activated by the presence of fructose-1-phosphate and fructose-6-phosphate ( ); however, activation of  M. jannaschii lactaldehyde dehydrogenase by these sugar-phosphates was not observed.	transcription
52010	3	334832	6	NULL	NULL	0	NULL	lactaldehyde dehydrogenase	NULL	M. jannaschii	is not activated by	NULL				fructose-1-phosphate	NULL	presence of 			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_8_2836_s_185	16585745	T. tenax glyceraldehyde-3-phosphate dehydrogenase was found to be activated by the presence of fructose-1-phosphate and fructose-6-phosphate ( ); however, activation of  M. jannaschii lactaldehyde dehydrogenase by these sugar-phosphates was not observed.	transcription
52011	4	334832	6	NULL	NULL	0	NULL	lactaldehyde dehydrogenase	NULL	M. jannaschii	is not activated by	NULL				fructose-6-phosphate	NULL	presence of 			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_188_8_2836_s_185	16585745	T. tenax glyceraldehyde-3-phosphate dehydrogenase was found to be activated by the presence of fructose-1-phosphate and fructose-6-phosphate ( ); however, activation of  M. jannaschii lactaldehyde dehydrogenase by these sugar-phosphates was not observed.	transcription
51626	1	334833	5	NULL	NULL	0	NULL	hyperglycemia	NULL		induce	NULL				superoxide	NULL	overproduction of;;mitochondrial			NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12222_s_21	11050244	In the present study, we show that hyperglycemia-induced mitochondrial superoxide overproduction inhibits glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity and activates the hexosamine pathway, presumably by diverting the upstream metabolite fructose-6-phosphate from glycolysis to glucosamine formation.	transcription
51627	2	334833	5	NULL	NULL	0	NULL	statement 1	NULL		inhibit	NULL				GAPDH	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12222_s_21	11050244	In the present study, we show that hyperglycemia-induced mitochondrial superoxide overproduction inhibits glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity and activates the hexosamine pathway, presumably by diverting the upstream metabolite fructose-6-phosphate from glycolysis to glucosamine formation.	transcription
51628	3	334833	5	NULL	NULL	0	NULL	GAPDH	NULL		is	NULL				glyceraldehyde-3-phosphate dehydrogenase	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12222_s_21	11050244	In the present study, we show that hyperglycemia-induced mitochondrial superoxide overproduction inhibits glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity and activates the hexosamine pathway, presumably by diverting the upstream metabolite fructose-6-phosphate from glycolysis to glucosamine formation.	transcription
51629	4	334833	5	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				hexosamine pathway	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12222_s_21	11050244	In the present study, we show that hyperglycemia-induced mitochondrial superoxide overproduction inhibits glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity and activates the hexosamine pathway, presumably by diverting the upstream metabolite fructose-6-phosphate from glycolysis to glucosamine formation.	transcription
51630	5	334833	5	NULL	NULL	0	NULL	fructose-6-phosphate	NULL		is a type of	NULL				upstream metabolite	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12222_s_21	11050244	In the present study, we show that hyperglycemia-induced mitochondrial superoxide overproduction inhibits glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity and activates the hexosamine pathway, presumably by diverting the upstream metabolite fructose-6-phosphate from glycolysis to glucosamine formation.	transcription
51631	6	334833	5	NULL	NULL	0	NULL	fructose-6-phosphate	NULL		is diverted from	NULL				glycolysis	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12222_s_21	11050244	In the present study, we show that hyperglycemia-induced mitochondrial superoxide overproduction inhibits glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity and activates the hexosamine pathway, presumably by diverting the upstream metabolite fructose-6-phosphate from glycolysis to glucosamine formation.	transcription
51632	7	334833	5	NULL	NULL	0	NULL	fructose-6-phosphate	NULL		is diverted to	NULL				glucosamine	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12222_s_21	11050244	In the present study, we show that hyperglycemia-induced mitochondrial superoxide overproduction inhibits glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity and activates the hexosamine pathway, presumably by diverting the upstream metabolite fructose-6-phosphate from glycolysis to glucosamine formation.	transcription
51633	8	334833	5	NULL	NULL	0	NULL	statement 4	NULL		occurs by	NULL	presumably			statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12222_s_21	11050244	In the present study, we show that hyperglycemia-induced mitochondrial superoxide overproduction inhibits glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity and activates the hexosamine pathway, presumably by diverting the upstream metabolite fructose-6-phosphate from glycolysis to glucosamine formation.	transcription
52012	1	334833	6	NULL	NULL	0	NULL	hyperglycemia	NULL		induces	NULL				mitochondrial superoxide	NULL	overproduction of 			NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12222_s_21	11050244	In the present study, we show that hyperglycemia-induced mitochondrial superoxide overproduction inhibits glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity and activates the hexosamine pathway, presumably by diverting the upstream metabolite fructose-6-phosphate from glycolysis to glucosamine formation.	transcription
52013	2	334833	6	NULL	NULL	0	NULL	statement 1	NULL		inhibits	NULL				GAPDH	NULL	activity of 			NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12222_s_21	11050244	In the present study, we show that hyperglycemia-induced mitochondrial superoxide overproduction inhibits glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity and activates the hexosamine pathway, presumably by diverting the upstream metabolite fructose-6-phosphate from glycolysis to glucosamine formation.	transcription
52014	3	334833	6	NULL	NULL	0	NULL	GAPDH	NULL		is	NULL				glyceraldehyde-3-phosphate dehydrogenase 	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12222_s_21	11050244	In the present study, we show that hyperglycemia-induced mitochondrial superoxide overproduction inhibits glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity and activates the hexosamine pathway, presumably by diverting the upstream metabolite fructose-6-phosphate from glycolysis to glucosamine formation.	transcription
52015	4	334833	6	NULL	NULL	0	NULL	statement 1	NULL		activates	NULL				hexosamine pathway	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12222_s_21	11050244	In the present study, we show that hyperglycemia-induced mitochondrial superoxide overproduction inhibits glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity and activates the hexosamine pathway, presumably by diverting the upstream metabolite fructose-6-phosphate from glycolysis to glucosamine formation.	transcription
52016	5	334833	6	NULL	NULL	0	NULL	fructose-6-phosphate	NULL		is diverted to	NULL				glucosamine	NULL	formation of 			NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12222_s_21	11050244	In the present study, we show that hyperglycemia-induced mitochondrial superoxide overproduction inhibits glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity and activates the hexosamine pathway, presumably by diverting the upstream metabolite fructose-6-phosphate from glycolysis to glucosamine formation.	transcription
52017	6	334833	6	NULL	NULL	0	NULL	statement 4	NULL		occurs by	NULL	presumably			statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_22_12222_s_21	11050244	In the present study, we show that hyperglycemia-induced mitochondrial superoxide overproduction inhibits glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity and activates the hexosamine pathway, presumably by diverting the upstream metabolite fructose-6-phosphate from glycolysis to glucosamine formation.	transcription
51634	1	334834	5	NULL	NULL	0	NULL	N, N-dimethylglycine	NULL		does not inhibit	NULL				betaine	NULL	transport of			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_17_5020_s_77	10940053	N, N-dimethylglycine did not inhibit [14]betaine transport (Table  1).	transcription
52018	1	334834	6	NULL	NULL	0	NULL	N, N-dimethylglycine	NULL		does not inhibit	NULL				betaine	NULL	transport of 			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_17_5020_s_77	10940053	N, N-dimethylglycine did not inhibit [14]betaine transport (Table  1).	transcription
52030	1	334835	5	NULL	NULL	0	NULL	glycine	NULL		is methylated to	NULL				sarcosine	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_4932_s_26	12466265	One of gene products catalyzed the methylation reactions of glycine and sarcosine to sarcosine and dimethylglycine, respectively (EcGSMT),1 whereas the other one catalyzed the methylations of sarcosine and dimethylglycine to dimethylglycine and betaine, respectively (EcSDMT) ( ,  ).	transcription
52031	2	334835	5	NULL	NULL	0	NULL	EcGSMT	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_4932_s_26	12466265	One of gene products catalyzed the methylation reactions of glycine and sarcosine to sarcosine and dimethylglycine, respectively (EcGSMT),1 whereas the other one catalyzed the methylations of sarcosine and dimethylglycine to dimethylglycine and betaine, respectively (EcSDMT) ( ,  ).	transcription
52032	3	334835	5	NULL	NULL	0	NULL	sarcosine	NULL		is methylated to	NULL				dimethylglycine	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_4932_s_26	12466265	One of gene products catalyzed the methylation reactions of glycine and sarcosine to sarcosine and dimethylglycine, respectively (EcGSMT),1 whereas the other one catalyzed the methylations of sarcosine and dimethylglycine to dimethylglycine and betaine, respectively (EcSDMT) ( ,  ).	transcription
52033	4	334835	5	NULL	NULL	0	NULL	EcGSMT	NULL		catalyzes	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_4932_s_26	12466265	One of gene products catalyzed the methylation reactions of glycine and sarcosine to sarcosine and dimethylglycine, respectively (EcGSMT),1 whereas the other one catalyzed the methylations of sarcosine and dimethylglycine to dimethylglycine and betaine, respectively (EcSDMT) ( ,  ).	transcription
52034	5	334835	5	NULL	NULL	0	NULL	EcSDMT	NULL		catalyzes	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_4932_s_26	12466265	One of gene products catalyzed the methylation reactions of glycine and sarcosine to sarcosine and dimethylglycine, respectively (EcGSMT),1 whereas the other one catalyzed the methylations of sarcosine and dimethylglycine to dimethylglycine and betaine, respectively (EcSDMT) ( ,  ).	transcription
52035	6	334835	5	NULL	NULL	0	NULL	dimethylglycine	NULL		is methylated to	NULL				betaine	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_4932_s_26	12466265	One of gene products catalyzed the methylation reactions of glycine and sarcosine to sarcosine and dimethylglycine, respectively (EcGSMT),1 whereas the other one catalyzed the methylations of sarcosine and dimethylglycine to dimethylglycine and betaine, respectively (EcSDMT) ( ,  ).	transcription
52036	7	334835	5	NULL	NULL	0	NULL	EcSDMT	NULL		catalyzes	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_4932_s_26	12466265	One of gene products catalyzed the methylation reactions of glycine and sarcosine to sarcosine and dimethylglycine, respectively (EcGSMT),1 whereas the other one catalyzed the methylations of sarcosine and dimethylglycine to dimethylglycine and betaine, respectively (EcSDMT) ( ,  ).	transcription
52019	1	334835	6	NULL	NULL	0	NULL	glycine	NULL		is methylated to 	NULL				sarcosine	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_7_4932_s_26	12466265	One of gene products catalyzed the methylation reactions of glycine and sarcosine to sarcosine and dimethylglycine, respectively (EcGSMT),1 whereas the other one catalyzed the methylations of sarcosine and dimethylglycine to dimethylglycine and betaine, respectively (EcSDMT) ( ,  ).	transcription
52020	2	334835	6	NULL	NULL	0	NULL	sarcosine	NULL		is methylated to 	NULL				dimethylglycine	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_7_4932_s_26	12466265	One of gene products catalyzed the methylation reactions of glycine and sarcosine to sarcosine and dimethylglycine, respectively (EcGSMT),1 whereas the other one catalyzed the methylations of sarcosine and dimethylglycine to dimethylglycine and betaine, respectively (EcSDMT) ( ,  ).	transcription
52021	3	334835	6	NULL	NULL	0	NULL	EcGSMT	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_4932_s_26	12466265	One of gene products catalyzed the methylation reactions of glycine and sarcosine to sarcosine and dimethylglycine, respectively (EcGSMT),1 whereas the other one catalyzed the methylations of sarcosine and dimethylglycine to dimethylglycine and betaine, respectively (EcSDMT) ( ,  ).	transcription
52022	4	334835	6	NULL	NULL	0	NULL	EcGSMT	NULL		catalyzes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_4932_s_26	12466265	One of gene products catalyzed the methylation reactions of glycine and sarcosine to sarcosine and dimethylglycine, respectively (EcGSMT),1 whereas the other one catalyzed the methylations of sarcosine and dimethylglycine to dimethylglycine and betaine, respectively (EcSDMT) ( ,  ).	transcription
52023	5	334835	6	NULL	NULL	0	NULL	dimethylglycine	NULL		is methylated to 	NULL				betaine	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_4932_s_26	12466265	One of gene products catalyzed the methylation reactions of glycine and sarcosine to sarcosine and dimethylglycine, respectively (EcGSMT),1 whereas the other one catalyzed the methylations of sarcosine and dimethylglycine to dimethylglycine and betaine, respectively (EcSDMT) ( ,  ).	transcription
52024	6	334835	6	NULL	NULL	0	NULL	EcSDMT	NULL		catalyzes	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_4932_s_26	12466265	One of gene products catalyzed the methylation reactions of glycine and sarcosine to sarcosine and dimethylglycine, respectively (EcGSMT),1 whereas the other one catalyzed the methylations of sarcosine and dimethylglycine to dimethylglycine and betaine, respectively (EcSDMT) ( ,  ).	transcription
52025	7	334835	6	NULL	NULL	0	NULL	EcSDMT	NULL		catalyzes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_7_4932_s_26	12466265	One of gene products catalyzed the methylation reactions of glycine and sarcosine to sarcosine and dimethylglycine, respectively (EcGSMT),1 whereas the other one catalyzed the methylations of sarcosine and dimethylglycine to dimethylglycine and betaine, respectively (EcSDMT) ( ,  ).	transcription
51635	1	334836	5	NULL	NULL	0	NULL	AmT1	NULL		mediate	NULL				proline 	NULL	uptake of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18373_s_174	11907031	Dimethylglycine, monomethylglycine, and GABA also showed less competition than did betaine for proline uptake mediated by AmT1.	transcription
51636	2	334836	5	NULL	NULL	0	NULL	AmT1	NULL		mediate	NULL				betaine	NULL	uptake of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_21_18373_s_174	11907031	Dimethylglycine, monomethylglycine, and GABA also showed less competition than did betaine for proline uptake mediated by AmT1.	transcription
51637	3	334836	5	NULL	NULL	0	NULL	statement 2	NULL		competes with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18373_s_174	11907031	Dimethylglycine, monomethylglycine, and GABA also showed less competition than did betaine for proline uptake mediated by AmT1.	transcription
51638	4	334836	5	NULL	NULL	0	NULL	AmT1	NULL		mediate	NULL				GABA	NULL	uptake of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18373_s_174	11907031	Dimethylglycine, monomethylglycine, and GABA also showed less competition than did betaine for proline uptake mediated by AmT1.	transcription
51639	5	334836	5	NULL	NULL	0	NULL	statement 4	NULL		competes with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18373_s_174	11907031	Dimethylglycine, monomethylglycine, and GABA also showed less competition than did betaine for proline uptake mediated by AmT1.	transcription
51640	6	334836	5	NULL	NULL	0	NULL	AmT1	NULL		mediate	NULL				monomethylglycine	NULL	uptake of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18373_s_174	11907031	Dimethylglycine, monomethylglycine, and GABA also showed less competition than did betaine for proline uptake mediated by AmT1.	transcription
51641	7	334836	5	NULL	NULL	0	NULL	statement 6	NULL		competes with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18373_s_174	11907031	Dimethylglycine, monomethylglycine, and GABA also showed less competition than did betaine for proline uptake mediated by AmT1.	transcription
51642	8	334836	5	NULL	NULL	0	NULL	AmT1	NULL		mediate	NULL				Dimethylglycine	NULL	uptake of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18373_s_174	11907031	Dimethylglycine, monomethylglycine, and GABA also showed less competition than did betaine for proline uptake mediated by AmT1.	transcription
51643	9	334836	5	NULL	NULL	0	NULL	statement 8	NULL		competes with	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18373_s_174	11907031	Dimethylglycine, monomethylglycine, and GABA also showed less competition than did betaine for proline uptake mediated by AmT1.	transcription
51644	10	334836	5	NULL	NULL	0	NULL	statement 5	NULL		lesser than	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18373_s_174	11907031	Dimethylglycine, monomethylglycine, and GABA also showed less competition than did betaine for proline uptake mediated by AmT1.	transcription
51645	11	334836	5	NULL	NULL	0	NULL	statement 7	NULL		lesser than	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18373_s_174	11907031	Dimethylglycine, monomethylglycine, and GABA also showed less competition than did betaine for proline uptake mediated by AmT1.	transcription
51646	12	334836	5	NULL	NULL	0	NULL	statement 9	NULL		lesser than	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18373_s_174	11907031	Dimethylglycine, monomethylglycine, and GABA also showed less competition than did betaine for proline uptake mediated by AmT1.	transcription
52112	1	334836	6	NULL	NULL	0	NULL	AmT1	NULL		mediates	NULL				proline	NULL	uptake of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_21_18373_s_174	11907031	Dimethylglycine, monomethylglycine, and GABA also showed less competition than did betaine for proline uptake mediated by AmT1.	transcription
51647	1	334837	5	NULL	NULL	0	NULL	glycine betaine	NULL		inhibit	NULL	effectively			PB	NULL	uptake of			NULL	betS mutant	NULL	NULL	NULL	NULL	gw70_jbacteriol_188_17_6308_s_183	16923898	In contrast, several other compounds (glycine betaine, gamma-butyrobetaine, choline,  N, N-dimethylglycine,  N-methylproline, and DMSA) effectively inhibited the uptake of PB in the  betS mutant.	transcription
51648	2	334837	5	NULL	NULL	0	NULL	gamma-butyrobetaine	NULL		inhibit	NULL	effectively			PB	NULL	uptake of			NULL	betS mutant	0	NULL	NULL	NULL	gw70_jbacteriol_188_17_6308_s_183	16923898	In contrast, several other compounds (glycine betaine, gamma-butyrobetaine, choline,  N, N-dimethylglycine,  N-methylproline, and DMSA) effectively inhibited the uptake of PB in the  betS mutant.	transcription
51649	3	334837	5	NULL	NULL	0	NULL	choline	NULL		inhibit	NULL	effectively			PB	NULL	uptake of			NULL	betS mutant	0	NULL	NULL	NULL	gw70_jbacteriol_188_17_6308_s_183	16923898	In contrast, several other compounds (glycine betaine, gamma-butyrobetaine, choline,  N, N-dimethylglycine,  N-methylproline, and DMSA) effectively inhibited the uptake of PB in the  betS mutant.	transcription
51650	4	334837	5	NULL	NULL	0	NULL	N, N-dimethylglycine	NULL		inhibit	NULL	effectively			PB	NULL	uptake of			NULL	betS mutant	0	NULL	NULL	NULL	gw70_jbacteriol_188_17_6308_s_183	16923898	In contrast, several other compounds (glycine betaine, gamma-butyrobetaine, choline,  N, N-dimethylglycine,  N-methylproline, and DMSA) effectively inhibited the uptake of PB in the  betS mutant.	transcription
51651	5	334837	5	NULL	NULL	0	NULL	N-methylproline	NULL		inhibit	NULL	effectively			PB	NULL	uptake of			NULL	betS mutant	0	NULL	NULL	NULL	gw70_jbacteriol_188_17_6308_s_183	16923898	In contrast, several other compounds (glycine betaine, gamma-butyrobetaine, choline,  N, N-dimethylglycine,  N-methylproline, and DMSA) effectively inhibited the uptake of PB in the  betS mutant.	transcription
51652	6	334837	5	NULL	NULL	0	NULL	DMSA	NULL		inhibit	NULL	effectively			PB	NULL	uptake of			NULL	betS mutant	0	NULL	NULL	NULL	gw70_jbacteriol_188_17_6308_s_183	16923898	In contrast, several other compounds (glycine betaine, gamma-butyrobetaine, choline,  N, N-dimethylglycine,  N-methylproline, and DMSA) effectively inhibited the uptake of PB in the  betS mutant.	transcription
52113	1	334837	6	NULL	NULL	0	NULL	glycine betaine	NULL		inhibits	NULL				PB	NULL	uptake of 			NULL	betS mutant	NULL	NULL	NULL	NULL	gw70_jbacteriol_188_17_6308_s_183	16923898	In contrast, several other compounds (glycine betaine, gamma-butyrobetaine, choline,  N, N-dimethylglycine,  N-methylproline, and DMSA) effectively inhibited the uptake of PB in the  betS mutant.	transcription
52114	2	334837	6	NULL	NULL	0	NULL	gamma-butyrobetaine	NULL		inhibits	NULL				PB	NULL	uptake of 			NULL	betS mutant	0	NULL	NULL	NULL	gw70_jbacteriol_188_17_6308_s_183	16923898	In contrast, several other compounds (glycine betaine, gamma-butyrobetaine, choline,  N, N-dimethylglycine,  N-methylproline, and DMSA) effectively inhibited the uptake of PB in the  betS mutant.	transcription
52115	3	334837	6	NULL	NULL	0	NULL	choline	NULL		inhibits	NULL				PB	NULL	uptake of 			NULL	betS mutant	0	NULL	NULL	NULL	gw70_jbacteriol_188_17_6308_s_183	16923898	In contrast, several other compounds (glycine betaine, gamma-butyrobetaine, choline,  N, N-dimethylglycine,  N-methylproline, and DMSA) effectively inhibited the uptake of PB in the  betS mutant.	transcription
52116	4	334837	6	NULL	NULL	0	NULL	N, N-dimethylglycine	NULL		inhibits	NULL				PB	NULL	uptake of 			NULL	betS mutant	0	NULL	NULL	NULL	gw70_jbacteriol_188_17_6308_s_183	16923898	In contrast, several other compounds (glycine betaine, gamma-butyrobetaine, choline,  N, N-dimethylglycine,  N-methylproline, and DMSA) effectively inhibited the uptake of PB in the  betS mutant.	transcription
52117	5	334837	6	NULL	NULL	0	NULL	N-methylproline	NULL		inhibits	NULL				PB	NULL	uptake of 			NULL	betS mutant	NULL	NULL	NULL	NULL	gw70_jbacteriol_188_17_6308_s_183	16923898	In contrast, several other compounds (glycine betaine, gamma-butyrobetaine, choline,  N, N-dimethylglycine,  N-methylproline, and DMSA) effectively inhibited the uptake of PB in the  betS mutant.	transcription
52118	6	334837	6	NULL	NULL	0	NULL	DMSA	NULL		inhibits	NULL				PB	NULL	uptake of 			NULL	betS mutant	0	NULL	NULL	NULL	gw70_jbacteriol_188_17_6308_s_183	16923898	In contrast, several other compounds (glycine betaine, gamma-butyrobetaine, choline,  N, N-dimethylglycine,  N-methylproline, and DMSA) effectively inhibited the uptake of PB in the  betS mutant.	transcription
51653	1	334838	5	NULL	NULL	0	NULL	betaine	NULL		is synthesized from	NULL				glycine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_29_22196_s_113	10896953	Further analysis of the reaction products by HPLC (Fig.  1 A) and activity measurement on sarcosine and dimethylglycine confirm that the organisms synthesize betaine from glycine in a three-step methylation reaction.	transcription
52119	1	334838	6	NULL	NULL	0	NULL	betaine	NULL		is synthesized from	NULL				glycine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_29_22196_s_113	10896953	Further analysis of the reaction products by HPLC (Fig.  1 A) and activity measurement on sarcosine and dimethylglycine confirm that the organisms synthesize betaine from glycine in a three-step methylation reaction.	transcription
51654	1	334839	5	NULL	NULL	0	NULL	dimethylglycine	NULL		inhibit	NULL	uncompetitively			BHMT	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_37_22831_s_242	8798461	Kinetic studies using the purified porcine enzyme indicate that dimethylglycine inhibits BHMT activity uncompetitively when Hcy is varied at either subsaturating (25 muM) or saturating (250 muM) levels of betaine.	transcription
52120	1	334839	6	NULL	NULL	0	NULL	dimethylglycine	NULL		inhibits	NULL				BHMT	NULL	activity of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_37_22831_s_242	8798461	Kinetic studies using the purified porcine enzyme indicate that dimethylglycine inhibits BHMT activity uncompetitively when Hcy is varied at either subsaturating (25 muM) or saturating (250 muM) levels of betaine.	transcription
51655	1	334840	5	NULL	NULL	0	NULL	glucose	NULL		is converted to	NULL				glucosamine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29179_s_128	10924527	Several studies have clearly established that the conversion of glucose into glucosamine, which is catalyzed by glutamine:fructose-6-phosphate amidotransferase (GFAT, EC 2.6.	transcription
51656	2	334840	5	NULL	NULL	0	NULL	GFAT	NULL		is	NULL				glutamine:fructose-6-phosphate amidotransferase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29179_s_128	10924527	Several studies have clearly established that the conversion of glucose into glucosamine, which is catalyzed by glutamine:fructose-6-phosphate amidotransferase (GFAT, EC 2.6.	transcription
51657	3	334840	5	NULL	NULL	0	NULL	GFAT	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29179_s_128	10924527	Several studies have clearly established that the conversion of glucose into glucosamine, which is catalyzed by glutamine:fructose-6-phosphate amidotransferase (GFAT, EC 2.6.	transcription
52121	1	334840	6	NULL	NULL	0	NULL	glucose	NULL		is converted to	NULL				glucosamine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29179_s_128	10924527	Several studies have clearly established that the conversion of glucose into glucosamine, which is catalyzed by glutamine:fructose-6-phosphate amidotransferase (GFAT, EC 2.6.	transcription
52122	2	334840	6	NULL	NULL	0	NULL	statement 1	NULL		is catalyzed by	NULL				GFAT	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29179_s_128	10924527	Several studies have clearly established that the conversion of glucose into glucosamine, which is catalyzed by glutamine:fructose-6-phosphate amidotransferase (GFAT, EC 2.6.	transcription
52123	3	334840	6	NULL	NULL	0	NULL	GFAT	NULL		is	NULL				glutamine:fructose-6-phosphate amidotransferase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29179_s_128	10924527	Several studies have clearly established that the conversion of glucose into glucosamine, which is catalyzed by glutamine:fructose-6-phosphate amidotransferase (GFAT, EC 2.6.	transcription
51658	1	334841	5	NULL	NULL	0	NULL	GFAT	NULL		is	NULL				glutamine:fructose-6-phosphate amidotransferase	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_11_2419_s_17	11679416	Glucose entry into this pathway is regulated by its first and rate-limiting enzyme, glutamine:fructose-6-phosphate amidotransferase (GFAT), which catalyzes the conversion of fructose-6-phosphate (F-6-P) and glutamine into glucosamine-6-phosphate (GlcN-6-P) and glutamate.	transcription
51659	2	334841	5	NULL	NULL	0	NULL	GFAT	NULL		is a type of	NULL				rate-limiting enzyme	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_11_2419_s_17	11679416	Glucose entry into this pathway is regulated by its first and rate-limiting enzyme, glutamine:fructose-6-phosphate amidotransferase (GFAT), which catalyzes the conversion of fructose-6-phosphate (F-6-P) and glutamine into glucosamine-6-phosphate (GlcN-6-P) and glutamate.	transcription
51660	3	334841	5	NULL	NULL	0	NULL	F-6-P	NULL		is	NULL				fructose-6-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_11_2419_s_17	11679416	Glucose entry into this pathway is regulated by its first and rate-limiting enzyme, glutamine:fructose-6-phosphate amidotransferase (GFAT), which catalyzes the conversion of fructose-6-phosphate (F-6-P) and glutamine into glucosamine-6-phosphate (GlcN-6-P) and glutamate.	transcription
51661	4	334841	5	NULL	NULL	0	NULL	F-6-P	NULL		is converted to	NULL				GlcN-6-P	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_11_2419_s_17	11679416	Glucose entry into this pathway is regulated by its first and rate-limiting enzyme, glutamine:fructose-6-phosphate amidotransferase (GFAT), which catalyzes the conversion of fructose-6-phosphate (F-6-P) and glutamine into glucosamine-6-phosphate (GlcN-6-P) and glutamate.	transcription
51662	5	334841	5	NULL	NULL	0	NULL	GlcN-6-P	NULL		is	NULL				glucosamine-6-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_11_2419_s_17	11679416	Glucose entry into this pathway is regulated by its first and rate-limiting enzyme, glutamine:fructose-6-phosphate amidotransferase (GFAT), which catalyzes the conversion of fructose-6-phosphate (F-6-P) and glutamine into glucosamine-6-phosphate (GlcN-6-P) and glutamate.	transcription
51663	6	334841	5	NULL	NULL	0	NULL	glutamine	NULL		is converted to	NULL				glutamate	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_11_2419_s_17	11679416	Glucose entry into this pathway is regulated by its first and rate-limiting enzyme, glutamine:fructose-6-phosphate amidotransferase (GFAT), which catalyzes the conversion of fructose-6-phosphate (F-6-P) and glutamine into glucosamine-6-phosphate (GlcN-6-P) and glutamate.	transcription
51664	7	334841	5	NULL	NULL	0	NULL	GFAT	NULL		catalyzes	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_11_2419_s_17	11679416	Glucose entry into this pathway is regulated by its first and rate-limiting enzyme, glutamine:fructose-6-phosphate amidotransferase (GFAT), which catalyzes the conversion of fructose-6-phosphate (F-6-P) and glutamine into glucosamine-6-phosphate (GlcN-6-P) and glutamate.	transcription
51665	8	334841	5	NULL	NULL	0	NULL	GFAT	NULL		catalyzes	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_11_2419_s_17	11679416	Glucose entry into this pathway is regulated by its first and rate-limiting enzyme, glutamine:fructose-6-phosphate amidotransferase (GFAT), which catalyzes the conversion of fructose-6-phosphate (F-6-P) and glutamine into glucosamine-6-phosphate (GlcN-6-P) and glutamate.	transcription
52131	1	334841	6	NULL	NULL	0	NULL	fructose-6-phosphate	NULL		is converted to	NULL				glucosamine-6-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_11_2419_s_17	11679416	Glucose entry into this pathway is regulated by its first and rate-limiting enzyme, glutamine:fructose-6-phosphate amidotransferase (GFAT), which catalyzes the conversion of fructose-6-phosphate (F-6-P) and glutamine into glucosamine-6-phosphate (GlcN-6-P) and glutamate.	transcription
52132	2	334841	6	NULL	NULL	0	NULL	glucosamine-6-phosphate	NULL		is	NULL				GlcN-6-P	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_11_2419_s_17	11679416	Glucose entry into this pathway is regulated by its first and rate-limiting enzyme, glutamine:fructose-6-phosphate amidotransferase (GFAT), which catalyzes the conversion of fructose-6-phosphate (F-6-P) and glutamine into glucosamine-6-phosphate (GlcN-6-P) and glutamate.	transcription
52133	3	334841	6	NULL	NULL	0	NULL	glutamine	NULL		is converted to	NULL				glutamate	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_11_2419_s_17	11679416	Glucose entry into this pathway is regulated by its first and rate-limiting enzyme, glutamine:fructose-6-phosphate amidotransferase (GFAT), which catalyzes the conversion of fructose-6-phosphate (F-6-P) and glutamine into glucosamine-6-phosphate (GlcN-6-P) and glutamate.	transcription
52134	4	334841	6	NULL	NULL	0	NULL	F-6-P	NULL		is	NULL				fructose-6-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_11_2419_s_17	11679416	Glucose entry into this pathway is regulated by its first and rate-limiting enzyme, glutamine:fructose-6-phosphate amidotransferase (GFAT), which catalyzes the conversion of fructose-6-phosphate (F-6-P) and glutamine into glucosamine-6-phosphate (GlcN-6-P) and glutamate.	transcription
52135	5	334841	6	NULL	NULL	0	NULL	GFAT	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_11_2419_s_17	11679416	Glucose entry into this pathway is regulated by its first and rate-limiting enzyme, glutamine:fructose-6-phosphate amidotransferase (GFAT), which catalyzes the conversion of fructose-6-phosphate (F-6-P) and glutamine into glucosamine-6-phosphate (GlcN-6-P) and glutamate.	transcription
52136	6	334841	6	NULL	NULL	0	NULL	GFAT	NULL		catalyzes	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_11_2419_s_17	11679416	Glucose entry into this pathway is regulated by its first and rate-limiting enzyme, glutamine:fructose-6-phosphate amidotransferase (GFAT), which catalyzes the conversion of fructose-6-phosphate (F-6-P) and glutamine into glucosamine-6-phosphate (GlcN-6-P) and glutamate.	transcription
52137	7	334841	6	NULL	NULL	0	NULL	GFAT	NULL		is	NULL				glutamine:fructose-6-phosphate amidotransferase	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_11_2419_s_17	11679416	Glucose entry into this pathway is regulated by its first and rate-limiting enzyme, glutamine:fructose-6-phosphate amidotransferase (GFAT), which catalyzes the conversion of fructose-6-phosphate (F-6-P) and glutamine into glucosamine-6-phosphate (GlcN-6-P) and glutamate.	transcription
51666	1	334842	5	NULL	NULL	0	NULL	glutamine:fructose-6-phosphate amidotransferase	NULL		is a type of	NULL				rate-limiting enzyme in hexosamine biosynthetic pathway 	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_311_2_610_s_138	15240824	The availability of glucose and the rate-limiting enzyme glutamine:fructose-6-phosphate amidotransferase of the hexosamine biosynthetic pathway contribute to the regulation of cellular metabolism by glucose (Singh et al., 2001 ).	transcription
51667	2	334842	5	NULL	NULL	0	NULL	glucose	NULL		plays a role in	NULL				cellular metabolism	NULL				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_311_2_610_s_138	15240824	The availability of glucose and the rate-limiting enzyme glutamine:fructose-6-phosphate amidotransferase of the hexosamine biosynthetic pathway contribute to the regulation of cellular metabolism by glucose (Singh et al., 2001 ).	transcription
51668	3	334842	5	NULL	NULL	0	NULL	glutamine:fructose-6-phosphate amidotransferase	NULL		regulates	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_311_2_610_s_138	15240824	The availability of glucose and the rate-limiting enzyme glutamine:fructose-6-phosphate amidotransferase of the hexosamine biosynthetic pathway contribute to the regulation of cellular metabolism by glucose (Singh et al., 2001 ).	transcription
51669	4	334842	5	NULL	NULL	0	NULL	glucose	NULL	availability of	regulates	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_311_2_610_s_138	15240824	The availability of glucose and the rate-limiting enzyme glutamine:fructose-6-phosphate amidotransferase of the hexosamine biosynthetic pathway contribute to the regulation of cellular metabolism by glucose (Singh et al., 2001 ).	transcription
52419	1	334842	6	NULL	NULL	0	NULL	glucose	NULL		regulates	NULL				cell metabolism	NULL				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_311_2_610_s_138	15240824	The availability of glucose and the rate-limiting enzyme glutamine:fructose-6-phosphate amidotransferase of the hexosamine biosynthetic pathway contribute to the regulation of cellular metabolism by glucose (Singh et al., 2001 ).	transcription
52468	2	334842	6	NULL	NULL	0	NULL	glucose	NULL	availability of 	contributes to	NULL				statement 1	NULL	regulation of 			NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_311_2_610_s_138	15240824	The availability of glucose and the rate-limiting enzyme glutamine:fructose-6-phosphate amidotransferase of the hexosamine biosynthetic pathway contribute to the regulation of cellular metabolism by glucose (Singh et al., 2001 ).	transcription
52469	3	334842	6	NULL	NULL	0	NULL	 glutamine:fructose-6-phosphate amidotransferase	NULL	availability of 	contributes to	NULL				statement 1	NULL	regulation of 			NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_311_2_610_s_138	15240824	The availability of glucose and the rate-limiting enzyme glutamine:fructose-6-phosphate amidotransferase of the hexosamine biosynthetic pathway contribute to the regulation of cellular metabolism by glucose (Singh et al., 2001 ).	transcription
51670	1	334843	5	NULL	NULL	0	NULL	hexokinase	NULL		is a type of	NULL				enzyme	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1626_1_57_s_102	12697330	The enzyme hexokinase phosphorylates both glucose and fructose to give respective  hexose-6-phosphate, while glucose-6-phosphate isomerase catalyzes the isomerization  of fructose-6-phosphate from/to glucose-6-phosphate.	transcription
51671	2	334843	5	NULL	NULL	0	NULL	hexokinase	NULL		phosphorylates	NULL				glucose	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1626_1_57_s_102	12697330	The enzyme hexokinase phosphorylates both glucose and fructose to give respective  hexose-6-phosphate, while glucose-6-phosphate isomerase catalyzes the isomerization  of fructose-6-phosphate from/to glucose-6-phosphate.	transcription
51672	3	334843	5	NULL	NULL	0	NULL	statement 2	NULL		forms	NULL				glucose-6-phosphate	NULL				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1626_1_57_s_102	12697330	The enzyme hexokinase phosphorylates both glucose and fructose to give respective  hexose-6-phosphate, while glucose-6-phosphate isomerase catalyzes the isomerization  of fructose-6-phosphate from/to glucose-6-phosphate.	transcription
51673	4	334843	5	NULL	NULL	0	NULL	hexokinase	NULL		phosphorylates	NULL				fructose	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1626_1_57_s_102	12697330	The enzyme hexokinase phosphorylates both glucose and fructose to give respective  hexose-6-phosphate, while glucose-6-phosphate isomerase catalyzes the isomerization  of fructose-6-phosphate from/to glucose-6-phosphate.	transcription
51674	5	334843	5	NULL	NULL	0	NULL	statement 4	NULL		forms	NULL				fructose-6-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1626_1_57_s_102	12697330	The enzyme hexokinase phosphorylates both glucose and fructose to give respective  hexose-6-phosphate, while glucose-6-phosphate isomerase catalyzes the isomerization  of fructose-6-phosphate from/to glucose-6-phosphate.	transcription
51675	6	334843	5	NULL	NULL	0	NULL	fructose-6-phosphate	NULL		is isomerized to	NULL				glucose-6-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1626_1_57_s_102	12697330	The enzyme hexokinase phosphorylates both glucose and fructose to give respective  hexose-6-phosphate, while glucose-6-phosphate isomerase catalyzes the isomerization  of fructose-6-phosphate from/to glucose-6-phosphate.	transcription
51676	7	334843	5	NULL	NULL	0	NULL	fructose-6-phosphate	NULL		is isomerized from	NULL				glucose-6-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1626_1_57_s_102	12697330	The enzyme hexokinase phosphorylates both glucose and fructose to give respective  hexose-6-phosphate, while glucose-6-phosphate isomerase catalyzes the isomerization  of fructose-6-phosphate from/to glucose-6-phosphate.	transcription
51677	8	334843	5	NULL	NULL	0	NULL	glucose-6-phosphate isomerase	NULL		catalyzes	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1626_1_57_s_102	12697330	The enzyme hexokinase phosphorylates both glucose and fructose to give respective  hexose-6-phosphate, while glucose-6-phosphate isomerase catalyzes the isomerization  of fructose-6-phosphate from/to glucose-6-phosphate.	transcription
51678	9	334843	5	NULL	NULL	0	NULL	glucose-6-phosphate isomerase	NULL		catalyzes	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1626_1_57_s_102	12697330	The enzyme hexokinase phosphorylates both glucose and fructose to give respective  hexose-6-phosphate, while glucose-6-phosphate isomerase catalyzes the isomerization  of fructose-6-phosphate from/to glucose-6-phosphate.	transcription
52470	1	334843	6	NULL	NULL	0	NULL	glucose	NULL		is phosphorylated to	NULL				glucose-6-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1626_1_57_s_102	12697330	The enzyme hexokinase phosphorylates both glucose and fructose to give respective  hexose-6-phosphate, while glucose-6-phosphate isomerase catalyzes the isomerization  of fructose-6-phosphate from/to glucose-6-phosphate.	transcription
52471	2	334843	6	NULL	NULL	0	NULL	fructose	NULL		is phosphorylated to	NULL				fructose-6-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1626_1_57_s_102	12697330	The enzyme hexokinase phosphorylates both glucose and fructose to give respective  hexose-6-phosphate, while glucose-6-phosphate isomerase catalyzes the isomerization  of fructose-6-phosphate from/to glucose-6-phosphate.	transcription
52472	3	334843	6	NULL	NULL	0	NULL	hexokinase	NULL		catalyzes	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1626_1_57_s_102	12697330	The enzyme hexokinase phosphorylates both glucose and fructose to give respective  hexose-6-phosphate, while glucose-6-phosphate isomerase catalyzes the isomerization  of fructose-6-phosphate from/to glucose-6-phosphate.	transcription
52473	4	334843	6	NULL	NULL	0	NULL	hexokinase	NULL		catalyzes	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1626_1_57_s_102	12697330	The enzyme hexokinase phosphorylates both glucose and fructose to give respective  hexose-6-phosphate, while glucose-6-phosphate isomerase catalyzes the isomerization  of fructose-6-phosphate from/to glucose-6-phosphate.	transcription
52474	5	334843	6	NULL	NULL	0	NULL	fructose-6-phosphate	NULL		is isomerized to	NULL				glucose-6-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1626_1_57_s_102	12697330	The enzyme hexokinase phosphorylates both glucose and fructose to give respective  hexose-6-phosphate, while glucose-6-phosphate isomerase catalyzes the isomerization  of fructose-6-phosphate from/to glucose-6-phosphate.	transcription
52475	6	334843	6	NULL	NULL	0	NULL	glucose-6-phosphate isomerase 	NULL		catalyzes	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1626_1_57_s_102	12697330	The enzyme hexokinase phosphorylates both glucose and fructose to give respective  hexose-6-phosphate, while glucose-6-phosphate isomerase catalyzes the isomerization  of fructose-6-phosphate from/to glucose-6-phosphate.	transcription
51679	1	334844	5	NULL	NULL	0	NULL	hexosamine	NULL		induces	NULL				insulin resistance	NULL				NULL	transgenic mice overexpressing glutamine: fructose-6-phosphate amidotransferase	NULL	NULL	NULL	NULL	gw60_gene_261_2_329_s_219	11167021	Mechanism of hexosamine-induced insulin resistance in transgenic mice overexpressing glutamine: fructose-6-phosphate amidotransferase: decreased glucose transporter GLUT4 translocation and reversal by treatment with thiazolidinedione.	transcription
52476	1	334844	6	NULL	NULL	0	NULL	hexosamine	NULL		induces	NULL				insulin	NULL	resistance to			NULL	transgenic mice overexpressing glutamine: fructose-6-phosphate amidotransferase	0	NULL	NULL	NULL	gw60_gene_261_2_329_s_219	11167021	Mechanism of hexosamine-induced insulin resistance in transgenic mice overexpressing glutamine: fructose-6-phosphate amidotransferase: decreased glucose transporter GLUT4 translocation and reversal by treatment with thiazolidinedione.	transcription
52477	2	334844	6	NULL	NULL	0	NULL	GLUT4	NULL		is a type of	NULL				glucose transporter	NULL				NULL		0	NULL	NULL	NULL	gw60_gene_261_2_329_s_219	11167021	Mechanism of hexosamine-induced insulin resistance in transgenic mice overexpressing glutamine: fructose-6-phosphate amidotransferase: decreased glucose transporter GLUT4 translocation and reversal by treatment with thiazolidinedione.	transcription
51680	1	334845	5	NULL	NULL	0	NULL	regulatory protein	NULL		bind	NULL				fructose-6-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_6_1263_s_16	11375325	lucokinase    activity is acutely regulated by interaction with a regulatory protein ( 1) that binds to fructose-6-phosphate (P) and allosterically inhibits glucokinase by lowering the enzyme s affinity for glucose.	transcription
51681	4	334845	5	NULL	NULL	0	NULL	statement 3	NULL		inhibit	NULL	allosterically			glucokinase	NULL				NULL		NULL	NULL	NULL	NULL	gw60_diabetes_50_6_1263_s_16	11375325	lucokinase    activity is acutely regulated by interaction with a regulatory protein ( 1) that binds to fructose-6-phosphate (P) and allosterically inhibits glucokinase by lowering the enzyme s affinity for glucose.	transcription
51682	2	334845	5	NULL	NULL	0	NULL	glucokinase	NULL		has affinity for	NULL				glucose	NULL				NULL		NULL	NULL	NULL	NULL	gw60_diabetes_50_6_1263_s_16	11375325	lucokinase    activity is acutely regulated by interaction with a regulatory protein ( 1) that binds to fructose-6-phosphate (P) and allosterically inhibits glucokinase by lowering the enzyme s affinity for glucose.	transcription
51683	3	334845	5	NULL	NULL	0	NULL	statement 1	NULL		lowers	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_diabetes_50_6_1263_s_16	11375325	lucokinase    activity is acutely regulated by interaction with a regulatory protein ( 1) that binds to fructose-6-phosphate (P) and allosterically inhibits glucokinase by lowering the enzyme s affinity for glucose.	transcription
52478	1	334845	6	NULL	NULL	0	NULL	regulatory protein	NULL		bind	NULL				fructose-6-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_6_1263_s_16	11375325	lucokinase    activity is acutely regulated by interaction with a regulatory protein ( 1) that binds to fructose-6-phosphate (P) and allosterically inhibits glucokinase by lowering the enzyme s affinity for glucose.	transcription
52479	2	334845	6	NULL	NULL	0	NULL	regulatory protein	NULL		inhibits	NULL	allosterically			glucokinase	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_6_1263_s_16	11375325	lucokinase    activity is acutely regulated by interaction with a regulatory protein ( 1) that binds to fructose-6-phosphate (P) and allosterically inhibits glucokinase by lowering the enzyme s affinity for glucose.	transcription
52480	3	334845	6	NULL	NULL	0	NULL	lucokinase	NULL		interacts with	NULL				regulatory protein	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_6_1263_s_16	11375325	lucokinase    activity is acutely regulated by interaction with a regulatory protein ( 1) that binds to fructose-6-phosphate (P) and allosterically inhibits glucokinase by lowering the enzyme s affinity for glucose.	transcription
52481	4	334845	6	NULL	NULL	0	NULL	statement 3	NULL		regulates	NULL				lucokinase	NULL	activity of 			NULL		0	NULL	NULL	NULL	gw60_diabetes_50_6_1263_s_16	11375325	lucokinase    activity is acutely regulated by interaction with a regulatory protein ( 1) that binds to fructose-6-phosphate (P) and allosterically inhibits glucokinase by lowering the enzyme s affinity for glucose.	transcription
51684	1	334846	5	NULL	NULL	0	NULL	glucose	NULL		induce	NULL					NULL	activation of		GlRE	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_7	14757763	The high glucose-induced activation of the GlRE is mediated by the HBP; increased flux through the HBP induced by high glucose concentrations, by glutamine, or by overexpression of the rate-limiting enzyme glutamine:fructose-6-phosphate aminotransferase (GFAT) particularly activated USF-2 expression.	transcription
51685	2	334846	5	NULL	NULL	0	NULL	HBP	NULL		mediate	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_7	14757763	The high glucose-induced activation of the GlRE is mediated by the HBP; increased flux through the HBP induced by high glucose concentrations, by glutamine, or by overexpression of the rate-limiting enzyme glutamine:fructose-6-phosphate aminotransferase (GFAT) particularly activated USF-2 expression.	transcription
51687	3	334846	5	NULL	NULL	0	NULL	GFAT	NULL		is	NULL				glutamine:fructose-6-phosphate aminotransferase	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_7	14757763	The high glucose-induced activation of the GlRE is mediated by the HBP; increased flux through the HBP induced by high glucose concentrations, by glutamine, or by overexpression of the rate-limiting enzyme glutamine:fructose-6-phosphate aminotransferase (GFAT) particularly activated USF-2 expression.	transcription
51688	4	334846	5	NULL	NULL	0	NULL	glucose	NULL	high concentration of	induce	NULL				HBP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_7	14757763	The high glucose-induced activation of the GlRE is mediated by the HBP; increased flux through the HBP induced by high glucose concentrations, by glutamine, or by overexpression of the rate-limiting enzyme glutamine:fructose-6-phosphate aminotransferase (GFAT) particularly activated USF-2 expression.	transcription
51689	5	334846	5	NULL	NULL	0	NULL	statement 4	NULL		increases	NULL				flux	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_7	14757763	The high glucose-induced activation of the GlRE is mediated by the HBP; increased flux through the HBP induced by high glucose concentrations, by glutamine, or by overexpression of the rate-limiting enzyme glutamine:fructose-6-phosphate aminotransferase (GFAT) particularly activated USF-2 expression.	transcription
51690	6	334846	5	NULL	NULL	0	NULL	statement 5	NULL		activates	NULL				USF-2	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_7	14757763	The high glucose-induced activation of the GlRE is mediated by the HBP; increased flux through the HBP induced by high glucose concentrations, by glutamine, or by overexpression of the rate-limiting enzyme glutamine:fructose-6-phosphate aminotransferase (GFAT) particularly activated USF-2 expression.	transcription
51691	7	334846	5	NULL	NULL	0	NULL	glutamine	NULL		induce	NULL				HBP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_7	14757763	The high glucose-induced activation of the GlRE is mediated by the HBP; increased flux through the HBP induced by high glucose concentrations, by glutamine, or by overexpression of the rate-limiting enzyme glutamine:fructose-6-phosphate aminotransferase (GFAT) particularly activated USF-2 expression.	transcription
51692	8	334846	5	NULL	NULL	0	NULL	statement 7	NULL		increases	NULL				flux	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_7	14757763	The high glucose-induced activation of the GlRE is mediated by the HBP; increased flux through the HBP induced by high glucose concentrations, by glutamine, or by overexpression of the rate-limiting enzyme glutamine:fructose-6-phosphate aminotransferase (GFAT) particularly activated USF-2 expression.	transcription
51693	9	334846	5	NULL	NULL	0	NULL	statement 8	NULL		activates	NULL				USF-2	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_7	14757763	The high glucose-induced activation of the GlRE is mediated by the HBP; increased flux through the HBP induced by high glucose concentrations, by glutamine, or by overexpression of the rate-limiting enzyme glutamine:fructose-6-phosphate aminotransferase (GFAT) particularly activated USF-2 expression.	transcription
51694	10	334846	5	NULL	NULL	0	NULL	GFAT	NULL	overexpression of	induce	NULL				HBP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_7	14757763	The high glucose-induced activation of the GlRE is mediated by the HBP; increased flux through the HBP induced by high glucose concentrations, by glutamine, or by overexpression of the rate-limiting enzyme glutamine:fructose-6-phosphate aminotransferase (GFAT) particularly activated USF-2 expression.	transcription
51695	11	334846	5	NULL	NULL	0	NULL	statement 10	NULL		increases	NULL				flux	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_7	14757763	The high glucose-induced activation of the GlRE is mediated by the HBP; increased flux through the HBP induced by high glucose concentrations, by glutamine, or by overexpression of the rate-limiting enzyme glutamine:fructose-6-phosphate aminotransferase (GFAT) particularly activated USF-2 expression.	transcription
51696	12	334846	5	NULL	NULL	0	NULL	statement 11	NULL		activates	NULL				USF-2	NULL	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_7	14757763	The high glucose-induced activation of the GlRE is mediated by the HBP; increased flux through the HBP induced by high glucose concentrations, by glutamine, or by overexpression of the rate-limiting enzyme glutamine:fructose-6-phosphate aminotransferase (GFAT) particularly activated USF-2 expression.	transcription
52482	1	334846	6	NULL	NULL	0	NULL	glucose	NULL		induces	NULL				GIRE	NULL	activation of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_7	14757763	The high glucose-induced activation of the GlRE is mediated by the HBP; increased flux through the HBP induced by high glucose concentrations, by glutamine, or by overexpression of the rate-limiting enzyme glutamine:fructose-6-phosphate aminotransferase (GFAT) particularly activated USF-2 expression.	transcription
52524	2	334846	6	NULL	NULL	0	NULL	HBP	NULL		mediates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_7	14757763	The high glucose-induced activation of the GlRE is mediated by the HBP; increased flux through the HBP induced by high glucose concentrations, by glutamine, or by overexpression of the rate-limiting enzyme glutamine:fructose-6-phosphate aminotransferase (GFAT) particularly activated USF-2 expression.	transcription
52525	3	334846	6	NULL	NULL	0	NULL	glucose	NULL	high concentration of 	induces	NULL				HBP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_7	14757763	The high glucose-induced activation of the GlRE is mediated by the HBP; increased flux through the HBP induced by high glucose concentrations, by glutamine, or by overexpression of the rate-limiting enzyme glutamine:fructose-6-phosphate aminotransferase (GFAT) particularly activated USF-2 expression.	transcription
52526	4	334846	6	NULL	NULL	0	NULL	statement 3	NULL		increases	NULL				flux	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_7	14757763	The high glucose-induced activation of the GlRE is mediated by the HBP; increased flux through the HBP induced by high glucose concentrations, by glutamine, or by overexpression of the rate-limiting enzyme glutamine:fructose-6-phosphate aminotransferase (GFAT) particularly activated USF-2 expression.	transcription
52527	5	334846	6	NULL	NULL	0	NULL	statement 4	NULL		activates	NULL				USF-2	NULL	expression of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_7	14757763	The high glucose-induced activation of the GlRE is mediated by the HBP; increased flux through the HBP induced by high glucose concentrations, by glutamine, or by overexpression of the rate-limiting enzyme glutamine:fructose-6-phosphate aminotransferase (GFAT) particularly activated USF-2 expression.	transcription
52528	6	334846	6	NULL	NULL	0	NULL	GFAT	NULL	overexpression of	activates	NULL				USF-2	NULL	expression of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_7	14757763	The high glucose-induced activation of the GlRE is mediated by the HBP; increased flux through the HBP induced by high glucose concentrations, by glutamine, or by overexpression of the rate-limiting enzyme glutamine:fructose-6-phosphate aminotransferase (GFAT) particularly activated USF-2 expression.	transcription
52529	7	334846	6	NULL	NULL	0	NULL	GFAT	NULL		is	NULL				glutamine:fructose-6-phosphate aminotransferase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_7	14757763	The high glucose-induced activation of the GlRE is mediated by the HBP; increased flux through the HBP induced by high glucose concentrations, by glutamine, or by overexpression of the rate-limiting enzyme glutamine:fructose-6-phosphate aminotransferase (GFAT) particularly activated USF-2 expression.	transcription
51697	1	334847	5	NULL	NULL	0	NULL	G3P & glucose	NULL	addition of	reduces	NULL				beta-galactosidase	NULL	activity of			NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-microbiol-lett_162_1_9595668_s_5	9595668	When G3P and glucose, glucose-6-phosphate or fructose-6-phosphate  were added, beta-galactosidase activity was reduced showing that GlpP  mediates catabolite repression of transcription from the glpD leader in  the absence of any other B. subtilis protein.	transcription
51698	2	334847	5	NULL	NULL	0	NULL	G3P & glucose-6-phosphate	NULL	addition of	reduces	NULL				beta-galactosidase	NULL	activity of			NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_fems-microbiol-lett_162_1_9595668_s_5	9595668	When G3P and glucose, glucose-6-phosphate or fructose-6-phosphate  were added, beta-galactosidase activity was reduced showing that GlpP  mediates catabolite repression of transcription from the glpD leader in  the absence of any other B. subtilis protein.	transcription
51699	3	334847	5	NULL	NULL	0	NULL	G3P & fructose-6-phosphate	NULL	addition of	reduces	NULL				beta-galactosidase	NULL	activity of			NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-microbiol-lett_162_1_9595668_s_5	9595668	When G3P and glucose, glucose-6-phosphate or fructose-6-phosphate  were added, beta-galactosidase activity was reduced showing that GlpP  mediates catabolite repression of transcription from the glpD leader in  the absence of any other B. subtilis protein.	transcription
51700	4	334847	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-microbiol-lett_162_1_9595668_s_5	9595668	When G3P and glucose, glucose-6-phosphate or fructose-6-phosphate  were added, beta-galactosidase activity was reduced showing that GlpP  mediates catabolite repression of transcription from the glpD leader in  the absence of any other B. subtilis protein.	transcription
51701	5	334847	5	NULL	NULL	0	NULL	statement 2	NULL		is an alternative to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-microbiol-lett_162_1_9595668_s_5	9595668	When G3P and glucose, glucose-6-phosphate or fructose-6-phosphate  were added, beta-galactosidase activity was reduced showing that GlpP  mediates catabolite repression of transcription from the glpD leader in  the absence of any other B. subtilis protein.	transcription
51702	6	334847	5	NULL	NULL	0	NULL	GlpP	NULL		mediates	NULL				glpD	NULL	catabolite repression of;;transcription of		leader	NULL		NULL	NULL	NULL	NULL	abs-batch0680-0699_fems-microbiol-lett_162_1_9595668_s_5	9595668	When G3P and glucose, glucose-6-phosphate or fructose-6-phosphate  were added, beta-galactosidase activity was reduced showing that GlpP  mediates catabolite repression of transcription from the glpD leader in  the absence of any other B. subtilis protein.	transcription
51703	7	334847	5	NULL	NULL	0	NULL	statement 6	NULL		in the absence of	NULL				protein	NULL	B. subtilis			NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-microbiol-lett_162_1_9595668_s_5	9595668	When G3P and glucose, glucose-6-phosphate or fructose-6-phosphate  were added, beta-galactosidase activity was reduced showing that GlpP  mediates catabolite repression of transcription from the glpD leader in  the absence of any other B. subtilis protein.	transcription
52530	1	334847	6	NULL	NULL	0	NULL	GlpP	NULL		mediates	NULL				transcription	NULL	catabolite repression of 			NULL		0	NULL	NULL	NULL	abs-batch0680-0699_fems-microbiol-lett_162_1_9595668_s_5	9595668	When G3P and glucose, glucose-6-phosphate or fructose-6-phosphate  were added, beta-galactosidase activity was reduced showing that GlpP  mediates catabolite repression of transcription from the glpD leader in  the absence of any other B. subtilis protein.	transcription
51704	1	334848	5	NULL	NULL	0	NULL	GFAT	NULL		is	NULL				glutamine:fructose-6-phosphate amidotransferase	NULL				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_1_93_s_91	16380481	The ability of 20 mumol/l azaserine, a potent inhibitor of GFAT (glutamine:fructose-6-phosphate amidotransferase), to attenuate glucose, but not glucosamine-induced ER stress, suggests that elevated concentrations of glucose cause ER stress through a glucosamine intermediate ( Fig. 1 B).	transcription
51705	2	334848	5	NULL	NULL	0	NULL	azaserine	NULL		is an inhibitor of	NULL	potent			GFAT	NULL				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_1_93_s_91	16380481	The ability of 20 mumol/l azaserine, a potent inhibitor of GFAT (glutamine:fructose-6-phosphate amidotransferase), to attenuate glucose, but not glucosamine-induced ER stress, suggests that elevated concentrations of glucose cause ER stress through a glucosamine intermediate ( Fig. 1 B).	transcription
51706	3	334848	5	NULL	NULL	0	NULL	azaserine	NULL		attenuate	NULL				glucose	NULL				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_1_93_s_91	16380481	The ability of 20 mumol/l azaserine, a potent inhibitor of GFAT (glutamine:fructose-6-phosphate amidotransferase), to attenuate glucose, but not glucosamine-induced ER stress, suggests that elevated concentrations of glucose cause ER stress through a glucosamine intermediate ( Fig. 1 B).	transcription
51707	4	334848	5	NULL	NULL	0	NULL	ER stress	NULL		is induced by	NULL				glucosamine	NULL				NULL		NULL	NULL	NULL	NULL	gw70_diabetes_55_1_93_s_91	16380481	The ability of 20 mumol/l azaserine, a potent inhibitor of GFAT (glutamine:fructose-6-phosphate amidotransferase), to attenuate glucose, but not glucosamine-induced ER stress, suggests that elevated concentrations of glucose cause ER stress through a glucosamine intermediate ( Fig. 1 B).	transcription
51708	5	334848	5	NULL	NULL	0	NULL	azaserine	NULL		does not attenuate	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_1_93_s_91	16380481	The ability of 20 mumol/l azaserine, a potent inhibitor of GFAT (glutamine:fructose-6-phosphate amidotransferase), to attenuate glucose, but not glucosamine-induced ER stress, suggests that elevated concentrations of glucose cause ER stress through a glucosamine intermediate ( Fig. 1 B).	transcription
51709	6	334848	5	NULL	NULL	0	NULL	glucose	NULL	elevated concentrations	causes	NULL				ER stress	NULL				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_1_93_s_91	16380481	The ability of 20 mumol/l azaserine, a potent inhibitor of GFAT (glutamine:fructose-6-phosphate amidotransferase), to attenuate glucose, but not glucosamine-induced ER stress, suggests that elevated concentrations of glucose cause ER stress through a glucosamine intermediate ( Fig. 1 B).	transcription
51710	7	334848	5	NULL	NULL	0	NULL	statement 6	NULL		occurs through	NULL				glucosamine intermediate	NULL				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_1_93_s_91	16380481	The ability of 20 mumol/l azaserine, a potent inhibitor of GFAT (glutamine:fructose-6-phosphate amidotransferase), to attenuate glucose, but not glucosamine-induced ER stress, suggests that elevated concentrations of glucose cause ER stress through a glucosamine intermediate ( Fig. 1 B).	transcription
52531	1	334848	6	NULL	NULL	0	NULL	glucose	NULL	elevated concentrations of	cause	NULL				ER stress	NULL				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_1_93_s_91	16380481	The ability of 20 mumol/l azaserine, a potent inhibitor of GFAT (glutamine:fructose-6-phosphate amidotransferase), to attenuate glucose, but not glucosamine-induced ER stress, suggests that elevated concentrations of glucose cause ER stress through a glucosamine intermediate ( Fig. 1 B).	transcription
52532	2	334848	6	NULL	NULL	0	NULL	statement 1	NULL		occurs through	NULL				glucosamine intermediate	NULL				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_1_93_s_91	16380481	The ability of 20 mumol/l azaserine, a potent inhibitor of GFAT (glutamine:fructose-6-phosphate amidotransferase), to attenuate glucose, but not glucosamine-induced ER stress, suggests that elevated concentrations of glucose cause ER stress through a glucosamine intermediate ( Fig. 1 B).	transcription
52533	3	334848	6	NULL	NULL	0	NULL	azaserine	NULL		is a type of 	NULL				inhibitor of GFAT	NULL				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_1_93_s_91	16380481	The ability of 20 mumol/l azaserine, a potent inhibitor of GFAT (glutamine:fructose-6-phosphate amidotransferase), to attenuate glucose, but not glucosamine-induced ER stress, suggests that elevated concentrations of glucose cause ER stress through a glucosamine intermediate ( Fig. 1 B).	transcription
52534	4	334848	6	NULL	NULL	0	NULL	GFAT	NULL		is	NULL				glutamine:fructose-6-phosphate amidotransferase	NULL				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_1_93_s_91	16380481	The ability of 20 mumol/l azaserine, a potent inhibitor of GFAT (glutamine:fructose-6-phosphate amidotransferase), to attenuate glucose, but not glucosamine-induced ER stress, suggests that elevated concentrations of glucose cause ER stress through a glucosamine intermediate ( Fig. 1 B).	transcription
52535	5	334848	6	NULL	NULL	0	NULL	azaserine	NULL		attenuates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_1_93_s_91	16380481	The ability of 20 mumol/l azaserine, a potent inhibitor of GFAT (glutamine:fructose-6-phosphate amidotransferase), to attenuate glucose, but not glucosamine-induced ER stress, suggests that elevated concentrations of glucose cause ER stress through a glucosamine intermediate ( Fig. 1 B).	transcription
52536	6	334848	6	NULL	NULL	0	NULL	glucosamine	NULL		induces	NULL				ER stress	NULL				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_1_93_s_91	16380481	The ability of 20 mumol/l azaserine, a potent inhibitor of GFAT (glutamine:fructose-6-phosphate amidotransferase), to attenuate glucose, but not glucosamine-induced ER stress, suggests that elevated concentrations of glucose cause ER stress through a glucosamine intermediate ( Fig. 1 B).	transcription
52537	7	334848	6	NULL	NULL	0	NULL	azaserine	NULL		does not attenuate	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_1_93_s_91	16380481	The ability of 20 mumol/l azaserine, a potent inhibitor of GFAT (glutamine:fructose-6-phosphate amidotransferase), to attenuate glucose, but not glucosamine-induced ER stress, suggests that elevated concentrations of glucose cause ER stress through a glucosamine intermediate ( Fig. 1 B).	transcription
51711	1	334849	5	NULL	NULL	0	NULL	azaserine	NULL		is an inhibitor of	NULL				glutamine/fructose-6-phosphate amidotransferase	NULL				NULL		0	NULL	NULL	NULL	gw70_diabetes_53_4_890_s_193	15047603	To evaluate whether the hexosamine pathway could mediate the induction of FXR expression by D-glucose, rat hepatocytes were cultured with azaserine (5 mumol/l), an inhibitor of glutamine/fructose-6-phosphate amidotransferase, the rate-limiting enzyme in the conversion of glucose to glucosamine.	transcription
51712	2	334849	5	NULL	NULL	0	NULL	glucose	NULL		is converted to	NULL				glucosamine	NULL				NULL		0	NULL	NULL	NULL	gw70_diabetes_53_4_890_s_193	15047603	To evaluate whether the hexosamine pathway could mediate the induction of FXR expression by D-glucose, rat hepatocytes were cultured with azaserine (5 mumol/l), an inhibitor of glutamine/fructose-6-phosphate amidotransferase, the rate-limiting enzyme in the conversion of glucose to glucosamine.	transcription
51713	3	334849	5	NULL	NULL	0	NULL	FXR	NULL	expression of	is induced by	NULL				D-glucose	NULL				NULL	rat hepatocytes	NULL	NULL	NULL	NULL	gw70_diabetes_53_4_890_s_193	15047603	To evaluate whether the hexosamine pathway could mediate the induction of FXR expression by D-glucose, rat hepatocytes were cultured with azaserine (5 mumol/l), an inhibitor of glutamine/fructose-6-phosphate amidotransferase, the rate-limiting enzyme in the conversion of glucose to glucosamine.	transcription
52037	4	334849	5	NULL	NULL	0	NULL	hexosamine pathway	NULL		mediate	NULL	may			statement 3	NULL				NULL	rat hepatocytes	0	NULL	NULL	NULL	gw70_diabetes_53_4_890_s_193	15047603	To evaluate whether the hexosamine pathway could mediate the induction of FXR expression by D-glucose, rat hepatocytes were cultured with azaserine (5 mumol/l), an inhibitor of glutamine/fructose-6-phosphate amidotransferase, the rate-limiting enzyme in the conversion of glucose to glucosamine.	transcription
52538	1	334849	6	NULL	NULL	0	NULL	glucose	NULL		is converted to	NULL				glucosamine	NULL				NULL		0	NULL	NULL	NULL	gw70_diabetes_53_4_890_s_193	15047603	To evaluate whether the hexosamine pathway could mediate the induction of FXR expression by D-glucose, rat hepatocytes were cultured with azaserine (5 mumol/l), an inhibitor of glutamine/fructose-6-phosphate amidotransferase, the rate-limiting enzyme in the conversion of glucose to glucosamine.	transcription
52539	2	334849	6	NULL	NULL	0	NULL	glutamine/fructose-6-phosphate amidotransferase	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_diabetes_53_4_890_s_193	15047603	To evaluate whether the hexosamine pathway could mediate the induction of FXR expression by D-glucose, rat hepatocytes were cultured with azaserine (5 mumol/l), an inhibitor of glutamine/fructose-6-phosphate amidotransferase, the rate-limiting enzyme in the conversion of glucose to glucosamine.	transcription
51714	1	334850	5	NULL	NULL	0	NULL	hexosamine	NULL		induce	NULL				insulin resistance	NULL				NULL	transgenic mice overexpressing glutamine:fructose-6-phosphate amidotransferase	0	NULL	NULL	NULL	gw60_diabetes_50_5_1093_s_411	11334413	Diabetes 45:1644 - 1654, 1996 [Abstract]    Cooksey RC, Hebert LF, Zhu JH, Wofford P, Garvey WT, McClain DA: Mechanism of hexosamine-induced insulin resistance in transgenic mice overexpressing glutamine:fructose-6-phosphate amidotransferase: decreased glucose transporter GLUT4 translocation and reversal by treatment with thiazolidinedione.	transcription
51715	2	334850	5	NULL	NULL	0	NULL	statement 1	NULL		decreases	NULL				GLUT4	NULL	translocation of			NULL		0	NULL	NULL	NULL	gw60_diabetes_50_5_1093_s_411	11334413	Diabetes 45:1644 - 1654, 1996 [Abstract]    Cooksey RC, Hebert LF, Zhu JH, Wofford P, Garvey WT, McClain DA: Mechanism of hexosamine-induced insulin resistance in transgenic mice overexpressing glutamine:fructose-6-phosphate amidotransferase: decreased glucose transporter GLUT4 translocation and reversal by treatment with thiazolidinedione.	transcription
51716	3	334850	5	NULL	NULL	0	NULL	GLUT4	NULL		is a type of	NULL				glucose transporter	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_5_1093_s_411	11334413	Diabetes 45:1644 - 1654, 1996 [Abstract]    Cooksey RC, Hebert LF, Zhu JH, Wofford P, Garvey WT, McClain DA: Mechanism of hexosamine-induced insulin resistance in transgenic mice overexpressing glutamine:fructose-6-phosphate amidotransferase: decreased glucose transporter GLUT4 translocation and reversal by treatment with thiazolidinedione.	transcription
51717	4	334850	5	NULL	NULL	0	NULL	thiazolidinedione	NULL	treatment	reverse	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_50_5_1093_s_411	11334413	Diabetes 45:1644 - 1654, 1996 [Abstract]    Cooksey RC, Hebert LF, Zhu JH, Wofford P, Garvey WT, McClain DA: Mechanism of hexosamine-induced insulin resistance in transgenic mice overexpressing glutamine:fructose-6-phosphate amidotransferase: decreased glucose transporter GLUT4 translocation and reversal by treatment with thiazolidinedione.	transcription
52540	1	334850	6	NULL	NULL	0	NULL	hexosamine	NULL		induces	NULL				insulin	NULL	resistance to			NULL	transgenic mice overexpressing glutamine:fructose-6-phosphate amidotransferase	0	NULL	NULL	NULL	gw60_diabetes_50_5_1093_s_411	11334413	Diabetes 45:1644 - 1654, 1996 [Abstract]    Cooksey RC, Hebert LF, Zhu JH, Wofford P, Garvey WT, McClain DA: Mechanism of hexosamine-induced insulin resistance in transgenic mice overexpressing glutamine:fructose-6-phosphate amidotransferase: decreased glucose transporter GLUT4 translocation and reversal by treatment with thiazolidinedione.	transcription
51718	1	334851	5	NULL	NULL	0	NULL	glucose	NULL	increase in;;levels of	increases	NULL				Id2	NULL	levels of			NULL	J774.2 macrophages	0	NULL	NULL	NULL	abs-batch0620-0649_am-j-physiol-endocrinol-metab_290_4_16234270_s_7	16234270	We demonstrate that increases in glucose levels cause  a rapid increase in levels of Id2 in J774.2 macrophages, and a number  of lines of evidence indicate that this is via the hexosamine pathway  because 1) the effect of glucose requires glutamine; 2) the effect of  glucose is mimicked by low levels of glucosamine; 3) the effect of glucose  is inhibited by azaserine, an inhibitor of glutamine:fructose-6-phosphate  amidotransferase (GFAT); and 4) adenoviral mediated overexpression of  GFAT increases levels of Id2.	transcription
51719	2	334851	5	NULL	NULL	0	NULL	statement 1	NULL		via	NULL				hexosamine pathway	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_am-j-physiol-endocrinol-metab_290_4_16234270_s_7	16234270	We demonstrate that increases in glucose levels cause  a rapid increase in levels of Id2 in J774.2 macrophages, and a number  of lines of evidence indicate that this is via the hexosamine pathway  because 1) the effect of glucose requires glutamine; 2) the effect of  glucose is mimicked by low levels of glucosamine; 3) the effect of glucose  is inhibited by azaserine, an inhibitor of glutamine:fructose-6-phosphate  amidotransferase (GFAT); and 4) adenoviral mediated overexpression of  GFAT increases levels of Id2.	transcription
51720	3	334851	5	NULL	NULL	0	NULL	glucose	NULL	effect of	requires	NULL				glutamine	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_am-j-physiol-endocrinol-metab_290_4_16234270_s_7	16234270	We demonstrate that increases in glucose levels cause  a rapid increase in levels of Id2 in J774.2 macrophages, and a number  of lines of evidence indicate that this is via the hexosamine pathway  because 1) the effect of glucose requires glutamine; 2) the effect of  glucose is mimicked by low levels of glucosamine; 3) the effect of glucose  is inhibited by azaserine, an inhibitor of glutamine:fructose-6-phosphate  amidotransferase (GFAT); and 4) adenoviral mediated overexpression of  GFAT increases levels of Id2.	transcription
51721	4	334851	5	NULL	NULL	0	NULL	glucose	NULL	effect of	is mimicked by	NULL				glucosamine	NULL	low levels of			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_am-j-physiol-endocrinol-metab_290_4_16234270_s_7	16234270	We demonstrate that increases in glucose levels cause  a rapid increase in levels of Id2 in J774.2 macrophages, and a number  of lines of evidence indicate that this is via the hexosamine pathway  because 1) the effect of glucose requires glutamine; 2) the effect of  glucose is mimicked by low levels of glucosamine; 3) the effect of glucose  is inhibited by azaserine, an inhibitor of glutamine:fructose-6-phosphate  amidotransferase (GFAT); and 4) adenoviral mediated overexpression of  GFAT increases levels of Id2.	transcription
51722	5	334851	5	NULL	NULL	0	NULL	glucose	NULL	effect of	is inhibited by	NULL				azaserine	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_am-j-physiol-endocrinol-metab_290_4_16234270_s_7	16234270	We demonstrate that increases in glucose levels cause  a rapid increase in levels of Id2 in J774.2 macrophages, and a number  of lines of evidence indicate that this is via the hexosamine pathway  because 1) the effect of glucose requires glutamine; 2) the effect of  glucose is mimicked by low levels of glucosamine; 3) the effect of glucose  is inhibited by azaserine, an inhibitor of glutamine:fructose-6-phosphate  amidotransferase (GFAT); and 4) adenoviral mediated overexpression of  GFAT increases levels of Id2.	transcription
51723	6	334851	5	NULL	NULL	0	NULL	azaserine	NULL		is an inhibitor of	NULL				GFAT	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_am-j-physiol-endocrinol-metab_290_4_16234270_s_7	16234270	We demonstrate that increases in glucose levels cause  a rapid increase in levels of Id2 in J774.2 macrophages, and a number  of lines of evidence indicate that this is via the hexosamine pathway  because 1) the effect of glucose requires glutamine; 2) the effect of  glucose is mimicked by low levels of glucosamine; 3) the effect of glucose  is inhibited by azaserine, an inhibitor of glutamine:fructose-6-phosphate  amidotransferase (GFAT); and 4) adenoviral mediated overexpression of  GFAT increases levels of Id2.	transcription
51724	7	334851	5	NULL	NULL	0	NULL	GFAT	NULL		is	NULL				glutamine:fructose-6-phosphate amidotransferase	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_am-j-physiol-endocrinol-metab_290_4_16234270_s_7	16234270	We demonstrate that increases in glucose levels cause  a rapid increase in levels of Id2 in J774.2 macrophages, and a number  of lines of evidence indicate that this is via the hexosamine pathway  because 1) the effect of glucose requires glutamine; 2) the effect of  glucose is mimicked by low levels of glucosamine; 3) the effect of glucose  is inhibited by azaserine, an inhibitor of glutamine:fructose-6-phosphate  amidotransferase (GFAT); and 4) adenoviral mediated overexpression of  GFAT increases levels of Id2.	transcription
51725	8	334851	5	NULL	NULL	0	NULL	adenovirus	NULL		mediate	NULL				GFAT	NULL	overexpression of			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_am-j-physiol-endocrinol-metab_290_4_16234270_s_7	16234270	We demonstrate that increases in glucose levels cause  a rapid increase in levels of Id2 in J774.2 macrophages, and a number  of lines of evidence indicate that this is via the hexosamine pathway  because 1) the effect of glucose requires glutamine; 2) the effect of  glucose is mimicked by low levels of glucosamine; 3) the effect of glucose  is inhibited by azaserine, an inhibitor of glutamine:fructose-6-phosphate  amidotransferase (GFAT); and 4) adenoviral mediated overexpression of  GFAT increases levels of Id2.	transcription
51726	9	334851	5	NULL	NULL	0	NULL	statement 8	NULL		increases	NULL				Id2	NULL	levels of			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_am-j-physiol-endocrinol-metab_290_4_16234270_s_7	16234270	We demonstrate that increases in glucose levels cause  a rapid increase in levels of Id2 in J774.2 macrophages, and a number  of lines of evidence indicate that this is via the hexosamine pathway  because 1) the effect of glucose requires glutamine; 2) the effect of  glucose is mimicked by low levels of glucosamine; 3) the effect of glucose  is inhibited by azaserine, an inhibitor of glutamine:fructose-6-phosphate  amidotransferase (GFAT); and 4) adenoviral mediated overexpression of  GFAT increases levels of Id2.	transcription
52541	1	334851	6	NULL	NULL	0	NULL	glucose	NULL	increased levels of 	increases	NULL				Id2	NULL	levels of 			NULL	J774.2 macrophages	0	NULL	NULL	NULL	abs-batch0620-0649_am-j-physiol-endocrinol-metab_290_4_16234270_s_7	16234270	We demonstrate that increases in glucose levels cause  a rapid increase in levels of Id2 in J774.2 macrophages, and a number  of lines of evidence indicate that this is via the hexosamine pathway  because 1) the effect of glucose requires glutamine; 2) the effect of  glucose is mimicked by low levels of glucosamine; 3) the effect of glucose  is inhibited by azaserine, an inhibitor of glutamine:fructose-6-phosphate  amidotransferase (GFAT); and 4) adenoviral mediated overexpression of  GFAT increases levels of Id2.	transcription
52542	2	334851	6	NULL	NULL	0	NULL	statement 1	NULL		occurs via	NULL				hexosamine pathway	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_am-j-physiol-endocrinol-metab_290_4_16234270_s_7	16234270	We demonstrate that increases in glucose levels cause  a rapid increase in levels of Id2 in J774.2 macrophages, and a number  of lines of evidence indicate that this is via the hexosamine pathway  because 1) the effect of glucose requires glutamine; 2) the effect of  glucose is mimicked by low levels of glucosamine; 3) the effect of glucose  is inhibited by azaserine, an inhibitor of glutamine:fructose-6-phosphate  amidotransferase (GFAT); and 4) adenoviral mediated overexpression of  GFAT increases levels of Id2.	transcription
52543	3	334851	6	NULL	NULL	0	NULL	glucose	NULL	effect of	requires	NULL				glutamine	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_am-j-physiol-endocrinol-metab_290_4_16234270_s_7	16234270	We demonstrate that increases in glucose levels cause  a rapid increase in levels of Id2 in J774.2 macrophages, and a number  of lines of evidence indicate that this is via the hexosamine pathway  because 1) the effect of glucose requires glutamine; 2) the effect of  glucose is mimicked by low levels of glucosamine; 3) the effect of glucose  is inhibited by azaserine, an inhibitor of glutamine:fructose-6-phosphate  amidotransferase (GFAT); and 4) adenoviral mediated overexpression of  GFAT increases levels of Id2.	transcription
52544	4	334851	6	NULL	NULL	0	NULL	glucose	NULL	effect of	is mimicked by	NULL				glucosamine	NULL	low levels of 			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_am-j-physiol-endocrinol-metab_290_4_16234270_s_7	16234270	We demonstrate that increases in glucose levels cause  a rapid increase in levels of Id2 in J774.2 macrophages, and a number  of lines of evidence indicate that this is via the hexosamine pathway  because 1) the effect of glucose requires glutamine; 2) the effect of  glucose is mimicked by low levels of glucosamine; 3) the effect of glucose  is inhibited by azaserine, an inhibitor of glutamine:fructose-6-phosphate  amidotransferase (GFAT); and 4) adenoviral mediated overexpression of  GFAT increases levels of Id2.	transcription
52545	5	334851	6	NULL	NULL	0	NULL	azaserine	NULL		inhibits	NULL				glucose	NULL	effect of 			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_am-j-physiol-endocrinol-metab_290_4_16234270_s_7	16234270	We demonstrate that increases in glucose levels cause  a rapid increase in levels of Id2 in J774.2 macrophages, and a number  of lines of evidence indicate that this is via the hexosamine pathway  because 1) the effect of glucose requires glutamine; 2) the effect of  glucose is mimicked by low levels of glucosamine; 3) the effect of glucose  is inhibited by azaserine, an inhibitor of glutamine:fructose-6-phosphate  amidotransferase (GFAT); and 4) adenoviral mediated overexpression of  GFAT increases levels of Id2.	transcription
52546	6	334851	6	NULL	NULL	0	NULL	azaserine	NULL		is a type of 	NULL				GFAT inhibitor	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_am-j-physiol-endocrinol-metab_290_4_16234270_s_7	16234270	We demonstrate that increases in glucose levels cause  a rapid increase in levels of Id2 in J774.2 macrophages, and a number  of lines of evidence indicate that this is via the hexosamine pathway  because 1) the effect of glucose requires glutamine; 2) the effect of  glucose is mimicked by low levels of glucosamine; 3) the effect of glucose  is inhibited by azaserine, an inhibitor of glutamine:fructose-6-phosphate  amidotransferase (GFAT); and 4) adenoviral mediated overexpression of  GFAT increases levels of Id2.	transcription
52547	7	334851	6	NULL	NULL	0	NULL	GFAT	NULL		is	NULL				glutamine:fructose-6-phosphate amidotransferase	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_am-j-physiol-endocrinol-metab_290_4_16234270_s_7	16234270	We demonstrate that increases in glucose levels cause  a rapid increase in levels of Id2 in J774.2 macrophages, and a number  of lines of evidence indicate that this is via the hexosamine pathway  because 1) the effect of glucose requires glutamine; 2) the effect of  glucose is mimicked by low levels of glucosamine; 3) the effect of glucose  is inhibited by azaserine, an inhibitor of glutamine:fructose-6-phosphate  amidotransferase (GFAT); and 4) adenoviral mediated overexpression of  GFAT increases levels of Id2.	transcription
51727	1	334852	5	NULL	NULL	0	NULL	glucose	NULL		up-regulates	NULL				USF-1 mRNA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_158	14757763	To assess whether the HBP mediates glucose-induced up-regulation of both USF-1 and USF-2 mRNA, we incubated porcine mesangial cells with 2 mM glucosamine or 30 mM glucose plus 16 mM glutamine for 24 h. GFAT, the rate-limiting enzyme of the HBP, requires glutamine for conversion of fructose-6-phosphate to glucosamine-6-phosphate, whereas glucosamine enters the HBP downstream of GFAT.	transcription
51728	2	334852	5	NULL	NULL	0	NULL	glucose	NULL		up-regulates	NULL				USF-2 mRNA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_158	14757763	To assess whether the HBP mediates glucose-induced up-regulation of both USF-1 and USF-2 mRNA, we incubated porcine mesangial cells with 2 mM glucosamine or 30 mM glucose plus 16 mM glutamine for 24 h. GFAT, the rate-limiting enzyme of the HBP, requires glutamine for conversion of fructose-6-phosphate to glucosamine-6-phosphate, whereas glucosamine enters the HBP downstream of GFAT.	transcription
51729	3	334852	5	NULL	NULL	0	NULL	GFAT	NULL		is a type of	NULL				rate-limiting enzyme of HBP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_158	14757763	To assess whether the HBP mediates glucose-induced up-regulation of both USF-1 and USF-2 mRNA, we incubated porcine mesangial cells with 2 mM glucosamine or 30 mM glucose plus 16 mM glutamine for 24 h. GFAT, the rate-limiting enzyme of the HBP, requires glutamine for conversion of fructose-6-phosphate to glucosamine-6-phosphate, whereas glucosamine enters the HBP downstream of GFAT.	transcription
51730	4	334852	5	NULL	NULL	0	NULL	fructose-6-phosphate	NULL		is converted to	NULL				glucosamine-6-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_158	14757763	To assess whether the HBP mediates glucose-induced up-regulation of both USF-1 and USF-2 mRNA, we incubated porcine mesangial cells with 2 mM glucosamine or 30 mM glucose plus 16 mM glutamine for 24 h. GFAT, the rate-limiting enzyme of the HBP, requires glutamine for conversion of fructose-6-phosphate to glucosamine-6-phosphate, whereas glucosamine enters the HBP downstream of GFAT.	transcription
51731	5	334852	5	NULL	NULL	0	NULL	GFAT	NULL		catalyzes	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_158	14757763	To assess whether the HBP mediates glucose-induced up-regulation of both USF-1 and USF-2 mRNA, we incubated porcine mesangial cells with 2 mM glucosamine or 30 mM glucose plus 16 mM glutamine for 24 h. GFAT, the rate-limiting enzyme of the HBP, requires glutamine for conversion of fructose-6-phosphate to glucosamine-6-phosphate, whereas glucosamine enters the HBP downstream of GFAT.	transcription
51732	6	334852	5	NULL	NULL	0	NULL	glutamine	NULL		is required for	NULL				statement 5	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_158	14757763	To assess whether the HBP mediates glucose-induced up-regulation of both USF-1 and USF-2 mRNA, we incubated porcine mesangial cells with 2 mM glucosamine or 30 mM glucose plus 16 mM glutamine for 24 h. GFAT, the rate-limiting enzyme of the HBP, requires glutamine for conversion of fructose-6-phosphate to glucosamine-6-phosphate, whereas glucosamine enters the HBP downstream of GFAT.	transcription
51733	7	334852	5	NULL	NULL	0	NULL	glucosamine	NULL		enters	NULL				HBP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_158	14757763	To assess whether the HBP mediates glucose-induced up-regulation of both USF-1 and USF-2 mRNA, we incubated porcine mesangial cells with 2 mM glucosamine or 30 mM glucose plus 16 mM glutamine for 24 h. GFAT, the rate-limiting enzyme of the HBP, requires glutamine for conversion of fructose-6-phosphate to glucosamine-6-phosphate, whereas glucosamine enters the HBP downstream of GFAT.	transcription
51734	8	334852	5	NULL	NULL	0	NULL	statement 7	NULL		occurs	NULL				GFAT	NULL	downstream of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_158	14757763	To assess whether the HBP mediates glucose-induced up-regulation of both USF-1 and USF-2 mRNA, we incubated porcine mesangial cells with 2 mM glucosamine or 30 mM glucose plus 16 mM glutamine for 24 h. GFAT, the rate-limiting enzyme of the HBP, requires glutamine for conversion of fructose-6-phosphate to glucosamine-6-phosphate, whereas glucosamine enters the HBP downstream of GFAT.	transcription
52548	1	334852	6	NULL	NULL	0	NULL	glucose	NULL		mediates	NULL				USF-1 mRNA	NULL	upregulation of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_158	14757763	To assess whether the HBP mediates glucose-induced up-regulation of both USF-1 and USF-2 mRNA, we incubated porcine mesangial cells with 2 mM glucosamine or 30 mM glucose plus 16 mM glutamine for 24 h. GFAT, the rate-limiting enzyme of the HBP, requires glutamine for conversion of fructose-6-phosphate to glucosamine-6-phosphate, whereas glucosamine enters the HBP downstream of GFAT.	transcription
52549	2	334852	6	NULL	NULL	0	NULL	glucose	NULL		induces	NULL				USF-2 mRNA	NULL	upregulation of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_158	14757763	To assess whether the HBP mediates glucose-induced up-regulation of both USF-1 and USF-2 mRNA, we incubated porcine mesangial cells with 2 mM glucosamine or 30 mM glucose plus 16 mM glutamine for 24 h. GFAT, the rate-limiting enzyme of the HBP, requires glutamine for conversion of fructose-6-phosphate to glucosamine-6-phosphate, whereas glucosamine enters the HBP downstream of GFAT.	transcription
52550	3	334852	6	NULL	NULL	0	NULL	GFAT	NULL		is a type of 	NULL				HBP enzyme	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_158	14757763	To assess whether the HBP mediates glucose-induced up-regulation of both USF-1 and USF-2 mRNA, we incubated porcine mesangial cells with 2 mM glucosamine or 30 mM glucose plus 16 mM glutamine for 24 h. GFAT, the rate-limiting enzyme of the HBP, requires glutamine for conversion of fructose-6-phosphate to glucosamine-6-phosphate, whereas glucosamine enters the HBP downstream of GFAT.	transcription
52551	4	334852	6	NULL	NULL	0	NULL	fructose-6-phosphate	NULL		is converted to	NULL				glucosamine-6-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_158	14757763	To assess whether the HBP mediates glucose-induced up-regulation of both USF-1 and USF-2 mRNA, we incubated porcine mesangial cells with 2 mM glucosamine or 30 mM glucose plus 16 mM glutamine for 24 h. GFAT, the rate-limiting enzyme of the HBP, requires glutamine for conversion of fructose-6-phosphate to glucosamine-6-phosphate, whereas glucosamine enters the HBP downstream of GFAT.	transcription
52552	5	334852	6	NULL	NULL	0	NULL	glutamine	NULL		is required for	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_158	14757763	To assess whether the HBP mediates glucose-induced up-regulation of both USF-1 and USF-2 mRNA, we incubated porcine mesangial cells with 2 mM glucosamine or 30 mM glucose plus 16 mM glutamine for 24 h. GFAT, the rate-limiting enzyme of the HBP, requires glutamine for conversion of fructose-6-phosphate to glucosamine-6-phosphate, whereas glucosamine enters the HBP downstream of GFAT.	transcription
52553	6	334852	6	NULL	NULL	0	NULL	glucosamine	NULL		enters	NULL				HBP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_158	14757763	To assess whether the HBP mediates glucose-induced up-regulation of both USF-1 and USF-2 mRNA, we incubated porcine mesangial cells with 2 mM glucosamine or 30 mM glucose plus 16 mM glutamine for 24 h. GFAT, the rate-limiting enzyme of the HBP, requires glutamine for conversion of fructose-6-phosphate to glucosamine-6-phosphate, whereas glucosamine enters the HBP downstream of GFAT.	transcription
52554	7	334852	6	NULL	NULL	0	NULL	statement 6	NULL		occurs downstream of	NULL				GFAT	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15908_s_158	14757763	To assess whether the HBP mediates glucose-induced up-regulation of both USF-1 and USF-2 mRNA, we incubated porcine mesangial cells with 2 mM glucosamine or 30 mM glucose plus 16 mM glutamine for 24 h. GFAT, the rate-limiting enzyme of the HBP, requires glutamine for conversion of fructose-6-phosphate to glucosamine-6-phosphate, whereas glucosamine enters the HBP downstream of GFAT.	transcription
51735	1	334853	5	NULL	NULL	0	NULL	hyperglycemia	NULL		induce	NULL				ED	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
51736	2	334853	5	NULL	NULL	0	NULL	statement 1	NULL		via	NULL				ROS	NULL	generation of			NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
51737	3	334853	5	NULL	NULL	0	NULL	statement 1	NULL		involves	NULL				protein kinase C	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
51738	4	334853	5	NULL	NULL	0	NULL	statement 1	NULL		involves	NULL				glycation end products	NULL	increased generation of;;advanced			NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
51739	5	334853	5	NULL	NULL	0	NULL	statement 1	NULL		involves	NULL				glucose flux	NULL	increased			NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
51740	6	334853	5	NULL	NULL	0	NULL	statement 5	NULL		occurs through	NULL				aldose reductase pathway	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
51741	7	334853	5	NULL	NULL	0	NULL	statement 1	NULL		involves	NULL				glutamine:fructose-6-phosphate amidotransferase 	NULL	increased activity of 			NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
51742	8	334853	5	NULL	NULL	0	NULL	statement 8	NULL		leads to	NULL				insulin resistance	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
51743	9	334853	5	NULL	NULL	0	NULL	statement 1	NULL		involves	NULL				NF-kappaB	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
51744	10	334853	5	NULL	NULL	0	NULL	statement 9	NULL		leads to	NULL				cytokines	NULL	nuclear transcription of			NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
51745	11	334853	5	NULL	NULL	0	NULL	statement 9	NULL		leads to	NULL				inflammatory mediators	NULL	nuclear transcription of			NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
52962	1	334853	6	NULL	NULL	0	NULL	hyperglycemia	NULL		induce	NULL				ED	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
52963	2	334853	6	NULL	NULL	0	NULL	statement 1	NULL		occurs via	NULL				ROS	NULL	generation of 			NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
52964	3	334853	6	NULL	NULL	0	NULL	statement 1	NULL		involve	NULL				protein kinase C	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
52965	4	334853	6	NULL	NULL	0	NULL	statement 1	NULL		involve	NULL				glycation end products	NULL	increased generation of;; advanced			NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
52966	5	334853	6	NULL	NULL	0	NULL	statement 1	NULL		involves	NULL				glucose flux	NULL	increased			NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
52967	6	334853	6	NULL	NULL	0	NULL	statement 5	NULL		occurs through	NULL				aldose reductase pathway	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
52968	7	334853	6	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				glutamine:fructose-6-phosphate amidotransferase	NULL	increased activity of 			NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
52969	8	334853	6	NULL	NULL	0	NULL	statement 7	NULL		leads to	NULL				insulin resistance	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
52970	9	334853	6	NULL	NULL	0	NULL	statement 1	NULL		involves	NULL				NFkappaB	NULL	activation of			NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
52971	10	334853	6	NULL	NULL	0	NULL	statement 9	NULL		leads to	NULL				cytokines	NULL	nuclear transcription of 			NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
52972	11	334853	6	NULL	NULL	0	NULL	statement 9	NULL		leads to	NULL				inflammatory cytokines	NULL	nuclear transcription of			NULL		0	NULL	NULL	NULL	gw70_pnas_103_1_218_s_36	16373499	Pathophysiological mechanisms for hyperglycemia-induced ED via generation of ROS involve: ( i) protein kinase C activation, ( ii) increased generation of advanced glycation end products, ( iii) increased glucose flux through the aldose reductase pathway, ( iv) increased activity of glutamine:fructose-6-phosphate amidotransferase leading to insulin resistance, and ( v) activation of NFkappaB leading to nuclear transcription of cytokines and inflammatory mediators.	transcription
51746	1	334854	5	NULL	NULL	0	NULL	OXA-10 enzyme	NULL		bind	NULL				metal	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1546_1_132_s_216	11257516	In both OXA-2 and -3, the histidine and one of the two glutamates involved in metal binding in OXA-10 enzyme are replaced by arginine and aspartate, respectively.	transcription
51747	2	334854	5	NULL	NULL	0	NULL	histidine	NULL		is involved in	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1546_1_132_s_216	11257516	In both OXA-2 and -3, the histidine and one of the two glutamates involved in metal binding in OXA-10 enzyme are replaced by arginine and aspartate, respectively.	transcription
51748	3	334854	5	NULL	NULL	0	NULL	glutamate	NULL		is involved in	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1546_1_132_s_216	11257516	In both OXA-2 and -3, the histidine and one of the two glutamates involved in metal binding in OXA-10 enzyme are replaced by arginine and aspartate, respectively.	transcription
52555	1	334855	6	NULL	NULL	0	NULL		NULL		produces	NULL		V67K		inhibitory effect	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_26_24108_s_95	11313347	On the other hand, an additional positive charge (V67K) produces a clear inhibitory effect (Fig.  3 c) consistent with the effects of the mutations replacing glutamates/aspartates with lysines/histidines ( 9).	transcription
51749	1	334856	5	NULL	NULL	0	NULL	L-glutamate	NULL	uptake of	is inhibited by	NULL				D-leucine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_15_4071_s_160	12107123	Uptake of L-glutamate was inhibited by D-leucine, D-alanine, D-histidine, and D-alpha-aminobutyrate, but not by D-glutamate.	transcription
51750	2	334856	5	NULL	NULL	0	NULL	L-glutamate	NULL	uptake of	is inhibited by	NULL				D-alanine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_15_4071_s_160	12107123	Uptake of L-glutamate was inhibited by D-leucine, D-alanine, D-histidine, and D-alpha-aminobutyrate, but not by D-glutamate.	transcription
51751	3	334856	5	NULL	NULL	0	NULL	L-glutamate	NULL	uptake of	is inhibited by	NULL				D-histidine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_15_4071_s_160	12107123	Uptake of L-glutamate was inhibited by D-leucine, D-alanine, D-histidine, and D-alpha-aminobutyrate, but not by D-glutamate.	transcription
51752	4	334856	5	NULL	NULL	0	NULL	L-glutamate	NULL	uptake of	is inhibited by	NULL				D-alpha-aminobutyrate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_15_4071_s_160	12107123	Uptake of L-glutamate was inhibited by D-leucine, D-alanine, D-histidine, and D-alpha-aminobutyrate, but not by D-glutamate.	transcription
51753	5	334856	5	NULL	NULL	0	NULL	L-glutamate	NULL	uptake of	is not inhibited by	NULL				D-glutamate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_15_4071_s_160	12107123	Uptake of L-glutamate was inhibited by D-leucine, D-alanine, D-histidine, and D-alpha-aminobutyrate, but not by D-glutamate.	transcription
52556	1	334856	6	NULL	NULL	0	NULL	D-leucine	NULL		inhibits	NULL				L-glutamate	NULL	uptake of 			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_15_4071_s_160	12107123	Uptake of L-glutamate was inhibited by D-leucine, D-alanine, D-histidine, and D-alpha-aminobutyrate, but not by D-glutamate.	transcription
52557	2	334856	6	NULL	NULL	0	NULL	D-alanine	NULL		inhibits	NULL				L-glutamate	NULL	uptake of 			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_15_4071_s_160	12107123	Uptake of L-glutamate was inhibited by D-leucine, D-alanine, D-histidine, and D-alpha-aminobutyrate, but not by D-glutamate.	transcription
52558	3	334856	6	NULL	NULL	0	NULL	D-histidine	NULL		inhibits	NULL				L-glutamate	NULL	uptake of 			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_15_4071_s_160	12107123	Uptake of L-glutamate was inhibited by D-leucine, D-alanine, D-histidine, and D-alpha-aminobutyrate, but not by D-glutamate.	transcription
52559	4	334856	6	NULL	NULL	0	NULL	 D-alpha-aminobutyrate	NULL		inhibits	NULL				L-glutamate	NULL	uptake of 			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_15_4071_s_160	12107123	Uptake of L-glutamate was inhibited by D-leucine, D-alanine, D-histidine, and D-alpha-aminobutyrate, but not by D-glutamate.	transcription
52560	5	334856	6	NULL	NULL	0	NULL	D-glutamate	NULL		does not inhibit	NULL				L-glutamate	NULL	uptake of 			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_15_4071_s_160	12107123	Uptake of L-glutamate was inhibited by D-leucine, D-alanine, D-histidine, and D-alpha-aminobutyrate, but not by D-glutamate.	transcription
51754	1	334857	5	NULL	NULL	0	NULL	RPE65	NULL	mutant	abolishes	NULL		histidine residues;;glutamate residues		RPE65	NULL	isomerohydrolase activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_5_2835_s_232	16319067	However, recent studies demonstrated that mutations at the conserved histidine and glutamate residues in RPE65 abolish its isomerohydrolase activity, suggesting that these conserved histidine and aspartate/glutamate residues may be located in the iron-binding site in RPE65 ( ,  ).	transcription
51755	2	334857	5	NULL	NULL	0	NULL	RPE65	NULL		is located in	NULL	may be	histidine residues;;glutamate residues		RPE65	NULL		iron-binding site		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_5_2835_s_232	16319067	However, recent studies demonstrated that mutations at the conserved histidine and glutamate residues in RPE65 abolish its isomerohydrolase activity, suggesting that these conserved histidine and aspartate/glutamate residues may be located in the iron-binding site in RPE65 ( ,  ).	transcription
52561	1	334857	6	NULL	NULL	0	NULL	RPE65	NULL		exhibits	NULL				isomerohydrolase activity	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_5_2835_s_232	16319067	However, recent studies demonstrated that mutations at the conserved histidine and glutamate residues in RPE65 abolish its isomerohydrolase activity, suggesting that these conserved histidine and aspartate/glutamate residues may be located in the iron-binding site in RPE65 ( ,  ).	transcription
52562	2	334857	6	NULL	NULL	0	NULL	RPE65	NULL	mutation of	abolishes	NULL		hisitdine residues		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_5_2835_s_232	16319067	However, recent studies demonstrated that mutations at the conserved histidine and glutamate residues in RPE65 abolish its isomerohydrolase activity, suggesting that these conserved histidine and aspartate/glutamate residues may be located in the iron-binding site in RPE65 ( ,  ).	transcription
52563	3	334857	6	NULL	NULL	0	NULL	RPE65	NULL	mutation of	abolishes	NULL		glutamate residues		statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_5_2835_s_232	16319067	However, recent studies demonstrated that mutations at the conserved histidine and glutamate residues in RPE65 abolish its isomerohydrolase activity, suggesting that these conserved histidine and aspartate/glutamate residues may be located in the iron-binding site in RPE65 ( ,  ).	transcription
51759	1	334858	5	NULL	NULL	0	NULL	histidine	NULL		block	NULL				3H-glutamine	NULL	transport of 			NULL	transfected cells	0	NULL	NULL	NULL	gw60_cell_99_7_769_s_158	10619430	Similar concentrations of  histidine block the transport of 3H-glutamine by transfected and untransfected cells whereas  glutamate has little effect on either.	transcription
51760	2	334858	5	NULL	NULL	0	NULL	histidine	NULL		block	NULL				3H-glutamine	NULL	transport of			NULL	untransfected cells	0	NULL	NULL	NULL	gw60_cell_99_7_769_s_158	10619430	Similar concentrations of  histidine block the transport of 3H-glutamine by transfected and untransfected cells whereas  glutamate has little effect on either.	transcription
52564	1	334858	6	NULL	NULL	0	NULL	hisitidine	NULL		blocks	NULL				3H-glutamine	NULL	transport of 			NULL		0	NULL	NULL	NULL	gw60_cell_99_7_769_s_158	10619430	Similar concentrations of  histidine block the transport of 3H-glutamine by transfected and untransfected cells whereas  glutamate has little effect on either.	transcription
51761	1	334859	5	NULL	NULL	0	NULL	L-histidine	NULL		does not inhibit	NULL				L-[14]leucine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_15_4071_s_253	12107123	Also, uptake of L-[14]leucine was not inhibited by L-histidine, L-glutamate, L-glutamine, or L-proline ( 23).	transcription
51762	2	334859	5	NULL	NULL	0	NULL	L-glutamate	NULL		does not inhibit	NULL				L-[14]leucine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_15_4071_s_253	12107123	Also, uptake of L-[14]leucine was not inhibited by L-histidine, L-glutamate, L-glutamine, or L-proline ( 23).	transcription
51763	3	334859	5	NULL	NULL	0	NULL	L-glutamine	NULL		does not inhibit	NULL				L-[14]leucine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_15_4071_s_253	12107123	Also, uptake of L-[14]leucine was not inhibited by L-histidine, L-glutamate, L-glutamine, or L-proline ( 23).	transcription
51764	4	334859	5	NULL	NULL	0	NULL	L-proline	NULL		does not inhibit	NULL				L-[14]leucine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_15_4071_s_253	12107123	Also, uptake of L-[14]leucine was not inhibited by L-histidine, L-glutamate, L-glutamine, or L-proline ( 23).	transcription
52565	1	334859	6	NULL	NULL	0	NULL	L-histidine	NULL		does not inhibit	NULL				L-[14]leucine	NULL	uptake of 			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_15_4071_s_253	12107123	Also, uptake of L-[14]leucine was not inhibited by L-histidine, L-glutamate, L-glutamine, or L-proline ( 23).	transcription
52566	2	334859	6	NULL	NULL	0	NULL	L-glutamate	NULL		does not inhibit	NULL				L-[14]leucine	NULL	uptake of 			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_15_4071_s_253	12107123	Also, uptake of L-[14]leucine was not inhibited by L-histidine, L-glutamate, L-glutamine, or L-proline ( 23).	transcription
52567	3	334859	6	NULL	NULL	0	NULL	L-glutamine	NULL		does not inhibit	NULL				L-[14]leucine	NULL	uptake of 			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_15_4071_s_253	12107123	Also, uptake of L-[14]leucine was not inhibited by L-histidine, L-glutamate, L-glutamine, or L-proline ( 23).	transcription
52568	4	334859	6	NULL	NULL	0	NULL	 L-proline	NULL		does not inhibit	NULL				L-[14]leucine	NULL	uptake of 			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_15_4071_s_253	12107123	Also, uptake of L-[14]leucine was not inhibited by L-histidine, L-glutamate, L-glutamine, or L-proline ( 23).	transcription
52569	1	334860	6	NULL	NULL	0	NULL	EAAT1	NULL		includes	NULL		Zn2+ binding site			NULL		histidine residues		NULL		0	NULL	NULL	NULL	gw60_molpharmacol_54_1_189_s_158	9658205	Thus, it may be concluded that the Zn2+ binding site on EAAT1 includes two histidine residues and the differential inhibition of glutamate transporter subtypes may be explained by the presence or absence of a histidine residue corresponding to position 156 of EAAT1.	transcription
51788	1	334861	5	NULL	NULL	0	NULL	glycine	NULL	conserved	allows	NULL				beta-turn	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_31_28280_s_250	12034745	The glutamate is required for catalysis, and the conserved glycine allows the formation of a beta-turn that brings the zinc ligands together; in addition, water is used as a nucleophile, which is bound by a single zinc ion ligated to the three histidines ( 26).	transcription
51789	2	334861	5	NULL	NULL	0	NULL	beta-turn	NULL		brings together	NULL				zinc ligands	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_31_28280_s_250	12034745	The glutamate is required for catalysis, and the conserved glycine allows the formation of a beta-turn that brings the zinc ligands together; in addition, water is used as a nucleophile, which is bound by a single zinc ion ligated to the three histidines ( 26).	transcription
51790	3	334861	5	NULL	NULL	0	NULL	water	NULL		acts as	NULL				nucleophile	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_31_28280_s_250	12034745	The glutamate is required for catalysis, and the conserved glycine allows the formation of a beta-turn that brings the zinc ligands together; in addition, water is used as a nucleophile, which is bound by a single zinc ion ligated to the three histidines ( 26).	transcription
51791	4	334861	5	NULL	NULL	0	NULL	zinc ion	NULL	single	is ligated to	NULL				histidines	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_31_28280_s_250	12034745	The glutamate is required for catalysis, and the conserved glycine allows the formation of a beta-turn that brings the zinc ligands together; in addition, water is used as a nucleophile, which is bound by a single zinc ion ligated to the three histidines ( 26).	transcription
51792	5	334861	5	NULL	NULL	0	NULL	water	NULL		is bound by	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_31_28280_s_250	12034745	The glutamate is required for catalysis, and the conserved glycine allows the formation of a beta-turn that brings the zinc ligands together; in addition, water is used as a nucleophile, which is bound by a single zinc ion ligated to the three histidines ( 26).	transcription
52570	1	334861	6	NULL	NULL	0	NULL	zinc ion	NULL	single	is ligated to	NULL				histidine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_31_28280_s_250	12034745	The glutamate is required for catalysis, and the conserved glycine allows the formation of a beta-turn that brings the zinc ligands together; in addition, water is used as a nucleophile, which is bound by a single zinc ion ligated to the three histidines ( 26).	transcription
52571	2	334861	6	NULL	NULL	0	NULL	water	NULL		bind	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_31_28280_s_250	12034745	The glutamate is required for catalysis, and the conserved glycine allows the formation of a beta-turn that brings the zinc ligands together; in addition, water is used as a nucleophile, which is bound by a single zinc ion ligated to the three histidines ( 26).	transcription
52572	3	334861	6	NULL	NULL	0	NULL	glycine	NULL	conserved	allows	NULL					NULL	formation of	beta-turn		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_31_28280_s_250	12034745	The glutamate is required for catalysis, and the conserved glycine allows the formation of a beta-turn that brings the zinc ligands together; in addition, water is used as a nucleophile, which is bound by a single zinc ion ligated to the three histidines ( 26).	transcription
52573	4	334861	6	NULL	NULL	0	NULL	statement 3	NULL		brings together	NULL				zinc ligands 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_31_28280_s_250	12034745	The glutamate is required for catalysis, and the conserved glycine allows the formation of a beta-turn that brings the zinc ligands together; in addition, water is used as a nucleophile, which is bound by a single zinc ion ligated to the three histidines ( 26).	transcription
51793	1	334862	5	NULL	NULL	0	NULL	glutamate	NULL		plays a role in	NULL				idiophase conditions	NULL	generation of			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_6_2596_s_175	11375168	Study of NAD- and NADP-glutamate dehydrogenase showed that glutamate and histidine play a key role in generation of idiophase conditions by the formation of alpha-ketoglutarate, which stimulates aflatoxin formation by inhibition of the tricarboxylic acid cycle ( 3).	transcription
51794	2	334862	5	NULL	NULL	0	NULL	histidine	NULL		plays a role in	NULL				idiophase conditions	NULL	generation of			NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_67_6_2596_s_175	11375168	Study of NAD- and NADP-glutamate dehydrogenase showed that glutamate and histidine play a key role in generation of idiophase conditions by the formation of alpha-ketoglutarate, which stimulates aflatoxin formation by inhibition of the tricarboxylic acid cycle ( 3).	transcription
51795	3	334862	5	NULL	NULL	0	NULL	statement 1	NULL		occurs by	NULL				alpha-ketoglutarate	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_6_2596_s_175	11375168	Study of NAD- and NADP-glutamate dehydrogenase showed that glutamate and histidine play a key role in generation of idiophase conditions by the formation of alpha-ketoglutarate, which stimulates aflatoxin formation by inhibition of the tricarboxylic acid cycle ( 3).	transcription
51796	4	334862	5	NULL	NULL	0	NULL	statement 2	NULL		occurs by	NULL				alpha-ketoglutarate	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_6_2596_s_175	11375168	Study of NAD- and NADP-glutamate dehydrogenase showed that glutamate and histidine play a key role in generation of idiophase conditions by the formation of alpha-ketoglutarate, which stimulates aflatoxin formation by inhibition of the tricarboxylic acid cycle ( 3).	transcription
51797	5	334862	5	NULL	NULL	0	NULL	alpha-ketoglutarate	NULL		inhibits	NULL				tricarboxylic acid cycle	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_6_2596_s_175	11375168	Study of NAD- and NADP-glutamate dehydrogenase showed that glutamate and histidine play a key role in generation of idiophase conditions by the formation of alpha-ketoglutarate, which stimulates aflatoxin formation by inhibition of the tricarboxylic acid cycle ( 3).	transcription
51798	6	334862	5	NULL	NULL	0	NULL	statement 5	NULL		stimulates	NULL				aflatoxin	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_6_2596_s_175	11375168	Study of NAD- and NADP-glutamate dehydrogenase showed that glutamate and histidine play a key role in generation of idiophase conditions by the formation of alpha-ketoglutarate, which stimulates aflatoxin formation by inhibition of the tricarboxylic acid cycle ( 3).	transcription
52574	1	334862	6	NULL	NULL	0	NULL	glutamate	NULL		plays a role in	NULL				alpha-ketoglutarate	NULL	formation of 			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_6_2596_s_175	11375168	Study of NAD- and NADP-glutamate dehydrogenase showed that glutamate and histidine play a key role in generation of idiophase conditions by the formation of alpha-ketoglutarate, which stimulates aflatoxin formation by inhibition of the tricarboxylic acid cycle ( 3).	transcription
52575	2	334862	6	NULL	NULL	0	NULL	histidine	NULL		plays a role in	NULL				alpha-ketoglutarate	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_6_2596_s_175	11375168	Study of NAD- and NADP-glutamate dehydrogenase showed that glutamate and histidine play a key role in generation of idiophase conditions by the formation of alpha-ketoglutarate, which stimulates aflatoxin formation by inhibition of the tricarboxylic acid cycle ( 3).	transcription
52576	3	334862	6	NULL	NULL	0	NULL	statement 1	NULL		stimulates	NULL				aflatoxin	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_6_2596_s_175	11375168	Study of NAD- and NADP-glutamate dehydrogenase showed that glutamate and histidine play a key role in generation of idiophase conditions by the formation of alpha-ketoglutarate, which stimulates aflatoxin formation by inhibition of the tricarboxylic acid cycle ( 3).	transcription
52577	4	334862	6	NULL	NULL	0	NULL	statement 3	NULL		occurs via 	NULL				tricarboxylic acid cycle	NULL	inhibition of 			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_6_2596_s_175	11375168	Study of NAD- and NADP-glutamate dehydrogenase showed that glutamate and histidine play a key role in generation of idiophase conditions by the formation of alpha-ketoglutarate, which stimulates aflatoxin formation by inhibition of the tricarboxylic acid cycle ( 3).	transcription
52578	5	334862	6	NULL	NULL	0	NULL	statement 2	NULL		stimulates	NULL				aflatoxin	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_6_2596_s_175	11375168	Study of NAD- and NADP-glutamate dehydrogenase showed that glutamate and histidine play a key role in generation of idiophase conditions by the formation of alpha-ketoglutarate, which stimulates aflatoxin formation by inhibition of the tricarboxylic acid cycle ( 3).	transcription
52579	6	334862	6	NULL	NULL	0	NULL	statement 4	NULL		occurs via	NULL				tricarboxylic acid cycle	NULL	inhibition of 			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_6_2596_s_175	11375168	Study of NAD- and NADP-glutamate dehydrogenase showed that glutamate and histidine play a key role in generation of idiophase conditions by the formation of alpha-ketoglutarate, which stimulates aflatoxin formation by inhibition of the tricarboxylic acid cycle ( 3).	transcription
51799	1	334863	5	NULL	NULL	0	NULL	glutamate	NULL		repress	NULL					NULL	expression of		GOGAT	NULL	Salmonella typhimurium	NULL	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
51800	2	334863	5	NULL	NULL	0	NULL	glutamate	NULL		repress	NULL					NULL	expression of		GOGAT	NULL	Klebsiella aerogenes	0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
51801	3	334863	5	NULL	NULL	0	NULL	statement 1	NULL		occurs during	NULL				N-limited growth	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
51802	4	334863	5	NULL	NULL	0	NULL	statement 2	NULL		occurs during	NULL				N-limited growth	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
51803	5	334863	5	NULL	NULL	0	NULL	arginine	NULL		is a type of	NULL				glutamate-generating nitrogen substrates	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
51804	6	334863	5	NULL	NULL	0	NULL	proline	NULL		is a type of	NULL				glutamate-generating nitrogen substrates	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
51805	7	334863	5	NULL	NULL	0	NULL	histidine	NULL		is a type of	NULL				glutamate-generating nitrogen substrates	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
51806	8	334863	5	NULL	NULL	0	NULL	arginine	NULL		repress	NULL					NULL	expression of		GOGAT	NULL	Salmonella typhimurium	NULL	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
51807	9	334863	5	NULL	NULL	0	NULL	arginine	NULL		repress	NULL					NULL	expression of		GOGAT	NULL	Klebsiella aerogenes	0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
51808	10	334863	5	NULL	NULL	0	NULL	statement 8	NULL		occurs during	NULL				N-limited growth	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
51809	11	334863	5	NULL	NULL	0	NULL	statement 9	NULL		occurs during	NULL				N-limited growth	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
51810	12	334863	5	NULL	NULL	0	NULL	proline	NULL		repress	NULL					NULL	expression of		GOGAT	NULL	Salmonella typhimurium	0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
51811	13	334863	5	NULL	NULL	0	NULL	proline	NULL		repress	NULL					NULL	expression of		GOGAT	NULL	Klebsiella aerogenes	0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
51812	14	334863	5	NULL	NULL	0	NULL	statement 12	NULL		occurs during	NULL				N-limited growth	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
51813	15	334863	5	NULL	NULL	0	NULL	statement 13	NULL		occurs during	NULL				N-limited growth	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
51814	16	334863	5	NULL	NULL	0	NULL	histidine	NULL		repress	NULL					NULL	expression of		GOGAT	NULL	Salmonella typhimurium	0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
51815	17	334863	5	NULL	NULL	0	NULL	histidine	NULL		repress	NULL					NULL	expression of		GOGAT	NULL	Klebsiella aerogenes	0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
51816	18	334863	5	NULL	NULL	0	NULL	statement 16	NULL		occurs during	NULL				N-limited growth	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
51817	19	334863	5	NULL	NULL	0	NULL	statement 17	NULL		occurs during	NULL				N-limited growth	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
52580	1	334863	6	NULL	NULL	0	NULL	glutamate	NULL		repress	NULL				GOGAT	NULL	expression of 			NULL	Salmonella typhimurium	0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
52581	2	334863	6	NULL	NULL	0	NULL	arginine	NULL		repress	NULL				GOGAT	NULL	expression of 			NULL	Salmonella typhimurium	0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
52582	3	334863	6	NULL	NULL	0	NULL	proline	NULL		repress	NULL				GOGAT	NULL	expression of 			NULL	Salmonella typhimurium	0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
52583	4	334863	6	NULL	NULL	0	NULL	histidine	NULL		repress	NULL				GOGAT	NULL	expression of 			NULL	Salmonella typhimurium	NULL	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
52584	5	334863	6	NULL	NULL	0	NULL	arginine	NULL		is a type of 	NULL				glutamate-generating nitrogen substrate	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
52585	6	334863	6	NULL	NULL	0	NULL	proline	NULL		is a type of 	NULL				glutamate-generating nitrogen substrate	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
52586	7	334863	6	NULL	NULL	0	NULL	histidine	NULL		is a type of 	NULL				glutamate-generating nitrogen substrate	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
52587	8	334863	6	NULL	NULL	0	NULL	glutamate	NULL		repress	NULL				GOGAT	NULL	expression of 			NULL	Klebsiella aerogenes 	0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
52588	9	334863	6	NULL	NULL	0	NULL	arginine	NULL		repress	NULL				GOGAT	NULL	expression of 			NULL	Klebsiella aerogenes 	0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
52589	10	334863	6	NULL	NULL	0	NULL	proline	NULL		repress	NULL				GOGAT	NULL	expression of 			NULL	Klebsiella aerogenes 	0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
52590	11	334863	6	NULL	NULL	0	NULL	histidine	NULL		repress	NULL				GOGAT	NULL	expression of 			NULL	Klebsiella aerogenes 	0	NULL	NULL	NULL	gw60_applenvironmicrob_65_3_1099_s_319	0010049869	The observation that glutamate or glutamate-generating nitrogen substrates (arginine, proline, or histidine) repress GOGAT expression in  Salmonella typhimurium and  Klebsiella aerogenes during N-limited growth ( 6,  7) is in agreement with this hypothesis.	transcription
52591	1	334864	6	NULL	NULL	0	NULL		NULL	mutation of	causes	NULL		active site histidine		allosteric interactions	NULL	loss of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_17701_s_103	15749695	Since the active site histidine and glutamate mutations caused a loss of allosteric interactions, we tested whether the mutant enzymes could still be activated by ATP and triphosphate.	transcription
52592	2	334864	6	NULL	NULL	0	NULL		NULL	mutation of	causes	NULL		active site glutamate		allosteric interactions	NULL	loss of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_17701_s_103	15749695	Since the active site histidine and glutamate mutations caused a loss of allosteric interactions, we tested whether the mutant enzymes could still be activated by ATP and triphosphate.	transcription
51818	1	334865	5	NULL	NULL	0	NULL	histidine	NULL		activates	NULL				aspartate	NULL		Q701H		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_37_27471_s_281	16864587	For example, one could envision that the histidine activates the aspartate (Q701H) or the glutamate (double mutant) and therefore induces different levels of ATPase activity in a distance-dependent manner.	transcription
51819	2	334865	5	NULL	NULL	0	NULL	histidine	NULL		activates	NULL				glutamate	NULL	double mutant			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_37_27471_s_281	16864587	For example, one could envision that the histidine activates the aspartate (Q701H) or the glutamate (double mutant) and therefore induces different levels of ATPase activity in a distance-dependent manner.	transcription
51820	3	334865	5	NULL	NULL	0	NULL	statement 1	NULL		induce	NULL				ATPase activity	NULL	different levels of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_37_27471_s_281	16864587	For example, one could envision that the histidine activates the aspartate (Q701H) or the glutamate (double mutant) and therefore induces different levels of ATPase activity in a distance-dependent manner.	transcription
51821	4	334865	5	NULL	NULL	0	NULL	statement 2	NULL		induce	NULL				ATPase activity	NULL	different levels of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_37_27471_s_281	16864587	For example, one could envision that the histidine activates the aspartate (Q701H) or the glutamate (double mutant) and therefore induces different levels of ATPase activity in a distance-dependent manner.	transcription
52593	1	334865	6	NULL	NULL	0	NULL	histidine	NULL		activates	NULL					NULL		aspartate (Q701H)		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_37_27471_s_281	16864587	For example, one could envision that the histidine activates the aspartate (Q701H) or the glutamate (double mutant) and therefore induces different levels of ATPase activity in a distance-dependent manner.	transcription
52594	2	334865	6	NULL	NULL	0	NULL	histidine	NULL		activates	NULL					NULL		glutamate		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_37_27471_s_281	16864587	For example, one could envision that the histidine activates the aspartate (Q701H) or the glutamate (double mutant) and therefore induces different levels of ATPase activity in a distance-dependent manner.	transcription
52595	3	334865	6	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_37_27471_s_281	16864587	For example, one could envision that the histidine activates the aspartate (Q701H) or the glutamate (double mutant) and therefore induces different levels of ATPase activity in a distance-dependent manner.	transcription
52596	4	334865	6	NULL	NULL	0	NULL	statement 1	NULL		induces	NULL				ATPase 	NULL	activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_37_27471_s_281	16864587	For example, one could envision that the histidine activates the aspartate (Q701H) or the glutamate (double mutant) and therefore induces different levels of ATPase activity in a distance-dependent manner.	transcription
52597	5	334865	6	NULL	NULL	0	NULL	statement 2	NULL		induces	NULL				ATPase 	NULL	activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_37_27471_s_281	16864587	For example, one could envision that the histidine activates the aspartate (Q701H) or the glutamate (double mutant) and therefore induces different levels of ATPase activity in a distance-dependent manner.	transcription
51822	1	334866	5	NULL	NULL	0	NULL	cysteine	NULL		is an active site in	NULL				glutamine	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_13_7599_s_32	12799468	The active-site cysteine  covalently binds glutamine, and the histidine, initially protonated, donates a  proton to the amide group of glutamine to produce ammonia and glutamate.	transcription
51823	2	334866	5	NULL	NULL	0	NULL	glutamine	NULL		bind	NULL	covalently	cysteine		histidine	NULL	protonated			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_13_7599_s_32	12799468	The active-site cysteine  covalently binds glutamine, and the histidine, initially protonated, donates a  proton to the amide group of glutamine to produce ammonia and glutamate.	transcription
51824	3	334866	5	NULL	NULL	0	NULL	histidine	NULL	protonated	donates	NULL				proton	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_100_13_7599_s_32	12799468	The active-site cysteine  covalently binds glutamine, and the histidine, initially protonated, donates a  proton to the amide group of glutamine to produce ammonia and glutamate.	transcription
51825	4	334866	5	NULL	NULL	0	NULL	proton	NULL		is donated to	NULL				glutamine	NULL		amide group		NULL		0	NULL	NULL	NULL	gw70_pnas_100_13_7599_s_32	12799468	The active-site cysteine  covalently binds glutamine, and the histidine, initially protonated, donates a  proton to the amide group of glutamine to produce ammonia and glutamate.	transcription
51826	5	334866	5	NULL	NULL	0	NULL	statement 4	NULL		produce	NULL				ammonia	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_100_13_7599_s_32	12799468	The active-site cysteine  covalently binds glutamine, and the histidine, initially protonated, donates a  proton to the amide group of glutamine to produce ammonia and glutamate.	transcription
51827	6	334866	5	NULL	NULL	0	NULL	statement 4	NULL		produce	NULL				glutamate	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_100_13_7599_s_32	12799468	The active-site cysteine  covalently binds glutamine, and the histidine, initially protonated, donates a  proton to the amide group of glutamine to produce ammonia and glutamate.	transcription
51828	7	334866	5	NULL	NULL	0	NULL	statement 5	NULL		occurs along with	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_100_13_7599_s_32	12799468	The active-site cysteine  covalently binds glutamine, and the histidine, initially protonated, donates a  proton to the amide group of glutamine to produce ammonia and glutamate.	transcription
52598	1	334866	6	NULL	NULL	0	NULL		NULL		bind	NULL	covalently	active-site cysteine		glutamine	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_100_13_7599_s_32	12799468	The active-site cysteine  covalently binds glutamine, and the histidine, initially protonated, donates a  proton to the amide group of glutamine to produce ammonia and glutamate.	transcription
52626	2	334866	6	NULL	NULL	0	NULL		NULL	protonated	donates 	NULL		histidine		proton	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_100_13_7599_s_32	12799468	The active-site cysteine  covalently binds glutamine, and the histidine, initially protonated, donates a  proton to the amide group of glutamine to produce ammonia and glutamate.	transcription
52627	3	334866	6	NULL	NULL	0	NULL	statement 2	NULL		occurs to	NULL				glutamine	NULL		amide group		NULL		0	NULL	NULL	NULL	gw70_pnas_100_13_7599_s_32	12799468	The active-site cysteine  covalently binds glutamine, and the histidine, initially protonated, donates a  proton to the amide group of glutamine to produce ammonia and glutamate.	transcription
52936	4	334866	6	NULL	NULL	0	NULL	statement 2	NULL		produce	NULL				ammonia	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_100_13_7599_s_32	12799468	The active-site cysteine  covalently binds glutamine, and the histidine, initially protonated, donates a  proton to the amide group of glutamine to produce ammonia and glutamate.	transcription
52937	5	334866	6	NULL	NULL	0	NULL	statement 2	NULL		produce	NULL				glutamate	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_100_13_7599_s_32	12799468	The active-site cysteine  covalently binds glutamine, and the histidine, initially protonated, donates a  proton to the amide group of glutamine to produce ammonia and glutamate.	transcription
51829	1	334867	5	NULL	NULL	0	NULL	Im gene	NULL		is homologous to	NULL				AOX	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_2_1190_s_30	11698414	The limited but significant homology of the  Im gene to the AOX includes several glutamate and histidine residues located in positions that could contribute to iron binding.	transcription
52628	1	334867	6	NULL	NULL	0	NULL	Im gene	NULL		is homologous to	NULL				AOX	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_2_1190_s_30	11698414	The limited but significant homology of the  Im gene to the AOX includes several glutamate and histidine residues located in positions that could contribute to iron binding.	transcription
51840	1	334868	5	NULL	NULL	0	NULL	Nt-FDH	NULL		is replaced with	NULL		histidine		Nt-FDH	NULL		alanine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_26_24030_s_8	11320079	Site-directed mutagenesis experiments showed that replacement of the histidine with alanine, asparagine, aspartate, glutamate, glutamine, or arginine in Nt-FDH resulted in expression of insoluble proteins.	transcription
51841	2	334868	5	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				insoluble proteins	NULL	expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_26_24030_s_8	11320079	Site-directed mutagenesis experiments showed that replacement of the histidine with alanine, asparagine, aspartate, glutamate, glutamine, or arginine in Nt-FDH resulted in expression of insoluble proteins.	transcription
51842	3	334868	5	NULL	NULL	0	NULL	Nt-FDH	NULL		is replaced with	NULL		histidine		Nt-FDH	NULL		asparagine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_26_24030_s_8	11320079	Site-directed mutagenesis experiments showed that replacement of the histidine with alanine, asparagine, aspartate, glutamate, glutamine, or arginine in Nt-FDH resulted in expression of insoluble proteins.	transcription
51843	4	334868	5	NULL	NULL	0	NULL	statement 3	NULL		results in	NULL				insoluble proteins	NULL	expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_26_24030_s_8	11320079	Site-directed mutagenesis experiments showed that replacement of the histidine with alanine, asparagine, aspartate, glutamate, glutamine, or arginine in Nt-FDH resulted in expression of insoluble proteins.	transcription
51844	5	334868	5	NULL	NULL	0	NULL	Nt-FDH	NULL		is replaced with	NULL		histidine		Nt-FDH	NULL		aspartate		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_26_24030_s_8	11320079	Site-directed mutagenesis experiments showed that replacement of the histidine with alanine, asparagine, aspartate, glutamate, glutamine, or arginine in Nt-FDH resulted in expression of insoluble proteins.	transcription
51845	6	334868	5	NULL	NULL	0	NULL	statement 5	NULL		results in	NULL				insoluble proteins	NULL	expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_26_24030_s_8	11320079	Site-directed mutagenesis experiments showed that replacement of the histidine with alanine, asparagine, aspartate, glutamate, glutamine, or arginine in Nt-FDH resulted in expression of insoluble proteins.	transcription
51846	7	334868	5	NULL	NULL	0	NULL	Nt-FDH	NULL		is replaced with	NULL		histidine		Nt-FDH	NULL		glutamate		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_26_24030_s_8	11320079	Site-directed mutagenesis experiments showed that replacement of the histidine with alanine, asparagine, aspartate, glutamate, glutamine, or arginine in Nt-FDH resulted in expression of insoluble proteins.	transcription
51847	8	334868	5	NULL	NULL	0	NULL	statement 7	NULL		results in	NULL				insoluble proteins	NULL	expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_26_24030_s_8	11320079	Site-directed mutagenesis experiments showed that replacement of the histidine with alanine, asparagine, aspartate, glutamate, glutamine, or arginine in Nt-FDH resulted in expression of insoluble proteins.	transcription
51848	9	334868	5	NULL	NULL	0	NULL	Nt-FDH	NULL		is replaced with	NULL		histidine		Nt-FDH	NULL		glutamine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_26_24030_s_8	11320079	Site-directed mutagenesis experiments showed that replacement of the histidine with alanine, asparagine, aspartate, glutamate, glutamine, or arginine in Nt-FDH resulted in expression of insoluble proteins.	transcription
51849	10	334868	5	NULL	NULL	0	NULL	statement 9	NULL		results in	NULL				insoluble proteins	NULL	expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_26_24030_s_8	11320079	Site-directed mutagenesis experiments showed that replacement of the histidine with alanine, asparagine, aspartate, glutamate, glutamine, or arginine in Nt-FDH resulted in expression of insoluble proteins.	transcription
51850	11	334868	5	NULL	NULL	0	NULL	Nt-FDH	NULL		is replaced with	NULL		histidine		Nt-FDH	NULL		arginine 		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_26_24030_s_8	11320079	Site-directed mutagenesis experiments showed that replacement of the histidine with alanine, asparagine, aspartate, glutamate, glutamine, or arginine in Nt-FDH resulted in expression of insoluble proteins.	transcription
51851	12	334868	5	NULL	NULL	0	NULL	statement 11	NULL		results in	NULL				insoluble proteins	NULL	expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_26_24030_s_8	11320079	Site-directed mutagenesis experiments showed that replacement of the histidine with alanine, asparagine, aspartate, glutamate, glutamine, or arginine in Nt-FDH resulted in expression of insoluble proteins.	transcription
51830	1	334869	5	NULL	NULL	0	NULL	GLYT1b	NULL		is homologous to	NULL				DAT	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_22_22983_s_120	15031290	Based on the homology between GLYT1b and DAT, we targeted histidine residues and a select number of glutamate residues, which are predicted to be on the extracellular domains of GLYT1b and in similar locations to the Zn2+-binding residues of DAT.	transcription
52465	1	334870	5	NULL	NULL	0	NULL	xylose	NULL		interacts with	NULL		O-2		asparagine	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_10_9597_s_24	14668328	The data show that at the -1 subsite the O-3 of xylose makes a hydrogen bond with a highly conserved lysine and histidine, whereas O-2 interacts with an asparagine and a glutamate (which acts as the catalytic nucleophile) that are invariant in GH10 xylanases.	transcription
52466	2	334870	5	NULL	NULL	0	NULL	xylose	NULL		interacts with	NULL		O-2		glutamate	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_10_9597_s_24	14668328	The data show that at the -1 subsite the O-3 of xylose makes a hydrogen bond with a highly conserved lysine and histidine, whereas O-2 interacts with an asparagine and a glutamate (which acts as the catalytic nucleophile) that are invariant in GH10 xylanases.	transcription
52467	3	334870	5	NULL	NULL	0	NULL	glutamate	NULL		acts as	NULL				catalytic nucleophile	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_10_9597_s_24	14668328	The data show that at the -1 subsite the O-3 of xylose makes a hydrogen bond with a highly conserved lysine and histidine, whereas O-2 interacts with an asparagine and a glutamate (which acts as the catalytic nucleophile) that are invariant in GH10 xylanases.	transcription
52522	4	334870	5	NULL	NULL	0	NULL	xylose	NULL		hydrogen-bonds with	NULL		O-3		lysine	NULL	highly conserved			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_10_9597_s_24	14668328	The data show that at the -1 subsite the O-3 of xylose makes a hydrogen bond with a highly conserved lysine and histidine, whereas O-2 interacts with an asparagine and a glutamate (which acts as the catalytic nucleophile) that are invariant in GH10 xylanases.	transcription
52523	5	334870	5	NULL	NULL	0	NULL	xylose	NULL		hydrogen-bonds with	NULL		O-3		histidine	NULL	highly conserved			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_10_9597_s_24	14668328	The data show that at the -1 subsite the O-3 of xylose makes a hydrogen bond with a highly conserved lysine and histidine, whereas O-2 interacts with an asparagine and a glutamate (which acts as the catalytic nucleophile) that are invariant in GH10 xylanases.	transcription
52629	1	334870	6	NULL	NULL	0	NULL	xylose	NULL		bind	NULL		1 subsite the O-3		lysine 	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_10_9597_s_24	14668328	The data show that at the -1 subsite the O-3 of xylose makes a hydrogen bond with a highly conserved lysine and histidine, whereas O-2 interacts with an asparagine and a glutamate (which acts as the catalytic nucleophile) that are invariant in GH10 xylanases.	transcription
52630	2	334870	6	NULL	NULL	0	NULL	xylose	NULL		bind	NULL		1 subsite the O-3		histidine	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_10_9597_s_24	14668328	The data show that at the -1 subsite the O-3 of xylose makes a hydrogen bond with a highly conserved lysine and histidine, whereas O-2 interacts with an asparagine and a glutamate (which acts as the catalytic nucleophile) that are invariant in GH10 xylanases.	transcription
52631	3	334870	6	NULL	NULL	0	NULL	O-2	NULL		interacts with	NULL				asparagine	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_10_9597_s_24	14668328	The data show that at the -1 subsite the O-3 of xylose makes a hydrogen bond with a highly conserved lysine and histidine, whereas O-2 interacts with an asparagine and a glutamate (which acts as the catalytic nucleophile) that are invariant in GH10 xylanases.	transcription
52632	4	334870	6	NULL	NULL	0	NULL	O-2	NULL		interacts with	NULL				glutamate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_10_9597_s_24	14668328	The data show that at the -1 subsite the O-3 of xylose makes a hydrogen bond with a highly conserved lysine and histidine, whereas O-2 interacts with an asparagine and a glutamate (which acts as the catalytic nucleophile) that are invariant in GH10 xylanases.	transcription
52633	1	334871	6	NULL	NULL	0	NULL		NULL		does not show	NULL		D668E		ATPase activity	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_37_27471_s_54	16864587	Although the D668E mutant like the wild-type enzyme did not show ATPase activity, reintroduction of the histidine in the absence of the glutamate (Q701H) resulted in an ATPase-active enzyme, although at a reduced level compared with the double mutant (D668E/Q701H).	transcription
52634	2	334871	6	NULL	NULL	0	NULL		NULL		shows	NULL		Q701H		ATPase activity	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_37_27471_s_54	16864587	Although the D668E mutant like the wild-type enzyme did not show ATPase activity, reintroduction of the histidine in the absence of the glutamate (Q701H) resulted in an ATPase-active enzyme, although at a reduced level compared with the double mutant (D668E/Q701H).	transcription
52635	3	334871	6	NULL	NULL	0	NULL		NULL		shows	NULL		D668E/Q701H		ATPase activity	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_37_27471_s_54	16864587	Although the D668E mutant like the wild-type enzyme did not show ATPase activity, reintroduction of the histidine in the absence of the glutamate (Q701H) resulted in an ATPase-active enzyme, although at a reduced level compared with the double mutant (D668E/Q701H).	transcription
52636	4	334871	6	NULL	NULL	0	NULL	statement 2	NULL		is reduced as compared to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_37_27471_s_54	16864587	Although the D668E mutant like the wild-type enzyme did not show ATPase activity, reintroduction of the histidine in the absence of the glutamate (Q701H) resulted in an ATPase-active enzyme, although at a reduced level compared with the double mutant (D668E/Q701H).	transcription
51852	1	334872	5	NULL	NULL	0	NULL	fumarylacetoacetate hydrolase	NULL		is composed of	NULL		active site		catalytic triad	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50091_s_233	14506266	As described in detail by Timm and co-workers ( ,  ), the active site of fumarylacetoacetate hydrolase is composed of a catalytic triad consisting of a glutamate carboxylate that stabilizes a histidine base that directly activates a nucleophilic water molecule.	transcription
51853	2	334872	5	NULL	NULL	0	NULL	catalytic triad	NULL		consists of	NULL				glutamate carboxylate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50091_s_233	14506266	As described in detail by Timm and co-workers ( ,  ), the active site of fumarylacetoacetate hydrolase is composed of a catalytic triad consisting of a glutamate carboxylate that stabilizes a histidine base that directly activates a nucleophilic water molecule.	transcription
51854	3	334872	5	NULL	NULL	0	NULL	glutamate carboxylate	NULL		stabilize	NULL				histidine base	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50091_s_233	14506266	As described in detail by Timm and co-workers ( ,  ), the active site of fumarylacetoacetate hydrolase is composed of a catalytic triad consisting of a glutamate carboxylate that stabilizes a histidine base that directly activates a nucleophilic water molecule.	transcription
51855	4	334872	5	NULL	NULL	0	NULL	histidine base	NULL		activates	NULL	directly			water molecule	NULL	nucleophilic			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50091_s_233	14506266	As described in detail by Timm and co-workers ( ,  ), the active site of fumarylacetoacetate hydrolase is composed of a catalytic triad consisting of a glutamate carboxylate that stabilizes a histidine base that directly activates a nucleophilic water molecule.	transcription
52973	1	334872	6	NULL	NULL	0	NULL	fumarylacetoacetate hydrolase	NULL		is composed of	NULL		active site		catalytic triad	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50091_s_233	14506266	As described in detail by Timm and co-workers ( ,  ), the active site of fumarylacetoacetate hydrolase is composed of a catalytic triad consisting of a glutamate carboxylate that stabilizes a histidine base that directly activates a nucleophilic water molecule.	transcription
52974	2	334872	6	NULL	NULL	0	NULL	catalytic site 	NULL		consists of	NULL				glutamate carboxylate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50091_s_233	14506266	As described in detail by Timm and co-workers ( ,  ), the active site of fumarylacetoacetate hydrolase is composed of a catalytic triad consisting of a glutamate carboxylate that stabilizes a histidine base that directly activates a nucleophilic water molecule.	transcription
52975	3	334872	6	NULL	NULL	0	NULL	glutamate carboxylate	NULL		stabilize	NULL				histidine base	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50091_s_233	14506266	As described in detail by Timm and co-workers ( ,  ), the active site of fumarylacetoacetate hydrolase is composed of a catalytic triad consisting of a glutamate carboxylate that stabilizes a histidine base that directly activates a nucleophilic water molecule.	transcription
52976	4	334872	6	NULL	NULL	0	NULL	histidine base	NULL		activates	NULL	directly			water molecule	NULL	nucleophilic			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50091_s_233	14506266	As described in detail by Timm and co-workers ( ,  ), the active site of fumarylacetoacetate hydrolase is composed of a catalytic triad consisting of a glutamate carboxylate that stabilizes a histidine base that directly activates a nucleophilic water molecule.	transcription
51856	1	334876	5	NULL	NULL	0	NULL	AHR	NULL		bind	NULL		glutamate;;arginine;;histidine		DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_49_31657_s_229	8940186	We have demonstrated that the amino acids involved in DNA binding of the AHR and ARNT, glutamate, arginine, and histidine residues, are similar to those involved in amino acid/nucleotide interactions of other bHLH proteins.	transcription
51857	2	334876	5	NULL	NULL	0	NULL	ARNT	NULL		bind	NULL		glutamate;;arginine;;histidine		DNA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_49_31657_s_229	8940186	We have demonstrated that the amino acids involved in DNA binding of the AHR and ARNT, glutamate, arginine, and histidine residues, are similar to those involved in amino acid/nucleotide interactions of other bHLH proteins.	transcription
52637	1	334876	6	NULL	NULL	0	NULL	DNA	NULL		bind	NULL				AHR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_49_31657_s_229	8940186	We have demonstrated that the amino acids involved in DNA binding of the AHR and ARNT, glutamate, arginine, and histidine residues, are similar to those involved in amino acid/nucleotide interactions of other bHLH proteins.	transcription
52638	2	334876	6	NULL	NULL	0	NULL	DNA	NULL		bind	NULL				ARNT	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_49_31657_s_229	8940186	We have demonstrated that the amino acids involved in DNA binding of the AHR and ARNT, glutamate, arginine, and histidine residues, are similar to those involved in amino acid/nucleotide interactions of other bHLH proteins.	transcription
52506	1	334877	5	NULL	NULL	0	NULL	PH1704	NULL		is similar to	NULL		catalytic triad		papain type cysteine proteases	NULL		triads		NULL		0	NULL	NULL	NULL	gw60_pnas_97_26_14079_s_144	11114201	The catalytic triad in PH1704 shares the same handedness with the triads in papain type cysteine proteases, namely the cysteine interacts with deltaN, whereas the glutamate hydrogen-bonds with  N of the histidine (Fig.  4 D).	transcription
52507	2	334877	5	NULL	NULL	0	NULL	cysteine	NULL		interacts with	NULL					NULL		deltaN		NULL		0	NULL	NULL	NULL	gw60_pnas_97_26_14079_s_144	11114201	The catalytic triad in PH1704 shares the same handedness with the triads in papain type cysteine proteases, namely the cysteine interacts with deltaN, whereas the glutamate hydrogen-bonds with  N of the histidine (Fig.  4 D).	transcription
52508	3	334877	5	NULL	NULL	0	NULL	glutamate	NULL		hydrogen-bonds with	NULL				histidine	NULL		N		NULL		0	NULL	NULL	NULL	gw60_pnas_97_26_14079_s_144	11114201	The catalytic triad in PH1704 shares the same handedness with the triads in papain type cysteine proteases, namely the cysteine interacts with deltaN, whereas the glutamate hydrogen-bonds with  N of the histidine (Fig.  4 D).	transcription
52639	1	334877	6	NULL	NULL	0	NULL	cysteine	NULL		interacts with	NULL				deltaN	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_97_26_14079_s_144	11114201	The catalytic triad in PH1704 shares the same handedness with the triads in papain type cysteine proteases, namely the cysteine interacts with deltaN, whereas the glutamate hydrogen-bonds with  N of the histidine (Fig.  4 D).	transcription
52640	2	334877	6	NULL	NULL	0	NULL		NULL		bind	NULL		glutamate hydrogen			NULL		N of histidine		NULL		0	NULL	NULL	NULL	gw60_pnas_97_26_14079_s_144	11114201	The catalytic triad in PH1704 shares the same handedness with the triads in papain type cysteine proteases, namely the cysteine interacts with deltaN, whereas the glutamate hydrogen-bonds with  N of the histidine (Fig.  4 D).	transcription
52509	1	334878	5	NULL	NULL	0	NULL	alanine	NULL		inhibit	NULL	strongly			glutamine	NULL	transport of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52510	2	334878	5	NULL	NULL	0	NULL	serine	NULL		inhibit	NULL	strongly			glutamine	NULL	transport of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52511	3	334878	5	NULL	NULL	0	NULL	threonine	NULL		inhibit	NULL	strongly			glutamine	NULL	transport of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52512	4	334878	5	NULL	NULL	0	NULL	cysteine	NULL		inhibit	NULL	strongly			glutamine	NULL	transport of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52513	5	334878	5	NULL	NULL	0	NULL	asparagine	NULL		inhibit	NULL	strongly			glutamine	NULL	transport of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52514	6	334878	5	NULL	NULL	0	NULL	methionine	NULL		inhibit	NULL	strongly			glutamine	NULL	transport of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52515	7	334878	5	NULL	NULL	0	NULL	valine	NULL		inhibit	NULL	strongly			glutamine	NULL	transport of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52516	8	334878	5	NULL	NULL	0	NULL	glycine	NULL		inhibit	NULL				glutamine	NULL	transport of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52517	9	334878	5	NULL	NULL	0	NULL	proline	NULL		inhibit	NULL				glutamine	NULL	transport of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52518	10	334878	5	NULL	NULL	0	NULL	arginine	NULL		inhibit	NULL				glutamine	NULL	transport of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52519	11	334878	5	NULL	NULL	0	NULL	histidine	NULL		inhibit	NULL				glutamine	NULL	transport of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52520	12	334878	5	NULL	NULL	0	NULL	glutamate	NULL		inhibit	NULL				glutamine	NULL	transport of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52521	13	334878	5	NULL	NULL	0	NULL	creatine	NULL		inhibit	NULL				glutamine	NULL	transport of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52641	1	334878	6	NULL	NULL	0	NULL	alanine	NULL		inhibits	NULL	strongly			glutamine	NULL	transport of 			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52642	2	334878	6	NULL	NULL	0	NULL	serine	NULL		inhibits	NULL	strongly			glutamine	NULL	transport of 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52643	3	334878	6	NULL	NULL	0	NULL	threonine	NULL		inhibits	NULL	strongly			glutamine	NULL	transport of 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52644	4	334878	6	NULL	NULL	0	NULL	cysteine	NULL		inhibits	NULL	strongly			glutamine	NULL	transport of 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52645	5	334878	6	NULL	NULL	0	NULL	asparagine	NULL		inhibits	NULL	strongly			glutamine	NULL	transport of 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52646	6	334878	6	NULL	NULL	0	NULL	methionine	NULL		inhibits	NULL	strongly			glutamine	NULL	transport of 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52647	7	334878	6	NULL	NULL	0	NULL	valine	NULL		inhibits	NULL	strongly			glutamine	NULL	transport of 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52648	8	334878	6	NULL	NULL	0	NULL	glycine	NULL		inhibits	NULL	weakly			glutamine	NULL	transport of 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52649	9	334878	6	NULL	NULL	0	NULL	proline	NULL		inhibits	NULL	weakly			glutamine	NULL	transport of 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52650	10	334878	6	NULL	NULL	0	NULL	arginine	NULL		inhibits	NULL	weakly			glutamine	NULL	transport of 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52651	11	334878	6	NULL	NULL	0	NULL	histidine	NULL		inhibits	NULL	weakly			glutamine	NULL	transport of 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52652	12	334878	6	NULL	NULL	0	NULL	glutamate	NULL		inhibits	NULL	weakly			glutamine	NULL	transport of 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
52653	13	334878	6	NULL	NULL	0	NULL	creatine	NULL		inhibits	NULL	weakly			glutamine	NULL	transport of 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_93	15581847	As shown in   Table 1, alanine, serine, threonine, cysteine, asparagine, methionine and valine strongly  inhibited the glutamine transport; the inhibition by these amino acids ranged from  54% to 70% at 1 mM and was virtually complete at a concentration of 10 mM. Glycine,  proline, arginine, histidine, glutamate and creatine had a low inhibitory effect.	transcription
51858	1	334879	5	NULL	NULL	0	NULL	pgiA	NULL		corresponds to	NULL		His311			NULL		active-site histidine		NULL		0	NULL	NULL	NULL	gw60_febslett_499_1_11_s_132	11418102	According to the binding position of the inhibitor, they proposed a different mechanism in which the active-site histidine and lysine (corresponding to His311 and Lys425 of pgiA) catalyze the opening of the cyclic form substrates, and the active-site glutamate (corresponding to Glu290 of pgiA) takes the responsibility for the isomerization.	transcription
51859	2	334879	5	NULL	NULL	0	NULL	pgiA	NULL		corresponds to	NULL		Lys425			NULL		active-site lysine		NULL		0	NULL	NULL	NULL	gw60_febslett_499_1_11_s_132	11418102	According to the binding position of the inhibitor, they proposed a different mechanism in which the active-site histidine and lysine (corresponding to His311 and Lys425 of pgiA) catalyze the opening of the cyclic form substrates, and the active-site glutamate (corresponding to Glu290 of pgiA) takes the responsibility for the isomerization.	transcription
51860	3	334879	5	NULL	NULL	0	NULL	statement 1	NULL		catalyze	NULL				cyclic form substrates	NULL	opening of			NULL		0	NULL	NULL	NULL	gw60_febslett_499_1_11_s_132	11418102	According to the binding position of the inhibitor, they proposed a different mechanism in which the active-site histidine and lysine (corresponding to His311 and Lys425 of pgiA) catalyze the opening of the cyclic form substrates, and the active-site glutamate (corresponding to Glu290 of pgiA) takes the responsibility for the isomerization.	transcription
51861	4	334879	5	NULL	NULL	0	NULL	statement 1	NULL		catalyze	NULL				cyclic form substrates	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_499_1_11_s_132	11418102	According to the binding position of the inhibitor, they proposed a different mechanism in which the active-site histidine and lysine (corresponding to His311 and Lys425 of pgiA) catalyze the opening of the cyclic form substrates, and the active-site glutamate (corresponding to Glu290 of pgiA) takes the responsibility for the isomerization.	transcription
51862	5	334879	5	NULL	NULL	0	NULL	pgiA	NULL		corresponds to	NULL		Glu290			NULL		active-site glutamate		NULL		0	NULL	NULL	NULL	gw60_febslett_499_1_11_s_132	11418102	According to the binding position of the inhibitor, they proposed a different mechanism in which the active-site histidine and lysine (corresponding to His311 and Lys425 of pgiA) catalyze the opening of the cyclic form substrates, and the active-site glutamate (corresponding to Glu290 of pgiA) takes the responsibility for the isomerization.	transcription
51863	6	334879	5	NULL	NULL	0	NULL	statement 5	NULL		is responsible for	NULL				isomerization	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_499_1_11_s_132	11418102	According to the binding position of the inhibitor, they proposed a different mechanism in which the active-site histidine and lysine (corresponding to His311 and Lys425 of pgiA) catalyze the opening of the cyclic form substrates, and the active-site glutamate (corresponding to Glu290 of pgiA) takes the responsibility for the isomerization.	transcription
51864	1	334880	5	NULL	NULL	0	NULL	methylisocitrate lyase	NULL		is important for	NULL		[KR-C-G-H[LMQR]		methylisocitrate lyase	NULL	catalytic activity of			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_1_271_s_126	11772636	[KR-C-G-H[LMQR]) was present, as it is in all known methylisocitrate lyase sequences; this signature includes highly conserved cysteine (C), glutamate (G), and histidine (H) residues which are important for the catalytic activity of isocitrate lyases ( http://www.expasy.	transcription
53713	1	334880	6	NULL	NULL	0	NULL	isocitrate lyases			exhibits					catalytic activity					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_1_271_s_126	11772636	[KR-C-G-H[LMQR]) was present, as it is in all known methylisocitrate lyase sequences; this signature includes highly conserved cysteine (C), glutamate (G), and histidine (H) residues which are important for the catalytic activity of isocitrate lyases ( http://www.expasy.	transcription
53715	2	334880	6	NULL	NULL	0	NULL				is important for			[KR-C-G-H[LMQR]		statement 1					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_1_271_s_126	11772636	[KR-C-G-H[LMQR]) was present, as it is in all known methylisocitrate lyase sequences; this signature includes highly conserved cysteine (C), glutamate (G), and histidine (H) residues which are important for the catalytic activity of isocitrate lyases ( http://www.expasy.	transcription
51865	1	334881	5	NULL	NULL	0	NULL	NixA	NULL		bind	NULL		histidine;;aspartate;;glutamate		nickel	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_jbacteriol_184_5_1438_s_36	11844775	In two previous papers, the consequences of amino acid replacements in high-affinity nickel transporters were studied: one concentrated on the conserved motif in TM II of the NixA homologue HoxN ( 7), and the other focused on conserved histidine, aspartate, and glutamate residues of NixA ( 12), well known to bind nickel in vitro.	transcription
52654	1	334881	6	NULL	NULL	0	NULL	NixA	NULL		bind	NULL				nickel	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw60_jbacteriol_184_5_1438_s_36	11844775	In two previous papers, the consequences of amino acid replacements in high-affinity nickel transporters were studied: one concentrated on the conserved motif in TM II of the NixA homologue HoxN ( 7), and the other focused on conserved histidine, aspartate, and glutamate residues of NixA ( 12), well known to bind nickel in vitro.	transcription
51866	1	334882	5	NULL	NULL	0	NULL		NULL	protonation of	is mediated by	NULL		Calpha			NULL		histidine residue		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_4_1939_s_163	9442028	An earlier study of the effects of D2O on the reaction catalyzed by glutamate decarboxylase has already shown large solvent isotope effects ( 25) and these have been cited in support of a proposal that, after the decarboxylation step, protonation at Calpha is mediated by a histidine residue ( 16).	transcription
51867	2	334882	5	NULL	NULL	0	NULL	statement 1	NULL		occurs after	NULL				decarboxylation step	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_4_1939_s_163	9442028	An earlier study of the effects of D2O on the reaction catalyzed by glutamate decarboxylase has already shown large solvent isotope effects ( 25) and these have been cited in support of a proposal that, after the decarboxylation step, protonation at Calpha is mediated by a histidine residue ( 16).	transcription
52800	1	334882	6	NULL	NULL	0	NULL	Calpha	NULL	protonation at	is mediated by	NULL					NULL		histidine residue		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_4_1939_s_163	9442028	An earlier study of the effects of D2O on the reaction catalyzed by glutamate decarboxylase has already shown large solvent isotope effects ( 25) and these have been cited in support of a proposal that, after the decarboxylation step, protonation at Calpha is mediated by a histidine residue ( 16).	transcription
52801	2	334882	6	NULL	NULL	0	NULL	statement 1	NULL		occurs after	NULL				decarboxylation step	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_4_1939_s_163	9442028	An earlier study of the effects of D2O on the reaction catalyzed by glutamate decarboxylase has already shown large solvent isotope effects ( 25) and these have been cited in support of a proposal that, after the decarboxylation step, protonation at Calpha is mediated by a histidine residue ( 16).	transcription
54306	1	334883	5	NULL	NULL	0	NULL	histidine			is a substrate for			E2-157		arginine			E2-157		NULL	newborn CD-1 mice	NULL	NULL	NULL	NULL	abs-batch0620-0649_virology_347_1_16380143_s_4	16380143	However, substitution of histidine  for arginine at E2-157 (R157H) or glutamate for lysine at E2-159 (K159E)  produces viruses with decreases in heparin-Sepharose binding and increases  in viremia but different levels of binding to HS-expressing cells and  virulence phenotypes in newborn CD-1 mice (Byrnes, A.P., Griffin, D.E.,  2000.	transcription
54307	2	334883	5	NULL	NULL	0	NULL	glutamate			is a substrate for			E2-159		lysine			E2-159		NULL	newborn CD-1 mice	0	NULL	NULL	NULL	abs-batch0620-0649_virology_347_1_16380143_s_4	16380143	However, substitution of histidine  for arginine at E2-157 (R157H) or glutamate for lysine at E2-159 (K159E)  produces viruses with decreases in heparin-Sepharose binding and increases  in viremia but different levels of binding to HS-expressing cells and  virulence phenotypes in newborn CD-1 mice (Byrnes, A.P., Griffin, D.E.,  2000.	transcription
54308	3	334883	5	NULL	NULL	0	NULL	R157H			is					statement 1					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_virology_347_1_16380143_s_4	16380143	However, substitution of histidine  for arginine at E2-157 (R157H) or glutamate for lysine at E2-159 (K159E)  produces viruses with decreases in heparin-Sepharose binding and increases  in viremia but different levels of binding to HS-expressing cells and  virulence phenotypes in newborn CD-1 mice (Byrnes, A.P., Griffin, D.E.,  2000.	transcription
54309	4	334883	5	NULL	NULL	0	NULL	K159E			is					statement 2					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_virology_347_1_16380143_s_4	16380143	However, substitution of histidine  for arginine at E2-157 (R157H) or glutamate for lysine at E2-159 (K159E)  produces viruses with decreases in heparin-Sepharose binding and increases  in viremia but different levels of binding to HS-expressing cells and  virulence phenotypes in newborn CD-1 mice (Byrnes, A.P., Griffin, D.E.,  2000.	transcription
54310	5	334883	5	NULL	NULL	0	NULL	statement 3			increases					viremia					NULL	newborn CD-1 mice	0	NULL	NULL	NULL	abs-batch0620-0649_virology_347_1_16380143_s_4	16380143	However, substitution of histidine  for arginine at E2-157 (R157H) or glutamate for lysine at E2-159 (K159E)  produces viruses with decreases in heparin-Sepharose binding and increases  in viremia but different levels of binding to HS-expressing cells and  virulence phenotypes in newborn CD-1 mice (Byrnes, A.P., Griffin, D.E.,  2000.	transcription
54311	6	334883	5	NULL	NULL	0	NULL	statement 4			increases					viremia 					NULL	newborn CD-1 mice	0	NULL	NULL	NULL	abs-batch0620-0649_virology_347_1_16380143_s_4	16380143	However, substitution of histidine  for arginine at E2-157 (R157H) or glutamate for lysine at E2-159 (K159E)  produces viruses with decreases in heparin-Sepharose binding and increases  in viremia but different levels of binding to HS-expressing cells and  virulence phenotypes in newborn CD-1 mice (Byrnes, A.P., Griffin, D.E.,  2000.	transcription
52815	1	334883	6	NULL	NULL	0	NULL	histidine	NULL		is substituted for	NULL				arginine	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_virology_347_1_16380143_s_4	16380143	However, substitution of histidine  for arginine at E2-157 (R157H) or glutamate for lysine at E2-159 (K159E)  produces viruses with decreases in heparin-Sepharose binding and increases  in viremia but different levels of binding to HS-expressing cells and  virulence phenotypes in newborn CD-1 mice (Byrnes, A.P., Griffin, D.E.,  2000.	transcription
52816	2	334883	6	NULL	NULL	0	NULL	glutamate	NULL		is substituted for	NULL				lysine	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_virology_347_1_16380143_s_4	16380143	However, substitution of histidine  for arginine at E2-157 (R157H) or glutamate for lysine at E2-159 (K159E)  produces viruses with decreases in heparin-Sepharose binding and increases  in viremia but different levels of binding to HS-expressing cells and  virulence phenotypes in newborn CD-1 mice (Byrnes, A.P., Griffin, D.E.,  2000.	transcription
52818	3	334883	6	NULL	NULL	0	NULL		NULL		is	NULL		R157H		statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_virology_347_1_16380143_s_4	16380143	However, substitution of histidine  for arginine at E2-157 (R157H) or glutamate for lysine at E2-159 (K159E)  produces viruses with decreases in heparin-Sepharose binding and increases  in viremia but different levels of binding to HS-expressing cells and  virulence phenotypes in newborn CD-1 mice (Byrnes, A.P., Griffin, D.E.,  2000.	transcription
52820	4	334883	6	NULL	NULL	0	NULL		NULL		is	NULL		K159E		statement 2	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_virology_347_1_16380143_s_4	16380143	However, substitution of histidine  for arginine at E2-157 (R157H) or glutamate for lysine at E2-159 (K159E)  produces viruses with decreases in heparin-Sepharose binding and increases  in viremia but different levels of binding to HS-expressing cells and  virulence phenotypes in newborn CD-1 mice (Byrnes, A.P., Griffin, D.E.,  2000.	transcription
52821	5	334883	6	NULL	NULL	0	NULL	statement 3	NULL		increases	NULL				viremia	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_virology_347_1_16380143_s_4	16380143	However, substitution of histidine  for arginine at E2-157 (R157H) or glutamate for lysine at E2-159 (K159E)  produces viruses with decreases in heparin-Sepharose binding and increases  in viremia but different levels of binding to HS-expressing cells and  virulence phenotypes in newborn CD-1 mice (Byrnes, A.P., Griffin, D.E.,  2000.	transcription
52822	6	334883	6	NULL	NULL	0	NULL	statement 4	NULL		increases	NULL				viremia	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_virology_347_1_16380143_s_4	16380143	However, substitution of histidine  for arginine at E2-157 (R157H) or glutamate for lysine at E2-159 (K159E)  produces viruses with decreases in heparin-Sepharose binding and increases  in viremia but different levels of binding to HS-expressing cells and  virulence phenotypes in newborn CD-1 mice (Byrnes, A.P., Griffin, D.E.,  2000.	transcription
52492	1	334884	5	NULL	NULL	0	NULL	alanine	NULL		stimulates	NULL	efficiently			glutamine	NULL	uptake of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52493	2	334884	5	NULL	NULL	0	NULL	alanine	NULL		stimulates	NULL	efficiently			efflux	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52494	3	334884	5	NULL	NULL	0	NULL	serine	NULL		stimulates	NULL	efficiently			glutamine	NULL	uptake of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52495	4	334884	5	NULL	NULL	0	NULL	serine	NULL		stimulates	NULL	efficiently			efflux	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52496	5	334884	5	NULL	NULL	0	NULL	asparagine	NULL		stimulates	NULL	efficiently			glutamine	NULL	uptake of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52497	6	334884	5	NULL	NULL	0	NULL	asparagine	NULL		stimulates	NULL	efficiently			efflux	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52498	7	334884	5	NULL	NULL	0	NULL	threonine	NULL		stimulates	NULL	efficiently			glutamine	NULL	uptake of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52499	8	334884	5	NULL	NULL	0	NULL	threonine	NULL		stimulates	NULL	efficiently			efflux	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52500	9	334884	5	NULL	NULL	0	NULL	cysteine	NULL		stimulates	NULL				efflux	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52501	10	334884	5	NULL	NULL	0	NULL	cysteine	NULL		stimulates	NULL				glutamine	NULL	uptake of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52502	11	334884	5	NULL	NULL	0	NULL	statement 9	NULL		is more than	NULL				statement 10	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52503	12	334884	5	NULL	NULL	0	NULL	valine	NULL		stimulates	NULL				efflux	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52504	13	334884	5	NULL	NULL	0	NULL	valine	NULL		stimulates	NULL				glutamine	NULL	uptake of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52505	14	334884	5	NULL	NULL	0	NULL	statement 12	NULL		is more than	NULL				statement 13	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52802	1	334884	6	NULL	NULL	0	NULL	alanine	NULL		stimulates	NULL	efficiently			glutamine	NULL	uptake of 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52803	2	334884	6	NULL	NULL	0	NULL	serine	NULL		stimulates	NULL	efficiently			glutamine	NULL	uptake of 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52804	3	334884	6	NULL	NULL	0	NULL	asparagine	NULL		stimulates	NULL	efficiently			glutamine	NULL	uptake of 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52823	4	334884	6	NULL	NULL	0	NULL	threonine	NULL		stimulates	NULL	efficiently			glutamine	NULL	uptake of 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52824	5	334884	6	NULL	NULL	0	NULL	alanine	NULL		stimulates	NULL	efficiently			glutamine efflux	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52825	6	334884	6	NULL	NULL	0	NULL	serine	NULL		stimulates	NULL	efficiently			glutamine efflux	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52827	7	334884	6	NULL	NULL	0	NULL	asparagine	NULL		stimulates	NULL	efficiently			glutamine efflux	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52828	8	334884	6	NULL	NULL	0	NULL	cysteine	NULL		stimulates	NULL	preferentially			glutamine efflux	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52829	9	334884	6	NULL	NULL	0	NULL	valine	NULL		stimulates	NULL	preferentially			glutamine efflux	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1667_2_122_s_108	15581847	As clearly demonstrated by the data in   Table 2, alanine, serine, asparagine and threonine efficiently stimulated both the [3]glutamine uptake and efflux; cysteine and valine stimulated the efflux much more  than the uptake of [3]glutamine, i.e., they are preferentially translocated from outside to inside; methionine,  glycine, histidine, glutamate, arginine, creatine and MeAIB were poorly or not transported.	transcription
52045	1	334885	5	NULL	NULL	0	NULL	Receptor 5.24	NULL		is activated by	NULL				L-amino acids	NULL	basic			NULL		NULL	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52046	2	334885	5	NULL	NULL	0	NULL	Receptor 5.24	NULL		is not activated by	NULL				D-arginine	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52047	3	334885	5	NULL	NULL	0	NULL	Receptor 5.24	NULL		is activated by	NULL				arginine	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52048	4	334885	5	NULL	NULL	0	NULL	Receptor 5.24	NULL		is activated by	NULL				lysine	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52049	5	334885	5	NULL	NULL	0	NULL	Receptor 5.24	NULL		is activated by	NULL	weakly			L-amino acids	NULL	neutral;;aliphatic			NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52050	6	334885	5	NULL	NULL	0	NULL	methionine	NULL		is a type of	NULL				L-amino acid	NULL	neutral;;aliphatic			NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52051	7	334885	5	NULL	NULL	0	NULL	isoleucine	NULL		is a type of	NULL				L-amino acid	NULL	neutral;;aliphatic			NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52052	8	334885	5	NULL	NULL	0	NULL	threonine	NULL		is a type of	NULL				L-amino acid	NULL	neutral;;aliphatic			NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52053	9	334885	5	NULL	NULL	0	NULL	serine	NULL		is a type of	NULL				L-amino acid	NULL	neutral;;aliphatic			NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52054	10	334885	5	NULL	NULL	0	NULL	alanine	NULL		is a type of	NULL				L-amino acid	NULL	neutral;;aliphatic			NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52055	11	334885	5	NULL	NULL	0	NULL	Receptor 5.24	NULL		is activated by	NULL	may			L-amino acids	NULL	acidic 			NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52056	12	334885	5	NULL	NULL	0	NULL	glutamate	NULL		is a type of	NULL				L-amino acid	NULL	acidic			NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52057	13	334885	5	NULL	NULL	0	NULL	aspartate	NULL		is a type of	NULL				L-amino acid	NULL	acidic			NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52058	14	334885	5	NULL	NULL	0	NULL	Receptor 5.24	NULL		is activated by	NULL	may			L-amino acids	NULL	aromatic			NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52059	15	334885	5	NULL	NULL	0	NULL	tyrosine	NULL		is a type of	NULL				L-amino acid	NULL	aromatic			NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52060	16	334885	5	NULL	NULL	0	NULL	phenylalanine	NULL		is a type of	NULL				L-amino acid	NULL	aromatic			NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52061	17	334885	5	NULL	NULL	0	NULL	tryptophan	NULL		is a type of	NULL				L-amino acid	NULL	aromatic			NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52062	18	334885	5	NULL	NULL	0	NULL	histidine	NULL		is a type of	NULL				L-amino acid	NULL	aromatic			NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52903	1	334885	6	NULL	NULL	0	NULL	Receptor 5.24	NULL		is not activated by	NULL				D-arginine	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52904	2	334885	6	NULL	NULL	0	NULL	arginine	NULL		activates	NULL				receptor 5.24	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52905	3	334885	6	NULL	NULL	0	NULL	lysine	NULL		activates	NULL				receptor 5.24	NULL				NULL		0	NULL	NULL	NULL	gw60_neuron_23_3_487_s_80	10433261	Receptor 5.24 responds best to basic L-amino acids, showing roughly equivalent currents upon activation by arginine and lysine, smaller responses to neutral aliphatic L-amino acids (e.g., methionine, isoleucine, threonine, serine, alanine) and little or no response to acidic and aromatic L-amino acids (e.g., glutamate, aspartate, tyrosine, phenylalanine, tryptophan, histidine); the receptor is not activated by D-arginine (all amino acids referred to hereafter are L-isomers unless stated otherwise).	transcription
52038	1	334886	5	NULL	NULL	0	NULL		NULL		contains	NULL			exon IIIb		NULL	dipeptide residues in		fl2 domain 	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_17_10222_s_123	7730326	Dipeptide Residues in the fl2 and E Domain of Alternate  Exon IIIb Indirectly Modify FGF-2 and FGF-7 Binding  The exon  IIIb sequence in both the FGFR1 and FGFR2 genes is distinguished from  exon IIIc and homologous sequences in the FGFR3 and FGFR4 genes by  histidine-serine (HS) residues at the NH terminus of the  fl2 domain combined with the absence of lysine-glutamate (KE) residues  within the E strand of Loop III ( Fig. 1).	transcription
52039	2	334886	5	NULL	NULL	0	NULL		NULL		contains	NULL			exon IIIb		NULL	dipeptide residues in		E Domain	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_17_10222_s_123	7730326	Dipeptide Residues in the fl2 and E Domain of Alternate  Exon IIIb Indirectly Modify FGF-2 and FGF-7 Binding  The exon  IIIb sequence in both the FGFR1 and FGFR2 genes is distinguished from  exon IIIc and homologous sequences in the FGFR3 and FGFR4 genes by  histidine-serine (HS) residues at the NH terminus of the  fl2 domain combined with the absence of lysine-glutamate (KE) residues  within the E strand of Loop III ( Fig. 1).	transcription
52040	3	334886	5	NULL	NULL	0	NULL	statement 1	NULL		modify	NULL	indirectly			FGF-2	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_17_10222_s_123	7730326	Dipeptide Residues in the fl2 and E Domain of Alternate  Exon IIIb Indirectly Modify FGF-2 and FGF-7 Binding  The exon  IIIb sequence in both the FGFR1 and FGFR2 genes is distinguished from  exon IIIc and homologous sequences in the FGFR3 and FGFR4 genes by  histidine-serine (HS) residues at the NH terminus of the  fl2 domain combined with the absence of lysine-glutamate (KE) residues  within the E strand of Loop III ( Fig. 1).	transcription
52041	4	334886	5	NULL	NULL	0	NULL	statement 1	NULL		modify	NULL	indirectly			FGF-2	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_17_10222_s_123	7730326	Dipeptide Residues in the fl2 and E Domain of Alternate  Exon IIIb Indirectly Modify FGF-2 and FGF-7 Binding  The exon  IIIb sequence in both the FGFR1 and FGFR2 genes is distinguished from  exon IIIc and homologous sequences in the FGFR3 and FGFR4 genes by  histidine-serine (HS) residues at the NH terminus of the  fl2 domain combined with the absence of lysine-glutamate (KE) residues  within the E strand of Loop III ( Fig. 1).	transcription
52042	5	334886	5	NULL	NULL	0	NULL	statement 1	NULL		modify	NULL	indirectly			FGF-7	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_17_10222_s_123	7730326	Dipeptide Residues in the fl2 and E Domain of Alternate  Exon IIIb Indirectly Modify FGF-2 and FGF-7 Binding  The exon  IIIb sequence in both the FGFR1 and FGFR2 genes is distinguished from  exon IIIc and homologous sequences in the FGFR3 and FGFR4 genes by  histidine-serine (HS) residues at the NH terminus of the  fl2 domain combined with the absence of lysine-glutamate (KE) residues  within the E strand of Loop III ( Fig. 1).	transcription
52043	6	334886	5	NULL	NULL	0	NULL	statement 2	NULL		modify	NULL	indirectly			FGF-7	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_17_10222_s_123	7730326	Dipeptide Residues in the fl2 and E Domain of Alternate  Exon IIIb Indirectly Modify FGF-2 and FGF-7 Binding  The exon  IIIb sequence in both the FGFR1 and FGFR2 genes is distinguished from  exon IIIc and homologous sequences in the FGFR3 and FGFR4 genes by  histidine-serine (HS) residues at the NH terminus of the  fl2 domain combined with the absence of lysine-glutamate (KE) residues  within the E strand of Loop III ( Fig. 1).	transcription
51887	1	334887	5	NULL	NULL	0	NULL	AChEs	NULL		interacts with	NULL		glutamate 347;;histidine 460			NULL		active site serine		NULL		0	NULL	NULL	NULL	gw60_insectbiochemmolbiol_28_8_581_s_121	9753768	Conservation of the primary structure to other AChEs was also indicated by the presence of key residues ( Fig. 2 and  Fig. 3) that are characteristic of cholinesterases ( B. microplus AChE amino acids are numbered from the start of the mature protein according to   Massoulie et al. (1992) and the corresponding amino acid residues for  T. californica are listed below in parentheses for reference): (i) the active site serine 222 (200) which is surrounded by the sequence FGESAG-this is present in all known cholinesterases; (ii) glutamate 347 (327) and histidine 460 (440) which interact with the active site serine to form the catalytic triad (  Sussman et al., 1991); and (iii) the choline binding site, tryptophan 103 (84).	transcription
51888	2	334887	5	NULL	NULL	0	NULL	statement 1	NULL		forms	NULL				catalytic triad	NULL				NULL		0	NULL	NULL	NULL	gw60_insectbiochemmolbiol_28_8_581_s_121	9753768	Conservation of the primary structure to other AChEs was also indicated by the presence of key residues ( Fig. 2 and  Fig. 3) that are characteristic of cholinesterases ( B. microplus AChE amino acids are numbered from the start of the mature protein according to   Massoulie et al. (1992) and the corresponding amino acid residues for  T. californica are listed below in parentheses for reference): (i) the active site serine 222 (200) which is surrounded by the sequence FGESAG-this is present in all known cholinesterases; (ii) glutamate 347 (327) and histidine 460 (440) which interact with the active site serine to form the catalytic triad (  Sussman et al., 1991); and (iii) the choline binding site, tryptophan 103 (84).	transcription
52901	1	334887	6	NULL	NULL	0	NULL		NULL		interacts with	NULL		histidine 460			NULL		active site serine		NULL		0	NULL	NULL	NULL	gw60_insectbiochemmolbiol_28_8_581_s_121	9753768	Conservation of the primary structure to other AChEs was also indicated by the presence of key residues ( Fig. 2 and  Fig. 3) that are characteristic of cholinesterases ( B. microplus AChE amino acids are numbered from the start of the mature protein according to   Massoulie et al. (1992) and the corresponding amino acid residues for  T. californica are listed below in parentheses for reference): (i) the active site serine 222 (200) which is surrounded by the sequence FGESAG-this is present in all known cholinesterases; (ii) glutamate 347 (327) and histidine 460 (440) which interact with the active site serine to form the catalytic triad (  Sussman et al., 1991); and (iii) the choline binding site, tryptophan 103 (84).	transcription
52902	2	334887	6	NULL	NULL	0	NULL	statement 1	NULL		forms 	NULL				catalytic triad	NULL				NULL		0	NULL	NULL	NULL	gw60_insectbiochemmolbiol_28_8_581_s_121	9753768	Conservation of the primary structure to other AChEs was also indicated by the presence of key residues ( Fig. 2 and  Fig. 3) that are characteristic of cholinesterases ( B. microplus AChE amino acids are numbered from the start of the mature protein according to   Massoulie et al. (1992) and the corresponding amino acid residues for  T. californica are listed below in parentheses for reference): (i) the active site serine 222 (200) which is surrounded by the sequence FGESAG-this is present in all known cholinesterases; (ii) glutamate 347 (327) and histidine 460 (440) which interact with the active site serine to form the catalytic triad (  Sussman et al., 1991); and (iii) the choline binding site, tryptophan 103 (84).	transcription
51885	1	334888	5	NULL	NULL	0	NULL	alpha-glucose-1-phosphate	NULL		is converted to	NULL				glucose-6-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_10_6935_s_64	16177373	The specific activity of PGM in cell extracts was measured as the conversion of alpha-glucose-1-phosphate to glucose-6-phosphate in a reaction coupled to reduction of glucose-6-phosphate by glucose-6-phosphate dehydrogenase and quantitated spectrophotometrically at 340 nm by monitoring the formation of NADPH from NADP+ at 30 degrees C.	transcription
51886	2	334888	5	NULL	NULL	0	NULL	glucose-6-phosphate dehydrogenase	NULL		reduces	NULL				glucose-6-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_10_6935_s_64	16177373	The specific activity of PGM in cell extracts was measured as the conversion of alpha-glucose-1-phosphate to glucose-6-phosphate in a reaction coupled to reduction of glucose-6-phosphate by glucose-6-phosphate dehydrogenase and quantitated spectrophotometrically at 340 nm by monitoring the formation of NADPH from NADP+ at 30 degrees C.	transcription
52899	1	334888	6	NULL	NULL	0	NULL	alpha-glucose-1-phosphate	NULL		is converted to	NULL				glucose-6-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_10_6935_s_64	16177373	The specific activity of PGM in cell extracts was measured as the conversion of alpha-glucose-1-phosphate to glucose-6-phosphate in a reaction coupled to reduction of glucose-6-phosphate by glucose-6-phosphate dehydrogenase and quantitated spectrophotometrically at 340 nm by monitoring the formation of NADPH from NADP+ at 30 degrees C.	transcription
52900	2	334888	6	NULL	NULL	0	NULL	glucose-6-phosphate dehydrogenase	NULL		reduces	NULL				glucose-6-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_73_10_6935_s_64	16177373	The specific activity of PGM in cell extracts was measured as the conversion of alpha-glucose-1-phosphate to glucose-6-phosphate in a reaction coupled to reduction of glucose-6-phosphate by glucose-6-phosphate dehydrogenase and quantitated spectrophotometrically at 340 nm by monitoring the formation of NADPH from NADP+ at 30 degrees C.	transcription
51868	1	334889	5	NULL	NULL	0	NULL	UDP-glucose	NULL		is synthesized from	NULL				glucose-1-phosphate & UTP	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_7_4224_s_191	15213167	While the  galU gene product is responsible for synthesis of UDP-glucose from glucose-1-phosphate and UTP, the  algC gene encodes a bifunctional enzyme with both a phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, and a phosphomannomutase activity ( ,  ).	transcription
51869	2	334889	5	NULL	NULL	0	NULL	galU gene product	NULL		is responsible for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_7_4224_s_191	15213167	While the  galU gene product is responsible for synthesis of UDP-glucose from glucose-1-phosphate and UTP, the  algC gene encodes a bifunctional enzyme with both a phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, and a phosphomannomutase activity ( ,  ).	transcription
51870	3	334889	5	NULL	NULL	0	NULL	algC gene	NULL		encodes	NULL				bifunctional enzyme	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_7_4224_s_191	15213167	While the  galU gene product is responsible for synthesis of UDP-glucose from glucose-1-phosphate and UTP, the  algC gene encodes a bifunctional enzyme with both a phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, and a phosphomannomutase activity ( ,  ).	transcription
52063	4	334889	5	NULL	NULL	0	NULL	algC gene	NULL		contains	NULL				phosphoglucomutase activity	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_7_4224_s_191	15213167	While the  galU gene product is responsible for synthesis of UDP-glucose from glucose-1-phosphate and UTP, the  algC gene encodes a bifunctional enzyme with both a phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, and a phosphomannomutase activity ( ,  ).	transcription
52064	5	334889	5	NULL	NULL	0	NULL	algC gene	NULL		contains	NULL				phosphomannomutase activity	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_7_4224_s_191	15213167	While the  galU gene product is responsible for synthesis of UDP-glucose from glucose-1-phosphate and UTP, the  algC gene encodes a bifunctional enzyme with both a phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, and a phosphomannomutase activity ( ,  ).	transcription
52065	6	334889	5	NULL	NULL	0	NULL	glucose-6-phosphate	NULL		is converted to	NULL				glucose-1-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_7_4224_s_191	15213167	While the  galU gene product is responsible for synthesis of UDP-glucose from glucose-1-phosphate and UTP, the  algC gene encodes a bifunctional enzyme with both a phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, and a phosphomannomutase activity ( ,  ).	transcription
52066	7	334889	5	NULL	NULL	0	NULL	glucose-1-phosphate	NULL		is converted to	NULL				glucose-6-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_7_4224_s_191	15213167	While the  galU gene product is responsible for synthesis of UDP-glucose from glucose-1-phosphate and UTP, the  algC gene encodes a bifunctional enzyme with both a phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, and a phosphomannomutase activity ( ,  ).	transcription
52067	8	334889	5	NULL	NULL	0	NULL	statement 3	NULL		catalyzes	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_7_4224_s_191	15213167	While the  galU gene product is responsible for synthesis of UDP-glucose from glucose-1-phosphate and UTP, the  algC gene encodes a bifunctional enzyme with both a phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, and a phosphomannomutase activity ( ,  ).	transcription
52068	9	334889	5	NULL	NULL	0	NULL	statement 3	NULL		catalyzes	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_7_4224_s_191	15213167	While the  galU gene product is responsible for synthesis of UDP-glucose from glucose-1-phosphate and UTP, the  algC gene encodes a bifunctional enzyme with both a phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, and a phosphomannomutase activity ( ,  ).	transcription
52881	1	334889	6	NULL	NULL	0	NULL	UDP-glucose	NULL		is synthesized from	NULL				glucose-1-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_7_4224_s_191	15213167	While the  galU gene product is responsible for synthesis of UDP-glucose from glucose-1-phosphate and UTP, the  algC gene encodes a bifunctional enzyme with both a phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, and a phosphomannomutase activity ( ,  ).	transcription
52882	2	334889	6	NULL	NULL	0	NULL	UDP-glucose	NULL		is synthesized from	NULL				UTP	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_7_4224_s_191	15213167	While the  galU gene product is responsible for synthesis of UDP-glucose from glucose-1-phosphate and UTP, the  algC gene encodes a bifunctional enzyme with both a phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, and a phosphomannomutase activity ( ,  ).	transcription
52883	3	334889	6	NULL	NULL	0	NULL	statement 1	NULL		occurs simultaneously with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_7_4224_s_191	15213167	While the  galU gene product is responsible for synthesis of UDP-glucose from glucose-1-phosphate and UTP, the  algC gene encodes a bifunctional enzyme with both a phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, and a phosphomannomutase activity ( ,  ).	transcription
52884	4	334889	6	NULL	NULL	0	NULL	galU gene product	NULL		is responsible for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_7_4224_s_191	15213167	While the  galU gene product is responsible for synthesis of UDP-glucose from glucose-1-phosphate and UTP, the  algC gene encodes a bifunctional enzyme with both a phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, and a phosphomannomutase activity ( ,  ).	transcription
52885	5	334889	6	NULL	NULL	0	NULL	galU gene product	NULL		is responsible for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_7_4224_s_191	15213167	While the  galU gene product is responsible for synthesis of UDP-glucose from glucose-1-phosphate and UTP, the  algC gene encodes a bifunctional enzyme with both a phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, and a phosphomannomutase activity ( ,  ).	transcription
52886	6	334889	6	NULL	NULL	0	NULL	algC gene product	NULL		encodes	NULL				bifunctional enzyme	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_7_4224_s_191	15213167	While the  galU gene product is responsible for synthesis of UDP-glucose from glucose-1-phosphate and UTP, the  algC gene encodes a bifunctional enzyme with both a phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, and a phosphomannomutase activity ( ,  ).	transcription
52887	7	334889	6	NULL	NULL	0	NULL	algC gene product	NULL		exhibits	NULL				phosphoglucomutase activity	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_7_4224_s_191	15213167	While the  galU gene product is responsible for synthesis of UDP-glucose from glucose-1-phosphate and UTP, the  algC gene encodes a bifunctional enzyme with both a phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, and a phosphomannomutase activity ( ,  ).	transcription
52888	8	334889	6	NULL	NULL	0	NULL	algC gene product	NULL		exhibits	NULL				phosphomannomutase activity	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_7_4224_s_191	15213167	While the  galU gene product is responsible for synthesis of UDP-glucose from glucose-1-phosphate and UTP, the  algC gene encodes a bifunctional enzyme with both a phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, and a phosphomannomutase activity ( ,  ).	transcription
52889	9	334889	6	NULL	NULL	0	NULL	glucose-6-phosphate	NULL		is interconverted to	NULL				glucose-1-phosphate	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_7_4224_s_191	15213167	While the  galU gene product is responsible for synthesis of UDP-glucose from glucose-1-phosphate and UTP, the  algC gene encodes a bifunctional enzyme with both a phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, and a phosphomannomutase activity ( ,  ).	transcription
52890	10	334889	6	NULL	NULL	0	NULL	algC gene product	NULL		plays a role in	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_72_7_4224_s_191	15213167	While the  galU gene product is responsible for synthesis of UDP-glucose from glucose-1-phosphate and UTP, the  algC gene encodes a bifunctional enzyme with both a phosphoglucomutase activity, which interconverts glucose-6-phosphate and glucose-1-phosphate, and a phosphomannomutase activity ( ,  ).	transcription
51871	1	334890	5	NULL	NULL	0	NULL	glucose-6-phosphate	NULL		is converted to	NULL				glucose-1-phosphate	NULL				NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-bacteriol_183_11_11344144_s_6	11344144	Pgm catalyzes the conversion of glucose-6-phosphate  to glucose-1-phosphate during growth on glucose, and therefore loss of  Pgm results in a deficiency in a variety of cellular constituents derived  from glucose-1-phosphate, including trehalose.	transcription
51872	2	334890	5	NULL	NULL	0	NULL	Pgm	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-bacteriol_183_11_11344144_s_6	11344144	Pgm catalyzes the conversion of glucose-6-phosphate  to glucose-1-phosphate during growth on glucose, and therefore loss of  Pgm results in a deficiency in a variety of cellular constituents derived  from glucose-1-phosphate, including trehalose.	transcription
51873	3	334890	5	NULL	NULL	0	NULL	statement 1	NULL		occurs during	NULL				growth on glucose	NULL				NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-bacteriol_183_11_11344144_s_6	11344144	Pgm catalyzes the conversion of glucose-6-phosphate  to glucose-1-phosphate during growth on glucose, and therefore loss of  Pgm results in a deficiency in a variety of cellular constituents derived  from glucose-1-phosphate, including trehalose.	transcription
51874	4	334890	5	NULL	NULL	0	NULL	Pgm	NULL	loss of	results in	NULL				trehalose	NULL	deficiency in			NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-bacteriol_183_11_11344144_s_6	11344144	Pgm catalyzes the conversion of glucose-6-phosphate  to glucose-1-phosphate during growth on glucose, and therefore loss of  Pgm results in a deficiency in a variety of cellular constituents derived  from glucose-1-phosphate, including trehalose.	transcription
52879	1	334890	6	NULL	NULL	0	NULL	glucose-6-phosphate	NULL		is converted to	NULL				glucose-1-phosphate	NULL				NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-bacteriol_183_11_11344144_s_6	11344144	Pgm catalyzes the conversion of glucose-6-phosphate  to glucose-1-phosphate during growth on glucose, and therefore loss of  Pgm results in a deficiency in a variety of cellular constituents derived  from glucose-1-phosphate, including trehalose.	transcription
52880	2	334890	6	NULL	NULL	0	NULL	Pgm	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-bacteriol_183_11_11344144_s_6	11344144	Pgm catalyzes the conversion of glucose-6-phosphate  to glucose-1-phosphate during growth on glucose, and therefore loss of  Pgm results in a deficiency in a variety of cellular constituents derived  from glucose-1-phosphate, including trehalose.	transcription
51875	1	334891	5	NULL	NULL	0	NULL	GAPDH	NULL		is	NULL				glyceraldehyde-3-phosphate dehydrogenase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_5_3091_s_36	9006960	There is experimental evidence indicating that accelerated NADH production by glyceraldehyde-3-phosphate dehydrogenase (GAPDH), linked to an effective glycerol 3-phosphate shuttle transferring cytosolic reducing equivalents to the mitochondria ( 26,  27), mediates this action of glucose ( 25).	transcription
51876	2	334891	5	NULL	NULL	0	NULL	NADH	NULL		is produced by	NULL				GAPDH	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_5_3091_s_36	9006960	There is experimental evidence indicating that accelerated NADH production by glyceraldehyde-3-phosphate dehydrogenase (GAPDH), linked to an effective glycerol 3-phosphate shuttle transferring cytosolic reducing equivalents to the mitochondria ( 26,  27), mediates this action of glucose ( 25).	transcription
51877	3	334891	5	NULL	NULL	0	NULL	cytosolic reducing equivalents	NULL		is transfered to	NULL				mitochondria	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_5_3091_s_36	9006960	There is experimental evidence indicating that accelerated NADH production by glyceraldehyde-3-phosphate dehydrogenase (GAPDH), linked to an effective glycerol 3-phosphate shuttle transferring cytosolic reducing equivalents to the mitochondria ( 26,  27), mediates this action of glucose ( 25).	transcription
51878	4	334891	5	NULL	NULL	0	NULL	glycerol 3-phosphate shuttle	NULL		is required for	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_5_3091_s_36	9006960	There is experimental evidence indicating that accelerated NADH production by glyceraldehyde-3-phosphate dehydrogenase (GAPDH), linked to an effective glycerol 3-phosphate shuttle transferring cytosolic reducing equivalents to the mitochondria ( 26,  27), mediates this action of glucose ( 25).	transcription
51879	5	334891	5	NULL	NULL	0	NULL	statement 1	NULL	accelerated	is linked to	NULL				statement 4	NULL	effective			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_5_3091_s_36	9006960	There is experimental evidence indicating that accelerated NADH production by glyceraldehyde-3-phosphate dehydrogenase (GAPDH), linked to an effective glycerol 3-phosphate shuttle transferring cytosolic reducing equivalents to the mitochondria ( 26,  27), mediates this action of glucose ( 25).	transcription
52877	1	334891	6	NULL	NULL	0	NULL	GAPDH	NULL		accelerates 	NULL				NADH	NULL	production of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_5_3091_s_36	9006960	There is experimental evidence indicating that accelerated NADH production by glyceraldehyde-3-phosphate dehydrogenase (GAPDH), linked to an effective glycerol 3-phosphate shuttle transferring cytosolic reducing equivalents to the mitochondria ( 26,  27), mediates this action of glucose ( 25).	transcription
52878	2	334891	6	NULL	NULL	0	NULL	GAPDH	NULL		is	NULL				glyceraldehyde-3-phosphate dehydrogenase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_5_3091_s_36	9006960	There is experimental evidence indicating that accelerated NADH production by glyceraldehyde-3-phosphate dehydrogenase (GAPDH), linked to an effective glycerol 3-phosphate shuttle transferring cytosolic reducing equivalents to the mitochondria ( 26,  27), mediates this action of glucose ( 25).	transcription
51880	1	334893	5	NULL	NULL	0	NULL	PII	NULL		interacts with	NULL				His6-NAGK	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_53_55202_s_227	15502156	C, interaction of PII with His6-NAGK in the presence of 1 mM ATP and 1 mM 2-oxoglutarate at various MgCl2 concentrations (1, 5, 10, and 20 mM).	transcription
51881	2	334893	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_53_55202_s_227	15502156	C, interaction of PII with His6-NAGK in the presence of 1 mM ATP and 1 mM 2-oxoglutarate at various MgCl2 concentrations (1, 5, 10, and 20 mM).	transcription
51882	3	334893	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				2-oxoglutarate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_53_55202_s_227	15502156	C, interaction of PII with His6-NAGK in the presence of 1 mM ATP and 1 mM 2-oxoglutarate at various MgCl2 concentrations (1, 5, 10, and 20 mM).	transcription
52874	1	334893	6	NULL	NULL	0	NULL	PII	NULL		interacts with	NULL				NAGK	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_53_55202_s_227	15502156	C, interaction of PII with His6-NAGK in the presence of 1 mM ATP and 1 mM 2-oxoglutarate at various MgCl2 concentrations (1, 5, 10, and 20 mM).	transcription
52875	2	334893	6	NULL	NULL	0	NULL	statement 1	NULL		occurs in presence of	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_53_55202_s_227	15502156	C, interaction of PII with His6-NAGK in the presence of 1 mM ATP and 1 mM 2-oxoglutarate at various MgCl2 concentrations (1, 5, 10, and 20 mM).	transcription
52876	3	334893	6	NULL	NULL	0	NULL	statement 1	NULL		occurs in presence of	NULL				2-oxoglutarate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_53_55202_s_227	15502156	C, interaction of PII with His6-NAGK in the presence of 1 mM ATP and 1 mM 2-oxoglutarate at various MgCl2 concentrations (1, 5, 10, and 20 mM).	transcription
51883	1	334894	5	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				PII	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_53_55202_s_255	15502156	In the presence of 5 mM CaCl2, ATP photolabeling to PII was not impaired by the presence of NAGK, and 2-oxoglutarate stimulated ATP binding to PII both in the presence or absence of NAGK.	transcription
51884	2	334894	5	NULL	NULL	0	NULL	2-oxoglutarate	NULL		stimulates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_53_55202_s_255	15502156	In the presence of 5 mM CaCl2, ATP photolabeling to PII was not impaired by the presence of NAGK, and 2-oxoglutarate stimulated ATP binding to PII both in the presence or absence of NAGK.	transcription
52870	1	334894	6	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				PII	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_53_55202_s_255	15502156	In the presence of 5 mM CaCl2, ATP photolabeling to PII was not impaired by the presence of NAGK, and 2-oxoglutarate stimulated ATP binding to PII both in the presence or absence of NAGK.	transcription
52871	2	334894	6	NULL	NULL	0	NULL	2-oxoglutarate	NULL		stimulates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_53_55202_s_255	15502156	In the presence of 5 mM CaCl2, ATP photolabeling to PII was not impaired by the presence of NAGK, and 2-oxoglutarate stimulated ATP binding to PII both in the presence or absence of NAGK.	transcription
52872	3	334894	6	NULL	NULL	0	NULL	ATP	NULL		is photolabeled to	NULL				PII	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_53_55202_s_255	15502156	In the presence of 5 mM CaCl2, ATP photolabeling to PII was not impaired by the presence of NAGK, and 2-oxoglutarate stimulated ATP binding to PII both in the presence or absence of NAGK.	transcription
52873	4	334894	6	NULL	NULL	0	NULL	NAGK	NULL		is not impaired by	NULL				statement 3	NULL	presence of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_53_55202_s_255	15502156	In the presence of 5 mM CaCl2, ATP photolabeling to PII was not impaired by the presence of NAGK, and 2-oxoglutarate stimulated ATP binding to PII both in the presence or absence of NAGK.	transcription
51889	1	334896	5	NULL	NULL	0	NULL	acetoacetyl:acyl CoA-transferase	NULL		catalyze	NULL				butyryl-CoA formation	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_16_4823_s_199	11466286	However, the genome encodes acetoacetyl:acyl CoA-transferase that catalyzes butyryl-CoA formation in solventogenesis (CAP0163-0164) and might also utilize succinate for the synthesis of succinyl-CoA and 2-oxoacid:ferredoxin oxidoreductase (CAC2458-2459) that could catalyze 2-oxoglutarate formation from succinyl-CoA (Fig.  5).	transcription
51890	2	334896	5	NULL	NULL	0	NULL	statement 1	NULL		occurs during	NULL				solventogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_16_4823_s_199	11466286	However, the genome encodes acetoacetyl:acyl CoA-transferase that catalyzes butyryl-CoA formation in solventogenesis (CAP0163-0164) and might also utilize succinate for the synthesis of succinyl-CoA and 2-oxoacid:ferredoxin oxidoreductase (CAC2458-2459) that could catalyze 2-oxoglutarate formation from succinyl-CoA (Fig.  5).	transcription
51891	3	334896	5	NULL	NULL	0	NULL	acetoacetyl:acyl CoA-transferase	NULL		utilize	NULL	might			succinate	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_16_4823_s_199	11466286	However, the genome encodes acetoacetyl:acyl CoA-transferase that catalyzes butyryl-CoA formation in solventogenesis (CAP0163-0164) and might also utilize succinate for the synthesis of succinyl-CoA and 2-oxoacid:ferredoxin oxidoreductase (CAC2458-2459) that could catalyze 2-oxoglutarate formation from succinyl-CoA (Fig.  5).	transcription
51892	4	334896	5	NULL	NULL	0	NULL	statement 3	NULL		is required for	NULL				succinyl-CoA	NULL	synthesis of			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_16_4823_s_199	11466286	However, the genome encodes acetoacetyl:acyl CoA-transferase that catalyzes butyryl-CoA formation in solventogenesis (CAP0163-0164) and might also utilize succinate for the synthesis of succinyl-CoA and 2-oxoacid:ferredoxin oxidoreductase (CAC2458-2459) that could catalyze 2-oxoglutarate formation from succinyl-CoA (Fig.  5).	transcription
51893	5	334896	5	NULL	NULL	0	NULL	2-oxoglutarate	NULL		is formed from	NULL				succinyl-CoA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_16_4823_s_199	11466286	However, the genome encodes acetoacetyl:acyl CoA-transferase that catalyzes butyryl-CoA formation in solventogenesis (CAP0163-0164) and might also utilize succinate for the synthesis of succinyl-CoA and 2-oxoacid:ferredoxin oxidoreductase (CAC2458-2459) that could catalyze 2-oxoglutarate formation from succinyl-CoA (Fig.  5).	transcription
51894	6	334896	5	NULL	NULL	0	NULL	2-oxoacid:ferredoxin oxidoreductase	NULL		catalyze	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_16_4823_s_199	11466286	However, the genome encodes acetoacetyl:acyl CoA-transferase that catalyzes butyryl-CoA formation in solventogenesis (CAP0163-0164) and might also utilize succinate for the synthesis of succinyl-CoA and 2-oxoacid:ferredoxin oxidoreductase (CAC2458-2459) that could catalyze 2-oxoglutarate formation from succinyl-CoA (Fig.  5).	transcription
51895	7	334896	5	NULL	NULL	0	NULL	2-oxoacid:ferredoxin oxidoreductase	NULL		is	NULL				CAC2458-2459	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_16_4823_s_199	11466286	However, the genome encodes acetoacetyl:acyl CoA-transferase that catalyzes butyryl-CoA formation in solventogenesis (CAP0163-0164) and might also utilize succinate for the synthesis of succinyl-CoA and 2-oxoacid:ferredoxin oxidoreductase (CAC2458-2459) that could catalyze 2-oxoglutarate formation from succinyl-CoA (Fig.  5).	transcription
51896	8	334896	5	NULL	NULL	0	NULL	acetoacetyl:acyl CoA-transferase	NULL		is	NULL				CAP0163-0164	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_16_4823_s_199	11466286	However, the genome encodes acetoacetyl:acyl CoA-transferase that catalyzes butyryl-CoA formation in solventogenesis (CAP0163-0164) and might also utilize succinate for the synthesis of succinyl-CoA and 2-oxoacid:ferredoxin oxidoreductase (CAC2458-2459) that could catalyze 2-oxoglutarate formation from succinyl-CoA (Fig.  5).	transcription
52864	1	334896	6	NULL	NULL	0	NULL	acetoacetyl:acyl CoA-transferase	NULL		catalyzes	NULL				butyryl-CoA	NULL	formation of 			NULL	solventogenesis (CAP0163-0164)	0	NULL	NULL	NULL	gw60_jbacteriol_183_16_4823_s_199	11466286	However, the genome encodes acetoacetyl:acyl CoA-transferase that catalyzes butyryl-CoA formation in solventogenesis (CAP0163-0164) and might also utilize succinate for the synthesis of succinyl-CoA and 2-oxoacid:ferredoxin oxidoreductase (CAC2458-2459) that could catalyze 2-oxoglutarate formation from succinyl-CoA (Fig.  5).	transcription
52865	2	334896	6	NULL	NULL	0	NULL	succinyl-CoA	NULL		forms	NULL				2-oxoglutarate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_16_4823_s_199	11466286	However, the genome encodes acetoacetyl:acyl CoA-transferase that catalyzes butyryl-CoA formation in solventogenesis (CAP0163-0164) and might also utilize succinate for the synthesis of succinyl-CoA and 2-oxoacid:ferredoxin oxidoreductase (CAC2458-2459) that could catalyze 2-oxoglutarate formation from succinyl-CoA (Fig.  5).	transcription
52866	3	334896	6	NULL	NULL	0	NULL	2-oxoacid:ferredoxin oxidoreductase	NULL		catalyzes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_16_4823_s_199	11466286	However, the genome encodes acetoacetyl:acyl CoA-transferase that catalyzes butyryl-CoA formation in solventogenesis (CAP0163-0164) and might also utilize succinate for the synthesis of succinyl-CoA and 2-oxoacid:ferredoxin oxidoreductase (CAC2458-2459) that could catalyze 2-oxoglutarate formation from succinyl-CoA (Fig.  5).	transcription
52867	4	334896	6	NULL	NULL	0	NULL	2-oxoacid:ferredoxin oxidoreductase	NULL		is	NULL				CAC2458-2459	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_16_4823_s_199	11466286	However, the genome encodes acetoacetyl:acyl CoA-transferase that catalyzes butyryl-CoA formation in solventogenesis (CAP0163-0164) and might also utilize succinate for the synthesis of succinyl-CoA and 2-oxoacid:ferredoxin oxidoreductase (CAC2458-2459) that could catalyze 2-oxoglutarate formation from succinyl-CoA (Fig.  5).	transcription
52868	5	334896	6	NULL	NULL	0	NULL	succinate	NULL		is used for	NULL				succinyl-CoA	NULL	synthesis of 			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_16_4823_s_199	11466286	However, the genome encodes acetoacetyl:acyl CoA-transferase that catalyzes butyryl-CoA formation in solventogenesis (CAP0163-0164) and might also utilize succinate for the synthesis of succinyl-CoA and 2-oxoacid:ferredoxin oxidoreductase (CAC2458-2459) that could catalyze 2-oxoglutarate formation from succinyl-CoA (Fig.  5).	transcription
52869	6	334896	6	NULL	NULL	0	NULL	acetoacetyl:acyl CoA-transferase	NULL		plays a role in	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_16_4823_s_199	11466286	However, the genome encodes acetoacetyl:acyl CoA-transferase that catalyzes butyryl-CoA formation in solventogenesis (CAP0163-0164) and might also utilize succinate for the synthesis of succinyl-CoA and 2-oxoacid:ferredoxin oxidoreductase (CAC2458-2459) that could catalyze 2-oxoglutarate formation from succinyl-CoA (Fig.  5).	transcription
51897	1	334897	5	NULL	NULL	0	NULL	DHQ	NULL	oxygenation of	leads to	NULL				quercetin	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21387_s_21	16702218	A recent  in vitro study on ANS revealed that ANS is capable of catalyzing the oxygenation of 2 R,3 R- trans-dihydroquercetin (DHQ)  5 toward quercetin  6; this reaction is also catalyzed by flavonol synthase (FLS), another member of the 2-oxoglutaratedependent dioxygenase family ( ).	transcription
51898	2	334897	5	NULL	NULL	0	NULL	ANS	NULL		catalyze	NULL				statement 1	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21387_s_21	16702218	A recent  in vitro study on ANS revealed that ANS is capable of catalyzing the oxygenation of 2 R,3 R- trans-dihydroquercetin (DHQ)  5 toward quercetin  6; this reaction is also catalyzed by flavonol synthase (FLS), another member of the 2-oxoglutaratedependent dioxygenase family ( ).	transcription
51899	3	334897	5	NULL	NULL	0	NULL	DHQ	NULL		is	NULL				2 R,3 R- trans-dihydroquercetin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21387_s_21	16702218	A recent  in vitro study on ANS revealed that ANS is capable of catalyzing the oxygenation of 2 R,3 R- trans-dihydroquercetin (DHQ)  5 toward quercetin  6; this reaction is also catalyzed by flavonol synthase (FLS), another member of the 2-oxoglutaratedependent dioxygenase family ( ).	transcription
51900	4	334897	5	NULL	NULL	0	NULL	FLS	NULL		is	NULL				flavonol synthase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21387_s_21	16702218	A recent  in vitro study on ANS revealed that ANS is capable of catalyzing the oxygenation of 2 R,3 R- trans-dihydroquercetin (DHQ)  5 toward quercetin  6; this reaction is also catalyzed by flavonol synthase (FLS), another member of the 2-oxoglutaratedependent dioxygenase family ( ).	transcription
51901	5	334897	5	NULL	NULL	0	NULL	FLS	NULL		is a member of	NULL				2-oxoglutaratedependent dioxygenase family	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21387_s_21	16702218	A recent  in vitro study on ANS revealed that ANS is capable of catalyzing the oxygenation of 2 R,3 R- trans-dihydroquercetin (DHQ)  5 toward quercetin  6; this reaction is also catalyzed by flavonol synthase (FLS), another member of the 2-oxoglutaratedependent dioxygenase family ( ).	transcription
51902	6	334897	5	NULL	NULL	0	NULL	FLS	NULL		catalyze	NULL				statement 1	NULL				NULL	in vitro	0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21387_s_21	16702218	A recent  in vitro study on ANS revealed that ANS is capable of catalyzing the oxygenation of 2 R,3 R- trans-dihydroquercetin (DHQ)  5 toward quercetin  6; this reaction is also catalyzed by flavonol synthase (FLS), another member of the 2-oxoglutaratedependent dioxygenase family ( ).	transcription
52858	1	334897	6	NULL	NULL	0	NULL	DHQ 5	NULL		is catalyzed towards	NULL				quercetin 6	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21387_s_21	16702218	A recent  in vitro study on ANS revealed that ANS is capable of catalyzing the oxygenation of 2 R,3 R- trans-dihydroquercetin (DHQ)  5 toward quercetin  6; this reaction is also catalyzed by flavonol synthase (FLS), another member of the 2-oxoglutaratedependent dioxygenase family ( ).	transcription
52859	2	334897	6	NULL	NULL	0	NULL	DHQ	NULL		is 	NULL				2 R,3 R- trans-dihydroquercetin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21387_s_21	16702218	A recent  in vitro study on ANS revealed that ANS is capable of catalyzing the oxygenation of 2 R,3 R- trans-dihydroquercetin (DHQ)  5 toward quercetin  6; this reaction is also catalyzed by flavonol synthase (FLS), another member of the 2-oxoglutaratedependent dioxygenase family ( ).	transcription
52860	3	334897	6	NULL	NULL	0	NULL	ANS	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21387_s_21	16702218	A recent  in vitro study on ANS revealed that ANS is capable of catalyzing the oxygenation of 2 R,3 R- trans-dihydroquercetin (DHQ)  5 toward quercetin  6; this reaction is also catalyzed by flavonol synthase (FLS), another member of the 2-oxoglutaratedependent dioxygenase family ( ).	transcription
52861	4	334897	6	NULL	NULL	0	NULL	FLS	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21387_s_21	16702218	A recent  in vitro study on ANS revealed that ANS is capable of catalyzing the oxygenation of 2 R,3 R- trans-dihydroquercetin (DHQ)  5 toward quercetin  6; this reaction is also catalyzed by flavonol synthase (FLS), another member of the 2-oxoglutaratedependent dioxygenase family ( ).	transcription
52862	5	334897	6	NULL	NULL	0	NULL	FLS	NULL		is	NULL				flavonol synthase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21387_s_21	16702218	A recent  in vitro study on ANS revealed that ANS is capable of catalyzing the oxygenation of 2 R,3 R- trans-dihydroquercetin (DHQ)  5 toward quercetin  6; this reaction is also catalyzed by flavonol synthase (FLS), another member of the 2-oxoglutaratedependent dioxygenase family ( ).	transcription
52863	6	334897	6	NULL	NULL	0	NULL	FLS	NULL		is a member of 	NULL				2-oxoglutaratedependent dioxygenase family	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21387_s_21	16702218	A recent  in vitro study on ANS revealed that ANS is capable of catalyzing the oxygenation of 2 R,3 R- trans-dihydroquercetin (DHQ)  5 toward quercetin  6; this reaction is also catalyzed by flavonol synthase (FLS), another member of the 2-oxoglutaratedependent dioxygenase family ( ).	transcription
51903	1	334898	5	NULL	NULL	0	NULL	NAD+ 	NULL		oxidizes	NULL				sorbitol	NULL				NULL		0	NULL	NULL	NULL	gw60_nature_414_6865_813_s_57	11742414	More recently, it has been proposed that oxidation of sorbitol by NAD+ increases the cytosolic NADH:NAD+ ratio, thereby inhibiting activity of the enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and increasing concentrations of triose phosphate 14.	transcription
51904	2	334898	5	NULL	NULL	0	NULL	statement 1	NULL		increases	NULL				NADH:NAD+ ratio	NULL	cytosolic			NULL		0	NULL	NULL	NULL	gw60_nature_414_6865_813_s_57	11742414	More recently, it has been proposed that oxidation of sorbitol by NAD+ increases the cytosolic NADH:NAD+ ratio, thereby inhibiting activity of the enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and increasing concentrations of triose phosphate 14.	transcription
51905	3	334898	5	NULL	NULL	0	NULL	statement 2	NULL		inhibit	NULL				GAPDH	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_nature_414_6865_813_s_57	11742414	More recently, it has been proposed that oxidation of sorbitol by NAD+ increases the cytosolic NADH:NAD+ ratio, thereby inhibiting activity of the enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and increasing concentrations of triose phosphate 14.	transcription
51906	4	334898	5	NULL	NULL	0	NULL	GAPDH	NULL		is	NULL				glyceraldehyde-3-phosphate dehydrogenase	NULL				NULL		0	NULL	NULL	NULL	gw60_nature_414_6865_813_s_57	11742414	More recently, it has been proposed that oxidation of sorbitol by NAD+ increases the cytosolic NADH:NAD+ ratio, thereby inhibiting activity of the enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and increasing concentrations of triose phosphate 14.	transcription
51907	5	334898	5	NULL	NULL	0	NULL	statement 2	NULL		increases	NULL				triose phosphate	NULL	concentration of			NULL		0	NULL	NULL	NULL	gw60_nature_414_6865_813_s_57	11742414	More recently, it has been proposed that oxidation of sorbitol by NAD+ increases the cytosolic NADH:NAD+ ratio, thereby inhibiting activity of the enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and increasing concentrations of triose phosphate 14.	transcription
52853	1	334898	6	NULL	NULL	0	NULL	NAD+	NULL		oxidizes	NULL				sorbitol	NULL				NULL		0	NULL	NULL	NULL	gw60_nature_414_6865_813_s_57	11742414	More recently, it has been proposed that oxidation of sorbitol by NAD+ increases the cytosolic NADH:NAD+ ratio, thereby inhibiting activity of the enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and increasing concentrations of triose phosphate 14.	transcription
52854	2	334898	6	NULL	NULL	0	NULL	statement 1	NULL		increases	NULL				NADH:NAD+ ratio	NULL	cytosolic			NULL		0	NULL	NULL	NULL	gw60_nature_414_6865_813_s_57	11742414	More recently, it has been proposed that oxidation of sorbitol by NAD+ increases the cytosolic NADH:NAD+ ratio, thereby inhibiting activity of the enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and increasing concentrations of triose phosphate 14.	transcription
52855	3	334898	6	NULL	NULL	0	NULL	statement 2	NULL		inhibits	NULL				GAPDH	NULL	activity of 			NULL		0	NULL	NULL	NULL	gw60_nature_414_6865_813_s_57	11742414	More recently, it has been proposed that oxidation of sorbitol by NAD+ increases the cytosolic NADH:NAD+ ratio, thereby inhibiting activity of the enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and increasing concentrations of triose phosphate 14.	transcription
52856	4	334898	6	NULL	NULL	0	NULL	GAPDH	NULL		is	NULL				glyceraldehyde-3-phosphate dehydrogenase	NULL				NULL		0	NULL	NULL	NULL	gw60_nature_414_6865_813_s_57	11742414	More recently, it has been proposed that oxidation of sorbitol by NAD+ increases the cytosolic NADH:NAD+ ratio, thereby inhibiting activity of the enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and increasing concentrations of triose phosphate 14.	transcription
52857	5	334898	6	NULL	NULL	0	NULL	statement 2	NULL		increases	NULL				triose phosphate 14	NULL	concentrations of 			NULL		0	NULL	NULL	NULL	gw60_nature_414_6865_813_s_57	11742414	More recently, it has been proposed that oxidation of sorbitol by NAD+ increases the cytosolic NADH:NAD+ ratio, thereby inhibiting activity of the enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and increasing concentrations of triose phosphate 14.	transcription
51908	1	334899	5	NULL	NULL	0	NULL	LCAT	NULL		is	NULL				lecithin:cholesterol acyltransferase	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_j-biomol-struct-dyn_24_1_16780378_s_2	16780378	Fluorescence spectroscopy has been used to investigate the conformational  changes that occur upon binding of wild type (WT) and mutant (Thr123Ile)  lecithin:cholesterol acyltransferase (LCAT) to the potential substrates  (dioleoyl-phosphatidyl choline [DOPC] and high density lipoprotein [HDL]).	transcription
51909	2	334899	5	NULL	NULL	0	NULL	DOPC	NULL		is	NULL				dioleoyl-phosphatidyl choline	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_j-biomol-struct-dyn_24_1_16780378_s_2	16780378	Fluorescence spectroscopy has been used to investigate the conformational  changes that occur upon binding of wild type (WT) and mutant (Thr123Ile)  lecithin:cholesterol acyltransferase (LCAT) to the potential substrates  (dioleoyl-phosphatidyl choline [DOPC] and high density lipoprotein [HDL]).	transcription
51910	3	334899	5	NULL	NULL	0	NULL	HDL	NULL		is	NULL				high density lipoprotein	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_j-biomol-struct-dyn_24_1_16780378_s_2	16780378	Fluorescence spectroscopy has been used to investigate the conformational  changes that occur upon binding of wild type (WT) and mutant (Thr123Ile)  lecithin:cholesterol acyltransferase (LCAT) to the potential substrates  (dioleoyl-phosphatidyl choline [DOPC] and high density lipoprotein [HDL]).	transcription
51911	4	334899	5	NULL	NULL	0	NULL	DOPC	NULL		is a substrate of	NULL	potential			LCAT	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_j-biomol-struct-dyn_24_1_16780378_s_2	16780378	Fluorescence spectroscopy has been used to investigate the conformational  changes that occur upon binding of wild type (WT) and mutant (Thr123Ile)  lecithin:cholesterol acyltransferase (LCAT) to the potential substrates  (dioleoyl-phosphatidyl choline [DOPC] and high density lipoprotein [HDL]).	transcription
51912	5	334899	5	NULL	NULL	0	NULL	HDL	NULL		is a substrate of	NULL	potential			LCAT	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_j-biomol-struct-dyn_24_1_16780378_s_2	16780378	Fluorescence spectroscopy has been used to investigate the conformational  changes that occur upon binding of wild type (WT) and mutant (Thr123Ile)  lecithin:cholesterol acyltransferase (LCAT) to the potential substrates  (dioleoyl-phosphatidyl choline [DOPC] and high density lipoprotein [HDL]).	transcription
52840	1	334899	6	NULL	NULL	0	NULL	LCAT	NULL	wild type	bind	NULL				DOPC	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_j-biomol-struct-dyn_24_1_16780378_s_2	16780378	Fluorescence spectroscopy has been used to investigate the conformational  changes that occur upon binding of wild type (WT) and mutant (Thr123Ile)  lecithin:cholesterol acyltransferase (LCAT) to the potential substrates  (dioleoyl-phosphatidyl choline [DOPC] and high density lipoprotein [HDL]).	transcription
52841	2	334899	6	NULL	NULL	0	NULL	LCAT	NULL		is	NULL				lecithin:cholesterol acyltransferase	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_j-biomol-struct-dyn_24_1_16780378_s_2	16780378	Fluorescence spectroscopy has been used to investigate the conformational  changes that occur upon binding of wild type (WT) and mutant (Thr123Ile)  lecithin:cholesterol acyltransferase (LCAT) to the potential substrates  (dioleoyl-phosphatidyl choline [DOPC] and high density lipoprotein [HDL]).	transcription
52842	3	334899	6	NULL	NULL	0	NULL	LCAT	NULL	mutant	bind	NULL		Thr123Ile		DOPC	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_j-biomol-struct-dyn_24_1_16780378_s_2	16780378	Fluorescence spectroscopy has been used to investigate the conformational  changes that occur upon binding of wild type (WT) and mutant (Thr123Ile)  lecithin:cholesterol acyltransferase (LCAT) to the potential substrates  (dioleoyl-phosphatidyl choline [DOPC] and high density lipoprotein [HDL]).	transcription
52849	4	334899	6	NULL	NULL	0	NULL	LCAT	NULL	wild type	bind	NULL				HDL	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_j-biomol-struct-dyn_24_1_16780378_s_2	16780378	Fluorescence spectroscopy has been used to investigate the conformational  changes that occur upon binding of wild type (WT) and mutant (Thr123Ile)  lecithin:cholesterol acyltransferase (LCAT) to the potential substrates  (dioleoyl-phosphatidyl choline [DOPC] and high density lipoprotein [HDL]).	transcription
52850	5	334899	6	NULL	NULL	0	NULL	LCAT	NULL	mutant	bind	NULL		Thr123Ile		HDL	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_j-biomol-struct-dyn_24_1_16780378_s_2	16780378	Fluorescence spectroscopy has been used to investigate the conformational  changes that occur upon binding of wild type (WT) and mutant (Thr123Ile)  lecithin:cholesterol acyltransferase (LCAT) to the potential substrates  (dioleoyl-phosphatidyl choline [DOPC] and high density lipoprotein [HDL]).	transcription
52851	6	334899	6	NULL	NULL	0	NULL	DOPC	NULL		is	NULL				dioleoyl-phosphatidyl choline	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_j-biomol-struct-dyn_24_1_16780378_s_2	16780378	Fluorescence spectroscopy has been used to investigate the conformational  changes that occur upon binding of wild type (WT) and mutant (Thr123Ile)  lecithin:cholesterol acyltransferase (LCAT) to the potential substrates  (dioleoyl-phosphatidyl choline [DOPC] and high density lipoprotein [HDL]).	transcription
52852	7	334899	6	NULL	NULL	0	NULL	HDL	NULL		is	NULL				high density lipoprotein	NULL				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_j-biomol-struct-dyn_24_1_16780378_s_2	16780378	Fluorescence spectroscopy has been used to investigate the conformational  changes that occur upon binding of wild type (WT) and mutant (Thr123Ile)  lecithin:cholesterol acyltransferase (LCAT) to the potential substrates  (dioleoyl-phosphatidyl choline [DOPC] and high density lipoprotein [HDL]).	transcription
51913	1	334900	5	NULL	NULL	0	NULL	PIP2	NULL		is	NULL				phosphatidylinositol 4, 5-biphosphate 	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_127_2_521_s_214	10385254	Stimulation of T cells through TCR results in the activation of PLCgammal which hydrolyzes the membrane phospholipid, phosphatidylinositol 4, 5-biphosphate (PIP2), into inositol 1, 4, 5-trisphosphate (IP3) and 1, 2-diacylglycerol (Isakov    et al.,  1987  ; Kikkawa & Nishizuka, 1986  ).	transcription
51914	2	334900	5	NULL	NULL	0	NULL	PIP2	NULL		is a type of	NULL				membrane phospholipid	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_127_2_521_s_214	10385254	Stimulation of T cells through TCR results in the activation of PLCgammal which hydrolyzes the membrane phospholipid, phosphatidylinositol 4, 5-biphosphate (PIP2), into inositol 1, 4, 5-trisphosphate (IP3) and 1, 2-diacylglycerol (Isakov    et al.,  1987  ; Kikkawa & Nishizuka, 1986  ).	transcription
51915	3	334900	5	NULL	NULL	0	NULL	IP3	NULL		is	NULL				inositol 1, 4, 5-trisphosphate	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_127_2_521_s_214	10385254	Stimulation of T cells through TCR results in the activation of PLCgammal which hydrolyzes the membrane phospholipid, phosphatidylinositol 4, 5-biphosphate (PIP2), into inositol 1, 4, 5-trisphosphate (IP3) and 1, 2-diacylglycerol (Isakov    et al.,  1987  ; Kikkawa & Nishizuka, 1986  ).	transcription
51916	4	334900	5	NULL	NULL	0	NULL	PIP2	NULL		is hydrolyzed to	NULL				IP3	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_127_2_521_s_214	10385254	Stimulation of T cells through TCR results in the activation of PLCgammal which hydrolyzes the membrane phospholipid, phosphatidylinositol 4, 5-biphosphate (PIP2), into inositol 1, 4, 5-trisphosphate (IP3) and 1, 2-diacylglycerol (Isakov    et al.,  1987  ; Kikkawa & Nishizuka, 1986  ).	transcription
51917	5	334900	5	NULL	NULL	0	NULL	PIP2	NULL		is hydrolyzed to	NULL				1, 2-diacylglycerol 	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_127_2_521_s_214	10385254	Stimulation of T cells through TCR results in the activation of PLCgammal which hydrolyzes the membrane phospholipid, phosphatidylinositol 4, 5-biphosphate (PIP2), into inositol 1, 4, 5-trisphosphate (IP3) and 1, 2-diacylglycerol (Isakov    et al.,  1987  ; Kikkawa & Nishizuka, 1986  ).	transcription
51918	6	334900	5	NULL	NULL	0	NULL	statement 4	NULL		occurs along with	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_127_2_521_s_214	10385254	Stimulation of T cells through TCR results in the activation of PLCgammal which hydrolyzes the membrane phospholipid, phosphatidylinositol 4, 5-biphosphate (PIP2), into inositol 1, 4, 5-trisphosphate (IP3) and 1, 2-diacylglycerol (Isakov    et al.,  1987  ; Kikkawa & Nishizuka, 1986  ).	transcription
51919	7	334900	5	NULL	NULL	0	NULL	PLCgammal	NULL	activated	catalyze	NULL				statement 6	NULL				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_127_2_521_s_214	10385254	Stimulation of T cells through TCR results in the activation of PLCgammal which hydrolyzes the membrane phospholipid, phosphatidylinositol 4, 5-biphosphate (PIP2), into inositol 1, 4, 5-trisphosphate (IP3) and 1, 2-diacylglycerol (Isakov    et al.,  1987  ; Kikkawa & Nishizuka, 1986  ).	transcription
51920	8	334900	5	NULL	NULL	0	NULL	T cells	NULL		is stimulated through	NULL				TCR	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_127_2_521_s_214	10385254	Stimulation of T cells through TCR results in the activation of PLCgammal which hydrolyzes the membrane phospholipid, phosphatidylinositol 4, 5-biphosphate (PIP2), into inositol 1, 4, 5-trisphosphate (IP3) and 1, 2-diacylglycerol (Isakov    et al.,  1987  ; Kikkawa & Nishizuka, 1986  ).	transcription
51921	9	334900	5	NULL	NULL	0	NULL	statement 8	NULL		activates	NULL				PLCgammal	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_127_2_521_s_214	10385254	Stimulation of T cells through TCR results in the activation of PLCgammal which hydrolyzes the membrane phospholipid, phosphatidylinositol 4, 5-biphosphate (PIP2), into inositol 1, 4, 5-trisphosphate (IP3) and 1, 2-diacylglycerol (Isakov    et al.,  1987  ; Kikkawa & Nishizuka, 1986  ).	transcription
52830	1	334900	6	NULL	NULL	0	NULL	TCR	NULL		stimulates	NULL				T cells	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_127_2_521_s_214	10385254	Stimulation of T cells through TCR results in the activation of PLCgammal which hydrolyzes the membrane phospholipid, phosphatidylinositol 4, 5-biphosphate (PIP2), into inositol 1, 4, 5-trisphosphate (IP3) and 1, 2-diacylglycerol (Isakov    et al.,  1987  ; Kikkawa & Nishizuka, 1986  ).	transcription
52831	2	334900	6	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				PLCgamma1	NULL	activation of 			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_127_2_521_s_214	10385254	Stimulation of T cells through TCR results in the activation of PLCgammal which hydrolyzes the membrane phospholipid, phosphatidylinositol 4, 5-biphosphate (PIP2), into inositol 1, 4, 5-trisphosphate (IP3) and 1, 2-diacylglycerol (Isakov    et al.,  1987  ; Kikkawa & Nishizuka, 1986  ).	transcription
52832	3	334900	6	NULL	NULL	0	NULL	statement 2	NULL		hydrolyzes	NULL				PIP2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_127_2_521_s_214	10385254	Stimulation of T cells through TCR results in the activation of PLCgammal which hydrolyzes the membrane phospholipid, phosphatidylinositol 4, 5-biphosphate (PIP2), into inositol 1, 4, 5-trisphosphate (IP3) and 1, 2-diacylglycerol (Isakov    et al.,  1987  ; Kikkawa & Nishizuka, 1986  ).	transcription
52833	4	334900	6	NULL	NULL	0	NULL	PIP2	NULL		is	NULL				phosphatidylinositol 4, 5-biphosphate	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_127_2_521_s_214	10385254	Stimulation of T cells through TCR results in the activation of PLCgammal which hydrolyzes the membrane phospholipid, phosphatidylinositol 4, 5-biphosphate (PIP2), into inositol 1, 4, 5-trisphosphate (IP3) and 1, 2-diacylglycerol (Isakov    et al.,  1987  ; Kikkawa & Nishizuka, 1986  ).	transcription
52834	5	334900	6	NULL	NULL	0	NULL	PIP2	NULL		is a type of	NULL				membrane phospholipid	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_127_2_521_s_214	10385254	Stimulation of T cells through TCR results in the activation of PLCgammal which hydrolyzes the membrane phospholipid, phosphatidylinositol 4, 5-biphosphate (PIP2), into inositol 1, 4, 5-trisphosphate (IP3) and 1, 2-diacylglycerol (Isakov    et al.,  1987  ; Kikkawa & Nishizuka, 1986  ).	transcription
52835	6	334900	6	NULL	NULL	0	NULL	PIP2	NULL		is hydrolyzed into	NULL				IP3	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_127_2_521_s_214	10385254	Stimulation of T cells through TCR results in the activation of PLCgammal which hydrolyzes the membrane phospholipid, phosphatidylinositol 4, 5-biphosphate (PIP2), into inositol 1, 4, 5-trisphosphate (IP3) and 1, 2-diacylglycerol (Isakov    et al.,  1987  ; Kikkawa & Nishizuka, 1986  ).	transcription
52836	7	334900	6	NULL	NULL	0	NULL	PIP2	NULL		is hydrolyzed into	NULL				1, 2-diacylglycerol	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_127_2_521_s_214	10385254	Stimulation of T cells through TCR results in the activation of PLCgammal which hydrolyzes the membrane phospholipid, phosphatidylinositol 4, 5-biphosphate (PIP2), into inositol 1, 4, 5-trisphosphate (IP3) and 1, 2-diacylglycerol (Isakov    et al.,  1987  ; Kikkawa & Nishizuka, 1986  ).	transcription
52837	8	334900	6	NULL	NULL	0	NULL	IP3	NULL		is	NULL				inositol 1, 4, 5-trisphosphate	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_127_2_521_s_214	10385254	Stimulation of T cells through TCR results in the activation of PLCgammal which hydrolyzes the membrane phospholipid, phosphatidylinositol 4, 5-biphosphate (PIP2), into inositol 1, 4, 5-trisphosphate (IP3) and 1, 2-diacylglycerol (Isakov    et al.,  1987  ; Kikkawa & Nishizuka, 1986  ).	transcription
52838	9	334900	6	NULL	NULL	0	NULL	statement 3	NULL		leads to	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_127_2_521_s_214	10385254	Stimulation of T cells through TCR results in the activation of PLCgammal which hydrolyzes the membrane phospholipid, phosphatidylinositol 4, 5-biphosphate (PIP2), into inositol 1, 4, 5-trisphosphate (IP3) and 1, 2-diacylglycerol (Isakov    et al.,  1987  ; Kikkawa & Nishizuka, 1986  ).	transcription
52839	10	334900	6	NULL	NULL	0	NULL	statement 3	NULL		leads to	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_127_2_521_s_214	10385254	Stimulation of T cells through TCR results in the activation of PLCgammal which hydrolyzes the membrane phospholipid, phosphatidylinositol 4, 5-biphosphate (PIP2), into inositol 1, 4, 5-trisphosphate (IP3) and 1, 2-diacylglycerol (Isakov    et al.,  1987  ; Kikkawa & Nishizuka, 1986  ).	transcription
51922	1	334901	5	NULL	NULL	0	NULL	Pyruvate 	NULL		interacts with	NULL	directly			HPHs	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_180	16223732	Pyruvate and Oxaloacetate Directly Interact with HPHs --	transcription
51923	2	334901	5	NULL	NULL	0	NULL	Oxaloacetate	NULL		interacts with	NULL	directly			HPHs	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_180	16223732	Pyruvate and Oxaloacetate Directly Interact with HPHs --	transcription
53716	1	334901	6	NULL	NULL	0	NULL	Pyruvate			interacts with		directly			HPH					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_180	16223732	Pyruvate and Oxaloacetate Directly Interact with HPHs --	transcription
53717	2	334901	6	NULL	NULL	0	NULL	Oxaloacetate			interacts with		directly			HPH					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_180	16223732	Pyruvate and Oxaloacetate Directly Interact with HPHs --	transcription
51924	1	334902	5	NULL	NULL	0	NULL	pyruvate	NULL		is carboxylated to	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw60_genomeres_12_11_1703_s_126	12421757	PYC2 catalyzes the carboxylation of pyruvate into oxaloacetate.	transcription
51925	2	334902	5	NULL	NULL	0	NULL	PYC2 	NULL		catalyze	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_genomeres_12_11_1703_s_126	12421757	PYC2 catalyzes the carboxylation of pyruvate into oxaloacetate.	transcription
53718	1	334902	6	NULL	NULL	0	NULL	pyruvate			is carboxylated to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw60_genomeres_12_11_1703_s_126	12421757	PYC2 catalyzes the carboxylation of pyruvate into oxaloacetate.	transcription
53719	2	334902	6	NULL	NULL	0	NULL	PYC2			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw60_genomeres_12_11_1703_s_126	12421757	PYC2 catalyzes the carboxylation of pyruvate into oxaloacetate.	transcription
51926	1	334903	5	NULL	NULL	0	NULL	Pyruvate	NULL	carboxylation of	is catalyzed by	NULL				pyruvate carboxylase	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_51_9_2669_s_11	12196457	Pyruvate carboxylation catalyzed by pyruvate carboxylase will supply oxaloacetate to mitochondrial aspartate aminotransferase.	transcription
51927	2	334903	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is supplied to	NULL				aspartate aminotransferase	NULL	mitochondrial			NULL		0	NULL	NULL	NULL	gw60_diabetes_51_9_2669_s_11	12196457	Pyruvate carboxylation catalyzed by pyruvate carboxylase will supply oxaloacetate to mitochondrial aspartate aminotransferase.	transcription
51928	3	334903	5	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_51_9_2669_s_11	12196457	Pyruvate carboxylation catalyzed by pyruvate carboxylase will supply oxaloacetate to mitochondrial aspartate aminotransferase.	transcription
53720	2	334903	6	NULL	NULL	0	NULL	pyruvate carboxylase			catalyzes					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_diabetes_51_9_2669_s_11	12196457	Pyruvate carboxylation catalyzed by pyruvate carboxylase will supply oxaloacetate to mitochondrial aspartate aminotransferase.	transcription
53721	1	334903	6	NULL	NULL	0	NULL	pyruvate			is carboxylated to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw60_diabetes_51_9_2669_s_11	12196457	Pyruvate carboxylation catalyzed by pyruvate carboxylase will supply oxaloacetate to mitochondrial aspartate aminotransferase.	transcription
53722	3	334903	6	NULL	NULL	0	NULL	Oxaloacetate			is supplied to					aspartate aminotransferase		mitochondrial			NULL		0	NULL	NULL	NULL	gw60_diabetes_51_9_2669_s_11	12196457	Pyruvate carboxylation catalyzed by pyruvate carboxylase will supply oxaloacetate to mitochondrial aspartate aminotransferase.	transcription
53723	4	334903	6	NULL	NULL	0	NULL	statement 3			occurs due to					statement 1					NULL		0	NULL	NULL	NULL	gw60_diabetes_51_9_2669_s_11	12196457	Pyruvate carboxylation catalyzed by pyruvate carboxylase will supply oxaloacetate to mitochondrial aspartate aminotransferase.	transcription
51929	1	334904	5	NULL	NULL	0	NULL	pyruvate	NULL		is carboxylated to	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_cell-mol-life-sci_63_7-8_16505973_s_2	16505973	Pyruvate carboxylase (PC) catalyzes the ATP-dependent carboxylation of  pyruvate to oxaloacetate.	transcription
51930	2	334904	5	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_cell-mol-life-sci_63_7-8_16505973_s_2	16505973	Pyruvate carboxylase (PC) catalyzes the ATP-dependent carboxylation of  pyruvate to oxaloacetate.	transcription
51931	3	334904	5	NULL	NULL	0	NULL	PC	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_cell-mol-life-sci_63_7-8_16505973_s_2	16505973	Pyruvate carboxylase (PC) catalyzes the ATP-dependent carboxylation of  pyruvate to oxaloacetate.	transcription
51932	4	334904	5	NULL	NULL	0	NULL	PC	NULL		is	NULL				pyruvate carboxylase	NULL				NULL		0	NULL	NULL	NULL	abs-batch0680-0699_cell-mol-life-sci_63_7-8_16505973_s_2	16505973	Pyruvate carboxylase (PC) catalyzes the ATP-dependent carboxylation of  pyruvate to oxaloacetate.	transcription
53724	1	334904	6	NULL	NULL	0	NULL	PC			is					pyruvate carboxylase					NULL		0	NULL	NULL	NULL	abs-batch0680-0699_cell-mol-life-sci_63_7-8_16505973_s_2	16505973	Pyruvate carboxylase (PC) catalyzes the ATP-dependent carboxylation of  pyruvate to oxaloacetate.	transcription
53725	2	334904	6	NULL	NULL	0	NULL	pyruvate			is carboxylated to					oxaloacetate					NULL		0	NULL	NULL	NULL	abs-batch0680-0699_cell-mol-life-sci_63_7-8_16505973_s_2	16505973	Pyruvate carboxylase (PC) catalyzes the ATP-dependent carboxylation of  pyruvate to oxaloacetate.	transcription
53726	3	334904	6	NULL	NULL	0	NULL	PC			catalyzes					statement 2					NULL		0	NULL	NULL	NULL	abs-batch0680-0699_cell-mol-life-sci_63_7-8_16505973_s_2	16505973	Pyruvate carboxylase (PC) catalyzes the ATP-dependent carboxylation of  pyruvate to oxaloacetate.	transcription
53727	4	334904	6	NULL	NULL	0	NULL	statement 2			is dependent on					ATP					NULL		0	NULL	NULL	NULL	abs-batch0680-0699_cell-mol-life-sci_63_7-8_16505973_s_2	16505973	Pyruvate carboxylase (PC) catalyzes the ATP-dependent carboxylation of  pyruvate to oxaloacetate.	transcription
51933	1	334905	5	NULL	NULL	0	NULL	CHA	NULL		is converted to	NULL				pyruvate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_9	12486039	Electrospray-ionization mass spectrometry indicated that LigK catalyzes not only the conversion of CHA to pyruvate and oxaloacetate but also that of oxaloacetate to pyruvate and CO2.	transcription
51934	2	334905	5	NULL	NULL	0	NULL	CHA	NULL		is converted to	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_9	12486039	Electrospray-ionization mass spectrometry indicated that LigK catalyzes not only the conversion of CHA to pyruvate and oxaloacetate but also that of oxaloacetate to pyruvate and CO2.	transcription
51935	3	334905	5	NULL	NULL	0	NULL	statement 1	NULL		occurs along with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_9	12486039	Electrospray-ionization mass spectrometry indicated that LigK catalyzes not only the conversion of CHA to pyruvate and oxaloacetate but also that of oxaloacetate to pyruvate and CO2.	transcription
51936	4	334905	5	NULL	NULL	0	NULL	LigK	NULL		catalyzes	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_9	12486039	Electrospray-ionization mass spectrometry indicated that LigK catalyzes not only the conversion of CHA to pyruvate and oxaloacetate but also that of oxaloacetate to pyruvate and CO2.	transcription
53728	1	334905	6	NULL	NULL	0	NULL	CHA			is converted to					pyruvate					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_9	12486039	Electrospray-ionization mass spectrometry indicated that LigK catalyzes not only the conversion of CHA to pyruvate and oxaloacetate but also that of oxaloacetate to pyruvate and CO2.	transcription
53729	2	334905	6	NULL	NULL	0	NULL	CHA			is converted to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_9	12486039	Electrospray-ionization mass spectrometry indicated that LigK catalyzes not only the conversion of CHA to pyruvate and oxaloacetate but also that of oxaloacetate to pyruvate and CO2.	transcription
53730	3	334905	6	NULL	NULL	0	NULL	LigK			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_9	12486039	Electrospray-ionization mass spectrometry indicated that LigK catalyzes not only the conversion of CHA to pyruvate and oxaloacetate but also that of oxaloacetate to pyruvate and CO2.	transcription
53731	4	334905	6	NULL	NULL	0	NULL	LigK			catalyzes					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_9	12486039	Electrospray-ionization mass spectrometry indicated that LigK catalyzes not only the conversion of CHA to pyruvate and oxaloacetate but also that of oxaloacetate to pyruvate and CO2.	transcription
53732	5	334905	6	NULL	NULL	0	NULL	Oxaloacetate			is catalyzed to					pyruvate					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_9	12486039	Electrospray-ionization mass spectrometry indicated that LigK catalyzes not only the conversion of CHA to pyruvate and oxaloacetate but also that of oxaloacetate to pyruvate and CO2.	transcription
53733	6	334905	6	NULL	NULL	0	NULL	Oxaloacetate			is catalyzed to					CO2					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_9	12486039	Electrospray-ionization mass spectrometry indicated that LigK catalyzes not only the conversion of CHA to pyruvate and oxaloacetate but also that of oxaloacetate to pyruvate and CO2.	transcription
53734	7	334905	6	NULL	NULL	0	NULL	LigK			catalyzes					statement 5					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_9	12486039	Electrospray-ionization mass spectrometry indicated that LigK catalyzes not only the conversion of CHA to pyruvate and oxaloacetate but also that of oxaloacetate to pyruvate and CO2.	transcription
53735	8	334905	6	NULL	NULL	0	NULL	LigK			catalyzes					statement 6					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_9	12486039	Electrospray-ionization mass spectrometry indicated that LigK catalyzes not only the conversion of CHA to pyruvate and oxaloacetate but also that of oxaloacetate to pyruvate and CO2.	transcription
52484	1	334906	5	NULL	NULL	0	NULL	citrate	NULL		is split into	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_4_665_s_432	16339740	The conversion involves the splitting of citrate into oxaloacetate and acetate catalyzed by citrate lyase and the decarboxylation of oxaloacetate to pyruvate and carbon dioxide catalyzed by oxaloacetate decarboxylase.	transcription
52485	2	334906	5	NULL	NULL	0	NULL	citrate	NULL		is split into	NULL				acetate	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_4_665_s_432	16339740	The conversion involves the splitting of citrate into oxaloacetate and acetate catalyzed by citrate lyase and the decarboxylation of oxaloacetate to pyruvate and carbon dioxide catalyzed by oxaloacetate decarboxylase.	transcription
52486	3	334906	5	NULL	NULL	0	NULL	statement 1	NULL		occurs along with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_4_665_s_432	16339740	The conversion involves the splitting of citrate into oxaloacetate and acetate catalyzed by citrate lyase and the decarboxylation of oxaloacetate to pyruvate and carbon dioxide catalyzed by oxaloacetate decarboxylase.	transcription
52487	4	334906	5	NULL	NULL	0	NULL	citrate lyase	NULL		catalyzes	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_4_665_s_432	16339740	The conversion involves the splitting of citrate into oxaloacetate and acetate catalyzed by citrate lyase and the decarboxylation of oxaloacetate to pyruvate and carbon dioxide catalyzed by oxaloacetate decarboxylase.	transcription
52488	5	334906	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is decarboxylatd to	NULL				pyruvate	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_4_665_s_432	16339740	The conversion involves the splitting of citrate into oxaloacetate and acetate catalyzed by citrate lyase and the decarboxylation of oxaloacetate to pyruvate and carbon dioxide catalyzed by oxaloacetate decarboxylase.	transcription
52489	6	334906	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is decarboxylatd to	NULL				carbon dioxide	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_4_665_s_432	16339740	The conversion involves the splitting of citrate into oxaloacetate and acetate catalyzed by citrate lyase and the decarboxylation of oxaloacetate to pyruvate and carbon dioxide catalyzed by oxaloacetate decarboxylase.	transcription
52490	7	334906	5	NULL	NULL	0	NULL	statement 5	NULL		occurs along with	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_4_665_s_432	16339740	The conversion involves the splitting of citrate into oxaloacetate and acetate catalyzed by citrate lyase and the decarboxylation of oxaloacetate to pyruvate and carbon dioxide catalyzed by oxaloacetate decarboxylase.	transcription
52491	8	334906	5	NULL	NULL	0	NULL	oxaloacetate decarboxylase	NULL		catalyzes	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_4_665_s_432	16339740	The conversion involves the splitting of citrate into oxaloacetate and acetate catalyzed by citrate lyase and the decarboxylation of oxaloacetate to pyruvate and carbon dioxide catalyzed by oxaloacetate decarboxylase.	transcription
53736	1	334906	6	NULL	NULL	0	NULL	citrate			is converted to					oxaloacetate					NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_4_665_s_432	16339740	The conversion involves the splitting of citrate into oxaloacetate and acetate catalyzed by citrate lyase and the decarboxylation of oxaloacetate to pyruvate and carbon dioxide catalyzed by oxaloacetate decarboxylase.	transcription
53737	2	334906	6	NULL	NULL	0	NULL	citrate			is converted to					acetate					NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_4_665_s_432	16339740	The conversion involves the splitting of citrate into oxaloacetate and acetate catalyzed by citrate lyase and the decarboxylation of oxaloacetate to pyruvate and carbon dioxide catalyzed by oxaloacetate decarboxylase.	transcription
53738	3	334906	6	NULL	NULL	0	NULL	citrate lyase			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_4_665_s_432	16339740	The conversion involves the splitting of citrate into oxaloacetate and acetate catalyzed by citrate lyase and the decarboxylation of oxaloacetate to pyruvate and carbon dioxide catalyzed by oxaloacetate decarboxylase.	transcription
53740	4	334906	6	NULL	NULL	0	NULL	citrate lyase			catalyzes					statement 2					NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_4_665_s_432	16339740	The conversion involves the splitting of citrate into oxaloacetate and acetate catalyzed by citrate lyase and the decarboxylation of oxaloacetate to pyruvate and carbon dioxide catalyzed by oxaloacetate decarboxylase.	transcription
53741	5	334906	6	NULL	NULL	0	NULL	Oxaloacetate			decarboxylated to					pyruvate					NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_4_665_s_432	16339740	The conversion involves the splitting of citrate into oxaloacetate and acetate catalyzed by citrate lyase and the decarboxylation of oxaloacetate to pyruvate and carbon dioxide catalyzed by oxaloacetate decarboxylase.	transcription
53742	6	334906	6	NULL	NULL	0	NULL	Oxaloacetate			decarboxylated to					carbon dioxide					NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_4_665_s_432	16339740	The conversion involves the splitting of citrate into oxaloacetate and acetate catalyzed by citrate lyase and the decarboxylation of oxaloacetate to pyruvate and carbon dioxide catalyzed by oxaloacetate decarboxylase.	transcription
53743	7	334906	6	NULL	NULL	0	NULL	oxaloacetate decarboxylase			catalyzes					statement 5					NULL		0	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_4_665_s_432	16339740	The conversion involves the splitting of citrate into oxaloacetate and acetate catalyzed by citrate lyase and the decarboxylation of oxaloacetate to pyruvate and carbon dioxide catalyzed by oxaloacetate decarboxylase.	transcription
53744	8	334906	6	NULL	NULL	0	NULL	oxaloacetate decarboxylase			catalyzes					statement 6					NULL		NULL	NULL	NULL	NULL	gw70_microbiolmolbiolr_69_4_665_s_432	16339740	The conversion involves the splitting of citrate into oxaloacetate and acetate catalyzed by citrate lyase and the decarboxylation of oxaloacetate to pyruvate and carbon dioxide catalyzed by oxaloacetate decarboxylase.	transcription
52069	1	334907	5	NULL	NULL	0	NULL	pyruvate	NULL		is carboxylated to	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_22_2_105_s_218	9729766	1.1) catalyzes the biotin-dependent carboxylation of  pyruvate to form oxaloacetate ( Fig. 2).	transcription
52070	2	334907	5	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				biotin	NULL				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_22_2_105_s_218	9729766	1.1) catalyzes the biotin-dependent carboxylation of  pyruvate to form oxaloacetate ( Fig. 2).	transcription
53745	1	334907	6	NULL	NULL	0	NULL	pyruvate			is carboxylated to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_22_2_105_s_218	9729766	1.1) catalyzes the biotin-dependent carboxylation of  pyruvate to form oxaloacetate ( Fig. 2).	transcription
53746	2	334907	6	NULL	NULL	0	NULL	statement 1			is dependent on					biotin					NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_22_2_105_s_218	9729766	1.1) catalyzes the biotin-dependent carboxylation of  pyruvate to form oxaloacetate ( Fig. 2).	transcription
52071	1	334908	5	NULL	NULL	0	NULL	CHA			is converted to					pyruvate					NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_178	12486039	This result indicated that LigK catalyzes the conversion of CHA to pyruvate and oxaloacetate.	transcription
52072	2	334908	5	NULL	NULL	0	NULL	LigK			is converted to					oxaloacetate					NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_178	12486039	This result indicated that LigK catalyzes the conversion of CHA to pyruvate and oxaloacetate.	transcription
54312	3	334908	5	NULL	NULL	0	NULL	statement 1			occurs along with					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_178	12486039	This result indicated that LigK catalyzes the conversion of CHA to pyruvate and oxaloacetate.	transcription
54313	4	334908	5	NULL	NULL	0	NULL	LigK			catalyzes					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_178	12486039	This result indicated that LigK catalyzes the conversion of CHA to pyruvate and oxaloacetate.	transcription
53747	1	334908	6	NULL	NULL	0	NULL	CHA			is converted to					pyruvate					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_178	12486039	This result indicated that LigK catalyzes the conversion of CHA to pyruvate and oxaloacetate.	transcription
53748	2	334908	6	NULL	NULL	0	NULL	CHA			is converted to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_178	12486039	This result indicated that LigK catalyzes the conversion of CHA to pyruvate and oxaloacetate.	transcription
53749	3	334908	6	NULL	NULL	0	NULL	LigK			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_178	12486039	This result indicated that LigK catalyzes the conversion of CHA to pyruvate and oxaloacetate.	transcription
53750	4	334908	6	NULL	NULL	0	NULL	LigK			catalyzes					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_1_41_s_178	12486039	This result indicated that LigK catalyzes the conversion of CHA to pyruvate and oxaloacetate.	transcription
52073	1	334909	5	NULL	NULL	0	NULL	citrate	NULL		is converted to	NULL				pyruvate	NULL				NULL	lactic acid bacteria	NULL	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
52074	2	334909	5	NULL	NULL	0	NULL	CitP	NULL		is required for	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
52075	3	334909	5	NULL	NULL	0	NULL	CL	NULL		is required for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
52076	4	334909	5	NULL	NULL	0	NULL	oxaloacetate decarboxylase	NULL		is required for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
52077	5	334909	5	NULL	NULL	0	NULL	CitP	NULL		is	NULL				citrate permease	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
52078	6	334909	5	NULL	NULL	0	NULL	CL	NULL		is	NULL				citrate lyase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
52079	7	334909	5	NULL	NULL	0	NULL	citrate		intracellular	is cleaved into					acetate					NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
52080	10	334909	5	NULL	NULL	0	NULL	CL			catalyzes					statement 9					NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
52081	11	334909	5	NULL	NULL	0	NULL	oxaloacetate			is decarboxylatd to					carbon dioxide					NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
52082	14	334909	5	NULL	NULL	0	NULL	oxaloacetate decarboxylase			catalyzes					statement 13					NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
54314	8	334909	5	NULL	NULL	0	NULL	citrate		intracellular	is cleaved into					oxaloacetate					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
54315	9	334909	5	NULL	NULL	0	NULL	statement 7			occurs along with					statement 8					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
54316	12	334909	5	NULL	NULL	0	NULL	oxaloacetate			is decarboxylatd to					pyruvate					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
54317	13	334909	5	NULL	NULL	0	NULL	statement 11			occurs along with					statement 12					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
53751	1	334909	6	NULL	NULL	0	NULL	citrate			is converted to					pyruvate					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
53752	2	334909	6	NULL	NULL	0	NULL	lactic acid bacteria			performs					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
53753	3	334909	6	NULL	NULL	0	NULL	statement 1			requires					CitP					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
53754	4	334909	6	NULL	NULL	0	NULL	statement 1			requires					CL					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
53755	5	334909	6	NULL	NULL	0	NULL	statement 1			requires					oxaloacetate decarboxylase					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
53756	6	334909	6	NULL	NULL	0	NULL	CitP			is					citrate permease					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
53757	7	334909	6	NULL	NULL	0	NULL	CL			is					citrate lyase					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
53758	8	334909	6	NULL	NULL	0	NULL	citrate		intracellular	is cleaved into					acetate					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
53759	9	334909	6	NULL	NULL	0	NULL	citrate		intracellular	is cleaved into					oxaloacetate					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
53760	10	334909	6	NULL	NULL	0	NULL	CL			catalyzes					statement 8					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
53761	11	334909	6	NULL	NULL	0	NULL	CL			catalyzes					statement 9					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
53762	12	334909	6	NULL	NULL	0	NULL	Oxaloacetate			is decarboxylated into					carbon dioxide					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
53763	13	334909	6	NULL	NULL	0	NULL	oxaloacetate			is decarboxylated into					pyruvate					NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
53764	14	334909	6	NULL	NULL	0	NULL	oxaloacetate decarboxylase			catalyzes					statement 12					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
53765	15	334909	6	NULL	NULL	0	NULL	oxaloacetate decarboxylase			catalyzes					statement 13					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_14_4411_s_9	10400601	Conversion of citrate into pyruvate by lactic acid bacteria requires three enzymes: a citrate permease (CitP), a citrate lyase (CL) that cleaves intracellular citrate into acetate and oxaloacetate, and an oxaloacetate decarboxylase that catalyzes the oxaloacetate decarboxylation into carbon dioxide and pyruvate.	transcription
52083	1	334910	5	NULL	NULL	0	NULL	pyruvate	NULL		is converted to	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevphysiol_65_0_401_s_142	12524459	Glutamate lost to the system by oxidation is replaced through anaplerosis, beginning  with pyruvate carboxylase catalyzed conversion of pyruvate to oxaloacetate.	transcription
52084	2	334910	5	NULL	NULL	0	NULL	pyruvate carboxylase	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevphysiol_65_0_401_s_142	12524459	Glutamate lost to the system by oxidation is replaced through anaplerosis, beginning  with pyruvate carboxylase catalyzed conversion of pyruvate to oxaloacetate.	transcription
52085	3	334910	5	NULL	NULL	0	NULL	glutamate	NULL	loss of	is caused by	NULL				oxidation	NULL				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_65_0_401_s_142	12524459	Glutamate lost to the system by oxidation is replaced through anaplerosis, beginning  with pyruvate carboxylase catalyzed conversion of pyruvate to oxaloacetate.	transcription
52087	5	334910	5	NULL	NULL	0	NULL	anaplerosis	NULL		replaces	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_annurevphysiol_65_0_401_s_142	12524459	Glutamate lost to the system by oxidation is replaced through anaplerosis, beginning  with pyruvate carboxylase catalyzed conversion of pyruvate to oxaloacetate.	transcription
53766	1	334910	6	NULL	NULL	0	NULL	pyruvate			is converted to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw70_annurevphysiol_65_0_401_s_142	12524459	Glutamate lost to the system by oxidation is replaced through anaplerosis, beginning  with pyruvate carboxylase catalyzed conversion of pyruvate to oxaloacetate.	transcription
53767	2	334910	6	NULL	NULL	0	NULL	pyruvate carboxylase			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw70_annurevphysiol_65_0_401_s_142	12524459	Glutamate lost to the system by oxidation is replaced through anaplerosis, beginning  with pyruvate carboxylase catalyzed conversion of pyruvate to oxaloacetate.	transcription
53768	3	334910	6	NULL	NULL	0	NULL	glutamate		lost	is replaced through					anaplerosis					NULL		0	NULL	NULL	NULL	gw70_annurevphysiol_65_0_401_s_142	12524459	Glutamate lost to the system by oxidation is replaced through anaplerosis, beginning  with pyruvate carboxylase catalyzed conversion of pyruvate to oxaloacetate.	transcription
52088	1	334911	5	NULL	NULL	0	NULL	B. subtilis	NULL		contains	NULL				PC	NULL				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_33	12839772	B. subtilis contains a pyruvate carboxylase (PC), encoded by  pycA, to convert pyruvate to oxaloacetate, and lacks phosphoenolpyruvate carboxylase activity ( ).	transcription
52089	2	334911	5	NULL	NULL	0	NULL	PC	NULL		is	NULL				pyruvate carboxylase	NULL				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_33	12839772	B. subtilis contains a pyruvate carboxylase (PC), encoded by  pycA, to convert pyruvate to oxaloacetate, and lacks phosphoenolpyruvate carboxylase activity ( ).	transcription
52090	3	334911	5	NULL	NULL	0	NULL	PC	NULL		is encoded by	NULL				pycA	NULL				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_33	12839772	B. subtilis contains a pyruvate carboxylase (PC), encoded by  pycA, to convert pyruvate to oxaloacetate, and lacks phosphoenolpyruvate carboxylase activity ( ).	transcription
52091	4	334911	5	NULL	NULL	0	NULL	pyruvate	NULL		is converted to	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_33	12839772	B. subtilis contains a pyruvate carboxylase (PC), encoded by  pycA, to convert pyruvate to oxaloacetate, and lacks phosphoenolpyruvate carboxylase activity ( ).	transcription
52092	5	334911	5	NULL	NULL	0	NULL	PC	NULL		catalyzes	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_33	12839772	B. subtilis contains a pyruvate carboxylase (PC), encoded by  pycA, to convert pyruvate to oxaloacetate, and lacks phosphoenolpyruvate carboxylase activity ( ).	transcription
52093	6	334911	5	NULL	NULL	0	NULL	PC	NULL		lacks	NULL				phosphoenolpyruvate carboxylase activity	NULL				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_33	12839772	B. subtilis contains a pyruvate carboxylase (PC), encoded by  pycA, to convert pyruvate to oxaloacetate, and lacks phosphoenolpyruvate carboxylase activity ( ).	transcription
53769	1	334911	6	NULL	NULL	0	NULL	PC			is					pyruvate carboxylase					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_33	12839772	B. subtilis contains a pyruvate carboxylase (PC), encoded by  pycA, to convert pyruvate to oxaloacetate, and lacks phosphoenolpyruvate carboxylase activity ( ).	transcription
53770	2	334911	6	NULL	NULL	0	NULL	pyruvate			is converted to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_33	12839772	B. subtilis contains a pyruvate carboxylase (PC), encoded by  pycA, to convert pyruvate to oxaloacetate, and lacks phosphoenolpyruvate carboxylase activity ( ).	transcription
53771	3	334911	6	NULL	NULL	0	NULL	PC			catalyzes					statement 2					NULL		NULL	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_33	12839772	B. subtilis contains a pyruvate carboxylase (PC), encoded by  pycA, to convert pyruvate to oxaloacetate, and lacks phosphoenolpyruvate carboxylase activity ( ).	transcription
53772	4	334911	6	NULL	NULL	0	NULL	PC			lacks					phosphoenolpyruvate carboxylase		activity of 			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_33	12839772	B. subtilis contains a pyruvate carboxylase (PC), encoded by  pycA, to convert pyruvate to oxaloacetate, and lacks phosphoenolpyruvate carboxylase activity ( ).	transcription
53773	5	334911	6	NULL	NULL	0	NULL	PC			is encoded by					pycA					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_33	12839772	B. subtilis contains a pyruvate carboxylase (PC), encoded by  pycA, to convert pyruvate to oxaloacetate, and lacks phosphoenolpyruvate carboxylase activity ( ).	transcription
53774	6	334911	6	NULL	NULL	0	NULL	B. subtilis			contains					PC					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_33	12839772	B. subtilis contains a pyruvate carboxylase (PC), encoded by  pycA, to convert pyruvate to oxaloacetate, and lacks phosphoenolpyruvate carboxylase activity ( ).	transcription
52094	1	334912	5	NULL	NULL	0	NULL	PycA	NULL		is	NULL				pyruvate carboxylase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_24_8478_s_281	15576798	Pyruvate carboxylase (PycA) catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate, a substrate for aspartate aminotransferase (AspB).	transcription
52095	2	334912	5	NULL	NULL	0	NULL	pyruvate	NULL		is carboxylated to	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_24_8478_s_281	15576798	Pyruvate carboxylase (PycA) catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate, a substrate for aspartate aminotransferase (AspB).	transcription
52096	3	334912	5	NULL	NULL	0	NULL	statement 2	NULL		is dependent on	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_24_8478_s_281	15576798	Pyruvate carboxylase (PycA) catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate, a substrate for aspartate aminotransferase (AspB).	transcription
52097	4	334912	5	NULL	NULL	0	NULL	PycA	NULL		catalyzes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_24_8478_s_281	15576798	Pyruvate carboxylase (PycA) catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate, a substrate for aspartate aminotransferase (AspB).	transcription
52098	5	334912	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is a substrate for	NULL				AspB	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_24_8478_s_281	15576798	Pyruvate carboxylase (PycA) catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate, a substrate for aspartate aminotransferase (AspB).	transcription
52099	6	334912	5	NULL	NULL	0	NULL	AspB	NULL		is	NULL				aspartate aminotransferase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_24_8478_s_281	15576798	Pyruvate carboxylase (PycA) catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate, a substrate for aspartate aminotransferase (AspB).	transcription
53784	1	334912	6	NULL	NULL	0	NULL	pyruvate			is carboxylated to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_24_8478_s_281	15576798	Pyruvate carboxylase (PycA) catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate, a substrate for aspartate aminotransferase (AspB).	transcription
53785	2	334912	6	NULL	NULL	0	NULL	statement 1			is dependent on					ATP					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_24_8478_s_281	15576798	Pyruvate carboxylase (PycA) catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate, a substrate for aspartate aminotransferase (AspB).	transcription
53786	3	334912	6	NULL	NULL	0	NULL	PycA			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_24_8478_s_281	15576798	Pyruvate carboxylase (PycA) catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate, a substrate for aspartate aminotransferase (AspB).	transcription
53787	4	334912	6	NULL	NULL	0	NULL	PycA			is					Pyruvate carboxylase					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_24_8478_s_281	15576798	Pyruvate carboxylase (PycA) catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate, a substrate for aspartate aminotransferase (AspB).	transcription
53788	5	334912	6	NULL	NULL	0	NULL	Oxaloacetate			is a substrate for					aspartate aminotransferase 					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_24_8478_s_281	15576798	Pyruvate carboxylase (PycA) catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate, a substrate for aspartate aminotransferase (AspB).	transcription
53789	6	334912	6	NULL	NULL	0	NULL	AspB			is					aspartate aminotransferase					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_24_8478_s_281	15576798	Pyruvate carboxylase (PycA) catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate, a substrate for aspartate aminotransferase (AspB).	transcription
52100	1	334913	5	NULL	NULL	0	NULL	PC	NULL		is	NULL				pyruvate carboxylase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27466_s_22	15917242	Pyruvate carboxylase (PC), a member of the biotin-containing enzyme family, catalyzes the ATP-dependent carboxylation of pyruvate to oxaloacetate ( ).	transcription
52101	2	334913	5	NULL	NULL	0	NULL	PC	NULL		is a member of	NULL				biotin-containing enzyme family	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27466_s_22	15917242	Pyruvate carboxylase (PC), a member of the biotin-containing enzyme family, catalyzes the ATP-dependent carboxylation of pyruvate to oxaloacetate ( ).	transcription
52102	3	334913	5	NULL	NULL	0	NULL	pyruvate	NULL		is carboxylated to	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27466_s_22	15917242	Pyruvate carboxylase (PC), a member of the biotin-containing enzyme family, catalyzes the ATP-dependent carboxylation of pyruvate to oxaloacetate ( ).	transcription
52103	4	334913	5	NULL	NULL	0	NULL	statement 3	NULL		is dependent on	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27466_s_22	15917242	Pyruvate carboxylase (PC), a member of the biotin-containing enzyme family, catalyzes the ATP-dependent carboxylation of pyruvate to oxaloacetate ( ).	transcription
52104	5	334913	5	NULL	NULL	0	NULL	PC	NULL		catalyzes	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27466_s_22	15917242	Pyruvate carboxylase (PC), a member of the biotin-containing enzyme family, catalyzes the ATP-dependent carboxylation of pyruvate to oxaloacetate ( ).	transcription
53790	1	334913	6	NULL	NULL	0	NULL	PC			is					pyruvate carboxylase					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27466_s_22	15917242	Pyruvate carboxylase (PC), a member of the biotin-containing enzyme family, catalyzes the ATP-dependent carboxylation of pyruvate to oxaloacetate ( ).	transcription
53791	2	334913	6	NULL	NULL	0	NULL	PC			is a member of					biotin-containing enzyme family					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27466_s_22	15917242	Pyruvate carboxylase (PC), a member of the biotin-containing enzyme family, catalyzes the ATP-dependent carboxylation of pyruvate to oxaloacetate ( ).	transcription
53792	3	334913	6	NULL	NULL	0	NULL	pyruvate			is carboxylated to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27466_s_22	15917242	Pyruvate carboxylase (PC), a member of the biotin-containing enzyme family, catalyzes the ATP-dependent carboxylation of pyruvate to oxaloacetate ( ).	transcription
53793	4	334913	6	NULL	NULL	0	NULL	statement 3			is dependent on					ATP					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27466_s_22	15917242	Pyruvate carboxylase (PC), a member of the biotin-containing enzyme family, catalyzes the ATP-dependent carboxylation of pyruvate to oxaloacetate ( ).	transcription
53794	5	334913	6	NULL	NULL	0	NULL	PC			catalyzes					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27466_s_22	15917242	Pyruvate carboxylase (PC), a member of the biotin-containing enzyme family, catalyzes the ATP-dependent carboxylation of pyruvate to oxaloacetate ( ).	transcription
52105	1	334914	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is formed from	NULL				pyruvate & HCO3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_30_27176_s_21	11986306	Pyruvate carboxylase catalyzes the ATP-driven formation of oxaloacetate from pyruvate and HCO3  and P-enolpyruvate carboxykinase (PEPCK) (EC 4.1.	transcription
52106	2	334914	5	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_30_27176_s_21	11986306	Pyruvate carboxylase catalyzes the ATP-driven formation of oxaloacetate from pyruvate and HCO3  and P-enolpyruvate carboxykinase (PEPCK) (EC 4.1.	transcription
52107	3	334914	5	NULL	NULL	0	NULL	pyruvate carboxylase	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_30_27176_s_21	11986306	Pyruvate carboxylase catalyzes the ATP-driven formation of oxaloacetate from pyruvate and HCO3  and P-enolpyruvate carboxykinase (PEPCK) (EC 4.1.	transcription
53795	1	334914	6	NULL	NULL	0	NULL	oxaloacetate			is formed from					pyruvate					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_30_27176_s_21	11986306	Pyruvate carboxylase catalyzes the ATP-driven formation of oxaloacetate from pyruvate and HCO3  and P-enolpyruvate carboxykinase (PEPCK) (EC 4.1.	transcription
53796	2	334914	6	NULL	NULL	0	NULL	Oxaloacetate			is formed from					HCO3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_30_27176_s_21	11986306	Pyruvate carboxylase catalyzes the ATP-driven formation of oxaloacetate from pyruvate and HCO3  and P-enolpyruvate carboxykinase (PEPCK) (EC 4.1.	transcription
53797	3	334914	6	NULL	NULL	0	NULL	oxaloacetate			is formed from					PEPCK					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_30_27176_s_21	11986306	Pyruvate carboxylase catalyzes the ATP-driven formation of oxaloacetate from pyruvate and HCO3  and P-enolpyruvate carboxykinase (PEPCK) (EC 4.1.	transcription
53798	4	334914	6	NULL	NULL	0	NULL	PEPCK			is					P-enolpyruvate carboxykinase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_30_27176_s_21	11986306	Pyruvate carboxylase catalyzes the ATP-driven formation of oxaloacetate from pyruvate and HCO3  and P-enolpyruvate carboxykinase (PEPCK) (EC 4.1.	transcription
53799	5	334914	6	NULL	NULL	0	NULL	statement 1			occurs simultaneously with					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_30_27176_s_21	11986306	Pyruvate carboxylase catalyzes the ATP-driven formation of oxaloacetate from pyruvate and HCO3  and P-enolpyruvate carboxykinase (PEPCK) (EC 4.1.	transcription
53809	6	334914	6	NULL	NULL	0	NULL	statement 2			occurs simultaneously with					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_30_27176_s_21	11986306	Pyruvate carboxylase catalyzes the ATP-driven formation of oxaloacetate from pyruvate and HCO3  and P-enolpyruvate carboxykinase (PEPCK) (EC 4.1.	transcription
53810	7	334914	6	NULL	NULL	0	NULL	Pyruvate carboxylase			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_30_27176_s_21	11986306	Pyruvate carboxylase catalyzes the ATP-driven formation of oxaloacetate from pyruvate and HCO3  and P-enolpyruvate carboxykinase (PEPCK) (EC 4.1.	transcription
53811	8	334914	6	NULL	NULL	0	NULL	Pyruvate carboxylase			catalyzes					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_30_27176_s_21	11986306	Pyruvate carboxylase catalyzes the ATP-driven formation of oxaloacetate from pyruvate and HCO3  and P-enolpyruvate carboxykinase (PEPCK) (EC 4.1.	transcription
53812	9	334914	6	NULL	NULL	0	NULL	Pyruvate carboxylase			catalyzes					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_30_27176_s_21	11986306	Pyruvate carboxylase catalyzes the ATP-driven formation of oxaloacetate from pyruvate and HCO3  and P-enolpyruvate carboxykinase (PEPCK) (EC 4.1.	transcription
53813	10	334914	6	NULL	NULL	0	NULL	statement 1			is dependent on					ATP					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_30_27176_s_21	11986306	Pyruvate carboxylase catalyzes the ATP-driven formation of oxaloacetate from pyruvate and HCO3  and P-enolpyruvate carboxykinase (PEPCK) (EC 4.1.	transcription
53814	11	334914	6	NULL	NULL	0	NULL	statement 2			is dependent on					ATP					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_30_27176_s_21	11986306	Pyruvate carboxylase catalyzes the ATP-driven formation of oxaloacetate from pyruvate and HCO3  and P-enolpyruvate carboxykinase (PEPCK) (EC 4.1.	transcription
53815	12	334914	6	NULL	NULL	0	NULL	statement 3			is dependent on					ATP					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_30_27176_s_21	11986306	Pyruvate carboxylase catalyzes the ATP-driven formation of oxaloacetate from pyruvate and HCO3  and P-enolpyruvate carboxykinase (PEPCK) (EC 4.1.	transcription
52108	1	334915	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is converted to	NULL				pyruvate	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_1_443_s_157	11756688	Similarly, conversion of oxaloacetate to pyruvate can be catalyzed by NADP-dependent malic enzyme and by pyruvate carboxylase.	transcription
52109	2	334915	5	NULL	NULL	0	NULL	malic enzyme	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_1_443_s_157	11756688	Similarly, conversion of oxaloacetate to pyruvate can be catalyzed by NADP-dependent malic enzyme and by pyruvate carboxylase.	transcription
52110	3	334915	5	NULL	NULL	0	NULL	malic enzyme	NULL		is dependent on	NULL				NADP	NULL				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_1_443_s_157	11756688	Similarly, conversion of oxaloacetate to pyruvate can be catalyzed by NADP-dependent malic enzyme and by pyruvate carboxylase.	transcription
52111	4	334915	5	NULL	NULL	0	NULL	pyruvate carboxylase	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_1_443_s_157	11756688	Similarly, conversion of oxaloacetate to pyruvate can be catalyzed by NADP-dependent malic enzyme and by pyruvate carboxylase.	transcription
53816	1	334915	6	NULL	NULL	0	NULL	oxaloacetate			is converted to					pyruvate					NULL		0	NULL	NULL	NULL	gw60_pnas_99_1_443_s_157	11756688	Similarly, conversion of oxaloacetate to pyruvate can be catalyzed by NADP-dependent malic enzyme and by pyruvate carboxylase.	transcription
53817	2	334915	6	NULL	NULL	0	NULL	malic enzyme			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw60_pnas_99_1_443_s_157	11756688	Similarly, conversion of oxaloacetate to pyruvate can be catalyzed by NADP-dependent malic enzyme and by pyruvate carboxylase.	transcription
53818	3	334915	6	NULL	NULL	0	NULL	malic enzyme			is dependent on					NADP					NULL		0	NULL	NULL	NULL	gw60_pnas_99_1_443_s_157	11756688	Similarly, conversion of oxaloacetate to pyruvate can be catalyzed by NADP-dependent malic enzyme and by pyruvate carboxylase.	transcription
53819	4	334915	6	NULL	NULL	0	NULL	pyruvate carboxylase			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw60_pnas_99_1_443_s_157	11756688	Similarly, conversion of oxaloacetate to pyruvate can be catalyzed by NADP-dependent malic enzyme and by pyruvate carboxylase.	transcription
52138	1	334916	5	NULL	NULL	0	NULL	pyruvate	NULL		is carboxylated to	NULL				oxaloacetate	NULL				NULL	B. subtilis	0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_242	12839772	In  B. subtilis ( ,  ), the major route for aspartate synthesis involves the carboxylation of pyruvate to oxaloacetate by PC and subsequent transamination to aspartate catalyzed by glutamate:oxaloacetate transaminase.	transcription
52139	2	334916	5	NULL	NULL	0	NULL	PC	NULL		catalyzes	NULL				statement 1	NULL				NULL	B. subtilis	NULL	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_242	12839772	In  B. subtilis ( ,  ), the major route for aspartate synthesis involves the carboxylation of pyruvate to oxaloacetate by PC and subsequent transamination to aspartate catalyzed by glutamate:oxaloacetate transaminase.	transcription
52140	3	334916	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is transaminated to	NULL				aspartate	NULL				NULL	B. subtilis	NULL	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_242	12839772	In  B. subtilis ( ,  ), the major route for aspartate synthesis involves the carboxylation of pyruvate to oxaloacetate by PC and subsequent transamination to aspartate catalyzed by glutamate:oxaloacetate transaminase.	transcription
52141	4	334916	5	NULL	NULL	0	NULL	glutamate:oxaloacetate transaminase	NULL		catalyzes	NULL				statement 3	NULL				NULL	B. subtilis	NULL	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_242	12839772	In  B. subtilis ( ,  ), the major route for aspartate synthesis involves the carboxylation of pyruvate to oxaloacetate by PC and subsequent transamination to aspartate catalyzed by glutamate:oxaloacetate transaminase.	transcription
53820	1	334916	6	NULL	NULL	0	NULL	pyruvate			is carboxylated to					oxaloacetate					NULL		NULL	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_242	12839772	In  B. subtilis ( ,  ), the major route for aspartate synthesis involves the carboxylation of pyruvate to oxaloacetate by PC and subsequent transamination to aspartate catalyzed by glutamate:oxaloacetate transaminase.	transcription
53821	2	334916	6	NULL	NULL	0	NULL	PC			performs					statement 1					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_242	12839772	In  B. subtilis ( ,  ), the major route for aspartate synthesis involves the carboxylation of pyruvate to oxaloacetate by PC and subsequent transamination to aspartate catalyzed by glutamate:oxaloacetate transaminase.	transcription
53822	3	334916	6	NULL	NULL	0	NULL	pyruvate			is converted to					aspartate					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_242	12839772	In  B. subtilis ( ,  ), the major route for aspartate synthesis involves the carboxylation of pyruvate to oxaloacetate by PC and subsequent transamination to aspartate catalyzed by glutamate:oxaloacetate transaminase.	transcription
53823	4	334916	6	NULL	NULL	0	NULL	glutamate:oxaloacetate transaminase			catalyzes					statement 3					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_242	12839772	In  B. subtilis ( ,  ), the major route for aspartate synthesis involves the carboxylation of pyruvate to oxaloacetate by PC and subsequent transamination to aspartate catalyzed by glutamate:oxaloacetate transaminase.	transcription
52142	1	334917	5	NULL	NULL	0	NULL	PC	NULL		is	NULL				pyruvate carboxylase	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_824_s_93	14741710	Biotin is the cofactor of pyruvate carboxylase (PC), which catalyzes pyruvate to oxaloacetate,  and acetyl CoA carboxylase (ACC), which catalyzes acetyl CoA to malonyl CoA.	transcription
52143	2	334917	5	NULL	NULL	0	NULL	biotin	NULL		is a cofactor of	NULL				PC	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_824_s_93	14741710	Biotin is the cofactor of pyruvate carboxylase (PC), which catalyzes pyruvate to oxaloacetate,  and acetyl CoA carboxylase (ACC), which catalyzes acetyl CoA to malonyl CoA.	transcription
52144	3	334917	5	NULL	NULL	0	NULL	pyruvate	NULL		is converted to	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_824_s_93	14741710	Biotin is the cofactor of pyruvate carboxylase (PC), which catalyzes pyruvate to oxaloacetate,  and acetyl CoA carboxylase (ACC), which catalyzes acetyl CoA to malonyl CoA.	transcription
52145	4	334917	5	NULL	NULL	0	NULL	ACC	NULL		is	NULL				acetyl CoA carboxylase	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_824_s_93	14741710	Biotin is the cofactor of pyruvate carboxylase (PC), which catalyzes pyruvate to oxaloacetate,  and acetyl CoA carboxylase (ACC), which catalyzes acetyl CoA to malonyl CoA.	transcription
52146	5	334917	5	NULL	NULL	0	NULL	biotin	NULL		is a cofactor of	NULL				ACC	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_824_s_93	14741710	Biotin is the cofactor of pyruvate carboxylase (PC), which catalyzes pyruvate to oxaloacetate,  and acetyl CoA carboxylase (ACC), which catalyzes acetyl CoA to malonyl CoA.	transcription
52147	6	334917	5	NULL	NULL	0	NULL	acetyl CoA	NULL		is converted to	NULL				malonyl CoA	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_824_s_93	14741710	Biotin is the cofactor of pyruvate carboxylase (PC), which catalyzes pyruvate to oxaloacetate,  and acetyl CoA carboxylase (ACC), which catalyzes acetyl CoA to malonyl CoA.	transcription
52148	7	334917	5	NULL	NULL	0	NULL	ACC	NULL		catalyzes	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_824_s_93	14741710	Biotin is the cofactor of pyruvate carboxylase (PC), which catalyzes pyruvate to oxaloacetate,  and acetyl CoA carboxylase (ACC), which catalyzes acetyl CoA to malonyl CoA.	transcription
53824	1	334917	6	NULL	NULL	0	NULL	PC			is					pyruvate carboxylase					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_824_s_93	14741710	Biotin is the cofactor of pyruvate carboxylase (PC), which catalyzes pyruvate to oxaloacetate,  and acetyl CoA carboxylase (ACC), which catalyzes acetyl CoA to malonyl CoA.	transcription
53825	2	334917	6	NULL	NULL	0	NULL	biotin			is cofactor of					PC					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_824_s_93	14741710	Biotin is the cofactor of pyruvate carboxylase (PC), which catalyzes pyruvate to oxaloacetate,  and acetyl CoA carboxylase (ACC), which catalyzes acetyl CoA to malonyl CoA.	transcription
53826	3	334917	6	NULL	NULL	0	NULL	pyruvate			is converted to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_824_s_93	14741710	Biotin is the cofactor of pyruvate carboxylase (PC), which catalyzes pyruvate to oxaloacetate,  and acetyl CoA carboxylase (ACC), which catalyzes acetyl CoA to malonyl CoA.	transcription
53827	4	334917	6	NULL	NULL	0	NULL	ACC			is					acetyl CoA carboxylase					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_824_s_93	14741710	Biotin is the cofactor of pyruvate carboxylase (PC), which catalyzes pyruvate to oxaloacetate,  and acetyl CoA carboxylase (ACC), which catalyzes acetyl CoA to malonyl CoA.	transcription
53828	5	334917	6	NULL	NULL	0	NULL	acetyl CoA			is converted to					malonyl CoA					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_824_s_93	14741710	Biotin is the cofactor of pyruvate carboxylase (PC), which catalyzes pyruvate to oxaloacetate,  and acetyl CoA carboxylase (ACC), which catalyzes acetyl CoA to malonyl CoA.	transcription
53829	6	334917	6	NULL	NULL	0	NULL	ACC			catalyzes					statement 5					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_824_s_93	14741710	Biotin is the cofactor of pyruvate carboxylase (PC), which catalyzes pyruvate to oxaloacetate,  and acetyl CoA carboxylase (ACC), which catalyzes acetyl CoA to malonyl CoA.	transcription
53830	7	334917	6	NULL	NULL	0	NULL	biotin			is cofactor of					ACC					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_824_s_93	14741710	Biotin is the cofactor of pyruvate carboxylase (PC), which catalyzes pyruvate to oxaloacetate,  and acetyl CoA carboxylase (ACC), which catalyzes acetyl CoA to malonyl CoA.	transcription
52149	1	334918	5	NULL	NULL	0	NULL	pyruvate	NULL		is carboxylated to	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevnutr_22_0_221_s_92	12055344	Pyruvate  carboxylase catalyzes the carboxylation of pyruvate to generate oxaloacetate and  therefore serves as an anapleurotic reaction that replenishes citric acid cycle intermediates  and catalyzes a required step in gluconeogenesis.	transcription
52150	2	334918	5	NULL	NULL	0	NULL	pyruvate carboxylase	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevnutr_22_0_221_s_92	12055344	Pyruvate  carboxylase catalyzes the carboxylation of pyruvate to generate oxaloacetate and  therefore serves as an anapleurotic reaction that replenishes citric acid cycle intermediates  and catalyzes a required step in gluconeogenesis.	transcription
52151	3	334918	5	NULL	NULL	0	NULL	statement 1	NULL		is a type of	NULL				anapleurotic reaction	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevnutr_22_0_221_s_92	12055344	Pyruvate  carboxylase catalyzes the carboxylation of pyruvate to generate oxaloacetate and  therefore serves as an anapleurotic reaction that replenishes citric acid cycle intermediates  and catalyzes a required step in gluconeogenesis.	transcription
52152	4	334918	5	NULL	NULL	0	NULL	statement 1	NULL		replenishes	NULL				citric acid cycle intermediates	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevnutr_22_0_221_s_92	12055344	Pyruvate  carboxylase catalyzes the carboxylation of pyruvate to generate oxaloacetate and  therefore serves as an anapleurotic reaction that replenishes citric acid cycle intermediates  and catalyzes a required step in gluconeogenesis.	transcription
52153	5	334918	5	NULL	NULL	0	NULL	statement 1	NULL		catalyzes	NULL				gluconeogenesis	NULL	required step in			NULL		0	NULL	NULL	NULL	gw70_annurevnutr_22_0_221_s_92	12055344	Pyruvate  carboxylase catalyzes the carboxylation of pyruvate to generate oxaloacetate and  therefore serves as an anapleurotic reaction that replenishes citric acid cycle intermediates  and catalyzes a required step in gluconeogenesis.	transcription
53831	1	334918	6	NULL	NULL	0	NULL	pyruvate			is carboxylated to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw70_annurevnutr_22_0_221_s_92	12055344	Pyruvate  carboxylase catalyzes the carboxylation of pyruvate to generate oxaloacetate and  therefore serves as an anapleurotic reaction that replenishes citric acid cycle intermediates  and catalyzes a required step in gluconeogenesis.	transcription
53832	2	334918	6	NULL	NULL	0	NULL	Pyruvate carboxylase			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw70_annurevnutr_22_0_221_s_92	12055344	Pyruvate  carboxylase catalyzes the carboxylation of pyruvate to generate oxaloacetate and  therefore serves as an anapleurotic reaction that replenishes citric acid cycle intermediates  and catalyzes a required step in gluconeogenesis.	transcription
53833	3	334918	6	NULL	NULL	0	NULL	Pyruvate carboxylase			serves as an					anapleurotic reaction					NULL		0	NULL	NULL	NULL	gw70_annurevnutr_22_0_221_s_92	12055344	Pyruvate  carboxylase catalyzes the carboxylation of pyruvate to generate oxaloacetate and  therefore serves as an anapleurotic reaction that replenishes citric acid cycle intermediates  and catalyzes a required step in gluconeogenesis.	transcription
53834	4	334918	6	NULL	NULL	0	NULL	Pyruvate carboxylase			replenishes					citric acid cycle intermediates					NULL		0	NULL	NULL	NULL	gw70_annurevnutr_22_0_221_s_92	12055344	Pyruvate  carboxylase catalyzes the carboxylation of pyruvate to generate oxaloacetate and  therefore serves as an anapleurotic reaction that replenishes citric acid cycle intermediates  and catalyzes a required step in gluconeogenesis.	transcription
52154	1	334919	5	NULL	NULL	0	NULL	PC	NULL		is important for	NULL				gluconeogenic pathway	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_23_18_3621_s_17	15329673	As the first enzyme in the gluconeogenic pathway, PC catalyzes  the ATP-driven conversion of pyruvate to oxaloacetate using HCO3- and Mg2+ (  et al).	transcription
52155	2	334919	5	NULL	NULL	0	NULL	pyruvate	NULL		is converted to	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_23_18_3621_s_17	15329673	As the first enzyme in the gluconeogenic pathway, PC catalyzes  the ATP-driven conversion of pyruvate to oxaloacetate using HCO3- and Mg2+ (  et al).	transcription
52156	3	334919	5	NULL	NULL	0	NULL	statement 1	NULL		is driven by	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_23_18_3621_s_17	15329673	As the first enzyme in the gluconeogenic pathway, PC catalyzes  the ATP-driven conversion of pyruvate to oxaloacetate using HCO3- and Mg2+ (  et al).	transcription
52157	4	334919	5	NULL	NULL	0	NULL	PC	NULL		catalyzes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_23_18_3621_s_17	15329673	As the first enzyme in the gluconeogenic pathway, PC catalyzes  the ATP-driven conversion of pyruvate to oxaloacetate using HCO3- and Mg2+ (  et al).	transcription
52158	5	334919	5	NULL	NULL	0	NULL	HCO3-	NULL		is required for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_23_18_3621_s_17	15329673	As the first enzyme in the gluconeogenic pathway, PC catalyzes  the ATP-driven conversion of pyruvate to oxaloacetate using HCO3- and Mg2+ (  et al).	transcription
52159	6	334919	5	NULL	NULL	0	NULL	Mg2+	NULL		is required for	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_embo_23_18_3621_s_17	15329673	As the first enzyme in the gluconeogenic pathway, PC catalyzes  the ATP-driven conversion of pyruvate to oxaloacetate using HCO3- and Mg2+ (  et al).	transcription
53835	1	334919	6	NULL	NULL	0	NULL	pyruvate			is converted to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw70_embo_23_18_3621_s_17	15329673	As the first enzyme in the gluconeogenic pathway, PC catalyzes  the ATP-driven conversion of pyruvate to oxaloacetate using HCO3- and Mg2+ (  et al).	transcription
53836	2	334919	6	NULL	NULL	0	NULL	statement 1			is dependent on					ATP					NULL		0	NULL	NULL	NULL	gw70_embo_23_18_3621_s_17	15329673	As the first enzyme in the gluconeogenic pathway, PC catalyzes  the ATP-driven conversion of pyruvate to oxaloacetate using HCO3- and Mg2+ (  et al).	transcription
53837	3	334919	6	NULL	NULL	0	NULL	PC			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw70_embo_23_18_3621_s_17	15329673	As the first enzyme in the gluconeogenic pathway, PC catalyzes  the ATP-driven conversion of pyruvate to oxaloacetate using HCO3- and Mg2+ (  et al).	transcription
53838	4	334919	6	NULL	NULL	0	NULL	PC			is 					enzyme in the gluconeogenic pathway		first			NULL		0	NULL	NULL	NULL	gw70_embo_23_18_3621_s_17	15329673	As the first enzyme in the gluconeogenic pathway, PC catalyzes  the ATP-driven conversion of pyruvate to oxaloacetate using HCO3- and Mg2+ (  et al).	transcription
53839	5	334919	6	NULL	NULL	0	NULL	statement 3			uses					HCO3-					NULL		0	NULL	NULL	NULL	gw70_embo_23_18_3621_s_17	15329673	As the first enzyme in the gluconeogenic pathway, PC catalyzes  the ATP-driven conversion of pyruvate to oxaloacetate using HCO3- and Mg2+ (  et al).	transcription
53840	6	334919	6	NULL	NULL	0	NULL	statement 3			uses					Mg2+					NULL		0	NULL	NULL	NULL	gw70_embo_23_18_3621_s_17	15329673	As the first enzyme in the gluconeogenic pathway, PC catalyzes  the ATP-driven conversion of pyruvate to oxaloacetate using HCO3- and Mg2+ (  et al).	transcription
52160	1	334920	5	NULL	NULL	0	NULL		NULL	luciferase activity of	is induced by	NULL			HRE	pyruvate	NULL				NULL	U251-HRE cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_144	16223732	Cysteine and histidine also lowered HRE-luciferase activity induced by pyruvate or oxaloacetate in the U251-HRE cells ( Fig. 2 D).	transcription
52161	2	334920	5	NULL	NULL	0	NULL		NULL	luciferase activity of	is induced by	NULL			HRE	oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_144	16223732	Cysteine and histidine also lowered HRE-luciferase activity induced by pyruvate or oxaloacetate in the U251-HRE cells ( Fig. 2 D).	transcription
52162	3	334920	5	NULL	NULL	0	NULL	cysteine	NULL		lowers	NULL				statement 1	NULL				NULL	U251-HRE cells	0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_144	16223732	Cysteine and histidine also lowered HRE-luciferase activity induced by pyruvate or oxaloacetate in the U251-HRE cells ( Fig. 2 D).	transcription
52163	4	334920	5	NULL	NULL	0	NULL	cysteine	NULL		lowers	NULL				statement 2	NULL				NULL	U251-HRE cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_144	16223732	Cysteine and histidine also lowered HRE-luciferase activity induced by pyruvate or oxaloacetate in the U251-HRE cells ( Fig. 2 D).	transcription
52164	5	334920	5	NULL	NULL	0	NULL	histidine	NULL		lowers	NULL				statement 1	NULL				NULL	U251-HRE cells	0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_144	16223732	Cysteine and histidine also lowered HRE-luciferase activity induced by pyruvate or oxaloacetate in the U251-HRE cells ( Fig. 2 D).	transcription
52165	6	334920	5	NULL	NULL	0	NULL	histidine	NULL		lowers	NULL				statement 2	NULL				NULL	U251-HRE cells	0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_144	16223732	Cysteine and histidine also lowered HRE-luciferase activity induced by pyruvate or oxaloacetate in the U251-HRE cells ( Fig. 2 D).	transcription
52166	7	334920	5	NULL	NULL	0	NULL	statement 1	NULL		is an alternative to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_144	16223732	Cysteine and histidine also lowered HRE-luciferase activity induced by pyruvate or oxaloacetate in the U251-HRE cells ( Fig. 2 D).	transcription
53841	1	334920	6	NULL	NULL	0	NULL	pyruvate			induces					HRE-luciferase		activity of			NULL	U251-HRE cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_144	16223732	Cysteine and histidine also lowered HRE-luciferase activity induced by pyruvate or oxaloacetate in the U251-HRE cells ( Fig. 2 D).	transcription
53842	2	334920	6	NULL	NULL	0	NULL	oxaloacetate			induces					HRE-luciferase		activity of			NULL	U251-HRE cells	0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_144	16223732	Cysteine and histidine also lowered HRE-luciferase activity induced by pyruvate or oxaloacetate in the U251-HRE cells ( Fig. 2 D).	transcription
53843	3	334920	6	NULL	NULL	0	NULL	cysteine			lowers					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_144	16223732	Cysteine and histidine also lowered HRE-luciferase activity induced by pyruvate or oxaloacetate in the U251-HRE cells ( Fig. 2 D).	transcription
53844	4	334920	6	NULL	NULL	0	NULL	cysteine			lowers					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_144	16223732	Cysteine and histidine also lowered HRE-luciferase activity induced by pyruvate or oxaloacetate in the U251-HRE cells ( Fig. 2 D).	transcription
53845	5	334920	6	NULL	NULL	0	NULL	histidine			lowers					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_144	16223732	Cysteine and histidine also lowered HRE-luciferase activity induced by pyruvate or oxaloacetate in the U251-HRE cells ( Fig. 2 D).	transcription
53846	6	334920	6	NULL	NULL	0	NULL	histidine			lowers					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_144	16223732	Cysteine and histidine also lowered HRE-luciferase activity induced by pyruvate or oxaloacetate in the U251-HRE cells ( Fig. 2 D).	transcription
52167	1	334921	5	NULL	NULL	0	NULL	HIF-1alpha	NULL		is induced by	NULL				pyruvate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_159	16223732	HIF-1alpha induced by pyruvate, oxaloacetate, or the HPH inhibitor DMOG did not contain hydroxyproline ( Fig. 3 D).	transcription
52168	2	334921	5	NULL	NULL	0	NULL	HIF-1alpha	NULL		is induced by	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_159	16223732	HIF-1alpha induced by pyruvate, oxaloacetate, or the HPH inhibitor DMOG did not contain hydroxyproline ( Fig. 3 D).	transcription
52169	3	334921	5	NULL	NULL	0	NULL	HIF-1alpha	NULL		is induced by	NULL				DMOG	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_159	16223732	HIF-1alpha induced by pyruvate, oxaloacetate, or the HPH inhibitor DMOG did not contain hydroxyproline ( Fig. 3 D).	transcription
52170	4	334921	5	NULL	NULL	0	NULL	DMOG	NULL		is an inhibitor of	NULL				HPH	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_159	16223732	HIF-1alpha induced by pyruvate, oxaloacetate, or the HPH inhibitor DMOG did not contain hydroxyproline ( Fig. 3 D).	transcription
52171	5	334921	5	NULL	NULL	0	NULL	HIF-1alpha	NULL		does not contain	NULL					NULL		hydroxyproline		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_159	16223732	HIF-1alpha induced by pyruvate, oxaloacetate, or the HPH inhibitor DMOG did not contain hydroxyproline ( Fig. 3 D).	transcription
53847	1	334921	6	NULL	NULL	0	NULL	pyruvate			induces					HIF-1alpha					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_159	16223732	HIF-1alpha induced by pyruvate, oxaloacetate, or the HPH inhibitor DMOG did not contain hydroxyproline ( Fig. 3 D).	transcription
53848	2	334921	6	NULL	NULL	0	NULL	oxaloacetate			induces					HIF-1alpha					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_159	16223732	HIF-1alpha induced by pyruvate, oxaloacetate, or the HPH inhibitor DMOG did not contain hydroxyproline ( Fig. 3 D).	transcription
53849	3	334921	6	NULL	NULL	0	NULL	DMOG			induces					HIF-1alpha					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_159	16223732	HIF-1alpha induced by pyruvate, oxaloacetate, or the HPH inhibitor DMOG did not contain hydroxyproline ( Fig. 3 D).	transcription
53850	4	334921	6	NULL	NULL	0	NULL	DMOG			is a type of					HPH inhibitor					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_159	16223732	HIF-1alpha induced by pyruvate, oxaloacetate, or the HPH inhibitor DMOG did not contain hydroxyproline ( Fig. 3 D).	transcription
53851	5	334921	6	NULL	NULL	0	NULL	HIF-1alpha			does not contain					hydroxyproline					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_159	16223732	HIF-1alpha induced by pyruvate, oxaloacetate, or the HPH inhibitor DMOG did not contain hydroxyproline ( Fig. 3 D).	transcription
52172	1	334922	5	NULL	NULL	0	NULL	pyruvate	NULL		induce	NULL				HIF-1alpha	NULL	accumulation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_241	16223732	The ascorbate reversibility of pyruvate- and oxaloacetate-induced HIF-1alpha accumulation thus suggested that these 2-oxoacids could somehow inactivate cellular HPHs.	transcription
52173	2	334922	5	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				ascorbate reversibility	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_241	16223732	The ascorbate reversibility of pyruvate- and oxaloacetate-induced HIF-1alpha accumulation thus suggested that these 2-oxoacids could somehow inactivate cellular HPHs.	transcription
52174	3	334922	5	NULL	NULL	0	NULL	oxaloacetate	NULL		induce	NULL				HIF-1alpha	NULL	accumulation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_241	16223732	The ascorbate reversibility of pyruvate- and oxaloacetate-induced HIF-1alpha accumulation thus suggested that these 2-oxoacids could somehow inactivate cellular HPHs.	transcription
52175	4	334922	5	NULL	NULL	0	NULL	statement 3	NULL		leads to	NULL				ascorbate reversibility	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_241	16223732	The ascorbate reversibility of pyruvate- and oxaloacetate-induced HIF-1alpha accumulation thus suggested that these 2-oxoacids could somehow inactivate cellular HPHs.	transcription
52176	5	334922	5	NULL	NULL	0	NULL	pyruvate	NULL		is a type of	NULL				2-oxoacids	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_241	16223732	The ascorbate reversibility of pyruvate- and oxaloacetate-induced HIF-1alpha accumulation thus suggested that these 2-oxoacids could somehow inactivate cellular HPHs.	transcription
52177	6	334922	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is a type of	NULL				2-oxoacids	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_241	16223732	The ascorbate reversibility of pyruvate- and oxaloacetate-induced HIF-1alpha accumulation thus suggested that these 2-oxoacids could somehow inactivate cellular HPHs.	transcription
52178	7	334922	5	NULL	NULL	0	NULL	pyruvate	NULL		inactivates	NULL				HPHs	NULL	cellular			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_241	16223732	The ascorbate reversibility of pyruvate- and oxaloacetate-induced HIF-1alpha accumulation thus suggested that these 2-oxoacids could somehow inactivate cellular HPHs.	transcription
52179	8	334922	5	NULL	NULL	0	NULL	oxaloacetate	NULL		inactivates	NULL				HPHs	NULL	cellular			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_241	16223732	The ascorbate reversibility of pyruvate- and oxaloacetate-induced HIF-1alpha accumulation thus suggested that these 2-oxoacids could somehow inactivate cellular HPHs.	transcription
53852	1	334922	6	NULL	NULL	0	NULL	pyruvate			induces					HIF-1alpha		accumulation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_241	16223732	The ascorbate reversibility of pyruvate- and oxaloacetate-induced HIF-1alpha accumulation thus suggested that these 2-oxoacids could somehow inactivate cellular HPHs.	transcription
53853	2	334922	6	NULL	NULL	0	NULL	oxaloacetate			induces					HIF-1alpha		accumulation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_241	16223732	The ascorbate reversibility of pyruvate- and oxaloacetate-induced HIF-1alpha accumulation thus suggested that these 2-oxoacids could somehow inactivate cellular HPHs.	transcription
53854	3	334922	6	NULL	NULL	0	NULL	oxoacids			inactivate					HPH					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_241	16223732	The ascorbate reversibility of pyruvate- and oxaloacetate-induced HIF-1alpha accumulation thus suggested that these 2-oxoacids could somehow inactivate cellular HPHs.	transcription
52180	1	334924	5	NULL	NULL	0	NULL	pyruvate	NULL		induce	NULL				HIF-1alpha	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_271	16223732	The addition of Fe(II) to cultured cells also prevented HIF-1alpha induction by pyruvate and oxaloacetate.	transcription
52181	2	334924	5	NULL	NULL	0	NULL	oxaloacetate	NULL		induce	NULL				HIF-1alpha	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_271	16223732	The addition of Fe(II) to cultured cells also prevented HIF-1alpha induction by pyruvate and oxaloacetate.	transcription
52182	3	334924	5	NULL	NULL	0	NULL	Fe(II)	NULL	addition of	prevents	NULL				statement 1	NULL				NULL	cultured cells	0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_271	16223732	The addition of Fe(II) to cultured cells also prevented HIF-1alpha induction by pyruvate and oxaloacetate.	transcription
53855	1	334924	6	NULL	NULL	0	NULL	pyruvate			induces					HIF-1alpha		induction of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_271	16223732	The addition of Fe(II) to cultured cells also prevented HIF-1alpha induction by pyruvate and oxaloacetate.	transcription
53857	2	334924	6	NULL	NULL	0	NULL	oxaloacetate			induces					HIF-1alpha		induction of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_271	16223732	The addition of Fe(II) to cultured cells also prevented HIF-1alpha induction by pyruvate and oxaloacetate.	transcription
52483	1	334925	5	NULL	NULL	0	NULL	metabolic pathways	NULL		regulates	NULL				HPH	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_358	16223732	The origin of pyruvate, oxaloacetate, and the branched chain 2-oxoacids via diverse metabolic routes underscores the potential for HPH regulation by metabolic pathways.	transcription
52183	1	334926	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is synthesized from	NULL				PEP	NULL				NULL	Escherichia coli	NULL	NULL	NULL	NULL	gw60_febslett_412_3_531_s_9	9276461	Escherichia coli synthesizes oxaloacetate not from pyruvate, but from phosphoenolpyruvate (PEP) in a reaction catalyzed by PEP carboxylase [ 2,   5].	transcription
52184	2	334926	5	NULL	NULL	0	NULL	PEP carboxylase	NULL		catalyzes	NULL				statement 1	NULL				NULL	Escherichia coli	0	NULL	NULL	NULL	gw60_febslett_412_3_531_s_9	9276461	Escherichia coli synthesizes oxaloacetate not from pyruvate, but from phosphoenolpyruvate (PEP) in a reaction catalyzed by PEP carboxylase [ 2,   5].	transcription
52185	3	334926	5	NULL	NULL	0	NULL	PEP	NULL		is	NULL				phosphoenolpyruvate	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_412_3_531_s_9	9276461	Escherichia coli synthesizes oxaloacetate not from pyruvate, but from phosphoenolpyruvate (PEP) in a reaction catalyzed by PEP carboxylase [ 2,   5].	transcription
53858	1	334926	6	NULL	NULL	0	NULL	oxaloacetate			is synthesized from					PEP					NULL	Escherichia coli	NULL	NULL	NULL	NULL	gw60_febslett_412_3_531_s_9	9276461	Escherichia coli synthesizes oxaloacetate not from pyruvate, but from phosphoenolpyruvate (PEP) in a reaction catalyzed by PEP carboxylase [ 2,   5].	transcription
53859	2	334926	6	NULL	NULL	0	NULL	PEP			is					phosphoenolpyruvate					NULL		0	NULL	NULL	NULL	gw60_febslett_412_3_531_s_9	9276461	Escherichia coli synthesizes oxaloacetate not from pyruvate, but from phosphoenolpyruvate (PEP) in a reaction catalyzed by PEP carboxylase [ 2,   5].	transcription
53860	3	334926	6	NULL	NULL	0	NULL	PEP carboxylase			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw60_febslett_412_3_531_s_9	9276461	Escherichia coli synthesizes oxaloacetate not from pyruvate, but from phosphoenolpyruvate (PEP) in a reaction catalyzed by PEP carboxylase [ 2,   5].	transcription
52186	1	334927	5	NULL	NULL	0	NULL	Pyc	NULL		is a type of	NULL				biotin-containing enzyme	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_66_3_1223_s_12	10698798	Pyc is a biotin-containing enzyme that catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate (OAA) ( 4).	transcription
52187	2	334927	5	NULL	NULL	0	NULL	pyruvate	NULL		is carboxylated to	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_66_3_1223_s_12	10698798	Pyc is a biotin-containing enzyme that catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate (OAA) ( 4).	transcription
52188	3	334927	5	NULL	NULL	0	NULL	statement 2	NULL		is dependent on	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_66_3_1223_s_12	10698798	Pyc is a biotin-containing enzyme that catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate (OAA) ( 4).	transcription
52189	4	334927	5	NULL	NULL	0	NULL	Pyc	NULL		catalyzes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_66_3_1223_s_12	10698798	Pyc is a biotin-containing enzyme that catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate (OAA) ( 4).	transcription
52190	5	334927	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is	NULL				OAA	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_66_3_1223_s_12	10698798	Pyc is a biotin-containing enzyme that catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate (OAA) ( 4).	transcription
53861	1	334927	6	NULL	NULL	0	NULL	pyruvate			is carboxylated to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_66_3_1223_s_12	10698798	Pyc is a biotin-containing enzyme that catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate (OAA) ( 4).	transcription
53862	2	334927	6	NULL	NULL	0	NULL	OAA			is					oxaloacetate					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_66_3_1223_s_12	10698798	Pyc is a biotin-containing enzyme that catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate (OAA) ( 4).	transcription
53863	3	334927	6	NULL	NULL	0	NULL	statement 1			is dependent on					ATP					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_66_3_1223_s_12	10698798	Pyc is a biotin-containing enzyme that catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate (OAA) ( 4).	transcription
53864	4	334927	6	NULL	NULL	0	NULL	Pyc			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_66_3_1223_s_12	10698798	Pyc is a biotin-containing enzyme that catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate (OAA) ( 4).	transcription
53865	5	334927	6	NULL	NULL	0	NULL	Pyc			is					biotin-containing enzyme family					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_66_3_1223_s_12	10698798	Pyc is a biotin-containing enzyme that catalyzes the ATP-dependent carboxylation of pyruvate to form oxaloacetate (OAA) ( 4).	transcription
52191	1	334929	5	NULL	NULL	0	NULL	succinate dehydrogenase	NULL		is inhibited by	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_40_25019_s_170	8798784	Such an interaction has been suggested to be responsible for the inhibition of succinate dehydrogenase by oxaloacetate ( 37), which, like pyruvate, is an alpha-keto acid.	transcription
52192	2	334929	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is a type of	NULL				alpha-keto acid	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_40_25019_s_170	8798784	Such an interaction has been suggested to be responsible for the inhibition of succinate dehydrogenase by oxaloacetate ( 37), which, like pyruvate, is an alpha-keto acid.	transcription
52193	3	334929	5	NULL	NULL	0	NULL	pyruvate	NULL		is a type of	NULL				alpha-keto acid	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_40_25019_s_170	8798784	Such an interaction has been suggested to be responsible for the inhibition of succinate dehydrogenase by oxaloacetate ( 37), which, like pyruvate, is an alpha-keto acid.	transcription
54320	1	334929	6	NULL	NULL	0	NULL	oxaloacetate			inhibits					succinate dehydrogenase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_40_25019_s_170	8798784	Such an interaction has been suggested to be responsible for the inhibition of succinate dehydrogenase by oxaloacetate ( 37), which, like pyruvate, is an alpha-keto acid.	transcription
54330	2	334929	6	NULL	NULL	0	NULL	succinate dehydrogenase			is a type of					alpha-keto acid					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_40_25019_s_170	8798784	Such an interaction has been suggested to be responsible for the inhibition of succinate dehydrogenase by oxaloacetate ( 37), which, like pyruvate, is an alpha-keto acid.	transcription
52194	1	334930	5	NULL	NULL	0	NULL	Oxalate	NULL		is a dead-end analogue of 	NULL				enolpyruvate	NULL				NULL		0	NULL	NULL	NULL	gw70_febslett_570_1_217_s_132	15251467	Oxalate (dead-end analogue of enolpyruvate) and malonate (dead-end analogue of oxaloacetate/pyruvate),  produced high inhibition on the activity ( Table 1).	transcription
52195	2	334930	5	NULL	NULL	0	NULL	malonate	NULL		is a dead-end analogue of	NULL				oxaloacetate/pyruvate	NULL				NULL		0	NULL	NULL	NULL	gw70_febslett_570_1_217_s_132	15251467	Oxalate (dead-end analogue of enolpyruvate) and malonate (dead-end analogue of oxaloacetate/pyruvate),  produced high inhibition on the activity ( Table 1).	transcription
52196	1	334931	5	NULL	NULL	0	NULL		NULL	absence of	allows	NULL	may	C5 carboxyl group		pyruvate	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_334	16223732	It is possible that the absence of a C5 carboxyl group allows pyruvate and oxaloacetate binding to interfere with allosteric enzyme mechanisms for the scheduled sequential binding of other reactants.	transcription
52197	2	334931	5	NULL	NULL	0	NULL		NULL	absence of	allows	NULL	may	C5 carboxyl group		oxaloacetate	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_334	16223732	It is possible that the absence of a C5 carboxyl group allows pyruvate and oxaloacetate binding to interfere with allosteric enzyme mechanisms for the scheduled sequential binding of other reactants.	transcription
52198	3	334931	5	NULL	NULL	0	NULL	statement 1	NULL		interfere with	NULL				allosteric enzyme	NULL	mechanism of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_334	16223732	It is possible that the absence of a C5 carboxyl group allows pyruvate and oxaloacetate binding to interfere with allosteric enzyme mechanisms for the scheduled sequential binding of other reactants.	transcription
52199	4	334931	5	NULL	NULL	0	NULL	statement 2	NULL		interfere with	NULL				allosteric enzyme	NULL	mechanism of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_334	16223732	It is possible that the absence of a C5 carboxyl group allows pyruvate and oxaloacetate binding to interfere with allosteric enzyme mechanisms for the scheduled sequential binding of other reactants.	transcription
52200	5	334931	5	NULL	NULL	0	NULL	statement 3	NULL		leads to	NULL				reactants	NULL	scheduled;;sequential binding of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_334	16223732	It is possible that the absence of a C5 carboxyl group allows pyruvate and oxaloacetate binding to interfere with allosteric enzyme mechanisms for the scheduled sequential binding of other reactants.	transcription
52201	6	334931	5	NULL	NULL	0	NULL	statement 4	NULL		leads to	NULL				reactants	NULL	scheduled;;sequential binding of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_334	16223732	It is possible that the absence of a C5 carboxyl group allows pyruvate and oxaloacetate binding to interfere with allosteric enzyme mechanisms for the scheduled sequential binding of other reactants.	transcription
52202	1	334932	5	NULL	NULL	0	NULL	acetyl-CoA	NULL		is carboxylated to	NULL				malonyl-CoA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_20	16533810	Acc1p catalyzes the first step of fatty acid biosynthesis ( i.e. the carboxylation of acetyl-CoA to malonyl-CoA), and Pyc1p and Pyc2p generate oxaloacetate from pyruvate.	transcription
52203	2	334932	5	NULL	NULL	0	NULL	statement 1	NULL		is first step of	NULL				fatty acid	NULL	biosynthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_20	16533810	Acc1p catalyzes the first step of fatty acid biosynthesis ( i.e. the carboxylation of acetyl-CoA to malonyl-CoA), and Pyc1p and Pyc2p generate oxaloacetate from pyruvate.	transcription
52204	3	334932	5	NULL	NULL	0	NULL	Acc1p	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_20	16533810	Acc1p catalyzes the first step of fatty acid biosynthesis ( i.e. the carboxylation of acetyl-CoA to malonyl-CoA), and Pyc1p and Pyc2p generate oxaloacetate from pyruvate.	transcription
52205	4	334932	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is generated from	NULL				pyruvate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_20	16533810	Acc1p catalyzes the first step of fatty acid biosynthesis ( i.e. the carboxylation of acetyl-CoA to malonyl-CoA), and Pyc1p and Pyc2p generate oxaloacetate from pyruvate.	transcription
52206	5	334932	5	NULL	NULL	0	NULL	Pyc1p	NULL		catalyzes	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_20	16533810	Acc1p catalyzes the first step of fatty acid biosynthesis ( i.e. the carboxylation of acetyl-CoA to malonyl-CoA), and Pyc1p and Pyc2p generate oxaloacetate from pyruvate.	transcription
52207	6	334932	5	NULL	NULL	0	NULL	Pyc2p	NULL		catalyzes	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_20	16533810	Acc1p catalyzes the first step of fatty acid biosynthesis ( i.e. the carboxylation of acetyl-CoA to malonyl-CoA), and Pyc1p and Pyc2p generate oxaloacetate from pyruvate.	transcription
54331	1	334932	6	NULL	NULL	0	NULL	acetyl-CoA			is carboxylated to					malonyl-CoA					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_20	16533810	Acc1p catalyzes the first step of fatty acid biosynthesis ( i.e. the carboxylation of acetyl-CoA to malonyl-CoA), and Pyc1p and Pyc2p generate oxaloacetate from pyruvate.	transcription
54332	2	334932	6	NULL	NULL	0	NULL	Acc1p			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_20	16533810	Acc1p catalyzes the first step of fatty acid biosynthesis ( i.e. the carboxylation of acetyl-CoA to malonyl-CoA), and Pyc1p and Pyc2p generate oxaloacetate from pyruvate.	transcription
54333	3	334932	6	NULL	NULL	0	NULL	oxaloacetate			is generated from					pyruvate					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_20	16533810	Acc1p catalyzes the first step of fatty acid biosynthesis ( i.e. the carboxylation of acetyl-CoA to malonyl-CoA), and Pyc1p and Pyc2p generate oxaloacetate from pyruvate.	transcription
54334	4	334932	6	NULL	NULL	0	NULL	Pyc1p			plays a role in					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_20	16533810	Acc1p catalyzes the first step of fatty acid biosynthesis ( i.e. the carboxylation of acetyl-CoA to malonyl-CoA), and Pyc1p and Pyc2p generate oxaloacetate from pyruvate.	transcription
54335	5	334932	6	NULL	NULL	0	NULL	Pyc2p			plays a role in					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_19_13513_s_20	16533810	Acc1p catalyzes the first step of fatty acid biosynthesis ( i.e. the carboxylation of acetyl-CoA to malonyl-CoA), and Pyc1p and Pyc2p generate oxaloacetate from pyruvate.	transcription
52208	1	334933	5	NULL	NULL	0	NULL	biotin	NULL	uptake of	is increased by	NULL				amino acid	NULL	starvation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_18_12381_s_347	16531611	Contrary to earlier speculations ( ), we propose that biotin uptake is increased by amino acid starvation to increase the activity of the biotin-dependent pyruvate carboxylases that generate oxaloacetate.	transcription
52209	2	334933	5	NULL	NULL	0	NULL	pyruvate carboxylases	NULL		generate	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_18_12381_s_347	16531611	Contrary to earlier speculations ( ), we propose that biotin uptake is increased by amino acid starvation to increase the activity of the biotin-dependent pyruvate carboxylases that generate oxaloacetate.	transcription
52210	3	334933	5	NULL	NULL	0	NULL	statement 2	NULL		is dependent on	NULL				biotin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_18_12381_s_347	16531611	Contrary to earlier speculations ( ), we propose that biotin uptake is increased by amino acid starvation to increase the activity of the biotin-dependent pyruvate carboxylases that generate oxaloacetate.	transcription
52211	4	334933	5	NULL	NULL	0	NULL	statement 1	NULL		increases	NULL				pyruvate carboxylases	NULL	activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_18_12381_s_347	16531611	Contrary to earlier speculations ( ), we propose that biotin uptake is increased by amino acid starvation to increase the activity of the biotin-dependent pyruvate carboxylases that generate oxaloacetate.	transcription
54337	1	334933	6	NULL	NULL	0	NULL	biotin		uptake of	is increased by					amino acid starvation					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_18_12381_s_347	16531611	Contrary to earlier speculations ( ), we propose that biotin uptake is increased by amino acid starvation to increase the activity of the biotin-dependent pyruvate carboxylases that generate oxaloacetate.	transcription
54339	2	334933	6	NULL	NULL	0	NULL	pyruvate carboxylase			generates					oxaloacetate					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_18_12381_s_347	16531611	Contrary to earlier speculations ( ), we propose that biotin uptake is increased by amino acid starvation to increase the activity of the biotin-dependent pyruvate carboxylases that generate oxaloacetate.	transcription
54340	3	334933	6	NULL	NULL	0	NULL	statement 1			increases					pyruvate carboxylase		activity of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_18_12381_s_347	16531611	Contrary to earlier speculations ( ), we propose that biotin uptake is increased by amino acid starvation to increase the activity of the biotin-dependent pyruvate carboxylases that generate oxaloacetate.	transcription
52212	1	334934	5	NULL	NULL	0	NULL	PEPCK	NULL		is	NULL				phosphoenolpyruvate carboxykinase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31475_s_15	9395482	In the liver, phosphoenolpyruvate carboxykinase (PEPCK) catalyzes the conversion of oxaloacetate to phosphoenolpyruvate and is considered the major rate-controlling enzyme in the pathway of gluconeogenesis from pyruvate, lactate, and alanine ( 8).	transcription
52213	2	334934	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is converted to	NULL				phosphoenolpyruvate	NULL				NULL	liver	0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31475_s_15	9395482	In the liver, phosphoenolpyruvate carboxykinase (PEPCK) catalyzes the conversion of oxaloacetate to phosphoenolpyruvate and is considered the major rate-controlling enzyme in the pathway of gluconeogenesis from pyruvate, lactate, and alanine ( 8).	transcription
52214	3	334934	5	NULL	NULL	0	NULL	PEPCK	NULL		catalyzes	NULL				statement 2	NULL				NULL	liver	0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31475_s_15	9395482	In the liver, phosphoenolpyruvate carboxykinase (PEPCK) catalyzes the conversion of oxaloacetate to phosphoenolpyruvate and is considered the major rate-controlling enzyme in the pathway of gluconeogenesis from pyruvate, lactate, and alanine ( 8).	transcription
54342	1	334934	6	NULL	NULL	0	NULL	oxaloacetate			is converted to					phosphoenolpyruvate					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31475_s_15	9395482	In the liver, phosphoenolpyruvate carboxykinase (PEPCK) catalyzes the conversion of oxaloacetate to phosphoenolpyruvate and is considered the major rate-controlling enzyme in the pathway of gluconeogenesis from pyruvate, lactate, and alanine ( 8).	transcription
54343	2	334934	6	NULL	NULL	0	NULL	PEPCK			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_50_31475_s_15	9395482	In the liver, phosphoenolpyruvate carboxykinase (PEPCK) catalyzes the conversion of oxaloacetate to phosphoenolpyruvate and is considered the major rate-controlling enzyme in the pathway of gluconeogenesis from pyruvate, lactate, and alanine ( 8).	transcription
52215	1	334935	5	NULL	NULL	0	NULL	pyruvate	NULL		inhibit	NULL	strongly			oxaloacetate	NULL	transamination of			NULL	brain homogenates	0	NULL	NULL	NULL	gw60_jneurosci_20_5_1809_s_192	10684882	Haslam and Krebs (1963)   found that 10 mM of pyruvate strongly inhibited oxaloacetate transamination in brain homogenates, and Dennis and Clark (1978)   observed the same in their nonsynaptic mitochondria.	transcription
52216	2	334935	5	NULL	NULL	0	NULL	pyruvate	NULL		inhibit	NULL	strongly			oxaloacetate	NULL	transamination of			NULL	nonsynaptic mitochondria	0	NULL	NULL	NULL	gw60_jneurosci_20_5_1809_s_192	10684882	Haslam and Krebs (1963)   found that 10 mM of pyruvate strongly inhibited oxaloacetate transamination in brain homogenates, and Dennis and Clark (1978)   observed the same in their nonsynaptic mitochondria.	transcription
54346	1	334935	6	NULL	NULL	0	NULL	pyruvate			inhibits		strongly			oxaloacetate		transamination of 			NULL	brain homogenates	NULL	NULL	NULL	NULL	gw60_jneurosci_20_5_1809_s_192	10684882	Haslam and Krebs (1963)   found that 10 mM of pyruvate strongly inhibited oxaloacetate transamination in brain homogenates, and Dennis and Clark (1978)   observed the same in their nonsynaptic mitochondria.	transcription
54347	2	334935	6	NULL	NULL	0	NULL	pyruvate			inhibits		strongly			oxaloacetate		transamination of 			NULL	nonsynaptic mitochondria	NULL	NULL	NULL	NULL	gw60_jneurosci_20_5_1809_s_192	10684882	Haslam and Krebs (1963)   found that 10 mM of pyruvate strongly inhibited oxaloacetate transamination in brain homogenates, and Dennis and Clark (1978)   observed the same in their nonsynaptic mitochondria.	transcription
52217	1	334937	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is converted to	NULL				malate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_7470_s_160	14660628	An alternate metabolic pathway for oxaloacetate besides conversion to malate is citrate synthase-induced production of citrate and distal metabolism through malonyl-CoA or recycling to pyruvate through the pyruvate-citrate shuttle.	transcription
52218	2	334937	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is converted to	NULL				citrate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_7470_s_160	14660628	An alternate metabolic pathway for oxaloacetate besides conversion to malate is citrate synthase-induced production of citrate and distal metabolism through malonyl-CoA or recycling to pyruvate through the pyruvate-citrate shuttle.	transcription
52219	3	334937	5	NULL	NULL	0	NULL	citrate synthase	NULL		catalyzes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_7470_s_160	14660628	An alternate metabolic pathway for oxaloacetate besides conversion to malate is citrate synthase-induced production of citrate and distal metabolism through malonyl-CoA or recycling to pyruvate through the pyruvate-citrate shuttle.	transcription
52220	4	334937	5	NULL	NULL	0	NULL	oxaloacetate	NULL	distal metabolism of	occurs through	NULL				malonyl-CoA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_7470_s_160	14660628	An alternate metabolic pathway for oxaloacetate besides conversion to malate is citrate synthase-induced production of citrate and distal metabolism through malonyl-CoA or recycling to pyruvate through the pyruvate-citrate shuttle.	transcription
52221	5	334937	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is recycled to	NULL				pyruvate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_7470_s_160	14660628	An alternate metabolic pathway for oxaloacetate besides conversion to malate is citrate synthase-induced production of citrate and distal metabolism through malonyl-CoA or recycling to pyruvate through the pyruvate-citrate shuttle.	transcription
52222	6	334937	5	NULL	NULL	0	NULL	statement 5	NULL		occurs through	NULL				pyruvate-citrate shuttle	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_7470_s_160	14660628	An alternate metabolic pathway for oxaloacetate besides conversion to malate is citrate synthase-induced production of citrate and distal metabolism through malonyl-CoA or recycling to pyruvate through the pyruvate-citrate shuttle.	transcription
52223	7	334937	5	NULL	NULL	0	NULL	statement 4	NULL		is an alternative to	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_7470_s_160	14660628	An alternate metabolic pathway for oxaloacetate besides conversion to malate is citrate synthase-induced production of citrate and distal metabolism through malonyl-CoA or recycling to pyruvate through the pyruvate-citrate shuttle.	transcription
54352	1	334937	6	NULL	NULL	0	NULL	citrate synthase			induces					citrate		production of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_7470_s_160	14660628	An alternate metabolic pathway for oxaloacetate besides conversion to malate is citrate synthase-induced production of citrate and distal metabolism through malonyl-CoA or recycling to pyruvate through the pyruvate-citrate shuttle.	transcription
52224	1	334938	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is synthesized from	NULL				pyruvate	NULL				NULL	S. cerevisiae	0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21044_s_23	10409655	In  S. cerevisiae, the anaplerotic synthesis of oxaloacetate from pyruvate is catalyzed by pyruvate carboxylase, an exclusively cytosolic enzyme, in contrast to many higher organisms in which this enzyme is mitochondrial ( 14,  18).	transcription
52225	2	334938	5	NULL	NULL	0	NULL	pyruvate carboxylase	NULL		catalyzes	NULL				statement 1	NULL				NULL	S. cerevisiae	0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21044_s_23	10409655	In  S. cerevisiae, the anaplerotic synthesis of oxaloacetate from pyruvate is catalyzed by pyruvate carboxylase, an exclusively cytosolic enzyme, in contrast to many higher organisms in which this enzyme is mitochondrial ( 14,  18).	transcription
52226	3	334938	5	NULL	NULL	0	NULL	statement 1	NULL		is a type of	NULL				anaplerotic reaction	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21044_s_23	10409655	In  S. cerevisiae, the anaplerotic synthesis of oxaloacetate from pyruvate is catalyzed by pyruvate carboxylase, an exclusively cytosolic enzyme, in contrast to many higher organisms in which this enzyme is mitochondrial ( 14,  18).	transcription
52227	4	334938	5	NULL	NULL	0	NULL	pyruvate carboxylase	NULL		is present in	NULL	exclusively			cytosol	NULL				NULL	S. cerevisiae	0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21044_s_23	10409655	In  S. cerevisiae, the anaplerotic synthesis of oxaloacetate from pyruvate is catalyzed by pyruvate carboxylase, an exclusively cytosolic enzyme, in contrast to many higher organisms in which this enzyme is mitochondrial ( 14,  18).	transcription
52228	5	334938	5	NULL	NULL	0	NULL	pyruvate carboxylase	NULL		is present in	NULL				mitochondria	NULL				NULL	higher organisms	0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21044_s_23	10409655	In  S. cerevisiae, the anaplerotic synthesis of oxaloacetate from pyruvate is catalyzed by pyruvate carboxylase, an exclusively cytosolic enzyme, in contrast to many higher organisms in which this enzyme is mitochondrial ( 14,  18).	transcription
54355	1	334938	6	NULL	NULL	0	NULL	oxaloacetate			is synthesized from					pyruvate					NULL	S. cerevisiae	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21044_s_23	10409655	In  S. cerevisiae, the anaplerotic synthesis of oxaloacetate from pyruvate is catalyzed by pyruvate carboxylase, an exclusively cytosolic enzyme, in contrast to many higher organisms in which this enzyme is mitochondrial ( 14,  18).	transcription
54356	2	334938	6	NULL	NULL	0	NULL	statement 1			is catalyzed by					pyruvate carboxylase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21044_s_23	10409655	In  S. cerevisiae, the anaplerotic synthesis of oxaloacetate from pyruvate is catalyzed by pyruvate carboxylase, an exclusively cytosolic enzyme, in contrast to many higher organisms in which this enzyme is mitochondrial ( 14,  18).	transcription
54357	3	334938	6	NULL	NULL	0	NULL	pyruvate carboxylase			is a type of					cytosolic enzyme					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21044_s_23	10409655	In  S. cerevisiae, the anaplerotic synthesis of oxaloacetate from pyruvate is catalyzed by pyruvate carboxylase, an exclusively cytosolic enzyme, in contrast to many higher organisms in which this enzyme is mitochondrial ( 14,  18).	transcription
52229	1	334939	5	NULL	NULL	0	NULL	mitochondria	NULL		oxidizes	NULL				pyruvate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21044_s_78	10409655	It is known that mitochondria do not oxidize pyruvate unless malate is added, since the oxaloacetate produced by malate dehydrogenase reacts with acetyl-CoA, a potent inhibitor of pyruvate dehydrogenase ( 6).	transcription
52230	2	334939	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL	only			malate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21044_s_78	10409655	It is known that mitochondria do not oxidize pyruvate unless malate is added, since the oxaloacetate produced by malate dehydrogenase reacts with acetyl-CoA, a potent inhibitor of pyruvate dehydrogenase ( 6).	transcription
52231	3	334939	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is produced by	NULL				malate dehydrogenase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21044_s_78	10409655	It is known that mitochondria do not oxidize pyruvate unless malate is added, since the oxaloacetate produced by malate dehydrogenase reacts with acetyl-CoA, a potent inhibitor of pyruvate dehydrogenase ( 6).	transcription
52232	4	334939	5	NULL	NULL	0	NULL	statement 3	NULL		reacts with	NULL				acetyl-CoA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21044_s_78	10409655	It is known that mitochondria do not oxidize pyruvate unless malate is added, since the oxaloacetate produced by malate dehydrogenase reacts with acetyl-CoA, a potent inhibitor of pyruvate dehydrogenase ( 6).	transcription
52233	5	334939	5	NULL	NULL	0	NULL	acetyl-CoA	NULL		is an inhibitor of	NULL	potent			pyruvate dehydrogenase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21044_s_78	10409655	It is known that mitochondria do not oxidize pyruvate unless malate is added, since the oxaloacetate produced by malate dehydrogenase reacts with acetyl-CoA, a potent inhibitor of pyruvate dehydrogenase ( 6).	transcription
54358	1	334939	6	NULL	NULL	0	NULL	oxaloacetate			is produced by					malate dehydrogenase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21044_s_78	10409655	It is known that mitochondria do not oxidize pyruvate unless malate is added, since the oxaloacetate produced by malate dehydrogenase reacts with acetyl-CoA, a potent inhibitor of pyruvate dehydrogenase ( 6).	transcription
54359	2	334939	6	NULL	NULL	0	NULL	oxaloacetate			reacts with					acetyl-CoA					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21044_s_78	10409655	It is known that mitochondria do not oxidize pyruvate unless malate is added, since the oxaloacetate produced by malate dehydrogenase reacts with acetyl-CoA, a potent inhibitor of pyruvate dehydrogenase ( 6).	transcription
54360	3	334939	6	NULL	NULL	0	NULL	acetyl-CoA			is an inhibitor of		potent			pyruvate dehydrogenase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21044_s_78	10409655	It is known that mitochondria do not oxidize pyruvate unless malate is added, since the oxaloacetate produced by malate dehydrogenase reacts with acetyl-CoA, a potent inhibitor of pyruvate dehydrogenase ( 6).	transcription
54361	4	334939	6	NULL	NULL	0	NULL	mitochondria			do not oxidize					pyruvate					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21044_s_78	10409655	It is known that mitochondria do not oxidize pyruvate unless malate is added, since the oxaloacetate produced by malate dehydrogenase reacts with acetyl-CoA, a potent inhibitor of pyruvate dehydrogenase ( 6).	transcription
54362	5	334939	6	NULL	NULL	0	NULL	statement 4			occurs in presence of					malate					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21044_s_78	10409655	It is known that mitochondria do not oxidize pyruvate unless malate is added, since the oxaloacetate produced by malate dehydrogenase reacts with acetyl-CoA, a potent inhibitor of pyruvate dehydrogenase ( 6).	transcription
52234	1	334940	5	NULL	NULL	0	NULL	palmitate	NULL	oxidation of	results in	NULL				acetyl-CoA	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_1_57_s_240	16375848	Thus, an increase in acetyl-CoA content from palmitate oxidation leads up to inhibition  of pyruvate dehydrogenase activity, decreasing the conversion of pyruvate to acetyl-CoA,  but also enhances pyruvate carboxylase activity, raising the conversion of pyruvate  to oxaloacetate that entries into the Krebs cycle being then oxidized   [57].	transcription
52235	2	334940	5	NULL	NULL	0	NULL	acetyl-CoA	NULL		inhibits	NULL				pyruvate dehydrogenase	NULL	activity of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_1_57_s_240	16375848	Thus, an increase in acetyl-CoA content from palmitate oxidation leads up to inhibition  of pyruvate dehydrogenase activity, decreasing the conversion of pyruvate to acetyl-CoA,  but also enhances pyruvate carboxylase activity, raising the conversion of pyruvate  to oxaloacetate that entries into the Krebs cycle being then oxidized   [57].	transcription
52236	3	334940	5	NULL	NULL	0	NULL	pyruvate	NULL		is converted to	NULL				acetyl-CoA	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_1_57_s_240	16375848	Thus, an increase in acetyl-CoA content from palmitate oxidation leads up to inhibition  of pyruvate dehydrogenase activity, decreasing the conversion of pyruvate to acetyl-CoA,  but also enhances pyruvate carboxylase activity, raising the conversion of pyruvate  to oxaloacetate that entries into the Krebs cycle being then oxidized   [57].	transcription
52237	4	334940	5	NULL	NULL	0	NULL	statement 2	NULL		decreases	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_1_57_s_240	16375848	Thus, an increase in acetyl-CoA content from palmitate oxidation leads up to inhibition  of pyruvate dehydrogenase activity, decreasing the conversion of pyruvate to acetyl-CoA,  but also enhances pyruvate carboxylase activity, raising the conversion of pyruvate  to oxaloacetate that entries into the Krebs cycle being then oxidized   [57].	transcription
52238	5	334940	5	NULL	NULL	0	NULL	acetyl-CoA	NULL		enhances	NULL				pyruvate carboxylase	NULL	activity of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_1_57_s_240	16375848	Thus, an increase in acetyl-CoA content from palmitate oxidation leads up to inhibition  of pyruvate dehydrogenase activity, decreasing the conversion of pyruvate to acetyl-CoA,  but also enhances pyruvate carboxylase activity, raising the conversion of pyruvate  to oxaloacetate that entries into the Krebs cycle being then oxidized   [57].	transcription
52239	6	334940	5	NULL	NULL	0	NULL	pyruvate	NULL		is converted to	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_1_57_s_240	16375848	Thus, an increase in acetyl-CoA content from palmitate oxidation leads up to inhibition  of pyruvate dehydrogenase activity, decreasing the conversion of pyruvate to acetyl-CoA,  but also enhances pyruvate carboxylase activity, raising the conversion of pyruvate  to oxaloacetate that entries into the Krebs cycle being then oxidized   [57].	transcription
52240	7	334940	5	NULL	NULL	0	NULL	statement 5	NULL		increases	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_1_57_s_240	16375848	Thus, an increase in acetyl-CoA content from palmitate oxidation leads up to inhibition  of pyruvate dehydrogenase activity, decreasing the conversion of pyruvate to acetyl-CoA,  but also enhances pyruvate carboxylase activity, raising the conversion of pyruvate  to oxaloacetate that entries into the Krebs cycle being then oxidized   [57].	transcription
52241	8	334940	5	NULL	NULL	0	NULL	oxaloacetate	NULL		enters into	NULL				Krebs cycle	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_1_57_s_240	16375848	Thus, an increase in acetyl-CoA content from palmitate oxidation leads up to inhibition  of pyruvate dehydrogenase activity, decreasing the conversion of pyruvate to acetyl-CoA,  but also enhances pyruvate carboxylase activity, raising the conversion of pyruvate  to oxaloacetate that entries into the Krebs cycle being then oxidized   [57].	transcription
52242	9	334940	5	NULL	NULL	0	NULL	statement 6	NULL		leads to	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_1_57_s_240	16375848	Thus, an increase in acetyl-CoA content from palmitate oxidation leads up to inhibition  of pyruvate dehydrogenase activity, decreasing the conversion of pyruvate to acetyl-CoA,  but also enhances pyruvate carboxylase activity, raising the conversion of pyruvate  to oxaloacetate that entries into the Krebs cycle being then oxidized   [57].	transcription
52243	10	334940	5	NULL	NULL	0	NULL	oxaloacetate 	NULL		undergoes	NULL				oxidation	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_1_57_s_240	16375848	Thus, an increase in acetyl-CoA content from palmitate oxidation leads up to inhibition  of pyruvate dehydrogenase activity, decreasing the conversion of pyruvate to acetyl-CoA,  but also enhances pyruvate carboxylase activity, raising the conversion of pyruvate  to oxaloacetate that entries into the Krebs cycle being then oxidized   [57].	transcription
52244	11	334940	5	NULL	NULL	0	NULL	statement 8	NULL		leads to	NULL				statement 10	NULL				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_1_57_s_240	16375848	Thus, an increase in acetyl-CoA content from palmitate oxidation leads up to inhibition  of pyruvate dehydrogenase activity, decreasing the conversion of pyruvate to acetyl-CoA,  but also enhances pyruvate carboxylase activity, raising the conversion of pyruvate  to oxaloacetate that entries into the Krebs cycle being then oxidized   [57].	transcription
54373	1	334940	6	NULL	NULL	0	NULL	palmitate		oxidation of	increases					acetyl-CoA 		content of 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_1_57_s_240	16375848	Thus, an increase in acetyl-CoA content from palmitate oxidation leads up to inhibition  of pyruvate dehydrogenase activity, decreasing the conversion of pyruvate to acetyl-CoA,  but also enhances pyruvate carboxylase activity, raising the conversion of pyruvate  to oxaloacetate that entries into the Krebs cycle being then oxidized   [57].	transcription
54374	2	334940	6	NULL	NULL	0	NULL	statement 1			leads to					pyruvate dehydrogenase		inhibition of;; activity of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_1_57_s_240	16375848	Thus, an increase in acetyl-CoA content from palmitate oxidation leads up to inhibition  of pyruvate dehydrogenase activity, decreasing the conversion of pyruvate to acetyl-CoA,  but also enhances pyruvate carboxylase activity, raising the conversion of pyruvate  to oxaloacetate that entries into the Krebs cycle being then oxidized   [57].	transcription
54375	3	334940	6	NULL	NULL	0	NULL	pyruvate			is converted to					acetyl-CoA					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_1_57_s_240	16375848	Thus, an increase in acetyl-CoA content from palmitate oxidation leads up to inhibition  of pyruvate dehydrogenase activity, decreasing the conversion of pyruvate to acetyl-CoA,  but also enhances pyruvate carboxylase activity, raising the conversion of pyruvate  to oxaloacetate that entries into the Krebs cycle being then oxidized   [57].	transcription
54376	4	334940	6	NULL	NULL	0	NULL	statement 1			decreases					statement 3					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_1_57_s_240	16375848	Thus, an increase in acetyl-CoA content from palmitate oxidation leads up to inhibition  of pyruvate dehydrogenase activity, decreasing the conversion of pyruvate to acetyl-CoA,  but also enhances pyruvate carboxylase activity, raising the conversion of pyruvate  to oxaloacetate that entries into the Krebs cycle being then oxidized   [57].	transcription
54377	5	334940	6	NULL	NULL	0	NULL	statement 1			enhances					pyruvate carboxylase		activity of 			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_1_57_s_240	16375848	Thus, an increase in acetyl-CoA content from palmitate oxidation leads up to inhibition  of pyruvate dehydrogenase activity, decreasing the conversion of pyruvate to acetyl-CoA,  but also enhances pyruvate carboxylase activity, raising the conversion of pyruvate  to oxaloacetate that entries into the Krebs cycle being then oxidized   [57].	transcription
54378	6	334940	6	NULL	NULL	0	NULL	pyruvate			is converted to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_1_57_s_240	16375848	Thus, an increase in acetyl-CoA content from palmitate oxidation leads up to inhibition  of pyruvate dehydrogenase activity, decreasing the conversion of pyruvate to acetyl-CoA,  but also enhances pyruvate carboxylase activity, raising the conversion of pyruvate  to oxaloacetate that entries into the Krebs cycle being then oxidized   [57].	transcription
54379	7	334940	6	NULL	NULL	0	NULL	statement 1			increases					statement 6					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1757_1_57_s_240	16375848	Thus, an increase in acetyl-CoA content from palmitate oxidation leads up to inhibition  of pyruvate dehydrogenase activity, decreasing the conversion of pyruvate to acetyl-CoA,  but also enhances pyruvate carboxylase activity, raising the conversion of pyruvate  to oxaloacetate that entries into the Krebs cycle being then oxidized   [57].	transcription
52245	1	334942	5	NULL	NULL	0	NULL	pyruvate	NULL		enters	NULL				tricarboxylic acid cycle	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
52246	2	334942	5	NULL	NULL	0	NULL	statement 1	NULL		via	NULL				PDH	NULL	reactions catalyzed by			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
52247	3	334942	5	NULL	NULL	0	NULL	statement 1	NULL		via	NULL				PYC	NULL	reactions catalyzed by			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
52248	4	334942	5	NULL	NULL	0	NULL	PYC	NULL		is	NULL				pyruvate carboxylase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
52249	5	334942	5	NULL	NULL	0	NULL	pyruvate	NULL		is utilized for	NULL				anabolism	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
52250	6	334942	5	NULL	NULL	0	NULL	PYC	NULL		produce	NULL	anaplerotic			oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
52251	7	334942	5	NULL	NULL	0	NULL	statement 5	NULL		via	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
52252	8	334942	5	NULL	NULL	0	NULL	pyruvate	NULL		is utilized for	NULL				catabolism	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
52253	9	334942	5	NULL	NULL	0	NULL	PDH	NULL		produce	NULL				acetyl-CoA	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
52254	10	334942	5	NULL	NULL	0	NULL	statement 8	NULL		via	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
52255	11	334942	5	NULL	NULL	0	NULL	acetyl-CoA	NULL		is	NULL				acetyl coenzyme A	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
52256	12	334942	5	NULL	NULL	0	NULL	PDH	NULL	regulation of	coordinates	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
52257	13	334942	5	NULL	NULL	0	NULL	PDH	NULL	regulation of	coordinates	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
52258	14	334942	5	NULL	NULL	0	NULL	PYC	NULL	regulation of	coordinates	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
52259	15	334942	5	NULL	NULL	0	NULL	PYC	NULL	regulation of	coordinates	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
54381	1	334942	6	NULL	NULL	0	NULL	pyruvate			enters 					tricarboxylic acid cycle					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
54382	2	334942	6	NULL	NULL	0	NULL	PDH			catalyzes					reactions					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
54383	3	334942	6	NULL	NULL	0	NULL	statement 1			occurs via					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
54384	4	334942	6	NULL	NULL	0	NULL	PYC			catalyzes					reactions					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
54385	5	334942	6	NULL	NULL	0	NULL	statement 4			occurs via					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
54386	6	334942	6	NULL	NULL	0	NULL	PYC			produces					oxaloacetate					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
54387	7	334942	6	NULL	NULL	0	NULL	statement 6			is					anaplerotic					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
54388	8	334942	6	NULL	NULL	0	NULL	PDH			produces					acetyl-CoA					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
54389	9	334942	6	NULL	NULL	0	NULL	acetyl-CoA			is					acetyl coenzyme A					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_8_2296_s_10	11914362	Pyruvate enters the tricarboxylic acid cycle via the reactions catalyzed by PDH and pyruvate carboxylase (PYC), which are regulated to coordinate the utilization of pyruvate for anabolism (via the anaplerotic production of oxaloacetate by PYC) and catabolism (via acetyl coenzyme A [acetyl-CoA] production by PDH) ( 26).	transcription
52260	1	334943	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is diverted from	NULL				phosphoenolpyruvate	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4705_s_229	9030522	Table  VIII also shows that the acetate-induced diversion of oxaloacetate from phosphoenolpyruvate formation to citrate synthesis was logically accompanied by a large decrease in flux through pyruvate kinase and therefore in a decreased availability of pyruvate leading to a diminution of fluxes through alanine aminotransferase and pyruvate dehydrogenase.	transcription
52261	2	334943	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is diverted to	NULL				citrate	NULL	synthesis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4705_s_229	9030522	Table  VIII also shows that the acetate-induced diversion of oxaloacetate from phosphoenolpyruvate formation to citrate synthesis was logically accompanied by a large decrease in flux through pyruvate kinase and therefore in a decreased availability of pyruvate leading to a diminution of fluxes through alanine aminotransferase and pyruvate dehydrogenase.	transcription
52262	3	334943	5	NULL	NULL	0	NULL	acetate	NULL		induce	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4705_s_229	9030522	Table  VIII also shows that the acetate-induced diversion of oxaloacetate from phosphoenolpyruvate formation to citrate synthesis was logically accompanied by a large decrease in flux through pyruvate kinase and therefore in a decreased availability of pyruvate leading to a diminution of fluxes through alanine aminotransferase and pyruvate dehydrogenase.	transcription
52263	4	334943	5	NULL	NULL	0	NULL	acetate	NULL		induce	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4705_s_229	9030522	Table  VIII also shows that the acetate-induced diversion of oxaloacetate from phosphoenolpyruvate formation to citrate synthesis was logically accompanied by a large decrease in flux through pyruvate kinase and therefore in a decreased availability of pyruvate leading to a diminution of fluxes through alanine aminotransferase and pyruvate dehydrogenase.	transcription
52264	5	334943	5	NULL	NULL	0	NULL	flux	NULL	decrease in	occurs through	NULL				pyruvate kinase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4705_s_229	9030522	Table  VIII also shows that the acetate-induced diversion of oxaloacetate from phosphoenolpyruvate formation to citrate synthesis was logically accompanied by a large decrease in flux through pyruvate kinase and therefore in a decreased availability of pyruvate leading to a diminution of fluxes through alanine aminotransferase and pyruvate dehydrogenase.	transcription
52265	6	334943	5	NULL	NULL	0	NULL	statement 4	NULL		is accompanied by	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4705_s_229	9030522	Table  VIII also shows that the acetate-induced diversion of oxaloacetate from phosphoenolpyruvate formation to citrate synthesis was logically accompanied by a large decrease in flux through pyruvate kinase and therefore in a decreased availability of pyruvate leading to a diminution of fluxes through alanine aminotransferase and pyruvate dehydrogenase.	transcription
52266	7	334943	5	NULL	NULL	0	NULL	statement 6	NULL		leads to	NULL				pyruvate	NULL	decreased availability of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4705_s_229	9030522	Table  VIII also shows that the acetate-induced diversion of oxaloacetate from phosphoenolpyruvate formation to citrate synthesis was logically accompanied by a large decrease in flux through pyruvate kinase and therefore in a decreased availability of pyruvate leading to a diminution of fluxes through alanine aminotransferase and pyruvate dehydrogenase.	transcription
52267	8	334943	5	NULL	NULL	0	NULL	statement 7	NULL		leads to	NULL				fluxes	NULL	diminution of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4705_s_229	9030522	Table  VIII also shows that the acetate-induced diversion of oxaloacetate from phosphoenolpyruvate formation to citrate synthesis was logically accompanied by a large decrease in flux through pyruvate kinase and therefore in a decreased availability of pyruvate leading to a diminution of fluxes through alanine aminotransferase and pyruvate dehydrogenase.	transcription
52268	9	334943	5	NULL	NULL	0	NULL	statement 8	NULL		occurs through	NULL				alanine aminotransferase 	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4705_s_229	9030522	Table  VIII also shows that the acetate-induced diversion of oxaloacetate from phosphoenolpyruvate formation to citrate synthesis was logically accompanied by a large decrease in flux through pyruvate kinase and therefore in a decreased availability of pyruvate leading to a diminution of fluxes through alanine aminotransferase and pyruvate dehydrogenase.	transcription
52269	10	334943	5	NULL	NULL	0	NULL	statement 8	NULL		occurs through	NULL				pyruvate dehydrogenase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4705_s_229	9030522	Table  VIII also shows that the acetate-induced diversion of oxaloacetate from phosphoenolpyruvate formation to citrate synthesis was logically accompanied by a large decrease in flux through pyruvate kinase and therefore in a decreased availability of pyruvate leading to a diminution of fluxes through alanine aminotransferase and pyruvate dehydrogenase.	transcription
55616	1	334943	6	NULL	NULL	0	NULL	oxaloacetate			forms					phosphoenolpyruvate					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4705_s_229	9030522	Table  VIII also shows that the acetate-induced diversion of oxaloacetate from phosphoenolpyruvate formation to citrate synthesis was logically accompanied by a large decrease in flux through pyruvate kinase and therefore in a decreased availability of pyruvate leading to a diminution of fluxes through alanine aminotransferase and pyruvate dehydrogenase.	transcription
55617	2	334943	6	NULL	NULL	0	NULL	oxaloacetate			forms					citrate					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4705_s_229	9030522	Table  VIII also shows that the acetate-induced diversion of oxaloacetate from phosphoenolpyruvate formation to citrate synthesis was logically accompanied by a large decrease in flux through pyruvate kinase and therefore in a decreased availability of pyruvate leading to a diminution of fluxes through alanine aminotransferase and pyruvate dehydrogenase.	transcription
55618	3	334943	6	NULL	NULL	0	NULL	acetate			induces					oxaloacetate		diversion of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4705_s_229	9030522	Table  VIII also shows that the acetate-induced diversion of oxaloacetate from phosphoenolpyruvate formation to citrate synthesis was logically accompanied by a large decrease in flux through pyruvate kinase and therefore in a decreased availability of pyruvate leading to a diminution of fluxes through alanine aminotransferase and pyruvate dehydrogenase.	transcription
55619	4	334943	6	NULL	NULL	0	NULL	statement 3			allows					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4705_s_229	9030522	Table  VIII also shows that the acetate-induced diversion of oxaloacetate from phosphoenolpyruvate formation to citrate synthesis was logically accompanied by a large decrease in flux through pyruvate kinase and therefore in a decreased availability of pyruvate leading to a diminution of fluxes through alanine aminotransferase and pyruvate dehydrogenase.	transcription
52270	1	334944	5	NULL	NULL	0	NULL	5S	NULL		is a type of	NULL				120 kDa dimer	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevphyschem_57_0_527_s_306	16599820	In  2000 our laboratory began Raman crystallographic studies on transcarboxylase's  second major subunit, the so-called 5S, a 120 kDa dimer that converts bound pyruvate  to oxaloacetate using -CO2  from carboxybiotin ( 21).	transcription
52271	2	334944	5	NULL	NULL	0	NULL	5S	NULL		is a subunit of	NULL	major			transcarboxylase	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevphyschem_57_0_527_s_306	16599820	In  2000 our laboratory began Raman crystallographic studies on transcarboxylase's  second major subunit, the so-called 5S, a 120 kDa dimer that converts bound pyruvate  to oxaloacetate using -CO2  from carboxybiotin ( 21).	transcription
52272	3	334944	5	NULL	NULL	0	NULL	pyruvate	NULL	bound	is converted to	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevphyschem_57_0_527_s_306	16599820	In  2000 our laboratory began Raman crystallographic studies on transcarboxylase's  second major subunit, the so-called 5S, a 120 kDa dimer that converts bound pyruvate  to oxaloacetate using -CO2  from carboxybiotin ( 21).	transcription
52273	4	334944	5	NULL	NULL	0	NULL	transcarboxylase	NULL		catalyzes	NULL		5S		statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_annurevphyschem_57_0_527_s_306	16599820	In  2000 our laboratory began Raman crystallographic studies on transcarboxylase's  second major subunit, the so-called 5S, a 120 kDa dimer that converts bound pyruvate  to oxaloacetate using -CO2  from carboxybiotin ( 21).	transcription
52274	5	334944	5	NULL	NULL	0	NULL	statement 4	NULL		uses	NULL				carboxybiotin	NULL		-CO2		NULL		0	NULL	NULL	NULL	gw70_annurevphyschem_57_0_527_s_306	16599820	In  2000 our laboratory began Raman crystallographic studies on transcarboxylase's  second major subunit, the so-called 5S, a 120 kDa dimer that converts bound pyruvate  to oxaloacetate using -CO2  from carboxybiotin ( 21).	transcription
54390	1	334944	6	NULL	NULL	0	NULL	pyruvate			is converted to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw70_annurevphyschem_57_0_527_s_306	16599820	In  2000 our laboratory began Raman crystallographic studies on transcarboxylase's  second major subunit, the so-called 5S, a 120 kDa dimer that converts bound pyruvate  to oxaloacetate using -CO2  from carboxybiotin ( 21).	transcription
54391	2	334944	6	NULL	NULL	0	NULL	5S subunit			converts					statement 1					NULL		0	NULL	NULL	NULL	gw70_annurevphyschem_57_0_527_s_306	16599820	In  2000 our laboratory began Raman crystallographic studies on transcarboxylase's  second major subunit, the so-called 5S, a 120 kDa dimer that converts bound pyruvate  to oxaloacetate using -CO2  from carboxybiotin ( 21).	transcription
54392	3	334944	6	NULL	NULL	0	NULL	5S subunit			is					transcarboxylase second major subunit					NULL		0	NULL	NULL	NULL	gw70_annurevphyschem_57_0_527_s_306	16599820	In  2000 our laboratory began Raman crystallographic studies on transcarboxylase's  second major subunit, the so-called 5S, a 120 kDa dimer that converts bound pyruvate  to oxaloacetate using -CO2  from carboxybiotin ( 21).	transcription
54393	4	334944	6	NULL	NULL	0	NULL	CO2			is used from					carboxybiotin					NULL		0	NULL	NULL	NULL	gw70_annurevphyschem_57_0_527_s_306	16599820	In  2000 our laboratory began Raman crystallographic studies on transcarboxylase's  second major subunit, the so-called 5S, a 120 kDa dimer that converts bound pyruvate  to oxaloacetate using -CO2  from carboxybiotin ( 21).	transcription
54394	5	334944	6	NULL	NULL	0	NULL	statement 1			occurs via					statement 4					NULL		0	NULL	NULL	NULL	gw70_annurevphyschem_57_0_527_s_306	16599820	In  2000 our laboratory began Raman crystallographic studies on transcarboxylase's  second major subunit, the so-called 5S, a 120 kDa dimer that converts bound pyruvate  to oxaloacetate using -CO2  from carboxybiotin ( 21).	transcription
52275	1	334945	5	NULL	NULL	0	NULL	U251-HRE cells	NULL		is	NULL				U251 cells stably expressing (HRE)-luciferase construct	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_126	16223732	Using U251 cells stably expressing a hypoxia regulatory element (HRE)-luciferase construct (U251-HRE cells;  Fig. 1 E), we found that pyruvate and oxaloacetate induced the HIF-1-regulated reporter gene as effectively as hypoxia or DMOG.	transcription
52276	2	334945	5	NULL	NULL	0	NULL	HRE	NULL		is	NULL				hypoxia regulatory element	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_126	16223732	Using U251 cells stably expressing a hypoxia regulatory element (HRE)-luciferase construct (U251-HRE cells;  Fig. 1 E), we found that pyruvate and oxaloacetate induced the HIF-1-regulated reporter gene as effectively as hypoxia or DMOG.	transcription
52277	3	334945	5	NULL	NULL	0	NULL	reporter gene	NULL		is regulated by	NULL				HIF-1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_126	16223732	Using U251 cells stably expressing a hypoxia regulatory element (HRE)-luciferase construct (U251-HRE cells;  Fig. 1 E), we found that pyruvate and oxaloacetate induced the HIF-1-regulated reporter gene as effectively as hypoxia or DMOG.	transcription
52278	4	334945	5	NULL	NULL	0	NULL	pyruvate	NULL		induce	NULL				statement 3	NULL				NULL	U251-HRE cells	0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_126	16223732	Using U251 cells stably expressing a hypoxia regulatory element (HRE)-luciferase construct (U251-HRE cells;  Fig. 1 E), we found that pyruvate and oxaloacetate induced the HIF-1-regulated reporter gene as effectively as hypoxia or DMOG.	transcription
52279	5	334945	5	NULL	NULL	0	NULL	oxaloacetate	NULL		induce	NULL				statement 3	NULL				NULL	U251-HRE cells	0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_126	16223732	Using U251 cells stably expressing a hypoxia regulatory element (HRE)-luciferase construct (U251-HRE cells;  Fig. 1 E), we found that pyruvate and oxaloacetate induced the HIF-1-regulated reporter gene as effectively as hypoxia or DMOG.	transcription
52280	6	334945	5	NULL	NULL	0	NULL	hypoxia	NULL		induce	NULL				statement 3	NULL				NULL	U251-HRE cells	0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_126	16223732	Using U251 cells stably expressing a hypoxia regulatory element (HRE)-luciferase construct (U251-HRE cells;  Fig. 1 E), we found that pyruvate and oxaloacetate induced the HIF-1-regulated reporter gene as effectively as hypoxia or DMOG.	transcription
52281	7	334945	5	NULL	NULL	0	NULL	DMOG	NULL		induce	NULL				statement 3	NULL				NULL	U251-HRE cells	0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_126	16223732	Using U251 cells stably expressing a hypoxia regulatory element (HRE)-luciferase construct (U251-HRE cells;  Fig. 1 E), we found that pyruvate and oxaloacetate induced the HIF-1-regulated reporter gene as effectively as hypoxia or DMOG.	transcription
52282	8	334945	5	NULL	NULL	0	NULL	statement 4	NULL		as effecective as	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_126	16223732	Using U251 cells stably expressing a hypoxia regulatory element (HRE)-luciferase construct (U251-HRE cells;  Fig. 1 E), we found that pyruvate and oxaloacetate induced the HIF-1-regulated reporter gene as effectively as hypoxia or DMOG.	transcription
52283	9	334945	5	NULL	NULL	0	NULL	statement 5	NULL		as effecective as	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_126	16223732	Using U251 cells stably expressing a hypoxia regulatory element (HRE)-luciferase construct (U251-HRE cells;  Fig. 1 E), we found that pyruvate and oxaloacetate induced the HIF-1-regulated reporter gene as effectively as hypoxia or DMOG.	transcription
52284	10	334945	5	NULL	NULL	0	NULL	statement 4	NULL		as effecective as	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_126	16223732	Using U251 cells stably expressing a hypoxia regulatory element (HRE)-luciferase construct (U251-HRE cells;  Fig. 1 E), we found that pyruvate and oxaloacetate induced the HIF-1-regulated reporter gene as effectively as hypoxia or DMOG.	transcription
52285	11	334945	5	NULL	NULL	0	NULL	statement 5	NULL		as effecective as	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_126	16223732	Using U251 cells stably expressing a hypoxia regulatory element (HRE)-luciferase construct (U251-HRE cells;  Fig. 1 E), we found that pyruvate and oxaloacetate induced the HIF-1-regulated reporter gene as effectively as hypoxia or DMOG.	transcription
54395	1	334945	6	NULL	NULL	0	NULL	HIF			regulates					reporter gene					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_126	16223732	Using U251 cells stably expressing a hypoxia regulatory element (HRE)-luciferase construct (U251-HRE cells;  Fig. 1 E), we found that pyruvate and oxaloacetate induced the HIF-1-regulated reporter gene as effectively as hypoxia or DMOG.	transcription
54396	2	334945	6	NULL	NULL	0	NULL	pyruvate			induces					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_126	16223732	Using U251 cells stably expressing a hypoxia regulatory element (HRE)-luciferase construct (U251-HRE cells;  Fig. 1 E), we found that pyruvate and oxaloacetate induced the HIF-1-regulated reporter gene as effectively as hypoxia or DMOG.	transcription
54397	3	334945	6	NULL	NULL	0	NULL	oxaloacetate			induces					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_126	16223732	Using U251 cells stably expressing a hypoxia regulatory element (HRE)-luciferase construct (U251-HRE cells;  Fig. 1 E), we found that pyruvate and oxaloacetate induced the HIF-1-regulated reporter gene as effectively as hypoxia or DMOG.	transcription
54398	4	334945	6	NULL	NULL	0	NULL	hypoxia			induces					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_126	16223732	Using U251 cells stably expressing a hypoxia regulatory element (HRE)-luciferase construct (U251-HRE cells;  Fig. 1 E), we found that pyruvate and oxaloacetate induced the HIF-1-regulated reporter gene as effectively as hypoxia or DMOG.	transcription
54399	5	334945	6	NULL	NULL	0	NULL	DMOG			induces					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_126	16223732	Using U251 cells stably expressing a hypoxia regulatory element (HRE)-luciferase construct (U251-HRE cells;  Fig. 1 E), we found that pyruvate and oxaloacetate induced the HIF-1-regulated reporter gene as effectively as hypoxia or DMOG.	transcription
54400	6	334945	6	NULL	NULL	0	NULL	statement 4			is an alternative to					statement 5					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_126	16223732	Using U251 cells stably expressing a hypoxia regulatory element (HRE)-luciferase construct (U251-HRE cells;  Fig. 1 E), we found that pyruvate and oxaloacetate induced the HIF-1-regulated reporter gene as effectively as hypoxia or DMOG.	transcription
52286	1	334946	5	NULL	NULL	0	NULL	2-oxoacids	NULL		induce	NULL				HIF-1 gene	NULL			reporter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_128	16223732	Induction of the HIF-1 reporter gene by the 2-oxoacids was also selectively reversed by ascorbate but not by 2-OG. Ascorbate did not reverse HRE-luciferase activation by hypoxia or by DMOG, again suggesting a unique mode of HIF-1alpha regulation by pyruvate and oxaloacetate.	transcription
52287	2	334946	5	NULL	NULL	0	NULL	statement 1	NULL		is reversed by	NULL	selectively			ascorbate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_128	16223732	Induction of the HIF-1 reporter gene by the 2-oxoacids was also selectively reversed by ascorbate but not by 2-OG. Ascorbate did not reverse HRE-luciferase activation by hypoxia or by DMOG, again suggesting a unique mode of HIF-1alpha regulation by pyruvate and oxaloacetate.	transcription
52288	3	334946	5	NULL	NULL	0	NULL	statement 1	NULL		is not reversed by	NULL				2-OG	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_128	16223732	Induction of the HIF-1 reporter gene by the 2-oxoacids was also selectively reversed by ascorbate but not by 2-OG. Ascorbate did not reverse HRE-luciferase activation by hypoxia or by DMOG, again suggesting a unique mode of HIF-1alpha regulation by pyruvate and oxaloacetate.	transcription
52289	4	334946	5	NULL	NULL	0	NULL	HIF-1alpha	NULL		is regulated by	NULL				pyruvate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_128	16223732	Induction of the HIF-1 reporter gene by the 2-oxoacids was also selectively reversed by ascorbate but not by 2-OG. Ascorbate did not reverse HRE-luciferase activation by hypoxia or by DMOG, again suggesting a unique mode of HIF-1alpha regulation by pyruvate and oxaloacetate.	transcription
52290	5	334946	5	NULL	NULL	0	NULL	HIF-1alpha	NULL		is regulated by	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_128	16223732	Induction of the HIF-1 reporter gene by the 2-oxoacids was also selectively reversed by ascorbate but not by 2-OG. Ascorbate did not reverse HRE-luciferase activation by hypoxia or by DMOG, again suggesting a unique mode of HIF-1alpha regulation by pyruvate and oxaloacetate.	transcription
52291	6	334946	5	NULL	NULL	0	NULL	hypoxia	NULL		activates	NULL				HRE-luciferase	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_128	16223732	Induction of the HIF-1 reporter gene by the 2-oxoacids was also selectively reversed by ascorbate but not by 2-OG. Ascorbate did not reverse HRE-luciferase activation by hypoxia or by DMOG, again suggesting a unique mode of HIF-1alpha regulation by pyruvate and oxaloacetate.	transcription
52292	7	334946	5	NULL	NULL	0	NULL	DMOG	NULL		activates	NULL				HRE-luciferase	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_128	16223732	Induction of the HIF-1 reporter gene by the 2-oxoacids was also selectively reversed by ascorbate but not by 2-OG. Ascorbate did not reverse HRE-luciferase activation by hypoxia or by DMOG, again suggesting a unique mode of HIF-1alpha regulation by pyruvate and oxaloacetate.	transcription
52293	8	334946	5	NULL	NULL	0	NULL	ascorbate	NULL		does not reverse	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_128	16223732	Induction of the HIF-1 reporter gene by the 2-oxoacids was also selectively reversed by ascorbate but not by 2-OG. Ascorbate did not reverse HRE-luciferase activation by hypoxia or by DMOG, again suggesting a unique mode of HIF-1alpha regulation by pyruvate and oxaloacetate.	transcription
52294	9	334946	5	NULL	NULL	0	NULL	ascorbate	NULL		does not reverse	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_128	16223732	Induction of the HIF-1 reporter gene by the 2-oxoacids was also selectively reversed by ascorbate but not by 2-OG. Ascorbate did not reverse HRE-luciferase activation by hypoxia or by DMOG, again suggesting a unique mode of HIF-1alpha regulation by pyruvate and oxaloacetate.	transcription
79259	1	334946	6	NULL	NULL	0	NULL	2-oxoacids	Chemical		induces					HIF-1 gene					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_128	16223732	Induction of the HIF-1 reporter gene by the 2-oxoacids was also selectively reversed by ascorbate but not by 2-OG. Ascorbate did not reverse HRE-luciferase activation by hypoxia or by DMOG, again suggesting a unique mode of HIF-1alpha regulation by pyruvate and oxaloacetate.	transcription
79260	2	334946	6	NULL	NULL	0	NULL	ascorbate	Chemical		reverses					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_128	16223732	Induction of the HIF-1 reporter gene by the 2-oxoacids was also selectively reversed by ascorbate but not by 2-OG. Ascorbate did not reverse HRE-luciferase activation by hypoxia or by DMOG, again suggesting a unique mode of HIF-1alpha regulation by pyruvate and oxaloacetate.	transcription
52295	1	334947	5	NULL	NULL	0	NULL	HIF-1alpha	NULL		is induced by	NULL				pyruvate	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
52296	2	334947	5	NULL	NULL	0	NULL	HIF-1alpha	NULL		is induced by	NULL				oxaloacetate	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
52297	3	334947	5	NULL	NULL	0	NULL	protein	NULL	acetylation of	is implicated in	NULL				HIF-1alpha	NULL	stabilization of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
52298	4	334947	5	NULL	NULL	0	NULL	protein	NULL	inhibition of;;acetylation of	does not alter	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
52299	5	334947	5	NULL	NULL	0	NULL	protein	NULL	inhibition of;;acetylation of	does not alter	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
52300	6	334947	5	NULL	NULL	0	NULL	phosphatidylinositol 3-kinase	NULL		is implicated in	NULL				HIF-1alpha	NULL	stabilization of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
52301	7	334947	5	NULL	NULL	0	NULL	phosphatidylinositol 3-kinase	NULL	inhibition of	does not alter	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
52302	8	334947	5	NULL	NULL	0	NULL	phosphatidylinositol 3-kinase	NULL	inhibition of	does not alter	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
52303	9	334947	5	NULL	NULL	0	NULL	mTOR	NULL		is implicated in	NULL				HIF-1alpha	NULL	stabilization of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
52304	10	334947	5	NULL	NULL	0	NULL	mTOR	NULL	inhibition of	does not alter	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
52305	11	334947	5	NULL	NULL	0	NULL	mTOR	NULL	inhibition of	does not alter	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
52306	12	334947	5	NULL	NULL	0	NULL	hsp70	NULL		is implicated in	NULL				HIF-1alpha	NULL	stabilization of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
52307	13	334947	5	NULL	NULL	0	NULL	hsp70	NULL	inhibition of	does not alter	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
52308	14	334947	5	NULL	NULL	0	NULL	hsp70	NULL	inhibition of	does not alter	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
54401	1	334947	6	NULL	NULL	0	NULL	pyruvate			induces					HIF-1alpha		induction of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
54402	2	334947	6	NULL	NULL	0	NULL	oxaloacetate			induces					HIF-1alpha		induction of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
54403	3	334947	6	NULL	NULL	0	NULL	phosphatidylinositol 3-kinase		inhibition of 	does not alter					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
54404	4	334947	6	NULL	NULL	0	NULL	phosphatidylinositol 3-kinase		inhibition of 	does not alter					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
54405	5	334947	6	NULL	NULL	0	NULL	mTOR		inhibition of 	does not alter					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
54406	6	334947	6	NULL	NULL	0	NULL	mTOR		inhibition of 	does not alter					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
54407	7	334947	6	NULL	NULL	0	NULL	hsp70		inhibition of 	does not alter					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
54408	8	334947	6	NULL	NULL	0	NULL	hsp70		inhibition of 	does not alter					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_154	16223732	Pharmacological inhibition of other signaling pathways implicated in HIF-1alpha stabilization, such as protein acetylation, phosphatidylinositol 3-kinase, mTOR, and hsp70, also failed to alter HIF-1alpha induction by pyruvate and oxaloacetate ( Fig. 3 C).	transcription
52309	1	334948	5	NULL	NULL	0	NULL	HPH1	NULL	in vitro translated	hydroxylates	NULL				HIF-1alpha peptide	NULL	biotinylated	Pro564		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_201	16223732	To determine whether HPH activity was directly modulated by pyruvate or oxaloacetate, we studied Pro564 hydroxylation in a biotinylated HIF-1alpha ODD peptide by  in vitro translated HPH1, HPH2, and HPH3.	transcription
52310	2	334948	5	NULL	NULL	0	NULL	HPH2	NULL	in vitro translated	hydroxylates	NULL				HIF-1alpha peptide	NULL	biotinylated	Pro564		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_201	16223732	To determine whether HPH activity was directly modulated by pyruvate or oxaloacetate, we studied Pro564 hydroxylation in a biotinylated HIF-1alpha ODD peptide by  in vitro translated HPH1, HPH2, and HPH3.	transcription
52311	3	334948	5	NULL	NULL	0	NULL	HPH3	NULL	in vitro translated	hydroxylates	NULL				HIF-1alpha peptide	NULL	biotinylated	Pro564		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_51_41928_s_201	16223732	To determine whether HPH activity was directly modulated by pyruvate or oxaloacetate, we studied Pro564 hydroxylation in a biotinylated HIF-1alpha ODD peptide by  in vitro translated HPH1, HPH2, and HPH3.	transcription
52312	1	334951	5	NULL	NULL	0	NULL	protocatechuate	NULL		is converted to	NULL				pyruvate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_12_3689_s_308	11371533	It is not required for the conversion of protocatechuate to pyruvate and oxaloacetate (above), and extracts of  E. coli strains carrying the  pcmF gene (on pRE1056, e.g.) did not have activity toward such substrates as 2-hydroxy-4-carboxymuconic semialdehyde and 2-pyrone-4,6-dicarboxylate.	transcription
52313	2	334951	5	NULL	NULL	0	NULL	protocatechuate	NULL		is converted to	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_12_3689_s_308	11371533	It is not required for the conversion of protocatechuate to pyruvate and oxaloacetate (above), and extracts of  E. coli strains carrying the  pcmF gene (on pRE1056, e.g.) did not have activity toward such substrates as 2-hydroxy-4-carboxymuconic semialdehyde and 2-pyrone-4,6-dicarboxylate.	transcription
52314	3	334951	5	NULL	NULL	0	NULL	statement 1	NULL		occurs along with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_12_3689_s_308	11371533	It is not required for the conversion of protocatechuate to pyruvate and oxaloacetate (above), and extracts of  E. coli strains carrying the  pcmF gene (on pRE1056, e.g.) did not have activity toward such substrates as 2-hydroxy-4-carboxymuconic semialdehyde and 2-pyrone-4,6-dicarboxylate.	transcription
52315	4	334951	5	NULL	NULL	0	NULL	E. coli strains	NULL	extracts of	carries	NULL				pcmF gene	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_12_3689_s_308	11371533	It is not required for the conversion of protocatechuate to pyruvate and oxaloacetate (above), and extracts of  E. coli strains carrying the  pcmF gene (on pRE1056, e.g.) did not have activity toward such substrates as 2-hydroxy-4-carboxymuconic semialdehyde and 2-pyrone-4,6-dicarboxylate.	transcription
52316	5	334951	5	NULL	NULL	0	NULL	statement 4	NULL		does have activity towards	NULL				2-hydroxy-4-carboxymuconic semialdehyde	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_12_3689_s_308	11371533	It is not required for the conversion of protocatechuate to pyruvate and oxaloacetate (above), and extracts of  E. coli strains carrying the  pcmF gene (on pRE1056, e.g.) did not have activity toward such substrates as 2-hydroxy-4-carboxymuconic semialdehyde and 2-pyrone-4,6-dicarboxylate.	transcription
52317	6	334951	5	NULL	NULL	0	NULL	statement 4	NULL		does have activity towards	NULL				2-pyrone-4,6-dicarboxylate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_12_3689_s_308	11371533	It is not required for the conversion of protocatechuate to pyruvate and oxaloacetate (above), and extracts of  E. coli strains carrying the  pcmF gene (on pRE1056, e.g.) did not have activity toward such substrates as 2-hydroxy-4-carboxymuconic semialdehyde and 2-pyrone-4,6-dicarboxylate.	transcription
52318	7	334951	5	NULL	NULL	0	NULL	2-pyrone-4,6-dicarboxylate	NULL		is a type of	NULL				substrate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_12_3689_s_308	11371533	It is not required for the conversion of protocatechuate to pyruvate and oxaloacetate (above), and extracts of  E. coli strains carrying the  pcmF gene (on pRE1056, e.g.) did not have activity toward such substrates as 2-hydroxy-4-carboxymuconic semialdehyde and 2-pyrone-4,6-dicarboxylate.	transcription
52319	8	334951	5	NULL	NULL	0	NULL	2-hydroxy-4-carboxymuconic semialdehyde	NULL		is a type of	NULL				substrate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_12_3689_s_308	11371533	It is not required for the conversion of protocatechuate to pyruvate and oxaloacetate (above), and extracts of  E. coli strains carrying the  pcmF gene (on pRE1056, e.g.) did not have activity toward such substrates as 2-hydroxy-4-carboxymuconic semialdehyde and 2-pyrone-4,6-dicarboxylate.	transcription
54409	1	334951	6	NULL	NULL	0	NULL	protocatechuate			is converted to					pyruvate					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_12_3689_s_308	11371533	It is not required for the conversion of protocatechuate to pyruvate and oxaloacetate (above), and extracts of  E. coli strains carrying the  pcmF gene (on pRE1056, e.g.) did not have activity toward such substrates as 2-hydroxy-4-carboxymuconic semialdehyde and 2-pyrone-4,6-dicarboxylate.	transcription
54410	2	334951	6	NULL	NULL	0	NULL	protocatechuate			is converted to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_12_3689_s_308	11371533	It is not required for the conversion of protocatechuate to pyruvate and oxaloacetate (above), and extracts of  E. coli strains carrying the  pcmF gene (on pRE1056, e.g.) did not have activity toward such substrates as 2-hydroxy-4-carboxymuconic semialdehyde and 2-pyrone-4,6-dicarboxylate.	transcription
54411	3	334951	6	NULL	NULL	0	NULL	statement 1			occurs simultaneously with					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_12_3689_s_308	11371533	It is not required for the conversion of protocatechuate to pyruvate and oxaloacetate (above), and extracts of  E. coli strains carrying the  pcmF gene (on pRE1056, e.g.) did not have activity toward such substrates as 2-hydroxy-4-carboxymuconic semialdehyde and 2-pyrone-4,6-dicarboxylate.	transcription
52320	1	334952	5	NULL	NULL	0	NULL	OAA	NULL		is	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_21_6679_s_126	10542169	These are the gluconeogenic conversion of oxaloacetate (OAA) to phosphoenolpyruvate (PEP) (Fig.  2G), catalyzed by the PEP carboxykinase ( 10,  11), and the conversion of malate (MAL) to pyruvate (PYR) (Fig.  2H and I) through the malic enzyme.	transcription
52321	2	334952	5	NULL	NULL	0	NULL	PEP	NULL		is	NULL				phosphoenolpyruvate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_21_6679_s_126	10542169	These are the gluconeogenic conversion of oxaloacetate (OAA) to phosphoenolpyruvate (PEP) (Fig.  2G), catalyzed by the PEP carboxykinase ( 10,  11), and the conversion of malate (MAL) to pyruvate (PYR) (Fig.  2H and I) through the malic enzyme.	transcription
52322	3	334952	5	NULL	NULL	0	NULL	MAL	NULL		is	NULL				malate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_21_6679_s_126	10542169	These are the gluconeogenic conversion of oxaloacetate (OAA) to phosphoenolpyruvate (PEP) (Fig.  2G), catalyzed by the PEP carboxykinase ( 10,  11), and the conversion of malate (MAL) to pyruvate (PYR) (Fig.  2H and I) through the malic enzyme.	transcription
52323	4	334952	5	NULL	NULL	0	NULL	PYR	NULL		is	NULL				pyruvate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_21_6679_s_126	10542169	These are the gluconeogenic conversion of oxaloacetate (OAA) to phosphoenolpyruvate (PEP) (Fig.  2G), catalyzed by the PEP carboxykinase ( 10,  11), and the conversion of malate (MAL) to pyruvate (PYR) (Fig.  2H and I) through the malic enzyme.	transcription
52324	5	334952	5	NULL	NULL	0	NULL	OAA	NULL		is converted to	NULL				PEP	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_21_6679_s_126	10542169	These are the gluconeogenic conversion of oxaloacetate (OAA) to phosphoenolpyruvate (PEP) (Fig.  2G), catalyzed by the PEP carboxykinase ( 10,  11), and the conversion of malate (MAL) to pyruvate (PYR) (Fig.  2H and I) through the malic enzyme.	transcription
52325	6	334952	5	NULL	NULL	0	NULL	PEP carboxykinase	NULL		catalyzes	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_21_6679_s_126	10542169	These are the gluconeogenic conversion of oxaloacetate (OAA) to phosphoenolpyruvate (PEP) (Fig.  2G), catalyzed by the PEP carboxykinase ( 10,  11), and the conversion of malate (MAL) to pyruvate (PYR) (Fig.  2H and I) through the malic enzyme.	transcription
52326	7	334952	5	NULL	NULL	0	NULL	MAL	NULL		is converted to	NULL				PYR	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_21_6679_s_126	10542169	These are the gluconeogenic conversion of oxaloacetate (OAA) to phosphoenolpyruvate (PEP) (Fig.  2G), catalyzed by the PEP carboxykinase ( 10,  11), and the conversion of malate (MAL) to pyruvate (PYR) (Fig.  2H and I) through the malic enzyme.	transcription
52327	8	334952	5	NULL	NULL	0	NULL	malic enzyme	NULL		catalyzes	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_21_6679_s_126	10542169	These are the gluconeogenic conversion of oxaloacetate (OAA) to phosphoenolpyruvate (PEP) (Fig.  2G), catalyzed by the PEP carboxykinase ( 10,  11), and the conversion of malate (MAL) to pyruvate (PYR) (Fig.  2H and I) through the malic enzyme.	transcription
54412	1	334952	6	NULL	NULL	0	NULL	oxaloacetate			is converted to					phosphoenolpyruvate					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_21_6679_s_126	10542169	These are the gluconeogenic conversion of oxaloacetate (OAA) to phosphoenolpyruvate (PEP) (Fig.  2G), catalyzed by the PEP carboxykinase ( 10,  11), and the conversion of malate (MAL) to pyruvate (PYR) (Fig.  2H and I) through the malic enzyme.	transcription
54413	2	334952	6	NULL	NULL	0	NULL	OAA			is					oxaloacetate					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_21_6679_s_126	10542169	These are the gluconeogenic conversion of oxaloacetate (OAA) to phosphoenolpyruvate (PEP) (Fig.  2G), catalyzed by the PEP carboxykinase ( 10,  11), and the conversion of malate (MAL) to pyruvate (PYR) (Fig.  2H and I) through the malic enzyme.	transcription
54414	3	334952	6	NULL	NULL	0	NULL	PEP			is					phosphoenolpyruvate					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_21_6679_s_126	10542169	These are the gluconeogenic conversion of oxaloacetate (OAA) to phosphoenolpyruvate (PEP) (Fig.  2G), catalyzed by the PEP carboxykinase ( 10,  11), and the conversion of malate (MAL) to pyruvate (PYR) (Fig.  2H and I) through the malic enzyme.	transcription
54415	4	334952	6	NULL	NULL	0	NULL	PEP carboxykinase			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_21_6679_s_126	10542169	These are the gluconeogenic conversion of oxaloacetate (OAA) to phosphoenolpyruvate (PEP) (Fig.  2G), catalyzed by the PEP carboxykinase ( 10,  11), and the conversion of malate (MAL) to pyruvate (PYR) (Fig.  2H and I) through the malic enzyme.	transcription
54416	5	334952	6	NULL	NULL	0	NULL	malate			is converted to					pyruvate					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_21_6679_s_126	10542169	These are the gluconeogenic conversion of oxaloacetate (OAA) to phosphoenolpyruvate (PEP) (Fig.  2G), catalyzed by the PEP carboxykinase ( 10,  11), and the conversion of malate (MAL) to pyruvate (PYR) (Fig.  2H and I) through the malic enzyme.	transcription
54417	6	334952	6	NULL	NULL	0	NULL	malic enzyme			catalyzes					statement 5					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_21_6679_s_126	10542169	These are the gluconeogenic conversion of oxaloacetate (OAA) to phosphoenolpyruvate (PEP) (Fig.  2G), catalyzed by the PEP carboxykinase ( 10,  11), and the conversion of malate (MAL) to pyruvate (PYR) (Fig.  2H and I) through the malic enzyme.	transcription
52328	1	334953	5	NULL	NULL	0	NULL	NAD(P)H	NULL		regulates	NULL	negatively			Bdh	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_3_849_s_260	9922248	Although there are several reports demonstrating that Bdh activity is negatively regulated by NAD(P)H, adenosine nucleotides, pyruvate, oxaloacetate, and 2-ketoglutarate ( 55,  71,  78), regulation of Bdh at the level of gene expression was not examined.	transcription
52329	2	334953	5	NULL	NULL	0	NULL	adenosine nucleotides	NULL		regulates	NULL	negatively			Bdh	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_3_849_s_260	9922248	Although there are several reports demonstrating that Bdh activity is negatively regulated by NAD(P)H, adenosine nucleotides, pyruvate, oxaloacetate, and 2-ketoglutarate ( 55,  71,  78), regulation of Bdh at the level of gene expression was not examined.	transcription
52330	3	334953	5	NULL	NULL	0	NULL	pyruvate	NULL		regulates	NULL	negatively			Bdh	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_3_849_s_260	9922248	Although there are several reports demonstrating that Bdh activity is negatively regulated by NAD(P)H, adenosine nucleotides, pyruvate, oxaloacetate, and 2-ketoglutarate ( 55,  71,  78), regulation of Bdh at the level of gene expression was not examined.	transcription
52331	4	334953	5	NULL	NULL	0	NULL	oxaloacetate	NULL		regulates	NULL	negatively			Bdh	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_3_849_s_260	9922248	Although there are several reports demonstrating that Bdh activity is negatively regulated by NAD(P)H, adenosine nucleotides, pyruvate, oxaloacetate, and 2-ketoglutarate ( 55,  71,  78), regulation of Bdh at the level of gene expression was not examined.	transcription
52332	5	334953	5	NULL	NULL	0	NULL	2-ketoglutarate	NULL		regulates	NULL	negatively			Bdh	NULL	activity of			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_3_849_s_260	9922248	Although there are several reports demonstrating that Bdh activity is negatively regulated by NAD(P)H, adenosine nucleotides, pyruvate, oxaloacetate, and 2-ketoglutarate ( 55,  71,  78), regulation of Bdh at the level of gene expression was not examined.	transcription
54418	1	334953	6	NULL	NULL	0	NULL	NAD(P)H			regulates		negatively			Bdh		activity of 			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_3_849_s_260	9922248	Although there are several reports demonstrating that Bdh activity is negatively regulated by NAD(P)H, adenosine nucleotides, pyruvate, oxaloacetate, and 2-ketoglutarate ( 55,  71,  78), regulation of Bdh at the level of gene expression was not examined.	transcription
54419	2	334953	6	NULL	NULL	0	NULL	adenosine nucleotides			regulates		negatively			Bdh		activity of 			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_3_849_s_260	9922248	Although there are several reports demonstrating that Bdh activity is negatively regulated by NAD(P)H, adenosine nucleotides, pyruvate, oxaloacetate, and 2-ketoglutarate ( 55,  71,  78), regulation of Bdh at the level of gene expression was not examined.	transcription
54420	3	334953	6	NULL	NULL	0	NULL	pyruvate			regulates		negatively			Bdh		activity of 			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_3_849_s_260	9922248	Although there are several reports demonstrating that Bdh activity is negatively regulated by NAD(P)H, adenosine nucleotides, pyruvate, oxaloacetate, and 2-ketoglutarate ( 55,  71,  78), regulation of Bdh at the level of gene expression was not examined.	transcription
54421	4	334953	6	NULL	NULL	0	NULL	oxaloacetate			regulates		negatively			Bdh		activity of 			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_3_849_s_260	9922248	Although there are several reports demonstrating that Bdh activity is negatively regulated by NAD(P)H, adenosine nucleotides, pyruvate, oxaloacetate, and 2-ketoglutarate ( 55,  71,  78), regulation of Bdh at the level of gene expression was not examined.	transcription
54422	5	334953	6	NULL	NULL	0	NULL	2-ketoglutarate			regulates		negatively			Bdh		activity of 			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_3_849_s_260	9922248	Although there are several reports demonstrating that Bdh activity is negatively regulated by NAD(P)H, adenosine nucleotides, pyruvate, oxaloacetate, and 2-ketoglutarate ( 55,  71,  78), regulation of Bdh at the level of gene expression was not examined.	transcription
52333	1	334954	5	NULL	NULL	0	NULL	pyruvate carboxylase	NULL	cytosolic	carboxylates	NULL				pyruvate	NULL				NULL		0	NULL	NULL	NULL	gw70_yeast_21_9_769_s_295	15282800	The mitochondrial malic enzyme, in conjunction with the cytosolic  enzymes pyruvate carboxylase, which carboxylates pyruvate producing oxaloacetate  and malate dehydrogenase, could effectively function as a futile cycle converting  NADH from cytosol at the expense of one ATP to mitochondrial NADPH, producing a transhydrogenase  effect.	transcription
52334	2	334954	5	NULL	NULL	0	NULL	statement 1	NULL		produce	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_yeast_21_9_769_s_295	15282800	The mitochondrial malic enzyme, in conjunction with the cytosolic  enzymes pyruvate carboxylase, which carboxylates pyruvate producing oxaloacetate  and malate dehydrogenase, could effectively function as a futile cycle converting  NADH from cytosol at the expense of one ATP to mitochondrial NADPH, producing a transhydrogenase  effect.	transcription
52335	3	334954	5	NULL	NULL	0	NULL	malic enzyme	NULL	mitochondrial	acts in conjunction with	NULL				pyruvate carboxylase	NULL	cytosolic			NULL		0	NULL	NULL	NULL	gw70_yeast_21_9_769_s_295	15282800	The mitochondrial malic enzyme, in conjunction with the cytosolic  enzymes pyruvate carboxylase, which carboxylates pyruvate producing oxaloacetate  and malate dehydrogenase, could effectively function as a futile cycle converting  NADH from cytosol at the expense of one ATP to mitochondrial NADPH, producing a transhydrogenase  effect.	transcription
52336	4	334954	5	NULL	NULL	0	NULL	malic enzyme	NULL	mitochondrial	acts in conjunction with	NULL				malate dehydrogenase	NULL	cytosolic			NULL		0	NULL	NULL	NULL	gw70_yeast_21_9_769_s_295	15282800	The mitochondrial malic enzyme, in conjunction with the cytosolic  enzymes pyruvate carboxylase, which carboxylates pyruvate producing oxaloacetate  and malate dehydrogenase, could effectively function as a futile cycle converting  NADH from cytosol at the expense of one ATP to mitochondrial NADPH, producing a transhydrogenase  effect.	transcription
52337	5	334954	5	NULL	NULL	0	NULL	statement 3	NULL		occurs along with	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_yeast_21_9_769_s_295	15282800	The mitochondrial malic enzyme, in conjunction with the cytosolic  enzymes pyruvate carboxylase, which carboxylates pyruvate producing oxaloacetate  and malate dehydrogenase, could effectively function as a futile cycle converting  NADH from cytosol at the expense of one ATP to mitochondrial NADPH, producing a transhydrogenase  effect.	transcription
52338	6	334954	5	NULL	NULL	0	NULL	statement 5	NULL		function as	NULL	effectively			futile cycle	NULL				NULL		0	NULL	NULL	NULL	gw70_yeast_21_9_769_s_295	15282800	The mitochondrial malic enzyme, in conjunction with the cytosolic  enzymes pyruvate carboxylase, which carboxylates pyruvate producing oxaloacetate  and malate dehydrogenase, could effectively function as a futile cycle converting  NADH from cytosol at the expense of one ATP to mitochondrial NADPH, producing a transhydrogenase  effect.	transcription
52339	7	334954	5	NULL	NULL	0	NULL	NADH	NULL	cytosolic	is converted to	NULL				NADPH	NULL	mitochondrial			NULL		0	NULL	NULL	NULL	gw70_yeast_21_9_769_s_295	15282800	The mitochondrial malic enzyme, in conjunction with the cytosolic  enzymes pyruvate carboxylase, which carboxylates pyruvate producing oxaloacetate  and malate dehydrogenase, could effectively function as a futile cycle converting  NADH from cytosol at the expense of one ATP to mitochondrial NADPH, producing a transhydrogenase  effect.	transcription
52340	8	334954	5	NULL	NULL	0	NULL	statement 6	NULL		leads to	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw70_yeast_21_9_769_s_295	15282800	The mitochondrial malic enzyme, in conjunction with the cytosolic  enzymes pyruvate carboxylase, which carboxylates pyruvate producing oxaloacetate  and malate dehydrogenase, could effectively function as a futile cycle converting  NADH from cytosol at the expense of one ATP to mitochondrial NADPH, producing a transhydrogenase  effect.	transcription
52341	9	334954	5	NULL	NULL	0	NULL	statement 7	NULL		requires	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_yeast_21_9_769_s_295	15282800	The mitochondrial malic enzyme, in conjunction with the cytosolic  enzymes pyruvate carboxylase, which carboxylates pyruvate producing oxaloacetate  and malate dehydrogenase, could effectively function as a futile cycle converting  NADH from cytosol at the expense of one ATP to mitochondrial NADPH, producing a transhydrogenase  effect.	transcription
52342	10	334954	5	NULL	NULL	0	NULL	statement 7	NULL		produce	NULL				transhydrogenase effect	NULL				NULL		0	NULL	NULL	NULL	gw70_yeast_21_9_769_s_295	15282800	The mitochondrial malic enzyme, in conjunction with the cytosolic  enzymes pyruvate carboxylase, which carboxylates pyruvate producing oxaloacetate  and malate dehydrogenase, could effectively function as a futile cycle converting  NADH from cytosol at the expense of one ATP to mitochondrial NADPH, producing a transhydrogenase  effect.	transcription
54426	1	334954	6	NULL	NULL	0	NULL	pyruvate			is carboxylated to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw70_yeast_21_9_769_s_295	15282800	The mitochondrial malic enzyme, in conjunction with the cytosolic  enzymes pyruvate carboxylase, which carboxylates pyruvate producing oxaloacetate  and malate dehydrogenase, could effectively function as a futile cycle converting  NADH from cytosol at the expense of one ATP to mitochondrial NADPH, producing a transhydrogenase  effect.	transcription
54427	2	334954	6	NULL	NULL	0	NULL	pyruvate			is carboxylated to					malate dehydrogenase					NULL		0	NULL	NULL	NULL	gw70_yeast_21_9_769_s_295	15282800	The mitochondrial malic enzyme, in conjunction with the cytosolic  enzymes pyruvate carboxylase, which carboxylates pyruvate producing oxaloacetate  and malate dehydrogenase, could effectively function as a futile cycle converting  NADH from cytosol at the expense of one ATP to mitochondrial NADPH, producing a transhydrogenase  effect.	transcription
54428	3	334954	6	NULL	NULL	0	NULL	statement 1			occurs simultaneously with					statement 2					NULL		0	NULL	NULL	NULL	gw70_yeast_21_9_769_s_295	15282800	The mitochondrial malic enzyme, in conjunction with the cytosolic  enzymes pyruvate carboxylase, which carboxylates pyruvate producing oxaloacetate  and malate dehydrogenase, could effectively function as a futile cycle converting  NADH from cytosol at the expense of one ATP to mitochondrial NADPH, producing a transhydrogenase  effect.	transcription
54442	4	334954	6	NULL	NULL	0	NULL	NADH		cytosol	is converted to					NADPH		mitochondria			NULL		0	NULL	NULL	NULL	gw70_yeast_21_9_769_s_295	15282800	The mitochondrial malic enzyme, in conjunction with the cytosolic  enzymes pyruvate carboxylase, which carboxylates pyruvate producing oxaloacetate  and malate dehydrogenase, could effectively function as a futile cycle converting  NADH from cytosol at the expense of one ATP to mitochondrial NADPH, producing a transhydrogenase  effect.	transcription
54443	5	334954	6	NULL	NULL	0	NULL	statement 4			produces					transhydrogenase effect					NULL		0	NULL	NULL	NULL	gw70_yeast_21_9_769_s_295	15282800	The mitochondrial malic enzyme, in conjunction with the cytosolic  enzymes pyruvate carboxylase, which carboxylates pyruvate producing oxaloacetate  and malate dehydrogenase, could effectively function as a futile cycle converting  NADH from cytosol at the expense of one ATP to mitochondrial NADPH, producing a transhydrogenase  effect.	transcription
52343	1	334955	5	NULL	NULL	0	NULL	PEP	NULL		is carboxylated to	NULL				oxaloacetate	NULL				NULL	R. eutropha	NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_212_2_159_s_6	12113928	In  R. eutropha three enzymes are known which mediate between the C3 and C4 compounds in the metabolism [  14 and   29]: (i) the PEP carboxykinase catalyzes the carboxylation of PEP to oxaloacetate and vice versa, (ii) the PEP synthetase catalyzes the phosphorylation of pyruvate to PEP, and (iii) the malic enzyme decarboxylates malate oxidatively to pyruvate.	transcription
52344	2	334955	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is carboxylated to	NULL				PEP	NULL				NULL	R. eutropha	NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_212_2_159_s_6	12113928	In  R. eutropha three enzymes are known which mediate between the C3 and C4 compounds in the metabolism [  14 and   29]: (i) the PEP carboxykinase catalyzes the carboxylation of PEP to oxaloacetate and vice versa, (ii) the PEP synthetase catalyzes the phosphorylation of pyruvate to PEP, and (iii) the malic enzyme decarboxylates malate oxidatively to pyruvate.	transcription
52345	3	334955	5	NULL	NULL	0	NULL	PEP carboxykinase	NULL		catalyzes	NULL				statement 1	NULL				NULL	R. eutropha	0	NULL	NULL	NULL	gw60_femsmicrobiollett_212_2_159_s_6	12113928	In  R. eutropha three enzymes are known which mediate between the C3 and C4 compounds in the metabolism [  14 and   29]: (i) the PEP carboxykinase catalyzes the carboxylation of PEP to oxaloacetate and vice versa, (ii) the PEP synthetase catalyzes the phosphorylation of pyruvate to PEP, and (iii) the malic enzyme decarboxylates malate oxidatively to pyruvate.	transcription
52346	4	334955	5	NULL	NULL	0	NULL	PEP carboxykinase	NULL		catalyzes	NULL				statement 2	NULL				NULL	R. eutropha	0	NULL	NULL	NULL	gw60_femsmicrobiollett_212_2_159_s_6	12113928	In  R. eutropha three enzymes are known which mediate between the C3 and C4 compounds in the metabolism [  14 and   29]: (i) the PEP carboxykinase catalyzes the carboxylation of PEP to oxaloacetate and vice versa, (ii) the PEP synthetase catalyzes the phosphorylation of pyruvate to PEP, and (iii) the malic enzyme decarboxylates malate oxidatively to pyruvate.	transcription
52347	5	334955	5	NULL	NULL	0	NULL	pyruvate	NULL		is phosphorylated to	NULL				PEP	NULL				NULL	R. eutropha	NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_212_2_159_s_6	12113928	In  R. eutropha three enzymes are known which mediate between the C3 and C4 compounds in the metabolism [  14 and   29]: (i) the PEP carboxykinase catalyzes the carboxylation of PEP to oxaloacetate and vice versa, (ii) the PEP synthetase catalyzes the phosphorylation of pyruvate to PEP, and (iii) the malic enzyme decarboxylates malate oxidatively to pyruvate.	transcription
52348	6	334955	5	NULL	NULL	0	NULL	PEP synthetase	NULL		catalyzes	NULL				statement 5	NULL				NULL	R. eutropha	0	NULL	NULL	NULL	gw60_femsmicrobiollett_212_2_159_s_6	12113928	In  R. eutropha three enzymes are known which mediate between the C3 and C4 compounds in the metabolism [  14 and   29]: (i) the PEP carboxykinase catalyzes the carboxylation of PEP to oxaloacetate and vice versa, (ii) the PEP synthetase catalyzes the phosphorylation of pyruvate to PEP, and (iii) the malic enzyme decarboxylates malate oxidatively to pyruvate.	transcription
52349	7	334955	5	NULL	NULL	0	NULL	malate	NULL		decarboxylated to	NULL	oxidatively			pyruvate	NULL				NULL	R. eutropha	0	NULL	NULL	NULL	gw60_femsmicrobiollett_212_2_159_s_6	12113928	In  R. eutropha three enzymes are known which mediate between the C3 and C4 compounds in the metabolism [  14 and   29]: (i) the PEP carboxykinase catalyzes the carboxylation of PEP to oxaloacetate and vice versa, (ii) the PEP synthetase catalyzes the phosphorylation of pyruvate to PEP, and (iii) the malic enzyme decarboxylates malate oxidatively to pyruvate.	transcription
52350	8	334955	5	NULL	NULL	0	NULL	malic enzyme	NULL		catalyzes	NULL				statement 7	NULL				NULL	R. eutropha	NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_212_2_159_s_6	12113928	In  R. eutropha three enzymes are known which mediate between the C3 and C4 compounds in the metabolism [  14 and   29]: (i) the PEP carboxykinase catalyzes the carboxylation of PEP to oxaloacetate and vice versa, (ii) the PEP synthetase catalyzes the phosphorylation of pyruvate to PEP, and (iii) the malic enzyme decarboxylates malate oxidatively to pyruvate.	transcription
54444	1	334955	6	NULL	NULL	0	NULL	PEP			is carboxylated to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_212_2_159_s_6	12113928	In  R. eutropha three enzymes are known which mediate between the C3 and C4 compounds in the metabolism [  14 and   29]: (i) the PEP carboxykinase catalyzes the carboxylation of PEP to oxaloacetate and vice versa, (ii) the PEP synthetase catalyzes the phosphorylation of pyruvate to PEP, and (iii) the malic enzyme decarboxylates malate oxidatively to pyruvate.	transcription
54445	2	334955	6	NULL	NULL	0	NULL	PEP carboxykinase			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_212_2_159_s_6	12113928	In  R. eutropha three enzymes are known which mediate between the C3 and C4 compounds in the metabolism [  14 and   29]: (i) the PEP carboxykinase catalyzes the carboxylation of PEP to oxaloacetate and vice versa, (ii) the PEP synthetase catalyzes the phosphorylation of pyruvate to PEP, and (iii) the malic enzyme decarboxylates malate oxidatively to pyruvate.	transcription
54446	3	334955	6	NULL	NULL	0	NULL	pyruvate			is phosphorylated to					PEP					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_212_2_159_s_6	12113928	In  R. eutropha three enzymes are known which mediate between the C3 and C4 compounds in the metabolism [  14 and   29]: (i) the PEP carboxykinase catalyzes the carboxylation of PEP to oxaloacetate and vice versa, (ii) the PEP synthetase catalyzes the phosphorylation of pyruvate to PEP, and (iii) the malic enzyme decarboxylates malate oxidatively to pyruvate.	transcription
54447	4	334955	6	NULL	NULL	0	NULL	PEP synthetase			catalyzes					statement 3					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_212_2_159_s_6	12113928	In  R. eutropha three enzymes are known which mediate between the C3 and C4 compounds in the metabolism [  14 and   29]: (i) the PEP carboxykinase catalyzes the carboxylation of PEP to oxaloacetate and vice versa, (ii) the PEP synthetase catalyzes the phosphorylation of pyruvate to PEP, and (iii) the malic enzyme decarboxylates malate oxidatively to pyruvate.	transcription
54448	5	334955	6	NULL	NULL	0	NULL	malate			decarboxylates		oxidatively			pyruvate					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_212_2_159_s_6	12113928	In  R. eutropha three enzymes are known which mediate between the C3 and C4 compounds in the metabolism [  14 and   29]: (i) the PEP carboxykinase catalyzes the carboxylation of PEP to oxaloacetate and vice versa, (ii) the PEP synthetase catalyzes the phosphorylation of pyruvate to PEP, and (iii) the malic enzyme decarboxylates malate oxidatively to pyruvate.	transcription
54449	6	334955	6	NULL	NULL	0	NULL	malic enzyme			catalyzes					statement 5					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_212_2_159_s_6	12113928	In  R. eutropha three enzymes are known which mediate between the C3 and C4 compounds in the metabolism [  14 and   29]: (i) the PEP carboxykinase catalyzes the carboxylation of PEP to oxaloacetate and vice versa, (ii) the PEP synthetase catalyzes the phosphorylation of pyruvate to PEP, and (iii) the malic enzyme decarboxylates malate oxidatively to pyruvate.	transcription
52372	1	334956	5	NULL	NULL	0	NULL	pyruvate	NULL	neuroprotective effects of;;addition of	is associated with	NULL				NAD+	NULL	normalization of;;cellular levels of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_9_3139_s_6	10777777	Favoring this indirect mechanism of GAPDH inhibition, the neuroprotective effects of pyruvate addition were associated with normalization of cellular levels of NAD+, DHAP, and FBP. Zn2+-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+ catabolism, niacinamide or benzamide.	transcription
52373	2	334956	5	NULL	NULL	0	NULL	pyruvate	NULL	neuroprotective effects of;;addition of	is associated with	NULL				DHAP	NULL	normalization of;;cellular levels of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_9_3139_s_6	10777777	Favoring this indirect mechanism of GAPDH inhibition, the neuroprotective effects of pyruvate addition were associated with normalization of cellular levels of NAD+, DHAP, and FBP. Zn2+-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+ catabolism, niacinamide or benzamide.	transcription
52374	3	334956	5	NULL	NULL	0	NULL	pyruvate	NULL	neuroprotective effects of;;addition of	is associated with	NULL				FBP	NULL	normalization of;;cellular levels of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_9_3139_s_6	10777777	Favoring this indirect mechanism of GAPDH inhibition, the neuroprotective effects of pyruvate addition were associated with normalization of cellular levels of NAD+, DHAP, and FBP. Zn2+-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+ catabolism, niacinamide or benzamide.	transcription
52375	4	334956	5	NULL	NULL	0	NULL	neuronal death	NULL		is induced by	NULL				Zn2+	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_20_9_3139_s_6	10777777	Favoring this indirect mechanism of GAPDH inhibition, the neuroprotective effects of pyruvate addition were associated with normalization of cellular levels of NAD+, DHAP, and FBP. Zn2+-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+ catabolism, niacinamide or benzamide.	transcription
52376	5	334956	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is a type of	NULL				energy substrate	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_9_3139_s_6	10777777	Favoring this indirect mechanism of GAPDH inhibition, the neuroprotective effects of pyruvate addition were associated with normalization of cellular levels of NAD+, DHAP, and FBP. Zn2+-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+ catabolism, niacinamide or benzamide.	transcription
52377	6	334956	5	NULL	NULL	0	NULL	oxaloacetate	NULL	addition of	attenuate	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_20_9_3139_s_6	10777777	Favoring this indirect mechanism of GAPDH inhibition, the neuroprotective effects of pyruvate addition were associated with normalization of cellular levels of NAD+, DHAP, and FBP. Zn2+-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+ catabolism, niacinamide or benzamide.	transcription
52378	7	334956	5	NULL	NULL	0	NULL	dichloroacetate	NULL		activates	NULL				pyruvate dehydrogenase	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_9_3139_s_6	10777777	Favoring this indirect mechanism of GAPDH inhibition, the neuroprotective effects of pyruvate addition were associated with normalization of cellular levels of NAD+, DHAP, and FBP. Zn2+-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+ catabolism, niacinamide or benzamide.	transcription
52379	8	334956	5	NULL	NULL	0	NULL	pyruvate dehydrogenase	NULL	addition of	attenuate	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_9_3139_s_6	10777777	Favoring this indirect mechanism of GAPDH inhibition, the neuroprotective effects of pyruvate addition were associated with normalization of cellular levels of NAD+, DHAP, and FBP. Zn2+-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+ catabolism, niacinamide or benzamide.	transcription
52380	9	334956	5	NULL	NULL	0	NULL	niacinamide	NULL		inhibit	NULL				NAD+	NULL	catabolism of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_9_3139_s_6	10777777	Favoring this indirect mechanism of GAPDH inhibition, the neuroprotective effects of pyruvate addition were associated with normalization of cellular levels of NAD+, DHAP, and FBP. Zn2+-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+ catabolism, niacinamide or benzamide.	transcription
52381	10	334956	5	NULL	NULL	0	NULL	benzamide	NULL		inhibit	NULL				NAD+	NULL	catabolism of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_9_3139_s_6	10777777	Favoring this indirect mechanism of GAPDH inhibition, the neuroprotective effects of pyruvate addition were associated with normalization of cellular levels of NAD+, DHAP, and FBP. Zn2+-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+ catabolism, niacinamide or benzamide.	transcription
52382	11	334956	5	NULL	NULL	0	NULL	niacinamide	NULL	addition of	attenuate	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_9_3139_s_6	10777777	Favoring this indirect mechanism of GAPDH inhibition, the neuroprotective effects of pyruvate addition were associated with normalization of cellular levels of NAD+, DHAP, and FBP. Zn2+-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+ catabolism, niacinamide or benzamide.	transcription
52383	12	334956	5	NULL	NULL	0	NULL	benzamide	NULL	addition of	attenuate	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_9_3139_s_6	10777777	Favoring this indirect mechanism of GAPDH inhibition, the neuroprotective effects of pyruvate addition were associated with normalization of cellular levels of NAD+, DHAP, and FBP. Zn2+-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+ catabolism, niacinamide or benzamide.	transcription
55279	1	334956	6	NULL	NULL	0	NULL	Zn2+			induces					neuronal death					NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_9_3139_s_6	10777777	Favoring this indirect mechanism of GAPDH inhibition, the neuroprotective effects of pyruvate addition were associated with normalization of cellular levels of NAD+, DHAP, and FBP. Zn2+-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+ catabolism, niacinamide or benzamide.	transcription
55280	2	334956	6	NULL	NULL	0	NULL	oxaloacetate			attenuates					statement 1					NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_9_3139_s_6	10777777	Favoring this indirect mechanism of GAPDH inhibition, the neuroprotective effects of pyruvate addition were associated with normalization of cellular levels of NAD+, DHAP, and FBP. Zn2+-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+ catabolism, niacinamide or benzamide.	transcription
55281	3	334956	6	NULL	NULL	0	NULL	pyruvate		addition of	effects					neuroprotection					NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_9_3139_s_6	10777777	Favoring this indirect mechanism of GAPDH inhibition, the neuroprotective effects of pyruvate addition were associated with normalization of cellular levels of NAD+, DHAP, and FBP. Zn2+-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+ catabolism, niacinamide or benzamide.	transcription
55282	4	334956	6	NULL	NULL	0	NULL	statement 3			is associated with					NAD+		normalization of 			NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_9_3139_s_6	10777777	Favoring this indirect mechanism of GAPDH inhibition, the neuroprotective effects of pyruvate addition were associated with normalization of cellular levels of NAD+, DHAP, and FBP. Zn2+-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+ catabolism, niacinamide or benzamide.	transcription
55283	5	334956	6	NULL	NULL	0	NULL	statement 3			is associated with					DHAP		normalization of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_9_3139_s_6	10777777	Favoring this indirect mechanism of GAPDH inhibition, the neuroprotective effects of pyruvate addition were associated with normalization of cellular levels of NAD+, DHAP, and FBP. Zn2+-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+ catabolism, niacinamide or benzamide.	transcription
55284	6	334956	6	NULL	NULL	0	NULL	statement 3			is associated with					FBP		normalization of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_9_3139_s_6	10777777	Favoring this indirect mechanism of GAPDH inhibition, the neuroprotective effects of pyruvate addition were associated with normalization of cellular levels of NAD+, DHAP, and FBP. Zn2+-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+ catabolism, niacinamide or benzamide.	transcription
52351	1	334957	5	NULL	NULL	0	NULL	PEP	NULL		is synthesized from	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52352	2	334957	5	NULL	NULL	0	NULL	PckA	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52353	3	334957	5	NULL	NULL	0	NULL	statement 1	NULL		refers to	NULL				PckA route	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52354	4	334957	5	NULL	NULL	0	NULL	malate	NULL		is converted to	NULL				pyruvate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52355	5	334957	5	NULL	NULL	0	NULL	MaeA	NULL		catalyzes	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52356	6	334957	5	NULL	NULL	0	NULL	MaeB	NULL		catalyzes	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52357	7	334957	5	NULL	NULL	0	NULL	statement 5	NULL		is an alternative to	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52358	8	334957	5	NULL	NULL	0	NULL	MaeA	NULL		is a type of	NULL				malic enzyme	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52359	9	334957	5	NULL	NULL	0	NULL	MaeB	NULL		is a type of	NULL				malic enzyme	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52360	10	334957	5	NULL	NULL	0	NULL	PEP	NULL		is synthesized from	NULL				pyruvate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52361	11	334957	5	NULL	NULL	0	NULL	PpsA	NULL		catalyzes	NULL				statement 10	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52362	12	334957	5	NULL	NULL	0	NULL	pyruvate	NULL		is a substrate for	NULL				PpsA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52363	13	334957	5	NULL	NULL	0	NULL	H2O	NULL		is a substrate for	NULL				PpsA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52364	14	334957	5	NULL	NULL	0	NULL	ATP	NULL		is a substrate for	NULL				PpsA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52365	15	334957	5	NULL	NULL	0	NULL	PPDK	NULL		catalyzes	NULL				statement 10	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52366	16	334957	5	NULL	NULL	0	NULL	pyruvate	NULL		is a substrate for	NULL				PPDK	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52367	17	334957	5	NULL	NULL	0	NULL	phosphate	NULL		is a substrate for	NULL				PPDK	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52368	18	334957	5	NULL	NULL	0	NULL	ATP	NULL		is a substrate for	NULL				PPDK	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52369	19	334957	5	NULL	NULL	0	NULL	statement 11	NULL		is an alternative to	NULL				statement 15	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52370	20	334957	5	NULL	NULL	0	NULL	statement 7	NULL		occurs simultaneously with	NULL				statement 19	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52371	21	334957	5	NULL	NULL	0	NULL	statement 20	NULL		refers to	NULL				malic enzyme-PpsA (or PPDK) route	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
55286	1	334957	6	NULL	NULL	0	NULL	oxaloacetate			synthesizes					PEP					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
55287	2	334957	6	NULL	NULL	0	NULL	PckA			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
55288	3	334957	6	NULL	NULL	0	NULL	malate			is converted to					pyruvate					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
55289	4	334957	6	NULL	NULL	0	NULL	MaeA			catalyzes					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
55290	5	334957	6	NULL	NULL	0	NULL	MaeB			catalyzes					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
55291	6	334957	6	NULL	NULL	0	NULL	pyruvate			synthesizes					PEP					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
55292	7	334957	6	NULL	NULL	0	NULL	PpsA			catalyzes					statement 6					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
55293	8	334957	6	NULL	NULL	0	NULL	PPDK			catalyzes					statement 6					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_17_6231_s_8	16109965	The PckA route is a one-step reaction in which PEP is synthesized from oxaloacetate catalyzed by PckA, and the malic enzyme-PpsA (or PPDK) route consists of two reactions: the first reaction is the conversion of malate to pyruvate catalyzed by the malic enzyme MaeA or MaeB and the second reaction is the synthesis of PEP from pyruvate catalyzed by PpsA using pyruvate, H2O, and ATP as substrates or by PPDK using pyruvate, phosphate, and ATP as substrates ( ,  ).	transcription
52384	1	334958	5	NULL	NULL	0	NULL	pyruvate	NULL	carboxylation of	is necessary for	NULL				oxygen	NULL	maximal consumption of			NULL	hamster brown adipose tissue	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_29_27466_s_29	15917242	Pyruvate carboxylation was shown to be necessary in hamster brown adipose tissue for maximal oxygen consumption in norepinephrine-stimulated respiration, even when drainage of the citric acid cycle for amino acid synthesis is eliminated, suggesting that the provision of oxaloacetate promotes the oxidation of acetyl-CoA from fatty acid degradation ( ,  ).	transcription
52385	2	334958	5	NULL	NULL	0	NULL	statement 1	NULL		occurs in	NULL				respiration	NULL	norepinephrine-stimulated			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27466_s_29	15917242	Pyruvate carboxylation was shown to be necessary in hamster brown adipose tissue for maximal oxygen consumption in norepinephrine-stimulated respiration, even when drainage of the citric acid cycle for amino acid synthesis is eliminated, suggesting that the provision of oxaloacetate promotes the oxidation of acetyl-CoA from fatty acid degradation ( ,  ).	transcription
52386	3	334958	5	NULL	NULL	0	NULL	acetyl-CoA	NULL	oxidation of	is promoted from	NULL				fatty acid	NULL	degradation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27466_s_29	15917242	Pyruvate carboxylation was shown to be necessary in hamster brown adipose tissue for maximal oxygen consumption in norepinephrine-stimulated respiration, even when drainage of the citric acid cycle for amino acid synthesis is eliminated, suggesting that the provision of oxaloacetate promotes the oxidation of acetyl-CoA from fatty acid degradation ( ,  ).	transcription
52387	4	334958	5	NULL	NULL	0	NULL	oxaloacetate	NULL		performs	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27466_s_29	15917242	Pyruvate carboxylation was shown to be necessary in hamster brown adipose tissue for maximal oxygen consumption in norepinephrine-stimulated respiration, even when drainage of the citric acid cycle for amino acid synthesis is eliminated, suggesting that the provision of oxaloacetate promotes the oxidation of acetyl-CoA from fatty acid degradation ( ,  ).	transcription
55302	1	334958	6	NULL	NULL	0	NULL	pyruvate		carboxylation of 	is necessary in					brown adipose tissue		hamster			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27466_s_29	15917242	Pyruvate carboxylation was shown to be necessary in hamster brown adipose tissue for maximal oxygen consumption in norepinephrine-stimulated respiration, even when drainage of the citric acid cycle for amino acid synthesis is eliminated, suggesting that the provision of oxaloacetate promotes the oxidation of acetyl-CoA from fatty acid degradation ( ,  ).	transcription
55303	2	334958	6	NULL	NULL	0	NULL	norepinephrine			stimulates					respiration					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27466_s_29	15917242	Pyruvate carboxylation was shown to be necessary in hamster brown adipose tissue for maximal oxygen consumption in norepinephrine-stimulated respiration, even when drainage of the citric acid cycle for amino acid synthesis is eliminated, suggesting that the provision of oxaloacetate promotes the oxidation of acetyl-CoA from fatty acid degradation ( ,  ).	transcription
55306	3	334958	6	NULL	NULL	0	NULL	statement 1			is required for					oxygen		consumption of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27466_s_29	15917242	Pyruvate carboxylation was shown to be necessary in hamster brown adipose tissue for maximal oxygen consumption in norepinephrine-stimulated respiration, even when drainage of the citric acid cycle for amino acid synthesis is eliminated, suggesting that the provision of oxaloacetate promotes the oxidation of acetyl-CoA from fatty acid degradation ( ,  ).	transcription
55309	4	334958	6	NULL	NULL	0	NULL	oxaloacetate			promotes					acetyl-CoA		oxidation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27466_s_29	15917242	Pyruvate carboxylation was shown to be necessary in hamster brown adipose tissue for maximal oxygen consumption in norepinephrine-stimulated respiration, even when drainage of the citric acid cycle for amino acid synthesis is eliminated, suggesting that the provision of oxaloacetate promotes the oxidation of acetyl-CoA from fatty acid degradation ( ,  ).	transcription
55311	5	334958	6	NULL	NULL	0	NULL	statement 4			occurs during					fatty acid		degradation of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_27466_s_29	15917242	Pyruvate carboxylation was shown to be necessary in hamster brown adipose tissue for maximal oxygen consumption in norepinephrine-stimulated respiration, even when drainage of the citric acid cycle for amino acid synthesis is eliminated, suggesting that the provision of oxaloacetate promotes the oxidation of acetyl-CoA from fatty acid degradation ( ,  ).	transcription
52388	1	334959	5	NULL	NULL	0	NULL	mitochondria	NULL		respires on	NULL				pyruvate & malate	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_23_12_4858_s_122	12832508	These measurements were similar  between the two tissue types whether the mitochondria were respiring on the  complex I substrates, pyruvate plus malate, or the complex II substrate,  succinate (plus glutamate to remove oxaloacetate, an inhibitor of succinate  dehydrogenase, by transamination)  (Lehninger et al., 1993 ).	transcription
52389	2	334959	5	NULL	NULL	0	NULL	pyruvate & malate	NULL		is a type of	NULL				complex I substrate	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_23_12_4858_s_122	12832508	These measurements were similar  between the two tissue types whether the mitochondria were respiring on the  complex I substrates, pyruvate plus malate, or the complex II substrate,  succinate (plus glutamate to remove oxaloacetate, an inhibitor of succinate  dehydrogenase, by transamination)  (Lehninger et al., 1993 ).	transcription
52390	3	334959	5	NULL	NULL	0	NULL	mitochondria	NULL		respires on	NULL				succinate & glutamate	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_23_12_4858_s_122	12832508	These measurements were similar  between the two tissue types whether the mitochondria were respiring on the  complex I substrates, pyruvate plus malate, or the complex II substrate,  succinate (plus glutamate to remove oxaloacetate, an inhibitor of succinate  dehydrogenase, by transamination)  (Lehninger et al., 1993 ).	transcription
52391	4	334959	5	NULL	NULL	0	NULL	succinate	NULL		is a type of	NULL				complex II substrate	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_23_12_4858_s_122	12832508	These measurements were similar  between the two tissue types whether the mitochondria were respiring on the  complex I substrates, pyruvate plus malate, or the complex II substrate,  succinate (plus glutamate to remove oxaloacetate, an inhibitor of succinate  dehydrogenase, by transamination)  (Lehninger et al., 1993 ).	transcription
52392	5	334959	5	NULL	NULL	0	NULL	statement 3	NULL		removes	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_23_12_4858_s_122	12832508	These measurements were similar  between the two tissue types whether the mitochondria were respiring on the  complex I substrates, pyruvate plus malate, or the complex II substrate,  succinate (plus glutamate to remove oxaloacetate, an inhibitor of succinate  dehydrogenase, by transamination)  (Lehninger et al., 1993 ).	transcription
52393	6	334959	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is an inhibitor of	NULL				succinate dehydrogenase	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_23_12_4858_s_122	12832508	These measurements were similar  between the two tissue types whether the mitochondria were respiring on the  complex I substrates, pyruvate plus malate, or the complex II substrate,  succinate (plus glutamate to remove oxaloacetate, an inhibitor of succinate  dehydrogenase, by transamination)  (Lehninger et al., 1993 ).	transcription
52394	7	334959	5	NULL	NULL	0	NULL	transamination	NULL		causes	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_23_12_4858_s_122	12832508	These measurements were similar  between the two tissue types whether the mitochondria were respiring on the  complex I substrates, pyruvate plus malate, or the complex II substrate,  succinate (plus glutamate to remove oxaloacetate, an inhibitor of succinate  dehydrogenase, by transamination)  (Lehninger et al., 1993 ).	transcription
52395	1	334960	5	NULL	NULL	0	NULL	E. coli	NULL		does not possess	NULL				pyruvate carboxylase	NULL				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_24_6892_s_273	11092847	Since  E. coli does not possess a pyruvate carboxylase and assuming, as seems to be the case in  C. glutamicum, that MQO catalyzes malate oxidation while MDH reduces oxaloacetate, the absence of a phenotype for the  mqo deletion mutant in  E. coli might be due to a PEP shunt taking over its function (Fig.  4).	transcription
52396	2	334960	5	NULL	NULL	0	NULL	MQO	NULL		catalyzes	NULL				malate	NULL	oxidation of			NULL	C. glutamicum	0	NULL	NULL	NULL	gw60_jbacteriol_182_24_6892_s_273	11092847	Since  E. coli does not possess a pyruvate carboxylase and assuming, as seems to be the case in  C. glutamicum, that MQO catalyzes malate oxidation while MDH reduces oxaloacetate, the absence of a phenotype for the  mqo deletion mutant in  E. coli might be due to a PEP shunt taking over its function (Fig.  4).	transcription
52397	3	334960	5	NULL	NULL	0	NULL	MDH	NULL		reduces	NULL				oxaloacetate	NULL				NULL	C. glutamicum	0	NULL	NULL	NULL	gw60_jbacteriol_182_24_6892_s_273	11092847	Since  E. coli does not possess a pyruvate carboxylase and assuming, as seems to be the case in  C. glutamicum, that MQO catalyzes malate oxidation while MDH reduces oxaloacetate, the absence of a phenotype for the  mqo deletion mutant in  E. coli might be due to a PEP shunt taking over its function (Fig.  4).	transcription
55320	1	334960	6	NULL	NULL	0	NULL	MQO			catalyzes					malate		oxidation of			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_24_6892_s_273	11092847	Since  E. coli does not possess a pyruvate carboxylase and assuming, as seems to be the case in  C. glutamicum, that MQO catalyzes malate oxidation while MDH reduces oxaloacetate, the absence of a phenotype for the  mqo deletion mutant in  E. coli might be due to a PEP shunt taking over its function (Fig.  4).	transcription
55322	2	334960	6	NULL	NULL	0	NULL	MDH			reduces					oxaloacetate					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_182_24_6892_s_273	11092847	Since  E. coli does not possess a pyruvate carboxylase and assuming, as seems to be the case in  C. glutamicum, that MQO catalyzes malate oxidation while MDH reduces oxaloacetate, the absence of a phenotype for the  mqo deletion mutant in  E. coli might be due to a PEP shunt taking over its function (Fig.  4).	transcription
52398	1	334961	5	NULL	NULL	0	NULL	ADP1	NULL	Acinetobacter sp. strain 	lacks	NULL				pyruvate kinase	NULL	gene encoding			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_2_1410_s_162	16461694	Since CGP biosynthesis in cells of  Acinetobacter sp. strain ADP1 using sugars or other carbohydrates as substrates gave only low amounts of CGP and since it was recently reported that  Acinetobacter sp. strain ADP1 is lacking a gene encoding pyruvate kinase, which is involved in the conversion of carbohydrates to pyruvate ( ), the phosphoenolpyruvate carboxylase encoded by  pepC catalyzing the conversion of phosphoenolpyruvate to oxaloacetate as one of the anaplerotic reactions was also overexpressed to augment the utilization of carbohydrates and to ultimately increase the metabolic flux towards 2-oxoglutarate, which is the substrate for glutamate and subsequently arginine biosynthesis.	transcription
52399	2	334961	5	NULL	NULL	0	NULL	carbohydrates	NULL		is converted to	NULL				pyruvate	NULL				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_2_1410_s_162	16461694	Since CGP biosynthesis in cells of  Acinetobacter sp. strain ADP1 using sugars or other carbohydrates as substrates gave only low amounts of CGP and since it was recently reported that  Acinetobacter sp. strain ADP1 is lacking a gene encoding pyruvate kinase, which is involved in the conversion of carbohydrates to pyruvate ( ), the phosphoenolpyruvate carboxylase encoded by  pepC catalyzing the conversion of phosphoenolpyruvate to oxaloacetate as one of the anaplerotic reactions was also overexpressed to augment the utilization of carbohydrates and to ultimately increase the metabolic flux towards 2-oxoglutarate, which is the substrate for glutamate and subsequently arginine biosynthesis.	transcription
52400	3	334961	5	NULL	NULL	0	NULL	pyruvate kinase	NULL		is involved in	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_2_1410_s_162	16461694	Since CGP biosynthesis in cells of  Acinetobacter sp. strain ADP1 using sugars or other carbohydrates as substrates gave only low amounts of CGP and since it was recently reported that  Acinetobacter sp. strain ADP1 is lacking a gene encoding pyruvate kinase, which is involved in the conversion of carbohydrates to pyruvate ( ), the phosphoenolpyruvate carboxylase encoded by  pepC catalyzing the conversion of phosphoenolpyruvate to oxaloacetate as one of the anaplerotic reactions was also overexpressed to augment the utilization of carbohydrates and to ultimately increase the metabolic flux towards 2-oxoglutarate, which is the substrate for glutamate and subsequently arginine biosynthesis.	transcription
52401	4	334961	5	NULL	NULL	0	NULL	phosphoenolpyruvate carboxylase	NULL		is encoded by	NULL				pepC	NULL				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_2_1410_s_162	16461694	Since CGP biosynthesis in cells of  Acinetobacter sp. strain ADP1 using sugars or other carbohydrates as substrates gave only low amounts of CGP and since it was recently reported that  Acinetobacter sp. strain ADP1 is lacking a gene encoding pyruvate kinase, which is involved in the conversion of carbohydrates to pyruvate ( ), the phosphoenolpyruvate carboxylase encoded by  pepC catalyzing the conversion of phosphoenolpyruvate to oxaloacetate as one of the anaplerotic reactions was also overexpressed to augment the utilization of carbohydrates and to ultimately increase the metabolic flux towards 2-oxoglutarate, which is the substrate for glutamate and subsequently arginine biosynthesis.	transcription
52402	5	334961	5	NULL	NULL	0	NULL	phosphoenolpyruvate	NULL		is converted to	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_2_1410_s_162	16461694	Since CGP biosynthesis in cells of  Acinetobacter sp. strain ADP1 using sugars or other carbohydrates as substrates gave only low amounts of CGP and since it was recently reported that  Acinetobacter sp. strain ADP1 is lacking a gene encoding pyruvate kinase, which is involved in the conversion of carbohydrates to pyruvate ( ), the phosphoenolpyruvate carboxylase encoded by  pepC catalyzing the conversion of phosphoenolpyruvate to oxaloacetate as one of the anaplerotic reactions was also overexpressed to augment the utilization of carbohydrates and to ultimately increase the metabolic flux towards 2-oxoglutarate, which is the substrate for glutamate and subsequently arginine biosynthesis.	transcription
52403	6	334961	5	NULL	NULL	0	NULL	pepC	NULL		catalyzes	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_2_1410_s_162	16461694	Since CGP biosynthesis in cells of  Acinetobacter sp. strain ADP1 using sugars or other carbohydrates as substrates gave only low amounts of CGP and since it was recently reported that  Acinetobacter sp. strain ADP1 is lacking a gene encoding pyruvate kinase, which is involved in the conversion of carbohydrates to pyruvate ( ), the phosphoenolpyruvate carboxylase encoded by  pepC catalyzing the conversion of phosphoenolpyruvate to oxaloacetate as one of the anaplerotic reactions was also overexpressed to augment the utilization of carbohydrates and to ultimately increase the metabolic flux towards 2-oxoglutarate, which is the substrate for glutamate and subsequently arginine biosynthesis.	transcription
52404	7	334961	5	NULL	NULL	0	NULL	statement 6	NULL		is a type of	NULL				anaplerotic reactions	NULL				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_2_1410_s_162	16461694	Since CGP biosynthesis in cells of  Acinetobacter sp. strain ADP1 using sugars or other carbohydrates as substrates gave only low amounts of CGP and since it was recently reported that  Acinetobacter sp. strain ADP1 is lacking a gene encoding pyruvate kinase, which is involved in the conversion of carbohydrates to pyruvate ( ), the phosphoenolpyruvate carboxylase encoded by  pepC catalyzing the conversion of phosphoenolpyruvate to oxaloacetate as one of the anaplerotic reactions was also overexpressed to augment the utilization of carbohydrates and to ultimately increase the metabolic flux towards 2-oxoglutarate, which is the substrate for glutamate and subsequently arginine biosynthesis.	transcription
52405	8	334961	5	NULL	NULL	0	NULL	2-oxoglutarate	NULL		is a substrate for	NULL				glutamate	NULL				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_2_1410_s_162	16461694	Since CGP biosynthesis in cells of  Acinetobacter sp. strain ADP1 using sugars or other carbohydrates as substrates gave only low amounts of CGP and since it was recently reported that  Acinetobacter sp. strain ADP1 is lacking a gene encoding pyruvate kinase, which is involved in the conversion of carbohydrates to pyruvate ( ), the phosphoenolpyruvate carboxylase encoded by  pepC catalyzing the conversion of phosphoenolpyruvate to oxaloacetate as one of the anaplerotic reactions was also overexpressed to augment the utilization of carbohydrates and to ultimately increase the metabolic flux towards 2-oxoglutarate, which is the substrate for glutamate and subsequently arginine biosynthesis.	transcription
52406	9	334961	5	NULL	NULL	0	NULL	2-oxoglutarate	NULL		is required for	NULL				arginine	NULL	biosynthesis of			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_2_1410_s_162	16461694	Since CGP biosynthesis in cells of  Acinetobacter sp. strain ADP1 using sugars or other carbohydrates as substrates gave only low amounts of CGP and since it was recently reported that  Acinetobacter sp. strain ADP1 is lacking a gene encoding pyruvate kinase, which is involved in the conversion of carbohydrates to pyruvate ( ), the phosphoenolpyruvate carboxylase encoded by  pepC catalyzing the conversion of phosphoenolpyruvate to oxaloacetate as one of the anaplerotic reactions was also overexpressed to augment the utilization of carbohydrates and to ultimately increase the metabolic flux towards 2-oxoglutarate, which is the substrate for glutamate and subsequently arginine biosynthesis.	transcription
55620	1	334961	6	NULL	NULL	0	NULL	Acinetobacter sp. strain ADP1			lacks					pyruvate kinase gene					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_2_1410_s_162	16461694	Since CGP biosynthesis in cells of  Acinetobacter sp. strain ADP1 using sugars or other carbohydrates as substrates gave only low amounts of CGP and since it was recently reported that  Acinetobacter sp. strain ADP1 is lacking a gene encoding pyruvate kinase, which is involved in the conversion of carbohydrates to pyruvate ( ), the phosphoenolpyruvate carboxylase encoded by  pepC catalyzing the conversion of phosphoenolpyruvate to oxaloacetate as one of the anaplerotic reactions was also overexpressed to augment the utilization of carbohydrates and to ultimately increase the metabolic flux towards 2-oxoglutarate, which is the substrate for glutamate and subsequently arginine biosynthesis.	transcription
55621	2	334961	6	NULL	NULL	0	NULL	carbohydrate			is converted to					pyruvate					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_2_1410_s_162	16461694	Since CGP biosynthesis in cells of  Acinetobacter sp. strain ADP1 using sugars or other carbohydrates as substrates gave only low amounts of CGP and since it was recently reported that  Acinetobacter sp. strain ADP1 is lacking a gene encoding pyruvate kinase, which is involved in the conversion of carbohydrates to pyruvate ( ), the phosphoenolpyruvate carboxylase encoded by  pepC catalyzing the conversion of phosphoenolpyruvate to oxaloacetate as one of the anaplerotic reactions was also overexpressed to augment the utilization of carbohydrates and to ultimately increase the metabolic flux towards 2-oxoglutarate, which is the substrate for glutamate and subsequently arginine biosynthesis.	transcription
55622	3	334961	6	NULL	NULL	0	NULL	pyruvate kinase			is involved in					statement 2					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_2_1410_s_162	16461694	Since CGP biosynthesis in cells of  Acinetobacter sp. strain ADP1 using sugars or other carbohydrates as substrates gave only low amounts of CGP and since it was recently reported that  Acinetobacter sp. strain ADP1 is lacking a gene encoding pyruvate kinase, which is involved in the conversion of carbohydrates to pyruvate ( ), the phosphoenolpyruvate carboxylase encoded by  pepC catalyzing the conversion of phosphoenolpyruvate to oxaloacetate as one of the anaplerotic reactions was also overexpressed to augment the utilization of carbohydrates and to ultimately increase the metabolic flux towards 2-oxoglutarate, which is the substrate for glutamate and subsequently arginine biosynthesis.	transcription
55623	4	334961	6	NULL	NULL	0	NULL	pepC			encodes for					phosphoenolpyruvate carboxylase					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_2_1410_s_162	16461694	Since CGP biosynthesis in cells of  Acinetobacter sp. strain ADP1 using sugars or other carbohydrates as substrates gave only low amounts of CGP and since it was recently reported that  Acinetobacter sp. strain ADP1 is lacking a gene encoding pyruvate kinase, which is involved in the conversion of carbohydrates to pyruvate ( ), the phosphoenolpyruvate carboxylase encoded by  pepC catalyzing the conversion of phosphoenolpyruvate to oxaloacetate as one of the anaplerotic reactions was also overexpressed to augment the utilization of carbohydrates and to ultimately increase the metabolic flux towards 2-oxoglutarate, which is the substrate for glutamate and subsequently arginine biosynthesis.	transcription
55624	5	334961	6	NULL	NULL	0	NULL	Phosphoenolpyruvate			is converted to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_2_1410_s_162	16461694	Since CGP biosynthesis in cells of  Acinetobacter sp. strain ADP1 using sugars or other carbohydrates as substrates gave only low amounts of CGP and since it was recently reported that  Acinetobacter sp. strain ADP1 is lacking a gene encoding pyruvate kinase, which is involved in the conversion of carbohydrates to pyruvate ( ), the phosphoenolpyruvate carboxylase encoded by  pepC catalyzing the conversion of phosphoenolpyruvate to oxaloacetate as one of the anaplerotic reactions was also overexpressed to augment the utilization of carbohydrates and to ultimately increase the metabolic flux towards 2-oxoglutarate, which is the substrate for glutamate and subsequently arginine biosynthesis.	transcription
55625	6	334961	6	NULL	NULL	0	NULL	pepC			catalyzes					statement 5					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_2_1410_s_162	16461694	Since CGP biosynthesis in cells of  Acinetobacter sp. strain ADP1 using sugars or other carbohydrates as substrates gave only low amounts of CGP and since it was recently reported that  Acinetobacter sp. strain ADP1 is lacking a gene encoding pyruvate kinase, which is involved in the conversion of carbohydrates to pyruvate ( ), the phosphoenolpyruvate carboxylase encoded by  pepC catalyzing the conversion of phosphoenolpyruvate to oxaloacetate as one of the anaplerotic reactions was also overexpressed to augment the utilization of carbohydrates and to ultimately increase the metabolic flux towards 2-oxoglutarate, which is the substrate for glutamate and subsequently arginine biosynthesis.	transcription
52407	1	334962	5	NULL	NULL	0	NULL	alanine	NULL		connected to	NULL	directly			pyruvate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_46_47881_s_180	15361523	Indeed, alanine is directly connected with pyruvate through aminotransferase activity, whereas the metabolic pathways leading to the other amino acids involve multisteps (the carbon in the pyruvate C3 position gives the C2 of acetyl-CoA, which becomes the C4 of 2-oxoglutarate and, further, the C3 or C2 of oxaloacetate in the first tricarboxylic acid cycle turn; from these intermediates, the carbon may be recovered either at glutamate C4, glutamine C4, GABA C2, or aspartate C2 or C3).	transcription
52408	2	334962	5	NULL	NULL	0	NULL	statement 1	NULL		occurs through	NULL				aminotransferase	NULL	activity of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_46_47881_s_180	15361523	Indeed, alanine is directly connected with pyruvate through aminotransferase activity, whereas the metabolic pathways leading to the other amino acids involve multisteps (the carbon in the pyruvate C3 position gives the C2 of acetyl-CoA, which becomes the C4 of 2-oxoglutarate and, further, the C3 or C2 of oxaloacetate in the first tricarboxylic acid cycle turn; from these intermediates, the carbon may be recovered either at glutamate C4, glutamine C4, GABA C2, or aspartate C2 or C3).	transcription
55325	1	334962	6	NULL	NULL	0	NULL	alanine			is connected to					pyruvate					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_46_47881_s_180	15361523	Indeed, alanine is directly connected with pyruvate through aminotransferase activity, whereas the metabolic pathways leading to the other amino acids involve multisteps (the carbon in the pyruvate C3 position gives the C2 of acetyl-CoA, which becomes the C4 of 2-oxoglutarate and, further, the C3 or C2 of oxaloacetate in the first tricarboxylic acid cycle turn; from these intermediates, the carbon may be recovered either at glutamate C4, glutamine C4, GABA C2, or aspartate C2 or C3).	transcription
55326	2	334962	6	NULL	NULL	0	NULL	statement 1			occurs through					aminotransferase activity					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_46_47881_s_180	15361523	Indeed, alanine is directly connected with pyruvate through aminotransferase activity, whereas the metabolic pathways leading to the other amino acids involve multisteps (the carbon in the pyruvate C3 position gives the C2 of acetyl-CoA, which becomes the C4 of 2-oxoglutarate and, further, the C3 or C2 of oxaloacetate in the first tricarboxylic acid cycle turn; from these intermediates, the carbon may be recovered either at glutamate C4, glutamine C4, GABA C2, or aspartate C2 or C3).	transcription
52420	1	334963	5	NULL	NULL	0	NULL	accA3	NULL		is a subunit of	NULL				acetyl CoA carboxylase	NULL				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_2_467_s_120	15626759	The two smaller species were identified as the biotin-containing subunit of acetyl CoA carboxylase (encoded by  accA3), which catalyzes the conversion of acetyl CoA to malonyl CoA, the first committed step in fatty acid biosynthesis, and pyruvate carboxylase (encoded by  pca), which catalyzes the conversion of pyruvate to oxaloacetate and serves an essential anaplerotic role during periods of metabolic shunting.	transcription
52421	2	334963	5	NULL	NULL	0	NULL	accA3	NULL		contains	NULL				biotin	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_2_467_s_120	15626759	The two smaller species were identified as the biotin-containing subunit of acetyl CoA carboxylase (encoded by  accA3), which catalyzes the conversion of acetyl CoA to malonyl CoA, the first committed step in fatty acid biosynthesis, and pyruvate carboxylase (encoded by  pca), which catalyzes the conversion of pyruvate to oxaloacetate and serves an essential anaplerotic role during periods of metabolic shunting.	transcription
52422	3	334963	5	NULL	NULL	0	NULL	acetyl CoA	NULL		is converted to	NULL				malonyl CoA	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_2_467_s_120	15626759	The two smaller species were identified as the biotin-containing subunit of acetyl CoA carboxylase (encoded by  accA3), which catalyzes the conversion of acetyl CoA to malonyl CoA, the first committed step in fatty acid biosynthesis, and pyruvate carboxylase (encoded by  pca), which catalyzes the conversion of pyruvate to oxaloacetate and serves an essential anaplerotic role during periods of metabolic shunting.	transcription
52423	4	334963	5	NULL	NULL	0	NULL	acetyl CoA carboxylase	NULL		catalyzes	NULL		accA3		statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_2_467_s_120	15626759	The two smaller species were identified as the biotin-containing subunit of acetyl CoA carboxylase (encoded by  accA3), which catalyzes the conversion of acetyl CoA to malonyl CoA, the first committed step in fatty acid biosynthesis, and pyruvate carboxylase (encoded by  pca), which catalyzes the conversion of pyruvate to oxaloacetate and serves an essential anaplerotic role during periods of metabolic shunting.	transcription
52424	5	334963	5	NULL	NULL	0	NULL	pyruvate carboxylase	NULL		is encoded by	NULL				pca	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_2_467_s_120	15626759	The two smaller species were identified as the biotin-containing subunit of acetyl CoA carboxylase (encoded by  accA3), which catalyzes the conversion of acetyl CoA to malonyl CoA, the first committed step in fatty acid biosynthesis, and pyruvate carboxylase (encoded by  pca), which catalyzes the conversion of pyruvate to oxaloacetate and serves an essential anaplerotic role during periods of metabolic shunting.	transcription
52425	6	334963	5	NULL	NULL	0	NULL	pyruvate	NULL		is converted to	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_2_467_s_120	15626759	The two smaller species were identified as the biotin-containing subunit of acetyl CoA carboxylase (encoded by  accA3), which catalyzes the conversion of acetyl CoA to malonyl CoA, the first committed step in fatty acid biosynthesis, and pyruvate carboxylase (encoded by  pca), which catalyzes the conversion of pyruvate to oxaloacetate and serves an essential anaplerotic role during periods of metabolic shunting.	transcription
52426	7	334963	5	NULL	NULL	0	NULL	pca	NULL		catalyzes	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_pnas_102_2_467_s_120	15626759	The two smaller species were identified as the biotin-containing subunit of acetyl CoA carboxylase (encoded by  accA3), which catalyzes the conversion of acetyl CoA to malonyl CoA, the first committed step in fatty acid biosynthesis, and pyruvate carboxylase (encoded by  pca), which catalyzes the conversion of pyruvate to oxaloacetate and serves an essential anaplerotic role during periods of metabolic shunting.	transcription
52427	8	334963	5	NULL	NULL	0	NULL	pca	NULL		serves as	NULL				anaplerotic	NULL	essential			NULL		0	NULL	NULL	NULL	gw70_pnas_102_2_467_s_120	15626759	The two smaller species were identified as the biotin-containing subunit of acetyl CoA carboxylase (encoded by  accA3), which catalyzes the conversion of acetyl CoA to malonyl CoA, the first committed step in fatty acid biosynthesis, and pyruvate carboxylase (encoded by  pca), which catalyzes the conversion of pyruvate to oxaloacetate and serves an essential anaplerotic role during periods of metabolic shunting.	transcription
52428	9	334963	5	NULL	NULL	0	NULL	statement 8	NULL		occurs during	NULL				metabolic shunting	NULL	periods of 			NULL		0	NULL	NULL	NULL	gw70_pnas_102_2_467_s_120	15626759	The two smaller species were identified as the biotin-containing subunit of acetyl CoA carboxylase (encoded by  accA3), which catalyzes the conversion of acetyl CoA to malonyl CoA, the first committed step in fatty acid biosynthesis, and pyruvate carboxylase (encoded by  pca), which catalyzes the conversion of pyruvate to oxaloacetate and serves an essential anaplerotic role during periods of metabolic shunting.	transcription
52429	10	334963	5	NULL	NULL	0	NULL	statement 4	NULL		leads to	NULL				fatty acids	NULL	biosynthesis of			NULL		0	NULL	NULL	NULL	gw70_pnas_102_2_467_s_120	15626759	The two smaller species were identified as the biotin-containing subunit of acetyl CoA carboxylase (encoded by  accA3), which catalyzes the conversion of acetyl CoA to malonyl CoA, the first committed step in fatty acid biosynthesis, and pyruvate carboxylase (encoded by  pca), which catalyzes the conversion of pyruvate to oxaloacetate and serves an essential anaplerotic role during periods of metabolic shunting.	transcription
55329	1	334963	6	NULL	NULL	0	NULL	acetyl CoA			is converted to					malonyl CoA					NULL		0	NULL	NULL	NULL	gw70_pnas_102_2_467_s_120	15626759	The two smaller species were identified as the biotin-containing subunit of acetyl CoA carboxylase (encoded by  accA3), which catalyzes the conversion of acetyl CoA to malonyl CoA, the first committed step in fatty acid biosynthesis, and pyruvate carboxylase (encoded by  pca), which catalyzes the conversion of pyruvate to oxaloacetate and serves an essential anaplerotic role during periods of metabolic shunting.	transcription
55331	2	334963	6	NULL	NULL	0	NULL	statement 1			occurs in					fatty acid		biosynthesis of 			NULL		0	NULL	NULL	NULL	gw70_pnas_102_2_467_s_120	15626759	The two smaller species were identified as the biotin-containing subunit of acetyl CoA carboxylase (encoded by  accA3), which catalyzes the conversion of acetyl CoA to malonyl CoA, the first committed step in fatty acid biosynthesis, and pyruvate carboxylase (encoded by  pca), which catalyzes the conversion of pyruvate to oxaloacetate and serves an essential anaplerotic role during periods of metabolic shunting.	transcription
55347	3	334963	6	NULL	NULL	0	NULL	accA3			is					acetyl CoA carboxylase					NULL		0	NULL	NULL	NULL	gw70_pnas_102_2_467_s_120	15626759	The two smaller species were identified as the biotin-containing subunit of acetyl CoA carboxylase (encoded by  accA3), which catalyzes the conversion of acetyl CoA to malonyl CoA, the first committed step in fatty acid biosynthesis, and pyruvate carboxylase (encoded by  pca), which catalyzes the conversion of pyruvate to oxaloacetate and serves an essential anaplerotic role during periods of metabolic shunting.	transcription
55356	4	334963	6	NULL	NULL	0	NULL	pca			is					pyruvate carboxylase					NULL		0	NULL	NULL	NULL	gw70_pnas_102_2_467_s_120	15626759	The two smaller species were identified as the biotin-containing subunit of acetyl CoA carboxylase (encoded by  accA3), which catalyzes the conversion of acetyl CoA to malonyl CoA, the first committed step in fatty acid biosynthesis, and pyruvate carboxylase (encoded by  pca), which catalyzes the conversion of pyruvate to oxaloacetate and serves an essential anaplerotic role during periods of metabolic shunting.	transcription
55357	5	334963	6	NULL	NULL	0	NULL	pyruvate			is converted to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw70_pnas_102_2_467_s_120	15626759	The two smaller species were identified as the biotin-containing subunit of acetyl CoA carboxylase (encoded by  accA3), which catalyzes the conversion of acetyl CoA to malonyl CoA, the first committed step in fatty acid biosynthesis, and pyruvate carboxylase (encoded by  pca), which catalyzes the conversion of pyruvate to oxaloacetate and serves an essential anaplerotic role during periods of metabolic shunting.	transcription
55359	6	334963	6	NULL	NULL	0	NULL	pca			catalyzes					statement 5					NULL		0	NULL	NULL	NULL	gw70_pnas_102_2_467_s_120	15626759	The two smaller species were identified as the biotin-containing subunit of acetyl CoA carboxylase (encoded by  accA3), which catalyzes the conversion of acetyl CoA to malonyl CoA, the first committed step in fatty acid biosynthesis, and pyruvate carboxylase (encoded by  pca), which catalyzes the conversion of pyruvate to oxaloacetate and serves an essential anaplerotic role during periods of metabolic shunting.	transcription
52409	1	334964	5	NULL	NULL	0	NULL	glycolate	NULL	provision of energy from	occur via	NULL	may			dicarboxylic acid cycle	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_9993_s_54	12556462	Jack and I were able to show that the provision of energy from glycolate could occur  via a dicarboxylic acid cycle, in which an isoform of malate synthetase catalyzed the condensation of glyoxylate and acetyl-coenzyme A as the first step in a sequence of reactions that led from malate via oxaloacetate and pyruvate to the loss of two carbons as CO2 and to the reformation of the acetyl-coenzyme A acceptor ( ).	transcription
52410	2	334964	5	NULL	NULL	0	NULL	isoform of malate synthetase	NULL		catalyzes	NULL				glyoxylate	NULL	condensation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_9993_s_54	12556462	Jack and I were able to show that the provision of energy from glycolate could occur  via a dicarboxylic acid cycle, in which an isoform of malate synthetase catalyzed the condensation of glyoxylate and acetyl-coenzyme A as the first step in a sequence of reactions that led from malate via oxaloacetate and pyruvate to the loss of two carbons as CO2 and to the reformation of the acetyl-coenzyme A acceptor ( ).	transcription
52411	3	334964	5	NULL	NULL	0	NULL	isoform of malate synthetase	NULL		catalyzes	NULL				acetyl-coenzyme A 	NULL	condensation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_9993_s_54	12556462	Jack and I were able to show that the provision of energy from glycolate could occur  via a dicarboxylic acid cycle, in which an isoform of malate synthetase catalyzed the condensation of glyoxylate and acetyl-coenzyme A as the first step in a sequence of reactions that led from malate via oxaloacetate and pyruvate to the loss of two carbons as CO2 and to the reformation of the acetyl-coenzyme A acceptor ( ).	transcription
52412	4	334964	5	NULL	NULL	0	NULL	statement 2	NULL		occurs along with	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_9993_s_54	12556462	Jack and I were able to show that the provision of energy from glycolate could occur  via a dicarboxylic acid cycle, in which an isoform of malate synthetase catalyzed the condensation of glyoxylate and acetyl-coenzyme A as the first step in a sequence of reactions that led from malate via oxaloacetate and pyruvate to the loss of two carbons as CO2 and to the reformation of the acetyl-coenzyme A acceptor ( ).	transcription
52413	5	334964	5	NULL	NULL	0	NULL	statement 4	NULL		led from	NULL				malate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_9993_s_54	12556462	Jack and I were able to show that the provision of energy from glycolate could occur  via a dicarboxylic acid cycle, in which an isoform of malate synthetase catalyzed the condensation of glyoxylate and acetyl-coenzyme A as the first step in a sequence of reactions that led from malate via oxaloacetate and pyruvate to the loss of two carbons as CO2 and to the reformation of the acetyl-coenzyme A acceptor ( ).	transcription
52414	6	334964	5	NULL	NULL	0	NULL	carbon	NULL		is lost as	NULL				CO2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_9993_s_54	12556462	Jack and I were able to show that the provision of energy from glycolate could occur  via a dicarboxylic acid cycle, in which an isoform of malate synthetase catalyzed the condensation of glyoxylate and acetyl-coenzyme A as the first step in a sequence of reactions that led from malate via oxaloacetate and pyruvate to the loss of two carbons as CO2 and to the reformation of the acetyl-coenzyme A acceptor ( ).	transcription
52415	7	334964	5	NULL	NULL	0	NULL	statement 4	NULL		led to	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_9993_s_54	12556462	Jack and I were able to show that the provision of energy from glycolate could occur  via a dicarboxylic acid cycle, in which an isoform of malate synthetase catalyzed the condensation of glyoxylate and acetyl-coenzyme A as the first step in a sequence of reactions that led from malate via oxaloacetate and pyruvate to the loss of two carbons as CO2 and to the reformation of the acetyl-coenzyme A acceptor ( ).	transcription
52416	8	334964	5	NULL	NULL	0	NULL	statement 7	NULL		via	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_9993_s_54	12556462	Jack and I were able to show that the provision of energy from glycolate could occur  via a dicarboxylic acid cycle, in which an isoform of malate synthetase catalyzed the condensation of glyoxylate and acetyl-coenzyme A as the first step in a sequence of reactions that led from malate via oxaloacetate and pyruvate to the loss of two carbons as CO2 and to the reformation of the acetyl-coenzyme A acceptor ( ).	transcription
52417	9	334964	5	NULL	NULL	0	NULL	statement 7	NULL		via	NULL				pyruvate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_9993_s_54	12556462	Jack and I were able to show that the provision of energy from glycolate could occur  via a dicarboxylic acid cycle, in which an isoform of malate synthetase catalyzed the condensation of glyoxylate and acetyl-coenzyme A as the first step in a sequence of reactions that led from malate via oxaloacetate and pyruvate to the loss of two carbons as CO2 and to the reformation of the acetyl-coenzyme A acceptor ( ).	transcription
52418	10	334964	5	NULL	NULL	0	NULL	statement 7	NULL		led to	NULL				acetyl-coenzyme A acceptor	NULL	reformation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_9993_s_54	12556462	Jack and I were able to show that the provision of energy from glycolate could occur  via a dicarboxylic acid cycle, in which an isoform of malate synthetase catalyzed the condensation of glyoxylate and acetyl-coenzyme A as the first step in a sequence of reactions that led from malate via oxaloacetate and pyruvate to the loss of two carbons as CO2 and to the reformation of the acetyl-coenzyme A acceptor ( ).	transcription
52430	1	334966	5	NULL	NULL	0	NULL	liver tumor	NULL		is induced by	NULL				DEN	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
52431	2	334966	5	NULL	NULL	0	NULL	Bauhinia variegata	NULL	extract of	suppress	NULL	effectively			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
52432	3	334966	5	NULL	NULL	0	NULL	DEN	NULL		induce	NULL				SGPT	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
52433	4	334966	5	NULL	NULL	0	NULL	SGPT	NULL		is	NULL				serum glutamate pyruvate transaminase	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
52434	5	334966	5	NULL	NULL	0	NULL	SGOT	NULL		is	NULL				serum glutamate oxaloacetate transaminase	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
52435	6	334966	5	NULL	NULL	0	NULL	DEN	NULL		induce	NULL				SGOT	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
52436	7	334966	5	NULL	NULL	0	NULL	DEN	NULL		induce	NULL				ALP	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
52437	8	334966	5	NULL	NULL	0	NULL	ALP	NULL		is	NULL				alkaline phosphatase	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
52438	9	334966	5	NULL	NULL	0	NULL	DEN	NULL		induce	NULL				bilirubin	NULL	total			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
52439	10	334966	5	NULL	NULL	0	NULL	DEN	NULL		induce	NULL				GGTP	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
52440	11	334966	5	NULL	NULL	0	NULL	GGTP	NULL		is	NULL				gamma glutamate transpeptidase	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
52441	12	334966	5	NULL	NULL	0	NULL	DEN	NULL		induce	NULL				LPO	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
52442	13	334966	5	NULL	NULL	0	NULL	LPO	NULL		is	NULL				lipid peroxidase	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
52443	14	334966	5	NULL	NULL	0	NULL	DEN	NULL		induce	NULL				GPx	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
52444	15	334966	5	NULL	NULL	0	NULL	GPx	NULL		is	NULL				glutathione peroxidase	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
52445	16	334966	5	NULL	NULL	0	NULL	DEN	NULL		induce	NULL				GST	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
52446	17	334966	5	NULL	NULL	0	NULL	GST	NULL		is	NULL				glutathione S-transferase	NULL				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55373	1	334966	6	NULL	NULL	0	NULL	DEN			induces					liver tumor					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55374	2	334966	6	NULL	NULL	0	NULL	Bauhinia variegata extracts			suppress					statement 1					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55375	3	334966	6	NULL	NULL	0	NULL	DEN			induces					SGPT		elevated levels of 			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55377	4	334966	6	NULL	NULL	0	NULL	Bauhinia variegata extracts		administration of	decreases					statement 3					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55378	5	334966	6	NULL	NULL	0	NULL	SGPT			is					serum glutamate pyruvate transaminase					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55379	6	334966	6	NULL	NULL	0	NULL	SGOT			is					serum glutamate oxaloacetate transaminase					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55380	7	334966	6	NULL	NULL	0	NULL	DEN			induces					SGOT		elevated levels of			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55381	8	334966	6	NULL	NULL	0	NULL	Bauhinia variegata extracts		administration of	decreases					statement 7					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55386	9	334966	6	NULL	NULL	0	NULL	DEN			induces					ALP					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55388	10	334966	6	NULL	NULL	0	NULL	Bauhinia variegata extracts		administration of	decreases					statement 9					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55389	11	334966	6	NULL	NULL	0	NULL	ALP			is					alkaline phosphatase					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55396	12	334966	6	NULL	NULL	0	NULL	DEN			induces					total bilirubin		elevated levels of			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55399	13	334966	6	NULL	NULL	0	NULL	Bauhinia variegata extracts		administration of	decreases					statement 12					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55400	14	334966	6	NULL	NULL	0	NULL	DEN			induces					GGTP		elevated levels of			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55401	15	334966	6	NULL	NULL	0	NULL	GGTP			is					gamma glutamate transpeptidase					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55402	16	334966	6	NULL	NULL	0	NULL	Bauhinia variegata extracts		administration of	decreases					statement 14					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55403	17	334966	6	NULL	NULL	0	NULL	LPO			is					lipid peroxidase					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55409	18	334966	6	NULL	NULL	0	NULL	DEN			induces					LPO		elevated levels of			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55410	19	334966	6	NULL	NULL	0	NULL	Bauhinia variegata extracts		administration of	decreases					statement 18					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55411	20	334966	6	NULL	NULL	0	NULL	GPx			is					glutathione peroxidase					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55412	21	334966	6	NULL	NULL	0	NULL	DEN			induces					GPx		elevated levels of			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
55413	22	334966	6	NULL	NULL	0	NULL	Bauhinia variegata extracts		administration of	decreases					statement 18					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-ethnopharmacol_104_3_16257158_s_3	16257158	Oral administration of ethanol extract of Bauhinia variegata (250mg/kg)  effectively suppressed liver tumor induced by DEN as revealed by decrease  in DEN induced elevated levels of serum glutamate pyruvate transaminase  (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase  (ALP), total bilirubin, gamma glutamate transpeptidase (GGTP), lipid peroxidase  (LPO), glutathione peroxidase (GPx) and glutathione S-transferase (GST).	transcription
52447	1	334968	5	NULL	NULL	0	NULL	ATP	NULL		bind	NULL				PII	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_8_2582_s_23	12670983	Conversely, the binding of ATP to PII inhibits phospho-PII dephosphorylation; this inhibition is greatly enhanced by 2-oxoglutarate and to a lesser extent by oxaloacetate ( ).	transcription
52448	2	334968	5	NULL	NULL	0	NULL	statement 1	NULL		inhibit	NULL				phospho-PII	NULL	dephosphorylation of			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_8_2582_s_23	12670983	Conversely, the binding of ATP to PII inhibits phospho-PII dephosphorylation; this inhibition is greatly enhanced by 2-oxoglutarate and to a lesser extent by oxaloacetate ( ).	transcription
52449	3	334968	5	NULL	NULL	0	NULL	2-oxoglutarate	NULL		enhance	NULL	greatly			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_8_2582_s_23	12670983	Conversely, the binding of ATP to PII inhibits phospho-PII dephosphorylation; this inhibition is greatly enhanced by 2-oxoglutarate and to a lesser extent by oxaloacetate ( ).	transcription
52450	4	334968	5	NULL	NULL	0	NULL	oxaloacetate	NULL		enhance	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_8_2582_s_23	12670983	Conversely, the binding of ATP to PII inhibits phospho-PII dephosphorylation; this inhibition is greatly enhanced by 2-oxoglutarate and to a lesser extent by oxaloacetate ( ).	transcription
55415	1	334968	6	NULL	NULL	0	NULL	ATP			bind					PII					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_8_2582_s_23	12670983	Conversely, the binding of ATP to PII inhibits phospho-PII dephosphorylation; this inhibition is greatly enhanced by 2-oxoglutarate and to a lesser extent by oxaloacetate ( ).	transcription
55417	2	334968	6	NULL	NULL	0	NULL	statement 1			inhibits					phospho-PII		dephosphorylation of 			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_8_2582_s_23	12670983	Conversely, the binding of ATP to PII inhibits phospho-PII dephosphorylation; this inhibition is greatly enhanced by 2-oxoglutarate and to a lesser extent by oxaloacetate ( ).	transcription
55420	3	334968	6	NULL	NULL	0	NULL	statement 2			is enhanced by					2-oxoglutarate					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_8_2582_s_23	12670983	Conversely, the binding of ATP to PII inhibits phospho-PII dephosphorylation; this inhibition is greatly enhanced by 2-oxoglutarate and to a lesser extent by oxaloacetate ( ).	transcription
55471	4	334968	6	NULL	NULL	0	NULL	statement 2			is enhanced by					oxaloacetate					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_185_8_2582_s_23	12670983	Conversely, the binding of ATP to PII inhibits phospho-PII dephosphorylation; this inhibition is greatly enhanced by 2-oxoglutarate and to a lesser extent by oxaloacetate ( ).	transcription
52451	1	334969	5	NULL	NULL	0	NULL	NtcA	NULL		bind	NULL				glnA	NULL	Synechococcus		promoter	NULL		0	NULL	NULL	NULL	gw60_febslett_512_1_71_s_69	11852054	Effect of different concentrations of 2-oxoglutarate, 3-oxoglutarate, glutamate or oxaloacetate on the binding of NtcA to the  Synechococcus glnA promoter.	transcription
55472	1	334969	6	NULL	NULL	0	NULL	NtcA			bind					glnA		Synechococcus		promoter	NULL		0	NULL	NULL	NULL	gw60_febslett_512_1_71_s_69	11852054	Effect of different concentrations of 2-oxoglutarate, 3-oxoglutarate, glutamate or oxaloacetate on the binding of NtcA to the  Synechococcus glnA promoter.	transcription
52452	1	334970	5	NULL	NULL	0	NULL	succinyl-CoA	NULL		is carboxylated to	NULL				2-oxoglutarate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_9_3020_s_23	15838028	2-Oxoglutarate:ferredoxin oxidoreductase catalyzes the carboxylation of succinyl-CoA to 2-oxoglutarate, ATP citrate lyase the ATP-dependent cleavage of citrate to acetyl-CoA and oxaloacetate, and fumarate reductase the reduction of fumarate forming succinate.	transcription
52453	2	334970	5	NULL	NULL	0	NULL	2-Oxoglutarate:ferredoxin oxidoreductase	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_9_3020_s_23	15838028	2-Oxoglutarate:ferredoxin oxidoreductase catalyzes the carboxylation of succinyl-CoA to 2-oxoglutarate, ATP citrate lyase the ATP-dependent cleavage of citrate to acetyl-CoA and oxaloacetate, and fumarate reductase the reduction of fumarate forming succinate.	transcription
52454	3	334970	5	NULL	NULL	0	NULL	citrate	NULL		is cleaved into	NULL				acetyl-CoA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_9_3020_s_23	15838028	2-Oxoglutarate:ferredoxin oxidoreductase catalyzes the carboxylation of succinyl-CoA to 2-oxoglutarate, ATP citrate lyase the ATP-dependent cleavage of citrate to acetyl-CoA and oxaloacetate, and fumarate reductase the reduction of fumarate forming succinate.	transcription
52455	4	334970	5	NULL	NULL	0	NULL	citrate	NULL		is cleaved into	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_9_3020_s_23	15838028	2-Oxoglutarate:ferredoxin oxidoreductase catalyzes the carboxylation of succinyl-CoA to 2-oxoglutarate, ATP citrate lyase the ATP-dependent cleavage of citrate to acetyl-CoA and oxaloacetate, and fumarate reductase the reduction of fumarate forming succinate.	transcription
52456	5	334970	5	NULL	NULL	0	NULL	statement 3	NULL		occurs along with	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_9_3020_s_23	15838028	2-Oxoglutarate:ferredoxin oxidoreductase catalyzes the carboxylation of succinyl-CoA to 2-oxoglutarate, ATP citrate lyase the ATP-dependent cleavage of citrate to acetyl-CoA and oxaloacetate, and fumarate reductase the reduction of fumarate forming succinate.	transcription
52457	6	334970	5	NULL	NULL	0	NULL	statement 5	NULL		is dependent on	NULL				ATP	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_9_3020_s_23	15838028	2-Oxoglutarate:ferredoxin oxidoreductase catalyzes the carboxylation of succinyl-CoA to 2-oxoglutarate, ATP citrate lyase the ATP-dependent cleavage of citrate to acetyl-CoA and oxaloacetate, and fumarate reductase the reduction of fumarate forming succinate.	transcription
52458	7	334970	5	NULL	NULL	0	NULL	ATP citrate lyase	NULL		catalyzes	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_9_3020_s_23	15838028	2-Oxoglutarate:ferredoxin oxidoreductase catalyzes the carboxylation of succinyl-CoA to 2-oxoglutarate, ATP citrate lyase the ATP-dependent cleavage of citrate to acetyl-CoA and oxaloacetate, and fumarate reductase the reduction of fumarate forming succinate.	transcription
52459	8	334970	5	NULL	NULL	0	NULL	fumarate	NULL	reduction of	leads to	NULL				succinate	NULL	formation of			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_9_3020_s_23	15838028	2-Oxoglutarate:ferredoxin oxidoreductase catalyzes the carboxylation of succinyl-CoA to 2-oxoglutarate, ATP citrate lyase the ATP-dependent cleavage of citrate to acetyl-CoA and oxaloacetate, and fumarate reductase the reduction of fumarate forming succinate.	transcription
52460	9	334970	5	NULL	NULL	0	NULL	fumarate reductase	NULL		catalyzes	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_9_3020_s_23	15838028	2-Oxoglutarate:ferredoxin oxidoreductase catalyzes the carboxylation of succinyl-CoA to 2-oxoglutarate, ATP citrate lyase the ATP-dependent cleavage of citrate to acetyl-CoA and oxaloacetate, and fumarate reductase the reduction of fumarate forming succinate.	transcription
55473	1	334970	6	NULL	NULL	0	NULL	succinyl-CoA			is carboxylated to					2-oxoglutarate					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_9_3020_s_23	15838028	2-Oxoglutarate:ferredoxin oxidoreductase catalyzes the carboxylation of succinyl-CoA to 2-oxoglutarate, ATP citrate lyase the ATP-dependent cleavage of citrate to acetyl-CoA and oxaloacetate, and fumarate reductase the reduction of fumarate forming succinate.	transcription
55474	2	334970	6	NULL	NULL	0	NULL	2-Oxoglutarate:ferredoxin oxidoreductase			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_9_3020_s_23	15838028	2-Oxoglutarate:ferredoxin oxidoreductase catalyzes the carboxylation of succinyl-CoA to 2-oxoglutarate, ATP citrate lyase the ATP-dependent cleavage of citrate to acetyl-CoA and oxaloacetate, and fumarate reductase the reduction of fumarate forming succinate.	transcription
55475	3	334970	6	NULL	NULL	0	NULL	citrate			is converted to					acetyl-CoA					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_9_3020_s_23	15838028	2-Oxoglutarate:ferredoxin oxidoreductase catalyzes the carboxylation of succinyl-CoA to 2-oxoglutarate, ATP citrate lyase the ATP-dependent cleavage of citrate to acetyl-CoA and oxaloacetate, and fumarate reductase the reduction of fumarate forming succinate.	transcription
55476	4	334970	6	NULL	NULL	0	NULL	citrate			is converted to					oxaloacetate					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_9_3020_s_23	15838028	2-Oxoglutarate:ferredoxin oxidoreductase catalyzes the carboxylation of succinyl-CoA to 2-oxoglutarate, ATP citrate lyase the ATP-dependent cleavage of citrate to acetyl-CoA and oxaloacetate, and fumarate reductase the reduction of fumarate forming succinate.	transcription
55477	5	334970	6	NULL	NULL	0	NULL	statement 3			is dependent on					ATP					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_9_3020_s_23	15838028	2-Oxoglutarate:ferredoxin oxidoreductase catalyzes the carboxylation of succinyl-CoA to 2-oxoglutarate, ATP citrate lyase the ATP-dependent cleavage of citrate to acetyl-CoA and oxaloacetate, and fumarate reductase the reduction of fumarate forming succinate.	transcription
55478	6	334970	6	NULL	NULL	0	NULL	statement 4			is dependent on					ATP					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_9_3020_s_23	15838028	2-Oxoglutarate:ferredoxin oxidoreductase catalyzes the carboxylation of succinyl-CoA to 2-oxoglutarate, ATP citrate lyase the ATP-dependent cleavage of citrate to acetyl-CoA and oxaloacetate, and fumarate reductase the reduction of fumarate forming succinate.	transcription
55479	7	334970	6	NULL	NULL	0	NULL	ATP citrate lyase			catalyzes					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_9_3020_s_23	15838028	2-Oxoglutarate:ferredoxin oxidoreductase catalyzes the carboxylation of succinyl-CoA to 2-oxoglutarate, ATP citrate lyase the ATP-dependent cleavage of citrate to acetyl-CoA and oxaloacetate, and fumarate reductase the reduction of fumarate forming succinate.	transcription
55480	8	334970	6	NULL	NULL	0	NULL	ATP citrate lyase			catalyzes					statement 4					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_9_3020_s_23	15838028	2-Oxoglutarate:ferredoxin oxidoreductase catalyzes the carboxylation of succinyl-CoA to 2-oxoglutarate, ATP citrate lyase the ATP-dependent cleavage of citrate to acetyl-CoA and oxaloacetate, and fumarate reductase the reduction of fumarate forming succinate.	transcription
55481	9	334970	6	NULL	NULL	0	NULL	fumarate			is converted to					succinate					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_9_3020_s_23	15838028	2-Oxoglutarate:ferredoxin oxidoreductase catalyzes the carboxylation of succinyl-CoA to 2-oxoglutarate, ATP citrate lyase the ATP-dependent cleavage of citrate to acetyl-CoA and oxaloacetate, and fumarate reductase the reduction of fumarate forming succinate.	transcription
55482	10	334970	6	NULL	NULL	0	NULL	fumarate reductase			catalyzes					statement 9					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_9_3020_s_23	15838028	2-Oxoglutarate:ferredoxin oxidoreductase catalyzes the carboxylation of succinyl-CoA to 2-oxoglutarate, ATP citrate lyase the ATP-dependent cleavage of citrate to acetyl-CoA and oxaloacetate, and fumarate reductase the reduction of fumarate forming succinate.	transcription
52461	1	334971	5	NULL	NULL	0	NULL	glyoxylate shunt	NULL	functional	regulates	NULL				isocitrate	NULL	levels of			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_261	12839772	A functional glyoxylate shunt would regulate isocitrate levels and may reduce intracellular 2-oxoglutarate accumulation by drawing off oxaloacetate via transamination to aspartate.	transcription
52462	2	334971	5	NULL	NULL	0	NULL	glyoxylate shunt	NULL	functional	reduce	NULL				2-oxoglutarate	NULL	accumulation of;;intracellular			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_261	12839772	A functional glyoxylate shunt would regulate isocitrate levels and may reduce intracellular 2-oxoglutarate accumulation by drawing off oxaloacetate via transamination to aspartate.	transcription
52463	3	334971	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is transaminated to	NULL				aspartate	NULL				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_261	12839772	A functional glyoxylate shunt would regulate isocitrate levels and may reduce intracellular 2-oxoglutarate accumulation by drawing off oxaloacetate via transamination to aspartate.	transcription
52464	4	334971	5	NULL	NULL	0	NULL	statement 2	NULL		via	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_261	12839772	A functional glyoxylate shunt would regulate isocitrate levels and may reduce intracellular 2-oxoglutarate accumulation by drawing off oxaloacetate via transamination to aspartate.	transcription
55508	1	334971	6	NULL	NULL	0	NULL	oxaloacetate			is transaminated to					aspartate					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_261	12839772	A functional glyoxylate shunt would regulate isocitrate levels and may reduce intracellular 2-oxoglutarate accumulation by drawing off oxaloacetate via transamination to aspartate.	transcription
55509	2	334971	6	NULL	NULL	0	NULL	glyoxylate shunt			regulates					isocitrate 		levels of 			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_7_3986_s_261	12839772	A functional glyoxylate shunt would regulate isocitrate levels and may reduce intracellular 2-oxoglutarate accumulation by drawing off oxaloacetate via transamination to aspartate.	transcription
52603	1	334972	5	NULL	NULL	0	NULL	HPSOT2 protein	NULL		catalyzes	NULL				oxaloacetate/malate	NULL	transport of			NULL		0	NULL	NULL	NULL	gw60_pnas_99_17_11487_s_185	12177442	Concomitant proteomic identification of two members of the 2-oxoglutarate/malate translocator family (Table  1) suggests that these two proteins may not be differentially expressed spatially or temporally but may differ in substrate specificity: the HPSOT2 protein may catalyze the transport of different dicarboxylic acids (oxaloacetate/malate, malate/glutamate, glutamate/glutamine).	transcription
52604	2	334972	5	NULL	NULL	0	NULL	HPSOT2 protein	NULL		catalyzes	NULL				malate/glutamate	NULL	transport of			NULL		0	NULL	NULL	NULL	gw60_pnas_99_17_11487_s_185	12177442	Concomitant proteomic identification of two members of the 2-oxoglutarate/malate translocator family (Table  1) suggests that these two proteins may not be differentially expressed spatially or temporally but may differ in substrate specificity: the HPSOT2 protein may catalyze the transport of different dicarboxylic acids (oxaloacetate/malate, malate/glutamate, glutamate/glutamine).	transcription
52605	3	334972	5	NULL	NULL	0	NULL	HPSOT2 protein	NULL		catalyzes	NULL				glutamate/glutamine	NULL	transport of			NULL		0	NULL	NULL	NULL	gw60_pnas_99_17_11487_s_185	12177442	Concomitant proteomic identification of two members of the 2-oxoglutarate/malate translocator family (Table  1) suggests that these two proteins may not be differentially expressed spatially or temporally but may differ in substrate specificity: the HPSOT2 protein may catalyze the transport of different dicarboxylic acids (oxaloacetate/malate, malate/glutamate, glutamate/glutamine).	transcription
52606	4	334972	5	NULL	NULL	0	NULL	HPSOT2 protein	NULL		is a member of	NULL				2-oxoglutarate/malate translocator family	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_17_11487_s_185	12177442	Concomitant proteomic identification of two members of the 2-oxoglutarate/malate translocator family (Table  1) suggests that these two proteins may not be differentially expressed spatially or temporally but may differ in substrate specificity: the HPSOT2 protein may catalyze the transport of different dicarboxylic acids (oxaloacetate/malate, malate/glutamate, glutamate/glutamine).	transcription
52607	5	334972	5	NULL	NULL	0	NULL	oxaloacetate/malate	NULL		is a type of	NULL				dicarboxylic acid	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_17_11487_s_185	12177442	Concomitant proteomic identification of two members of the 2-oxoglutarate/malate translocator family (Table  1) suggests that these two proteins may not be differentially expressed spatially or temporally but may differ in substrate specificity: the HPSOT2 protein may catalyze the transport of different dicarboxylic acids (oxaloacetate/malate, malate/glutamate, glutamate/glutamine).	transcription
52608	6	334972	5	NULL	NULL	0	NULL	malate/glutamate	NULL		is a type of	NULL				dicarboxylic acid	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_17_11487_s_185	12177442	Concomitant proteomic identification of two members of the 2-oxoglutarate/malate translocator family (Table  1) suggests that these two proteins may not be differentially expressed spatially or temporally but may differ in substrate specificity: the HPSOT2 protein may catalyze the transport of different dicarboxylic acids (oxaloacetate/malate, malate/glutamate, glutamate/glutamine).	transcription
52609	7	334972	5	NULL	NULL	0	NULL	glutamate/glutamine	NULL		is a type of	NULL				dicarboxylic acids	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_99_17_11487_s_185	12177442	Concomitant proteomic identification of two members of the 2-oxoglutarate/malate translocator family (Table  1) suggests that these two proteins may not be differentially expressed spatially or temporally but may differ in substrate specificity: the HPSOT2 protein may catalyze the transport of different dicarboxylic acids (oxaloacetate/malate, malate/glutamate, glutamate/glutamine).	transcription
55510	1	334972	6	NULL	NULL	0	NULL	HPSOT2 protein			catalyze		may			oxaloacetate/malate		transport of 			NULL		0	NULL	NULL	NULL	gw60_pnas_99_17_11487_s_185	12177442	Concomitant proteomic identification of two members of the 2-oxoglutarate/malate translocator family (Table  1) suggests that these two proteins may not be differentially expressed spatially or temporally but may differ in substrate specificity: the HPSOT2 protein may catalyze the transport of different dicarboxylic acids (oxaloacetate/malate, malate/glutamate, glutamate/glutamine).	transcription
55511	2	334972	6	NULL	NULL	0	NULL	HPSOT2 protein			catalyze		may			malate/glutamate		transport of			NULL		0	NULL	NULL	NULL	gw60_pnas_99_17_11487_s_185	12177442	Concomitant proteomic identification of two members of the 2-oxoglutarate/malate translocator family (Table  1) suggests that these two proteins may not be differentially expressed spatially or temporally but may differ in substrate specificity: the HPSOT2 protein may catalyze the transport of different dicarboxylic acids (oxaloacetate/malate, malate/glutamate, glutamate/glutamine).	transcription
55512	3	334972	6	NULL	NULL	0	NULL	HPSOT2 protein			catalyze		may			glutamate/glutamine		transport of			NULL		0	NULL	NULL	NULL	gw60_pnas_99_17_11487_s_185	12177442	Concomitant proteomic identification of two members of the 2-oxoglutarate/malate translocator family (Table  1) suggests that these two proteins may not be differentially expressed spatially or temporally but may differ in substrate specificity: the HPSOT2 protein may catalyze the transport of different dicarboxylic acids (oxaloacetate/malate, malate/glutamate, glutamate/glutamine).	transcription
52610	1	334973	5	NULL	NULL	0	NULL	homocitrate	NULL		is synthesized from	NULL				2-oxoglutarate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
52611	2	334973	5	NULL	NULL	0	NULL	homocitrate	NULL		is synthesized from	NULL				acetyl-CoA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
52612	3	334973	5	NULL	NULL	0	NULL	statement 1	NULL		occurs along with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
52613	4	334973	5	NULL	NULL	0	NULL	homocitrate synthase	NULL		catalyzes	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
52655	5	334973	5	NULL	NULL	0	NULL	statement 4	NULL		plays a role in	NULL				lysine	NULL	biosynthesis of			NULL	T. thermophilus HB27	0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
52656	6	334973	5	NULL	NULL	0	NULL	citrate	NULL		is synthesized from	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
52657	7	334973	5	NULL	NULL	0	NULL	citrate	NULL		is synthesized from	NULL				acetyl-CoA	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
52658	8	334973	5	NULL	NULL	0	NULL	statement 6	NULL		occurs along with	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
52659	9	334973	5	NULL	NULL	0	NULL	citrate synthase	NULL		catalyzes	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
52660	10	334973	5	NULL	NULL	0	NULL	homocitrate synthase	NULL		catalyzes	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
52661	11	334973	5	NULL	NULL	0	NULL	homocitrate synthase	NULL		is not similar to	NULL	structurally			citrate synthase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
55513	1	334973	6	NULL	NULL	0	NULL	2-oxoglutarate			synthesizes					homocitrate					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
55515	2	334973	6	NULL	NULL	0	NULL	acetyl-CoA			synthesizes					homocitrate					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
55516	3	334973	6	NULL	NULL	0	NULL	statement 1			occurs simultaneously with					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
55517	4	334973	6	NULL	NULL	0	NULL	homocitrate synthase			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
55518	5	334973	6	NULL	NULL	0	NULL	homocitrate synthase			catalyzes					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
55519	6	334973	6	NULL	NULL	0	NULL	statement 3			occurs during					lysine		biosynthesis of			NULL	T. thermophilus HB27	0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
55520	7	334973	6	NULL	NULL	0	NULL	oxaloacetate			synthesizes					citrate					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
55554	8	334973	6	NULL	NULL	0	NULL	acetyl-CoA			synthesizes					citrate					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
55555	9	334973	6	NULL	NULL	0	NULL	statement 7			occurs simultaneously with					statement 8					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
55556	10	334973	6	NULL	NULL	0	NULL	homocitrate synthase			catalyzes					statement 7					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
55557	11	334973	6	NULL	NULL	0	NULL	homocitrate synthase			catalyzes					statement 8					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
55558	12	334973	6	NULL	NULL	0	NULL	homocitrate synthase			is dissimilar to		structurally			citrate synthase					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_3_1864_s_215	12427751	It should be noted that we recently found that homocitrate synthase, which catalyzes synthesis of homocitrate from 2-oxoglutarate and acetyl-CoA, the first reaction in lysine biosynthesis of  T. thermophilus HB27, was able to catalyze the synthesis of citrate from oxaloacetate and acetyl-CoA, the corresponding reaction by citrate synthase in the tricarboxylic acid cycle, although homocitrate synthase has no structural similarity to citrate synthase ( ).	transcription
52662	1	334974	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is converted to	NULL				phosphoenolpyruvate	NULL				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_309_1_328_s_28	14722324	Phosphoenolpyruvate carboxykinase catalyzes the conversion of oxaloacetate to phosphoenolpyruvate, the rate-limiting step in gluconeogenesis.	transcription
52663	2	334974	5	NULL	NULL	0	NULL	Phosphoenolpyruvate carboxykinase			catalyzes					rate-limiting step					NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_309_1_328_s_28	14722324	Phosphoenolpyruvate carboxykinase catalyzes the conversion of oxaloacetate to phosphoenolpyruvate, the rate-limiting step in gluconeogenesis.	transcription
52664	3	334974	5	NULL	NULL	0	NULL	statement 2			conversion of		for			statement 1					NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_309_1_328_s_28	14722324	Phosphoenolpyruvate carboxykinase catalyzes the conversion of oxaloacetate to phosphoenolpyruvate, the rate-limiting step in gluconeogenesis.	transcription
54319	4	334974	5	NULL	NULL	0	NULL	statement 1			occurs in					gluconeogenesis					NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_309_1_328_s_28	14722324	Phosphoenolpyruvate carboxykinase catalyzes the conversion of oxaloacetate to phosphoenolpyruvate, the rate-limiting step in gluconeogenesis.	transcription
55559	1	334974	6	NULL	NULL	0	NULL	oxaloacetate			is converted to					phosphoenolpyruvate					NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_309_1_328_s_28	14722324	Phosphoenolpyruvate carboxykinase catalyzes the conversion of oxaloacetate to phosphoenolpyruvate, the rate-limiting step in gluconeogenesis.	transcription
55560	2	334974	6	NULL	NULL	0	NULL	Phosphoenolpyruvate carboxykinase			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_309_1_328_s_28	14722324	Phosphoenolpyruvate carboxykinase catalyzes the conversion of oxaloacetate to phosphoenolpyruvate, the rate-limiting step in gluconeogenesis.	transcription
55561	3	334974	6	NULL	NULL	0	NULL	statement 1			is an important step in					gluconeogenesis					NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_309_1_328_s_28	14722324	Phosphoenolpyruvate carboxykinase catalyzes the conversion of oxaloacetate to phosphoenolpyruvate, the rate-limiting step in gluconeogenesis.	transcription
52665	1	334975	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is converted to	NULL				phosphoenolpyruvate	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1454_2_133_s_102	10381558	Phosphoenolpyruvate carboxykinase catalyzes the conversion of oxaloacetate to phosphoenolpyruvate which is then utilized by the gluconeogenic pathway.	transcription
52666	2	334975	5	NULL	NULL	0	NULL	Phosphoenolpyruvate carboxykinase	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1454_2_133_s_102	10381558	Phosphoenolpyruvate carboxykinase catalyzes the conversion of oxaloacetate to phosphoenolpyruvate which is then utilized by the gluconeogenic pathway.	transcription
52667	3	334975	5	NULL	NULL	0	NULL	phosphoenolpyruvate	NULL		is utilized by	NULL				gluconeogenic pathway	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1454_2_133_s_102	10381558	Phosphoenolpyruvate carboxykinase catalyzes the conversion of oxaloacetate to phosphoenolpyruvate which is then utilized by the gluconeogenic pathway.	transcription
55562	1	334975	6	NULL	NULL	0	NULL	oxaloacetate			is converted to					phosphoenolpyruvate					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1454_2_133_s_102	10381558	Phosphoenolpyruvate carboxykinase catalyzes the conversion of oxaloacetate to phosphoenolpyruvate which is then utilized by the gluconeogenic pathway.	transcription
55563	2	334975	6	NULL	NULL	0	NULL	Phosphoenolpyruvate carboxykinase			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1454_2_133_s_102	10381558	Phosphoenolpyruvate carboxykinase catalyzes the conversion of oxaloacetate to phosphoenolpyruvate which is then utilized by the gluconeogenic pathway.	transcription
55564	3	334975	6	NULL	NULL	0	NULL	Phosphoenolpyruvate			is utilized by					gluconeogenic pathway					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1454_2_133_s_102	10381558	Phosphoenolpyruvate carboxykinase catalyzes the conversion of oxaloacetate to phosphoenolpyruvate which is then utilized by the gluconeogenic pathway.	transcription
52668	1	334976	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is converted to	NULL				phosphoenolpyruvate	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_51_3_624_s_17	11872659	A regulatory step of this pathway is the conversion of oxaloacetate to phosphoenolpyruvate catalyzed by PEPCK ( 2).	transcription
52669	2	334976	5	NULL	NULL	0	NULL	PEPCK	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_diabetes_51_3_624_s_17	11872659	A regulatory step of this pathway is the conversion of oxaloacetate to phosphoenolpyruvate catalyzed by PEPCK ( 2).	transcription
55565	1	334976	6	NULL	NULL	0	NULL	oxaloacetate			is converted to					phosphoenolpyruvate					NULL		0	NULL	NULL	NULL	gw60_diabetes_51_3_624_s_17	11872659	A regulatory step of this pathway is the conversion of oxaloacetate to phosphoenolpyruvate catalyzed by PEPCK ( 2).	transcription
55566	2	334976	6	NULL	NULL	0	NULL	PEPCK			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw60_diabetes_51_3_624_s_17	11872659	A regulatory step of this pathway is the conversion of oxaloacetate to phosphoenolpyruvate catalyzed by PEPCK ( 2).	transcription
52670	1	334977	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is converted to	NULL				phosphoenolpyruvate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3446_s_37	10652338	PEPCK catalyzes the conversion of oxaloacetate to phosphoenolpyruvate, a rate-controlling step in hepatic gluconeogenesis.	transcription
52671	2	334977	5	NULL	NULL	0	NULL	PEPCK	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3446_s_37	10652338	PEPCK catalyzes the conversion of oxaloacetate to phosphoenolpyruvate, a rate-controlling step in hepatic gluconeogenesis.	transcription
52672	3	334977	5	NULL	NULL	0	NULL	statement 1	NULL		is a type of	NULL				rate-controlling step in hepatic gluconeogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3446_s_37	10652338	PEPCK catalyzes the conversion of oxaloacetate to phosphoenolpyruvate, a rate-controlling step in hepatic gluconeogenesis.	transcription
52673	1	334978	5	NULL	NULL	0	NULL	PEPCK	NULL		is	NULL				phosphoenolpyruvate carboxykinase	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_31_28272_s_13	15951444	Phosphoenolpyruvate carboxykinase (PEPCK)  1 catalyzes the conversion of oxaloacetate to phosphoenolpyruvate, a rate-limiting step in gluconeogenesis.	transcription
52674	2	334978	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is converted to	NULL				phosphoenolpyruvate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_31_28272_s_13	15951444	Phosphoenolpyruvate carboxykinase (PEPCK)  1 catalyzes the conversion of oxaloacetate to phosphoenolpyruvate, a rate-limiting step in gluconeogenesis.	transcription
52675	3	334978	5	NULL	NULL	0	NULL	PEPCK	NULL		catalyzes	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_31_28272_s_13	15951444	Phosphoenolpyruvate carboxykinase (PEPCK)  1 catalyzes the conversion of oxaloacetate to phosphoenolpyruvate, a rate-limiting step in gluconeogenesis.	transcription
52676	4	334978	5	NULL	NULL	0	NULL	statement 2	NULL		is a type of	NULL				rate-limiting step in gluconeogenesis	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_31_28272_s_13	15951444	Phosphoenolpyruvate carboxykinase (PEPCK)  1 catalyzes the conversion of oxaloacetate to phosphoenolpyruvate, a rate-limiting step in gluconeogenesis.	transcription
55569	1	334978	6	NULL	NULL	0	NULL	PEPCK			is					Phosphoenolpyruvate carboxykinase					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_31_28272_s_13	15951444	Phosphoenolpyruvate carboxykinase (PEPCK)  1 catalyzes the conversion of oxaloacetate to phosphoenolpyruvate, a rate-limiting step in gluconeogenesis.	transcription
55570	2	334978	6	NULL	NULL	0	NULL	oxaloacetate			is converted to					phosphoenolpyruvate					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_31_28272_s_13	15951444	Phosphoenolpyruvate carboxykinase (PEPCK)  1 catalyzes the conversion of oxaloacetate to phosphoenolpyruvate, a rate-limiting step in gluconeogenesis.	transcription
55571	3	334978	6	NULL	NULL	0	NULL	PEPCK			catalyzes					statement  2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_31_28272_s_13	15951444	Phosphoenolpyruvate carboxykinase (PEPCK)  1 catalyzes the conversion of oxaloacetate to phosphoenolpyruvate, a rate-limiting step in gluconeogenesis.	transcription
55572	4	334978	6	NULL	NULL	0	NULL	statement 1			is a step in					gluconeogenesis					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_31_28272_s_13	15951444	Phosphoenolpyruvate carboxykinase (PEPCK)  1 catalyzes the conversion of oxaloacetate to phosphoenolpyruvate, a rate-limiting step in gluconeogenesis.	transcription
52677	1	334979	5	NULL	NULL	0	NULL	oxaloacetate	NULL		is converted to	NULL				phosphoenolpyruvate	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6508_s_11	10938127	A key step in gluconeogenesis is the formation of phosphoenolpyruvate from oxaloacetate, which is catalyzed by phosphoenolpyruvate carboxykinase (PEPCK).	transcription
52678	2	334979	5	NULL	NULL	0	NULL	statement 1	NULL		is a key step in	NULL				gluconeogenesis	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6508_s_11	10938127	A key step in gluconeogenesis is the formation of phosphoenolpyruvate from oxaloacetate, which is catalyzed by phosphoenolpyruvate carboxykinase (PEPCK).	transcription
52679	3	334979	5	NULL	NULL	0	NULL	PEPCK	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6508_s_11	10938127	A key step in gluconeogenesis is the formation of phosphoenolpyruvate from oxaloacetate, which is catalyzed by phosphoenolpyruvate carboxykinase (PEPCK).	transcription
52680	4	334979	5	NULL	NULL	0	NULL	PEPCK	NULL		is	NULL				phosphoenolpyruvate carboxykinase	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_17_6508_s_11	10938127	A key step in gluconeogenesis is the formation of phosphoenolpyruvate from oxaloacetate, which is catalyzed by phosphoenolpyruvate carboxykinase (PEPCK).	transcription
52681	1	334980	5	NULL	NULL	0	NULL	PEP	NULL		is	NULL				phosphoenolpyruvate	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1546_1_242_s_4	11257527	1.31) catalyzes the essentially irreversible formation of oxaloacetate and inorganic phosphate from phosphoenolpyruvate (PEP) and bicarbonate, in the presence of Mg2+ [  1.	transcription
52682	2	334980	5	NULL	NULL	0	NULL	PEP			forms		irreversibly			oxaloacetate					NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1546_1_242_s_4	11257527	1.31) catalyzes the essentially irreversible formation of oxaloacetate and inorganic phosphate from phosphoenolpyruvate (PEP) and bicarbonate, in the presence of Mg2+ [  1.	transcription
52683	3	334980	5	NULL	NULL	0	NULL	bicarbonate			forms		irreversibly			oxaloacetate					NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1546_1_242_s_4	11257527	1.31) catalyzes the essentially irreversible formation of oxaloacetate and inorganic phosphate from phosphoenolpyruvate (PEP) and bicarbonate, in the presence of Mg2+ [  1.	transcription
58483	4	334980	5	NULL	NULL	0	NULL	statement 2			occurs simultaneously with					statement 3					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1546_1_242_s_4	11257527	1.31) catalyzes the essentially irreversible formation of oxaloacetate and inorganic phosphate from phosphoenolpyruvate (PEP) and bicarbonate, in the presence of Mg2+ [  1.	transcription
58484	5	334980	5	NULL	NULL	0	NULL	PEP			forms		irreversibly			inorganic phosphate					NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1546_1_242_s_4	11257527	1.31) catalyzes the essentially irreversible formation of oxaloacetate and inorganic phosphate from phosphoenolpyruvate (PEP) and bicarbonate, in the presence of Mg2+ [  1.	transcription
58485	6	334980	5	NULL	NULL	0	NULL	bicarbonate			forms		irreversibly			inorganic phosphate					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1546_1_242_s_4	11257527	1.31) catalyzes the essentially irreversible formation of oxaloacetate and inorganic phosphate from phosphoenolpyruvate (PEP) and bicarbonate, in the presence of Mg2+ [  1.	transcription
58486	7	334980	5	NULL	NULL	0	NULL	statement 5			occurs simultaneously with					statement 6					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1546_1_242_s_4	11257527	1.31) catalyzes the essentially irreversible formation of oxaloacetate and inorganic phosphate from phosphoenolpyruvate (PEP) and bicarbonate, in the presence of Mg2+ [  1.	transcription
58487	8	334980	5	NULL	NULL	0	NULL	statement 4			in the presence of					Mg2+					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1546_1_242_s_4	11257527	1.31) catalyzes the essentially irreversible formation of oxaloacetate and inorganic phosphate from phosphoenolpyruvate (PEP) and bicarbonate, in the presence of Mg2+ [  1.	transcription
58488	9	334980	5	NULL	NULL	0	NULL	statement 7			in the presence of					Mg2+					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1546_1_242_s_4	11257527	1.31) catalyzes the essentially irreversible formation of oxaloacetate and inorganic phosphate from phosphoenolpyruvate (PEP) and bicarbonate, in the presence of Mg2+ [  1.	transcription
55576	1	334980	6	NULL	NULL	0	NULL	PEP			forms					oxaloacetate					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1546_1_242_s_4	11257527	1.31) catalyzes the essentially irreversible formation of oxaloacetate and inorganic phosphate from phosphoenolpyruvate (PEP) and bicarbonate, in the presence of Mg2+ [  1.	transcription
55577	2	334980	6	NULL	NULL	0	NULL	PEP			is					phosphoenolpyruvate					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1546_1_242_s_4	11257527	1.31) catalyzes the essentially irreversible formation of oxaloacetate and inorganic phosphate from phosphoenolpyruvate (PEP) and bicarbonate, in the presence of Mg2+ [  1.	transcription
55578	3	334980	6	NULL	NULL	0	NULL	bicarbonate			forms					oxaloacetate					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1546_1_242_s_4	11257527	1.31) catalyzes the essentially irreversible formation of oxaloacetate and inorganic phosphate from phosphoenolpyruvate (PEP) and bicarbonate, in the presence of Mg2+ [  1.	transcription
55579	4	334980	6	NULL	NULL	0	NULL	statement 1			occurs in the presence of					Mg2+					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1546_1_242_s_4	11257527	1.31) catalyzes the essentially irreversible formation of oxaloacetate and inorganic phosphate from phosphoenolpyruvate (PEP) and bicarbonate, in the presence of Mg2+ [  1.	transcription
55580	5	334980	6	NULL	NULL	0	NULL	statement 3			occurs in the presence of					Mg2+					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1546_1_242_s_4	11257527	1.31) catalyzes the essentially irreversible formation of oxaloacetate and inorganic phosphate from phosphoenolpyruvate (PEP) and bicarbonate, in the presence of Mg2+ [  1.	transcription
52684	1	334981	5	NULL	NULL	0	NULL	HCO3	NULL		is fixed to	NULL				phosphoenolpyruvate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27917_s_11	10871630	1.31; PEPC)1 catalyzes the fixation of HCO3  to the receptor phosphoenolpyruvate resulting in the formation of oxaloacetate and inorganic phosphate.	transcription
52685	2	334981	5	NULL	NULL	0	NULL	phosphoenolpyruvate	NULL		is a type of	NULL				receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27917_s_11	10871630	1.31; PEPC)1 catalyzes the fixation of HCO3  to the receptor phosphoenolpyruvate resulting in the formation of oxaloacetate and inorganic phosphate.	transcription
52686	3	334981	5	NULL	NULL	0	NULL	PEPC	NULL		catalyzes	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27917_s_11	10871630	1.31; PEPC)1 catalyzes the fixation of HCO3  to the receptor phosphoenolpyruvate resulting in the formation of oxaloacetate and inorganic phosphate.	transcription
52687	4	334981	5	NULL	NULL	0	NULL	statement 3	NULL		results in	NULL				oxaloacetate	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27917_s_11	10871630	1.31; PEPC)1 catalyzes the fixation of HCO3  to the receptor phosphoenolpyruvate resulting in the formation of oxaloacetate and inorganic phosphate.	transcription
52688	5	334981	5	NULL	NULL	0	NULL	statement 3	NULL		results in	NULL				inorganic phosphate	NULL	formation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27917_s_11	10871630	1.31; PEPC)1 catalyzes the fixation of HCO3  to the receptor phosphoenolpyruvate resulting in the formation of oxaloacetate and inorganic phosphate.	transcription
52689	6	334981	5	NULL	NULL	0	NULL	statement 4	NULL		occurs along with	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27917_s_11	10871630	1.31; PEPC)1 catalyzes the fixation of HCO3  to the receptor phosphoenolpyruvate resulting in the formation of oxaloacetate and inorganic phosphate.	transcription
55581	1	334981	6	NULL	NULL	0	NULL	HCO3			fixes					phosphoenolpyruvate receptor					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27917_s_11	10871630	1.31; PEPC)1 catalyzes the fixation of HCO3  to the receptor phosphoenolpyruvate resulting in the formation of oxaloacetate and inorganic phosphate.	transcription
55582	2	334981	6	NULL	NULL	0	NULL	PEPC1			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27917_s_11	10871630	1.31; PEPC)1 catalyzes the fixation of HCO3  to the receptor phosphoenolpyruvate resulting in the formation of oxaloacetate and inorganic phosphate.	transcription
55583	3	334981	6	NULL	NULL	0	NULL	statement 1			results in 					oxaloacetate		formation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27917_s_11	10871630	1.31; PEPC)1 catalyzes the fixation of HCO3  to the receptor phosphoenolpyruvate resulting in the formation of oxaloacetate and inorganic phosphate.	transcription
55584	4	334981	6	NULL	NULL	0	NULL	statement 1			results in					inorganic phosphate		formation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27917_s_11	10871630	1.31; PEPC)1 catalyzes the fixation of HCO3  to the receptor phosphoenolpyruvate resulting in the formation of oxaloacetate and inorganic phosphate.	transcription
58489	1	334983	5	NULL	NULL	0	NULL	C4-decarboxylating backflux			occurs from					TCA cycle					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_12_5843_s_265	12450803	It is known that  C. glutamicum has several enzymes, such as phosphoenolpyruvate carboxykinase and oxaloacetate decarboxylase, that catalyze a C4-decarboxylating backflux from the TCA cycle to glycolysis ( 14).	transcription
58490	2	334983	5	NULL	NULL	0	NULL	C4-decarboxylating backflux			to					glycolysis					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_12_5843_s_265	12450803	It is known that  C. glutamicum has several enzymes, such as phosphoenolpyruvate carboxykinase and oxaloacetate decarboxylase, that catalyze a C4-decarboxylating backflux from the TCA cycle to glycolysis ( 14).	transcription
58491	3	334983	5	NULL	NULL	0	NULL	statement 1			occurs along with					statement 2					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_12_5843_s_265	12450803	It is known that  C. glutamicum has several enzymes, such as phosphoenolpyruvate carboxykinase and oxaloacetate decarboxylase, that catalyze a C4-decarboxylating backflux from the TCA cycle to glycolysis ( 14).	transcription
58492	4	334983	5	NULL	NULL	0	NULL	phosphoenolpyruvate carboxykinase		C. glutamicum	catalyzes					statement 3					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_12_5843_s_265	12450803	It is known that  C. glutamicum has several enzymes, such as phosphoenolpyruvate carboxykinase and oxaloacetate decarboxylase, that catalyze a C4-decarboxylating backflux from the TCA cycle to glycolysis ( 14).	transcription
58493	5	334983	5	NULL	NULL	0	NULL	oxaloacetate decarboxylase		C. glutamicum	catalyzes					statement 3					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_12_5843_s_265	12450803	It is known that  C. glutamicum has several enzymes, such as phosphoenolpyruvate carboxykinase and oxaloacetate decarboxylase, that catalyze a C4-decarboxylating backflux from the TCA cycle to glycolysis ( 14).	transcription
55585	1	334983	6	NULL	NULL	0	NULL	phosphoenolpyruvate carboxykinase			catalyze					C4-decarboxylating backflux					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_12_5843_s_265	12450803	It is known that  C. glutamicum has several enzymes, such as phosphoenolpyruvate carboxykinase and oxaloacetate decarboxylase, that catalyze a C4-decarboxylating backflux from the TCA cycle to glycolysis ( 14).	transcription
55586	2	334983	6	NULL	NULL	0	NULL	statement 1			occurs from					TCA cycle					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_12_5843_s_265	12450803	It is known that  C. glutamicum has several enzymes, such as phosphoenolpyruvate carboxykinase and oxaloacetate decarboxylase, that catalyze a C4-decarboxylating backflux from the TCA cycle to glycolysis ( 14).	transcription
55587	3	334983	6	NULL	NULL	0	NULL	statement 1			occurs to					glycolysis					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_12_5843_s_265	12450803	It is known that  C. glutamicum has several enzymes, such as phosphoenolpyruvate carboxykinase and oxaloacetate decarboxylase, that catalyze a C4-decarboxylating backflux from the TCA cycle to glycolysis ( 14).	transcription
55588	4	334983	6	NULL	NULL	0	NULL	oxaloacetate decarboxylase			catalyze					C4-decarboxylating backflux					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_12_5843_s_265	12450803	It is known that  C. glutamicum has several enzymes, such as phosphoenolpyruvate carboxykinase and oxaloacetate decarboxylase, that catalyze a C4-decarboxylating backflux from the TCA cycle to glycolysis ( 14).	transcription
52690	1	334984	5	NULL	NULL	0	NULL	PEP	NULL		is	NULL				phosphoenolpyruvate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_17238_s_14	16624802	It catalyzes the irreversible, biotin-independent carboxylation of phosphoenolpyruvate (PEP) in the presence of   and Mg2+ (or Mn2+) to yield Pi and oxaloacetate and, thus, is involved intimately in photosynthetic and/or anaplerotic C4 dicarboxylic acid metabolism in these organisms.	transcription
52691	2	334984	5	NULL	NULL	0	NULL	PEP	NULL		undergoes	NULL				carboxylation	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_17238_s_14	16624802	It catalyzes the irreversible, biotin-independent carboxylation of phosphoenolpyruvate (PEP) in the presence of   and Mg2+ (or Mn2+) to yield Pi and oxaloacetate and, thus, is involved intimately in photosynthetic and/or anaplerotic C4 dicarboxylic acid metabolism in these organisms.	transcription
52692	3	334984	5	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				biotin	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_17238_s_14	16624802	It catalyzes the irreversible, biotin-independent carboxylation of phosphoenolpyruvate (PEP) in the presence of   and Mg2+ (or Mn2+) to yield Pi and oxaloacetate and, thus, is involved intimately in photosynthetic and/or anaplerotic C4 dicarboxylic acid metabolism in these organisms.	transcription
52693	4	334984	5	NULL	NULL	0	NULL	statement 2	NULL		in the presence of	NULL				Mg2+	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_17238_s_14	16624802	It catalyzes the irreversible, biotin-independent carboxylation of phosphoenolpyruvate (PEP) in the presence of   and Mg2+ (or Mn2+) to yield Pi and oxaloacetate and, thus, is involved intimately in photosynthetic and/or anaplerotic C4 dicarboxylic acid metabolism in these organisms.	transcription
52694	5	334984	5	NULL	NULL	0	NULL	statement 2	NULL		in the presence of	NULL				Mn2+	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_17238_s_14	16624802	It catalyzes the irreversible, biotin-independent carboxylation of phosphoenolpyruvate (PEP) in the presence of   and Mg2+ (or Mn2+) to yield Pi and oxaloacetate and, thus, is involved intimately in photosynthetic and/or anaplerotic C4 dicarboxylic acid metabolism in these organisms.	transcription
52695	6	334984	5	NULL	NULL	0	NULL	statement 4	NULL		is an alternative to	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_17238_s_14	16624802	It catalyzes the irreversible, biotin-independent carboxylation of phosphoenolpyruvate (PEP) in the presence of   and Mg2+ (or Mn2+) to yield Pi and oxaloacetate and, thus, is involved intimately in photosynthetic and/or anaplerotic C4 dicarboxylic acid metabolism in these organisms.	transcription
52696	7	334984	5	NULL	NULL	0	NULL	statement 2	NULL		yields	NULL				oxaloacetate	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_17238_s_14	16624802	It catalyzes the irreversible, biotin-independent carboxylation of phosphoenolpyruvate (PEP) in the presence of   and Mg2+ (or Mn2+) to yield Pi and oxaloacetate and, thus, is involved intimately in photosynthetic and/or anaplerotic C4 dicarboxylic acid metabolism in these organisms.	transcription
52697	8	334984	5	NULL	NULL	0	NULL	statement 2	NULL		yields	NULL				Pi	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_17238_s_14	16624802	It catalyzes the irreversible, biotin-independent carboxylation of phosphoenolpyruvate (PEP) in the presence of   and Mg2+ (or Mn2+) to yield Pi and oxaloacetate and, thus, is involved intimately in photosynthetic and/or anaplerotic C4 dicarboxylic acid metabolism in these organisms.	transcription
52698	9	334984	5	NULL	NULL	0	NULL	statement 7	NULL		occurs along with	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_17238_s_14	16624802	It catalyzes the irreversible, biotin-independent carboxylation of phosphoenolpyruvate (PEP) in the presence of   and Mg2+ (or Mn2+) to yield Pi and oxaloacetate and, thus, is involved intimately in photosynthetic and/or anaplerotic C4 dicarboxylic acid metabolism in these organisms.	transcription
52699	10	334984	5	NULL	NULL	0	NULL	statement 2	NULL		is involved in	NULL	intimately			photosynthetic C4 dicarboxylic acid metabolism	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_17238_s_14	16624802	It catalyzes the irreversible, biotin-independent carboxylation of phosphoenolpyruvate (PEP) in the presence of   and Mg2+ (or Mn2+) to yield Pi and oxaloacetate and, thus, is involved intimately in photosynthetic and/or anaplerotic C4 dicarboxylic acid metabolism in these organisms.	transcription
52700	11	334984	5	NULL	NULL	0	NULL	statement 2	NULL		is involved in	NULL	intimately			anaplerotic C4 dicarboxylic acid metabolism	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_17238_s_14	16624802	It catalyzes the irreversible, biotin-independent carboxylation of phosphoenolpyruvate (PEP) in the presence of   and Mg2+ (or Mn2+) to yield Pi and oxaloacetate and, thus, is involved intimately in photosynthetic and/or anaplerotic C4 dicarboxylic acid metabolism in these organisms.	transcription
55589	1	334985	6	NULL	NULL	0	NULL	PEP			forms		reversibly			oxaloacetate					NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_biochimie_88_6_16469427_s_2	16469427	Saccharomyces cerevisiae phosphoenolpyruvate (PEP) carboxykinase catalyzes  the reversible formation of oxaloacetate and adenosine triphosphate from  PEP, adenosine diphosphate and carbon dioxide, and uses Mn(2+) as the  activating metal ion.	transcription
55590	2	334985	6	NULL	NULL	0	NULL	PEP			forms		reversibly			adenosine triphosphate					NULL		NULL	NULL	NULL	NULL	abs-batch0740-0759_biochimie_88_6_16469427_s_2	16469427	Saccharomyces cerevisiae phosphoenolpyruvate (PEP) carboxykinase catalyzes  the reversible formation of oxaloacetate and adenosine triphosphate from  PEP, adenosine diphosphate and carbon dioxide, and uses Mn(2+) as the  activating metal ion.	transcription
55591	3	334985	6	NULL	NULL	0	NULL	PEP carboxykinase 			catalyzes					statement 1					NULL	Saccharomyces cerevisiae	0	NULL	NULL	NULL	abs-batch0740-0759_biochimie_88_6_16469427_s_2	16469427	Saccharomyces cerevisiae phosphoenolpyruvate (PEP) carboxykinase catalyzes  the reversible formation of oxaloacetate and adenosine triphosphate from  PEP, adenosine diphosphate and carbon dioxide, and uses Mn(2+) as the  activating metal ion.	transcription
55592	4	334985	6	NULL	NULL	0	NULL	PEP carboxykinase			catalyzes					statement 2					NULL	Saccharomyces cerevisiae	NULL	NULL	NULL	NULL	abs-batch0740-0759_biochimie_88_6_16469427_s_2	16469427	Saccharomyces cerevisiae phosphoenolpyruvate (PEP) carboxykinase catalyzes  the reversible formation of oxaloacetate and adenosine triphosphate from  PEP, adenosine diphosphate and carbon dioxide, and uses Mn(2+) as the  activating metal ion.	transcription
55593	5	334985	6	NULL	NULL	0	NULL	statement 1			occurs simultaneously with					statement 2					NULL		0	NULL	NULL	NULL	abs-batch0740-0759_biochimie_88_6_16469427_s_2	16469427	Saccharomyces cerevisiae phosphoenolpyruvate (PEP) carboxykinase catalyzes  the reversible formation of oxaloacetate and adenosine triphosphate from  PEP, adenosine diphosphate and carbon dioxide, and uses Mn(2+) as the  activating metal ion.	transcription
52706	1	334987	5	NULL	NULL	0	NULL	PC	NULL		interacts with	NULL				cholesterol	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_chem-phys-lipids_22_3_719817_s_3	719817	The interactions of these  PC with cholesterol or desmosterol were studied.	transcription
52707	2	334987	5	NULL	NULL	0	NULL	PC	NULL		interacts with	NULL				desmosterol	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_chem-phys-lipids_22_3_719817_s_3	719817	The interactions of these  PC with cholesterol or desmosterol were studied.	transcription
55594	1	334987	6	NULL	NULL	0	NULL	PC			interacts with					cholesterol					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_chem-phys-lipids_22_3_719817_s_3	719817	The interactions of these  PC with cholesterol or desmosterol were studied.	transcription
55595	2	334987	6	NULL	NULL	0	NULL	PC			interacts with					desmosterol					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_chem-phys-lipids_22_3_719817_s_3	719817	The interactions of these  PC with cholesterol or desmosterol were studied.	transcription
52708	1	334988	5	NULL	NULL	0	NULL	IR	NULL	ligand-bound	associate with	NULL	selectively			DRMs	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_348_s_239	16249181	This may be related to the weaker membrane-ordering properties of desmosterol as suggested by the selective association of the ligand-bound IR with DRMs in the presence of cholesterol.	transcription
52709	2	334988	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				cholesterol	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_348_s_239	16249181	This may be related to the weaker membrane-ordering properties of desmosterol as suggested by the selective association of the ligand-bound IR with DRMs in the presence of cholesterol.	transcription
55596	1	334988	6	NULL	NULL	0	NULL	IR		ligand bound	interacts with					DRMs					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_348_s_239	16249181	This may be related to the weaker membrane-ordering properties of desmosterol as suggested by the selective association of the ligand-bound IR with DRMs in the presence of cholesterol.	transcription
55597	2	334988	6	NULL	NULL	0	NULL	statement 1			occurs in the presence of					cholesterol					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_348_s_239	16249181	This may be related to the weaker membrane-ordering properties of desmosterol as suggested by the selective association of the ligand-bound IR with DRMs in the presence of cholesterol.	transcription
52710	1	334989	5	NULL	NULL	0	NULL	IR	NULL	ligand-occupied	associate with	NULL				DRMs	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_348_s_234	16249181	To study whether desmosterol interfered with the association of the ligand-occupied IR with DRMs, we stimulated cholesterol- or desmosterol-repleted HuH7 with insulin, lysed the cells in cold Triton X-100, and fractionated the material in an Optiprep gradient as described previously ( ).	transcription
52711	2	334989	5	NULL	NULL	0	NULL	desmosterol	NULL		interfere with	NULL	possibly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_348_s_234	16249181	To study whether desmosterol interfered with the association of the ligand-occupied IR with DRMs, we stimulated cholesterol- or desmosterol-repleted HuH7 with insulin, lysed the cells in cold Triton X-100, and fractionated the material in an Optiprep gradient as described previously ( ).	transcription
52712	1	334990	5	NULL	NULL	0	NULL	LXR	NULL		activates	NULL				stigmasterol	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_38_27816_s_264	16857673	We found that unsaturation of the cholesterol side chain was necessary and sufficient for the LXR-activating effects of stigmasterol: the presence of a double bond at C-20, C-22, and C-24 of cholesterol was associated with activation of LXR, with the delta24 bond in desmosterol having the most potent effect ( Fig. 2 B).	transcription
52713	2	334990	5	NULL	NULL	0	NULL	cholesterol	NULL	unsaturation of;;side chain of	is necessary for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_38_27816_s_264	16857673	We found that unsaturation of the cholesterol side chain was necessary and sufficient for the LXR-activating effects of stigmasterol: the presence of a double bond at C-20, C-22, and C-24 of cholesterol was associated with activation of LXR, with the delta24 bond in desmosterol having the most potent effect ( Fig. 2 B).	transcription
52714	3	334990	5	NULL	NULL	0	NULL	cholesterol	NULL	unsaturation of;;side chain of	is sufficient for	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_38_27816_s_264	16857673	We found that unsaturation of the cholesterol side chain was necessary and sufficient for the LXR-activating effects of stigmasterol: the presence of a double bond at C-20, C-22, and C-24 of cholesterol was associated with activation of LXR, with the delta24 bond in desmosterol having the most potent effect ( Fig. 2 B).	transcription
55598	1	334990	6	NULL	NULL	0	NULL	LXR			activates					stigmasterol					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_38_27816_s_264	16857673	We found that unsaturation of the cholesterol side chain was necessary and sufficient for the LXR-activating effects of stigmasterol: the presence of a double bond at C-20, C-22, and C-24 of cholesterol was associated with activation of LXR, with the delta24 bond in desmosterol having the most potent effect ( Fig. 2 B).	transcription
55599	2	334990	6	NULL	NULL	0	NULL	cholesterol		unsaturation of	is necessary for			side chain		statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_38_27816_s_264	16857673	We found that unsaturation of the cholesterol side chain was necessary and sufficient for the LXR-activating effects of stigmasterol: the presence of a double bond at C-20, C-22, and C-24 of cholesterol was associated with activation of LXR, with the delta24 bond in desmosterol having the most potent effect ( Fig. 2 B).	transcription
52715	1	334992	5	NULL	NULL	0	NULL	taurine	NULL		inhibit	NULL				GlyRs	NULL	glycine current of	E53K;;D57K		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50151_s_136	14525990	Co-application of taurine in the presence of 5 mM glycine demonstrated that taurine inhibited the glycine current of the E53K and D57K GlyRs.	transcription
52716	2	334992	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				glycine	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50151_s_136	14525990	Co-application of taurine in the presence of 5 mM glycine demonstrated that taurine inhibited the glycine current of the E53K and D57K GlyRs.	transcription
55600	1	334992	6	NULL	NULL	0	NULL	GlyR			exhibits			E53K		glycine current					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_50_50151_s_136	14525990	Co-application of taurine in the presence of 5 mM glycine demonstrated that taurine inhibited the glycine current of the E53K and D57K GlyRs.	transcription
55601	2	334992	6	NULL	NULL	0	NULL	GlyR			exhibits			D57K		glycine current					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50151_s_136	14525990	Co-application of taurine in the presence of 5 mM glycine demonstrated that taurine inhibited the glycine current of the E53K and D57K GlyRs.	transcription
55602	3	334992	6	NULL	NULL	0	NULL	taurine			inhibits					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50151_s_136	14525990	Co-application of taurine in the presence of 5 mM glycine demonstrated that taurine inhibited the glycine current of the E53K and D57K GlyRs.	transcription
55603	4	334992	6	NULL	NULL	0	NULL	taurine			inhibits					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50151_s_136	14525990	Co-application of taurine in the presence of 5 mM glycine demonstrated that taurine inhibited the glycine current of the E53K and D57K GlyRs.	transcription
52717	1	334993	5	NULL	NULL	0	NULL	glycine	NULL		activates	NULL				current	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_136_4_629_s_136	12055142	Figure 5 illustrates that although ethanol significantly inhibited the glycine-activated current, decanol had virtually no effect on the glycine current.	transcription
52718	2	334993	5	NULL	NULL	0	NULL	ethanol	NULL		inhibit	NULL	significantly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_136_4_629_s_136	12055142	Figure 5 illustrates that although ethanol significantly inhibited the glycine-activated current, decanol had virtually no effect on the glycine current.	transcription
52719	3	334993	5	NULL	NULL	0	NULL	decanol	NULL		does not effect	NULL				glycine current	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_136_4_629_s_136	12055142	Figure 5 illustrates that although ethanol significantly inhibited the glycine-activated current, decanol had virtually no effect on the glycine current.	transcription
55604	1	334993	6	NULL	NULL	0	NULL	ethanol			inhibits					glycine-activated current					NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_136_4_629_s_136	12055142	Figure 5 illustrates that although ethanol significantly inhibited the glycine-activated current, decanol had virtually no effect on the glycine current.	transcription
55605	2	334993	6	NULL	NULL	0	NULL	decanol			has no effect on					glycine-activated current					NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_136_4_629_s_136	12055142	Figure 5 illustrates that although ethanol significantly inhibited the glycine-activated current, decanol had virtually no effect on the glycine current.	transcription
52720	1	334994	5	NULL	NULL	0	NULL	glycine	NULL		is a component within	NULL				GpA	NULL		dimerization motif		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_49_50864_s_235	15448134	Substitution of these glycines (an important component within the dimerization motif in GpA) with alanines did not affect dimerization of N1 in the TOX-CAT assay ( Fig. 5 B and not shown).	transcription
52721	2	334994	5	NULL	NULL	0	NULL	statement 1	NULL		is substituted with	NULL				alanine	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_49_50864_s_235	15448134	Substitution of these glycines (an important component within the dimerization motif in GpA) with alanines did not affect dimerization of N1 in the TOX-CAT assay ( Fig. 5 B and not shown).	transcription
52722	3	334994	5	NULL	NULL	0	NULL	statement 2	NULL		does not affect	NULL				N1	NULL	dimerization of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_49_50864_s_235	15448134	Substitution of these glycines (an important component within the dimerization motif in GpA) with alanines did not affect dimerization of N1 in the TOX-CAT assay ( Fig. 5 B and not shown).	transcription
52723	1	334996	5	NULL	NULL	0	NULL	glycine	NULL		induce	NULL				ADE1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_7072_s_160	14645232	Glycine induction of  ADE1 and  SHM2 was confirmed by Northern analysis ( Fig. 5).	transcription
52724	2	334996	5	NULL	NULL	0	NULL	glycine	NULL		induce	NULL				SHM2	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_7072_s_160	14645232	Glycine induction of  ADE1 and  SHM2 was confirmed by Northern analysis ( Fig. 5).	transcription
55606	1	334996	6	NULL	NULL	0	NULL	glycine			induces					ADE1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_7072_s_160	14645232	Glycine induction of  ADE1 and  SHM2 was confirmed by Northern analysis ( Fig. 5).	transcription
55607	2	334996	6	NULL	NULL	0	NULL	glycine			induces					SHM2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_7072_s_160	14645232	Glycine induction of  ADE1 and  SHM2 was confirmed by Northern analysis ( Fig. 5).	transcription
52725	1	334997	5	NULL	NULL	0	NULL	Wy-14,643	NULL		induce	NULL				cells	NULL	proliferation of			NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_119	9934846	Since dietary glycine has been shown to inhibit Wy-14,643-induced cell proliferation and TNFalpha production ( 5), Kupffer cells were incubated with glycine prior to stimulation with Wy-14,643 to test the hypothesis that glycine inhibits superoxide production.	transcription
52726	2	334997	5	NULL	NULL	0	NULL	Wy-14,643	NULL		induce	NULL				TNFalpha	NULL	production of			NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_119	9934846	Since dietary glycine has been shown to inhibit Wy-14,643-induced cell proliferation and TNFalpha production ( 5), Kupffer cells were incubated with glycine prior to stimulation with Wy-14,643 to test the hypothesis that glycine inhibits superoxide production.	transcription
52727	3	334997	5	NULL	NULL	0	NULL	glycine	NULL	dietary	inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_119	9934846	Since dietary glycine has been shown to inhibit Wy-14,643-induced cell proliferation and TNFalpha production ( 5), Kupffer cells were incubated with glycine prior to stimulation with Wy-14,643 to test the hypothesis that glycine inhibits superoxide production.	transcription
52728	4	334997	5	NULL	NULL	0	NULL	glycine	NULL	dietary	inhibit	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_119	9934846	Since dietary glycine has been shown to inhibit Wy-14,643-induced cell proliferation and TNFalpha production ( 5), Kupffer cells were incubated with glycine prior to stimulation with Wy-14,643 to test the hypothesis that glycine inhibits superoxide production.	transcription
52729	5	334997	5	NULL	NULL	0	NULL	glycine	NULL		inhibit	NULL	possibly			superoxide	NULL	production of			NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_119	9934846	Since dietary glycine has been shown to inhibit Wy-14,643-induced cell proliferation and TNFalpha production ( 5), Kupffer cells were incubated with glycine prior to stimulation with Wy-14,643 to test the hypothesis that glycine inhibits superoxide production.	transcription
55608	1	334997	6	NULL	NULL	0	NULL	Wy-14,643			induces					cell proliferation					NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_119	9934846	Since dietary glycine has been shown to inhibit Wy-14,643-induced cell proliferation and TNFalpha production ( 5), Kupffer cells were incubated with glycine prior to stimulation with Wy-14,643 to test the hypothesis that glycine inhibits superoxide production.	transcription
55609	2	334997	6	NULL	NULL	0	NULL	dietary glycine			inhibits					statement 1					NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_119	9934846	Since dietary glycine has been shown to inhibit Wy-14,643-induced cell proliferation and TNFalpha production ( 5), Kupffer cells were incubated with glycine prior to stimulation with Wy-14,643 to test the hypothesis that glycine inhibits superoxide production.	transcription
55610	3	334997	6	NULL	NULL	0	NULL	Wy-14,643			induces					TNFalpha		production of 			NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_119	9934846	Since dietary glycine has been shown to inhibit Wy-14,643-induced cell proliferation and TNFalpha production ( 5), Kupffer cells were incubated with glycine prior to stimulation with Wy-14,643 to test the hypothesis that glycine inhibits superoxide production.	transcription
55611	4	334997	6	NULL	NULL	0	NULL	dietary glycine			inhibits					statement 2					NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_119	9934846	Since dietary glycine has been shown to inhibit Wy-14,643-induced cell proliferation and TNFalpha production ( 5), Kupffer cells were incubated with glycine prior to stimulation with Wy-14,643 to test the hypothesis that glycine inhibits superoxide production.	transcription
52730	1	334999	5	NULL	NULL	0	NULL	zmgrp5	NULL		is	NULL				Zea mays glycine-rich protein 5	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_plant-cell-rep_25_8_16528565_s_3	16528565	zmgrp5 (Zea mays glycine-rich protein  5) encodes a 187 amino acid glycine-rich protein that displays developmentally  regulated silk-specific expression.	transcription
52731	2	334999	5	NULL	NULL	0	NULL	zmgrp5	NULL		encodes	NULL				187 amino acid glycine-rich protein	NULL				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_plant-cell-rep_25_8_16528565_s_3	16528565	zmgrp5 (Zea mays glycine-rich protein  5) encodes a 187 amino acid glycine-rich protein that displays developmentally  regulated silk-specific expression.	transcription
52732	3	334999	5	NULL	NULL	0	NULL	zmgrp5	NULL		displays	NULL				silk-specific expression	NULL	developmentally regulated			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_plant-cell-rep_25_8_16528565_s_3	16528565	zmgrp5 (Zea mays glycine-rich protein  5) encodes a 187 amino acid glycine-rich protein that displays developmentally  regulated silk-specific expression.	transcription
55612	1	334999	6	NULL	NULL	0	NULL	zmgrp5			is					Zea mays glycine-rich protein 5					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_plant-cell-rep_25_8_16528565_s_3	16528565	zmgrp5 (Zea mays glycine-rich protein  5) encodes a 187 amino acid glycine-rich protein that displays developmentally  regulated silk-specific expression.	transcription
55613	2	334999	6	NULL	NULL	0	NULL	zmgrp5			displays					silk-specific expression		developmentally regulated			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_plant-cell-rep_25_8_16528565_s_3	16528565	zmgrp5 (Zea mays glycine-rich protein  5) encodes a 187 amino acid glycine-rich protein that displays developmentally  regulated silk-specific expression.	transcription
55614	3	334999	6	NULL	NULL	0	NULL	zmgrp5			encodes					187 amino acid glycine-rich protein					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_plant-cell-rep_25_8_16528565_s_3	16528565	zmgrp5 (Zea mays glycine-rich protein  5) encodes a 187 amino acid glycine-rich protein that displays developmentally  regulated silk-specific expression.	transcription
52733	1	335000	5	NULL	NULL	0	NULL	glycine	NULL		has affinity for	NULL				NMDA receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_57_1_10_s_219	9630479	Moreover, our results support the model that the effect of glycine on desensitization is a result of the affinity of glycine for the NMDA receptor because the rank order of glycine's ability to inhibit desensitization matched the rank order of the affinity of glycine determined for each combination [ 12,  30] (cf.  Table 1,  Fig. 5).	transcription
52734	1	335002	5	NULL	NULL	0	NULL	CYT1	NULL		is a type of	NULL				respiratory gene	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_7072_s_137	14645232	The glycine induction of a representative respiratory gene  CYT1, encoding cytochrome  c1, was confirmed by separate Northern analysis ( Fig. 5).	transcription
52735	2	335002	5	NULL	NULL	0	NULL	glycine	NULL		induce	NULL				CYT1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_7072_s_137	14645232	The glycine induction of a representative respiratory gene  CYT1, encoding cytochrome  c1, was confirmed by separate Northern analysis ( Fig. 5).	transcription
52736	3	335002	5	NULL	NULL	0	NULL	CYT1	NULL		encodes	NULL				cytochrome c1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_7072_s_137	14645232	The glycine induction of a representative respiratory gene  CYT1, encoding cytochrome  c1, was confirmed by separate Northern analysis ( Fig. 5).	transcription
56035	1	335002	6	NULL	NULL	0	NULL	CYT1			encodes for					cytochrome c1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_7072_s_137	14645232	The glycine induction of a representative respiratory gene  CYT1, encoding cytochrome  c1, was confirmed by separate Northern analysis ( Fig. 5).	transcription
56036	2	335002	6	NULL	NULL	0	NULL	CYT1			is a type of					respiratory gene					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_7072_s_137	14645232	The glycine induction of a representative respiratory gene  CYT1, encoding cytochrome  c1, was confirmed by separate Northern analysis ( Fig. 5).	transcription
56037	3	335002	6	NULL	NULL	0	NULL	glycine			induces					CYT1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_7072_s_137	14645232	The glycine induction of a representative respiratory gene  CYT1, encoding cytochrome  c1, was confirmed by separate Northern analysis ( Fig. 5).	transcription
52737	1	335003	5	NULL	NULL	0	NULL	ODC	NULL		is involved in	NULL		Lys-69		pyridoxal 5''-phosphate	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_41_30896_s_149	16916800	To note that the residue Lys-69 that in ODC is involved in the binding of pyridoxal 5''-phosphate is conserved in human ODCp, but it is substituted by glycine in murine ODCp.	transcription
52738	2	335003	5	NULL	NULL	0	NULL	statement 1	NULL		is conserved in	NULL				ODCp	NULL	human			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_41_30896_s_149	16916800	To note that the residue Lys-69 that in ODC is involved in the binding of pyridoxal 5''-phosphate is conserved in human ODCp, but it is substituted by glycine in murine ODCp.	transcription
52739	3	335003	5	NULL	NULL	0	NULL	statement 1	NULL		is substituted by	NULL				ODCp	NULL	murine	glycine		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_41_30896_s_149	16916800	To note that the residue Lys-69 that in ODC is involved in the binding of pyridoxal 5''-phosphate is conserved in human ODCp, but it is substituted by glycine in murine ODCp.	transcription
56038	1	335003	6	NULL	NULL	0	NULL	ODC			is involved in			Lys-69		pyridoxal 5''-phosphate		binding of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_41_30896_s_149	16916800	To note that the residue Lys-69 that in ODC is involved in the binding of pyridoxal 5''-phosphate is conserved in human ODCp, but it is substituted by glycine in murine ODCp.	transcription
52740	1	335004	5	NULL	NULL	0	NULL	GABAA blockers	NULL		induce	NULL				TH-P	NULL	strong			NULL		0	NULL	NULL	NULL	gw70_jneurosci_24_17_4242_s_164	15115820	In the absence of TTX, the GABAA and glycine blockers induced strong TH-P ( Fig. 5 b,f,j).	transcription
52741	2	335004	5	NULL	NULL	0	NULL	glycine blockers	NULL		induce	NULL				TH-P	NULL	strong			NULL		0	NULL	NULL	NULL	gw70_jneurosci_24_17_4242_s_164	15115820	In the absence of TTX, the GABAA and glycine blockers induced strong TH-P ( Fig. 5 b,f,j).	transcription
52742	3	335004	5	NULL	NULL	0	NULL	statement 1	NULL		in the absence of	NULL				TTX	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_24_17_4242_s_164	15115820	In the absence of TTX, the GABAA and glycine blockers induced strong TH-P ( Fig. 5 b,f,j).	transcription
52743	4	335004	5	NULL	NULL	0	NULL	statement 2	NULL		in the absence of	NULL				TTX	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_24_17_4242_s_164	15115820	In the absence of TTX, the GABAA and glycine blockers induced strong TH-P ( Fig. 5 b,f,j).	transcription
56039	1	335004	6	NULL	NULL	0	NULL	GABAA blockers			induce					TH-P		strong			NULL		0	NULL	NULL	NULL	gw70_jneurosci_24_17_4242_s_164	15115820	In the absence of TTX, the GABAA and glycine blockers induced strong TH-P ( Fig. 5 b,f,j).	transcription
56040	2	335004	6	NULL	NULL	0	NULL	glycine blockers			induce					TH-P		strong			NULL		0	NULL	NULL	NULL	gw70_jneurosci_24_17_4242_s_164	15115820	In the absence of TTX, the GABAA and glycine blockers induced strong TH-P ( Fig. 5 b,f,j).	transcription
56041	3	335004	6	NULL	NULL	0	NULL	statement 1			occurs in absence of					TTX					NULL		0	NULL	NULL	NULL	gw70_jneurosci_24_17_4242_s_164	15115820	In the absence of TTX, the GABAA and glycine blockers induced strong TH-P ( Fig. 5 b,f,j).	transcription
52744	1	335005	5	NULL	NULL	0	NULL	E. coli GJ146 derivatives	NULL		contain	NULL				pAT1	NULL				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_162_2_241_s_96	9627959	Similarly,  E. coli GJ146 derivatives containing pAT1 and pAT7 also showed osmoprotective effect of glycine betaine ( Fig. 5).	transcription
52745	2	335005	5	NULL	NULL	0	NULL	E. coli GJ146 derivatives	NULL		contain	NULL				pAT7	NULL				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_162_2_241_s_96	9627959	Similarly,  E. coli GJ146 derivatives containing pAT1 and pAT7 also showed osmoprotective effect of glycine betaine ( Fig. 5).	transcription
52746	3	335005	5	NULL	NULL	0	NULL	statement 1	NULL		displays	NULL				glycine betaine	NULL	osmoprotective effect of			NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_162_2_241_s_96	9627959	Similarly,  E. coli GJ146 derivatives containing pAT1 and pAT7 also showed osmoprotective effect of glycine betaine ( Fig. 5).	transcription
52747	4	335005	5	NULL	NULL	0	NULL	statement 2	NULL		displays	NULL				glycine betaine	NULL	osmoprotective effect of			NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_162_2_241_s_96	9627959	Similarly,  E. coli GJ146 derivatives containing pAT1 and pAT7 also showed osmoprotective effect of glycine betaine ( Fig. 5).	transcription
56042	1	335005	6	NULL	NULL	0	NULL	glycine betaine			shows					osmoprotective effects					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_162_2_241_s_96	9627959	Similarly,  E. coli GJ146 derivatives containing pAT1 and pAT7 also showed osmoprotective effect of glycine betaine ( Fig. 5).	transcription
56043	2	335005	6	NULL	NULL	0	NULL	pAT1			is a type of					E.coli GJ146 derivative					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_162_2_241_s_96	9627959	Similarly,  E. coli GJ146 derivatives containing pAT1 and pAT7 also showed osmoprotective effect of glycine betaine ( Fig. 5).	transcription
56044	3	335005	6	NULL	NULL	0	NULL	pAT7			is a type of					E.coli GJ146 derivative					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_162_2_241_s_96	9627959	Similarly,  E. coli GJ146 derivatives containing pAT1 and pAT7 also showed osmoprotective effect of glycine betaine ( Fig. 5).	transcription
56045	4	335005	6	NULL	NULL	0	NULL	pAT1			shows					statement 1					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_162_2_241_s_96	9627959	Similarly,  E. coli GJ146 derivatives containing pAT1 and pAT7 also showed osmoprotective effect of glycine betaine ( Fig. 5).	transcription
56046	5	335005	6	NULL	NULL	0	NULL	pAT7			shows					statement 1					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_162_2_241_s_96	9627959	Similarly,  E. coli GJ146 derivatives containing pAT1 and pAT7 also showed osmoprotective effect of glycine betaine ( Fig. 5).	transcription
52748	1	335006	5	NULL	NULL	0	NULL	taurine	NULL	release of	is induced by	NULL				hyposmosis	NULL				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_1_s_104	10536255	The hyposmotically induced releases of taurine, glutamate, glycine or phosphoethanolamine were not affected by PMA ( Fig. 4,  Fig. 5 and  Fig. 6).	transcription
52749	2	335006	5	NULL	NULL	0	NULL	glutamate	NULL	release of	is induced by	NULL				hyposmosis	NULL				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_1_s_104	10536255	The hyposmotically induced releases of taurine, glutamate, glycine or phosphoethanolamine were not affected by PMA ( Fig. 4,  Fig. 5 and  Fig. 6).	transcription
52750	3	335006	5	NULL	NULL	0	NULL	glycine	NULL	release of	is induced by	NULL				hyposmosis	NULL				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_1_s_104	10536255	The hyposmotically induced releases of taurine, glutamate, glycine or phosphoethanolamine were not affected by PMA ( Fig. 4,  Fig. 5 and  Fig. 6).	transcription
52751	4	335006	5	NULL	NULL	0	NULL	phosphoethanolamine	NULL	release of	is induced by	NULL				hyposmosis	NULL				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_1_s_104	10536255	The hyposmotically induced releases of taurine, glutamate, glycine or phosphoethanolamine were not affected by PMA ( Fig. 4,  Fig. 5 and  Fig. 6).	transcription
52752	5	335006	5	NULL	NULL	0	NULL	PMA	NULL		does not affect	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_1_s_104	10536255	The hyposmotically induced releases of taurine, glutamate, glycine or phosphoethanolamine were not affected by PMA ( Fig. 4,  Fig. 5 and  Fig. 6).	transcription
52753	6	335006	5	NULL	NULL	0	NULL	PMA	NULL		does not affect	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_1_s_104	10536255	The hyposmotically induced releases of taurine, glutamate, glycine or phosphoethanolamine were not affected by PMA ( Fig. 4,  Fig. 5 and  Fig. 6).	transcription
52754	7	335006	5	NULL	NULL	0	NULL	PMA	NULL		does not affect	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_1_s_104	10536255	The hyposmotically induced releases of taurine, glutamate, glycine or phosphoethanolamine were not affected by PMA ( Fig. 4,  Fig. 5 and  Fig. 6).	transcription
52755	8	335006	5	NULL	NULL	0	NULL	PMA	NULL		does not affect	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_1_s_104	10536255	The hyposmotically induced releases of taurine, glutamate, glycine or phosphoethanolamine were not affected by PMA ( Fig. 4,  Fig. 5 and  Fig. 6).	transcription
56047	1	335006	6	NULL	NULL	0	NULL	hyposomosis			induces					taurine		release of			NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_1_s_104	10536255	The hyposmotically induced releases of taurine, glutamate, glycine or phosphoethanolamine were not affected by PMA ( Fig. 4,  Fig. 5 and  Fig. 6).	transcription
56048	2	335006	6	NULL	NULL	0	NULL	hyposomosis			induces					glutamate		release of			NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_1_s_104	10536255	The hyposmotically induced releases of taurine, glutamate, glycine or phosphoethanolamine were not affected by PMA ( Fig. 4,  Fig. 5 and  Fig. 6).	transcription
56049	3	335006	6	NULL	NULL	0	NULL	hyposomosis			induces					glycine		release of			NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_1_s_104	10536255	The hyposmotically induced releases of taurine, glutamate, glycine or phosphoethanolamine were not affected by PMA ( Fig. 4,  Fig. 5 and  Fig. 6).	transcription
56050	4	335006	6	NULL	NULL	0	NULL	hyposomosis			induces					phosphoethanolamine		release of			NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_1_s_104	10536255	The hyposmotically induced releases of taurine, glutamate, glycine or phosphoethanolamine were not affected by PMA ( Fig. 4,  Fig. 5 and  Fig. 6).	transcription
56051	5	335006	6	NULL	NULL	0	NULL	statement 1			is not affected by					PMA					NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_1_s_104	10536255	The hyposmotically induced releases of taurine, glutamate, glycine or phosphoethanolamine were not affected by PMA ( Fig. 4,  Fig. 5 and  Fig. 6).	transcription
56052	6	335006	6	NULL	NULL	0	NULL	statement 2			is not affected by					PMA					NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_1_s_104	10536255	The hyposmotically induced releases of taurine, glutamate, glycine or phosphoethanolamine were not affected by PMA ( Fig. 4,  Fig. 5 and  Fig. 6).	transcription
56053	7	335006	6	NULL	NULL	0	NULL	statement 3			is not affected by					PMA					NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_1_s_104	10536255	The hyposmotically induced releases of taurine, glutamate, glycine or phosphoethanolamine were not affected by PMA ( Fig. 4,  Fig. 5 and  Fig. 6).	transcription
56054	8	335006	6	NULL	NULL	0	NULL	statement 4			is not affected by					PMA					NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_1_s_104	10536255	The hyposmotically induced releases of taurine, glutamate, glycine or phosphoethanolamine were not affected by PMA ( Fig. 4,  Fig. 5 and  Fig. 6).	transcription
52756	1	335007	5	NULL	NULL	0	NULL	glycine	NULL		is added to	NULL				WY-14,643 diet	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_11_2075_s_97	10545408	The addition of 5% glycine to the WY-14,643 diet did not affect the development of preneoplastic foci in either of these groups.	transcription
52757	2	335007	5	NULL	NULL	0	NULL	statement 1	NULL		does not affect	NULL				preneoplastic foci	NULL	development of			NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_11_2075_s_97	10545408	The addition of 5% glycine to the WY-14,643 diet did not affect the development of preneoplastic foci in either of these groups.	transcription
52758	1	335008	5	NULL	NULL	0	NULL	glycine	NULL		inhibit	NULL				tumors	NULL	growth of;;large			NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_11_2075_s_181	10545408	In these studies, glycine inhibited the growth of larger tumors to a greater extent than smaller tumors (Figure 5  ).	transcription
52759	2	335008	5	NULL	NULL	0	NULL	glycine	NULL		inhibit	NULL				tumors	NULL	growth of;;small			NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_11_2075_s_181	10545408	In these studies, glycine inhibited the growth of larger tumors to a greater extent than smaller tumors (Figure 5  ).	transcription
52760	3	335008	5	NULL	NULL	0	NULL	statement 1	NULL		greater extent than	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_11_2075_s_181	10545408	In these studies, glycine inhibited the growth of larger tumors to a greater extent than smaller tumors (Figure 5  ).	transcription
56055	1	335008	6	NULL	NULL	0	NULL	glycine			inhibits					tumors		growth of;; larger			NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_11_2075_s_181	10545408	In these studies, glycine inhibited the growth of larger tumors to a greater extent than smaller tumors (Figure 5  ).	transcription
56056	2	335008	6	NULL	NULL	0	NULL	glycine			inhibits					tumors		growth of;; smaller			NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_11_2075_s_181	10545408	In these studies, glycine inhibited the growth of larger tumors to a greater extent than smaller tumors (Figure 5  ).	transcription
56057	3	335008	6	NULL	NULL	0	NULL	statement 1			is greater than					statement 2					NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_11_2075_s_181	10545408	In these studies, glycine inhibited the growth of larger tumors to a greater extent than smaller tumors (Figure 5  ).	transcription
52761	1	335009	5	NULL	NULL	0	NULL	Kupffer cells	NULL		produce	NULL				superoxide	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_120	9934846	Indeed, glycine prevented Wy-14,643-stimulated superoxide production by Kupffer cells (Figure 5  ).	transcription
52762	2	335009	5	NULL	NULL	0	NULL	Wy-14,643	NULL		stimulates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_120	9934846	Indeed, glycine prevented Wy-14,643-stimulated superoxide production by Kupffer cells (Figure 5  ).	transcription
52763	3	335009	5	NULL	NULL	0	NULL	glycine	NULL		prevents	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_120	9934846	Indeed, glycine prevented Wy-14,643-stimulated superoxide production by Kupffer cells (Figure 5  ).	transcription
56058	1	335009	6	NULL	NULL	0	NULL	Wy-14,643			stimulates					superoxide		production of			NULL	Kupffer cells	0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_120	9934846	Indeed, glycine prevented Wy-14,643-stimulated superoxide production by Kupffer cells (Figure 5  ).	transcription
56059	2	335009	6	NULL	NULL	0	NULL	glycine			prevents					statement 1					NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_120	9934846	Indeed, glycine prevented Wy-14,643-stimulated superoxide production by Kupffer cells (Figure 5  ).	transcription
52764	1	335010	5	NULL	NULL	0	NULL	proline porter II	NULL		is a type of	NULL				transporter	NULL				NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_230_s_2110	10066837	Insertion  proQ220::Tn 5 alters regulation of proline porter II, a transporter of proline and glycine betaine in  Escherichia coli.	transcription
52765	2	335010	5	NULL	NULL	0	NULL	proline porter II	NULL		transports	NULL				proline	NULL				NULL	Escherichia coli	0	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_230_s_2110	10066837	Insertion  proQ220::Tn 5 alters regulation of proline porter II, a transporter of proline and glycine betaine in  Escherichia coli.	transcription
52766	3	335010	5	NULL	NULL	0	NULL	proline porter II	NULL		transports	NULL				glycine betaine	NULL				NULL	Escherichia coli	0	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_230_s_2110	10066837	Insertion  proQ220::Tn 5 alters regulation of proline porter II, a transporter of proline and glycine betaine in  Escherichia coli.	transcription
52767	4	335010	5	NULL	NULL	0	NULL	proQ220::Tn 5	NULL	insertion of	alters	NULL				proline porter II	NULL	regulation of			NULL	Escherichia coli	NULL	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_230_s_2110	10066837	Insertion  proQ220::Tn 5 alters regulation of proline porter II, a transporter of proline and glycine betaine in  Escherichia coli.	transcription
56062	1	335010	6	NULL	NULL	0	NULL	proline porter II			is a type of					proline transporter					NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_230_s_2110	10066837	Insertion  proQ220::Tn 5 alters regulation of proline porter II, a transporter of proline and glycine betaine in  Escherichia coli.	transcription
56063	2	335010	6	NULL	NULL	0	NULL	proline porter II			is a type of					glycine betaine transporter					NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_230_s_2110	10066837	Insertion  proQ220::Tn 5 alters regulation of proline porter II, a transporter of proline and glycine betaine in  Escherichia coli.	transcription
56064	3	335010	6	NULL	NULL	0	NULL	proQ220::Tn 5		insertion of 	alters 					proline porter II		regulation of 			NULL		0	NULL	NULL	NULL	gw60_microbiolmolbiolr_63_1_230_s_2110	10066837	Insertion  proQ220::Tn 5 alters regulation of proline porter II, a transporter of proline and glycine betaine in  Escherichia coli.	transcription
52768	1	335011	5	NULL	NULL	0	NULL	E7	NULL		stimulates	NULL				VAI	NULL	expression of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4927_s_194	10373542	Indeed, substitution of the C24 residue to glycine is sufficient to abrogate the ability of E7 to stimulate VAI expression (lane 5).	transcription
52769	2	335011	5	NULL	NULL	0	NULL		NULL		is substituted to	NULL		C24 residue			NULL		glycine		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4927_s_194	10373542	Indeed, substitution of the C24 residue to glycine is sufficient to abrogate the ability of E7 to stimulate VAI expression (lane 5).	transcription
52770	3	335011	5	NULL	NULL	0	NULL	statement 2	NULL		abrogates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4927_s_194	10373542	Indeed, substitution of the C24 residue to glycine is sufficient to abrogate the ability of E7 to stimulate VAI expression (lane 5).	transcription
56065	1	335011	6	NULL	NULL	0	NULL	E7			stimulate					VAI		expression of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4927_s_194	10373542	Indeed, substitution of the C24 residue to glycine is sufficient to abrogate the ability of E7 to stimulate VAI expression (lane 5).	transcription
56066	2	335011	6	NULL	NULL	0	NULL			substitution of 	abrogates			C24		statement 1					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_7_4927_s_194	10373542	Indeed, substitution of the C24 residue to glycine is sufficient to abrogate the ability of E7 to stimulate VAI expression (lane 5).	transcription
52771	1	335012	5	NULL	NULL	0	NULL	GFRs	NULL	decrease in	is caused by	NULL				CsA	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_56_3_455_s_97	10462532	This effect appears specific for glycine, because dietary valine (5%) did not block decreases in GFRs caused by CsA.	transcription
52772	2	335012	5	NULL	NULL	0	NULL	valine	NULL	dietary	does not block	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_56_3_455_s_97	10462532	This effect appears specific for glycine, because dietary valine (5%) did not block decreases in GFRs caused by CsA.	transcription
56067	1	335012	6	NULL	NULL	0	NULL	CsA			causes					GFR		decrease in			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_56_3_455_s_97	10462532	This effect appears specific for glycine, because dietary valine (5%) did not block decreases in GFRs caused by CsA.	transcription
56068	2	335012	6	NULL	NULL	0	NULL			dietary 	does not block			valine		statement 1					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_56_3_455_s_97	10462532	This effect appears specific for glycine, because dietary valine (5%) did not block decreases in GFRs caused by CsA.	transcription
52773	1	335013	5	NULL	NULL	0	NULL	glycine	NULL	medium	effect	NULL	may			thymidylate	NULL	biosynthesis of			NULL	MCF-7 cells	0	NULL	NULL	NULL	gw60_jbiolchem_277_41_38381_s_194	12161434	The effect of medium glycine on thymidylate biosynthesis was determined for MCF-7 cells and MCF-7 cells that express GlyT (Fig.  5).	transcription
52774	2	335013	5	NULL	NULL	0	NULL	glycine	NULL	medium	effect	NULL	may			thymidylate	NULL	biosynthesis of			NULL	MCF-7 cells that express GlyT	0	NULL	NULL	NULL	gw60_jbiolchem_277_41_38381_s_194	12161434	The effect of medium glycine on thymidylate biosynthesis was determined for MCF-7 cells and MCF-7 cells that express GlyT (Fig.  5).	transcription
56069	1	335013	6	NULL	NULL	0	NULL	MCF-7 cells			express					GlyT					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_41_38381_s_194	12161434	The effect of medium glycine on thymidylate biosynthesis was determined for MCF-7 cells and MCF-7 cells that express GlyT (Fig.  5).	transcription
52775	1	335014	5	NULL	NULL	0	NULL	leucine	NULL	uptake of	is inhibited by	NULL				glycine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_28_19745_s_124	10391916	As shown in Fig.  5 a, the leucine uptake was inhibited by glycine and L-isomers of the neutral amino acids and histidine.	transcription
52776	2	335014	5	NULL	NULL	0	NULL	leucine	NULL	uptake of	is inhibited by	NULL				L-isomers of neutral amino acids	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_28_19745_s_124	10391916	As shown in Fig.  5 a, the leucine uptake was inhibited by glycine and L-isomers of the neutral amino acids and histidine.	transcription
52777	3	335014	5	NULL	NULL	0	NULL	leucine	NULL	uptake of	is inhibited by	NULL				histidine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_28_19745_s_124	10391916	As shown in Fig.  5 a, the leucine uptake was inhibited by glycine and L-isomers of the neutral amino acids and histidine.	transcription
56070	1	335014	6	NULL	NULL	0	NULL	glycine			inhibits					leucine		uptake of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_28_19745_s_124	10391916	As shown in Fig.  5 a, the leucine uptake was inhibited by glycine and L-isomers of the neutral amino acids and histidine.	transcription
56071	2	335014	6	NULL	NULL	0	NULL	histidine			inhibits					leucine		uptake of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_28_19745_s_124	10391916	As shown in Fig.  5 a, the leucine uptake was inhibited by glycine and L-isomers of the neutral amino acids and histidine.	transcription
52778	1	335015	5	NULL	NULL	0	NULL		NULL	MTSET modification of	increases	NULL	dramatically	R271C		glycine	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_8_2589_s_385	11306612	MTSET modification of R271C, A272C, S273C, L274C, and K276C dramatically increased the apparent glycine affinity (Fig.  5 B).	transcription
52779	2	335015	5	NULL	NULL	0	NULL		NULL	MTSET modification of	increases	NULL	dramatically	A272C		glycine	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_8_2589_s_385	11306612	MTSET modification of R271C, A272C, S273C, L274C, and K276C dramatically increased the apparent glycine affinity (Fig.  5 B).	transcription
52780	3	335015	5	NULL	NULL	0	NULL		NULL	MTSET modification of	increases	NULL	dramatically	S273C		glycine	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_8_2589_s_385	11306612	MTSET modification of R271C, A272C, S273C, L274C, and K276C dramatically increased the apparent glycine affinity (Fig.  5 B).	transcription
52781	4	335015	5	NULL	NULL	0	NULL		NULL	MTSET modification of	increases	NULL	dramatically	L274C		glycine	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_8_2589_s_385	11306612	MTSET modification of R271C, A272C, S273C, L274C, and K276C dramatically increased the apparent glycine affinity (Fig.  5 B).	transcription
52782	5	335015	5	NULL	NULL	0	NULL		NULL	MTSET modification of	increases	NULL	dramatically	K276C 		glycine	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_8_2589_s_385	11306612	MTSET modification of R271C, A272C, S273C, L274C, and K276C dramatically increased the apparent glycine affinity (Fig.  5 B).	transcription
56072	1	335015	6	NULL	NULL	0	NULL			modification of 	increases			R271C		glycine		affinity of 			NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_8_2589_s_385	11306612	MTSET modification of R271C, A272C, S273C, L274C, and K276C dramatically increased the apparent glycine affinity (Fig.  5 B).	transcription
56073	2	335015	6	NULL	NULL	0	NULL			modification of	increases			A272C		glycine		affinity of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_8_2589_s_385	11306612	MTSET modification of R271C, A272C, S273C, L274C, and K276C dramatically increased the apparent glycine affinity (Fig.  5 B).	transcription
56074	3	335015	6	NULL	NULL	0	NULL			modification of	increases			S273C		glycine		affinity of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_8_2589_s_385	11306612	MTSET modification of R271C, A272C, S273C, L274C, and K276C dramatically increased the apparent glycine affinity (Fig.  5 B).	transcription
56075	4	335015	6	NULL	NULL	0	NULL			modification of	increases			L274C		glycine		affinity of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_8_2589_s_385	11306612	MTSET modification of R271C, A272C, S273C, L274C, and K276C dramatically increased the apparent glycine affinity (Fig.  5 B).	transcription
56082	5	335015	6	NULL	NULL	0	NULL			modification of	increases			K276C		glycine		affinity of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_8_2589_s_385	11306612	MTSET modification of R271C, A272C, S273C, L274C, and K276C dramatically increased the apparent glycine affinity (Fig.  5 B).	transcription
52783	1	335016	5	NULL	NULL	0	NULL	L-threonine	NULL		is interconverted to	NULL				glycine	NULL				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_appl-microbiol-biotechnol_68_4_15726349_s_3	15726349	This aldolase is a pyridoxal 5''-phosphate-dependent enzyme  that stereospecifically catalyzes the interconversion of L-threonine to  glycine and acetaldehyde.	transcription
52784	2	335016	5	NULL	NULL	0	NULL	L-threonine	NULL		is interconverted to	NULL				acetaldehyde	NULL				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_appl-microbiol-biotechnol_68_4_15726349_s_3	15726349	This aldolase is a pyridoxal 5''-phosphate-dependent enzyme  that stereospecifically catalyzes the interconversion of L-threonine to  glycine and acetaldehyde.	transcription
56083	1	335016	6	NULL	NULL	0	NULL	L-threonine			is converted to					glycine					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_appl-microbiol-biotechnol_68_4_15726349_s_3	15726349	This aldolase is a pyridoxal 5''-phosphate-dependent enzyme  that stereospecifically catalyzes the interconversion of L-threonine to  glycine and acetaldehyde.	transcription
56084	2	335016	6	NULL	NULL	0	NULL	L-threonine			is converted to					acetaldehyde					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_appl-microbiol-biotechnol_68_4_15726349_s_3	15726349	This aldolase is a pyridoxal 5''-phosphate-dependent enzyme  that stereospecifically catalyzes the interconversion of L-threonine to  glycine and acetaldehyde.	transcription
56085	3	335016	6	NULL	NULL	0	NULL	pyridoxal 5''-phosphate-dependent enzyme			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_appl-microbiol-biotechnol_68_4_15726349_s_3	15726349	This aldolase is a pyridoxal 5''-phosphate-dependent enzyme  that stereospecifically catalyzes the interconversion of L-threonine to  glycine and acetaldehyde.	transcription
56086	4	335016	6	NULL	NULL	0	NULL	pyridoxal 5''-phosphate-dependent enzyme			catalyzes					statement 2					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_appl-microbiol-biotechnol_68_4_15726349_s_3	15726349	This aldolase is a pyridoxal 5''-phosphate-dependent enzyme  that stereospecifically catalyzes the interconversion of L-threonine to  glycine and acetaldehyde.	transcription
56087	5	335016	6	NULL	NULL	0	NULL	pyridoxal 5''-phosphate-dependent enzyme			is a type of					aldolase					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_appl-microbiol-biotechnol_68_4_15726349_s_3	15726349	This aldolase is a pyridoxal 5''-phosphate-dependent enzyme  that stereospecifically catalyzes the interconversion of L-threonine to  glycine and acetaldehyde.	transcription
52785	1	335017	5	NULL	NULL	0	NULL	NMDA receptors	NULL	activation of	requires	NULL				glycine	NULL	presence of			NULL		0	NULL	NULL	NULL	gw70_brainres_1020_1_178_s_146	15312801	Finally, the activation of NMDA receptors often requires the presence of glycine  [  15], but bath application of glycine (20  M) in these experiments produced no significant  changes in mean sEPSC amplitude or shape ( n=5).	transcription
56088	1	335017	6	NULL	NULL	0	NULL	NMDA receptor		activation of 	requires					glycine		presence of 			NULL		0	NULL	NULL	NULL	gw70_brainres_1020_1_178_s_146	15312801	Finally, the activation of NMDA receptors often requires the presence of glycine  [  15], but bath application of glycine (20  M) in these experiments produced no significant  changes in mean sEPSC amplitude or shape ( n=5).	transcription
52786	1	335018	5	NULL	NULL	0	NULL	currents	NULL		is induced by	NULL				glycine	NULL				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_69_3_991_s_149	16332990	As illustrated in  Fig. 6C, whereas the currents induced by 5 muM glycine were markedly enhanced by 300 nM THC, the  IGly level induced by 30 muM glycine remained unchanged in the presence of THC ( Fig. 6C).	transcription
52787	2	335018	5	NULL	NULL	0	NULL	THC	NULL		enhance	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_69_3_991_s_149	16332990	As illustrated in  Fig. 6C, whereas the currents induced by 5 muM glycine were markedly enhanced by 300 nM THC, the  IGly level induced by 30 muM glycine remained unchanged in the presence of THC ( Fig. 6C).	transcription
52788	3	335018	5	NULL	NULL	0	NULL	IGly	NULL	levels of	is induced by	NULL				glycine	NULL				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_69_3_991_s_149	16332990	As illustrated in  Fig. 6C, whereas the currents induced by 5 muM glycine were markedly enhanced by 300 nM THC, the  IGly level induced by 30 muM glycine remained unchanged in the presence of THC ( Fig. 6C).	transcription
52789	4	335018	5	NULL	NULL	0	NULL	THC	NULL		does not effect	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_69_3_991_s_149	16332990	As illustrated in  Fig. 6C, whereas the currents induced by 5 muM glycine were markedly enhanced by 300 nM THC, the  IGly level induced by 30 muM glycine remained unchanged in the presence of THC ( Fig. 6C).	transcription
56089	1	335018	6	NULL	NULL	0	NULL	glycine			induces					currents					NULL		0	NULL	NULL	NULL	gw70_molpharmacol_69_3_991_s_149	16332990	As illustrated in  Fig. 6C, whereas the currents induced by 5 muM glycine were markedly enhanced by 300 nM THC, the  IGly level induced by 30 muM glycine remained unchanged in the presence of THC ( Fig. 6C).	transcription
56090	2	335018	6	NULL	NULL	0	NULL	THC			enhances					statement 1					NULL		0	NULL	NULL	NULL	gw70_molpharmacol_69_3_991_s_149	16332990	As illustrated in  Fig. 6C, whereas the currents induced by 5 muM glycine were markedly enhanced by 300 nM THC, the  IGly level induced by 30 muM glycine remained unchanged in the presence of THC ( Fig. 6C).	transcription
52790	1	335019	5	NULL	NULL	0	NULL	MTX	NULL		induce	NULL				K+ 	NULL	release of			NULL		0	NULL	NULL	NULL	gw70_molpharmacol_66_4_909_s_213	15385641	We also tested the ability of MTX to induce K+ release in the presence or absence of glycine and found that 5 mM extracellular glycine did not affect the MTX-induced cation fluxes ( Fig. 5E).	transcription
52791	2	335019	5	NULL	NULL	0	NULL	MTX	NULL		induce	NULL				cation fluxes	NULL				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_66_4_909_s_213	15385641	We also tested the ability of MTX to induce K+ release in the presence or absence of glycine and found that 5 mM extracellular glycine did not affect the MTX-induced cation fluxes ( Fig. 5E).	transcription
52792	3	335019	5	NULL	NULL	0	NULL	glycine	NULL		does not affect	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_66_4_909_s_213	15385641	We also tested the ability of MTX to induce K+ release in the presence or absence of glycine and found that 5 mM extracellular glycine did not affect the MTX-induced cation fluxes ( Fig. 5E).	transcription
56091	1	335019	6	NULL	NULL	0	NULL	MTX			induces					cation flux					NULL		0	NULL	NULL	NULL	gw70_molpharmacol_66_4_909_s_213	15385641	We also tested the ability of MTX to induce K+ release in the presence or absence of glycine and found that 5 mM extracellular glycine did not affect the MTX-induced cation fluxes ( Fig. 5E).	transcription
56092	2	335019	6	NULL	NULL	0	NULL	glycine		extracellular	does not affect					statement 1					NULL		0	NULL	NULL	NULL	gw70_molpharmacol_66_4_909_s_213	15385641	We also tested the ability of MTX to induce K+ release in the presence or absence of glycine and found that 5 mM extracellular glycine did not affect the MTX-induced cation fluxes ( Fig. 5E).	transcription
52793	1	335020	5	NULL	NULL	0	NULL	glycine	NULL		activates	NULL				glycine receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_9_5883_s_277	11500467	These data are consistent with the hypothesis that glycine activates a glycine receptor (Fig.  5), leading to the influx of chloride which hyperpolarizes the macrophage membrane and decreases the opening time of voltage-dependent calcium channels.	transcription
52794	2	335020	5	NULL	NULL	0	NULL	statement 1	NULL		leads to	NULL				chloride	NULL	influx of			NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_9_5883_s_277	11500467	These data are consistent with the hypothesis that glycine activates a glycine receptor (Fig.  5), leading to the influx of chloride which hyperpolarizes the macrophage membrane and decreases the opening time of voltage-dependent calcium channels.	transcription
52795	3	335020	5	NULL	NULL	0	NULL	chloride	NULL		hyperpolarizes	NULL				macrophage membrane	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_9_5883_s_277	11500467	These data are consistent with the hypothesis that glycine activates a glycine receptor (Fig.  5), leading to the influx of chloride which hyperpolarizes the macrophage membrane and decreases the opening time of voltage-dependent calcium channels.	transcription
52796	4	335020	5	NULL	NULL	0	NULL	chloride	NULL		decreases	NULL				calcium channels	NULL	opening time of			NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_9_5883_s_277	11500467	These data are consistent with the hypothesis that glycine activates a glycine receptor (Fig.  5), leading to the influx of chloride which hyperpolarizes the macrophage membrane and decreases the opening time of voltage-dependent calcium channels.	transcription
52797	5	335020	5	NULL	NULL	0	NULL	calcium channels	NULL		is dependent on	NULL				voltage	NULL				NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_9_5883_s_277	11500467	These data are consistent with the hypothesis that glycine activates a glycine receptor (Fig.  5), leading to the influx of chloride which hyperpolarizes the macrophage membrane and decreases the opening time of voltage-dependent calcium channels.	transcription
56093	1	335020	6	NULL	NULL	0	NULL	glycine			activates					glycine receptor					NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_9_5883_s_277	11500467	These data are consistent with the hypothesis that glycine activates a glycine receptor (Fig.  5), leading to the influx of chloride which hyperpolarizes the macrophage membrane and decreases the opening time of voltage-dependent calcium channels.	transcription
56094	2	335020	6	NULL	NULL	0	NULL	statement 1			leads to					chloride		influx of 			NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_9_5883_s_277	11500467	These data are consistent with the hypothesis that glycine activates a glycine receptor (Fig.  5), leading to the influx of chloride which hyperpolarizes the macrophage membrane and decreases the opening time of voltage-dependent calcium channels.	transcription
56095	3	335020	6	NULL	NULL	0	NULL	chloride		influx of	hyperpolarizes					macrophage membrane					NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_9_5883_s_277	11500467	These data are consistent with the hypothesis that glycine activates a glycine receptor (Fig.  5), leading to the influx of chloride which hyperpolarizes the macrophage membrane and decreases the opening time of voltage-dependent calcium channels.	transcription
56096	4	335020	6	NULL	NULL	0	NULL	chloride		influx of	decreases					calcium channels		opening time;; voltage dependent			NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_9_5883_s_277	11500467	These data are consistent with the hypothesis that glycine activates a glycine receptor (Fig.  5), leading to the influx of chloride which hyperpolarizes the macrophage membrane and decreases the opening time of voltage-dependent calcium channels.	transcription
52798	1	335021	5	NULL	NULL	0	NULL	DCS	NULL	increased efficacy of	is elicited through	NULL	solely				NULL		glycine binding site		NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_41_2_151_s_155	11489451	Interestingly,  Fig. 5 also indicates that the increased efficacy of DCS in comparison to glycine controls for NMDA receptors containing NR2C subunits is elicited solely through the glycine binding site.	transcription
53350	1	335023	7	NULL	NULL	0	NULL	receptor glycine	NULL	affinity of	is reduced in	NULL				acutely dissociated hippocampal neurons	NULL				NULL	mice carrying Grin1 D481N mutations	NULL	NULL	NULL	NULL	gw60_jneurosci_20_11_4037_s_3	10818139	Glycine concentration-response curves from acutely dissociated hippocampal neurons revealed a 5- and 86-fold reduction in receptor glycine affinity in mice carrying  Grin1 D481N and  Grin1K483Qmutations, respectively, whereas receptor glutamate affinity remained unaffected.	transcription
53351	2	335023	7	NULL	NULL	0	NULL	receptor glycine	NULL	affinity of	reduced in	NULL				acutely dissociated hippocampal neurons	NULL				NULL	 mice carrying Grin1K483Qmutations	0	NULL	NULL	NULL	gw60_jneurosci_20_11_4037_s_3	10818139	Glycine concentration-response curves from acutely dissociated hippocampal neurons revealed a 5- and 86-fold reduction in receptor glycine affinity in mice carrying  Grin1 D481N and  Grin1K483Qmutations, respectively, whereas receptor glutamate affinity remained unaffected.	transcription
53352	3	335023	7	NULL	NULL	0	NULL	receptor glutamate	NULL	affinity of	is not affected in	NULL				 acutely dissociated hippocampal neurons	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_11_4037_s_3	10818139	Glycine concentration-response curves from acutely dissociated hippocampal neurons revealed a 5- and 86-fold reduction in receptor glycine affinity in mice carrying  Grin1 D481N and  Grin1K483Qmutations, respectively, whereas receptor glutamate affinity remained unaffected.	transcription
53368	1	335024	5	NULL	NULL	0	NULL	ischemia	NULL		induce	NULL				glycine	NULL	release of			NULL	in vitro	0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_553_s_69	15020253	The present finding that in vitro ischemia induces glycine release with an extent  comparable to that of GABA release demonstrates that no involvement of glycine receptors  in inhibiting the release of  -glutamate following in vitro ischemia [ 5] is due to the absence of presynaptic glycine receptors leading to the inhibition.	transcription
53369	2	335024	5	NULL	NULL	0	NULL	ischemia	NULL		induce	NULL				GABA	NULL	release of			NULL	in vitro	0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_553_s_69	15020253	The present finding that in vitro ischemia induces glycine release with an extent  comparable to that of GABA release demonstrates that no involvement of glycine receptors  in inhibiting the release of  -glutamate following in vitro ischemia [ 5] is due to the absence of presynaptic glycine receptors leading to the inhibition.	transcription
53370	3	335024	5	NULL	NULL	0	NULL	glutamate	NULL		is released following	NULL				ischemia	NULL				NULL	in vitro	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_553_s_69	15020253	The present finding that in vitro ischemia induces glycine release with an extent  comparable to that of GABA release demonstrates that no involvement of glycine receptors  in inhibiting the release of  -glutamate following in vitro ischemia [ 5] is due to the absence of presynaptic glycine receptors leading to the inhibition.	transcription
53371	4	335024	5	NULL	NULL	0	NULL	glycine receptors	NULL		is not involved in	NULL				statement 3	NULL	inhibition of			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_553_s_69	15020253	The present finding that in vitro ischemia induces glycine release with an extent  comparable to that of GABA release demonstrates that no involvement of glycine receptors  in inhibiting the release of  -glutamate following in vitro ischemia [ 5] is due to the absence of presynaptic glycine receptors leading to the inhibition.	transcription
53372	5	335024	5	NULL	NULL	0	NULL	presynaptic glycine receptors	NULL	absence of	leads to	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_553_s_69	15020253	The present finding that in vitro ischemia induces glycine release with an extent  comparable to that of GABA release demonstrates that no involvement of glycine receptors  in inhibiting the release of  -glutamate following in vitro ischemia [ 5] is due to the absence of presynaptic glycine receptors leading to the inhibition.	transcription
53139	1	335024	7	NULL	NULL	0	NULL	in vitro ischemia	NULL		induce	NULL				glycine	NULL	release of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_553_s_69	15020253	The present finding that in vitro ischemia induces glycine release with an extent  comparable to that of GABA release demonstrates that no involvement of glycine receptors  in inhibiting the release of  -glutamate following in vitro ischemia [ 5] is due to the absence of presynaptic glycine receptors leading to the inhibition.	transcription
53140	2	335024	7	NULL	NULL	0	NULL	in vitro ischemia	NULL		induce	NULL				GABA	NULL	release of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_553_s_69	15020253	The present finding that in vitro ischemia induces glycine release with an extent  comparable to that of GABA release demonstrates that no involvement of glycine receptors  in inhibiting the release of  -glutamate following in vitro ischemia [ 5] is due to the absence of presynaptic glycine receptors leading to the inhibition.	transcription
53141	3	335024	7	NULL	NULL	0	NULL	in vitro ischemia	NULL		release	NULL				glutamate	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_553_s_69	15020253	The present finding that in vitro ischemia induces glycine release with an extent  comparable to that of GABA release demonstrates that no involvement of glycine receptors  in inhibiting the release of  -glutamate following in vitro ischemia [ 5] is due to the absence of presynaptic glycine receptors leading to the inhibition.	transcription
53142	4	335024	7	NULL	NULL	0	NULL	glycine receptors	NULL		is not involved in	NULL				statement 3	NULL	inhibition of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_553_s_69	15020253	The present finding that in vitro ischemia induces glycine release with an extent  comparable to that of GABA release demonstrates that no involvement of glycine receptors  in inhibiting the release of  -glutamate following in vitro ischemia [ 5] is due to the absence of presynaptic glycine receptors leading to the inhibition.	transcription
53143	5	335024	7	NULL	NULL	0	NULL	statement 4	NULL		due to	NULL				presynaptic glycine receptors	NULL	absence of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_553_s_69	15020253	The present finding that in vitro ischemia induces glycine release with an extent  comparable to that of GABA release demonstrates that no involvement of glycine receptors  in inhibiting the release of  -glutamate following in vitro ischemia [ 5] is due to the absence of presynaptic glycine receptors leading to the inhibition.	transcription
53144	6	335024	7	NULL	NULL	0	NULL	statement 1	NULL		demonstrate	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_553_s_69	15020253	The present finding that in vitro ischemia induces glycine release with an extent  comparable to that of GABA release demonstrates that no involvement of glycine receptors  in inhibiting the release of  -glutamate following in vitro ischemia [ 5] is due to the absence of presynaptic glycine receptors leading to the inhibition.	transcription
53145	7	335024	7	NULL	NULL	0	NULL	statement 2	NULL		demonstrate	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_553_s_69	15020253	The present finding that in vitro ischemia induces glycine release with an extent  comparable to that of GABA release demonstrates that no involvement of glycine receptors  in inhibiting the release of  -glutamate following in vitro ischemia [ 5] is due to the absence of presynaptic glycine receptors leading to the inhibition.	transcription
53374	1	335026	5	NULL	NULL	0	NULL	Zn2+	NULL		inhibits	NULL	competitively			glycine receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_6_3234_s_101	10077667	In contrast, 100 muM Zn2+ did not affect the maximum glycine responses, but it acted as a competitive inhibitor for glycine receptors, lowered the apparent glycine affinity, and shifted EC50 to the right (Fig.  5 B; EC50,Ctr = 40 muM, EC50,Zn2+ = 74 muM).	transcription
53375	2	335026	5	NULL	NULL	0	NULL	Zn2+	NULL		lowers	NULL				glycine	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_pnas_96_6_3234_s_101	10077667	In contrast, 100 muM Zn2+ did not affect the maximum glycine responses, but it acted as a competitive inhibitor for glycine receptors, lowered the apparent glycine affinity, and shifted EC50 to the right (Fig.  5 B; EC50,Ctr = 40 muM, EC50,Zn2+ = 74 muM).	transcription
53146	1	335026	7	NULL	NULL	0	NULL	Zn2+	NULL		inhibits	NULL	competitively			glycine receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_6_3234_s_101	10077667	In contrast, 100 muM Zn2+ did not affect the maximum glycine responses, but it acted as a competitive inhibitor for glycine receptors, lowered the apparent glycine affinity, and shifted EC50 to the right (Fig.  5 B; EC50,Ctr = 40 muM, EC50,Zn2+ = 74 muM).	transcription
53147	2	335026	7	NULL	NULL	0	NULL	Zn2+	NULL		lowers	NULL				glycine affinity	NULL				NULL		0	NULL	NULL	NULL	gw60_pnas_96_6_3234_s_101	10077667	In contrast, 100 muM Zn2+ did not affect the maximum glycine responses, but it acted as a competitive inhibitor for glycine receptors, lowered the apparent glycine affinity, and shifted EC50 to the right (Fig.  5 B; EC50,Ctr = 40 muM, EC50,Zn2+ = 74 muM).	transcription
53376	1	335027	5	NULL	NULL	0	NULL	trigonelline	NULL		inhibits	NULL				LTG59 strain	NULL	growth of			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_11_5647_s_124	12406761	The growth of strain LTG59 was inhibited by both 5 mM trigonelline and 5 mM triethylglycine in the presence of 100 muM glycine betaine (Table  2).	transcription
53377	2	335027	5	NULL	NULL	0	NULL	triethylglycine	NULL		inhibits	NULL				LTG59 strain	NULL	growth of			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_11_5647_s_124	12406761	The growth of strain LTG59 was inhibited by both 5 mM trigonelline and 5 mM triethylglycine in the presence of 100 muM glycine betaine (Table  2).	transcription
53378	3	335027	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				glycine betaine	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_11_5647_s_124	12406761	The growth of strain LTG59 was inhibited by both 5 mM trigonelline and 5 mM triethylglycine in the presence of 100 muM glycine betaine (Table  2).	transcription
53379	4	335027	5	NULL	NULL	0	NULL	statement 2	NULL		in the presence of	NULL				glycine betaine	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_11_5647_s_124	12406761	The growth of strain LTG59 was inhibited by both 5 mM trigonelline and 5 mM triethylglycine in the presence of 100 muM glycine betaine (Table  2).	transcription
53148	1	335027	7	NULL	NULL	0	NULL	 trigonelline	NULL		inhibit	NULL				 LTG59	NULL	growth of			NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_68_11_5647_s_124	12406761	The growth of strain LTG59 was inhibited by both 5 mM trigonelline and 5 mM triethylglycine in the presence of 100 muM glycine betaine (Table  2).	transcription
53149	2	335027	7	NULL	NULL	0	NULL	triethylglycine	NULL		inhibit	NULL				LTG59	NULL	growth of			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_11_5647_s_124	12406761	The growth of strain LTG59 was inhibited by both 5 mM trigonelline and 5 mM triethylglycine in the presence of 100 muM glycine betaine (Table  2).	transcription
53150	3	335027	7	NULL	NULL	0	NULL	statement 1	NULL		in presence of	NULL				glycine betaine	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_11_5647_s_124	12406761	The growth of strain LTG59 was inhibited by both 5 mM trigonelline and 5 mM triethylglycine in the presence of 100 muM glycine betaine (Table  2).	transcription
53151	4	335027	7	NULL	NULL	0	NULL	statement 2	NULL		in presence of	NULL				glycine betaine	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_11_5647_s_124	12406761	The growth of strain LTG59 was inhibited by both 5 mM trigonelline and 5 mM triethylglycine in the presence of 100 muM glycine betaine (Table  2).	transcription
53380	1	335029	5	NULL	NULL	0	NULL	proQ220::Tn 5	NULL	insertion of	alters	NULL				proline porter II	NULL	regulation of			NULL	Escherichia coli	NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_1_49_s_1573	12007642	J.L. Milner and J.M. Wood, Insertion  proQ220::Tn 5 alters regulation of proline porter II, a transporter of proline and glycine betaine  in  Escherichia coli.	transcription
53381	2	335029	5	NULL	NULL	0	NULL	proline porter II	NULL		is a transporter of	NULL				proline	NULL				NULL	Escherichia coli	0	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_1_49_s_1573	12007642	J.L. Milner and J.M. Wood, Insertion  proQ220::Tn 5 alters regulation of proline porter II, a transporter of proline and glycine betaine  in  Escherichia coli.	transcription
53382	3	335029	5	NULL	NULL	0	NULL	proline porter II	NULL		is a transporter of	NULL				glycine betaine	NULL				NULL	Escherichia coli	0	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_1_49_s_1573	12007642	J.L. Milner and J.M. Wood, Insertion  proQ220::Tn 5 alters regulation of proline porter II, a transporter of proline and glycine betaine  in  Escherichia coli.	transcription
53152	1	335029	7	NULL	NULL	0	NULL	 proQ220::Tn 5	NULL		alters	NULL				proline porter II	NULL	regulation of			NULL	Escherichia coli	0	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_1_49_s_1573	12007642	J.L. Milner and J.M. Wood, Insertion  proQ220::Tn 5 alters regulation of proline porter II, a transporter of proline and glycine betaine  in  Escherichia coli.	transcription
53153	2	335029	7	NULL	NULL	0	NULL	proline porter II	NULL		is a transporter of	NULL				proline	NULL				NULL	Escherichia coli	0	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_1_49_s_1573	12007642	J.L. Milner and J.M. Wood, Insertion  proQ220::Tn 5 alters regulation of proline porter II, a transporter of proline and glycine betaine  in  Escherichia coli.	transcription
53154	3	335029	7	NULL	NULL	0	NULL	proline porter II	NULL		is a transporter of	NULL				glycine betaine 	NULL				NULL	Escherichia coli	0	NULL	NULL	NULL	gw70_femsmicrobiolrev_26_1_49_s_1573	12007642	J.L. Milner and J.M. Wood, Insertion  proQ220::Tn 5 alters regulation of proline porter II, a transporter of proline and glycine betaine  in  Escherichia coli.	transcription
53383	1	335032	5	NULL	NULL	0	NULL	TNFalpha	NULL	secretion of	is induced by	NULL				LPS	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53384	2	335032	5	NULL	NULL	0	NULL	LCA	NULL		reduces	NULL	significantly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53385	3	335032	5	NULL	NULL	0	NULL	DCA	NULL		reduces	NULL	significantly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53386	4	335032	5	NULL	NULL	0	NULL	CDCA	NULL		reduces	NULL	significantly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53387	5	335032	5	NULL	NULL	0	NULL	taurine-conjugated LCA	NULL		reduces	NULL	significantly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53388	6	335032	5	NULL	NULL	0	NULL	taurine-conjugated DCA	NULL		reduces	NULL	significantly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53389	7	335032	5	NULL	NULL	0	NULL	taurine-conjugated CDCA	NULL		reduces	NULL	significantly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53390	8	335032	5	NULL	NULL	0	NULL	glycine-conjugated LCA	NULL		reduces	NULL	significantly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53391	9	335032	5	NULL	NULL	0	NULL	glycine-conjugated DCA	NULL		reduces	NULL	significantly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53392	10	335032	5	NULL	NULL	0	NULL	glycine-conjugated CDCA	NULL		reduces	NULL	significantly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53393	11	335032	5	NULL	NULL	0	NULL	statement 5	NULL		is an alternative to	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53394	12	335032	5	NULL	NULL	0	NULL	statement 6	NULL		is an alternative to	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53395	13	335032	5	NULL	NULL	0	NULL	statement 7	NULL		is an alternative to	NULL				statement 10	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53155	1	335032	7	NULL	NULL	0	NULL	LPS	NULL		induce	NULL				TNFalpha 	NULL	secretion of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53156	2	335032	7	NULL	NULL	0	NULL	LCA	NULL		reduce	NULL	significantly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53157	3	335032	7	NULL	NULL	0	NULL	DCA	NULL		reduce	NULL	significantly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53158	4	335032	7	NULL	NULL	0	NULL	CDCA	NULL		reduce	NULL	significantly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53159	5	335032	7	NULL	NULL	0	NULL	taurine-conjugated form	NULL		reduce	NULL	significantly			statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53160	6	335032	7	NULL	NULL	0	NULL	glycine-conjugated form	NULL		reduce	NULL	significantly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53161	7	335032	7	NULL	NULL	0	NULL	statement 5	NULL		is an alternative to	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_11_9435_s_137	12524422	Finally, LPS-induced TNFalpha secretion was significantly reduced with LCA, DCA, and CDCA and their taurine- or glycine-conjugated forms (Fig.  5 D).	transcription
53396	1	335033	5	NULL	NULL	0	NULL	Apg10p	NULL		interacts with	NULL				Apg12p	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_41_39517_s_108	12890687	These results indicate that the interaction of Apg10p with Apg12p in the presence of Apg7p is dependent on the carboxyl-terminal glycine of Apg12p that is essential for the conjugation reaction ( Fig. 2 A,  lane 5).	transcription
53397	2	335033	5	NULL	NULL	0	NULL	statement 1	NULL		in the presence of	NULL				Apg7p	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_41_39517_s_108	12890687	These results indicate that the interaction of Apg10p with Apg12p in the presence of Apg7p is dependent on the carboxyl-terminal glycine of Apg12p that is essential for the conjugation reaction ( Fig. 2 A,  lane 5).	transcription
53398	3	335033	5	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				Apg12p	NULL		carboxyl-terminal glycine		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_41_39517_s_108	12890687	These results indicate that the interaction of Apg10p with Apg12p in the presence of Apg7p is dependent on the carboxyl-terminal glycine of Apg12p that is essential for the conjugation reaction ( Fig. 2 A,  lane 5).	transcription
53399	4	335033	5	NULL	NULL	0	NULL	Apg12p	NULL		is dependent on	NULL		carboxyl-terminal glycine		conjugation reaction	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_41_39517_s_108	12890687	These results indicate that the interaction of Apg10p with Apg12p in the presence of Apg7p is dependent on the carboxyl-terminal glycine of Apg12p that is essential for the conjugation reaction ( Fig. 2 A,  lane 5).	transcription
53162	1	335033	7	NULL	NULL	0	NULL	Apg10p	NULL		interacts with	NULL				Apg12p	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_41_39517_s_108	12890687	These results indicate that the interaction of Apg10p with Apg12p in the presence of Apg7p is dependent on the carboxyl-terminal glycine of Apg12p that is essential for the conjugation reaction ( Fig. 2 A,  lane 5).	transcription
53163	2	335033	7	NULL	NULL	0	NULL	statement 1	NULL		in presence of	NULL				Apg7p	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_41_39517_s_108	12890687	These results indicate that the interaction of Apg10p with Apg12p in the presence of Apg7p is dependent on the carboxyl-terminal glycine of Apg12p that is essential for the conjugation reaction ( Fig. 2 A,  lane 5).	transcription
53164	3	335033	7	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				Apg12p	NULL		 carboxyl-terminal glycine 		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_41_39517_s_108	12890687	These results indicate that the interaction of Apg10p with Apg12p in the presence of Apg7p is dependent on the carboxyl-terminal glycine of Apg12p that is essential for the conjugation reaction ( Fig. 2 A,  lane 5).	transcription
53165	4	335033	7	NULL	NULL	0	NULL	statement 3	NULL		essential for	NULL				conjugation reaction	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_41_39517_s_108	12890687	These results indicate that the interaction of Apg10p with Apg12p in the presence of Apg7p is dependent on the carboxyl-terminal glycine of Apg12p that is essential for the conjugation reaction ( Fig. 2 A,  lane 5).	transcription
53400	1	335034	5	NULL	NULL	0	NULL	A1	NULL		contains	NULL		UP1			NULL		RNA-binding domains		NULL		0	NULL	NULL	NULL	gw60_embo_18_7_1939_s_113	10202157	The N-terminal portion of A1 (called UP1) contains two RNA-binding domains but lacks the C-terminal glycine-rich domain (Figure  5).	transcription
53401	2	335034	5	NULL	NULL	0	NULL	A1	NULL		lacks	NULL		UP1			NULL		C-terminal glycine-rich domain		NULL		0	NULL	NULL	NULL	gw60_embo_18_7_1939_s_113	10202157	The N-terminal portion of A1 (called UP1) contains two RNA-binding domains but lacks the C-terminal glycine-rich domain (Figure  5).	transcription
53402	3	335034	5	NULL	NULL	0	NULL	UP1	NULL		is	NULL				N-terminal portion of A1	NULL				NULL		0	NULL	NULL	NULL	gw60_embo_18_7_1939_s_113	10202157	The N-terminal portion of A1 (called UP1) contains two RNA-binding domains but lacks the C-terminal glycine-rich domain (Figure  5).	transcription
53353	1	335034	7	NULL	NULL	0	NULL	A1	NULL		contains	NULL		N-terminal portion			NULL		two RNA-binding domains		NULL		0	NULL	NULL	NULL	gw60_embo_18_7_1939_s_113	10202157	The N-terminal portion of A1 (called UP1) contains two RNA-binding domains but lacks the C-terminal glycine-rich domain (Figure  5).	transcription
53354	2	335034	7	NULL	NULL	0	NULL	A1	NULL		lacks	NULL		N-terminal portion of 			NULL		C-terminal glycine-rich domain		NULL		0	NULL	NULL	NULL	gw60_embo_18_7_1939_s_113	10202157	The N-terminal portion of A1 (called UP1) contains two RNA-binding domains but lacks the C-terminal glycine-rich domain (Figure  5).	transcription
53355	3	335034	7	NULL	NULL	0	NULL	A1	NULL		is	NULL		N-terminal portion 		UP1	NULL	synonym of			NULL		0	NULL	NULL	NULL	gw60_embo_18_7_1939_s_113	10202157	The N-terminal portion of A1 (called UP1) contains two RNA-binding domains but lacks the C-terminal glycine-rich domain (Figure  5).	transcription
53403	1	335036	5	NULL	NULL	0	NULL	glycine	NULL		stimulates	NULL				spermatozoa	NULL	acrosomal exocytosis of;;human			NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_306_2_376_s_110	12804573	It is worth to mention that glycine stimulates acrosomal exocytosis of several mammalian spermatozoa including human, an effect blocked by strychnine [ 5,  6 and  10].	transcription
53404	2	335036	5	NULL	NULL	0	NULL	spermatozoa	NULL	acrosomal exocytosis of;;human	is blocked by	NULL				strychnine	NULL				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_306_2_376_s_110	12804573	It is worth to mention that glycine stimulates acrosomal exocytosis of several mammalian spermatozoa including human, an effect blocked by strychnine [ 5,  6 and  10].	transcription
53166	1	335036	7	NULL	NULL	0	NULL	glycine	NULL		stimulate	NULL				acrosomal exocytosis	NULL	human			NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_306_2_376_s_110	12804573	It is worth to mention that glycine stimulates acrosomal exocytosis of several mammalian spermatozoa including human, an effect blocked by strychnine [ 5,  6 and  10].	transcription
53167	2	335036	7	NULL	NULL	0	NULL	strychnine	NULL		blocks	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_306_2_376_s_110	12804573	It is worth to mention that glycine stimulates acrosomal exocytosis of several mammalian spermatozoa including human, an effect blocked by strychnine [ 5,  6 and  10].	transcription
53405	1	335037	5	NULL	NULL	0	NULL	TNFalpha mRNA	NULL	increase in	is caused by	NULL				Wy-14,643	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_176	9934846	Additionally, inactivation of Kupffer cells with either methyl palmitate or dietary glycine prevented the increase in TNFalpha mRNA caused by Wy-14,643 ( 4, 5).	transcription
53406	2	335037	5	NULL	NULL	0	NULL	Kupffer cells	NULL		is inactivated by	NULL				methyl palmitate	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_176	9934846	Additionally, inactivation of Kupffer cells with either methyl palmitate or dietary glycine prevented the increase in TNFalpha mRNA caused by Wy-14,643 ( 4, 5).	transcription
53407	3	335037	5	NULL	NULL	0	NULL	Kupffer cells	NULL		is inactivated by	NULL				glycine	NULL	dietary			NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_176	9934846	Additionally, inactivation of Kupffer cells with either methyl palmitate or dietary glycine prevented the increase in TNFalpha mRNA caused by Wy-14,643 ( 4, 5).	transcription
53408	4	335037	5	NULL	NULL	0	NULL	statement 2	NULL		is an alternative to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_176	9934846	Additionally, inactivation of Kupffer cells with either methyl palmitate or dietary glycine prevented the increase in TNFalpha mRNA caused by Wy-14,643 ( 4, 5).	transcription
53409	5	335037	5	NULL	NULL	0	NULL	statement 2	NULL		prevents	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_176	9934846	Additionally, inactivation of Kupffer cells with either methyl palmitate or dietary glycine prevented the increase in TNFalpha mRNA caused by Wy-14,643 ( 4, 5).	transcription
53410	6	335037	5	NULL	NULL	0	NULL	statement 3	NULL		prevents	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_176	9934846	Additionally, inactivation of Kupffer cells with either methyl palmitate or dietary glycine prevented the increase in TNFalpha mRNA caused by Wy-14,643 ( 4, 5).	transcription
53168	1	335037	7	NULL	NULL	0	NULL	Wy-14,643	NULL		increase	NULL				TNFalpha mRNA	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_176	9934846	Additionally, inactivation of Kupffer cells with either methyl palmitate or dietary glycine prevented the increase in TNFalpha mRNA caused by Wy-14,643 ( 4, 5).	transcription
53169	2	335037	7	NULL	NULL	0	NULL	Kupffer cells	NULL	 inactivation of 	prevents	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_176	9934846	Additionally, inactivation of Kupffer cells with either methyl palmitate or dietary glycine prevented the increase in TNFalpha mRNA caused by Wy-14,643 ( 4, 5).	transcription
53170	3	335037	7	NULL	NULL	0	NULL	statement 2	NULL		in presence of	NULL				methyl palmitate	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_176	9934846	Additionally, inactivation of Kupffer cells with either methyl palmitate or dietary glycine prevented the increase in TNFalpha mRNA caused by Wy-14,643 ( 4, 5).	transcription
53171	4	335037	7	NULL	NULL	0	NULL	statement 2	NULL		in presence of	NULL				dietary glycine	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_176	9934846	Additionally, inactivation of Kupffer cells with either methyl palmitate or dietary glycine prevented the increase in TNFalpha mRNA caused by Wy-14,643 ( 4, 5).	transcription
53172	5	335037	7	NULL	NULL	0	NULL	statement 3	NULL		is an alternative to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_176	9934846	Additionally, inactivation of Kupffer cells with either methyl palmitate or dietary glycine prevented the increase in TNFalpha mRNA caused by Wy-14,643 ( 4, 5).	transcription
53411	1	335038	5	NULL	NULL	0	NULL	hepatocyte	NULL	replication of	is induced by	NULL				Wy-14,643	NULL				NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_194	9934846	In addition, dietary glycine has been shown to prevent Wy-14,643-induced hepatocyte replication by inhibiting Kupffer cell production of TNFalpha ( 5).	transcription
53412	2	335038	5	NULL	NULL	0	NULL	glycine	NULL	dietary	prevents	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_194	9934846	In addition, dietary glycine has been shown to prevent Wy-14,643-induced hepatocyte replication by inhibiting Kupffer cell production of TNFalpha ( 5).	transcription
53413	3	335038	5	NULL	NULL	0	NULL	Kupffer cell	NULL		is produced by	NULL				TNFalpha	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_194	9934846	In addition, dietary glycine has been shown to prevent Wy-14,643-induced hepatocyte replication by inhibiting Kupffer cell production of TNFalpha ( 5).	transcription
53414	4	335038	5	NULL	NULL	0	NULL	glycine	NULL	dietary	inhibits	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_194	9934846	In addition, dietary glycine has been shown to prevent Wy-14,643-induced hepatocyte replication by inhibiting Kupffer cell production of TNFalpha ( 5).	transcription
53415	5	335038	5	NULL	NULL	0	NULL	statement 4	NULL		leads to	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_194	9934846	In addition, dietary glycine has been shown to prevent Wy-14,643-induced hepatocyte replication by inhibiting Kupffer cell production of TNFalpha ( 5).	transcription
53173	1	335038	7	NULL	NULL	0	NULL	Wy-14,643	NULL		induce	NULL				 hepatocyte 	NULL	replication of			NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_194	9934846	In addition, dietary glycine has been shown to prevent Wy-14,643-induced hepatocyte replication by inhibiting Kupffer cell production of TNFalpha ( 5).	transcription
53174	2	335038	7	NULL	NULL	0	NULL	Kupffer cell 	NULL		produce	NULL				TNFalpha	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_194	9934846	In addition, dietary glycine has been shown to prevent Wy-14,643-induced hepatocyte replication by inhibiting Kupffer cell production of TNFalpha ( 5).	transcription
53175	3	335038	7	NULL	NULL	0	NULL	dietary glycine	NULL		prevent	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_194	9934846	In addition, dietary glycine has been shown to prevent Wy-14,643-induced hepatocyte replication by inhibiting Kupffer cell production of TNFalpha ( 5).	transcription
53176	4	335038	7	NULL	NULL	0	NULL	statement 3	NULL		occur by	NULL				statement 2	NULL	inhibition of			NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_20_1_27_s_194	9934846	In addition, dietary glycine has been shown to prevent Wy-14,643-induced hepatocyte replication by inhibiting Kupffer cell production of TNFalpha ( 5).	transcription
53416	1	335039	5	NULL	NULL	0	NULL	alanine	NULL		inhibit	NULL				GS enzymes	NULL	archaeal			NULL	Methanobacterium ivanovi	0	NULL	NULL	NULL	gw60_applenvironmicrob_67_10_4458_s_87	11571143	For comparison, 5 mM alanine or glycine inhibited the archaeal GS enzymes from  Methanobacterium ivanovi ( 2) and  A. fulgidus (H. Schreier, unpublished results) to a similar extent.	transcription
53417	2	335039	5	NULL	NULL	0	NULL	alanine	NULL		inhibit	NULL				GS enzymes	NULL	archaeal			NULL	A. fulgidus	0	NULL	NULL	NULL	gw60_applenvironmicrob_67_10_4458_s_87	11571143	For comparison, 5 mM alanine or glycine inhibited the archaeal GS enzymes from  Methanobacterium ivanovi ( 2) and  A. fulgidus (H. Schreier, unpublished results) to a similar extent.	transcription
53418	3	335039	5	NULL	NULL	0	NULL	glycine	NULL		inhibit	NULL				GS enzymes	NULL	archaeal			NULL	Methanobacterium ivanovi	0	NULL	NULL	NULL	gw60_applenvironmicrob_67_10_4458_s_87	11571143	For comparison, 5 mM alanine or glycine inhibited the archaeal GS enzymes from  Methanobacterium ivanovi ( 2) and  A. fulgidus (H. Schreier, unpublished results) to a similar extent.	transcription
53419	4	335039	5	NULL	NULL	0	NULL	glycine	NULL		inhibit	NULL				GS enzymes	NULL	archaeal			NULL	A. fulgidus	NULL	NULL	NULL	NULL	gw60_applenvironmicrob_67_10_4458_s_87	11571143	For comparison, 5 mM alanine or glycine inhibited the archaeal GS enzymes from  Methanobacterium ivanovi ( 2) and  A. fulgidus (H. Schreier, unpublished results) to a similar extent.	transcription
53420	5	335039	5	NULL	NULL	0	NULL	statement 1	NULL		is similar to	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_10_4458_s_87	11571143	For comparison, 5 mM alanine or glycine inhibited the archaeal GS enzymes from  Methanobacterium ivanovi ( 2) and  A. fulgidus (H. Schreier, unpublished results) to a similar extent.	transcription
53421	6	335039	5	NULL	NULL	0	NULL	statement 2	NULL		is similar to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_10_4458_s_87	11571143	For comparison, 5 mM alanine or glycine inhibited the archaeal GS enzymes from  Methanobacterium ivanovi ( 2) and  A. fulgidus (H. Schreier, unpublished results) to a similar extent.	transcription
53177	1	335039	7	NULL	NULL	0	NULL	alanine	NULL		inhibit	NULL				archaeal GS enzymes	NULL	Methanobacterium ivanovi 			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_10_4458_s_87	11571143	For comparison, 5 mM alanine or glycine inhibited the archaeal GS enzymes from  Methanobacterium ivanovi ( 2) and  A. fulgidus (H. Schreier, unpublished results) to a similar extent.	transcription
53178	2	335039	7	NULL	NULL	0	NULL	alanine	NULL		inhibit	NULL				 archaeal GS enzymes	NULL	A. fulgidus			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_10_4458_s_87	11571143	For comparison, 5 mM alanine or glycine inhibited the archaeal GS enzymes from  Methanobacterium ivanovi ( 2) and  A. fulgidus (H. Schreier, unpublished results) to a similar extent.	transcription
53179	3	335039	7	NULL	NULL	0	NULL	glycine	NULL		inhibit	NULL				archaeal GS enzymes	NULL	Methanobacterium ivanovi			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_10_4458_s_87	11571143	For comparison, 5 mM alanine or glycine inhibited the archaeal GS enzymes from  Methanobacterium ivanovi ( 2) and  A. fulgidus (H. Schreier, unpublished results) to a similar extent.	transcription
53180	4	335039	7	NULL	NULL	0	NULL	 glycine	NULL		inhibit	NULL				archaeal GS enzymes	NULL	A. fulgidus			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_67_10_4458_s_87	11571143	For comparison, 5 mM alanine or glycine inhibited the archaeal GS enzymes from  Methanobacterium ivanovi ( 2) and  A. fulgidus (H. Schreier, unpublished results) to a similar extent.	transcription
53181	5	335039	7	NULL	NULL	0	NULL	statement 1	NULL		is similar to	NULL				statement 2	NULL				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_67_10_4458_s_87	11571143	For comparison, 5 mM alanine or glycine inhibited the archaeal GS enzymes from  Methanobacterium ivanovi ( 2) and  A. fulgidus (H. Schreier, unpublished results) to a similar extent.	transcription
53182	6	335039	7	NULL	NULL	0	NULL	statement 3	NULL		is similar to	NULL				statement 4	NULL				NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_67_10_4458_s_87	11571143	For comparison, 5 mM alanine or glycine inhibited the archaeal GS enzymes from  Methanobacterium ivanovi ( 2) and  A. fulgidus (H. Schreier, unpublished results) to a similar extent.	transcription
53183	1	335041	7	NULL	NULL	0	NULL	glycine	NULL		mediates	NULL				current	NULL				NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_37_3_391_s_74	9681937	Colchicine inhibition of glycine mediated currents did not vary between oocytes maintained at room or cold temperatures ( n=5, Student's  t-test).	transcription
53184	2	335041	7	NULL	NULL	0	NULL	Colchicine	NULL		inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_37_3_391_s_74	9681937	Colchicine inhibition of glycine mediated currents did not vary between oocytes maintained at room or cold temperatures ( n=5, Student's  t-test).	transcription
53185	3	335041	7	NULL	NULL	0	NULL	statement 2	NULL		does not vary between	NULL				oocytes	NULL				NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_37_3_391_s_74	9681937	Colchicine inhibition of glycine mediated currents did not vary between oocytes maintained at room or cold temperatures ( n=5, Student's  t-test).	transcription
53422	1	335042	5	NULL	NULL	0	NULL	NFPS	NULL		abolishes	NULL	totally			glycine	NULL	effects of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_41_1_88_s_117	11445189	In contrast, NFPS alone had no effect on [3] content, but the effects of glycine and sarcosine were totally abolished by 1  M NFPS ( Fig. 5).	transcription
53423	2	335042	5	NULL	NULL	0	NULL	NFPS	NULL		abolishes	NULL	totally			sarcosine	NULL	effects of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_41_1_88_s_117	11445189	In contrast, NFPS alone had no effect on [3] content, but the effects of glycine and sarcosine were totally abolished by 1  M NFPS ( Fig. 5).	transcription
53186	1	335042	7	NULL	NULL	0	NULL	NFPS 	NULL		abolish	NULL	totally			 glycine	NULL	effect of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_41_1_88_s_117	11445189	In contrast, NFPS alone had no effect on [3] content, but the effects of glycine and sarcosine were totally abolished by 1  M NFPS ( Fig. 5).	transcription
53187	2	335042	7	NULL	NULL	0	NULL	NFPS 	NULL		abolish	NULL	totally			sarcosine	NULL	effect of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_41_1_88_s_117	11445189	In contrast, NFPS alone had no effect on [3] content, but the effects of glycine and sarcosine were totally abolished by 1  M NFPS ( Fig. 5).	transcription
53424	1	335043	5	NULL	NULL	0	NULL	synaptic events	NULL		is activated in	NULL				5 DIV neurons	NULL				NULL		0	NULL	NULL	NULL	gw60_neuroscience_108_3_493_s_168	11738262	The data shown in  Fig. 2 indicate that the synaptic events activated in 5 DIV neurons are mediated by glycine, GABAA, and, to a lesser extent, AMPA receptors.	transcription
53425	2	335043	5	NULL	NULL	0	NULL	glycine	NULL		mediates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_neuroscience_108_3_493_s_168	11738262	The data shown in  Fig. 2 indicate that the synaptic events activated in 5 DIV neurons are mediated by glycine, GABAA, and, to a lesser extent, AMPA receptors.	transcription
53426	3	335043	5	NULL	NULL	0	NULL	GABAA	NULL		mediates	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_108_3_493_s_168	11738262	The data shown in  Fig. 2 indicate that the synaptic events activated in 5 DIV neurons are mediated by glycine, GABAA, and, to a lesser extent, AMPA receptors.	transcription
53427	4	335043	5	NULL	NULL	0	NULL	AMPA receptors	NULL		mediates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_neuroscience_108_3_493_s_168	11738262	The data shown in  Fig. 2 indicate that the synaptic events activated in 5 DIV neurons are mediated by glycine, GABAA, and, to a lesser extent, AMPA receptors.	transcription
53194	1	335043	7	NULL	NULL	0	NULL	 glycine	NULL		mediates	NULL				synaptic events	NULL	activation of			NULL	DIV neurons	0	NULL	NULL	NULL	gw60_neuroscience_108_3_493_s_168	11738262	The data shown in  Fig. 2 indicate that the synaptic events activated in 5 DIV neurons are mediated by glycine, GABAA, and, to a lesser extent, AMPA receptors.	transcription
53195	2	335043	7	NULL	NULL	0	NULL	GABAA	NULL		mediates	NULL				synaptic events	NULL	activation of			NULL	DIV neurons	0	NULL	NULL	NULL	gw60_neuroscience_108_3_493_s_168	11738262	The data shown in  Fig. 2 indicate that the synaptic events activated in 5 DIV neurons are mediated by glycine, GABAA, and, to a lesser extent, AMPA receptors.	transcription
53196	3	335043	7	NULL	NULL	0	NULL	AMPA receptors	NULL		mediates	NULL				synaptic events	NULL	activation of			NULL	DIV neurons	NULL	NULL	NULL	NULL	gw60_neuroscience_108_3_493_s_168	11738262	The data shown in  Fig. 2 indicate that the synaptic events activated in 5 DIV neurons are mediated by glycine, GABAA, and, to a lesser extent, AMPA receptors.	transcription
53428	1	335045	5	NULL	NULL	0	NULL	Lsm4	NULL		interacts with	NULL	directly	carboxyl terminus		SMN	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_34_26370_s_167	10851237	The carboxyl terminus of Lsm4 contains an arginine-and glycine-rich domain that, when expressed on its own, is sufficient for direct interaction with SMN (Fig.  5 B).	transcription
53429	2	335045	5	NULL	NULL	0	NULL	Lsm4	NULL		contains	NULL		carboxyl terminus			NULL		glycine-rich domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_34_26370_s_167	10851237	The carboxyl terminus of Lsm4 contains an arginine-and glycine-rich domain that, when expressed on its own, is sufficient for direct interaction with SMN (Fig.  5 B).	transcription
53430	3	335045	5	NULL	NULL	0	NULL	Lsm4	NULL		contains	NULL		carboxyl terminus			NULL		arginine-rich domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_34_26370_s_167	10851237	The carboxyl terminus of Lsm4 contains an arginine-and glycine-rich domain that, when expressed on its own, is sufficient for direct interaction with SMN (Fig.  5 B).	transcription
53197	1	335045	7	NULL	NULL	0	NULL	Lsm4 	NULL		contains	NULL		carboxyl terminus			NULL		arginine-rich domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_34_26370_s_167	10851237	The carboxyl terminus of Lsm4 contains an arginine-and glycine-rich domain that, when expressed on its own, is sufficient for direct interaction with SMN (Fig.  5 B).	transcription
53198	2	335045	7	NULL	NULL	0	NULL	Lsm4	NULL		contains	NULL		carboxyl terminus			NULL		glycine-rich domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_34_26370_s_167	10851237	The carboxyl terminus of Lsm4 contains an arginine-and glycine-rich domain that, when expressed on its own, is sufficient for direct interaction with SMN (Fig.  5 B).	transcription
53199	3	335045	7	NULL	NULL	0	NULL	Lsm4	NULL		interacts with	NULL	directly	carboxyl terminus		SMN	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_34_26370_s_167	10851237	The carboxyl terminus of Lsm4 contains an arginine-and glycine-rich domain that, when expressed on its own, is sufficient for direct interaction with SMN (Fig.  5 B).	transcription
53200	4	335045	7	NULL	NULL	0	NULL	statement 1	NULL		is required for	NULL				statement 3	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_34_26370_s_167	10851237	The carboxyl terminus of Lsm4 contains an arginine-and glycine-rich domain that, when expressed on its own, is sufficient for direct interaction with SMN (Fig.  5 B).	transcription
53201	5	335045	7	NULL	NULL	0	NULL	statement 2	NULL		is required for	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_34_26370_s_167	10851237	The carboxyl terminus of Lsm4 contains an arginine-and glycine-rich domain that, when expressed on its own, is sufficient for direct interaction with SMN (Fig.  5 B).	transcription
53431	1	335047	5	NULL	NULL	0	NULL	Osteopontin	NULL		bind	NULL		RGD motif		alphavbeta3	NULL				NULL	surface of cells	NULL	NULL	NULL	NULL	gw60_jclininvest_98_10_2218_s_23	8941637	Osteopontin contains an arginine-glycine-aspartate  (RGD) motif which allows the molecule to bind to alphavbeta3 and  other integrins on the surface of cells ( 5,  6).	transcription
53432	2	335047	5	NULL	NULL	0	NULL	RGD	NULL		is	NULL				arginine-glycine-aspartate 	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_10_2218_s_23	8941637	Osteopontin contains an arginine-glycine-aspartate  (RGD) motif which allows the molecule to bind to alphavbeta3 and  other integrins on the surface of cells ( 5,  6).	transcription
53433	3	335047	5	NULL	NULL	0	NULL	Osteopontin	NULL		bind	NULL		RGD motif		integrins	NULL				NULL	surface of cells	0	NULL	NULL	NULL	gw60_jclininvest_98_10_2218_s_23	8941637	Osteopontin contains an arginine-glycine-aspartate  (RGD) motif which allows the molecule to bind to alphavbeta3 and  other integrins on the surface of cells ( 5,  6).	transcription
53202	1	335047	7	NULL	NULL	0	NULL	Osteopontin 	NULL		bind	NULL		RGD motif		alphavbeta3	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_10_2218_s_23	8941637	Osteopontin contains an arginine-glycine-aspartate  (RGD) motif which allows the molecule to bind to alphavbeta3 and  other integrins on the surface of cells ( 5,  6).	transcription
53203	2	335047	7	NULL	NULL	0	NULL	Osteopontin	NULL		bind	NULL		RGD motif		integrins	NULL				NULL	surface of cells	0	NULL	NULL	NULL	gw60_jclininvest_98_10_2218_s_23	8941637	Osteopontin contains an arginine-glycine-aspartate  (RGD) motif which allows the molecule to bind to alphavbeta3 and  other integrins on the surface of cells ( 5,  6).	transcription
53204	3	335047	7	NULL	NULL	0	NULL		NULL		is	NULL		RGD motif		arginine-glycine-aspartate	NULL				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_10_2218_s_23	8941637	Osteopontin contains an arginine-glycine-aspartate  (RGD) motif which allows the molecule to bind to alphavbeta3 and  other integrins on the surface of cells ( 5,  6).	transcription
53434	1	335049	5	NULL	NULL	0	NULL	SGAT	NULL		is	NULL				Serine-glyoxylate aminotransferase	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53435	2	335049	5	NULL	NULL	0	NULL	PLP	NULL		is	NULL				pyridoxal 5''-phosphate	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53436	3	335049	5	NULL	NULL	0	NULL	SGAT	NULL		is a type of	NULL				PLP enzyme	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53437	4	335049	5	NULL	NULL	0	NULL	l-serine	NULL		is converted to	NULL				hydroxypyruvate	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53438	5	335049	5	NULL	NULL	0	NULL	l-serine	NULL		is converted to	NULL				glycine	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53439	6	335049	5	NULL	NULL	0	NULL	glyoxylate	NULL		is converted to	NULL				hydroxypyruvate	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53440	7	335049	5	NULL	NULL	0	NULL	glyoxylate	NULL		is converted to	NULL				glycine	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53441	8	335049	5	NULL	NULL	0	NULL	statement 4	NULL		occurs along with	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53442	9	335049	5	NULL	NULL	0	NULL	statement 5	NULL		occurs along with	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53443	10	335049	5	NULL	NULL	0	NULL	statement 8	NULL		occurs along with	NULL				statement 9	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53444	11	335049	5	NULL	NULL	0	NULL	SGAT	NULL	Hyphomicrobium methylovorum	catalyzes	NULL				statement 10	NULL	interconversion of			NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53205	1	335049	7	NULL	NULL	0	NULL	 l-serine 	NULL		converted to	NULL				hydroxypyruvate	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53206	2	335049	7	NULL	NULL	0	NULL	l-serine	NULL		converted to	NULL				glycine	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53207	3	335049	7	NULL	NULL	0	NULL	glyoxylate	NULL		converted to	NULL				hydroxypyruvate	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53208	4	335049	7	NULL	NULL	0	NULL	glyoxylate	NULL		converted to	NULL				glycine	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53209	5	335049	7	NULL	NULL	0	NULL	statement 1	NULL		occur along with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53210	6	335049	7	NULL	NULL	0	NULL	statement 3	NULL		occur along with	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53211	7	335049	7	NULL	NULL	0	NULL	statement 5	NULL		occur along with	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53212	8	335049	7	NULL	NULL	0	NULL	SGAT	NULL	Hyphomicrobium methylovorum	catalyzes	NULL				statement 7	NULL	interconversion of			NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53213	9	335049	7	NULL	NULL	0	NULL	SGAT	NULL		is	NULL				Serine-glyoxylate aminotransferase	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53225	10	335049	7	NULL	NULL	0	NULL	SGAT	NULL		is a type of	NULL				PLP enzyme	NULL				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53226	11	335049	7	NULL	NULL	0	NULL	PLP	NULL		is	NULL				pyridoxal 5''-phosphate	NULL				NULL		NULL	NULL	NULL	NULL	abs-batch0540-0549_biochemistry_44_48_16313196_s_2	16313196	Serine-glyoxylate aminotransferase (SGAT) from Hyphomicrobium methylovorum  is a pyridoxal 5''-phosphate (PLP) enzyme that catalyzes the interconversion  of l-serine and glyoxylate to hydroxypyruvate and glycine.	transcription
53445	1	335052	5	NULL	NULL	0	NULL	lysine-56	NULL		bind	NULL	potentially			serine racemase	NULL		pyridoxal 5' phosphate		NULL		0	NULL	NULL	NULL	gw60_pnas_96_23_13409_s_93	10557334	To explore the dependence on pyridoxal 5' phosphate binding, we constructed a mutant in which lysine-56, predicted to bind pyridoxal 5' phosphate in serine racemase (Fig.  1 C), was replaced by glycine (K56G mutant).	transcription
53214	1	335052	7	NULL	NULL	0	NULL		NULL		bind	NULL	may	 lysine-56		serine racemase	NULL		pyridoxal 5' phosphate		NULL		0	NULL	NULL	NULL	gw60_pnas_96_23_13409_s_93	10557334	To explore the dependence on pyridoxal 5' phosphate binding, we constructed a mutant in which lysine-56, predicted to bind pyridoxal 5' phosphate in serine racemase (Fig.  1 C), was replaced by glycine (K56G mutant).	transcription
53446	1	335053	5	NULL	NULL	0	NULL	GlyR	NULL	WT	is inhibited by	NULL				PTX	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_43_35836_s_226	16109711	C, currents activated by 30 muM glycine in the WT GlyR are completely inhibited by 100 muM PTX ( left panel), whereas those activated by 5 muM glycine in the T6'F GlyR are little affected by 300 muM PTX ( center panel).	transcription
53447	2	335053	5	NULL	NULL	0	NULL	GlyR	NULL		is affected by	NULL	little	T6'F		PTX	NULL				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_43_35836_s_226	16109711	C, currents activated by 30 muM glycine in the WT GlyR are completely inhibited by 100 muM PTX ( left panel), whereas those activated by 5 muM glycine in the T6'F GlyR are little affected by 300 muM PTX ( center panel).	transcription
53215	1	335053	7	NULL	NULL	0	NULL	PTX	NULL		inhibit	NULL	completely			GlyR	NULL	WT			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_43_35836_s_226	16109711	C, currents activated by 30 muM glycine in the WT GlyR are completely inhibited by 100 muM PTX ( left panel), whereas those activated by 5 muM glycine in the T6'F GlyR are little affected by 300 muM PTX ( center panel).	transcription
53216	2	335053	7	NULL	NULL	0	NULL	PTX	NULL		affect	NULL	little			GlyR	NULL		T6'F		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_43_35836_s_226	16109711	C, currents activated by 30 muM glycine in the WT GlyR are completely inhibited by 100 muM PTX ( left panel), whereas those activated by 5 muM glycine in the T6'F GlyR are little affected by 300 muM PTX ( center panel).	transcription
53448	1	335054	5	NULL	NULL	0	NULL	glycine	NULL		is a type of	NULL				neurotransmitter	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_8_5_283_s_70	9501073	We were unable to demonstrate any rise in [Ca2+]i upon application of the neurotransmitter glycine ( n = 5), but currents induced by glycine were apparent in 20% of ganglion cell layer neurons ( n = 16), as recorded whole-cell patch-clamping (V.B., unpublished observation).	transcription
53449	2	335054	5	NULL	NULL	0	NULL	glycine	NULL	addition of	does not rise	NULL	potentially			[Ca2+]i	NULL				NULL		0	NULL	NULL	NULL	gw60_currbiol_8_5_283_s_70	9501073	We were unable to demonstrate any rise in [Ca2+]i upon application of the neurotransmitter glycine ( n = 5), but currents induced by glycine were apparent in 20% of ganglion cell layer neurons ( n = 16), as recorded whole-cell patch-clamping (V.B., unpublished observation).	transcription
53450	1	335055	5	NULL	NULL	0	NULL	spermine	NULL	stimulation of	is independent of	NULL				glycine	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_4_701_s_16	9380034	The glycine-independent form of spermine stimulation (Fig.  1A,  1), seen with saturating concentrations of glycine, may involve relief of proton inhibition (Fig.  1A,  6), processes that are also influenced by the alternatively spliced insert encoded by exon 5 in the NR1 subunit (Fig.  1A,  9).	transcription
53451	2	335055	5	NULL	NULL	0	NULL	statement 1	NULL		involves	NULL	may			proton	NULL	relief of;;inhibition of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_4_701_s_16	9380034	The glycine-independent form of spermine stimulation (Fig.  1A,  1), seen with saturating concentrations of glycine, may involve relief of proton inhibition (Fig.  1A,  6), processes that are also influenced by the alternatively spliced insert encoded by exon 5 in the NR1 subunit (Fig.  1A,  9).	transcription
53217	1	335055	7	NULL	NULL	0	NULL	spermine	NULL	stimulation of	is independent of	NULL				glycine	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_4_701_s_16	9380034	The glycine-independent form of spermine stimulation (Fig.  1A,  1), seen with saturating concentrations of glycine, may involve relief of proton inhibition (Fig.  1A,  6), processes that are also influenced by the alternatively spliced insert encoded by exon 5 in the NR1 subunit (Fig.  1A,  9).	transcription
53218	2	335055	7	NULL	NULL	0	NULL	statement 1	NULL		involve	NULL	may			proton inhibition	NULL	relief of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_4_701_s_16	9380034	The glycine-independent form of spermine stimulation (Fig.  1A,  1), seen with saturating concentrations of glycine, may involve relief of proton inhibition (Fig.  1A,  6), processes that are also influenced by the alternatively spliced insert encoded by exon 5 in the NR1 subunit (Fig.  1A,  9).	transcription
53219	3	335055	7	NULL	NULL	0	NULL	NR1 subunit 	NULL		influence	NULL			exon 5	proton inhibition	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_4_701_s_16	9380034	The glycine-independent form of spermine stimulation (Fig.  1A,  1), seen with saturating concentrations of glycine, may involve relief of proton inhibition (Fig.  1A,  6), processes that are also influenced by the alternatively spliced insert encoded by exon 5 in the NR1 subunit (Fig.  1A,  9).	transcription
53453	1	335056	5	NULL	NULL	0	NULL	glycine	NULL	concentration of	elevates within	NULL				synapse	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_1_129_s_209	10860934	The elevation in glycine concentrations within the synapse caused by pH inhibition of glycine transport may lead to increased activity of NMDA receptors containing the exon 5 in the NR-1 subunits and may be one of the factors triggering the subsequent destructive phase of ischemia.	transcription
53454	2	335056	5	NULL	NULL	0	NULL	glycine	NULL	transport of	is inhibited by	NULL				pH	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_1_129_s_209	10860934	The elevation in glycine concentrations within the synapse caused by pH inhibition of glycine transport may lead to increased activity of NMDA receptors containing the exon 5 in the NR-1 subunits and may be one of the factors triggering the subsequent destructive phase of ischemia.	transcription
53455	3	335056	5	NULL	NULL	0	NULL	statement 2	NULL		causes	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_58_1_129_s_209	10860934	The elevation in glycine concentrations within the synapse caused by pH inhibition of glycine transport may lead to increased activity of NMDA receptors containing the exon 5 in the NR-1 subunits and may be one of the factors triggering the subsequent destructive phase of ischemia.	transcription
53456	4	335056	5	NULL	NULL	0	NULL	NMDA receptors	NULL		contains	NULL					NULL		NR-1 subunits	exon 5	NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_1_129_s_209	10860934	The elevation in glycine concentrations within the synapse caused by pH inhibition of glycine transport may lead to increased activity of NMDA receptors containing the exon 5 in the NR-1 subunits and may be one of the factors triggering the subsequent destructive phase of ischemia.	transcription
53458	5	335056	5	NULL	NULL	0	NULL	statement 1	NULL		increases	NULL	may			statement 4	NULL	activity of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_58_1_129_s_209	10860934	The elevation in glycine concentrations within the synapse caused by pH inhibition of glycine transport may lead to increased activity of NMDA receptors containing the exon 5 in the NR-1 subunits and may be one of the factors triggering the subsequent destructive phase of ischemia.	transcription
53459	6	335056	5	NULL	NULL	0	NULL	statement 1	NULL		triggers	NULL	may			ischemia	NULL	subsequent destructive phase of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_58_1_129_s_209	10860934	The elevation in glycine concentrations within the synapse caused by pH inhibition of glycine transport may lead to increased activity of NMDA receptors containing the exon 5 in the NR-1 subunits and may be one of the factors triggering the subsequent destructive phase of ischemia.	transcription
53220	2	335056	7	NULL	NULL	0	NULL	statement 1	NULL		elevates	NULL				glycine	NULL	concentration of			NULL	within synapse	NULL	NULL	NULL	NULL	gw60_molpharmacol_58_1_129_s_209	10860934	The elevation in glycine concentrations within the synapse caused by pH inhibition of glycine transport may lead to increased activity of NMDA receptors containing the exon 5 in the NR-1 subunits and may be one of the factors triggering the subsequent destructive phase of ischemia.	transcription
53221	1	335056	7	NULL	NULL	0	NULL	glycine transport 	NULL		inhibited by	NULL				pH	NULL				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_1_129_s_209	10860934	The elevation in glycine concentrations within the synapse caused by pH inhibition of glycine transport may lead to increased activity of NMDA receptors containing the exon 5 in the NR-1 subunits and may be one of the factors triggering the subsequent destructive phase of ischemia.	transcription
53222	4	335056	7	NULL	NULL	0	NULL	statement 2	NULL		increase	NULL	may			statement 3	NULL	activity of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_58_1_129_s_209	10860934	The elevation in glycine concentrations within the synapse caused by pH inhibition of glycine transport may lead to increased activity of NMDA receptors containing the exon 5 in the NR-1 subunits and may be one of the factors triggering the subsequent destructive phase of ischemia.	transcription
53223	3	335056	7	NULL	NULL	0	NULL	NMDA receptor	NULL		contain	NULL					NULL		NR-1 subunits 	exon 5	NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_58_1_129_s_209	10860934	The elevation in glycine concentrations within the synapse caused by pH inhibition of glycine transport may lead to increased activity of NMDA receptors containing the exon 5 in the NR-1 subunits and may be one of the factors triggering the subsequent destructive phase of ischemia.	transcription
53224	5	335056	7	NULL	NULL	0	NULL	statement 4	NULL		trigger	NULL	may			ischemia	NULL	destructive phase of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_58_1_129_s_209	10860934	The elevation in glycine concentrations within the synapse caused by pH inhibition of glycine transport may lead to increased activity of NMDA receptors containing the exon 5 in the NR-1 subunits and may be one of the factors triggering the subsequent destructive phase of ischemia.	transcription
53460	1	335058	5	NULL	NULL	0	NULL	CPE	NULL	lower dose of	induce	NULL				DNA	NULL	cleavage of			NULL		0	NULL	NULL	NULL	gw70_infectimmun_71_8_4260_s_177	12874301	That lower CPE dose-induced DNA cleavage was blocked by a 50 muM concentration of the broad-spectrum caspase inhibitor Z-VAD-FMK but not by a 5 mM concentration of the oncosis inhibitor glycine (Fig.  3A).	transcription
53461	2	335058	5	NULL	NULL	0	NULL	Z-VAD-FMK	NULL		blocks	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_71_8_4260_s_177	12874301	That lower CPE dose-induced DNA cleavage was blocked by a 50 muM concentration of the broad-spectrum caspase inhibitor Z-VAD-FMK but not by a 5 mM concentration of the oncosis inhibitor glycine (Fig.  3A).	transcription
53462	3	335058	5	NULL	NULL	0	NULL	Z-VAD-FMK	NULL		is an inhibitor of	NULL				caspase	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_71_8_4260_s_177	12874301	That lower CPE dose-induced DNA cleavage was blocked by a 50 muM concentration of the broad-spectrum caspase inhibitor Z-VAD-FMK but not by a 5 mM concentration of the oncosis inhibitor glycine (Fig.  3A).	transcription
53463	4	335058	5	NULL	NULL	0	NULL	glycine	NULL		does not block	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_71_8_4260_s_177	12874301	That lower CPE dose-induced DNA cleavage was blocked by a 50 muM concentration of the broad-spectrum caspase inhibitor Z-VAD-FMK but not by a 5 mM concentration of the oncosis inhibitor glycine (Fig.  3A).	transcription
53464	5	335058	5	NULL	NULL	0	NULL	glycine	NULL		is an inhibitor of	NULL				oncosis	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_71_8_4260_s_177	12874301	That lower CPE dose-induced DNA cleavage was blocked by a 50 muM concentration of the broad-spectrum caspase inhibitor Z-VAD-FMK but not by a 5 mM concentration of the oncosis inhibitor glycine (Fig.  3A).	transcription
53227	1	335058	7	NULL	NULL	0	NULL	CPE	NULL		induce	NULL				DNA cleavage	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_71_8_4260_s_177	12874301	That lower CPE dose-induced DNA cleavage was blocked by a 50 muM concentration of the broad-spectrum caspase inhibitor Z-VAD-FMK but not by a 5 mM concentration of the oncosis inhibitor glycine (Fig.  3A).	transcription
53228	2	335058	7	NULL	NULL	0	NULL	Z-VAD-FMK	NULL		inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_71_8_4260_s_177	12874301	That lower CPE dose-induced DNA cleavage was blocked by a 50 muM concentration of the broad-spectrum caspase inhibitor Z-VAD-FMK but not by a 5 mM concentration of the oncosis inhibitor glycine (Fig.  3A).	transcription
53229	3	335058	7	NULL	NULL	0	NULL	Z-VAD-FMK	NULL		is a type of	NULL				broad-spectrum caspase inhibitor	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_71_8_4260_s_177	12874301	That lower CPE dose-induced DNA cleavage was blocked by a 50 muM concentration of the broad-spectrum caspase inhibitor Z-VAD-FMK but not by a 5 mM concentration of the oncosis inhibitor glycine (Fig.  3A).	transcription
53230	4	335058	7	NULL	NULL	0	NULL	glycine	NULL		does not inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_71_8_4260_s_177	12874301	That lower CPE dose-induced DNA cleavage was blocked by a 50 muM concentration of the broad-spectrum caspase inhibitor Z-VAD-FMK but not by a 5 mM concentration of the oncosis inhibitor glycine (Fig.  3A).	transcription
53231	5	335058	7	NULL	NULL	0	NULL	glycine	NULL		is a type of	NULL				oncosis inhibitor	NULL				NULL		0	NULL	NULL	NULL	gw70_infectimmun_71_8_4260_s_177	12874301	That lower CPE dose-induced DNA cleavage was blocked by a 50 muM concentration of the broad-spectrum caspase inhibitor Z-VAD-FMK but not by a 5 mM concentration of the oncosis inhibitor glycine (Fig.  3A).	transcription
53483	1	335059	5	NULL	NULL	0	NULL	tetrahydrofolate-responsive protein	NULL		bind	NULL					NULL			glycine regulatory region	NULL		0	NULL	NULL	NULL	gw70_annurevplantbiol_52_0_119_s_479	null	Control of expression of  one-carbon metabolism genes of  Saccharomyces cerevisiae is mediated by a tetrahydrofolate-responsive protein binding to a glycine regulatory  region including a core 5''-CTTCTT-3'' motif.	transcription
53484	2	335059	5	NULL	NULL	0	NULL	glycine regulatory region	NULL		includes	NULL					NULL			core 5''-CTTCTT-3'' motif	NULL		0	NULL	NULL	NULL	gw70_annurevplantbiol_52_0_119_s_479	null	Control of expression of  one-carbon metabolism genes of  Saccharomyces cerevisiae is mediated by a tetrahydrofolate-responsive protein binding to a glycine regulatory  region including a core 5''-CTTCTT-3'' motif.	transcription
53485	3	335059	5	NULL	NULL	0	NULL	statement 1	NULL		mediate	NULL				one-carbon metabolism genes	NULL	control of;;expression of;;Saccharomyces cerevisiae			NULL		0	NULL	NULL	NULL	gw70_annurevplantbiol_52_0_119_s_479	null	Control of expression of  one-carbon metabolism genes of  Saccharomyces cerevisiae is mediated by a tetrahydrofolate-responsive protein binding to a glycine regulatory  region including a core 5''-CTTCTT-3'' motif.	transcription
53232	1	335059	7	NULL	NULL	0	NULL	tetrahydrofolate-responsive protein	NULL		bind	NULL					NULL		glycine regulatory region		NULL		0	NULL	NULL	NULL	gw70_annurevplantbiol_52_0_119_s_479	null	Control of expression of  one-carbon metabolism genes of  Saccharomyces cerevisiae is mediated by a tetrahydrofolate-responsive protein binding to a glycine regulatory  region including a core 5''-CTTCTT-3'' motif.	transcription
53233	2	335059	7	NULL	NULL	0	NULL	glycine regulatory region	NULL		include	NULL					NULL		core 5''-CTTCTT-3'' motif		NULL		0	NULL	NULL	NULL	gw70_annurevplantbiol_52_0_119_s_479	null	Control of expression of  one-carbon metabolism genes of  Saccharomyces cerevisiae is mediated by a tetrahydrofolate-responsive protein binding to a glycine regulatory  region including a core 5''-CTTCTT-3'' motif.	transcription
53234	3	335059	7	NULL	NULL	0	NULL	tetrahydrofolate-responsive protein	NULL		mediate	NULL				one-carbon metabolism genes	NULL	expression of;;Saccharomyces cerevisiae			NULL		0	NULL	NULL	NULL	gw70_annurevplantbiol_52_0_119_s_479	null	Control of expression of  one-carbon metabolism genes of  Saccharomyces cerevisiae is mediated by a tetrahydrofolate-responsive protein binding to a glycine regulatory  region including a core 5''-CTTCTT-3'' motif.	transcription
53235	1	335060	7	NULL	NULL	0	NULL	ApoL-I	NULL		bind	NULL				anti-apoL-I	NULL				NULL		0	NULL	NULL	NULL	gw70_nature_422_6927_83_s_131	12621437	ApoL-I was obtained by elution of the NHS material bound to anti-apoL-I-Sepharose,  using 5% CHAPS, 0.1 M glycine (pH 2.8) followed by neutralization with 1 M Tris (pH  8.0).	transcription
53486	1	335061	5	NULL	NULL	0	NULL	glycine	NULL		induces	NULL				Cl currents	NULL				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_51_4_701_s_42	16842826	Glycine-induced Cl  currents were low-pass filtered at 5 kHz, monitored on an oscilloscope and a chart  recorder (Gould TA240), and stored on a computer (pClamp 6.0, Axon Instruments) for  subsequent analysis.	transcription
53236	1	335061	7	NULL	NULL	0	NULL	Glycine	NULL		induce	NULL				Cl currents 	NULL				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_51_4_701_s_42	16842826	Glycine-induced Cl  currents were low-pass filtered at 5 kHz, monitored on an oscilloscope and a chart  recorder (Gould TA240), and stored on a computer (pClamp 6.0, Axon Instruments) for  subsequent analysis.	transcription
53487	1	335062	5	NULL	NULL	0	NULL		NULL		is substituted for	NULL		octarepeat histidine residues			NULL		glycine (PHGG(G/S)WGQ4 PGGG(G/S)WGQ4) 		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_53_55443_s_217	15459186	Missense mutations substituting octarepeat histidine residues for glycine (PHGG(G/S)WGQ4   PGGG(G/S)WGQ4) also inactivated the protective effect of PrPC ( Fig. 5).	transcription
53488	2	335062	5	NULL	NULL	0	NULL	statement 1	NULL		inactivates	NULL				PrPC	NULL	protective effect of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_53_55443_s_217	15459186	Missense mutations substituting octarepeat histidine residues for glycine (PHGG(G/S)WGQ4   PGGG(G/S)WGQ4) also inactivated the protective effect of PrPC ( Fig. 5).	transcription
53237	1	335062	7	NULL	NULL	0	NULL		NULL	Missense mutant	substituted for	NULL		octarepeat histidine residues			NULL		 glycine		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_53_55443_s_217	15459186	Missense mutations substituting octarepeat histidine residues for glycine (PHGG(G/S)WGQ4   PGGG(G/S)WGQ4) also inactivated the protective effect of PrPC ( Fig. 5).	transcription
53238	3	335062	7	NULL	NULL	0	NULL	statement 1	NULL		inactivate	NULL				PrPC	NULL	protective effect of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_53_55443_s_217	15459186	Missense mutations substituting octarepeat histidine residues for glycine (PHGG(G/S)WGQ4   PGGG(G/S)WGQ4) also inactivated the protective effect of PrPC ( Fig. 5).	transcription
53239	2	335062	7	NULL	NULL	0	NULL	statement 1	NULL		contains	NULL					NULL		(PHGG(G/S)WGQ4 PGGG(G/S)WGQ4)		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_53_55443_s_217	15459186	Missense mutations substituting octarepeat histidine residues for glycine (PHGG(G/S)WGQ4   PGGG(G/S)WGQ4) also inactivated the protective effect of PrPC ( Fig. 5).	transcription
53489	1	335063	5	NULL	NULL	0	NULL	NE	NULL		is relased from	NULL				hippocampal synaptosomes	NULL				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_313_1_242_s_115	15608072	As shown in  Fig. 2, addition to the superfusion medium of PP2 (1 muM) or lavendustin A (5 muM) inhibited in part the [3]NE release induced by SRIF-14/NMDA/glycine from hippocampal synaptosomes.	transcription
53490	2	335063	5	NULL	NULL	0	NULL	SRIF-14/NMDA/glycine	NULL		induces	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_313_1_242_s_115	15608072	As shown in  Fig. 2, addition to the superfusion medium of PP2 (1 muM) or lavendustin A (5 muM) inhibited in part the [3]NE release induced by SRIF-14/NMDA/glycine from hippocampal synaptosomes.	transcription
53491	3	335063	5	NULL	NULL	0	NULL	PP2	NULL		inhibits	NULL	partly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_313_1_242_s_115	15608072	As shown in  Fig. 2, addition to the superfusion medium of PP2 (1 muM) or lavendustin A (5 muM) inhibited in part the [3]NE release induced by SRIF-14/NMDA/glycine from hippocampal synaptosomes.	transcription
53492	4	335063	5	NULL	NULL	0	NULL	lavendustin A	NULL		inhibits	NULL	partly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_313_1_242_s_115	15608072	As shown in  Fig. 2, addition to the superfusion medium of PP2 (1 muM) or lavendustin A (5 muM) inhibited in part the [3]NE release induced by SRIF-14/NMDA/glycine from hippocampal synaptosomes.	transcription
53493	5	335063	5	NULL	NULL	0	NULL	statement 3	NULL		is an alternative to	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_313_1_242_s_115	15608072	As shown in  Fig. 2, addition to the superfusion medium of PP2 (1 muM) or lavendustin A (5 muM) inhibited in part the [3]NE release induced by SRIF-14/NMDA/glycine from hippocampal synaptosomes.	transcription
53240	1	335063	7	NULL	NULL	0	NULL	SRIF-14/NMDA/glycine	NULL	 hippocampal synaptosomes	induce	NULL				NE	NULL	release of			NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_313_1_242_s_115	15608072	As shown in  Fig. 2, addition to the superfusion medium of PP2 (1 muM) or lavendustin A (5 muM) inhibited in part the [3]NE release induced by SRIF-14/NMDA/glycine from hippocampal synaptosomes.	transcription
53241	2	335063	7	NULL	NULL	0	NULL	 PP2 	NULL		inhibit	NULL	partly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_313_1_242_s_115	15608072	As shown in  Fig. 2, addition to the superfusion medium of PP2 (1 muM) or lavendustin A (5 muM) inhibited in part the [3]NE release induced by SRIF-14/NMDA/glycine from hippocampal synaptosomes.	transcription
53242	3	335063	7	NULL	NULL	0	NULL	 lavendustin A	NULL		inhibit	NULL	partly			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_313_1_242_s_115	15608072	As shown in  Fig. 2, addition to the superfusion medium of PP2 (1 muM) or lavendustin A (5 muM) inhibited in part the [3]NE release induced by SRIF-14/NMDA/glycine from hippocampal synaptosomes.	transcription
53494	1	335064	5	NULL	NULL	0	NULL	ETC	NULL		is	NULL				electron transport chain	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_412_2_265_s_8	9256232	It was shown that oxidation of glycine coupled with NADH oxidation in mitochondrial electron transport chain (ETC) is less inhibited by the inhibitor of Complex I rotenone than oxidation of other mitochondrial substrates  [ 5.	transcription
53495	2	335064	5	NULL	NULL	0	NULL	glycine	NULL	oxidation of	is coupled with	NULL				NADH	NULL	oxidation of			NULL	mitochondrial ETC	0	NULL	NULL	NULL	gw60_febslett_412_2_265_s_8	9256232	It was shown that oxidation of glycine coupled with NADH oxidation in mitochondrial electron transport chain (ETC) is less inhibited by the inhibitor of Complex I rotenone than oxidation of other mitochondrial substrates  [ 5.	transcription
53496	3	335064	5	NULL	NULL	0	NULL	rotenone	NULL		is an inhibitor of	NULL				Complex I	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_412_2_265_s_8	9256232	It was shown that oxidation of glycine coupled with NADH oxidation in mitochondrial electron transport chain (ETC) is less inhibited by the inhibitor of Complex I rotenone than oxidation of other mitochondrial substrates  [ 5.	transcription
53497	4	335064	5	NULL	NULL	0	NULL	rotenone	NULL		inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_412_2_265_s_8	9256232	It was shown that oxidation of glycine coupled with NADH oxidation in mitochondrial electron transport chain (ETC) is less inhibited by the inhibitor of Complex I rotenone than oxidation of other mitochondrial substrates  [ 5.	transcription
53498	5	335064	5	NULL	NULL	0	NULL	rotenone	NULL		inhibits	NULL				substrates	NULL	oxidation of;;mitochondrial			NULL		0	NULL	NULL	NULL	gw60_febslett_412_2_265_s_8	9256232	It was shown that oxidation of glycine coupled with NADH oxidation in mitochondrial electron transport chain (ETC) is less inhibited by the inhibitor of Complex I rotenone than oxidation of other mitochondrial substrates  [ 5.	transcription
53499	6	335064	5	NULL	NULL	0	NULL	statement 4	NULL		lesser than	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_412_2_265_s_8	9256232	It was shown that oxidation of glycine coupled with NADH oxidation in mitochondrial electron transport chain (ETC) is less inhibited by the inhibitor of Complex I rotenone than oxidation of other mitochondrial substrates  [ 5.	transcription
53243	1	335064	7	NULL	NULL	0	NULL	glycine 	NULL	oxidation of	coupled with	NULL				NADH	NULL	oxidation of			NULL	mitochondrial ETC	NULL	NULL	NULL	NULL	gw60_febslett_412_2_265_s_8	9256232	It was shown that oxidation of glycine coupled with NADH oxidation in mitochondrial electron transport chain (ETC) is less inhibited by the inhibitor of Complex I rotenone than oxidation of other mitochondrial substrates  [ 5.	transcription
53270	2	335064	7	NULL	NULL	0	NULL	Complex I rotenone	NULL	inhibitor of	inhibit	NULL				statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw60_febslett_412_2_265_s_8	9256232	It was shown that oxidation of glycine coupled with NADH oxidation in mitochondrial electron transport chain (ETC) is less inhibited by the inhibitor of Complex I rotenone than oxidation of other mitochondrial substrates  [ 5.	transcription
53271	3	335064	7	NULL	NULL	0	NULL	substrates	NULL	oxidation of;;mitochondrial	inhibit	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_412_2_265_s_8	9256232	It was shown that oxidation of glycine coupled with NADH oxidation in mitochondrial electron transport chain (ETC) is less inhibited by the inhibitor of Complex I rotenone than oxidation of other mitochondrial substrates  [ 5.	transcription
53272	4	335064	7	NULL	NULL	0	NULL	statement 2	NULL	inhibition of	is less than	NULL				statement 3	NULL	inhibition of			NULL		NULL	NULL	NULL	NULL	gw60_febslett_412_2_265_s_8	9256232	It was shown that oxidation of glycine coupled with NADH oxidation in mitochondrial electron transport chain (ETC) is less inhibited by the inhibitor of Complex I rotenone than oxidation of other mitochondrial substrates  [ 5.	transcription
53273	5	335064	7	NULL	NULL	0	NULL	ETC	NULL		is	NULL				electron transport chain	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_412_2_265_s_8	9256232	It was shown that oxidation of glycine coupled with NADH oxidation in mitochondrial electron transport chain (ETC) is less inhibited by the inhibitor of Complex I rotenone than oxidation of other mitochondrial substrates  [ 5.	transcription
53500	1	335065	5	NULL	NULL	0	NULL	Class III ribonucleotide reductase	NULL		catalyzes	NULL				AdoMet	NULL	reductive cleavage of			NULL		0	NULL	NULL	NULL	gw60_febslett_529_2_237_s_183	12372607	Class III ribonucleotide reductase also catalyzes reductive cleavage of AdoMet to generate 5''-deoxyadenosine, in this case as an oxidant for a polypeptide glycine residue, generating a glycyl radical that is required for initiating ribonucleotide reduction [  38].	transcription
53501	2	335065	5	NULL	NULL	0	NULL	statement 1	NULL		generates	NULL				5''-deoxyadenosine	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_529_2_237_s_183	12372607	Class III ribonucleotide reductase also catalyzes reductive cleavage of AdoMet to generate 5''-deoxyadenosine, in this case as an oxidant for a polypeptide glycine residue, generating a glycyl radical that is required for initiating ribonucleotide reduction [  38].	transcription
53502	3	335065	5	NULL	NULL	0	NULL	Class III ribonucleotide reductase	NULL		acts as	NULL				polypeptide glycine residue	NULL	oxidant for			NULL		0	NULL	NULL	NULL	gw60_febslett_529_2_237_s_183	12372607	Class III ribonucleotide reductase also catalyzes reductive cleavage of AdoMet to generate 5''-deoxyadenosine, in this case as an oxidant for a polypeptide glycine residue, generating a glycyl radical that is required for initiating ribonucleotide reduction [  38].	transcription
53503	4	335065	5	NULL	NULL	0	NULL	statement 3	NULL		generates	NULL				glycyl radical	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_529_2_237_s_183	12372607	Class III ribonucleotide reductase also catalyzes reductive cleavage of AdoMet to generate 5''-deoxyadenosine, in this case as an oxidant for a polypeptide glycine residue, generating a glycyl radical that is required for initiating ribonucleotide reduction [  38].	transcription
53504	5	335065	5	NULL	NULL	0	NULL	glycyl radical	NULL		is required for	NULL				ribonucleotide	NULL	initiating;;reduction of			NULL		NULL	NULL	NULL	NULL	gw60_febslett_529_2_237_s_183	12372607	Class III ribonucleotide reductase also catalyzes reductive cleavage of AdoMet to generate 5''-deoxyadenosine, in this case as an oxidant for a polypeptide glycine residue, generating a glycyl radical that is required for initiating ribonucleotide reduction [  38].	transcription
53274	1	335065	7	NULL	NULL	0	NULL	Class III ribonucleotide reductase	NULL		catalyse	NULL				AdoMet	NULL	 reductive cleavage of 			NULL		0	NULL	NULL	NULL	gw60_febslett_529_2_237_s_183	12372607	Class III ribonucleotide reductase also catalyzes reductive cleavage of AdoMet to generate 5''-deoxyadenosine, in this case as an oxidant for a polypeptide glycine residue, generating a glycyl radical that is required for initiating ribonucleotide reduction [  38].	transcription
53275	2	335065	7	NULL	NULL	0	NULL	statement 1	NULL		generate	NULL				5''-deoxyadenosine	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_529_2_237_s_183	12372607	Class III ribonucleotide reductase also catalyzes reductive cleavage of AdoMet to generate 5''-deoxyadenosine, in this case as an oxidant for a polypeptide glycine residue, generating a glycyl radical that is required for initiating ribonucleotide reduction [  38].	transcription
53276	3	335065	7	NULL	NULL	0	NULL	Class III ribonucleotide reductase	NULL		generates	NULL				glycyl radical	NULL				NULL		0	NULL	NULL	NULL	gw60_febslett_529_2_237_s_183	12372607	Class III ribonucleotide reductase also catalyzes reductive cleavage of AdoMet to generate 5''-deoxyadenosine, in this case as an oxidant for a polypeptide glycine residue, generating a glycyl radical that is required for initiating ribonucleotide reduction [  38].	transcription
53277	4	335065	7	NULL	NULL	0	NULL	Class III ribonucleotide reductase	NULL		acts as a 	NULL				polypeptide glycine residue	NULL	oxidant for			NULL		0	NULL	NULL	NULL	gw60_febslett_529_2_237_s_183	12372607	Class III ribonucleotide reductase also catalyzes reductive cleavage of AdoMet to generate 5''-deoxyadenosine, in this case as an oxidant for a polypeptide glycine residue, generating a glycyl radical that is required for initiating ribonucleotide reduction [  38].	transcription
53278	5	335065	7	NULL	NULL	0	NULL	statement 3	NULL		is required for	NULL				ribonucleotide	NULL	initiating;;  reduction of			NULL		0	NULL	NULL	NULL	gw60_febslett_529_2_237_s_183	12372607	Class III ribonucleotide reductase also catalyzes reductive cleavage of AdoMet to generate 5''-deoxyadenosine, in this case as an oxidant for a polypeptide glycine residue, generating a glycyl radical that is required for initiating ribonucleotide reduction [  38].	transcription
53505	1	335067	5	NULL	NULL	0	NULL	MPO	NULL		induce	NULL				LDL	NULL	modification of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1481_1_109_s_167	11004581	Methionine showed an even stronger retarding effect on MPO-induced LDL modification among the HOCl traps used (factor 103), while glycine was the least effective (factor 13,  Fig. 5).	transcription
53506	2	335067	5	NULL	NULL	0	NULL	methionine	NULL		retard	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1481_1_109_s_167	11004581	Methionine showed an even stronger retarding effect on MPO-induced LDL modification among the HOCl traps used (factor 103), while glycine was the least effective (factor 13,  Fig. 5).	transcription
53507	3	335067	5	NULL	NULL	0	NULL	glycine	NULL		retard	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1481_1_109_s_167	11004581	Methionine showed an even stronger retarding effect on MPO-induced LDL modification among the HOCl traps used (factor 103), while glycine was the least effective (factor 13,  Fig. 5).	transcription
53508	4	335067	5	NULL	NULL	0	NULL	statement 2	NULL		stronger than	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1481_1_109_s_167	11004581	Methionine showed an even stronger retarding effect on MPO-induced LDL modification among the HOCl traps used (factor 103), while glycine was the least effective (factor 13,  Fig. 5).	transcription
53279	1	335067	7	NULL	NULL	0	NULL	MPO	NULL		induce	NULL				LDL	NULL	modification of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1481_1_109_s_167	11004581	Methionine showed an even stronger retarding effect on MPO-induced LDL modification among the HOCl traps used (factor 103), while glycine was the least effective (factor 13,  Fig. 5).	transcription
53280	2	335067	7	NULL	NULL	0	NULL	Methionine	NULL		retard	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1481_1_109_s_167	11004581	Methionine showed an even stronger retarding effect on MPO-induced LDL modification among the HOCl traps used (factor 103), while glycine was the least effective (factor 13,  Fig. 5).	transcription
53281	3	335067	7	NULL	NULL	0	NULL	glycine	NULL		retard	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1481_1_109_s_167	11004581	Methionine showed an even stronger retarding effect on MPO-induced LDL modification among the HOCl traps used (factor 103), while glycine was the least effective (factor 13,  Fig. 5).	transcription
53282	4	335067	7	NULL	NULL	0	NULL	statement 2	NULL	retarding effect of	is stronger than	NULL				statement 3	NULL	retarding effect of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1481_1_109_s_167	11004581	Methionine showed an even stronger retarding effect on MPO-induced LDL modification among the HOCl traps used (factor 103), while glycine was the least effective (factor 13,  Fig. 5).	transcription
53509	1	335070	5	NULL	NULL	0	NULL	glutamate	NULL		activates	NULL				NR1/NR2A receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53510	2	335070	5	NULL	NULL	0	NULL	glutamate	NULL		activates	NULL				NR1/NR2B receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53511	3	335070	5	NULL	NULL	0	NULL	glutamate	NULL		activates	NULL				NR1/NR2C receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53512	4	335070	5	NULL	NULL	0	NULL	glutamate	NULL		activates	NULL				NR1/NR2D receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53513	5	335070	5	NULL	NULL	0	NULL	glycine	NULL		activates	NULL				NR1/NR2A receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53514	6	335070	5	NULL	NULL	0	NULL	glycine	NULL		activates	NULL				NR1/NR2B receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53515	7	335070	5	NULL	NULL	0	NULL	glycine	NULL		activates	NULL				NR1/NR2C receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53516	8	335070	5	NULL	NULL	0	NULL	glycine	NULL		activates	NULL				NR1/NR2D receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53517	9	335070	5	NULL	NULL	0	NULL	3alpha5betaS	NULL		decreases	NULL				statement 1	NULL	efficacy of			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53518	10	335070	5	NULL	NULL	0	NULL	3alpha5betaS	NULL		decreases	NULL				statement 2	NULL	efficacy of			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53519	11	335070	5	NULL	NULL	0	NULL	3alpha5betaS	NULL		decreases	NULL				statement 3	NULL	efficacy of			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53520	12	335070	5	NULL	NULL	0	NULL	3alpha5betaS	NULL		decreases	NULL				statement 4	NULL	efficacy of			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53521	13	335070	5	NULL	NULL	0	NULL	3alpha5betaS	NULL		decreases	NULL				statement 5	NULL	efficacy of			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53522	14	335070	5	NULL	NULL	0	NULL	3alpha5betaS	NULL		decreases	NULL				statement 6	NULL	efficacy of			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53523	15	335070	5	NULL	NULL	0	NULL	3alpha5betaS	NULL		decreases	NULL				statement 7	NULL	efficacy of			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53524	16	335070	5	NULL	NULL	0	NULL	3alpha5betaS	NULL		decreases	NULL				statement 8	NULL	efficacy of			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53283	1	335070	7	NULL	NULL	0	NULL	glutamate	NULL		activate	NULL				NR1/NR2A receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53284	2	335070	7	NULL	NULL	0	NULL	glutamate	NULL		activate	NULL				NR1/NR2B receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53285	3	335070	7	NULL	NULL	0	NULL	glutamate 	NULL		activate	NULL				NR1/NR2C receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53286	4	335070	7	NULL	NULL	0	NULL	glutamate	NULL		activate	NULL				NR1/NR2D receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53287	5	335070	7	NULL	NULL	0	NULL	glycine	NULL		activate	NULL				NR1/NR2A receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53288	6	335070	7	NULL	NULL	0	NULL	glycine	NULL		activate	NULL				NR1/NR2B receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53289	7	335070	7	NULL	NULL	0	NULL	glycine	NULL		activate	NULL				NR1/NR2C receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53290	8	335070	7	NULL	NULL	0	NULL	glycine	NULL		activate	NULL				NR1/NR2D receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53291	9	335070	7	NULL	NULL	0	NULL	3alpha5betaS	NULL		decrease	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53292	10	335070	7	NULL	NULL	0	NULL	3alpha5betaS	NULL		decrease	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53293	11	335070	7	NULL	NULL	0	NULL	3alpha5betaS	NULL		decrease	NULL				statement 3	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53294	12	335070	7	NULL	NULL	0	NULL	3alpha5betaS	NULL		decrease	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53295	13	335070	7	NULL	NULL	0	NULL	3alpha5betaS	NULL		decrease	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53296	14	335070	7	NULL	NULL	0	NULL	3alpha5betaS	NULL		decrease	NULL				statement 6	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53297	15	335070	7	NULL	NULL	0	NULL	3alpha5betaS	NULL		decrease	NULL				statement 7	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53298	16	335070	7	NULL	NULL	0	NULL	3alpha5betaS	NULL		decrease	NULL				statement 8	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_4_901_s_135	11861317	As shown in  Figure 5, 3alpha5betaS decreases the efficacy with which glutamate and glycine activate NR1/NR2A ( Figure 5a,b), NR1/NR2B ( Figure 5c,d), NR1/NR2C ( Figure 5e,f), and NR1/NR2D ( Figure 5g,h) receptors.	transcription
53525	1	335071	5	NULL	NULL	0	NULL	5-HT1A receptor	NULL		affinity for	NULL	high	binding sites		8-OH-DPAT	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_137_3_345_s_7	12237254	5 The proportion of 5-HT1A receptor binding sites detected by [3]-MPPF that displayed high affinity for 8-OH-DPAT was significantly greater when the interacting G protein contained isoleucine rather than glycine at residue351.	transcription
53526	2	335071	5	NULL	NULL	0	NULL	interacting G protein	NULL		contains	NULL					NULL		isoleucine residue 351		NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_137_3_345_s_7	12237254	5 The proportion of 5-HT1A receptor binding sites detected by [3]-MPPF that displayed high affinity for 8-OH-DPAT was significantly greater when the interacting G protein contained isoleucine rather than glycine at residue351.	transcription
53527	3	335071	5	NULL	NULL	0	NULL	interacting G protein	NULL		contains	NULL					NULL		glycine residue351		NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_137_3_345_s_7	12237254	5 The proportion of 5-HT1A receptor binding sites detected by [3]-MPPF that displayed high affinity for 8-OH-DPAT was significantly greater when the interacting G protein contained isoleucine rather than glycine at residue351.	transcription
53299	1	335071	7	NULL	NULL	0	NULL	5-HT1A receptor	NULL		high affinity for	NULL		binding sites		8-OH-DPAT	NULL				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_137_3_345_s_7	12237254	5 The proportion of 5-HT1A receptor binding sites detected by [3]-MPPF that displayed high affinity for 8-OH-DPAT was significantly greater when the interacting G protein contained isoleucine rather than glycine at residue351.	transcription
53300	2	335071	7	NULL	NULL	0	NULL	interacting G protein	NULL		contains	NULL					NULL		isoleucine residue 351		NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_137_3_345_s_7	12237254	5 The proportion of 5-HT1A receptor binding sites detected by [3]-MPPF that displayed high affinity for 8-OH-DPAT was significantly greater when the interacting G protein contained isoleucine rather than glycine at residue351.	transcription
53301	3	335071	7	NULL	NULL	0	NULL	interacting G protein	NULL		contains	NULL					NULL		glycine residue 351		NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_137_3_345_s_7	12237254	5 The proportion of 5-HT1A receptor binding sites detected by [3]-MPPF that displayed high affinity for 8-OH-DPAT was significantly greater when the interacting G protein contained isoleucine rather than glycine at residue351.	transcription
53305	4	335071	7	NULL	NULL	0	NULL	statement 2	NULL	affinity of	is higher than	NULL				statement 3	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_137_3_345_s_7	12237254	5 The proportion of 5-HT1A receptor binding sites detected by [3]-MPPF that displayed high affinity for 8-OH-DPAT was significantly greater when the interacting G protein contained isoleucine rather than glycine at residue351.	transcription
53528	1	335072	5	NULL	NULL	0	NULL	glycine	NULL	substitution of	affects	NULL	may				NULL	secondary structure of	region following the helix 5		NULL		0	NULL	NULL	NULL	gw60_chembiol_7_9_709_s_114	10980451	Their substitution for glycine may affect the secondary structure of the region following the helix  5, not only because of an increased flexibility, but also because of the loss of hydrogen bonds between the side chains of S149 and Ser164, and nearby residues.	transcription
53529	2	335072	5	NULL	NULL	0	NULL	flexibility	NULL	increased	leads to	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_chembiol_7_9_709_s_114	10980451	Their substitution for glycine may affect the secondary structure of the region following the helix  5, not only because of an increased flexibility, but also because of the loss of hydrogen bonds between the side chains of S149 and Ser164, and nearby residues.	transcription
53530	3	335072	5	NULL	NULL	0	NULL	hydrogen bonds	NULL		is lost between	NULL					NULL	side chains of	S149;;Ser164		NULL		0	NULL	NULL	NULL	gw60_chembiol_7_9_709_s_114	10980451	Their substitution for glycine may affect the secondary structure of the region following the helix  5, not only because of an increased flexibility, but also because of the loss of hydrogen bonds between the side chains of S149 and Ser164, and nearby residues.	transcription
53531	4	335072	5	NULL	NULL	0	NULL	statement 3	NULL		leads to	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_chembiol_7_9_709_s_114	10980451	Their substitution for glycine may affect the secondary structure of the region following the helix  5, not only because of an increased flexibility, but also because of the loss of hydrogen bonds between the side chains of S149 and Ser164, and nearby residues.	transcription
53306	1	335072	7	NULL	NULL	0	NULL	glycine	NULL	 substitution for	affect	NULL					NULL	secondary structure of 	region following helix 5		NULL		0	NULL	NULL	NULL	gw60_chembiol_7_9_709_s_114	10980451	Their substitution for glycine may affect the secondary structure of the region following the helix  5, not only because of an increased flexibility, but also because of the loss of hydrogen bonds between the side chains of S149 and Ser164, and nearby residues.	transcription
53307	2	335072	7	NULL	NULL	0	NULL	statement 1	NULL		because of	NULL				increased flexibility	NULL				NULL		0	NULL	NULL	NULL	gw60_chembiol_7_9_709_s_114	10980451	Their substitution for glycine may affect the secondary structure of the region following the helix  5, not only because of an increased flexibility, but also because of the loss of hydrogen bonds between the side chains of S149 and Ser164, and nearby residues.	transcription
53308	3	335072	7	NULL	NULL	0	NULL	statement 1	NULL		because of	NULL				hydrogen bonds	NULL	loss of	between side chains of S149 and Ser164		NULL		NULL	NULL	NULL	NULL	gw60_chembiol_7_9_709_s_114	10980451	Their substitution for glycine may affect the secondary structure of the region following the helix  5, not only because of an increased flexibility, but also because of the loss of hydrogen bonds between the side chains of S149 and Ser164, and nearby residues.	transcription
53532	1	335080	5	NULL	NULL	0	NULL	ivermectin	NULL		induce	NULL				GlyR	NULL	direct;;activation of;;mutant	R271Q		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_16_12556_s_174	11278873	Although 0.03 muM ivermectin induced little direct activation of the R271Q mutant GlyR, it potentiated the magnitude of currents activated by a 7 mM (EC50) concentration of glycine (Fig.  5 A).	transcription
53309	1	335080	7	NULL	NULL	0	NULL	ivermectin	NULL		induce	NULL				GlyR	NULL	direct activation of ;;mutant	R271Q 		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_16_12556_s_174	11278873	Although 0.03 muM ivermectin induced little direct activation of the R271Q mutant GlyR, it potentiated the magnitude of currents activated by a 7 mM (EC50) concentration of glycine (Fig.  5 A).	transcription
53533	1	335082	5	NULL	NULL	0	NULL	EGF-R peptide	NULL	aromatic residues of	is mutated to	NULL				EGF-R peptide	NULL		glycine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_48_30429_s_160	9374534	In accordance with these observations, a mutated EGF-R peptide in which all aromatic residues were changed to glycine failed to interact with the caveolin 1 scaffolding domain (Fig.  5 A).	transcription
53534	2	335082	5	NULL	NULL	0	NULL	statement 1	NULL		does not interact with	NULL				caveolin 1	NULL		scaffolding domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_48_30429_s_160	9374534	In accordance with these observations, a mutated EGF-R peptide in which all aromatic residues were changed to glycine failed to interact with the caveolin 1 scaffolding domain (Fig.  5 A).	transcription
53310	1	335082	7	NULL	NULL	0	NULL	EGF-R peptide	NULL		changed to	NULL		aromatic residues 		EGF-R peptide	NULL	mutant	glycine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_48_30429_s_160	9374534	In accordance with these observations, a mutated EGF-R peptide in which all aromatic residues were changed to glycine failed to interact with the caveolin 1 scaffolding domain (Fig.  5 A).	transcription
53311	2	335082	7	NULL	NULL	0	NULL	statement 1	NULL		does not interact with	NULL				caveolin 1 	NULL		 scaffolding domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_48_30429_s_160	9374534	In accordance with these observations, a mutated EGF-R peptide in which all aromatic residues were changed to glycine failed to interact with the caveolin 1 scaffolding domain (Fig.  5 A).	transcription
53535	1	335084	5	NULL	NULL	0	NULL	polyamine	NULL	stimulation of	is independent of	NULL				glycine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_40_24971_s_128	9312102	Because glycine-independent polyamine stimulation may result from the relief of the tonic inhibition of the NMDA receptor by protons ( 39), the proton inhibition of the Glu-201 mutant receptors was investigated (Fig.  5,  A and  B).	transcription
53536	2	335084	5	NULL	NULL	0	NULL	protons	NULL		inhibit	NULL				NMDA receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_40_24971_s_128	9312102	Because glycine-independent polyamine stimulation may result from the relief of the tonic inhibition of the NMDA receptor by protons ( 39), the proton inhibition of the Glu-201 mutant receptors was investigated (Fig.  5,  A and  B).	transcription
53537	3	335084	5	NULL	NULL	0	NULL	statement 2	NULL	relief of	results in	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_40_24971_s_128	9312102	Because glycine-independent polyamine stimulation may result from the relief of the tonic inhibition of the NMDA receptor by protons ( 39), the proton inhibition of the Glu-201 mutant receptors was investigated (Fig.  5,  A and  B).	transcription
53312	1	335084	7	NULL	NULL	0	NULL	protons	NULL		inhibit	NULL				NMDA receptor	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_40_24971_s_128	9312102	Because glycine-independent polyamine stimulation may result from the relief of the tonic inhibition of the NMDA receptor by protons ( 39), the proton inhibition of the Glu-201 mutant receptors was investigated (Fig.  5,  A and  B).	transcription
53313	2	335084	7	NULL	NULL	0	NULL	statement 1	NULL		is a type of	NULL				tonic inhibition	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_40_24971_s_128	9312102	Because glycine-independent polyamine stimulation may result from the relief of the tonic inhibition of the NMDA receptor by protons ( 39), the proton inhibition of the Glu-201 mutant receptors was investigated (Fig.  5,  A and  B).	transcription
53314	3	335084	7	NULL	NULL	0	NULL	polyamine	NULL	stimulation of	independent of	NULL				glycine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_40_24971_s_128	9312102	Because glycine-independent polyamine stimulation may result from the relief of the tonic inhibition of the NMDA receptor by protons ( 39), the proton inhibition of the Glu-201 mutant receptors was investigated (Fig.  5,  A and  B).	transcription
53315	4	335084	7	NULL	NULL	0	NULL	statement 3	NULL		result from	NULL	may			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_40_24971_s_128	9312102	Because glycine-independent polyamine stimulation may result from the relief of the tonic inhibition of the NMDA receptor by protons ( 39), the proton inhibition of the Glu-201 mutant receptors was investigated (Fig.  5,  A and  B).	transcription
53316	5	335084	7	NULL	NULL	0	NULL	protons	NULL		inhibit	NULL				receptors	NULL	mutant	Glu-201		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_40_24971_s_128	9312102	Because glycine-independent polyamine stimulation may result from the relief of the tonic inhibition of the NMDA receptor by protons ( 39), the proton inhibition of the Glu-201 mutant receptors was investigated (Fig.  5,  A and  B).	transcription
53538	1	335085	5	NULL	NULL	0	NULL	glutamate	NULL		stimulates	NULL				NMDA receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34252_s_238	10950953	Subsequent addition of 100 muML-glutamate and 10 muM glycine (stimulating both NMDA receptors and mGluRs)  reduced [Ca2+] i (Fig.  4 b;  n = 5).	transcription
53539	2	335085	5	NULL	NULL	0	NULL	glutamate	NULL		stimulates	NULL				mGluRs	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34252_s_238	10950953	Subsequent addition of 100 muML-glutamate and 10 muM glycine (stimulating both NMDA receptors and mGluRs)  reduced [Ca2+] i (Fig.  4 b;  n = 5).	transcription
53540	3	335085	5	NULL	NULL	0	NULL	glycine	NULL		stimulates	NULL				NMDA receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34252_s_238	10950953	Subsequent addition of 100 muML-glutamate and 10 muM glycine (stimulating both NMDA receptors and mGluRs)  reduced [Ca2+] i (Fig.  4 b;  n = 5).	transcription
53541	4	335085	5	NULL	NULL	0	NULL	glycine	NULL		stimulates	NULL				mGluRs	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34252_s_238	10950953	Subsequent addition of 100 muML-glutamate and 10 muM glycine (stimulating both NMDA receptors and mGluRs)  reduced [Ca2+] i (Fig.  4 b;  n = 5).	transcription
53542	5	335085	5	NULL	NULL	0	NULL	statement 1	NULL		occurs along with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34252_s_238	10950953	Subsequent addition of 100 muML-glutamate and 10 muM glycine (stimulating both NMDA receptors and mGluRs)  reduced [Ca2+] i (Fig.  4 b;  n = 5).	transcription
53543	6	335085	5	NULL	NULL	0	NULL	statement 5	NULL		reduces	NULL				[Ca2+] i	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34252_s_238	10950953	Subsequent addition of 100 muML-glutamate and 10 muM glycine (stimulating both NMDA receptors and mGluRs)  reduced [Ca2+] i (Fig.  4 b;  n = 5).	transcription
53544	7	335085	5	NULL	NULL	0	NULL	statement 3	NULL		occurs along with	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34252_s_238	10950953	Subsequent addition of 100 muML-glutamate and 10 muM glycine (stimulating both NMDA receptors and mGluRs)  reduced [Ca2+] i (Fig.  4 b;  n = 5).	transcription
53545	8	335085	5	NULL	NULL	0	NULL	statement 7	NULL		reduces	NULL				[Ca2+] i	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34252_s_238	10950953	Subsequent addition of 100 muML-glutamate and 10 muM glycine (stimulating both NMDA receptors and mGluRs)  reduced [Ca2+] i (Fig.  4 b;  n = 5).	transcription
53317	1	335085	7	NULL	NULL	0	NULL	NMDA receptor	NULL	stimulation of	reduce	NULL				Ca2+	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34252_s_238	10950953	Subsequent addition of 100 muML-glutamate and 10 muM glycine (stimulating both NMDA receptors and mGluRs)  reduced [Ca2+] i (Fig.  4 b;  n = 5).	transcription
53318	2	335085	7	NULL	NULL	0	NULL	mGluRs	NULL	stimulation of	reduce	NULL				Ca2+	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34252_s_238	10950953	Subsequent addition of 100 muML-glutamate and 10 muM glycine (stimulating both NMDA receptors and mGluRs)  reduced [Ca2+] i (Fig.  4 b;  n = 5).	transcription
53319	3	335085	7	NULL	NULL	0	NULL	statement 1	NULL		occur along with	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34252_s_238	10950953	Subsequent addition of 100 muML-glutamate and 10 muM glycine (stimulating both NMDA receptors and mGluRs)  reduced [Ca2+] i (Fig.  4 b;  n = 5).	transcription
53546	1	335086	5	NULL	NULL	0	NULL	OATP2	NULL	human	transports	NULL				cholyl taurine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_30_23161_s_278	10779507	In contrast to human OATP2, which transports cholyl taurine and whose 17beta-glucuronosyl estradiol transport was inhibited by cholate ( 5), OATP8 did neither transport cholyl taurine nor cholate nor cholyl glycine.	transcription
53547	2	335086	5	NULL	NULL	0	NULL	OATP2	NULL	human	transports	NULL				17beta-glucuronosyl estradiol	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_30_23161_s_278	10779507	In contrast to human OATP2, which transports cholyl taurine and whose 17beta-glucuronosyl estradiol transport was inhibited by cholate ( 5), OATP8 did neither transport cholyl taurine nor cholate nor cholyl glycine.	transcription
53548	3	335086	5	NULL	NULL	0	NULL	cholate	NULL		inhibits	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_30_23161_s_278	10779507	In contrast to human OATP2, which transports cholyl taurine and whose 17beta-glucuronosyl estradiol transport was inhibited by cholate ( 5), OATP8 did neither transport cholyl taurine nor cholate nor cholyl glycine.	transcription
53549	4	335086	5	NULL	NULL	0	NULL	OATP8	NULL		does not transport	NULL				cholyl taurine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_30_23161_s_278	10779507	In contrast to human OATP2, which transports cholyl taurine and whose 17beta-glucuronosyl estradiol transport was inhibited by cholate ( 5), OATP8 did neither transport cholyl taurine nor cholate nor cholyl glycine.	transcription
53550	5	335086	5	NULL	NULL	0	NULL	OATP8	NULL		does not transport	NULL				cholate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_30_23161_s_278	10779507	In contrast to human OATP2, which transports cholyl taurine and whose 17beta-glucuronosyl estradiol transport was inhibited by cholate ( 5), OATP8 did neither transport cholyl taurine nor cholate nor cholyl glycine.	transcription
53551	6	335086	5	NULL	NULL	0	NULL	OATP8	NULL		does not transport	NULL				cholyl glycine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_30_23161_s_278	10779507	In contrast to human OATP2, which transports cholyl taurine and whose 17beta-glucuronosyl estradiol transport was inhibited by cholate ( 5), OATP8 did neither transport cholyl taurine nor cholate nor cholyl glycine.	transcription
53320	1	335086	7	NULL	NULL	0	NULL	OATP2	NULL	human	transports	NULL				cholyl taurine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_30_23161_s_278	10779507	In contrast to human OATP2, which transports cholyl taurine and whose 17beta-glucuronosyl estradiol transport was inhibited by cholate ( 5), OATP8 did neither transport cholyl taurine nor cholate nor cholyl glycine.	transcription
53321	2	335086	7	NULL	NULL	0	NULL	cholate	NULL		inhibit	NULL				17beta-glucuronosyl estradiol	NULL	transport of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_30_23161_s_278	10779507	In contrast to human OATP2, which transports cholyl taurine and whose 17beta-glucuronosyl estradiol transport was inhibited by cholate ( 5), OATP8 did neither transport cholyl taurine nor cholate nor cholyl glycine.	transcription
53322	3	335086	7	NULL	NULL	0	NULL	OATP8	NULL		does not transport	NULL				cholyl taurine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_30_23161_s_278	10779507	In contrast to human OATP2, which transports cholyl taurine and whose 17beta-glucuronosyl estradiol transport was inhibited by cholate ( 5), OATP8 did neither transport cholyl taurine nor cholate nor cholyl glycine.	transcription
53323	4	335086	7	NULL	NULL	0	NULL	OATP8	NULL		does not transport	NULL				cholate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_30_23161_s_278	10779507	In contrast to human OATP2, which transports cholyl taurine and whose 17beta-glucuronosyl estradiol transport was inhibited by cholate ( 5), OATP8 did neither transport cholyl taurine nor cholate nor cholyl glycine.	transcription
53324	5	335086	7	NULL	NULL	0	NULL	OATP8	NULL		does not transport	NULL				cholyl glycine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_30_23161_s_278	10779507	In contrast to human OATP2, which transports cholyl taurine and whose 17beta-glucuronosyl estradiol transport was inhibited by cholate ( 5), OATP8 did neither transport cholyl taurine nor cholate nor cholyl glycine.	transcription
53552	1	335088	5	NULL	NULL	0	NULL	NMDA receptors	NULL		is a type of	NULL				heteromers	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_1_276_s_11	12414797	NMDA receptors are heteromers containing NR1 subunits, which bind the co-agonist glycine ( 2,  3), and NR2 subunits, which bind the agonist glutamate ( 4,  5).	transcription
53553	2	335088	5	NULL	NULL	0	NULL	NMDA receptors	NULL		contains	NULL					NULL		NR1 subunits		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_1_276_s_11	12414797	NMDA receptors are heteromers containing NR1 subunits, which bind the co-agonist glycine ( 2,  3), and NR2 subunits, which bind the agonist glutamate ( 4,  5).	transcription
53554	3	335088	5	NULL	NULL	0	NULL	NMDA receptors	NULL		bind	NULL		NR1 subunits		glycine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_1_276_s_11	12414797	NMDA receptors are heteromers containing NR1 subunits, which bind the co-agonist glycine ( 2,  3), and NR2 subunits, which bind the agonist glutamate ( 4,  5).	transcription
53555	4	335088	5	NULL	NULL	0	NULL	glycine	NULL		is a type of	NULL				co-agonist	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_1_276_s_11	12414797	NMDA receptors are heteromers containing NR1 subunits, which bind the co-agonist glycine ( 2,  3), and NR2 subunits, which bind the agonist glutamate ( 4,  5).	transcription
53556	5	335088	5	NULL	NULL	0	NULL	NMDA receptors	NULL		contains	NULL					NULL		NR2 subunits		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_1_276_s_11	12414797	NMDA receptors are heteromers containing NR1 subunits, which bind the co-agonist glycine ( 2,  3), and NR2 subunits, which bind the agonist glutamate ( 4,  5).	transcription
53557	6	335088	5	NULL	NULL	0	NULL	NMDA receptors	NULL		bind	NULL		NR2 subunits		glutamate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_1_276_s_11	12414797	NMDA receptors are heteromers containing NR1 subunits, which bind the co-agonist glycine ( 2,  3), and NR2 subunits, which bind the agonist glutamate ( 4,  5).	transcription
53558	7	335088	5	NULL	NULL	0	NULL	glutamate	NULL		is a type of	NULL				agonist	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_1_276_s_11	12414797	NMDA receptors are heteromers containing NR1 subunits, which bind the co-agonist glycine ( 2,  3), and NR2 subunits, which bind the agonist glutamate ( 4,  5).	transcription
53325	1	335088	7	NULL	NULL	0	NULL	NMDA receptors	NULL		contains	NULL					NULL		NR1 subunits		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_1_276_s_11	12414797	NMDA receptors are heteromers containing NR1 subunits, which bind the co-agonist glycine ( 2,  3), and NR2 subunits, which bind the agonist glutamate ( 4,  5).	transcription
53326	2	335088	7	NULL	NULL	0	NULL	statement 1	NULL		bind	NULL				glycine	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_1_276_s_11	12414797	NMDA receptors are heteromers containing NR1 subunits, which bind the co-agonist glycine ( 2,  3), and NR2 subunits, which bind the agonist glutamate ( 4,  5).	transcription
53327	3	335088	7	NULL	NULL	0	NULL	NMDA receptors	NULL		is a type of	NULL				heteromer	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_1_276_s_11	12414797	NMDA receptors are heteromers containing NR1 subunits, which bind the co-agonist glycine ( 2,  3), and NR2 subunits, which bind the agonist glutamate ( 4,  5).	transcription
53328	4	335088	7	NULL	NULL	0	NULL	NMDA receptors	NULL		contain	NULL					NULL		NR2 subunits		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_1_276_s_11	12414797	NMDA receptors are heteromers containing NR1 subunits, which bind the co-agonist glycine ( 2,  3), and NR2 subunits, which bind the agonist glutamate ( 4,  5).	transcription
53329	5	335088	7	NULL	NULL	0	NULL	statement 4	NULL		bind	NULL				glutamate	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_1_276_s_11	12414797	NMDA receptors are heteromers containing NR1 subunits, which bind the co-agonist glycine ( 2,  3), and NR2 subunits, which bind the agonist glutamate ( 4,  5).	transcription
53330	6	335088	7	NULL	NULL	0	NULL	glycine	NULL		is a type of	NULL				co-agonist	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_1_276_s_11	12414797	NMDA receptors are heteromers containing NR1 subunits, which bind the co-agonist glycine ( 2,  3), and NR2 subunits, which bind the agonist glutamate ( 4,  5).	transcription
53331	7	335088	7	NULL	NULL	0	NULL	 glutamate	NULL		is a type of	NULL				agonist	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_1_276_s_11	12414797	NMDA receptors are heteromers containing NR1 subunits, which bind the co-agonist glycine ( 2,  3), and NR2 subunits, which bind the agonist glutamate ( 4,  5).	transcription
53559	1	335092	5	NULL	NULL	0	NULL	GABAA receptors		mutation of	affects					anesthetic 		action of;;volatile			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8248_s_202	9525931	Because mutations of GABAA and glycine receptors that affect volatile anesthetic actions also affect alcohol (but not barbiturate) actions ( 5), we asked if mutation of Gly-819 would change ethanol and pentobarbital inhibition of GluR6.	transcription
54027	2	335092	5	NULL	NULL	0	NULL	GABAA receptors		mutation of	affects					alcohol		action of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8248_s_202	9525931	Because mutations of GABAA and glycine receptors that affect volatile anesthetic actions also affect alcohol (but not barbiturate) actions ( 5), we asked if mutation of Gly-819 would change ethanol and pentobarbital inhibition of GluR6.	transcription
54028	3	335092	5	NULL	NULL	0	NULL	GABAA receptors		mutation of	does not affect					barbiturate		action of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8248_s_202	9525931	Because mutations of GABAA and glycine receptors that affect volatile anesthetic actions also affect alcohol (but not barbiturate) actions ( 5), we asked if mutation of Gly-819 would change ethanol and pentobarbital inhibition of GluR6.	transcription
54029	4	335092	5	NULL	NULL	0	NULL	glycine receptors		mutation of	affects					anesthetic		action of;;volatile			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8248_s_202	9525931	Because mutations of GABAA and glycine receptors that affect volatile anesthetic actions also affect alcohol (but not barbiturate) actions ( 5), we asked if mutation of Gly-819 would change ethanol and pentobarbital inhibition of GluR6.	transcription
54030	5	335092	5	NULL	NULL	0	NULL	glycine receptors		mutation of	affects					alcohol		action of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8248_s_202	9525931	Because mutations of GABAA and glycine receptors that affect volatile anesthetic actions also affect alcohol (but not barbiturate) actions ( 5), we asked if mutation of Gly-819 would change ethanol and pentobarbital inhibition of GluR6.	transcription
54031	6	335092	5	NULL	NULL	0	NULL	glycine receptors			does not affect					barbiturate		action of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8248_s_202	9525931	Because mutations of GABAA and glycine receptors that affect volatile anesthetic actions also affect alcohol (but not barbiturate) actions ( 5), we asked if mutation of Gly-819 would change ethanol and pentobarbital inhibition of GluR6.	transcription
53332	1	335092	7	NULL	NULL	0	NULL	GABAA receptors		mutation of	affect					 volatile anesthetic 		action of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8248_s_202	9525931	Because mutations of GABAA and glycine receptors that affect volatile anesthetic actions also affect alcohol (but not barbiturate) actions ( 5), we asked if mutation of Gly-819 would change ethanol and pentobarbital inhibition of GluR6.	transcription
53333	2	335092	7	NULL	NULL	0	NULL	GABAA receptors		mutation of	affect					alcohol		action of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8248_s_202	9525931	Because mutations of GABAA and glycine receptors that affect volatile anesthetic actions also affect alcohol (but not barbiturate) actions ( 5), we asked if mutation of Gly-819 would change ethanol and pentobarbital inhibition of GluR6.	transcription
53334	3	335092	7	NULL	NULL	0	NULL	GABAA receptors		mutation of	does not affect					barbiturate		action of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8248_s_202	9525931	Because mutations of GABAA and glycine receptors that affect volatile anesthetic actions also affect alcohol (but not barbiturate) actions ( 5), we asked if mutation of Gly-819 would change ethanol and pentobarbital inhibition of GluR6.	transcription
53335	4	335092	7	NULL	NULL	0	NULL	glycine receptors		mutation of	affect					volatile anesthetic 		action of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8248_s_202	9525931	Because mutations of GABAA and glycine receptors that affect volatile anesthetic actions also affect alcohol (but not barbiturate) actions ( 5), we asked if mutation of Gly-819 would change ethanol and pentobarbital inhibition of GluR6.	transcription
53336	5	335092	7	NULL	NULL	0	NULL	glycine receptors		mutation of	affect					alchol		action of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8248_s_202	9525931	Because mutations of GABAA and glycine receptors that affect volatile anesthetic actions also affect alcohol (but not barbiturate) actions ( 5), we asked if mutation of Gly-819 would change ethanol and pentobarbital inhibition of GluR6.	transcription
53337	6	335092	7	NULL	NULL	0	NULL	glycine receptors		mutation of	does not affect					barbiturate		action of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_14_8248_s_202	9525931	Because mutations of GABAA and glycine receptors that affect volatile anesthetic actions also affect alcohol (but not barbiturate) actions ( 5), we asked if mutation of Gly-819 would change ethanol and pentobarbital inhibition of GluR6.	transcription
53560	1	335093	5	NULL	NULL	0	NULL	NMDA receptors	NULL		permeable to	NULL	highly			Ca2+	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_19933_s_11	9685327	NMDA receptors are highly permeable to Ca2+ ( 3), they are regulated by a voltage-dependent Mg2+ block ( 4), and simultaneous binding of both glutamate and the co-agonist glycine is required for efficient activation of NMDA receptors ( 5,  6).	transcription
53561	2	335093	5	NULL	NULL	0	NULL	Mg2+	NULL	blocking of	is dependent on	NULL				voltage	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_19933_s_11	9685327	NMDA receptors are highly permeable to Ca2+ ( 3), they are regulated by a voltage-dependent Mg2+ block ( 4), and simultaneous binding of both glutamate and the co-agonist glycine is required for efficient activation of NMDA receptors ( 5,  6).	transcription
53562	3	335093	5	NULL	NULL	0	NULL	statement 2	NULL		regulates	NULL				NMDA receptors	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_19933_s_11	9685327	NMDA receptors are highly permeable to Ca2+ ( 3), they are regulated by a voltage-dependent Mg2+ block ( 4), and simultaneous binding of both glutamate and the co-agonist glycine is required for efficient activation of NMDA receptors ( 5,  6).	transcription
53563	4	335093	5	NULL	NULL	0	NULL	glutamate	NULL	binding of	occurs simultaneously with	NULL				glycine	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_19933_s_11	9685327	NMDA receptors are highly permeable to Ca2+ ( 3), they are regulated by a voltage-dependent Mg2+ block ( 4), and simultaneous binding of both glutamate and the co-agonist glycine is required for efficient activation of NMDA receptors ( 5,  6).	transcription
53564	5	335093	5	NULL	NULL	0	NULL	statement 4	NULL		is required for	NULL				NMDA receptors	NULL	efficient activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_19933_s_11	9685327	NMDA receptors are highly permeable to Ca2+ ( 3), they are regulated by a voltage-dependent Mg2+ block ( 4), and simultaneous binding of both glutamate and the co-agonist glycine is required for efficient activation of NMDA receptors ( 5,  6).	transcription
53565	6	335093	5	NULL	NULL	0	NULL	glycine	NULL		is a type of	NULL				co-agonist	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_19933_s_11	9685327	NMDA receptors are highly permeable to Ca2+ ( 3), they are regulated by a voltage-dependent Mg2+ block ( 4), and simultaneous binding of both glutamate and the co-agonist glycine is required for efficient activation of NMDA receptors ( 5,  6).	transcription
53338	1	335093	7	NULL	NULL	0	NULL	NMDA receptors	NULL		permeable to	NULL	highly			Ca2+	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_19933_s_11	9685327	NMDA receptors are highly permeable to Ca2+ ( 3), they are regulated by a voltage-dependent Mg2+ block ( 4), and simultaneous binding of both glutamate and the co-agonist glycine is required for efficient activation of NMDA receptors ( 5,  6).	transcription
53339	2	335093	7	NULL	NULL	0	NULL	Mg2+	NULL	blocking of	depends on	NULL				voltage	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_19933_s_11	9685327	NMDA receptors are highly permeable to Ca2+ ( 3), they are regulated by a voltage-dependent Mg2+ block ( 4), and simultaneous binding of both glutamate and the co-agonist glycine is required for efficient activation of NMDA receptors ( 5,  6).	transcription
53340	3	335093	7	NULL	NULL	0	NULL	NMDA receptors	NULL		regulated by	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_19933_s_11	9685327	NMDA receptors are highly permeable to Ca2+ ( 3), they are regulated by a voltage-dependent Mg2+ block ( 4), and simultaneous binding of both glutamate and the co-agonist glycine is required for efficient activation of NMDA receptors ( 5,  6).	transcription
53341	4	335093	7	NULL	NULL	0	NULL	glutamate	NULL	binding of	is required for	NULL				NMDA receptors	NULL	efficient activation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_19933_s_11	9685327	NMDA receptors are highly permeable to Ca2+ ( 3), they are regulated by a voltage-dependent Mg2+ block ( 4), and simultaneous binding of both glutamate and the co-agonist glycine is required for efficient activation of NMDA receptors ( 5,  6).	transcription
53342	5	335093	7	NULL	NULL	0	NULL	glycine	NULL	binding of	is required for	NULL				NMDA receptors	NULL	efficient activation of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_32_19933_s_11	9685327	NMDA receptors are highly permeable to Ca2+ ( 3), they are regulated by a voltage-dependent Mg2+ block ( 4), and simultaneous binding of both glutamate and the co-agonist glycine is required for efficient activation of NMDA receptors ( 5,  6).	transcription
53343	6	335093	7	NULL	NULL	0	NULL	statement 4	NULL		occur simultaneously with	NULL				statement 5	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_32_19933_s_11	9685327	NMDA receptors are highly permeable to Ca2+ ( 3), they are regulated by a voltage-dependent Mg2+ block ( 4), and simultaneous binding of both glutamate and the co-agonist glycine is required for efficient activation of NMDA receptors ( 5,  6).	transcription
53344	2	335095	7	NULL	NULL	0	NULL	FSS	NULL	Mg2+-free	stimulate	NULL				NMDA receptors	NULL				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_10_3725_s_57	9570803	For stimulation of NMDA receptors, 100 muM NMDA in Mg2+-free FSS containing 5 muM glycine was perfused through the chamber for 80 sec, followed by FSS for 3 min.	transcription
53345	1	335095	7	NULL	NULL	0	NULL	FSS	NULL		contains	NULL				glycine	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_10_3725_s_57	9570803	For stimulation of NMDA receptors, 100 muM NMDA in Mg2+-free FSS containing 5 muM glycine was perfused through the chamber for 80 sec, followed by FSS for 3 min.	transcription
53566	1	335096	5	NULL	NULL	0	NULL	bicuculline	NULL		block	NULL	selectively			GABAA receptor-mediated responses	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_21_8482_s_195	11606637	These data show that 5 muM bicuculline can selectively block the majority of GABAA receptor-mediated responses, without having a large effect on the glycine receptor-mediated responses.	transcription
53567	2	335096	5	NULL	NULL	0	NULL	bicuculline	NULL		effect	NULL	may			glycine receptor-mediated responses	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_21_8482_s_195	11606637	These data show that 5 muM bicuculline can selectively block the majority of GABAA receptor-mediated responses, without having a large effect on the glycine receptor-mediated responses.	transcription
53346	1	335096	7	NULL	NULL	0	NULL	bicuculline	NULL		block	NULL	selectively			GABAA receptor-mediated responses	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_21_8482_s_195	11606637	These data show that 5 muM bicuculline can selectively block the majority of GABAA receptor-mediated responses, without having a large effect on the glycine receptor-mediated responses.	transcription
53347	2	335096	7	NULL	NULL	0	NULL	bicuculline	NULL		does not effect	NULL				glycine receptor-mediated responses	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_21_8482_s_195	11606637	These data show that 5 muM bicuculline can selectively block the majority of GABAA receptor-mediated responses, without having a large effect on the glycine receptor-mediated responses.	transcription
53568	1	335098	5	NULL	NULL	0	NULL	PMA	NULL		enhance	NULL				Ip	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_12_4452_s_173	10844014	In recordings made with EGTA, applications of PMA enhanced  Ip but had little effect on  Iss evoked by applying relatively intermediate concentrations of agonist and coagonist (50 muM NMDA and 0.5 muM glycine; Fig.  5 A).	transcription
53569	2	335098	5	NULL	NULL	0	NULL	PMA	NULL		effect	NULL	little			Iss	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_12_4452_s_173	10844014	In recordings made with EGTA, applications of PMA enhanced  Ip but had little effect on  Iss evoked by applying relatively intermediate concentrations of agonist and coagonist (50 muM NMDA and 0.5 muM glycine; Fig.  5 A).	transcription
53348	1	335098	7	NULL	NULL	0	NULL	PMA	NULL		enhance	NULL				Ip	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_12_4452_s_173	10844014	In recordings made with EGTA, applications of PMA enhanced  Ip but had little effect on  Iss evoked by applying relatively intermediate concentrations of agonist and coagonist (50 muM NMDA and 0.5 muM glycine; Fig.  5 A).	transcription
53349	2	335098	7	NULL	NULL	0	NULL	PMA	NULL		effect	NULL	little			Iss	NULL				NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_12_4452_s_173	10844014	In recordings made with EGTA, applications of PMA enhanced  Ip but had little effect on  Iss evoked by applying relatively intermediate concentrations of agonist and coagonist (50 muM NMDA and 0.5 muM glycine; Fig.  5 A).	transcription
53570	1	335101	5	NULL	NULL	0	NULL	Kupffer cells	NULL	activation of	is induced by	NULL				CsA	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_299_3_858_s_10	11714869	Importantly, dietary glycine (5%) largely blocked chronic CsA-induced activation of Kupffer cells, blunted production of PGE2, prevented the hypermetabolic state, and minimized tissue hypoxia.	transcription
53571	2	335101	5	NULL	NULL	0	NULL	glycine	NULL	dietary	block	NULL	largely			statement 1	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_299_3_858_s_10	11714869	Importantly, dietary glycine (5%) largely blocked chronic CsA-induced activation of Kupffer cells, blunted production of PGE2, prevented the hypermetabolic state, and minimized tissue hypoxia.	transcription
53573	3	335101	5	NULL	NULL	0	NULL	glycine	NULL	dietary	blunted	NULL				PGE2	NULL	production of			NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_299_3_858_s_10	11714869	Importantly, dietary glycine (5%) largely blocked chronic CsA-induced activation of Kupffer cells, blunted production of PGE2, prevented the hypermetabolic state, and minimized tissue hypoxia.	transcription
53574	4	335101	5	NULL	NULL	0	NULL	glycine	NULL	dietary	prevents	NULL				hypermetabolic state	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_299_3_858_s_10	11714869	Importantly, dietary glycine (5%) largely blocked chronic CsA-induced activation of Kupffer cells, blunted production of PGE2, prevented the hypermetabolic state, and minimized tissue hypoxia.	transcription
53575	5	335101	5	NULL	NULL	0	NULL	glycine	NULL	dietary	minimize	NULL				tissue hypoxia	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_299_3_858_s_10	11714869	Importantly, dietary glycine (5%) largely blocked chronic CsA-induced activation of Kupffer cells, blunted production of PGE2, prevented the hypermetabolic state, and minimized tissue hypoxia.	transcription
54018	1	335101	7	NULL	NULL	0	NULL	chronic CsA			induce					Kupffer cells		activation of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_299_3_858_s_10	11714869	Importantly, dietary glycine (5%) largely blocked chronic CsA-induced activation of Kupffer cells, blunted production of PGE2, prevented the hypermetabolic state, and minimized tissue hypoxia.	transcription
54019	2	335101	7	NULL	NULL	0	NULL	dietary glycine			blocks		largely			statement 1					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_299_3_858_s_10	11714869	Importantly, dietary glycine (5%) largely blocked chronic CsA-induced activation of Kupffer cells, blunted production of PGE2, prevented the hypermetabolic state, and minimized tissue hypoxia.	transcription
54020	3	335101	7	NULL	NULL	0	NULL	dietary glycine			blunt					PGE2		production of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_299_3_858_s_10	11714869	Importantly, dietary glycine (5%) largely blocked chronic CsA-induced activation of Kupffer cells, blunted production of PGE2, prevented the hypermetabolic state, and minimized tissue hypoxia.	transcription
54021	4	335101	7	NULL	NULL	0	NULL	dietary glycine			prevents					hypermetabolic state					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_299_3_858_s_10	11714869	Importantly, dietary glycine (5%) largely blocked chronic CsA-induced activation of Kupffer cells, blunted production of PGE2, prevented the hypermetabolic state, and minimized tissue hypoxia.	transcription
54022	5	335101	7	NULL	NULL	0	NULL	dietary glycine			minimize					tissue hypoxia					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_299_3_858_s_10	11714869	Importantly, dietary glycine (5%) largely blocked chronic CsA-induced activation of Kupffer cells, blunted production of PGE2, prevented the hypermetabolic state, and minimized tissue hypoxia.	transcription
54024	1	335102	5	NULL	NULL	0	NULL	disulphide bridge			is formed between					plasminogen			P4 (cysteine);;P 5 (cysteine)		NULL		0	NULL	NULL	NULL	gw60_structure_6_9_1195_s_227	9753698	The following P 3 and P 4 glycine residues of the plasminogen activation loop must fold back to allow disulphide bridge formation between P4 (cysteine) and P 5 (cysteine) of plasminogen (  Figure 4).	transcription
54025	2	335102	5	NULL	NULL	0	NULL	plasminogen 			resides in			P3glycine;;P4 glycine		plasminogen 			activation loop		NULL		0	NULL	NULL	NULL	gw60_structure_6_9_1195_s_227	9753698	The following P 3 and P 4 glycine residues of the plasminogen activation loop must fold back to allow disulphide bridge formation between P4 (cysteine) and P 5 (cysteine) of plasminogen (  Figure 4).	transcription
54026	3	335102	5	NULL	NULL	0	NULL	statement 2		folding back of	allows					statement 1					NULL		0	NULL	NULL	NULL	gw60_structure_6_9_1195_s_227	9753698	The following P 3 and P 4 glycine residues of the plasminogen activation loop must fold back to allow disulphide bridge formation between P4 (cysteine) and P 5 (cysteine) of plasminogen (  Figure 4).	transcription
54023	1	335102	7	NULL	NULL	0	NULL	plasminogen activation loop			allow			P 3 and P 4 glycine residues		plasminogen			disulphide bridge formation between P4 (cysteine) and P 5 (cysteine)		NULL		0	NULL	NULL	NULL	gw60_structure_6_9_1195_s_227	9753698	The following P 3 and P 4 glycine residues of the plasminogen activation loop must fold back to allow disulphide bridge formation between P4 (cysteine) and P 5 (cysteine) of plasminogen (  Figure 4).	transcription
54032	1	335109	7	NULL	NULL	0	NULL	CO-			bind					DNA					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_4_2333_s_78	12433917	For the measurement of DNA binding of CO-, imidazole-and CN -bound deltaP3R4 CooA at pH 9.5, the following assay buffer (high pH anisotropy buffer) was used: 40 mM glycine-NaOH, pH 9.5, 6 mM CaCl2, 50 mM KCl, 5% (v/v) glycerol, and 5 mM dithiothreitol.	transcription
54033	2	335109	7	NULL	NULL	0	NULL	imidazole			bind					deltaP3R4 CooA					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_4_2333_s_78	12433917	For the measurement of DNA binding of CO-, imidazole-and CN -bound deltaP3R4 CooA at pH 9.5, the following assay buffer (high pH anisotropy buffer) was used: 40 mM glycine-NaOH, pH 9.5, 6 mM CaCl2, 50 mM KCl, 5% (v/v) glycerol, and 5 mM dithiothreitol.	transcription
54034	3	335109	7	NULL	NULL	0	NULL	CN			bind					deltaP3R4 CooA					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_4_2333_s_78	12433917	For the measurement of DNA binding of CO-, imidazole-and CN -bound deltaP3R4 CooA at pH 9.5, the following assay buffer (high pH anisotropy buffer) was used: 40 mM glycine-NaOH, pH 9.5, 6 mM CaCl2, 50 mM KCl, 5% (v/v) glycerol, and 5 mM dithiothreitol.	transcription
53576	1	335110	5	NULL	NULL	0	NULL	(2 S,1' S,2' S)-2-(carboxycyclopropyl)-glycine	NULL		is a type of	NULL				group II selective mGluR agonist	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_25_40_9213_s_265	16207881	Application of the group II selective mGluR agonist (2 S,1' S,2' S)-2-(carboxycyclopropyl)-glycine (20 muM) did not depress EPSCs evoked by stimulation at CA1 stratum radiatum (102  plus-or-minus  7% of control;  n = 5 from 5 animals), verifying that the currents were not contaminated by pp inputs.	transcription
53577	2	335110	5	NULL	NULL	0	NULL	EPSCs	NULL		is evoked by	NULL				CA1 stratum radiatum	NULL	stimulation of			NULL		0	NULL	NULL	NULL	gw70_jneurosci_25_40_9213_s_265	16207881	Application of the group II selective mGluR agonist (2 S,1' S,2' S)-2-(carboxycyclopropyl)-glycine (20 muM) did not depress EPSCs evoked by stimulation at CA1 stratum radiatum (102  plus-or-minus  7% of control;  n = 5 from 5 animals), verifying that the currents were not contaminated by pp inputs.	transcription
53578	3	335110	5	NULL	NULL	0	NULL	(2 S,1' S,2' S)-2-(carboxycyclopropyl)-glycine	NULL		does not depress	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_jneurosci_25_40_9213_s_265	16207881	Application of the group II selective mGluR agonist (2 S,1' S,2' S)-2-(carboxycyclopropyl)-glycine (20 muM) did not depress EPSCs evoked by stimulation at CA1 stratum radiatum (102  plus-or-minus  7% of control;  n = 5 from 5 animals), verifying that the currents were not contaminated by pp inputs.	transcription
54035	1	335110	7	NULL	NULL	0	NULL	(2 S,1' S,2' S)-2-(carboxycyclopropyl)-glycine			did not depress					EPSCs					NULL		0	NULL	NULL	NULL	gw70_jneurosci_25_40_9213_s_265	16207881	Application of the group II selective mGluR agonist (2 S,1' S,2' S)-2-(carboxycyclopropyl)-glycine (20 muM) did not depress EPSCs evoked by stimulation at CA1 stratum radiatum (102  plus-or-minus  7% of control;  n = 5 from 5 animals), verifying that the currents were not contaminated by pp inputs.	transcription
54036	2	335110	7	NULL	NULL	0	NULL	statement 1			evoked by					CA1 stratum radiatum		stimulation at			NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_25_40_9213_s_265	16207881	Application of the group II selective mGluR agonist (2 S,1' S,2' S)-2-(carboxycyclopropyl)-glycine (20 muM) did not depress EPSCs evoked by stimulation at CA1 stratum radiatum (102  plus-or-minus  7% of control;  n = 5 from 5 animals), verifying that the currents were not contaminated by pp inputs.	transcription
54037	3	335110	7	NULL	NULL	0	NULL	(2 S,1' S,2' S)-2-(carboxycyclopropyl)-glycine			is a type of					group II selective mGluR agonist					NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_25_40_9213_s_265	16207881	Application of the group II selective mGluR agonist (2 S,1' S,2' S)-2-(carboxycyclopropyl)-glycine (20 muM) did not depress EPSCs evoked by stimulation at CA1 stratum radiatum (102  plus-or-minus  7% of control;  n = 5 from 5 animals), verifying that the currents were not contaminated by pp inputs.	transcription
53579	1	335113	5	NULL	NULL	0	NULL	IGF-1R-LexA construct	NULL		is expressed with	NULL				proline-glycine spacer	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_36_33419_s_35	11445579	Expression of the IGF-1R-LexA construct with a proline-glycine spacer resulted in the highest autokinase activity and the strongest interaction with p85alpha (PCR was performed with the following oligonucleotides: sense primer with an  EcoRI/ SmaI adaptor: 5''-TCCGGAATTCCCGGGGAGAAAGAGAAATAACAGCAGGCTGG3-'', reverse primer with an  SalI/ BamHI adaptor: 5''-TCCGGTCGACGGATCCAAGGATCAGCAGGTCGAA-3'').	transcription
53580	2	335113	5	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				autokinase activity	NULL	highest			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_36_33419_s_35	11445579	Expression of the IGF-1R-LexA construct with a proline-glycine spacer resulted in the highest autokinase activity and the strongest interaction with p85alpha (PCR was performed with the following oligonucleotides: sense primer with an  EcoRI/ SmaI adaptor: 5''-TCCGGAATTCCCGGGGAGAAAGAGAAATAACAGCAGGCTGG3-'', reverse primer with an  SalI/ BamHI adaptor: 5''-TCCGGTCGACGGATCCAAGGATCAGCAGGTCGAA-3'').	transcription
53581	3	335113	5	NULL	NULL	0	NULL	statement 1	NULL		results in	NULL				p85alpha	NULL	strongest interaction with			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_36_33419_s_35	11445579	Expression of the IGF-1R-LexA construct with a proline-glycine spacer resulted in the highest autokinase activity and the strongest interaction with p85alpha (PCR was performed with the following oligonucleotides: sense primer with an  EcoRI/ SmaI adaptor: 5''-TCCGGAATTCCCGGGGAGAAAGAGAAATAACAGCAGGCTGG3-'', reverse primer with an  SalI/ BamHI adaptor: 5''-TCCGGTCGACGGATCCAAGGATCAGCAGGTCGAA-3'').	transcription
54038	1	335113	7	NULL	NULL	0	NULL	IGF-1R-LexA construct			is expressed with					proline-glycine spacer					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_36_33419_s_35	11445579	Expression of the IGF-1R-LexA construct with a proline-glycine spacer resulted in the highest autokinase activity and the strongest interaction with p85alpha (PCR was performed with the following oligonucleotides: sense primer with an  EcoRI/ SmaI adaptor: 5''-TCCGGAATTCCCGGGGAGAAAGAGAAATAACAGCAGGCTGG3-'', reverse primer with an  SalI/ BamHI adaptor: 5''-TCCGGTCGACGGATCCAAGGATCAGCAGGTCGAA-3'').	transcription
54039	2	335113	7	NULL	NULL	0	NULL	statement 1			results in					 autokinase 		highest activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_36_33419_s_35	11445579	Expression of the IGF-1R-LexA construct with a proline-glycine spacer resulted in the highest autokinase activity and the strongest interaction with p85alpha (PCR was performed with the following oligonucleotides: sense primer with an  EcoRI/ SmaI adaptor: 5''-TCCGGAATTCCCGGGGAGAAAGAGAAATAACAGCAGGCTGG3-'', reverse primer with an  SalI/ BamHI adaptor: 5''-TCCGGTCGACGGATCCAAGGATCAGCAGGTCGAA-3'').	transcription
54040	3	335113	7	NULL	NULL	0	NULL	statement 1			interacts with		strongly			 p85alpha					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_36_33419_s_35	11445579	Expression of the IGF-1R-LexA construct with a proline-glycine spacer resulted in the highest autokinase activity and the strongest interaction with p85alpha (PCR was performed with the following oligonucleotides: sense primer with an  EcoRI/ SmaI adaptor: 5''-TCCGGAATTCCCGGGGAGAAAGAGAAATAACAGCAGGCTGG3-'', reverse primer with an  SalI/ BamHI adaptor: 5''-TCCGGTCGACGGATCCAAGGATCAGCAGGTCGAA-3'').	transcription
53582	1	335114	5	NULL	NULL	0	NULL	NMDA receptor	NULL	activation of	is dependent on	NULL				glycine	NULL				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_302_1_163_s_184	12065713	As depicted in Fig.  5A, the glycine-dependent activation of the NMDA receptor exhibited an EC50 of 0.8  plus-or-minus  0.1 muM ( n = 5) that was not significantly changed by the presence of 20 muM N20C in the medium (EC50 = 1.1  plus-or-minus  0.3 muM,  n = 5).	transcription
54041	1	335114	7	NULL	NULL	0	NULL	NMDA receptor		activation of	depends on					glycine					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_302_1_163_s_184	12065713	As depicted in Fig.  5A, the glycine-dependent activation of the NMDA receptor exhibited an EC50 of 0.8  plus-or-minus  0.1 muM ( n = 5) that was not significantly changed by the presence of 20 muM N20C in the medium (EC50 = 1.1  plus-or-minus  0.3 muM,  n = 5).	transcription
53583	1	335116	5	NULL	NULL	0	NULL	glycine	NULL		activates	NULL				NMDA receptor	NULL		glycine-binding site		NULL		0	NULL	NULL	NULL	gw70_nature_438_7071_1162_s_127	16372011	Slices were superfused at  33   1  degrees C with bicarbonate-buffered solution (for ischaemia experiments) containing  126 mM NaCl, 24 mM NaHCO3, 1 mM NaH2PO4, 2.5 mM KCl, 2 mM MgCl2, 2.5 mM CaCl2, 10 mM glucose, 0.1 mM glycine (which activates the NMDA receptor glycine-binding  site) and 0.005 mM strychnine (which blocks glycine receptors), bubbled with 95%  O2, 5% CO2 (pH 7.4); or at 24   1  degrees C with HEPES-buffered solution (for non-ischaemia experiments) containing  144 mM NaCl, 2.5 mM KCl, 2 mM MgCl2, 10 mM HEPES, 1 mM NaH2PO4, 2.5 mM CaCl2, 10 mM glucose, 0.1 mM glycine and 0.005 mM strychnine, with the pH set to 7.4 using  NaOH.	transcription
53584	2	335116	5	NULL	NULL	0	NULL	strychnine	NULL		blocks	NULL				glycine receptors	NULL				NULL		0	NULL	NULL	NULL	gw70_nature_438_7071_1162_s_127	16372011	Slices were superfused at  33   1  degrees C with bicarbonate-buffered solution (for ischaemia experiments) containing  126 mM NaCl, 24 mM NaHCO3, 1 mM NaH2PO4, 2.5 mM KCl, 2 mM MgCl2, 2.5 mM CaCl2, 10 mM glucose, 0.1 mM glycine (which activates the NMDA receptor glycine-binding  site) and 0.005 mM strychnine (which blocks glycine receptors), bubbled with 95%  O2, 5% CO2 (pH 7.4); or at 24   1  degrees C with HEPES-buffered solution (for non-ischaemia experiments) containing  144 mM NaCl, 2.5 mM KCl, 2 mM MgCl2, 10 mM HEPES, 1 mM NaH2PO4, 2.5 mM CaCl2, 10 mM glucose, 0.1 mM glycine and 0.005 mM strychnine, with the pH set to 7.4 using  NaOH.	transcription
54042	1	335116	7	NULL	NULL	0	NULL	bicarbonate-buffered solution			activates					NMDA receptor			glycine-binding site		NULL		0	NULL	NULL	NULL	gw70_nature_438_7071_1162_s_127	16372011	Slices were superfused at  33   1  degrees C with bicarbonate-buffered solution (for ischaemia experiments) containing  126 mM NaCl, 24 mM NaHCO3, 1 mM NaH2PO4, 2.5 mM KCl, 2 mM MgCl2, 2.5 mM CaCl2, 10 mM glucose, 0.1 mM glycine (which activates the NMDA receptor glycine-binding  site) and 0.005 mM strychnine (which blocks glycine receptors), bubbled with 95%  O2, 5% CO2 (pH 7.4); or at 24   1  degrees C with HEPES-buffered solution (for non-ischaemia experiments) containing  144 mM NaCl, 2.5 mM KCl, 2 mM MgCl2, 10 mM HEPES, 1 mM NaH2PO4, 2.5 mM CaCl2, 10 mM glucose, 0.1 mM glycine and 0.005 mM strychnine, with the pH set to 7.4 using  NaOH.	transcription
54043	2	335116	7	NULL	NULL	0	NULL	strychnine			block					glycine receptors					NULL		0	NULL	NULL	NULL	gw70_nature_438_7071_1162_s_127	16372011	Slices were superfused at  33   1  degrees C with bicarbonate-buffered solution (for ischaemia experiments) containing  126 mM NaCl, 24 mM NaHCO3, 1 mM NaH2PO4, 2.5 mM KCl, 2 mM MgCl2, 2.5 mM CaCl2, 10 mM glucose, 0.1 mM glycine (which activates the NMDA receptor glycine-binding  site) and 0.005 mM strychnine (which blocks glycine receptors), bubbled with 95%  O2, 5% CO2 (pH 7.4); or at 24   1  degrees C with HEPES-buffered solution (for non-ischaemia experiments) containing  144 mM NaCl, 2.5 mM KCl, 2 mM MgCl2, 10 mM HEPES, 1 mM NaH2PO4, 2.5 mM CaCl2, 10 mM glucose, 0.1 mM glycine and 0.005 mM strychnine, with the pH set to 7.4 using  NaOH.	transcription
53585	1	335117	5	NULL	NULL	0	NULL	glycine	NULL		reduces	NULL				NFPS	NULL	binding of			NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_5_585_s_135	12941372	As illustrated in  Fig. 4A by saturation plot and Scatchard transformation, glycine reduced maximal [3]NFPS binding (58 plus-or-minus 5% at 1 mM glycine;  P<0.05;  t-test paired, two-tailed) without significantly changing the affinity of [3]NFPS for its binding site ( Kd=4.2 plus-or-minus 0.4 nM, compared to 6.2 plus-or-minus 2.3 nM for control).	transcription
53586	2	335117	5	NULL	NULL	0	NULL	statement 1	NULL		without changing	NULL	significantly			NFPS	NULL	affinity of			NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_5_585_s_135	12941372	As illustrated in  Fig. 4A by saturation plot and Scatchard transformation, glycine reduced maximal [3]NFPS binding (58 plus-or-minus 5% at 1 mM glycine;  P<0.05;  t-test paired, two-tailed) without significantly changing the affinity of [3]NFPS for its binding site ( Kd=4.2 plus-or-minus 0.4 nM, compared to 6.2 plus-or-minus 2.3 nM for control).	transcription
54044	1	335117	7	NULL	NULL	0	NULL	glycine			reduce					NFPS		binding of			NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_5_585_s_135	12941372	As illustrated in  Fig. 4A by saturation plot and Scatchard transformation, glycine reduced maximal [3]NFPS binding (58 plus-or-minus 5% at 1 mM glycine;  P<0.05;  t-test paired, two-tailed) without significantly changing the affinity of [3]NFPS for its binding site ( Kd=4.2 plus-or-minus 0.4 nM, compared to 6.2 plus-or-minus 2.3 nM for control).	transcription
53587	1	335118	5	NULL	NULL	0	NULL	deoxyhemoglobin	NULL		bind	NULL	avidly			CO	NULL				NULL		0	NULL	NULL	NULL	gw60_circulationres_83_5_568_s_93	9734480	The lower chamber contained 5 muCi of [2-14C]L-glycine, a heme precursor, and the upper chamber contained a solution of deoxyhemoglobin (15 mumol/L), which is known to avidly bind CO. Aortas were removed from rats at various times after surgery, trimmed of adventitial tissue, and transferred into the lower chamber containing [2-14C]L-glycine in oxygenated Krebs-Henseleit buffer (1:20 [vol/vol]) containing (mmol/L) NaCl 118, KCl 4.7, KH2PO4 1.2, MgSO4 .	transcription
54045	1	335118	7	NULL	NULL	0	NULL	deoxyhemoglobin			bind		avidly			CO					NULL		0	NULL	NULL	NULL	gw60_circulationres_83_5_568_s_93	9734480	The lower chamber contained 5 muCi of [2-14C]L-glycine, a heme precursor, and the upper chamber contained a solution of deoxyhemoglobin (15 mumol/L), which is known to avidly bind CO. Aortas were removed from rats at various times after surgery, trimmed of adventitial tissue, and transferred into the lower chamber containing [2-14C]L-glycine in oxygenated Krebs-Henseleit buffer (1:20 [vol/vol]) containing (mmol/L) NaCl 118, KCl 4.7, KH2PO4 1.2, MgSO4 .	transcription
53588	1	335119	5	NULL	NULL	0	NULL	glycine	NULL		is mutated to	NULL		position 269		cysteine	NULL		position 269		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_37_21659_s_138	7665581	Mutation of the glycine residues at positions  269 and 271 to cysteine and arginine respectively, had no effect on ATP  binding, although both of these mutations resulted in decreased  selenium labeling of 5``-deiodinase ( Fig. 4 b  and data  not shown), suggesting that the glycine residues at these positions  have roles in normal selenophosphate synthetase activity other than ATP  binding.	transcription
53589	2	335119	5	NULL	NULL	0	NULL	glycine	NULL		is mutated to	NULL		position 271		arginine	NULL		position 271		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_37_21659_s_138	7665581	Mutation of the glycine residues at positions  269 and 271 to cysteine and arginine respectively, had no effect on ATP  binding, although both of these mutations resulted in decreased  selenium labeling of 5``-deiodinase ( Fig. 4 b  and data  not shown), suggesting that the glycine residues at these positions  have roles in normal selenophosphate synthetase activity other than ATP  binding.	transcription
53590	3	335119	5	NULL	NULL	0	NULL	statement 1	NULL		does not effect	NULL				ATP	NULL	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_37_21659_s_138	7665581	Mutation of the glycine residues at positions  269 and 271 to cysteine and arginine respectively, had no effect on ATP  binding, although both of these mutations resulted in decreased  selenium labeling of 5``-deiodinase ( Fig. 4 b  and data  not shown), suggesting that the glycine residues at these positions  have roles in normal selenophosphate synthetase activity other than ATP  binding.	transcription
53591	4	335119	5	NULL	NULL	0	NULL	statement 2	NULL		does not effect	NULL				ATP	NULL	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_37_21659_s_138	7665581	Mutation of the glycine residues at positions  269 and 271 to cysteine and arginine respectively, had no effect on ATP  binding, although both of these mutations resulted in decreased  selenium labeling of 5``-deiodinase ( Fig. 4 b  and data  not shown), suggesting that the glycine residues at these positions  have roles in normal selenophosphate synthetase activity other than ATP  binding.	transcription
53592	5	335119	5	NULL	NULL	0	NULL	glycine	NULL		plays a role in	NULL		position 269		selenophosphate synthetase activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_37_21659_s_138	7665581	Mutation of the glycine residues at positions  269 and 271 to cysteine and arginine respectively, had no effect on ATP  binding, although both of these mutations resulted in decreased  selenium labeling of 5``-deiodinase ( Fig. 4 b  and data  not shown), suggesting that the glycine residues at these positions  have roles in normal selenophosphate synthetase activity other than ATP  binding.	transcription
53593	6	335119	5	NULL	NULL	0	NULL	glycine	NULL		plays a role in	NULL		position 271		selenophosphate synthetase activity	NULL				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_37_21659_s_138	7665581	Mutation of the glycine residues at positions  269 and 271 to cysteine and arginine respectively, had no effect on ATP  binding, although both of these mutations resulted in decreased  selenium labeling of 5``-deiodinase ( Fig. 4 b  and data  not shown), suggesting that the glycine residues at these positions  have roles in normal selenophosphate synthetase activity other than ATP  binding.	transcription
54046	1	335119	7	NULL	NULL	0	NULL				mutated to			glycine residue at position 269					cysteine at position 269		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_37_21659_s_138	7665581	Mutation of the glycine residues at positions  269 and 271 to cysteine and arginine respectively, had no effect on ATP  binding, although both of these mutations resulted in decreased  selenium labeling of 5``-deiodinase ( Fig. 4 b  and data  not shown), suggesting that the glycine residues at these positions  have roles in normal selenophosphate synthetase activity other than ATP  binding.	transcription
54047	2	335119	7	NULL	NULL	0	NULL	statement 1			does not effect					ATP		binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_37_21659_s_138	7665581	Mutation of the glycine residues at positions  269 and 271 to cysteine and arginine respectively, had no effect on ATP  binding, although both of these mutations resulted in decreased  selenium labeling of 5``-deiodinase ( Fig. 4 b  and data  not shown), suggesting that the glycine residues at these positions  have roles in normal selenophosphate synthetase activity other than ATP  binding.	transcription
54048	3	335119	7	NULL	NULL	0	NULL				mutated to			glycine residue at position 271					arginine at position 271		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_37_21659_s_138	7665581	Mutation of the glycine residues at positions  269 and 271 to cysteine and arginine respectively, had no effect on ATP  binding, although both of these mutations resulted in decreased  selenium labeling of 5``-deiodinase ( Fig. 4 b  and data  not shown), suggesting that the glycine residues at these positions  have roles in normal selenophosphate synthetase activity other than ATP  binding.	transcription
54049	4	335119	7	NULL	NULL	0	NULL	statement 3			does not effect					ATP		binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_37_21659_s_138	7665581	Mutation of the glycine residues at positions  269 and 271 to cysteine and arginine respectively, had no effect on ATP  binding, although both of these mutations resulted in decreased  selenium labeling of 5``-deiodinase ( Fig. 4 b  and data  not shown), suggesting that the glycine residues at these positions  have roles in normal selenophosphate synthetase activity other than ATP  binding.	transcription
54050	5	335119	7	NULL	NULL	0	NULL	statement 1			decrease					5``-deiodinase		selenium labeling of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_37_21659_s_138	7665581	Mutation of the glycine residues at positions  269 and 271 to cysteine and arginine respectively, had no effect on ATP  binding, although both of these mutations resulted in decreased  selenium labeling of 5``-deiodinase ( Fig. 4 b  and data  not shown), suggesting that the glycine residues at these positions  have roles in normal selenophosphate synthetase activity other than ATP  binding.	transcription
54051	6	335119	7	NULL	NULL	0	NULL	statement 3			decrease					5``-deiodinase		selenium labeling of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_37_21659_s_138	7665581	Mutation of the glycine residues at positions  269 and 271 to cysteine and arginine respectively, had no effect on ATP  binding, although both of these mutations resulted in decreased  selenium labeling of 5``-deiodinase ( Fig. 4 b  and data  not shown), suggesting that the glycine residues at these positions  have roles in normal selenophosphate synthetase activity other than ATP  binding.	transcription
54052	7	335119	7	NULL	NULL	0	NULL				play a role in			glycine residue at position 269 		selenophosphate synthetase 		normal;;activity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_37_21659_s_138	7665581	Mutation of the glycine residues at positions  269 and 271 to cysteine and arginine respectively, had no effect on ATP  binding, although both of these mutations resulted in decreased  selenium labeling of 5``-deiodinase ( Fig. 4 b  and data  not shown), suggesting that the glycine residues at these positions  have roles in normal selenophosphate synthetase activity other than ATP  binding.	transcription
54053	8	335119	7	NULL	NULL	0	NULL				play a role in			glycine residue at position 271		selenophosphate synthetase 		normal;;activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_37_21659_s_138	7665581	Mutation of the glycine residues at positions  269 and 271 to cysteine and arginine respectively, had no effect on ATP  binding, although both of these mutations resulted in decreased  selenium labeling of 5``-deiodinase ( Fig. 4 b  and data  not shown), suggesting that the glycine residues at these positions  have roles in normal selenophosphate synthetase activity other than ATP  binding.	transcription
54054	9	335119	7	NULL	NULL	0	NULL	statement 2			suggest					statement 7					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_37_21659_s_138	7665581	Mutation of the glycine residues at positions  269 and 271 to cysteine and arginine respectively, had no effect on ATP  binding, although both of these mutations resulted in decreased  selenium labeling of 5``-deiodinase ( Fig. 4 b  and data  not shown), suggesting that the glycine residues at these positions  have roles in normal selenophosphate synthetase activity other than ATP  binding.	transcription
54055	10	335119	7	NULL	NULL	0	NULL	statement 4			suggests					statement 8					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_37_21659_s_138	7665581	Mutation of the glycine residues at positions  269 and 271 to cysteine and arginine respectively, had no effect on ATP  binding, although both of these mutations resulted in decreased  selenium labeling of 5``-deiodinase ( Fig. 4 b  and data  not shown), suggesting that the glycine residues at these positions  have roles in normal selenophosphate synthetase activity other than ATP  binding.	transcription
53594	1	335120	5	NULL	NULL	0	NULL	GlyRs	NULL		decreases	NULL		D148E		strychnine	NULL	affinity of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mol-pharmacol_44_1_8393521_s_14	8393521	The D148E GlyRs showed a 1 order of magnitude decrease in strychnine affinity  (Kd, 8.1 +/- 1.4 nM versus 82 +/- 21 nM), without any change in the glycine  displacement of strychnine binding (Ki, 25 +/- 5 microM versus 29 +/-  8 microM) or glycine activation of chloride currents (EC50, 27 +/- 6 microM  versus 20 +/- 1 microM).	transcription
53595	2	335120	5	NULL	NULL	0	NULL	glycine	NULL		activates	NULL				chloride currents	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mol-pharmacol_44_1_8393521_s_14	8393521	The D148E GlyRs showed a 1 order of magnitude decrease in strychnine affinity  (Kd, 8.1 +/- 1.4 nM versus 82 +/- 21 nM), without any change in the glycine  displacement of strychnine binding (Ki, 25 +/- 5 microM versus 29 +/-  8 microM) or glycine activation of chloride currents (EC50, 27 +/- 6 microM  versus 20 +/- 1 microM).	transcription
53596	3	335120	5	NULL	NULL	0	NULL	statement 1	NULL		does not change	NULL				statement 2	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mol-pharmacol_44_1_8393521_s_14	8393521	The D148E GlyRs showed a 1 order of magnitude decrease in strychnine affinity  (Kd, 8.1 +/- 1.4 nM versus 82 +/- 21 nM), without any change in the glycine  displacement of strychnine binding (Ki, 25 +/- 5 microM versus 29 +/-  8 microM) or glycine activation of chloride currents (EC50, 27 +/- 6 microM  versus 20 +/- 1 microM).	transcription
53597	4	335120	5	NULL	NULL	0	NULL	glycine	NULL		displaced in	NULL				strychnine	NULL	binding of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mol-pharmacol_44_1_8393521_s_14	8393521	The D148E GlyRs showed a 1 order of magnitude decrease in strychnine affinity  (Kd, 8.1 +/- 1.4 nM versus 82 +/- 21 nM), without any change in the glycine  displacement of strychnine binding (Ki, 25 +/- 5 microM versus 29 +/-  8 microM) or glycine activation of chloride currents (EC50, 27 +/- 6 microM  versus 20 +/- 1 microM).	transcription
53598	5	335120	5	NULL	NULL	0	NULL	statement 1	NULL		does not change	NULL				statement 4	NULL				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mol-pharmacol_44_1_8393521_s_14	8393521	The D148E GlyRs showed a 1 order of magnitude decrease in strychnine affinity  (Kd, 8.1 +/- 1.4 nM versus 82 +/- 21 nM), without any change in the glycine  displacement of strychnine binding (Ki, 25 +/- 5 microM versus 29 +/-  8 microM) or glycine activation of chloride currents (EC50, 27 +/- 6 microM  versus 20 +/- 1 microM).	transcription
54056	1	335120	7	NULL	NULL	0	NULL	GlyRs			decrease			D148E		strychnine		affinity of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mol-pharmacol_44_1_8393521_s_14	8393521	The D148E GlyRs showed a 1 order of magnitude decrease in strychnine affinity  (Kd, 8.1 +/- 1.4 nM versus 82 +/- 21 nM), without any change in the glycine  displacement of strychnine binding (Ki, 25 +/- 5 microM versus 29 +/-  8 microM) or glycine activation of chloride currents (EC50, 27 +/- 6 microM  versus 20 +/- 1 microM).	transcription
54057	2	335120	7	NULL	NULL	0	NULL	glycine			activate					chloride currents					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mol-pharmacol_44_1_8393521_s_14	8393521	The D148E GlyRs showed a 1 order of magnitude decrease in strychnine affinity  (Kd, 8.1 +/- 1.4 nM versus 82 +/- 21 nM), without any change in the glycine  displacement of strychnine binding (Ki, 25 +/- 5 microM versus 29 +/-  8 microM) or glycine activation of chloride currents (EC50, 27 +/- 6 microM  versus 20 +/- 1 microM).	transcription
54058	3	335120	7	NULL	NULL	0	NULL	GlyRs			does not change			D148E		statement 2					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mol-pharmacol_44_1_8393521_s_14	8393521	The D148E GlyRs showed a 1 order of magnitude decrease in strychnine affinity  (Kd, 8.1 +/- 1.4 nM versus 82 +/- 21 nM), without any change in the glycine  displacement of strychnine binding (Ki, 25 +/- 5 microM versus 29 +/-  8 microM) or glycine activation of chloride currents (EC50, 27 +/- 6 microM  versus 20 +/- 1 microM).	transcription
53599	1	335122	5	NULL	NULL	0	NULL	CCBD	NULL		is	NULL				central cell-binding domain	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_260_2_449_s_23	12921745	The central cell-binding domain (CCBD) of fibronectin contains the RGD (Arginine-Glycine-Aspartic  acid) sequence and an adjacent site that acts in synergy with RGD to allow  5 1-dependent  cell spreading and cell migration [  Mould et al 1997 and   Obara and Yoshizato 1995].	transcription
53600	2	335122	5	NULL	NULL	0	NULL	RGD	NULL		is	NULL				Arginine-Glycine-Aspartic acid	NULL				NULL		0	NULL	NULL	NULL	gw70_devbiol_260_2_449_s_23	12921745	The central cell-binding domain (CCBD) of fibronectin contains the RGD (Arginine-Glycine-Aspartic  acid) sequence and an adjacent site that acts in synergy with RGD to allow  5 1-dependent  cell spreading and cell migration [  Mould et al 1997 and   Obara and Yoshizato 1995].	transcription
53601	3	335122	5	NULL	NULL	0	NULL	fibronectin	NULL		contains	NULL		CCBD		fibronectin \t	NULL		RGD		NULL		NULL	NULL	NULL	NULL	gw70_devbiol_260_2_449_s_23	12921745	The central cell-binding domain (CCBD) of fibronectin contains the RGD (Arginine-Glycine-Aspartic  acid) sequence and an adjacent site that acts in synergy with RGD to allow  5 1-dependent  cell spreading and cell migration [  Mould et al 1997 and   Obara and Yoshizato 1995].	transcription
53602	4	335122	5	NULL	NULL	0	NULL	fibronectin \t	NULL	adjacent site of	acts in synergy with	NULL		RGD		fibronectin \t	NULL		RGD		NULL		NULL	NULL	NULL	NULL	gw70_devbiol_260_2_449_s_23	12921745	The central cell-binding domain (CCBD) of fibronectin contains the RGD (Arginine-Glycine-Aspartic  acid) sequence and an adjacent site that acts in synergy with RGD to allow  5 1-dependent  cell spreading and cell migration [  Mould et al 1997 and   Obara and Yoshizato 1995].	transcription
53603	5	335122	5	NULL	NULL	0	NULL	statement 4	NULL		allows	NULL				cell	NULL	spreading of			NULL		0	NULL	NULL	NULL	gw70_devbiol_260_2_449_s_23	12921745	The central cell-binding domain (CCBD) of fibronectin contains the RGD (Arginine-Glycine-Aspartic  acid) sequence and an adjacent site that acts in synergy with RGD to allow  5 1-dependent  cell spreading and cell migration [  Mould et al 1997 and   Obara and Yoshizato 1995].	transcription
53604	6	335122	5	NULL	NULL	0	NULL	statement 4	NULL		allows	NULL				cell	NULL	migration of			NULL		0	NULL	NULL	NULL	gw70_devbiol_260_2_449_s_23	12921745	The central cell-binding domain (CCBD) of fibronectin contains the RGD (Arginine-Glycine-Aspartic  acid) sequence and an adjacent site that acts in synergy with RGD to allow  5 1-dependent  cell spreading and cell migration [  Mould et al 1997 and   Obara and Yoshizato 1995].	transcription
54059	1	335122	7	NULL	NULL	0	NULL	fibronectin			contains			CCBD					RGD sequence 		NULL		0	NULL	NULL	NULL	gw70_devbiol_260_2_449_s_23	12921745	The central cell-binding domain (CCBD) of fibronectin contains the RGD (Arginine-Glycine-Aspartic  acid) sequence and an adjacent site that acts in synergy with RGD to allow  5 1-dependent  cell spreading and cell migration [  Mould et al 1997 and   Obara and Yoshizato 1995].	transcription
54060	2	335122	7	NULL	NULL	0	NULL	statement 1			allow					cell spreading					NULL		0	NULL	NULL	NULL	gw70_devbiol_260_2_449_s_23	12921745	The central cell-binding domain (CCBD) of fibronectin contains the RGD (Arginine-Glycine-Aspartic  acid) sequence and an adjacent site that acts in synergy with RGD to allow  5 1-dependent  cell spreading and cell migration [  Mould et al 1997 and   Obara and Yoshizato 1995].	transcription
54061	3	335122	7	NULL	NULL	0	NULL	statement 1			allow					cell migration					NULL		0	NULL	NULL	NULL	gw70_devbiol_260_2_449_s_23	12921745	The central cell-binding domain (CCBD) of fibronectin contains the RGD (Arginine-Glycine-Aspartic  acid) sequence and an adjacent site that acts in synergy with RGD to allow  5 1-dependent  cell spreading and cell migration [  Mould et al 1997 and   Obara and Yoshizato 1995].	transcription
54062	4	335122	7	NULL	NULL	0	NULL	CCBD			is					central cell-binding domain					NULL		0	NULL	NULL	NULL	gw70_devbiol_260_2_449_s_23	12921745	The central cell-binding domain (CCBD) of fibronectin contains the RGD (Arginine-Glycine-Aspartic  acid) sequence and an adjacent site that acts in synergy with RGD to allow  5 1-dependent  cell spreading and cell migration [  Mould et al 1997 and   Obara and Yoshizato 1995].	transcription
54063	5	335122	7	NULL	NULL	0	NULL	RGD			is					Arginine-Glycine-Aspartic acid					NULL		0	NULL	NULL	NULL	gw70_devbiol_260_2_449_s_23	12921745	The central cell-binding domain (CCBD) of fibronectin contains the RGD (Arginine-Glycine-Aspartic  acid) sequence and an adjacent site that acts in synergy with RGD to allow  5 1-dependent  cell spreading and cell migration [  Mould et al 1997 and   Obara and Yoshizato 1995].	transcription
53605	1	335123	5	NULL	NULL	0	NULL	HAT	NULL	enzymatic activity of	plays a role in	NULL	critical			X chromosome	NULL	increased transcription of;;male			NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_70_0_81_s_141	11395403	Indeed, mutation of the single underlined glycine (Gly) to  glutamic acid in motif A (Arg/ln-X-X- Gly-X-Glyla; see  Figure 5 D) led to the original discovery of MOF, supporting a critical role for HAT enzymatic  activity in the twofold increased transcription of the male X chromosome (reviewed  in  47,  92).	transcription
54064	1	335123	7	NULL	NULL	0	NULL	HAT		enzymatic activity of	play a critical role in					male X chromosome		increased transcription of			NULL		NULL	NULL	NULL	NULL	gw70_annurevbiochem_70_0_81_s_141	11395403	Indeed, mutation of the single underlined glycine (Gly) to  glutamic acid in motif A (Arg/ln-X-X- Gly-X-Glyla; see  Figure 5 D) led to the original discovery of MOF, supporting a critical role for HAT enzymatic  activity in the twofold increased transcription of the male X chromosome (reviewed  in  47,  92).	transcription
54065	2	335123	7	NULL	NULL	0	NULL				mutated to			Gly in motif A					glutamic acid in motif A		NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_70_0_81_s_141	11395403	Indeed, mutation of the single underlined glycine (Gly) to  glutamic acid in motif A (Arg/ln-X-X- Gly-X-Glyla; see  Figure 5 D) led to the original discovery of MOF, supporting a critical role for HAT enzymatic  activity in the twofold increased transcription of the male X chromosome (reviewed  in  47,  92).	transcription
54066	3	335123	7	NULL	NULL	0	NULL	statement 2			support					statement 1					NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_70_0_81_s_141	11395403	Indeed, mutation of the single underlined glycine (Gly) to  glutamic acid in motif A (Arg/ln-X-X- Gly-X-Glyla; see  Figure 5 D) led to the original discovery of MOF, supporting a critical role for HAT enzymatic  activity in the twofold increased transcription of the male X chromosome (reviewed  in  47,  92).	transcription
54067	4	335123	7	NULL	NULL	0	NULL	Gly			is					glycine					NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_70_0_81_s_141	11395403	Indeed, mutation of the single underlined glycine (Gly) to  glutamic acid in motif A (Arg/ln-X-X- Gly-X-Glyla; see  Figure 5 D) led to the original discovery of MOF, supporting a critical role for HAT enzymatic  activity in the twofold increased transcription of the male X chromosome (reviewed  in  47,  92).	transcription
53606	1	335124	5	NULL	NULL	0	NULL	NMDARs	NULL	internalization of	occurs after	NULL				glycine	NULL	priming of			NULL		0	NULL	NULL	NULL	gw70_nature_422_6929_302_s_138	12646920	To determine whether the internalization of NMDARs after glycine priming was mediated  through clathrin-dependent endocytosis, we made use of a dynamin inhibitory peptide,  QVPSRPNRAP, which competitively binds with the amphiphysin SH3 domain 15 and prevents endocytosis when administered intracellularly 5,  10.	transcription
53607	2	335124	5	NULL	NULL	0	NULL	endocytosis	NULL		is dependent on	NULL				clathrin	NULL				NULL		0	NULL	NULL	NULL	gw70_nature_422_6929_302_s_138	12646920	To determine whether the internalization of NMDARs after glycine priming was mediated  through clathrin-dependent endocytosis, we made use of a dynamin inhibitory peptide,  QVPSRPNRAP, which competitively binds with the amphiphysin SH3 domain 15 and prevents endocytosis when administered intracellularly 5,  10.	transcription
53608	3	335124	5	NULL	NULL	0	NULL	statement 1	NULL		is mediated through	NULL	possibly			statement 2	NULL				NULL		0	NULL	NULL	NULL	gw70_nature_422_6929_302_s_138	12646920	To determine whether the internalization of NMDARs after glycine priming was mediated  through clathrin-dependent endocytosis, we made use of a dynamin inhibitory peptide,  QVPSRPNRAP, which competitively binds with the amphiphysin SH3 domain 15 and prevents endocytosis when administered intracellularly 5,  10.	transcription
53609	4	335124	5	NULL	NULL	0	NULL	QVPSRPNRAP	NULL		is an inhibitory peptide of	NULL				dynamin	NULL				NULL		0	NULL	NULL	NULL	gw70_nature_422_6929_302_s_138	12646920	To determine whether the internalization of NMDARs after glycine priming was mediated  through clathrin-dependent endocytosis, we made use of a dynamin inhibitory peptide,  QVPSRPNRAP, which competitively binds with the amphiphysin SH3 domain 15 and prevents endocytosis when administered intracellularly 5,  10.	transcription
53610	5	335124	5	NULL	NULL	0	NULL		NULL		bind	NULL	competitively	QVPSRPNRAP		amphiphysin	NULL		SH3 domain		NULL		0	NULL	NULL	NULL	gw70_nature_422_6929_302_s_138	12646920	To determine whether the internalization of NMDARs after glycine priming was mediated  through clathrin-dependent endocytosis, we made use of a dynamin inhibitory peptide,  QVPSRPNRAP, which competitively binds with the amphiphysin SH3 domain 15 and prevents endocytosis when administered intracellularly 5,  10.	transcription
53611	6	335124	5	NULL	NULL	0	NULL	statement 5	NULL		prevents	NULL				endocytosis	NULL				NULL		NULL	NULL	NULL	NULL	gw70_nature_422_6929_302_s_138	12646920	To determine whether the internalization of NMDARs after glycine priming was mediated  through clathrin-dependent endocytosis, we made use of a dynamin inhibitory peptide,  QVPSRPNRAP, which competitively binds with the amphiphysin SH3 domain 15 and prevents endocytosis when administered intracellularly 5,  10.	transcription
54068	1	335124	7	NULL	NULL	0	NULL	dynamin inhibitory peptide			bind		competitively			amphiphysin			SH3 domain		NULL		0	NULL	NULL	NULL	gw70_nature_422_6929_302_s_138	12646920	To determine whether the internalization of NMDARs after glycine priming was mediated  through clathrin-dependent endocytosis, we made use of a dynamin inhibitory peptide,  QVPSRPNRAP, which competitively binds with the amphiphysin SH3 domain 15 and prevents endocytosis when administered intracellularly 5,  10.	transcription
54069	2	335124	7	NULL	NULL	0	NULL	statement 1			prevents					endocytosis 					NULL	intracellularly	NULL	NULL	NULL	NULL	gw70_nature_422_6929_302_s_138	12646920	To determine whether the internalization of NMDARs after glycine priming was mediated  through clathrin-dependent endocytosis, we made use of a dynamin inhibitory peptide,  QVPSRPNRAP, which competitively binds with the amphiphysin SH3 domain 15 and prevents endocytosis when administered intracellularly 5,  10.	transcription
54070	3	335124	7	NULL	NULL	0	NULL	 NMDARs		internalization of	occurs after					 glycine		priming of			NULL		0	NULL	NULL	NULL	gw70_nature_422_6929_302_s_138	12646920	To determine whether the internalization of NMDARs after glycine priming was mediated  through clathrin-dependent endocytosis, we made use of a dynamin inhibitory peptide,  QVPSRPNRAP, which competitively binds with the amphiphysin SH3 domain 15 and prevents endocytosis when administered intracellularly 5,  10.	transcription
54071	4	335124	7	NULL	NULL	0	NULL	dynamin inhibitory peptide			is					QVPSRPNRAP					NULL		0	NULL	NULL	NULL	gw70_nature_422_6929_302_s_138	12646920	To determine whether the internalization of NMDARs after glycine priming was mediated  through clathrin-dependent endocytosis, we made use of a dynamin inhibitory peptide,  QVPSRPNRAP, which competitively binds with the amphiphysin SH3 domain 15 and prevents endocytosis when administered intracellularly 5,  10.	transcription
53612	2	335126	5	NULL	NULL	0	NULL	Z1	NULL	mRNA splicing of	generates	NULL				statement 1	NULL				NULL		0	NULL	NULL	NULL	gw70_neuroscience_122_2_449_s_198	14614909	Of more interest is the fact that alternative mRNA splicing of  Z1 generates glycine  receptors that differ in their anatomical distribution;  Z1L transcript expression  is highly restricted to the rostral part of the telencephalon while  Z1 mRNA is expressed  all over the CNS ( Fig. 5).	transcription
53613	1	335126	5	NULL	NULL	0	NULL	glycine receptors	NULL		differ in	NULL				anatomical distribution	NULL				NULL		0	NULL	NULL	NULL	gw70_neuroscience_122_2_449_s_198	14614909	Of more interest is the fact that alternative mRNA splicing of  Z1 generates glycine  receptors that differ in their anatomical distribution;  Z1L transcript expression  is highly restricted to the rostral part of the telencephalon while  Z1 mRNA is expressed  all over the CNS ( Fig. 5).	transcription
53614	3	335126	5	NULL	NULL	0	NULL	Z1L transcript	NULL	expression of	is restricted to	NULL	highly			telencephalon	NULL	rostral part of			NULL		0	NULL	NULL	NULL	gw70_neuroscience_122_2_449_s_198	14614909	Of more interest is the fact that alternative mRNA splicing of  Z1 generates glycine  receptors that differ in their anatomical distribution;  Z1L transcript expression  is highly restricted to the rostral part of the telencephalon while  Z1 mRNA is expressed  all over the CNS ( Fig. 5).	transcription
53615	4	335126	5	NULL	NULL	0	NULL	Z1 mRNA	NULL		is expressed all over	NULL				CNS	NULL				NULL		0	NULL	NULL	NULL	gw70_neuroscience_122_2_449_s_198	14614909	Of more interest is the fact that alternative mRNA splicing of  Z1 generates glycine  receptors that differ in their anatomical distribution;  Z1L transcript expression  is highly restricted to the rostral part of the telencephalon while  Z1 mRNA is expressed  all over the CNS ( Fig. 5).	transcription
54072	1	335126	7	NULL	NULL	0	NULL	Z1		alternative mRNA splicing of	generates					glycine receptors					NULL		0	NULL	NULL	NULL	gw70_neuroscience_122_2_449_s_198	14614909	Of more interest is the fact that alternative mRNA splicing of  Z1 generates glycine  receptors that differ in their anatomical distribution;  Z1L transcript expression  is highly restricted to the rostral part of the telencephalon while  Z1 mRNA is expressed  all over the CNS ( Fig. 5).	transcription
54073	2	335126	7	NULL	NULL	0	NULL	Z1L transcript		expression of	is restricted to					 telencephalon		rostral part of			NULL		0	NULL	NULL	NULL	gw70_neuroscience_122_2_449_s_198	14614909	Of more interest is the fact that alternative mRNA splicing of  Z1 generates glycine  receptors that differ in their anatomical distribution;  Z1L transcript expression  is highly restricted to the rostral part of the telencephalon while  Z1 mRNA is expressed  all over the CNS ( Fig. 5).	transcription
54074	3	335126	7	NULL	NULL	0	NULL	Z1 mRNA			is expressed in					CNS		entire			NULL		NULL	NULL	NULL	NULL	gw70_neuroscience_122_2_449_s_198	14614909	Of more interest is the fact that alternative mRNA splicing of  Z1 generates glycine  receptors that differ in their anatomical distribution;  Z1L transcript expression  is highly restricted to the rostral part of the telencephalon while  Z1 mRNA is expressed  all over the CNS ( Fig. 5).	transcription
53616	1	335127	5	NULL	NULL	0	NULL	beta-TrCP	NULL		bind	NULL				mPER2	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_7_2795_s_335	15767683	Mutation of serine 477 and glycine 479 to alanine [mPER2(S477A/G479A)] abolished almost all detectable CKI -dependent beta-TrCP binding to mPER2 (Fig.  8B, lane 5), indicating that these residues function as a novel beta-TrCP binding motif.	transcription
53617	2	335127	5	NULL	NULL	0	NULL	statement 1	NULL		is dependent on	NULL				CKI	NULL				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_7_2795_s_335	15767683	Mutation of serine 477 and glycine 479 to alanine [mPER2(S477A/G479A)] abolished almost all detectable CKI -dependent beta-TrCP binding to mPER2 (Fig.  8B, lane 5), indicating that these residues function as a novel beta-TrCP binding motif.	transcription
53618	3	335127	5	NULL	NULL	0	NULL	mPER2	NULL	mutant	abolishes	NULL		(S477A/G479A)		statement 1	NULL				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_7_2795_s_335	15767683	Mutation of serine 477 and glycine 479 to alanine [mPER2(S477A/G479A)] abolished almost all detectable CKI -dependent beta-TrCP binding to mPER2 (Fig.  8B, lane 5), indicating that these residues function as a novel beta-TrCP binding motif.	transcription
53619	4	335127	5	NULL	NULL	0	NULL	mPER2	NULL		function as	NULL		S477		beta-TrCP binding motif	NULL	novel			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_7_2795_s_335	15767683	Mutation of serine 477 and glycine 479 to alanine [mPER2(S477A/G479A)] abolished almost all detectable CKI -dependent beta-TrCP binding to mPER2 (Fig.  8B, lane 5), indicating that these residues function as a novel beta-TrCP binding motif.	transcription
53620	5	335127	5	NULL	NULL	0	NULL	mPER2	NULL		function as	NULL		G479		beta-TrCP binding motif	NULL	novel			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_7_2795_s_335	15767683	Mutation of serine 477 and glycine 479 to alanine [mPER2(S477A/G479A)] abolished almost all detectable CKI -dependent beta-TrCP binding to mPER2 (Fig.  8B, lane 5), indicating that these residues function as a novel beta-TrCP binding motif.	transcription
54075	1	335127	7	NULL	NULL	0	NULL	beta-TrCP			bind					mPER2					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_7_2795_s_335	15767683	Mutation of serine 477 and glycine 479 to alanine [mPER2(S477A/G479A)] abolished almost all detectable CKI -dependent beta-TrCP binding to mPER2 (Fig.  8B, lane 5), indicating that these residues function as a novel beta-TrCP binding motif.	transcription
54076	2	335127	7	NULL	NULL	0	NULL	statement 1			depends on					CKI					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_7_2795_s_335	15767683	Mutation of serine 477 and glycine 479 to alanine [mPER2(S477A/G479A)] abolished almost all detectable CKI -dependent beta-TrCP binding to mPER2 (Fig.  8B, lane 5), indicating that these residues function as a novel beta-TrCP binding motif.	transcription
54077	3	335127	7	NULL	NULL	0	NULL	mPER2		mutant	abolish			S477A		statement 1					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_7_2795_s_335	15767683	Mutation of serine 477 and glycine 479 to alanine [mPER2(S477A/G479A)] abolished almost all detectable CKI -dependent beta-TrCP binding to mPER2 (Fig.  8B, lane 5), indicating that these residues function as a novel beta-TrCP binding motif.	transcription
54078	4	335127	7	NULL	NULL	0	NULL	mPER2		mutant	abolish			G479A		statement 1					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_7_2795_s_335	15767683	Mutation of serine 477 and glycine 479 to alanine [mPER2(S477A/G479A)] abolished almost all detectable CKI -dependent beta-TrCP binding to mPER2 (Fig.  8B, lane 5), indicating that these residues function as a novel beta-TrCP binding motif.	transcription
54079	5	335127	7	NULL	NULL	0	NULL	mPER2			function as			serine 477		mPER2			novel beta-TrCP binding motif		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_7_2795_s_335	15767683	Mutation of serine 477 and glycine 479 to alanine [mPER2(S477A/G479A)] abolished almost all detectable CKI -dependent beta-TrCP binding to mPER2 (Fig.  8B, lane 5), indicating that these residues function as a novel beta-TrCP binding motif.	transcription
54080	6	335127	7	NULL	NULL	0	NULL	mPER2			function as			glycine 479		mPER2			novel beta-TrCP binding motif		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_7_2795_s_335	15767683	Mutation of serine 477 and glycine 479 to alanine [mPER2(S477A/G479A)] abolished almost all detectable CKI -dependent beta-TrCP binding to mPER2 (Fig.  8B, lane 5), indicating that these residues function as a novel beta-TrCP binding motif.	transcription
53621	1	335128	5	NULL	NULL	0	NULL	insulin-like growth factor-binding protein 5	NULL	rat	is mutated to	NULL		glycine		insulin-like growth factor-binding protein 5	NULL	rat	glutamine		NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_9_2841_s_312	15090526	Another study, involving a mutation in rat insulin-like growth factor-binding protein 5, has also shown that replacement of a critical glycine with glutamine causes the protein to lose activity, although the mutation did not result in gross conformational changes in the protein ( ).	transcription
53622	2	335128	5	NULL	NULL	0	NULL	statement 1	NULL		causes	NULL				insulin-like growth factor-binding protein 5	NULL	loss of activity of;;rat			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_9_2841_s_312	15090526	Another study, involving a mutation in rat insulin-like growth factor-binding protein 5, has also shown that replacement of a critical glycine with glutamine causes the protein to lose activity, although the mutation did not result in gross conformational changes in the protein ( ).	transcription
53623	3	335128	5	NULL	NULL	0	NULL	statement 1	NULL		does not result in	NULL				insulin-like growth factor-binding protein 5	NULL	gross conformational change of;;rat			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_9_2841_s_312	15090526	Another study, involving a mutation in rat insulin-like growth factor-binding protein 5, has also shown that replacement of a critical glycine with glutamine causes the protein to lose activity, although the mutation did not result in gross conformational changes in the protein ( ).	transcription
54081	1	335128	7	NULL	NULL	0	NULL	insulin-like growth factor-binding protein 5		rat	is mutated to			glycine		insulin-like growth factor-binding protein 5		rat	glutamine		NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_9_2841_s_312	15090526	Another study, involving a mutation in rat insulin-like growth factor-binding protein 5, has also shown that replacement of a critical glycine with glutamine causes the protein to lose activity, although the mutation did not result in gross conformational changes in the protein ( ).	transcription
54082	2	335128	7	NULL	NULL	0	NULL	statement 1			cause					protein		loss of;; activity of			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_9_2841_s_312	15090526	Another study, involving a mutation in rat insulin-like growth factor-binding protein 5, has also shown that replacement of a critical glycine with glutamine causes the protein to lose activity, although the mutation did not result in gross conformational changes in the protein ( ).	transcription
54083	3	335128	7	NULL	NULL	0	NULL	statement 1			does not result in					protein		gross conformational changes in			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_9_2841_s_312	15090526	Another study, involving a mutation in rat insulin-like growth factor-binding protein 5, has also shown that replacement of a critical glycine with glutamine causes the protein to lose activity, although the mutation did not result in gross conformational changes in the protein ( ).	transcription
53624	1	335129	5	NULL	NULL	0	NULL	phage A1-9	NULL		bind	NULL				OppA-1	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_1_51_s_175	14679224	To investigate whether changes in pH affect the affinity of OppA for its peptide substrates, phage A1-9, which binds to both OppA-1 and OppA-3, was diluted to the final concentration of 109 PFU in different pH buffers (0.2 M glycine-HCl for pHs 2.2 and 3; 100 mM Tris-HCl for pHs 5, 6, 7.	transcription
53625	2	335129	5	NULL	NULL	0	NULL	phage A1-9	NULL		bind	NULL				OppA-3	NULL				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_1_51_s_175	14679224	To investigate whether changes in pH affect the affinity of OppA for its peptide substrates, phage A1-9, which binds to both OppA-1 and OppA-3, was diluted to the final concentration of 109 PFU in different pH buffers (0.2 M glycine-HCl for pHs 2.2 and 3; 100 mM Tris-HCl for pHs 5, 6, 7.	transcription
54084	1	335129	7	NULL	NULL	0	NULL	OppA			has affinity for					peptide substrates					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_1_51_s_175	14679224	To investigate whether changes in pH affect the affinity of OppA for its peptide substrates, phage A1-9, which binds to both OppA-1 and OppA-3, was diluted to the final concentration of 109 PFU in different pH buffers (0.2 M glycine-HCl for pHs 2.2 and 3; 100 mM Tris-HCl for pHs 5, 6, 7.	transcription
54085	2	335129	7	NULL	NULL	0	NULL	phage A1-9			bind					OppA-1					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_1_51_s_175	14679224	To investigate whether changes in pH affect the affinity of OppA for its peptide substrates, phage A1-9, which binds to both OppA-1 and OppA-3, was diluted to the final concentration of 109 PFU in different pH buffers (0.2 M glycine-HCl for pHs 2.2 and 3; 100 mM Tris-HCl for pHs 5, 6, 7.	transcription
54086	3	335129	7	NULL	NULL	0	NULL	phage A1-9			bind					OppA-3					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_1_51_s_175	14679224	To investigate whether changes in pH affect the affinity of OppA for its peptide substrates, phage A1-9, which binds to both OppA-1 and OppA-3, was diluted to the final concentration of 109 PFU in different pH buffers (0.2 M glycine-HCl for pHs 2.2 and 3; 100 mM Tris-HCl for pHs 5, 6, 7.	transcription
53626	1	335130	5	NULL	NULL	0	NULL	PMTS	NULL		enhances	NULL				GlyR	NULL	function of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_6_3305_s_66	16361257	However, before using this approach to examine binding pocket occupancy, we showed that 5 mM PMTS enhances GlyR function like alcohols or anesthetics when directly co-applied to wt and S267C GlyRs with an EC10 concentration of glycine ( Fig. 2).	transcription
54763	1	335130	7	NULL	NULL	0	NULL	PMTS			enhance					GlyR		function of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_6_3305_s_66	16361257	However, before using this approach to examine binding pocket occupancy, we showed that 5 mM PMTS enhances GlyR function like alcohols or anesthetics when directly co-applied to wt and S267C GlyRs with an EC10 concentration of glycine ( Fig. 2).	transcription
54764	2	335130	7	NULL	NULL	0	NULL	alcohols			enhance					GlyR		function of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_6_3305_s_66	16361257	However, before using this approach to examine binding pocket occupancy, we showed that 5 mM PMTS enhances GlyR function like alcohols or anesthetics when directly co-applied to wt and S267C GlyRs with an EC10 concentration of glycine ( Fig. 2).	transcription
54765	3	335130	7	NULL	NULL	0	NULL	anesthetics			enhance					GlyR		function of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_6_3305_s_66	16361257	However, before using this approach to examine binding pocket occupancy, we showed that 5 mM PMTS enhances GlyR function like alcohols or anesthetics when directly co-applied to wt and S267C GlyRs with an EC10 concentration of glycine ( Fig. 2).	transcription
54766	4	335130	7	NULL	NULL	0	NULL	statement 2			is an alternative to					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_6_3305_s_66	16361257	However, before using this approach to examine binding pocket occupancy, we showed that 5 mM PMTS enhances GlyR function like alcohols or anesthetics when directly co-applied to wt and S267C GlyRs with an EC10 concentration of glycine ( Fig. 2).	transcription
53665	1	335132	5	NULL	NULL	0	NULL	amino acid		specific composition of	plays a role in		central					binding of	ALE-1-targeting domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_549_s_261	16257954	Evidently, the specific amino acid composition and the length of the interpeptide bridge play central roles in ALE-1-targeting domain binding; substitution of glycine by serine at position 3 or 5 significantly impairs the gross binding of the targeting domain to staphylococcal PGs, while the length of the interpeptide bridges,  i.e. pentaglycine, confers the maximum binding of the targeting domain to PGs.	transcription
53666	2	335132	5	NULL	NULL	0	NULL	interpeptide bridge		length of	plays a role in		central					binding of	ALE-1-targeting domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_549_s_261	16257954	Evidently, the specific amino acid composition and the length of the interpeptide bridge play central roles in ALE-1-targeting domain binding; substitution of glycine by serine at position 3 or 5 significantly impairs the gross binding of the targeting domain to staphylococcal PGs, while the length of the interpeptide bridges,  i.e. pentaglycine, confers the maximum binding of the targeting domain to PGs.	transcription
53667	3	335132	5	NULL	NULL	0	NULL				bind			targeting domain		PGs		staphylococcal			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_549_s_261	16257954	Evidently, the specific amino acid composition and the length of the interpeptide bridge play central roles in ALE-1-targeting domain binding; substitution of glycine by serine at position 3 or 5 significantly impairs the gross binding of the targeting domain to staphylococcal PGs, while the length of the interpeptide bridges,  i.e. pentaglycine, confers the maximum binding of the targeting domain to PGs.	transcription
53668	4	335132	5	NULL	NULL	0	NULL	glycine			is substituted to			position 3		serine					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_1_549_s_261	16257954	Evidently, the specific amino acid composition and the length of the interpeptide bridge play central roles in ALE-1-targeting domain binding; substitution of glycine by serine at position 3 or 5 significantly impairs the gross binding of the targeting domain to staphylococcal PGs, while the length of the interpeptide bridges,  i.e. pentaglycine, confers the maximum binding of the targeting domain to PGs.	transcription
53669	5	335132	5	NULL	NULL	0	NULL	glycine			is substituted to			position 5		serine					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_549_s_261	16257954	Evidently, the specific amino acid composition and the length of the interpeptide bridge play central roles in ALE-1-targeting domain binding; substitution of glycine by serine at position 3 or 5 significantly impairs the gross binding of the targeting domain to staphylococcal PGs, while the length of the interpeptide bridges,  i.e. pentaglycine, confers the maximum binding of the targeting domain to PGs.	transcription
53670	6	335132	5	NULL	NULL	0	NULL	statement 4			impairs					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_549_s_261	16257954	Evidently, the specific amino acid composition and the length of the interpeptide bridge play central roles in ALE-1-targeting domain binding; substitution of glycine by serine at position 3 or 5 significantly impairs the gross binding of the targeting domain to staphylococcal PGs, while the length of the interpeptide bridges,  i.e. pentaglycine, confers the maximum binding of the targeting domain to PGs.	transcription
53671	7	335132	5	NULL	NULL	0	NULL	statement 5			impairs					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_549_s_261	16257954	Evidently, the specific amino acid composition and the length of the interpeptide bridge play central roles in ALE-1-targeting domain binding; substitution of glycine by serine at position 3 or 5 significantly impairs the gross binding of the targeting domain to staphylococcal PGs, while the length of the interpeptide bridges,  i.e. pentaglycine, confers the maximum binding of the targeting domain to PGs.	transcription
53672	8	335132	5	NULL	NULL	0	NULL	pentaglycine			confers					statement 3		maximum binding of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_549_s_261	16257954	Evidently, the specific amino acid composition and the length of the interpeptide bridge play central roles in ALE-1-targeting domain binding; substitution of glycine by serine at position 3 or 5 significantly impairs the gross binding of the targeting domain to staphylococcal PGs, while the length of the interpeptide bridges,  i.e. pentaglycine, confers the maximum binding of the targeting domain to PGs.	transcription
54767	1	335132	7	NULL	NULL	0	NULL				bind			ALE-1-targeting domain		PGs				staphylococcal	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_549_s_261	16257954	Evidently, the specific amino acid composition and the length of the interpeptide bridge play central roles in ALE-1-targeting domain binding; substitution of glycine by serine at position 3 or 5 significantly impairs the gross binding of the targeting domain to staphylococcal PGs, while the length of the interpeptide bridges,  i.e. pentaglycine, confers the maximum binding of the targeting domain to PGs.	transcription
54768	2	335132	7	NULL	NULL	0	NULL				substituted for			ALE-1-targeting domain;;glycine 3					ALE-1-targeting domain;;serine 3		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_549_s_261	16257954	Evidently, the specific amino acid composition and the length of the interpeptide bridge play central roles in ALE-1-targeting domain binding; substitution of glycine by serine at position 3 or 5 significantly impairs the gross binding of the targeting domain to staphylococcal PGs, while the length of the interpeptide bridges,  i.e. pentaglycine, confers the maximum binding of the targeting domain to PGs.	transcription
54769	3	335132	7	NULL	NULL	0	NULL				substituted for			ALE-1-targeting domain;;glycine 5					ALE-1-targeting domain;;serine 5		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_549_s_261	16257954	Evidently, the specific amino acid composition and the length of the interpeptide bridge play central roles in ALE-1-targeting domain binding; substitution of glycine by serine at position 3 or 5 significantly impairs the gross binding of the targeting domain to staphylococcal PGs, while the length of the interpeptide bridges,  i.e. pentaglycine, confers the maximum binding of the targeting domain to PGs.	transcription
54770	4	335132	7	NULL	NULL	0	NULL	statement 2			impairs		significantly			statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_549_s_261	16257954	Evidently, the specific amino acid composition and the length of the interpeptide bridge play central roles in ALE-1-targeting domain binding; substitution of glycine by serine at position 3 or 5 significantly impairs the gross binding of the targeting domain to staphylococcal PGs, while the length of the interpeptide bridges,  i.e. pentaglycine, confers the maximum binding of the targeting domain to PGs.	transcription
54771	5	335132	7	NULL	NULL	0	NULL	statement 3			impairs		significantly			statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_549_s_261	16257954	Evidently, the specific amino acid composition and the length of the interpeptide bridge play central roles in ALE-1-targeting domain binding; substitution of glycine by serine at position 3 or 5 significantly impairs the gross binding of the targeting domain to staphylococcal PGs, while the length of the interpeptide bridges,  i.e. pentaglycine, confers the maximum binding of the targeting domain to PGs.	transcription
54772	6	335132	7	NULL	NULL	0	NULL	pentaglycine		interpeptide bridge of	confers					statement 1		maximum binding of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_1_549_s_261	16257954	Evidently, the specific amino acid composition and the length of the interpeptide bridge play central roles in ALE-1-targeting domain binding; substitution of glycine by serine at position 3 or 5 significantly impairs the gross binding of the targeting domain to staphylococcal PGs, while the length of the interpeptide bridges,  i.e. pentaglycine, confers the maximum binding of the targeting domain to PGs.	transcription
53673	1	335133	5	NULL	NULL	0	NULL	NMDA			induce					[Ca2+]i		increase in			NULL		0	NULL	NULL	NULL	gw70_jneurosci_26_13_3404_s_85	16571747	E, Administration of 500 muM NMDA (in Mg2+-free KRH, containing 5 muM glycine) induces both a [Ca2+]i increase and a PKCgamma-EGFP translocation that are completely reverted by a NMDAR blocker (100 muM APV, in the presence of 1.2 mM Mg2+).	transcription
53674	2	335133	5	NULL	NULL	0	NULL	NMDA			induce					PKCgamma-EGFP		translocation of			NULL		0	NULL	NULL	NULL	gw70_jneurosci_26_13_3404_s_85	16571747	E, Administration of 500 muM NMDA (in Mg2+-free KRH, containing 5 muM glycine) induces both a [Ca2+]i increase and a PKCgamma-EGFP translocation that are completely reverted by a NMDAR blocker (100 muM APV, in the presence of 1.2 mM Mg2+).	transcription
53675	3	335133	5	NULL	NULL	0	NULL	NMDAR blocker			reverts		completely			statement 1					NULL		0	NULL	NULL	NULL	gw70_jneurosci_26_13_3404_s_85	16571747	E, Administration of 500 muM NMDA (in Mg2+-free KRH, containing 5 muM glycine) induces both a [Ca2+]i increase and a PKCgamma-EGFP translocation that are completely reverted by a NMDAR blocker (100 muM APV, in the presence of 1.2 mM Mg2+).	transcription
53676	4	335133	5	NULL	NULL	0	NULL	NMDAR blocker			reverts		completely			statement 2					NULL		0	NULL	NULL	NULL	gw70_jneurosci_26_13_3404_s_85	16571747	E, Administration of 500 muM NMDA (in Mg2+-free KRH, containing 5 muM glycine) induces both a [Ca2+]i increase and a PKCgamma-EGFP translocation that are completely reverted by a NMDAR blocker (100 muM APV, in the presence of 1.2 mM Mg2+).	transcription
54773	1	335133	7	NULL	NULL	0	NULL	 PKCgamma			translocates					EGFP					NULL		0	NULL	NULL	NULL	gw70_jneurosci_26_13_3404_s_85	16571747	E, Administration of 500 muM NMDA (in Mg2+-free KRH, containing 5 muM glycine) induces both a [Ca2+]i increase and a PKCgamma-EGFP translocation that are completely reverted by a NMDAR blocker (100 muM APV, in the presence of 1.2 mM Mg2+).	transcription
54774	2	335133	7	NULL	NULL	0	NULL	NMDA 			induce					[Ca2+]i		increase of			NULL		0	NULL	NULL	NULL	gw70_jneurosci_26_13_3404_s_85	16571747	E, Administration of 500 muM NMDA (in Mg2+-free KRH, containing 5 muM glycine) induces both a [Ca2+]i increase and a PKCgamma-EGFP translocation that are completely reverted by a NMDAR blocker (100 muM APV, in the presence of 1.2 mM Mg2+).	transcription
54775	3	335133	7	NULL	NULL	0	NULL	NMDA			induce					statement 1					NULL		0	NULL	NULL	NULL	gw70_jneurosci_26_13_3404_s_85	16571747	E, Administration of 500 muM NMDA (in Mg2+-free KRH, containing 5 muM glycine) induces both a [Ca2+]i increase and a PKCgamma-EGFP translocation that are completely reverted by a NMDAR blocker (100 muM APV, in the presence of 1.2 mM Mg2+).	transcription
54776	4	335133	7	NULL	NULL	0	NULL	NMDAR blocker			reverts		completely			statement 2					NULL		0	NULL	NULL	NULL	gw70_jneurosci_26_13_3404_s_85	16571747	E, Administration of 500 muM NMDA (in Mg2+-free KRH, containing 5 muM glycine) induces both a [Ca2+]i increase and a PKCgamma-EGFP translocation that are completely reverted by a NMDAR blocker (100 muM APV, in the presence of 1.2 mM Mg2+).	transcription
54777	5	335133	7	NULL	NULL	0	NULL	NMDAR blocker			reverts		completely			statement 4					NULL		NULL	NULL	NULL	NULL	gw70_jneurosci_26_13_3404_s_85	16571747	E, Administration of 500 muM NMDA (in Mg2+-free KRH, containing 5 muM glycine) induces both a [Ca2+]i increase and a PKCgamma-EGFP translocation that are completely reverted by a NMDAR blocker (100 muM APV, in the presence of 1.2 mM Mg2+).	transcription
54822	1	335134	7	NULL	NULL	0	NULL	HF-Cui1 			bind					Cdc48 proteins					NULL		0	NULL	NULL	NULL	gw70_yeast_21_2_127_s_76	14755638	The column was then washed with 3 x 5 ml TBS buffer (150 mM NaCl, 50 mM Tris-HCl, pH 7.5) and the bound HF-Cui1 and Cdc48 proteins eluted using 3 x 0.25  ml of 0.1 M glycine, pH 3.5.	transcription
53677	1	335135	5	NULL	NULL	0	NULL	RPS19 protein		mature	replaces		functionally;;possibly	RNA-binding portion		ribosomal protein					NULL		NULL	NULL	NULL	NULL	gw60_genetics_158_3_1289_s_214	11454775	Most of the RNA-binding protein, minus the glycine-rich C terminus, is found at the 5' end of  rps19, and the RNA-binding portion of the mature RPS19 protein has been proposed to functionally replace another ribosomal protein ( S ANCHEZ et al. 1996   ).	transcription
56140	1	335135	7	NULL	NULL	0	NULL	RNA-binding protein			bind					rps19			 5' end of		NULL		0	NULL	NULL	NULL	gw60_genetics_158_3_1289_s_214	11454775	Most of the RNA-binding protein, minus the glycine-rich C terminus, is found at the 5' end of  rps19, and the RNA-binding portion of the mature RPS19 protein has been proposed to functionally replace another ribosomal protein ( S ANCHEZ et al. 1996   ).	transcription
53678	1	335138	5	NULL	NULL	0	NULL	NMDA			induce					seizures					NULL	mice	0	NULL	NULL	NULL	gw60_brainres_944_1_165_s_172	12106676	Comparison of the anticonvulsant activities of NMDA receptor glycine-binding site antagonists on NMDA-induced seizures in mice      (<1K) Drugs were administered intravenously via the tail vein 20 min before intracerebroventricular injection of NMDA (5 nmol/10  l per mouse).	transcription
54823	1	335138	7	NULL	NULL	0	NULL	NMDA			induce					seizure					NULL	mice	0	NULL	NULL	NULL	gw60_brainres_944_1_165_s_172	12106676	Comparison of the anticonvulsant activities of NMDA receptor glycine-binding site antagonists on NMDA-induced seizures in mice      (<1K) Drugs were administered intravenously via the tail vein 20 min before intracerebroventricular injection of NMDA (5 nmol/10  l per mouse).	transcription
53679	1	335140	5	NULL	NULL	0	NULL	chlormethiazole			does not affect					glycine responses					NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_3_801_s_160	10188994	The inability of chlormethiazole to affect glycine responses (on either side of ECl) was confirmed by using a higher concentration (100 muM) in seven additional cells, continuously perfused with bicuculline (5 muM) in order to block GABA responses and to prevent the leak current increase usually induced by chlormethiazole ( Figure 5f).	transcription
54824	1	335140	7	NULL	NULL	0	NULL	chlormethiazole			does not affect					glycine		response of			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_126_3_801_s_160	10188994	The inability of chlormethiazole to affect glycine responses (on either side of ECl) was confirmed by using a higher concentration (100 muM) in seven additional cells, continuously perfused with bicuculline (5 muM) in order to block GABA responses and to prevent the leak current increase usually induced by chlormethiazole ( Figure 5f).	transcription
54825	2	335140	7	NULL	NULL	0	NULL	bicuculline			block					GABA 		response of			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_126_3_801_s_160	10188994	The inability of chlormethiazole to affect glycine responses (on either side of ECl) was confirmed by using a higher concentration (100 muM) in seven additional cells, continuously perfused with bicuculline (5 muM) in order to block GABA responses and to prevent the leak current increase usually induced by chlormethiazole ( Figure 5f).	transcription
53680	1	335143	5	NULL	NULL	0	NULL	LDL			is mutated to			Asp235		LDL			glycine		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1392_s_160	9261272	2  Interestingly, another point mutation in the same codon as FH-Keuruu, changing aspartic acid to the neutral amino acid glycine (Asp235 Gly or FH Nevers), was found to result in an LDL receptor with only 5% to 15% of activity compared to the normal one.	transcription
53681	2	335143	5	NULL	NULL	0	NULL			point mutation of	leads to			FH-Keuruu		statement 1					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1392_s_160	9261272	2  Interestingly, another point mutation in the same codon as FH-Keuruu, changing aspartic acid to the neutral amino acid glycine (Asp235 Gly or FH Nevers), was found to result in an LDL receptor with only 5% to 15% of activity compared to the normal one.	transcription
53682	3	335143	5	NULL	NULL	0	NULL	statement 1		activity of	lesser than					LDL		normal			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1392_s_160	9261272	2  Interestingly, another point mutation in the same codon as FH-Keuruu, changing aspartic acid to the neutral amino acid glycine (Asp235 Gly or FH Nevers), was found to result in an LDL receptor with only 5% to 15% of activity compared to the normal one.	transcription
53683	4	335143	5	NULL	NULL	0	NULL	glycine			is a type of					neutral amino acid					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1392_s_160	9261272	2  Interestingly, another point mutation in the same codon as FH-Keuruu, changing aspartic acid to the neutral amino acid glycine (Asp235 Gly or FH Nevers), was found to result in an LDL receptor with only 5% to 15% of activity compared to the normal one.	transcription
56141	1	335143	7	NULL	NULL	0	NULL	LDL			is mutated to			Asp235 		LDL			glycine		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1392_s_160	9261272	2  Interestingly, another point mutation in the same codon as FH-Keuruu, changing aspartic acid to the neutral amino acid glycine (Asp235 Gly or FH Nevers), was found to result in an LDL receptor with only 5% to 15% of activity compared to the normal one.	transcription
56142	2	335143	7	NULL	NULL	0	NULL	FH-Keuruu		 point mutation of	leads to 					statement 1					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1392_s_160	9261272	2  Interestingly, another point mutation in the same codon as FH-Keuruu, changing aspartic acid to the neutral amino acid glycine (Asp235 Gly or FH Nevers), was found to result in an LDL receptor with only 5% to 15% of activity compared to the normal one.	transcription
56143	3	335143	7	NULL	NULL	0	NULL	statement 1		activity of	is lesser than					LDL		normal			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1392_s_160	9261272	2  Interestingly, another point mutation in the same codon as FH-Keuruu, changing aspartic acid to the neutral amino acid glycine (Asp235 Gly or FH Nevers), was found to result in an LDL receptor with only 5% to 15% of activity compared to the normal one.	transcription
56144	4	335143	7	NULL	NULL	0	NULL	glycine			is a type of					neutral amino acid					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_17_7_1392_s_160	9261272	2  Interestingly, another point mutation in the same codon as FH-Keuruu, changing aspartic acid to the neutral amino acid glycine (Asp235 Gly or FH Nevers), was found to result in an LDL receptor with only 5% to 15% of activity compared to the normal one.	transcription
53684	1	335145	5	NULL	NULL	0	NULL	bicuculline			is an antagonist of					GABAA receptor					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
53685	2	335145	5	NULL	NULL	0	NULL	picrotoxin			is an antagonist of					GABAA receptor					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
53686	3	335145	5	NULL	NULL	0	NULL	strychnine			is an antagonist of					glycine receptor					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
53687	4	335145	5	NULL	NULL	0	NULL	bicuculline			increases					EPSPs		duration of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
53688	5	335145	5	NULL	NULL	0	NULL	picrotoxin			increases					EPSPs		duration of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
53689	6	335145	5	NULL	NULL	0	NULL	strychnine			increases					EPSPs		duration of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
53690	7	335145	5	NULL	NULL	0	NULL	bicuculline			increases					EPSCs		duration of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
53691	8	335145	5	NULL	NULL	0	NULL	picrotoxin			increases					EPSCs		duration of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
53692	9	335145	5	NULL	NULL	0	NULL	strychnine			increases					EPSCs		duration of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
53693	10	335145	5	NULL	NULL	0	NULL	bicuculline			increases					cell		excitability of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
53694	11	335145	5	NULL	NULL	0	NULL	picrotoxin			increases					cell		excitability of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
53695	12	335145	5	NULL	NULL	0	NULL	strychnine			increases					cell		excitability of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
54837	1	335145	7	NULL	NULL	0	NULL	bicuculline 			increase 					EPSPs		duration of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
54838	2	335145	7	NULL	NULL	0	NULL	bicuculline			increase					EPSCs		duration of			NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
54839	3	335145	7	NULL	NULL	0	NULL	 bicuculline			increase					cell excitability		duration of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
54840	4	335145	7	NULL	NULL	0	NULL	picrotoxin			increase					EPSPs		duration of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
54841	5	335145	7	NULL	NULL	0	NULL	picrotoxin			increase					EPSCs		duration of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
54842	6	335145	7	NULL	NULL	0	NULL	picrotoxin			increase					cell excitability		duration of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
54843	7	335145	7	NULL	NULL	0	NULL	strychnine			increase					EPSPs		duration of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
54844	8	335145	7	NULL	NULL	0	NULL	strychnine			increase					EPSCs		duration of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
55136	9	335145	7	NULL	NULL	0	NULL	strychnine			increase					cell excitability		duration of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
55137	10	335145	7	NULL	NULL	0	NULL	bicuculline			is a type of					GABAA receptor antagonist					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
55138	11	335145	7	NULL	NULL	0	NULL	picrotoxin			is a type of					GABAA receptor antagonist					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
55139	12	335145	7	NULL	NULL	0	NULL	strychnine			is a type of					 glycine receptor antagonist					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_39_12_2231_s_54	10974307	Bath application of the GABAA receptor antagonists bicuculline or picrotoxin and the glycine receptor antagonist strychnine typically increased the duration of EPSPs and EPSCs and the cell excitability but had little or no effect on the amplitude and slope of the initial component of both responses (see the traces in  Fig. 3,  Fig. 4 and  Fig. 5).	transcription
53696	1	335148	5	NULL	NULL	0	NULL	VirD2		mutant	mediates			R129G		T-DNA		integration of			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_18_5758_s_221	10482518	These data are reminiscent of the properties of T-DNA integration mediated by a mutant form of VirD2, VirD2R129G (created by replacement of arginine 129 with glycine;  44); in both cases, the efficiency of integration is unaltered compared to the respective wild-type situation while the pattern of integration indicates deletions at the 5' end.	transcription
55149	1	335148	7	NULL	NULL	0	NULL	VirD2		mutant	mediate					T-DNA		integration of			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_18_5758_s_221	10482518	These data are reminiscent of the properties of T-DNA integration mediated by a mutant form of VirD2, VirD2R129G (created by replacement of arginine 129 with glycine;  44); in both cases, the efficiency of integration is unaltered compared to the respective wild-type situation while the pattern of integration indicates deletions at the 5' end.	transcription
55150	2	335148	7	NULL	NULL	0	NULL	VirD2		mutant	mediate			R129G		T-DNA		integration of			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_18_5758_s_221	10482518	These data are reminiscent of the properties of T-DNA integration mediated by a mutant form of VirD2, VirD2R129G (created by replacement of arginine 129 with glycine;  44); in both cases, the efficiency of integration is unaltered compared to the respective wild-type situation while the pattern of integration indicates deletions at the 5' end.	transcription
55151	3	335148	7	NULL	NULL	0	NULL	T-DNA		pattern of;;integration of	indicates									deletion at 5' end	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_18_5758_s_221	10482518	These data are reminiscent of the properties of T-DNA integration mediated by a mutant form of VirD2, VirD2R129G (created by replacement of arginine 129 with glycine;  44); in both cases, the efficiency of integration is unaltered compared to the respective wild-type situation while the pattern of integration indicates deletions at the 5' end.	transcription
53697	1	335149	5	NULL	NULL	0	NULL	SMN			interacts with					fibrillarin			GAR domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_38645_s_210	11509571	We have found that SMN interacts with the GAR domain of fibrillarin (Figs.  4 and  5), and other studies indicate that SMN also interacts with hnRNP U ( 34), several Sm and Sm-like (Lsm) proteins ( 23,  36,  41,  44,  62), and RNA helicase A ( 30) via glycine/arginine-rich domains.	transcription
53698	2	335149	5	NULL	NULL	0	NULL	SMN			interacts with			glycine/arginine-rich domains		hnRNP U					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38645_s_210	11509571	We have found that SMN interacts with the GAR domain of fibrillarin (Figs.  4 and  5), and other studies indicate that SMN also interacts with hnRNP U ( 34), several Sm and Sm-like (Lsm) proteins ( 23,  36,  41,  44,  62), and RNA helicase A ( 30) via glycine/arginine-rich domains.	transcription
53699	3	335149	5	NULL	NULL	0	NULL	SMN			interacts with			glycine/arginine-rich domains		Sm proteins					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38645_s_210	11509571	We have found that SMN interacts with the GAR domain of fibrillarin (Figs.  4 and  5), and other studies indicate that SMN also interacts with hnRNP U ( 34), several Sm and Sm-like (Lsm) proteins ( 23,  36,  41,  44,  62), and RNA helicase A ( 30) via glycine/arginine-rich domains.	transcription
53700	4	335149	5	NULL	NULL	0	NULL	SMN			interacts with			glycine/arginine-rich domains		Sm-like proteins					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38645_s_210	11509571	We have found that SMN interacts with the GAR domain of fibrillarin (Figs.  4 and  5), and other studies indicate that SMN also interacts with hnRNP U ( 34), several Sm and Sm-like (Lsm) proteins ( 23,  36,  41,  44,  62), and RNA helicase A ( 30) via glycine/arginine-rich domains.	transcription
53701	5	335149	5	NULL	NULL	0	NULL	SMN			interacts with			glycine/arginine-rich domain		RNA helicase A					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_38645_s_210	11509571	We have found that SMN interacts with the GAR domain of fibrillarin (Figs.  4 and  5), and other studies indicate that SMN also interacts with hnRNP U ( 34), several Sm and Sm-like (Lsm) proteins ( 23,  36,  41,  44,  62), and RNA helicase A ( 30) via glycine/arginine-rich domains.	transcription
53702	6	335149	5	NULL	NULL	0	NULL	Lsm			is					Sm-like proteins					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_38645_s_210	11509571	We have found that SMN interacts with the GAR domain of fibrillarin (Figs.  4 and  5), and other studies indicate that SMN also interacts with hnRNP U ( 34), several Sm and Sm-like (Lsm) proteins ( 23,  36,  41,  44,  62), and RNA helicase A ( 30) via glycine/arginine-rich domains.	transcription
55152	1	335149	7	NULL	NULL	0	NULL	SMN			interacts with					fibrillarin			GAR domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_38645_s_210	11509571	We have found that SMN interacts with the GAR domain of fibrillarin (Figs.  4 and  5), and other studies indicate that SMN also interacts with hnRNP U ( 34), several Sm and Sm-like (Lsm) proteins ( 23,  36,  41,  44,  62), and RNA helicase A ( 30) via glycine/arginine-rich domains.	transcription
55153	2	335149	7	NULL	NULL	0	NULL	SMN			interacts with					 hnRNP U			glycine/arginine-rich domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_42_38645_s_210	11509571	We have found that SMN interacts with the GAR domain of fibrillarin (Figs.  4 and  5), and other studies indicate that SMN also interacts with hnRNP U ( 34), several Sm and Sm-like (Lsm) proteins ( 23,  36,  41,  44,  62), and RNA helicase A ( 30) via glycine/arginine-rich domains.	transcription
55169	3	335149	7	NULL	NULL	0	NULL	SMN			interacts with					SM protein			glycine/arginine-rich domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_38645_s_210	11509571	We have found that SMN interacts with the GAR domain of fibrillarin (Figs.  4 and  5), and other studies indicate that SMN also interacts with hnRNP U ( 34), several Sm and Sm-like (Lsm) proteins ( 23,  36,  41,  44,  62), and RNA helicase A ( 30) via glycine/arginine-rich domains.	transcription
55170	4	335149	7	NULL	NULL	0	NULL	SMN			interacts with					Lsm			glycine/arginine-rich domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_38645_s_210	11509571	We have found that SMN interacts with the GAR domain of fibrillarin (Figs.  4 and  5), and other studies indicate that SMN also interacts with hnRNP U ( 34), several Sm and Sm-like (Lsm) proteins ( 23,  36,  41,  44,  62), and RNA helicase A ( 30) via glycine/arginine-rich domains.	transcription
55171	5	335149	7	NULL	NULL	0	NULL	SMN			interacts with					RNA helicase A			glycine/arginine-rich domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_38645_s_210	11509571	We have found that SMN interacts with the GAR domain of fibrillarin (Figs.  4 and  5), and other studies indicate that SMN also interacts with hnRNP U ( 34), several Sm and Sm-like (Lsm) proteins ( 23,  36,  41,  44,  62), and RNA helicase A ( 30) via glycine/arginine-rich domains.	transcription
55172	6	335149	7	NULL	NULL	0	NULL	Lsm			is a type of					Sm-like protein					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_38645_s_210	11509571	We have found that SMN interacts with the GAR domain of fibrillarin (Figs.  4 and  5), and other studies indicate that SMN also interacts with hnRNP U ( 34), several Sm and Sm-like (Lsm) proteins ( 23,  36,  41,  44,  62), and RNA helicase A ( 30) via glycine/arginine-rich domains.	transcription
55173	1	335151	7	NULL	NULL	0	NULL	GCC			encode					glycine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_37_23130_s_46	9287315	The 3 -primer, 5 -gggcggccgcTCAGAAGAGGCC GCCGTCCTTCAGCGTTGTTCTTGATGATGACGT-3 , contains the  NotI site, a stop codon, and 14 amino acids in the C-terminal region of Gi2alpha, except for GCC (underlined), which encodes glycine instead of cysteine at position 352 from the N terminus.	transcription
55174	1	335152	7	NULL	NULL	0	NULL	GCC			encode					glycine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_37_23130_s_49	9287315	The 3 -primer, 5 -gggcggccgcTCAGTAAAGCCC GCCTTCCTTTAAGTTGTT-3 , contains the  NotI site, a stop codon, and nine amino acids in the C-terminal region of Gi3alpha, except for GCC (underlined), which encodes glycine instead of cysteine at position 351 from the N terminus.	transcription
53703	1	335153	5	NULL	NULL	0	NULL	scallop omega-crystallin			forms			Glycine 254;;valine 278;;valine 282		scallop omega-crystallin		altered	NAD pocket		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41064_s_204	10961997	Glycine 254, valine 278, and especially, valine 282 (marked by  arrows and   in Fig.  5) may form an altered NAD pocket in scallop omega-crystallin limiting the binding of NAD required for enzymatic activity (see below and Fig.  8).	transcription
53704	2	335153	5	NULL	NULL	0	NULL	NAD		binding of	is required for					scallop omega-crystallin		enzymatic activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41064_s_204	10961997	Glycine 254, valine 278, and especially, valine 282 (marked by  arrows and   in Fig.  5) may form an altered NAD pocket in scallop omega-crystallin limiting the binding of NAD required for enzymatic activity (see below and Fig.  8).	transcription
53705	3	335153	5	NULL	NULL	0	NULL	statement 1			limits					NAD		binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41064_s_204	10961997	Glycine 254, valine 278, and especially, valine 282 (marked by  arrows and   in Fig.  5) may form an altered NAD pocket in scallop omega-crystallin limiting the binding of NAD required for enzymatic activity (see below and Fig.  8).	transcription
55175	1	335153	7	NULL	NULL	0	NULL				form		may	Glycine 254, valine 278, valine 282		omega-crystallin		scallop	altered NAD pocket  		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41064_s_204	10961997	Glycine 254, valine 278, and especially, valine 282 (marked by  arrows and   in Fig.  5) may form an altered NAD pocket in scallop omega-crystallin limiting the binding of NAD required for enzymatic activity (see below and Fig.  8).	transcription
55176	2	335153	7	NULL	NULL	0	NULL	statement 1			limit					NAD		binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41064_s_204	10961997	Glycine 254, valine 278, and especially, valine 282 (marked by  arrows and   in Fig.  5) may form an altered NAD pocket in scallop omega-crystallin limiting the binding of NAD required for enzymatic activity (see below and Fig.  8).	transcription
55177	3	335153	7	NULL	NULL	0	NULL	statement 2			is required for					enzymatic activity					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41064_s_204	10961997	Glycine 254, valine 278, and especially, valine 282 (marked by  arrows and   in Fig.  5) may form an altered NAD pocket in scallop omega-crystallin limiting the binding of NAD required for enzymatic activity (see below and Fig.  8).	transcription
53706	1	335155	5	NULL	NULL	0	NULL	glycine			stimulates					pre-MG		activation of	D151G		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9695_s_248	9545304	4) Instead of inhibition of the activation, glycine actually stimulated the activation of pre-MG(D151G) (Fig.  5), which is very similar to the observation that methylamine inhibits trypsin hydrolysis of specific substrates and stimulates the enzyme activity toward nonspecific substrates ( 26).	transcription
53707	2	335155	5	NULL	NULL	0	NULL	methylamine			inhibits					substrates		hydrolysis of;;specific			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9695_s_248	9545304	4) Instead of inhibition of the activation, glycine actually stimulated the activation of pre-MG(D151G) (Fig.  5), which is very similar to the observation that methylamine inhibits trypsin hydrolysis of specific substrates and stimulates the enzyme activity toward nonspecific substrates ( 26).	transcription
53708	3	335155	5	NULL	NULL	0	NULL	statement 2			stimulates					substrates		enzyme activity toward;;nonspecific			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9695_s_248	9545304	4) Instead of inhibition of the activation, glycine actually stimulated the activation of pre-MG(D151G) (Fig.  5), which is very similar to the observation that methylamine inhibits trypsin hydrolysis of specific substrates and stimulates the enzyme activity toward nonspecific substrates ( 26).	transcription
55178	1	335155	7	NULL	NULL	0	NULL	glycine			stimulate					 pre-MG(D151G)		activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9695_s_248	9545304	4) Instead of inhibition of the activation, glycine actually stimulated the activation of pre-MG(D151G) (Fig.  5), which is very similar to the observation that methylamine inhibits trypsin hydrolysis of specific substrates and stimulates the enzyme activity toward nonspecific substrates ( 26).	transcription
55179	3	335155	7	NULL	NULL	0	NULL	methylamine 			inhibits					statement 2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_16_9695_s_248	9545304	4) Instead of inhibition of the activation, glycine actually stimulated the activation of pre-MG(D151G) (Fig.  5), which is very similar to the observation that methylamine inhibits trypsin hydrolysis of specific substrates and stimulates the enzyme activity toward nonspecific substrates ( 26).	transcription
55180	2	335155	7	NULL	NULL	0	NULL	trypsin			hydrolyse					substrates					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9695_s_248	9545304	4) Instead of inhibition of the activation, glycine actually stimulated the activation of pre-MG(D151G) (Fig.  5), which is very similar to the observation that methylamine inhibits trypsin hydrolysis of specific substrates and stimulates the enzyme activity toward nonspecific substrates ( 26).	transcription
55181	4	335155	7	NULL	NULL	0	NULL	statement 2			stimulate					enzyme activity					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9695_s_248	9545304	4) Instead of inhibition of the activation, glycine actually stimulated the activation of pre-MG(D151G) (Fig.  5), which is very similar to the observation that methylamine inhibits trypsin hydrolysis of specific substrates and stimulates the enzyme activity toward nonspecific substrates ( 26).	transcription
53709	1	335156	5	NULL	NULL	0	NULL	Li+			is substituted for					Na+					NULL	external medium	0	NULL	NULL	NULL	gw60_jneurosci_17_12_4580_s_145	9169519	This does not occur (1) in oocytes in which GLYT1b was not expressed; (2) when the GLYT1b is inhibited by substituting Li+ for Na+ in the external medium; (3) when glycine is replaced by D-serine in the external medium; (4) when GLYT1b is saturated by sarcosine; or (5) when membrane voltage changes alter the carrier function.	transcription
53710	2	335156	5	NULL	NULL	0	NULL	statement 1			inhibits					GLYT1b					NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_12_4580_s_145	9169519	This does not occur (1) in oocytes in which GLYT1b was not expressed; (2) when the GLYT1b is inhibited by substituting Li+ for Na+ in the external medium; (3) when glycine is replaced by D-serine in the external medium; (4) when GLYT1b is saturated by sarcosine; or (5) when membrane voltage changes alter the carrier function.	transcription
53711	3	335156	5	NULL	NULL	0	NULL	GLYT1b			is saturated by					sarcosine					NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_17_12_4580_s_145	9169519	This does not occur (1) in oocytes in which GLYT1b was not expressed; (2) when the GLYT1b is inhibited by substituting Li+ for Na+ in the external medium; (3) when glycine is replaced by D-serine in the external medium; (4) when GLYT1b is saturated by sarcosine; or (5) when membrane voltage changes alter the carrier function.	transcription
53712	4	335156	5	NULL	NULL	0	NULL	membrane voltage		changes in	alter					carrier		function of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_12_4580_s_145	9169519	This does not occur (1) in oocytes in which GLYT1b was not expressed; (2) when the GLYT1b is inhibited by substituting Li+ for Na+ in the external medium; (3) when glycine is replaced by D-serine in the external medium; (4) when GLYT1b is saturated by sarcosine; or (5) when membrane voltage changes alter the carrier function.	transcription
53800	1	335158	5	NULL	NULL	0	NULL	NMDA			activates					NMDARs					NULL	cerebrocortical neurons	0	NULL	NULL	NULL	gw60_jneurosci_21_20_7985_s_63	11588171	Activation of NMDARs in cerebrocortical neurons and transfected HEK 293 cells expressing heteromeric NMDARs was induced by adding 200 muM NMDA, 10 muM glycine, and 2.5 mM calcium in nominally Mg2+-free Hank's solution at 37 degrees C for 5 min.	transcription
53801	2	335158	5	NULL	NULL	0	NULL	NMDA			activates					NMDARs					NULL	transfected HEK 293 cells expressing heteromeric NMDARs 	0	NULL	NULL	NULL	gw60_jneurosci_21_20_7985_s_63	11588171	Activation of NMDARs in cerebrocortical neurons and transfected HEK 293 cells expressing heteromeric NMDARs was induced by adding 200 muM NMDA, 10 muM glycine, and 2.5 mM calcium in nominally Mg2+-free Hank's solution at 37 degrees C for 5 min.	transcription
53802	3	335158	5	NULL	NULL	0	NULL	glycine			activates					NMDARs					NULL	cerebrocortical neurons	0	NULL	NULL	NULL	gw60_jneurosci_21_20_7985_s_63	11588171	Activation of NMDARs in cerebrocortical neurons and transfected HEK 293 cells expressing heteromeric NMDARs was induced by adding 200 muM NMDA, 10 muM glycine, and 2.5 mM calcium in nominally Mg2+-free Hank's solution at 37 degrees C for 5 min.	transcription
53803	4	335158	5	NULL	NULL	0	NULL	glycine			activates					NMDARs					NULL	transfected HEK 293 cells expressing heteromeric NMDARs	0	NULL	NULL	NULL	gw60_jneurosci_21_20_7985_s_63	11588171	Activation of NMDARs in cerebrocortical neurons and transfected HEK 293 cells expressing heteromeric NMDARs was induced by adding 200 muM NMDA, 10 muM glycine, and 2.5 mM calcium in nominally Mg2+-free Hank's solution at 37 degrees C for 5 min.	transcription
53804	5	335158	5	NULL	NULL	0	NULL	calcium			activates					NMDARs					NULL	cerebrocortical neurons	0	NULL	NULL	NULL	gw60_jneurosci_21_20_7985_s_63	11588171	Activation of NMDARs in cerebrocortical neurons and transfected HEK 293 cells expressing heteromeric NMDARs was induced by adding 200 muM NMDA, 10 muM glycine, and 2.5 mM calcium in nominally Mg2+-free Hank's solution at 37 degrees C for 5 min.	transcription
53805	6	335158	5	NULL	NULL	0	NULL	calcium			activates					NMDARs					NULL	transfected HEK 293 cells expressing heteromeric NMDARs	0	NULL	NULL	NULL	gw60_jneurosci_21_20_7985_s_63	11588171	Activation of NMDARs in cerebrocortical neurons and transfected HEK 293 cells expressing heteromeric NMDARs was induced by adding 200 muM NMDA, 10 muM glycine, and 2.5 mM calcium in nominally Mg2+-free Hank's solution at 37 degrees C for 5 min.	transcription
56145	1	335158	7	NULL	NULL	0	NULL	HEK 293 cells 			express					heteromeric NMDARs					NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_20_7985_s_63	11588171	Activation of NMDARs in cerebrocortical neurons and transfected HEK 293 cells expressing heteromeric NMDARs was induced by adding 200 muM NMDA, 10 muM glycine, and 2.5 mM calcium in nominally Mg2+-free Hank's solution at 37 degrees C for 5 min.	transcription
53806	1	335159	5	NULL	NULL	0	NULL	group II metabotropic glutamate receptors			is coupled with					Gi					NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_4_1257_s_220	11160396	The enhancement because of forskolin treatment was inhibited by a 5 min pretreatment with (2S, 1'R, 2'R, 3'R)-2-2(2,3-dicarboxyclopropyl)glycine, an agonist of group II metabotropic glutamate receptors that is coupled with Gi and negatively regulates adenylate cyclase (data not shown).	transcription
53807	2	335159	5	NULL	NULL	0	NULL	(2S, 1'R, 2'R, 3'R)-2-2(2,3-dicarboxyclopropyl)glycine			is an agonist of					statement 1					NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_4_1257_s_220	11160396	The enhancement because of forskolin treatment was inhibited by a 5 min pretreatment with (2S, 1'R, 2'R, 3'R)-2-2(2,3-dicarboxyclopropyl)glycine, an agonist of group II metabotropic glutamate receptors that is coupled with Gi and negatively regulates adenylate cyclase (data not shown).	transcription
53808	3	335159	5	NULL	NULL	0	NULL	statement 1			regulates		negatively			adenylate cyclase					NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_4_1257_s_220	11160396	The enhancement because of forskolin treatment was inhibited by a 5 min pretreatment with (2S, 1'R, 2'R, 3'R)-2-2(2,3-dicarboxyclopropyl)glycine, an agonist of group II metabotropic glutamate receptors that is coupled with Gi and negatively regulates adenylate cyclase (data not shown).	transcription
55182	1	335159	7	NULL	NULL	0	NULL	glutamate receptors			coupled with					Gi					NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_4_1257_s_220	11160396	The enhancement because of forskolin treatment was inhibited by a 5 min pretreatment with (2S, 1'R, 2'R, 3'R)-2-2(2,3-dicarboxyclopropyl)glycine, an agonist of group II metabotropic glutamate receptors that is coupled with Gi and negatively regulates adenylate cyclase (data not shown).	transcription
55183	2	335159	7	NULL	NULL	0	NULL	glutamate receptors			is a type of					group II metabotropic receptor					NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_4_1257_s_220	11160396	The enhancement because of forskolin treatment was inhibited by a 5 min pretreatment with (2S, 1'R, 2'R, 3'R)-2-2(2,3-dicarboxyclopropyl)glycine, an agonist of group II metabotropic glutamate receptors that is coupled with Gi and negatively regulates adenylate cyclase (data not shown).	transcription
55184	3	335159	7	NULL	NULL	0	NULL	(2S, 1'R, 2'R, 3'R)-2-2(2,3-dicarboxyclopropyl)glycine			is an agonist of					statement 1					NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_4_1257_s_220	11160396	The enhancement because of forskolin treatment was inhibited by a 5 min pretreatment with (2S, 1'R, 2'R, 3'R)-2-2(2,3-dicarboxyclopropyl)glycine, an agonist of group II metabotropic glutamate receptors that is coupled with Gi and negatively regulates adenylate cyclase (data not shown).	transcription
55185	4	335159	7	NULL	NULL	0	NULL	statement 1			regulates		negatively			adenylate cyclase					NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_4_1257_s_220	11160396	The enhancement because of forskolin treatment was inhibited by a 5 min pretreatment with (2S, 1'R, 2'R, 3'R)-2-2(2,3-dicarboxyclopropyl)glycine, an agonist of group II metabotropic glutamate receptors that is coupled with Gi and negatively regulates adenylate cyclase (data not shown).	transcription
55186	1	335160	7	NULL	NULL	0	NULL	GABA			induce					[Ca2+]i 		increase of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_21_7905_s_191	11050110	However, on average, 24.5  plus-or-minus  6% ( n = 5) of the GABA-induced [Ca2+]i increase and 21.0  plus-or-minus  3.8% ( n = 4) of the glycine-induced [Ca2+]i transient persisted even during exposure to the drug for time periods of >1 hr (Fig.  8 A, B).	transcription
55187	2	335160	7	NULL	NULL	0	NULL	 glycine			induce					[Ca2+]i					NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_21_7905_s_191	11050110	However, on average, 24.5  plus-or-minus  6% ( n = 5) of the GABA-induced [Ca2+]i increase and 21.0  plus-or-minus  3.8% ( n = 4) of the glycine-induced [Ca2+]i transient persisted even during exposure to the drug for time periods of >1 hr (Fig.  8 A, B).	transcription
53856	1	335161	5	NULL	NULL	0	NULL	spermine		stimulation of	is independent of					glycine					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1026_s_22	10454474	The glycine-independent form of spermine stimulation may involve relief of proton inhibition, and both processes are influenced by the alternatively spliced insert encoded by exon 5 in the NR1 subunit (Zheng et al., 1994  ; Traynelis et al., 1995  ).	transcription
53866	2	335161	5	NULL	NULL	0	NULL	statement 1			involves		may			proton		relief of;;inhibition of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1026_s_22	10454474	The glycine-independent form of spermine stimulation may involve relief of proton inhibition, and both processes are influenced by the alternatively spliced insert encoded by exon 5 in the NR1 subunit (Zheng et al., 1994  ; Traynelis et al., 1995  ).	transcription
53867	3	335161	5	NULL	NULL	0	NULL	alternatively spliced insert			is encoded by					NR1 subunit				exon 5	NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1026_s_22	10454474	The glycine-independent form of spermine stimulation may involve relief of proton inhibition, and both processes are influenced by the alternatively spliced insert encoded by exon 5 in the NR1 subunit (Zheng et al., 1994  ; Traynelis et al., 1995  ).	transcription
53868	4	335161	5	NULL	NULL	0	NULL	statement 3			influences					statement 1					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1026_s_22	10454474	The glycine-independent form of spermine stimulation may involve relief of proton inhibition, and both processes are influenced by the alternatively spliced insert encoded by exon 5 in the NR1 subunit (Zheng et al., 1994  ; Traynelis et al., 1995  ).	transcription
53869	5	335161	5	NULL	NULL	0	NULL	statement 3			influences					statement 2					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1026_s_22	10454474	The glycine-independent form of spermine stimulation may involve relief of proton inhibition, and both processes are influenced by the alternatively spliced insert encoded by exon 5 in the NR1 subunit (Zheng et al., 1994  ; Traynelis et al., 1995  ).	transcription
55188	1	335161	7	NULL	NULL	0	NULL	spermine		stimulation of	is independent of					glycine					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1026_s_22	10454474	The glycine-independent form of spermine stimulation may involve relief of proton inhibition, and both processes are influenced by the alternatively spliced insert encoded by exon 5 in the NR1 subunit (Zheng et al., 1994  ; Traynelis et al., 1995  ).	transcription
55189	2	335161	7	NULL	NULL	0	NULL	statement 1			involve		may			proton 		relief of;; inhibition of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1026_s_22	10454474	The glycine-independent form of spermine stimulation may involve relief of proton inhibition, and both processes are influenced by the alternatively spliced insert encoded by exon 5 in the NR1 subunit (Zheng et al., 1994  ; Traynelis et al., 1995  ).	transcription
55190	3	335161	7	NULL	NULL	0	NULL				encode				exon 5				NR1 subunit	alternatively spliced insert	NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1026_s_22	10454474	The glycine-independent form of spermine stimulation may involve relief of proton inhibition, and both processes are influenced by the alternatively spliced insert encoded by exon 5 in the NR1 subunit (Zheng et al., 1994  ; Traynelis et al., 1995  ).	transcription
55191	4	335161	7	NULL	NULL	0	NULL	statement 3			influence					statement 1					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1026_s_22	10454474	The glycine-independent form of spermine stimulation may involve relief of proton inhibition, and both processes are influenced by the alternatively spliced insert encoded by exon 5 in the NR1 subunit (Zheng et al., 1994  ; Traynelis et al., 1995  ).	transcription
55192	5	335161	7	NULL	NULL	0	NULL	statement 3			influence					statement 2					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1026_s_22	10454474	The glycine-independent form of spermine stimulation may involve relief of proton inhibition, and both processes are influenced by the alternatively spliced insert encoded by exon 5 in the NR1 subunit (Zheng et al., 1994  ; Traynelis et al., 1995  ).	transcription
53870	1	335162	5	NULL	NULL	0	NULL	NMDA receptors		functional	gates					inward currents					NULL	Xenopus oocytes	NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_292_1_215_s_289	10604951	As previously reported (Hess et al., 1996  ), expression of human NR1a/NR2A or NR1a/NR2B subunits in  Xenopus oocytes resulted in functional NMDA receptors that gated inward currents of 50 to 500 nA on coperfusion of 100 muM NMDA and 1 muM glycine (Fig.  5) when oocytes were voltage-clamped at negative potentials.	transcription
53871	2	335162	5	NULL	NULL	0	NULL	NR1a/NR2A subunits		expression of	results in					NMDA receptors		functional			NULL	Xenopus oocytes	0	NULL	NULL	NULL	gw60_jpharmacolexpther_292_1_215_s_289	10604951	As previously reported (Hess et al., 1996  ), expression of human NR1a/NR2A or NR1a/NR2B subunits in  Xenopus oocytes resulted in functional NMDA receptors that gated inward currents of 50 to 500 nA on coperfusion of 100 muM NMDA and 1 muM glycine (Fig.  5) when oocytes were voltage-clamped at negative potentials.	transcription
53872	3	335162	5	NULL	NULL	0	NULL	NR1a/NR2B subunits		expression of	results in					NMDA receptors		functional			NULL	Xenopus oocytes	0	NULL	NULL	NULL	gw60_jpharmacolexpther_292_1_215_s_289	10604951	As previously reported (Hess et al., 1996  ), expression of human NR1a/NR2A or NR1a/NR2B subunits in  Xenopus oocytes resulted in functional NMDA receptors that gated inward currents of 50 to 500 nA on coperfusion of 100 muM NMDA and 1 muM glycine (Fig.  5) when oocytes were voltage-clamped at negative potentials.	transcription
55193	1	335162	7	NULL	NULL	0	NULL			human	expressed in			NR1a/NR2A subunit		oocytes		Xenopus			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_292_1_215_s_289	10604951	As previously reported (Hess et al., 1996  ), expression of human NR1a/NR2A or NR1a/NR2B subunits in  Xenopus oocytes resulted in functional NMDA receptors that gated inward currents of 50 to 500 nA on coperfusion of 100 muM NMDA and 1 muM glycine (Fig.  5) when oocytes were voltage-clamped at negative potentials.	transcription
55194	2	335162	7	NULL	NULL	0	NULL			human	expressed in			NR1a/NR2B subunit		oocytes		Xenopus			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_292_1_215_s_289	10604951	As previously reported (Hess et al., 1996  ), expression of human NR1a/NR2A or NR1a/NR2B subunits in  Xenopus oocytes resulted in functional NMDA receptors that gated inward currents of 50 to 500 nA on coperfusion of 100 muM NMDA and 1 muM glycine (Fig.  5) when oocytes were voltage-clamped at negative potentials.	transcription
55195	3	335162	7	NULL	NULL	0	NULL	statement 1			result in					NMDA receptors		functional			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_292_1_215_s_289	10604951	As previously reported (Hess et al., 1996  ), expression of human NR1a/NR2A or NR1a/NR2B subunits in  Xenopus oocytes resulted in functional NMDA receptors that gated inward currents of 50 to 500 nA on coperfusion of 100 muM NMDA and 1 muM glycine (Fig.  5) when oocytes were voltage-clamped at negative potentials.	transcription
55196	4	335162	7	NULL	NULL	0	NULL	statement 2			result in					NMDA receptor		functional			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_292_1_215_s_289	10604951	As previously reported (Hess et al., 1996  ), expression of human NR1a/NR2A or NR1a/NR2B subunits in  Xenopus oocytes resulted in functional NMDA receptors that gated inward currents of 50 to 500 nA on coperfusion of 100 muM NMDA and 1 muM glycine (Fig.  5) when oocytes were voltage-clamped at negative potentials.	transcription
53873	1	335163	5	NULL	NULL	0	NULL	BP		transport of	is induced by					epinephrine					NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_293_1_128_s_141	10734162	After perfusion of the lumen with Ringer's solution containing BP in the presence of these compounds, epinephrine was added to the perfusate at a concentration of 0.1 mM and perfusion was continued for an additional 30 min. Glycyl-L-alanine, glycyl-L-leucine, glycylsarcosine, and glycyl-glycyl-glycine reduced the extent of epinephrine-induced BP transport by 80 to 90% (Table  5).	transcription
53874	2	335163	5	NULL	NULL	0	NULL	Glycyl-L-alanine			reduces					statement 1					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_293_1_128_s_141	10734162	After perfusion of the lumen with Ringer's solution containing BP in the presence of these compounds, epinephrine was added to the perfusate at a concentration of 0.1 mM and perfusion was continued for an additional 30 min. Glycyl-L-alanine, glycyl-L-leucine, glycylsarcosine, and glycyl-glycyl-glycine reduced the extent of epinephrine-induced BP transport by 80 to 90% (Table  5).	transcription
53875	3	335163	5	NULL	NULL	0	NULL	glycyl-L-leucine			reduces					statement 1					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_293_1_128_s_141	10734162	After perfusion of the lumen with Ringer's solution containing BP in the presence of these compounds, epinephrine was added to the perfusate at a concentration of 0.1 mM and perfusion was continued for an additional 30 min. Glycyl-L-alanine, glycyl-L-leucine, glycylsarcosine, and glycyl-glycyl-glycine reduced the extent of epinephrine-induced BP transport by 80 to 90% (Table  5).	transcription
53876	4	335163	5	NULL	NULL	0	NULL	glycylsarcosine			reduces					statement 1					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_293_1_128_s_141	10734162	After perfusion of the lumen with Ringer's solution containing BP in the presence of these compounds, epinephrine was added to the perfusate at a concentration of 0.1 mM and perfusion was continued for an additional 30 min. Glycyl-L-alanine, glycyl-L-leucine, glycylsarcosine, and glycyl-glycyl-glycine reduced the extent of epinephrine-induced BP transport by 80 to 90% (Table  5).	transcription
53877	5	335163	5	NULL	NULL	0	NULL	glycyl-glycyl-glycine			reduces					statement 1					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_293_1_128_s_141	10734162	After perfusion of the lumen with Ringer's solution containing BP in the presence of these compounds, epinephrine was added to the perfusate at a concentration of 0.1 mM and perfusion was continued for an additional 30 min. Glycyl-L-alanine, glycyl-L-leucine, glycylsarcosine, and glycyl-glycyl-glycine reduced the extent of epinephrine-induced BP transport by 80 to 90% (Table  5).	transcription
55197	1	335163	7	NULL	NULL	0	NULL	epinephrine			induce					BP		transport of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_293_1_128_s_141	10734162	After perfusion of the lumen with Ringer's solution containing BP in the presence of these compounds, epinephrine was added to the perfusate at a concentration of 0.1 mM and perfusion was continued for an additional 30 min. Glycyl-L-alanine, glycyl-L-leucine, glycylsarcosine, and glycyl-glycyl-glycine reduced the extent of epinephrine-induced BP transport by 80 to 90% (Table  5).	transcription
55198	2	335163	7	NULL	NULL	0	NULL	Glycyl-L-alanine			reduce					statement 1					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_293_1_128_s_141	10734162	After perfusion of the lumen with Ringer's solution containing BP in the presence of these compounds, epinephrine was added to the perfusate at a concentration of 0.1 mM and perfusion was continued for an additional 30 min. Glycyl-L-alanine, glycyl-L-leucine, glycylsarcosine, and glycyl-glycyl-glycine reduced the extent of epinephrine-induced BP transport by 80 to 90% (Table  5).	transcription
55199	3	335163	7	NULL	NULL	0	NULL	glycyl-L-leucine			reduce					statement 1					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_293_1_128_s_141	10734162	After perfusion of the lumen with Ringer's solution containing BP in the presence of these compounds, epinephrine was added to the perfusate at a concentration of 0.1 mM and perfusion was continued for an additional 30 min. Glycyl-L-alanine, glycyl-L-leucine, glycylsarcosine, and glycyl-glycyl-glycine reduced the extent of epinephrine-induced BP transport by 80 to 90% (Table  5).	transcription
55200	4	335163	7	NULL	NULL	0	NULL	glycylsarcosine			reduce					statement 1					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_293_1_128_s_141	10734162	After perfusion of the lumen with Ringer's solution containing BP in the presence of these compounds, epinephrine was added to the perfusate at a concentration of 0.1 mM and perfusion was continued for an additional 30 min. Glycyl-L-alanine, glycyl-L-leucine, glycylsarcosine, and glycyl-glycyl-glycine reduced the extent of epinephrine-induced BP transport by 80 to 90% (Table  5).	transcription
55201	5	335163	7	NULL	NULL	0	NULL	glycyl-glycyl-glycine			reduce					statement 1					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_293_1_128_s_141	10734162	After perfusion of the lumen with Ringer's solution containing BP in the presence of these compounds, epinephrine was added to the perfusate at a concentration of 0.1 mM and perfusion was continued for an additional 30 min. Glycyl-L-alanine, glycyl-L-leucine, glycylsarcosine, and glycyl-glycyl-glycine reduced the extent of epinephrine-induced BP transport by 80 to 90% (Table  5).	transcription
55202	1	335164	7	NULL	NULL	0	NULL			Arabidopsis thaliana	encode				Atgrp7 	glycine-rich RNA-binding proteins					NULL		0	NULL	NULL	NULL	gw60_pnas_94_16_8515_s_27	9238008	Gene- and strand-specific antisense probes that distinguish between the  Arabidopsis thaliana genes  Atgrp7 ( 23), also designated  ccr2 ( 24), and  Atgrp8 ( 23), also designated ccr1 ( 24), both encoding glycine-rich RNA-binding proteins with 75% sequence identity ( 23,  24), were derived from the 5  untranslated regions.	transcription
55203	2	335164	7	NULL	NULL	0	NULL			Arabidopsis thaliana	encode				Atgrp8	glycine-rich RNA-binding proteins					NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_16_8515_s_27	9238008	Gene- and strand-specific antisense probes that distinguish between the  Arabidopsis thaliana genes  Atgrp7 ( 23), also designated  ccr2 ( 24), and  Atgrp8 ( 23), also designated ccr1 ( 24), both encoding glycine-rich RNA-binding proteins with 75% sequence identity ( 23,  24), were derived from the 5  untranslated regions.	transcription
55204	3	335164	7	NULL	NULL	0	NULL				is designated as				Atgrp7	ccr2					NULL		0	NULL	NULL	NULL	gw60_pnas_94_16_8515_s_27	9238008	Gene- and strand-specific antisense probes that distinguish between the  Arabidopsis thaliana genes  Atgrp7 ( 23), also designated  ccr2 ( 24), and  Atgrp8 ( 23), also designated ccr1 ( 24), both encoding glycine-rich RNA-binding proteins with 75% sequence identity ( 23,  24), were derived from the 5  untranslated regions.	transcription
55205	4	335164	7	NULL	NULL	0	NULL				is designated as				Atgrp8	ccr1					NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_16_8515_s_27	9238008	Gene- and strand-specific antisense probes that distinguish between the  Arabidopsis thaliana genes  Atgrp7 ( 23), also designated  ccr2 ( 24), and  Atgrp8 ( 23), also designated ccr1 ( 24), both encoding glycine-rich RNA-binding proteins with 75% sequence identity ( 23,  24), were derived from the 5  untranslated regions.	transcription
53878	1	335165	5	NULL	NULL	0	NULL	glycine betaine			is a type of					stabilizing cosolutes					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53879	2	335165	5	NULL	NULL	0	NULL	sucrose			is a type of					stabilizing cosolutes					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53880	3	335165	5	NULL	NULL	0	NULL	bicarbonate			is a type of					donor-side cofactors					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53881	4	335165	5	NULL	NULL	0	NULL	chloride			is a type of					donor-side cofactors					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53882	5	335165	5	NULL	NULL	0	NULL	calcium			is a type of					donor-side cofactors					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53884	6	335165	5	NULL	NULL	0	NULL	glycine betaine		presence of	diminishes					J-P phase		suppression of			NULL	PS II membranes	NULL	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53885	7	335165	5	NULL	NULL	0	NULL	statement 6			occurs before					heating					NULL	PS II membranes	NULL	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53886	8	335165	5	NULL	NULL	0	NULL	statement 6			prevents					dip appearance					NULL	PS II membranes	NULL	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53887	9	335165	5	NULL	NULL	0	NULL	sucrose		presence of	diminishes					J-P phase		suppression of			NULL	PS II membranes	0	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53888	10	335165	5	NULL	NULL	0	NULL	statement 9			occurs before					heating					NULL	PS II membranes	0	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53889	11	335165	5	NULL	NULL	0	NULL	statement 9			prevents					dip appearance					NULL	PS II membranes	NULL	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53890	12	335165	5	NULL	NULL	0	NULL	bicarbonate		addition of	diminishes					J-P phase		suppression of			NULL	PS II membranes	NULL	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53891	13	335165	5	NULL	NULL	0	NULL	statement 12			occurs before					heating					NULL	PS II membranes	NULL	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53892	14	335165	5	NULL	NULL	0	NULL	statement 12			prevents					dip appearance					NULL	PS II membranes	0	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53893	15	335165	5	NULL	NULL	0	NULL	chloride		addition of	diminishes					J-P phase		suppression of			NULL	PS II membranes	0	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53894	16	335165	5	NULL	NULL	0	NULL	statement 15			occurs before					heating					NULL	PS II membranes	0	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53895	17	335165	5	NULL	NULL	0	NULL	statement 17			prevents					dip appearance					NULL	PS II membranes	0	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53896	18	335165	5	NULL	NULL	0	NULL	calcium		addition of	diminishes					J-P phase		suppression of			NULL	PS II membranes	0	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53897	19	335165	5	NULL	NULL	0	NULL	statement 18			occurs before					heating					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53898	20	335165	5	NULL	NULL	0	NULL	statement 18			prevents					dip appearance					NULL	PS II membranes	0	NULL	NULL	NULL	abs-batch0530-0539_photosynth-res_65_1_16228469_s_6	16228469	Presence of stabilizing cosolutes (glycine  betaine, sucrose) or addition of donor-side cofactors (bicarbonate, chloride,  calcium) to PS II membranes before heating (47 degrees C, 5 min) diminishes  J-P phase suppression and prevents dip appearance, whereas the addition  after heating is without effect.	transcription
53899	1	335166	5	NULL	NULL	0	NULL	FIB		human	interacts with			N-terminal glycine- and arginine-rich domain (residues 1-77)		SF2A-p32					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_279_3_14583623_s_4	14583623	Here, we demonstrate that the human  FIB N-terminal glycine- and arginine-rich domain (residues 1-77) and its  spacer region 1 (78-132) interact with splicing factor 2-associated p32  (SF2A-p32) and that the FIB methyltransferase-like domain (133-321) interacts  with protein-arginine methyltransferase 5 (PRMT5, Janus kinase-binding  protein 1).	transcription
53900	2	335166	5	NULL	NULL	0	NULL	FIB		human	interacts with			spacer region 1 (78-132)		SF2A-p32					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_279_3_14583623_s_4	14583623	Here, we demonstrate that the human  FIB N-terminal glycine- and arginine-rich domain (residues 1-77) and its  spacer region 1 (78-132) interact with splicing factor 2-associated p32  (SF2A-p32) and that the FIB methyltransferase-like domain (133-321) interacts  with protein-arginine methyltransferase 5 (PRMT5, Janus kinase-binding  protein 1).	transcription
53901	3	335166	5	NULL	NULL	0	NULL	FIB		human	interacts with			methyltransferase-like domain (133-321)		PRMT5					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_279_3_14583623_s_4	14583623	Here, we demonstrate that the human  FIB N-terminal glycine- and arginine-rich domain (residues 1-77) and its  spacer region 1 (78-132) interact with splicing factor 2-associated p32  (SF2A-p32) and that the FIB methyltransferase-like domain (133-321) interacts  with protein-arginine methyltransferase 5 (PRMT5, Janus kinase-binding  protein 1).	transcription
53902	4	335166	5	NULL	NULL	0	NULL	SF2A-p32			is					splicing factor 2-associated p32					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_279_3_14583623_s_4	14583623	Here, we demonstrate that the human  FIB N-terminal glycine- and arginine-rich domain (residues 1-77) and its  spacer region 1 (78-132) interact with splicing factor 2-associated p32  (SF2A-p32) and that the FIB methyltransferase-like domain (133-321) interacts  with protein-arginine methyltransferase 5 (PRMT5, Janus kinase-binding  protein 1).	transcription
53903	5	335166	5	NULL	NULL	0	NULL	PRMT5			is					protein-arginine methyltransferase 5					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_279_3_14583623_s_4	14583623	Here, we demonstrate that the human  FIB N-terminal glycine- and arginine-rich domain (residues 1-77) and its  spacer region 1 (78-132) interact with splicing factor 2-associated p32  (SF2A-p32) and that the FIB methyltransferase-like domain (133-321) interacts  with protein-arginine methyltransferase 5 (PRMT5, Janus kinase-binding  protein 1).	transcription
53904	6	335166	5	NULL	NULL	0	NULL	PRMT5			is					Janus kinase-binding protein 1		synonym of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_279_3_14583623_s_4	14583623	Here, we demonstrate that the human  FIB N-terminal glycine- and arginine-rich domain (residues 1-77) and its  spacer region 1 (78-132) interact with splicing factor 2-associated p32  (SF2A-p32) and that the FIB methyltransferase-like domain (133-321) interacts  with protein-arginine methyltransferase 5 (PRMT5, Janus kinase-binding  protein 1).	transcription
55206	1	335166	7	NULL	NULL	0	NULL	FIB		human	interacts with			N-terminal glycine rich domain (residues 1-77)		SF2A-p32					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_279_3_14583623_s_4	14583623	Here, we demonstrate that the human  FIB N-terminal glycine- and arginine-rich domain (residues 1-77) and its  spacer region 1 (78-132) interact with splicing factor 2-associated p32  (SF2A-p32) and that the FIB methyltransferase-like domain (133-321) interacts  with protein-arginine methyltransferase 5 (PRMT5, Janus kinase-binding  protein 1).	transcription
55207	2	335166	7	NULL	NULL	0	NULL	FIB		human	interacts with			N-terminal arginine-rich domain (residues 1-77)		SF2A-p32					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_279_3_14583623_s_4	14583623	Here, we demonstrate that the human  FIB N-terminal glycine- and arginine-rich domain (residues 1-77) and its  spacer region 1 (78-132) interact with splicing factor 2-associated p32  (SF2A-p32) and that the FIB methyltransferase-like domain (133-321) interacts  with protein-arginine methyltransferase 5 (PRMT5, Janus kinase-binding  protein 1).	transcription
55208	3	335166	7	NULL	NULL	0	NULL	FIB		human	interacts with			spacer region 1 (78-132)		SF2A-p32					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_279_3_14583623_s_4	14583623	Here, we demonstrate that the human  FIB N-terminal glycine- and arginine-rich domain (residues 1-77) and its  spacer region 1 (78-132) interact with splicing factor 2-associated p32  (SF2A-p32) and that the FIB methyltransferase-like domain (133-321) interacts  with protein-arginine methyltransferase 5 (PRMT5, Janus kinase-binding  protein 1).	transcription
55209	4	335166	7	NULL	NULL	0	NULL	 FIB			interacts with			methyltransferase-like domain (133-321)		PRMT5					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_279_3_14583623_s_4	14583623	Here, we demonstrate that the human  FIB N-terminal glycine- and arginine-rich domain (residues 1-77) and its  spacer region 1 (78-132) interact with splicing factor 2-associated p32  (SF2A-p32) and that the FIB methyltransferase-like domain (133-321) interacts  with protein-arginine methyltransferase 5 (PRMT5, Janus kinase-binding  protein 1).	transcription
55210	5	335166	7	NULL	NULL	0	NULL	FIB			interacts with			methyltransferase-like domain (133-321)		Janus kinase-binding protein 1					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_279_3_14583623_s_4	14583623	Here, we demonstrate that the human  FIB N-terminal glycine- and arginine-rich domain (residues 1-77) and its  spacer region 1 (78-132) interact with splicing factor 2-associated p32  (SF2A-p32) and that the FIB methyltransferase-like domain (133-321) interacts  with protein-arginine methyltransferase 5 (PRMT5, Janus kinase-binding  protein 1).	transcription
55211	6	335166	7	NULL	NULL	0	NULL	SF2A-p32			is					splicing factor 2-associated p32					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_279_3_14583623_s_4	14583623	Here, we demonstrate that the human  FIB N-terminal glycine- and arginine-rich domain (residues 1-77) and its  spacer region 1 (78-132) interact with splicing factor 2-associated p32  (SF2A-p32) and that the FIB methyltransferase-like domain (133-321) interacts  with protein-arginine methyltransferase 5 (PRMT5, Janus kinase-binding  protein 1).	transcription
55212	7	335166	7	NULL	NULL	0	NULL	PRMT5			is					protein-arginine methyltransferase 5					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-biol-chem_279_3_14583623_s_4	14583623	Here, we demonstrate that the human  FIB N-terminal glycine- and arginine-rich domain (residues 1-77) and its  spacer region 1 (78-132) interact with splicing factor 2-associated p32  (SF2A-p32) and that the FIB methyltransferase-like domain (133-321) interacts  with protein-arginine methyltransferase 5 (PRMT5, Janus kinase-binding  protein 1).	transcription
53907	1	335167	5	NULL	NULL	0	NULL	GlyRs			is activated by					glycine					NULL		0	NULL	NULL	NULL	gw70_jneurophysiol_95_4_2366_s_160	16381810	In voltage-clamp recordings, we found that activation of GlyRs by bath application of glycine (300 muM; CsCl pipette solution) elicited a >50% depression of both EPSCs (68  plus-or-minus  15%  n = 5 pyramidal cells; 64  plus-or-minus  5%  n = 10 interneurons) and IPSCs (52  plus-or-minus  5%,  n = 5 pyramidal cells; 64  plus-or-minus  6%,  n = 7 interneurons) that quickly recovered after washout ( Fig. 4).	transcription
53908	2	335167	5	NULL	NULL	0	NULL	statement 1			elicits					EPSCs		depression of			NULL		0	NULL	NULL	NULL	gw70_jneurophysiol_95_4_2366_s_160	16381810	In voltage-clamp recordings, we found that activation of GlyRs by bath application of glycine (300 muM; CsCl pipette solution) elicited a >50% depression of both EPSCs (68  plus-or-minus  15%  n = 5 pyramidal cells; 64  plus-or-minus  5%  n = 10 interneurons) and IPSCs (52  plus-or-minus  5%,  n = 5 pyramidal cells; 64  plus-or-minus  6%,  n = 7 interneurons) that quickly recovered after washout ( Fig. 4).	transcription
53909	3	335167	5	NULL	NULL	0	NULL	statement 1			elicits					IPSCs		depression of			NULL		0	NULL	NULL	NULL	gw70_jneurophysiol_95_4_2366_s_160	16381810	In voltage-clamp recordings, we found that activation of GlyRs by bath application of glycine (300 muM; CsCl pipette solution) elicited a >50% depression of both EPSCs (68  plus-or-minus  15%  n = 5 pyramidal cells; 64  plus-or-minus  5%  n = 10 interneurons) and IPSCs (52  plus-or-minus  5%,  n = 5 pyramidal cells; 64  plus-or-minus  6%,  n = 7 interneurons) that quickly recovered after washout ( Fig. 4).	transcription
55213	1	335167	7	NULL	NULL	0	NULL	glycine			activates					GlyRs					NULL		0	NULL	NULL	NULL	gw70_jneurophysiol_95_4_2366_s_160	16381810	In voltage-clamp recordings, we found that activation of GlyRs by bath application of glycine (300 muM; CsCl pipette solution) elicited a >50% depression of both EPSCs (68  plus-or-minus  15%  n = 5 pyramidal cells; 64  plus-or-minus  5%  n = 10 interneurons) and IPSCs (52  plus-or-minus  5%,  n = 5 pyramidal cells; 64  plus-or-minus  6%,  n = 7 interneurons) that quickly recovered after washout ( Fig. 4).	transcription
55214	2	335167	7	NULL	NULL	0	NULL	statement 1			elicits					EPSCs		depression of			NULL		0	NULL	NULL	NULL	gw70_jneurophysiol_95_4_2366_s_160	16381810	In voltage-clamp recordings, we found that activation of GlyRs by bath application of glycine (300 muM; CsCl pipette solution) elicited a >50% depression of both EPSCs (68  plus-or-minus  15%  n = 5 pyramidal cells; 64  plus-or-minus  5%  n = 10 interneurons) and IPSCs (52  plus-or-minus  5%,  n = 5 pyramidal cells; 64  plus-or-minus  6%,  n = 7 interneurons) that quickly recovered after washout ( Fig. 4).	transcription
55215	3	335167	7	NULL	NULL	0	NULL	statement 1			elicits					IPSCs		depression of			NULL		0	NULL	NULL	NULL	gw70_jneurophysiol_95_4_2366_s_160	16381810	In voltage-clamp recordings, we found that activation of GlyRs by bath application of glycine (300 muM; CsCl pipette solution) elicited a >50% depression of both EPSCs (68  plus-or-minus  15%  n = 5 pyramidal cells; 64  plus-or-minus  5%  n = 10 interneurons) and IPSCs (52  plus-or-minus  5%,  n = 5 pyramidal cells; 64  plus-or-minus  6%,  n = 7 interneurons) that quickly recovered after washout ( Fig. 4).	transcription
53910	1	335174	5	NULL	NULL	0	NULL	DCS			is					D-cycloserine					NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_11_4011_s_127	10818136	C, D-cycloserine ( DCS), a partial agonist at the glycine site of the NMDA receptor enhanced at 1 mg/kg haloperidol (0.3 mg/kg)-mediated  c-fos induction (compare  H 0.3 with  DCS 1 H 0.3) but had no significant effect at 5 mg/kg (compare  H 0.3 with  DCS 5 H 0.3).	transcription
53911	2	335174	5	NULL	NULL	0	NULL	DCS			is an agonist of		partial			NMDA receptor			glycine site		NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_11_4011_s_127	10818136	C, D-cycloserine ( DCS), a partial agonist at the glycine site of the NMDA receptor enhanced at 1 mg/kg haloperidol (0.3 mg/kg)-mediated  c-fos induction (compare  H 0.3 with  DCS 1 H 0.3) but had no significant effect at 5 mg/kg (compare  H 0.3 with  DCS 5 H 0.3).	transcription
53912	3	335174	5	NULL	NULL	0	NULL	c-fos		induction of	is mediated by					haloperidol					NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_11_4011_s_127	10818136	C, D-cycloserine ( DCS), a partial agonist at the glycine site of the NMDA receptor enhanced at 1 mg/kg haloperidol (0.3 mg/kg)-mediated  c-fos induction (compare  H 0.3 with  DCS 1 H 0.3) but had no significant effect at 5 mg/kg (compare  H 0.3 with  DCS 5 H 0.3).	transcription
53913	4	335174	5	NULL	NULL	0	NULL	DCS			enhance					statement 3					NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_11_4011_s_127	10818136	C, D-cycloserine ( DCS), a partial agonist at the glycine site of the NMDA receptor enhanced at 1 mg/kg haloperidol (0.3 mg/kg)-mediated  c-fos induction (compare  H 0.3 with  DCS 1 H 0.3) but had no significant effect at 5 mg/kg (compare  H 0.3 with  DCS 5 H 0.3).	transcription
55216	1	335174	7	NULL	NULL	0	NULL	DCS			agonist of		partial			NMDA receptor			glycine site of		NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_11_4011_s_127	10818136	C, D-cycloserine ( DCS), a partial agonist at the glycine site of the NMDA receptor enhanced at 1 mg/kg haloperidol (0.3 mg/kg)-mediated  c-fos induction (compare  H 0.3 with  DCS 1 H 0.3) but had no significant effect at 5 mg/kg (compare  H 0.3 with  DCS 5 H 0.3).	transcription
55217	2	335174	7	NULL	NULL	0	NULL	haloperidol			mediates					c-fos		induction of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_11_4011_s_127	10818136	C, D-cycloserine ( DCS), a partial agonist at the glycine site of the NMDA receptor enhanced at 1 mg/kg haloperidol (0.3 mg/kg)-mediated  c-fos induction (compare  H 0.3 with  DCS 1 H 0.3) but had no significant effect at 5 mg/kg (compare  H 0.3 with  DCS 5 H 0.3).	transcription
55218	3	335174	7	NULL	NULL	0	NULL	statement 1			enhanced upon					statement 2					NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_11_4011_s_127	10818136	C, D-cycloserine ( DCS), a partial agonist at the glycine site of the NMDA receptor enhanced at 1 mg/kg haloperidol (0.3 mg/kg)-mediated  c-fos induction (compare  H 0.3 with  DCS 1 H 0.3) but had no significant effect at 5 mg/kg (compare  H 0.3 with  DCS 5 H 0.3).	transcription
55219	4	335174	7	NULL	NULL	0	NULL	DCS			is					D-cycloserine					NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_11_4011_s_127	10818136	C, D-cycloserine ( DCS), a partial agonist at the glycine site of the NMDA receptor enhanced at 1 mg/kg haloperidol (0.3 mg/kg)-mediated  c-fos induction (compare  H 0.3 with  DCS 1 H 0.3) but had no significant effect at 5 mg/kg (compare  H 0.3 with  DCS 5 H 0.3).	transcription
53916	1	335179	5	NULL	NULL	0	NULL	D,L-APV			block					NMDA receptors		potential activation of			NULL		0	NULL	NULL	NULL	gw70_jneurophysiol_95_4_2366_s_273	16381810	When D,L-APV (100 muM) was included in the bath solution to block potential activation of  NMDA receptors by increased local glycine concentrations during GlyT1 blockade with  NFPS, the percentage of trials that elicited suprathreshold EPSPs was still not significantly  decreased compared with control (without D-APV; 5  plus-or-minus  4%,  n = 4,  P > 0.05, data not shown).	transcription
53917	2	335179	5	NULL	NULL	0	NULL	NFPS			block					GlyT1					NULL		0	NULL	NULL	NULL	gw70_jneurophysiol_95_4_2366_s_273	16381810	When D,L-APV (100 muM) was included in the bath solution to block potential activation of  NMDA receptors by increased local glycine concentrations during GlyT1 blockade with  NFPS, the percentage of trials that elicited suprathreshold EPSPs was still not significantly  decreased compared with control (without D-APV; 5  plus-or-minus  4%,  n = 4,  P > 0.05, data not shown).	transcription
53918	3	335179	5	NULL	NULL	0	NULL	statement 2			results in					glycine		increase in;;concentration of;;local			NULL		0	NULL	NULL	NULL	gw70_jneurophysiol_95_4_2366_s_273	16381810	When D,L-APV (100 muM) was included in the bath solution to block potential activation of  NMDA receptors by increased local glycine concentrations during GlyT1 blockade with  NFPS, the percentage of trials that elicited suprathreshold EPSPs was still not significantly  decreased compared with control (without D-APV; 5  plus-or-minus  4%,  n = 4,  P > 0.05, data not shown).	transcription
53919	4	335179	5	NULL	NULL	0	NULL	statement 3			leads to					statement 1					NULL		0	NULL	NULL	NULL	gw70_jneurophysiol_95_4_2366_s_273	16381810	When D,L-APV (100 muM) was included in the bath solution to block potential activation of  NMDA receptors by increased local glycine concentrations during GlyT1 blockade with  NFPS, the percentage of trials that elicited suprathreshold EPSPs was still not significantly  decreased compared with control (without D-APV; 5  plus-or-minus  4%,  n = 4,  P > 0.05, data not shown).	transcription
55355	1	335179	7	NULL	NULL	0	NULL	D,L-APV			block					NMDA receptor		potential activation of			NULL		0	NULL	NULL	NULL	gw70_jneurophysiol_95_4_2366_s_273	16381810	When D,L-APV (100 muM) was included in the bath solution to block potential activation of  NMDA receptors by increased local glycine concentrations during GlyT1 blockade with  NFPS, the percentage of trials that elicited suprathreshold EPSPs was still not significantly  decreased compared with control (without D-APV; 5  plus-or-minus  4%,  n = 4,  P > 0.05, data not shown).	transcription
55363	2	335179	7	NULL	NULL	0	NULL	statement 1			occur by					glycine		increased concentration of			NULL		0	NULL	NULL	NULL	gw70_jneurophysiol_95_4_2366_s_273	16381810	When D,L-APV (100 muM) was included in the bath solution to block potential activation of  NMDA receptors by increased local glycine concentrations during GlyT1 blockade with  NFPS, the percentage of trials that elicited suprathreshold EPSPs was still not significantly  decreased compared with control (without D-APV; 5  plus-or-minus  4%,  n = 4,  P > 0.05, data not shown).	transcription
55365	3	335179	7	NULL	NULL	0	NULL	NFPS			blocks					GlyT1					NULL		0	NULL	NULL	NULL	gw70_jneurophysiol_95_4_2366_s_273	16381810	When D,L-APV (100 muM) was included in the bath solution to block potential activation of  NMDA receptors by increased local glycine concentrations during GlyT1 blockade with  NFPS, the percentage of trials that elicited suprathreshold EPSPs was still not significantly  decreased compared with control (without D-APV; 5  plus-or-minus  4%,  n = 4,  P > 0.05, data not shown).	transcription
55367	4	335179	7	NULL	NULL	0	NULL	statement 1			occur during					statement 3					NULL		0	NULL	NULL	NULL	gw70_jneurophysiol_95_4_2366_s_273	16381810	When D,L-APV (100 muM) was included in the bath solution to block potential activation of  NMDA receptors by increased local glycine concentrations during GlyT1 blockade with  NFPS, the percentage of trials that elicited suprathreshold EPSPs was still not significantly  decreased compared with control (without D-APV; 5  plus-or-minus  4%,  n = 4,  P > 0.05, data not shown).	transcription
53924	1	335180	5	NULL	NULL	0	NULL	glycine			effects					VZ cells					NULL		0	NULL	NULL	NULL	gw70_pnas_102_52_19174_s_195	16357207	Most important, the effect of glycine on VZ cells is blocked by TTX (9.0  plus-or-minus  1.4%;  P < 0.05;  n = 5; data not shown), indicating that GlyR activation is sufficient to trigger both the activation of PP cells that express Na+ channels and the propagation of the Ca2+ signal to other cells in a manner that is similar to that observed with direct activation of the Na+ channels with veratridine.	transcription
53925	2	335180	5	NULL	NULL	0	NULL	TTX			blocks					statement 1					NULL		0	NULL	NULL	NULL	gw70_pnas_102_52_19174_s_195	16357207	Most important, the effect of glycine on VZ cells is blocked by TTX (9.0  plus-or-minus  1.4%;  P < 0.05;  n = 5; data not shown), indicating that GlyR activation is sufficient to trigger both the activation of PP cells that express Na+ channels and the propagation of the Ca2+ signal to other cells in a manner that is similar to that observed with direct activation of the Na+ channels with veratridine.	transcription
53926	3	335180	5	NULL	NULL	0	NULL	PP cells			express					Na+ channels					NULL		0	NULL	NULL	NULL	gw70_pnas_102_52_19174_s_195	16357207	Most important, the effect of glycine on VZ cells is blocked by TTX (9.0  plus-or-minus  1.4%;  P < 0.05;  n = 5; data not shown), indicating that GlyR activation is sufficient to trigger both the activation of PP cells that express Na+ channels and the propagation of the Ca2+ signal to other cells in a manner that is similar to that observed with direct activation of the Na+ channels with veratridine.	transcription
53927	4	335180	5	NULL	NULL	0	NULL	GlyR		activation of	triggers					statement 3		activation of			NULL		0	NULL	NULL	NULL	gw70_pnas_102_52_19174_s_195	16357207	Most important, the effect of glycine on VZ cells is blocked by TTX (9.0  plus-or-minus  1.4%;  P < 0.05;  n = 5; data not shown), indicating that GlyR activation is sufficient to trigger both the activation of PP cells that express Na+ channels and the propagation of the Ca2+ signal to other cells in a manner that is similar to that observed with direct activation of the Na+ channels with veratridine.	transcription
53928	5	335180	5	NULL	NULL	0	NULL	Ca2+ signal			is propagated to					cells					NULL		0	NULL	NULL	NULL	gw70_pnas_102_52_19174_s_195	16357207	Most important, the effect of glycine on VZ cells is blocked by TTX (9.0  plus-or-minus  1.4%;  P < 0.05;  n = 5; data not shown), indicating that GlyR activation is sufficient to trigger both the activation of PP cells that express Na+ channels and the propagation of the Ca2+ signal to other cells in a manner that is similar to that observed with direct activation of the Na+ channels with veratridine.	transcription
53929	6	335180	5	NULL	NULL	0	NULL	GlyR		activation of	triggers					statement 6					NULL		0	NULL	NULL	NULL	gw70_pnas_102_52_19174_s_195	16357207	Most important, the effect of glycine on VZ cells is blocked by TTX (9.0  plus-or-minus  1.4%;  P < 0.05;  n = 5; data not shown), indicating that GlyR activation is sufficient to trigger both the activation of PP cells that express Na+ channels and the propagation of the Ca2+ signal to other cells in a manner that is similar to that observed with direct activation of the Na+ channels with veratridine.	transcription
53930	7	335180	5	NULL	NULL	0	NULL	veratridine			activates		directly			Na+ channels					NULL		0	NULL	NULL	NULL	gw70_pnas_102_52_19174_s_195	16357207	Most important, the effect of glycine on VZ cells is blocked by TTX (9.0  plus-or-minus  1.4%;  P < 0.05;  n = 5; data not shown), indicating that GlyR activation is sufficient to trigger both the activation of PP cells that express Na+ channels and the propagation of the Ca2+ signal to other cells in a manner that is similar to that observed with direct activation of the Na+ channels with veratridine.	transcription
55370	1	335180	7	NULL	NULL	0	NULL	TTX			blocks					glycine		effect of			NULL	VZ cells	0	NULL	NULL	NULL	gw70_pnas_102_52_19174_s_195	16357207	Most important, the effect of glycine on VZ cells is blocked by TTX (9.0  plus-or-minus  1.4%;  P < 0.05;  n = 5; data not shown), indicating that GlyR activation is sufficient to trigger both the activation of PP cells that express Na+ channels and the propagation of the Ca2+ signal to other cells in a manner that is similar to that observed with direct activation of the Na+ channels with veratridine.	transcription
55371	2	335180	7	NULL	NULL	0	NULL	PP cells			express					Na+ channels					NULL		0	NULL	NULL	NULL	gw70_pnas_102_52_19174_s_195	16357207	Most important, the effect of glycine on VZ cells is blocked by TTX (9.0  plus-or-minus  1.4%;  P < 0.05;  n = 5; data not shown), indicating that GlyR activation is sufficient to trigger both the activation of PP cells that express Na+ channels and the propagation of the Ca2+ signal to other cells in a manner that is similar to that observed with direct activation of the Na+ channels with veratridine.	transcription
55372	3	335180	7	NULL	NULL	0	NULL	GlyR		activation of	trigger					statement 2					NULL		0	NULL	NULL	NULL	gw70_pnas_102_52_19174_s_195	16357207	Most important, the effect of glycine on VZ cells is blocked by TTX (9.0  plus-or-minus  1.4%;  P < 0.05;  n = 5; data not shown), indicating that GlyR activation is sufficient to trigger both the activation of PP cells that express Na+ channels and the propagation of the Ca2+ signal to other cells in a manner that is similar to that observed with direct activation of the Na+ channels with veratridine.	transcription
55376	4	335180	7	NULL	NULL	0	NULL	GlyR		activation of	trigger					Ca2+ signal		propogation of			NULL		0	NULL	NULL	NULL	gw70_pnas_102_52_19174_s_195	16357207	Most important, the effect of glycine on VZ cells is blocked by TTX (9.0  plus-or-minus  1.4%;  P < 0.05;  n = 5; data not shown), indicating that GlyR activation is sufficient to trigger both the activation of PP cells that express Na+ channels and the propagation of the Ca2+ signal to other cells in a manner that is similar to that observed with direct activation of the Na+ channels with veratridine.	transcription
55382	5	335180	7	NULL	NULL	0	NULL	veratridine			activates		directly			Na+ channels					NULL		0	NULL	NULL	NULL	gw70_pnas_102_52_19174_s_195	16357207	Most important, the effect of glycine on VZ cells is blocked by TTX (9.0  plus-or-minus  1.4%;  P < 0.05;  n = 5; data not shown), indicating that GlyR activation is sufficient to trigger both the activation of PP cells that express Na+ channels and the propagation of the Ca2+ signal to other cells in a manner that is similar to that observed with direct activation of the Na+ channels with veratridine.	transcription
53937	1	335189	5	NULL	NULL	0	NULL	Propofol			induce					GABA currents		enhancement of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_20_17438_s_112	11877425	Mutation of TM1 Glycine on alpha1 and beta2 Subunit Diminishes Propofol-induced Enhancement of GABA Currents-- The modulating effect of propofol on currents induced by GABA at EC20 in the wild type and mutant receptors is summarized in Table  II, which shows the effect of the highest propofol concentration tested for each receptor combination without inducing direct activation: 50 muM for the alpha1beta2gamma2 and alpha1(G223F)beta2gamma2 and 5 muM for the alpha1beta2(G219F)gamma2 combinations.	transcription
53938	2	335189	5	NULL	NULL	0	NULL	TM1 Glycine			is mutated in								alpha1 subunit		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_20_17438_s_112	11877425	Mutation of TM1 Glycine on alpha1 and beta2 Subunit Diminishes Propofol-induced Enhancement of GABA Currents-- The modulating effect of propofol on currents induced by GABA at EC20 in the wild type and mutant receptors is summarized in Table  II, which shows the effect of the highest propofol concentration tested for each receptor combination without inducing direct activation: 50 muM for the alpha1beta2gamma2 and alpha1(G223F)beta2gamma2 and 5 muM for the alpha1beta2(G219F)gamma2 combinations.	transcription
53939	3	335189	5	NULL	NULL	0	NULL	TM1 Glycine			is mutated in								beta2 subunit		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_20_17438_s_112	11877425	Mutation of TM1 Glycine on alpha1 and beta2 Subunit Diminishes Propofol-induced Enhancement of GABA Currents-- The modulating effect of propofol on currents induced by GABA at EC20 in the wild type and mutant receptors is summarized in Table  II, which shows the effect of the highest propofol concentration tested for each receptor combination without inducing direct activation: 50 muM for the alpha1beta2gamma2 and alpha1(G223F)beta2gamma2 and 5 muM for the alpha1beta2(G219F)gamma2 combinations.	transcription
53940	4	335189	5	NULL	NULL	0	NULL	statement 2			diminishes					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_20_17438_s_112	11877425	Mutation of TM1 Glycine on alpha1 and beta2 Subunit Diminishes Propofol-induced Enhancement of GABA Currents-- The modulating effect of propofol on currents induced by GABA at EC20 in the wild type and mutant receptors is summarized in Table  II, which shows the effect of the highest propofol concentration tested for each receptor combination without inducing direct activation: 50 muM for the alpha1beta2gamma2 and alpha1(G223F)beta2gamma2 and 5 muM for the alpha1beta2(G219F)gamma2 combinations.	transcription
53941	5	335189	5	NULL	NULL	0	NULL	statement 3			diminishes					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_20_17438_s_112	11877425	Mutation of TM1 Glycine on alpha1 and beta2 Subunit Diminishes Propofol-induced Enhancement of GABA Currents-- The modulating effect of propofol on currents induced by GABA at EC20 in the wild type and mutant receptors is summarized in Table  II, which shows the effect of the highest propofol concentration tested for each receptor combination without inducing direct activation: 50 muM for the alpha1beta2gamma2 and alpha1(G223F)beta2gamma2 and 5 muM for the alpha1beta2(G219F)gamma2 combinations.	transcription
55390	1	335189	7	NULL	NULL	0	NULL	 Propofol			induce					GABA currents		enhancement of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_20_17438_s_112	11877425	Mutation of TM1 Glycine on alpha1 and beta2 Subunit Diminishes Propofol-induced Enhancement of GABA Currents-- The modulating effect of propofol on currents induced by GABA at EC20 in the wild type and mutant receptors is summarized in Table  II, which shows the effect of the highest propofol concentration tested for each receptor combination without inducing direct activation: 50 muM for the alpha1beta2gamma2 and alpha1(G223F)beta2gamma2 and 5 muM for the alpha1beta2(G219F)gamma2 combinations.	transcription
55483	2	335189	7	NULL	NULL	0	NULL	TM1		mutation of	diminishes			Glycine on alpha1 subunit		statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_20_17438_s_112	11877425	Mutation of TM1 Glycine on alpha1 and beta2 Subunit Diminishes Propofol-induced Enhancement of GABA Currents-- The modulating effect of propofol on currents induced by GABA at EC20 in the wild type and mutant receptors is summarized in Table  II, which shows the effect of the highest propofol concentration tested for each receptor combination without inducing direct activation: 50 muM for the alpha1beta2gamma2 and alpha1(G223F)beta2gamma2 and 5 muM for the alpha1beta2(G219F)gamma2 combinations.	transcription
55484	3	335189	7	NULL	NULL	0	NULL	TM1		mutation of	diminishes			Glycine beta2 subunit		statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_20_17438_s_112	11877425	Mutation of TM1 Glycine on alpha1 and beta2 Subunit Diminishes Propofol-induced Enhancement of GABA Currents-- The modulating effect of propofol on currents induced by GABA at EC20 in the wild type and mutant receptors is summarized in Table  II, which shows the effect of the highest propofol concentration tested for each receptor combination without inducing direct activation: 50 muM for the alpha1beta2gamma2 and alpha1(G223F)beta2gamma2 and 5 muM for the alpha1beta2(G219F)gamma2 combinations.	transcription
53942	1	335191	5	NULL	NULL	0	NULL	p53		MT	activates					MDR1				promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39359_s_114	11483599	We found that although other MT p53s activated the  MDR1 promoter (see Fig.  5), the p53 aspartate to glycine 281 MT (p53-281) was the most potent activator of  MDR1 and that transcriptional activation required an intact transactivation domain because p53-281 containing mutations at amino acids 14 and 19 was ineffective in up-regulating the  MDR1 promoter (Fig.  2 A).	transcription
53943	2	335191	5	NULL	NULL	0	NULL	p53-281		MT	is					p53 aspartate to glycine 281					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39359_s_114	11483599	We found that although other MT p53s activated the  MDR1 promoter (see Fig.  5), the p53 aspartate to glycine 281 MT (p53-281) was the most potent activator of  MDR1 and that transcriptional activation required an intact transactivation domain because p53-281 containing mutations at amino acids 14 and 19 was ineffective in up-regulating the  MDR1 promoter (Fig.  2 A).	transcription
53944	3	335191	5	NULL	NULL	0	NULL	p53-281		MT	activates		potent			MDR1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39359_s_114	11483599	We found that although other MT p53s activated the  MDR1 promoter (see Fig.  5), the p53 aspartate to glycine 281 MT (p53-281) was the most potent activator of  MDR1 and that transcriptional activation required an intact transactivation domain because p53-281 containing mutations at amino acids 14 and 19 was ineffective in up-regulating the  MDR1 promoter (Fig.  2 A).	transcription
53945	4	335191	5	NULL	NULL	0	NULL	p53-281			conatins							mutation of	amino acids 14 and 19		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39359_s_114	11483599	We found that although other MT p53s activated the  MDR1 promoter (see Fig.  5), the p53 aspartate to glycine 281 MT (p53-281) was the most potent activator of  MDR1 and that transcriptional activation required an intact transactivation domain because p53-281 containing mutations at amino acids 14 and 19 was ineffective in up-regulating the  MDR1 promoter (Fig.  2 A).	transcription
53946	5	335191	5	NULL	NULL	0	NULL	statement 1			does not upregulate					MDR1				promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39359_s_114	11483599	We found that although other MT p53s activated the  MDR1 promoter (see Fig.  5), the p53 aspartate to glycine 281 MT (p53-281) was the most potent activator of  MDR1 and that transcriptional activation required an intact transactivation domain because p53-281 containing mutations at amino acids 14 and 19 was ineffective in up-regulating the  MDR1 promoter (Fig.  2 A).	transcription
53947	6	335191	5	NULL	NULL	0	NULL	transcription		activation of	requires							intact	 transactivation domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39359_s_114	11483599	We found that although other MT p53s activated the  MDR1 promoter (see Fig.  5), the p53 aspartate to glycine 281 MT (p53-281) was the most potent activator of  MDR1 and that transcriptional activation required an intact transactivation domain because p53-281 containing mutations at amino acids 14 and 19 was ineffective in up-regulating the  MDR1 promoter (Fig.  2 A).	transcription
55485	1	335191	7	NULL	NULL	0	NULL	p53		MT	activate					MDR1				promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39359_s_114	11483599	We found that although other MT p53s activated the  MDR1 promoter (see Fig.  5), the p53 aspartate to glycine 281 MT (p53-281) was the most potent activator of  MDR1 and that transcriptional activation required an intact transactivation domain because p53-281 containing mutations at amino acids 14 and 19 was ineffective in up-regulating the  MDR1 promoter (Fig.  2 A).	transcription
55486	2	335191	7	NULL	NULL	0	NULL	p53		MT	activate		potently	aspartate to glycine 281		MDR1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39359_s_114	11483599	We found that although other MT p53s activated the  MDR1 promoter (see Fig.  5), the p53 aspartate to glycine 281 MT (p53-281) was the most potent activator of  MDR1 and that transcriptional activation required an intact transactivation domain because p53-281 containing mutations at amino acids 14 and 19 was ineffective in up-regulating the  MDR1 promoter (Fig.  2 A).	transcription
55487	3	335191	7	NULL	NULL	0	NULL	p53-281			is					p53		MT	aspartate to glycine 281		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39359_s_114	11483599	We found that although other MT p53s activated the  MDR1 promoter (see Fig.  5), the p53 aspartate to glycine 281 MT (p53-281) was the most potent activator of  MDR1 and that transcriptional activation required an intact transactivation domain because p53-281 containing mutations at amino acids 14 and 19 was ineffective in up-regulating the  MDR1 promoter (Fig.  2 A).	transcription
55488	4	335191	7	NULL	NULL	0	NULL	statement 2			require							intact	transactivation domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39359_s_114	11483599	We found that although other MT p53s activated the  MDR1 promoter (see Fig.  5), the p53 aspartate to glycine 281 MT (p53-281) was the most potent activator of  MDR1 and that transcriptional activation required an intact transactivation domain because p53-281 containing mutations at amino acids 14 and 19 was ineffective in up-regulating the  MDR1 promoter (Fig.  2 A).	transcription
55489	5	335191	7	NULL	NULL	0	NULL	p53-281 		MT	does not upregulate			mutations at amino acids 14 and 19		MDR1				promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39359_s_114	11483599	We found that although other MT p53s activated the  MDR1 promoter (see Fig.  5), the p53 aspartate to glycine 281 MT (p53-281) was the most potent activator of  MDR1 and that transcriptional activation required an intact transactivation domain because p53-281 containing mutations at amino acids 14 and 19 was ineffective in up-regulating the  MDR1 promoter (Fig.  2 A).	transcription
53948	1	335196	5	NULL	NULL	0	NULL	dGK/dAK			is associated with			glycine- and arginine-rich motifs		nucleotide-binding proteins			ATP-binding site		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_12_6602_s_21	7896799	Scanning for homology with structural  elements shown to be related to function in other kinases reveals that  dGK/dAK contains the glycine- and arginine-rich motifs associated with  the ATP- or GTP-binding sites of many nucleotide-binding proteins ( 9,  10) and which are also highly conserved in the  adenylate kinases ( 11) and herpesviral thymidine kinases (HSV  sites 1 and 5)( 12,  13) .	transcription
53949	2	335196	5	NULL	NULL	0	NULL	dGK/dAK			is associated with			glycine- and arginine-rich motifs		nucleotide-binding proteins			GTP-binding sites		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_12_6602_s_21	7896799	Scanning for homology with structural  elements shown to be related to function in other kinases reveals that  dGK/dAK contains the glycine- and arginine-rich motifs associated with  the ATP- or GTP-binding sites of many nucleotide-binding proteins ( 9,  10) and which are also highly conserved in the  adenylate kinases ( 11) and herpesviral thymidine kinases (HSV  sites 1 and 5)( 12,  13) .	transcription
53950	3	335196	5	NULL	NULL	0	NULL	dGK/dAK			is conserved in		highly	glycine- and arginine-rich motifs		adenylate kinases					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_12_6602_s_21	7896799	Scanning for homology with structural  elements shown to be related to function in other kinases reveals that  dGK/dAK contains the glycine- and arginine-rich motifs associated with  the ATP- or GTP-binding sites of many nucleotide-binding proteins ( 9,  10) and which are also highly conserved in the  adenylate kinases ( 11) and herpesviral thymidine kinases (HSV  sites 1 and 5)( 12,  13) .	transcription
53951	4	335196	5	NULL	NULL	0	NULL	dGK/dAK			is conserved in			glycine- and arginine-rich motifs		herpesviral thymidine kinases					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_12_6602_s_21	7896799	Scanning for homology with structural  elements shown to be related to function in other kinases reveals that  dGK/dAK contains the glycine- and arginine-rich motifs associated with  the ATP- or GTP-binding sites of many nucleotide-binding proteins ( 9,  10) and which are also highly conserved in the  adenylate kinases ( 11) and herpesviral thymidine kinases (HSV  sites 1 and 5)( 12,  13) .	transcription
55490	1	335196	7	NULL	NULL	0	NULL	dGK			contains								glycine rich motifs		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_12_6602_s_21	7896799	Scanning for homology with structural  elements shown to be related to function in other kinases reveals that  dGK/dAK contains the glycine- and arginine-rich motifs associated with  the ATP- or GTP-binding sites of many nucleotide-binding proteins ( 9,  10) and which are also highly conserved in the  adenylate kinases ( 11) and herpesviral thymidine kinases (HSV  sites 1 and 5)( 12,  13) .	transcription
55491	2	335196	7	NULL	NULL	0	NULL	dAK			contains								arginine-rich motifs		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_12_6602_s_21	7896799	Scanning for homology with structural  elements shown to be related to function in other kinases reveals that  dGK/dAK contains the glycine- and arginine-rich motifs associated with  the ATP- or GTP-binding sites of many nucleotide-binding proteins ( 9,  10) and which are also highly conserved in the  adenylate kinases ( 11) and herpesviral thymidine kinases (HSV  sites 1 and 5)( 12,  13) .	transcription
55492	3	335196	7	NULL	NULL	0	NULL	statement 1			associated with					nucleotide-binding proteins			ATP-binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_12_6602_s_21	7896799	Scanning for homology with structural  elements shown to be related to function in other kinases reveals that  dGK/dAK contains the glycine- and arginine-rich motifs associated with  the ATP- or GTP-binding sites of many nucleotide-binding proteins ( 9,  10) and which are also highly conserved in the  adenylate kinases ( 11) and herpesviral thymidine kinases (HSV  sites 1 and 5)( 12,  13) .	transcription
55493	4	335196	7	NULL	NULL	0	NULL	statement 1			associated with					nucleotide-binding proteins			GTP-binding sites		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_12_6602_s_21	7896799	Scanning for homology with structural  elements shown to be related to function in other kinases reveals that  dGK/dAK contains the glycine- and arginine-rich motifs associated with  the ATP- or GTP-binding sites of many nucleotide-binding proteins ( 9,  10) and which are also highly conserved in the  adenylate kinases ( 11) and herpesviral thymidine kinases (HSV  sites 1 and 5)( 12,  13) .	transcription
55494	5	335196	7	NULL	NULL	0	NULL	statement 2			associated with					nucleotide-binding proteins			ATP-binding site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_12_6602_s_21	7896799	Scanning for homology with structural  elements shown to be related to function in other kinases reveals that  dGK/dAK contains the glycine- and arginine-rich motifs associated with  the ATP- or GTP-binding sites of many nucleotide-binding proteins ( 9,  10) and which are also highly conserved in the  adenylate kinases ( 11) and herpesviral thymidine kinases (HSV  sites 1 and 5)( 12,  13) .	transcription
55495	6	335196	7	NULL	NULL	0	NULL	statement 2			associated with					nucleotide-binding proteins			GTP-binding sites		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_12_6602_s_21	7896799	Scanning for homology with structural  elements shown to be related to function in other kinases reveals that  dGK/dAK contains the glycine- and arginine-rich motifs associated with  the ATP- or GTP-binding sites of many nucleotide-binding proteins ( 9,  10) and which are also highly conserved in the  adenylate kinases ( 11) and herpesviral thymidine kinases (HSV  sites 1 and 5)( 12,  13) .	transcription
55496	7	335196	7	NULL	NULL	0	NULL				is highly conserved in			glycine-rich motifs		adenylate kinases					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_12_6602_s_21	7896799	Scanning for homology with structural  elements shown to be related to function in other kinases reveals that  dGK/dAK contains the glycine- and arginine-rich motifs associated with  the ATP- or GTP-binding sites of many nucleotide-binding proteins ( 9,  10) and which are also highly conserved in the  adenylate kinases ( 11) and herpesviral thymidine kinases (HSV  sites 1 and 5)( 12,  13) .	transcription
55497	8	335196	7	NULL	NULL	0	NULL				is highly conserved in			arginine-rich motifs		adenylate kinases					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_12_6602_s_21	7896799	Scanning for homology with structural  elements shown to be related to function in other kinases reveals that  dGK/dAK contains the glycine- and arginine-rich motifs associated with  the ATP- or GTP-binding sites of many nucleotide-binding proteins ( 9,  10) and which are also highly conserved in the  adenylate kinases ( 11) and herpesviral thymidine kinases (HSV  sites 1 and 5)( 12,  13) .	transcription
55498	9	335196	7	NULL	NULL	0	NULL				is highly conserved in			glycine-rich motifs		thymidine kinases		herpesviral 	HSV sites 1		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_12_6602_s_21	7896799	Scanning for homology with structural  elements shown to be related to function in other kinases reveals that  dGK/dAK contains the glycine- and arginine-rich motifs associated with  the ATP- or GTP-binding sites of many nucleotide-binding proteins ( 9,  10) and which are also highly conserved in the  adenylate kinases ( 11) and herpesviral thymidine kinases (HSV  sites 1 and 5)( 12,  13) .	transcription
55499	10	335196	7	NULL	NULL	0	NULL				is highly conserved in			glycine-rich motifs		 thymidine kinases		herpesviral	HSV sites 5		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_12_6602_s_21	7896799	Scanning for homology with structural  elements shown to be related to function in other kinases reveals that  dGK/dAK contains the glycine- and arginine-rich motifs associated with  the ATP- or GTP-binding sites of many nucleotide-binding proteins ( 9,  10) and which are also highly conserved in the  adenylate kinases ( 11) and herpesviral thymidine kinases (HSV  sites 1 and 5)( 12,  13) .	transcription
55500	11	335196	7	NULL	NULL	0	NULL				is highly conserved in			arginine-rich motifs		 thymidine kinases		herpesviral	HSV sites 1		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_12_6602_s_21	7896799	Scanning for homology with structural  elements shown to be related to function in other kinases reveals that  dGK/dAK contains the glycine- and arginine-rich motifs associated with  the ATP- or GTP-binding sites of many nucleotide-binding proteins ( 9,  10) and which are also highly conserved in the  adenylate kinases ( 11) and herpesviral thymidine kinases (HSV  sites 1 and 5)( 12,  13) .	transcription
55501	12	335196	7	NULL	NULL	0	NULL				is highly conserved in			arginine-rich motifs		thymidine kinases		herpesviral	HSV sites 5		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_12_6602_s_21	7896799	Scanning for homology with structural  elements shown to be related to function in other kinases reveals that  dGK/dAK contains the glycine- and arginine-rich motifs associated with  the ATP- or GTP-binding sites of many nucleotide-binding proteins ( 9,  10) and which are also highly conserved in the  adenylate kinases ( 11) and herpesviral thymidine kinases (HSV  sites 1 and 5)( 12,  13) .	transcription
53952	1	335199	5	NULL	NULL	0	NULL	mecamylamine stereoisomers			inhibits		transiently			NMDA receptor		response of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_297_2_646_s_145	11303054	As shown in Fig.  5, whereas both mecamylamine stereoisomers applied at a concentration of 100 muM could produce a transient inhibition of NMDA receptor responses to the coapplication of 10 muM glutamate + 10 muM glycine ( p < 0.001), this effect was reversible after a 5-min wash. NMDA receptor responses obtained in the presence of mecamylamine were also analyzed in terms of net charge.	transcription
55502	1	335199	7	NULL	NULL	0	NULL	mecamylamine stereoisomers			inhibits		transiently			NMDA receptor					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_297_2_646_s_145	11303054	As shown in Fig.  5, whereas both mecamylamine stereoisomers applied at a concentration of 100 muM could produce a transient inhibition of NMDA receptor responses to the coapplication of 10 muM glutamate + 10 muM glycine ( p < 0.001), this effect was reversible after a 5-min wash. NMDA receptor responses obtained in the presence of mecamylamine were also analyzed in terms of net charge.	transcription
53953	1	335201	5	NULL	NULL	0	NULL	class II enzymes			cleaves		homolytically			adenosylcobalamin					NULL		0	NULL	NULL	NULL	gw60_structure_2_9_793_s_91	7812713	Class I enzymes (subunit composition   2  2) carry the stable tyrosyl radical on a component different from the substrate binding component  [11  , class II enzymes (subunit composition usually   ) can cleave adenosylcobalamin homolytically to produce a transient 5 -deoxyadenosyl radical   [18,3]  , and class III enzymes (subunit composition   2) carry a stable glycine radical  [4  .	transcription
53954	2	335201	5	NULL	NULL	0	NULL	statement 1			produce					5 -deoxyadenosyl radical		transient			NULL		0	NULL	NULL	NULL	gw60_structure_2_9_793_s_91	7812713	Class I enzymes (subunit composition   2  2) carry the stable tyrosyl radical on a component different from the substrate binding component  [11  , class II enzymes (subunit composition usually   ) can cleave adenosylcobalamin homolytically to produce a transient 5 -deoxyadenosyl radical   [18,3]  , and class III enzymes (subunit composition   2) carry a stable glycine radical  [4  .	transcription
55503	1	335201	7	NULL	NULL	0	NULL	Class I enzymes			carry							stable	tyrosyl radical 		NULL		0	NULL	NULL	NULL	gw60_structure_2_9_793_s_91	7812713	Class I enzymes (subunit composition   2  2) carry the stable tyrosyl radical on a component different from the substrate binding component  [11  , class II enzymes (subunit composition usually   ) can cleave adenosylcobalamin homolytically to produce a transient 5 -deoxyadenosyl radical   [18,3]  , and class III enzymes (subunit composition   2) carry a stable glycine radical  [4  .	transcription
55504	2	335201	7	NULL	NULL	0	NULL	class II enzymes			cleave		could;;homolytically			adenosylcobalamin					NULL		0	NULL	NULL	NULL	gw60_structure_2_9_793_s_91	7812713	Class I enzymes (subunit composition   2  2) carry the stable tyrosyl radical on a component different from the substrate binding component  [11  , class II enzymes (subunit composition usually   ) can cleave adenosylcobalamin homolytically to produce a transient 5 -deoxyadenosyl radical   [18,3]  , and class III enzymes (subunit composition   2) carry a stable glycine radical  [4  .	transcription
55505	3	335201	7	NULL	NULL	0	NULL	statement 2			produce		transiently			5 -deoxyadenosyl radical					NULL		0	NULL	NULL	NULL	gw60_structure_2_9_793_s_91	7812713	Class I enzymes (subunit composition   2  2) carry the stable tyrosyl radical on a component different from the substrate binding component  [11  , class II enzymes (subunit composition usually   ) can cleave adenosylcobalamin homolytically to produce a transient 5 -deoxyadenosyl radical   [18,3]  , and class III enzymes (subunit composition   2) carry a stable glycine radical  [4  .	transcription
55506	4	335201	7	NULL	NULL	0	NULL	class III enzymes			carry					glycine radical		stable			NULL		0	NULL	NULL	NULL	gw60_structure_2_9_793_s_91	7812713	Class I enzymes (subunit composition   2  2) carry the stable tyrosyl radical on a component different from the substrate binding component  [11  , class II enzymes (subunit composition usually   ) can cleave adenosylcobalamin homolytically to produce a transient 5 -deoxyadenosyl radical   [18,3]  , and class III enzymes (subunit composition   2) carry a stable glycine radical  [4  .	transcription
55507	5	335201	7	NULL	NULL	0	NULL	statement 1			is not present in								substrate binding component		NULL		0	NULL	NULL	NULL	gw60_structure_2_9_793_s_91	7812713	Class I enzymes (subunit composition   2  2) carry the stable tyrosyl radical on a component different from the substrate binding component  [11  , class II enzymes (subunit composition usually   ) can cleave adenosylcobalamin homolytically to produce a transient 5 -deoxyadenosyl radical   [18,3]  , and class III enzymes (subunit composition   2) carry a stable glycine radical  [4  .	transcription
53955	1	335202	5	NULL	NULL	0	NULL	IGF-1		stimulation of	maintains					C/EBP		low nuclear levels of			NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
53956	2	335202	5	NULL	NULL	0	NULL	C/EBP		nuclear levels of	increase upon					growth factor support		removal of			NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
53957	3	335202	5	NULL	NULL	0	NULL	L channel		inhibition of;;activity of	increases					C/EBP		nuclear levels of			NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
53958	4	335202	5	NULL	NULL	0	NULL	CaMK		inhibition of;;activity of	increases					C/EBP		nuclear levels of			NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
53959	5	335202	5	NULL	NULL	0	NULL	NMDA receptor		activity of	increases					C/EBP		nuclear levels of			NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
53960	6	335202	5	NULL	NULL	0	NULL	statement 5			is dependent on					calcineurin					NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
53961	7	335202	5	NULL	NULL	0	NULL	NMDA receptors			is blocked by					APV					NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
53962	8	335202	5	NULL	NULL	0	NULL	statement 7			reduces					C/EBP		nuclear levels of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
53963	9	335202	5	NULL	NULL	0	NULL	NMDA			stimulates					NMDA receptors					NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
53964	10	335202	5	NULL	NULL	0	NULL	glycine			stimulates					NMDA receptors					NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
53965	11	335202	5	NULL	NULL	0	NULL	statement 9			occurs along with					statement 10					NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
53966	12	335202	5	NULL	NULL	0	NULL	statement 11			increases					C/EBP		nuclear levels of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
53967	13	335202	5	NULL	NULL	0	NULL	deltamethrin			declines					C/EBP		nuclear levels of			NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
55514	1	335202	7	NULL	NULL	0	NULL	IGF-1 		stimulation of	maintains					C/EBP		 low nuclear levels of 			NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
55521	2	335202	7	NULL	NULL	0	NULL	L channel 		inhibition of	increase					C/EBP		nuclear levels of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
55522	3	335202	7	NULL	NULL	0	NULL	CaMK		inhibition of;;activities of	increase					C/EBP		nuclear levels of			NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
55523	4	335202	7	NULL	NULL	0	NULL	 APV 			blocks					NMDA receptor					NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
55524	5	335202	7	NULL	NULL	0	NULL	statement 4			reduce					C/EBP		nuclear			NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
55626	6	335202	7	NULL	NULL	0	NULL	NMDA receptor		activity of	increase					C/EBP		nuclear levels of			NULL		NULL	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
55627	7	335202	7	NULL	NULL	0	NULL	statement 6			depends on					calcineurin					NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
55628	8	335202	7	NULL	NULL	0	NULL	NMDA		stimulation with	increases in					C/EBP		nuclear levels of			NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
55629	9	335202	7	NULL	NULL	0	NULL	glycine			increases more than					C/EBP		nuclear levels of			NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
55630	10	335202	7	NULL	NULL	0	NULL	statement 8			occur along with					statement 9					NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
55631	11	335202	7	NULL	NULL	0	NULL	deltamethrin			decrease					C/EBP		nuclear levels of			NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
55632	12	335202	7	NULL	NULL	0	NULL	statement 8			occur along with					statement 11					NULL		0	NULL	NULL	NULL	gw60_neuron_39_4_625_s_194	12925277	(a1) IGF-1 stimulation maintains low nuclear levels of C/EBP  (lane 2), but levels increase when growth factor support is removed (lane 1) or when L channel or CaMK activities are inhibited (lanes 3 and 4); nimodipine, 5  M; KN62, 10  M. Conversely, NMDA receptor activity increases the levels in a calcineurin-dependent manner: blocking NMDA receptors with 100  M APV reduces nuclear C/EBP  (lane 5), stimulation with 300  M NMDA + 1  M glycine increases it (lane 6), but when 1  M deltamethrin is coapplied, nuclear levels decline (lane 7).	transcription
53968	1	335205	5	NULL	NULL	0	NULL	APV			inhibit		selectively			NMDA		responses to			NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_93_1_8_s_129	11532333	By comparison, responses to 100  M NMDA plus 10  M glycine, which were inhibited selectively by 100  M APV, were of similar amplitude in oocytes injected with cerebellar mRNA from +/+ and wv/wv mice at P5-6 (+/+ 10 plus-or-minus 5 nA,  n=8 and wv/wv 12 plus-or-minus 5 nA,  n=8), P10 (+/+ 35 plus-or-minus 5 nA,  n=8 and wv/wv 31 plus-or-minus 4 nA,  n=8) or P23 (+/+ 70 plus-or-minus 3 nA,  n=8 and wv/wv 60 plus-or-minus 5 nA,  n=8; second and fourth set of traces in  Fig. 4).	transcription
53969	2	335205	5	NULL	NULL	0	NULL	APV			inhibit		selectively			glycine		responses to			NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_93_1_8_s_129	11532333	By comparison, responses to 100  M NMDA plus 10  M glycine, which were inhibited selectively by 100  M APV, were of similar amplitude in oocytes injected with cerebellar mRNA from +/+ and wv/wv mice at P5-6 (+/+ 10 plus-or-minus 5 nA,  n=8 and wv/wv 12 plus-or-minus 5 nA,  n=8), P10 (+/+ 35 plus-or-minus 5 nA,  n=8 and wv/wv 31 plus-or-minus 4 nA,  n=8) or P23 (+/+ 70 plus-or-minus 3 nA,  n=8 and wv/wv 60 plus-or-minus 5 nA,  n=8; second and fourth set of traces in  Fig. 4).	transcription
53970	3	335205	5	NULL	NULL	0	NULL	statement 1			occurs along with					statement 2					NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_93_1_8_s_129	11532333	By comparison, responses to 100  M NMDA plus 10  M glycine, which were inhibited selectively by 100  M APV, were of similar amplitude in oocytes injected with cerebellar mRNA from +/+ and wv/wv mice at P5-6 (+/+ 10 plus-or-minus 5 nA,  n=8 and wv/wv 12 plus-or-minus 5 nA,  n=8), P10 (+/+ 35 plus-or-minus 5 nA,  n=8 and wv/wv 31 plus-or-minus 4 nA,  n=8) or P23 (+/+ 70 plus-or-minus 3 nA,  n=8 and wv/wv 60 plus-or-minus 5 nA,  n=8; second and fourth set of traces in  Fig. 4).	transcription
55633	1	335205	7	NULL	NULL	0	NULL	APV			inhibit					NMDA					NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_93_1_8_s_129	11532333	By comparison, responses to 100  M NMDA plus 10  M glycine, which were inhibited selectively by 100  M APV, were of similar amplitude in oocytes injected with cerebellar mRNA from +/+ and wv/wv mice at P5-6 (+/+ 10 plus-or-minus 5 nA,  n=8 and wv/wv 12 plus-or-minus 5 nA,  n=8), P10 (+/+ 35 plus-or-minus 5 nA,  n=8 and wv/wv 31 plus-or-minus 4 nA,  n=8) or P23 (+/+ 70 plus-or-minus 3 nA,  n=8 and wv/wv 60 plus-or-minus 5 nA,  n=8; second and fourth set of traces in  Fig. 4).	transcription
55634	2	335205	7	NULL	NULL	0	NULL	APV			inhibit					glycine					NULL		0	NULL	NULL	NULL	gw60_brainresmolbrainres_93_1_8_s_129	11532333	By comparison, responses to 100  M NMDA plus 10  M glycine, which were inhibited selectively by 100  M APV, were of similar amplitude in oocytes injected with cerebellar mRNA from +/+ and wv/wv mice at P5-6 (+/+ 10 plus-or-minus 5 nA,  n=8 and wv/wv 12 plus-or-minus 5 nA,  n=8), P10 (+/+ 35 plus-or-minus 5 nA,  n=8 and wv/wv 31 plus-or-minus 4 nA,  n=8) or P23 (+/+ 70 plus-or-minus 3 nA,  n=8 and wv/wv 60 plus-or-minus 5 nA,  n=8; second and fourth set of traces in  Fig. 4).	transcription
53972	1	335210	5	NULL	NULL	0	NULL	ATP			does not increase					mIPSC		frequency of			NULL	glycinergic presynaptic nerve terminals	NULL	NULL	NULL	NULL	gw60_jneurosci_21_9_2983_s_147	11312282	In the presence of both KT5720 and SP, however, ATP failed to increase the mIPSC frequency (Fig.  5 A,B), indicating that the effect of SP on P2X receptors are not mediated through the PKA pathway in the glycinergic presynaptic nerve terminals.	transcription
53973	2	335210	5	NULL	NULL	0	NULL	statement 1			in the presence of					KT5720 & SP					NULL	glycinergic presynaptic nerve terminals	NULL	NULL	NULL	NULL	gw60_jneurosci_21_9_2983_s_147	11312282	In the presence of both KT5720 and SP, however, ATP failed to increase the mIPSC frequency (Fig.  5 A,B), indicating that the effect of SP on P2X receptors are not mediated through the PKA pathway in the glycinergic presynaptic nerve terminals.	transcription
53976	3	335210	5	NULL	NULL	0	NULL	SP			effects					P2X receptors					NULL	glycinergic presynaptic nerve terminals	NULL	NULL	NULL	NULL	gw60_jneurosci_21_9_2983_s_147	11312282	In the presence of both KT5720 and SP, however, ATP failed to increase the mIPSC frequency (Fig.  5 A,B), indicating that the effect of SP on P2X receptors are not mediated through the PKA pathway in the glycinergic presynaptic nerve terminals.	transcription
53977	4	335210	5	NULL	NULL	0	NULL	statement 3			is not mediated through					PKA pathway					NULL	glycinergic presynaptic nerve terminals	NULL	NULL	NULL	NULL	gw60_jneurosci_21_9_2983_s_147	11312282	In the presence of both KT5720 and SP, however, ATP failed to increase the mIPSC frequency (Fig.  5 A,B), indicating that the effect of SP on P2X receptors are not mediated through the PKA pathway in the glycinergic presynaptic nerve terminals.	transcription
55635	1	335210	7	NULL	NULL	0	NULL	ATP 			does not increase					mIPSC		frequency of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_9_2983_s_147	11312282	In the presence of both KT5720 and SP, however, ATP failed to increase the mIPSC frequency (Fig.  5 A,B), indicating that the effect of SP on P2X receptors are not mediated through the PKA pathway in the glycinergic presynaptic nerve terminals.	transcription
55636	2	335210	7	NULL	NULL	0	NULL	statement 1			in the presence of					KT5720					NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_9_2983_s_147	11312282	In the presence of both KT5720 and SP, however, ATP failed to increase the mIPSC frequency (Fig.  5 A,B), indicating that the effect of SP on P2X receptors are not mediated through the PKA pathway in the glycinergic presynaptic nerve terminals.	transcription
55637	3	335210	7	NULL	NULL	0	NULL	statement 1			in the presence of					SP					NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_9_2983_s_147	11312282	In the presence of both KT5720 and SP, however, ATP failed to increase the mIPSC frequency (Fig.  5 A,B), indicating that the effect of SP on P2X receptors are not mediated through the PKA pathway in the glycinergic presynaptic nerve terminals.	transcription
55638	4	335210	7	NULL	NULL	0	NULL	SP			effect					P2X receptors					NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_9_2983_s_147	11312282	In the presence of both KT5720 and SP, however, ATP failed to increase the mIPSC frequency (Fig.  5 A,B), indicating that the effect of SP on P2X receptors are not mediated through the PKA pathway in the glycinergic presynaptic nerve terminals.	transcription
55639	5	335210	7	NULL	NULL	0	NULL	statement 4			not mediated through					PKA pathway					NULL	glycinergic presynaptic nerve terminals	0	NULL	NULL	NULL	gw60_jneurosci_21_9_2983_s_147	11312282	In the presence of both KT5720 and SP, however, ATP failed to increase the mIPSC frequency (Fig.  5 A,B), indicating that the effect of SP on P2X receptors are not mediated through the PKA pathway in the glycinergic presynaptic nerve terminals.	transcription
53978	1	335213	5	NULL	NULL	0	NULL	3-phosphoglycerate dehydrogenase			is encoded by					serA					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
53979	2	335213	5	NULL	NULL	0	NULL	Lrp			activates					serA					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
53980	3	335213	5	NULL	NULL	0	NULL	3-phosphoglycerate			is a type of					glycolytic intermediate					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
53981	4	335213	5	NULL	NULL	0	NULL	3-phosphoglycerate			is converted to					serine					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
53982	5	335213	5	NULL	NULL	0	NULL	serA			catalyzes					statement 4					NULL		NULL	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
53983	6	335213	5	NULL	NULL	0	NULL	serine hydroxymethyltransferase			is encoded by					glyA					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
53984	7	335213	5	NULL	NULL	0	NULL	Lrp			repress					glyA					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
53985	8	335213	5	NULL	NULL	0	NULL	Lrp			repress					sdaA					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
53986	9	335213	5	NULL	NULL	0	NULL	serine deaminase			is encoded by					sdaA					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
53987	10	335213	5	NULL	NULL	0	NULL	sdaA			plays a role in					serine degradation pathway					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
53988	11	335213	5	NULL	NULL	0	NULL	glyA			plays a role in					serine degradation pathway					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
55640	1	335213	7	NULL	NULL	0	NULL	Lrp			activates					 3-phosphoglycerate dehydrogenase					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
55641	2	335213	7	NULL	NULL	0	NULL	serA			encodes					 3-phosphoglycerate dehydrogenase					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
55642	3	335213	7	NULL	NULL	0	NULL	glycolytic intermediate 3-phosphoglycerate 			converted to					serine					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
55643	4	335213	7	NULL	NULL	0	NULL	Lrp			repress					serine hydroxymethyltransferase					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
55644	5	335213	7	NULL	NULL	0	NULL	glyA			encode					serine hydroxymethyltransferase					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
55645	6	335213	7	NULL	NULL	0	NULL	3-phosphoglycerate dehydrogenase			catalyse					statement 3					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
55646	7	335213	7	NULL	NULL	0	NULL	Lrp			repress					serine deaminase					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
55647	8	335213	7	NULL	NULL	0	NULL	sdaA			encode					serine deaminase					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
55648	9	335213	7	NULL	NULL	0	NULL	serine hydroxymethyltransferase			belongs to					serine degradation pathway					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
55649	10	335213	7	NULL	NULL	0	NULL	serine deaminase			belongs to					serine degradation pathway					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_10_5772_s_155	14532024	Lrp activates 3-phosphoglycerate dehydrogenase (encoded by  serA), which converts the glycolytic intermediate 3-phosphoglycerate to serine, while it represses serine hydroxymethyltransferase (encoded by  glyA) and serine deaminase (encoded by  sdaA) of the serine degradation pathway.	transcription
53989	1	335214	5	NULL	NULL	0	NULL	PGDH		Escherichia coli	catalyzes					serine biosynthesis		first step of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_eur-j-biochem_269_17_12199695_s_2	12199695	Escherichia coli 3-phosphoglycerate dehydrogenase (PGDH) catalyzes the  first step in serine biosynthesis, and is allosterically inhibited by  serine.	transcription
53990	2	335214	5	NULL	NULL	0	NULL	serine			inhibits		allosterically			PGDH		Escherichia coli			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_eur-j-biochem_269_17_12199695_s_2	12199695	Escherichia coli 3-phosphoglycerate dehydrogenase (PGDH) catalyzes the  first step in serine biosynthesis, and is allosterically inhibited by  serine.	transcription
53991	3	335214	5	NULL	NULL	0	NULL	PGDH			is					3-phosphoglycerate dehydrogenase					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_eur-j-biochem_269_17_12199695_s_2	12199695	Escherichia coli 3-phosphoglycerate dehydrogenase (PGDH) catalyzes the  first step in serine biosynthesis, and is allosterically inhibited by  serine.	transcription
55650	1	335214	7	NULL	NULL	0	NULL	PGDH		Escherichia coli	catalyze					serine		first step in biosynthesis of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_eur-j-biochem_269_17_12199695_s_2	12199695	Escherichia coli 3-phosphoglycerate dehydrogenase (PGDH) catalyzes the  first step in serine biosynthesis, and is allosterically inhibited by  serine.	transcription
55651	2	335214	7	NULL	NULL	0	NULL	serine			inhibits		allosterically			statement 1					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_eur-j-biochem_269_17_12199695_s_2	12199695	Escherichia coli 3-phosphoglycerate dehydrogenase (PGDH) catalyzes the  first step in serine biosynthesis, and is allosterically inhibited by  serine.	transcription
55652	3	335214	7	NULL	NULL	0	NULL	PGDH			is					3-phosphoglycerate dehydrogenase 					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_eur-j-biochem_269_17_12199695_s_2	12199695	Escherichia coli 3-phosphoglycerate dehydrogenase (PGDH) catalyzes the  first step in serine biosynthesis, and is allosterically inhibited by  serine.	transcription
53992	1	335215	5	NULL	NULL	0	NULL	3-phosphoglycerate			is a type of					glycolytic metabolite					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10264_s_3	12525494	These dehydrogenases catalyze the first reaction of serine and glycine biosynthesis from the glycolytic metabolite 3-phosphoglycerate.	transcription
53993	2	335215	5	NULL	NULL	0	NULL	serine			is synthesized from					3-phosphoglycerate					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10264_s_3	12525494	These dehydrogenases catalyze the first reaction of serine and glycine biosynthesis from the glycolytic metabolite 3-phosphoglycerate.	transcription
53994	3	335215	5	NULL	NULL	0	NULL	glycine			is synthesized from					3-phosphoglycerate					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10264_s_3	12525494	These dehydrogenases catalyze the first reaction of serine and glycine biosynthesis from the glycolytic metabolite 3-phosphoglycerate.	transcription
53995	4	335215	5	NULL	NULL	0	NULL	dehydrogenases			catalyzes					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10264_s_3	12525494	These dehydrogenases catalyze the first reaction of serine and glycine biosynthesis from the glycolytic metabolite 3-phosphoglycerate.	transcription
53996	5	335215	5	NULL	NULL	0	NULL	dehydrogenases			catalyzes					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10264_s_3	12525494	These dehydrogenases catalyze the first reaction of serine and glycine biosynthesis from the glycolytic metabolite 3-phosphoglycerate.	transcription
55653	1	335215	7	NULL	NULL	0	NULL	 3-phosphoglycerate			is involved in					glycine		biosynthesis of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_12_10264_s_3	12525494	These dehydrogenases catalyze the first reaction of serine and glycine biosynthesis from the glycolytic metabolite 3-phosphoglycerate.	transcription
55654	2	335215	7	NULL	NULL	0	NULL	3-phosphoglycerate			is a type of					glycolytic metabolite					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_12_10264_s_3	12525494	These dehydrogenases catalyze the first reaction of serine and glycine biosynthesis from the glycolytic metabolite 3-phosphoglycerate.	transcription
53997	1	335216	5	NULL	NULL	0	NULL	threonine deaminase		structure of	resembles			C-domain		3-phosphoglycerate dehydrogenase			serine binding domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_18_12855_s_256	10212273	The structure of the C-domain of threonine deaminase resembles that of the serine binding domain of 3-phosphoglycerate dehydrogenase.	transcription
56146	1	335216	7	NULL	NULL	0	NULL	threonine deaminase			resembles			C-domain 		3-phosphoglycerate dehydrogenase			serine binding domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_18_12855_s_256	10212273	The structure of the C-domain of threonine deaminase resembles that of the serine binding domain of 3-phosphoglycerate dehydrogenase.	transcription
53998	1	335217	5	NULL	NULL	0	NULL	3-phosphoglycerate			is oxidized to					phosphohydroxypyruvate					NULL		0	NULL	NULL	NULL	gw70_pnas_100_1_370_s_175	12509500	An enzyme of nitrogen metabolism has been identified as a potential target for thioredoxin:  phosphoglycerate dehydrogenase, which catalyzes the oxidation of 3-phosphoglycerate to phosphohydroxypyruvate in the first step of the serine biosynthesis.	transcription
53999	2	335217	5	NULL	NULL	0	NULL	statement 1			is first step of					serine		biosynthesis of			NULL		0	NULL	NULL	NULL	gw70_pnas_100_1_370_s_175	12509500	An enzyme of nitrogen metabolism has been identified as a potential target for thioredoxin:  phosphoglycerate dehydrogenase, which catalyzes the oxidation of 3-phosphoglycerate to phosphohydroxypyruvate in the first step of the serine biosynthesis.	transcription
54000	3	335217	5	NULL	NULL	0	NULL	phosphoglycerate dehydrogenase			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw70_pnas_100_1_370_s_175	12509500	An enzyme of nitrogen metabolism has been identified as a potential target for thioredoxin:  phosphoglycerate dehydrogenase, which catalyzes the oxidation of 3-phosphoglycerate to phosphohydroxypyruvate in the first step of the serine biosynthesis.	transcription
54001	4	335217	5	NULL	NULL	0	NULL	phosphoglycerate dehydrogenase			target for		potential			thioredoxin					NULL		0	NULL	NULL	NULL	gw70_pnas_100_1_370_s_175	12509500	An enzyme of nitrogen metabolism has been identified as a potential target for thioredoxin:  phosphoglycerate dehydrogenase, which catalyzes the oxidation of 3-phosphoglycerate to phosphohydroxypyruvate in the first step of the serine biosynthesis.	transcription
55655	1	335217	7	NULL	NULL	0	NULL	3-phosphoglycerate			oxidizes to					phosphohydroxypyruvate					NULL		0	NULL	NULL	NULL	gw70_pnas_100_1_370_s_175	12509500	An enzyme of nitrogen metabolism has been identified as a potential target for thioredoxin:  phosphoglycerate dehydrogenase, which catalyzes the oxidation of 3-phosphoglycerate to phosphohydroxypyruvate in the first step of the serine biosynthesis.	transcription
55656	2	335217	7	NULL	NULL	0	NULL	statement 1			first step in the					serine		biosynthesis of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_1_370_s_175	12509500	An enzyme of nitrogen metabolism has been identified as a potential target for thioredoxin:  phosphoglycerate dehydrogenase, which catalyzes the oxidation of 3-phosphoglycerate to phosphohydroxypyruvate in the first step of the serine biosynthesis.	transcription
55657	3	335217	7	NULL	NULL	0	NULL	nitrogen metabolism enzyme			potential target for					thioredoxin					NULL		0	NULL	NULL	NULL	gw70_pnas_100_1_370_s_175	12509500	An enzyme of nitrogen metabolism has been identified as a potential target for thioredoxin:  phosphoglycerate dehydrogenase, which catalyzes the oxidation of 3-phosphoglycerate to phosphohydroxypyruvate in the first step of the serine biosynthesis.	transcription
54002	1	335218	5	NULL	NULL	0	NULL	Upp			is					uracil phosphoribosyltransferase					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_39_29131_s_217	16893888	Uracil phosphoribosyltransferase (Upp) functions to regulate entry into the pyrimidine salvage pathway commonly induced by starvation conditions, whereas SerA (D-3-phosphoglycerate dehydrogenase) regulates the cellular levels of 3-phosphoglycerate from serine.	transcription
54003	2	335218	5	NULL	NULL	0	NULL	Upp			regulates					pyrimidine salvage pathway		entry into			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_39_29131_s_217	16893888	Uracil phosphoribosyltransferase (Upp) functions to regulate entry into the pyrimidine salvage pathway commonly induced by starvation conditions, whereas SerA (D-3-phosphoglycerate dehydrogenase) regulates the cellular levels of 3-phosphoglycerate from serine.	transcription
54004	3	335218	5	NULL	NULL	0	NULL	pyrimidine salvage pathway			is induced by		commonly			starvation					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_39_29131_s_217	16893888	Uracil phosphoribosyltransferase (Upp) functions to regulate entry into the pyrimidine salvage pathway commonly induced by starvation conditions, whereas SerA (D-3-phosphoglycerate dehydrogenase) regulates the cellular levels of 3-phosphoglycerate from serine.	transcription
54005	4	335218	5	NULL	NULL	0	NULL	SerA			is					D-3-phosphoglycerate dehydrogenase					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_39_29131_s_217	16893888	Uracil phosphoribosyltransferase (Upp) functions to regulate entry into the pyrimidine salvage pathway commonly induced by starvation conditions, whereas SerA (D-3-phosphoglycerate dehydrogenase) regulates the cellular levels of 3-phosphoglycerate from serine.	transcription
54006	5	335218	5	NULL	NULL	0	NULL	3-phosphoglycerate			is obtained from					serine					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_39_29131_s_217	16893888	Uracil phosphoribosyltransferase (Upp) functions to regulate entry into the pyrimidine salvage pathway commonly induced by starvation conditions, whereas SerA (D-3-phosphoglycerate dehydrogenase) regulates the cellular levels of 3-phosphoglycerate from serine.	transcription
54007	6	335218	5	NULL	NULL	0	NULL	SerA			regulates					statement 5		cellular levels of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_39_29131_s_217	16893888	Uracil phosphoribosyltransferase (Upp) functions to regulate entry into the pyrimidine salvage pathway commonly induced by starvation conditions, whereas SerA (D-3-phosphoglycerate dehydrogenase) regulates the cellular levels of 3-phosphoglycerate from serine.	transcription
55658	1	335218	7	NULL	NULL	0	NULL	D-3-phosphoglycerate			is obtained from					serine					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_39_29131_s_217	16893888	Uracil phosphoribosyltransferase (Upp) functions to regulate entry into the pyrimidine salvage pathway commonly induced by starvation conditions, whereas SerA (D-3-phosphoglycerate dehydrogenase) regulates the cellular levels of 3-phosphoglycerate from serine.	transcription
55659	2	335218	7	NULL	NULL	0	NULL	SerA			regulates					statement 1		cellular levels of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_39_29131_s_217	16893888	Uracil phosphoribosyltransferase (Upp) functions to regulate entry into the pyrimidine salvage pathway commonly induced by starvation conditions, whereas SerA (D-3-phosphoglycerate dehydrogenase) regulates the cellular levels of 3-phosphoglycerate from serine.	transcription
55660	3	335218	7	NULL	NULL	0	NULL	Upp			regulate					pyrimidine salvage pathway		entry into			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_39_29131_s_217	16893888	Uracil phosphoribosyltransferase (Upp) functions to regulate entry into the pyrimidine salvage pathway commonly induced by starvation conditions, whereas SerA (D-3-phosphoglycerate dehydrogenase) regulates the cellular levels of 3-phosphoglycerate from serine.	transcription
55661	4	335218	7	NULL	NULL	0	NULL	statement 3			induced by					starvation condition					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_39_29131_s_217	16893888	Uracil phosphoribosyltransferase (Upp) functions to regulate entry into the pyrimidine salvage pathway commonly induced by starvation conditions, whereas SerA (D-3-phosphoglycerate dehydrogenase) regulates the cellular levels of 3-phosphoglycerate from serine.	transcription
55662	5	335218	7	NULL	NULL	0	NULL	UPP			is					Uracil phosphoribosyltransferase					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_39_29131_s_217	16893888	Uracil phosphoribosyltransferase (Upp) functions to regulate entry into the pyrimidine salvage pathway commonly induced by starvation conditions, whereas SerA (D-3-phosphoglycerate dehydrogenase) regulates the cellular levels of 3-phosphoglycerate from serine.	transcription
55663	6	335218	7	NULL	NULL	0	NULL	SerA			is					D-3-phosphoglycerate dehydrogenase					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_39_29131_s_217	16893888	Uracil phosphoribosyltransferase (Upp) functions to regulate entry into the pyrimidine salvage pathway commonly induced by starvation conditions, whereas SerA (D-3-phosphoglycerate dehydrogenase) regulates the cellular levels of 3-phosphoglycerate from serine.	transcription
54008	1	335219	5	NULL	NULL	0	NULL	p105			processed to					p50					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_4_980_s_107	13679070	Casper inhibits the processing of p105 to p50	transcription
54009	2	335219	5	NULL	NULL	0	NULL	Casper			inhibits					statement 1					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_4_980_s_107	13679070	Casper inhibits the processing of p105 to p50	transcription
55664	1	335219	7	NULL	NULL	0	NULL	p105			processed to					p50					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_4_980_s_107	13679070	Casper inhibits the processing of p105 to p50	transcription
55665	2	335219	7	NULL	NULL	0	NULL	Casper			inhibits					statement 1					NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_4_980_s_107	13679070	Casper inhibits the processing of p105 to p50	transcription
54010	1	335220	5	NULL	NULL	0	NULL	p105.p50 complex			is retained in					cytoplasm					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_1_556_s_421	12399470	Expression of p105 or both p105 and p50 results in a p105.p50 complex that is retained in the cytoplasm.	transcription
54011	2	335220	5	NULL	NULL	0	NULL	p105 & p50		expression of	results in					p105.p50 complex					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_1_556_s_421	12399470	Expression of p105 or both p105 and p50 results in a p105.p50 complex that is retained in the cytoplasm.	transcription
55666	1	335220	7	NULL	NULL	0	NULL	p105		expression of	results in					p105.p50 complex					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_1_556_s_421	12399470	Expression of p105 or both p105 and p50 results in a p105.p50 complex that is retained in the cytoplasm.	transcription
55667	2	335220	7	NULL	NULL	0	NULL	p50		expression of	results in					p105.p50 complex					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_1_556_s_421	12399470	Expression of p105 or both p105 and p50 results in a p105.p50 complex that is retained in the cytoplasm.	transcription
55668	3	335220	7	NULL	NULL	0	NULL	statement 1			occur along with					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_1_556_s_421	12399470	Expression of p105 or both p105 and p50 results in a p105.p50 complex that is retained in the cytoplasm.	transcription
55669	4	335220	7	NULL	NULL	0	NULL	statement 3			results in					p105.p50 complex					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_1_556_s_421	12399470	Expression of p105 or both p105 and p50 results in a p105.p50 complex that is retained in the cytoplasm.	transcription
55670	5	335220	7	NULL	NULL	0	NULL	statement 4			is an alternative to					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_1_556_s_421	12399470	Expression of p105 or both p105 and p50 results in a p105.p50 complex that is retained in the cytoplasm.	transcription
55671	6	335220	7	NULL	NULL	0	NULL	p105.p50 complex			retained in					cytoplasm					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_1_556_s_421	12399470	Expression of p105 or both p105 and p50 results in a p105.p50 complex that is retained in the cytoplasm.	transcription
54013	1	335221	5	NULL	NULL	0	NULL	proteolysis			leads to					p50		generation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_126	12807880	Proteolysis Leading to p50 Generation Initiates at an Internal Site of  the p105 Protein --	transcription
55672	1	335221	7	NULL	NULL	0	NULL	proteolysis			leads to					p50		generation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_126	12807880	Proteolysis Leading to p50 Generation Initiates at an Internal Site of  the p105 Protein --	transcription
55673	2	335221	7	NULL	NULL	0	NULL	statement 1			initiates					p105 Protein			Internal Site of		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_126	12807880	Proteolysis Leading to p50 Generation Initiates at an Internal Site of  the p105 Protein --	transcription
54014	1	335222	5	NULL	NULL	0	NULL	IKK			stimulates					p105		processing of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_222	11350967	Panel A, IKK stimulates processing of p105 and subsequent translocation of the resulting p50 to the nucleus.	transcription
54015	2	335222	5	NULL	NULL	0	NULL	p50			is translocated to					nucleus					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_222	11350967	Panel A, IKK stimulates processing of p105 and subsequent translocation of the resulting p50 to the nucleus.	transcription
54016	3	335222	5	NULL	NULL	0	NULL	IKK			stimulates		subsequently			statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_222	11350967	Panel A, IKK stimulates processing of p105 and subsequent translocation of the resulting p50 to the nucleus.	transcription
55674	1	335222	7	NULL	NULL	0	NULL	 IKK 			stimulates					p105		processing of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_222	11350967	Panel A, IKK stimulates processing of p105 and subsequent translocation of the resulting p50 to the nucleus.	transcription
55675	2	335222	7	NULL	NULL	0	NULL	p50			translocated to					nucleus					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_222	11350967	Panel A, IKK stimulates processing of p105 and subsequent translocation of the resulting p50 to the nucleus.	transcription
55676	3	335222	7	NULL	NULL	0	NULL	statement 1			leads to					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_222	11350967	Panel A, IKK stimulates processing of p105 and subsequent translocation of the resulting p50 to the nucleus.	transcription
54566	1	335223	5	NULL	NULL	0	NULL	Casper			interacts with					p105					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_4_980_s_108	13679070	Since Casper interacts with p105, we examined whether Casper has any effects on p105  processing into p50.	transcription
54567	2	335223	5	NULL	NULL	0	NULL	p105			is processed into					p50					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_4_980_s_108	13679070	Since Casper interacts with p105, we examined whether Casper has any effects on p105  processing into p50.	transcription
54568	3	335223	5	NULL	NULL	0	NULL	Casper			effect		may			statement 2					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_4_980_s_108	13679070	Since Casper interacts with p105, we examined whether Casper has any effects on p105  processing into p50.	transcription
55677	1	335223	7	NULL	NULL	0	NULL	Casper			interacts with					p105					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_4_980_s_108	13679070	Since Casper interacts with p105, we examined whether Casper has any effects on p105  processing into p50.	transcription
54569	1	335224	5	NULL	NULL	0	NULL	Tpl-2			interacts with		directly			p105					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_32465_s_206	12801933	Tpl-2 directly  interacts with p105, and its overexpression leads to increased turnover of  p105 into p50 subunits ( ).	transcription
54570	2	335224	5	NULL	NULL	0	NULL	p105			is converted to					p50 subunits					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_32465_s_206	12801933	Tpl-2 directly  interacts with p105, and its overexpression leads to increased turnover of  p105 into p50 subunits ( ).	transcription
54571	3	335224	5	NULL	NULL	0	NULL	Tpl-2		overexpression of	leads to					statement 2		increased			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_34_32465_s_206	12801933	Tpl-2 directly  interacts with p105, and its overexpression leads to increased turnover of  p105 into p50 subunits ( ).	transcription
55678	1	335224	7	NULL	NULL	0	NULL	Tpl-2			interacts with		directly			p105					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_32465_s_206	12801933	Tpl-2 directly  interacts with p105, and its overexpression leads to increased turnover of  p105 into p50 subunits ( ).	transcription
55679	2	335224	7	NULL	NULL	0	NULL	p105			converted to					p50 subunits					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_32465_s_206	12801933	Tpl-2 directly  interacts with p105, and its overexpression leads to increased turnover of  p105 into p50 subunits ( ).	transcription
55680	3	335224	7	NULL	NULL	0	NULL	Tpl-2		overexpression of	increase					statement 2		turnover of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_34_32465_s_206	12801933	Tpl-2 directly  interacts with p105, and its overexpression leads to increased turnover of  p105 into p50 subunits ( ).	transcription
54572	1	335226	5	NULL	NULL	0	NULL	p50			inhibits					p105		processing of	ankyrin repeat		NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_189	11350967	p50 inhibits  in vivo processing of ankyrin repeat-containing, but not of ankyrin repeat-lacking p105s.	transcription
54573	2	335226	5	NULL	NULL	0	NULL	p105			lacks								ankyrin repeat		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_189	11350967	p50 inhibits  in vivo processing of ankyrin repeat-containing, but not of ankyrin repeat-lacking p105s.	transcription
54574	3	335226	5	NULL	NULL	0	NULL	p50			does not inhibit					statement 2		processing of			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_189	11350967	p50 inhibits  in vivo processing of ankyrin repeat-containing, but not of ankyrin repeat-lacking p105s.	transcription
55681	1	335226	7	NULL	NULL	0	NULL	 p105			contains					ankyrin repeat					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_189	11350967	p50 inhibits  in vivo processing of ankyrin repeat-containing, but not of ankyrin repeat-lacking p105s.	transcription
55682	2	335226	7	NULL	NULL	0	NULL	p50			inhibits					statement 1		in vivo processing of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_189	11350967	p50 inhibits  in vivo processing of ankyrin repeat-containing, but not of ankyrin repeat-lacking p105s.	transcription
55683	3	335226	7	NULL	NULL	0	NULL	p105			lacks								ankyrin repeat		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_189	11350967	p50 inhibits  in vivo processing of ankyrin repeat-containing, but not of ankyrin repeat-lacking p105s.	transcription
55684	4	335226	7	NULL	NULL	0	NULL	p50			does not inhibit					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_189	11350967	p50 inhibits  in vivo processing of ankyrin repeat-containing, but not of ankyrin repeat-lacking p105s.	transcription
54575	1	335227	5	NULL	NULL	0	NULL	p105			is processed into					p50					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_52_54841_s_33	15485831	Processing of p105 into p50 is constitutively regulated, and p50 is most commonly associated with p65 and the inhibitor protein IkappaBalpha in an inactive complex in the cytosol.	transcription
54576	2	335227	5	NULL	NULL	0	NULL	p50			is associated with		most commonly			p65					NULL	cytosol	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_52_54841_s_33	15485831	Processing of p105 into p50 is constitutively regulated, and p50 is most commonly associated with p65 and the inhibitor protein IkappaBalpha in an inactive complex in the cytosol.	transcription
54577	3	335227	5	NULL	NULL	0	NULL	p50			is associated with		most commonly			IkappaBalpha					NULL	cytosol	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_52_54841_s_33	15485831	Processing of p105 into p50 is constitutively regulated, and p50 is most commonly associated with p65 and the inhibitor protein IkappaBalpha in an inactive complex in the cytosol.	transcription
54578	4	335227	5	NULL	NULL	0	NULL	statement 2			occurs along with					statement 3					NULL	cytosol	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_52_54841_s_33	15485831	Processing of p105 into p50 is constitutively regulated, and p50 is most commonly associated with p65 and the inhibitor protein IkappaBalpha in an inactive complex in the cytosol.	transcription
54579	5	335227	5	NULL	NULL	0	NULL	statement 4			forms					complex		inactive			NULL	cytosol	0	NULL	NULL	NULL	gw70_jbiolchem_279_52_54841_s_33	15485831	Processing of p105 into p50 is constitutively regulated, and p50 is most commonly associated with p65 and the inhibitor protein IkappaBalpha in an inactive complex in the cytosol.	transcription
54580	6	335227	5	NULL	NULL	0	NULL	IkappaBalpha			is a type of					inhibitor protein					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_52_54841_s_33	15485831	Processing of p105 into p50 is constitutively regulated, and p50 is most commonly associated with p65 and the inhibitor protein IkappaBalpha in an inactive complex in the cytosol.	transcription
55685	1	335227	7	NULL	NULL	0	NULL	p105			processed to					p50					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_52_54841_s_33	15485831	Processing of p105 into p50 is constitutively regulated, and p50 is most commonly associated with p65 and the inhibitor protein IkappaBalpha in an inactive complex in the cytosol.	transcription
55686	2	335227	7	NULL	NULL	0	NULL	p50			associate with					p65					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_52_54841_s_33	15485831	Processing of p105 into p50 is constitutively regulated, and p50 is most commonly associated with p65 and the inhibitor protein IkappaBalpha in an inactive complex in the cytosol.	transcription
55687	3	335227	7	NULL	NULL	0	NULL	p50			associate with					IkappaBalpha					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_52_54841_s_33	15485831	Processing of p105 into p50 is constitutively regulated, and p50 is most commonly associated with p65 and the inhibitor protein IkappaBalpha in an inactive complex in the cytosol.	transcription
55688	4	335227	7	NULL	NULL	0	NULL	statement 2			occur in an					inactive complex					NULL	cytosol	0	NULL	NULL	NULL	gw70_jbiolchem_279_52_54841_s_33	15485831	Processing of p105 into p50 is constitutively regulated, and p50 is most commonly associated with p65 and the inhibitor protein IkappaBalpha in an inactive complex in the cytosol.	transcription
55689	5	335227	7	NULL	NULL	0	NULL	statement 3			occur in an					inactive complex					NULL	cytosol	0	NULL	NULL	NULL	gw70_jbiolchem_279_52_54841_s_33	15485831	Processing of p105 into p50 is constitutively regulated, and p50 is most commonly associated with p65 and the inhibitor protein IkappaBalpha in an inactive complex in the cytosol.	transcription
55690	6	335227	7	NULL	NULL	0	NULL	statement 1		processing of	regulated					constitutively					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_52_54841_s_33	15485831	Processing of p105 into p50 is constitutively regulated, and p50 is most commonly associated with p65 and the inhibitor protein IkappaBalpha in an inactive complex in the cytosol.	transcription
55691	7	335227	7	NULL	NULL	0	NULL	IkappaBalpha			is a type of					inhibitor protein					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_52_54841_s_33	15485831	Processing of p105 into p50 is constitutively regulated, and p50 is most commonly associated with p65 and the inhibitor protein IkappaBalpha in an inactive complex in the cytosol.	transcription
54581	1	335228	5	NULL	NULL	0	NULL	p50			is generated by		cotranslationally			proteasome-mediated process					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_27	9529257	Rather, p50 is generated cotranslationally by a proteasome-mediated process that ensures the  production of both p50 and p105 and preserves their independent functions.	transcription
54582	2	335228	5	NULL	NULL	0	NULL	statement 1			ensures					p50		production of			NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_27	9529257	Rather, p50 is generated cotranslationally by a proteasome-mediated process that ensures the  production of both p50 and p105 and preserves their independent functions.	transcription
54583	3	335228	5	NULL	NULL	0	NULL	statement 1			ensures					p105		production of			NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_27	9529257	Rather, p50 is generated cotranslationally by a proteasome-mediated process that ensures the  production of both p50 and p105 and preserves their independent functions.	transcription
54584	4	335228	5	NULL	NULL	0	NULL	statement 2			occurs along with					statement 3					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_27	9529257	Rather, p50 is generated cotranslationally by a proteasome-mediated process that ensures the  production of both p50 and p105 and preserves their independent functions.	transcription
55692	1	335228	7	NULL	NULL	0	NULL	proteasome-mediated process 			generates		cotranslationally			p50					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_27	9529257	Rather, p50 is generated cotranslationally by a proteasome-mediated process that ensures the  production of both p50 and p105 and preserves their independent functions.	transcription
55693	2	335228	7	NULL	NULL	0	NULL	statement 1			ensures					p50		production of			NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_27	9529257	Rather, p50 is generated cotranslationally by a proteasome-mediated process that ensures the  production of both p50 and p105 and preserves their independent functions.	transcription
55694	3	335228	7	NULL	NULL	0	NULL	statement 1			ensures					p105		production of			NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_27	9529257	Rather, p50 is generated cotranslationally by a proteasome-mediated process that ensures the  production of both p50 and p105 and preserves their independent functions.	transcription
55695	4	335228	7	NULL	NULL	0	NULL	statement 1			preserves					p50		independent function of			NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_27	9529257	Rather, p50 is generated cotranslationally by a proteasome-mediated process that ensures the  production of both p50 and p105 and preserves their independent functions.	transcription
55696	5	335228	7	NULL	NULL	0	NULL	statement 1			preserves					p105		independent function of			NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_27	9529257	Rather, p50 is generated cotranslationally by a proteasome-mediated process that ensures the  production of both p50 and p105 and preserves their independent functions.	transcription
54585	1	335229	5	NULL	NULL	0	NULL	p105			is a type of					NF- B p50 precursor					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_472	9529257	The NF- B p50 precursor, p105, contains an internal I B-like inhibitor that preferentially inhibits p50.	transcription
54586	2	335229	5	NULL	NULL	0	NULL	p105			contains					I B-like inhibitor		internal			NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_472	9529257	The NF- B p50 precursor, p105, contains an internal I B-like inhibitor that preferentially inhibits p50.	transcription
54587	3	335229	5	NULL	NULL	0	NULL	statement 2			inhibits		preferentially			p50					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_472	9529257	The NF- B p50 precursor, p105, contains an internal I B-like inhibitor that preferentially inhibits p50.	transcription
55697	1	335229	7	NULL	NULL	0	NULL	NF- B p50			precursor of					p105					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_472	9529257	The NF- B p50 precursor, p105, contains an internal I B-like inhibitor that preferentially inhibits p50.	transcription
55698	2	335229	7	NULL	NULL	0	NULL	p105			contains					internal I B-like inhibitor					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_472	9529257	The NF- B p50 precursor, p105, contains an internal I B-like inhibitor that preferentially inhibits p50.	transcription
55699	3	335229	7	NULL	NULL	0	NULL	p105			inhibits		preferentially			p50					NULL		NULL	NULL	NULL	NULL	gw60_cell_92_6_819_s_472	9529257	The NF- B p50 precursor, p105, contains an internal I B-like inhibitor that preferentially inhibits p50.	transcription
54588	1	335230	5	NULL	NULL	0	NULL	p50			is translocated to					nucleus					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_69	9950430	Thus, TPL2-mediated activation of nuclear translocation of p50 does not require stimulation of p105 processing to p50.	transcription
54589	2	335230	5	NULL	NULL	0	NULL	TPL2			mediates					statement 1		activation of			NULL		NULL	NULL	NULL	NULL	gw60_nature_397_6717_363_s_69	9950430	Thus, TPL2-mediated activation of nuclear translocation of p50 does not require stimulation of p105 processing to p50.	transcription
54590	3	335230	5	NULL	NULL	0	NULL	p105			is processed to					p50					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_69	9950430	Thus, TPL2-mediated activation of nuclear translocation of p50 does not require stimulation of p105 processing to p50.	transcription
54591	4	335230	5	NULL	NULL	0	NULL	statement 2			does not require					statement 3		stimulation of			NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_69	9950430	Thus, TPL2-mediated activation of nuclear translocation of p50 does not require stimulation of p105 processing to p50.	transcription
55700	1	335230	7	NULL	NULL	0	NULL	p105			processed to					p50					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_69	9950430	Thus, TPL2-mediated activation of nuclear translocation of p50 does not require stimulation of p105 processing to p50.	transcription
55701	2	335230	7	NULL	NULL	0	NULL	TPL2			mediates					p50		activation of ;; nuclear translocation of			NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_69	9950430	Thus, TPL2-mediated activation of nuclear translocation of p50 does not require stimulation of p105 processing to p50.	transcription
55702	3	335230	7	NULL	NULL	0	NULL	statement 2			does not require					statement 1		stimulation of			NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_69	9950430	Thus, TPL2-mediated activation of nuclear translocation of p50 does not require stimulation of p105 processing to p50.	transcription
54601	1	335231	5	NULL	NULL	0	NULL	p105			undergoes					processing					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_190	11350967	Panel A, processing of p105 and nuclear translocation of p50 are inhibited by the presence of an ankyrin repeat domain that binds p50.	transcription
54602	2	335231	5	NULL	NULL	0	NULL	p50			is translocated to					nucleus					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_190	11350967	Panel A, processing of p105 and nuclear translocation of p50 are inhibited by the presence of an ankyrin repeat domain that binds p50.	transcription
54603	3	335231	5	NULL	NULL	0	NULL				bind			ankyrin repeat domain		p50					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_190	11350967	Panel A, processing of p105 and nuclear translocation of p50 are inhibited by the presence of an ankyrin repeat domain that binds p50.	transcription
54604	4	335231	5	NULL	NULL	0	NULL	statement 3		presence of	inhibits					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_190	11350967	Panel A, processing of p105 and nuclear translocation of p50 are inhibited by the presence of an ankyrin repeat domain that binds p50.	transcription
54605	5	335231	5	NULL	NULL	0	NULL	statement 3		presence of	inhibits					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_190	11350967	Panel A, processing of p105 and nuclear translocation of p50 are inhibited by the presence of an ankyrin repeat domain that binds p50.	transcription
55703	1	335231	7	NULL	NULL	0	NULL				bind			 ankyrin repeat domain		p50					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_190	11350967	Panel A, processing of p105 and nuclear translocation of p50 are inhibited by the presence of an ankyrin repeat domain that binds p50.	transcription
55704	2	335231	7	NULL	NULL	0	NULL			presence of	inhibits			ankyrin repeat domain		p105		processing of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_190	11350967	Panel A, processing of p105 and nuclear translocation of p50 are inhibited by the presence of an ankyrin repeat domain that binds p50.	transcription
55705	3	335231	7	NULL	NULL	0	NULL			presence of	inhibits			ankyrin repeat domain		p50		nuclear translocation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_190	11350967	Panel A, processing of p105 and nuclear translocation of p50 are inhibited by the presence of an ankyrin repeat domain that binds p50.	transcription
54606	1	335232	5	NULL	NULL	0	NULL	Bcl-3			bind					p50 dimers					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_270	10469655	Bcl-3-bound p50 dimers are in fact a suitable readout system for p105-controlled Rel activity: in contrast to Bcl-3, neither IkappaBalpha, beta nor   binds to p50 efficiently and p50 is produced from processed p105 and sequestered by p105.	transcription
54607	2	335232	5	NULL	NULL	0	NULL	Rel		activity of	is controlled by					p105					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_270	10469655	Bcl-3-bound p50 dimers are in fact a suitable readout system for p105-controlled Rel activity: in contrast to Bcl-3, neither IkappaBalpha, beta nor   binds to p50 efficiently and p50 is produced from processed p105 and sequestered by p105.	transcription
54608	3	335232	5	NULL	NULL	0	NULL	IkappaBalpha			does not bind		efficiently			p50					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_270	10469655	Bcl-3-bound p50 dimers are in fact a suitable readout system for p105-controlled Rel activity: in contrast to Bcl-3, neither IkappaBalpha, beta nor   binds to p50 efficiently and p50 is produced from processed p105 and sequestered by p105.	transcription
54609	4	335232	5	NULL	NULL	0	NULL	IkappaBbeta			does not bind		efficiently			p50					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_270	10469655	Bcl-3-bound p50 dimers are in fact a suitable readout system for p105-controlled Rel activity: in contrast to Bcl-3, neither IkappaBalpha, beta nor   binds to p50 efficiently and p50 is produced from processed p105 and sequestered by p105.	transcription
54610	5	335232	5	NULL	NULL	0	NULL	p50			is produced from					p105		processed			NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_270	10469655	Bcl-3-bound p50 dimers are in fact a suitable readout system for p105-controlled Rel activity: in contrast to Bcl-3, neither IkappaBalpha, beta nor   binds to p50 efficiently and p50 is produced from processed p105 and sequestered by p105.	transcription
54611	6	335232	5	NULL	NULL	0	NULL	p50			is sequestered by					p105					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_270	10469655	Bcl-3-bound p50 dimers are in fact a suitable readout system for p105-controlled Rel activity: in contrast to Bcl-3, neither IkappaBalpha, beta nor   binds to p50 efficiently and p50 is produced from processed p105 and sequestered by p105.	transcription
55706	1	335232	7	NULL	NULL	0	NULL	Bcl-3-			bind					p50 dimers					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_270	10469655	Bcl-3-bound p50 dimers are in fact a suitable readout system for p105-controlled Rel activity: in contrast to Bcl-3, neither IkappaBalpha, beta nor   binds to p50 efficiently and p50 is produced from processed p105 and sequestered by p105.	transcription
55707	2	335232	7	NULL	NULL	0	NULL	IkappaBalpha			does not bind		efficiently			p50					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_270	10469655	Bcl-3-bound p50 dimers are in fact a suitable readout system for p105-controlled Rel activity: in contrast to Bcl-3, neither IkappaBalpha, beta nor   binds to p50 efficiently and p50 is produced from processed p105 and sequestered by p105.	transcription
55708	3	335232	7	NULL	NULL	0	NULL	IkappaBbeta			does not bind		efficiently			p50					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_270	10469655	Bcl-3-bound p50 dimers are in fact a suitable readout system for p105-controlled Rel activity: in contrast to Bcl-3, neither IkappaBalpha, beta nor   binds to p50 efficiently and p50 is produced from processed p105 and sequestered by p105.	transcription
55709	4	335232	7	NULL	NULL	0	NULL	p105			controls					Rel		activity of			NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_270	10469655	Bcl-3-bound p50 dimers are in fact a suitable readout system for p105-controlled Rel activity: in contrast to Bcl-3, neither IkappaBalpha, beta nor   binds to p50 efficiently and p50 is produced from processed p105 and sequestered by p105.	transcription
55710	5	335232	7	NULL	NULL	0	NULL	p50			produced from					p105		processed			NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_270	10469655	Bcl-3-bound p50 dimers are in fact a suitable readout system for p105-controlled Rel activity: in contrast to Bcl-3, neither IkappaBalpha, beta nor   binds to p50 efficiently and p50 is produced from processed p105 and sequestered by p105.	transcription
55711	6	335232	7	NULL	NULL	0	NULL	p50			sequestered by					p105					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_270	10469655	Bcl-3-bound p50 dimers are in fact a suitable readout system for p105-controlled Rel activity: in contrast to Bcl-3, neither IkappaBalpha, beta nor   binds to p50 efficiently and p50 is produced from processed p105 and sequestered by p105.	transcription
54612	1	335233	5	NULL	NULL	0	NULL	p105 protein			undergoes					proteolysis					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_135	12807880	To demonstrate that proteolysis leading to p50 generation initiates at the  internal site of the p105 protein, we expressed the N-terminal 530 residues of  p105 in the cell.	transcription
54613	2	335233	5	NULL	NULL	0	NULL	statement 1			generates					p50					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_135	12807880	To demonstrate that proteolysis leading to p50 generation initiates at the  internal site of the p105 protein, we expressed the N-terminal 530 residues of  p105 in the cell.	transcription
55713	1	335233	7	NULL	NULL	0	NULL	proteloysis			generates					p50					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_135	12807880	To demonstrate that proteolysis leading to p50 generation initiates at the  internal site of the p105 protein, we expressed the N-terminal 530 residues of  p105 in the cell.	transcription
55714	2	335233	7	NULL	NULL	0	NULL	statement 1			initiates					p105 protein		internal site of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_135	12807880	To demonstrate that proteolysis leading to p50 generation initiates at the  internal site of the p105 protein, we expressed the N-terminal 530 residues of  p105 in the cell.	transcription
54614	1	335234	5	NULL	NULL	0	NULL	p105			associates with					p50					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_1_556_s_373	12399470	A possible mode of sequestration could be binding to another cytoplasmic protein(s)  through the scaffold formed because of the association of p105 and p50 and the death  domain of p105.	transcription
55715	1	335234	7	NULL	NULL	0	NULL	p105			associate with			death domain		p50					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_1_556_s_373	12399470	A possible mode of sequestration could be binding to another cytoplasmic protein(s)  through the scaffold formed because of the association of p105 and p50 and the death  domain of p105.	transcription
54615	1	335235	5	NULL	NULL	0	NULL	NF-kappaB1 gene			encodes					p105					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_8	9950430	The NF-kappaB1 gene encodes a larger precursor protein, p105, from which p50 is produced constitutively by proteasome-mediated removal of the p105 carboxy terminus 2-5.	transcription
54616	2	335235	5	NULL	NULL	0	NULL	p105			is a type of					large precursor protein					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_8	9950430	The NF-kappaB1 gene encodes a larger precursor protein, p105, from which p50 is produced constitutively by proteasome-mediated removal of the p105 carboxy terminus 2-5.	transcription
54617	3	335235	5	NULL	NULL	0	NULL	p105		removal of	is mediated by			carboxy terminus		proteasome					NULL		NULL	NULL	NULL	NULL	gw60_nature_397_6717_363_s_8	9950430	The NF-kappaB1 gene encodes a larger precursor protein, p105, from which p50 is produced constitutively by proteasome-mediated removal of the p105 carboxy terminus 2-5.	transcription
54618	4	335235	5	NULL	NULL	0	NULL	statement 3			generates					p50					NULL		NULL	NULL	NULL	NULL	gw60_nature_397_6717_363_s_8	9950430	The NF-kappaB1 gene encodes a larger precursor protein, p105, from which p50 is produced constitutively by proteasome-mediated removal of the p105 carboxy terminus 2-5.	transcription
55716	1	335235	7	NULL	NULL	0	NULL	 NF-kappaB1 gene			encode					p105					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_8	9950430	The NF-kappaB1 gene encodes a larger precursor protein, p105, from which p50 is produced constitutively by proteasome-mediated removal of the p105 carboxy terminus 2-5.	transcription
55717	2	335235	7	NULL	NULL	0	NULL	p105			is a type of					large precursor protein					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_8	9950430	The NF-kappaB1 gene encodes a larger precursor protein, p105, from which p50 is produced constitutively by proteasome-mediated removal of the p105 carboxy terminus 2-5.	transcription
55718	3	335235	7	NULL	NULL	0	NULL	p50			produced from		constitutively			p105					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_8	9950430	The NF-kappaB1 gene encodes a larger precursor protein, p105, from which p50 is produced constitutively by proteasome-mediated removal of the p105 carboxy terminus 2-5.	transcription
55719	4	335235	7	NULL	NULL	0	NULL	 proteasome			mediates					p105		removal of	carboxy terminus 2-5		NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_8	9950430	The NF-kappaB1 gene encodes a larger precursor protein, p105, from which p50 is produced constitutively by proteasome-mediated removal of the p105 carboxy terminus 2-5.	transcription
55720	5	335235	7	NULL	NULL	0	NULL	statement 3			occurs by					statement 4					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_8	9950430	The NF-kappaB1 gene encodes a larger precursor protein, p105, from which p50 is produced constitutively by proteasome-mediated removal of the p105 carboxy terminus 2-5.	transcription
54619	1	335236	5	NULL	NULL	0	NULL	p105													NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_223	11158290	By physically interacting with the p105 mutants at an early step in the biogenesis of p105 and p50, unable to dissociate upon substrate phosphorylation due to lack of phosphorylation sites, it could hinder access of the proteasome or other processing components or affect p105 folding.	transcription
54620	1	335237	5	NULL	NULL	0	NULL	p50			associate with					p105					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_326	10469655	Since a significant proportion of total p50 but less p65 is associated with p105, p105 plays a unique role in controlling p50 dimer activity (Ishikawa  et al., 1996  ).	transcription
54621	2	335237	5	NULL	NULL	0	NULL	p65			associate with					p105					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_326	10469655	Since a significant proportion of total p50 but less p65 is associated with p105, p105 plays a unique role in controlling p50 dimer activity (Ishikawa  et al., 1996  ).	transcription
54622	3	335237	5	NULL	NULL	0	NULL	statement 1			is more than		significantly			statement 2					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_326	10469655	Since a significant proportion of total p50 but less p65 is associated with p105, p105 plays a unique role in controlling p50 dimer activity (Ishikawa  et al., 1996  ).	transcription
54623	4	335237	5	NULL	NULL	0	NULL	p105			controls					p50 dimer		activity of			NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_326	10469655	Since a significant proportion of total p50 but less p65 is associated with p105, p105 plays a unique role in controlling p50 dimer activity (Ishikawa  et al., 1996  ).	transcription
55721	1	335237	7	NULL	NULL	0	NULL	 total p50		significant proportion of	associate with					p105					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_326	10469655	Since a significant proportion of total p50 but less p65 is associated with p105, p105 plays a unique role in controlling p50 dimer activity (Ishikawa  et al., 1996  ).	transcription
55722	2	335237	7	NULL	NULL	0	NULL	p65			associate with					p105					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_326	10469655	Since a significant proportion of total p50 but less p65 is associated with p105, p105 plays a unique role in controlling p50 dimer activity (Ishikawa  et al., 1996  ).	transcription
55724	3	335237	7	NULL	NULL	0	NULL	p105			controls					p50 dimer		activity of			NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_326	10469655	Since a significant proportion of total p50 but less p65 is associated with p105, p105 plays a unique role in controlling p50 dimer activity (Ishikawa  et al., 1996  ).	transcription
54628	1	335238	5	NULL	NULL	0	NULL	IKKbeta		expression of	increases					p50					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_318	11158290	We demonstrated that the expression of IKKbeta alone led to an increase in p50, but this effect is ascribed to IKKbeta-induced expression of p105, resulting in increased amounts of p50 produced by processing and loss of p105 by simultaneous IKKbeta-induced degradation.	transcription
54629	2	335238	5	NULL	NULL	0	NULL	p105		expression of	is induced by					IKKbeta					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_318	11158290	We demonstrated that the expression of IKKbeta alone led to an increase in p50, but this effect is ascribed to IKKbeta-induced expression of p105, resulting in increased amounts of p50 produced by processing and loss of p105 by simultaneous IKKbeta-induced degradation.	transcription
54630	3	335238	5	NULL	NULL	0	NULL	statement 2			ascribe					statement 1					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_318	11158290	We demonstrated that the expression of IKKbeta alone led to an increase in p50, but this effect is ascribed to IKKbeta-induced expression of p105, resulting in increased amounts of p50 produced by processing and loss of p105 by simultaneous IKKbeta-induced degradation.	transcription
54631	4	335238	5	NULL	NULL	0	NULL	statement 2			results in					p50		increased amounts of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_318	11158290	We demonstrated that the expression of IKKbeta alone led to an increase in p50, but this effect is ascribed to IKKbeta-induced expression of p105, resulting in increased amounts of p50 produced by processing and loss of p105 by simultaneous IKKbeta-induced degradation.	transcription
54632	5	335238	5	NULL	NULL	0	NULL	p50			is produced by					p105		processing of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_318	11158290	We demonstrated that the expression of IKKbeta alone led to an increase in p50, but this effect is ascribed to IKKbeta-induced expression of p105, resulting in increased amounts of p50 produced by processing and loss of p105 by simultaneous IKKbeta-induced degradation.	transcription
54633	6	335238	5	NULL	NULL	0	NULL	p50			is produced by					p105		loss of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_318	11158290	We demonstrated that the expression of IKKbeta alone led to an increase in p50, but this effect is ascribed to IKKbeta-induced expression of p105, resulting in increased amounts of p50 produced by processing and loss of p105 by simultaneous IKKbeta-induced degradation.	transcription
54634	7	335238	5	NULL	NULL	0	NULL	statement 5			occurs simultaneously with					statement 6					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_318	11158290	We demonstrated that the expression of IKKbeta alone led to an increase in p50, but this effect is ascribed to IKKbeta-induced expression of p105, resulting in increased amounts of p50 produced by processing and loss of p105 by simultaneous IKKbeta-induced degradation.	transcription
54635	8	335238	5	NULL	NULL	0	NULL	IKKbeta			induce					degradation					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_318	11158290	We demonstrated that the expression of IKKbeta alone led to an increase in p50, but this effect is ascribed to IKKbeta-induced expression of p105, resulting in increased amounts of p50 produced by processing and loss of p105 by simultaneous IKKbeta-induced degradation.	transcription
54636	9	335238	5	NULL	NULL	0	NULL	statement 8			occurs simultaneously with					statement 7					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_318	11158290	We demonstrated that the expression of IKKbeta alone led to an increase in p50, but this effect is ascribed to IKKbeta-induced expression of p105, resulting in increased amounts of p50 produced by processing and loss of p105 by simultaneous IKKbeta-induced degradation.	transcription
55725	1	335238	7	NULL	NULL	0	NULL	IKKbeta			induce					p105		expression of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_318	11158290	We demonstrated that the expression of IKKbeta alone led to an increase in p50, but this effect is ascribed to IKKbeta-induced expression of p105, resulting in increased amounts of p50 produced by processing and loss of p105 by simultaneous IKKbeta-induced degradation.	transcription
55726	2	335238	7	NULL	NULL	0	NULL	statement 1			result in					p50		increased amounts of 			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_318	11158290	We demonstrated that the expression of IKKbeta alone led to an increase in p50, but this effect is ascribed to IKKbeta-induced expression of p105, resulting in increased amounts of p50 produced by processing and loss of p105 by simultaneous IKKbeta-induced degradation.	transcription
55727	3	335238	7	NULL	NULL	0	NULL	p50			produced by					p105		processing of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_318	11158290	We demonstrated that the expression of IKKbeta alone led to an increase in p50, but this effect is ascribed to IKKbeta-induced expression of p105, resulting in increased amounts of p50 produced by processing and loss of p105 by simultaneous IKKbeta-induced degradation.	transcription
55728	5	335238	7	NULL	NULL	0	NULL	p50			produced by					p105		loss of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_318	11158290	We demonstrated that the expression of IKKbeta alone led to an increase in p50, but this effect is ascribed to IKKbeta-induced expression of p105, resulting in increased amounts of p50 produced by processing and loss of p105 by simultaneous IKKbeta-induced degradation.	transcription
55729	4	335238	7	NULL	NULL	0	NULL	IKKbeta			induce					p105		degradation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_318	11158290	We demonstrated that the expression of IKKbeta alone led to an increase in p50, but this effect is ascribed to IKKbeta-induced expression of p105, resulting in increased amounts of p50 produced by processing and loss of p105 by simultaneous IKKbeta-induced degradation.	transcription
55730	6	335238	7	NULL	NULL	0	NULL	statement 4			leads to					statement 5					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_318	11158290	We demonstrated that the expression of IKKbeta alone led to an increase in p50, but this effect is ascribed to IKKbeta-induced expression of p105, resulting in increased amounts of p50 produced by processing and loss of p105 by simultaneous IKKbeta-induced degradation.	transcription
54637	1	335239	5	NULL	NULL	0	NULL	p50			is synthesized from		de novo			p105					NULL	tolerant CD4+ T cells 	0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_214	14668329	Thus, the increased expression of p50 in tolerant CD4+ T cells could reflect  de novo synthesis of p50 from p105 following tolerance induction.	transcription
55731	1	335239	7	NULL	NULL	0	NULL	p50			produced by					p105		de novo synthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_214	14668329	Thus, the increased expression of p50 in tolerant CD4+ T cells could reflect  de novo synthesis of p50 from p105 following tolerance induction.	transcription
55732	2	335239	7	NULL	NULL	0	NULL	p50		increased expression of	reflect					statement 1					NULL	tolerant CD4+ T cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_214	14668329	Thus, the increased expression of p50 in tolerant CD4+ T cells could reflect  de novo synthesis of p50 from p105 following tolerance induction.	transcription
55733	3	335239	7	NULL	NULL	0	NULL	statement 1			occurs following					tolerance		induction of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_214	14668329	Thus, the increased expression of p50 in tolerant CD4+ T cells could reflect  de novo synthesis of p50 from p105 following tolerance induction.	transcription
54638	1	335240	5	NULL	NULL	0	NULL	p50		cotranslational folding of	regulates		might			p50		primary ratio of			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4712_s_35	10970863	In our previous work, we proposed that cotranslational folding of p50 might regulate the primary ratio of p50 and p105 ( Lin   et al., 1998).	transcription
54639	2	335240	5	NULL	NULL	0	NULL	p50		cotranslational folding of	regulates		might			p105		primary ratio of			NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_35	10970863	In our previous work, we proposed that cotranslational folding of p50 might regulate the primary ratio of p50 and p105 ( Lin   et al., 1998).	transcription
54640	3	335240	5	NULL	NULL	0	NULL	statement 1			occurs along with					statement 2					NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_35	10970863	In our previous work, we proposed that cotranslational folding of p50 might regulate the primary ratio of p50 and p105 ( Lin   et al., 1998).	transcription
55734	1	335240	7	NULL	NULL	0	NULL	p50		cotranslational folding of	regulate		might			p50		primary ratio of			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4712_s_35	10970863	In our previous work, we proposed that cotranslational folding of p50 might regulate the primary ratio of p50 and p105 ( Lin   et al., 1998).	transcription
55735	2	335240	7	NULL	NULL	0	NULL	p50		cotranslational folding of	regulate		might			p105		primary ratio of			NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_35	10970863	In our previous work, we proposed that cotranslational folding of p50 might regulate the primary ratio of p50 and p105 ( Lin   et al., 1998).	transcription
55736	3	335240	7	NULL	NULL	0	NULL	statement 1			occur along with					statement 2					NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_35	10970863	In our previous work, we proposed that cotranslational folding of p50 might regulate the primary ratio of p50 and p105 ( Lin   et al., 1998).	transcription
54641	1	335241	5	NULL	NULL	0	NULL	p105			is substituted with			ankyrin repeats		DHFR					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_201	11350967	Panel B, substitution of four ankyrin repeats with DHFR abrogates the ability of p50 to inhibit processing of p105 and does not prevent nuclear translocation of free p50.	transcription
54642	2	335241	5	NULL	NULL	0	NULL	p50			inhibits					p105		processing of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_201	11350967	Panel B, substitution of four ankyrin repeats with DHFR abrogates the ability of p50 to inhibit processing of p105 and does not prevent nuclear translocation of free p50.	transcription
54643	3	335241	5	NULL	NULL	0	NULL	statement 1			abrogates					statement 2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_201	11350967	Panel B, substitution of four ankyrin repeats with DHFR abrogates the ability of p50 to inhibit processing of p105 and does not prevent nuclear translocation of free p50.	transcription
54644	4	335241	5	NULL	NULL	0	NULL	p50		free	is translocated to					nucleus					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_201	11350967	Panel B, substitution of four ankyrin repeats with DHFR abrogates the ability of p50 to inhibit processing of p105 and does not prevent nuclear translocation of free p50.	transcription
54645	5	335241	5	NULL	NULL	0	NULL	statement 1			does not prevent					statement 4					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_201	11350967	Panel B, substitution of four ankyrin repeats with DHFR abrogates the ability of p50 to inhibit processing of p105 and does not prevent nuclear translocation of free p50.	transcription
55737	1	335241	7	NULL	NULL	0	NULL	p50			inhibit					p105		processing of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_201	11350967	Panel B, substitution of four ankyrin repeats with DHFR abrogates the ability of p50 to inhibit processing of p105 and does not prevent nuclear translocation of free p50.	transcription
55738	2	335241	7	NULL	NULL	0	NULL				substituted with			 four ankyrin repeats		DHFR					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_201	11350967	Panel B, substitution of four ankyrin repeats with DHFR abrogates the ability of p50 to inhibit processing of p105 and does not prevent nuclear translocation of free p50.	transcription
55739	3	335241	7	NULL	NULL	0	NULL	statement 2			abrogates					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_201	11350967	Panel B, substitution of four ankyrin repeats with DHFR abrogates the ability of p50 to inhibit processing of p105 and does not prevent nuclear translocation of free p50.	transcription
55740	4	335241	7	NULL	NULL	0	NULL	statement 2			does not prevent					p50		nuclear translocation of free			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_201	11350967	Panel B, substitution of four ankyrin repeats with DHFR abrogates the ability of p50 to inhibit processing of p105 and does not prevent nuclear translocation of free p50.	transcription
54646	1	335242	5	NULL	NULL	0	NULL	p50			is generated from					p105					NULL	T2 cell extracts	0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_196	10671572	Impaired Processing of p50 in T2 Cell Extracts-- The generation of p50 from p105 is mediated by the ubiquitin-proteasome processing pathway ( 28,  44,  46,  61).	transcription
54647	2	335242	5	NULL	NULL	0	NULL	statement 1			is mediated by					ubiquitin-proteasome processing pathway					NULL	T2 cell extracts	0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_196	10671572	Impaired Processing of p50 in T2 Cell Extracts-- The generation of p50 from p105 is mediated by the ubiquitin-proteasome processing pathway ( 28,  44,  46,  61).	transcription
55741	1	335242	7	NULL	NULL	0	NULL	 p50 			generated from					p105					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_196	10671572	Impaired Processing of p50 in T2 Cell Extracts-- The generation of p50 from p105 is mediated by the ubiquitin-proteasome processing pathway ( 28,  44,  46,  61).	transcription
55742	2	335242	7	NULL	NULL	0	NULL	statement 1			mediated by					ubiquitin-proteasome processing pathway					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_196	10671572	Impaired Processing of p50 in T2 Cell Extracts-- The generation of p50 from p105 is mediated by the ubiquitin-proteasome processing pathway ( 28,  44,  46,  61).	transcription
55743	3	335242	7	NULL	NULL	0	NULL	p50		processing of	impaired in					T2 Cell Extracts					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_196	10671572	Impaired Processing of p50 in T2 Cell Extracts-- The generation of p50 from p105 is mediated by the ubiquitin-proteasome processing pathway ( 28,  44,  46,  61).	transcription
54648	1	335243	5	NULL	NULL	0	NULL	p105			is processed to					p50					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_545_s_147	15020252	This is because  degradation of I B and processing of p105 to p50 are mediated by the ubiquitin/proteasome  system [ 3.	transcription
54649	2	335243	5	NULL	NULL	0	NULL	ubiquitin/proteasome system			mediates					statement 1					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_545_s_147	15020252	This is because  degradation of I B and processing of p105 to p50 are mediated by the ubiquitin/proteasome  system [ 3.	transcription
54650	3	335243	5	NULL	NULL	0	NULL	ubiquitin/proteasome system			mediates					I B		degradation of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_545_s_147	15020252	This is because  degradation of I B and processing of p105 to p50 are mediated by the ubiquitin/proteasome  system [ 3.	transcription
55744	1	335243	7	NULL	NULL	0	NULL	I B		 degradation of	is mediated by					ubiquitin/proteasome system					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_545_s_147	15020252	This is because  degradation of I B and processing of p105 to p50 are mediated by the ubiquitin/proteasome  system [ 3.	transcription
55745	2	335243	7	NULL	NULL	0	NULL	p105			processed to					p50					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_545_s_147	15020252	This is because  degradation of I B and processing of p105 to p50 are mediated by the ubiquitin/proteasome  system [ 3.	transcription
55746	3	335243	7	NULL	NULL	0	NULL	statement 2			mediated by					ubiquitin/proteasome system					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_316_2_545_s_147	15020252	This is because  degradation of I B and processing of p105 to p50 are mediated by the ubiquitin/proteasome  system [ 3.	transcription
54651	1	335244	5	NULL	NULL	0	NULL	GSK-3beta			regulates					NF-kappaB					NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_23	16192643	GSK-3beta regulates NF-kappaB by phosphorylating its p65 transactivation subunit   and by phosphorylating and stabilizing p105, the precursor of its p50 subunit.	transcription
54652	2	335244	5	NULL	NULL	0	NULL	GSK-3beta			phosphorylates					NF-kappaB			p65 subuint		NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_23	16192643	GSK-3beta regulates NF-kappaB by phosphorylating its p65 transactivation subunit   and by phosphorylating and stabilizing p105, the precursor of its p50 subunit.	transcription
54653	3	335244	5	NULL	NULL	0	NULL	statement 2			leads to					statement 1					NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_23	16192643	GSK-3beta regulates NF-kappaB by phosphorylating its p65 transactivation subunit   and by phosphorylating and stabilizing p105, the precursor of its p50 subunit.	transcription
54654	4	335244	5	NULL	NULL	0	NULL	NF-kappaB			is a type of			p65 subunit		transactivation subunit					NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_23	16192643	GSK-3beta regulates NF-kappaB by phosphorylating its p65 transactivation subunit   and by phosphorylating and stabilizing p105, the precursor of its p50 subunit.	transcription
54655	5	335244	5	NULL	NULL	0	NULL	p105			is a precursor of								p50 subunit		NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_23	16192643	GSK-3beta regulates NF-kappaB by phosphorylating its p65 transactivation subunit   and by phosphorylating and stabilizing p105, the precursor of its p50 subunit.	transcription
54656	6	335244	5	NULL	NULL	0	NULL	GSK-3beta			stabilize					p105					NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_23	16192643	GSK-3beta regulates NF-kappaB by phosphorylating its p65 transactivation subunit   and by phosphorylating and stabilizing p105, the precursor of its p50 subunit.	transcription
55747	1	335244	7	NULL	NULL	0	NULL	GSK-3beta			regulates					NF-kappaB					NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_23	16192643	GSK-3beta regulates NF-kappaB by phosphorylating its p65 transactivation subunit   and by phosphorylating and stabilizing p105, the precursor of its p50 subunit.	transcription
55748	2	335244	7	NULL	NULL	0	NULL	statement 1			occur by					p65		phosphorylation of	transactivation subunit		NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_23	16192643	GSK-3beta regulates NF-kappaB by phosphorylating its p65 transactivation subunit   and by phosphorylating and stabilizing p105, the precursor of its p50 subunit.	transcription
55749	3	335244	7	NULL	NULL	0	NULL	statement 1			occur by					p105		phosphorylating;;stabilizing			NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_23	16192643	GSK-3beta regulates NF-kappaB by phosphorylating its p65 transactivation subunit   and by phosphorylating and stabilizing p105, the precursor of its p50 subunit.	transcription
55750	4	335244	7	NULL	NULL	0	NULL	p105			is a precursor of					p50 subunit					NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_23	16192643	GSK-3beta regulates NF-kappaB by phosphorylating its p65 transactivation subunit   and by phosphorylating and stabilizing p105, the precursor of its p50 subunit.	transcription
54657	1	335245	5	NULL	NULL	0	NULL	p105			is a regulator of		negative			TPL-2					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_26	15169888	Thus, in addition to its roles as a precursor for p50 and an IkappaB, p105 functions as a negative regulator of TPL-2.	transcription
54658	2	335245	5	NULL	NULL	0	NULL	p105			is a precursor of					p50					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_26	15169888	Thus, in addition to its roles as a precursor for p50 and an IkappaB, p105 functions as a negative regulator of TPL-2.	transcription
54659	3	335245	5	NULL	NULL	0	NULL	p105			is a precursor of					IkappaB					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_26	15169888	Thus, in addition to its roles as a precursor for p50 and an IkappaB, p105 functions as a negative regulator of TPL-2.	transcription
55751	1	335245	7	NULL	NULL	0	NULL	p105			is a precursor of					p50					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_26	15169888	Thus, in addition to its roles as a precursor for p50 and an IkappaB, p105 functions as a negative regulator of TPL-2.	transcription
55752	2	335245	7	NULL	NULL	0	NULL	p105			is a precursor of					IkappaB					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_26	15169888	Thus, in addition to its roles as a precursor for p50 and an IkappaB, p105 functions as a negative regulator of TPL-2.	transcription
55753	3	335245	7	NULL	NULL	0	NULL	p105			regulates		negatively			 TPL-2					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_26	15169888	Thus, in addition to its roles as a precursor for p50 and an IkappaB, p105 functions as a negative regulator of TPL-2.	transcription
54660	1	335246	5	NULL	NULL	0	NULL	nfkb1 gene			encodes					p50					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_2	12807880	he NF-kappaB transcription factor p50 and the Rel protein-specific  transcription inhibitor p105 are both encoded by the  nfkb1 gene.	transcription
54661	2	335246	5	NULL	NULL	0	NULL	nfkb1 gene			encodes					p105					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_2	12807880	he NF-kappaB transcription factor p50 and the Rel protein-specific  transcription inhibitor p105 are both encoded by the  nfkb1 gene.	transcription
54662	3	335246	5	NULL	NULL	0	NULL	p105			is a type of					Rel protein-specific transcription inhibitor					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_2	12807880	he NF-kappaB transcription factor p50 and the Rel protein-specific  transcription inhibitor p105 are both encoded by the  nfkb1 gene.	transcription
54663	4	335246	5	NULL	NULL	0	NULL	p50			is a type of					NF-kappaB transcription factor					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_2	12807880	he NF-kappaB transcription factor p50 and the Rel protein-specific  transcription inhibitor p105 are both encoded by the  nfkb1 gene.	transcription
55754	1	335246	7	NULL	NULL	0	NULL	 nfkb1 gene			encode					p50					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_2	12807880	he NF-kappaB transcription factor p50 and the Rel protein-specific  transcription inhibitor p105 are both encoded by the  nfkb1 gene.	transcription
55755	2	335246	7	NULL	NULL	0	NULL	 nfkb1 gene			encode					p105					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_2	12807880	he NF-kappaB transcription factor p50 and the Rel protein-specific  transcription inhibitor p105 are both encoded by the  nfkb1 gene.	transcription
55756	3	335246	7	NULL	NULL	0	NULL	p50			is a type of					NF-kappaB transcription factor					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_2	12807880	he NF-kappaB transcription factor p50 and the Rel protein-specific  transcription inhibitor p105 are both encoded by the  nfkb1 gene.	transcription
55757	4	335246	7	NULL	NULL	0	NULL	p105			is a type of					Rel protein-specific transcription inhibitor					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_2	12807880	he NF-kappaB transcription factor p50 and the Rel protein-specific  transcription inhibitor p105 are both encoded by the  nfkb1 gene.	transcription
54664	1	335247	5	NULL	NULL	0	NULL	SCFbetaTrCP complex			bind					p105					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_20	12807880	The binding of the SCFbetaTrCP complex to p105 was  originally attributed to enhancement of p50 generation upon stimulation  ( ,   ).	transcription
55758	1	335247	7	NULL	NULL	0	NULL	SCFbetaTrCP complex			bind					p105					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_20	12807880	The binding of the SCFbetaTrCP complex to p105 was  originally attributed to enhancement of p50 generation upon stimulation  ( ,   ).	transcription
55759	2	335247	7	NULL	NULL	0	NULL	statement 1			occurs upon					p50		enhancement of;; generation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_20	12807880	The binding of the SCFbetaTrCP complex to p105 was  originally attributed to enhancement of p50 generation upon stimulation  ( ,   ).	transcription
55760	3	335247	7	NULL	NULL	0	NULL	statement 2			occurs upon					stimulation					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_20	12807880	The binding of the SCFbetaTrCP complex to p105 was  originally attributed to enhancement of p50 generation upon stimulation  ( ,   ).	transcription
54665	1	335248	5	NULL	NULL	0	NULL	p105		deletion mutant	does not effect			C terminus		p50		level of			NULL	resting cells	0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_184	12807880	B, deletion of the C terminus of p105 does not affect p50 level in  resting cells.	transcription
55761	1	335248	7	NULL	NULL	0	NULL	p105		deletion of	does not affect			C terminus		p50		level of			NULL	resting cells	0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_184	12807880	B, deletion of the C terminus of p105 does not affect p50 level in  resting cells.	transcription
54666	1	335249	5	NULL	NULL	0	NULL	TNF-alpha			fails to induce					p105		degradation of			NULL	GSK-3beta - / - fibroblasts	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_41_39583_s_186	12871932	On the contrary, in  GSK-3beta - / -  fibroblasts p50 appears to accumulate significantly in the control chase, while TNF-alpha fails to induce p105 degradation.	transcription
55762	1	335249	7	NULL	NULL	0	NULL	TNF-alpha			does not induce					p105		degradation of			NULL	GSK-3beta - / - fibroblasts 	0	NULL	NULL	NULL	gw70_jbiolchem_278_41_39583_s_186	12871932	On the contrary, in  GSK-3beta - / -  fibroblasts p50 appears to accumulate significantly in the control chase, while TNF-alpha fails to induce p105 degradation.	transcription
54678	1	335250	5	NULL	NULL	0	NULL	p105			is associated with		predominantly			p50					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_322	10469655	Depending on relative expression levels, p105 is associated predominantly with p50, generated by constitutive processing, or with other NF-kappaB subunits.	transcription
54679	2	335250	5	NULL	NULL	0	NULL	p50			is generated by					p105		constitutive processing of			NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_322	10469655	Depending on relative expression levels, p105 is associated predominantly with p50, generated by constitutive processing, or with other NF-kappaB subunits.	transcription
54680	3	335250	5	NULL	NULL	0	NULL	p105			is associated with					NF-kappaB subunits					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_322	10469655	Depending on relative expression levels, p105 is associated predominantly with p50, generated by constitutive processing, or with other NF-kappaB subunits.	transcription
55763	1	335250	7	NULL	NULL	0	NULL	p105			associate with		predominantly			p50					NULL		NULL	NULL	NULL	NULL	gw60_embo_18_17_4766_s_322	10469655	Depending on relative expression levels, p105 is associated predominantly with p50, generated by constitutive processing, or with other NF-kappaB subunits.	transcription
55764	2	335250	7	NULL	NULL	0	NULL	p50			generated by					constitutive processing					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_322	10469655	Depending on relative expression levels, p105 is associated predominantly with p50, generated by constitutive processing, or with other NF-kappaB subunits.	transcription
55765	3	335250	7	NULL	NULL	0	NULL	p105			associate with					NF-kappaB 			subunits		NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_322	10469655	Depending on relative expression levels, p105 is associated predominantly with p50, generated by constitutive processing, or with other NF-kappaB subunits.	transcription
54681	1	335251	5	NULL	NULL	0	NULL	p105 gene		expression of	is regulated by					NF-kappaB					NULL		0	NULL	NULL	NULL	gw60_genesdev_15_18_2321_s_214	11562344	Regulated processing is difficult to demonstrate for p50 because expression of the p105 gene is itself regulated by NF-kappaB.	transcription
55766	1	335251	7	NULL	NULL	0	NULL	 NF-kappaB			regulates					p105 gene		expression of			NULL		0	NULL	NULL	NULL	gw60_genesdev_15_18_2321_s_214	11562344	Regulated processing is difficult to demonstrate for p50 because expression of the p105 gene is itself regulated by NF-kappaB.	transcription
54682	1	335252	5	NULL	NULL	0	NULL	p50			corresponds to					p105			N terminus		NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_3	9529257	p50  corresponds to the N terminus of p105 and with p65 (RelA) forms the  prototypical NF- B transcription factor complex.	transcription
54683	2	335252	5	NULL	NULL	0	NULL	p65			is a synonym of					RelA					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_3	9529257	p50  corresponds to the N terminus of p105 and with p65 (RelA) forms the  prototypical NF- B transcription factor complex.	transcription
54684	3	335252	5	NULL	NULL	0	NULL	p65			forms					NF- B transcription factor complex		prototypical			NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_3	9529257	p50  corresponds to the N terminus of p105 and with p65 (RelA) forms the  prototypical NF- B transcription factor complex.	transcription
55767	1	335252	7	NULL	NULL	0	NULL	p50			corresponds to					p105			N terminus		NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_3	9529257	p50  corresponds to the N terminus of p105 and with p65 (RelA) forms the  prototypical NF- B transcription factor complex.	transcription
55768	2	335252	7	NULL	NULL	0	NULL	p50			associate with					p65					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_3	9529257	p50  corresponds to the N terminus of p105 and with p65 (RelA) forms the  prototypical NF- B transcription factor complex.	transcription
55769	3	335252	7	NULL	NULL	0	NULL	statement 2			forms					NF- B transcription factor complex		prototypical			NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_3	9529257	p50  corresponds to the N terminus of p105 and with p65 (RelA) forms the  prototypical NF- B transcription factor complex.	transcription
54685	1	335253	5	NULL	NULL	0	NULL	NF- B			is a type of					transcription factor					NULL		0	NULL	NULL	NULL	gw60_molcell_7_3_627_s_30	11463387	The transcription factor NF- B subunit p50 is produced by partial proteolysis of the p105 precursor protein by the proteasome.	transcription
54686	2	335253	5	NULL	NULL	0	NULL	p105 precursor protein			undergoes					proteolysis		partial			NULL		0	NULL	NULL	NULL	gw60_molcell_7_3_627_s_30	11463387	The transcription factor NF- B subunit p50 is produced by partial proteolysis of the p105 precursor protein by the proteasome.	transcription
54687	3	335253	5	NULL	NULL	0	NULL	proteasome			is required for					statement 1					NULL		0	NULL	NULL	NULL	gw60_molcell_7_3_627_s_30	11463387	The transcription factor NF- B subunit p50 is produced by partial proteolysis of the p105 precursor protein by the proteasome.	transcription
54689	4	335253	5	NULL	NULL	0	NULL	statement 2			produces					NF- B			p50 subunit		NULL		0	NULL	NULL	NULL	gw60_molcell_7_3_627_s_30	11463387	The transcription factor NF- B subunit p50 is produced by partial proteolysis of the p105 precursor protein by the proteasome.	transcription
55770	1	335253	7	NULL	NULL	0	NULL	p50 			produced by					p105 precursor protein		partial proteolysis of 			NULL		0	NULL	NULL	NULL	gw60_molcell_7_3_627_s_30	11463387	The transcription factor NF- B subunit p50 is produced by partial proteolysis of the p105 precursor protein by the proteasome.	transcription
55771	2	335253	7	NULL	NULL	0	NULL	statement 1			occur by					proteasome					NULL		0	NULL	NULL	NULL	gw60_molcell_7_3_627_s_30	11463387	The transcription factor NF- B subunit p50 is produced by partial proteolysis of the p105 precursor protein by the proteasome.	transcription
55772	3	335253	7	NULL	NULL	0	NULL	 p50			is subunit of					NF- B transcription factor					NULL		0	NULL	NULL	NULL	gw60_molcell_7_3_627_s_30	11463387	The transcription factor NF- B subunit p50 is produced by partial proteolysis of the p105 precursor protein by the proteasome.	transcription
54690	1	335254	5	NULL	NULL	0	NULL	TNF-alpha			induces					p105		degradation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_42	11158290	TNF-alpha-induced p105 degradation rapidly releases p105-bound p50, which is detected in the nucleus as dimers complexed with Bcl-3 ( 13).	transcription
54691	3	335254	5	NULL	NULL	0	NULL	statement 1			releases		rapidly			statement 2					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_42	11158290	TNF-alpha-induced p105 degradation rapidly releases p105-bound p50, which is detected in the nucleus as dimers complexed with Bcl-3 ( 13).	transcription
54692	2	335254	5	NULL	NULL	0	NULL	p50			bind					p105					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_42	11158290	TNF-alpha-induced p105 degradation rapidly releases p105-bound p50, which is detected in the nucleus as dimers complexed with Bcl-3 ( 13).	transcription
54693	4	335254	5	NULL	NULL	0	NULL	statement 2			complexes with					Bcl-3					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_42	11158290	TNF-alpha-induced p105 degradation rapidly releases p105-bound p50, which is detected in the nucleus as dimers complexed with Bcl-3 ( 13).	transcription
55773	1	335254	7	NULL	NULL	0	NULL	TNF-alpha			induce					p105		degradation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_42	11158290	TNF-alpha-induced p105 degradation rapidly releases p105-bound p50, which is detected in the nucleus as dimers complexed with Bcl-3 ( 13).	transcription
55774	2	335254	7	NULL	NULL	0	NULL	p50			bind					p105					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_42	11158290	TNF-alpha-induced p105 degradation rapidly releases p105-bound p50, which is detected in the nucleus as dimers complexed with Bcl-3 ( 13).	transcription
55775	3	335254	7	NULL	NULL	0	NULL	statement 1			release		rapidly			statement 2					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_42	11158290	TNF-alpha-induced p105 degradation rapidly releases p105-bound p50, which is detected in the nucleus as dimers complexed with Bcl-3 ( 13).	transcription
55776	4	335254	7	NULL	NULL	0	NULL	statement 2			complexed with					Bcl-3					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_42	11158290	TNF-alpha-induced p105 degradation rapidly releases p105-bound p50, which is detected in the nucleus as dimers complexed with Bcl-3 ( 13).	transcription
55777	5	335254	7	NULL	NULL	0	NULL	statement 4			detected as					dimers					NULL	nucleus	0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_42	11158290	TNF-alpha-induced p105 degradation rapidly releases p105-bound p50, which is detected in the nucleus as dimers complexed with Bcl-3 ( 13).	transcription
54694	1	335255	5	NULL	NULL	0	NULL	p105			is a regulator of		negative			TPL-2					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_14_4739_s_9	12832462	Thus, in addition to its role as a precursor for p50 and cytoplasmic inhibitor of NF-kappaB, p105 is a negative regulator of TPL-2.	transcription
54695	2	335255	5	NULL	NULL	0	NULL	p105			is a precursor for					p50					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_14_4739_s_9	12832462	Thus, in addition to its role as a precursor for p50 and cytoplasmic inhibitor of NF-kappaB, p105 is a negative regulator of TPL-2.	transcription
54696	3	335255	5	NULL	NULL	0	NULL	p105			is an inhibitor of					NF-kappaB					NULL	cytoplasm	0	NULL	NULL	NULL	gw60_molcellbiol_23_14_4739_s_9	12832462	Thus, in addition to its role as a precursor for p50 and cytoplasmic inhibitor of NF-kappaB, p105 is a negative regulator of TPL-2.	transcription
55778	1	335255	7	NULL	NULL	0	NULL	p105			is a precursor of					p50					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_14_4739_s_9	12832462	Thus, in addition to its role as a precursor for p50 and cytoplasmic inhibitor of NF-kappaB, p105 is a negative regulator of TPL-2.	transcription
55779	2	335255	7	NULL	NULL	0	NULL	p105			is a precursor of					NF-kappaB					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_14_4739_s_9	12832462	Thus, in addition to its role as a precursor for p50 and cytoplasmic inhibitor of NF-kappaB, p105 is a negative regulator of TPL-2.	transcription
55780	3	335255	7	NULL	NULL	0	NULL	p105			regulates		negatively			TPL-2					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_14_4739_s_9	12832462	Thus, in addition to its role as a precursor for p50 and cytoplasmic inhibitor of NF-kappaB, p105 is a negative regulator of TPL-2.	transcription
55781	4	335255	7	NULL	NULL	0	NULL	NF-kappaB			is a type of					cytoplasmic inhibitor					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_14_4739_s_9	12832462	Thus, in addition to its role as a precursor for p50 and cytoplasmic inhibitor of NF-kappaB, p105 is a negative regulator of TPL-2.	transcription
54697	1	335256	5	NULL	NULL	0	NULL	NF-kappaB1			is a regulator of		negative	p105		TPL-2					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_14_4739_s_363	12832462	NF-kappaB1 p105 is therefore a negative regulator of TPL-2 MEK kinase, in addition to its functions as a precursor for p50 and an IkappaB protein ( 18).	transcription
54698	2	335256	5	NULL	NULL	0	NULL	TPL-2			is a type of					MEK kinase					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_14_4739_s_363	12832462	NF-kappaB1 p105 is therefore a negative regulator of TPL-2 MEK kinase, in addition to its functions as a precursor for p50 and an IkappaB protein ( 18).	transcription
54699	3	335256	5	NULL	NULL	0	NULL	NF-kappaB1			function as			p105		p50		precursor of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_14_4739_s_363	12832462	NF-kappaB1 p105 is therefore a negative regulator of TPL-2 MEK kinase, in addition to its functions as a precursor for p50 and an IkappaB protein ( 18).	transcription
54700	4	335256	5	NULL	NULL	0	NULL	NF-kappaB1			is a type of			p105		IkappaB protein					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_14_4739_s_363	12832462	NF-kappaB1 p105 is therefore a negative regulator of TPL-2 MEK kinase, in addition to its functions as a precursor for p50 and an IkappaB protein ( 18).	transcription
55782	1	335256	7	NULL	NULL	0	NULL	NF-kappaB1 p105			regulates		negatively			TPL-2 MEK kinase					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_14_4739_s_363	12832462	NF-kappaB1 p105 is therefore a negative regulator of TPL-2 MEK kinase, in addition to its functions as a precursor for p50 and an IkappaB protein ( 18).	transcription
55783	2	335256	7	NULL	NULL	0	NULL	NF-kappaB1 p105			is a precursor of					p50 dimer					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_14_4739_s_363	12832462	NF-kappaB1 p105 is therefore a negative regulator of TPL-2 MEK kinase, in addition to its functions as a precursor for p50 and an IkappaB protein ( 18).	transcription
55784	3	335256	7	NULL	NULL	0	NULL	NF-kappaB1 p105			is a precursor of					IkappaB protein					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_14_4739_s_363	12832462	NF-kappaB1 p105 is therefore a negative regulator of TPL-2 MEK kinase, in addition to its functions as a precursor for p50 and an IkappaB protein ( 18).	transcription
54701	1	335257	5	NULL	NULL	0	NULL	NF-kappaB1			function as			p105		NF-kappaB1		precursor of	p50		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_1_402_s_2	12482991	F-kappaB1 p105 functions both as a precursor of NF-kappaB1 p50 and as a cytoplasmic inhibitor of NF-kappaB.	transcription
54702	2	335257	5	NULL	NULL	0	NULL	NF-kappaB1			is an inhibitor of			p105		NF-kappaB					NULL	cytoplasm	0	NULL	NULL	NULL	gw60_molcellbiol_23_1_402_s_2	12482991	F-kappaB1 p105 functions both as a precursor of NF-kappaB1 p50 and as a cytoplasmic inhibitor of NF-kappaB.	transcription
55785	1	335257	7	NULL	NULL	0	NULL	F-kappaB1 p105			is a precursor of					NF-kappaB1 p50					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_1_402_s_2	12482991	F-kappaB1 p105 functions both as a precursor of NF-kappaB1 p50 and as a cytoplasmic inhibitor of NF-kappaB.	transcription
55786	2	335257	7	NULL	NULL	0	NULL	F-kappaB1 p105			is a precursor of					NF-kappaB					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_1_402_s_2	12482991	F-kappaB1 p105 functions both as a precursor of NF-kappaB1 p50 and as a cytoplasmic inhibitor of NF-kappaB.	transcription
55787	3	335257	7	NULL	NULL	0	NULL	NF-kappaB			is a type of					cytoplasmic inhibitor					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_1_402_s_2	12482991	F-kappaB1 p105 functions both as a precursor of NF-kappaB1 p50 and as a cytoplasmic inhibitor of NF-kappaB.	transcription
55788	1	335258	7	NULL	NULL	0	NULL	TNF			stimulate					LNCaP cells					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_13_11116_s_178	11799112	D, p50 activity was measured as a function of p105 processing in TNF-stimulated LNCaP cells expressing either GFP or PTEN.	transcription
55789	2	335258	7	NULL	NULL	0	NULL	statement 1			express					GFP					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_13_11116_s_178	11799112	D, p50 activity was measured as a function of p105 processing in TNF-stimulated LNCaP cells expressing either GFP or PTEN.	transcription
55790	3	335258	7	NULL	NULL	0	NULL	statement 1			express					PTEN					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_13_11116_s_178	11799112	D, p50 activity was measured as a function of p105 processing in TNF-stimulated LNCaP cells expressing either GFP or PTEN.	transcription
55791	4	335258	7	NULL	NULL	0	NULL	statement 2			is an alternative to					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_13_11116_s_178	11799112	D, p50 activity was measured as a function of p105 processing in TNF-stimulated LNCaP cells expressing either GFP or PTEN.	transcription
54703	1	335259	5	NULL	NULL	0	NULL	p105		cleavage of	is mediated by					proteasome					NULL	T2 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_231	10671572	Overall, these data suggest that the defect in p50 generation in T2 cells is due to a failure of proteasome-mediated cleavage of p105.	transcription
54704	2	335259	5	NULL	NULL	0	NULL	statement 1		failure of	leads to					p50		defect in generation of			NULL	T2 cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_231	10671572	Overall, these data suggest that the defect in p50 generation in T2 cells is due to a failure of proteasome-mediated cleavage of p105.	transcription
55793	1	335259	7	NULL	NULL	0	NULL	proteasome			mediates					p105		cleavage of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_231	10671572	Overall, these data suggest that the defect in p50 generation in T2 cells is due to a failure of proteasome-mediated cleavage of p105.	transcription
55794	2	335259	7	NULL	NULL	0	NULL	p50		defect in generation of	is due to					statement 1		failure of			NULL	T2 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_231	10671572	Overall, these data suggest that the defect in p50 generation in T2 cells is due to a failure of proteasome-mediated cleavage of p105.	transcription
54705	1	335261	5	NULL	NULL	0	NULL	p105			is a synonym of					NF-kappaB1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_5	8537390	Here, we report a  novel mechanism of NF-kappaB regulation mediated by p105 (NF-kappaB1)  precursor of p50 directly at the nuclear level.	transcription
54706	2	335261	5	NULL	NULL	0	NULL	p105			is a precursor of					p50					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_5	8537390	Here, we report a  novel mechanism of NF-kappaB regulation mediated by p105 (NF-kappaB1)  precursor of p50 directly at the nuclear level.	transcription
54707	3	335261	5	NULL	NULL	0	NULL	NF-kappaB		regulation of	is mediated by		directly			p105					NULL	nuclear level	0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_5	8537390	Here, we report a  novel mechanism of NF-kappaB regulation mediated by p105 (NF-kappaB1)  precursor of p50 directly at the nuclear level.	transcription
55795	1	335261	7	NULL	NULL	0	NULL	p105			mediates					NF-kappaB 		regulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_5	8537390	Here, we report a  novel mechanism of NF-kappaB regulation mediated by p105 (NF-kappaB1)  precursor of p50 directly at the nuclear level.	transcription
55806	2	335261	7	NULL	NULL	0	NULL	p105			is a precursor of					p50					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_5	8537390	Here, we report a  novel mechanism of NF-kappaB regulation mediated by p105 (NF-kappaB1)  precursor of p50 directly at the nuclear level.	transcription
55807	3	335261	7	NULL	NULL	0	NULL	p105			is					NF-kappaB1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_5	8537390	Here, we report a  novel mechanism of NF-kappaB regulation mediated by p105 (NF-kappaB1)  precursor of p50 directly at the nuclear level.	transcription
55808	4	335261	7	NULL	NULL	0	NULL	statement 1			occurs at					nuclear level					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_5	8537390	Here, we report a  novel mechanism of NF-kappaB regulation mediated by p105 (NF-kappaB1)  precursor of p50 directly at the nuclear level.	transcription
54708	1	335262	5	NULL	NULL	0	NULL	mitomycin C			activates					NF-kappaB					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_157	8537390	Interestingly, concomitantly with  NF-kappaB activation by mitomycin C, p105 was processed to p50 in the  nucleus but not in the cytoplasm.	transcription
54709	2	335262	5	NULL	NULL	0	NULL	p105			is processed to					p50					NULL	nucleus	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_157	8537390	Interestingly, concomitantly with  NF-kappaB activation by mitomycin C, p105 was processed to p50 in the  nucleus but not in the cytoplasm.	transcription
54710	3	335262	5	NULL	NULL	0	NULL	statement 1			is concomitant to					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_157	8537390	Interestingly, concomitantly with  NF-kappaB activation by mitomycin C, p105 was processed to p50 in the  nucleus but not in the cytoplasm.	transcription
55809	1	335262	7	NULL	NULL	0	NULL	mitomycin C			activate					NF-kappaB					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_157	8537390	Interestingly, concomitantly with  NF-kappaB activation by mitomycin C, p105 was processed to p50 in the  nucleus but not in the cytoplasm.	transcription
55810	2	335262	7	NULL	NULL	0	NULL	p105			processed to					p50					NULL	nucleus	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_157	8537390	Interestingly, concomitantly with  NF-kappaB activation by mitomycin C, p105 was processed to p50 in the  nucleus but not in the cytoplasm.	transcription
55811	3	335262	7	NULL	NULL	0	NULL	statement 2			occurs upon					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_157	8537390	Interestingly, concomitantly with  NF-kappaB activation by mitomycin C, p105 was processed to p50 in the  nucleus but not in the cytoplasm.	transcription
55812	4	335262	7	NULL	NULL	0	NULL	p105			not processed to					p50					NULL	cytoplasm	0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_157	8537390	Interestingly, concomitantly with  NF-kappaB activation by mitomycin C, p105 was processed to p50 in the  nucleus but not in the cytoplasm.	transcription
54711	1	335263	5	NULL	NULL	0	NULL	C2-ceramide			induce					p105		processing of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15494_s_43	9624136	However, C2-ceramide can induce p105 processing, with NFkappaB complexes predominantly comprising p50 homodimers.	transcription
54712	2	335263	5	NULL	NULL	0	NULL	NFkappaB complexes			compromises		predominantly			p50 homodimers					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15494_s_43	9624136	However, C2-ceramide can induce p105 processing, with NFkappaB complexes predominantly comprising p50 homodimers.	transcription
55837	1	335263	7	NULL	NULL	0	NULL	C2-ceramide			induce					p105		processing of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15494_s_43	9624136	However, C2-ceramide can induce p105 processing, with NFkappaB complexes predominantly comprising p50 homodimers.	transcription
55838	2	335263	7	NULL	NULL	0	NULL	NFkappaB complexes			comprise		predominantly			p50 homodimers					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15494_s_43	9624136	However, C2-ceramide can induce p105 processing, with NFkappaB complexes predominantly comprising p50 homodimers.	transcription
54713	1	335264	5	NULL	NULL	0	NULL	NFkappaB1 gene			is autoregulated by		positively			NF-kappaB					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_27	9430676	Since the NFkappaB1 gene is positively autoregulated by NF-kappaB, the increase in p50 could result in the presence of more p105 ( 31).	transcription
54714	2	335264	5	NULL	NULL	0	NULL	p50		increase in	results in					p105		presence of more			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_27	9430676	Since the NFkappaB1 gene is positively autoregulated by NF-kappaB, the increase in p50 could result in the presence of more p105 ( 31).	transcription
54715	3	335264	5	NULL	NULL	0	NULL	statement 1			leads to					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_27	9430676	Since the NFkappaB1 gene is positively autoregulated by NF-kappaB, the increase in p50 could result in the presence of more p105 ( 31).	transcription
55839	1	335264	7	NULL	NULL	0	NULL	NF-kappaB			autoregulates		positively			NFkappaB1 gene					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_27	9430676	Since the NFkappaB1 gene is positively autoregulated by NF-kappaB, the increase in p50 could result in the presence of more p105 ( 31).	transcription
55840	2	335264	7	NULL	NULL	0	NULL	p50		increase in	in the presence of					p105					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_27	9430676	Since the NFkappaB1 gene is positively autoregulated by NF-kappaB, the increase in p50 could result in the presence of more p105 ( 31).	transcription
55841	3	335264	7	NULL	NULL	0	NULL	statement 2			follows					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_27	9430676	Since the NFkappaB1 gene is positively autoregulated by NF-kappaB, the increase in p50 could result in the presence of more p105 ( 31).	transcription
54716	1	335265	5	NULL	NULL	0	NULL	p105			is processed to					p50					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_150	9430676	The  cim5-1 strain also inhibited processing of p105 to p50 at the non-permissive temperature (Fig.  2,  lane 5).	transcription
54717	2	335265	5	NULL	NULL	0	NULL	cim5-1 strain			inhibits					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_150	9430676	The  cim5-1 strain also inhibited processing of p105 to p50 at the non-permissive temperature (Fig.  2,  lane 5).	transcription
55842	1	335265	7	NULL	NULL	0	NULL	p105			processed to					p50					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_150	9430676	The  cim5-1 strain also inhibited processing of p105 to p50 at the non-permissive temperature (Fig.  2,  lane 5).	transcription
55843	2	335265	7	NULL	NULL	0	NULL	cim5-1 strain			inhibits					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_150	9430676	The  cim5-1 strain also inhibited processing of p105 to p50 at the non-permissive temperature (Fig.  2,  lane 5).	transcription
55844	3	335265	7	NULL	NULL	0	NULL	statement 2			occurs at					non-permissive temperature 					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_150	9430676	The  cim5-1 strain also inhibited processing of p105 to p50 at the non-permissive temperature (Fig.  2,  lane 5).	transcription
54718	1	335266	5	NULL	NULL	0	NULL	NF-kappaB1			is a precursor of			p105		NF-kappaB1			p50		NULL		0	NULL	NULL	NULL	abs-batch0680-0699_mol-cell-biol_23_1_12482991_s_2	12482991	NF-kappaB1 p105 functions both as a precursor of NF-kappaB1 p50 and as  a cytoplasmic inhibitor of NF-kappaB.	transcription
54719	2	335266	5	NULL	NULL	0	NULL	NF-kappaB1			is an inhibitor of			p105		NF-kappaB					NULL	cytoplasm	0	NULL	NULL	NULL	abs-batch0680-0699_mol-cell-biol_23_1_12482991_s_2	12482991	NF-kappaB1 p105 functions both as a precursor of NF-kappaB1 p50 and as  a cytoplasmic inhibitor of NF-kappaB.	transcription
55845	1	335266	7	NULL	NULL	0	NULL	NF-kappaB1 p105			functions as a					NF-kappaB1 p50		precursor of			NULL		0	NULL	NULL	NULL	abs-batch0680-0699_mol-cell-biol_23_1_12482991_s_2	12482991	NF-kappaB1 p105 functions both as a precursor of NF-kappaB1 p50 and as  a cytoplasmic inhibitor of NF-kappaB.	transcription
55846	2	335266	7	NULL	NULL	0	NULL	NF-kappaB1 p105 			functions as a					NF-kappaB		 cytoplasmic inhibitor of			NULL		0	NULL	NULL	NULL	abs-batch0680-0699_mol-cell-biol_23_1_12482991_s_2	12482991	NF-kappaB1 p105 functions both as a precursor of NF-kappaB1 p50 and as  a cytoplasmic inhibitor of NF-kappaB.	transcription
54720	1	335267	5	NULL	NULL	0	NULL	p50			corresponds to					p105			N terminus		NULL		0	NULL	NULL	NULL	abs-batch0720-0739_cell_92_6_9529257_s_3	9529257	p50 corresponds to the N terminus of p105 and with p65 (RelA)  forms the prototypical NF-kappaB transcription factor complex.	transcription
54721	2	335267	5	NULL	NULL	0	NULL	p65			is a synonym of					RelA					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_cell_92_6_9529257_s_3	9529257	p50 corresponds to the N terminus of p105 and with p65 (RelA)  forms the prototypical NF-kappaB transcription factor complex.	transcription
54722	3	335267	5	NULL	NULL	0	NULL	p50			is a part of					NF-kappaB complex		prototypical			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_cell_92_6_9529257_s_3	9529257	p50 corresponds to the N terminus of p105 and with p65 (RelA)  forms the prototypical NF-kappaB transcription factor complex.	transcription
54723	4	335267	5	NULL	NULL	0	NULL	p65			is a part of					NF-kappaB complex		prototypical			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_cell_92_6_9529257_s_3	9529257	p50 corresponds to the N terminus of p105 and with p65 (RelA)  forms the prototypical NF-kappaB transcription factor complex.	transcription
54724	5	335267	5	NULL	NULL	0	NULL	statement 3			occurs along with					statement 4					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_cell_92_6_9529257_s_3	9529257	p50 corresponds to the N terminus of p105 and with p65 (RelA)  forms the prototypical NF-kappaB transcription factor complex.	transcription
54725	6	335267	5	NULL	NULL	0	NULL	NF-kappaB			is a type of					transcription factor					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_cell_92_6_9529257_s_3	9529257	p50 corresponds to the N terminus of p105 and with p65 (RelA)  forms the prototypical NF-kappaB transcription factor complex.	transcription
55847	1	335267	7	NULL	NULL	0	NULL	p50			corresponds to					p105			N terminus		NULL		0	NULL	NULL	NULL	abs-batch0720-0739_cell_92_6_9529257_s_3	9529257	p50 corresponds to the N terminus of p105 and with p65 (RelA)  forms the prototypical NF-kappaB transcription factor complex.	transcription
55848	2	335267	7	NULL	NULL	0	NULL	p50			associate with					p65					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_cell_92_6_9529257_s_3	9529257	p50 corresponds to the N terminus of p105 and with p65 (RelA)  forms the prototypical NF-kappaB transcription factor complex.	transcription
55849	3	335267	7	NULL	NULL	0	NULL	statement 2			forms					prototypical NF-kappaB transcription factor complex					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_cell_92_6_9529257_s_3	9529257	p50 corresponds to the N terminus of p105 and with p65 (RelA)  forms the prototypical NF-kappaB transcription factor complex.	transcription
55850	4	335267	7	NULL	NULL	0	NULL	p65			is					RelA					NULL		0	NULL	NULL	NULL	abs-batch0720-0739_cell_92_6_9529257_s_3	9529257	p50 corresponds to the N terminus of p105 and with p65 (RelA)  forms the prototypical NF-kappaB transcription factor complex.	transcription
54726	1	335268	5	NULL	NULL	0	NULL	GSK-3beta			phosphorylates					p105					NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_261	16192643	In addition, GSK-3beta phosphorylates the p105 precursor of the p50 member of the NF-kappaB dimer; this has the dual effect of slowing constitutive processing to p50 and accelerating the degradation of p50 on stimulation with TNF-alpha.	transcription
54727	2	335268	5	NULL	NULL	0	NULL	p105			is a precursor of					p50					NULL		NULL	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_261	16192643	In addition, GSK-3beta phosphorylates the p105 precursor of the p50 member of the NF-kappaB dimer; this has the dual effect of slowing constitutive processing to p50 and accelerating the degradation of p50 on stimulation with TNF-alpha.	transcription
54728	3	335268	5	NULL	NULL	0	NULL	p50			is a member of					NF-kappaB dimer					NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_261	16192643	In addition, GSK-3beta phosphorylates the p105 precursor of the p50 member of the NF-kappaB dimer; this has the dual effect of slowing constitutive processing to p50 and accelerating the degradation of p50 on stimulation with TNF-alpha.	transcription
54729	4	335268	5	NULL	NULL	0	NULL	p105			is processed to		constitutive			p50					NULL		NULL	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_261	16192643	In addition, GSK-3beta phosphorylates the p105 precursor of the p50 member of the NF-kappaB dimer; this has the dual effect of slowing constitutive processing to p50 and accelerating the degradation of p50 on stimulation with TNF-alpha.	transcription
54730	5	335268	5	NULL	NULL	0	NULL	statement 1			slows					statement 4					NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_261	16192643	In addition, GSK-3beta phosphorylates the p105 precursor of the p50 member of the NF-kappaB dimer; this has the dual effect of slowing constitutive processing to p50 and accelerating the degradation of p50 on stimulation with TNF-alpha.	transcription
54731	6	335268	5	NULL	NULL	0	NULL	statement 1			accelerates					p50		degradation of			NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_261	16192643	In addition, GSK-3beta phosphorylates the p105 precursor of the p50 member of the NF-kappaB dimer; this has the dual effect of slowing constitutive processing to p50 and accelerating the degradation of p50 on stimulation with TNF-alpha.	transcription
54732	7	335268	5	NULL	NULL	0	NULL	TNF-alpha		stimulation	leads to					statement 6					NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_261	16192643	In addition, GSK-3beta phosphorylates the p105 precursor of the p50 member of the NF-kappaB dimer; this has the dual effect of slowing constitutive processing to p50 and accelerating the degradation of p50 on stimulation with TNF-alpha.	transcription
55851	1	335268	7	NULL	NULL	0	NULL	 GSK-3beta			phosphorylates					NF-kappaB dimer		p105 precursor of;; p50 member of 			NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_261	16192643	In addition, GSK-3beta phosphorylates the p105 precursor of the p50 member of the NF-kappaB dimer; this has the dual effect of slowing constitutive processing to p50 and accelerating the degradation of p50 on stimulation with TNF-alpha.	transcription
55852	2	335268	7	NULL	NULL	0	NULL	statement 1			slows					p50		 constitutive processing to 			NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_261	16192643	In addition, GSK-3beta phosphorylates the p105 precursor of the p50 member of the NF-kappaB dimer; this has the dual effect of slowing constitutive processing to p50 and accelerating the degradation of p50 on stimulation with TNF-alpha.	transcription
55853	3	335268	7	NULL	NULL	0	NULL	TNF-alpha		stimulation with 	degrades					p50					NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_261	16192643	In addition, GSK-3beta phosphorylates the p105 precursor of the p50 member of the NF-kappaB dimer; this has the dual effect of slowing constitutive processing to p50 and accelerating the degradation of p50 on stimulation with TNF-alpha.	transcription
55854	4	335268	7	NULL	NULL	0	NULL	statement 1			accelerates					statement 3					NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_261	16192643	In addition, GSK-3beta phosphorylates the p105 precursor of the p50 member of the NF-kappaB dimer; this has the dual effect of slowing constitutive processing to p50 and accelerating the degradation of p50 on stimulation with TNF-alpha.	transcription
54733	1	335269	5	NULL	NULL	0	NULL	p105			bind					NF-kappaB protein					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_1_556_s_131	12399470	The fact that p105 binds to all NF-kappaB proteins and IkappaBgamma binds only to p50 dimers (any NF-kappaB dimer that contains at least one p50 subunit) suggests that the required p50 subunit in IkappaBgamma.	transcription
54734	2	335269	5	NULL	NULL	0	NULL	IkappaBgamma			bind					p50 dimers					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_1_556_s_131	12399470	The fact that p105 binds to all NF-kappaB proteins and IkappaBgamma binds only to p50 dimers (any NF-kappaB dimer that contains at least one p50 subunit) suggests that the required p50 subunit in IkappaBgamma.	transcription
55855	1	335269	7	NULL	NULL	0	NULL	 p105			bind					NF-kappaB proteins					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_1_556_s_131	12399470	The fact that p105 binds to all NF-kappaB proteins and IkappaBgamma binds only to p50 dimers (any NF-kappaB dimer that contains at least one p50 subunit) suggests that the required p50 subunit in IkappaBgamma.	transcription
55856	2	335269	7	NULL	NULL	0	NULL	 IkappaBgamma			bind		only			p50 dimer					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_1_556_s_131	12399470	The fact that p105 binds to all NF-kappaB proteins and IkappaBgamma binds only to p50 dimers (any NF-kappaB dimer that contains at least one p50 subunit) suggests that the required p50 subunit in IkappaBgamma.	transcription
55857	3	335269	7	NULL	NULL	0	NULL	statement 2			requires					 IkappaBgamma			p50 subunit		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_1_556_s_131	12399470	The fact that p105 binds to all NF-kappaB proteins and IkappaBgamma binds only to p50 dimers (any NF-kappaB dimer that contains at least one p50 subunit) suggests that the required p50 subunit in IkappaBgamma.	transcription
54735	1	335270	5	NULL	NULL	0	NULL	BCL-3			acts as					chaperone					NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_252	10970863	BCL-3 could act as a chaperone binding the p50 - p105 complex and promoting its disassembly while preserving the proper conformation in p50 for dimerization with other disassembled p50 monomers.	transcription
54736	2	335270	5	NULL	NULL	0	NULL	BCL-3			bind					p50 - p105 complex					NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_252	10970863	BCL-3 could act as a chaperone binding the p50 - p105 complex and promoting its disassembly while preserving the proper conformation in p50 for dimerization with other disassembled p50 monomers.	transcription
54737	3	335270	5	NULL	NULL	0	NULL	BCL-3			promotes					p50 - p105 complex		disassembly of			NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_252	10970863	BCL-3 could act as a chaperone binding the p50 - p105 complex and promoting its disassembly while preserving the proper conformation in p50 for dimerization with other disassembled p50 monomers.	transcription
54738	4	335270	5	NULL	NULL	0	NULL	statement 3			preserves					p50		proper conformation of			NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_252	10970863	BCL-3 could act as a chaperone binding the p50 - p105 complex and promoting its disassembly while preserving the proper conformation in p50 for dimerization with other disassembled p50 monomers.	transcription
54739	5	335270	5	NULL	NULL	0	NULL	p50			dimerize with					p50 monomers		disassembled			NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_252	10970863	BCL-3 could act as a chaperone binding the p50 - p105 complex and promoting its disassembly while preserving the proper conformation in p50 for dimerization with other disassembled p50 monomers.	transcription
54740	6	335270	5	NULL	NULL	0	NULL	statement 4			leads to					statement 5					NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_252	10970863	BCL-3 could act as a chaperone binding the p50 - p105 complex and promoting its disassembly while preserving the proper conformation in p50 for dimerization with other disassembled p50 monomers.	transcription
55858	1	335270	7	NULL	NULL	0	NULL	BCL-3			bind					p50 - p105 complex 					NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_252	10970863	BCL-3 could act as a chaperone binding the p50 - p105 complex and promoting its disassembly while preserving the proper conformation in p50 for dimerization with other disassembled p50 monomers.	transcription
55859	2	335270	7	NULL	NULL	0	NULL	BCL-3			act as a 					chaperone					NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_252	10970863	BCL-3 could act as a chaperone binding the p50 - p105 complex and promoting its disassembly while preserving the proper conformation in p50 for dimerization with other disassembled p50 monomers.	transcription
55860	3	335270	7	NULL	NULL	0	NULL	statement 1			promote					p50 - p105 complex		disassembly of			NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_252	10970863	BCL-3 could act as a chaperone binding the p50 - p105 complex and promoting its disassembly while preserving the proper conformation in p50 for dimerization with other disassembled p50 monomers.	transcription
55861	4	335270	7	NULL	NULL	0	NULL	BCL-3			preserve					p50		proper conformation of			NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_252	10970863	BCL-3 could act as a chaperone binding the p50 - p105 complex and promoting its disassembly while preserving the proper conformation in p50 for dimerization with other disassembled p50 monomers.	transcription
55862	5	335270	7	NULL	NULL	0	NULL	p50 			dimerize with					p50 monomers		disassembled			NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_252	10970863	BCL-3 could act as a chaperone binding the p50 - p105 complex and promoting its disassembly while preserving the proper conformation in p50 for dimerization with other disassembled p50 monomers.	transcription
55863	6	335270	7	NULL	NULL	0	NULL	statement 4			required for					statement 5					NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_252	10970863	BCL-3 could act as a chaperone binding the p50 - p105 complex and promoting its disassembly while preserving the proper conformation in p50 for dimerization with other disassembled p50 monomers.	transcription
54741	1	335271	5	NULL	NULL	0	NULL	p50			inhibits					p105		processing of			NULL	in vivo	0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_177	11350967	p50 Inhibits Processing of p105 in Vivo, and Inhibition Is Dependent on the Presence of the Ankyrin Repeat-containing Domain-- To test the effect of the ankyrin repeat domain and anchored p50 subunits on processing of p105  in vivo, we overexpressed p50- XbaI in cells that do not express the NF-kappaB cascade proteins.	transcription
54742	2	335271	5	NULL	NULL	0	NULL	statement 1			is dependent on							presence of	ankyrin repeat-containing domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_177	11350967	p50 Inhibits Processing of p105 in Vivo, and Inhibition Is Dependent on the Presence of the Ankyrin Repeat-containing Domain-- To test the effect of the ankyrin repeat domain and anchored p50 subunits on processing of p105  in vivo, we overexpressed p50- XbaI in cells that do not express the NF-kappaB cascade proteins.	transcription
55864	1	335271	7	NULL	NULL	0	NULL	p50			inhibits					p105		processing of			NULL	in vivo	0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_177	11350967	p50 Inhibits Processing of p105 in Vivo, and Inhibition Is Dependent on the Presence of the Ankyrin Repeat-containing Domain-- To test the effect of the ankyrin repeat domain and anchored p50 subunits on processing of p105  in vivo, we overexpressed p50- XbaI in cells that do not express the NF-kappaB cascade proteins.	transcription
55865	2	335271	7	NULL	NULL	0	NULL	statement 1			depends on							presence of	Ankyrin Repeat-containing Domain-		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_177	11350967	p50 Inhibits Processing of p105 in Vivo, and Inhibition Is Dependent on the Presence of the Ankyrin Repeat-containing Domain-- To test the effect of the ankyrin repeat domain and anchored p50 subunits on processing of p105  in vivo, we overexpressed p50- XbaI in cells that do not express the NF-kappaB cascade proteins.	transcription
54743	1	335272	5	NULL	NULL	0	NULL	BCL3			increases					p50 homodimers		quantity of			NULL	nucleus	0	NULL	NULL	NULL	gw60_jbiolchem_272_52_33132_s_290	9407099	Recently, it has been shown that BCL3 can increase the quantity of nuclear p50 homodimers by inducing a redistribution of the subunits of cytoplasmic heterodimers containing p50 and its precursor p105 to yield p50 homodimers that translocate to the nucleus; this occurs without an effect on processing of p105 ( 54).	transcription
54744	3	335272	5	NULL	NULL	0	NULL	BCL3			redistributes					statement 2					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_33132_s_290	9407099	Recently, it has been shown that BCL3 can increase the quantity of nuclear p50 homodimers by inducing a redistribution of the subunits of cytoplasmic heterodimers containing p50 and its precursor p105 to yield p50 homodimers that translocate to the nucleus; this occurs without an effect on processing of p105 ( 54).	transcription
54745	4	335272	5	NULL	NULL	0	NULL	statement 3			leads to					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_52_33132_s_290	9407099	Recently, it has been shown that BCL3 can increase the quantity of nuclear p50 homodimers by inducing a redistribution of the subunits of cytoplasmic heterodimers containing p50 and its precursor p105 to yield p50 homodimers that translocate to the nucleus; this occurs without an effect on processing of p105 ( 54).	transcription
54746	2	335272	5	NULL	NULL	0	NULL	p105 precursor			bind					p50					NULL	cytoplasm	0	NULL	NULL	NULL	gw60_jbiolchem_272_52_33132_s_290	9407099	Recently, it has been shown that BCL3 can increase the quantity of nuclear p50 homodimers by inducing a redistribution of the subunits of cytoplasmic heterodimers containing p50 and its precursor p105 to yield p50 homodimers that translocate to the nucleus; this occurs without an effect on processing of p105 ( 54).	transcription
54747	5	335272	5	NULL	NULL	0	NULL	statement 3			yields					p50 homodimers					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_33132_s_290	9407099	Recently, it has been shown that BCL3 can increase the quantity of nuclear p50 homodimers by inducing a redistribution of the subunits of cytoplasmic heterodimers containing p50 and its precursor p105 to yield p50 homodimers that translocate to the nucleus; this occurs without an effect on processing of p105 ( 54).	transcription
54748	6	335272	5	NULL	NULL	0	NULL	p50 homodimers			translocates to					nucleus					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_33132_s_290	9407099	Recently, it has been shown that BCL3 can increase the quantity of nuclear p50 homodimers by inducing a redistribution of the subunits of cytoplasmic heterodimers containing p50 and its precursor p105 to yield p50 homodimers that translocate to the nucleus; this occurs without an effect on processing of p105 ( 54).	transcription
54749	7	335272	5	NULL	NULL	0	NULL	statement 1			does not effect					p105		processing of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_33132_s_290	9407099	Recently, it has been shown that BCL3 can increase the quantity of nuclear p50 homodimers by inducing a redistribution of the subunits of cytoplasmic heterodimers containing p50 and its precursor p105 to yield p50 homodimers that translocate to the nucleus; this occurs without an effect on processing of p105 ( 54).	transcription
55866	1	335272	7	NULL	NULL	0	NULL	BCL3			increase					 p50 homodimers		quantity of;; nuclear			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_33132_s_290	9407099	Recently, it has been shown that BCL3 can increase the quantity of nuclear p50 homodimers by inducing a redistribution of the subunits of cytoplasmic heterodimers containing p50 and its precursor p105 to yield p50 homodimers that translocate to the nucleus; this occurs without an effect on processing of p105 ( 54).	transcription
55867	2	335272	7	NULL	NULL	0	NULL	p50			heterodimerize with					p105					NULL	cytoplasm	0	NULL	NULL	NULL	gw60_jbiolchem_272_52_33132_s_290	9407099	Recently, it has been shown that BCL3 can increase the quantity of nuclear p50 homodimers by inducing a redistribution of the subunits of cytoplasmic heterodimers containing p50 and its precursor p105 to yield p50 homodimers that translocate to the nucleus; this occurs without an effect on processing of p105 ( 54).	transcription
55868	3	335272	7	NULL	NULL	0	NULL	BCL3			induce					statement 2		redistribution of	subunits 		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_33132_s_290	9407099	Recently, it has been shown that BCL3 can increase the quantity of nuclear p50 homodimers by inducing a redistribution of the subunits of cytoplasmic heterodimers containing p50 and its precursor p105 to yield p50 homodimers that translocate to the nucleus; this occurs without an effect on processing of p105 ( 54).	transcription
55869	4	335272	7	NULL	NULL	0	NULL	statement 3			yield					p50 homodimers					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_33132_s_290	9407099	Recently, it has been shown that BCL3 can increase the quantity of nuclear p50 homodimers by inducing a redistribution of the subunits of cytoplasmic heterodimers containing p50 and its precursor p105 to yield p50 homodimers that translocate to the nucleus; this occurs without an effect on processing of p105 ( 54).	transcription
55870	5	335272	7	NULL	NULL	0	NULL	p50 homodimers			translocate to					nucleus					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_33132_s_290	9407099	Recently, it has been shown that BCL3 can increase the quantity of nuclear p50 homodimers by inducing a redistribution of the subunits of cytoplasmic heterodimers containing p50 and its precursor p105 to yield p50 homodimers that translocate to the nucleus; this occurs without an effect on processing of p105 ( 54).	transcription
55871	6	335272	7	NULL	NULL	0	NULL	statement 5			does not effect					p105		processing of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_33132_s_290	9407099	Recently, it has been shown that BCL3 can increase the quantity of nuclear p50 homodimers by inducing a redistribution of the subunits of cytoplasmic heterodimers containing p50 and its precursor p105 to yield p50 homodimers that translocate to the nucleus; this occurs without an effect on processing of p105 ( 54).	transcription
55872	7	335272	7	NULL	NULL	0	NULL	p105			is a precursor of					p50					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_33132_s_290	9407099	Recently, it has been shown that BCL3 can increase the quantity of nuclear p50 homodimers by inducing a redistribution of the subunits of cytoplasmic heterodimers containing p50 and its precursor p105 to yield p50 homodimers that translocate to the nucleus; this occurs without an effect on processing of p105 ( 54).	transcription
54750	1	335273	5	NULL	NULL	0	NULL				resides in			serines		p105			PEST domain		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_18	15169888	However, following cellular stimulation with ligands, such as TNF-alpha, two serines in the p105 PEST domain are rapidly phosphorylated by the IkappaB kinase (IKK) complex, triggering complete p105 degradation with little effect on processing to p50 ( ,  ,  ).	transcription
54751	2	335273	5	NULL	NULL	0	NULL	IKK			phosphorylates		rapidly			statement 1					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_18	15169888	However, following cellular stimulation with ligands, such as TNF-alpha, two serines in the p105 PEST domain are rapidly phosphorylated by the IkappaB kinase (IKK) complex, triggering complete p105 degradation with little effect on processing to p50 ( ,  ,  ).	transcription
54753	3	335273	5	NULL	NULL	0	NULL	IKK			is					IkappaB kinase complex					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_18	15169888	However, following cellular stimulation with ligands, such as TNF-alpha, two serines in the p105 PEST domain are rapidly phosphorylated by the IkappaB kinase (IKK) complex, triggering complete p105 degradation with little effect on processing to p50 ( ,  ,  ).	transcription
54754	4	335273	5	NULL	NULL	0	NULL	TNF-alpha			is a type of					ligand					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_18	15169888	However, following cellular stimulation with ligands, such as TNF-alpha, two serines in the p105 PEST domain are rapidly phosphorylated by the IkappaB kinase (IKK) complex, triggering complete p105 degradation with little effect on processing to p50 ( ,  ,  ).	transcription
54755	5	335273	5	NULL	NULL	0	NULL	TNF-alpha			stimulates					statement 2					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_18	15169888	However, following cellular stimulation with ligands, such as TNF-alpha, two serines in the p105 PEST domain are rapidly phosphorylated by the IkappaB kinase (IKK) complex, triggering complete p105 degradation with little effect on processing to p50 ( ,  ,  ).	transcription
54756	6	335273	5	NULL	NULL	0	NULL	statement 2			triggers					p105		complete degradation of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_18	15169888	However, following cellular stimulation with ligands, such as TNF-alpha, two serines in the p105 PEST domain are rapidly phosphorylated by the IkappaB kinase (IKK) complex, triggering complete p105 degradation with little effect on processing to p50 ( ,  ,  ).	transcription
54757	7	335273	5	NULL	NULL	0	NULL	p105			is processed to					p50					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_18	15169888	However, following cellular stimulation with ligands, such as TNF-alpha, two serines in the p105 PEST domain are rapidly phosphorylated by the IkappaB kinase (IKK) complex, triggering complete p105 degradation with little effect on processing to p50 ( ,  ,  ).	transcription
54758	8	335273	5	NULL	NULL	0	NULL	statement 6			does not effect					statement 7					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_18	15169888	However, following cellular stimulation with ligands, such as TNF-alpha, two serines in the p105 PEST domain are rapidly phosphorylated by the IkappaB kinase (IKK) complex, triggering complete p105 degradation with little effect on processing to p50 ( ,  ,  ).	transcription
55873	1	335273	7	NULL	NULL	0	NULL	TNF-alpha			stimulate					cells					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_18	15169888	However, following cellular stimulation with ligands, such as TNF-alpha, two serines in the p105 PEST domain are rapidly phosphorylated by the IkappaB kinase (IKK) complex, triggering complete p105 degradation with little effect on processing to p50 ( ,  ,  ).	transcription
55874	2	335273	7	NULL	NULL	0	NULL	IKK complex			phosphorylate		rapidly			p105			two serines in the PEST domain		NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_18	15169888	However, following cellular stimulation with ligands, such as TNF-alpha, two serines in the p105 PEST domain are rapidly phosphorylated by the IkappaB kinase (IKK) complex, triggering complete p105 degradation with little effect on processing to p50 ( ,  ,  ).	transcription
55875	3	335273	7	NULL	NULL	0	NULL	statement 2			is followed by 					statement 1					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_18	15169888	However, following cellular stimulation with ligands, such as TNF-alpha, two serines in the p105 PEST domain are rapidly phosphorylated by the IkappaB kinase (IKK) complex, triggering complete p105 degradation with little effect on processing to p50 ( ,  ,  ).	transcription
55876	4	335273	7	NULL	NULL	0	NULL	statement 2			trigger					p105		complete degradation of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_18	15169888	However, following cellular stimulation with ligands, such as TNF-alpha, two serines in the p105 PEST domain are rapidly phosphorylated by the IkappaB kinase (IKK) complex, triggering complete p105 degradation with little effect on processing to p50 ( ,  ,  ).	transcription
55877	5	335273	7	NULL	NULL	0	NULL	statement 2			effect on		little			p50		processing to			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_18	15169888	However, following cellular stimulation with ligands, such as TNF-alpha, two serines in the p105 PEST domain are rapidly phosphorylated by the IkappaB kinase (IKK) complex, triggering complete p105 degradation with little effect on processing to p50 ( ,  ,  ).	transcription
55878	6	335273	7	NULL	NULL	0	NULL	IKK			is					IkappaB kinase 					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_12_5235_s_18	15169888	However, following cellular stimulation with ligands, such as TNF-alpha, two serines in the p105 PEST domain are rapidly phosphorylated by the IkappaB kinase (IKK) complex, triggering complete p105 degradation with little effect on processing to p50 ( ,  ,  ).	transcription
54759	1	335274	5	NULL	NULL	0	NULL	TPL-2			increase		may			Myc - p105		efficiency of;;processing of			NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_77	9950430	As Myc - p50 was generated at a similar rate in cells co-transfected with TPL-2 as in control cells, but from progressively decreasing amounts of Myc - p105 ( Fig. 6c), TPL-2 may increase the efficiency of Myc - p105 processing.	transcription
55879	1	335274	7	NULL	NULL	0	NULL	TPL-2 			increase		may			Myc - p105		efficiency of;; processing of			NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_77	9950430	As Myc - p50 was generated at a similar rate in cells co-transfected with TPL-2 as in control cells, but from progressively decreasing amounts of Myc - p105 ( Fig. 6c), TPL-2 may increase the efficiency of Myc - p105 processing.	transcription
55880	2	335274	7	NULL	NULL	0	NULL	statement 1			occurs upon					Myc - p105 		progressively decreasing amounts of			NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_77	9950430	As Myc - p50 was generated at a similar rate in cells co-transfected with TPL-2 as in control cells, but from progressively decreasing amounts of Myc - p105 ( Fig. 6c), TPL-2 may increase the efficiency of Myc - p105 processing.	transcription
54760	1	335275	5	NULL	NULL	0	NULL	MG132			is an inhibitor of		potent			proteasome 4					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_83	9950430	Treatment with MG132, a potent inhibitor of the proteasome 4, blocked increased turnover of Myc - p105 ( Fig. 6f) and completely prevented Myc - p50 production (data not shown) in cells co-expressing TPL-2 and Myc - p105.	transcription
54761	2	335275	5	NULL	NULL	0	NULL	MG132		treatment	blocks					Myc - p105		increased turnover of			NULL	cells co-expressing TPL-2 and Myc - p105	NULL	NULL	NULL	NULL	gw60_nature_397_6717_363_s_83	9950430	Treatment with MG132, a potent inhibitor of the proteasome 4, blocked increased turnover of Myc - p105 ( Fig. 6f) and completely prevented Myc - p50 production (data not shown) in cells co-expressing TPL-2 and Myc - p105.	transcription
54762	3	335275	5	NULL	NULL	0	NULL	MG132		treatment	prevented		completely			Myc - p50		production of			NULL	cells co-expressing TPL-2 and Myc - p105	0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_83	9950430	Treatment with MG132, a potent inhibitor of the proteasome 4, blocked increased turnover of Myc - p105 ( Fig. 6f) and completely prevented Myc - p50 production (data not shown) in cells co-expressing TPL-2 and Myc - p105.	transcription
55881	1	335275	7	NULL	NULL	0	NULL	MG132			blocks					Myc - p105 		increased turnover of			NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_83	9950430	Treatment with MG132, a potent inhibitor of the proteasome 4, blocked increased turnover of Myc - p105 ( Fig. 6f) and completely prevented Myc - p50 production (data not shown) in cells co-expressing TPL-2 and Myc - p105.	transcription
55882	2	335275	7	NULL	NULL	0	NULL	MG132			is a type of					proteasome 4 inhibitor					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_83	9950430	Treatment with MG132, a potent inhibitor of the proteasome 4, blocked increased turnover of Myc - p105 ( Fig. 6f) and completely prevented Myc - p50 production (data not shown) in cells co-expressing TPL-2 and Myc - p105.	transcription
55883	3	335275	7	NULL	NULL	0	NULL	MG132			prevents		completely			Myc - p50		production of			NULL	cells co-expressing TPL-2 and Myc - p105	NULL	NULL	NULL	NULL	gw60_nature_397_6717_363_s_83	9950430	Treatment with MG132, a potent inhibitor of the proteasome 4, blocked increased turnover of Myc - p105 ( Fig. 6f) and completely prevented Myc - p50 production (data not shown) in cells co-expressing TPL-2 and Myc - p105.	transcription
54778	1	335276	5	NULL	NULL	0	NULL	Myc - p105			is degraded by					proteasome					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_84	9950430	Thus, the results of the metabolic labelling experiments (above) indicate that the predominant effect of TPL-2 expression is to increase the rate of Myc - p105 degradation by the proteasome while maintaining the overall rate of production of Myc - p50 from Myc - p105.	transcription
54779	2	335276	5	NULL	NULL	0	NULL	Myc - p50			is produced from					Myc - p105					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_84	9950430	Thus, the results of the metabolic labelling experiments (above) indicate that the predominant effect of TPL-2 expression is to increase the rate of Myc - p105 degradation by the proteasome while maintaining the overall rate of production of Myc - p50 from Myc - p105.	transcription
54780	3	335276	5	NULL	NULL	0	NULL	TPL-2		expression of	increases					statement 1		rate of			NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_84	9950430	Thus, the results of the metabolic labelling experiments (above) indicate that the predominant effect of TPL-2 expression is to increase the rate of Myc - p105 degradation by the proteasome while maintaining the overall rate of production of Myc - p50 from Myc - p105.	transcription
54781	4	335276	5	NULL	NULL	0	NULL	TPL-2		expression of	maintains					statement 2		overall rate of			NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_84	9950430	Thus, the results of the metabolic labelling experiments (above) indicate that the predominant effect of TPL-2 expression is to increase the rate of Myc - p105 degradation by the proteasome while maintaining the overall rate of production of Myc - p50 from Myc - p105.	transcription
54782	5	335276	5	NULL	NULL	0	NULL	statement 3			occurs simultaneously with					statement 4					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_84	9950430	Thus, the results of the metabolic labelling experiments (above) indicate that the predominant effect of TPL-2 expression is to increase the rate of Myc - p105 degradation by the proteasome while maintaining the overall rate of production of Myc - p50 from Myc - p105.	transcription
55884	1	335276	7	NULL	NULL	0	NULL	proteasome 			degrades					Myc - p105					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_84	9950430	Thus, the results of the metabolic labelling experiments (above) indicate that the predominant effect of TPL-2 expression is to increase the rate of Myc - p105 degradation by the proteasome while maintaining the overall rate of production of Myc - p50 from Myc - p105.	transcription
55885	2	335276	7	NULL	NULL	0	NULL	TPL-2		expression of	increase					statement 1					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_84	9950430	Thus, the results of the metabolic labelling experiments (above) indicate that the predominant effect of TPL-2 expression is to increase the rate of Myc - p105 degradation by the proteasome while maintaining the overall rate of production of Myc - p50 from Myc - p105.	transcription
55886	3	335276	7	NULL	NULL	0	NULL	Myc - p50			produced from					Myc - p105					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_84	9950430	Thus, the results of the metabolic labelling experiments (above) indicate that the predominant effect of TPL-2 expression is to increase the rate of Myc - p105 degradation by the proteasome while maintaining the overall rate of production of Myc - p50 from Myc - p105.	transcription
55887	4	335276	7	NULL	NULL	0	NULL	TPL-2 		expression of	maintains					statement 3					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_84	9950430	Thus, the results of the metabolic labelling experiments (above) indicate that the predominant effect of TPL-2 expression is to increase the rate of Myc - p105 degradation by the proteasome while maintaining the overall rate of production of Myc - p50 from Myc - p105.	transcription
54783	1	335277	5	NULL	NULL	0	NULL	Tpl2			forms a complex with		stable			p105					NULL		0	NULL	NULL	NULL	gw60_molcell_11_3_685_s_169	12667451	Interestingly, the coIP assays revealed that while Tpl2 formed a stable complex with p105 (  Figure 4C, top panel, lane 2) and p105 N (lane 6), it did not interact with p50 (lane 3) or p100 (lane 4).	transcription
54784	2	335277	5	NULL	NULL	0	NULL	Tpl2			forms a complex with		stable			p105 N					NULL		0	NULL	NULL	NULL	gw60_molcell_11_3_685_s_169	12667451	Interestingly, the coIP assays revealed that while Tpl2 formed a stable complex with p105 (  Figure 4C, top panel, lane 2) and p105 N (lane 6), it did not interact with p50 (lane 3) or p100 (lane 4).	transcription
54785	3	335277	5	NULL	NULL	0	NULL	Tpl2			does not interact with					p50					NULL		0	NULL	NULL	NULL	gw60_molcell_11_3_685_s_169	12667451	Interestingly, the coIP assays revealed that while Tpl2 formed a stable complex with p105 (  Figure 4C, top panel, lane 2) and p105 N (lane 6), it did not interact with p50 (lane 3) or p100 (lane 4).	transcription
54786	4	335277	5	NULL	NULL	0	NULL	Tpl2			does not interact with					p100					NULL		0	NULL	NULL	NULL	gw60_molcell_11_3_685_s_169	12667451	Interestingly, the coIP assays revealed that while Tpl2 formed a stable complex with p105 (  Figure 4C, top panel, lane 2) and p105 N (lane 6), it did not interact with p50 (lane 3) or p100 (lane 4).	transcription
54787	5	335277	5	NULL	NULL	0	NULL	statement 3			is an alternative to					statement 4					NULL		0	NULL	NULL	NULL	gw60_molcell_11_3_685_s_169	12667451	Interestingly, the coIP assays revealed that while Tpl2 formed a stable complex with p105 (  Figure 4C, top panel, lane 2) and p105 N (lane 6), it did not interact with p50 (lane 3) or p100 (lane 4).	transcription
55888	1	335277	7	NULL	NULL	0	NULL	Tpl2			forms stable complex with					p105					NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_3_685_s_169	12667451	Interestingly, the coIP assays revealed that while Tpl2 formed a stable complex with p105 (  Figure 4C, top panel, lane 2) and p105 N (lane 6), it did not interact with p50 (lane 3) or p100 (lane 4).	transcription
55889	2	335277	7	NULL	NULL	0	NULL	Tpl2			forms stable complex with					p105 N					NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_3_685_s_169	12667451	Interestingly, the coIP assays revealed that while Tpl2 formed a stable complex with p105 (  Figure 4C, top panel, lane 2) and p105 N (lane 6), it did not interact with p50 (lane 3) or p100 (lane 4).	transcription
55890	3	335277	7	NULL	NULL	0	NULL	Tpl2			does not interact with					p50					NULL		0	NULL	NULL	NULL	gw60_molcell_11_3_685_s_169	12667451	Interestingly, the coIP assays revealed that while Tpl2 formed a stable complex with p105 (  Figure 4C, top panel, lane 2) and p105 N (lane 6), it did not interact with p50 (lane 3) or p100 (lane 4).	transcription
55891	4	335277	7	NULL	NULL	0	NULL	Tpl2			does not interact with					p100					NULL		0	NULL	NULL	NULL	gw60_molcell_11_3_685_s_169	12667451	Interestingly, the coIP assays revealed that while Tpl2 formed a stable complex with p105 (  Figure 4C, top panel, lane 2) and p105 N (lane 6), it did not interact with p50 (lane 3) or p100 (lane 4).	transcription
54788	1	335278	5	NULL	NULL	0	NULL	p105			is processed to					p50					NULL	nucleus	0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_7	8537390	In concomitance with NF-kappaB activation,  mitomycin C induced the processing of p105 to p50 in the nucleus, while  it did not affect the steady-state protein levels of IkappaBalpha  and  p105 in the cytoplasm.	transcription
54789	2	335278	5	NULL	NULL	0	NULL	mitomycin C			induce					statement 1					NULL	nucleus	0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_7	8537390	In concomitance with NF-kappaB activation,  mitomycin C induced the processing of p105 to p50 in the nucleus, while  it did not affect the steady-state protein levels of IkappaBalpha  and  p105 in the cytoplasm.	transcription
54790	3	335278	5	NULL	NULL	0	NULL	NF-kappaB		activation of	is concomitant to					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_7	8537390	In concomitance with NF-kappaB activation,  mitomycin C induced the processing of p105 to p50 in the nucleus, while  it did not affect the steady-state protein levels of IkappaBalpha  and  p105 in the cytoplasm.	transcription
54791	4	335278	5	NULL	NULL	0	NULL	mitomycin C			does not affect					IkappaBalpha		protein levels of			NULL	cytoplasm	0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_7	8537390	In concomitance with NF-kappaB activation,  mitomycin C induced the processing of p105 to p50 in the nucleus, while  it did not affect the steady-state protein levels of IkappaBalpha  and  p105 in the cytoplasm.	transcription
54793	5	335278	5	NULL	NULL	0	NULL	mitomycin C			does not affect					p105		protein levels of			NULL	cytoplasm	0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_7	8537390	In concomitance with NF-kappaB activation,  mitomycin C induced the processing of p105 to p50 in the nucleus, while  it did not affect the steady-state protein levels of IkappaBalpha  and  p105 in the cytoplasm.	transcription
55892	1	335278	7	NULL	NULL	0	NULL	p105			processed to					p50					NULL	nucleus	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_7	8537390	In concomitance with NF-kappaB activation,  mitomycin C induced the processing of p105 to p50 in the nucleus, while  it did not affect the steady-state protein levels of IkappaBalpha  and  p105 in the cytoplasm.	transcription
55893	2	335278	7	NULL	NULL	0	NULL	 mitomycin C			induce					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_7	8537390	In concomitance with NF-kappaB activation,  mitomycin C induced the processing of p105 to p50 in the nucleus, while  it did not affect the steady-state protein levels of IkappaBalpha  and  p105 in the cytoplasm.	transcription
55894	3	335278	7	NULL	NULL	0	NULL	statement 2			occurs upon					NF-kappaB		activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_7	8537390	In concomitance with NF-kappaB activation,  mitomycin C induced the processing of p105 to p50 in the nucleus, while  it did not affect the steady-state protein levels of IkappaBalpha  and  p105 in the cytoplasm.	transcription
55895	4	335278	7	NULL	NULL	0	NULL	mitomycin C			does not affect					IkappaBalpha		steady-state protein levels of 			NULL	cytoplasm	0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_7	8537390	In concomitance with NF-kappaB activation,  mitomycin C induced the processing of p105 to p50 in the nucleus, while  it did not affect the steady-state protein levels of IkappaBalpha  and  p105 in the cytoplasm.	transcription
55896	5	335278	7	NULL	NULL	0	NULL	mitomycin C			does not affect					p105		steady-state protein levels of			NULL	cytoplasm	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_7	8537390	In concomitance with NF-kappaB activation,  mitomycin C induced the processing of p105 to p50 in the nucleus, while  it did not affect the steady-state protein levels of IkappaBalpha  and  p105 in the cytoplasm.	transcription
54794	1	335280	5	NULL	NULL	0	NULL	transactivation			is dependent on					NF-kappaB					NULL		0	NULL	NULL	NULL	gw70_jclininvest_114_10_1504_s_48	15546001	To investigate a potential role of p50 and Bcl-3 in this NF-kappaB - dependent transactivation during disuse atrophy, we studied mice with a knockout of  Nfkb1 (which encodes the p105 and p50 protein) or  Bcl3.	transcription
54795	2	335280	5	NULL	NULL	0	NULL	statement 1			occurs during					disuse atrophy					NULL		0	NULL	NULL	NULL	gw70_jclininvest_114_10_1504_s_48	15546001	To investigate a potential role of p50 and Bcl-3 in this NF-kappaB - dependent transactivation during disuse atrophy, we studied mice with a knockout of  Nfkb1 (which encodes the p105 and p50 protein) or  Bcl3.	transcription
54796	3	335280	5	NULL	NULL	0	NULL	p50			plays a role in		potentially			statement 1					NULL		0	NULL	NULL	NULL	gw70_jclininvest_114_10_1504_s_48	15546001	To investigate a potential role of p50 and Bcl-3 in this NF-kappaB - dependent transactivation during disuse atrophy, we studied mice with a knockout of  Nfkb1 (which encodes the p105 and p50 protein) or  Bcl3.	transcription
54797	4	335280	5	NULL	NULL	0	NULL	Bcl-3			plays a role in		potentially			statement 1					NULL		0	NULL	NULL	NULL	gw70_jclininvest_114_10_1504_s_48	15546001	To investigate a potential role of p50 and Bcl-3 in this NF-kappaB - dependent transactivation during disuse atrophy, we studied mice with a knockout of  Nfkb1 (which encodes the p105 and p50 protein) or  Bcl3.	transcription
54798	5	335280	5	NULL	NULL	0	NULL	Nfkb1			encodes					p105 protein					NULL		0	NULL	NULL	NULL	gw70_jclininvest_114_10_1504_s_48	15546001	To investigate a potential role of p50 and Bcl-3 in this NF-kappaB - dependent transactivation during disuse atrophy, we studied mice with a knockout of  Nfkb1 (which encodes the p105 and p50 protein) or  Bcl3.	transcription
54799	6	335280	5	NULL	NULL	0	NULL	Nfkb1			encodes					p50 protein					NULL		0	NULL	NULL	NULL	gw70_jclininvest_114_10_1504_s_48	15546001	To investigate a potential role of p50 and Bcl-3 in this NF-kappaB - dependent transactivation during disuse atrophy, we studied mice with a knockout of  Nfkb1 (which encodes the p105 and p50 protein) or  Bcl3.	transcription
56147	1	335280	7	NULL	NULL	0	NULL	Nfkb1			encode					p105					NULL		0	NULL	NULL	NULL	gw70_jclininvest_114_10_1504_s_48	15546001	To investigate a potential role of p50 and Bcl-3 in this NF-kappaB - dependent transactivation during disuse atrophy, we studied mice with a knockout of  Nfkb1 (which encodes the p105 and p50 protein) or  Bcl3.	transcription
56148	2	335280	7	NULL	NULL	0	NULL	Nfkb1			encode					p50 protein					NULL		0	NULL	NULL	NULL	gw70_jclininvest_114_10_1504_s_48	15546001	To investigate a potential role of p50 and Bcl-3 in this NF-kappaB - dependent transactivation during disuse atrophy, we studied mice with a knockout of  Nfkb1 (which encodes the p105 and p50 protein) or  Bcl3.	transcription
54800	1	335281	5	NULL	NULL	0	NULL	p50		newly synthesized	is encoded by					p50 expression vector					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_165	9529257	However, newly synthesized p50 encoded by a p50  expression vector was effectively coimmunoprecipitated by the E446-1 antibody (lane 12), suggesting that  the interaction of p105 fragments with the proteasome may occur during translation.	transcription
54801	2	335281	5	NULL	NULL	0	NULL	E446-1 antibody			coimmunoprecipitates with		effectively			statement 1					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_165	9529257	However, newly synthesized p50 encoded by a p50  expression vector was effectively coimmunoprecipitated by the E446-1 antibody (lane 12), suggesting that  the interaction of p105 fragments with the proteasome may occur during translation.	transcription
54802	3	335281	5	NULL	NULL	0	NULL	p105 fragments 			interacts with					proteasome					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_165	9529257	However, newly synthesized p50 encoded by a p50  expression vector was effectively coimmunoprecipitated by the E446-1 antibody (lane 12), suggesting that  the interaction of p105 fragments with the proteasome may occur during translation.	transcription
54803	4	335281	5	NULL	NULL	0	NULL	statement 3			occurs during		may			translation					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_165	9529257	However, newly synthesized p50 encoded by a p50  expression vector was effectively coimmunoprecipitated by the E446-1 antibody (lane 12), suggesting that  the interaction of p105 fragments with the proteasome may occur during translation.	transcription
55897	1	335281	7	NULL	NULL	0	NULL	p50		newly synthesized	bind					E446-1 antibody					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_165	9529257	However, newly synthesized p50 encoded by a p50  expression vector was effectively coimmunoprecipitated by the E446-1 antibody (lane 12), suggesting that  the interaction of p105 fragments with the proteasome may occur during translation.	transcription
55898	2	335281	7	NULL	NULL	0	NULL	p105 fragments 			interacts with					proteasome					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_165	9529257	However, newly synthesized p50 encoded by a p50  expression vector was effectively coimmunoprecipitated by the E446-1 antibody (lane 12), suggesting that  the interaction of p105 fragments with the proteasome may occur during translation.	transcription
55899	3	335281	7	NULL	NULL	0	NULL	statement 2			occur during		may			translation					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_165	9529257	However, newly synthesized p50 encoded by a p50  expression vector was effectively coimmunoprecipitated by the E446-1 antibody (lane 12), suggesting that  the interaction of p105 fragments with the proteasome may occur during translation.	transcription
54804	1	335282	5	NULL	NULL	0	NULL	p105		proteolytic processing of	leads to					p50		nuclear translocation of			NULL	transfected 3T3cells	0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_65	9950430	To determine whether TPL-2 must induce proteolytic processing of p105 to promote nuclear translocation of p50, we transfected 3T3cells with a vector encoding Myc - p105deltaGRR 18, together with haemagglutinin (HA) - p50 on a separate plasmid.	transcription
54805	2	335282	5	NULL	NULL	0	NULL	TPL-2			induce		might			statement 1					NULL	transfected 3T3cells	NULL	NULL	NULL	NULL	gw60_nature_397_6717_363_s_65	9950430	To determine whether TPL-2 must induce proteolytic processing of p105 to promote nuclear translocation of p50, we transfected 3T3cells with a vector encoding Myc - p105deltaGRR 18, together with haemagglutinin (HA) - p50 on a separate plasmid.	transcription
56174	1	335282	7	NULL	NULL	0	NULL	p105		proteolytic processing of	promote					p50		nuclear translocation of 			NULL	transfected 3T3cells	0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_65	9950430	To determine whether TPL-2 must induce proteolytic processing of p105 to promote nuclear translocation of p50, we transfected 3T3cells with a vector encoding Myc - p105deltaGRR 18, together with haemagglutinin (HA) - p50 on a separate plasmid.	transcription
56175	2	335282	7	NULL	NULL	0	NULL	TPL-2			induce		might			statement 1					NULL	transfected 3T3cells	0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_65	9950430	To determine whether TPL-2 must induce proteolytic processing of p105 to promote nuclear translocation of p50, we transfected 3T3cells with a vector encoding Myc - p105deltaGRR 18, together with haemagglutinin (HA) - p50 on a separate plasmid.	transcription
54806	1	335284	5	NULL	NULL	0	NULL	NF-kappaB-1 p105			resides in			PEST sequence		NF-kappaB-1 p105			C-terminus		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_52_35201_s_220	9857058	Moreover, the C-terminal PEST sequence of NF-kappaB-1 p105 also plays an important role in its processing; it was shown by MacKichan  et al. ( 46) that phosphorylation of the PEST sequences of p105 up-regulates the proteolytic processing of p105 into the active p50.	transcription
54807	2	335284	5	NULL	NULL	0	NULL	statement 1			plays a role in					NF-kappaB-1 p105		processing of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_35201_s_220	9857058	Moreover, the C-terminal PEST sequence of NF-kappaB-1 p105 also plays an important role in its processing; it was shown by MacKichan  et al. ( 46) that phosphorylation of the PEST sequences of p105 up-regulates the proteolytic processing of p105 into the active p50.	transcription
54808	4	335284	5	NULL	NULL	0	NULL	NF-kappaB-1 p105		phosphorylation of	upregulates			PEST sequence		statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_35201_s_220	9857058	Moreover, the C-terminal PEST sequence of NF-kappaB-1 p105 also plays an important role in its processing; it was shown by MacKichan  et al. ( 46) that phosphorylation of the PEST sequences of p105 up-regulates the proteolytic processing of p105 into the active p50.	transcription
54809	3	335284	5	NULL	NULL	0	NULL	p105		proteolytic processing of	forms					p50		active			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_35201_s_220	9857058	Moreover, the C-terminal PEST sequence of NF-kappaB-1 p105 also plays an important role in its processing; it was shown by MacKichan  et al. ( 46) that phosphorylation of the PEST sequences of p105 up-regulates the proteolytic processing of p105 into the active p50.	transcription
55900	1	335284	7	NULL	NULL	0	NULL	NF-kappaB-1 p105 			plays an important role in			C-terminal PEST sequence		NF-kappaB-1 p105 		processing of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_35201_s_220	9857058	Moreover, the C-terminal PEST sequence of NF-kappaB-1 p105 also plays an important role in its processing; it was shown by MacKichan  et al. ( 46) that phosphorylation of the PEST sequences of p105 up-regulates the proteolytic processing of p105 into the active p50.	transcription
55901	2	335284	7	NULL	NULL	0	NULL	p105 			processed to		proteolytically			p50		active			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_35201_s_220	9857058	Moreover, the C-terminal PEST sequence of NF-kappaB-1 p105 also plays an important role in its processing; it was shown by MacKichan  et al. ( 46) that phosphorylation of the PEST sequences of p105 up-regulates the proteolytic processing of p105 into the active p50.	transcription
55902	3	335284	7	NULL	NULL	0	NULL	p105		phosphorylation of 	upregulates			PEST sequences		statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_52_35201_s_220	9857058	Moreover, the C-terminal PEST sequence of NF-kappaB-1 p105 also plays an important role in its processing; it was shown by MacKichan  et al. ( 46) that phosphorylation of the PEST sequences of p105 up-regulates the proteolytic processing of p105 into the active p50.	transcription
54810	1	335285	5	NULL	NULL	0	NULL	BCL-3			is a type of					oncoprotein					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_218	9529257	While the biological function of these  Rel-p105 complexes remains to be elucidated, the candidate oncoprotein BCL-3 may mobilize p50  molecules bound to p105 without enhancing p105 processing (Watanabe et al., 1997   ), suggesting that p105/p50 complexes could function as a source of p50 homodimers.	transcription
54811	2	335285	5	NULL	NULL	0	NULL	p50			bind					p105					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_218	9529257	While the biological function of these  Rel-p105 complexes remains to be elucidated, the candidate oncoprotein BCL-3 may mobilize p50  molecules bound to p105 without enhancing p105 processing (Watanabe et al., 1997   ), suggesting that p105/p50 complexes could function as a source of p50 homodimers.	transcription
54812	3	335285	5	NULL	NULL	0	NULL	BCL-3			mobilize		may			statement 2					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_218	9529257	While the biological function of these  Rel-p105 complexes remains to be elucidated, the candidate oncoprotein BCL-3 may mobilize p50  molecules bound to p105 without enhancing p105 processing (Watanabe et al., 1997   ), suggesting that p105/p50 complexes could function as a source of p50 homodimers.	transcription
54813	4	335285	5	NULL	NULL	0	NULL	statement 3			does not enhance					p105		processing of			NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_218	9529257	While the biological function of these  Rel-p105 complexes remains to be elucidated, the candidate oncoprotein BCL-3 may mobilize p50  molecules bound to p105 without enhancing p105 processing (Watanabe et al., 1997   ), suggesting that p105/p50 complexes could function as a source of p50 homodimers.	transcription
54814	5	335285	5	NULL	NULL	0	NULL	p105/p50 complexes			function as		may			p50 homodimers		source of			NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_218	9529257	While the biological function of these  Rel-p105 complexes remains to be elucidated, the candidate oncoprotein BCL-3 may mobilize p50  molecules bound to p105 without enhancing p105 processing (Watanabe et al., 1997   ), suggesting that p105/p50 complexes could function as a source of p50 homodimers.	transcription
55903	1	335285	7	NULL	NULL	0	NULL	p50 molecules			bind					p105					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_218	9529257	While the biological function of these  Rel-p105 complexes remains to be elucidated, the candidate oncoprotein BCL-3 may mobilize p50  molecules bound to p105 without enhancing p105 processing (Watanabe et al., 1997   ), suggesting that p105/p50 complexes could function as a source of p50 homodimers.	transcription
55904	2	335285	7	NULL	NULL	0	NULL	BCL-3 			mobilize		may			statement 1					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_218	9529257	While the biological function of these  Rel-p105 complexes remains to be elucidated, the candidate oncoprotein BCL-3 may mobilize p50  molecules bound to p105 without enhancing p105 processing (Watanabe et al., 1997   ), suggesting that p105/p50 complexes could function as a source of p50 homodimers.	transcription
55905	3	335285	7	NULL	NULL	0	NULL	statement 2			occurs without					p105		enhancing;;processing of			NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_218	9529257	While the biological function of these  Rel-p105 complexes remains to be elucidated, the candidate oncoprotein BCL-3 may mobilize p50  molecules bound to p105 without enhancing p105 processing (Watanabe et al., 1997   ), suggesting that p105/p50 complexes could function as a source of p50 homodimers.	transcription
55906	4	335285	7	NULL	NULL	0	NULL	p105/p50 complexes			function as					p50 homodimers		source of			NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_218	9529257	While the biological function of these  Rel-p105 complexes remains to be elucidated, the candidate oncoprotein BCL-3 may mobilize p50  molecules bound to p105 without enhancing p105 processing (Watanabe et al., 1997   ), suggesting that p105/p50 complexes could function as a source of p50 homodimers.	transcription
55907	5	335285	7	NULL	NULL	0	NULL	statement 3			suggest					statement 4					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_218	9529257	While the biological function of these  Rel-p105 complexes remains to be elucidated, the candidate oncoprotein BCL-3 may mobilize p50  molecules bound to p105 without enhancing p105 processing (Watanabe et al., 1997   ), suggesting that p105/p50 complexes could function as a source of p50 homodimers.	transcription
55908	6	335285	7	NULL	NULL	0	NULL	BCL-3			is a type of					oncoprotein					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_218	9529257	While the biological function of these  Rel-p105 complexes remains to be elucidated, the candidate oncoprotein BCL-3 may mobilize p50  molecules bound to p105 without enhancing p105 processing (Watanabe et al., 1997   ), suggesting that p105/p50 complexes could function as a source of p50 homodimers.	transcription
54815	1	335286	5	NULL	NULL	0	NULL	IKKbeta		expression of;;wild-type	increases					p50					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_226	11158290	While expression of wild-type IKKbeta led to increased p50, presumably by increasing p105 expression and concomitant p105 degradation, inactive IKKbeta reduced the amounts of p50 (Fig.  6B, left panel, compare lane 1 with 2 and 3).	transcription
54816	2	335286	5	NULL	NULL	0	NULL	IKKbeta		expression of;;wild-type	increases					p105		expression of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_226	11158290	While expression of wild-type IKKbeta led to increased p50, presumably by increasing p105 expression and concomitant p105 degradation, inactive IKKbeta reduced the amounts of p50 (Fig.  6B, left panel, compare lane 1 with 2 and 3).	transcription
54817	3	335286	5	NULL	NULL	0	NULL	statement 2			is concomitant to					p105		degradation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_226	11158290	While expression of wild-type IKKbeta led to increased p50, presumably by increasing p105 expression and concomitant p105 degradation, inactive IKKbeta reduced the amounts of p50 (Fig.  6B, left panel, compare lane 1 with 2 and 3).	transcription
54826	4	335286	5	NULL	NULL	0	NULL	statement 2			leads to					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_226	11158290	While expression of wild-type IKKbeta led to increased p50, presumably by increasing p105 expression and concomitant p105 degradation, inactive IKKbeta reduced the amounts of p50 (Fig.  6B, left panel, compare lane 1 with 2 and 3).	transcription
54827	5	335286	5	NULL	NULL	0	NULL	statement 3			leads to					statement 1					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_226	11158290	While expression of wild-type IKKbeta led to increased p50, presumably by increasing p105 expression and concomitant p105 degradation, inactive IKKbeta reduced the amounts of p50 (Fig.  6B, left panel, compare lane 1 with 2 and 3).	transcription
54828	6	335286	5	NULL	NULL	0	NULL	IKKbeta		inactive	reduces					p50		amounts of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_226	11158290	While expression of wild-type IKKbeta led to increased p50, presumably by increasing p105 expression and concomitant p105 degradation, inactive IKKbeta reduced the amounts of p50 (Fig.  6B, left panel, compare lane 1 with 2 and 3).	transcription
55909	1	335286	7	NULL	NULL	0	NULL	IKKbeta		 expression of wild-type	increased					p50					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_226	11158290	While expression of wild-type IKKbeta led to increased p50, presumably by increasing p105 expression and concomitant p105 degradation, inactive IKKbeta reduced the amounts of p50 (Fig.  6B, left panel, compare lane 1 with 2 and 3).	transcription
55910	2	335286	7	NULL	NULL	0	NULL	statement 1			occur by increasing		presumably			p105		expression of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_226	11158290	While expression of wild-type IKKbeta led to increased p50, presumably by increasing p105 expression and concomitant p105 degradation, inactive IKKbeta reduced the amounts of p50 (Fig.  6B, left panel, compare lane 1 with 2 and 3).	transcription
55911	3	335286	7	NULL	NULL	0	NULL	statement 1			occur by increasing					p105		degradation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_226	11158290	While expression of wild-type IKKbeta led to increased p50, presumably by increasing p105 expression and concomitant p105 degradation, inactive IKKbeta reduced the amounts of p50 (Fig.  6B, left panel, compare lane 1 with 2 and 3).	transcription
55912	4	335286	7	NULL	NULL	0	NULL	IKKbeta		inactive	reduce					p50		amount of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_226	11158290	While expression of wild-type IKKbeta led to increased p50, presumably by increasing p105 expression and concomitant p105 degradation, inactive IKKbeta reduced the amounts of p50 (Fig.  6B, left panel, compare lane 1 with 2 and 3).	transcription
54829	1	335287	5	NULL	NULL	0	NULL	p105 precursor protein		phosphorylation of	is dependent on					IKK					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_13_11116_s_197	11799112	Because p50 activity is regulated predominantly through IKK-dependent phosphorylation and proteolysis of the p105 precursor protein ( 49-51), we analyzed whether PTEN blocked p50 activity by inhibiting p105 processing in LNCaP cells following TNF stimulation.	transcription
54830	2	335287	5	NULL	NULL	0	NULL	p105 precursor protein		proteolysis of	is dependent on					IKK					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_13_11116_s_197	11799112	Because p50 activity is regulated predominantly through IKK-dependent phosphorylation and proteolysis of the p105 precursor protein ( 49-51), we analyzed whether PTEN blocked p50 activity by inhibiting p105 processing in LNCaP cells following TNF stimulation.	transcription
54831	3	335287	5	NULL	NULL	0	NULL	p50		activity of	is regulated through		predominantly			statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_13_11116_s_197	11799112	Because p50 activity is regulated predominantly through IKK-dependent phosphorylation and proteolysis of the p105 precursor protein ( 49-51), we analyzed whether PTEN blocked p50 activity by inhibiting p105 processing in LNCaP cells following TNF stimulation.	transcription
54832	4	335287	5	NULL	NULL	0	NULL	p50		activity of	is regulated through		predominantly			statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_13_11116_s_197	11799112	Because p50 activity is regulated predominantly through IKK-dependent phosphorylation and proteolysis of the p105 precursor protein ( 49-51), we analyzed whether PTEN blocked p50 activity by inhibiting p105 processing in LNCaP cells following TNF stimulation.	transcription
54833	5	335287	5	NULL	NULL	0	NULL	PTEN			block		potentially			p50		activity of			NULL	LNCaP cells	0	NULL	NULL	NULL	gw60_jbiolchem_277_13_11116_s_197	11799112	Because p50 activity is regulated predominantly through IKK-dependent phosphorylation and proteolysis of the p105 precursor protein ( 49-51), we analyzed whether PTEN blocked p50 activity by inhibiting p105 processing in LNCaP cells following TNF stimulation.	transcription
54834	6	335287	5	NULL	NULL	0	NULL	PTEN			inhibits		potentially			p105		degradation of			NULL	LNCaP cells	0	NULL	NULL	NULL	gw60_jbiolchem_277_13_11116_s_197	11799112	Because p50 activity is regulated predominantly through IKK-dependent phosphorylation and proteolysis of the p105 precursor protein ( 49-51), we analyzed whether PTEN blocked p50 activity by inhibiting p105 processing in LNCaP cells following TNF stimulation.	transcription
54835	7	335287	5	NULL	NULL	0	NULL	statement 5			leads to		potentially			statement 6					NULL	LNCaP cells	0	NULL	NULL	NULL	gw60_jbiolchem_277_13_11116_s_197	11799112	Because p50 activity is regulated predominantly through IKK-dependent phosphorylation and proteolysis of the p105 precursor protein ( 49-51), we analyzed whether PTEN blocked p50 activity by inhibiting p105 processing in LNCaP cells following TNF stimulation.	transcription
54836	8	335287	5	NULL	NULL	0	NULL	TNF		stimulation	leads to		potentially			statement 7					NULL	LNCaP cells	0	NULL	NULL	NULL	gw60_jbiolchem_277_13_11116_s_197	11799112	Because p50 activity is regulated predominantly through IKK-dependent phosphorylation and proteolysis of the p105 precursor protein ( 49-51), we analyzed whether PTEN blocked p50 activity by inhibiting p105 processing in LNCaP cells following TNF stimulation.	transcription
55913	1	335287	7	NULL	NULL	0	NULL	p50		activity of	regulated through		predominantly			IKK-dependent phosphorylation 					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_13_11116_s_197	11799112	Because p50 activity is regulated predominantly through IKK-dependent phosphorylation and proteolysis of the p105 precursor protein ( 49-51), we analyzed whether PTEN blocked p50 activity by inhibiting p105 processing in LNCaP cells following TNF stimulation.	transcription
55914	2	335287	7	NULL	NULL	0	NULL	p50		activity of	regulated through		predominantly			p105 precursor protein 		proteolysis of	49-51		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_13_11116_s_197	11799112	Because p50 activity is regulated predominantly through IKK-dependent phosphorylation and proteolysis of the p105 precursor protein ( 49-51), we analyzed whether PTEN blocked p50 activity by inhibiting p105 processing in LNCaP cells following TNF stimulation.	transcription
55926	3	335287	7	NULL	NULL	0	NULL	statement 1			occur along with					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_13_11116_s_197	11799112	Because p50 activity is regulated predominantly through IKK-dependent phosphorylation and proteolysis of the p105 precursor protein ( 49-51), we analyzed whether PTEN blocked p50 activity by inhibiting p105 processing in LNCaP cells following TNF stimulation.	transcription
56781	1	335288	5	NULL	NULL	0	NULL	SCFbeta-TrCP ubiquitin ligase		stimulated	is recruited to								IKK-mediated phosphorylation motif at the C-terminal domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23253_s_241	11953428	Following stimulation, the SCFbeta-TrCP ubiquitin ligase is recruited to the IKK-mediated phosphorylation motif at the C-terminal domain, leading to rapid polyubiquitination and subsequent processing/degradation of p105 with release of the docked p50 molecules and an additional p50 subunit released from processed p105 ( 11,  12,  22).	transcription
56782	2	335288	5	NULL	NULL	0	NULL	statement 1			leads to					p105		rapid polyubiquitination of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23253_s_241	11953428	Following stimulation, the SCFbeta-TrCP ubiquitin ligase is recruited to the IKK-mediated phosphorylation motif at the C-terminal domain, leading to rapid polyubiquitination and subsequent processing/degradation of p105 with release of the docked p50 molecules and an additional p50 subunit released from processed p105 ( 11,  12,  22).	transcription
56783	3	335288	5	NULL	NULL	0	NULL	statement 2			leads to		subsequently			p105		processing/degradation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23253_s_241	11953428	Following stimulation, the SCFbeta-TrCP ubiquitin ligase is recruited to the IKK-mediated phosphorylation motif at the C-terminal domain, leading to rapid polyubiquitination and subsequent processing/degradation of p105 with release of the docked p50 molecules and an additional p50 subunit released from processed p105 ( 11,  12,  22).	transcription
56784	4	335288	5	NULL	NULL	0	NULL	statement 3			release					p50 molecules		docked			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_26_23253_s_241	11953428	Following stimulation, the SCFbeta-TrCP ubiquitin ligase is recruited to the IKK-mediated phosphorylation motif at the C-terminal domain, leading to rapid polyubiquitination and subsequent processing/degradation of p105 with release of the docked p50 molecules and an additional p50 subunit released from processed p105 ( 11,  12,  22).	transcription
56785	5	335288	5	NULL	NULL	0	NULL	p50 subunit			is relased from					p105		processed			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23253_s_241	11953428	Following stimulation, the SCFbeta-TrCP ubiquitin ligase is recruited to the IKK-mediated phosphorylation motif at the C-terminal domain, leading to rapid polyubiquitination and subsequent processing/degradation of p105 with release of the docked p50 molecules and an additional p50 subunit released from processed p105 ( 11,  12,  22).	transcription
56786	6	335288	5	NULL	NULL	0	NULL	statement 3			leads to					statement 5					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23253_s_241	11953428	Following stimulation, the SCFbeta-TrCP ubiquitin ligase is recruited to the IKK-mediated phosphorylation motif at the C-terminal domain, leading to rapid polyubiquitination and subsequent processing/degradation of p105 with release of the docked p50 molecules and an additional p50 subunit released from processed p105 ( 11,  12,  22).	transcription
55915	1	335288	7	NULL	NULL	0	NULL	SCFbeta-TrCP ubiquitin ligase 			recruited to								IKK-mediated phosphorylation motif at the C-terminal domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23253_s_241	11953428	Following stimulation, the SCFbeta-TrCP ubiquitin ligase is recruited to the IKK-mediated phosphorylation motif at the C-terminal domain, leading to rapid polyubiquitination and subsequent processing/degradation of p105 with release of the docked p50 molecules and an additional p50 subunit released from processed p105 ( 11,  12,  22).	transcription
55916	2	335288	7	NULL	NULL	0	NULL	statement 1			leads to		rapidly			polyubiquitination					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23253_s_241	11953428	Following stimulation, the SCFbeta-TrCP ubiquitin ligase is recruited to the IKK-mediated phosphorylation motif at the C-terminal domain, leading to rapid polyubiquitination and subsequent processing/degradation of p105 with release of the docked p50 molecules and an additional p50 subunit released from processed p105 ( 11,  12,  22).	transcription
55917	3	335288	7	NULL	NULL	0	NULL	statement 1			leads to		rapidly			p105		processing/degradation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23253_s_241	11953428	Following stimulation, the SCFbeta-TrCP ubiquitin ligase is recruited to the IKK-mediated phosphorylation motif at the C-terminal domain, leading to rapid polyubiquitination and subsequent processing/degradation of p105 with release of the docked p50 molecules and an additional p50 subunit released from processed p105 ( 11,  12,  22).	transcription
55918	4	335288	7	NULL	NULL	0	NULL	statement 3			release					p50 molecules 		docked			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23253_s_241	11953428	Following stimulation, the SCFbeta-TrCP ubiquitin ligase is recruited to the IKK-mediated phosphorylation motif at the C-terminal domain, leading to rapid polyubiquitination and subsequent processing/degradation of p105 with release of the docked p50 molecules and an additional p50 subunit released from processed p105 ( 11,  12,  22).	transcription
55919	5	335288	7	NULL	NULL	0	NULL	p50 subunit			released from					p105		processed			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23253_s_241	11953428	Following stimulation, the SCFbeta-TrCP ubiquitin ligase is recruited to the IKK-mediated phosphorylation motif at the C-terminal domain, leading to rapid polyubiquitination and subsequent processing/degradation of p105 with release of the docked p50 molecules and an additional p50 subunit released from processed p105 ( 11,  12,  22).	transcription
55920	6	335288	7	NULL	NULL	0	NULL	statement 3			leads to					statement 5					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23253_s_241	11953428	Following stimulation, the SCFbeta-TrCP ubiquitin ligase is recruited to the IKK-mediated phosphorylation motif at the C-terminal domain, leading to rapid polyubiquitination and subsequent processing/degradation of p105 with release of the docked p50 molecules and an additional p50 subunit released from processed p105 ( 11,  12,  22).	transcription
55921	7	335288	7	NULL	NULL	0	NULL	statement 1			occur upon					stimulation					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23253_s_241	11953428	Following stimulation, the SCFbeta-TrCP ubiquitin ligase is recruited to the IKK-mediated phosphorylation motif at the C-terminal domain, leading to rapid polyubiquitination and subsequent processing/degradation of p105 with release of the docked p50 molecules and an additional p50 subunit released from processed p105 ( 11,  12,  22).	transcription
54845	1	335289	5	NULL	NULL	0	NULL	LTbetaR		signaling of	induces					p105 precursor		processingof;;degradation of 			NULL		0	NULL	NULL	NULL	gw70_embo_22_1_121_s_224	12505990	We observed that LTbetaR signaling also induces processing/degradation of the p105 precursor with similar  kinetics to p100, but without altering p50 levels.	transcription
54846	2	335289	5	NULL	NULL	0	NULL	statement 1			does not alter					p50		levels of			NULL		0	NULL	NULL	NULL	gw70_embo_22_1_121_s_224	12505990	We observed that LTbetaR signaling also induces processing/degradation of the p105 precursor with similar  kinetics to p100, but without altering p50 levels.	transcription
54847	3	335289	5	NULL	NULL	0	NULL	LTbetaR		signaling of	induces					p100		processingof;;degradation of			NULL		0	NULL	NULL	NULL	gw70_embo_22_1_121_s_224	12505990	We observed that LTbetaR signaling also induces processing/degradation of the p105 precursor with similar  kinetics to p100, but without altering p50 levels.	transcription
54848	4	335289	5	NULL	NULL	0	NULL	statement 1		kinetics of	similar to					statement 3		kinetics of			NULL		0	NULL	NULL	NULL	gw70_embo_22_1_121_s_224	12505990	We observed that LTbetaR signaling also induces processing/degradation of the p105 precursor with similar  kinetics to p100, but without altering p50 levels.	transcription
55922	1	335289	7	NULL	NULL	0	NULL	 LTbetaR 		signaling of	induce					p105 precursor		processing/degradation of			NULL		NULL	NULL	NULL	NULL	gw70_embo_22_1_121_s_224	12505990	We observed that LTbetaR signaling also induces processing/degradation of the p105 precursor with similar  kinetics to p100, but without altering p50 levels.	transcription
55923	2	335289	7	NULL	NULL	0	NULL	LTbetaR		signaling of	induce					p100		processing/degradation of			NULL		0	NULL	NULL	NULL	gw70_embo_22_1_121_s_224	12505990	We observed that LTbetaR signaling also induces processing/degradation of the p105 precursor with similar  kinetics to p100, but without altering p50 levels.	transcription
55924	3	335289	7	NULL	NULL	0	NULL	statement 1			does not alter					p50		levels of			NULL		0	NULL	NULL	NULL	gw70_embo_22_1_121_s_224	12505990	We observed that LTbetaR signaling also induces processing/degradation of the p105 precursor with similar  kinetics to p100, but without altering p50 levels.	transcription
55925	4	335289	7	NULL	NULL	0	NULL	statement 2			does not alter					p50		levels of			NULL		0	NULL	NULL	NULL	gw70_embo_22_1_121_s_224	12505990	We observed that LTbetaR signaling also induces processing/degradation of the p105 precursor with similar  kinetics to p100, but without altering p50 levels.	transcription
54849	1	335290	5	NULL	NULL	0	NULL	p105			is a precursor of					p50					NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	transcription
54850	2	335290	5	NULL	NULL	0	NULL	1,25-VD			reduces					p50		levels of			NULL	human lymphocytes	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	transcription
54851	3	335290	5	NULL	NULL	0	NULL	1,25-VD			reduces					p105		levels of			NULL	human lymphocytes	NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	transcription
54852	4	335290	5	NULL	NULL	0	NULL	NF-kappaB			bind					IL-6				promoter	NULL	human lymphocytes	0	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	transcription
54853	5	335290	5	NULL	NULL	0	NULL	PMA			induces					statement 4					NULL	human lymphocytes	0	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	transcription
54854	6	335290	5	NULL	NULL	0	NULL	1,25-VD			decreases					statement 5					NULL	human lymphocytes	0	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	transcription
54855	7	335290	5	NULL	NULL	0	NULL	statement 2			leads to					statement 6					NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	transcription
54856	8	335290	5	NULL	NULL	0	NULL	statement 3			leads to					statement 6					NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	transcription
55927	1	335290	7	NULL	NULL	0	NULL	1,25-VD 			reduce					p50		levels of			NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	transcription
55928	2	335290	7	NULL	NULL	0	NULL	1,25-VD 			reduce					p105		levels of			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	transcription
55929	3	335290	7	NULL	NULL	0	NULL	NF-kappaB			bind					IL-6				promoter	NULL	human lymphocytes	0	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	transcription
55930	4	335290	7	NULL	NULL	0	NULL	PMA			induce					statement 3					NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	transcription
55931	5	335290	7	NULL	NULL	0	NULL	1,25-VD			decrease					statement 4					NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_9_1883_s_257	16624828	1,25-VD has been shown to reduce levels of p50 and its precursor p105 and then decrease PMA-induced NF-kappaB binding to the IL-6promoter in human lymphocytes ( ).	transcription
54857	1	335292	5	NULL	NULL	0	NULL	IKK			mediates					p105		phosphorylation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_282	14668329	Signal-induced degradation of p105 could result from IKK-mediated phosphorylation and targeting by the proteasome ( ,  ,  ); then released p50 might be sequestered and transported to the nucleus by Bcl-3.	transcription
54858	2	335292	5	NULL	NULL	0	NULL	p105			is targeted by					proteasome					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_282	14668329	Signal-induced degradation of p105 could result from IKK-mediated phosphorylation and targeting by the proteasome ( ,  ,  ); then released p50 might be sequestered and transported to the nucleus by Bcl-3.	transcription
54859	3	335292	5	NULL	NULL	0	NULL	statement 1			leads to					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_282	14668329	Signal-induced degradation of p105 could result from IKK-mediated phosphorylation and targeting by the proteasome ( ,  ,  ); then released p50 might be sequestered and transported to the nucleus by Bcl-3.	transcription
54860	4	335292	5	NULL	NULL	0	NULL	statement 3			results in					p105		degradation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_282	14668329	Signal-induced degradation of p105 could result from IKK-mediated phosphorylation and targeting by the proteasome ( ,  ,  ); then released p50 might be sequestered and transported to the nucleus by Bcl-3.	transcription
54861	5	335292	5	NULL	NULL	0	NULL	statement 4			releases					p50					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_282	14668329	Signal-induced degradation of p105 could result from IKK-mediated phosphorylation and targeting by the proteasome ( ,  ,  ); then released p50 might be sequestered and transported to the nucleus by Bcl-3.	transcription
54862	6	335292	5	NULL	NULL	0	NULL	p50		released	undergoes					sequestration					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_282	14668329	Signal-induced degradation of p105 could result from IKK-mediated phosphorylation and targeting by the proteasome ( ,  ,  ); then released p50 might be sequestered and transported to the nucleus by Bcl-3.	transcription
54863	7	335292	5	NULL	NULL	0	NULL	p50			is transported to					nucleus					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_282	14668329	Signal-induced degradation of p105 could result from IKK-mediated phosphorylation and targeting by the proteasome ( ,  ,  ); then released p50 might be sequestered and transported to the nucleus by Bcl-3.	transcription
54864	8	335292	5	NULL	NULL	0	NULL	Bcl-3			is required for					statement 7					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_282	14668329	Signal-induced degradation of p105 could result from IKK-mediated phosphorylation and targeting by the proteasome ( ,  ,  ); then released p50 might be sequestered and transported to the nucleus by Bcl-3.	transcription
55955	1	335292	7	NULL	NULL	0	NULL	Signal			induce					p105		degradation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_282	14668329	Signal-induced degradation of p105 could result from IKK-mediated phosphorylation and targeting by the proteasome ( ,  ,  ); then released p50 might be sequestered and transported to the nucleus by Bcl-3.	transcription
55956	2	335292	7	NULL	NULL	0	NULL	IKK			mediate					phosphorylation					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_282	14668329	Signal-induced degradation of p105 could result from IKK-mediated phosphorylation and targeting by the proteasome ( ,  ,  ); then released p50 might be sequestered and transported to the nucleus by Bcl-3.	transcription
55957	3	335292	7	NULL	NULL	0	NULL	statement 1			result from					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_282	14668329	Signal-induced degradation of p105 could result from IKK-mediated phosphorylation and targeting by the proteasome ( ,  ,  ); then released p50 might be sequestered and transported to the nucleus by Bcl-3.	transcription
55958	4	335292	7	NULL	NULL	0	NULL	statement 1			result from					proteasome		targeting by			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_282	14668329	Signal-induced degradation of p105 could result from IKK-mediated phosphorylation and targeting by the proteasome ( ,  ,  ); then released p50 might be sequestered and transported to the nucleus by Bcl-3.	transcription
55959	5	335292	7	NULL	NULL	0	NULL	statement 3			occur along with					statement 4					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_282	14668329	Signal-induced degradation of p105 could result from IKK-mediated phosphorylation and targeting by the proteasome ( ,  ,  ); then released p50 might be sequestered and transported to the nucleus by Bcl-3.	transcription
55960	6	335292	7	NULL	NULL	0	NULL	Bcl-3			sequester		may			p50					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_282	14668329	Signal-induced degradation of p105 could result from IKK-mediated phosphorylation and targeting by the proteasome ( ,  ,  ); then released p50 might be sequestered and transported to the nucleus by Bcl-3.	transcription
55961	7	335292	7	NULL	NULL	0	NULL	p50			be transpored to		may			nucleus					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_282	14668329	Signal-induced degradation of p105 could result from IKK-mediated phosphorylation and targeting by the proteasome ( ,  ,  ); then released p50 might be sequestered and transported to the nucleus by Bcl-3.	transcription
55962	8	335292	7	NULL	NULL	0	NULL	Bcl-3			support					statement 7					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_282	14668329	Signal-induced degradation of p105 could result from IKK-mediated phosphorylation and targeting by the proteasome ( ,  ,  ); then released p50 might be sequestered and transported to the nucleus by Bcl-3.	transcription
54865	1	335293	5	NULL	NULL	0	NULL	NF-kappaB			is a family of					transcription factors					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
54926	2	335293	5	NULL	NULL	0	NULL	statement 1			includes					RelA					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
54927	3	335293	5	NULL	NULL	0	NULL	statement 1			includes					NF-kappaB1 p50					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
54928	4	335293	5	NULL	NULL	0	NULL	statement 1			includes					NF-kappaB1 p105					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
54929	5	335293	5	NULL	NULL	0	NULL	statement 1			includes					NF-kappaB2 p52					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
54930	6	335293	5	NULL	NULL	0	NULL	statement 1			includes					NF-kappaB2 p100					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
54931	7	335293	5	NULL	NULL	0	NULL	statement 1			includes					c-Rel					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
54932	8	335293	5	NULL	NULL	0	NULL	statement 1			includes					RelB					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
54933	9	335293	5	NULL	NULL	0	NULL	RelA			is a synonym of					p65					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
55963	1	335293	7	NULL	NULL	0	NULL	NF-kappaB 			is a type of					transcription factors					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
55964	2	335293	7	NULL	NULL	0	NULL	NF-kappaB family			include					RelA					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
55965	3	335293	7	NULL	NULL	0	NULL	NF-kappaB family			include					NF-kappaB1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
55966	4	335293	7	NULL	NULL	0	NULL	NF-kappaB family			include					NF-kappaB2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
55967	5	335293	7	NULL	NULL	0	NULL	NF-kappaB family			include					c-Rel					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
55968	6	335293	7	NULL	NULL	0	NULL	NF-kappaB family			include					RelB					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
55969	7	335293	7	NULL	NULL	0	NULL	RelA 			is					p65					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
55970	8	335293	7	NULL	NULL	0	NULL	NF-kappaB1			include					p50					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
55971	9	335293	7	NULL	NULL	0	NULL	NF-kappaB1			include					p105					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
55972	10	335293	7	NULL	NULL	0	NULL	NF-kappaB2 			include					p52					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
55973	11	335293	7	NULL	NULL	0	NULL	NF-kappaB2 			include					p100					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_30	16835236	NF-kappaB is a family of transcription factors that includes RelA (p65), NF-kappaB1 (p50 and p105), NF-kappaB2 (p52 and p100), c-Rel, and RelB.	transcription
54866	1	335294	5	NULL	NULL	0	NULL	gp 10		bacteriophage T7	is a type of					capsid protein					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_148	12807880	Replacement of a large  portion of p105 starting from the end of the GRR with either IkappaBalpha  or bacteriophage T7 capsid protein gp 10 does not affect p50  production ( ).	transcription
54867	2	335294	5	NULL	NULL	0	NULL	p105		large portion of	is replaced with					IkappaBalpha					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_148	12807880	Replacement of a large  portion of p105 starting from the end of the GRR with either IkappaBalpha  or bacteriophage T7 capsid protein gp 10 does not affect p50  production ( ).	transcription
54868	3	335294	5	NULL	NULL	0	NULL	p105		large portion of	is replaced with					gp 10		bacteriophage T7			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_148	12807880	Replacement of a large  portion of p105 starting from the end of the GRR with either IkappaBalpha  or bacteriophage T7 capsid protein gp 10 does not affect p50  production ( ).	transcription
54869	4	335294	5	NULL	NULL	0	NULL	statement 2			is an alternative to					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_148	12807880	Replacement of a large  portion of p105 starting from the end of the GRR with either IkappaBalpha  or bacteriophage T7 capsid protein gp 10 does not affect p50  production ( ).	transcription
54870	5	335294	5	NULL	NULL	0	NULL	statement 2			does not affect					p50		production of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_148	12807880	Replacement of a large  portion of p105 starting from the end of the GRR with either IkappaBalpha  or bacteriophage T7 capsid protein gp 10 does not affect p50  production ( ).	transcription
54871	6	335294	5	NULL	NULL	0	NULL	statement 3			does not affect					p50		production of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_148	12807880	Replacement of a large  portion of p105 starting from the end of the GRR with either IkappaBalpha  or bacteriophage T7 capsid protein gp 10 does not affect p50  production ( ).	transcription
55974	1	335294	7	NULL	NULL	0	NULL	 IkappaBalpha			replace					p105 			 large portion from the end of GRR		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_148	12807880	Replacement of a large  portion of p105 starting from the end of the GRR with either IkappaBalpha  or bacteriophage T7 capsid protein gp 10 does not affect p50  production ( ).	transcription
55975	2	335294	7	NULL	NULL	0	NULL	gp 10			replace					p105 			large portion from the end of the GRR		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_148	12807880	Replacement of a large  portion of p105 starting from the end of the GRR with either IkappaBalpha  or bacteriophage T7 capsid protein gp 10 does not affect p50  production ( ).	transcription
55976	3	335294	7	NULL	NULL	0	NULL	gp 10			is a type of					 capsid protein		bacteriophage T7			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_148	12807880	Replacement of a large  portion of p105 starting from the end of the GRR with either IkappaBalpha  or bacteriophage T7 capsid protein gp 10 does not affect p50  production ( ).	transcription
55977	4	335294	7	NULL	NULL	0	NULL	statement 1			does not affect					p50		production of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_148	12807880	Replacement of a large  portion of p105 starting from the end of the GRR with either IkappaBalpha  or bacteriophage T7 capsid protein gp 10 does not affect p50  production ( ).	transcription
55978	5	335294	7	NULL	NULL	0	NULL	statement 2			does not affect					p50		production of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_148	12807880	Replacement of a large  portion of p105 starting from the end of the GRR with either IkappaBalpha  or bacteriophage T7 capsid protein gp 10 does not affect p50  production ( ).	transcription
54872	1	335295	5	NULL	NULL	0	NULL	p105 protein		proteolysis of	leads to					p50		production of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_196	12807880	Our work further confirmed that proteolysis leading to p50 production  initiates at an internal site, rather than at the C terminus of the p105  protein.	transcription
55979	1	335295	7	NULL	NULL	0	NULL	proteolysis			lead to					p50		production of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_196	12807880	Our work further confirmed that proteolysis leading to p50 production  initiates at an internal site, rather than at the C terminus of the p105  protein.	transcription
55980	2	335295	7	NULL	NULL	0	NULL	statement 1			initiates at an					internal site					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_196	12807880	Our work further confirmed that proteolysis leading to p50 production  initiates at an internal site, rather than at the C terminus of the p105  protein.	transcription
55981	3	335295	7	NULL	NULL	0	NULL	statement 1			does not initiate from					p105 			C terminus of		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_31479_s_196	12807880	Our work further confirmed that proteolysis leading to p50 production  initiates at an internal site, rather than at the C terminus of the p105  protein.	transcription
54873	1	335296	5	NULL	NULL	0	NULL	p105			is processed to					p50					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_41_39583_s_180	12871932	Indeed, some reports demonstrate that TNF-alpha induces p105 processing to p50 ( ,  ), others show that TNF-alpha induces complete degradation of the protein ( ,  ).	transcription
54874	2	335296	5	NULL	NULL	0	NULL	TNF-alpha			induces					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_41_39583_s_180	12871932	Indeed, some reports demonstrate that TNF-alpha induces p105 processing to p50 ( ,  ), others show that TNF-alpha induces complete degradation of the protein ( ,  ).	transcription
54875	3	335296	5	NULL	NULL	0	NULL	TNF-alpha			induces					p105		complete degradation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_41_39583_s_180	12871932	Indeed, some reports demonstrate that TNF-alpha induces p105 processing to p50 ( ,  ), others show that TNF-alpha induces complete degradation of the protein ( ,  ).	transcription
55982	1	335296	7	NULL	NULL	0	NULL	 p105			processed to					p50					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_41_39583_s_180	12871932	Indeed, some reports demonstrate that TNF-alpha induces p105 processing to p50 ( ,  ), others show that TNF-alpha induces complete degradation of the protein ( ,  ).	transcription
55983	2	335296	7	NULL	NULL	0	NULL	TNF-alpha			induce					statement 1					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_41_39583_s_180	12871932	Indeed, some reports demonstrate that TNF-alpha induces p105 processing to p50 ( ,  ), others show that TNF-alpha induces complete degradation of the protein ( ,  ).	transcription
55984	3	335296	7	NULL	NULL	0	NULL	 TNF-alpha			induce					p105		complete degradation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_41_39583_s_180	12871932	Indeed, some reports demonstrate that TNF-alpha induces p105 processing to p50 ( ,  ), others show that TNF-alpha induces complete degradation of the protein ( ,  ).	transcription
54876	1	335297	5	NULL	NULL	0	NULL	NFkappaB			is a precursor of			p105		NFkappaB			p50 subunit		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_48839_s_184	14514692	However, NFkappaB p105 is the precursor form of the NFkappaB p50 subunit that, in our study, did not appear to be the major subunit involved in the TNFalpha-dependent transcription of  MEFV.	transcription
54877	2	335297	5	NULL	NULL	0	NULL	MEFV		transcription of	is dependent on					TNFalpha					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_48839_s_184	14514692	However, NFkappaB p105 is the precursor form of the NFkappaB p50 subunit that, in our study, did not appear to be the major subunit involved in the TNFalpha-dependent transcription of  MEFV.	transcription
54878	3	335297	5	NULL	NULL	0	NULL	NFkappaB			not involved in		may	p105		statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_48839_s_184	14514692	However, NFkappaB p105 is the precursor form of the NFkappaB p50 subunit that, in our study, did not appear to be the major subunit involved in the TNFalpha-dependent transcription of  MEFV.	transcription
55985	1	335297	7	NULL	NULL	0	NULL	NFkappaB p105 			is precursor of					NFkappaB p50 subunit					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_48839_s_184	14514692	However, NFkappaB p105 is the precursor form of the NFkappaB p50 subunit that, in our study, did not appear to be the major subunit involved in the TNFalpha-dependent transcription of  MEFV.	transcription
55986	2	335297	7	NULL	NULL	0	NULL	MEFV		transcription of	depends on					 TNFalpha					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_48839_s_184	14514692	However, NFkappaB p105 is the precursor form of the NFkappaB p50 subunit that, in our study, did not appear to be the major subunit involved in the TNFalpha-dependent transcription of  MEFV.	transcription
55987	3	335297	7	NULL	NULL	0	NULL	 NFkappaB p50 subunit 			 not be involved in		may			statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_49_48839_s_184	14514692	However, NFkappaB p105 is the precursor form of the NFkappaB p50 subunit that, in our study, did not appear to be the major subunit involved in the TNFalpha-dependent transcription of  MEFV.	transcription
54879	1	335298	5	NULL	NULL	0	NULL	p105 inhibitor			gains					p50		early control of			NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_40	10970863	These results highlight a mechanism by which the p105 inhibitor gains very early control of the p50 transcription factor and provide a new perspective on Rel protein assembly.	transcription
54880	2	335298	5	NULL	NULL	0	NULL	p50			is a type of					transcription factor					NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_40	10970863	These results highlight a mechanism by which the p105 inhibitor gains very early control of the p50 transcription factor and provide a new perspective on Rel protein assembly.	transcription
55988	1	335298	7	NULL	NULL	0	NULL	p105 inhibitor			gains early control of					p50 transcription factor					NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_40	10970863	These results highlight a mechanism by which the p105 inhibitor gains very early control of the p50 transcription factor and provide a new perspective on Rel protein assembly.	transcription
55989	2	335298	7	NULL	NULL	0	NULL	statement 1			provide					Rel protein assembly		new prespective on			NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_40	10970863	These results highlight a mechanism by which the p105 inhibitor gains very early control of the p50 transcription factor and provide a new perspective on Rel protein assembly.	transcription
54881	1	335299	5	NULL	NULL	0	NULL	p105			is processed to					p50					NULL		0	NULL	NULL	NULL	gw60_embo_19_11_2580_s_49	10835356	Here we show that IkappaKbeta-mediated phosphorylation at the C-terminal domain results in accelerated processing of p105 to p50, a process that is mediated by the SCFbeta-TrCP E3.	transcription
54882	2	335299	5	NULL	NULL	0	NULL	IkappaKbeta			mediates					p105		phosphorylation of	C-terminus		NULL		0	NULL	NULL	NULL	gw60_embo_19_11_2580_s_49	10835356	Here we show that IkappaKbeta-mediated phosphorylation at the C-terminal domain results in accelerated processing of p105 to p50, a process that is mediated by the SCFbeta-TrCP E3.	transcription
54883	3	335299	5	NULL	NULL	0	NULL	statement 2			results in					statement 1		accelerated			NULL		0	NULL	NULL	NULL	gw60_embo_19_11_2580_s_49	10835356	Here we show that IkappaKbeta-mediated phosphorylation at the C-terminal domain results in accelerated processing of p105 to p50, a process that is mediated by the SCFbeta-TrCP E3.	transcription
54884	4	335299	5	NULL	NULL	0	NULL	SCFbeta-TrCP E3			mediates					statement 1		accelerated			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_11_2580_s_49	10835356	Here we show that IkappaKbeta-mediated phosphorylation at the C-terminal domain results in accelerated processing of p105 to p50, a process that is mediated by the SCFbeta-TrCP E3.	transcription
55990	1	335299	7	NULL	NULL	0	NULL	 IkappaKbeta			mediates							phosphorylation at	C-terminal domain		NULL		0	NULL	NULL	NULL	gw60_embo_19_11_2580_s_49	10835356	Here we show that IkappaKbeta-mediated phosphorylation at the C-terminal domain results in accelerated processing of p105 to p50, a process that is mediated by the SCFbeta-TrCP E3.	transcription
55991	2	335299	7	NULL	NULL	0	NULL	p105			processed to					p50					NULL		0	NULL	NULL	NULL	gw60_embo_19_11_2580_s_49	10835356	Here we show that IkappaKbeta-mediated phosphorylation at the C-terminal domain results in accelerated processing of p105 to p50, a process that is mediated by the SCFbeta-TrCP E3.	transcription
55992	3	335299	7	NULL	NULL	0	NULL	statement 1			accelerates					statement 2					NULL		0	NULL	NULL	NULL	gw60_embo_19_11_2580_s_49	10835356	Here we show that IkappaKbeta-mediated phosphorylation at the C-terminal domain results in accelerated processing of p105 to p50, a process that is mediated by the SCFbeta-TrCP E3.	transcription
55993	4	335299	7	NULL	NULL	0	NULL	SCFbeta-TrCP E3			mediates					statement 3					NULL		0	NULL	NULL	NULL	gw60_embo_19_11_2580_s_49	10835356	Here we show that IkappaKbeta-mediated phosphorylation at the C-terminal domain results in accelerated processing of p105 to p50, a process that is mediated by the SCFbeta-TrCP E3.	transcription
54885	1	335300	5	NULL	NULL	0	NULL	p105			is targeted of		may	glycine-rich region		endoprotease					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_31	10469655	C-terminal to the p50 moiety, p105 contains a glycine-rich region which is required for processing in mammalian cells and may be the target of an endoprotease (Lin and Ghosh, 1996  ).	transcription
55994	1	335300	7	NULL	NULL	0	NULL	p105			contains								glycine-rich region		NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_31	10469655	C-terminal to the p50 moiety, p105 contains a glycine-rich region which is required for processing in mammalian cells and may be the target of an endoprotease (Lin and Ghosh, 1996  ).	transcription
55995	2	335300	7	NULL	NULL	0	NULL	statement 1			is required for					mammalian cells		processing in			NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_31	10469655	C-terminal to the p50 moiety, p105 contains a glycine-rich region which is required for processing in mammalian cells and may be the target of an endoprotease (Lin and Ghosh, 1996  ).	transcription
55996	3	335300	7	NULL	NULL	0	NULL	statement 1			be target for		may			endoprotease					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_31	10469655	C-terminal to the p50 moiety, p105 contains a glycine-rich region which is required for processing in mammalian cells and may be the target of an endoprotease (Lin and Ghosh, 1996  ).	transcription
54886	1	335301	5	NULL	NULL	0	NULL	BCL-3			is a type of					oncoprotein					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_19	9529257	Additionally, the candidate oncoprotein BCL-3 induces p50 homodimers from cytosolic p105/p50 complexes without  enhancing the processing of p105 (Watanabe et al., 1997   ).	transcription
54887	2	335301	5	NULL	NULL	0	NULL	p50 homodimers			formed from					p105/p50 complexes		cytosolic			NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_19	9529257	Additionally, the candidate oncoprotein BCL-3 induces p50 homodimers from cytosolic p105/p50 complexes without  enhancing the processing of p105 (Watanabe et al., 1997   ).	transcription
54888	3	335301	5	NULL	NULL	0	NULL	statement 2			does not enhance					p105		processing of			NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_19	9529257	Additionally, the candidate oncoprotein BCL-3 induces p50 homodimers from cytosolic p105/p50 complexes without  enhancing the processing of p105 (Watanabe et al., 1997   ).	transcription
54889	4	335301	5	NULL	NULL	0	NULL	BCL-3			induces					statement 3					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_19	9529257	Additionally, the candidate oncoprotein BCL-3 induces p50 homodimers from cytosolic p105/p50 complexes without  enhancing the processing of p105 (Watanabe et al., 1997   ).	transcription
55997	1	335301	7	NULL	NULL	0	NULL	p50 homodimers			obtained from					p105/p50 complexes		cytosolic			NULL		NULL	NULL	NULL	NULL	gw60_cell_92_6_819_s_19	9529257	Additionally, the candidate oncoprotein BCL-3 induces p50 homodimers from cytosolic p105/p50 complexes without  enhancing the processing of p105 (Watanabe et al., 1997   ).	transcription
55998	2	335301	7	NULL	NULL	0	NULL	BCL-3 			induce					statement 1					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_19	9529257	Additionally, the candidate oncoprotein BCL-3 induces p50 homodimers from cytosolic p105/p50 complexes without  enhancing the processing of p105 (Watanabe et al., 1997   ).	transcription
55999	3	335301	7	NULL	NULL	0	NULL	BCL-3 			does not enhance					p105		processing of			NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_19	9529257	Additionally, the candidate oncoprotein BCL-3 induces p50 homodimers from cytosolic p105/p50 complexes without  enhancing the processing of p105 (Watanabe et al., 1997   ).	transcription
56000	4	335301	7	NULL	NULL	0	NULL	BCL-3 			is a type of					oncoprotein					NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_19	9529257	Additionally, the candidate oncoprotein BCL-3 induces p50 homodimers from cytosolic p105/p50 complexes without  enhancing the processing of p105 (Watanabe et al., 1997   ).	transcription
54890	1	335302	5	NULL	NULL	0	NULL	Ang II			effect		delayed			NF-kappaB1		processing of			NULL	VSMCs	0	NULL	NULL	NULL	gw60_circulationres_84_6_695_s_253	10189357	Our data also implicate a delayed effect of Ang II on NF-kappaB1 processing in VSMCs. NF-kappaB1 p50 is the NH2-terminal DNA-binding product of p105 precursor processing.	transcription
54891	2	335302	5	NULL	NULL	0	NULL	NF-kappaB1 p50			is a product of					p105 precursor		processing of			NULL		0	NULL	NULL	NULL	gw60_circulationres_84_6_695_s_253	10189357	Our data also implicate a delayed effect of Ang II on NF-kappaB1 processing in VSMCs. NF-kappaB1 p50 is the NH2-terminal DNA-binding product of p105 precursor processing.	transcription
56001	1	335302	7	NULL	NULL	0	NULL	NF-kappaB1 p50			is a type of								NH2-terminal DNA-binding product		NULL		0	NULL	NULL	NULL	gw60_circulationres_84_6_695_s_253	10189357	Our data also implicate a delayed effect of Ang II on NF-kappaB1 processing in VSMCs. NF-kappaB1 p50 is the NH2-terminal DNA-binding product of p105 precursor processing.	transcription
56002	2	335302	7	NULL	NULL	0	NULL	statement 1			is obtained from					p105 precursor		processing of			NULL		0	NULL	NULL	NULL	gw60_circulationres_84_6_695_s_253	10189357	Our data also implicate a delayed effect of Ang II on NF-kappaB1 processing in VSMCs. NF-kappaB1 p50 is the NH2-terminal DNA-binding product of p105 precursor processing.	transcription
54892	1	335303	5	NULL	NULL	0	NULL	TPL-2			co-immunoprecipitates with		specifically			p50					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_109	9950430	As TPL-2 specifically co-immunoprecipitates with p50, Rel-A and c-Rel ( Fig.3a), it may regulate proteolysis of all of the major p105 complexes present in cells 6, 7.	transcription
54893	2	335303	5	NULL	NULL	0	NULL	TPL-2			co-immunoprecipitates with		specifically			Rel-A					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_109	9950430	As TPL-2 specifically co-immunoprecipitates with p50, Rel-A and c-Rel ( Fig.3a), it may regulate proteolysis of all of the major p105 complexes present in cells 6, 7.	transcription
54894	3	335303	5	NULL	NULL	0	NULL	TPL-2			co-immunoprecipitates with		specifically			c-Rel					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_109	9950430	As TPL-2 specifically co-immunoprecipitates with p50, Rel-A and c-Rel ( Fig.3a), it may regulate proteolysis of all of the major p105 complexes present in cells 6, 7.	transcription
54895	4	335303	5	NULL	NULL	0	NULL	TPL-2			regulates		may			p105 complexes		proteolysis of major 			NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_109	9950430	As TPL-2 specifically co-immunoprecipitates with p50, Rel-A and c-Rel ( Fig.3a), it may regulate proteolysis of all of the major p105 complexes present in cells 6, 7.	transcription
56003	1	335303	7	NULL	NULL	0	NULL	TPL-2			bind		specifically			p50					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_109	9950430	As TPL-2 specifically co-immunoprecipitates with p50, Rel-A and c-Rel ( Fig.3a), it may regulate proteolysis of all of the major p105 complexes present in cells 6, 7.	transcription
56004	2	335303	7	NULL	NULL	0	NULL	TPL-2			bind		specifically			Rel-A					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_109	9950430	As TPL-2 specifically co-immunoprecipitates with p50, Rel-A and c-Rel ( Fig.3a), it may regulate proteolysis of all of the major p105 complexes present in cells 6, 7.	transcription
56005	3	335303	7	NULL	NULL	0	NULL	TPL-2 			bind		specifically			c-Rel					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_109	9950430	As TPL-2 specifically co-immunoprecipitates with p50, Rel-A and c-Rel ( Fig.3a), it may regulate proteolysis of all of the major p105 complexes present in cells 6, 7.	transcription
56006	4	335303	7	NULL	NULL	0	NULL	statement 1			regulate		may			p105 complex		proteolysis of			NULL	cells	0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_109	9950430	As TPL-2 specifically co-immunoprecipitates with p50, Rel-A and c-Rel ( Fig.3a), it may regulate proteolysis of all of the major p105 complexes present in cells 6, 7.	transcription
56007	5	335303	7	NULL	NULL	0	NULL	statement 2			regulate		may			p105 complex		proteolysis of			NULL	cells	0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_109	9950430	As TPL-2 specifically co-immunoprecipitates with p50, Rel-A and c-Rel ( Fig.3a), it may regulate proteolysis of all of the major p105 complexes present in cells 6, 7.	transcription
56008	6	335303	7	NULL	NULL	0	NULL	statement 3			regulate		may			p105 complex		proteolysis of			NULL	cells	0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_109	9950430	As TPL-2 specifically co-immunoprecipitates with p50, Rel-A and c-Rel ( Fig.3a), it may regulate proteolysis of all of the major p105 complexes present in cells 6, 7.	transcription
54896	1	335304	5	NULL	NULL	0	NULL	p105			interacts with			C-terminal region		p50			nuclear localization signal		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_512_s_641	9418898	Interaction of the C-terminal region of p105 with the nuclear localization signal of p50 is required for inhibition of NF-kappa B DNA binding activity.	transcription
54897	2	335304	5	NULL	NULL	0	NULL	NF-kappa B			bind					DNA					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_512_s_641	9418898	Interaction of the C-terminal region of p105 with the nuclear localization signal of p50 is required for inhibition of NF-kappa B DNA binding activity.	transcription
54898	3	335304	5	NULL	NULL	0	NULL	statement 1			is required for					statement 2		inhibition of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_512_s_641	9418898	Interaction of the C-terminal region of p105 with the nuclear localization signal of p50 is required for inhibition of NF-kappa B DNA binding activity.	transcription
56009	1	335304	7	NULL	NULL	0	NULL	p105 			interacts with			C-terminal region		p50			nuclear localization signal		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_512_s_641	9418898	Interaction of the C-terminal region of p105 with the nuclear localization signal of p50 is required for inhibition of NF-kappa B DNA binding activity.	transcription
56010	2	335304	7	NULL	NULL	0	NULL	NF-kappa B 			bind					DNA					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_512_s_641	9418898	Interaction of the C-terminal region of p105 with the nuclear localization signal of p50 is required for inhibition of NF-kappa B DNA binding activity.	transcription
56011	3	335304	7	NULL	NULL	0	NULL	statement 1			is required for					statement 2		inhibition of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_512_s_641	9418898	Interaction of the C-terminal region of p105 with the nuclear localization signal of p50 is required for inhibition of NF-kappa B DNA binding activity.	transcription
54899	1	335305	5	NULL	NULL	0	NULL	LPS			is					lipopolysaccharide					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_12	11158290	In line with this and as a physiologically relevant model, lipopolysaccharide (LPS) induced degradation of endogenous p105 and p50 homodimer formation, but not processing in pre-B cells.	transcription
54900	2	335305	5	NULL	NULL	0	NULL	LPS			induces					p105		degradation of;;endogenous			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_12	11158290	In line with this and as a physiologically relevant model, lipopolysaccharide (LPS) induced degradation of endogenous p105 and p50 homodimer formation, but not processing in pre-B cells.	transcription
54901	3	335305	5	NULL	NULL	0	NULL	LPS			induces					p50 homodimer		formation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_12	11158290	In line with this and as a physiologically relevant model, lipopolysaccharide (LPS) induced degradation of endogenous p105 and p50 homodimer formation, but not processing in pre-B cells.	transcription
56012	1	335305	7	NULL	NULL	0	NULL	p105		endogenous	homodimerize with					p105		endogenous			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_12	11158290	In line with this and as a physiologically relevant model, lipopolysaccharide (LPS) induced degradation of endogenous p105 and p50 homodimer formation, but not processing in pre-B cells.	transcription
56013	2	335305	7	NULL	NULL	0	NULL	p50		endogenous	homodimerize with					p50		endogenous			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_12	11158290	In line with this and as a physiologically relevant model, lipopolysaccharide (LPS) induced degradation of endogenous p105 and p50 homodimer formation, but not processing in pre-B cells.	transcription
56014	3	335305	7	NULL	NULL	0	NULL	LPS			induce					statement 1		degradation of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_12	11158290	In line with this and as a physiologically relevant model, lipopolysaccharide (LPS) induced degradation of endogenous p105 and p50 homodimer formation, but not processing in pre-B cells.	transcription
56015	4	335305	7	NULL	NULL	0	NULL	LPS			induce					statement 2		degradation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_12	11158290	In line with this and as a physiologically relevant model, lipopolysaccharide (LPS) induced degradation of endogenous p105 and p50 homodimer formation, but not processing in pre-B cells.	transcription
56016	5	335305	7	NULL	NULL	0	NULL	LPS			is					lipopolysaccharide					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_12	11158290	In line with this and as a physiologically relevant model, lipopolysaccharide (LPS) induced degradation of endogenous p105 and p50 homodimer formation, but not processing in pre-B cells.	transcription
56017	6	335305	7	NULL	NULL	0	NULL	LPS			does not induce					p105		processing of			NULL	pre-B cells	0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_12	11158290	In line with this and as a physiologically relevant model, lipopolysaccharide (LPS) induced degradation of endogenous p105 and p50 homodimer formation, but not processing in pre-B cells.	transcription
56018	7	335305	7	NULL	NULL	0	NULL	LPS			does not induce					p50		processing of			NULL	pre-B cells	0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_12	11158290	In line with this and as a physiologically relevant model, lipopolysaccharide (LPS) induced degradation of endogenous p105 and p50 homodimer formation, but not processing in pre-B cells.	transcription
54902	1	335306	5	NULL	NULL	0	NULL	IKK complex		functional;;endogenous	contains					IKKgamma					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_257	11158290	Taken together, these data demonstrate that a functional endogenous IKK complex containing IKKgamma is required for LPS-induced p105 degradation and p50 release.	transcription
54903	2	335306	5	NULL	NULL	0	NULL	LPS			induces					p105		degradation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_257	11158290	Taken together, these data demonstrate that a functional endogenous IKK complex containing IKKgamma is required for LPS-induced p105 degradation and p50 release.	transcription
54904	3	335306	5	NULL	NULL	0	NULL	statement 2			releases					p50					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_257	11158290	Taken together, these data demonstrate that a functional endogenous IKK complex containing IKKgamma is required for LPS-induced p105 degradation and p50 release.	transcription
54905	4	335306	5	NULL	NULL	0	NULL	statement 1			is required for					statement 2					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_257	11158290	Taken together, these data demonstrate that a functional endogenous IKK complex containing IKKgamma is required for LPS-induced p105 degradation and p50 release.	transcription
54906	5	335306	5	NULL	NULL	0	NULL	statement 1			is required for					statement 3					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_257	11158290	Taken together, these data demonstrate that a functional endogenous IKK complex containing IKKgamma is required for LPS-induced p105 degradation and p50 release.	transcription
56019	1	335306	7	NULL	NULL	0	NULL	LPS			induce					p105		degradation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_257	11158290	Taken together, these data demonstrate that a functional endogenous IKK complex containing IKKgamma is required for LPS-induced p105 degradation and p50 release.	transcription
56020	2	335306	7	NULL	NULL	0	NULL	LPS			induce					p50		release of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_257	11158290	Taken together, these data demonstrate that a functional endogenous IKK complex containing IKKgamma is required for LPS-induced p105 degradation and p50 release.	transcription
56021	3	335306	7	NULL	NULL	0	NULL	IKK complex		 functional;;endogenous	contains					IKKgamma					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_257	11158290	Taken together, these data demonstrate that a functional endogenous IKK complex containing IKKgamma is required for LPS-induced p105 degradation and p50 release.	transcription
56022	4	335306	7	NULL	NULL	0	NULL	statement 3			is required for					statement 1					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_257	11158290	Taken together, these data demonstrate that a functional endogenous IKK complex containing IKKgamma is required for LPS-induced p105 degradation and p50 release.	transcription
56023	5	335306	7	NULL	NULL	0	NULL	statement 3			is required for					statement 2					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_257	11158290	Taken together, these data demonstrate that a functional endogenous IKK complex containing IKKgamma is required for LPS-induced p105 degradation and p50 release.	transcription
54907	1	335307	5	NULL	NULL	0	NULL	p50		overexpressed	does not affect					p105- Tth111		processing of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_180	11350967	As can be seen in Fig.  5 A, overexpressed p50 does not affect processing of p105- Tth111 (11%; compare  lanes 1 and  2 with  lanes 3 and  4).	transcription
56024	1	335307	7	NULL	NULL	0	NULL	 p50		overexpressed	does not affect					p105- Tth111		processing of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_180	11350967	As can be seen in Fig.  5 A, overexpressed p50 does not affect processing of p105- Tth111 (11%; compare  lanes 1 and  2 with  lanes 3 and  4).	transcription
54908	1	335308	5	NULL	NULL	0	NULL	IKK			mediates					p105		degradation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_238	11350967	Heissmeyer and colleagues ( 15) have shown that IKK-mediated degradation of p105 releases docked p50 that interacts with Bcl-3 to generate the trimeric p50.p50.Bcl-3 active transcription factor.	transcription
54909	2	335308	5	NULL	NULL	0	NULL	statement 1			releases					p50		docked			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_238	11350967	Heissmeyer and colleagues ( 15) have shown that IKK-mediated degradation of p105 releases docked p50 that interacts with Bcl-3 to generate the trimeric p50.p50.Bcl-3 active transcription factor.	transcription
54910	3	335308	5	NULL	NULL	0	NULL	p50			interacts with					Bcl-3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_238	11350967	Heissmeyer and colleagues ( 15) have shown that IKK-mediated degradation of p105 releases docked p50 that interacts with Bcl-3 to generate the trimeric p50.p50.Bcl-3 active transcription factor.	transcription
54911	4	335308	5	NULL	NULL	0	NULL	statement 3			generates					p50.p50.Bcl-3 timer					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_238	11350967	Heissmeyer and colleagues ( 15) have shown that IKK-mediated degradation of p105 releases docked p50 that interacts with Bcl-3 to generate the trimeric p50.p50.Bcl-3 active transcription factor.	transcription
54912	5	335308	5	NULL	NULL	0	NULL	p50.p50.Bcl-3 trimer			is a type of					active transcription factor					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_238	11350967	Heissmeyer and colleagues ( 15) have shown that IKK-mediated degradation of p105 releases docked p50 that interacts with Bcl-3 to generate the trimeric p50.p50.Bcl-3 active transcription factor.	transcription
56025	1	335308	7	NULL	NULL	0	NULL	IKK			mediate					p105		degradation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_238	11350967	Heissmeyer and colleagues ( 15) have shown that IKK-mediated degradation of p105 releases docked p50 that interacts with Bcl-3 to generate the trimeric p50.p50.Bcl-3 active transcription factor.	transcription
56026	2	335308	7	NULL	NULL	0	NULL	statement 1			release					p50		docked			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_238	11350967	Heissmeyer and colleagues ( 15) have shown that IKK-mediated degradation of p105 releases docked p50 that interacts with Bcl-3 to generate the trimeric p50.p50.Bcl-3 active transcription factor.	transcription
56027	3	335308	7	NULL	NULL	0	NULL	p50			interacts with					Bcl-3 					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_238	11350967	Heissmeyer and colleagues ( 15) have shown that IKK-mediated degradation of p105 releases docked p50 that interacts with Bcl-3 to generate the trimeric p50.p50.Bcl-3 active transcription factor.	transcription
56028	4	335308	7	NULL	NULL	0	NULL	statement 3			generate					p50.p50.Bcl-3		trimeric			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_238	11350967	Heissmeyer and colleagues ( 15) have shown that IKK-mediated degradation of p105 releases docked p50 that interacts with Bcl-3 to generate the trimeric p50.p50.Bcl-3 active transcription factor.	transcription
56029	5	335308	7	NULL	NULL	0	NULL	p50.p50.Bcl-3			is a type of					active transcription factor					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_238	11350967	Heissmeyer and colleagues ( 15) have shown that IKK-mediated degradation of p105 releases docked p50 that interacts with Bcl-3 to generate the trimeric p50.p50.Bcl-3 active transcription factor.	transcription
54913	1	335309	5	NULL	NULL	0	NULL	p105		transcription of	is induced by					IKK					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_302	11350967	The researchers argue, although they do not provide direct experimental evidence, that the increased amount of p50 observed under these conditions is attributed to increased transcription of p105 induced by IKK.	transcription
54914	1	335309	5	NULL	NULL	0	NULL	p105		transcription of	is induced by					IKK					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_302	11350967	The researchers argue, although they do not provide direct experimental evidence, that the increased amount of p50 observed under these conditions is attributed to increased transcription of p105 induced by IKK.	transcription
54915	2	335309	5	NULL	NULL	0	NULL	statement 1		increased	leads to					p50		increased			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_302	11350967	The researchers argue, although they do not provide direct experimental evidence, that the increased amount of p50 observed under these conditions is attributed to increased transcription of p105 induced by IKK.	transcription
56030	1	335309	7	NULL	NULL	0	NULL	 IKK			induce					p105		increased transcription of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_302	11350967	The researchers argue, although they do not provide direct experimental evidence, that the increased amount of p50 observed under these conditions is attributed to increased transcription of p105 induced by IKK.	transcription
54916	1	335310	5	NULL	NULL	0	NULL	proteasome			activates		proteolytically			NFkappaB					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_16802_s_218	12615917	For example, the first step in the proteolytic activation of NFkappaB from its precursor protein p105 to yield p50 is catalyzed by the proteasome ( 37,  46).	transcription
54917	2	335310	5	NULL	NULL	0	NULL	p105 precursor protein			yields					p50					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_16802_s_218	12615917	For example, the first step in the proteolytic activation of NFkappaB from its precursor protein p105 to yield p50 is catalyzed by the proteasome ( 37,  46).	transcription
54918	3	335310	5	NULL	NULL	0	NULL	statement 1			leads to					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_16802_s_218	12615917	For example, the first step in the proteolytic activation of NFkappaB from its precursor protein p105 to yield p50 is catalyzed by the proteasome ( 37,  46).	transcription
56031	2	335310	7	NULL	NULL	0	NULL	statement 1			is obtained from					p105					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_19_16802_s_218	12615917	For example, the first step in the proteolytic activation of NFkappaB from its precursor protein p105 to yield p50 is catalyzed by the proteasome ( 37,  46).	transcription
56032	1	335310	7	NULL	NULL	0	NULL	proteasome 			catalyze					NFkappaB		proteolytic activation of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_19_16802_s_218	12615917	For example, the first step in the proteolytic activation of NFkappaB from its precursor protein p105 to yield p50 is catalyzed by the proteasome ( 37,  46).	transcription
56033	4	335310	7	NULL	NULL	0	NULL	p105			is a precursor of					NFkappaB					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_19_16802_s_218	12615917	For example, the first step in the proteolytic activation of NFkappaB from its precursor protein p105 to yield p50 is catalyzed by the proteasome ( 37,  46).	transcription
56034	3	335310	7	NULL	NULL	0	NULL	statement 1			yield					p50					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_16802_s_218	12615917	For example, the first step in the proteolytic activation of NFkappaB from its precursor protein p105 to yield p50 is catalyzed by the proteasome ( 37,  46).	transcription
54919	1	335311	5	NULL	NULL	0	NULL	NF-kappaB inducers		treatment	results in					p105		phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_25	9430676	Analogous to the situation for IkappaB-alpha, treatment of cells with inducers of NF-kappaB results in the phosphorylation of p105 ( 23-26), and an increase in the level of p50 is observed ( 27-29).	transcription
54920	2	335311	5	NULL	NULL	0	NULL	statement 1			leads to					p50		increase in level of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_25	9430676	Analogous to the situation for IkappaB-alpha, treatment of cells with inducers of NF-kappaB results in the phosphorylation of p105 ( 23-26), and an increase in the level of p50 is observed ( 27-29).	transcription
56913	1	335311	7	NULL	NULL	0	NULL	 NF-kappaB 		inducers of	result in					p105		phosphorylation of			NULL	cells	0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_25	9430676	Analogous to the situation for IkappaB-alpha, treatment of cells with inducers of NF-kappaB results in the phosphorylation of p105 ( 23-26), and an increase in the level of p50 is observed ( 27-29).	transcription
56914	2	335311	7	NULL	NULL	0	NULL	 NF-kappaB 		inducers of	increase					p50		level of			NULL	cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_25	9430676	Analogous to the situation for IkappaB-alpha, treatment of cells with inducers of NF-kappaB results in the phosphorylation of p105 ( 23-26), and an increase in the level of p50 is observed ( 27-29).	transcription
54921	1	335312	5	NULL	NULL	0	NULL	p105			is cleaved to					p50					NULL		0	NULL	NULL	NULL	gw60_science_295_5556_813_s_172	11823631	Thus, two proteolytic events--the cleavage of p105 to p50 and  the destruction of IkappaB governed by serine  phosphorylation--are required to produce the proteins and then activate them.	transcription
54922	2	335312	5	NULL	NULL	0	NULL	IkappaB		destruction of	is governed by					serine		phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_science_295_5556_813_s_172	11823631	Thus, two proteolytic events--the cleavage of p105 to p50 and  the destruction of IkappaB governed by serine  phosphorylation--are required to produce the proteins and then activate them.	transcription
56915	1	335312	7	NULL	NULL	0	NULL	 p105			cleaved to					p50					NULL		0	NULL	NULL	NULL	gw60_science_295_5556_813_s_172	11823631	Thus, two proteolytic events--the cleavage of p105 to p50 and  the destruction of IkappaB governed by serine  phosphorylation--are required to produce the proteins and then activate them.	transcription
56916	2	335312	7	NULL	NULL	0	NULL	serine 		phosphorylation of	governs					statement 1					NULL		0	NULL	NULL	NULL	gw60_science_295_5556_813_s_172	11823631	Thus, two proteolytic events--the cleavage of p105 to p50 and  the destruction of IkappaB governed by serine  phosphorylation--are required to produce the proteins and then activate them.	transcription
56917	3	335312	7	NULL	NULL	0	NULL	serine		phosphorylation of	governs					IkappaB		destruction of			NULL		0	NULL	NULL	NULL	gw60_science_295_5556_813_s_172	11823631	Thus, two proteolytic events--the cleavage of p105 to p50 and  the destruction of IkappaB governed by serine  phosphorylation--are required to produce the proteins and then activate them.	transcription
54923	1	335313	5	NULL	NULL	0	NULL	p105sr			inhibits		efficiently			NF-kappaB		activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_113	16835236	Consequently, p105sr efficiently inhibits all NF-kappaB activities, including p50 homodimers ( ).	transcription
54924	2	335313	5	NULL	NULL	0	NULL	p105sr			inhibits		efficiently			p50 homodimer					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_113	16835236	Consequently, p105sr efficiently inhibits all NF-kappaB activities, including p50 homodimers ( ).	transcription
56918	1	335313	7	NULL	NULL	0	NULL	 p105sr			inhibits		efficiently			NF-kappaB 		all activities of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_113	16835236	Consequently, p105sr efficiently inhibits all NF-kappaB activities, including p50 homodimers ( ).	transcription
56919	2	335313	7	NULL	NULL	0	NULL	NF-kappaB			include					p50 homodimers					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_36_26041_s_113	16835236	Consequently, p105sr efficiently inhibits all NF-kappaB activities, including p50 homodimers ( ).	transcription
56931	1	335314	7	NULL	NULL	0	NULL	p50			generated by					proteasome					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_12_8646_s_209	10567588	To investigate whether the reduced expression of p50 in NOD mouse spleen cells is attributable to defective p50 generation by the proteasome, we examined p50 generation by cytosolic extracts by using an in vitro assay in which 35S-labeled recombinant p105, or the truncated version, p60Tth, was used as the substrate ( 19,  61).	transcription
56932	2	335314	7	NULL	NULL	0	NULL	p50		reduced expression of	is attributed to					statement 1		defective			NULL	NOD mouse spleen cells	0	NULL	NULL	NULL	gw60_molcellbiol_19_12_8646_s_209	10567588	To investigate whether the reduced expression of p50 in NOD mouse spleen cells is attributable to defective p50 generation by the proteasome, we examined p50 generation by cytosolic extracts by using an in vitro assay in which 35S-labeled recombinant p105, or the truncated version, p60Tth, was used as the substrate ( 19,  61).	transcription
54925	1	335315	5	NULL	NULL	0	NULL	p105 protein		post-translational modifications of	leads to					p50		increase in level of			NULL	tolerant T cells	0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_30	14668329	Because transcriptional induction of the precursor protein p105 did not differ between tolerant and activated T cells, our data suggest that the overall increased levels of p50 in tolerant T cells may be due to post-translational modifications of the p105 protein.	transcription
56933	1	335315	7	NULL	NULL	0	NULL	p50		increased levels of;;tolerant T cells	due to					p105 protein		 post-translational modifications of 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_30	14668329	Because transcriptional induction of the precursor protein p105 did not differ between tolerant and activated T cells, our data suggest that the overall increased levels of p50 in tolerant T cells may be due to post-translational modifications of the p105 protein.	transcription
56934	2	335315	7	NULL	NULL	0	NULL	p105		transcriptional induction of ;;tolerant T cells	does not differ  from					p105		transcriptional induction of ;;activated T cells			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_30	14668329	Because transcriptional induction of the precursor protein p105 did not differ between tolerant and activated T cells, our data suggest that the overall increased levels of p50 in tolerant T cells may be due to post-translational modifications of the p105 protein.	transcription
56935	3	335315	7	NULL	NULL	0	NULL	p105			is a type of					precursor protein					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_30	14668329	Because transcriptional induction of the precursor protein p105 did not differ between tolerant and activated T cells, our data suggest that the overall increased levels of p50 in tolerant T cells may be due to post-translational modifications of the p105 protein.	transcription
54934	1	335316	5	NULL	NULL	0	NULL	p50			constitutes					p105			NH2-terminus		NULL		0	NULL	NULL	NULL	gw70_science_299_5605_408_s_8	12481023	Because p50 constitutes the NH2-terminus of p105 and the COOH-terminus is presumably blocked by the ribosome, the proteasome must either wait for release of nascent p105 from the ribosome or activate another protease that catalyzes the initial endoproteolytic step, as in the proteasome-dependent activation of Esp1 protease during sister chromatid exchange ( 9).	transcription
54935	2	335316	5	NULL	NULL	0	NULL	p105			is blocked by		presumably	COOH-terminus		ribosome					NULL		0	NULL	NULL	NULL	gw70_science_299_5605_408_s_8	12481023	Because p50 constitutes the NH2-terminus of p105 and the COOH-terminus is presumably blocked by the ribosome, the proteasome must either wait for release of nascent p105 from the ribosome or activate another protease that catalyzes the initial endoproteolytic step, as in the proteasome-dependent activation of Esp1 protease during sister chromatid exchange ( 9).	transcription
54936	3	335316	5	NULL	NULL	0	NULL	p105		nascent	is released from					ribosome					NULL		NULL	NULL	NULL	NULL	gw70_science_299_5605_408_s_8	12481023	Because p50 constitutes the NH2-terminus of p105 and the COOH-terminus is presumably blocked by the ribosome, the proteasome must either wait for release of nascent p105 from the ribosome or activate another protease that catalyzes the initial endoproteolytic step, as in the proteasome-dependent activation of Esp1 protease during sister chromatid exchange ( 9).	transcription
54937	4	335316	5	NULL	NULL	0	NULL	proteasome			waits for		may			statement 3					NULL		0	NULL	NULL	NULL	gw70_science_299_5605_408_s_8	12481023	Because p50 constitutes the NH2-terminus of p105 and the COOH-terminus is presumably blocked by the ribosome, the proteasome must either wait for release of nascent p105 from the ribosome or activate another protease that catalyzes the initial endoproteolytic step, as in the proteasome-dependent activation of Esp1 protease during sister chromatid exchange ( 9).	transcription
54938	5	335316	5	NULL	NULL	0	NULL	proteasome			activates		may			protease					NULL		0	NULL	NULL	NULL	gw70_science_299_5605_408_s_8	12481023	Because p50 constitutes the NH2-terminus of p105 and the COOH-terminus is presumably blocked by the ribosome, the proteasome must either wait for release of nascent p105 from the ribosome or activate another protease that catalyzes the initial endoproteolytic step, as in the proteasome-dependent activation of Esp1 protease during sister chromatid exchange ( 9).	transcription
54939	6	335316	5	NULL	NULL	0	NULL	statement 5			catalyze					endoproteolytic step		initial			NULL		0	NULL	NULL	NULL	gw70_science_299_5605_408_s_8	12481023	Because p50 constitutes the NH2-terminus of p105 and the COOH-terminus is presumably blocked by the ribosome, the proteasome must either wait for release of nascent p105 from the ribosome or activate another protease that catalyzes the initial endoproteolytic step, as in the proteasome-dependent activation of Esp1 protease during sister chromatid exchange ( 9).	transcription
54940	7	335316	5	NULL	NULL	0	NULL	statement 4			is an alternative to					statement 5					NULL		0	NULL	NULL	NULL	gw70_science_299_5605_408_s_8	12481023	Because p50 constitutes the NH2-terminus of p105 and the COOH-terminus is presumably blocked by the ribosome, the proteasome must either wait for release of nascent p105 from the ribosome or activate another protease that catalyzes the initial endoproteolytic step, as in the proteasome-dependent activation of Esp1 protease during sister chromatid exchange ( 9).	transcription
54941	8	335316	5	NULL	NULL	0	NULL	Esp1			is a type of					protease					NULL		0	NULL	NULL	NULL	gw70_science_299_5605_408_s_8	12481023	Because p50 constitutes the NH2-terminus of p105 and the COOH-terminus is presumably blocked by the ribosome, the proteasome must either wait for release of nascent p105 from the ribosome or activate another protease that catalyzes the initial endoproteolytic step, as in the proteasome-dependent activation of Esp1 protease during sister chromatid exchange ( 9).	transcription
54942	9	335316	5	NULL	NULL	0	NULL	Esp1		activation of	is dependent on					proteasome					NULL		0	NULL	NULL	NULL	gw70_science_299_5605_408_s_8	12481023	Because p50 constitutes the NH2-terminus of p105 and the COOH-terminus is presumably blocked by the ribosome, the proteasome must either wait for release of nascent p105 from the ribosome or activate another protease that catalyzes the initial endoproteolytic step, as in the proteasome-dependent activation of Esp1 protease during sister chromatid exchange ( 9).	transcription
54943	10	335316	5	NULL	NULL	0	NULL	statement 9			occurs during					sister chromatid exchange					NULL		0	NULL	NULL	NULL	gw70_science_299_5605_408_s_8	12481023	Because p50 constitutes the NH2-terminus of p105 and the COOH-terminus is presumably blocked by the ribosome, the proteasome must either wait for release of nascent p105 from the ribosome or activate another protease that catalyzes the initial endoproteolytic step, as in the proteasome-dependent activation of Esp1 protease during sister chromatid exchange ( 9).	transcription
56936	1	335316	7	NULL	NULL	0	NULL	p50			constitute					p105			NH2-terminus		NULL		0	NULL	NULL	NULL	gw70_science_299_5605_408_s_8	12481023	Because p50 constitutes the NH2-terminus of p105 and the COOH-terminus is presumably blocked by the ribosome, the proteasome must either wait for release of nascent p105 from the ribosome or activate another protease that catalyzes the initial endoproteolytic step, as in the proteasome-dependent activation of Esp1 protease during sister chromatid exchange ( 9).	transcription
56937	2	335316	7	NULL	NULL	0	NULL	p105			blocked by		presumably	COOH-terminus		ribosome					NULL		0	NULL	NULL	NULL	gw70_science_299_5605_408_s_8	12481023	Because p50 constitutes the NH2-terminus of p105 and the COOH-terminus is presumably blocked by the ribosome, the proteasome must either wait for release of nascent p105 from the ribosome or activate another protease that catalyzes the initial endoproteolytic step, as in the proteasome-dependent activation of Esp1 protease during sister chromatid exchange ( 9).	transcription
56938	3	335316	7	NULL	NULL	0	NULL	p105		nascent	released from					ribosome					NULL		NULL	NULL	NULL	NULL	gw70_science_299_5605_408_s_8	12481023	Because p50 constitutes the NH2-terminus of p105 and the COOH-terminus is presumably blocked by the ribosome, the proteasome must either wait for release of nascent p105 from the ribosome or activate another protease that catalyzes the initial endoproteolytic step, as in the proteasome-dependent activation of Esp1 protease during sister chromatid exchange ( 9).	transcription
56939	4	335316	7	NULL	NULL	0	NULL	protease			catalyze					endoproteolytic step		initial 			NULL		NULL	NULL	NULL	NULL	gw70_science_299_5605_408_s_8	12481023	Because p50 constitutes the NH2-terminus of p105 and the COOH-terminus is presumably blocked by the ribosome, the proteasome must either wait for release of nascent p105 from the ribosome or activate another protease that catalyzes the initial endoproteolytic step, as in the proteasome-dependent activation of Esp1 protease during sister chromatid exchange ( 9).	transcription
56940	5	335316	7	NULL	NULL	0	NULL	proteasome			activate					statement 4					NULL		0	NULL	NULL	NULL	gw70_science_299_5605_408_s_8	12481023	Because p50 constitutes the NH2-terminus of p105 and the COOH-terminus is presumably blocked by the ribosome, the proteasome must either wait for release of nascent p105 from the ribosome or activate another protease that catalyzes the initial endoproteolytic step, as in the proteasome-dependent activation of Esp1 protease during sister chromatid exchange ( 9).	transcription
56941	9	335316	7	NULL	NULL	0	NULL	statement 5			is an alternative to					statement 6					NULL		NULL	NULL	NULL	NULL	gw70_science_299_5605_408_s_8	12481023	Because p50 constitutes the NH2-terminus of p105 and the COOH-terminus is presumably blocked by the ribosome, the proteasome must either wait for release of nascent p105 from the ribosome or activate another protease that catalyzes the initial endoproteolytic step, as in the proteasome-dependent activation of Esp1 protease during sister chromatid exchange ( 9).	transcription
56942	7	335316	7	NULL	NULL	0	NULL	Esp1 protease		activation of	depends on					proteasome					NULL		0	NULL	NULL	NULL	gw70_science_299_5605_408_s_8	12481023	Because p50 constitutes the NH2-terminus of p105 and the COOH-terminus is presumably blocked by the ribosome, the proteasome must either wait for release of nascent p105 from the ribosome or activate another protease that catalyzes the initial endoproteolytic step, as in the proteasome-dependent activation of Esp1 protease during sister chromatid exchange ( 9).	transcription
56943	8	335316	7	NULL	NULL	0	NULL	statement 7			during					sister chromatid		exchange of			NULL		0	NULL	NULL	NULL	gw70_science_299_5605_408_s_8	12481023	Because p50 constitutes the NH2-terminus of p105 and the COOH-terminus is presumably blocked by the ribosome, the proteasome must either wait for release of nascent p105 from the ribosome or activate another protease that catalyzes the initial endoproteolytic step, as in the proteasome-dependent activation of Esp1 protease during sister chromatid exchange ( 9).	transcription
56944	6	335316	7	NULL	NULL	0	NULL	proteasome			wait for					statement 3					NULL		NULL	NULL	NULL	NULL	gw70_science_299_5605_408_s_8	12481023	Because p50 constitutes the NH2-terminus of p105 and the COOH-terminus is presumably blocked by the ribosome, the proteasome must either wait for release of nascent p105 from the ribosome or activate another protease that catalyzes the initial endoproteolytic step, as in the proteasome-dependent activation of Esp1 protease during sister chromatid exchange ( 9).	transcription
54944	1	335318	5	NULL	NULL	0	NULL				is synthesized as			p50 subunits		p105					NULL		NULL	NULL	NULL	NULL	gw70_embo_25_20_4820_s_14	16990795	The p50 and p52 subunits are synthesized as longer precursor proteins, p105 and  p100 that contain ankyrin repeats in their C-termini, similar to those possessed  by the inhibitor of NF-kappaB (IkappaB) family of proteins ( ).	transcription
54945	2	335318	5	NULL	NULL	0	NULL	p105			is a type of					long precursor protein					NULL		0	NULL	NULL	NULL	gw70_embo_25_20_4820_s_14	16990795	The p50 and p52 subunits are synthesized as longer precursor proteins, p105 and  p100 that contain ankyrin repeats in their C-termini, similar to those possessed  by the inhibitor of NF-kappaB (IkappaB) family of proteins ( ).	transcription
54946	3	335318	5	NULL	NULL	0	NULL	p105			contains					p105			ankyrin repeats in C-termini		NULL		0	NULL	NULL	NULL	gw70_embo_25_20_4820_s_14	16990795	The p50 and p52 subunits are synthesized as longer precursor proteins, p105 and  p100 that contain ankyrin repeats in their C-termini, similar to those possessed  by the inhibitor of NF-kappaB (IkappaB) family of proteins ( ).	transcription
54947	4	335318	5	NULL	NULL	0	NULL				is synthesized as			p52 subunits		p100					NULL		0	NULL	NULL	NULL	gw70_embo_25_20_4820_s_14	16990795	The p50 and p52 subunits are synthesized as longer precursor proteins, p105 and  p100 that contain ankyrin repeats in their C-termini, similar to those possessed  by the inhibitor of NF-kappaB (IkappaB) family of proteins ( ).	transcription
54948	5	335318	5	NULL	NULL	0	NULL	p100			is a type of					long precursor protein					NULL		0	NULL	NULL	NULL	gw70_embo_25_20_4820_s_14	16990795	The p50 and p52 subunits are synthesized as longer precursor proteins, p105 and  p100 that contain ankyrin repeats in their C-termini, similar to those possessed  by the inhibitor of NF-kappaB (IkappaB) family of proteins ( ).	transcription
54949	6	335318	5	NULL	NULL	0	NULL	p100			contains								ankyrin repeats in C-termini		NULL		0	NULL	NULL	NULL	gw70_embo_25_20_4820_s_14	16990795	The p50 and p52 subunits are synthesized as longer precursor proteins, p105 and  p100 that contain ankyrin repeats in their C-termini, similar to those possessed  by the inhibitor of NF-kappaB (IkappaB) family of proteins ( ).	transcription
56945	1	335318	7	NULL	NULL	0	NULL				is synthesized as			p50 subunit		p105					NULL		0	NULL	NULL	NULL	gw70_embo_25_20_4820_s_14	16990795	The p50 and p52 subunits are synthesized as longer precursor proteins, p105 and  p100 that contain ankyrin repeats in their C-termini, similar to those possessed  by the inhibitor of NF-kappaB (IkappaB) family of proteins ( ).	transcription
56946	2	335318	7	NULL	NULL	0	NULL				is synthesized as			p52 subunit		p100					NULL		0	NULL	NULL	NULL	gw70_embo_25_20_4820_s_14	16990795	The p50 and p52 subunits are synthesized as longer precursor proteins, p105 and  p100 that contain ankyrin repeats in their C-termini, similar to those possessed  by the inhibitor of NF-kappaB (IkappaB) family of proteins ( ).	transcription
56947	3	335318	7	NULL	NULL	0	NULL	p105			contains								ankyrin repeats in their C-termini		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_20_4820_s_14	16990795	The p50 and p52 subunits are synthesized as longer precursor proteins, p105 and  p100 that contain ankyrin repeats in their C-termini, similar to those possessed  by the inhibitor of NF-kappaB (IkappaB) family of proteins ( ).	transcription
56948	4	335318	7	NULL	NULL	0	NULL	p100			contains								ankyrin repeats in their C-termini		NULL		NULL	NULL	NULL	NULL	gw70_embo_25_20_4820_s_14	16990795	The p50 and p52 subunits are synthesized as longer precursor proteins, p105 and  p100 that contain ankyrin repeats in their C-termini, similar to those possessed  by the inhibitor of NF-kappaB (IkappaB) family of proteins ( ).	transcription
56949	5	335318	7	NULL	NULL	0	NULL	NF-kappaB  family		inhibitor of	contains								ankyrin repeats in their C-termini		NULL		0	NULL	NULL	NULL	gw70_embo_25_20_4820_s_14	16990795	The p50 and p52 subunits are synthesized as longer precursor proteins, p105 and  p100 that contain ankyrin repeats in their C-termini, similar to those possessed  by the inhibitor of NF-kappaB (IkappaB) family of proteins ( ).	transcription
56950	6	335318	7	NULL	NULL	0	NULL	NF-kappaB			is					IkappaB					NULL		0	NULL	NULL	NULL	gw70_embo_25_20_4820_s_14	16990795	The p50 and p52 subunits are synthesized as longer precursor proteins, p105 and  p100 that contain ankyrin repeats in their C-termini, similar to those possessed  by the inhibitor of NF-kappaB (IkappaB) family of proteins ( ).	transcription
56956	7	335318	7	NULL	NULL	0	NULL	p105			is a type of					longer precursor protein					NULL		0	NULL	NULL	NULL	gw70_embo_25_20_4820_s_14	16990795	The p50 and p52 subunits are synthesized as longer precursor proteins, p105 and  p100 that contain ankyrin repeats in their C-termini, similar to those possessed  by the inhibitor of NF-kappaB (IkappaB) family of proteins ( ).	transcription
56957	8	335318	7	NULL	NULL	0	NULL	p100			is a type of					longer precursor protein					NULL		0	NULL	NULL	NULL	gw70_embo_25_20_4820_s_14	16990795	The p50 and p52 subunits are synthesized as longer precursor proteins, p105 and  p100 that contain ankyrin repeats in their C-termini, similar to those possessed  by the inhibitor of NF-kappaB (IkappaB) family of proteins ( ).	transcription
54950	1	335319	5	NULL	NULL	0	NULL	Casper			induces					NF- B		activation of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_4_980_s_140	13679070	Based on these data, an additional  explanation for p105-mediated inhibition of Casper-induced NF- B activation is that  Casper causes inhibition of p105 processing and subsequent lack of p50 and therefore  inhibition of NF- B activation.	transcription
54951	2	335319	5	NULL	NULL	0	NULL	p105			mediates					statement 1		inhibition of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_4_980_s_140	13679070	Based on these data, an additional  explanation for p105-mediated inhibition of Casper-induced NF- B activation is that  Casper causes inhibition of p105 processing and subsequent lack of p50 and therefore  inhibition of NF- B activation.	transcription
54952	3	335319	5	NULL	NULL	0	NULL	Casper			inhibits					p105		processing of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_4_980_s_140	13679070	Based on these data, an additional  explanation for p105-mediated inhibition of Casper-induced NF- B activation is that  Casper causes inhibition of p105 processing and subsequent lack of p50 and therefore  inhibition of NF- B activation.	transcription
54953	4	335319	5	NULL	NULL	0	NULL	statement 3			leads to		subsequently			p50		lack of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_4_980_s_140	13679070	Based on these data, an additional  explanation for p105-mediated inhibition of Casper-induced NF- B activation is that  Casper causes inhibition of p105 processing and subsequent lack of p50 and therefore  inhibition of NF- B activation.	transcription
54954	5	335319	5	NULL	NULL	0	NULL	statement 4			inhibits					NF- B		activation of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_4_980_s_140	13679070	Based on these data, an additional  explanation for p105-mediated inhibition of Casper-induced NF- B activation is that  Casper causes inhibition of p105 processing and subsequent lack of p50 and therefore  inhibition of NF- B activation.	transcription
56951	1	335319	7	NULL	NULL	0	NULL	Casper			induce					NF-B		activation of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_4_980_s_140	13679070	Based on these data, an additional  explanation for p105-mediated inhibition of Casper-induced NF- B activation is that  Casper causes inhibition of p105 processing and subsequent lack of p50 and therefore  inhibition of NF- B activation.	transcription
56952	2	335319	7	NULL	NULL	0	NULL	Casper			inhibits					p105		processing of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_4_980_s_140	13679070	Based on these data, an additional  explanation for p105-mediated inhibition of Casper-induced NF- B activation is that  Casper causes inhibition of p105 processing and subsequent lack of p50 and therefore  inhibition of NF- B activation.	transcription
56953	3	335319	7	NULL	NULL	0	NULL	statement 2			leads to		subsequently			p50		lack of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_4_980_s_140	13679070	Based on these data, an additional  explanation for p105-mediated inhibition of Casper-induced NF- B activation is that  Casper causes inhibition of p105 processing and subsequent lack of p50 and therefore  inhibition of NF- B activation.	transcription
56954	4	335319	7	NULL	NULL	0	NULL	statement 3			leads to					NF-B		inhibition of;;activation of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_4_980_s_140	13679070	Based on these data, an additional  explanation for p105-mediated inhibition of Casper-induced NF- B activation is that  Casper causes inhibition of p105 processing and subsequent lack of p50 and therefore  inhibition of NF- B activation.	transcription
56955	5	335319	7	NULL	NULL	0	NULL	p105			mediates					statement 1		inhibition of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_309_4_980_s_140	13679070	Based on these data, an additional  explanation for p105-mediated inhibition of Casper-induced NF- B activation is that  Casper causes inhibition of p105 processing and subsequent lack of p50 and therefore  inhibition of NF- B activation.	transcription
54955	1	335320	5	NULL	NULL	0	NULL	TNF-alpha			is overexpressed by					nfkappab1 - / - HSCs					NULL		0	NULL	NULL	NULL	gw70_amjpathol_166_3_695_s_323	15743782	Overexpression of TNF-alpha by  nfkappab1 - / -  HSCs is therefore because of absence of p50 (rather than a function attributed to the precursor protein p105) and specifically arises as a consequence of the loss of p50-dependent HDAC-mediated transcriptional repression of the TNF-alpha gene.	transcription
54956	2	335320	5	NULL	NULL	0	NULL	p50		absence of	leads to					statement 1					NULL		0	NULL	NULL	NULL	gw70_amjpathol_166_3_695_s_323	15743782	Overexpression of TNF-alpha by  nfkappab1 - / -  HSCs is therefore because of absence of p50 (rather than a function attributed to the precursor protein p105) and specifically arises as a consequence of the loss of p50-dependent HDAC-mediated transcriptional repression of the TNF-alpha gene.	transcription
54957	3	335320	5	NULL	NULL	0	NULL	TNF-alpha gene		transcriptional repression of	is mediated by					HDAC					NULL		0	NULL	NULL	NULL	gw70_amjpathol_166_3_695_s_323	15743782	Overexpression of TNF-alpha by  nfkappab1 - / -  HSCs is therefore because of absence of p50 (rather than a function attributed to the precursor protein p105) and specifically arises as a consequence of the loss of p50-dependent HDAC-mediated transcriptional repression of the TNF-alpha gene.	transcription
54958	4	335320	5	NULL	NULL	0	NULL	statement 3			is dependent on					p50					NULL		0	NULL	NULL	NULL	gw70_amjpathol_166_3_695_s_323	15743782	Overexpression of TNF-alpha by  nfkappab1 - / -  HSCs is therefore because of absence of p50 (rather than a function attributed to the precursor protein p105) and specifically arises as a consequence of the loss of p50-dependent HDAC-mediated transcriptional repression of the TNF-alpha gene.	transcription
54959	5	335320	5	NULL	NULL	0	NULL	p50		loss of	leads to					statement 3		loss of			NULL		0	NULL	NULL	NULL	gw70_amjpathol_166_3_695_s_323	15743782	Overexpression of TNF-alpha by  nfkappab1 - / -  HSCs is therefore because of absence of p50 (rather than a function attributed to the precursor protein p105) and specifically arises as a consequence of the loss of p50-dependent HDAC-mediated transcriptional repression of the TNF-alpha gene.	transcription
54960	6	335320	5	NULL	NULL	0	NULL	statement 5			leads to					statement 1					NULL		0	NULL	NULL	NULL	gw70_amjpathol_166_3_695_s_323	15743782	Overexpression of TNF-alpha by  nfkappab1 - / -  HSCs is therefore because of absence of p50 (rather than a function attributed to the precursor protein p105) and specifically arises as a consequence of the loss of p50-dependent HDAC-mediated transcriptional repression of the TNF-alpha gene.	transcription
56958	1	335320	7	NULL	NULL	0	NULL	HDAC			mediate					TNF-alpha gene		transcriptional repression of 			NULL		0	NULL	NULL	NULL	gw70_amjpathol_166_3_695_s_323	15743782	Overexpression of TNF-alpha by  nfkappab1 - / -  HSCs is therefore because of absence of p50 (rather than a function attributed to the precursor protein p105) and specifically arises as a consequence of the loss of p50-dependent HDAC-mediated transcriptional repression of the TNF-alpha gene.	transcription
56959	2	335320	7	NULL	NULL	0	NULL	statement 1			depends on					p50					NULL		0	NULL	NULL	NULL	gw70_amjpathol_166_3_695_s_323	15743782	Overexpression of TNF-alpha by  nfkappab1 - / -  HSCs is therefore because of absence of p50 (rather than a function attributed to the precursor protein p105) and specifically arises as a consequence of the loss of p50-dependent HDAC-mediated transcriptional repression of the TNF-alpha gene.	transcription
56960	3	335320	7	NULL	NULL	0	NULL	nfkappab1 - / - HSCs			overexpress					TNF-alpha					NULL		0	NULL	NULL	NULL	gw70_amjpathol_166_3_695_s_323	15743782	Overexpression of TNF-alpha by  nfkappab1 - / -  HSCs is therefore because of absence of p50 (rather than a function attributed to the precursor protein p105) and specifically arises as a consequence of the loss of p50-dependent HDAC-mediated transcriptional repression of the TNF-alpha gene.	transcription
56961	4	335320	7	NULL	NULL	0	NULL	statement 3			because					p50		absence of			NULL		NULL	NULL	NULL	NULL	gw70_amjpathol_166_3_695_s_323	15743782	Overexpression of TNF-alpha by  nfkappab1 - / -  HSCs is therefore because of absence of p50 (rather than a function attributed to the precursor protein p105) and specifically arises as a consequence of the loss of p50-dependent HDAC-mediated transcriptional repression of the TNF-alpha gene.	transcription
56962	5	335320	7	NULL	NULL	0	NULL	statement 3			arises		specifically			statement 2		due to loss of			NULL		0	NULL	NULL	NULL	gw70_amjpathol_166_3_695_s_323	15743782	Overexpression of TNF-alpha by  nfkappab1 - / -  HSCs is therefore because of absence of p50 (rather than a function attributed to the precursor protein p105) and specifically arises as a consequence of the loss of p50-dependent HDAC-mediated transcriptional repression of the TNF-alpha gene.	transcription
54961	1	335321	5	NULL	NULL	0	NULL	IKK			mediates					NF- B component		phosphorylation of			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_18_0_621_s_657	10837071	The basis for this difference in DNA-binding activity is not yet known,  although it may result from IKK -mediated phosphorylation of an NF- B component or  from an effect on the processing of p105 to p50.	transcription
54962	2	335321	5	NULL	NULL	0	NULL	p105			is processed to					p50					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_18_0_621_s_657	10837071	The basis for this difference in DNA-binding activity is not yet known,  although it may result from IKK -mediated phosphorylation of an NF- B component or  from an effect on the processing of p105 to p50.	transcription
56963	1	335321	7	NULL	NULL	0	NULL	IKK			mediate					NF- B component		phosphorylation of			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_18_0_621_s_657	10837071	The basis for this difference in DNA-binding activity is not yet known,  although it may result from IKK -mediated phosphorylation of an NF- B component or  from an effect on the processing of p105 to p50.	transcription
56964	2	335321	7	NULL	NULL	0	NULL	p105			processed to					p50					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_18_0_621_s_657	10837071	The basis for this difference in DNA-binding activity is not yet known,  although it may result from IKK -mediated phosphorylation of an NF- B component or  from an effect on the processing of p105 to p50.	transcription
54963	1	335322	5	NULL	NULL	0	NULL	p105		degradation of	is mediated by					IKK					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_1_475_s_181	14673179	As was noted earlier ( ), IKK-mediated degradation of p105 results in disappearance of the cytosolic anchor of free p50 that now migrates to the nucleus (Fig.  4A, compare lane 5 to lane 3 and lane 9 to lane 7).	transcription
54964	2	335322	5	NULL	NULL	0	NULL	statement 1			results in					p50		disappearance of;;cytosolic anchor of;;free 			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_1_475_s_181	14673179	As was noted earlier ( ), IKK-mediated degradation of p105 results in disappearance of the cytosolic anchor of free p50 that now migrates to the nucleus (Fig.  4A, compare lane 5 to lane 3 and lane 9 to lane 7).	transcription
54965	3	335322	5	NULL	NULL	0	NULL	p50		free	migrates to					nucleus					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_1_475_s_181	14673179	As was noted earlier ( ), IKK-mediated degradation of p105 results in disappearance of the cytosolic anchor of free p50 that now migrates to the nucleus (Fig.  4A, compare lane 5 to lane 3 and lane 9 to lane 7).	transcription
54966	4	335322	5	NULL	NULL	0	NULL	statement 2			leads to					statement 3					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_1_475_s_181	14673179	As was noted earlier ( ), IKK-mediated degradation of p105 results in disappearance of the cytosolic anchor of free p50 that now migrates to the nucleus (Fig.  4A, compare lane 5 to lane 3 and lane 9 to lane 7).	transcription
56965	1	335322	7	NULL	NULL	0	NULL	IKK			mediates					p105		degradation of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_1_475_s_181	14673179	As was noted earlier ( ), IKK-mediated degradation of p105 results in disappearance of the cytosolic anchor of free p50 that now migrates to the nucleus (Fig.  4A, compare lane 5 to lane 3 and lane 9 to lane 7).	transcription
56966	2	335322	7	NULL	NULL	0	NULL	statement 1			result in					free p50		disappearance of 	 cytosolic anchor of		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_1_475_s_181	14673179	As was noted earlier ( ), IKK-mediated degradation of p105 results in disappearance of the cytosolic anchor of free p50 that now migrates to the nucleus (Fig.  4A, compare lane 5 to lane 3 and lane 9 to lane 7).	transcription
56967	3	335322	7	NULL	NULL	0	NULL	p50			migrates to					nucleus					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_1_475_s_181	14673179	As was noted earlier ( ), IKK-mediated degradation of p105 results in disappearance of the cytosolic anchor of free p50 that now migrates to the nucleus (Fig.  4A, compare lane 5 to lane 3 and lane 9 to lane 7).	transcription
56968	4	335322	7	NULL	NULL	0	NULL	statement 2			leads to					statement 3					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_1_475_s_181	14673179	As was noted earlier ( ), IKK-mediated degradation of p105 results in disappearance of the cytosolic anchor of free p50 that now migrates to the nucleus (Fig.  4A, compare lane 5 to lane 3 and lane 9 to lane 7).	transcription
56969	1	335323	7	NULL	NULL	0	NULL	Kinase			process		rapidly			p105		synthesized			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_1_475_s_203	14673179	The reason is that during the 24 h of transfection in the presence of IKKbeta that precedes the analysis, the synthesized p105 is rapidly processed and degraded under the effect of the kinase, and a stable p50 is accumulated continuously.	transcription
56970	2	335323	7	NULL	NULL	0	NULL	kinase			degrades		rapidly			statement 1					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_1_475_s_203	14673179	The reason is that during the 24 h of transfection in the presence of IKKbeta that precedes the analysis, the synthesized p105 is rapidly processed and degraded under the effect of the kinase, and a stable p50 is accumulated continuously.	transcription
56971	3	335323	7	NULL	NULL	0	NULL	statement 2			leads to					p50		continuous accumulation of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_1_475_s_203	14673179	The reason is that during the 24 h of transfection in the presence of IKKbeta that precedes the analysis, the synthesized p105 is rapidly processed and degraded under the effect of the kinase, and a stable p50 is accumulated continuously.	transcription
56097	1	335324	6	NULL	NULL	0	NULL	IKKbeta		stimulation by	results in					p105		complete degradation of 			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_1_475_s_310	14673179	Heissmeyer and colleagues ( ,  ) have shown that stimulation by IKKbeta with subsequent ubiquitination by beta-TrCP results in almost complete degradation of p105, while the increased generation of p50 is slight and inconsistent.	transcription
56098	2	335324	6	NULL	NULL	0	NULL	beta-TrCP		ubiquitination by	results in					p105		complete degradation of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_1_475_s_310	14673179	Heissmeyer and colleagues ( ,  ) have shown that stimulation by IKKbeta with subsequent ubiquitination by beta-TrCP results in almost complete degradation of p105, while the increased generation of p50 is slight and inconsistent.	transcription
56972	1	335324	7	NULL	NULL	0	NULL	IKKbeta		stimulation by	results in					p105		complete degradation of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_1_475_s_310	14673179	Heissmeyer and colleagues ( ,  ) have shown that stimulation by IKKbeta with subsequent ubiquitination by beta-TrCP results in almost complete degradation of p105, while the increased generation of p50 is slight and inconsistent.	transcription
56973	2	335324	7	NULL	NULL	0	NULL	beta-TrCP		ubiquitination by	results in					p105		complete degradation of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_1_475_s_310	14673179	Heissmeyer and colleagues ( ,  ) have shown that stimulation by IKKbeta with subsequent ubiquitination by beta-TrCP results in almost complete degradation of p105, while the increased generation of p50 is slight and inconsistent.	transcription
56974	3	335324	7	NULL	NULL	0	NULL	statement 1			occur simulataneous with					statement 2					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_1_475_s_310	14673179	Heissmeyer and colleagues ( ,  ) have shown that stimulation by IKKbeta with subsequent ubiquitination by beta-TrCP results in almost complete degradation of p105, while the increased generation of p50 is slight and inconsistent.	transcription
56975	4	335324	7	NULL	NULL	0	NULL	statement 3			leads to					p50		slightly increased generation of 			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_1_475_s_310	14673179	Heissmeyer and colleagues ( ,  ) have shown that stimulation by IKKbeta with subsequent ubiquitination by beta-TrCP results in almost complete degradation of p105, while the increased generation of p50 is slight and inconsistent.	transcription
56976	5	335324	7	NULL	NULL	0	NULL	statement 3			leads to					p50		inconsistent generation of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_1_475_s_310	14673179	Heissmeyer and colleagues ( ,  ) have shown that stimulation by IKKbeta with subsequent ubiquitination by beta-TrCP results in almost complete degradation of p105, while the increased generation of p50 is slight and inconsistent.	transcription
56977	1	335325	7	NULL	NULL	0	NULL	 p105 heterodimers			recruits		non-proteolytically			p50					NULL	cytosol	0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_290	14668329	The induction of Bcl-3 in tolerant T cells may be relevant in the nuclear shuttling of p50-p50 homodimers, which could be the result from a non-proteolytic recruitment of p50 from p105 heterodimers in the cytosol.	transcription
56978	2	335325	7	NULL	NULL	0	NULL	Bcl-3		 induction of 	relevant in		may be			p50-p50 homodimers		nuclear shuttling of			NULL	tolerant T cells	0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_290	14668329	The induction of Bcl-3 in tolerant T cells may be relevant in the nuclear shuttling of p50-p50 homodimers, which could be the result from a non-proteolytic recruitment of p50 from p105 heterodimers in the cytosol.	transcription
56979	3	335325	7	NULL	NULL	0	NULL	statement 2			result from					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8460_s_290	14668329	The induction of Bcl-3 in tolerant T cells may be relevant in the nuclear shuttling of p50-p50 homodimers, which could be the result from a non-proteolytic recruitment of p50 from p105 heterodimers in the cytosol.	transcription
56099	1	335326	6	NULL	NULL	0	NULL	MEK/ERK pathway		activation of	controls					p105		processing of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_32465_s_189	12801933	By a similar mechanism,  the constitutive p50 homodimer signal in LY-ar cells may not be a result of  MEK/ERK-induced Bcl-3 activity but rather a result of increased p105  processing directly or indirectly controlled by activation of the MEK/ERK  pathway.	transcription
56980	1	335326	7	NULL	NULL	0	NULL	MEK/ERK			induce					Bcl-3		activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_32465_s_189	12801933	By a similar mechanism,  the constitutive p50 homodimer signal in LY-ar cells may not be a result of  MEK/ERK-induced Bcl-3 activity but rather a result of increased p105  processing directly or indirectly controlled by activation of the MEK/ERK  pathway.	transcription
56981	2	335326	7	NULL	NULL	0	NULL	statement 1			does not result in					p50 homodimer		constitutive signal of			NULL	LY-ar cells	0	NULL	NULL	NULL	gw70_jbiolchem_278_34_32465_s_189	12801933	By a similar mechanism,  the constitutive p50 homodimer signal in LY-ar cells may not be a result of  MEK/ERK-induced Bcl-3 activity but rather a result of increased p105  processing directly or indirectly controlled by activation of the MEK/ERK  pathway.	transcription
56982	3	335326	7	NULL	NULL	0	NULL	MEK/ERK pathway		activation of	controls		directly			p105		increased processing of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_32465_s_189	12801933	By a similar mechanism,  the constitutive p50 homodimer signal in LY-ar cells may not be a result of  MEK/ERK-induced Bcl-3 activity but rather a result of increased p105  processing directly or indirectly controlled by activation of the MEK/ERK  pathway.	transcription
56983	4	335326	7	NULL	NULL	0	NULL	MEK/ERK pathway		activation of	controls		indirectly			p105		increased processing of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_32465_s_189	12801933	By a similar mechanism,  the constitutive p50 homodimer signal in LY-ar cells may not be a result of  MEK/ERK-induced Bcl-3 activity but rather a result of increased p105  processing directly or indirectly controlled by activation of the MEK/ERK  pathway.	transcription
56984	5	335326	7	NULL	NULL	0	NULL	statement 3			is an alternative to					statement 4					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_32465_s_189	12801933	By a similar mechanism,  the constitutive p50 homodimer signal in LY-ar cells may not be a result of  MEK/ERK-induced Bcl-3 activity but rather a result of increased p105  processing directly or indirectly controlled by activation of the MEK/ERK  pathway.	transcription
56985	6	335326	7	NULL	NULL	0	NULL	statement 5			result in					p50 homodimer		constitutive signal of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_34_32465_s_189	12801933	By a similar mechanism,  the constitutive p50 homodimer signal in LY-ar cells may not be a result of  MEK/ERK-induced Bcl-3 activity but rather a result of increased p105  processing directly or indirectly controlled by activation of the MEK/ERK  pathway.	transcription
56100	1	335327	6	NULL	NULL	0	NULL	NF-kappaB			is sequestered to					cytoplasm					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56101	2	335327	6	NULL	NULL	0	NULL	IkappaB			performs					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56102	3	335327	6	NULL	NULL	0	NULL	p105			performs					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56103	4	335327	6	NULL	NULL	0	NULL	p100			performs					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56104	5	335327	6	NULL	NULL	0	NULL	p105			is a type of					NF-kappaB precursor protein					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56105	6	335327	6	NULL	NULL	0	NULL	p100			is a type of					NF-kappaB precursor protein					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56986	1	335327	7	NULL	NULL	0	NULL	NF-kappaB 			is composed of					p50 dimer					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56987	2	335327	7	NULL	NULL	0	NULL	NF-kappaB 			is composed of					p52 dimer					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56988	3	335327	7	NULL	NULL	0	NULL	NF-kappaB 			is composed of					RelA dimer					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56989	4	335327	7	NULL	NULL	0	NULL	NF-kappaB			is composed of					RelB dimer					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56990	5	335327	7	NULL	NULL	0	NULL	NF-kappaB			is composed of					c-Rel dimer					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56991	6	335327	7	NULL	NULL	0	NULL	p50 dimer			complexed to		endogenously			p105					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56992	7	335327	7	NULL	NULL	0	NULL	p50 dimer			complexed to		endogenously			p100					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56993	8	335327	7	NULL	NULL	0	NULL	p52 dimer			complexed to		endogenously			p105					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56994	9	335327	7	NULL	NULL	0	NULL	p52 dimer			complexed to		endogenously			p100					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56995	10	335327	7	NULL	NULL	0	NULL	RelA dimer			complexed to		endogenously			p105					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56996	11	335327	7	NULL	NULL	0	NULL	RelA dimer			complexed to		endogenously			p100					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56997	12	335327	7	NULL	NULL	0	NULL	RelB dimer			complexed to		endogenously			p105					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56998	13	335327	7	NULL	NULL	0	NULL	RelB dimer			complexed to		endogenously			p100					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56999	14	335327	7	NULL	NULL	0	NULL	c-Rel dimer			complexed to		endogenously			p105					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
57000	15	335327	7	NULL	NULL	0	NULL	c-Rel dimer			complexed to		endogenously			p100					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
57001	16	335327	7	NULL	NULL	0	NULL	p105			is a precursor of					IkappaB protein					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
57002	17	335327	7	NULL	NULL	0	NULL	p105			is a precursor of					NF-kappaB protein					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
57003	18	335327	7	NULL	NULL	0	NULL	p100			is a precursor of					IkappaB protein					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
57004	19	335327	7	NULL	NULL	0	NULL	p100			is a precursor of					NF-kappaB protein					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
57005	20	335327	7	NULL	NULL	0	NULL	IkappaB			is a type of					inhibitory protein					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
57006	21	335327	7	NULL	NULL	0	NULL	NF-kappaB			is a type of					inhibitory protein					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
57007	22	335327	7	NULL	NULL	0	NULL	p105			sequester					NF-kappaB					NULL	cytoplasm	0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
57008	23	335327	7	NULL	NULL	0	NULL	p100			sequester					NF-kappaB					NULL	cytoplasm	0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
57017	24	335327	7	NULL	NULL	0	NULL	statement 6			is an alternative to					statement 7					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
57018	25	335327	7	NULL	NULL	0	NULL	statement 8			is an alternative to					statement 9					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
57019	26	335327	7	NULL	NULL	0	NULL	statement 10			is an alternative to					statement 11					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
57020	27	335327	7	NULL	NULL	0	NULL	statement 12			is an alternative to					statement 13					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
57021	28	335327	7	NULL	NULL	0	NULL	statement 14			is an alternative to					statement 15					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_47_46565_s_17	12968033	NF-kappaB is composed of dimers of p50, p52, RelA, RelB, or c-Rel that are endogenously complexed to inhibitor proteins called IkappaB and NF-kappaB precursor proteins p105 or p100, which sequester NF-kappaB in the cytoplasm.	transcription
56106	1	335328	6	NULL	NULL	0	NULL	p50			interacts with					IkappaBalpha					NULL		0	NULL	NULL	NULL	gw70_pnas_103_40_14767_s_135	17003112	Manipulations of FIH levels in this setting resulted in no major effects on interactions of p50 with either IkappaBalpha or p105, on nuclear abundance of the proteins, or on NF-kappaB DNA-binding activity (data not shown).	transcription
56107	2	335328	6	NULL	NULL	0	NULL	p50			interacts with					p105					NULL		0	NULL	NULL	NULL	gw70_pnas_103_40_14767_s_135	17003112	Manipulations of FIH levels in this setting resulted in no major effects on interactions of p50 with either IkappaBalpha or p105, on nuclear abundance of the proteins, or on NF-kappaB DNA-binding activity (data not shown).	transcription
56108	3	335328	6	NULL	NULL	0	NULL	statement 1			is an alternative to					statement 2					NULL		0	NULL	NULL	NULL	gw70_pnas_103_40_14767_s_135	17003112	Manipulations of FIH levels in this setting resulted in no major effects on interactions of p50 with either IkappaBalpha or p105, on nuclear abundance of the proteins, or on NF-kappaB DNA-binding activity (data not shown).	transcription
57009	1	335328	7	NULL	NULL	0	NULL	p50			interacts with					IkappaBalpha					NULL		0	NULL	NULL	NULL	gw70_pnas_103_40_14767_s_135	17003112	Manipulations of FIH levels in this setting resulted in no major effects on interactions of p50 with either IkappaBalpha or p105, on nuclear abundance of the proteins, or on NF-kappaB DNA-binding activity (data not shown).	transcription
57010	2	335328	7	NULL	NULL	0	NULL	p50			interacts with					p105					NULL		0	NULL	NULL	NULL	gw70_pnas_103_40_14767_s_135	17003112	Manipulations of FIH levels in this setting resulted in no major effects on interactions of p50 with either IkappaBalpha or p105, on nuclear abundance of the proteins, or on NF-kappaB DNA-binding activity (data not shown).	transcription
57011	3	335328	7	NULL	NULL	0	NULL	FIH		levels of	does not effect					statement 1					NULL		0	NULL	NULL	NULL	gw70_pnas_103_40_14767_s_135	17003112	Manipulations of FIH levels in this setting resulted in no major effects on interactions of p50 with either IkappaBalpha or p105, on nuclear abundance of the proteins, or on NF-kappaB DNA-binding activity (data not shown).	transcription
57012	4	335328	7	NULL	NULL	0	NULL	FIH		levels of	does not effect					statement 2					NULL		0	NULL	NULL	NULL	gw70_pnas_103_40_14767_s_135	17003112	Manipulations of FIH levels in this setting resulted in no major effects on interactions of p50 with either IkappaBalpha or p105, on nuclear abundance of the proteins, or on NF-kappaB DNA-binding activity (data not shown).	transcription
57013	5	335328	7	NULL	NULL	0	NULL	FIH		levels of	does not effect on					proteins		nuclear abundance of			NULL		0	NULL	NULL	NULL	gw70_pnas_103_40_14767_s_135	17003112	Manipulations of FIH levels in this setting resulted in no major effects on interactions of p50 with either IkappaBalpha or p105, on nuclear abundance of the proteins, or on NF-kappaB DNA-binding activity (data not shown).	transcription
57014	6	335328	7	NULL	NULL	0	NULL	NF-kappaB			bind					DNA					NULL		0	NULL	NULL	NULL	gw70_pnas_103_40_14767_s_135	17003112	Manipulations of FIH levels in this setting resulted in no major effects on interactions of p50 with either IkappaBalpha or p105, on nuclear abundance of the proteins, or on NF-kappaB DNA-binding activity (data not shown).	transcription
57015	7	335328	7	NULL	NULL	0	NULL	FIH		levels of	does not effect					statement 6					NULL		0	NULL	NULL	NULL	gw70_pnas_103_40_14767_s_135	17003112	Manipulations of FIH levels in this setting resulted in no major effects on interactions of p50 with either IkappaBalpha or p105, on nuclear abundance of the proteins, or on NF-kappaB DNA-binding activity (data not shown).	transcription
57016	8	335328	7	NULL	NULL	0	NULL	statement 3			is an alternative to					statement 4					NULL		0	NULL	NULL	NULL	gw70_pnas_103_40_14767_s_135	17003112	Manipulations of FIH levels in this setting resulted in no major effects on interactions of p50 with either IkappaBalpha or p105, on nuclear abundance of the proteins, or on NF-kappaB DNA-binding activity (data not shown).	transcription
77626	1	335329	6	NULL	NULL	0	NULL	p100 	GP		processes into					p52	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_1_141_s_29	14691250	LMP1 induces p100 and p105 NF-kappaB precursors and up-regulates their processing into p52 and p50, respectively ( ), implicating LMP1 in both canonical NF-kappaB up-regulation and noncanonical p100 processing into p52.	transcription
77627	2	335329	6	NULL	NULL	0	NULL	p105	GP		processes into					p50	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_1_141_s_29	14691250	LMP1 induces p100 and p105 NF-kappaB precursors and up-regulates their processing into p52 and p50, respectively ( ), implicating LMP1 in both canonical NF-kappaB up-regulation and noncanonical p100 processing into p52.	transcription
77628	3	335329	6	NULL	NULL	0	NULL	p100	GP		is a type of					NF-kappaB precursor	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_1_141_s_29	14691250	LMP1 induces p100 and p105 NF-kappaB precursors and up-regulates their processing into p52 and p50, respectively ( ), implicating LMP1 in both canonical NF-kappaB up-regulation and noncanonical p100 processing into p52.	transcription
77629	4	335329	6	NULL	NULL	0	NULL	p105	GP		is a type of					NF-kappaB precursor	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_1_141_s_29	14691250	LMP1 induces p100 and p105 NF-kappaB precursors and up-regulates their processing into p52 and p50, respectively ( ), implicating LMP1 in both canonical NF-kappaB up-regulation and noncanonical p100 processing into p52.	transcription
77630	5	335329	6	NULL	NULL	0	NULL	LMP1	GP		induces					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_1_141_s_29	14691250	LMP1 induces p100 and p105 NF-kappaB precursors and up-regulates their processing into p52 and p50, respectively ( ), implicating LMP1 in both canonical NF-kappaB up-regulation and noncanonical p100 processing into p52.	transcription
57022	1	335329	7	NULL	NULL	0	NULL	p100			processed to					p52					NULL		0	NULL	NULL	NULL	gw70_pnas_101_1_141_s_29	14691250	LMP1 induces p100 and p105 NF-kappaB precursors and up-regulates their processing into p52 and p50, respectively ( ), implicating LMP1 in both canonical NF-kappaB up-regulation and noncanonical p100 processing into p52.	transcription
57023	2	335329	7	NULL	NULL	0	NULL	p105			processed to					p50					NULL		0	NULL	NULL	NULL	gw70_pnas_101_1_141_s_29	14691250	LMP1 induces p100 and p105 NF-kappaB precursors and up-regulates their processing into p52 and p50, respectively ( ), implicating LMP1 in both canonical NF-kappaB up-regulation and noncanonical p100 processing into p52.	transcription
57024	3	335329	7	NULL	NULL	0	NULL	LMP1			induce					p100					NULL		0	NULL	NULL	NULL	gw70_pnas_101_1_141_s_29	14691250	LMP1 induces p100 and p105 NF-kappaB precursors and up-regulates their processing into p52 and p50, respectively ( ), implicating LMP1 in both canonical NF-kappaB up-regulation and noncanonical p100 processing into p52.	transcription
57025	4	335329	7	NULL	NULL	0	NULL	LMP1			induce					p105					NULL		0	NULL	NULL	NULL	gw70_pnas_101_1_141_s_29	14691250	LMP1 induces p100 and p105 NF-kappaB precursors and up-regulates their processing into p52 and p50, respectively ( ), implicating LMP1 in both canonical NF-kappaB up-regulation and noncanonical p100 processing into p52.	transcription
57026	5	335329	7	NULL	NULL	0	NULL	LMP1			upregulates					statement 1					NULL		0	NULL	NULL	NULL	gw70_pnas_101_1_141_s_29	14691250	LMP1 induces p100 and p105 NF-kappaB precursors and up-regulates their processing into p52 and p50, respectively ( ), implicating LMP1 in both canonical NF-kappaB up-regulation and noncanonical p100 processing into p52.	transcription
57027	6	335329	7	NULL	NULL	0	NULL	LMP1			upregulates					statement 2					NULL		0	NULL	NULL	NULL	gw70_pnas_101_1_141_s_29	14691250	LMP1 induces p100 and p105 NF-kappaB precursors and up-regulates their processing into p52 and p50, respectively ( ), implicating LMP1 in both canonical NF-kappaB up-regulation and noncanonical p100 processing into p52.	transcription
57028	7	335329	7	NULL	NULL	0	NULL	LMP1			implicated in					NF-kappaB		up-regulation of;;canonical			NULL		0	NULL	NULL	NULL	gw70_pnas_101_1_141_s_29	14691250	LMP1 induces p100 and p105 NF-kappaB precursors and up-regulates their processing into p52 and p50, respectively ( ), implicating LMP1 in both canonical NF-kappaB up-regulation and noncanonical p100 processing into p52.	transcription
57029	8	335329	7	NULL	NULL	0	NULL	LMP1			implicated in					statement 1		noncanonical			NULL		0	NULL	NULL	NULL	gw70_pnas_101_1_141_s_29	14691250	LMP1 induces p100 and p105 NF-kappaB precursors and up-regulates their processing into p52 and p50, respectively ( ), implicating LMP1 in both canonical NF-kappaB up-regulation and noncanonical p100 processing into p52.	transcription
57030	9	335329	7	NULL	NULL	0	NULL	p100			is a type of					NF-kappaB precursor					NULL		0	NULL	NULL	NULL	gw70_pnas_101_1_141_s_29	14691250	LMP1 induces p100 and p105 NF-kappaB precursors and up-regulates their processing into p52 and p50, respectively ( ), implicating LMP1 in both canonical NF-kappaB up-regulation and noncanonical p100 processing into p52.	transcription
57031	10	335329	7	NULL	NULL	0	NULL	p105			is a type of					NF-kappaB precursor					NULL		0	NULL	NULL	NULL	gw70_pnas_101_1_141_s_29	14691250	LMP1 induces p100 and p105 NF-kappaB precursors and up-regulates their processing into p52 and p50, respectively ( ), implicating LMP1 in both canonical NF-kappaB up-regulation and noncanonical p100 processing into p52.	transcription
77631	1	335330	6	NULL	NULL	0	NULL	p105	GP		modulates					p50 homodimer	GP				NULL	in vivo	0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_254	10970863	p105 modulates p50 homodimer in vivo   The formation of homo- or heterodimers is a common intracellular event involving many proteins; however, the rules that regulate such assemblies are not well understood ( Lamb and McKnight, 1991;  Tjian and Maniatis, 1994).	transcription
57032	1	335330	7	NULL	NULL	0	NULL	p105			modulate					p50 homodimer					NULL	in vivo	0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_254	10970863	p105 modulates p50 homodimer in vivo   The formation of homo- or heterodimers is a common intracellular event involving many proteins; however, the rules that regulate such assemblies are not well understood ( Lamb and McKnight, 1991;  Tjian and Maniatis, 1994).	transcription
57033	2	335330	7	NULL	NULL	0	NULL	homo-dimer		formation of	is a type of					intracellular event					NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_254	10970863	p105 modulates p50 homodimer in vivo   The formation of homo- or heterodimers is a common intracellular event involving many proteins; however, the rules that regulate such assemblies are not well understood ( Lamb and McKnight, 1991;  Tjian and Maniatis, 1994).	transcription
57034	3	335330	7	NULL	NULL	0	NULL	heterodimer		formation of	is a type of					intracellular event					NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_254	10970863	p105 modulates p50 homodimer in vivo   The formation of homo- or heterodimers is a common intracellular event involving many proteins; however, the rules that regulate such assemblies are not well understood ( Lamb and McKnight, 1991;  Tjian and Maniatis, 1994).	transcription
78185	1	335331	6	NULL	NULL	0	NULL	BCL-3	GP		is a type of					oncoprotein	GP				NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_483	10970863	Watanabe,N., Iwamura,T., Shinoda,T. and Fujita,T. (1997) Regulation of NF-kappaB1 proteins by candidate oncoprotein BCL-3: generation of NF-kappaB homodimers from the cytoplasmic pool of p50 - p105 and nuclear translocation.	transcription
78186	2	335331	6	NULL	NULL	0	NULL	BCL-3	GP		regulate					NF-kappaB1 proteins	GP				NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_483	10970863	Watanabe,N., Iwamura,T., Shinoda,T. and Fujita,T. (1997) Regulation of NF-kappaB1 proteins by candidate oncoprotein BCL-3: generation of NF-kappaB homodimers from the cytoplasmic pool of p50 - p105 and nuclear translocation.	transcription
57035	1	335331	7	NULL	NULL	0	NULL	BCL-3			regulate					NF-kappaB1 protein					NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_483	10970863	Watanabe,N., Iwamura,T., Shinoda,T. and Fujita,T. (1997) Regulation of NF-kappaB1 proteins by candidate oncoprotein BCL-3: generation of NF-kappaB homodimers from the cytoplasmic pool of p50 - p105 and nuclear translocation.	transcription
57036	2	335331	7	NULL	NULL	0	NULL	BCL-3			is a type of					oncoprotein					NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4712_s_483	10970863	Watanabe,N., Iwamura,T., Shinoda,T. and Fujita,T. (1997) Regulation of NF-kappaB1 proteins by candidate oncoprotein BCL-3: generation of NF-kappaB homodimers from the cytoplasmic pool of p50 - p105 and nuclear translocation.	transcription
78187	1	335332	6	NULL	NULL	0	NULL	TNF-alpha	GP		induces					p105	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_198	10469655	The finding that TNF-alpha induces p105 phosphorylation by IKKalpha (Figures  4 and  5) suggests that this is a rate-limiting step for precursor proteolysis and release of p50 or other associated NF-kappaB subunits.	transcription
78188	2	335332	6	NULL	NULL	0	NULL	statement 1	process		occurs by					IKKalpha	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_198	10469655	The finding that TNF-alpha induces p105 phosphorylation by IKKalpha (Figures  4 and  5) suggests that this is a rate-limiting step for precursor proteolysis and release of p50 or other associated NF-kappaB subunits.	transcription
57037	1	335332	7	NULL	NULL	0	NULL	IKKalpha 			phosphorylates					p105					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_198	10469655	The finding that TNF-alpha induces p105 phosphorylation by IKKalpha (Figures  4 and  5) suggests that this is a rate-limiting step for precursor proteolysis and release of p50 or other associated NF-kappaB subunits.	transcription
57038	2	335332	7	NULL	NULL	0	NULL	TNF-alpha			induce					statement 1					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_198	10469655	The finding that TNF-alpha induces p105 phosphorylation by IKKalpha (Figures  4 and  5) suggests that this is a rate-limiting step for precursor proteolysis and release of p50 or other associated NF-kappaB subunits.	transcription
57039	3	335332	7	NULL	NULL	0	NULL	statement 2			rate limiting step for					precursor		 proteolysis of			NULL		NULL	NULL	NULL	NULL	gw60_embo_18_17_4766_s_198	10469655	The finding that TNF-alpha induces p105 phosphorylation by IKKalpha (Figures  4 and  5) suggests that this is a rate-limiting step for precursor proteolysis and release of p50 or other associated NF-kappaB subunits.	transcription
57040	4	335332	7	NULL	NULL	0	NULL	statement 2			rate limiting step for					p50		release of			NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_198	10469655	The finding that TNF-alpha induces p105 phosphorylation by IKKalpha (Figures  4 and  5) suggests that this is a rate-limiting step for precursor proteolysis and release of p50 or other associated NF-kappaB subunits.	transcription
57041	5	335332	7	NULL	NULL	0	NULL	statement 2			rate limiting step for					NF-kappaB			subunits		NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_198	10469655	The finding that TNF-alpha induces p105 phosphorylation by IKKalpha (Figures  4 and  5) suggests that this is a rate-limiting step for precursor proteolysis and release of p50 or other associated NF-kappaB subunits.	transcription
57042	1	335333	7	NULL	NULL	0	NULL	MEFs			lack					p105			C-terminal ankyrin domain of 		NULL		0	NULL	NULL	NULL	gw60_embo_22_1_121_s_152	12505990	In striking contrast, kappaB binding in MEFs from mice lacking the C-terminal ankyrin domain of p105, but still expressing p50 ( Ishikawa  et al., 1998), consisted almost exclusively of RelA complexes (Figure  7A).	transcription
57043	2	335333	7	NULL	NULL	0	NULL	MEFs			express					p50 					NULL		0	NULL	NULL	NULL	gw60_embo_22_1_121_s_152	12505990	In striking contrast, kappaB binding in MEFs from mice lacking the C-terminal ankyrin domain of p105, but still expressing p50 ( Ishikawa  et al., 1998), consisted almost exclusively of RelA complexes (Figure  7A).	transcription
57044	3	335333	7	NULL	NULL	0	NULL	MEFs			consist					RelA complexes		exclusively of			NULL		0	NULL	NULL	NULL	gw60_embo_22_1_121_s_152	12505990	In striking contrast, kappaB binding in MEFs from mice lacking the C-terminal ankyrin domain of p105, but still expressing p50 ( Ishikawa  et al., 1998), consisted almost exclusively of RelA complexes (Figure  7A).	transcription
57045	4	335333	7	NULL	NULL	0	NULL	kappaB		binding of	occur in 					MEFs					NULL		0	NULL	NULL	NULL	gw60_embo_22_1_121_s_152	12505990	In striking contrast, kappaB binding in MEFs from mice lacking the C-terminal ankyrin domain of p105, but still expressing p50 ( Ishikawa  et al., 1998), consisted almost exclusively of RelA complexes (Figure  7A).	transcription
78189	1	335334	6	NULL	NULL	0	NULL	CER	GP		activates					AP1	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_507_2_163_s_160	11684091	It has been reported that CER activates AP1 by increasing c-jun mRNA synthesis [  27], or NF- B by inducing the processing of p105 to p50, a component of the NF- B transcription factor [  28].	transcription
78190	2	335334	6	NULL	NULL	0	NULL	CER	GP		increases					c-jun mRNA	NucleicAcid	synthesis of			NULL		0	NULL	NULL	NULL	gw60_febslett_507_2_163_s_160	11684091	It has been reported that CER activates AP1 by increasing c-jun mRNA synthesis [  27], or NF- B by inducing the processing of p105 to p50, a component of the NF- B transcription factor [  28].	transcription
78191	3	335334	6	NULL	NULL	0	NULL	p105	GP		is processed to					p50	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_507_2_163_s_160	11684091	It has been reported that CER activates AP1 by increasing c-jun mRNA synthesis [  27], or NF- B by inducing the processing of p105 to p50, a component of the NF- B transcription factor [  28].	transcription
78192	4	335334	6	NULL	NULL	0	NULL	CER	GP		activates					NF-B	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_507_2_163_s_160	11684091	It has been reported that CER activates AP1 by increasing c-jun mRNA synthesis [  27], or NF- B by inducing the processing of p105 to p50, a component of the NF- B transcription factor [  28].	transcription
78193	5	335334	6	NULL	NULL	0	NULL	statement 4	process		occurs via					statement 3	process				NULL		0	NULL	NULL	NULL	gw60_febslett_507_2_163_s_160	11684091	It has been reported that CER activates AP1 by increasing c-jun mRNA synthesis [  27], or NF- B by inducing the processing of p105 to p50, a component of the NF- B transcription factor [  28].	transcription
57046	1	335334	7	NULL	NULL	0	NULL	CER			activates					AP1					NULL		0	NULL	NULL	NULL	gw60_febslett_507_2_163_s_160	11684091	It has been reported that CER activates AP1 by increasing c-jun mRNA synthesis [  27], or NF- B by inducing the processing of p105 to p50, a component of the NF- B transcription factor [  28].	transcription
57047	2	335334	7	NULL	NULL	0	NULL	statement 1			occur by					c-jun mRNA		increasing synthesis of			NULL		0	NULL	NULL	NULL	gw60_febslett_507_2_163_s_160	11684091	It has been reported that CER activates AP1 by increasing c-jun mRNA synthesis [  27], or NF- B by inducing the processing of p105 to p50, a component of the NF- B transcription factor [  28].	transcription
57048	3	335334	7	NULL	NULL	0	NULL	statement 1			occur through					NF-B					NULL		NULL	NULL	NULL	NULL	gw60_febslett_507_2_163_s_160	11684091	It has been reported that CER activates AP1 by increasing c-jun mRNA synthesis [  27], or NF- B by inducing the processing of p105 to p50, a component of the NF- B transcription factor [  28].	transcription
57049	4	335334	7	NULL	NULL	0	NULL	p105			processed to					p50					NULL		0	NULL	NULL	NULL	gw60_febslett_507_2_163_s_160	11684091	It has been reported that CER activates AP1 by increasing c-jun mRNA synthesis [  27], or NF- B by inducing the processing of p105 to p50, a component of the NF- B transcription factor [  28].	transcription
57050	5	335334	7	NULL	NULL	0	NULL	statement 3			occur by					statement 4		inducing			NULL		0	NULL	NULL	NULL	gw60_febslett_507_2_163_s_160	11684091	It has been reported that CER activates AP1 by increasing c-jun mRNA synthesis [  27], or NF- B by inducing the processing of p105 to p50, a component of the NF- B transcription factor [  28].	transcription
57051	6	335334	7	NULL	NULL	0	NULL	p50			is a component of					NF- B transcription factor					NULL		0	NULL	NULL	NULL	gw60_febslett_507_2_163_s_160	11684091	It has been reported that CER activates AP1 by increasing c-jun mRNA synthesis [  27], or NF- B by inducing the processing of p105 to p50, a component of the NF- B transcription factor [  28].	transcription
78194	1	335335	6	NULL	NULL	0	NULL	ASMase	GP		activate		may			I B kinase complex	OrganismPart				NULL		0	NULL	NULL	NULL	gw60_febslett_526_1_15_s_180	12208496	Hence, it is conceivable that ASMase may activate the I B kinase complex, which in turn leads to phosphorylation and proteasome-limited proteolysis of p105, the precursor form of p50 [  39].	transcription
78195	2	335335	6	NULL	NULL	0	NULL	statement 1	process		leads to					p105	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_febslett_526_1_15_s_180	12208496	Hence, it is conceivable that ASMase may activate the I B kinase complex, which in turn leads to phosphorylation and proteasome-limited proteolysis of p105, the precursor form of p50 [  39].	transcription
78196	3	335335	6	NULL	NULL	0	NULL	statement 1	process		leads to					p105	GP	proteolysis of			NULL		0	NULL	NULL	NULL	gw60_febslett_526_1_15_s_180	12208496	Hence, it is conceivable that ASMase may activate the I B kinase complex, which in turn leads to phosphorylation and proteasome-limited proteolysis of p105, the precursor form of p50 [  39].	transcription
78197	4	335335	6	NULL	NULL	0	NULL	p105	GP	proteolysis of	is limited to					proteasome	CellComponent				NULL		0	NULL	NULL	NULL	gw60_febslett_526_1_15_s_180	12208496	Hence, it is conceivable that ASMase may activate the I B kinase complex, which in turn leads to phosphorylation and proteasome-limited proteolysis of p105, the precursor form of p50 [  39].	transcription
57052	1	335335	7	NULL	NULL	0	NULL	ASMase			activate		may			 I B kinase complex					NULL		0	NULL	NULL	NULL	gw60_febslett_526_1_15_s_180	12208496	Hence, it is conceivable that ASMase may activate the I B kinase complex, which in turn leads to phosphorylation and proteasome-limited proteolysis of p105, the precursor form of p50 [  39].	transcription
57053	2	335335	7	NULL	NULL	0	NULL	statement 1			leads to					phosphorylation					NULL		0	NULL	NULL	NULL	gw60_febslett_526_1_15_s_180	12208496	Hence, it is conceivable that ASMase may activate the I B kinase complex, which in turn leads to phosphorylation and proteasome-limited proteolysis of p105, the precursor form of p50 [  39].	transcription
57054	3	335335	7	NULL	NULL	0	NULL	statement 1			leads to					p105		proteasome-limited proteolysis of 			NULL		0	NULL	NULL	NULL	gw60_febslett_526_1_15_s_180	12208496	Hence, it is conceivable that ASMase may activate the I B kinase complex, which in turn leads to phosphorylation and proteasome-limited proteolysis of p105, the precursor form of p50 [  39].	transcription
57055	4	335335	7	NULL	NULL	0	NULL	p105			is a precursor of					p50					NULL		0	NULL	NULL	NULL	gw60_febslett_526_1_15_s_180	12208496	Hence, it is conceivable that ASMase may activate the I B kinase complex, which in turn leads to phosphorylation and proteasome-limited proteolysis of p105, the precursor form of p50 [  39].	transcription
78198	1	335336	6	NULL	NULL	0	NULL	NF-B	GP		is a type of					Transcription factor	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_529_1_22_s_62	12354607	The first example of this type of regulator was found in the p105 precursor of the transcription factor NF- B which contains a Gly rich region (GRR) that is required for processing to the active p50 [  17].	transcription
78199	2	335336	6	NULL	NULL	0	NULL	NF-B	GP		contains						AminoAcid		Gly rich region		NULL		0	NULL	NULL	NULL	gw60_febslett_529_1_22_s_62	12354607	The first example of this type of regulator was found in the p105 precursor of the transcription factor NF- B which contains a Gly rich region (GRR) that is required for processing to the active p50 [  17].	transcription
78200	3	335336	6	NULL	NULL	0	NULL	GRR	AminoAcid		is					Gly rich region	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_febslett_529_1_22_s_62	12354607	The first example of this type of regulator was found in the p105 precursor of the transcription factor NF- B which contains a Gly rich region (GRR) that is required for processing to the active p50 [  17].	transcription
78201	4	335336	6	NULL	NULL	0	NULL	p105 precursor	GP		is processed to					p50	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_529_1_22_s_62	12354607	The first example of this type of regulator was found in the p105 precursor of the transcription factor NF- B which contains a Gly rich region (GRR) that is required for processing to the active p50 [  17].	transcription
57056	1	335336	7	NULL	NULL	0	NULL	p105			is a precursor of					NF-B					NULL		0	NULL	NULL	NULL	gw60_febslett_529_1_22_s_62	12354607	The first example of this type of regulator was found in the p105 precursor of the transcription factor NF- B which contains a Gly rich region (GRR) that is required for processing to the active p50 [  17].	transcription
57057	2	335336	7	NULL	NULL	0	NULL	NF-B			is a type of					transcription factor					NULL		0	NULL	NULL	NULL	gw60_febslett_529_1_22_s_62	12354607	The first example of this type of regulator was found in the p105 precursor of the transcription factor NF- B which contains a Gly rich region (GRR) that is required for processing to the active p50 [  17].	transcription
57058	3	335336	7	NULL	NULL	0	NULL	NF-B			contains								Gly rich region (GRR)		NULL		0	NULL	NULL	NULL	gw60_febslett_529_1_22_s_62	12354607	The first example of this type of regulator was found in the p105 precursor of the transcription factor NF- B which contains a Gly rich region (GRR) that is required for processing to the active p50 [  17].	transcription
57059	4	335336	7	NULL	NULL	0	NULL	statement 3			is required for					p50		processing to active			NULL		0	NULL	NULL	NULL	gw60_febslett_529_1_22_s_62	12354607	The first example of this type of regulator was found in the p105 precursor of the transcription factor NF- B which contains a Gly rich region (GRR) that is required for processing to the active p50 [  17].	transcription
57060	1	335337	7	NULL	NULL	0	NULL	clasto-lactacystin beta-lactone			inhibits					p50		generation of			NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_152	9529257	The addition of  clasto-lactacystin beta-lactone at concentrations as low as 10  muM inhibited the generation of p50 while not altering the production of  p105 (  Figure 6, compare lanes 1 - 4 with lanes 5 - 8).	transcription
57061	2	335337	7	NULL	NULL	0	NULL	clasto-lactacystin beta-lactone			does not alter					p105		production of			NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_152	9529257	The addition of  clasto-lactacystin beta-lactone at concentrations as low as 10  muM inhibited the generation of p50 while not altering the production of  p105 (  Figure 6, compare lanes 1 - 4 with lanes 5 - 8).	transcription
57062	1	335338	7	NULL	NULL	0	NULL	Proteasome inhibitor			blocks					p50		Cotranslational Generation of			NULL		0	NULL	NULL	NULL	gw60_cell_92_6_819_s_155	9529257	Cotranslational Generation of p50 Is Blocked by a Specific  Inhibitor of the Proteasome CHO-CD14 cells were transfected with a p105 expression vector  containing an N-terminal gp 10 epitope tag.	transcription
57063	1	335339	7	NULL	NULL	0	NULL	Myc			bind					p50					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_62	9950430	An anti-Myc monoclonal antibody caused a supershift of the induced smaller NF-kappaB complex in cells that had been co-transfected with TPL-2 and Myc - p105 (  Fig. 4c, lane 8), confirming the presence of Myc - p50 in this complex.	transcription
78202	1	335340	6	NULL	NULL	0	NULL	TNF-alpha	GP		stimulates					p105	GP	degradation of 			NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_89	9950430	In Jurkat T cells stably transfected with control vector, tumour-necrosis factor-alpha (TNF-alpha) stimulated p105 degradation ( Fig. 7a) while having no detectable effect on p50 production (data not shown).	transcription
78203	2	335340	6	NULL	NULL	0	NULL	TNF-alpha	GP		is					 tumour-necrosis factor-alpha	GP				NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_89	9950430	In Jurkat T cells stably transfected with control vector, tumour-necrosis factor-alpha (TNF-alpha) stimulated p105 degradation ( Fig. 7a) while having no detectable effect on p50 production (data not shown).	transcription
57064	1	335340	7	NULL	NULL	0	NULL	TNF-alpha			stimulates					p105		degradation of			NULL	Jurkat T cells	0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_89	9950430	In Jurkat T cells stably transfected with control vector, tumour-necrosis factor-alpha (TNF-alpha) stimulated p105 degradation ( Fig. 7a) while having no detectable effect on p50 production (data not shown).	transcription
57065	2	335340	7	NULL	NULL	0	NULL	TNF-alpha			is					tumour-necrosis factor-alpha					NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_89	9950430	In Jurkat T cells stably transfected with control vector, tumour-necrosis factor-alpha (TNF-alpha) stimulated p105 degradation ( Fig. 7a) while having no detectable effect on p50 production (data not shown).	transcription
57066	3	335340	7	NULL	NULL	0	NULL	TNF-alpha			does not effect					p50		production of			NULL		0	NULL	NULL	NULL	gw60_nature_397_6717_363_s_89	9950430	In Jurkat T cells stably transfected with control vector, tumour-necrosis factor-alpha (TNF-alpha) stimulated p105 degradation ( Fig. 7a) while having no detectable effect on p50 production (data not shown).	transcription
78204	1	335341	6	NULL	NULL	0	NULL	DA-IKK	GP		induces					p105	GP	loss of			NULL		0	NULL	NULL	NULL	gw60_molcell_7_2_401_s_105	11239468	Consistent with one recent report  (Heissmeyer et al., 1999  ), DA-IKK  induced significant loss of p105 without significantly enhancing the production of p50 (lane 2).	transcription
78205	2	335341	6	NULL	NULL	0	NULL	DA-IKK	GP		does not enhance					p50	GP	production of 			NULL		0	NULL	NULL	NULL	gw60_molcell_7_2_401_s_105	11239468	Consistent with one recent report  (Heissmeyer et al., 1999  ), DA-IKK  induced significant loss of p105 without significantly enhancing the production of p50 (lane 2).	transcription
57067	1	335341	7	NULL	NULL	0	NULL	DA-IKK			induce					p105		significant loss of 			NULL		0	NULL	NULL	NULL	gw60_molcell_7_2_401_s_105	11239468	Consistent with one recent report  (Heissmeyer et al., 1999  ), DA-IKK  induced significant loss of p105 without significantly enhancing the production of p50 (lane 2).	transcription
57068	2	335341	7	NULL	NULL	0	NULL	statement 1			does not enhance		significantly			p50		production of			NULL		0	NULL	NULL	NULL	gw60_molcell_7_2_401_s_105	11239468	Consistent with one recent report  (Heissmeyer et al., 1999  ), DA-IKK  induced significant loss of p105 without significantly enhancing the production of p50 (lane 2).	transcription
78206	1	335342	6	NULL	NULL	0	NULL	NFKB1	GP		encodes					p105	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_421	11158290	The complete exon-intron structure of the 156-kb human gene NFKB1, which encodes the p105 and p50 proteins of transcription factors NF-kappaB and IkappaBgamma: implications for NF-kappaB-mediated signal transduction.	transcription
78207	2	335342	6	NULL	NULL	0	NULL	NFKB1	GP		encodes					p50	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_421	11158290	The complete exon-intron structure of the 156-kb human gene NFKB1, which encodes the p105 and p50 proteins of transcription factors NF-kappaB and IkappaBgamma: implications for NF-kappaB-mediated signal transduction.	transcription
78208	3	335342	6	NULL	NULL	NULL	NULL	p105	GP		is a type of					Transcription factor	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_421	11158290	The complete exon-intron structure of the 156-kb human gene NFKB1, which encodes the p105 and p50 proteins of transcription factors NF-kappaB and IkappaBgamma: implications for NF-kappaB-mediated signal transduction.	transcription
78209	4	335342	6	NULL	NULL	0	NULL	p50	GP		is a type of					Transcription factor	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_421	11158290	The complete exon-intron structure of the 156-kb human gene NFKB1, which encodes the p105 and p50 proteins of transcription factors NF-kappaB and IkappaBgamma: implications for NF-kappaB-mediated signal transduction.	transcription
57069	1	335342	7	NULL	NULL	0	NULL	NFKB1 gene		human	encode					p105 protein					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_421	11158290	The complete exon-intron structure of the 156-kb human gene NFKB1, which encodes the p105 and p50 proteins of transcription factors NF-kappaB and IkappaBgamma: implications for NF-kappaB-mediated signal transduction.	transcription
57070	2	335342	7	NULL	NULL	0	NULL	NFKB1 gene		human	encode					p50 protein					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_421	11158290	The complete exon-intron structure of the 156-kb human gene NFKB1, which encodes the p105 and p50 proteins of transcription factors NF-kappaB and IkappaBgamma: implications for NF-kappaB-mediated signal transduction.	transcription
57071	3	335342	7	NULL	NULL	0	NULL	NF-kappaB 			is a type of					transcription factor					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_421	11158290	The complete exon-intron structure of the 156-kb human gene NFKB1, which encodes the p105 and p50 proteins of transcription factors NF-kappaB and IkappaBgamma: implications for NF-kappaB-mediated signal transduction.	transcription
57072	4	335342	7	NULL	NULL	0	NULL	IkappaBgamma			is a type of					transcription factor					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1024_s_421	11158290	The complete exon-intron structure of the 156-kb human gene NFKB1, which encodes the p105 and p50 proteins of transcription factors NF-kappaB and IkappaBgamma: implications for NF-kappaB-mediated signal transduction.	transcription
78210	1	335344	6	NULL	NULL	0	NULL	p105 molecule	GP		contain								ankyrin repeats		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_5	11350967	Here we show that processing of p105 molecules that contain more then four ankyrin repeats, but lack the C-terminal phosphorylation/ubiquitin ligase binding domain, is strongly inhibited by docked p50 subunits.	transcription
78211	2	335344	6	NULL	NULL	0	NULL	p105 molecule	GP		lack								 C-terminal phosphorylation/ubiquitin ligase binding domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_5	11350967	Here we show that processing of p105 molecules that contain more then four ankyrin repeats, but lack the C-terminal phosphorylation/ubiquitin ligase binding domain, is strongly inhibited by docked p50 subunits.	transcription
78212	3	335344	6	NULL	NULL	0	NULL	p105 molecule 	GP	processing of	is inhibited by		strongly			p50 subunit	GP	docked			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_5	11350967	Here we show that processing of p105 molecules that contain more then four ankyrin repeats, but lack the C-terminal phosphorylation/ubiquitin ligase binding domain, is strongly inhibited by docked p50 subunits.	transcription
57073	1	335344	7	NULL	NULL	0	NULL	p105 molecules			contain								four ankyrin repeats		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_5	11350967	Here we show that processing of p105 molecules that contain more then four ankyrin repeats, but lack the C-terminal phosphorylation/ubiquitin ligase binding domain, is strongly inhibited by docked p50 subunits.	transcription
57074	2	335344	7	NULL	NULL	0	NULL	p105 molecules			lack								C-terminal phosphorylation/ubiquitin ligase binding domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_5	11350967	Here we show that processing of p105 molecules that contain more then four ankyrin repeats, but lack the C-terminal phosphorylation/ubiquitin ligase binding domain, is strongly inhibited by docked p50 subunits.	transcription
57075	3	335344	7	NULL	NULL	0	NULL	statement 1			occur simulataneous with					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_5	11350967	Here we show that processing of p105 molecules that contain more then four ankyrin repeats, but lack the C-terminal phosphorylation/ubiquitin ligase binding domain, is strongly inhibited by docked p50 subunits.	transcription
57076	4	335344	7	NULL	NULL	0	NULL			docked	inhibits		strongly	p50 subunits		statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_5	11350967	Here we show that processing of p105 molecules that contain more then four ankyrin repeats, but lack the C-terminal phosphorylation/ubiquitin ligase binding domain, is strongly inhibited by docked p50 subunits.	transcription
57077	1	335345	7	NULL	NULL	0	NULL	p105 			contain							more than	four ankyrin repeats		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_147	11350967	Exogenous p50 inhibits  in vitro processing of p105 species that contain more than four ankyrin repeats but lack the C-terminal  IKK  phosphorylation and beta-TrCP binding domain.	transcription
57078	2	335345	7	NULL	NULL	0	NULL	p105			lack								C-terminal IKK phosphorylation domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_147	11350967	Exogenous p50 inhibits  in vitro processing of p105 species that contain more than four ankyrin repeats but lack the C-terminal  IKK  phosphorylation and beta-TrCP binding domain.	transcription
57079	3	335345	7	NULL	NULL	0	NULL	p105			lack								beta-TrCP binding domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_147	11350967	Exogenous p50 inhibits  in vitro processing of p105 species that contain more than four ankyrin repeats but lack the C-terminal  IKK  phosphorylation and beta-TrCP binding domain.	transcription
57080	4	335345	7	NULL	NULL	0	NULL	statement 1			occur simulataneous with					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_147	11350967	Exogenous p50 inhibits  in vitro processing of p105 species that contain more than four ankyrin repeats but lack the C-terminal  IKK  phosphorylation and beta-TrCP binding domain.	transcription
57081	5	335345	7	NULL	NULL	0	NULL	statement 2			occur simulataneous with					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_147	11350967	Exogenous p50 inhibits  in vitro processing of p105 species that contain more than four ankyrin repeats but lack the C-terminal  IKK  phosphorylation and beta-TrCP binding domain.	transcription
57082	6	335345	7	NULL	NULL	0	NULL	p50		exogenous	inhibits					statement 4		processing of			NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_147	11350967	Exogenous p50 inhibits  in vitro processing of p105 species that contain more than four ankyrin repeats but lack the C-terminal  IKK  phosphorylation and beta-TrCP binding domain.	transcription
57083	7	335345	7	NULL	NULL	0	NULL	p50		exogenous	inhibits					statement 5		processing of			NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_147	11350967	Exogenous p50 inhibits  in vitro processing of p105 species that contain more than four ankyrin repeats but lack the C-terminal  IKK  phosphorylation and beta-TrCP binding domain.	transcription
78730	1	335346	6	NULL	NULL	0	NULL	mice	Organism		express					p50	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_34_31479_s_13	12807880	However, mice expressing  p50 but lacking p105 suffer severe defects that include lymphocyte  infiltration in multiple organs and a lack of normal cytokine expression in  macrophages, leading to their high postnatal fatality  ( 5).	transcription
78731	2	335346	6	NULL	NULL	0	NULL	mice	Organism		lack					p105	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_34_31479_s_13	12807880	However, mice expressing  p50 but lacking p105 suffer severe defects that include lymphocyte  infiltration in multiple organs and a lack of normal cytokine expression in  macrophages, leading to their high postnatal fatality  ( 5).	transcription
78732	3	335346	6	NULL	NULL	0	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_34_31479_s_13	12807880	However, mice expressing  p50 but lacking p105 suffer severe defects that include lymphocyte  infiltration in multiple organs and a lack of normal cytokine expression in  macrophages, leading to their high postnatal fatality  ( 5).	transcription
78733	4	335346	6	NULL	NULL	0	NULL	statement 3	Process		leads to					lymphocyte infiltration	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_34_31479_s_13	12807880	However, mice expressing  p50 but lacking p105 suffer severe defects that include lymphocyte  infiltration in multiple organs and a lack of normal cytokine expression in  macrophages, leading to their high postnatal fatality  ( 5).	transcription
78734	5	335346	6	NULL	NULL	0	NULL	cytokine	Chemical		is expressed in					macrophages	Cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_34_31479_s_13	12807880	However, mice expressing  p50 but lacking p105 suffer severe defects that include lymphocyte  infiltration in multiple organs and a lack of normal cytokine expression in  macrophages, leading to their high postnatal fatality  ( 5).	transcription
78735	6	335346	6	NULL	NULL	0	NULL	statement 3	Process		causes					statement 5	Process	lack of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_34_31479_s_13	12807880	However, mice expressing  p50 but lacking p105 suffer severe defects that include lymphocyte  infiltration in multiple organs and a lack of normal cytokine expression in  macrophages, leading to their high postnatal fatality  ( 5).	transcription
57084	1	335346	7	NULL	NULL	0	NULL	mice 			express					p50					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_34_31479_s_13	12807880	However, mice expressing  p50 but lacking p105 suffer severe defects that include lymphocyte  infiltration in multiple organs and a lack of normal cytokine expression in  macrophages, leading to their high postnatal fatality  ( 5).	transcription
57085	2	335346	7	NULL	NULL	0	NULL	statement 1			lacks					p105					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_34_31479_s_13	12807880	However, mice expressing  p50 but lacking p105 suffer severe defects that include lymphocyte  infiltration in multiple organs and a lack of normal cytokine expression in  macrophages, leading to their high postnatal fatality  ( 5).	transcription
57086	3	335346	7	NULL	NULL	0	NULL	statement 2			suffer from					lymphocyte infiltration					NULL	multiple organs	0	NULL	NULL	NULL	gw60_jbiolchem_278_34_31479_s_13	12807880	However, mice expressing  p50 but lacking p105 suffer severe defects that include lymphocyte  infiltration in multiple organs and a lack of normal cytokine expression in  macrophages, leading to their high postnatal fatality  ( 5).	transcription
57087	4	335346	7	NULL	NULL	0	NULL	statement 2			leads to					cytokine		 lack of normal expression of			NULL	macrophages	0	NULL	NULL	NULL	gw60_jbiolchem_278_34_31479_s_13	12807880	However, mice expressing  p50 but lacking p105 suffer severe defects that include lymphocyte  infiltration in multiple organs and a lack of normal cytokine expression in  macrophages, leading to their high postnatal fatality  ( 5).	transcription
57088	5	335346	7	NULL	NULL	0	NULL	statement 3			leads to					high postnatal fatality					NULL	mice	NULL	NULL	NULL	NULL	gw60_jbiolchem_278_34_31479_s_13	12807880	However, mice expressing  p50 but lacking p105 suffer severe defects that include lymphocyte  infiltration in multiple organs and a lack of normal cytokine expression in  macrophages, leading to their high postnatal fatality  ( 5).	transcription
57089	6	335346	7	NULL	NULL	0	NULL	statement 4			leads to					high postnatal fatality					NULL	mice	0	NULL	NULL	NULL	gw60_jbiolchem_278_34_31479_s_13	12807880	However, mice expressing  p50 but lacking p105 suffer severe defects that include lymphocyte  infiltration in multiple organs and a lack of normal cytokine expression in  macrophages, leading to their high postnatal fatality  ( 5).	transcription
78213	1	335348	6	NULL	NULL	0	NULL	PMA	Chemical		activates					NF-kappaB	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_94	8537390	In concomitance with NF-kappaB  activation by PMA, the processing of p105 did not occur in the nucleus ( Fig. 3,  B  and  C), and the nuclear content of  p50 was unchanged ( Fig. 3 B).	transcription
57090	1	335348	7	NULL	NULL	0	NULL	PMA			activates					NF-kappaB					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_94	8537390	In concomitance with NF-kappaB  activation by PMA, the processing of p105 did not occur in the nucleus ( Fig. 3,  B  and  C), and the nuclear content of  p50 was unchanged ( Fig. 3 B).	transcription
57091	2	335348	7	NULL	NULL	0	NULL	p105		processing of	does not occur in					nucleus					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_94	8537390	In concomitance with NF-kappaB  activation by PMA, the processing of p105 did not occur in the nucleus ( Fig. 3,  B  and  C), and the nuclear content of  p50 was unchanged ( Fig. 3 B).	transcription
57092	3	335348	7	NULL	NULL	0	NULL	p50		nuclear content of	remains					unchanged					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_94	8537390	In concomitance with NF-kappaB  activation by PMA, the processing of p105 did not occur in the nucleus ( Fig. 3,  B  and  C), and the nuclear content of  p50 was unchanged ( Fig. 3 B).	transcription
57093	4	335348	7	NULL	NULL	0	NULL	statement 2			in concomitance with					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_94	8537390	In concomitance with NF-kappaB  activation by PMA, the processing of p105 did not occur in the nucleus ( Fig. 3,  B  and  C), and the nuclear content of  p50 was unchanged ( Fig. 3 B).	transcription
57094	5	335348	7	NULL	NULL	0	NULL	statement 3			in concomitance with					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_52_31244_s_94	8537390	In concomitance with NF-kappaB  activation by PMA, the processing of p105 did not occur in the nucleus ( Fig. 3,  B  and  C), and the nuclear content of  p50 was unchanged ( Fig. 3 B).	transcription
78214	1	335349	6	NULL	NULL	0	NULL	p105	GP		is processed to					p50	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_21	7814425	Here we demonstrate that treatment of human monocytic cells with either  bacterial lipopolysaccharide (LPS) or tumor necrosis factor-alpha  (TNF)  stimulates p105 processing to p50 via an ATP-dependent pathway.	transcription
78215	2	335349	6	NULL	NULL	0	NULL	statement 1	process		is dependent on					ATP	process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_21	7814425	Here we demonstrate that treatment of human monocytic cells with either  bacterial lipopolysaccharide (LPS) or tumor necrosis factor-alpha  (TNF)  stimulates p105 processing to p50 via an ATP-dependent pathway.	transcription
78216	3	335349	6	NULL	NULL	0	NULL	LPS	Chemical		stimulates					statement 1	process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_21	7814425	Here we demonstrate that treatment of human monocytic cells with either  bacterial lipopolysaccharide (LPS) or tumor necrosis factor-alpha  (TNF)  stimulates p105 processing to p50 via an ATP-dependent pathway.	transcription
78217	4	335349	6	NULL	NULL	0	NULL	TNF	Chemical		stimulates					statement 1	process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_21	7814425	Here we demonstrate that treatment of human monocytic cells with either  bacterial lipopolysaccharide (LPS) or tumor necrosis factor-alpha  (TNF)  stimulates p105 processing to p50 via an ATP-dependent pathway.	transcription
57095	1	335349	7	NULL	NULL	0	NULL	p105			processed to					p50					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_21	7814425	Here we demonstrate that treatment of human monocytic cells with either  bacterial lipopolysaccharide (LPS) or tumor necrosis factor-alpha  (TNF)  stimulates p105 processing to p50 via an ATP-dependent pathway.	transcription
57096	2	335349	7	NULL	NULL	0	NULL	LPS			stimulates					statement 1					NULL	human monocytic cells	0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_21	7814425	Here we demonstrate that treatment of human monocytic cells with either  bacterial lipopolysaccharide (LPS) or tumor necrosis factor-alpha  (TNF)  stimulates p105 processing to p50 via an ATP-dependent pathway.	transcription
57097	3	335349	7	NULL	NULL	0	NULL	TNF-alpha			stimulates					statement 1					NULL	human monocytic cells	0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_21	7814425	Here we demonstrate that treatment of human monocytic cells with either  bacterial lipopolysaccharide (LPS) or tumor necrosis factor-alpha  (TNF)  stimulates p105 processing to p50 via an ATP-dependent pathway.	transcription
57098	4	335349	7	NULL	NULL	0	NULL	statement 1			via an					ATP-dependent pathway					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_21	7814425	Here we demonstrate that treatment of human monocytic cells with either  bacterial lipopolysaccharide (LPS) or tumor necrosis factor-alpha  (TNF)  stimulates p105 processing to p50 via an ATP-dependent pathway.	transcription
57099	5	335349	7	NULL	NULL	0	NULL	LPS			is					bacterial lipopolysaccharide					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_21	7814425	Here we demonstrate that treatment of human monocytic cells with either  bacterial lipopolysaccharide (LPS) or tumor necrosis factor-alpha  (TNF)  stimulates p105 processing to p50 via an ATP-dependent pathway.	transcription
57100	6	335349	7	NULL	NULL	0	NULL	TNF			is					tumor necrosis factor					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_21	7814425	Here we demonstrate that treatment of human monocytic cells with either  bacterial lipopolysaccharide (LPS) or tumor necrosis factor-alpha  (TNF)  stimulates p105 processing to p50 via an ATP-dependent pathway.	transcription
57101	7	335349	7	NULL	NULL	0	NULL	statement 2			is an alternative to					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_21	7814425	Here we demonstrate that treatment of human monocytic cells with either  bacterial lipopolysaccharide (LPS) or tumor necrosis factor-alpha  (TNF)  stimulates p105 processing to p50 via an ATP-dependent pathway.	transcription
57102	1	335350	7	NULL	NULL	0	NULL	p105			forms					p50					NULL		0	NULL	NULL	NULL	abs-batch0740-0759_febs-j_273_16_16911524_s_10	16911524	Western blot analysis revealed transient activation of p38 mitogen-activated  protein kinase, extracellular signal-related kinase 1/2, and nuclear factor  kappaB1 and possibly new formation of p50 from its precursor p105.	transcription
57103	2	335350	7	NULL	NULL	0	NULL	p105			is a precursor of					p50					NULL		0	NULL	NULL	NULL	abs-batch0740-0759_febs-j_273_16_16911524_s_10	16911524	Western blot analysis revealed transient activation of p38 mitogen-activated  protein kinase, extracellular signal-related kinase 1/2, and nuclear factor  kappaB1 and possibly new formation of p50 from its precursor p105.	transcription
78218	1	335351	6	NULL	NULL	0	NULL	TNF-alpha	GP		activates					PI3K/Akt	GP				NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
78219	2	335351	6	NULL	NULL	0	NULL	TNF-alpha	GP		is a type of					cytokine	GP				NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
78220	3	335351	6	NULL	NULL	NULL	NULL	statement 1	process		induces					GSK-3beta	GP	phosphorylation of			NULL	neurons	NULL	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
78221	4	335351	6	NULL	NULL	0	NULL	statement 1	process		induces					GSK-3beta	GP	inactivation of			NULL	neurons	0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
78222	5	335351	6	NULL	NULL	0	NULL	p65	GP		is imported to					nucleus	CellComponent				NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
78223	6	335351	6	NULL	NULL	0	NULL	statement 3	process		impairs					statement 5	process				NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
78224	7	335351	6	NULL	NULL	0	NULL	p50	GP		is processed to					p105	GP				NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
78225	8	335351	6	NULL	NULL	0	NULL	statement 3	process		decreases					statement 7	process				NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
78226	9	335351	6	NULL	NULL	0	NULL	proteasome	CellComponent		mediates					p50	GP	degradation of 			NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
78227	10	335351	6	NULL	NULL	0	NULL	statement 3	process		reduces					statement 9	process				NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
57106	1	335351	7	NULL	NULL	0	NULL	TNF-alpha			activates					PI3K/Akt 					NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
57107	2	335351	7	NULL	NULL	0	NULL	statement 1			induces					GSK-3beta 		phosphorylation of			NULL	neurons	0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
57108	3	335351	7	NULL	NULL	0	NULL	statement 1			induces					GSK-3beta 		inactivation of			NULL	neurons	0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
57109	4	335351	7	NULL	NULL	0	NULL	statement 2			occur simulataneous with					statement 3					NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
57110	5	335351	7	NULL	NULL	0	NULL	statement 4			impairs					p65		nuclear import of 			NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
57111	6	335351	7	NULL	NULL	0	NULL	p150			processed to					p50					NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
57112	7	335351	7	NULL	NULL	0	NULL	statement 4			decreases					statement 6					NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
57113	8	335351	7	NULL	NULL	0	NULL	proteasome			mediate					p50		degradation of			NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
57114	9	335351	7	NULL	NULL	0	NULL	statement 4			reduces					statement 6					NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
57115	10	335351	7	NULL	NULL	0	NULL	TNF-alpha			is a type of					cytokine					NULL		0	NULL	NULL	NULL	gw70_amjpathol_167_4_1081_s_282	16192643	Activation of PI3K/Akt by the cytokine TNF-alpha or other factors, induces the phosphorylation and inactivation of GSK-3beta in neurons,  which in turn 1) impairs nuclear import of p65, 2) decreases the processing of p105  to p50, and 3) reduces proteasome (prot)-mediated degradation of p50.	transcription
78228	1	335352	6	NULL	NULL	0	NULL	p100	GP		processed into					p52	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_2_1217_s_11	15536066	Limited proteolytic processing of the p100 and p105 proteins generates p52 and p50, respectively, and NF-kappaB DNA binding and transactivation is carried out by heterodimers of p50 or p52 with one of the transactivation-domain containing Rel proteins (RelA, RelB, or c-Rel) ( ).	transcription
78229	2	335352	6	NULL	NULL	0	NULL	p105	GP		processed into					p50	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_2_1217_s_11	15536066	Limited proteolytic processing of the p100 and p105 proteins generates p52 and p50, respectively, and NF-kappaB DNA binding and transactivation is carried out by heterodimers of p50 or p52 with one of the transactivation-domain containing Rel proteins (RelA, RelB, or c-Rel) ( ).	transcription
78230	3	335352	6	NULL	NULL	0	NULL	NF-kappaB	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_2_1217_s_11	15536066	Limited proteolytic processing of the p100 and p105 proteins generates p52 and p50, respectively, and NF-kappaB DNA binding and transactivation is carried out by heterodimers of p50 or p52 with one of the transactivation-domain containing Rel proteins (RelA, RelB, or c-Rel) ( ).	transcription
78231	4	335352	6	NULL	NULL	NULL	NULL	p50	GP		bind					RelA	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_2_1217_s_11	15536066	Limited proteolytic processing of the p100 and p105 proteins generates p52 and p50, respectively, and NF-kappaB DNA binding and transactivation is carried out by heterodimers of p50 or p52 with one of the transactivation-domain containing Rel proteins (RelA, RelB, or c-Rel) ( ).	transcription
78232	5	335352	6	NULL	NULL	0	NULL	p50	GP		bind					RelB	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_2_1217_s_11	15536066	Limited proteolytic processing of the p100 and p105 proteins generates p52 and p50, respectively, and NF-kappaB DNA binding and transactivation is carried out by heterodimers of p50 or p52 with one of the transactivation-domain containing Rel proteins (RelA, RelB, or c-Rel) ( ).	transcription
78233	6	335352	6	NULL	NULL	0	NULL	p50	GP		bind					c-Rel	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_2_1217_s_11	15536066	Limited proteolytic processing of the p100 and p105 proteins generates p52 and p50, respectively, and NF-kappaB DNA binding and transactivation is carried out by heterodimers of p50 or p52 with one of the transactivation-domain containing Rel proteins (RelA, RelB, or c-Rel) ( ).	transcription
78234	7	335352	6	NULL	NULL	0	NULL	p52	GP		bind					RelA	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_2_1217_s_11	15536066	Limited proteolytic processing of the p100 and p105 proteins generates p52 and p50, respectively, and NF-kappaB DNA binding and transactivation is carried out by heterodimers of p50 or p52 with one of the transactivation-domain containing Rel proteins (RelA, RelB, or c-Rel) ( ).	transcription
78235	8	335352	6	NULL	NULL	0	NULL	p52	GP		bind					RelB	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_2_1217_s_11	15536066	Limited proteolytic processing of the p100 and p105 proteins generates p52 and p50, respectively, and NF-kappaB DNA binding and transactivation is carried out by heterodimers of p50 or p52 with one of the transactivation-domain containing Rel proteins (RelA, RelB, or c-Rel) ( ).	transcription
78236	9	335352	6	NULL	NULL	0	NULL	p52	GP		bind					c-Rel	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_2_1217_s_11	15536066	Limited proteolytic processing of the p100 and p105 proteins generates p52 and p50, respectively, and NF-kappaB DNA binding and transactivation is carried out by heterodimers of p50 or p52 with one of the transactivation-domain containing Rel proteins (RelA, RelB, or c-Rel) ( ).	transcription
57116	1	335352	7	NULL	NULL	0	NULL	p100			proteolyse		limited			p52					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_2_1217_s_11	15536066	Limited proteolytic processing of the p100 and p105 proteins generates p52 and p50, respectively, and NF-kappaB DNA binding and transactivation is carried out by heterodimers of p50 or p52 with one of the transactivation-domain containing Rel proteins (RelA, RelB, or c-Rel) ( ).	transcription
57117	2	335352	7	NULL	NULL	0	NULL	p105			proteolyse		limited			p50					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_2_1217_s_11	15536066	Limited proteolytic processing of the p100 and p105 proteins generates p52 and p50, respectively, and NF-kappaB DNA binding and transactivation is carried out by heterodimers of p50 or p52 with one of the transactivation-domain containing Rel proteins (RelA, RelB, or c-Rel) ( ).	transcription
57118	3	335352	7	NULL	NULL	0	NULL	NF-kappaB			bind					DNA					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_2_1217_s_11	15536066	Limited proteolytic processing of the p100 and p105 proteins generates p52 and p50, respectively, and NF-kappaB DNA binding and transactivation is carried out by heterodimers of p50 or p52 with one of the transactivation-domain containing Rel proteins (RelA, RelB, or c-Rel) ( ).	transcription
57119	4	335352	7	NULL	NULL	0	NULL	p50 heterodimer			carries out					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_2_1217_s_11	15536066	Limited proteolytic processing of the p100 and p105 proteins generates p52 and p50, respectively, and NF-kappaB DNA binding and transactivation is carried out by heterodimers of p50 or p52 with one of the transactivation-domain containing Rel proteins (RelA, RelB, or c-Rel) ( ).	transcription
57120	5	335352	7	NULL	NULL	0	NULL	p52			carries out					NF-kappaB		transactivation of	transactivation-domain containing RelA		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_2_1217_s_11	15536066	Limited proteolytic processing of the p100 and p105 proteins generates p52 and p50, respectively, and NF-kappaB DNA binding and transactivation is carried out by heterodimers of p50 or p52 with one of the transactivation-domain containing Rel proteins (RelA, RelB, or c-Rel) ( ).	transcription
57121	6	335352	7	NULL	NULL	0	NULL	p52			carries out					NF-kappaB		transactivation of	transactivation-domain containing RelB		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_2_1217_s_11	15536066	Limited proteolytic processing of the p100 and p105 proteins generates p52 and p50, respectively, and NF-kappaB DNA binding and transactivation is carried out by heterodimers of p50 or p52 with one of the transactivation-domain containing Rel proteins (RelA, RelB, or c-Rel) ( ).	transcription
57122	7	335352	7	NULL	NULL	0	NULL	p52			carries out					NF-kappaB		transactivation of	transactivation-domain containing c-Rel		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_2_1217_s_11	15536066	Limited proteolytic processing of the p100 and p105 proteins generates p52 and p50, respectively, and NF-kappaB DNA binding and transactivation is carried out by heterodimers of p50 or p52 with one of the transactivation-domain containing Rel proteins (RelA, RelB, or c-Rel) ( ).	transcription
57123	8	335352	7	NULL	NULL	0	NULL	p50 heterodimer			carries out					NF-kappaB		transactivation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_2_1217_s_11	15536066	Limited proteolytic processing of the p100 and p105 proteins generates p52 and p50, respectively, and NF-kappaB DNA binding and transactivation is carried out by heterodimers of p50 or p52 with one of the transactivation-domain containing Rel proteins (RelA, RelB, or c-Rel) ( ).	transcription
78724	1	335353	6	NULL	NULL	NULL	NULL	p105	GP	cleavage of	results in					RelB	GP				NULL		NULL	NULL	NULL	NULL	gw60_neurobiolaging_23_5_899_s_14	12392794	Unlike p65, RelB and c-Rel, the p50 and p49 subunits result from proteolytic cleavage of their p105 and p100 precursor molecules, respectively, which include C-terminal I B-like ankyrin repeats that inhibit p50 and p49 activity.	transcription
78725	2	335353	6	NULL	NULL	0	NULL	p105	GP	cleavage of	results in					c-Rel	GP				NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_23_5_899_s_14	12392794	Unlike p65, RelB and c-Rel, the p50 and p49 subunits result from proteolytic cleavage of their p105 and p100 precursor molecules, respectively, which include C-terminal I B-like ankyrin repeats that inhibit p50 and p49 activity.	transcription
78726	3	335353	6	NULL	NULL	0	NULL	p100	GP	cleavage of	results in					p50	GP				NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_23_5_899_s_14	12392794	Unlike p65, RelB and c-Rel, the p50 and p49 subunits result from proteolytic cleavage of their p105 and p100 precursor molecules, respectively, which include C-terminal I B-like ankyrin repeats that inhibit p50 and p49 activity.	transcription
78727	4	335353	6	NULL	NULL	0	NULL	p100	GP	cleavage of	results in					p49	GP				NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_23_5_899_s_14	12392794	Unlike p65, RelB and c-Rel, the p50 and p49 subunits result from proteolytic cleavage of their p105 and p100 precursor molecules, respectively, which include C-terminal I B-like ankyrin repeats that inhibit p50 and p49 activity.	transcription
78728	5	335353	6	NULL	NULL	0	NULL				inhibits			C-terminal I B-like ankyrin repeat		p50	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_23_5_899_s_14	12392794	Unlike p65, RelB and c-Rel, the p50 and p49 subunits result from proteolytic cleavage of their p105 and p100 precursor molecules, respectively, which include C-terminal I B-like ankyrin repeats that inhibit p50 and p49 activity.	transcription
78729	6	335353	6	NULL	NULL	0	NULL				inhibits			C-terminal I B-like ankyrin repeat		p49	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_23_5_899_s_14	12392794	Unlike p65, RelB and c-Rel, the p50 and p49 subunits result from proteolytic cleavage of their p105 and p100 precursor molecules, respectively, which include C-terminal I B-like ankyrin repeats that inhibit p50 and p49 activity.	transcription
57126	1	335353	7	NULL	NULL	0	NULL				result from			p50 subunits		p105 precursor molecules		proteolytic cleavage of			NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_23_5_899_s_14	12392794	Unlike p65, RelB and c-Rel, the p50 and p49 subunits result from proteolytic cleavage of their p105 and p100 precursor molecules, respectively, which include C-terminal I B-like ankyrin repeats that inhibit p50 and p49 activity.	transcription
57127	2	335353	7	NULL	NULL	0	NULL				result from			p49 subunits		p100 precursor molecules		proteolytic cleavage of			NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_23_5_899_s_14	12392794	Unlike p65, RelB and c-Rel, the p50 and p49 subunits result from proteolytic cleavage of their p105 and p100 precursor molecules, respectively, which include C-terminal I B-like ankyrin repeats that inhibit p50 and p49 activity.	transcription
57128	3	335353	7	NULL	NULL	0	NULL	p105 precursor molecule			include								C-terminal I B-like ankyrin repeats		NULL		NULL	NULL	NULL	NULL	gw60_neurobiolaging_23_5_899_s_14	12392794	Unlike p65, RelB and c-Rel, the p50 and p49 subunits result from proteolytic cleavage of their p105 and p100 precursor molecules, respectively, which include C-terminal I B-like ankyrin repeats that inhibit p50 and p49 activity.	transcription
57129	4	335353	7	NULL	NULL	0	NULL	p100 precursor molecule			include								C-terminal I B-like ankyrin repeats		NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_23_5_899_s_14	12392794	Unlike p65, RelB and c-Rel, the p50 and p49 subunits result from proteolytic cleavage of their p105 and p100 precursor molecules, respectively, which include C-terminal I B-like ankyrin repeats that inhibit p50 and p49 activity.	transcription
57130	5	335353	7	NULL	NULL	0	NULL	statement 3			inhibit					p50		activity of			NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_23_5_899_s_14	12392794	Unlike p65, RelB and c-Rel, the p50 and p49 subunits result from proteolytic cleavage of their p105 and p100 precursor molecules, respectively, which include C-terminal I B-like ankyrin repeats that inhibit p50 and p49 activity.	transcription
57131	6	335353	7	NULL	NULL	0	NULL	statement 4			inhibit					p49		activity of			NULL		0	NULL	NULL	NULL	gw60_neurobiolaging_23_5_899_s_14	12392794	Unlike p65, RelB and c-Rel, the p50 and p49 subunits result from proteolytic cleavage of their p105 and p100 precursor molecules, respectively, which include C-terminal I B-like ankyrin repeats that inhibit p50 and p49 activity.	transcription
78237	1	335354	6	NULL	NULL	0	NULL	NF-kappaB	GP		regulate		transcriptionally			beta interferon	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_24_9113_s_145	11094063	It has also been observed that expression of beta interferon, which is transcriptionally regulated by NF-kappaB, is increased in mice with disruptions of the p50 gene ( 19), while in mice with elevated constitutive levels of p50 due to p105 gene disruption, NF-kappaB-regulated cytokine production is increased in some cell types and suppressed in others ( 9).	transcription
78238	2	335354	6	NULL	NULL	NULL	NULL	p50	GP	disruption of	increases					statement 1	process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9113_s_145	11094063	It has also been observed that expression of beta interferon, which is transcriptionally regulated by NF-kappaB, is increased in mice with disruptions of the p50 gene ( 19), while in mice with elevated constitutive levels of p50 due to p105 gene disruption, NF-kappaB-regulated cytokine production is increased in some cell types and suppressed in others ( 9).	transcription
78239	3	335354	6	NULL	NULL	0	NULL	p105	GP	disruption of	increases					p50	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_24_9113_s_145	11094063	It has also been observed that expression of beta interferon, which is transcriptionally regulated by NF-kappaB, is increased in mice with disruptions of the p50 gene ( 19), while in mice with elevated constitutive levels of p50 due to p105 gene disruption, NF-kappaB-regulated cytokine production is increased in some cell types and suppressed in others ( 9).	transcription
78240	4	335354	6	NULL	NULL	0	NULL	NF-kappaB	GP		regulates					cytokine	Chemical	production of 			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_24_9113_s_145	11094063	It has also been observed that expression of beta interferon, which is transcriptionally regulated by NF-kappaB, is increased in mice with disruptions of the p50 gene ( 19), while in mice with elevated constitutive levels of p50 due to p105 gene disruption, NF-kappaB-regulated cytokine production is increased in some cell types and suppressed in others ( 9).	transcription
57132	1	335354	7	NULL	NULL	0	NULL	NF-kappaB			regulates		transcriptionally			beta interferon		expression of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_24_9113_s_145	11094063	It has also been observed that expression of beta interferon, which is transcriptionally regulated by NF-kappaB, is increased in mice with disruptions of the p50 gene ( 19), while in mice with elevated constitutive levels of p50 due to p105 gene disruption, NF-kappaB-regulated cytokine production is increased in some cell types and suppressed in others ( 9).	transcription
57133	2	335354	7	NULL	NULL	0	NULL	p50 gene		disruption of	increase					beta interferon		expression of			NULL	mice	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9113_s_145	11094063	It has also been observed that expression of beta interferon, which is transcriptionally regulated by NF-kappaB, is increased in mice with disruptions of the p50 gene ( 19), while in mice with elevated constitutive levels of p50 due to p105 gene disruption, NF-kappaB-regulated cytokine production is increased in some cell types and suppressed in others ( 9).	transcription
57134	3	335354	7	NULL	NULL	0	NULL	p105 gene		disruption of	elevates					p50		constitutive levels of			NULL	mice	NULL	NULL	NULL	NULL	gw60_molcellbiol_20_24_9113_s_145	11094063	It has also been observed that expression of beta interferon, which is transcriptionally regulated by NF-kappaB, is increased in mice with disruptions of the p50 gene ( 19), while in mice with elevated constitutive levels of p50 due to p105 gene disruption, NF-kappaB-regulated cytokine production is increased in some cell types and suppressed in others ( 9).	transcription
57135	4	335354	7	NULL	NULL	0	NULL	NF-kappaB			regulates					cytokine		production of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_24_9113_s_145	11094063	It has also been observed that expression of beta interferon, which is transcriptionally regulated by NF-kappaB, is increased in mice with disruptions of the p50 gene ( 19), while in mice with elevated constitutive levels of p50 due to p105 gene disruption, NF-kappaB-regulated cytokine production is increased in some cell types and suppressed in others ( 9).	transcription
57136	5	335354	7	NULL	NULL	0	NULL	statement 3			leads to					statement 4					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_24_9113_s_145	11094063	It has also been observed that expression of beta interferon, which is transcriptionally regulated by NF-kappaB, is increased in mice with disruptions of the p50 gene ( 19), while in mice with elevated constitutive levels of p50 due to p105 gene disruption, NF-kappaB-regulated cytokine production is increased in some cell types and suppressed in others ( 9).	transcription
78241	1	335356	6	NULL	NULL	0	NULL	p105	GP		is processed to					p50					NULL	Yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_117	9430676	As shown previously, p105 is processed to p50 in yeast (Fig.  1,  lane 1), but a mutation in the beta-type subunit,  pre1-1 ( 59), that decreases the chymotrypsin-like peptide hydrolysis activity of the proteasome blocks the formation of the mature p50 product (Fig.  1,  lane 2; Fig.  6).	transcription
78279	2	335356	6	NULL	NULL	0	NULL	proteasome	CellComponent		hydrolyze					chymotrypsin-like peptide	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_117	9430676	As shown previously, p105 is processed to p50 in yeast (Fig.  1,  lane 1), but a mutation in the beta-type subunit,  pre1-1 ( 59), that decreases the chymotrypsin-like peptide hydrolysis activity of the proteasome blocks the formation of the mature p50 product (Fig.  1,  lane 2; Fig.  6).	transcription
78280	3	335356	6	NULL	NULL	0	NULL	pre1-1	GP	mutation of	decreases					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_117	9430676	As shown previously, p105 is processed to p50 in yeast (Fig.  1,  lane 1), but a mutation in the beta-type subunit,  pre1-1 ( 59), that decreases the chymotrypsin-like peptide hydrolysis activity of the proteasome blocks the formation of the mature p50 product (Fig.  1,  lane 2; Fig.  6).	transcription
78281	4	335356	6	NULL	NULL	0	NULL	statement 2	process		decreases					p50 	GP	formation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_117	9430676	As shown previously, p105 is processed to p50 in yeast (Fig.  1,  lane 1), but a mutation in the beta-type subunit,  pre1-1 ( 59), that decreases the chymotrypsin-like peptide hydrolysis activity of the proteasome blocks the formation of the mature p50 product (Fig.  1,  lane 2; Fig.  6).	transcription
57137	1	335356	7	NULL	NULL	0	NULL	 p105			processed to					p50					NULL	yeast	0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_117	9430676	As shown previously, p105 is processed to p50 in yeast (Fig.  1,  lane 1), but a mutation in the beta-type subunit,  pre1-1 ( 59), that decreases the chymotrypsin-like peptide hydrolysis activity of the proteasome blocks the formation of the mature p50 product (Fig.  1,  lane 2; Fig.  6).	transcription
57138	2	335356	7	NULL	NULL	0	NULL	pre1-1		mutant	decreases			 beta-type subunit		proteasome		chymotrypsin-like peptide hydrolysis activity of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_117	9430676	As shown previously, p105 is processed to p50 in yeast (Fig.  1,  lane 1), but a mutation in the beta-type subunit,  pre1-1 ( 59), that decreases the chymotrypsin-like peptide hydrolysis activity of the proteasome blocks the formation of the mature p50 product (Fig.  1,  lane 2; Fig.  6).	transcription
57139	3	335356	7	NULL	NULL	0	NULL	statement 2			blocks					p50		formation of mature			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_3_1409_s_117	9430676	As shown previously, p105 is processed to p50 in yeast (Fig.  1,  lane 1), but a mutation in the beta-type subunit,  pre1-1 ( 59), that decreases the chymotrypsin-like peptide hydrolysis activity of the proteasome blocks the formation of the mature p50 product (Fig.  1,  lane 2; Fig.  6).	transcription
78282	1	335357	6	NULL	NULL	0	NULL	BCL-3	GP		mediates					p50 homodimer	GP	formation of 			NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_243	10970863	However, after the primary cotranslational event, the intracellular ratio of p50 and p105 may also be influenced either by cellular factors such as BCL-3, which mediates p50 homodimer formation ( Naumann  et al., 1993;  Watanabe  et al., 1997), or by phosphorylation of p105, which triggers degradation of this protein ( MacKichan  et al., 1996;  Belich  et al., 1999;  Heissmeyer  et al., 1999).	transcription
78283	2	335357	6	NULL	NULL	0	NULL	p105 	GP	phosphorylation of 	triggers					p105	GP	degradation of 			NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_243	10970863	However, after the primary cotranslational event, the intracellular ratio of p50 and p105 may also be influenced either by cellular factors such as BCL-3, which mediates p50 homodimer formation ( Naumann  et al., 1993;  Watanabe  et al., 1997), or by phosphorylation of p105, which triggers degradation of this protein ( MacKichan  et al., 1996;  Belich  et al., 1999;  Heissmeyer  et al., 1999).	transcription
57140	1	335357	7	NULL	NULL	0	NULL	BCL-3			influence		may			p50		intracellular ratio of			NULL		NULL	NULL	NULL	NULL	gw60_embo_19_17_4712_s_243	10970863	However, after the primary cotranslational event, the intracellular ratio of p50 and p105 may also be influenced either by cellular factors such as BCL-3, which mediates p50 homodimer formation ( Naumann  et al., 1993;  Watanabe  et al., 1997), or by phosphorylation of p105, which triggers degradation of this protein ( MacKichan  et al., 1996;  Belich  et al., 1999;  Heissmeyer  et al., 1999).	transcription
57141	2	335357	7	NULL	NULL	0	NULL	BCL-3			influence		may			p105		intracellular ratio of			NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_243	10970863	However, after the primary cotranslational event, the intracellular ratio of p50 and p105 may also be influenced either by cellular factors such as BCL-3, which mediates p50 homodimer formation ( Naumann  et al., 1993;  Watanabe  et al., 1997), or by phosphorylation of p105, which triggers degradation of this protein ( MacKichan  et al., 1996;  Belich  et al., 1999;  Heissmeyer  et al., 1999).	transcription
57142	3	335357	7	NULL	NULL	0	NULL	statement 1			occur simulataneous with					statement 2					NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_243	10970863	However, after the primary cotranslational event, the intracellular ratio of p50 and p105 may also be influenced either by cellular factors such as BCL-3, which mediates p50 homodimer formation ( Naumann  et al., 1993;  Watanabe  et al., 1997), or by phosphorylation of p105, which triggers degradation of this protein ( MacKichan  et al., 1996;  Belich  et al., 1999;  Heissmeyer  et al., 1999).	transcription
57143	4	335357	7	NULL	NULL	0	NULL	statement 3			occur after					primary cotranslational event					NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_243	10970863	However, after the primary cotranslational event, the intracellular ratio of p50 and p105 may also be influenced either by cellular factors such as BCL-3, which mediates p50 homodimer formation ( Naumann  et al., 1993;  Watanabe  et al., 1997), or by phosphorylation of p105, which triggers degradation of this protein ( MacKichan  et al., 1996;  Belich  et al., 1999;  Heissmeyer  et al., 1999).	transcription
57144	5	335357	7	NULL	NULL	0	NULL	BCL-3			mediates					p50 homodimer		formation of			NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_243	10970863	However, after the primary cotranslational event, the intracellular ratio of p50 and p105 may also be influenced either by cellular factors such as BCL-3, which mediates p50 homodimer formation ( Naumann  et al., 1993;  Watanabe  et al., 1997), or by phosphorylation of p105, which triggers degradation of this protein ( MacKichan  et al., 1996;  Belich  et al., 1999;  Heissmeyer  et al., 1999).	transcription
57145	6	335357	7	NULL	NULL	0	NULL	p105		phosphorylation of 	triggers					BCL-3		degradation of			NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_243	10970863	However, after the primary cotranslational event, the intracellular ratio of p50 and p105 may also be influenced either by cellular factors such as BCL-3, which mediates p50 homodimer formation ( Naumann  et al., 1993;  Watanabe  et al., 1997), or by phosphorylation of p105, which triggers degradation of this protein ( MacKichan  et al., 1996;  Belich  et al., 1999;  Heissmeyer  et al., 1999).	transcription
57146	7	335357	7	NULL	NULL	0	NULL	statement 6			influence		may			statement 3					NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_243	10970863	However, after the primary cotranslational event, the intracellular ratio of p50 and p105 may also be influenced either by cellular factors such as BCL-3, which mediates p50 homodimer formation ( Naumann  et al., 1993;  Watanabe  et al., 1997), or by phosphorylation of p105, which triggers degradation of this protein ( MacKichan  et al., 1996;  Belich  et al., 1999;  Heissmeyer  et al., 1999).	transcription
57147	8	335357	7	NULL	NULL	0	NULL	statement 3			is an alternative to					statement 7					NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_243	10970863	However, after the primary cotranslational event, the intracellular ratio of p50 and p105 may also be influenced either by cellular factors such as BCL-3, which mediates p50 homodimer formation ( Naumann  et al., 1993;  Watanabe  et al., 1997), or by phosphorylation of p105, which triggers degradation of this protein ( MacKichan  et al., 1996;  Belich  et al., 1999;  Heissmeyer  et al., 1999).	transcription
57148	9	335357	7	NULL	NULL	0	NULL	BCL-3			is a type of					cellular factor					NULL		0	NULL	NULL	NULL	gw60_embo_19_17_4712_s_243	10970863	However, after the primary cotranslational event, the intracellular ratio of p50 and p105 may also be influenced either by cellular factors such as BCL-3, which mediates p50 homodimer formation ( Naumann  et al., 1993;  Watanabe  et al., 1997), or by phosphorylation of p105, which triggers degradation of this protein ( MacKichan  et al., 1996;  Belich  et al., 1999;  Heissmeyer  et al., 1999).	transcription
78284	1	335358	6	NULL	NULL	0	NULL	p105 	GP		resides in					cytosol	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
78285	2	335358	6	NULL	NULL	0	NULL	p105	GP		contains								ankyrin motif-rich carboxyl-terminal domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
78475	3	335358	6	NULL	NULL	0	NULL		AminoAcid		degrades into			IkappaBalpha-related domain		NF-kappaB	GP		p50 DNA binding subunit 		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
78476	4	335358	6	NULL	NULL	0	NULL	RelA	GP		sequestered into					cytoplasm	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
78477	5	335358	6	NULL	NULL	0	NULL	p105	GP		sequesters					RelA					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
78478	6	335358	6	NULL	NULL	0	NULL	IkappaBalpha	GP		sequesters					RelA	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
57149	1	335358	7	NULL	NULL	0	NULL	p105			resides in		exclusively			cytosolic compartment					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
57150	2	335358	7	NULL	NULL	0	NULL	statement 1			independent of					cellular activation		status of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
57151	3	335358	7	NULL	NULL	0	NULL	p105			contains								ankyrin motif-rich carboxyl-terminal domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
57152	4	335358	7	NULL	NULL	0	NULL	statement 3			inhibit					p105		 nuclear expression of	amino-terminal half		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
57153	5	335358	7	NULL	NULL	0	NULL	statement 3			inhibit					p105		DNA binding activity of	amino-terminal half		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
57154	6	335358	7	NULL	NULL	0	NULL	 IkappaBalpha-related domain			constitutively					degraded					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
57155	7	335358	7	NULL	NULL	0	NULL	statement 6			generate					NF-kappaB			p50 DNA binding subunit of		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
57156	8	335358	7	NULL	NULL	0	NULL	p105			sequesters		physically			RelA 					NULL	cytoplasmic compartment	0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
57157	9	335358	7	NULL	NULL	0	NULL	IkappaBalpha			sequesters		physically			RelA 					NULL	cytoplasmic compartment	0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
57158	10	335358	7	NULL	NULL	0	NULL	statement 8			is similar to					statement 9					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
57159	11	335358	7	NULL	NULL	0	NULL	inducible genes			encode					p105 protein					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
57160	12	335358	7	NULL	NULL	0	NULL	inducible genes			encode					IkappaBalpha					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
57161	13	335358	7	NULL	NULL	0	NULL	statement 11			contain							functional	NF-kappaB binding sites		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
57162	14	335358	7	NULL	NULL	0	NULL	statement 12			contain							functional	NF-kappaB binding sites		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_1_9_s_18	7814425	(i) p105 resides exclusively in the cytosolic compartment  independent of the status of cellular  activation( 8 ,  9 ) ; (ii) p105 contains an ankyrin  motif-rich carboxyl-terminal domain that inhibits the nuclear  expression and DNA binding activity of its amino-terminal  half( 8 ,  9 ,  10 ,  11 ,  12 ) ;  this IkappaBalpha-related domain is constitutively degraded in order to  generate the p50 DNA binding subunit of NF-kappaB( 13 ) ; (iii)  p105, like IkappaBalpha, physically sequesters RelA in the cytoplasmic  compartment ( 14 ) ; and (iv) the inducible genes encoding p105  and IkappaBalpha  both contain functional NF-kappaB binding  sites( 15 ,  16 ,  17 ,  18 ) .	transcription
78479	1	335359	6	NULL	NULL	0	NULL	TSA	Chemical		represses					p105 precursor gene	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1693_3_167_s_172	15363630	Since our data show that TSA represses the gene for the p105 precursor of p50 NF- B and activates the STAT1 gene, it may be that the up-regulation of TNF and its receptor  by TSA may represent additional factors that contribute to the apoptotic cell death  induced by TSA.	transcription
78480	2	335359	6	NULL	NULL	0	NULL	TSA	Chemical		activates					STAT1 gene	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1693_3_167_s_172	15363630	Since our data show that TSA represses the gene for the p105 precursor of p50 NF- B and activates the STAT1 gene, it may be that the up-regulation of TNF and its receptor  by TSA may represent additional factors that contribute to the apoptotic cell death  induced by TSA.	transcription
78481	3	335359	6	NULL	NULL	0	NULL	TNF	GP	upregulation of	contribute to					apoptotic cell death	Process				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1693_3_167_s_172	15363630	Since our data show that TSA represses the gene for the p105 precursor of p50 NF- B and activates the STAT1 gene, it may be that the up-regulation of TNF and its receptor  by TSA may represent additional factors that contribute to the apoptotic cell death  induced by TSA.	transcription
78482	4	335359	6	NULL	NULL	0	NULL	TSA	Chemical		induces					apoptotic cell death	Process				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1693_3_167_s_172	15363630	Since our data show that TSA represses the gene for the p105 precursor of p50 NF- B and activates the STAT1 gene, it may be that the up-regulation of TNF and its receptor  by TSA may represent additional factors that contribute to the apoptotic cell death  induced by TSA.	transcription
57163	1	335359	7	NULL	NULL	0	NULL	p105			precursor of					NF-B			p50		NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1693_3_167_s_172	15363630	Since our data show that TSA represses the gene for the p105 precursor of p50 NF- B and activates the STAT1 gene, it may be that the up-regulation of TNF and its receptor  by TSA may represent additional factors that contribute to the apoptotic cell death  induced by TSA.	transcription
57164	2	335359	7	NULL	NULL	0	NULL	TSA			represses					statement 1					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1693_3_167_s_172	15363630	Since our data show that TSA represses the gene for the p105 precursor of p50 NF- B and activates the STAT1 gene, it may be that the up-regulation of TNF and its receptor  by TSA may represent additional factors that contribute to the apoptotic cell death  induced by TSA.	transcription
57165	3	335359	7	NULL	NULL	0	NULL	TSA			activates					STAT1 gene					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1693_3_167_s_172	15363630	Since our data show that TSA represses the gene for the p105 precursor of p50 NF- B and activates the STAT1 gene, it may be that the up-regulation of TNF and its receptor  by TSA may represent additional factors that contribute to the apoptotic cell death  induced by TSA.	transcription
57166	4	335359	7	NULL	NULL	0	NULL	TSA			up-regulate					TNF					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1693_3_167_s_172	15363630	Since our data show that TSA represses the gene for the p105 precursor of p50 NF- B and activates the STAT1 gene, it may be that the up-regulation of TNF and its receptor  by TSA may represent additional factors that contribute to the apoptotic cell death  induced by TSA.	transcription
57167	5	335359	7	NULL	NULL	0	NULL	TSA			up-regulate					TNF receptor					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1693_3_167_s_172	15363630	Since our data show that TSA represses the gene for the p105 precursor of p50 NF- B and activates the STAT1 gene, it may be that the up-regulation of TNF and its receptor  by TSA may represent additional factors that contribute to the apoptotic cell death  induced by TSA.	transcription
57168	6	335359	7	NULL	NULL	0	NULL	TSA			induce					apoptotic cell death					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1693_3_167_s_172	15363630	Since our data show that TSA represses the gene for the p105 precursor of p50 NF- B and activates the STAT1 gene, it may be that the up-regulation of TNF and its receptor  by TSA may represent additional factors that contribute to the apoptotic cell death  induced by TSA.	transcription
57169	7	335359	7	NULL	NULL	0	NULL	statement 4			contribute to		may			statement 6					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1693_3_167_s_172	15363630	Since our data show that TSA represses the gene for the p105 precursor of p50 NF- B and activates the STAT1 gene, it may be that the up-regulation of TNF and its receptor  by TSA may represent additional factors that contribute to the apoptotic cell death  induced by TSA.	transcription
57170	8	335359	7	NULL	NULL	0	NULL	statement 5			contribute to		may			statement 6					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1693_3_167_s_172	15363630	Since our data show that TSA represses the gene for the p105 precursor of p50 NF- B and activates the STAT1 gene, it may be that the up-regulation of TNF and its receptor  by TSA may represent additional factors that contribute to the apoptotic cell death  induced by TSA.	transcription
78483	1	335360	6	NULL	NULL	0	NULL	NF-B1	GP		play a role in					immune response	Process	regulation of 			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78484	2	335360	6	NULL	NULL	NULL	NULL	NF-B1	GP		play a role in					inflammatory response	Process	regulation of 			NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78485	3	335360	6	NULL	NULL	0	NULL	NF-B1	GP		is					p50/ p105	GP				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78486	4	335360	6	NULL	NULL	0	NULL	NF-B2	GP		play a role in					inflammatory response	Process	regulation of 			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78487	5	335360	6	NULL	NULL	0	NULL	NF-B2	GP		play a role in					immune response	Process	regulation of 			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78488	6	335360	6	NULL	NULL	0	NULL	NF-B2	GP		is					p52/p100	GP				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78489	7	335360	6	NULL	NULL	0	NULL	RelA	GP		play a role in					immune response	Process	regulation of 			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78490	8	335360	6	NULL	NULL	0	NULL	RelA	GP		play a role in					inflammatory response	Process	regulation of 			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78491	9	335360	6	NULL	NULL	0	NULL	RelA	GP		is					p65	GP				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78492	10	335360	6	NULL	NULL	0	NULL	c-Rel	GP		play a role in					immune response	Process	regulation of 			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78493	11	335360	6	NULL	NULL	0	NULL	c-Rel	GP		play a role in					inflammatory response	Process	regulation of 			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78494	12	335360	6	NULL	NULL	0	NULL	RelB	GP		play a role in					immune response	Process	regulation of 			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78495	13	335360	6	NULL	NULL	NULL	NULL	RelB	GP		play a role in					inflammatory response	Process	regulation of 			NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78496	14	335360	6	NULL	NULL	0	NULL	NF-B1	GP		play a role in					cell proliferation	Process				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78497	15	335360	6	NULL	NULL	0	NULL	NF-B1	GP		play a role in					cell death	Process				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78498	16	335360	6	NULL	NULL	0	NULL	NF-B2	GP		play a role in					cell death	Process				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78499	17	335360	6	NULL	NULL	0	NULL	NF-B2	GP		play a role in					cell proliferation	Process				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78500	18	335360	6	NULL	NULL	0	NULL	RelA	GP		play a role in					cell death	Process				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78501	19	335360	6	NULL	NULL	0	NULL	RelA	GP		play a role in					cell proliferation	Process				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78502	20	335360	6	NULL	NULL	0	NULL	c-Rel	GP		play a role in					cell death	Process				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
78503	21	335360	6	NULL	NULL	0	NULL	RelB	GP		play a role in					cell proliferation	Process				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57171	1	335360	7	NULL	NULL	0	NULL	NF- B transcription factors		mammalian	include					NF- B1					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57172	2	335360	7	NULL	NULL	0	NULL	NF- B transcription factors		mammalian	include					NF- B2					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57173	3	335360	7	NULL	NULL	0	NULL	NF- B transcription factors		mammalian	include					 RelA					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57174	4	335360	7	NULL	NULL	0	NULL	NF- B transcription factors		mammalian	include					c-Rel					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57175	5	335360	7	NULL	NULL	0	NULL	NF- B transcription factors		mammalian	include					RelB					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57176	6	335360	7	NULL	NULL	0	NULL	NF- B1			play important role in					immune response		regulation of			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57177	7	335360	7	NULL	NULL	0	NULL	NF- B2			play important role in					immune response		regulation of			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57178	8	335360	7	NULL	NULL	0	NULL	 RelA			play important role in					immune response		regulation of			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57179	9	335360	7	NULL	NULL	0	NULL	c-Rel			play important role in					immune response		regulation of			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57180	10	335360	7	NULL	NULL	0	NULL	RelB			play important role in					immune response		regulation of			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57181	11	335360	7	NULL	NULL	0	NULL	NF- B1			play important role in					inflammatory response		regulation of			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57182	12	335360	7	NULL	NULL	0	NULL	NF- B2			play important role in					inflammatory response		regulation of			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57183	13	335360	7	NULL	NULL	0	NULL	RelA			play important role in					inflammatory response		regulation of			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57184	14	335360	7	NULL	NULL	0	NULL	 c-Rel			play important role in					inflammatory response		regulation of			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57185	15	335360	7	NULL	NULL	0	NULL	RelB			play important role in					inflammatory response		regulation of			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57186	16	335360	7	NULL	NULL	0	NULL	NF- B1			play important role in					cellular proliferation					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57187	17	335360	7	NULL	NULL	0	NULL	NF- B2			play important role in					cellular proliferation					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57188	18	335360	7	NULL	NULL	0	NULL	RelA			play important role in					cellular proliferation					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57189	19	335360	7	NULL	NULL	0	NULL	c-Rel			play important role in					cellular proliferation					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57190	20	335360	7	NULL	NULL	0	NULL	RelB 			play important role in					cellular proliferation					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57191	21	335360	7	NULL	NULL	0	NULL	NF- B1			play important role in					cell death					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57192	22	335360	7	NULL	NULL	0	NULL	NF- B2			play important role in					cell death					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57193	23	335360	7	NULL	NULL	0	NULL	RelA			play important role in					cell death					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57194	24	335360	7	NULL	NULL	0	NULL	c-Rel			play important role in					cell death					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57195	25	335360	7	NULL	NULL	0	NULL	RelB			play important role in					cell death					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57196	26	335360	7	NULL	NULL	0	NULL	NF- B1			consist of					p50/ p105					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57197	27	335360	7	NULL	NULL	0	NULL	NF- B2			consist of					p52/p100					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57198	28	335360	7	NULL	NULL	0	NULL	RelA			consist of					p65					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_17_0_149_s_282	10358756	The mammalian NF- B transcription factors, which include NF- B1 (p50/ p105), NF- B2  (p52/p100), RelA (p65), c-Rel, and RelB, play important roles in the regulation of  immune and inflammatory responses, cellular proliferation, and cell death (reviewed  in  109,  110,  111).	transcription
57199	1	335361	7	NULL	NULL	0	NULL	NF-kappaBel family of TFs			include					RELA					NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3154_s_128	15933209	Known NF-kappaB target genes   he NF-kappaBel family of TFs, which includes RELA (p65), NF-kappaB1 (p50, p105), NF-kappaB2 (p52, p100), c-REL and RELB, plays a central role in regulating the immune response ( ).	transcription
57200	2	335361	7	NULL	NULL	0	NULL	 NF-kappaBel family of TFs			include					NF-kappaB1					NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3154_s_128	15933209	Known NF-kappaB target genes   he NF-kappaBel family of TFs, which includes RELA (p65), NF-kappaB1 (p50, p105), NF-kappaB2 (p52, p100), c-REL and RELB, plays a central role in regulating the immune response ( ).	transcription
57201	3	335361	7	NULL	NULL	0	NULL	NF-kappaBel family of TFs			include					NF-kappaB2					NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3154_s_128	15933209	Known NF-kappaB target genes   he NF-kappaBel family of TFs, which includes RELA (p65), NF-kappaB1 (p50, p105), NF-kappaB2 (p52, p100), c-REL and RELB, plays a central role in regulating the immune response ( ).	transcription
57202	4	335361	7	NULL	NULL	0	NULL	NF-kappaBel family of TFs			include					c-REL					NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3154_s_128	15933209	Known NF-kappaB target genes   he NF-kappaBel family of TFs, which includes RELA (p65), NF-kappaB1 (p50, p105), NF-kappaB2 (p52, p100), c-REL and RELB, plays a central role in regulating the immune response ( ).	transcription
57203	5	335361	7	NULL	NULL	0	NULL	NF-kappaBel family of TFs			include					RELB					NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3154_s_128	15933209	Known NF-kappaB target genes   he NF-kappaBel family of TFs, which includes RELA (p65), NF-kappaB1 (p50, p105), NF-kappaB2 (p52, p100), c-REL and RELB, plays a central role in regulating the immune response ( ).	transcription
57204	6	335361	7	NULL	NULL	0	NULL	RELA			plays a central role in					immune response		regulating			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3154_s_128	15933209	Known NF-kappaB target genes   he NF-kappaBel family of TFs, which includes RELA (p65), NF-kappaB1 (p50, p105), NF-kappaB2 (p52, p100), c-REL and RELB, plays a central role in regulating the immune response ( ).	transcription
57205	7	335361	7	NULL	NULL	0	NULL	NF-kappaB1			plays a central role in					immune response		regulating			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3154_s_128	15933209	Known NF-kappaB target genes   he NF-kappaBel family of TFs, which includes RELA (p65), NF-kappaB1 (p50, p105), NF-kappaB2 (p52, p100), c-REL and RELB, plays a central role in regulating the immune response ( ).	transcription
57206	8	335361	7	NULL	NULL	0	NULL	NF-kappaB2			plays a central role in					immune response		regulating			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3154_s_128	15933209	Known NF-kappaB target genes   he NF-kappaBel family of TFs, which includes RELA (p65), NF-kappaB1 (p50, p105), NF-kappaB2 (p52, p100), c-REL and RELB, plays a central role in regulating the immune response ( ).	transcription
57207	9	335361	7	NULL	NULL	0	NULL	c-REL			plays a central role in					immune response		regulating			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3154_s_128	15933209	Known NF-kappaB target genes   he NF-kappaBel family of TFs, which includes RELA (p65), NF-kappaB1 (p50, p105), NF-kappaB2 (p52, p100), c-REL and RELB, plays a central role in regulating the immune response ( ).	transcription
57208	10	335361	7	NULL	NULL	0	NULL	RELB			plays a central role in					immune response		regulating			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3154_s_128	15933209	Known NF-kappaB target genes   he NF-kappaBel family of TFs, which includes RELA (p65), NF-kappaB1 (p50, p105), NF-kappaB2 (p52, p100), c-REL and RELB, plays a central role in regulating the immune response ( ).	transcription
57209	11	335361	7	NULL	NULL	0	NULL	RelA 			consist of					p65					NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3154_s_128	15933209	Known NF-kappaB target genes   he NF-kappaBel family of TFs, which includes RELA (p65), NF-kappaB1 (p50, p105), NF-kappaB2 (p52, p100), c-REL and RELB, plays a central role in regulating the immune response ( ).	transcription
57210	12	335361	7	NULL	NULL	0	NULL	NF-kappaB1			consist of					p50					NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3154_s_128	15933209	Known NF-kappaB target genes   he NF-kappaBel family of TFs, which includes RELA (p65), NF-kappaB1 (p50, p105), NF-kappaB2 (p52, p100), c-REL and RELB, plays a central role in regulating the immune response ( ).	transcription
57211	13	335361	7	NULL	NULL	0	NULL	NF-kappaB1			consist of					p105					NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3154_s_128	15933209	Known NF-kappaB target genes   he NF-kappaBel family of TFs, which includes RELA (p65), NF-kappaB1 (p50, p105), NF-kappaB2 (p52, p100), c-REL and RELB, plays a central role in regulating the immune response ( ).	transcription
57212	14	335361	7	NULL	NULL	0	NULL	statement 12			occur simulataneous with					statement 13					NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3154_s_128	15933209	Known NF-kappaB target genes   he NF-kappaBel family of TFs, which includes RELA (p65), NF-kappaB1 (p50, p105), NF-kappaB2 (p52, p100), c-REL and RELB, plays a central role in regulating the immune response ( ).	transcription
57213	15	335361	7	NULL	NULL	0	NULL	NF-kappaB2			consist of					p52					NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3154_s_128	15933209	Known NF-kappaB target genes   he NF-kappaBel family of TFs, which includes RELA (p65), NF-kappaB1 (p50, p105), NF-kappaB2 (p52, p100), c-REL and RELB, plays a central role in regulating the immune response ( ).	transcription
57214	16	335361	7	NULL	NULL	0	NULL	NF-kappaB2			consist of					p100					NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3154_s_128	15933209	Known NF-kappaB target genes   he NF-kappaBel family of TFs, which includes RELA (p65), NF-kappaB1 (p50, p105), NF-kappaB2 (p52, p100), c-REL and RELB, plays a central role in regulating the immune response ( ).	transcription
57215	17	335361	7	NULL	NULL	0	NULL	statement 15			occur simulataneous with					statement 16					NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_10_3154_s_128	15933209	Known NF-kappaB target genes   he NF-kappaBel family of TFs, which includes RELA (p65), NF-kappaB1 (p50, p105), NF-kappaB2 (p52, p100), c-REL and RELB, plays a central role in regulating the immune response ( ).	transcription
78683	1	335364	6	NULL	NULL	0	NULL	TLR	GP		induces					IL-10	GP	expression of			NULL	BMDM	0	NULL	NULL	NULL	gw70_pnas_103_9_3274_s_168	16484370	Finally, the finding that p50  NF-kappaB1 and its precursor, p105 NF-kappaB1, contribute to  TLR-induced IL-10 expression in BMDMs in a direct and indirect  ERK-dependent manner, respectively, highlights the utility of the  model described here to study the joint contribution of the  NF-kappaB and ERK pathways in controlling TLR-mediated gene  expression.	transcription
78684	2	335364	6	NULL	NULL	0	NULL	p50 NF-kappaB1	GP		contribute to					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3274_s_168	16484370	Finally, the finding that p50  NF-kappaB1 and its precursor, p105 NF-kappaB1, contribute to  TLR-induced IL-10 expression in BMDMs in a direct and indirect  ERK-dependent manner, respectively, highlights the utility of the  model described here to study the joint contribution of the  NF-kappaB and ERK pathways in controlling TLR-mediated gene  expression.	transcription
78685	3	335364	6	NULL	NULL	0	NULL	p105 NF-kappaB1	GP		contribute to					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3274_s_168	16484370	Finally, the finding that p50  NF-kappaB1 and its precursor, p105 NF-kappaB1, contribute to  TLR-induced IL-10 expression in BMDMs in a direct and indirect  ERK-dependent manner, respectively, highlights the utility of the  model described here to study the joint contribution of the  NF-kappaB and ERK pathways in controlling TLR-mediated gene  expression.	transcription
78686	4	335364	6	NULL	NULL	0	NULL	p105 NF-kappaB1	GP		is 					p50 NF-kappaB1 precursor	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3274_s_168	16484370	Finally, the finding that p50  NF-kappaB1 and its precursor, p105 NF-kappaB1, contribute to  TLR-induced IL-10 expression in BMDMs in a direct and indirect  ERK-dependent manner, respectively, highlights the utility of the  model described here to study the joint contribution of the  NF-kappaB and ERK pathways in controlling TLR-mediated gene  expression.	transcription
57216	1	335364	7	NULL	NULL	0	NULL	TLR			induce					IL-10		expression of			NULL	BMDMs	NULL	NULL	NULL	NULL	gw70_pnas_103_9_3274_s_168	16484370	Finally, the finding that p50  NF-kappaB1 and its precursor, p105 NF-kappaB1, contribute to  TLR-induced IL-10 expression in BMDMs in a direct and indirect  ERK-dependent manner, respectively, highlights the utility of the  model described here to study the joint contribution of the  NF-kappaB and ERK pathways in controlling TLR-mediated gene  expression.	transcription
57217	2	335364	7	NULL	NULL	0	NULL	p50 NF-kappaB1			contribute to					statement 1					NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3274_s_168	16484370	Finally, the finding that p50  NF-kappaB1 and its precursor, p105 NF-kappaB1, contribute to  TLR-induced IL-10 expression in BMDMs in a direct and indirect  ERK-dependent manner, respectively, highlights the utility of the  model described here to study the joint contribution of the  NF-kappaB and ERK pathways in controlling TLR-mediated gene  expression.	transcription
57218	3	335364	7	NULL	NULL	0	NULL	statement 2			occur through		directly			ERK-dependent manner					NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3274_s_168	16484370	Finally, the finding that p50  NF-kappaB1 and its precursor, p105 NF-kappaB1, contribute to  TLR-induced IL-10 expression in BMDMs in a direct and indirect  ERK-dependent manner, respectively, highlights the utility of the  model described here to study the joint contribution of the  NF-kappaB and ERK pathways in controlling TLR-mediated gene  expression.	transcription
57219	4	335364	7	NULL	NULL	0	NULL	p105 NF-kappaB1			contribute to					statement 1					NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3274_s_168	16484370	Finally, the finding that p50  NF-kappaB1 and its precursor, p105 NF-kappaB1, contribute to  TLR-induced IL-10 expression in BMDMs in a direct and indirect  ERK-dependent manner, respectively, highlights the utility of the  model described here to study the joint contribution of the  NF-kappaB and ERK pathways in controlling TLR-mediated gene  expression.	transcription
57220	5	335364	7	NULL	NULL	0	NULL	statement 4			occur through		indirectly			ERK-dependent manner					NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3274_s_168	16484370	Finally, the finding that p50  NF-kappaB1 and its precursor, p105 NF-kappaB1, contribute to  TLR-induced IL-10 expression in BMDMs in a direct and indirect  ERK-dependent manner, respectively, highlights the utility of the  model described here to study the joint contribution of the  NF-kappaB and ERK pathways in controlling TLR-mediated gene  expression.	transcription
57221	6	335364	7	NULL	NULL	0	NULL	TLR			mediates					gene expression					NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3274_s_168	16484370	Finally, the finding that p50  NF-kappaB1 and its precursor, p105 NF-kappaB1, contribute to  TLR-induced IL-10 expression in BMDMs in a direct and indirect  ERK-dependent manner, respectively, highlights the utility of the  model described here to study the joint contribution of the  NF-kappaB and ERK pathways in controlling TLR-mediated gene  expression.	transcription
57222	7	335364	7	NULL	NULL	0	NULL	 NF-kappaB 			controls					statement 6					NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3274_s_168	16484370	Finally, the finding that p50  NF-kappaB1 and its precursor, p105 NF-kappaB1, contribute to  TLR-induced IL-10 expression in BMDMs in a direct and indirect  ERK-dependent manner, respectively, highlights the utility of the  model described here to study the joint contribution of the  NF-kappaB and ERK pathways in controlling TLR-mediated gene  expression.	transcription
57223	8	335364	7	NULL	NULL	0	NULL	ERK pathways			controls					statement 6					NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3274_s_168	16484370	Finally, the finding that p50  NF-kappaB1 and its precursor, p105 NF-kappaB1, contribute to  TLR-induced IL-10 expression in BMDMs in a direct and indirect  ERK-dependent manner, respectively, highlights the utility of the  model described here to study the joint contribution of the  NF-kappaB and ERK pathways in controlling TLR-mediated gene  expression.	transcription
57224	9	335364	7	NULL	NULL	0	NULL	p105 NF-kappaB1			is a precursor of					p50 NF-kappaB1					NULL		0	NULL	NULL	NULL	gw70_pnas_103_9_3274_s_168	16484370	Finally, the finding that p50  NF-kappaB1 and its precursor, p105 NF-kappaB1, contribute to  TLR-induced IL-10 expression in BMDMs in a direct and indirect  ERK-dependent manner, respectively, highlights the utility of the  model described here to study the joint contribution of the  NF-kappaB and ERK pathways in controlling TLR-mediated gene  expression.	transcription
78687	1	335365	6	NULL	NULL	0	NULL	NF-kappaB subunit	GP		retained in					cytosol	CellComponent				NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_265	10469655	The precursor molecules p105 and p100 retain NF-kappaB subunits in the cytosol (Rice  et al., 1992  ; Mercurio  et al., 1993  ; Naumann  et al., 1993a  ,b) and are critical for the generation of p50 and p52 homodimers, which are bound specifically by the predominantly nuclear IkappaB homologue Bcl-3.	transcription
78688	2	335365	6	NULL	NULL	0	NULL	p105	GP		participate in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_265	10469655	The precursor molecules p105 and p100 retain NF-kappaB subunits in the cytosol (Rice  et al., 1992  ; Mercurio  et al., 1993  ; Naumann  et al., 1993a  ,b) and are critical for the generation of p50 and p52 homodimers, which are bound specifically by the predominantly nuclear IkappaB homologue Bcl-3.	transcription
78689	3	335365	6	NULL	NULL	0	NULL	p100	GP		participate in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_265	10469655	The precursor molecules p105 and p100 retain NF-kappaB subunits in the cytosol (Rice  et al., 1992  ; Mercurio  et al., 1993  ; Naumann  et al., 1993a  ,b) and are critical for the generation of p50 and p52 homodimers, which are bound specifically by the predominantly nuclear IkappaB homologue Bcl-3.	transcription
78690	4	335365	6	NULL	NULL	0	NULL	statement 1	Process		is critical for					p50 homodimer	GP	generation of 			NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_265	10469655	The precursor molecules p105 and p100 retain NF-kappaB subunits in the cytosol (Rice  et al., 1992  ; Mercurio  et al., 1993  ; Naumann  et al., 1993a  ,b) and are critical for the generation of p50 and p52 homodimers, which are bound specifically by the predominantly nuclear IkappaB homologue Bcl-3.	transcription
78691	5	335365	6	NULL	NULL	0	NULL	statement 1	Process		is critical for					p52 homodimer	GP	generation of 			NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_265	10469655	The precursor molecules p105 and p100 retain NF-kappaB subunits in the cytosol (Rice  et al., 1992  ; Mercurio  et al., 1993  ; Naumann  et al., 1993a  ,b) and are critical for the generation of p50 and p52 homodimers, which are bound specifically by the predominantly nuclear IkappaB homologue Bcl-3.	transcription
57225	1	335365	7	NULL	NULL	0	NULL	p105			retain					NF-kappaB subunits					NULL	cytosol	0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_265	10469655	The precursor molecules p105 and p100 retain NF-kappaB subunits in the cytosol (Rice  et al., 1992  ; Mercurio  et al., 1993  ; Naumann  et al., 1993a  ,b) and are critical for the generation of p50 and p52 homodimers, which are bound specifically by the predominantly nuclear IkappaB homologue Bcl-3.	transcription
57226	2	335365	7	NULL	NULL	0	NULL	p100			retain					NF-kappaB subunits					NULL	cytosol	0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_265	10469655	The precursor molecules p105 and p100 retain NF-kappaB subunits in the cytosol (Rice  et al., 1992  ; Mercurio  et al., 1993  ; Naumann  et al., 1993a  ,b) and are critical for the generation of p50 and p52 homodimers, which are bound specifically by the predominantly nuclear IkappaB homologue Bcl-3.	transcription
57227	3	335365	7	NULL	NULL	0	NULL	p105			is critical for					p50 homodimer		generation of			NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_265	10469655	The precursor molecules p105 and p100 retain NF-kappaB subunits in the cytosol (Rice  et al., 1992  ; Mercurio  et al., 1993  ; Naumann  et al., 1993a  ,b) and are critical for the generation of p50 and p52 homodimers, which are bound specifically by the predominantly nuclear IkappaB homologue Bcl-3.	transcription
57228	4	335365	7	NULL	NULL	0	NULL	p100 			is critical for					p50 homodimer		generation of			NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_265	10469655	The precursor molecules p105 and p100 retain NF-kappaB subunits in the cytosol (Rice  et al., 1992  ; Mercurio  et al., 1993  ; Naumann  et al., 1993a  ,b) and are critical for the generation of p50 and p52 homodimers, which are bound specifically by the predominantly nuclear IkappaB homologue Bcl-3.	transcription
57229	5	335365	7	NULL	NULL	0	NULL	p105			is critical for					p52 homodimer		generation of			NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_265	10469655	The precursor molecules p105 and p100 retain NF-kappaB subunits in the cytosol (Rice  et al., 1992  ; Mercurio  et al., 1993  ; Naumann  et al., 1993a  ,b) and are critical for the generation of p50 and p52 homodimers, which are bound specifically by the predominantly nuclear IkappaB homologue Bcl-3.	transcription
57230	6	335365	7	NULL	NULL	0	NULL	p100			is critical for					p52 homodimer		generation of			NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_265	10469655	The precursor molecules p105 and p100 retain NF-kappaB subunits in the cytosol (Rice  et al., 1992  ; Mercurio  et al., 1993  ; Naumann  et al., 1993a  ,b) and are critical for the generation of p50 and p52 homodimers, which are bound specifically by the predominantly nuclear IkappaB homologue Bcl-3.	transcription
57231	7	335365	7	NULL	NULL	0	NULL	p50 homodimer			bind		specifically			Bcl-3					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_265	10469655	The precursor molecules p105 and p100 retain NF-kappaB subunits in the cytosol (Rice  et al., 1992  ; Mercurio  et al., 1993  ; Naumann  et al., 1993a  ,b) and are critical for the generation of p50 and p52 homodimers, which are bound specifically by the predominantly nuclear IkappaB homologue Bcl-3.	transcription
57232	8	335365	7	NULL	NULL	0	NULL	p52 homodimer			bind		specifically			Bcl-3					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_265	10469655	The precursor molecules p105 and p100 retain NF-kappaB subunits in the cytosol (Rice  et al., 1992  ; Mercurio  et al., 1993  ; Naumann  et al., 1993a  ,b) and are critical for the generation of p50 and p52 homodimers, which are bound specifically by the predominantly nuclear IkappaB homologue Bcl-3.	transcription
57233	9	335365	7	NULL	NULL	0	NULL	Bcl-3			is a type of					nuclear IkappaB homologue					NULL		NULL	NULL	NULL	NULL	gw60_embo_18_17_4766_s_265	10469655	The precursor molecules p105 and p100 retain NF-kappaB subunits in the cytosol (Rice  et al., 1992  ; Mercurio  et al., 1993  ; Naumann  et al., 1993a  ,b) and are critical for the generation of p50 and p52 homodimers, which are bound specifically by the predominantly nuclear IkappaB homologue Bcl-3.	transcription
57234	10	335365	7	NULL	NULL	0	NULL	p105			is a type of					precursor molecule					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_265	10469655	The precursor molecules p105 and p100 retain NF-kappaB subunits in the cytosol (Rice  et al., 1992  ; Mercurio  et al., 1993  ; Naumann  et al., 1993a  ,b) and are critical for the generation of p50 and p52 homodimers, which are bound specifically by the predominantly nuclear IkappaB homologue Bcl-3.	transcription
57235	11	335365	7	NULL	NULL	0	NULL	p100			is a type of					precursor molecule					NULL		0	NULL	NULL	NULL	gw60_embo_18_17_4766_s_265	10469655	The precursor molecules p105 and p100 retain NF-kappaB subunits in the cytosol (Rice  et al., 1992  ; Mercurio  et al., 1993  ; Naumann  et al., 1993a  ,b) and are critical for the generation of p50 and p52 homodimers, which are bound specifically by the predominantly nuclear IkappaB homologue Bcl-3.	transcription
78692	1	335366	6	NULL	NULL	0	NULL	1,25-(OH)2-D3	Chemical		reduce					p50	GP	levels of 			NULL	human lymphocytes	0	NULL	NULL	NULL	gw60_febslett_436_3_329_s_128	9801142	Yu et al. have shown that 1,25-(OH)2-D3 can reduce levels of p50 and its precursor p105 in human lymphocytes and they observed reduced binding of PMA-induced nuclear factors to the NF- B binding site of the IL-6 promoter [ 20].	transcription
78693	2	335366	6	NULL	NULL	0	NULL	1,25-(OH)2-D3	Chemical		reduce					p105 precursor gene	GP	levels of 			NULL		0	NULL	NULL	NULL	gw60_febslett_436_3_329_s_128	9801142	Yu et al. have shown that 1,25-(OH)2-D3 can reduce levels of p50 and its precursor p105 in human lymphocytes and they observed reduced binding of PMA-induced nuclear factors to the NF- B binding site of the IL-6 promoter [ 20].	transcription
78694	3	335366	6	NULL	NULL	0	NULL	nuclear factors	GP	PMA-induced	bind					IL-6	GP			NF-B binding site of promoter	NULL		0	NULL	NULL	NULL	gw60_febslett_436_3_329_s_128	9801142	Yu et al. have shown that 1,25-(OH)2-D3 can reduce levels of p50 and its precursor p105 in human lymphocytes and they observed reduced binding of PMA-induced nuclear factors to the NF- B binding site of the IL-6 promoter [ 20].	transcription
57246	1	335366	7	NULL	NULL	0	NULL	1,25-(OH)2-D3			reduce					p50		levels of			NULL	human lymphocytes	NULL	NULL	NULL	NULL	gw60_febslett_436_3_329_s_128	9801142	Yu et al. have shown that 1,25-(OH)2-D3 can reduce levels of p50 and its precursor p105 in human lymphocytes and they observed reduced binding of PMA-induced nuclear factors to the NF- B binding site of the IL-6 promoter [ 20].	transcription
57247	2	335366	7	NULL	NULL	0	NULL	1,25-(OH)2-D3			reduce					precursor p105		levels of			NULL	human lymphocytes	NULL	NULL	NULL	NULL	gw60_febslett_436_3_329_s_128	9801142	Yu et al. have shown that 1,25-(OH)2-D3 can reduce levels of p50 and its precursor p105 in human lymphocytes and they observed reduced binding of PMA-induced nuclear factors to the NF- B binding site of the IL-6 promoter [ 20].	transcription
57248	3	335366	7	NULL	NULL	0	NULL	PMA			induce					nuclear factors					NULL		0	NULL	NULL	NULL	gw60_febslett_436_3_329_s_128	9801142	Yu et al. have shown that 1,25-(OH)2-D3 can reduce levels of p50 and its precursor p105 in human lymphocytes and they observed reduced binding of PMA-induced nuclear factors to the NF- B binding site of the IL-6 promoter [ 20].	transcription
57249	4	335366	7	NULL	NULL	0	NULL	statement 3			bind		reduced			IL-6				NF- B binding site of promoter	NULL		0	NULL	NULL	NULL	gw60_febslett_436_3_329_s_128	9801142	Yu et al. have shown that 1,25-(OH)2-D3 can reduce levels of p50 and its precursor p105 in human lymphocytes and they observed reduced binding of PMA-induced nuclear factors to the NF- B binding site of the IL-6 promoter [ 20].	transcription
57250	1	335367	7	NULL	NULL	0	NULL	v-Abl			induce					cyclin D1		transcription of;;mouse			NULL	293T cells	0	NULL	NULL	NULL	gw60_molcellbiol_22_15_5563_s_233	12101248	The role of NF-kappaB1 in v-Abl-induced cyclin D1 transcription was assessed by cotransfecting 293T cells with mouse  cyclin D1 promoter reporter constructs (Fig.  10A) and expression vectors encoding v-Abl and the p50 or p105 form of NF-kappaB1.	transcription
78695	1	335368	6	NULL	NULL	0	NULL	v-Abl	GP		induces					cyclin D1	GP	transcription of 			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_15_5563_s_237	12101248	In contrast to RelA (lane 9), expression vectors for either the p105 or p50 form of NF-kappaB1 inhibited v-Abl-induced  cyclin D1 transcription (compare lanes 16 and 17 with lane 7), and this repression was mediated predominantly through the kappaB element (compare lanes 20 and 21 with lane 11).	transcription
78696	2	335368	6	NULL	NULL	0	NULL		GP		represses				kappa B element	statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_15_5563_s_237	12101248	In contrast to RelA (lane 9), expression vectors for either the p105 or p50 form of NF-kappaB1 inhibited v-Abl-induced  cyclin D1 transcription (compare lanes 16 and 17 with lane 7), and this repression was mediated predominantly through the kappaB element (compare lanes 20 and 21 with lane 11).	transcription
57251	1	335368	7	NULL	NULL	0	NULL	v-Abl			induce					cyclin D1		transcription of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_15_5563_s_237	12101248	In contrast to RelA (lane 9), expression vectors for either the p105 or p50 form of NF-kappaB1 inhibited v-Abl-induced  cyclin D1 transcription (compare lanes 16 and 17 with lane 7), and this repression was mediated predominantly through the kappaB element (compare lanes 20 and 21 with lane 11).	transcription
57252	2	335368	7	NULL	NULL	0	NULL	NF-kappaB1			inhibits					statement 1					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_15_5563_s_237	12101248	In contrast to RelA (lane 9), expression vectors for either the p105 or p50 form of NF-kappaB1 inhibited v-Abl-induced  cyclin D1 transcription (compare lanes 16 and 17 with lane 7), and this repression was mediated predominantly through the kappaB element (compare lanes 20 and 21 with lane 11).	transcription
57253	3	335368	7	NULL	NULL	0	NULL	statement 2			mediated by		predominantly							kappaB element	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_22_15_5563_s_237	12101248	In contrast to RelA (lane 9), expression vectors for either the p105 or p50 form of NF-kappaB1 inhibited v-Abl-induced  cyclin D1 transcription (compare lanes 16 and 17 with lane 7), and this repression was mediated predominantly through the kappaB element (compare lanes 20 and 21 with lane 11).	transcription
78697	1	335369	6	NULL	NULL	0	NULL	RelB	GP		bind					p100	GP		inhibitory ankyrin containing region		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_2_1405_s_116	11687592	We chose to examine the interaction of RelB with only the inhibitory ankyrin containing regions of p100 and p105, to dissect it from the potential interaction of RelB with the Rel homology domain present in the amino-terminal portions of these atypical inhibitor proteins,  i.e. p52 and p50, respectively.	transcription
78698	2	335369	6	NULL	NULL	0	NULL	RelB	GP		bind					p105	GP		inhibitory ankyrin containing region		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_2_1405_s_116	11687592	We chose to examine the interaction of RelB with only the inhibitory ankyrin containing regions of p100 and p105, to dissect it from the potential interaction of RelB with the Rel homology domain present in the amino-terminal portions of these atypical inhibitor proteins,  i.e. p52 and p50, respectively.	transcription
78699	3	335369	6	NULL	NULL	0	NULL	RelB	GP		bind					p52	GP		Rel homology domain in amino-terminal		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_2_1405_s_116	11687592	We chose to examine the interaction of RelB with only the inhibitory ankyrin containing regions of p100 and p105, to dissect it from the potential interaction of RelB with the Rel homology domain present in the amino-terminal portions of these atypical inhibitor proteins,  i.e. p52 and p50, respectively.	transcription
78700	4	335369	6	NULL	NULL	0	NULL	RelB	GP		bind					p50 	GP		Rel homology domain in amino-terminal		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_2_1405_s_116	11687592	We chose to examine the interaction of RelB with only the inhibitory ankyrin containing regions of p100 and p105, to dissect it from the potential interaction of RelB with the Rel homology domain present in the amino-terminal portions of these atypical inhibitor proteins,  i.e. p52 and p50, respectively.	transcription
57254	1	335369	7	NULL	NULL	0	NULL	RelB			interacts with					p100			inhibitory ankyrin containing regions		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_2_1405_s_116	11687592	We chose to examine the interaction of RelB with only the inhibitory ankyrin containing regions of p100 and p105, to dissect it from the potential interaction of RelB with the Rel homology domain present in the amino-terminal portions of these atypical inhibitor proteins,  i.e. p52 and p50, respectively.	transcription
57255	2	335369	7	NULL	NULL	0	NULL	RelB			interacts with					p105			inhibitory ankyrin containing regions		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_2_1405_s_116	11687592	We chose to examine the interaction of RelB with only the inhibitory ankyrin containing regions of p100 and p105, to dissect it from the potential interaction of RelB with the Rel homology domain present in the amino-terminal portions of these atypical inhibitor proteins,  i.e. p52 and p50, respectively.	transcription
57256	3	335369	7	NULL	NULL	0	NULL	RelB			interacts with					p52			Rel homology domain present in the amino-terminal portions of 		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_2_1405_s_116	11687592	We chose to examine the interaction of RelB with only the inhibitory ankyrin containing regions of p100 and p105, to dissect it from the potential interaction of RelB with the Rel homology domain present in the amino-terminal portions of these atypical inhibitor proteins,  i.e. p52 and p50, respectively.	transcription
57257	4	335369	7	NULL	NULL	0	NULL	RelB			interacts with					p50			Rel homology domain present in the amino-terminal portions of 		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_2_1405_s_116	11687592	We chose to examine the interaction of RelB with only the inhibitory ankyrin containing regions of p100 and p105, to dissect it from the potential interaction of RelB with the Rel homology domain present in the amino-terminal portions of these atypical inhibitor proteins,  i.e. p52 and p50, respectively.	transcription
57258	1	335370	7	NULL	NULL	0	NULL	p105		phosphorylated	bind			tyrosine		phosphatase			active site		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_18_12158_s_189	9115287	Although tyrosine-phosphorylated p105, p62, and p50 most likely bind to the active site of the phosphatase, consistent with the idea of being substrates of DEP-1, we could demonstrate that DEP-1 also engages in protein-protein interactions that require binding determinants other than the catalytic center.	transcription
57259	2	335370	7	NULL	NULL	0	NULL	p62		phosphorylated	bind			tyrosine		phosphatase			active site		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_18_12158_s_189	9115287	Although tyrosine-phosphorylated p105, p62, and p50 most likely bind to the active site of the phosphatase, consistent with the idea of being substrates of DEP-1, we could demonstrate that DEP-1 also engages in protein-protein interactions that require binding determinants other than the catalytic center.	transcription
57260	3	335370	7	NULL	NULL	0	NULL	p50		phosphorylated	bind			tyrosine		phosphatase			active site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_18_12158_s_189	9115287	Although tyrosine-phosphorylated p105, p62, and p50 most likely bind to the active site of the phosphatase, consistent with the idea of being substrates of DEP-1, we could demonstrate that DEP-1 also engages in protein-protein interactions that require binding determinants other than the catalytic center.	transcription
57261	5	335370	7	NULL	NULL	0	NULL	DEP-1			engages in					statement 4					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_18_12158_s_189	9115287	Although tyrosine-phosphorylated p105, p62, and p50 most likely bind to the active site of the phosphatase, consistent with the idea of being substrates of DEP-1, we could demonstrate that DEP-1 also engages in protein-protein interactions that require binding determinants other than the catalytic center.	transcription
57262	4	335370	7	NULL	NULL	0	NULL	protein			interacts with					protein					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_18_12158_s_189	9115287	Although tyrosine-phosphorylated p105, p62, and p50 most likely bind to the active site of the phosphatase, consistent with the idea of being substrates of DEP-1, we could demonstrate that DEP-1 also engages in protein-protein interactions that require binding determinants other than the catalytic center.	transcription
57263	6	335370	7	NULL	NULL	0	NULL	statement 5			require					binding determinants					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_18_12158_s_189	9115287	Although tyrosine-phosphorylated p105, p62, and p50 most likely bind to the active site of the phosphatase, consistent with the idea of being substrates of DEP-1, we could demonstrate that DEP-1 also engages in protein-protein interactions that require binding determinants other than the catalytic center.	transcription
57264	7	335370	7	NULL	NULL	0	NULL	p105		phosphorylated	is a substrate of			tyrosine		DEP-1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_18_12158_s_189	9115287	Although tyrosine-phosphorylated p105, p62, and p50 most likely bind to the active site of the phosphatase, consistent with the idea of being substrates of DEP-1, we could demonstrate that DEP-1 also engages in protein-protein interactions that require binding determinants other than the catalytic center.	transcription
57265	8	335370	7	NULL	NULL	0	NULL	p62		phosphorylated	is a substrate of			tyrosine		DEP-1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_18_12158_s_189	9115287	Although tyrosine-phosphorylated p105, p62, and p50 most likely bind to the active site of the phosphatase, consistent with the idea of being substrates of DEP-1, we could demonstrate that DEP-1 also engages in protein-protein interactions that require binding determinants other than the catalytic center.	transcription
57266	9	335370	7	NULL	NULL	0	NULL	p50		phosphorylated	is a substrate of			tyrosine		DEP-1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_18_12158_s_189	9115287	Although tyrosine-phosphorylated p105, p62, and p50 most likely bind to the active site of the phosphatase, consistent with the idea of being substrates of DEP-1, we could demonstrate that DEP-1 also engages in protein-protein interactions that require binding determinants other than the catalytic center.	transcription
78701	1	335371	6	NULL	NULL	0	NULL	p105	GP	removal of	produces			COOH termini		p50	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_19	10671572	In mammalian cells, the NF-kappaB family of proteins can be divided into two classes as follows: one class includes p50 and p52, both of which are produced constitutively by the proteasome-mediated removal of the COOH termini of the precursor proteins p105 and p100, respectively ( 22,  25-27).	transcription
78702	2	335371	6	NULL	NULL	0	NULL	p100	GP	removal of	produces			COOH termini		p52	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_19	10671572	In mammalian cells, the NF-kappaB family of proteins can be divided into two classes as follows: one class includes p50 and p52, both of which are produced constitutively by the proteasome-mediated removal of the COOH termini of the precursor proteins p105 and p100, respectively ( 22,  25-27).	transcription
78703	3	335371	6	NULL	NULL	0	NULL	statement 1	Process		is mediated by					proteasome	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_19	10671572	In mammalian cells, the NF-kappaB family of proteins can be divided into two classes as follows: one class includes p50 and p52, both of which are produced constitutively by the proteasome-mediated removal of the COOH termini of the precursor proteins p105 and p100, respectively ( 22,  25-27).	transcription
78704	4	335371	6	NULL	NULL	0	NULL	statement 2	Process		is mediated by					proteasome	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_19	10671572	In mammalian cells, the NF-kappaB family of proteins can be divided into two classes as follows: one class includes p50 and p52, both of which are produced constitutively by the proteasome-mediated removal of the COOH termini of the precursor proteins p105 and p100, respectively ( 22,  25-27).	transcription
78705	5	335371	6	NULL	NULL	0	NULL	p50	GP		belongs to					NF-kappaB family	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_19	10671572	In mammalian cells, the NF-kappaB family of proteins can be divided into two classes as follows: one class includes p50 and p52, both of which are produced constitutively by the proteasome-mediated removal of the COOH termini of the precursor proteins p105 and p100, respectively ( 22,  25-27).	transcription
78706	6	335371	6	NULL	NULL	0	NULL	p52	GP		belongs to					NF-kappaB family	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_19	10671572	In mammalian cells, the NF-kappaB family of proteins can be divided into two classes as follows: one class includes p50 and p52, both of which are produced constitutively by the proteasome-mediated removal of the COOH termini of the precursor proteins p105 and p100, respectively ( 22,  25-27).	transcription
57268	1	335371	7	NULL	NULL	0	NULL	NF-kappaB family			include					p50					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_19	10671572	In mammalian cells, the NF-kappaB family of proteins can be divided into two classes as follows: one class includes p50 and p52, both of which are produced constitutively by the proteasome-mediated removal of the COOH termini of the precursor proteins p105 and p100, respectively ( 22,  25-27).	transcription
57269	2	335371	7	NULL	NULL	0	NULL	NF-kappaB family			include					p52					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_19	10671572	In mammalian cells, the NF-kappaB family of proteins can be divided into two classes as follows: one class includes p50 and p52, both of which are produced constitutively by the proteasome-mediated removal of the COOH termini of the precursor proteins p105 and p100, respectively ( 22,  25-27).	transcription
57270	3	335371	7	NULL	NULL	0	NULL	proteasome			mediates					p105		removal of	COOH terminus		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_19	10671572	In mammalian cells, the NF-kappaB family of proteins can be divided into two classes as follows: one class includes p50 and p52, both of which are produced constitutively by the proteasome-mediated removal of the COOH termini of the precursor proteins p105 and p100, respectively ( 22,  25-27).	transcription
57271	4	335371	7	NULL	NULL	0	NULL	proteasome			mediates					p100		removal of	COOH terminus		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_19	10671572	In mammalian cells, the NF-kappaB family of proteins can be divided into two classes as follows: one class includes p50 and p52, both of which are produced constitutively by the proteasome-mediated removal of the COOH termini of the precursor proteins p105 and p100, respectively ( 22,  25-27).	transcription
57272	5	335371	7	NULL	NULL	0	NULL	p50			produced by		constitutively			statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_19	10671572	In mammalian cells, the NF-kappaB family of proteins can be divided into two classes as follows: one class includes p50 and p52, both of which are produced constitutively by the proteasome-mediated removal of the COOH termini of the precursor proteins p105 and p100, respectively ( 22,  25-27).	transcription
57273	6	335371	7	NULL	NULL	0	NULL	p52			produced by		constitutively			statement 4					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_19	10671572	In mammalian cells, the NF-kappaB family of proteins can be divided into two classes as follows: one class includes p50 and p52, both of which are produced constitutively by the proteasome-mediated removal of the COOH termini of the precursor proteins p105 and p100, respectively ( 22,  25-27).	transcription
57274	7	335371	7	NULL	NULL	0	NULL	p105			is a type of					precursor protein					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_19	10671572	In mammalian cells, the NF-kappaB family of proteins can be divided into two classes as follows: one class includes p50 and p52, both of which are produced constitutively by the proteasome-mediated removal of the COOH termini of the precursor proteins p105 and p100, respectively ( 22,  25-27).	transcription
57275	8	335371	7	NULL	NULL	0	NULL	p100			is a type of					precursor protein					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_7_5238_s_19	10671572	In mammalian cells, the NF-kappaB family of proteins can be divided into two classes as follows: one class includes p50 and p52, both of which are produced constitutively by the proteasome-mediated removal of the COOH termini of the precursor proteins p105 and p100, respectively ( 22,  25-27).	transcription
78707	1	335372	6	NULL	NULL	0	NULL	RelA	GP		belongs to					NF-kappaB family	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_19_13010_s_22	10224051	NF-kappaB consists of five family members including RelA and c-Rel, which contain transcriptional activation domains p100 and p105 precursor proteins, which are cleaved to the active members, p52 and p50, respectively, and RelB (reviewed in Refs.	transcription
78708	2	335372	6	NULL	NULL	0	NULL	c-Rel	GP		belongs to					NF-kappaB family	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_19_13010_s_22	10224051	NF-kappaB consists of five family members including RelA and c-Rel, which contain transcriptional activation domains p100 and p105 precursor proteins, which are cleaved to the active members, p52 and p50, respectively, and RelB (reviewed in Refs.	transcription
78709	3	335372	6	NULL	NULL	0	NULL	p100	GP		is cleaved to					p52	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_19_13010_s_22	10224051	NF-kappaB consists of five family members including RelA and c-Rel, which contain transcriptional activation domains p100 and p105 precursor proteins, which are cleaved to the active members, p52 and p50, respectively, and RelB (reviewed in Refs.	transcription
78710	4	335372	6	NULL	NULL	0	NULL	p105	GP		is cleaved to					p50	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_19_13010_s_22	10224051	NF-kappaB consists of five family members including RelA and c-Rel, which contain transcriptional activation domains p100 and p105 precursor proteins, which are cleaved to the active members, p52 and p50, respectively, and RelB (reviewed in Refs.	transcription
57276	1	335372	7	NULL	NULL	0	NULL	NF-kappaB			consist of					RelA					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_19_13010_s_22	10224051	NF-kappaB consists of five family members including RelA and c-Rel, which contain transcriptional activation domains p100 and p105 precursor proteins, which are cleaved to the active members, p52 and p50, respectively, and RelB (reviewed in Refs.	transcription
57277	2	335372	7	NULL	NULL	0	NULL	NF-kappaB			consist of					c-Rel					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_19_13010_s_22	10224051	NF-kappaB consists of five family members including RelA and c-Rel, which contain transcriptional activation domains p100 and p105 precursor proteins, which are cleaved to the active members, p52 and p50, respectively, and RelB (reviewed in Refs.	transcription
57278	3	335372	7	NULL	NULL	0	NULL	RelA			contain					p100			transcriptional activation domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_19_13010_s_22	10224051	NF-kappaB consists of five family members including RelA and c-Rel, which contain transcriptional activation domains p100 and p105 precursor proteins, which are cleaved to the active members, p52 and p50, respectively, and RelB (reviewed in Refs.	transcription
57279	4	335372	7	NULL	NULL	0	NULL	c-Rel			contain					p105			transcriptional activation domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_19_13010_s_22	10224051	NF-kappaB consists of five family members including RelA and c-Rel, which contain transcriptional activation domains p100 and p105 precursor proteins, which are cleaved to the active members, p52 and p50, respectively, and RelB (reviewed in Refs.	transcription
57280	5	335372	7	NULL	NULL	0	NULL	p100			is cleaved to			transcriptional activation domain		p52					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_19_13010_s_22	10224051	NF-kappaB consists of five family members including RelA and c-Rel, which contain transcriptional activation domains p100 and p105 precursor proteins, which are cleaved to the active members, p52 and p50, respectively, and RelB (reviewed in Refs.	transcription
57281	6	335372	7	NULL	NULL	0	NULL	p105			is cleaved to			transcriptional activation domain		p50					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_19_13010_s_22	10224051	NF-kappaB consists of five family members including RelA and c-Rel, which contain transcriptional activation domains p100 and p105 precursor proteins, which are cleaved to the active members, p52 and p50, respectively, and RelB (reviewed in Refs.	transcription
78711	1	335373	6	NULL	NULL	0	NULL		GP		inhibits			Ankyrin Repeat		p105	GP	processing of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_138	11350967	Ankyrin Repeat-dependent Inhibition of p105 Processing in Vitro Is Probably Mediated by Anchored p50 Subunits, and Inhibition Is Alleviated by the Presence of the C-terminal Signaling Motif--  We surmised that inhibition of processing which is observed with the increasing number of ankyrin repeats (Fig.  2) is caused by the presence of free p50 and other active NF-kappaB subunits in the HeLa cell extract in which the processing reactions are carried out.	transcription
78712	2	335373	6	NULL	NULL	NULL	NULL	p50 subunit	GP	anchored	mediates					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_138	11350967	Ankyrin Repeat-dependent Inhibition of p105 Processing in Vitro Is Probably Mediated by Anchored p50 Subunits, and Inhibition Is Alleviated by the Presence of the C-terminal Signaling Motif--  We surmised that inhibition of processing which is observed with the increasing number of ankyrin repeats (Fig.  2) is caused by the presence of free p50 and other active NF-kappaB subunits in the HeLa cell extract in which the processing reactions are carried out.	transcription
78713	3	335373	6	NULL	NULL	0	NULL	statement 2	Process		is alleviated by							presence of	C-terminal Signaling Motif		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_138	11350967	Ankyrin Repeat-dependent Inhibition of p105 Processing in Vitro Is Probably Mediated by Anchored p50 Subunits, and Inhibition Is Alleviated by the Presence of the C-terminal Signaling Motif--  We surmised that inhibition of processing which is observed with the increasing number of ankyrin repeats (Fig.  2) is caused by the presence of free p50 and other active NF-kappaB subunits in the HeLa cell extract in which the processing reactions are carried out.	transcription
57282	1	335373	7	NULL	NULL	0	NULL	p105		inhibition of;;processing of	depends on								Ankyrin Repeat		NULL	in vitro;;HeLa cell extract	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_138	11350967	Ankyrin Repeat-dependent Inhibition of p105 Processing in Vitro Is Probably Mediated by Anchored p50 Subunits, and Inhibition Is Alleviated by the Presence of the C-terminal Signaling Motif--  We surmised that inhibition of processing which is observed with the increasing number of ankyrin repeats (Fig.  2) is caused by the presence of free p50 and other active NF-kappaB subunits in the HeLa cell extract in which the processing reactions are carried out.	transcription
57283	2	335373	7	NULL	NULL	0	NULL	statement 1			mediated by		probably			p50 subunits		anchored			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_138	11350967	Ankyrin Repeat-dependent Inhibition of p105 Processing in Vitro Is Probably Mediated by Anchored p50 Subunits, and Inhibition Is Alleviated by the Presence of the C-terminal Signaling Motif--  We surmised that inhibition of processing which is observed with the increasing number of ankyrin repeats (Fig.  2) is caused by the presence of free p50 and other active NF-kappaB subunits in the HeLa cell extract in which the processing reactions are carried out.	transcription
57284	3	335373	7	NULL	NULL	0	NULL	p105		inhibition of	is alleviated by							presence of	C-terminal Signaling Motif		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_138	11350967	Ankyrin Repeat-dependent Inhibition of p105 Processing in Vitro Is Probably Mediated by Anchored p50 Subunits, and Inhibition Is Alleviated by the Presence of the C-terminal Signaling Motif--  We surmised that inhibition of processing which is observed with the increasing number of ankyrin repeats (Fig.  2) is caused by the presence of free p50 and other active NF-kappaB subunits in the HeLa cell extract in which the processing reactions are carried out.	transcription
57285	4	335373	7	NULL	NULL	0	NULL	statement 1			caused by					p50		presence of free			NULL	HeLa cell extract	0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_138	11350967	Ankyrin Repeat-dependent Inhibition of p105 Processing in Vitro Is Probably Mediated by Anchored p50 Subunits, and Inhibition Is Alleviated by the Presence of the C-terminal Signaling Motif--  We surmised that inhibition of processing which is observed with the increasing number of ankyrin repeats (Fig.  2) is caused by the presence of free p50 and other active NF-kappaB subunits in the HeLa cell extract in which the processing reactions are carried out.	transcription
57286	5	335373	7	NULL	NULL	0	NULL	statement 1			caused by					NF-kappaB subunits		active			NULL	HeLa cell extract	0	NULL	NULL	NULL	gw60_jbiolchem_276_29_26769_s_138	11350967	Ankyrin Repeat-dependent Inhibition of p105 Processing in Vitro Is Probably Mediated by Anchored p50 Subunits, and Inhibition Is Alleviated by the Presence of the C-terminal Signaling Motif--  We surmised that inhibition of processing which is observed with the increasing number of ankyrin repeats (Fig.  2) is caused by the presence of free p50 and other active NF-kappaB subunits in the HeLa cell extract in which the processing reactions are carried out.	transcription
57287	1	335376	7	NULL	NULL	0	NULL	NF-kappaB1		mammalian	belongs to					class I members					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
57288	2	335376	7	NULL	NULL	0	NULL	NF-kappaB1		mammalian	consist of					p105/p50					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
57289	3	335376	7	NULL	NULL	0	NULL	NF-kappaB2		mammalian	belongs to					class I members					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
57290	4	335376	7	NULL	NULL	0	NULL	NF-kappaB2		mammalian	consist of					p100/p52					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
57291	5	335376	7	NULL	NULL	0	NULL	p105			is a precursor of					NF-kappaB1					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
57292	6	335376	7	NULL	NULL	0	NULL	p100			is a precursor of					NF-kappaB2					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
57293	7	335376	7	NULL	NULL	0	NULL	NF-kappaB1			processed to		proteolytically			p50					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
57294	8	335376	7	NULL	NULL	0	NULL	NF-kappaB2			processed to		proteolytically			p52					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
57295	9	335376	7	NULL	NULL	0	NULL	p50			bind					DNA					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
57296	10	335376	7	NULL	NULL	0	NULL	p52			bind					DNA					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
57297	11	335376	7	NULL	NULL	0	NULL	RelA		mammalian	belongs to					class II members					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
57298	12	335376	7	NULL	NULL	0	NULL	c-Rel		mammalian	belongs to					class II members					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
57299	13	335376	7	NULL	NULL	0	NULL	RelB		mammalian	belongs to					class II members					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
57300	14	335376	7	NULL	NULL	0	NULL	RelA			consist of					p65					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
57301	15	335376	7	NULL	NULL	0	NULL	RelA			does not undergo					proteolytic processing					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
57302	16	335376	7	NULL	NULL	0	NULL	c-Rel			does not undergo					proteolytic processing					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
57303	17	335376	7	NULL	NULL	0	NULL	RelB			does not undergo					proteolytic processing					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
57304	18	335376	7	NULL	NULL	0	NULL	RelA			contains								transcriptional activation domain in C terminus		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
57305	19	335376	7	NULL	NULL	0	NULL	c-Rel			contains								transcriptional activation domain in C terminus		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
57306	20	335376	7	NULL	NULL	0	NULL	RelB			contains								transcriptional activation domain in C terminus		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_1_477_s_14	9418895	The mammalian members of this family can be grouped into two classes: class I members, which include NF-kappaB1 (p105/p50) and NF-kappaB2 (p100/p52), are transcribed as precursors (p105 and p100) and then proteolytically processed to yield the DNA binding subunits p50 and p52, respectively, and class II members, which include RelA (p65), c-Rel, and RelB, are not proteolytically processed and contain a transcriptional activation domain in their C termini.	transcription
78714	1	335377	6	NULL	NULL	0	NULL	v-Abl	GP		induces					cyclin D1	GP	transcription of 			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_15_5563_s_262	12101248	While these findings indicate that NF-kappaB1 downregulates v-Abl-induced  cyclin D1 transcription, an inability to obtain  nfkb1-/- pre-B cells that express only an NF-kappaB1 p50-encoded transgene (Nakamura, unpublished) prevented us from determining if the inhibition of  cyclin D1 transcription induced by v-Abl is mediated through the p50 or p105 form of NF-kappaB1.	transcription
78715	2	335377	6	NULL	NULL	0	NULL	NF-kappaB1	GP		downregulates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_15_5563_s_262	12101248	While these findings indicate that NF-kappaB1 downregulates v-Abl-induced  cyclin D1 transcription, an inability to obtain  nfkb1-/- pre-B cells that express only an NF-kappaB1 p50-encoded transgene (Nakamura, unpublished) prevented us from determining if the inhibition of  cyclin D1 transcription induced by v-Abl is mediated through the p50 or p105 form of NF-kappaB1.	transcription
57307	1	335377	7	NULL	NULL	0	NULL	v-Abl			induce					cyclin D1		transcription of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_15_5563_s_262	12101248	While these findings indicate that NF-kappaB1 downregulates v-Abl-induced  cyclin D1 transcription, an inability to obtain  nfkb1-/- pre-B cells that express only an NF-kappaB1 p50-encoded transgene (Nakamura, unpublished) prevented us from determining if the inhibition of  cyclin D1 transcription induced by v-Abl is mediated through the p50 or p105 form of NF-kappaB1.	transcription
57308	2	335377	7	NULL	NULL	0	NULL	NF-kappaB1			downregulates					statement 1					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_15_5563_s_262	12101248	While these findings indicate that NF-kappaB1 downregulates v-Abl-induced  cyclin D1 transcription, an inability to obtain  nfkb1-/- pre-B cells that express only an NF-kappaB1 p50-encoded transgene (Nakamura, unpublished) prevented us from determining if the inhibition of  cyclin D1 transcription induced by v-Abl is mediated through the p50 or p105 form of NF-kappaB1.	transcription
78286	1	335378	6	NULL	NULL	NULL	NULL	Uracil phosphoribosyltransferase	GP		catalyzes					uracil	Chemical	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_17_6681_s_181	15090651	Uracil phosphoribosyltransferase catalyzes the phosphorylation of uracil or cytidine (step 1 in  Fig. 2).	transcription
78287	2	335378	6	NULL	NULL	0	NULL	Uracil phosphoribosyltransferase	GP		catalyzes					cytidine	NucleicAcid	phosphorylation of			NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6681_s_181	15090651	Uracil phosphoribosyltransferase catalyzes the phosphorylation of uracil or cytidine (step 1 in  Fig. 2).	transcription
57309	1	335378	7	NULL	NULL	0	NULL	Uracil phosphoribosyltransferase			catalyzes					uracil		phosphorylation of 			NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6681_s_181	15090651	Uracil phosphoribosyltransferase catalyzes the phosphorylation of uracil or cytidine (step 1 in  Fig. 2).	transcription
57310	2	335378	7	NULL	NULL	0	NULL	Uracil phosphoribosyltransferase			catalyze					cytidine		phosphorylation of			NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6681_s_181	15090651	Uracil phosphoribosyltransferase catalyzes the phosphorylation of uracil or cytidine (step 1 in  Fig. 2).	transcription
57311	3	335378	7	NULL	NULL	0	NULL	statement 1			is an alternative to					statement 2					NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6681_s_181	15090651	Uracil phosphoribosyltransferase catalyzes the phosphorylation of uracil or cytidine (step 1 in  Fig. 2).	transcription
78717	1	335379	6	NULL	NULL	0	NULL	cytidine	Chemical		is deaminated to		site specific			uracil	Chemical				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_8_4426_s_2	9671452	The editing of apolipoprotein B (apo-B) mRNA involves the site-specific deamination of cytidine to uracil.	transcription
78718	2	335379	6	NULL	NULL	0	NULL	apo-B mRNA	NucleicAcid	editing of	involves					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_8_4426_s_2	9671452	The editing of apolipoprotein B (apo-B) mRNA involves the site-specific deamination of cytidine to uracil.	transcription
57312	2	335379	7	NULL	NULL	0	NULL	apo-B mRNA		editing of	involves					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_8_4426_s_2	9671452	The editing of apolipoprotein B (apo-B) mRNA involves the site-specific deamination of cytidine to uracil.	transcription
57313	1	335379	7	NULL	NULL	0	NULL	cytidine			deaminated to		site-specifically			uracil					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_18_8_4426_s_2	9671452	The editing of apolipoprotein B (apo-B) mRNA involves the site-specific deamination of cytidine to uracil.	transcription
57314	3	335379	7	NULL	NULL	0	NULL	apo-B			is					apolipoprotein B					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_8_4426_s_2	9671452	The editing of apolipoprotein B (apo-B) mRNA involves the site-specific deamination of cytidine to uracil.	transcription
57315	1	335380	7	NULL	NULL	0	NULL	uracil plus uridine			repress					pyrG					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_19_5513_s_175	11544212	Addition of pyrimidines to this strain brought about repression of  pyrG, twofold repression by uracil plus uridine, and almost threefold repression by cytidine.	transcription
57316	2	335380	7	NULL	NULL	0	NULL	cytidine			repress					pyrG					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_19_5513_s_175	11544212	Addition of pyrimidines to this strain brought about repression of  pyrG, twofold repression by uracil plus uridine, and almost threefold repression by cytidine.	transcription
57322	1	335381	7	NULL	NULL	0	NULL	cdd		mutation	does not alter					uracil plus uridine		repression by			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_19_5513_s_177	11544212	Repression by uracil plus uridine was not altered by the  cdd mutation, but cytidine became a more effective repressor (seven- to eightfold repression).	transcription
57323	2	335381	7	NULL	NULL	0	NULL	cytidine			became					effective repressor					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_19_5513_s_177	11544212	Repression by uracil plus uridine was not altered by the  cdd mutation, but cytidine became a more effective repressor (seven- to eightfold repression).	transcription
57324	3	335381	7	NULL	NULL	0	NULL	statement 2			because of					cdd		mutation			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_19_5513_s_177	11544212	Repression by uracil plus uridine was not altered by the  cdd mutation, but cytidine became a more effective repressor (seven- to eightfold repression).	transcription
78288	1	335382	6	NULL	NULL	0	NULL	Uracil	NucleicAcid		is removed from					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-virol_80_2_16378989_s_4	16378989	UNG initiates the removal of uracils from DNA,  and this has been proposed to be important both for reverse transcription  and as a mediator to the antiviral effect of virion-incorporated Apobec3G,  a cytidine deaminase that generates numerous uracils in the viral DNA  during virus replication.	transcription
78719	2	335382	6	NULL	NULL	0	NULL	UNG	Chemical		initiates					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-virol_80_2_16378989_s_4	16378989	UNG initiates the removal of uracils from DNA,  and this has been proposed to be important both for reverse transcription  and as a mediator to the antiviral effect of virion-incorporated Apobec3G,  a cytidine deaminase that generates numerous uracils in the viral DNA  during virus replication.	transcription
78720	3	335382	6	NULL	NULL	0	NULL	virion-incorporated Apobec3G,	GP		generates					uracil	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-virol_80_2_16378989_s_4	16378989	UNG initiates the removal of uracils from DNA,  and this has been proposed to be important both for reverse transcription  and as a mediator to the antiviral effect of virion-incorporated Apobec3G,  a cytidine deaminase that generates numerous uracils in the viral DNA  during virus replication.	transcription
78721	4	335382	6	NULL	NULL	0	NULL	statement 3	Process		occurs during					virus	Organism	replication of 			NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-virol_80_2_16378989_s_4	16378989	UNG initiates the removal of uracils from DNA,  and this has been proposed to be important both for reverse transcription  and as a mediator to the antiviral effect of virion-incorporated Apobec3G,  a cytidine deaminase that generates numerous uracils in the viral DNA  during virus replication.	transcription
78722	5	335382	6	NULL	NULL	0	NULL	virion-incorporated Apobec3G,	GP		is a type of					cytidine deaminase	GP				NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-virol_80_2_16378989_s_4	16378989	UNG initiates the removal of uracils from DNA,  and this has been proposed to be important both for reverse transcription  and as a mediator to the antiviral effect of virion-incorporated Apobec3G,  a cytidine deaminase that generates numerous uracils in the viral DNA  during virus replication.	transcription
57325	1	335382	7	NULL	NULL	0	NULL	Uracils			removed from					DNA					NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-virol_80_2_16378989_s_4	16378989	UNG initiates the removal of uracils from DNA,  and this has been proposed to be important both for reverse transcription  and as a mediator to the antiviral effect of virion-incorporated Apobec3G,  a cytidine deaminase that generates numerous uracils in the viral DNA  during virus replication.	transcription
57326	2	335382	7	NULL	NULL	0	NULL	UNG			initiates					statement 1					NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-virol_80_2_16378989_s_4	16378989	UNG initiates the removal of uracils from DNA,  and this has been proposed to be important both for reverse transcription  and as a mediator to the antiviral effect of virion-incorporated Apobec3G,  a cytidine deaminase that generates numerous uracils in the viral DNA  during virus replication.	transcription
57327	3	335382	7	NULL	NULL	0	NULL	statement 2			is important for					reverse transcription					NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-virol_80_2_16378989_s_4	16378989	UNG initiates the removal of uracils from DNA,  and this has been proposed to be important both for reverse transcription  and as a mediator to the antiviral effect of virion-incorporated Apobec3G,  a cytidine deaminase that generates numerous uracils in the viral DNA  during virus replication.	transcription
57328	4	335382	7	NULL	NULL	0	NULL	virion			incorporate					Apobec3G					NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-virol_80_2_16378989_s_4	16378989	UNG initiates the removal of uracils from DNA,  and this has been proposed to be important both for reverse transcription  and as a mediator to the antiviral effect of virion-incorporated Apobec3G,  a cytidine deaminase that generates numerous uracils in the viral DNA  during virus replication.	transcription
57329	5	335382	7	NULL	NULL	0	NULL	statement 2			mediate					statement 4		antiviral effect of 			NULL		NULL	NULL	NULL	NULL	abs-batch0560-0569_j-virol_80_2_16378989_s_4	16378989	UNG initiates the removal of uracils from DNA,  and this has been proposed to be important both for reverse transcription  and as a mediator to the antiviral effect of virion-incorporated Apobec3G,  a cytidine deaminase that generates numerous uracils in the viral DNA  during virus replication.	transcription
57330	6	335382	7	NULL	NULL	0	NULL	Apobec3G			is a type of					 cytidine deaminase					NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-virol_80_2_16378989_s_4	16378989	UNG initiates the removal of uracils from DNA,  and this has been proposed to be important both for reverse transcription  and as a mediator to the antiviral effect of virion-incorporated Apobec3G,  a cytidine deaminase that generates numerous uracils in the viral DNA  during virus replication.	transcription
57331	7	335382	7	NULL	NULL	0	NULL	Apobec3G			generates					viral DNA		numerous uracils in			NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-virol_80_2_16378989_s_4	16378989	UNG initiates the removal of uracils from DNA,  and this has been proposed to be important both for reverse transcription  and as a mediator to the antiviral effect of virion-incorporated Apobec3G,  a cytidine deaminase that generates numerous uracils in the viral DNA  during virus replication.	transcription
57332	8	335382	7	NULL	NULL	0	NULL	statement 7			occur during					virus replication					NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-virol_80_2_16378989_s_4	16378989	UNG initiates the removal of uracils from DNA,  and this has been proposed to be important both for reverse transcription  and as a mediator to the antiviral effect of virion-incorporated Apobec3G,  a cytidine deaminase that generates numerous uracils in the viral DNA  during virus replication.	transcription
78681	1	335383	6	NULL	NULL	0	NULL	AID	GP		is					activation-induced cytidine deaminase	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_103_32_12081_s_18	16873544	The transcription-coupled deamination of cytosines by activation-induced cytidine deaminase (AID) leads to uracil that may be processed to abasic sites or strand breaks by the excision repair pathway, i.e., uracil- N-glycosylase ( ,  ).	transcription
78682	2	335383	6	NULL	NULL	0	NULL	AID	GP		leads to					cytosine	Chemical	deamination of			NULL		0	NULL	NULL	NULL	gw70_pnas_103_32_12081_s_18	16873544	The transcription-coupled deamination of cytosines by activation-induced cytidine deaminase (AID) leads to uracil that may be processed to abasic sites or strand breaks by the excision repair pathway, i.e., uracil- N-glycosylase ( ,  ).	transcription
78723	3	335383	6	NULL	NULL	0	NULL	statement 2	Process		leads to					uracil	Chemical				NULL		0	NULL	NULL	NULL	gw70_pnas_103_32_12081_s_18	16873544	The transcription-coupled deamination of cytosines by activation-induced cytidine deaminase (AID) leads to uracil that may be processed to abasic sites or strand breaks by the excision repair pathway, i.e., uracil- N-glycosylase ( ,  ).	transcription
57333	1	335383	7	NULL	NULL	0	NULL	activation			induce					cytidine deaminase					NULL		0	NULL	NULL	NULL	gw70_pnas_103_32_12081_s_18	16873544	The transcription-coupled deamination of cytosines by activation-induced cytidine deaminase (AID) leads to uracil that may be processed to abasic sites or strand breaks by the excision repair pathway, i.e., uracil- N-glycosylase ( ,  ).	transcription
57334	2	335383	7	NULL	NULL	0	NULL	cytosines		transcription-coupled deamination of	leads to					uracil					NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_32_12081_s_18	16873544	The transcription-coupled deamination of cytosines by activation-induced cytidine deaminase (AID) leads to uracil that may be processed to abasic sites or strand breaks by the excision repair pathway, i.e., uracil- N-glycosylase ( ,  ).	transcription
57335	3	335383	7	NULL	NULL	0	NULL	uracil			be processed to		may							abasic sites	NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_32_12081_s_18	16873544	The transcription-coupled deamination of cytosines by activation-induced cytidine deaminase (AID) leads to uracil that may be processed to abasic sites or strand breaks by the excision repair pathway, i.e., uracil- N-glycosylase ( ,  ).	transcription
57336	4	335383	7	NULL	NULL	0	NULL	uracil			be processed to		may			strand breaks by the excision repair pathway					NULL		0	NULL	NULL	NULL	gw70_pnas_103_32_12081_s_18	16873544	The transcription-coupled deamination of cytosines by activation-induced cytidine deaminase (AID) leads to uracil that may be processed to abasic sites or strand breaks by the excision repair pathway, i.e., uracil- N-glycosylase ( ,  ).	transcription
57338	6	335383	7	NULL	NULL	0	NULL	statement 1			is					AID					NULL		0	NULL	NULL	NULL	gw70_pnas_103_32_12081_s_18	16873544	The transcription-coupled deamination of cytosines by activation-induced cytidine deaminase (AID) leads to uracil that may be processed to abasic sites or strand breaks by the excision repair pathway, i.e., uracil- N-glycosylase ( ,  ).	transcription
57339	5	335383	7	NULL	NULL	0	NULL	statement 2			is carried out by					AID					NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_32_12081_s_18	16873544	The transcription-coupled deamination of cytosines by activation-induced cytidine deaminase (AID) leads to uracil that may be processed to abasic sites or strand breaks by the excision repair pathway, i.e., uracil- N-glycosylase ( ,  ).	transcription
57340	1	335384	7	NULL	NULL	0	NULL	Pol		 polymerase activity of 	mediates					C/G mutations 		generation of			NULL		0	NULL	NULL	NULL	gw70_pnas_102_39_13986_s_35	16172387	We propose that the polymerase activity of Pol  mediates the generation of C/G mutations by replicating over abasic sites formed by uracil-DNA glycosylase-catalyzed excision of the uracil residues generated by activation-induced cytidine deaminase.	transcription
57341	2	335384	7	NULL	NULL	0	NULL	statement 1			occur by							replicating over		abasic sites	NULL		0	NULL	NULL	NULL	gw70_pnas_102_39_13986_s_35	16172387	We propose that the polymerase activity of Pol  mediates the generation of C/G mutations by replicating over abasic sites formed by uracil-DNA glycosylase-catalyzed excision of the uracil residues generated by activation-induced cytidine deaminase.	transcription
57342	3	335384	7	NULL	NULL	0	NULL	uracil-DNA glycosylase			catalyze					uracil residues		excision of			NULL		0	NULL	NULL	NULL	gw70_pnas_102_39_13986_s_35	16172387	We propose that the polymerase activity of Pol  mediates the generation of C/G mutations by replicating over abasic sites formed by uracil-DNA glycosylase-catalyzed excision of the uracil residues generated by activation-induced cytidine deaminase.	transcription
57343	4	335384	7	NULL	NULL	0	NULL				formed by				abasic sites	statement 3					NULL		0	NULL	NULL	NULL	gw70_pnas_102_39_13986_s_35	16172387	We propose that the polymerase activity of Pol  mediates the generation of C/G mutations by replicating over abasic sites formed by uracil-DNA glycosylase-catalyzed excision of the uracil residues generated by activation-induced cytidine deaminase.	transcription
57344	5	335384	7	NULL	NULL	0	NULL	statement 3			generated by					activation-induced cytidine deaminase					NULL		0	NULL	NULL	NULL	gw70_pnas_102_39_13986_s_35	16172387	We propose that the polymerase activity of Pol  mediates the generation of C/G mutations by replicating over abasic sites formed by uracil-DNA glycosylase-catalyzed excision of the uracil residues generated by activation-induced cytidine deaminase.	transcription
78645	1	335385	6	NULL	NULL	0	NULL	Uracil	Chemical		replaces					cytosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_nature_424_6944_99_s_122	12808466	These results are consistent with a model in which the previously demonstrated cytidine  deaminase activity of APOBEC3G leads to the replacement of cytosine by uracil in  the nascent retroviral DNA.	transcription
78646	2	335385	6	NULL	NULL	0	NULL	APOBEC3G	GP		deaminates					cytidine	Chemical				NULL		0	NULL	NULL	NULL	gw70_nature_424_6944_99_s_122	12808466	These results are consistent with a model in which the previously demonstrated cytidine  deaminase activity of APOBEC3G leads to the replacement of cytosine by uracil in  the nascent retroviral DNA.	transcription
78647	3	335385	6	NULL	NULL	0	NULL	statement 2	Process		leads to					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_nature_424_6944_99_s_122	12808466	These results are consistent with a model in which the previously demonstrated cytidine  deaminase activity of APOBEC3G leads to the replacement of cytosine by uracil in  the nascent retroviral DNA.	transcription
57345	1	335385	7	NULL	NULL	0	NULL	APOBEC3G			possess					cytidine deaminase activity					NULL		0	NULL	NULL	NULL	gw70_nature_424_6944_99_s_122	12808466	These results are consistent with a model in which the previously demonstrated cytidine  deaminase activity of APOBEC3G leads to the replacement of cytosine by uracil in  the nascent retroviral DNA.	transcription
57346	3	335385	7	NULL	NULL	0	NULL	statement 1			leads to					statement 3					NULL		NULL	NULL	NULL	NULL	gw70_nature_424_6944_99_s_122	12808466	These results are consistent with a model in which the previously demonstrated cytidine  deaminase activity of APOBEC3G leads to the replacement of cytosine by uracil in  the nascent retroviral DNA.	transcription
57347	2	335385	7	NULL	NULL	0	NULL	cytosine			replaced with					uracil					NULL	nascent retroviral DNA	0	NULL	NULL	NULL	gw70_nature_424_6944_99_s_122	12808466	These results are consistent with a model in which the previously demonstrated cytidine  deaminase activity of APOBEC3G leads to the replacement of cytosine by uracil in  the nascent retroviral DNA.	transcription
78641	1	335386	6	NULL	NULL	0	NULL	cytidine	Chemical		changed to					deoxycytidine	Chemical				NULL		0	NULL	NULL	NULL	gw60_molcell_6_5_1077_s_169	11106747	Modification of cytidine to deoxycytidine (or uracil to thymidine) on either the sense or the antisense strand of the trigger was sufficient to produce a substantial decrease in interference activity (  Figure 5B).	transcription
78642	2	335386	6	NULL	NULL	0	NULL	statement 1	Process		decreases					interference activity	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_6_5_1077_s_169	11106747	Modification of cytidine to deoxycytidine (or uracil to thymidine) on either the sense or the antisense strand of the trigger was sufficient to produce a substantial decrease in interference activity (  Figure 5B).	transcription
78643	3	335386	6	NULL	NULL	0	NULL	Uracil	Chemical		changed to					thymidine	Chemical				NULL		0	NULL	NULL	NULL	gw60_molcell_6_5_1077_s_169	11106747	Modification of cytidine to deoxycytidine (or uracil to thymidine) on either the sense or the antisense strand of the trigger was sufficient to produce a substantial decrease in interference activity (  Figure 5B).	transcription
78644	4	335386	6	NULL	NULL	0	NULL	statement 3	Process		decreases					interference activity	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_6_5_1077_s_169	11106747	Modification of cytidine to deoxycytidine (or uracil to thymidine) on either the sense or the antisense strand of the trigger was sufficient to produce a substantial decrease in interference activity (  Figure 5B).	transcription
57348	1	335386	7	NULL	NULL	0	NULL	cytidine			modified to					deoxycytidine					NULL		0	NULL	NULL	NULL	gw60_molcell_6_5_1077_s_169	11106747	Modification of cytidine to deoxycytidine (or uracil to thymidine) on either the sense or the antisense strand of the trigger was sufficient to produce a substantial decrease in interference activity (  Figure 5B).	transcription
57349	2	335386	7	NULL	NULL	0	NULL	uracil			modified to					thymidine					NULL		0	NULL	NULL	NULL	gw60_molcell_6_5_1077_s_169	11106747	Modification of cytidine to deoxycytidine (or uracil to thymidine) on either the sense or the antisense strand of the trigger was sufficient to produce a substantial decrease in interference activity (  Figure 5B).	transcription
57350	3	335386	7	NULL	NULL	0	NULL	statement 1			produce					interference activity		substantial decrease in			NULL		0	NULL	NULL	NULL	gw60_molcell_6_5_1077_s_169	11106747	Modification of cytidine to deoxycytidine (or uracil to thymidine) on either the sense or the antisense strand of the trigger was sufficient to produce a substantial decrease in interference activity (  Figure 5B).	transcription
57351	4	335386	7	NULL	NULL	0	NULL	statement 2			produce					interference activity		substantial decrease in			NULL		0	NULL	NULL	NULL	gw60_molcell_6_5_1077_s_169	11106747	Modification of cytidine to deoxycytidine (or uracil to thymidine) on either the sense or the antisense strand of the trigger was sufficient to produce a substantial decrease in interference activity (  Figure 5B).	transcription
57352	5	335386	7	NULL	NULL	0	NULL	statement 1			occur in					sense strand					NULL		0	NULL	NULL	NULL	gw60_molcell_6_5_1077_s_169	11106747	Modification of cytidine to deoxycytidine (or uracil to thymidine) on either the sense or the antisense strand of the trigger was sufficient to produce a substantial decrease in interference activity (  Figure 5B).	transcription
57353	6	335386	7	NULL	NULL	0	NULL	statement 1			occur in					antisense strand					NULL		0	NULL	NULL	NULL	gw60_molcell_6_5_1077_s_169	11106747	Modification of cytidine to deoxycytidine (or uracil to thymidine) on either the sense or the antisense strand of the trigger was sufficient to produce a substantial decrease in interference activity (  Figure 5B).	transcription
57354	7	335386	7	NULL	NULL	0	NULL	statement 5			is an alternative to					statement 6					NULL		0	NULL	NULL	NULL	gw60_molcell_6_5_1077_s_169	11106747	Modification of cytidine to deoxycytidine (or uracil to thymidine) on either the sense or the antisense strand of the trigger was sufficient to produce a substantial decrease in interference activity (  Figure 5B).	transcription
57355	8	335386	7	NULL	NULL	0	NULL	statement 2			occur in					sense strand					NULL		0	NULL	NULL	NULL	gw60_molcell_6_5_1077_s_169	11106747	Modification of cytidine to deoxycytidine (or uracil to thymidine) on either the sense or the antisense strand of the trigger was sufficient to produce a substantial decrease in interference activity (  Figure 5B).	transcription
57356	9	335386	7	NULL	NULL	0	NULL	statement 2			occur in					antisense strand					NULL		0	NULL	NULL	NULL	gw60_molcell_6_5_1077_s_169	11106747	Modification of cytidine to deoxycytidine (or uracil to thymidine) on either the sense or the antisense strand of the trigger was sufficient to produce a substantial decrease in interference activity (  Figure 5B).	transcription
57357	10	335386	7	NULL	NULL	0	NULL	statement 8			is an alternative to					statement 9					NULL		0	NULL	NULL	NULL	gw60_molcell_6_5_1077_s_169	11106747	Modification of cytidine to deoxycytidine (or uracil to thymidine) on either the sense or the antisense strand of the trigger was sufficient to produce a substantial decrease in interference activity (  Figure 5B).	transcription
57358	1	335387	7	NULL	NULL	0	NULL	Uracil 			removed in					U-G mismatch					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8765_s_117	15611076	The absence of UDG activity in the cells facilitates subsequent analysis, once it prevents the removal of uracil in U-G mismatch resulting from cytidine deamination, allowing the increase of mutation frequency caused by the activity of deaminase expression.	transcription
57359	2	335387	7	NULL	NULL	0	NULL	statement 1			result from					cytidine deamination					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8765_s_117	15611076	The absence of UDG activity in the cells facilitates subsequent analysis, once it prevents the removal of uracil in U-G mismatch resulting from cytidine deamination, allowing the increase of mutation frequency caused by the activity of deaminase expression.	transcription
57360	3	335387	7	NULL	NULL	0	NULL	UDG activity		absence of	prevents					statement 1					NULL	cells	0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8765_s_117	15611076	The absence of UDG activity in the cells facilitates subsequent analysis, once it prevents the removal of uracil in U-G mismatch resulting from cytidine deamination, allowing the increase of mutation frequency caused by the activity of deaminase expression.	transcription
57361	4	335387	7	NULL	NULL	0	NULL	statement 2			allows					mutation frequency		increase of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8765_s_117	15611076	The absence of UDG activity in the cells facilitates subsequent analysis, once it prevents the removal of uracil in U-G mismatch resulting from cytidine deamination, allowing the increase of mutation frequency caused by the activity of deaminase expression.	transcription
57362	5	335387	7	NULL	NULL	0	NULL	statement 4			caused by					deaminase		activation of;;expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8765_s_117	15611076	The absence of UDG activity in the cells facilitates subsequent analysis, once it prevents the removal of uracil in U-G mismatch resulting from cytidine deamination, allowing the increase of mutation frequency caused by the activity of deaminase expression.	transcription
78635	1	335388	6	NULL	NULL	0	NULL	NTPs	GP		activate					GTP	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_19_19955_s_309	14981084	In previous studies we showed that NTPs activate Gs-proteins in the order of potency GTP > ITP > UTP > XTP > CTP ( ,  ), rendering hypoxanthine, uracil, xanthine, and cytidine nucleotides potential candidates for AC inhibitors.	transcription
78636	2	335388	6	NULL	NULL	0	NULL	NTPs	Chemical		activate					ITP	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_19_19955_s_309	14981084	In previous studies we showed that NTPs activate Gs-proteins in the order of potency GTP > ITP > UTP > XTP > CTP ( ,  ), rendering hypoxanthine, uracil, xanthine, and cytidine nucleotides potential candidates for AC inhibitors.	transcription
78637	3	335388	6	NULL	NULL	0	NULL	NTPs	Chemical		activate					UTP	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_19_19955_s_309	14981084	In previous studies we showed that NTPs activate Gs-proteins in the order of potency GTP > ITP > UTP > XTP > CTP ( ,  ), rendering hypoxanthine, uracil, xanthine, and cytidine nucleotides potential candidates for AC inhibitors.	transcription
78638	4	335388	6	NULL	NULL	0	NULL	NTPs	Chemical		activate					CTP	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_19_19955_s_309	14981084	In previous studies we showed that NTPs activate Gs-proteins in the order of potency GTP > ITP > UTP > XTP > CTP ( ,  ), rendering hypoxanthine, uracil, xanthine, and cytidine nucleotides potential candidates for AC inhibitors.	transcription
57363	1	335388	7	NULL	NULL	0	NULL	NTPs 			activate					Gs-proteins					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_19_19955_s_309	14981084	In previous studies we showed that NTPs activate Gs-proteins in the order of potency GTP > ITP > UTP > XTP > CTP ( ,  ), rendering hypoxanthine, uracil, xanthine, and cytidine nucleotides potential candidates for AC inhibitors.	transcription
57364	2	335388	7	NULL	NULL	0	NULL	hypoxanthine			candidate for		potential			AC inhibitors					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_19_19955_s_309	14981084	In previous studies we showed that NTPs activate Gs-proteins in the order of potency GTP > ITP > UTP > XTP > CTP ( ,  ), rendering hypoxanthine, uracil, xanthine, and cytidine nucleotides potential candidates for AC inhibitors.	transcription
57365	3	335388	7	NULL	NULL	0	NULL	uracil			candidate for		potential			AC inhibitors					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_19_19955_s_309	14981084	In previous studies we showed that NTPs activate Gs-proteins in the order of potency GTP > ITP > UTP > XTP > CTP ( ,  ), rendering hypoxanthine, uracil, xanthine, and cytidine nucleotides potential candidates for AC inhibitors.	transcription
57366	4	335388	7	NULL	NULL	0	NULL	xanthine			candidate for		potential			AC inhibitors					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_19_19955_s_309	14981084	In previous studies we showed that NTPs activate Gs-proteins in the order of potency GTP > ITP > UTP > XTP > CTP ( ,  ), rendering hypoxanthine, uracil, xanthine, and cytidine nucleotides potential candidates for AC inhibitors.	transcription
57367	5	335388	7	NULL	NULL	0	NULL	cytidine nucleotides 			candidate for		potential			AC inhibitors					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_19_19955_s_309	14981084	In previous studies we showed that NTPs activate Gs-proteins in the order of potency GTP > ITP > UTP > XTP > CTP ( ,  ), rendering hypoxanthine, uracil, xanthine, and cytidine nucleotides potential candidates for AC inhibitors.	transcription
57368	1	335389	7	NULL	NULL	0	NULL	ATP			mediate					Cytosine Salvage 					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_9865_s_136	11782482	ATP-mediated Cytosine Salvage-- Strikingly, cytosine was not utilized at all during ATP breakdown (results not shown), showing that the base is not deaminated to uracil and confirming the absence of cytidine phosphorylase and cytosine phosphoribosyltransferase activities in rat brain ( 13).	transcription
57369	2	335389	7	NULL	NULL	0	NULL	cytosine			not utilized during					ATP 		breakdown of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_9865_s_136	11782482	ATP-mediated Cytosine Salvage-- Strikingly, cytosine was not utilized at all during ATP breakdown (results not shown), showing that the base is not deaminated to uracil and confirming the absence of cytidine phosphorylase and cytosine phosphoribosyltransferase activities in rat brain ( 13).	transcription
57370	3	335389	7	NULL	NULL	0	NULL	cytosine			is not deaminated to					uracil					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_9865_s_136	11782482	ATP-mediated Cytosine Salvage-- Strikingly, cytosine was not utilized at all during ATP breakdown (results not shown), showing that the base is not deaminated to uracil and confirming the absence of cytidine phosphorylase and cytosine phosphoribosyltransferase activities in rat brain ( 13).	transcription
57371	4	335389	7	NULL	NULL	0	NULL	statement 3			confirms					cytidine phosphorylase		absence of			NULL	rat brain	0	NULL	NULL	NULL	gw60_jbiolchem_277_12_9865_s_136	11782482	ATP-mediated Cytosine Salvage-- Strikingly, cytosine was not utilized at all during ATP breakdown (results not shown), showing that the base is not deaminated to uracil and confirming the absence of cytidine phosphorylase and cytosine phosphoribosyltransferase activities in rat brain ( 13).	transcription
57372	5	335389	7	NULL	NULL	0	NULL	statement 3			confirms					cytosine phosphoribosyltransferase		absence of;;activities of			NULL	rat brain	0	NULL	NULL	NULL	gw60_jbiolchem_277_12_9865_s_136	11782482	ATP-mediated Cytosine Salvage-- Strikingly, cytosine was not utilized at all during ATP breakdown (results not shown), showing that the base is not deaminated to uracil and confirming the absence of cytidine phosphorylase and cytosine phosphoribosyltransferase activities in rat brain ( 13).	transcription
78629	1	335390	6	NULL	NULL	0	NULL	APOBEC-1	GP		forms a complex with					ACF	GP				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_20_0_165_s_431	11861601	APOBEC-1 forms a complex with an RNA-binding protein ACF and converts the specific  cytosine at position 6666 of apolipoprotein B mRNA to uracil by its intrinsic cytidine  deaminase activity, giving rise to mRNA encoding the chylomicron component ( 250,  251).	transcription
78630	2	335390	6	NULL	NULL	NULL	NULL	ACF	GP		is a type of					RNA-binding protein	GP				NULL		NULL	NULL	NULL	NULL	gw70_annurevimmunol_20_0_165_s_431	11861601	APOBEC-1 forms a complex with an RNA-binding protein ACF and converts the specific  cytosine at position 6666 of apolipoprotein B mRNA to uracil by its intrinsic cytidine  deaminase activity, giving rise to mRNA encoding the chylomicron component ( 250,  251).	transcription
78631	3	335390	6	NULL	NULL	0	NULL	apolipoprotein B mRNA	NucleicAcid		is converted to					uracil	Chemical				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_20_0_165_s_431	11861601	APOBEC-1 forms a complex with an RNA-binding protein ACF and converts the specific  cytosine at position 6666 of apolipoprotein B mRNA to uracil by its intrinsic cytidine  deaminase activity, giving rise to mRNA encoding the chylomicron component ( 250,  251).	transcription
78632	4	335390	6	NULL	NULL	0	NULL	APOBEC-1	GP		performs					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_20_0_165_s_431	11861601	APOBEC-1 forms a complex with an RNA-binding protein ACF and converts the specific  cytosine at position 6666 of apolipoprotein B mRNA to uracil by its intrinsic cytidine  deaminase activity, giving rise to mRNA encoding the chylomicron component ( 250,  251).	transcription
78633	5	335390	6	NULL	NULL	0	NULL	APOBEC-1	GP		deaminates					cytidine	Chemical				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_20_0_165_s_431	11861601	APOBEC-1 forms a complex with an RNA-binding protein ACF and converts the specific  cytosine at position 6666 of apolipoprotein B mRNA to uracil by its intrinsic cytidine  deaminase activity, giving rise to mRNA encoding the chylomicron component ( 250,  251).	transcription
78634	6	335390	6	NULL	NULL	0	NULL	mRNA	NucleicAcid		encodes					chylomicron component	CellComponent				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_20_0_165_s_431	11861601	APOBEC-1 forms a complex with an RNA-binding protein ACF and converts the specific  cytosine at position 6666 of apolipoprotein B mRNA to uracil by its intrinsic cytidine  deaminase activity, giving rise to mRNA encoding the chylomicron component ( 250,  251).	transcription
57373	1	335390	7	NULL	NULL	0	NULL	APOBEC-1			forms a complex with					ACF					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_20_0_165_s_431	11861601	APOBEC-1 forms a complex with an RNA-binding protein ACF and converts the specific  cytosine at position 6666 of apolipoprotein B mRNA to uracil by its intrinsic cytidine  deaminase activity, giving rise to mRNA encoding the chylomicron component ( 250,  251).	transcription
57374	2	335390	7	NULL	NULL	0	NULL	ACF			is a type of					RNA-binding protein					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_20_0_165_s_431	11861601	APOBEC-1 forms a complex with an RNA-binding protein ACF and converts the specific  cytosine at position 6666 of apolipoprotein B mRNA to uracil by its intrinsic cytidine  deaminase activity, giving rise to mRNA encoding the chylomicron component ( 250,  251).	transcription
57375	3	335390	7	NULL	NULL	0	NULL	apolipoprotein B mRNA			converted to				cytosine at position 6666	uracil					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_20_0_165_s_431	11861601	APOBEC-1 forms a complex with an RNA-binding protein ACF and converts the specific  cytosine at position 6666 of apolipoprotein B mRNA to uracil by its intrinsic cytidine  deaminase activity, giving rise to mRNA encoding the chylomicron component ( 250,  251).	transcription
57376	4	335390	7	NULL	NULL	0	NULL	statement 1			leads to					statement 3					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_20_0_165_s_431	11861601	APOBEC-1 forms a complex with an RNA-binding protein ACF and converts the specific  cytosine at position 6666 of apolipoprotein B mRNA to uracil by its intrinsic cytidine  deaminase activity, giving rise to mRNA encoding the chylomicron component ( 250,  251).	transcription
57377	5	335390	7	NULL	NULL	0	NULL	statement 3			occur by					cytidine deaminase 		intrinsic activity of			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_20_0_165_s_431	11861601	APOBEC-1 forms a complex with an RNA-binding protein ACF and converts the specific  cytosine at position 6666 of apolipoprotein B mRNA to uracil by its intrinsic cytidine  deaminase activity, giving rise to mRNA encoding the chylomicron component ( 250,  251).	transcription
57378	6	335390	7	NULL	NULL	0	NULL	statement 5			generates					mRNA					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_20_0_165_s_431	11861601	APOBEC-1 forms a complex with an RNA-binding protein ACF and converts the specific  cytosine at position 6666 of apolipoprotein B mRNA to uracil by its intrinsic cytidine  deaminase activity, giving rise to mRNA encoding the chylomicron component ( 250,  251).	transcription
57379	7	335390	7	NULL	NULL	0	NULL	mRNA			encodes					chylomicron component					NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_20_0_165_s_431	11861601	APOBEC-1 forms a complex with an RNA-binding protein ACF and converts the specific  cytosine at position 6666 of apolipoprotein B mRNA to uracil by its intrinsic cytidine  deaminase activity, giving rise to mRNA encoding the chylomicron component ( 250,  251).	transcription
57380	1	335391	7	NULL	NULL	0	NULL	adenosine			inhibits		marginally			[3]D-inosine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57381	2	335391	7	NULL	NULL	0	NULL	xanthosine			inhibits		marginally			[3]D-inosine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57382	3	335391	7	NULL	NULL	0	NULL	uridine			inhibits		marginally			[3]D-inosine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57383	4	335391	7	NULL	NULL	0	NULL	cytidine			inhibits		marginally			[3]D-inosine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57384	5	335391	7	NULL	NULL	0	NULL	thymidine			inhibits		marginally			[3]D-inosine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57385	6	335391	7	NULL	NULL	0	NULL	adenine			inhibits		marginally			[3]D-inosine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57386	7	335391	7	NULL	NULL	0	NULL	hypoxanthine			inhibits		marginally			[3]D-inosine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57387	8	335391	7	NULL	NULL	0	NULL	guanine			inhibits		marginally			[3]D-inosine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57388	9	335391	7	NULL	NULL	0	NULL	xanthine			inhibits		marginally			[3]D-inosine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57389	10	335391	7	NULL	NULL	0	NULL	thymine			inhibits		marginally			[3]D-inosine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57390	11	335391	7	NULL	NULL	0	NULL	uracil 			inhibits		marginally			[3]D-inosine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57391	12	335391	7	NULL	NULL	0	NULL	adenosine			is a type of					naturally occuring nucleoside					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57392	13	335391	7	NULL	NULL	0	NULL	xanthosine			is a type of					naturally occuring nucleoside					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57393	14	335391	7	NULL	NULL	0	NULL	uridine			is a type of					naturally occuring nucleoside					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57394	15	335391	7	NULL	NULL	0	NULL	cytidine			is a type of					naturally occuring nucleoside					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57395	16	335391	7	NULL	NULL	0	NULL	thymidine			is a type of					naturally occuring nucleoside					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57396	17	335391	7	NULL	NULL	0	NULL	adenine			is a type of					nucleobase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57397	18	335391	7	NULL	NULL	0	NULL	hypoxanthine			is a type of					nucleobase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57398	19	335391	7	NULL	NULL	0	NULL	guanine			is a type of					nucleobase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57399	20	335391	7	NULL	NULL	0	NULL	xanthine			is a type of					nucleobase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57400	21	335391	7	NULL	NULL	0	NULL	thymine			is a type of					nucleobase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
57401	22	335391	7	NULL	NULL	0	NULL	uracil			is a type of					nucleobase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20935_s_142	10783393	By contrast a 100-fold excess of the naturally occurring nucleosides, adenosine (<1%), xanthosine (35%), uridine (33%), cytidine (<1%), and thymidine (14%), as well as the nucleobases, adenine (6%), hypoxanthine (24%), guanine (26%), xanthine (12%), thymine (<1%), and uracil (1%), only inhibited 1 muM [3]D-inosine marginally (Fig.  7).	transcription
78626	1	335392	6	NULL	NULL	0	NULL	RNase-4	GP		prefers					Uracil	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_14902_s_116	10329690	Uracil was selected as the base because RNase-4, one of the targets for the inhibitors under development (see below), strongly prefers this pyrimidine over cytosine ( 17), and most of the other mammalian RNases bind uridine and cytidine nucleotides with similar affinity ( 1,  23,  27).	transcription
78627	2	335392	6	NULL	NULL	0	NULL	Uracil	Chemical		is a type of					pyrimidine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_14902_s_116	10329690	Uracil was selected as the base because RNase-4, one of the targets for the inhibitors under development (see below), strongly prefers this pyrimidine over cytosine ( 17), and most of the other mammalian RNases bind uridine and cytidine nucleotides with similar affinity ( 1,  23,  27).	transcription
57402	1	335392	7	NULL	NULL	0	NULL	RNases		mammalian	bind					uridine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_14902_s_116	10329690	Uracil was selected as the base because RNase-4, one of the targets for the inhibitors under development (see below), strongly prefers this pyrimidine over cytosine ( 17), and most of the other mammalian RNases bind uridine and cytidine nucleotides with similar affinity ( 1,  23,  27).	transcription
57403	2	335392	7	NULL	NULL	0	NULL	RNases		mammalian	bind					cytidine					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_14902_s_116	10329690	Uracil was selected as the base because RNase-4, one of the targets for the inhibitors under development (see below), strongly prefers this pyrimidine over cytosine ( 17), and most of the other mammalian RNases bind uridine and cytidine nucleotides with similar affinity ( 1,  23,  27).	transcription
57404	3	335392	7	NULL	NULL	0	NULL	statement 1			similar affinity to					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_14902_s_116	10329690	Uracil was selected as the base because RNase-4, one of the targets for the inhibitors under development (see below), strongly prefers this pyrimidine over cytosine ( 17), and most of the other mammalian RNases bind uridine and cytidine nucleotides with similar affinity ( 1,  23,  27).	transcription
78622	1	335393	6	NULL	NULL	0	NULL	APOBEC3	GP		is					apolipoprotein B-editing catalytic polypeptide 3	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_22161_s_27	16735504	As APOBEC3G, a member of the recently discovered human cytidine deaminase family named apolipoprotein B-editing catalytic polypeptide 3 (APOBEC3), deaminates cytosine residues to uracil in the growing minus strand viral DNA during retroviral reverse transcription, we wanted to evaluate whether members of the APOBEC3 family also interfere with L1 retrotransposition, which is also dependent on reverse transcription of template RNA.	transcription
78623	2	335393	6	NULL	NULL	0	NULL	APOBEC3	GP		belongs to					cytidine deaminase family		human			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_22161_s_27	16735504	As APOBEC3G, a member of the recently discovered human cytidine deaminase family named apolipoprotein B-editing catalytic polypeptide 3 (APOBEC3), deaminates cytosine residues to uracil in the growing minus strand viral DNA during retroviral reverse transcription, we wanted to evaluate whether members of the APOBEC3 family also interfere with L1 retrotransposition, which is also dependent on reverse transcription of template RNA.	transcription
78624	3	335393	6	NULL	NULL	0	NULL	cytosine			is converted to					Uracil					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_22161_s_27	16735504	As APOBEC3G, a member of the recently discovered human cytidine deaminase family named apolipoprotein B-editing catalytic polypeptide 3 (APOBEC3), deaminates cytosine residues to uracil in the growing minus strand viral DNA during retroviral reverse transcription, we wanted to evaluate whether members of the APOBEC3 family also interfere with L1 retrotransposition, which is also dependent on reverse transcription of template RNA.	transcription
78625	4	335393	6	NULL	NULL	0	NULL	statement 3	Process		occurs during					reverse transcription	Process	retroviral 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_22161_s_27	16735504	As APOBEC3G, a member of the recently discovered human cytidine deaminase family named apolipoprotein B-editing catalytic polypeptide 3 (APOBEC3), deaminates cytosine residues to uracil in the growing minus strand viral DNA during retroviral reverse transcription, we wanted to evaluate whether members of the APOBEC3 family also interfere with L1 retrotransposition, which is also dependent on reverse transcription of template RNA.	transcription
57405	1	335393	7	NULL	NULL	0	NULL	APOBEC3G			belongs to					cytidine deaminase family		human			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_22161_s_27	16735504	As APOBEC3G, a member of the recently discovered human cytidine deaminase family named apolipoprotein B-editing catalytic polypeptide 3 (APOBEC3), deaminates cytosine residues to uracil in the growing minus strand viral DNA during retroviral reverse transcription, we wanted to evaluate whether members of the APOBEC3 family also interfere with L1 retrotransposition, which is also dependent on reverse transcription of template RNA.	transcription
57406	2	335393	7	NULL	NULL	0	NULL	APOBEC3G			is					apolipoprotein B-editing catalytic polypeptide 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_22161_s_27	16735504	As APOBEC3G, a member of the recently discovered human cytidine deaminase family named apolipoprotein B-editing catalytic polypeptide 3 (APOBEC3), deaminates cytosine residues to uracil in the growing minus strand viral DNA during retroviral reverse transcription, we wanted to evaluate whether members of the APOBEC3 family also interfere with L1 retrotransposition, which is also dependent on reverse transcription of template RNA.	transcription
57407	3	335393	7	NULL	NULL	0	NULL	cytosine residues			deaminates to					uracil					NULL	growing minus strand viral DNA	0	NULL	NULL	NULL	gw70_jbiolchem_281_31_22161_s_27	16735504	As APOBEC3G, a member of the recently discovered human cytidine deaminase family named apolipoprotein B-editing catalytic polypeptide 3 (APOBEC3), deaminates cytosine residues to uracil in the growing minus strand viral DNA during retroviral reverse transcription, we wanted to evaluate whether members of the APOBEC3 family also interfere with L1 retrotransposition, which is also dependent on reverse transcription of template RNA.	transcription
57408	4	335393	7	NULL	NULL	0	NULL	APOBEC3			deaminates 					statement 3					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_31_22161_s_27	16735504	As APOBEC3G, a member of the recently discovered human cytidine deaminase family named apolipoprotein B-editing catalytic polypeptide 3 (APOBEC3), deaminates cytosine residues to uracil in the growing minus strand viral DNA during retroviral reverse transcription, we wanted to evaluate whether members of the APOBEC3 family also interfere with L1 retrotransposition, which is also dependent on reverse transcription of template RNA.	transcription
57409	5	335393	7	NULL	NULL	0	NULL	statement 3			during					retroviral reverse transcription					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_22161_s_27	16735504	As APOBEC3G, a member of the recently discovered human cytidine deaminase family named apolipoprotein B-editing catalytic polypeptide 3 (APOBEC3), deaminates cytosine residues to uracil in the growing minus strand viral DNA during retroviral reverse transcription, we wanted to evaluate whether members of the APOBEC3 family also interfere with L1 retrotransposition, which is also dependent on reverse transcription of template RNA.	transcription
57410	6	335393	7	NULL	NULL	0	NULL	L1 retrotransposition			depends on					template RNA		 reverse transcription of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_31_22161_s_27	16735504	As APOBEC3G, a member of the recently discovered human cytidine deaminase family named apolipoprotein B-editing catalytic polypeptide 3 (APOBEC3), deaminates cytosine residues to uracil in the growing minus strand viral DNA during retroviral reverse transcription, we wanted to evaluate whether members of the APOBEC3 family also interfere with L1 retrotransposition, which is also dependent on reverse transcription of template RNA.	transcription
78617	1	335395	6	NULL	NULL	0	NULL	L-tyrosine	AminoAcid		is converted to					L-dopa	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21225_s_235	16714291	The conversion of L-tyrosine to L-dopa by TH is the rate-limiting step for catecholamine biosynthesis ( ,  ), and PNMT catalyzes the synthesis of epinephrine from nor epinephrine ( ) ( Fig. 7 A).	transcription
78618	2	335395	6	NULL	NULL	0	NULL	TH	GP		performs					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21225_s_235	16714291	The conversion of L-tyrosine to L-dopa by TH is the rate-limiting step for catecholamine biosynthesis ( ,  ), and PNMT catalyzes the synthesis of epinephrine from nor epinephrine ( ) ( Fig. 7 A).	transcription
78619	3	335395	6	NULL	NULL	0	NULL	statement 1	Process		is a step for					catecholamine	Chemical	biosynthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21225_s_235	16714291	The conversion of L-tyrosine to L-dopa by TH is the rate-limiting step for catecholamine biosynthesis ( ,  ), and PNMT catalyzes the synthesis of epinephrine from nor epinephrine ( ) ( Fig. 7 A).	transcription
78620	4	335395	6	NULL	NULL	0	NULL	nor epinephrine	Chemical		is converted to					epinephrine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21225_s_235	16714291	The conversion of L-tyrosine to L-dopa by TH is the rate-limiting step for catecholamine biosynthesis ( ,  ), and PNMT catalyzes the synthesis of epinephrine from nor epinephrine ( ) ( Fig. 7 A).	transcription
78621	5	335395	6	NULL	NULL	0	NULL	PNMT	GP		catalyzes					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21225_s_235	16714291	The conversion of L-tyrosine to L-dopa by TH is the rate-limiting step for catecholamine biosynthesis ( ,  ), and PNMT catalyzes the synthesis of epinephrine from nor epinephrine ( ) ( Fig. 7 A).	transcription
57411	1	335395	7	NULL	NULL	0	NULL	 L-tyrosine			converted to					 L-dopa					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21225_s_235	16714291	The conversion of L-tyrosine to L-dopa by TH is the rate-limiting step for catecholamine biosynthesis ( ,  ), and PNMT catalyzes the synthesis of epinephrine from nor epinephrine ( ) ( Fig. 7 A).	transcription
57412	2	335395	7	NULL	NULL	0	NULL	TH			catalyze					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21225_s_235	16714291	The conversion of L-tyrosine to L-dopa by TH is the rate-limiting step for catecholamine biosynthesis ( ,  ), and PNMT catalyzes the synthesis of epinephrine from nor epinephrine ( ) ( Fig. 7 A).	transcription
57413	3	335395	7	NULL	NULL	0	NULL	statement 1			rate-limiting step for					catecholamine		biosynthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21225_s_235	16714291	The conversion of L-tyrosine to L-dopa by TH is the rate-limiting step for catecholamine biosynthesis ( ,  ), and PNMT catalyzes the synthesis of epinephrine from nor epinephrine ( ) ( Fig. 7 A).	transcription
57414	4	335395	7	NULL	NULL	0	NULL	epinephrine			synthesized from					nor epinephrine					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21225_s_235	16714291	The conversion of L-tyrosine to L-dopa by TH is the rate-limiting step for catecholamine biosynthesis ( ,  ), and PNMT catalyzes the synthesis of epinephrine from nor epinephrine ( ) ( Fig. 7 A).	transcription
57415	5	335395	7	NULL	NULL	0	NULL	PNMT			catalyze					statement 4					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21225_s_235	16714291	The conversion of L-tyrosine to L-dopa by TH is the rate-limiting step for catecholamine biosynthesis ( ,  ), and PNMT catalyzes the synthesis of epinephrine from nor epinephrine ( ) ( Fig. 7 A).	transcription
78607	1	335396	6	NULL	NULL	0	NULL	thrombin	GP		stimulates					platelets	cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
78608	2	335396	6	NULL	NULL	0	NULL	collagen	GP		stimulates					platelets	cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
78609	3	335396	6	NULL	NULL	0	NULL	ADP	Chemical		stimulates					platelets	cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
78610	4	335396	6	NULL	NULL	0	NULL	epinephrine	Chemical		stimulates					platelets	cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
78611	5	335396	6	NULL	NULL	0	NULL	calcium ionophore A23187	Chemical		stimulates					platelets	cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
78612	6	335396	6	NULL	NULL	0	NULL	thrombin	GP		induces					RAFTK	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
78613	7	335396	6	NULL	NULL	0	NULL	collagen	GP		induces					RAFTK	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
78614	8	335396	6	NULL	NULL	0	NULL	ADP	Chemical		induces					RAFTK	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
78615	9	335396	6	NULL	NULL	0	NULL	epinephrine	Chemical		induces					RAFTK	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
78616	10	335396	6	NULL	NULL	0	NULL	calcium ionophore A23187	Chemical		induces					RAFTK	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
57416	1	335396	7	NULL	NULL	0	NULL	thrombin			stimulates					platelets					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
57417	2	335396	7	NULL	NULL	0	NULL	collagen			stimulates					platelets					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
57418	3	335396	7	NULL	NULL	0	NULL	ADP			stimulates					platelets					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
57419	4	335396	7	NULL	NULL	0	NULL	epinephrine			stimulates					platelets					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
57420	5	335396	7	NULL	NULL	0	NULL	A23187 			stimulates					platelets					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
57421	6	335396	7	NULL	NULL	0	NULL	statement 1			induce					RAFTK		phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
57422	7	335396	7	NULL	NULL	0	NULL	statement 2			induce					RAFTK		phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
57423	8	335396	7	NULL	NULL	0	NULL	statement 3			induce					RAFTK		phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
57424	9	335396	7	NULL	NULL	0	NULL	statement 4			induce					RAFTK		phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
57425	10	335396	7	NULL	NULL	0	NULL	statement 5			induce					RAFTK		phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
57426	11	335396	7	NULL	NULL	0	NULL	A23187 			is a type of					calcium ionophore					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10941_s_40	9099753	Stimulation of platelets by several agonists including thrombin, collagen, ADP, epinephrine, and the calcium ionophore A23187 induced the tyrosine phosphorylation of RAFTK.	transcription
78516	1	335397	6	NULL	NULL	0	NULL	ADP			induces					beta3	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_22_13878_s_95	9593734	Thus, ADP and ADP + epinephrine induced tyrosine phosphorylation of beta3 in an aggregation-dependent manner.	transcription
78517	2	335397	6	NULL	NULL	0	NULL	ADP + epinephrine	Chemical		induces					beta3	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_22_13878_s_95	9593734	Thus, ADP and ADP + epinephrine induced tyrosine phosphorylation of beta3 in an aggregation-dependent manner.	transcription
57427	1	335397	7	NULL	NULL	0	NULL	ADP			induce					beta3		phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_22_13878_s_95	9593734	Thus, ADP and ADP + epinephrine induced tyrosine phosphorylation of beta3 in an aggregation-dependent manner.	transcription
57428	2	335397	7	NULL	NULL	0	NULL	ADP + epinephrine			induce					beta3		phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_22_13878_s_95	9593734	Thus, ADP and ADP + epinephrine induced tyrosine phosphorylation of beta3 in an aggregation-dependent manner.	transcription
57429	3	335397	7	NULL	NULL	0	NULL	statement 1			depends on					aggregation					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_22_13878_s_95	9593734	Thus, ADP and ADP + epinephrine induced tyrosine phosphorylation of beta3 in an aggregation-dependent manner.	transcription
57430	4	335397	7	NULL	NULL	0	NULL	statement 2			depends on					aggregation					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_22_13878_s_95	9593734	Thus, ADP and ADP + epinephrine induced tyrosine phosphorylation of beta3 in an aggregation-dependent manner.	transcription
78513	1	335398	6	NULL	NULL	0	NULL	thrombin	GP		induces					platelets	cell	aggregation of;; epinephrine-potentiated			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-biochem-(tokyo)_121_2_9089407_s_1	9089407	Tyrosine phosphorylation and Syk activation are involved in thrombin-induced aggregation of epinephrine-potentiated platelets..	transcription
78514	2	335398	6	NULL	NULL	0	NULL	Tyrosine	AminoAcid	phosphorylation of	is involved in					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-biochem-(tokyo)_121_2_9089407_s_1	9089407	Tyrosine phosphorylation and Syk activation are involved in thrombin-induced aggregation of epinephrine-potentiated platelets..	transcription
78515	3	335398	6	NULL	NULL	0	NULL	Syk	GP	activation of	is involved in					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-biochem-(tokyo)_121_2_9089407_s_1	9089407	Tyrosine phosphorylation and Syk activation are involved in thrombin-induced aggregation of epinephrine-potentiated platelets..	transcription
57431	1	335398	7	NULL	NULL	0	NULL	epinephrine			potentiate					platelets					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-biochem-(tokyo)_121_2_9089407_s_1	9089407	Tyrosine phosphorylation and Syk activation are involved in thrombin-induced aggregation of epinephrine-potentiated platelets..	transcription
57432	2	335398	7	NULL	NULL	0	NULL	thrombin			induce					statement 1		aggregation of 			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-biochem-(tokyo)_121_2_9089407_s_1	9089407	Tyrosine phosphorylation and Syk activation are involved in thrombin-induced aggregation of epinephrine-potentiated platelets..	transcription
57433	3	335398	7	NULL	NULL	0	NULL			phosphorylation of	is involved in			tyrosine		statement 2					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-biochem-(tokyo)_121_2_9089407_s_1	9089407	Tyrosine phosphorylation and Syk activation are involved in thrombin-induced aggregation of epinephrine-potentiated platelets..	transcription
57434	4	335398	7	NULL	NULL	0	NULL	Syk		activation of	is involved in					statement 2					NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-biochem-(tokyo)_121_2_9089407_s_1	9089407	Tyrosine phosphorylation and Syk activation are involved in thrombin-induced aggregation of epinephrine-potentiated platelets..	transcription
78509	1	335399	6	NULL	NULL	0	NULL	epinephrine	Chemical		phosphorylates					Insulin receptor	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_5_3254_s_257	14602724	Preincubation with sodium vanadate, an inhibitor of protein-tyrosine phosphatases, partially reversed the effects of epinephrine on the tyrosine phosphorylation of the insulin receptor ( Fig. 8 D).	transcription
78512	2	335399	6	NULL	NULL	0	NULL	sodium vanadate	Chemical		reverses					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_5_3254_s_257	14602724	Preincubation with sodium vanadate, an inhibitor of protein-tyrosine phosphatases, partially reversed the effects of epinephrine on the tyrosine phosphorylation of the insulin receptor ( Fig. 8 D).	transcription
57435	1	335399	7	NULL	NULL	0	NULL	epinephrine 			effect					insulin receptor		phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_5_3254_s_257	14602724	Preincubation with sodium vanadate, an inhibitor of protein-tyrosine phosphatases, partially reversed the effects of epinephrine on the tyrosine phosphorylation of the insulin receptor ( Fig. 8 D).	transcription
57436	2	335399	7	NULL	NULL	0	NULL	sodium vanadate			reverse		partially			statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_5_3254_s_257	14602724	Preincubation with sodium vanadate, an inhibitor of protein-tyrosine phosphatases, partially reversed the effects of epinephrine on the tyrosine phosphorylation of the insulin receptor ( Fig. 8 D).	transcription
57437	3	335399	7	NULL	NULL	0	NULL	sodium vanadate			is an inhibitor of					 protein-tyrosine phosphatases					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_5_3254_s_257	14602724	Preincubation with sodium vanadate, an inhibitor of protein-tyrosine phosphatases, partially reversed the effects of epinephrine on the tyrosine phosphorylation of the insulin receptor ( Fig. 8 D).	transcription
78505	1	335400	6	NULL	NULL	0	NULL	epinephrine	Chemical		induces					tyrosine	AminoAcid	phosphorylation of			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-biochem-(tokyo)_121_2_9089407_s_5	9089407	Although  epinephrine alone (4 microM) slightly induced protein-tyrosine phosphorylation  and Syk activation, the presence of epinephrine caused a shift to the  left in the dose-dependence of thrombin (0.01-0.5 U/ml)-induced tyrosine  phosphorylation and Syk activation, as well as platelet aggregation.	transcription
78506	2	335400	6	NULL	NULL	0	NULL	epinephrine	Chemical		induces					Syk	GP	activation of 			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-biochem-(tokyo)_121_2_9089407_s_5	9089407	Although  epinephrine alone (4 microM) slightly induced protein-tyrosine phosphorylation  and Syk activation, the presence of epinephrine caused a shift to the  left in the dose-dependence of thrombin (0.01-0.5 U/ml)-induced tyrosine  phosphorylation and Syk activation, as well as platelet aggregation.	transcription
78507	3	335400	6	NULL	NULL	0	NULL	epinephrine	Chemical		induces					platelet aggregation 	Process				NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-biochem-(tokyo)_121_2_9089407_s_5	9089407	Although  epinephrine alone (4 microM) slightly induced protein-tyrosine phosphorylation  and Syk activation, the presence of epinephrine caused a shift to the  left in the dose-dependence of thrombin (0.01-0.5 U/ml)-induced tyrosine  phosphorylation and Syk activation, as well as platelet aggregation.	transcription
57438	1	335400	7	NULL	NULL	0	NULL	epinephrine			induce		slightly			protein-tyrosine		phosphorylation of			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-biochem-(tokyo)_121_2_9089407_s_5	9089407	Although  epinephrine alone (4 microM) slightly induced protein-tyrosine phosphorylation  and Syk activation, the presence of epinephrine caused a shift to the  left in the dose-dependence of thrombin (0.01-0.5 U/ml)-induced tyrosine  phosphorylation and Syk activation, as well as platelet aggregation.	transcription
57439	2	335400	7	NULL	NULL	0	NULL	epinephrine			induce		slightly			Syk		activation of			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-biochem-(tokyo)_121_2_9089407_s_5	9089407	Although  epinephrine alone (4 microM) slightly induced protein-tyrosine phosphorylation  and Syk activation, the presence of epinephrine caused a shift to the  left in the dose-dependence of thrombin (0.01-0.5 U/ml)-induced tyrosine  phosphorylation and Syk activation, as well as platelet aggregation.	transcription
57440	3	335400	7	NULL	NULL	0	NULL	thrombin			induce							phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-biochem-(tokyo)_121_2_9089407_s_5	9089407	Although  epinephrine alone (4 microM) slightly induced protein-tyrosine phosphorylation  and Syk activation, the presence of epinephrine caused a shift to the  left in the dose-dependence of thrombin (0.01-0.5 U/ml)-induced tyrosine  phosphorylation and Syk activation, as well as platelet aggregation.	transcription
57441	4	335400	7	NULL	NULL	0	NULL	thrombin			induce					Syk		activation of			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-biochem-(tokyo)_121_2_9089407_s_5	9089407	Although  epinephrine alone (4 microM) slightly induced protein-tyrosine phosphorylation  and Syk activation, the presence of epinephrine caused a shift to the  left in the dose-dependence of thrombin (0.01-0.5 U/ml)-induced tyrosine  phosphorylation and Syk activation, as well as platelet aggregation.	transcription
57442	5	335400	7	NULL	NULL	0	NULL	thrombin			induce					platelet		aggregation of 			NULL		0	NULL	NULL	NULL	abs-batch0620-0649_j-biochem-(tokyo)_121_2_9089407_s_5	9089407	Although  epinephrine alone (4 microM) slightly induced protein-tyrosine phosphorylation  and Syk activation, the presence of epinephrine caused a shift to the  left in the dose-dependence of thrombin (0.01-0.5 U/ml)-induced tyrosine  phosphorylation and Syk activation, as well as platelet aggregation.	transcription
78736	1	335401	6	NULL	NULL	NULL	NULL	angiotensin II	GP		stimulates					p120/p125	GP	phosphorylation of;; tyrosine			NULL	liver endothelial cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_916_s_219	14741724	A similar finding was made in liver endothelial cells, in which  angiotensin II, vasopressin, and epinephrine stimulated tyrosine phosphorylation  of p120/125, p75/p78, and p66 proteins [ 2.	transcription
78737	2	335401	6	NULL	NULL	NULL	NULL	vasopressin	GP		stimulates					p75/p78	GP	phosphorylation of;; tyrosine			NULL	liver endothelial cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_916_s_219	14741724	A similar finding was made in liver endothelial cells, in which  angiotensin II, vasopressin, and epinephrine stimulated tyrosine phosphorylation  of p120/125, p75/p78, and p66 proteins [ 2.	transcription
78738	3	335401	6	NULL	NULL	0	NULL	epinephrine	GP		stimulates					p66	GP	phosphorylation of;; tyrosine			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_916_s_219	14741724	A similar finding was made in liver endothelial cells, in which  angiotensin II, vasopressin, and epinephrine stimulated tyrosine phosphorylation  of p120/125, p75/p78, and p66 proteins [ 2.	transcription
57443	1	335401	7	NULL	NULL	0	NULL	 angiotensin II			stimulate					p120/125		phosphorylation of 	tyrosine		NULL	liver endothelial cells	0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_916_s_219	14741724	A similar finding was made in liver endothelial cells, in which  angiotensin II, vasopressin, and epinephrine stimulated tyrosine phosphorylation  of p120/125, p75/p78, and p66 proteins [ 2.	transcription
57444	2	335401	7	NULL	NULL	0	NULL	angiotensin II			stimulate					 p75/p78		phosphorylation of	tyrosine		NULL	liver endothelial cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_916_s_219	14741724	A similar finding was made in liver endothelial cells, in which  angiotensin II, vasopressin, and epinephrine stimulated tyrosine phosphorylation  of p120/125, p75/p78, and p66 proteins [ 2.	transcription
57445	3	335401	7	NULL	NULL	0	NULL	angiotensin II			stimulate					p66 protein		phosphorylation of	tyrosine		NULL	liver endothelial cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_916_s_219	14741724	A similar finding was made in liver endothelial cells, in which  angiotensin II, vasopressin, and epinephrine stimulated tyrosine phosphorylation  of p120/125, p75/p78, and p66 proteins [ 2.	transcription
57446	4	335401	7	NULL	NULL	0	NULL	vasopressin			stimulate					p120/125		phosphorylation of	tyrosine		NULL	liver endothelial cells	0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_916_s_219	14741724	A similar finding was made in liver endothelial cells, in which  angiotensin II, vasopressin, and epinephrine stimulated tyrosine phosphorylation  of p120/125, p75/p78, and p66 proteins [ 2.	transcription
57447	5	335401	7	NULL	NULL	0	NULL	vasopressin			stimulate					p75/p78		phosphorylation of	tyrosine		NULL	liver endothelial cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_916_s_219	14741724	A similar finding was made in liver endothelial cells, in which  angiotensin II, vasopressin, and epinephrine stimulated tyrosine phosphorylation  of p120/125, p75/p78, and p66 proteins [ 2.	transcription
57448	6	335401	7	NULL	NULL	0	NULL	vasopressin			stimulate					p66 protein		phosphorylation of	tyrosine		NULL	liver endothelial cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_916_s_219	14741724	A similar finding was made in liver endothelial cells, in which  angiotensin II, vasopressin, and epinephrine stimulated tyrosine phosphorylation  of p120/125, p75/p78, and p66 proteins [ 2.	transcription
57449	7	335401	7	NULL	NULL	0	NULL	epinephrine			stimulate					p120/125		phosphorylation of	tyrosine		NULL	liver endothelial cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_916_s_219	14741724	A similar finding was made in liver endothelial cells, in which  angiotensin II, vasopressin, and epinephrine stimulated tyrosine phosphorylation  of p120/125, p75/p78, and p66 proteins [ 2.	transcription
57450	8	335401	7	NULL	NULL	0	NULL	epinephrine			stimulate					p75/p78		phosphorylation of	tyrosine		NULL	liver endothelial cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_916_s_219	14741724	A similar finding was made in liver endothelial cells, in which  angiotensin II, vasopressin, and epinephrine stimulated tyrosine phosphorylation  of p120/125, p75/p78, and p66 proteins [ 2.	transcription
57451	9	335401	7	NULL	NULL	0	NULL	epinephrine			stimulate					p66 protein		phosphorylation of	tyrosine		NULL	liver endothelial cells	NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_314_3_916_s_219	14741724	A similar finding was made in liver endothelial cells, in which  angiotensin II, vasopressin, and epinephrine stimulated tyrosine phosphorylation  of p120/125, p75/p78, and p66 proteins [ 2.	transcription
78739	1	335402	6	NULL	NULL	0	NULL	insulin	GP		induces					IRS-1	GP	phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_febslett_421_3_191_s_172	9468304	We have shown that chronic GH or acute epinephrine treatment can specifically decrease insulin-induced IRS-1 tyrosine phosphorylation and association with PI 3-kinase.	transcription
78740	2	335402	6	NULL	NULL	0	NULL	epinephrine	GP		decrease					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_421_3_191_s_172	9468304	We have shown that chronic GH or acute epinephrine treatment can specifically decrease insulin-induced IRS-1 tyrosine phosphorylation and association with PI 3-kinase.	transcription
78741	3	335402	6	NULL	NULL	0	NULL	GH	GP		decreases					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_421_3_191_s_172	9468304	We have shown that chronic GH or acute epinephrine treatment can specifically decrease insulin-induced IRS-1 tyrosine phosphorylation and association with PI 3-kinase.	transcription
57452	1	335402	7	NULL	NULL	0	NULL	insulin			induce					IRS-1		phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_febslett_421_3_191_s_172	9468304	We have shown that chronic GH or acute epinephrine treatment can specifically decrease insulin-induced IRS-1 tyrosine phosphorylation and association with PI 3-kinase.	transcription
57453	2	335402	7	NULL	NULL	0	NULL	insulin			induce					PI 3-kinase		association with			NULL		0	NULL	NULL	NULL	gw60_febslett_421_3_191_s_172	9468304	We have shown that chronic GH or acute epinephrine treatment can specifically decrease insulin-induced IRS-1 tyrosine phosphorylation and association with PI 3-kinase.	transcription
57454	3	335402	7	NULL	NULL	0	NULL	chronic GH		treatment with	decrease		specifically			statement 1					NULL		NULL	NULL	NULL	NULL	gw60_febslett_421_3_191_s_172	9468304	We have shown that chronic GH or acute epinephrine treatment can specifically decrease insulin-induced IRS-1 tyrosine phosphorylation and association with PI 3-kinase.	transcription
57455	4	335402	7	NULL	NULL	0	NULL	chronic GH		treatment with	decrease		specifically			statement 2					NULL		NULL	NULL	NULL	NULL	gw60_febslett_421_3_191_s_172	9468304	We have shown that chronic GH or acute epinephrine treatment can specifically decrease insulin-induced IRS-1 tyrosine phosphorylation and association with PI 3-kinase.	transcription
57456	5	335402	7	NULL	NULL	0	NULL	acute epinephrine 		treatment with	decrease		specifically			statement 1					NULL		NULL	NULL	NULL	NULL	gw60_febslett_421_3_191_s_172	9468304	We have shown that chronic GH or acute epinephrine treatment can specifically decrease insulin-induced IRS-1 tyrosine phosphorylation and association with PI 3-kinase.	transcription
57457	6	335402	7	NULL	NULL	0	NULL	acute epinephrine 		treatment with	decrease		specifically			statement 2					NULL		0	NULL	NULL	NULL	gw60_febslett_421_3_191_s_172	9468304	We have shown that chronic GH or acute epinephrine treatment can specifically decrease insulin-induced IRS-1 tyrosine phosphorylation and association with PI 3-kinase.	transcription
78742	1	335403	6	NULL	NULL	0	NULL	ST	Chemical		induces					Myocyte 	Cell	apoptosis of 			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_109	11093795	Tyrosine-kinase inhibition by 50 muM genistein blunted the protective effects of 0.1 muM epinephrine and serum against ST-induced myocyte apoptosis.	transcription
78743	2	335403	6	NULL	NULL	NULL	NULL	epinephrine	Chemical		protects					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_109	11093795	Tyrosine-kinase inhibition by 50 muM genistein blunted the protective effects of 0.1 muM epinephrine and serum against ST-induced myocyte apoptosis.	transcription
78744	3	335403	6	NULL	NULL	0	NULL	serum	CellComponent		protects					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_109	11093795	Tyrosine-kinase inhibition by 50 muM genistein blunted the protective effects of 0.1 muM epinephrine and serum against ST-induced myocyte apoptosis.	transcription
78745	4	335403	6	NULL	NULL	0	NULL	genistein	Chemical		inhibits					tyrosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_109	11093795	Tyrosine-kinase inhibition by 50 muM genistein blunted the protective effects of 0.1 muM epinephrine and serum against ST-induced myocyte apoptosis.	transcription
78746	5	335403	6	NULL	NULL	0	NULL	statement 4	Process		blunts					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_109	11093795	Tyrosine-kinase inhibition by 50 muM genistein blunted the protective effects of 0.1 muM epinephrine and serum against ST-induced myocyte apoptosis.	transcription
78747	6	335403	6	NULL	NULL	0	NULL	statement 4	Process		blunts					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_109	11093795	Tyrosine-kinase inhibition by 50 muM genistein blunted the protective effects of 0.1 muM epinephrine and serum against ST-induced myocyte apoptosis.	transcription
57458	1	335403	7	NULL	NULL	0	NULL	genistein			inhibits					Tyrosine-kinase					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_109	11093795	Tyrosine-kinase inhibition by 50 muM genistein blunted the protective effects of 0.1 muM epinephrine and serum against ST-induced myocyte apoptosis.	transcription
57459	2	335403	7	NULL	NULL	0	NULL	ST			induce					myocyte 		apoptosis of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_109	11093795	Tyrosine-kinase inhibition by 50 muM genistein blunted the protective effects of 0.1 muM epinephrine and serum against ST-induced myocyte apoptosis.	transcription
57460	3	335403	7	NULL	NULL	0	NULL	epinephrine 			protects					statement 2					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_109	11093795	Tyrosine-kinase inhibition by 50 muM genistein blunted the protective effects of 0.1 muM epinephrine and serum against ST-induced myocyte apoptosis.	transcription
57461	4	335403	7	NULL	NULL	0	NULL	serum			protects					statement 2					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_109	11093795	Tyrosine-kinase inhibition by 50 muM genistein blunted the protective effects of 0.1 muM epinephrine and serum against ST-induced myocyte apoptosis.	transcription
57462	5	335403	7	NULL	NULL	0	NULL	statement 1			blunts					statement 3					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_109	11093795	Tyrosine-kinase inhibition by 50 muM genistein blunted the protective effects of 0.1 muM epinephrine and serum against ST-induced myocyte apoptosis.	transcription
57463	6	335403	7	NULL	NULL	0	NULL	statement 1			blunts					statement 4					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_109	11093795	Tyrosine-kinase inhibition by 50 muM genistein blunted the protective effects of 0.1 muM epinephrine and serum against ST-induced myocyte apoptosis.	transcription
78748	1	335404	6	NULL	NULL	0	NULL	ST	Chemical		induces					cardiac myocytes	cell	adult, apoptosis of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_123	11093795	Altogether, these results suggested that the protective effect of epinephrine and serum on ST-induced apoptosis of adult cardiac myocytes could involve tyrosine-kinase-mediated ERK activation.	transcription
78749	2	335404	6	NULL	NULL	0	NULL	serum	CellComponent		protects					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_123	11093795	Altogether, these results suggested that the protective effect of epinephrine and serum on ST-induced apoptosis of adult cardiac myocytes could involve tyrosine-kinase-mediated ERK activation.	transcription
78750	3	335404	6	NULL	NULL	0	NULL	epinephrine	Chemical		protects					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_123	11093795	Altogether, these results suggested that the protective effect of epinephrine and serum on ST-induced apoptosis of adult cardiac myocytes could involve tyrosine-kinase-mediated ERK activation.	transcription
78751	4	335404	6	NULL	NULL	0	NULL	Tyrosine kinase	GP		mediates					ERK	GP	activation of 			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_123	11093795	Altogether, these results suggested that the protective effect of epinephrine and serum on ST-induced apoptosis of adult cardiac myocytes could involve tyrosine-kinase-mediated ERK activation.	transcription
78752	5	335404	6	NULL	NULL	0	NULL	statement 2	Process		involve		could			statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_123	11093795	Altogether, these results suggested that the protective effect of epinephrine and serum on ST-induced apoptosis of adult cardiac myocytes could involve tyrosine-kinase-mediated ERK activation.	transcription
78753	6	335404	6	NULL	NULL	0	NULL	statement 3	Process		involve		could			statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_123	11093795	Altogether, these results suggested that the protective effect of epinephrine and serum on ST-induced apoptosis of adult cardiac myocytes could involve tyrosine-kinase-mediated ERK activation.	transcription
57464	1	335404	7	NULL	NULL	0	NULL	ST			induce					cardiac myocytes		apoptosis of adult			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_123	11093795	Altogether, these results suggested that the protective effect of epinephrine and serum on ST-induced apoptosis of adult cardiac myocytes could involve tyrosine-kinase-mediated ERK activation.	transcription
57465	2	335404	7	NULL	NULL	0	NULL	tyrosine-kinase			mediates					ERK		activation of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_123	11093795	Altogether, these results suggested that the protective effect of epinephrine and serum on ST-induced apoptosis of adult cardiac myocytes could involve tyrosine-kinase-mediated ERK activation.	transcription
57466	3	335404	7	NULL	NULL	0	NULL	epinephrine			protects					statement 1					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_123	11093795	Altogether, these results suggested that the protective effect of epinephrine and serum on ST-induced apoptosis of adult cardiac myocytes could involve tyrosine-kinase-mediated ERK activation.	transcription
57467	4	335404	7	NULL	NULL	0	NULL	serum			protects					statement 1					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_123	11093795	Altogether, these results suggested that the protective effect of epinephrine and serum on ST-induced apoptosis of adult cardiac myocytes could involve tyrosine-kinase-mediated ERK activation.	transcription
57468	5	335404	7	NULL	NULL	0	NULL	statement 1			involves					statement 2					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_58_6_1546_s_123	11093795	Altogether, these results suggested that the protective effect of epinephrine and serum on ST-induced apoptosis of adult cardiac myocytes could involve tyrosine-kinase-mediated ERK activation.	transcription
78754	1	335405	6	NULL	NULL	0	NULL	Tyrosine hydroxylase 1	GP		is					TH 1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_26683_s_11	10842166	The first and major rate-limiting regulatory step in the biosynthesis of the catecholamines (dopamine, norepinephrine, and epinephrine) is catalyzed by tyrosine hydroxylase (TH)1 ( 1).	transcription
78755	2	335405	6	NULL	NULL	0	NULL	dopamine	Chemical		is a type of					catecholamine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_26683_s_11	10842166	The first and major rate-limiting regulatory step in the biosynthesis of the catecholamines (dopamine, norepinephrine, and epinephrine) is catalyzed by tyrosine hydroxylase (TH)1 ( 1).	transcription
78757	3	335405	6	NULL	NULL	0	NULL	norepinephrine	Chemical		is a type of					catecholamine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_26683_s_11	10842166	The first and major rate-limiting regulatory step in the biosynthesis of the catecholamines (dopamine, norepinephrine, and epinephrine) is catalyzed by tyrosine hydroxylase (TH)1 ( 1).	transcription
78758	4	335405	6	NULL	NULL	0	NULL	epinephrine	Chemical		is a type of					catecholamine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_26683_s_11	10842166	The first and major rate-limiting regulatory step in the biosynthesis of the catecholamines (dopamine, norepinephrine, and epinephrine) is catalyzed by tyrosine hydroxylase (TH)1 ( 1).	transcription
78759	5	335405	6	NULL	NULL	0	NULL	TH 1	GP		catalyzes					dopamine	Chemical	biosynthesis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_26683_s_11	10842166	The first and major rate-limiting regulatory step in the biosynthesis of the catecholamines (dopamine, norepinephrine, and epinephrine) is catalyzed by tyrosine hydroxylase (TH)1 ( 1).	transcription
78760	6	335405	6	NULL	NULL	NULL	NULL	TH 1	GP		catalyzes					norepinephrine	Chemical	biosynthesis of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_35_26683_s_11	10842166	The first and major rate-limiting regulatory step in the biosynthesis of the catecholamines (dopamine, norepinephrine, and epinephrine) is catalyzed by tyrosine hydroxylase (TH)1 ( 1).	transcription
78761	7	335405	6	NULL	NULL	0	NULL	TH 1	GP		catalyzes					epinephrine	Chemical	biosynthesis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_26683_s_11	10842166	The first and major rate-limiting regulatory step in the biosynthesis of the catecholamines (dopamine, norepinephrine, and epinephrine) is catalyzed by tyrosine hydroxylase (TH)1 ( 1).	transcription
57469	1	335405	7	NULL	NULL	0	NULL	(TH)1			catalyze					dopamine		major rate-limiting regulatory step in biosynthesis of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_35_26683_s_11	10842166	The first and major rate-limiting regulatory step in the biosynthesis of the catecholamines (dopamine, norepinephrine, and epinephrine) is catalyzed by tyrosine hydroxylase (TH)1 ( 1).	transcription
57470	2	335405	7	NULL	NULL	0	NULL	(TH)1			catalyze					norepinephrine		major rate-limiting regulatory step in biosynthesis of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_35_26683_s_11	10842166	The first and major rate-limiting regulatory step in the biosynthesis of the catecholamines (dopamine, norepinephrine, and epinephrine) is catalyzed by tyrosine hydroxylase (TH)1 ( 1).	transcription
57471	3	335405	7	NULL	NULL	0	NULL	(TH)1			catalyze					epinephrine		major rate-limiting regulatory step in biosynthesis of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_35_26683_s_11	10842166	The first and major rate-limiting regulatory step in the biosynthesis of the catecholamines (dopamine, norepinephrine, and epinephrine) is catalyzed by tyrosine hydroxylase (TH)1 ( 1).	transcription
57472	4	335405	7	NULL	NULL	0	NULL	TH			is					tyrosine hydroxylase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_26683_s_11	10842166	The first and major rate-limiting regulatory step in the biosynthesis of the catecholamines (dopamine, norepinephrine, and epinephrine) is catalyzed by tyrosine hydroxylase (TH)1 ( 1).	transcription
57473	5	335405	7	NULL	NULL	0	NULL	dopamine			is a type of					catecholamine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_26683_s_11	10842166	The first and major rate-limiting regulatory step in the biosynthesis of the catecholamines (dopamine, norepinephrine, and epinephrine) is catalyzed by tyrosine hydroxylase (TH)1 ( 1).	transcription
57474	6	335405	7	NULL	NULL	0	NULL	norepinephrine			is a type of					catecholamine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_26683_s_11	10842166	The first and major rate-limiting regulatory step in the biosynthesis of the catecholamines (dopamine, norepinephrine, and epinephrine) is catalyzed by tyrosine hydroxylase (TH)1 ( 1).	transcription
57475	7	335405	7	NULL	NULL	0	NULL	epinephrine 			is a type of					catecholamine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_35_26683_s_11	10842166	The first and major rate-limiting regulatory step in the biosynthesis of the catecholamines (dopamine, norepinephrine, and epinephrine) is catalyzed by tyrosine hydroxylase (TH)1 ( 1).	transcription
78762	1	335406	6	NULL	NULL	0	NULL	epinephrine receptor	GP		activates					adenylcyclase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5226_s_260	9478978	The signal transduction pathway by which this is accomplished, involving transactivation of the EGF receptor and other tyrosine kinases, offers the opportunity for amplification of the signals and a prolonged response, much like the activation of adenylcyclase by the epinephrine receptor.	transcription
57476	1	335406	7	NULL	NULL	0	NULL	epinephrine receptor			activates					adenylcyclase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5226_s_260	9478978	The signal transduction pathway by which this is accomplished, involving transactivation of the EGF receptor and other tyrosine kinases, offers the opportunity for amplification of the signals and a prolonged response, much like the activation of adenylcyclase by the epinephrine receptor.	transcription
57477	2	335406	7	NULL	NULL	0	NULL	EGF receptor		transactivation of 	offers					amplification of signals		opportunity for			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5226_s_260	9478978	The signal transduction pathway by which this is accomplished, involving transactivation of the EGF receptor and other tyrosine kinases, offers the opportunity for amplification of the signals and a prolonged response, much like the activation of adenylcyclase by the epinephrine receptor.	transcription
57478	3	335406	7	NULL	NULL	0	NULL	statement 2			leads to					prolonged response					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5226_s_260	9478978	The signal transduction pathway by which this is accomplished, involving transactivation of the EGF receptor and other tyrosine kinases, offers the opportunity for amplification of the signals and a prolonged response, much like the activation of adenylcyclase by the epinephrine receptor.	transcription
78763	1	335407	6	NULL	NULL	0	NULL	thrombin	GP		induces					Vav	GP	phosphorylation of;; tyrosine			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_13_7544_s_88	8631786	Tyrosine Phosphorylation of Vav Is Induced by Thrombin  and Collagen, but Not by Other AgonistsIn order to determine if  other platelet agonists that work through G protein-coupled receptors  can cause Vav phosphorylation, we next stimulated platelets with either  U46619, epinephrine, or ADP. U46619 activates platelet TxA   receptors, epinephrine activates platelet  alpha -adrenergic receptors, and ADP is believed to activate  an unidentified purinergic receptor ( Fig. 3,  A  and  B).	transcription
78764	2	335407	6	NULL	NULL	0	NULL	collagen	GP		induces					Vav	GP	phosphorylation of;; tyrosine			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_13_7544_s_88	8631786	Tyrosine Phosphorylation of Vav Is Induced by Thrombin  and Collagen, but Not by Other AgonistsIn order to determine if  other platelet agonists that work through G protein-coupled receptors  can cause Vav phosphorylation, we next stimulated platelets with either  U46619, epinephrine, or ADP. U46619 activates platelet TxA   receptors, epinephrine activates platelet  alpha -adrenergic receptors, and ADP is believed to activate  an unidentified purinergic receptor ( Fig. 3,  A  and  B).	transcription
78765	3	335407	6	NULL	NULL	0	NULL	U46619	Chemical		activates					platelet TxA receptors	Cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_13_7544_s_88	8631786	Tyrosine Phosphorylation of Vav Is Induced by Thrombin  and Collagen, but Not by Other AgonistsIn order to determine if  other platelet agonists that work through G protein-coupled receptors  can cause Vav phosphorylation, we next stimulated platelets with either  U46619, epinephrine, or ADP. U46619 activates platelet TxA   receptors, epinephrine activates platelet  alpha -adrenergic receptors, and ADP is believed to activate  an unidentified purinergic receptor ( Fig. 3,  A  and  B).	transcription
78766	4	335407	6	NULL	NULL	0	NULL	epinephrine	GP		activates					platelet alpha -adrenergic receptor	cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_13_7544_s_88	8631786	Tyrosine Phosphorylation of Vav Is Induced by Thrombin  and Collagen, but Not by Other AgonistsIn order to determine if  other platelet agonists that work through G protein-coupled receptors  can cause Vav phosphorylation, we next stimulated platelets with either  U46619, epinephrine, or ADP. U46619 activates platelet TxA   receptors, epinephrine activates platelet  alpha -adrenergic receptors, and ADP is believed to activate  an unidentified purinergic receptor ( Fig. 3,  A  and  B).	transcription
57491	1	335407	7	NULL	NULL	0	NULL	Thrombin			induce					Vav		Phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_13_7544_s_88	8631786	Tyrosine Phosphorylation of Vav Is Induced by Thrombin  and Collagen, but Not by Other AgonistsIn order to determine if  other platelet agonists that work through G protein-coupled receptors  can cause Vav phosphorylation, we next stimulated platelets with either  U46619, epinephrine, or ADP. U46619 activates platelet TxA   receptors, epinephrine activates platelet  alpha -adrenergic receptors, and ADP is believed to activate  an unidentified purinergic receptor ( Fig. 3,  A  and  B).	transcription
57492	2	335407	7	NULL	NULL	0	NULL	collagen			induce					Vav		phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_13_7544_s_88	8631786	Tyrosine Phosphorylation of Vav Is Induced by Thrombin  and Collagen, but Not by Other AgonistsIn order to determine if  other platelet agonists that work through G protein-coupled receptors  can cause Vav phosphorylation, we next stimulated platelets with either  U46619, epinephrine, or ADP. U46619 activates platelet TxA   receptors, epinephrine activates platelet  alpha -adrenergic receptors, and ADP is believed to activate  an unidentified purinergic receptor ( Fig. 3,  A  and  B).	transcription
57493	3	335407	7	NULL	NULL	0	NULL	U46619			activates					TxA receptor		platelet			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_13_7544_s_88	8631786	Tyrosine Phosphorylation of Vav Is Induced by Thrombin  and Collagen, but Not by Other AgonistsIn order to determine if  other platelet agonists that work through G protein-coupled receptors  can cause Vav phosphorylation, we next stimulated platelets with either  U46619, epinephrine, or ADP. U46619 activates platelet TxA   receptors, epinephrine activates platelet  alpha -adrenergic receptors, and ADP is believed to activate  an unidentified purinergic receptor ( Fig. 3,  A  and  B).	transcription
57494	4	335407	7	NULL	NULL	0	NULL	epinephrine			activates					alpha -adrenergic receptor		platelet			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_13_7544_s_88	8631786	Tyrosine Phosphorylation of Vav Is Induced by Thrombin  and Collagen, but Not by Other AgonistsIn order to determine if  other platelet agonists that work through G protein-coupled receptors  can cause Vav phosphorylation, we next stimulated platelets with either  U46619, epinephrine, or ADP. U46619 activates platelet TxA   receptors, epinephrine activates platelet  alpha -adrenergic receptors, and ADP is believed to activate  an unidentified purinergic receptor ( Fig. 3,  A  and  B).	transcription
57495	5	335407	7	NULL	NULL	0	NULL	ADP			activates					unidentified purinergic receptor					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_13_7544_s_88	8631786	Tyrosine Phosphorylation of Vav Is Induced by Thrombin  and Collagen, but Not by Other AgonistsIn order to determine if  other platelet agonists that work through G protein-coupled receptors  can cause Vav phosphorylation, we next stimulated platelets with either  U46619, epinephrine, or ADP. U46619 activates platelet TxA   receptors, epinephrine activates platelet  alpha -adrenergic receptors, and ADP is believed to activate  an unidentified purinergic receptor ( Fig. 3,  A  and  B).	transcription
57502	1	335409	7	NULL	NULL	0	NULL	tyrosine			converted to					dopa					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27051_s_60	9765218	We initially examined the functional role of V-1 in the regulation of expression of genes encoding TH ( 36), AADC ( 37), DBH ( 38), and PNMT ( 39,  40), which catalyze the four synthetic successive steps from tyrosine to dopa, dopamine, norepinephrine, and epinephrine.	transcription
57503	2	335409	7	NULL	NULL	0	NULL	TH 			catalyze					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27051_s_60	9765218	We initially examined the functional role of V-1 in the regulation of expression of genes encoding TH ( 36), AADC ( 37), DBH ( 38), and PNMT ( 39,  40), which catalyze the four synthetic successive steps from tyrosine to dopa, dopamine, norepinephrine, and epinephrine.	transcription
57504	3	335409	7	NULL	NULL	0	NULL	dopa			converted to					dopamine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27051_s_60	9765218	We initially examined the functional role of V-1 in the regulation of expression of genes encoding TH ( 36), AADC ( 37), DBH ( 38), and PNMT ( 39,  40), which catalyze the four synthetic successive steps from tyrosine to dopa, dopamine, norepinephrine, and epinephrine.	transcription
57505	4	335409	7	NULL	NULL	0	NULL	AADC			catalyze					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27051_s_60	9765218	We initially examined the functional role of V-1 in the regulation of expression of genes encoding TH ( 36), AADC ( 37), DBH ( 38), and PNMT ( 39,  40), which catalyze the four synthetic successive steps from tyrosine to dopa, dopamine, norepinephrine, and epinephrine.	transcription
57506	5	335409	7	NULL	NULL	0	NULL	dopamine			converted to					norepinephrine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27051_s_60	9765218	We initially examined the functional role of V-1 in the regulation of expression of genes encoding TH ( 36), AADC ( 37), DBH ( 38), and PNMT ( 39,  40), which catalyze the four synthetic successive steps from tyrosine to dopa, dopamine, norepinephrine, and epinephrine.	transcription
57507	6	335409	7	NULL	NULL	0	NULL	DBH			catalyze					statement 5					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27051_s_60	9765218	We initially examined the functional role of V-1 in the regulation of expression of genes encoding TH ( 36), AADC ( 37), DBH ( 38), and PNMT ( 39,  40), which catalyze the four synthetic successive steps from tyrosine to dopa, dopamine, norepinephrine, and epinephrine.	transcription
57508	7	335409	7	NULL	NULL	0	NULL	norepinephrine			converted to					epinephrine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27051_s_60	9765218	We initially examined the functional role of V-1 in the regulation of expression of genes encoding TH ( 36), AADC ( 37), DBH ( 38), and PNMT ( 39,  40), which catalyze the four synthetic successive steps from tyrosine to dopa, dopamine, norepinephrine, and epinephrine.	transcription
57509	8	335409	7	NULL	NULL	0	NULL	PNMT			catalyze					statement 7					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27051_s_60	9765218	We initially examined the functional role of V-1 in the regulation of expression of genes encoding TH ( 36), AADC ( 37), DBH ( 38), and PNMT ( 39,  40), which catalyze the four synthetic successive steps from tyrosine to dopa, dopamine, norepinephrine, and epinephrine.	transcription
57510	9	335409	7	NULL	NULL	0	NULL	V-1 			regulates					TH gene		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27051_s_60	9765218	We initially examined the functional role of V-1 in the regulation of expression of genes encoding TH ( 36), AADC ( 37), DBH ( 38), and PNMT ( 39,  40), which catalyze the four synthetic successive steps from tyrosine to dopa, dopamine, norepinephrine, and epinephrine.	transcription
57511	10	335409	7	NULL	NULL	0	NULL	V-1			regulates					AADC gene		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27051_s_60	9765218	We initially examined the functional role of V-1 in the regulation of expression of genes encoding TH ( 36), AADC ( 37), DBH ( 38), and PNMT ( 39,  40), which catalyze the four synthetic successive steps from tyrosine to dopa, dopamine, norepinephrine, and epinephrine.	transcription
57512	11	335409	7	NULL	NULL	0	NULL	V-1 			regulates					DBH gene		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27051_s_60	9765218	We initially examined the functional role of V-1 in the regulation of expression of genes encoding TH ( 36), AADC ( 37), DBH ( 38), and PNMT ( 39,  40), which catalyze the four synthetic successive steps from tyrosine to dopa, dopamine, norepinephrine, and epinephrine.	transcription
57513	12	335409	7	NULL	NULL	0	NULL	V-1			regulates					PNMT gene		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_42_27051_s_60	9765218	We initially examined the functional role of V-1 in the regulation of expression of genes encoding TH ( 36), AADC ( 37), DBH ( 38), and PNMT ( 39,  40), which catalyze the four synthetic successive steps from tyrosine to dopa, dopamine, norepinephrine, and epinephrine.	transcription
78773	1	335410	6	NULL	NULL	0	NULL	catecholamine	Chemical		response to					hypoglycemia	MedicalFinding				NULL		0	NULL	NULL	NULL	gw70_diabetes_54_12_3592_s_131	16306382	Assuming that the catecholamine biosynthetic enzyme protein and enzymatic activities paralleled the mRNA levels and that the reduced biosynthetic enzyme activities were sufficient to reduce adrenomedullary catecholamine contents, these data are consistent with the hypotheses that  1) reduced tyrosine hydroxylase activity contributes to reduced catecholamine responses to hypoglycemia in diabetes and  2) reduced phenylethanolamine  N-methyltransferase activity contributes to further reduced epinephrine responses to hypoglycemia following recent hypoglycemia.	transcription
78774	2	335410	6	NULL	NULL	0	NULL	tyrosine hydroxylase activity 	Process	reduction of 	contributes to					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_diabetes_54_12_3592_s_131	16306382	Assuming that the catecholamine biosynthetic enzyme protein and enzymatic activities paralleled the mRNA levels and that the reduced biosynthetic enzyme activities were sufficient to reduce adrenomedullary catecholamine contents, these data are consistent with the hypotheses that  1) reduced tyrosine hydroxylase activity contributes to reduced catecholamine responses to hypoglycemia in diabetes and  2) reduced phenylethanolamine  N-methyltransferase activity contributes to further reduced epinephrine responses to hypoglycemia following recent hypoglycemia.	transcription
78775	3	335410	6	NULL	NULL	0	NULL	epinephrine	Chemical		is responsive to					hypoglycemia	MedicalFinding				NULL		0	NULL	NULL	NULL	gw70_diabetes_54_12_3592_s_131	16306382	Assuming that the catecholamine biosynthetic enzyme protein and enzymatic activities paralleled the mRNA levels and that the reduced biosynthetic enzyme activities were sufficient to reduce adrenomedullary catecholamine contents, these data are consistent with the hypotheses that  1) reduced tyrosine hydroxylase activity contributes to reduced catecholamine responses to hypoglycemia in diabetes and  2) reduced phenylethanolamine  N-methyltransferase activity contributes to further reduced epinephrine responses to hypoglycemia following recent hypoglycemia.	transcription
78776	4	335410	6	NULL	NULL	0	NULL	phenylethanolamine N-methyltransferase activity	Process		contributes to					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_diabetes_54_12_3592_s_131	16306382	Assuming that the catecholamine biosynthetic enzyme protein and enzymatic activities paralleled the mRNA levels and that the reduced biosynthetic enzyme activities were sufficient to reduce adrenomedullary catecholamine contents, these data are consistent with the hypotheses that  1) reduced tyrosine hydroxylase activity contributes to reduced catecholamine responses to hypoglycemia in diabetes and  2) reduced phenylethanolamine  N-methyltransferase activity contributes to further reduced epinephrine responses to hypoglycemia following recent hypoglycemia.	transcription
57514	1	335410	7	NULL	NULL	0	NULL	tyrosine hydroxylase		reduced activity of	contributes to					catecholamine 		reduced response of			NULL		0	NULL	NULL	NULL	gw70_diabetes_54_12_3592_s_131	16306382	Assuming that the catecholamine biosynthetic enzyme protein and enzymatic activities paralleled the mRNA levels and that the reduced biosynthetic enzyme activities were sufficient to reduce adrenomedullary catecholamine contents, these data are consistent with the hypotheses that  1) reduced tyrosine hydroxylase activity contributes to reduced catecholamine responses to hypoglycemia in diabetes and  2) reduced phenylethanolamine  N-methyltransferase activity contributes to further reduced epinephrine responses to hypoglycemia following recent hypoglycemia.	transcription
57515	2	335410	7	NULL	NULL	0	NULL	statement 1			in response to					hypoglycemia					NULL	diabetes	NULL	NULL	NULL	NULL	gw70_diabetes_54_12_3592_s_131	16306382	Assuming that the catecholamine biosynthetic enzyme protein and enzymatic activities paralleled the mRNA levels and that the reduced biosynthetic enzyme activities were sufficient to reduce adrenomedullary catecholamine contents, these data are consistent with the hypotheses that  1) reduced tyrosine hydroxylase activity contributes to reduced catecholamine responses to hypoglycemia in diabetes and  2) reduced phenylethanolamine  N-methyltransferase activity contributes to further reduced epinephrine responses to hypoglycemia following recent hypoglycemia.	transcription
57516	3	335410	7	NULL	NULL	0	NULL	phenylethanolamine N-methyltransferase		reduced activity of	contribute to					epinephrine		reduced response of			NULL		0	NULL	NULL	NULL	gw70_diabetes_54_12_3592_s_131	16306382	Assuming that the catecholamine biosynthetic enzyme protein and enzymatic activities paralleled the mRNA levels and that the reduced biosynthetic enzyme activities were sufficient to reduce adrenomedullary catecholamine contents, these data are consistent with the hypotheses that  1) reduced tyrosine hydroxylase activity contributes to reduced catecholamine responses to hypoglycemia in diabetes and  2) reduced phenylethanolamine  N-methyltransferase activity contributes to further reduced epinephrine responses to hypoglycemia following recent hypoglycemia.	transcription
57517	4	335410	7	NULL	NULL	0	NULL	statement 3			in response to					hypoglycemia					NULL		0	NULL	NULL	NULL	gw70_diabetes_54_12_3592_s_131	16306382	Assuming that the catecholamine biosynthetic enzyme protein and enzymatic activities paralleled the mRNA levels and that the reduced biosynthetic enzyme activities were sufficient to reduce adrenomedullary catecholamine contents, these data are consistent with the hypotheses that  1) reduced tyrosine hydroxylase activity contributes to reduced catecholamine responses to hypoglycemia in diabetes and  2) reduced phenylethanolamine  N-methyltransferase activity contributes to further reduced epinephrine responses to hypoglycemia following recent hypoglycemia.	transcription
78777	1	335411	6	NULL	NULL	0	NULL	PKC	GP		induces					p125FAK	GP	phosphorylation of;; serine			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
78778	2	335411	6	NULL	NULL	0	NULL	statement 1	Process		regulate					focal adhesion kinase	GP	intracellular stability of			NULL	mouse 3T3 cells	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
78779	3	335411	6	NULL	NULL	0	NULL	p125FAK	GP		is activated					PKC	GP	downstream of 			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57518	1	335411	7	NULL	NULL	0	NULL	epinephrine			stimulate					 p125FAK		phosphorylation of	tyrosine		NULL	platelets	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57519	2	335411	7	NULL	NULL	0	NULL	anti-LIBS6 antibody 30			stimulate					p125FAK		phosphorylation of	tyrosine		NULL	platelets	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57520	3	335411	7	NULL	NULL	0	NULL	statement 1			occur simulataneous with					statement 2					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57521	4	335411	7	NULL	NULL	0	NULL	fibrinogen		platelets adherent  to	stimulate					p125FAK		phosphorylation of	tyrosine		NULL	platelets	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57522	5	335411	7	NULL	NULL	0	NULL	IgG		platelets adherent  to immobilized	stimulate					p125FAK		phosphorylation of	tyrosine		NULL	platelets	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57523	6	335411	7	NULL	NULL	0	NULL	statement 3			is an alternative to					statement 4					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57524	7	335411	7	NULL	NULL	0	NULL	bisindolylmaleimide			inhibits					PKC		activity of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57525	8	335411	7	NULL	NULL	0	NULL	GF 109203X			inhibits					PKC		activity of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57526	9	335411	7	NULL	NULL	0	NULL	statement 3			is an alternative to					statement 5					NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57527	10	335411	7	NULL	NULL	0	NULL	statement 4			is an alternative to					statement 5					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57528	11	335411	7	NULL	NULL	0	NULL	statement 7			blocks					statement 3					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57529	12	335411	7	NULL	NULL	0	NULL	statement 7			blocks					statement 4					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57530	13	335411	7	NULL	NULL	0	NULL	statement 7			blocks					statement 5					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57531	14	335411	7	NULL	NULL	0	NULL	statement 8			blocks					statement 3					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57532	15	335411	7	NULL	NULL	0	NULL	statement 8			blocks					statement 4					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57533	16	335411	7	NULL	NULL	0	NULL	statement 8			blocks					statement 5					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57534	17	335411	7	NULL	NULL	0	NULL	bisindolylmaleimide			is a type of					PKC inhibitor					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57535	18	335411	7	NULL	NULL	0	NULL	GF 109203X			is a type of					PKC inhibitor					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57536	19	335411	7	NULL	NULL	0	NULL	p125FAK			activated					PKC		downstream of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57537	20	335411	7	NULL	NULL	0	NULL	PKC			induce					p125FAK		phosphorylation of	serine		NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57538	21	335411	7	NULL	NULL	0	NULL	statement 20			regulate					 focal adhesion kinase		intracellular stability of 			NULL	mouse 3T3 cells	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57539	22	335411	7	NULL	NULL	0	NULL	statement 11			suggest					statement 19					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57540	23	335411	7	NULL	NULL	0	NULL	statement 12			suggest					statement 19					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57541	24	335411	7	NULL	NULL	0	NULL	statement 13			suggest					statement 19					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57542	25	335411	7	NULL	NULL	0	NULL	statement 14			suggest					statement 19					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57543	26	335411	7	NULL	NULL	0	NULL	statement 15			suggest					statement 19					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57544	27	335411	7	NULL	NULL	0	NULL	statement 16			suggest					statement 19					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_12_3044_s_33	10591686	Tyrosine phosphorylation of p125FAK in platelets stimulated with a mixture of epinephrine and anti-LIBS6 antibody 30  or in platelets adherent either to fibrinogen or to immobilized immunoglobulin IgG 31 32  is blocked when PKC activity was inhibited with a specific PKC inhibitor, bisindolylmaleimide GF 109203X, suggesting that p125FAK is activated downstream of PKC. PKC-induced serine phosphorylation of p125FAK has been suggested to regulate the intracellular stability of focal adhesion kinase in mouse 3T3 cells.	transcription
57545	1	335412	7	NULL	NULL	0	NULL	L-DOPA			induce					melanin		excess production of			NULL	 highly melanized organisms 	NULL	NULL	NULL	NULL	gw70_eukaryotcell_5_6_916_s_189	16757739	To address this, we exposed native melanized  Pneumocystis (basal amounts of melanins) and highly melanized organisms (excessive melanin production induced by L-DOPA) to either UV irradiation or desiccation.	transcription
78767	1	335413	6	NULL	NULL	0	NULL	riboflavin	GP		bind					DOPA-melanin	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_282_3_1228_s_732	9316830	Studies on equilibrium binding of riboflavin to DOPA-melanin and some spectroscopic characteristics of flavin-melanin complex.	transcription
57546	1	335413	7	NULL	NULL	0	NULL	riboflavin 			bind					DOPA-melanin 					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_282_3_1228_s_732	9316830	Studies on equilibrium binding of riboflavin to DOPA-melanin and some spectroscopic characteristics of flavin-melanin complex.	transcription
78768	1	335414	6	NULL	NULL	0	NULL	DDC	GP		is					dopa decarboxylase	GP				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_10_591_s_20	10837223	Thus, dopa decarboxylase (DDC) catalyzes the conversion of dopa to dopamine, which is a precursor for both melanin and papiliochrome synthesis (  Figure 1c).	transcription
78769	2	335414	6	NULL	NULL	0	NULL	dopa	Chemical		is converted to					dopamine	Chemical				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_10_591_s_20	10837223	Thus, dopa decarboxylase (DDC) catalyzes the conversion of dopa to dopamine, which is a precursor for both melanin and papiliochrome synthesis (  Figure 1c).	transcription
78770	3	335414	6	NULL	NULL	0	NULL	DDC	GP		catalyzes					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_10_591_s_20	10837223	Thus, dopa decarboxylase (DDC) catalyzes the conversion of dopa to dopamine, which is a precursor for both melanin and papiliochrome synthesis (  Figure 1c).	transcription
78771	4	335414	6	NULL	NULL	0	NULL	dopamine	Chemical		is a precursor for					melanin 	Chemical	synthesis of 			NULL		0	NULL	NULL	NULL	gw60_currbiol_10_10_591_s_20	10837223	Thus, dopa decarboxylase (DDC) catalyzes the conversion of dopa to dopamine, which is a precursor for both melanin and papiliochrome synthesis (  Figure 1c).	transcription
78772	5	335414	6	NULL	NULL	0	NULL	dopamine	Chemical		is a precursor for					papiliochrome	Chemical	synthesis of 			NULL		0	NULL	NULL	NULL	gw60_currbiol_10_10_591_s_20	10837223	Thus, dopa decarboxylase (DDC) catalyzes the conversion of dopa to dopamine, which is a precursor for both melanin and papiliochrome synthesis (  Figure 1c).	transcription
57547	1	335414	7	NULL	NULL	0	NULL	dopa			converted to					dopamine					NULL		0	NULL	NULL	NULL	gw60_currbiol_10_10_591_s_20	10837223	Thus, dopa decarboxylase (DDC) catalyzes the conversion of dopa to dopamine, which is a precursor for both melanin and papiliochrome synthesis (  Figure 1c).	transcription
57548	2	335414	7	NULL	NULL	0	NULL	DDC			catalyze					statement 1					NULL		0	NULL	NULL	NULL	gw60_currbiol_10_10_591_s_20	10837223	Thus, dopa decarboxylase (DDC) catalyzes the conversion of dopa to dopamine, which is a precursor for both melanin and papiliochrome synthesis (  Figure 1c).	transcription
57549	3	335414	7	NULL	NULL	0	NULL	statement 1			is a precursor of					melanin		biosynthesis of			NULL		0	NULL	NULL	NULL	gw60_currbiol_10_10_591_s_20	10837223	Thus, dopa decarboxylase (DDC) catalyzes the conversion of dopa to dopamine, which is a precursor for both melanin and papiliochrome synthesis (  Figure 1c).	transcription
57550	4	335414	7	NULL	NULL	0	NULL	statement 1			is a precursor of					papiliochrome		biosynthesis of			NULL		0	NULL	NULL	NULL	gw60_currbiol_10_10_591_s_20	10837223	Thus, dopa decarboxylase (DDC) catalyzes the conversion of dopa to dopamine, which is a precursor for both melanin and papiliochrome synthesis (  Figure 1c).	transcription
57551	5	335414	7	NULL	NULL	0	NULL	DDC			is					dopa decarboxylase					NULL		0	NULL	NULL	NULL	gw60_currbiol_10_10_591_s_20	10837223	Thus, dopa decarboxylase (DDC) catalyzes the conversion of dopa to dopamine, which is a precursor for both melanin and papiliochrome synthesis (  Figure 1c).	transcription
57552	1	335415	7	NULL	NULL	0	NULL	melanin		cell wall of melanized yeast cells 	reacts with					L-dopa Abs		C. neoformans melanin			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_160_12_9637518_s_7	9637518	Furthermore, the  experiments demonstrate 1) a sensitive ELISA for the measurement of Ab  to melanin, 2) that mice mount an intense Ab response to fungal melanin  that includes Abs of IgM and IgG isotypes, 3) that melanins from different  sources have cross-reactive epitopes, and 4) melanin in the cell wall  of melanized yeast cells reacts with Abs raised to L-dopa C. neoformans  melanin.	transcription
57553	2	335415	7	NULL	NULL	0	NULL	melanin		fungal	mounts					IgM antibody					NULL	mice	0	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_160_12_9637518_s_7	9637518	Furthermore, the  experiments demonstrate 1) a sensitive ELISA for the measurement of Ab  to melanin, 2) that mice mount an intense Ab response to fungal melanin  that includes Abs of IgM and IgG isotypes, 3) that melanins from different  sources have cross-reactive epitopes, and 4) melanin in the cell wall  of melanized yeast cells reacts with Abs raised to L-dopa C. neoformans  melanin.	transcription
57554	3	335415	7	NULL	NULL	0	NULL	melanin		fungal	mounts					IgG antibody					NULL	mice	NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_160_12_9637518_s_7	9637518	Furthermore, the  experiments demonstrate 1) a sensitive ELISA for the measurement of Ab  to melanin, 2) that mice mount an intense Ab response to fungal melanin  that includes Abs of IgM and IgG isotypes, 3) that melanins from different  sources have cross-reactive epitopes, and 4) melanin in the cell wall  of melanized yeast cells reacts with Abs raised to L-dopa C. neoformans  melanin.	transcription
78780	1	335416	6	NULL	NULL	0	NULL	glyphosate	Chemical		inhibits					phenoloxidase activity	Process	Pneumocystis			NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_6_916_s_144	16757739	Panel D shows that glyphosate inhibition of  Pneumocystis phenoloxidase activity impairs the L-DOPA-driven generation of  Pneumocystis melanin pigment.	transcription
78781	2	335416	6	NULL	NULL	0	NULL	L-DOPA	Chemical		drives					melanin pigment	Chemical	generation of;; Pneumocystis			NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_6_916_s_144	16757739	Panel D shows that glyphosate inhibition of  Pneumocystis phenoloxidase activity impairs the L-DOPA-driven generation of  Pneumocystis melanin pigment.	transcription
78782	3	335416	6	NULL	NULL	0	NULL	statement 1	Process		impairs					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_6_916_s_144	16757739	Panel D shows that glyphosate inhibition of  Pneumocystis phenoloxidase activity impairs the L-DOPA-driven generation of  Pneumocystis melanin pigment.	transcription
57555	1	335416	7	NULL	NULL	0	NULL	glyphosate			inhibits					Pneumocystis phenoloxidase		activity of			NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_6_916_s_144	16757739	Panel D shows that glyphosate inhibition of  Pneumocystis phenoloxidase activity impairs the L-DOPA-driven generation of  Pneumocystis melanin pigment.	transcription
57556	2	335416	7	NULL	NULL	0	NULL	L-DOPA			drives					Pneumocystis melanin pigment		generation of			NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_6_916_s_144	16757739	Panel D shows that glyphosate inhibition of  Pneumocystis phenoloxidase activity impairs the L-DOPA-driven generation of  Pneumocystis melanin pigment.	transcription
57557	3	335416	7	NULL	NULL	0	NULL	statement 1			impairs					statement 2					NULL		0	NULL	NULL	NULL	gw70_eukaryotcell_5_6_916_s_144	16757739	Panel D shows that glyphosate inhibition of  Pneumocystis phenoloxidase activity impairs the L-DOPA-driven generation of  Pneumocystis melanin pigment.	transcription
78783	1	335417	6	NULL	NULL	0	NULL	tyrosine	GP		is converted to					DOPA	Chemical				NULL		0	NULL	NULL	NULL	gw70_pnas_103_2_353_s_28	16384915	Tyr catalyzes the conversion of tyrosine to DOPA, which is an essential and rate-limiting step in melanin synthesis.	transcription
78784	2	335417	6	NULL	NULL	0	NULL	Tyr	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_103_2_353_s_28	16384915	Tyr catalyzes the conversion of tyrosine to DOPA, which is an essential and rate-limiting step in melanin synthesis.	transcription
78785	3	335417	6	NULL	NULL	0	NULL	statement 1	Process		plays a role in					melanin 	Chemical	synthesis of 			NULL		0	NULL	NULL	NULL	gw70_pnas_103_2_353_s_28	16384915	Tyr catalyzes the conversion of tyrosine to DOPA, which is an essential and rate-limiting step in melanin synthesis.	transcription
57558	1	335417	7	NULL	NULL	0	NULL	 tyrosine			converted to					DOPA					NULL		0	NULL	NULL	NULL	gw70_pnas_103_2_353_s_28	16384915	Tyr catalyzes the conversion of tyrosine to DOPA, which is an essential and rate-limiting step in melanin synthesis.	transcription
57559	2	335417	7	NULL	NULL	0	NULL	Tyr			catalyze					statement 1					NULL		0	NULL	NULL	NULL	gw70_pnas_103_2_353_s_28	16384915	Tyr catalyzes the conversion of tyrosine to DOPA, which is an essential and rate-limiting step in melanin synthesis.	transcription
57560	3	335417	7	NULL	NULL	0	NULL	statement 1			rate limiting step in					melanin		synthesis of			NULL		0	NULL	NULL	NULL	gw70_pnas_103_2_353_s_28	16384915	Tyr catalyzes the conversion of tyrosine to DOPA, which is an essential and rate-limiting step in melanin synthesis.	transcription
57561	1	335418	7	NULL	NULL	0	NULL	melanin			synthesized from					L-DOPA					NULL	cytoplasmic yeast extract	0	NULL	NULL	NULL	gw60_infectimmun_69_9_5760_s_8	11500453	Nonreducing polyacrylamide gel electrophoresis of cytoplasmic yeast extract revealed a protein that catalyzed melanin synthesis from L-DOPA.	transcription
78786	1	335419	6	NULL	NULL	0	NULL	melanin-binding peptides	GP		inhibits					C. neoformans	Organism	growth of 			NULL		0	NULL	NULL	NULL	gw70_microbesinfect_7_4_789_s_53	15823515	The growth of  C. neoformans was also inhibited by melanin-binding peptides   [13] and glyphosate   [14], which inhibited autopolymerization of  l-dopa and oxidation of  l-epinephrine by cryptococcal cells.	transcription
78787	2	335419	6	NULL	NULL	0	NULL	glyphosate	Chemical		inhibits					C. neoformans	Organism	growth of 			NULL		0	NULL	NULL	NULL	gw70_microbesinfect_7_4_789_s_53	15823515	The growth of  C. neoformans was also inhibited by melanin-binding peptides   [13] and glyphosate   [14], which inhibited autopolymerization of  l-dopa and oxidation of  l-epinephrine by cryptococcal cells.	transcription
78788	3	335419	6	NULL	NULL	NULL	NULL	cryptococcal cells	Cell		autopolymerizes					l-dopa	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_microbesinfect_7_4_789_s_53	15823515	The growth of  C. neoformans was also inhibited by melanin-binding peptides   [13] and glyphosate   [14], which inhibited autopolymerization of  l-dopa and oxidation of  l-epinephrine by cryptococcal cells.	transcription
78789	4	335419	6	NULL	NULL	0	NULL	cryptococcal cells	Cell		autopolymerizes					l-epinephrine	Chemical				NULL		0	NULL	NULL	NULL	gw70_microbesinfect_7_4_789_s_53	15823515	The growth of  C. neoformans was also inhibited by melanin-binding peptides   [13] and glyphosate   [14], which inhibited autopolymerization of  l-dopa and oxidation of  l-epinephrine by cryptococcal cells.	transcription
78790	5	335419	6	NULL	NULL	0	NULL	statement 1	Process		inhibits					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_microbesinfect_7_4_789_s_53	15823515	The growth of  C. neoformans was also inhibited by melanin-binding peptides   [13] and glyphosate   [14], which inhibited autopolymerization of  l-dopa and oxidation of  l-epinephrine by cryptococcal cells.	transcription
78791	6	335419	6	NULL	NULL	0	NULL	statement 1	Process		inhibits					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_microbesinfect_7_4_789_s_53	15823515	The growth of  C. neoformans was also inhibited by melanin-binding peptides   [13] and glyphosate   [14], which inhibited autopolymerization of  l-dopa and oxidation of  l-epinephrine by cryptococcal cells.	transcription
78792	7	335419	6	NULL	NULL	0	NULL	statement 2	Process		inhibits					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_microbesinfect_7_4_789_s_53	15823515	The growth of  C. neoformans was also inhibited by melanin-binding peptides   [13] and glyphosate   [14], which inhibited autopolymerization of  l-dopa and oxidation of  l-epinephrine by cryptococcal cells.	transcription
78793	8	335419	6	NULL	NULL	0	NULL	statement 2	Process		inhibits					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_microbesinfect_7_4_789_s_53	15823515	The growth of  C. neoformans was also inhibited by melanin-binding peptides   [13] and glyphosate   [14], which inhibited autopolymerization of  l-dopa and oxidation of  l-epinephrine by cryptococcal cells.	transcription
57562	1	335419	7	NULL	NULL	0	NULL	 melanin-binding peptides			inhibits					C. neoformans		growth of			NULL		0	NULL	NULL	NULL	gw70_microbesinfect_7_4_789_s_53	15823515	The growth of  C. neoformans was also inhibited by melanin-binding peptides   [13] and glyphosate   [14], which inhibited autopolymerization of  l-dopa and oxidation of  l-epinephrine by cryptococcal cells.	transcription
57563	2	335419	7	NULL	NULL	0	NULL	glyphosate			inhibits					C. neoformans		growth of			NULL		0	NULL	NULL	NULL	gw70_microbesinfect_7_4_789_s_53	15823515	The growth of  C. neoformans was also inhibited by melanin-binding peptides   [13] and glyphosate   [14], which inhibited autopolymerization of  l-dopa and oxidation of  l-epinephrine by cryptococcal cells.	transcription
57564	3	335419	7	NULL	NULL	0	NULL	 l-dopa			undergoes					autopolymerization					NULL		0	NULL	NULL	NULL	gw70_microbesinfect_7_4_789_s_53	15823515	The growth of  C. neoformans was also inhibited by melanin-binding peptides   [13] and glyphosate   [14], which inhibited autopolymerization of  l-dopa and oxidation of  l-epinephrine by cryptococcal cells.	transcription
57565	4	335419	7	NULL	NULL	0	NULL	cryptococcal cells			oxidize					l-epinephrine					NULL		0	NULL	NULL	NULL	gw70_microbesinfect_7_4_789_s_53	15823515	The growth of  C. neoformans was also inhibited by melanin-binding peptides   [13] and glyphosate   [14], which inhibited autopolymerization of  l-dopa and oxidation of  l-epinephrine by cryptococcal cells.	transcription
57566	5	335419	7	NULL	NULL	0	NULL	melanin-binding peptides			inhibits					statement 3					NULL		NULL	NULL	NULL	NULL	gw70_microbesinfect_7_4_789_s_53	15823515	The growth of  C. neoformans was also inhibited by melanin-binding peptides   [13] and glyphosate   [14], which inhibited autopolymerization of  l-dopa and oxidation of  l-epinephrine by cryptococcal cells.	transcription
57567	6	335419	7	NULL	NULL	0	NULL	melanin-binding peptides			inhibits					statement 4					NULL		NULL	NULL	NULL	NULL	gw70_microbesinfect_7_4_789_s_53	15823515	The growth of  C. neoformans was also inhibited by melanin-binding peptides   [13] and glyphosate   [14], which inhibited autopolymerization of  l-dopa and oxidation of  l-epinephrine by cryptococcal cells.	transcription
57568	7	335419	7	NULL	NULL	0	NULL	glyphosate 			inhibits					statement 3					NULL		NULL	NULL	NULL	NULL	gw70_microbesinfect_7_4_789_s_53	15823515	The growth of  C. neoformans was also inhibited by melanin-binding peptides   [13] and glyphosate   [14], which inhibited autopolymerization of  l-dopa and oxidation of  l-epinephrine by cryptococcal cells.	transcription
57569	8	335419	7	NULL	NULL	0	NULL	glyphosate 			inhibits					statement 4					NULL		0	NULL	NULL	NULL	gw70_microbesinfect_7_4_789_s_53	15823515	The growth of  C. neoformans was also inhibited by melanin-binding peptides   [13] and glyphosate   [14], which inhibited autopolymerization of  l-dopa and oxidation of  l-epinephrine by cryptococcal cells.	transcription
78794	1	335420	6	NULL	NULL	0	NULL	MelC2	GP		forms					DOPA melanin	Chemical				NULL	Streptomyces	0	NULL	NULL	NULL	gw70_jbacteriol_187_23_8149_s_15	16291687	The representative of the tyrosinases responsible for the formation of DOPA melanin in  Streptomyces is MelC2 ( ), which is a copper-containing monooxygenase that catalyzes the  o-hydroxylation of monophenols and the oxidation of  o-diphenols to yield  o-quinones using molecular oxygen ( ).	transcription
78795	2	335420	6	NULL	NULL	0	NULL	MelC2	Chemical		is a type of					copper-containing monooxygenase 					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_23_8149_s_15	16291687	The representative of the tyrosinases responsible for the formation of DOPA melanin in  Streptomyces is MelC2 ( ), which is a copper-containing monooxygenase that catalyzes the  o-hydroxylation of monophenols and the oxidation of  o-diphenols to yield  o-quinones using molecular oxygen ( ).	transcription
78796	3	335420	6	NULL	NULL	0	NULL	MelC2	GP		catalyzes					monophenols	Chemical	o-hydroxylation of 			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_23_8149_s_15	16291687	The representative of the tyrosinases responsible for the formation of DOPA melanin in  Streptomyces is MelC2 ( ), which is a copper-containing monooxygenase that catalyzes the  o-hydroxylation of monophenols and the oxidation of  o-diphenols to yield  o-quinones using molecular oxygen ( ).	transcription
78797	4	335420	6	NULL	NULL	0	NULL	o-diphenol	Chemical		is oxidized to					o-quinone	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_23_8149_s_15	16291687	The representative of the tyrosinases responsible for the formation of DOPA melanin in  Streptomyces is MelC2 ( ), which is a copper-containing monooxygenase that catalyzes the  o-hydroxylation of monophenols and the oxidation of  o-diphenols to yield  o-quinones using molecular oxygen ( ).	transcription
57570	1	335420	7	NULL	NULL	0	NULL	MelC2 			responsible for					DOPA melanin		formation of			NULL	Streptomyces	NULL	NULL	NULL	NULL	gw70_jbacteriol_187_23_8149_s_15	16291687	The representative of the tyrosinases responsible for the formation of DOPA melanin in  Streptomyces is MelC2 ( ), which is a copper-containing monooxygenase that catalyzes the  o-hydroxylation of monophenols and the oxidation of  o-diphenols to yield  o-quinones using molecular oxygen ( ).	transcription
57571	2	335420	7	NULL	NULL	0	NULL	MelC2			is a type of					tyrosinases					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_23_8149_s_15	16291687	The representative of the tyrosinases responsible for the formation of DOPA melanin in  Streptomyces is MelC2 ( ), which is a copper-containing monooxygenase that catalyzes the  o-hydroxylation of monophenols and the oxidation of  o-diphenols to yield  o-quinones using molecular oxygen ( ).	transcription
57572	3	335420	7	NULL	NULL	0	NULL	MelC2 			is a type of					copper-containing monooxygenase					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_23_8149_s_15	16291687	The representative of the tyrosinases responsible for the formation of DOPA melanin in  Streptomyces is MelC2 ( ), which is a copper-containing monooxygenase that catalyzes the  o-hydroxylation of monophenols and the oxidation of  o-diphenols to yield  o-quinones using molecular oxygen ( ).	transcription
57573	4	335420	7	NULL	NULL	0	NULL	monophenols		o-hydroxylation of	yield					o-quinones					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_23_8149_s_15	16291687	The representative of the tyrosinases responsible for the formation of DOPA melanin in  Streptomyces is MelC2 ( ), which is a copper-containing monooxygenase that catalyzes the  o-hydroxylation of monophenols and the oxidation of  o-diphenols to yield  o-quinones using molecular oxygen ( ).	transcription
57574	5	335420	7	NULL	NULL	0	NULL	o-diphenols 		oxidation of	yield					o-quinones					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_23_8149_s_15	16291687	The representative of the tyrosinases responsible for the formation of DOPA melanin in  Streptomyces is MelC2 ( ), which is a copper-containing monooxygenase that catalyzes the  o-hydroxylation of monophenols and the oxidation of  o-diphenols to yield  o-quinones using molecular oxygen ( ).	transcription
57575	6	335420	7	NULL	NULL	0	NULL	statement 4			involves					molecular oxygen					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_23_8149_s_15	16291687	The representative of the tyrosinases responsible for the formation of DOPA melanin in  Streptomyces is MelC2 ( ), which is a copper-containing monooxygenase that catalyzes the  o-hydroxylation of monophenols and the oxidation of  o-diphenols to yield  o-quinones using molecular oxygen ( ).	transcription
57576	7	335420	7	NULL	NULL	0	NULL	statement 5			involves					molecular oxygen					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_23_8149_s_15	16291687	The representative of the tyrosinases responsible for the formation of DOPA melanin in  Streptomyces is MelC2 ( ), which is a copper-containing monooxygenase that catalyzes the  o-hydroxylation of monophenols and the oxidation of  o-diphenols to yield  o-quinones using molecular oxygen ( ).	transcription
78798	1	335421	6	NULL	NULL	0	NULL	BrY	GP		excretes					HGA	Chemical				NULL	S. algae	0	NULL	NULL	NULL	gw60_applenvironmicrob_68_5_2436_s_218	11976119	In addition previous work demonstrated that HGA, but not DOPA, is excreted by  S. algae BrY and melanin production by  S. algae BrY is inhibited by sulcotrione, a specific inhibitor of the enzyme  p-hydroxyphenylpyruvate dioxygenase, which produces HGA ( 39).	transcription
78799	2	335421	6	NULL	NULL	0	NULL	BrY	GP		produces					melanin	Chemical				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_5_2436_s_218	11976119	In addition previous work demonstrated that HGA, but not DOPA, is excreted by  S. algae BrY and melanin production by  S. algae BrY is inhibited by sulcotrione, a specific inhibitor of the enzyme  p-hydroxyphenylpyruvate dioxygenase, which produces HGA ( 39).	transcription
78800	3	335421	6	NULL	NULL	0	NULL	sulcotrione	Chemical		inhibits					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_5_2436_s_218	11976119	In addition previous work demonstrated that HGA, but not DOPA, is excreted by  S. algae BrY and melanin production by  S. algae BrY is inhibited by sulcotrione, a specific inhibitor of the enzyme  p-hydroxyphenylpyruvate dioxygenase, which produces HGA ( 39).	transcription
78801	4	335421	6	NULL	NULL	0	NULL	sulcotrione	Chemical		is an					p-hydroxyphenylpyruvate dioxygenase	GP	inhibitor of 			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_5_2436_s_218	11976119	In addition previous work demonstrated that HGA, but not DOPA, is excreted by  S. algae BrY and melanin production by  S. algae BrY is inhibited by sulcotrione, a specific inhibitor of the enzyme  p-hydroxyphenylpyruvate dioxygenase, which produces HGA ( 39).	transcription
78802	5	335421	6	NULL	NULL	0	NULL	p-hydroxyphenylpyruvate dioxygenase	GP		produces					HGA	Chemical				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_5_2436_s_218	11976119	In addition previous work demonstrated that HGA, but not DOPA, is excreted by  S. algae BrY and melanin production by  S. algae BrY is inhibited by sulcotrione, a specific inhibitor of the enzyme  p-hydroxyphenylpyruvate dioxygenase, which produces HGA ( 39).	transcription
57577	1	335421	7	NULL	NULL	0	NULL	HGA			is excreted by					BrY		S. algae			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_5_2436_s_218	11976119	In addition previous work demonstrated that HGA, but not DOPA, is excreted by  S. algae BrY and melanin production by  S. algae BrY is inhibited by sulcotrione, a specific inhibitor of the enzyme  p-hydroxyphenylpyruvate dioxygenase, which produces HGA ( 39).	transcription
57578	2	335421	7	NULL	NULL	0	NULL	BrY		 S. algae 	produce					melanin					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_5_2436_s_218	11976119	In addition previous work demonstrated that HGA, but not DOPA, is excreted by  S. algae BrY and melanin production by  S. algae BrY is inhibited by sulcotrione, a specific inhibitor of the enzyme  p-hydroxyphenylpyruvate dioxygenase, which produces HGA ( 39).	transcription
57579	3	335421	7	NULL	NULL	0	NULL	sulcotrione			inhibit					statement 2					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_5_2436_s_218	11976119	In addition previous work demonstrated that HGA, but not DOPA, is excreted by  S. algae BrY and melanin production by  S. algae BrY is inhibited by sulcotrione, a specific inhibitor of the enzyme  p-hydroxyphenylpyruvate dioxygenase, which produces HGA ( 39).	transcription
57580	4	335421	7	NULL	NULL	0	NULL	p-hydroxyphenylpyruvate dioxygenase			produce					HGA					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_5_2436_s_218	11976119	In addition previous work demonstrated that HGA, but not DOPA, is excreted by  S. algae BrY and melanin production by  S. algae BrY is inhibited by sulcotrione, a specific inhibitor of the enzyme  p-hydroxyphenylpyruvate dioxygenase, which produces HGA ( 39).	transcription
57581	5	335421	7	NULL	NULL	0	NULL	sulcotrione			inhibitor of		specific			 p-hydroxyphenylpyruvate dioxygenase					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_5_2436_s_218	11976119	In addition previous work demonstrated that HGA, but not DOPA, is excreted by  S. algae BrY and melanin production by  S. algae BrY is inhibited by sulcotrione, a specific inhibitor of the enzyme  p-hydroxyphenylpyruvate dioxygenase, which produces HGA ( 39).	transcription
57582	6	335421	7	NULL	NULL	0	NULL	DOPA			is not excreted by					BrY		S. algae			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_68_5_2436_s_218	11976119	In addition previous work demonstrated that HGA, but not DOPA, is excreted by  S. algae BrY and melanin production by  S. algae BrY is inhibited by sulcotrione, a specific inhibitor of the enzyme  p-hydroxyphenylpyruvate dioxygenase, which produces HGA ( 39).	transcription
78803	1	335422	6	NULL	NULL	0	NULL	dopa	Chemical		regulates					retinal mitosis	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_23_9948_s_255	9822750	Ilia M, Jeffery G (1998) Retinal mitosis is regulated by dopa, a melanin precursor that may influence the time at which cells exit the cell cycle: analysis of patterns of cell production in pigmented and albino retinae.	transcription
78804	2	335422	6	NULL	NULL	0	NULL	dopa	Chemical		is a precursor for					melanin 	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_23_9948_s_255	9822750	Ilia M, Jeffery G (1998) Retinal mitosis is regulated by dopa, a melanin precursor that may influence the time at which cells exit the cell cycle: analysis of patterns of cell production in pigmented and albino retinae.	transcription
57583	1	335422	7	NULL	NULL	0	NULL	Retinal mitosis			is regulated by					dopa					NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_23_9948_s_255	9822750	Ilia M, Jeffery G (1998) Retinal mitosis is regulated by dopa, a melanin precursor that may influence the time at which cells exit the cell cycle: analysis of patterns of cell production in pigmented and albino retinae.	transcription
57584	2	335422	7	NULL	NULL	0	NULL	dopa			is a precursor of					melanin					NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_23_9948_s_255	9822750	Ilia M, Jeffery G (1998) Retinal mitosis is regulated by dopa, a melanin precursor that may influence the time at which cells exit the cell cycle: analysis of patterns of cell production in pigmented and albino retinae.	transcription
57585	3	335422	7	NULL	NULL	0	NULL	dopa			influence					cell cycle		time at which cells exit 			NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_23_9948_s_255	9822750	Ilia M, Jeffery G (1998) Retinal mitosis is regulated by dopa, a melanin precursor that may influence the time at which cells exit the cell cycle: analysis of patterns of cell production in pigmented and albino retinae.	transcription
57586	1	335423	7	NULL	NULL	0	NULL	L-dopa			added to					Cryptococcus					NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_11_6034_s_5	10531264	Addition of L-dopa to  Cryptococcus to produce melanin in a laccase-positive strain resulted in a slight increase in protection of  C. neoformans from the antifungal activity of macrophages ([25.4  plus-or-minus  3.4]% versus [28.9  plus-or-minus  1.2]% killing).	transcription
57587	2	335423	7	NULL	NULL	0	NULL	statement 1			produce					melanin					NULL	laccase-positive strain	0	NULL	NULL	NULL	gw60_infectimmun_67_11_6034_s_5	10531264	Addition of L-dopa to  Cryptococcus to produce melanin in a laccase-positive strain resulted in a slight increase in protection of  C. neoformans from the antifungal activity of macrophages ([25.4  plus-or-minus  3.4]% versus [28.9  plus-or-minus  1.2]% killing).	transcription
57588	4	335423	7	NULL	NULL	0	NULL	statement 2			increase					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_67_11_6034_s_5	10531264	Addition of L-dopa to  Cryptococcus to produce melanin in a laccase-positive strain resulted in a slight increase in protection of  C. neoformans from the antifungal activity of macrophages ([25.4  plus-or-minus  3.4]% versus [28.9  plus-or-minus  1.2]% killing).	transcription
57589	3	335423	7	NULL	NULL	0	NULL	C. neoformans			protected from					macrophages		antifungal activity of			NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_11_6034_s_5	10531264	Addition of L-dopa to  Cryptococcus to produce melanin in a laccase-positive strain resulted in a slight increase in protection of  C. neoformans from the antifungal activity of macrophages ([25.4  plus-or-minus  3.4]% versus [28.9  plus-or-minus  1.2]% killing).	transcription
78805	1	335424	6	NULL	NULL	0	NULL	NB-DNJ	Chemical		is					N-butyldeoxynojirimycin	Chemical				NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_3_369_s_65	11673476	Indeed, treatment of MEB4 cells with  N-butyldeoxynojirimycin (NB-DNJ), a potent inhibitor of the ER alpha-glucosidases and of maturation of tyrosinase into the active conformation ( Petrescu et al., 1997), completely inhibited melanin formation unless exogenous L-DOPA was added to bypass the requirement for tyrosinase ( Fig. 2 B).	transcription
78806	2	335424	6	NULL	NULL	0	NULL	NB-DNJ	Chemical		inhibits					ER alpha-glucosidases	Chemical				NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_3_369_s_65	11673476	Indeed, treatment of MEB4 cells with  N-butyldeoxynojirimycin (NB-DNJ), a potent inhibitor of the ER alpha-glucosidases and of maturation of tyrosinase into the active conformation ( Petrescu et al., 1997), completely inhibited melanin formation unless exogenous L-DOPA was added to bypass the requirement for tyrosinase ( Fig. 2 B).	transcription
57590	1	335424	7	NULL	NULL	0	NULL	NB-DNJ			inhibitor of		potent			ER alpha-glucosidases					NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_3_369_s_65	11673476	Indeed, treatment of MEB4 cells with  N-butyldeoxynojirimycin (NB-DNJ), a potent inhibitor of the ER alpha-glucosidases and of maturation of tyrosinase into the active conformation ( Petrescu et al., 1997), completely inhibited melanin formation unless exogenous L-DOPA was added to bypass the requirement for tyrosinase ( Fig. 2 B).	transcription
57591	2	335424	7	NULL	NULL	0	NULL	tyrosinase			matures to					active conformation					NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_3_369_s_65	11673476	Indeed, treatment of MEB4 cells with  N-butyldeoxynojirimycin (NB-DNJ), a potent inhibitor of the ER alpha-glucosidases and of maturation of tyrosinase into the active conformation ( Petrescu et al., 1997), completely inhibited melanin formation unless exogenous L-DOPA was added to bypass the requirement for tyrosinase ( Fig. 2 B).	transcription
57592	3	335424	7	NULL	NULL	0	NULL	NB-DNJ			inhibits		completely			melanin		formation of			NULL	MEB4 cells	NULL	NULL	NULL	NULL	gw60_cellbiol_155_3_369_s_65	11673476	Indeed, treatment of MEB4 cells with  N-butyldeoxynojirimycin (NB-DNJ), a potent inhibitor of the ER alpha-glucosidases and of maturation of tyrosinase into the active conformation ( Petrescu et al., 1997), completely inhibited melanin formation unless exogenous L-DOPA was added to bypass the requirement for tyrosinase ( Fig. 2 B).	transcription
57593	4	335424	7	NULL	NULL	0	NULL	statement 2			inhibits		completely			melanin		formation of			NULL	MEB4 cells	NULL	NULL	NULL	NULL	gw60_cellbiol_155_3_369_s_65	11673476	Indeed, treatment of MEB4 cells with  N-butyldeoxynojirimycin (NB-DNJ), a potent inhibitor of the ER alpha-glucosidases and of maturation of tyrosinase into the active conformation ( Petrescu et al., 1997), completely inhibited melanin formation unless exogenous L-DOPA was added to bypass the requirement for tyrosinase ( Fig. 2 B).	transcription
57594	5	335424	7	NULL	NULL	0	NULL	L-DOPA		exogenous	reverse					statement 3					NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_3_369_s_65	11673476	Indeed, treatment of MEB4 cells with  N-butyldeoxynojirimycin (NB-DNJ), a potent inhibitor of the ER alpha-glucosidases and of maturation of tyrosinase into the active conformation ( Petrescu et al., 1997), completely inhibited melanin formation unless exogenous L-DOPA was added to bypass the requirement for tyrosinase ( Fig. 2 B).	transcription
57595	6	335424	7	NULL	NULL	0	NULL	L-DOPA		exogenous	reverse					statement 4					NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_3_369_s_65	11673476	Indeed, treatment of MEB4 cells with  N-butyldeoxynojirimycin (NB-DNJ), a potent inhibitor of the ER alpha-glucosidases and of maturation of tyrosinase into the active conformation ( Petrescu et al., 1997), completely inhibited melanin formation unless exogenous L-DOPA was added to bypass the requirement for tyrosinase ( Fig. 2 B).	transcription
57596	7	335424	7	NULL	NULL	0	NULL	L-DOPA		addition of	bypass 					tyrosinase		requirement for			NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_3_369_s_65	11673476	Indeed, treatment of MEB4 cells with  N-butyldeoxynojirimycin (NB-DNJ), a potent inhibitor of the ER alpha-glucosidases and of maturation of tyrosinase into the active conformation ( Petrescu et al., 1997), completely inhibited melanin formation unless exogenous L-DOPA was added to bypass the requirement for tyrosinase ( Fig. 2 B).	transcription
57597	8	335424	7	NULL	NULL	0	NULL	NB-DNJ			is					N-butyldeoxynojirimycin					NULL		0	NULL	NULL	NULL	gw60_cellbiol_155_3_369_s_65	11673476	Indeed, treatment of MEB4 cells with  N-butyldeoxynojirimycin (NB-DNJ), a potent inhibitor of the ER alpha-glucosidases and of maturation of tyrosinase into the active conformation ( Petrescu et al., 1997), completely inhibited melanin formation unless exogenous L-DOPA was added to bypass the requirement for tyrosinase ( Fig. 2 B).	transcription
78807	1	335425	6	NULL	NULL	0	NULL	melanin	Chemical		is produced by					C. neoformans	Organism				NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_11_6034_s_97	10531264	While melanin produced by  C. neoformans in the presence of L-dopa inhibited phagocytosis by AMs ([10.0  plus-or-minus  2.0]% with the laccase-positive strain versus [19.4  plus-or-minus  0.4]% with the laccase-deficient strain), the phagocytosis indices of the two strains were similar in the absence of L-dopa substrate ([17.0  plus-or-minus  1.0]% versus [18.2  plus-or-minus  1.3]%) (Fig.  2).	transcription
78808	2	335425	6	NULL	NULL	0	NULL	statement 1	Process		occurs in presence of					L-dopa	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_11_6034_s_97	10531264	While melanin produced by  C. neoformans in the presence of L-dopa inhibited phagocytosis by AMs ([10.0  plus-or-minus  2.0]% with the laccase-positive strain versus [19.4  plus-or-minus  0.4]% with the laccase-deficient strain), the phagocytosis indices of the two strains were similar in the absence of L-dopa substrate ([17.0  plus-or-minus  1.0]% versus [18.2  plus-or-minus  1.3]%) (Fig.  2).	transcription
78809	3	335425	6	NULL	NULL	0	NULL	AM	CellComponent		plays a role in					phagocytosis	Process				NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_11_6034_s_97	10531264	While melanin produced by  C. neoformans in the presence of L-dopa inhibited phagocytosis by AMs ([10.0  plus-or-minus  2.0]% with the laccase-positive strain versus [19.4  plus-or-minus  0.4]% with the laccase-deficient strain), the phagocytosis indices of the two strains were similar in the absence of L-dopa substrate ([17.0  plus-or-minus  1.0]% versus [18.2  plus-or-minus  1.3]%) (Fig.  2).	transcription
78810	4	335425	6	NULL	NULL	0	NULL	statement 1	Process		inhibits					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_11_6034_s_97	10531264	While melanin produced by  C. neoformans in the presence of L-dopa inhibited phagocytosis by AMs ([10.0  plus-or-minus  2.0]% with the laccase-positive strain versus [19.4  plus-or-minus  0.4]% with the laccase-deficient strain), the phagocytosis indices of the two strains were similar in the absence of L-dopa substrate ([17.0  plus-or-minus  1.0]% versus [18.2  plus-or-minus  1.3]%) (Fig.  2).	transcription
57599	1	335425	7	NULL	NULL	0	NULL	C. neoformans			produce					melanin					NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_11_6034_s_97	10531264	While melanin produced by  C. neoformans in the presence of L-dopa inhibited phagocytosis by AMs ([10.0  plus-or-minus  2.0]% with the laccase-positive strain versus [19.4  plus-or-minus  0.4]% with the laccase-deficient strain), the phagocytosis indices of the two strains were similar in the absence of L-dopa substrate ([17.0  plus-or-minus  1.0]% versus [18.2  plus-or-minus  1.3]%) (Fig.  2).	transcription
57600	2	335425	7	NULL	NULL	0	NULL	statement 1			in the presence of					L-dopa					NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_11_6034_s_97	10531264	While melanin produced by  C. neoformans in the presence of L-dopa inhibited phagocytosis by AMs ([10.0  plus-or-minus  2.0]% with the laccase-positive strain versus [19.4  plus-or-minus  0.4]% with the laccase-deficient strain), the phagocytosis indices of the two strains were similar in the absence of L-dopa substrate ([17.0  plus-or-minus  1.0]% versus [18.2  plus-or-minus  1.3]%) (Fig.  2).	transcription
57621	3	335425	7	NULL	NULL	0	NULL	melanin			inhibits					AMs		phagocytosis by			NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_11_6034_s_97	10531264	While melanin produced by  C. neoformans in the presence of L-dopa inhibited phagocytosis by AMs ([10.0  plus-or-minus  2.0]% with the laccase-positive strain versus [19.4  plus-or-minus  0.4]% with the laccase-deficient strain), the phagocytosis indices of the two strains were similar in the absence of L-dopa substrate ([17.0  plus-or-minus  1.0]% versus [18.2  plus-or-minus  1.3]%) (Fig.  2).	transcription
78811	1	335426	6	NULL	NULL	0	NULL	trimethyllysine	AminoAcid		is an intermediate for					L-carnitine	AminoAcid	biosynthesis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_39_36262_s_298	12089149	In contrast, trimethyllysine and lysine, an intermediate and a precursor of L-carnitine biosynthesis, respectively, had no apparent inhibitory effect on CT2-mediated carnitine uptake.	transcription
78812	2	335426	6	NULL	NULL	0	NULL	lysine	AminoAcid		is a precursor for					L-carnitine	AminoAcid	biosynthesis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_39_36262_s_298	12089149	In contrast, trimethyllysine and lysine, an intermediate and a precursor of L-carnitine biosynthesis, respectively, had no apparent inhibitory effect on CT2-mediated carnitine uptake.	transcription
57622	1	335426	7	NULL	NULL	0	NULL	 trimethyllysine			intermediate of					L-carnitine		biosynthesis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_39_36262_s_298	12089149	In contrast, trimethyllysine and lysine, an intermediate and a precursor of L-carnitine biosynthesis, respectively, had no apparent inhibitory effect on CT2-mediated carnitine uptake.	transcription
57623	2	335426	7	NULL	NULL	0	NULL	lysine			precursor of					L-carnitine		biosynthesis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_39_36262_s_298	12089149	In contrast, trimethyllysine and lysine, an intermediate and a precursor of L-carnitine biosynthesis, respectively, had no apparent inhibitory effect on CT2-mediated carnitine uptake.	transcription
57624	3	335426	7	NULL	NULL	0	NULL	CT2			mediates					carnitine		uptake of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_39_36262_s_298	12089149	In contrast, trimethyllysine and lysine, an intermediate and a precursor of L-carnitine biosynthesis, respectively, had no apparent inhibitory effect on CT2-mediated carnitine uptake.	transcription
57625	4	335426	7	NULL	NULL	0	NULL	statement 1			has no inhibitory effect on					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_39_36262_s_298	12089149	In contrast, trimethyllysine and lysine, an intermediate and a precursor of L-carnitine biosynthesis, respectively, had no apparent inhibitory effect on CT2-mediated carnitine uptake.	transcription
57626	5	335426	7	NULL	NULL	0	NULL	statement 2			has no inhibitory effect on					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_39_36262_s_298	12089149	In contrast, trimethyllysine and lysine, an intermediate and a precursor of L-carnitine biosynthesis, respectively, had no apparent inhibitory effect on CT2-mediated carnitine uptake.	transcription
78813	1	335427	6	NULL	NULL	0	NULL	lysine	AminoAcid		did not affect					L-carnitine	AminoAcid	uptake of 			NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_179	10545096	Amino acids including lysine, serine, leucine and threonine did not affect the uptake of L-carnitine.	transcription
78814	2	335427	6	NULL	NULL	0	NULL	serine	AminoAcid		did not affect					L-carnitine	AminoAcid	uptake of 			NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_179	10545096	Amino acids including lysine, serine, leucine and threonine did not affect the uptake of L-carnitine.	transcription
78815	3	335427	6	NULL	NULL	0	NULL	leucine	AminoAcid		did not affect					L-carnitine	AminoAcid	uptake of 			NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_179	10545096	Amino acids including lysine, serine, leucine and threonine did not affect the uptake of L-carnitine.	transcription
78816	4	335427	6	NULL	NULL	0	NULL	threonine	AminoAcid		did not affect					L-carnitine	AminoAcid	uptake of 			NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_179	10545096	Amino acids including lysine, serine, leucine and threonine did not affect the uptake of L-carnitine.	transcription
57627	1	335427	7	NULL	NULL	0	NULL	lysine			does not affect					L-carnitine		uptake of			NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_179	10545096	Amino acids including lysine, serine, leucine and threonine did not affect the uptake of L-carnitine.	transcription
57628	2	335427	7	NULL	NULL	0	NULL	serine			does not affect					L-carnitine		uptake of			NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_179	10545096	Amino acids including lysine, serine, leucine and threonine did not affect the uptake of L-carnitine.	transcription
57629	3	335427	7	NULL	NULL	0	NULL	leucine			does not affect					L-carnitine		uptake of			NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_179	10545096	Amino acids including lysine, serine, leucine and threonine did not affect the uptake of L-carnitine.	transcription
57630	4	335427	7	NULL	NULL	0	NULL	threonine			does not affect					L-carnitine		uptake of			NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_179	10545096	Amino acids including lysine, serine, leucine and threonine did not affect the uptake of L-carnitine.	transcription
57631	5	335427	7	NULL	NULL	0	NULL	lysine			is a type of					amino acid					NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_179	10545096	Amino acids including lysine, serine, leucine and threonine did not affect the uptake of L-carnitine.	transcription
57632	6	335427	7	NULL	NULL	0	NULL	serine			is a type of					amino acid					NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_179	10545096	Amino acids including lysine, serine, leucine and threonine did not affect the uptake of L-carnitine.	transcription
57633	7	335427	7	NULL	NULL	0	NULL	leucine			is a type of					amino acid					NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_179	10545096	Amino acids including lysine, serine, leucine and threonine did not affect the uptake of L-carnitine.	transcription
57634	8	335427	7	NULL	NULL	0	NULL	threonine			is a type of					amino acid					NULL		0	NULL	NULL	NULL	gw60_embo_18_21_5843_s_179	10545096	Amino acids including lysine, serine, leucine and threonine did not affect the uptake of L-carnitine.	transcription
57635	1	335428	7	NULL	NULL	0	NULL	gamma-butyrobetaine			inhibit					carnitine transport activity		free			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_289_1_93_s_229	10086992	As examples of inhibition of free carnitine transport activity by carnitine analogs, gamma-butyrobetaine, acetylcarnitine, and lysine are known to function as inhibitors (Huth and Shug, 1980  ; Bahl et al., 1981  ).	transcription
57636	2	335428	7	NULL	NULL	0	NULL	acetylcarnitine			inhibit					carnitine transport activity		free			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_289_1_93_s_229	10086992	As examples of inhibition of free carnitine transport activity by carnitine analogs, gamma-butyrobetaine, acetylcarnitine, and lysine are known to function as inhibitors (Huth and Shug, 1980  ; Bahl et al., 1981  ).	transcription
57637	3	335428	7	NULL	NULL	0	NULL	lysine			inhibit					carnitine transport activity		free			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_289_1_93_s_229	10086992	As examples of inhibition of free carnitine transport activity by carnitine analogs, gamma-butyrobetaine, acetylcarnitine, and lysine are known to function as inhibitors (Huth and Shug, 1980  ; Bahl et al., 1981  ).	transcription
57638	4	335428	7	NULL	NULL	0	NULL	gamma-butyrobetaine			is a type of					carnitine analog					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_289_1_93_s_229	10086992	As examples of inhibition of free carnitine transport activity by carnitine analogs, gamma-butyrobetaine, acetylcarnitine, and lysine are known to function as inhibitors (Huth and Shug, 1980  ; Bahl et al., 1981  ).	transcription
57639	5	335428	7	NULL	NULL	0	NULL	acetylcarnitine			is a type of					carnitine analog					NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_289_1_93_s_229	10086992	As examples of inhibition of free carnitine transport activity by carnitine analogs, gamma-butyrobetaine, acetylcarnitine, and lysine are known to function as inhibitors (Huth and Shug, 1980  ; Bahl et al., 1981  ).	transcription
57640	6	335428	7	NULL	NULL	0	NULL	 lysine			is a type of					carnitine transport activity		free			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_289_1_93_s_229	10086992	As examples of inhibition of free carnitine transport activity by carnitine analogs, gamma-butyrobetaine, acetylcarnitine, and lysine are known to function as inhibitors (Huth and Shug, 1980  ; Bahl et al., 1981  ).	transcription
78817	1	335429	6	NULL	NULL	0	NULL	lysine	AminoAcid		is converted to					Carnitine	AminoAcid				NULL		0	NULL	NULL	NULL	gw70_pnas_103_7_2434_s_41	16467150	ALDH9 is a key enzyme in converting lysine to carnitine ( ), which provides substrates for the carnitine shuttle system mediated by CPT1 and Slc25a20, whereas peroxisomal enoyl-CoA isomerase and hydratase play important roles in peroxisomal fatty acid beta-oxidation.	transcription
78818	2	335429	6	NULL	NULL	0	NULL	ALDH9	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_103_7_2434_s_41	16467150	ALDH9 is a key enzyme in converting lysine to carnitine ( ), which provides substrates for the carnitine shuttle system mediated by CPT1 and Slc25a20, whereas peroxisomal enoyl-CoA isomerase and hydratase play important roles in peroxisomal fatty acid beta-oxidation.	transcription
78819	3	335429	6	NULL	NULL	0	NULL	peroxisomal enoyl-CoA isomerase	GP		plays a role in					fatty acid beta-oxidation	Process	peroxisomal			NULL		0	NULL	NULL	NULL	gw70_pnas_103_7_2434_s_41	16467150	ALDH9 is a key enzyme in converting lysine to carnitine ( ), which provides substrates for the carnitine shuttle system mediated by CPT1 and Slc25a20, whereas peroxisomal enoyl-CoA isomerase and hydratase play important roles in peroxisomal fatty acid beta-oxidation.	transcription
78820	4	335429	6	NULL	NULL	0	NULL	peroxisomal enoyl-CoA hydratase	GP		plays a role in					peroxisomal fatty acid beta-oxidation	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_103_7_2434_s_41	16467150	ALDH9 is a key enzyme in converting lysine to carnitine ( ), which provides substrates for the carnitine shuttle system mediated by CPT1 and Slc25a20, whereas peroxisomal enoyl-CoA isomerase and hydratase play important roles in peroxisomal fatty acid beta-oxidation.	transcription
57641	1	335429	7	NULL	NULL	0	NULL	lysine			converted to					carnitine					NULL		0	NULL	NULL	NULL	gw70_pnas_103_7_2434_s_41	16467150	ALDH9 is a key enzyme in converting lysine to carnitine ( ), which provides substrates for the carnitine shuttle system mediated by CPT1 and Slc25a20, whereas peroxisomal enoyl-CoA isomerase and hydratase play important roles in peroxisomal fatty acid beta-oxidation.	transcription
57642	2	335429	7	NULL	NULL	0	NULL	ALDH9			carries out					statement 1					NULL		0	NULL	NULL	NULL	gw70_pnas_103_7_2434_s_41	16467150	ALDH9 is a key enzyme in converting lysine to carnitine ( ), which provides substrates for the carnitine shuttle system mediated by CPT1 and Slc25a20, whereas peroxisomal enoyl-CoA isomerase and hydratase play important roles in peroxisomal fatty acid beta-oxidation.	transcription
57643	3	335429	7	NULL	NULL	0	NULL	carinitine			substrate for					 carnitine shuttle system					NULL		0	NULL	NULL	NULL	gw70_pnas_103_7_2434_s_41	16467150	ALDH9 is a key enzyme in converting lysine to carnitine ( ), which provides substrates for the carnitine shuttle system mediated by CPT1 and Slc25a20, whereas peroxisomal enoyl-CoA isomerase and hydratase play important roles in peroxisomal fatty acid beta-oxidation.	transcription
57644	4	335429	7	NULL	NULL	0	NULL	CPT1			mediates					statement 3					NULL		0	NULL	NULL	NULL	gw70_pnas_103_7_2434_s_41	16467150	ALDH9 is a key enzyme in converting lysine to carnitine ( ), which provides substrates for the carnitine shuttle system mediated by CPT1 and Slc25a20, whereas peroxisomal enoyl-CoA isomerase and hydratase play important roles in peroxisomal fatty acid beta-oxidation.	transcription
57645	5	335429	7	NULL	NULL	0	NULL	Slc25a20			mediates					statement 3					NULL		0	NULL	NULL	NULL	gw70_pnas_103_7_2434_s_41	16467150	ALDH9 is a key enzyme in converting lysine to carnitine ( ), which provides substrates for the carnitine shuttle system mediated by CPT1 and Slc25a20, whereas peroxisomal enoyl-CoA isomerase and hydratase play important roles in peroxisomal fatty acid beta-oxidation.	transcription
57646	6	335429	7	NULL	NULL	0	NULL	peroxisomal enoyl-CoA isomerase			play important role in					fatty acid beta-oxidation		peroxisomal			NULL		0	NULL	NULL	NULL	gw70_pnas_103_7_2434_s_41	16467150	ALDH9 is a key enzyme in converting lysine to carnitine ( ), which provides substrates for the carnitine shuttle system mediated by CPT1 and Slc25a20, whereas peroxisomal enoyl-CoA isomerase and hydratase play important roles in peroxisomal fatty acid beta-oxidation.	transcription
57647	7	335429	7	NULL	NULL	0	NULL	hydratase			play important role in					fatty acid beta-oxidation		peroxisomal			NULL		0	NULL	NULL	NULL	gw70_pnas_103_7_2434_s_41	16467150	ALDH9 is a key enzyme in converting lysine to carnitine ( ), which provides substrates for the carnitine shuttle system mediated by CPT1 and Slc25a20, whereas peroxisomal enoyl-CoA isomerase and hydratase play important roles in peroxisomal fatty acid beta-oxidation.	transcription
57648	1	335430	7	NULL	NULL	0	NULL	OCTN2		rat	mediates					carnitine transport					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_51_40064_s_229	11010964	Strong inhibitory effects were observed with carnitine-related compounds, including acylcarnitines and gamma-butyrobetaine, whereas lysine, gamma-aminobutyrate, or choline showed negligible or weak inhibitory effect; these are consistent with observations in human and rat OCTN2-mediated carnitine transport ( 9,  23,  42).	transcription
57649	2	335430	7	NULL	NULL	0	NULL	OCTN2		human	mediates					carnitine transport					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_51_40064_s_229	11010964	Strong inhibitory effects were observed with carnitine-related compounds, including acylcarnitines and gamma-butyrobetaine, whereas lysine, gamma-aminobutyrate, or choline showed negligible or weak inhibitory effect; these are consistent with observations in human and rat OCTN2-mediated carnitine transport ( 9,  23,  42).	transcription
57650	3	335430	7	NULL	NULL	0	NULL	acylcarnitines			shows					strong inhibitory effect					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_51_40064_s_229	11010964	Strong inhibitory effects were observed with carnitine-related compounds, including acylcarnitines and gamma-butyrobetaine, whereas lysine, gamma-aminobutyrate, or choline showed negligible or weak inhibitory effect; these are consistent with observations in human and rat OCTN2-mediated carnitine transport ( 9,  23,  42).	transcription
57651	4	335430	7	NULL	NULL	0	NULL	gamma-butyrobetaine			shows					strong inhibitory effect					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_51_40064_s_229	11010964	Strong inhibitory effects were observed with carnitine-related compounds, including acylcarnitines and gamma-butyrobetaine, whereas lysine, gamma-aminobutyrate, or choline showed negligible or weak inhibitory effect; these are consistent with observations in human and rat OCTN2-mediated carnitine transport ( 9,  23,  42).	transcription
57652	5	335430	7	NULL	NULL	0	NULL	lysine			shows					weak inhibitory effect					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_51_40064_s_229	11010964	Strong inhibitory effects were observed with carnitine-related compounds, including acylcarnitines and gamma-butyrobetaine, whereas lysine, gamma-aminobutyrate, or choline showed negligible or weak inhibitory effect; these are consistent with observations in human and rat OCTN2-mediated carnitine transport ( 9,  23,  42).	transcription
57653	6	335430	7	NULL	NULL	0	NULL	 gamma-aminobutyrate			shows					weak inhibitory effect					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_51_40064_s_229	11010964	Strong inhibitory effects were observed with carnitine-related compounds, including acylcarnitines and gamma-butyrobetaine, whereas lysine, gamma-aminobutyrate, or choline showed negligible or weak inhibitory effect; these are consistent with observations in human and rat OCTN2-mediated carnitine transport ( 9,  23,  42).	transcription
57654	7	335430	7	NULL	NULL	0	NULL	choline			shows					weak inhibitory effect					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_51_40064_s_229	11010964	Strong inhibitory effects were observed with carnitine-related compounds, including acylcarnitines and gamma-butyrobetaine, whereas lysine, gamma-aminobutyrate, or choline showed negligible or weak inhibitory effect; these are consistent with observations in human and rat OCTN2-mediated carnitine transport ( 9,  23,  42).	transcription
57655	1	335431	7	NULL	NULL	0	NULL	Ant1p		reconstituted 	does not catalyze					phosphate		homo-exchanges of			NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_154	11566870	Furthermore, reconstituted Ant1p did not catalyze the homo-exchanges of phosphate, pyruvate, malonate, succinate, malate, oxoglutarate, ketoisocaproate, citrate, carnitine, ornithine, lysine, arginine, histidine, glutathione, choline, spermine, proline and threonine (external concentration 1 mM, internal concentration 10 mM; data not shown), all being substrates for various known mitochondrial transporters.	transcription
57656	2	335431	7	NULL	NULL	0	NULL	Ant1p		reconstituted 	does not catalyze					pyruvate		homo-exchanges of			NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_154	11566870	Furthermore, reconstituted Ant1p did not catalyze the homo-exchanges of phosphate, pyruvate, malonate, succinate, malate, oxoglutarate, ketoisocaproate, citrate, carnitine, ornithine, lysine, arginine, histidine, glutathione, choline, spermine, proline and threonine (external concentration 1 mM, internal concentration 10 mM; data not shown), all being substrates for various known mitochondrial transporters.	transcription
57657	3	335431	7	NULL	NULL	0	NULL	Ant1p		reconstituted 	does not catalyze					malonate		homo-exchanges of			NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_154	11566870	Furthermore, reconstituted Ant1p did not catalyze the homo-exchanges of phosphate, pyruvate, malonate, succinate, malate, oxoglutarate, ketoisocaproate, citrate, carnitine, ornithine, lysine, arginine, histidine, glutathione, choline, spermine, proline and threonine (external concentration 1 mM, internal concentration 10 mM; data not shown), all being substrates for various known mitochondrial transporters.	transcription
57658	4	335431	7	NULL	NULL	0	NULL	Ant1p		reconstituted 	does not catalyze					succinate		homo-exchanges of			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_18_5049_s_154	11566870	Furthermore, reconstituted Ant1p did not catalyze the homo-exchanges of phosphate, pyruvate, malonate, succinate, malate, oxoglutarate, ketoisocaproate, citrate, carnitine, ornithine, lysine, arginine, histidine, glutathione, choline, spermine, proline and threonine (external concentration 1 mM, internal concentration 10 mM; data not shown), all being substrates for various known mitochondrial transporters.	transcription
57659	5	335431	7	NULL	NULL	0	NULL	Ant1p		reconstituted 	does not catalyze					malate		homo-exchanges of			NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_154	11566870	Furthermore, reconstituted Ant1p did not catalyze the homo-exchanges of phosphate, pyruvate, malonate, succinate, malate, oxoglutarate, ketoisocaproate, citrate, carnitine, ornithine, lysine, arginine, histidine, glutathione, choline, spermine, proline and threonine (external concentration 1 mM, internal concentration 10 mM; data not shown), all being substrates for various known mitochondrial transporters.	transcription
57660	6	335431	7	NULL	NULL	0	NULL	Ant1p		reconstituted 	does not catalyze					oxoglutarate		homo-exchanges of			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_18_5049_s_154	11566870	Furthermore, reconstituted Ant1p did not catalyze the homo-exchanges of phosphate, pyruvate, malonate, succinate, malate, oxoglutarate, ketoisocaproate, citrate, carnitine, ornithine, lysine, arginine, histidine, glutathione, choline, spermine, proline and threonine (external concentration 1 mM, internal concentration 10 mM; data not shown), all being substrates for various known mitochondrial transporters.	transcription
57661	7	335431	7	NULL	NULL	0	NULL	Ant1p		reconstituted 	does not catalyze					ketoisocaproate		homo-exchanges of			NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_154	11566870	Furthermore, reconstituted Ant1p did not catalyze the homo-exchanges of phosphate, pyruvate, malonate, succinate, malate, oxoglutarate, ketoisocaproate, citrate, carnitine, ornithine, lysine, arginine, histidine, glutathione, choline, spermine, proline and threonine (external concentration 1 mM, internal concentration 10 mM; data not shown), all being substrates for various known mitochondrial transporters.	transcription
57662	8	335431	7	NULL	NULL	0	NULL	Ant1p		reconstituted 	does not catalyze					citrate		homo-exchanges of			NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_154	11566870	Furthermore, reconstituted Ant1p did not catalyze the homo-exchanges of phosphate, pyruvate, malonate, succinate, malate, oxoglutarate, ketoisocaproate, citrate, carnitine, ornithine, lysine, arginine, histidine, glutathione, choline, spermine, proline and threonine (external concentration 1 mM, internal concentration 10 mM; data not shown), all being substrates for various known mitochondrial transporters.	transcription
57663	9	335431	7	NULL	NULL	0	NULL	Ant1p		reconstituted 	does not catalyze					carnitine		homo-exchanges of			NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_154	11566870	Furthermore, reconstituted Ant1p did not catalyze the homo-exchanges of phosphate, pyruvate, malonate, succinate, malate, oxoglutarate, ketoisocaproate, citrate, carnitine, ornithine, lysine, arginine, histidine, glutathione, choline, spermine, proline and threonine (external concentration 1 mM, internal concentration 10 mM; data not shown), all being substrates for various known mitochondrial transporters.	transcription
57664	10	335431	7	NULL	NULL	0	NULL	Ant1p		reconstituted 	does not catalyze					ornithine		homo-exchanges of			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_18_5049_s_154	11566870	Furthermore, reconstituted Ant1p did not catalyze the homo-exchanges of phosphate, pyruvate, malonate, succinate, malate, oxoglutarate, ketoisocaproate, citrate, carnitine, ornithine, lysine, arginine, histidine, glutathione, choline, spermine, proline and threonine (external concentration 1 mM, internal concentration 10 mM; data not shown), all being substrates for various known mitochondrial transporters.	transcription
57665	11	335431	7	NULL	NULL	0	NULL	Ant1p		reconstituted 	does not catalyze					lysine		homo-exchanges of			NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_154	11566870	Furthermore, reconstituted Ant1p did not catalyze the homo-exchanges of phosphate, pyruvate, malonate, succinate, malate, oxoglutarate, ketoisocaproate, citrate, carnitine, ornithine, lysine, arginine, histidine, glutathione, choline, spermine, proline and threonine (external concentration 1 mM, internal concentration 10 mM; data not shown), all being substrates for various known mitochondrial transporters.	transcription
57666	12	335431	7	NULL	NULL	0	NULL	Ant1p		reconstituted 	does not catalyze					arginine		homo-exchanges of			NULL		NULL	NULL	NULL	NULL	gw60_embo_20_18_5049_s_154	11566870	Furthermore, reconstituted Ant1p did not catalyze the homo-exchanges of phosphate, pyruvate, malonate, succinate, malate, oxoglutarate, ketoisocaproate, citrate, carnitine, ornithine, lysine, arginine, histidine, glutathione, choline, spermine, proline and threonine (external concentration 1 mM, internal concentration 10 mM; data not shown), all being substrates for various known mitochondrial transporters.	transcription
57667	13	335431	7	NULL	NULL	0	NULL	Ant1p		reconstituted 	does not catalyze					histidine		homo-exchanges of			NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_154	11566870	Furthermore, reconstituted Ant1p did not catalyze the homo-exchanges of phosphate, pyruvate, malonate, succinate, malate, oxoglutarate, ketoisocaproate, citrate, carnitine, ornithine, lysine, arginine, histidine, glutathione, choline, spermine, proline and threonine (external concentration 1 mM, internal concentration 10 mM; data not shown), all being substrates for various known mitochondrial transporters.	transcription
57668	14	335431	7	NULL	NULL	0	NULL	Ant1p		reconstituted 	does not catalyze					glutathione		homo-exchanges of			NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_154	11566870	Furthermore, reconstituted Ant1p did not catalyze the homo-exchanges of phosphate, pyruvate, malonate, succinate, malate, oxoglutarate, ketoisocaproate, citrate, carnitine, ornithine, lysine, arginine, histidine, glutathione, choline, spermine, proline and threonine (external concentration 1 mM, internal concentration 10 mM; data not shown), all being substrates for various known mitochondrial transporters.	transcription
57669	15	335431	7	NULL	NULL	0	NULL	Ant1p		reconstituted 	does not catalyze					choline		homo-exchanges of			NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_154	11566870	Furthermore, reconstituted Ant1p did not catalyze the homo-exchanges of phosphate, pyruvate, malonate, succinate, malate, oxoglutarate, ketoisocaproate, citrate, carnitine, ornithine, lysine, arginine, histidine, glutathione, choline, spermine, proline and threonine (external concentration 1 mM, internal concentration 10 mM; data not shown), all being substrates for various known mitochondrial transporters.	transcription
57670	16	335431	7	NULL	NULL	0	NULL	Ant1p		reconstituted 	does not catalyze					spermine		homo-exchanges of			NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_154	11566870	Furthermore, reconstituted Ant1p did not catalyze the homo-exchanges of phosphate, pyruvate, malonate, succinate, malate, oxoglutarate, ketoisocaproate, citrate, carnitine, ornithine, lysine, arginine, histidine, glutathione, choline, spermine, proline and threonine (external concentration 1 mM, internal concentration 10 mM; data not shown), all being substrates for various known mitochondrial transporters.	transcription
57671	17	335431	7	NULL	NULL	0	NULL	Ant1p		reconstituted 	does not catalyze					proline		homo-exchanges of			NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_154	11566870	Furthermore, reconstituted Ant1p did not catalyze the homo-exchanges of phosphate, pyruvate, malonate, succinate, malate, oxoglutarate, ketoisocaproate, citrate, carnitine, ornithine, lysine, arginine, histidine, glutathione, choline, spermine, proline and threonine (external concentration 1 mM, internal concentration 10 mM; data not shown), all being substrates for various known mitochondrial transporters.	transcription
57672	18	335431	7	NULL	NULL	0	NULL	Ant1p		reconstituted 	does not catalyze					threonine		homo-exchanges of			NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_154	11566870	Furthermore, reconstituted Ant1p did not catalyze the homo-exchanges of phosphate, pyruvate, malonate, succinate, malate, oxoglutarate, ketoisocaproate, citrate, carnitine, ornithine, lysine, arginine, histidine, glutathione, choline, spermine, proline and threonine (external concentration 1 mM, internal concentration 10 mM; data not shown), all being substrates for various known mitochondrial transporters.	transcription
78821	1	335432	6	NULL	NULL	0	NULL	cholate	GP		did not increase					G5G8		expression of			NULL	Fxr - / - mice	0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_220	15611112	Cholate did not increase G5G8 expression in  Fxr - / -  mice, indicating that the effect of cholate on biliary cholesterol secretion is mediated by FXR.	transcription
78822	2	335432	6	NULL	NULL	0	NULL	cholate	Chemical		effects					biliary cholesterol	Chemical	secretion of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_220	15611112	Cholate did not increase G5G8 expression in  Fxr - / -  mice, indicating that the effect of cholate on biliary cholesterol secretion is mediated by FXR.	transcription
78823	3	335432	6	NULL	NULL	0	NULL	FXR	GP		mediates					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_220	15611112	Cholate did not increase G5G8 expression in  Fxr - / -  mice, indicating that the effect of cholate on biliary cholesterol secretion is mediated by FXR.	transcription
57673	1	335432	7	NULL	NULL	0	NULL	cholate 			does not increase					G5G8		expression of			NULL	Fxr - / - mice	0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_220	15611112	Cholate did not increase G5G8 expression in  Fxr - / -  mice, indicating that the effect of cholate on biliary cholesterol secretion is mediated by FXR.	transcription
57674	2	335432	7	NULL	NULL	0	NULL	FXR			mediates					biliary cholesterol		secretion of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_220	15611112	Cholate did not increase G5G8 expression in  Fxr - / -  mice, indicating that the effect of cholate on biliary cholesterol secretion is mediated by FXR.	transcription
57675	3	335432	7	NULL	NULL	0	NULL	cholate			effect					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_220	15611112	Cholate did not increase G5G8 expression in  Fxr - / -  mice, indicating that the effect of cholate on biliary cholesterol secretion is mediated by FXR.	transcription
57676	4	335432	7	NULL	NULL	0	NULL	statement 1			indicate					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_220	15611112	Cholate did not increase G5G8 expression in  Fxr - / -  mice, indicating that the effect of cholate on biliary cholesterol secretion is mediated by FXR.	transcription
57677	1	335433	7	NULL	NULL	0	NULL	taurine			induce					CYP7A1					NULL		0	NULL	NULL	NULL	abs-batch0580-0599_life-sci_77_7_15936349_s_14	15936349	The overall results suggest that there are differences between  mice and rats in susceptibility of the three enzymes to dietary cholesterol  and cholate, and taurine induced CYP7A1 to produce its cholesterol-lowering  effect only in the presence of cholate in the cholesterol diet.	transcription
57678	2	335433	7	NULL	NULL	0	NULL	statement 1			produce					cholesterol-lowering effect					NULL		0	NULL	NULL	NULL	abs-batch0580-0599_life-sci_77_7_15936349_s_14	15936349	The overall results suggest that there are differences between  mice and rats in susceptibility of the three enzymes to dietary cholesterol  and cholate, and taurine induced CYP7A1 to produce its cholesterol-lowering  effect only in the presence of cholate in the cholesterol diet.	transcription
57679	3	335433	7	NULL	NULL	0	NULL	statement 2			in the presence of					cholate					NULL	cholesterol diet	0	NULL	NULL	NULL	abs-batch0580-0599_life-sci_77_7_15936349_s_14	15936349	The overall results suggest that there are differences between  mice and rats in susceptibility of the three enzymes to dietary cholesterol  and cholate, and taurine induced CYP7A1 to produce its cholesterol-lowering  effect only in the presence of cholate in the cholesterol diet.	transcription
78824	1	335434	6	NULL	NULL	NULL	NULL	chow	Chemical	feeding on	increases					HMG-CoA synthase mRNA	NucleicAcid	intestinal 			NULL	NPC1L1 null mice	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_32_33586_s_232	15173162	Intestinal HMG-CoA synthase mRNA was increased in both chow and cholesterol/cholate-fed NPC1L1 null mice, in contrast to NPC1L1 (+/-) and (+/+) mice, where HMG-CoA synthase was down-regulated with cholesterol/cholate feeding.	transcription
78825	2	335434	6	NULL	NULL	0	NULL	cholesterol/cholate	Chemical	feeding on	increases					HMG-CoA synthase mRNA	NucleicAcid				NULL	NPC1L1 null mice	0	NULL	NULL	NULL	gw70_jbiolchem_279_32_33586_s_232	15173162	Intestinal HMG-CoA synthase mRNA was increased in both chow and cholesterol/cholate-fed NPC1L1 null mice, in contrast to NPC1L1 (+/-) and (+/+) mice, where HMG-CoA synthase was down-regulated with cholesterol/cholate feeding.	transcription
57680	1	335434	7	NULL	NULL	0	NULL	HMG-CoA synthase mRNA		intestinal	is increased in					NPC1L1 null mice		chow-fed			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_32_33586_s_232	15173162	Intestinal HMG-CoA synthase mRNA was increased in both chow and cholesterol/cholate-fed NPC1L1 null mice, in contrast to NPC1L1 (+/-) and (+/+) mice, where HMG-CoA synthase was down-regulated with cholesterol/cholate feeding.	transcription
57681	2	335434	7	NULL	NULL	0	NULL	HMG-CoA synthase mRNA		intestinal	is increased in					NPC1L1 null mice		cholesterol/cholate-fed			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_32_33586_s_232	15173162	Intestinal HMG-CoA synthase mRNA was increased in both chow and cholesterol/cholate-fed NPC1L1 null mice, in contrast to NPC1L1 (+/-) and (+/+) mice, where HMG-CoA synthase was down-regulated with cholesterol/cholate feeding.	transcription
57682	3	335434	7	NULL	NULL	0	NULL	HMG-CoA synthase			is down-regulated in					NPC1L1 (+/-) mice		cholesterol/cholate-fed			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_32_33586_s_232	15173162	Intestinal HMG-CoA synthase mRNA was increased in both chow and cholesterol/cholate-fed NPC1L1 null mice, in contrast to NPC1L1 (+/-) and (+/+) mice, where HMG-CoA synthase was down-regulated with cholesterol/cholate feeding.	transcription
57683	4	335434	7	NULL	NULL	0	NULL	HMG-CoA synthase			is down-regulated in					NPC1L1 (+/+) mice		cholesterol/cholate-fed			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_32_33586_s_232	15173162	Intestinal HMG-CoA synthase mRNA was increased in both chow and cholesterol/cholate-fed NPC1L1 null mice, in contrast to NPC1L1 (+/-) and (+/+) mice, where HMG-CoA synthase was down-regulated with cholesterol/cholate feeding.	transcription
78826	1	335435	6	NULL	NULL	0	NULL	ABC	GP		is					ATP-binding cassette	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_3	15611112	Biliary cholesterol secretion is mediated by the ATP-binding cassette (ABC) transporters ABCG5 (G5) and ABCG8 (G8) and is stimulated by cholesterol and by the non-cholesterol steroids cholate and diosgenin.	transcription
78827	2	335435	6	NULL	NULL	0	NULL	ABCG5	GP		is a type of					ABC transporter	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_3	15611112	Biliary cholesterol secretion is mediated by the ATP-binding cassette (ABC) transporters ABCG5 (G5) and ABCG8 (G8) and is stimulated by cholesterol and by the non-cholesterol steroids cholate and diosgenin.	transcription
78828	3	335435	6	NULL	NULL	0	NULL	ABCG8	GP		is a type of					ABC transporter	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_3	15611112	Biliary cholesterol secretion is mediated by the ATP-binding cassette (ABC) transporters ABCG5 (G5) and ABCG8 (G8) and is stimulated by cholesterol and by the non-cholesterol steroids cholate and diosgenin.	transcription
78829	4	335435	6	NULL	NULL	0	NULL	ABCG5	GP		mediates					cholesterol	Chemical	secretion of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_3	15611112	Biliary cholesterol secretion is mediated by the ATP-binding cassette (ABC) transporters ABCG5 (G5) and ABCG8 (G8) and is stimulated by cholesterol and by the non-cholesterol steroids cholate and diosgenin.	transcription
78830	5	335435	6	NULL	NULL	0	NULL	ABCG8	GP		mediates					cholesterol	Chemical	secretion of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_3	15611112	Biliary cholesterol secretion is mediated by the ATP-binding cassette (ABC) transporters ABCG5 (G5) and ABCG8 (G8) and is stimulated by cholesterol and by the non-cholesterol steroids cholate and diosgenin.	transcription
78831	6	335435	6	NULL	NULL	0	NULL	diosgenin	Chemical		mediates					cholesterol	Chemical	secretion of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_3	15611112	Biliary cholesterol secretion is mediated by the ATP-binding cassette (ABC) transporters ABCG5 (G5) and ABCG8 (G8) and is stimulated by cholesterol and by the non-cholesterol steroids cholate and diosgenin.	transcription
57684	1	335435	7	NULL	NULL	0	NULL	ABCG5			mediates					Biliary cholesterol		secretion of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_3	15611112	Biliary cholesterol secretion is mediated by the ATP-binding cassette (ABC) transporters ABCG5 (G5) and ABCG8 (G8) and is stimulated by cholesterol and by the non-cholesterol steroids cholate and diosgenin.	transcription
57685	2	335435	7	NULL	NULL	0	NULL	ABCG8			mediates					Biliary cholesterol		secretion of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_3	15611112	Biliary cholesterol secretion is mediated by the ATP-binding cassette (ABC) transporters ABCG5 (G5) and ABCG8 (G8) and is stimulated by cholesterol and by the non-cholesterol steroids cholate and diosgenin.	transcription
57686	3	335435	7	NULL	NULL	0	NULL	ABC			is					ATP-binding cassette					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_3	15611112	Biliary cholesterol secretion is mediated by the ATP-binding cassette (ABC) transporters ABCG5 (G5) and ABCG8 (G8) and is stimulated by cholesterol and by the non-cholesterol steroids cholate and diosgenin.	transcription
57687	4	335435	7	NULL	NULL	0	NULL	ABCG5			is a type of					ABC transporter					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_3	15611112	Biliary cholesterol secretion is mediated by the ATP-binding cassette (ABC) transporters ABCG5 (G5) and ABCG8 (G8) and is stimulated by cholesterol and by the non-cholesterol steroids cholate and diosgenin.	transcription
57688	5	335435	7	NULL	NULL	0	NULL	ABCG8			is a type of					ABC transporter					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_3	15611112	Biliary cholesterol secretion is mediated by the ATP-binding cassette (ABC) transporters ABCG5 (G5) and ABCG8 (G8) and is stimulated by cholesterol and by the non-cholesterol steroids cholate and diosgenin.	transcription
57689	6	335435	7	NULL	NULL	0	NULL	cholate			stimulate					Biliary cholesterol		secretion of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_3	15611112	Biliary cholesterol secretion is mediated by the ATP-binding cassette (ABC) transporters ABCG5 (G5) and ABCG8 (G8) and is stimulated by cholesterol and by the non-cholesterol steroids cholate and diosgenin.	transcription
57690	7	335435	7	NULL	NULL	0	NULL	diosgenin			stimulate					Biliary cholesterol		secretion of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_3	15611112	Biliary cholesterol secretion is mediated by the ATP-binding cassette (ABC) transporters ABCG5 (G5) and ABCG8 (G8) and is stimulated by cholesterol and by the non-cholesterol steroids cholate and diosgenin.	transcription
57691	8	335435	7	NULL	NULL	0	NULL	cholate			is a type of					cholesterol steroid					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_3	15611112	Biliary cholesterol secretion is mediated by the ATP-binding cassette (ABC) transporters ABCG5 (G5) and ABCG8 (G8) and is stimulated by cholesterol and by the non-cholesterol steroids cholate and diosgenin.	transcription
57692	9	335435	7	NULL	NULL	0	NULL	 diosgenin			is a type of					non-cholesterol steroid					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_3	15611112	Biliary cholesterol secretion is mediated by the ATP-binding cassette (ABC) transporters ABCG5 (G5) and ABCG8 (G8) and is stimulated by cholesterol and by the non-cholesterol steroids cholate and diosgenin.	transcription
78974	1	335436	6	NULL	NULL	0	NULL	atherogenic diet			induces					hypercholesterolemia	MedicalFinding				NULL		0	NULL	NULL	NULL	gw70_amjpathol_163_6_2155_s_182	14633589	A cholate-containing high fat/high cholesterol atherogenic diet induces hypercholesterolemia and atherosclerosis in susceptible strains of mice including C57BL/6.	transcription
78975	2	335436	6	NULL	NULL	0	NULL	atherogenic diet			induces					atherosclerosis	MedicalFinding				NULL		0	NULL	NULL	NULL	gw70_amjpathol_163_6_2155_s_182	14633589	A cholate-containing high fat/high cholesterol atherogenic diet induces hypercholesterolemia and atherosclerosis in susceptible strains of mice including C57BL/6.	transcription
57693	1	335436	7	NULL	NULL	0	NULL	cholate-containing high fat/high cholesterol atherogenic diet			induce					hypercholesterolemia					NULL	C57BL/6 mice	0	NULL	NULL	NULL	gw70_amjpathol_163_6_2155_s_182	14633589	A cholate-containing high fat/high cholesterol atherogenic diet induces hypercholesterolemia and atherosclerosis in susceptible strains of mice including C57BL/6.	transcription
57694	2	335436	7	NULL	NULL	0	NULL	cholate-containing high fat/high cholesterol atherogenic diet			induce					atherosclerosis					NULL	C57BL/6 mice	0	NULL	NULL	NULL	gw70_amjpathol_163_6_2155_s_182	14633589	A cholate-containing high fat/high cholesterol atherogenic diet induces hypercholesterolemia and atherosclerosis in susceptible strains of mice including C57BL/6.	transcription
78976	1	335437	6	NULL	NULL	0	NULL	Inflammatory gene	GP	activation of	is dependent on					cholesterol	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_44_42774_s_218	12923166	Inflammatory gene activation was dependent on the presence of cholesterol in the diet, whereas the collagen gene family members were induced specifically by cholate.	transcription
78977	2	335437	6	NULL	NULL	0	NULL	cholate	Chemical		induces					collagen gene family members	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_44_42774_s_218	12923166	Inflammatory gene activation was dependent on the presence of cholesterol in the diet, whereas the collagen gene family members were induced specifically by cholate.	transcription
57696	1	335437	7	NULL	NULL	0	NULL	Inflammatory gene		activation of	depends on					cholesterol diet					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_44_42774_s_218	12923166	Inflammatory gene activation was dependent on the presence of cholesterol in the diet, whereas the collagen gene family members were induced specifically by cholate.	transcription
57697	2	335437	7	NULL	NULL	0	NULL	cholate			induce		specifically			collagen gene family					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_44_42774_s_218	12923166	Inflammatory gene activation was dependent on the presence of cholesterol in the diet, whereas the collagen gene family members were induced specifically by cholate.	transcription
57698	1	335438	7	NULL	NULL	0	NULL	cholate			stimulate					biliary cholesterol		secretion of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_202	15611112	Expression of G5 and G8 was required for the stimulation of biliary cholesterol secretion by either cholate or diosgenin, but the two choleretic agents activated G5G8-mediated cholesterol secretion by different mechanisms.	transcription
57699	2	335438	7	NULL	NULL	0	NULL	diosgenin			stimulate					biliary cholesterol		secretion of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_202	15611112	Expression of G5 and G8 was required for the stimulation of biliary cholesterol secretion by either cholate or diosgenin, but the two choleretic agents activated G5G8-mediated cholesterol secretion by different mechanisms.	transcription
57700	3	335438	7	NULL	NULL	0	NULL	G5		expression of	is required for					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_202	15611112	Expression of G5 and G8 was required for the stimulation of biliary cholesterol secretion by either cholate or diosgenin, but the two choleretic agents activated G5G8-mediated cholesterol secretion by different mechanisms.	transcription
57701	4	335438	7	NULL	NULL	0	NULL	G8		expression of	is required for					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_202	15611112	Expression of G5 and G8 was required for the stimulation of biliary cholesterol secretion by either cholate or diosgenin, but the two choleretic agents activated G5G8-mediated cholesterol secretion by different mechanisms.	transcription
57702	5	335438	7	NULL	NULL	0	NULL	G5		expression of	is required for					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_202	15611112	Expression of G5 and G8 was required for the stimulation of biliary cholesterol secretion by either cholate or diosgenin, but the two choleretic agents activated G5G8-mediated cholesterol secretion by different mechanisms.	transcription
57703	6	335438	7	NULL	NULL	0	NULL	G8		expression of	is required for					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_202	15611112	Expression of G5 and G8 was required for the stimulation of biliary cholesterol secretion by either cholate or diosgenin, but the two choleretic agents activated G5G8-mediated cholesterol secretion by different mechanisms.	transcription
57704	7	335438	7	NULL	NULL	0	NULL	G5G8			mediates					cholesterol		secretion of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_202	15611112	Expression of G5 and G8 was required for the stimulation of biliary cholesterol secretion by either cholate or diosgenin, but the two choleretic agents activated G5G8-mediated cholesterol secretion by different mechanisms.	transcription
57705	8	335438	7	NULL	NULL	0	NULL	cholate			activates					statement 7					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_202	15611112	Expression of G5 and G8 was required for the stimulation of biliary cholesterol secretion by either cholate or diosgenin, but the two choleretic agents activated G5G8-mediated cholesterol secretion by different mechanisms.	transcription
57706	9	335438	7	NULL	NULL	0	NULL	diosgenin			activates					statement 7					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_202	15611112	Expression of G5 and G8 was required for the stimulation of biliary cholesterol secretion by either cholate or diosgenin, but the two choleretic agents activated G5G8-mediated cholesterol secretion by different mechanisms.	transcription
57707	10	335438	7	NULL	NULL	0	NULL	cholate			is a type of					choleretic agents					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_202	15611112	Expression of G5 and G8 was required for the stimulation of biliary cholesterol secretion by either cholate or diosgenin, but the two choleretic agents activated G5G8-mediated cholesterol secretion by different mechanisms.	transcription
57708	11	335438	7	NULL	NULL	0	NULL	diosgenin			is a type of					choleretic agents					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_8742_s_202	15611112	Expression of G5 and G8 was required for the stimulation of biliary cholesterol secretion by either cholate or diosgenin, but the two choleretic agents activated G5G8-mediated cholesterol secretion by different mechanisms.	transcription
78978	1	335439	6	NULL	NULL	0	NULL	cholesterol	Chemical		induces					SAA gene	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_44_42774_s_159	12923166	The data above demonstrated that cholesterol was required for the large induction of SAA gene expression, whereas cholate was required for induction of collagen gene expression.	transcription
78979	2	335439	6	NULL	NULL	0	NULL	cholate	Chemical		induces					collagen gene	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_44_42774_s_159	12923166	The data above demonstrated that cholesterol was required for the large induction of SAA gene expression, whereas cholate was required for induction of collagen gene expression.	transcription
57709	1	335439	7	NULL	NULL	0	NULL	cholesterol			is required for					SAA gene		large induction of;;expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_44_42774_s_159	12923166	The data above demonstrated that cholesterol was required for the large induction of SAA gene expression, whereas cholate was required for induction of collagen gene expression.	transcription
57710	2	335439	7	NULL	NULL	0	NULL	cholate 			is required for					collagen gene		induction of;;expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_44_42774_s_159	12923166	The data above demonstrated that cholesterol was required for the large induction of SAA gene expression, whereas cholate was required for induction of collagen gene expression.	transcription
57711	1	335440	7	NULL	NULL	0	NULL	mice			express		constitutively			7alpha-hydroxylase gene		exogenous			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_1_126_s_180	9417056	Effect of cholate or cholestyramine on hepatic 7alpha-hydroxylase activity and plasma LDL cholesterol concentrations in LDL receptor /  mice constitutively expressing an exogenous 7alpha-hydroxylase gene.	transcription
57712	1	335441	7	NULL	NULL	0	NULL	cholate			does not induce					collagen family member					NULL	C57BL/6ByJ mice	0	NULL	NULL	NULL	gw70_jbiolchem_278_44_42774_s_197	12923166	Thus, the two C57BL/6 substrains differ substantially in their gene expression response to dietary cholesterol, and C57BL/6ByJ mice also fail to induce collagen family members to the levels seen in C57BL/6J mice in response to cholate.	transcription
57713	2	335441	7	NULL	NULL	0	NULL	cholate			 induce					collagen family member					NULL	C57BL/6J mice	0	NULL	NULL	NULL	gw70_jbiolchem_278_44_42774_s_197	12923166	Thus, the two C57BL/6 substrains differ substantially in their gene expression response to dietary cholesterol, and C57BL/6ByJ mice also fail to induce collagen family members to the levels seen in C57BL/6J mice in response to cholate.	transcription
57714	1	335442	7	NULL	NULL	0	NULL	 SR-BI			facilitate					atherosclerosis					NULL	LDLr - / - mice	0	NULL	NULL	NULL	gw70_amjpathol_165_3_785_s_129	15331403	Because SR-BI facilitated atherosclerosis in LDLr - / -  mice after only 4 weeks of Western-type diet feeding, in contrast to the protective role at 9 and 12 weeks, this prompted us to study the effect in a second model of atherosclerosis with small fatty streak lesions: WT mice on a high-cholesterol/cholate diet.	transcription
78980	1	335446	6	NULL	NULL	0	NULL	LDLr	GP		facilitates					foam cell	cell	formation of 			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_8_1961_s_180	10938018	13  Although different animal models were used to analyze diet-induced (with and without the addition of cholate) atherosclerosis in these studies, which could make direct comparisons difficult, the present data strongly suggest that the LDLr can facilitate foam cell formation only under conditions of moderate cholesterol levels.	transcription
78981	2	335446	6	NULL	NULL	0	NULL	statement 1	Process		occurs under					cholesterol levels	Chemical	moderate			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_8_1961_s_180	10938018	13  Although different animal models were used to analyze diet-induced (with and without the addition of cholate) atherosclerosis in these studies, which could make direct comparisons difficult, the present data strongly suggest that the LDLr can facilitate foam cell formation only under conditions of moderate cholesterol levels.	transcription
57715	1	335446	7	NULL	NULL	0	NULL	LDLr			facilitate		could			foam cell		formation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_8_1961_s_180	10938018	13  Although different animal models were used to analyze diet-induced (with and without the addition of cholate) atherosclerosis in these studies, which could make direct comparisons difficult, the present data strongly suggest that the LDLr can facilitate foam cell formation only under conditions of moderate cholesterol levels.	transcription
57716	2	335446	7	NULL	NULL	0	NULL	statement 1			under conditions of					cholesterol		moderate			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_20_8_1961_s_180	10938018	13  Although different animal models were used to analyze diet-induced (with and without the addition of cholate) atherosclerosis in these studies, which could make direct comparisons difficult, the present data strongly suggest that the LDLr can facilitate foam cell formation only under conditions of moderate cholesterol levels.	transcription
57717	1	335447	7	NULL	NULL	0	NULL	 dietary cholate			elevates					RIP140		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_20_15482_s_260	10809780	The marked elevation of RIP140 expression induced by dietary cholate also suggested a bile acid/FXR-mediated feedback regulation at the feed-forward stage of cholesterol disposal, in addition to direct repression of Cyp7a through  cis-acting elements in the  cyp7a gene ( 37).	transcription
57718	2	335447	7	NULL	NULL	0	NULL	bile acid			mediates					feedback regulation					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_20_15482_s_260	10809780	The marked elevation of RIP140 expression induced by dietary cholate also suggested a bile acid/FXR-mediated feedback regulation at the feed-forward stage of cholesterol disposal, in addition to direct repression of Cyp7a through  cis-acting elements in the  cyp7a gene ( 37).	transcription
57719	3	335447	7	NULL	NULL	0	NULL	FXR			mediates					feedback regulation					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_20_15482_s_260	10809780	The marked elevation of RIP140 expression induced by dietary cholate also suggested a bile acid/FXR-mediated feedback regulation at the feed-forward stage of cholesterol disposal, in addition to direct repression of Cyp7a through  cis-acting elements in the  cyp7a gene ( 37).	transcription
57720	4	335447	7	NULL	NULL	0	NULL	statement 2			occur during					cholesterol		feed-forward stage of;;disposal of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_20_15482_s_260	10809780	The marked elevation of RIP140 expression induced by dietary cholate also suggested a bile acid/FXR-mediated feedback regulation at the feed-forward stage of cholesterol disposal, in addition to direct repression of Cyp7a through  cis-acting elements in the  cyp7a gene ( 37).	transcription
57721	5	335447	7	NULL	NULL	0	NULL	statement 3			occur during					cholesterol		feed-forward stage of;;disposal of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_20_15482_s_260	10809780	The marked elevation of RIP140 expression induced by dietary cholate also suggested a bile acid/FXR-mediated feedback regulation at the feed-forward stage of cholesterol disposal, in addition to direct repression of Cyp7a through  cis-acting elements in the  cyp7a gene ( 37).	transcription
57722	6	335447	7	NULL	NULL	0	NULL	 cyp7a gene			repress		directly	cis-acting elements		Cyp7a					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_20_15482_s_260	10809780	The marked elevation of RIP140 expression induced by dietary cholate also suggested a bile acid/FXR-mediated feedback regulation at the feed-forward stage of cholesterol disposal, in addition to direct repression of Cyp7a through  cis-acting elements in the  cyp7a gene ( 37).	transcription
57723	7	335447	7	NULL	NULL	0	NULL	statement 1			suggest					statement 4					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_20_15482_s_260	10809780	The marked elevation of RIP140 expression induced by dietary cholate also suggested a bile acid/FXR-mediated feedback regulation at the feed-forward stage of cholesterol disposal, in addition to direct repression of Cyp7a through  cis-acting elements in the  cyp7a gene ( 37).	transcription
57724	8	335447	7	NULL	NULL	0	NULL	statement 1			suggest					statement 5					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_20_15482_s_260	10809780	The marked elevation of RIP140 expression induced by dietary cholate also suggested a bile acid/FXR-mediated feedback regulation at the feed-forward stage of cholesterol disposal, in addition to direct repression of Cyp7a through  cis-acting elements in the  cyp7a gene ( 37).	transcription
57725	9	335447	7	NULL	NULL	0	NULL	statement 1			suggest					statement 6					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_20_15482_s_260	10809780	The marked elevation of RIP140 expression induced by dietary cholate also suggested a bile acid/FXR-mediated feedback regulation at the feed-forward stage of cholesterol disposal, in addition to direct repression of Cyp7a through  cis-acting elements in the  cyp7a gene ( 37).	transcription
57726	1	335448	7	NULL	NULL	0	NULL	high-cholesterol diet			elevates					transaminase		liver			NULL	mice	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1960_s_24	10446078	10  Although no murine model fully recapitulates all of the features of human atherosclerosis, a potential drawback to using mice fed a high-fat, high-cholesterol, cholate-containing diet is that the diet itself is inflammatory when fed to certain strains of mice, and results in liver transaminase elevations, activation of hepatic NFkappaB, increases in acute-phase reactants such as serum amyloid A, and liberation of inflammatory cytokines.	transcription
57727	2	335448	7	NULL	NULL	0	NULL	high-cholesterol diet			activates					NFkappaB		hepatic			NULL	mice	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1960_s_24	10446078	10  Although no murine model fully recapitulates all of the features of human atherosclerosis, a potential drawback to using mice fed a high-fat, high-cholesterol, cholate-containing diet is that the diet itself is inflammatory when fed to certain strains of mice, and results in liver transaminase elevations, activation of hepatic NFkappaB, increases in acute-phase reactants such as serum amyloid A, and liberation of inflammatory cytokines.	transcription
57728	3	335448	7	NULL	NULL	0	NULL	high-cholesterol diet			increase					serum amyloid A					NULL	mice	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1960_s_24	10446078	10  Although no murine model fully recapitulates all of the features of human atherosclerosis, a potential drawback to using mice fed a high-fat, high-cholesterol, cholate-containing diet is that the diet itself is inflammatory when fed to certain strains of mice, and results in liver transaminase elevations, activation of hepatic NFkappaB, increases in acute-phase reactants such as serum amyloid A, and liberation of inflammatory cytokines.	transcription
57729	4	335448	7	NULL	NULL	0	NULL	high-cholesterol diet			increase					inflammatory cytokines		liberation of			NULL	mice	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1960_s_24	10446078	10  Although no murine model fully recapitulates all of the features of human atherosclerosis, a potential drawback to using mice fed a high-fat, high-cholesterol, cholate-containing diet is that the diet itself is inflammatory when fed to certain strains of mice, and results in liver transaminase elevations, activation of hepatic NFkappaB, increases in acute-phase reactants such as serum amyloid A, and liberation of inflammatory cytokines.	transcription
57730	5	335448	7	NULL	NULL	0	NULL	cholate-containing diet			elevates					transaminase		liver			NULL	mice	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1960_s_24	10446078	10  Although no murine model fully recapitulates all of the features of human atherosclerosis, a potential drawback to using mice fed a high-fat, high-cholesterol, cholate-containing diet is that the diet itself is inflammatory when fed to certain strains of mice, and results in liver transaminase elevations, activation of hepatic NFkappaB, increases in acute-phase reactants such as serum amyloid A, and liberation of inflammatory cytokines.	transcription
57731	6	335448	7	NULL	NULL	0	NULL	cholate-containing diet			activates					NFkappaB		hepatic			NULL	mice	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1960_s_24	10446078	10  Although no murine model fully recapitulates all of the features of human atherosclerosis, a potential drawback to using mice fed a high-fat, high-cholesterol, cholate-containing diet is that the diet itself is inflammatory when fed to certain strains of mice, and results in liver transaminase elevations, activation of hepatic NFkappaB, increases in acute-phase reactants such as serum amyloid A, and liberation of inflammatory cytokines.	transcription
57732	7	335448	7	NULL	NULL	0	NULL	cholate-containing diet			increase					serum amyloid A					NULL	mice	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1960_s_24	10446078	10  Although no murine model fully recapitulates all of the features of human atherosclerosis, a potential drawback to using mice fed a high-fat, high-cholesterol, cholate-containing diet is that the diet itself is inflammatory when fed to certain strains of mice, and results in liver transaminase elevations, activation of hepatic NFkappaB, increases in acute-phase reactants such as serum amyloid A, and liberation of inflammatory cytokines.	transcription
57733	8	335448	7	NULL	NULL	0	NULL	cholate-containing diet			increase					inflammatory cytokines		liberation of			NULL	mice	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_8_1960_s_24	10446078	10  Although no murine model fully recapitulates all of the features of human atherosclerosis, a potential drawback to using mice fed a high-fat, high-cholesterol, cholate-containing diet is that the diet itself is inflammatory when fed to certain strains of mice, and results in liver transaminase elevations, activation of hepatic NFkappaB, increases in acute-phase reactants such as serum amyloid A, and liberation of inflammatory cytokines.	transcription
78982	1	335452	6	NULL	NULL	0	NULL	Cbp1	GP		bind					COB	GP			CCG region of UTR	NULL		0	NULL	NULL	NULL	gw70_genetics_171_3_949_s_26	16118200	Recovery of a dominant suppressor in  CBP1 that suppresses the  ACG mutation supports the hypothesis that Cbp1 interacts with the CCG region of the  COB 5''-UTR.	transcription
57734	1	335452	7	NULL	NULL	0	NULL	Cbp1			interacts with					COB				CCG region of the 5''-UTR	NULL		0	NULL	NULL	NULL	gw70_genetics_171_3_949_s_26	16118200	Recovery of a dominant suppressor in  CBP1 that suppresses the  ACG mutation supports the hypothesis that Cbp1 interacts with the CCG region of the  COB 5''-UTR.	transcription
57735	2	335452	7	NULL	NULL	0	NULL	CBP1 		dominant suppressor in	suppress							mutation		 ACG 	NULL		0	NULL	NULL	NULL	gw70_genetics_171_3_949_s_26	16118200	Recovery of a dominant suppressor in  CBP1 that suppresses the  ACG mutation supports the hypothesis that Cbp1 interacts with the CCG region of the  COB 5''-UTR.	transcription
57736	3	335452	7	NULL	NULL	0	NULL	statement 2			support					statement 1					NULL		0	NULL	NULL	NULL	gw70_genetics_171_3_949_s_26	16118200	Recovery of a dominant suppressor in  CBP1 that suppresses the  ACG mutation supports the hypothesis that Cbp1 interacts with the CCG region of the  COB 5''-UTR.	transcription
57737	1	335453	7	NULL	NULL	0	NULL	adenosylcobalamin			reacts with			Cys 408		coenzyme B12					NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_70_0_121_s_362	11395404	Radical chemistry is projected into the substrate binding site from adenosylcobalamin  through Cys 408, which reacts with coenzyme B12 to produce cob(II)alamin, 5''-deoxyadenosine, and the Cys 408-thiyl radical.	transcription
57738	2	335453	7	NULL	NULL	0	NULL	statement 1			produce					cob(II)alamin, 5''-deoxyadenosine					NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_70_0_121_s_362	11395404	Radical chemistry is projected into the substrate binding site from adenosylcobalamin  through Cys 408, which reacts with coenzyme B12 to produce cob(II)alamin, 5''-deoxyadenosine, and the Cys 408-thiyl radical.	transcription
57739	3	335453	7	NULL	NULL	0	NULL	statement 1			produce								Cys 408-thiyl radical		NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_70_0_121_s_362	11395404	Radical chemistry is projected into the substrate binding site from adenosylcobalamin  through Cys 408, which reacts with coenzyme B12 to produce cob(II)alamin, 5''-deoxyadenosine, and the Cys 408-thiyl radical.	transcription
57740	1	335454	7	NULL	NULL	0	NULL				is present at				CCG trinucleotide	COB mRNA		mature		11 nucleotides downstream of the 5' end 	NULL	yeast strains with mutations in the AU-rich COB 5'' UTR	NULL	NULL	NULL	NULL	gw70_molbiolcell_15_6_2674_s_21	15047869	Analyses of yeast strains with mutations in the AU-rich  COB 5'' UTR have shown that a CCG trinucleotide 11 nucleotides downstream of the 5' end of the mature mRNA plays a key role in the interaction with Cbp1; mutations that change this sequence to  ACG, CC U, or C AG result in decreased stability of the  COB mRNA (Chen and Dieckmann, 1997 ).	transcription
57741	2	335454	7	NULL	NULL	0	NULL				plays a key role in				CCG trinucleotide	Cbp1		interaction with			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_6_2674_s_21	15047869	Analyses of yeast strains with mutations in the AU-rich  COB 5'' UTR have shown that a CCG trinucleotide 11 nucleotides downstream of the 5' end of the mature mRNA plays a key role in the interaction with Cbp1; mutations that change this sequence to  ACG, CC U, or C AG result in decreased stability of the  COB mRNA (Chen and Dieckmann, 1997 ).	transcription
57742	3	335454	7	NULL	NULL	0	NULL				mutated to				CCG trinucleotide					 ACG	NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_6_2674_s_21	15047869	Analyses of yeast strains with mutations in the AU-rich  COB 5'' UTR have shown that a CCG trinucleotide 11 nucleotides downstream of the 5' end of the mature mRNA plays a key role in the interaction with Cbp1; mutations that change this sequence to  ACG, CC U, or C AG result in decreased stability of the  COB mRNA (Chen and Dieckmann, 1997 ).	transcription
57743	4	335454	7	NULL	NULL	0	NULL				mutated to				CCG trinucleotide					CC U	NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_6_2674_s_21	15047869	Analyses of yeast strains with mutations in the AU-rich  COB 5'' UTR have shown that a CCG trinucleotide 11 nucleotides downstream of the 5' end of the mature mRNA plays a key role in the interaction with Cbp1; mutations that change this sequence to  ACG, CC U, or C AG result in decreased stability of the  COB mRNA (Chen and Dieckmann, 1997 ).	transcription
57744	5	335454	7	NULL	NULL	0	NULL				mutated to				CCG trinucleotide					C AG	NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_6_2674_s_21	15047869	Analyses of yeast strains with mutations in the AU-rich  COB 5'' UTR have shown that a CCG trinucleotide 11 nucleotides downstream of the 5' end of the mature mRNA plays a key role in the interaction with Cbp1; mutations that change this sequence to  ACG, CC U, or C AG result in decreased stability of the  COB mRNA (Chen and Dieckmann, 1997 ).	transcription
57745	6	335454	7	NULL	NULL	0	NULL	statement 3			result in					COB mRNA		decreased stability of			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_6_2674_s_21	15047869	Analyses of yeast strains with mutations in the AU-rich  COB 5'' UTR have shown that a CCG trinucleotide 11 nucleotides downstream of the 5' end of the mature mRNA plays a key role in the interaction with Cbp1; mutations that change this sequence to  ACG, CC U, or C AG result in decreased stability of the  COB mRNA (Chen and Dieckmann, 1997 ).	transcription
57746	7	335454	7	NULL	NULL	0	NULL	statement 4			result in					COB mRNA		decreased stability of			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_6_2674_s_21	15047869	Analyses of yeast strains with mutations in the AU-rich  COB 5'' UTR have shown that a CCG trinucleotide 11 nucleotides downstream of the 5' end of the mature mRNA plays a key role in the interaction with Cbp1; mutations that change this sequence to  ACG, CC U, or C AG result in decreased stability of the  COB mRNA (Chen and Dieckmann, 1997 ).	transcription
57747	8	335454	7	NULL	NULL	0	NULL	statement 5			result in					COB mRNA		decreased stability of			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_15_6_2674_s_21	15047869	Analyses of yeast strains with mutations in the AU-rich  COB 5'' UTR have shown that a CCG trinucleotide 11 nucleotides downstream of the 5' end of the mature mRNA plays a key role in the interaction with Cbp1; mutations that change this sequence to  ACG, CC U, or C AG result in decreased stability of the  COB mRNA (Chen and Dieckmann, 1997 ).	transcription
78983	1	335455	6	NULL	NULL	0	NULL	Co(II)	Chemical		is reduced to					Co(I)	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_49_40948_s_32	16207720	As mentioned above, we previously hypothesized that FldA reduces Co(II) to Co(I) in the CobA active site, triggering the attack of the Co(I) nucleophile on the 5' carbon of the ribosyl moiety of ATP ( ).	transcription
78984	2	335455	6	NULL	NULL	0	NULL	FldA	GP		play a role in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_49_40948_s_32	16207720	As mentioned above, we previously hypothesized that FldA reduces Co(II) to Co(I) in the CobA active site, triggering the attack of the Co(I) nucleophile on the 5' carbon of the ribosyl moiety of ATP ( ).	transcription
57748	1	335455	7	NULL	NULL	0	NULL	Co(II)			converted to					Co(I)			CobA active site		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_49_40948_s_32	16207720	As mentioned above, we previously hypothesized that FldA reduces Co(II) to Co(I) in the CobA active site, triggering the attack of the Co(I) nucleophile on the 5' carbon of the ribosyl moiety of ATP ( ).	transcription
57749	2	335455	7	NULL	NULL	0	NULL	FldA			reduces					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_49_40948_s_32	16207720	As mentioned above, we previously hypothesized that FldA reduces Co(II) to Co(I) in the CobA active site, triggering the attack of the Co(I) nucleophile on the 5' carbon of the ribosyl moiety of ATP ( ).	transcription
57750	3	335455	7	NULL	NULL	0	NULL	Co(I) nucleophile			attack					ATP			5' carbon of the ribosyl moiety 		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_49_40948_s_32	16207720	As mentioned above, we previously hypothesized that FldA reduces Co(II) to Co(I) in the CobA active site, triggering the attack of the Co(I) nucleophile on the 5' carbon of the ribosyl moiety of ATP ( ).	transcription
57751	4	335455	7	NULL	NULL	0	NULL	statement 2			triggers					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_49_40948_s_32	16207720	As mentioned above, we previously hypothesized that FldA reduces Co(II) to Co(I) in the CobA active site, triggering the attack of the Co(I) nucleophile on the 5' carbon of the ribosyl moiety of ATP ( ).	transcription
78985	1	335457	6	NULL	NULL	0	NULL	GTP	Chemical		does not increase					CobU	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27576_s_265	10869342	The addition of GTP to the ATP:AdoCbi kinase reaction after 30 min did not restore the reaction rate to the level seen when GTP was added at the start of the reaction (Fig.  5), suggesting that GTP could no longer increase the activity of CobU.	transcription
59041	1	335457	7	NULL	NULL	0	NULL	GTP			does not increase					CobU		activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_36_27576_s_265	10869342	The addition of GTP to the ATP:AdoCbi kinase reaction after 30 min did not restore the reaction rate to the level seen when GTP was added at the start of the reaction (Fig.  5), suggesting that GTP could no longer increase the activity of CobU.	transcription
78986	1	335458	6	NULL	NULL	NULL	NULL	PD98059	Chemical		is a type of					MEK inhibitor	GP				NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_139_3_475_s_162	12788807	We used PD98059 (IC50=5 - 10  muM), a highly selective MEK inhibitor that binds to the inactive forms of MEK and prevents its activation by upstream activators (English & Cobb, 2002  ).	transcription
59042	1	335458	7	NULL	NULL	0	NULL	MEK inhibitor		highly selective	bind					MEK		inactive			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_139_3_475_s_162	12788807	We used PD98059 (IC50=5 - 10  muM), a highly selective MEK inhibitor that binds to the inactive forms of MEK and prevents its activation by upstream activators (English & Cobb, 2002  ).	transcription
59043	2	335458	7	NULL	NULL	0	NULL	statement 1			prevent					upstream activators		activation by			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_139_3_475_s_162	12788807	We used PD98059 (IC50=5 - 10  muM), a highly selective MEK inhibitor that binds to the inactive forms of MEK and prevents its activation by upstream activators (English & Cobb, 2002  ).	transcription
78987	1	335463	6	NULL	NULL	0	NULL	guanosine phosphorylase	GP		catalyzes					purine bases	Chemical	recycling of 			NULL		0	NULL	NULL	NULL	gw70_annurevplantbiol_57_0_805_s_421	16669783	Another route to recycle purine bases is catalyzed by adenine  or inosine/guanosine phosphorylases.	transcription
78988	2	335463	6	NULL	NULL	0	NULL	inosine phosphorylase	GP		catalyzes					purine bases	Chemical	recycling of 			NULL		0	NULL	NULL	NULL	gw70_annurevplantbiol_57_0_805_s_421	16669783	Another route to recycle purine bases is catalyzed by adenine  or inosine/guanosine phosphorylases.	transcription
59044	1	335463	7	NULL	NULL	0	NULL	adenine phosphorylase			catalyze					purine bases		recycling of			NULL		NULL	NULL	NULL	NULL	gw70_annurevplantbiol_57_0_805_s_421	16669783	Another route to recycle purine bases is catalyzed by adenine  or inosine/guanosine phosphorylases.	transcription
59045	2	335463	7	NULL	NULL	0	NULL	 inosine phosphorylase			catalyze					purine bases		recycling of			NULL		NULL	NULL	NULL	NULL	gw70_annurevplantbiol_57_0_805_s_421	16669783	Another route to recycle purine bases is catalyzed by adenine  or inosine/guanosine phosphorylases.	transcription
59046	3	335463	7	NULL	NULL	0	NULL	guanosine phosphorylase			catalyze					purine bases		recycling of			NULL		0	NULL	NULL	NULL	gw70_annurevplantbiol_57_0_805_s_421	16669783	Another route to recycle purine bases is catalyzed by adenine  or inosine/guanosine phosphorylases.	transcription
59047	4	335463	7	NULL	NULL	0	NULL	statement 1			is an alternative to					statement 2					NULL		0	NULL	NULL	NULL	gw70_annurevplantbiol_57_0_805_s_421	16669783	Another route to recycle purine bases is catalyzed by adenine  or inosine/guanosine phosphorylases.	transcription
59048	5	335463	7	NULL	NULL	0	NULL	statement 1			is an alternative to					statement 3					NULL		0	NULL	NULL	NULL	gw70_annurevplantbiol_57_0_805_s_421	16669783	Another route to recycle purine bases is catalyzed by adenine  or inosine/guanosine phosphorylases.	transcription
59049	1	335464	7	NULL	NULL	0	NULL	 inosine			inhibit		specifically			P1					NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_29_5_987_s_18	16040150	They identified two high-affinity adenosine  transporters, designated P1 and P2, which could be specifically inhibited by inosine  and adenine, respectively   .	transcription
59050	2	335464	7	NULL	NULL	0	NULL	adenine 			inhibit		specifically			P2					NULL		NULL	NULL	NULL	NULL	gw70_femsmicrobiolrev_29_5_987_s_18	16040150	They identified two high-affinity adenosine  transporters, designated P1 and P2, which could be specifically inhibited by inosine  and adenine, respectively   .	transcription
59051	3	335464	7	NULL	NULL	0	NULL	P1			is a type of					adenosine transporter		high-affinity			NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_29_5_987_s_18	16040150	They identified two high-affinity adenosine  transporters, designated P1 and P2, which could be specifically inhibited by inosine  and adenine, respectively   .	transcription
59052	4	335464	7	NULL	NULL	0	NULL	P2			is a type of					adenosine transporter		high-affinity			NULL		0	NULL	NULL	NULL	gw70_femsmicrobiolrev_29_5_987_s_18	16040150	They identified two high-affinity adenosine  transporters, designated P1 and P2, which could be specifically inhibited by inosine  and adenine, respectively   .	transcription
78989	1	335465	6	NULL	NULL	0	NULL	inosine	Chemical		inhibits					adenosine	Chemical	uptake of 			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_56_6_1162_s_76	10570043	Conversely, inosine completely inhibited [3]adenosine uptake in the presence of 100 muM adenine (not shown).	transcription
59053	1	335465	7	NULL	NULL	0	NULL	inosine			inhibit		completely			adenosine		uptake of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_56_6_1162_s_76	10570043	Conversely, inosine completely inhibited [3]adenosine uptake in the presence of 100 muM adenine (not shown).	transcription
59054	2	335465	7	NULL	NULL	0	NULL	statement 1			in the presence of					adenine					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_56_6_1162_s_76	10570043	Conversely, inosine completely inhibited [3]adenosine uptake in the presence of 100 muM adenine (not shown).	transcription
78990	1	335466	6	NULL	NULL	0	NULL	P1 system	GP		is inhibited by					inosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9486_s_21	9545276	The P1 system was selectively inhibited by inosine, whereas the P2 transporter was specifically blocked by adenine.	transcription
78991	2	335466	6	NULL	NULL	0	NULL	P2 transporter	GP		is blocked by					adenine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9486_s_21	9545276	The P1 system was selectively inhibited by inosine, whereas the P2 transporter was specifically blocked by adenine.	transcription
59055	1	335466	7	NULL	NULL	0	NULL	inosine			inhibit		selectively			P1 system					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9486_s_21	9545276	The P1 system was selectively inhibited by inosine, whereas the P2 transporter was specifically blocked by adenine.	transcription
59056	2	335466	7	NULL	NULL	0	NULL	adenine			blocks		specifically			P2 transporter					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_16_9486_s_21	9545276	The P1 system was selectively inhibited by inosine, whereas the P2 transporter was specifically blocked by adenine.	transcription
59057	1	335467	7	NULL	NULL	0	NULL	fructose			induce					adenine nucleotides		degradation of			NULL	humans	0	NULL	NULL	NULL	abs-batch0720-0739_clin-chem_32_5_3698269_s_1	3698269	Liquid-chromatographic measurements of inosine, hypoxanthine, and xanthine in studies of fructose-induced degradation of adenine nucleotides in humans and rats..	transcription
59058	2	335467	7	NULL	NULL	0	NULL	fructose			induce					adenine nucleotides		degradation of			NULL	rats	0	NULL	NULL	NULL	abs-batch0720-0739_clin-chem_32_5_3698269_s_1	3698269	Liquid-chromatographic measurements of inosine, hypoxanthine, and xanthine in studies of fructose-induced degradation of adenine nucleotides in humans and rats..	transcription
78992	1	335468	6	NULL	NULL	0	NULL	dCTP	Chemical		is formed from					dUTP	Chemical				NULL		0	NULL	NULL	NULL	gw60_chembiol_9_2_245_s_64	11880039	URA7 is a CTP synthase that catalyzes the formation of dCTP from dUTP, the final step in pyrimidine biosynthesis, whereas AAH1 is an adenine deaminase (adenine aminohydrolase), an enzyme of the purine salvage pathway, and converts adenosine to inosine     [33-36]  .	transcription
78993	2	335468	6	NULL	NULL	0	NULL	URA7	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_chembiol_9_2_245_s_64	11880039	URA7 is a CTP synthase that catalyzes the formation of dCTP from dUTP, the final step in pyrimidine biosynthesis, whereas AAH1 is an adenine deaminase (adenine aminohydrolase), an enzyme of the purine salvage pathway, and converts adenosine to inosine     [33-36]  .	transcription
78994	3	335468	6	NULL	NULL	0	NULL	URA7	GP		is a type of					CTP synthase	GP				NULL		0	NULL	NULL	NULL	gw60_chembiol_9_2_245_s_64	11880039	URA7 is a CTP synthase that catalyzes the formation of dCTP from dUTP, the final step in pyrimidine biosynthesis, whereas AAH1 is an adenine deaminase (adenine aminohydrolase), an enzyme of the purine salvage pathway, and converts adenosine to inosine     [33-36]  .	transcription
78995	4	335468	6	NULL	NULL	0	NULL	AAH1	GP		is					adenine deaminase	GP				NULL		0	NULL	NULL	NULL	gw60_chembiol_9_2_245_s_64	11880039	URA7 is a CTP synthase that catalyzes the formation of dCTP from dUTP, the final step in pyrimidine biosynthesis, whereas AAH1 is an adenine deaminase (adenine aminohydrolase), an enzyme of the purine salvage pathway, and converts adenosine to inosine     [33-36]  .	transcription
78996	5	335468	6	NULL	NULL	0	NULL	adenosine	Chemical		is converted to					inosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_chembiol_9_2_245_s_64	11880039	URA7 is a CTP synthase that catalyzes the formation of dCTP from dUTP, the final step in pyrimidine biosynthesis, whereas AAH1 is an adenine deaminase (adenine aminohydrolase), an enzyme of the purine salvage pathway, and converts adenosine to inosine     [33-36]  .	transcription
78997	6	335468	6	NULL	NULL	0	NULL	AAH1	GP		catalyzes					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_chembiol_9_2_245_s_64	11880039	URA7 is a CTP synthase that catalyzes the formation of dCTP from dUTP, the final step in pyrimidine biosynthesis, whereas AAH1 is an adenine deaminase (adenine aminohydrolase), an enzyme of the purine salvage pathway, and converts adenosine to inosine     [33-36]  .	transcription
59059	1	335468	7	NULL	NULL	0	NULL	dUTP			converted to					dCTP					NULL		0	NULL	NULL	NULL	gw60_chembiol_9_2_245_s_64	11880039	URA7 is a CTP synthase that catalyzes the formation of dCTP from dUTP, the final step in pyrimidine biosynthesis, whereas AAH1 is an adenine deaminase (adenine aminohydrolase), an enzyme of the purine salvage pathway, and converts adenosine to inosine     [33-36]  .	transcription
59060	2	335468	7	NULL	NULL	0	NULL	URA7			catalyze					statement 1					NULL		0	NULL	NULL	NULL	gw60_chembiol_9_2_245_s_64	11880039	URA7 is a CTP synthase that catalyzes the formation of dCTP from dUTP, the final step in pyrimidine biosynthesis, whereas AAH1 is an adenine deaminase (adenine aminohydrolase), an enzyme of the purine salvage pathway, and converts adenosine to inosine     [33-36]  .	transcription
59061	3	335468	7	NULL	NULL	0	NULL	URA7			is a type of					CTP synthase					NULL		0	NULL	NULL	NULL	gw60_chembiol_9_2_245_s_64	11880039	URA7 is a CTP synthase that catalyzes the formation of dCTP from dUTP, the final step in pyrimidine biosynthesis, whereas AAH1 is an adenine deaminase (adenine aminohydrolase), an enzyme of the purine salvage pathway, and converts adenosine to inosine     [33-36]  .	transcription
59062	4	335468	7	NULL	NULL	0	NULL	statement 1			final step in					pyrimidine		biosynthesis of			NULL		0	NULL	NULL	NULL	gw60_chembiol_9_2_245_s_64	11880039	URA7 is a CTP synthase that catalyzes the formation of dCTP from dUTP, the final step in pyrimidine biosynthesis, whereas AAH1 is an adenine deaminase (adenine aminohydrolase), an enzyme of the purine salvage pathway, and converts adenosine to inosine     [33-36]  .	transcription
59063	5	335468	7	NULL	NULL	0	NULL	AAH1			is a type of					adenine deaminase					NULL		NULL	NULL	NULL	NULL	gw60_chembiol_9_2_245_s_64	11880039	URA7 is a CTP synthase that catalyzes the formation of dCTP from dUTP, the final step in pyrimidine biosynthesis, whereas AAH1 is an adenine deaminase (adenine aminohydrolase), an enzyme of the purine salvage pathway, and converts adenosine to inosine     [33-36]  .	transcription
59064	6	335468	7	NULL	NULL	0	NULL	AAH1			is 					adenine aminohydrolase					NULL		NULL	NULL	NULL	NULL	gw60_chembiol_9_2_245_s_64	11880039	URA7 is a CTP synthase that catalyzes the formation of dCTP from dUTP, the final step in pyrimidine biosynthesis, whereas AAH1 is an adenine deaminase (adenine aminohydrolase), an enzyme of the purine salvage pathway, and converts adenosine to inosine     [33-36]  .	transcription
59065	7	335468	7	NULL	NULL	0	NULL	adenosine			converted to					inosine					NULL		0	NULL	NULL	NULL	gw60_chembiol_9_2_245_s_64	11880039	URA7 is a CTP synthase that catalyzes the formation of dCTP from dUTP, the final step in pyrimidine biosynthesis, whereas AAH1 is an adenine deaminase (adenine aminohydrolase), an enzyme of the purine salvage pathway, and converts adenosine to inosine     [33-36]  .	transcription
59066	8	335468	7	NULL	NULL	0	NULL	AAH1			converts					statement 7					NULL		0	NULL	NULL	NULL	gw60_chembiol_9_2_245_s_64	11880039	URA7 is a CTP synthase that catalyzes the formation of dCTP from dUTP, the final step in pyrimidine biosynthesis, whereas AAH1 is an adenine deaminase (adenine aminohydrolase), an enzyme of the purine salvage pathway, and converts adenosine to inosine     [33-36]  .	transcription
59067	9	335468	7	NULL	NULL	0	NULL	AAH1			is an enzyme of					 purine salvage pathway					NULL		0	NULL	NULL	NULL	gw60_chembiol_9_2_245_s_64	11880039	URA7 is a CTP synthase that catalyzes the formation of dCTP from dUTP, the final step in pyrimidine biosynthesis, whereas AAH1 is an adenine deaminase (adenine aminohydrolase), an enzyme of the purine salvage pathway, and converts adenosine to inosine     [33-36]  .	transcription
78998	1	335469	6	NULL	NULL	NULL	NULL	ATP	Chemical	depletion of	leads to					adenine nucleotides	Chemical	accumulation of			NULL	myocardial ischemia	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_17_10096_s_62	8626567	Effect of EHNA on the Adenine Nucleotide Pool in the  Postischemic HeartIt is well established that ATP depletion  during myocardial ischemia leads to accumulation of the diffusible  adenine nucleotides, adenosine and inosine, as well as the  nucleopurines, hypoxanthine and xanthine ( Fig. 1).	transcription
78999	2	335469	6	NULL	NULL	NULL	NULL	ATP	Chemical	depletion of	leads to					adenosine	Chemical	accumulation of 			NULL	myocardial ischemia	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_17_10096_s_62	8626567	Effect of EHNA on the Adenine Nucleotide Pool in the  Postischemic HeartIt is well established that ATP depletion  during myocardial ischemia leads to accumulation of the diffusible  adenine nucleotides, adenosine and inosine, as well as the  nucleopurines, hypoxanthine and xanthine ( Fig. 1).	transcription
79000	3	335469	6	NULL	NULL	NULL	NULL	ATP	Chemical	depletion of	leads to					inosine	Chemical	accumulation of 			NULL	myocardial ischemia	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_17_10096_s_62	8626567	Effect of EHNA on the Adenine Nucleotide Pool in the  Postischemic HeartIt is well established that ATP depletion  during myocardial ischemia leads to accumulation of the diffusible  adenine nucleotides, adenosine and inosine, as well as the  nucleopurines, hypoxanthine and xanthine ( Fig. 1).	transcription
79001	4	335469	6	NULL	NULL	0	NULL	ATP	Chemical	depletion of	leads to					hypoxanthine	Chemical	accumulation of 			NULL	myocardial ischemia	0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10096_s_62	8626567	Effect of EHNA on the Adenine Nucleotide Pool in the  Postischemic HeartIt is well established that ATP depletion  during myocardial ischemia leads to accumulation of the diffusible  adenine nucleotides, adenosine and inosine, as well as the  nucleopurines, hypoxanthine and xanthine ( Fig. 1).	transcription
79002	5	335469	6	NULL	NULL	0	NULL	ATP	Chemical	depletion of	leads to					xanthine	Chemical	accumulation of 			NULL	myocardial ischemia	0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10096_s_62	8626567	Effect of EHNA on the Adenine Nucleotide Pool in the  Postischemic HeartIt is well established that ATP depletion  during myocardial ischemia leads to accumulation of the diffusible  adenine nucleotides, adenosine and inosine, as well as the  nucleopurines, hypoxanthine and xanthine ( Fig. 1).	transcription
59068	1	335469	7	NULL	NULL	0	NULL	ATP		depletion of	leads to					adenine nucleotides		accumulation of;;diffusible 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_17_10096_s_62	8626567	Effect of EHNA on the Adenine Nucleotide Pool in the  Postischemic HeartIt is well established that ATP depletion  during myocardial ischemia leads to accumulation of the diffusible  adenine nucleotides, adenosine and inosine, as well as the  nucleopurines, hypoxanthine and xanthine ( Fig. 1).	transcription
59069	2	335469	7	NULL	NULL	0	NULL	statement 1			occur during					myocardial ischemia					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10096_s_62	8626567	Effect of EHNA on the Adenine Nucleotide Pool in the  Postischemic HeartIt is well established that ATP depletion  during myocardial ischemia leads to accumulation of the diffusible  adenine nucleotides, adenosine and inosine, as well as the  nucleopurines, hypoxanthine and xanthine ( Fig. 1).	transcription
59070	3	335469	7	NULL	NULL	0	NULL	ATP		depletion of	leads to					adenosine		accumulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10096_s_62	8626567	Effect of EHNA on the Adenine Nucleotide Pool in the  Postischemic HeartIt is well established that ATP depletion  during myocardial ischemia leads to accumulation of the diffusible  adenine nucleotides, adenosine and inosine, as well as the  nucleopurines, hypoxanthine and xanthine ( Fig. 1).	transcription
59071	4	335469	7	NULL	NULL	0	NULL	statement 3			occur during					myocardial ischemia					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10096_s_62	8626567	Effect of EHNA on the Adenine Nucleotide Pool in the  Postischemic HeartIt is well established that ATP depletion  during myocardial ischemia leads to accumulation of the diffusible  adenine nucleotides, adenosine and inosine, as well as the  nucleopurines, hypoxanthine and xanthine ( Fig. 1).	transcription
59072	5	335469	7	NULL	NULL	0	NULL	ATP		depletion of	leads to					inosine		accumulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10096_s_62	8626567	Effect of EHNA on the Adenine Nucleotide Pool in the  Postischemic HeartIt is well established that ATP depletion  during myocardial ischemia leads to accumulation of the diffusible  adenine nucleotides, adenosine and inosine, as well as the  nucleopurines, hypoxanthine and xanthine ( Fig. 1).	transcription
59073	6	335469	7	NULL	NULL	0	NULL	statement 5			occur during					myocardial ischemia					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10096_s_62	8626567	Effect of EHNA on the Adenine Nucleotide Pool in the  Postischemic HeartIt is well established that ATP depletion  during myocardial ischemia leads to accumulation of the diffusible  adenine nucleotides, adenosine and inosine, as well as the  nucleopurines, hypoxanthine and xanthine ( Fig. 1).	transcription
59074	7	335469	7	NULL	NULL	0	NULL	ATP		depletion of	leads to					hypoxanthine		accumulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10096_s_62	8626567	Effect of EHNA on the Adenine Nucleotide Pool in the  Postischemic HeartIt is well established that ATP depletion  during myocardial ischemia leads to accumulation of the diffusible  adenine nucleotides, adenosine and inosine, as well as the  nucleopurines, hypoxanthine and xanthine ( Fig. 1).	transcription
59075	8	335469	7	NULL	NULL	0	NULL	statement 7			occur during					myocardial ischemia					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10096_s_62	8626567	Effect of EHNA on the Adenine Nucleotide Pool in the  Postischemic HeartIt is well established that ATP depletion  during myocardial ischemia leads to accumulation of the diffusible  adenine nucleotides, adenosine and inosine, as well as the  nucleopurines, hypoxanthine and xanthine ( Fig. 1).	transcription
59076	9	335469	7	NULL	NULL	0	NULL	ATP		depletion of	leads to					xanthine		accumulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10096_s_62	8626567	Effect of EHNA on the Adenine Nucleotide Pool in the  Postischemic HeartIt is well established that ATP depletion  during myocardial ischemia leads to accumulation of the diffusible  adenine nucleotides, adenosine and inosine, as well as the  nucleopurines, hypoxanthine and xanthine ( Fig. 1).	transcription
59077	10	335469	7	NULL	NULL	0	NULL	statement 9			occur during					myocardial ischemia					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10096_s_62	8626567	Effect of EHNA on the Adenine Nucleotide Pool in the  Postischemic HeartIt is well established that ATP depletion  during myocardial ischemia leads to accumulation of the diffusible  adenine nucleotides, adenosine and inosine, as well as the  nucleopurines, hypoxanthine and xanthine ( Fig. 1).	transcription
59078	11	335469	7	NULL	NULL	0	NULL	hypoxanthine			is a type of					nucleopurine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10096_s_62	8626567	Effect of EHNA on the Adenine Nucleotide Pool in the  Postischemic HeartIt is well established that ATP depletion  during myocardial ischemia leads to accumulation of the diffusible  adenine nucleotides, adenosine and inosine, as well as the  nucleopurines, hypoxanthine and xanthine ( Fig. 1).	transcription
59079	12	335469	7	NULL	NULL	0	NULL	xanthine			is a type of					nucleopurine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10096_s_62	8626567	Effect of EHNA on the Adenine Nucleotide Pool in the  Postischemic HeartIt is well established that ATP depletion  during myocardial ischemia leads to accumulation of the diffusible  adenine nucleotides, adenosine and inosine, as well as the  nucleopurines, hypoxanthine and xanthine ( Fig. 1).	transcription
79003	1	335471	6	NULL	NULL	0	NULL	adenosine			is deaminated to					inosine					NULL	viral RNA	0	NULL	NULL	NULL	gw70_pnas_103_5_1440_s_168	16434471	Although expression of A3G is not stimulated by IFN in T cell line H9 ( ), one of the ISGs, adenine deaminase, catalyzes deamination of adenosine to inosine  in viral RNAs ( ).	transcription
79004	2	335471	6	NULL	NULL	0	NULL	IFN	GP		does not stimulate					A3G	GP	expression of			NULL	T cell line H9	0	NULL	NULL	NULL	gw70_pnas_103_5_1440_s_168	16434471	Although expression of A3G is not stimulated by IFN in T cell line H9 ( ), one of the ISGs, adenine deaminase, catalyzes deamination of adenosine to inosine  in viral RNAs ( ).	transcription
79005	3	335471	6	NULL	NULL	0	NULL	adenine deaminase	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_103_5_1440_s_168	16434471	Although expression of A3G is not stimulated by IFN in T cell line H9 ( ), one of the ISGs, adenine deaminase, catalyzes deamination of adenosine to inosine  in viral RNAs ( ).	transcription
59098	1	335471	7	NULL	NULL	0	NULL	IFN 			does not stimulate					A3G		expression of			NULL	T cell line H9	0	NULL	NULL	NULL	gw70_pnas_103_5_1440_s_168	16434471	Although expression of A3G is not stimulated by IFN in T cell line H9 ( ), one of the ISGs, adenine deaminase, catalyzes deamination of adenosine to inosine  in viral RNAs ( ).	transcription
59099	2	335471	7	NULL	NULL	0	NULL	adenosine 			converted to					inosine					NULL	viral RNAs	0	NULL	NULL	NULL	gw70_pnas_103_5_1440_s_168	16434471	Although expression of A3G is not stimulated by IFN in T cell line H9 ( ), one of the ISGs, adenine deaminase, catalyzes deamination of adenosine to inosine  in viral RNAs ( ).	transcription
59100	3	335471	7	NULL	NULL	0	NULL	adenine deaminase			catalyze					statement 2		deamination of			NULL		0	NULL	NULL	NULL	gw70_pnas_103_5_1440_s_168	16434471	Although expression of A3G is not stimulated by IFN in T cell line H9 ( ), one of the ISGs, adenine deaminase, catalyzes deamination of adenosine to inosine  in viral RNAs ( ).	transcription
59101	4	335471	7	NULL	NULL	0	NULL	adenine deaminase			is a type of					ISGs					NULL		0	NULL	NULL	NULL	gw70_pnas_103_5_1440_s_168	16434471	Although expression of A3G is not stimulated by IFN in T cell line H9 ( ), one of the ISGs, adenine deaminase, catalyzes deamination of adenosine to inosine  in viral RNAs ( ).	transcription
59102	1	335472	7	NULL	NULL	0	NULL	hypoxanthine			incorporated into					cell lines					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_31_19488_s_150	9235951	100 muM concentrations of either hypoxanthine, adenine, adenosine, inosine, or guanine inhibited the incorporation of 1.8 muM [14]hypoxanthine into all cell lines tested by 80-90%.	transcription
59103	2	335472	7	NULL	NULL	0	NULL	hypoxanthine			inhibit					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_31_19488_s_150	9235951	100 muM concentrations of either hypoxanthine, adenine, adenosine, inosine, or guanine inhibited the incorporation of 1.8 muM [14]hypoxanthine into all cell lines tested by 80-90%.	transcription
59104	3	335472	7	NULL	NULL	0	NULL	adenine			inhibit					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_31_19488_s_150	9235951	100 muM concentrations of either hypoxanthine, adenine, adenosine, inosine, or guanine inhibited the incorporation of 1.8 muM [14]hypoxanthine into all cell lines tested by 80-90%.	transcription
59105	4	335472	7	NULL	NULL	0	NULL	adenosine 			inhibit					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_31_19488_s_150	9235951	100 muM concentrations of either hypoxanthine, adenine, adenosine, inosine, or guanine inhibited the incorporation of 1.8 muM [14]hypoxanthine into all cell lines tested by 80-90%.	transcription
59106	5	335472	7	NULL	NULL	0	NULL	inosine			inhibit					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_31_19488_s_150	9235951	100 muM concentrations of either hypoxanthine, adenine, adenosine, inosine, or guanine inhibited the incorporation of 1.8 muM [14]hypoxanthine into all cell lines tested by 80-90%.	transcription
59107	6	335472	7	NULL	NULL	0	NULL	guanine			inhibit					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_31_19488_s_150	9235951	100 muM concentrations of either hypoxanthine, adenine, adenosine, inosine, or guanine inhibited the incorporation of 1.8 muM [14]hypoxanthine into all cell lines tested by 80-90%.	transcription
79006	1	335473	6	NULL	NULL	0	NULL	EHNA	Chemical		is					Erythro-9-(2-hydroxy-3-nonyl)adenine	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_mol-cell-biochem_281_1-2_16328964_s_8	16328964	Erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA),  an adenosine deaminase inhibitor, abolished the TNF-alpha induced inosine  increase, nitrite accumulation and nitric oxide synthase activity.	transcription
79007	2	335473	6	NULL	NULL	0	NULL	EHNA	Chemical		is a type of					adenosine deaminase inhibitor	GP				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_mol-cell-biochem_281_1-2_16328964_s_8	16328964	Erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA),  an adenosine deaminase inhibitor, abolished the TNF-alpha induced inosine  increase, nitrite accumulation and nitric oxide synthase activity.	transcription
79008	3	335473	6	NULL	NULL	0	NULL	TNF-alpha	GP		induces					inosine	Chemical	increase of 			NULL		0	NULL	NULL	NULL	abs-batch0540-0549_mol-cell-biochem_281_1-2_16328964_s_8	16328964	Erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA),  an adenosine deaminase inhibitor, abolished the TNF-alpha induced inosine  increase, nitrite accumulation and nitric oxide synthase activity.	transcription
79009	4	335473	6	NULL	NULL	0	NULL	TNF-alpha	GP		induces					nitrite	Chemical	accumulation of 			NULL		0	NULL	NULL	NULL	abs-batch0540-0549_mol-cell-biochem_281_1-2_16328964_s_8	16328964	Erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA),  an adenosine deaminase inhibitor, abolished the TNF-alpha induced inosine  increase, nitrite accumulation and nitric oxide synthase activity.	transcription
79010	5	335473	6	NULL	NULL	0	NULL	TNF-alpha	GP		induces					nitric oxide synthase activity	Process				NULL		0	NULL	NULL	NULL	abs-batch0540-0549_mol-cell-biochem_281_1-2_16328964_s_8	16328964	Erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA),  an adenosine deaminase inhibitor, abolished the TNF-alpha induced inosine  increase, nitrite accumulation and nitric oxide synthase activity.	transcription
59108	1	335473	7	NULL	NULL	0	NULL	TNF-alpha			induce					inosine		increase in			NULL		0	NULL	NULL	NULL	abs-batch0540-0549_mol-cell-biochem_281_1-2_16328964_s_8	16328964	Erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA),  an adenosine deaminase inhibitor, abolished the TNF-alpha induced inosine  increase, nitrite accumulation and nitric oxide synthase activity.	transcription
59109	2	335473	7	NULL	NULL	0	NULL	TNF-alpha			induce					nitrite		accumulation of			NULL		0	NULL	NULL	NULL	abs-batch0540-0549_mol-cell-biochem_281_1-2_16328964_s_8	16328964	Erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA),  an adenosine deaminase inhibitor, abolished the TNF-alpha induced inosine  increase, nitrite accumulation and nitric oxide synthase activity.	transcription
59110	3	335473	7	NULL	NULL	0	NULL	TNF-alpha			induce					nitric oxide synthase		activity of			NULL		0	NULL	NULL	NULL	abs-batch0540-0549_mol-cell-biochem_281_1-2_16328964_s_8	16328964	Erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA),  an adenosine deaminase inhibitor, abolished the TNF-alpha induced inosine  increase, nitrite accumulation and nitric oxide synthase activity.	transcription
59111	4	335473	7	NULL	NULL	0	NULL	EHNA			abolish					statement 1					NULL		0	NULL	NULL	NULL	abs-batch0540-0549_mol-cell-biochem_281_1-2_16328964_s_8	16328964	Erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA),  an adenosine deaminase inhibitor, abolished the TNF-alpha induced inosine  increase, nitrite accumulation and nitric oxide synthase activity.	transcription
59112	5	335473	7	NULL	NULL	0	NULL	EHNA			abolish					statement 2					NULL		0	NULL	NULL	NULL	abs-batch0540-0549_mol-cell-biochem_281_1-2_16328964_s_8	16328964	Erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA),  an adenosine deaminase inhibitor, abolished the TNF-alpha induced inosine  increase, nitrite accumulation and nitric oxide synthase activity.	transcription
59113	6	335473	7	NULL	NULL	0	NULL	EHNA			abolish					statement 3					NULL		0	NULL	NULL	NULL	abs-batch0540-0549_mol-cell-biochem_281_1-2_16328964_s_8	16328964	Erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA),  an adenosine deaminase inhibitor, abolished the TNF-alpha induced inosine  increase, nitrite accumulation and nitric oxide synthase activity.	transcription
59114	7	335473	7	NULL	NULL	0	NULL	EHNA			is					Erythro-9-(2-hydroxy-3-nonyl)adenine					NULL		0	NULL	NULL	NULL	abs-batch0540-0549_mol-cell-biochem_281_1-2_16328964_s_8	16328964	Erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA),  an adenosine deaminase inhibitor, abolished the TNF-alpha induced inosine  increase, nitrite accumulation and nitric oxide synthase activity.	transcription
59116	8	335473	7	NULL	NULL	0	NULL	EHNA			is a type of					adenosine deaminase inhibitor					NULL		0	NULL	NULL	NULL	abs-batch0540-0549_mol-cell-biochem_281_1-2_16328964_s_8	16328964	Erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA),  an adenosine deaminase inhibitor, abolished the TNF-alpha induced inosine  increase, nitrite accumulation and nitric oxide synthase activity.	transcription
59117	1	335474	7	NULL	NULL	0	NULL	T. b. brucei			salvage					adenosine					NULL		0	NULL	NULL	NULL	gw60_microbesinfect_3_9_763_s_151	11489425	T. b. brucei were reported to salvage adenosine via the transporters, P1, which is specific for adenosine and inosine, and P2, which mediates transport of adenosine, adenine, melanophenyl arsenicals and diamidines  38;   51 and   52.	transcription
59118	2	335474	7	NULL	NULL	0	NULL	statement 1			via					P1 transporter					NULL		0	NULL	NULL	NULL	gw60_microbesinfect_3_9_763_s_151	11489425	T. b. brucei were reported to salvage adenosine via the transporters, P1, which is specific for adenosine and inosine, and P2, which mediates transport of adenosine, adenine, melanophenyl arsenicals and diamidines  38;   51 and   52.	transcription
59119	3	335474	7	NULL	NULL	0	NULL	P1 transporter			is specific for					adenosine					NULL		0	NULL	NULL	NULL	gw60_microbesinfect_3_9_763_s_151	11489425	T. b. brucei were reported to salvage adenosine via the transporters, P1, which is specific for adenosine and inosine, and P2, which mediates transport of adenosine, adenine, melanophenyl arsenicals and diamidines  38;   51 and   52.	transcription
59120	4	335474	7	NULL	NULL	0	NULL	P1 transporter			is specific for					inosine					NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_3_9_763_s_151	11489425	T. b. brucei were reported to salvage adenosine via the transporters, P1, which is specific for adenosine and inosine, and P2, which mediates transport of adenosine, adenine, melanophenyl arsenicals and diamidines  38;   51 and   52.	transcription
59124	5	335474	7	NULL	NULL	0	NULL	P2			mediates					adenosine		transport of			NULL		0	NULL	NULL	NULL	gw60_microbesinfect_3_9_763_s_151	11489425	T. b. brucei were reported to salvage adenosine via the transporters, P1, which is specific for adenosine and inosine, and P2, which mediates transport of adenosine, adenine, melanophenyl arsenicals and diamidines  38;   51 and   52.	transcription
59129	6	335474	7	NULL	NULL	0	NULL	P2			mediates					adenine		transport of			NULL		0	NULL	NULL	NULL	gw60_microbesinfect_3_9_763_s_151	11489425	T. b. brucei were reported to salvage adenosine via the transporters, P1, which is specific for adenosine and inosine, and P2, which mediates transport of adenosine, adenine, melanophenyl arsenicals and diamidines  38;   51 and   52.	transcription
59134	7	335474	7	NULL	NULL	0	NULL	P2			mediates					melanophenyl arsenicals		transport of			NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_3_9_763_s_151	11489425	T. b. brucei were reported to salvage adenosine via the transporters, P1, which is specific for adenosine and inosine, and P2, which mediates transport of adenosine, adenine, melanophenyl arsenicals and diamidines  38;   51 and   52.	transcription
59138	8	335474	7	NULL	NULL	0	NULL	P2			mediates					diamidines		transport of			NULL		0	NULL	NULL	NULL	gw60_microbesinfect_3_9_763_s_151	11489425	T. b. brucei were reported to salvage adenosine via the transporters, P1, which is specific for adenosine and inosine, and P2, which mediates transport of adenosine, adenine, melanophenyl arsenicals and diamidines  38;   51 and   52.	transcription
79011	1	335475	6	NULL	NULL	0	NULL	adenosine	Chemical		is formed from					adenine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_3_457_s_230	9457844	The enzyme activities present in both halobacteria suggest that this conversion implies formation of adenosine from adenine and ribose-1-phosphate catalyzed by adenosine phosphorylase, followed by deamination of adenosine to inosine catalyzed by adenosine deaminase.	transcription
79012	2	335475	6	NULL	NULL	0	NULL	adenosine	Chemical		is formed from					ribose-1-phosphate	GP				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_3_457_s_230	9457844	The enzyme activities present in both halobacteria suggest that this conversion implies formation of adenosine from adenine and ribose-1-phosphate catalyzed by adenosine phosphorylase, followed by deamination of adenosine to inosine catalyzed by adenosine deaminase.	transcription
79013	3	335475	6	NULL	NULL	0	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_3_457_s_230	9457844	The enzyme activities present in both halobacteria suggest that this conversion implies formation of adenosine from adenine and ribose-1-phosphate catalyzed by adenosine phosphorylase, followed by deamination of adenosine to inosine catalyzed by adenosine deaminase.	transcription
79014	4	335475	6	NULL	NULL	0	NULL	adenosine phosphorylase	GP		catalyzes					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_3_457_s_230	9457844	The enzyme activities present in both halobacteria suggest that this conversion implies formation of adenosine from adenine and ribose-1-phosphate catalyzed by adenosine phosphorylase, followed by deamination of adenosine to inosine catalyzed by adenosine deaminase.	transcription
79015	5	335475	6	NULL	NULL	0	NULL	adenosine	Chemical		is deaminated to					inosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_3_457_s_230	9457844	The enzyme activities present in both halobacteria suggest that this conversion implies formation of adenosine from adenine and ribose-1-phosphate catalyzed by adenosine phosphorylase, followed by deamination of adenosine to inosine catalyzed by adenosine deaminase.	transcription
79016	6	335475	6	NULL	NULL	0	NULL	statement 5	Process		is catalyzed by					adenosine deaminase	GP				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_3_457_s_230	9457844	The enzyme activities present in both halobacteria suggest that this conversion implies formation of adenosine from adenine and ribose-1-phosphate catalyzed by adenosine phosphorylase, followed by deamination of adenosine to inosine catalyzed by adenosine deaminase.	transcription
59143	1	335475	7	NULL	NULL	0	NULL	adenosine			formed from					adenine					NULL	halobacteria	NULL	NULL	NULL	NULL	gw60_jbacteriol_180_3_457_s_230	9457844	The enzyme activities present in both halobacteria suggest that this conversion implies formation of adenosine from adenine and ribose-1-phosphate catalyzed by adenosine phosphorylase, followed by deamination of adenosine to inosine catalyzed by adenosine deaminase.	transcription
59145	2	335475	7	NULL	NULL	0	NULL	adenosine			formed from					ribose-1-phosphate					NULL	halobacteria	NULL	NULL	NULL	NULL	gw60_jbacteriol_180_3_457_s_230	9457844	The enzyme activities present in both halobacteria suggest that this conversion implies formation of adenosine from adenine and ribose-1-phosphate catalyzed by adenosine phosphorylase, followed by deamination of adenosine to inosine catalyzed by adenosine deaminase.	transcription
59146	3	335475	7	NULL	NULL	0	NULL	statement 1			occur simulataneous with					statement 2					NULL	halobacteria	NULL	NULL	NULL	NULL	gw60_jbacteriol_180_3_457_s_230	9457844	The enzyme activities present in both halobacteria suggest that this conversion implies formation of adenosine from adenine and ribose-1-phosphate catalyzed by adenosine phosphorylase, followed by deamination of adenosine to inosine catalyzed by adenosine deaminase.	transcription
59174	4	335475	7	NULL	NULL	0	NULL	adenosine phosphorylase			catalyze					statement 3					NULL	halobacteria	NULL	NULL	NULL	NULL	gw60_jbacteriol_180_3_457_s_230	9457844	The enzyme activities present in both halobacteria suggest that this conversion implies formation of adenosine from adenine and ribose-1-phosphate catalyzed by adenosine phosphorylase, followed by deamination of adenosine to inosine catalyzed by adenosine deaminase.	transcription
59175	5	335475	7	NULL	NULL	0	NULL	adenosine			deaminates to					inosine					NULL	halobacteria	NULL	NULL	NULL	NULL	gw60_jbacteriol_180_3_457_s_230	9457844	The enzyme activities present in both halobacteria suggest that this conversion implies formation of adenosine from adenine and ribose-1-phosphate catalyzed by adenosine phosphorylase, followed by deamination of adenosine to inosine catalyzed by adenosine deaminase.	transcription
59176	6	335475	7	NULL	NULL	0	NULL	adenosine deaminase			catalyze					statement 5					NULL	halobacteria	NULL	NULL	NULL	NULL	gw60_jbacteriol_180_3_457_s_230	9457844	The enzyme activities present in both halobacteria suggest that this conversion implies formation of adenosine from adenine and ribose-1-phosphate catalyzed by adenosine phosphorylase, followed by deamination of adenosine to inosine catalyzed by adenosine deaminase.	transcription
59177	7	335475	7	NULL	NULL	0	NULL	statement 5			is followed by					statement 4					NULL	halobacteria	NULL	NULL	NULL	NULL	gw60_jbacteriol_180_3_457_s_230	9457844	The enzyme activities present in both halobacteria suggest that this conversion implies formation of adenosine from adenine and ribose-1-phosphate catalyzed by adenosine phosphorylase, followed by deamination of adenosine to inosine catalyzed by adenosine deaminase.	transcription
79017	1	335476	6	NULL	NULL	0	NULL	IMP	Chemical		is oxidized to					XMP	Chemical				NULL		0	NULL	NULL	NULL	gw60_cell_85_6_921_s_10	8681386	IMPDH catalyzes the nicotinamide adenine dinucleotide (NAD)-dependent oxidation of inosine-5''-monophosphate  (IMP) to xanthosine-5''-monophosphate (XMP), which is the committed step in de novo guanosine nucleotide  biosynthesis (Crabtree and Henderson, 1971   ;  Snyder et al., 1972   ;  Jackson  et al., 1975   ;  Weber, 1983   ).	transcription
79018	2	335476	6	NULL	NULL	0	NULL	IMPDH	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cell_85_6_921_s_10	8681386	IMPDH catalyzes the nicotinamide adenine dinucleotide (NAD)-dependent oxidation of inosine-5''-monophosphate  (IMP) to xanthosine-5''-monophosphate (XMP), which is the committed step in de novo guanosine nucleotide  biosynthesis (Crabtree and Henderson, 1971   ;  Snyder et al., 1972   ;  Jackson  et al., 1975   ;  Weber, 1983   ).	transcription
79019	3	335476	6	NULL	NULL	0	NULL	statement 1	Process		is dependent on					NAD	Chemical				NULL		0	NULL	NULL	NULL	gw60_cell_85_6_921_s_10	8681386	IMPDH catalyzes the nicotinamide adenine dinucleotide (NAD)-dependent oxidation of inosine-5''-monophosphate  (IMP) to xanthosine-5''-monophosphate (XMP), which is the committed step in de novo guanosine nucleotide  biosynthesis (Crabtree and Henderson, 1971   ;  Snyder et al., 1972   ;  Jackson  et al., 1975   ;  Weber, 1983   ).	transcription
79020	4	335476	6	NULL	NULL	0	NULL	NAD	Chemical		is					nicotinamide adenine dinucleotide	Chemical				NULL		0	NULL	NULL	NULL	gw60_cell_85_6_921_s_10	8681386	IMPDH catalyzes the nicotinamide adenine dinucleotide (NAD)-dependent oxidation of inosine-5''-monophosphate  (IMP) to xanthosine-5''-monophosphate (XMP), which is the committed step in de novo guanosine nucleotide  biosynthesis (Crabtree and Henderson, 1971   ;  Snyder et al., 1972   ;  Jackson  et al., 1975   ;  Weber, 1983   ).	transcription
79021	5	335476	6	NULL	NULL	0	NULL	IMP	Chemical		is					inosine-5''-monophosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_cell_85_6_921_s_10	8681386	IMPDH catalyzes the nicotinamide adenine dinucleotide (NAD)-dependent oxidation of inosine-5''-monophosphate  (IMP) to xanthosine-5''-monophosphate (XMP), which is the committed step in de novo guanosine nucleotide  biosynthesis (Crabtree and Henderson, 1971   ;  Snyder et al., 1972   ;  Jackson  et al., 1975   ;  Weber, 1983   ).	transcription
79022	6	335476	6	NULL	NULL	0	NULL	XMP	Chemical		is					xanthosine-5''-monophosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_cell_85_6_921_s_10	8681386	IMPDH catalyzes the nicotinamide adenine dinucleotide (NAD)-dependent oxidation of inosine-5''-monophosphate  (IMP) to xanthosine-5''-monophosphate (XMP), which is the committed step in de novo guanosine nucleotide  biosynthesis (Crabtree and Henderson, 1971   ;  Snyder et al., 1972   ;  Jackson  et al., 1975   ;  Weber, 1983   ).	transcription
59178	1	335476	7	NULL	NULL	0	NULL	IMP			oxidizes to					XMP					NULL		0	NULL	NULL	NULL	gw60_cell_85_6_921_s_10	8681386	IMPDH catalyzes the nicotinamide adenine dinucleotide (NAD)-dependent oxidation of inosine-5''-monophosphate  (IMP) to xanthosine-5''-monophosphate (XMP), which is the committed step in de novo guanosine nucleotide  biosynthesis (Crabtree and Henderson, 1971   ;  Snyder et al., 1972   ;  Jackson  et al., 1975   ;  Weber, 1983   ).	transcription
59179	2	335476	7	NULL	NULL	0	NULL	statement 1			depends on					NAD					NULL		0	NULL	NULL	NULL	gw60_cell_85_6_921_s_10	8681386	IMPDH catalyzes the nicotinamide adenine dinucleotide (NAD)-dependent oxidation of inosine-5''-monophosphate  (IMP) to xanthosine-5''-monophosphate (XMP), which is the committed step in de novo guanosine nucleotide  biosynthesis (Crabtree and Henderson, 1971   ;  Snyder et al., 1972   ;  Jackson  et al., 1975   ;  Weber, 1983   ).	transcription
59180	3	335476	7	NULL	NULL	0	NULL	IMPDH			catalyzes					statement 2					NULL		0	NULL	NULL	NULL	gw60_cell_85_6_921_s_10	8681386	IMPDH catalyzes the nicotinamide adenine dinucleotide (NAD)-dependent oxidation of inosine-5''-monophosphate  (IMP) to xanthosine-5''-monophosphate (XMP), which is the committed step in de novo guanosine nucleotide  biosynthesis (Crabtree and Henderson, 1971   ;  Snyder et al., 1972   ;  Jackson  et al., 1975   ;  Weber, 1983   ).	transcription
59181	4	335476	7	NULL	NULL	0	NULL	statement 1			committed step in					de novo guanosine nucleotide biosynthesis					NULL		0	NULL	NULL	NULL	gw60_cell_85_6_921_s_10	8681386	IMPDH catalyzes the nicotinamide adenine dinucleotide (NAD)-dependent oxidation of inosine-5''-monophosphate  (IMP) to xanthosine-5''-monophosphate (XMP), which is the committed step in de novo guanosine nucleotide  biosynthesis (Crabtree and Henderson, 1971   ;  Snyder et al., 1972   ;  Jackson  et al., 1975   ;  Weber, 1983   ).	transcription
59182	5	335476	7	NULL	NULL	0	NULL	NAD			is					nicotinamide adenine dinucleotide					NULL		0	NULL	NULL	NULL	gw60_cell_85_6_921_s_10	8681386	IMPDH catalyzes the nicotinamide adenine dinucleotide (NAD)-dependent oxidation of inosine-5''-monophosphate  (IMP) to xanthosine-5''-monophosphate (XMP), which is the committed step in de novo guanosine nucleotide  biosynthesis (Crabtree and Henderson, 1971   ;  Snyder et al., 1972   ;  Jackson  et al., 1975   ;  Weber, 1983   ).	transcription
59183	6	335476	7	NULL	NULL	0	NULL	IMP			is					inosine-5''-monophosphate					NULL		0	NULL	NULL	NULL	gw60_cell_85_6_921_s_10	8681386	IMPDH catalyzes the nicotinamide adenine dinucleotide (NAD)-dependent oxidation of inosine-5''-monophosphate  (IMP) to xanthosine-5''-monophosphate (XMP), which is the committed step in de novo guanosine nucleotide  biosynthesis (Crabtree and Henderson, 1971   ;  Snyder et al., 1972   ;  Jackson  et al., 1975   ;  Weber, 1983   ).	transcription
59184	7	335476	7	NULL	NULL	0	NULL	XMP			is					xanthosine-5''-monophosphate					NULL		0	NULL	NULL	NULL	gw60_cell_85_6_921_s_10	8681386	IMPDH catalyzes the nicotinamide adenine dinucleotide (NAD)-dependent oxidation of inosine-5''-monophosphate  (IMP) to xanthosine-5''-monophosphate (XMP), which is the committed step in de novo guanosine nucleotide  biosynthesis (Crabtree and Henderson, 1971   ;  Snyder et al., 1972   ;  Jackson  et al., 1975   ;  Weber, 1983   ).	transcription
59185	1	335479	7	NULL	NULL	0	NULL	P1 type system 			mediates					adenosine		uptake of			NULL	BF life cycle stage	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_24_21499_s_14	11937511	The P1 type system mediates the uptake of purine nucleosides (adenosine, inosine, and guanosine) and is detected in both BF and PF life cycle stages, and the P2 type system mediates the uptake of adenosine and adenine, as well as several anti-trypanosomal drugs, and is detected only in the BF ( 6,  7) parasites.	transcription
59186	2	335479	7	NULL	NULL	0	NULL	P1 type system 			mediates					inosine		uptake of			NULL	BF life cycle stage	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_24_21499_s_14	11937511	The P1 type system mediates the uptake of purine nucleosides (adenosine, inosine, and guanosine) and is detected in both BF and PF life cycle stages, and the P2 type system mediates the uptake of adenosine and adenine, as well as several anti-trypanosomal drugs, and is detected only in the BF ( 6,  7) parasites.	transcription
59187	3	335479	7	NULL	NULL	0	NULL	P1 type system 			mediates					guanosine		uptake of			NULL	BF life cycle stage	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_24_21499_s_14	11937511	The P1 type system mediates the uptake of purine nucleosides (adenosine, inosine, and guanosine) and is detected in both BF and PF life cycle stages, and the P2 type system mediates the uptake of adenosine and adenine, as well as several anti-trypanosomal drugs, and is detected only in the BF ( 6,  7) parasites.	transcription
59188	4	335479	7	NULL	NULL	0	NULL	adenosine 			is a type of					purine nucleoside					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_24_21499_s_14	11937511	The P1 type system mediates the uptake of purine nucleosides (adenosine, inosine, and guanosine) and is detected in both BF and PF life cycle stages, and the P2 type system mediates the uptake of adenosine and adenine, as well as several anti-trypanosomal drugs, and is detected only in the BF ( 6,  7) parasites.	transcription
59189	5	335479	7	NULL	NULL	0	NULL	inosine			is a type of					purine nucleoside					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_24_21499_s_14	11937511	The P1 type system mediates the uptake of purine nucleosides (adenosine, inosine, and guanosine) and is detected in both BF and PF life cycle stages, and the P2 type system mediates the uptake of adenosine and adenine, as well as several anti-trypanosomal drugs, and is detected only in the BF ( 6,  7) parasites.	transcription
59190	6	335479	7	NULL	NULL	0	NULL	guanosine			is a type of					purine nucleoside					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_24_21499_s_14	11937511	The P1 type system mediates the uptake of purine nucleosides (adenosine, inosine, and guanosine) and is detected in both BF and PF life cycle stages, and the P2 type system mediates the uptake of adenosine and adenine, as well as several anti-trypanosomal drugs, and is detected only in the BF ( 6,  7) parasites.	transcription
59191	7	335479	7	NULL	NULL	0	NULL	P1 type system 			mediates					adenosine		uptake of			NULL	PF life cycle stage	0	NULL	NULL	NULL	gw60_jbiolchem_277_24_21499_s_14	11937511	The P1 type system mediates the uptake of purine nucleosides (adenosine, inosine, and guanosine) and is detected in both BF and PF life cycle stages, and the P2 type system mediates the uptake of adenosine and adenine, as well as several anti-trypanosomal drugs, and is detected only in the BF ( 6,  7) parasites.	transcription
59192	8	335479	7	NULL	NULL	0	NULL	P1 type system 			mediate					inosine		uptake of			NULL	PF life cycle stage	0	NULL	NULL	NULL	gw60_jbiolchem_277_24_21499_s_14	11937511	The P1 type system mediates the uptake of purine nucleosides (adenosine, inosine, and guanosine) and is detected in both BF and PF life cycle stages, and the P2 type system mediates the uptake of adenosine and adenine, as well as several anti-trypanosomal drugs, and is detected only in the BF ( 6,  7) parasites.	transcription
59193	9	335479	7	NULL	NULL	0	NULL	P1 type system 			mediates					guanosine		uptake of			NULL	PF life cycle stage	0	NULL	NULL	NULL	gw60_jbiolchem_277_24_21499_s_14	11937511	The P1 type system mediates the uptake of purine nucleosides (adenosine, inosine, and guanosine) and is detected in both BF and PF life cycle stages, and the P2 type system mediates the uptake of adenosine and adenine, as well as several anti-trypanosomal drugs, and is detected only in the BF ( 6,  7) parasites.	transcription
59194	10	335479	7	NULL	NULL	0	NULL	P2 type system			mediates					adenosine		uptake of			NULL	BF parasites	0	NULL	NULL	NULL	gw60_jbiolchem_277_24_21499_s_14	11937511	The P1 type system mediates the uptake of purine nucleosides (adenosine, inosine, and guanosine) and is detected in both BF and PF life cycle stages, and the P2 type system mediates the uptake of adenosine and adenine, as well as several anti-trypanosomal drugs, and is detected only in the BF ( 6,  7) parasites.	transcription
59195	11	335479	7	NULL	NULL	0	NULL	P2 type system			mediates					adenine		uptake of			NULL	BF parasites	0	NULL	NULL	NULL	gw60_jbiolchem_277_24_21499_s_14	11937511	The P1 type system mediates the uptake of purine nucleosides (adenosine, inosine, and guanosine) and is detected in both BF and PF life cycle stages, and the P2 type system mediates the uptake of adenosine and adenine, as well as several anti-trypanosomal drugs, and is detected only in the BF ( 6,  7) parasites.	transcription
59196	12	335479	7	NULL	NULL	0	NULL	P2 type system			mediates					anti-trypanosomal drugs		uptake of			NULL	BF parasites	0	NULL	NULL	NULL	gw60_jbiolchem_277_24_21499_s_14	11937511	The P1 type system mediates the uptake of purine nucleosides (adenosine, inosine, and guanosine) and is detected in both BF and PF life cycle stages, and the P2 type system mediates the uptake of adenosine and adenine, as well as several anti-trypanosomal drugs, and is detected only in the BF ( 6,  7) parasites.	transcription
79097	1	335481	6	NULL	NULL	0	NULL	astrocytes	Cell		release					adenine nucleotides	Chemical				NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
79098	2	335481	6	NULL	NULL	0	NULL	astrocytes	Chemical		release					adenosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
79099	3	335481	6	NULL	NULL	0	NULL	neurons	CellComponent		release					purines	Chemical				NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
79100	4	335481	6	NULL	NULL	0	NULL	statement 3	Process		occurs during					glycolysis	Process	inhibition of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
79101	5	335481	6	NULL	NULL	0	NULL	statement 3	Process		occurs during					oxidative phosphorylation	Process	inhibition of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59200	1	335481	7	NULL	NULL	0	NULL	astrocytes			release					adenine nucleotides					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59201	2	335481	7	NULL	NULL	0	NULL	astrocytes			release					adenosine					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59202	3	335481	7	NULL	NULL	0	NULL	neurons			release					adenine nucleotides					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59203	4	335481	7	NULL	NULL	0	NULL	neurons			release					adenosine					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59204	5	335481	7	NULL	NULL	0	NULL	statement 1			more significantly than					statement 3					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59205	6	335481	7	NULL	NULL	0	NULL	statement 2			more significantly than					statement 4					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59206	7	335481	7	NULL	NULL	0	NULL	neurons			release					purines					NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59207	8	335481	7	NULL	NULL	0	NULL	statement 7			during					glycolysis		inhibition of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59208	9	335481	7	NULL	NULL	0	NULL	statement 7			during					oxidative phosphorylation 		inhibition of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59209	10	335481	7	NULL	NULL	0	NULL	statement 8		release from	is greater than					statement 9		release from			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59210	11	335481	7	NULL	NULL	0	NULL	astrocytes			release					purines					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59211	12	335481	7	NULL	NULL	0	NULL	statement 11			during					glycolysis		inhibition of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59212	13	335481	7	NULL	NULL	0	NULL	statement 11			during					oxidative phosphorylation 		inhibition of			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59213	14	335481	7	NULL	NULL	0	NULL	statement 12		release from	is same as					statement 13		release from			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59214	15	335481	7	NULL	NULL	0	NULL	neurons			release					inosine					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59285	16	335481	7	NULL	NULL	0	NULL	neurons			release					hypoxanthine					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59286	17	335481	7	NULL	NULL	0	NULL	NaCN			induce					statement 15					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59287	18	335481	7	NULL	NULL	0	NULL	NACN			induce					statement 16					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59288	19	335481	7	NULL	NULL	0	NULL	IAA			induce					statement 15					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59289	20	335481	7	NULL	NULL	0	NULL	IAA			induce					statement 16					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59290	21	335481	7	NULL	NULL	0	NULL	statement 17		release from	is same as					statement 19		release from			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59291	22	335481	7	NULL	NULL	0	NULL	statement 18		release from	is same as					statement 20		release from			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59292	23	335481	7	NULL	NULL	0	NULL	astrocytes			release					hypoxanthine					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59293	24	335481	7	NULL	NULL	0	NULL	astrocytes			release					inosine					NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59294	25	335481	7	NULL	NULL	0	NULL	NACN			induce					statement 23					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59295	26	335481	7	NULL	NULL	0	NULL	IAA			induce					statement 23					NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59296	27	335481	7	NULL	NULL	0	NULL	NACN			induce					statement 24					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59297	28	335481	7	NULL	NULL	0	NULL	IAA			induce					statement 24					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59298	29	335481	7	NULL	NULL	0	NULL	statement 25		release from	is greater than					statement 18		release from			NULL		NULL	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59299	30	335481	7	NULL	NULL	0	NULL	statement 28		release from	is greater than					statement 20		release from			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59300	31	335481	7	NULL	NULL	0	NULL	statement 27		release from	is greater than					statement 17		release from			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59301	32	335481	7	NULL	NULL	0	NULL	statement 26		release from	is greater than					statement 19		release from			NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59302	33	335481	7	NULL	NULL	0	NULL	OGD			increase		significantly			statement 4					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59303	34	335481	7	NULL	NULL	0	NULL	NaCN 			increase		significantly			statement 4					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59304	35	335481	7	NULL	NULL	0	NULL	 IAA			increase		significantly			statement 4					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59305	36	335481	7	NULL	NULL	0	NULL	OGD			does not increase					statement 2					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59306	37	335481	7	NULL	NULL	0	NULL	NACN			does not increase					statement 2					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59307	38	335481	7	NULL	NULL	0	NULL	IAA			does not increase					statement 2					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59308	39	335481	7	NULL	NULL	0	NULL	DPR			blocks					statement 15					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59309	40	335481	7	NULL	NULL	0	NULL	DPR			blocks					statement 24					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59310	41	335481	7	NULL	NULL	0	NULL	DPR			blocks					statement 4					NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_43_5_836_s_216	12384169	The primary findings of this study are that (a) astrocytes released significantly more [3]adenine nucleotides and [3]adenosine than neurons, (b) neurons released greater amounts of [3]purines during inhibition of glycolysis compared to inhibition of oxidative phosphorylation while astrocytes released similar amounts with both stimuli, (c) NaCN and IAA treatments induced the release of similar amounts of [3]inosine and [3]hypoxanthine from neurons and ~2-4 fold more [3]hypoxanthine than [3]inosine from astrocytes, (d) OGD, NaCN and IAA conditions produced significant increases in [3]adenosine release from neurons but not astrocytes, and (e) DPR blocked [3]inosine release from both astrocytes and neurons but only blocked [3]adenosine release from neurons.	transcription
59311	1	335483	7	NULL	NULL	0	NULL	P1			mediates					adenosine		uptake of			NULL	T. b. brucei bloodstream	NULL	NULL	NULL	NULL	gw60_molpharmacol_56_6_1162_s_102	10570043	View this table:   [in this window]   [in a new window]     [[ TABLE 1        Ki ]] values for potential inhibitors of P1- and P2-mediated adenosine uptake in  T. b. brucei bloodstream forms    Initial rates of transport were measured by incubating 107 cells for 10 s with [3]adenosine in the presence of increasing amounts of inhibitor (at least 8 points) and 100 muM adenine (P1 mediated) or 100 muM inosine (P2 mediated).	transcription
59312	2	335483	7	NULL	NULL	0	NULL	P2			mediates					adenosine		uptake of			NULL	T. b. brucei bloodstream	0	NULL	NULL	NULL	gw60_molpharmacol_56_6_1162_s_102	10570043	View this table:   [in this window]   [in a new window]     [[ TABLE 1        Ki ]] values for potential inhibitors of P1- and P2-mediated adenosine uptake in  T. b. brucei bloodstream forms    Initial rates of transport were measured by incubating 107 cells for 10 s with [3]adenosine in the presence of increasing amounts of inhibitor (at least 8 points) and 100 muM adenine (P1 mediated) or 100 muM inosine (P2 mediated).	transcription
79117	1	335484	6	NULL	NULL	0	NULL	adenosine	Chemical		is converted to					inosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
79118	2	335484	6	NULL	NULL	0	NULL	adenosine deaminase	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
79119	3	335484	6	NULL	NULL	0	NULL	DPCPX	Chemical		is a type of					adenosine A1 receptor antagonist	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
79120	4	335484	6	NULL	NULL	0	NULL	adenine nucleotides	Chemical		forms					adenosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
79121	5	335484	6	NULL	NULL	0	NULL	AOPCP	Chemical		inhibits					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
59313	1	335484	7	NULL	NULL	0	NULL	AOPCP			inhibits					ATP		synaptic transmission of 			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
59314	2	335484	7	NULL	NULL	0	NULL	AOPCP			inhibits					gamma-substituted ATP analogs		synaptic transmission of 			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
59315	3	335484	7	NULL	NULL	0	NULL	AOPCP			an inhibitor of					ecto-5'-nucleotidase					NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
59316	4	335484	7	NULL	NULL	0	NULL	adenosine			formed from					adenine nucleotides		extracellular			NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
59317	5	335484	7	NULL	NULL	0	NULL	ecto-5'-nucleotidase			catalyze					statement 4					NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
59318	6	335484	7	NULL	NULL	0	NULL	adenosine deaminase			inhibits					ATP 		synaptic transmission of 			NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
59319	7	335484	7	NULL	NULL	0	NULL	adenosine deaminase			inhibits					gamma-substituted ATP analogs		synaptic transmission of 			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
59320	8	335484	7	NULL	NULL	0	NULL	adenosine			converted to					inosine					NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
59321	9	335484	7	NULL	NULL	0	NULL	adenosine deaminase			catalyze					statement 8					NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
59322	10	335484	7	NULL	NULL	0	NULL	inosine			is a type of					inactive metabolite					NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
59323	11	335484	7	NULL	NULL	0	NULL	DPCPX			inhibits					ATP		synaptic transmission of 			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
59324	12	335484	7	NULL	NULL	0	NULL	DPCPX			inhibits					 gamma-substituted ATP analogs		synaptic transmission of 			NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
59325	13	335484	7	NULL	NULL	0	NULL	DPCPX			is a antagonist of					adenosine A1 receptor 					NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
59326	14	335484	7	NULL	NULL	0	NULL	dipyridamole			potentiate					ATP 		synaptic transmission of 			NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
59327	15	335484	7	NULL	NULL	0	NULL	dipyridamole			potentiate					gamma-substituted ATP analogs		synaptic transmission of 			NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
59328	16	335484	7	NULL	NULL	0	NULL	dipyridamole			is an inhibitor of					adenosine uptake					NULL		0	NULL	NULL	NULL	gw60_jneurosci_18_6_1987_s_168	9482785	Thus, the inhibitory effect on synaptic transmission of ATP and gamma-substituted ATP analogs was inhibited (1) by AOPCP, an inhibitor of ecto-5'-nucleotidase, the enzyme that forms adenosine from extracellular adenine nucleotides, (2) by adenosine deaminase, which converts adenosine into its inactive metabolite inosine, and (3) by DPCPX, an adenosine A1 receptor antagonist, whereas (4) it was potentiated by the adenosine uptake inhibitor dipyridamole.	transcription
79122	1	335485	6	NULL	NULL	0	NULL	Fe3+	Chemical		bind					adenine N7	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_43_42495_s_181	12913009	5, whereas binding of Fe3+ to the adenine N7 is favored at neutral pH ( ).	transcription
59329	1	335485	7	NULL	NULL	0	NULL	Fe3+			bind					adenine N7					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_43_42495_s_181	12913009	5, whereas binding of Fe3+ to the adenine N7 is favored at neutral pH ( ).	transcription
59330	2	335485	7	NULL	NULL	0	NULL	neurtral pH			favours					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_43_42495_s_181	12913009	5, whereas binding of Fe3+ to the adenine N7 is favored at neutral pH ( ).	transcription
59331	1	335488	7	NULL	NULL	0	NULL	M.EcoRI			modifies					recognition hexanucleotide				adenine on the 5''-half of	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_35_37049_s_539	15210696	Further, all but M.EcoRI methylate an adenine either at the 3''-end of the site, or the penultimate base, whereas M.EcoRI modifies the adenine on the 5''-half of the recognition hexanucleotide.	transcription
79123	1	335489	6	NULL	NULL	NULL	NULL	GCAP-2/Ca	GP		regulates					RetGC-1	GP		ICD		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_20_11646_s_176	8662612	Regulation of ICD RetGC-1 by GCAP-2/Ca   and Adenine NucleotidesThe catalytic activity of ICD  RetGC-1 is regulated by GCAP-2, Ca , and adenine  nucleotides ( Fig. 5,  B  and  C).	transcription
79124	2	335489	6	NULL	NULL	0	NULL	GCAP-2	GP		regulates					RetGC-1	GP	catalytic activity of	ICD		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_20_11646_s_176	8662612	Regulation of ICD RetGC-1 by GCAP-2/Ca   and Adenine NucleotidesThe catalytic activity of ICD  RetGC-1 is regulated by GCAP-2, Ca , and adenine  nucleotides ( Fig. 5,  B  and  C).	transcription
59332	1	335489	7	NULL	NULL	0	NULL	GCAP-2			regulates					ICD RetGC-1		catalytic activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_20_11646_s_176	8662612	Regulation of ICD RetGC-1 by GCAP-2/Ca   and Adenine NucleotidesThe catalytic activity of ICD  RetGC-1 is regulated by GCAP-2, Ca , and adenine  nucleotides ( Fig. 5,  B  and  C).	transcription
59333	2	335489	7	NULL	NULL	0	NULL	Ca			regulates					ICD RetGC-1		catalytic activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_20_11646_s_176	8662612	Regulation of ICD RetGC-1 by GCAP-2/Ca   and Adenine NucleotidesThe catalytic activity of ICD  RetGC-1 is regulated by GCAP-2, Ca , and adenine  nucleotides ( Fig. 5,  B  and  C).	transcription
59334	3	335489	7	NULL	NULL	0	NULL	adenine nucleotides			regulates					ICD RetGC-1		catalytic activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_20_11646_s_176	8662612	Regulation of ICD RetGC-1 by GCAP-2/Ca   and Adenine NucleotidesThe catalytic activity of ICD  RetGC-1 is regulated by GCAP-2, Ca , and adenine  nucleotides ( Fig. 5,  B  and  C).	transcription
59335	1	335490	7	NULL	NULL	0	NULL	DEPC			mediates					ANF 5''-FS		modification of		adenines at positions -113, -112, -111, -110, and -105 on the + strand	NULL		0	NULL	NULL	NULL	gw60_circulationres_77_6_1060_s_117	7586217	DEPC-mediated modification of adenines at positions -113, -112, -111, -110, and -105 on the + strand of the ANF 5''-FS interfered with complex formation (Fig 5A  , DEPC +), as did modification of adenines -114 and -116 on the - strand (Fig 5A  , DEPC -).	transcription
59336	2	335490	7	NULL	NULL	0	NULL	DEPC			mediates					ANF 5''-FS		modification of		adenines -114 and -116 on the - strand	NULL		0	NULL	NULL	NULL	gw60_circulationres_77_6_1060_s_117	7586217	DEPC-mediated modification of adenines at positions -113, -112, -111, -110, and -105 on the + strand of the ANF 5''-FS interfered with complex formation (Fig 5A  , DEPC +), as did modification of adenines -114 and -116 on the - strand (Fig 5A  , DEPC -).	transcription
79125	1	335491	6	NULL	NULL	0	NULL	AMP	Chemical		bind					Mg2+	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_35_37163_s_186	15210687	In the case of product complex with AMP and Mg2+ ( Fig. 5 A), the adenine was recognized by Ile-19 and Tyr-28* through stacking interactions and adenine N1 made a hydrogen bond with Glu-29*, and adenine N6 made hydrogen bonds with Glu-29* and Gly-104*, although positions of adenine and alpha-phosphate of AMP were located away from residues in the Nudix motif.	transcription
59337	1	335491	7	NULL	NULL	0	NULL	AMP			complex with					Mg2+					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_35_37163_s_186	15210687	In the case of product complex with AMP and Mg2+ ( Fig. 5 A), the adenine was recognized by Ile-19 and Tyr-28* through stacking interactions and adenine N1 made a hydrogen bond with Glu-29*, and adenine N6 made hydrogen bonds with Glu-29* and Gly-104*, although positions of adenine and alpha-phosphate of AMP were located away from residues in the Nudix motif.	transcription
59338	2	335491	7	NULL	NULL	0	NULL	adenine			recognized by					Ile-19					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_35_37163_s_186	15210687	In the case of product complex with AMP and Mg2+ ( Fig. 5 A), the adenine was recognized by Ile-19 and Tyr-28* through stacking interactions and adenine N1 made a hydrogen bond with Glu-29*, and adenine N6 made hydrogen bonds with Glu-29* and Gly-104*, although positions of adenine and alpha-phosphate of AMP were located away from residues in the Nudix motif.	transcription
59339	3	335491	7	NULL	NULL	0	NULL	adenine			recognized by					Tyr-28					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_35_37163_s_186	15210687	In the case of product complex with AMP and Mg2+ ( Fig. 5 A), the adenine was recognized by Ile-19 and Tyr-28* through stacking interactions and adenine N1 made a hydrogen bond with Glu-29*, and adenine N6 made hydrogen bonds with Glu-29* and Gly-104*, although positions of adenine and alpha-phosphate of AMP were located away from residues in the Nudix motif.	transcription
59340	4	335491	7	NULL	NULL	0	NULL	statement 2			through					stacking interactions					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_35_37163_s_186	15210687	In the case of product complex with AMP and Mg2+ ( Fig. 5 A), the adenine was recognized by Ile-19 and Tyr-28* through stacking interactions and adenine N1 made a hydrogen bond with Glu-29*, and adenine N6 made hydrogen bonds with Glu-29* and Gly-104*, although positions of adenine and alpha-phosphate of AMP were located away from residues in the Nudix motif.	transcription
59341	5	335491	7	NULL	NULL	0	NULL	statement 3			through					stacking interactions					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_35_37163_s_186	15210687	In the case of product complex with AMP and Mg2+ ( Fig. 5 A), the adenine was recognized by Ile-19 and Tyr-28* through stacking interactions and adenine N1 made a hydrogen bond with Glu-29*, and adenine N6 made hydrogen bonds with Glu-29* and Gly-104*, although positions of adenine and alpha-phosphate of AMP were located away from residues in the Nudix motif.	transcription
59342	6	335491	7	NULL	NULL	0	NULL	adenine N1			hydrogen bond with					Glu-29					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_35_37163_s_186	15210687	In the case of product complex with AMP and Mg2+ ( Fig. 5 A), the adenine was recognized by Ile-19 and Tyr-28* through stacking interactions and adenine N1 made a hydrogen bond with Glu-29*, and adenine N6 made hydrogen bonds with Glu-29* and Gly-104*, although positions of adenine and alpha-phosphate of AMP were located away from residues in the Nudix motif.	transcription
59343	7	335491	7	NULL	NULL	0	NULL	adenine N6			hydrogen bond with					Gly-104					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_35_37163_s_186	15210687	In the case of product complex with AMP and Mg2+ ( Fig. 5 A), the adenine was recognized by Ile-19 and Tyr-28* through stacking interactions and adenine N1 made a hydrogen bond with Glu-29*, and adenine N6 made hydrogen bonds with Glu-29* and Gly-104*, although positions of adenine and alpha-phosphate of AMP were located away from residues in the Nudix motif.	transcription
59344	1	335492	7	NULL	NULL	0	NULL	adenine 			mutated to				at position 5(-5)	cytosine				at position 5(-5)	NULL		0	NULL	NULL	NULL	gw60_cell_84_5_791_s_174	8625416	By contrast, mutation of  the adenine at position 5(-5) dramatically affects EBNA1 binding; the EBNA1 affinity for its  binding site drops 30-fold if position 5 is changed from an adenine  to a cytosine or a guanine (Ambinder et al., 1990   ).	transcription
59345	2	335492	7	NULL	NULL	0	NULL	adenine			mutated to				at position 5(-5)	guanine				at position 5(-5)	NULL		0	NULL	NULL	NULL	gw60_cell_84_5_791_s_174	8625416	By contrast, mutation of  the adenine at position 5(-5) dramatically affects EBNA1 binding; the EBNA1 affinity for its  binding site drops 30-fold if position 5 is changed from an adenine  to a cytosine or a guanine (Ambinder et al., 1990   ).	transcription
59346	3	335492	7	NULL	NULL	0	NULL	statement 1			affects					EBNA1		binding of			NULL		0	NULL	NULL	NULL	gw60_cell_84_5_791_s_174	8625416	By contrast, mutation of  the adenine at position 5(-5) dramatically affects EBNA1 binding; the EBNA1 affinity for its  binding site drops 30-fold if position 5 is changed from an adenine  to a cytosine or a guanine (Ambinder et al., 1990   ).	transcription
59347	4	335492	7	NULL	NULL	0	NULL	statement 2			affects					EBNA1		binding of			NULL		0	NULL	NULL	NULL	gw60_cell_84_5_791_s_174	8625416	By contrast, mutation of  the adenine at position 5(-5) dramatically affects EBNA1 binding; the EBNA1 affinity for its  binding site drops 30-fold if position 5 is changed from an adenine  to a cytosine or a guanine (Ambinder et al., 1990   ).	transcription
59348	1	335493	7	NULL	NULL	0	NULL	common polymorphism			affect					MMP-3		promoter			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_11_1254_s_29	12750310	A naturally occurring and common polymorphism affects the MMP-3 promoter, where either 5 or 6 consecutive adenines (5A/6A) alter transcription factor binding and affect MMP-3 promoter activity.	transcription
59349	2	335493	7	NULL	NULL	0	NULL	5A			alter					transcription factor		binding of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_11_1254_s_29	12750310	A naturally occurring and common polymorphism affects the MMP-3 promoter, where either 5 or 6 consecutive adenines (5A/6A) alter transcription factor binding and affect MMP-3 promoter activity.	transcription
59350	3	335493	7	NULL	NULL	0	NULL	6A			alter					transcription factor		binding of			NULL		0	NULL	NULL	NULL	gw70_circulationres_92_11_1254_s_29	12750310	A naturally occurring and common polymorphism affects the MMP-3 promoter, where either 5 or 6 consecutive adenines (5A/6A) alter transcription factor binding and affect MMP-3 promoter activity.	transcription
59351	4	335493	7	NULL	NULL	0	NULL	5A			affect					MMP-3		activity of		promoter	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_11_1254_s_29	12750310	A naturally occurring and common polymorphism affects the MMP-3 promoter, where either 5 or 6 consecutive adenines (5A/6A) alter transcription factor binding and affect MMP-3 promoter activity.	transcription
59352	5	335493	7	NULL	NULL	0	NULL	6A			affect					MMP-3		activity of		promoter	NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_11_1254_s_29	12750310	A naturally occurring and common polymorphism affects the MMP-3 promoter, where either 5 or 6 consecutive adenines (5A/6A) alter transcription factor binding and affect MMP-3 promoter activity.	transcription
59353	6	335493	7	NULL	NULL	0	NULL	5A			is					5 consecutive adenines					NULL		NULL	NULL	NULL	NULL	gw70_circulationres_92_11_1254_s_29	12750310	A naturally occurring and common polymorphism affects the MMP-3 promoter, where either 5 or 6 consecutive adenines (5A/6A) alter transcription factor binding and affect MMP-3 promoter activity.	transcription
59361	7	335493	7	NULL	NULL	0	NULL	6A			is					6 consecutive adenines					NULL		0	NULL	NULL	NULL	gw70_circulationres_92_11_1254_s_29	12750310	A naturally occurring and common polymorphism affects the MMP-3 promoter, where either 5 or 6 consecutive adenines (5A/6A) alter transcription factor binding and affect MMP-3 promoter activity.	transcription
79126	1	335495	6	NULL	NULL	0	NULL	PABPN1	GP		recognizes					adenine bases	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_19_16916_s_413	12637556	The selection experiment (Fig.  5) suggests that PABPN1 recognizes adenine bases in a specific fashion throughout its  binding site.	transcription
59366	1	335495	7	NULL	NULL	0	NULL	PABPN1			recognizes		specifically			adenine bases				binding site	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_19_16916_s_413	12637556	The selection experiment (Fig.  5) suggests that PABPN1 recognizes adenine bases in a specific fashion throughout its  binding site.	transcription
79127	1	335496	6	NULL	NULL	0	NULL	BVR	GP		phosphorylates					IRS	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_102_20_7109_s_230	15870194	A point mutation introduced in the adenine-binding domain ( ) of BVR (GXGXXG) significantly decreased phosphorylation of IRS by BVR ( Fig. 5).	transcription
79128	2	335496	6	NULL	NULL	0	NULL	BVR	GP	mutation of 	decreases during					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_102_20_7109_s_230	15870194	A point mutation introduced in the adenine-binding domain ( ) of BVR (GXGXXG) significantly decreased phosphorylation of IRS by BVR ( Fig. 5).	transcription
59367	1	335496	7	NULL	NULL	0	NULL	BVR			phosphorylates					IRS					NULL		0	NULL	NULL	NULL	gw70_pnas_102_20_7109_s_230	15870194	A point mutation introduced in the adenine-binding domain ( ) of BVR (GXGXXG) significantly decreased phosphorylation of IRS by BVR ( Fig. 5).	transcription
59368	2	335496	7	NULL	NULL	0	NULL	BVR		point mutant	decrease		significantly	adenine-binding domain GXGXXG		statement 1					NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_20_7109_s_230	15870194	A point mutation introduced in the adenine-binding domain ( ) of BVR (GXGXXG) significantly decreased phosphorylation of IRS by BVR ( Fig. 5).	transcription
59369	1	335497	7	NULL	NULL	0	NULL	Stx1			complex with					ribosome					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2383_s_95	10871371	From such increase a value of  Kiu of 66 muM for the binding of adenine to the Stx1 - ribosome complex was obtained in the previous paper ( 5).	transcription
59370	2	335497	7	NULL	NULL	0	NULL	adenine			bind					statement 1					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2383_s_95	10871371	From such increase a value of  Kiu of 66 muM for the binding of adenine to the Stx1 - ribosome complex was obtained in the previous paper ( 5).	transcription
79129	1	335498	6	NULL	NULL	0	NULL	BAS2p	GP		plays a role in					adenine	Chemical	regulation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_47_29637_s_34	8939895	Finally, together with BAS1p, BAS2p is involved in the adenine regulation of either purine ( 5) or amino acid biosynthetic genes.	transcription
79130	2	335498	6	NULL	NULL	0	NULL	statement 1	Process		occurs together with					BAS1p	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_47_29637_s_34	8939895	Finally, together with BAS1p, BAS2p is involved in the adenine regulation of either purine ( 5) or amino acid biosynthetic genes.	transcription
59371	1	335498	7	NULL	NULL	0	NULL	BAS1p			is involved in					adenine		regulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_47_29637_s_34	8939895	Finally, together with BAS1p, BAS2p is involved in the adenine regulation of either purine ( 5) or amino acid biosynthetic genes.	transcription
59372	2	335498	7	NULL	NULL	0	NULL	BAS2p			is involved in					adenine		regulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_47_29637_s_34	8939895	Finally, together with BAS1p, BAS2p is involved in the adenine regulation of either purine ( 5) or amino acid biosynthetic genes.	transcription
59373	3	335498	7	NULL	NULL	0	NULL	statement 1			occur simulataneous with					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_47_29637_s_34	8939895	Finally, together with BAS1p, BAS2p is involved in the adenine regulation of either purine ( 5) or amino acid biosynthetic genes.	transcription
59374	4	335498	7	NULL	NULL	0	NULL	BAS1p			is involved in					amino acid biosynthetic genes		regulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_47_29637_s_34	8939895	Finally, together with BAS1p, BAS2p is involved in the adenine regulation of either purine ( 5) or amino acid biosynthetic genes.	transcription
59375	5	335498	7	NULL	NULL	0	NULL	BAS2p			is involved in					amino acid biosynthetic genes		regulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_47_29637_s_34	8939895	Finally, together with BAS1p, BAS2p is involved in the adenine regulation of either purine ( 5) or amino acid biosynthetic genes.	transcription
59376	6	335498	7	NULL	NULL	0	NULL	statement 4			occur simulataneous with					statement 5					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_47_29637_s_34	8939895	Finally, together with BAS1p, BAS2p is involved in the adenine regulation of either purine ( 5) or amino acid biosynthetic genes.	transcription
59377	7	335498	7	NULL	NULL	0	NULL	statement 3			is an alternative to					statement 6					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_47_29637_s_34	8939895	Finally, together with BAS1p, BAS2p is involved in the adenine regulation of either purine ( 5) or amino acid biosynthetic genes.	transcription
79131	1	335499	6	NULL	NULL	0	NULL	adenine nucleotides	Chemical		regulates					5 ''-nucleotidase	GP				NULL	rat heart	0	NULL	NULL	NULL	gw60_jpharmacolexpther_298_1_71_s_268	11408527	Sullivan JM and Alpers JB (1971) In vitro regulation of rat heart 5 ''-nucleotidaseby adenine nucleotides and magnesium.	transcription
59378	1	335499	7	NULL	NULL	0	NULL	adenine nucleotides			regulates					5 ''-nucleotidase		rat;;heart			NULL	in vitro	0	NULL	NULL	NULL	gw60_jpharmacolexpther_298_1_71_s_268	11408527	Sullivan JM and Alpers JB (1971) In vitro regulation of rat heart 5 ''-nucleotidaseby adenine nucleotides and magnesium.	transcription
59379	2	335499	7	NULL	NULL	0	NULL	magnesium			regulates					5 ''-nucleotidase		rat;;heart			NULL	in vitro	0	NULL	NULL	NULL	gw60_jpharmacolexpther_298_1_71_s_268	11408527	Sullivan JM and Alpers JB (1971) In vitro regulation of rat heart 5 ''-nucleotidaseby adenine nucleotides and magnesium.	transcription
79132	1	335501	6	NULL	NULL	0	NULL	Stx-1	Chemical		induces					adenine	Chemical	release of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2383_s_80	10871371	Similarly, 4-APP was more effective than adenine in protecting the DNA substrate from the [3]adenine release induced by 200 nM Stx1 (38  plus-or-minus  9 pmol,  n = 5).	transcription
79133	2	335501	6	NULL	NULL	0	NULL	APP	Chemical		protects from					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2383_s_80	10871371	Similarly, 4-APP was more effective than adenine in protecting the DNA substrate from the [3]adenine release induced by 200 nM Stx1 (38  plus-or-minus  9 pmol,  n = 5).	transcription
59380	2	335501	7	NULL	NULL	0	NULL	Stx1 			induce					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2383_s_80	10871371	Similarly, 4-APP was more effective than adenine in protecting the DNA substrate from the [3]adenine release induced by 200 nM Stx1 (38  plus-or-minus  9 pmol,  n = 5).	transcription
59381	3	335501	7	NULL	NULL	0	NULL	4-APP			protects					statement 2					NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2383_s_80	10871371	Similarly, 4-APP was more effective than adenine in protecting the DNA substrate from the [3]adenine release induced by 200 nM Stx1 (38  plus-or-minus  9 pmol,  n = 5).	transcription
59382	1	335501	7	NULL	NULL	0	NULL	adenine			released from					DNA substrate					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2383_s_80	10871371	Similarly, 4-APP was more effective than adenine in protecting the DNA substrate from the [3]adenine release induced by 200 nM Stx1 (38  plus-or-minus  9 pmol,  n = 5).	transcription
59383	4	335501	7	NULL	NULL	0	NULL	adenine			protects					statement 2					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2383_s_80	10871371	Similarly, 4-APP was more effective than adenine in protecting the DNA substrate from the [3]adenine release induced by 200 nM Stx1 (38  plus-or-minus  9 pmol,  n = 5).	transcription
59384	5	335501	7	NULL	NULL	0	NULL	statement 3			more effective than					statement 4					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2383_s_80	10871371	Similarly, 4-APP was more effective than adenine in protecting the DNA substrate from the [3]adenine release induced by 200 nM Stx1 (38  plus-or-minus  9 pmol,  n = 5).	transcription
79134	1	335503	6	NULL	NULL	0	NULL	NADH	Chemical		bind					Th	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10103_s_7	8626568	NADH and reduced acetylpyridine adenine  dinucleotide bound tightly to Th , whereas  NAD , oxidized acetylpyridine adenine dinucleotide,  deamino-NADH, 5``-AMP and adenosine bound less tightly.	transcription
79135	2	335503	6	NULL	NULL	0	NULL	acetylpyridine adenine dinucleotide	Chemical	reduced	bind					Th	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10103_s_7	8626568	NADH and reduced acetylpyridine adenine  dinucleotide bound tightly to Th , whereas  NAD , oxidized acetylpyridine adenine dinucleotide,  deamino-NADH, 5``-AMP and adenosine bound less tightly.	transcription
79136	3	335503	6	NULL	NULL	0	NULL	NAD	Chemical		bind					Th	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10103_s_7	8626568	NADH and reduced acetylpyridine adenine  dinucleotide bound tightly to Th , whereas  NAD , oxidized acetylpyridine adenine dinucleotide,  deamino-NADH, 5``-AMP and adenosine bound less tightly.	transcription
79137	4	335503	6	NULL	NULL	0	NULL	acetylpyridine adenine dinucleotide	Chemical	oxidized	bind					Th	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10103_s_7	8626568	NADH and reduced acetylpyridine adenine  dinucleotide bound tightly to Th , whereas  NAD , oxidized acetylpyridine adenine dinucleotide,  deamino-NADH, 5``-AMP and adenosine bound less tightly.	transcription
79138	5	335503	6	NULL	NULL	0	NULL	deamino-NADH	Chemical		bind					Th	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10103_s_7	8626568	NADH and reduced acetylpyridine adenine  dinucleotide bound tightly to Th , whereas  NAD , oxidized acetylpyridine adenine dinucleotide,  deamino-NADH, 5``-AMP and adenosine bound less tightly.	transcription
79139	6	335503	6	NULL	NULL	0	NULL	AMP	Chemical		bind					Th	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10103_s_7	8626568	NADH and reduced acetylpyridine adenine  dinucleotide bound tightly to Th , whereas  NAD , oxidized acetylpyridine adenine dinucleotide,  deamino-NADH, 5``-AMP and adenosine bound less tightly.	transcription
79140	7	335503	6	NULL	NULL	0	NULL	adenosine	Chemical		bind					Th	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10103_s_7	8626568	NADH and reduced acetylpyridine adenine  dinucleotide bound tightly to Th , whereas  NAD , oxidized acetylpyridine adenine dinucleotide,  deamino-NADH, 5``-AMP and adenosine bound less tightly.	transcription
59619	1	335503	7	NULL	NULL	0	NULL	NADH	Chemical		bind		tightly			Th	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10103_s_7	8626568	NADH and reduced acetylpyridine adenine  dinucleotide bound tightly to Th , whereas  NAD , oxidized acetylpyridine adenine dinucleotide,  deamino-NADH, 5``-AMP and adenosine bound less tightly.	transcription
59620	2	335503	7	NULL	NULL	0	NULL	acetylpyridine adenine dinucleotide	Chemical	reduced	bind		tightly			Th	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_17_10103_s_7	8626568	NADH and reduced acetylpyridine adenine  dinucleotide bound tightly to Th , whereas  NAD , oxidized acetylpyridine adenine dinucleotide,  deamino-NADH, 5``-AMP and adenosine bound less tightly.	transcription
59621	3	335503	7	NULL	NULL	0	NULL	NAD	Chemical		bind		less tightly			Th	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10103_s_7	8626568	NADH and reduced acetylpyridine adenine  dinucleotide bound tightly to Th , whereas  NAD , oxidized acetylpyridine adenine dinucleotide,  deamino-NADH, 5``-AMP and adenosine bound less tightly.	transcription
59622	4	335503	7	NULL	NULL	0	NULL	acetylpyridine adenine dinucleotide	Chemical	oxidized	bind		less tightly			Th	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10103_s_7	8626568	NADH and reduced acetylpyridine adenine  dinucleotide bound tightly to Th , whereas  NAD , oxidized acetylpyridine adenine dinucleotide,  deamino-NADH, 5``-AMP and adenosine bound less tightly.	transcription
59623	5	335503	7	NULL	NULL	0	NULL	deamino-NADH	Chemical		bind		less tightly			Th	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10103_s_7	8626568	NADH and reduced acetylpyridine adenine  dinucleotide bound tightly to Th , whereas  NAD , oxidized acetylpyridine adenine dinucleotide,  deamino-NADH, 5``-AMP and adenosine bound less tightly.	transcription
59624	6	335503	7	NULL	NULL	0	NULL	 5``-AMP	Chemical		bind		less tightly			Th	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10103_s_7	8626568	NADH and reduced acetylpyridine adenine  dinucleotide bound tightly to Th , whereas  NAD , oxidized acetylpyridine adenine dinucleotide,  deamino-NADH, 5``-AMP and adenosine bound less tightly.	transcription
59625	7	335503	7	NULL	NULL	0	NULL	adenosine 	Chemical		bind		less tightly			Th	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10103_s_7	8626568	NADH and reduced acetylpyridine adenine  dinucleotide bound tightly to Th , whereas  NAD , oxidized acetylpyridine adenine dinucleotide,  deamino-NADH, 5``-AMP and adenosine bound less tightly.	transcription
79141	1	335505	6	NULL	NULL	0	NULL	adenine nucleotides	Chemical		inhibits					NK cell	cell	proliferation of 			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_162_12_10358189_s_5	10358189	Adenine nucleotides inhibited NK cell proliferation, with ATP = ADP >  5''-adenylylimidodiphosphate > AMP = adenosine; ADP-ribose and nicotinamide  adenine dinucleotide, but not nicotinamide or UTP, caused a dose-dependent  suppression of thymidine uptake.	transcription
59626	1	335505	7	NULL	NULL	0	NULL	Adenine nucleotides	NucleicAcid		inhibit					NK cell	Cell	cell proliferation of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_162_12_10358189_s_5	10358189	Adenine nucleotides inhibited NK cell proliferation, with ATP = ADP >  5''-adenylylimidodiphosphate > AMP = adenosine; ADP-ribose and nicotinamide  adenine dinucleotide, but not nicotinamide or UTP, caused a dose-dependent  suppression of thymidine uptake.	transcription
59627	2	335505	7	NULL	NULL	0	NULL	ADP-ribose	NucleicAcid		suppress		dose-dependently			thymidine	NucleicAcid	uptake of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_162_12_10358189_s_5	10358189	Adenine nucleotides inhibited NK cell proliferation, with ATP = ADP >  5''-adenylylimidodiphosphate > AMP = adenosine; ADP-ribose and nicotinamide  adenine dinucleotide, but not nicotinamide or UTP, caused a dose-dependent  suppression of thymidine uptake.	transcription
59628	3	335505	7	NULL	NULL	0	NULL	nicotinamide adenine dinucleotide	Chemical		suppress		dose-dependently			thymidine	NucleicAcid	uptake of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_162_12_10358189_s_5	10358189	Adenine nucleotides inhibited NK cell proliferation, with ATP = ADP >  5''-adenylylimidodiphosphate > AMP = adenosine; ADP-ribose and nicotinamide  adenine dinucleotide, but not nicotinamide or UTP, caused a dose-dependent  suppression of thymidine uptake.	transcription
59629	4	335505	7	NULL	NULL	0	NULL	nicotinamide	Chemical		does not suppress					thymidine	NucleicAcid	uptake of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_162_12_10358189_s_5	10358189	Adenine nucleotides inhibited NK cell proliferation, with ATP = ADP >  5''-adenylylimidodiphosphate > AMP = adenosine; ADP-ribose and nicotinamide  adenine dinucleotide, but not nicotinamide or UTP, caused a dose-dependent  suppression of thymidine uptake.	transcription
59630	5	335505	7	NULL	NULL	0	NULL	UTP	NucleicAcid		does not suppress					thymidine	NucleicAcid	uptake of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_j-immunol_162_12_10358189_s_5	10358189	Adenine nucleotides inhibited NK cell proliferation, with ATP = ADP >  5''-adenylylimidodiphosphate > AMP = adenosine; ADP-ribose and nicotinamide  adenine dinucleotide, but not nicotinamide or UTP, caused a dose-dependent  suppression of thymidine uptake.	transcription
79142	1	335506	6	NULL	NULL	0	NULL	Allopurinol	Chemical		inhibits					adenine	Chemical	transport of			NULL		0	NULL	NULL	NULL	gw70_molpharmacol_63_4_814_s_48	12644582	The adenine transporter generally displayed far higher affinity for nucleobases than for their corresponding nucleosides, as illustrated in Fig.  1B for adenine and adenosine, which displayed a  Ki value of >5 mM. Allopurinol was a moderately effective inhibitor of [3]adenine transport (Fig.  1B) with a  Ki of 56  plus-or-minus  2 muM ( n = 3).	transcription
59631	1	335506	7	NULL	NULL	0	NULL	adenine transporter	GP		affinity for					adenine	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_63_4_814_s_48	12644582	The adenine transporter generally displayed far higher affinity for nucleobases than for their corresponding nucleosides, as illustrated in Fig.  1B for adenine and adenosine, which displayed a  Ki value of >5 mM. Allopurinol was a moderately effective inhibitor of [3]adenine transport (Fig.  1B) with a  Ki of 56  plus-or-minus  2 muM ( n = 3).	transcription
59632	2	335506	7	NULL	NULL	0	NULL	adenine transporter	GP		affinity for					adenosine	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_63_4_814_s_48	12644582	The adenine transporter generally displayed far higher affinity for nucleobases than for their corresponding nucleosides, as illustrated in Fig.  1B for adenine and adenosine, which displayed a  Ki value of >5 mM. Allopurinol was a moderately effective inhibitor of [3]adenine transport (Fig.  1B) with a  Ki of 56  plus-or-minus  2 muM ( n = 3).	transcription
59633	3	335506	7	NULL	NULL	0	NULL	statement 1	Process	affinity of	is higher than					statement 2	Process	affinity of			NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_63_4_814_s_48	12644582	The adenine transporter generally displayed far higher affinity for nucleobases than for their corresponding nucleosides, as illustrated in Fig.  1B for adenine and adenosine, which displayed a  Ki value of >5 mM. Allopurinol was a moderately effective inhibitor of [3]adenine transport (Fig.  1B) with a  Ki of 56  plus-or-minus  2 muM ( n = 3).	transcription
59634	4	335506	7	NULL	NULL	0	NULL	Allopurinol	Chemical		inhibitor of		effective			adenine transport	GP				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_63_4_814_s_48	12644582	The adenine transporter generally displayed far higher affinity for nucleobases than for their corresponding nucleosides, as illustrated in Fig.  1B for adenine and adenosine, which displayed a  Ki value of >5 mM. Allopurinol was a moderately effective inhibitor of [3]adenine transport (Fig.  1B) with a  Ki of 56  plus-or-minus  2 muM ( n = 3).	transcription
59635	7	335507	7	NULL	NULL	0	NULL	adenine	NucleicAcid		protects 					U31	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59636	8	335507	7	NULL	NULL	0	NULL	adenine	NucleicAcid		protects					U33	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59637	9	335507	7	NULL	NULL	0	NULL	adenine	NucleicAcid		protects					G35	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59638	4	335507	7	NULL	NULL	0	NULL	U31	NucleicAcid		belongs to									loop I	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59639	5	335507	7	NULL	NULL	0	NULL	U33	NucleicAcid		belongs to									Ioop I	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59640	6	335507	7	NULL	NULL	0	NULL	G35	NucleicAcid		belongs to									loop I	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59641	1	335507	7	NULL	NULL	0	NULL	single strand-specific RNase 	GP		attack					U31	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59642	2	335507	7	NULL	NULL	0	NULL	single strand-specific RNase 	GP		attack					U33	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59643	3	335507	7	NULL	NULL	0	NULL	single strand-specific RNase 	GP		attack					G35	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59644	10	335507	7	NULL	NULL	0	NULL	statement 7	Process		protected from					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59645	11	335507	7	NULL	NULL	0	NULL	statement 8	Process		protected from					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59646	12	335507	7	NULL	NULL	0	NULL	statement 9	Process		protected from					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59647	13	335507	7	NULL	NULL	0	NULL	adenine	NucleicAcid		induce					U31	NucleicAcid	structural stabilization of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59648	14	335507	7	NULL	NULL	0	NULL	statement 10	Process		because of					statement 13	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59649	15	335507	7	NULL	NULL	0	NULL	adenine	NucleicAcid		induce					U33	NucleicAcid	structural stabilization of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59650	16	335507	7	NULL	NULL	0	NULL	statement 11	Process		because of					statement 15	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59651	17	335507	7	NULL	NULL	0	NULL	adenine	NucleicAcid		induce					G35	NucleicAcid	structural stabilization of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59652	18	335507	7	NULL	NULL	0	NULL	statement 12	Process		because of					statement 17	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59653	19	335507	7	NULL	NULL	0	NULL	U31	NucleicAcid		interact with		directly			adenine target	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59654	20	335507	7	NULL	NULL	0	NULL	U33	NucleicAcid		interact with		directly			adenine target	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59655	21	335507	7	NULL	NULL	0	NULL	G35	NucleicAcid		interact with		directly			adenine target	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59656	22	335507	7	NULL	NULL	0	NULL	statement 10	Process		because of					statement 19	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59657	23	335507	7	NULL	NULL	0	NULL	statement 11	Process		because of					statement 20	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59658	24	335507	7	NULL	NULL	0	NULL	statement 12	Process		because of					statement 21	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59659	25	335507	7	NULL	NULL	0	NULL	statement 14	Process		is an alternative to					statement 22	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59660	26	335507	7	NULL	NULL	0	NULL	statement 16	Process		is an alternative to					statement 23	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59661	27	335507	7	NULL	NULL	0	NULL	statement 18	Process		is an alternative to					statement 24	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59662	28	335507	7	NULL	NULL	0	NULL	U31	NucleicAcid		is a type of					unpaired nucleotide	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59663	29	335507	7	NULL	NULL	0	NULL	U33	NucleicAcid		is a type of					unpaired nucleotide	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
59664	30	335507	7	NULL	NULL	0	NULL	G35	NucleicAcid		is a type of					unpaired nucleotide	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_3_2104_s_257	11705996	Three unpaired nucleotides (U31, U33, and G35) of the first loop (loop I) are clearly protected by adenine against single strand-specific RNase attack, either because of a structural stabilization induced by adenine or simply because they interact directly with the adenine target (Fig.  5).	transcription
79143	1	335508	6	NULL	NULL	0	NULL	SAH	GP		forms					SRH	GP				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_13_3450_s_43	12057938	Pfs catalyzes two reactions in bacterial cells: the formation of  S-ribosylhomocysteine (SRH) from  S-adenosylhomocysteine (SAH) to release adenine and the production of 5''-methylthioribose (MTR) from 5''-methylthioadenosine (MTA), also releasing adenine ( 11,  19,  28).	transcription
79144	2	335508	6	NULL	NULL	0	NULL	SAH	GP		is					S-adenosylhomocysteine	GP				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_13_3450_s_43	12057938	Pfs catalyzes two reactions in bacterial cells: the formation of  S-ribosylhomocysteine (SRH) from  S-adenosylhomocysteine (SAH) to release adenine and the production of 5''-methylthioribose (MTR) from 5''-methylthioadenosine (MTA), also releasing adenine ( 11,  19,  28).	transcription
79145	3	335508	6	NULL	NULL	0	NULL	SRH	GP		is					S-ribosylhomocysteine	GP				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_13_3450_s_43	12057938	Pfs catalyzes two reactions in bacterial cells: the formation of  S-ribosylhomocysteine (SRH) from  S-adenosylhomocysteine (SAH) to release adenine and the production of 5''-methylthioribose (MTR) from 5''-methylthioadenosine (MTA), also releasing adenine ( 11,  19,  28).	transcription
79146	4	335508	6	NULL	NULL	0	NULL	Pf	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_13_3450_s_43	12057938	Pfs catalyzes two reactions in bacterial cells: the formation of  S-ribosylhomocysteine (SRH) from  S-adenosylhomocysteine (SAH) to release adenine and the production of 5''-methylthioribose (MTR) from 5''-methylthioadenosine (MTA), also releasing adenine ( 11,  19,  28).	transcription
79147	5	335508	6	NULL	NULL	0	NULL	statement 1	Process		releases					adenine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_13_3450_s_43	12057938	Pfs catalyzes two reactions in bacterial cells: the formation of  S-ribosylhomocysteine (SRH) from  S-adenosylhomocysteine (SAH) to release adenine and the production of 5''-methylthioribose (MTR) from 5''-methylthioadenosine (MTA), also releasing adenine ( 11,  19,  28).	transcription
79148	6	335508	6	NULL	NULL	0	NULL	MTR	GP		is produced from					MTA	GP				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_13_3450_s_43	12057938	Pfs catalyzes two reactions in bacterial cells: the formation of  S-ribosylhomocysteine (SRH) from  S-adenosylhomocysteine (SAH) to release adenine and the production of 5''-methylthioribose (MTR) from 5''-methylthioadenosine (MTA), also releasing adenine ( 11,  19,  28).	transcription
79149	7	335508	6	NULL	NULL	0	NULL	MTR	GP		is					5''-methylthioribose	GP				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_13_3450_s_43	12057938	Pfs catalyzes two reactions in bacterial cells: the formation of  S-ribosylhomocysteine (SRH) from  S-adenosylhomocysteine (SAH) to release adenine and the production of 5''-methylthioribose (MTR) from 5''-methylthioadenosine (MTA), also releasing adenine ( 11,  19,  28).	transcription
79150	8	335508	6	NULL	NULL	0	NULL	MTA	GP		is					5''-methylthioadenosine	GP				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_13_3450_s_43	12057938	Pfs catalyzes two reactions in bacterial cells: the formation of  S-ribosylhomocysteine (SRH) from  S-adenosylhomocysteine (SAH) to release adenine and the production of 5''-methylthioribose (MTR) from 5''-methylthioadenosine (MTA), also releasing adenine ( 11,  19,  28).	transcription
79151	9	335508	6	NULL	NULL	0	NULL	statement 6	Process		releases					adenine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_13_3450_s_43	12057938	Pfs catalyzes two reactions in bacterial cells: the formation of  S-ribosylhomocysteine (SRH) from  S-adenosylhomocysteine (SAH) to release adenine and the production of 5''-methylthioribose (MTR) from 5''-methylthioadenosine (MTA), also releasing adenine ( 11,  19,  28).	transcription
59706	1	335508	7	NULL	NULL	0	NULL	SRH	Chemical		formed from					SAH	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_13_3450_s_43	12057938	Pfs catalyzes two reactions in bacterial cells: the formation of  S-ribosylhomocysteine (SRH) from  S-adenosylhomocysteine (SAH) to release adenine and the production of 5''-methylthioribose (MTR) from 5''-methylthioadenosine (MTA), also releasing adenine ( 11,  19,  28).	transcription
59809	2	335508	7	NULL	NULL	0	NULL	statement 1	Process		release					Adenine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_13_3450_s_43	12057938	Pfs catalyzes two reactions in bacterial cells: the formation of  S-ribosylhomocysteine (SRH) from  S-adenosylhomocysteine (SAH) to release adenine and the production of 5''-methylthioribose (MTR) from 5''-methylthioadenosine (MTA), also releasing adenine ( 11,  19,  28).	transcription
59810	3	335508	7	NULL	NULL	0	NULL	Pfs	Chemical		catalyze					statement 1	Process				NULL	bacterial cells	0	NULL	NULL	NULL	gw60_jbacteriol_184_13_3450_s_43	12057938	Pfs catalyzes two reactions in bacterial cells: the formation of  S-ribosylhomocysteine (SRH) from  S-adenosylhomocysteine (SAH) to release adenine and the production of 5''-methylthioribose (MTR) from 5''-methylthioadenosine (MTA), also releasing adenine ( 11,  19,  28).	transcription
59811	4	335508	7	NULL	NULL	0	NULL	MTR	Chemical		formed from					MTA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_13_3450_s_43	12057938	Pfs catalyzes two reactions in bacterial cells: the formation of  S-ribosylhomocysteine (SRH) from  S-adenosylhomocysteine (SAH) to release adenine and the production of 5''-methylthioribose (MTR) from 5''-methylthioadenosine (MTA), also releasing adenine ( 11,  19,  28).	transcription
59812	5	335508	7	NULL	NULL	0	NULL	statement 4	Process		release					Adenine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_13_3450_s_43	12057938	Pfs catalyzes two reactions in bacterial cells: the formation of  S-ribosylhomocysteine (SRH) from  S-adenosylhomocysteine (SAH) to release adenine and the production of 5''-methylthioribose (MTR) from 5''-methylthioadenosine (MTA), also releasing adenine ( 11,  19,  28).	transcription
59813	6	335508	7	NULL	NULL	0	NULL	Pfs	Chemical		catalyze					statement 5	Process				NULL	bacterial cells	0	NULL	NULL	NULL	gw60_jbacteriol_184_13_3450_s_43	12057938	Pfs catalyzes two reactions in bacterial cells: the formation of  S-ribosylhomocysteine (SRH) from  S-adenosylhomocysteine (SAH) to release adenine and the production of 5''-methylthioribose (MTR) from 5''-methylthioadenosine (MTA), also releasing adenine ( 11,  19,  28).	transcription
59814	7	335508	7	NULL	NULL	0	NULL	SRH	Chemical		is					S-ribosylhomocysteine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_13_3450_s_43	12057938	Pfs catalyzes two reactions in bacterial cells: the formation of  S-ribosylhomocysteine (SRH) from  S-adenosylhomocysteine (SAH) to release adenine and the production of 5''-methylthioribose (MTR) from 5''-methylthioadenosine (MTA), also releasing adenine ( 11,  19,  28).	transcription
59815	8	335508	7	NULL	NULL	0	NULL	SAH	Chemical		is					S-adenosylhomocysteine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_13_3450_s_43	12057938	Pfs catalyzes two reactions in bacterial cells: the formation of  S-ribosylhomocysteine (SRH) from  S-adenosylhomocysteine (SAH) to release adenine and the production of 5''-methylthioribose (MTR) from 5''-methylthioadenosine (MTA), also releasing adenine ( 11,  19,  28).	transcription
59816	9	335508	7	NULL	NULL	0	NULL	MTR	Chemical		is					5''-methylthioadenosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_13_3450_s_43	12057938	Pfs catalyzes two reactions in bacterial cells: the formation of  S-ribosylhomocysteine (SRH) from  S-adenosylhomocysteine (SAH) to release adenine and the production of 5''-methylthioribose (MTR) from 5''-methylthioadenosine (MTA), also releasing adenine ( 11,  19,  28).	transcription
79152	1	335509	6	NULL	NULL	0	NULL	palmitoyl-CoA	Chemical		inhibits					adenine nucleotide translocator	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_54_4_944_s_3	15793231	We found that 5 mumol/l palmitoyl-CoA inhibited adenine nucleotide translocator, without direct effect on other components of oxidative phosphorylation.	transcription
79153	2	335509	6	NULL	NULL	0	NULL	statement 1	Process		does not effect					oxidative phosphorylation	Process				NULL		0	NULL	NULL	NULL	gw70_diabetes_54_4_944_s_3	15793231	We found that 5 mumol/l palmitoyl-CoA inhibited adenine nucleotide translocator, without direct effect on other components of oxidative phosphorylation.	transcription
59817	1	335509	7	NULL	NULL	0	NULL	 palmitoyl-CoA	Chemical		inhibit					adenine nucleotide translocator	Chemical				NULL		0	NULL	NULL	NULL	gw70_diabetes_54_4_944_s_3	15793231	We found that 5 mumol/l palmitoyl-CoA inhibited adenine nucleotide translocator, without direct effect on other components of oxidative phosphorylation.	transcription
59818	2	335509	7	NULL	NULL	0	NULL	statement 1	Process		does not effect		directly			oxidative phosphorylation	Process	other components of			NULL		NULL	NULL	NULL	NULL	gw70_diabetes_54_4_944_s_3	15793231	We found that 5 mumol/l palmitoyl-CoA inhibited adenine nucleotide translocator, without direct effect on other components of oxidative phosphorylation.	transcription
59819	1	335510	7	NULL	NULL	0	NULL	MrgA family	GP	murine	respond to					RF-amide peptides	GP				NULL		0	NULL	NULL	NULL	gw70_brainresmolbrainres_142_1_58_s_146	16246453	In contrast, the only  ligand described for rMrgA is adenine   [1, although two members of the murine MrgA family respond to a number of RF-amide peptides    [5] and   [8.	transcription
59820	2	335510	7	NULL	NULL	0	NULL	adenine	Chemical		ligand for					rMrgA	GP				NULL		0	NULL	NULL	NULL	gw70_brainresmolbrainres_142_1_58_s_146	16246453	In contrast, the only  ligand described for rMrgA is adenine   [1, although two members of the murine MrgA family respond to a number of RF-amide peptides    [5] and   [8.	transcription
79154	1	335511	6	NULL	NULL	0	NULL	GTP/dGTP	Chemical		does not activate					Apaf-1	GP				NULL		0	NULL	NULL	NULL	gw70_nature_434_7035_926_s_109	15829969	These two hydrogen bonds are specific  for the adenine base but not the guanine, explaining why GTP/dGTP fails to activate  Apaf-1 (refs  3,  5).	transcription
59821	1	335511	7	NULL	NULL	0	NULL	GTP/dGTP	NucleicAcid		fails to activate					Apaf-1	GP				NULL		NULL	NULL	NULL	NULL	gw70_nature_434_7035_926_s_109	15829969	These two hydrogen bonds are specific  for the adenine base but not the guanine, explaining why GTP/dGTP fails to activate  Apaf-1 (refs  3,  5).	transcription
59822	1	335512	7	NULL	NULL	0	NULL	 5''-aziridine adenylate 1	Chemical		substitute for					SAM	Chemical				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1644_s_18	15778434	The 5''-aziridine adenylate  1 is a substitute for SAM in the M.TaqI catalyzed alkylation of adenine within the recognition sequence d(TCGA) as depicted in  Scheme 1 (  -  ).	transcription
59823	2	335512	7	NULL	NULL	0	NULL	statement 1	Process		present in					 M.TaqI 	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1644_s_18	15778434	The 5''-aziridine adenylate  1 is a substitute for SAM in the M.TaqI catalyzed alkylation of adenine within the recognition sequence d(TCGA) as depicted in  Scheme 1 (  -  ).	transcription
59824	3	335512	7	NULL	NULL	0	NULL	 M.TaqI 	GP		catalyze					adenine	Chemical	alkylation of 			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1644_s_18	15778434	The 5''-aziridine adenylate  1 is a substitute for SAM in the M.TaqI catalyzed alkylation of adenine within the recognition sequence d(TCGA) as depicted in  Scheme 1 (  -  ).	transcription
59825	4	335512	7	NULL	NULL	0	NULL	statement 3	Process		occurs within									recognition sequence d(TCGA)	NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_5_1644_s_18	15778434	The 5''-aziridine adenylate  1 is a substitute for SAM in the M.TaqI catalyzed alkylation of adenine within the recognition sequence d(TCGA) as depicted in  Scheme 1 (  -  ).	transcription
79155	1	335513	6	NULL	NULL	0	NULL	PABP	GP		bind					PABP mRNA	NucleicAcid			ARS in 5''-untranslated region	NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_4	16356927	(A)-binding protein (PABP) mRNA translation involves the binding of PABP to the adenine-rich autoregulatory sequence (ARS) in the 5''-untranslated region of its own mRNA.	transcription
79156	2	335513	6	NULL	NULL	0	NULL	ARS	GP		is					adenine-rich autoregulatory sequence	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_4	16356927	(A)-binding protein (PABP) mRNA translation involves the binding of PABP to the adenine-rich autoregulatory sequence (ARS) in the 5''-untranslated region of its own mRNA.	transcription
59826	1	335513	7	NULL	NULL	0	NULL	PABP	GP		bind									ARS	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_4	16356927	(A)-binding protein (PABP) mRNA translation involves the binding of PABP to the adenine-rich autoregulatory sequence (ARS) in the 5''-untranslated region of its own mRNA.	transcription
59827	2	335513	7	NULL	NULL	0	NULL	statement 1	Process		occur in the					PABP mRNA	GP	5''-untranslated region of			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_4	16356927	(A)-binding protein (PABP) mRNA translation involves the binding of PABP to the adenine-rich autoregulatory sequence (ARS) in the 5''-untranslated region of its own mRNA.	transcription
59828	3	335513	7	NULL	NULL	0	NULL	PABP mRNA	GP	translation of	involves					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_22_7074_s_4	16356927	(A)-binding protein (PABP) mRNA translation involves the binding of PABP to the adenine-rich autoregulatory sequence (ARS) in the 5''-untranslated region of its own mRNA.	transcription
59829	1	335514	7	NULL	NULL	0	NULL	Dir.956-1	GP		changed to				5''-GGCCGC	Dir.956-1	GP			5''-GACCAC	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_6_2042_s_98	15817568	The IGS of Dir.956-1 was therefore changed from 5''-GGCCGC to 5''-GACCAC ( Figure 1) to allow correct base pairing between the IGS and the  E.coli SSU target sequence.	transcription
59830	2	335514	7	NULL	NULL	0	NULL				is a type of				 5''-GGCCGC	IGS	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_6_2042_s_98	15817568	The IGS of Dir.956-1 was therefore changed from 5''-GGCCGC to 5''-GACCAC ( Figure 1) to allow correct base pairing between the IGS and the  E.coli SSU target sequence.	transcription
59831	3	335514	7	NULL	NULL	0	NULL				is a type of				5''-GACCAC	IGS	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_6_2042_s_98	15817568	The IGS of Dir.956-1 was therefore changed from 5''-GGCCGC to 5''-GACCAC ( Figure 1) to allow correct base pairing between the IGS and the  E.coli SSU target sequence.	transcription
59832	4	335514	7	NULL	NULL	0	NULL				base pair with				IGS			E.coli		SSU target sequence	NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_33_6_2042_s_98	15817568	The IGS of Dir.956-1 was therefore changed from 5''-GGCCGC to 5''-GACCAC ( Figure 1) to allow correct base pairing between the IGS and the  E.coli SSU target sequence.	transcription
59833	5	335514	7	NULL	NULL	0	NULL	statement 1	Process		allows					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_33_6_2042_s_98	15817568	The IGS of Dir.956-1 was therefore changed from 5''-GGCCGC to 5''-GACCAC ( Figure 1) to allow correct base pairing between the IGS and the  E.coli SSU target sequence.	transcription
79024	1	335516	6	NULL	NULL	0	NULL	adenine	Chemical		activates					RyR	GP				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_130_7_1618_s_131	10928966	Analysis of the open and closed lifetime distributions confirms our understanding of the mechanisms underlying adenine activation of RyR and can be seen in  Figure 5.	transcription
59849	1	335516	7	NULL	NULL	0	NULL	adenine	Chemical		activates					RyR	GP				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_130_7_1618_s_131	10928966	Analysis of the open and closed lifetime distributions confirms our understanding of the mechanisms underlying adenine activation of RyR and can be seen in  Figure 5.	transcription
59850	1	335517	7	NULL	NULL	0	NULL	adenine	Chemical		regulates					Bas1p target genes	GP				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_23_4665_s_222	11095676	The identification of BIRD function in Bas1p allows us to propose a specific model for adenine regulation of Bas1p target genes, as illustrated in Figure  5.	transcription
59851	2	335517	7	NULL	NULL	0	NULL				identified in			BIRD function		Bas1p	GP				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_23_4665_s_222	11095676	The identification of BIRD function in Bas1p allows us to propose a specific model for adenine regulation of Bas1p target genes, as illustrated in Figure  5.	transcription
79025	1	335518	6	NULL	NULL	0	NULL	thymidine	Chemical		interacts with					adenine	Chemical				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_10_2183_s_3	12000838	The structure of 5''-ApTpApT-3'' has been shown to be stabilized by the 5-methyl group in the thymidine moiety that favorably interacts with the adenine pi-ring preceding it.	transcription
59852	1	335518	7	NULL	NULL	0	NULL	 5''-ApTpApT-3''	NucleicAcid	structure of	stabilized by					thymidine	NucleicAcid			5-methyl group in	NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_30_10_2183_s_3	12000838	The structure of 5''-ApTpApT-3'' has been shown to be stabilized by the 5-methyl group in the thymidine moiety that favorably interacts with the adenine pi-ring preceding it.	transcription
59853	2	335518	7	NULL	NULL	0	NULL	thymidine	NucleicAcid		interacts with		favorably		5-methyl group in	adenine	Chemical			pi-ring	NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_30_10_2183_s_3	12000838	The structure of 5''-ApTpApT-3'' has been shown to be stabilized by the 5-methyl group in the thymidine moiety that favorably interacts with the adenine pi-ring preceding it.	transcription
79026	1	335520	6	NULL	NULL	0	NULL	Aer energy taxis protein	GP	E.coli	bind			PAS domain		flavin adenine dinucleotide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_24_7206_s_25	11717280	It is particularly noteworthy that the PAS domain of the Aer energy taxis protein of  E. coli binds a flavin adenine dinucleotide to sense changes in cellular redox ( 5,  34).	transcription
59854	1	335520	7	NULL	NULL	0	NULL	Aer energy taxis protein	GP	E.coli	bind			PAS domain		flavin adenine dinucleotide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_24_7206_s_25	11717280	It is particularly noteworthy that the PAS domain of the Aer energy taxis protein of  E. coli binds a flavin adenine dinucleotide to sense changes in cellular redox ( 5,  34).	transcription
59855	2	335520	7	NULL	NULL	0	NULL	statement 1	Process		occurs to					cellular redox	Process	sense changes in			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_24_7206_s_25	11717280	It is particularly noteworthy that the PAS domain of the Aer energy taxis protein of  E. coli binds a flavin adenine dinucleotide to sense changes in cellular redox ( 5,  34).	transcription
79027	1	335521	6	NULL	NULL	NULL	NULL	adenine	Chemical		activates					SDH	GP				NULL	cauliflower mitochondria	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_35_32567_s_271	11350973	It has been observed previously, however, that SDH activation by adenine nucleotides in cauliflower mitochondria is negatively affected by sonication or freeze-thawing treatments ( 5).	transcription
59856	1	335521	7	NULL	NULL	0	NULL	adenine nucleotides	NucleicAcid	cauliflower mitochondria	activates					SDH	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32567_s_271	11350973	It has been observed previously, however, that SDH activation by adenine nucleotides in cauliflower mitochondria is negatively affected by sonication or freeze-thawing treatments ( 5).	transcription
59857	2	335521	7	NULL	NULL	0	NULL	sonication	Process		affect		negatively			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32567_s_271	11350973	It has been observed previously, however, that SDH activation by adenine nucleotides in cauliflower mitochondria is negatively affected by sonication or freeze-thawing treatments ( 5).	transcription
59858	3	335521	7	NULL	NULL	0	NULL	freeze-thawing	Process		affect		negatively			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32567_s_271	11350973	It has been observed previously, however, that SDH activation by adenine nucleotides in cauliflower mitochondria is negatively affected by sonication or freeze-thawing treatments ( 5).	transcription
59862	4	335521	7	NULL	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32567_s_271	11350973	It has been observed previously, however, that SDH activation by adenine nucleotides in cauliflower mitochondria is negatively affected by sonication or freeze-thawing treatments ( 5).	transcription
59859	1	335522	7	NULL	NULL	0	NULL	3'',5''-ADP	NucleicAcid		hydrogen bond with				Atoms N6 of adenosine				Asn-70		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_18_15009_s_233	11154698	Atoms N6 and N1 of the adenosine of 3'',5''-ADP form hydrogen bonds with Asn-70, and the adenine ring is engaged in stacking interactions with the imidazole of His-129.	transcription
59860	2	335522	7	NULL	NULL	0	NULL	3'',5''-ADP	NucleicAcid		hydrogen bond with				Atom N1 of the adenosine				Asn-70		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_18_15009_s_233	11154698	Atoms N6 and N1 of the adenosine of 3'',5''-ADP form hydrogen bonds with Asn-70, and the adenine ring is engaged in stacking interactions with the imidazole of His-129.	transcription
59861	3	335522	7	NULL	NULL	0	NULL	adenine ring 	Chemical		is engaged in							stacking interactions with	imidazole of His-129		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_18_15009_s_233	11154698	Atoms N6 and N1 of the adenosine of 3'',5''-ADP form hydrogen bonds with Asn-70, and the adenine ring is engaged in stacking interactions with the imidazole of His-129.	transcription
54967	1	335523	5	NULL	NULL	0	NULL	adenylyl cyclase			bind					AMP					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_26_16332_s_19	9632695	The crystal structure of adenylyl cyclase with bound 2'd3'AMP reveals the amino acid residues that interact with the adenine ring of the inhibitor ( 5).	transcription
59863	1	335523	7	NULL	NULL	0	NULL	adenylyl cyclase	GP		bind					2'd3'AMP	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_26_16332_s_19	9632695	The crystal structure of adenylyl cyclase with bound 2'd3'AMP reveals the amino acid residues that interact with the adenine ring of the inhibitor ( 5).	transcription
59864	1	335524	7	NULL	NULL	0	NULL	antisense oligonucleotide	NucleicAcid		targeted to					hTR	GP			16 nucleotides of the J2a/3 loop	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_23502_s_303	15811851	A recent study ( ) shows that an antisense oligonucleotide targeting 16 nucleotides of the J2a/3 loop of hTR, including the first three adenines of the 5''- AAACAAA3'' sequence, caused a 26% decrease in telomerase activity  in vitro and an increase in hTR-DNA telomeric sequence complex formation ( ).	transcription
59865	2	335524	7	NULL	NULL	0	NULL	statement 1	Process		include					5''- AAACAAA3'' sequence	NucleicAcid			 first three adenines of	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_25_23502_s_303	15811851	A recent study ( ) shows that an antisense oligonucleotide targeting 16 nucleotides of the J2a/3 loop of hTR, including the first three adenines of the 5''- AAACAAA3'' sequence, caused a 26% decrease in telomerase activity  in vitro and an increase in hTR-DNA telomeric sequence complex formation ( ).	transcription
59866	3	335524	7	NULL	NULL	0	NULL	statement 2	Process		decrease					telomerase	GP	activity of			NULL	in vitro	0	NULL	NULL	NULL	gw70_jbiolchem_280_25_23502_s_303	15811851	A recent study ( ) shows that an antisense oligonucleotide targeting 16 nucleotides of the J2a/3 loop of hTR, including the first three adenines of the 5''- AAACAAA3'' sequence, caused a 26% decrease in telomerase activity  in vitro and an increase in hTR-DNA telomeric sequence complex formation ( ).	transcription
59867	4	335524	7	NULL	NULL	0	NULL	hTR	GP		complex with					DNA	NucleicAcid			telomeric sequence	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_25_23502_s_303	15811851	A recent study ( ) shows that an antisense oligonucleotide targeting 16 nucleotides of the J2a/3 loop of hTR, including the first three adenines of the 5''- AAACAAA3'' sequence, caused a 26% decrease in telomerase activity  in vitro and an increase in hTR-DNA telomeric sequence complex formation ( ).	transcription
59868	5	335524	7	NULL	NULL	0	NULL	statement 2	Process		increase					statement 4	Process	formation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_25_23502_s_303	15811851	A recent study ( ) shows that an antisense oligonucleotide targeting 16 nucleotides of the J2a/3 loop of hTR, including the first three adenines of the 5''- AAACAAA3'' sequence, caused a 26% decrease in telomerase activity  in vitro and an increase in hTR-DNA telomeric sequence complex formation ( ).	transcription
59894	1	335525	7	NULL	NULL	0	NULL	5-methylcytosines	Chemical	number of	is identical in					G-d5 oligomer	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_14_4099_s_207	12853627	Since the number of 5-methylcytosines is identical in  G-d5,  G-d6 and  G-d7, and each oligomer contains one commonly positioned 5-methylcytosine, the relative arrangement of the 8-oxo-adenines and 5-methylcytosine in the 5' region of the oligomer must influence triplex stability, possibly as a consequence of different interactions between the bases in the third strand.	transcription
59895	2	335525	7	NULL	NULL	0	NULL	5-methylcytosines	Chemical	number of	is identical in					G-d6 oligomer	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_14_4099_s_207	12853627	Since the number of 5-methylcytosines is identical in  G-d5,  G-d6 and  G-d7, and each oligomer contains one commonly positioned 5-methylcytosine, the relative arrangement of the 8-oxo-adenines and 5-methylcytosine in the 5' region of the oligomer must influence triplex stability, possibly as a consequence of different interactions between the bases in the third strand.	transcription
59896	3	335525	7	NULL	NULL	0	NULL	5-methylcytosines	Chemical	number of	is identical in					G-d7 oligomer	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_31_14_4099_s_207	12853627	Since the number of 5-methylcytosines is identical in  G-d5,  G-d6 and  G-d7, and each oligomer contains one commonly positioned 5-methylcytosine, the relative arrangement of the 8-oxo-adenines and 5-methylcytosine in the 5' region of the oligomer must influence triplex stability, possibly as a consequence of different interactions between the bases in the third strand.	transcription
59897	4	335525	7	NULL	NULL	0	NULL	oligomer		relative arrangement of 	influence				8-oxo-adenines in the 5' region 	triplex 		stability of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_14_4099_s_207	12853627	Since the number of 5-methylcytosines is identical in  G-d5,  G-d6 and  G-d7, and each oligomer contains one commonly positioned 5-methylcytosine, the relative arrangement of the 8-oxo-adenines and 5-methylcytosine in the 5' region of the oligomer must influence triplex stability, possibly as a consequence of different interactions between the bases in the third strand.	transcription
59898	5	335525	7	NULL	NULL	0	NULL	oligomer		relative arrangement of	influence				5-methylcytosine in the 5' region of 	triplex		stability of			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_31_14_4099_s_207	12853627	Since the number of 5-methylcytosines is identical in  G-d5,  G-d6 and  G-d7, and each oligomer contains one commonly positioned 5-methylcytosine, the relative arrangement of the 8-oxo-adenines and 5-methylcytosine in the 5' region of the oligomer must influence triplex stability, possibly as a consequence of different interactions between the bases in the third strand.	transcription
54968	1	335526	5	NULL	NULL	0	NULL	Po		increase of	higher level than					adenine					NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_130_7_1618_s_130	10928966	Not only does ATP increase Po to much higher levels than adenine (optimal activation =0.95 with 2 mM ATP compared with 0.24 with 5 mM adenine) but a dose-dependent increase in mean open lifetimes is observed together with the dose-dependent reduction in mean closed times.	transcription
54969	2	335526	5	NULL	NULL	0	NULL	ATP			is required for					statement 1					NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_130_7_1618_s_130	10928966	Not only does ATP increase Po to much higher levels than adenine (optimal activation =0.95 with 2 mM ATP compared with 0.24 with 5 mM adenine) but a dose-dependent increase in mean open lifetimes is observed together with the dose-dependent reduction in mean closed times.	transcription
54970	1	335527	5	NULL	NULL	0	NULL	ribosomes			is inactivated by					RIPs					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2383_s_14	10871371	It is well established that adenine added to cell-free protein synthesising systems protects ribosomes from inactivation by RIPs ( 2 -  4) and that protection results from an inhibition of the RNA- N-glycosidase reaction of the uncompetitive type, adenine binding more tightly to the enzyme - substrate complex than to the free enzyme ( 5).	transcription
54971	2	335527	5	NULL	NULL	0	NULL	adenine			protects					statement 1					NULL	cell-free protein synthesising systems	0	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2383_s_14	10871371	It is well established that adenine added to cell-free protein synthesising systems protects ribosomes from inactivation by RIPs ( 2 -  4) and that protection results from an inhibition of the RNA- N-glycosidase reaction of the uncompetitive type, adenine binding more tightly to the enzyme - substrate complex than to the free enzyme ( 5).	transcription
54972	3	335527	5	NULL	NULL	0	NULL	statement 2			results from					RNA- N-glycosidase reaction		inhibition of;;uncompetitive			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2383_s_14	10871371	It is well established that adenine added to cell-free protein synthesising systems protects ribosomes from inactivation by RIPs ( 2 -  4) and that protection results from an inhibition of the RNA- N-glycosidase reaction of the uncompetitive type, adenine binding more tightly to the enzyme - substrate complex than to the free enzyme ( 5).	transcription
54973	4	335527	5	NULL	NULL	0	NULL	adenine			bind					enzyme - substrate complex					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2383_s_14	10871371	It is well established that adenine added to cell-free protein synthesising systems protects ribosomes from inactivation by RIPs ( 2 -  4) and that protection results from an inhibition of the RNA- N-glycosidase reaction of the uncompetitive type, adenine binding more tightly to the enzyme - substrate complex than to the free enzyme ( 5).	transcription
54974	5	335527	5	NULL	NULL	0	NULL	adenine			bind					enzyme		free			NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2383_s_14	10871371	It is well established that adenine added to cell-free protein synthesising systems protects ribosomes from inactivation by RIPs ( 2 -  4) and that protection results from an inhibition of the RNA- N-glycosidase reaction of the uncompetitive type, adenine binding more tightly to the enzyme - substrate complex than to the free enzyme ( 5).	transcription
54975	6	335527	5	NULL	NULL	0	NULL	statement 4			tighter than					statement 5					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2383_s_14	10871371	It is well established that adenine added to cell-free protein synthesising systems protects ribosomes from inactivation by RIPs ( 2 -  4) and that protection results from an inhibition of the RNA- N-glycosidase reaction of the uncompetitive type, adenine binding more tightly to the enzyme - substrate complex than to the free enzyme ( 5).	transcription
59900	1	335527	7	NULL	NULL	0	NULL	RIPs	GP		inactivate					ribosomes	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2383_s_14	10871371	It is well established that adenine added to cell-free protein synthesising systems protects ribosomes from inactivation by RIPs ( 2 -  4) and that protection results from an inhibition of the RNA- N-glycosidase reaction of the uncompetitive type, adenine binding more tightly to the enzyme - substrate complex than to the free enzyme ( 5).	transcription
59902	2	335527	7	NULL	NULL	0	NULL	adenine	Chemical		added to					cell-free protein synthesising systems	Cell				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2383_s_14	10871371	It is well established that adenine added to cell-free protein synthesising systems protects ribosomes from inactivation by RIPs ( 2 -  4) and that protection results from an inhibition of the RNA- N-glycosidase reaction of the uncompetitive type, adenine binding more tightly to the enzyme - substrate complex than to the free enzyme ( 5).	transcription
59903	3	335527	7	NULL	NULL	0	NULL	statement 2	Process		protects					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2383_s_14	10871371	It is well established that adenine added to cell-free protein synthesising systems protects ribosomes from inactivation by RIPs ( 2 -  4) and that protection results from an inhibition of the RNA- N-glycosidase reaction of the uncompetitive type, adenine binding more tightly to the enzyme - substrate complex than to the free enzyme ( 5).	transcription
59905	4	335527	7	NULL	NULL	0	NULL	statement 3	Process		results from					RNA- N-glycosidase reaction	Process	uncompetitive inhibition of			NULL		NULL	NULL	NULL	NULL	gw60_nucleicacidsres_28_12_2383_s_14	10871371	It is well established that adenine added to cell-free protein synthesising systems protects ribosomes from inactivation by RIPs ( 2 -  4) and that protection results from an inhibition of the RNA- N-glycosidase reaction of the uncompetitive type, adenine binding more tightly to the enzyme - substrate complex than to the free enzyme ( 5).	transcription
54976	1	335528	5	NULL	NULL	0	NULL	CFTR currents			is induced by					adenine					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_606_s_8	11854441	Although adenine nucleotide-induced CFTR currents were inhibited by XAC, they were highly resistant to ADA treatment; 5 U/ml ADA was required for inhibition of adenine nucleotide-induced CFTR current, whereas 1 U/ml ADA was sufficient to abolish the Ade-induced response.	transcription
54977	2	335528	5	NULL	NULL	0	NULL	XAC			inhibits					statement 1					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_606_s_8	11854441	Although adenine nucleotide-induced CFTR currents were inhibited by XAC, they were highly resistant to ADA treatment; 5 U/ml ADA was required for inhibition of adenine nucleotide-induced CFTR current, whereas 1 U/ml ADA was sufficient to abolish the Ade-induced response.	transcription
54978	3	335528	5	NULL	NULL	0	NULL	statement 1			is resistant to					ADA		treatment			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_606_s_8	11854441	Although adenine nucleotide-induced CFTR currents were inhibited by XAC, they were highly resistant to ADA treatment; 5 U/ml ADA was required for inhibition of adenine nucleotide-induced CFTR current, whereas 1 U/ml ADA was sufficient to abolish the Ade-induced response.	transcription
54979	4	335528	5	NULL	NULL	0	NULL	ADA		large quantity of	is required for					statement 1		inhibition of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_606_s_8	11854441	Although adenine nucleotide-induced CFTR currents were inhibited by XAC, they were highly resistant to ADA treatment; 5 U/ml ADA was required for inhibition of adenine nucleotide-induced CFTR current, whereas 1 U/ml ADA was sufficient to abolish the Ade-induced response.	transcription
54980	5	335528	5	NULL	NULL	0	NULL	ADA		small quantity of	abolishes					Ade-induced response					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_606_s_8	11854441	Although adenine nucleotide-induced CFTR currents were inhibited by XAC, they were highly resistant to ADA treatment; 5 U/ml ADA was required for inhibition of adenine nucleotide-induced CFTR current, whereas 1 U/ml ADA was sufficient to abolish the Ade-induced response.	transcription
59906	1	335528	7	NULL	NULL	0	NULL	adenine nucleotide	Chemical		induce					CFTR current	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_606_s_8	11854441	Although adenine nucleotide-induced CFTR currents were inhibited by XAC, they were highly resistant to ADA treatment; 5 U/ml ADA was required for inhibition of adenine nucleotide-induced CFTR current, whereas 1 U/ml ADA was sufficient to abolish the Ade-induced response.	transcription
59907	2	335528	7	NULL	NULL	0	NULL	XAC	Chemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_606_s_8	11854441	Although adenine nucleotide-induced CFTR currents were inhibited by XAC, they were highly resistant to ADA treatment; 5 U/ml ADA was required for inhibition of adenine nucleotide-induced CFTR current, whereas 1 U/ml ADA was sufficient to abolish the Ade-induced response.	transcription
59908	3	335528	7	NULL	NULL	0	NULL	statement 1	Process		resistant to					ADA	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_606_s_8	11854441	Although adenine nucleotide-induced CFTR currents were inhibited by XAC, they were highly resistant to ADA treatment; 5 U/ml ADA was required for inhibition of adenine nucleotide-induced CFTR current, whereas 1 U/ml ADA was sufficient to abolish the Ade-induced response.	transcription
59909	4	335528	7	NULL	NULL	0	NULL	Ade	Chemical		induce					response	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_606_s_8	11854441	Although adenine nucleotide-induced CFTR currents were inhibited by XAC, they were highly resistant to ADA treatment; 5 U/ml ADA was required for inhibition of adenine nucleotide-induced CFTR current, whereas 1 U/ml ADA was sufficient to abolish the Ade-induced response.	transcription
59910	5	335528	7	NULL	NULL	0	NULL	ADA	Chemical		abolish					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_606_s_8	11854441	Although adenine nucleotide-induced CFTR currents were inhibited by XAC, they were highly resistant to ADA treatment; 5 U/ml ADA was required for inhibition of adenine nucleotide-induced CFTR current, whereas 1 U/ml ADA was sufficient to abolish the Ade-induced response.	transcription
54981	1	335529	5	NULL	NULL	0	NULL	palmitoyl-CoA			inhibits		exclusively			adenine nucleotide translocator					NULL		0	NULL	NULL	NULL	gw70_diabetes_54_4_944_s_156	15793231	Figures 4 and  5 together show that 5 mumol/l palmitoyl-CoA exclusively inhibits the adenine nucleotide translocator and has no direct effect on any other component of oxidative phosphorylation.	transcription
54982	2	335529	5	NULL	NULL	0	NULL	palmitoyl-CoA			does not effect		directly			oxidative phosphorylation		component of			NULL		0	NULL	NULL	NULL	gw70_diabetes_54_4_944_s_156	15793231	Figures 4 and  5 together show that 5 mumol/l palmitoyl-CoA exclusively inhibits the adenine nucleotide translocator and has no direct effect on any other component of oxidative phosphorylation.	transcription
59911	1	335529	7	NULL	NULL	0	NULL	palmitoyl-CoA 	Chemical		inhibits		exclusively			adenine nucleotide translocator	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_54_4_944_s_156	15793231	Figures 4 and  5 together show that 5 mumol/l palmitoyl-CoA exclusively inhibits the adenine nucleotide translocator and has no direct effect on any other component of oxidative phosphorylation.	transcription
59912	2	335529	7	NULL	NULL	0	NULL	statement 1	Process		no direct effect on					oxidative phosphorylation	Process	component of			NULL		NULL	NULL	NULL	NULL	gw70_diabetes_54_4_944_s_156	15793231	Figures 4 and  5 together show that 5 mumol/l palmitoyl-CoA exclusively inhibits the adenine nucleotide translocator and has no direct effect on any other component of oxidative phosphorylation.	transcription
54983	1	335530	5	NULL	NULL	0	NULL	AMP			is					adenosine 5 -triphosphate					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
54984	2	335530	5	NULL	NULL	0	NULL	NAD+			is					nicotinamide adenine dinucleotide					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
54985	3	335530	5	NULL	NULL	0	NULL	ATP			is					adenosine 5 -triphosphate					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
54986	4	335530	5	NULL	NULL	0	NULL	AMP			is transferred from					NAD+					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
54987	5	335530	5	NULL	NULL	0	NULL	AMP			is transferred from					ATP					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
54988	6	335530	5	NULL	NULL	0	NULL	statement 4			is an alternative to					statement 5					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
54989	7	335530	5	NULL	NULL	0	NULL	AMP			is transferred to					DNA ligase			lysine residue		NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
54990	8	335530	5	NULL	NULL	0	NULL	statement 6			occurs along with					statement 7					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
54991	9	335530	5	NULL	NULL	0	NULL	DNA ligase			resides in			lysine residue		DNA ligase			active site		NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
54992	10	335530	5	NULL	NULL	0	NULL	statement 7			forms					phosphoamide bond					NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
54993	11	335530	5	NULL	NULL	0	NULL	phosphoamide bond			is a type of					protein-nucleotide bond					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
59913	1	335530	7	NULL	NULL	0	NULL	AMP	Chemical		is transferred from					NAD+	Chemical				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
59914	2	335530	7	NULL	NULL	0	NULL	AMP	Chemical		is transferred from					ATP	Chemical				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
59915	3	335530	7	NULL	NULL	0	NULL	statement 1	Process		transferred to					DNA ligase	GP		lysine residue at the active site		NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
59916	4	335530	7	NULL	NULL	0	NULL	statement 2	Process		transferred to					DNA ligase	GP		lysine residue at the active site		NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
59917	5	335530	7	NULL	NULL	0	NULL	statement 3	Process		forms					 phosphoamide protein-nucleotide bond	Process				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
59918	6	335530	7	NULL	NULL	0	NULL	statement 4	Process		forms					phosphoamide protein-nucleotide bond	Process				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
59919	7	335530	7	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
59920	8	335530	7	NULL	NULL	0	NULL	NAD+	Chemical		is					nicotinamide adenine dinucleotide	Chemical				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
59921	9	335530	7	NULL	NULL	0	NULL	ATP	Chemical		is					adenosine 5 -triphosphate	Chemical				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1701_1_37_s_5	15450174	In the first step, an adenosine 5 -triphosphate  (AMP) moiety is transferred from nicotinamide adenine dinucleotide (NAD+) or adenosine 5 -triphosphate (ATP) to a lysine residue at the active site of DNA  ligase, forming a phosphoamide protein-nucleotide bond.	transcription
60045	1	335531	7	NULL	NULL	0	NULL	adenylyl cyclases	GP		contains								adenine nucleotide binding domains		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_5_2380_s_60	8576194	Thus, the evidence supports the conclusion that  adenylyl cyclases contain distinct and interacting adenine nucleotide  binding domains for catalysis (5``-ATP) and inhibition  (2``,5``-dd-3``-ATP).	transcription
60046	2	335531	7	NULL	NULL	0	NULL	adenylyl cyclases	GP		catalyze					5``-ATP	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_5_2380_s_60	8576194	Thus, the evidence supports the conclusion that  adenylyl cyclases contain distinct and interacting adenine nucleotide  binding domains for catalysis (5``-ATP) and inhibition  (2``,5``-dd-3``-ATP).	transcription
60047	3	335531	7	NULL	NULL	0	NULL	adenylyl cyclases	GP		inhibit					2``,5``-dd-3``-ATP	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_5_2380_s_60	8576194	Thus, the evidence supports the conclusion that  adenylyl cyclases contain distinct and interacting adenine nucleotide  binding domains for catalysis (5``-ATP) and inhibition  (2``,5``-dd-3``-ATP).	transcription
54994	1	335532	5	NULL	NULL	0	NULL	DEN			stimulates					taste membranes					NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9903_s_70	10449792	As with GMP (Fig.  1 e), adenosine 5''-carboxylate, adenosine 5''-monosulfate, theophylline, adenine, adenosine, cAMP, and caffeine did not block activation of transducin by DEN-stimulated taste membranes (Fig.  2).	transcription
54995	2	335532	5	NULL	NULL	0	NULL	transducin			is activated by					statement 1					NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9903_s_70	10449792	As with GMP (Fig.  1 e), adenosine 5''-carboxylate, adenosine 5''-monosulfate, theophylline, adenine, adenosine, cAMP, and caffeine did not block activation of transducin by DEN-stimulated taste membranes (Fig.  2).	transcription
54996	3	335532	5	NULL	NULL	0	NULL	adenosine 5''-carboxylate			does not block					statement 2					NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9903_s_70	10449792	As with GMP (Fig.  1 e), adenosine 5''-carboxylate, adenosine 5''-monosulfate, theophylline, adenine, adenosine, cAMP, and caffeine did not block activation of transducin by DEN-stimulated taste membranes (Fig.  2).	transcription
54997	4	335532	5	NULL	NULL	0	NULL	adenosine 5''-monosulfate			does not block					statement 2					NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9903_s_70	10449792	As with GMP (Fig.  1 e), adenosine 5''-carboxylate, adenosine 5''-monosulfate, theophylline, adenine, adenosine, cAMP, and caffeine did not block activation of transducin by DEN-stimulated taste membranes (Fig.  2).	transcription
54998	5	335532	5	NULL	NULL	0	NULL	theophylline			does not block					statement 2					NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9903_s_70	10449792	As with GMP (Fig.  1 e), adenosine 5''-carboxylate, adenosine 5''-monosulfate, theophylline, adenine, adenosine, cAMP, and caffeine did not block activation of transducin by DEN-stimulated taste membranes (Fig.  2).	transcription
54999	6	335532	5	NULL	NULL	0	NULL	adenine			does not block					statement 2					NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9903_s_70	10449792	As with GMP (Fig.  1 e), adenosine 5''-carboxylate, adenosine 5''-monosulfate, theophylline, adenine, adenosine, cAMP, and caffeine did not block activation of transducin by DEN-stimulated taste membranes (Fig.  2).	transcription
55000	7	335532	5	NULL	NULL	0	NULL	adenosine			does not block					statement 2					NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9903_s_70	10449792	As with GMP (Fig.  1 e), adenosine 5''-carboxylate, adenosine 5''-monosulfate, theophylline, adenine, adenosine, cAMP, and caffeine did not block activation of transducin by DEN-stimulated taste membranes (Fig.  2).	transcription
55001	8	335532	5	NULL	NULL	0	NULL	cAMP			does not block					statement 2					NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9903_s_70	10449792	As with GMP (Fig.  1 e), adenosine 5''-carboxylate, adenosine 5''-monosulfate, theophylline, adenine, adenosine, cAMP, and caffeine did not block activation of transducin by DEN-stimulated taste membranes (Fig.  2).	transcription
55002	9	335532	5	NULL	NULL	0	NULL	caffeine			does not block					statement 2					NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9903_s_70	10449792	As with GMP (Fig.  1 e), adenosine 5''-carboxylate, adenosine 5''-monosulfate, theophylline, adenine, adenosine, cAMP, and caffeine did not block activation of transducin by DEN-stimulated taste membranes (Fig.  2).	transcription
59922	1	335532	7	NULL	NULL	0	NULL	DEN	Chemical		stimulate					taste membranes	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9903_s_70	10449792	As with GMP (Fig.  1 e), adenosine 5''-carboxylate, adenosine 5''-monosulfate, theophylline, adenine, adenosine, cAMP, and caffeine did not block activation of transducin by DEN-stimulated taste membranes (Fig.  2).	transcription
59923	2	335532	7	NULL	NULL	0	NULL	statement 1	Process		activates					transducin	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9903_s_70	10449792	As with GMP (Fig.  1 e), adenosine 5''-carboxylate, adenosine 5''-monosulfate, theophylline, adenine, adenosine, cAMP, and caffeine did not block activation of transducin by DEN-stimulated taste membranes (Fig.  2).	transcription
59924	3	335532	7	NULL	NULL	0	NULL	GMP	Chemical		does not block					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9903_s_70	10449792	As with GMP (Fig.  1 e), adenosine 5''-carboxylate, adenosine 5''-monosulfate, theophylline, adenine, adenosine, cAMP, and caffeine did not block activation of transducin by DEN-stimulated taste membranes (Fig.  2).	transcription
59925	4	335532	7	NULL	NULL	0	NULL	adenosine 5''-carboxylate	Chemical		does not block					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9903_s_70	10449792	As with GMP (Fig.  1 e), adenosine 5''-carboxylate, adenosine 5''-monosulfate, theophylline, adenine, adenosine, cAMP, and caffeine did not block activation of transducin by DEN-stimulated taste membranes (Fig.  2).	transcription
59926	5	335532	7	NULL	NULL	0	NULL	adenosine 5''-monosulfate	Chemical		does not block					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9903_s_70	10449792	As with GMP (Fig.  1 e), adenosine 5''-carboxylate, adenosine 5''-monosulfate, theophylline, adenine, adenosine, cAMP, and caffeine did not block activation of transducin by DEN-stimulated taste membranes (Fig.  2).	transcription
59927	6	335532	7	NULL	NULL	0	NULL	theophylline	Chemical		does not block					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9903_s_70	10449792	As with GMP (Fig.  1 e), adenosine 5''-carboxylate, adenosine 5''-monosulfate, theophylline, adenine, adenosine, cAMP, and caffeine did not block activation of transducin by DEN-stimulated taste membranes (Fig.  2).	transcription
59928	7	335532	7	NULL	NULL	0	NULL	adenine	Chemical		does not block					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9903_s_70	10449792	As with GMP (Fig.  1 e), adenosine 5''-carboxylate, adenosine 5''-monosulfate, theophylline, adenine, adenosine, cAMP, and caffeine did not block activation of transducin by DEN-stimulated taste membranes (Fig.  2).	transcription
59929	8	335532	7	NULL	NULL	0	NULL	adenosine	Chemical		does not block					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9903_s_70	10449792	As with GMP (Fig.  1 e), adenosine 5''-carboxylate, adenosine 5''-monosulfate, theophylline, adenine, adenosine, cAMP, and caffeine did not block activation of transducin by DEN-stimulated taste membranes (Fig.  2).	transcription
59930	9	335532	7	NULL	NULL	0	NULL	 cAMP	Chemical		does not block					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9903_s_70	10449792	As with GMP (Fig.  1 e), adenosine 5''-carboxylate, adenosine 5''-monosulfate, theophylline, adenine, adenosine, cAMP, and caffeine did not block activation of transducin by DEN-stimulated taste membranes (Fig.  2).	transcription
59931	10	335532	7	NULL	NULL	0	NULL	caffeine	Chemical		does not block					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_96_17_9903_s_70	10449792	As with GMP (Fig.  1 e), adenosine 5''-carboxylate, adenosine 5''-monosulfate, theophylline, adenine, adenosine, cAMP, and caffeine did not block activation of transducin by DEN-stimulated taste membranes (Fig.  2).	transcription
55003	1	335533	5	NULL	NULL	0	NULL	NAD			is incorporated into					GAPDH					NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_1_259_s_109	9864224	To determine whether the residual ADP-ribosylation reflected the addition of ADP-ribose to the proteins or the covalent attachment of NAD as was observed for the nitroprusside-stimulated incorporation of [32]NAD into GAPDH ( 16), V53D and Y104K were activated with trypsin and incubated with ARF, DTT, and either [ adenine-14]NAD or [ nicotinamide-14]NAD (Fig.  5).	transcription
55004	2	335533	5	NULL	NULL	0	NULL	nitroprusside			stimulates					statement 1					NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_1_259_s_109	9864224	To determine whether the residual ADP-ribosylation reflected the addition of ADP-ribose to the proteins or the covalent attachment of NAD as was observed for the nitroprusside-stimulated incorporation of [32]NAD into GAPDH ( 16), V53D and Y104K were activated with trypsin and incubated with ARF, DTT, and either [ adenine-14]NAD or [ nicotinamide-14]NAD (Fig.  5).	transcription
59932	1	335533	7	NULL	NULL	0	NULL	NAD	Chemical		incorporated into					GAPDH	GP				NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_1_259_s_109	9864224	To determine whether the residual ADP-ribosylation reflected the addition of ADP-ribose to the proteins or the covalent attachment of NAD as was observed for the nitroprusside-stimulated incorporation of [32]NAD into GAPDH ( 16), V53D and Y104K were activated with trypsin and incubated with ARF, DTT, and either [ adenine-14]NAD or [ nicotinamide-14]NAD (Fig.  5).	transcription
59933	2	335533	7	NULL	NULL	0	NULL	nitroprusside	Chemical		stimulate					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_1_259_s_109	9864224	To determine whether the residual ADP-ribosylation reflected the addition of ADP-ribose to the proteins or the covalent attachment of NAD as was observed for the nitroprusside-stimulated incorporation of [32]NAD into GAPDH ( 16), V53D and Y104K were activated with trypsin and incubated with ARF, DTT, and either [ adenine-14]NAD or [ nicotinamide-14]NAD (Fig.  5).	transcription
59934	3	335533	7	NULL	NULL	0	NULL	trypsin	GP		activates								V53D		NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_1_259_s_109	9864224	To determine whether the residual ADP-ribosylation reflected the addition of ADP-ribose to the proteins or the covalent attachment of NAD as was observed for the nitroprusside-stimulated incorporation of [32]NAD into GAPDH ( 16), V53D and Y104K were activated with trypsin and incubated with ARF, DTT, and either [ adenine-14]NAD or [ nicotinamide-14]NAD (Fig.  5).	transcription
59935	4	335533	7	NULL	NULL	0	NULL	trypsin	GP		activates								Y104K		NULL		0	NULL	NULL	NULL	gw60_infectimmun_67_1_259_s_109	9864224	To determine whether the residual ADP-ribosylation reflected the addition of ADP-ribose to the proteins or the covalent attachment of NAD as was observed for the nitroprusside-stimulated incorporation of [32]NAD into GAPDH ( 16), V53D and Y104K were activated with trypsin and incubated with ARF, DTT, and either [ adenine-14]NAD or [ nicotinamide-14]NAD (Fig.  5).	transcription
55005	1	335534	5	NULL	NULL	0	NULL	Slr1134			hydrolyze					ADP-ribose					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
55006	2	335534	5	NULL	NULL	0	NULL	Slr1134			hydrolyze					NADH					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
55007	3	335534	5	NULL	NULL	0	NULL	Slr1134			hydrolyze					FAD					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
55008	4	335534	5	NULL	NULL	0	NULL	FAD			is					flavin adenine dinucleotide 					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
55009	5	335534	5	NULL	NULL	0	NULL	Sll1054			specific for		highly			ADP-ribose					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
55010	6	335534	5	NULL	NULL	0	NULL	Sll1054			activity for		low			Ap4A					NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
55011	7	335534	5	NULL	NULL	0	NULL	Ap4A			is					adenosine(5'')-tetraphospho-(5'')-adenosine					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
55012	8	335534	5	NULL	NULL	0	NULL	Sll1054			activity for		low			Ap5A					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
55013	9	335534	5	NULL	NULL	0	NULL	Ap5A			is					adenosine(5'')-pentaphospho-(5'')-adenosine					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
55014	10	335534	5	NULL	NULL	0	NULL	Sll1054			activity for		low			NADH					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
59936	1	335534	7	NULL	NULL	0	NULL	Sll1054	Chemical		specific for		highly			ADP-ribose	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
59937	2	335534	7	NULL	NULL	0	NULL	Sll1054	Chemical		activity for		low			Ap4A	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
59938	3	335534	7	NULL	NULL	0	NULL	Sll1054	Chemical		activity for		low			Ap5A	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
59939	4	335534	7	NULL	NULL	0	NULL	Sll1054	Chemical		activity for		low			NADH	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
59940	5	335534	7	NULL	NULL	0	NULL	Slr1134	Chemical		hydrolyze					ADP-ribose	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
59941	6	335534	7	NULL	NULL	0	NULL	Slr1134	Chemical		hydrolyze					NADH	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
59942	7	335534	7	NULL	NULL	0	NULL	Slr1134	Chemical		hydrolyze					FAD	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
59943	8	335534	7	NULL	NULL	0	NULL	Ap4A	Chemical		is					adenosine(5'')-tetraphospho-(5'')-adenosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
59944	9	335534	7	NULL	NULL	0	NULL	Ap5A	Chemical		is					adenosine(5'')-pentaphospho-(5'')-adenosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
59945	10	335534	7	NULL	NULL	0	NULL	FAD	Chemical		is					flavin adenine dinucleotide	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_14_4984_s_117	15995214	Sll1054 was also highly specific for ADP-ribose but it had low activity for adenosine(5'')-tetraphospho-(5'')-adenosine (Ap4A), adenosine(5'')-pentaphospho-(5'')-adenosine (Ap5A), and NADH. Slr1134 hydrolyzed not only ADP-ribose but also NADH and flavin adenine dinucleotide (FAD).	transcription
55015	1	335535	5	NULL	NULL	0	NULL				resides within				5''-GATC-3'' sites					pac sequence	NULL		0	NULL	NULL	NULL	gw70_genetics_165_1_11_s_331	14504214	STERNBERG and COULBY 1988  ,   STERNBERG and COULBY 1990   found that cleavage of the bacteriophage P1 packaging site ( pac) was regulated by adenine methylation of seven 5''-GATC-3'' sites within the  pac sequence.	transcription
55016	2	335535	5	NULL	NULL	0	NULL	statement 1		adenine methylation of 	regulates							cleavage of;;bacteriophage P1		pac	NULL		0	NULL	NULL	NULL	gw70_genetics_165_1_11_s_331	14504214	STERNBERG and COULBY 1988  ,   STERNBERG and COULBY 1990   found that cleavage of the bacteriophage P1 packaging site ( pac) was regulated by adenine methylation of seven 5''-GATC-3'' sites within the  pac sequence.	transcription
55017	3	335535	5	NULL	NULL	0	NULL	pac			is					packaging site					NULL		0	NULL	NULL	NULL	gw70_genetics_165_1_11_s_331	14504214	STERNBERG and COULBY 1988  ,   STERNBERG and COULBY 1990   found that cleavage of the bacteriophage P1 packaging site ( pac) was regulated by adenine methylation of seven 5''-GATC-3'' sites within the  pac sequence.	transcription
59946	1	335535	7	NULL	NULL	0	NULL			cleavage of bacteriophage	regulated by				pac site	adenine	Chemical	methylation of		seven 5''-GATC-3'' sites within the pac sequence	NULL		NULL	NULL	NULL	NULL	gw70_genetics_165_1_11_s_331	14504214	STERNBERG and COULBY 1988  ,   STERNBERG and COULBY 1990   found that cleavage of the bacteriophage P1 packaging site ( pac) was regulated by adenine methylation of seven 5''-GATC-3'' sites within the  pac sequence.	transcription
59947	2	335535	7	NULL	NULL	0	NULL				is				pac site			bacteriophage		P1 packaging site	NULL		0	NULL	NULL	NULL	gw70_genetics_165_1_11_s_331	14504214	STERNBERG and COULBY 1988  ,   STERNBERG and COULBY 1990   found that cleavage of the bacteriophage P1 packaging site ( pac) was regulated by adenine methylation of seven 5''-GATC-3'' sites within the  pac sequence.	transcription
55021	1	335536	5	NULL	NULL	0	NULL	palmitoyl-CoA			inhibits		exclusively			adenine nucleotide translocator					NULL	mitochondrial matrix	NULL	NULL	NULL	NULL	gw70_diabetes_54_4_944_s_208	15793231	Under the experimental conditions used, 5 mumol/l palmitoyl-CoA exclusively inhibited adenine nucleotide translocator, and this inhibition led to an increase in deltapsi and ATP concentration in the mitochondrial matrix.	transcription
55022	2	335536	5	NULL	NULL	0	NULL	statement 1			increases					ATP		concentration of			NULL	mitochondrial matrix	0	NULL	NULL	NULL	gw70_diabetes_54_4_944_s_208	15793231	Under the experimental conditions used, 5 mumol/l palmitoyl-CoA exclusively inhibited adenine nucleotide translocator, and this inhibition led to an increase in deltapsi and ATP concentration in the mitochondrial matrix.	transcription
59948	1	335536	7	NULL	NULL	0	NULL	 palmitoyl-CoA	Chemical		inhibit		exclusively			adenine nucleotide translocator	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_54_4_944_s_208	15793231	Under the experimental conditions used, 5 mumol/l palmitoyl-CoA exclusively inhibited adenine nucleotide translocator, and this inhibition led to an increase in deltapsi and ATP concentration in the mitochondrial matrix.	transcription
59949	2	335536	7	NULL	NULL	0	NULL	statement 1	Process		leads to					deltapsi 	Process	increase in concentration of			NULL	mitochondrial matrix	NULL	NULL	NULL	NULL	gw70_diabetes_54_4_944_s_208	15793231	Under the experimental conditions used, 5 mumol/l palmitoyl-CoA exclusively inhibited adenine nucleotide translocator, and this inhibition led to an increase in deltapsi and ATP concentration in the mitochondrial matrix.	transcription
59950	3	335536	7	NULL	NULL	0	NULL	statement 1	Process		leads to					ATP	Chemical	increase in concentration of 			NULL	mitochondrial matrix	NULL	NULL	NULL	NULL	gw70_diabetes_54_4_944_s_208	15793231	Under the experimental conditions used, 5 mumol/l palmitoyl-CoA exclusively inhibited adenine nucleotide translocator, and this inhibition led to an increase in deltapsi and ATP concentration in the mitochondrial matrix.	transcription
55023	1	335537	5	NULL	NULL	0	NULL	Transglutaminase 5			is regulated by					guanine/adenine nucleotides					NULL		0	NULL	NULL	NULL	gw70_brainresmolbrainres_135_1_122_s_258	15857675	[12] E. Candi, A. Paradisi, A. Terrinoni, V. Pietroni, S. Oddi, B. Cadot, V. Jogini, M.  Meiyappan, J. Clardy, A. Finazzi-Agro and G. Melino, Transglutaminase 5 is regulated  by guanine/adenine nucleotides,  Biochem.	transcription
59951	1	335537	7	NULL	NULL	0	NULL	Transglutaminase 5	GP		is regulated by					guanine nucleotides	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_brainresmolbrainres_135_1_122_s_258	15857675	[12] E. Candi, A. Paradisi, A. Terrinoni, V. Pietroni, S. Oddi, B. Cadot, V. Jogini, M.  Meiyappan, J. Clardy, A. Finazzi-Agro and G. Melino, Transglutaminase 5 is regulated  by guanine/adenine nucleotides,  Biochem.	transcription
59952	2	335537	7	NULL	NULL	0	NULL	Transglutaminase 5	GP		is regulated by					adenine nucleotides	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_brainresmolbrainres_135_1_122_s_258	15857675	[12] E. Candi, A. Paradisi, A. Terrinoni, V. Pietroni, S. Oddi, B. Cadot, V. Jogini, M.  Meiyappan, J. Clardy, A. Finazzi-Agro and G. Melino, Transglutaminase 5 is regulated  by guanine/adenine nucleotides,  Biochem.	transcription
55024	1	335538	5	NULL	NULL	0	NULL	methylene ADP			is an inhibitor of					ectonucleotidase		extracellular			NULL		NULL	NULL	NULL	NULL	gw70_neuropharmacology_47_3_427_s_200	15275832	Considering the possibility that endogenous adenosine was key to explain our findings  here, we interfered with the normal metabolic flux of adenine nucleotides using   , -methylene ADP, an inhibitor of the extracellular 5 -ectonucleotidase.	transcription
59953	1	335538	7	NULL	NULL	0	NULL	methylene ADP	Chemical		is an inhibitor of					5 -ectonucleotidase	GP	extracellular			NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_47_3_427_s_200	15275832	Considering the possibility that endogenous adenosine was key to explain our findings  here, we interfered with the normal metabolic flux of adenine nucleotides using   , -methylene ADP, an inhibitor of the extracellular 5 -ectonucleotidase.	transcription
55025	1	335539	5	NULL	NULL	0	NULL	adenosine			inhibits					adenylyl cyclases					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_7253_s_17	15591060	Adenylyl cyclases are inhibited by adenosine and certain adenosine derivatives such as 2''-5''-dideoxyadenosine and 2''-deoxyadenosine 3''-monophosphate that possess intact adenine rings and are known as "`P-site"` inhibitors (  -  ).	transcription
55026	2	335539	5	NULL	NULL	0	NULL	2''-5''-dideoxyadenosine			is a derivative of					adenosine					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_7253_s_17	15591060	Adenylyl cyclases are inhibited by adenosine and certain adenosine derivatives such as 2''-5''-dideoxyadenosine and 2''-deoxyadenosine 3''-monophosphate that possess intact adenine rings and are known as "`P-site"` inhibitors (  -  ).	transcription
55027	3	335539	5	NULL	NULL	0	NULL	2''-deoxyadenosine 3''-monophosphate			is a derivative of					adenosine					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_7253_s_17	15591060	Adenylyl cyclases are inhibited by adenosine and certain adenosine derivatives such as 2''-5''-dideoxyadenosine and 2''-deoxyadenosine 3''-monophosphate that possess intact adenine rings and are known as "`P-site"` inhibitors (  -  ).	transcription
55030	4	335539	5	NULL	NULL	0	NULL	2''-5''-dideoxyadenosine			inhibits					adenylyl cyclases					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_7253_s_17	15591060	Adenylyl cyclases are inhibited by adenosine and certain adenosine derivatives such as 2''-5''-dideoxyadenosine and 2''-deoxyadenosine 3''-monophosphate that possess intact adenine rings and are known as "`P-site"` inhibitors (  -  ).	transcription
55031	5	335539	5	NULL	NULL	0	NULL	2''-deoxyadenosine 3''-monophosphate			inhibits					adenylyl cyclases					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_7253_s_17	15591060	Adenylyl cyclases are inhibited by adenosine and certain adenosine derivatives such as 2''-5''-dideoxyadenosine and 2''-deoxyadenosine 3''-monophosphate that possess intact adenine rings and are known as "`P-site"` inhibitors (  -  ).	transcription
55032	6	335539	5	NULL	NULL	0	NULL	2''-5''-dideoxyadenosine			possess								adenine rings		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_7253_s_17	15591060	Adenylyl cyclases are inhibited by adenosine and certain adenosine derivatives such as 2''-5''-dideoxyadenosine and 2''-deoxyadenosine 3''-monophosphate that possess intact adenine rings and are known as "`P-site"` inhibitors (  -  ).	transcription
55034	7	335539	5	NULL	NULL	0	NULL	2''-deoxyadenosine 3''-monophosphate			possess								adenine rings		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_7253_s_17	15591060	Adenylyl cyclases are inhibited by adenosine and certain adenosine derivatives such as 2''-5''-dideoxyadenosine and 2''-deoxyadenosine 3''-monophosphate that possess intact adenine rings and are known as "`P-site"` inhibitors (  -  ).	transcription
55038	8	335539	5	NULL	NULL	0	NULL	2''-5''-dideoxyadenosine			is known as					"`P-site"` inhibitors					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_7253_s_17	15591060	Adenylyl cyclases are inhibited by adenosine and certain adenosine derivatives such as 2''-5''-dideoxyadenosine and 2''-deoxyadenosine 3''-monophosphate that possess intact adenine rings and are known as "`P-site"` inhibitors (  -  ).	transcription
55040	9	335539	5	NULL	NULL	0	NULL	2''-deoxyadenosine 3''-monophosphate			is known as					"`P-site"` inhibitors					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_7253_s_17	15591060	Adenylyl cyclases are inhibited by adenosine and certain adenosine derivatives such as 2''-5''-dideoxyadenosine and 2''-deoxyadenosine 3''-monophosphate that possess intact adenine rings and are known as "`P-site"` inhibitors (  -  ).	transcription
59954	1	335539	7	NULL	NULL	0	NULL	adenosine	Chemical		inhibit					Adenylyl cyclases	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_7253_s_17	15591060	Adenylyl cyclases are inhibited by adenosine and certain adenosine derivatives such as 2''-5''-dideoxyadenosine and 2''-deoxyadenosine 3''-monophosphate that possess intact adenine rings and are known as "`P-site"` inhibitors (  -  ).	transcription
59955	2	335539	7	NULL	NULL	0	NULL	2''-5''-dideoxyadenosine	Chemical		possess					adenine rings	Chemical	intact			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_7253_s_17	15591060	Adenylyl cyclases are inhibited by adenosine and certain adenosine derivatives such as 2''-5''-dideoxyadenosine and 2''-deoxyadenosine 3''-monophosphate that possess intact adenine rings and are known as "`P-site"` inhibitors (  -  ).	transcription
59956	3	335539	7	NULL	NULL	0	NULL	2''-deoxyadenosine 3''-monophosphate	Chemical		possess					adenine rings	Chemical	intact			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_7253_s_17	15591060	Adenylyl cyclases are inhibited by adenosine and certain adenosine derivatives such as 2''-5''-dideoxyadenosine and 2''-deoxyadenosine 3''-monophosphate that possess intact adenine rings and are known as "`P-site"` inhibitors (  -  ).	transcription
59957	4	335539	7	NULL	NULL	0	NULL	2''-5''-dideoxyadenosine	Chemical		is an inhibitor of								"`P-site"		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_8_7253_s_17	15591060	Adenylyl cyclases are inhibited by adenosine and certain adenosine derivatives such as 2''-5''-dideoxyadenosine and 2''-deoxyadenosine 3''-monophosphate that possess intact adenine rings and are known as "`P-site"` inhibitors (  -  ).	transcription
59958	5	335539	7	NULL	NULL	0	NULL	2''-deoxyadenosine 3''-monophosphate	Chemical		is an inhibitor of								"`P-site"		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_7253_s_17	15591060	Adenylyl cyclases are inhibited by adenosine and certain adenosine derivatives such as 2''-5''-dideoxyadenosine and 2''-deoxyadenosine 3''-monophosphate that possess intact adenine rings and are known as "`P-site"` inhibitors (  -  ).	transcription
59959	6	335539	7	NULL	NULL	0	NULL	2''-5''-dideoxyadenosine	Chemical		is a type of					adenosine derivative	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_7253_s_17	15591060	Adenylyl cyclases are inhibited by adenosine and certain adenosine derivatives such as 2''-5''-dideoxyadenosine and 2''-deoxyadenosine 3''-monophosphate that possess intact adenine rings and are known as "`P-site"` inhibitors (  -  ).	transcription
59960	7	335539	7	NULL	NULL	0	NULL	2''-deoxyadenosine 3''-monophosphate	Chemical		is a type of					adenosine derivative	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_8_7253_s_17	15591060	Adenylyl cyclases are inhibited by adenosine and certain adenosine derivatives such as 2''-5''-dideoxyadenosine and 2''-deoxyadenosine 3''-monophosphate that possess intact adenine rings and are known as "`P-site"` inhibitors (  -  ).	transcription
55041	1	335540	5	NULL	NULL	0	NULL	fat		inguinal	contains					ATP		enhanced turnover of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_42_31894_s_266	16914547	Up-regulation of the adenine nucleotide translocator (ANT2) also indicates that inguinal fat has an enhanced turnover of ATP as expected for a more thermogenically active tissue ( Table 5).	transcription
55042	2	335540	5	NULL	NULL	0	NULL	ANT2			is					adenine nucleotide translocator					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_42_31894_s_266	16914547	Up-regulation of the adenine nucleotide translocator (ANT2) also indicates that inguinal fat has an enhanced turnover of ATP as expected for a more thermogenically active tissue ( Table 5).	transcription
55043	3	335540	5	NULL	NULL	0	NULL	ANT2		upregulation of	indicates					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_42_31894_s_266	16914547	Up-regulation of the adenine nucleotide translocator (ANT2) also indicates that inguinal fat has an enhanced turnover of ATP as expected for a more thermogenically active tissue ( Table 5).	transcription
59961	1	335540	7	NULL	NULL	0	NULL	ANT2	GP	Up-regulation of	indicates					ATP	Chemical	enhanced turnover of;;inguinal fat			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_42_31894_s_266	16914547	Up-regulation of the adenine nucleotide translocator (ANT2) also indicates that inguinal fat has an enhanced turnover of ATP as expected for a more thermogenically active tissue ( Table 5).	transcription
59962	2	335540	7	NULL	NULL	0	NULL	statement 1	Process		occur in					 tissue	OrganismPart	thermogenically active			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_42_31894_s_266	16914547	Up-regulation of the adenine nucleotide translocator (ANT2) also indicates that inguinal fat has an enhanced turnover of ATP as expected for a more thermogenically active tissue ( Table 5).	transcription
59963	3	335540	7	NULL	NULL	0	NULL	ANT2	GP		is					adenine nucleotide translocator	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_42_31894_s_266	16914547	Up-regulation of the adenine nucleotide translocator (ANT2) also indicates that inguinal fat has an enhanced turnover of ATP as expected for a more thermogenically active tissue ( Table 5).	transcription
55046	1	335541	5	NULL	NULL	0	NULL	EHNA			is					erythro-9-(2-hydroxy-3-nonyl)adenine hydrochloride					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_27_24888_s_136	12707258	Inhibitor of adenosine deaminase  erythro-9-(2-hydroxy-3-nonyl)adenine hydrochloride (EHNA) blocked further  conversion of adenosine in the experiments with HUVEC, either alone ( lane  3) or in combination with lymphocytes ( lane 5).	transcription
55047	2	335541	5	NULL	NULL	0	NULL	EHNA			is an inhibitor of					adenosine deaminase					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_27_24888_s_136	12707258	Inhibitor of adenosine deaminase  erythro-9-(2-hydroxy-3-nonyl)adenine hydrochloride (EHNA) blocked further  conversion of adenosine in the experiments with HUVEC, either alone ( lane  3) or in combination with lymphocytes ( lane 5).	transcription
55048	3	335541	5	NULL	NULL	0	NULL	EHNA			blocks					adenosine		further conversion of			NULL	HUVEC	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_27_24888_s_136	12707258	Inhibitor of adenosine deaminase  erythro-9-(2-hydroxy-3-nonyl)adenine hydrochloride (EHNA) blocked further  conversion of adenosine in the experiments with HUVEC, either alone ( lane  3) or in combination with lymphocytes ( lane 5).	transcription
55049	4	335541	5	NULL	NULL	0	NULL	EHNA			blocks					adenosine		further conversion of			NULL	HUVEC in combination with lymphocytes	0	NULL	NULL	NULL	gw70_jbiolchem_278_27_24888_s_136	12707258	Inhibitor of adenosine deaminase  erythro-9-(2-hydroxy-3-nonyl)adenine hydrochloride (EHNA) blocked further  conversion of adenosine in the experiments with HUVEC, either alone ( lane  3) or in combination with lymphocytes ( lane 5).	transcription
55050	5	335541	5	NULL	NULL	0	NULL	statement 3			is an alternative to					statement 4					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_27_24888_s_136	12707258	Inhibitor of adenosine deaminase  erythro-9-(2-hydroxy-3-nonyl)adenine hydrochloride (EHNA) blocked further  conversion of adenosine in the experiments with HUVEC, either alone ( lane  3) or in combination with lymphocytes ( lane 5).	transcription
59964	1	335541	7	NULL	NULL	0	NULL	EHNA	Chemical		is an inhibitor of					adenosine deaminase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_27_24888_s_136	12707258	Inhibitor of adenosine deaminase  erythro-9-(2-hydroxy-3-nonyl)adenine hydrochloride (EHNA) blocked further  conversion of adenosine in the experiments with HUVEC, either alone ( lane  3) or in combination with lymphocytes ( lane 5).	transcription
59965	2	335541	7	NULL	NULL	0	NULL	EHNA	Chemical		is					erythro-9-(2-hydroxy-3-nonyl)adenine hydrochloride	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_27_24888_s_136	12707258	Inhibitor of adenosine deaminase  erythro-9-(2-hydroxy-3-nonyl)adenine hydrochloride (EHNA) blocked further  conversion of adenosine in the experiments with HUVEC, either alone ( lane  3) or in combination with lymphocytes ( lane 5).	transcription
59966	3	335541	7	NULL	NULL	0	NULL	EHNA	Chemical		blocks					adenosine	Chemical	conversion of			NULL	HUVEC	0	NULL	NULL	NULL	gw70_jbiolchem_278_27_24888_s_136	12707258	Inhibitor of adenosine deaminase  erythro-9-(2-hydroxy-3-nonyl)adenine hydrochloride (EHNA) blocked further  conversion of adenosine in the experiments with HUVEC, either alone ( lane  3) or in combination with lymphocytes ( lane 5).	transcription
59967	4	335541	7	NULL	NULL	0	NULL	EHNA	Chemical		blocks					adenosine	Chemical	conversion of			NULL	HUVEC and lymphocytes	0	NULL	NULL	NULL	gw70_jbiolchem_278_27_24888_s_136	12707258	Inhibitor of adenosine deaminase  erythro-9-(2-hydroxy-3-nonyl)adenine hydrochloride (EHNA) blocked further  conversion of adenosine in the experiments with HUVEC, either alone ( lane  3) or in combination with lymphocytes ( lane 5).	transcription
55051	1	335543	5	NULL	NULL	0	NULL	Ant1p			is a type of					novel adenine nucleotide transporter					NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_152	11566870	Ant1p is a novel adenine nucleotide transporter   Upon reconstitution into liposomes, recombinant Ant1p catalyzed an active [14]ATP/ATP exchange that was completely inhibited by a mixture of pyridoxal 5''-phosphate and bathophenanthroline.	transcription
55052	2	335543	5	NULL	NULL	0	NULL	Ant1p		recombinant	catalyzes					ATP/ATP exchange		active			NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_152	11566870	Ant1p is a novel adenine nucleotide transporter   Upon reconstitution into liposomes, recombinant Ant1p catalyzed an active [14]ATP/ATP exchange that was completely inhibited by a mixture of pyridoxal 5''-phosphate and bathophenanthroline.	transcription
55053	3	335543	5	NULL	NULL	0	NULL	pyridoxal 5''-phosphate			mixed with					bathophenanthroline					NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_152	11566870	Ant1p is a novel adenine nucleotide transporter   Upon reconstitution into liposomes, recombinant Ant1p catalyzed an active [14]ATP/ATP exchange that was completely inhibited by a mixture of pyridoxal 5''-phosphate and bathophenanthroline.	transcription
55054	4	335543	5	NULL	NULL	0	NULL	ATP/ATP exchange		active	is inhibited by		completely			statement 3					NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_152	11566870	Ant1p is a novel adenine nucleotide transporter   Upon reconstitution into liposomes, recombinant Ant1p catalyzed an active [14]ATP/ATP exchange that was completely inhibited by a mixture of pyridoxal 5''-phosphate and bathophenanthroline.	transcription
59968	1	335543	7	NULL	NULL	0	NULL	Ant1p	GP		is a type of					adenine nucleotide transporter	GP	novel			NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_152	11566870	Ant1p is a novel adenine nucleotide transporter   Upon reconstitution into liposomes, recombinant Ant1p catalyzed an active [14]ATP/ATP exchange that was completely inhibited by a mixture of pyridoxal 5''-phosphate and bathophenanthroline.	transcription
59969	2	335543	7	NULL	NULL	0	NULL	Ant1p	GP		is reconstituted into					liposomes	CellComponent				NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_152	11566870	Ant1p is a novel adenine nucleotide transporter   Upon reconstitution into liposomes, recombinant Ant1p catalyzed an active [14]ATP/ATP exchange that was completely inhibited by a mixture of pyridoxal 5''-phosphate and bathophenanthroline.	transcription
59970	3	335543	7	NULL	NULL	0	NULL	Ant1p	GP	recombinant	catalyze					activeATP/ATP	Chemical	exchange of			NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_152	11566870	Ant1p is a novel adenine nucleotide transporter   Upon reconstitution into liposomes, recombinant Ant1p catalyzed an active [14]ATP/ATP exchange that was completely inhibited by a mixture of pyridoxal 5''-phosphate and bathophenanthroline.	transcription
59971	4	335543	7	NULL	NULL	0	NULL	pyridoxal 5''-phosphate	Chemical		mixed with					bathophenanthroline	Chemical				NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_152	11566870	Ant1p is a novel adenine nucleotide transporter   Upon reconstitution into liposomes, recombinant Ant1p catalyzed an active [14]ATP/ATP exchange that was completely inhibited by a mixture of pyridoxal 5''-phosphate and bathophenanthroline.	transcription
59972	5	335543	7	NULL	NULL	0	NULL	statement 4	Process		inhibits		completely			statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_embo_20_18_5049_s_152	11566870	Ant1p is a novel adenine nucleotide transporter   Upon reconstitution into liposomes, recombinant Ant1p catalyzed an active [14]ATP/ATP exchange that was completely inhibited by a mixture of pyridoxal 5''-phosphate and bathophenanthroline.	transcription
55055	1	335544	5	NULL	NULL	0	NULL	7-chloro-4-nitrobenzo-2-oxa-1,3-diazole			is an analog of					adenine					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1465_1_17_s_70	10748245	It contains a nucleotide-binding site, and the binding of the adenine analogue 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole [  32], of fluorescein 5''-isothiocyanate [  33] or of  N-ethylmaleimide [ 32 and   34] to subunit A inhibits ATP-hydrolysis activity.	transcription
55056	2	335544	5	NULL	NULL	0	NULL	7-chloro-4-nitrobenzo-2-oxa-1,3-diazole			bind								subunit A		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1465_1_17_s_70	10748245	It contains a nucleotide-binding site, and the binding of the adenine analogue 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole [  32], of fluorescein 5''-isothiocyanate [  33] or of  N-ethylmaleimide [ 32 and   34] to subunit A inhibits ATP-hydrolysis activity.	transcription
55057	3	335544	5	NULL	NULL	0	NULL	statement 1			inhibits					ATP		hydrolysis of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1465_1_17_s_70	10748245	It contains a nucleotide-binding site, and the binding of the adenine analogue 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole [  32], of fluorescein 5''-isothiocyanate [  33] or of  N-ethylmaleimide [ 32 and   34] to subunit A inhibits ATP-hydrolysis activity.	transcription
55058	4	335544	5	NULL	NULL	0	NULL	fluorescein 5''-isothiocyanate			bind								subunit A		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1465_1_17_s_70	10748245	It contains a nucleotide-binding site, and the binding of the adenine analogue 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole [  32], of fluorescein 5''-isothiocyanate [  33] or of  N-ethylmaleimide [ 32 and   34] to subunit A inhibits ATP-hydrolysis activity.	transcription
55059	5	335544	5	NULL	NULL	0	NULL	statement 4			inhibits					ATP		hydrolysis of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1465_1_17_s_70	10748245	It contains a nucleotide-binding site, and the binding of the adenine analogue 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole [  32], of fluorescein 5''-isothiocyanate [  33] or of  N-ethylmaleimide [ 32 and   34] to subunit A inhibits ATP-hydrolysis activity.	transcription
55060	6	335544	5	NULL	NULL	0	NULL	N-ethylmaleimide			bind								subunit A		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1465_1_17_s_70	10748245	It contains a nucleotide-binding site, and the binding of the adenine analogue 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole [  32], of fluorescein 5''-isothiocyanate [  33] or of  N-ethylmaleimide [ 32 and   34] to subunit A inhibits ATP-hydrolysis activity.	transcription
55061	7	335544	5	NULL	NULL	0	NULL	statement 6			inhibits					ATP		hydrolysis of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1465_1_17_s_70	10748245	It contains a nucleotide-binding site, and the binding of the adenine analogue 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole [  32], of fluorescein 5''-isothiocyanate [  33] or of  N-ethylmaleimide [ 32 and   34] to subunit A inhibits ATP-hydrolysis activity.	transcription
55062	8	335544	5	NULL	NULL	0	NULL	statement 2			is an alternative to					statement 4					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1465_1_17_s_70	10748245	It contains a nucleotide-binding site, and the binding of the adenine analogue 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole [  32], of fluorescein 5''-isothiocyanate [  33] or of  N-ethylmaleimide [ 32 and   34] to subunit A inhibits ATP-hydrolysis activity.	transcription
55063	9	335544	5	NULL	NULL	0	NULL	statement 4			is an alternative to					statement 6					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1465_1_17_s_70	10748245	It contains a nucleotide-binding site, and the binding of the adenine analogue 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole [  32], of fluorescein 5''-isothiocyanate [  33] or of  N-ethylmaleimide [ 32 and   34] to subunit A inhibits ATP-hydrolysis activity.	transcription
59973	1	335544	7	NULL	NULL	0	NULL	7-chloro-4-nitrobenzo-2-oxa-1,3-diazole	Chemical		bind								subunit A		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1465_1_17_s_70	10748245	It contains a nucleotide-binding site, and the binding of the adenine analogue 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole [  32], of fluorescein 5''-isothiocyanate [  33] or of  N-ethylmaleimide [ 32 and   34] to subunit A inhibits ATP-hydrolysis activity.	transcription
59974	2	335544	7	NULL	NULL	0	NULL	fluorescein 5''-isothiocyanate	Chemical		bind								subunit A		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1465_1_17_s_70	10748245	It contains a nucleotide-binding site, and the binding of the adenine analogue 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole [  32], of fluorescein 5''-isothiocyanate [  33] or of  N-ethylmaleimide [ 32 and   34] to subunit A inhibits ATP-hydrolysis activity.	transcription
59975	3	335544	7	NULL	NULL	0	NULL	N-ethylmaleimide	Chemical		bind								subunit A		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1465_1_17_s_70	10748245	It contains a nucleotide-binding site, and the binding of the adenine analogue 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole [  32], of fluorescein 5''-isothiocyanate [  33] or of  N-ethylmaleimide [ 32 and   34] to subunit A inhibits ATP-hydrolysis activity.	transcription
59976	4	335544	7	NULL	NULL	0	NULL	statement 1	Process		inhibit					ATP-hydrolysis activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1465_1_17_s_70	10748245	It contains a nucleotide-binding site, and the binding of the adenine analogue 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole [  32], of fluorescein 5''-isothiocyanate [  33] or of  N-ethylmaleimide [ 32 and   34] to subunit A inhibits ATP-hydrolysis activity.	transcription
59977	5	335544	7	NULL	NULL	0	NULL	statement 2	Process		inhibit					ATP-hydrolysis activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1465_1_17_s_70	10748245	It contains a nucleotide-binding site, and the binding of the adenine analogue 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole [  32], of fluorescein 5''-isothiocyanate [  33] or of  N-ethylmaleimide [ 32 and   34] to subunit A inhibits ATP-hydrolysis activity.	transcription
59978	6	335544	7	NULL	NULL	0	NULL	statement 3	Process		inhibit					ATP-hydrolysis activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1465_1_17_s_70	10748245	It contains a nucleotide-binding site, and the binding of the adenine analogue 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole [  32], of fluorescein 5''-isothiocyanate [  33] or of  N-ethylmaleimide [ 32 and   34] to subunit A inhibits ATP-hydrolysis activity.	transcription
59979	7	335544	7	NULL	NULL	0	NULL	7-chloro-4-nitrobenzo-2-oxa-1,3-diazole	Chemical		is an analogue of					adenine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1465_1_17_s_70	10748245	It contains a nucleotide-binding site, and the binding of the adenine analogue 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole [  32], of fluorescein 5''-isothiocyanate [  33] or of  N-ethylmaleimide [ 32 and   34] to subunit A inhibits ATP-hydrolysis activity.	transcription
59980	8	335544	7	NULL	NULL	0	NULL	fluorescein 5''-isothiocyanate	Chemical		is an analogue of					adenine	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1465_1_17_s_70	10748245	It contains a nucleotide-binding site, and the binding of the adenine analogue 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole [  32], of fluorescein 5''-isothiocyanate [  33] or of  N-ethylmaleimide [ 32 and   34] to subunit A inhibits ATP-hydrolysis activity.	transcription
59981	9	335544	7	NULL	NULL	0	NULL	N-ethylmaleimide	Chemical		is an analogue of					adenine	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1465_1_17_s_70	10748245	It contains a nucleotide-binding site, and the binding of the adenine analogue 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole [  32], of fluorescein 5''-isothiocyanate [  33] or of  N-ethylmaleimide [ 32 and   34] to subunit A inhibits ATP-hydrolysis activity.	transcription
55064	1	335546	5	NULL	NULL	0	NULL	profilin		low concentrations of	increases					adenine nucleotide		rate of;;exchange of			NULL	actin monomers	0	NULL	NULL	NULL	gw60_currbiol_4_5_465_s_37	7922367	This effect may be further enhanced by a second property of profilin -- its ability at low concentrations to increase the rate of adenine nucleotide exchange (replacement of ADP by ATP) on actin monomers  [5  .	transcription
59982	1	335546	7	NULL	NULL	0	NULL	ADP	Chemical		replaced by					ATP	Chemical				NULL		0	NULL	NULL	NULL	gw60_currbiol_4_5_465_s_37	7922367	This effect may be further enhanced by a second property of profilin -- its ability at low concentrations to increase the rate of adenine nucleotide exchange (replacement of ADP by ATP) on actin monomers  [5  .	transcription
59983	2	335546	7	NULL	NULL	0	NULL	statement 1			occur on					actin monomers					NULL		0	NULL	NULL	NULL	gw60_currbiol_4_5_465_s_37	7922367	This effect may be further enhanced by a second property of profilin -- its ability at low concentrations to increase the rate of adenine nucleotide exchange (replacement of ADP by ATP) on actin monomers  [5  .	transcription
59984	3	335546	7	NULL	NULL	0	NULL	profilin	Chemical		increase					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_currbiol_4_5_465_s_37	7922367	This effect may be further enhanced by a second property of profilin -- its ability at low concentrations to increase the rate of adenine nucleotide exchange (replacement of ADP by ATP) on actin monomers  [5  .	transcription
55065	1	335547	5	NULL	NULL	0	NULL	ecto-5''-nucleotidase inhibitor			effects		may			adenosine		production of			NULL	canine coronary arteries	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_12_2298_s_50	7489256	Protocol 2: Effect of an Ecto-5''-Nucleotidase Inhibitor on Adenosine Production in Canine Coronary Arteries   Adenosine can be produced intracellularly by cytosolic 5''-nucleotidase and by  S-adenosylhomocysteine, and extracellularly by ecto-5''-nucleotidase acting on released adenine nucleotides.	transcription
59985	1	335547	7	NULL	NULL	0	NULL	Adenosine	Chemical		produced by					  5''-nucleotidase	GP	cytosolic			NULL	intracellular;;Canine Coronary Arteries	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_12_2298_s_50	7489256	Protocol 2: Effect of an Ecto-5''-Nucleotidase Inhibitor on Adenosine Production in Canine Coronary Arteries   Adenosine can be produced intracellularly by cytosolic 5''-nucleotidase and by  S-adenosylhomocysteine, and extracellularly by ecto-5''-nucleotidase acting on released adenine nucleotides.	transcription
59986	2	335547	7	NULL	NULL	0	NULL	Adenosine	Chemical		produced by					S-adenosylhomocysteine	Chemical				NULL	intracellular;;Canine Coronary Arteries	NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_12_2298_s_50	7489256	Protocol 2: Effect of an Ecto-5''-Nucleotidase Inhibitor on Adenosine Production in Canine Coronary Arteries   Adenosine can be produced intracellularly by cytosolic 5''-nucleotidase and by  S-adenosylhomocysteine, and extracellularly by ecto-5''-nucleotidase acting on released adenine nucleotides.	transcription
59987	3	335547	7	NULL	NULL	0	NULL	statement 1	Process		occur simulataneous with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_12_2298_s_50	7489256	Protocol 2: Effect of an Ecto-5''-Nucleotidase Inhibitor on Adenosine Production in Canine Coronary Arteries   Adenosine can be produced intracellularly by cytosolic 5''-nucleotidase and by  S-adenosylhomocysteine, and extracellularly by ecto-5''-nucleotidase acting on released adenine nucleotides.	transcription
59988	4	335547	7	NULL	NULL	0	NULL	Adenosine	Chemical		produced by					ecto-5''-nucleotidase	GP				NULL	extracellular	0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_12_2298_s_50	7489256	Protocol 2: Effect of an Ecto-5''-Nucleotidase Inhibitor on Adenosine Production in Canine Coronary Arteries   Adenosine can be produced intracellularly by cytosolic 5''-nucleotidase and by  S-adenosylhomocysteine, and extracellularly by ecto-5''-nucleotidase acting on released adenine nucleotides.	transcription
59989	5	335547	7	NULL	NULL	0	NULL	ecto-5''-nucleotidase	GP		act on					adenine nucleotides		released			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_15_12_2298_s_50	7489256	Protocol 2: Effect of an Ecto-5''-Nucleotidase Inhibitor on Adenosine Production in Canine Coronary Arteries   Adenosine can be produced intracellularly by cytosolic 5''-nucleotidase and by  S-adenosylhomocysteine, and extracellularly by ecto-5''-nucleotidase acting on released adenine nucleotides.	transcription
55066	1	335550	5	NULL	NULL	0	NULL	Pfu			is a type of					polymerase					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_11_2914_s_69	12003931	The 3''-5' exonuclease activity of  Pfu polymerase removes nucleotide residues from both 3' ends of the PCR product and stops on the first adenine residue because of the dATP present in the reaction.	transcription
55067	2	335550	5	NULL	NULL	0	NULL	nucleotide residues			removed from					PCR product				3' ends	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_11_2914_s_69	12003931	The 3''-5' exonuclease activity of  Pfu polymerase removes nucleotide residues from both 3' ends of the PCR product and stops on the first adenine residue because of the dATP present in the reaction.	transcription
55068	3	335550	5	NULL	NULL	0	NULL	statement 2			stops at					adenine residue					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_11_2914_s_69	12003931	The 3''-5' exonuclease activity of  Pfu polymerase removes nucleotide residues from both 3' ends of the PCR product and stops on the first adenine residue because of the dATP present in the reaction.	transcription
55069	4	335550	5	NULL	NULL	0	NULL	statement 3			because of					dATP		presence of			NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_11_2914_s_69	12003931	The 3''-5' exonuclease activity of  Pfu polymerase removes nucleotide residues from both 3' ends of the PCR product and stops on the first adenine residue because of the dATP present in the reaction.	transcription
55070	5	335550	5	NULL	NULL	0	NULL	Pfu		3''-5' exonuclease activity of	is required for					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_11_2914_s_69	12003931	The 3''-5' exonuclease activity of  Pfu polymerase removes nucleotide residues from both 3' ends of the PCR product and stops on the first adenine residue because of the dATP present in the reaction.	transcription
59990	1	335550	7	NULL	NULL	0	NULL	Pfu polymerase	GP		possess					3''-5' exonuclease activity	Process				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_11_2914_s_69	12003931	The 3''-5' exonuclease activity of  Pfu polymerase removes nucleotide residues from both 3' ends of the PCR product and stops on the first adenine residue because of the dATP present in the reaction.	transcription
59991	2	335550	7	NULL	NULL	0	NULL	statement 1	Process		removes					nucleotide residues	NucleicAcid			from 3' end	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_184_11_2914_s_69	12003931	The 3''-5' exonuclease activity of  Pfu polymerase removes nucleotide residues from both 3' ends of the PCR product and stops on the first adenine residue because of the dATP present in the reaction.	transcription
59992	3	335550	7	NULL	NULL	0	NULL	statement 1	Process		stops					adenine residue	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_184_11_2914_s_69	12003931	The 3''-5' exonuclease activity of  Pfu polymerase removes nucleotide residues from both 3' ends of the PCR product and stops on the first adenine residue because of the dATP present in the reaction.	transcription
55071	1	335551	5	NULL	NULL	0	NULL	Oocytes			express					TbNBT1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_26_23502_s_119	12707261	Oocytes expressing  TbNBT1 rapidly accumulated  [3]adenine and, to a lesser extent, [3]uracil, but no  significant mediated transport of [3]adenosine or  [3]uridine was observed at pH 7.5  ( Fig. 5).	transcription
55072	2	335551	5	NULL	NULL	0	NULL	statement 1			accumulates		rapidly			adenine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_26_23502_s_119	12707261	Oocytes expressing  TbNBT1 rapidly accumulated  [3]adenine and, to a lesser extent, [3]uracil, but no  significant mediated transport of [3]adenosine or  [3]uridine was observed at pH 7.5  ( Fig. 5).	transcription
55073	3	335551	5	NULL	NULL	0	NULL	statement 1			accumulates					uracil					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_26_23502_s_119	12707261	Oocytes expressing  TbNBT1 rapidly accumulated  [3]adenine and, to a lesser extent, [3]uracil, but no  significant mediated transport of [3]adenosine or  [3]uridine was observed at pH 7.5  ( Fig. 5).	transcription
55074	4	335551	5	NULL	NULL	0	NULL	statement 3			lesser extent than					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_26_23502_s_119	12707261	Oocytes expressing  TbNBT1 rapidly accumulated  [3]adenine and, to a lesser extent, [3]uracil, but no  significant mediated transport of [3]adenosine or  [3]uridine was observed at pH 7.5  ( Fig. 5).	transcription
59993	1	335551	7	NULL	NULL	0	NULL	Oocytes	Cell		express					TbNBT1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_26_23502_s_119	12707261	Oocytes expressing  TbNBT1 rapidly accumulated  [3]adenine and, to a lesser extent, [3]uracil, but no  significant mediated transport of [3]adenosine or  [3]uridine was observed at pH 7.5  ( Fig. 5).	transcription
59994	2	335551	7	NULL	NULL	0	NULL	statement 1	Process		accumulate		rapidly			adenine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_26_23502_s_119	12707261	Oocytes expressing  TbNBT1 rapidly accumulated  [3]adenine and, to a lesser extent, [3]uracil, but no  significant mediated transport of [3]adenosine or  [3]uridine was observed at pH 7.5  ( Fig. 5).	transcription
59995	3	335551	7	NULL	NULL	0	NULL	statement 1	Process		accumulate					Uracil	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_26_23502_s_119	12707261	Oocytes expressing  TbNBT1 rapidly accumulated  [3]adenine and, to a lesser extent, [3]uracil, but no  significant mediated transport of [3]adenosine or  [3]uridine was observed at pH 7.5  ( Fig. 5).	transcription
59996	4	335551	7	NULL	NULL	0	NULL	statement 3	Process	accumulation of	is lesser than					statement 2	Process	accumulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_26_23502_s_119	12707261	Oocytes expressing  TbNBT1 rapidly accumulated  [3]adenine and, to a lesser extent, [3]uracil, but no  significant mediated transport of [3]adenosine or  [3]uridine was observed at pH 7.5  ( Fig. 5).	transcription
59997	5	335551	7	NULL	NULL	0	NULL	statement 1	Process		does not mediate					adenosine	Chemical	transport of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_26_23502_s_119	12707261	Oocytes expressing  TbNBT1 rapidly accumulated  [3]adenine and, to a lesser extent, [3]uracil, but no  significant mediated transport of [3]adenosine or  [3]uridine was observed at pH 7.5  ( Fig. 5).	transcription
59998	6	335551	7	NULL	NULL	0	NULL	statement 1	Process		does not mediate					uridine	Chemical	transport of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_26_23502_s_119	12707261	Oocytes expressing  TbNBT1 rapidly accumulated  [3]adenine and, to a lesser extent, [3]uracil, but no  significant mediated transport of [3]adenosine or  [3]uridine was observed at pH 7.5  ( Fig. 5).	transcription
55075	1	335552	5	NULL	NULL	0	NULL	mdr1a gene product			bind					adenine nucleotide					NULL	ZGM	0	NULL	NULL	NULL	gw60_jbiolchem_271_6_3300_s_156	8621734	As  summarized in the model in  Fig. 5, we propose that a  mdr1a  gene product in ZGM is an adenine nucleotide binding protein that  regulates both Cl   and K   conductances  in a coupled but inverse manner.	transcription
55076	2	335552	5	NULL	NULL	0	NULL	mdr1a gene product			regulates					Cl conductance					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_6_3300_s_156	8621734	As  summarized in the model in  Fig. 5, we propose that a  mdr1a  gene product in ZGM is an adenine nucleotide binding protein that  regulates both Cl   and K   conductances  in a coupled but inverse manner.	transcription
55077	3	335552	5	NULL	NULL	0	NULL	mdr1a gene product			regulates					K conductance					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_6_3300_s_156	8621734	As  summarized in the model in  Fig. 5, we propose that a  mdr1a  gene product in ZGM is an adenine nucleotide binding protein that  regulates both Cl   and K   conductances  in a coupled but inverse manner.	transcription
59999	1	335552	7	NULL	NULL	0	NULL	mdr1a gene	GP	product of	is a type of					adenine nucleotide binding protein					NULL	ZGM	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_6_3300_s_156	8621734	As  summarized in the model in  Fig. 5, we propose that a  mdr1a  gene product in ZGM is an adenine nucleotide binding protein that  regulates both Cl   and K   conductances  in a coupled but inverse manner.	transcription
60000	2	335552	7	NULL	NULL	0	NULL	mdr1a gene	GP	product of	regulates					Cl conductance	Process				NULL	ZGM	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_6_3300_s_156	8621734	As  summarized in the model in  Fig. 5, we propose that a  mdr1a  gene product in ZGM is an adenine nucleotide binding protein that  regulates both Cl   and K   conductances  in a coupled but inverse manner.	transcription
60001	3	335552	7	NULL	NULL	0	NULL	mdr1a gene	GP	product of	regulates					K conductance	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_6_3300_s_156	8621734	As  summarized in the model in  Fig. 5, we propose that a  mdr1a  gene product in ZGM is an adenine nucleotide binding protein that  regulates both Cl   and K   conductances  in a coupled but inverse manner.	transcription
60002	4	335552	7	NULL	NULL	0	NULL	statement 2	Process		coupled with					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_6_3300_s_156	8621734	As  summarized in the model in  Fig. 5, we propose that a  mdr1a  gene product in ZGM is an adenine nucleotide binding protein that  regulates both Cl   and K   conductances  in a coupled but inverse manner.	transcription
60003	5	335552	7	NULL	NULL	0	NULL	statement 2	Process		occur inversely to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_6_3300_s_156	8621734	As  summarized in the model in  Fig. 5, we propose that a  mdr1a  gene product in ZGM is an adenine nucleotide binding protein that  regulates both Cl   and K   conductances  in a coupled but inverse manner.	transcription
55078	1	335553	5	NULL	NULL	0	NULL	HAL2			encodes					3 (2 ),5 -bisphosphate nucleotidase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_12859_s_177	8662738	HAL2 encodes a 3 (2 ),5 -bisphosphate nucleotidase required for recycling of adenine nucleotides in sulfate transfer reactions, and its phosphatase activity was inhibited by Li+ and to a lesser extend by Na+ ions ( 59).	transcription
55079	2	335553	5	NULL	NULL	0	NULL	HAL2			recycles					adenine nucleotides					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_12859_s_177	8662738	HAL2 encodes a 3 (2 ),5 -bisphosphate nucleotidase required for recycling of adenine nucleotides in sulfate transfer reactions, and its phosphatase activity was inhibited by Li+ and to a lesser extend by Na+ ions ( 59).	transcription
55080	3	335553	5	NULL	NULL	0	NULL	statement 2			occurs in					sulfate transfer reactions					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_12859_s_177	8662738	HAL2 encodes a 3 (2 ),5 -bisphosphate nucleotidase required for recycling of adenine nucleotides in sulfate transfer reactions, and its phosphatase activity was inhibited by Li+ and to a lesser extend by Na+ ions ( 59).	transcription
55081	4	335553	5	NULL	NULL	0	NULL	Li+ ions			inhibit					HAL2		phosphatase activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_12859_s_177	8662738	HAL2 encodes a 3 (2 ),5 -bisphosphate nucleotidase required for recycling of adenine nucleotides in sulfate transfer reactions, and its phosphatase activity was inhibited by Li+ and to a lesser extend by Na+ ions ( 59).	transcription
55082	5	335553	5	NULL	NULL	0	NULL	Na+ ion			inhibit					HAL2		phosphatase activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_12859_s_177	8662738	HAL2 encodes a 3 (2 ),5 -bisphosphate nucleotidase required for recycling of adenine nucleotides in sulfate transfer reactions, and its phosphatase activity was inhibited by Li+ and to a lesser extend by Na+ ions ( 59).	transcription
55083	6	335553	5	NULL	NULL	0	NULL	statement 5			lesser extent than					statement 4					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_12859_s_177	8662738	HAL2 encodes a 3 (2 ),5 -bisphosphate nucleotidase required for recycling of adenine nucleotides in sulfate transfer reactions, and its phosphatase activity was inhibited by Li+ and to a lesser extend by Na+ ions ( 59).	transcription
60004	1	335553	7	NULL	NULL	0	NULL	HAL2	GP		encode					3 (2 ),5 -bisphosphate nucleotidase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_12859_s_177	8662738	HAL2 encodes a 3 (2 ),5 -bisphosphate nucleotidase required for recycling of adenine nucleotides in sulfate transfer reactions, and its phosphatase activity was inhibited by Li+ and to a lesser extend by Na+ ions ( 59).	transcription
60005	2	335553	7	NULL	NULL	0	NULL	3 (2 ),5 -bisphosphate nucleotidase	GP		required for					adenine nucleotides	NucleicAcid	recycling of			NULL	sulfate transfer reactions	0	NULL	NULL	NULL	gw60_jbiolchem_271_22_12859_s_177	8662738	HAL2 encodes a 3 (2 ),5 -bisphosphate nucleotidase required for recycling of adenine nucleotides in sulfate transfer reactions, and its phosphatase activity was inhibited by Li+ and to a lesser extend by Na+ ions ( 59).	transcription
60006	3	335553	7	NULL	NULL	0	NULL	Li+ 	Chemical		inhibit					 3 (2 ),5 -bisphosphate nucleotidase	GP	phosphatase activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_12859_s_177	8662738	HAL2 encodes a 3 (2 ),5 -bisphosphate nucleotidase required for recycling of adenine nucleotides in sulfate transfer reactions, and its phosphatase activity was inhibited by Li+ and to a lesser extend by Na+ ions ( 59).	transcription
60007	4	335553	7	NULL	NULL	0	NULL	Na+ ions	Chemical		inhibit					3 (2 ),5 -bisphosphate nucleotidase	Chemical	phosphatase activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_12859_s_177	8662738	HAL2 encodes a 3 (2 ),5 -bisphosphate nucleotidase required for recycling of adenine nucleotides in sulfate transfer reactions, and its phosphatase activity was inhibited by Li+ and to a lesser extend by Na+ ions ( 59).	transcription
60008	5	335553	7	NULL	NULL	0	NULL	statement 4	Process	inhibition of	is lesser than					statement 3	Process	inhibition of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_22_12859_s_177	8662738	HAL2 encodes a 3 (2 ),5 -bisphosphate nucleotidase required for recycling of adenine nucleotides in sulfate transfer reactions, and its phosphatase activity was inhibited by Li+ and to a lesser extend by Na+ ions ( 59).	transcription
55084	1	335554	5	NULL	NULL	0	NULL	adenine group			contains								nitrogen atoms ( N1, N3, N6, N7, and N9)		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3617_s_147	9920910	The adenine group contains five nitrogen atoms ( N1,  N3,  N6,  N7, and  N9) that can interact with receptor sites, whereas the ribose moiety contains three hydroxyl groups (2'', 3'', 5'') ( 8).	transcription
55085	2	335554	5	NULL	NULL	0	NULL	statement 1			interacts with								receptor sites		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3617_s_147	9920910	The adenine group contains five nitrogen atoms ( N1,  N3,  N6,  N7, and  N9) that can interact with receptor sites, whereas the ribose moiety contains three hydroxyl groups (2'', 3'', 5'') ( 8).	transcription
55086	3	335554	5	NULL	NULL	0	NULL	ribose moiety			contains					hydroxyl groups					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_6_3617_s_147	9920910	The adenine group contains five nitrogen atoms ( N1,  N3,  N6,  N7, and  N9) that can interact with receptor sites, whereas the ribose moiety contains three hydroxyl groups (2'', 3'', 5'') ( 8).	transcription
55087	1	335555	5	NULL	NULL	0	NULL	AC			is					adenylyl cyclase					NULL		0	NULL	NULL	NULL	gw60_science_294_5545_1299_s_149	11701921	The stimulation of adenylyl cyclase (AC) by heterotrimeric G proteins  is the classic example for an allosteric effector interaction mediating  the conversion of ATP to the second messenger cyclic adenine  3''-5''-monophosphate (cAMP).	transcription
55088	2	335555	5	NULL	NULL	0	NULL	adenylyl cyclase			is stimulated by					heterotrimeric G proteins					NULL		0	NULL	NULL	NULL	gw60_science_294_5545_1299_s_149	11701921	The stimulation of adenylyl cyclase (AC) by heterotrimeric G proteins  is the classic example for an allosteric effector interaction mediating  the conversion of ATP to the second messenger cyclic adenine  3''-5''-monophosphate (cAMP).	transcription
55089	3	335555	5	NULL	NULL	0	NULL	statement 2			is an example of					allosteric effector interaction					NULL		0	NULL	NULL	NULL	gw60_science_294_5545_1299_s_149	11701921	The stimulation of adenylyl cyclase (AC) by heterotrimeric G proteins  is the classic example for an allosteric effector interaction mediating  the conversion of ATP to the second messenger cyclic adenine  3''-5''-monophosphate (cAMP).	transcription
55090	4	335555	5	NULL	NULL	0	NULL	ATP			is converted to					cAMP					NULL		0	NULL	NULL	NULL	gw60_science_294_5545_1299_s_149	11701921	The stimulation of adenylyl cyclase (AC) by heterotrimeric G proteins  is the classic example for an allosteric effector interaction mediating  the conversion of ATP to the second messenger cyclic adenine  3''-5''-monophosphate (cAMP).	transcription
55091	5	335555	5	NULL	NULL	0	NULL	cAMP			is					cyclic adenine 3''-5''-monophosphate					NULL		0	NULL	NULL	NULL	gw60_science_294_5545_1299_s_149	11701921	The stimulation of adenylyl cyclase (AC) by heterotrimeric G proteins  is the classic example for an allosteric effector interaction mediating  the conversion of ATP to the second messenger cyclic adenine  3''-5''-monophosphate (cAMP).	transcription
55092	6	335555	5	NULL	NULL	0	NULL	cAMP			is a type of					second messenger					NULL		0	NULL	NULL	NULL	gw60_science_294_5545_1299_s_149	11701921	The stimulation of adenylyl cyclase (AC) by heterotrimeric G proteins  is the classic example for an allosteric effector interaction mediating  the conversion of ATP to the second messenger cyclic adenine  3''-5''-monophosphate (cAMP).	transcription
55093	7	335555	5	NULL	NULL	0	NULL	statement 2			mediates					statement 4					NULL		0	NULL	NULL	NULL	gw60_science_294_5545_1299_s_149	11701921	The stimulation of adenylyl cyclase (AC) by heterotrimeric G proteins  is the classic example for an allosteric effector interaction mediating  the conversion of ATP to the second messenger cyclic adenine  3''-5''-monophosphate (cAMP).	transcription
60009	1	335555	7	NULL	NULL	0	NULL	heterotrimeric G proteins	GP		stimulate					AC	GP				NULL		0	NULL	NULL	NULL	gw60_science_294_5545_1299_s_149	11701921	The stimulation of adenylyl cyclase (AC) by heterotrimeric G proteins  is the classic example for an allosteric effector interaction mediating  the conversion of ATP to the second messenger cyclic adenine  3''-5''-monophosphate (cAMP).	transcription
60010	2	335555	7	NULL	NULL	0	NULL	statement 1	Process		is an example of					allosteric effector interaction	Process				NULL		0	NULL	NULL	NULL	gw60_science_294_5545_1299_s_149	11701921	The stimulation of adenylyl cyclase (AC) by heterotrimeric G proteins  is the classic example for an allosteric effector interaction mediating  the conversion of ATP to the second messenger cyclic adenine  3''-5''-monophosphate (cAMP).	transcription
60011	3	335555	7	NULL	NULL	0	NULL	AC	GP		is					adenylyl cyclase	GP				NULL		0	NULL	NULL	NULL	gw60_science_294_5545_1299_s_149	11701921	The stimulation of adenylyl cyclase (AC) by heterotrimeric G proteins  is the classic example for an allosteric effector interaction mediating  the conversion of ATP to the second messenger cyclic adenine  3''-5''-monophosphate (cAMP).	transcription
60012	4	335555	7	NULL	NULL	0	NULL	ATP	Chemical		converted to					cAMP	Chemical				NULL		0	NULL	NULL	NULL	gw60_science_294_5545_1299_s_149	11701921	The stimulation of adenylyl cyclase (AC) by heterotrimeric G proteins  is the classic example for an allosteric effector interaction mediating  the conversion of ATP to the second messenger cyclic adenine  3''-5''-monophosphate (cAMP).	transcription
60013	5	335555	7	NULL	NULL	0	NULL	cAMP	Chemical		is					cyclic adenine 3''-5''-monophosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_science_294_5545_1299_s_149	11701921	The stimulation of adenylyl cyclase (AC) by heterotrimeric G proteins  is the classic example for an allosteric effector interaction mediating  the conversion of ATP to the second messenger cyclic adenine  3''-5''-monophosphate (cAMP).	transcription
60014	6	335555	7	NULL	NULL	0	NULL	statement 1	Process		mediates					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_science_294_5545_1299_s_149	11701921	The stimulation of adenylyl cyclase (AC) by heterotrimeric G proteins  is the classic example for an allosteric effector interaction mediating  the conversion of ATP to the second messenger cyclic adenine  3''-5''-monophosphate (cAMP).	transcription
55094	1	335556	5	NULL	NULL	0	NULL	oligos			conatins					adenine					NULL		0	NULL	NULL	NULL	gw60_structure_4_10_1171_s_103	8939742	Competition experiments and  Kd determinations also show that Zif268 binds oligos with adenine or cytosine at these positions about 5 to 10-fold more tightly than oligos containing guanine or thymine ( [13]  ; Bryan Wang and COP, unpublished data).	transcription
55095	2	335556	5	NULL	NULL	0	NULL	oligos			contains					cytosine					NULL		0	NULL	NULL	NULL	gw60_structure_4_10_1171_s_103	8939742	Competition experiments and  Kd determinations also show that Zif268 binds oligos with adenine or cytosine at these positions about 5 to 10-fold more tightly than oligos containing guanine or thymine ( [13]  ; Bryan Wang and COP, unpublished data).	transcription
55096	3	335556	5	NULL	NULL	0	NULL	oligos			contains					guanine					NULL		0	NULL	NULL	NULL	gw60_structure_4_10_1171_s_103	8939742	Competition experiments and  Kd determinations also show that Zif268 binds oligos with adenine or cytosine at these positions about 5 to 10-fold more tightly than oligos containing guanine or thymine ( [13]  ; Bryan Wang and COP, unpublished data).	transcription
55097	4	335556	5	NULL	NULL	0	NULL	oligos			contains					thymine					NULL		0	NULL	NULL	NULL	gw60_structure_4_10_1171_s_103	8939742	Competition experiments and  Kd determinations also show that Zif268 binds oligos with adenine or cytosine at these positions about 5 to 10-fold more tightly than oligos containing guanine or thymine ( [13]  ; Bryan Wang and COP, unpublished data).	transcription
55098	5	335556	5	NULL	NULL	0	NULL	Zif268			bind					statement 1					NULL		0	NULL	NULL	NULL	gw60_structure_4_10_1171_s_103	8939742	Competition experiments and  Kd determinations also show that Zif268 binds oligos with adenine or cytosine at these positions about 5 to 10-fold more tightly than oligos containing guanine or thymine ( [13]  ; Bryan Wang and COP, unpublished data).	transcription
55099	6	335556	5	NULL	NULL	0	NULL	Zif268			bind					statement 2					NULL		0	NULL	NULL	NULL	gw60_structure_4_10_1171_s_103	8939742	Competition experiments and  Kd determinations also show that Zif268 binds oligos with adenine or cytosine at these positions about 5 to 10-fold more tightly than oligos containing guanine or thymine ( [13]  ; Bryan Wang and COP, unpublished data).	transcription
55100	7	335556	5	NULL	NULL	0	NULL	Zif268			bind					statement 3					NULL		0	NULL	NULL	NULL	gw60_structure_4_10_1171_s_103	8939742	Competition experiments and  Kd determinations also show that Zif268 binds oligos with adenine or cytosine at these positions about 5 to 10-fold more tightly than oligos containing guanine or thymine ( [13]  ; Bryan Wang and COP, unpublished data).	transcription
55101	8	335556	5	NULL	NULL	0	NULL	Zif268			bind					statement 4					NULL		0	NULL	NULL	NULL	gw60_structure_4_10_1171_s_103	8939742	Competition experiments and  Kd determinations also show that Zif268 binds oligos with adenine or cytosine at these positions about 5 to 10-fold more tightly than oligos containing guanine or thymine ( [13]  ; Bryan Wang and COP, unpublished data).	transcription
55102	9	335556	5	NULL	NULL	0	NULL	statement 5			is an alternative to					statement 6					NULL		0	NULL	NULL	NULL	gw60_structure_4_10_1171_s_103	8939742	Competition experiments and  Kd determinations also show that Zif268 binds oligos with adenine or cytosine at these positions about 5 to 10-fold more tightly than oligos containing guanine or thymine ( [13]  ; Bryan Wang and COP, unpublished data).	transcription
55103	10	335556	5	NULL	NULL	0	NULL	statement 7			is an alternative to					statement 8					NULL		0	NULL	NULL	NULL	gw60_structure_4_10_1171_s_103	8939742	Competition experiments and  Kd determinations also show that Zif268 binds oligos with adenine or cytosine at these positions about 5 to 10-fold more tightly than oligos containing guanine or thymine ( [13]  ; Bryan Wang and COP, unpublished data).	transcription
55104	11	335556	5	NULL	NULL	0	NULL	statement 9			more tightly than					statement 10					NULL		0	NULL	NULL	NULL	gw60_structure_4_10_1171_s_103	8939742	Competition experiments and  Kd determinations also show that Zif268 binds oligos with adenine or cytosine at these positions about 5 to 10-fold more tightly than oligos containing guanine or thymine ( [13]  ; Bryan Wang and COP, unpublished data).	transcription
60015	1	335556	7	NULL	NULL	0	NULL	Zif268	Chemical		bind					adenine oligos	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_structure_4_10_1171_s_103	8939742	Competition experiments and  Kd determinations also show that Zif268 binds oligos with adenine or cytosine at these positions about 5 to 10-fold more tightly than oligos containing guanine or thymine ( [13]  ; Bryan Wang and COP, unpublished data).	transcription
60016	2	335556	7	NULL	NULL	0	NULL	Zif268	Chemical		bind					cytosine oligos	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_structure_4_10_1171_s_103	8939742	Competition experiments and  Kd determinations also show that Zif268 binds oligos with adenine or cytosine at these positions about 5 to 10-fold more tightly than oligos containing guanine or thymine ( [13]  ; Bryan Wang and COP, unpublished data).	transcription
60017	3	335556	7	NULL	NULL	0	NULL	Zif268	Chemical		bind					guanine oligos	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_structure_4_10_1171_s_103	8939742	Competition experiments and  Kd determinations also show that Zif268 binds oligos with adenine or cytosine at these positions about 5 to 10-fold more tightly than oligos containing guanine or thymine ( [13]  ; Bryan Wang and COP, unpublished data).	transcription
60018	4	335556	7	NULL	NULL	0	NULL	Zif268	Chemical		bind					thymine oligos	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_structure_4_10_1171_s_103	8939742	Competition experiments and  Kd determinations also show that Zif268 binds oligos with adenine or cytosine at these positions about 5 to 10-fold more tightly than oligos containing guanine or thymine ( [13]  ; Bryan Wang and COP, unpublished data).	transcription
60019	5	335556	7	NULL	NULL	0	NULL	statement 1	Process	binding of	is stronger than					statement 3	Process	binding of			NULL		0	NULL	NULL	NULL	gw60_structure_4_10_1171_s_103	8939742	Competition experiments and  Kd determinations also show that Zif268 binds oligos with adenine or cytosine at these positions about 5 to 10-fold more tightly than oligos containing guanine or thymine ( [13]  ; Bryan Wang and COP, unpublished data).	transcription
60020	6	335556	7	NULL	NULL	0	NULL	statement 1	Process	binding of	is stronger than					statement 4	Process	binding of			NULL		0	NULL	NULL	NULL	gw60_structure_4_10_1171_s_103	8939742	Competition experiments and  Kd determinations also show that Zif268 binds oligos with adenine or cytosine at these positions about 5 to 10-fold more tightly than oligos containing guanine or thymine ( [13]  ; Bryan Wang and COP, unpublished data).	transcription
60021	7	335556	7	NULL	NULL	0	NULL	statement 2	Process	binding of	is stronger than					statement 3	Process	binding of			NULL		0	NULL	NULL	NULL	gw60_structure_4_10_1171_s_103	8939742	Competition experiments and  Kd determinations also show that Zif268 binds oligos with adenine or cytosine at these positions about 5 to 10-fold more tightly than oligos containing guanine or thymine ( [13]  ; Bryan Wang and COP, unpublished data).	transcription
60022	8	335556	7	NULL	NULL	0	NULL	statement 2	Process	binding of	is stronger than					statement 4	Process	binding of			NULL		0	NULL	NULL	NULL	gw60_structure_4_10_1171_s_103	8939742	Competition experiments and  Kd determinations also show that Zif268 binds oligos with adenine or cytosine at these positions about 5 to 10-fold more tightly than oligos containing guanine or thymine ( [13]  ; Bryan Wang and COP, unpublished data).	transcription
55105	1	335557	5	NULL	NULL	0	NULL	cytochrome c		released	work together with					Apaf-1					NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_173	9689121	The released cytochrome  c could work together with Apaf-1, caspase-9, and increasing concentrations of adenine deoxynuclesoside 5''-triphosphates to start a feed forward amplification cascade of caspase activation.	transcription
55106	2	335557	5	NULL	NULL	0	NULL	cytochrome c		released	work together with					caspase-9					NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_173	9689121	The released cytochrome  c could work together with Apaf-1, caspase-9, and increasing concentrations of adenine deoxynuclesoside 5''-triphosphates to start a feed forward amplification cascade of caspase activation.	transcription
55107	3	335557	5	NULL	NULL	0	NULL	cytochrome c		released	work together with					adenine deoxynuclesoside 5''-triphosphates		increasing concentrations of			NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_173	9689121	The released cytochrome  c could work together with Apaf-1, caspase-9, and increasing concentrations of adenine deoxynuclesoside 5''-triphosphates to start a feed forward amplification cascade of caspase activation.	transcription
55108	4	335557	5	NULL	NULL	0	NULL	statement 1			occurs along with					statement 2					NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_173	9689121	The released cytochrome  c could work together with Apaf-1, caspase-9, and increasing concentrations of adenine deoxynuclesoside 5''-triphosphates to start a feed forward amplification cascade of caspase activation.	transcription
55109	5	335557	5	NULL	NULL	0	NULL	statement 2			occurs along with					statement 3					NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_173	9689121	The released cytochrome  c could work together with Apaf-1, caspase-9, and increasing concentrations of adenine deoxynuclesoside 5''-triphosphates to start a feed forward amplification cascade of caspase activation.	transcription
55110	6	335557	5	NULL	NULL	0	NULL	statement 4			starts					caspase		feed forward amplification cascade of;;activation of			NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_173	9689121	The released cytochrome  c could work together with Apaf-1, caspase-9, and increasing concentrations of adenine deoxynuclesoside 5''-triphosphates to start a feed forward amplification cascade of caspase activation.	transcription
55111	7	335557	5	NULL	NULL	0	NULL	statement 5			starts					caspase		feed forward amplification cascade of;;activation of			NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_173	9689121	The released cytochrome  c could work together with Apaf-1, caspase-9, and increasing concentrations of adenine deoxynuclesoside 5''-triphosphates to start a feed forward amplification cascade of caspase activation.	transcription
60023	1	335557	7	NULL	NULL	0	NULL	cytochrome c	GP		start					caspase activation	Process	feed forward amplification cascade of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_173	9689121	The released cytochrome  c could work together with Apaf-1, caspase-9, and increasing concentrations of adenine deoxynuclesoside 5''-triphosphates to start a feed forward amplification cascade of caspase activation.	transcription
60024	2	335557	7	NULL	NULL	0	NULL	statement 1	Process		work along with					Apaf-1	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_173	9689121	The released cytochrome  c could work together with Apaf-1, caspase-9, and increasing concentrations of adenine deoxynuclesoside 5''-triphosphates to start a feed forward amplification cascade of caspase activation.	transcription
60025	3	335557	7	NULL	NULL	0	NULL	statement 1	Process		work along with					caspase-9	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_173	9689121	The released cytochrome  c could work together with Apaf-1, caspase-9, and increasing concentrations of adenine deoxynuclesoside 5''-triphosphates to start a feed forward amplification cascade of caspase activation.	transcription
60026	4	335557	7	NULL	NULL	0	NULL	statement 1	Process		work along with					adenine deoxynuclesoside 5''-triphosphates	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_173	9689121	The released cytochrome  c could work together with Apaf-1, caspase-9, and increasing concentrations of adenine deoxynuclesoside 5''-triphosphates to start a feed forward amplification cascade of caspase activation.	transcription
55112	1	335558	5	NULL	NULL	0	NULL	Apaf-1			bind					caspase-9					NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
55113	2	335558	5	NULL	NULL	0	NULL	Apaf-1			bind					caspase-3					NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
55114	3	335558	5	NULL	NULL	0	NULL	statement 1			in the presence of					adenine deoxynucleoside 5''-triphosphates		high concentrations of			NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
55115	4	335558	5	NULL	NULL	0	NULL	statement 2			in the presence of					adenine deoxynucleoside 5''-triphosphates		high concentrations of			NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
55116	5	335558	5	NULL	NULL	0	NULL	statement 1			in the presence of					cytochrome c		small amounts of;;released			NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
55117	6	335558	5	NULL	NULL	0	NULL	statement 2			in the presence of					cytochrome c		small amounts of;;released			NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
55118	7	335558	5	NULL	NULL	0	NULL	caspase-3			undergoes					cleavage					NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
55119	8	335558	5	NULL	NULL	0	NULL	statement 7			is converted to					protease		active;;autocatalytic			NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
55120	9	335558	5	NULL	NULL	0	NULL	statement 8			is analogous to					blood		clotting of			NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
55121	10	335558	5	NULL	NULL	0	NULL	statement 3			leads to					statement 7					NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
55122	11	335558	5	NULL	NULL	0	NULL	statement 4			leads to					statement 7					NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
55123	12	335558	5	NULL	NULL	0	NULL	statement 5			leads to					statement 7					NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
55124	13	335558	5	NULL	NULL	0	NULL	statement 6			leads to					statement 7					NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
60027	1	335558	7	NULL	NULL	0	NULL	Apaf-1	GP		bind					caspase-9	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
60028	2	335558	7	NULL	NULL	0	NULL	 Apaf-1	GP		bind					caspase-3	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
60029	3	335558	7	NULL	NULL	0	NULL	statement 1	Process		in the presence of					adenine deoxynucleoside 5''-triphosphates	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
60030	4	335558	7	NULL	NULL	0	NULL	statement 2	Process		in the presence of					adenine deoxynucleoside 5''-triphosphates	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
60031	5	335558	7	NULL	NULL	0	NULL	 cytochrome c	GP		leads to					caspase-3	GP	cleavage of			NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
60032	6	335558	7	NULL	NULL	0	NULL	statement 5	Process		converts it to					autocatalytic protease	GP	active			NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
60033	7	335558	7	NULL	NULL	0	NULL	statement 6	Process		is analogous to					blood clotting	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_16_9567_s_178	9689121	However, the binding of Apaf-1 to caspase-9, and caspase-3, in the presence of high concentrations of adenine deoxynucleoside 5''-triphosphates and small amounts of released cytochrome  c, leads to the cleavage of caspase-3, converting it to an active autocatalytic protease, in a process analogous to blood clotting.	transcription
60034	1	335559	7	NULL	NULL	0	NULL	adenine 7	Chemical		modified to					purine	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9244_s_179	9689065	Modification of adenine  7 to a purine or hypoxanthine only slightly affects protein binding ( 2), and even the Tyr85His protein binds with similar affinity, provided that the histidine ring is protonated to make the hydrogen bond with phosphate  5 ( 18).	transcription
60035	2	335559	7	NULL	NULL	0	NULL	adenine 7 	Chemical		modified to					hypoxanthine	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9244_s_179	9689065	Modification of adenine  7 to a purine or hypoxanthine only slightly affects protein binding ( 2), and even the Tyr85His protein binds with similar affinity, provided that the histidine ring is protonated to make the hydrogen bond with phosphate  5 ( 18).	transcription
60036	3	335559	7	NULL	NULL	0	NULL	statement 1	Process		affects		slightly			protein	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_16_9244_s_179	9689065	Modification of adenine  7 to a purine or hypoxanthine only slightly affects protein binding ( 2), and even the Tyr85His protein binds with similar affinity, provided that the histidine ring is protonated to make the hydrogen bond with phosphate  5 ( 18).	transcription
60037	4	335559	7	NULL	NULL	0	NULL	statement 2	Process		affects		slightly			protein	GP	binding of			NULL		0	NULL	NULL	NULL	gw60_pnas_95_16_9244_s_179	9689065	Modification of adenine  7 to a purine or hypoxanthine only slightly affects protein binding ( 2), and even the Tyr85His protein binds with similar affinity, provided that the histidine ring is protonated to make the hydrogen bond with phosphate  5 ( 18).	transcription
55127	1	335560	5	NULL	NULL	0	NULL	TSA			is an inhibitor of					HDAC					NULL		0	NULL	NULL	NULL	gw60_pnas_97_25_13708_s_25	11095743	Of these, Rpd3p and Hda1p are sensitive to the HDAC inhibitor TSA. Hos3p and Sir2p are TSA-insensitive, Sir2p is activated by nicotinamide adenine dinucleotide (NAD), and little is known about Hos1p and Hos2p ( 5,  6).	transcription
55128	2	335560	5	NULL	NULL	0	NULL	Rpd3p			is sensitive to					TSA					NULL		0	NULL	NULL	NULL	gw60_pnas_97_25_13708_s_25	11095743	Of these, Rpd3p and Hda1p are sensitive to the HDAC inhibitor TSA. Hos3p and Sir2p are TSA-insensitive, Sir2p is activated by nicotinamide adenine dinucleotide (NAD), and little is known about Hos1p and Hos2p ( 5,  6).	transcription
55129	3	335560	5	NULL	NULL	0	NULL	Hda1p			is sensitive to					TSA					NULL		0	NULL	NULL	NULL	gw60_pnas_97_25_13708_s_25	11095743	Of these, Rpd3p and Hda1p are sensitive to the HDAC inhibitor TSA. Hos3p and Sir2p are TSA-insensitive, Sir2p is activated by nicotinamide adenine dinucleotide (NAD), and little is known about Hos1p and Hos2p ( 5,  6).	transcription
55130	4	335560	5	NULL	NULL	0	NULL	Hos3p			is insensitive to					TSA					NULL		0	NULL	NULL	NULL	gw60_pnas_97_25_13708_s_25	11095743	Of these, Rpd3p and Hda1p are sensitive to the HDAC inhibitor TSA. Hos3p and Sir2p are TSA-insensitive, Sir2p is activated by nicotinamide adenine dinucleotide (NAD), and little is known about Hos1p and Hos2p ( 5,  6).	transcription
55131	5	335560	5	NULL	NULL	0	NULL	Sir2p			is insensitive to					TSA					NULL		0	NULL	NULL	NULL	gw60_pnas_97_25_13708_s_25	11095743	Of these, Rpd3p and Hda1p are sensitive to the HDAC inhibitor TSA. Hos3p and Sir2p are TSA-insensitive, Sir2p is activated by nicotinamide adenine dinucleotide (NAD), and little is known about Hos1p and Hos2p ( 5,  6).	transcription
55132	6	335560	5	NULL	NULL	0	NULL	Sir2p			is activated by					NAD					NULL		0	NULL	NULL	NULL	gw60_pnas_97_25_13708_s_25	11095743	Of these, Rpd3p and Hda1p are sensitive to the HDAC inhibitor TSA. Hos3p and Sir2p are TSA-insensitive, Sir2p is activated by nicotinamide adenine dinucleotide (NAD), and little is known about Hos1p and Hos2p ( 5,  6).	transcription
55133	7	335560	5	NULL	NULL	0	NULL	NAD			is					nicotinamide adenine dinucleotide					NULL		0	NULL	NULL	NULL	gw60_pnas_97_25_13708_s_25	11095743	Of these, Rpd3p and Hda1p are sensitive to the HDAC inhibitor TSA. Hos3p and Sir2p are TSA-insensitive, Sir2p is activated by nicotinamide adenine dinucleotide (NAD), and little is known about Hos1p and Hos2p ( 5,  6).	transcription
60038	1	335560	7	NULL	NULL	0	NULL	Rpd3p	GP		is sensitive to					TSA	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_97_25_13708_s_25	11095743	Of these, Rpd3p and Hda1p are sensitive to the HDAC inhibitor TSA. Hos3p and Sir2p are TSA-insensitive, Sir2p is activated by nicotinamide adenine dinucleotide (NAD), and little is known about Hos1p and Hos2p ( 5,  6).	transcription
60039	2	335560	7	NULL	NULL	0	NULL	Hda1p	GP		is sensitive to					TSA	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_97_25_13708_s_25	11095743	Of these, Rpd3p and Hda1p are sensitive to the HDAC inhibitor TSA. Hos3p and Sir2p are TSA-insensitive, Sir2p is activated by nicotinamide adenine dinucleotide (NAD), and little is known about Hos1p and Hos2p ( 5,  6).	transcription
60040	3	335560	7	NULL	NULL	0	NULL	TSA	Chemical		is a type of					HDAC inhibitor	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_97_25_13708_s_25	11095743	Of these, Rpd3p and Hda1p are sensitive to the HDAC inhibitor TSA. Hos3p and Sir2p are TSA-insensitive, Sir2p is activated by nicotinamide adenine dinucleotide (NAD), and little is known about Hos1p and Hos2p ( 5,  6).	transcription
60041	4	335560	7	NULL	NULL	0	NULL	Hos3p	GP		is insensitive to					TSA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_25_13708_s_25	11095743	Of these, Rpd3p and Hda1p are sensitive to the HDAC inhibitor TSA. Hos3p and Sir2p are TSA-insensitive, Sir2p is activated by nicotinamide adenine dinucleotide (NAD), and little is known about Hos1p and Hos2p ( 5,  6).	transcription
60042	5	335560	7	NULL	NULL	0	NULL	Sir2p	GP		is insensitive to					TSA	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_25_13708_s_25	11095743	Of these, Rpd3p and Hda1p are sensitive to the HDAC inhibitor TSA. Hos3p and Sir2p are TSA-insensitive, Sir2p is activated by nicotinamide adenine dinucleotide (NAD), and little is known about Hos1p and Hos2p ( 5,  6).	transcription
60043	6	335560	7	NULL	NULL	0	NULL	NAD	Chemical		activates					Sir2p	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_25_13708_s_25	11095743	Of these, Rpd3p and Hda1p are sensitive to the HDAC inhibitor TSA. Hos3p and Sir2p are TSA-insensitive, Sir2p is activated by nicotinamide adenine dinucleotide (NAD), and little is known about Hos1p and Hos2p ( 5,  6).	transcription
60044	7	335560	7	NULL	NULL	0	NULL	NAD	Chemical		is					nicotinamide adenine dinucleotide	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_97_25_13708_s_25	11095743	Of these, Rpd3p and Hda1p are sensitive to the HDAC inhibitor TSA. Hos3p and Sir2p are TSA-insensitive, Sir2p is activated by nicotinamide adenine dinucleotide (NAD), and little is known about Hos1p and Hos2p ( 5,  6).	transcription
55134	1	335561	5	NULL	NULL	0	NULL	guanosine			incorporated into					nucleic acids					NULL		0	NULL	NULL	NULL	gw60_pnas_98_8_4593_s_171	11287638	Imm-H suppressed only the incorporation of guanosine into nucleic acids (Fig.  5) with no effect on adenine and guanine phosphoribosyltransferases, dCK, adenosine kinase, or the enzymes of RNA and DNA synthesis, consistent with selective inhibition of PNP.	transcription
55135	2	335561	5	NULL	NULL	0	NULL	Imm-H			suppress					statement 1					NULL		0	NULL	NULL	NULL	gw60_pnas_98_8_4593_s_171	11287638	Imm-H suppressed only the incorporation of guanosine into nucleic acids (Fig.  5) with no effect on adenine and guanine phosphoribosyltransferases, dCK, adenosine kinase, or the enzymes of RNA and DNA synthesis, consistent with selective inhibition of PNP.	transcription
55140	3	335561	5	NULL	NULL	0	NULL	statement 2			does not effect					adenine phosphoribosyltransferases					NULL		0	NULL	NULL	NULL	gw60_pnas_98_8_4593_s_171	11287638	Imm-H suppressed only the incorporation of guanosine into nucleic acids (Fig.  5) with no effect on adenine and guanine phosphoribosyltransferases, dCK, adenosine kinase, or the enzymes of RNA and DNA synthesis, consistent with selective inhibition of PNP.	transcription
55141	4	335561	5	NULL	NULL	0	NULL	statement 2			does not effect					guanine phosphoribosyltransferases					NULL		0	NULL	NULL	NULL	gw60_pnas_98_8_4593_s_171	11287638	Imm-H suppressed only the incorporation of guanosine into nucleic acids (Fig.  5) with no effect on adenine and guanine phosphoribosyltransferases, dCK, adenosine kinase, or the enzymes of RNA and DNA synthesis, consistent with selective inhibition of PNP.	transcription
55142	5	335561	5	NULL	NULL	0	NULL	statement 2			does not effect					dCK					NULL		0	NULL	NULL	NULL	gw60_pnas_98_8_4593_s_171	11287638	Imm-H suppressed only the incorporation of guanosine into nucleic acids (Fig.  5) with no effect on adenine and guanine phosphoribosyltransferases, dCK, adenosine kinase, or the enzymes of RNA and DNA synthesis, consistent with selective inhibition of PNP.	transcription
55143	6	335561	5	NULL	NULL	0	NULL	statement 2			does not effect					adenosine kinase					NULL		0	NULL	NULL	NULL	gw60_pnas_98_8_4593_s_171	11287638	Imm-H suppressed only the incorporation of guanosine into nucleic acids (Fig.  5) with no effect on adenine and guanine phosphoribosyltransferases, dCK, adenosine kinase, or the enzymes of RNA and DNA synthesis, consistent with selective inhibition of PNP.	transcription
55144	7	335561	5	NULL	NULL	0	NULL	statement 2			does not effect					enzymes of RNA synthesis					NULL		0	NULL	NULL	NULL	gw60_pnas_98_8_4593_s_171	11287638	Imm-H suppressed only the incorporation of guanosine into nucleic acids (Fig.  5) with no effect on adenine and guanine phosphoribosyltransferases, dCK, adenosine kinase, or the enzymes of RNA and DNA synthesis, consistent with selective inhibition of PNP.	transcription
55145	8	335561	5	NULL	NULL	0	NULL	statement 2			does not effect					enzymes of DNA synthesis					NULL		0	NULL	NULL	NULL	gw60_pnas_98_8_4593_s_171	11287638	Imm-H suppressed only the incorporation of guanosine into nucleic acids (Fig.  5) with no effect on adenine and guanine phosphoribosyltransferases, dCK, adenosine kinase, or the enzymes of RNA and DNA synthesis, consistent with selective inhibition of PNP.	transcription
55146	9	335561	5	NULL	NULL	0	NULL	statement 2			inhibits		selectively			PNP					NULL		0	NULL	NULL	NULL	gw60_pnas_98_8_4593_s_171	11287638	Imm-H suppressed only the incorporation of guanosine into nucleic acids (Fig.  5) with no effect on adenine and guanine phosphoribosyltransferases, dCK, adenosine kinase, or the enzymes of RNA and DNA synthesis, consistent with selective inhibition of PNP.	transcription
60078	1	335561	7	NULL	NULL	0	NULL	guanosine	NucleicAcid		incorporated into					nucleic acids	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_pnas_98_8_4593_s_171	11287638	Imm-H suppressed only the incorporation of guanosine into nucleic acids (Fig.  5) with no effect on adenine and guanine phosphoribosyltransferases, dCK, adenosine kinase, or the enzymes of RNA and DNA synthesis, consistent with selective inhibition of PNP.	transcription
60079	2	335561	7	NULL	NULL	0	NULL	Imm-H	Chemical		suppress					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_98_8_4593_s_171	11287638	Imm-H suppressed only the incorporation of guanosine into nucleic acids (Fig.  5) with no effect on adenine and guanine phosphoribosyltransferases, dCK, adenosine kinase, or the enzymes of RNA and DNA synthesis, consistent with selective inhibition of PNP.	transcription
60080	3	335561	7	NULL	NULL	0	NULL	statement 2	Process		does not effect					adenine  phosphoribosyltransferase	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_98_8_4593_s_171	11287638	Imm-H suppressed only the incorporation of guanosine into nucleic acids (Fig.  5) with no effect on adenine and guanine phosphoribosyltransferases, dCK, adenosine kinase, or the enzymes of RNA and DNA synthesis, consistent with selective inhibition of PNP.	transcription
60081	4	335561	7	NULL	NULL	0	NULL	statement 2	Process		does not effect					guanine phosphoribosyltransferase	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_98_8_4593_s_171	11287638	Imm-H suppressed only the incorporation of guanosine into nucleic acids (Fig.  5) with no effect on adenine and guanine phosphoribosyltransferases, dCK, adenosine kinase, or the enzymes of RNA and DNA synthesis, consistent with selective inhibition of PNP.	transcription
60082	5	335561	7	NULL	NULL	0	NULL	statement 2	Process		does not effect					dCK	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_98_8_4593_s_171	11287638	Imm-H suppressed only the incorporation of guanosine into nucleic acids (Fig.  5) with no effect on adenine and guanine phosphoribosyltransferases, dCK, adenosine kinase, or the enzymes of RNA and DNA synthesis, consistent with selective inhibition of PNP.	transcription
60083	6	335561	7	NULL	NULL	0	NULL	statement 2	Process		does not effect					adenosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_98_8_4593_s_171	11287638	Imm-H suppressed only the incorporation of guanosine into nucleic acids (Fig.  5) with no effect on adenine and guanine phosphoribosyltransferases, dCK, adenosine kinase, or the enzymes of RNA and DNA synthesis, consistent with selective inhibition of PNP.	transcription
55147	1	335562	5	NULL	NULL	0	NULL	CtrA			controls		directly			ccrM gene		expression of			NULL	late in the cell cycle	NULL	NULL	NULL	NULL	gw60_pnas_99_7_4632_s_205	11930012	Consistent with previous results ( 5,  8), we found that CtrA directly controls expression of the essential gene  ccrM, encoding an adenine DNA methyltransferase, late in the cell cycle.	transcription
55148	2	335562	5	NULL	NULL	0	NULL	ccrM gene			encodes					adenine DNA methyltransferase					NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_7_4632_s_205	11930012	Consistent with previous results ( 5,  8), we found that CtrA directly controls expression of the essential gene  ccrM, encoding an adenine DNA methyltransferase, late in the cell cycle.	transcription
60084	1	335562	7	NULL	NULL	0	NULL	CtrA	GP		controls expression of		directly			ccrM gene	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_99_7_4632_s_205	11930012	Consistent with previous results ( 5,  8), we found that CtrA directly controls expression of the essential gene  ccrM, encoding an adenine DNA methyltransferase, late in the cell cycle.	transcription
60085	2	335562	7	NULL	NULL	0	NULL	ccrM gene	GP		encode					adenine DNA methyltransferase	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_99_7_4632_s_205	11930012	Consistent with previous results ( 5,  8), we found that CtrA directly controls expression of the essential gene  ccrM, encoding an adenine DNA methyltransferase, late in the cell cycle.	transcription
60086	3	335562	7	NULL	NULL	0	NULL	statement 2	Process		occur during					late cell cycle	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_99_7_4632_s_205	11930012	Consistent with previous results ( 5,  8), we found that CtrA directly controls expression of the essential gene  ccrM, encoding an adenine DNA methyltransferase, late in the cell cycle.	transcription
55154	1	335563	5	NULL	NULL	0	NULL	erythro-9-(2-hydroxy-3-nonyl-)-adenine			block					adenosine deaminase					NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
55155	2	335563	5	NULL	NULL	0	NULL	statement 1			increases					adenosine		interstitial			NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
55156	3	335563	5	NULL	NULL	0	NULL	statement 2			unrelated to					hypoxia					NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
55157	4	335563	5	NULL	NULL	0	NULL	statement 2			unrelated to					diameter					NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
55158	5	335563	5	NULL	NULL	0	NULL	statement 3			is an alternative to					statement 4					NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
55159	6	335563	5	NULL	NULL	0	NULL	iodotubericidine			block					adenosine kinase					NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
55160	7	335563	5	NULL	NULL	0	NULL	statement 6			increases					adenosine		interstitial			NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
55161	8	335563	5	NULL	NULL	0	NULL	statement 7			unrelated to					hypoxia					NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
55162	9	335563	5	NULL	NULL	0	NULL	statement 7			unrelated to					diameter					NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
55163	10	335563	5	NULL	NULL	0	NULL	statement 8			is an alternative to					statement 9					NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
55164	11	335563	5	NULL	NULL	0	NULL	n-nitrobenzylthioinosine			block					adenosine transport					NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
55165	12	335563	5	NULL	NULL	0	NULL	statement 11			increases					adenosine		interstitial			NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
55166	13	335563	5	NULL	NULL	0	NULL	statement 12			unrelated to					hypoxia					NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
55167	14	335563	5	NULL	NULL	0	NULL	statement 12			unrelated to					diameter					NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
55168	15	335563	5	NULL	NULL	0	NULL	statement 13			is an alternative to					statement 14					NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
60087	1	335563	7	NULL	NULL	0	NULL	erythro-9-(2-hydroxy-3-nonyl-)-adenine	Chemical		blocks					adenosine deaminase	GP				NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
60088	2	335563	7	NULL	NULL	0	NULL	iodotubericidine	Chemical		blocks					adenosine kinase	GP				NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
60089	3	335563	7	NULL	NULL	0	NULL	 n-nitrobenzylthioinosine	Chemical		blocks					adenosine 	Process	transport of			NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
60090	4	335563	7	NULL	NULL	0	NULL	statement 1	Process		increase					 adenosine	NucleicAcid	interstitial			NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
60152	5	335563	7	NULL	NULL	0	NULL	statement 2	Process		increase					adenosine	NucleicAcid	interstitial			NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
60153	6	335563	7	NULL	NULL	0	NULL	statement 3	Process		increase					adenosine	NucleicAcid	interstitial			NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
60154	7	335563	7	NULL	NULL	0	NULL	statement 4	Process		is unrelated to					hypoxia	Process				NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
60155	8	335563	7	NULL	NULL	0	NULL	statement 5	Process		is unrelated to					hypoxia	Process				NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
60156	9	335563	7	NULL	NULL	0	NULL	statement 6	Process		is unrelated to					hypoxia	Process				NULL		0	NULL	NULL	NULL	abs-batch0580-0599_j-physiol_570_pt-2_16284071_s_9	16284071	Blockade of adenosine deaminase (with erythro-9-(2-hydroxy-3-nonyl-)-adenine,  5 microM), adenosine kinase (with iodotubericidine, 10 microM) and adenosine  transport (with n-nitrobenzylthioinosine, 1 microM) increased interstitial  adenosine but the increase was unrelated to hypoxia or diameter.	transcription
55220	1	335564	5	NULL	NULL	0	NULL	RNase L			undergoes		effectively			dimerization					NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-(tokyo)_132_4_12359081_s_8	12359081	The results  suggest that 2-5A molecules modified at the 8-position of the third (from  the 5' terminus) adenine ring cause effective dimerization of RNase L  and thus increase the ability of RNase L activation.	transcription
55221	2	335564	5	NULL	NULL	0	NULL	2-5A molecules			is modified at								adenine ring		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-(tokyo)_132_4_12359081_s_8	12359081	The results  suggest that 2-5A molecules modified at the 8-position of the third (from  the 5' terminus) adenine ring cause effective dimerization of RNase L  and thus increase the ability of RNase L activation.	transcription
55222	3	335564	5	NULL	NULL	0	NULL	statement 2			results in					statement 1					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-(tokyo)_132_4_12359081_s_8	12359081	The results  suggest that 2-5A molecules modified at the 8-position of the third (from  the 5' terminus) adenine ring cause effective dimerization of RNase L  and thus increase the ability of RNase L activation.	transcription
55223	4	335564	5	NULL	NULL	0	NULL	statement 1			increases					RNase L		activation of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-(tokyo)_132_4_12359081_s_8	12359081	The results  suggest that 2-5A molecules modified at the 8-position of the third (from  the 5' terminus) adenine ring cause effective dimerization of RNase L  and thus increase the ability of RNase L activation.	transcription
60157	1	335564	7	NULL	NULL	0	NULL				cause				2-5A molecules modified at the 8-position of the third adenine ring	RNase L	GP	effective dimerization of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-(tokyo)_132_4_12359081_s_8	12359081	The results  suggest that 2-5A molecules modified at the 8-position of the third (from  the 5' terminus) adenine ring cause effective dimerization of RNase L  and thus increase the ability of RNase L activation.	transcription
60158	2	335564	7	NULL	NULL	0	NULL	statement 1	Process		increase					RNase L	GP	activation of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-(tokyo)_132_4_12359081_s_8	12359081	The results  suggest that 2-5A molecules modified at the 8-position of the third (from  the 5' terminus) adenine ring cause effective dimerization of RNase L  and thus increase the ability of RNase L activation.	transcription
55224	1	335565	5	NULL	NULL	0	NULL	5 -AMP			bind					phosphorylase		liver			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_44_27569_s_200	8910343	The delta H b on 5 -AMP binding to liver phosphorylase  a is not so negative as when 5 -AMP binds to muscle isozyme ( 24), and the absence of some hydrogen bonds between the adenine N6 amino group of 5 -AMP and amino acids in the 315 to 325 loop might contribute to this.	transcription
55225	2	335565	5	NULL	NULL	0	NULL	5 -AMP			bind					isozyme		muscle			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_44_27569_s_200	8910343	The delta H b on 5 -AMP binding to liver phosphorylase  a is not so negative as when 5 -AMP binds to muscle isozyme ( 24), and the absence of some hydrogen bonds between the adenine N6 amino group of 5 -AMP and amino acids in the 315 to 325 loop might contribute to this.	transcription
60159	1	335565	7	NULL	NULL	0	NULL	5 -AMP	Chemical		bind					phosphorylase a	GP	liver			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_44_27569_s_200	8910343	The delta H b on 5 -AMP binding to liver phosphorylase  a is not so negative as when 5 -AMP binds to muscle isozyme ( 24), and the absence of some hydrogen bonds between the adenine N6 amino group of 5 -AMP and amino acids in the 315 to 325 loop might contribute to this.	transcription
60160	1	335566	7	NULL	NULL	0	NULL	G-protein	GP		is					heterotrimeric guanine nucleotide-binding protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_47785_s_341	11602596	The abbreviations used are:   G-protein, heterotrimeric guanine nucleotide-binding protein;  Gsalpha, the alpha subunit of G protein that stimulates adenylyl cyclase;  GTPgammaS, guanosine 5''-(gamma-thio) triphosphate;  THFA, 9-(tetrahydro-2-furyl) adenine;  CPA, 9-(cyclopentyl) adenine;  Ap(CH2)pp, alpha,beta-methylene adenosine 5''-triphosphate;  2''-d-3''-AMP, 2''-deoxyadenosine 3''-monophosphate;  3''-AMP, adenosine 3''-monophosphate.	transcription
60161	2	335566	7	NULL	NULL	0	NULL	Gsalpha	GP		is 					G protein	GP		alpha subunit of		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_47785_s_341	11602596	The abbreviations used are:   G-protein, heterotrimeric guanine nucleotide-binding protein;  Gsalpha, the alpha subunit of G protein that stimulates adenylyl cyclase;  GTPgammaS, guanosine 5''-(gamma-thio) triphosphate;  THFA, 9-(tetrahydro-2-furyl) adenine;  CPA, 9-(cyclopentyl) adenine;  Ap(CH2)pp, alpha,beta-methylene adenosine 5''-triphosphate;  2''-d-3''-AMP, 2''-deoxyadenosine 3''-monophosphate;  3''-AMP, adenosine 3''-monophosphate.	transcription
60162	3	335566	7	NULL	NULL	0	NULL	Gsalpha	GP		stimulates					adenylyl cyclase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_47785_s_341	11602596	The abbreviations used are:   G-protein, heterotrimeric guanine nucleotide-binding protein;  Gsalpha, the alpha subunit of G protein that stimulates adenylyl cyclase;  GTPgammaS, guanosine 5''-(gamma-thio) triphosphate;  THFA, 9-(tetrahydro-2-furyl) adenine;  CPA, 9-(cyclopentyl) adenine;  Ap(CH2)pp, alpha,beta-methylene adenosine 5''-triphosphate;  2''-d-3''-AMP, 2''-deoxyadenosine 3''-monophosphate;  3''-AMP, adenosine 3''-monophosphate.	transcription
60163	4	335566	7	NULL	NULL	0	NULL	GTPgammaS	GP		is					guanosine 5''-(gamma-thio) triphosphate	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_47785_s_341	11602596	The abbreviations used are:   G-protein, heterotrimeric guanine nucleotide-binding protein;  Gsalpha, the alpha subunit of G protein that stimulates adenylyl cyclase;  GTPgammaS, guanosine 5''-(gamma-thio) triphosphate;  THFA, 9-(tetrahydro-2-furyl) adenine;  CPA, 9-(cyclopentyl) adenine;  Ap(CH2)pp, alpha,beta-methylene adenosine 5''-triphosphate;  2''-d-3''-AMP, 2''-deoxyadenosine 3''-monophosphate;  3''-AMP, adenosine 3''-monophosphate.	transcription
60164	5	335566	7	NULL	NULL	0	NULL	THFA	Chemical		is					9-(tetrahydro-2-furyl) adenine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_47785_s_341	11602596	The abbreviations used are:   G-protein, heterotrimeric guanine nucleotide-binding protein;  Gsalpha, the alpha subunit of G protein that stimulates adenylyl cyclase;  GTPgammaS, guanosine 5''-(gamma-thio) triphosphate;  THFA, 9-(tetrahydro-2-furyl) adenine;  CPA, 9-(cyclopentyl) adenine;  Ap(CH2)pp, alpha,beta-methylene adenosine 5''-triphosphate;  2''-d-3''-AMP, 2''-deoxyadenosine 3''-monophosphate;  3''-AMP, adenosine 3''-monophosphate.	transcription
60165	6	335566	7	NULL	NULL	0	NULL	CPA	Chemical		is					9-(cyclopentyl) adenine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_47785_s_341	11602596	The abbreviations used are:   G-protein, heterotrimeric guanine nucleotide-binding protein;  Gsalpha, the alpha subunit of G protein that stimulates adenylyl cyclase;  GTPgammaS, guanosine 5''-(gamma-thio) triphosphate;  THFA, 9-(tetrahydro-2-furyl) adenine;  CPA, 9-(cyclopentyl) adenine;  Ap(CH2)pp, alpha,beta-methylene adenosine 5''-triphosphate;  2''-d-3''-AMP, 2''-deoxyadenosine 3''-monophosphate;  3''-AMP, adenosine 3''-monophosphate.	transcription
60166	7	335566	7	NULL	NULL	0	NULL	Ap(CH2)pp	Chemical		is					alpha,beta-methylene adenosine 5''-triphosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_47785_s_341	11602596	The abbreviations used are:   G-protein, heterotrimeric guanine nucleotide-binding protein;  Gsalpha, the alpha subunit of G protein that stimulates adenylyl cyclase;  GTPgammaS, guanosine 5''-(gamma-thio) triphosphate;  THFA, 9-(tetrahydro-2-furyl) adenine;  CPA, 9-(cyclopentyl) adenine;  Ap(CH2)pp, alpha,beta-methylene adenosine 5''-triphosphate;  2''-d-3''-AMP, 2''-deoxyadenosine 3''-monophosphate;  3''-AMP, adenosine 3''-monophosphate.	transcription
60167	8	335566	7	NULL	NULL	0	NULL	2''-d-3''-AMP	Chemical		is					2''-deoxyadenosine 3''-monophosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_47785_s_341	11602596	The abbreviations used are:   G-protein, heterotrimeric guanine nucleotide-binding protein;  Gsalpha, the alpha subunit of G protein that stimulates adenylyl cyclase;  GTPgammaS, guanosine 5''-(gamma-thio) triphosphate;  THFA, 9-(tetrahydro-2-furyl) adenine;  CPA, 9-(cyclopentyl) adenine;  Ap(CH2)pp, alpha,beta-methylene adenosine 5''-triphosphate;  2''-d-3''-AMP, 2''-deoxyadenosine 3''-monophosphate;  3''-AMP, adenosine 3''-monophosphate.	transcription
60168	9	335566	7	NULL	NULL	0	NULL	3''-AMP	Chemical		is					adenosine 3''-monophosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_47785_s_341	11602596	The abbreviations used are:   G-protein, heterotrimeric guanine nucleotide-binding protein;  Gsalpha, the alpha subunit of G protein that stimulates adenylyl cyclase;  GTPgammaS, guanosine 5''-(gamma-thio) triphosphate;  THFA, 9-(tetrahydro-2-furyl) adenine;  CPA, 9-(cyclopentyl) adenine;  Ap(CH2)pp, alpha,beta-methylene adenosine 5''-triphosphate;  2''-d-3''-AMP, 2''-deoxyadenosine 3''-monophosphate;  3''-AMP, adenosine 3''-monophosphate.	transcription
55226	1	335567	5	NULL	NULL	0	NULL	ecto-5''-nucleotidase			is a type of					enzyme					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_48_37572_s_216	10978314	In contrast, Fig.  6 B shows that the formation of adenosine from released adenine nucleotides might be more efficient in AA (30 muM)-treated synaptosomes since the activity of ecto-5''-nucleotidase (the enzyme that forms adenosine from extracellular adenine nucleotides) was greater in AA (30 muM)-treated synaptosomes (2.06  plus-or-minus  0.08 nmol of AMP catabolized per min per mg protein,  n = 5) than in control synaptosomes (0.69  plus-or-minus  0.05 nmol/min/mg of protein,  n = 5).	transcription
55227	2	335567	5	NULL	NULL	0	NULL	adenosine			is formed from					adenine nucleotides		extracellular			NULL	AA treated synaptosomes	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_37572_s_216	10978314	In contrast, Fig.  6 B shows that the formation of adenosine from released adenine nucleotides might be more efficient in AA (30 muM)-treated synaptosomes since the activity of ecto-5''-nucleotidase (the enzyme that forms adenosine from extracellular adenine nucleotides) was greater in AA (30 muM)-treated synaptosomes (2.06  plus-or-minus  0.08 nmol of AMP catabolized per min per mg protein,  n = 5) than in control synaptosomes (0.69  plus-or-minus  0.05 nmol/min/mg of protein,  n = 5).	transcription
55228	3	335567	5	NULL	NULL	0	NULL	ecto-5''-nucleotidase			is required for					statement 2					NULL	AA treated synaptosomes	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_37572_s_216	10978314	In contrast, Fig.  6 B shows that the formation of adenosine from released adenine nucleotides might be more efficient in AA (30 muM)-treated synaptosomes since the activity of ecto-5''-nucleotidase (the enzyme that forms adenosine from extracellular adenine nucleotides) was greater in AA (30 muM)-treated synaptosomes (2.06  plus-or-minus  0.08 nmol of AMP catabolized per min per mg protein,  n = 5) than in control synaptosomes (0.69  plus-or-minus  0.05 nmol/min/mg of protein,  n = 5).	transcription
55229	4	335567	5	NULL	NULL	0	NULL	adenosine			is formed from					adenine nucleotides		extracellular			NULL	control synaptosomes	0	NULL	NULL	NULL	gw60_jbiolchem_275_48_37572_s_216	10978314	In contrast, Fig.  6 B shows that the formation of adenosine from released adenine nucleotides might be more efficient in AA (30 muM)-treated synaptosomes since the activity of ecto-5''-nucleotidase (the enzyme that forms adenosine from extracellular adenine nucleotides) was greater in AA (30 muM)-treated synaptosomes (2.06  plus-or-minus  0.08 nmol of AMP catabolized per min per mg protein,  n = 5) than in control synaptosomes (0.69  plus-or-minus  0.05 nmol/min/mg of protein,  n = 5).	transcription
55230	5	335567	5	NULL	NULL	0	NULL	ecto-5''-nucleotidase			is required for					statement 4					NULL	control synaptosomes	0	NULL	NULL	NULL	gw60_jbiolchem_275_48_37572_s_216	10978314	In contrast, Fig.  6 B shows that the formation of adenosine from released adenine nucleotides might be more efficient in AA (30 muM)-treated synaptosomes since the activity of ecto-5''-nucleotidase (the enzyme that forms adenosine from extracellular adenine nucleotides) was greater in AA (30 muM)-treated synaptosomes (2.06  plus-or-minus  0.08 nmol of AMP catabolized per min per mg protein,  n = 5) than in control synaptosomes (0.69  plus-or-minus  0.05 nmol/min/mg of protein,  n = 5).	transcription
55231	6	335567	5	NULL	NULL	0	NULL	statement 2			more efficient than					statement 4					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_48_37572_s_216	10978314	In contrast, Fig.  6 B shows that the formation of adenosine from released adenine nucleotides might be more efficient in AA (30 muM)-treated synaptosomes since the activity of ecto-5''-nucleotidase (the enzyme that forms adenosine from extracellular adenine nucleotides) was greater in AA (30 muM)-treated synaptosomes (2.06  plus-or-minus  0.08 nmol of AMP catabolized per min per mg protein,  n = 5) than in control synaptosomes (0.69  plus-or-minus  0.05 nmol/min/mg of protein,  n = 5).	transcription
55232	7	335567	5	NULL	NULL	0	NULL	statement 3			greater activity than					statement 5					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_48_37572_s_216	10978314	In contrast, Fig.  6 B shows that the formation of adenosine from released adenine nucleotides might be more efficient in AA (30 muM)-treated synaptosomes since the activity of ecto-5''-nucleotidase (the enzyme that forms adenosine from extracellular adenine nucleotides) was greater in AA (30 muM)-treated synaptosomes (2.06  plus-or-minus  0.08 nmol of AMP catabolized per min per mg protein,  n = 5) than in control synaptosomes (0.69  plus-or-minus  0.05 nmol/min/mg of protein,  n = 5).	transcription
55233	8	335567	5	NULL	NULL	0	NULL	statement 7			leads to					statement 6					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_48_37572_s_216	10978314	In contrast, Fig.  6 B shows that the formation of adenosine from released adenine nucleotides might be more efficient in AA (30 muM)-treated synaptosomes since the activity of ecto-5''-nucleotidase (the enzyme that forms adenosine from extracellular adenine nucleotides) was greater in AA (30 muM)-treated synaptosomes (2.06  plus-or-minus  0.08 nmol of AMP catabolized per min per mg protein,  n = 5) than in control synaptosomes (0.69  plus-or-minus  0.05 nmol/min/mg of protein,  n = 5).	transcription
60169	1	335567	7	NULL	NULL	0	NULL	adenosine	NucleicAcid		formed from					adenine nucleotides	NucleicAcid	extracellular			NULL	AA treated synaptosomes	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_37572_s_216	10978314	In contrast, Fig.  6 B shows that the formation of adenosine from released adenine nucleotides might be more efficient in AA (30 muM)-treated synaptosomes since the activity of ecto-5''-nucleotidase (the enzyme that forms adenosine from extracellular adenine nucleotides) was greater in AA (30 muM)-treated synaptosomes (2.06  plus-or-minus  0.08 nmol of AMP catabolized per min per mg protein,  n = 5) than in control synaptosomes (0.69  plus-or-minus  0.05 nmol/min/mg of protein,  n = 5).	transcription
60233	2	335567	7	NULL	NULL	0	NULL	ecto-5''-nucleotidase	GP		catalyze					statement 1	Process				NULL	AA treated synaptosomes	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_48_37572_s_216	10978314	In contrast, Fig.  6 B shows that the formation of adenosine from released adenine nucleotides might be more efficient in AA (30 muM)-treated synaptosomes since the activity of ecto-5''-nucleotidase (the enzyme that forms adenosine from extracellular adenine nucleotides) was greater in AA (30 muM)-treated synaptosomes (2.06  plus-or-minus  0.08 nmol of AMP catabolized per min per mg protein,  n = 5) than in control synaptosomes (0.69  plus-or-minus  0.05 nmol/min/mg of protein,  n = 5).	transcription
55234	1	335568	5	NULL	NULL	0	NULL	9-(cyclopentyl)adenine			inhibits		selectively			type 5 AC					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_39_40938_s_149	15262973	For comparison, 9-(cyclopentyl)adenine also inhibited type 5 AC in a similarly selective manner as PMC-6 (632 for type 2 AC and 79 for type 3 AC), as already reported by us ( ) and others ( ), although the IC50 value for type 5 AC (3.2 muM) was greater than that of PMC-6 (0.32 muM).	transcription
55235	2	335568	5	NULL	NULL	0	NULL	PMC-6			inhibits		selectively			type 5 AC					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_39_40938_s_149	15262973	For comparison, 9-(cyclopentyl)adenine also inhibited type 5 AC in a similarly selective manner as PMC-6 (632 for type 2 AC and 79 for type 3 AC), as already reported by us ( ) and others ( ), although the IC50 value for type 5 AC (3.2 muM) was greater than that of PMC-6 (0.32 muM).	transcription
60234	1	335568	7	NULL	NULL	0	NULL	9-(cyclopentyl)adenine 	Chemical		inhibit					 type 5 AC	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_39_40938_s_149	15262973	For comparison, 9-(cyclopentyl)adenine also inhibited type 5 AC in a similarly selective manner as PMC-6 (632 for type 2 AC and 79 for type 3 AC), as already reported by us ( ) and others ( ), although the IC50 value for type 5 AC (3.2 muM) was greater than that of PMC-6 (0.32 muM).	transcription
60235	2	335568	7	NULL	NULL	0	NULL	PMC-6	Chemical		inhibit					type 5 AC	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_39_40938_s_149	15262973	For comparison, 9-(cyclopentyl)adenine also inhibited type 5 AC in a similarly selective manner as PMC-6 (632 for type 2 AC and 79 for type 3 AC), as already reported by us ( ) and others ( ), although the IC50 value for type 5 AC (3.2 muM) was greater than that of PMC-6 (0.32 muM).	transcription
60236	3	335568	7	NULL	NULL	0	NULL	statement 1	Process	inhibition of	is similar to					statement 2	Process	inhibition of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_39_40938_s_149	15262973	For comparison, 9-(cyclopentyl)adenine also inhibited type 5 AC in a similarly selective manner as PMC-6 (632 for type 2 AC and 79 for type 3 AC), as already reported by us ( ) and others ( ), although the IC50 value for type 5 AC (3.2 muM) was greater than that of PMC-6 (0.32 muM).	transcription
55236	1	335570	5	NULL	NULL	0	NULL	YPH-A cells		growth of;;prototrophic	requires					uracil					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
55237	2	335570	5	NULL	NULL	0	NULL	YPH-A cells		growth of;;prototrophic	requires					adenine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
55238	3	335570	5	NULL	NULL	0	NULL	YPH-E cells		growth of;;prototrophic	requires					uracil					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
55239	4	335570	5	NULL	NULL	0	NULL	YPH-E cells		growth of;;prototrophic	requires					adenine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
55240	5	335570	5	NULL	NULL	0	NULL	PHS		high concentration of	inhibits					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
55241	6	335570	5	NULL	NULL	0	NULL	PHS		high concentration of	inhibits					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
55242	7	335570	5	NULL	NULL	0	NULL	PHS		high concentration of	inhibits					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
55243	8	335570	5	NULL	NULL	0	NULL	PHS		high concentration of	inhibits					statement 4					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
55244	9	335570	5	NULL	NULL	0	NULL	proline			is the source of					nitrogen					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
55245	10	335570	5	NULL	NULL	0	NULL	ammonium ions 			is the source of					nitrogen					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
55246	11	335570	5	NULL	NULL	0	NULL	statement 9			is preferred over					statement 10					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60237	1	335570	7	NULL	NULL	0	NULL	YPH-A cells	Cell	growth of	require					Uracil	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60238	2	335570	7	NULL	NULL	0	NULL	YPH-A cells	Cell	growth of	require					adenine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60239	3	335570	7	NULL	NULL	0	NULL	YPH-E cells	Cell	growth of	require					Uracil	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60240	4	335570	7	NULL	NULL	0	NULL	YPH-E cells	Cell	growth of	require					adenine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60241	5	335570	7	NULL	NULL	0	NULL	PHS	Chemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60242	6	335570	7	NULL	NULL	0	NULL	PHS	Chemical		inhibit					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60243	7	335570	7	NULL	NULL	0	NULL	PHS	Chemical		inhibit					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60244	8	335570	7	NULL	NULL	0	NULL	PHS	Chemical		inhibit					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60250	9	335570	7	NULL	NULL	0	NULL	proline	AminoAcid		used as a					nitrogen source	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60251	10	335570	7	NULL	NULL	0	NULL	Ammonium ions	Chemical		used as a					nitrogen source	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60252	11	335570	7	NULL	NULL	0	NULL	statement 5	Process		occur upon					statement 9	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60253	12	335570	7	NULL	NULL	0	NULL	statement 6	Process		occur upon					statement 9	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60254	13	335570	7	NULL	NULL	0	NULL	statement 7	Process		occur upon					statement 9	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60255	14	335570	7	NULL	NULL	0	NULL	statement 8	Process		occur upon					statement 9	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60256	15	335570	7	NULL	NULL	0	NULL	statement 5	Process		occur upon					statement 10	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60257	16	335570	7	NULL	NULL	0	NULL	statement 6	Process		occur upon					statement 10	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60258	17	335570	7	NULL	NULL	0	NULL	statement 7	Process		occur upon					statement 10	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60263	18	335570	7	NULL	NULL	0	NULL	statement 8	Process		occur upon					statement 10	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60269	19	335570	7	NULL	NULL	0	NULL	statement 11	Process	inhibition of	is more than					statement 15	Process	inhibition of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60270	20	335570	7	NULL	NULL	0	NULL	statement 12	Process	inhibition of	is more than					statement 16	Process	inhibition of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60271	21	335570	7	NULL	NULL	0	NULL	statement 13	Process	inhibition of	is more than					statement 17	Process	inhibition of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60272	22	335570	7	NULL	NULL	0	NULL	statement 14	Process	inhibition of	is more than					statement 18	Process	inhibition of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60273	23	335570	7	NULL	NULL	0	NULL	YPH-A cell	Cell		is a type of					prototrophic cell	Cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
60274	24	335570	7	NULL	NULL	0	NULL	YPH-E cell	Cell		is a type of					prototrophic cell	Cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_153	9446592	Growth of prototrophic YPH-A and YPH-E cells requiring uracil and adenine was slightly more inhibited by high concentrations of PHS when proline (Fig.  5 B) rather than ammonium ions were the nitrogen source (Fig.  5 A).	transcription
55247	1	335572	5	NULL	NULL	0	NULL	AFB1 exo-8,9-epoxide			reacts with					adenine bases					NULL		0	NULL	NULL	NULL	gw60_pnas_94_12_6121_s_98	9177180	Because AFB1  exo-8,9-epoxide reacts with adenine bases only 1% as effectively as Gua ( 22), we also investigated the effect of poly d(AT), which is necessarily duplex helical DNA and shown to intercalate AFB1 ( 5); its presence produced a 33% rate enhancement (Fig.  5).	transcription
55248	2	335572	5	NULL	NULL	0	NULL	poly d(AT)			is a type of					duplex helical DNA					NULL		0	NULL	NULL	NULL	gw60_pnas_94_12_6121_s_98	9177180	Because AFB1  exo-8,9-epoxide reacts with adenine bases only 1% as effectively as Gua ( 22), we also investigated the effect of poly d(AT), which is necessarily duplex helical DNA and shown to intercalate AFB1 ( 5); its presence produced a 33% rate enhancement (Fig.  5).	transcription
55249	3	335572	5	NULL	NULL	0	NULL	poly d(AT)			intercalate					AFB1					NULL		0	NULL	NULL	NULL	gw60_pnas_94_12_6121_s_98	9177180	Because AFB1  exo-8,9-epoxide reacts with adenine bases only 1% as effectively as Gua ( 22), we also investigated the effect of poly d(AT), which is necessarily duplex helical DNA and shown to intercalate AFB1 ( 5); its presence produced a 33% rate enhancement (Fig.  5).	transcription
60280	1	335572	7	NULL	NULL	0	NULL	AFB1 exo-8,9-epoxide	Chemical		reacts with					adenine bases	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_94_12_6121_s_98	9177180	Because AFB1  exo-8,9-epoxide reacts with adenine bases only 1% as effectively as Gua ( 22), we also investigated the effect of poly d(AT), which is necessarily duplex helical DNA and shown to intercalate AFB1 ( 5); its presence produced a 33% rate enhancement (Fig.  5).	transcription
60283	2	335572	7	NULL	NULL	0	NULL	AFB1 exo-8,9-epoxide	Chemical		reacts with					Gua	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_94_12_6121_s_98	9177180	Because AFB1  exo-8,9-epoxide reacts with adenine bases only 1% as effectively as Gua ( 22), we also investigated the effect of poly d(AT), which is necessarily duplex helical DNA and shown to intercalate AFB1 ( 5); its presence produced a 33% rate enhancement (Fig.  5).	transcription
60288	3	335572	7	NULL	NULL	0	NULL	poly d(AT)	NucleicAcid		intercalate					AFB1	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_12_6121_s_98	9177180	Because AFB1  exo-8,9-epoxide reacts with adenine bases only 1% as effectively as Gua ( 22), we also investigated the effect of poly d(AT), which is necessarily duplex helical DNA and shown to intercalate AFB1 ( 5); its presence produced a 33% rate enhancement (Fig.  5).	transcription
60289	4	335572	7	NULL	NULL	0	NULL	poly d(AT)	NucleicAcid		is a type of					duplex helical DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_pnas_94_12_6121_s_98	9177180	Because AFB1  exo-8,9-epoxide reacts with adenine bases only 1% as effectively as Gua ( 22), we also investigated the effect of poly d(AT), which is necessarily duplex helical DNA and shown to intercalate AFB1 ( 5); its presence produced a 33% rate enhancement (Fig.  5).	transcription
55250	1	335573	5	NULL	NULL	0	NULL	Choline			does not affect					yeast		vitality of			NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_84	10359089	Choline did not affect yeast vitality or the electrochemical gradient, since the transport of [U-14]adenine by endogenous yeast H+-cotransport systems [  24] was uninhibited by the presence of 0, 5 or 25 mM choline (783 plus-or-minus 97, 778 plus-or-minus 63 and 800 plus-or-minus 34 nmol adenine min~1 g~1 yeast DW).	transcription
55251	2	335573	5	NULL	NULL	0	NULL	[U-14]adenine			is transported by					H+-cotransport systems		endogenous;;yeast			NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_84	10359089	Choline did not affect yeast vitality or the electrochemical gradient, since the transport of [U-14]adenine by endogenous yeast H+-cotransport systems [  24] was uninhibited by the presence of 0, 5 or 25 mM choline (783 plus-or-minus 97, 778 plus-or-minus 63 and 800 plus-or-minus 34 nmol adenine min~1 g~1 yeast DW).	transcription
55252	3	335573	5	NULL	NULL	0	NULL	choline		presence of	inhibits					statement 2					NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_84	10359089	Choline did not affect yeast vitality or the electrochemical gradient, since the transport of [U-14]adenine by endogenous yeast H+-cotransport systems [  24] was uninhibited by the presence of 0, 5 or 25 mM choline (783 plus-or-minus 97, 778 plus-or-minus 63 and 800 plus-or-minus 34 nmol adenine min~1 g~1 yeast DW).	transcription
60290	1	335573	7	NULL	NULL	0	NULL	Choline	Chemical		does not affect					yeast vitality	Organism				NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_84	10359089	Choline did not affect yeast vitality or the electrochemical gradient, since the transport of [U-14]adenine by endogenous yeast H+-cotransport systems [  24] was uninhibited by the presence of 0, 5 or 25 mM choline (783 plus-or-minus 97, 778 plus-or-minus 63 and 800 plus-or-minus 34 nmol adenine min~1 g~1 yeast DW).	transcription
60291	2	335573	7	NULL	NULL	0	NULL	Choline	Chemical		does not affect					electrochemical gradient	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_450_3_280_s_84	10359089	Choline did not affect yeast vitality or the electrochemical gradient, since the transport of [U-14]adenine by endogenous yeast H+-cotransport systems [  24] was uninhibited by the presence of 0, 5 or 25 mM choline (783 plus-or-minus 97, 778 plus-or-minus 63 and 800 plus-or-minus 34 nmol adenine min~1 g~1 yeast DW).	transcription
60292	3	335573	7	NULL	NULL	0	NULL	H+-cotransport system	Process	yeast;;endogenous	transport					[U-14]adenine	Chemical				NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_84	10359089	Choline did not affect yeast vitality or the electrochemical gradient, since the transport of [U-14]adenine by endogenous yeast H+-cotransport systems [  24] was uninhibited by the presence of 0, 5 or 25 mM choline (783 plus-or-minus 97, 778 plus-or-minus 63 and 800 plus-or-minus 34 nmol adenine min~1 g~1 yeast DW).	transcription
60293	4	335573	7	NULL	NULL	0	NULL	Choline	Chemical		does not inhibit					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_84	10359089	Choline did not affect yeast vitality or the electrochemical gradient, since the transport of [U-14]adenine by endogenous yeast H+-cotransport systems [  24] was uninhibited by the presence of 0, 5 or 25 mM choline (783 plus-or-minus 97, 778 plus-or-minus 63 and 800 plus-or-minus 34 nmol adenine min~1 g~1 yeast DW).	transcription
55253	1	335575	5	NULL	NULL	0	NULL	MYH			catalyzes					adenine base 		excision of			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_19_5928_s_77	15531653	Adenine base excision catalyzed by MYH and APE1   The reaction mixture (20 mul) contained 50 mM Tris - HCl (pH 7.5), 5 mM MgCl2, 5 mM DTT, 50 mug/ml BSA, 1 nM 5''-labeled 40mer duplex DNA and MYH (0, 2.5, 5 or 10 nM) and was incubated at 37 degrees C for 15 min followed by incubation with APE1 (0, 10 or 50 nM) in the presence of 150 mM KCl at 37 degrees C for 15 min ( Figure 5).	transcription
55254	2	335575	5	NULL	NULL	0	NULL	APE1			catalyzes					adenine base		excision of			NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_19_5928_s_77	15531653	Adenine base excision catalyzed by MYH and APE1   The reaction mixture (20 mul) contained 50 mM Tris - HCl (pH 7.5), 5 mM MgCl2, 5 mM DTT, 50 mug/ml BSA, 1 nM 5''-labeled 40mer duplex DNA and MYH (0, 2.5, 5 or 10 nM) and was incubated at 37 degrees C for 15 min followed by incubation with APE1 (0, 10 or 50 nM) in the presence of 150 mM KCl at 37 degrees C for 15 min ( Figure 5).	transcription
60294	1	335575	7	NULL	NULL	0	NULL	Adenine base	Chemical	excision of	catalyzed by					MYH	GP				NULL		0	NULL	NULL	NULL	gw70_nucleicacidsres_32_19_5928_s_77	15531653	Adenine base excision catalyzed by MYH and APE1   The reaction mixture (20 mul) contained 50 mM Tris - HCl (pH 7.5), 5 mM MgCl2, 5 mM DTT, 50 mug/ml BSA, 1 nM 5''-labeled 40mer duplex DNA and MYH (0, 2.5, 5 or 10 nM) and was incubated at 37 degrees C for 15 min followed by incubation with APE1 (0, 10 or 50 nM) in the presence of 150 mM KCl at 37 degrees C for 15 min ( Figure 5).	transcription
60295	2	335575	7	NULL	NULL	0	NULL	Adenine base	Chemical	excision of	catalyzed by					APE1	GP				NULL		NULL	NULL	NULL	NULL	gw70_nucleicacidsres_32_19_5928_s_77	15531653	Adenine base excision catalyzed by MYH and APE1   The reaction mixture (20 mul) contained 50 mM Tris - HCl (pH 7.5), 5 mM MgCl2, 5 mM DTT, 50 mug/ml BSA, 1 nM 5''-labeled 40mer duplex DNA and MYH (0, 2.5, 5 or 10 nM) and was incubated at 37 degrees C for 15 min followed by incubation with APE1 (0, 10 or 50 nM) in the presence of 150 mM KCl at 37 degrees C for 15 min ( Figure 5).	transcription
60296	1	335576	7	NULL	NULL	0	NULL	 IRF-3	GP		bind								Arg 81	 3' site opposite guanine	NULL		0	NULL	NULL	NULL	gw70_embo_23_22_4384_s_95	15510218	We find that IRF-3 binds the 3' site in the standard fashion, with  Arg 81 opposite the guanine ( Figure 2), but it binds the 5' site 1 bp 'out of phase'', with Arg 81 opposite  the first adenine, thus preserving the canonical 2 bp intersite spacing, at the expense  of the usually conserved contact of Arg 81 with guanine.	transcription
60297	2	335576	7	NULL	NULL	0	NULL	IRF-3	GP		bind								Arg 81	5' site opposite first adenine	NULL		0	NULL	NULL	NULL	gw70_embo_23_22_4384_s_95	15510218	We find that IRF-3 binds the 3' site in the standard fashion, with  Arg 81 opposite the guanine ( Figure 2), but it binds the 5' site 1 bp 'out of phase'', with Arg 81 opposite  the first adenine, thus preserving the canonical 2 bp intersite spacing, at the expense  of the usually conserved contact of Arg 81 with guanine.	transcription
60298	3	335576	7	NULL	NULL	0	NULL	statement 2	Process		occurs					out of phase	Process				NULL		0	NULL	NULL	NULL	gw70_embo_23_22_4384_s_95	15510218	We find that IRF-3 binds the 3' site in the standard fashion, with  Arg 81 opposite the guanine ( Figure 2), but it binds the 5' site 1 bp 'out of phase'', with Arg 81 opposite  the first adenine, thus preserving the canonical 2 bp intersite spacing, at the expense  of the usually conserved contact of Arg 81 with guanine.	transcription
60299	4	335576	7	NULL	NULL	0	NULL	statement 3	Process		preserves					 intersite spacing	QuantityOrMeasure				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_22_4384_s_95	15510218	We find that IRF-3 binds the 3' site in the standard fashion, with  Arg 81 opposite the guanine ( Figure 2), but it binds the 5' site 1 bp 'out of phase'', with Arg 81 opposite  the first adenine, thus preserving the canonical 2 bp intersite spacing, at the expense  of the usually conserved contact of Arg 81 with guanine.	transcription
60300	5	335576	7	NULL	NULL	0	NULL				contact with		conserved	Arg 81		guanine	Chemical				NULL		0	NULL	NULL	NULL	gw70_embo_23_22_4384_s_95	15510218	We find that IRF-3 binds the 3' site in the standard fashion, with  Arg 81 opposite the guanine ( Figure 2), but it binds the 5' site 1 bp 'out of phase'', with Arg 81 opposite  the first adenine, thus preserving the canonical 2 bp intersite spacing, at the expense  of the usually conserved contact of Arg 81 with guanine.	transcription
60301	6	335576	7	NULL	NULL	0	NULL	statement 4	Process		at the expense of					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_embo_23_22_4384_s_95	15510218	We find that IRF-3 binds the 3' site in the standard fashion, with  Arg 81 opposite the guanine ( Figure 2), but it binds the 5' site 1 bp 'out of phase'', with Arg 81 opposite  the first adenine, thus preserving the canonical 2 bp intersite spacing, at the expense  of the usually conserved contact of Arg 81 with guanine.	transcription
55255	1	335577	5	NULL	NULL	0	NULL	ATP			is a type of					adenine-based nucleotides					NULL		0	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_395_s_281	11378300	In  cultures of rat astrocytes, exogenous GTP substantially increases the extracellular  levels of adenine-based nucleotides (mainly ATP and AMP) from rat astrocytes, an  effect at least in part ascribable to the blockade of 5 -ectonucleotidase (   Rathbone et al., 1998b , 1999).	transcription
55256	2	335577	5	NULL	NULL	0	NULL	AMP			is a type of					adenine-based nucleotides					NULL		0	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_395_s_281	11378300	In  cultures of rat astrocytes, exogenous GTP substantially increases the extracellular  levels of adenine-based nucleotides (mainly ATP and AMP) from rat astrocytes, an  effect at least in part ascribable to the blockade of 5 -ectonucleotidase (   Rathbone et al., 1998b , 1999).	transcription
55257	3	335577	5	NULL	NULL	0	NULL	GTP		exogenous	increases		substantially			ATP		extracellular levels of			NULL	cultures of rat astrocytes	0	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_395_s_281	11378300	In  cultures of rat astrocytes, exogenous GTP substantially increases the extracellular  levels of adenine-based nucleotides (mainly ATP and AMP) from rat astrocytes, an  effect at least in part ascribable to the blockade of 5 -ectonucleotidase (   Rathbone et al., 1998b , 1999).	transcription
55258	4	335577	5	NULL	NULL	0	NULL	GTP		exogenous	increases		substantially			AMP		extracellular levels of			NULL	cultures of rat astrocytes	0	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_395_s_281	11378300	In  cultures of rat astrocytes, exogenous GTP substantially increases the extracellular  levels of adenine-based nucleotides (mainly ATP and AMP) from rat astrocytes, an  effect at least in part ascribable to the blockade of 5 -ectonucleotidase (   Rathbone et al., 1998b , 1999).	transcription
55259	5	335577	5	NULL	NULL	0	NULL	statement 3			ascribable to		partly			5 -ectonucleotidase		blockade of			NULL	cultures of rat astrocytes	NULL	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_395_s_281	11378300	In  cultures of rat astrocytes, exogenous GTP substantially increases the extracellular  levels of adenine-based nucleotides (mainly ATP and AMP) from rat astrocytes, an  effect at least in part ascribable to the blockade of 5 -ectonucleotidase (   Rathbone et al., 1998b , 1999).	transcription
55260	6	335577	5	NULL	NULL	0	NULL	statement 4			ascribable to		partly			5 -ectonucleotidase		blockade of			NULL	cultures of rat astrocytes	NULL	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_395_s_281	11378300	In  cultures of rat astrocytes, exogenous GTP substantially increases the extracellular  levels of adenine-based nucleotides (mainly ATP and AMP) from rat astrocytes, an  effect at least in part ascribable to the blockade of 5 -ectonucleotidase (   Rathbone et al., 1998b , 1999).	transcription
60302	1	335577	7	NULL	NULL	0	NULL	 GTP	Chemical	exogenous	increase					ATP	Chemical	extracellular levels of			NULL	rat astrocytes	0	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_395_s_281	11378300	In  cultures of rat astrocytes, exogenous GTP substantially increases the extracellular  levels of adenine-based nucleotides (mainly ATP and AMP) from rat astrocytes, an  effect at least in part ascribable to the blockade of 5 -ectonucleotidase (   Rathbone et al., 1998b , 1999).	transcription
60303	2	335577	7	NULL	NULL	0	NULL	GTP	Chemical	exogenous	increase					AMP	Chemical	extracellular levels of			NULL	rat astrocytes	NULL	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_395_s_281	11378300	In  cultures of rat astrocytes, exogenous GTP substantially increases the extracellular  levels of adenine-based nucleotides (mainly ATP and AMP) from rat astrocytes, an  effect at least in part ascribable to the blockade of 5 -ectonucleotidase (   Rathbone et al., 1998b , 1999).	transcription
60304	3	335577	7	NULL	NULL	0	NULL	statement 1	Process		ascribable to		partly			5 -ectonucleotidase	GP	blockade of			NULL		0	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_395_s_281	11378300	In  cultures of rat astrocytes, exogenous GTP substantially increases the extracellular  levels of adenine-based nucleotides (mainly ATP and AMP) from rat astrocytes, an  effect at least in part ascribable to the blockade of 5 -ectonucleotidase (   Rathbone et al., 1998b , 1999).	transcription
60305	4	335577	7	NULL	NULL	0	NULL	statement 2	Process		ascribable to		partly			5 -ectonucleotidase	GP	blockade of			NULL		NULL	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_395_s_281	11378300	In  cultures of rat astrocytes, exogenous GTP substantially increases the extracellular  levels of adenine-based nucleotides (mainly ATP and AMP) from rat astrocytes, an  effect at least in part ascribable to the blockade of 5 -ectonucleotidase (   Rathbone et al., 1998b , 1999).	transcription
60306	5	335577	7	NULL	NULL	0	NULL	ATP	Chemical		is a type of					adenine-based nucleotide	Chemical				NULL		0	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_395_s_281	11378300	In  cultures of rat astrocytes, exogenous GTP substantially increases the extracellular  levels of adenine-based nucleotides (mainly ATP and AMP) from rat astrocytes, an  effect at least in part ascribable to the blockade of 5 -ectonucleotidase (   Rathbone et al., 1998b , 1999).	transcription
60307	6	335577	7	NULL	NULL	0	NULL	AMP	Chemical		is a type of					adenine-based nucleotide	Chemical				NULL		0	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_395_s_281	11378300	In  cultures of rat astrocytes, exogenous GTP substantially increases the extracellular  levels of adenine-based nucleotides (mainly ATP and AMP) from rat astrocytes, an  effect at least in part ascribable to the blockade of 5 -ectonucleotidase (   Rathbone et al., 1998b , 1999).	transcription
55261	1	335578	5	NULL	NULL	0	NULL	HDAC 1			is related to					RPD3		yeast			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
55262	2	335578	5	NULL	NULL	0	NULL	HDAC 2			is related to					RPD3		yeast			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
55263	3	335578	5	NULL	NULL	0	NULL	HDAC 3			is related to					RPD3		yeast			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
55264	4	335578	5	NULL	NULL	0	NULL	HDAC 8			is related to					RPD3		yeast			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
55265	5	335578	5	NULL	NULL	0	NULL	HDAC 4			is related to					Had1					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
55266	6	335578	5	NULL	NULL	0	NULL	HDAC 5			is related to					Had1					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
55267	7	335578	5	NULL	NULL	0	NULL	HDAC 6			is related to					Had1					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
55268	8	335578	5	NULL	NULL	0	NULL	HDAC 7			is related to					Had1					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
55269	9	335578	5	NULL	NULL	0	NULL	class III HDACs			is related to					Sir2 family					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
55270	10	335578	5	NULL	NULL	0	NULL	Sir2 family		activity of	is dependent on					nicotinamide-adenine-dinucleotide					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
55271	11	335578	5	NULL	NULL	0	NULL	HDAC 1			is a type of					Class 1 HDAC					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
55272	12	335578	5	NULL	NULL	0	NULL	HDAC 2			is a type of					Class 1 HDAC					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
55273	13	335578	5	NULL	NULL	0	NULL	HDAC 3			is a type of					Class 1 HDAC					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
55274	14	335578	5	NULL	NULL	0	NULL	HDAC 8			is a type of					Class 1 HDAC					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
55275	15	335578	5	NULL	NULL	0	NULL	HDAC 4			is a type of					class II HDAC					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
55276	16	335578	5	NULL	NULL	0	NULL	HDAC 5			is a type of					class II HDAC					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
55277	17	335578	5	NULL	NULL	0	NULL	HDAC 6			is a type of					class II HDAC					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
55278	18	335578	5	NULL	NULL	0	NULL	HDAC 7			is a type of					class II HDAC					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
60308	1	335578	7	NULL	NULL	0	NULL	HDAC 1	GP		is related to					RPD3	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
60309	2	335578	7	NULL	NULL	0	NULL	HDAC 2	GP		is related to					RPD3	GP	yeast			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
60310	3	335578	7	NULL	NULL	0	NULL	HDAC 3	GP		is related to					RPD3	GP	yeast			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
60311	4	335578	7	NULL	NULL	0	NULL	HDAC 8	GP		is related to					RPD3	GP	yeast			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
60312	5	335578	7	NULL	NULL	0	NULL	HDAC 4	GP		is related to					Had1	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
60313	6	335578	7	NULL	NULL	0	NULL	HDAC 5	GP		is related to					Had1	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
60314	7	335578	7	NULL	NULL	0	NULL	HDAC 6	GP		is related to					Had1	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
60315	8	335578	7	NULL	NULL	0	NULL	HDAC 7	GP		is related to					Had1	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
60316	9	335578	7	NULL	NULL	0	NULL	class III HDAC 	GP		is related to					 Sir2 family	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
60317	10	335578	7	NULL	NULL	0	NULL	Sir2 family	GP	activity of	depends on					nicotinamide-adenine-dinucleotide	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
60318	11	335578	7	NULL	NULL	0	NULL	HDAC 1	GP		is a type of					Class I molecule	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
60319	12	335578	7	NULL	NULL	0	NULL	HDAC 2	GP		is a type of					Class I molecule	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
60320	13	335578	7	NULL	NULL	0	NULL	HDAC 3	GP		is a type of					Class I molecule	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
60321	14	335578	7	NULL	NULL	0	NULL	HDAC 8	GP		is a type of					Class I molecule	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
60322	15	335578	7	NULL	NULL	0	NULL	HDAC 4	GP		is a type of					Class II molecule	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
60323	16	335578	7	NULL	NULL	0	NULL	HDAC 5	GP		is a type of					Class II molecule	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
60324	17	335578	7	NULL	NULL	0	NULL	HDAC 6	GP		is a type of					Class II molecule	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
60325	18	335578	7	NULL	NULL	0	NULL	HDAC 7	GP		is a type of					Class II molecule	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1677_1_30_s_204	15020043	Class 1 (HDAC 1, 2, 3  and 8) are related to yeast RPD3, class II (HDAC 4, 5, 6 and 7) are related to Had1  and class III HDACs are related to Sir2 family whose activity depends on nicotinamide-adenine-dinucleotide  [  137].	transcription
56504	1	335579	5	NULL	NULL	0	NULL	adenine base		phosphates 5' to alkylated	interacts with					AlkBs		eubacterial	Thr 51;;Tyr 76 ;;Arg 161		NULL		0	NULL	NULL	NULL	gw70_nature_439_7078_879_s_60	16482161	The nucleotide backbone is bound in a cooperative hydrogen-bonding (H-bonding) network  in which the two phosphates 5' to the alkylated adenine base interact with Thr  51, Tyr 76 and Arg 161 ( Fig. 2b), which are invariant in eubacterial AlkBs ( Supplementary Fig. S2A).	transcription
60342	1	335579	7	NULL	NULL	0	NULL	nucleotide	NucleicAcid	binding of backbone of	occur as a 					H-bonding network	Process	cooperative			NULL		NULL	NULL	NULL	NULL	gw70_nature_439_7078_879_s_60	16482161	The nucleotide backbone is bound in a cooperative hydrogen-bonding (H-bonding) network  in which the two phosphates 5' to the alkylated adenine base interact with Thr  51, Tyr 76 and Arg 161 ( Fig. 2b), which are invariant in eubacterial AlkBs ( Supplementary Fig. S2A).	transcription
60343	2	335579	7	NULL	NULL	0	NULL	adenine base	Chemical	alkylated	interacts with				two phosphates 5' 				Thr51		NULL	eubacterial AlkBs 	0	NULL	NULL	NULL	gw70_nature_439_7078_879_s_60	16482161	The nucleotide backbone is bound in a cooperative hydrogen-bonding (H-bonding) network  in which the two phosphates 5' to the alkylated adenine base interact with Thr  51, Tyr 76 and Arg 161 ( Fig. 2b), which are invariant in eubacterial AlkBs ( Supplementary Fig. S2A).	transcription
60344	3	335579	7	NULL	NULL	0	NULL	adenine base	Chemical	alkylated	interacts with				two phosphates 5'				Tyr 76		NULL	eubacterial AlkBs	NULL	NULL	NULL	NULL	gw70_nature_439_7078_879_s_60	16482161	The nucleotide backbone is bound in a cooperative hydrogen-bonding (H-bonding) network  in which the two phosphates 5' to the alkylated adenine base interact with Thr  51, Tyr 76 and Arg 161 ( Fig. 2b), which are invariant in eubacterial AlkBs ( Supplementary Fig. S2A).	transcription
60345	4	335579	7	NULL	NULL	0	NULL	adenine base	Chemical	alkylated	interacts with				two phosphates 5'				Arg 161		NULL	eubacterial AlkBs	0	NULL	NULL	NULL	gw70_nature_439_7078_879_s_60	16482161	The nucleotide backbone is bound in a cooperative hydrogen-bonding (H-bonding) network  in which the two phosphates 5' to the alkylated adenine base interact with Thr  51, Tyr 76 and Arg 161 ( Fig. 2b), which are invariant in eubacterial AlkBs ( Supplementary Fig. S2A).	transcription
60346	5	335579	7	NULL	NULL	0	NULL	statement 2	Process		occur as					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_nature_439_7078_879_s_60	16482161	The nucleotide backbone is bound in a cooperative hydrogen-bonding (H-bonding) network  in which the two phosphates 5' to the alkylated adenine base interact with Thr  51, Tyr 76 and Arg 161 ( Fig. 2b), which are invariant in eubacterial AlkBs ( Supplementary Fig. S2A).	transcription
60347	6	335579	7	NULL	NULL	0	NULL	statement 3	Process		occur as					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_nature_439_7078_879_s_60	16482161	The nucleotide backbone is bound in a cooperative hydrogen-bonding (H-bonding) network  in which the two phosphates 5' to the alkylated adenine base interact with Thr  51, Tyr 76 and Arg 161 ( Fig. 2b), which are invariant in eubacterial AlkBs ( Supplementary Fig. S2A).	transcription
60348	7	335579	7	NULL	NULL	0	NULL	statement 4	Process		occur as					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_nature_439_7078_879_s_60	16482161	The nucleotide backbone is bound in a cooperative hydrogen-bonding (H-bonding) network  in which the two phosphates 5' to the alkylated adenine base interact with Thr  51, Tyr 76 and Arg 161 ( Fig. 2b), which are invariant in eubacterial AlkBs ( Supplementary Fig. S2A).	transcription
60349	8	335579	7	NULL	NULL	0	NULL	H-bonding	Process		is					hydrogen-bonding	Process				NULL		NULL	NULL	NULL	NULL	gw70_nature_439_7078_879_s_60	16482161	The nucleotide backbone is bound in a cooperative hydrogen-bonding (H-bonding) network  in which the two phosphates 5' to the alkylated adenine base interact with Thr  51, Tyr 76 and Arg 161 ( Fig. 2b), which are invariant in eubacterial AlkBs ( Supplementary Fig. S2A).	transcription
55296	1	335580	5	NULL	NULL	0	NULL	ade2 cells			harbor					AtENT1		coding sequences of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35732_s_242	12810710	After inducing the expression of the cloned sequences by  galactose, the  ade2 cells harboring AtENT1 or AtENT3 coding sequences  could grow in the presence of 150 muM adenosine  ( Fig. 5 and data not shown),  indicating that adenine dependence of the  ade2 cells was rescued by  adenosine transport activities of the proteins expressed from the cloned  sequences in the four expression constructs.	transcription
55297	2	335580	5	NULL	NULL	0	NULL	ade2 cells			harbor					AtENT3		coding sequences of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35732_s_242	12810710	After inducing the expression of the cloned sequences by  galactose, the  ade2 cells harboring AtENT1 or AtENT3 coding sequences  could grow in the presence of 150 muM adenosine  ( Fig. 5 and data not shown),  indicating that adenine dependence of the  ade2 cells was rescued by  adenosine transport activities of the proteins expressed from the cloned  sequences in the four expression constructs.	transcription
55298	3	335580	5	NULL	NULL	0	NULL	statement 1			grows					adenosine		in the presence of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_37_35732_s_242	12810710	After inducing the expression of the cloned sequences by  galactose, the  ade2 cells harboring AtENT1 or AtENT3 coding sequences  could grow in the presence of 150 muM adenosine  ( Fig. 5 and data not shown),  indicating that adenine dependence of the  ade2 cells was rescued by  adenosine transport activities of the proteins expressed from the cloned  sequences in the four expression constructs.	transcription
55299	4	335580	5	NULL	NULL	0	NULL	statement 2			grows					adenosine		in the presence of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35732_s_242	12810710	After inducing the expression of the cloned sequences by  galactose, the  ade2 cells harboring AtENT1 or AtENT3 coding sequences  could grow in the presence of 150 muM adenosine  ( Fig. 5 and data not shown),  indicating that adenine dependence of the  ade2 cells was rescued by  adenosine transport activities of the proteins expressed from the cloned  sequences in the four expression constructs.	transcription
55300	5	335580	5	NULL	NULL	0	NULL	ade2 cells			is dependent on					adenine					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35732_s_242	12810710	After inducing the expression of the cloned sequences by  galactose, the  ade2 cells harboring AtENT1 or AtENT3 coding sequences  could grow in the presence of 150 muM adenosine  ( Fig. 5 and data not shown),  indicating that adenine dependence of the  ade2 cells was rescued by  adenosine transport activities of the proteins expressed from the cloned  sequences in the four expression constructs.	transcription
55301	6	335580	5	NULL	NULL	0	NULL	proteins		adenosine transport activities of;;expressed	rescues					statement 5					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35732_s_242	12810710	After inducing the expression of the cloned sequences by  galactose, the  ade2 cells harboring AtENT1 or AtENT3 coding sequences  could grow in the presence of 150 muM adenosine  ( Fig. 5 and data not shown),  indicating that adenine dependence of the  ade2 cells was rescued by  adenosine transport activities of the proteins expressed from the cloned  sequences in the four expression constructs.	transcription
60350	1	335580	7	NULL	NULL	0	NULL	ade2 cells	Cell		depend on					adenine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_37_35732_s_242	12810710	After inducing the expression of the cloned sequences by  galactose, the  ade2 cells harboring AtENT1 or AtENT3 coding sequences  could grow in the presence of 150 muM adenosine  ( Fig. 5 and data not shown),  indicating that adenine dependence of the  ade2 cells was rescued by  adenosine transport activities of the proteins expressed from the cloned  sequences in the four expression constructs.	transcription
60351	1	335581	7	NULL	NULL	0	NULL	ROR 	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1494_3_236_s_85	11121580	Because the DNA-binding affinities of ROR  and ROR  reportedly depend on sequences 5' of the consensus half site [ 2,  3,  11 and  16], the ROREs contained a thymine at position -1 and an adenine at position -4 of the nuclear receptor half site.	transcription
60352	2	335581	7	NULL	NULL	0	NULL	statement 1	Process		depend on									sequences 5' of the consensus half site 	NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1494_3_236_s_85	11121580	Because the DNA-binding affinities of ROR  and ROR  reportedly depend on sequences 5' of the consensus half site [ 2,  3,  11 and  16], the ROREs contained a thymine at position -1 and an adenine at position -4 of the nuclear receptor half site.	transcription
60353	3	335581	7	NULL	NULL	0	NULL	statement 1	Process		depend on					 nuclear receptor 	GP			ROREs containing  thymine at position -1 at half site	NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1494_3_236_s_85	11121580	Because the DNA-binding affinities of ROR  and ROR  reportedly depend on sequences 5' of the consensus half site [ 2,  3,  11 and  16], the ROREs contained a thymine at position -1 and an adenine at position -4 of the nuclear receptor half site.	transcription
60354	4	335581	7	NULL	NULL	0	NULL	statement 1	Process		depend on					nuclear receptor	GP			ROREs containing adenine at position -4 at half site	NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1494_3_236_s_85	11121580	Because the DNA-binding affinities of ROR  and ROR  reportedly depend on sequences 5' of the consensus half site [ 2,  3,  11 and  16], the ROREs contained a thymine at position -1 and an adenine at position -4 of the nuclear receptor half site.	transcription
55304	1	335582	5	NULL	NULL	0	NULL	NifL			bind					adenine nucleotides					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1594_2_243_s_212	11904220	We obtained strong evidence that (i) NifL is able to bind and hydrolyze adenine nucleotides at significant rates (  Fig. 2,  Fig. 3,  Fig. 4 and  Fig. 5), and (ii) the presence of ATP or ADP prior to open complex formation stimulates NifL inhibition of NifA transcriptional activity in vitro (  Fig. 1).	transcription
55305	2	335582	5	NULL	NULL	0	NULL	statement 1			hydrolyze					adenine nucleotides					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1594_2_243_s_212	11904220	We obtained strong evidence that (i) NifL is able to bind and hydrolyze adenine nucleotides at significant rates (  Fig. 2,  Fig. 3,  Fig. 4 and  Fig. 5), and (ii) the presence of ATP or ADP prior to open complex formation stimulates NifL inhibition of NifA transcriptional activity in vitro (  Fig. 1).	transcription
55307	3	335582	5	NULL	NULL	0	NULL	NifL			inhibits					NifA		transcriptional activity of			NULL	in vitro	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1594_2_243_s_212	11904220	We obtained strong evidence that (i) NifL is able to bind and hydrolyze adenine nucleotides at significant rates (  Fig. 2,  Fig. 3,  Fig. 4 and  Fig. 5), and (ii) the presence of ATP or ADP prior to open complex formation stimulates NifL inhibition of NifA transcriptional activity in vitro (  Fig. 1).	transcription
55308	4	335582	5	NULL	NULL	0	NULL	ATP		presence of	stimulates					statement 3					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1594_2_243_s_212	11904220	We obtained strong evidence that (i) NifL is able to bind and hydrolyze adenine nucleotides at significant rates (  Fig. 2,  Fig. 3,  Fig. 4 and  Fig. 5), and (ii) the presence of ATP or ADP prior to open complex formation stimulates NifL inhibition of NifA transcriptional activity in vitro (  Fig. 1).	transcription
55310	5	335582	5	NULL	NULL	0	NULL	statement 4			occurs prior to					open complex		formation of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1594_2_243_s_212	11904220	We obtained strong evidence that (i) NifL is able to bind and hydrolyze adenine nucleotides at significant rates (  Fig. 2,  Fig. 3,  Fig. 4 and  Fig. 5), and (ii) the presence of ATP or ADP prior to open complex formation stimulates NifL inhibition of NifA transcriptional activity in vitro (  Fig. 1).	transcription
55312	6	335582	5	NULL	NULL	0	NULL	ADP		presence of	stimulates					statement 3					NULL	in vitro	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1594_2_243_s_212	11904220	We obtained strong evidence that (i) NifL is able to bind and hydrolyze adenine nucleotides at significant rates (  Fig. 2,  Fig. 3,  Fig. 4 and  Fig. 5), and (ii) the presence of ATP or ADP prior to open complex formation stimulates NifL inhibition of NifA transcriptional activity in vitro (  Fig. 1).	transcription
55313	7	335582	5	NULL	NULL	0	NULL	statement 6			occurs prior to					open complex		formation of			NULL	in vitro	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1594_2_243_s_212	11904220	We obtained strong evidence that (i) NifL is able to bind and hydrolyze adenine nucleotides at significant rates (  Fig. 2,  Fig. 3,  Fig. 4 and  Fig. 5), and (ii) the presence of ATP or ADP prior to open complex formation stimulates NifL inhibition of NifA transcriptional activity in vitro (  Fig. 1).	transcription
60355	1	335582	7	NULL	NULL	0	NULL	NifL	GP		bind					adenine nucleotides	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1594_2_243_s_212	11904220	We obtained strong evidence that (i) NifL is able to bind and hydrolyze adenine nucleotides at significant rates (  Fig. 2,  Fig. 3,  Fig. 4 and  Fig. 5), and (ii) the presence of ATP or ADP prior to open complex formation stimulates NifL inhibition of NifA transcriptional activity in vitro (  Fig. 1).	transcription
60356	2	335582	7	NULL	NULL	0	NULL	statement 1	Process		hydrolyze					adenine nucleotides	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1594_2_243_s_212	11904220	We obtained strong evidence that (i) NifL is able to bind and hydrolyze adenine nucleotides at significant rates (  Fig. 2,  Fig. 3,  Fig. 4 and  Fig. 5), and (ii) the presence of ATP or ADP prior to open complex formation stimulates NifL inhibition of NifA transcriptional activity in vitro (  Fig. 1).	transcription
60357	3	335582	7	NULL	NULL	0	NULL	NifL	GP		inhibit					NifA 	GP	transcriptional activity of			NULL	in vitro	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1594_2_243_s_212	11904220	We obtained strong evidence that (i) NifL is able to bind and hydrolyze adenine nucleotides at significant rates (  Fig. 2,  Fig. 3,  Fig. 4 and  Fig. 5), and (ii) the presence of ATP or ADP prior to open complex formation stimulates NifL inhibition of NifA transcriptional activity in vitro (  Fig. 1).	transcription
60358	4	335582	7	NULL	NULL	0	NULL	ATP	Chemical	presence of	stimulate					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1594_2_243_s_212	11904220	We obtained strong evidence that (i) NifL is able to bind and hydrolyze adenine nucleotides at significant rates (  Fig. 2,  Fig. 3,  Fig. 4 and  Fig. 5), and (ii) the presence of ATP or ADP prior to open complex formation stimulates NifL inhibition of NifA transcriptional activity in vitro (  Fig. 1).	transcription
60359	5	335582	7	NULL	NULL	0	NULL	ADP	Chemical	presence of	stimulate					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1594_2_243_s_212	11904220	We obtained strong evidence that (i) NifL is able to bind and hydrolyze adenine nucleotides at significant rates (  Fig. 2,  Fig. 3,  Fig. 4 and  Fig. 5), and (ii) the presence of ATP or ADP prior to open complex formation stimulates NifL inhibition of NifA transcriptional activity in vitro (  Fig. 1).	transcription
60360	6	335582	7	NULL	NULL	0	NULL	statement 4	Process		occur prior to					open complex	Process	formation of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1594_2_243_s_212	11904220	We obtained strong evidence that (i) NifL is able to bind and hydrolyze adenine nucleotides at significant rates (  Fig. 2,  Fig. 3,  Fig. 4 and  Fig. 5), and (ii) the presence of ATP or ADP prior to open complex formation stimulates NifL inhibition of NifA transcriptional activity in vitro (  Fig. 1).	transcription
60361	7	335582	7	NULL	NULL	0	NULL	statement 5	Process		occur prior to					open complex	Process	formation of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1594_2_243_s_212	11904220	We obtained strong evidence that (i) NifL is able to bind and hydrolyze adenine nucleotides at significant rates (  Fig. 2,  Fig. 3,  Fig. 4 and  Fig. 5), and (ii) the presence of ATP or ADP prior to open complex formation stimulates NifL inhibition of NifA transcriptional activity in vitro (  Fig. 1).	transcription
60362	8	335582	7	NULL	NULL	0	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1594_2_243_s_212	11904220	We obtained strong evidence that (i) NifL is able to bind and hydrolyze adenine nucleotides at significant rates (  Fig. 2,  Fig. 3,  Fig. 4 and  Fig. 5), and (ii) the presence of ATP or ADP prior to open complex formation stimulates NifL inhibition of NifA transcriptional activity in vitro (  Fig. 1).	transcription
55314	1	335583	5	NULL	NULL	0	NULL	nucleoside transporters			is sensitive to					NBMPR					NULL		0	NULL	NULL	NULL	gw60_circulationres_90_5_570_s_146	11909821	5, 38, 39 Thus, the inhibition of adenosine transport by elevated D-glucose and adenine or uridine nucleotides could be due to the reduced number rather than the activity of an existing pool of NBMPR-sensitive nucleoside transporters in the plasma membrane of HUVECs.	transcription
55315	2	335583	5	NULL	NULL	0	NULL	statement 1			is present in					HUVECs		plasma membrane			NULL		0	NULL	NULL	NULL	gw60_circulationres_90_5_570_s_146	11909821	5, 38, 39 Thus, the inhibition of adenosine transport by elevated D-glucose and adenine or uridine nucleotides could be due to the reduced number rather than the activity of an existing pool of NBMPR-sensitive nucleoside transporters in the plasma membrane of HUVECs.	transcription
55316	3	335583	5	NULL	NULL	0	NULL	D-glucose		elevated 	inhibits					adenosine		transport of			NULL	plasma membrane of HUVECs	NULL	NULL	NULL	NULL	gw60_circulationres_90_5_570_s_146	11909821	5, 38, 39 Thus, the inhibition of adenosine transport by elevated D-glucose and adenine or uridine nucleotides could be due to the reduced number rather than the activity of an existing pool of NBMPR-sensitive nucleoside transporters in the plasma membrane of HUVECs.	transcription
55317	4	335583	5	NULL	NULL	0	NULL	statement 1		reduced number of	leads to					statement 3					NULL	plasma membrane of HUVECs	0	NULL	NULL	NULL	gw60_circulationres_90_5_570_s_146	11909821	5, 38, 39 Thus, the inhibition of adenosine transport by elevated D-glucose and adenine or uridine nucleotides could be due to the reduced number rather than the activity of an existing pool of NBMPR-sensitive nucleoside transporters in the plasma membrane of HUVECs.	transcription
55318	5	335583	5	NULL	NULL	0	NULL	adenine nucleotides		elevated	inhibits					adenosine		transport of			NULL	plasma membrane of HUVECs	0	NULL	NULL	NULL	gw60_circulationres_90_5_570_s_146	11909821	5, 38, 39 Thus, the inhibition of adenosine transport by elevated D-glucose and adenine or uridine nucleotides could be due to the reduced number rather than the activity of an existing pool of NBMPR-sensitive nucleoside transporters in the plasma membrane of HUVECs.	transcription
55319	6	335583	5	NULL	NULL	0	NULL	uridine nucleotides		elevated	inhibits					adenosine		transport of			NULL	plasma membrane of HUVECs	0	NULL	NULL	NULL	gw60_circulationres_90_5_570_s_146	11909821	5, 38, 39 Thus, the inhibition of adenosine transport by elevated D-glucose and adenine or uridine nucleotides could be due to the reduced number rather than the activity of an existing pool of NBMPR-sensitive nucleoside transporters in the plasma membrane of HUVECs.	transcription
55321	7	335583	5	NULL	NULL	0	NULL	statement 5			is an alternative to					statement 6					NULL		0	NULL	NULL	NULL	gw60_circulationres_90_5_570_s_146	11909821	5, 38, 39 Thus, the inhibition of adenosine transport by elevated D-glucose and adenine or uridine nucleotides could be due to the reduced number rather than the activity of an existing pool of NBMPR-sensitive nucleoside transporters in the plasma membrane of HUVECs.	transcription
55323	8	335583	5	NULL	NULL	0	NULL	statement 1		reduced number of	leads to					statement 7					NULL	plasma membrane of HUVECs	0	NULL	NULL	NULL	gw60_circulationres_90_5_570_s_146	11909821	5, 38, 39 Thus, the inhibition of adenosine transport by elevated D-glucose and adenine or uridine nucleotides could be due to the reduced number rather than the activity of an existing pool of NBMPR-sensitive nucleoside transporters in the plasma membrane of HUVECs.	transcription
60363	1	335583	7	NULL	NULL	0	NULL	D-glucose	Chemical	elevated	inhibit					adenosine 	Chemical	transport of			NULL		0	NULL	NULL	NULL	gw60_circulationres_90_5_570_s_146	11909821	5, 38, 39 Thus, the inhibition of adenosine transport by elevated D-glucose and adenine or uridine nucleotides could be due to the reduced number rather than the activity of an existing pool of NBMPR-sensitive nucleoside transporters in the plasma membrane of HUVECs.	transcription
60364	2	335583	7	NULL	NULL	0	NULL	adenine nucleotide	NucleicAcid	elevated	inhibit					adenosine	Chemical	transport of			NULL		NULL	NULL	NULL	NULL	gw60_circulationres_90_5_570_s_146	11909821	5, 38, 39 Thus, the inhibition of adenosine transport by elevated D-glucose and adenine or uridine nucleotides could be due to the reduced number rather than the activity of an existing pool of NBMPR-sensitive nucleoside transporters in the plasma membrane of HUVECs.	transcription
60365	3	335583	7	NULL	NULL	0	NULL	uridine nucleotide	NucleicAcid	elevated	inhibit					adenosine	Chemical	transport of			NULL		0	NULL	NULL	NULL	gw60_circulationres_90_5_570_s_146	11909821	5, 38, 39 Thus, the inhibition of adenosine transport by elevated D-glucose and adenine or uridine nucleotides could be due to the reduced number rather than the activity of an existing pool of NBMPR-sensitive nucleoside transporters in the plasma membrane of HUVECs.	transcription
60366	4	335583	7	NULL	NULL	0	NULL	statement 1	Process		is not due to					NBMPR-sensitive nucleoside transporters	Chemical	activity of			NULL	plasma membrane of HUVECs	NULL	NULL	NULL	NULL	gw60_circulationres_90_5_570_s_146	11909821	5, 38, 39 Thus, the inhibition of adenosine transport by elevated D-glucose and adenine or uridine nucleotides could be due to the reduced number rather than the activity of an existing pool of NBMPR-sensitive nucleoside transporters in the plasma membrane of HUVECs.	transcription
60367	5	335583	7	NULL	NULL	0	NULL	statement 2	Process		is not due to					NBMPR-sensitive nucleoside transporters	Chemical	activity of			NULL	plasma membrane of HUVECs	0	NULL	NULL	NULL	gw60_circulationres_90_5_570_s_146	11909821	5, 38, 39 Thus, the inhibition of adenosine transport by elevated D-glucose and adenine or uridine nucleotides could be due to the reduced number rather than the activity of an existing pool of NBMPR-sensitive nucleoside transporters in the plasma membrane of HUVECs.	transcription
60368	6	335583	7	NULL	NULL	0	NULL	statement 3	Process		is not due to					NBMPR-sensitive nucleoside transporters	Chemical	activity of			NULL	plasma membrane of HUVECs	0	NULL	NULL	NULL	gw60_circulationres_90_5_570_s_146	11909821	5, 38, 39 Thus, the inhibition of adenosine transport by elevated D-glucose and adenine or uridine nucleotides could be due to the reduced number rather than the activity of an existing pool of NBMPR-sensitive nucleoside transporters in the plasma membrane of HUVECs.	transcription
55324	2	335584	5	NULL	NULL	0	NULL	Oct-1			bind			Asn-429		statement 1					NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_333	10409735	The crystal structure of Oct-1 bound to DNA has shown that critical contact is made between a specific amino acid (Asn-429) of Oct-1 and the adenine nucleotide which base pairs with the second thymine of the Octamer motif (5''-A TTA/TGCAT-3'') ( 19).	transcription
55327	1	335584	5	NULL	NULL	0	NULL	DNA			base pairs with			adenine nucleotide		DNA			thymine of Octamer motif (5''-A TTA/TGCAT-3'')		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_333	10409735	The crystal structure of Oct-1 bound to DNA has shown that critical contact is made between a specific amino acid (Asn-429) of Oct-1 and the adenine nucleotide which base pairs with the second thymine of the Octamer motif (5''-A TTA/TGCAT-3'') ( 19).	transcription
60369	1	335584	7	NULL	NULL	0	NULL	Oct-1	GP		bind					DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_333	10409735	The crystal structure of Oct-1 bound to DNA has shown that critical contact is made between a specific amino acid (Asn-429) of Oct-1 and the adenine nucleotide which base pairs with the second thymine of the Octamer motif (5''-A TTA/TGCAT-3'') ( 19).	transcription
60370	2	335584	7	NULL	NULL	0	NULL	Oct-1	GP		contact with			Asn-429		adenine nucleotide	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_333	10409735	The crystal structure of Oct-1 bound to DNA has shown that critical contact is made between a specific amino acid (Asn-429) of Oct-1 and the adenine nucleotide which base pairs with the second thymine of the Octamer motif (5''-A TTA/TGCAT-3'') ( 19).	transcription
60371	3	335584	7	NULL	NULL	0	NULL	adenine nucleotide	NucleicAcid		base pair with					thymine	NucleicAcid			Octamer motif (5''-A TTA/TGCAT-3'')	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_8_5453_s_333	10409735	The crystal structure of Oct-1 bound to DNA has shown that critical contact is made between a specific amino acid (Asn-429) of Oct-1 and the adenine nucleotide which base pairs with the second thymine of the Octamer motif (5''-A TTA/TGCAT-3'') ( 19).	transcription
55328	1	335585	5	NULL	NULL	0	NULL	Tg			pairs with					adenine					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6111_s_298	12167705	Furthermore, under our conditions  E. coli endonuclease IV did not efficiently cleave Tg paired either with adenine or guanine (Fig.  5, lanes 2 and 13), thereby making it unlikely that a mammalian endonuclease IV-like enzyme is responsible for the residual activity ( 16).	transcription
55330	2	335585	5	NULL	NULL	0	NULL	Tg			pairs with					guanine					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6111_s_298	12167705	Furthermore, under our conditions  E. coli endonuclease IV did not efficiently cleave Tg paired either with adenine or guanine (Fig.  5, lanes 2 and 13), thereby making it unlikely that a mammalian endonuclease IV-like enzyme is responsible for the residual activity ( 16).	transcription
55332	3	335585	5	NULL	NULL	0	NULL	endonuclease IV		E. coli	does not cleave		efficiently			statement 1					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6111_s_298	12167705	Furthermore, under our conditions  E. coli endonuclease IV did not efficiently cleave Tg paired either with adenine or guanine (Fig.  5, lanes 2 and 13), thereby making it unlikely that a mammalian endonuclease IV-like enzyme is responsible for the residual activity ( 16).	transcription
55333	4	335585	5	NULL	NULL	0	NULL	endonuclease IV		E. coli	does not cleave		efficiently			statement 2					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6111_s_298	12167705	Furthermore, under our conditions  E. coli endonuclease IV did not efficiently cleave Tg paired either with adenine or guanine (Fig.  5, lanes 2 and 13), thereby making it unlikely that a mammalian endonuclease IV-like enzyme is responsible for the residual activity ( 16).	transcription
55334	5	335585	5	NULL	NULL	0	NULL	statement 1			is an alternative to					statement 2					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6111_s_298	12167705	Furthermore, under our conditions  E. coli endonuclease IV did not efficiently cleave Tg paired either with adenine or guanine (Fig.  5, lanes 2 and 13), thereby making it unlikely that a mammalian endonuclease IV-like enzyme is responsible for the residual activity ( 16).	transcription
60372	1	335585	7	NULL	NULL	0	NULL	Tg 	Chemical		pair with					adenine	Chemical				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6111_s_298	12167705	Furthermore, under our conditions  E. coli endonuclease IV did not efficiently cleave Tg paired either with adenine or guanine (Fig.  5, lanes 2 and 13), thereby making it unlikely that a mammalian endonuclease IV-like enzyme is responsible for the residual activity ( 16).	transcription
60373	2	335585	7	NULL	NULL	0	NULL	Tg	Chemical		pair with					guanine	Chemical				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6111_s_298	12167705	Furthermore, under our conditions  E. coli endonuclease IV did not efficiently cleave Tg paired either with adenine or guanine (Fig.  5, lanes 2 and 13), thereby making it unlikely that a mammalian endonuclease IV-like enzyme is responsible for the residual activity ( 16).	transcription
60374	3	335585	7	NULL	NULL	0	NULL	endonuclease IV	GP	E.coli	does not cleave		efficiently			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6111_s_298	12167705	Furthermore, under our conditions  E. coli endonuclease IV did not efficiently cleave Tg paired either with adenine or guanine (Fig.  5, lanes 2 and 13), thereby making it unlikely that a mammalian endonuclease IV-like enzyme is responsible for the residual activity ( 16).	transcription
60375	4	335585	7	NULL	NULL	0	NULL	endonuclease IV	GP	E.coli	does not cleave		efficiently			statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6111_s_298	12167705	Furthermore, under our conditions  E. coli endonuclease IV did not efficiently cleave Tg paired either with adenine or guanine (Fig.  5, lanes 2 and 13), thereby making it unlikely that a mammalian endonuclease IV-like enzyme is responsible for the residual activity ( 16).	transcription
60376	5	335585	7	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6111_s_298	12167705	Furthermore, under our conditions  E. coli endonuclease IV did not efficiently cleave Tg paired either with adenine or guanine (Fig.  5, lanes 2 and 13), thereby making it unlikely that a mammalian endonuclease IV-like enzyme is responsible for the residual activity ( 16).	transcription
60377	6	335585	7	NULL	NULL	0	NULL	endonuclease IV-like enzyme	GP 	mammalian	is not responsible for					residual activity	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6111_s_298	12167705	Furthermore, under our conditions  E. coli endonuclease IV did not efficiently cleave Tg paired either with adenine or guanine (Fig.  5, lanes 2 and 13), thereby making it unlikely that a mammalian endonuclease IV-like enzyme is responsible for the residual activity ( 16).	transcription
60378	7	335585	7	NULL	NULL	0	NULL	statement 3	Process		indicate					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6111_s_298	12167705	Furthermore, under our conditions  E. coli endonuclease IV did not efficiently cleave Tg paired either with adenine or guanine (Fig.  5, lanes 2 and 13), thereby making it unlikely that a mammalian endonuclease IV-like enzyme is responsible for the residual activity ( 16).	transcription
60379	8	335585	7	NULL	NULL	0	NULL	statement 4	Process		indicate					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6111_s_298	12167705	Furthermore, under our conditions  E. coli endonuclease IV did not efficiently cleave Tg paired either with adenine or guanine (Fig.  5, lanes 2 and 13), thereby making it unlikely that a mammalian endonuclease IV-like enzyme is responsible for the residual activity ( 16).	transcription
55335	1	335587	5	NULL	NULL	0	NULL	genomic DNA		Sodalis	methylated at		extensively			adenine residues					NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_15_4517_s_128	11443086	Neither the plasmid nor the chromosomal DNA could be digested with Dam-sensitive restriction enzyme  MboI (Fig.  6, lanes 5), while the same DNAs were cleaved with its isoschizomer  Sau3AI (Fig.  6, lanes 4), indicating that  Sodalis genomic as well as plasmid DNAs are extensively methylated at the adenine residues.	transcription
55336	2	335587	5	NULL	NULL	0	NULL	plasmid DNA		Sodalis	methylated at		extensively			adenine residues					NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_183_15_4517_s_128	11443086	Neither the plasmid nor the chromosomal DNA could be digested with Dam-sensitive restriction enzyme  MboI (Fig.  6, lanes 5), while the same DNAs were cleaved with its isoschizomer  Sau3AI (Fig.  6, lanes 4), indicating that  Sodalis genomic as well as plasmid DNAs are extensively methylated at the adenine residues.	transcription
60380	1	335587	7	NULL	NULL	0	NULL	MboI	GP		does not digest					plasmid DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_15_4517_s_128	11443086	Neither the plasmid nor the chromosomal DNA could be digested with Dam-sensitive restriction enzyme  MboI (Fig.  6, lanes 5), while the same DNAs were cleaved with its isoschizomer  Sau3AI (Fig.  6, lanes 4), indicating that  Sodalis genomic as well as plasmid DNAs are extensively methylated at the adenine residues.	transcription
60381	2	335587	7	NULL	NULL	0	NULL	MboI	GP		does not digest					chromosomal DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_15_4517_s_128	11443086	Neither the plasmid nor the chromosomal DNA could be digested with Dam-sensitive restriction enzyme  MboI (Fig.  6, lanes 5), while the same DNAs were cleaved with its isoschizomer  Sau3AI (Fig.  6, lanes 4), indicating that  Sodalis genomic as well as plasmid DNAs are extensively methylated at the adenine residues.	transcription
60382	3	335587	7	NULL	NULL	0	NULL	MboI	GP		is sensitive to					Dam	GP				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_15_4517_s_128	11443086	Neither the plasmid nor the chromosomal DNA could be digested with Dam-sensitive restriction enzyme  MboI (Fig.  6, lanes 5), while the same DNAs were cleaved with its isoschizomer  Sau3AI (Fig.  6, lanes 4), indicating that  Sodalis genomic as well as plasmid DNAs are extensively methylated at the adenine residues.	transcription
60383	4	335587	7	NULL	NULL	0	NULL	Sau3AI	GP		cleaves					plasmid DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_15_4517_s_128	11443086	Neither the plasmid nor the chromosomal DNA could be digested with Dam-sensitive restriction enzyme  MboI (Fig.  6, lanes 5), while the same DNAs were cleaved with its isoschizomer  Sau3AI (Fig.  6, lanes 4), indicating that  Sodalis genomic as well as plasmid DNAs are extensively methylated at the adenine residues.	transcription
60384	5	335587	7	NULL	NULL	0	NULL	Sau3AI	GP		cleaves					chromosomal DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_15_4517_s_128	11443086	Neither the plasmid nor the chromosomal DNA could be digested with Dam-sensitive restriction enzyme  MboI (Fig.  6, lanes 5), while the same DNAs were cleaved with its isoschizomer  Sau3AI (Fig.  6, lanes 4), indicating that  Sodalis genomic as well as plasmid DNAs are extensively methylated at the adenine residues.	transcription
60385	6	335587	7	NULL	NULL	0	NULL	 genomic DNA	NucleicAcid	Sodalis	is methylated at					adenine residues	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_15_4517_s_128	11443086	Neither the plasmid nor the chromosomal DNA could be digested with Dam-sensitive restriction enzyme  MboI (Fig.  6, lanes 5), while the same DNAs were cleaved with its isoschizomer  Sau3AI (Fig.  6, lanes 4), indicating that  Sodalis genomic as well as plasmid DNAs are extensively methylated at the adenine residues.	transcription
60386	7	335587	7	NULL	NULL	0	NULL	plasmid DNAs	NucleicAcid	Sodalis	is methylated at					adenine residues	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_15_4517_s_128	11443086	Neither the plasmid nor the chromosomal DNA could be digested with Dam-sensitive restriction enzyme  MboI (Fig.  6, lanes 5), while the same DNAs were cleaved with its isoschizomer  Sau3AI (Fig.  6, lanes 4), indicating that  Sodalis genomic as well as plasmid DNAs are extensively methylated at the adenine residues.	transcription
60387	8	335587	7	NULL	NULL	0	NULL	statement 4	Process		indicate					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_15_4517_s_128	11443086	Neither the plasmid nor the chromosomal DNA could be digested with Dam-sensitive restriction enzyme  MboI (Fig.  6, lanes 5), while the same DNAs were cleaved with its isoschizomer  Sau3AI (Fig.  6, lanes 4), indicating that  Sodalis genomic as well as plasmid DNAs are extensively methylated at the adenine residues.	transcription
60388	9	335587	7	NULL	NULL	0	NULL	statement 5	Process		indicate					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_15_4517_s_128	11443086	Neither the plasmid nor the chromosomal DNA could be digested with Dam-sensitive restriction enzyme  MboI (Fig.  6, lanes 5), while the same DNAs were cleaved with its isoschizomer  Sau3AI (Fig.  6, lanes 4), indicating that  Sodalis genomic as well as plasmid DNAs are extensively methylated at the adenine residues.	transcription
60389	10	335587	7	NULL	NULL	0	NULL	Sau3AI	GP		is an isoschizomer of 					MboI 	GP				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_183_15_4517_s_128	11443086	Neither the plasmid nor the chromosomal DNA could be digested with Dam-sensitive restriction enzyme  MboI (Fig.  6, lanes 5), while the same DNAs were cleaved with its isoschizomer  Sau3AI (Fig.  6, lanes 4), indicating that  Sodalis genomic as well as plasmid DNAs are extensively methylated at the adenine residues.	transcription
55337	1	335588	5	NULL	NULL	0	NULL	ACh			is					acetylcholine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
55338	2	335588	5	NULL	NULL	0	NULL	ACh			is a type of					neurotransmitter					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
55339	3	335588	5	NULL	NULL	0	NULL	Ca2+			is relased from					ER					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
55340	4	335588	5	NULL	NULL	0	NULL	statement 3			via					IP3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
55341	5	335588	5	NULL	NULL	0	NULL	ACh			stimulates					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
55342	6	335588	5	NULL	NULL	0	NULL	IP3			is					inositol 1,4,5-trisphosphate					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
55343	7	335588	5	NULL	NULL	0	NULL	CCK			is					cholecystokinin					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
55344	8	335588	5	NULL	NULL	0	NULL	CCK			is a type of					hormone					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
55345	9	335588	5	NULL	NULL	0	NULL	IP3			is a type of					messenger					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
55346	10	335588	5	NULL	NULL	0	NULL	cyclic ADP- ribose			is a type of					messenger					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
55348	11	335588	5	NULL	NULL	0	NULL	NAADP			is a type of					messenger					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
55349	12	335588	5	NULL	NULL	0	NULL	NAADP			is					nicotinic acid adenine dinucleotide phosphate					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
55350	13	335588	5	NULL	NULL	0	NULL	IP3			interacts with					cyclic ADP- ribose					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
55351	14	335588	5	NULL	NULL	0	NULL	IP3			interacts with					NAADP					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
55352	15	335588	5	NULL	NULL	0	NULL	statement 13			occurs simultaneously with					statement 14					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
55353	16	335588	5	NULL	NULL	0	NULL	Ca2+			is released by					statement 15					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
55354	17	335588	5	NULL	NULL	0	NULL	CCK			evokes					statement 16					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
60390	1	335588	7	NULL	NULL	0	NULL	ACh	Chemical		stimulates					Ca2+	Chemical	release of			NULL	pancreatic acinar cell 	0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
60391	2	335588	7	NULL	NULL	0	NULL	statement 1	Process		occur from					ER	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
60392	3	335588	7	NULL	NULL	0	NULL	statement 2	Process		occur via					IP3	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
60393	4	335588	7	NULL	NULL	0	NULL	CCK	GP		evokes					Ca2+	Chemical	release of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
60394	5	335588	7	NULL	NULL	0	NULL	IP3	Chemical		interacts with					cyclic ADP- ribose	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
60395	6	335588	7	NULL	NULL	0	NULL	statement 5	Process		interacts with					NAADP	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
60396	7	335588	7	NULL	NULL	0	NULL	statement 4	Process		occur by					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
60397	8	335588	7	NULL	NULL	0	NULL	statement 4	Process		occur by					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
60398	9	335588	7	NULL	NULL	0	NULL	ACh	Chemical		is a type of					neurotransmitter	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
60399	10	335588	7	NULL	NULL	0	NULL	ACh	Chemical		is					acetylcholine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
60400	11	335588	7	NULL	NULL	0	NULL	IP3	Chemical		is					inositol 1,4,5-trisphosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
60401	12	335588	7	NULL	NULL	0	NULL	CCK	GP		is					cholecystokinin	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
60402	13	335588	7	NULL	NULL	0	NULL	NAADP	Chemical		is					nicotinic acid adenine dinucleotide phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_26479_s_12	11994289	Thus, in the pancreatic acinar cell the neurotransmitter acetylcholine (ACh) stimulates the release of Ca2+ from the ER via inositol 1,4,5-trisphosphate (IP3), while the hormone cholecystokinin (CCK) evokes Ca2+ release by a complex interaction between the messengers IP3, cyclic ADP- ribose, and nicotinic acid adenine dinucleotide phosphate (NAADP) ( 5).	transcription
55358	1	335589	5	NULL	NULL	0	NULL	succinate dehydrogenase			is activated by					adenine nucleotides					NULL	cauliflower mitochondria	0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32567_s_233	11350973	This observation agrees well with the earlier findings that activation of succinate dehydrogenase by adenine nucleotides in cauliflower mitochondria is negatively affected by sonication or freeze-thawing treatments ( 5) and that the mammalian succinate dehydrogenase is not at all activated by ATP when studied in a solubilized form or in sub-mitochondrial particles ( 3).	transcription
55360	2	335589	5	NULL	NULL	0	NULL	sonication		treatment	affects		negatively			statement 1					NULL	cauliflower mitochondria	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_35_32567_s_233	11350973	This observation agrees well with the earlier findings that activation of succinate dehydrogenase by adenine nucleotides in cauliflower mitochondria is negatively affected by sonication or freeze-thawing treatments ( 5) and that the mammalian succinate dehydrogenase is not at all activated by ATP when studied in a solubilized form or in sub-mitochondrial particles ( 3).	transcription
55361	3	335589	5	NULL	NULL	0	NULL	freeze-thawing		treatment	affects		negatively			statement 1					NULL	cauliflower mitochondria	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_35_32567_s_233	11350973	This observation agrees well with the earlier findings that activation of succinate dehydrogenase by adenine nucleotides in cauliflower mitochondria is negatively affected by sonication or freeze-thawing treatments ( 5) and that the mammalian succinate dehydrogenase is not at all activated by ATP when studied in a solubilized form or in sub-mitochondrial particles ( 3).	transcription
55362	4	335589	5	NULL	NULL	0	NULL	statement 2			is an alternative to					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32567_s_233	11350973	This observation agrees well with the earlier findings that activation of succinate dehydrogenase by adenine nucleotides in cauliflower mitochondria is negatively affected by sonication or freeze-thawing treatments ( 5) and that the mammalian succinate dehydrogenase is not at all activated by ATP when studied in a solubilized form or in sub-mitochondrial particles ( 3).	transcription
55364	5	335589	5	NULL	NULL	0	NULL	succinate dehydrogenase		mammalian;;soluble	is not activated by					ATP					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32567_s_233	11350973	This observation agrees well with the earlier findings that activation of succinate dehydrogenase by adenine nucleotides in cauliflower mitochondria is negatively affected by sonication or freeze-thawing treatments ( 5) and that the mammalian succinate dehydrogenase is not at all activated by ATP when studied in a solubilized form or in sub-mitochondrial particles ( 3).	transcription
55366	6	335589	5	NULL	NULL	0	NULL	succinate dehydrogenase		mammalian	is not activated by					ATP					NULL	sub-mitochondrial particles	0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32567_s_233	11350973	This observation agrees well with the earlier findings that activation of succinate dehydrogenase by adenine nucleotides in cauliflower mitochondria is negatively affected by sonication or freeze-thawing treatments ( 5) and that the mammalian succinate dehydrogenase is not at all activated by ATP when studied in a solubilized form or in sub-mitochondrial particles ( 3).	transcription
60403	1	335589	7	NULL	NULL	0	NULL	adenine nucleotides	NucleicAcid		activates					succinate dehydrogenase	GP				NULL	cauliflower mitochondria	0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32567_s_233	11350973	This observation agrees well with the earlier findings that activation of succinate dehydrogenase by adenine nucleotides in cauliflower mitochondria is negatively affected by sonication or freeze-thawing treatments ( 5) and that the mammalian succinate dehydrogenase is not at all activated by ATP when studied in a solubilized form or in sub-mitochondrial particles ( 3).	transcription
60404	2	335589	7	NULL	NULL	0	NULL	statement 1	Process		affected by		negatively			sonication	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32567_s_233	11350973	This observation agrees well with the earlier findings that activation of succinate dehydrogenase by adenine nucleotides in cauliflower mitochondria is negatively affected by sonication or freeze-thawing treatments ( 5) and that the mammalian succinate dehydrogenase is not at all activated by ATP when studied in a solubilized form or in sub-mitochondrial particles ( 3).	transcription
60405	3	335589	7	NULL	NULL	0	NULL	statement 1	Process		affected by		negatively			freeze-thawing	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32567_s_233	11350973	This observation agrees well with the earlier findings that activation of succinate dehydrogenase by adenine nucleotides in cauliflower mitochondria is negatively affected by sonication or freeze-thawing treatments ( 5) and that the mammalian succinate dehydrogenase is not at all activated by ATP when studied in a solubilized form or in sub-mitochondrial particles ( 3).	transcription
60406	4	335589	7	NULL	NULL	0	NULL	 ATP	Chemical		does not activate					succinate dehydrogenase	GP	mammalian			NULL	sub-mitochondrial particles 	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_35_32567_s_233	11350973	This observation agrees well with the earlier findings that activation of succinate dehydrogenase by adenine nucleotides in cauliflower mitochondria is negatively affected by sonication or freeze-thawing treatments ( 5) and that the mammalian succinate dehydrogenase is not at all activated by ATP when studied in a solubilized form or in sub-mitochondrial particles ( 3).	transcription
60407	5	335589	7	NULL	NULL	0	NULL	ATP	Chemical		does not activate					succinate dehydrogenase	GP	mammalian;;solubilized			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_35_32567_s_233	11350973	This observation agrees well with the earlier findings that activation of succinate dehydrogenase by adenine nucleotides in cauliflower mitochondria is negatively affected by sonication or freeze-thawing treatments ( 5) and that the mammalian succinate dehydrogenase is not at all activated by ATP when studied in a solubilized form or in sub-mitochondrial particles ( 3).	transcription
55368	1	335590	5	NULL	NULL	0	NULL	oligonucleotide duplex		synthetic	carries									abasic site	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_25_15650_s_165	9188454	A recent methylation interference analysis of Ape interaction with a synthetic oligonucleotide duplex carrying an abasic site on one strand displayed a substantial interference signal from an adenine two nucleotides 5  to the abasic site (equivalent to the guanine lying between the two thymines marked in Fig.  7) ( 35).	transcription
55369	2	335590	5	NULL	NULL	0	NULL	Ape			interacts with					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_25_15650_s_165	9188454	A recent methylation interference analysis of Ape interaction with a synthetic oligonucleotide duplex carrying an abasic site on one strand displayed a substantial interference signal from an adenine two nucleotides 5  to the abasic site (equivalent to the guanine lying between the two thymines marked in Fig.  7) ( 35).	transcription
60408	1	335590	7	NULL	NULL	0	NULL	oligonucleotide duplex 	NucleicAcid		carry									abasic site on one strand 	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_25_15650_s_165	9188454	A recent methylation interference analysis of Ape interaction with a synthetic oligonucleotide duplex carrying an abasic site on one strand displayed a substantial interference signal from an adenine two nucleotides 5  to the abasic site (equivalent to the guanine lying between the two thymines marked in Fig.  7) ( 35).	transcription
60409	2	335590	7	NULL	NULL	0	NULL	Ape	Chemical		interacts with					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_25_15650_s_165	9188454	A recent methylation interference analysis of Ape interaction with a synthetic oligonucleotide duplex carrying an abasic site on one strand displayed a substantial interference signal from an adenine two nucleotides 5  to the abasic site (equivalent to the guanine lying between the two thymines marked in Fig.  7) ( 35).	transcription
60410	3	335590	7	NULL	NULL	0	NULL	statement 2	Process		is interferred by					adenine	Chemical	signal from			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_25_15650_s_165	9188454	A recent methylation interference analysis of Ape interaction with a synthetic oligonucleotide duplex carrying an abasic site on one strand displayed a substantial interference signal from an adenine two nucleotides 5  to the abasic site (equivalent to the guanine lying between the two thymines marked in Fig.  7) ( 35).	transcription
60411	4	335590	7	NULL	NULL	0	NULL	adenine	Chemical		is located at									two nucleotides 5 to the abasic site	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_25_15650_s_165	9188454	A recent methylation interference analysis of Ape interaction with a synthetic oligonucleotide duplex carrying an abasic site on one strand displayed a substantial interference signal from an adenine two nucleotides 5  to the abasic site (equivalent to the guanine lying between the two thymines marked in Fig.  7) ( 35).	transcription
55383	1	335591	5	NULL	NULL	0	NULL	ScCKmit			couple with		functionally			ATP-ADP carrier					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6937_s_24	10702255	Considering the functional coupling of the ScCKmit with the ATP-ADP carrier and the restricted permeability of the outer mitochondrial membrane for adenine nucleotides ( 5,  14), the ADP produced in the intermembrane space by ScCKmit could be more efficient to stimulate the respiration than ADP produced directly in the cytoplasm ( 15).	transcription
55384	2	335591	5	NULL	NULL	0	NULL	mitochondrial membrane		outer	permiable to		restricted			adenine nucleotides					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6937_s_24	10702255	Considering the functional coupling of the ScCKmit with the ATP-ADP carrier and the restricted permeability of the outer mitochondrial membrane for adenine nucleotides ( 5,  14), the ADP produced in the intermembrane space by ScCKmit could be more efficient to stimulate the respiration than ADP produced directly in the cytoplasm ( 15).	transcription
55385	3	335591	5	NULL	NULL	0	NULL	ADP			is produced by					ScCKmit					NULL	intermembrane space	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_10_6937_s_24	10702255	Considering the functional coupling of the ScCKmit with the ATP-ADP carrier and the restricted permeability of the outer mitochondrial membrane for adenine nucleotides ( 5,  14), the ADP produced in the intermembrane space by ScCKmit could be more efficient to stimulate the respiration than ADP produced directly in the cytoplasm ( 15).	transcription
55387	4	335591	5	NULL	NULL	0	NULL	ADP			is produced in		directly			cytoplasm					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6937_s_24	10702255	Considering the functional coupling of the ScCKmit with the ATP-ADP carrier and the restricted permeability of the outer mitochondrial membrane for adenine nucleotides ( 5,  14), the ADP produced in the intermembrane space by ScCKmit could be more efficient to stimulate the respiration than ADP produced directly in the cytoplasm ( 15).	transcription
55391	5	335591	5	NULL	NULL	0	NULL	statement 3			stimulates					respiration					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6937_s_24	10702255	Considering the functional coupling of the ScCKmit with the ATP-ADP carrier and the restricted permeability of the outer mitochondrial membrane for adenine nucleotides ( 5,  14), the ADP produced in the intermembrane space by ScCKmit could be more efficient to stimulate the respiration than ADP produced directly in the cytoplasm ( 15).	transcription
55392	6	335591	5	NULL	NULL	0	NULL	statement 4			stimulates					respiration					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6937_s_24	10702255	Considering the functional coupling of the ScCKmit with the ATP-ADP carrier and the restricted permeability of the outer mitochondrial membrane for adenine nucleotides ( 5,  14), the ADP produced in the intermembrane space by ScCKmit could be more efficient to stimulate the respiration than ADP produced directly in the cytoplasm ( 15).	transcription
55393	7	335591	5	NULL	NULL	0	NULL	statement 5			more efficient than					statement 8					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6937_s_24	10702255	Considering the functional coupling of the ScCKmit with the ATP-ADP carrier and the restricted permeability of the outer mitochondrial membrane for adenine nucleotides ( 5,  14), the ADP produced in the intermembrane space by ScCKmit could be more efficient to stimulate the respiration than ADP produced directly in the cytoplasm ( 15).	transcription
60412	1	335591	7	NULL	NULL	0	NULL	ScCKmit	GP		coupled with		functionally			ATP-ADP carrier	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6937_s_24	10702255	Considering the functional coupling of the ScCKmit with the ATP-ADP carrier and the restricted permeability of the outer mitochondrial membrane for adenine nucleotides ( 5,  14), the ADP produced in the intermembrane space by ScCKmit could be more efficient to stimulate the respiration than ADP produced directly in the cytoplasm ( 15).	transcription
60413	2	335591	7	NULL	NULL	0	NULL	adenine nucleotides	Chemical	permeability of	restricted to					outer mitochondrial membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6937_s_24	10702255	Considering the functional coupling of the ScCKmit with the ATP-ADP carrier and the restricted permeability of the outer mitochondrial membrane for adenine nucleotides ( 5,  14), the ADP produced in the intermembrane space by ScCKmit could be more efficient to stimulate the respiration than ADP produced directly in the cytoplasm ( 15).	transcription
60414	3	335591	7	NULL	NULL	0	NULL	 ScCKmit	GP		produce					ADP	Chemical				NULL	 intermembrane space	0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6937_s_24	10702255	Considering the functional coupling of the ScCKmit with the ATP-ADP carrier and the restricted permeability of the outer mitochondrial membrane for adenine nucleotides ( 5,  14), the ADP produced in the intermembrane space by ScCKmit could be more efficient to stimulate the respiration than ADP produced directly in the cytoplasm ( 15).	transcription
60415	4	335591	7	NULL	NULL	0	NULL	statement 3	Process		stimulate					respiration	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6937_s_24	10702255	Considering the functional coupling of the ScCKmit with the ATP-ADP carrier and the restricted permeability of the outer mitochondrial membrane for adenine nucleotides ( 5,  14), the ADP produced in the intermembrane space by ScCKmit could be more efficient to stimulate the respiration than ADP produced directly in the cytoplasm ( 15).	transcription
60416	5	335591	7	NULL	NULL	0	NULL	ADP	Chemical		produced in		directly			cytoplasm	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6937_s_24	10702255	Considering the functional coupling of the ScCKmit with the ATP-ADP carrier and the restricted permeability of the outer mitochondrial membrane for adenine nucleotides ( 5,  14), the ADP produced in the intermembrane space by ScCKmit could be more efficient to stimulate the respiration than ADP produced directly in the cytoplasm ( 15).	transcription
60417	6	335591	7	NULL	NULL	0	NULL	statement 5	Process		stimulate					respiration	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6937_s_24	10702255	Considering the functional coupling of the ScCKmit with the ATP-ADP carrier and the restricted permeability of the outer mitochondrial membrane for adenine nucleotides ( 5,  14), the ADP produced in the intermembrane space by ScCKmit could be more efficient to stimulate the respiration than ADP produced directly in the cytoplasm ( 15).	transcription
60418	7	335591	7	NULL	NULL	0	NULL	statement 4	Process		is more efficient than					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6937_s_24	10702255	Considering the functional coupling of the ScCKmit with the ATP-ADP carrier and the restricted permeability of the outer mitochondrial membrane for adenine nucleotides ( 5,  14), the ADP produced in the intermembrane space by ScCKmit could be more efficient to stimulate the respiration than ADP produced directly in the cytoplasm ( 15).	transcription
55394	1	335592	5	NULL	NULL	0	NULL	adenine nucleotide			promotes					Cl channel activation					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_46_29080_s_7	8910562	Although injection of oocytes with either GDPbetaS (guanyl-5 -yl thiophosphate) or GTPgammaS (guanosine 5 -3- O-(thio)triphosphate) resulted in loss of adenine nucleotide-promoted Cl  channel activation, neither guanine nucleotide altered the 2MeSATP-stimulated cation current.	transcription
55395	2	335592	5	NULL	NULL	0	NULL	oocytes			is injected with					GDPbetaS (guanyl-5 -yl thiophosphate)					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_46_29080_s_7	8910562	Although injection of oocytes with either GDPbetaS (guanyl-5 -yl thiophosphate) or GTPgammaS (guanosine 5 -3- O-(thio)triphosphate) resulted in loss of adenine nucleotide-promoted Cl  channel activation, neither guanine nucleotide altered the 2MeSATP-stimulated cation current.	transcription
55397	3	335592	5	NULL	NULL	0	NULL	oocytes			is injected with					GTPgammaS (guanosine 5 -3- O-(thio)triphosphate)					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_46_29080_s_7	8910562	Although injection of oocytes with either GDPbetaS (guanyl-5 -yl thiophosphate) or GTPgammaS (guanosine 5 -3- O-(thio)triphosphate) resulted in loss of adenine nucleotide-promoted Cl  channel activation, neither guanine nucleotide altered the 2MeSATP-stimulated cation current.	transcription
55398	4	335592	5	NULL	NULL	0	NULL	statement 2			is an alternative to					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_46_29080_s_7	8910562	Although injection of oocytes with either GDPbetaS (guanyl-5 -yl thiophosphate) or GTPgammaS (guanosine 5 -3- O-(thio)triphosphate) resulted in loss of adenine nucleotide-promoted Cl  channel activation, neither guanine nucleotide altered the 2MeSATP-stimulated cation current.	transcription
55404	5	335592	5	NULL	NULL	0	NULL	statement 2			results in					statement 1		loss of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_46_29080_s_7	8910562	Although injection of oocytes with either GDPbetaS (guanyl-5 -yl thiophosphate) or GTPgammaS (guanosine 5 -3- O-(thio)triphosphate) resulted in loss of adenine nucleotide-promoted Cl  channel activation, neither guanine nucleotide altered the 2MeSATP-stimulated cation current.	transcription
55405	6	335592	5	NULL	NULL	0	NULL	statement 3			results in					statement 1		loss of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_46_29080_s_7	8910562	Although injection of oocytes with either GDPbetaS (guanyl-5 -yl thiophosphate) or GTPgammaS (guanosine 5 -3- O-(thio)triphosphate) resulted in loss of adenine nucleotide-promoted Cl  channel activation, neither guanine nucleotide altered the 2MeSATP-stimulated cation current.	transcription
55406	7	335592	5	NULL	NULL	0	NULL	2MeSATP			stimulates					cation current					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_46_29080_s_7	8910562	Although injection of oocytes with either GDPbetaS (guanyl-5 -yl thiophosphate) or GTPgammaS (guanosine 5 -3- O-(thio)triphosphate) resulted in loss of adenine nucleotide-promoted Cl  channel activation, neither guanine nucleotide altered the 2MeSATP-stimulated cation current.	transcription
55407	8	335592	5	NULL	NULL	0	NULL	GDPbetaS (guanyl-5 -yl thiophosphate)			does not alter					statement 7					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_46_29080_s_7	8910562	Although injection of oocytes with either GDPbetaS (guanyl-5 -yl thiophosphate) or GTPgammaS (guanosine 5 -3- O-(thio)triphosphate) resulted in loss of adenine nucleotide-promoted Cl  channel activation, neither guanine nucleotide altered the 2MeSATP-stimulated cation current.	transcription
55408	9	335592	5	NULL	NULL	0	NULL	GTPgammaS (guanosine 5 -3- O-(thio)triphosphate)			does not alter					statement 7					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_46_29080_s_7	8910562	Although injection of oocytes with either GDPbetaS (guanyl-5 -yl thiophosphate) or GTPgammaS (guanosine 5 -3- O-(thio)triphosphate) resulted in loss of adenine nucleotide-promoted Cl  channel activation, neither guanine nucleotide altered the 2MeSATP-stimulated cation current.	transcription
60419	1	335592	7	NULL	NULL	0	NULL	adenine nucleotide	NucleicAcid		promote					Cl channel	CellComponent	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_46_29080_s_7	8910562	Although injection of oocytes with either GDPbetaS (guanyl-5 -yl thiophosphate) or GTPgammaS (guanosine 5 -3- O-(thio)triphosphate) resulted in loss of adenine nucleotide-promoted Cl  channel activation, neither guanine nucleotide altered the 2MeSATP-stimulated cation current.	transcription
60420	2	335592	7	NULL	NULL	0	NULL	GDPbetaS (guanyl-5 -yl thiophosphate)	Chemical	treatment with	results in					statement 1	Process	loss of			NULL	oocytes	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_46_29080_s_7	8910562	Although injection of oocytes with either GDPbetaS (guanyl-5 -yl thiophosphate) or GTPgammaS (guanosine 5 -3- O-(thio)triphosphate) resulted in loss of adenine nucleotide-promoted Cl  channel activation, neither guanine nucleotide altered the 2MeSATP-stimulated cation current.	transcription
60421	3	335592	7	NULL	NULL	0	NULL	GTPgammaS (guanosine 5 -3- O-(thio)triphosphate)	Chemical	treatment with	results in					statement 1	Process	loss of			NULL	oocytes	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_46_29080_s_7	8910562	Although injection of oocytes with either GDPbetaS (guanyl-5 -yl thiophosphate) or GTPgammaS (guanosine 5 -3- O-(thio)triphosphate) resulted in loss of adenine nucleotide-promoted Cl  channel activation, neither guanine nucleotide altered the 2MeSATP-stimulated cation current.	transcription
60422	4	335592	7	NULL	NULL	0	NULL	MeSATP	Chemical		stimulate					cation current	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_46_29080_s_7	8910562	Although injection of oocytes with either GDPbetaS (guanyl-5 -yl thiophosphate) or GTPgammaS (guanosine 5 -3- O-(thio)triphosphate) resulted in loss of adenine nucleotide-promoted Cl  channel activation, neither guanine nucleotide altered the 2MeSATP-stimulated cation current.	transcription
60423	5	335592	7	NULL	NULL	0	NULL	guanine nucleotide	NucleicAcid		does not alter					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_46_29080_s_7	8910562	Although injection of oocytes with either GDPbetaS (guanyl-5 -yl thiophosphate) or GTPgammaS (guanosine 5 -3- O-(thio)triphosphate) resulted in loss of adenine nucleotide-promoted Cl  channel activation, neither guanine nucleotide altered the 2MeSATP-stimulated cation current.	transcription
60424	6	335592	7	NULL	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_46_29080_s_7	8910562	Although injection of oocytes with either GDPbetaS (guanyl-5 -yl thiophosphate) or GTPgammaS (guanosine 5 -3- O-(thio)triphosphate) resulted in loss of adenine nucleotide-promoted Cl  channel activation, neither guanine nucleotide altered the 2MeSATP-stimulated cation current.	transcription
56502	1	335593	5	NULL	NULL	0	NULL	adenine			interacts with			methyl group at position N6		glucocorticoid receptor			Val-482		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11679_s_219	10206981	This is probably related to the fact that the methyl group at position  N6 of adenine can mimic the 5''-methyl group of the thymine ( i.e. establish hydrophobic interaction with residue Val-482 of the glucocorticoid receptor) ( 47) and enables strong specific interaction of the GR with the major groove, although the positions of these methyl groups differ in the major groove ( 29).	transcription
60426	1	335593	7	NULL	NULL	0	NULL	adenine	Chemical	methyl group at position N6	interacts with		hydrophobically		 	glucocorticoid receptor	GP		residue Val-482		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_17_11679_s_219	10206981	This is probably related to the fact that the methyl group at position  N6 of adenine can mimic the 5''-methyl group of the thymine ( i.e. establish hydrophobic interaction with residue Val-482 of the glucocorticoid receptor) ( 47) and enables strong specific interaction of the GR with the major groove, although the positions of these methyl groups differ in the major groove ( 29).	transcription
60428	2	335593	7	NULL	NULL	0	NULL	thymine	Chemical	5''-methyl group of	interacts with		hydrophobically			glucocorticoid receptor	GP		residue Val-482		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_17_11679_s_219	10206981	This is probably related to the fact that the methyl group at position  N6 of adenine can mimic the 5''-methyl group of the thymine ( i.e. establish hydrophobic interaction with residue Val-482 of the glucocorticoid receptor) ( 47) and enables strong specific interaction of the GR with the major groove, although the positions of these methyl groups differ in the major groove ( 29).	transcription
60430	3	335593	7	NULL	NULL	0	NULL	adenine	Chemical	methyl group at position N6 of	mimic					thymine	Chemical	5''-methyl group of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11679_s_219	10206981	This is probably related to the fact that the methyl group at position  N6 of adenine can mimic the 5''-methyl group of the thymine ( i.e. establish hydrophobic interaction with residue Val-482 of the glucocorticoid receptor) ( 47) and enables strong specific interaction of the GR with the major groove, although the positions of these methyl groups differ in the major groove ( 29).	transcription
60432	4	335593	7	NULL	NULL	0	NULL	GR	GP		interacts with		strongly;;specifically							major groove	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11679_s_219	10206981	This is probably related to the fact that the methyl group at position  N6 of adenine can mimic the 5''-methyl group of the thymine ( i.e. establish hydrophobic interaction with residue Val-482 of the glucocorticoid receptor) ( 47) and enables strong specific interaction of the GR with the major groove, although the positions of these methyl groups differ in the major groove ( 29).	transcription
60433	5	335593	7	NULL	NULL	0	NULL	adenine	Chemical	methyl group at position N6 of	enables					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11679_s_219	10206981	This is probably related to the fact that the methyl group at position  N6 of adenine can mimic the 5''-methyl group of the thymine ( i.e. establish hydrophobic interaction with residue Val-482 of the glucocorticoid receptor) ( 47) and enables strong specific interaction of the GR with the major groove, although the positions of these methyl groups differ in the major groove ( 29).	transcription
60434	6	335593	7	NULL	NULL	0	NULL	thymine	Chemical	5''-methyl group of	enables					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_17_11679_s_219	10206981	This is probably related to the fact that the methyl group at position  N6 of adenine can mimic the 5''-methyl group of the thymine ( i.e. establish hydrophobic interaction with residue Val-482 of the glucocorticoid receptor) ( 47) and enables strong specific interaction of the GR with the major groove, although the positions of these methyl groups differ in the major groove ( 29).	transcription
55414	1	335594	5	NULL	NULL	0	NULL	PHS			does not inhibit					uracil		transport of			NULL	nitrogen-repressing condition	0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_190	9446592	PHS did not inhibit uracil or adenine transport under nitrogen-repressing (ammonia ions in the culture medium), partially nitrogen-repressing (PYED medium), or nitrogen-derepressing (proline in the culture medium) conditions (Figs.  1 and  5), indicating that PHS does not affect these two families of major facilitator superfamily of membrane-bound transporters.	transcription
55416	2	335594	5	NULL	NULL	0	NULL	PHS			does not inhibit					adenine		transport of			NULL	nitrogen-repressing condition	0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_190	9446592	PHS did not inhibit uracil or adenine transport under nitrogen-repressing (ammonia ions in the culture medium), partially nitrogen-repressing (PYED medium), or nitrogen-derepressing (proline in the culture medium) conditions (Figs.  1 and  5), indicating that PHS does not affect these two families of major facilitator superfamily of membrane-bound transporters.	transcription
55418	3	335594	5	NULL	NULL	0	NULL	PHS			does not inhibit					uracil		transport of			NULL	partially nitrogen-repressing condition	0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_190	9446592	PHS did not inhibit uracil or adenine transport under nitrogen-repressing (ammonia ions in the culture medium), partially nitrogen-repressing (PYED medium), or nitrogen-derepressing (proline in the culture medium) conditions (Figs.  1 and  5), indicating that PHS does not affect these two families of major facilitator superfamily of membrane-bound transporters.	transcription
55419	4	335594	5	NULL	NULL	0	NULL	PHS			does not inhibit					adenine		transport of			NULL	partially nitrogen-repressing condition	0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_190	9446592	PHS did not inhibit uracil or adenine transport under nitrogen-repressing (ammonia ions in the culture medium), partially nitrogen-repressing (PYED medium), or nitrogen-derepressing (proline in the culture medium) conditions (Figs.  1 and  5), indicating that PHS does not affect these two families of major facilitator superfamily of membrane-bound transporters.	transcription
55421	5	335594	5	NULL	NULL	0	NULL	PHS			does not inhibit					uracil		transport of			NULL	nitrogen-derepressing condition	0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_190	9446592	PHS did not inhibit uracil or adenine transport under nitrogen-repressing (ammonia ions in the culture medium), partially nitrogen-repressing (PYED medium), or nitrogen-derepressing (proline in the culture medium) conditions (Figs.  1 and  5), indicating that PHS does not affect these two families of major facilitator superfamily of membrane-bound transporters.	transcription
55422	6	335594	5	NULL	NULL	0	NULL	PHS			does not inhibit					adenine		transport of			NULL	nitrogen-derepressing condition	0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_190	9446592	PHS did not inhibit uracil or adenine transport under nitrogen-repressing (ammonia ions in the culture medium), partially nitrogen-repressing (PYED medium), or nitrogen-derepressing (proline in the culture medium) conditions (Figs.  1 and  5), indicating that PHS does not affect these two families of major facilitator superfamily of membrane-bound transporters.	transcription
60435	1	335594	7	NULL	NULL	0	NULL	PHS	Chemical		does not inhibit					uracil	Chemical	transport of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_190	9446592	PHS did not inhibit uracil or adenine transport under nitrogen-repressing (ammonia ions in the culture medium), partially nitrogen-repressing (PYED medium), or nitrogen-derepressing (proline in the culture medium) conditions (Figs.  1 and  5), indicating that PHS does not affect these two families of major facilitator superfamily of membrane-bound transporters.	transcription
60436	2	335594	7	NULL	NULL	0	NULL	PHS	Chemical		does not inhibit					adenine	Chemical	transport of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_190	9446592	PHS did not inhibit uracil or adenine transport under nitrogen-repressing (ammonia ions in the culture medium), partially nitrogen-repressing (PYED medium), or nitrogen-derepressing (proline in the culture medium) conditions (Figs.  1 and  5), indicating that PHS does not affect these two families of major facilitator superfamily of membrane-bound transporters.	transcription
60437	3	335594	7	NULL	NULL	0	NULL	statement 1	Process		occur upon					nitrogen	Chemical	repressing			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_190	9446592	PHS did not inhibit uracil or adenine transport under nitrogen-repressing (ammonia ions in the culture medium), partially nitrogen-repressing (PYED medium), or nitrogen-derepressing (proline in the culture medium) conditions (Figs.  1 and  5), indicating that PHS does not affect these two families of major facilitator superfamily of membrane-bound transporters.	transcription
60438	4	335594	7	NULL	NULL	0	NULL	statement 2	Process		occur upon					nitrogen 	Chemical	repressing			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_190	9446592	PHS did not inhibit uracil or adenine transport under nitrogen-repressing (ammonia ions in the culture medium), partially nitrogen-repressing (PYED medium), or nitrogen-derepressing (proline in the culture medium) conditions (Figs.  1 and  5), indicating that PHS does not affect these two families of major facilitator superfamily of membrane-bound transporters.	transcription
60439	5	335594	7	NULL	NULL	0	NULL	statement 1	Process		occur upon					 nitrogen	Chemical	partially repressing			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_190	9446592	PHS did not inhibit uracil or adenine transport under nitrogen-repressing (ammonia ions in the culture medium), partially nitrogen-repressing (PYED medium), or nitrogen-derepressing (proline in the culture medium) conditions (Figs.  1 and  5), indicating that PHS does not affect these two families of major facilitator superfamily of membrane-bound transporters.	transcription
60440	6	335594	7	NULL	NULL	0	NULL	statement 2	Process		occur upon					nitrogen	Chemical	partially repressing			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_190	9446592	PHS did not inhibit uracil or adenine transport under nitrogen-repressing (ammonia ions in the culture medium), partially nitrogen-repressing (PYED medium), or nitrogen-derepressing (proline in the culture medium) conditions (Figs.  1 and  5), indicating that PHS does not affect these two families of major facilitator superfamily of membrane-bound transporters.	transcription
60441	7	335594	7	NULL	NULL	0	NULL	statement 1	Process		occur upon					nitrogen	Chemical	derepressing			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_190	9446592	PHS did not inhibit uracil or adenine transport under nitrogen-repressing (ammonia ions in the culture medium), partially nitrogen-repressing (PYED medium), or nitrogen-derepressing (proline in the culture medium) conditions (Figs.  1 and  5), indicating that PHS does not affect these two families of major facilitator superfamily of membrane-bound transporters.	transcription
60442	8	335594	7	NULL	NULL	0	NULL	statement 2	Process		occur upon					nitrogen	Chemical	derepressing			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2829_s_190	9446592	PHS did not inhibit uracil or adenine transport under nitrogen-repressing (ammonia ions in the culture medium), partially nitrogen-repressing (PYED medium), or nitrogen-derepressing (proline in the culture medium) conditions (Figs.  1 and  5), indicating that PHS does not affect these two families of major facilitator superfamily of membrane-bound transporters.	transcription
55423	1	335595	5	NULL	NULL	0	NULL	DnaA protein			initiates					chromosomal DNA		replication of;;Escherichia coli			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_33_20847_s_11	9694830	DnaA protein, the initiator of chromosomal DNA replication in  Escherichia coli ( 1-4), has a high affinity for adenine nucleotides; the ATP-binding form of DnaA protein is active, whereas the ADP-binding form is inactive in an  oriC DNA replication system  in vitro ( 5).	transcription
55424	2	335595	5	NULL	NULL	0	NULL	DnaA protein			has affinity for		high			adenine nucleotides					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_33_20847_s_11	9694830	DnaA protein, the initiator of chromosomal DNA replication in  Escherichia coli ( 1-4), has a high affinity for adenine nucleotides; the ATP-binding form of DnaA protein is active, whereas the ADP-binding form is inactive in an  oriC DNA replication system  in vitro ( 5).	transcription
55425	3	335595	5	NULL	NULL	0	NULL	DnaA protein			bind					ATP					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_33_20847_s_11	9694830	DnaA protein, the initiator of chromosomal DNA replication in  Escherichia coli ( 1-4), has a high affinity for adenine nucleotides; the ATP-binding form of DnaA protein is active, whereas the ADP-binding form is inactive in an  oriC DNA replication system  in vitro ( 5).	transcription
55426	4	335595	5	NULL	NULL	0	NULL	statement 3			is active in					oriC DNA replication system					NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_273_33_20847_s_11	9694830	DnaA protein, the initiator of chromosomal DNA replication in  Escherichia coli ( 1-4), has a high affinity for adenine nucleotides; the ATP-binding form of DnaA protein is active, whereas the ADP-binding form is inactive in an  oriC DNA replication system  in vitro ( 5).	transcription
55427	5	335595	5	NULL	NULL	0	NULL	DnaA protein			bind					ADP					NULL	in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_33_20847_s_11	9694830	DnaA protein, the initiator of chromosomal DNA replication in  Escherichia coli ( 1-4), has a high affinity for adenine nucleotides; the ATP-binding form of DnaA protein is active, whereas the ADP-binding form is inactive in an  oriC DNA replication system  in vitro ( 5).	transcription
55428	6	335595	5	NULL	NULL	0	NULL	statement 5			is inactivate in					oriC DNA replication system					NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_273_33_20847_s_11	9694830	DnaA protein, the initiator of chromosomal DNA replication in  Escherichia coli ( 1-4), has a high affinity for adenine nucleotides; the ATP-binding form of DnaA protein is active, whereas the ADP-binding form is inactive in an  oriC DNA replication system  in vitro ( 5).	transcription
60443	1	335595	7	NULL	NULL	0	NULL	DnaA protein	GP		is the initiator of					chromosomal DNA	NucleicAcid	replication of			NULL	Escherichia coli 	0	NULL	NULL	NULL	gw60_jbiolchem_273_33_20847_s_11	9694830	DnaA protein, the initiator of chromosomal DNA replication in  Escherichia coli ( 1-4), has a high affinity for adenine nucleotides; the ATP-binding form of DnaA protein is active, whereas the ADP-binding form is inactive in an  oriC DNA replication system  in vitro ( 5).	transcription
60444	2	335595	7	NULL	NULL	0	NULL	DnaA protein	GP		high affinity for					adenine nucleotides	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_33_20847_s_11	9694830	DnaA protein, the initiator of chromosomal DNA replication in  Escherichia coli ( 1-4), has a high affinity for adenine nucleotides; the ATP-binding form of DnaA protein is active, whereas the ADP-binding form is inactive in an  oriC DNA replication system  in vitro ( 5).	transcription
60445	3	335595	7	NULL	NULL	0	NULL	DnaA protein	GP		bind					ATP	Chemical				NULL	oriC DNA replication system in vitro	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_33_20847_s_11	9694830	DnaA protein, the initiator of chromosomal DNA replication in  Escherichia coli ( 1-4), has a high affinity for adenine nucleotides; the ATP-binding form of DnaA protein is active, whereas the ADP-binding form is inactive in an  oriC DNA replication system  in vitro ( 5).	transcription
60446	4	335595	7	NULL	NULL	0	NULL	DnaA protein	GP		bind					ADP	Chemical				NULL	oriC DNA replication system in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_273_33_20847_s_11	9694830	DnaA protein, the initiator of chromosomal DNA replication in  Escherichia coli ( 1-4), has a high affinity for adenine nucleotides; the ATP-binding form of DnaA protein is active, whereas the ADP-binding form is inactive in an  oriC DNA replication system  in vitro ( 5).	transcription
60447	5	335595	7	NULL	NULL	0	NULL	statement 3	Process		is					active	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_33_20847_s_11	9694830	DnaA protein, the initiator of chromosomal DNA replication in  Escherichia coli ( 1-4), has a high affinity for adenine nucleotides; the ATP-binding form of DnaA protein is active, whereas the ADP-binding form is inactive in an  oriC DNA replication system  in vitro ( 5).	transcription
60448	6	335595	7	NULL	NULL	0	NULL	statement 4	Process		is					inactive	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_33_20847_s_11	9694830	DnaA protein, the initiator of chromosomal DNA replication in  Escherichia coli ( 1-4), has a high affinity for adenine nucleotides; the ATP-binding form of DnaA protein is active, whereas the ADP-binding form is inactive in an  oriC DNA replication system  in vitro ( 5).	transcription
55429	1	335596	5	NULL	NULL	0	NULL	iodotubercidine			is an inhibitor of					adenosine kinase					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_988_s_39	10565815	The probes were connected to a CMA/100 microinfusion pump (Carnergie Medicine, Stockholm, Sweden) and were perfused with isotonic saline solution with heparin (30 U/ml) containing iodotubercidine (10 muM), an inhibitor of adenosine kinase, and  erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA) (100 muM), an inhibitor of adenosine deaminase, at a rate of 5 mul/min.	transcription
55430	2	335596	5	NULL	NULL	0	NULL	EHNA			is					erythro-9-(2-hydroxy-3-nonyl)adenine					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_988_s_39	10565815	The probes were connected to a CMA/100 microinfusion pump (Carnergie Medicine, Stockholm, Sweden) and were perfused with isotonic saline solution with heparin (30 U/ml) containing iodotubercidine (10 muM), an inhibitor of adenosine kinase, and  erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA) (100 muM), an inhibitor of adenosine deaminase, at a rate of 5 mul/min.	transcription
55431	3	335596	5	NULL	NULL	0	NULL	EHNA			inhibit					adenosine deaminase					NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_988_s_39	10565815	The probes were connected to a CMA/100 microinfusion pump (Carnergie Medicine, Stockholm, Sweden) and were perfused with isotonic saline solution with heparin (30 U/ml) containing iodotubercidine (10 muM), an inhibitor of adenosine kinase, and  erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA) (100 muM), an inhibitor of adenosine deaminase, at a rate of 5 mul/min.	transcription
60449	1	335596	7	NULL	NULL	0	NULL	iodotubercidine	Chemical		is an inhibitor of					adenosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_988_s_39	10565815	The probes were connected to a CMA/100 microinfusion pump (Carnergie Medicine, Stockholm, Sweden) and were perfused with isotonic saline solution with heparin (30 U/ml) containing iodotubercidine (10 muM), an inhibitor of adenosine kinase, and  erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA) (100 muM), an inhibitor of adenosine deaminase, at a rate of 5 mul/min.	transcription
60450	2	335596	7	NULL	NULL	0	NULL	EHNA	Chemical		is an inhibitor of					adenosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_988_s_39	10565815	The probes were connected to a CMA/100 microinfusion pump (Carnergie Medicine, Stockholm, Sweden) and were perfused with isotonic saline solution with heparin (30 U/ml) containing iodotubercidine (10 muM), an inhibitor of adenosine kinase, and  erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA) (100 muM), an inhibitor of adenosine deaminase, at a rate of 5 mul/min.	transcription
60451	3	335596	7	NULL	NULL	0	NULL	EHNA	Chemical		is					erythro-9-(2-hydroxy-3-nonyl)adenine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_291_3_988_s_39	10565815	The probes were connected to a CMA/100 microinfusion pump (Carnergie Medicine, Stockholm, Sweden) and were perfused with isotonic saline solution with heparin (30 U/ml) containing iodotubercidine (10 muM), an inhibitor of adenosine kinase, and  erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA) (100 muM), an inhibitor of adenosine deaminase, at a rate of 5 mul/min.	transcription
55432	1	335597	5	NULL	NULL	0	NULL	Escherichia coli			is a type of					enteric bacterium					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
55433	2	335597	5	NULL	NULL	0	NULL	Dam			is present in					Escherichia coli					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
55434	3	335597	5	NULL	NULL	0	NULL	Dcm			is present in					Escherichia coli					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
55435	4	335597	5	NULL	NULL	0	NULL	M. EcoK			is present in					Escherichia coli					NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
55436	5	335597	5	NULL	NULL	0	NULL	Dam			is					DNA adenine methyltransferase					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
55437	6	335597	5	NULL	NULL	0	NULL	Dcm			is					DNA cytosine methyltransferase					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
55438	7	335597	5	NULL	NULL	0	NULL	N6-methyladenosine			is created in							specific;;target sequence		5''-GmATC-3''	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
55439	8	335597	5	NULL	NULL	0	NULL	Dam			is required for					statement 7					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
55440	9	335597	5	NULL	NULL	0	NULL	C5-methylcytosine		internal	is created in							specific;;target sequence		5''-CmC(A/T)GG-3''	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
55441	10	335597	5	NULL	NULL	0	NULL	Dcm			is required for					statement 9					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
55442	11	335597	5	NULL	NULL	0	NULL	adenine			is modified in									AmAC(N6)GTCG	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
55443	12	335597	5	NULL	NULL	0	NULL	M. EcoK			is required for					statement 11					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
55444	13	335597	5	NULL	NULL	0	NULL				is recognized as		specifically		AmAC(N6)GTCG	unmethylated sequence					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
55445	14	335597	5	NULL	NULL	0	NULL	EcoK			is a type of					endonuclease					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
55446	15	335597	5	NULL	NULL	0	NULL	EcoK			is required for					statement 13					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
55447	16	335597	5	NULL	NULL	0	NULL	R-M system			is					restriction-modification system					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
55448	17	335597	5	NULL	NULL	0	NULL	R-M system			is specific to					host					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
55449	18	335597	5	NULL	NULL	0	NULL	statement 13			is a part of					R-M system					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
60452	1	335597	7	NULL	NULL	0	NULL	Dam	GP		creates					N6-methyladenosine 	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
60453	2	335597	7	NULL	NULL	0	NULL	statement 1	Process		occur in							target sequence		5''-GmATC-3''	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
60454	3	335597	7	NULL	NULL	0	NULL	Dcm	GP		leads to					C5-methylcytosine	Chemical	internal			NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
60455	4	335597	7	NULL	NULL	0	NULL	statement 3	Process		occur in							target sequence		5''-CmC(A/T)GG-3''	NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
60456	5	335597	7	NULL	NULL	0	NULL	M. EcoK	GP		modifies							second adenine in		AmAC(N6)GTCG	NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
60457	6	335597	7	NULL	NULL	0	NULL				recognized as		specifically		AmAC(N6)GTCG	unmethylated sequence					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
60458	7	335597	7	NULL	NULL	0	NULL	statement 6	Process		recognized by					EcoK	GP				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
60459	8	335597	7	NULL	NULL	0	NULL	EcoK	GP		is part of					host-specific restriction-modification system	Process				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
60460	9	335597	7	NULL	NULL	0	NULL	EcoK	GP		is a type of					restriction endonuclease	GP				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
60461	10	335597	7	NULL	NULL	0	NULL	Dam	GP		is					DNA adenine methyltransferase	GP				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
60462	11	335597	7	NULL	NULL	0	NULL	Dcm	GP		is					DNA cytosine methyltransferase	GP				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
60463	12	335597	7	NULL	NULL	0	NULL	M. EcoK	GP		is a type of					methyltransferase	GP				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_180_16_4116_s_17	9696758	In the enteric bacterium  Escherichia coli, three methyltransferases are present: (i) Dam (DNA adenine methyltransferase), creating N6-methyladenosine in the specific target sequence 5''-GmATC-3''; (ii) Dcm (DNA cytosine methyltransferase), leading to an internal C5-methylcytosine in the specific target sequence 5''-CmC(A/T)GG-3''; and (iii) methyltransferase M.   EcoK, modifying the second adenine in the sequence AmAC(N6)GTCG, which is specifically recognized as an unmethylated sequence by restriction endonuclease  EcoK, which is part of the host-specific restriction-modification (R-M) system (for a review, see reference  22).	transcription
55450	1	335598	5	NULL	NULL	0	NULL	GMP			is converted to					adenine nucleotides					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
55451	2	335598	5	NULL	NULL	0	NULL	statement 1			via					GMP reductase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
55452	3	335598	5	NULL	NULL	0	NULL	GMP reductase			is encoded by					guaC gene					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
55453	4	335598	5	NULL	NULL	0	NULL	phosphoribosylpyrophosphate synthetase			is inhibited by		presumably 			ADP					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
55454	5	335598	5	NULL	NULL	0	NULL	ADP			is a type of					adenine nucleotide					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
55455	6	335598	5	NULL	NULL	0	NULL	statement 4			causes					histidine		starvation for			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
55456	7	335598	5	NULL	NULL	0	NULL	statement 4			causes					tryptophan		starvation for			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
55457	8	335598	5	NULL	NULL	0	NULL	statement 4			causes					pyrimidines		starvation for			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
55458	9	335598	5	NULL	NULL	0	NULL	PRPP			is required for					histidine		synthesis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
55459	10	335598	5	NULL	NULL	0	NULL	PRPP			is required for					tryptophan		synthesis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
55460	11	335598	5	NULL	NULL	0	NULL	PRPP			is required for					pyrimidines		synthesis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
55461	12	335598	5	NULL	NULL	0	NULL	ppGpp			is					guanosine 5'',3''-bispyrophosphate					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
55462	13	335598	5	NULL	NULL	0	NULL	ppGpp			is a type of					nucleotide					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
55463	14	335598	5	NULL	NULL	0	NULL	ppGpp			is a type of					transcriptional inhibitor					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
55464	15	335598	5	NULL	NULL	0	NULL	ppGpp			is synthesized by					relA gene product					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
55465	16	335598	5	NULL	NULL	0	NULL	statement 15			in response to					amino acid		starvation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
60473	1	335598	7	NULL	NULL	0	NULL	GMP	Chemical		converted to					adenine nucleotides 	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
60474	2	335598	7	NULL	NULL	0	NULL	statement 1	Process		via					GMP reductase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
60475	3	335598	7	NULL	NULL	0	NULL	GMP reductase	GP		encoded by					guaC gene	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
60476	4	335598	7	NULL	NULL	0	NULL	ADP	Chemical		inhibit					 phosphoribosylpyrophosphate synthetase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
60477	5	335598	7	NULL	NULL	0	NULL	statement 4	Process		cause					histidine	AminoAcid	starvation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
60478	6	335598	7	NULL	NULL	0	NULL	statement 4	Process		cause					tryptophan	AminoAcid	starvation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
60479	7	335598	7	NULL	NULL	0	NULL	statement 4	Process		cause					pyrimidines	Chemical	starvation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
60482	8	335598	7	NULL	NULL	0	NULL	histidine	AminoAcid	synthesis of	require					PRPP	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
60486	9	335598	7	NULL	NULL	0	NULL	tryptophan	AminoAcid	synthesis of	require					PRPP	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
60490	10	335598	7	NULL	NULL	0	NULL	pyrimidines	Chemical	synthesis of	require					PRPP	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
60496	11	335598	7	NULL	NULL	0	NULL	ppGpp	Chemical		is a type of					transcriptional inhibitor	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
60500	12	335598	7	NULL	NULL	0	NULL	relA gene product	GP		synthesize					ppGpp	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
60501	13	335598	7	NULL	NULL	0	NULL	statement 12	Process		in response to					amino acid	AminoAcid	starvation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
60502	14	335598	7	NULL	NULL	0	NULL	ppGpp	NucleicAcid		is a type of					regulatory nucleotide	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
60503	15	335598	7	NULL	NULL	0	NULL	ppGPpp	NucleicAcid		is					guanosine 5'',3''-bispyrophosphate	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_9_5348_s_7	10026143	By isolation and characterization of guanosine-resistant derivatives of the  gsk-3 mutant, some of the crucial steps in this deleterious cascade of events were found to include the following: first, conversion of GMP to adenine nucleotides via GMP reductase, encoded by the  guaC gene; second, inhibition of phosphoribosylpyrophosphate synthetase by an adenine nucleotide, presumably ADP, causing starvation for histidine, tryptophan, and pyrimidines, all of which require PRPP for their synthesis; third, accumulation of the regulatory nucleotide guanosine 5'',3''-bispyrophosphate (ppGpp), a general transcriptional inhibitor synthesized by the  relA gene product in response to amino acid starvation.	transcription
55466	1	335603	5	NULL	NULL	0	NULL				bind			modular zinc finger domains						subsites containing a 5''-adenine	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_31_29466_s_288	11340073	Phage display selection of modular zinc finger domains that bind to subsites containing a 5''-adenine or -cytosine from our previously described finger-2 library based on the 3-finger protein C7 ( 7) failed due to the limitations imposed by Asp2 of finger 3 of this protein which makes a cross-subsite contact to the nucleotide complementary to the 5''-position of the finger-2 subsite (Fig.  1 A).	transcription
55467	2	335603	5	NULL	NULL	0	NULL				bind			modular zinc finger domains					subsites containing a 5''-cytosine		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_31_29466_s_288	11340073	Phage display selection of modular zinc finger domains that bind to subsites containing a 5''-adenine or -cytosine from our previously described finger-2 library based on the 3-finger protein C7 ( 7) failed due to the limitations imposed by Asp2 of finger 3 of this protein which makes a cross-subsite contact to the nucleotide complementary to the 5''-position of the finger-2 subsite (Fig.  1 A).	transcription
60505	1	335603	7	NULL	NULL	0	NULL			Phage	bind			modular zinc finger domain						subsites containing a 5''-adenine	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_31_29466_s_288	11340073	Phage display selection of modular zinc finger domains that bind to subsites containing a 5''-adenine or -cytosine from our previously described finger-2 library based on the 3-finger protein C7 ( 7) failed due to the limitations imposed by Asp2 of finger 3 of this protein which makes a cross-subsite contact to the nucleotide complementary to the 5''-position of the finger-2 subsite (Fig.  1 A).	transcription
60506	2	335603	7	NULL	NULL	0	NULL			Phage	bind			modular zinc finger domain						subsites containing a 5''-cytosine	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_31_29466_s_288	11340073	Phage display selection of modular zinc finger domains that bind to subsites containing a 5''-adenine or -cytosine from our previously described finger-2 library based on the 3-finger protein C7 ( 7) failed due to the limitations imposed by Asp2 of finger 3 of this protein which makes a cross-subsite contact to the nucleotide complementary to the 5''-position of the finger-2 subsite (Fig.  1 A).	transcription
55468	1	335607	5	NULL	NULL	0	NULL	complex III			is present in					electron transport chain					NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
55469	2	335607	5	NULL	NULL	0	NULL	Ec			targets					statement 1					NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
55470	3	335607	5	NULL	NULL	0	NULL	statement 2			results in					mitochondrial membrane		hyperpolarization of			NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
56168	4	335607	5	NULL	NULL	0	NULL	electron transport			is decoupled from					adenine nucleotide transport					NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
56169	5	335607	5	NULL	NULL	0	NULL	Ca2+ 			is release from					ER					NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
56170	6	335607	5	NULL	NULL	0	NULL	ROS			stimulates					statement 5					NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
56171	7	335607	5	NULL	NULL	0	NULL	Ec			block					Ca2+		influx of			NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
56172	8	335607	5	NULL	NULL	0	NULL	statement 7			results in					ER stress response					NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
60507	1	335607	7	NULL	NULL	0	NULL	Ec	Process		targets					complex III	GP				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
60508	2	335607	7	NULL	NULL	0	NULL	statement 1	Process		result in					mitochondrial membrane	CellComponent	hyperpolarization of			NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
60509	3	335607	7	NULL	NULL	0	NULL	electron transport	Process		decoupled from					adenine nucleotide transport 	Process				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
60510	4	335607	7	NULL	NULL	0	NULL	electron transport	Process		decoupled from					ATP	Chemical	production of			NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
60511	5	335607	7	NULL	NULL	0	NULL	statement 1	Process		leads to					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
60512	6	335607	7	NULL	NULL	0	NULL	statement 1	Process		leads to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
60513	7	335607	7	NULL	NULL	0	NULL	statement 1	Process		leads to					ANT	Chemical	inhibition of			NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
60514	8	335607	7	NULL	NULL	0	NULL	statement 1	Process		leads to					ROS	Chemical	generation of			NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
60515	9	335607	7	NULL	NULL	0	NULL	ROS	Chemical		stimulate					Ca2+	Chemical	release of;;ER			NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
60516	10	335607	7	NULL	NULL	0	NULL	Ec	Process		blocks					Ca2+ influx	Process				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
60517	11	335607	7	NULL	NULL	0	NULL	statement 10	Process		results in					stress response	Process				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
60518	12	335607	7	NULL	NULL	0	NULL	statement 1	Process		leads to					statement 9	Process				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_70_4_1424_s_269	16849592	1) Ec targets  complex III in the electron transport chain resulting in hyperpolarization of the  mitochondrial membrane; 2) decoupling of electron transport from adenine nucleotide  transport and ATP production; 3) inhibition of ANT and ROS generation; 4) ROS stimulates  ER Ca2+ release; and 5) Ec also blocks Ca2+ influx, resulting in an ER stress response.	transcription
60519	1	335609	7	NULL	NULL	0	NULL	GDP	Chemical		inhibit					ATP synthase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_16_15534_s_207	15695816	Fig. 6 A shows that the nonphosphorylating oxygen consumption rates (state 4; expressed as nanomoles of oxygen atoms/min/mg of mitochondrial protein) of non-Dowex-treated BAT mitochondria from rats kept at room temperature in the presence of inhibitors of the adenine nucleotide carrier and ATP synthase is inhibited by addition of 1 mM GDP (from 175  plus-or-minus  6 to 128  plus-or-minus  5;  p = 0.0038).	transcription
60520	1	335612	7	NULL	NULL	0	NULL	2''-deoxyribose oligonucleotide	NucleicAcid		contain					adenine	Chemical				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6111_s_232	12167705	Because of the relative insensitivity of the 3H-based DNA  N-glycosylase release assay, DNA  N-glycosylase activity was measured by the more sensitive method, i.e., cleavage of a Tg residue-containing 2''-deoxyribose oligonucleotide which had been 5' end labeled with [gamma-32] and paired with a complementary 2''-deoxyribose oligonucleotide containing either an adenine or a guanine opposite Tg.	transcription
60521	2	335612	7	NULL	NULL	0	NULL	2''-deoxyribose oligonucleotide	NucleicAcid		contain					guanine	Chemical				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6111_s_232	12167705	Because of the relative insensitivity of the 3H-based DNA  N-glycosylase release assay, DNA  N-glycosylase activity was measured by the more sensitive method, i.e., cleavage of a Tg residue-containing 2''-deoxyribose oligonucleotide which had been 5' end labeled with [gamma-32] and paired with a complementary 2''-deoxyribose oligonucleotide containing either an adenine or a guanine opposite Tg.	transcription
60522	3	335612	7	NULL	NULL	0	NULL	Tg residue	Chemical		contain					2''-deoxyribose oligonucleotide	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6111_s_232	12167705	Because of the relative insensitivity of the 3H-based DNA  N-glycosylase release assay, DNA  N-glycosylase activity was measured by the more sensitive method, i.e., cleavage of a Tg residue-containing 2''-deoxyribose oligonucleotide which had been 5' end labeled with [gamma-32] and paired with a complementary 2''-deoxyribose oligonucleotide containing either an adenine or a guanine opposite Tg.	transcription
60523	4	335612	7	NULL	NULL	0	NULL	statement 3	Process		pair with					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6111_s_232	12167705	Because of the relative insensitivity of the 3H-based DNA  N-glycosylase release assay, DNA  N-glycosylase activity was measured by the more sensitive method, i.e., cleavage of a Tg residue-containing 2''-deoxyribose oligonucleotide which had been 5' end labeled with [gamma-32] and paired with a complementary 2''-deoxyribose oligonucleotide containing either an adenine or a guanine opposite Tg.	transcription
60524	5	335612	7	NULL	NULL	0	NULL	statement 3	Process		pair with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6111_s_232	12167705	Because of the relative insensitivity of the 3H-based DNA  N-glycosylase release assay, DNA  N-glycosylase activity was measured by the more sensitive method, i.e., cleavage of a Tg residue-containing 2''-deoxyribose oligonucleotide which had been 5' end labeled with [gamma-32] and paired with a complementary 2''-deoxyribose oligonucleotide containing either an adenine or a guanine opposite Tg.	transcription
60525	6	335612	7	NULL	NULL	0	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_17_6111_s_232	12167705	Because of the relative insensitivity of the 3H-based DNA  N-glycosylase release assay, DNA  N-glycosylase activity was measured by the more sensitive method, i.e., cleavage of a Tg residue-containing 2''-deoxyribose oligonucleotide which had been 5' end labeled with [gamma-32] and paired with a complementary 2''-deoxyribose oligonucleotide containing either an adenine or a guanine opposite Tg.	transcription
56173	1	335613	5	NULL	NULL	0	NULL	MutM			inhibit		severely			adenine		intrinsic rate of;;removal of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_25_22605_s_231	11960995	Conditions: DNA, 20 nM; active MutY, 5 nM; MutY alone ( closed circles), 480 nM MutM ( open circles), 480 nM Endo IV ( open triangles), 37  degrees C. Note that MutM severely inhibits the intrinsic rate of adenine removal, whereas similar concentrations of Endo IV only affect turnover.	transcription
60526	1	335613	7	NULL	NULL	0	NULL	 MutM	GP		inhibit		severely			adenine	Chemical	intrinsic rate of removal of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_25_22605_s_231	11960995	Conditions: DNA, 20 nM; active MutY, 5 nM; MutY alone ( closed circles), 480 nM MutM ( open circles), 480 nM Endo IV ( open triangles), 37  degrees C. Note that MutM severely inhibits the intrinsic rate of adenine removal, whereas similar concentrations of Endo IV only affect turnover.	transcription
60527	2	335613	7	NULL	NULL	0	NULL	Endo IV	GP		affect					adenine	Chemical	turnover of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_25_22605_s_231	11960995	Conditions: DNA, 20 nM; active MutY, 5 nM; MutY alone ( closed circles), 480 nM MutM ( open circles), 480 nM Endo IV ( open triangles), 37  degrees C. Note that MutM severely inhibits the intrinsic rate of adenine removal, whereas similar concentrations of Endo IV only affect turnover.	transcription
56185	2	335618	5	NULL	NULL	0	NULL	N6-adenine DNA Mtases M. TaqI		Thermus aquaticus	methylate					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_15066_s_36	10329711	In this publication we show that the  N6-adenine DNA Mtases M. TaqI from  Thermus aquaticus ( 23,  24) and M. CviBIII from the  Chlorella virus NC-1A ( 25), which both methylate adenine within the double-stranded 5''-TCGA-3' DNA sequence, give high photo-cross-linking yields with duplex ODNs containing 5-iodouracil at the target position (Scheme  1).	transcription
56186	1	335618	5	NULL	NULL	0	NULL	adenine			is present within					DNA sequence		double-stranded		5''-TCGA-3' 	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_15066_s_36	10329711	In this publication we show that the  N6-adenine DNA Mtases M. TaqI from  Thermus aquaticus ( 23,  24) and M. CviBIII from the  Chlorella virus NC-1A ( 25), which both methylate adenine within the double-stranded 5''-TCGA-3' DNA sequence, give high photo-cross-linking yields with duplex ODNs containing 5-iodouracil at the target position (Scheme  1).	transcription
56187	3	335618	5	NULL	NULL	0	NULL	M. CviBIII		Chlorella virus NC-1A	methylate					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_15066_s_36	10329711	In this publication we show that the  N6-adenine DNA Mtases M. TaqI from  Thermus aquaticus ( 23,  24) and M. CviBIII from the  Chlorella virus NC-1A ( 25), which both methylate adenine within the double-stranded 5''-TCGA-3' DNA sequence, give high photo-cross-linking yields with duplex ODNs containing 5-iodouracil at the target position (Scheme  1).	transcription
60528	1	335618	7	NULL	NULL	0	NULL	M. TaqI	GP	Thermus aquaticus	methylate					adenine 	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_21_15066_s_36	10329711	In this publication we show that the  N6-adenine DNA Mtases M. TaqI from  Thermus aquaticus ( 23,  24) and M. CviBIII from the  Chlorella virus NC-1A ( 25), which both methylate adenine within the double-stranded 5''-TCGA-3' DNA sequence, give high photo-cross-linking yields with duplex ODNs containing 5-iodouracil at the target position (Scheme  1).	transcription
60529	2	335618	7	NULL	NULL	0	NULL	statement 1	Process		occur within							double-stranded		5''-TCGA-3' DNA sequence	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_15066_s_36	10329711	In this publication we show that the  N6-adenine DNA Mtases M. TaqI from  Thermus aquaticus ( 23,  24) and M. CviBIII from the  Chlorella virus NC-1A ( 25), which both methylate adenine within the double-stranded 5''-TCGA-3' DNA sequence, give high photo-cross-linking yields with duplex ODNs containing 5-iodouracil at the target position (Scheme  1).	transcription
60530	3	335618	7	NULL	NULL	0	NULL	M. CviBIII	GP	Chlorella virus NC-1A	methylate					adenine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_15066_s_36	10329711	In this publication we show that the  N6-adenine DNA Mtases M. TaqI from  Thermus aquaticus ( 23,  24) and M. CviBIII from the  Chlorella virus NC-1A ( 25), which both methylate adenine within the double-stranded 5''-TCGA-3' DNA sequence, give high photo-cross-linking yields with duplex ODNs containing 5-iodouracil at the target position (Scheme  1).	transcription
60531	4	335618	7	NULL	NULL	0	NULL	statement 3	Process		occur within							double-stranded		5''-TCGA-3' DNA sequence	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_15066_s_36	10329711	In this publication we show that the  N6-adenine DNA Mtases M. TaqI from  Thermus aquaticus ( 23,  24) and M. CviBIII from the  Chlorella virus NC-1A ( 25), which both methylate adenine within the double-stranded 5''-TCGA-3' DNA sequence, give high photo-cross-linking yields with duplex ODNs containing 5-iodouracil at the target position (Scheme  1).	transcription
60532	5	335618	7	NULL	NULL	0	NULL	M. TaqI	GP	Thermus aquaticus	is a type of					N6-adenine DNA Mtases	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_15066_s_36	10329711	In this publication we show that the  N6-adenine DNA Mtases M. TaqI from  Thermus aquaticus ( 23,  24) and M. CviBIII from the  Chlorella virus NC-1A ( 25), which both methylate adenine within the double-stranded 5''-TCGA-3' DNA sequence, give high photo-cross-linking yields with duplex ODNs containing 5-iodouracil at the target position (Scheme  1).	transcription
60533	6	335618	7	NULL	NULL	0	NULL	M. CviBIII	GP	Chlorella virus NC-1A	is a type of					N6-adenine DNA Mtases	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_21_15066_s_36	10329711	In this publication we show that the  N6-adenine DNA Mtases M. TaqI from  Thermus aquaticus ( 23,  24) and M. CviBIII from the  Chlorella virus NC-1A ( 25), which both methylate adenine within the double-stranded 5''-TCGA-3' DNA sequence, give high photo-cross-linking yields with duplex ODNs containing 5-iodouracil at the target position (Scheme  1).	transcription
56188	1	335619	5	NULL	NULL	0	NULL	apoptosis			is mediated by					TNF-alpha					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
56189	2	335619	5	NULL	NULL	0	NULL	ceramides			is involved in					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
56190	3	335619	5	NULL	NULL	0	NULL	protein-phosphatase			is activated by					ceramide					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
56191	4	335619	5	NULL	NULL	0	NULL	statement 3			is involved in					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
56192	5	335619	5	NULL	NULL	0	NULL	protein kinase II			is dependent on					calmodulin					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
56193	6	335619	5	NULL	NULL	0	NULL	statement 5			is involved in					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
56194	7	335619	5	NULL	NULL	0	NULL	nicotinamide adenine dinucleotide			is involved in					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
56195	8	335619	5	NULL	NULL	0	NULL	P24			is involved in					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
56196	9	335619	5	NULL	NULL	0	NULL	P21/WAF-1			is involved in					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
56197	10	335619	5	NULL	NULL	0	NULL	mitochondrial respiratory insufficiency			is involved in					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
56198	11	335619	5	NULL	NULL	0	NULL	NFkB			is involved in					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
56199	12	335619	5	NULL	NULL	0	NULL	phospholipase D			is involved in					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60534	1	335619	7	NULL	NULL	0	NULL	TNF-alpha	GP		mediate					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60535	2	335619	7	NULL	NULL	0	NULL	ceramides 	Chemical		is involved in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60536	3	335619	7	NULL	NULL	0	NULL	ceramide	Chemical		activate					protein-phosphatase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60537	4	335619	7	NULL	NULL	0	NULL	statement 3	Process		is involved in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60538	5	335619	7	NULL	NULL	0	NULL	calmodulin-dependent protein kinase II 	GP		is involved in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60539	6	335619	7	NULL	NULL	0	NULL	 nicotinamide adenine dinucleotide	Chemical		is involved in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60540	7	335619	7	NULL	NULL	0	NULL	P24	GP		is involved in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60541	8	335619	7	NULL	NULL	0	NULL	P21/WAF-1	GP		is involved in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60542	9	335619	7	NULL	NULL	0	NULL	mitochondrial respiratory insufficiency 	Process		is involved in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60543	10	335619	7	NULL	NULL	0	NULL	NFkB	GP		is involved in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60544	11	335619	7	NULL	NULL	0	NULL	phospholipase D	GP		is involved in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60545	12	335619	7	NULL	NULL	0	NULL	ceramides	Chemical		is a type of					signaling factor	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60546	13	335619	7	NULL	NULL	0	NULL	ceramide-activated protein-phosphatase	GP		is a type of					signaling factor	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60547	14	335619	7	NULL	NULL	0	NULL	calmodulin-dependent protein kinase II	GP		is a type of					signaling factor	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60548	15	335619	7	NULL	NULL	0	NULL	nicotinamide adenine dinucleotide	Chemical		is a type of					signaling factor	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60549	16	335619	7	NULL	NULL	0	NULL	P24	GP		is a type of					signaling factor	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60550	17	335619	7	NULL	NULL	0	NULL	P21/WAF-1	GP		is a type of					signaling factor	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60551	18	335619	7	NULL	NULL	0	NULL	mitochondrial respiratory insufficiency	Process		is a type of					signaling factor	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60552	19	335619	7	NULL	NULL	0	NULL	NFkB	GP		is a type of					signaling factor	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
60553	20	335619	7	NULL	NULL	0	NULL	phospholipase D	GP		is a type of					signaling factor	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23526_s_11	10438532	Numerous signaling factors have been reported to be involved in the apoptosis process mediated by TNF-alpha, including ceramides and ceramide-activated protein-phosphatase ( 3), calmodulin-dependent protein kinase II ( 4), nicotinamide adenine dinucleotide and P24 ( 5), P21/WAF-1 ( 6), mitochondrial respiratory insufficiency ( 7), NFkB ( 8), and phospholipase D ( 9).	transcription
56485	1	335623	5	NULL	NULL	0	NULL	PDGF			induces					DNA		synthesis of			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58494	2	335623	5	NULL	NULL	0	NULL	antisense oligonucleotides to A(2B) receptor			increases					DNA synthesis		basal			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58495	3	335623	5	NULL	NULL	0	NULL	antisense oligonucleotides to A(2B) receptor			increases					statement 1					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58496	4	335623	5	NULL	NULL	0	NULL	sense oligonucleotides to A(2B) receptor			does not increase					statement 1					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58497	5	335623	5	NULL	NULL	0	NULL	sense oligonucleotides to A(2B) receptor			does not increase					DNA synthesis		basal			NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58498	6	335623	5	NULL	NULL	0	NULL	scrambled oligonucleotides to A(2B) receptor			does not increase					statement 1					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58499	7	335623	5	NULL	NULL	0	NULL	scrambled oligonucleotides to A(2B) receptor			does not increase					DNA synthesis		basal			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58500	8	335623	5	NULL	NULL	0	NULL	antisense oligonucleotides to A(2B) receptor			increases					cell proliferation					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58501	9	335623	5	NULL	NULL	0	NULL	sense oligonucleotides to A(2B) receptor			does not increase					cell proliferation					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58502	10	335623	5	NULL	NULL	0	NULL	scrambled oligonucleotides to A(2B) receptor			does not increase					cell proliferation					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58503	11	335623	5	NULL	NULL	0	NULL	antisense oligonucleotides to A(2B) receptor			increases					collagen		synthesis of			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58504	12	335623	5	NULL	NULL	0	NULL	sense oligonucleotides to A(2B) receptor			does not increase					collagen		synthesis of			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58505	13	335623	5	NULL	NULL	0	NULL	antisense oligonucleotides to A(2B) receptor			abolishes					2-chloroadenosine		growth-inhibitory effects of 			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58506	14	335623	5	NULL	NULL	0	NULL	sense oligonucleotides to A(2B) receptor			does not abolish					2-chloroadenosine		growth-inhibitory effects of 			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58507	15	335623	5	NULL	NULL	0	NULL	scrambled oligonucleotides to A(2B) receptor			does not abolish					2-chloroadenosine		growth-inhibitory effects of			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58508	16	335623	5	NULL	NULL	0	NULL	antisense oligonucleotides to A(2B) receptor			abolishes					5''-N-MECA		growth-inhibitory effects of			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58509	17	335623	5	NULL	NULL	0	NULL	sense oligonucleotides to A(2B) receptor			does not abolish					5''-N-MECA		growth-inhibitory effects of			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58510	18	335623	5	NULL	NULL	0	NULL	scrambled oligonucleotides to A(2B) receptor			does not abolish					5''-N-MECA		growth-inhibitory effects of			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58511	19	335623	5	NULL	NULL	0	NULL	antisense oligonucleotides to A(2B) receptor			abolishes					erythro-9-(2-hydroxy-3-nonyl)adenine		growth-inhibitory effects of			NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58512	20	335623	5	NULL	NULL	0	NULL	sense oligonucleotides to A(2B) receptor			does not abolish					erythro-9-(2-hydroxy-3-nonyl)adenine		growth-inhibitory effects of			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58513	21	335623	5	NULL	NULL	0	NULL	scrambled oligonucleotides to A(2B) receptor			does not abolish					erythro-9-(2-hydroxy-3-nonyl)adenine		growth-inhibitory effects of			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58514	22	335623	5	NULL	NULL	0	NULL	antisense oligonucleotides to A(2B) receptor			abolishes					iodotubercidin		growth-inhibitory effects of			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58515	23	335623	5	NULL	NULL	0	NULL	sense oligonucleotides to A(2B) receptor			does not abolish					iodotubercidin		growth-inhibitory effects of			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58516	24	335623	5	NULL	NULL	0	NULL	scrambled oligonucleotides to A(2B) receptor			does not abolish					iodotubercidin		growth-inhibitory effects of			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58517	25	335623	5	NULL	NULL	0	NULL	iodotubercidin			is an inhibitor of					adenosine kinase					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
58518	26	335623	5	NULL	NULL	0	NULL	erythro-9-(2-hydroxy-3-nonyl)adenine			is an inhibitor of					adenosine deaminase					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60555	1	335623	7	NULL	NULL	0	NULL	PDGF	GP		induce					DNA 	NucleicAcid	synthesis of			NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60556	2	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	antisense oligonucleotides to 	increase					DNA	NucleicAcid	basal synthesis of			NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60557	3	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	antisense oligonucleotides to 	increase					statement 1	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60558	4	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	antisense oligonucleotides to 	increase					cell proliferation	Process				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60559	5	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	antisense oligonucleotides to 	increase					collagen	GP	synthesis of			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60560	6	335623	7	NULL	NULL	0	NULL	2-chloroadenosine	Chemical		inhibit					growth	Process				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60561	7	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	antisense oligonucleotides to 	abolish					statement 6	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60562	9	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	antisense oligonucleotides to 	abolish					statement 8	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60563	11	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	antisense oligonucleotides to 	abolish					statement 10	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60564	8	335623	7	NULL	NULL	0	NULL	 5''-N-MECA	Chemical		inhibit					growth	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60565	10	335623	7	NULL	NULL	0	NULL	erythro-9-(2-hydroxy-3-nonyl)adenine	Chemical		inhibit					growth	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60566	12	335623	7	NULL	NULL	0	NULL	 5''-N-MECA	Chemical		is an inhibitor of					adenosine deaminase	GP				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60567	13	335623	7	NULL	NULL	0	NULL	erythro-9-(2-hydroxy-3-nonyl)adenine	Chemical		is an inhibitor of					adenosine deaminase	GP				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60568	14	335623	7	NULL	NULL	0	NULL	iodotubercidin	Chemical		inhibit					growth	Process				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60569	15	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	 antisense oligonucleotide to	abolish					statement 14	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60570	16	335623	7	NULL	NULL	0	NULL	iodotubercidin	Chemical		is an inhibitor of					adenosine kinase	GP				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60574	17	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	sense oligonucleotide to	does not increase					DNA	NucleicAcid	synthesis of basal			NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60575	18	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	sense oligonucleotide to	does not increase					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60576	19	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	sense oligonucleotide to	does not increase					cell proliferation	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60577	20	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	sense oligonucleotide to	does not increase					collagen	GP	synthesis of			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60578	21	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	sense oligonucleotide to	does not abolish					statement 6	Process				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60579	22	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	sense oligonucleotide to	does not abolish					statement 8	Process				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60580	23	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	sense oligonucleotide to	does not abolish					statement 10	Process				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60581	24	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	sense oligonucleotide to	does not abolish					statement 14	Process				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60582	25	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	scrambled oligonucleotide to	does not increase					DNA	NucleicAcid	synthesis of basal			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60583	26	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	scrambled oligonucleotide to	does not increase					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60584	27	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	scrambled oligonucleotide to	does not increase					cell proliferation	Process				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60585	28	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	scrambled oligonucleotide to	does not increase					collagen	GP	synthesis of			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60586	29	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	scrambled oligonucleotide to	does not abolish					statement 6	Process				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60587	30	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	scrambled oligonucleotide to	does not abolish					statement 8	Process				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60588	31	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	scrambled oligonucleotide to	does not abolish					statement 10	Process				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
60589	32	335623	7	NULL	NULL	0	NULL	A(2B) receptor	GP	scrambled oligonucleotide to	does not abolish					statement 14	Process				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_hypertension_46_3_16103269_s_4	16103269	Antisense, but not sense or scrambled,  oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced  DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory  effects of 2-chloroadenosine, 5''-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine  (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine  kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides  to the A(2B) receptor.	transcription
56486	1	335626	5	NULL	NULL	0	NULL	BH3 only proteins			induces		autonomously			cytochrome c		release of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
56487	2	335626	5	NULL	NULL	0	NULL	BCL-2 family			does not participate in					statement 1					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
56488	3	335626	5	NULL	NULL	0	NULL	mitochondrial proteins		intrinsic	does not participate in					statement 1					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
56489	4	335626	5	NULL	NULL	0	NULL	cardiolipin			is required for					statement 1					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
56490	5	335626	5	NULL	NULL	0	NULL	cardiolipin			is a type of					negatively charged lipids					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
56491	6	335626	5	NULL	NULL	0	NULL	BAX			is a type of					proapoptotic protein					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
56492	7	335626	5	NULL	NULL	0	NULL	BAK			is a type of					proapoptotic protein					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
56493	8	335626	5	NULL	NULL	0	NULL	BAX		activated	mediates					cytochrome c		release of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
56494	9	335626	5	NULL	NULL	0	NULL	BAK		activated	mediates					cytochrome c		release of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
56495	10	335626	5	NULL	NULL	0	NULL	ANT			is					adenine nucleotide exchanger					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
56496	11	335626	5	NULL	NULL	0	NULL	VDAC			is					voltage dependent anion channel					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60590	1	335626	7	NULL	NULL	0	NULL	BH3 only proteins	GP		induce		autonomously			cytochrome c	GP	release of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60591	2	335626	7	NULL	NULL	0	NULL	statement 1	Process		does not involve					BCL-2 family	GP				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60592	3	335626	7	NULL	NULL	0	NULL	statement 1	Process		does not involve					intrinsic mitochondrial proteins	GP				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60593	4	335626	7	NULL	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60594	5	335626	7	NULL	NULL	0	NULL	statement 1	Process		require					cardiolipin	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60595	6	335626	7	NULL	NULL	0	NULL	cardiolipin	Chemical		is a type of					negatively charged lipid	Chemical				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60596	7	335626	7	NULL	NULL	0	NULL	BH3 only proteins	GP		interact with					antiapoptotic BCL-2 family members	GP				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60597	8	335626	7	NULL	NULL	0	NULL	BH3 only proteins	GP		inhibit					antiapoptotic BCL-2 family members	GP				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60598	9	335626	7	NULL	NULL	0	NULL	BH3 only proteins	GP		activate					proapoptotic BAX	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60599	10	335626	7	NULL	NULL	0	NULL	BH3 only proteins	GP		activate					proapoptotic BAK	GP				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60600	11	335626	7	NULL	NULL	0	NULL	statement 9	Process		mediate					cytochrome	GP	release of			NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60601	12	335626	7	NULL	NULL	0	NULL	statement 10	Process		mediate					cytochrome	GP	release of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60602	13	335626	7	NULL	NULL	0	NULL	BH3 only proteins	GP		interact with					ANT	GP				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60603	14	335626	7	NULL	NULL	0	NULL	BH3 only proteins	GP		interact with					VDAC	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60604	15	335626	7	NULL	NULL	0	NULL	statement 13	Process		induce					mitochondrial dysfunction	CellComponent				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60605	16	335626	7	NULL	NULL	0	NULL	statement 14	Process		induce					mitochondrial dysfunction	CellComponent				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60606	17	335626	7	NULL	NULL	0	NULL	statement 13	Process		induce					cytochrome c	GP	release of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60607	18	335626	7	NULL	NULL	0	NULL	statement 14	Process		induce					cytochrome c	GP	release of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60608	19	335626	7	NULL	NULL	0	NULL	statement 13	Process		is an alternative to					statement 14	Process				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60609	20	335626	7	NULL	NULL	0	NULL	ANT	GP		is					adenine nucleotide exchanger 	GP				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60610	21	335626	7	NULL	NULL	0	NULL	VDAC	GP		is					voltage dependent anion channel 	GP				NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60611	22	335626	7	NULL	NULL	0	NULL	ANT	GP		is a type of					 intrinsic mitochondrial proteins 	GP				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
60612	23	335626	7	NULL	NULL	0	NULL	VDAC	GP		is a type of					intrinsic mitochondrial proteins	GP				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_304_3_437_s_7	12729577	At least four main different models have been put  forth: (i) BH3 only proteins autonomously induce cytochrome  c release, without the participation of BCL-2 family or intrinsic mitochondrial proteins  but with a marked requirement for negatively charged lipids such as cardiolipin [  15 and   16]; (ii) they interact and inhibit antiapoptotic BCL-2 family members [  17,   18,   19,   20 and   21]; (iii) they activate the multidomain proapoptotic BAX and BAK to mediate cytochrome   c release [ 5,   22 and   23]; (iv) they interact with intrinsic mitochondrial proteins such as the adenine nucleotide  exchanger (ANT) or the voltage dependent anion channel (VDAC) to induce mitochondrial  dysfunction and cytochrome  c release [  24 and   25].	transcription
56499	3	335629	5	NULL	NULL	0	NULL	long chain fatty acyl-CoAs			regulates		may			metabolism		intermediary			NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
56500	4	335629	5	NULL	NULL	0	NULL	glucokinase		modulation of;;activity of	leads to					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58519	1	335629	5	NULL	NULL	0	NULL	free acids		CoA-thioesterification of;;xenobiotic	produces		endogenously			acyl-CoAs		xenobiotic			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58520	2	335629	5	NULL	NULL	0	NULL	statement 1			is dependent on					ATP					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58521	5	335629	5	NULL	NULL	0	NULL	pyruvate dehydrogenase		modulation of;;activity of	leads to					statement 3					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58522	6	335629	5	NULL	NULL	0	NULL	acetyl-CoA carboxylase		modulation of;;activity of	leads to					statement 3					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58523	7	335629	5	NULL	NULL	0	NULL	delta9-desaturase		modulation of;;activity of	leads to					statement 3					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58524	8	335629	5	NULL	NULL	0	NULL	protein kinase C		modulation of;;activity of	leads to					statement 3					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58525	9	335629	5	NULL	NULL	0	NULL	adenine nucleotide translocase		modulation of;;activity of;;mitochondrial	leads to					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58526	10	335629	5	NULL	NULL	0	NULL	citrate transporter		modulation of;;activity of;;mitochondrial	leads to					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58527	11	335629	5	NULL	NULL	0	NULL	Na/K ATPase		modulation of;;activity of	leads to					statement 3					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58528	12	335629	5	NULL	NULL	0	NULL	ATP-sensitive K-channels		modulation of;;activity of	leads to					statement 3					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58529	13	335629	5	NULL	NULL	0	NULL	Ca-ATPase		modulation of;;activity of;;endoplasmic reticulum	leads to					statement 3					NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58530	14	335629	5	NULL	NULL	0	NULL	transcription factors		modulation of;;activity of	leads to					statement 3					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58531	15	335629	5	NULL	NULL	0	NULL	acyl-CoAs		xenobiotic	regulates		may			metabolism		intermediary			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58532	16	335629	5	NULL	NULL	0	NULL	glucokinase		modulation of;;activity of	leads to					statement 15					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58533	17	335629	5	NULL	NULL	0	NULL	pyruvate dehydrogenase		modulation of;;activity of	leads to					statement 15					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58534	18	335629	5	NULL	NULL	0	NULL	acetyl-CoA carboxylase		modulation of;;activity of	leads to					statement 15					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58535	19	335629	5	NULL	NULL	0	NULL	delta9-desaturase		modulation of;;activity of	leads to					statement 15					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58536	20	335629	5	NULL	NULL	0	NULL	protein kinase C		modulation of;;activity of	leads to					statement 15					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58537	21	335629	5	NULL	NULL	0	NULL	adenine nucleotide translocase		modulation of;;activity of;;mitochondrial	leads to					statement 15					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58538	22	335629	5	NULL	NULL	0	NULL	citrate transporter		modulation of;;activity of;;mitochondrial	leads to					statement 15					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58539	23	335629	5	NULL	NULL	0	NULL	Na/K ATPase		modulation of;;activity of	leads to					statement 15					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58540	24	335629	5	NULL	NULL	0	NULL	ATP-sensitive K-channels		modulation of;;activity of	leads to					statement 15					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58541	25	335629	5	NULL	NULL	0	NULL	Ca-ATPase		modulation of;;activity of;;endoplasmic reticulum	leads to					statement 15					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58542	26	335629	5	NULL	NULL	0	NULL	transcription factors		modulation of;;activity of	leads to					statement 15					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58543	27	335629	5	NULL	NULL	0	NULL	adenine nucleotide translocase		mitochondrial	is a type of					transporter					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58544	28	335629	5	NULL	NULL	0	NULL	citrate transporter		mitochondrial	is a type of					transporter					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58545	29	335629	5	NULL	NULL	0	NULL	Na/K ATPase			is a type of					transporter					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58546	30	335629	5	NULL	NULL	0	NULL	ATP-sensitive K-channels			is a type of					ion channel					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
58547	31	335629	5	NULL	NULL	0	NULL	Ca-ATPase		endoplasmic reticulum	is a type of					ion channel					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60613	1	335629	7	NULL	NULL	0	NULL	long chain fatty acyl-CoA 	Chemical		regulate		may			intermediary metabolism	Process				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60614	2	335629	7	NULL	NULL	0	NULL	statement 1	Process		occur by					glucokinase	GP	modulating			NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60615	3	335629	7	NULL	NULL	0	NULL	statement 1	Process		occur by					pyruvate dehydrogenase	GP	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60616	4	335629	7	NULL	NULL	0	NULL	statement 1	Process		occur by					acetyl-CoA carboxylase	GP	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60617	5	335629	7	NULL	NULL	0	NULL	statement 1	Process		occur by					delta9-desaturase	GP	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60618	6	335629	7	NULL	NULL	0	NULL	statement 1	Process		occur by					protein kinase C	GP	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60619	7	335629	7	NULL	NULL	0	NULL	statement 1	Process		occur by					mitochondrial adenine nucleotide translocase	GP	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60620	8	335629	7	NULL	NULL	0	NULL	statement 1	Process		occur by					mitochondrial citrate transporter	GP	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60621	9	335629	7	NULL	NULL	0	NULL	statement 1	Process		occur by					Na/K ATPase	GP	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60622	10	335629	7	NULL	NULL	0	NULL	statement 1	Process		occur by					ATP-sensitive K-channels	CellComponent	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60623	11	335629	7	NULL	NULL	0	NULL	statement 1	Process		occur by					endoplasmic reticulum Ca-ATPase	GP	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60624	12	335629	7	NULL	NULL	0	NULL	statement 1	Process		occur by					transcription factors	GP	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60625	13	335629	7	NULL	NULL	0	NULL	xenobiotic acyl-CoAs	Chemical		produced by					xenobiotic free acids	Chemical				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60626	14	335629	7	NULL	NULL	0	NULL	statement 13	Process		produced by		endogenously			ATP-dependent CoA-thioesterification	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60627	15	335629	7	NULL	NULL	0	NULL	statement 13	Process		regulate		may			intermediary metabolism	Process				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60628	16	335629	7	NULL	NULL	0	NULL	statement 15	Process		occur by					glucokinase	GP	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60629	17	335629	7	NULL	NULL	0	NULL	statement 15	Process		occur by					pyruvate dehydrogenase	GP	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60630	18	335629	7	NULL	NULL	0	NULL	statement 15	Process		occur by					acetyl-CoA carboxylase	GP	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60631	19	335629	7	NULL	NULL	0	NULL	statement 15	Process		occur by					delta9-desaturase	GP	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60632	20	335629	7	NULL	NULL	0	NULL	statement 15	Process		occur by					protein kinase C	GP	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60633	21	335629	7	NULL	NULL	0	NULL	statement 15	Process		occur by					mitochondrial adenine nucleotide translocase	GP	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60634	22	335629	7	NULL	NULL	0	NULL	statement 15	Process		occur by					mitochondrial citrate transporter	GP	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60635	23	335629	7	NULL	NULL	0	NULL	statement 15	Process		occur by					 Na/K ATPase	GP	modulating			NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60636	24	335629	7	NULL	NULL	0	NULL	statement 15	Process		occur by					ATP-sensitive K-channels	CellComponent	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60637	25	335629	7	NULL	NULL	0	NULL	statement 15	Process		occur by					endoplasmic reticulum Ca-ATPase	GP	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60638	26	335629	7	NULL	NULL	0	NULL	statement 15	Process		occur by					transcription factors	GP	modulating			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60639	27	335629	7	NULL	NULL	0	NULL	mitochondrial adenine nucleotide translocase	GP		is a type of					transporter	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60640	28	335629	7	NULL	NULL	0	NULL	mitochondrial citrate transporter	GP		is a type of					transporter	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60641	29	335629	7	NULL	NULL	0	NULL	Na/K ATPase	GP		is a type of					transporter	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60642	30	335629	7	NULL	NULL	0	NULL	ATP-sensitive K-channels	CellComponent		is a type of					ion channel	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
60643	31	335629	7	NULL	NULL	0	NULL	endoplasmic reticulum Ca-ATPase	GP		is a type of					ion channel	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_7_1125_s_12	12091497	In addition to their substrate role, long chain fatty acyl-CoAs, as well as xenobiotic acyl-CoAs endogenously produced by ATP-dependent CoA-thioesterification of the respective xenobiotic free acids ( 1), may regulate intermediary metabolism by modulating the activity of enzymes (e.g., glucokinase, pyruvate dehydrogenase, acetyl-CoA carboxylase, delta9-desaturase, protein kinase C), transporters (e.g., mitochondrial adenine nucleotide translocase, mitochondrial citrate transporter, Na/K ATPase), ion channels (e.g., ATP-sensitive K-channels, endoplasmic reticulum Ca-ATPase) ( 2 -  4), or transcription factors ( 5 -  9).	transcription
56234	1	335630	5	NULL	NULL	0	NULL	NOS isozymes			is activated by					calcium		intracellular 			NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
56235	2	335630	5	NULL	NULL	0	NULL	iNOS			bind			NOSox		heme					NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
56236	3	335630	5	NULL	NULL	0	NULL	NOSox			is					NH2-terminal catalytic oxygenase domain					NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
56237	4	335630	5	NULL	NULL	0	NULL	iNOS			resides in			NOSox		iNOS			residues 1 to 498		NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
56238	5	335630	5	NULL	NULL	0	NULL	heme			is					iron protoporphyrin IX					NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
56239	6	335630	5	NULL	NULL	0	NULL	iNOS			bind			NOSox		tetrahydrobiopterin					NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
56240	7	335630	5	NULL	NULL	0	NULL	tetrahydrobiopterin			is					H4B					NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
56241	8	335630	5	NULL	NULL	0	NULL	iNOS			bind			NOSox		L-Arg					NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
56242	9	335630	5	NULL	NULL	0	NULL	L-Arg			is a type of					substrate					NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
56243	10	335630	5	NULL	NULL	0	NULL	iNOS			bind			NOSred		FMN					NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
56244	11	335630	5	NULL	NULL	0	NULL	FMN			is					flavin mononucleotide 					NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
56245	12	335630	5	NULL	NULL	0	NULL	NOSred			is					COOH-terminal reductase domain					NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
56246	13	335630	5	NULL	NULL	0	NULL	iNOS			resides in			NOSred		iNOS			residues 531 to 1144		NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
56247	14	335630	5	NULL	NULL	0	NULL	iNOS			bind			NOSred		FAD					NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
56248	15	335630	5	NULL	NULL	0	NULL	FAD			is					flavin adenine dinucleotide					NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
56249	16	335630	5	NULL	NULL	0	NULL	iNOS			bind			NOSred		NADPH					NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
56250	17	335630	5	NULL	NULL	0	NULL	iNOS			communicates with		electronic	NOSox		iNOS			NOSred		NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
56251	18	335630	5	NULL	NULL	0	NULL	iNOS			resides in			calmodulin-binding region		iNOS			residues 499 to 530		NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
56252	19	335630	5	NULL	NULL	0	NULL	iNOS			regulates			calmodulin-binding region		statement 17					NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
60644	1	335630	7	NULL	NULL	0	NULL	iNOS	GP		bind			NOSox, residues 1 to 498		iron protoporphyrin IX	Chemical				NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
60645	2	335630	7	NULL	NULL	0	NULL	i NOS	GP		bind			NOSox, residues 1 to 498		H4B	Chemical				NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
60646	3	335630	7	NULL	NULL	0	NULL	iNOS	GP		bind			NOSox, residues 1 to 498		L-Arg	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
60647	4	335630	7	NULL	NULL	0	NULL	iNOS			is a type of			NOSox, residues 1 to 498					NH2-terminal catalytic oxygenase domain		NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
60648	5	335630	7	NULL	NULL	0	NULL	H4B	Chemical		is					tetrahydrobiopterin	Chemical				NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
60649	6	335630	7	NULL	NULL	0	NULL	iNOS	GP		bind			NOSred, residues 531 to 1144		FMN	Chemical				NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
60650	7	335630	7	NULL	NULL	0	NULL	iNOS			bind			NOSred, residues 531 to 1144		FAD	Chemical				NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
60651	8	335630	7	NULL	NULL	0	NULL	iNOS	GP		bind			NOSred, residues 531 to 1144		NADPH	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
60652	9	335630	7	NULL	NULL	0	NULL	FMN	Chemical		is					flavin mononucleotide 	Chemical				NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
60653	10	335630	7	NULL	NULL	0	NULL	FAD	Chemical		is					flavin adenine dinucleotide	Chemical				NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
60654	11	335630	7	NULL	NULL	0	NULL	NOSox	GP		communicate with		electronically			NOSred	GP				NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
60655	12	335630	7	NULL	NULL	0	NULL	iNOS	GP		regulates			intervening calmodulin-binding region (residues 499 to 530)		statement 11	Process				NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
60656	13	335630	7	NULL	NULL	0	NULL	iron protoporphyrin IX	Chemical		is a type of					heme	Chemical				NULL		0	NULL	NULL	NULL	gw60_science_278_5337_425_s_22	9334294	NOS isozymes differ in size (130 to 160 kD), amino acid sequence (50 to 60% identity between any two isozymes), tissue distribution, transcriptional regulation, and activation by intracellular calcium ( 1), but they share an overall three-component construction ( 1,  2,  4,  5): (i) an NH2-terminal catalytic oxygenase domain (NOSox, residues 1 to 498 for iNOS) that binds heme (iron protoporphyrin IX), tetrahydrobiopterin (H4B), and the substrate L-Arg; (ii) a COOH-terminal reductase domain (NOSred, residues 531 to 1144 for iNOS) that binds flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and NADPH; and (iii) an intervening calmodulin-binding region (residues 499 to 530 for iNOS) that regulates electronic communication between NOSox and NOSred ( 5,  9).	transcription
56253	1	335631	5	NULL	NULL	0	NULL	ATP			is transported to					mitochondrion					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
56254	2	335631	5	NULL	NULL	0	NULL	statement 1			via					translocase					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
56255	3	335631	5	NULL	NULL	0	NULL	translocase			is similar to					adenine nucleotide transporter					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
56256	4	335631	5	NULL	NULL	0	NULL	adenine nucleotide transporter			sensitive to					carboxyatractyloside					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
56257	5	335631	5	NULL	NULL	0	NULL	ATPase			is associated with					RIC					NULL	mitochondria	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
56258	6	335631	5	NULL	NULL	0	NULL	statement 5		activation of	catalyze					ATP		hydrolysis of			NULL	mitochondria	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
56259	7	335631	5	NULL	NULL	0	NULL	tRNA-receptor		binding of	leads to					statement 6					NULL	mitochondria 	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
56260	8	335631	5	NULL	NULL	0	NULL	protons			pumped from					membrane		inside			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
56261	9	335631	5	NULL	NULL	0	NULL	protons			pumped to					membrane		outside			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
56262	10	335631	5	NULL	NULL	0	NULL	statement 8			occurs simultaneously with					statement 9					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
56263	11	335631	5	NULL	NULL	0	NULL	statement 10			occurs through					oligomycin-sensitive channel					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
56264	12	335631	5	NULL	NULL	0	NULL	statement 10			generates					membrane potential					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
56265	13	335631	5	NULL	NULL	0	NULL	ATP		hydrolysis of	is accompanied by					statement 10					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
56266	14	335631	5	NULL	NULL	0	NULL	proton gradient		establishment of	opens					import channel					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
56267	15	335631	5	NULL	NULL	0	NULL	statement 14			occurs by		possibly			voltage gating					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
56268	16	335631	5	NULL	NULL	0	NULL	tRNA			transported through					import pore					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
60758	1	335631	7	NULL	NULL	0	NULL	ATP	Chemical		is transported into					mitochondrion	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
60759	2	335631	7	NULL	NULL	0	NULL	statement 1	Process		via					translocase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
60760	3	335631	7	NULL	NULL	0	NULL	translocase	GP		is similar to					carboxyatractyloside-sensitive adenine nucleotide transporter	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
60761	4	335631	7	NULL	NULL	0	NULL	RIC	GP		associate with					ATPase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
60762	5	335631	7	NULL	NULL	0	NULL	tRNA-receptor	GP	binding of	leads to					statement 4	Process	activation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
60763	6	335631	7	NULL	NULL	0	NULL	ATP	Chemical		hydrolyze within					mitochondrion	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
60764	7	335631	7	NULL	NULL	0	NULL	statement 4	Process		catalyze					statement 6	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
60766	8	335631	7	NULL	NULL	0	NULL	protons	Chemical		pumped from					inside membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
60767	9	335631	7	NULL	NULL	0	NULL	protons	Chemical		pumped to					outside membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
60769	10	335631	7	NULL	NULL	0	NULL	statement 8	Process		occur along with					statement 9	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
60770	11	335631	7	NULL	NULL	0	NULL	statement 10	Process		occur through					oligomycin-sensitive channel	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
60771	12	335631	7	NULL	NULL	0	NULL	statement 6	Process		is accompanied by					statement 10	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
60772	13	335631	7	NULL	NULL	0	NULL	statement 10	Process		result in					membrane potential	Process	generation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
60773	14	335631	7	NULL	NULL	0	NULL	Proton gradient	Process		leads to					import channel	CellComponent	opening of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
60774	15	335631	7	NULL	NULL	0	NULL	statement 14	Process		occur by		may			voltage gating	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
60775	16	335631	7	NULL	NULL	0	NULL	statement 15	Process		explain					deltapsi	Process	requirement of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
60776	17	335631	7	NULL	NULL	0	NULL	tRNA	NucleicAcid		is transported through					import pore	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
60777	18	335631	7	NULL	NULL	0	NULL	deltapsi	Process		is a type of					membrane potential	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_12_11259_s_142	14739289	Our current results are consistent with a multistep pathway of energy transduction within the complex leading, ultimately, to tRNA translocation; 1) substrate tRNA binds to its receptor; 2) ATP is transported into the mitochondrion via a translocase, which is similar or identical to the carboxyatractyloside-sensitive adenine nucleotide transporter; 3) tRNA-receptor binding leads to the activation of an RIC-associated ATPase which catalyzes ATP hydrolysis within the mitochondrion; 4) ATP hydrolysis is accompanied by pumping of protons through an oligomycin-sensitive channel from inside to outside the membrane, resulting in the generation of a membrane potential; 5) establishment of the proton gradient leads to opening of the import channel, possibly by voltage gating; this would explain the requirement for the membrane potential, deltapsi; 6) the tRNA is transported through the import pore.	transcription
58548	1	335632	5	NULL	NULL	0	NULL	target			undergoes					alteration					NULL	ribosomes	0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
58549	3	335632	5	NULL	NULL	0	NULL	statement 2			leads to					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
58550	2	335632	5	NULL	NULL	0	NULL	product of the erm gene			dimethylates					23S ribosomal RNA 				specific adenine residue \t	NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
58551	4	335632	5	NULL	NULL	0	NULL	statement 3			decreases					MLS antibiotics		binding of			NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
58552	5	335632	5	NULL	NULL	0	NULL	STG-B			is					streptogramin B					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
58553	6	335632	5	NULL	NULL	0	NULL	sbh gene			encodes					streptogramin B hydrolase					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
58554	7	335632	5	NULL	NULL	0	NULL	streptogramin B hydrolase			inactivates					STG-B					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
58555	8	335632	5	NULL	NULL	0	NULL	streptogramin B hydrolase			inactivates					lincosamide					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
58556	9	335632	5	NULL	NULL	0	NULL	linA''			encodes					3-lincomycin 4-clindamycin O-nucleotidyltransferase					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
58557	10	335632	5	NULL	NULL	0	NULL	3-lincomycin 4-clindamycin O-nucleotidyltransferase			inactivates					STG-B					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
58558	11	335632	5	NULL	NULL	0	NULL	3-lincomycin 4-clindamycin O-nucleotidyltransferase			inactivates					lincosamide					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
58559	12	335632	5	NULL	NULL	0	NULL	Mac antibiotics		active efflux of	determined by					msrA gene		Staphylococcus epidermidis			NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
58560	13	335632	5	NULL	NULL	0	NULL	STG-B antibiotics		active efflux of	determined by					msrB gene		Staphylococcus xylosus			NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
58561	15	335632	5	NULL	NULL	0	NULL	msrA gene		Staphylococcus epidermidis	acts as					statement 14					NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
58562	14	335632	5	NULL	NULL	0	NULL	efflux pump			is dependent on					ATP					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
58563	16	335632	5	NULL	NULL	0	NULL	msrB gene		Staphylococcus xylosus	acts as					statement 14					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
58564	17	335632	5	NULL	NULL	0	NULL	MLS antibiotics			is					macrolide, lincosamide, and streptogramin B antibiotics  					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
58565	18	335632	5	NULL	NULL	0	NULL	streptogramin B			is a type of					antibiotic					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
58566	19	335632	5	NULL	NULL	0	NULL	lincosamide			is a type of					antibiotic					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
58567	20	335632	5	NULL	NULL	0	NULL	macrolide			is a type of					antibiotic					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60778	1	335632	7	NULL	NULL	0	NULL	staphylococci 	Organism		resistant to					macrolide	Chemical				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60779	2	335632	7	NULL	NULL	0	NULL	staphylococci 	Organism		resistant to					lincosamide	Chemical				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60780	3	335632	7	NULL	NULL	0	NULL	staphylococci 	Organism		resistant to					streptogramin B	Chemical				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60781	4	335632	7	NULL	NULL	0	NULL	erm gene	GP	product of	dimethylates					adenine residues	NucleicAcid				NULL	23S ribosomal RNA	0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60782	5	335632	7	NULL	NULL	0	NULL	ribosome	CellComponent	alteration of target on	due to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60783	6	335632	7	NULL	NULL	0	NULL	statement 5	Process		decrease					MLS antibiotics	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60784	7	335632	7	NULL	NULL	0	NULL	statement 5	Process		leads to					STG-B	Chemical	inactivation of			NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60785	8	335632	7	NULL	NULL	0	NULL	statement 5	Process		leads to					lincosamide	Chemical	inactivation of			NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60786	9	335632	7	NULL	NULL	0	NULL	sbh	GP		catalyze					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60789	10	335632	7	NULL	NULL	0	NULL	linA	GP		catalyze					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60790	11	335632	7	NULL	NULL	0	NULL	sbh	GP		encode					streptogramin B hydrolase	GP				NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60791	12	335632	7	NULL	NULL	0	NULL	linA	GP		encode					3-lincomycin 4-clindamycin O-nucleotidyltransferase	GP				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60792	13	335632	7	NULL	NULL	0	NULL	STG-B	Chemical		is					streptogramin B	Chemical				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60799	14	335632	7	NULL	NULL	0	NULL	Mac	Chemical	active efflux of	determined by					msrA gene					NULL	Staphylococcus epidermidis	NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60808	15	335632	7	NULL	NULL	0	NULL	STG-B antibiotics	Chemical	active efflux of	determined by					msrB genes	GP				NULL	Staphylococcus xylosus	0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60811	16	335632	7	NULL	NULL	0	NULL	Mac	Chemical	active efflux of	act as					ATP-dependent efflux pumps	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60812	17	335632	7	NULL	NULL	0	NULL	STG-B antibiotics	Chemical	active efflux of	act as					ATP-dependent efflux pumps	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60813	18	335632	7	NULL	NULL	0	NULL	statement 1	Process		reflect					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60814	19	335632	7	NULL	NULL	0	NULL	statement 2	Process		reflect					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60815	20	335632	7	NULL	NULL	0	NULL	statement 3	Process		reflect					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60816	21	335632	7	NULL	NULL	0	NULL	statement 1	Process		reflect					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60817	22	335632	7	NULL	NULL	0	NULL	statement 2	Process		reflect					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60818	23	335632	7	NULL	NULL	0	NULL	statement 3	Process		reflect					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60819	24	335632	7	NULL	NULL	0	NULL	statement 1	Process		reflect					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60820	25	335632	7	NULL	NULL	0	NULL	statement 2	Process		reflect					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60821	26	335632	7	NULL	NULL	0	NULL	statement 3	Process		reflect					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60822	27	335632	7	NULL	NULL	0	NULL	statement 1	Process		reflect					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60823	28	335632	7	NULL	NULL	0	NULL	statement 2	Process		reflect					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60824	29	335632	7	NULL	NULL	0	NULL	statement 3	Process		reflect					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60825	30	335632	7	NULL	NULL	0	NULL	statement 1	Process		reflect					statement 16	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60826	31	335632	7	NULL	NULL	0	NULL	statement 2	Process		reflect					statement 16	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60827	32	335632	7	NULL	NULL	0	NULL	statement 3	Process		reflect					statement 16	Process				NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60828	33	335632	7	NULL	NULL	0	NULL	statement 1	Process		reflect					statement 17	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60829	34	335632	7	NULL	NULL	0	NULL	statement 2	Process		reflect					statement 17	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
60830	35	335632	7	NULL	NULL	0	NULL	statement 3	Process		reflect					statement 17	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_181_1_91_s_6	10564793	Resistance to macrolide, lincosamide, and streptogramin B (MLS) antibiotics in staphylococci is known to have the following mechanisms: (1) alteration of the target on ribosome due to dimethylation of a specific adenine residue in the 23S ribosomal RNA by the product of the  erm gene, and consequently a decrease in binding of MLS antibiotics [  4,   5 and   6]; (2) inactivation of streptogramin B (STG-B) and lincosamide by the products of the  sbh (encoding streptogramin B hydrolase) [  7] and  linA'' (encoding 3-lincomycin 4-clindamycin  O-nucleotidyltransferase) [  8 genes, respectively; and (3) active efflux of Mac and STG-B antibiotics determined by the  msrA and  msrB genes in  Staphylococcus epidermidis and  Staphylococcus xylosus, respectively [  9 and   10], both of which appear to act as ATP-dependent efflux pumps.	transcription
56269	1	335634	5	NULL	NULL	0	NULL	choline			is oxidized to					glycine-betaine					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_36	12676692	Oxidation of choline to glycine-betaine catalyzed by choline dehydrogenase.	transcription
56270	2	335634	5	NULL	NULL	0	NULL	choline dehydrogenase			catalyze					statement 1					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_36	12676692	Oxidation of choline to glycine-betaine catalyzed by choline dehydrogenase.	transcription
60831	1	335634	7	NULL	NULL	0	NULL	choline	Chemical		oxidizes to					glycine-betaine	AminoAcid				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_36	12676692	Oxidation of choline to glycine-betaine catalyzed by choline dehydrogenase.	transcription
60832	2	335634	7	NULL	NULL	0	NULL	choline dehydrogenase	GP		catalyze					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_36	12676692	Oxidation of choline to glycine-betaine catalyzed by choline dehydrogenase.	transcription
56271	1	335635	5	NULL	NULL	0	NULL	choline			is converted to					glycine betaine					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_7_2273_s_62	10094709	CudA and CudB catalyze the conversion of choline to glycine betaine.	transcription
56272	2	335635	5	NULL	NULL	0	NULL	CudB			catalyze					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_7_2273_s_62	10094709	CudA and CudB catalyze the conversion of choline to glycine betaine.	transcription
56273	3	335635	5	NULL	NULL	0	NULL	CudA			catalyze					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_7_2273_s_62	10094709	CudA and CudB catalyze the conversion of choline to glycine betaine.	transcription
60833	1	335635	7	NULL	NULL	0	NULL	choline	Chemical		converted to					glycine betaine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbacteriol_181_7_2273_s_62	10094709	CudA and CudB catalyze the conversion of choline to glycine betaine.	transcription
60834	2	335635	7	NULL	NULL	0	NULL	CudA 	GP		catalyze					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_7_2273_s_62	10094709	CudA and CudB catalyze the conversion of choline to glycine betaine.	transcription
60835	3	335635	7	NULL	NULL	0	NULL	CudB	GP		catalyze					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbacteriol_181_7_2273_s_62	10094709	CudA and CudB catalyze the conversion of choline to glycine betaine.	transcription
56274	1	335636	5	NULL	NULL	0	NULL	bet genes			is induced by					choline					NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_158	8905077	The  bet genes are also induced by choline and repressed by glycine betaine.	transcription
56275	2	335636	5	NULL	NULL	0	NULL	bet genes			repressed by					glycine betaine					NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_158	8905077	The  bet genes are also induced by choline and repressed by glycine betaine.	transcription
60836	1	335636	7	NULL	NULL	0	NULL	 choline	Chemical		induce					bet genes	GP				NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_158	8905077	The  bet genes are also induced by choline and repressed by glycine betaine.	transcription
60837	2	335636	7	NULL	NULL	0	NULL	glycine betaine	AminoAcid		repress					bet genes	GP				NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_158	8905077	The  bet genes are also induced by choline and repressed by glycine betaine.	transcription
56276	1	335637	5	NULL	NULL	0	NULL	choline			is oxidized to					glycine betaine					NULL	cytoplasm	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1420_1_30_s_18	10446288	Enzymes BetB and BetA catalyze the cytoplasmic oxidation of choline to glycine betaine.	transcription
56277	2	335637	5	NULL	NULL	0	NULL	BetB enzyme			catalyze					statement 1					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1420_1_30_s_18	10446288	Enzymes BetB and BetA catalyze the cytoplasmic oxidation of choline to glycine betaine.	transcription
56278	3	335637	5	NULL	NULL	0	NULL	BetA enzyme			catalyze					statement 1					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1420_1_30_s_18	10446288	Enzymes BetB and BetA catalyze the cytoplasmic oxidation of choline to glycine betaine.	transcription
60838	1	335637	7	NULL	NULL	0	NULL	Choline	Chemical		oxidizes to					glycine betaine	AminoAcid				NULL	cytoplasm	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1420_1_30_s_18	10446288	Enzymes BetB and BetA catalyze the cytoplasmic oxidation of choline to glycine betaine.	transcription
60839	2	335637	7	NULL	NULL	0	NULL	BetB	GP		catalyze					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1420_1_30_s_18	10446288	Enzymes BetB and BetA catalyze the cytoplasmic oxidation of choline to glycine betaine.	transcription
60840	3	335637	7	NULL	NULL	0	NULL	BetA	GP		catalyze					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1420_1_30_s_18	10446288	Enzymes BetB and BetA catalyze the cytoplasmic oxidation of choline to glycine betaine.	transcription
56279	1	335638	5	NULL	NULL	0	NULL	choline			is oxidized to					glycine-betaine					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_2_296_s_131	14702297	Choline is an osmoprotectant for  E. coli K-12 because BetT mediates choline uptake while BetB and BetA mediate choline oxidation to glycine-betaine ( ).	transcription
56280	2	335638	5	NULL	NULL	0	NULL	BetB			mediates					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_2_296_s_131	14702297	Choline is an osmoprotectant for  E. coli K-12 because BetT mediates choline uptake while BetB and BetA mediate choline oxidation to glycine-betaine ( ).	transcription
56281	3	335638	5	NULL	NULL	0	NULL	BetA			mediates					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_2_296_s_131	14702297	Choline is an osmoprotectant for  E. coli K-12 because BetT mediates choline uptake while BetB and BetA mediate choline oxidation to glycine-betaine ( ).	transcription
56282	4	335638	5	NULL	NULL	0	NULL	BetT			mediates					choline		uptake of			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_2_296_s_131	14702297	Choline is an osmoprotectant for  E. coli K-12 because BetT mediates choline uptake while BetB and BetA mediate choline oxidation to glycine-betaine ( ).	transcription
56283	5	335638	5	NULL	NULL	0	NULL	choline			acts as					osmoprotectant		E. coli K-12			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_2_296_s_131	14702297	Choline is an osmoprotectant for  E. coli K-12 because BetT mediates choline uptake while BetB and BetA mediate choline oxidation to glycine-betaine ( ).	transcription
60841	1	335638	7	NULL	NULL	0	NULL	choline	Chemical		is a type of					osmoprotectant	Chemical				NULL	E. coli K-12	0	NULL	NULL	NULL	gw70_jbacteriol_186_2_296_s_131	14702297	Choline is an osmoprotectant for  E. coli K-12 because BetT mediates choline uptake while BetB and BetA mediate choline oxidation to glycine-betaine ( ).	transcription
60842	2	335638	7	NULL	NULL	0	NULL	BetT	GP		mediates					choline	Chemical	uptake of			NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_2_296_s_131	14702297	Choline is an osmoprotectant for  E. coli K-12 because BetT mediates choline uptake while BetB and BetA mediate choline oxidation to glycine-betaine ( ).	transcription
60843	3	335638	7	NULL	NULL	0	NULL	statement 1	Process		because of					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_2_296_s_131	14702297	Choline is an osmoprotectant for  E. coli K-12 because BetT mediates choline uptake while BetB and BetA mediate choline oxidation to glycine-betaine ( ).	transcription
60844	4	335638	7	NULL	NULL	0	NULL	choline	Chemical		oxidizes to					glycine-betaine	Aminoacid				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_2_296_s_131	14702297	Choline is an osmoprotectant for  E. coli K-12 because BetT mediates choline uptake while BetB and BetA mediate choline oxidation to glycine-betaine ( ).	transcription
60845	5	335638	7	NULL	NULL	0	NULL	BetB	GP		mediate					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_2_296_s_131	14702297	Choline is an osmoprotectant for  E. coli K-12 because BetT mediates choline uptake while BetB and BetA mediate choline oxidation to glycine-betaine ( ).	transcription
60846	6	335638	7	NULL	NULL	0	NULL	BetA	GP		mediate					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_2_296_s_131	14702297	Choline is an osmoprotectant for  E. coli K-12 because BetT mediates choline uptake while BetB and BetA mediate choline oxidation to glycine-betaine ( ).	transcription
56284	1	335639	5	NULL	NULL	0	NULL	choline sulfate			hydrolyzed to					choline					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiolrev_24_2_135_s_349	10717312	The BetC protein catalyzes the hydrolysis of choline sulfate to choline, and is part of a pathway that synthesizes the osmoprotectant glycine betaine.	transcription
56285	2	335639	5	NULL	NULL	0	NULL	BetC protein			catalyze					statement 1					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiolrev_24_2_135_s_349	10717312	The BetC protein catalyzes the hydrolysis of choline sulfate to choline, and is part of a pathway that synthesizes the osmoprotectant glycine betaine.	transcription
56286	3	335639	5	NULL	NULL	0	NULL	glycine betaine			is a type of					osmoprotectant					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiolrev_24_2_135_s_349	10717312	The BetC protein catalyzes the hydrolysis of choline sulfate to choline, and is part of a pathway that synthesizes the osmoprotectant glycine betaine.	transcription
56287	4	335639	5	NULL	NULL	0	NULL	BetC protein			plays a role in					glycine betaine		synthesis of			NULL		0	NULL	NULL	NULL	gw60_femsmicrobiolrev_24_2_135_s_349	10717312	The BetC protein catalyzes the hydrolysis of choline sulfate to choline, and is part of a pathway that synthesizes the osmoprotectant glycine betaine.	transcription
60847	1	335639	7	NULL	NULL	0	NULL	choline sulfate	Chemical		hydrolyze to					Choline	Chemical				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiolrev_24_2_135_s_349	10717312	The BetC protein catalyzes the hydrolysis of choline sulfate to choline, and is part of a pathway that synthesizes the osmoprotectant glycine betaine.	transcription
60848	2	335639	7	NULL	NULL	0	NULL	BetC protein 	GP		catalyze					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiolrev_24_2_135_s_349	10717312	The BetC protein catalyzes the hydrolysis of choline sulfate to choline, and is part of a pathway that synthesizes the osmoprotectant glycine betaine.	transcription
60849	3	335639	7	NULL	NULL	0	NULL	BetC protein 	GP		is part of					glycine betaine	AminoAcid	pathway that synthesizes			NULL		0	NULL	NULL	NULL	gw60_femsmicrobiolrev_24_2_135_s_349	10717312	The BetC protein catalyzes the hydrolysis of choline sulfate to choline, and is part of a pathway that synthesizes the osmoprotectant glycine betaine.	transcription
60850	4	335639	7	NULL	NULL	0	NULL	glycine betaine	AminoAcid		is a type of					osmoprotectant	Chemical				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiolrev_24_2_135_s_349	10717312	The BetC protein catalyzes the hydrolysis of choline sulfate to choline, and is part of a pathway that synthesizes the osmoprotectant glycine betaine.	transcription
56288	1	335640	5	NULL	NULL	0	NULL	choline			is oxidized to					glycine betaine					NULL		0	NULL	NULL	NULL	abs-batch0550-0559_j-am-chem-soc_127_50_16351127_s_2	16351127	Choline oxidase catalyzes the flavin-linked oxidation of choline to glycine  betaine, with betaine aldehyde as intermediate and oxygen as electron  acceptor.	transcription
56289	2	335640	5	NULL	NULL	0	NULL	statement 1			linked to					flavin					NULL		0	NULL	NULL	NULL	abs-batch0550-0559_j-am-chem-soc_127_50_16351127_s_2	16351127	Choline oxidase catalyzes the flavin-linked oxidation of choline to glycine  betaine, with betaine aldehyde as intermediate and oxygen as electron  acceptor.	transcription
56290	3	335640	5	NULL	NULL	0	NULL	choline oxidase			catalyze					statement 1					NULL		0	NULL	NULL	NULL	abs-batch0550-0559_j-am-chem-soc_127_50_16351127_s_2	16351127	Choline oxidase catalyzes the flavin-linked oxidation of choline to glycine  betaine, with betaine aldehyde as intermediate and oxygen as electron  acceptor.	transcription
56291	4	335640	5	NULL	NULL	0	NULL	betaine aldehyde			is produced as					intermediate					NULL		0	NULL	NULL	NULL	abs-batch0550-0559_j-am-chem-soc_127_50_16351127_s_2	16351127	Choline oxidase catalyzes the flavin-linked oxidation of choline to glycine  betaine, with betaine aldehyde as intermediate and oxygen as electron  acceptor.	transcription
56292	5	335640	5	NULL	NULL	0	NULL	statement 4			occurs simultaneously with					statement 1					NULL		0	NULL	NULL	NULL	abs-batch0550-0559_j-am-chem-soc_127_50_16351127_s_2	16351127	Choline oxidase catalyzes the flavin-linked oxidation of choline to glycine  betaine, with betaine aldehyde as intermediate and oxygen as electron  acceptor.	transcription
56293	6	335640	5	NULL	NULL	0	NULL	oxygen			acts as					electron acceptor					NULL		0	NULL	NULL	NULL	abs-batch0550-0559_j-am-chem-soc_127_50_16351127_s_2	16351127	Choline oxidase catalyzes the flavin-linked oxidation of choline to glycine  betaine, with betaine aldehyde as intermediate and oxygen as electron  acceptor.	transcription
60851	1	335640	7	NULL	NULL	0	NULL	Choline	Chemical		oxidizes to					glycine betaine	AminoAcid				NULL		0	NULL	NULL	NULL	abs-batch0550-0559_j-am-chem-soc_127_50_16351127_s_2	16351127	Choline oxidase catalyzes the flavin-linked oxidation of choline to glycine  betaine, with betaine aldehyde as intermediate and oxygen as electron  acceptor.	transcription
60852	2	335640	7	NULL	NULL	0	NULL	Choline oxidase	GP		catalyze					statement 1	Process	flavin-linked oxidation of			NULL		0	NULL	NULL	NULL	abs-batch0550-0559_j-am-chem-soc_127_50_16351127_s_2	16351127	Choline oxidase catalyzes the flavin-linked oxidation of choline to glycine  betaine, with betaine aldehyde as intermediate and oxygen as electron  acceptor.	transcription
60853	3	335640	7	NULL	NULL	0	NULL	betaine aldehyde	Chemical		acts as a					statement 1	Chemical	intermediate of			NULL		NULL	NULL	NULL	NULL	abs-batch0550-0559_j-am-chem-soc_127_50_16351127_s_2	16351127	Choline oxidase catalyzes the flavin-linked oxidation of choline to glycine  betaine, with betaine aldehyde as intermediate and oxygen as electron  acceptor.	transcription
60854	4	335640	7	NULL	NULL	0	NULL	oxygen	Chemical		acts as a					statement 1	Process	electron acceptor of			NULL		0	NULL	NULL	NULL	abs-batch0550-0559_j-am-chem-soc_127_50_16351127_s_2	16351127	Choline oxidase catalyzes the flavin-linked oxidation of choline to glycine  betaine, with betaine aldehyde as intermediate and oxygen as electron  acceptor.	transcription
56294	1	335641	5	NULL	NULL	0	NULL	choline			is oxidized to					glycine betaine					NULL		0	NULL	NULL	NULL	abs-batch0600-0619_biochemistry_45_6_16460045_s_2	16460045	Choline oxidase catalyzes the four-electron oxidation of choline to glycine  betaine via two sequential FAD-dependent reactions in which betaine aldehyde  is formed as an intermediate.	transcription
56295	2	335641	5	NULL	NULL	0	NULL	statement 1			via					FAD-dependent reactions		sequential			NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_biochemistry_45_6_16460045_s_2	16460045	Choline oxidase catalyzes the four-electron oxidation of choline to glycine  betaine via two sequential FAD-dependent reactions in which betaine aldehyde  is formed as an intermediate.	transcription
56296	3	335641	5	NULL	NULL	0	NULL	choline oxidase			catalyze					statement 1					NULL		0	NULL	NULL	NULL	abs-batch0600-0619_biochemistry_45_6_16460045_s_2	16460045	Choline oxidase catalyzes the four-electron oxidation of choline to glycine  betaine via two sequential FAD-dependent reactions in which betaine aldehyde  is formed as an intermediate.	transcription
56297	4	335641	5	NULL	NULL	0	NULL	betaine aldehyde			formed as					intermediate					NULL		0	NULL	NULL	NULL	abs-batch0600-0619_biochemistry_45_6_16460045_s_2	16460045	Choline oxidase catalyzes the four-electron oxidation of choline to glycine  betaine via two sequential FAD-dependent reactions in which betaine aldehyde  is formed as an intermediate.	transcription
56298	5	335641	5	NULL	NULL	0	NULL	statement 4			occurs simultaneously with					statement 1					NULL		0	NULL	NULL	NULL	abs-batch0600-0619_biochemistry_45_6_16460045_s_2	16460045	Choline oxidase catalyzes the four-electron oxidation of choline to glycine  betaine via two sequential FAD-dependent reactions in which betaine aldehyde  is formed as an intermediate.	transcription
60855	1	335641	7	NULL	NULL	0	NULL	choline	Chemical		oxidizes to					glycine betaine	AminoAcid				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_biochemistry_45_6_16460045_s_2	16460045	Choline oxidase catalyzes the four-electron oxidation of choline to glycine  betaine via two sequential FAD-dependent reactions in which betaine aldehyde  is formed as an intermediate.	transcription
60856	2	335641	7	NULL	NULL	0	NULL	Choline oxidase	GP		catalyze					statement 1	Process	four-electron oxidation of			NULL		0	NULL	NULL	NULL	abs-batch0600-0619_biochemistry_45_6_16460045_s_2	16460045	Choline oxidase catalyzes the four-electron oxidation of choline to glycine  betaine via two sequential FAD-dependent reactions in which betaine aldehyde  is formed as an intermediate.	transcription
60857	3	335641	7	NULL	NULL	0	NULL	statement 2	Process		via					sequential FAD-dependent reactions	Process				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_biochemistry_45_6_16460045_s_2	16460045	Choline oxidase catalyzes the four-electron oxidation of choline to glycine  betaine via two sequential FAD-dependent reactions in which betaine aldehyde  is formed as an intermediate.	transcription
60858	4	335641	7	NULL	NULL	0	NULL	betaine aldehyde	Chemical		is formed as a					statement 1	Process	intermediate of			NULL		0	NULL	NULL	NULL	abs-batch0600-0619_biochemistry_45_6_16460045_s_2	16460045	Choline oxidase catalyzes the four-electron oxidation of choline to glycine  betaine via two sequential FAD-dependent reactions in which betaine aldehyde  is formed as an intermediate.	transcription
56299	1	335642	5	NULL	NULL	0	NULL	choline			is converted to					glycine betaine					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_6_1683_s_137	14996799	To test whether the thermoprotective effect of choline was dependent on its GbsA- and GbsB-mediated enzymatic conversion to glycine betaine ( ), we grew the delta( gbsAB:: neo) 2 strain JBB5 in the presence of either glycine betaine or choline.	transcription
56300	2	335642	5	NULL	NULL	0	NULL	GbsA enzyme			mediates					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_6_1683_s_137	14996799	To test whether the thermoprotective effect of choline was dependent on its GbsA- and GbsB-mediated enzymatic conversion to glycine betaine ( ), we grew the delta( gbsAB:: neo) 2 strain JBB5 in the presence of either glycine betaine or choline.	transcription
56301	3	335642	5	NULL	NULL	0	NULL	GbsB enzyme			mediates					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_6_1683_s_137	14996799	To test whether the thermoprotective effect of choline was dependent on its GbsA- and GbsB-mediated enzymatic conversion to glycine betaine ( ), we grew the delta( gbsAB:: neo) 2 strain JBB5 in the presence of either glycine betaine or choline.	transcription
56302	4	335642	5	NULL	NULL	0	NULL	choline		thermoprotective effect of	is dependent on		possibly			statement 2					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_6_1683_s_137	14996799	To test whether the thermoprotective effect of choline was dependent on its GbsA- and GbsB-mediated enzymatic conversion to glycine betaine ( ), we grew the delta( gbsAB:: neo) 2 strain JBB5 in the presence of either glycine betaine or choline.	transcription
56303	5	335642	5	NULL	NULL	0	NULL	choline		thermoprotective effect of	is dependent on		possibly			statement 3					NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_6_1683_s_137	14996799	To test whether the thermoprotective effect of choline was dependent on its GbsA- and GbsB-mediated enzymatic conversion to glycine betaine ( ), we grew the delta( gbsAB:: neo) 2 strain JBB5 in the presence of either glycine betaine or choline.	transcription
60859	1	335642	7	NULL	NULL	0	NULL	GbsA	GP		mediate					glycine betaine	AminoAcid	enzymatic conversion to			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_6_1683_s_137	14996799	To test whether the thermoprotective effect of choline was dependent on its GbsA- and GbsB-mediated enzymatic conversion to glycine betaine ( ), we grew the delta( gbsAB:: neo) 2 strain JBB5 in the presence of either glycine betaine or choline.	transcription
60860	2	335642	7	NULL	NULL	0	NULL	GbsB	GP		mediate					glycine betaine	AminoAcid	enzymatic conversion to			NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_6_1683_s_137	14996799	To test whether the thermoprotective effect of choline was dependent on its GbsA- and GbsB-mediated enzymatic conversion to glycine betaine ( ), we grew the delta( gbsAB:: neo) 2 strain JBB5 in the presence of either glycine betaine or choline.	transcription
56314	1	335643	5	NULL	NULL	0	NULL	BetB			is					choline dehydrogenase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_28_20011_s_74	10391951	The proposed pathway of choline degradation ( 17) is initiated by two subsequent oxidation steps catalyzed by choline dehydrogenase (BetB) and glycine betaine aldehyde dehydrogenase (BetA) leading to the formation of glycine betaine, which can be metabolized further ( 16).	transcription
56315	2	335643	5	NULL	NULL	0	NULL	BetA			is					glycine betaine aldehyde dehydrogenase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_28_20011_s_74	10391951	The proposed pathway of choline degradation ( 17) is initiated by two subsequent oxidation steps catalyzed by choline dehydrogenase (BetB) and glycine betaine aldehyde dehydrogenase (BetA) leading to the formation of glycine betaine, which can be metabolized further ( 16).	transcription
56316	3	335643	5	NULL	NULL	0	NULL	BetB			catalyze					glycine betaine		formation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_28_20011_s_74	10391951	The proposed pathway of choline degradation ( 17) is initiated by two subsequent oxidation steps catalyzed by choline dehydrogenase (BetB) and glycine betaine aldehyde dehydrogenase (BetA) leading to the formation of glycine betaine, which can be metabolized further ( 16).	transcription
56317	4	335643	5	NULL	NULL	0	NULL	BetA			catalyze					glycine betaine		formation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_28_20011_s_74	10391951	The proposed pathway of choline degradation ( 17) is initiated by two subsequent oxidation steps catalyzed by choline dehydrogenase (BetB) and glycine betaine aldehyde dehydrogenase (BetA) leading to the formation of glycine betaine, which can be metabolized further ( 16).	transcription
56318	5	335643	5	NULL	NULL	0	NULL	statement 3			subsequent to					statement 4					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_28_20011_s_74	10391951	The proposed pathway of choline degradation ( 17) is initiated by two subsequent oxidation steps catalyzed by choline dehydrogenase (BetB) and glycine betaine aldehyde dehydrogenase (BetA) leading to the formation of glycine betaine, which can be metabolized further ( 16).	transcription
56319	6	335643	5	NULL	NULL	0	NULL	statement 5			initiates					choline degradation pathway					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_28_20011_s_74	10391951	The proposed pathway of choline degradation ( 17) is initiated by two subsequent oxidation steps catalyzed by choline dehydrogenase (BetB) and glycine betaine aldehyde dehydrogenase (BetA) leading to the formation of glycine betaine, which can be metabolized further ( 16).	transcription
56320	7	335643	5	NULL	NULL	0	NULL	glycine betaine			undergoes					metabolism					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_28_20011_s_74	10391951	The proposed pathway of choline degradation ( 17) is initiated by two subsequent oxidation steps catalyzed by choline dehydrogenase (BetB) and glycine betaine aldehyde dehydrogenase (BetA) leading to the formation of glycine betaine, which can be metabolized further ( 16).	transcription
60861	1	335643	7	NULL	NULL	0	NULL	choline 	Chemical		degraded to					glycine betaine	AminoAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_28_20011_s_74	10391951	The proposed pathway of choline degradation ( 17) is initiated by two subsequent oxidation steps catalyzed by choline dehydrogenase (BetB) and glycine betaine aldehyde dehydrogenase (BetA) leading to the formation of glycine betaine, which can be metabolized further ( 16).	transcription
60862	2	335643	7	NULL	NULL	0	NULL	choline dehydrogenase	GP		catalyze					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_28_20011_s_74	10391951	The proposed pathway of choline degradation ( 17) is initiated by two subsequent oxidation steps catalyzed by choline dehydrogenase (BetB) and glycine betaine aldehyde dehydrogenase (BetA) leading to the formation of glycine betaine, which can be metabolized further ( 16).	transcription
60863	3	335643	7	NULL	NULL	0	NULL	glycine betaine aldehyde dehydrogenase 	GP		catalyze					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_28_20011_s_74	10391951	The proposed pathway of choline degradation ( 17) is initiated by two subsequent oxidation steps catalyzed by choline dehydrogenase (BetB) and glycine betaine aldehyde dehydrogenase (BetA) leading to the formation of glycine betaine, which can be metabolized further ( 16).	transcription
60864	4	335643	7	NULL	NULL	0	NULL	BetB	GP		is					choline dehydrogenase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_28_20011_s_74	10391951	The proposed pathway of choline degradation ( 17) is initiated by two subsequent oxidation steps catalyzed by choline dehydrogenase (BetB) and glycine betaine aldehyde dehydrogenase (BetA) leading to the formation of glycine betaine, which can be metabolized further ( 16).	transcription
60865	5	335643	7	NULL	NULL	0	NULL	BetA	GP		is					glycine betaine aldehyde dehydrogenase 	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_28_20011_s_74	10391951	The proposed pathway of choline degradation ( 17) is initiated by two subsequent oxidation steps catalyzed by choline dehydrogenase (BetB) and glycine betaine aldehyde dehydrogenase (BetA) leading to the formation of glycine betaine, which can be metabolized further ( 16).	transcription
60866	6	335643	7	NULL	NULL	0	NULL	statement 2	Process		is a type of					oxidation step	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_28_20011_s_74	10391951	The proposed pathway of choline degradation ( 17) is initiated by two subsequent oxidation steps catalyzed by choline dehydrogenase (BetB) and glycine betaine aldehyde dehydrogenase (BetA) leading to the formation of glycine betaine, which can be metabolized further ( 16).	transcription
60867	7	335643	7	NULL	NULL	0	NULL	statement 3	Process		is a type of					oxidation step	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_28_20011_s_74	10391951	The proposed pathway of choline degradation ( 17) is initiated by two subsequent oxidation steps catalyzed by choline dehydrogenase (BetB) and glycine betaine aldehyde dehydrogenase (BetA) leading to the formation of glycine betaine, which can be metabolized further ( 16).	transcription
60868	1	335645	7	NULL	NULL	0	NULL	fixA-lacZ transcriptional fusion	GP	expression of	induced by					l-carnitine	Chemical				NULL		0	NULL	NULL	NULL	gw70_annurevnutr_18_0_39_s_114	9706218	Expression of a  fixA-lacZ transcriptional fusion was induced by  l-carnitine and crotonobetaine, but not by  d-carnitine,  -butyrobetaine, glycine betaine, or choline.	transcription
60869	2	335645	7	NULL	NULL	0	NULL	fixA-lacZ transcriptional fusion	GP	expression of	induced by					crotonobetaine	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_annurevnutr_18_0_39_s_114	9706218	Expression of a  fixA-lacZ transcriptional fusion was induced by  l-carnitine and crotonobetaine, but not by  d-carnitine,  -butyrobetaine, glycine betaine, or choline.	transcription
60870	3	335645	7	NULL	NULL	0	NULL	d-carnitine	Chemical		does not induce					fixA-lacZ transcriptional fusion	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_annurevnutr_18_0_39_s_114	9706218	Expression of a  fixA-lacZ transcriptional fusion was induced by  l-carnitine and crotonobetaine, but not by  d-carnitine,  -butyrobetaine, glycine betaine, or choline.	transcription
60871	4	335645	7	NULL	NULL	0	NULL	butyrobetaine	Chemical		does not induce					fixA-lacZ transcriptional fusion	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_annurevnutr_18_0_39_s_114	9706218	Expression of a  fixA-lacZ transcriptional fusion was induced by  l-carnitine and crotonobetaine, but not by  d-carnitine,  -butyrobetaine, glycine betaine, or choline.	transcription
60872	5	335645	7	NULL	NULL	0	NULL	glycine betaine	AminoAcid		does not induce					fixA-lacZ transcriptional fusion	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_annurevnutr_18_0_39_s_114	9706218	Expression of a  fixA-lacZ transcriptional fusion was induced by  l-carnitine and crotonobetaine, but not by  d-carnitine,  -butyrobetaine, glycine betaine, or choline.	transcription
60873	6	335645	7	NULL	NULL	0	NULL	choline	Chemical		does not induce					fixA-lacZ transcriptional fusion	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_annurevnutr_18_0_39_s_114	9706218	Expression of a  fixA-lacZ transcriptional fusion was induced by  l-carnitine and crotonobetaine, but not by  d-carnitine,  -butyrobetaine, glycine betaine, or choline.	transcription
56321	1	335646	5	NULL	NULL	0	NULL	choline			is oxidized to					glycine betaine					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_3	12676692	99.1) catalyzes the four-electron oxidation of choline to glycine-betaine via a betaine-aldehyde intermediate.	transcription
56322	2	335646	5	NULL	NULL	0	NULL	statement 1			via					betaine-aldehyde intermediate					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_3	12676692	99.1) catalyzes the four-electron oxidation of choline to glycine-betaine via a betaine-aldehyde intermediate.	transcription
60874	1	335646	7	NULL	NULL	0	NULL	choline	Chemical		oxidizes to					glycine-betaine	AminoAcid				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_3	12676692	99.1) catalyzes the four-electron oxidation of choline to glycine-betaine via a betaine-aldehyde intermediate.	transcription
60875	2	335646	7	NULL	NULL	0	NULL	statement 1	Process		via					betaine-aldehyde intermediate	Chemical				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_3	12676692	99.1) catalyzes the four-electron oxidation of choline to glycine-betaine via a betaine-aldehyde intermediate.	transcription
56323	1	335647	5	NULL	NULL	0	NULL	ABC transporters			mediates					choline		uptake of			NULL	Bacillus subtilis	NULL	NULL	NULL	NULL	gw60_genomeres_11_9_1484_s_448	11544192	Two evolutionarily closely related ABC transporters mediate the uptake of choline for synthesis of the osmoprotectant glycine betaine in  Bacillus subtilis.	transcription
56324	2	335647	5	NULL	NULL	0	NULL	statement 1			is required for					glycine betaine		synthesis of			NULL	Bacillus subtilis	0	NULL	NULL	NULL	gw60_genomeres_11_9_1484_s_448	11544192	Two evolutionarily closely related ABC transporters mediate the uptake of choline for synthesis of the osmoprotectant glycine betaine in  Bacillus subtilis.	transcription
56325	3	335647	5	NULL	NULL	0	NULL	glycine betaine			is a type of					osmoprotectant					NULL		0	NULL	NULL	NULL	gw60_genomeres_11_9_1484_s_448	11544192	Two evolutionarily closely related ABC transporters mediate the uptake of choline for synthesis of the osmoprotectant glycine betaine in  Bacillus subtilis.	transcription
60876	1	335647	7	NULL	NULL	0	NULL	ABC transporters	GP		mediate					choline	Chemical	uptake of			NULL	Bacillus subtilis	NULL	NULL	NULL	NULL	gw60_genomeres_11_9_1484_s_448	11544192	Two evolutionarily closely related ABC transporters mediate the uptake of choline for synthesis of the osmoprotectant glycine betaine in  Bacillus subtilis.	transcription
60877	2	335647	7	NULL	NULL	0	NULL	statement 1	Process		for synthesis of					glycine betaine	AminoAcid				NULL	Bacillus subtilis	0	NULL	NULL	NULL	gw60_genomeres_11_9_1484_s_448	11544192	Two evolutionarily closely related ABC transporters mediate the uptake of choline for synthesis of the osmoprotectant glycine betaine in  Bacillus subtilis.	transcription
60878	3	335647	7	NULL	NULL	0	NULL	glycine betaine	AminoAcid		is a type of					osmoprotectant	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_genomeres_11_9_1484_s_448	11544192	Two evolutionarily closely related ABC transporters mediate the uptake of choline for synthesis of the osmoprotectant glycine betaine in  Bacillus subtilis.	transcription
56326	1	335650	5	NULL	NULL	0	NULL	glycine			induces					steady-state currents					NULL	wild type transporters	0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13856_s_174	10788509	Replacement of sodium by choline abolished glycine induced steady-state currents in wild type and mutant transporters.	transcription
56327	2	335650	5	NULL	NULL	0	NULL	glycine			induces					steady-state currents					NULL	mutant transporters	0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13856_s_174	10788509	Replacement of sodium by choline abolished glycine induced steady-state currents in wild type and mutant transporters.	transcription
56328	3	335650	5	NULL	NULL	0	NULL	sodium			is replaced with					choline					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13856_s_174	10788509	Replacement of sodium by choline abolished glycine induced steady-state currents in wild type and mutant transporters.	transcription
56329	4	335650	5	NULL	NULL	0	NULL	statement 3			abolishes					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13856_s_174	10788509	Replacement of sodium by choline abolished glycine induced steady-state currents in wild type and mutant transporters.	transcription
56330	5	335650	5	NULL	NULL	0	NULL	statement 3			abolishes					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13856_s_174	10788509	Replacement of sodium by choline abolished glycine induced steady-state currents in wild type and mutant transporters.	transcription
60881	1	335650	7	NULL	NULL	0	NULL	glycine	AminoAcid		induce					transporter	GP	steady-state current;; wild type			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_18_13856_s_174	10788509	Replacement of sodium by choline abolished glycine induced steady-state currents in wild type and mutant transporters.	transcription
60882	2	335650	7	NULL	NULL	0	NULL	glycine	AminoAcid		induce					transporter	GP	steady-state current;;mutant			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_18_13856_s_174	10788509	Replacement of sodium by choline abolished glycine induced steady-state currents in wild type and mutant transporters.	transcription
60883	3	335650	7	NULL	NULL	0	NULL	sodium	Chemical		replaced by					choline	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13856_s_174	10788509	Replacement of sodium by choline abolished glycine induced steady-state currents in wild type and mutant transporters.	transcription
60884	4	335650	7	NULL	NULL	0	NULL	statement 3	Process		abolish					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13856_s_174	10788509	Replacement of sodium by choline abolished glycine induced steady-state currents in wild type and mutant transporters.	transcription
60885	5	335650	7	NULL	NULL	0	NULL	statement 3	Process		abolish					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13856_s_174	10788509	Replacement of sodium by choline abolished glycine induced steady-state currents in wild type and mutant transporters.	transcription
56331	1	335651	5	NULL	NULL	0	NULL	choline- O-sulfate			hydrolyzed to					choline					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_227	0009925583	Recently, Osteraos et al. ( 50) reported the presence of a choline sulfatase activity (BetC) in the rhizosphere bacterium  Sinorhizobium meliloti that catalyzed the hydrolysis of choline- O-sulfate into choline and sulfate; the produced choline was then further oxidized into glycine betaine by the BetA and BetB enzymes.	transcription
56332	2	335651	5	NULL	NULL	0	NULL	choline- O-sulfate			hydrolyzed to					sulfate					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_227	0009925583	Recently, Osteraos et al. ( 50) reported the presence of a choline sulfatase activity (BetC) in the rhizosphere bacterium  Sinorhizobium meliloti that catalyzed the hydrolysis of choline- O-sulfate into choline and sulfate; the produced choline was then further oxidized into glycine betaine by the BetA and BetB enzymes.	transcription
56333	3	335651	5	NULL	NULL	0	NULL	statement 1			occurs along with					statement 2					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_227	0009925583	Recently, Osteraos et al. ( 50) reported the presence of a choline sulfatase activity (BetC) in the rhizosphere bacterium  Sinorhizobium meliloti that catalyzed the hydrolysis of choline- O-sulfate into choline and sulfate; the produced choline was then further oxidized into glycine betaine by the BetA and BetB enzymes.	transcription
56334	4	335651	5	NULL	NULL	0	NULL	BetC		Sinorhizobium meliloti	catalyze					statement 3					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_227	0009925583	Recently, Osteraos et al. ( 50) reported the presence of a choline sulfatase activity (BetC) in the rhizosphere bacterium  Sinorhizobium meliloti that catalyzed the hydrolysis of choline- O-sulfate into choline and sulfate; the produced choline was then further oxidized into glycine betaine by the BetA and BetB enzymes.	transcription
56335	5	335651	5	NULL	NULL	0	NULL	Sinorhizobium meliloti			is a type of					rhizosphere bacterium					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_227	0009925583	Recently, Osteraos et al. ( 50) reported the presence of a choline sulfatase activity (BetC) in the rhizosphere bacterium  Sinorhizobium meliloti that catalyzed the hydrolysis of choline- O-sulfate into choline and sulfate; the produced choline was then further oxidized into glycine betaine by the BetA and BetB enzymes.	transcription
56364	6	335651	5	NULL	NULL	0	NULL	choline			is oxidized to					glycine betaine					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_227	0009925583	Recently, Osteraos et al. ( 50) reported the presence of a choline sulfatase activity (BetC) in the rhizosphere bacterium  Sinorhizobium meliloti that catalyzed the hydrolysis of choline- O-sulfate into choline and sulfate; the produced choline was then further oxidized into glycine betaine by the BetA and BetB enzymes.	transcription
56365	7	335651	5	NULL	NULL	0	NULL	BetA enzyme			catalyzes					statement 6					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_227	0009925583	Recently, Osteraos et al. ( 50) reported the presence of a choline sulfatase activity (BetC) in the rhizosphere bacterium  Sinorhizobium meliloti that catalyzed the hydrolysis of choline- O-sulfate into choline and sulfate; the produced choline was then further oxidized into glycine betaine by the BetA and BetB enzymes.	transcription
56366	8	335651	5	NULL	NULL	0	NULL	BetB enzyme			catalyzes					statement 6					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_227	0009925583	Recently, Osteraos et al. ( 50) reported the presence of a choline sulfatase activity (BetC) in the rhizosphere bacterium  Sinorhizobium meliloti that catalyzed the hydrolysis of choline- O-sulfate into choline and sulfate; the produced choline was then further oxidized into glycine betaine by the BetA and BetB enzymes.	transcription
60886	1	335651	7	NULL	NULL	0	NULL	choline- O-sulfate	Chemical		hydrolyzed to					choline	Chemical				NULL	Sinorhizobium meliloti 	NULL	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_227	0009925583	Recently, Osteraos et al. ( 50) reported the presence of a choline sulfatase activity (BetC) in the rhizosphere bacterium  Sinorhizobium meliloti that catalyzed the hydrolysis of choline- O-sulfate into choline and sulfate; the produced choline was then further oxidized into glycine betaine by the BetA and BetB enzymes.	transcription
60887	2	335651	7	NULL	NULL	0	NULL	choline- O-sulfate	Chemical		hydrolyzed to					sulfate	Chemical				NULL	Sinorhizobium meliloti	NULL	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_227	0009925583	Recently, Osteraos et al. ( 50) reported the presence of a choline sulfatase activity (BetC) in the rhizosphere bacterium  Sinorhizobium meliloti that catalyzed the hydrolysis of choline- O-sulfate into choline and sulfate; the produced choline was then further oxidized into glycine betaine by the BetA and BetB enzymes.	transcription
60888	3	335651	7	NULL	NULL	0	NULL	statement 1	Process		occur simultaneous with					statement 2	Process				NULL	Sinorhizobium meliloti 	NULL	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_227	0009925583	Recently, Osteraos et al. ( 50) reported the presence of a choline sulfatase activity (BetC) in the rhizosphere bacterium  Sinorhizobium meliloti that catalyzed the hydrolysis of choline- O-sulfate into choline and sulfate; the produced choline was then further oxidized into glycine betaine by the BetA and BetB enzymes.	transcription
60889	4	335651	7	NULL	NULL	0	NULL	BetC	GP		catalyze					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_227	0009925583	Recently, Osteraos et al. ( 50) reported the presence of a choline sulfatase activity (BetC) in the rhizosphere bacterium  Sinorhizobium meliloti that catalyzed the hydrolysis of choline- O-sulfate into choline and sulfate; the produced choline was then further oxidized into glycine betaine by the BetA and BetB enzymes.	transcription
60890	5	335651	7	NULL	NULL	0	NULL	BetC	GP		catalyze					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_227	0009925583	Recently, Osteraos et al. ( 50) reported the presence of a choline sulfatase activity (BetC) in the rhizosphere bacterium  Sinorhizobium meliloti that catalyzed the hydrolysis of choline- O-sulfate into choline and sulfate; the produced choline was then further oxidized into glycine betaine by the BetA and BetB enzymes.	transcription
60891	6	335651	7	NULL	NULL	0	NULL	BetC	GP		is					choline sulfatase	GP				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_227	0009925583	Recently, Osteraos et al. ( 50) reported the presence of a choline sulfatase activity (BetC) in the rhizosphere bacterium  Sinorhizobium meliloti that catalyzed the hydrolysis of choline- O-sulfate into choline and sulfate; the produced choline was then further oxidized into glycine betaine by the BetA and BetB enzymes.	transcription
60895	7	335651	7	NULL	NULL	0	NULL	choline	Chemical		oxidizes to					glycine betaine	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_227	0009925583	Recently, Osteraos et al. ( 50) reported the presence of a choline sulfatase activity (BetC) in the rhizosphere bacterium  Sinorhizobium meliloti that catalyzed the hydrolysis of choline- O-sulfate into choline and sulfate; the produced choline was then further oxidized into glycine betaine by the BetA and BetB enzymes.	transcription
60899	8	335651	7	NULL	NULL	0	NULL	BetA	GP		catalyze					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_227	0009925583	Recently, Osteraos et al. ( 50) reported the presence of a choline sulfatase activity (BetC) in the rhizosphere bacterium  Sinorhizobium meliloti that catalyzed the hydrolysis of choline- O-sulfate into choline and sulfate; the produced choline was then further oxidized into glycine betaine by the BetA and BetB enzymes.	transcription
60902	9	335651	7	NULL	NULL	0	NULL	BetB	GP		catalyze					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_227	0009925583	Recently, Osteraos et al. ( 50) reported the presence of a choline sulfatase activity (BetC) in the rhizosphere bacterium  Sinorhizobium meliloti that catalyzed the hydrolysis of choline- O-sulfate into choline and sulfate; the produced choline was then further oxidized into glycine betaine by the BetA and BetB enzymes.	transcription
60905	10	335651	7	NULL	NULL	0	NULL	Sinorhizobium meliloti	Organism		is a type of					rhizosphere bacterium	Organism				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_227	0009925583	Recently, Osteraos et al. ( 50) reported the presence of a choline sulfatase activity (BetC) in the rhizosphere bacterium  Sinorhizobium meliloti that catalyzed the hydrolysis of choline- O-sulfate into choline and sulfate; the produced choline was then further oxidized into glycine betaine by the BetA and BetB enzymes.	transcription
56367	1	335652	5	NULL	NULL	0	NULL	choline transport system		A. halophytica	has affinity for		low			choline					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1621_1_102_s_186	12667616	The data in  Fig. 3B revealed that the choline transport system of  A. halophytica had a low affinity for choline ( Km, 272  M) which is in contrast to a rather high affinity for glycine betaine transporter  ( Km, 2  M) [ 15].	transcription
56368	2	335652	5	NULL	NULL	0	NULL	glycine betaine transporter		A. halophytica	has affinity for		high			choline					NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1621_1_102_s_186	12667616	The data in  Fig. 3B revealed that the choline transport system of  A. halophytica had a low affinity for choline ( Km, 272  M) which is in contrast to a rather high affinity for glycine betaine transporter  ( Km, 2  M) [ 15].	transcription
60906	1	335652	7	NULL	NULL	0	NULL	choline transport system	GP	A. halophytica	has low affinity for					choline	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1621_1_102_s_186	12667616	The data in  Fig. 3B revealed that the choline transport system of  A. halophytica had a low affinity for choline ( Km, 272  M) which is in contrast to a rather high affinity for glycine betaine transporter  ( Km, 2  M) [ 15].	transcription
60907	2	335652	7	NULL	NULL	0	NULL	glycine betaine transporter	GP	A. halophytica	high affinity for					choline	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1621_1_102_s_186	12667616	The data in  Fig. 3B revealed that the choline transport system of  A. halophytica had a low affinity for choline ( Km, 272  M) which is in contrast to a rather high affinity for glycine betaine transporter  ( Km, 2  M) [ 15].	transcription
56369	1	335653	5	NULL	NULL	0	NULL	choline			is oxidized to					glycine-betaine					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_32	12676692	Choline dehydrogenase catalyzes the four-electron oxidation of choline to glycine-betaine via a betaine-aldehyde intermediate ( ) (Fig.  1) and shows an absolute requirement for an electron acceptor other than molecular oxygen for catalysis ( ,  ).	transcription
56370	2	335653	5	NULL	NULL	0	NULL	statement 1			via					betaine-aldehyde intermediate					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_32	12676692	Choline dehydrogenase catalyzes the four-electron oxidation of choline to glycine-betaine via a betaine-aldehyde intermediate ( ) (Fig.  1) and shows an absolute requirement for an electron acceptor other than molecular oxygen for catalysis ( ,  ).	transcription
56371	3	335653	5	NULL	NULL	0	NULL	choline dehydrogenase			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_32	12676692	Choline dehydrogenase catalyzes the four-electron oxidation of choline to glycine-betaine via a betaine-aldehyde intermediate ( ) (Fig.  1) and shows an absolute requirement for an electron acceptor other than molecular oxygen for catalysis ( ,  ).	transcription
56372	4	335653	5	NULL	NULL	0	NULL	electron acceptor			is required for					statement 3					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_32	12676692	Choline dehydrogenase catalyzes the four-electron oxidation of choline to glycine-betaine via a betaine-aldehyde intermediate ( ) (Fig.  1) and shows an absolute requirement for an electron acceptor other than molecular oxygen for catalysis ( ,  ).	transcription
60908	1	335653	7	NULL	NULL	0	NULL	choline	Chemical		oxidizes to					glycine-betaine	AminoAcid				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_32	12676692	Choline dehydrogenase catalyzes the four-electron oxidation of choline to glycine-betaine via a betaine-aldehyde intermediate ( ) (Fig.  1) and shows an absolute requirement for an electron acceptor other than molecular oxygen for catalysis ( ,  ).	transcription
60909	2	335653	7	NULL	NULL	0	NULL	statement 1	Process		via					betaine-aldehyde intermediate	Chemical				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_32	12676692	Choline dehydrogenase catalyzes the four-electron oxidation of choline to glycine-betaine via a betaine-aldehyde intermediate ( ) (Fig.  1) and shows an absolute requirement for an electron acceptor other than molecular oxygen for catalysis ( ,  ).	transcription
60910	3	335653	7	NULL	NULL	0	NULL	Choline dehydrogenase	GP		catalyze					statement 1	Process	four-electron oxidation of			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_32	12676692	Choline dehydrogenase catalyzes the four-electron oxidation of choline to glycine-betaine via a betaine-aldehyde intermediate ( ) (Fig.  1) and shows an absolute requirement for an electron acceptor other than molecular oxygen for catalysis ( ,  ).	transcription
60914	4	335653	7	NULL	NULL	0	NULL	statement 3	Process		require					electron acceptor	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_32	12676692	Choline dehydrogenase catalyzes the four-electron oxidation of choline to glycine-betaine via a betaine-aldehyde intermediate ( ) (Fig.  1) and shows an absolute requirement for an electron acceptor other than molecular oxygen for catalysis ( ,  ).	transcription
60918	5	335653	7	NULL	NULL	0	NULL	statement 3	Process		require					molecular oxygen	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_32	12676692	Choline dehydrogenase catalyzes the four-electron oxidation of choline to glycine-betaine via a betaine-aldehyde intermediate ( ) (Fig.  1) and shows an absolute requirement for an electron acceptor other than molecular oxygen for catalysis ( ,  ).	transcription
56373	1	335654	5	NULL	NULL	0	NULL	glycine-betaine			is produced from					choline					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
56374	2	335654	5	NULL	NULL	0	NULL	betA gene			clustered in									bet operon	NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
56375	3	335654	5	NULL	NULL	0	NULL	betB gene			clustered in									bet operon	NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
56376	4	335654	5	NULL	NULL	0	NULL	betI gene			clustered in									bet operon	NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
56377	5	335654	5	NULL	NULL	0	NULL	betT gene			clustered in									bet operon	NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
56378	6	335654	5	NULL	NULL	0	NULL	statement 2			occurs simultaneously with					statement 3					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
56379	7	335654	5	NULL	NULL	0	NULL	statement 4			occurs simultaneously with					statement 5					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
56380	8	335654	5	NULL	NULL	0	NULL	betA gene			encodes					choline dehydrogenase					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
56381	9	335654	5	NULL	NULL	0	NULL	betB gene			encodes					betaine-aldehyde dehydrogenase					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
56382	10	335654	5	NULL	NULL	0	NULL	betI gene			is a type of					putative regulator					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
56383	11	335654	5	NULL	NULL	0	NULL	betT gene			encodes					choline transporter					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
60920	1	335654	7	NULL	NULL	0	NULL	glycine-betaine	AminoAcid		produced from					choline	Chemical				NULL	E.coli	0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
60921	2	335654	7	NULL	NULL	0	NULL	betA	GP		encode					choline dehydrogenase	GP				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
60922	3	335654	7	NULL	NULL	0	NULL	 betB	GP		encode					betaine-aldehyde dehydrogenase	GP				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
60923	4	335654	7	NULL	NULL	0	NULL	betI	GP		encode					putative regulator	GP				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
60924	5	335654	7	NULL	NULL	0	NULL	betT	GP		encode					choline transporter	GP				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
60925	6	335654	7	NULL	NULL	0	NULL	betA	GP		clustered in					bet operon	GP				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
60926	7	335654	7	NULL	NULL	0	NULL	betB	GP		clustered in					bet operon	GP				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
60927	8	335654	7	NULL	NULL	0	NULL	betI	GP		clustered in					bet operon	GP				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
60928	9	335654	7	NULL	NULL	0	NULL	betT	GP		clustered in					bet operon	GP				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_4_2126_s_24	12676692	In  E. coli, the biosynthetic pathway for the production of glycine-betaine from choline has been well characterized at the genetic level, where it has been shown that four genes encoding choline dehydrogenase ( betA), betaine-aldehyde dehydrogenase ( betB), a putative regulator ( betI), and a choline transporter ( betT) are clustered in the  bet operon ( ).	transcription
56384	1	335655	5	NULL	NULL	0	NULL	choline		uptake of	occurs by					transport activity		constitutive low-affinity			NULL	R. meliloti	0	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_272	8905077	However, Pocard et al ( 111) also showed that glycine betaine is not a potent inhibitor of choline uptake by  the constitutive low-affinity transport activity of  R. meliloti.	transcription
56385	2	335655	5	NULL	NULL	0	NULL	glycine betaine			is not an inhibitor of		potent			statement 1					NULL	R. meliloti	0	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_272	8905077	However, Pocard et al ( 111) also showed that glycine betaine is not a potent inhibitor of choline uptake by  the constitutive low-affinity transport activity of  R. meliloti.	transcription
60929	1	335655	7	NULL	NULL	0	NULL	glycine betaine	AminoAcid		is not potent inhibitor of					choline	Chemical	uptake of			NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_272	8905077	However, Pocard et al ( 111) also showed that glycine betaine is not a potent inhibitor of choline uptake by  the constitutive low-affinity transport activity of  R. meliloti.	transcription
60930	2	335655	7	NULL	NULL	0	NULL	R. meliloti	Organism		possess					transport activity	Process	 constitutive low-affinity 			NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_272	8905077	However, Pocard et al ( 111) also showed that glycine betaine is not a potent inhibitor of choline uptake by  the constitutive low-affinity transport activity of  R. meliloti.	transcription
56386	1	335656	5	NULL	NULL	0	NULL	alanine			reduce		slightly			GABA		rates of;;transport of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
56387	2	335656	5	NULL	NULL	0	NULL	histidine			does not reduce					GABA		uptake of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
56388	3	335656	5	NULL	NULL	0	NULL	D-proline			does not reduce					GABA		uptake of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
56389	4	335656	5	NULL	NULL	0	NULL	L-proline			does not reduce					GABA		uptake of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
56390	5	335656	5	NULL	NULL	0	NULL	glycine betaine			does not reduce					GABA		uptake of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
56391	6	335656	5	NULL	NULL	0	NULL	choline			does not reduce					GABA		uptake of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
56392	7	335656	5	NULL	NULL	0	NULL	ProT			mediate					GABA		transport of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
56393	8	335656	5	NULL	NULL	0	NULL	histidine			mediate					GABA		transport of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
56394	9	335656	5	NULL	NULL	0	NULL	statement 8			competes with					statement 7					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
56395	10	335656	5	NULL	NULL	0	NULL	D-proline			mediate					GABA		transport of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
56396	11	335656	5	NULL	NULL	0	NULL	statement 10			competes with					statement 7					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
56397	12	335656	5	NULL	NULL	0	NULL	L-proline			mediate					GABA		transport of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
56398	13	335656	5	NULL	NULL	0	NULL	statement 12			competes with					statement 7					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
56399	14	335656	5	NULL	NULL	0	NULL	glycine betaine			mediate					GABA		transport of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
56400	15	335656	5	NULL	NULL	0	NULL	statement 14			competes with					statement 7					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
56401	16	335656	5	NULL	NULL	0	NULL	choline			mediate					GABA		transport of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
56402	17	335656	5	NULL	NULL	0	NULL	statement 16			competes with					statement 7					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
60931	1	335656	7	NULL	NULL	0	NULL	Alanine	AminoAcid		reduce		slightly			GABA 	Process	rate of transport of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
60932	2	335656	7	NULL	NULL	0	NULL	ProT	GP		mediate					GABA 	Process	transport of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
60933	3	335656	7	NULL	NULL	0	NULL	histidine 	AminoAcid		compete with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
60934	4	335656	7	NULL	NULL	0	NULL	D-proline	AminoAcid		does not reduce					GABA	Chemical	uptake activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
60935	5	335656	7	NULL	NULL	0	NULL	L-proline	AminoAcid		does not reduce					GABA	Chemical	uptake activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
60936	6	335656	7	NULL	NULL	0	NULL	glycine betaine	AminoAcid		does not reduce					GABA	Chemical	uptake activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
60937	7	335656	7	NULL	NULL	0	NULL	choline	Chemical		does not reduce					GABA 	Chemical	uptake activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7197_s_115	16407306	Alanine slightly reduced GABA transport rates, whereas histidine as well as compounds that were good competitors for ProT-mediated GABA transport ( i.e.D- and L-proline, glycine betaine, and choline) did not reduce GABA uptake activity ( ).	transcription
56403	1	335657	5	NULL	NULL	0	NULL	glycine betaine			inhibits		strongly			GABA		transport of			NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
56404	2	335657	5	NULL	NULL	0	NULL	betaine aldehyde			inhibits		strongly			GABA		transport of			NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
56405	3	335657	5	NULL	NULL	0	NULL	choline			inhibits		strongly			GABA		transport of			NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
56406	4	335657	5	NULL	NULL	0	NULL	betaine aldehyde			is a metabolic precursor of					glycine betaine					NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
56407	5	335657	5	NULL	NULL	0	NULL	choline			is a metabolic precursor of					glycine betaine					NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
56408	6	335657	5	NULL	NULL	0	NULL	carnitine			is a type of					betaines					NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
56409	7	335657	5	NULL	NULL	0	NULL	trigonelline			is a type of					betaines					NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
56410	8	335657	5	NULL	NULL	0	NULL	betonicine			is a type of					betaines					NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
56411	9	335657	5	NULL	NULL	0	NULL	carnitine			inhibits					GABA		transport of			NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
56412	10	335657	5	NULL	NULL	0	NULL	trigonelline			inhibits					GABA		transport of			NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
56413	11	335657	5	NULL	NULL	0	NULL	betonicine			inhibits					GABA		transport of			NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
60938	1	335657	7	NULL	NULL	0	NULL	Glycine betaine	AminoAcid		inhibit		strongly			GABA	Chemical	transport of			NULL		NULL	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
60939	2	335657	7	NULL	NULL	0	NULL	betaine aldehyde	Chemical		inhibit		strongly			GABA	Chemical	transport of			NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
60940	3	335657	7	NULL	NULL	0	NULL	choline	Chemical		inhibit		strongly			GABA	Chemical	transport of			NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
60941	4	335657	7	NULL	NULL	0	NULL	carnitine	Chemical		inhibit					GABA	Chemical	transport of			NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
60942	5	335657	7	NULL	NULL	0	NULL	 trigonelline	Chemical		inhibit					GABA	Chemical	transport of			NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
60943	6	335657	7	NULL	NULL	0	NULL	betonicine	Chemical		inhibit					GABA	Chemical	transport of			NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
60944	7	335657	7	NULL	NULL	0	NULL	statement 4	Process		is not as effective as					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
60945	8	335657	7	NULL	NULL	0	NULL	statement 4	Process		is not as effective as					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
60946	9	335657	7	NULL	NULL	0	NULL	statement 4	Process		is not as effective as					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
60947	10	335657	7	NULL	NULL	0	NULL	statement 5	Process		is not as effective as					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
60948	11	335657	7	NULL	NULL	0	NULL	statement 5	Process		is not as effective as					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
60949	12	335657	7	NULL	NULL	0	NULL	statement 5	Process		is not as effective as					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
60950	13	335657	7	NULL	NULL	0	NULL	statement 6	Process		is not as effective as					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
60951	14	335657	7	NULL	NULL	0	NULL	statement 6	Process		is not as effective as					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
60952	15	335657	7	NULL	NULL	0	NULL	statement 6	Process		is not as effective as					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
60953	16	335657	7	NULL	NULL	0	NULL	carnitine	Chemical		is a type of					betaine	Chemical				NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
60954	17	335657	7	NULL	NULL	0	NULL	trigonelline	Chemical		is a type of					betaine	Chemical				NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
60955	18	335657	7	NULL	NULL	0	NULL	betonicine	Chemical		is a type of					betaine	Chemical				NULL		0	NULL	NULL	NULL	gw60_febslett_450_3_280_s_99	10359089	Glycine betaine and its immediate metabolic precursors, betaine aldehyde and choline, were strong inhibitors; other betaines, including carnitine, trigonelline and betonicine, also inhibited GABA transport, but were not as effective.	transcription
56414	1	335658	5	NULL	NULL	0	NULL	glycine betaine			stimulates					E.coli		growth of			NULL	hypertonic media	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1420_1_30_s_335	10446288	Glycine betaine, choline and other urine constituents with dietary origins (e.g. proline betaine) stimulate growth of  E. coli, the primary causative agent of ascending urinary tract infections, in hypertonic media [  46].	transcription
56415	2	335658	5	NULL	NULL	0	NULL	choline			stimulates					E.coli		growth of			NULL	hypertonic media	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1420_1_30_s_335	10446288	Glycine betaine, choline and other urine constituents with dietary origins (e.g. proline betaine) stimulate growth of  E. coli, the primary causative agent of ascending urinary tract infections, in hypertonic media [  46].	transcription
56416	3	335658	5	NULL	NULL	0	NULL	proline betaine			stimulates					E.coli		growth of			NULL	hypertonic media	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1420_1_30_s_335	10446288	Glycine betaine, choline and other urine constituents with dietary origins (e.g. proline betaine) stimulate growth of  E. coli, the primary causative agent of ascending urinary tract infections, in hypertonic media [  46].	transcription
56417	4	335658	5	NULL	NULL	0	NULL	E. coli			is causative agent of		primary			ascending urinary tract infections					NULL	hypertonic media	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1420_1_30_s_335	10446288	Glycine betaine, choline and other urine constituents with dietary origins (e.g. proline betaine) stimulate growth of  E. coli, the primary causative agent of ascending urinary tract infections, in hypertonic media [  46].	transcription
60956	1	335658	7	NULL	NULL	0	NULL	Glycine betaine	AminoAcid		stimulate					E.coli	Organism	growth of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1420_1_30_s_335	10446288	Glycine betaine, choline and other urine constituents with dietary origins (e.g. proline betaine) stimulate growth of  E. coli, the primary causative agent of ascending urinary tract infections, in hypertonic media [  46].	transcription
60957	2	335658	7	NULL	NULL	0	NULL	choline	chemical		stimulate					E.coli	Organism	growth of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1420_1_30_s_335	10446288	Glycine betaine, choline and other urine constituents with dietary origins (e.g. proline betaine) stimulate growth of  E. coli, the primary causative agent of ascending urinary tract infections, in hypertonic media [  46].	transcription
60958	3	335658	7	NULL	NULL	0	NULL	proline betaine	AminoAcid		stimulate					E.coli	Organism	growth of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1420_1_30_s_335	10446288	Glycine betaine, choline and other urine constituents with dietary origins (e.g. proline betaine) stimulate growth of  E. coli, the primary causative agent of ascending urinary tract infections, in hypertonic media [  46].	transcription
60959	4	335658	7	NULL	NULL	0	NULL	E.coli	Organism		causative agent of					ascending urinary tract infections	medical finding				NULL	hypertonic media	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1420_1_30_s_335	10446288	Glycine betaine, choline and other urine constituents with dietary origins (e.g. proline betaine) stimulate growth of  E. coli, the primary causative agent of ascending urinary tract infections, in hypertonic media [  46].	transcription
56418	1	335659	5	NULL	NULL	0	NULL	OpuC			transports		efficiently			glycine betaine					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_10	0009925583	OpuC mediates the efficient transport not only of glycine betaine and choline- O-sulfate but also of carnitine, crotonobetaine, and gamma-butyrobetaine (R. Kappes and E. Bremer, Microbiology 144:83-90, 1998).	transcription
56419	2	335659	5	NULL	NULL	0	NULL	OpuC			transports		efficiently			choline- O-sulfate					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_10	0009925583	OpuC mediates the efficient transport not only of glycine betaine and choline- O-sulfate but also of carnitine, crotonobetaine, and gamma-butyrobetaine (R. Kappes and E. Bremer, Microbiology 144:83-90, 1998).	transcription
56420	3	335659	5	NULL	NULL	0	NULL	OpuC			transports		efficiently			carnitine					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_10	0009925583	OpuC mediates the efficient transport not only of glycine betaine and choline- O-sulfate but also of carnitine, crotonobetaine, and gamma-butyrobetaine (R. Kappes and E. Bremer, Microbiology 144:83-90, 1998).	transcription
56421	4	335659	5	NULL	NULL	0	NULL	OpuC			transports		efficiently			crotonobetaine					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_10	0009925583	OpuC mediates the efficient transport not only of glycine betaine and choline- O-sulfate but also of carnitine, crotonobetaine, and gamma-butyrobetaine (R. Kappes and E. Bremer, Microbiology 144:83-90, 1998).	transcription
56422	5	335659	5	NULL	NULL	0	NULL	OpuC			transports		efficiently			gamma-butyrobetaine					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_10	0009925583	OpuC mediates the efficient transport not only of glycine betaine and choline- O-sulfate but also of carnitine, crotonobetaine, and gamma-butyrobetaine (R. Kappes and E. Bremer, Microbiology 144:83-90, 1998).	transcription
60960	1	335659	7	NULL	NULL	0	NULL	OpuC	GP		mediates					glycine betaine	AminoAcid	efficient transport of			NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_10	0009925583	OpuC mediates the efficient transport not only of glycine betaine and choline- O-sulfate but also of carnitine, crotonobetaine, and gamma-butyrobetaine (R. Kappes and E. Bremer, Microbiology 144:83-90, 1998).	transcription
60961	2	335659	7	NULL	NULL	0	NULL	OpuC	GP		mediate					choline- O-sulfate	Chemical	efficient transport of			NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_10	0009925583	OpuC mediates the efficient transport not only of glycine betaine and choline- O-sulfate but also of carnitine, crotonobetaine, and gamma-butyrobetaine (R. Kappes and E. Bremer, Microbiology 144:83-90, 1998).	transcription
60962	3	335659	7	NULL	NULL	0	NULL	OpuC	GP		mediate					carnitine	Chemical	efficient transport of			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_10	0009925583	OpuC mediates the efficient transport not only of glycine betaine and choline- O-sulfate but also of carnitine, crotonobetaine, and gamma-butyrobetaine (R. Kappes and E. Bremer, Microbiology 144:83-90, 1998).	transcription
60963	4	335659	7	NULL	NULL	0	NULL	OpuC	GP		mediate					crotonobetaine	Chemical	efficient transport of			NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_10	0009925583	OpuC mediates the efficient transport not only of glycine betaine and choline- O-sulfate but also of carnitine, crotonobetaine, and gamma-butyrobetaine (R. Kappes and E. Bremer, Microbiology 144:83-90, 1998).	transcription
60964	5	335659	7	NULL	NULL	0	NULL	OpuC	GP		mediate					gamma-butyrobetaine	Chemical	efficient transport of			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_560_s_10	0009925583	OpuC mediates the efficient transport not only of glycine betaine and choline- O-sulfate but also of carnitine, crotonobetaine, and gamma-butyrobetaine (R. Kappes and E. Bremer, Microbiology 144:83-90, 1998).	transcription
60965	1	335660	7	NULL	NULL	0	NULL	glycine betaine gene	GP	neutrophilic;;Bacillus subtilis	is similar to					glycine betaine gene	GP	halotolerant;;Bacillus subtilis			NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_235_2_393_s_14	15183890	Comparative analysis of this genome with that of the neutrophilic and halotolerant   Bacillus subtilis showed that there were no great differences in the genes of the glycine betaine and  choline ABC (ATP binding cassette) transport systems; however, a difference was found  in the glycine betaine secondary transporter genes [  18].	transcription
60966	2	335660	7	NULL	NULL	0	NULL	choline ABC gene	GP	neutrophilic;;Bacillus subtilis	is similar to					choline ABC gene	GP	halotolerant;;Bacillus subtilis			NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_235_2_393_s_14	15183890	Comparative analysis of this genome with that of the neutrophilic and halotolerant   Bacillus subtilis showed that there were no great differences in the genes of the glycine betaine and  choline ABC (ATP binding cassette) transport systems; however, a difference was found  in the glycine betaine secondary transporter genes [  18].	transcription
60967	3	335660	7	NULL	NULL	0	NULL	glycine betaine secondary transporter genes	GP	neutrophilic;;Bacillus subtilis	is different from					glycine betaine secondary transporter genes	GP	halotolerant;;Bacillus subtilis			NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_235_2_393_s_14	15183890	Comparative analysis of this genome with that of the neutrophilic and halotolerant   Bacillus subtilis showed that there were no great differences in the genes of the glycine betaine and  choline ABC (ATP binding cassette) transport systems; however, a difference was found  in the glycine betaine secondary transporter genes [  18].	transcription
60968	4	335660	7	NULL	NULL	0	NULL	ABC	GP		is					ATP binding cassette	GP				NULL		0	NULL	NULL	NULL	gw70_femsmicrobiollett_235_2_393_s_14	15183890	Comparative analysis of this genome with that of the neutrophilic and halotolerant   Bacillus subtilis showed that there were no great differences in the genes of the glycine betaine and  choline ABC (ATP binding cassette) transport systems; however, a difference was found  in the glycine betaine secondary transporter genes [  18].	transcription
56423	1	335661	5	NULL	NULL	0	NULL	ProX protein		E. coli	bind		high affinity			proline betaine					NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_244	8905077	The  E.  coli ProX protein binds both proline betaine and glycine betaine with high affinity [e.g.   Kd 5.2  M for proline betaine and 1.4  M for glycine betaine ( 57)], yet ProX does not bind the low affinity ProU substrates proline and choline ( 26).	transcription
56424	2	335661	5	NULL	NULL	0	NULL	ProX protein		E. coli	bind		high affinity			glycine betaine					NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_244	8905077	The  E.  coli ProX protein binds both proline betaine and glycine betaine with high affinity [e.g.   Kd 5.2  M for proline betaine and 1.4  M for glycine betaine ( 57)], yet ProX does not bind the low affinity ProU substrates proline and choline ( 26).	transcription
56425	3	335661	5	NULL	NULL	0	NULL	proline			substrate of					ProU					NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_244	8905077	The  E.  coli ProX protein binds both proline betaine and glycine betaine with high affinity [e.g.   Kd 5.2  M for proline betaine and 1.4  M for glycine betaine ( 57)], yet ProX does not bind the low affinity ProU substrates proline and choline ( 26).	transcription
56427	4	335661	5	NULL	NULL	0	NULL	choline			substrate of					ProU 					NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_244	8905077	The  E.  coli ProX protein binds both proline betaine and glycine betaine with high affinity [e.g.   Kd 5.2  M for proline betaine and 1.4  M for glycine betaine ( 57)], yet ProX does not bind the low affinity ProU substrates proline and choline ( 26).	transcription
56428	5	335661	5	NULL	NULL	0	NULL	ProX protein		E. coli	does not bind					proline					NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_244	8905077	The  E.  coli ProX protein binds both proline betaine and glycine betaine with high affinity [e.g.   Kd 5.2  M for proline betaine and 1.4  M for glycine betaine ( 57)], yet ProX does not bind the low affinity ProU substrates proline and choline ( 26).	transcription
56429	6	335661	5	NULL	NULL	0	NULL	ProX protein		E. coli	does not bind					choline					NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_244	8905077	The  E.  coli ProX protein binds both proline betaine and glycine betaine with high affinity [e.g.   Kd 5.2  M for proline betaine and 1.4  M for glycine betaine ( 57)], yet ProX does not bind the low affinity ProU substrates proline and choline ( 26).	transcription
60969	1	335661	7	NULL	NULL	0	NULL	ProX protein	GP	E.coli	bind		high affinity			proline betaine	AminoAcid				NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_244	8905077	The  E.  coli ProX protein binds both proline betaine and glycine betaine with high affinity [e.g.   Kd 5.2  M for proline betaine and 1.4  M for glycine betaine ( 57)], yet ProX does not bind the low affinity ProU substrates proline and choline ( 26).	transcription
60970	2	335661	7	NULL	NULL	0	NULL	ProX protein	GP	E.coli	bind		high affinity			glycine betaine	AminoAcid				NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_244	8905077	The  E.  coli ProX protein binds both proline betaine and glycine betaine with high affinity [e.g.   Kd 5.2  M for proline betaine and 1.4  M for glycine betaine ( 57)], yet ProX does not bind the low affinity ProU substrates proline and choline ( 26).	transcription
60971	3	335661	7	NULL	NULL	0	NULL	ProX	GP		does not bind					proline	AminoAcid				NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_244	8905077	The  E.  coli ProX protein binds both proline betaine and glycine betaine with high affinity [e.g.   Kd 5.2  M for proline betaine and 1.4  M for glycine betaine ( 57)], yet ProX does not bind the low affinity ProU substrates proline and choline ( 26).	transcription
60972	4	335661	7	NULL	NULL	0	NULL	ProX	GP		does not bind					choline	Chemical				NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_244	8905077	The  E.  coli ProX protein binds both proline betaine and glycine betaine with high affinity [e.g.   Kd 5.2  M for proline betaine and 1.4  M for glycine betaine ( 57)], yet ProX does not bind the low affinity ProU substrates proline and choline ( 26).	transcription
60973	5	335661	7	NULL	NULL	0	NULL	proline	AminoAcid		is a type of					ProU substrate	GP	low affinity			NULL		NULL	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_244	8905077	The  E.  coli ProX protein binds both proline betaine and glycine betaine with high affinity [e.g.   Kd 5.2  M for proline betaine and 1.4  M for glycine betaine ( 57)], yet ProX does not bind the low affinity ProU substrates proline and choline ( 26).	transcription
60974	6	335661	7	NULL	NULL	0	NULL	choline	Chemical		is a type of					ProU substrate	GP	low affinity			NULL		0	NULL	NULL	NULL	gw70_annurevmicrobiol_50_0_101_s_244	8905077	The  E.  coli ProX protein binds both proline betaine and glycine betaine with high affinity [e.g.   Kd 5.2  M for proline betaine and 1.4  M for glycine betaine ( 57)], yet ProX does not bind the low affinity ProU substrates proline and choline ( 26).	transcription
60975	1	335662	7	NULL	NULL	0	NULL	RpoS	GP	expression of	regulate					osmY	GP				NULL		NULL	NULL	NULL	NULL	gw70_applenvironmicrob_69_3_1759_s_273	12620868	Besides the expression of RpoS-regulated  osmY, the expression of the  betIBA operon for the synthesis of the compatible solute glycine betaine from choline, of the  proVWX operon for the uptake of proline and glycine betaine, and of the  otsAB operon for the synthesis of the compatible solute trehalose was increased after adaptation to acetate or propionate.	transcription
60976	2	335662	7	NULL	NULL	0	NULL	glycine betaine	AminoAcid		synthesized from					choline	Chemical				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_3_1759_s_273	12620868	Besides the expression of RpoS-regulated  osmY, the expression of the  betIBA operon for the synthesis of the compatible solute glycine betaine from choline, of the  proVWX operon for the uptake of proline and glycine betaine, and of the  otsAB operon for the synthesis of the compatible solute trehalose was increased after adaptation to acetate or propionate.	transcription
60977	3	335662	7	NULL	NULL	0	NULL	betIBA operon	GP	expression of	is required for					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_3_1759_s_273	12620868	Besides the expression of RpoS-regulated  osmY, the expression of the  betIBA operon for the synthesis of the compatible solute glycine betaine from choline, of the  proVWX operon for the uptake of proline and glycine betaine, and of the  otsAB operon for the synthesis of the compatible solute trehalose was increased after adaptation to acetate or propionate.	transcription
60978	4	335662	7	NULL	NULL	0	NULL	proVWX operon	GP	expression of	is required for					proline	AminoAcid	uptake of			NULL		NULL	NULL	NULL	NULL	gw70_applenvironmicrob_69_3_1759_s_273	12620868	Besides the expression of RpoS-regulated  osmY, the expression of the  betIBA operon for the synthesis of the compatible solute glycine betaine from choline, of the  proVWX operon for the uptake of proline and glycine betaine, and of the  otsAB operon for the synthesis of the compatible solute trehalose was increased after adaptation to acetate or propionate.	transcription
60979	5	335662	7	NULL	NULL	0	NULL	proVWX operon	GP	expression of	is required for					glycine betaine	AminoAcid	uptake of			NULL		NULL	NULL	NULL	NULL	gw70_applenvironmicrob_69_3_1759_s_273	12620868	Besides the expression of RpoS-regulated  osmY, the expression of the  betIBA operon for the synthesis of the compatible solute glycine betaine from choline, of the  proVWX operon for the uptake of proline and glycine betaine, and of the  otsAB operon for the synthesis of the compatible solute trehalose was increased after adaptation to acetate or propionate.	transcription
60980	6	335662	7	NULL	NULL	0	NULL	otsAB operon	GP	expression of	is required for					trehalose	Chemical	synthesis of;;compatible solute			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_3_1759_s_273	12620868	Besides the expression of RpoS-regulated  osmY, the expression of the  betIBA operon for the synthesis of the compatible solute glycine betaine from choline, of the  proVWX operon for the uptake of proline and glycine betaine, and of the  otsAB operon for the synthesis of the compatible solute trehalose was increased after adaptation to acetate or propionate.	transcription
60981	7	335662	7	NULL	NULL	0	NULL	acetate	Chemical		increase					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_3_1759_s_273	12620868	Besides the expression of RpoS-regulated  osmY, the expression of the  betIBA operon for the synthesis of the compatible solute glycine betaine from choline, of the  proVWX operon for the uptake of proline and glycine betaine, and of the  otsAB operon for the synthesis of the compatible solute trehalose was increased after adaptation to acetate or propionate.	transcription
60982	8	335662	7	NULL	NULL	0	NULL	propionate	Chemical		increase					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_3_1759_s_273	12620868	Besides the expression of RpoS-regulated  osmY, the expression of the  betIBA operon for the synthesis of the compatible solute glycine betaine from choline, of the  proVWX operon for the uptake of proline and glycine betaine, and of the  otsAB operon for the synthesis of the compatible solute trehalose was increased after adaptation to acetate or propionate.	transcription
60983	9	335662	7	NULL	NULL	0	NULL	acetate	Chemical		increase					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_3_1759_s_273	12620868	Besides the expression of RpoS-regulated  osmY, the expression of the  betIBA operon for the synthesis of the compatible solute glycine betaine from choline, of the  proVWX operon for the uptake of proline and glycine betaine, and of the  otsAB operon for the synthesis of the compatible solute trehalose was increased after adaptation to acetate or propionate.	transcription
60984	10	335662	7	NULL	NULL	0	NULL	propionate	Chemical		increase					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_3_1759_s_273	12620868	Besides the expression of RpoS-regulated  osmY, the expression of the  betIBA operon for the synthesis of the compatible solute glycine betaine from choline, of the  proVWX operon for the uptake of proline and glycine betaine, and of the  otsAB operon for the synthesis of the compatible solute trehalose was increased after adaptation to acetate or propionate.	transcription
60985	11	335662	7	NULL	NULL	0	NULL	acetate	Chemical		increase					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_3_1759_s_273	12620868	Besides the expression of RpoS-regulated  osmY, the expression of the  betIBA operon for the synthesis of the compatible solute glycine betaine from choline, of the  proVWX operon for the uptake of proline and glycine betaine, and of the  otsAB operon for the synthesis of the compatible solute trehalose was increased after adaptation to acetate or propionate.	transcription
60986	12	335662	7	NULL	NULL	0	NULL	propionate	Chemical		increase					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_3_1759_s_273	12620868	Besides the expression of RpoS-regulated  osmY, the expression of the  betIBA operon for the synthesis of the compatible solute glycine betaine from choline, of the  proVWX operon for the uptake of proline and glycine betaine, and of the  otsAB operon for the synthesis of the compatible solute trehalose was increased after adaptation to acetate or propionate.	transcription
60987	13	335662	7	NULL	NULL	0	NULL	acetate	Chemical		increase					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_applenvironmicrob_69_3_1759_s_273	12620868	Besides the expression of RpoS-regulated  osmY, the expression of the  betIBA operon for the synthesis of the compatible solute glycine betaine from choline, of the  proVWX operon for the uptake of proline and glycine betaine, and of the  otsAB operon for the synthesis of the compatible solute trehalose was increased after adaptation to acetate or propionate.	transcription
60988	14	335662	7	NULL	NULL	0	NULL	propionate	Chemical		increase					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_3_1759_s_273	12620868	Besides the expression of RpoS-regulated  osmY, the expression of the  betIBA operon for the synthesis of the compatible solute glycine betaine from choline, of the  proVWX operon for the uptake of proline and glycine betaine, and of the  otsAB operon for the synthesis of the compatible solute trehalose was increased after adaptation to acetate or propionate.	transcription
60989	15	335662	7	NULL	NULL	0	NULL	acetate	Chemical		increase					statement 6	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_3_1759_s_273	12620868	Besides the expression of RpoS-regulated  osmY, the expression of the  betIBA operon for the synthesis of the compatible solute glycine betaine from choline, of the  proVWX operon for the uptake of proline and glycine betaine, and of the  otsAB operon for the synthesis of the compatible solute trehalose was increased after adaptation to acetate or propionate.	transcription
60990	16	335662	7	NULL	NULL	0	NULL	propionate	Chemical		increase					statement 6	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_69_3_1759_s_273	12620868	Besides the expression of RpoS-regulated  osmY, the expression of the  betIBA operon for the synthesis of the compatible solute glycine betaine from choline, of the  proVWX operon for the uptake of proline and glycine betaine, and of the  otsAB operon for the synthesis of the compatible solute trehalose was increased after adaptation to acetate or propionate.	transcription
56431	1	335664	5	NULL	NULL	0	NULL	Hut system			is transport system for					betaines					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_10_5916_s_27	15466533	Two transport systems for betaines have been fully characterized: the Hut system, an ATP-binding cassette histidine transporter also involved in low-affinity glycine betaine transport ( ), and the BetS system, a betaine choline carnitine transporter (BCCT) required for early osmotic adjustment ( ).	transcription
56432	2	335664	5	NULL	NULL	0	NULL	BetS system			is transport system for					betaines					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_10_5916_s_27	15466533	Two transport systems for betaines have been fully characterized: the Hut system, an ATP-binding cassette histidine transporter also involved in low-affinity glycine betaine transport ( ), and the BetS system, a betaine choline carnitine transporter (BCCT) required for early osmotic adjustment ( ).	transcription
56433	3	335664	5	NULL	NULL	0	NULL	Hut system			is a type of					ATP-binding cassette histidine transporter					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_10_5916_s_27	15466533	Two transport systems for betaines have been fully characterized: the Hut system, an ATP-binding cassette histidine transporter also involved in low-affinity glycine betaine transport ( ), and the BetS system, a betaine choline carnitine transporter (BCCT) required for early osmotic adjustment ( ).	transcription
56434	4	335664	5	NULL	NULL	0	NULL	Hut system			is involved in					glycine betaine		transport of;;low-affinity			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_10_5916_s_27	15466533	Two transport systems for betaines have been fully characterized: the Hut system, an ATP-binding cassette histidine transporter also involved in low-affinity glycine betaine transport ( ), and the BetS system, a betaine choline carnitine transporter (BCCT) required for early osmotic adjustment ( ).	transcription
56435	5	335664	5	NULL	NULL	0	NULL	BetS system			is a type of					betaine choline carnitine transporter					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_10_5916_s_27	15466533	Two transport systems for betaines have been fully characterized: the Hut system, an ATP-binding cassette histidine transporter also involved in low-affinity glycine betaine transport ( ), and the BetS system, a betaine choline carnitine transporter (BCCT) required for early osmotic adjustment ( ).	transcription
56436	6	335664	5	NULL	NULL	0	NULL	BCC			is
\n					betaine choline carnitine transporter					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_10_5916_s_27	15466533	Two transport systems for betaines have been fully characterized: the Hut system, an ATP-binding cassette histidine transporter also involved in low-affinity glycine betaine transport ( ), and the BetS system, a betaine choline carnitine transporter (BCCT) required for early osmotic adjustment ( ).	transcription
56437	7	335664	5	NULL	NULL	0	NULL	BetS system			is required for					osmotic adjustment 		early			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_10_5916_s_27	15466533	Two transport systems for betaines have been fully characterized: the Hut system, an ATP-binding cassette histidine transporter also involved in low-affinity glycine betaine transport ( ), and the BetS system, a betaine choline carnitine transporter (BCCT) required for early osmotic adjustment ( ).	transcription
60991	1	335664	7	NULL	NULL	0	NULL	Hut system	GP		is a type of					ATP-binding cassette histidine transporter	GP				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_10_5916_s_27	15466533	Two transport systems for betaines have been fully characterized: the Hut system, an ATP-binding cassette histidine transporter also involved in low-affinity glycine betaine transport ( ), and the BetS system, a betaine choline carnitine transporter (BCCT) required for early osmotic adjustment ( ).	transcription
60992	2	335664	7	NULL	NULL	0	NULL	statement 1	Process		is involved in					glycine betaine	AminoAcid	low-affinity transport of			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_10_5916_s_27	15466533	Two transport systems for betaines have been fully characterized: the Hut system, an ATP-binding cassette histidine transporter also involved in low-affinity glycine betaine transport ( ), and the BetS system, a betaine choline carnitine transporter (BCCT) required for early osmotic adjustment ( ).	transcription
60993	3	335664	7	NULL	NULL	0	NULL	BetS system	GP		is a type of					BCCT	GP				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_10_5916_s_27	15466533	Two transport systems for betaines have been fully characterized: the Hut system, an ATP-binding cassette histidine transporter also involved in low-affinity glycine betaine transport ( ), and the BetS system, a betaine choline carnitine transporter (BCCT) required for early osmotic adjustment ( ).	transcription
60994	4	335664	7	NULL	NULL	0	NULL	statement 3	Process		is required for					early osmotic adjustment	Process				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_10_5916_s_27	15466533	Two transport systems for betaines have been fully characterized: the Hut system, an ATP-binding cassette histidine transporter also involved in low-affinity glycine betaine transport ( ), and the BetS system, a betaine choline carnitine transporter (BCCT) required for early osmotic adjustment ( ).	transcription
60995	5	335664	7	NULL	NULL	0	NULL	BCCT	GP		is 					betaine choline carnitine transporter	GP				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_70_10_5916_s_27	15466533	Two transport systems for betaines have been fully characterized: the Hut system, an ATP-binding cassette histidine transporter also involved in low-affinity glycine betaine transport ( ), and the BetS system, a betaine choline carnitine transporter (BCCT) required for early osmotic adjustment ( ).	transcription
56438	1	335665	5	NULL	NULL	0	NULL	ABC transporters			mediates					choline		uptake of			NULL	Bacillus subtilis	0	NULL	NULL	NULL	gw60_femsmicrobiolrev_26_1_49_s_918	12007642	R.M. Kappes, B. Kempf, S. Kneip, J. Boch, J. Gade, J. Meier-Wagner and E. Bremer, Two evolutionary closely related ABC transporters mediate the uptake of choline for synthesis of the osmoprotectant glycine betaine in  Bacillus subtilis.	transcription
56439	2	335665	5	NULL	NULL	0	NULL	statement 1			is required for					glycine betaine		synthesis of			NULL	Bacillus subtilis	0	NULL	NULL	NULL	gw60_femsmicrobiolrev_26_1_49_s_918	12007642	R.M. Kappes, B. Kempf, S. Kneip, J. Boch, J. Gade, J. Meier-Wagner and E. Bremer, Two evolutionary closely related ABC transporters mediate the uptake of choline for synthesis of the osmoprotectant glycine betaine in  Bacillus subtilis.	transcription
56440	3	335665	5	NULL	NULL	0	NULL	glycine betaine			is a type of					osmoprotectant					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiolrev_26_1_49_s_918	12007642	R.M. Kappes, B. Kempf, S. Kneip, J. Boch, J. Gade, J. Meier-Wagner and E. Bremer, Two evolutionary closely related ABC transporters mediate the uptake of choline for synthesis of the osmoprotectant glycine betaine in  Bacillus subtilis.	transcription
60996	1	335665	7	NULL	NULL	0	NULL	ABC transporters	GP		mediate					choline	Chemical	uptake of			NULL		0	NULL	NULL	NULL	gw60_femsmicrobiolrev_26_1_49_s_918	12007642	R.M. Kappes, B. Kempf, S. Kneip, J. Boch, J. Gade, J. Meier-Wagner and E. Bremer, Two evolutionary closely related ABC transporters mediate the uptake of choline for synthesis of the osmoprotectant glycine betaine in  Bacillus subtilis.	transcription
60997	2	335665	7	NULL	NULL	0	NULL	statement 1	Process		is required for 					glycine betaine	AminoAcid	synthesis of			NULL	Bacillus subtilis	NULL	NULL	NULL	NULL	gw60_femsmicrobiolrev_26_1_49_s_918	12007642	R.M. Kappes, B. Kempf, S. Kneip, J. Boch, J. Gade, J. Meier-Wagner and E. Bremer, Two evolutionary closely related ABC transporters mediate the uptake of choline for synthesis of the osmoprotectant glycine betaine in  Bacillus subtilis.	transcription
60998	3	335665	7	NULL	NULL	0	NULL	glycine betaine	AminoAcid		is a type of					osmoprotectant	Process				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiolrev_26_1_49_s_918	12007642	R.M. Kappes, B. Kempf, S. Kneip, J. Boch, J. Gade, J. Meier-Wagner and E. Bremer, Two evolutionary closely related ABC transporters mediate the uptake of choline for synthesis of the osmoprotectant glycine betaine in  Bacillus subtilis.	transcription
56441	1	335667	5	NULL	NULL	0	NULL	mAChRs			is present in					glycinergic amacrine cells					NULL	rabbit retina	0	NULL	NULL	NULL	gw60_jneurosci_20_22_8417_s_208	11069949	For instance, in rabbit retina, mAChRs on glycinergic amacrine cells stimulate the release of glycine, which then inhibits release of ACh from cholinergic amacrine cells (Cunningham et al., 1983  ; Neal and Cunningham, 1995  ; Linn, 1998  ).	transcription
56442	2	335667	5	NULL	NULL	0	NULL	statement 1			stimulates					glycine		release of			NULL	rabbit retina	0	NULL	NULL	NULL	gw60_jneurosci_20_22_8417_s_208	11069949	For instance, in rabbit retina, mAChRs on glycinergic amacrine cells stimulate the release of glycine, which then inhibits release of ACh from cholinergic amacrine cells (Cunningham et al., 1983  ; Neal and Cunningham, 1995  ; Linn, 1998  ).	transcription
56443	3	335667	5	NULL	NULL	0	NULL	ACh			is released from					cholinergic amacrine cells					NULL	rabbit retina	NULL	NULL	NULL	NULL	gw60_jneurosci_20_22_8417_s_208	11069949	For instance, in rabbit retina, mAChRs on glycinergic amacrine cells stimulate the release of glycine, which then inhibits release of ACh from cholinergic amacrine cells (Cunningham et al., 1983  ; Neal and Cunningham, 1995  ; Linn, 1998  ).	transcription
56444	4	335667	5	NULL	NULL	0	NULL	statement 3			inhibits					statement 2					NULL		0	NULL	NULL	NULL	gw60_jneurosci_20_22_8417_s_208	11069949	For instance, in rabbit retina, mAChRs on glycinergic amacrine cells stimulate the release of glycine, which then inhibits release of ACh from cholinergic amacrine cells (Cunningham et al., 1983  ; Neal and Cunningham, 1995  ; Linn, 1998  ).	transcription
60999	1	335667	7	NULL	NULL	0	NULL	mAChRs	GP	rabbit retina	stimulate					glycine	AminoAcid	release of			NULL	glycinergic amacrine cells	0	NULL	NULL	NULL	gw60_jneurosci_20_22_8417_s_208	11069949	For instance, in rabbit retina, mAChRs on glycinergic amacrine cells stimulate the release of glycine, which then inhibits release of ACh from cholinergic amacrine cells (Cunningham et al., 1983  ; Neal and Cunningham, 1995  ; Linn, 1998  ).	transcription
61000	2	335667	7	NULL	NULL	0	NULL	glycine	AminoAcid		inhibit					ACh	GP	release of			NULL	cholinergic amacrine cells 	0	NULL	NULL	NULL	gw60_jneurosci_20_22_8417_s_208	11069949	For instance, in rabbit retina, mAChRs on glycinergic amacrine cells stimulate the release of glycine, which then inhibits release of ACh from cholinergic amacrine cells (Cunningham et al., 1983  ; Neal and Cunningham, 1995  ; Linn, 1998  ).	transcription
56445	1	335668	5	NULL	NULL	0	NULL	opuCA			encodes					glycine/betaine/carnitine/choline ABC transporter					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_8_5197_s_29	16885265	To do this, transcript levels were determined for  opuCA, which encodes a glycine/betaine/carnitine/choline ABC transporter ( ,  ,  ,  ,  ), and for  clpC, which encodes endopeptidase Clp ATP-binding chain C, a stress response protein that contributes to  L. monocytogenes phagosomal escape ( ,  ,  ), in the  L. monocytogenes wild-type, delta sigB, delta rsbT, and delta rsbV strains under different stress conditions.	transcription
56446	2	335668	5	NULL	NULL	0	NULL	clpC			encodes					endopeptidase Clp			ATP-binding chain C		NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_8_5197_s_29	16885265	To do this, transcript levels were determined for  opuCA, which encodes a glycine/betaine/carnitine/choline ABC transporter ( ,  ,  ,  ,  ), and for  clpC, which encodes endopeptidase Clp ATP-binding chain C, a stress response protein that contributes to  L. monocytogenes phagosomal escape ( ,  ,  ), in the  L. monocytogenes wild-type, delta sigB, delta rsbT, and delta rsbV strains under different stress conditions.	transcription
56447	3	335668	5	NULL	NULL	0	NULL	endopeptidase Clp			is a type of			ATP-binding chain C		stress response protein					NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_8_5197_s_29	16885265	To do this, transcript levels were determined for  opuCA, which encodes a glycine/betaine/carnitine/choline ABC transporter ( ,  ,  ,  ,  ), and for  clpC, which encodes endopeptidase Clp ATP-binding chain C, a stress response protein that contributes to  L. monocytogenes phagosomal escape ( ,  ,  ), in the  L. monocytogenes wild-type, delta sigB, delta rsbT, and delta rsbV strains under different stress conditions.	transcription
56448	4	335668	5	NULL	NULL	0	NULL	endopeptidase Clp			contributes to			ATP-binding chain C		L. monocytogenes		phagosomal escape of			NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_8_5197_s_29	16885265	To do this, transcript levels were determined for  opuCA, which encodes a glycine/betaine/carnitine/choline ABC transporter ( ,  ,  ,  ,  ), and for  clpC, which encodes endopeptidase Clp ATP-binding chain C, a stress response protein that contributes to  L. monocytogenes phagosomal escape ( ,  ,  ), in the  L. monocytogenes wild-type, delta sigB, delta rsbT, and delta rsbV strains under different stress conditions.	transcription
61001	1	335668	7	NULL	NULL	0	NULL	opuCA	GP		encode					glycine ABC transporter	GP				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_8_5197_s_29	16885265	To do this, transcript levels were determined for  opuCA, which encodes a glycine/betaine/carnitine/choline ABC transporter ( ,  ,  ,  ,  ), and for  clpC, which encodes endopeptidase Clp ATP-binding chain C, a stress response protein that contributes to  L. monocytogenes phagosomal escape ( ,  ,  ), in the  L. monocytogenes wild-type, delta sigB, delta rsbT, and delta rsbV strains under different stress conditions.	transcription
61002	2	335668	7	NULL	NULL	0	NULL	opuCA	GP		encode					betaine ABC transporter	GP				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_8_5197_s_29	16885265	To do this, transcript levels were determined for  opuCA, which encodes a glycine/betaine/carnitine/choline ABC transporter ( ,  ,  ,  ,  ), and for  clpC, which encodes endopeptidase Clp ATP-binding chain C, a stress response protein that contributes to  L. monocytogenes phagosomal escape ( ,  ,  ), in the  L. monocytogenes wild-type, delta sigB, delta rsbT, and delta rsbV strains under different stress conditions.	transcription
61003	3	335668	7	NULL	NULL	0	NULL	opuCA	GP		encode					carnitine ABC transporter	GP				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_8_5197_s_29	16885265	To do this, transcript levels were determined for  opuCA, which encodes a glycine/betaine/carnitine/choline ABC transporter ( ,  ,  ,  ,  ), and for  clpC, which encodes endopeptidase Clp ATP-binding chain C, a stress response protein that contributes to  L. monocytogenes phagosomal escape ( ,  ,  ), in the  L. monocytogenes wild-type, delta sigB, delta rsbT, and delta rsbV strains under different stress conditions.	transcription
61004	4	335668	7	NULL	NULL	0	NULL	opuCA	GP		encode					choline ABC transporter	GP				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_8_5197_s_29	16885265	To do this, transcript levels were determined for  opuCA, which encodes a glycine/betaine/carnitine/choline ABC transporter ( ,  ,  ,  ,  ), and for  clpC, which encodes endopeptidase Clp ATP-binding chain C, a stress response protein that contributes to  L. monocytogenes phagosomal escape ( ,  ,  ), in the  L. monocytogenes wild-type, delta sigB, delta rsbT, and delta rsbV strains under different stress conditions.	transcription
61005	5	335668	7	NULL	NULL	0	NULL	clpC	GP		encode					endopeptidase Clp ATP-binding chain C	GP				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_8_5197_s_29	16885265	To do this, transcript levels were determined for  opuCA, which encodes a glycine/betaine/carnitine/choline ABC transporter ( ,  ,  ,  ,  ), and for  clpC, which encodes endopeptidase Clp ATP-binding chain C, a stress response protein that contributes to  L. monocytogenes phagosomal escape ( ,  ,  ), in the  L. monocytogenes wild-type, delta sigB, delta rsbT, and delta rsbV strains under different stress conditions.	transcription
61006	6	335668	7	NULL	NULL	0	NULL	endopeptidase Clp ATP-binding chain C	GP		contributes to					phagosomal escape	Process				NULL	wild-type L. monocytogenes	0	NULL	NULL	NULL	gw70_applenvironmicrob_72_8_5197_s_29	16885265	To do this, transcript levels were determined for  opuCA, which encodes a glycine/betaine/carnitine/choline ABC transporter ( ,  ,  ,  ,  ), and for  clpC, which encodes endopeptidase Clp ATP-binding chain C, a stress response protein that contributes to  L. monocytogenes phagosomal escape ( ,  ,  ), in the  L. monocytogenes wild-type, delta sigB, delta rsbT, and delta rsbV strains under different stress conditions.	transcription
61007	7	335668	7	NULL	NULL	0	NULL	endopeptidase Clp ATP-binding chain C	GP		contributes to					phagosomal escape	Process				NULL	delta sigB L. monocytogenes	0	NULL	NULL	NULL	gw70_applenvironmicrob_72_8_5197_s_29	16885265	To do this, transcript levels were determined for  opuCA, which encodes a glycine/betaine/carnitine/choline ABC transporter ( ,  ,  ,  ,  ), and for  clpC, which encodes endopeptidase Clp ATP-binding chain C, a stress response protein that contributes to  L. monocytogenes phagosomal escape ( ,  ,  ), in the  L. monocytogenes wild-type, delta sigB, delta rsbT, and delta rsbV strains under different stress conditions.	transcription
61008	8	335668	7	NULL	NULL	0	NULL	endopeptidase Clp ATP-binding chain C	GP		contributes to					phagosomal escape	Process				NULL	delta rsbT L. monocytogenes	0	NULL	NULL	NULL	gw70_applenvironmicrob_72_8_5197_s_29	16885265	To do this, transcript levels were determined for  opuCA, which encodes a glycine/betaine/carnitine/choline ABC transporter ( ,  ,  ,  ,  ), and for  clpC, which encodes endopeptidase Clp ATP-binding chain C, a stress response protein that contributes to  L. monocytogenes phagosomal escape ( ,  ,  ), in the  L. monocytogenes wild-type, delta sigB, delta rsbT, and delta rsbV strains under different stress conditions.	transcription
61009	9	335668	7	NULL	NULL	0	NULL	endopeptidase Clp ATP-binding chain C	GP		contributes to					phagosomal escape	Process				NULL	delta rsbV L. monocytogenes	0	NULL	NULL	NULL	gw70_applenvironmicrob_72_8_5197_s_29	16885265	To do this, transcript levels were determined for  opuCA, which encodes a glycine/betaine/carnitine/choline ABC transporter ( ,  ,  ,  ,  ), and for  clpC, which encodes endopeptidase Clp ATP-binding chain C, a stress response protein that contributes to  L. monocytogenes phagosomal escape ( ,  ,  ), in the  L. monocytogenes wild-type, delta sigB, delta rsbT, and delta rsbV strains under different stress conditions.	transcription
61010	10	335668	7	NULL	NULL	0	NULL	endopeptidase Clp ATP-binding chain C	GP		is a type of					stress response protein	GP				NULL		0	NULL	NULL	NULL	gw70_applenvironmicrob_72_8_5197_s_29	16885265	To do this, transcript levels were determined for  opuCA, which encodes a glycine/betaine/carnitine/choline ABC transporter ( ,  ,  ,  ,  ), and for  clpC, which encodes endopeptidase Clp ATP-binding chain C, a stress response protein that contributes to  L. monocytogenes phagosomal escape ( ,  ,  ), in the  L. monocytogenes wild-type, delta sigB, delta rsbT, and delta rsbV strains under different stress conditions.	transcription
56450	1	335670	5	NULL	NULL	0	NULL	rCBF response			abolished by					scopolamine					NULL		0	NULL	NULL	NULL	gw60_brainres_832_1_118_s_98	10375657	-Cycloserine significantly recovered the rCBF response abolished by scopolamine in our previous study without affecting neuronal activity, suggesting that the activation of NMDA receptors through the glycine site by  -cycloserine could reverse the dysfunction in the coupling between neuronal activation and the rCBF response that is associated with a cholinergic blockade [ 43].	transcription
56451	2	335670	5	NULL	NULL	0	NULL	statement 1			does not affect					neuronal activity					NULL		0	NULL	NULL	NULL	gw60_brainres_832_1_118_s_98	10375657	-Cycloserine significantly recovered the rCBF response abolished by scopolamine in our previous study without affecting neuronal activity, suggesting that the activation of NMDA receptors through the glycine site by  -cycloserine could reverse the dysfunction in the coupling between neuronal activation and the rCBF response that is associated with a cholinergic blockade [ 43].	transcription
56452	3	335670	5	NULL	NULL	0	NULL	Cycloserine			recover		significantly			statement 1					NULL		0	NULL	NULL	NULL	gw60_brainres_832_1_118_s_98	10375657	-Cycloserine significantly recovered the rCBF response abolished by scopolamine in our previous study without affecting neuronal activity, suggesting that the activation of NMDA receptors through the glycine site by  -cycloserine could reverse the dysfunction in the coupling between neuronal activation and the rCBF response that is associated with a cholinergic blockade [ 43].	transcription
56453	4	335670	5	NULL	NULL	0	NULL	cycloserine			activates					NMDA receptor					NULL		0	NULL	NULL	NULL	gw60_brainres_832_1_118_s_98	10375657	-Cycloserine significantly recovered the rCBF response abolished by scopolamine in our previous study without affecting neuronal activity, suggesting that the activation of NMDA receptors through the glycine site by  -cycloserine could reverse the dysfunction in the coupling between neuronal activation and the rCBF response that is associated with a cholinergic blockade [ 43].	transcription
56454	5	335670	5	NULL	NULL	0	NULL	statement 4			through					glycine site					NULL		0	NULL	NULL	NULL	gw60_brainres_832_1_118_s_98	10375657	-Cycloserine significantly recovered the rCBF response abolished by scopolamine in our previous study without affecting neuronal activity, suggesting that the activation of NMDA receptors through the glycine site by  -cycloserine could reverse the dysfunction in the coupling between neuronal activation and the rCBF response that is associated with a cholinergic blockade [ 43].	transcription
56455	6	335670	5	NULL	NULL	0	NULL	rCBF response			is associated with					cholinergic blockade					NULL		0	NULL	NULL	NULL	gw60_brainres_832_1_118_s_98	10375657	-Cycloserine significantly recovered the rCBF response abolished by scopolamine in our previous study without affecting neuronal activity, suggesting that the activation of NMDA receptors through the glycine site by  -cycloserine could reverse the dysfunction in the coupling between neuronal activation and the rCBF response that is associated with a cholinergic blockade [ 43].	transcription
56456	7	335670	5	NULL	NULL	0	NULL	neuronal activation			is coupled to					rCBF response					NULL		0	NULL	NULL	NULL	gw60_brainres_832_1_118_s_98	10375657	-Cycloserine significantly recovered the rCBF response abolished by scopolamine in our previous study without affecting neuronal activity, suggesting that the activation of NMDA receptors through the glycine site by  -cycloserine could reverse the dysfunction in the coupling between neuronal activation and the rCBF response that is associated with a cholinergic blockade [ 43].	transcription
56457	8	335670	5	NULL	NULL	0	NULL	statement 4			reverse					statement 7		dysfunction of			NULL		0	NULL	NULL	NULL	gw60_brainres_832_1_118_s_98	10375657	-Cycloserine significantly recovered the rCBF response abolished by scopolamine in our previous study without affecting neuronal activity, suggesting that the activation of NMDA receptors through the glycine site by  -cycloserine could reverse the dysfunction in the coupling between neuronal activation and the rCBF response that is associated with a cholinergic blockade [ 43].	transcription
61038	1	335670	7	NULL	NULL	0	NULL	scopolamine	Chemical		abolish					 rCBF response	Process				NULL		0	NULL	NULL	NULL	gw60_brainres_832_1_118_s_98	10375657	-Cycloserine significantly recovered the rCBF response abolished by scopolamine in our previous study without affecting neuronal activity, suggesting that the activation of NMDA receptors through the glycine site by  -cycloserine could reverse the dysfunction in the coupling between neuronal activation and the rCBF response that is associated with a cholinergic blockade [ 43].	transcription
61039	2	335670	7	NULL	NULL	0	NULL	Cycloserine 	Chemical		recovers		significantly			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_brainres_832_1_118_s_98	10375657	-Cycloserine significantly recovered the rCBF response abolished by scopolamine in our previous study without affecting neuronal activity, suggesting that the activation of NMDA receptors through the glycine site by  -cycloserine could reverse the dysfunction in the coupling between neuronal activation and the rCBF response that is associated with a cholinergic blockade [ 43].	transcription
61040	3	335670	7	NULL	NULL	0	NULL	statement 2	Process		does not affect					neuronal activity	Process				NULL		0	NULL	NULL	NULL	gw60_brainres_832_1_118_s_98	10375657	-Cycloserine significantly recovered the rCBF response abolished by scopolamine in our previous study without affecting neuronal activity, suggesting that the activation of NMDA receptors through the glycine site by  -cycloserine could reverse the dysfunction in the coupling between neuronal activation and the rCBF response that is associated with a cholinergic blockade [ 43].	transcription
61041	4	335670	7	NULL	NULL	0	NULL	cycloserine	Chemical		activate					NMDA receptors	GP		glycine site		NULL		0	NULL	NULL	NULL	gw60_brainres_832_1_118_s_98	10375657	-Cycloserine significantly recovered the rCBF response abolished by scopolamine in our previous study without affecting neuronal activity, suggesting that the activation of NMDA receptors through the glycine site by  -cycloserine could reverse the dysfunction in the coupling between neuronal activation and the rCBF response that is associated with a cholinergic blockade [ 43].	transcription
61042	5	335670	7	NULL	NULL	0	NULL	neuronal activation	Process		coupled to					 rCBF response	Process				NULL		0	NULL	NULL	NULL	gw60_brainres_832_1_118_s_98	10375657	-Cycloserine significantly recovered the rCBF response abolished by scopolamine in our previous study without affecting neuronal activity, suggesting that the activation of NMDA receptors through the glycine site by  -cycloserine could reverse the dysfunction in the coupling between neuronal activation and the rCBF response that is associated with a cholinergic blockade [ 43].	transcription
61043	6	335670	7	NULL	NULL	0	NULL	statement 5	Process		associated with					choline	Chemical	blockade of			NULL		0	NULL	NULL	NULL	gw60_brainres_832_1_118_s_98	10375657	-Cycloserine significantly recovered the rCBF response abolished by scopolamine in our previous study without affecting neuronal activity, suggesting that the activation of NMDA receptors through the glycine site by  -cycloserine could reverse the dysfunction in the coupling between neuronal activation and the rCBF response that is associated with a cholinergic blockade [ 43].	transcription
61044	7	335670	7	NULL	NULL	0	NULL	statement 4	Process		reverse					statement 5	Process	dysfunction in			NULL		NULL	NULL	NULL	NULL	gw60_brainres_832_1_118_s_98	10375657	-Cycloserine significantly recovered the rCBF response abolished by scopolamine in our previous study without affecting neuronal activity, suggesting that the activation of NMDA receptors through the glycine site by  -cycloserine could reverse the dysfunction in the coupling between neuronal activation and the rCBF response that is associated with a cholinergic blockade [ 43].	transcription
61045	1	335671	7	NULL	NULL	0	NULL	NMDA	GP		stimulate					GABA	Chemical				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61046	2	335671	7	NULL	NULL	0	NULL	PCP	Chemical		release					ACh	Chemical				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61047	3	335671	7	NULL	NULL	0	NULL	MK801	Chemical		release from					ACh	Chemical				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61048	4	335671	7	NULL	NULL	0	NULL	mecamylamine	Chemical		release					ACh	Chemical				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61049	5	335671	7	NULL	NULL	0	NULL	CNQX	Chemical		release					ACh	Chemical				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61050	6	335671	7	NULL	NULL	0	NULL	DNQX	Chemical		release					ACh	Chemical				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61051	7	335671	7	NULL	NULL	0	NULL	7-chlorokynurenic acid	Chemical		release					ACh	Chemical				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61052	8	335671	7	NULL	NULL	0	NULL	NMDA receptor	GP	cholinergic neuron	differs from			subunit		NMDA receptor	GP	GABAergic neuron	subunit		NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61053	9	335671	7	NULL	NULL	0	NULL	statement 1	Process	sensitivity of	differs with					statement 2	Process	sensitivity of			NULL		NULL	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61054	10	335671	7	NULL	NULL	0	NULL	statement 1	Process	sensitivity of	differs with					statement 3	Process	sensitivity of			NULL		NULL	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61055	11	335671	7	NULL	NULL	0	NULL	statement 1	Process	sensitivity of	differs with					statement 4	Process	sensitivity of			NULL		NULL	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61056	12	335671	7	NULL	NULL	0	NULL	statement 1	Process	sensitivity of	differs with					statement 5	Process	sensitivity of			NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61057	13	335671	7	NULL	NULL	0	NULL	statement 1	Process	sensitivity of	differs with					statement 6	Process	sensitivity of			NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61058	14	335671	7	NULL	NULL	0	NULL	statement 1	Process	sensitivity of	differs with					statement 7	Process	sensitivity of			NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61059	15	335671	7	NULL	NULL	0	NULL	statement 9	Process		because of					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61060	16	335671	7	NULL	NULL	0	NULL	statement 10	Process		because of					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61061	17	335671	7	NULL	NULL	0	NULL	statement 11	Process		because of					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61062	18	335671	7	NULL	NULL	0	NULL	statement 12	Process		because of					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61063	19	335671	7	NULL	NULL	0	NULL	statement 13	Process		because of					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61064	20	335671	7	NULL	NULL	0	NULL	statement 14	Process		because of					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61065	21	335671	7	NULL	NULL	0	NULL	PCP	Chemical		is a type of					NMDA antagonist	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61066	22	335671	7	NULL	NULL	0	NULL	MK801	Chemical		is a type of					NMDA antagonist	Chemical				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61067	23	335671	7	NULL	NULL	0	NULL	mecamylamine	Chemical		is a type of					NMDA antagonist	Chemical				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61068	24	335671	7	NULL	NULL	0	NULL	CNQX	Chemical		is a type of					NMDA antagonist	Chemical				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61069	25	335671	7	NULL	NULL	0	NULL	DNQX	Chemical		is a type of					NMDA antagonist	Chemical				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
61070	26	335671	7	NULL	NULL	0	NULL	7-chlorokynurenic acid	Chemical		is a type of					NMDA antagonist	Chemical				NULL		0	NULL	NULL	NULL	gw60_brainres_844_1_106_s_252	10536266	The difference in sensitivity between NMDA-stimulated [14]GABA and [3]ACh release to the NMDA antagonists, PCP, MK801 and mecamylamine, and to the glycine antagonists, CNQX, DNQX and 7-chlorokynurenic acid, might result from a difference in the subunit composition of the NMDA receptors found on cholinergic and on GABAergic neurons.	transcription
56506	1	335672	5	NULL	NULL	0	NULL	heme			stimulates					globin		synthesis of			NULL		0	NULL	NULL	NULL	gw60_jlipidres_40_7_1222_s_271	10393207	The stimulation of globin synthesis by heme.	transcription
61071	1	335672	7	NULL	NULL	0	NULL	heme	Chemical		stimulate					globin	GP	synthesis of			NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_40_7_1222_s_271	10393207	The stimulation of globin synthesis by heme.	transcription
61072	1	335673	7	NULL	NULL	0	NULL	globin	GP		interacts with					heme	Chemical				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1749_2_148_s_84	15927874	Dynamics of globin and the heme-globin interaction,  J. Mol.	transcription
56507	1	335674	5	NULL	NULL	0	NULL	heme			bind					globin chains		nascent			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10646_s_100	9099713	On the grounds of these data we suggest that heme binding to the nascent globin chains can be used as a test of cotranslational folding of globins.	transcription
61073	1	335674	7	NULL	NULL	0	NULL	heme	Chemical		bind					globin chains	GP	nascent			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10646_s_100	9099713	On the grounds of these data we suggest that heme binding to the nascent globin chains can be used as a test of cotranslational folding of globins.	transcription
56508	1	335675	5	NULL	NULL	0	NULL	heme			induces					beta-globin gene		transcription of			NULL		0	NULL	NULL	NULL	gw70_embo_23_13_2544_s_34	15175654	Importantly, heme induces transcription of the beta-globin gene ( ).	transcription
61074	1	335675	7	NULL	NULL	0	NULL	heme	Chemical		induce					beta-globin gene	GP	transcription of			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_13_2544_s_34	15175654	Importantly, heme induces transcription of the beta-globin gene ( ).	transcription
56509	1	335676	5	NULL	NULL	0	NULL	HRI			regulates					alpha-globin		synthesis of			NULL		0	NULL	NULL	NULL	gw60_embo_20_23_6909_s_251	11726526	( A) Regulation of alpha- and beta-globin synthesis by HRI and heme.	transcription
56510	2	335676	5	NULL	NULL	0	NULL	HRI			regulates					beta-globin		synthesis of			NULL		0	NULL	NULL	NULL	gw60_embo_20_23_6909_s_251	11726526	( A) Regulation of alpha- and beta-globin synthesis by HRI and heme.	transcription
56511	3	335676	5	NULL	NULL	0	NULL	heme			regulates					alpha-globin		synthesis of			NULL		0	NULL	NULL	NULL	gw60_embo_20_23_6909_s_251	11726526	( A) Regulation of alpha- and beta-globin synthesis by HRI and heme.	transcription
56512	4	335676	5	NULL	NULL	0	NULL	heme			regulates					beta-globin		synthesis of			NULL		0	NULL	NULL	NULL	gw60_embo_20_23_6909_s_251	11726526	( A) Regulation of alpha- and beta-globin synthesis by HRI and heme.	transcription
61075	1	335676	7	NULL	NULL	0	NULL	HRI	GP		regulate					alpha-globin	GP	synthesis of			NULL		0	NULL	NULL	NULL	gw60_embo_20_23_6909_s_251	11726526	( A) Regulation of alpha- and beta-globin synthesis by HRI and heme.	transcription
61076	2	335676	7	NULL	NULL	0	NULL	HRI	GP		regulate					beta-globin	GP	synthesis of			NULL		0	NULL	NULL	NULL	gw60_embo_20_23_6909_s_251	11726526	( A) Regulation of alpha- and beta-globin synthesis by HRI and heme.	transcription
61077	3	335676	7	NULL	NULL	0	NULL	heme	Chemical		regulate					alpha-globin	GP	synthesis of			NULL		0	NULL	NULL	NULL	gw60_embo_20_23_6909_s_251	11726526	( A) Regulation of alpha- and beta-globin synthesis by HRI and heme.	transcription
61078	4	335676	7	NULL	NULL	0	NULL	heme	Chemical		regulate					beta-globin	GP	synthesis of			NULL		0	NULL	NULL	NULL	gw60_embo_20_23_6909_s_251	11726526	( A) Regulation of alpha- and beta-globin synthesis by HRI and heme.	transcription
56513	1	335677	5	NULL	NULL	0	NULL	AHSP			bind					alpha-globin					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_43_40602_s_234	12192002	B, AHSP binds alpha-globin in the absence of heme.	transcription
56514	2	335677	5	NULL	NULL	0	NULL	statement 1			in absence of					heme					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_43_40602_s_234	12192002	B, AHSP binds alpha-globin in the absence of heme.	transcription
61079	1	335677	7	NULL	NULL	0	NULL	AHSP	GP		bind					alpha-globin	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_43_40602_s_234	12192002	B, AHSP binds alpha-globin in the absence of heme.	transcription
61080	2	335677	7	NULL	NULL	0	NULL	statement 1	Process		in the absence of					heme	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_43_40602_s_234	12192002	B, AHSP binds alpha-globin in the absence of heme.	transcription
61081	1	335678	7	NULL	NULL	0	NULL	Heme	Chemical		regulates					kinase	GP				NULL		0	NULL	NULL	NULL	gw70_jclininvest_114_10_1457_s_272	15545996	Heme-regulated kinase inhibits globin translation when heme availability is limited ( ).	transcription
61082	2	335678	7	NULL	NULL	0	NULL	statement 1	Process		inhibit					globin	GP	translation of			NULL		0	NULL	NULL	NULL	gw70_jclininvest_114_10_1457_s_272	15545996	Heme-regulated kinase inhibits globin translation when heme availability is limited ( ).	transcription
61083	3	335678	7	NULL	NULL	0	NULL	statement 1	Process		occur upon					heme	Chemical	limited availability of			NULL		0	NULL	NULL	NULL	gw70_jclininvest_114_10_1457_s_272	15545996	Heme-regulated kinase inhibits globin translation when heme availability is limited ( ).	transcription
56515	1	335679	5	NULL	NULL	0	NULL	globin			hydrolyzed by					THAP					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_37_28659_s_5	10896678	Hydrolysis of globin by THAP increased as increasing amounts of heme were added to globin, with maximum activation at a heme-to-globin 1:1 ratio.	transcription
61084	1	335679	7	NULL	NULL	0	NULL	THAP	GP		hydrolyze					globin	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_37_28659_s_5	10896678	Hydrolysis of globin by THAP increased as increasing amounts of heme were added to globin, with maximum activation at a heme-to-globin 1:1 ratio.	transcription
61085	1	335680	7	NULL	NULL	0	NULL	CooA	GP		does not resemble			heme-binding region of 					PAS domain		NULL		NULL	NULL	NULL	NULL	gw70_jbacteriol_186_5_1320_s_193	14973040	The heme-binding region of CooA does not resemble those of other common heme regions, such as the PAS domain ( ) or the heme domain found in globins ( ).	transcription
61086	2	335680	7	NULL	NULL	0	NULL	CooA	GP		does not resemble			heme-binding region of 		globins	GP		heme domain		NULL		0	NULL	NULL	NULL	gw70_jbacteriol_186_5_1320_s_193	14973040	The heme-binding region of CooA does not resemble those of other common heme regions, such as the PAS domain ( ) or the heme domain found in globins ( ).	transcription
56516	1	335681	5	NULL	NULL	0	NULL	globin		increase of;;synthesis of	leads to					globin		accumulation of			NULL	erythroid cells from iron-deficient HRI / mice	0	NULL	NULL	NULL	gw70_annurevnutr_24_0_105_s_479	15189115	However, in erythroid cells from iron-deficient HRI /  mice, a marked increase in both  - and  -globin synthesis led to accumulated globins  that were devoid of heme and aggregated within the erythrocytes and their precursors.	transcription
56517	2	335681	5	NULL	NULL	0	NULL	globin		accumulated	is devoid of					heme					NULL		0	NULL	NULL	NULL	gw70_annurevnutr_24_0_105_s_479	15189115	However, in erythroid cells from iron-deficient HRI /  mice, a marked increase in both  - and  -globin synthesis led to accumulated globins  that were devoid of heme and aggregated within the erythrocytes and their precursors.	transcription
56518	3	335681	5	NULL	NULL	0	NULL	statement 2			is aggregated within					erythrocytes					NULL		0	NULL	NULL	NULL	gw70_annurevnutr_24_0_105_s_479	15189115	However, in erythroid cells from iron-deficient HRI /  mice, a marked increase in both  - and  -globin synthesis led to accumulated globins  that were devoid of heme and aggregated within the erythrocytes and their precursors.	transcription
61087	1	335681	7	NULL	NULL	0	NULL	globin	GP	increase in synthesis of	leads to					globins	GP	accumulation of			NULL	erythroid cells from iron-deficient HRI / mice	0	NULL	NULL	NULL	gw70_annurevnutr_24_0_105_s_479	15189115	However, in erythroid cells from iron-deficient HRI /  mice, a marked increase in both  - and  -globin synthesis led to accumulated globins  that were devoid of heme and aggregated within the erythrocytes and their precursors.	transcription
61088	2	335681	7	NULL	NULL	0	NULL	globins	GP		devoid of					heme	Chemical				NULL		0	NULL	NULL	NULL	gw70_annurevnutr_24_0_105_s_479	15189115	However, in erythroid cells from iron-deficient HRI /  mice, a marked increase in both  - and  -globin synthesis led to accumulated globins  that were devoid of heme and aggregated within the erythrocytes and their precursors.	transcription
61089	3	335681	7	NULL	NULL	0	NULL	statement 2	Process		aggregates within					erythrocytes	Cell				NULL		0	NULL	NULL	NULL	gw70_annurevnutr_24_0_105_s_479	15189115	However, in erythroid cells from iron-deficient HRI /  mice, a marked increase in both  - and  -globin synthesis led to accumulated globins  that were devoid of heme and aggregated within the erythrocytes and their precursors.	transcription
66477	1	335682	7	NULL	NULL	0	NULL	HRI	GP		evolved from			NT-HBD		globin gene	GP			second exon of	NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1725_2_174_s_68	16109458	However, while the analyses suggest  that the NT-HBD of HRI may have evolved from the second exon of the  -globin gene    [12], the finding that His123 may be one of the axial heme-binding ligands   [17] suggests that the tertiary fold of the NT-HBD may be different from that of globin  chains, as H123 is predicted to be part of what would be equivalent to the H-helix of globins: a  helix located outside the heme-binding core of globins   [12].	transcription
66478	2	335682	7	NULL	NULL	0	NULL	His123	GP		is a type of					axial heme-binding ligands	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1725_2_174_s_68	16109458	However, while the analyses suggest  that the NT-HBD of HRI may have evolved from the second exon of the  -globin gene    [12], the finding that His123 may be one of the axial heme-binding ligands   [17] suggests that the tertiary fold of the NT-HBD may be different from that of globin  chains, as H123 is predicted to be part of what would be equivalent to the H-helix of globins: a  helix located outside the heme-binding core of globins   [12].	transcription
66479	3	335682	7	NULL	NULL	0	NULL	HRI	GP		different from		may be	NT-HBD 		globin chains	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1725_2_174_s_68	16109458	However, while the analyses suggest  that the NT-HBD of HRI may have evolved from the second exon of the  -globin gene    [12], the finding that His123 may be one of the axial heme-binding ligands   [17] suggests that the tertiary fold of the NT-HBD may be different from that of globin  chains, as H123 is predicted to be part of what would be equivalent to the H-helix of globins: a  helix located outside the heme-binding core of globins   [12].	transcription
66480	4	335682	7	NULL	NULL	0	NULL	H123	GP		is equivalent to					globins	GP	part of	H-helix of 		NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1725_2_174_s_68	16109458	However, while the analyses suggest  that the NT-HBD of HRI may have evolved from the second exon of the  -globin gene    [12], the finding that His123 may be one of the axial heme-binding ligands   [17] suggests that the tertiary fold of the NT-HBD may be different from that of globin  chains, as H123 is predicted to be part of what would be equivalent to the H-helix of globins: a  helix located outside the heme-binding core of globins   [12].	transcription
56664	1	335683	5	NULL	NULL	0	NULL	HRI			regulates					globin		synthesis of			NULL	reticulocytes	0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15752_s_17	14752110	HRI regulates globin synthesis in reticulocytes in response to heme availability.	transcription
56665	2	335683	5	NULL	NULL	0	NULL	statement 1			in response to					heme		availability of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15752_s_17	14752110	HRI regulates globin synthesis in reticulocytes in response to heme availability.	transcription
66481	1	335683	7	NULL	NULL	0	NULL	HRI 	GP		regulates					globin	GP	synthesis of			NULL	reticulocytes	0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15752_s_17	14752110	HRI regulates globin synthesis in reticulocytes in response to heme availability.	transcription
66482	2	335683	7	NULL	NULL	0	NULL	statement 1	Process		in response to					heme	GP	availability of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_16_15752_s_17	14752110	HRI regulates globin synthesis in reticulocytes in response to heme availability.	transcription
56666	1	335684	5	NULL	NULL	0	NULL	heme			bind					globin					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_22_22944_s_247	15016813	Remarkably, as in murine Ngb, the heme binds to the globin in two orientations in  Chironomus Hb ( ,  ).	transcription
56667	2	335684	5	NULL	NULL	0	NULL	statement 1			occurs in					Hb		Chironomus			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_22_22944_s_247	15016813	Remarkably, as in murine Ngb, the heme binds to the globin in two orientations in  Chironomus Hb ( ,  ).	transcription
56668	3	335684	5	NULL	NULL	0	NULL	statement 1			occurs in					Ngb		murine			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_22_22944_s_247	15016813	Remarkably, as in murine Ngb, the heme binds to the globin in two orientations in  Chironomus Hb ( ,  ).	transcription
66483	1	335684	7	NULL	NULL	0	NULL	heme	Chemical		bind					globin	GP				NULL	Chironomus Hb	0	NULL	NULL	NULL	gw70_jbiolchem_279_22_22944_s_247	15016813	Remarkably, as in murine Ngb, the heme binds to the globin in two orientations in  Chironomus Hb ( ,  ).	transcription
66484	2	335684	7	NULL	NULL	0	NULL	statement 1	Process		occur in					two orientations	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_22_22944_s_247	15016813	Remarkably, as in murine Ngb, the heme binds to the globin in two orientations in  Chironomus Hb ( ,  ).	transcription
66485	3	335684	7	NULL	NULL	0	NULL	Heme	Chemical		bind					globin	GP				NULL	murine Ngb	0	NULL	NULL	NULL	gw70_jbiolchem_279_22_22944_s_247	15016813	Remarkably, as in murine Ngb, the heme binds to the globin in two orientations in  Chironomus Hb ( ,  ).	transcription
56669	1	335685	5	NULL	NULL	0	NULL	Bach1			departs from					beta-Globin LCR					NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_179	14747657	Heme Induces the Departure of Bach1 from the beta-Globin LCR.	transcription
56670	2	335685	5	NULL	NULL	0	NULL	heme			induce					statement 1					NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_179	14747657	Heme Induces the Departure of Bach1 from the beta-Globin LCR.	transcription
66486	1	335685	7	NULL	NULL	0	NULL	Bach1	GP		depart from					beta-Globin	GP		LCR		NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_179	14747657	Heme Induces the Departure of Bach1 from the beta-Globin LCR.	transcription
66487	2	335685	7	NULL	NULL	0	NULL	Heme	Chemical		induce					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_179	14747657	Heme Induces the Departure of Bach1 from the beta-Globin LCR.	transcription
56671	1	335686	5	NULL	NULL	0	NULL	globin			undergoes					translation					NULL		0	NULL	NULL	NULL	gw60_embo_20_23_6909_s_235	11726526	The lack of HRI relieves the normal feedback regulation of globin translation in heme deficiency.	transcription
56672	2	335686	5	NULL	NULL	0	NULL	statement 1			in deficiency of					heme					NULL		0	NULL	NULL	NULL	gw60_embo_20_23_6909_s_235	11726526	The lack of HRI relieves the normal feedback regulation of globin translation in heme deficiency.	transcription
56673	3	335686	5	NULL	NULL	0	NULL	HRI		absence of	relieves					statement 1		normal feedback regulation of			NULL		0	NULL	NULL	NULL	gw60_embo_20_23_6909_s_235	11726526	The lack of HRI relieves the normal feedback regulation of globin translation in heme deficiency.	transcription
66488	1	335686	7	NULL	NULL	0	NULL	HRI	GP	lack of	relieves					globin translation	Process	normal feedback regulation of			NULL		0	NULL	NULL	NULL	gw60_embo_20_23_6909_s_235	11726526	The lack of HRI relieves the normal feedback regulation of globin translation in heme deficiency.	transcription
66489	2	335686	7	NULL	NULL	0	NULL	statement 1	Process		occurs in					heme deficiency	MedicalFinding				NULL		0	NULL	NULL	NULL	gw60_embo_20_23_6909_s_235	11726526	The lack of HRI relieves the normal feedback regulation of globin translation in heme deficiency.	transcription
56674	1	335687	5	NULL	NULL	0	NULL	HRI			is a feedback inhibitor of					globin		synthesis of			NULL		0	NULL	NULL	NULL	gw60_embo_20_23_6909_s_245	11726526	HRI serves as a feedback inhibitor of globin synthesis by sensing heme.	transcription
56675	2	335687	5	NULL	NULL	0	NULL	statement 1			occurs by					heme		sensing of			NULL		0	NULL	NULL	NULL	gw60_embo_20_23_6909_s_245	11726526	HRI serves as a feedback inhibitor of globin synthesis by sensing heme.	transcription
66490	1	335687	7	NULL	NULL	0	NULL	HRI	GP		is a feedback inhibitor of					globin synthesis	Process				NULL		0	NULL	NULL	NULL	gw60_embo_20_23_6909_s_245	11726526	HRI serves as a feedback inhibitor of globin synthesis by sensing heme.	transcription
66491	2	335687	7	NULL	NULL	0	NULL	statement 1	Process		occur by 					heme	Chemical	sensing			NULL		0	NULL	NULL	NULL	gw60_embo_20_23_6909_s_245	11726526	HRI serves as a feedback inhibitor of globin synthesis by sensing heme.	transcription
56676	1	335688	5	NULL	NULL	0	NULL	heme			bind					globin					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_640_s_301	9925594	The association rate constant for heme binding to globin is independent of protein structure.	transcription
66492	1	335688	7	NULL	NULL	0	NULL	heme	Chemical		bind					globin	GP				NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_640_s_301	9925594	The association rate constant for heme binding to globin is independent of protein structure.	transcription
56677	1	335689	5	NULL	NULL	0	NULL	alpha-globin			is not required for			heme group		AHSP		interaction with			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_43_40602_s_33	12192002	In addition, we find that the heme group of alpha-globin is not required for AHSP interaction.	transcription
66493	1	335689	7	NULL	NULL	0	NULL	 alpha-globin	GP		is not required for			heme group		AHSP	GP	interaction of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_43_40602_s_33	12192002	In addition, we find that the heme group of alpha-globin is not required for AHSP interaction.	transcription
56678	1	335690	5	NULL	NULL	0	NULL	globin			contains								heme-binding domain		NULL		0	NULL	NULL	NULL	gw70_jneurosci_23_28_9418_s_323	14561870	Globins contain a heme-binding domain and participate in diverse processes such as oxygen transport, oxygen storage, and nitric oxide detoxification.	transcription
56679	2	335690	5	NULL	NULL	0	NULL	statement 1			participates in					oxygen		transport of			NULL		0	NULL	NULL	NULL	gw70_jneurosci_23_28_9418_s_323	14561870	Globins contain a heme-binding domain and participate in diverse processes such as oxygen transport, oxygen storage, and nitric oxide detoxification.	transcription
56680	3	335690	5	NULL	NULL	0	NULL	statement 1			participates in					oxygen		storage of			NULL		0	NULL	NULL	NULL	gw70_jneurosci_23_28_9418_s_323	14561870	Globins contain a heme-binding domain and participate in diverse processes such as oxygen transport, oxygen storage, and nitric oxide detoxification.	transcription
56681	4	335690	5	NULL	NULL	0	NULL	statement 1			participates in					nitric oxide		detoxification of			NULL		0	NULL	NULL	NULL	gw70_jneurosci_23_28_9418_s_323	14561870	Globins contain a heme-binding domain and participate in diverse processes such as oxygen transport, oxygen storage, and nitric oxide detoxification.	transcription
66494	1	335690	7	NULL	NULL	0	NULL	Globins	GP		contains					heme-binding domain	GP				NULL		0	NULL	NULL	NULL	gw70_jneurosci_23_28_9418_s_323	14561870	Globins contain a heme-binding domain and participate in diverse processes such as oxygen transport, oxygen storage, and nitric oxide detoxification.	transcription
66495	2	335690	7	NULL	NULL	0	NULL	Globins	GP		participate in					oxygen transport	Process				NULL		0	NULL	NULL	NULL	gw70_jneurosci_23_28_9418_s_323	14561870	Globins contain a heme-binding domain and participate in diverse processes such as oxygen transport, oxygen storage, and nitric oxide detoxification.	transcription
66496	3	335690	7	NULL	NULL	0	NULL	globins	GP		participate in					oxygen storage	Process				NULL		0	NULL	NULL	NULL	gw70_jneurosci_23_28_9418_s_323	14561870	Globins contain a heme-binding domain and participate in diverse processes such as oxygen transport, oxygen storage, and nitric oxide detoxification.	transcription
66497	4	335690	7	NULL	NULL	0	NULL	Globins	GP		participate in					nitric oxide detoxification	Process				NULL		0	NULL	NULL	NULL	gw70_jneurosci_23_28_9418_s_323	14561870	Globins contain a heme-binding domain and participate in diverse processes such as oxygen transport, oxygen storage, and nitric oxide detoxification.	transcription
56682	1	335691	5	NULL	NULL	0	NULL	heme			induce					beta-globin gene		expression of			NULL	erythroid cells	0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_121	14660636	Thus, heme induces the expression of the beta-globin gene by stimulating the enhancer activity of the beta-globin LCR in erythroid cells.	transcription
56683	2	335691	5	NULL	NULL	0	NULL	heme			stimulates					beta-globin LCR		activity of		enhancer	NULL	erythroid cells	0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_121	14660636	Thus, heme induces the expression of the beta-globin gene by stimulating the enhancer activity of the beta-globin LCR in erythroid cells.	transcription
56684	3	335691	5	NULL	NULL	0	NULL	statement 2			leads to					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_121	14660636	Thus, heme induces the expression of the beta-globin gene by stimulating the enhancer activity of the beta-globin LCR in erythroid cells.	transcription
66498	1	335691	7	NULL	NULL	0	NULL	heme	Chemical		induce					beta-globin gene	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_121	14660636	Thus, heme induces the expression of the beta-globin gene by stimulating the enhancer activity of the beta-globin LCR in erythroid cells.	transcription
66499	2	335691	7	NULL	NULL	NULL	NULL	statement 1	Process		occur by 					beta-globin	GP	stimulating;;enhancer activity of	LCR		NULL	erythroid cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_121	14660636	Thus, heme induces the expression of the beta-globin gene by stimulating the enhancer activity of the beta-globin LCR in erythroid cells.	transcription
66500	1	335692	7	NULL	NULL	0	NULL	Mutations	Process		result in					globin 	GP	instability of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_43_26931_s_26	8900178	Mutations that result in globin instability either affect structure of globin and heme subunit or hemoglobin tetramer.	transcription
66501	2	335692	7	NULL	NULL	0	NULL	statement 1	Process		affect					globin	GP	structure of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_43_26931_s_26	8900178	Mutations that result in globin instability either affect structure of globin and heme subunit or hemoglobin tetramer.	transcription
66502	3	335692	7	NULL	NULL	NULL	NULL	statement 1	Process		affect					heme subunit	Chemical	structure of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_43_26931_s_26	8900178	Mutations that result in globin instability either affect structure of globin and heme subunit or hemoglobin tetramer.	transcription
66503	4	335692	7	NULL	NULL	0	NULL	statement 1	Process		affect					hemoglobin tetramer	GP	structure of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_43_26931_s_26	8900178	Mutations that result in globin instability either affect structure of globin and heme subunit or hemoglobin tetramer.	transcription
66504	5	335692	7	NULL	NULL	0	NULL	statement 2	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_43_26931_s_26	8900178	Mutations that result in globin instability either affect structure of globin and heme subunit or hemoglobin tetramer.	transcription
66505	6	335692	7	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_43_26931_s_26	8900178	Mutations that result in globin instability either affect structure of globin and heme subunit or hemoglobin tetramer.	transcription
56685	1	335693	5	NULL	NULL	0	NULL	heme		synthesis of	is coupled with					beta-globin mRNA		transcription of			NULL		0	NULL	NULL	NULL	gw70_embo_23_13_2544_s_259	15175654	In this  view, synthesis of heme is coupled with transcription of beta-globin mRNA by the heme response of Bach1.	transcription
56686	2	335693	5	NULL	NULL	0	NULL	Bach1		heme response of	is required for					statement 1					NULL		0	NULL	NULL	NULL	gw70_embo_23_13_2544_s_259	15175654	In this  view, synthesis of heme is coupled with transcription of beta-globin mRNA by the heme response of Bach1.	transcription
66506	1	335693	7	NULL	NULL	0	NULL	heme	Chemical	synthesis of	is coupled with					beta-globin mRNA	GP	transcription of			NULL		0	NULL	NULL	NULL	gw70_embo_23_13_2544_s_259	15175654	In this  view, synthesis of heme is coupled with transcription of beta-globin mRNA by the heme response of Bach1.	transcription
66507	2	335693	7	NULL	NULL	0	NULL	statement 1	Process		occur by					Bach1	GP	heme response of			NULL		0	NULL	NULL	NULL	gw70_embo_23_13_2544_s_259	15175654	In this  view, synthesis of heme is coupled with transcription of beta-globin mRNA by the heme response of Bach1.	transcription
56687	1	335694	5	NULL	NULL	0	NULL	globin mRNA		translation of	is controlled by					heme					NULL	mammalian reticulocytes	0	NULL	NULL	NULL	gw70_jbacteriol_187_15_5084_s_20	16030200	Translation of globin mRNA in mammalian reticulocytes is controlled by heme via the heme-controlled inhibitor ( ).	transcription
56688	2	335694	5	NULL	NULL	0	NULL	statement 1			via					heme-controlled inhibitor					NULL	mammalian reticulocytes	NULL	NULL	NULL	NULL	gw70_jbacteriol_187_15_5084_s_20	16030200	Translation of globin mRNA in mammalian reticulocytes is controlled by heme via the heme-controlled inhibitor ( ).	transcription
66508	1	335694	7	NULL	NULL	0	NULL	globin mRNA	GP	translation of	is controlled by					heme	Chemical				NULL	mammalian reticulocytes	0	NULL	NULL	NULL	gw70_jbacteriol_187_15_5084_s_20	16030200	Translation of globin mRNA in mammalian reticulocytes is controlled by heme via the heme-controlled inhibitor ( ).	transcription
66509	2	335694	7	NULL	NULL	0	NULL	statement 1	Process		via					heme-controlled inhibitor	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbacteriol_187_15_5084_s_20	16030200	Translation of globin mRNA in mammalian reticulocytes is controlled by heme via the heme-controlled inhibitor ( ).	transcription
56689	1	335695	5	NULL	NULL	0	NULL	HRI			is					Heme-regulated eukaryotic initiation factor (eIF)-2 kinase					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_99_s_3	12922173	Heme-regulated eukaryotic initiation factor (eIF)-2  kinase (HRI) regulates the synthesis of globin chains in reticulocytes with heme availability.	transcription
56690	2	335695	5	NULL	NULL	0	NULL	HRI			regulates					globin chains		synthesis of			NULL	reticulocytes with heme availability	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_99_s_3	12922173	Heme-regulated eukaryotic initiation factor (eIF)-2  kinase (HRI) regulates the synthesis of globin chains in reticulocytes with heme availability.	transcription
66510	1	335695	7	NULL	NULL	0	NULL	HRI	GP		regulate 					globin chains	GP	synthesis of			NULL	reticulocytes	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_99_s_3	12922173	Heme-regulated eukaryotic initiation factor (eIF)-2  kinase (HRI) regulates the synthesis of globin chains in reticulocytes with heme availability.	transcription
66511	2	335695	7	NULL	NULL	0	NULL	statement 1	Process		occur with					heme 	Chemical	availability of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_99_s_3	12922173	Heme-regulated eukaryotic initiation factor (eIF)-2  kinase (HRI) regulates the synthesis of globin chains in reticulocytes with heme availability.	transcription
66512	3	335695	7	NULL	NULL	NULL	NULL	Heme-regulated eukaryotic initiation factor (eIF)-2 kinase	GP		is a type of					HRI	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_99_s_3	12922173	Heme-regulated eukaryotic initiation factor (eIF)-2  kinase (HRI) regulates the synthesis of globin chains in reticulocytes with heme availability.	transcription
66513	1	335696	7	NULL	NULL	0	NULL	heme binding module	GP		regulate					heme binding structure	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_17_12438_s_33	10777528	This structural conversion in the Mbalpha(HBM)-globin clearly demonstrated that the heme binding structure is regulated by the heme binding module.	transcription
56691	2	335697	5	NULL	NULL	0	NULL	linkers			does not bind					statement 1					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_47_29999_s_189	8939946	We conclude that the linkers do not bind heme under conditions where heme is not lost by the globin chains.	transcription
56692	1	335697	5	NULL	NULL	0	NULL	heme			is not lost by					globin chains					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_47_29999_s_189	8939946	We conclude that the linkers do not bind heme under conditions where heme is not lost by the globin chains.	transcription
66514	1	335697	7	NULL	NULL	0	NULL	linkers	GP		does not bind					heme	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_47_29999_s_189	8939946	We conclude that the linkers do not bind heme under conditions where heme is not lost by the globin chains.	transcription
66515	2	335697	7	NULL	NULL	0	NULL	heme	Chemical		is not lost by					globin chain	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_47_29999_s_189	8939946	We conclude that the linkers do not bind heme under conditions where heme is not lost by the globin chains.	transcription
66516	3	335697	7	NULL	NULL	0	NULL	statement 1	Process		occur upon					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_47_29999_s_189	8939946	We conclude that the linkers do not bind heme under conditions where heme is not lost by the globin chains.	transcription
56693	1	335698	5	NULL	NULL	0	NULL	heme			regulates					globin gene		transcription of			NULL	erythroleukemia cells	0	NULL	NULL	NULL	abs-batch0600-0619_antioxid-redox-signal_8_1-2_16487039_s_1	16487039	Regulation of Globin Gene Transcription by Heme in Erythroleukemia Cells: Analysis of Putative Heme Regulatory Motifs in the p45 NF-E2 Transcription Factor..	transcription
66517	1	335698	7	NULL	NULL	NULL	NULL	Heme	Chemical		regulate					Globin gene	GP	transcription of			NULL	Erythroleukemia Cells	NULL	NULL	NULL	NULL	abs-batch0600-0619_antioxid-redox-signal_8_1-2_16487039_s_1	16487039	Regulation of Globin Gene Transcription by Heme in Erythroleukemia Cells: Analysis of Putative Heme Regulatory Motifs in the p45 NF-E2 Transcription Factor..	transcription
56694	1	335699	5	NULL	NULL	0	NULL	HRI			is					Heme-regulated eIF2alpha kinase					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_12_5205_s_255	15923635	Heme-regulated eIF2alpha kinase (HRI) phosphorylates and inactivates eukaryotic initiation factor 2alpha (eIF2alpha) in the absence of heme ( ), thereby coordinating heme and globin synthesis ( ).	transcription
56695	2	335699	5	NULL	NULL	0	NULL	eIF2alpha			is					eukaryotic initiation factor 2alpha					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_12_5205_s_255	15923635	Heme-regulated eIF2alpha kinase (HRI) phosphorylates and inactivates eukaryotic initiation factor 2alpha (eIF2alpha) in the absence of heme ( ), thereby coordinating heme and globin synthesis ( ).	transcription
56696	3	335699	5	NULL	NULL	0	NULL	HRI			phosphorylates					eIF2alpha					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_12_5205_s_255	15923635	Heme-regulated eIF2alpha kinase (HRI) phosphorylates and inactivates eukaryotic initiation factor 2alpha (eIF2alpha) in the absence of heme ( ), thereby coordinating heme and globin synthesis ( ).	transcription
56697	4	335699	5	NULL	NULL	0	NULL	statement 3			inactivates					eIF2alpha					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_12_5205_s_255	15923635	Heme-regulated eIF2alpha kinase (HRI) phosphorylates and inactivates eukaryotic initiation factor 2alpha (eIF2alpha) in the absence of heme ( ), thereby coordinating heme and globin synthesis ( ).	transcription
56698	5	335699	5	NULL	NULL	0	NULL	statement 3			in the absence of					heme					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_12_5205_s_255	15923635	Heme-regulated eIF2alpha kinase (HRI) phosphorylates and inactivates eukaryotic initiation factor 2alpha (eIF2alpha) in the absence of heme ( ), thereby coordinating heme and globin synthesis ( ).	transcription
56699	6	335699	5	NULL	NULL	0	NULL	statement 4			coordinates with					heme		synthesis of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_12_5205_s_255	15923635	Heme-regulated eIF2alpha kinase (HRI) phosphorylates and inactivates eukaryotic initiation factor 2alpha (eIF2alpha) in the absence of heme ( ), thereby coordinating heme and globin synthesis ( ).	transcription
56700	7	335699	5	NULL	NULL	0	NULL	statement 4			coordinates with					globin		synthesis of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_12_5205_s_255	15923635	Heme-regulated eIF2alpha kinase (HRI) phosphorylates and inactivates eukaryotic initiation factor 2alpha (eIF2alpha) in the absence of heme ( ), thereby coordinating heme and globin synthesis ( ).	transcription
66518	1	335699	7	NULL	NULL	NULL	NULL	HRI	GP		is					Heme-regulated eIF2alpha kinase	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_5205_s_255	15923635	Heme-regulated eIF2alpha kinase (HRI) phosphorylates and inactivates eukaryotic initiation factor 2alpha (eIF2alpha) in the absence of heme ( ), thereby coordinating heme and globin synthesis ( ).	transcription
66519	2	335699	7	NULL	NULL	NULL	NULL	HRI	GP		phosphorylates					eIF2alpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_5205_s_255	15923635	Heme-regulated eIF2alpha kinase (HRI) phosphorylates and inactivates eukaryotic initiation factor 2alpha (eIF2alpha) in the absence of heme ( ), thereby coordinating heme and globin synthesis ( ).	transcription
66520	3	335699	7	NULL	NULL	0	NULL	HRI	GP		inactivates					eIF2alpha	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_12_5205_s_255	15923635	Heme-regulated eIF2alpha kinase (HRI) phosphorylates and inactivates eukaryotic initiation factor 2alpha (eIF2alpha) in the absence of heme ( ), thereby coordinating heme and globin synthesis ( ).	transcription
66521	4	335699	7	NULL	NULL	0	NULL	statement 2	Process		in the absence of					heme	Chemical				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_12_5205_s_255	15923635	Heme-regulated eIF2alpha kinase (HRI) phosphorylates and inactivates eukaryotic initiation factor 2alpha (eIF2alpha) in the absence of heme ( ), thereby coordinating heme and globin synthesis ( ).	transcription
66522	5	335699	7	NULL	NULL	0	NULL	statement 3	Process		in the absence of					heme	Chemical				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_12_5205_s_255	15923635	Heme-regulated eIF2alpha kinase (HRI) phosphorylates and inactivates eukaryotic initiation factor 2alpha (eIF2alpha) in the absence of heme ( ), thereby coordinating heme and globin synthesis ( ).	transcription
66523	6	335699	7	NULL	NULL	0	NULL	statement 2	Process		coordinate					heme synthesis	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_12_5205_s_255	15923635	Heme-regulated eIF2alpha kinase (HRI) phosphorylates and inactivates eukaryotic initiation factor 2alpha (eIF2alpha) in the absence of heme ( ), thereby coordinating heme and globin synthesis ( ).	transcription
66524	7	335699	7	NULL	NULL	0	NULL	statement 3	Process		coordinate					heme synthesis	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_12_5205_s_255	15923635	Heme-regulated eIF2alpha kinase (HRI) phosphorylates and inactivates eukaryotic initiation factor 2alpha (eIF2alpha) in the absence of heme ( ), thereby coordinating heme and globin synthesis ( ).	transcription
66525	8	335699	7	NULL	NULL	0	NULL	statement 2	Process		coordinate					globin synthesis	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_12_5205_s_255	15923635	Heme-regulated eIF2alpha kinase (HRI) phosphorylates and inactivates eukaryotic initiation factor 2alpha (eIF2alpha) in the absence of heme ( ), thereby coordinating heme and globin synthesis ( ).	transcription
66526	9	335699	7	NULL	NULL	0	NULL	statement 3	Process		coordinate					globin synthesis	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_12_5205_s_255	15923635	Heme-regulated eIF2alpha kinase (HRI) phosphorylates and inactivates eukaryotic initiation factor 2alpha (eIF2alpha) in the absence of heme ( ), thereby coordinating heme and globin synthesis ( ).	transcription
66528	10	335699	7	NULL	NULL	NULL	NULL	eIF2alpha	GP		is					eukaryotic initiation factor 2alpha	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_12_5205_s_255	15923635	Heme-regulated eIF2alpha kinase (HRI) phosphorylates and inactivates eukaryotic initiation factor 2alpha (eIF2alpha) in the absence of heme ( ), thereby coordinating heme and globin synthesis ( ).	transcription
56701	1	335700	5	NULL	NULL	0	NULL	N-RsbR		B. subtilis	is a member of					globins family					NULL		0	NULL	NULL	NULL	gw70_pnas_102_48_17320_s_230	16301540	It is thus possible that globins with functions other than binding of gaseous diatomic molecules are yet to be discovered and that N-RsbR of  B. subtilis is the first member to be described of what could prove to be a large family of globins that do not bind heme.	transcription
56702	2	335700	5	NULL	NULL	0	NULL	N-RsbR		B. subtilis	does not bind					heme					NULL		0	NULL	NULL	NULL	gw70_pnas_102_48_17320_s_230	16301540	It is thus possible that globins with functions other than binding of gaseous diatomic molecules are yet to be discovered and that N-RsbR of  B. subtilis is the first member to be described of what could prove to be a large family of globins that do not bind heme.	transcription
66529	1	335700	7	NULL	NULL	0	NULL	N-RsbR	GP	B. subtilis	belongs to					globin family	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_102_48_17320_s_230	16301540	It is thus possible that globins with functions other than binding of gaseous diatomic molecules are yet to be discovered and that N-RsbR of  B. subtilis is the first member to be described of what could prove to be a large family of globins that do not bind heme.	transcription
66530	2	335700	7	NULL	NULL	NULL	NULL	N-RsbR	GP	B.subtilis	does not bind					heme	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_48_17320_s_230	16301540	It is thus possible that globins with functions other than binding of gaseous diatomic molecules are yet to be discovered and that N-RsbR of  B. subtilis is the first member to be described of what could prove to be a large family of globins that do not bind heme.	transcription
56703	1	335701	5	NULL	NULL	0	NULL	heme			bind					globin					NULL		0	NULL	NULL	NULL	gw70_embo_22_8_1824_s_202	12682015	Also similar to TipAS antibiotic binding, heme  binding to globins induces the folding of additional alpha-helices that are in contact with the ligand ( ;   et al;   et al).	transcription
56704	2	335701	5	NULL	NULL	0	NULL	statement 1			induces					alpha-helices		folding of			NULL		0	NULL	NULL	NULL	gw70_embo_22_8_1824_s_202	12682015	Also similar to TipAS antibiotic binding, heme  binding to globins induces the folding of additional alpha-helices that are in contact with the ligand ( ;   et al;   et al).	transcription
66531	1	335701	7	NULL	NULL	0	NULL	heme	Chemical		bind					globin	GP				NULL		0	NULL	NULL	NULL	gw70_embo_22_8_1824_s_202	12682015	Also similar to TipAS antibiotic binding, heme  binding to globins induces the folding of additional alpha-helices that are in contact with the ligand ( ;   et al;   et al).	transcription
66532	2	335701	7	NULL	NULL	0	NULL	heme	Chemical		induce					alpha-helices	GP	folding of			NULL		0	NULL	NULL	NULL	gw70_embo_22_8_1824_s_202	12682015	Also similar to TipAS antibiotic binding, heme  binding to globins induces the folding of additional alpha-helices that are in contact with the ligand ( ;   et al;   et al).	transcription
66533	1	335702	7	NULL	NULL	0	NULL	heme	Chemical		bind								NTD		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_12	14672943	His78 appears to play the primary role in the specific binding of heme to the NTD, acting analogously to the "`proximal histidine"` ligand of globins, while His123 appears to act as the "`distal"` heme ligand.	transcription
66534	2	335702	7	NULL	NULL	0	NULL				primary role in			His78		statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_12	14672943	His78 appears to play the primary role in the specific binding of heme to the NTD, acting analogously to the "`proximal histidine"` ligand of globins, while His123 appears to act as the "`distal"` heme ligand.	transcription
66535	3	335702	7	NULL	NULL	0	NULL				act analogously to			His78 		globins	GP	ligand of	proximal histidine		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_12	14672943	His78 appears to play the primary role in the specific binding of heme to the NTD, acting analogously to the "`proximal histidine"` ligand of globins, while His123 appears to act as the "`distal"` heme ligand.	transcription
66536	4	335702	7	NULL	NULL	0	NULL				act as			His123		heme ligand	GP		distal		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_12	14672943	His78 appears to play the primary role in the specific binding of heme to the NTD, acting analogously to the "`proximal histidine"` ligand of globins, while His123 appears to act as the "`distal"` heme ligand.	transcription
56726	1	335703	5	NULL	NULL	0	NULL	globin genes		transcriptional activation of	results in					globin chains		synthesis of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_51_4_558_s_28	9106619	The synthesis of globin chains primarily results from transcriptional activation of the globin genes ( 16), and the enhanced heme production is ensured by activation of the enzymes responsible for its biosynthesis.	transcription
56727	2	335703	5	NULL	NULL	0	NULL	statement 1			enhances					heme		production of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_51_4_558_s_28	9106619	The synthesis of globin chains primarily results from transcriptional activation of the globin genes ( 16), and the enhanced heme production is ensured by activation of the enzymes responsible for its biosynthesis.	transcription
66537	1	335703	7	NULL	NULL	0	NULL	globin chains	GP	synthesis of	result from					globin genes	GP	transcriptional activation of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_51_4_558_s_28	9106619	The synthesis of globin chains primarily results from transcriptional activation of the globin genes ( 16), and the enhanced heme production is ensured by activation of the enzymes responsible for its biosynthesis.	transcription
56728	1	335704	5	NULL	NULL	0	NULL	beta-globin chains		expressed	bind					heme					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_43_26677_s_147	8900144	Expressed beta-globin chains bound heme and spectrophotometric properties were similar to that of authentic beta-globin from human red blood cells.	transcription
66538	1	335704	7	NULL	NULL	0	NULL	beta-globin chains	GP	expressed	bind					heme	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_43_26677_s_147	8900144	Expressed beta-globin chains bound heme and spectrophotometric properties were similar to that of authentic beta-globin from human red blood cells.	transcription
56729	1	335705	5	NULL	NULL	0	NULL	beta-globin gene		regulation of;;expression of	is dependent on					heme					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_4	14660636	To investigate the involvement of Bach1 in the heme-dependent regulation of the expression of the beta-globin gene, mouse erythroleukemia (MEL) cells were cultured with succinylacetone (SA), a specific inhibitor of heme biosynthesis, and the level of beta-globin mRNA was examined.	transcription
56730	2	335705	5	NULL	NULL	0	NULL	Bach1			is involved in		potentially			statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_4	14660636	To investigate the involvement of Bach1 in the heme-dependent regulation of the expression of the beta-globin gene, mouse erythroleukemia (MEL) cells were cultured with succinylacetone (SA), a specific inhibitor of heme biosynthesis, and the level of beta-globin mRNA was examined.	transcription
66539	1	335705	7	NULL	NULL	0	NULL	SA	Chemical		is an inhibitor of					heme biosynthesis	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_4	14660636	To investigate the involvement of Bach1 in the heme-dependent regulation of the expression of the beta-globin gene, mouse erythroleukemia (MEL) cells were cultured with succinylacetone (SA), a specific inhibitor of heme biosynthesis, and the level of beta-globin mRNA was examined.	transcription
66540	2	335705	7	NULL	NULL	0	NULL	SA	Chemical		is					succinylacetone 	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_4	14660636	To investigate the involvement of Bach1 in the heme-dependent regulation of the expression of the beta-globin gene, mouse erythroleukemia (MEL) cells were cultured with succinylacetone (SA), a specific inhibitor of heme biosynthesis, and the level of beta-globin mRNA was examined.	transcription
56731	1	335706	5	NULL	NULL	0	NULL	Bach1			regulates		potentially			beta-globin gene		expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_40	14660636	To clarify whether Bach1 regulates beta-globin gene expression, we examined heme-dependent expression of the beta-globin gene in human erythroleukemia K562 and MEL cells and the regulation of the interaction of Bach1 with the LCR by heme.	transcription
56732	2	335706	5	NULL	NULL	0	NULL	Bach1			interacts with					LCR					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_40	14660636	To clarify whether Bach1 regulates beta-globin gene expression, we examined heme-dependent expression of the beta-globin gene in human erythroleukemia K562 and MEL cells and the regulation of the interaction of Bach1 with the LCR by heme.	transcription
66541	1	335706	7	NULL	NULL	0	NULL	 beta-globin gene	GP	expression of	depends on					heme	Chemical				NULL	human erythroleukemia K562 cells	0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_40	14660636	To clarify whether Bach1 regulates beta-globin gene expression, we examined heme-dependent expression of the beta-globin gene in human erythroleukemia K562 and MEL cells and the regulation of the interaction of Bach1 with the LCR by heme.	transcription
66542	2	335706	7	NULL	NULL	0	NULL	beta-globin gene	GP	expression of	depends on					heme	Chemical				NULL	MEL cells	0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_40	14660636	To clarify whether Bach1 regulates beta-globin gene expression, we examined heme-dependent expression of the beta-globin gene in human erythroleukemia K562 and MEL cells and the regulation of the interaction of Bach1 with the LCR by heme.	transcription
66543	3	335706	7	NULL	NULL	0	NULL	Bach1	GP		interacts with					LCR	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_40	14660636	To clarify whether Bach1 regulates beta-globin gene expression, we examined heme-dependent expression of the beta-globin gene in human erythroleukemia K562 and MEL cells and the regulation of the interaction of Bach1 with the LCR by heme.	transcription
66544	4	335706	7	NULL	NULL	0	NULL	heme	Chemical		regulates					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_40	14660636	To clarify whether Bach1 regulates beta-globin gene expression, we examined heme-dependent expression of the beta-globin gene in human erythroleukemia K562 and MEL cells and the regulation of the interaction of Bach1 with the LCR by heme.	transcription
56733	1	335707	5	NULL	NULL	0	NULL	heme		inhibition of;;biosynthesis of	decreases					beta-globin		expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_101	14660636	The decreased beta-globin expression by the inhibition of heme biosynthesis was reversed by culture with 50 muM hemin, suggesting that the expression of beta-globin mRNA in MEL cells is controlled by heme in both uninduced and induced cells.	transcription
56734	2	335707	5	NULL	NULL	0	NULL	hemin			reverses					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_101	14660636	The decreased beta-globin expression by the inhibition of heme biosynthesis was reversed by culture with 50 muM hemin, suggesting that the expression of beta-globin mRNA in MEL cells is controlled by heme in both uninduced and induced cells.	transcription
56735	3	335707	5	NULL	NULL	0	NULL	beta-globin mRNA			is expressed in					MEL cells					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_101	14660636	The decreased beta-globin expression by the inhibition of heme biosynthesis was reversed by culture with 50 muM hemin, suggesting that the expression of beta-globin mRNA in MEL cells is controlled by heme in both uninduced and induced cells.	transcription
56736	4	335707	5	NULL	NULL	0	NULL	heme			controls					statement 3					NULL	uninduced cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_101	14660636	The decreased beta-globin expression by the inhibition of heme biosynthesis was reversed by culture with 50 muM hemin, suggesting that the expression of beta-globin mRNA in MEL cells is controlled by heme in both uninduced and induced cells.	transcription
56737	5	335707	5	NULL	NULL	0	NULL	heme			controls					statement 3					NULL	induced cells	0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_101	14660636	The decreased beta-globin expression by the inhibition of heme biosynthesis was reversed by culture with 50 muM hemin, suggesting that the expression of beta-globin mRNA in MEL cells is controlled by heme in both uninduced and induced cells.	transcription
66545	1	335707	7	NULL	NULL	0	NULL	beta-globin mRNA	GP	expression of	is controlled by					heme	Chemical				NULL	induced MEL cells	0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_101	14660636	The decreased beta-globin expression by the inhibition of heme biosynthesis was reversed by culture with 50 muM hemin, suggesting that the expression of beta-globin mRNA in MEL cells is controlled by heme in both uninduced and induced cells.	transcription
66546	2	335707	7	NULL	NULL	NULL	NULL	beta-globin mRNA	GP	expression of	is controlled by					heme	Chemical				NULL	uninduced MEL cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_101	14660636	The decreased beta-globin expression by the inhibition of heme biosynthesis was reversed by culture with 50 muM hemin, suggesting that the expression of beta-globin mRNA in MEL cells is controlled by heme in both uninduced and induced cells.	transcription
66547	3	335707	7	NULL	NULL	0	NULL	heme biosynthesis	Process	inhibition of	decrease					beta-globin	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_101	14660636	The decreased beta-globin expression by the inhibition of heme biosynthesis was reversed by culture with 50 muM hemin, suggesting that the expression of beta-globin mRNA in MEL cells is controlled by heme in both uninduced and induced cells.	transcription
66548	4	335707	7	NULL	NULL	0	NULL	heme	Chemical		reverse					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_101	14660636	The decreased beta-globin expression by the inhibition of heme biosynthesis was reversed by culture with 50 muM hemin, suggesting that the expression of beta-globin mRNA in MEL cells is controlled by heme in both uninduced and induced cells.	transcription
56738	1	335708	5	NULL	NULL	0	NULL	heme			not incorporated into					beta-globin					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_43_26677_s_138	8900144	From these results they suggested that heme was not incorporated into beta-globin and that interaction between alpha-and beta-globin chains may affect correct folding of the two globin polypeptides in  E. coli ( 4).	transcription
56739	2	335708	5	NULL	NULL	0	NULL	alpha-globin chains			interacts with					beta-globin chains					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_43_26677_s_138	8900144	From these results they suggested that heme was not incorporated into beta-globin and that interaction between alpha-and beta-globin chains may affect correct folding of the two globin polypeptides in  E. coli ( 4).	transcription
56740	3	335708	5	NULL	NULL	0	NULL	statement 2			affects		may			globin polypeptides		correct folding of			NULL	E. coli	0	NULL	NULL	NULL	gw60_jbiolchem_271_43_26677_s_138	8900144	From these results they suggested that heme was not incorporated into beta-globin and that interaction between alpha-and beta-globin chains may affect correct folding of the two globin polypeptides in  E. coli ( 4).	transcription
66549	1	335708	7	NULL	NULL	0	NULL	alpha-globin chain	GP		interacts with					beta-globin chain	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_43_26677_s_138	8900144	From these results they suggested that heme was not incorporated into beta-globin and that interaction between alpha-and beta-globin chains may affect correct folding of the two globin polypeptides in  E. coli ( 4).	transcription
66550	2	335708	7	NULL	NULL	0	NULL	statement 1	Process		affect		may			two globin polypeptides	GP	correct folding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_43_26677_s_138	8900144	From these results they suggested that heme was not incorporated into beta-globin and that interaction between alpha-and beta-globin chains may affect correct folding of the two globin polypeptides in  E. coli ( 4).	transcription
56741	1	335709	5	NULL	NULL	0	NULL	heme group			is a constituent of		intimate			globin molecule					NULL		0	NULL	NULL	NULL	gw70_pnas_102_48_17320_s_133	16301540	The heme group is an intimate constituent of the globin molecule, and mutations of amino acids that line the heme-binding site in myoglobin affect protein folding and stability ( ).	transcription
66551	1	335709	7	NULL	NULL	0	NULL	heme group	GP		intimate constituent of					globin molecule	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_102_48_17320_s_133	16301540	The heme group is an intimate constituent of the globin molecule, and mutations of amino acids that line the heme-binding site in myoglobin affect protein folding and stability ( ).	transcription
66552	2	335709	7	NULL	NULL	NULL	NULL	myoglobin	GP	mutations in	affect			aminoacid lining heme-binding site		protein folding	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_48_17320_s_133	16301540	The heme group is an intimate constituent of the globin molecule, and mutations of amino acids that line the heme-binding site in myoglobin affect protein folding and stability ( ).	transcription
66553	3	335709	7	NULL	NULL	NULL	NULL	myoglobin	GP	mutations in	affect			aminoacid lining heme-binding site		protein stability	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_102_48_17320_s_133	16301540	The heme group is an intimate constituent of the globin molecule, and mutations of amino acids that line the heme-binding site in myoglobin affect protein folding and stability ( ).	transcription
56742	1	335710	5	NULL	NULL	0	NULL	heme			is synthesized during					erythroid		differentiation of			NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_182	14747657	Because heme is synthesized at high levels during erythroid differentiation, we investigated whether heme induces displacement of Bach1 from the beta-globin LCR.	transcription
56743	2	335710	5	NULL	NULL	0	NULL	Bach1			displaced from					beta-globin				LCR	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_182	14747657	Because heme is synthesized at high levels during erythroid differentiation, we investigated whether heme induces displacement of Bach1 from the beta-globin LCR.	transcription
56744	3	335710	5	NULL	NULL	0	NULL	heme			induces		potentially			statement 2					NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_182	14747657	Because heme is synthesized at high levels during erythroid differentiation, we investigated whether heme induces displacement of Bach1 from the beta-globin LCR.	transcription
66554	1	335710	7	NULL	NULL	0	NULL	heme	Chemical	high levels of	synthesized during					erythroid differentiation	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_182	14747657	Because heme is synthesized at high levels during erythroid differentiation, we investigated whether heme induces displacement of Bach1 from the beta-globin LCR.	transcription
56759	1	335711	5	NULL	NULL	0	NULL	globin		proximal side of	contains			heme pocket					side chains at Leu89(F4)		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_12_9093_s_4	11084036	Globin side chains at the Leu89(F4), His97(FG3), Ile99(FG5), and Leu104(G5) positions on the proximal side of the heme pocket strongly influence heme affinity.	transcription
56760	2	335711	5	NULL	NULL	0	NULL	globin		proximal side of	contains			heme pocket					side chains at His97(FG3)		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_12_9093_s_4	11084036	Globin side chains at the Leu89(F4), His97(FG3), Ile99(FG5), and Leu104(G5) positions on the proximal side of the heme pocket strongly influence heme affinity.	transcription
56761	3	335711	5	NULL	NULL	0	NULL	globin		proximal side of	contains			heme pocket					side chains at Ile99(FG5)		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_12_9093_s_4	11084036	Globin side chains at the Leu89(F4), His97(FG3), Ile99(FG5), and Leu104(G5) positions on the proximal side of the heme pocket strongly influence heme affinity.	transcription
56763	4	335711	5	NULL	NULL	0	NULL	globin		proximal side of	contains			heme pocket					side chains at Leu104(G5)		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_12_9093_s_4	11084036	Globin side chains at the Leu89(F4), His97(FG3), Ile99(FG5), and Leu104(G5) positions on the proximal side of the heme pocket strongly influence heme affinity.	transcription
56764	5	335711	5	NULL	NULL	0	NULL	statement 1			influences		strongly			heme		affinity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_12_9093_s_4	11084036	Globin side chains at the Leu89(F4), His97(FG3), Ile99(FG5), and Leu104(G5) positions on the proximal side of the heme pocket strongly influence heme affinity.	transcription
56765	6	335711	5	NULL	NULL	0	NULL	statement 2			influences		strongly			heme		affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_12_9093_s_4	11084036	Globin side chains at the Leu89(F4), His97(FG3), Ile99(FG5), and Leu104(G5) positions on the proximal side of the heme pocket strongly influence heme affinity.	transcription
56766	7	335711	5	NULL	NULL	0	NULL	statement 3			influences		strongly			heme		affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_12_9093_s_4	11084036	Globin side chains at the Leu89(F4), His97(FG3), Ile99(FG5), and Leu104(G5) positions on the proximal side of the heme pocket strongly influence heme affinity.	transcription
56767	8	335711	5	NULL	NULL	0	NULL	statement 4			influences		strongly			heme		affinity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_12_9093_s_4	11084036	Globin side chains at the Leu89(F4), His97(FG3), Ile99(FG5), and Leu104(G5) positions on the proximal side of the heme pocket strongly influence heme affinity.	transcription
66555	1	335711	7	NULL	NULL	NULL	NULL	Globin	GP		influence		strongly	 side chain Leu89(F4) positions on the proximal side of the heme pocket		heme affinity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_12_9093_s_4	11084036	Globin side chains at the Leu89(F4), His97(FG3), Ile99(FG5), and Leu104(G5) positions on the proximal side of the heme pocket strongly influence heme affinity.	transcription
66556	2	335711	7	NULL	NULL	NULL	NULL	Globin	GP		influence		strongly	side chain His97(FG3) positions on the proximal side of the heme pocket		heme affinity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_12_9093_s_4	11084036	Globin side chains at the Leu89(F4), His97(FG3), Ile99(FG5), and Leu104(G5) positions on the proximal side of the heme pocket strongly influence heme affinity.	transcription
66557	3	335711	7	NULL	NULL	NULL	NULL	Globin	GP		influence		strongly	side chain Ile99(FG5) positions on the proximal side of the heme pocket		heme affinity	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_12_9093_s_4	11084036	Globin side chains at the Leu89(F4), His97(FG3), Ile99(FG5), and Leu104(G5) positions on the proximal side of the heme pocket strongly influence heme affinity.	transcription
66558	4	335711	7	NULL	NULL	0	NULL	Globin	GP		influence		strongly	side chain Leu104(G5) positions on the proximal side of the heme pocket		heme affinity	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_12_9093_s_4	11084036	Globin side chains at the Leu89(F4), His97(FG3), Ile99(FG5), and Leu104(G5) positions on the proximal side of the heme pocket strongly influence heme affinity.	transcription
56745	1	335712	5	NULL	NULL	0	NULL	HRI			is					heme- regulated inhibitor					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_206_s_12	11036079	The  heme- regulated  inhibitor (HRI)1 of protein synthesis is a protein-serine kinase which coordinates the synthesis of globin chains with the availability of heme in reticulocytes (reviewed in Refs.	transcription
56746	2	335712	5	NULL	NULL	0	NULL	(HRI)1			is a type of					protein-serine kinase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_206_s_12	11036079	The  heme- regulated  inhibitor (HRI)1 of protein synthesis is a protein-serine kinase which coordinates the synthesis of globin chains with the availability of heme in reticulocytes (reviewed in Refs.	transcription
56747	3	335712	5	NULL	NULL	0	NULL	globin chains		synthesis of	coordinates with					heme		availability of			NULL	reticulocytes	0	NULL	NULL	NULL	gw60_jbiolchem_276_1_206_s_12	11036079	The  heme- regulated  inhibitor (HRI)1 of protein synthesis is a protein-serine kinase which coordinates the synthesis of globin chains with the availability of heme in reticulocytes (reviewed in Refs.	transcription
56748	4	335712	5	NULL	NULL	0	NULL	(HRI)1			is required for					statement 3					NULL	reticulocytes	0	NULL	NULL	NULL	gw60_jbiolchem_276_1_206_s_12	11036079	The  heme- regulated  inhibitor (HRI)1 of protein synthesis is a protein-serine kinase which coordinates the synthesis of globin chains with the availability of heme in reticulocytes (reviewed in Refs.	transcription
66559	1	335712	7	NULL	NULL	0	NULL	HRI	GP		is a type of					protein-serine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_206_s_12	11036079	The  heme- regulated  inhibitor (HRI)1 of protein synthesis is a protein-serine kinase which coordinates the synthesis of globin chains with the availability of heme in reticulocytes (reviewed in Refs.	transcription
66560	2	335712	7	NULL	NULL	0	NULL	HRI	GP		coordinate					globin chains	GP	synthesis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_206_s_12	11036079	The  heme- regulated  inhibitor (HRI)1 of protein synthesis is a protein-serine kinase which coordinates the synthesis of globin chains with the availability of heme in reticulocytes (reviewed in Refs.	transcription
66561	3	335712	7	NULL	NULL	0	NULL	statement 1	Process		depends on					heme	Chemical	availability of			NULL	reticulocytes	0	NULL	NULL	NULL	gw60_jbiolchem_276_1_206_s_12	11036079	The  heme- regulated  inhibitor (HRI)1 of protein synthesis is a protein-serine kinase which coordinates the synthesis of globin chains with the availability of heme in reticulocytes (reviewed in Refs.	transcription
66562	4	335712	7	NULL	NULL	0	NULL	HRI	GP		is					heme- regulated inhibitor	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_206_s_12	11036079	The  heme- regulated  inhibitor (HRI)1 of protein synthesis is a protein-serine kinase which coordinates the synthesis of globin chains with the availability of heme in reticulocytes (reviewed in Refs.	transcription
66563	1	335713	7	NULL	NULL	0	NULL	heme binding module	GP		regulates					globin family	GP		heme proximal structure in		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_17_12438_s_20	10777528	In our previous paper ( 13), we have proposed the heme binding module, a protein continuous segment regulating the heme proximal structure in the globin family.	transcription
56749	1	335714	5	NULL	NULL	0	NULL	globin			has affinity for		high			heme					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_47937_s_190	11602592	No heme exchange reaction was demonstrated between ferrous and ferric Hb because of the high affinity of globin for the heme ( 19); such an exchange would involve a concomitant heme dissociation from both types of subunit.	transcription
66564	1	335714	7	NULL	NULL	0	NULL	globin	GP		high affinity for					heme	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_51_47937_s_190	11602592	No heme exchange reaction was demonstrated between ferrous and ferric Hb because of the high affinity of globin for the heme ( 19); such an exchange would involve a concomitant heme dissociation from both types of subunit.	transcription
56750	1	335715	5	NULL	NULL	0	NULL	heme			bind					cytochromes					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_51_32605_s_173	8955088	The loose association of heme with these proteins is quite different from the situation observed for heme binding to cytochromes, globin, or other heme-binding proteins (see  e.g. 38), where a stable interaction is needed to ensure proper biochemical function.	transcription
56751	2	335715	5	NULL	NULL	0	NULL	heme			bind					globin					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_51_32605_s_173	8955088	The loose association of heme with these proteins is quite different from the situation observed for heme binding to cytochromes, globin, or other heme-binding proteins (see  e.g. 38), where a stable interaction is needed to ensure proper biochemical function.	transcription
66565	1	335715	7	NULL	NULL	0	NULL	heme	Chemical		bind					cytochromes	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_51_32605_s_173	8955088	The loose association of heme with these proteins is quite different from the situation observed for heme binding to cytochromes, globin, or other heme-binding proteins (see  e.g. 38), where a stable interaction is needed to ensure proper biochemical function.	transcription
66566	2	335715	7	NULL	NULL	0	NULL	heme	Chemical		bind					globin	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_51_32605_s_173	8955088	The loose association of heme with these proteins is quite different from the situation observed for heme binding to cytochromes, globin, or other heme-binding proteins (see  e.g. 38), where a stable interaction is needed to ensure proper biochemical function.	transcription
66567	3	335715	7	NULL	NULL	0	NULL	statement 1	Process	stable interaction of	is required for					biochemical function	Process	proper			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_51_32605_s_173	8955088	The loose association of heme with these proteins is quite different from the situation observed for heme binding to cytochromes, globin, or other heme-binding proteins (see  e.g. 38), where a stable interaction is needed to ensure proper biochemical function.	transcription
66568	4	335715	7	NULL	NULL	0	NULL	statement 2	Process	stable interaction of	is required for					biochemical function	Process	proper			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_51_32605_s_173	8955088	The loose association of heme with these proteins is quite different from the situation observed for heme binding to cytochromes, globin, or other heme-binding proteins (see  e.g. 38), where a stable interaction is needed to ensure proper biochemical function.	transcription
56752	1	335716	5	NULL	NULL	0	NULL	globin			bind			chain a		heme					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_47_29999_s_181	8939946	The conclusion that the stoichiometry is ( abcd)2L implies that the calculation of heme content hinges on whether the linkers bind any heme because the globin chains  a,  b,  c, and  d each bind heme.	transcription
56753	2	335716	5	NULL	NULL	0	NULL	globin			bind			chain b		heme					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_47_29999_s_181	8939946	The conclusion that the stoichiometry is ( abcd)2L implies that the calculation of heme content hinges on whether the linkers bind any heme because the globin chains  a,  b,  c, and  d each bind heme.	transcription
56754	3	335716	5	NULL	NULL	0	NULL	globin			bind			chain c		heme					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_47_29999_s_181	8939946	The conclusion that the stoichiometry is ( abcd)2L implies that the calculation of heme content hinges on whether the linkers bind any heme because the globin chains  a,  b,  c, and  d each bind heme.	transcription
56755	4	335716	5	NULL	NULL	0	NULL	globin			bind			chain d		heme					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_47_29999_s_181	8939946	The conclusion that the stoichiometry is ( abcd)2L implies that the calculation of heme content hinges on whether the linkers bind any heme because the globin chains  a,  b,  c, and  d each bind heme.	transcription
66569	1	335716	7	NULL	NULL	NULL	NULL	 globin 	GP		bind			chain a		heme	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_47_29999_s_181	8939946	The conclusion that the stoichiometry is ( abcd)2L implies that the calculation of heme content hinges on whether the linkers bind any heme because the globin chains  a,  b,  c, and  d each bind heme.	transcription
66570	2	335716	7	NULL	NULL	NULL	NULL	globin	GP		bind			chain b		heme	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_47_29999_s_181	8939946	The conclusion that the stoichiometry is ( abcd)2L implies that the calculation of heme content hinges on whether the linkers bind any heme because the globin chains  a,  b,  c, and  d each bind heme.	transcription
66571	3	335716	7	NULL	NULL	0	NULL	globin	GP		bind			chain c		heme	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_47_29999_s_181	8939946	The conclusion that the stoichiometry is ( abcd)2L implies that the calculation of heme content hinges on whether the linkers bind any heme because the globin chains  a,  b,  c, and  d each bind heme.	transcription
56756	1	335717	5	NULL	NULL	0	NULL	globin gene		stimulation of;;expression of	is dependent on					heme					NULL	erythroid precursor cells	0	NULL	NULL	NULL	gw70_biochimbiophysacta_1619_2_113_s_141	12527106	Increased NF-E2 binding probably accounts for heme-dependent stimulation of globin  gene expression in erythroid precursor cells [ 71 and  82].	transcription
56757	2	335717	5	NULL	NULL	0	NULL	NF-E2		increased binding of	accounts for		probably			statement 1					NULL	erythroid precursor cells	NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1619_2_113_s_141	12527106	Increased NF-E2 binding probably accounts for heme-dependent stimulation of globin  gene expression in erythroid precursor cells [ 71 and  82].	transcription
66582	1	335717	7	NULL	NULL	0	NULL	globin gene	GP	stimulation of;;expression of	depends on					heme	Chemical				NULL	erythroid precursor cells	0	NULL	NULL	NULL	gw70_biochimbiophysacta_1619_2_113_s_141	12527106	Increased NF-E2 binding probably accounts for heme-dependent stimulation of globin  gene expression in erythroid precursor cells [ 71 and  82].	transcription
66585	2	335717	7	NULL	NULL	NULL	NULL	statement 1	Process		increase					NF-E2	GP	binding of			NULL		NULL	NULL	NULL	NULL	gw70_biochimbiophysacta_1619_2_113_s_141	12527106	Increased NF-E2 binding probably accounts for heme-dependent stimulation of globin  gene expression in erythroid precursor cells [ 71 and  82].	transcription
66586	1	335718	7	NULL	NULL	0	NULL	heme	Chemical		bind					globin	GP				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_305_4_840_s_284	12767907	M.S. Hargrove, D. Barrick and J.S. Olson, The association rate constant for heme  binding to globin is independent of protein structure.	transcription
66587	2	335718	7	NULL	NULL	0	NULL	statement 1	Process		is independent of					protein structure					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_305_4_840_s_284	12767907	M.S. Hargrove, D. Barrick and J.S. Olson, The association rate constant for heme  binding to globin is independent of protein structure.	transcription
56768	1	335719	5	NULL	NULL	0	NULL	Transthyretin			interacts with					globin					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_2_344_s_354	14592420	R. Martone and J. Herbert, Transthyretin interacts with globin to form protein complexes  with heme dependent solubility.	transcription
66588	1	335719	7	NULL	NULL	0	NULL	Transthyretin	GP		interacts with					globin	GP				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_2_344_s_354	14592420	R. Martone and J. Herbert, Transthyretin interacts with globin to form protein complexes  with heme dependent solubility.	transcription
66589	2	335719	7	NULL	NULL	0	NULL	statement 1	Process		form					protein complexes	GP				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_2_344_s_354	14592420	R. Martone and J. Herbert, Transthyretin interacts with globin to form protein complexes  with heme dependent solubility.	transcription
66590	3	335719	7	NULL	NULL	0	NULL	solubility	Process		depends on					heme 	Chemical				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_2_344_s_354	14592420	R. Martone and J. Herbert, Transthyretin interacts with globin to form protein complexes  with heme dependent solubility.	transcription
66591	4	335719	7	NULL	NULL	0	NULL	statement 2	Process		occur with					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_2_344_s_354	14592420	R. Martone and J. Herbert, Transthyretin interacts with globin to form protein complexes  with heme dependent solubility.	transcription
56769	1	335720	5	NULL	NULL	0	NULL	heme			regulates		positively			beta-globin		expression of		locus control region	NULL	erythroid cells	0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_1	14660636	Heme positively regulates the expression of beta-globin at the locus control region via the transcriptional factor Bach1 in erythroid cells.	transcription
56770	2	335720	5	NULL	NULL	0	NULL	statement 1			via					Bach1					NULL	erythroid cells	0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_1	14660636	Heme positively regulates the expression of beta-globin at the locus control region via the transcriptional factor Bach1 in erythroid cells.	transcription
56771	3	335720	5	NULL	NULL	0	NULL	Bach1			is a type of					transcription factor					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_1	14660636	Heme positively regulates the expression of beta-globin at the locus control region via the transcriptional factor Bach1 in erythroid cells.	transcription
66592	1	335720	7	NULL	NULL	0	NULL	Heme	Chemical		regulates		positively			beta-globin	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_1	14660636	Heme positively regulates the expression of beta-globin at the locus control region via the transcriptional factor Bach1 in erythroid cells.	transcription
66593	2	335720	7	NULL	NULL	NULL	NULL	statement 1	Process		occur at					locus control region	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_1	14660636	Heme positively regulates the expression of beta-globin at the locus control region via the transcriptional factor Bach1 in erythroid cells.	transcription
66594	3	335720	7	NULL	NULL	0	NULL	statement 1	Process		via					Bach1	GP				NULL	erythroid cells	0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_1	14660636	Heme positively regulates the expression of beta-globin at the locus control region via the transcriptional factor Bach1 in erythroid cells.	transcription
66595	4	335720	7	NULL	NULL	0	NULL	Bach1	GP		is a type of					transcription factor	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_1	14660636	Heme positively regulates the expression of beta-globin at the locus control region via the transcriptional factor Bach1 in erythroid cells.	transcription
56772	1	335721	5	NULL	NULL	0	NULL	Bach1			interacts with									MARE in LCR	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_14	14660636	We propose that heme positively regulates the beta-globin gene expression by blocking the interaction of Bach1 with the MARE in the LCR.	transcription
56773	2	335721	5	NULL	NULL	0	NULL	heme			regulates		positively			beta-globin gene		expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_14	14660636	We propose that heme positively regulates the beta-globin gene expression by blocking the interaction of Bach1 with the MARE in the LCR.	transcription
56774	3	335721	5	NULL	NULL	0	NULL	heme			blocks					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_14	14660636	We propose that heme positively regulates the beta-globin gene expression by blocking the interaction of Bach1 with the MARE in the LCR.	transcription
56775	4	335721	5	NULL	NULL	0	NULL	statement 3			leads to					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_14	14660636	We propose that heme positively regulates the beta-globin gene expression by blocking the interaction of Bach1 with the MARE in the LCR.	transcription
66625	1	335721	7	NULL	NULL	0	NULL	heme	Chemical		regulates		positively			beta-globin gene	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_14	14660636	We propose that heme positively regulates the beta-globin gene expression by blocking the interaction of Bach1 with the MARE in the LCR.	transcription
66626	2	335721	7	NULL	NULL	NULL	NULL	Bach1	GP		interacts with									MARE	NULL	LCR	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_14	14660636	We propose that heme positively regulates the beta-globin gene expression by blocking the interaction of Bach1 with the MARE in the LCR.	transcription
66662	3	335721	7	NULL	NULL	0	NULL	statement 1	Process		occur by					statement 2	Process	blocking 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_14	14660636	We propose that heme positively regulates the beta-globin gene expression by blocking the interaction of Bach1 with the MARE in the LCR.	transcription
56776	1	335722	5	NULL	NULL	0	NULL	Bach1			interacts with									LCR	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_41	14660636	Here we demonstrated that heme positively regulates the beta-globin gene expression by disrupting the interaction of Bach1 with the LCR.	transcription
56777	2	335722	5	NULL	NULL	0	NULL	heme			disrupts					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_41	14660636	Here we demonstrated that heme positively regulates the beta-globin gene expression by disrupting the interaction of Bach1 with the LCR.	transcription
56778	3	335722	5	NULL	NULL	0	NULL	heme			regulates		positively			beta-globin gene		expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_41	14660636	Here we demonstrated that heme positively regulates the beta-globin gene expression by disrupting the interaction of Bach1 with the LCR.	transcription
56779	4	335722	5	NULL	NULL	0	NULL	statement 2			leads to					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_41	14660636	Here we demonstrated that heme positively regulates the beta-globin gene expression by disrupting the interaction of Bach1 with the LCR.	transcription
66663	1	335722	7	NULL	NULL	0	NULL	heme	Chemical		regulates		positively			beta-globin gene	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_41	14660636	Here we demonstrated that heme positively regulates the beta-globin gene expression by disrupting the interaction of Bach1 with the LCR.	transcription
66664	2	335722	7	NULL	NULL	0	NULL	Bach1	GP		interacts with					LCR	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_41	14660636	Here we demonstrated that heme positively regulates the beta-globin gene expression by disrupting the interaction of Bach1 with the LCR.	transcription
66667	3	335722	7	NULL	NULL	0	NULL	statement 1	Process		occur by					statement 2	Process	disrupting			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_41	14660636	Here we demonstrated that heme positively regulates the beta-globin gene expression by disrupting the interaction of Bach1 with the LCR.	transcription
56800	1	335723	5	NULL	NULL	0	NULL	heme			bind		covalently			apo-globin			His-120		NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6675_s_166	15096613	Mutagenesis experiments coupled with our 3D homology model of  ApPgb indicate that heme is covalently bound to the apo-globin by means of His-120.	transcription
79028	1	335723	6	NULL	NULL	0	NULL	heme	GP		bind			His-120		apo-globin	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6675_s_166	15096613	Mutagenesis experiments coupled with our 3D homology model of  ApPgb indicate that heme is covalently bound to the apo-globin by means of His-120.	transcription
56801	1	335724	5	NULL	NULL	0	NULL	Bach1			departs from		selectively			beta-globin				MAREs	NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_189	14747657	Thus, heme induced the selective departure of Bach1 from the beta-globin MAREs without affecting the binding of MafK.	transcription
56802	2	335724	5	NULL	NULL	0	NULL	heme			induce					statement 1					NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_189	14747657	Thus, heme induced the selective departure of Bach1 from the beta-globin MAREs without affecting the binding of MafK.	transcription
56803	3	335724	5	NULL	NULL	0	NULL	statement 2			does not affect					MafK		binding of			NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_189	14747657	Thus, heme induced the selective departure of Bach1 from the beta-globin MAREs without affecting the binding of MafK.	transcription
79029	1	335724	6	NULL	NULL	0	NULL	Bach1	GP		bind					beta-globin	GP			MARE	NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_189	14747657	Thus, heme induced the selective departure of Bach1 from the beta-globin MAREs without affecting the binding of MafK.	transcription
56804	1	335727	5	NULL	NULL	0	NULL	heme			bind					globin					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_12_9093_s_14	11084036	Heme binding causes the globin to form a more compact structure with an approximately 20% increase in helicity ( 1).	transcription
56805	1	335728	5	NULL	NULL	0	NULL	heme			bind					alpha-globin		rabbit			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_32715_s_38	9407040	Binding of heme to rabbit alpha-globin begins when the emerging polypeptide achieves a length of 86 residues ( 19).	transcription
79030	1	335728	6	NULL	NULL	0	NULL	heme	GP		bind					alpha-globin	GP	rabbit			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_52_32715_s_38	9407040	Binding of heme to rabbit alpha-globin begins when the emerging polypeptide achieves a length of 86 residues ( 19).	transcription
56806	1	335729	5	NULL	NULL	0	NULL	heme		binding of	induce					globin molecule		conformational shift of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_37_28659_s_179	10896678	This observation could mean that the binding of heme induced a conformational shift in the globin molecule leading to exposure of susceptible peptide bonds.	transcription
56807	2	335729	5	NULL	NULL	0	NULL	statement 1			exposes					peptide bonds		susceptible			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_37_28659_s_179	10896678	This observation could mean that the binding of heme induced a conformational shift in the globin molecule leading to exposure of susceptible peptide bonds.	transcription
56808	1	335730	5	NULL	NULL	0	NULL	heme			bind					globin					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_23_13785_s_11	7775434	This suggested that binding of heme to  globin and binding of     dimers to each other are yet another  example of linked functions.	transcription
56809	1	335732	5	NULL	NULL	0	NULL	globin gene			is activated by					heme					NULL		0	NULL	NULL	NULL	abs-batch0600-0619_antioxid-redox-signal_8_1-2_16487039_s_9	16487039	Our results suggest that globin  gene activation by heme appears to be independent of the putative HRMs  in the p45 subunit of the NF-E2 transcription factor.	transcription
56810	2	335732	5	NULL	NULL	0	NULL	NF-E2			is a type of					transcription factor					NULL		0	NULL	NULL	NULL	abs-batch0600-0619_antioxid-redox-signal_8_1-2_16487039_s_9	16487039	Our results suggest that globin  gene activation by heme appears to be independent of the putative HRMs  in the p45 subunit of the NF-E2 transcription factor.	transcription
56811	3	335732	5	NULL	NULL	0	NULL	NF-E2			contains			p45 subunit				putative	HRMs		NULL		0	NULL	NULL	NULL	abs-batch0600-0619_antioxid-redox-signal_8_1-2_16487039_s_9	16487039	Our results suggest that globin  gene activation by heme appears to be independent of the putative HRMs  in the p45 subunit of the NF-E2 transcription factor.	transcription
56812	4	335732	5	NULL	NULL	0	NULL	statement 1			is independent of					statement 3					NULL		0	NULL	NULL	NULL	abs-batch0600-0619_antioxid-redox-signal_8_1-2_16487039_s_9	16487039	Our results suggest that globin  gene activation by heme appears to be independent of the putative HRMs  in the p45 subunit of the NF-E2 transcription factor.	transcription
79031	1	335732	6	NULL	NULL	0	NULL	heme	GP		activates					globin gene	GP				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_antioxid-redox-signal_8_1-2_16487039_s_9	16487039	Our results suggest that globin  gene activation by heme appears to be independent of the putative HRMs  in the p45 subunit of the NF-E2 transcription factor.	transcription
79032	2	335732	6	NULL	NULL	0	NULL	statement 1	Process		is independent of					NF-E2 transcription factor	GP		HRMs in the p45 subunit		NULL		0	NULL	NULL	NULL	abs-batch0600-0619_antioxid-redox-signal_8_1-2_16487039_s_9	16487039	Our results suggest that globin  gene activation by heme appears to be independent of the putative HRMs  in the p45 subunit of the NF-E2 transcription factor.	transcription
56813	1	335733	5	NULL	NULL	0	NULL	Ngb			bind		reversibly			O2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_21_20660_s_25	15793311	Like other globins, Ngb binds O2 reversibly via an iron (Fe2+) ion of the heme group with an affinity ( P50) of about 1 Torr, which is in the range of that of Mb ( ).	transcription
56814	2	335733	5	NULL	NULL	0	NULL	Fe2+			is					iron ion					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_21_20660_s_25	15793311	Like other globins, Ngb binds O2 reversibly via an iron (Fe2+) ion of the heme group with an affinity ( P50) of about 1 Torr, which is in the range of that of Mb ( ).	transcription
56815	3	335733	5	NULL	NULL	0	NULL	statement 1			via					Fe2+					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_21_20660_s_25	15793311	Like other globins, Ngb binds O2 reversibly via an iron (Fe2+) ion of the heme group with an affinity ( P50) of about 1 Torr, which is in the range of that of Mb ( ).	transcription
56816	4	335733	5	NULL	NULL	0	NULL	Fe2+			is present in					heme group					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_21_20660_s_25	15793311	Like other globins, Ngb binds O2 reversibly via an iron (Fe2+) ion of the heme group with an affinity ( P50) of about 1 Torr, which is in the range of that of Mb ( ).	transcription
56817	5	335733	5	NULL	NULL	0	NULL	Ngb			is a type of					globin					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_21_20660_s_25	15793311	Like other globins, Ngb binds O2 reversibly via an iron (Fe2+) ion of the heme group with an affinity ( P50) of about 1 Torr, which is in the range of that of Mb ( ).	transcription
79033	1	335733	6	NULL	NULL	0	NULL	Ngb	GP		bind					O2	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_21_20660_s_25	15793311	Like other globins, Ngb binds O2 reversibly via an iron (Fe2+) ion of the heme group with an affinity ( P50) of about 1 Torr, which is in the range of that of Mb ( ).	transcription
79034	2	335733	6	NULL	NULL	0	NULL	statement 1	Process		occurs via					Fe2+	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_21_20660_s_25	15793311	Like other globins, Ngb binds O2 reversibly via an iron (Fe2+) ion of the heme group with an affinity ( P50) of about 1 Torr, which is in the range of that of Mb ( ).	transcription
56818	1	335734	5	NULL	NULL	0	NULL	GATA-1			is a type of					transcription factor					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_23_22385_s_10	15817467	ranscription factor GATA-1 recognizes conserved GATA motifs ((T/A)GATA(A/G)) in the regulatory regions of many genes encoding erythroid-restricted proteins, such as globins, heme biosynthetic enzymes, membrane proteins, and transcription factors ( ,  ).	transcription
56819	2	335734	5	NULL	NULL	0	NULL	((T/A)GATA(A/G))			is					GATA motifs					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_23_22385_s_10	15817467	ranscription factor GATA-1 recognizes conserved GATA motifs ((T/A)GATA(A/G)) in the regulatory regions of many genes encoding erythroid-restricted proteins, such as globins, heme biosynthetic enzymes, membrane proteins, and transcription factors ( ,  ).	transcription
56820	3	335734	5	NULL	NULL	0	NULL	GATA-1			recognizes					globin gene				GATA motifs	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_23_22385_s_10	15817467	ranscription factor GATA-1 recognizes conserved GATA motifs ((T/A)GATA(A/G)) in the regulatory regions of many genes encoding erythroid-restricted proteins, such as globins, heme biosynthetic enzymes, membrane proteins, and transcription factors ( ,  ).	transcription
56821	4	335734	5	NULL	NULL	0	NULL	globin gene			is present in				GATA motifs	globin gene				regulatory region	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_23_22385_s_10	15817467	ranscription factor GATA-1 recognizes conserved GATA motifs ((T/A)GATA(A/G)) in the regulatory regions of many genes encoding erythroid-restricted proteins, such as globins, heme biosynthetic enzymes, membrane proteins, and transcription factors ( ,  ).	transcription
56822	1	335735	5	NULL	NULL	0	NULL	heme			bind								NTD		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_98	14672943	Such drastic changes in the CD spectra of His78 mutant lead us to conclude that His78 is the essential axial ligand, which is required for the specific binding of heme to the NTD, corresponding to the proximal histidine in globins.	transcription
56823	2	335735	5	NULL	NULL	0	NULL				is required for			His78		statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_98	14672943	Such drastic changes in the CD spectra of His78 mutant lead us to conclude that His78 is the essential axial ligand, which is required for the specific binding of heme to the NTD, corresponding to the proximal histidine in globins.	transcription
79035	1	335735	6	NULL	NULL	0	NULL	Heme	GP		bind								NTD		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_98	14672943	Such drastic changes in the CD spectra of His78 mutant lead us to conclude that His78 is the essential axial ligand, which is required for the specific binding of heme to the NTD, corresponding to the proximal histidine in globins.	transcription
56824	1	335737	5	NULL	NULL	0	NULL	heme			bind					globin					NULL		0	NULL	NULL	NULL	gw60_embo_22_8_1824_s_198	12682015	Also similar to TipAS antibiotic binding, heme binding to globins induces the folding of additional alpha-helices that are in contact with the ligand ( Eliezer and Wright, 1996;  Wakasugi  et al., 1997;  Eliezer  et al., 1998).	transcription
56825	2	335737	5	NULL	NULL	0	NULL	statement 1			induce							folding of	alpha-helices		NULL		0	NULL	NULL	NULL	gw60_embo_22_8_1824_s_198	12682015	Also similar to TipAS antibiotic binding, heme binding to globins induces the folding of additional alpha-helices that are in contact with the ligand ( Eliezer and Wright, 1996;  Wakasugi  et al., 1997;  Eliezer  et al., 1998).	transcription
79036	1	335737	6	NULL	NULL	0	NULL	heme	GP		bind					globin	GP				NULL		0	NULL	NULL	NULL	gw60_embo_22_8_1824_s_198	12682015	Also similar to TipAS antibiotic binding, heme binding to globins induces the folding of additional alpha-helices that are in contact with the ligand ( Eliezer and Wright, 1996;  Wakasugi  et al., 1997;  Eliezer  et al., 1998).	transcription
79037	1	335739	6	NULL	NULL	0	NULL				bind			beta Lys-66		heme			propionic acid group of pyrrole IV		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_27_16998_s_263	9642264	Additional stabilization of the hemin in  C. lacteus globins is provided by the interaction of residue Lys-47 (E10) corresponding to human beta Lys-66 (E10) which is known to form an electrostatic link with the propionic acid group of pyrrole IV of the heme ( 26).	transcription
56826	1	335740	5	NULL	NULL	0	NULL	globin			does not leave					ribosome					NULL		0	NULL	NULL	NULL	gw60_cell_108_5_591_s_51	11893330	Since competence to bind the heme group requires formation of the heme binding site, and since folding in the exit tunnel is precluded by its small size, this suggests that globin cannot leave the ribosome via the exit tunnel.	transcription
56827	2	335740	5	NULL	NULL	0	NULL	statement 1			via					exit tunnel					NULL		0	NULL	NULL	NULL	gw60_cell_108_5_591_s_51	11893330	Since competence to bind the heme group requires formation of the heme binding site, and since folding in the exit tunnel is precluded by its small size, this suggests that globin cannot leave the ribosome via the exit tunnel.	transcription
79038	1	335740	6	NULL	NULL	0	NULL	globin	GP		cannot leave					ribosome	CellComponent				NULL		0	NULL	NULL	NULL	gw60_cell_108_5_591_s_51	11893330	Since competence to bind the heme group requires formation of the heme binding site, and since folding in the exit tunnel is precluded by its small size, this suggests that globin cannot leave the ribosome via the exit tunnel.	transcription
79039	2	335740	6	NULL	NULL	0	NULL	statement 1	Process		occurs via					exit tunnel					NULL		0	NULL	NULL	NULL	gw60_cell_108_5_591_s_51	11893330	Since competence to bind the heme group requires formation of the heme binding site, and since folding in the exit tunnel is precluded by its small size, this suggests that globin cannot leave the ribosome via the exit tunnel.	transcription
56828	1	335741	5	NULL	NULL	0	NULL	alpha-globin chains			bind					ribosome					NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_70_0_603_s_305	11395418	For instance, ribosome-bound alpha-globin chains can bind heme after synthesis of only 86 amino acids, possibly reflecting the formation of a folded heme-binding pocket ( 156).	transcription
56829	2	335741	5	NULL	NULL	0	NULL	statement 1			bind					heme					NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_70_0_603_s_305	11395418	For instance, ribosome-bound alpha-globin chains can bind heme after synthesis of only 86 amino acids, possibly reflecting the formation of a folded heme-binding pocket ( 156).	transcription
79040	1	335741	6	NULL	NULL	0	NULL	ribosome	CellComponent		bind					alpha-globin	GP				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_70_0_603_s_305	11395418	For instance, ribosome-bound alpha-globin chains can bind heme after synthesis of only 86 amino acids, possibly reflecting the formation of a folded heme-binding pocket ( 156).	transcription
79041	2	335741	6	NULL	NULL	0	NULL	statement 1	Process		bind					Heme	GP				NULL		0	NULL	NULL	NULL	gw60_annrevbiochem_70_0_603_s_305	11395418	For instance, ribosome-bound alpha-globin chains can bind heme after synthesis of only 86 amino acids, possibly reflecting the formation of a folded heme-binding pocket ( 156).	transcription
79042	1	335742	6	NULL	NULL	0	NULL	Heme	GP		bind								beta chain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10130_s_9	8626572	These results  indicate that in human hemoglobin the heme-globin linkage in the alpha   chains is stabilized by interactions between unlike chains at the  alpha beta   interface, whereas heme binding to  the beta  chains is stabilized by interactions at the  alpha beta   interface.	transcription
79043	2	335742	6	NULL	NULL	0	NULL	statement 1	Process		is stablized by								alpha beta interface		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10130_s_9	8626572	These results  indicate that in human hemoglobin the heme-globin linkage in the alpha   chains is stabilized by interactions between unlike chains at the  alpha beta   interface, whereas heme binding to  the beta  chains is stabilized by interactions at the  alpha beta   interface.	transcription
56830	1	335743	5	NULL	NULL	0	NULL	heme			bind					globin					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_40_24564_s_84	8798719	The side chain of Leu-beta88 (F4) contacts the heme side chain ( 13), and binding of heme to globin involves a specific stereochemical fit that helps stabilize tertiary conformation of the subunit.	transcription
56831	1	335746	5	NULL	NULL	0	NULL	Me2SO			mediates					beta-globin mRNA		increase in			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5358_s_144	9478996	Inhibition of Serine/hreonine Phosphorylation Also Inhibits the Me2SO- mediated Increase in beta -Globin and ALAS-E mRNA Levels and Heme Content-- To examine the effect of inhibition of serine/threonine phosphorylation on erythroid differentiation, the effect of 2-AP on Me2SO-mediated induction of  beta-globin and  ALAS-E mRNAs and heme content was examined.	transcription
56832	2	335746	5	NULL	NULL	0	NULL	Me2SO			mediates					ALAS-E mRNA		increase in			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5358_s_144	9478996	Inhibition of Serine/hreonine Phosphorylation Also Inhibits the Me2SO- mediated Increase in beta -Globin and ALAS-E mRNA Levels and Heme Content-- To examine the effect of inhibition of serine/threonine phosphorylation on erythroid differentiation, the effect of 2-AP on Me2SO-mediated induction of  beta-globin and  ALAS-E mRNAs and heme content was examined.	transcription
56833	3	335746	5	NULL	NULL	0	NULL	Me2SO			mediates					heme		increase in			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5358_s_144	9478996	Inhibition of Serine/hreonine Phosphorylation Also Inhibits the Me2SO- mediated Increase in beta -Globin and ALAS-E mRNA Levels and Heme Content-- To examine the effect of inhibition of serine/threonine phosphorylation on erythroid differentiation, the effect of 2-AP on Me2SO-mediated induction of  beta-globin and  ALAS-E mRNAs and heme content was examined.	transcription
56834	4	335746	5	NULL	NULL	0	NULL	serine/threonine		inhibition of;;phosphorylation of	inhibits					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5358_s_144	9478996	Inhibition of Serine/hreonine Phosphorylation Also Inhibits the Me2SO- mediated Increase in beta -Globin and ALAS-E mRNA Levels and Heme Content-- To examine the effect of inhibition of serine/threonine phosphorylation on erythroid differentiation, the effect of 2-AP on Me2SO-mediated induction of  beta-globin and  ALAS-E mRNAs and heme content was examined.	transcription
56835	5	335746	5	NULL	NULL	0	NULL	serine/threonine		inhibition of;;phosphorylation of	inhibits					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5358_s_144	9478996	Inhibition of Serine/hreonine Phosphorylation Also Inhibits the Me2SO- mediated Increase in beta -Globin and ALAS-E mRNA Levels and Heme Content-- To examine the effect of inhibition of serine/threonine phosphorylation on erythroid differentiation, the effect of 2-AP on Me2SO-mediated induction of  beta-globin and  ALAS-E mRNAs and heme content was examined.	transcription
56836	6	335746	5	NULL	NULL	0	NULL	serine/threonine		inhibition of;;phosphorylation of	inhibits					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5358_s_144	9478996	Inhibition of Serine/hreonine Phosphorylation Also Inhibits the Me2SO- mediated Increase in beta -Globin and ALAS-E mRNA Levels and Heme Content-- To examine the effect of inhibition of serine/threonine phosphorylation on erythroid differentiation, the effect of 2-AP on Me2SO-mediated induction of  beta-globin and  ALAS-E mRNAs and heme content was examined.	transcription
79044	1	335746	6	NULL	NULL	0	NULL	Me2SO	Chemical		mediates					beta-globin	GP	increase in			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5358_s_144	9478996	Inhibition of Serine/hreonine Phosphorylation Also Inhibits the Me2SO- mediated Increase in beta -Globin and ALAS-E mRNA Levels and Heme Content-- To examine the effect of inhibition of serine/threonine phosphorylation on erythroid differentiation, the effect of 2-AP on Me2SO-mediated induction of  beta-globin and  ALAS-E mRNAs and heme content was examined.	transcription
79045	2	335746	6	NULL	NULL	0	NULL	Me2SO	Chemical		mediates					ALAS-E mRNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5358_s_144	9478996	Inhibition of Serine/hreonine Phosphorylation Also Inhibits the Me2SO- mediated Increase in beta -Globin and ALAS-E mRNA Levels and Heme Content-- To examine the effect of inhibition of serine/threonine phosphorylation on erythroid differentiation, the effect of 2-AP on Me2SO-mediated induction of  beta-globin and  ALAS-E mRNAs and heme content was examined.	transcription
79046	3	335746	6	NULL	NULL	0	NULL	Me2SO	Chemical		mediates					Heme	GP	increase in			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5358_s_144	9478996	Inhibition of Serine/hreonine Phosphorylation Also Inhibits the Me2SO- mediated Increase in beta -Globin and ALAS-E mRNA Levels and Heme Content-- To examine the effect of inhibition of serine/threonine phosphorylation on erythroid differentiation, the effect of 2-AP on Me2SO-mediated induction of  beta-globin and  ALAS-E mRNAs and heme content was examined.	transcription
79047	4	335746	6	NULL	NULL	0	NULL	Serine/hreonine	AminoAcid	inhibition of;; phosphorylation of 	inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5358_s_144	9478996	Inhibition of Serine/hreonine Phosphorylation Also Inhibits the Me2SO- mediated Increase in beta -Globin and ALAS-E mRNA Levels and Heme Content-- To examine the effect of inhibition of serine/threonine phosphorylation on erythroid differentiation, the effect of 2-AP on Me2SO-mediated induction of  beta-globin and  ALAS-E mRNAs and heme content was examined.	transcription
79048	5	335746	6	NULL	NULL	0	NULL	Serine/hreonine	AminoAcid	inhibition of;; phosphorylation of 	inhibits					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5358_s_144	9478996	Inhibition of Serine/hreonine Phosphorylation Also Inhibits the Me2SO- mediated Increase in beta -Globin and ALAS-E mRNA Levels and Heme Content-- To examine the effect of inhibition of serine/threonine phosphorylation on erythroid differentiation, the effect of 2-AP on Me2SO-mediated induction of  beta-globin and  ALAS-E mRNAs and heme content was examined.	transcription
79049	6	335746	6	NULL	NULL	0	NULL	Serine/hreonine	AminoAcid	inhibition of;; phosphorylation of 	inhibits					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5358_s_144	9478996	Inhibition of Serine/hreonine Phosphorylation Also Inhibits the Me2SO- mediated Increase in beta -Globin and ALAS-E mRNA Levels and Heme Content-- To examine the effect of inhibition of serine/threonine phosphorylation on erythroid differentiation, the effect of 2-AP on Me2SO-mediated induction of  beta-globin and  ALAS-E mRNAs and heme content was examined.	transcription
56837	1	335747	5	NULL	NULL	0	NULL	heme			stimulates					globin gene		transcription of			NULL		0	NULL	NULL	NULL	gw70_annurevnutr_24_0_105_s_458	15189115	Numerous reports indicate that heme stimulates globin gene transcription and is  probably involved in promoting some other aspects of erythroid differentiation ( 105).	transcription
56838	2	335747	5	NULL	NULL	0	NULL	heme			promotes		probably			erythroid		differentiation of			NULL		0	NULL	NULL	NULL	gw70_annurevnutr_24_0_105_s_458	15189115	Numerous reports indicate that heme stimulates globin gene transcription and is  probably involved in promoting some other aspects of erythroid differentiation ( 105).	transcription
56839	1	335748	5	NULL	NULL	0	NULL	heme			bind					HRI					NULL	erythroid cells	NULL	NULL	NULL	NULL	gw70_annurevnutr_24_0_105_s_469	15189115	Heme binding to  HRI inhibits the phosphorylation of eIF-2  by HRI, resulting in an efficient translation  of globin and probably other proteins in erythroid cells ( 23, 113).	transcription
56840	2	335748	5	NULL	NULL	0	NULL	HRI			phosphorylates					eIF-2					NULL	erythroid cells	NULL	NULL	NULL	NULL	gw70_annurevnutr_24_0_105_s_469	15189115	Heme binding to  HRI inhibits the phosphorylation of eIF-2  by HRI, resulting in an efficient translation  of globin and probably other proteins in erythroid cells ( 23, 113).	transcription
56841	3	335748	5	NULL	NULL	0	NULL	statement 1			inhibits					statement 2					NULL	erythroid cells	NULL	NULL	NULL	NULL	gw70_annurevnutr_24_0_105_s_469	15189115	Heme binding to  HRI inhibits the phosphorylation of eIF-2  by HRI, resulting in an efficient translation  of globin and probably other proteins in erythroid cells ( 23, 113).	transcription
56842	4	335748	5	NULL	NULL	0	NULL	statement 3			results in					globin		efficient translation			NULL	erythroid cells	0	NULL	NULL	NULL	gw70_annurevnutr_24_0_105_s_469	15189115	Heme binding to  HRI inhibits the phosphorylation of eIF-2  by HRI, resulting in an efficient translation  of globin and probably other proteins in erythroid cells ( 23, 113).	transcription
79050	1	335748	6	NULL	NULL	0	NULL	Heme	GP		bind					HRI	GP				NULL		0	NULL	NULL	NULL	gw70_annurevnutr_24_0_105_s_469	15189115	Heme binding to  HRI inhibits the phosphorylation of eIF-2  by HRI, resulting in an efficient translation  of globin and probably other proteins in erythroid cells ( 23, 113).	transcription
56843	1	335749	5	NULL	NULL	0	NULL	HRI			regulates					globin		synthesis of			NULL	developing reticulocytes	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_21_20331_s_312	15788408	HRI regulates globin synthesis to match heme availability in developing reticulocytes ( ) and may regulate eIF2alpha phosphorylation in response to certain oxidative stresses.	transcription
56844	2	335749	5	NULL	NULL	0	NULL	statement 1			match					heme		availability of			NULL	developing reticulocytes	0	NULL	NULL	NULL	gw70_jbiolchem_280_21_20331_s_312	15788408	HRI regulates globin synthesis to match heme availability in developing reticulocytes ( ) and may regulate eIF2alpha phosphorylation in response to certain oxidative stresses.	transcription
56845	3	335749	5	NULL	NULL	0	NULL	HRI			regulates		may			eIF2alpha		phosphorylation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_21_20331_s_312	15788408	HRI regulates globin synthesis to match heme availability in developing reticulocytes ( ) and may regulate eIF2alpha phosphorylation in response to certain oxidative stresses.	transcription
56846	4	335749	5	NULL	NULL	0	NULL	statement 3			in response to					oxidative stress					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_21_20331_s_312	15788408	HRI regulates globin synthesis to match heme availability in developing reticulocytes ( ) and may regulate eIF2alpha phosphorylation in response to certain oxidative stresses.	transcription
79051	1	335749	6	NULL	NULL	0	NULL	HRI	GP		regulates					globin	GP	synthesis of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_21_20331_s_312	15788408	HRI regulates globin synthesis to match heme availability in developing reticulocytes ( ) and may regulate eIF2alpha phosphorylation in response to certain oxidative stresses.	transcription
79052	2	335749	6	NULL	NULL	0	NULL	HRI	GP		regulates		may			eIF2alpha	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_21_20331_s_312	15788408	HRI regulates globin synthesis to match heme availability in developing reticulocytes ( ) and may regulate eIF2alpha phosphorylation in response to certain oxidative stresses.	transcription
56847	1	335750	5	NULL	NULL	0	NULL	heme			controls					muLCR-beta-globin promoter reporter gene					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_9	14660636	The control of the muLCR-beta-globin promoter reporter gene by heme was dependent on DNase I-hypersensitive site 2 (HS2), which contains MARE.	transcription
56848	2	335750	5	NULL	NULL	0	NULL	statement 1			is dependent on					DNase I				HS2	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_9	14660636	The control of the muLCR-beta-globin promoter reporter gene by heme was dependent on DNase I-hypersensitive site 2 (HS2), which contains MARE.	transcription
56849	3	335750	5	NULL	NULL	0	NULL	DNase I			contains				HS2					MARE	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_9	14660636	The control of the muLCR-beta-globin promoter reporter gene by heme was dependent on DNase I-hypersensitive site 2 (HS2), which contains MARE.	transcription
56850	4	335750	5	NULL	NULL	0	NULL	HS2			is					hypersensitive site 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_9	14660636	The control of the muLCR-beta-globin promoter reporter gene by heme was dependent on DNase I-hypersensitive site 2 (HS2), which contains MARE.	transcription
56851	1	335751	5	NULL	NULL	0	NULL	AHSP			bind					Fe(II) alphaHb					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32611_s_5	16901899	Binding of AHSP to Fe(II) alphaHb induces an unusual configuration in which the F helix of the globin becomes disordered and the heme ring becomes solvent-exposed.	transcription
56852	2	335751	5	NULL	NULL	0	NULL	globin			becomes			F helix		disordered					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32611_s_5	16901899	Binding of AHSP to Fe(II) alphaHb induces an unusual configuration in which the F helix of the globin becomes disordered and the heme ring becomes solvent-exposed.	transcription
56853	3	335751	5	NULL	NULL	0	NULL	heme ring			is exposed to					solvent					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32611_s_5	16901899	Binding of AHSP to Fe(II) alphaHb induces an unusual configuration in which the F helix of the globin becomes disordered and the heme ring becomes solvent-exposed.	transcription
56854	4	335751	5	NULL	NULL	0	NULL	statement 1			leads to					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32611_s_5	16901899	Binding of AHSP to Fe(II) alphaHb induces an unusual configuration in which the F helix of the globin becomes disordered and the heme ring becomes solvent-exposed.	transcription
56855	5	335751	5	NULL	NULL	0	NULL	statement 1			leads to					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32611_s_5	16901899	Binding of AHSP to Fe(II) alphaHb induces an unusual configuration in which the F helix of the globin becomes disordered and the heme ring becomes solvent-exposed.	transcription
79053	1	335751	6	NULL	NULL	0	NULL	AHSP	GP		bind					Fe(II) alphaHb	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32611_s_5	16901899	Binding of AHSP to Fe(II) alphaHb induces an unusual configuration in which the F helix of the globin becomes disordered and the heme ring becomes solvent-exposed.	transcription
56856	1	335752	5	NULL	NULL	0	NULL	AHSP			bind					apo alpha globin protein					NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_281_43_32611_s_337	16901899	For example, AHSP binds apo (non heme-bound) alpha globin protein  in vitro ( ) and facilitates its folding and expression in  Escherichia coli and in eukaryotic cells ( ,  ).	transcription
56857	2	335752	5	NULL	NULL	0	NULL	statement 1			facilitates					apo alpha globin protein		folding of			NULL	in vitro	0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32611_s_337	16901899	For example, AHSP binds apo (non heme-bound) alpha globin protein  in vitro ( ) and facilitates its folding and expression in  Escherichia coli and in eukaryotic cells ( ,  ).	transcription
56858	3	335752	5	NULL	NULL	0	NULL	statement 1			facilitates					apo alpha globin protein		expression of			NULL	Escherichia coli, eukaryotic cells	0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32611_s_337	16901899	For example, AHSP binds apo (non heme-bound) alpha globin protein  in vitro ( ) and facilitates its folding and expression in  Escherichia coli and in eukaryotic cells ( ,  ).	transcription
79054	1	335752	6	NULL	NULL	0	NULL	AHSP	GP		bind					apo alpha globin protein	GP				NULL	in vitro	0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32611_s_337	16901899	For example, AHSP binds apo (non heme-bound) alpha globin protein  in vitro ( ) and facilitates its folding and expression in  Escherichia coli and in eukaryotic cells ( ,  ).	transcription
56859	1	335753	5	NULL	NULL	0	NULL	RsbR			does not bind					heme					NULL		0	NULL	NULL	NULL	gw70_pnas_102_48_17320_s_127	16301540	Despite the globin fold of N-RsbR, there is no evidence, through spectroscopy or careful inspection of the electron density maps of N-RsbR, for heme binding by RsbR.	transcription
56860	1	335754	5	NULL	NULL	0	NULL	Bach1			displaced from					beta-globin				locus control region	NULL	murine erythroleukemia cells	NULL	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_10	14747657	Heme also promotes displacement of Bach1 from the beta-globin locus control region without affecting MafK binding in murine erythroleukemia cells.	transcription
56861	2	335754	5	NULL	NULL	0	NULL	heme			promotes					statement 1					NULL	murine erythroleukemia cells	0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_10	14747657	Heme also promotes displacement of Bach1 from the beta-globin locus control region without affecting MafK binding in murine erythroleukemia cells.	transcription
56862	3	335754	5	NULL	NULL	0	NULL	statement 2			does not affect					MafK		binding of			NULL	murine erythroleukemia cells	0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_10	14747657	Heme also promotes displacement of Bach1 from the beta-globin locus control region without affecting MafK binding in murine erythroleukemia cells.	transcription
79055	1	335754	6	NULL	NULL	0	NULL	heme	GP		promotes					Bach1	GP	displacement of			NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_10	14747657	Heme also promotes displacement of Bach1 from the beta-globin locus control region without affecting MafK binding in murine erythroleukemia cells.	transcription
79056	2	335754	6	NULL	NULL	NULL	NULL	statement 1	Process		does not affect					MafK	GP	binding of 			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_10	14747657	Heme also promotes displacement of Bach1 from the beta-globin locus control region without affecting MafK binding in murine erythroleukemia cells.	transcription
56863	1	335755	5	NULL	NULL	0	NULL	Bach1			departs from									LCR	NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_194	14747657	These results indicate that the heme-mediated departure of Bach1 from the LCR is not sufficient for the activation of beta-globin expression or the induction of MEL cell differentiation.	transcription
56864	2	335755	5	NULL	NULL	0	NULL	heme			mediates					statement 1					NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_194	14747657	These results indicate that the heme-mediated departure of Bach1 from the LCR is not sufficient for the activation of beta-globin expression or the induction of MEL cell differentiation.	transcription
56865	3	335755	5	NULL	NULL	0	NULL	statement 2			is not sufficient for					beta-globin		activation of;;expression of			NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_194	14747657	These results indicate that the heme-mediated departure of Bach1 from the LCR is not sufficient for the activation of beta-globin expression or the induction of MEL cell differentiation.	transcription
56866	4	335755	5	NULL	NULL	0	NULL	statement 2			is not sufficient for					MEL cell		induction of;;differentiation of			NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_194	14747657	These results indicate that the heme-mediated departure of Bach1 from the LCR is not sufficient for the activation of beta-globin expression or the induction of MEL cell differentiation.	transcription
79057	1	335755	6	NULL	NULL	0	NULL	Bach1	GP		is removed from					LCR	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_194	14747657	These results indicate that the heme-mediated departure of Bach1 from the LCR is not sufficient for the activation of beta-globin expression or the induction of MEL cell differentiation.	transcription
79058	2	335755	6	NULL	NULL	0	NULL	statement 1	Process		is dependent on					Heme	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_194	14747657	These results indicate that the heme-mediated departure of Bach1 from the LCR is not sufficient for the activation of beta-globin expression or the induction of MEL cell differentiation.	transcription
79059	3	335755	6	NULL	NULL	0	NULL	statement 1	Process		is not sufficient for					beta-globin	GP	activation of;; expression of			NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_194	14747657	These results indicate that the heme-mediated departure of Bach1 from the LCR is not sufficient for the activation of beta-globin expression or the induction of MEL cell differentiation.	transcription
79060	4	335755	6	NULL	NULL	0	NULL	statement 1	Process		is not sufficient for					MEL cell	Process	differentiation of			NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_194	14747657	These results indicate that the heme-mediated departure of Bach1 from the LCR is not sufficient for the activation of beta-globin expression or the induction of MEL cell differentiation.	transcription
56867	1	335757	5	NULL	NULL	0	NULL	heme			regulates					HO-1		expression of			NULL		0	NULL	NULL	NULL	abs-batch0600-0619_antioxid-redox-signal_8_1-2_16487043_s_8	16487043	By modulating the equilibrium  of the small Maf heterodimer network, heme regulates expression of the  cytoprotective enzyme HO-1 during the stress response and of beta-globin  during erythroid differentiation.	transcription
56868	2	335757	5	NULL	NULL	0	NULL	HO-1			is a type of					cytoprotective enzyme					NULL		0	NULL	NULL	NULL	abs-batch0600-0619_antioxid-redox-signal_8_1-2_16487043_s_8	16487043	By modulating the equilibrium  of the small Maf heterodimer network, heme regulates expression of the  cytoprotective enzyme HO-1 during the stress response and of beta-globin  during erythroid differentiation.	transcription
56869	3	335757	5	NULL	NULL	0	NULL	Maf heterodimer network		modulating the equilibrium of;;small	leads to					statement 1					NULL		0	NULL	NULL	NULL	abs-batch0600-0619_antioxid-redox-signal_8_1-2_16487043_s_8	16487043	By modulating the equilibrium  of the small Maf heterodimer network, heme regulates expression of the  cytoprotective enzyme HO-1 during the stress response and of beta-globin  during erythroid differentiation.	transcription
56870	4	335757	5	NULL	NULL	0	NULL	statement 1			occurs during					stress response					NULL		0	NULL	NULL	NULL	abs-batch0600-0619_antioxid-redox-signal_8_1-2_16487043_s_8	16487043	By modulating the equilibrium  of the small Maf heterodimer network, heme regulates expression of the  cytoprotective enzyme HO-1 during the stress response and of beta-globin  during erythroid differentiation.	transcription
56871	5	335757	5	NULL	NULL	0	NULL	heme			regulates					beta-globin		expression of			NULL		0	NULL	NULL	NULL	abs-batch0600-0619_antioxid-redox-signal_8_1-2_16487043_s_8	16487043	By modulating the equilibrium  of the small Maf heterodimer network, heme regulates expression of the  cytoprotective enzyme HO-1 during the stress response and of beta-globin  during erythroid differentiation.	transcription
56872	6	335757	5	NULL	NULL	0	NULL	statement 5			occurs during					erythroid		differentiation of			NULL		0	NULL	NULL	NULL	abs-batch0600-0619_antioxid-redox-signal_8_1-2_16487043_s_8	16487043	By modulating the equilibrium  of the small Maf heterodimer network, heme regulates expression of the  cytoprotective enzyme HO-1 during the stress response and of beta-globin  during erythroid differentiation.	transcription
56873	7	335757	5	NULL	NULL	0	NULL	Maf heterodimer network		modulating the equilibrium of;;small	leads to					statement 5					NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_antioxid-redox-signal_8_1-2_16487043_s_8	16487043	By modulating the equilibrium  of the small Maf heterodimer network, heme regulates expression of the  cytoprotective enzyme HO-1 during the stress response and of beta-globin  during erythroid differentiation.	transcription
79061	1	335757	6	NULL	NULL	0	NULL	heme	GP		regulates					HO-1	GP	expression of			NULL		0	NULL	NULL	NULL	abs-batch0600-0619_antioxid-redox-signal_8_1-2_16487043_s_8	16487043	By modulating the equilibrium  of the small Maf heterodimer network, heme regulates expression of the  cytoprotective enzyme HO-1 during the stress response and of beta-globin  during erythroid differentiation.	transcription
79062	2	335757	6	NULL	NULL	0	NULL	HO-1	GP		is a type of					cytoprotective enzyme					NULL		0	NULL	NULL	NULL	abs-batch0600-0619_antioxid-redox-signal_8_1-2_16487043_s_8	16487043	By modulating the equilibrium  of the small Maf heterodimer network, heme regulates expression of the  cytoprotective enzyme HO-1 during the stress response and of beta-globin  during erythroid differentiation.	transcription
79063	3	335757	6	NULL	NULL	0	NULL	heme	GP		regulates					beta-globin	GP	expression of			NULL		0	NULL	NULL	NULL	abs-batch0600-0619_antioxid-redox-signal_8_1-2_16487043_s_8	16487043	By modulating the equilibrium  of the small Maf heterodimer network, heme regulates expression of the  cytoprotective enzyme HO-1 during the stress response and of beta-globin  during erythroid differentiation.	transcription
79064	4	335757	6	NULL	NULL	0	NULL	statement 3	GP		occurs during					erythroid differentiation	Process				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_antioxid-redox-signal_8_1-2_16487043_s_8	16487043	By modulating the equilibrium  of the small Maf heterodimer network, heme regulates expression of the  cytoprotective enzyme HO-1 during the stress response and of beta-globin  during erythroid differentiation.	transcription
56874	1	335758	5	NULL	NULL	0	NULL	heme			controls					microLCR-beta-globin promoter reporter gene					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_7_14660636_s_9	14660636	The control of the microLCR-beta-globin  promoter reporter gene by heme was dependent on DNase I-hypersensitive  site 2 (HS2), which contains MARE.	transcription
56875	2	335758	5	NULL	NULL	0	NULL	statement 1			is dependent on					DNase I				HS2	NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_7_14660636_s_9	14660636	The control of the microLCR-beta-globin  promoter reporter gene by heme was dependent on DNase I-hypersensitive  site 2 (HS2), which contains MARE.	transcription
56876	3	335758	5	NULL	NULL	0	NULL	DNase I			contains				HS2					MARE	NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_7_14660636_s_9	14660636	The control of the microLCR-beta-globin  promoter reporter gene by heme was dependent on DNase I-hypersensitive  site 2 (HS2), which contains MARE.	transcription
56877	4	335758	5	NULL	NULL	0	NULL	HS2			is					hypersensitive site 2					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_7_14660636_s_9	14660636	The control of the microLCR-beta-globin  promoter reporter gene by heme was dependent on DNase I-hypersensitive  site 2 (HS2), which contains MARE.	transcription
79065	1	335758	6	NULL	NULL	0	NULL	Heme	GP		controls					microLCR-beta-globin promoter	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_279_7_14660636_s_9	14660636	The control of the microLCR-beta-globin  promoter reporter gene by heme was dependent on DNase I-hypersensitive  site 2 (HS2), which contains MARE.	transcription
56878	1	335759	5	NULL	NULL	0	NULL	heme			split from					globin					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_zh-evol-biokhim-fiziol_13_2_868393_s_4	868393	It was shown that splitting of heme from  the globin results in an increase of the area occupied by the molecule  on the phase boarderline from 36-10(2) to 47-10(2) A2.	transcription
57104	1	335761	5	NULL	NULL	0	NULL	globin mRNA		regulation of;;translation of	is dependent on					heme					NULL		0	NULL	NULL	NULL	gw70_embo_23_13_2544_s_260	15175654	This type of regulation, together with  the heme-dependent regulation of globin mRNA translation (  et al), may be important in avoiding toxicity due to the pro-oxidant nature of free heme  during erythroid differentiation, since such a mechanistic link furthers the incorporation  of heme into hemoglobin.	transcription
57105	2	335761	5	NULL	NULL	0	NULL	heme			is incorporated into					hemoglobin					NULL		0	NULL	NULL	NULL	gw70_embo_23_13_2544_s_260	15175654	This type of regulation, together with  the heme-dependent regulation of globin mRNA translation (  et al), may be important in avoiding toxicity due to the pro-oxidant nature of free heme  during erythroid differentiation, since such a mechanistic link furthers the incorporation  of heme into hemoglobin.	transcription
56879	1	335762	5	NULL	NULL	0	NULL	AHSP			bind					oxy-alphaHb		free			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32611_s_26	16901899	The initial binding of AHSP to free oxy-alphaHb causes disordering of the globin F helix, movement of the heme group, displacement of the F8 histidine, coordination of the Fe(II) heme iron by the distal histidine (E7), and binding of O2 to the proximal side of the heme group ( ).	transcription
56880	2	335762	5	NULL	NULL	0	NULL	statement 1			causes					globin		disordering of	F helix		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32611_s_26	16901899	The initial binding of AHSP to free oxy-alphaHb causes disordering of the globin F helix, movement of the heme group, displacement of the F8 histidine, coordination of the Fe(II) heme iron by the distal histidine (E7), and binding of O2 to the proximal side of the heme group ( ).	transcription
56881	3	335762	5	NULL	NULL	0	NULL	statement 1			causes					heme group		movement of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32611_s_26	16901899	The initial binding of AHSP to free oxy-alphaHb causes disordering of the globin F helix, movement of the heme group, displacement of the F8 histidine, coordination of the Fe(II) heme iron by the distal histidine (E7), and binding of O2 to the proximal side of the heme group ( ).	transcription
56882	4	335762	5	NULL	NULL	0	NULL	statement 1			causes					F8 histidine		displacement of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32611_s_26	16901899	The initial binding of AHSP to free oxy-alphaHb causes disordering of the globin F helix, movement of the heme group, displacement of the F8 histidine, coordination of the Fe(II) heme iron by the distal histidine (E7), and binding of O2 to the proximal side of the heme group ( ).	transcription
56883	5	335762	5	NULL	NULL	0	NULL	Fe(II) heme iron			is coordinated by					histidine (E7)		distal			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32611_s_26	16901899	The initial binding of AHSP to free oxy-alphaHb causes disordering of the globin F helix, movement of the heme group, displacement of the F8 histidine, coordination of the Fe(II) heme iron by the distal histidine (E7), and binding of O2 to the proximal side of the heme group ( ).	transcription
56884	6	335762	5	NULL	NULL	0	NULL	statement 1			causes					statement 5					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32611_s_26	16901899	The initial binding of AHSP to free oxy-alphaHb causes disordering of the globin F helix, movement of the heme group, displacement of the F8 histidine, coordination of the Fe(II) heme iron by the distal histidine (E7), and binding of O2 to the proximal side of the heme group ( ).	transcription
56885	7	335762	5	NULL	NULL	0	NULL	O2			bind					heme group		proximal side of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32611_s_26	16901899	The initial binding of AHSP to free oxy-alphaHb causes disordering of the globin F helix, movement of the heme group, displacement of the F8 histidine, coordination of the Fe(II) heme iron by the distal histidine (E7), and binding of O2 to the proximal side of the heme group ( ).	transcription
56886	8	335762	5	NULL	NULL	0	NULL	statement 1			causes					statement 7					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32611_s_26	16901899	The initial binding of AHSP to free oxy-alphaHb causes disordering of the globin F helix, movement of the heme group, displacement of the F8 histidine, coordination of the Fe(II) heme iron by the distal histidine (E7), and binding of O2 to the proximal side of the heme group ( ).	transcription
79066	1	335762	6	NULL	NULL	0	NULL	AHSP	GP		bind					oxy-alphaHb	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_43_32611_s_26	16901899	The initial binding of AHSP to free oxy-alphaHb causes disordering of the globin F helix, movement of the heme group, displacement of the F8 histidine, coordination of the Fe(II) heme iron by the distal histidine (E7), and binding of O2 to the proximal side of the heme group ( ).	transcription
56887	1	335763	5	NULL	NULL	0	NULL	rHbs		high soluble expression of	requires					heme		excess of			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_640_s_206	9925594	Since very high soluble expression of rHbs always required a >2.5-fold molar excess of heme, this excess may be required for sufficient diffusion across the cell membrane to maintain an intracellular heme concentration high enough to drive the bimolecular reaction of heme with globin.	transcription
56888	2	335763	5	NULL	NULL	0	NULL	heme		excess	is diffussed across					cell membrane					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_640_s_206	9925594	Since very high soluble expression of rHbs always required a >2.5-fold molar excess of heme, this excess may be required for sufficient diffusion across the cell membrane to maintain an intracellular heme concentration high enough to drive the bimolecular reaction of heme with globin.	transcription
56890	3	335763	5	NULL	NULL	0	NULL	statement 2			maintains					heme		high concentration of;;intracellular			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_640_s_206	9925594	Since very high soluble expression of rHbs always required a >2.5-fold molar excess of heme, this excess may be required for sufficient diffusion across the cell membrane to maintain an intracellular heme concentration high enough to drive the bimolecular reaction of heme with globin.	transcription
56891	4	335763	5	NULL	NULL	0	NULL	heme			bind					globin					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_640_s_206	9925594	Since very high soluble expression of rHbs always required a >2.5-fold molar excess of heme, this excess may be required for sufficient diffusion across the cell membrane to maintain an intracellular heme concentration high enough to drive the bimolecular reaction of heme with globin.	transcription
56892	5	335763	5	NULL	NULL	0	NULL	statement 3			drives					statement 4					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_2_640_s_206	9925594	Since very high soluble expression of rHbs always required a >2.5-fold molar excess of heme, this excess may be required for sufficient diffusion across the cell membrane to maintain an intracellular heme concentration high enough to drive the bimolecular reaction of heme with globin.	transcription
56893	1	335765	5	NULL	NULL	0	NULL	CO2			bind		covalently			Hb alpha-globin chains			amino terminus		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_22_16738_s_233	10747928	For example, the covalent binding of CO2 to the amino terminus of Hb alpha-globin chains lowers O2 affinity, and accordingly, O2 binding at the hemes triggers the dissociation of CO2 (the Haldane effect) ( 58).	transcription
56894	2	335765	5	NULL	NULL	0	NULL	statement 1			lowers					O2		affinity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_22_16738_s_233	10747928	For example, the covalent binding of CO2 to the amino terminus of Hb alpha-globin chains lowers O2 affinity, and accordingly, O2 binding at the hemes triggers the dissociation of CO2 (the Haldane effect) ( 58).	transcription
56895	3	335765	5	NULL	NULL	0	NULL	O2			bind					heme					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_22_16738_s_233	10747928	For example, the covalent binding of CO2 to the amino terminus of Hb alpha-globin chains lowers O2 affinity, and accordingly, O2 binding at the hemes triggers the dissociation of CO2 (the Haldane effect) ( 58).	transcription
56896	4	335765	5	NULL	NULL	0	NULL	statement 3			triggers					CO2		dissociation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_22_16738_s_233	10747928	For example, the covalent binding of CO2 to the amino terminus of Hb alpha-globin chains lowers O2 affinity, and accordingly, O2 binding at the hemes triggers the dissociation of CO2 (the Haldane effect) ( 58).	transcription
79067	1	335765	6	NULL	NULL	0	NULL	CO2	Chemical		bind					Hb alpha-globin			amino terminus		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_22_16738_s_233	10747928	For example, the covalent binding of CO2 to the amino terminus of Hb alpha-globin chains lowers O2 affinity, and accordingly, O2 binding at the hemes triggers the dissociation of CO2 (the Haldane effect) ( 58).	transcription
79068	2	335765	6	NULL	NULL	0	NULL	O2	Chemical		bind					heme	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_22_16738_s_233	10747928	For example, the covalent binding of CO2 to the amino terminus of Hb alpha-globin chains lowers O2 affinity, and accordingly, O2 binding at the hemes triggers the dissociation of CO2 (the Haldane effect) ( 58).	transcription
57886	1	335766	5	NULL	NULL	0	NULL	Ngb			coordinates to			proximal histidine residue		heme					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_39_36377_s_22	11473111	Nevertheless, according to multiple sequence alignment, key amino acid residues that are required for the function of these proteins and are conserved among a great variety of globins are present in the primary amino acid sequence of Ngb: namely a proximal histidine residue that coordinates to the heme (helical position F8), a distal histidine residue that might be involved in interactions with heme-bound ligands (E7), and a phenylalanine residue at CD1 that is involved in pi-pi interactions with the heme ( 4).	transcription
57887	2	335766	5	NULL	NULL	0	NULL	Ngb			is involved in		might be	distal histidine residue		heme-bound ligands		interaction with			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_39_36377_s_22	11473111	Nevertheless, according to multiple sequence alignment, key amino acid residues that are required for the function of these proteins and are conserved among a great variety of globins are present in the primary amino acid sequence of Ngb: namely a proximal histidine residue that coordinates to the heme (helical position F8), a distal histidine residue that might be involved in interactions with heme-bound ligands (E7), and a phenylalanine residue at CD1 that is involved in pi-pi interactions with the heme ( 4).	transcription
57888	3	335766	5	NULL	NULL	0	NULL	Ngb			is involved in			phenylalanine residue at CD1		heme		pi-pi interactions with			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_39_36377_s_22	11473111	Nevertheless, according to multiple sequence alignment, key amino acid residues that are required for the function of these proteins and are conserved among a great variety of globins are present in the primary amino acid sequence of Ngb: namely a proximal histidine residue that coordinates to the heme (helical position F8), a distal histidine residue that might be involved in interactions with heme-bound ligands (E7), and a phenylalanine residue at CD1 that is involved in pi-pi interactions with the heme ( 4).	transcription
57889	1	335768	5	NULL	NULL	0	NULL	K562 cells			is a type of					human erythroleukemia cells					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_7	14660636	The heme-dependent expression of beta-globin is a transcriptional event since the expression of the human beta-globin gene promoter-reporter gene containing the microlocus control region (muLCR) was inhibited when human erythroleukemia K562 cells and MEL cells were cultured with SA.	transcription
57890	2	335768	5	NULL	NULL	0	NULL	K562 cells			is cultured with					SA					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_7	14660636	The heme-dependent expression of beta-globin is a transcriptional event since the expression of the human beta-globin gene promoter-reporter gene containing the microlocus control region (muLCR) was inhibited when human erythroleukemia K562 cells and MEL cells were cultured with SA.	transcription
57891	3	335768	5	NULL	NULL	0	NULL	MEL cells			is cultured with					SA					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_7	14660636	The heme-dependent expression of beta-globin is a transcriptional event since the expression of the human beta-globin gene promoter-reporter gene containing the microlocus control region (muLCR) was inhibited when human erythroleukemia K562 cells and MEL cells were cultured with SA.	transcription
57892	4	335768	5	NULL	NULL	0	NULL	beta-globin gene promoter-reporter gene		human	contains									muLCR	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_7	14660636	The heme-dependent expression of beta-globin is a transcriptional event since the expression of the human beta-globin gene promoter-reporter gene containing the microlocus control region (muLCR) was inhibited when human erythroleukemia K562 cells and MEL cells were cultured with SA.	transcription
57893	5	335768	5	NULL	NULL	0	NULL	muLCR			is					microlocus control region					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_7	14660636	The heme-dependent expression of beta-globin is a transcriptional event since the expression of the human beta-globin gene promoter-reporter gene containing the microlocus control region (muLCR) was inhibited when human erythroleukemia K562 cells and MEL cells were cultured with SA.	transcription
57894	6	335768	5	NULL	NULL	0	NULL	statement 2			inhibits					statement 4					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_7	14660636	The heme-dependent expression of beta-globin is a transcriptional event since the expression of the human beta-globin gene promoter-reporter gene containing the microlocus control region (muLCR) was inhibited when human erythroleukemia K562 cells and MEL cells were cultured with SA.	transcription
57895	7	335768	5	NULL	NULL	0	NULL	statement 3			inhibits					statement 4					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_7	14660636	The heme-dependent expression of beta-globin is a transcriptional event since the expression of the human beta-globin gene promoter-reporter gene containing the microlocus control region (muLCR) was inhibited when human erythroleukemia K562 cells and MEL cells were cultured with SA.	transcription
57896	8	335768	5	NULL	NULL	0	NULL	beta-globin		expression of	is dependent on					heme					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_7	14660636	The heme-dependent expression of beta-globin is a transcriptional event since the expression of the human beta-globin gene promoter-reporter gene containing the microlocus control region (muLCR) was inhibited when human erythroleukemia K562 cells and MEL cells were cultured with SA.	transcription
57897	1	335770	5	NULL	NULL	0	NULL	globin			interacts with					heme					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_1_65_s_18	14630020	By means of various optical methods (ORD, CD, MORD) the interaction of globin with  heme was analysed to understand the specific function of hemoproteins such as reversible  oxygen binding (hemoglobin), splitting of hydrogen peroxide (catalase), and electron  transfer (cytochrome  c).	transcription
57898	2	335770	5	NULL	NULL	0	NULL	hemoglobin			is a type of					hemoproteins					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_1_65_s_18	14630020	By means of various optical methods (ORD, CD, MORD) the interaction of globin with  heme was analysed to understand the specific function of hemoproteins such as reversible  oxygen binding (hemoglobin), splitting of hydrogen peroxide (catalase), and electron  transfer (cytochrome  c).	transcription
57899	3	335770	5	NULL	NULL	0	NULL	catalase			is a type of					hemoproteins					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_1_65_s_18	14630020	By means of various optical methods (ORD, CD, MORD) the interaction of globin with  heme was analysed to understand the specific function of hemoproteins such as reversible  oxygen binding (hemoglobin), splitting of hydrogen peroxide (catalase), and electron  transfer (cytochrome  c).	transcription
57900	4	335770	5	NULL	NULL	0	NULL	cytochrome c			is a type of					hemoproteins					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_1_65_s_18	14630020	By means of various optical methods (ORD, CD, MORD) the interaction of globin with  heme was analysed to understand the specific function of hemoproteins such as reversible  oxygen binding (hemoglobin), splitting of hydrogen peroxide (catalase), and electron  transfer (cytochrome  c).	transcription
57901	5	335770	5	NULL	NULL	0	NULL	hemoglobin			bind		reversibly			oxygen					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_1_65_s_18	14630020	By means of various optical methods (ORD, CD, MORD) the interaction of globin with  heme was analysed to understand the specific function of hemoproteins such as reversible  oxygen binding (hemoglobin), splitting of hydrogen peroxide (catalase), and electron  transfer (cytochrome  c).	transcription
57902	6	335770	5	NULL	NULL	0	NULL	catalase			splits					hydrogen peroxide					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_1_65_s_18	14630020	By means of various optical methods (ORD, CD, MORD) the interaction of globin with  heme was analysed to understand the specific function of hemoproteins such as reversible  oxygen binding (hemoglobin), splitting of hydrogen peroxide (catalase), and electron  transfer (cytochrome  c).	transcription
57903	7	335770	5	NULL	NULL	0	NULL	cytochrome c			is involved in					electron transfer					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_312_1_65_s_18	14630020	By means of various optical methods (ORD, CD, MORD) the interaction of globin with  heme was analysed to understand the specific function of hemoproteins such as reversible  oxygen binding (hemoglobin), splitting of hydrogen peroxide (catalase), and electron  transfer (cytochrome  c).	transcription
57904	1	335771	5	NULL	NULL	0	NULL	GATA-1			bind		specifically			GSTP1-1				promoter	NULL		NULL	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_4_815_s_115	14623254	Specific GATA-1 binding to the GSTP1-1 promoter is  shown here by EMSA competition and supershift experiments as it was previously described  for erythroid-specific genes such as globin [  42] and genes involved in heme biosynthesis [  43].	transcription
79069	1	335771	6	NULL	NULL	0	NULL	GATA-1	GP		bind					GSTP1-1 	GP			promoter	NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_311_4_815_s_115	14623254	Specific GATA-1 binding to the GSTP1-1 promoter is  shown here by EMSA competition and supershift experiments as it was previously described  for erythroid-specific genes such as globin [  42] and genes involved in heme biosynthesis [  43].	transcription
57905	1	335772	5	NULL	NULL	0	NULL	heme			bind		directly			Bach1					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_16_5857_s_16	12897155	Notably, heme directly binds to and inhibits the mammalian transcriptional repressor Bach1 ( ), a dimerization partner of the Maf family proteins, which controls the expression of a wide array of genes, including oxidative stress-responsive genes and globin genes ( ,  - ,  ,  ,  ).	transcription
57906	2	335772	5	NULL	NULL	0	NULL	statement 1			inhibits					Bach1					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_16_5857_s_16	12897155	Notably, heme directly binds to and inhibits the mammalian transcriptional repressor Bach1 ( ), a dimerization partner of the Maf family proteins, which controls the expression of a wide array of genes, including oxidative stress-responsive genes and globin genes ( ,  - ,  ,  ,  ).	transcription
57907	3	335772	5	NULL	NULL	0	NULL	Bach1			is a type of					mammalian transcriptional repressor					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_16_5857_s_16	12897155	Notably, heme directly binds to and inhibits the mammalian transcriptional repressor Bach1 ( ), a dimerization partner of the Maf family proteins, which controls the expression of a wide array of genes, including oxidative stress-responsive genes and globin genes ( ,  - ,  ,  ,  ).	transcription
57908	4	335772	5	NULL	NULL	0	NULL	Bach1			is a dimerization partner of					Maf family proteins					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_16_5857_s_16	12897155	Notably, heme directly binds to and inhibits the mammalian transcriptional repressor Bach1 ( ), a dimerization partner of the Maf family proteins, which controls the expression of a wide array of genes, including oxidative stress-responsive genes and globin genes ( ,  - ,  ,  ,  ).	transcription
57909	1	335774	5	NULL	NULL	0	NULL	alpha-globin chain			assemble into					hemoglobin					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_15	14672943	A deficiency of heme, which is required for the assembly of alpha- and beta-globin chains into hemoglobin, induces the activation of HRI, which subsequently phosphorylates the alpha-subunit of eIF2, leading to the inhibition of polypeptide chain initiation and the arrest of protein synthesis.	transcription
57910	2	335774	5	NULL	NULL	0	NULL	beta-globin chain			assemble into					hemoglobin					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_15	14672943	A deficiency of heme, which is required for the assembly of alpha- and beta-globin chains into hemoglobin, induces the activation of HRI, which subsequently phosphorylates the alpha-subunit of eIF2, leading to the inhibition of polypeptide chain initiation and the arrest of protein synthesis.	transcription
57911	3	335774	5	NULL	NULL	0	NULL	heme			is required for					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_15	14672943	A deficiency of heme, which is required for the assembly of alpha- and beta-globin chains into hemoglobin, induces the activation of HRI, which subsequently phosphorylates the alpha-subunit of eIF2, leading to the inhibition of polypeptide chain initiation and the arrest of protein synthesis.	transcription
57912	4	335774	5	NULL	NULL	0	NULL	heme			is required for					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_15	14672943	A deficiency of heme, which is required for the assembly of alpha- and beta-globin chains into hemoglobin, induces the activation of HRI, which subsequently phosphorylates the alpha-subunit of eIF2, leading to the inhibition of polypeptide chain initiation and the arrest of protein synthesis.	transcription
57913	5	335774	5	NULL	NULL	0	NULL	heme		deficiency of	induces					HRI		activation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_15	14672943	A deficiency of heme, which is required for the assembly of alpha- and beta-globin chains into hemoglobin, induces the activation of HRI, which subsequently phosphorylates the alpha-subunit of eIF2, leading to the inhibition of polypeptide chain initiation and the arrest of protein synthesis.	transcription
57914	6	335774	5	NULL	NULL	0	NULL	HRI		activated	phosphorylates		subsequently			eIF2			alpha-subunit		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_15	14672943	A deficiency of heme, which is required for the assembly of alpha- and beta-globin chains into hemoglobin, induces the activation of HRI, which subsequently phosphorylates the alpha-subunit of eIF2, leading to the inhibition of polypeptide chain initiation and the arrest of protein synthesis.	transcription
57915	7	335774	5	NULL	NULL	0	NULL	statement 6			inhibits					polypeptide chain		initiation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_15	14672943	A deficiency of heme, which is required for the assembly of alpha- and beta-globin chains into hemoglobin, induces the activation of HRI, which subsequently phosphorylates the alpha-subunit of eIF2, leading to the inhibition of polypeptide chain initiation and the arrest of protein synthesis.	transcription
57916	8	335774	5	NULL	NULL	0	NULL	statement 7			arrests					protein		synthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_15	14672943	A deficiency of heme, which is required for the assembly of alpha- and beta-globin chains into hemoglobin, induces the activation of HRI, which subsequently phosphorylates the alpha-subunit of eIF2, leading to the inhibition of polypeptide chain initiation and the arrest of protein synthesis.	transcription
79072	1	335774	6	NULL	NULL	0	NULL	heme	GP	deficiency of	induces					HRI	GP	activation of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_15	14672943	A deficiency of heme, which is required for the assembly of alpha- and beta-globin chains into hemoglobin, induces the activation of HRI, which subsequently phosphorylates the alpha-subunit of eIF2, leading to the inhibition of polypeptide chain initiation and the arrest of protein synthesis.	transcription
57917	1	335775	5	NULL	NULL	0	NULL	Bach1		endogenous	bind					DNA					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_148	14660636	We then conducted a conventional gel-shift assay using a synthetic oligonucleotide probe containing a MARE from the chicken beta-globin 3' enhancer to examine whether the DNA binding activity of endogenous Bach1 is indeed regulated by heme.	transcription
57918	2	335775	5	NULL	NULL	0	NULL	heme			regulates		potentially			statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_7_5480_s_148	14660636	We then conducted a conventional gel-shift assay using a synthetic oligonucleotide probe containing a MARE from the chicken beta-globin 3' enhancer to examine whether the DNA binding activity of endogenous Bach1 is indeed regulated by heme.	transcription
58416	1	335777	5	NULL	NULL	0	NULL	H93G (+Imd)		mutant	mimics					Mb		NT			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24637_s_236	16774917	The H93G (+Imd) mutant serves as a mimic of NT Mb in which the covalent bond between heme and globin is cleaved and an exogenous imidazole binds to iron freely in the proximal cavity ( ).	transcription
58417	2	335777	5	NULL	NULL	0	NULL	heme			bind		covalently			globin					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24637_s_236	16774917	The H93G (+Imd) mutant serves as a mimic of NT Mb in which the covalent bond between heme and globin is cleaved and an exogenous imidazole binds to iron freely in the proximal cavity ( ).	transcription
58418	3	335777	5	NULL	NULL	0	NULL	statement 2			occurs in					Mb		NT			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24637_s_236	16774917	The H93G (+Imd) mutant serves as a mimic of NT Mb in which the covalent bond between heme and globin is cleaved and an exogenous imidazole binds to iron freely in the proximal cavity ( ).	transcription
58419	4	335777	5	NULL	NULL	0	NULL	statement 2			undergoes					cleavage					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24637_s_236	16774917	The H93G (+Imd) mutant serves as a mimic of NT Mb in which the covalent bond between heme and globin is cleaved and an exogenous imidazole binds to iron freely in the proximal cavity ( ).	transcription
58420	5	335777	5	NULL	NULL	0	NULL	imidazole		exogenous	bind		freely			iron					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24637_s_236	16774917	The H93G (+Imd) mutant serves as a mimic of NT Mb in which the covalent bond between heme and globin is cleaved and an exogenous imidazole binds to iron freely in the proximal cavity ( ).	transcription
58421	6	335777	5	NULL	NULL	0	NULL	statement 5			occurs in					Mb		NT	proximal cavity		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_34_24637_s_236	16774917	The H93G (+Imd) mutant serves as a mimic of NT Mb in which the covalent bond between heme and globin is cleaved and an exogenous imidazole binds to iron freely in the proximal cavity ( ).	transcription
58422	7	335777	5	NULL	NULL	0	NULL	statement 4			leads to					statement 5					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24637_s_236	16774917	The H93G (+Imd) mutant serves as a mimic of NT Mb in which the covalent bond between heme and globin is cleaved and an exogenous imidazole binds to iron freely in the proximal cavity ( ).	transcription
79073	1	335777	6	NULL	NULL	0	NULL	imidazole	Chemical		bind					iron	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24637_s_236	16774917	The H93G (+Imd) mutant serves as a mimic of NT Mb in which the covalent bond between heme and globin is cleaved and an exogenous imidazole binds to iron freely in the proximal cavity ( ).	transcription
58424	1	335779	5	NULL	NULL	0	NULL	ApPgb		Archaea Aeropyrum pernix	bind					O2					NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6675_s_16	15096613	Here, we show that two proteins  ApPgb and  MaPgb, identified from the  Archaea Aeropyrum pernix and  Methanosarcina acetivorans, respectively, conform to the globin sequence motifs, contain heme, and demonstrably bind O2, CO, and NO.	transcription
58425	2	335779	5	NULL	NULL	0	NULL	ApPgb		Archaea Aeropyrum pernix	bind					CO					NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6675_s_16	15096613	Here, we show that two proteins  ApPgb and  MaPgb, identified from the  Archaea Aeropyrum pernix and  Methanosarcina acetivorans, respectively, conform to the globin sequence motifs, contain heme, and demonstrably bind O2, CO, and NO.	transcription
58426	3	335779	5	NULL	NULL	0	NULL	ApPgb		Archaea Aeropyrum pernix	bind					NO					NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6675_s_16	15096613	Here, we show that two proteins  ApPgb and  MaPgb, identified from the  Archaea Aeropyrum pernix and  Methanosarcina acetivorans, respectively, conform to the globin sequence motifs, contain heme, and demonstrably bind O2, CO, and NO.	transcription
58427	4	335779	5	NULL	NULL	0	NULL	MaPgb		Methanosarcina acetivorans	bind					O2					NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6675_s_16	15096613	Here, we show that two proteins  ApPgb and  MaPgb, identified from the  Archaea Aeropyrum pernix and  Methanosarcina acetivorans, respectively, conform to the globin sequence motifs, contain heme, and demonstrably bind O2, CO, and NO.	transcription
58428	5	335779	5	NULL	NULL	0	NULL	MaPgb		Methanosarcina acetivorans	bind					CO					NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6675_s_16	15096613	Here, we show that two proteins  ApPgb and  MaPgb, identified from the  Archaea Aeropyrum pernix and  Methanosarcina acetivorans, respectively, conform to the globin sequence motifs, contain heme, and demonstrably bind O2, CO, and NO.	transcription
58429	6	335779	5	NULL	NULL	0	NULL	MaPgb		Methanosarcina acetivorans	bind					NO					NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6675_s_16	15096613	Here, we show that two proteins  ApPgb and  MaPgb, identified from the  Archaea Aeropyrum pernix and  Methanosarcina acetivorans, respectively, conform to the globin sequence motifs, contain heme, and demonstrably bind O2, CO, and NO.	transcription
79074	1	335779	6	NULL	NULL	0	NULL	ApPgb	GP		bind					O2	Chemical				NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6675_s_16	15096613	Here, we show that two proteins  ApPgb and  MaPgb, identified from the  Archaea Aeropyrum pernix and  Methanosarcina acetivorans, respectively, conform to the globin sequence motifs, contain heme, and demonstrably bind O2, CO, and NO.	transcription
79075	2	335779	6	NULL	NULL	0	NULL	ApPgb	GP		bind					CO	Chemical				NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6675_s_16	15096613	Here, we show that two proteins  ApPgb and  MaPgb, identified from the  Archaea Aeropyrum pernix and  Methanosarcina acetivorans, respectively, conform to the globin sequence motifs, contain heme, and demonstrably bind O2, CO, and NO.	transcription
79076	3	335779	6	NULL	NULL	0	NULL	ApPgb	Chemical		bind					NO	Chemical				NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6675_s_16	15096613	Here, we show that two proteins  ApPgb and  MaPgb, identified from the  Archaea Aeropyrum pernix and  Methanosarcina acetivorans, respectively, conform to the globin sequence motifs, contain heme, and demonstrably bind O2, CO, and NO.	transcription
79077	4	335779	6	NULL	NULL	0	NULL	MaPgb	GP		bind					O2	Chemical				NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6675_s_16	15096613	Here, we show that two proteins  ApPgb and  MaPgb, identified from the  Archaea Aeropyrum pernix and  Methanosarcina acetivorans, respectively, conform to the globin sequence motifs, contain heme, and demonstrably bind O2, CO, and NO.	transcription
79078	5	335779	6	NULL	NULL	0	NULL	MaPgb	GP		bind					CO	Chemical				NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6675_s_16	15096613	Here, we show that two proteins  ApPgb and  MaPgb, identified from the  Archaea Aeropyrum pernix and  Methanosarcina acetivorans, respectively, conform to the globin sequence motifs, contain heme, and demonstrably bind O2, CO, and NO.	transcription
79079	6	335779	6	NULL	NULL	0	NULL	MaPgb	GP		bind					NO	Chemical				NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6675_s_16	15096613	Here, we show that two proteins  ApPgb and  MaPgb, identified from the  Archaea Aeropyrum pernix and  Methanosarcina acetivorans, respectively, conform to the globin sequence motifs, contain heme, and demonstrably bind O2, CO, and NO.	transcription
58430	1	335780	5	NULL	NULL	0	NULL	HemAT- Hs			bind		reversibly			O2					NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6675_s_96	15096613	The archaeal Pgbs,  ApPgb and  MaPgb, were exactly 195 aa long: the minimum length found to be required for heme and reversible O2 binding by the globin-coupled aerotaxis transducer HemAT- Hs (9 ).	transcription
58431	2	335780	5	NULL	NULL	0	NULL	HemAT- Hs			is coupled to					globin					NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6675_s_96	15096613	The archaeal Pgbs,  ApPgb and  MaPgb, were exactly 195 aa long: the minimum length found to be required for heme and reversible O2 binding by the globin-coupled aerotaxis transducer HemAT- Hs (9 ).	transcription
58432	3	335780	5	NULL	NULL	0	NULL	HemAT- Hs			is a type of					aerotaxis transducer					NULL		0	NULL	NULL	NULL	gw70_pnas_101_17_6675_s_96	15096613	The archaeal Pgbs,  ApPgb and  MaPgb, were exactly 195 aa long: the minimum length found to be required for heme and reversible O2 binding by the globin-coupled aerotaxis transducer HemAT- Hs (9 ).	transcription
58433	1	335781	5	NULL	NULL	0	NULL	heme		intracellular levels of	regulates					Maf protein partners		exchange of;;small			NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_215	14747657	Our results suggest that intracellular levels of heme regulate the exchange of small Maf protein partners in not only the stress-responsive control of HO-1 but also the differentiation-associated control of beta-globin expression.	transcription
58434	2	335781	5	NULL	NULL	0	NULL	statement 1			occurs in					HO-1		stress-responsive control of			NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_215	14747657	Our results suggest that intracellular levels of heme regulate the exchange of small Maf protein partners in not only the stress-responsive control of HO-1 but also the differentiation-associated control of beta-globin expression.	transcription
58435	3	335781	5	NULL	NULL	0	NULL	statement 1			occurs in					beta-globin		differentiation-associated control of;;expression of			NULL		0	NULL	NULL	NULL	gw70_pnas_101_6_1461_s_215	14747657	Our results suggest that intracellular levels of heme regulate the exchange of small Maf protein partners in not only the stress-responsive control of HO-1 but also the differentiation-associated control of beta-globin expression.	transcription
58436	1	335782	5	NULL	NULL	0	NULL	N. meningitidis			bind					hemoglobin		biotinylated			NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_162_2_227_s_96	9627957	The results are consistent with other studies which show that the binding of  N. meningitidis to biotinylated hemoglobin is inhibited by unlabeled hemoglobin but not heme, suggesting that the hemoglobin binding protein of  N. meningitidis recognizes the globin moiety of hemoglobin  [ 18].	transcription
58437	2	335782	5	NULL	NULL	0	NULL	hemoglobin		unlabeled	inhibits					statement 1					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_162_2_227_s_96	9627957	The results are consistent with other studies which show that the binding of  N. meningitidis to biotinylated hemoglobin is inhibited by unlabeled hemoglobin but not heme, suggesting that the hemoglobin binding protein of  N. meningitidis recognizes the globin moiety of hemoglobin  [ 18].	transcription
58438	3	335782	5	NULL	NULL	0	NULL	heme			does not inhibit					statement 1					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_162_2_227_s_96	9627957	The results are consistent with other studies which show that the binding of  N. meningitidis to biotinylated hemoglobin is inhibited by unlabeled hemoglobin but not heme, suggesting that the hemoglobin binding protein of  N. meningitidis recognizes the globin moiety of hemoglobin  [ 18].	transcription
58439	4	335782	5	NULL	NULL	0	NULL	hemoglobin binding protein		N. meningitidis	recognizes					hemoglobin			globin moiety		NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_162_2_227_s_96	9627957	The results are consistent with other studies which show that the binding of  N. meningitidis to biotinylated hemoglobin is inhibited by unlabeled hemoglobin but not heme, suggesting that the hemoglobin binding protein of  N. meningitidis recognizes the globin moiety of hemoglobin  [ 18].	transcription
58440	5	335782	5	NULL	NULL	0	NULL	statement 2			suggest					statement 4					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_162_2_227_s_96	9627957	The results are consistent with other studies which show that the binding of  N. meningitidis to biotinylated hemoglobin is inhibited by unlabeled hemoglobin but not heme, suggesting that the hemoglobin binding protein of  N. meningitidis recognizes the globin moiety of hemoglobin  [ 18].	transcription
58441	6	335782	5	NULL	NULL	0	NULL	statement 3			suggest					statement 4					NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_162_2_227_s_96	9627957	The results are consistent with other studies which show that the binding of  N. meningitidis to biotinylated hemoglobin is inhibited by unlabeled hemoglobin but not heme, suggesting that the hemoglobin binding protein of  N. meningitidis recognizes the globin moiety of hemoglobin  [ 18].	transcription
79080	1	335782	6	NULL	NULL	0	NULL	N. meningitidis	Organism		bind					hemoglobin	GP	bioytinylated			NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_162_2_227_s_96	9627957	The results are consistent with other studies which show that the binding of  N. meningitidis to biotinylated hemoglobin is inhibited by unlabeled hemoglobin but not heme, suggesting that the hemoglobin binding protein of  N. meningitidis recognizes the globin moiety of hemoglobin  [ 18].	transcription
58442	1	335783	5	NULL	NULL	0	NULL	NF-E2			bind									TGCTGA(G/C)TCA	NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_14_10715_s_12	11154691	NF-E2 binds to an extended AP-1-like element, TGCTGA(G/C)TCA, which is found in the locus control regions (LCRs) of the alpha- and beta-globin genes and in the promoters of several heme biosynthetic enzyme genes (for review see Refs.	transcription
58443	2	335783	5	NULL	NULL	0	NULL	TGCTGA(G/C)TCA			is					AP-1-like element					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_14_10715_s_12	11154691	NF-E2 binds to an extended AP-1-like element, TGCTGA(G/C)TCA, which is found in the locus control regions (LCRs) of the alpha- and beta-globin genes and in the promoters of several heme biosynthetic enzyme genes (for review see Refs.	transcription
58444	3	335783	5	NULL	NULL	0	NULL	AP-1-like element			is located in					alpha-globin gene				LCRs	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_14_10715_s_12	11154691	NF-E2 binds to an extended AP-1-like element, TGCTGA(G/C)TCA, which is found in the locus control regions (LCRs) of the alpha- and beta-globin genes and in the promoters of several heme biosynthetic enzyme genes (for review see Refs.	transcription
58445	4	335783	5	NULL	NULL	0	NULL	AP-1-like element			is located in					beta-globin gene				LCRs	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_14_10715_s_12	11154691	NF-E2 binds to an extended AP-1-like element, TGCTGA(G/C)TCA, which is found in the locus control regions (LCRs) of the alpha- and beta-globin genes and in the promoters of several heme biosynthetic enzyme genes (for review see Refs.	transcription
79081	1	335783	6	NULL	NULL	0	NULL	NF-E2	GP		bind									AP-1-like element	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_14_10715_s_12	11154691	NF-E2 binds to an extended AP-1-like element, TGCTGA(G/C)TCA, which is found in the locus control regions (LCRs) of the alpha- and beta-globin genes and in the promoters of several heme biosynthetic enzyme genes (for review see Refs.	transcription
58446	1	335784	5	NULL	NULL	0	NULL	globin		Vitreoscilla	contains		only						heme protein domain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_46_35868_s_239	10915782	Interestingly, the well studied globin from  Vitreoscilla, which contains only a heme protein domain and no bound flavin, is a homodimer and the ferric protein displays anticooperative ligand binding behavior in solution ( 57).	transcription
58447	2	335784	5	NULL	NULL	0	NULL	globin		Vitreoscilla	does not bind					flavin					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_46_35868_s_239	10915782	Interestingly, the well studied globin from  Vitreoscilla, which contains only a heme protein domain and no bound flavin, is a homodimer and the ferric protein displays anticooperative ligand binding behavior in solution ( 57).	transcription
58448	3	335784	5	NULL	NULL	0	NULL	globin		Vitreoscilla	forms					homodimer					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_46_35868_s_239	10915782	Interestingly, the well studied globin from  Vitreoscilla, which contains only a heme protein domain and no bound flavin, is a homodimer and the ferric protein displays anticooperative ligand binding behavior in solution ( 57).	transcription
58449	4	335784	5	NULL	NULL	0	NULL	ferric protein			bind					ligand		anticooperative			NULL	solution	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_46_35868_s_239	10915782	Interestingly, the well studied globin from  Vitreoscilla, which contains only a heme protein domain and no bound flavin, is a homodimer and the ferric protein displays anticooperative ligand binding behavior in solution ( 57).	transcription
58450	1	335785	5	NULL	NULL	0	NULL	globin		structure of	controls					hemoglobins		redox potential of	heme site		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39048_s_10	10984477	The globin structure controls the redox potential of the heme site of hemoglobins (Hbs)1 and myoglobins (Mbs), protects them from rapid oxidation, and thereby allows for reversible oxygen binding.	transcription
58451	2	335785	5	NULL	NULL	0	NULL	globin		structure of	controls					myoglobins		redox potential of	heme site		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39048_s_10	10984477	The globin structure controls the redox potential of the heme site of hemoglobins (Hbs)1 and myoglobins (Mbs), protects them from rapid oxidation, and thereby allows for reversible oxygen binding.	transcription
58452	3	335785	5	NULL	NULL	0	NULL	globin		structure of	protects					hemoglobins		rapid oxidation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39048_s_10	10984477	The globin structure controls the redox potential of the heme site of hemoglobins (Hbs)1 and myoglobins (Mbs), protects them from rapid oxidation, and thereby allows for reversible oxygen binding.	transcription
58453	4	335785	5	NULL	NULL	0	NULL	statement 3			allows					oxygen		reversible binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39048_s_10	10984477	The globin structure controls the redox potential of the heme site of hemoglobins (Hbs)1 and myoglobins (Mbs), protects them from rapid oxidation, and thereby allows for reversible oxygen binding.	transcription
58454	5	335785	5	NULL	NULL	0	NULL	globin		structure of	protects					myoglobins		rapid oxidation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39048_s_10	10984477	The globin structure controls the redox potential of the heme site of hemoglobins (Hbs)1 and myoglobins (Mbs), protects them from rapid oxidation, and thereby allows for reversible oxygen binding.	transcription
58455	6	335785	5	NULL	NULL	0	NULL	statement 5			allows					oxygen		reversible binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39048_s_10	10984477	The globin structure controls the redox potential of the heme site of hemoglobins (Hbs)1 and myoglobins (Mbs), protects them from rapid oxidation, and thereby allows for reversible oxygen binding.	transcription
79082	1	335785	6	NULL	NULL	0	NULL	hemoglobin	GP		bind					oxygen	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39048_s_10	10984477	The globin structure controls the redox potential of the heme site of hemoglobins (Hbs)1 and myoglobins (Mbs), protects them from rapid oxidation, and thereby allows for reversible oxygen binding.	transcription
79083	2	335785	6	NULL	NULL	0	NULL	myoglobin	GP		bind					oxygen	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_50_39048_s_10	10984477	The globin structure controls the redox potential of the heme site of hemoglobins (Hbs)1 and myoglobins (Mbs), protects them from rapid oxidation, and thereby allows for reversible oxygen binding.	transcription
58456	1	335786	5	NULL	NULL	0	NULL	EKLF protein			decrease during					erythroid		terminal differentiation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_37_23793_s_181	9726989	Although EKLF protein decreased during erythroid terminal differentiation, down-regulation of EKLF by the antisense construct prior to induction by epo severely inhibited transcription of globin and heme enzyme genes.	transcription
58457	2	335786	5	NULL	NULL	0	NULL	EKLF		down-regulation of	inhibit		severely			globin gene		transcription of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_37_23793_s_181	9726989	Although EKLF protein decreased during erythroid terminal differentiation, down-regulation of EKLF by the antisense construct prior to induction by epo severely inhibited transcription of globin and heme enzyme genes.	transcription
58458	3	335786	5	NULL	NULL	0	NULL	EKLF		down-regulation of	inhibit		severely			heme enzyme gene		transcription of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_37_23793_s_181	9726989	Although EKLF protein decreased during erythroid terminal differentiation, down-regulation of EKLF by the antisense construct prior to induction by epo severely inhibited transcription of globin and heme enzyme genes.	transcription
58459	4	335786	5	NULL	NULL	0	NULL	statement 2			occurs prior to					epo		induction by			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_37_23793_s_181	9726989	Although EKLF protein decreased during erythroid terminal differentiation, down-regulation of EKLF by the antisense construct prior to induction by epo severely inhibited transcription of globin and heme enzyme genes.	transcription
58460	5	335786	5	NULL	NULL	0	NULL	statement 3			occurs prior to					epo		induction by			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_37_23793_s_181	9726989	Although EKLF protein decreased during erythroid terminal differentiation, down-regulation of EKLF by the antisense construct prior to induction by epo severely inhibited transcription of globin and heme enzyme genes.	transcription
79084	1	335786	6	NULL	NULL	0	NULL	EKLF protein	GP		decreases during					erythroid terminal	cell	differentiation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_37_23793_s_181	9726989	Although EKLF protein decreased during erythroid terminal differentiation, down-regulation of EKLF by the antisense construct prior to induction by epo severely inhibited transcription of globin and heme enzyme genes.	transcription
58570	1	335787	5	NULL	NULL	0	NULL	cyanide ion			bind					heme Fe atom					NULL		0	NULL	NULL	NULL	gw60_pnas_100_10_5766_s_8	12719529	All 12 subunits display a cyanide ion bound to the heme Fe atom, stabilized by a tight hydrogen-bonded network based on the (globin very rare) TyrCD1 and TrpG8 residues.	transcription
79085	1	335787	6	NULL	NULL	0	NULL	cyanide ion	Chemical		bind					heme Fe atom	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_100_10_5766_s_8	12719529	All 12 subunits display a cyanide ion bound to the heme Fe atom, stabilized by a tight hydrogen-bonded network based on the (globin very rare) TyrCD1 and TrpG8 residues.	transcription
58571	1	335789	5	NULL	NULL	0	NULL	iron chelation/DFO			inhibits					heme		biosynthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_34_36048_s_181	15169765	To confirm that this differential expression pattern is HIF-derived, rather than from an iron chelation/DFO-mediated inhibition of heme biosynthesis, which, in turn, could lead to moderate down-regulation of fly globin transcription, it was necessary to look for similar responses in other HRE-flanked genes encoding heme-free products.	transcription
58572	2	335789	5	NULL	NULL	0	NULL	statement 1			down-regulates		moderately			globin		transcription of;;fly			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_34_36048_s_181	15169765	To confirm that this differential expression pattern is HIF-derived, rather than from an iron chelation/DFO-mediated inhibition of heme biosynthesis, which, in turn, could lead to moderate down-regulation of fly globin transcription, it was necessary to look for similar responses in other HRE-flanked genes encoding heme-free products.	transcription
58574	1	335790	5	NULL	NULL	0	NULL	HRI			bind			NTD		CO					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_99_s_146	12922173	The present study suggests that (1) the CO binding behavior of HRI-NTD is unusual for a globin-type heme protein, and (2) the CO molecule binds to the heme in HRI-NTD in an upright manner, forming weak interactions with nearby amino acids, according to the resonance Raman spectroscopy.	transcription
58575	2	335790	5	NULL	NULL	0	NULL	globin-type heme protein			does not bind					CO					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_99_s_146	12922173	The present study suggests that (1) the CO binding behavior of HRI-NTD is unusual for a globin-type heme protein, and (2) the CO molecule binds to the heme in HRI-NTD in an upright manner, forming weak interactions with nearby amino acids, according to the resonance Raman spectroscopy.	transcription
58576	3	335790	5	NULL	NULL	0	NULL	heme			is present in					HRI			NTD		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_99_s_146	12922173	The present study suggests that (1) the CO binding behavior of HRI-NTD is unusual for a globin-type heme protein, and (2) the CO molecule binds to the heme in HRI-NTD in an upright manner, forming weak interactions with nearby amino acids, according to the resonance Raman spectroscopy.	transcription
58577	4	335790	5	NULL	NULL	0	NULL	CO			bind					statement 3					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_99_s_146	12922173	The present study suggests that (1) the CO binding behavior of HRI-NTD is unusual for a globin-type heme protein, and (2) the CO molecule binds to the heme in HRI-NTD in an upright manner, forming weak interactions with nearby amino acids, according to the resonance Raman spectroscopy.	transcription
79086	1	335790	6	NULL	NULL	0	NULL	CO	Chemical		bind					HRI	GP		NTD		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_99_s_146	12922173	The present study suggests that (1) the CO binding behavior of HRI-NTD is unusual for a globin-type heme protein, and (2) the CO molecule binds to the heme in HRI-NTD in an upright manner, forming weak interactions with nearby amino acids, according to the resonance Raman spectroscopy.	transcription
79087	2	335790	6	NULL	NULL	0	NULL	CO	GP		bind					heme	GP		HRI-NTD		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1650_1_99_s_146	12922173	The present study suggests that (1) the CO binding behavior of HRI-NTD is unusual for a globin-type heme protein, and (2) the CO molecule binds to the heme in HRI-NTD in an upright manner, forming weak interactions with nearby amino acids, according to the resonance Raman spectroscopy.	transcription
58578	1	335791	5	NULL	NULL	0	NULL	heme			stimulates					globin chains		expression of			NULL	erythroid cells	0	NULL	NULL	NULL	gw60_molcellbiol_18_7_3819_s_14	9632766	For example, heme stimulates the expression of globin chains in erythroid cells and cytochrome P-450 in hepatic cells ( 6,  9,  36), activates protein synthesis through the heme-regulated inhibitor kinase ( 7), and regulates the transport of numerous enzymes and the assembly of hemoglobin and cytochrome complexes ( 24,  31).	transcription
58579	2	335791	5	NULL	NULL	0	NULL	heme			stimulates					cytochrome P-450					NULL	hepatic cells 	0	NULL	NULL	NULL	gw60_molcellbiol_18_7_3819_s_14	9632766	For example, heme stimulates the expression of globin chains in erythroid cells and cytochrome P-450 in hepatic cells ( 6,  9,  36), activates protein synthesis through the heme-regulated inhibitor kinase ( 7), and regulates the transport of numerous enzymes and the assembly of hemoglobin and cytochrome complexes ( 24,  31).	transcription
58580	3	335791	5	NULL	NULL	0	NULL	inhibitor kinase			is regulated by					heme					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_3819_s_14	9632766	For example, heme stimulates the expression of globin chains in erythroid cells and cytochrome P-450 in hepatic cells ( 6,  9,  36), activates protein synthesis through the heme-regulated inhibitor kinase ( 7), and regulates the transport of numerous enzymes and the assembly of hemoglobin and cytochrome complexes ( 24,  31).	transcription
58581	4	335791	5	NULL	NULL	0	NULL	heme			activates					protein synthesis					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_3819_s_14	9632766	For example, heme stimulates the expression of globin chains in erythroid cells and cytochrome P-450 in hepatic cells ( 6,  9,  36), activates protein synthesis through the heme-regulated inhibitor kinase ( 7), and regulates the transport of numerous enzymes and the assembly of hemoglobin and cytochrome complexes ( 24,  31).	transcription
58582	5	335791	5	NULL	NULL	0	NULL	statement 4			occurs through					statement 3					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_3819_s_14	9632766	For example, heme stimulates the expression of globin chains in erythroid cells and cytochrome P-450 in hepatic cells ( 6,  9,  36), activates protein synthesis through the heme-regulated inhibitor kinase ( 7), and regulates the transport of numerous enzymes and the assembly of hemoglobin and cytochrome complexes ( 24,  31).	transcription
58583	6	335791	5	NULL	NULL	0	NULL	heme			regulates					hemoglobin		assembly of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_3819_s_14	9632766	For example, heme stimulates the expression of globin chains in erythroid cells and cytochrome P-450 in hepatic cells ( 6,  9,  36), activates protein synthesis through the heme-regulated inhibitor kinase ( 7), and regulates the transport of numerous enzymes and the assembly of hemoglobin and cytochrome complexes ( 24,  31).	transcription
58584	7	335791	5	NULL	NULL	0	NULL	heme			regulates					cytochrome complexes		assembly of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_3819_s_14	9632766	For example, heme stimulates the expression of globin chains in erythroid cells and cytochrome P-450 in hepatic cells ( 6,  9,  36), activates protein synthesis through the heme-regulated inhibitor kinase ( 7), and regulates the transport of numerous enzymes and the assembly of hemoglobin and cytochrome complexes ( 24,  31).	transcription
79088	1	335791	6	NULL	NULL	0	NULL	heme	GP		stimulates					hepatic cells	cell	expression of	globin chains		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_18_7_3819_s_14	9632766	For example, heme stimulates the expression of globin chains in erythroid cells and cytochrome P-450 in hepatic cells ( 6,  9,  36), activates protein synthesis through the heme-regulated inhibitor kinase ( 7), and regulates the transport of numerous enzymes and the assembly of hemoglobin and cytochrome complexes ( 24,  31).	transcription
79089	2	335791	6	NULL	NULL	0	NULL	heme	GP		stimulates					cytochrome P-450	GP	expression of			NULL	hepatic cells	0	NULL	NULL	NULL	gw60_molcellbiol_18_7_3819_s_14	9632766	For example, heme stimulates the expression of globin chains in erythroid cells and cytochrome P-450 in hepatic cells ( 6,  9,  36), activates protein synthesis through the heme-regulated inhibitor kinase ( 7), and regulates the transport of numerous enzymes and the assembly of hemoglobin and cytochrome complexes ( 24,  31).	transcription
58585	1	335792	5	NULL	NULL	0	NULL	alpha chains		nascent	interacts with					heme					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13415_s_154	11827978	This indicates that nascent alpha chains having 86 amino acids possess a structure that allows interaction with heme or that heme binding to nascent globin chains promotes formation of the proper tertiary structure of the growing polypeptide chain on polyribosomes ( 19,  20).	transcription
58586	2	335792	5	NULL	NULL	0	NULL	heme			bind					globin chains		nascent			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13415_s_154	11827978	This indicates that nascent alpha chains having 86 amino acids possess a structure that allows interaction with heme or that heme binding to nascent globin chains promotes formation of the proper tertiary structure of the growing polypeptide chain on polyribosomes ( 19,  20).	transcription
58587	3	335792	5	NULL	NULL	0	NULL	polypeptide chain		growing	forms					tertiary structure					NULL	polyribosomes	0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13415_s_154	11827978	This indicates that nascent alpha chains having 86 amino acids possess a structure that allows interaction with heme or that heme binding to nascent globin chains promotes formation of the proper tertiary structure of the growing polypeptide chain on polyribosomes ( 19,  20).	transcription
58588	4	335792	5	NULL	NULL	0	NULL	statement 2			promotes					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13415_s_154	11827978	This indicates that nascent alpha chains having 86 amino acids possess a structure that allows interaction with heme or that heme binding to nascent globin chains promotes formation of the proper tertiary structure of the growing polypeptide chain on polyribosomes ( 19,  20).	transcription
79090	1	335792	6	NULL	NULL	0	NULL	Heme	GP		bind					globin chains	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_16_13415_s_154	11827978	This indicates that nascent alpha chains having 86 amino acids possess a structure that allows interaction with heme or that heme binding to nascent globin chains promotes formation of the proper tertiary structure of the growing polypeptide chain on polyribosomes ( 19,  20).	transcription
58594	1	335794	5	NULL	NULL	0	NULL	heme-globin linkage			is present in					hemoglobin			alpha chains		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10130_s_225	8626572	In conclusion, the present data bring out that in  hemoglobin the heme-globin linkage in the alpha  chains is stabilized by  interactions between unlike chains at the alpha beta   interface, whereas heme binding to the beta  chains is stabilized  by interactions at the alpha beta   interface.	transcription
58595	2	335794	5	NULL	NULL	0	NULL	statement 1			is stabilized by					alpha beta interface		interactions between	unlike chains		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10130_s_225	8626572	In conclusion, the present data bring out that in  hemoglobin the heme-globin linkage in the alpha  chains is stabilized by  interactions between unlike chains at the alpha beta   interface, whereas heme binding to the beta  chains is stabilized  by interactions at the alpha beta   interface.	transcription
58596	3	335794	5	NULL	NULL	0	NULL	heme			bind					beta chains					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10130_s_225	8626572	In conclusion, the present data bring out that in  hemoglobin the heme-globin linkage in the alpha  chains is stabilized by  interactions between unlike chains at the alpha beta   interface, whereas heme binding to the beta  chains is stabilized  by interactions at the alpha beta   interface.	transcription
58597	4	335794	5	NULL	NULL	0	NULL	alpha beta interface		interactions at	stabilize					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10130_s_225	8626572	In conclusion, the present data bring out that in  hemoglobin the heme-globin linkage in the alpha  chains is stabilized by  interactions between unlike chains at the alpha beta   interface, whereas heme binding to the beta  chains is stabilized  by interactions at the alpha beta   interface.	transcription
79091	1	335794	6	NULL	NULL	0	NULL	Heme	GP		bind								beta chain		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_17_10130_s_225	8626572	In conclusion, the present data bring out that in  hemoglobin the heme-globin linkage in the alpha  chains is stabilized by  interactions between unlike chains at the alpha beta   interface, whereas heme binding to the beta  chains is stabilized  by interactions at the alpha beta   interface.	transcription
58598	1	335795	5	NULL	NULL	0	NULL	heme			bind					cytochrome b5			His63		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_104	14672943	Based on the heme binding and spectroscopic data for the two axial mutants of cytochrome  b5, we had proposed that His63 plays a primary role for the binding of heme to cytochrome  b5 and acts in a manner analogous to the proximal histidine in globin, while His39 would correspond to the "`distal histidine"`, with ligation of His39 to the heme iron being critical for the electron transfer reaction catalyzed by cytochrome  b5 and not for heme binding ( ).	transcription
58599	2	335795	5	NULL	NULL	0	NULL	cytochrome b5			acts as			His63		globin		proximal	histidine		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_104	14672943	Based on the heme binding and spectroscopic data for the two axial mutants of cytochrome  b5, we had proposed that His63 plays a primary role for the binding of heme to cytochrome  b5 and acts in a manner analogous to the proximal histidine in globin, while His39 would correspond to the "`distal histidine"`, with ligation of His39 to the heme iron being critical for the electron transfer reaction catalyzed by cytochrome  b5 and not for heme binding ( ).	transcription
58600	3	335795	5	NULL	NULL	0	NULL	cytochrome b5			corresponds to			His39 		distal histidine					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_104	14672943	Based on the heme binding and spectroscopic data for the two axial mutants of cytochrome  b5, we had proposed that His63 plays a primary role for the binding of heme to cytochrome  b5 and acts in a manner analogous to the proximal histidine in globin, while His39 would correspond to the "`distal histidine"`, with ligation of His39 to the heme iron being critical for the electron transfer reaction catalyzed by cytochrome  b5 and not for heme binding ( ).	transcription
58601	4	335795	5	NULL	NULL	0	NULL	electron transfer reaction			is catalyzed by					cytochrome b5					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_104	14672943	Based on the heme binding and spectroscopic data for the two axial mutants of cytochrome  b5, we had proposed that His63 plays a primary role for the binding of heme to cytochrome  b5 and acts in a manner analogous to the proximal histidine in globin, while His39 would correspond to the "`distal histidine"`, with ligation of His39 to the heme iron being critical for the electron transfer reaction catalyzed by cytochrome  b5 and not for heme binding ( ).	transcription
58602	5	335795	5	NULL	NULL	0	NULL	cytochrome b5		ligation of	is critical for			His39		statement 4					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_8_6778_s_104	14672943	Based on the heme binding and spectroscopic data for the two axial mutants of cytochrome  b5, we had proposed that His63 plays a primary role for the binding of heme to cytochrome  b5 and acts in a manner analogous to the proximal histidine in globin, while His39 would correspond to the "`distal histidine"`, with ligation of His39 to the heme iron being critical for the electron transfer reaction catalyzed by cytochrome  b5 and not for heme binding ( ).	transcription
58603	1	335800	5	NULL	NULL	0	NULL	bacteria			produce					monocot globin protein					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_27_16746_s_193	9201978	The distinct red color of the recombinant bacteria and the purified protein, as well as its absorbance spectra, is strong evidence that the bacteria can properly produce a monocot globin protein capable of binding heme and constitute definitive evidence that the cloned Hb cDNA does in fact represent a Hb gene.	transcription
58604	2	335800	5	NULL	NULL	0	NULL	monocot globin protein			bind					heme					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_27_16746_s_193	9201978	The distinct red color of the recombinant bacteria and the purified protein, as well as its absorbance spectra, is strong evidence that the bacteria can properly produce a monocot globin protein capable of binding heme and constitute definitive evidence that the cloned Hb cDNA does in fact represent a Hb gene.	transcription
58605	1	335801	5	NULL	NULL	0	NULL	protein kinases			phosphorylates					eIF2alpha			Ser51		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21458_s_21	16717090	Four protein kinases phosphorylate eIF2alpha at Ser51 in response to different stress stimuli: 1) the dsRNA-activated protein kinase PKR is a major component of the interferonmediated antiviral response and is activated by binding to dsRNA produced during viral infection ( ); 2) the general control of nitrogen metabolism kinase GCN2 responds to amino acid depletion ( ); 3) the heme-regulated inhibitor kinase HRI responds to heme deprivation to couple globin synthesis with available heme ( ); and 4) the PKR-related endoplasmic reticulum (ER) kinase PERK responds to the accumulation of unfolded proteins in the ER in a subpathway of the unfolded protein response ( ).	transcription
58606	2	335801	5	NULL	NULL	0	NULL	statement 1			in response to					stress stimuli					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21458_s_21	16717090	Four protein kinases phosphorylate eIF2alpha at Ser51 in response to different stress stimuli: 1) the dsRNA-activated protein kinase PKR is a major component of the interferonmediated antiviral response and is activated by binding to dsRNA produced during viral infection ( ); 2) the general control of nitrogen metabolism kinase GCN2 responds to amino acid depletion ( ); 3) the heme-regulated inhibitor kinase HRI responds to heme deprivation to couple globin synthesis with available heme ( ); and 4) the PKR-related endoplasmic reticulum (ER) kinase PERK responds to the accumulation of unfolded proteins in the ER in a subpathway of the unfolded protein response ( ).	transcription
58607	3	335801	5	NULL	NULL	0	NULL	PKR			is a type of					protein kinase					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21458_s_21	16717090	Four protein kinases phosphorylate eIF2alpha at Ser51 in response to different stress stimuli: 1) the dsRNA-activated protein kinase PKR is a major component of the interferonmediated antiviral response and is activated by binding to dsRNA produced during viral infection ( ); 2) the general control of nitrogen metabolism kinase GCN2 responds to amino acid depletion ( ); 3) the heme-regulated inhibitor kinase HRI responds to heme deprivation to couple globin synthesis with available heme ( ); and 4) the PKR-related endoplasmic reticulum (ER) kinase PERK responds to the accumulation of unfolded proteins in the ER in a subpathway of the unfolded protein response ( ).	transcription
58608	4	335801	5	NULL	NULL	0	NULL	PKR			is activated by					dsRNA					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21458_s_21	16717090	Four protein kinases phosphorylate eIF2alpha at Ser51 in response to different stress stimuli: 1) the dsRNA-activated protein kinase PKR is a major component of the interferonmediated antiviral response and is activated by binding to dsRNA produced during viral infection ( ); 2) the general control of nitrogen metabolism kinase GCN2 responds to amino acid depletion ( ); 3) the heme-regulated inhibitor kinase HRI responds to heme deprivation to couple globin synthesis with available heme ( ); and 4) the PKR-related endoplasmic reticulum (ER) kinase PERK responds to the accumulation of unfolded proteins in the ER in a subpathway of the unfolded protein response ( ).	transcription
58609	5	335801	5	NULL	NULL	0	NULL	antiviral response			is mediated by					interferon					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21458_s_21	16717090	Four protein kinases phosphorylate eIF2alpha at Ser51 in response to different stress stimuli: 1) the dsRNA-activated protein kinase PKR is a major component of the interferonmediated antiviral response and is activated by binding to dsRNA produced during viral infection ( ); 2) the general control of nitrogen metabolism kinase GCN2 responds to amino acid depletion ( ); 3) the heme-regulated inhibitor kinase HRI responds to heme deprivation to couple globin synthesis with available heme ( ); and 4) the PKR-related endoplasmic reticulum (ER) kinase PERK responds to the accumulation of unfolded proteins in the ER in a subpathway of the unfolded protein response ( ).	transcription
58610	6	335801	5	NULL	NULL	0	NULL	PKR			is a component of		major			statement 5					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21458_s_21	16717090	Four protein kinases phosphorylate eIF2alpha at Ser51 in response to different stress stimuli: 1) the dsRNA-activated protein kinase PKR is a major component of the interferonmediated antiviral response and is activated by binding to dsRNA produced during viral infection ( ); 2) the general control of nitrogen metabolism kinase GCN2 responds to amino acid depletion ( ); 3) the heme-regulated inhibitor kinase HRI responds to heme deprivation to couple globin synthesis with available heme ( ); and 4) the PKR-related endoplasmic reticulum (ER) kinase PERK responds to the accumulation of unfolded proteins in the ER in a subpathway of the unfolded protein response ( ).	transcription
58611	7	335801	5	NULL	NULL	0	NULL	dsRNA			is produced during					virus		infection of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21458_s_21	16717090	Four protein kinases phosphorylate eIF2alpha at Ser51 in response to different stress stimuli: 1) the dsRNA-activated protein kinase PKR is a major component of the interferonmediated antiviral response and is activated by binding to dsRNA produced during viral infection ( ); 2) the general control of nitrogen metabolism kinase GCN2 responds to amino acid depletion ( ); 3) the heme-regulated inhibitor kinase HRI responds to heme deprivation to couple globin synthesis with available heme ( ); and 4) the PKR-related endoplasmic reticulum (ER) kinase PERK responds to the accumulation of unfolded proteins in the ER in a subpathway of the unfolded protein response ( ).	transcription
58612	8	335801	5	NULL	NULL	0	NULL	PKR			bind					statement 7					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21458_s_21	16717090	Four protein kinases phosphorylate eIF2alpha at Ser51 in response to different stress stimuli: 1) the dsRNA-activated protein kinase PKR is a major component of the interferonmediated antiviral response and is activated by binding to dsRNA produced during viral infection ( ); 2) the general control of nitrogen metabolism kinase GCN2 responds to amino acid depletion ( ); 3) the heme-regulated inhibitor kinase HRI responds to heme deprivation to couple globin synthesis with available heme ( ); and 4) the PKR-related endoplasmic reticulum (ER) kinase PERK responds to the accumulation of unfolded proteins in the ER in a subpathway of the unfolded protein response ( ).	transcription
58613	9	335801	5	NULL	NULL	0	NULL	statement 8			activates					PKR					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21458_s_21	16717090	Four protein kinases phosphorylate eIF2alpha at Ser51 in response to different stress stimuli: 1) the dsRNA-activated protein kinase PKR is a major component of the interferonmediated antiviral response and is activated by binding to dsRNA produced during viral infection ( ); 2) the general control of nitrogen metabolism kinase GCN2 responds to amino acid depletion ( ); 3) the heme-regulated inhibitor kinase HRI responds to heme deprivation to couple globin synthesis with available heme ( ); and 4) the PKR-related endoplasmic reticulum (ER) kinase PERK responds to the accumulation of unfolded proteins in the ER in a subpathway of the unfolded protein response ( ).	transcription
58614	10	335801	5	NULL	NULL	0	NULL	GCN2			is a type of					nitrogen metabolism					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21458_s_21	16717090	Four protein kinases phosphorylate eIF2alpha at Ser51 in response to different stress stimuli: 1) the dsRNA-activated protein kinase PKR is a major component of the interferonmediated antiviral response and is activated by binding to dsRNA produced during viral infection ( ); 2) the general control of nitrogen metabolism kinase GCN2 responds to amino acid depletion ( ); 3) the heme-regulated inhibitor kinase HRI responds to heme deprivation to couple globin synthesis with available heme ( ); and 4) the PKR-related endoplasmic reticulum (ER) kinase PERK responds to the accumulation of unfolded proteins in the ER in a subpathway of the unfolded protein response ( ).	transcription
58615	11	335801	5	NULL	NULL	0	NULL	GCN2		control of	respond to					amino acid		depletion of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21458_s_21	16717090	Four protein kinases phosphorylate eIF2alpha at Ser51 in response to different stress stimuli: 1) the dsRNA-activated protein kinase PKR is a major component of the interferonmediated antiviral response and is activated by binding to dsRNA produced during viral infection ( ); 2) the general control of nitrogen metabolism kinase GCN2 responds to amino acid depletion ( ); 3) the heme-regulated inhibitor kinase HRI responds to heme deprivation to couple globin synthesis with available heme ( ); and 4) the PKR-related endoplasmic reticulum (ER) kinase PERK responds to the accumulation of unfolded proteins in the ER in a subpathway of the unfolded protein response ( ).	transcription
58616	12	335801	5	NULL	NULL	0	NULL	HRI 			is					heme-regulated inhibitor kinase					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21458_s_21	16717090	Four protein kinases phosphorylate eIF2alpha at Ser51 in response to different stress stimuli: 1) the dsRNA-activated protein kinase PKR is a major component of the interferonmediated antiviral response and is activated by binding to dsRNA produced during viral infection ( ); 2) the general control of nitrogen metabolism kinase GCN2 responds to amino acid depletion ( ); 3) the heme-regulated inhibitor kinase HRI responds to heme deprivation to couple globin synthesis with available heme ( ); and 4) the PKR-related endoplasmic reticulum (ER) kinase PERK responds to the accumulation of unfolded proteins in the ER in a subpathway of the unfolded protein response ( ).	transcription
58617	13	335801	5	NULL	NULL	0	NULL	PERK			is					PKR-related endoplasmic reticulum (ER) kinase					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_30_21458_s_21	16717090	Four protein kinases phosphorylate eIF2alpha at Ser51 in response to different stress stimuli: 1) the dsRNA-activated protein kinase PKR is a major component of the interferonmediated antiviral response and is activated by binding to dsRNA produced during viral infection ( ); 2) the general control of nitrogen metabolism kinase GCN2 responds to amino acid depletion ( ); 3) the heme-regulated inhibitor kinase HRI responds to heme deprivation to couple globin synthesis with available heme ( ); and 4) the PKR-related endoplasmic reticulum (ER) kinase PERK responds to the accumulation of unfolded proteins in the ER in a subpathway of the unfolded protein response ( ).	transcription
58618	14	335801	5	NULL	NULL	0	NULL	HRI			respond to					heme		deprivation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21458_s_21	16717090	Four protein kinases phosphorylate eIF2alpha at Ser51 in response to different stress stimuli: 1) the dsRNA-activated protein kinase PKR is a major component of the interferonmediated antiviral response and is activated by binding to dsRNA produced during viral infection ( ); 2) the general control of nitrogen metabolism kinase GCN2 responds to amino acid depletion ( ); 3) the heme-regulated inhibitor kinase HRI responds to heme deprivation to couple globin synthesis with available heme ( ); and 4) the PKR-related endoplasmic reticulum (ER) kinase PERK responds to the accumulation of unfolded proteins in the ER in a subpathway of the unfolded protein response ( ).	transcription
58619	15	335801	5	NULL	NULL	0	NULL	HRI			is coupled to					globin synthesis					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21458_s_21	16717090	Four protein kinases phosphorylate eIF2alpha at Ser51 in response to different stress stimuli: 1) the dsRNA-activated protein kinase PKR is a major component of the interferonmediated antiviral response and is activated by binding to dsRNA produced during viral infection ( ); 2) the general control of nitrogen metabolism kinase GCN2 responds to amino acid depletion ( ); 3) the heme-regulated inhibitor kinase HRI responds to heme deprivation to couple globin synthesis with available heme ( ); and 4) the PKR-related endoplasmic reticulum (ER) kinase PERK responds to the accumulation of unfolded proteins in the ER in a subpathway of the unfolded protein response ( ).	transcription
58620	16	335801	5	NULL	NULL	0	NULL	statement 15			occurs with					heme		available			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21458_s_21	16717090	Four protein kinases phosphorylate eIF2alpha at Ser51 in response to different stress stimuli: 1) the dsRNA-activated protein kinase PKR is a major component of the interferonmediated antiviral response and is activated by binding to dsRNA produced during viral infection ( ); 2) the general control of nitrogen metabolism kinase GCN2 responds to amino acid depletion ( ); 3) the heme-regulated inhibitor kinase HRI responds to heme deprivation to couple globin synthesis with available heme ( ); and 4) the PKR-related endoplasmic reticulum (ER) kinase PERK responds to the accumulation of unfolded proteins in the ER in a subpathway of the unfolded protein response ( ).	transcription
58621	17	335801	5	NULL	NULL	0	NULL	statement 16			occurs simultaneously with					statement 14					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21458_s_21	16717090	Four protein kinases phosphorylate eIF2alpha at Ser51 in response to different stress stimuli: 1) the dsRNA-activated protein kinase PKR is a major component of the interferonmediated antiviral response and is activated by binding to dsRNA produced during viral infection ( ); 2) the general control of nitrogen metabolism kinase GCN2 responds to amino acid depletion ( ); 3) the heme-regulated inhibitor kinase HRI responds to heme deprivation to couple globin synthesis with available heme ( ); and 4) the PKR-related endoplasmic reticulum (ER) kinase PERK responds to the accumulation of unfolded proteins in the ER in a subpathway of the unfolded protein response ( ).	transcription
58622	18	335801	5	NULL	NULL	0	NULL	PERK			respond to					unfolded proteins		accumulation of			NULL	ER	0	NULL	NULL	NULL	gw70_jbiolchem_281_30_21458_s_21	16717090	Four protein kinases phosphorylate eIF2alpha at Ser51 in response to different stress stimuli: 1) the dsRNA-activated protein kinase PKR is a major component of the interferonmediated antiviral response and is activated by binding to dsRNA produced during viral infection ( ); 2) the general control of nitrogen metabolism kinase GCN2 responds to amino acid depletion ( ); 3) the heme-regulated inhibitor kinase HRI responds to heme deprivation to couple globin synthesis with available heme ( ); and 4) the PKR-related endoplasmic reticulum (ER) kinase PERK responds to the accumulation of unfolded proteins in the ER in a subpathway of the unfolded protein response ( ).	transcription
58623	1	335802	5	NULL	NULL	0	NULL	globin		synthesis of	modulated by					heme-regulated translational inhibitor					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biol-res_39_1_16629165_s_3	16629165	For example, three enzymes involved in erythrocyte  development are regulated by three different control mechanisms: globin  synthesis is modulated by heme-regulated translational inhibitor, erythroid  5-aminolevulinate synthase translation is inhibited by binding of the  iron regulatory protein to the iron response element in the 5''-untranslated  region (UTR); and 15-lipoxygenase is regulated by specific proteins binding  to the 3''-UTR.	transcription
58624	2	335802	5	NULL	NULL	0	NULL	iron regulatory protein			bind									iron response element in 5'' -UTR	NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_biol-res_39_1_16629165_s_3	16629165	For example, three enzymes involved in erythrocyte  development are regulated by three different control mechanisms: globin  synthesis is modulated by heme-regulated translational inhibitor, erythroid  5-aminolevulinate synthase translation is inhibited by binding of the  iron regulatory protein to the iron response element in the 5''-untranslated  region (UTR); and 15-lipoxygenase is regulated by specific proteins binding  to the 3''-UTR.	transcription
58625	3	335802	5	NULL	NULL	0	NULL	statement 2			inhibits					5-aminolevulinate synthase		erythroid			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biol-res_39_1_16629165_s_3	16629165	For example, three enzymes involved in erythrocyte  development are regulated by three different control mechanisms: globin  synthesis is modulated by heme-regulated translational inhibitor, erythroid  5-aminolevulinate synthase translation is inhibited by binding of the  iron regulatory protein to the iron response element in the 5''-untranslated  region (UTR); and 15-lipoxygenase is regulated by specific proteins binding  to the 3''-UTR.	transcription
58626	4	335802	5	NULL	NULL	0	NULL	proteins 		specific 	bind									3''-UTR	NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biol-res_39_1_16629165_s_3	16629165	For example, three enzymes involved in erythrocyte  development are regulated by three different control mechanisms: globin  synthesis is modulated by heme-regulated translational inhibitor, erythroid  5-aminolevulinate synthase translation is inhibited by binding of the  iron regulatory protein to the iron response element in the 5''-untranslated  region (UTR); and 15-lipoxygenase is regulated by specific proteins binding  to the 3''-UTR.	transcription
58627	5	335802	5	NULL	NULL	0	NULL	statement 4			regulates					15-lipoxygenase					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biol-res_39_1_16629165_s_3	16629165	For example, three enzymes involved in erythrocyte  development are regulated by three different control mechanisms: globin  synthesis is modulated by heme-regulated translational inhibitor, erythroid  5-aminolevulinate synthase translation is inhibited by binding of the  iron regulatory protein to the iron response element in the 5''-untranslated  region (UTR); and 15-lipoxygenase is regulated by specific proteins binding  to the 3''-UTR.	transcription
79103	1	335802	6	NULL	NULL	0	NULL	globin	GP	synthesis of	is modulated by					heme-regulated translational inhibitor					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biol-res_39_1_16629165_s_3	16629165	For example, three enzymes involved in erythrocyte  development are regulated by three different control mechanisms: globin  synthesis is modulated by heme-regulated translational inhibitor, erythroid  5-aminolevulinate synthase translation is inhibited by binding of the  iron regulatory protein to the iron response element in the 5''-untranslated  region (UTR); and 15-lipoxygenase is regulated by specific proteins binding  to the 3''-UTR.	transcription
79104	3	335802	6	NULL	NULL	0	NULL	erythroid 5-aminolevulinate synthase	GP	translation of 	is inhibited by					statement 2	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biol-res_39_1_16629165_s_3	16629165	For example, three enzymes involved in erythrocyte  development are regulated by three different control mechanisms: globin  synthesis is modulated by heme-regulated translational inhibitor, erythroid  5-aminolevulinate synthase translation is inhibited by binding of the  iron regulatory protein to the iron response element in the 5''-untranslated  region (UTR); and 15-lipoxygenase is regulated by specific proteins binding  to the 3''-UTR.	transcription
79105	2	335802	6	NULL	NULL	0	NULL	iron regulatory protein	GP		bind									iron response element in the 5''-untranslated region (UTR)	NULL		0	NULL	NULL	NULL	abs-batch0650-0679_biol-res_39_1_16629165_s_3	16629165	For example, three enzymes involved in erythrocyte  development are regulated by three different control mechanisms: globin  synthesis is modulated by heme-regulated translational inhibitor, erythroid  5-aminolevulinate synthase translation is inhibited by binding of the  iron regulatory protein to the iron response element in the 5''-untranslated  region (UTR); and 15-lipoxygenase is regulated by specific proteins binding  to the 3''-UTR.	transcription
58628	1	335803	5	NULL	NULL	0	NULL	taurine			interacts with					hypochlorite anion					NULL		0	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_114_11_1337841_s_1	1337841	[The interaction of taurine and beta-alanyl-L-histidine (carnosine) with hypochlorite anion (ClO-)].	transcription
58629	2	335803	5	NULL	NULL	0	NULL	beta-alanyl-L-histidine			interacts with					hypochlorite anion					NULL		0	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_114_11_1337841_s_1	1337841	[The interaction of taurine and beta-alanyl-L-histidine (carnosine) with hypochlorite anion (ClO-)].	transcription
58630	3	335803	5	NULL	NULL	0	NULL	beta-alanyl-L-histidine			is					carnosine					NULL		0	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_114_11_1337841_s_1	1337841	[The interaction of taurine and beta-alanyl-L-histidine (carnosine) with hypochlorite anion (ClO-)].	transcription
58631	4	335803	5	NULL	NULL	0	NULL	hypochlorite anion			is					ClO-					NULL		0	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_114_11_1337841_s_1	1337841	[The interaction of taurine and beta-alanyl-L-histidine (carnosine) with hypochlorite anion (ClO-)].	transcription
79157	1	335803	6	NULL	NULL	0	NULL	taurine	AminoAcid		bind					beta-alanyl-L-histidine	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_114_11_1337841_s_1	1337841	[The interaction of taurine and beta-alanyl-L-histidine (carnosine) with hypochlorite anion (ClO-)].	transcription
79158	2	335803	6	NULL	NULL	0	NULL	beta-alanyl-L-histidine	Chemical		is					carnosine	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_114_11_1337841_s_1	1337841	[The interaction of taurine and beta-alanyl-L-histidine (carnosine) with hypochlorite anion (ClO-)].	transcription
58632	1	335804	5	NULL	NULL	0	NULL	CE		activity of	release					beta-alanine					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_8_3540_s_161	10427046	The activity of CE mainly released beta-alanine, histidine, alanine, and anserine, while the levels of glycine, glutamine, and carnosine decreased.	transcription
58633	2	335804	5	NULL	NULL	0	NULL	CE		activity of	release					histidine					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_8_3540_s_161	10427046	The activity of CE mainly released beta-alanine, histidine, alanine, and anserine, while the levels of glycine, glutamine, and carnosine decreased.	transcription
58634	3	335804	5	NULL	NULL	0	NULL	CE		activity of	release					alanine					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_8_3540_s_161	10427046	The activity of CE mainly released beta-alanine, histidine, alanine, and anserine, while the levels of glycine, glutamine, and carnosine decreased.	transcription
58635	4	335804	5	NULL	NULL	0	NULL	CE		activity of	release					anserine					NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_8_3540_s_161	10427046	The activity of CE mainly released beta-alanine, histidine, alanine, and anserine, while the levels of glycine, glutamine, and carnosine decreased.	transcription
58636	5	335804	5	NULL	NULL	0	NULL	CE		activity of	decreases					glycine		level of			NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_65_8_3540_s_161	10427046	The activity of CE mainly released beta-alanine, histidine, alanine, and anserine, while the levels of glycine, glutamine, and carnosine decreased.	transcription
58637	6	335804	5	NULL	NULL	0	NULL	CE		activity of	decreases					glutamine		level of			NULL		NULL	NULL	NULL	NULL	gw60_applenvironmicrob_65_8_3540_s_161	10427046	The activity of CE mainly released beta-alanine, histidine, alanine, and anserine, while the levels of glycine, glutamine, and carnosine decreased.	transcription
58638	7	335804	5	NULL	NULL	0	NULL	CE		activity of	decreases					carnosine 		level of			NULL		0	NULL	NULL	NULL	gw60_applenvironmicrob_65_8_3540_s_161	10427046	The activity of CE mainly released beta-alanine, histidine, alanine, and anserine, while the levels of glycine, glutamine, and carnosine decreased.	transcription
58639	1	335805	5	NULL	NULL	0	NULL	Carnosine			is					beta-alanyl-L-histidine					NULL		0	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_107_2_2923966_s_2	2923966	Carnosine (beta-alanyl-L-histidine) injected to intact albino rats (20  mg/kg body weight) induces depletion of lipid peroxidation (LPO) products  in brain and blood serum, an increase of superoxide scavenging activity  in brain and serum, decrease of cholesterol: phospholipid ratio and increase  of easy oxidizable phospholipid portion in brain lipid extracts.	transcription
58640	2	335805	5	NULL	NULL	0	NULL	Carnosine			is injected to					albino rats		intact			NULL		0	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_107_2_2923966_s_2	2923966	Carnosine (beta-alanyl-L-histidine) injected to intact albino rats (20  mg/kg body weight) induces depletion of lipid peroxidation (LPO) products  in brain and blood serum, an increase of superoxide scavenging activity  in brain and serum, decrease of cholesterol: phospholipid ratio and increase  of easy oxidizable phospholipid portion in brain lipid extracts.	transcription
58641	3	335805	5	NULL	NULL	0	NULL	statement 2			induce					LPO products		depletion of			NULL	brain, blood serum	NULL	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_107_2_2923966_s_2	2923966	Carnosine (beta-alanyl-L-histidine) injected to intact albino rats (20  mg/kg body weight) induces depletion of lipid peroxidation (LPO) products  in brain and blood serum, an increase of superoxide scavenging activity  in brain and serum, decrease of cholesterol: phospholipid ratio and increase  of easy oxidizable phospholipid portion in brain lipid extracts.	transcription
58642	4	335805	5	NULL	NULL	0	NULL	LPO products			is					lipid peroxidation products					NULL		0	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_107_2_2923966_s_2	2923966	Carnosine (beta-alanyl-L-histidine) injected to intact albino rats (20  mg/kg body weight) induces depletion of lipid peroxidation (LPO) products  in brain and blood serum, an increase of superoxide scavenging activity  in brain and serum, decrease of cholesterol: phospholipid ratio and increase  of easy oxidizable phospholipid portion in brain lipid extracts.	transcription
58643	5	335805	5	NULL	NULL	0	NULL	statement 2			increases					superoxide		scavenging activity of			NULL	brain, blood serum	0	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_107_2_2923966_s_2	2923966	Carnosine (beta-alanyl-L-histidine) injected to intact albino rats (20  mg/kg body weight) induces depletion of lipid peroxidation (LPO) products  in brain and blood serum, an increase of superoxide scavenging activity  in brain and serum, decrease of cholesterol: phospholipid ratio and increase  of easy oxidizable phospholipid portion in brain lipid extracts.	transcription
58644	6	335805	5	NULL	NULL	0	NULL	statement 2			decreases					cholesterol: phospholipid ratio					NULL		NULL	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_107_2_2923966_s_2	2923966	Carnosine (beta-alanyl-L-histidine) injected to intact albino rats (20  mg/kg body weight) induces depletion of lipid peroxidation (LPO) products  in brain and blood serum, an increase of superoxide scavenging activity  in brain and serum, decrease of cholesterol: phospholipid ratio and increase  of easy oxidizable phospholipid portion in brain lipid extracts.	transcription
58645	7	335805	5	NULL	NULL	0	NULL	statement 2			increases					phospholipid portion		easy oxidizable			NULL	brain lipid extracts	0	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_107_2_2923966_s_2	2923966	Carnosine (beta-alanyl-L-histidine) injected to intact albino rats (20  mg/kg body weight) induces depletion of lipid peroxidation (LPO) products  in brain and blood serum, an increase of superoxide scavenging activity  in brain and serum, decrease of cholesterol: phospholipid ratio and increase  of easy oxidizable phospholipid portion in brain lipid extracts.	transcription
79159	1	335805	6	NULL	NULL	0	NULL	beta-alanyl-L-histidine	AminoAcid		induces					LPO	Process	depletion of 			NULL		0	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_107_2_2923966_s_2	2923966	Carnosine (beta-alanyl-L-histidine) injected to intact albino rats (20  mg/kg body weight) induces depletion of lipid peroxidation (LPO) products  in brain and blood serum, an increase of superoxide scavenging activity  in brain and serum, decrease of cholesterol: phospholipid ratio and increase  of easy oxidizable phospholipid portion in brain lipid extracts.	transcription
79160	2	335805	6	NULL	NULL	0	NULL	beta-alanyl-L-histidine	AminoAcid		is					carnosine	AminoAcid				NULL		0	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_107_2_2923966_s_2	2923966	Carnosine (beta-alanyl-L-histidine) injected to intact albino rats (20  mg/kg body weight) induces depletion of lipid peroxidation (LPO) products  in brain and blood serum, an increase of superoxide scavenging activity  in brain and serum, decrease of cholesterol: phospholipid ratio and increase  of easy oxidizable phospholipid portion in brain lipid extracts.	transcription
79161	3	335805	6	NULL	NULL	NULL	NULL	beta-alanyl-L-histidine	AminoAcid		increases					superoxide scavenging activity	Process				NULL	brain	NULL	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_107_2_2923966_s_2	2923966	Carnosine (beta-alanyl-L-histidine) injected to intact albino rats (20  mg/kg body weight) induces depletion of lipid peroxidation (LPO) products  in brain and blood serum, an increase of superoxide scavenging activity  in brain and serum, decrease of cholesterol: phospholipid ratio and increase  of easy oxidizable phospholipid portion in brain lipid extracts.	transcription
79162	4	335805	6	NULL	NULL	0	NULL	beta-alanyl-L-histidine	AminoAcid		increases					superoxide scavenging activity	Process				NULL	serum	0	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_107_2_2923966_s_2	2923966	Carnosine (beta-alanyl-L-histidine) injected to intact albino rats (20  mg/kg body weight) induces depletion of lipid peroxidation (LPO) products  in brain and blood serum, an increase of superoxide scavenging activity  in brain and serum, decrease of cholesterol: phospholipid ratio and increase  of easy oxidizable phospholipid portion in brain lipid extracts.	transcription
79163	5	335805	6	NULL	NULL	0	NULL	beta-alanyl-L-histidine	AminoAcid		induces					cholesterol	Chemical	decrease of 			NULL		0	NULL	NULL	NULL	abs-batch0760-0779_biull-eksp-biol-med_107_2_2923966_s_2	2923966	Carnosine (beta-alanyl-L-histidine) injected to intact albino rats (20  mg/kg body weight) induces depletion of lipid peroxidation (LPO) products  in brain and blood serum, an increase of superoxide scavenging activity  in brain and serum, decrease of cholesterol: phospholipid ratio and increase  of easy oxidizable phospholipid portion in brain lipid extracts.	transcription
58646	1	335806	5	NULL	NULL	0	NULL	fimbriae		purified	bind					glucosylceramide					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58647	2	335806	5	NULL	NULL	0	NULL	glucosylceramide			is					GlcCer					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58648	3	335806	5	NULL	NULL	0	NULL	fimbriae		purified	bind					galactosylceramide 2					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58649	4	335806	5	NULL	NULL	0	NULL	galactosylceramide 2			is a type of					nonhydroxylated fatty acids					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58650	5	335806	5	NULL	NULL	0	NULL	fimbriae		purified	bind					lactosylceramide					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58651	6	335806	5	NULL	NULL	0	NULL	lactosylceramide			is					LacCer					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58652	7	335806	5	NULL	NULL	0	NULL	fimbriae		purified	bind					paragloboside					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58653	8	335806	5	NULL	NULL	0	NULL	paragloboside			is					nLc4Cer					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58654	9	335806	5	NULL	NULL	0	NULL	fimbriae		purified	bind					lactotriaosylceramide					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58655	10	335806	5	NULL	NULL	0	NULL	lactotriaosylceramide			is					Lc3Cer					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58656	11	335806	5	NULL	NULL	0	NULL	fimbriae		purified	bind					asialo-GM1					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58657	12	335806	5	NULL	NULL	0	NULL	asialo-GM1			is					GgO4Cer					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58658	13	335806	5	NULL	NULL	0	NULL	fimbriae		purified	bind					asialo-GM2					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58659	14	335806	5	NULL	NULL	0	NULL	asialo-GM2			is					GgO3Cer					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58660	15	335806	5	NULL	NULL	0	NULL	fimbriae		purified	bind					globotriaosylceramide					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58661	16	335806	5	NULL	NULL	0	NULL	globotriaosylceramide			is					Gb3Cer					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58662	17	335806	5	NULL	NULL	0	NULL	fimbriae		purified	does not bind					sulfatide 					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58663	18	335806	5	NULL	NULL	0	NULL	sulfatide 			is					SFT					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58664	19	335806	5	NULL	NULL	0	NULL	fimbriae		purified	does not bind					globotetraosylceramide					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58665	20	335806	5	NULL	NULL	0	NULL	globotetraosylceramide 			is					Gb4Cer					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58666	21	335806	5	NULL	NULL	0	NULL	fimbriae		purified	does not bind					Forssman antigen					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58667	22	335806	5	NULL	NULL	0	NULL	fimbriae		purified	does not bind					GM1 					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58668	23	335806	5	NULL	NULL	0	NULL	fimbriae		purified	does not bind					GM2					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58669	24	335806	5	NULL	NULL	0	NULL	fimbriae		purified	does not bind					GM3					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58670	25	335806	5	NULL	NULL	0	NULL	fimbriae		purified	does not bind					GD2					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58671	26	335806	5	NULL	NULL	0	NULL	fimbriae		purified	does not bind					GD3 					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58672	27	335806	5	NULL	NULL	0	NULL	fimbriae		purified	does not bind					DSPG					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58673	28	335806	5	NULL	NULL	0	NULL	fimbriae		purified	does not bind					DSnHC					NULL		NULL	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58674	29	335806	5	NULL	NULL	0	NULL	fimbriae		purified	does not bind					DSnOC 					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58675	30	335806	5	NULL	NULL	0	NULL	fimbriae		purified	does not bind					ceramide 					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58676	31	335806	5	NULL	NULL	0	NULL	ceramide 			is					Cer					NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79164	1	335806	6	NULL	NULL	0	NULL	fimbriae	CellComponent	purified	bind					GlcCer	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79165	2	335806	6	NULL	NULL	0	NULL	fimbriae	CellComponent	purified	bind					nonhydroxylated fatty acids	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79166	3	335806	6	NULL	NULL	0	NULL	fimbriae	CellComponent	purified	bind					LacCer	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79167	4	335806	6	NULL	NULL	0	NULL	fimbriae	CellComponent	purified	bind					nLc4Cer	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79168	5	335806	6	NULL	NULL	0	NULL	fimbriae	CellComponent	purified	bind					Lc3Cer	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79169	6	335806	6	NULL	NULL	0	NULL	fimbriae	CellComponent	purified	bind					GgO4Cer	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79170	7	335806	6	NULL	NULL	0	NULL	fimbriae	CellComponent	purified	bind					GgO3Cer	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79171	8	335806	6	NULL	NULL	0	NULL	fimbriae	CellComponent	purified	bind					Gb3Cer	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79172	9	335806	6	NULL	NULL	0	NULL	GlcCer	Chemical		is					glucosylceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79173	10	335806	6	NULL	NULL	0	NULL	nonhydroxylated fatty acids	Chemical		is					galactosylceramide 2	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79174	11	335806	6	NULL	NULL	0	NULL	LacCer	Chemical		is					lactosylceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79175	12	335806	6	NULL	NULL	0	NULL	nLc4Cer	Chemical		is					paragloboside	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79176	13	335806	6	NULL	NULL	0	NULL	Lc3Cer	Chemical		is					lactotriaosylceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79177	14	335806	6	NULL	NULL	0	NULL	GgO4Cer	Chemical		is					asialo-GM1	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79178	15	335806	6	NULL	NULL	0	NULL	GgO3Cer	Chemical		is					asialo-GM2	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79179	16	335806	6	NULL	NULL	0	NULL	Gb3Cer	Chemical		is					globotriaosylceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79180	17	335806	6	NULL	NULL	0	NULL	sulfatide	Chemical		is					SFT	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79181	18	335806	6	NULL	NULL	0	NULL	Gb4Cer	Chemical		is					globotetraosylceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79182	19	335806	6	NULL	NULL	0	NULL	fimbriae	CellComponent	purified	does not bind					Forssman antigen	GP				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79183	20	335806	6	NULL	NULL	0	NULL	fimbriae	CellComponent	purified	does not bind					SFT	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79184	21	335806	6	NULL	NULL	0	NULL	fimbriae	CellComponent	purified	does not bind					Gb4Cer	GP				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79185	22	335806	6	NULL	NULL	0	NULL	fimbriae	CellComponent	purified	does not bind					GM1	GP				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79186	23	335806	6	NULL	NULL	0	NULL	fimbriae	CellComponent	purified	does not bind					GM2	GP				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79187	24	335806	6	NULL	NULL	0	NULL	fimbriae	CellComponent	purified	does not bind					GM3	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79188	25	335806	6	NULL	NULL	0	NULL	fimbriae	CellComponent	purified	does not bind					GD2	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79189	26	335806	6	NULL	NULL	0	NULL	fimbriae	CellComponent	purified	does not bind					GD2	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79190	27	335806	6	NULL	NULL	0	NULL	fimbriae	CellComponent	purified	does not bind					DSPG	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79191	28	335806	6	NULL	NULL	0	NULL	fimbriae	CellComponent	purified	does not bind					DSnHC	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
79192	29	335806	6	NULL	NULL	0	NULL	fimbriae	CellComponent	purified	does not bind					DSnOC	Chemical				NULL		0	NULL	NULL	NULL	gw60_infectimmun_68_6_3541_s_109	10816509	Purified fimbriae bound to glucosylceramide (GlcCer), galactosylceramide 2 (nonhydroxylated fatty acids), lactosylceramide (LacCer), paragloboside (nLc4Cer), lactotriaosylceramide (Lc3Cer), asialo-GM1 (GgO4Cer), asialo-GM2 (GgO3Cer), and globotriaosylceramide (Gb3Cer) (Table  1) but did not bind to sulfatide (SFT), globotetraosylceramide (Gb4Cer), the Forssman antigen (Table  1), GM1 (Fig.  1), GM2, GM3, GD2, GD3 (Table  1), DSPG, DSnHC, DSnOC (see Fig.  3), or ceramide (Cer) (Table  1).	transcription
58677	1	335807	5	NULL	NULL	0	NULL	p73			induce					Bax		up-regulation of			NULL	Saos-2 cells	0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_96	14634023	p73 induces Bax up-regulation in Saos-2 cells.	transcription
79193	1	335807	6	NULL	NULL	0	NULL	p73	GP		induces					Bax	GP	upregulation of			NULL	Saos-2 cells	0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_96	14634023	p73 induces Bax up-regulation in Saos-2 cells.	transcription
58678	1	335808	5	NULL	NULL	0	NULL	p73 isoforms			activates		transcriptionaly			Bax					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_97	14634023	A, Bax transcriptional activation by different p73 isoforms.	transcription
79194	1	335808	6	NULL	NULL	0	NULL	p73	GP		activates					Bax	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_97	14634023	A, Bax transcriptional activation by different p73 isoforms.	transcription
58679	1	335809	5	NULL	NULL	0	NULL	Bax			is translocated from					cytosol					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_122	14634023	p73 induces Bax translocation from cytosol to mitochondria.	transcription
58680	2	335809	5	NULL	NULL	0	NULL	Bax			is translocated to					mitochondria					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_122	14634023	p73 induces Bax translocation from cytosol to mitochondria.	transcription
58681	3	335809	5	NULL	NULL	0	NULL	statement 1			occurs simultaneously with					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_122	14634023	p73 induces Bax translocation from cytosol to mitochondria.	transcription
58682	4	335809	5	NULL	NULL	0	NULL	p73			induce					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_122	14634023	p73 induces Bax translocation from cytosol to mitochondria.	transcription
79195	1	335809	6	NULL	NULL	0	NULL	Bax	GP		is translocated from					cytosol	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_122	14634023	p73 induces Bax translocation from cytosol to mitochondria.	transcription
79196	2	335809	6	NULL	NULL	0	NULL	Bax	GP		is translocated to					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_122	14634023	p73 induces Bax translocation from cytosol to mitochondria.	transcription
79197	3	335809	6	NULL	NULL	0	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_122	14634023	p73 induces Bax translocation from cytosol to mitochondria.	transcription
79198	4	335809	6	NULL	NULL	0	NULL	p73	GP		induces					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_122	14634023	p73 induces Bax translocation from cytosol to mitochondria.	transcription
58683	1	335810	5	NULL	NULL	0	NULL	p73			regulates		transcriptionaly			Bax					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_262	14634023	p73 transcriptionally regulates both Bax and PUMA.	transcription
58684	2	335810	5	NULL	NULL	0	NULL	p73			regulates		transcriptionaly			PUMA					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_262	14634023	p73 transcriptionally regulates both Bax and PUMA.	transcription
79199	1	335810	6	NULL	NULL	0	NULL	p73	GP		regulates					Bax	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_262	14634023	p73 transcriptionally regulates both Bax and PUMA.	transcription
79200	2	335810	6	NULL	NULL	0	NULL	p73	GP		regulates					PUMA	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_262	14634023	p73 transcriptionally regulates both Bax and PUMA.	transcription
58685	1	335811	5	NULL	NULL	0	NULL	p73			induce		strongly			Bax				promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_269	10207112	It is possible that the induction of the Bax promoter by p73 is via a synergism between p73 and another putative transcription factor also binding to the Bax promoter, which also might explain the strong induction of the Bax promoter by p73.	transcription
58690	1	335812	5	NULL	NULL	0	NULL	PIAS-1			mediates					p73		sumoylation of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_24_10593_s_6	15572666	PIAS-1-mediated sumoylation decreases p73 transcriptional activity on several target promoters, such as Bax. p73 is colocalized in the nucleus with PIAS-1, and sumoylated p73 is located exclusively in the nuclear matrix.	transcription
58691	2	335812	5	NULL	NULL	0	NULL	p73			activates		transcriptionaly			Bax				promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_24_10593_s_6	15572666	PIAS-1-mediated sumoylation decreases p73 transcriptional activity on several target promoters, such as Bax. p73 is colocalized in the nucleus with PIAS-1, and sumoylated p73 is located exclusively in the nuclear matrix.	transcription
58692	3	335812	5	NULL	NULL	0	NULL	statement 1			decreases					statement 2					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_24_10593_s_6	15572666	PIAS-1-mediated sumoylation decreases p73 transcriptional activity on several target promoters, such as Bax. p73 is colocalized in the nucleus with PIAS-1, and sumoylated p73 is located exclusively in the nuclear matrix.	transcription
58693	4	335812	5	NULL	NULL	0	NULL	p73			colocalize with					PIAS-1					NULL	nucleus	0	NULL	NULL	NULL	gw70_molcellbiol_24_24_10593_s_6	15572666	PIAS-1-mediated sumoylation decreases p73 transcriptional activity on several target promoters, such as Bax. p73 is colocalized in the nucleus with PIAS-1, and sumoylated p73 is located exclusively in the nuclear matrix.	transcription
58694	5	335812	5	NULL	NULL	0	NULL	p73		sumoylated	is located in		exclusively			nuclear matrix					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_24_10593_s_6	15572666	PIAS-1-mediated sumoylation decreases p73 transcriptional activity on several target promoters, such as Bax. p73 is colocalized in the nucleus with PIAS-1, and sumoylated p73 is located exclusively in the nuclear matrix.	transcription
79201	1	335812	6	NULL	NULL	0	NULL	PIAS-1	GP		mediates					sumoylation	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_24_10593_s_6	15572666	PIAS-1-mediated sumoylation decreases p73 transcriptional activity on several target promoters, such as Bax. p73 is colocalized in the nucleus with PIAS-1, and sumoylated p73 is located exclusively in the nuclear matrix.	transcription
79202	2	335812	6	NULL	NULL	0	NULL	statement 1	Process		decreases					p73	GP	transcriptional activity of 			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_24_10593_s_6	15572666	PIAS-1-mediated sumoylation decreases p73 transcriptional activity on several target promoters, such as Bax. p73 is colocalized in the nucleus with PIAS-1, and sumoylated p73 is located exclusively in the nuclear matrix.	transcription
79203	3	335812	6	NULL	NULL	0	NULL	p73	GP		is localized in					nucleus	CellComponent				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_24_10593_s_6	15572666	PIAS-1-mediated sumoylation decreases p73 transcriptional activity on several target promoters, such as Bax. p73 is colocalized in the nucleus with PIAS-1, and sumoylated p73 is located exclusively in the nuclear matrix.	transcription
79204	4	335812	6	NULL	NULL	0	NULL	PIAS-1	GP		is localized in					nucleus	CellComponent				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_24_10593_s_6	15572666	PIAS-1-mediated sumoylation decreases p73 transcriptional activity on several target promoters, such as Bax. p73 is colocalized in the nucleus with PIAS-1, and sumoylated p73 is located exclusively in the nuclear matrix.	transcription
79205	5	335812	6	NULL	NULL	0	NULL	p73	GP	sumoylated	is localized in					nuclear matrix	CellComponent				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_24_10593_s_6	15572666	PIAS-1-mediated sumoylation decreases p73 transcriptional activity on several target promoters, such as Bax. p73 is colocalized in the nucleus with PIAS-1, and sumoylated p73 is located exclusively in the nuclear matrix.	transcription
58686	1	335813	5	NULL	NULL	0	NULL	Bax			is translocated to					mitochondria					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_1	14634023	p73 Induces apoptosis via PUMA transactivation and Bax mitochondrial translocation.	transcription
58687	2	335813	5	NULL	NULL	0	NULL	p73			induce					apoptosis					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_1	14634023	p73 Induces apoptosis via PUMA transactivation and Bax mitochondrial translocation.	transcription
58688	3	335813	5	NULL	NULL	0	NULL	statement 2			via					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_1	14634023	p73 Induces apoptosis via PUMA transactivation and Bax mitochondrial translocation.	transcription
58689	4	335813	5	NULL	NULL	0	NULL	statement 2			via					PUMA		transactivation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_1	14634023	p73 Induces apoptosis via PUMA transactivation and Bax mitochondrial translocation.	transcription
79206	1	335813	6	NULL	NULL	0	NULL	p73	GP		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_1	14634023	p73 Induces apoptosis via PUMA transactivation and Bax mitochondrial translocation.	transcription
79207	2	335813	6	NULL	NULL	0	NULL	statement 1	Process		occurs via					PUMA	GP	transactivation of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_1	14634023	p73 Induces apoptosis via PUMA transactivation and Bax mitochondrial translocation.	transcription
79208	3	335813	6	NULL	NULL	0	NULL	Bax	GP		is translocated to					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_1	14634023	p73 Induces apoptosis via PUMA transactivation and Bax mitochondrial translocation.	transcription
79209	4	335813	6	NULL	NULL	0	NULL	statement 1	Process		occurs via					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_1	14634023	p73 Induces apoptosis via PUMA transactivation and Bax mitochondrial translocation.	transcription
58695	1	335814	5	NULL	NULL	0	NULL	Bax			is translocated to					mitochondria					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_151	14634023	These results indicate that p73 induces the mitochondrial translocation of Bax through indirect mechanisms.	transcription
58696	2	335814	5	NULL	NULL	0	NULL	p73			induce		indirectly			statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_151	14634023	These results indicate that p73 induces the mitochondrial translocation of Bax through indirect mechanisms.	transcription
79210	1	335814	6	NULL	NULL	0	NULL	Bax	GP		is translocated to					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_151	14634023	These results indicate that p73 induces the mitochondrial translocation of Bax through indirect mechanisms.	transcription
79211	2	335814	6	NULL	NULL	0	NULL	p73	GP		induces					statement 1	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_151	14634023	These results indicate that p73 induces the mitochondrial translocation of Bax through indirect mechanisms.	transcription
58697	1	335815	5	NULL	NULL	0	NULL	Bax			is translocated to					mitochondria					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_260	14634023	p73 induces apoptosis via PUMA-mediated Bax mitochondrial translocation.	transcription
58698	2	335815	5	NULL	NULL	0	NULL	PUMA			mediates					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_260	14634023	p73 induces apoptosis via PUMA-mediated Bax mitochondrial translocation.	transcription
58699	3	335815	5	NULL	NULL	0	NULL	p73			induce					apoptosis					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_260	14634023	p73 induces apoptosis via PUMA-mediated Bax mitochondrial translocation.	transcription
58700	4	335815	5	NULL	NULL	0	NULL	statement 3			via					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_260	14634023	p73 induces apoptosis via PUMA-mediated Bax mitochondrial translocation.	transcription
79212	1	335815	6	NULL	NULL	0	NULL	Bax	GP		is translocated to					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_260	14634023	p73 induces apoptosis via PUMA-mediated Bax mitochondrial translocation.	transcription
79213	2	335815	6	NULL	NULL	0	NULL	PUMA	Chemical		mediates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_260	14634023	p73 induces apoptosis via PUMA-mediated Bax mitochondrial translocation.	transcription
79214	3	335815	6	NULL	NULL	0	NULL	p73	GP		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_260	14634023	p73 induces apoptosis via PUMA-mediated Bax mitochondrial translocation.	transcription
79215	4	335815	6	NULL	NULL	0	NULL	statement 3	Process		occurs via					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_260	14634023	p73 induces apoptosis via PUMA-mediated Bax mitochondrial translocation.	transcription
79216	1	335816	6	NULL	NULL	0	NULL	Bax	GP		activates					transcription	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10202_s_354	10744705	WT1 represses p73- and p53-dependent transcription activation from the  bax and the  mdm2 promoters.	transcription
79217	2	335816	6	NULL	NULL	0	NULL	statement 1	Process		is dependent on					p73	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10202_s_354	10744705	WT1 represses p73- and p53-dependent transcription activation from the  bax and the  mdm2 promoters.	transcription
79218	3	335816	6	NULL	NULL	0	NULL	WT1	GP		represses					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10202_s_354	10744705	WT1 represses p73- and p53-dependent transcription activation from the  bax and the  mdm2 promoters.	transcription
79219	4	335816	6	NULL	NULL	0	NULL	mdm2	GP		activates					transcription	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10202_s_354	10744705	WT1 represses p73- and p53-dependent transcription activation from the  bax and the  mdm2 promoters.	transcription
79220	5	335816	6	NULL	NULL	0	NULL	statement 4	Process		is dependent on					p53	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10202_s_354	10744705	WT1 represses p73- and p53-dependent transcription activation from the  bax and the  mdm2 promoters.	transcription
79221	6	335816	6	NULL	NULL	0	NULL	WT1	GP		represses					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10202_s_354	10744705	WT1 represses p73- and p53-dependent transcription activation from the  bax and the  mdm2 promoters.	transcription
58701	1	335817	5	NULL	NULL	0	NULL	Bax			is translocated from					cytosol					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_112	14634023	p73 Indirectly Induces Bax Mitochondrial Relocalization --  Bax translocation from cytosol to mitochondria is a critical step in p53-mediated apoptosis ( ).	transcription
58702	2	335817	5	NULL	NULL	0	NULL	Bax			is translocated to					mitochondria					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_112	14634023	p73 Indirectly Induces Bax Mitochondrial Relocalization --  Bax translocation from cytosol to mitochondria is a critical step in p53-mediated apoptosis ( ).	transcription
58703	3	335817	5	NULL	NULL	0	NULL	statement 1			occurs simultaneously with					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_112	14634023	p73 Indirectly Induces Bax Mitochondrial Relocalization --  Bax translocation from cytosol to mitochondria is a critical step in p53-mediated apoptosis ( ).	transcription
58704	4	335817	5	NULL	NULL	0	NULL	p53			mediates					apoptosis					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_112	14634023	p73 Indirectly Induces Bax Mitochondrial Relocalization --  Bax translocation from cytosol to mitochondria is a critical step in p53-mediated apoptosis ( ).	transcription
58705	5	335817	5	NULL	NULL	0	NULL	statement 3			is critical for					statement 4					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_112	14634023	p73 Indirectly Induces Bax Mitochondrial Relocalization --  Bax translocation from cytosol to mitochondria is a critical step in p53-mediated apoptosis ( ).	transcription
58706	6	335817	5	NULL	NULL	0	NULL	p73			induce		indirectly			statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_112	14634023	p73 Indirectly Induces Bax Mitochondrial Relocalization --  Bax translocation from cytosol to mitochondria is a critical step in p53-mediated apoptosis ( ).	transcription
79222	1	335817	6	NULL	NULL	0	NULL	Bax	GP		is translocated to					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_112	14634023	p73 Indirectly Induces Bax Mitochondrial Relocalization --  Bax translocation from cytosol to mitochondria is a critical step in p53-mediated apoptosis ( ).	transcription
79223	2	335817	6	NULL	NULL	0	NULL	Bax	GP		is translocated from					cytosol	CellComponent				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_112	14634023	p73 Indirectly Induces Bax Mitochondrial Relocalization --  Bax translocation from cytosol to mitochondria is a critical step in p53-mediated apoptosis ( ).	transcription
79224	3	335817	6	NULL	NULL	0	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_112	14634023	p73 Indirectly Induces Bax Mitochondrial Relocalization --  Bax translocation from cytosol to mitochondria is a critical step in p53-mediated apoptosis ( ).	transcription
79225	4	335817	6	NULL	NULL	0	NULL	p73	GP		induces					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_112	14634023	p73 Indirectly Induces Bax Mitochondrial Relocalization --  Bax translocation from cytosol to mitochondria is a critical step in p53-mediated apoptosis ( ).	transcription
58707	1	335819	5	NULL	NULL	0	NULL	p53 virus		infection of	induce					p21		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_195	11706030	Apparently, expression of p21 and Bax was induced by infection of the p53 and p73 viruses (Fig.  6,  A and  B,  p21 and  Bax panels,  lanes 1 and  2).	transcription
58708	2	335819	5	NULL	NULL	0	NULL	p73 virus		infection of	induce					p21		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_195	11706030	Apparently, expression of p21 and Bax was induced by infection of the p53 and p73 viruses (Fig.  6,  A and  B,  p21 and  Bax panels,  lanes 1 and  2).	transcription
58709	3	335819	5	NULL	NULL	0	NULL	p73 virus		infection of	induce					Bax		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_195	11706030	Apparently, expression of p21 and Bax was induced by infection of the p53 and p73 viruses (Fig.  6,  A and  B,  p21 and  Bax panels,  lanes 1 and  2).	transcription
58710	4	335819	5	NULL	NULL	0	NULL	p53 virus		infection of	induce					Bax		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_195	11706030	Apparently, expression of p21 and Bax was induced by infection of the p53 and p73 viruses (Fig.  6,  A and  B,  p21 and  Bax panels,  lanes 1 and  2).	transcription
79226	1	335819	6	NULL	NULL	0	NULL	p53	GP		induces					p21	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_195	11706030	Apparently, expression of p21 and Bax was induced by infection of the p53 and p73 viruses (Fig.  6,  A and  B,  p21 and  Bax panels,  lanes 1 and  2).	transcription
79227	2	335819	6	NULL	NULL	0	NULL	p73	GP		induces					Bax	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_195	11706030	Apparently, expression of p21 and Bax was induced by infection of the p53 and p73 viruses (Fig.  6,  A and  B,  p21 and  Bax panels,  lanes 1 and  2).	transcription
58711	1	335820	5	NULL	NULL	0	NULL	p73			cooperates with					p53					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_7_5945_s_21	15572378	p73 cooperates with p53 to induce specific targets such as PERP, Bax, and Noxa, which are involved in the p53-mediated induction of apoptosis.	transcription
58712	2	335820	5	NULL	NULL	0	NULL	statement 1			induce					PERP					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_7_5945_s_21	15572378	p73 cooperates with p53 to induce specific targets such as PERP, Bax, and Noxa, which are involved in the p53-mediated induction of apoptosis.	transcription
58713	3	335820	5	NULL	NULL	0	NULL	statement 1			induce					Bax					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_7_5945_s_21	15572378	p73 cooperates with p53 to induce specific targets such as PERP, Bax, and Noxa, which are involved in the p53-mediated induction of apoptosis.	transcription
58714	4	335820	5	NULL	NULL	0	NULL	statement 1			induce					Noxa					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_7_5945_s_21	15572378	p73 cooperates with p53 to induce specific targets such as PERP, Bax, and Noxa, which are involved in the p53-mediated induction of apoptosis.	transcription
58715	5	335820	5	NULL	NULL	0	NULL	p53			induce					apoptosis					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_7_5945_s_21	15572378	p73 cooperates with p53 to induce specific targets such as PERP, Bax, and Noxa, which are involved in the p53-mediated induction of apoptosis.	transcription
58716	6	335820	5	NULL	NULL	0	NULL	PERP			is involved in					statement 5					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_7_5945_s_21	15572378	p73 cooperates with p53 to induce specific targets such as PERP, Bax, and Noxa, which are involved in the p53-mediated induction of apoptosis.	transcription
58717	7	335820	5	NULL	NULL	0	NULL	Bax			is involved in					statement 5					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_7_5945_s_21	15572378	p73 cooperates with p53 to induce specific targets such as PERP, Bax, and Noxa, which are involved in the p53-mediated induction of apoptosis.	transcription
58718	8	335820	5	NULL	NULL	0	NULL	Noxa			is involved in					statement 5					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_7_5945_s_21	15572378	p73 cooperates with p53 to induce specific targets such as PERP, Bax, and Noxa, which are involved in the p53-mediated induction of apoptosis.	transcription
79228	1	335820	6	NULL	NULL	0	NULL	p53	GP		mediates					apoptosis	Process	induction of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_7_5945_s_21	15572378	p73 cooperates with p53 to induce specific targets such as PERP, Bax, and Noxa, which are involved in the p53-mediated induction of apoptosis.	transcription
79229	2	335820	6	NULL	NULL	0	NULL	PERP	GP		is involved in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_7_5945_s_21	15572378	p73 cooperates with p53 to induce specific targets such as PERP, Bax, and Noxa, which are involved in the p53-mediated induction of apoptosis.	transcription
79230	3	335820	6	NULL	NULL	0	NULL	Bax	GP		is involved in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_7_5945_s_21	15572378	p73 cooperates with p53 to induce specific targets such as PERP, Bax, and Noxa, which are involved in the p53-mediated induction of apoptosis.	transcription
79231	4	335820	6	NULL	NULL	0	NULL	Noxa	GP		is involved in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_7_5945_s_21	15572378	p73 cooperates with p53 to induce specific targets such as PERP, Bax, and Noxa, which are involved in the p53-mediated induction of apoptosis.	transcription
58719	1	335821	5	NULL	NULL	0	NULL	Bax			is apoptotic target of					p53					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_7_5945_s_364	15572378	Exogenous expression of both p53 and p73 in Saos-2 cells resulted in the activation of p53 apoptotic target Bax ( Fig. 9 A).	transcription
58720	2	335821	5	NULL	NULL	0	NULL	p53		exogenous expression of	activates					statement 1					NULL	Saos-2 cells	0	NULL	NULL	NULL	gw70_jbiolchem_280_7_5945_s_364	15572378	Exogenous expression of both p53 and p73 in Saos-2 cells resulted in the activation of p53 apoptotic target Bax ( Fig. 9 A).	transcription
58721	3	335821	5	NULL	NULL	0	NULL	p73		exogenous expression of	activates					statement 1					NULL	Saos-2 cells	0	NULL	NULL	NULL	gw70_jbiolchem_280_7_5945_s_364	15572378	Exogenous expression of both p53 and p73 in Saos-2 cells resulted in the activation of p53 apoptotic target Bax ( Fig. 9 A).	transcription
79232	1	335821	6	NULL	NULL	0	NULL	p53	GP	expression of	results in					Bax	GP	activation of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_7_5945_s_364	15572378	Exogenous expression of both p53 and p73 in Saos-2 cells resulted in the activation of p53 apoptotic target Bax ( Fig. 9 A).	transcription
79233	2	335821	6	NULL	NULL	0	NULL	p73	GP	expression of	results in					Bax	GP	activation of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_7_5945_s_364	15572378	Exogenous expression of both p53 and p73 in Saos-2 cells resulted in the activation of p53 apoptotic target Bax ( Fig. 9 A).	transcription
58722	1	335822	5	NULL	NULL	0	NULL	p73 isoforms		overexpression of	promotes					cell death					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_5	14634023	Overexpression of p73 isoforms promotes cell death and  bax promoter transactivation in a time-dependent manner.	transcription
58723	2	335822	5	NULL	NULL	0	NULL	p73 isoforms		overexpression of	transactivates					Bax				promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_5	14634023	Overexpression of p73 isoforms promotes cell death and  bax promoter transactivation in a time-dependent manner.	transcription
79234	1	335822	6	NULL	NULL	0	NULL	p73 isoforms	GP	overexpression of	promotes					cell death	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_5	14634023	Overexpression of p73 isoforms promotes cell death and  bax promoter transactivation in a time-dependent manner.	transcription
79235	2	335822	6	NULL	NULL	0	NULL	p73 isoforms	GP	overexpression of	results in					Bax 	GP	transactivation of 		promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_5	14634023	Overexpression of p73 isoforms promotes cell death and  bax promoter transactivation in a time-dependent manner.	transcription
58724	1	335823	5	NULL	NULL	0	NULL	Bax		translocation of	is induced by		may;;directly			p73 protein					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_139	14634023	At the same time, the experiment would elucidate if Bax translocation is directly induced by the p73 protein  per se.	transcription
58725	1	335824	5	NULL	NULL	0	NULL	bax-Pruc		transactivation of	is dependent on					p73					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_214	14634023	The results show that delta84p73beta strongly inhibited both p73- and p53-dependent transactivation of the  bax-Pruc ( Fig. 7 A).	transcription
58726	2	335824	5	NULL	NULL	0	NULL	bax-Pruc		transactivation of	is dependent on					p53					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_214	14634023	The results show that delta84p73beta strongly inhibited both p73- and p53-dependent transactivation of the  bax-Pruc ( Fig. 7 A).	transcription
58727	3	335824	5	NULL	NULL	0	NULL	delta84p73beta			inhibits		strongly			statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_214	14634023	The results show that delta84p73beta strongly inhibited both p73- and p53-dependent transactivation of the  bax-Pruc ( Fig. 7 A).	transcription
58728	4	335824	5	NULL	NULL	0	NULL	delta84p73beta			inhibits		strongly			statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_214	14634023	The results show that delta84p73beta strongly inhibited both p73- and p53-dependent transactivation of the  bax-Pruc ( Fig. 7 A).	transcription
79236	1	335824	6	NULL	NULL	0	NULL	p73	GP		transactivates					Bax-Prunc	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_214	14634023	The results show that delta84p73beta strongly inhibited both p73- and p53-dependent transactivation of the  bax-Pruc ( Fig. 7 A).	transcription
79237	2	335824	6	NULL	NULL	0	NULL	p53	GP		transactivates					Bax-Prunc	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_214	14634023	The results show that delta84p73beta strongly inhibited both p73- and p53-dependent transactivation of the  bax-Pruc ( Fig. 7 A).	transcription
79238	3	335824	6	NULL	NULL	0	NULL	delta84p73beta	GP		inhibits		strongly			statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_214	14634023	The results show that delta84p73beta strongly inhibited both p73- and p53-dependent transactivation of the  bax-Pruc ( Fig. 7 A).	transcription
79239	4	335824	6	NULL	NULL	0	NULL	delta84p73beta	GP		inhibits		strongly			statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_214	14634023	The results show that delta84p73beta strongly inhibited both p73- and p53-dependent transactivation of the  bax-Pruc ( Fig. 7 A).	transcription
58729	1	335825	5	NULL	NULL	0	NULL	deltaNp73			does not activate					transcription					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_236	14634023	As shown in  Fig. 7 B, deltaNp73 did not have transcriptional activity but efficiently inhibited p73- and p53-dependent transactivation of  bax-PrLuc.	transcription
58730	2	335825	5	NULL	NULL	0	NULL	bax-PrLuc		transactivation of	is dependent on					p53					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_236	14634023	As shown in  Fig. 7 B, deltaNp73 did not have transcriptional activity but efficiently inhibited p73- and p53-dependent transactivation of  bax-PrLuc.	transcription
58731	3	335825	5	NULL	NULL	0	NULL	bax-PrLuc		transactivation of	is dependent on					p73					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_236	14634023	As shown in  Fig. 7 B, deltaNp73 did not have transcriptional activity but efficiently inhibited p73- and p53-dependent transactivation of  bax-PrLuc.	transcription
58732	4	335825	5	NULL	NULL	0	NULL	deltaNp73			inhibit		efficiently			statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_236	14634023	As shown in  Fig. 7 B, deltaNp73 did not have transcriptional activity but efficiently inhibited p73- and p53-dependent transactivation of  bax-PrLuc.	transcription
58733	5	335825	5	NULL	NULL	0	NULL	deltaNp73			inhibit		efficiently			statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_236	14634023	As shown in  Fig. 7 B, deltaNp73 did not have transcriptional activity but efficiently inhibited p73- and p53-dependent transactivation of  bax-PrLuc.	transcription
58734	1	335826	5	NULL	NULL	0	NULL	p73			induce					cell death					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_249	14634023	Therefore, p73-induced cell death cannot rely only on the ability of p73 to up-regulate  bax expression.	transcription
58735	2	335826	5	NULL	NULL	0	NULL	p73			up-regulates					bax		expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_249	14634023	Therefore, p73-induced cell death cannot rely only on the ability of p73 to up-regulate  bax expression.	transcription
58736	3	335826	5	NULL	NULL	0	NULL	statement 1			does not rely on					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_249	14634023	Therefore, p73-induced cell death cannot rely only on the ability of p73 to up-regulate  bax expression.	transcription
79240	1	335826	6	NULL	NULL	0	NULL	p73	GP		up-regulates					bax	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_249	14634023	Therefore, p73-induced cell death cannot rely only on the ability of p73 to up-regulate  bax expression.	transcription
58737	1	335827	5	NULL	NULL	0	NULL	p53			regulates					BAX					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_4_2249_s_20	12427762	For example, p73 induces p53-regulated  BAX in A2870 ovarian cells but not in H1229 lung cancer cells ( ,  ).	transcription
58738	2	335827	5	NULL	NULL	0	NULL	p73			induces					statement 1					NULL	A2870 ovarian cells	0	NULL	NULL	NULL	gw70_jbiolchem_278_4_2249_s_20	12427762	For example, p73 induces p53-regulated  BAX in A2870 ovarian cells but not in H1229 lung cancer cells ( ,  ).	transcription
58739	3	335827	5	NULL	NULL	0	NULL	p73			does not induce					statement 1					NULL	H1229 lung cancer cells	0	NULL	NULL	NULL	gw70_jbiolchem_278_4_2249_s_20	12427762	For example, p73 induces p53-regulated  BAX in A2870 ovarian cells but not in H1229 lung cancer cells ( ,  ).	transcription
79241	1	335827	6	NULL	NULL	0	NULL	p53	GP		regulates					BAX	GP				NULL	A2870 ovarian cells	0	NULL	NULL	NULL	gw70_jbiolchem_278_4_2249_s_20	12427762	For example, p73 induces p53-regulated  BAX in A2870 ovarian cells but not in H1229 lung cancer cells ( ,  ).	transcription
79242	2	335827	6	NULL	NULL	0	NULL	p73	GP		induces					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_4_2249_s_20	12427762	For example, p73 induces p53-regulated  BAX in A2870 ovarian cells but not in H1229 lung cancer cells ( ,  ).	transcription
79243	3	335827	6	NULL	NULL	0	NULL	p73	GP		does not induce					statement 1	Process				NULL	H1229 lung cancer cells	0	NULL	NULL	NULL	gw70_jbiolchem_278_4_2249_s_20	12427762	For example, p73 induces p53-regulated  BAX in A2870 ovarian cells but not in H1229 lung cancer cells ( ,  ).	transcription
58740	1	335828	5	NULL	NULL	0	NULL	apoptosis			is dependent on					p53					NULL		0	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_28	12086844	Remarkably, however, loss of p63 and p73 severely affected the induction of  bax and  PERP, two genes thought to mediate p53-dependent apoptosis.	transcription
58741	2	335828	5	NULL	NULL	0	NULL	bax gene			mediates					statement 1					NULL		0	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_28	12086844	Remarkably, however, loss of p63 and p73 severely affected the induction of  bax and  PERP, two genes thought to mediate p53-dependent apoptosis.	transcription
58742	3	335828	5	NULL	NULL	0	NULL	PERP gene			mediates					statement 1					NULL		0	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_28	12086844	Remarkably, however, loss of p63 and p73 severely affected the induction of  bax and  PERP, two genes thought to mediate p53-dependent apoptosis.	transcription
58743	4	335828	5	NULL	NULL	0	NULL	p63		loss of	affects		severely			bax gene		induction of			NULL		0	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_28	12086844	Remarkably, however, loss of p63 and p73 severely affected the induction of  bax and  PERP, two genes thought to mediate p53-dependent apoptosis.	transcription
58744	5	335828	5	NULL	NULL	0	NULL	p63		loss of	affects		severely			PERP gene		induction of			NULL		NULL	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_28	12086844	Remarkably, however, loss of p63 and p73 severely affected the induction of  bax and  PERP, two genes thought to mediate p53-dependent apoptosis.	transcription
58745	6	335828	5	NULL	NULL	0	NULL	p73		loss of	affects		severely			bax gene		induction of			NULL		0	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_28	12086844	Remarkably, however, loss of p63 and p73 severely affected the induction of  bax and  PERP, two genes thought to mediate p53-dependent apoptosis.	transcription
58746	7	335828	5	NULL	NULL	0	NULL	p73		loss of	affects		severely			PERP gene		induction of			NULL		NULL	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_28	12086844	Remarkably, however, loss of p63 and p73 severely affected the induction of  bax and  PERP, two genes thought to mediate p53-dependent apoptosis.	transcription
58747	1	335829	5	NULL	NULL	0	NULL	p21			is a type of					p53 target gene					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_2_513_s_17	10606650	p73 can transcriptionally activate p53 target genes such as p21 or BAX and induces apoptosis in p53-null Saos-2 cells ( 12, 13).	transcription
58748	2	335829	5	NULL	NULL	0	NULL	BAX			is a type of					p53 target gene					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_2_513_s_17	10606650	p73 can transcriptionally activate p53 target genes such as p21 or BAX and induces apoptosis in p53-null Saos-2 cells ( 12, 13).	transcription
58749	3	335829	5	NULL	NULL	0	NULL	p73			activates		transcriptionaly			p21 gene					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_2_513_s_17	10606650	p73 can transcriptionally activate p53 target genes such as p21 or BAX and induces apoptosis in p53-null Saos-2 cells ( 12, 13).	transcription
58750	4	335829	5	NULL	NULL	0	NULL	p73			activates		transcriptionaly			BAX gene					NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_2_513_s_17	10606650	p73 can transcriptionally activate p53 target genes such as p21 or BAX and induces apoptosis in p53-null Saos-2 cells ( 12, 13).	transcription
58751	5	335829	5	NULL	NULL	0	NULL	p73			induces					apoptosis					NULL	p53-null Saos-2 cells	0	NULL	NULL	NULL	gw60_nucleicacidsres_28_2_513_s_17	10606650	p73 can transcriptionally activate p53 target genes such as p21 or BAX and induces apoptosis in p53-null Saos-2 cells ( 12, 13).	transcription
79244	1	335829	6	NULL	NULL	0	NULL	p73	GP		activates					p21	GP				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_2_513_s_17	10606650	p73 can transcriptionally activate p53 target genes such as p21 or BAX and induces apoptosis in p53-null Saos-2 cells ( 12, 13).	transcription
79245	2	335829	6	NULL	NULL	0	NULL	p73	GP		activates					BAX	GP				NULL		0	NULL	NULL	NULL	gw60_nucleicacidsres_28_2_513_s_17	10606650	p73 can transcriptionally activate p53 target genes such as p21 or BAX and induces apoptosis in p53-null Saos-2 cells ( 12, 13).	transcription
79246	3	335829	6	NULL	NULL	0	NULL	p73	GP		induces					apoptosis	Process				NULL	p53-null Saos-2 cells	0	NULL	NULL	NULL	gw60_nucleicacidsres_28_2_513_s_17	10606650	p73 can transcriptionally activate p53 target genes such as p21 or BAX and induces apoptosis in p53-null Saos-2 cells ( 12, 13).	transcription
58752	1	335830	5	NULL	NULL	0	NULL	ik3-1		co-infection of	does not alter		significantly			p53		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_201	11706030	Co-infection of ik3-1 or ik3-1-deltaC does not significantly alter expression of p53, p73, p21, or Bax.	transcription
58753	2	335830	5	NULL	NULL	0	NULL	ik3-1		co-infection of	does not alter		significantly			p73		expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_201	11706030	Co-infection of ik3-1 or ik3-1-deltaC does not significantly alter expression of p53, p73, p21, or Bax.	transcription
58754	3	335830	5	NULL	NULL	0	NULL	ik3-1		co-infection of	does not alter		significantly			p21		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_201	11706030	Co-infection of ik3-1 or ik3-1-deltaC does not significantly alter expression of p53, p73, p21, or Bax.	transcription
58755	4	335830	5	NULL	NULL	0	NULL	ik3-1		co-infection of	does not alter		significantly			Bax		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_201	11706030	Co-infection of ik3-1 or ik3-1-deltaC does not significantly alter expression of p53, p73, p21, or Bax.	transcription
58756	5	335830	5	NULL	NULL	0	NULL	ik3-1-deltaC		co-infection of	does not alter		significantly			p53		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_201	11706030	Co-infection of ik3-1 or ik3-1-deltaC does not significantly alter expression of p53, p73, p21, or Bax.	transcription
58757	6	335830	5	NULL	NULL	0	NULL	ik3-1-deltaC		co-infection of	does not alter		significantly			p73		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_201	11706030	Co-infection of ik3-1 or ik3-1-deltaC does not significantly alter expression of p53, p73, p21, or Bax.	transcription
58758	7	335830	5	NULL	NULL	0	NULL	ik3-1-deltaC		co-infection of	does not alter		significantly			p21		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_201	11706030	Co-infection of ik3-1 or ik3-1-deltaC does not significantly alter expression of p53, p73, p21, or Bax.	transcription
58759	8	335830	5	NULL	NULL	0	NULL	ik3-1-deltaC		co-infection of	does not alter		significantly			Bax		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_201	11706030	Co-infection of ik3-1 or ik3-1-deltaC does not significantly alter expression of p53, p73, p21, or Bax.	transcription
58760	1	335831	5	NULL	NULL	0	NULL	p73			is a homolog of					p53					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33747_s_251	10559267	The p53 homolog p73 does not selectively inhibit the ability of p53 to activate transcription through the  bax promoter.	transcription
58761	2	335831	5	NULL	NULL	0	NULL	p53			activates					transcription					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33747_s_251	10559267	The p53 homolog p73 does not selectively inhibit the ability of p53 to activate transcription through the  bax promoter.	transcription
58762	3	335831	5	NULL	NULL	0	NULL	statement 2			through					bax				promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33747_s_251	10559267	The p53 homolog p73 does not selectively inhibit the ability of p53 to activate transcription through the  bax promoter.	transcription
58763	4	335831	5	NULL	NULL	0	NULL	p73			does not inhibit		selectively			statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33747_s_251	10559267	The p53 homolog p73 does not selectively inhibit the ability of p53 to activate transcription through the  bax promoter.	transcription
79257	1	335831	6	NULL	NULL	0	NULL	p53	GP		transactivates					bax	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33747_s_251	10559267	The p53 homolog p73 does not selectively inhibit the ability of p53 to activate transcription through the  bax promoter.	transcription
79258	2	335831	6	NULL	NULL	0	NULL	p73	GP		does not inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33747_s_251	10559267	The p53 homolog p73 does not selectively inhibit the ability of p53 to activate transcription through the  bax promoter.	transcription
58764	1	335832	5	NULL	NULL	0	NULL	p63		loss of	affects		severely			bax gene		induction of			NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_25_6_857_s_68	15033906	While induction of  p21 and  MDM2 occurred normally in p63 - / - , p73 - / - , and double-null E1A-expressing MEFs, loss of p63 and p73 severely affected the induction of  bax,  NOXA and  PERP, genes thought to mediate p53-dependent apoptosis.	transcription
58765	2	335832	5	NULL	NULL	0	NULL	p63		loss of	affects		severely			NOXA gene		induction of			NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_25_6_857_s_68	15033906	While induction of  p21 and  MDM2 occurred normally in p63 - / - , p73 - / - , and double-null E1A-expressing MEFs, loss of p63 and p73 severely affected the induction of  bax,  NOXA and  PERP, genes thought to mediate p53-dependent apoptosis.	transcription
58766	3	335832	5	NULL	NULL	0	NULL	p63		loss of	affects		severely			PERP gene		induction of			NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_25_6_857_s_68	15033906	While induction of  p21 and  MDM2 occurred normally in p63 - / - , p73 - / - , and double-null E1A-expressing MEFs, loss of p63 and p73 severely affected the induction of  bax,  NOXA and  PERP, genes thought to mediate p53-dependent apoptosis.	transcription
58767	4	335832	5	NULL	NULL	0	NULL	p73 		loss of	affects		severely			bax gene		induction of			NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_25_6_857_s_68	15033906	While induction of  p21 and  MDM2 occurred normally in p63 - / - , p73 - / - , and double-null E1A-expressing MEFs, loss of p63 and p73 severely affected the induction of  bax,  NOXA and  PERP, genes thought to mediate p53-dependent apoptosis.	transcription
58768	5	335832	5	NULL	NULL	0	NULL	p73		loss of	affects		severely			NOXA gene		induction of			NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_25_6_857_s_68	15033906	While induction of  p21 and  MDM2 occurred normally in p63 - / - , p73 - / - , and double-null E1A-expressing MEFs, loss of p63 and p73 severely affected the induction of  bax,  NOXA and  PERP, genes thought to mediate p53-dependent apoptosis.	transcription
58769	6	335832	5	NULL	NULL	0	NULL	p73		loss of	affects		severely			PERP gene		induction of			NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_25_6_857_s_68	15033906	While induction of  p21 and  MDM2 occurred normally in p63 - / - , p73 - / - , and double-null E1A-expressing MEFs, loss of p63 and p73 severely affected the induction of  bax,  NOXA and  PERP, genes thought to mediate p53-dependent apoptosis.	transcription
58770	7	335832	5	NULL	NULL	0	NULL	apoptosis			is dependent on					p53					NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_25_6_857_s_68	15033906	While induction of  p21 and  MDM2 occurred normally in p63 - / - , p73 - / - , and double-null E1A-expressing MEFs, loss of p63 and p73 severely affected the induction of  bax,  NOXA and  PERP, genes thought to mediate p53-dependent apoptosis.	transcription
58771	8	335832	5	NULL	NULL	0	NULL	bax gene			mediates		may			statement 7					NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_25_6_857_s_68	15033906	While induction of  p21 and  MDM2 occurred normally in p63 - / - , p73 - / - , and double-null E1A-expressing MEFs, loss of p63 and p73 severely affected the induction of  bax,  NOXA and  PERP, genes thought to mediate p53-dependent apoptosis.	transcription
58772	9	335832	5	NULL	NULL	0	NULL	NOXA gene			mediates		may			statement 7					NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_25_6_857_s_68	15033906	While induction of  p21 and  MDM2 occurred normally in p63 - / - , p73 - / - , and double-null E1A-expressing MEFs, loss of p63 and p73 severely affected the induction of  bax,  NOXA and  PERP, genes thought to mediate p53-dependent apoptosis.	transcription
58773	10	335832	5	NULL	NULL	0	NULL	PERP gene			mediates		may			statement 7					NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_25_6_857_s_68	15033906	While induction of  p21 and  MDM2 occurred normally in p63 - / - , p73 - / - , and double-null E1A-expressing MEFs, loss of p63 and p73 severely affected the induction of  bax,  NOXA and  PERP, genes thought to mediate p53-dependent apoptosis.	transcription
58774	1	335833	5	NULL	NULL	0	NULL	Bax			is a type of					proapoptotic gene					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58775	2	335833	5	NULL	NULL	0	NULL	PIG3			is a type of					proapoptotic gene					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58776	3	335833	5	NULL	NULL	0	NULL	PUMA			is a type of					proapoptotic gene					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58777	4	335833	5	NULL	NULL	0	NULL	p63			transactivates					Bax				promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58778	5	335833	5	NULL	NULL	0	NULL	p63			transactivates					PIG3				promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58779	6	335833	5	NULL	NULL	0	NULL	p63			transactivates					PUMA				promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58780	7	335833	5	NULL	NULL	0	NULL	p73			transactivates					Bax				promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58781	8	335833	5	NULL	NULL	0	NULL	p73			transactivates					PIG3				promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58782	9	335833	5	NULL	NULL	0	NULL	p73			transactivates					PUMA				promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58783	10	335833	5	NULL	NULL	0	NULL	ASPP1			stimulates					statement 4					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58784	11	335833	5	NULL	NULL	0	NULL	ASPP1			stimulates					statement 5					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58785	12	335833	5	NULL	NULL	0	NULL	ASPP1			stimulates					statement 6					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58786	13	335833	5	NULL	NULL	0	NULL	ASPP1			stimulates					statement 7					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58787	14	335833	5	NULL	NULL	0	NULL	ASPP1			stimulates					statement 8					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58788	15	335833	5	NULL	NULL	0	NULL	ASPP1			stimulates					statement 9					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58789	16	335833	5	NULL	NULL	0	NULL	ASPP2 			stimulates					statement 4					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58790	17	335833	5	NULL	NULL	0	NULL	ASPP2			stimulates					statement 5					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58791	18	335833	5	NULL	NULL	0	NULL	ASPP2			stimulates					statement 6					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58792	19	335833	5	NULL	NULL	0	NULL	ASPP2			stimulates					statement 7					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58793	20	335833	5	NULL	NULL	0	NULL	ASPP2			stimulates					statement 8					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58794	21	335833	5	NULL	NULL	0	NULL	ASPP2			stimulates					statement 9					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58795	22	335833	5	NULL	NULL	0	NULL	ASPP1			stimulates					p63		apoptotic function of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58796	23	335833	5	NULL	NULL	0	NULL	ASPP2			stimulates					p63		apoptotic function of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58797	24	335833	5	NULL	NULL	0	NULL	ASPP1			stimulates					p73		apoptotic function of			NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58798	25	335833	5	NULL	NULL	0	NULL	ASPP2			stimulates					p73		apoptotic function of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
79553	1	335833	6	NULL	NULL	0	NULL	ASPP1	GP		stimulates					p63	GP	apoptotic activity of 			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
79554	2	335833	6	NULL	NULL	0	NULL	ASPP2	GP		activates					p63	GP	apoptotic activity of 			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
79555	3	335833	6	NULL	NULL	0	NULL	ASPP1	GP		stimulates					p73	GP	apoptotic activity of 			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
79556	4	335833	6	NULL	NULL	0	NULL	ASPP2	GP		stimulates					p73	GP	apoptotic activity of 			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1341_s_188	14729977	Since expression of ASPP1 or ASPP2 stimulated the transactivation function of p63 and p73 on promoters of proapoptotic genes, such as Bax, PIG3, and PUMA, it is likely that ASPP1 and ASPP2 also stimulate the apoptotic function of p63 and p73.	transcription
58799	1	335834	5	NULL	NULL	0	NULL	bax gene			is a target of		endogenous			p53					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10202_s_292	10744705	WT1 Inhibits the Induction of Endogenous Mdm2 Protein by p73 and p53-- The  bax ( 48) and  mdm2 ( 57,  58) genes have been documented to be endogenous targets of p53, and p73 is also known to stimulate the expression of Mdm2 ( 45).	transcription
58800	2	335834	5	NULL	NULL	0	NULL	bax gene			is a target of		endogenous			p73					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10202_s_292	10744705	WT1 Inhibits the Induction of Endogenous Mdm2 Protein by p73 and p53-- The  bax ( 48) and  mdm2 ( 57,  58) genes have been documented to be endogenous targets of p53, and p73 is also known to stimulate the expression of Mdm2 ( 45).	transcription
58801	3	335834	5	NULL	NULL	0	NULL	mdm2 gene			is a target of		endogenous			p63					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10202_s_292	10744705	WT1 Inhibits the Induction of Endogenous Mdm2 Protein by p73 and p53-- The  bax ( 48) and  mdm2 ( 57,  58) genes have been documented to be endogenous targets of p53, and p73 is also known to stimulate the expression of Mdm2 ( 45).	transcription
58802	4	335834	5	NULL	NULL	0	NULL	mdm2 gene			is a target of		endogenous			p73					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10202_s_292	10744705	WT1 Inhibits the Induction of Endogenous Mdm2 Protein by p73 and p53-- The  bax ( 48) and  mdm2 ( 57,  58) genes have been documented to be endogenous targets of p53, and p73 is also known to stimulate the expression of Mdm2 ( 45).	transcription
58803	5	335834	5	NULL	NULL	0	NULL	mdm2 gene			stimulates					Mdm2		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10202_s_292	10744705	WT1 Inhibits the Induction of Endogenous Mdm2 Protein by p73 and p53-- The  bax ( 48) and  mdm2 ( 57,  58) genes have been documented to be endogenous targets of p53, and p73 is also known to stimulate the expression of Mdm2 ( 45).	transcription
58804	6	335834	5	NULL	NULL	0	NULL	bax gene			stimulates					Mdm2		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10202_s_292	10744705	WT1 Inhibits the Induction of Endogenous Mdm2 Protein by p73 and p53-- The  bax ( 48) and  mdm2 ( 57,  58) genes have been documented to be endogenous targets of p53, and p73 is also known to stimulate the expression of Mdm2 ( 45).	transcription
58805	7	335834	5	NULL	NULL	0	NULL	p73			induce					Mdm2 Protein		endogenous			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10202_s_292	10744705	WT1 Inhibits the Induction of Endogenous Mdm2 Protein by p73 and p53-- The  bax ( 48) and  mdm2 ( 57,  58) genes have been documented to be endogenous targets of p53, and p73 is also known to stimulate the expression of Mdm2 ( 45).	transcription
58806	8	335834	5	NULL	NULL	0	NULL	p53			induce					Mdm2 Protein		endogenous			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10202_s_292	10744705	WT1 Inhibits the Induction of Endogenous Mdm2 Protein by p73 and p53-- The  bax ( 48) and  mdm2 ( 57,  58) genes have been documented to be endogenous targets of p53, and p73 is also known to stimulate the expression of Mdm2 ( 45).	transcription
58807	9	335834	5	NULL	NULL	0	NULL	WT1			inhibits					statement 7					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10202_s_292	10744705	WT1 Inhibits the Induction of Endogenous Mdm2 Protein by p73 and p53-- The  bax ( 48) and  mdm2 ( 57,  58) genes have been documented to be endogenous targets of p53, and p73 is also known to stimulate the expression of Mdm2 ( 45).	transcription
58808	10	335834	5	NULL	NULL	0	NULL	WT1			inhibits					statement 8					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10202_s_292	10744705	WT1 Inhibits the Induction of Endogenous Mdm2 Protein by p73 and p53-- The  bax ( 48) and  mdm2 ( 57,  58) genes have been documented to be endogenous targets of p53, and p73 is also known to stimulate the expression of Mdm2 ( 45).	transcription
79550	1	335834	6	NULL	NULL	0	NULL	p73	GP		induces					Mdm2	GP	induction of;; endogenous			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10202_s_292	10744705	WT1 Inhibits the Induction of Endogenous Mdm2 Protein by p73 and p53-- The  bax ( 48) and  mdm2 ( 57,  58) genes have been documented to be endogenous targets of p53, and p73 is also known to stimulate the expression of Mdm2 ( 45).	transcription
79552	2	335834	6	NULL	NULL	0	NULL	p53	GP		induces					mdm2	GP	endogenous			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_14_10202_s_292	10744705	WT1 Inhibits the Induction of Endogenous Mdm2 Protein by p73 and p53-- The  bax ( 48) and  mdm2 ( 57,  58) genes have been documented to be endogenous targets of p53, and p73 is also known to stimulate the expression of Mdm2 ( 45).	transcription
58817	1	335835	5	NULL	NULL	0	NULL	cisplatin		transfection	upregulates					Bax		expression of			NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_193	12535517	Both cisplatin and YAP transfection-induced upregulation of Bax expression are almost completely reversed by treatment of the cells with siRNA oligonucleotides to human p73   (Figure 6A), revealing that they both require p73 function to induce the expression of the proapoptotic Bax protein in this system.	transcription
58818	2	335835	5	NULL	NULL	0	NULL	YAP		transfection	upregulates					Bax		expression of			NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_193	12535517	Both cisplatin and YAP transfection-induced upregulation of Bax expression are almost completely reversed by treatment of the cells with siRNA oligonucleotides to human p73   (Figure 6A), revealing that they both require p73 function to induce the expression of the proapoptotic Bax protein in this system.	transcription
58819	3	335835	5	NULL	NULL	0	NULL	p73 siRNA oligonucleotides		human	reverse		completely			statement 1					NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_193	12535517	Both cisplatin and YAP transfection-induced upregulation of Bax expression are almost completely reversed by treatment of the cells with siRNA oligonucleotides to human p73   (Figure 6A), revealing that they both require p73 function to induce the expression of the proapoptotic Bax protein in this system.	transcription
58820	4	335835	5	NULL	NULL	0	NULL	p73 siRNA oligonucleotides		human	reverse		completely			statement 2					NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_193	12535517	Both cisplatin and YAP transfection-induced upregulation of Bax expression are almost completely reversed by treatment of the cells with siRNA oligonucleotides to human p73   (Figure 6A), revealing that they both require p73 function to induce the expression of the proapoptotic Bax protein in this system.	transcription
58821	5	335835	5	NULL	NULL	0	NULL	statement 1			requires					p73		function of			NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_193	12535517	Both cisplatin and YAP transfection-induced upregulation of Bax expression are almost completely reversed by treatment of the cells with siRNA oligonucleotides to human p73   (Figure 6A), revealing that they both require p73 function to induce the expression of the proapoptotic Bax protein in this system.	transcription
58822	6	335835	5	NULL	NULL	0	NULL	statement 2			requires					p73		function of			NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_193	12535517	Both cisplatin and YAP transfection-induced upregulation of Bax expression are almost completely reversed by treatment of the cells with siRNA oligonucleotides to human p73   (Figure 6A), revealing that they both require p73 function to induce the expression of the proapoptotic Bax protein in this system.	transcription
58823	7	335835	5	NULL	NULL	0	NULL	Bax protein			is a type of					proapoptotic protein					NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_1_11_s_193	12535517	Both cisplatin and YAP transfection-induced upregulation of Bax expression are almost completely reversed by treatment of the cells with siRNA oligonucleotides to human p73   (Figure 6A), revealing that they both require p73 function to induce the expression of the proapoptotic Bax protein in this system.	transcription
79546	1	335835	6	NULL	NULL	0	NULL	cisplatin	Chemical		induces					Bax	GP	upregulation of			NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_193	12535517	Both cisplatin and YAP transfection-induced upregulation of Bax expression are almost completely reversed by treatment of the cells with siRNA oligonucleotides to human p73   (Figure 6A), revealing that they both require p73 function to induce the expression of the proapoptotic Bax protein in this system.	transcription
79547	2	335835	6	NULL	NULL	0	NULL	YAP	GP		induces					Bax	GP	upregulation of			NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_193	12535517	Both cisplatin and YAP transfection-induced upregulation of Bax expression are almost completely reversed by treatment of the cells with siRNA oligonucleotides to human p73   (Figure 6A), revealing that they both require p73 function to induce the expression of the proapoptotic Bax protein in this system.	transcription
79548	3	335835	6	NULL	NULL	0	NULL	p73	GP		reverses					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_193	12535517	Both cisplatin and YAP transfection-induced upregulation of Bax expression are almost completely reversed by treatment of the cells with siRNA oligonucleotides to human p73   (Figure 6A), revealing that they both require p73 function to induce the expression of the proapoptotic Bax protein in this system.	transcription
79549	4	335835	6	NULL	NULL	0	NULL	p73	GP		reverses					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_193	12535517	Both cisplatin and YAP transfection-induced upregulation of Bax expression are almost completely reversed by treatment of the cells with siRNA oligonucleotides to human p73   (Figure 6A), revealing that they both require p73 function to induce the expression of the proapoptotic Bax protein in this system.	transcription
58824	1	335836	5	NULL	NULL	0	NULL	p73			is a homolog of					p53					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33747_s_246	10559267	The p53 Homolog p73 Does Not Selectively Inhibit the Ability of p53 to Activate Transcription through the bax Promoter--  In addition to BoB1 and BoB2, the p53 homolog p73 was examined as a potential explanation for the inability of wild-type p53 to activate transcription through the  bax promoter in MDA-MB-453 cells.	transcription
58825	2	335836	5	NULL	NULL	0	NULL	p53			activates					transcription					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33747_s_246	10559267	The p53 Homolog p73 Does Not Selectively Inhibit the Ability of p53 to Activate Transcription through the bax Promoter--  In addition to BoB1 and BoB2, the p53 homolog p73 was examined as a potential explanation for the inability of wild-type p53 to activate transcription through the  bax promoter in MDA-MB-453 cells.	transcription
58826	3	335836	5	NULL	NULL	0	NULL	statement 2			through					bax				promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33747_s_246	10559267	The p53 Homolog p73 Does Not Selectively Inhibit the Ability of p53 to Activate Transcription through the bax Promoter--  In addition to BoB1 and BoB2, the p53 homolog p73 was examined as a potential explanation for the inability of wild-type p53 to activate transcription through the  bax promoter in MDA-MB-453 cells.	transcription
58827	4	335836	5	NULL	NULL	0	NULL	p73			does not inhibit		selectively			statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33747_s_246	10559267	The p53 Homolog p73 Does Not Selectively Inhibit the Ability of p53 to Activate Transcription through the bax Promoter--  In addition to BoB1 and BoB2, the p53 homolog p73 was examined as a potential explanation for the inability of wild-type p53 to activate transcription through the  bax promoter in MDA-MB-453 cells.	transcription
58828	5	335836	5	NULL	NULL	0	NULL	p53		wild-type	does not activate					transcription					NULL	MDA-MB-453 cells	0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33747_s_246	10559267	The p53 Homolog p73 Does Not Selectively Inhibit the Ability of p53 to Activate Transcription through the bax Promoter--  In addition to BoB1 and BoB2, the p53 homolog p73 was examined as a potential explanation for the inability of wild-type p53 to activate transcription through the  bax promoter in MDA-MB-453 cells.	transcription
58829	6	335836	5	NULL	NULL	0	NULL	statement 5			through					bax				promoter	NULL	MDA-MB-453 cells	0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33747_s_246	10559267	The p53 Homolog p73 Does Not Selectively Inhibit the Ability of p53 to Activate Transcription through the bax Promoter--  In addition to BoB1 and BoB2, the p53 homolog p73 was examined as a potential explanation for the inability of wild-type p53 to activate transcription through the  bax promoter in MDA-MB-453 cells.	transcription
58830	7	335836	5	NULL	NULL	0	NULL	p73			is responsible for					statement 5					NULL	MDA-MB-453 cells	0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33747_s_246	10559267	The p53 Homolog p73 Does Not Selectively Inhibit the Ability of p53 to Activate Transcription through the bax Promoter--  In addition to BoB1 and BoB2, the p53 homolog p73 was examined as a potential explanation for the inability of wild-type p53 to activate transcription through the  bax promoter in MDA-MB-453 cells.	transcription
58831	8	335836	5	NULL	NULL	0	NULL	BoB1			is responsible for					statement 5					NULL	MDA-MB-453 cells	0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33747_s_246	10559267	The p53 Homolog p73 Does Not Selectively Inhibit the Ability of p53 to Activate Transcription through the bax Promoter--  In addition to BoB1 and BoB2, the p53 homolog p73 was examined as a potential explanation for the inability of wild-type p53 to activate transcription through the  bax promoter in MDA-MB-453 cells.	transcription
58832	9	335836	5	NULL	NULL	0	NULL	BoB2			is responsible for					statement 5					NULL	MDA-MB-453 cells	0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33747_s_246	10559267	The p53 Homolog p73 Does Not Selectively Inhibit the Ability of p53 to Activate Transcription through the bax Promoter--  In addition to BoB1 and BoB2, the p53 homolog p73 was examined as a potential explanation for the inability of wild-type p53 to activate transcription through the  bax promoter in MDA-MB-453 cells.	transcription
79544	1	335836	6	NULL	NULL	0	NULL	p53	GP		activates					Bax	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33747_s_246	10559267	The p53 Homolog p73 Does Not Selectively Inhibit the Ability of p53 to Activate Transcription through the bax Promoter--  In addition to BoB1 and BoB2, the p53 homolog p73 was examined as a potential explanation for the inability of wild-type p53 to activate transcription through the  bax promoter in MDA-MB-453 cells.	transcription
79545	2	335836	6	NULL	NULL	0	NULL	p73	GP		does not inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_47_33747_s_246	10559267	The p53 Homolog p73 Does Not Selectively Inhibit the Ability of p53 to Activate Transcription through the bax Promoter--  In addition to BoB1 and BoB2, the p53 homolog p73 was examined as a potential explanation for the inability of wild-type p53 to activate transcription through the  bax promoter in MDA-MB-453 cells.	transcription
58833	1	335837	5	NULL	NULL	0	NULL	p73			induces					apoptosis					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_248	14634023	However, transactivation of the  bax promoter by p73gamma or p53 was observed only after 72-96 h, much later than p73- and p53-mediated induction of apoptosis.	transcription
58834	2	335837	5	NULL	NULL	0	NULL	p53			induces					apoptosis					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_248	14634023	However, transactivation of the  bax promoter by p73gamma or p53 was observed only after 72-96 h, much later than p73- and p53-mediated induction of apoptosis.	transcription
58835	3	335837	5	NULL	NULL	0	NULL	p73gamma			transactivates					bax				promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_248	14634023	However, transactivation of the  bax promoter by p73gamma or p53 was observed only after 72-96 h, much later than p73- and p53-mediated induction of apoptosis.	transcription
58836	4	335837	5	NULL	NULL	0	NULL	p53			transactivates					bax				promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_248	14634023	However, transactivation of the  bax promoter by p73gamma or p53 was observed only after 72-96 h, much later than p73- and p53-mediated induction of apoptosis.	transcription
58837	5	335837	5	NULL	NULL	0	NULL	statement 3			occurs after					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_248	14634023	However, transactivation of the  bax promoter by p73gamma or p53 was observed only after 72-96 h, much later than p73- and p53-mediated induction of apoptosis.	transcription
58838	6	335837	5	NULL	NULL	0	NULL	statement 4			occurs after					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_248	14634023	However, transactivation of the  bax promoter by p73gamma or p53 was observed only after 72-96 h, much later than p73- and p53-mediated induction of apoptosis.	transcription
79542	1	335837	6	NULL	NULL	0	NULL	p73gamma	GP		transactivates					bax	GP			promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_248	14634023	However, transactivation of the  bax promoter by p73gamma or p53 was observed only after 72-96 h, much later than p73- and p53-mediated induction of apoptosis.	transcription
79543	2	335837	6	NULL	NULL	0	NULL	p53	GP		activates					Bax	GP			promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_248	14634023	However, transactivation of the  bax promoter by p73gamma or p53 was observed only after 72-96 h, much later than p73- and p53-mediated induction of apoptosis.	transcription
58839	1	335838	5	NULL	NULL	0	NULL	RDCs			activates					p53					NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_235	16169939	We further identified several molecular mechanisms induced by RDCs, such as activation of p53 and p73, expression of p21 and Bax, induction of caspase-3, and nuclear fragmentation.	transcription
58840	2	335838	5	NULL	NULL	0	NULL	RDCs			activates					p73					NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_235	16169939	We further identified several molecular mechanisms induced by RDCs, such as activation of p53 and p73, expression of p21 and Bax, induction of caspase-3, and nuclear fragmentation.	transcription
58841	3	335838	5	NULL	NULL	0	NULL	RDCs			induce					p21		expression of			NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_235	16169939	We further identified several molecular mechanisms induced by RDCs, such as activation of p53 and p73, expression of p21 and Bax, induction of caspase-3, and nuclear fragmentation.	transcription
58842	4	335838	5	NULL	NULL	0	NULL	RDCs			induce					Bax		expression of			NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_235	16169939	We further identified several molecular mechanisms induced by RDCs, such as activation of p53 and p73, expression of p21 and Bax, induction of caspase-3, and nuclear fragmentation.	transcription
58843	5	335838	5	NULL	NULL	0	NULL	RDCs			induce					caspase-3					NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_235	16169939	We further identified several molecular mechanisms induced by RDCs, such as activation of p53 and p73, expression of p21 and Bax, induction of caspase-3, and nuclear fragmentation.	transcription
58844	6	335838	5	NULL	NULL	0	NULL	RDCs			induce					nuclear fragmentation					NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_235	16169939	We further identified several molecular mechanisms induced by RDCs, such as activation of p53 and p73, expression of p21 and Bax, induction of caspase-3, and nuclear fragmentation.	transcription
79536	1	335838	6	NULL	NULL	0	NULL	RDC	GP		activates					p53	GP				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_235	16169939	We further identified several molecular mechanisms induced by RDCs, such as activation of p53 and p73, expression of p21 and Bax, induction of caspase-3, and nuclear fragmentation.	transcription
79537	2	335838	6	NULL	NULL	0	NULL	RDC	GP		activates					p73	GP				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_235	16169939	We further identified several molecular mechanisms induced by RDCs, such as activation of p53 and p73, expression of p21 and Bax, induction of caspase-3, and nuclear fragmentation.	transcription
79538	3	335838	6	NULL	NULL	0	NULL	RDC	GP		activates					p21	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_235	16169939	We further identified several molecular mechanisms induced by RDCs, such as activation of p53 and p73, expression of p21 and Bax, induction of caspase-3, and nuclear fragmentation.	transcription
79539	4	335838	6	NULL	NULL	0	NULL	RDC	GP		activates					Bax	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_235	16169939	We further identified several molecular mechanisms induced by RDCs, such as activation of p53 and p73, expression of p21 and Bax, induction of caspase-3, and nuclear fragmentation.	transcription
79540	5	335838	6	NULL	NULL	0	NULL	RDC	GP		activates					caspase-3	GP	induction of			NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_235	16169939	We further identified several molecular mechanisms induced by RDCs, such as activation of p53 and p73, expression of p21 and Bax, induction of caspase-3, and nuclear fragmentation.	transcription
79541	6	335838	6	NULL	NULL	0	NULL	RDC	GP		activates					nuclear fragmentation	Process				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_235	16169939	We further identified several molecular mechanisms induced by RDCs, such as activation of p53 and p73, expression of p21 and Bax, induction of caspase-3, and nuclear fragmentation.	transcription
58845	1	335839	5	NULL	NULL	0	NULL	CDDP			is					cisplatin					NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_199	12535517	(A) Bax protein expression induced by both cisplatin (CDDP) treatment and YAP expression is dramatically reduced by treatment with human p73 siRNA (hp73) but not control siRNA (cont).	transcription
58846	2	335839	5	NULL	NULL	0	NULL	cisplatin 		treatment	induce					Bax protein		expression of			NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_199	12535517	(A) Bax protein expression induced by both cisplatin (CDDP) treatment and YAP expression is dramatically reduced by treatment with human p73 siRNA (hp73) but not control siRNA (cont).	transcription
58847	3	335839	5	NULL	NULL	0	NULL	YAP		expression of	induce					Bax protein		expression of			NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_199	12535517	(A) Bax protein expression induced by both cisplatin (CDDP) treatment and YAP expression is dramatically reduced by treatment with human p73 siRNA (hp73) but not control siRNA (cont).	transcription
58848	4	335839	5	NULL	NULL	0	NULL	p73 siRNA		treatment;;human	reduce		dramatically			statement 2					NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_199	12535517	(A) Bax protein expression induced by both cisplatin (CDDP) treatment and YAP expression is dramatically reduced by treatment with human p73 siRNA (hp73) but not control siRNA (cont).	transcription
58849	5	335839	5	NULL	NULL	0	NULL	p73 siRNA		treatment;;human	reduce		dramatically			statement 3					NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_199	12535517	(A) Bax protein expression induced by both cisplatin (CDDP) treatment and YAP expression is dramatically reduced by treatment with human p73 siRNA (hp73) but not control siRNA (cont).	transcription
58850	6	335839	5	NULL	NULL	0	NULL	siRNA		treatment;;control	does not reduce					statement 2					NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_199	12535517	(A) Bax protein expression induced by both cisplatin (CDDP) treatment and YAP expression is dramatically reduced by treatment with human p73 siRNA (hp73) but not control siRNA (cont).	transcription
58851	7	335839	5	NULL	NULL	0	NULL	siRNA		treatment;;control	does not reduce					statement 3					NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_199	12535517	(A) Bax protein expression induced by both cisplatin (CDDP) treatment and YAP expression is dramatically reduced by treatment with human p73 siRNA (hp73) but not control siRNA (cont).	transcription
79532	1	335839	6	NULL	NULL	0	NULL	CDDP	Chemical		is					cisplatin	Chemical				NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_199	12535517	(A) Bax protein expression induced by both cisplatin (CDDP) treatment and YAP expression is dramatically reduced by treatment with human p73 siRNA (hp73) but not control siRNA (cont).	transcription
79533	2	335839	6	NULL	NULL	0	NULL	YAP	GP		increases					Bax	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_199	12535517	(A) Bax protein expression induced by both cisplatin (CDDP) treatment and YAP expression is dramatically reduced by treatment with human p73 siRNA (hp73) but not control siRNA (cont).	transcription
79534	3	335839	6	NULL	NULL	0	NULL	p73	GP		reduces					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_199	12535517	(A) Bax protein expression induced by both cisplatin (CDDP) treatment and YAP expression is dramatically reduced by treatment with human p73 siRNA (hp73) but not control siRNA (cont).	transcription
79535	4	335839	6	NULL	NULL	0	NULL	p73	GP		reduces					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_199	12535517	(A) Bax protein expression induced by both cisplatin (CDDP) treatment and YAP expression is dramatically reduced by treatment with human p73 siRNA (hp73) but not control siRNA (cont).	transcription
58852	1	335840	5	NULL	NULL	0	NULL	p53			transactivates					p21				promoter	NULL	mammalian cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1438_s_255	9891077	In mammalian cells, the  GADD45 and  Bax promoters are stimulated to the same extent by all three proteins, but p53 is a more potent transactivator of  p21 and  mdm2 promoters than p73.	transcription
58853	2	335840	5	NULL	NULL	0	NULL	p53			transactivates					mdm2				promoter	NULL	mammalian cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1438_s_255	9891077	In mammalian cells, the  GADD45 and  Bax promoters are stimulated to the same extent by all three proteins, but p53 is a more potent transactivator of  p21 and  mdm2 promoters than p73.	transcription
58854	3	335840	5	NULL	NULL	0	NULL	p73			transactivates					p21				promoter	NULL	mammalian cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1438_s_255	9891077	In mammalian cells, the  GADD45 and  Bax promoters are stimulated to the same extent by all three proteins, but p53 is a more potent transactivator of  p21 and  mdm2 promoters than p73.	transcription
58855	4	335840	5	NULL	NULL	0	NULL	p73			transactivates					mdm2				promoter	NULL	mammalian cells	NULL	NULL	NULL	NULL	gw60_molcellbiol_19_2_1438_s_255	9891077	In mammalian cells, the  GADD45 and  Bax promoters are stimulated to the same extent by all three proteins, but p53 is a more potent transactivator of  p21 and  mdm2 promoters than p73.	transcription
58856	5	335840	5	NULL	NULL	0	NULL	statement 1			more potent than					statement 3					NULL	mammalian cells	0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1438_s_255	9891077	In mammalian cells, the  GADD45 and  Bax promoters are stimulated to the same extent by all three proteins, but p53 is a more potent transactivator of  p21 and  mdm2 promoters than p73.	transcription
58857	6	335840	5	NULL	NULL	0	NULL	statement 2			more potent than					statement 4					NULL	mammalian cells	0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1438_s_255	9891077	In mammalian cells, the  GADD45 and  Bax promoters are stimulated to the same extent by all three proteins, but p53 is a more potent transactivator of  p21 and  mdm2 promoters than p73.	transcription
79528	1	335840	6	NULL	NULL	0	NULL	p53	GP		transactivates					p21	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1438_s_255	9891077	In mammalian cells, the  GADD45 and  Bax promoters are stimulated to the same extent by all three proteins, but p53 is a more potent transactivator of  p21 and  mdm2 promoters than p73.	transcription
79529	2	335840	6	NULL	NULL	0	NULL	p53	GP		transactivates					mdm2	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1438_s_255	9891077	In mammalian cells, the  GADD45 and  Bax promoters are stimulated to the same extent by all three proteins, but p53 is a more potent transactivator of  p21 and  mdm2 promoters than p73.	transcription
79530	3	335840	6	NULL	NULL	0	NULL	p73	GP		transactivates					p21	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1438_s_255	9891077	In mammalian cells, the  GADD45 and  Bax promoters are stimulated to the same extent by all three proteins, but p53 is a more potent transactivator of  p21 and  mdm2 promoters than p73.	transcription
79531	4	335840	6	NULL	NULL	0	NULL	p73	GP		transactivates					mdm2	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1438_s_255	9891077	In mammalian cells, the  GADD45 and  Bax promoters are stimulated to the same extent by all three proteins, but p53 is a more potent transactivator of  p21 and  mdm2 promoters than p73.	transcription
58858	1	335841	5	NULL	NULL	0	NULL	p53			activates		efficiently			Bax				reporter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_259	10207112	We first compared the effects of CMV-p53 and CMV-p73 on different reporter constructs and found that both p53 and p73 could very efficiently activate the Bax and IGF-BP3 reporter constructs, while the activation of the p21Waf1 and cyclin G reporter constructs by p73 was significantly lower than that by p53.	transcription
58859	2	335841	5	NULL	NULL	0	NULL	p53			activates		efficiently			IGF-BP3				reporter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_259	10207112	We first compared the effects of CMV-p53 and CMV-p73 on different reporter constructs and found that both p53 and p73 could very efficiently activate the Bax and IGF-BP3 reporter constructs, while the activation of the p21Waf1 and cyclin G reporter constructs by p73 was significantly lower than that by p53.	transcription
58860	3	335841	5	NULL	NULL	0	NULL	p73			activates		efficiently			Bax				reporter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_259	10207112	We first compared the effects of CMV-p53 and CMV-p73 on different reporter constructs and found that both p53 and p73 could very efficiently activate the Bax and IGF-BP3 reporter constructs, while the activation of the p21Waf1 and cyclin G reporter constructs by p73 was significantly lower than that by p53.	transcription
58861	4	335841	5	NULL	NULL	0	NULL	p73			activates		efficiently			IGF-BP3				reporter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_259	10207112	We first compared the effects of CMV-p53 and CMV-p73 on different reporter constructs and found that both p53 and p73 could very efficiently activate the Bax and IGF-BP3 reporter constructs, while the activation of the p21Waf1 and cyclin G reporter constructs by p73 was significantly lower than that by p53.	transcription
58862	5	335841	5	NULL	NULL	0	NULL	p73			activates					p21Waf1				reporter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_259	10207112	We first compared the effects of CMV-p53 and CMV-p73 on different reporter constructs and found that both p53 and p73 could very efficiently activate the Bax and IGF-BP3 reporter constructs, while the activation of the p21Waf1 and cyclin G reporter constructs by p73 was significantly lower than that by p53.	transcription
58863	6	335841	5	NULL	NULL	0	NULL	p73			activates					cyclin G				reporter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_259	10207112	We first compared the effects of CMV-p53 and CMV-p73 on different reporter constructs and found that both p53 and p73 could very efficiently activate the Bax and IGF-BP3 reporter constructs, while the activation of the p21Waf1 and cyclin G reporter constructs by p73 was significantly lower than that by p53.	transcription
58864	7	335841	5	NULL	NULL	0	NULL	p53			activates					p21Waf1				reporter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_259	10207112	We first compared the effects of CMV-p53 and CMV-p73 on different reporter constructs and found that both p53 and p73 could very efficiently activate the Bax and IGF-BP3 reporter constructs, while the activation of the p21Waf1 and cyclin G reporter constructs by p73 was significantly lower than that by p53.	transcription
58865	8	335841	5	NULL	NULL	0	NULL	p53			activates					cyclin G				reporter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_259	10207112	We first compared the effects of CMV-p53 and CMV-p73 on different reporter constructs and found that both p53 and p73 could very efficiently activate the Bax and IGF-BP3 reporter constructs, while the activation of the p21Waf1 and cyclin G reporter constructs by p73 was significantly lower than that by p53.	transcription
58866	9	335841	5	NULL	NULL	0	NULL	statement 5			lower than		significantly			statement 7					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_259	10207112	We first compared the effects of CMV-p53 and CMV-p73 on different reporter constructs and found that both p53 and p73 could very efficiently activate the Bax and IGF-BP3 reporter constructs, while the activation of the p21Waf1 and cyclin G reporter constructs by p73 was significantly lower than that by p53.	transcription
58867	10	335841	5	NULL	NULL	0	NULL	statement 6			lower than		significantly			statement 8					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_259	10207112	We first compared the effects of CMV-p53 and CMV-p73 on different reporter constructs and found that both p53 and p73 could very efficiently activate the Bax and IGF-BP3 reporter constructs, while the activation of the p21Waf1 and cyclin G reporter constructs by p73 was significantly lower than that by p53.	transcription
79522	1	335841	6	NULL	NULL	0	NULL	p53	GP		activates					Bax 	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_259	10207112	We first compared the effects of CMV-p53 and CMV-p73 on different reporter constructs and found that both p53 and p73 could very efficiently activate the Bax and IGF-BP3 reporter constructs, while the activation of the p21Waf1 and cyclin G reporter constructs by p73 was significantly lower than that by p53.	transcription
79523	2	335841	6	NULL	NULL	0	NULL	p73	GP		activates					IGF-BP3	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_259	10207112	We first compared the effects of CMV-p53 and CMV-p73 on different reporter constructs and found that both p53 and p73 could very efficiently activate the Bax and IGF-BP3 reporter constructs, while the activation of the p21Waf1 and cyclin G reporter constructs by p73 was significantly lower than that by p53.	transcription
79524	3	335841	6	NULL	NULL	0	NULL	p73	GP		activates					p21Waf1	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_259	10207112	We first compared the effects of CMV-p53 and CMV-p73 on different reporter constructs and found that both p53 and p73 could very efficiently activate the Bax and IGF-BP3 reporter constructs, while the activation of the p21Waf1 and cyclin G reporter constructs by p73 was significantly lower than that by p53.	transcription
79525	4	335841	6	NULL	NULL	NULL	NULL	p73	GP		activates					cyclin G	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_259	10207112	We first compared the effects of CMV-p53 and CMV-p73 on different reporter constructs and found that both p53 and p73 could very efficiently activate the Bax and IGF-BP3 reporter constructs, while the activation of the p21Waf1 and cyclin G reporter constructs by p73 was significantly lower than that by p53.	transcription
79526	5	335841	6	NULL	NULL	0	NULL	p53	GP		activates					p21Waf1	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_259	10207112	We first compared the effects of CMV-p53 and CMV-p73 on different reporter constructs and found that both p53 and p73 could very efficiently activate the Bax and IGF-BP3 reporter constructs, while the activation of the p21Waf1 and cyclin G reporter constructs by p73 was significantly lower than that by p53.	transcription
79527	6	335841	6	NULL	NULL	0	NULL	p53	GP		activates					cyclin G	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_259	10207112	We first compared the effects of CMV-p53 and CMV-p73 on different reporter constructs and found that both p53 and p73 could very efficiently activate the Bax and IGF-BP3 reporter constructs, while the activation of the p21Waf1 and cyclin G reporter constructs by p73 was significantly lower than that by p53.	transcription
58868	1	335842	5	NULL	NULL	0	NULL	CDDP			induce					DNA		damage of			NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_4_589_s_157	16461361	In this case, DNA damage induced by CDDP leads to activation of p73, and the transcription cofactor YAP promotes p73-mediated transactivation of cell death genes, including Bax and possibly PUMA ( ).	transcription
58869	2	335842	5	NULL	NULL	0	NULL	statement 1			activates					p73					NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_4_589_s_157	16461361	In this case, DNA damage induced by CDDP leads to activation of p73, and the transcription cofactor YAP promotes p73-mediated transactivation of cell death genes, including Bax and possibly PUMA ( ).	transcription
58870	3	335842	5	NULL	NULL	0	NULL	p73			mediates					Bax		transactivation of			NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_4_589_s_157	16461361	In this case, DNA damage induced by CDDP leads to activation of p73, and the transcription cofactor YAP promotes p73-mediated transactivation of cell death genes, including Bax and possibly PUMA ( ).	transcription
58871	4	335842	5	NULL	NULL	0	NULL	p73			mediates					PUMA		transactivation of			NULL		NULL	NULL	NULL	NULL	gw70_cellbiol_172_4_589_s_157	16461361	In this case, DNA damage induced by CDDP leads to activation of p73, and the transcription cofactor YAP promotes p73-mediated transactivation of cell death genes, including Bax and possibly PUMA ( ).	transcription
58872	5	335842	5	NULL	NULL	0	NULL	YAP			promotes					statement 3					NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_4_589_s_157	16461361	In this case, DNA damage induced by CDDP leads to activation of p73, and the transcription cofactor YAP promotes p73-mediated transactivation of cell death genes, including Bax and possibly PUMA ( ).	transcription
58873	6	335842	5	NULL	NULL	0	NULL	YAP			promotes		possibly			statement 4					NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_4_589_s_157	16461361	In this case, DNA damage induced by CDDP leads to activation of p73, and the transcription cofactor YAP promotes p73-mediated transactivation of cell death genes, including Bax and possibly PUMA ( ).	transcription
58874	7	335842	5	NULL	NULL	0	NULL	YAP			is a type of					transcription cofactor					NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_4_589_s_157	16461361	In this case, DNA damage induced by CDDP leads to activation of p73, and the transcription cofactor YAP promotes p73-mediated transactivation of cell death genes, including Bax and possibly PUMA ( ).	transcription
58875	8	335842	5	NULL	NULL	0	NULL	Bax			is a type of					cell death gene					NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_4_589_s_157	16461361	In this case, DNA damage induced by CDDP leads to activation of p73, and the transcription cofactor YAP promotes p73-mediated transactivation of cell death genes, including Bax and possibly PUMA ( ).	transcription
58876	9	335842	5	NULL	NULL	0	NULL	PUMA			is a type of					cell death gene					NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_4_589_s_157	16461361	In this case, DNA damage induced by CDDP leads to activation of p73, and the transcription cofactor YAP promotes p73-mediated transactivation of cell death genes, including Bax and possibly PUMA ( ).	transcription
79517	1	335842	6	NULL	NULL	0	NULL	CDDP	GP		induces					DNA	NucleicAcid	damage to			NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_4_589_s_157	16461361	In this case, DNA damage induced by CDDP leads to activation of p73, and the transcription cofactor YAP promotes p73-mediated transactivation of cell death genes, including Bax and possibly PUMA ( ).	transcription
79518	2	335842	6	NULL	NULL	0	NULL	statement 1	Process		leads to					p73	GP	activation of 			NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_4_589_s_157	16461361	In this case, DNA damage induced by CDDP leads to activation of p73, and the transcription cofactor YAP promotes p73-mediated transactivation of cell death genes, including Bax and possibly PUMA ( ).	transcription
79519	3	335842	6	NULL	NULL	0	NULL	YAP	GP		is a type of					transcription cofactor	GP				NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_4_589_s_157	16461361	In this case, DNA damage induced by CDDP leads to activation of p73, and the transcription cofactor YAP promotes p73-mediated transactivation of cell death genes, including Bax and possibly PUMA ( ).	transcription
79520	4	335842	6	NULL	NULL	0	NULL	p73	GP		mediates					Bax	GP	transactivation of 			NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_4_589_s_157	16461361	In this case, DNA damage induced by CDDP leads to activation of p73, and the transcription cofactor YAP promotes p73-mediated transactivation of cell death genes, including Bax and possibly PUMA ( ).	transcription
79521	5	335842	6	NULL	NULL	0	NULL	YAP	GP		promotes					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_cellbiol_172_4_589_s_157	16461361	In this case, DNA damage induced by CDDP leads to activation of p73, and the transcription cofactor YAP promotes p73-mediated transactivation of cell death genes, including Bax and possibly PUMA ( ).	transcription
58877	1	335843	5	NULL	NULL	0	NULL	TNF-alpha-CHX			activates		possibly			p73		transcription function of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_10_4438_s_134	15121862	To determine if TNF-alpha-CHX activated the transcription function of p73, we performed luciferase reporter assays using promoters of either  p21CIP1 or  BAX in transient-cotransfection experiments.	transcription
58878	1	335844	5	NULL	NULL	0	NULL	YAP			stimulates					Bax		expression of			NULL	HeLa cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_25_26300_s_171	15096513	Because HeLa cells express significant amounts of p73 ( ), we tested whether co-expression of hnRNP U had an effect on the ability of YAP to stimulate the expression of Bax.	transcription
58879	2	335844	5	NULL	NULL	0	NULL	HeLa cells			express					p73					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_25_26300_s_171	15096513	Because HeLa cells express significant amounts of p73 ( ), we tested whether co-expression of hnRNP U had an effect on the ability of YAP to stimulate the expression of Bax.	transcription
58880	3	335844	5	NULL	NULL	0	NULL	hnRNP U		co-expression of	effects		possibly			statement 1					NULL	HeLa cells	0	NULL	NULL	NULL	gw70_jbiolchem_279_25_26300_s_171	15096513	Because HeLa cells express significant amounts of p73 ( ), we tested whether co-expression of hnRNP U had an effect on the ability of YAP to stimulate the expression of Bax.	transcription
79516	1	335844	6	NULL	NULL	0	NULL	YAP	GP		stimulates					Bax	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_25_26300_s_171	15096513	Because HeLa cells express significant amounts of p73 ( ), we tested whether co-expression of hnRNP U had an effect on the ability of YAP to stimulate the expression of Bax.	transcription
58881	1	335845	5	NULL	NULL	0	NULL	Bax			is translocated to					mitochondria					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_153	14634023	To identify the mediators through which p73 indirectly induces Bax mitochondrial translocation, we examined the modulation of several BH3-only proteins (data not shown) that bind to Bcl2/Xl via their BH3 domain, thereby inactivating their protective functions ( ,  ).	transcription
58882	2	335845	5	NULL	NULL	0	NULL	p73			induce		indirectly			statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_9_8076_s_153	14634023	To identify the mediators through which p73 indirectly induces Bax mitochondrial translocation, we examined the modulation of several BH3-only proteins (data not shown) that bind to Bcl2/Xl via their BH3 domain, thereby inactivating their protective functions ( ,  ).	transcription
58883	1	335846	5	NULL	NULL	0	NULL	p21/WAF-1			is a type of					p53 target gene					NULL		0	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_12	12086844	Moreover, at least in overexpression assays, p63 and p73 were shown to transactivate many p53 target genes including p21/WAF-1 and Bax, and they were able to induce cell cycle arrest and apoptosis ( Yang and McKeon, 2000  ).	transcription
58884	2	335846	5	NULL	NULL	0	NULL	Bax			is a type of					p53 target gene					NULL		0	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_12	12086844	Moreover, at least in overexpression assays, p63 and p73 were shown to transactivate many p53 target genes including p21/WAF-1 and Bax, and they were able to induce cell cycle arrest and apoptosis ( Yang and McKeon, 2000  ).	transcription
58885	3	335846	5	NULL	NULL	0	NULL	p63		overexpression of	transactivates					p21/WAF-1					NULL		0	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_12	12086844	Moreover, at least in overexpression assays, p63 and p73 were shown to transactivate many p53 target genes including p21/WAF-1 and Bax, and they were able to induce cell cycle arrest and apoptosis ( Yang and McKeon, 2000  ).	transcription
58886	4	335846	5	NULL	NULL	0	NULL	p73		overexpression of	transactivates					p21/WAF-1					NULL		0	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_12	12086844	Moreover, at least in overexpression assays, p63 and p73 were shown to transactivate many p53 target genes including p21/WAF-1 and Bax, and they were able to induce cell cycle arrest and apoptosis ( Yang and McKeon, 2000  ).	transcription
58887	5	335846	5	NULL	NULL	0	NULL	p63		overexpression of	transactivates					Bax					NULL		0	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_12	12086844	Moreover, at least in overexpression assays, p63 and p73 were shown to transactivate many p53 target genes including p21/WAF-1 and Bax, and they were able to induce cell cycle arrest and apoptosis ( Yang and McKeon, 2000  ).	transcription
58888	6	335846	5	NULL	NULL	0	NULL	p73		overexpression of	transactivates					Bax					NULL		0	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_12	12086844	Moreover, at least in overexpression assays, p63 and p73 were shown to transactivate many p53 target genes including p21/WAF-1 and Bax, and they were able to induce cell cycle arrest and apoptosis ( Yang and McKeon, 2000  ).	transcription
58889	7	335846	5	NULL	NULL	0	NULL	p63			induce					cell cycle arrest					NULL		0	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_12	12086844	Moreover, at least in overexpression assays, p63 and p73 were shown to transactivate many p53 target genes including p21/WAF-1 and Bax, and they were able to induce cell cycle arrest and apoptosis ( Yang and McKeon, 2000  ).	transcription
58890	8	335846	5	NULL	NULL	0	NULL	p63			induce					apoptosis					NULL		0	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_12	12086844	Moreover, at least in overexpression assays, p63 and p73 were shown to transactivate many p53 target genes including p21/WAF-1 and Bax, and they were able to induce cell cycle arrest and apoptosis ( Yang and McKeon, 2000  ).	transcription
58891	9	335846	5	NULL	NULL	0	NULL	p73			induce					cell cycle arrest					NULL		0	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_12	12086844	Moreover, at least in overexpression assays, p63 and p73 were shown to transactivate many p53 target genes including p21/WAF-1 and Bax, and they were able to induce cell cycle arrest and apoptosis ( Yang and McKeon, 2000  ).	transcription
58892	10	335846	5	NULL	NULL	0	NULL	p73			induce					apoptosis					NULL		0	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_12	12086844	Moreover, at least in overexpression assays, p63 and p73 were shown to transactivate many p53 target genes including p21/WAF-1 and Bax, and they were able to induce cell cycle arrest and apoptosis ( Yang and McKeon, 2000  ).	transcription
79512	1	335846	6	NULL	NULL	0	NULL	p63	GP		induces					cell cycle arrest	Process				NULL		0	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_12	12086844	Moreover, at least in overexpression assays, p63 and p73 were shown to transactivate many p53 target genes including p21/WAF-1 and Bax, and they were able to induce cell cycle arrest and apoptosis ( Yang and McKeon, 2000  ).	transcription
79513	2	335846	6	NULL	NULL	0	NULL	p63	GP		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_12	12086844	Moreover, at least in overexpression assays, p63 and p73 were shown to transactivate many p53 target genes including p21/WAF-1 and Bax, and they were able to induce cell cycle arrest and apoptosis ( Yang and McKeon, 2000  ).	transcription
79514	3	335846	6	NULL	NULL	0	NULL	p73	GP		induces					cell cycle arrest	Process				NULL		0	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_12	12086844	Moreover, at least in overexpression assays, p63 and p73 were shown to transactivate many p53 target genes including p21/WAF-1 and Bax, and they were able to induce cell cycle arrest and apoptosis ( Yang and McKeon, 2000  ).	transcription
79515	4	335846	6	NULL	NULL	0	NULL	p73	GP		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_cancercell_1_4_311_s_12	12086844	Moreover, at least in overexpression assays, p63 and p73 were shown to transactivate many p53 target genes including p21/WAF-1 and Bax, and they were able to induce cell cycle arrest and apoptosis ( Yang and McKeon, 2000  ).	transcription
58893	1	335847	5	NULL	NULL	0	NULL	ik3-1		co-expression of	does not affect					Bax protein		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_194	11706030	Protein Expression of Bax and p21 Are Not Affected by Coexpression of ik3-1 or ik3-1-deltaC-- Because p53 and p73 exert their activities by transactivating and transrepressing downstream genes, we examined expression of representative downstream gene products by immunoblotting (Fig.  6).	transcription
58894	2	335847	5	NULL	NULL	0	NULL	ik3-1-deltaC		co-expression of	does not affect					Bax protein		expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_194	11706030	Protein Expression of Bax and p21 Are Not Affected by Coexpression of ik3-1 or ik3-1-deltaC-- Because p53 and p73 exert their activities by transactivating and transrepressing downstream genes, we examined expression of representative downstream gene products by immunoblotting (Fig.  6).	transcription
58895	3	335847	5	NULL	NULL	0	NULL	statement 1			is an alternative to					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_194	11706030	Protein Expression of Bax and p21 Are Not Affected by Coexpression of ik3-1 or ik3-1-deltaC-- Because p53 and p73 exert their activities by transactivating and transrepressing downstream genes, we examined expression of representative downstream gene products by immunoblotting (Fig.  6).	transcription
58896	4	335847	5	NULL	NULL	0	NULL	ik3-1		co-expression of	does not affect					p21 protein		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_194	11706030	Protein Expression of Bax and p21 Are Not Affected by Coexpression of ik3-1 or ik3-1-deltaC-- Because p53 and p73 exert their activities by transactivating and transrepressing downstream genes, we examined expression of representative downstream gene products by immunoblotting (Fig.  6).	transcription
58897	5	335847	5	NULL	NULL	0	NULL	ik3-1-deltaC		co-expression of	does not affect					p21 protein		expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_194	11706030	Protein Expression of Bax and p21 Are Not Affected by Coexpression of ik3-1 or ik3-1-deltaC-- Because p53 and p73 exert their activities by transactivating and transrepressing downstream genes, we examined expression of representative downstream gene products by immunoblotting (Fig.  6).	transcription
58898	6	335847	5	NULL	NULL	0	NULL	statement 4			is an alternative to					statement 5					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_4_2951_s_194	11706030	Protein Expression of Bax and p21 Are Not Affected by Coexpression of ik3-1 or ik3-1-deltaC-- Because p53 and p73 exert their activities by transactivating and transrepressing downstream genes, we examined expression of representative downstream gene products by immunoblotting (Fig.  6).	transcription
58899	1	335848	5	NULL	NULL	0	NULL	p73		ectopically expressed	transactivates					p21				promoter	NULL	p53-deficient cell lines	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_19_15720_s_38	11279015	Furthermore, when ectopically expressed, p73 can trans-activate a variety of p53 promoters ( p21,  bax,  mdm2, and  GADD45) and induce apoptosis in p53-deficient cell lines ( 45,  48,  52,  56-59).	transcription
58900	2	335848	5	NULL	NULL	0	NULL	p73		ectopically expressed	transactivates					bax				promoter	NULL	p53-deficient cell lines	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_19_15720_s_38	11279015	Furthermore, when ectopically expressed, p73 can trans-activate a variety of p53 promoters ( p21,  bax,  mdm2, and  GADD45) and induce apoptosis in p53-deficient cell lines ( 45,  48,  52,  56-59).	transcription
58901	3	335848	5	NULL	NULL	0	NULL	p73		ectopically expressed	transactivates					mdm2				promoter	NULL	p53-deficient cell lines	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_19_15720_s_38	11279015	Furthermore, when ectopically expressed, p73 can trans-activate a variety of p53 promoters ( p21,  bax,  mdm2, and  GADD45) and induce apoptosis in p53-deficient cell lines ( 45,  48,  52,  56-59).	transcription
58902	4	335848	5	NULL	NULL	0	NULL	p73		ectopically expressed	transactivates					GADD45				promoter	NULL	p53-deficient cell lines	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_19_15720_s_38	11279015	Furthermore, when ectopically expressed, p73 can trans-activate a variety of p53 promoters ( p21,  bax,  mdm2, and  GADD45) and induce apoptosis in p53-deficient cell lines ( 45,  48,  52,  56-59).	transcription
58903	5	335848	5	NULL	NULL	0	NULL	statement 1			induce					apoptosis					NULL	p53-deficient cell lines	0	NULL	NULL	NULL	gw60_jbiolchem_276_19_15720_s_38	11279015	Furthermore, when ectopically expressed, p73 can trans-activate a variety of p53 promoters ( p21,  bax,  mdm2, and  GADD45) and induce apoptosis in p53-deficient cell lines ( 45,  48,  52,  56-59).	transcription
58904	6	335848	5	NULL	NULL	0	NULL	statement 2			induce					apoptosis					NULL	p53-deficient cell lines	0	NULL	NULL	NULL	gw60_jbiolchem_276_19_15720_s_38	11279015	Furthermore, when ectopically expressed, p73 can trans-activate a variety of p53 promoters ( p21,  bax,  mdm2, and  GADD45) and induce apoptosis in p53-deficient cell lines ( 45,  48,  52,  56-59).	transcription
58905	7	335848	5	NULL	NULL	0	NULL	statement 3			induce					apoptosis					NULL	p53-deficient cell lines	0	NULL	NULL	NULL	gw60_jbiolchem_276_19_15720_s_38	11279015	Furthermore, when ectopically expressed, p73 can trans-activate a variety of p53 promoters ( p21,  bax,  mdm2, and  GADD45) and induce apoptosis in p53-deficient cell lines ( 45,  48,  52,  56-59).	transcription
58906	8	335848	5	NULL	NULL	0	NULL	statement 4			induce					apoptosis					NULL	p53-deficient cell lines	0	NULL	NULL	NULL	gw60_jbiolchem_276_19_15720_s_38	11279015	Furthermore, when ectopically expressed, p73 can trans-activate a variety of p53 promoters ( p21,  bax,  mdm2, and  GADD45) and induce apoptosis in p53-deficient cell lines ( 45,  48,  52,  56-59).	transcription
79508	1	335848	6	NULL	NULL	0	NULL	p73	GP		transactivates					p53 	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_19_15720_s_38	11279015	Furthermore, when ectopically expressed, p73 can trans-activate a variety of p53 promoters ( p21,  bax,  mdm2, and  GADD45) and induce apoptosis in p53-deficient cell lines ( 45,  48,  52,  56-59).	transcription
79509	2	335848	6	NULL	NULL	0	NULL	p73	GP		transactivates					bax	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_19_15720_s_38	11279015	Furthermore, when ectopically expressed, p73 can trans-activate a variety of p53 promoters ( p21,  bax,  mdm2, and  GADD45) and induce apoptosis in p53-deficient cell lines ( 45,  48,  52,  56-59).	transcription
79510	3	335848	6	NULL	NULL	0	NULL	p73	GP		transactivates					mdm2	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_19_15720_s_38	11279015	Furthermore, when ectopically expressed, p73 can trans-activate a variety of p53 promoters ( p21,  bax,  mdm2, and  GADD45) and induce apoptosis in p53-deficient cell lines ( 45,  48,  52,  56-59).	transcription
79511	4	335848	6	NULL	NULL	0	NULL	p73	GP		transactivates					GADD45	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_19_15720_s_38	11279015	Furthermore, when ectopically expressed, p73 can trans-activate a variety of p53 promoters ( p21,  bax,  mdm2, and  GADD45) and induce apoptosis in p53-deficient cell lines ( 45,  48,  52,  56-59).	transcription
58907	1	335849	5	NULL	NULL	0	NULL	p53			activates					Bax				reporter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_5	10207112	Our results show that the large E1B proteins very efficiently inhibited the activity of p53 on the Bax, p21Waf1, cyclin G, and MDM2 reporter constructs but had no effect on the activation of the same reporter constructs by p73, with the exception of some inhibition of the Bax promoter by Ad12 E1B.	transcription
58908	2	335849	5	NULL	NULL	0	NULL	p53			activates					p21Waf1				reporter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_5	10207112	Our results show that the large E1B proteins very efficiently inhibited the activity of p53 on the Bax, p21Waf1, cyclin G, and MDM2 reporter constructs but had no effect on the activation of the same reporter constructs by p73, with the exception of some inhibition of the Bax promoter by Ad12 E1B.	transcription
58909	3	335849	5	NULL	NULL	0	NULL	p53			activates					cyclin G				reporter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_5	10207112	Our results show that the large E1B proteins very efficiently inhibited the activity of p53 on the Bax, p21Waf1, cyclin G, and MDM2 reporter constructs but had no effect on the activation of the same reporter constructs by p73, with the exception of some inhibition of the Bax promoter by Ad12 E1B.	transcription
58910	4	335849	5	NULL	NULL	0	NULL	p53			activates					MDM2				reporter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_5	10207112	Our results show that the large E1B proteins very efficiently inhibited the activity of p53 on the Bax, p21Waf1, cyclin G, and MDM2 reporter constructs but had no effect on the activation of the same reporter constructs by p73, with the exception of some inhibition of the Bax promoter by Ad12 E1B.	transcription
58911	5	335849	5	NULL	NULL	0	NULL	E1B proteins		large	inhibits		efficiently			statement 1					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_5	10207112	Our results show that the large E1B proteins very efficiently inhibited the activity of p53 on the Bax, p21Waf1, cyclin G, and MDM2 reporter constructs but had no effect on the activation of the same reporter constructs by p73, with the exception of some inhibition of the Bax promoter by Ad12 E1B.	transcription
58912	6	335849	5	NULL	NULL	0	NULL	E1B proteins		large	inhibits		efficiently			statement 2					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_5	10207112	Our results show that the large E1B proteins very efficiently inhibited the activity of p53 on the Bax, p21Waf1, cyclin G, and MDM2 reporter constructs but had no effect on the activation of the same reporter constructs by p73, with the exception of some inhibition of the Bax promoter by Ad12 E1B.	transcription
58913	7	335849	5	NULL	NULL	0	NULL	E1B proteins		large	inhibits		efficiently			statement 3					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_5	10207112	Our results show that the large E1B proteins very efficiently inhibited the activity of p53 on the Bax, p21Waf1, cyclin G, and MDM2 reporter constructs but had no effect on the activation of the same reporter constructs by p73, with the exception of some inhibition of the Bax promoter by Ad12 E1B.	transcription
58914	8	335849	5	NULL	NULL	0	NULL	E1B proteins		large	inhibits		efficiently			statement 4					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_5	10207112	Our results show that the large E1B proteins very efficiently inhibited the activity of p53 on the Bax, p21Waf1, cyclin G, and MDM2 reporter constructs but had no effect on the activation of the same reporter constructs by p73, with the exception of some inhibition of the Bax promoter by Ad12 E1B.	transcription
58915	9	335849	5	NULL	NULL	0	NULL	p73			activates					Bax				reporter	NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_5	10207112	Our results show that the large E1B proteins very efficiently inhibited the activity of p53 on the Bax, p21Waf1, cyclin G, and MDM2 reporter constructs but had no effect on the activation of the same reporter constructs by p73, with the exception of some inhibition of the Bax promoter by Ad12 E1B.	transcription
58916	10	335849	5	NULL	NULL	0	NULL	p73			activates					p21Waf1				reporter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_5	10207112	Our results show that the large E1B proteins very efficiently inhibited the activity of p53 on the Bax, p21Waf1, cyclin G, and MDM2 reporter constructs but had no effect on the activation of the same reporter constructs by p73, with the exception of some inhibition of the Bax promoter by Ad12 E1B.	transcription
58917	11	335849	5	NULL	NULL	0	NULL	p73			activates					cyclin G 				reporter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_5	10207112	Our results show that the large E1B proteins very efficiently inhibited the activity of p53 on the Bax, p21Waf1, cyclin G, and MDM2 reporter constructs but had no effect on the activation of the same reporter constructs by p73, with the exception of some inhibition of the Bax promoter by Ad12 E1B.	transcription
58918	12	335849	5	NULL	NULL	0	NULL	p73			activates					MDM2				reporter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_5	10207112	Our results show that the large E1B proteins very efficiently inhibited the activity of p53 on the Bax, p21Waf1, cyclin G, and MDM2 reporter constructs but had no effect on the activation of the same reporter constructs by p73, with the exception of some inhibition of the Bax promoter by Ad12 E1B.	transcription
58919	13	335849	5	NULL	NULL	0	NULL	E1B proteins \t		large	does not effect					statement 10					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_5	10207112	Our results show that the large E1B proteins very efficiently inhibited the activity of p53 on the Bax, p21Waf1, cyclin G, and MDM2 reporter constructs but had no effect on the activation of the same reporter constructs by p73, with the exception of some inhibition of the Bax promoter by Ad12 E1B.	transcription
58920	14	335849	5	NULL	NULL	0	NULL	E1B proteins \t		large	does not effect					statement 11					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_5	10207112	Our results show that the large E1B proteins very efficiently inhibited the activity of p53 on the Bax, p21Waf1, cyclin G, and MDM2 reporter constructs but had no effect on the activation of the same reporter constructs by p73, with the exception of some inhibition of the Bax promoter by Ad12 E1B.	transcription
58921	15	335849	5	NULL	NULL	0	NULL	E1B proteins \t		large	does not effect					statement 12					NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_5	10207112	Our results show that the large E1B proteins very efficiently inhibited the activity of p53 on the Bax, p21Waf1, cyclin G, and MDM2 reporter constructs but had no effect on the activation of the same reporter constructs by p73, with the exception of some inhibition of the Bax promoter by Ad12 E1B.	transcription
58922	16	335849	5	NULL	NULL	0	NULL	Ad12 E1B			inhibits					Bax				promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3885_s_5	10207112	Our results show that the large E1B proteins very efficiently inhibited the activity of p53 on the Bax, p21Waf1, cyclin G, and MDM2 reporter constructs but had no effect on the activation of the same reporter constructs by p73, with the exception of some inhibition of the Bax promoter by Ad12 E1B.	transcription
58923	1	335850	5	NULL	NULL	0	NULL	p21			is a type of					p53 target gene					NULL		0	NULL	NULL	NULL	gw60_pnas_95_12_6681_s_29	9618472	P73 can transcriptionally activate p53 target genes such as p21 or bax-1, and induce growth suppression or apoptosis ( 34,  35).	transcription
58924	2	335850	5	NULL	NULL	0	NULL	bax-1			is a type of					p53 target gene					NULL		0	NULL	NULL	NULL	gw60_pnas_95_12_6681_s_29	9618472	P73 can transcriptionally activate p53 target genes such as p21 or bax-1, and induce growth suppression or apoptosis ( 34,  35).	transcription
58925	3	335850	5	NULL	NULL	0	NULL	p73			activates		transcriptionaly			p21					NULL		0	NULL	NULL	NULL	gw60_pnas_95_12_6681_s_29	9618472	P73 can transcriptionally activate p53 target genes such as p21 or bax-1, and induce growth suppression or apoptosis ( 34,  35).	transcription
58926	4	335850	5	NULL	NULL	0	NULL	p73			activates		transcriptionaly			bax-1					NULL		0	NULL	NULL	NULL	gw60_pnas_95_12_6681_s_29	9618472	P73 can transcriptionally activate p53 target genes such as p21 or bax-1, and induce growth suppression or apoptosis ( 34,  35).	transcription
58927	5	335850	5	NULL	NULL	0	NULL	statement 3			induce					growth suppression					NULL		NULL	NULL	NULL	NULL	gw60_pnas_95_12_6681_s_29	9618472	P73 can transcriptionally activate p53 target genes such as p21 or bax-1, and induce growth suppression or apoptosis ( 34,  35).	transcription
58928	6	335850	5	NULL	NULL	0	NULL	statement 4			induce					growth suppression					NULL		0	NULL	NULL	NULL	gw60_pnas_95_12_6681_s_29	9618472	P73 can transcriptionally activate p53 target genes such as p21 or bax-1, and induce growth suppression or apoptosis ( 34,  35).	transcription
58929	7	335850	5	NULL	NULL	0	NULL	statement 3			induce					apoptosis					NULL		0	NULL	NULL	NULL	gw60_pnas_95_12_6681_s_29	9618472	P73 can transcriptionally activate p53 target genes such as p21 or bax-1, and induce growth suppression or apoptosis ( 34,  35).	transcription
58930	8	335850	5	NULL	NULL	0	NULL	statement 4			induce					apoptosis					NULL		0	NULL	NULL	NULL	gw60_pnas_95_12_6681_s_29	9618472	P73 can transcriptionally activate p53 target genes such as p21 or bax-1, and induce growth suppression or apoptosis ( 34,  35).	transcription
79506	1	335850	6	NULL	NULL	0	NULL	p73	GP		activates					p21	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_95_12_6681_s_29	9618472	P73 can transcriptionally activate p53 target genes such as p21 or bax-1, and induce growth suppression or apoptosis ( 34,  35).	transcription
79507	2	335850	6	NULL	NULL	0	NULL	p73	GP		activates					bax-1	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_95_12_6681_s_29	9618472	P73 can transcriptionally activate p53 target genes such as p21 or bax-1, and induce growth suppression or apoptosis ( 34,  35).	transcription
58931	1	335851	5	NULL	NULL	0	NULL	RDCs		treatment	activates		may			p73					NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_178	16169939	To confirm whether RDCs treatment leads to p53 and p73 activation, we analyzed the expression of two p53 target genes, p21 and Bax, that can account for cell growth arrest and apoptosis (Xiong et al., 1993 ; Brady and Gil-Gomez, 1998 ).	transcription
58932	2	335851	5	NULL	NULL	0	NULL	RDCs		treatment	activates		may			p53					NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_178	16169939	To confirm whether RDCs treatment leads to p53 and p73 activation, we analyzed the expression of two p53 target genes, p21 and Bax, that can account for cell growth arrest and apoptosis (Xiong et al., 1993 ; Brady and Gil-Gomez, 1998 ).	transcription
58933	3	335851	5	NULL	NULL	0	NULL	p21			accounts for					cell growth arrest					NULL		NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_178	16169939	To confirm whether RDCs treatment leads to p53 and p73 activation, we analyzed the expression of two p53 target genes, p21 and Bax, that can account for cell growth arrest and apoptosis (Xiong et al., 1993 ; Brady and Gil-Gomez, 1998 ).	transcription
58934	4	335851	5	NULL	NULL	0	NULL	p21			accounts for					apoptosis					NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_178	16169939	To confirm whether RDCs treatment leads to p53 and p73 activation, we analyzed the expression of two p53 target genes, p21 and Bax, that can account for cell growth arrest and apoptosis (Xiong et al., 1993 ; Brady and Gil-Gomez, 1998 ).	transcription
58935	5	335851	5	NULL	NULL	0	NULL	Bax			accounts for					cell growth arrest					NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_178	16169939	To confirm whether RDCs treatment leads to p53 and p73 activation, we analyzed the expression of two p53 target genes, p21 and Bax, that can account for cell growth arrest and apoptosis (Xiong et al., 1993 ; Brady and Gil-Gomez, 1998 ).	transcription
58936	6	335851	5	NULL	NULL	0	NULL	Bax			accounts for					apoptosis					NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_178	16169939	To confirm whether RDCs treatment leads to p53 and p73 activation, we analyzed the expression of two p53 target genes, p21 and Bax, that can account for cell growth arrest and apoptosis (Xiong et al., 1993 ; Brady and Gil-Gomez, 1998 ).	transcription
58937	7	335851	5	NULL	NULL	0	NULL	Bax			is a type of					p53 target gene					NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_178	16169939	To confirm whether RDCs treatment leads to p53 and p73 activation, we analyzed the expression of two p53 target genes, p21 and Bax, that can account for cell growth arrest and apoptosis (Xiong et al., 1993 ; Brady and Gil-Gomez, 1998 ).	transcription
58938	8	335851	5	NULL	NULL	0	NULL	p21			is a type of					p53 target gene					NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_315_3_1403_s_178	16169939	To confirm whether RDCs treatment leads to p53 and p73 activation, we analyzed the expression of two p53 target genes, p21 and Bax, that can account for cell growth arrest and apoptosis (Xiong et al., 1993 ; Brady and Gil-Gomez, 1998 ).	transcription
58939	1	335852	5	NULL	NULL	0	NULL	U2OS cells			treated with					cisplatin					NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_191	12535517	Treatment of U2OS cells with the DNA-damaging agent cisplatin (CDDP), an activator of p73 and p53 signaling   (Gong et al., 1999  ; Ono et al., 2001  ), results in an increase in endogenous Bax protein expression as visualized by Western blot   (Figure 6A) .	transcription
58940	2	335852	5	NULL	NULL	0	NULL	statement 1			increases					Bax protein		expression of;;endogenous			NULL	U2OS cells	NULL	NULL	NULL	NULL	gw60_molcell_11_1_11_s_191	12535517	Treatment of U2OS cells with the DNA-damaging agent cisplatin (CDDP), an activator of p73 and p53 signaling   (Gong et al., 1999  ; Ono et al., 2001  ), results in an increase in endogenous Bax protein expression as visualized by Western blot   (Figure 6A) .	transcription
58941	3	335852	5	NULL	NULL	0	NULL	cisplatin			is					CDDP					NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_191	12535517	Treatment of U2OS cells with the DNA-damaging agent cisplatin (CDDP), an activator of p73 and p53 signaling   (Gong et al., 1999  ; Ono et al., 2001  ), results in an increase in endogenous Bax protein expression as visualized by Western blot   (Figure 6A) .	transcription
58942	4	335852	5	NULL	NULL	0	NULL	cisplatin			is a type of					DNA-damaging agent					NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_191	12535517	Treatment of U2OS cells with the DNA-damaging agent cisplatin (CDDP), an activator of p73 and p53 signaling   (Gong et al., 1999  ; Ono et al., 2001  ), results in an increase in endogenous Bax protein expression as visualized by Western blot   (Figure 6A) .	transcription
58943	5	335852	5	NULL	NULL	0	NULL	cisplatin			activates					p73 signaling					NULL		NULL	NULL	NULL	NULL	gw60_molcell_11_1_11_s_191	12535517	Treatment of U2OS cells with the DNA-damaging agent cisplatin (CDDP), an activator of p73 and p53 signaling   (Gong et al., 1999  ; Ono et al., 2001  ), results in an increase in endogenous Bax protein expression as visualized by Western blot   (Figure 6A) .	transcription
58944	6	335852	5	NULL	NULL	0	NULL	cisplatin			activates					p53 signaling					NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_191	12535517	Treatment of U2OS cells with the DNA-damaging agent cisplatin (CDDP), an activator of p73 and p53 signaling   (Gong et al., 1999  ; Ono et al., 2001  ), results in an increase in endogenous Bax protein expression as visualized by Western blot   (Figure 6A) .	transcription
79501	1	335852	6	NULL	NULL	0	NULL	CDDP	Chemical		is					DNA-damaging agent cisplatin	Chemical				NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_191	12535517	Treatment of U2OS cells with the DNA-damaging agent cisplatin (CDDP), an activator of p73 and p53 signaling   (Gong et al., 1999  ; Ono et al., 2001  ), results in an increase in endogenous Bax protein expression as visualized by Western blot   (Figure 6A) .	transcription
79502	2	335852	6	NULL	NULL	0	NULL	CDDP	Chemical		activates					p73 signaling	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_191	12535517	Treatment of U2OS cells with the DNA-damaging agent cisplatin (CDDP), an activator of p73 and p53 signaling   (Gong et al., 1999  ; Ono et al., 2001  ), results in an increase in endogenous Bax protein expression as visualized by Western blot   (Figure 6A) .	transcription
79503	3	335852	6	NULL	NULL	0	NULL	CDDP	Chemical		activates					p53 signaling	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_191	12535517	Treatment of U2OS cells with the DNA-damaging agent cisplatin (CDDP), an activator of p73 and p53 signaling   (Gong et al., 1999  ; Ono et al., 2001  ), results in an increase in endogenous Bax protein expression as visualized by Western blot   (Figure 6A) .	transcription
79504	4	335852	6	NULL	NULL	0	NULL	CDDP	Chemical		increases					Bax protein	GP	expression of			NULL	U2OS cells	0	NULL	NULL	NULL	gw60_molcell_11_1_11_s_191	12535517	Treatment of U2OS cells with the DNA-damaging agent cisplatin (CDDP), an activator of p73 and p53 signaling   (Gong et al., 1999  ; Ono et al., 2001  ), results in an increase in endogenous Bax protein expression as visualized by Western blot   (Figure 6A) .	transcription
58945	1	335853	5	NULL	NULL	0	NULL	p63			interacts with					p21				p53-binding sites in promoter	NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_2_615_s_56	15120643	Furthermore, the factor demonstrated binding specificity different from those of  p63 and p73, proteins with high homology to p53; p63 and p73 interact with p53-binding  sites in the p21 and Bax promoters with similar affinity [  37,   38,   39 and   40] whereas the BC-binding factor discriminated these two sites showing much higher  affinity for the p21Waf1 site ( Fig. 1B).	transcription
58946	2	335853	5	NULL	NULL	0	NULL	p63			interacts with					Bax				p53-binding sites in promoter	NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_2_615_s_56	15120643	Furthermore, the factor demonstrated binding specificity different from those of  p63 and p73, proteins with high homology to p53; p63 and p73 interact with p53-binding  sites in the p21 and Bax promoters with similar affinity [  37,   38,   39 and   40] whereas the BC-binding factor discriminated these two sites showing much higher  affinity for the p21Waf1 site ( Fig. 1B).	transcription
58947	3	335853	5	NULL	NULL	0	NULL	statement 1			similar affinity as					statement 2					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_2_615_s_56	15120643	Furthermore, the factor demonstrated binding specificity different from those of  p63 and p73, proteins with high homology to p53; p63 and p73 interact with p53-binding  sites in the p21 and Bax promoters with similar affinity [  37,   38,   39 and   40] whereas the BC-binding factor discriminated these two sites showing much higher  affinity for the p21Waf1 site ( Fig. 1B).	transcription
58948	4	335853	5	NULL	NULL	0	NULL	p73			interacts with					p21				p53-binding sites in promoter	NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_2_615_s_56	15120643	Furthermore, the factor demonstrated binding specificity different from those of  p63 and p73, proteins with high homology to p53; p63 and p73 interact with p53-binding  sites in the p21 and Bax promoters with similar affinity [  37,   38,   39 and   40] whereas the BC-binding factor discriminated these two sites showing much higher  affinity for the p21Waf1 site ( Fig. 1B).	transcription
58949	5	335853	5	NULL	NULL	0	NULL	p73			interacts with					Bax				p53-binding sites in promoter	NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_2_615_s_56	15120643	Furthermore, the factor demonstrated binding specificity different from those of  p63 and p73, proteins with high homology to p53; p63 and p73 interact with p53-binding  sites in the p21 and Bax promoters with similar affinity [  37,   38,   39 and   40] whereas the BC-binding factor discriminated these two sites showing much higher  affinity for the p21Waf1 site ( Fig. 1B).	transcription
58950	6	335853	5	NULL	NULL	0	NULL	statement 4			similar affinity as					statement 5					NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_2_615_s_56	15120643	Furthermore, the factor demonstrated binding specificity different from those of  p63 and p73, proteins with high homology to p53; p63 and p73 interact with p53-binding  sites in the p21 and Bax promoters with similar affinity [  37,   38,   39 and   40] whereas the BC-binding factor discriminated these two sites showing much higher  affinity for the p21Waf1 site ( Fig. 1B).	transcription
79499	1	335853	6	NULL	NULL	0	NULL	p63	GP		bind					p21	GP			p53-binding site of promoter	NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_2_615_s_56	15120643	Furthermore, the factor demonstrated binding specificity different from those of  p63 and p73, proteins with high homology to p53; p63 and p73 interact with p53-binding  sites in the p21 and Bax promoters with similar affinity [  37,   38,   39 and   40] whereas the BC-binding factor discriminated these two sites showing much higher  affinity for the p21Waf1 site ( Fig. 1B).	transcription
79500	2	335853	6	NULL	NULL	0	NULL	p73	GP		bind					Bax	GP			p53-binding site of promoter	NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_318_2_615_s_56	15120643	Furthermore, the factor demonstrated binding specificity different from those of  p63 and p73, proteins with high homology to p53; p63 and p73 interact with p53-binding  sites in the p21 and Bax promoters with similar affinity [  37,   38,   39 and   40] whereas the BC-binding factor discriminated these two sites showing much higher  affinity for the p21Waf1 site ( Fig. 1B).	transcription
58951	1	335854	5	NULL	NULL	0	NULL	p73			activates					transcription					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_17_15113_s_215	11844794	Effect of MM1 on the p73-mediated Transcriptional Activation and Growth Suppression-- To determine whether or not MM1 affects the p73- or p53-dependent transcriptional activation in cells, p53/p73-responsive  Bax,  PG13, which carries 13 copies of the consensus p53-responsive element,  p21 waf1, or  MDM2-luciferase reporter construct was co-transfected with the expression plasmid for HA-p73alpha, HA-p73beta, HA-p73alpha-(1-427), or p53 in the presence or absence of the increasing amounts of FLAG-MM1 expression plasmid into p53-deficient human osteosarcoma SAOS-2 cells.	transcription
58952	2	335854	5	NULL	NULL	0	NULL	MM1			effects		may			statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_17_15113_s_215	11844794	Effect of MM1 on the p73-mediated Transcriptional Activation and Growth Suppression-- To determine whether or not MM1 affects the p73- or p53-dependent transcriptional activation in cells, p53/p73-responsive  Bax,  PG13, which carries 13 copies of the consensus p53-responsive element,  p21 waf1, or  MDM2-luciferase reporter construct was co-transfected with the expression plasmid for HA-p73alpha, HA-p73beta, HA-p73alpha-(1-427), or p53 in the presence or absence of the increasing amounts of FLAG-MM1 expression plasmid into p53-deficient human osteosarcoma SAOS-2 cells.	transcription
58953	1	335856	5	NULL	NULL	0	NULL	Gatm			catalyzes					creatine		rate-limiting step in synthesis of			NULL		0	NULL	NULL	NULL	gw70_pnas_100_8_4622_s_3	12671064	We identified  Gatm, a gene that encodes L-arginine:glycine amidinotransferase, which catalyzes the rate-limiting step in the synthesis of creatine.	transcription
58954	2	335856	5	NULL	NULL	0	NULL	Gatm			encodes					L-arginine:glycine amidinotransferase					NULL		0	NULL	NULL	NULL	gw70_pnas_100_8_4622_s_3	12671064	We identified  Gatm, a gene that encodes L-arginine:glycine amidinotransferase, which catalyzes the rate-limiting step in the synthesis of creatine.	transcription
79497	1	335856	6	NULL	NULL	0	NULL	Gatm	GP		encodes for					L-arginine:glycine amidinotransferase	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_100_8_4622_s_3	12671064	We identified  Gatm, a gene that encodes L-arginine:glycine amidinotransferase, which catalyzes the rate-limiting step in the synthesis of creatine.	transcription
79498	2	335856	6	NULL	NULL	0	NULL	Gatm	GP		catalyzes					creatine	Chemical	synthesis of 			NULL		0	NULL	NULL	NULL	gw70_pnas_100_8_4622_s_3	12671064	We identified  Gatm, a gene that encodes L-arginine:glycine amidinotransferase, which catalyzes the rate-limiting step in the synthesis of creatine.	transcription
58955	1	335857	5	NULL	NULL	0	NULL	prednisolone			inhibit					muscle contractile proteins		proteolysis			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_13_9452_s_226	10734092	Measurements of serum creatine kinase and myoglobin, along with measurements of urinary excretion of 3-methylhistidine and glycine from these patients, suggest that prednisolone inhibits proteolysis of muscle contractile proteins ( 30).	transcription
79496	1	335857	6	NULL	NULL	0	NULL	prednisolone	Chemical		inhibits					muscle contractile proteins 	GP	proteolysis of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_13_9452_s_226	10734092	Measurements of serum creatine kinase and myoglobin, along with measurements of urinary excretion of 3-methylhistidine and glycine from these patients, suggest that prednisolone inhibits proteolysis of muscle contractile proteins ( 30).	transcription
58956	1	335862	5	NULL	NULL	0	NULL	Leydig cells		primary;;immature;;porcine	secrete					dehydroepiandrosterone					NULL		0	NULL	NULL	NULL	gw60_biolreprod_69_2_592_s_353	12700195	Biochem Biophys Acta  1994 1222:71-80 [Medline]   Mauduit C, Chauvin MA, de Peretti E, Morera AM, Benahmed M.  Effect of activin A on dehydroepiandrosterone and testosterone secretion by primary immature porcine Leydig cells.	transcription
58957	2	335862	5	NULL	NULL	0	NULL	activin A			effects		potentially			statement 1					NULL		0	NULL	NULL	NULL	gw60_biolreprod_69_2_592_s_353	12700195	Biochem Biophys Acta  1994 1222:71-80 [Medline]   Mauduit C, Chauvin MA, de Peretti E, Morera AM, Benahmed M.  Effect of activin A on dehydroepiandrosterone and testosterone secretion by primary immature porcine Leydig cells.	transcription
58958	3	335862	5	NULL	NULL	0	NULL	Leydig cells		primary;;immature;;porcine	secrete					testosterone					NULL		0	NULL	NULL	NULL	gw60_biolreprod_69_2_592_s_353	12700195	Biochem Biophys Acta  1994 1222:71-80 [Medline]   Mauduit C, Chauvin MA, de Peretti E, Morera AM, Benahmed M.  Effect of activin A on dehydroepiandrosterone and testosterone secretion by primary immature porcine Leydig cells.	transcription
58959	4	335862	5	NULL	NULL	0	NULL	activin A			effects		potentially			statement 3					NULL		0	NULL	NULL	NULL	gw60_biolreprod_69_2_592_s_353	12700195	Biochem Biophys Acta  1994 1222:71-80 [Medline]   Mauduit C, Chauvin MA, de Peretti E, Morera AM, Benahmed M.  Effect of activin A on dehydroepiandrosterone and testosterone secretion by primary immature porcine Leydig cells.	transcription
58960	1	335863	5	NULL	NULL	0	NULL	DHT			is					dihydrotestosterone					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol-endocrinol-metab_290_5_16368782_s_4	16368782	Dihydrotestosterone  (DHT) and testosterone (T) stimulate prostate cancer cell growth, development,  and function, whereas the effects of DHT and T in prostate stromal cells,  and of dehydroepiandrosterone (DHEA) in prostate cancer or stromal cells,  are uncertain.	transcription
58961	2	335863	5	NULL	NULL	0	NULL	T			is					testosterone					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol-endocrinol-metab_290_5_16368782_s_4	16368782	Dihydrotestosterone  (DHT) and testosterone (T) stimulate prostate cancer cell growth, development,  and function, whereas the effects of DHT and T in prostate stromal cells,  and of dehydroepiandrosterone (DHEA) in prostate cancer or stromal cells,  are uncertain.	transcription
58962	3	335863	5	NULL	NULL	0	NULL	testosterone			stimulates					prostate cancer cell		growth of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol-endocrinol-metab_290_5_16368782_s_4	16368782	Dihydrotestosterone  (DHT) and testosterone (T) stimulate prostate cancer cell growth, development,  and function, whereas the effects of DHT and T in prostate stromal cells,  and of dehydroepiandrosterone (DHEA) in prostate cancer or stromal cells,  are uncertain.	transcription
58963	4	335863	5	NULL	NULL	0	NULL	testosterone			stimulates					prostate cancer cell		development of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol-endocrinol-metab_290_5_16368782_s_4	16368782	Dihydrotestosterone  (DHT) and testosterone (T) stimulate prostate cancer cell growth, development,  and function, whereas the effects of DHT and T in prostate stromal cells,  and of dehydroepiandrosterone (DHEA) in prostate cancer or stromal cells,  are uncertain.	transcription
58964	5	335863	5	NULL	NULL	0	NULL	testosterone			stimulates					prostate cancer cell		function of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol-endocrinol-metab_290_5_16368782_s_4	16368782	Dihydrotestosterone  (DHT) and testosterone (T) stimulate prostate cancer cell growth, development,  and function, whereas the effects of DHT and T in prostate stromal cells,  and of dehydroepiandrosterone (DHEA) in prostate cancer or stromal cells,  are uncertain.	transcription
58965	6	335863	5	NULL	NULL	0	NULL	dihydrotestosterone			stimulates					prostate cancer cell		growth of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol-endocrinol-metab_290_5_16368782_s_4	16368782	Dihydrotestosterone  (DHT) and testosterone (T) stimulate prostate cancer cell growth, development,  and function, whereas the effects of DHT and T in prostate stromal cells,  and of dehydroepiandrosterone (DHEA) in prostate cancer or stromal cells,  are uncertain.	transcription
58966	7	335863	5	NULL	NULL	0	NULL	dihydrotestosterone			stimulates					prostate cancer cell		development of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol-endocrinol-metab_290_5_16368782_s_4	16368782	Dihydrotestosterone  (DHT) and testosterone (T) stimulate prostate cancer cell growth, development,  and function, whereas the effects of DHT and T in prostate stromal cells,  and of dehydroepiandrosterone (DHEA) in prostate cancer or stromal cells,  are uncertain.	transcription
58967	8	335863	5	NULL	NULL	0	NULL	dihydrotestosterone			stimulates					prostate cancer cell		function of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol-endocrinol-metab_290_5_16368782_s_4	16368782	Dihydrotestosterone  (DHT) and testosterone (T) stimulate prostate cancer cell growth, development,  and function, whereas the effects of DHT and T in prostate stromal cells,  and of dehydroepiandrosterone (DHEA) in prostate cancer or stromal cells,  are uncertain.	transcription
79492	1	335863	6	NULL	NULL	0	NULL	Dihydrotestosterone	GP		stimulate					prostate cancer cell	cell	growth of 			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol-endocrinol-metab_290_5_16368782_s_4	16368782	Dihydrotestosterone  (DHT) and testosterone (T) stimulate prostate cancer cell growth, development,  and function, whereas the effects of DHT and T in prostate stromal cells,  and of dehydroepiandrosterone (DHEA) in prostate cancer or stromal cells,  are uncertain.	transcription
79493	2	335863	6	NULL	NULL	0	NULL	testosterone	GP		stimulates					prostate cancer cell	cell	growth of 			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol-endocrinol-metab_290_5_16368782_s_4	16368782	Dihydrotestosterone  (DHT) and testosterone (T) stimulate prostate cancer cell growth, development,  and function, whereas the effects of DHT and T in prostate stromal cells,  and of dehydroepiandrosterone (DHEA) in prostate cancer or stromal cells,  are uncertain.	transcription
79494	3	335863	6	NULL	NULL	0	NULL	testosterone	GP		is					T	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol-endocrinol-metab_290_5_16368782_s_4	16368782	Dihydrotestosterone  (DHT) and testosterone (T) stimulate prostate cancer cell growth, development,  and function, whereas the effects of DHT and T in prostate stromal cells,  and of dehydroepiandrosterone (DHEA) in prostate cancer or stromal cells,  are uncertain.	transcription
79495	4	335863	6	NULL	NULL	0	NULL	DHT	GP		is					Dihydrotestosterone	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_am-j-physiol-endocrinol-metab_290_5_16368782_s_4	16368782	Dihydrotestosterone  (DHT) and testosterone (T) stimulate prostate cancer cell growth, development,  and function, whereas the effects of DHT and T in prostate stromal cells,  and of dehydroepiandrosterone (DHEA) in prostate cancer or stromal cells,  are uncertain.	transcription
58968	1	335865	5	NULL	NULL	0	NULL	CRH			does not modulate					CRH-R		expression of			NULL		0	NULL	NULL	NULL	gw60_pnas_99_10_7148_s_8	12011471	CRH, dehydroepiandrosterone, and 17beta-estradiol did not modulate CRH-R expression, whereas testosterone at 10 7 M down-regulated CRH-R1 and CRH-R2 mRNA expression at 6 to 24 h, and growth hormone (GH) switched CRH-R1 mRNA expression to CRH-R2 at 24 h.	transcription
58969	2	335865	5	NULL	NULL	0	NULL	dehydroepiandrosterone			does not modulate					CRH-R		expression of			NULL		0	NULL	NULL	NULL	gw60_pnas_99_10_7148_s_8	12011471	CRH, dehydroepiandrosterone, and 17beta-estradiol did not modulate CRH-R expression, whereas testosterone at 10 7 M down-regulated CRH-R1 and CRH-R2 mRNA expression at 6 to 24 h, and growth hormone (GH) switched CRH-R1 mRNA expression to CRH-R2 at 24 h.	transcription
58970	3	335865	5	NULL	NULL	0	NULL	17beta-estradiol			does not modulate					CRH-R		expression of			NULL		0	NULL	NULL	NULL	gw60_pnas_99_10_7148_s_8	12011471	CRH, dehydroepiandrosterone, and 17beta-estradiol did not modulate CRH-R expression, whereas testosterone at 10 7 M down-regulated CRH-R1 and CRH-R2 mRNA expression at 6 to 24 h, and growth hormone (GH) switched CRH-R1 mRNA expression to CRH-R2 at 24 h.	transcription
58971	4	335865	5	NULL	NULL	0	NULL	testosterone			down-regulates					CRH-R1 mRNA		expression of			NULL		0	NULL	NULL	NULL	gw60_pnas_99_10_7148_s_8	12011471	CRH, dehydroepiandrosterone, and 17beta-estradiol did not modulate CRH-R expression, whereas testosterone at 10 7 M down-regulated CRH-R1 and CRH-R2 mRNA expression at 6 to 24 h, and growth hormone (GH) switched CRH-R1 mRNA expression to CRH-R2 at 24 h.	transcription
58972	5	335865	5	NULL	NULL	0	NULL	testosterone			down-regulates					CRH-R2 mRNA		expression of			NULL		0	NULL	NULL	NULL	gw60_pnas_99_10_7148_s_8	12011471	CRH, dehydroepiandrosterone, and 17beta-estradiol did not modulate CRH-R expression, whereas testosterone at 10 7 M down-regulated CRH-R1 and CRH-R2 mRNA expression at 6 to 24 h, and growth hormone (GH) switched CRH-R1 mRNA expression to CRH-R2 at 24 h.	transcription
58973	6	335865	5	NULL	NULL	0	NULL	CRH-R1 mRNA		expression of	switched to					CRH-R2					NULL		0	NULL	NULL	NULL	gw60_pnas_99_10_7148_s_8	12011471	CRH, dehydroepiandrosterone, and 17beta-estradiol did not modulate CRH-R expression, whereas testosterone at 10 7 M down-regulated CRH-R1 and CRH-R2 mRNA expression at 6 to 24 h, and growth hormone (GH) switched CRH-R1 mRNA expression to CRH-R2 at 24 h.	transcription
58974	7	335865	5	NULL	NULL	0	NULL	growth hormone			is required for					statement 6					NULL		0	NULL	NULL	NULL	gw60_pnas_99_10_7148_s_8	12011471	CRH, dehydroepiandrosterone, and 17beta-estradiol did not modulate CRH-R expression, whereas testosterone at 10 7 M down-regulated CRH-R1 and CRH-R2 mRNA expression at 6 to 24 h, and growth hormone (GH) switched CRH-R1 mRNA expression to CRH-R2 at 24 h.	transcription
58975	8	335865	5	NULL	NULL	0	NULL	growth hormone			is					GH					NULL		0	NULL	NULL	NULL	gw60_pnas_99_10_7148_s_8	12011471	CRH, dehydroepiandrosterone, and 17beta-estradiol did not modulate CRH-R expression, whereas testosterone at 10 7 M down-regulated CRH-R1 and CRH-R2 mRNA expression at 6 to 24 h, and growth hormone (GH) switched CRH-R1 mRNA expression to CRH-R2 at 24 h.	transcription
79487	1	335865	6	NULL	NULL	NULL	NULL	testosterone	GP		downregulates					CRH-R1 mRNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_pnas_99_10_7148_s_8	12011471	CRH, dehydroepiandrosterone, and 17beta-estradiol did not modulate CRH-R expression, whereas testosterone at 10 7 M down-regulated CRH-R1 and CRH-R2 mRNA expression at 6 to 24 h, and growth hormone (GH) switched CRH-R1 mRNA expression to CRH-R2 at 24 h.	transcription
79488	2	335865	6	NULL	NULL	0	NULL	testosterone	Chemical		downregulates					CRH-R2 mRNA	NucleicAcid	expression of			NULL		0	NULL	NULL	NULL	gw60_pnas_99_10_7148_s_8	12011471	CRH, dehydroepiandrosterone, and 17beta-estradiol did not modulate CRH-R expression, whereas testosterone at 10 7 M down-regulated CRH-R1 and CRH-R2 mRNA expression at 6 to 24 h, and growth hormone (GH) switched CRH-R1 mRNA expression to CRH-R2 at 24 h.	transcription
79489	3	335865	6	NULL	NULL	0	NULL	CRH	GP		does not modulate					CRH-R	NucleicAcid	expression of			NULL		0	NULL	NULL	NULL	gw60_pnas_99_10_7148_s_8	12011471	CRH, dehydroepiandrosterone, and 17beta-estradiol did not modulate CRH-R expression, whereas testosterone at 10 7 M down-regulated CRH-R1 and CRH-R2 mRNA expression at 6 to 24 h, and growth hormone (GH) switched CRH-R1 mRNA expression to CRH-R2 at 24 h.	transcription
79490	4	335865	6	NULL	NULL	0	NULL	dehydroepiandrosterone	Chemical		does not modulate					CRH-R	NucleicAcid	expression of			NULL		0	NULL	NULL	NULL	gw60_pnas_99_10_7148_s_8	12011471	CRH, dehydroepiandrosterone, and 17beta-estradiol did not modulate CRH-R expression, whereas testosterone at 10 7 M down-regulated CRH-R1 and CRH-R2 mRNA expression at 6 to 24 h, and growth hormone (GH) switched CRH-R1 mRNA expression to CRH-R2 at 24 h.	transcription
79491	5	335865	6	NULL	NULL	0	NULL	17beta-estradiol	Chemical		does not modulate					CRH-R	NucleicAcid	expression of			NULL		0	NULL	NULL	NULL	gw60_pnas_99_10_7148_s_8	12011471	CRH, dehydroepiandrosterone, and 17beta-estradiol did not modulate CRH-R expression, whereas testosterone at 10 7 M down-regulated CRH-R1 and CRH-R2 mRNA expression at 6 to 24 h, and growth hormone (GH) switched CRH-R1 mRNA expression to CRH-R2 at 24 h.	transcription
58976	1	335869	5	NULL	NULL	0	NULL	cyclization reactions		concerted	fabricates					four-fused-ring steroid nucleus					NULL	Drosophila	NULL	NULL	NULL	NULL	gw70_annurevnutr_25_0_499_s_247	16011476	In the case of  Drosophila this metabolic inability was recently shown to be due to the absence from the genome  of coding regions for seven enzymes in the sterol branch, including lanosterol synthase,  which catalyzes the concerted cyclization reactions required to fabricate the four-fused-ring  steroid nucleus, and 7-dehydrocholesterol reductase, which synthesizes the definitive  cholesterol molecule ( 88).	transcription
58977	2	335869	5	NULL	NULL	0	NULL	lanosterol synthase			catalyzes					statement 1					NULL	Drosophila	NULL	NULL	NULL	NULL	gw70_annurevnutr_25_0_499_s_247	16011476	In the case of  Drosophila this metabolic inability was recently shown to be due to the absence from the genome  of coding regions for seven enzymes in the sterol branch, including lanosterol synthase,  which catalyzes the concerted cyclization reactions required to fabricate the four-fused-ring  steroid nucleus, and 7-dehydrocholesterol reductase, which synthesizes the definitive  cholesterol molecule ( 88).	transcription
58978	3	335869	5	NULL	NULL	0	NULL	7-dehydrocholesterol reductase			synthesize					cholesterol molecule		definitive			NULL	Drosophila	NULL	NULL	NULL	NULL	gw70_annurevnutr_25_0_499_s_247	16011476	In the case of  Drosophila this metabolic inability was recently shown to be due to the absence from the genome  of coding regions for seven enzymes in the sterol branch, including lanosterol synthase,  which catalyzes the concerted cyclization reactions required to fabricate the four-fused-ring  steroid nucleus, and 7-dehydrocholesterol reductase, which synthesizes the definitive  cholesterol molecule ( 88).	transcription
58979	1	335870	5	NULL	NULL	0	NULL	7-ketocholesterol			is a type of					oxysterol					NULL		0	NULL	NULL	NULL	gw70_annurevcelldevbiol_22_0_129_s_396	16753029	( d) Cholesterol activates ACAT1 when an oxysterol (7-ketocholesterol) is the substrate.	transcription
58980	2	335870	5	NULL	NULL	0	NULL	cholesterol			activates					ACAT1					NULL		0	NULL	NULL	NULL	gw70_annurevcelldevbiol_22_0_129_s_396	16753029	( d) Cholesterol activates ACAT1 when an oxysterol (7-ketocholesterol) is the substrate.	transcription
58981	3	335870	5	NULL	NULL	0	NULL	7-ketocholesterol			is a substrate for					statement 2					NULL		0	NULL	NULL	NULL	gw70_annurevcelldevbiol_22_0_129_s_396	16753029	( d) Cholesterol activates ACAT1 when an oxysterol (7-ketocholesterol) is the substrate.	transcription
79485	1	335870	6	NULL	NULL	0	NULL	cholesterol	Chemical		activates					ACAT1	GP				NULL		0	NULL	NULL	NULL	gw70_annurevcelldevbiol_22_0_129_s_396	16753029	( d) Cholesterol activates ACAT1 when an oxysterol (7-ketocholesterol) is the substrate.	transcription
79486	2	335870	6	NULL	NULL	0	NULL	statement 1	Process		occurs in presence of					oxysterol	Chemical				NULL		0	NULL	NULL	NULL	gw70_annurevcelldevbiol_22_0_129_s_396	16753029	( d) Cholesterol activates ACAT1 when an oxysterol (7-ketocholesterol) is the substrate.	transcription
58982	1	335871	5	NULL	NULL	0	NULL	cholesterol efflux		macrophage foam cells	is induced by					apoA-I					NULL		0	NULL	NULL	NULL	gw60_jlipidres_40_9_1636_s_3	10484610	For example, 7-ketocholesterol (7KC) inhibits cholesterol efflux from macrophage foam cells induced by apolipoprotein A-I (apoA-I).	transcription
58983	2	335871	5	NULL	NULL	0	NULL	apoA-I			is					apolipoprotein A-I					NULL		0	NULL	NULL	NULL	gw60_jlipidres_40_9_1636_s_3	10484610	For example, 7-ketocholesterol (7KC) inhibits cholesterol efflux from macrophage foam cells induced by apolipoprotein A-I (apoA-I).	transcription
58984	3	335871	5	NULL	NULL	0	NULL	7KC			is					7-ketocholesterol					NULL		0	NULL	NULL	NULL	gw60_jlipidres_40_9_1636_s_3	10484610	For example, 7-ketocholesterol (7KC) inhibits cholesterol efflux from macrophage foam cells induced by apolipoprotein A-I (apoA-I).	transcription
58985	4	335871	5	NULL	NULL	0	NULL	7KC			inhibit					statement 1					NULL		0	NULL	NULL	NULL	gw60_jlipidres_40_9_1636_s_3	10484610	For example, 7-ketocholesterol (7KC) inhibits cholesterol efflux from macrophage foam cells induced by apolipoprotein A-I (apoA-I).	transcription
79481	1	335871	6	NULL	NULL	0	NULL	apolipoprotein A-I	GP		induces					macrophage foam cells 	Cell				NULL		0	NULL	NULL	NULL	gw60_jlipidres_40_9_1636_s_3	10484610	For example, 7-ketocholesterol (7KC) inhibits cholesterol efflux from macrophage foam cells induced by apolipoprotein A-I (apoA-I).	transcription
79482	2	335871	6	NULL	NULL	0	NULL	7-ketocholesterol	Chemical		inhibits					cholesterol	Chemical	efflux of 			NULL	macrophage foam cell	0	NULL	NULL	NULL	gw60_jlipidres_40_9_1636_s_3	10484610	For example, 7-ketocholesterol (7KC) inhibits cholesterol efflux from macrophage foam cells induced by apolipoprotein A-I (apoA-I).	transcription
79483	3	335871	6	NULL	NULL	0	NULL	7-ketocholesterol	Chemical		is					7KC	Chemical				NULL		0	NULL	NULL	NULL	gw60_jlipidres_40_9_1636_s_3	10484610	For example, 7-ketocholesterol (7KC) inhibits cholesterol efflux from macrophage foam cells induced by apolipoprotein A-I (apoA-I).	transcription
79484	4	335871	6	NULL	NULL	0	NULL	apoA-I	GP		is					apolipoprotein A-I 	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_40_9_1636_s_3	10484610	For example, 7-ketocholesterol (7KC) inhibits cholesterol efflux from macrophage foam cells induced by apolipoprotein A-I (apoA-I).	transcription
58986	1	335872	5	NULL	NULL	0	NULL	death pathway			is mediated by					Fas					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-mol-cell-cardiol_39_5_16198370_s_4	16198370	In  this study, we investigated whether 7-ketocholesterol, one of the major  cholesterol oxides in the lesions, altered resistance of HVSMC to Fas-mediated  death pathway.	transcription
58987	2	335872	5	NULL	NULL	0	NULL	HVSMC			resistant to					statement 1					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-mol-cell-cardiol_39_5_16198370_s_4	16198370	In  this study, we investigated whether 7-ketocholesterol, one of the major  cholesterol oxides in the lesions, altered resistance of HVSMC to Fas-mediated  death pathway.	transcription
58988	3	335872	5	NULL	NULL	0	NULL	7-ketocholesterol			alter		may			statement 2					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-mol-cell-cardiol_39_5_16198370_s_4	16198370	In  this study, we investigated whether 7-ketocholesterol, one of the major  cholesterol oxides in the lesions, altered resistance of HVSMC to Fas-mediated  death pathway.	transcription
58989	4	335872	5	NULL	NULL	0	NULL	7-ketocholesterol			is a type of					cholesterol oxides					NULL	lesions	0	NULL	NULL	NULL	abs-batch0530-0539_j-mol-cell-cardiol_39_5_16198370_s_4	16198370	In  this study, we investigated whether 7-ketocholesterol, one of the major  cholesterol oxides in the lesions, altered resistance of HVSMC to Fas-mediated  death pathway.	transcription
79480	1	335872	6	NULL	NULL	0	NULL	HVSMC	Cell		is resistant to					Fas-mediated death pathway	Process				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-mol-cell-cardiol_39_5_16198370_s_4	16198370	In  this study, we investigated whether 7-ketocholesterol, one of the major  cholesterol oxides in the lesions, altered resistance of HVSMC to Fas-mediated  death pathway.	transcription
58990	1	335873	5	NULL	NULL	0	NULL	oxysterols			effects		may			SMC DNA		synthesis of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_194_s_150	8620332	Effect of Oxysterols on SMC DNA Synthesis    xidation of LDL is associated with increased accumulation of a number of oxysterols, such as 5alpha,6alpha-epoxy cholesterol, cholestane-3beta,5alpha,6beta-triol, 7alpha-hydroxycholesterol, 7beta-hydroxycholesterol, 7-ketocholesterol, 24-hydroxycholesterol, 25-hydroxycholesterol, and 27-hydroxycholesterol.	transcription
58991	2	335873	5	NULL	NULL	0	NULL	LDL		oxidation of	is associated with					5alpha,6alpha-epoxy cholesterol		increased accumulation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_194_s_150	8620332	Effect of Oxysterols on SMC DNA Synthesis    xidation of LDL is associated with increased accumulation of a number of oxysterols, such as 5alpha,6alpha-epoxy cholesterol, cholestane-3beta,5alpha,6beta-triol, 7alpha-hydroxycholesterol, 7beta-hydroxycholesterol, 7-ketocholesterol, 24-hydroxycholesterol, 25-hydroxycholesterol, and 27-hydroxycholesterol.	transcription
58992	3	335873	5	NULL	NULL	0	NULL	LDL		oxidation of	is associated with					cholestane-3beta,5alpha,6beta-triol		increased accumulation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_194_s_150	8620332	Effect of Oxysterols on SMC DNA Synthesis    xidation of LDL is associated with increased accumulation of a number of oxysterols, such as 5alpha,6alpha-epoxy cholesterol, cholestane-3beta,5alpha,6beta-triol, 7alpha-hydroxycholesterol, 7beta-hydroxycholesterol, 7-ketocholesterol, 24-hydroxycholesterol, 25-hydroxycholesterol, and 27-hydroxycholesterol.	transcription
58993	4	335873	5	NULL	NULL	0	NULL	LDL		oxidation of	is associated with					7alpha-hydroxycholesterol		increased accumulation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_194_s_150	8620332	Effect of Oxysterols on SMC DNA Synthesis    xidation of LDL is associated with increased accumulation of a number of oxysterols, such as 5alpha,6alpha-epoxy cholesterol, cholestane-3beta,5alpha,6beta-triol, 7alpha-hydroxycholesterol, 7beta-hydroxycholesterol, 7-ketocholesterol, 24-hydroxycholesterol, 25-hydroxycholesterol, and 27-hydroxycholesterol.	transcription
58994	5	335873	5	NULL	NULL	0	NULL	LDL		oxidation of	is associated with					7beta-hydroxycholesterol		increased accumulation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_194_s_150	8620332	Effect of Oxysterols on SMC DNA Synthesis    xidation of LDL is associated with increased accumulation of a number of oxysterols, such as 5alpha,6alpha-epoxy cholesterol, cholestane-3beta,5alpha,6beta-triol, 7alpha-hydroxycholesterol, 7beta-hydroxycholesterol, 7-ketocholesterol, 24-hydroxycholesterol, 25-hydroxycholesterol, and 27-hydroxycholesterol.	transcription
58995	6	335873	5	NULL	NULL	0	NULL	LDL		oxidation of	is associated with					7-ketocholesterol		increased accumulation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_194_s_150	8620332	Effect of Oxysterols on SMC DNA Synthesis    xidation of LDL is associated with increased accumulation of a number of oxysterols, such as 5alpha,6alpha-epoxy cholesterol, cholestane-3beta,5alpha,6beta-triol, 7alpha-hydroxycholesterol, 7beta-hydroxycholesterol, 7-ketocholesterol, 24-hydroxycholesterol, 25-hydroxycholesterol, and 27-hydroxycholesterol.	transcription
58996	7	335873	5	NULL	NULL	0	NULL	LDL		oxidation of	is associated with					24-hydroxycholesterol		increased accumulation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_194_s_150	8620332	Effect of Oxysterols on SMC DNA Synthesis    xidation of LDL is associated with increased accumulation of a number of oxysterols, such as 5alpha,6alpha-epoxy cholesterol, cholestane-3beta,5alpha,6beta-triol, 7alpha-hydroxycholesterol, 7beta-hydroxycholesterol, 7-ketocholesterol, 24-hydroxycholesterol, 25-hydroxycholesterol, and 27-hydroxycholesterol.	transcription
58997	8	335873	5	NULL	NULL	0	NULL	LDL		oxidation of	is associated with					25-hydroxycholesterol		increased accumulation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_194_s_150	8620332	Effect of Oxysterols on SMC DNA Synthesis    xidation of LDL is associated with increased accumulation of a number of oxysterols, such as 5alpha,6alpha-epoxy cholesterol, cholestane-3beta,5alpha,6beta-triol, 7alpha-hydroxycholesterol, 7beta-hydroxycholesterol, 7-ketocholesterol, 24-hydroxycholesterol, 25-hydroxycholesterol, and 27-hydroxycholesterol.	transcription
58998	9	335873	5	NULL	NULL	0	NULL	LDL		oxidation of	is associated with					27-hydroxycholesterol		increased accumulation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_194_s_150	8620332	Effect of Oxysterols on SMC DNA Synthesis    xidation of LDL is associated with increased accumulation of a number of oxysterols, such as 5alpha,6alpha-epoxy cholesterol, cholestane-3beta,5alpha,6beta-triol, 7alpha-hydroxycholesterol, 7beta-hydroxycholesterol, 7-ketocholesterol, 24-hydroxycholesterol, 25-hydroxycholesterol, and 27-hydroxycholesterol.	transcription
58999	10	335873	5	NULL	NULL	0	NULL	5alpha,6alpha-epoxy cholesterol			is a type of					oxysterol					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_194_s_150	8620332	Effect of Oxysterols on SMC DNA Synthesis    xidation of LDL is associated with increased accumulation of a number of oxysterols, such as 5alpha,6alpha-epoxy cholesterol, cholestane-3beta,5alpha,6beta-triol, 7alpha-hydroxycholesterol, 7beta-hydroxycholesterol, 7-ketocholesterol, 24-hydroxycholesterol, 25-hydroxycholesterol, and 27-hydroxycholesterol.	transcription
59000	11	335873	5	NULL	NULL	0	NULL	cholestane-3beta,5alpha,6beta-triol			is a type of					oxysterol					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_194_s_150	8620332	Effect of Oxysterols on SMC DNA Synthesis    xidation of LDL is associated with increased accumulation of a number of oxysterols, such as 5alpha,6alpha-epoxy cholesterol, cholestane-3beta,5alpha,6beta-triol, 7alpha-hydroxycholesterol, 7beta-hydroxycholesterol, 7-ketocholesterol, 24-hydroxycholesterol, 25-hydroxycholesterol, and 27-hydroxycholesterol.	transcription
59001	12	335873	5	NULL	NULL	0	NULL	7alpha-hydroxycholesterol			is a type of					oxysterol					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_194_s_150	8620332	Effect of Oxysterols on SMC DNA Synthesis    xidation of LDL is associated with increased accumulation of a number of oxysterols, such as 5alpha,6alpha-epoxy cholesterol, cholestane-3beta,5alpha,6beta-triol, 7alpha-hydroxycholesterol, 7beta-hydroxycholesterol, 7-ketocholesterol, 24-hydroxycholesterol, 25-hydroxycholesterol, and 27-hydroxycholesterol.	transcription
59002	13	335873	5	NULL	NULL	0	NULL	7beta-hydroxycholesterol			is a type of					oxysterol					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_194_s_150	8620332	Effect of Oxysterols on SMC DNA Synthesis    xidation of LDL is associated with increased accumulation of a number of oxysterols, such as 5alpha,6alpha-epoxy cholesterol, cholestane-3beta,5alpha,6beta-triol, 7alpha-hydroxycholesterol, 7beta-hydroxycholesterol, 7-ketocholesterol, 24-hydroxycholesterol, 25-hydroxycholesterol, and 27-hydroxycholesterol.	transcription
59003	14	335873	5	NULL	NULL	0	NULL	7-ketocholesterol			is a type of					oxysterol					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_194_s_150	8620332	Effect of Oxysterols on SMC DNA Synthesis    xidation of LDL is associated with increased accumulation of a number of oxysterols, such as 5alpha,6alpha-epoxy cholesterol, cholestane-3beta,5alpha,6beta-triol, 7alpha-hydroxycholesterol, 7beta-hydroxycholesterol, 7-ketocholesterol, 24-hydroxycholesterol, 25-hydroxycholesterol, and 27-hydroxycholesterol.	transcription
59004	15	335873	5	NULL	NULL	0	NULL	24-hydroxycholesterol			is a type of					oxysterol					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_194_s_150	8620332	Effect of Oxysterols on SMC DNA Synthesis    xidation of LDL is associated with increased accumulation of a number of oxysterols, such as 5alpha,6alpha-epoxy cholesterol, cholestane-3beta,5alpha,6beta-triol, 7alpha-hydroxycholesterol, 7beta-hydroxycholesterol, 7-ketocholesterol, 24-hydroxycholesterol, 25-hydroxycholesterol, and 27-hydroxycholesterol.	transcription
59005	16	335873	5	NULL	NULL	0	NULL	25-hydroxycholesterol			is a type of					oxysterol					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_194_s_150	8620332	Effect of Oxysterols on SMC DNA Synthesis    xidation of LDL is associated with increased accumulation of a number of oxysterols, such as 5alpha,6alpha-epoxy cholesterol, cholestane-3beta,5alpha,6beta-triol, 7alpha-hydroxycholesterol, 7beta-hydroxycholesterol, 7-ketocholesterol, 24-hydroxycholesterol, 25-hydroxycholesterol, and 27-hydroxycholesterol.	transcription
59006	17	335873	5	NULL	NULL	0	NULL	27-hydroxycholesterol			is a type of					oxysterol					NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_194_s_150	8620332	Effect of Oxysterols on SMC DNA Synthesis    xidation of LDL is associated with increased accumulation of a number of oxysterols, such as 5alpha,6alpha-epoxy cholesterol, cholestane-3beta,5alpha,6beta-triol, 7alpha-hydroxycholesterol, 7beta-hydroxycholesterol, 7-ketocholesterol, 24-hydroxycholesterol, 25-hydroxycholesterol, and 27-hydroxycholesterol.	transcription
79479	1	335873	6	NULL	NULL	0	NULL	LDL	Chemical	oxidation of 	is associated with					oxysterol	Chemical	accumulation of 			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_16_2_194_s_150	8620332	Effect of Oxysterols on SMC DNA Synthesis    xidation of LDL is associated with increased accumulation of a number of oxysterols, such as 5alpha,6alpha-epoxy cholesterol, cholestane-3beta,5alpha,6beta-triol, 7alpha-hydroxycholesterol, 7beta-hydroxycholesterol, 7-ketocholesterol, 24-hydroxycholesterol, 25-hydroxycholesterol, and 27-hydroxycholesterol.	transcription
59007	1	335874	5	NULL	NULL	0	NULL	ACAT			is					acyl-CoA:cholesterol acyltransferase					NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_9_1844_s_144	9741697	To determine whether the acyl-CoA:cholesterol acyltransferase (ACAT) activity was inhibited by CPHS, we tested the effect of this steroid in the presence of 7-ketocholesterol which is known to be an ACAT substrate  ( 16).	transcription
59008	2	335874	5	NULL	NULL	0	NULL	ACAT		activity of	is inhibited by		may be			CPHS					NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_9_1844_s_144	9741697	To determine whether the acyl-CoA:cholesterol acyltransferase (ACAT) activity was inhibited by CPHS, we tested the effect of this steroid in the presence of 7-ketocholesterol which is known to be an ACAT substrate  ( 16).	transcription
59009	3	335874	5	NULL	NULL	0	NULL	7-ketocholesterol			is a substrate of					ACAT 					NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_9_1844_s_144	9741697	To determine whether the acyl-CoA:cholesterol acyltransferase (ACAT) activity was inhibited by CPHS, we tested the effect of this steroid in the presence of 7-ketocholesterol which is known to be an ACAT substrate  ( 16).	transcription
59010	1	335876	5	NULL	NULL	0	NULL	sphingosine			activates					PLD					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_25_15579_s_93	9188441	In contrast to ceramides, sphingosine and its metabolite sphingosine-1-P activate PLD ( 58).	transcription
59011	2	335876	5	NULL	NULL	0	NULL	sphingosine-1-P			activates					PLD					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_25_15579_s_93	9188441	In contrast to ceramides, sphingosine and its metabolite sphingosine-1-P activate PLD ( 58).	transcription
59012	3	335876	5	NULL	NULL	0	NULL	sphingosine-1-P			is a metabolite of					sphingosine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_25_15579_s_93	9188441	In contrast to ceramides, sphingosine and its metabolite sphingosine-1-P activate PLD ( 58).	transcription
59013	4	335876	5	NULL	NULL	0	NULL	ceramides			does not activate					PLD					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_25_15579_s_93	9188441	In contrast to ceramides, sphingosine and its metabolite sphingosine-1-P activate PLD ( 58).	transcription
59014	1	335877	5	NULL	NULL	0	NULL	sphingosine			induce					ceramide		accumulation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_165	15774472	Sphingosine induces ceramide accumulation.	transcription
79478	1	335877	6	NULL	NULL	0	NULL	sphingosine	Chemical		induces					Ceramide	Chemical	accumulation of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_165	15774472	Sphingosine induces ceramide accumulation.	transcription
59015	1	335878	5	NULL	NULL	0	NULL	SPP			is degraded to					sphingosine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_297	7592842	Ceramides  stimulate the degradation of SPP to sphingosine and ceramide and  stimulate the production of ceramides from endogenous lipids.	transcription
59016	2	335878	5	NULL	NULL	0	NULL	SPP			is degraded to					ceramide					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_297	7592842	Ceramides  stimulate the degradation of SPP to sphingosine and ceramide and  stimulate the production of ceramides from endogenous lipids.	transcription
59017	3	335878	5	NULL	NULL	0	NULL	statement 1			occurs simultaneously with					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_297	7592842	Ceramides  stimulate the degradation of SPP to sphingosine and ceramide and  stimulate the production of ceramides from endogenous lipids.	transcription
59018	4	335878	5	NULL	NULL	0	NULL	ceramides			stimulates					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_297	7592842	Ceramides  stimulate the degradation of SPP to sphingosine and ceramide and  stimulate the production of ceramides from endogenous lipids.	transcription
59019	5	335878	5	NULL	NULL	0	NULL	ceramides			is produced from					lipids		endogenous			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_297	7592842	Ceramides  stimulate the degradation of SPP to sphingosine and ceramide and  stimulate the production of ceramides from endogenous lipids.	transcription
59020	6	335878	5	NULL	NULL	0	NULL	ceramides			stimulates					statement 5					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_297	7592842	Ceramides  stimulate the degradation of SPP to sphingosine and ceramide and  stimulate the production of ceramides from endogenous lipids.	transcription
79473	1	335878	6	NULL	NULL	0	NULL	SPP	GP		degrades into					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_297	7592842	Ceramides  stimulate the degradation of SPP to sphingosine and ceramide and  stimulate the production of ceramides from endogenous lipids.	transcription
79474	2	335878	6	NULL	NULL	0	NULL	SPP	GP		degrades into					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_297	7592842	Ceramides  stimulate the degradation of SPP to sphingosine and ceramide and  stimulate the production of ceramides from endogenous lipids.	transcription
79475	3	335878	6	NULL	NULL	0	NULL	Ceramides	Chemical		stimulates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_297	7592842	Ceramides  stimulate the degradation of SPP to sphingosine and ceramide and  stimulate the production of ceramides from endogenous lipids.	transcription
79476	4	335878	6	NULL	NULL	0	NULL	Ceramides	Chemical		stimulates					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_297	7592842	Ceramides  stimulate the degradation of SPP to sphingosine and ceramide and  stimulate the production of ceramides from endogenous lipids.	transcription
79477	5	335878	6	NULL	NULL	0	NULL	lipids	Chemical	endogenous	produces					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_297	7592842	Ceramides  stimulate the degradation of SPP to sphingosine and ceramide and  stimulate the production of ceramides from endogenous lipids.	transcription
59021	1	335879	5	NULL	NULL	0	NULL	palmitate			stimulates					ceramide		accumulation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_80	15774472	Palmitate stimulates ceramide and sphingosine accumulation.	transcription
59022	2	335879	5	NULL	NULL	0	NULL	palmitate			stimulates					sphingosine		accumulation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_80	15774472	Palmitate stimulates ceramide and sphingosine accumulation.	transcription
79471	1	335879	6	NULL	NULL	0	NULL	Palmitate	Chemical		stimulates					ceramide	Chemical	accumulation of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_80	15774472	Palmitate stimulates ceramide and sphingosine accumulation.	transcription
79472	2	335879	6	NULL	NULL	0	NULL	palmitate	Chemical		stimulates					sphingosine	Chemical	accumulation of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_80	15774472	Palmitate stimulates ceramide and sphingosine accumulation.	transcription
59023	1	335880	5	NULL	NULL	0	NULL	PLD			is stimulated by					sphingosine 1-phosphate					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_200	7592842	Figure 5:Effect of okadaic acid on the stimulation  of PLD by sphingosine 1-phosphate and the production of endogenous  ceramides by C -ceramide.	transcription
59024	2	335880	5	NULL	NULL	0	NULL	okadaic acid			effects		potentially			statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_200	7592842	Figure 5:Effect of okadaic acid on the stimulation  of PLD by sphingosine 1-phosphate and the production of endogenous  ceramides by C -ceramide.	transcription
59025	3	335880	5	NULL	NULL	0	NULL	ceramides		endogenous	is produced by					C -ceramide					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_200	7592842	Figure 5:Effect of okadaic acid on the stimulation  of PLD by sphingosine 1-phosphate and the production of endogenous  ceramides by C -ceramide.	transcription
59026	4	335880	5	NULL	NULL	0	NULL	okadaic acid			effects		potentially			statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_200	7592842	Figure 5:Effect of okadaic acid on the stimulation  of PLD by sphingosine 1-phosphate and the production of endogenous  ceramides by C -ceramide.	transcription
79469	1	335880	6	NULL	NULL	0	NULL	sphingosine 1-phosphate	GP		stimulates					PLD	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_200	7592842	Figure 5:Effect of okadaic acid on the stimulation  of PLD by sphingosine 1-phosphate and the production of endogenous  ceramides by C -ceramide.	transcription
79470	2	335880	6	NULL	NULL	0	NULL	C-ceramide	Chemical		produces					ceramides	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_200	7592842	Figure 5:Effect of okadaic acid on the stimulation  of PLD by sphingosine 1-phosphate and the production of endogenous  ceramides by C -ceramide.	transcription
59027	1	335881	5	NULL	NULL	0	NULL	sphingosine			induce					apoptosis					NULL		0	NULL	NULL	NULL	gw60_febslett_425_1_61_s_46	9541007	Sphingosine and ceramide induce apoptosis without interconversion of the lipids	transcription
59028	2	335881	5	NULL	NULL	0	NULL	statement 1			without interconversion of					lipids					NULL		0	NULL	NULL	NULL	gw60_febslett_425_1_61_s_46	9541007	Sphingosine and ceramide induce apoptosis without interconversion of the lipids	transcription
59029	3	335881	5	NULL	NULL	0	NULL	ceramide			induce					apoptosis					NULL		0	NULL	NULL	NULL	gw60_febslett_425_1_61_s_46	9541007	Sphingosine and ceramide induce apoptosis without interconversion of the lipids	transcription
59030	4	335881	5	NULL	NULL	0	NULL	statement 3			without interconversion of					lipids					NULL		0	NULL	NULL	NULL	gw60_febslett_425_1_61_s_46	9541007	Sphingosine and ceramide induce apoptosis without interconversion of the lipids	transcription
79467	1	335881	6	NULL	NULL	0	NULL	sphingosine	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_425_1_61_s_46	9541007	Sphingosine and ceramide induce apoptosis without interconversion of the lipids	transcription
79468	2	335881	6	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_425_1_61_s_46	9541007	Sphingosine and ceramide induce apoptosis without interconversion of the lipids	transcription
59031	1	335882	5	NULL	NULL	0	NULL	sphingosine			induce					apoptosis					NULL	WEHI 231	0	NULL	NULL	NULL	gw60_molpharmacol_61_1_177_s_346	11752219	Sphingosine and ceramide induce apoptosis in WEHI 231.	transcription
59032	2	335882	5	NULL	NULL	0	NULL	ceramide			induce					apoptosis					NULL	WEHI 231	0	NULL	NULL	NULL	gw60_molpharmacol_61_1_177_s_346	11752219	Sphingosine and ceramide induce apoptosis in WEHI 231.	transcription
79465	1	335882	6	NULL	NULL	NULL	NULL	sphingosine	Chemical		induces					apoptosis	Process				NULL	WEHI 231	NULL	NULL	NULL	NULL	gw60_molpharmacol_61_1_177_s_346	11752219	Sphingosine and ceramide induce apoptosis in WEHI 231.	transcription
79466	2	335882	6	NULL	NULL	NULL	NULL	ceramide	Chemical		induces					apoptosis	Process				NULL	WEHI 231	NULL	NULL	NULL	NULL	gw60_molpharmacol_61_1_177_s_346	11752219	Sphingosine and ceramide induce apoptosis in WEHI 231.	transcription
59033	1	335883	5	NULL	NULL	0	NULL	apoptosis			is induced by					ceramide					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_199	8626522	Figure 7: Potentiation of ceramide-induced apoptosis  by sphingosine.	transcription
59034	2	335883	5	NULL	NULL	0	NULL	sphingosine			potentiate					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_199	8626522	Figure 7: Potentiation of ceramide-induced apoptosis  by sphingosine.	transcription
79463	1	335883	6	NULL	NULL	0	NULL	ceramide	Chemical		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_199	8626522	Figure 7: Potentiation of ceramide-induced apoptosis  by sphingosine.	transcription
79464	2	335883	6	NULL	NULL	0	NULL	sphingosine	Chemical		potentiates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_199	8626522	Figure 7: Potentiation of ceramide-induced apoptosis  by sphingosine.	transcription
59035	1	335884	5	NULL	NULL	0	NULL	dSREBP		cleavage of	is inhibited by					palmitate					NULL		0	NULL	NULL	NULL	gw60_science_296_5569_879_s_76	11988566	( A) Cleavage of dSREBP is inhibited by palmitate, ceramide, or sphingosine.	transcription
59036	2	335884	5	NULL	NULL	0	NULL	dSREBP		cleavage of	is inhibited by					ceramide					NULL		0	NULL	NULL	NULL	gw60_science_296_5569_879_s_76	11988566	( A) Cleavage of dSREBP is inhibited by palmitate, ceramide, or sphingosine.	transcription
59037	3	335884	5	NULL	NULL	0	NULL	dSREBP		cleavage of	is inhibited by					sphingosine					NULL		0	NULL	NULL	NULL	gw60_science_296_5569_879_s_76	11988566	( A) Cleavage of dSREBP is inhibited by palmitate, ceramide, or sphingosine.	transcription
79460	1	335884	6	NULL	NULL	0	NULL	palmitate	Chemical		inhibits					dSREBP	GP	cleavage of 			NULL		0	NULL	NULL	NULL	gw60_science_296_5569_879_s_76	11988566	( A) Cleavage of dSREBP is inhibited by palmitate, ceramide, or sphingosine.	transcription
79461	2	335884	6	NULL	NULL	0	NULL	ceramide	Chemical		inhibits					dSREBP	GP	cleavage of 			NULL		0	NULL	NULL	NULL	gw60_science_296_5569_879_s_76	11988566	( A) Cleavage of dSREBP is inhibited by palmitate, ceramide, or sphingosine.	transcription
79462	3	335884	6	NULL	NULL	0	NULL	sphingosine	Chemical		inhibits					dSREBP	GP	cleavage of 			NULL		0	NULL	NULL	NULL	gw60_science_296_5569_879_s_76	11988566	( A) Cleavage of dSREBP is inhibited by palmitate, ceramide, or sphingosine.	transcription
59038	1	335885	5	NULL	NULL	0	NULL	ceramide			is converted to					sphingosine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_34_30784_s_7	12072440	Inhibition of ceramide conversion to sphingosine had no effect on this ceramide-induced effect.	transcription
79459	1	335885	6	NULL	NULL	0	NULL	ceramide	Chemical		is converted to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_34_30784_s_7	12072440	Inhibition of ceramide conversion to sphingosine had no effect on this ceramide-induced effect.	transcription
59039	1	335886	5	NULL	NULL	0	NULL	sphingosine		increase in	results from		may			ceramide		degradation of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_42	12531549	The ceramide increase preceded that of sphingosine, suggesting that the increase in sphingosine could result from degradation of the ceramide.	transcription
59080	1	335887	5	NULL	NULL	0	NULL	SM			is hydrolyzed by					SMase					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_340	14702348	It has been reported that the catabolic generation of ceramide is mediated by the hydrolysis of SM by SMase, that ceramide is deamidated to sphingosine by ceramidase, and that sphingosine is phosphorylated to S1P by sphingosine kinase ( ).	transcription
59081	2	335887	5	NULL	NULL	0	NULL	statement 1			generates		catabolically			ceramide					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_340	14702348	It has been reported that the catabolic generation of ceramide is mediated by the hydrolysis of SM by SMase, that ceramide is deamidated to sphingosine by ceramidase, and that sphingosine is phosphorylated to S1P by sphingosine kinase ( ).	transcription
59082	3	335887	5	NULL	NULL	0	NULL	ceramide			deamidated to					sphingosine					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_340	14702348	It has been reported that the catabolic generation of ceramide is mediated by the hydrolysis of SM by SMase, that ceramide is deamidated to sphingosine by ceramidase, and that sphingosine is phosphorylated to S1P by sphingosine kinase ( ).	transcription
59083	4	335887	5	NULL	NULL	0	NULL	ceramidase			catalyzes					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_340	14702348	It has been reported that the catabolic generation of ceramide is mediated by the hydrolysis of SM by SMase, that ceramide is deamidated to sphingosine by ceramidase, and that sphingosine is phosphorylated to S1P by sphingosine kinase ( ).	transcription
59084	5	335887	5	NULL	NULL	0	NULL	sphingosine			is phosphorylated to					S1P					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_340	14702348	It has been reported that the catabolic generation of ceramide is mediated by the hydrolysis of SM by SMase, that ceramide is deamidated to sphingosine by ceramidase, and that sphingosine is phosphorylated to S1P by sphingosine kinase ( ).	transcription
59085	6	335887	5	NULL	NULL	0	NULL	sphingosine kinase			catalyzes					statement 5					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_340	14702348	It has been reported that the catabolic generation of ceramide is mediated by the hydrolysis of SM by SMase, that ceramide is deamidated to sphingosine by ceramidase, and that sphingosine is phosphorylated to S1P by sphingosine kinase ( ).	transcription
79453	1	335887	6	NULL	NULL	0	NULL	SM	Chemical		is hydrolysed to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_340	14702348	It has been reported that the catabolic generation of ceramide is mediated by the hydrolysis of SM by SMase, that ceramide is deamidated to sphingosine by ceramidase, and that sphingosine is phosphorylated to S1P by sphingosine kinase ( ).	transcription
79454	2	335887	6	NULL	NULL	0	NULL	SMase	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_340	14702348	It has been reported that the catabolic generation of ceramide is mediated by the hydrolysis of SM by SMase, that ceramide is deamidated to sphingosine by ceramidase, and that sphingosine is phosphorylated to S1P by sphingosine kinase ( ).	transcription
79455	3	335887	6	NULL	NULL	0	NULL	ceramide	Chemical		is deaminated to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_340	14702348	It has been reported that the catabolic generation of ceramide is mediated by the hydrolysis of SM by SMase, that ceramide is deamidated to sphingosine by ceramidase, and that sphingosine is phosphorylated to S1P by sphingosine kinase ( ).	transcription
79456	4	335887	6	NULL	NULL	0	NULL	ceramidase	GP		catalyzes					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_340	14702348	It has been reported that the catabolic generation of ceramide is mediated by the hydrolysis of SM by SMase, that ceramide is deamidated to sphingosine by ceramidase, and that sphingosine is phosphorylated to S1P by sphingosine kinase ( ).	transcription
79457	5	335887	6	NULL	NULL	0	NULL	sphingosine	Chemical		phosphorylates to					S1P	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_340	14702348	It has been reported that the catabolic generation of ceramide is mediated by the hydrolysis of SM by SMase, that ceramide is deamidated to sphingosine by ceramidase, and that sphingosine is phosphorylated to S1P by sphingosine kinase ( ).	transcription
79458	6	335887	6	NULL	NULL	0	NULL	statement 5	Process		occurs by					sphingosine kinase	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_340	14702348	It has been reported that the catabolic generation of ceramide is mediated by the hydrolysis of SM by SMase, that ceramide is deamidated to sphingosine by ceramidase, and that sphingosine is phosphorylated to S1P by sphingosine kinase ( ).	transcription
59086	1	335888	5	NULL	NULL	0	NULL	ceramide synthase			is a type of					ceramidase					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_46	12531549	Together with ceramide synthase and glucosylceramide synthase, ceramidases, by catalyzing the hydrolysis of ceramide to sphingosine, regulate the available supply of ceramide.	transcription
59087	2	335888	5	NULL	NULL	0	NULL	glucosylceramide synthase			is a type of					ceramidase					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_46	12531549	Together with ceramide synthase and glucosylceramide synthase, ceramidases, by catalyzing the hydrolysis of ceramide to sphingosine, regulate the available supply of ceramide.	transcription
59088	3	335888	5	NULL	NULL	0	NULL	ceramide			is hydrolyzed to					sphingosine					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_46	12531549	Together with ceramide synthase and glucosylceramide synthase, ceramidases, by catalyzing the hydrolysis of ceramide to sphingosine, regulate the available supply of ceramide.	transcription
59089	4	335888	5	NULL	NULL	0	NULL	ceramide synthase			catalyzes					statement 3					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_46	12531549	Together with ceramide synthase and glucosylceramide synthase, ceramidases, by catalyzing the hydrolysis of ceramide to sphingosine, regulate the available supply of ceramide.	transcription
59090	5	335888	5	NULL	NULL	0	NULL	glucosylceramide synthase \t			catalyzes					statement 3					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_46	12531549	Together with ceramide synthase and glucosylceramide synthase, ceramidases, by catalyzing the hydrolysis of ceramide to sphingosine, regulate the available supply of ceramide.	transcription
59091	6	335888	5	NULL	NULL	0	NULL	statement 4			regulates					ceramide		available supply of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_46	12531549	Together with ceramide synthase and glucosylceramide synthase, ceramidases, by catalyzing the hydrolysis of ceramide to sphingosine, regulate the available supply of ceramide.	transcription
59092	7	335888	5	NULL	NULL	0	NULL	statement 5			regulates					ceramide		available supply of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_46	12531549	Together with ceramide synthase and glucosylceramide synthase, ceramidases, by catalyzing the hydrolysis of ceramide to sphingosine, regulate the available supply of ceramide.	transcription
79450	1	335888	6	NULL	NULL	0	NULL	ceramide	Chemical		is converted to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_46	12531549	Together with ceramide synthase and glucosylceramide synthase, ceramidases, by catalyzing the hydrolysis of ceramide to sphingosine, regulate the available supply of ceramide.	transcription
79451	2	335888	6	NULL	NULL	0	NULL	ceramide synthase 	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_46	12531549	Together with ceramide synthase and glucosylceramide synthase, ceramidases, by catalyzing the hydrolysis of ceramide to sphingosine, regulate the available supply of ceramide.	transcription
79452	3	335888	6	NULL	NULL	0	NULL	glucosylceramide synthase	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_46	12531549	Together with ceramide synthase and glucosylceramide synthase, ceramidases, by catalyzing the hydrolysis of ceramide to sphingosine, regulate the available supply of ceramide.	transcription
59093	1	335889	5	NULL	NULL	0	NULL	ceramide			is a type of					sphingolipid metabolite					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_247	10747891	Ceramide and sphingosine are interconvertable sphingolipid metabolites; however, we have shown that sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 did not affect sphingosine- or Fas-induced apoptosis.	transcription
59094	2	335889	5	NULL	NULL	0	NULL	sphingosine			is a type of					sphingolipid metabolite					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_247	10747891	Ceramide and sphingosine are interconvertable sphingolipid metabolites; however, we have shown that sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 did not affect sphingosine- or Fas-induced apoptosis.	transcription
59095	3	335889	5	NULL	NULL	0	NULL	sphingosine			induce					apoptosis					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_247	10747891	Ceramide and sphingosine are interconvertable sphingolipid metabolites; however, we have shown that sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 did not affect sphingosine- or Fas-induced apoptosis.	transcription
59096	4	335889	5	NULL	NULL	0	NULL	sphingosine			is not converted to					ceramide					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_247	10747891	Ceramide and sphingosine are interconvertable sphingolipid metabolites; however, we have shown that sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 did not affect sphingosine- or Fas-induced apoptosis.	transcription
59097	5	335889	5	NULL	NULL	0	NULL	statement 4			is necessary for					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_247	10747891	Ceramide and sphingosine are interconvertable sphingolipid metabolites; however, we have shown that sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 did not affect sphingosine- or Fas-induced apoptosis.	transcription
59115	6	335889	5	NULL	NULL	0	NULL	fumonisin B1			is an inhibitor of					ceramide synthase 					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_247	10747891	Ceramide and sphingosine are interconvertable sphingolipid metabolites; however, we have shown that sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 did not affect sphingosine- or Fas-induced apoptosis.	transcription
59121	7	335889	5	NULL	NULL	0	NULL	apoptosis			is induced by					sphingosine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_247	10747891	Ceramide and sphingosine are interconvertable sphingolipid metabolites; however, we have shown that sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 did not affect sphingosine- or Fas-induced apoptosis.	transcription
59122	8	335889	5	NULL	NULL	0	NULL	fumonisin B1			does not affect					statement 7					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_247	10747891	Ceramide and sphingosine are interconvertable sphingolipid metabolites; however, we have shown that sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 did not affect sphingosine- or Fas-induced apoptosis.	transcription
59123	9	335889	5	NULL	NULL	0	NULL	apoptosis			is induced by					Fas					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_247	10747891	Ceramide and sphingosine are interconvertable sphingolipid metabolites; however, we have shown that sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 did not affect sphingosine- or Fas-induced apoptosis.	transcription
59125	10	335889	5	NULL	NULL	0	NULL	fumonisin B1			does not affect					statement 9					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_247	10747891	Ceramide and sphingosine are interconvertable sphingolipid metabolites; however, we have shown that sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 did not affect sphingosine- or Fas-induced apoptosis.	transcription
59126	1	335890	5	NULL	NULL	0	NULL	PAI-1 gene			is induced by					ceramide					NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_192	16936207	Genes such as PAI-1 and KC were induced by ceramide, sphingosine, and S1P.	transcription
59127	2	335890	5	NULL	NULL	0	NULL	PAI-1 gene			is induced by					sphingosine					NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_192	16936207	Genes such as PAI-1 and KC were induced by ceramide, sphingosine, and S1P.	transcription
59128	3	335890	5	NULL	NULL	0	NULL	PAI-1 gene			is induced by					S1P					NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_192	16936207	Genes such as PAI-1 and KC were induced by ceramide, sphingosine, and S1P.	transcription
59130	4	335890	5	NULL	NULL	0	NULL	KC gene			is induced by					ceramide					NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_192	16936207	Genes such as PAI-1 and KC were induced by ceramide, sphingosine, and S1P.	transcription
59131	5	335890	5	NULL	NULL	0	NULL	KC gene			is induced by					sphingosine					NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_192	16936207	Genes such as PAI-1 and KC were induced by ceramide, sphingosine, and S1P.	transcription
59132	6	335890	5	NULL	NULL	0	NULL	KC gene			is induced by					S1P					NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_192	16936207	Genes such as PAI-1 and KC were induced by ceramide, sphingosine, and S1P.	transcription
79444	1	335890	6	NULL	NULL	0	NULL	ceramide	Chemical		induces					PAI-1	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_192	16936207	Genes such as PAI-1 and KC were induced by ceramide, sphingosine, and S1P.	transcription
79445	2	335890	6	NULL	NULL	0	NULL	ceramide	Chemical		induces					KC	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_192	16936207	Genes such as PAI-1 and KC were induced by ceramide, sphingosine, and S1P.	transcription
79446	3	335890	6	NULL	NULL	0	NULL	sphingosine	Chemical		induces					PAI-1	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_192	16936207	Genes such as PAI-1 and KC were induced by ceramide, sphingosine, and S1P.	transcription
79447	4	335890	6	NULL	NULL	0	NULL	sphingosine	Chemical		induces					KC	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_192	16936207	Genes such as PAI-1 and KC were induced by ceramide, sphingosine, and S1P.	transcription
79448	5	335890	6	NULL	NULL	0	NULL	S1P	GP		induces					PAI-1	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_192	16936207	Genes such as PAI-1 and KC were induced by ceramide, sphingosine, and S1P.	transcription
79449	6	335890	6	NULL	NULL	0	NULL	S1P	GP		induces					KC	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_192	16936207	Genes such as PAI-1 and KC were induced by ceramide, sphingosine, and S1P.	transcription
59133	1	335891	5	NULL	NULL	0	NULL	ceramide			is hydrolyzed to					sphingosine					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_16	12815059	1.23 [EC]) catalyzes the hydrolysis of  ceramide to sphingosine and fatty acid.	transcription
59135	2	335891	5	NULL	NULL	0	NULL	ceramide			is hydrolyzed to					fatty acid					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_16	12815059	1.23 [EC]) catalyzes the hydrolysis of  ceramide to sphingosine and fatty acid.	transcription
59136	3	335891	5	NULL	NULL	0	NULL	statement 1			occurs along with					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_16	12815059	1.23 [EC]) catalyzes the hydrolysis of  ceramide to sphingosine and fatty acid.	transcription
79442	1	335891	6	NULL	NULL	0	NULL	ceramide	Chemical		is hydrolysed to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_16	12815059	1.23 [EC]) catalyzes the hydrolysis of  ceramide to sphingosine and fatty acid.	transcription
79443	2	335891	6	NULL	NULL	0	NULL	ceramide	Chemical		is hydrolysed to					fatty acid 	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_16	12815059	1.23 [EC]) catalyzes the hydrolysis of  ceramide to sphingosine and fatty acid.	transcription
59137	1	335892	5	NULL	NULL	0	NULL	L-Cycloserine			blocks					sphingosine		biosynthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_184	12424251	L-Cycloserine blocks sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity.	transcription
59139	2	335892	5	NULL	NULL	0	NULL	L-Cycloserine			blocks					ceramide		biosynthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_184	12424251	L-Cycloserine blocks sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity.	transcription
59140	3	335892	5	NULL	NULL	0	NULL	L-Cycloserine			inhibit					serine palmitoyltransferase		activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_184	12424251	L-Cycloserine blocks sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity.	transcription
59141	4	335892	5	NULL	NULL	0	NULL	L-Cycloserine			inhibit					serine palmitoyltransferase		activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_184	12424251	L-Cycloserine blocks sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity.	transcription
59142	5	335892	5	NULL	NULL	0	NULL	statement 3			leads to					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_184	12424251	L-Cycloserine blocks sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity.	transcription
59144	6	335892	5	NULL	NULL	0	NULL	statement 5			leads to					statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_184	12424251	L-Cycloserine blocks sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity.	transcription
79440	1	335892	6	NULL	NULL	0	NULL	L-Cycloserine	Chemical		blocks					sphingosine	Chemical	biosynthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_184	12424251	L-Cycloserine blocks sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity.	transcription
79441	2	335892	6	NULL	NULL	0	NULL	L-Cycloserine	Chemical		blocks					ceramide	Chemical	biosynthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_184	12424251	L-Cycloserine blocks sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity.	transcription
59147	1	335893	5	NULL	NULL	0	NULL	sphingosine			activates					PLD					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_128	10425402	Ceramide was shown to inhibit sphingosine and sphingosine-1-phosphate activation of PLD but not of cyclic AMP generation.	transcription
59148	2	335893	5	NULL	NULL	0	NULL	sphingosine-1-phosphate			activates					PLD					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_128	10425402	Ceramide was shown to inhibit sphingosine and sphingosine-1-phosphate activation of PLD but not of cyclic AMP generation.	transcription
59149	3	335893	5	NULL	NULL	0	NULL	ceramide			inhibit					statement 1					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_128	10425402	Ceramide was shown to inhibit sphingosine and sphingosine-1-phosphate activation of PLD but not of cyclic AMP generation.	transcription
59150	4	335893	5	NULL	NULL	0	NULL	ceramide			inhibit					statement 2					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_128	10425402	Ceramide was shown to inhibit sphingosine and sphingosine-1-phosphate activation of PLD but not of cyclic AMP generation.	transcription
59151	5	335893	5	NULL	NULL	0	NULL	sphingosine			activates					cyclic AMP		generation of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_128	10425402	Ceramide was shown to inhibit sphingosine and sphingosine-1-phosphate activation of PLD but not of cyclic AMP generation.	transcription
59152	6	335893	5	NULL	NULL	0	NULL	sphingosine-1-phosphate			activates					cyclic AMP		generation of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_128	10425402	Ceramide was shown to inhibit sphingosine and sphingosine-1-phosphate activation of PLD but not of cyclic AMP generation.	transcription
59153	7	335893	5	NULL	NULL	0	NULL	ceramide			inhibit					statement 5					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_128	10425402	Ceramide was shown to inhibit sphingosine and sphingosine-1-phosphate activation of PLD but not of cyclic AMP generation.	transcription
59154	8	335893	5	NULL	NULL	0	NULL	ceramide			inhibit					statement 6					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_128	10425402	Ceramide was shown to inhibit sphingosine and sphingosine-1-phosphate activation of PLD but not of cyclic AMP generation.	transcription
79438	1	335893	6	NULL	NULL	0	NULL	ceramide	Chemical		inhibits					sphingosine	Chemical	activation of 			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_128	10425402	Ceramide was shown to inhibit sphingosine and sphingosine-1-phosphate activation of PLD but not of cyclic AMP generation.	transcription
79439	2	335893	6	NULL	NULL	0	NULL	ceramide	Chemical		inhibits					sphingosine 1-phosphate	GP	activation of 			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_128	10425402	Ceramide was shown to inhibit sphingosine and sphingosine-1-phosphate activation of PLD but not of cyclic AMP generation.	transcription
59155	1	335894	5	NULL	NULL	0	NULL	ceramide			is cleaved into					sphingosine		nonradiolabeled			NULL		0	NULL	NULL	NULL	gw60_clindiagnlabimmun_6_1_101_s_68	9874672	CDase catalyzed the cleavage of [14]ceramide to nonradiolabeled sphingosine and 14C-radiolabeled palmitic acid.	transcription
59156	2	335894	5	NULL	NULL	0	NULL	ceramide			is cleaved into					palmitic acid		14C-radiolabeled			NULL		0	NULL	NULL	NULL	gw60_clindiagnlabimmun_6_1_101_s_68	9874672	CDase catalyzed the cleavage of [14]ceramide to nonradiolabeled sphingosine and 14C-radiolabeled palmitic acid.	transcription
59157	3	335894	5	NULL	NULL	0	NULL	statement 1			occurs along with					statement 2					NULL		0	NULL	NULL	NULL	gw60_clindiagnlabimmun_6_1_101_s_68	9874672	CDase catalyzed the cleavage of [14]ceramide to nonradiolabeled sphingosine and 14C-radiolabeled palmitic acid.	transcription
59158	4	335894	5	NULL	NULL	0	NULL	CDase			catalyzes					statement 3					NULL		0	NULL	NULL	NULL	gw60_clindiagnlabimmun_6_1_101_s_68	9874672	CDase catalyzed the cleavage of [14]ceramide to nonradiolabeled sphingosine and 14C-radiolabeled palmitic acid.	transcription
79436	1	335894	6	NULL	NULL	0	NULL	ceramide	Chemical		is converted to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_clindiagnlabimmun_6_1_101_s_68	9874672	CDase catalyzed the cleavage of [14]ceramide to nonradiolabeled sphingosine and 14C-radiolabeled palmitic acid.	transcription
79437	2	335894	6	NULL	NULL	0	NULL	CDase	Chemical		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_clindiagnlabimmun_6_1_101_s_68	9874672	CDase catalyzed the cleavage of [14]ceramide to nonradiolabeled sphingosine and 14C-radiolabeled palmitic acid.	transcription
59159	1	335895	5	NULL	NULL	0	NULL	ceramide		elevation of;;endogenous	induce					apoptosis					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_1_177_s_13	10617602	In particular, apoptosis is known to be induced by elevation of endogenous ceramide or sphingosine ( 1-10).	transcription
59160	2	335895	5	NULL	NULL	0	NULL	sphingosine		elevation of;;endogenous	induce					apoptosis					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_1_177_s_13	10617602	In particular, apoptosis is known to be induced by elevation of endogenous ceramide or sphingosine ( 1-10).	transcription
59161	3	335895	5	NULL	NULL	0	NULL	statement 1			is an alternative to					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_1_177_s_13	10617602	In particular, apoptosis is known to be induced by elevation of endogenous ceramide or sphingosine ( 1-10).	transcription
79434	1	335895	6	NULL	NULL	0	NULL	ceramide	Chemical	elevation of	induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_1_177_s_13	10617602	In particular, apoptosis is known to be induced by elevation of endogenous ceramide or sphingosine ( 1-10).	transcription
79435	2	335895	6	NULL	NULL	0	NULL	sphingosine	Chemical	elevation of	induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_1_177_s_13	10617602	In particular, apoptosis is known to be induced by elevation of endogenous ceramide or sphingosine ( 1-10).	transcription
59162	1	335896	5	NULL	NULL	0	NULL	sphingosine 1-phosphate			stimulates					PLD					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_179	7592842	Figure 4:Effect of C -ceramide on the  stimulation of PLD by sphingosine 1-phosphate.	transcription
59163	2	335896	5	NULL	NULL	0	NULL	C -ceramide			effects		may			statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_179	7592842	Figure 4:Effect of C -ceramide on the  stimulation of PLD by sphingosine 1-phosphate.	transcription
79433	1	335896	6	NULL	NULL	0	NULL	sphingosine 1-phosphate	GP		stimulates					PLD	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_179	7592842	Figure 4:Effect of C -ceramide on the  stimulation of PLD by sphingosine 1-phosphate.	transcription
59164	1	335897	5	NULL	NULL	0	NULL	p55TNFR		signaling of	stimulates					sphingomyelinase		neutral			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_14_9539_s_290	10092639	Signaling by the p55TNFR stimulates a neutral sphingomyelinase, which in turn generates ceramide and sphingosine.	transcription
59165	2	335897	5	NULL	NULL	0	NULL	statement 1			generates					ceramide					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_14_9539_s_290	10092639	Signaling by the p55TNFR stimulates a neutral sphingomyelinase, which in turn generates ceramide and sphingosine.	transcription
59166	3	335897	5	NULL	NULL	0	NULL	statement 1			generates					sphingosine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_14_9539_s_290	10092639	Signaling by the p55TNFR stimulates a neutral sphingomyelinase, which in turn generates ceramide and sphingosine.	transcription
79430	1	335897	6	NULL	NULL	0	NULL	p55TNFR	GP	signaling by	stimulates					sphingomyelinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_14_9539_s_290	10092639	Signaling by the p55TNFR stimulates a neutral sphingomyelinase, which in turn generates ceramide and sphingosine.	transcription
79431	2	335897	6	NULL	NULL	0	NULL	sphingomyelinase	GP		generates					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_14_9539_s_290	10092639	Signaling by the p55TNFR stimulates a neutral sphingomyelinase, which in turn generates ceramide and sphingosine.	transcription
79432	3	335897	6	NULL	NULL	0	NULL	sphingomyelinase	GP		generates					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_14_9539_s_290	10092639	Signaling by the p55TNFR stimulates a neutral sphingomyelinase, which in turn generates ceramide and sphingosine.	transcription
59167	1	335898	5	NULL	NULL	0	NULL	ceramide			is formed in					ER					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_227	16782891	It is still not clear whether the formation of ceramide in the ER depends directly on the availability of its substrate sphingosine or whether sphingosine activates specific ceramide synthase(s).	transcription
59168	2	335898	5	NULL	NULL	0	NULL	sphingosine			is a substrate of					ceramide					NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_227	16782891	It is still not clear whether the formation of ceramide in the ER depends directly on the availability of its substrate sphingosine or whether sphingosine activates specific ceramide synthase(s).	transcription
59169	3	335898	5	NULL	NULL	0	NULL	statement 1			depends on		potentially;;directly			sphingosine		availability of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_227	16782891	It is still not clear whether the formation of ceramide in the ER depends directly on the availability of its substrate sphingosine or whether sphingosine activates specific ceramide synthase(s).	transcription
59170	4	335898	5	NULL	NULL	0	NULL	sphingosine			activates		potentially			ceramide synthase		specific			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_227	16782891	It is still not clear whether the formation of ceramide in the ER depends directly on the availability of its substrate sphingosine or whether sphingosine activates specific ceramide synthase(s).	transcription
59171	5	335898	5	NULL	NULL	0	NULL	statement 1			depends on		potentially;;directly			statement 4					NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_227	16782891	It is still not clear whether the formation of ceramide in the ER depends directly on the availability of its substrate sphingosine or whether sphingosine activates specific ceramide synthase(s).	transcription
59172	1	335899	5	NULL	NULL	0	NULL	S1P			is dephosphorylated to					sphingosine					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_110	15180992	Dephosphorylation of S1P to sphingosine by SPP-1 has been associated with a large increase of ceramide levels resulting mainly from acylation of increased sphingosine by ceramide synthase ( ,  ).	transcription
59173	2	335899	5	NULL	NULL	0	NULL	SPP-1			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_110	15180992	Dephosphorylation of S1P to sphingosine by SPP-1 has been associated with a large increase of ceramide levels resulting mainly from acylation of increased sphingosine by ceramide synthase ( ,  ).	transcription
59197	3	335899	5	NULL	NULL	0	NULL	ceramide synthase			acylates					sphingosine		increased			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_110	15180992	Dephosphorylation of S1P to sphingosine by SPP-1 has been associated with a large increase of ceramide levels resulting mainly from acylation of increased sphingosine by ceramide synthase ( ,  ).	transcription
59198	4	335899	5	NULL	NULL	0	NULL	statement 3			increases					ceramide		level of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_110	15180992	Dephosphorylation of S1P to sphingosine by SPP-1 has been associated with a large increase of ceramide levels resulting mainly from acylation of increased sphingosine by ceramide synthase ( ,  ).	transcription
59199	5	335899	5	NULL	NULL	0	NULL	statement 1			is associated with					statement 4					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_110	15180992	Dephosphorylation of S1P to sphingosine by SPP-1 has been associated with a large increase of ceramide levels resulting mainly from acylation of increased sphingosine by ceramide synthase ( ,  ).	transcription
79427	1	335899	6	NULL	NULL	0	NULL	S1P	GP		is converted to					sphingosine	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_110	15180992	Dephosphorylation of S1P to sphingosine by SPP-1 has been associated with a large increase of ceramide levels resulting mainly from acylation of increased sphingosine by ceramide synthase ( ,  ).	transcription
79428	2	335899	6	NULL	NULL	0	NULL	statement 1	Process		occurs by					SPP-1	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_110	15180992	Dephosphorylation of S1P to sphingosine by SPP-1 has been associated with a large increase of ceramide levels resulting mainly from acylation of increased sphingosine by ceramide synthase ( ,  ).	transcription
79429	3	335899	6	NULL	NULL	0	NULL	ceramide synthase	GP		acylates					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_110	15180992	Dephosphorylation of S1P to sphingosine by SPP-1 has been associated with a large increase of ceramide levels resulting mainly from acylation of increased sphingosine by ceramide synthase ( ,  ).	transcription
59215	1	335900	5	NULL	NULL	0	NULL	apoptosis			is mediated by					sphingosine					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_154	9415703	Similarly, sphingosine-mediated apoptosis was unaffected by the ceramide synthase inhibitor fumonisin B1 (Table  3), indicating that acylation to ceramide did not contribute to the bioactivity of sphingosine.	transcription
59216	2	335900	5	NULL	NULL	0	NULL	fumonisin B1			does not affect					statement 1					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_154	9415703	Similarly, sphingosine-mediated apoptosis was unaffected by the ceramide synthase inhibitor fumonisin B1 (Table  3), indicating that acylation to ceramide did not contribute to the bioactivity of sphingosine.	transcription
59217	3	335900	5	NULL	NULL	0	NULL	fumonisin B1			is an inhibitor of					ceramide synthase					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_154	9415703	Similarly, sphingosine-mediated apoptosis was unaffected by the ceramide synthase inhibitor fumonisin B1 (Table  3), indicating that acylation to ceramide did not contribute to the bioactivity of sphingosine.	transcription
59218	4	335900	5	NULL	NULL	0	NULL	ceramide		acylation to	does not contribute to					sphingosine		bioactivity of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_154	9415703	Similarly, sphingosine-mediated apoptosis was unaffected by the ceramide synthase inhibitor fumonisin B1 (Table  3), indicating that acylation to ceramide did not contribute to the bioactivity of sphingosine.	transcription
79424	1	335900	6	NULL	NULL	0	NULL	sphingosine	Chemical		mediates					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_154	9415703	Similarly, sphingosine-mediated apoptosis was unaffected by the ceramide synthase inhibitor fumonisin B1 (Table  3), indicating that acylation to ceramide did not contribute to the bioactivity of sphingosine.	transcription
79425	2	335900	6	NULL	NULL	0	NULL	fumonisin B1	Chemical		does not affect					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_154	9415703	Similarly, sphingosine-mediated apoptosis was unaffected by the ceramide synthase inhibitor fumonisin B1 (Table  3), indicating that acylation to ceramide did not contribute to the bioactivity of sphingosine.	transcription
79426	3	335900	6	NULL	NULL	0	NULL	ceramide	Chemical	acylation to	does not contribute to					sphingosine	Chemical	bioactivity of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_154	9415703	Similarly, sphingosine-mediated apoptosis was unaffected by the ceramide synthase inhibitor fumonisin B1 (Table  3), indicating that acylation to ceramide did not contribute to the bioactivity of sphingosine.	transcription
59219	1	335901	5	NULL	NULL	0	NULL	ceramide		initial increase in	preceded					sphingosine		increase in			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_147	10747891	The initial ceramide increase preceded that of sphingosine, suggesting that the increase in sphingosine might result from degradation of the ceramide formed upon Fas ligation.	transcription
59220	2	335901	5	NULL	NULL	0	NULL	ceramide			formed upon					Fas		ligation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_147	10747891	The initial ceramide increase preceded that of sphingosine, suggesting that the increase in sphingosine might result from degradation of the ceramide formed upon Fas ligation.	transcription
59221	3	335901	5	NULL	NULL	0	NULL	sphingosine		increase in	results from		might			ceramide		degradation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_147	10747891	The initial ceramide increase preceded that of sphingosine, suggesting that the increase in sphingosine might result from degradation of the ceramide formed upon Fas ligation.	transcription
59222	1	335902	5	NULL	NULL	0	NULL	ceramide			activates					cell death pathway					NULL	GST-P-positive cells in vitro	0	NULL	NULL	NULL	gw70_carcinogenesis_24_6_1077_s_210	12807752	Ceramide, sphingosine and an inhibitor of sphingosine kinase all activate a cell death pathway in such GST-P-positive cells  in vitro.	transcription
59223	2	335902	5	NULL	NULL	0	NULL	sphingosine			activates					cell death pathway					NULL	GST-P-positive cells in vitro	0	NULL	NULL	NULL	gw70_carcinogenesis_24_6_1077_s_210	12807752	Ceramide, sphingosine and an inhibitor of sphingosine kinase all activate a cell death pathway in such GST-P-positive cells  in vitro.	transcription
59224	3	335902	5	NULL	NULL	0	NULL	inhibitor of sphingosine kinase			activates					cell death pathway					NULL	GST-P-positive cells in vitro	0	NULL	NULL	NULL	gw70_carcinogenesis_24_6_1077_s_210	12807752	Ceramide, sphingosine and an inhibitor of sphingosine kinase all activate a cell death pathway in such GST-P-positive cells  in vitro.	transcription
79419	1	335902	6	NULL	NULL	0	NULL	ceramide	GP		activates					cell death pathway	Process				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_24_6_1077_s_210	12807752	Ceramide, sphingosine and an inhibitor of sphingosine kinase all activate a cell death pathway in such GST-P-positive cells  in vitro.	transcription
79420	2	335902	6	NULL	NULL	0	NULL	sphingosine	Chemical		activates					cell death pathway	Process				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_24_6_1077_s_210	12807752	Ceramide, sphingosine and an inhibitor of sphingosine kinase all activate a cell death pathway in such GST-P-positive cells  in vitro.	transcription
79421	3	335902	6	NULL	NULL	0	NULL	sphingosine kinase	GP	inhibitor of 	activates					cell death pathway	Process				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_24_6_1077_s_210	12807752	Ceramide, sphingosine and an inhibitor of sphingosine kinase all activate a cell death pathway in such GST-P-positive cells  in vitro.	transcription
59225	1	335903	5	NULL	NULL	0	NULL	sphingosine		exogenous	increases					ceramide		synthesis of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_943_s_8	15132973	When ceramide synthesis is increased through exogenous sphingosine or inhibition of sphingosine kinase, SRE-mediated gene transcription is increased.	transcription
59226	2	335903	5	NULL	NULL	0	NULL	sphingosine kinase		inhibition of	increases					ceramide		synthesis of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_943_s_8	15132973	When ceramide synthesis is increased through exogenous sphingosine or inhibition of sphingosine kinase, SRE-mediated gene transcription is increased.	transcription
59227	3	335903	5	NULL	NULL	0	NULL	SRE			mediates					gene transcription					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_943_s_8	15132973	When ceramide synthesis is increased through exogenous sphingosine or inhibition of sphingosine kinase, SRE-mediated gene transcription is increased.	transcription
59228	4	335903	5	NULL	NULL	0	NULL	statement 1			increases					statement 3					NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_943_s_8	15132973	When ceramide synthesis is increased through exogenous sphingosine or inhibition of sphingosine kinase, SRE-mediated gene transcription is increased.	transcription
59229	5	335903	5	NULL	NULL	0	NULL	statement 2			increases					statement 3					NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_943_s_8	15132973	When ceramide synthesis is increased through exogenous sphingosine or inhibition of sphingosine kinase, SRE-mediated gene transcription is increased.	transcription
59230	1	335904	5	NULL	NULL	0	NULL	sphingosine			induce					apoptosis					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50624_s_37	14522966	Whereas sphingosine induces apoptosis in various cell types ( ), sphingosine 1-phosphate antagonizes the apoptotic actions of ceramide ( ).	transcription
59231	2	335904	5	NULL	NULL	0	NULL	sphingosine 1-phosphate			antagonize					ceramide		apoptotic actions of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50624_s_37	14522966	Whereas sphingosine induces apoptosis in various cell types ( ), sphingosine 1-phosphate antagonizes the apoptotic actions of ceramide ( ).	transcription
79416	1	335904	6	NULL	NULL	0	NULL	sphingosine	Chemical		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50624_s_37	14522966	Whereas sphingosine induces apoptosis in various cell types ( ), sphingosine 1-phosphate antagonizes the apoptotic actions of ceramide ( ).	transcription
79417	2	335904	6	NULL	NULL	0	NULL	sphingosine 1-phosphat	GP		suppresses					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50624_s_37	14522966	Whereas sphingosine induces apoptosis in various cell types ( ), sphingosine 1-phosphate antagonizes the apoptotic actions of ceramide ( ).	transcription
79418	3	335904	6	NULL	NULL	0	NULL	ceramide	Chemical		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_50_50624_s_37	14522966	Whereas sphingosine induces apoptosis in various cell types ( ), sphingosine 1-phosphate antagonizes the apoptotic actions of ceramide ( ).	transcription
59232	1	335905	5	NULL	NULL	0	NULL	TNF-alpha			stimulates					sphingosine kinase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_3	11815603	TNF-alpha also stimulates sphingosine kinase, the enzyme that phosphorylates sphingosine to form sphingosine-1-phosphate (SPP), a further metabolite of ceramide.	transcription
59233	2	335905	5	NULL	NULL	0	NULL	sphingosine			is phosphorylated to					SPP					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_3	11815603	TNF-alpha also stimulates sphingosine kinase, the enzyme that phosphorylates sphingosine to form sphingosine-1-phosphate (SPP), a further metabolite of ceramide.	transcription
59234	3	335905	5	NULL	NULL	0	NULL	sphingosine kinase			catalyzes					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_3	11815603	TNF-alpha also stimulates sphingosine kinase, the enzyme that phosphorylates sphingosine to form sphingosine-1-phosphate (SPP), a further metabolite of ceramide.	transcription
59235	4	335905	5	NULL	NULL	0	NULL	SPP			is					sphingosine-1-phosphate					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_3	11815603	TNF-alpha also stimulates sphingosine kinase, the enzyme that phosphorylates sphingosine to form sphingosine-1-phosphate (SPP), a further metabolite of ceramide.	transcription
59236	5	335905	5	NULL	NULL	0	NULL	SPP			is a metabolite of					ceramide					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_3	11815603	TNF-alpha also stimulates sphingosine kinase, the enzyme that phosphorylates sphingosine to form sphingosine-1-phosphate (SPP), a further metabolite of ceramide.	transcription
79412	1	335905	6	NULL	NULL	0	NULL	TNF-alpha	GP		stimulates					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_3	11815603	TNF-alpha also stimulates sphingosine kinase, the enzyme that phosphorylates sphingosine to form sphingosine-1-phosphate (SPP), a further metabolite of ceramide.	transcription
79413	2	335905	6	NULL	NULL	0	NULL	sphingosine	GP		forms					sphingosine 1-phosphate	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_3	11815603	TNF-alpha also stimulates sphingosine kinase, the enzyme that phosphorylates sphingosine to form sphingosine-1-phosphate (SPP), a further metabolite of ceramide.	transcription
79414	3	335905	6	NULL	NULL	0	NULL	sphingosine kinase	GP		catalyzes					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_3	11815603	TNF-alpha also stimulates sphingosine kinase, the enzyme that phosphorylates sphingosine to form sphingosine-1-phosphate (SPP), a further metabolite of ceramide.	transcription
79415	4	335905	6	NULL	NULL	0	NULL	SPP	GP		is					sphingosine-1-phosphate	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_3	11815603	TNF-alpha also stimulates sphingosine kinase, the enzyme that phosphorylates sphingosine to form sphingosine-1-phosphate (SPP), a further metabolite of ceramide.	transcription
59237	1	335906	5	NULL	NULL	0	NULL	apoptosis			is induced by		directly			sphingosine					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_188	8626522	Consistent with the direct induction of apoptosis  by sphingosine described above, potentiation of ceramide-related  apoptosis by sphingosine was not stereoselective ( Table 3 ).	transcription
59238	2	335906	5	NULL	NULL	0	NULL	apoptosis			is related to					ceramide					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_188	8626522	Consistent with the direct induction of apoptosis  by sphingosine described above, potentiation of ceramide-related  apoptosis by sphingosine was not stereoselective ( Table 3 ).	transcription
59239	3	335906	5	NULL	NULL	0	NULL	sphingosine			potentiate					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_188	8626522	Consistent with the direct induction of apoptosis  by sphingosine described above, potentiation of ceramide-related  apoptosis by sphingosine was not stereoselective ( Table 3 ).	transcription
79411	1	335906	6	NULL	NULL	0	NULL	sphingosine	Chemical		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_188	8626522	Consistent with the direct induction of apoptosis  by sphingosine described above, potentiation of ceramide-related  apoptosis by sphingosine was not stereoselective ( Table 3 ).	transcription
59240	1	335907	5	NULL	NULL	0	NULL	PLD			is activated by					ATP					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_175	12177168	Therefore, it can be concluded that PLD activation by ATP is not mediated through the generation of ceramide or its further metabolism to sphingosine or sphingosine 1-phosphate.	transcription
59241	2	335907	5	NULL	NULL	0	NULL	statement 1			is not mediated through					ceramide		generation of			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_175	12177168	Therefore, it can be concluded that PLD activation by ATP is not mediated through the generation of ceramide or its further metabolism to sphingosine or sphingosine 1-phosphate.	transcription
59242	3	335907	5	NULL	NULL	0	NULL	ceramide			metabolized to					sphingosine					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_175	12177168	Therefore, it can be concluded that PLD activation by ATP is not mediated through the generation of ceramide or its further metabolism to sphingosine or sphingosine 1-phosphate.	transcription
59243	4	335907	5	NULL	NULL	0	NULL	statement 1			is not mediated through					statement 3					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_175	12177168	Therefore, it can be concluded that PLD activation by ATP is not mediated through the generation of ceramide or its further metabolism to sphingosine or sphingosine 1-phosphate.	transcription
59244	5	335907	5	NULL	NULL	0	NULL	ceramide			metabolized to					sphingosine 1-phosphate					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_175	12177168	Therefore, it can be concluded that PLD activation by ATP is not mediated through the generation of ceramide or its further metabolism to sphingosine or sphingosine 1-phosphate.	transcription
59245	6	335907	5	NULL	NULL	0	NULL	statement 1			is not mediated through					statement 5					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_175	12177168	Therefore, it can be concluded that PLD activation by ATP is not mediated through the generation of ceramide or its further metabolism to sphingosine or sphingosine 1-phosphate.	transcription
79409	1	335907	6	NULL	NULL	0	NULL	ATP	Chemical		activates					PLD	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_175	12177168	Therefore, it can be concluded that PLD activation by ATP is not mediated through the generation of ceramide or its further metabolism to sphingosine or sphingosine 1-phosphate.	transcription
79410	2	335907	6	NULL	NULL	0	NULL	statement 1	Process		is not mediated through					ceramide	Chemical	generation of 			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_175	12177168	Therefore, it can be concluded that PLD activation by ATP is not mediated through the generation of ceramide or its further metabolism to sphingosine or sphingosine 1-phosphate.	transcription
59246	1	335908	5	NULL	NULL	0	NULL	sphingosine			is phosphorylated to					S1P					NULL		0	NULL	NULL	NULL	gw70_circulationres_98_11_1381_s_20	16675717	2 - 5    S1P is derived from the phosphorylation of sphingosine catalyzed by sphingosine kinase, sphingosine being from ceramide and ceramide from sphingomyelin, a constituent lipid of signaling microdomains of plasma membrane lipid rafts and caveolae.	transcription
59247	2	335908	5	NULL	NULL	0	NULL	sphingosine kinase			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw70_circulationres_98_11_1381_s_20	16675717	2 - 5    S1P is derived from the phosphorylation of sphingosine catalyzed by sphingosine kinase, sphingosine being from ceramide and ceramide from sphingomyelin, a constituent lipid of signaling microdomains of plasma membrane lipid rafts and caveolae.	transcription
59248	3	335908	5	NULL	NULL	0	NULL	sphingosine			is derived from					ceramide					NULL		0	NULL	NULL	NULL	gw70_circulationres_98_11_1381_s_20	16675717	2 - 5    S1P is derived from the phosphorylation of sphingosine catalyzed by sphingosine kinase, sphingosine being from ceramide and ceramide from sphingomyelin, a constituent lipid of signaling microdomains of plasma membrane lipid rafts and caveolae.	transcription
59249	4	335908	5	NULL	NULL	0	NULL	ceramide			is derived from					sphingomyelin					NULL		0	NULL	NULL	NULL	gw70_circulationres_98_11_1381_s_20	16675717	2 - 5    S1P is derived from the phosphorylation of sphingosine catalyzed by sphingosine kinase, sphingosine being from ceramide and ceramide from sphingomyelin, a constituent lipid of signaling microdomains of plasma membrane lipid rafts and caveolae.	transcription
59250	5	335908	5	NULL	NULL	0	NULL	sphingomyelin			is a type of					lipid					NULL		0	NULL	NULL	NULL	gw70_circulationres_98_11_1381_s_20	16675717	2 - 5    S1P is derived from the phosphorylation of sphingosine catalyzed by sphingosine kinase, sphingosine being from ceramide and ceramide from sphingomyelin, a constituent lipid of signaling microdomains of plasma membrane lipid rafts and caveolae.	transcription
79404	1	335908	6	NULL	NULL	0	NULL	sphingosine	Chemical	phosphorylation of	forms					S1P	GP				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_11_1381_s_20	16675717	2 - 5    S1P is derived from the phosphorylation of sphingosine catalyzed by sphingosine kinase, sphingosine being from ceramide and ceramide from sphingomyelin, a constituent lipid of signaling microdomains of plasma membrane lipid rafts and caveolae.	transcription
79405	2	335908	6	NULL	NULL	0	NULL	statement 1	Process		is catalyzed by					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_11_1381_s_20	16675717	2 - 5    S1P is derived from the phosphorylation of sphingosine catalyzed by sphingosine kinase, sphingosine being from ceramide and ceramide from sphingomyelin, a constituent lipid of signaling microdomains of plasma membrane lipid rafts and caveolae.	transcription
79406	3	335908	6	NULL	NULL	0	NULL	sphingosine	Chemical		is formed from					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_11_1381_s_20	16675717	2 - 5    S1P is derived from the phosphorylation of sphingosine catalyzed by sphingosine kinase, sphingosine being from ceramide and ceramide from sphingomyelin, a constituent lipid of signaling microdomains of plasma membrane lipid rafts and caveolae.	transcription
79407	4	335908	6	NULL	NULL	0	NULL	ceramide	Chemical		is formed from					sphingomyelin	Chemical				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_11_1381_s_20	16675717	2 - 5    S1P is derived from the phosphorylation of sphingosine catalyzed by sphingosine kinase, sphingosine being from ceramide and ceramide from sphingomyelin, a constituent lipid of signaling microdomains of plasma membrane lipid rafts and caveolae.	transcription
79408	5	335908	6	NULL	NULL	0	NULL	sphingomyelin	Chemical		is a type of					lipid molecule	Chemical				NULL		0	NULL	NULL	NULL	gw70_circulationres_98_11_1381_s_20	16675717	2 - 5    S1P is derived from the phosphorylation of sphingosine catalyzed by sphingosine kinase, sphingosine being from ceramide and ceramide from sphingomyelin, a constituent lipid of signaling microdomains of plasma membrane lipid rafts and caveolae.	transcription
59251	1	335909	5	NULL	NULL	0	NULL	sphingosine			does not activate					phospholipase D		activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_10	7592842	Sphingosine did not activate  phospholipase D activity significantly after 10 min.  C -ceramide stimulated the conversion of exogenous  [ H]sphingosine 1-phosphate to sphingosine and  ceramide in fibroblasts.	transcription
59252	2	335909	5	NULL	NULL	0	NULL	sphingosine 1-phosphate		exogenous	is converted to					sphingosine					NULL	fibroblasts	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_10	7592842	Sphingosine did not activate  phospholipase D activity significantly after 10 min.  C -ceramide stimulated the conversion of exogenous  [ H]sphingosine 1-phosphate to sphingosine and  ceramide in fibroblasts.	transcription
59253	3	335909	5	NULL	NULL	0	NULL	sphingosine 1-phosphate		exogenous	is converted to					ceramide					NULL	fibroblasts	0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_10	7592842	Sphingosine did not activate  phospholipase D activity significantly after 10 min.  C -ceramide stimulated the conversion of exogenous  [ H]sphingosine 1-phosphate to sphingosine and  ceramide in fibroblasts.	transcription
59254	4	335909	5	NULL	NULL	0	NULL	C -ceramide			stimulates					statement 2					NULL	fibroblasts	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_10	7592842	Sphingosine did not activate  phospholipase D activity significantly after 10 min.  C -ceramide stimulated the conversion of exogenous  [ H]sphingosine 1-phosphate to sphingosine and  ceramide in fibroblasts.	transcription
59255	5	335909	5	NULL	NULL	0	NULL	C -ceramide			stimulates					statement 3					NULL	fibroblasts	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_10	7592842	Sphingosine did not activate  phospholipase D activity significantly after 10 min.  C -ceramide stimulated the conversion of exogenous  [ H]sphingosine 1-phosphate to sphingosine and  ceramide in fibroblasts.	transcription
79399	1	335909	6	NULL	NULL	0	NULL	sphingosine	Chemical		does not activate					phospholipase D	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_10	7592842	Sphingosine did not activate  phospholipase D activity significantly after 10 min.  C -ceramide stimulated the conversion of exogenous  [ H]sphingosine 1-phosphate to sphingosine and  ceramide in fibroblasts.	transcription
79400	2	335909	6	NULL	NULL	0	NULL	sphingosine 1-phosphate	GP		is converted to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_10	7592842	Sphingosine did not activate  phospholipase D activity significantly after 10 min.  C -ceramide stimulated the conversion of exogenous  [ H]sphingosine 1-phosphate to sphingosine and  ceramide in fibroblasts.	transcription
79401	3	335909	6	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		is converted to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_10	7592842	Sphingosine did not activate  phospholipase D activity significantly after 10 min.  C -ceramide stimulated the conversion of exogenous  [ H]sphingosine 1-phosphate to sphingosine and  ceramide in fibroblasts.	transcription
79402	4	335909	6	NULL	NULL	0	NULL	ceramide	Chemical		catalyzes					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_10	7592842	Sphingosine did not activate  phospholipase D activity significantly after 10 min.  C -ceramide stimulated the conversion of exogenous  [ H]sphingosine 1-phosphate to sphingosine and  ceramide in fibroblasts.	transcription
79403	5	335909	6	NULL	NULL	0	NULL	ceramide	GP		catalyzes					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_10	7592842	Sphingosine did not activate  phospholipase D activity significantly after 10 min.  C -ceramide stimulated the conversion of exogenous  [ H]sphingosine 1-phosphate to sphingosine and  ceramide in fibroblasts.	transcription
59256	1	335910	5	NULL	NULL	0	NULL	sphingosine-1 phosphate			is a type of					lipid					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_32_22532_s_219	10428830	Incidentally, another lipid that was shown to counteract the effects of ceramide and to inhibit CD95-mediated apoptosis, sphingosine-1 phosphate, was also shown to be active in Jurkat T cells ( 17,  62).	transcription
59257	2	335910	5	NULL	NULL	0	NULL	sphingosine-1 phosphate			counteracts					ceramide		effects of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_32_22532_s_219	10428830	Incidentally, another lipid that was shown to counteract the effects of ceramide and to inhibit CD95-mediated apoptosis, sphingosine-1 phosphate, was also shown to be active in Jurkat T cells ( 17,  62).	transcription
59258	3	335910	5	NULL	NULL	0	NULL	apoptosis			is mediated by					CD95					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_32_22532_s_219	10428830	Incidentally, another lipid that was shown to counteract the effects of ceramide and to inhibit CD95-mediated apoptosis, sphingosine-1 phosphate, was also shown to be active in Jurkat T cells ( 17,  62).	transcription
59259	4	335910	5	NULL	NULL	0	NULL	sphingosine-1 phosphate			inhibits					statement 4					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_32_22532_s_219	10428830	Incidentally, another lipid that was shown to counteract the effects of ceramide and to inhibit CD95-mediated apoptosis, sphingosine-1 phosphate, was also shown to be active in Jurkat T cells ( 17,  62).	transcription
59260	5	335910	5	NULL	NULL	0	NULL	sphingosine-1 phosphate			active in					Jurkat T cells					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_32_22532_s_219	10428830	Incidentally, another lipid that was shown to counteract the effects of ceramide and to inhibit CD95-mediated apoptosis, sphingosine-1 phosphate, was also shown to be active in Jurkat T cells ( 17,  62).	transcription
59261	1	335912	5	NULL	NULL	0	NULL	ceramide			deamidated to					sphingosine					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_193	14702348	Effect of Ceramide Metabolism on the Toxin-induced Hemolysis of Sheep Erythrocytes -- Ceramide is known to be deamidated to sphingosine by ceramidase.	transcription
59262	2	335912	5	NULL	NULL	0	NULL	ceramidase			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_193	14702348	Effect of Ceramide Metabolism on the Toxin-induced Hemolysis of Sheep Erythrocytes -- Ceramide is known to be deamidated to sphingosine by ceramidase.	transcription
59263	3	335912	5	NULL	NULL	0	NULL	erythrocytes 		sheep	undergoes					hemolysis					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_193	14702348	Effect of Ceramide Metabolism on the Toxin-induced Hemolysis of Sheep Erythrocytes -- Ceramide is known to be deamidated to sphingosine by ceramidase.	transcription
59264	4	335912	5	NULL	NULL	0	NULL	toxin			induce					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_193	14702348	Effect of Ceramide Metabolism on the Toxin-induced Hemolysis of Sheep Erythrocytes -- Ceramide is known to be deamidated to sphingosine by ceramidase.	transcription
59265	5	335912	5	NULL	NULL	0	NULL	ceramide		metabolism of	effects		potentially			statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_193	14702348	Effect of Ceramide Metabolism on the Toxin-induced Hemolysis of Sheep Erythrocytes -- Ceramide is known to be deamidated to sphingosine by ceramidase.	transcription
79397	1	335912	6	NULL	NULL	0	NULL	ceramide	Chemical		is deaminated to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_193	14702348	Effect of Ceramide Metabolism on the Toxin-induced Hemolysis of Sheep Erythrocytes -- Ceramide is known to be deamidated to sphingosine by ceramidase.	transcription
79398	2	335912	6	NULL	NULL	0	NULL	statement 1	Process		is catalyzed by					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_193	14702348	Effect of Ceramide Metabolism on the Toxin-induced Hemolysis of Sheep Erythrocytes -- Ceramide is known to be deamidated to sphingosine by ceramidase.	transcription
59266	1	335913	5	NULL	NULL	0	NULL	ceramide			deamidated to					sphingosine					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_212	14702348	These results suggested that  N-oleoylethanolamine specifically blocked the toxin-stimulated deamidation of ceramide to sphingosine, resulting in the accumulation of ceramide.	transcription
59267	2	335913	5	NULL	NULL	0	NULL	statement 1			is stimulated by					toxin					NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_212	14702348	These results suggested that  N-oleoylethanolamine specifically blocked the toxin-stimulated deamidation of ceramide to sphingosine, resulting in the accumulation of ceramide.	transcription
59268	3	335913	5	NULL	NULL	0	NULL	N-oleoylethanolamine			blocks		specifically			statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_212	14702348	These results suggested that  N-oleoylethanolamine specifically blocked the toxin-stimulated deamidation of ceramide to sphingosine, resulting in the accumulation of ceramide.	transcription
59269	4	335913	5	NULL	NULL	0	NULL	statement 3			accumulates					ceramide					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_212	14702348	These results suggested that  N-oleoylethanolamine specifically blocked the toxin-stimulated deamidation of ceramide to sphingosine, resulting in the accumulation of ceramide.	transcription
79395	1	335913	6	NULL	NULL	0	NULL	ceramide	Chemical		is deaminated to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_212	14702348	These results suggested that  N-oleoylethanolamine specifically blocked the toxin-stimulated deamidation of ceramide to sphingosine, resulting in the accumulation of ceramide.	transcription
79396	2	335913	6	NULL	NULL	0	NULL	N-oleoylethanolamine	Chemical		blocks					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_212	14702348	These results suggested that  N-oleoylethanolamine specifically blocked the toxin-stimulated deamidation of ceramide to sphingosine, resulting in the accumulation of ceramide.	transcription
59270	1	335914	5	NULL	NULL	0	NULL	dihydrosphingosine			N-acylated to					ceramide					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_10	12424251	The formation of ceramide resulting from the  N-acylation of dihydrosphingosine or sphingosine by ceramide synthase is inhibited by the fungal toxin fumonisin B1.	transcription
59271	2	335914	5	NULL	NULL	0	NULL	ceramide synthase			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_10	12424251	The formation of ceramide resulting from the  N-acylation of dihydrosphingosine or sphingosine by ceramide synthase is inhibited by the fungal toxin fumonisin B1.	transcription
59272	3	335914	5	NULL	NULL	0	NULL	sphingosine			N-acylated to					ceramide					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_10	12424251	The formation of ceramide resulting from the  N-acylation of dihydrosphingosine or sphingosine by ceramide synthase is inhibited by the fungal toxin fumonisin B1.	transcription
59273	4	335914	5	NULL	NULL	0	NULL	ceramide synthase			catalyzes					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_10	12424251	The formation of ceramide resulting from the  N-acylation of dihydrosphingosine or sphingosine by ceramide synthase is inhibited by the fungal toxin fumonisin B1.	transcription
59274	5	335914	5	NULL	NULL	0	NULL	fumonisin B1			inhibits					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_10	12424251	The formation of ceramide resulting from the  N-acylation of dihydrosphingosine or sphingosine by ceramide synthase is inhibited by the fungal toxin fumonisin B1.	transcription
59275	6	335914	5	NULL	NULL	0	NULL	fumonisin B1			inhibits					statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_10	12424251	The formation of ceramide resulting from the  N-acylation of dihydrosphingosine or sphingosine by ceramide synthase is inhibited by the fungal toxin fumonisin B1.	transcription
59276	7	335914	5	NULL	NULL	0	NULL	fumonisin B1			is a type of					fungal toxin					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_10	12424251	The formation of ceramide resulting from the  N-acylation of dihydrosphingosine or sphingosine by ceramide synthase is inhibited by the fungal toxin fumonisin B1.	transcription
59277	1	335915	5	NULL	NULL	0	NULL	sphingosine			is converted to					dihydroceramide					NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_253	15772421	The pathways  discussed in this study include the de novo pathway involving the conversion of sphinganine  to dihydroceramide or sphingosine to ceramide catalyzed by ceramide synthase	transcription
59278	2	335915	5	NULL	NULL	0	NULL	ceramide synthase			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_253	15772421	The pathways  discussed in this study include the de novo pathway involving the conversion of sphinganine  to dihydroceramide or sphingosine to ceramide catalyzed by ceramide synthase	transcription
59279	3	335915	5	NULL	NULL	0	NULL	sphingosine			is converted to					ceramide					NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_253	15772421	The pathways  discussed in this study include the de novo pathway involving the conversion of sphinganine  to dihydroceramide or sphingosine to ceramide catalyzed by ceramide synthase	transcription
59280	4	335915	5	NULL	NULL	0	NULL	ceramide synthase			catalyzes					statement 3					NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_253	15772421	The pathways  discussed in this study include the de novo pathway involving the conversion of sphinganine  to dihydroceramide or sphingosine to ceramide catalyzed by ceramide synthase	transcription
79391	1	335915	6	NULL	NULL	0	NULL	sphinganine	Chemical		is converted to					dihydroceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_253	15772421	The pathways  discussed in this study include the de novo pathway involving the conversion of sphinganine  to dihydroceramide or sphingosine to ceramide catalyzed by ceramide synthase	transcription
79392	2	335915	6	NULL	NULL	0	NULL	sphingosine	Chemical		is converted to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_253	15772421	The pathways  discussed in this study include the de novo pathway involving the conversion of sphinganine  to dihydroceramide or sphingosine to ceramide catalyzed by ceramide synthase	transcription
79393	3	335915	6	NULL	NULL	0	NULL	ceramide synthase	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_253	15772421	The pathways  discussed in this study include the de novo pathway involving the conversion of sphinganine  to dihydroceramide or sphingosine to ceramide catalyzed by ceramide synthase	transcription
79394	4	335915	6	NULL	NULL	0	NULL	ceramide synthase	GP		catalyzes					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_253	15772421	The pathways  discussed in this study include the de novo pathway involving the conversion of sphinganine  to dihydroceramide or sphingosine to ceramide catalyzed by ceramide synthase	transcription
59354	1	335916	5	NULL	NULL	0	NULL	sphinganine			N-acylated to					dihydroceramide					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_33_20373_s_113	9252342	Ceramide synthase catalyzes the  N-acylation of sphinganine or sphingosine with a long chain fatty acyl-CoA to form dihydroceramide or ceramide.	transcription
59355	2	335916	5	NULL	NULL	0	NULL	sphinganine			N-acylated to					ceramide					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_33_20373_s_113	9252342	Ceramide synthase catalyzes the  N-acylation of sphinganine or sphingosine with a long chain fatty acyl-CoA to form dihydroceramide or ceramide.	transcription
59356	3	335916	5	NULL	NULL	0	NULL	statement 1			is an alternative to					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_33_20373_s_113	9252342	Ceramide synthase catalyzes the  N-acylation of sphinganine or sphingosine with a long chain fatty acyl-CoA to form dihydroceramide or ceramide.	transcription
59357	4	335916	5	NULL	NULL	0	NULL	ceramide synthase			catalyzes					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_33_20373_s_113	9252342	Ceramide synthase catalyzes the  N-acylation of sphinganine or sphingosine with a long chain fatty acyl-CoA to form dihydroceramide or ceramide.	transcription
59358	5	335916	5	NULL	NULL	0	NULL	ceramide synthase			catalyzes					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_33_20373_s_113	9252342	Ceramide synthase catalyzes the  N-acylation of sphinganine or sphingosine with a long chain fatty acyl-CoA to form dihydroceramide or ceramide.	transcription
59359	6	335916	5	NULL	NULL	0	NULL	sphingosine			contains					long chain fatty acyl-CoA					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_33_20373_s_113	9252342	Ceramide synthase catalyzes the  N-acylation of sphinganine or sphingosine with a long chain fatty acyl-CoA to form dihydroceramide or ceramide.	transcription
59360	7	335916	5	NULL	NULL	0	NULL	sphingosine			N-acylated to					dihydroceramide					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_33_20373_s_113	9252342	Ceramide synthase catalyzes the  N-acylation of sphinganine or sphingosine with a long chain fatty acyl-CoA to form dihydroceramide or ceramide.	transcription
59362	8	335916	5	NULL	NULL	0	NULL	sphingosine			N-acylated to					ceramide					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_33_20373_s_113	9252342	Ceramide synthase catalyzes the  N-acylation of sphinganine or sphingosine with a long chain fatty acyl-CoA to form dihydroceramide or ceramide.	transcription
59363	9	335916	5	NULL	NULL	0	NULL	statement 7			is an alternative to					statement 8					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_33_20373_s_113	9252342	Ceramide synthase catalyzes the  N-acylation of sphinganine or sphingosine with a long chain fatty acyl-CoA to form dihydroceramide or ceramide.	transcription
59364	10	335916	5	NULL	NULL	0	NULL	ceramide synthase \t			catalyzes					statement 7					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_33_20373_s_113	9252342	Ceramide synthase catalyzes the  N-acylation of sphinganine or sphingosine with a long chain fatty acyl-CoA to form dihydroceramide or ceramide.	transcription
59365	11	335916	5	NULL	NULL	0	NULL	ceramide synthase			catalyzes					statement 8					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_33_20373_s_113	9252342	Ceramide synthase catalyzes the  N-acylation of sphinganine or sphingosine with a long chain fatty acyl-CoA to form dihydroceramide or ceramide.	transcription
79388	1	335916	6	NULL	NULL	0	NULL	sphinganine	Chemical		forms					dihydroceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_33_20373_s_113	9252342	Ceramide synthase catalyzes the  N-acylation of sphinganine or sphingosine with a long chain fatty acyl-CoA to form dihydroceramide or ceramide.	transcription
79389	2	335916	6	NULL	NULL	0	NULL	Ceramide synthase	GP		catalyzes					sphingosine	GP	N-acylation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_33_20373_s_113	9252342	Ceramide synthase catalyzes the  N-acylation of sphinganine or sphingosine with a long chain fatty acyl-CoA to form dihydroceramide or ceramide.	transcription
79390	3	335916	6	NULL	NULL	0	NULL	ceramide synthase	GP		catalyzes					sphinganine	GP	N-acylation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_33_20373_s_113	9252342	Ceramide synthase catalyzes the  N-acylation of sphinganine or sphingosine with a long chain fatty acyl-CoA to form dihydroceramide or ceramide.	transcription
59281	1	335917	5	NULL	NULL	0	NULL	apoptosis			is mediated by					sphingosine					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_261	10747891	Sphingosine- and Ceramide-mediated Apoptosis Is Mitochondria-dependent-- Mitochondrial dysfunction appears to be important in ceramide signaling of apoptosis ( 77).	transcription
59282	2	335917	5	NULL	NULL	0	NULL	statement 1			is dependent on					mitochondria					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_261	10747891	Sphingosine- and Ceramide-mediated Apoptosis Is Mitochondria-dependent-- Mitochondrial dysfunction appears to be important in ceramide signaling of apoptosis ( 77).	transcription
59283	3	335917	5	NULL	NULL	0	NULL	apoptosis			is mediated by					ceramide					NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_261	10747891	Sphingosine- and Ceramide-mediated Apoptosis Is Mitochondria-dependent-- Mitochondrial dysfunction appears to be important in ceramide signaling of apoptosis ( 77).	transcription
59284	4	335917	5	NULL	NULL	0	NULL	statement 3			is dependent on					mitochondria					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_261	10747891	Sphingosine- and Ceramide-mediated Apoptosis Is Mitochondria-dependent-- Mitochondrial dysfunction appears to be important in ceramide signaling of apoptosis ( 77).	transcription
59385	5	335917	5	NULL	NULL	0	NULL	mitochondria		dysfunction of	is important for		may be			statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_261	10747891	Sphingosine- and Ceramide-mediated Apoptosis Is Mitochondria-dependent-- Mitochondrial dysfunction appears to be important in ceramide signaling of apoptosis ( 77).	transcription
79384	1	335917	6	NULL	NULL	0	NULL	sphingosine	Chemical		mediates					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_261	10747891	Sphingosine- and Ceramide-mediated Apoptosis Is Mitochondria-dependent-- Mitochondrial dysfunction appears to be important in ceramide signaling of apoptosis ( 77).	transcription
79385	2	335917	6	NULL	NULL	0	NULL	ceramide	Chemical		mediates					apoptosis	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_261	10747891	Sphingosine- and Ceramide-mediated Apoptosis Is Mitochondria-dependent-- Mitochondrial dysfunction appears to be important in ceramide signaling of apoptosis ( 77).	transcription
79386	3	335917	6	NULL	NULL	0	NULL	statement 1	Process		is dependent on					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_261	10747891	Sphingosine- and Ceramide-mediated Apoptosis Is Mitochondria-dependent-- Mitochondrial dysfunction appears to be important in ceramide signaling of apoptosis ( 77).	transcription
79387	4	335917	6	NULL	NULL	0	NULL	statement 2	Process		is dependent on					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_261	10747891	Sphingosine- and Ceramide-mediated Apoptosis Is Mitochondria-dependent-- Mitochondrial dysfunction appears to be important in ceramide signaling of apoptosis ( 77).	transcription
59386	1	335918	5	NULL	NULL	0	NULL	FB1			inhibits					ceramide synthase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_18_12367_s_26	10212208	FB1 inhibits ceramide synthase, which alters sphinganine:sphingosine ratios ( 16,  17) and inhibits the synthesis of ceramide.	transcription
59387	2	335918	5	NULL	NULL	0	NULL	ceramide synthase			alters					sphinganine:sphingosine ratios					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_18_12367_s_26	10212208	FB1 inhibits ceramide synthase, which alters sphinganine:sphingosine ratios ( 16,  17) and inhibits the synthesis of ceramide.	transcription
59388	3	335918	5	NULL	NULL	0	NULL	FB1			inhibits					ceramide		synthesis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_18_12367_s_26	10212208	FB1 inhibits ceramide synthase, which alters sphinganine:sphingosine ratios ( 16,  17) and inhibits the synthesis of ceramide.	transcription
79383	1	335918	6	NULL	NULL	0	NULL	FB1	Chemical		inhibits					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_18_12367_s_26	10212208	FB1 inhibits ceramide synthase, which alters sphinganine:sphingosine ratios ( 16,  17) and inhibits the synthesis of ceramide.	transcription
59389	1	335919	5	NULL	NULL	0	NULL	sphingosine 1-phosphate			is a catabolite of					ceramide					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21121_s_17	10409665	On the other hand, ceramide catabolites, such as sphingosine 1-phosphate, stimulate cell growth and suppress ceramide-mediated cell death ( 5).	transcription
59390	2	335919	5	NULL	NULL	0	NULL	sphingosine 1-phosphate			stimulates					cell growth					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21121_s_17	10409665	On the other hand, ceramide catabolites, such as sphingosine 1-phosphate, stimulate cell growth and suppress ceramide-mediated cell death ( 5).	transcription
59391	3	335919	5	NULL	NULL	0	NULL	ceramide			mediates					cell death					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21121_s_17	10409665	On the other hand, ceramide catabolites, such as sphingosine 1-phosphate, stimulate cell growth and suppress ceramide-mediated cell death ( 5).	transcription
59392	4	335919	5	NULL	NULL	0	NULL	sphingosine 1-phosphate			supress					statement 3					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21121_s_17	10409665	On the other hand, ceramide catabolites, such as sphingosine 1-phosphate, stimulate cell growth and suppress ceramide-mediated cell death ( 5).	transcription
79380	1	335919	6	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		stimulates					cell growth	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21121_s_17	10409665	On the other hand, ceramide catabolites, such as sphingosine 1-phosphate, stimulate cell growth and suppress ceramide-mediated cell death ( 5).	transcription
79381	2	335919	6	NULL	NULL	NULL	NULL	sphingosine 1-phosphate	GP		suppresses					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_21121_s_17	10409665	On the other hand, ceramide catabolites, such as sphingosine 1-phosphate, stimulate cell growth and suppress ceramide-mediated cell death ( 5).	transcription
79382	3	335919	6	NULL	NULL	0	NULL	ceramide	Chemical		mediates					cell death	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_21121_s_17	10409665	On the other hand, ceramide catabolites, such as sphingosine 1-phosphate, stimulate cell growth and suppress ceramide-mediated cell death ( 5).	transcription
59393	1	335920	5	NULL	NULL	0	NULL	fumonisin B1			is an inhibitor of					ceramide synthase					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-bioenerg-biomembr_37_4_16167178_s_7	16167178	The ceramide synthase inhibitor, fumonisin B1 failed to prevent sphingosine  metabolism to ceramide and actually increased it.	transcription
59394	2	335920	5	NULL	NULL	0	NULL	sphingosine			metabolized to					ceramide					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-bioenerg-biomembr_37_4_16167178_s_7	16167178	The ceramide synthase inhibitor, fumonisin B1 failed to prevent sphingosine  metabolism to ceramide and actually increased it.	transcription
59395	3	335920	5	NULL	NULL	0	NULL	fumonisin B1			does not prevent					statement 2					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-bioenerg-biomembr_37_4_16167178_s_7	16167178	The ceramide synthase inhibitor, fumonisin B1 failed to prevent sphingosine  metabolism to ceramide and actually increased it.	transcription
59396	4	335920	5	NULL	NULL	0	NULL	fumonisin B1			increases					statement 2					NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-bioenerg-biomembr_37_4_16167178_s_7	16167178	The ceramide synthase inhibitor, fumonisin B1 failed to prevent sphingosine  metabolism to ceramide and actually increased it.	transcription
79377	1	335920	6	NULL	NULL	0	NULL	sphingosine	Chemical		is converted to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-bioenerg-biomembr_37_4_16167178_s_7	16167178	The ceramide synthase inhibitor, fumonisin B1 failed to prevent sphingosine  metabolism to ceramide and actually increased it.	transcription
79378	2	335920	6	NULL	NULL	0	NULL	fumonisin B1	Chemical		prevents					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-bioenerg-biomembr_37_4_16167178_s_7	16167178	The ceramide synthase inhibitor, fumonisin B1 failed to prevent sphingosine  metabolism to ceramide and actually increased it.	transcription
79379	3	335920	6	NULL	NULL	0	NULL	fumonisin B1	Chemical		is a type of					ceramide synthase inhibitor	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-bioenerg-biomembr_37_4_16167178_s_7	16167178	The ceramide synthase inhibitor, fumonisin B1 failed to prevent sphingosine  metabolism to ceramide and actually increased it.	transcription
59397	1	335921	5	NULL	NULL	0	NULL	C2-Cer			induces					ceramides		accumulation of;;endogenous;;long chain			NULL	HT-29 cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_279_18_18384_s_144	14970205	From these results we concluded that C2-Cer induces an accumulation of endogenous long chain ceramides in HT-29 cells, and this accumulation is dependent on the recycling of the sphingosine moiety and the activity of ceramide synthase.	transcription
59398	2	335921	5	NULL	NULL	0	NULL	ceramides		accumulation of;;endogenous;;long chain	is dependent on					sphingosine moiety		recycling of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_18384_s_144	14970205	From these results we concluded that C2-Cer induces an accumulation of endogenous long chain ceramides in HT-29 cells, and this accumulation is dependent on the recycling of the sphingosine moiety and the activity of ceramide synthase.	transcription
59399	3	335921	5	NULL	NULL	0	NULL	ceramides		accumulation of;;endogenous;;long chain	is dependent on					ceramide synthase		activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_18384_s_144	14970205	From these results we concluded that C2-Cer induces an accumulation of endogenous long chain ceramides in HT-29 cells, and this accumulation is dependent on the recycling of the sphingosine moiety and the activity of ceramide synthase.	transcription
79374	1	335921	6	NULL	NULL	0	NULL	C2-cer	Chemical		induces					long chain ceramides	Chemical	accumulation of;; endogenous			NULL	HT-29 cells	0	NULL	NULL	NULL	gw70_jbiolchem_279_18_18384_s_144	14970205	From these results we concluded that C2-Cer induces an accumulation of endogenous long chain ceramides in HT-29 cells, and this accumulation is dependent on the recycling of the sphingosine moiety and the activity of ceramide synthase.	transcription
79375	2	335921	6	NULL	NULL	0	NULL	statement 1	Process		is dependent on					ceramide synthase	GP	activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_18384_s_144	14970205	From these results we concluded that C2-Cer induces an accumulation of endogenous long chain ceramides in HT-29 cells, and this accumulation is dependent on the recycling of the sphingosine moiety and the activity of ceramide synthase.	transcription
79376	3	335921	6	NULL	NULL	0	NULL	statement 1	Process		is dependent on					sphingosine	Chemical	recycling of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_18_18384_s_144	14970205	From these results we concluded that C2-Cer induces an accumulation of endogenous long chain ceramides in HT-29 cells, and this accumulation is dependent on the recycling of the sphingosine moiety and the activity of ceramide synthase.	transcription
59400	1	335922	5	NULL	NULL	0	NULL	sphingosine			is converted to					ceramide					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_3_1255_s_74	8576106	However, Fumonisin B1, which  inhibits the conversion of sphingosine to ceramide( 24) , did  not inhibit the effect of exogenously added sphingosine on the ISP-1  action ( 14) , suggesting that ceramide is not the downstream  effector and that sphingosine derivatives with a free amino group such  as sphingosine and sphingosine 1-phosphate are possible candidates.	transcription
59401	2	335922	5	NULL	NULL	0	NULL	Fumonisin B1			inhibits					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_3_1255_s_74	8576106	However, Fumonisin B1, which  inhibits the conversion of sphingosine to ceramide( 24) , did  not inhibit the effect of exogenously added sphingosine on the ISP-1  action ( 14) , suggesting that ceramide is not the downstream  effector and that sphingosine derivatives with a free amino group such  as sphingosine and sphingosine 1-phosphate are possible candidates.	transcription
79372	1	335922	6	NULL	NULL	0	NULL	sphingosine	Chemical		is converted to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_3_1255_s_74	8576106	However, Fumonisin B1, which  inhibits the conversion of sphingosine to ceramide( 24) , did  not inhibit the effect of exogenously added sphingosine on the ISP-1  action ( 14) , suggesting that ceramide is not the downstream  effector and that sphingosine derivatives with a free amino group such  as sphingosine and sphingosine 1-phosphate are possible candidates.	transcription
79373	2	335922	6	NULL	NULL	0	NULL	Fumonisin B1	Chemical		inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_3_1255_s_74	8576106	However, Fumonisin B1, which  inhibits the conversion of sphingosine to ceramide( 24) , did  not inhibit the effect of exogenously added sphingosine on the ISP-1  action ( 14) , suggesting that ceramide is not the downstream  effector and that sphingosine derivatives with a free amino group such  as sphingosine and sphingosine 1-phosphate are possible candidates.	transcription
59402	1	335923	5	NULL	NULL	0	NULL	sphingosine			N-acylated to					ceramide					NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_78	12135749	Because sphingosine could be converted to ceramide by  N-acylation and ceramide could induce c-jun expression, we used fumonisin B1, an inhibitor of ceramide synthase, to investigate whether sphingosine itself induced c-jun expression.	transcription
59403	2	335923	5	NULL	NULL	0	NULL	ceramide			induce					c-jun		expression of			NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_78	12135749	Because sphingosine could be converted to ceramide by  N-acylation and ceramide could induce c-jun expression, we used fumonisin B1, an inhibitor of ceramide synthase, to investigate whether sphingosine itself induced c-jun expression.	transcription
59404	3	335923	5	NULL	NULL	0	NULL	fumonisin B1			is an inhibitor of					ceramide synthase					NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_78	12135749	Because sphingosine could be converted to ceramide by  N-acylation and ceramide could induce c-jun expression, we used fumonisin B1, an inhibitor of ceramide synthase, to investigate whether sphingosine itself induced c-jun expression.	transcription
59405	4	335923	5	NULL	NULL	0	NULL	sphingosine			induce		potentially			c-jun		expression of			NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_78	12135749	Because sphingosine could be converted to ceramide by  N-acylation and ceramide could induce c-jun expression, we used fumonisin B1, an inhibitor of ceramide synthase, to investigate whether sphingosine itself induced c-jun expression.	transcription
79369	1	335923	6	NULL	NULL	0	NULL	sphingosine	Chemical		is converted to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_78	12135749	Because sphingosine could be converted to ceramide by  N-acylation and ceramide could induce c-jun expression, we used fumonisin B1, an inhibitor of ceramide synthase, to investigate whether sphingosine itself induced c-jun expression.	transcription
79370	2	335923	6	NULL	NULL	0	NULL	statement 1	Process		occurs by					N-acylation	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_78	12135749	Because sphingosine could be converted to ceramide by  N-acylation and ceramide could induce c-jun expression, we used fumonisin B1, an inhibitor of ceramide synthase, to investigate whether sphingosine itself induced c-jun expression.	transcription
79371	3	335923	6	NULL	NULL	0	NULL	ceramide	Chemical		induces					c-jun	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_78	12135749	Because sphingosine could be converted to ceramide by  N-acylation and ceramide could induce c-jun expression, we used fumonisin B1, an inhibitor of ceramide synthase, to investigate whether sphingosine itself induced c-jun expression.	transcription
59406	1	335924	5	NULL	NULL	0	NULL	apoptosis			is mediated by					ceramide					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_152	9415703	Ceramide-mediated apoptosis was unaffected by the ceramide acylhydrolase inhibitor oleoylethanolamine (Table  3), indicating that deacylation to sphingosine did not underlie the bioactivity of ceramide.	transcription
59407	2	335924	5	NULL	NULL	0	NULL	oleoylethanolamine			does not affect					statement 1					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_152	9415703	Ceramide-mediated apoptosis was unaffected by the ceramide acylhydrolase inhibitor oleoylethanolamine (Table  3), indicating that deacylation to sphingosine did not underlie the bioactivity of ceramide.	transcription
59408	3	335924	5	NULL	NULL	0	NULL	oleoylethanolamine			is an inhibitor of					ceramide acylhydrolase					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_152	9415703	Ceramide-mediated apoptosis was unaffected by the ceramide acylhydrolase inhibitor oleoylethanolamine (Table  3), indicating that deacylation to sphingosine did not underlie the bioactivity of ceramide.	transcription
59409	4	335924	5	NULL	NULL	0	NULL	sphingosine		deacylation to	does not underlie					ceramide		bioactivity of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_152	9415703	Ceramide-mediated apoptosis was unaffected by the ceramide acylhydrolase inhibitor oleoylethanolamine (Table  3), indicating that deacylation to sphingosine did not underlie the bioactivity of ceramide.	transcription
59410	5	335924	5	NULL	NULL	0	NULL	statement 3			indicates					statement 4					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_152	9415703	Ceramide-mediated apoptosis was unaffected by the ceramide acylhydrolase inhibitor oleoylethanolamine (Table  3), indicating that deacylation to sphingosine did not underlie the bioactivity of ceramide.	transcription
79366	1	335924	6	NULL	NULL	0	NULL	ceramide	Chemical		mediates					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_152	9415703	Ceramide-mediated apoptosis was unaffected by the ceramide acylhydrolase inhibitor oleoylethanolamine (Table  3), indicating that deacylation to sphingosine did not underlie the bioactivity of ceramide.	transcription
79367	2	335924	6	NULL	NULL	0	NULL	oleoylethanolamine	Chemical		does not affect					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_152	9415703	Ceramide-mediated apoptosis was unaffected by the ceramide acylhydrolase inhibitor oleoylethanolamine (Table  3), indicating that deacylation to sphingosine did not underlie the bioactivity of ceramide.	transcription
79368	3	335924	6	NULL	NULL	0	NULL	oleoylethanolamine	Chemical		is a type of					ceramide acylhydrolase inhibitor	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_152	9415703	Ceramide-mediated apoptosis was unaffected by the ceramide acylhydrolase inhibitor oleoylethanolamine (Table  3), indicating that deacylation to sphingosine did not underlie the bioactivity of ceramide.	transcription
59411	1	335925	5	NULL	NULL	0	NULL	phospholipase D			is activated by					sphingosine 1-phosphate					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_7	7592842	C - and  C -ceramides blocked the activation of phospholipase D by  sphingosine 1-phosphate, and this inhibition was not affected by  insulin.	transcription
59412	2	335925	5	NULL	NULL	0	NULL	C -ceramides			blocks					statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_7	7592842	C - and  C -ceramides blocked the activation of phospholipase D by  sphingosine 1-phosphate, and this inhibition was not affected by  insulin.	transcription
59413	3	335925	5	NULL	NULL	0	NULL	insulin			does not affect					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_7	7592842	C - and  C -ceramides blocked the activation of phospholipase D by  sphingosine 1-phosphate, and this inhibition was not affected by  insulin.	transcription
79363	1	335925	6	NULL	NULL	0	NULL	C-ceramides	Chemical		blocks					phospholipase D	GP	activation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_7	7592842	C - and  C -ceramides blocked the activation of phospholipase D by  sphingosine 1-phosphate, and this inhibition was not affected by  insulin.	transcription
79364	2	335925	6	NULL	NULL	0	NULL	sphingosine 1-phosphate	GP		blocks					phospholipase D	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_7	7592842	C - and  C -ceramides blocked the activation of phospholipase D by  sphingosine 1-phosphate, and this inhibition was not affected by  insulin.	transcription
79365	3	335925	6	NULL	NULL	0	NULL	Insulin	GP		does not affect					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_7	7592842	C - and  C -ceramides blocked the activation of phospholipase D by  sphingosine 1-phosphate, and this inhibition was not affected by  insulin.	transcription
59414	1	335926	5	NULL	NULL	0	NULL	C6-ceramide			is					N-hexanoyl sphingosine					NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-biochem-(tokyo)_139_2_16452313_s_5	16452313	We found that N-hexanoyl sphingosine (C6-ceramide)  induced apoptosis efficiently through the accumulation of long chain ceramides.	transcription
59415	2	335926	5	NULL	NULL	0	NULL	C6-ceramide			induce		efficiently			apoptosis					NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-biochem-(tokyo)_139_2_16452313_s_5	16452313	We found that N-hexanoyl sphingosine (C6-ceramide)  induced apoptosis efficiently through the accumulation of long chain ceramides.	transcription
59416	3	335926	5	NULL	NULL	0	NULL	statement 2			occurs through					long chain ceramides		accumulation of			NULL		NULL	NULL	NULL	NULL	abs-batch0600-0619_j-biochem-(tokyo)_139_2_16452313_s_5	16452313	We found that N-hexanoyl sphingosine (C6-ceramide)  induced apoptosis efficiently through the accumulation of long chain ceramides.	transcription
79361	1	335926	6	NULL	NULL	0	NULL	N-hexanoyl sphingosine	Chemical		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-biochem-(tokyo)_139_2_16452313_s_5	16452313	We found that N-hexanoyl sphingosine (C6-ceramide)  induced apoptosis efficiently through the accumulation of long chain ceramides.	transcription
79362	2	335926	6	NULL	NULL	0	NULL	N-hexanoyl sphingosine	Chemical		is					C6-ceramide	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-biochem-(tokyo)_139_2_16452313_s_5	16452313	We found that N-hexanoyl sphingosine (C6-ceramide)  induced apoptosis efficiently through the accumulation of long chain ceramides.	transcription
59417	1	335927	5	NULL	NULL	0	NULL	C2-ceramide			is					N-acetyl sphingosine					NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-biochem-(tokyo)_139_2_16452313_s_6	16452313	On the other hand, N-acetyl sphingosine (C2-ceramide) induced neither  apoptosis nor accumulation of long chain ceramides.	transcription
59418	2	335927	5	NULL	NULL	0	NULL	C2-ceramide			does not induce					apoptosis					NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-biochem-(tokyo)_139_2_16452313_s_6	16452313	On the other hand, N-acetyl sphingosine (C2-ceramide) induced neither  apoptosis nor accumulation of long chain ceramides.	transcription
59419	3	335927	5	NULL	NULL	0	NULL	C2-ceramide			does not induce					long chain ceramides		accumulation of			NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-biochem-(tokyo)_139_2_16452313_s_6	16452313	On the other hand, N-acetyl sphingosine (C2-ceramide) induced neither  apoptosis nor accumulation of long chain ceramides.	transcription
79359	1	335927	6	NULL	NULL	0	NULL	N-acetyl sphingosine	Chemical		does not induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-biochem-(tokyo)_139_2_16452313_s_6	16452313	On the other hand, N-acetyl sphingosine (C2-ceramide) induced neither  apoptosis nor accumulation of long chain ceramides.	transcription
79360	2	335927	6	NULL	NULL	0	NULL	N-acetyl sphingosine	Chemical		does not induce					ceramide	Chemical	accumulation of;; long chain			NULL		0	NULL	NULL	NULL	abs-batch0600-0619_j-biochem-(tokyo)_139_2_16452313_s_6	16452313	On the other hand, N-acetyl sphingosine (C2-ceramide) induced neither  apoptosis nor accumulation of long chain ceramides.	transcription
59420	1	335928	5	NULL	NULL	0	NULL	haCER2			is					human ceramidase					NULL		0	NULL	NULL	NULL	abs-batch0760-0779_faseb-j_20_11_16940153_s_4	16940153	Here we identify a novel human ceramidase (haCER2) that regulates the  levels of both sphingosine and S1P by controlling the hydrolysis of ceramides.	transcription
59421	2	335928	5	NULL	NULL	0	NULL	haCER2			regulates					sphingosine		level of			NULL		NULL	NULL	NULL	NULL	abs-batch0760-0779_faseb-j_20_11_16940153_s_4	16940153	Here we identify a novel human ceramidase (haCER2) that regulates the  levels of both sphingosine and S1P by controlling the hydrolysis of ceramides.	transcription
59422	3	335928	5	NULL	NULL	0	NULL	haCER2			controls					ceramide		hydrolysis of			NULL		0	NULL	NULL	NULL	abs-batch0760-0779_faseb-j_20_11_16940153_s_4	16940153	Here we identify a novel human ceramidase (haCER2) that regulates the  levels of both sphingosine and S1P by controlling the hydrolysis of ceramides.	transcription
59423	4	335928	5	NULL	NULL	0	NULL	statement 3			leads to					statement 2					NULL		0	NULL	NULL	NULL	abs-batch0760-0779_faseb-j_20_11_16940153_s_4	16940153	Here we identify a novel human ceramidase (haCER2) that regulates the  levels of both sphingosine and S1P by controlling the hydrolysis of ceramides.	transcription
59424	5	335928	5	NULL	NULL	0	NULL	haCER2			regulates					S1P		level of			NULL		0	NULL	NULL	NULL	abs-batch0760-0779_faseb-j_20_11_16940153_s_4	16940153	Here we identify a novel human ceramidase (haCER2) that regulates the  levels of both sphingosine and S1P by controlling the hydrolysis of ceramides.	transcription
59425	6	335928	5	NULL	NULL	0	NULL	statement 3			leads to					statement 5					NULL		0	NULL	NULL	NULL	abs-batch0760-0779_faseb-j_20_11_16940153_s_4	16940153	Here we identify a novel human ceramidase (haCER2) that regulates the  levels of both sphingosine and S1P by controlling the hydrolysis of ceramides.	transcription
79355	1	335928	6	NULL	NULL	NULL	NULL	haCER2	GP		controls					ceramide	Chemical	hydrolysis of 			NULL		NULL	NULL	NULL	NULL	abs-batch0760-0779_faseb-j_20_11_16940153_s_4	16940153	Here we identify a novel human ceramidase (haCER2) that regulates the  levels of both sphingosine and S1P by controlling the hydrolysis of ceramides.	transcription
79356	2	335928	6	NULL	NULL	0	NULL	haCER2	GP		regulates					sphingosine	Chemical	levels of 			NULL		0	NULL	NULL	NULL	abs-batch0760-0779_faseb-j_20_11_16940153_s_4	16940153	Here we identify a novel human ceramidase (haCER2) that regulates the  levels of both sphingosine and S1P by controlling the hydrolysis of ceramides.	transcription
79357	3	335928	6	NULL	NULL	0	NULL	haCER2	GP		regulates					S1P	GP	levels of 			NULL		0	NULL	NULL	NULL	abs-batch0760-0779_faseb-j_20_11_16940153_s_4	16940153	Here we identify a novel human ceramidase (haCER2) that regulates the  levels of both sphingosine and S1P by controlling the hydrolysis of ceramides.	transcription
79358	4	335928	6	NULL	NULL	0	NULL	haCER2	GP		is					human ceramidase	GP				NULL		0	NULL	NULL	NULL	abs-batch0760-0779_faseb-j_20_11_16940153_s_4	16940153	Here we identify a novel human ceramidase (haCER2) that regulates the  levels of both sphingosine and S1P by controlling the hydrolysis of ceramides.	transcription
59426	1	335929	5	NULL	NULL	0	NULL	ceramide			induce					apoptosis					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_30_19060_s_144	9668088	Although PAP1 might also be toxic as a ceramide analog because ceramides can induce apoptosis, this probably does not play a role in the toxicity of PAP1 because the effects of N-acylsphingosines (ceramides) are usually stereoselective and require the 4,5- trans-double bond of the sphingosine backbone ( 28).	transcription
59427	2	335929	5	NULL	NULL	0	NULL	sphingosine			does not play a role in					PAP1		toxicity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_30_19060_s_144	9668088	Although PAP1 might also be toxic as a ceramide analog because ceramides can induce apoptosis, this probably does not play a role in the toxicity of PAP1 because the effects of N-acylsphingosines (ceramides) are usually stereoselective and require the 4,5- trans-double bond of the sphingosine backbone ( 28).	transcription
59428	1	335930	5	NULL	NULL	0	NULL	serum		deprivation of	is an inducer of					stress					NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
59429	2	335930	5	NULL	NULL	0	NULL	Fas		ligation of	is an inducer of					stress					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
59430	3	335930	5	NULL	NULL	0	NULL	sphingomyelinase		bacterial	is an inducer of					stress					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
59431	4	335930	5	NULL	NULL	0	NULL	ceramide		cell-permeable	is an inducer of					stress					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
59432	5	335930	5	NULL	NULL	0	NULL	serum		deprivation of	increases					ceramide		cellular levels of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
59433	6	335930	5	NULL	NULL	0	NULL	Fas		ligation of	increases					ceramide		cellular levels of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
59434	7	335930	5	NULL	NULL	0	NULL	sphingomyelinase		bacterial	increases					ceramide		cellular levels of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
59435	8	335930	5	NULL	NULL	0	NULL	ceramide		cell-permeable	increases					ceramide		cellular levels of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
59436	9	335930	5	NULL	NULL	0	NULL	serum		deprivation of	increases					sphingosine		cellular levels of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
59437	10	335930	5	NULL	NULL	0	NULL	Fas`		ligation of	increases					sphingosine		cellular levels of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
59438	11	335930	5	NULL	NULL	0	NULL	sphingomyelinase		bacterial	increases					sphingosine		cellular levels of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
59439	12	335930	5	NULL	NULL	0	NULL	ceramide		cell-permeable	increases					sphingosine		cellular levels of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
79347	1	335930	6	NULL	NULL	0	NULL	serum	GP	deprivation of 	induces					ceramide	Chemical	levels of 			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
79348	2	335930	6	NULL	NULL	0	NULL	Fas	GP	ligation of 	induces					ceramide	Chemical	levels of 			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
79349	3	335930	6	NULL	NULL	0	NULL	sphingomyelinase	GP	bacterial	induces					ceramide	Chemical	levels of 			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
79350	4	335930	6	NULL	NULL	0	NULL	cell-permeable ceramides	Chemical		induces					ceramide	Chemical	levels of 			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
79351	5	335930	6	NULL	NULL	0	NULL	serum	Chemical	deprivation of 	induces					sphingosine	Chemical	levels of 			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
79352	6	335930	6	NULL	NULL	0	NULL	Fas	GP	ligation of 	induces					sphingosine	Chemical	levels of 			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
79353	7	335930	6	NULL	NULL	0	NULL	sphingomyelinase	GP		increases					sphingosine	Chemical	levels of 			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
79354	8	335930	6	NULL	NULL	0	NULL	cell-permeable ceramides	Chemical		increases					sphingosine	Chemical	levels of 			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_156	12531549	Accordingly, enforced expression of sphingosine kinase markedly enhanced survival in NIH3T3 [  90], HEK293 [ 90], Jurkat [ 90], and PC12 cells [ 88] in response to several stress inducers such as serum deprivation, Fas ligation, bacterial sphingomyelinase, and cell-permeable ceramides known to increase cellular ceramide and sphingosine levels.	transcription
59440	1	335932	5	NULL	NULL	0	NULL	palmitate			is incorporated into					ceramide					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_312	16118219	Importantly, sphingosine-induced incorporation of [3]palmitate into ceramide ( Fig. 11 D) and sphingosine-induced increases in the major ceramide species were sharply curtailed by down-regulation of SphK2 ( Fig. 11 F), further suggesting a role for SphK2 in reutilization of sphingosine and its conversion to ceramide.	transcription
59441	2	335932	5	NULL	NULL	0	NULL	sphingosine			induce					statement 1					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_312	16118219	Importantly, sphingosine-induced incorporation of [3]palmitate into ceramide ( Fig. 11 D) and sphingosine-induced increases in the major ceramide species were sharply curtailed by down-regulation of SphK2 ( Fig. 11 F), further suggesting a role for SphK2 in reutilization of sphingosine and its conversion to ceramide.	transcription
59442	3	335932	5	NULL	NULL	0	NULL	sphingosine			induce					ceramide species		increase in			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_312	16118219	Importantly, sphingosine-induced incorporation of [3]palmitate into ceramide ( Fig. 11 D) and sphingosine-induced increases in the major ceramide species were sharply curtailed by down-regulation of SphK2 ( Fig. 11 F), further suggesting a role for SphK2 in reutilization of sphingosine and its conversion to ceramide.	transcription
59443	4	335932	5	NULL	NULL	0	NULL	SphK2		down-regulation of	curtails		sharply			statement 2					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_312	16118219	Importantly, sphingosine-induced incorporation of [3]palmitate into ceramide ( Fig. 11 D) and sphingosine-induced increases in the major ceramide species were sharply curtailed by down-regulation of SphK2 ( Fig. 11 F), further suggesting a role for SphK2 in reutilization of sphingosine and its conversion to ceramide.	transcription
59444	5	335932	5	NULL	NULL	0	NULL	SphK2		down-regulation of	curtails		sharply			statement 3					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_312	16118219	Importantly, sphingosine-induced incorporation of [3]palmitate into ceramide ( Fig. 11 D) and sphingosine-induced increases in the major ceramide species were sharply curtailed by down-regulation of SphK2 ( Fig. 11 F), further suggesting a role for SphK2 in reutilization of sphingosine and its conversion to ceramide.	transcription
59445	6	335932	5	NULL	NULL	0	NULL	SphK2			plays a role in		may			sphingosine		reutilization of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_312	16118219	Importantly, sphingosine-induced incorporation of [3]palmitate into ceramide ( Fig. 11 D) and sphingosine-induced increases in the major ceramide species were sharply curtailed by down-regulation of SphK2 ( Fig. 11 F), further suggesting a role for SphK2 in reutilization of sphingosine and its conversion to ceramide.	transcription
59446	7	335932	5	NULL	NULL	0	NULL	sphingosine			is converted to					ceramide					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_312	16118219	Importantly, sphingosine-induced incorporation of [3]palmitate into ceramide ( Fig. 11 D) and sphingosine-induced increases in the major ceramide species were sharply curtailed by down-regulation of SphK2 ( Fig. 11 F), further suggesting a role for SphK2 in reutilization of sphingosine and its conversion to ceramide.	transcription
59447	8	335932	5	NULL	NULL	0	NULL	SphK2		down-regulation of	plays a role in		may			statement 7					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_312	16118219	Importantly, sphingosine-induced incorporation of [3]palmitate into ceramide ( Fig. 11 D) and sphingosine-induced increases in the major ceramide species were sharply curtailed by down-regulation of SphK2 ( Fig. 11 F), further suggesting a role for SphK2 in reutilization of sphingosine and its conversion to ceramide.	transcription
79342	1	335932	6	NULL	NULL	0	NULL	palmitate	Chemical		is converted to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_312	16118219	Importantly, sphingosine-induced incorporation of [3]palmitate into ceramide ( Fig. 11 D) and sphingosine-induced increases in the major ceramide species were sharply curtailed by down-regulation of SphK2 ( Fig. 11 F), further suggesting a role for SphK2 in reutilization of sphingosine and its conversion to ceramide.	transcription
79343	2	335932	6	NULL	NULL	0	NULL	sphingosine	Chemical		induces					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_312	16118219	Importantly, sphingosine-induced incorporation of [3]palmitate into ceramide ( Fig. 11 D) and sphingosine-induced increases in the major ceramide species were sharply curtailed by down-regulation of SphK2 ( Fig. 11 F), further suggesting a role for SphK2 in reutilization of sphingosine and its conversion to ceramide.	transcription
79344	3	335932	6	NULL	NULL	0	NULL	SphK2	GP		plays a role in					sphingosine	Chemical	reutilization of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_312	16118219	Importantly, sphingosine-induced incorporation of [3]palmitate into ceramide ( Fig. 11 D) and sphingosine-induced increases in the major ceramide species were sharply curtailed by down-regulation of SphK2 ( Fig. 11 F), further suggesting a role for SphK2 in reutilization of sphingosine and its conversion to ceramide.	transcription
79345	4	335932	6	NULL	NULL	0	NULL	sphingosine	Chemical		is converted to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_312	16118219	Importantly, sphingosine-induced incorporation of [3]palmitate into ceramide ( Fig. 11 D) and sphingosine-induced increases in the major ceramide species were sharply curtailed by down-regulation of SphK2 ( Fig. 11 F), further suggesting a role for SphK2 in reutilization of sphingosine and its conversion to ceramide.	transcription
79346	5	335932	6	NULL	NULL	0	NULL	SphK2	GP		plays a role in					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_312	16118219	Importantly, sphingosine-induced incorporation of [3]palmitate into ceramide ( Fig. 11 D) and sphingosine-induced increases in the major ceramide species were sharply curtailed by down-regulation of SphK2 ( Fig. 11 F), further suggesting a role for SphK2 in reutilization of sphingosine and its conversion to ceramide.	transcription
59448	1	335933	5	NULL	NULL	0	NULL	ceramide			is a type of					metabolite					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_57	12531549	Ceramide and sphingosine are interconvertible metabolites; however, sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 does not affect sphingosine-induced apoptosis in HL-60 [  20,   21 and   22], U937 [  23], Jurkat [ 6, TF1 erythroleukemic [  24], and Hep3B hepatoma cells [  25].	transcription
59449	1	335933	5	NULL	NULL	0	NULL	ceramide			is a type of					metabolite					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_57	12531549	Ceramide and sphingosine are interconvertible metabolites; however, sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 does not affect sphingosine-induced apoptosis in HL-60 [  20,   21 and   22], U937 [  23], Jurkat [ 6, TF1 erythroleukemic [  24], and Hep3B hepatoma cells [  25].	transcription
59450	2	335933	5	NULL	NULL	0	NULL	sphingosine			is a type of					metabolite					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_57	12531549	Ceramide and sphingosine are interconvertible metabolites; however, sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 does not affect sphingosine-induced apoptosis in HL-60 [  20,   21 and   22], U937 [  23], Jurkat [ 6, TF1 erythroleukemic [  24], and Hep3B hepatoma cells [  25].	transcription
59451	3	335933	5	NULL	NULL	0	NULL	ceramide			is interconvertible to					sphingosine					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_57	12531549	Ceramide and sphingosine are interconvertible metabolites; however, sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 does not affect sphingosine-induced apoptosis in HL-60 [  20,   21 and   22], U937 [  23], Jurkat [ 6, TF1 erythroleukemic [  24], and Hep3B hepatoma cells [  25].	transcription
59452	4	335933	5	NULL	NULL	0	NULL	sphingosine			induce					apoptosis					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_57	12531549	Ceramide and sphingosine are interconvertible metabolites; however, sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 does not affect sphingosine-induced apoptosis in HL-60 [  20,   21 and   22], U937 [  23], Jurkat [ 6, TF1 erythroleukemic [  24], and Hep3B hepatoma cells [  25].	transcription
59453	5	335933	5	NULL	NULL	0	NULL	sphingosine			is not converted to					ceramide					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_57	12531549	Ceramide and sphingosine are interconvertible metabolites; however, sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 does not affect sphingosine-induced apoptosis in HL-60 [  20,   21 and   22], U937 [  23], Jurkat [ 6, TF1 erythroleukemic [  24], and Hep3B hepatoma cells [  25].	transcription
59454	6	335933	5	NULL	NULL	0	NULL	statement 5			is necessary for					statement 4					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_57	12531549	Ceramide and sphingosine are interconvertible metabolites; however, sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 does not affect sphingosine-induced apoptosis in HL-60 [  20,   21 and   22], U937 [  23], Jurkat [ 6, TF1 erythroleukemic [  24], and Hep3B hepatoma cells [  25].	transcription
59455	7	335933	5	NULL	NULL	0	NULL	fumonisin B1			is an inhibitor of					ceramide synthase					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_57	12531549	Ceramide and sphingosine are interconvertible metabolites; however, sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 does not affect sphingosine-induced apoptosis in HL-60 [  20,   21 and   22], U937 [  23], Jurkat [ 6, TF1 erythroleukemic [  24], and Hep3B hepatoma cells [  25].	transcription
59456	8	335933	5	NULL	NULL	0	NULL	fumonisin B1			does not affect					statement 4					NULL	HL-60 cells	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_57	12531549	Ceramide and sphingosine are interconvertible metabolites; however, sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 does not affect sphingosine-induced apoptosis in HL-60 [  20,   21 and   22], U937 [  23], Jurkat [ 6, TF1 erythroleukemic [  24], and Hep3B hepatoma cells [  25].	transcription
59457	9	335933	5	NULL	NULL	0	NULL	fumonisin B1			does not affect					statement 4					NULL	U937 cells	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_57	12531549	Ceramide and sphingosine are interconvertible metabolites; however, sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 does not affect sphingosine-induced apoptosis in HL-60 [  20,   21 and   22], U937 [  23], Jurkat [ 6, TF1 erythroleukemic [  24], and Hep3B hepatoma cells [  25].	transcription
59458	10	335933	5	NULL	NULL	0	NULL	fumonisin B1			does not affect					statement 4					NULL	Jurkat cells	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_57	12531549	Ceramide and sphingosine are interconvertible metabolites; however, sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 does not affect sphingosine-induced apoptosis in HL-60 [  20,   21 and   22], U937 [  23], Jurkat [ 6, TF1 erythroleukemic [  24], and Hep3B hepatoma cells [  25].	transcription
59459	11	335933	5	NULL	NULL	0	NULL	fumonisin B1			does not affect					statement 4					NULL	Hep3B hepatoma cells	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_57	12531549	Ceramide and sphingosine are interconvertible metabolites; however, sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 does not affect sphingosine-induced apoptosis in HL-60 [  20,   21 and   22], U937 [  23], Jurkat [ 6, TF1 erythroleukemic [  24], and Hep3B hepatoma cells [  25].	transcription
79336	1	335933	6	NULL	NULL	0	NULL	sphingosine	Chemical		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_57	12531549	Ceramide and sphingosine are interconvertible metabolites; however, sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 does not affect sphingosine-induced apoptosis in HL-60 [  20,   21 and   22], U937 [  23], Jurkat [ 6, TF1 erythroleukemic [  24], and Hep3B hepatoma cells [  25].	transcription
79337	2	335933	6	NULL	NULL	NULL	NULL	fumonisin B1	Chemical		does not affect					statement 1	Process				NULL	HL-60 cells	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_57	12531549	Ceramide and sphingosine are interconvertible metabolites; however, sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 does not affect sphingosine-induced apoptosis in HL-60 [  20,   21 and   22], U937 [  23], Jurkat [ 6, TF1 erythroleukemic [  24], and Hep3B hepatoma cells [  25].	transcription
79338	3	335933	6	NULL	NULL	NULL	NULL	fumonisin B1	Chemical		does not affect					statement 1	Process				NULL	U937 cells	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_57	12531549	Ceramide and sphingosine are interconvertible metabolites; however, sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 does not affect sphingosine-induced apoptosis in HL-60 [  20,   21 and   22], U937 [  23], Jurkat [ 6, TF1 erythroleukemic [  24], and Hep3B hepatoma cells [  25].	transcription
79339	4	335933	6	NULL	NULL	NULL	NULL	fumonisin B1	Chemical		does not affect					statement 1	Process				NULL	Jurkat cells	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_57	12531549	Ceramide and sphingosine are interconvertible metabolites; however, sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 does not affect sphingosine-induced apoptosis in HL-60 [  20,   21 and   22], U937 [  23], Jurkat [ 6, TF1 erythroleukemic [  24], and Hep3B hepatoma cells [  25].	transcription
79340	5	335933	6	NULL	NULL	0	NULL	fumonisin B1	Chemical		does not affect					statement 1	Process				NULL	TF1 erythroleukemic cells	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_57	12531549	Ceramide and sphingosine are interconvertible metabolites; however, sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 does not affect sphingosine-induced apoptosis in HL-60 [  20,   21 and   22], U937 [  23], Jurkat [ 6, TF1 erythroleukemic [  24], and Hep3B hepatoma cells [  25].	transcription
79341	6	335933	6	NULL	NULL	0	NULL	fumonisin B1	Chemical		does not affect					statement 1	Process				NULL	Hep3B hepatoma cells	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_57	12531549	Ceramide and sphingosine are interconvertible metabolites; however, sphingosine induces apoptosis without being converted to ceramide inasmuch as the ceramide synthase inhibitor fumonisin B1 does not affect sphingosine-induced apoptosis in HL-60 [  20,   21 and   22], U937 [  23], Jurkat [ 6, TF1 erythroleukemic [  24], and Hep3B hepatoma cells [  25].	transcription
59460	1	335934	5	NULL	NULL	0	NULL	safingol			is an inhibitor of		competitive			sphingosine kinase					NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_44_9_1772_s_30	12777464	As a competitive inhibitor of sphingosine kinase ( ), safingol could prevent the formation of S1P from sphingosine, which in turn is exclusively formed from ceramide ( ).	transcription
59461	2	335934	5	NULL	NULL	0	NULL	S1P			is formed from					sphingosine					NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_9_1772_s_30	12777464	As a competitive inhibitor of sphingosine kinase ( ), safingol could prevent the formation of S1P from sphingosine, which in turn is exclusively formed from ceramide ( ).	transcription
59462	3	335934	5	NULL	NULL	0	NULL	safingol			prevents					statement 2					NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_9_1772_s_30	12777464	As a competitive inhibitor of sphingosine kinase ( ), safingol could prevent the formation of S1P from sphingosine, which in turn is exclusively formed from ceramide ( ).	transcription
59463	4	335934	5	NULL	NULL	0	NULL	sphingosine			is formed from		exclusively			ceramide					NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_9_1772_s_30	12777464	As a competitive inhibitor of sphingosine kinase ( ), safingol could prevent the formation of S1P from sphingosine, which in turn is exclusively formed from ceramide ( ).	transcription
79334	1	335934	6	NULL	NULL	0	NULL	sphingosine	Chemical		is formed from					S1P	GP				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_9_1772_s_30	12777464	As a competitive inhibitor of sphingosine kinase ( ), safingol could prevent the formation of S1P from sphingosine, which in turn is exclusively formed from ceramide ( ).	transcription
79335	2	335934	6	NULL	NULL	0	NULL	safingol	Chemical		prevents					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_9_1772_s_30	12777464	As a competitive inhibitor of sphingosine kinase ( ), safingol could prevent the formation of S1P from sphingosine, which in turn is exclusively formed from ceramide ( ).	transcription
59464	1	335935	5	NULL	NULL	0	NULL	S1P			is a downstream metabolite of					ceramide					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34628_s_25	10942778	In contrast, S1P, a downstream metabolite of ceramide, produced by phosphorylation of sphingosine following activation of sphingosine kinase, is mitogenic and regulates apoptosis in diverse cell types ( 12).	transcription
59465	2	335935	5	NULL	NULL	0	NULL	sphingosine			is phosphorylated to					S1P					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34628_s_25	10942778	In contrast, S1P, a downstream metabolite of ceramide, produced by phosphorylation of sphingosine following activation of sphingosine kinase, is mitogenic and regulates apoptosis in diverse cell types ( 12).	transcription
59466	3	335935	5	NULL	NULL	0	NULL	sphingosine kinase			catalyzes					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34628_s_25	10942778	In contrast, S1P, a downstream metabolite of ceramide, produced by phosphorylation of sphingosine following activation of sphingosine kinase, is mitogenic and regulates apoptosis in diverse cell types ( 12).	transcription
59467	4	335935	5	NULL	NULL	0	NULL	S1P			regulates					apoptosis					NULL	diverse cell types	0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34628_s_25	10942778	In contrast, S1P, a downstream metabolite of ceramide, produced by phosphorylation of sphingosine following activation of sphingosine kinase, is mitogenic and regulates apoptosis in diverse cell types ( 12).	transcription
79330	1	335935	6	NULL	NULL	0	NULL	S1P	GP		produced by					sphingosine	Chemical	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34628_s_25	10942778	In contrast, S1P, a downstream metabolite of ceramide, produced by phosphorylation of sphingosine following activation of sphingosine kinase, is mitogenic and regulates apoptosis in diverse cell types ( 12).	transcription
79331	2	335935	6	NULL	NULL	0	NULL	statement 1	Process		activates					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34628_s_25	10942778	In contrast, S1P, a downstream metabolite of ceramide, produced by phosphorylation of sphingosine following activation of sphingosine kinase, is mitogenic and regulates apoptosis in diverse cell types ( 12).	transcription
79332	3	335935	6	NULL	NULL	0	NULL	S1P	GP		is					mitogenic	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34628_s_25	10942778	In contrast, S1P, a downstream metabolite of ceramide, produced by phosphorylation of sphingosine following activation of sphingosine kinase, is mitogenic and regulates apoptosis in diverse cell types ( 12).	transcription
79333	4	335935	6	NULL	NULL	0	NULL	S1P	GP		regulates					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_44_34628_s_25	10942778	In contrast, S1P, a downstream metabolite of ceramide, produced by phosphorylation of sphingosine following activation of sphingosine kinase, is mitogenic and regulates apoptosis in diverse cell types ( 12).	transcription
59468	1	335936	5	NULL	NULL	0	NULL	ceramide			induce					apoptosis					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6876_s_336	10702247	In addition cellular levels of sphingosine (the product of ceramidase) and sphingosine phosphate are critical for cellular well being in that they may mediate proliferation and oppose ceramide-induced apoptosis ( 41).	transcription
59469	2	335936	5	NULL	NULL	0	NULL	sphingosine		cellular levels of	oppose		may			statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6876_s_336	10702247	In addition cellular levels of sphingosine (the product of ceramidase) and sphingosine phosphate are critical for cellular well being in that they may mediate proliferation and oppose ceramide-induced apoptosis ( 41).	transcription
59470	3	335936	5	NULL	NULL	0	NULL	sphingosine phosphate			oppose		may			statement 1					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6876_s_336	10702247	In addition cellular levels of sphingosine (the product of ceramidase) and sphingosine phosphate are critical for cellular well being in that they may mediate proliferation and oppose ceramide-induced apoptosis ( 41).	transcription
59471	4	335936	5	NULL	NULL	0	NULL	sphingosine			is a product of					ceramidase					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6876_s_336	10702247	In addition cellular levels of sphingosine (the product of ceramidase) and sphingosine phosphate are critical for cellular well being in that they may mediate proliferation and oppose ceramide-induced apoptosis ( 41).	transcription
79327	1	335936	6	NULL	NULL	0	NULL	sphingosine	Chemical		mediates					proliferation	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6876_s_336	10702247	In addition cellular levels of sphingosine (the product of ceramidase) and sphingosine phosphate are critical for cellular well being in that they may mediate proliferation and oppose ceramide-induced apoptosis ( 41).	transcription
79328	2	335936	6	NULL	NULL	0	NULL	sphingosine phosphate	GP		mediates					proliferation	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6876_s_336	10702247	In addition cellular levels of sphingosine (the product of ceramidase) and sphingosine phosphate are critical for cellular well being in that they may mediate proliferation and oppose ceramide-induced apoptosis ( 41).	transcription
79329	3	335936	6	NULL	NULL	0	NULL	ceramide	Chemical		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_10_6876_s_336	10702247	In addition cellular levels of sphingosine (the product of ceramidase) and sphingosine phosphate are critical for cellular well being in that they may mediate proliferation and oppose ceramide-induced apoptosis ( 41).	transcription
59472	1	335937	5	NULL	NULL	0	NULL	ceramide		cell-permeable	does not stimulate					PLD					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_346	12177168	Also, the cell-permeable [C2]ceramide, exogenous sphingomyelinase, or sphingosine failed to stimulate PLD, and sphingosine 1-phosphate was a weak activator of this enzyme activity in the acini.	transcription
59473	2	335937	5	NULL	NULL	0	NULL	sphingomyelinase		exogenous	does not stimulate					PLD					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_346	12177168	Also, the cell-permeable [C2]ceramide, exogenous sphingomyelinase, or sphingosine failed to stimulate PLD, and sphingosine 1-phosphate was a weak activator of this enzyme activity in the acini.	transcription
59474	3	335937	5	NULL	NULL	0	NULL	sphingosine			does not stimulate					PLD					NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_346	12177168	Also, the cell-permeable [C2]ceramide, exogenous sphingomyelinase, or sphingosine failed to stimulate PLD, and sphingosine 1-phosphate was a weak activator of this enzyme activity in the acini.	transcription
59475	4	335937	5	NULL	NULL	0	NULL	sphingosine 1-phosphate			activates		weakly			PLD		activity of			NULL	acini	0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_346	12177168	Also, the cell-permeable [C2]ceramide, exogenous sphingomyelinase, or sphingosine failed to stimulate PLD, and sphingosine 1-phosphate was a weak activator of this enzyme activity in the acini.	transcription
79324	1	335937	6	NULL	NULL	0	NULL	ceramide	Chemical		does not stimulate					PLD	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_346	12177168	Also, the cell-permeable [C2]ceramide, exogenous sphingomyelinase, or sphingosine failed to stimulate PLD, and sphingosine 1-phosphate was a weak activator of this enzyme activity in the acini.	transcription
79325	2	335937	6	NULL	NULL	0	NULL	sphingosine	Chemical		does not stimulate					PLD	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_346	12177168	Also, the cell-permeable [C2]ceramide, exogenous sphingomyelinase, or sphingosine failed to stimulate PLD, and sphingosine 1-phosphate was a weak activator of this enzyme activity in the acini.	transcription
79326	3	335937	6	NULL	NULL	0	NULL	sphingosine 1-phosphate	GP		does not stimulate					PLD	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_346	12177168	Also, the cell-permeable [C2]ceramide, exogenous sphingomyelinase, or sphingosine failed to stimulate PLD, and sphingosine 1-phosphate was a weak activator of this enzyme activity in the acini.	transcription
59476	1	335938	5	NULL	NULL	0	NULL	ceramide	Chemical	cell-permeable	inhibit					sphingosine kinase-1	GP				NULL	chemoresistant cells	NULL	NULL	NULL	NULL	abs-batch0650-0679_leukemia_20_1_16281067_s_7	16281067	Incubation with cell-permeable ceramide of chemoresistant cells  led to a sphingosine kinase-1 inhibition and apoptosis both prevented  by sphingosine kinase-1 over-expression.	transcription
59477	2	335938	5	NULL	NULL	0	NULL	ceramide	Chemical	cell-permeable	leads to					apoptosis	Process				NULL	chemoresistant cells	0	NULL	NULL	NULL	abs-batch0650-0679_leukemia_20_1_16281067_s_7	16281067	Incubation with cell-permeable ceramide of chemoresistant cells  led to a sphingosine kinase-1 inhibition and apoptosis both prevented  by sphingosine kinase-1 over-expression.	transcription
59478	3	335938	5	NULL	NULL	0	NULL	statement 1	Process		prevented by					sphingosine kinase-1	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_leukemia_20_1_16281067_s_7	16281067	Incubation with cell-permeable ceramide of chemoresistant cells  led to a sphingosine kinase-1 inhibition and apoptosis both prevented  by sphingosine kinase-1 over-expression.	transcription
59479	4	335938	5	NULL	NULL	0	NULL	statement 2	Process		prevented by					sphingosine kinase-1	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_leukemia_20_1_16281067_s_7	16281067	Incubation with cell-permeable ceramide of chemoresistant cells  led to a sphingosine kinase-1 inhibition and apoptosis both prevented  by sphingosine kinase-1 over-expression.	transcription
79320	1	335938	6	NULL	NULL	0	NULL	ceramide	Chemical		leads to					sphingosine kinase-1	GP	inhibition of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_leukemia_20_1_16281067_s_7	16281067	Incubation with cell-permeable ceramide of chemoresistant cells  led to a sphingosine kinase-1 inhibition and apoptosis both prevented  by sphingosine kinase-1 over-expression.	transcription
79321	2	335938	6	NULL	NULL	0	NULL	ceramide	Chemical		leads to					apoptosis	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_leukemia_20_1_16281067_s_7	16281067	Incubation with cell-permeable ceramide of chemoresistant cells  led to a sphingosine kinase-1 inhibition and apoptosis both prevented  by sphingosine kinase-1 over-expression.	transcription
79322	3	335938	6	NULL	NULL	0	NULL	sphingosine kinase-1	GP		prevents					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_leukemia_20_1_16281067_s_7	16281067	Incubation with cell-permeable ceramide of chemoresistant cells  led to a sphingosine kinase-1 inhibition and apoptosis both prevented  by sphingosine kinase-1 over-expression.	transcription
79323	4	335938	6	NULL	NULL	0	NULL	sphingosine kinase-1	GP		prevents					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_leukemia_20_1_16281067_s_7	16281067	Incubation with cell-permeable ceramide of chemoresistant cells  led to a sphingosine kinase-1 inhibition and apoptosis both prevented  by sphingosine kinase-1 over-expression.	transcription
59480	1	335939	5	NULL	NULL	0	NULL	TNF-alpha	GP		changes					ceramide	Chemical	levels of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_72	16269668	Cell transfection with N-SMase2 siRNA inhibited the changes induced by TNF-alpha in the levels not only of ceramide but also of sphingosine and Sph1P ( Figure 2A), whereas transfection with SK1-DN blocked generation of Sph1P with accumulation of sphingosine and ceramide ( Figure 2B).	transcription
59481	2	335939	5	NULL	NULL	0	NULL	TNF-alpha	GP		changes					sphingosine	Chemical	levels of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_72	16269668	Cell transfection with N-SMase2 siRNA inhibited the changes induced by TNF-alpha in the levels not only of ceramide but also of sphingosine and Sph1P ( Figure 2A), whereas transfection with SK1-DN blocked generation of Sph1P with accumulation of sphingosine and ceramide ( Figure 2B).	transcription
59482	3	335939	5	NULL	NULL	0	NULL	TNF-alpha	GP		changes					Sph1P	Chemical	levels of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_72	16269668	Cell transfection with N-SMase2 siRNA inhibited the changes induced by TNF-alpha in the levels not only of ceramide but also of sphingosine and Sph1P ( Figure 2A), whereas transfection with SK1-DN blocked generation of Sph1P with accumulation of sphingosine and ceramide ( Figure 2B).	transcription
59483	4	335939	5	NULL	NULL	0	NULL	N-SMase2 siRNA	NucleicAcid		inhibits					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_72	16269668	Cell transfection with N-SMase2 siRNA inhibited the changes induced by TNF-alpha in the levels not only of ceramide but also of sphingosine and Sph1P ( Figure 2A), whereas transfection with SK1-DN blocked generation of Sph1P with accumulation of sphingosine and ceramide ( Figure 2B).	transcription
59484	5	335939	5	NULL	NULL	0	NULL	N-SMase2 siRNA	NucleicAcid		inhibits					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_72	16269668	Cell transfection with N-SMase2 siRNA inhibited the changes induced by TNF-alpha in the levels not only of ceramide but also of sphingosine and Sph1P ( Figure 2A), whereas transfection with SK1-DN blocked generation of Sph1P with accumulation of sphingosine and ceramide ( Figure 2B).	transcription
59485	6	335939	5	NULL	NULL	0	NULL	N-SMase2 siRNA	NucleicAcid		inhibits					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_72	16269668	Cell transfection with N-SMase2 siRNA inhibited the changes induced by TNF-alpha in the levels not only of ceramide but also of sphingosine and Sph1P ( Figure 2A), whereas transfection with SK1-DN blocked generation of Sph1P with accumulation of sphingosine and ceramide ( Figure 2B).	transcription
59486	7	335939	5	NULL	NULL	0	NULL	SK1-DN	GP		block					Sph1P	Chemical	generation of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_72	16269668	Cell transfection with N-SMase2 siRNA inhibited the changes induced by TNF-alpha in the levels not only of ceramide but also of sphingosine and Sph1P ( Figure 2A), whereas transfection with SK1-DN blocked generation of Sph1P with accumulation of sphingosine and ceramide ( Figure 2B).	transcription
59487	8	335939	5	NULL	NULL	0	NULL	SK1-DN	GP		accumulates					sphingosine	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_72	16269668	Cell transfection with N-SMase2 siRNA inhibited the changes induced by TNF-alpha in the levels not only of ceramide but also of sphingosine and Sph1P ( Figure 2A), whereas transfection with SK1-DN blocked generation of Sph1P with accumulation of sphingosine and ceramide ( Figure 2B).	transcription
59488	9	335939	5	NULL	NULL	0	NULL	statement 8	Process		leads to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_72	16269668	Cell transfection with N-SMase2 siRNA inhibited the changes induced by TNF-alpha in the levels not only of ceramide but also of sphingosine and Sph1P ( Figure 2A), whereas transfection with SK1-DN blocked generation of Sph1P with accumulation of sphingosine and ceramide ( Figure 2B).	transcription
59489	10	335939	5	NULL	NULL	0	NULL	SK1-DN	GP		accumulates					ceramide	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_72	16269668	Cell transfection with N-SMase2 siRNA inhibited the changes induced by TNF-alpha in the levels not only of ceramide but also of sphingosine and Sph1P ( Figure 2A), whereas transfection with SK1-DN blocked generation of Sph1P with accumulation of sphingosine and ceramide ( Figure 2B).	transcription
59490	11	335939	5	NULL	NULL	0	NULL	statement 10	Process		leads to					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_72	16269668	Cell transfection with N-SMase2 siRNA inhibited the changes induced by TNF-alpha in the levels not only of ceramide but also of sphingosine and Sph1P ( Figure 2A), whereas transfection with SK1-DN blocked generation of Sph1P with accumulation of sphingosine and ceramide ( Figure 2B).	transcription
59491	1	335940	5	NULL	NULL	0	NULL	ceramide	Chemical	increase in	more rapid than					sphingosine	Chemical	increase in			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_27	12531549	The increase in ceramide content was more rapid than that of sphingosine, suggesting that the increase of sphingosine levels could be resulting from the degradation of ceramide formed after TNF  treatment [ 5.	transcription
59492	2	335940	5	NULL	NULL	0	NULL	sphingosine	Chemical	increase in;;levels of	results from		may			ceramide	Chemical	degradation of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_27	12531549	The increase in ceramide content was more rapid than that of sphingosine, suggesting that the increase of sphingosine levels could be resulting from the degradation of ceramide formed after TNF  treatment [ 5.	transcription
59493	3	335940	5	NULL	NULL	0	NULL	statement 2	Process		occurs after					TNF	GP	treatment			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_27	12531549	The increase in ceramide content was more rapid than that of sphingosine, suggesting that the increase of sphingosine levels could be resulting from the degradation of ceramide formed after TNF  treatment [ 5.	transcription
59494	4	335940	5	NULL	NULL	0	NULL	statement 1	Process		suggest					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_27	12531549	The increase in ceramide content was more rapid than that of sphingosine, suggesting that the increase of sphingosine levels could be resulting from the degradation of ceramide formed after TNF  treatment [ 5.	transcription
79318	1	335940	6	NULL	NULL	0	NULL	TNF	GP		degrades					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_27	12531549	The increase in ceramide content was more rapid than that of sphingosine, suggesting that the increase of sphingosine levels could be resulting from the degradation of ceramide formed after TNF  treatment [ 5.	transcription
79319	2	335940	6	NULL	NULL	0	NULL	statement 1	Process		increases					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_27	12531549	The increase in ceramide content was more rapid than that of sphingosine, suggesting that the increase of sphingosine levels could be resulting from the degradation of ceramide formed after TNF  treatment [ 5.	transcription
59495	1	335941	5	NULL	NULL	0	NULL	S1P	Chemical	dephosphorylation of;;exogenous	generates					sphingosine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_94	12235122	Thus, it is most likely that as a consequence of overexpression of mSPP-1, the increased sphingosine generated by dephosphorylation of exogenous S1P has been diverted to ceramide generation by ceramide synthase - catalyzed N-acylation of sphingosine.	transcription
59496	3	335941	5	NULL	NULL	0	NULL	statement 2	Process		generates					ceramide	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_94	12235122	Thus, it is most likely that as a consequence of overexpression of mSPP-1, the increased sphingosine generated by dephosphorylation of exogenous S1P has been diverted to ceramide generation by ceramide synthase - catalyzed N-acylation of sphingosine.	transcription
59497	2	335941	5	NULL	NULL	0	NULL	sphingosine	Chemical	N-acylation of	is catalyzed by					ceramide synthase	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_94	12235122	Thus, it is most likely that as a consequence of overexpression of mSPP-1, the increased sphingosine generated by dephosphorylation of exogenous S1P has been diverted to ceramide generation by ceramide synthase - catalyzed N-acylation of sphingosine.	transcription
59498	4	335941	5	NULL	NULL	0	NULL	mSPP-1	GP	overexpression of	leads to					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_94	12235122	Thus, it is most likely that as a consequence of overexpression of mSPP-1, the increased sphingosine generated by dephosphorylation of exogenous S1P has been diverted to ceramide generation by ceramide synthase - catalyzed N-acylation of sphingosine.	transcription
59499	1	335942	5	NULL	NULL	0	NULL	sphingosine	Chemical	addition of;;exogenous	elevates		rapidly			ceramide	Chemical	cellular levels of			NULL	A431 cells, Neuro2a cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_5_3028_s_253	9006952	Addition of exogenous sphingosine rapidly elevates cellular ceramide levels in A431 cells and Neuro2a cells ( 66,  67) suggesting that some effects of sphingosine may be mediated by its conversion to ceramide.	transcription
59500	2	335942	5	NULL	NULL	0	NULL	sphingosine	Chemical		is converted to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_5_3028_s_253	9006952	Addition of exogenous sphingosine rapidly elevates cellular ceramide levels in A431 cells and Neuro2a cells ( 66,  67) suggesting that some effects of sphingosine may be mediated by its conversion to ceramide.	transcription
59501	3	335942	5	NULL	NULL	0	NULL	sphingosine	Chemical	effect of	is mediated by		may be			statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_5_3028_s_253	9006952	Addition of exogenous sphingosine rapidly elevates cellular ceramide levels in A431 cells and Neuro2a cells ( 66,  67) suggesting that some effects of sphingosine may be mediated by its conversion to ceramide.	transcription
79316	1	335942	6	NULL	NULL	0	NULL	sphingosine	Chemical		elevates					ceramide	Chemical				NULL	A431 cells	0	NULL	NULL	NULL	gw60_jbiolchem_272_5_3028_s_253	9006952	Addition of exogenous sphingosine rapidly elevates cellular ceramide levels in A431 cells and Neuro2a cells ( 66,  67) suggesting that some effects of sphingosine may be mediated by its conversion to ceramide.	transcription
79317	2	335942	6	NULL	NULL	0	NULL	sphingosine	Chemical		elevates					ceramide	Chemical	levels of 			NULL	Neuro2a cells	0	NULL	NULL	NULL	gw60_jbiolchem_272_5_3028_s_253	9006952	Addition of exogenous sphingosine rapidly elevates cellular ceramide levels in A431 cells and Neuro2a cells ( 66,  67) suggesting that some effects of sphingosine may be mediated by its conversion to ceramide.	transcription
59502	1	335943	5	NULL	NULL	0	NULL	PLD	GP		is activated by					ATP	Chemical				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_345	12177168	Our results indicate that it is unlikely that PLD activation by ATP is mediated by ceramide or its possible metabolism to sphingosine or sphingosine 1-phosphate, as ATP does not cause ceramide accumulation in the acini.	transcription
59503	2	335943	5	NULL	NULL	0	NULL	ceramide	Chemical		does not mediate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_345	12177168	Our results indicate that it is unlikely that PLD activation by ATP is mediated by ceramide or its possible metabolism to sphingosine or sphingosine 1-phosphate, as ATP does not cause ceramide accumulation in the acini.	transcription
59504	3	335943	5	NULL	NULL	0	NULL	ceramide	Chemical		metabolized to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_345	12177168	Our results indicate that it is unlikely that PLD activation by ATP is mediated by ceramide or its possible metabolism to sphingosine or sphingosine 1-phosphate, as ATP does not cause ceramide accumulation in the acini.	transcription
59505	4	335943	5	NULL	NULL	0	NULL	statement 3	Process		does not mediate					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_345	12177168	Our results indicate that it is unlikely that PLD activation by ATP is mediated by ceramide or its possible metabolism to sphingosine or sphingosine 1-phosphate, as ATP does not cause ceramide accumulation in the acini.	transcription
59506	5	335943	5	NULL	NULL	0	NULL	ceramide	Chemical		metabolized to					sphingosine 1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_345	12177168	Our results indicate that it is unlikely that PLD activation by ATP is mediated by ceramide or its possible metabolism to sphingosine or sphingosine 1-phosphate, as ATP does not cause ceramide accumulation in the acini.	transcription
59507	6	335943	5	NULL	NULL	0	NULL	statement 5	Process		does not mediate					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_345	12177168	Our results indicate that it is unlikely that PLD activation by ATP is mediated by ceramide or its possible metabolism to sphingosine or sphingosine 1-phosphate, as ATP does not cause ceramide accumulation in the acini.	transcription
59508	7	335943	5	NULL	NULL	0	NULL	ATP	Chemical		does not cause					ceramide	Chemical	accumulation of			NULL	acini	NULL	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_345	12177168	Our results indicate that it is unlikely that PLD activation by ATP is mediated by ceramide or its possible metabolism to sphingosine or sphingosine 1-phosphate, as ATP does not cause ceramide accumulation in the acini.	transcription
79314	1	335943	6	NULL	NULL	0	NULL	ATP	Chemical		activates					PLD	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_345	12177168	Our results indicate that it is unlikely that PLD activation by ATP is mediated by ceramide or its possible metabolism to sphingosine or sphingosine 1-phosphate, as ATP does not cause ceramide accumulation in the acini.	transcription
79315	2	335943	6	NULL	NULL	0	NULL	ATP	Chemical		does not cause					ceramide	Chemical	accumulation of 			NULL	acini	0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_345	12177168	Our results indicate that it is unlikely that PLD activation by ATP is mediated by ceramide or its possible metabolism to sphingosine or sphingosine 1-phosphate, as ATP does not cause ceramide accumulation in the acini.	transcription
59509	1	335944	5	NULL	NULL	0	NULL	TNF-alpha	GP		signals					cell death	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_30_27879_s_2	15946935	umor necrosis factor (TNF)-alpha signals cell death and simultaneously induces the generation of ceramide, which is metabolized to sphingosine and sphingosine 1-phosphate (S1P) by ceramidase (CDase) and sphingosine kinase.	transcription
59510	2	335944	5	NULL	NULL	0	NULL	TNF	GP		is					tumor necrosis factor	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_30_27879_s_2	15946935	umor necrosis factor (TNF)-alpha signals cell death and simultaneously induces the generation of ceramide, which is metabolized to sphingosine and sphingosine 1-phosphate (S1P) by ceramidase (CDase) and sphingosine kinase.	transcription
59511	3	335944	5	NULL	NULL	0	NULL	TNF-alpha	GP		induce					ceramide	Chemical	generation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_30_27879_s_2	15946935	umor necrosis factor (TNF)-alpha signals cell death and simultaneously induces the generation of ceramide, which is metabolized to sphingosine and sphingosine 1-phosphate (S1P) by ceramidase (CDase) and sphingosine kinase.	transcription
59512	4	335944	5	NULL	NULL	0	NULL	statement 1	Process		occurs simultaneously with					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_30_27879_s_2	15946935	umor necrosis factor (TNF)-alpha signals cell death and simultaneously induces the generation of ceramide, which is metabolized to sphingosine and sphingosine 1-phosphate (S1P) by ceramidase (CDase) and sphingosine kinase.	transcription
59513	5	335944	5	NULL	NULL	0	NULL	ceramide	Chemical		metabolized to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_30_27879_s_2	15946935	umor necrosis factor (TNF)-alpha signals cell death and simultaneously induces the generation of ceramide, which is metabolized to sphingosine and sphingosine 1-phosphate (S1P) by ceramidase (CDase) and sphingosine kinase.	transcription
59514	6	335944	5	NULL	NULL	0	NULL	ceramidase	GP		catalyzes					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_30_27879_s_2	15946935	umor necrosis factor (TNF)-alpha signals cell death and simultaneously induces the generation of ceramide, which is metabolized to sphingosine and sphingosine 1-phosphate (S1P) by ceramidase (CDase) and sphingosine kinase.	transcription
59515	7	335944	5	NULL	NULL	0	NULL	ceramide	Chemical		metabolized to					sphingosine 1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_30_27879_s_2	15946935	umor necrosis factor (TNF)-alpha signals cell death and simultaneously induces the generation of ceramide, which is metabolized to sphingosine and sphingosine 1-phosphate (S1P) by ceramidase (CDase) and sphingosine kinase.	transcription
59516	8	335944	5	NULL	NULL	0	NULL	sphingosine kinase	GP		catalyzes					statement 7	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_30_27879_s_2	15946935	umor necrosis factor (TNF)-alpha signals cell death and simultaneously induces the generation of ceramide, which is metabolized to sphingosine and sphingosine 1-phosphate (S1P) by ceramidase (CDase) and sphingosine kinase.	transcription
59517	9	335944	5	NULL	NULL	0	NULL	S1P	Chemical		is					sphingosine 1-phosphate	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_30_27879_s_2	15946935	umor necrosis factor (TNF)-alpha signals cell death and simultaneously induces the generation of ceramide, which is metabolized to sphingosine and sphingosine 1-phosphate (S1P) by ceramidase (CDase) and sphingosine kinase.	transcription
59518	10	335944	5	NULL	NULL	0	NULL	CDase	GP		is					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_30_27879_s_2	15946935	umor necrosis factor (TNF)-alpha signals cell death and simultaneously induces the generation of ceramide, which is metabolized to sphingosine and sphingosine 1-phosphate (S1P) by ceramidase (CDase) and sphingosine kinase.	transcription
59519	1	335945	5	NULL	NULL	0	NULL	protein kinase C	GP	activation of	activates					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_289	10747891	Interestingly, activation of protein kinase C can lead to the activation of sphingosine kinase ( 91), the enzyme responsible for the conversion of sphingosine into sphingosine 1-phosphate, a sphingolipid metabolite known to antagonize ceramide-mediated apoptosis ( 35,  37,  91-93).	transcription
59520	2	335945	5	NULL	NULL	0	NULL	sphingosine	Chemical		is converted to					sphingosine 1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_289	10747891	Interestingly, activation of protein kinase C can lead to the activation of sphingosine kinase ( 91), the enzyme responsible for the conversion of sphingosine into sphingosine 1-phosphate, a sphingolipid metabolite known to antagonize ceramide-mediated apoptosis ( 35,  37,  91-93).	transcription
59521	3	335945	5	NULL	NULL	0	NULL	sphingosine kinase	GP		catalyzes					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_289	10747891	Interestingly, activation of protein kinase C can lead to the activation of sphingosine kinase ( 91), the enzyme responsible for the conversion of sphingosine into sphingosine 1-phosphate, a sphingolipid metabolite known to antagonize ceramide-mediated apoptosis ( 35,  37,  91-93).	transcription
59522	4	335945	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		is a metabolite of					sphingolipid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_289	10747891	Interestingly, activation of protein kinase C can lead to the activation of sphingosine kinase ( 91), the enzyme responsible for the conversion of sphingosine into sphingosine 1-phosphate, a sphingolipid metabolite known to antagonize ceramide-mediated apoptosis ( 35,  37,  91-93).	transcription
59523	5	335945	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_289	10747891	Interestingly, activation of protein kinase C can lead to the activation of sphingosine kinase ( 91), the enzyme responsible for the conversion of sphingosine into sphingosine 1-phosphate, a sphingolipid metabolite known to antagonize ceramide-mediated apoptosis ( 35,  37,  91-93).	transcription
59524	6	335945	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		antagonize					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_289	10747891	Interestingly, activation of protein kinase C can lead to the activation of sphingosine kinase ( 91), the enzyme responsible for the conversion of sphingosine into sphingosine 1-phosphate, a sphingolipid metabolite known to antagonize ceramide-mediated apoptosis ( 35,  37,  91-93).	transcription
79311	1	335945	6	NULL	NULL	0	NULL	protein kinase C	GP	activation of	activates					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_289	10747891	Interestingly, activation of protein kinase C can lead to the activation of sphingosine kinase ( 91), the enzyme responsible for the conversion of sphingosine into sphingosine 1-phosphate, a sphingolipid metabolite known to antagonize ceramide-mediated apoptosis ( 35,  37,  91-93).	transcription
79312	2	335945	6	NULL	NULL	0	NULL	sphingosine	GP		is converted to					sphingosine 1-phosphate	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_289	10747891	Interestingly, activation of protein kinase C can lead to the activation of sphingosine kinase ( 91), the enzyme responsible for the conversion of sphingosine into sphingosine 1-phosphate, a sphingolipid metabolite known to antagonize ceramide-mediated apoptosis ( 35,  37,  91-93).	transcription
79313	3	335945	6	NULL	NULL	0	NULL	sphingosine kinase	GP		catalyzes					statement 2					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_289	10747891	Interestingly, activation of protein kinase C can lead to the activation of sphingosine kinase ( 91), the enzyme responsible for the conversion of sphingosine into sphingosine 1-phosphate, a sphingolipid metabolite known to antagonize ceramide-mediated apoptosis ( 35,  37,  91-93).	transcription
59525	1	335946	5	NULL	NULL	0	NULL	fumonisin B	GP		is an inhibitor of					N-acyltransferase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_22_13541_s_123	7768956	Futhermore, in support  of ceramide as the mediator, the sphingosine  N-acyltransferase  inhibitor fumonisin B   inhibited sphingosine acylation and  blocked sphingosine-induced GVBD without affecting progesterone-induced  GVBD.	transcription
59526	2	335946	5	NULL	NULL	0	NULL	fumonisin B	GP		inhibits					sphingosine	Chemical	acylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_22_13541_s_123	7768956	Futhermore, in support  of ceramide as the mediator, the sphingosine  N-acyltransferase  inhibitor fumonisin B   inhibited sphingosine acylation and  blocked sphingosine-induced GVBD without affecting progesterone-induced  GVBD.	transcription
59527	3	335946	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					GVBD	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_22_13541_s_123	7768956	Futhermore, in support  of ceramide as the mediator, the sphingosine  N-acyltransferase  inhibitor fumonisin B   inhibited sphingosine acylation and  blocked sphingosine-induced GVBD without affecting progesterone-induced  GVBD.	transcription
59528	4	335946	5	NULL	NULL	0	NULL	fumonisin B	GP		blocks					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_22_13541_s_123	7768956	Futhermore, in support  of ceramide as the mediator, the sphingosine  N-acyltransferase  inhibitor fumonisin B   inhibited sphingosine acylation and  blocked sphingosine-induced GVBD without affecting progesterone-induced  GVBD.	transcription
59529	5	335946	5	NULL	NULL	0	NULL	progesterone	GP		induce					GVBD	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_22_13541_s_123	7768956	Futhermore, in support  of ceramide as the mediator, the sphingosine  N-acyltransferase  inhibitor fumonisin B   inhibited sphingosine acylation and  blocked sphingosine-induced GVBD without affecting progesterone-induced  GVBD.	transcription
59530	6	335946	5	NULL	NULL	0	NULL	statement 4	Process		does not affect					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_22_13541_s_123	7768956	Futhermore, in support  of ceramide as the mediator, the sphingosine  N-acyltransferase  inhibitor fumonisin B   inhibited sphingosine acylation and  blocked sphingosine-induced GVBD without affecting progesterone-induced  GVBD.	transcription
79306	1	335946	6	NULL	NULL	0	NULL	sphingosine N-acyltransferase inhibitor	GP		inhibits					sphingosine	Chemical	acylation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_22_13541_s_123	7768956	Futhermore, in support  of ceramide as the mediator, the sphingosine  N-acyltransferase  inhibitor fumonisin B   inhibited sphingosine acylation and  blocked sphingosine-induced GVBD without affecting progesterone-induced  GVBD.	transcription
79307	2	335946	6	NULL	NULL	0	NULL	sphingosine	Chemical		induces					GVBD	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_22_13541_s_123	7768956	Futhermore, in support  of ceramide as the mediator, the sphingosine  N-acyltransferase  inhibitor fumonisin B   inhibited sphingosine acylation and  blocked sphingosine-induced GVBD without affecting progesterone-induced  GVBD.	transcription
79308	3	335946	6	NULL	NULL	0	NULL	progesterone	GP		induces					GVBD	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_22_13541_s_123	7768956	Futhermore, in support  of ceramide as the mediator, the sphingosine  N-acyltransferase  inhibitor fumonisin B   inhibited sphingosine acylation and  blocked sphingosine-induced GVBD without affecting progesterone-induced  GVBD.	transcription
79309	4	335946	6	NULL	NULL	0	NULL	fumonisin B	Chemical		inhibits					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_22_13541_s_123	7768956	Futhermore, in support  of ceramide as the mediator, the sphingosine  N-acyltransferase  inhibitor fumonisin B   inhibited sphingosine acylation and  blocked sphingosine-induced GVBD without affecting progesterone-induced  GVBD.	transcription
79310	5	335946	6	NULL	NULL	0	NULL	fumonisin B	Chemical		is a type of					sphingosine N-acyltransferase inhibitor	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_22_13541_s_123	7768956	Futhermore, in support  of ceramide as the mediator, the sphingosine  N-acyltransferase  inhibitor fumonisin B   inhibited sphingosine acylation and  blocked sphingosine-induced GVBD without affecting progesterone-induced  GVBD.	transcription
59531	1	335947	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					SMC	Cell	proliferation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_31_21533_s_183	10419457	Last, sphingosine-induced SMC proliferation was not blocked by FB1 (155  plus-or-minus  7%) (data not shown), indicating that re-acylation of sphingosine to ceramide is not required for the effect of sphingosine.	transcription
59532	2	335947	5	NULL	NULL	0	NULL	FB1	GP		does not block					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_31_21533_s_183	10419457	Last, sphingosine-induced SMC proliferation was not blocked by FB1 (155  plus-or-minus  7%) (data not shown), indicating that re-acylation of sphingosine to ceramide is not required for the effect of sphingosine.	transcription
59533	3	335947	5	NULL	NULL	0	NULL	sphingosine	Chemical		is re-acylated to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_31_21533_s_183	10419457	Last, sphingosine-induced SMC proliferation was not blocked by FB1 (155  plus-or-minus  7%) (data not shown), indicating that re-acylation of sphingosine to ceramide is not required for the effect of sphingosine.	transcription
59534	4	335947	5	NULL	NULL	0	NULL	statement 3	Process		is not required for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_31_21533_s_183	10419457	Last, sphingosine-induced SMC proliferation was not blocked by FB1 (155  plus-or-minus  7%) (data not shown), indicating that re-acylation of sphingosine to ceramide is not required for the effect of sphingosine.	transcription
79304	1	335947	6	NULL	NULL	0	NULL	sphingosine	Chemical		induces					SMC	cell	proliferation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_31_21533_s_183	10419457	Last, sphingosine-induced SMC proliferation was not blocked by FB1 (155  plus-or-minus  7%) (data not shown), indicating that re-acylation of sphingosine to ceramide is not required for the effect of sphingosine.	transcription
79305	2	335947	6	NULL	NULL	0	NULL	statement 1	Process		is not blocked by					FB1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_31_21533_s_183	10419457	Last, sphingosine-induced SMC proliferation was not blocked by FB1 (155  plus-or-minus  7%) (data not shown), indicating that re-acylation of sphingosine to ceramide is not required for the effect of sphingosine.	transcription
59535	1	335948	5	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_28_26577_s_316	11356846	It has been shown that both ceramide and its intermediate breakdown product sphingosine induce apoptosis or growth suppression of many cancerous cell lines ( 36-38), whereas its subsequent product sphingosine-1-P has a proliferative effect on fibroblast or endothelial cells ( 39).	transcription
59536	2	335948	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_28_26577_s_316	11356846	It has been shown that both ceramide and its intermediate breakdown product sphingosine induce apoptosis or growth suppression of many cancerous cell lines ( 36-38), whereas its subsequent product sphingosine-1-P has a proliferative effect on fibroblast or endothelial cells ( 39).	transcription
59537	3	335948	5	NULL	NULL	0	NULL	ceramide	Chemical		suppress					cancerous cell lines	Cell	growth of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_28_26577_s_316	11356846	It has been shown that both ceramide and its intermediate breakdown product sphingosine induce apoptosis or growth suppression of many cancerous cell lines ( 36-38), whereas its subsequent product sphingosine-1-P has a proliferative effect on fibroblast or endothelial cells ( 39).	transcription
59538	4	335948	5	NULL	NULL	0	NULL	sphingosine	Chemical		suppress					cancerous cell lines	Cell	growth of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_28_26577_s_316	11356846	It has been shown that both ceramide and its intermediate breakdown product sphingosine induce apoptosis or growth suppression of many cancerous cell lines ( 36-38), whereas its subsequent product sphingosine-1-P has a proliferative effect on fibroblast or endothelial cells ( 39).	transcription
59539	5	335948	5	NULL	NULL	0	NULL	sphingosine	Chemical		is a breakdown product of		intermediate			ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_28_26577_s_316	11356846	It has been shown that both ceramide and its intermediate breakdown product sphingosine induce apoptosis or growth suppression of many cancerous cell lines ( 36-38), whereas its subsequent product sphingosine-1-P has a proliferative effect on fibroblast or endothelial cells ( 39).	transcription
59540	6	335948	5	NULL	NULL	0	NULL	sphingosine-1-P	Chemical		proliferates					fibroblast	Cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_28_26577_s_316	11356846	It has been shown that both ceramide and its intermediate breakdown product sphingosine induce apoptosis or growth suppression of many cancerous cell lines ( 36-38), whereas its subsequent product sphingosine-1-P has a proliferative effect on fibroblast or endothelial cells ( 39).	transcription
59541	7	335948	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		proliferates					endothelial cells	Cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_28_26577_s_316	11356846	It has been shown that both ceramide and its intermediate breakdown product sphingosine induce apoptosis or growth suppression of many cancerous cell lines ( 36-38), whereas its subsequent product sphingosine-1-P has a proliferative effect on fibroblast or endothelial cells ( 39).	transcription
79300	1	335948	6	NULL	NULL	0	NULL	ceramide	Chemical		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_28_26577_s_316	11356846	It has been shown that both ceramide and its intermediate breakdown product sphingosine induce apoptosis or growth suppression of many cancerous cell lines ( 36-38), whereas its subsequent product sphingosine-1-P has a proliferative effect on fibroblast or endothelial cells ( 39).	transcription
79301	2	335948	6	NULL	NULL	0	NULL	sphingosine	Chemical		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_28_26577_s_316	11356846	It has been shown that both ceramide and its intermediate breakdown product sphingosine induce apoptosis or growth suppression of many cancerous cell lines ( 36-38), whereas its subsequent product sphingosine-1-P has a proliferative effect on fibroblast or endothelial cells ( 39).	transcription
79302	3	335948	6	NULL	NULL	0	NULL	sphingosine-1-P	GP		proliferates					fibroblast cells	cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_28_26577_s_316	11356846	It has been shown that both ceramide and its intermediate breakdown product sphingosine induce apoptosis or growth suppression of many cancerous cell lines ( 36-38), whereas its subsequent product sphingosine-1-P has a proliferative effect on fibroblast or endothelial cells ( 39).	transcription
79303	4	335948	6	NULL	NULL	0	NULL	sphingosine-1 phosphate	GP		proliferates					endothelial cells	Cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_28_26577_s_316	11356846	It has been shown that both ceramide and its intermediate breakdown product sphingosine induce apoptosis or growth suppression of many cancerous cell lines ( 36-38), whereas its subsequent product sphingosine-1-P has a proliferative effect on fibroblast or endothelial cells ( 39).	transcription
59542	1	335949	5	NULL	NULL	0	NULL	S1P	Chemical		regulates					cellular growth	Process				NULL		0	NULL	NULL	NULL	gw70_biolreprod_70_3_759_s_24	14613902	In contrast with the growth-inhibitory and proapoptotic actions of ceramide and sphingosine, S1P regulates diverse processes such as cellular growth, inhibition of ceramide-mediated apoptosis, and cell migration [ ].	transcription
59543	2	335949	5	NULL	NULL	0	NULL	ceramide	Chemical		mediates					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_biolreprod_70_3_759_s_24	14613902	In contrast with the growth-inhibitory and proapoptotic actions of ceramide and sphingosine, S1P regulates diverse processes such as cellular growth, inhibition of ceramide-mediated apoptosis, and cell migration [ ].	transcription
59544	3	335949	5	NULL	NULL	0	NULL	S1P	Chemical		regulates					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_biolreprod_70_3_759_s_24	14613902	In contrast with the growth-inhibitory and proapoptotic actions of ceramide and sphingosine, S1P regulates diverse processes such as cellular growth, inhibition of ceramide-mediated apoptosis, and cell migration [ ].	transcription
59545	4	335949	5	NULL	NULL	0	NULL	S1P	Chemical		regulates					cell migration	Process				NULL		0	NULL	NULL	NULL	gw70_biolreprod_70_3_759_s_24	14613902	In contrast with the growth-inhibitory and proapoptotic actions of ceramide and sphingosine, S1P regulates diverse processes such as cellular growth, inhibition of ceramide-mediated apoptosis, and cell migration [ ].	transcription
79296	1	335949	6	NULL	NULL	0	NULL	S1p	GP		regulates					cell growth	Process				NULL		0	NULL	NULL	NULL	gw70_biolreprod_70_3_759_s_24	14613902	In contrast with the growth-inhibitory and proapoptotic actions of ceramide and sphingosine, S1P regulates diverse processes such as cellular growth, inhibition of ceramide-mediated apoptosis, and cell migration [ ].	transcription
79297	2	335949	6	NULL	NULL	0	NULL	S1P	GP		regulates					cell migration	Process				NULL		0	NULL	NULL	NULL	gw70_biolreprod_70_3_759_s_24	14613902	In contrast with the growth-inhibitory and proapoptotic actions of ceramide and sphingosine, S1P regulates diverse processes such as cellular growth, inhibition of ceramide-mediated apoptosis, and cell migration [ ].	transcription
79298	3	335949	6	NULL	NULL	0	NULL	ceramide	Chemical		mediates					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_biolreprod_70_3_759_s_24	14613902	In contrast with the growth-inhibitory and proapoptotic actions of ceramide and sphingosine, S1P regulates diverse processes such as cellular growth, inhibition of ceramide-mediated apoptosis, and cell migration [ ].	transcription
79299	4	335949	6	NULL	NULL	0	NULL	S1P	GP		regulates					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_biolreprod_70_3_759_s_24	14613902	In contrast with the growth-inhibitory and proapoptotic actions of ceramide and sphingosine, S1P regulates diverse processes such as cellular growth, inhibition of ceramide-mediated apoptosis, and cell migration [ ].	transcription
59546	1	335950	5	NULL	NULL	0	NULL	ceramide	Chemical		induce					cell death	Process				NULL	sensory neurons	0	NULL	NULL	NULL	gw70_neuropharmacology_45_8_1130_s_998	14614956	S.E. Ping and G.L. Barrett, Ceramide can induce cell death in sensory neurons, whereas  ceramide analogues and sphingosine promote survival.	transcription
59547	2	335950	5	NULL	NULL	0	NULL	ceramide analogues	Chemical		promotes					cell survival	Process				NULL	sensory neurons	0	NULL	NULL	NULL	gw70_neuropharmacology_45_8_1130_s_998	14614956	S.E. Ping and G.L. Barrett, Ceramide can induce cell death in sensory neurons, whereas  ceramide analogues and sphingosine promote survival.	transcription
59548	3	335950	5	NULL	NULL	0	NULL	sphingosine	Chemical		promotes					cell survival	Process				NULL	sensory neurons	0	NULL	NULL	NULL	gw70_neuropharmacology_45_8_1130_s_998	14614956	S.E. Ping and G.L. Barrett, Ceramide can induce cell death in sensory neurons, whereas  ceramide analogues and sphingosine promote survival.	transcription
79294	1	335950	6	NULL	NULL	0	NULL	ceramide	Chemical		induces					cell death	Process				NULL	sensory neurons	0	NULL	NULL	NULL	gw70_neuropharmacology_45_8_1130_s_998	14614956	S.E. Ping and G.L. Barrett, Ceramide can induce cell death in sensory neurons, whereas  ceramide analogues and sphingosine promote survival.	transcription
79295	2	335950	6	NULL	NULL	0	NULL	sphingosine	Chemical		promotes					cell survival	Process				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_8_1130_s_998	14614956	S.E. Ping and G.L. Barrett, Ceramide can induce cell death in sensory neurons, whereas  ceramide analogues and sphingosine promote survival.	transcription
59549	1	335951	5	NULL	NULL	0	NULL	ceramide	Chemical	natural	induce					c-jun	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_75	12135749	Because the time-course of c-jun induction by natural ceramide was much slower than that by sphingosine or C2-ceramide, natural ceramide was not used in the experiments described below.	transcription
59550	2	335951	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					c-jun	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_75	12135749	Because the time-course of c-jun induction by natural ceramide was much slower than that by sphingosine or C2-ceramide, natural ceramide was not used in the experiments described below.	transcription
59551	3	335951	5	NULL	NULL	0	NULL	C2-ceramide	Chemical		induce					c-jun	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_75	12135749	Because the time-course of c-jun induction by natural ceramide was much slower than that by sphingosine or C2-ceramide, natural ceramide was not used in the experiments described below.	transcription
59552	4	335951	5	NULL	NULL	0	NULL	statement 1	Process		slower than					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_75	12135749	Because the time-course of c-jun induction by natural ceramide was much slower than that by sphingosine or C2-ceramide, natural ceramide was not used in the experiments described below.	transcription
59553	5	335951	5	NULL	NULL	0	NULL	statement 1	Process		slower than					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_75	12135749	Because the time-course of c-jun induction by natural ceramide was much slower than that by sphingosine or C2-ceramide, natural ceramide was not used in the experiments described below.	transcription
59554	1	335952	5	NULL	NULL	0	NULL	ceramide	Chemical		stimulates					epidermal growth factor receptor	GP	phosphorylation of			NULL	A431 cells	0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_476	9415703	Ceramide stimulates epidermal growth factor receptor phosphorylation in A431 human epidermoid carcinoma cells: evidence that ceramide may mediate sphingosine action.	transcription
59555	2	335952	5	NULL	NULL	0	NULL	A431 cells	Cell		is					human epidermoid carcinoma cells	Cell				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_476	9415703	Ceramide stimulates epidermal growth factor receptor phosphorylation in A431 human epidermoid carcinoma cells: evidence that ceramide may mediate sphingosine action.	transcription
59556	3	335952	5	NULL	NULL	0	NULL	ceramide	Chemical		mediates		may			sphingosine	Chemical	action of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_476	9415703	Ceramide stimulates epidermal growth factor receptor phosphorylation in A431 human epidermoid carcinoma cells: evidence that ceramide may mediate sphingosine action.	transcription
79292	1	335952	6	NULL	NULL	0	NULL	ceramide	Chemical		stimulates					epidermal growth factor receptor	GP	phosphorylation of			NULL	A431 human epidermoid carcinoma cells	0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_476	9415703	Ceramide stimulates epidermal growth factor receptor phosphorylation in A431 human epidermoid carcinoma cells: evidence that ceramide may mediate sphingosine action.	transcription
79293	2	335952	6	NULL	NULL	0	NULL	ceramide	Chemical		mediates					sphingosine	Chemical	action of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_476	9415703	Ceramide stimulates epidermal growth factor receptor phosphorylation in A431 human epidermoid carcinoma cells: evidence that ceramide may mediate sphingosine action.	transcription
59557	1	335953	5	NULL	NULL	0	NULL	ceramide	Chemical		is a type of					sphingolipid	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_27129_s_188	11369765	To determine whether sphingolipids such as ceramide and sphingosine could affect the accumulation of p53, LM cells were treated with ceramide, and their cellular p53 protein levels were measured.	transcription
59558	2	335953	5	NULL	NULL	0	NULL	sphingosine	Chemical		is a type of					sphingolipid	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_27129_s_188	11369765	To determine whether sphingolipids such as ceramide and sphingosine could affect the accumulation of p53, LM cells were treated with ceramide, and their cellular p53 protein levels were measured.	transcription
59559	3	335953	5	NULL	NULL	0	NULL	ceramide	Chemical		affects		may			p53	GP	accumulation of			NULL	LM cells	0	NULL	NULL	NULL	gw60_jbiolchem_276_29_27129_s_188	11369765	To determine whether sphingolipids such as ceramide and sphingosine could affect the accumulation of p53, LM cells were treated with ceramide, and their cellular p53 protein levels were measured.	transcription
59560	4	335953	5	NULL	NULL	0	NULL	sphingosine	Chemical		affects		may			p53	GP	accumulation of			NULL	LM cells	0	NULL	NULL	NULL	gw60_jbiolchem_276_29_27129_s_188	11369765	To determine whether sphingolipids such as ceramide and sphingosine could affect the accumulation of p53, LM cells were treated with ceramide, and their cellular p53 protein levels were measured.	transcription
59561	1	335954	5	NULL	NULL	0	NULL	ceramide	Chemical		is an inhibitor of		potent			PLD	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_344	12177168	Although ceramides are potent inhibitors of PLD activity in a variety of cell types ( 13,  14,  18,  26,  28,  30 -  33), in human fibroblasts, ceramides or sphingosine can activate PLD ( 34).	transcription
59562	2	335954	5	NULL	NULL	0	NULL	ceramide	Chemical		activates					PLD	GP				NULL	human fibroblasts	0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_344	12177168	Although ceramides are potent inhibitors of PLD activity in a variety of cell types ( 13,  14,  18,  26,  28,  30 -  33), in human fibroblasts, ceramides or sphingosine can activate PLD ( 34).	transcription
59563	3	335954	5	NULL	NULL	0	NULL	sphingosine	Chemical		activates					PLD	GP				NULL	human fibroblasts	0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_344	12177168	Although ceramides are potent inhibitors of PLD activity in a variety of cell types ( 13,  14,  18,  26,  28,  30 -  33), in human fibroblasts, ceramides or sphingosine can activate PLD ( 34).	transcription
59564	4	335954	5	NULL	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_344	12177168	Although ceramides are potent inhibitors of PLD activity in a variety of cell types ( 13,  14,  18,  26,  28,  30 -  33), in human fibroblasts, ceramides or sphingosine can activate PLD ( 34).	transcription
79291	1	335954	6	NULL	NULL	0	NULL	ceramide	Chemical		inhibits					PLD activity	Process				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_8_1244_s_344	12177168	Although ceramides are potent inhibitors of PLD activity in a variety of cell types ( 13,  14,  18,  26,  28,  30 -  33), in human fibroblasts, ceramides or sphingosine can activate PLD ( 34).	transcription
59565	1	335955	5	NULL	NULL	0	NULL	ceramide	Chemical		mediates					programmed cell death	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_54_1_70_s_247	9658191	Cuvillier O, Pirianov G, Kleuser B, Vanek PG, Coso OA, Gutkind S and Spiegel S (1996) Suppression of ceramide-mediated programmed cell death by sphingosine-1 phosphate.	transcription
59566	2	335955	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		suppress					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_54_1_70_s_247	9658191	Cuvillier O, Pirianov G, Kleuser B, Vanek PG, Coso OA, Gutkind S and Spiegel S (1996) Suppression of ceramide-mediated programmed cell death by sphingosine-1 phosphate.	transcription
79289	1	335955	6	NULL	NULL	0	NULL	ceramide	Chemical		mediates					programmed cell death	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_54_1_70_s_247	9658191	Cuvillier O, Pirianov G, Kleuser B, Vanek PG, Coso OA, Gutkind S and Spiegel S (1996) Suppression of ceramide-mediated programmed cell death by sphingosine-1 phosphate.	transcription
79290	2	335955	6	NULL	NULL	0	NULL	sphingosine-1 phosphate	GP		suppresses					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_54_1_70_s_247	9658191	Cuvillier O, Pirianov G, Kleuser B, Vanek PG, Coso OA, Gutkind S and Spiegel S (1996) Suppression of ceramide-mediated programmed cell death by sphingosine-1 phosphate.	transcription
59567	1	335956	5	NULL	NULL	0	NULL	JNK	GP		is activated by					TNF	GP				NULL		0	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_427_s_259	11378302	Other studies have confirmed the activation of JNK by TNF- , as well as by ceramide,  sphingosine and sphingomyelinase (  Fig. 2).	transcription
59568	2	335956	5	NULL	NULL	0	NULL	JNK	GP		is activated by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_427_s_259	11378302	Other studies have confirmed the activation of JNK by TNF- , as well as by ceramide,  sphingosine and sphingomyelinase (  Fig. 2).	transcription
59569	3	335956	5	NULL	NULL	0	NULL	JNK	GP		is activated by					sphingosine	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_427_s_259	11378302	Other studies have confirmed the activation of JNK by TNF- , as well as by ceramide,  sphingosine and sphingomyelinase (  Fig. 2).	transcription
59570	4	335956	5	NULL	NULL	0	NULL	JNK	GP		is activated by					sphingomyelinase	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_427_s_259	11378302	Other studies have confirmed the activation of JNK by TNF- , as well as by ceramide,  sphingosine and sphingomyelinase (  Fig. 2).	transcription
79285	1	335956	6	NULL	NULL	0	NULL	TNF	GP		activates					JNK	GP				NULL		0	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_427_s_259	11378302	Other studies have confirmed the activation of JNK by TNF- , as well as by ceramide,  sphingosine and sphingomyelinase (  Fig. 2).	transcription
79286	2	335956	6	NULL	NULL	0	NULL	ceramide	Chemical		activates					JNK	GP				NULL		0	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_427_s_259	11378302	Other studies have confirmed the activation of JNK by TNF- , as well as by ceramide,  sphingosine and sphingomyelinase (  Fig. 2).	transcription
79287	3	335956	6	NULL	NULL	0	NULL	sphingosine	Chemical		activates					JNK	GP				NULL		0	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_427_s_259	11378302	Other studies have confirmed the activation of JNK by TNF- , as well as by ceramide,  sphingosine and sphingomyelinase (  Fig. 2).	transcription
79288	4	335956	6	NULL	NULL	0	NULL	sphingomyelinase	GP		activates					JNK	GP				NULL		0	NULL	NULL	NULL	gw70_intjdevneurosci_19_4_427_s_259	11378302	Other studies have confirmed the activation of JNK by TNF- , as well as by ceramide,  sphingosine and sphingomyelinase (  Fig. 2).	transcription
59571	1	335957	5	NULL	NULL	0	NULL	TNF-alpha	GP		is not induced by					C2 ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_194	16936207	TNF-alpha and IL-6 were not induced by C2 ceramide but were induced by sphingosine and S1P.	transcription
59572	2	335957	5	NULL	NULL	0	NULL	TNF-alpha	GP		is induced by					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_194	16936207	TNF-alpha and IL-6 were not induced by C2 ceramide but were induced by sphingosine and S1P.	transcription
59573	3	335957	5	NULL	NULL	0	NULL	TNF-alpha	GP		is induced by					S1P	Chemical				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_194	16936207	TNF-alpha and IL-6 were not induced by C2 ceramide but were induced by sphingosine and S1P.	transcription
59574	4	335957	5	NULL	NULL	0	NULL	IL-6	GP		is not induced by					C2 ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_194	16936207	TNF-alpha and IL-6 were not induced by C2 ceramide but were induced by sphingosine and S1P.	transcription
59575	5	335957	5	NULL	NULL	0	NULL	IL-6	GP		is induced by					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_194	16936207	TNF-alpha and IL-6 were not induced by C2 ceramide but were induced by sphingosine and S1P.	transcription
59576	6	335957	5	NULL	NULL	0	NULL	IL-6	GP		is induced by					S1P	Chemical				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_194	16936207	TNF-alpha and IL-6 were not induced by C2 ceramide but were induced by sphingosine and S1P.	transcription
59577	1	335959	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					ceramide	Chemical				NULL	tumor cells	0	NULL	NULL	NULL	gw70_biolreprod_71_6_2072_s_159	15317688	Some cancer therapies are based on inhibition of sphingosine-kinase activity to amplify ceramide-mediated apoptosis in tumor cells [ ].	transcription
59578	2	335959	5	NULL	NULL	0	NULL	sphingosine-kinase	GP	inhibition of;;activity of	amplify					statement 1	Process				NULL	tumor cells	0	NULL	NULL	NULL	gw70_biolreprod_71_6_2072_s_159	15317688	Some cancer therapies are based on inhibition of sphingosine-kinase activity to amplify ceramide-mediated apoptosis in tumor cells [ ].	transcription
79277	1	335959	6	NULL	NULL	0	NULL	sphingosine-kinase activity	Process	inhibition of 	amplify					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_biolreprod_71_6_2072_s_159	15317688	Some cancer therapies are based on inhibition of sphingosine-kinase activity to amplify ceramide-mediated apoptosis in tumor cells [ ].	transcription
79278	2	335959	6	NULL	NULL	0	NULL	ceramide	Chemical		mediates					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_biolreprod_71_6_2072_s_159	15317688	Some cancer therapies are based on inhibition of sphingosine-kinase activity to amplify ceramide-mediated apoptosis in tumor cells [ ].	transcription
59579	1	335960	5	NULL	NULL	0	NULL	ASM	GP		is					acidic sphingomyelinase	GP				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_19_0_497_s_217	11244045	The effect requires the expression of acidic sphingomyelinase (ASM), which is activated  by CD95 stimulation to produce ceramide and its metabolite, sphingosine.	transcription
59580	2	335960	5	NULL	NULL	0	NULL	ASM	GP	expression of	is activated by					CD95	GP	stimulation of			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_19_0_497_s_217	11244045	The effect requires the expression of acidic sphingomyelinase (ASM), which is activated  by CD95 stimulation to produce ceramide and its metabolite, sphingosine.	transcription
59581	3	335960	5	NULL	NULL	0	NULL	statement 2	Process		produce					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_19_0_497_s_217	11244045	The effect requires the expression of acidic sphingomyelinase (ASM), which is activated  by CD95 stimulation to produce ceramide and its metabolite, sphingosine.	transcription
59582	4	335960	5	NULL	NULL	0	NULL	statement 2	Process		produce					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_19_0_497_s_217	11244045	The effect requires the expression of acidic sphingomyelinase (ASM), which is activated  by CD95 stimulation to produce ceramide and its metabolite, sphingosine.	transcription
59583	5	335960	5	NULL	NULL	0	NULL	sphingosine	Chemical		is a metabolite of					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_19_0_497_s_217	11244045	The effect requires the expression of acidic sphingomyelinase (ASM), which is activated  by CD95 stimulation to produce ceramide and its metabolite, sphingosine.	transcription
79273	1	335960	6	NULL	NULL	0	NULL	ASM	Chemical		is					acidic sphingomyelinase	Chemical				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_19_0_497_s_217	11244045	The effect requires the expression of acidic sphingomyelinase (ASM), which is activated  by CD95 stimulation to produce ceramide and its metabolite, sphingosine.	transcription
79274	2	335960	6	NULL	NULL	0	NULL	CD95	GP	stimulation of 	produces					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_19_0_497_s_217	11244045	The effect requires the expression of acidic sphingomyelinase (ASM), which is activated  by CD95 stimulation to produce ceramide and its metabolite, sphingosine.	transcription
79275	3	335960	6	NULL	NULL	0	NULL	CD95	GP	stimulation of 	produces					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_19_0_497_s_217	11244045	The effect requires the expression of acidic sphingomyelinase (ASM), which is activated  by CD95 stimulation to produce ceramide and its metabolite, sphingosine.	transcription
79276	4	335960	6	NULL	NULL	0	NULL	CD95	GP		activates					ASM	Chemical				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_19_0_497_s_217	11244045	The effect requires the expression of acidic sphingomyelinase (ASM), which is activated  by CD95 stimulation to produce ceramide and its metabolite, sphingosine.	transcription
59584	1	335961	5	NULL	NULL	0	NULL	sphingosine	Chemical	addition of	stimulates					ceramide	Chemical	fomation of			NULL		0	NULL	NULL	NULL	gw70_atherosclerosis_167_1_159_s_107	12618281	Conversely the stimulation  of ceramide formation by the addition of sphingosine resulted in increased SRE mediated  transcription.	transcription
59585	2	335961	5	NULL	NULL	0	NULL	transcription	Process		is mediated by					SRE	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_atherosclerosis_167_1_159_s_107	12618281	Conversely the stimulation  of ceramide formation by the addition of sphingosine resulted in increased SRE mediated  transcription.	transcription
59586	3	335961	5	NULL	NULL	0	NULL	statement 1	Process		results in					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_atherosclerosis_167_1_159_s_107	12618281	Conversely the stimulation  of ceramide formation by the addition of sphingosine resulted in increased SRE mediated  transcription.	transcription
79271	1	335961	6	NULL	NULL	0	NULL	SRE	GP		mediates					transcription	Process				NULL		0	NULL	NULL	NULL	gw70_atherosclerosis_167_1_159_s_107	12618281	Conversely the stimulation  of ceramide formation by the addition of sphingosine resulted in increased SRE mediated  transcription.	transcription
79272	2	335961	6	NULL	NULL	0	NULL	ceramide	GP	formation by	results in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_atherosclerosis_167_1_159_s_107	12618281	Conversely the stimulation  of ceramide formation by the addition of sphingosine resulted in increased SRE mediated  transcription.	transcription
59587	1	335962	5	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL	sensory neurons	0	NULL	NULL	NULL	gw70_neuropharmacology_45_8_1130_s_298	14614956	In addition, ceramide induces apoptosis in sensory neurons whereas sphingosine  induces survival ( [ Ping and Barrett, 1998]).	transcription
59588	2	335962	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					cell survival	Process				NULL	sensory neurons	0	NULL	NULL	NULL	gw70_neuropharmacology_45_8_1130_s_298	14614956	In addition, ceramide induces apoptosis in sensory neurons whereas sphingosine  induces survival ( [ Ping and Barrett, 1998]).	transcription
79269	1	335962	6	NULL	NULL	0	NULL	ceramide	Chemical		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_8_1130_s_298	14614956	In addition, ceramide induces apoptosis in sensory neurons whereas sphingosine  induces survival ( [ Ping and Barrett, 1998]).	transcription
79270	2	335962	6	NULL	NULL	0	NULL	sphingosine	Chemical		induces					survival	Process				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_8_1130_s_298	14614956	In addition, ceramide induces apoptosis in sensory neurons whereas sphingosine  induces survival ( [ Ping and Barrett, 1998]).	transcription
59589	1	335963	5	NULL	NULL	0	NULL	ceramide	Chemical	degradation of	increases		slightly			sphingosine	Chemical	level of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_17_7359_s_363	15314148	In our studies, the slight increase in the sphingosine level could also result from ceramide degradation.	transcription
79268	1	335963	6	NULL	NULL	0	NULL	ceramide	Chemical	degradation of 	results in					sphingosine	Chemical	rise of 			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_17_7359_s_363	15314148	In our studies, the slight increase in the sphingosine level could also result from ceramide degradation.	transcription
59590	1	335964	5	NULL	NULL	0	NULL	bFGF	GP		activates					eNOS	GP				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_63_2_297_s_237	12527801	bFGF Activation of eNOS via Ceramide Production Does [[ Not Involve Sphingosine 1-Phosphate  Production ]].	transcription
59591	2	335964	5	NULL	NULL	0	NULL	statement 1	Process		via					ceramide	Chemical	production of			NULL		0	NULL	NULL	NULL	gw70_molpharmacol_63_2_297_s_237	12527801	bFGF Activation of eNOS via Ceramide Production Does [[ Not Involve Sphingosine 1-Phosphate  Production ]].	transcription
59592	3	335964	5	NULL	NULL	0	NULL	statement 2	Process		does not involve					sphingosine 1-phosphate	Chemical	production of			NULL		0	NULL	NULL	NULL	gw70_molpharmacol_63_2_297_s_237	12527801	bFGF Activation of eNOS via Ceramide Production Does [[ Not Involve Sphingosine 1-Phosphate  Production ]].	transcription
79266	1	335964	6	NULL	NULL	0	NULL	bFGF	GP		activates					eNOS	Chemical				NULL		0	NULL	NULL	NULL	gw70_molpharmacol_63_2_297_s_237	12527801	bFGF Activation of eNOS via Ceramide Production Does [[ Not Involve Sphingosine 1-Phosphate  Production ]].	transcription
79267	2	335964	6	NULL	NULL	0	NULL	statement 1	Process		occurs via					ceramide	Chemical	production of 			NULL		0	NULL	NULL	NULL	gw70_molpharmacol_63_2_297_s_237	12527801	bFGF Activation of eNOS via Ceramide Production Does [[ Not Involve Sphingosine 1-Phosphate  Production ]].	transcription
59593	1	335965	5	NULL	NULL	0	NULL	FFAs	Chemical		stimulates					ceramide	Chemical	de novo synthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_10	15774472	Moreover, these FFAs stimulated the  de novo synthesis of ceramide and sphingosine, two sphingolipids shown previously to inhibit insulin action.	transcription
59594	2	335965	5	NULL	NULL	0	NULL	FFAs	Chemical		stimulates					sphingosine	Chemical	de novo synthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_10	15774472	Moreover, these FFAs stimulated the  de novo synthesis of ceramide and sphingosine, two sphingolipids shown previously to inhibit insulin action.	transcription
59595	3	335965	5	NULL	NULL	0	NULL	ceramide	Chemical		is a type of					sphingolipid	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_10	15774472	Moreover, these FFAs stimulated the  de novo synthesis of ceramide and sphingosine, two sphingolipids shown previously to inhibit insulin action.	transcription
59596	4	335965	5	NULL	NULL	0	NULL	sphingosine	Chemical		is a type of					sphingolipid	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_10	15774472	Moreover, these FFAs stimulated the  de novo synthesis of ceramide and sphingosine, two sphingolipids shown previously to inhibit insulin action.	transcription
59597	5	335965	5	NULL	NULL	0	NULL	ceramide	Chemical		inhibit					insulin	GP	action of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_10	15774472	Moreover, these FFAs stimulated the  de novo synthesis of ceramide and sphingosine, two sphingolipids shown previously to inhibit insulin action.	transcription
59598	6	335965	5	NULL	NULL	0	NULL	sphingosine	Chemical		inhibit					insulin	GP	action of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_10	15774472	Moreover, these FFAs stimulated the  de novo synthesis of ceramide and sphingosine, two sphingolipids shown previously to inhibit insulin action.	transcription
79264	1	335965	6	NULL	NULL	0	NULL	FFA	Chemical		stimulates					ceramide	Chemical	de novo synthesis of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_10	15774472	Moreover, these FFAs stimulated the  de novo synthesis of ceramide and sphingosine, two sphingolipids shown previously to inhibit insulin action.	transcription
79265	2	335965	6	NULL	NULL	0	NULL	FFA	Chemical		stimulates					sphingosine	Chemical	de novo synthesis of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_10	15774472	Moreover, these FFAs stimulated the  de novo synthesis of ceramide and sphingosine, two sphingolipids shown previously to inhibit insulin action.	transcription
59599	1	335966	5	NULL	NULL	0	NULL	ceramide	Chemical		is hydrolyzed to					sphingosine	Chemical				NULL	lysosome	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_38	15774472	Acid ceramidase (AC) catalyzes the lysosomal hydrolysis of ceramide to sphingosine and free fatty acid ( ).	transcription
59600	2	335966	5	NULL	NULL	0	NULL	ceramide	Chemical		is hydrolyzed to					fatty acids	Chemical	free			NULL	lysosome	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_38	15774472	Acid ceramidase (AC) catalyzes the lysosomal hydrolysis of ceramide to sphingosine and free fatty acid ( ).	transcription
59601	3	335966	5	NULL	NULL	0	NULL	statement 1	Process		occurs along with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_38	15774472	Acid ceramidase (AC) catalyzes the lysosomal hydrolysis of ceramide to sphingosine and free fatty acid ( ).	transcription
59602	4	335966	5	NULL	NULL	0	NULL	AC	GP		catalyzes					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_38	15774472	Acid ceramidase (AC) catalyzes the lysosomal hydrolysis of ceramide to sphingosine and free fatty acid ( ).	transcription
59603	5	335966	5	NULL	NULL	0	NULL	AC	GP		is					acid ceramidase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_38	15774472	Acid ceramidase (AC) catalyzes the lysosomal hydrolysis of ceramide to sphingosine and free fatty acid ( ).	transcription
79262	1	335966	6	NULL	NULL	0	NULL	ceramide	Chemical		is converted to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_38	15774472	Acid ceramidase (AC) catalyzes the lysosomal hydrolysis of ceramide to sphingosine and free fatty acid ( ).	transcription
79263	2	335966	6	NULL	NULL	0	NULL	Acid ceramidase	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_38	15774472	Acid ceramidase (AC) catalyzes the lysosomal hydrolysis of ceramide to sphingosine and free fatty acid ( ).	transcription
59607	1	335967	5	NULL	NULL	0	NULL	AC	GP	overexpression of	prevents					ceramide	Chemical	accrual of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_40	15774472	As shown herein, overexpressing AC prevented the accrual of ceramide, but not DAG or sphingosine, induced by long-chain saturated FFAs.	transcription
59608	2	335967	5	NULL	NULL	0	NULL	AC	GP	overexpression of	does not prevent					DAG	Chemical	accrual of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_40	15774472	As shown herein, overexpressing AC prevented the accrual of ceramide, but not DAG or sphingosine, induced by long-chain saturated FFAs.	transcription
59609	3	335967	5	NULL	NULL	0	NULL	AC	GP	overexpression of	does not prevent					sphingosine	Chemical	accrual of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_40	15774472	As shown herein, overexpressing AC prevented the accrual of ceramide, but not DAG or sphingosine, induced by long-chain saturated FFAs.	transcription
59610	4	335967	5	NULL	NULL	0	NULL	ceramide	Chemical	accrual of	is induced by					FFAs	Chemical	long-chain;;saturated			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_40	15774472	As shown herein, overexpressing AC prevented the accrual of ceramide, but not DAG or sphingosine, induced by long-chain saturated FFAs.	transcription
59611	5	335967	5	NULL	NULL	0	NULL	DAG	Chemical	accrual of	is induced by					FFAs	Chemical	long-chain;;saturated 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_40	15774472	As shown herein, overexpressing AC prevented the accrual of ceramide, but not DAG or sphingosine, induced by long-chain saturated FFAs.	transcription
59612	6	335967	5	NULL	NULL	0	NULL	sphingosine	Chemical	accrual of	is induced by					FFAs	Chemical	long-chain;;saturated			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_40	15774472	As shown herein, overexpressing AC prevented the accrual of ceramide, but not DAG or sphingosine, induced by long-chain saturated FFAs.	transcription
59613	1	335968	5	NULL	NULL	0	NULL	ceramide	Chemical		is degraded to					sphingosine bases	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_239	15546881	For example, sphingosine levels increase with FB1, ruling out a role for further degradation of ceramide to sphingoid bases.	transcription
59614	2	335968	5	NULL	NULL	0	NULL	sphingosine	Chemical	levels of	increase with					FB1	NucleicAcid	increase in;;levels of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_239	15546881	For example, sphingosine levels increase with FB1, ruling out a role for further degradation of ceramide to sphingoid bases.	transcription
79261	1	335968	6	NULL	NULL	0	NULL	FB1	GP		increase					sphingosine 	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_239	15546881	For example, sphingosine levels increase with FB1, ruling out a role for further degradation of ceramide to sphingoid bases.	transcription
59615	1	335969	5	NULL	NULL	0	NULL	SPL	GP	expression of	regulates					S1P	Chemical	intracellular			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_2_1281_s_273	14570870	First, SPL expression regulates not only intracellular S1P and sphingosine but also appears to increase ceramide generation under stress conditions.	transcription
59616	2	335969	5	NULL	NULL	0	NULL	SPL	GP	expression of	regulates					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_2_1281_s_273	14570870	First, SPL expression regulates not only intracellular S1P and sphingosine but also appears to increase ceramide generation under stress conditions.	transcription
59617	3	335969	5	NULL	NULL	0	NULL	ceramide	Chemical		is generated under					stress condition	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_2_1281_s_273	14570870	First, SPL expression regulates not only intracellular S1P and sphingosine but also appears to increase ceramide generation under stress conditions.	transcription
59618	4	335969	5	NULL	NULL	0	NULL	SPL	GP	expression of	increases					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_2_1281_s_273	14570870	First, SPL expression regulates not only intracellular S1P and sphingosine but also appears to increase ceramide generation under stress conditions.	transcription
78971	1	335969	6	NULL	NULL	0	NULL	SPL	GP	expression of	regulates					S1P	GP	intracellular			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_2_1281_s_273	14570870	First, SPL expression regulates not only intracellular S1P and sphingosine but also appears to increase ceramide generation under stress conditions.	transcription
78972	2	335969	6	NULL	NULL	0	NULL	SPL	GP	expression of	regulates					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_2_1281_s_273	14570870	First, SPL expression regulates not only intracellular S1P and sphingosine but also appears to increase ceramide generation under stress conditions.	transcription
78973	3	335969	6	NULL	NULL	0	NULL	SPL	GP	expression of	increases					ceramide	Chemical	generation of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_2_1281_s_273	14570870	First, SPL expression regulates not only intracellular S1P and sphingosine but also appears to increase ceramide generation under stress conditions.	transcription
59604	1	335970	5	NULL	NULL	0	NULL	ceramide	Chemical	hydrolysis of;;N-acyl group of	yields					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7324_s_16	16380386	1.23 [EC]) catalyze the hydrolysis of the  N-acyl group of ceramide to yield sphingosine and fatty acids.	transcription
59605	2	335970	5	NULL	NULL	0	NULL	ceramide	Chemical	hydrolysis of;;N-acyl group of	yields					fatty acids	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7324_s_16	16380386	1.23 [EC]) catalyze the hydrolysis of the  N-acyl group of ceramide to yield sphingosine and fatty acids.	transcription
59606	3	335970	5	NULL	NULL	0	NULL	statement 1	Process		occurs along with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7324_s_16	16380386	1.23 [EC]) catalyze the hydrolysis of the  N-acyl group of ceramide to yield sphingosine and fatty acids.	transcription
78969	1	335970	6	NULL	NULL	0	NULL	ceramide	Chemical	hydrolysis of	yields			N-acyl 		sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7324_s_16	16380386	1.23 [EC]) catalyze the hydrolysis of the  N-acyl group of ceramide to yield sphingosine and fatty acids.	transcription
78970	2	335970	6	NULL	NULL	0	NULL	ceramide	Chemical	hydrolysis of	yields			N-acyl 		fatty acids	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_11_7324_s_16	16380386	1.23 [EC]) catalyze the hydrolysis of the  N-acyl group of ceramide to yield sphingosine and fatty acids.	transcription
59665	1	335971	5	NULL	NULL	0	NULL	AC	GP	recombinant	catalyzes					ceramide	Chemical	synthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_194	12815059	We therefore evaluated whether recombinant AC could catalyze ceramide  synthesis using [14]lauric acid and sphingosine as the substrates.	transcription
59666	2	335971	5	NULL	NULL	0	NULL	lauric acid	Chemical		is a substrate of					AC	GP	recombinant			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_194	12815059	We therefore evaluated whether recombinant AC could catalyze ceramide  synthesis using [14]lauric acid and sphingosine as the substrates.	transcription
59667	3	335971	5	NULL	NULL	0	NULL	sphingosine	Chemical		is a substrate of					AC	GP	recombinant			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_194	12815059	We therefore evaluated whether recombinant AC could catalyze ceramide  synthesis using [14]lauric acid and sphingosine as the substrates.	transcription
59668	1	335972	5	NULL	NULL	0	NULL	ceramide	Chemical		is cleaved into					fatty acids	Chemical				NULL	normal epidermis	NULL	NULL	NULL	NULL	gw70_vetmicrobiol_99_1_67_s_139	15019113	In normal epidermis, ceramidase catalyzes the cleavage of ceramide to fatty acids  and sphingosine (  Ohnishi et al., 1999).	transcription
59669	2	335972	5	NULL	NULL	0	NULL	ceramide	Chemical		is cleaved into					sphingosine	Chemical				NULL	normal epidermis	NULL	NULL	NULL	NULL	gw70_vetmicrobiol_99_1_67_s_139	15019113	In normal epidermis, ceramidase catalyzes the cleavage of ceramide to fatty acids  and sphingosine (  Ohnishi et al., 1999).	transcription
59670	3	335972	5	NULL	NULL	0	NULL	statement 1	Process		occurs along with					statement 2	Process				NULL	normal epidermis	NULL	NULL	NULL	NULL	gw70_vetmicrobiol_99_1_67_s_139	15019113	In normal epidermis, ceramidase catalyzes the cleavage of ceramide to fatty acids  and sphingosine (  Ohnishi et al., 1999).	transcription
59671	4	335972	5	NULL	NULL	0	NULL	ceramidase	Chemical		catalyzes					statement 1	Process				NULL	normal epidermis	NULL	NULL	NULL	NULL	gw70_vetmicrobiol_99_1_67_s_139	15019113	In normal epidermis, ceramidase catalyzes the cleavage of ceramide to fatty acids  and sphingosine (  Ohnishi et al., 1999).	transcription
59672	5	335972	5	NULL	NULL	0	NULL	ceramidase	Chemical		catalyzes					statement 2	Process				NULL	normal epidermis	0	NULL	NULL	NULL	gw70_vetmicrobiol_99_1_67_s_139	15019113	In normal epidermis, ceramidase catalyzes the cleavage of ceramide to fatty acids  and sphingosine (  Ohnishi et al., 1999).	transcription
78965	1	335972	6	NULL	NULL	0	NULL	ceramide	Chemical		is cleaved to					fatty acids	Chemical				NULL		0	NULL	NULL	NULL	gw70_vetmicrobiol_99_1_67_s_139	15019113	In normal epidermis, ceramidase catalyzes the cleavage of ceramide to fatty acids  and sphingosine (  Ohnishi et al., 1999).	transcription
78966	2	335972	6	NULL	NULL	0	NULL	ceramide	Chemical		is cleaved to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_vetmicrobiol_99_1_67_s_139	15019113	In normal epidermis, ceramidase catalyzes the cleavage of ceramide to fatty acids  and sphingosine (  Ohnishi et al., 1999).	transcription
78967	3	335972	6	NULL	NULL	NULL	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL	normal epidermis	NULL	NULL	NULL	NULL	gw70_vetmicrobiol_99_1_67_s_139	15019113	In normal epidermis, ceramidase catalyzes the cleavage of ceramide to fatty acids  and sphingosine (  Ohnishi et al., 1999).	transcription
78968	4	335972	6	NULL	NULL	0	NULL	ceramidase	GP		catalyzes					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_vetmicrobiol_99_1_67_s_139	15019113	In normal epidermis, ceramidase catalyzes the cleavage of ceramide to fatty acids  and sphingosine (  Ohnishi et al., 1999).	transcription
59673	1	335973	5	NULL	NULL	0	NULL	TID-ceramide	Chemical		bind					CTSD	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_194	10508159	Notably, D- erythro-sphingosine, but not the fatty acid palmitate, competed for TID-ceramide binding to CTSD.	transcription
59674	2	335973	5	NULL	NULL	0	NULL	D- erythro-sphingosine	Chemical		bind					CTSD	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_194	10508159	Notably, D- erythro-sphingosine, but not the fatty acid palmitate, competed for TID-ceramide binding to CTSD.	transcription
59675	3	335973	5	NULL	NULL	0	NULL	statement 2	Process		competes with					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_194	10508159	Notably, D- erythro-sphingosine, but not the fatty acid palmitate, competed for TID-ceramide binding to CTSD.	transcription
59676	4	335973	5	NULL	NULL	0	NULL	palmitate	Chemical		does not compete with					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_194	10508159	Notably, D- erythro-sphingosine, but not the fatty acid palmitate, competed for TID-ceramide binding to CTSD.	transcription
59677	5	335973	5	NULL	NULL	0	NULL	palmitate	Chemical		is a type of					fatty acid	Chemical				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_194	10508159	Notably, D- erythro-sphingosine, but not the fatty acid palmitate, competed for TID-ceramide binding to CTSD.	transcription
78963	1	335973	6	NULL	NULL	0	NULL	D- erythro-sphingosine	Chemical		bind					CTSD	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_194	10508159	Notably, D- erythro-sphingosine, but not the fatty acid palmitate, competed for TID-ceramide binding to CTSD.	transcription
78964	2	335973	6	NULL	NULL	0	NULL	TID-ceramide	Chemical		bind					CTSD	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_194	10508159	Notably, D- erythro-sphingosine, but not the fatty acid palmitate, competed for TID-ceramide binding to CTSD.	transcription
59678	1	335974	5	NULL	NULL	0	NULL	sphingosine	Chemical		is a type of					N-deacylated ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_10	12135749	Sphingosine, an  N-deacylated form of ceramide, is a potent inhibitor of protein kinase C (PKC) [  9].	transcription
59679	2	335974	5	NULL	NULL	0	NULL	sphingosine	Chemical		is an inhibitor of		potent			PKC	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_10	12135749	Sphingosine, an  N-deacylated form of ceramide, is a potent inhibitor of protein kinase C (PKC) [  9].	transcription
59680	3	335974	5	NULL	NULL	0	NULL	PKC	GP		is					protein kinase C	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_10	12135749	Sphingosine, an  N-deacylated form of ceramide, is a potent inhibitor of protein kinase C (PKC) [  9].	transcription
78960	1	335974	6	NULL	NULL	0	NULL	sphingosine	Chemical		is an inhibitor for					PKC	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_10	12135749	Sphingosine, an  N-deacylated form of ceramide, is a potent inhibitor of protein kinase C (PKC) [  9].	transcription
78961	2	335974	6	NULL	NULL	0	NULL	PKC	GP		is					protein kinase C	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_10	12135749	Sphingosine, an  N-deacylated form of ceramide, is a potent inhibitor of protein kinase C (PKC) [  9].	transcription
78962	3	335974	6	NULL	NULL	0	NULL	sphingosine	Chemical		is 					N-deacylated form of ceramide					NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_10	12135749	Sphingosine, an  N-deacylated form of ceramide, is a potent inhibitor of protein kinase C (PKC) [  9].	transcription
59681	1	335975	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					c-jun	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_83	12135749	These results suggest that sphingosine itself could induce c-jun expression and apoptosis without conversion to ceramide.	transcription
59682	2	335975	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_83	12135749	These results suggest that sphingosine itself could induce c-jun expression and apoptosis without conversion to ceramide.	transcription
59683	3	335975	5	NULL	NULL	0	NULL	sphingosine	Chemical		is not converted to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_83	12135749	These results suggest that sphingosine itself could induce c-jun expression and apoptosis without conversion to ceramide.	transcription
59684	4	335975	5	NULL	NULL	0	NULL	statement 3	Process		is required for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_83	12135749	These results suggest that sphingosine itself could induce c-jun expression and apoptosis without conversion to ceramide.	transcription
59685	5	335975	5	NULL	NULL	0	NULL	statement 3	Process		is required for					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_83	12135749	These results suggest that sphingosine itself could induce c-jun expression and apoptosis without conversion to ceramide.	transcription
78958	1	335975	6	NULL	NULL	0	NULL	sphingosine	Chemical		induces					c-jun	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_83	12135749	These results suggest that sphingosine itself could induce c-jun expression and apoptosis without conversion to ceramide.	transcription
78959	2	335975	6	NULL	NULL	0	NULL	sphingosine	Chemical		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_83	12135749	These results suggest that sphingosine itself could induce c-jun expression and apoptosis without conversion to ceramide.	transcription
59704	1	335976	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					c-jun	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_142	12135749	Further studies will be needed to elucidate the signaling pathways in c-jun expression induced by sphingosine and ceramide.	transcription
59705	2	335976	5	NULL	NULL	0	NULL	ceramide	Chemical		induce					c-jun	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_142	12135749	Further studies will be needed to elucidate the signaling pathways in c-jun expression induced by sphingosine and ceramide.	transcription
78956	1	335976	6	NULL	NULL	0	NULL	sphingosine	Chemical		induces					c-jun	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_142	12135749	Further studies will be needed to elucidate the signaling pathways in c-jun expression induced by sphingosine and ceramide.	transcription
78957	2	335976	6	NULL	NULL	0	NULL	ceramide	Chemical		induces					c-jun	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_142	12135749	Further studies will be needed to elucidate the signaling pathways in c-jun expression induced by sphingosine and ceramide.	transcription
59701	1	335977	5	NULL	NULL	0	NULL	fumonisin	Chemical		is related to		structurally			sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_177_1_109_s_11	10436928	Fumonisin is structurally related to sphingosine, and FB1 is a competitive inhibitor of sphinganine  N-acyltransferase (ceramide synthase) [  12].	transcription
59702	2	335977	5	NULL	NULL	0	NULL	FB1	Chemical		is an inhibitor of		competitive			ceramide synthase	GP				NULL		NULL	NULL	NULL	NULL	gw60_femsmicrobiollett_177_1_109_s_11	10436928	Fumonisin is structurally related to sphingosine, and FB1 is a competitive inhibitor of sphinganine  N-acyltransferase (ceramide synthase) [  12].	transcription
59703	3	335977	5	NULL	NULL	0	NULL	ceramide synthase	GP		is					sphinganine N-acyltransferase	GP				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_177_1_109_s_11	10436928	Fumonisin is structurally related to sphingosine, and FB1 is a competitive inhibitor of sphinganine  N-acyltransferase (ceramide synthase) [  12].	transcription
78953	1	335977	6	NULL	NULL	0	NULL	Fumonisin	Chemical		is related to		structurally			sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_177_1_109_s_11	10436928	Fumonisin is structurally related to sphingosine, and FB1 is a competitive inhibitor of sphinganine  N-acyltransferase (ceramide synthase) [  12].	transcription
78954	2	335977	6	NULL	NULL	0	NULL	FB1	Chemical		is an inhibitor for		competitive			sphinganine N-acyltransferase	GP				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_177_1_109_s_11	10436928	Fumonisin is structurally related to sphingosine, and FB1 is a competitive inhibitor of sphinganine  N-acyltransferase (ceramide synthase) [  12].	transcription
78955	3	335977	6	NULL	NULL	0	NULL	sphinganine N-acyltransferase	GP		is					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_femsmicrobiollett_177_1_109_s_11	10436928	Fumonisin is structurally related to sphingosine, and FB1 is a competitive inhibitor of sphinganine  N-acyltransferase (ceramide synthase) [  12].	transcription
59698	1	335978	5	NULL	NULL	0	NULL	sphingosine	Chemical		acylated to					PAP1	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_188_s_52	12531553	Schematic representation of the inhibition of the acylation of sphingosine by AP1, which is acylated to PAP1, a more potent inhibitor of ceramide synthase.	transcription
59699	2	335978	5	NULL	NULL	0	NULL	AP1	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_188_s_52	12531553	Schematic representation of the inhibition of the acylation of sphingosine by AP1, which is acylated to PAP1, a more potent inhibitor of ceramide synthase.	transcription
59700	3	335978	5	NULL	NULL	0	NULL	PAP1	Chemical		is an inhibitor of		potent			ceramide synthase					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_188_s_52	12531553	Schematic representation of the inhibition of the acylation of sphingosine by AP1, which is acylated to PAP1, a more potent inhibitor of ceramide synthase.	transcription
78950	1	335978	6	NULL	NULL	0	NULL	AP1	GP		acylates					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_188_s_52	12531553	Schematic representation of the inhibition of the acylation of sphingosine by AP1, which is acylated to PAP1, a more potent inhibitor of ceramide synthase.	transcription
78951	2	335978	6	NULL	NULL	0	NULL	sphingosine	Chemical		is acylated into					PAP1	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_188_s_52	12531553	Schematic representation of the inhibition of the acylation of sphingosine by AP1, which is acylated to PAP1, a more potent inhibitor of ceramide synthase.	transcription
78952	3	335978	6	NULL	NULL	0	NULL	PAP1	GP		is an inhibitor for					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_188_s_52	12531553	Schematic representation of the inhibition of the acylation of sphingosine by AP1, which is acylated to PAP1, a more potent inhibitor of ceramide synthase.	transcription
59693	1	335979	5	NULL	NULL	0	NULL	LH	GP		induce					progesterone	GP	production of			NULL	hen granulosa cells	NULL	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_160	9915989	The effect of ceramide analogues and sphingosine on basal and LH-induced progesterone production in hen granulosa cells during follicular development.	transcription
59694	2	335979	5	NULL	NULL	0	NULL	ceramide analogues	Chemical		effects		potentially			statement 1					NULL	hen granulosa cells 	NULL	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_160	9915989	The effect of ceramide analogues and sphingosine on basal and LH-induced progesterone production in hen granulosa cells during follicular development.	transcription
59695	3	335979	5	NULL	NULL	0	NULL	statement 2	Process		occurs during					follicle	CellComponent	development of			NULL	hen granulosa cells 	NULL	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_160	9915989	The effect of ceramide analogues and sphingosine on basal and LH-induced progesterone production in hen granulosa cells during follicular development.	transcription
59696	4	335979	5	NULL	NULL	0	NULL	sphingosine	Chemical		effects		potentially			statement 1	Process				NULL	hen granulosa cells 	0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_160	9915989	The effect of ceramide analogues and sphingosine on basal and LH-induced progesterone production in hen granulosa cells during follicular development.	transcription
59697	5	335979	5	NULL	NULL	0	NULL	statement 4	Process		occurs during					follicle	CellComponent	development of			NULL	hen granulosa cells 	0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_160	9915989	The effect of ceramide analogues and sphingosine on basal and LH-induced progesterone production in hen granulosa cells during follicular development.	transcription
59686	1	335980	5	NULL	NULL	0	NULL	CDase	GP		is					ceramidase	GP				NULL		NULL	NULL	NULL	NULL	gw60_clindiagnlabimmun_6_1_101_s_11	9874672	Ceramidase (CDase), which catalyzes the cleavage of ceramide to fatty acids and sphingosine, is a known inhibitor of the protein kinase C.	transcription
59687	2	335980	5	NULL	NULL	0	NULL	ceramide	Chemical		is cleaved into					fatty acid	Chemical				NULL		0	NULL	NULL	NULL	gw60_clindiagnlabimmun_6_1_101_s_11	9874672	Ceramidase (CDase), which catalyzes the cleavage of ceramide to fatty acids and sphingosine, is a known inhibitor of the protein kinase C.	transcription
59688	3	335980	5	NULL	NULL	0	NULL	ceramide	Chemical		is cleaved into					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_clindiagnlabimmun_6_1_101_s_11	9874672	Ceramidase (CDase), which catalyzes the cleavage of ceramide to fatty acids and sphingosine, is a known inhibitor of the protein kinase C.	transcription
59689	4	335980	5	NULL	NULL	0	NULL	statement 2	Process		occurs along with					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_clindiagnlabimmun_6_1_101_s_11	9874672	Ceramidase (CDase), which catalyzes the cleavage of ceramide to fatty acids and sphingosine, is a known inhibitor of the protein kinase C.	transcription
59690	5	335980	5	NULL	NULL	0	NULL	CDase	GP		catalyzes					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_clindiagnlabimmun_6_1_101_s_11	9874672	Ceramidase (CDase), which catalyzes the cleavage of ceramide to fatty acids and sphingosine, is a known inhibitor of the protein kinase C.	transcription
59691	6	335980	5	NULL	NULL	0	NULL	CDase	GP		catalyzes					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_clindiagnlabimmun_6_1_101_s_11	9874672	Ceramidase (CDase), which catalyzes the cleavage of ceramide to fatty acids and sphingosine, is a known inhibitor of the protein kinase C.	transcription
59692	7	335980	5	NULL	NULL	0	NULL	CDase	GP		is an inhibitor of					protein kinase C	GP				NULL		0	NULL	NULL	NULL	gw60_clindiagnlabimmun_6_1_101_s_11	9874672	Ceramidase (CDase), which catalyzes the cleavage of ceramide to fatty acids and sphingosine, is a known inhibitor of the protein kinase C.	transcription
78944	1	335980	6	NULL	NULL	0	NULL	ceramide	Chemical		is cleaved to					fatty acids	Chemical				NULL		0	NULL	NULL	NULL	gw60_clindiagnlabimmun_6_1_101_s_11	9874672	Ceramidase (CDase), which catalyzes the cleavage of ceramide to fatty acids and sphingosine, is a known inhibitor of the protein kinase C.	transcription
78945	2	335980	6	NULL	NULL	0	NULL	ceramide	Chemical		is cleaved to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_clindiagnlabimmun_6_1_101_s_11	9874672	Ceramidase (CDase), which catalyzes the cleavage of ceramide to fatty acids and sphingosine, is a known inhibitor of the protein kinase C.	transcription
78946	3	335980	6	NULL	NULL	0	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_clindiagnlabimmun_6_1_101_s_11	9874672	Ceramidase (CDase), which catalyzes the cleavage of ceramide to fatty acids and sphingosine, is a known inhibitor of the protein kinase C.	transcription
78947	4	335980	6	NULL	NULL	0	NULL	Ceramidase	GP		catalyzes					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_clindiagnlabimmun_6_1_101_s_11	9874672	Ceramidase (CDase), which catalyzes the cleavage of ceramide to fatty acids and sphingosine, is a known inhibitor of the protein kinase C.	transcription
78948	5	335980	6	NULL	NULL	0	NULL	Ceramidase	GP		is					CDase	GP				NULL		0	NULL	NULL	NULL	gw60_clindiagnlabimmun_6_1_101_s_11	9874672	Ceramidase (CDase), which catalyzes the cleavage of ceramide to fatty acids and sphingosine, is a known inhibitor of the protein kinase C.	transcription
78949	6	335980	6	NULL	NULL	0	NULL	CDase	GP		is an inhibitor for					protein kinase C	GP				NULL		0	NULL	NULL	NULL	gw60_clindiagnlabimmun_6_1_101_s_11	9874672	Ceramidase (CDase), which catalyzes the cleavage of ceramide to fatty acids and sphingosine, is a known inhibitor of the protein kinase C.	transcription
59707	1	335981	5	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL	U937 cells	0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_28	9415703	The current study was undertaken to compare the relative involvement of SAPK activities in the induction of apoptosis by ceramide and sphingosine in U937 cells.	transcription
59708	2	335981	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					apoptosis	Process				NULL	U937 cells	NULL	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_28	9415703	The current study was undertaken to compare the relative involvement of SAPK activities in the induction of apoptosis by ceramide and sphingosine in U937 cells.	transcription
59709	3	335981	5	NULL	NULL	0	NULL	SAPK	GP	activity of	is involved in					statement 1	Process				NULL	U937 cells	NULL	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_28	9415703	The current study was undertaken to compare the relative involvement of SAPK activities in the induction of apoptosis by ceramide and sphingosine in U937 cells.	transcription
59710	4	335981	5	NULL	NULL	0	NULL	SAPK	GP	activity of	is involved in					statement 2	Process				NULL	U937 cells	NULL	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_28	9415703	The current study was undertaken to compare the relative involvement of SAPK activities in the induction of apoptosis by ceramide and sphingosine in U937 cells.	transcription
78942	1	335981	6	NULL	NULL	0	NULL	ceramide	Chemical		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_28	9415703	The current study was undertaken to compare the relative involvement of SAPK activities in the induction of apoptosis by ceramide and sphingosine in U937 cells.	transcription
78943	2	335981	6	NULL	NULL	0	NULL	sphingosine	GP		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_28	9415703	The current study was undertaken to compare the relative involvement of SAPK activities in the induction of apoptosis by ceramide and sphingosine in U937 cells.	transcription
59711	1	335982	5	NULL	NULL	0	NULL	ceramide	Chemical		induce					cell death	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_298	9415703	Increased expression and activation of the SAPK substrate c-Jun were absolutely necessary for the induction of cell death by ceramide but not by sphingosine.	transcription
59712	2	335982	5	NULL	NULL	0	NULL	c-Jun	GP		is a substrate of					SAPK	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_298	9415703	Increased expression and activation of the SAPK substrate c-Jun were absolutely necessary for the induction of cell death by ceramide but not by sphingosine.	transcription
59713	3	335982	5	NULL	NULL	0	NULL	c-Jun	GP	increased expression;;activation of	is necessary for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_298	9415703	Increased expression and activation of the SAPK substrate c-Jun were absolutely necessary for the induction of cell death by ceramide but not by sphingosine.	transcription
59714	4	335982	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_298	9415703	Increased expression and activation of the SAPK substrate c-Jun were absolutely necessary for the induction of cell death by ceramide but not by sphingosine.	transcription
59715	5	335982	5	NULL	NULL	0	NULL	c-Jun	GP	increased expression;;activation of	is not necessary for					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_298	9415703	Increased expression and activation of the SAPK substrate c-Jun were absolutely necessary for the induction of cell death by ceramide but not by sphingosine.	transcription
78939	1	335982	6	NULL	NULL	0	NULL	ceramide	Chemical		induces					cell death	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_298	9415703	Increased expression and activation of the SAPK substrate c-Jun were absolutely necessary for the induction of cell death by ceramide but not by sphingosine.	transcription
78940	2	335982	6	NULL	NULL	0	NULL	c-jun	GP	activation of	is necessary for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_298	9415703	Increased expression and activation of the SAPK substrate c-Jun were absolutely necessary for the induction of cell death by ceramide but not by sphingosine.	transcription
78941	3	335982	6	NULL	NULL	0	NULL	c-jun	GP	expression of	is necessary for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_298	9415703	Increased expression and activation of the SAPK substrate c-Jun were absolutely necessary for the induction of cell death by ceramide but not by sphingosine.	transcription
59716	1	335983	5	NULL	NULL	0	NULL	N, N-dimethylsphingosine	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12724_s_371	11821388	Similarly, in the study of Sweeney  et al. ( 28),  N, N-dimethylsphingosine and sphingosine induced apoptosis in the absence of ceramide generation.	transcription
59717	2	335983	5	NULL	NULL	0	NULL	statement 1	Process		in the absence of					ceramide	Chemical	generation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12724_s_371	11821388	Similarly, in the study of Sweeney  et al. ( 28),  N, N-dimethylsphingosine and sphingosine induced apoptosis in the absence of ceramide generation.	transcription
59718	3	335983	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12724_s_371	11821388	Similarly, in the study of Sweeney  et al. ( 28),  N, N-dimethylsphingosine and sphingosine induced apoptosis in the absence of ceramide generation.	transcription
59719	4	335983	5	NULL	NULL	0	NULL	statement 3	Process		in the absence of					ceramide	Chemical	generation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12724_s_371	11821388	Similarly, in the study of Sweeney  et al. ( 28),  N, N-dimethylsphingosine and sphingosine induced apoptosis in the absence of ceramide generation.	transcription
78935	1	335983	6	NULL	NULL	0	NULL	N, N-dimethylsphingosine	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12724_s_371	11821388	Similarly, in the study of Sweeney  et al. ( 28),  N, N-dimethylsphingosine and sphingosine induced apoptosis in the absence of ceramide generation.	transcription
78936	2	335983	6	NULL	NULL	0	NULL	sphingosine	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12724_s_371	11821388	Similarly, in the study of Sweeney  et al. ( 28),  N, N-dimethylsphingosine and sphingosine induced apoptosis in the absence of ceramide generation.	transcription
78937	3	335983	6	NULL	NULL	0	NULL	statement 1	Process		occurs in absence of					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12724_s_371	11821388	Similarly, in the study of Sweeney  et al. ( 28),  N, N-dimethylsphingosine and sphingosine induced apoptosis in the absence of ceramide generation.	transcription
78938	4	335983	6	NULL	NULL	0	NULL	statement 2	Process		occurs in absence of					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12724_s_371	11821388	Similarly, in the study of Sweeney  et al. ( 28),  N, N-dimethylsphingosine and sphingosine induced apoptosis in the absence of ceramide generation.	transcription
59720	1	335984	5	NULL	NULL	0	NULL	ceramide	Chemical		induce					cell death	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_27129_s_121	11369765	These results indicated that ceramide and sphingosine can induce cell death regardless of the presence or absence of p53.	transcription
59721	2	335984	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					cell death	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_27129_s_121	11369765	These results indicated that ceramide and sphingosine can induce cell death regardless of the presence or absence of p53.	transcription
78933	1	335984	6	NULL	NULL	0	NULL	ceramide	Chemical		induce					cell death	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_27129_s_121	11369765	These results indicated that ceramide and sphingosine can induce cell death regardless of the presence or absence of p53.	transcription
78934	2	335984	6	NULL	NULL	0	NULL	sphingosine	Chemical		induce					cell death	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_29_27129_s_121	11369765	These results indicated that ceramide and sphingosine can induce cell death regardless of the presence or absence of p53.	transcription
59722	1	335985	5	NULL	NULL	0	NULL	Fas	GP		induce					ceramide	Chemical	generation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_62	10747891	Fas induces generation of ceramide and sphingosine prior to activation of caspases and formation of apoptotic nuclei.	transcription
59723	2	335985	5	NULL	NULL	0	NULL	Fas	GP		induce					sphingosine	Chemical	generation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_62	10747891	Fas induces generation of ceramide and sphingosine prior to activation of caspases and formation of apoptotic nuclei.	transcription
59724	3	335985	5	NULL	NULL	0	NULL	statement 1	Process		occurs prior to					caspases	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_62	10747891	Fas induces generation of ceramide and sphingosine prior to activation of caspases and formation of apoptotic nuclei.	transcription
59725	4	335985	5	NULL	NULL	0	NULL	statement 1	Process		occurs prior to					apoptotic nuclei	CellComponent	formation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_62	10747891	Fas induces generation of ceramide and sphingosine prior to activation of caspases and formation of apoptotic nuclei.	transcription
59726	5	335985	5	NULL	NULL	0	NULL	statement 2	Process		occurs prior to					caspases	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_62	10747891	Fas induces generation of ceramide and sphingosine prior to activation of caspases and formation of apoptotic nuclei.	transcription
59727	6	335985	5	NULL	NULL	0	NULL	statement 2	Process		occurs prior to					apoptotic nuclei	CellComponent	formation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_62	10747891	Fas induces generation of ceramide and sphingosine prior to activation of caspases and formation of apoptotic nuclei.	transcription
78927	1	335985	6	NULL	NULL	0	NULL	Fas	GP		induces					ceramide	Chemical	generation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_62	10747891	Fas induces generation of ceramide and sphingosine prior to activation of caspases and formation of apoptotic nuclei.	transcription
78928	2	335985	6	NULL	NULL	0	NULL	Fas	GP		induces					sphingosine	Chemical	generation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_62	10747891	Fas induces generation of ceramide and sphingosine prior to activation of caspases and formation of apoptotic nuclei.	transcription
78929	3	335985	6	NULL	NULL	0	NULL	statement 1	Process		occurs prior to					caspases	GP	activation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_62	10747891	Fas induces generation of ceramide and sphingosine prior to activation of caspases and formation of apoptotic nuclei.	transcription
78930	4	335985	6	NULL	NULL	0	NULL	statement 2	Process		occurs prior to					caspases	GP	activation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_62	10747891	Fas induces generation of ceramide and sphingosine prior to activation of caspases and formation of apoptotic nuclei.	transcription
78931	5	335985	6	NULL	NULL	0	NULL	statement 1	Process		occurs prior to					apoptotic nuclei	CellComponent	formation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_62	10747891	Fas induces generation of ceramide and sphingosine prior to activation of caspases and formation of apoptotic nuclei.	transcription
78932	6	335985	6	NULL	NULL	0	NULL	statement 2	Process		occurs prior to					apoptotic nuclei	CellComponent	formation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_62	10747891	Fas induces generation of ceramide and sphingosine prior to activation of caspases and formation of apoptotic nuclei.	transcription
59728	1	335986	5	NULL	NULL	0	NULL	sphingosine	Chemical	increase in;;generation of	is triggerd by					Fas	GP	ligation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_130	10747891	In agreement, we found that overexpression of Bcl-xL did not inhibit the early increase in ceramide or sphingosine generation triggered by Fas ligation.	transcription
59729	2	335986	5	NULL	NULL	0	NULL	ceramide	Chemical	increase in;;generation of	is triggerd by					Fas	GP	ligation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_130	10747891	In agreement, we found that overexpression of Bcl-xL did not inhibit the early increase in ceramide or sphingosine generation triggered by Fas ligation.	transcription
59730	3	335986	5	NULL	NULL	0	NULL	Bcl-xL	GP	overexpression of	does not inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_130	10747891	In agreement, we found that overexpression of Bcl-xL did not inhibit the early increase in ceramide or sphingosine generation triggered by Fas ligation.	transcription
59731	4	335986	5	NULL	NULL	0	NULL	Bcl-xL	GP	overexpression of	does not inhibit					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_130	10747891	In agreement, we found that overexpression of Bcl-xL did not inhibit the early increase in ceramide or sphingosine generation triggered by Fas ligation.	transcription
59732	1	335987	5	NULL	NULL	0	NULL	cyt c	GP		is translocated from					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_183	10747891	These results demonstrate that sphingosine and ceramide induce translocation of cyt  c from mitochondria to cytosol in a caspase-independent manner.	transcription
59733	2	335987	5	NULL	NULL	0	NULL	cyt c	GP		is translocated to					cytosol	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_183	10747891	These results demonstrate that sphingosine and ceramide induce translocation of cyt  c from mitochondria to cytosol in a caspase-independent manner.	transcription
59734	3	335987	5	NULL	NULL	0	NULL	statement 1	Process		occurs along with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_183	10747891	These results demonstrate that sphingosine and ceramide induce translocation of cyt  c from mitochondria to cytosol in a caspase-independent manner.	transcription
59735	4	335987	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_183	10747891	These results demonstrate that sphingosine and ceramide induce translocation of cyt  c from mitochondria to cytosol in a caspase-independent manner.	transcription
59736	5	335987	5	NULL	NULL	0	NULL	statement 4	Process		is independent of					caspase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_183	10747891	These results demonstrate that sphingosine and ceramide induce translocation of cyt  c from mitochondria to cytosol in a caspase-independent manner.	transcription
59737	6	335987	5	NULL	NULL	0	NULL	ceramide	Chemical		induce					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_183	10747891	These results demonstrate that sphingosine and ceramide induce translocation of cyt  c from mitochondria to cytosol in a caspase-independent manner.	transcription
59738	7	335987	5	NULL	NULL	0	NULL	statement 6	Process		is independent of					caspase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_183	10747891	These results demonstrate that sphingosine and ceramide induce translocation of cyt  c from mitochondria to cytosol in a caspase-independent manner.	transcription
78922	1	335987	6	NULL	NULL	0	NULL	cyt c	GP		is translocated from					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_183	10747891	These results demonstrate that sphingosine and ceramide induce translocation of cyt  c from mitochondria to cytosol in a caspase-independent manner.	transcription
78923	2	335987	6	NULL	NULL	0	NULL	cyt c	GP		is translocated to					cytosol	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_183	10747891	These results demonstrate that sphingosine and ceramide induce translocation of cyt  c from mitochondria to cytosol in a caspase-independent manner.	transcription
78924	3	335987	6	NULL	NULL	0	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_183	10747891	These results demonstrate that sphingosine and ceramide induce translocation of cyt  c from mitochondria to cytosol in a caspase-independent manner.	transcription
78925	4	335987	6	NULL	NULL	0	NULL	sphingosine	Chemical		induces					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_183	10747891	These results demonstrate that sphingosine and ceramide induce translocation of cyt  c from mitochondria to cytosol in a caspase-independent manner.	transcription
78926	5	335987	6	NULL	NULL	0	NULL	ceramide	Chemical		induces					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_183	10747891	These results demonstrate that sphingosine and ceramide induce translocation of cyt  c from mitochondria to cytosol in a caspase-independent manner.	transcription
59739	1	335988	5	NULL	NULL	0	NULL	ceramide	Chemical	formation of	is mediated by					cytokine	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_48_37365_s_246	10956644	B, cytokine-mediated formation of [3]ceramide and [3]sphingosine from the newly delivered [3]sphingomyelin.	transcription
59740	2	335988	5	NULL	NULL	0	NULL	sphingosine	Chemical	formation of	is mediated by					cytokine	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_48_37365_s_246	10956644	B, cytokine-mediated formation of [3]ceramide and [3]sphingosine from the newly delivered [3]sphingomyelin.	transcription
59741	3	335988	5	NULL	NULL	0	NULL	ceramide	Chemical		is formed from					sphingomyelin	Chemical	newly delivered			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_48_37365_s_246	10956644	B, cytokine-mediated formation of [3]ceramide and [3]sphingosine from the newly delivered [3]sphingomyelin.	transcription
59742	4	335988	5	NULL	NULL	0	NULL	sphingosine	Chemical		is formed from					sphingomyelin	Chemical	newly delivered			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_48_37365_s_246	10956644	B, cytokine-mediated formation of [3]ceramide and [3]sphingosine from the newly delivered [3]sphingomyelin.	transcription
78920	1	335988	6	NULL	NULL	0	NULL	sphingomyelin	Chemical		forms					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_48_37365_s_246	10956644	B, cytokine-mediated formation of [3]ceramide and [3]sphingosine from the newly delivered [3]sphingomyelin.	transcription
78921	2	335988	6	NULL	NULL	0	NULL	sphingomyelin	Chemical		forms					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_48_37365_s_246	10956644	B, cytokine-mediated formation of [3]ceramide and [3]sphingosine from the newly delivered [3]sphingomyelin.	transcription
59743	1	335989	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					ceramide	Chemical				NULL	U937 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_182	8626522	Ceramide-induced apoptosis was comparably enhanced by sphingosine and  sphinganine in U937 cells (data not shown).	transcription
59744	2	335989	5	NULL	NULL	0	NULL	sphingosine	Chemical		enhances					statement 1	Process				NULL	U937 cells	0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_182	8626522	Ceramide-induced apoptosis was comparably enhanced by sphingosine and  sphinganine in U937 cells (data not shown).	transcription
59745	3	335989	5	NULL	NULL	0	NULL	sphinganine	Chemical		enhances					statement 1	Process				NULL	U937 cells	0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_182	8626522	Ceramide-induced apoptosis was comparably enhanced by sphingosine and  sphinganine in U937 cells (data not shown).	transcription
78917	1	335989	6	NULL	NULL	0	NULL	ceramide	Chemical		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_182	8626522	Ceramide-induced apoptosis was comparably enhanced by sphingosine and  sphinganine in U937 cells (data not shown).	transcription
78918	2	335989	6	NULL	NULL	0	NULL	sphingosine	Chemical		enhances					statement 1	Process				NULL	U937 cells	0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_182	8626522	Ceramide-induced apoptosis was comparably enhanced by sphingosine and  sphinganine in U937 cells (data not shown).	transcription
78919	3	335989	6	NULL	NULL	NULL	NULL	sphinganine	Chemical		enhances					statement 1	Process				NULL	U937 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_182	8626522	Ceramide-induced apoptosis was comparably enhanced by sphingosine and  sphinganine in U937 cells (data not shown).	transcription
59746	1	335991	5	NULL	NULL	0	NULL	phospholipase D	GP		is activated by					sphingosine 1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_8	7592842	Okadaic acid decreased the activation of phospholipase D by  sphingosine 1-phosphate and did not reverse the inhibitory effect of  C -ceramide on this activation.	transcription
59747	2	335991	5	NULL	NULL	0	NULL	okadaic acid	Chemical		decreases					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_8	7592842	Okadaic acid decreased the activation of phospholipase D by  sphingosine 1-phosphate and did not reverse the inhibitory effect of  C -ceramide on this activation.	transcription
59748	3	335991	5	NULL	NULL	0	NULL	C -ceramide	Chemical		inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_8	7592842	Okadaic acid decreased the activation of phospholipase D by  sphingosine 1-phosphate and did not reverse the inhibitory effect of  C -ceramide on this activation.	transcription
59749	4	335991	5	NULL	NULL	0	NULL	okadaic acid	Chemical		does not reverse					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_8	7592842	Okadaic acid decreased the activation of phospholipase D by  sphingosine 1-phosphate and did not reverse the inhibitory effect of  C -ceramide on this activation.	transcription
78915	1	335991	6	NULL	NULL	NULL	NULL	Okadaic acid	Chemical		decreases					phospholipase D	GP	activation of 			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_8	7592842	Okadaic acid decreased the activation of phospholipase D by  sphingosine 1-phosphate and did not reverse the inhibitory effect of  C -ceramide on this activation.	transcription
78916	2	335991	6	NULL	NULL	0	NULL	statement 1	Process		occurs via					sphingosine 1-phosphate	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_8	7592842	Okadaic acid decreased the activation of phospholipase D by  sphingosine 1-phosphate and did not reverse the inhibitory effect of  C -ceramide on this activation.	transcription
59750	1	335992	5	NULL	NULL	0	NULL	cAMP	Chemical		is produced by					SPP	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_171	7592842	However, there was no significant effect of  C -ceramide on the percentage decrease in cAMP that was  produced by SPP, sphingosine, and lysophosphatidate ( Table 1).	transcription
59751	2	335992	5	NULL	NULL	0	NULL	cAMP	Chemical		is produced by					sphingosine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_171	7592842	However, there was no significant effect of  C -ceramide on the percentage decrease in cAMP that was  produced by SPP, sphingosine, and lysophosphatidate ( Table 1).	transcription
59752	3	335992	5	NULL	NULL	0	NULL	cAMP	Chemical		is produced by					lysophosphatidate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_171	7592842	However, there was no significant effect of  C -ceramide on the percentage decrease in cAMP that was  produced by SPP, sphingosine, and lysophosphatidate ( Table 1).	transcription
59753	4	335992	5	NULL	NULL	0	NULL	C -ceramide	Chemical		does not effect		significantly			statement 1	Process	decrease in			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_171	7592842	However, there was no significant effect of  C -ceramide on the percentage decrease in cAMP that was  produced by SPP, sphingosine, and lysophosphatidate ( Table 1).	transcription
59754	5	335992	5	NULL	NULL	0	NULL	C -ceramide	Chemical		does not effect		significantly			statement 2	Process	decrease in			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_171	7592842	However, there was no significant effect of  C -ceramide on the percentage decrease in cAMP that was  produced by SPP, sphingosine, and lysophosphatidate ( Table 1).	transcription
59755	6	335992	5	NULL	NULL	0	NULL	C -ceramide	Chemical		does not effect		significantly			statement 3	Process	decrease in			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_171	7592842	However, there was no significant effect of  C -ceramide on the percentage decrease in cAMP that was  produced by SPP, sphingosine, and lysophosphatidate ( Table 1).	transcription
78912	1	335992	6	NULL	NULL	0	NULL	SPP	Chemical		produces					cAMP	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_171	7592842	However, there was no significant effect of  C -ceramide on the percentage decrease in cAMP that was  produced by SPP, sphingosine, and lysophosphatidate ( Table 1).	transcription
78913	2	335992	6	NULL	NULL	0	NULL	sphingosine	Chemical		produces					cAMP	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_171	7592842	However, there was no significant effect of  C -ceramide on the percentage decrease in cAMP that was  produced by SPP, sphingosine, and lysophosphatidate ( Table 1).	transcription
78914	3	335992	6	NULL	NULL	0	NULL	lysophosphatidate	Chemical		produces					cAMP	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_171	7592842	However, there was no significant effect of  C -ceramide on the percentage decrease in cAMP that was  produced by SPP, sphingosine, and lysophosphatidate ( Table 1).	transcription
59756	1	335993	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					apoptosis	Process				NULL	in cells in culture 	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_48_33875_s_177	10567348	If so, the formation of sphingosine and ceramide, which are well known to induce apoptosis in cells in culture ( 1-4), might participate in the toxicity of NH4+.	transcription
59757	2	335993	5	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL	in cells in culture	0	NULL	NULL	NULL	gw60_jbiolchem_274_48_33875_s_177	10567348	If so, the formation of sphingosine and ceramide, which are well known to induce apoptosis in cells in culture ( 1-4), might participate in the toxicity of NH4+.	transcription
59758	3	335993	5	NULL	NULL	0	NULL	sphingosine	Chemical	formation of	participates in		might			NH4+	Chemical	toxicity of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_48_33875_s_177	10567348	If so, the formation of sphingosine and ceramide, which are well known to induce apoptosis in cells in culture ( 1-4), might participate in the toxicity of NH4+.	transcription
59759	4	335993	5	NULL	NULL	0	NULL	ceramide	Chemical	formation of	participates in		might			NH4+	Chemical	toxicity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_48_33875_s_177	10567348	If so, the formation of sphingosine and ceramide, which are well known to induce apoptosis in cells in culture ( 1-4), might participate in the toxicity of NH4+.	transcription
78910	1	335993	6	NULL	NULL	0	NULL	sphingosine	Chemical		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_48_33875_s_177	10567348	If so, the formation of sphingosine and ceramide, which are well known to induce apoptosis in cells in culture ( 1-4), might participate in the toxicity of NH4+.	transcription
78911	2	335993	6	NULL	NULL	0	NULL	ceramide	Chemical		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_48_33875_s_177	10567348	If so, the formation of sphingosine and ceramide, which are well known to induce apoptosis in cells in culture ( 1-4), might participate in the toxicity of NH4+.	transcription
59760	1	335994	5	NULL	NULL	0	NULL	TNF-alpha	g		increases					ceramide	Chemical	cellular concentration of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15345_s_194	9624115	TNF-alpha increased the cellular concentration of ceramide, but TNF-alpha had no effect on the amount of basal sphingosine.	transcription
59761	2	335994	5	NULL	NULL	0	NULL	TNF-alpha	GP		does not effect					sphingosine	Chemical	basal amount of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_25_15345_s_194	9624115	TNF-alpha increased the cellular concentration of ceramide, but TNF-alpha had no effect on the amount of basal sphingosine.	transcription
78908	1	335994	6	NULL	NULL	0	NULL	TNF-alpha	Chemical		increases					ceramide	Chemical	levels of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15345_s_194	9624115	TNF-alpha increased the cellular concentration of ceramide, but TNF-alpha had no effect on the amount of basal sphingosine.	transcription
78909	2	335994	6	NULL	NULL	0	NULL	TNF-alpha	GP		has no effect on					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15345_s_194	9624115	TNF-alpha increased the cellular concentration of ceramide, but TNF-alpha had no effect on the amount of basal sphingosine.	transcription
59762	1	335995	5	NULL	NULL	0	NULL	PMA	Chemical		increases					sphingosine	Chemical	level of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15345_s_196	9624115	In contrast to TNF-alpha, PMA increased sphingosine levels but did not increase basal levels of ceramide, even in the presence of TNF-alpha.	transcription
59763	2	335995	5	NULL	NULL	0	NULL	PMA	Chemical		does not increase					ceramide	Chemical	basal level of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15345_s_196	9624115	In contrast to TNF-alpha, PMA increased sphingosine levels but did not increase basal levels of ceramide, even in the presence of TNF-alpha.	transcription
59764	3	335995	5	NULL	NULL	0	NULL	statement 2	Process		in the presence of					TNF-alpha	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15345_s_196	9624115	In contrast to TNF-alpha, PMA increased sphingosine levels but did not increase basal levels of ceramide, even in the presence of TNF-alpha.	transcription
78906	1	335995	6	NULL	NULL	0	NULL	PMA	Chemical		increases					sphingosine	Chemical	levels of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15345_s_196	9624115	In contrast to TNF-alpha, PMA increased sphingosine levels but did not increase basal levels of ceramide, even in the presence of TNF-alpha.	transcription
78907	2	335995	6	NULL	NULL	0	NULL	PMA	Chemical		does not increase					ceramide	Chemical	levels of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15345_s_196	9624115	In contrast to TNF-alpha, PMA increased sphingosine levels but did not increase basal levels of ceramide, even in the presence of TNF-alpha.	transcription
59765	1	335996	5	NULL	NULL	0	NULL	LPP1 gene product	GP	PA phosphatase activity of	is independent of					Mg2+	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14331_s_170	9603941	We examined the effects of ceramide 1-phosphate and sphingosine 1-phosphate on the Mg2+-independent PA phosphatase activity encoded by the  LPP1 gene.	transcription
59766	2	335996	5	NULL	NULL	0	NULL	ceramide 1-phosphate	Chemical		effects		potentially			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14331_s_170	9603941	We examined the effects of ceramide 1-phosphate and sphingosine 1-phosphate on the Mg2+-independent PA phosphatase activity encoded by the  LPP1 gene.	transcription
59767	3	335996	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		effects		potentially			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14331_s_170	9603941	We examined the effects of ceramide 1-phosphate and sphingosine 1-phosphate on the Mg2+-independent PA phosphatase activity encoded by the  LPP1 gene.	transcription
78904	1	335996	6	NULL	NULL	0	NULL	LPP1 gene	GP		encodes					PA phosphatase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14331_s_170	9603941	We examined the effects of ceramide 1-phosphate and sphingosine 1-phosphate on the Mg2+-independent PA phosphatase activity encoded by the  LPP1 gene.	transcription
78905	2	335996	6	NULL	NULL	0	NULL	statement 1	Process		is independent of					Mg2+	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14331_s_170	9603941	We examined the effects of ceramide 1-phosphate and sphingosine 1-phosphate on the Mg2+-independent PA phosphatase activity encoded by the  LPP1 gene.	transcription
59768	1	335997	5	NULL	NULL	0	NULL	PKC	GP		activates					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_17	9446602	These results indicate that PKC may inhibit ceramide-induced apoptosis by activating sphingosine kinase.	transcription
59769	2	335997	5	NULL	NULL	0	NULL	apoptosis	Process		is inhibited by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_17	9446602	These results indicate that PKC may inhibit ceramide-induced apoptosis by activating sphingosine kinase.	transcription
59770	3	335997	5	NULL	NULL	0	NULL	statement 1	Process		inhibit		may			statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_17	9446602	These results indicate that PKC may inhibit ceramide-induced apoptosis by activating sphingosine kinase.	transcription
78900	1	335997	6	NULL	NULL	0	NULL	PKC	GP		activates					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_17	9446602	These results indicate that PKC may inhibit ceramide-induced apoptosis by activating sphingosine kinase.	transcription
78901	2	335997	6	NULL	NULL	0	NULL	ceramide	Chemical		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_17	9446602	These results indicate that PKC may inhibit ceramide-induced apoptosis by activating sphingosine kinase.	transcription
78902	3	335997	6	NULL	NULL	0	NULL	PKC	GP		inhibits					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_17	9446602	These results indicate that PKC may inhibit ceramide-induced apoptosis by activating sphingosine kinase.	transcription
78903	4	335997	6	NULL	NULL	0	NULL	statement 3	Process		occurs via					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_17	9446602	These results indicate that PKC may inhibit ceramide-induced apoptosis by activating sphingosine kinase.	transcription
59771	1	335998	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_1_1_s_107	9469581	Ceramide-mediated apoptosis is subject to reciprocal modulation by diglyceride and sphingosine in HL-60 and U937 human leukemia cells.	transcription
59772	2	335998	5	NULL	NULL	0	NULL	diglyceride	Chemical		modulate		reciprocally			statement 1	Process				NULL	HL-60 cells	0	NULL	NULL	NULL	gw60_jlipidres_39_1_1_s_107	9469581	Ceramide-mediated apoptosis is subject to reciprocal modulation by diglyceride and sphingosine in HL-60 and U937 human leukemia cells.	transcription
59773	3	335998	5	NULL	NULL	0	NULL	sphingosine	Chemical		modulate		reciprocally			statement 1	Process				NULL	HL-60 cells	0	NULL	NULL	NULL	gw60_jlipidres_39_1_1_s_107	9469581	Ceramide-mediated apoptosis is subject to reciprocal modulation by diglyceride and sphingosine in HL-60 and U937 human leukemia cells.	transcription
59774	6	335998	5	NULL	NULL	0	NULL	U937 cells	Cell		is a type of					human leukemia cells	Cell				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_1_1_s_107	9469581	Ceramide-mediated apoptosis is subject to reciprocal modulation by diglyceride and sphingosine in HL-60 and U937 human leukemia cells.	transcription
59775	4	335998	5	NULL	NULL	0	NULL	diglyceride	Chemical		modulate		reciprocally			statement 1	Process				NULL	U937 cells	NULL	NULL	NULL	NULL	gw60_jlipidres_39_1_1_s_107	9469581	Ceramide-mediated apoptosis is subject to reciprocal modulation by diglyceride and sphingosine in HL-60 and U937 human leukemia cells.	transcription
59776	5	335998	5	NULL	NULL	0	NULL	sphingosine	Chemical		modulate		reciprocally			statement 1	Process				NULL	U937 cells	NULL	NULL	NULL	NULL	gw60_jlipidres_39_1_1_s_107	9469581	Ceramide-mediated apoptosis is subject to reciprocal modulation by diglyceride and sphingosine in HL-60 and U937 human leukemia cells.	transcription
78899	1	335998	6	NULL	NULL	0	NULL	ceramide	Chemical		mediates					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_1_1_s_107	9469581	Ceramide-mediated apoptosis is subject to reciprocal modulation by diglyceride and sphingosine in HL-60 and U937 human leukemia cells.	transcription
59777	1	335999	5	NULL	NULL	0	NULL	DMS	Chemical		is					dimethylsphingosine	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_j-physiol_575_pt-1_16740613_s_8	16740613	This sensitizing action of NGF,  ceramide and internally perfused Sph was abolished by dimethylsphingosine  (DMS), an inhibitor of sphingosine kinase.	transcription
59778	2	335999	5	NULL	NULL	0	NULL	DMS	Chemical		is an inhibitor of					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_j-physiol_575_pt-1_16740613_s_8	16740613	This sensitizing action of NGF,  ceramide and internally perfused Sph was abolished by dimethylsphingosine  (DMS), an inhibitor of sphingosine kinase.	transcription
59779	3	335999	5	NULL	NULL	0	NULL	DMS	Chemical		abolishes					NGF	GP	sensitizing action of			NULL		0	NULL	NULL	NULL	abs-batch0740-0759_j-physiol_575_pt-1_16740613_s_8	16740613	This sensitizing action of NGF,  ceramide and internally perfused Sph was abolished by dimethylsphingosine  (DMS), an inhibitor of sphingosine kinase.	transcription
59780	4	335999	5	NULL	NULL	0	NULL	DMS	Chemical		abolishes					ceramide	Chemical	sensitizing action of			NULL		0	NULL	NULL	NULL	abs-batch0740-0759_j-physiol_575_pt-1_16740613_s_8	16740613	This sensitizing action of NGF,  ceramide and internally perfused Sph was abolished by dimethylsphingosine  (DMS), an inhibitor of sphingosine kinase.	transcription
59781	5	335999	5	NULL	NULL	0	NULL	DMS	Chemical		abolishes					Sph	Chemical	sensitizing action of;;internally perfused			NULL		0	NULL	NULL	NULL	abs-batch0740-0759_j-physiol_575_pt-1_16740613_s_8	16740613	This sensitizing action of NGF,  ceramide and internally perfused Sph was abolished by dimethylsphingosine  (DMS), an inhibitor of sphingosine kinase.	transcription
78897	1	335999	6	NULL	NULL	0	NULL	DMS	Chemical		is					dimethylsphingosine	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_j-physiol_575_pt-1_16740613_s_8	16740613	This sensitizing action of NGF,  ceramide and internally perfused Sph was abolished by dimethylsphingosine  (DMS), an inhibitor of sphingosine kinase.	transcription
78898	2	335999	6	NULL	NULL	0	NULL	DMS	Chemical		inhibits					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_j-physiol_575_pt-1_16740613_s_8	16740613	This sensitizing action of NGF,  ceramide and internally perfused Sph was abolished by dimethylsphingosine  (DMS), an inhibitor of sphingosine kinase.	transcription
59782	1	336000	5	NULL	NULL	0	NULL	sphingosine	Chemical		is phosphorylated to					SPP	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_17	10760461	In contrast to the growth-inhibitory and pro-apoptotic effects of ceramide and sphingosine, SPP, which is produced by sphingosine kinase-dependent phosphorylation of sphingosine, has been implicated in cell growth [  8] and is able to inhibit ceramide-mediated apoptosis [  9,   10,   11 and   12].	transcription
59783	2	336000	5	NULL	NULL	0	NULL	statement 1	Process		is dependent on					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_17	10760461	In contrast to the growth-inhibitory and pro-apoptotic effects of ceramide and sphingosine, SPP, which is produced by sphingosine kinase-dependent phosphorylation of sphingosine, has been implicated in cell growth [  8] and is able to inhibit ceramide-mediated apoptosis [  9,   10,   11 and   12].	transcription
59784	3	336000	5	NULL	NULL	0	NULL	SPP	Chemical		is implicated in					cell growth	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_17	10760461	In contrast to the growth-inhibitory and pro-apoptotic effects of ceramide and sphingosine, SPP, which is produced by sphingosine kinase-dependent phosphorylation of sphingosine, has been implicated in cell growth [  8] and is able to inhibit ceramide-mediated apoptosis [  9,   10,   11 and   12].	transcription
59785	4	336000	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_17	10760461	In contrast to the growth-inhibitory and pro-apoptotic effects of ceramide and sphingosine, SPP, which is produced by sphingosine kinase-dependent phosphorylation of sphingosine, has been implicated in cell growth [  8] and is able to inhibit ceramide-mediated apoptosis [  9,   10,   11 and   12].	transcription
59786	5	336000	5	NULL	NULL	0	NULL	SPP	Chemical		inhibit					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_17	10760461	In contrast to the growth-inhibitory and pro-apoptotic effects of ceramide and sphingosine, SPP, which is produced by sphingosine kinase-dependent phosphorylation of sphingosine, has been implicated in cell growth [  8] and is able to inhibit ceramide-mediated apoptosis [  9,   10,   11 and   12].	transcription
78890	1	336000	6	NULL	NULL	0	NULL	ceramide	Chemical		inhibits					growth	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_17	10760461	In contrast to the growth-inhibitory and pro-apoptotic effects of ceramide and sphingosine, SPP, which is produced by sphingosine kinase-dependent phosphorylation of sphingosine, has been implicated in cell growth [  8] and is able to inhibit ceramide-mediated apoptosis [  9,   10,   11 and   12].	transcription
78891	2	336000	6	NULL	NULL	0	NULL	sphingosine	Chemical		inhibits					growth	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_17	10760461	In contrast to the growth-inhibitory and pro-apoptotic effects of ceramide and sphingosine, SPP, which is produced by sphingosine kinase-dependent phosphorylation of sphingosine, has been implicated in cell growth [  8] and is able to inhibit ceramide-mediated apoptosis [  9,   10,   11 and   12].	transcription
78892	3	336000	6	NULL	NULL	0	NULL	sphingosine	Chemical	phosphorylation of	is dependent on					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_17	10760461	In contrast to the growth-inhibitory and pro-apoptotic effects of ceramide and sphingosine, SPP, which is produced by sphingosine kinase-dependent phosphorylation of sphingosine, has been implicated in cell growth [  8] and is able to inhibit ceramide-mediated apoptosis [  9,   10,   11 and   12].	transcription
78893	4	336000	6	NULL	NULL	0	NULL	statement 3	Process		produces					SPP	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_17	10760461	In contrast to the growth-inhibitory and pro-apoptotic effects of ceramide and sphingosine, SPP, which is produced by sphingosine kinase-dependent phosphorylation of sphingosine, has been implicated in cell growth [  8] and is able to inhibit ceramide-mediated apoptosis [  9,   10,   11 and   12].	transcription
78894	5	336000	6	NULL	NULL	0	NULL	SPP	GP		plays a role in					cell growth	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_17	10760461	In contrast to the growth-inhibitory and pro-apoptotic effects of ceramide and sphingosine, SPP, which is produced by sphingosine kinase-dependent phosphorylation of sphingosine, has been implicated in cell growth [  8] and is able to inhibit ceramide-mediated apoptosis [  9,   10,   11 and   12].	transcription
78895	6	336000	6	NULL	NULL	0	NULL	ceramide	Chemical		mediates					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_17	10760461	In contrast to the growth-inhibitory and pro-apoptotic effects of ceramide and sphingosine, SPP, which is produced by sphingosine kinase-dependent phosphorylation of sphingosine, has been implicated in cell growth [  8] and is able to inhibit ceramide-mediated apoptosis [  9,   10,   11 and   12].	transcription
78896	7	336000	6	NULL	NULL	0	NULL	SPP	Chemical		inhibits					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1484_2_107_s_17	10760461	In contrast to the growth-inhibitory and pro-apoptotic effects of ceramide and sphingosine, SPP, which is produced by sphingosine kinase-dependent phosphorylation of sphingosine, has been implicated in cell growth [  8] and is able to inhibit ceramide-mediated apoptosis [  9,   10,   11 and   12].	transcription
59787	1	336001	5	NULL	NULL	0	NULL	ceramide	Chemical	apoptotic capacity of	augmented by					D-erythro-sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_259	8626522	Thus, the findings that  the apoptotic capacity of ceramide was ( a) comparably  augmented by both D- and L- forms of  erythro-sphingosine and  threo-sphingosine, but ( b) selectively abolished by  sn-1,2-substituted (but  not  sn-2,3-substituted or  rac-1,3-substituted) forms  of diglyceride additionally supports an involvement of PKC activity in  the reciprocal modulation of ceramide action by sphingosine and  diglyceride.	transcription
59788	2	336001	5	NULL	NULL	0	NULL	ceramide	Chemical	apoptotic capacity of	augmented by					L-erythro-sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_259	8626522	Thus, the findings that  the apoptotic capacity of ceramide was ( a) comparably  augmented by both D- and L- forms of  erythro-sphingosine and  threo-sphingosine, but ( b) selectively abolished by  sn-1,2-substituted (but  not  sn-2,3-substituted or  rac-1,3-substituted) forms  of diglyceride additionally supports an involvement of PKC activity in  the reciprocal modulation of ceramide action by sphingosine and  diglyceride.	transcription
59789	3	336001	5	NULL	NULL	0	NULL	ceramide	Chemical	apoptotic capacity of	augmented by					threo-sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_259	8626522	Thus, the findings that  the apoptotic capacity of ceramide was ( a) comparably  augmented by both D- and L- forms of  erythro-sphingosine and  threo-sphingosine, but ( b) selectively abolished by  sn-1,2-substituted (but  not  sn-2,3-substituted or  rac-1,3-substituted) forms  of diglyceride additionally supports an involvement of PKC activity in  the reciprocal modulation of ceramide action by sphingosine and  diglyceride.	transcription
59790	4	336001	5	NULL	NULL	0	NULL	ceramide	Chemical	apoptotic capacity of	abolished by		selectively			sn-1,2-substituted diglyceride	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_259	8626522	Thus, the findings that  the apoptotic capacity of ceramide was ( a) comparably  augmented by both D- and L- forms of  erythro-sphingosine and  threo-sphingosine, but ( b) selectively abolished by  sn-1,2-substituted (but  not  sn-2,3-substituted or  rac-1,3-substituted) forms  of diglyceride additionally supports an involvement of PKC activity in  the reciprocal modulation of ceramide action by sphingosine and  diglyceride.	transcription
59791	5	336001	5	NULL	NULL	0	NULL	ceramide	Chemical	apoptotic capacity of	not abolished by					sn-2,3-substituted diglyceride	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_259	8626522	Thus, the findings that  the apoptotic capacity of ceramide was ( a) comparably  augmented by both D- and L- forms of  erythro-sphingosine and  threo-sphingosine, but ( b) selectively abolished by  sn-1,2-substituted (but  not  sn-2,3-substituted or  rac-1,3-substituted) forms  of diglyceride additionally supports an involvement of PKC activity in  the reciprocal modulation of ceramide action by sphingosine and  diglyceride.	transcription
59792	6	336001	5	NULL	NULL	0	NULL	ceramide	Chemical	apoptotic capacity of	not abolished by					rac-1,3-substituted diglyceride	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_259	8626522	Thus, the findings that  the apoptotic capacity of ceramide was ( a) comparably  augmented by both D- and L- forms of  erythro-sphingosine and  threo-sphingosine, but ( b) selectively abolished by  sn-1,2-substituted (but  not  sn-2,3-substituted or  rac-1,3-substituted) forms  of diglyceride additionally supports an involvement of PKC activity in  the reciprocal modulation of ceramide action by sphingosine and  diglyceride.	transcription
59793	7	336001	5	NULL	NULL	0	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_259	8626522	Thus, the findings that  the apoptotic capacity of ceramide was ( a) comparably  augmented by both D- and L- forms of  erythro-sphingosine and  threo-sphingosine, but ( b) selectively abolished by  sn-1,2-substituted (but  not  sn-2,3-substituted or  rac-1,3-substituted) forms  of diglyceride additionally supports an involvement of PKC activity in  the reciprocal modulation of ceramide action by sphingosine and  diglyceride.	transcription
59794	8	336001	5	NULL	NULL	0	NULL	sphingosine	Chemical		modulate		reciprocally			ceramide	Chemical	action of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_259	8626522	Thus, the findings that  the apoptotic capacity of ceramide was ( a) comparably  augmented by both D- and L- forms of  erythro-sphingosine and  threo-sphingosine, but ( b) selectively abolished by  sn-1,2-substituted (but  not  sn-2,3-substituted or  rac-1,3-substituted) forms  of diglyceride additionally supports an involvement of PKC activity in  the reciprocal modulation of ceramide action by sphingosine and  diglyceride.	transcription
59795	9	336001	5	NULL	NULL	0	NULL	diglyceride	Chemical		modulate		reciprocally			ceramide	Chemical	action of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_259	8626522	Thus, the findings that  the apoptotic capacity of ceramide was ( a) comparably  augmented by both D- and L- forms of  erythro-sphingosine and  threo-sphingosine, but ( b) selectively abolished by  sn-1,2-substituted (but  not  sn-2,3-substituted or  rac-1,3-substituted) forms  of diglyceride additionally supports an involvement of PKC activity in  the reciprocal modulation of ceramide action by sphingosine and  diglyceride.	transcription
59796	10	336001	5	NULL	NULL	0	NULL	PKC	GP	activity of	is involved in					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_259	8626522	Thus, the findings that  the apoptotic capacity of ceramide was ( a) comparably  augmented by both D- and L- forms of  erythro-sphingosine and  threo-sphingosine, but ( b) selectively abolished by  sn-1,2-substituted (but  not  sn-2,3-substituted or  rac-1,3-substituted) forms  of diglyceride additionally supports an involvement of PKC activity in  the reciprocal modulation of ceramide action by sphingosine and  diglyceride.	transcription
59797	11	336001	5	NULL	NULL	0	NULL	PKC	GP	activity of	is involved in					statement 9	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_259	8626522	Thus, the findings that  the apoptotic capacity of ceramide was ( a) comparably  augmented by both D- and L- forms of  erythro-sphingosine and  threo-sphingosine, but ( b) selectively abolished by  sn-1,2-substituted (but  not  sn-2,3-substituted or  rac-1,3-substituted) forms  of diglyceride additionally supports an involvement of PKC activity in  the reciprocal modulation of ceramide action by sphingosine and  diglyceride.	transcription
78887	1	336001	6	NULL	NULL	0	NULL	ceramide	Chemical		plays a role in					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_259	8626522	Thus, the findings that  the apoptotic capacity of ceramide was ( a) comparably  augmented by both D- and L- forms of  erythro-sphingosine and  threo-sphingosine, but ( b) selectively abolished by  sn-1,2-substituted (but  not  sn-2,3-substituted or  rac-1,3-substituted) forms  of diglyceride additionally supports an involvement of PKC activity in  the reciprocal modulation of ceramide action by sphingosine and  diglyceride.	transcription
78888	2	336001	6	NULL	NULL	0	NULL	statement 1	Process		is augmented by					erythro-sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_259	8626522	Thus, the findings that  the apoptotic capacity of ceramide was ( a) comparably  augmented by both D- and L- forms of  erythro-sphingosine and  threo-sphingosine, but ( b) selectively abolished by  sn-1,2-substituted (but  not  sn-2,3-substituted or  rac-1,3-substituted) forms  of diglyceride additionally supports an involvement of PKC activity in  the reciprocal modulation of ceramide action by sphingosine and  diglyceride.	transcription
78889	3	336001	6	NULL	NULL	0	NULL	statement 1	Process		is augmented by					threo-sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_259	8626522	Thus, the findings that  the apoptotic capacity of ceramide was ( a) comparably  augmented by both D- and L- forms of  erythro-sphingosine and  threo-sphingosine, but ( b) selectively abolished by  sn-1,2-substituted (but  not  sn-2,3-substituted or  rac-1,3-substituted) forms  of diglyceride additionally supports an involvement of PKC activity in  the reciprocal modulation of ceramide action by sphingosine and  diglyceride.	transcription
59798	1	336002	5	NULL	NULL	0	NULL	PAK1	GP		is activated by					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_6	9525917	We observed concentration- and time-dependent activation of PAK1 by sphingosine and several related long chain sphingoid bases but not by ceramides or a variety of other lipids.	transcription
59799	2	336002	5	NULL	NULL	0	NULL	statement 1	Process		is dependent on					concentration	QuantityOrMeasure				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_6	9525917	We observed concentration- and time-dependent activation of PAK1 by sphingosine and several related long chain sphingoid bases but not by ceramides or a variety of other lipids.	transcription
59800	3	336002	5	NULL	NULL	0	NULL	statement 1	Process		is dependent on					time	Time				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_6	9525917	We observed concentration- and time-dependent activation of PAK1 by sphingosine and several related long chain sphingoid bases but not by ceramides or a variety of other lipids.	transcription
59801	4	336002	5	NULL	NULL	0	NULL	PAK1	GP		is activated by					sphingoid bases	Chemical	sphingosine related;;long chain			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_6	9525917	We observed concentration- and time-dependent activation of PAK1 by sphingosine and several related long chain sphingoid bases but not by ceramides or a variety of other lipids.	transcription
59802	5	336002	5	NULL	NULL	0	NULL	statement 4	Process		is dependent on					concentration	QuantityOrMeasure				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_6	9525917	We observed concentration- and time-dependent activation of PAK1 by sphingosine and several related long chain sphingoid bases but not by ceramides or a variety of other lipids.	transcription
59803	6	336002	5	NULL	NULL	0	NULL	statement 4	Process		is dependent on					time	Time				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_6	9525917	We observed concentration- and time-dependent activation of PAK1 by sphingosine and several related long chain sphingoid bases but not by ceramides or a variety of other lipids.	transcription
59804	7	336002	5	NULL	NULL	0	NULL	PAK1	GP		is not activated by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_6	9525917	We observed concentration- and time-dependent activation of PAK1 by sphingosine and several related long chain sphingoid bases but not by ceramides or a variety of other lipids.	transcription
59805	8	336002	5	NULL	NULL	0	NULL	PAK1	GP		is not activated by					lipids	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_6	9525917	We observed concentration- and time-dependent activation of PAK1 by sphingosine and several related long chain sphingoid bases but not by ceramides or a variety of other lipids.	transcription
78886	1	336002	6	NULL	NULL	0	NULL	sphingosine	Chemical		activates					PAK1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_6	9525917	We observed concentration- and time-dependent activation of PAK1 by sphingosine and several related long chain sphingoid bases but not by ceramides or a variety of other lipids.	transcription
59806	1	336004	5	NULL	NULL	0	NULL	sphingosine	Chemical		acylated to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_5	15180992	To determine whether the inhibitory effect on EGF-induced migration was because of decreased S1P or increased ceramide as a consequence of acylation of increased sphingosine by ceramide synthase, we used fumonisin B1, a specific inhibitor of ceramide synthase.	transcription
59807	2	336004	5	NULL	NULL	0	NULL	ceramide synthase	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_5	15180992	To determine whether the inhibitory effect on EGF-induced migration was because of decreased S1P or increased ceramide as a consequence of acylation of increased sphingosine by ceramide synthase, we used fumonisin B1, a specific inhibitor of ceramide synthase.	transcription
59808	3	336004	5	NULL	NULL	0	NULL	fumonisin B1			is an inhibitor of		specific			ceramide synthase					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_5	15180992	To determine whether the inhibitory effect on EGF-induced migration was because of decreased S1P or increased ceramide as a consequence of acylation of increased sphingosine by ceramide synthase, we used fumonisin B1, a specific inhibitor of ceramide synthase.	transcription
78884	1	336004	6	NULL	NULL	0	NULL	fumonisin B1	Chemical		inhibits					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_5	15180992	To determine whether the inhibitory effect on EGF-induced migration was because of decreased S1P or increased ceramide as a consequence of acylation of increased sphingosine by ceramide synthase, we used fumonisin B1, a specific inhibitor of ceramide synthase.	transcription
78885	2	336004	6	NULL	NULL	0	NULL	ceramide synthase	GP		increases					sphingosine	Chemical	acylation of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_5	15180992	To determine whether the inhibitory effect on EGF-induced migration was because of decreased S1P or increased ceramide as a consequence of acylation of increased sphingosine by ceramide synthase, we used fumonisin B1, a specific inhibitor of ceramide synthase.	transcription
59835	1	336005	5	NULL	NULL	0	NULL	ceramide	Chemical		bind		directly;;specific			CTSD	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_68	10508159	Direct and specific binding of ceramide to CTSD was additionally assessed using the radiolabeled photo-crosslinking ceramide analog, 3-trifluoromethyl-3-( m-iodophenyl) diazirine D- erythro-sphingosine ([125]TID-ceramide) as the ligand (Weber and Brunner, 1995  ).	transcription
78883	1	336005	6	NULL	NULL	0	NULL	ceramide	Chemical		bind					CTSD	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_68	10508159	Direct and specific binding of ceramide to CTSD was additionally assessed using the radiolabeled photo-crosslinking ceramide analog, 3-trifluoromethyl-3-( m-iodophenyl) diazirine D- erythro-sphingosine ([125]TID-ceramide) as the ligand (Weber and Brunner, 1995  ).	transcription
59836	1	336006	5	NULL	NULL	0	NULL	ceramide	Chemical		bind					CTSD	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_71	10508159	Labeling of CTSD with [125]TID-ceramide allowed us to perform specificity analysis of ceramide binding to CTSD using different ceramide and sphingosine isomers and various unrelated lipids.	transcription
59837	1	336007	5	NULL	NULL	0	NULL	ceramide	Chemical		does not originate from					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12724_s_10	11821388	A rise in total ceramide levels was also observed; however, ceramide did not originate from [3]sphingosine, and S1P-induced apoptosis was not inhibited by fumonisin B, precluding involvement of  de novo ceramide synthesis in apoptosis.	transcription
59838	2	336007	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					S1P	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12724_s_10	11821388	A rise in total ceramide levels was also observed; however, ceramide did not originate from [3]sphingosine, and S1P-induced apoptosis was not inhibited by fumonisin B, precluding involvement of  de novo ceramide synthesis in apoptosis.	transcription
59839	3	336007	5	NULL	NULL	0	NULL	fumonisin B	Chemical		does not inhibit					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12724_s_10	11821388	A rise in total ceramide levels was also observed; however, ceramide did not originate from [3]sphingosine, and S1P-induced apoptosis was not inhibited by fumonisin B, precluding involvement of  de novo ceramide synthesis in apoptosis.	transcription
59840	4	336007	5	NULL	NULL	0	NULL	ceramide	Chemical	de novo synthesis of	is not involved in					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12724_s_10	11821388	A rise in total ceramide levels was also observed; however, ceramide did not originate from [3]sphingosine, and S1P-induced apoptosis was not inhibited by fumonisin B, precluding involvement of  de novo ceramide synthesis in apoptosis.	transcription
78881	1	336007	6	NULL	NULL	0	NULL	ceramide	Chemical		does not originate from					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12724_s_10	11821388	A rise in total ceramide levels was also observed; however, ceramide did not originate from [3]sphingosine, and S1P-induced apoptosis was not inhibited by fumonisin B, precluding involvement of  de novo ceramide synthesis in apoptosis.	transcription
78882	2	336007	6	NULL	NULL	0	NULL	fumonisin B	Chemical		does not inhibit					S1P-induced apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12724_s_10	11821388	A rise in total ceramide levels was also observed; however, ceramide did not originate from [3]sphingosine, and S1P-induced apoptosis was not inhibited by fumonisin B, precluding involvement of  de novo ceramide synthesis in apoptosis.	transcription
59841	1	336008	5	NULL	NULL	0	NULL	ceramide	Chemical	levels of	is regulated in		tightly			DCs	Cell	human			NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-leukoc-biol_79_1_16244104_s_4	16244104	We found  that ceramide levels are tightly regulated in human DCs and that the pharmacological  inhibition of enzymes responsible for ceramide catabolism, such as ceramidases  and sphingosine kinases, sensitizes DCs to ceramide-induced cell death.	transcription
59842	2	336008	5	NULL	NULL	0	NULL	cell death	Process		is induced by					ceramide	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0560-0569_j-leukoc-biol_79_1_16244104_s_4	16244104	We found  that ceramide levels are tightly regulated in human DCs and that the pharmacological  inhibition of enzymes responsible for ceramide catabolism, such as ceramidases  and sphingosine kinases, sensitizes DCs to ceramide-induced cell death.	transcription
59843	3	336008	5	NULL	NULL	0	NULL	ceramidases	GP		is responsible for					ceramide	Chemical	catabolism of			NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-leukoc-biol_79_1_16244104_s_4	16244104	We found  that ceramide levels are tightly regulated in human DCs and that the pharmacological  inhibition of enzymes responsible for ceramide catabolism, such as ceramidases  and sphingosine kinases, sensitizes DCs to ceramide-induced cell death.	transcription
59844	4	336008	5	NULL	NULL	0	NULL	sphingosine kinases	GP		is responsible for					ceramide	Chemical	catabolism of			NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-leukoc-biol_79_1_16244104_s_4	16244104	We found  that ceramide levels are tightly regulated in human DCs and that the pharmacological  inhibition of enzymes responsible for ceramide catabolism, such as ceramidases  and sphingosine kinases, sensitizes DCs to ceramide-induced cell death.	transcription
59845	5	336008	5	NULL	NULL	0	NULL	DCs	Cell	human	is sensitive to					statement 2	Process				NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-leukoc-biol_79_1_16244104_s_4	16244104	We found  that ceramide levels are tightly regulated in human DCs and that the pharmacological  inhibition of enzymes responsible for ceramide catabolism, such as ceramidases  and sphingosine kinases, sensitizes DCs to ceramide-induced cell death.	transcription
59846	6	336008	5	NULL	NULL	0	NULL	ceramidases	GP	pharmacological inhibition of	results in					statement 5	Process				NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-leukoc-biol_79_1_16244104_s_4	16244104	We found  that ceramide levels are tightly regulated in human DCs and that the pharmacological  inhibition of enzymes responsible for ceramide catabolism, such as ceramidases  and sphingosine kinases, sensitizes DCs to ceramide-induced cell death.	transcription
59847	7	336008	5	NULL	NULL	0	NULL	sphingosine kinase	GP	pharmacological inhibition of	results in					statement 5	Process				NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-leukoc-biol_79_1_16244104_s_4	16244104	We found  that ceramide levels are tightly regulated in human DCs and that the pharmacological  inhibition of enzymes responsible for ceramide catabolism, such as ceramidases  and sphingosine kinases, sensitizes DCs to ceramide-induced cell death.	transcription
78880	1	336008	6	NULL	NULL	0	NULL	ceramide	Chemical	levels of	are regulated in					DC	cell	human			NULL		0	NULL	NULL	NULL	abs-batch0560-0569_j-leukoc-biol_79_1_16244104_s_4	16244104	We found  that ceramide levels are tightly regulated in human DCs and that the pharmacological  inhibition of enzymes responsible for ceramide catabolism, such as ceramidases  and sphingosine kinases, sensitizes DCs to ceramide-induced cell death.	transcription
59848	1	336009	5	NULL	NULL	0	NULL	C -ceramide	Chemical		stimulates					Sphingosine 1-Phosphate	Chemical	metabolism of			NULL	fibroblasts	NULL	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_208	7592842	C  -ceramide Stimulates the Metabolism of  Sphingosine 1-Phosphate by FibroblastsRecently, we  demonstrated that at least part of the mechanism by which ceramides  block the effects of PA and lyso-PA on the stimulation of DNA synthesis  and PLD activity is by interfering with the interaction of the latter  two mitogens with the cells and by increasing their rates of metabolism ( 20) .	transcription
59869	2	336009	5	NULL	NULL	0	NULL	PA	Chemical		stimulates					DNA	NucleicAcid	synthesis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_208	7592842	C  -ceramide Stimulates the Metabolism of  Sphingosine 1-Phosphate by FibroblastsRecently, we  demonstrated that at least part of the mechanism by which ceramides  block the effects of PA and lyso-PA on the stimulation of DNA synthesis  and PLD activity is by interfering with the interaction of the latter  two mitogens with the cells and by increasing their rates of metabolism ( 20) .	transcription
59870	3	336009	5	NULL	NULL	0	NULL	lyso-PA	Chemical		stimulates					DNA	NucleicAcid	synthesis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_208	7592842	C  -ceramide Stimulates the Metabolism of  Sphingosine 1-Phosphate by FibroblastsRecently, we  demonstrated that at least part of the mechanism by which ceramides  block the effects of PA and lyso-PA on the stimulation of DNA synthesis  and PLD activity is by interfering with the interaction of the latter  two mitogens with the cells and by increasing their rates of metabolism ( 20) .	transcription
59871	4	336009	5	NULL	NULL	0	NULL	ceramide	Chemical		blocks					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_208	7592842	C  -ceramide Stimulates the Metabolism of  Sphingosine 1-Phosphate by FibroblastsRecently, we  demonstrated that at least part of the mechanism by which ceramides  block the effects of PA and lyso-PA on the stimulation of DNA synthesis  and PLD activity is by interfering with the interaction of the latter  two mitogens with the cells and by increasing their rates of metabolism ( 20) .	transcription
59872	5	336009	5	NULL	NULL	0	NULL	ceramide	Chemical		blocks					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_208	7592842	C  -ceramide Stimulates the Metabolism of  Sphingosine 1-Phosphate by FibroblastsRecently, we  demonstrated that at least part of the mechanism by which ceramides  block the effects of PA and lyso-PA on the stimulation of DNA synthesis  and PLD activity is by interfering with the interaction of the latter  two mitogens with the cells and by increasing their rates of metabolism ( 20) .	transcription
59873	6	336009	5	NULL	NULL	0	NULL	PA	Chemical		stimulates					PLD	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_208	7592842	C  -ceramide Stimulates the Metabolism of  Sphingosine 1-Phosphate by FibroblastsRecently, we  demonstrated that at least part of the mechanism by which ceramides  block the effects of PA and lyso-PA on the stimulation of DNA synthesis  and PLD activity is by interfering with the interaction of the latter  two mitogens with the cells and by increasing their rates of metabolism ( 20) .	transcription
59874	7	336009	5	NULL	NULL	0	NULL	lyso-PA	Chemical		stimulates					PLD	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_208	7592842	C  -ceramide Stimulates the Metabolism of  Sphingosine 1-Phosphate by FibroblastsRecently, we  demonstrated that at least part of the mechanism by which ceramides  block the effects of PA and lyso-PA on the stimulation of DNA synthesis  and PLD activity is by interfering with the interaction of the latter  two mitogens with the cells and by increasing their rates of metabolism ( 20) .	transcription
59875	8	336009	5	NULL	NULL	0	NULL	ceramide	Chemical		blocks					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_208	7592842	C  -ceramide Stimulates the Metabolism of  Sphingosine 1-Phosphate by FibroblastsRecently, we  demonstrated that at least part of the mechanism by which ceramides  block the effects of PA and lyso-PA on the stimulation of DNA synthesis  and PLD activity is by interfering with the interaction of the latter  two mitogens with the cells and by increasing their rates of metabolism ( 20) .	transcription
59876	9	336009	5	NULL	NULL	0	NULL	ceramide	Chemical		blocks					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_208	7592842	C  -ceramide Stimulates the Metabolism of  Sphingosine 1-Phosphate by FibroblastsRecently, we  demonstrated that at least part of the mechanism by which ceramides  block the effects of PA and lyso-PA on the stimulation of DNA synthesis  and PLD activity is by interfering with the interaction of the latter  two mitogens with the cells and by increasing their rates of metabolism ( 20) .	transcription
59877	10	336009	5	NULL	NULL	0	NULL	PA	Chemical		is a type of					mitogen	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_208	7592842	C  -ceramide Stimulates the Metabolism of  Sphingosine 1-Phosphate by FibroblastsRecently, we  demonstrated that at least part of the mechanism by which ceramides  block the effects of PA and lyso-PA on the stimulation of DNA synthesis  and PLD activity is by interfering with the interaction of the latter  two mitogens with the cells and by increasing their rates of metabolism ( 20) .	transcription
59878	11	336009	5	NULL	NULL	0	NULL	lyso-PA	Chemical		is a type of					mitogen	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_208	7592842	C  -ceramide Stimulates the Metabolism of  Sphingosine 1-Phosphate by FibroblastsRecently, we  demonstrated that at least part of the mechanism by which ceramides  block the effects of PA and lyso-PA on the stimulation of DNA synthesis  and PLD activity is by interfering with the interaction of the latter  two mitogens with the cells and by increasing their rates of metabolism ( 20) .	transcription
78875	1	336009	6	NULL	NULL	0	NULL	ceramide	Chemical		stimulates					Sphingosine 1-Phosphate	Chemical	metabolism of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_208	7592842	C  -ceramide Stimulates the Metabolism of  Sphingosine 1-Phosphate by FibroblastsRecently, we  demonstrated that at least part of the mechanism by which ceramides  block the effects of PA and lyso-PA on the stimulation of DNA synthesis  and PLD activity is by interfering with the interaction of the latter  two mitogens with the cells and by increasing their rates of metabolism ( 20) .	transcription
78876	2	336009	6	NULL	NULL	0	NULL	PA	Chemical		effects					DNA	NucleicAcid	synthesis of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_208	7592842	C  -ceramide Stimulates the Metabolism of  Sphingosine 1-Phosphate by FibroblastsRecently, we  demonstrated that at least part of the mechanism by which ceramides  block the effects of PA and lyso-PA on the stimulation of DNA synthesis  and PLD activity is by interfering with the interaction of the latter  two mitogens with the cells and by increasing their rates of metabolism ( 20) .	transcription
78877	3	336009	6	NULL	NULL	0	NULL	lyso-PA	Chemical		effects					PLD	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_208	7592842	C  -ceramide Stimulates the Metabolism of  Sphingosine 1-Phosphate by FibroblastsRecently, we  demonstrated that at least part of the mechanism by which ceramides  block the effects of PA and lyso-PA on the stimulation of DNA synthesis  and PLD activity is by interfering with the interaction of the latter  two mitogens with the cells and by increasing their rates of metabolism ( 20) .	transcription
78878	4	336009	6	NULL	NULL	0	NULL	ceramide	Chemical		blocks					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_208	7592842	C  -ceramide Stimulates the Metabolism of  Sphingosine 1-Phosphate by FibroblastsRecently, we  demonstrated that at least part of the mechanism by which ceramides  block the effects of PA and lyso-PA on the stimulation of DNA synthesis  and PLD activity is by interfering with the interaction of the latter  two mitogens with the cells and by increasing their rates of metabolism ( 20) .	transcription
78879	5	336009	6	NULL	NULL	0	NULL	ceramide	Chemical		blocks					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_208	7592842	C  -ceramide Stimulates the Metabolism of  Sphingosine 1-Phosphate by FibroblastsRecently, we  demonstrated that at least part of the mechanism by which ceramides  block the effects of PA and lyso-PA on the stimulation of DNA synthesis  and PLD activity is by interfering with the interaction of the latter  two mitogens with the cells and by increasing their rates of metabolism ( 20) .	transcription
59879	1	336010	5	NULL	NULL	0	NULL	sphingosine	Chemical		is converted to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_83	10747891	It should be noted that similar to addition of sphingosine, treatment with C2-ceramide also resulted in the appearance of a late peak of endogenous ceramide (Fig.  2 B), which could be due in part to conversion of sphingosine (Fig.  1 B) to ceramide by ceramide synthase, inasmuch as fumonisin B1 was capable of inhibiting the late increase.	transcription
59880	2	336010	5	NULL	NULL	0	NULL	ceramide synthase	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_83	10747891	It should be noted that similar to addition of sphingosine, treatment with C2-ceramide also resulted in the appearance of a late peak of endogenous ceramide (Fig.  2 B), which could be due in part to conversion of sphingosine (Fig.  1 B) to ceramide by ceramide synthase, inasmuch as fumonisin B1 was capable of inhibiting the late increase.	transcription
59881	3	336010	5	NULL	NULL	0	NULL	C2-ceramide	Chemical	treatment	results in					ceramide	Chemical	appearance of;;endogenous			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_83	10747891	It should be noted that similar to addition of sphingosine, treatment with C2-ceramide also resulted in the appearance of a late peak of endogenous ceramide (Fig.  2 B), which could be due in part to conversion of sphingosine (Fig.  1 B) to ceramide by ceramide synthase, inasmuch as fumonisin B1 was capable of inhibiting the late increase.	transcription
59882	4	336010	5	NULL	NULL	0	NULL	fumonisin B1	Chemical		inhibit					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_83	10747891	It should be noted that similar to addition of sphingosine, treatment with C2-ceramide also resulted in the appearance of a late peak of endogenous ceramide (Fig.  2 B), which could be due in part to conversion of sphingosine (Fig.  1 B) to ceramide by ceramide synthase, inasmuch as fumonisin B1 was capable of inhibiting the late increase.	transcription
78872	1	336010	6	NULL	NULL	0	NULL	sphingosine	Chemical		is converted to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_83	10747891	It should be noted that similar to addition of sphingosine, treatment with C2-ceramide also resulted in the appearance of a late peak of endogenous ceramide (Fig.  2 B), which could be due in part to conversion of sphingosine (Fig.  1 B) to ceramide by ceramide synthase, inasmuch as fumonisin B1 was capable of inhibiting the late increase.	transcription
78873	2	336010	6	NULL	NULL	0	NULL	statement 1	Process		is catalyzed by					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_83	10747891	It should be noted that similar to addition of sphingosine, treatment with C2-ceramide also resulted in the appearance of a late peak of endogenous ceramide (Fig.  2 B), which could be due in part to conversion of sphingosine (Fig.  1 B) to ceramide by ceramide synthase, inasmuch as fumonisin B1 was capable of inhibiting the late increase.	transcription
78874	3	336010	6	NULL	NULL	0	NULL	fumonisin B1	Chemical		inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_83	10747891	It should be noted that similar to addition of sphingosine, treatment with C2-ceramide also resulted in the appearance of a late peak of endogenous ceramide (Fig.  2 B), which could be due in part to conversion of sphingosine (Fig.  1 B) to ceramide by ceramide synthase, inasmuch as fumonisin B1 was capable of inhibiting the late increase.	transcription
59883	1	336011	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					growth suppression	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_21_12646_s_281	8647877	In many cell systems, sphingosine and  ceramide induce similar activities such as growth suppression, and  induction of Rb dephosphorylation( 37,  62) , whereas in  other situations, sphingosine may have effects opposite to those of  ceramide such as activation of phospholipase D ( 63,  64) which is inhibited by  ceramide( 65,  66,  67,  68,  69) .	transcription
59884	2	336011	5	NULL	NULL	0	NULL	ceramide	Chemical		induce					growth suppression	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_21_12646_s_281	8647877	In many cell systems, sphingosine and  ceramide induce similar activities such as growth suppression, and  induction of Rb dephosphorylation( 37,  62) , whereas in  other situations, sphingosine may have effects opposite to those of  ceramide such as activation of phospholipase D ( 63,  64) which is inhibited by  ceramide( 65,  66,  67,  68,  69) .	transcription
59885	3	336011	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					Rb	GP	dephosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_21_12646_s_281	8647877	In many cell systems, sphingosine and  ceramide induce similar activities such as growth suppression, and  induction of Rb dephosphorylation( 37,  62) , whereas in  other situations, sphingosine may have effects opposite to those of  ceramide such as activation of phospholipase D ( 63,  64) which is inhibited by  ceramide( 65,  66,  67,  68,  69) .	transcription
59886	4	336011	5	NULL	NULL	0	NULL	ceramide	Chemical		induce					Rb	GP	dephosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_21_12646_s_281	8647877	In many cell systems, sphingosine and  ceramide induce similar activities such as growth suppression, and  induction of Rb dephosphorylation( 37,  62) , whereas in  other situations, sphingosine may have effects opposite to those of  ceramide such as activation of phospholipase D ( 63,  64) which is inhibited by  ceramide( 65,  66,  67,  68,  69) .	transcription
59887	5	336011	5	NULL	NULL	0	NULL	sphingosine	Chemical		activates					phospholipase D	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_21_12646_s_281	8647877	In many cell systems, sphingosine and  ceramide induce similar activities such as growth suppression, and  induction of Rb dephosphorylation( 37,  62) , whereas in  other situations, sphingosine may have effects opposite to those of  ceramide such as activation of phospholipase D ( 63,  64) which is inhibited by  ceramide( 65,  66,  67,  68,  69) .	transcription
59888	6	336011	5	NULL	NULL	0	NULL	ceramide	Chemical		inhibit					phospholipase D	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_21_12646_s_281	8647877	In many cell systems, sphingosine and  ceramide induce similar activities such as growth suppression, and  induction of Rb dephosphorylation( 37,  62) , whereas in  other situations, sphingosine may have effects opposite to those of  ceramide such as activation of phospholipase D ( 63,  64) which is inhibited by  ceramide( 65,  66,  67,  68,  69) .	transcription
59889	1	336012	5	NULL	NULL	0	NULL	ceramide	Chemical		metabolized to		easily			sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_146	16936207	Because ceramide is easily metabolized to sphingosine, which, in turn, is readily converted to S1P, we also determined whether sphingosine and S1P can regulate the expression of proinflammatory cytokines in adipocytes ( Figs. 5 B -  E).	transcription
59890	2	336012	5	NULL	NULL	0	NULL	sphingosine	Chemical		is converted to		readily			S1P	Chemical				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_146	16936207	Because ceramide is easily metabolized to sphingosine, which, in turn, is readily converted to S1P, we also determined whether sphingosine and S1P can regulate the expression of proinflammatory cytokines in adipocytes ( Figs. 5 B -  E).	transcription
59891	3	336012	5	NULL	NULL	0	NULL	sphingosine	Chemical		regulates		potentially			cytokines	GP	expression of;;proinflammatory			NULL	adipocytes	0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_146	16936207	Because ceramide is easily metabolized to sphingosine, which, in turn, is readily converted to S1P, we also determined whether sphingosine and S1P can regulate the expression of proinflammatory cytokines in adipocytes ( Figs. 5 B -  E).	transcription
59892	4	336012	5	NULL	NULL	0	NULL	S1P	Chemical		regulates		potentially			cytokines	GP	expression of;;proinflammatory			NULL	adipocytes	NULL	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_146	16936207	Because ceramide is easily metabolized to sphingosine, which, in turn, is readily converted to S1P, we also determined whether sphingosine and S1P can regulate the expression of proinflammatory cytokines in adipocytes ( Figs. 5 B -  E).	transcription
78870	1	336012	6	NULL	NULL	0	NULL	ceramide	Chemical		is metabolized into					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_146	16936207	Because ceramide is easily metabolized to sphingosine, which, in turn, is readily converted to S1P, we also determined whether sphingosine and S1P can regulate the expression of proinflammatory cytokines in adipocytes ( Figs. 5 B -  E).	transcription
78871	2	336012	6	NULL	NULL	0	NULL	sphingosine	Chemical		is converted to					S1P	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_146	16936207	Because ceramide is easily metabolized to sphingosine, which, in turn, is readily converted to S1P, we also determined whether sphingosine and S1P can regulate the expression of proinflammatory cytokines in adipocytes ( Figs. 5 B -  E).	transcription
59893	1	336013	5	NULL	NULL	0	NULL	gene transcription	Process		is mediated by									SRE	NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_943_s_167	15132973	32,36  SRE-mediated gene transcription and mature SREBP levels are increased when ceramide synthesis is increased by sphingosine either added exogenously or increased endogenously through inhibition of sphingosine kinase ( Figure 4).	transcription
59899	2	336013	5	NULL	NULL	0	NULL	sphingosine	Chemical	addition of;;exogenous	increases					ceramide	Chemical	synthesis of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_943_s_167	15132973	32,36  SRE-mediated gene transcription and mature SREBP levels are increased when ceramide synthesis is increased by sphingosine either added exogenously or increased endogenously through inhibition of sphingosine kinase ( Figure 4).	transcription
59901	3	336013	5	NULL	NULL	0	NULL	sphingosine kinase	Chemical		increases		endogenously			ceramide	Chemical	synthesis of			NULL		NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_943_s_167	15132973	32,36  SRE-mediated gene transcription and mature SREBP levels are increased when ceramide synthesis is increased by sphingosine either added exogenously or increased endogenously through inhibition of sphingosine kinase ( Figure 4).	transcription
59904	4	336013	5	NULL	NULL	0	NULL	statement 2	Process		increases					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_943_s_167	15132973	32,36  SRE-mediated gene transcription and mature SREBP levels are increased when ceramide synthesis is increased by sphingosine either added exogenously or increased endogenously through inhibition of sphingosine kinase ( Figure 4).	transcription
60048	5	336013	5	NULL	NULL	0	NULL	statement 3	Process		occurs through					sphingosine kinase	GP	inhibition of			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_943_s_167	15132973	32,36  SRE-mediated gene transcription and mature SREBP levels are increased when ceramide synthesis is increased by sphingosine either added exogenously or increased endogenously through inhibition of sphingosine kinase ( Figure 4).	transcription
60049	6	336013	5	NULL	NULL	0	NULL	statement 3	Process		increases					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_943_s_167	15132973	32,36  SRE-mediated gene transcription and mature SREBP levels are increased when ceramide synthesis is increased by sphingosine either added exogenously or increased endogenously through inhibition of sphingosine kinase ( Figure 4).	transcription
60050	7	336013	5	NULL	NULL	0	NULL	statement 2	Process		increases					SREBP	GP	level of;;mature			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_943_s_167	15132973	32,36  SRE-mediated gene transcription and mature SREBP levels are increased when ceramide synthesis is increased by sphingosine either added exogenously or increased endogenously through inhibition of sphingosine kinase ( Figure 4).	transcription
60051	8	336013	5	NULL	NULL	0	NULL	statement 3	Process		increases					SREBP	GP	level of;;mature			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_943_s_167	15132973	32,36  SRE-mediated gene transcription and mature SREBP levels are increased when ceramide synthesis is increased by sphingosine either added exogenously or increased endogenously through inhibition of sphingosine kinase ( Figure 4).	transcription
78867	1	336013	6	NULL	NULL	0	NULL	sphingosine	Chemical		increases					ceramide	Chemical	synthesis of 			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_943_s_167	15132973	32,36  SRE-mediated gene transcription and mature SREBP levels are increased when ceramide synthesis is increased by sphingosine either added exogenously or increased endogenously through inhibition of sphingosine kinase ( Figure 4).	transcription
78868	2	336013	6	NULL	NULL	0	NULL	statement 1	Process		increases					SREBP	GP	levels of 			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_943_s_167	15132973	32,36  SRE-mediated gene transcription and mature SREBP levels are increased when ceramide synthesis is increased by sphingosine either added exogenously or increased endogenously through inhibition of sphingosine kinase ( Figure 4).	transcription
78869	3	336013	6	NULL	NULL	0	NULL	sphingosine kinase	GP	inhibition of 	increases					ceramide	Chemical	synthesis of 			NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_24_5_943_s_167	15132973	32,36  SRE-mediated gene transcription and mature SREBP levels are increased when ceramide synthesis is increased by sphingosine either added exogenously or increased endogenously through inhibition of sphingosine kinase ( Figure 4).	transcription
60052	1	336014	5	NULL	NULL	0	NULL	TNF-alpha	GP		induce					ceramide	Chemical	change in;;level of			NULL	HUVECs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_31	16269668	ctivation of N-SMase and sphingosine-kinase (SK) and changes in ceramide, sphingosine, and Sph1P levels induced by TNF-alpha are time dependent and precede activation of Akt and eNOS in HUVECs.	transcription
60053	2	336014	5	NULL	NULL	0	NULL	TNF-alpha	GP		induce					sphingosine	Chemical	change in;;level of			NULL	HUVECs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_31	16269668	ctivation of N-SMase and sphingosine-kinase (SK) and changes in ceramide, sphingosine, and Sph1P levels induced by TNF-alpha are time dependent and precede activation of Akt and eNOS in HUVECs.	transcription
60054	3	336014	5	NULL	NULL	0	NULL	TNF-alpha	GP		induce					Sph1P	Chemical	change in;;level of			NULL	HUVECs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_31	16269668	ctivation of N-SMase and sphingosine-kinase (SK) and changes in ceramide, sphingosine, and Sph1P levels induced by TNF-alpha are time dependent and precede activation of Akt and eNOS in HUVECs.	transcription
60055	4	336014	5	NULL	NULL	0	NULL	statement 1	Process		precede					Akt	GP	activation of			NULL	HUVECs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_31	16269668	ctivation of N-SMase and sphingosine-kinase (SK) and changes in ceramide, sphingosine, and Sph1P levels induced by TNF-alpha are time dependent and precede activation of Akt and eNOS in HUVECs.	transcription
60056	5	336014	5	NULL	NULL	0	NULL	statement 1	Process		precede					eNOS	GP	activation of			NULL	HUVECs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_31	16269668	ctivation of N-SMase and sphingosine-kinase (SK) and changes in ceramide, sphingosine, and Sph1P levels induced by TNF-alpha are time dependent and precede activation of Akt and eNOS in HUVECs.	transcription
60057	6	336014	5	NULL	NULL	0	NULL	statement 2	Process		precede					Akt	GP	activation of			NULL	HUVECs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_31	16269668	ctivation of N-SMase and sphingosine-kinase (SK) and changes in ceramide, sphingosine, and Sph1P levels induced by TNF-alpha are time dependent and precede activation of Akt and eNOS in HUVECs.	transcription
60058	7	336014	5	NULL	NULL	0	NULL	statement 2	Process		precede					eNOS	GP	activation of			NULL	HUVECs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_31	16269668	ctivation of N-SMase and sphingosine-kinase (SK) and changes in ceramide, sphingosine, and Sph1P levels induced by TNF-alpha are time dependent and precede activation of Akt and eNOS in HUVECs.	transcription
60059	8	336014	5	NULL	NULL	0	NULL	statement 3	Process		precede					Akt	GP	activation of			NULL	HUVECs	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_31	16269668	ctivation of N-SMase and sphingosine-kinase (SK) and changes in ceramide, sphingosine, and Sph1P levels induced by TNF-alpha are time dependent and precede activation of Akt and eNOS in HUVECs.	transcription
60060	9	336014	5	NULL	NULL	0	NULL	statement 3	Process		precede					eNOS	GP	activation of			NULL	HUVECs	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_31	16269668	ctivation of N-SMase and sphingosine-kinase (SK) and changes in ceramide, sphingosine, and Sph1P levels induced by TNF-alpha are time dependent and precede activation of Akt and eNOS in HUVECs.	transcription
60061	10	336014	5	NULL	NULL	0	NULL	N-SMase	GP	activation of	precede					Akt	GP	activation of			NULL	HUVECs	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_31	16269668	ctivation of N-SMase and sphingosine-kinase (SK) and changes in ceramide, sphingosine, and Sph1P levels induced by TNF-alpha are time dependent and precede activation of Akt and eNOS in HUVECs.	transcription
60062	11	336014	5	NULL	NULL	0	NULL	N-SMase	GP	activation of	precede					eNOS	GP	activation of			NULL	HUVECs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_31	16269668	ctivation of N-SMase and sphingosine-kinase (SK) and changes in ceramide, sphingosine, and Sph1P levels induced by TNF-alpha are time dependent and precede activation of Akt and eNOS in HUVECs.	transcription
60063	12	336014	5	NULL	NULL	0	NULL	sphingosine-kinase	GP	activation of	precede					Akt	GP	activation of			NULL	HUVECs	NULL	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_31	16269668	ctivation of N-SMase and sphingosine-kinase (SK) and changes in ceramide, sphingosine, and Sph1P levels induced by TNF-alpha are time dependent and precede activation of Akt and eNOS in HUVECs.	transcription
60064	13	336014	5	NULL	NULL	0	NULL	sphingosine-kinase	GP	activation of	precede					eNOS	GP	activation of			NULL	HUVECs	0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_31	16269668	ctivation of N-SMase and sphingosine-kinase (SK) and changes in ceramide, sphingosine, and Sph1P levels induced by TNF-alpha are time dependent and precede activation of Akt and eNOS in HUVECs.	transcription
60065	14	336014	5	NULL	NULL	0	NULL	SK	GP		is					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_31	16269668	ctivation of N-SMase and sphingosine-kinase (SK) and changes in ceramide, sphingosine, and Sph1P levels induced by TNF-alpha are time dependent and precede activation of Akt and eNOS in HUVECs.	transcription
78864	1	336014	6	NULL	NULL	0	NULL	TNF-alpha	GP		induces					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_31	16269668	ctivation of N-SMase and sphingosine-kinase (SK) and changes in ceramide, sphingosine, and Sph1P levels induced by TNF-alpha are time dependent and precede activation of Akt and eNOS in HUVECs.	transcription
78865	2	336014	6	NULL	NULL	0	NULL	TNF-alpha	GP		induces					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_31	16269668	ctivation of N-SMase and sphingosine-kinase (SK) and changes in ceramide, sphingosine, and Sph1P levels induced by TNF-alpha are time dependent and precede activation of Akt and eNOS in HUVECs.	transcription
78866	3	336014	6	NULL	NULL	0	NULL	TNF-alpha	GP		induces					Sph1P	GP				NULL		0	NULL	NULL	NULL	gw70_arterthrombvascbiol_26_1_99_s_31	16269668	ctivation of N-SMase and sphingosine-kinase (SK) and changes in ceramide, sphingosine, and Sph1P levels induced by TNF-alpha are time dependent and precede activation of Akt and eNOS in HUVECs.	transcription
60066	1	336015	5	NULL	NULL	0	NULL	S1P	Chemical		is generated by					sphingosine kinase	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34541_s_203	12815058	Tipping  the balance toward S1P generation by sphingosine kinase activation precludes  induction of apoptosis ( ),  whereas overexpression of SPPase leads to the breakdown of S1P into  sphingosine and ceramide, thereby promoting induction of apoptosis  ( ).	transcription
60067	2	336015	5	NULL	NULL	0	NULL	statement 1	Process		precludes					apoptosis	Process	induction of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34541_s_203	12815058	Tipping  the balance toward S1P generation by sphingosine kinase activation precludes  induction of apoptosis ( ),  whereas overexpression of SPPase leads to the breakdown of S1P into  sphingosine and ceramide, thereby promoting induction of apoptosis  ( ).	transcription
60068	3	336015	5	NULL	NULL	0	NULL	S1P	Chemical		broken down into					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34541_s_203	12815058	Tipping  the balance toward S1P generation by sphingosine kinase activation precludes  induction of apoptosis ( ),  whereas overexpression of SPPase leads to the breakdown of S1P into  sphingosine and ceramide, thereby promoting induction of apoptosis  ( ).	transcription
60069	4	336015	5	NULL	NULL	0	NULL	S1P	Chemical		broken down into					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34541_s_203	12815058	Tipping  the balance toward S1P generation by sphingosine kinase activation precludes  induction of apoptosis ( ),  whereas overexpression of SPPase leads to the breakdown of S1P into  sphingosine and ceramide, thereby promoting induction of apoptosis  ( ).	transcription
60070	5	336015	5	NULL	NULL	0	NULL	statement 3	Process		occurs along with					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34541_s_203	12815058	Tipping  the balance toward S1P generation by sphingosine kinase activation precludes  induction of apoptosis ( ),  whereas overexpression of SPPase leads to the breakdown of S1P into  sphingosine and ceramide, thereby promoting induction of apoptosis  ( ).	transcription
60071	6	336015	5	NULL	NULL	0	NULL	SPPase	GP	overexpression of	leads to					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34541_s_203	12815058	Tipping  the balance toward S1P generation by sphingosine kinase activation precludes  induction of apoptosis ( ),  whereas overexpression of SPPase leads to the breakdown of S1P into  sphingosine and ceramide, thereby promoting induction of apoptosis  ( ).	transcription
60072	7	336015	5	NULL	NULL	0	NULL	statement 6	Process		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34541_s_203	12815058	Tipping  the balance toward S1P generation by sphingosine kinase activation precludes  induction of apoptosis ( ),  whereas overexpression of SPPase leads to the breakdown of S1P into  sphingosine and ceramide, thereby promoting induction of apoptosis  ( ).	transcription
78858	1	336015	6	NULL	NULL	NULL	NULL	sphingosine kinase	GP	activation of	generates					S1P	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_36_34541_s_203	12815058	Tipping  the balance toward S1P generation by sphingosine kinase activation precludes  induction of apoptosis ( ),  whereas overexpression of SPPase leads to the breakdown of S1P into  sphingosine and ceramide, thereby promoting induction of apoptosis  ( ).	transcription
78859	2	336015	6	NULL	NULL	0	NULL	statement 1	Process		precludes					apoptosis	Process	induction of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34541_s_203	12815058	Tipping  the balance toward S1P generation by sphingosine kinase activation precludes  induction of apoptosis ( ),  whereas overexpression of SPPase leads to the breakdown of S1P into  sphingosine and ceramide, thereby promoting induction of apoptosis  ( ).	transcription
78860	3	336015	6	NULL	NULL	0	NULL	S1P	GP		generates					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34541_s_203	12815058	Tipping  the balance toward S1P generation by sphingosine kinase activation precludes  induction of apoptosis ( ),  whereas overexpression of SPPase leads to the breakdown of S1P into  sphingosine and ceramide, thereby promoting induction of apoptosis  ( ).	transcription
78861	4	336015	6	NULL	NULL	0	NULL	S1P	Chemical		generates					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34541_s_203	12815058	Tipping  the balance toward S1P generation by sphingosine kinase activation precludes  induction of apoptosis ( ),  whereas overexpression of SPPase leads to the breakdown of S1P into  sphingosine and ceramide, thereby promoting induction of apoptosis  ( ).	transcription
78862	6	336015	6	NULL	NULL	0	NULL	SPPase	GP	overexpression of	leads to					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34541_s_203	12815058	Tipping  the balance toward S1P generation by sphingosine kinase activation precludes  induction of apoptosis ( ),  whereas overexpression of SPPase leads to the breakdown of S1P into  sphingosine and ceramide, thereby promoting induction of apoptosis  ( ).	transcription
78863	5	336015	6	NULL	NULL	0	NULL	statement 3	Process		occurs simultaneously with					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_36_34541_s_203	12815058	Tipping  the balance toward S1P generation by sphingosine kinase activation precludes  induction of apoptosis ( ),  whereas overexpression of SPPase leads to the breakdown of S1P into  sphingosine and ceramide, thereby promoting induction of apoptosis  ( ).	transcription
60073	1	336016	5	NULL	NULL	0	NULL	SPC	Chemical		is an analog of					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_317_2_685_s_113	16415087	Of the sphingosine analogs tested, SPC and dihydrosphingosine 1-phosphate (at concentrations of 5 muM) were as effective as S1P, whereas the addition of sphingosine, dihydrosphingosine, dimethylsphingosine, or ceramide had little or no effect on taurine efflux ( Table 1).	transcription
60074	2	336016	5	NULL	NULL	0	NULL	dihydrosphingosine 1-phosphate	Chemical		is an analog of					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_317_2_685_s_113	16415087	Of the sphingosine analogs tested, SPC and dihydrosphingosine 1-phosphate (at concentrations of 5 muM) were as effective as S1P, whereas the addition of sphingosine, dihydrosphingosine, dimethylsphingosine, or ceramide had little or no effect on taurine efflux ( Table 1).	transcription
60075	3	336016	5	NULL	NULL	0	NULL	SPC	Chemical		is as effective as					S1P	Chemical				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_317_2_685_s_113	16415087	Of the sphingosine analogs tested, SPC and dihydrosphingosine 1-phosphate (at concentrations of 5 muM) were as effective as S1P, whereas the addition of sphingosine, dihydrosphingosine, dimethylsphingosine, or ceramide had little or no effect on taurine efflux ( Table 1).	transcription
60076	4	336016	5	NULL	NULL	0	NULL	dihydrosphingosine 1-phosphate	Chemical		is as effective as					S1P	Chemical				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_317_2_685_s_113	16415087	Of the sphingosine analogs tested, SPC and dihydrosphingosine 1-phosphate (at concentrations of 5 muM) were as effective as S1P, whereas the addition of sphingosine, dihydrosphingosine, dimethylsphingosine, or ceramide had little or no effect on taurine efflux ( Table 1).	transcription
60077	5	336016	5	NULL	NULL	0	NULL	sphingosine	Chemical		does not effect					taurine	Chemical	efflux of			NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_317_2_685_s_113	16415087	Of the sphingosine analogs tested, SPC and dihydrosphingosine 1-phosphate (at concentrations of 5 muM) were as effective as S1P, whereas the addition of sphingosine, dihydrosphingosine, dimethylsphingosine, or ceramide had little or no effect on taurine efflux ( Table 1).	transcription
60091	6	336016	5	NULL	NULL	0	NULL	dihydrosphingosine	Chemical		does not effect					taurine	Chemical	efflux of			NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_317_2_685_s_113	16415087	Of the sphingosine analogs tested, SPC and dihydrosphingosine 1-phosphate (at concentrations of 5 muM) were as effective as S1P, whereas the addition of sphingosine, dihydrosphingosine, dimethylsphingosine, or ceramide had little or no effect on taurine efflux ( Table 1).	transcription
60092	7	336016	5	NULL	NULL	0	NULL	dimethylsphingosine	Chemical		does not effect					taurine	Chemical	efflux of			NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_317_2_685_s_113	16415087	Of the sphingosine analogs tested, SPC and dihydrosphingosine 1-phosphate (at concentrations of 5 muM) were as effective as S1P, whereas the addition of sphingosine, dihydrosphingosine, dimethylsphingosine, or ceramide had little or no effect on taurine efflux ( Table 1).	transcription
60093	8	336016	5	NULL	NULL	0	NULL	ceramide	Chemical		does not effect					taurine	Chemical	efflux of			NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_317_2_685_s_113	16415087	Of the sphingosine analogs tested, SPC and dihydrosphingosine 1-phosphate (at concentrations of 5 muM) were as effective as S1P, whereas the addition of sphingosine, dihydrosphingosine, dimethylsphingosine, or ceramide had little or no effect on taurine efflux ( Table 1).	transcription
60101	1	336018	5	NULL	NULL	0	NULL	ceramide	Chemical		is synthesized from					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_febslett_425_1_61_s_48	9541007	As we previously reported [ 8, blocking ceramide synthesis from sphingosine by the addition of the fungal agent Fumonisin B1 (25  M) did not inhibit sphingosine from inducing apoptosis ( Fig. 1A).	transcription
60102	2	336018	5	NULL	NULL	0	NULL	Fumonisin B1	Chemical		blocks					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_425_1_61_s_48	9541007	As we previously reported [ 8, blocking ceramide synthesis from sphingosine by the addition of the fungal agent Fumonisin B1 (25  M) did not inhibit sphingosine from inducing apoptosis ( Fig. 1A).	transcription
60103	3	336018	5	NULL	NULL	0	NULL	Fumonisin B1	Chemical		is a type of					fungal agent	Chemical				NULL		0	NULL	NULL	NULL	gw60_febslett_425_1_61_s_48	9541007	As we previously reported [ 8, blocking ceramide synthesis from sphingosine by the addition of the fungal agent Fumonisin B1 (25  M) did not inhibit sphingosine from inducing apoptosis ( Fig. 1A).	transcription
60104	4	336018	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_febslett_425_1_61_s_48	9541007	As we previously reported [ 8, blocking ceramide synthesis from sphingosine by the addition of the fungal agent Fumonisin B1 (25  M) did not inhibit sphingosine from inducing apoptosis ( Fig. 1A).	transcription
60105	5	336018	5	NULL	NULL	0	NULL	statement 2	Process		does not inhibit					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_425_1_61_s_48	9541007	As we previously reported [ 8, blocking ceramide synthesis from sphingosine by the addition of the fungal agent Fumonisin B1 (25  M) did not inhibit sphingosine from inducing apoptosis ( Fig. 1A).	transcription
78847	1	336018	6	NULL	NULL	0	NULL	sphingosine	Chemical		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_425_1_61_s_48	9541007	As we previously reported [ 8, blocking ceramide synthesis from sphingosine by the addition of the fungal agent Fumonisin B1 (25  M) did not inhibit sphingosine from inducing apoptosis ( Fig. 1A).	transcription
78848	2	336018	6	NULL	NULL	0	NULL	sphingosine 	Chemical		induces					ceramide	Chemical	synthesis of 			NULL		0	NULL	NULL	NULL	gw60_febslett_425_1_61_s_48	9541007	As we previously reported [ 8, blocking ceramide synthesis from sphingosine by the addition of the fungal agent Fumonisin B1 (25  M) did not inhibit sphingosine from inducing apoptosis ( Fig. 1A).	transcription
78849	3	336018	6	NULL	NULL	0	NULL	Fumonisin B1	Chemical		blocks					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_425_1_61_s_48	9541007	As we previously reported [ 8, blocking ceramide synthesis from sphingosine by the addition of the fungal agent Fumonisin B1 (25  M) did not inhibit sphingosine from inducing apoptosis ( Fig. 1A).	transcription
78850	4	336018	6	NULL	NULL	0	NULL	statement 3	Process		does not inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_425_1_61_s_48	9541007	As we previously reported [ 8, blocking ceramide synthesis from sphingosine by the addition of the fungal agent Fumonisin B1 (25  M) did not inhibit sphingosine from inducing apoptosis ( Fig. 1A).	transcription
60106	1	336019	5	NULL	NULL	0	NULL	ceramide	Chemical		is converted to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_170	10051135	Therefore there appears to be a link between the sphingosine and cyclo-oxygenase pathways in the TNF-mediated coronary constriction, but the direct cardiac depressant actions of TNF are dependant on the conversion of ceramide of sphingosine, and do not involve the cyclo-oxygenase pathway.	transcription
60107	2	336019	5	NULL	NULL	0	NULL	TNF	GP	direct cardiac depressant actions of	is dependent on					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_170	10051135	Therefore there appears to be a link between the sphingosine and cyclo-oxygenase pathways in the TNF-mediated coronary constriction, but the direct cardiac depressant actions of TNF are dependant on the conversion of ceramide of sphingosine, and do not involve the cyclo-oxygenase pathway.	transcription
60108	3	336019	5	NULL	NULL	0	NULL	TNF	GP	direct cardiac depressant actions of	does not involve					cyclo-oxygenase pathway	Process				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_170	10051135	Therefore there appears to be a link between the sphingosine and cyclo-oxygenase pathways in the TNF-mediated coronary constriction, but the direct cardiac depressant actions of TNF are dependant on the conversion of ceramide of sphingosine, and do not involve the cyclo-oxygenase pathway.	transcription
60109	4	336019	5	NULL	NULL	0	NULL	TNF	GP		mediates					coronary constriction	Process				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_170	10051135	Therefore there appears to be a link between the sphingosine and cyclo-oxygenase pathways in the TNF-mediated coronary constriction, but the direct cardiac depressant actions of TNF are dependant on the conversion of ceramide of sphingosine, and do not involve the cyclo-oxygenase pathway.	transcription
60110	5	336019	5	NULL	NULL	0	NULL	sphingosine	Chemical		is linked to		possibly			cyclo-oxygenase pathway	Process				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_170	10051135	Therefore there appears to be a link between the sphingosine and cyclo-oxygenase pathways in the TNF-mediated coronary constriction, but the direct cardiac depressant actions of TNF are dependant on the conversion of ceramide of sphingosine, and do not involve the cyclo-oxygenase pathway.	transcription
78843	1	336019	6	NULL	NULL	0	NULL	TNF	GP		depresses					cardiac actions	Process				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_170	10051135	Therefore there appears to be a link between the sphingosine and cyclo-oxygenase pathways in the TNF-mediated coronary constriction, but the direct cardiac depressant actions of TNF are dependant on the conversion of ceramide of sphingosine, and do not involve the cyclo-oxygenase pathway.	transcription
78844	2	336019	6	NULL	NULL	0	NULL	statement 1	Process		does not involve					cyclo-oxygenase pathway	Process				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_170	10051135	Therefore there appears to be a link between the sphingosine and cyclo-oxygenase pathways in the TNF-mediated coronary constriction, but the direct cardiac depressant actions of TNF are dependant on the conversion of ceramide of sphingosine, and do not involve the cyclo-oxygenase pathway.	transcription
78845	3	336019	6	NULL	NULL	0	NULL	ceramide	Chemical		is converted to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_170	10051135	Therefore there appears to be a link between the sphingosine and cyclo-oxygenase pathways in the TNF-mediated coronary constriction, but the direct cardiac depressant actions of TNF are dependant on the conversion of ceramide of sphingosine, and do not involve the cyclo-oxygenase pathway.	transcription
78846	4	336019	6	NULL	NULL	0	NULL	statement 1	Process		is dependent on					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_170	10051135	Therefore there appears to be a link between the sphingosine and cyclo-oxygenase pathways in the TNF-mediated coronary constriction, but the direct cardiac depressant actions of TNF are dependant on the conversion of ceramide of sphingosine, and do not involve the cyclo-oxygenase pathway.	transcription
60111	1	336020	5	NULL	NULL	0	NULL	S1P	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_254	12138095	Whereas S1P-induced apoptosis was caspase-dependent, the cytotoxic effect of sphingosine was caspase-independent, raising the possibility that sphingosine may trigger apoptosis via a caspase-independent release of apoptosis-inducing factor, as described for ceramide in lymphoid cells ( 31).	transcription
60112	2	336020	5	NULL	NULL	0	NULL	statement 1			is dependent on					caspase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_254	12138095	Whereas S1P-induced apoptosis was caspase-dependent, the cytotoxic effect of sphingosine was caspase-independent, raising the possibility that sphingosine may trigger apoptosis via a caspase-independent release of apoptosis-inducing factor, as described for ceramide in lymphoid cells ( 31).	transcription
60113	3	336020	5	NULL	NULL	0	NULL	sphingosine	Chemical	cytotoxic effect of	is independent of					caspase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_254	12138095	Whereas S1P-induced apoptosis was caspase-dependent, the cytotoxic effect of sphingosine was caspase-independent, raising the possibility that sphingosine may trigger apoptosis via a caspase-independent release of apoptosis-inducing factor, as described for ceramide in lymphoid cells ( 31).	transcription
60114	4	336020	5	NULL	NULL	0	NULL	sphingosine	Chemical		triggers		may			apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_254	12138095	Whereas S1P-induced apoptosis was caspase-dependent, the cytotoxic effect of sphingosine was caspase-independent, raising the possibility that sphingosine may trigger apoptosis via a caspase-independent release of apoptosis-inducing factor, as described for ceramide in lymphoid cells ( 31).	transcription
60115	5	336020	5	NULL	NULL	0	NULL	apoptosis-inducing factor	Chemical	release of	is independent of					caspase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_254	12138095	Whereas S1P-induced apoptosis was caspase-dependent, the cytotoxic effect of sphingosine was caspase-independent, raising the possibility that sphingosine may trigger apoptosis via a caspase-independent release of apoptosis-inducing factor, as described for ceramide in lymphoid cells ( 31).	transcription
60116	6	336020	5	NULL	NULL	0	NULL	statement 4	Process		via					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_254	12138095	Whereas S1P-induced apoptosis was caspase-dependent, the cytotoxic effect of sphingosine was caspase-independent, raising the possibility that sphingosine may trigger apoptosis via a caspase-independent release of apoptosis-inducing factor, as described for ceramide in lymphoid cells ( 31).	transcription
60117	7	336020	5	NULL	NULL	0	NULL	ceramide	Chemical		triggers					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_254	12138095	Whereas S1P-induced apoptosis was caspase-dependent, the cytotoxic effect of sphingosine was caspase-independent, raising the possibility that sphingosine may trigger apoptosis via a caspase-independent release of apoptosis-inducing factor, as described for ceramide in lymphoid cells ( 31).	transcription
60118	8	336020	5	NULL	NULL	0	NULL	statement 7	Process		via					statement 5	Process				NULL	lymphoid cells	0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_254	12138095	Whereas S1P-induced apoptosis was caspase-dependent, the cytotoxic effect of sphingosine was caspase-independent, raising the possibility that sphingosine may trigger apoptosis via a caspase-independent release of apoptosis-inducing factor, as described for ceramide in lymphoid cells ( 31).	transcription
78839	1	336020	6	NULL	NULL	0	NULL	S1P	GP		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_254	12138095	Whereas S1P-induced apoptosis was caspase-dependent, the cytotoxic effect of sphingosine was caspase-independent, raising the possibility that sphingosine may trigger apoptosis via a caspase-independent release of apoptosis-inducing factor, as described for ceramide in lymphoid cells ( 31).	transcription
78840	2	336020	6	NULL	NULL	0	NULL	statement 1	Process		is dependent on					caspase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_254	12138095	Whereas S1P-induced apoptosis was caspase-dependent, the cytotoxic effect of sphingosine was caspase-independent, raising the possibility that sphingosine may trigger apoptosis via a caspase-independent release of apoptosis-inducing factor, as described for ceramide in lymphoid cells ( 31).	transcription
78841	3	336020	6	NULL	NULL	0	NULL	sphingosine	Chemical		exhibits					cytotoxic effect	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_254	12138095	Whereas S1P-induced apoptosis was caspase-dependent, the cytotoxic effect of sphingosine was caspase-independent, raising the possibility that sphingosine may trigger apoptosis via a caspase-independent release of apoptosis-inducing factor, as described for ceramide in lymphoid cells ( 31).	transcription
78842	4	336020	6	NULL	NULL	0	NULL	statement 3	Process		does not depend on					caspase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_254	12138095	Whereas S1P-induced apoptosis was caspase-dependent, the cytotoxic effect of sphingosine was caspase-independent, raising the possibility that sphingosine may trigger apoptosis via a caspase-independent release of apoptosis-inducing factor, as described for ceramide in lymphoid cells ( 31).	transcription
60119	1	336021	5	NULL	NULL	0	NULL	TNF signaling	Process		via					sphingolipids	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_7996_s_19	11777919	TNF signaling via sphingolipids is exemplified by two distinct pathways: the formation of ceramide resulting from the activation of sphingomyelinase or  de novo synthesis and the production of sphingosine 1-phosphate (S1P) upon sphingosine kinase (SphK) activation.	transcription
60120	2	336021	5	NULL	NULL	0	NULL	sphingomyelinase	Chemical	activation of	results in					ceramide	Chemical	fomation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_7996_s_19	11777919	TNF signaling via sphingolipids is exemplified by two distinct pathways: the formation of ceramide resulting from the activation of sphingomyelinase or  de novo synthesis and the production of sphingosine 1-phosphate (S1P) upon sphingosine kinase (SphK) activation.	transcription
60121	3	336021	5	NULL	NULL	0	NULL	statement 2	Process		exemplifies					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_7996_s_19	11777919	TNF signaling via sphingolipids is exemplified by two distinct pathways: the formation of ceramide resulting from the activation of sphingomyelinase or  de novo synthesis and the production of sphingosine 1-phosphate (S1P) upon sphingosine kinase (SphK) activation.	transcription
60122	4	336021	5	NULL	NULL	0	NULL	SphK	GP	activation of	produce					S1P	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_7996_s_19	11777919	TNF signaling via sphingolipids is exemplified by two distinct pathways: the formation of ceramide resulting from the activation of sphingomyelinase or  de novo synthesis and the production of sphingosine 1-phosphate (S1P) upon sphingosine kinase (SphK) activation.	transcription
60123	5	336021	5	NULL	NULL	0	NULL	statement 4	Process		exemplifies					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_7996_s_19	11777919	TNF signaling via sphingolipids is exemplified by two distinct pathways: the formation of ceramide resulting from the activation of sphingomyelinase or  de novo synthesis and the production of sphingosine 1-phosphate (S1P) upon sphingosine kinase (SphK) activation.	transcription
60124	6	336021	5	NULL	NULL	0	NULL	SphK	GP		is					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_7996_s_19	11777919	TNF signaling via sphingolipids is exemplified by two distinct pathways: the formation of ceramide resulting from the activation of sphingomyelinase or  de novo synthesis and the production of sphingosine 1-phosphate (S1P) upon sphingosine kinase (SphK) activation.	transcription
60125	7	336021	5	NULL	NULL	0	NULL	S1P	Chemical		is					sphingosine 1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_7996_s_19	11777919	TNF signaling via sphingolipids is exemplified by two distinct pathways: the formation of ceramide resulting from the activation of sphingomyelinase or  de novo synthesis and the production of sphingosine 1-phosphate (S1P) upon sphingosine kinase (SphK) activation.	transcription
78835	1	336021	6	NULL	NULL	0	NULL	sphingomyelinase	GP	activation of	results in					ceramide	Chemical	formation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_7996_s_19	11777919	TNF signaling via sphingolipids is exemplified by two distinct pathways: the formation of ceramide resulting from the activation of sphingomyelinase or  de novo synthesis and the production of sphingosine 1-phosphate (S1P) upon sphingosine kinase (SphK) activation.	transcription
78836	2	336021	6	NULL	NULL	0	NULL	S1P	Chemical		is					sphingosine 1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_7996_s_19	11777919	TNF signaling via sphingolipids is exemplified by two distinct pathways: the formation of ceramide resulting from the activation of sphingomyelinase or  de novo synthesis and the production of sphingosine 1-phosphate (S1P) upon sphingosine kinase (SphK) activation.	transcription
78837	3	336021	6	NULL	NULL	0	NULL	SphK	GP		is					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_7996_s_19	11777919	TNF signaling via sphingolipids is exemplified by two distinct pathways: the formation of ceramide resulting from the activation of sphingomyelinase or  de novo synthesis and the production of sphingosine 1-phosphate (S1P) upon sphingosine kinase (SphK) activation.	transcription
78838	4	336021	6	NULL	NULL	0	NULL	SphK	GP	activation of	results in					S1P	GP	production of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_10_7996_s_19	11777919	TNF signaling via sphingolipids is exemplified by two distinct pathways: the formation of ceramide resulting from the activation of sphingomyelinase or  de novo synthesis and the production of sphingosine 1-phosphate (S1P) upon sphingosine kinase (SphK) activation.	transcription
60126	1	336022	5	NULL	NULL	0	NULL	ceramide	Chemical	elevation of	is induced by					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_82	10747891	Moreover, a higher concentration of fumonisin B1 (100 muM) not only inhibited elevation of ceramide induced by 5 muM sphingosine by more than 70% after 5 h of treatment, it also markedly enhanced apoptosis induced by sphingosine.	transcription
60127	2	336022	5	NULL	NULL	0	NULL	fumonisin B1	Chemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_82	10747891	Moreover, a higher concentration of fumonisin B1 (100 muM) not only inhibited elevation of ceramide induced by 5 muM sphingosine by more than 70% after 5 h of treatment, it also markedly enhanced apoptosis induced by sphingosine.	transcription
60128	3	336022	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_82	10747891	Moreover, a higher concentration of fumonisin B1 (100 muM) not only inhibited elevation of ceramide induced by 5 muM sphingosine by more than 70% after 5 h of treatment, it also markedly enhanced apoptosis induced by sphingosine.	transcription
60129	4	336022	5	NULL	NULL	0	NULL	fumonisin B1	Chemical		enhances		markedly			statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_82	10747891	Moreover, a higher concentration of fumonisin B1 (100 muM) not only inhibited elevation of ceramide induced by 5 muM sphingosine by more than 70% after 5 h of treatment, it also markedly enhanced apoptosis induced by sphingosine.	transcription
78832	1	336022	6	NULL	NULL	0	NULL	sphingosine	Chemical		induces					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_82	10747891	Moreover, a higher concentration of fumonisin B1 (100 muM) not only inhibited elevation of ceramide induced by 5 muM sphingosine by more than 70% after 5 h of treatment, it also markedly enhanced apoptosis induced by sphingosine.	transcription
78833	2	336022	6	NULL	NULL	0	NULL	fumonisin B1 	Chemical		inhibits					ceramide	Chemical	elevation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_82	10747891	Moreover, a higher concentration of fumonisin B1 (100 muM) not only inhibited elevation of ceramide induced by 5 muM sphingosine by more than 70% after 5 h of treatment, it also markedly enhanced apoptosis induced by sphingosine.	transcription
78834	3	336022	6	NULL	NULL	0	NULL	sphingosine	Chemical		induces					ceramide	Chemical	elevation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_82	10747891	Moreover, a higher concentration of fumonisin B1 (100 muM) not only inhibited elevation of ceramide induced by 5 muM sphingosine by more than 70% after 5 h of treatment, it also markedly enhanced apoptosis induced by sphingosine.	transcription
60130	1	336023	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
60131	2	336023	5	NULL	NULL	0	NULL	statement 1	Process		is dependent on					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
60132	3	336023	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
60133	4	336023	5	NULL	NULL	0	NULL	statement 3	Process		is dependent on					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
60134	5	336023	5	NULL	NULL	0	NULL	Bcl-xL	GP		abolishes		completely			apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
60135	6	336023	5	NULL	NULL	0	NULL	Bcl-xL	GP		abolishes		completely			DEVDase	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
60136	7	336023	5	NULL	NULL	0	NULL	cyt c	GP	release of	is induced by					C2-ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
60137	8	336023	5	NULL	NULL	0	NULL	cyt c	GP	release of	is induced by					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
60138	9	336023	5	NULL	NULL	0	NULL	statement 7	Process		is an alternative to					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
60139	10	336023	5	NULL	NULL	0	NULL	Bcl-xL	GP		abolishes		completely			statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
60140	11	336023	5	NULL	NULL	0	NULL	Bcl-xL	GP		abolishes		completely			statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
66669	1	336023	7	NULL	NULL	0	NULL	sphingosine	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
66670	2	336023	7	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
66671	3	336023	7	NULL	NULL	0	NULL	statement 1	Process		depends on					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
66672	4	336023	7	NULL	NULL	0	NULL	statement 2	Process		depends on					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
66673	5	336023	7	NULL	NULL	0	NULL	Bcl-xL	GP		abolishes		completely			apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
66674	6	336023	7	NULL	NULL	0	NULL	Bcl-xL	GP		abolishes		completely			DEVDase	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
66675	7	336023	7	NULL	NULL	0	NULL	 C2-ceramide	Chemical		induce					cyt c	GP	release of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
66676	8	336023	7	NULL	NULL	NULL	NULL	sphingosine	Chemical		induce					cyt c	GP	release of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
66677	9	336023	7	NULL	NULL	0	NULL	statement 7	Process		is an alternative to					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
66678	10	336023	7	NULL	NULL	0	NULL	Bcl-xL	GP		abolishes		completely			statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
66679	11	336023	7	NULL	NULL	0	NULL	Bcl-xL	GP		abolishes		completely			statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_266	10747891	Herein, we suggest that sphingosine, as well as ceramide, induces apoptosis in a mitochondria-dependent fashion, as Bcl-xL completely abolishes apoptosis, DEVDase activity, and release of cyt  c induced by C2-ceramide or by sphingosine.	transcription
60141	1	336024	5	NULL	NULL	0	NULL	sphingosine	Chemical		increases					Ca2+	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
60142	2	336024	5	NULL	NULL	0	NULL	sphingosine	Chemical		increases					DG kinase	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
60143	3	336024	5	NULL	NULL	0	NULL	stearylamine	Chemical		increases					Ca2+	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
60144	4	336024	5	NULL	NULL	0	NULL	stearylamine	Chemical		increases					DG kinase	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
60145	5	336024	5	NULL	NULL	0	NULL	psychosine	Chemical		increases					Ca2+	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
60146	6	336024	5	NULL	NULL	0	NULL	psychosine	Chemical		increases					DG kinase	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
60147	7	336024	5	NULL	NULL	0	NULL	DG kinase	GP		is					diacylglycerol kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
60148	8	336024	5	NULL	NULL	0	NULL	ceramide	Chemical		does not increase					Ca2+	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
60149	9	336024	5	NULL	NULL	0	NULL	ceramide	Chemical		does not increase					DG kinase	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
60150	10	336024	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		activates		slightly			DG kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
60151	11	336024	5	NULL	NULL	0	NULL	statement 10	Process		occurs without elevation of					Ca2+	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
66680	1	336024	7	NULL	NULL	0	NULL	Sphingosine	Chemical		increase					Ca	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
66681	2	336024	7	NULL	NULL	0	NULL	stearylamine	Chemical		increase					Ca	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
66682	3	336024	7	NULL	NULL	NULL	NULL	psychosine	Chemical		increase					Ca	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
66683	4	336024	7	NULL	NULL	0	NULL	Sphingosine	Chemical		increase					DG kinase	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
66684	5	336024	7	NULL	NULL	0	NULL	stearylamine	Chemical		increase					DG kinase	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
66685	6	336024	7	NULL	NULL	0	NULL	psychosine	Chemical		increase					DG kinase	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
66686	7	336024	7	NULL	NULL	NULL	NULL	ceramide	Chemical		does not activate					DG kinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
66687	8	336024	7	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		activates		slightly			DG kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
66688	9	336024	7	NULL	NULL	0	NULL	statement 8	Process		occur without					Ca	Chemical	elevation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
66689	10	336024	7	NULL	NULL	0	NULL	DG	Chemical		is					diacylglycerol	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_19_11148_s_10	8626660	Sphingosine,  stearylamine, and psychosine increased  [Ca ]   and  diacylglycerol (DG) kinase activation; however, ceramide did not,  whereas sphingosine 1-phosphate slightly activated DG kinase without  elevation of [Ca ] .	transcription
60170	1	336025	5	NULL	NULL	0	NULL	ceramide	Chemical		is formed from		directly			sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_21_12646_s_269	8647877	The inhibitor can also be used to distinguish  those effects of sphingosine that are mediated through the direct  formation of ceramide from sphingosine since those effects would be  anticipated to be inhibitable by fumonisin B1.	transcription
66690	1	336025	7	NULL	NULL	0	NULL	ceramide	Chemical		formed from					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_21_12646_s_269	8647877	The inhibitor can also be used to distinguish  those effects of sphingosine that are mediated through the direct  formation of ceramide from sphingosine since those effects would be  anticipated to be inhibitable by fumonisin B1.	transcription
66691	2	336025	7	NULL	NULL	0	NULL	fumonisin B1	Chemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_21_12646_s_269	8647877	The inhibitor can also be used to distinguish  those effects of sphingosine that are mediated through the direct  formation of ceramide from sphingosine since those effects would be  anticipated to be inhibitable by fumonisin B1.	transcription
60171	1	336026	5	NULL	NULL	0	NULL	sphingosine	Chemical		does not inhibit					PLD	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_40_24800_s_155	8798752	It is unlikely that ceramide acts via its metabolism to sphingosine since our intact cell data demonstrate that sphingosine does not inhibit PLD as potently as C6-ceramide, and in the cell-free assay, no preincubation is necessary for maximal effect.	transcription
60172	2	336026	5	NULL	NULL	0	NULL	C6-ceramide	Chemical		does not inhibit					PLD	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_40_24800_s_155	8798752	It is unlikely that ceramide acts via its metabolism to sphingosine since our intact cell data demonstrate that sphingosine does not inhibit PLD as potently as C6-ceramide, and in the cell-free assay, no preincubation is necessary for maximal effect.	transcription
60173	3	336026	5	NULL	NULL	0	NULL	statement 1	Process		not as potent as					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_40_24800_s_155	8798752	It is unlikely that ceramide acts via its metabolism to sphingosine since our intact cell data demonstrate that sphingosine does not inhibit PLD as potently as C6-ceramide, and in the cell-free assay, no preincubation is necessary for maximal effect.	transcription
66692	1	336026	7	NULL	NULL	0	NULL	sphingosine	Chemical		does not inhibit					PLD	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_40_24800_s_155	8798752	It is unlikely that ceramide acts via its metabolism to sphingosine since our intact cell data demonstrate that sphingosine does not inhibit PLD as potently as C6-ceramide, and in the cell-free assay, no preincubation is necessary for maximal effect.	transcription
66693	2	336026	7	NULL	NULL	0	NULL	C6-ceramide	Chemical		does not inhibit					PLD	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_40_24800_s_155	8798752	It is unlikely that ceramide acts via its metabolism to sphingosine since our intact cell data demonstrate that sphingosine does not inhibit PLD as potently as C6-ceramide, and in the cell-free assay, no preincubation is necessary for maximal effect.	transcription
66694	3	336026	7	NULL	NULL	0	NULL	statement 1	Process		is not as potent as					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_40_24800_s_155	8798752	It is unlikely that ceramide acts via its metabolism to sphingosine since our intact cell data demonstrate that sphingosine does not inhibit PLD as potently as C6-ceramide, and in the cell-free assay, no preincubation is necessary for maximal effect.	transcription
60174	1	336027	5	NULL	NULL	0	NULL	SPT	GP		is					serine palmitoyltransferase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_49_32487_s_28	9829981	The first step in the pathway involves serine palmitoyltransferase (SPT), the enzyme that catalyzes the condensation of palmitoyl-CoA and serine to form dehydrosphinganine, a precursor of sphingosine ( 9,  10); sphingosine is then acylated to form ceramide ( 11,  12).	transcription
60175	2	336027	5	NULL	NULL	0	NULL	palmitoyl-CoA	Chemical		is condensed to					dehydrosphinganine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_49_32487_s_28	9829981	The first step in the pathway involves serine palmitoyltransferase (SPT), the enzyme that catalyzes the condensation of palmitoyl-CoA and serine to form dehydrosphinganine, a precursor of sphingosine ( 9,  10); sphingosine is then acylated to form ceramide ( 11,  12).	transcription
60176	3	336027	5	NULL	NULL	0	NULL	serine	AminoAcid		is condensed to					dehydrosphinganine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32487_s_28	9829981	The first step in the pathway involves serine palmitoyltransferase (SPT), the enzyme that catalyzes the condensation of palmitoyl-CoA and serine to form dehydrosphinganine, a precursor of sphingosine ( 9,  10); sphingosine is then acylated to form ceramide ( 11,  12).	transcription
60177	4	336027	5	NULL	NULL	0	NULL	SPT	GP		catalyzes					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32487_s_28	9829981	The first step in the pathway involves serine palmitoyltransferase (SPT), the enzyme that catalyzes the condensation of palmitoyl-CoA and serine to form dehydrosphinganine, a precursor of sphingosine ( 9,  10); sphingosine is then acylated to form ceramide ( 11,  12).	transcription
60178	5	336027	5	NULL	NULL	0	NULL	SPT	GP		catalyzes					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32487_s_28	9829981	The first step in the pathway involves serine palmitoyltransferase (SPT), the enzyme that catalyzes the condensation of palmitoyl-CoA and serine to form dehydrosphinganine, a precursor of sphingosine ( 9,  10); sphingosine is then acylated to form ceramide ( 11,  12).	transcription
60179	6	336027	5	NULL	NULL	0	NULL	dehydrosphinganine	Chemical		is a precursor of					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32487_s_28	9829981	The first step in the pathway involves serine palmitoyltransferase (SPT), the enzyme that catalyzes the condensation of palmitoyl-CoA and serine to form dehydrosphinganine, a precursor of sphingosine ( 9,  10); sphingosine is then acylated to form ceramide ( 11,  12).	transcription
60180	7	336027	5	NULL	NULL	0	NULL	sphingosine	Chemical		acylated to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32487_s_28	9829981	The first step in the pathway involves serine palmitoyltransferase (SPT), the enzyme that catalyzes the condensation of palmitoyl-CoA and serine to form dehydrosphinganine, a precursor of sphingosine ( 9,  10); sphingosine is then acylated to form ceramide ( 11,  12).	transcription
66695	1	336027	7	NULL	NULL	0	NULL	palmitoyl-CoA	Chemical		condense to form					dehydrosphinganine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32487_s_28	9829981	The first step in the pathway involves serine palmitoyltransferase (SPT), the enzyme that catalyzes the condensation of palmitoyl-CoA and serine to form dehydrosphinganine, a precursor of sphingosine ( 9,  10); sphingosine is then acylated to form ceramide ( 11,  12).	transcription
66696	2	336027	7	NULL	NULL	0	NULL	serine	AminoAcid		condense to form					dehydrosphinganine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32487_s_28	9829981	The first step in the pathway involves serine palmitoyltransferase (SPT), the enzyme that catalyzes the condensation of palmitoyl-CoA and serine to form dehydrosphinganine, a precursor of sphingosine ( 9,  10); sphingosine is then acylated to form ceramide ( 11,  12).	transcription
66697	3	336027	7	NULL	NULL	0	NULL	statement 1	Process		occur along with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32487_s_28	9829981	The first step in the pathway involves serine palmitoyltransferase (SPT), the enzyme that catalyzes the condensation of palmitoyl-CoA and serine to form dehydrosphinganine, a precursor of sphingosine ( 9,  10); sphingosine is then acylated to form ceramide ( 11,  12).	transcription
66698	4	336027	7	NULL	NULL	0	NULL	SPT	GP		catalyze					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32487_s_28	9829981	The first step in the pathway involves serine palmitoyltransferase (SPT), the enzyme that catalyzes the condensation of palmitoyl-CoA and serine to form dehydrosphinganine, a precursor of sphingosine ( 9,  10); sphingosine is then acylated to form ceramide ( 11,  12).	transcription
66699	5	336027	7	NULL	NULL	0	NULL	dehydrosphinganine	Chemical		is a precursor of					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32487_s_28	9829981	The first step in the pathway involves serine palmitoyltransferase (SPT), the enzyme that catalyzes the condensation of palmitoyl-CoA and serine to form dehydrosphinganine, a precursor of sphingosine ( 9,  10); sphingosine is then acylated to form ceramide ( 11,  12).	transcription
66700	6	336027	7	NULL	NULL	0	NULL	sphingosine	Chemical		undergoes					acylation	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32487_s_28	9829981	The first step in the pathway involves serine palmitoyltransferase (SPT), the enzyme that catalyzes the condensation of palmitoyl-CoA and serine to form dehydrosphinganine, a precursor of sphingosine ( 9,  10); sphingosine is then acylated to form ceramide ( 11,  12).	transcription
66701	7	336027	7	NULL	NULL	0	NULL	statement 6	Process		leads to					ceramide	Chemical	formation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32487_s_28	9829981	The first step in the pathway involves serine palmitoyltransferase (SPT), the enzyme that catalyzes the condensation of palmitoyl-CoA and serine to form dehydrosphinganine, a precursor of sphingosine ( 9,  10); sphingosine is then acylated to form ceramide ( 11,  12).	transcription
66702	8	336027	7	NULL	NULL	0	NULL	SPT	GP		is					serine palmitoyltransferase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32487_s_28	9829981	The first step in the pathway involves serine palmitoyltransferase (SPT), the enzyme that catalyzes the condensation of palmitoyl-CoA and serine to form dehydrosphinganine, a precursor of sphingosine ( 9,  10); sphingosine is then acylated to form ceramide ( 11,  12).	transcription
60181	1	336028	5	NULL	NULL	0	NULL	SPP	Chemical		is a metabolite of					ceramide	Chemical				NULL	PC12 cells	NULL	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_176	9278531	In this study, we found that in PC12 cells NGF stimulated the formation of a further metabolite of ceramide, SPP, by markedly activating sphingosine kinase, the enzyme that catalyzes the phosphorylation of sphingosine to SPP.	transcription
60182	2	336028	5	NULL	NULL	0	NULL	sphingosine	Chemical		is phosphorylated to					SPP	Chemical				NULL	PC12 cells	NULL	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_176	9278531	In this study, we found that in PC12 cells NGF stimulated the formation of a further metabolite of ceramide, SPP, by markedly activating sphingosine kinase, the enzyme that catalyzes the phosphorylation of sphingosine to SPP.	transcription
60183	3	336028	5	NULL	NULL	0	NULL	sphingosine kinase	GP	activated	catalyzes					statement 2	Process				NULL	PC12 cells	NULL	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_176	9278531	In this study, we found that in PC12 cells NGF stimulated the formation of a further metabolite of ceramide, SPP, by markedly activating sphingosine kinase, the enzyme that catalyzes the phosphorylation of sphingosine to SPP.	transcription
60184	4	336028	5	NULL	NULL	0	NULL	NGF	GP		activates		markedly			sphingosine kinase	GP				NULL	PC12 cells	NULL	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_176	9278531	In this study, we found that in PC12 cells NGF stimulated the formation of a further metabolite of ceramide, SPP, by markedly activating sphingosine kinase, the enzyme that catalyzes the phosphorylation of sphingosine to SPP.	transcription
60185	5	336028	5	NULL	NULL	0	NULL	statement 4	Process		leads to					statement 3	Process				NULL	PC12 cells	NULL	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_176	9278531	In this study, we found that in PC12 cells NGF stimulated the formation of a further metabolite of ceramide, SPP, by markedly activating sphingosine kinase, the enzyme that catalyzes the phosphorylation of sphingosine to SPP.	transcription
60186	6	336028	5	NULL	NULL	0	NULL	NGF	GP		stimulates					SPP	Chemical	fomation of			NULL	PC12 cells	0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_176	9278531	In this study, we found that in PC12 cells NGF stimulated the formation of a further metabolite of ceramide, SPP, by markedly activating sphingosine kinase, the enzyme that catalyzes the phosphorylation of sphingosine to SPP.	transcription
66703	1	336028	7	NULL	NULL	0	NULL	NGF	GP		stimulate					SPP	Chemical	formation of			NULL	PC12 cells	0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_176	9278531	In this study, we found that in PC12 cells NGF stimulated the formation of a further metabolite of ceramide, SPP, by markedly activating sphingosine kinase, the enzyme that catalyzes the phosphorylation of sphingosine to SPP.	transcription
66704	2	336028	7	NULL	NULL	0	NULL	statement 1	Process		occur by					sphingosine kinase	GP	activating			NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_176	9278531	In this study, we found that in PC12 cells NGF stimulated the formation of a further metabolite of ceramide, SPP, by markedly activating sphingosine kinase, the enzyme that catalyzes the phosphorylation of sphingosine to SPP.	transcription
66705	3	336028	7	NULL	NULL	0	NULL	sphingosine	Chemical		phosphorylated to					SPP	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_176	9278531	In this study, we found that in PC12 cells NGF stimulated the formation of a further metabolite of ceramide, SPP, by markedly activating sphingosine kinase, the enzyme that catalyzes the phosphorylation of sphingosine to SPP.	transcription
66706	4	336028	7	NULL	NULL	0	NULL	sphingosine kinase	GP		catalyze					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_176	9278531	In this study, we found that in PC12 cells NGF stimulated the formation of a further metabolite of ceramide, SPP, by markedly activating sphingosine kinase, the enzyme that catalyzes the phosphorylation of sphingosine to SPP.	transcription
60187	1	336029	5	NULL	NULL	0	NULL	PLD	GP		is activated by					ET-1	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_292_2_629_s_9	10640300	Inhibition by genistein and D-erythro- N-hexanoyl-sphingosine was additive, whereas inhibition by Ro-31-8220 and D-erythro- N-hexanoyl-sphingosine was not, indicating that ceramide affected the PKC-dependent process involved in PLD activation by ET-1.	transcription
60188	2	336029	5	NULL	NULL	0	NULL	statement 1	Process		is dependent on					PKC	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_292_2_629_s_9	10640300	Inhibition by genistein and D-erythro- N-hexanoyl-sphingosine was additive, whereas inhibition by Ro-31-8220 and D-erythro- N-hexanoyl-sphingosine was not, indicating that ceramide affected the PKC-dependent process involved in PLD activation by ET-1.	transcription
60189	3	336029	5	NULL	NULL	0	NULL	ceramide	Chemical		affects					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_292_2_629_s_9	10640300	Inhibition by genistein and D-erythro- N-hexanoyl-sphingosine was additive, whereas inhibition by Ro-31-8220 and D-erythro- N-hexanoyl-sphingosine was not, indicating that ceramide affected the PKC-dependent process involved in PLD activation by ET-1.	transcription
66707	1	336029	7	NULL	NULL	0	NULL	ET-1	GP		activate					PLD	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_292_2_629_s_9	10640300	Inhibition by genistein and D-erythro- N-hexanoyl-sphingosine was additive, whereas inhibition by Ro-31-8220 and D-erythro- N-hexanoyl-sphingosine was not, indicating that ceramide affected the PKC-dependent process involved in PLD activation by ET-1.	transcription
66708	2	336029	7	NULL	NULL	0	NULL	ceramide	Chemical		affects					PKC-dependent process	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_292_2_629_s_9	10640300	Inhibition by genistein and D-erythro- N-hexanoyl-sphingosine was additive, whereas inhibition by Ro-31-8220 and D-erythro- N-hexanoyl-sphingosine was not, indicating that ceramide affected the PKC-dependent process involved in PLD activation by ET-1.	transcription
66709	3	336029	7	NULL	NULL	0	NULL	PKC-dependent process	Process		involved in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_292_2_629_s_9	10640300	Inhibition by genistein and D-erythro- N-hexanoyl-sphingosine was additive, whereas inhibition by Ro-31-8220 and D-erythro- N-hexanoyl-sphingosine was not, indicating that ceramide affected the PKC-dependent process involved in PLD activation by ET-1.	transcription
60190	1	336030	5	NULL	NULL	0	NULL	D- erythro-sphingosine, N-acetyl-(C2-ceramides) 1	Chemical		is a type of					cell-permeant ceramide	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_48_47498_s_14	12952965	By stimulating NHEK with cell-permeant ceramides ( e.g.D- erythro-sphingosine,  N-acetyl-(C2-ceramides)  1 or D-erythrosphingosine,  N-hexanoyl-(C6-ceramides)) it has recently been observed that ceramide-induced expression of the human ICAM-1 gene is mediated through activation of AP-2, indicating that ceramides are capable of activating transcription factors in human cells through a yet unknown mechanism ( ).	transcription
60191	2	336030	5	NULL	NULL	0	NULL	D-erythrosphingosine, N-hexanoyl-(C6-ceramides)	Chemical		is a type of					cell-permeant ceramide	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_48_47498_s_14	12952965	By stimulating NHEK with cell-permeant ceramides ( e.g.D- erythro-sphingosine,  N-acetyl-(C2-ceramides)  1 or D-erythrosphingosine,  N-hexanoyl-(C6-ceramides)) it has recently been observed that ceramide-induced expression of the human ICAM-1 gene is mediated through activation of AP-2, indicating that ceramides are capable of activating transcription factors in human cells through a yet unknown mechanism ( ).	transcription
60192	3	336030	5	NULL	NULL	0	NULL	D-erythrosphingosine, N-hexanoyl-(C6-ceramides)	Chemical		stimulates					NHEK	Cell				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_48_47498_s_14	12952965	By stimulating NHEK with cell-permeant ceramides ( e.g.D- erythro-sphingosine,  N-acetyl-(C2-ceramides)  1 or D-erythrosphingosine,  N-hexanoyl-(C6-ceramides)) it has recently been observed that ceramide-induced expression of the human ICAM-1 gene is mediated through activation of AP-2, indicating that ceramides are capable of activating transcription factors in human cells through a yet unknown mechanism ( ).	transcription
60193	4	336030	5	NULL	NULL	0	NULL	D- erythro-sphingosine, N-acetyl-(C2-ceramides) 1	Chemical		stimulates					NHEK	Cell				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_48_47498_s_14	12952965	By stimulating NHEK with cell-permeant ceramides ( e.g.D- erythro-sphingosine,  N-acetyl-(C2-ceramides)  1 or D-erythrosphingosine,  N-hexanoyl-(C6-ceramides)) it has recently been observed that ceramide-induced expression of the human ICAM-1 gene is mediated through activation of AP-2, indicating that ceramides are capable of activating transcription factors in human cells through a yet unknown mechanism ( ).	transcription
60194	5	336030	5	NULL	NULL	0	NULL	ceramide	Chemical		induce					ICAM-1 gene	GP	expression of;;human			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_48_47498_s_14	12952965	By stimulating NHEK with cell-permeant ceramides ( e.g.D- erythro-sphingosine,  N-acetyl-(C2-ceramides)  1 or D-erythrosphingosine,  N-hexanoyl-(C6-ceramides)) it has recently been observed that ceramide-induced expression of the human ICAM-1 gene is mediated through activation of AP-2, indicating that ceramides are capable of activating transcription factors in human cells through a yet unknown mechanism ( ).	transcription
60195	6	336030	5	NULL	NULL	0	NULL	statement 5	Process		is mediated through					AP-2	GP	activation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_48_47498_s_14	12952965	By stimulating NHEK with cell-permeant ceramides ( e.g.D- erythro-sphingosine,  N-acetyl-(C2-ceramides)  1 or D-erythrosphingosine,  N-hexanoyl-(C6-ceramides)) it has recently been observed that ceramide-induced expression of the human ICAM-1 gene is mediated through activation of AP-2, indicating that ceramides are capable of activating transcription factors in human cells through a yet unknown mechanism ( ).	transcription
60196	7	336030	5	NULL	NULL	0	NULL	ceramide	Chemical		activates					transcription factor	GP				NULL	human cells	0	NULL	NULL	NULL	gw70_jbiolchem_278_48_47498_s_14	12952965	By stimulating NHEK with cell-permeant ceramides ( e.g.D- erythro-sphingosine,  N-acetyl-(C2-ceramides)  1 or D-erythrosphingosine,  N-hexanoyl-(C6-ceramides)) it has recently been observed that ceramide-induced expression of the human ICAM-1 gene is mediated through activation of AP-2, indicating that ceramides are capable of activating transcription factors in human cells through a yet unknown mechanism ( ).	transcription
60197	8	336030	5	NULL	NULL	0	NULL	statement 6	Process		indicates					statement 7	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_48_47498_s_14	12952965	By stimulating NHEK with cell-permeant ceramides ( e.g.D- erythro-sphingosine,  N-acetyl-(C2-ceramides)  1 or D-erythrosphingosine,  N-hexanoyl-(C6-ceramides)) it has recently been observed that ceramide-induced expression of the human ICAM-1 gene is mediated through activation of AP-2, indicating that ceramides are capable of activating transcription factors in human cells through a yet unknown mechanism ( ).	transcription
66710	1	336030	7	NULL	NULL	0	NULL	ceramide	Chemical		induce					ICAM-1 gene	GP	human;;expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_48_47498_s_14	12952965	By stimulating NHEK with cell-permeant ceramides ( e.g.D- erythro-sphingosine,  N-acetyl-(C2-ceramides)  1 or D-erythrosphingosine,  N-hexanoyl-(C6-ceramides)) it has recently been observed that ceramide-induced expression of the human ICAM-1 gene is mediated through activation of AP-2, indicating that ceramides are capable of activating transcription factors in human cells through a yet unknown mechanism ( ).	transcription
66711	2	336030	7	NULL	NULL	0	NULL	statement 1	Process		mediated through					AP-2	GP	activation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_48_47498_s_14	12952965	By stimulating NHEK with cell-permeant ceramides ( e.g.D- erythro-sphingosine,  N-acetyl-(C2-ceramides)  1 or D-erythrosphingosine,  N-hexanoyl-(C6-ceramides)) it has recently been observed that ceramide-induced expression of the human ICAM-1 gene is mediated through activation of AP-2, indicating that ceramides are capable of activating transcription factors in human cells through a yet unknown mechanism ( ).	transcription
66712	3	336030	7	NULL	NULL	0	NULL	ceramides	Chemical		activate					transcription factors	GP				NULL	human cells	0	NULL	NULL	NULL	gw70_jbiolchem_278_48_47498_s_14	12952965	By stimulating NHEK with cell-permeant ceramides ( e.g.D- erythro-sphingosine,  N-acetyl-(C2-ceramides)  1 or D-erythrosphingosine,  N-hexanoyl-(C6-ceramides)) it has recently been observed that ceramide-induced expression of the human ICAM-1 gene is mediated through activation of AP-2, indicating that ceramides are capable of activating transcription factors in human cells through a yet unknown mechanism ( ).	transcription
66713	4	336030	7	NULL	NULL	NULL	NULL	D- erythro-sphingosine	Chemical		stimulate					NHEK 	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_48_47498_s_14	12952965	By stimulating NHEK with cell-permeant ceramides ( e.g.D- erythro-sphingosine,  N-acetyl-(C2-ceramides)  1 or D-erythrosphingosine,  N-hexanoyl-(C6-ceramides)) it has recently been observed that ceramide-induced expression of the human ICAM-1 gene is mediated through activation of AP-2, indicating that ceramides are capable of activating transcription factors in human cells through a yet unknown mechanism ( ).	transcription
66714	5	336030	7	NULL	NULL	NULL	NULL	N-acetyl-(C2-ceramides)1-erythrosphingosine 	Chemical		stimulate					NHEK	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_48_47498_s_14	12952965	By stimulating NHEK with cell-permeant ceramides ( e.g.D- erythro-sphingosine,  N-acetyl-(C2-ceramides)  1 or D-erythrosphingosine,  N-hexanoyl-(C6-ceramides)) it has recently been observed that ceramide-induced expression of the human ICAM-1 gene is mediated through activation of AP-2, indicating that ceramides are capable of activating transcription factors in human cells through a yet unknown mechanism ( ).	transcription
66715	6	336030	7	NULL	NULL	NULL	NULL	N-acetyl-(C2-ceramides) D-erythrosphingosine	Chemical		stimulate					NHEK	Cell				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_48_47498_s_14	12952965	By stimulating NHEK with cell-permeant ceramides ( e.g.D- erythro-sphingosine,  N-acetyl-(C2-ceramides)  1 or D-erythrosphingosine,  N-hexanoyl-(C6-ceramides)) it has recently been observed that ceramide-induced expression of the human ICAM-1 gene is mediated through activation of AP-2, indicating that ceramides are capable of activating transcription factors in human cells through a yet unknown mechanism ( ).	transcription
66716	7	336030	7	NULL	NULL	0	NULL	N-hexanoyl-(C6-ceramides)	Chemical		stimulate					NHEK	Cell				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_48_47498_s_14	12952965	By stimulating NHEK with cell-permeant ceramides ( e.g.D- erythro-sphingosine,  N-acetyl-(C2-ceramides)  1 or D-erythrosphingosine,  N-hexanoyl-(C6-ceramides)) it has recently been observed that ceramide-induced expression of the human ICAM-1 gene is mediated through activation of AP-2, indicating that ceramides are capable of activating transcription factors in human cells through a yet unknown mechanism ( ).	transcription
66717	8	336030	7	NULL	NULL	0	NULL	D- erythro-sphingosine	Chemical		is a type of					ceramides	Chemical	cell-permeant 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_48_47498_s_14	12952965	By stimulating NHEK with cell-permeant ceramides ( e.g.D- erythro-sphingosine,  N-acetyl-(C2-ceramides)  1 or D-erythrosphingosine,  N-hexanoyl-(C6-ceramides)) it has recently been observed that ceramide-induced expression of the human ICAM-1 gene is mediated through activation of AP-2, indicating that ceramides are capable of activating transcription factors in human cells through a yet unknown mechanism ( ).	transcription
66718	9	336030	7	NULL	NULL	NULL	NULL	N-acetyl-(C2-ceramides)1-erythrosphingosine	Chemical		is a type of					ceramides	Chemical	cell-permeant 			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_48_47498_s_14	12952965	By stimulating NHEK with cell-permeant ceramides ( e.g.D- erythro-sphingosine,  N-acetyl-(C2-ceramides)  1 or D-erythrosphingosine,  N-hexanoyl-(C6-ceramides)) it has recently been observed that ceramide-induced expression of the human ICAM-1 gene is mediated through activation of AP-2, indicating that ceramides are capable of activating transcription factors in human cells through a yet unknown mechanism ( ).	transcription
66719	10	336030	7	NULL	NULL	0	NULL	N-acetyl-(C2-ceramides)D-erythrosphingosine	Chemical		is a type of					ceramides	Chemical	cell-permeant 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_48_47498_s_14	12952965	By stimulating NHEK with cell-permeant ceramides ( e.g.D- erythro-sphingosine,  N-acetyl-(C2-ceramides)  1 or D-erythrosphingosine,  N-hexanoyl-(C6-ceramides)) it has recently been observed that ceramide-induced expression of the human ICAM-1 gene is mediated through activation of AP-2, indicating that ceramides are capable of activating transcription factors in human cells through a yet unknown mechanism ( ).	transcription
66720	11	336030	7	NULL	NULL	0	NULL	N-hexanoyl-(C6-ceramides)	Chemical		is a type of					ceramide	Chemical	cell-permeant 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_48_47498_s_14	12952965	By stimulating NHEK with cell-permeant ceramides ( e.g.D- erythro-sphingosine,  N-acetyl-(C2-ceramides)  1 or D-erythrosphingosine,  N-hexanoyl-(C6-ceramides)) it has recently been observed that ceramide-induced expression of the human ICAM-1 gene is mediated through activation of AP-2, indicating that ceramides are capable of activating transcription factors in human cells through a yet unknown mechanism ( ).	transcription
60198	1	336031	5	NULL	NULL	0	NULL	hemolysis	Process		is induced by					alpha-toxin	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_196	14702348	To clarify the relationship between alpha-toxin-induced hemolysis and the deamidation of ceramide to sphingosine, the effect of  N-oleoylethanolamine ( ), a ceramidase inhibitor, on the toxin-induced hemolysis and formation of phosphorylcholine and ceramide was investigated ( Fig. 5).	transcription
60199	2	336031	5	NULL	NULL	0	NULL	ceramide	Chemical		deamidated to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_196	14702348	To clarify the relationship between alpha-toxin-induced hemolysis and the deamidation of ceramide to sphingosine, the effect of  N-oleoylethanolamine ( ), a ceramidase inhibitor, on the toxin-induced hemolysis and formation of phosphorylcholine and ceramide was investigated ( Fig. 5).	transcription
60200	3	336031	5	NULL	NULL	0	NULL	N-oleoylethanolamine	Chemical		is an inhibitor of					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_196	14702348	To clarify the relationship between alpha-toxin-induced hemolysis and the deamidation of ceramide to sphingosine, the effect of  N-oleoylethanolamine ( ), a ceramidase inhibitor, on the toxin-induced hemolysis and formation of phosphorylcholine and ceramide was investigated ( Fig. 5).	transcription
60201	4	336031	5	NULL	NULL	0	NULL	N-oleoylethanolamine	Chemical		effects		potentially			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_196	14702348	To clarify the relationship between alpha-toxin-induced hemolysis and the deamidation of ceramide to sphingosine, the effect of  N-oleoylethanolamine ( ), a ceramidase inhibitor, on the toxin-induced hemolysis and formation of phosphorylcholine and ceramide was investigated ( Fig. 5).	transcription
60202	5	336031	5	NULL	NULL	0	NULL	N-oleoylethanolamine	Chemical		effects		potentially			phosphorylcholine	Chemical	formation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_196	14702348	To clarify the relationship between alpha-toxin-induced hemolysis and the deamidation of ceramide to sphingosine, the effect of  N-oleoylethanolamine ( ), a ceramidase inhibitor, on the toxin-induced hemolysis and formation of phosphorylcholine and ceramide was investigated ( Fig. 5).	transcription
60203	6	336031	5	NULL	NULL	0	NULL	N-oleoylethanolamine	Chemical		effects		potentially			ceramide	Chemical	formation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_196	14702348	To clarify the relationship between alpha-toxin-induced hemolysis and the deamidation of ceramide to sphingosine, the effect of  N-oleoylethanolamine ( ), a ceramidase inhibitor, on the toxin-induced hemolysis and formation of phosphorylcholine and ceramide was investigated ( Fig. 5).	transcription
66721	1	336031	7	NULL	NULL	0	NULL	alpha-toxin	GP		induce					hemolysis	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_196	14702348	To clarify the relationship between alpha-toxin-induced hemolysis and the deamidation of ceramide to sphingosine, the effect of  N-oleoylethanolamine ( ), a ceramidase inhibitor, on the toxin-induced hemolysis and formation of phosphorylcholine and ceramide was investigated ( Fig. 5).	transcription
66722	2	336031	7	NULL	NULL	0	NULL	ceramide	Chemical		deamidated to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_196	14702348	To clarify the relationship between alpha-toxin-induced hemolysis and the deamidation of ceramide to sphingosine, the effect of  N-oleoylethanolamine ( ), a ceramidase inhibitor, on the toxin-induced hemolysis and formation of phosphorylcholine and ceramide was investigated ( Fig. 5).	transcription
66723	3	336031	7	NULL	NULL	NULL	NULL	N-oleoylethanolamine	Chemical		is an inhibitor of					ceramidase 	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_13_12181_s_196	14702348	To clarify the relationship between alpha-toxin-induced hemolysis and the deamidation of ceramide to sphingosine, the effect of  N-oleoylethanolamine ( ), a ceramidase inhibitor, on the toxin-induced hemolysis and formation of phosphorylcholine and ceramide was investigated ( Fig. 5).	transcription
60204	1	336032	5	NULL	NULL	0	NULL	ceramide	Chemical		stimulates					phosphatidic acid phosphohydrolase	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_130	10425402	Also, ceramide stimulates the phosphatidic acid phosphohydrolase which breaks down PA as well as lyso-PA, ceramide phosphate and sphingosine thereby ablating these antagonistic signals [  62].	transcription
60205	2	336032	5	NULL	NULL	0	NULL	phosphatidic acid phosphohydrolase	GP		breaks down					PA	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_130	10425402	Also, ceramide stimulates the phosphatidic acid phosphohydrolase which breaks down PA as well as lyso-PA, ceramide phosphate and sphingosine thereby ablating these antagonistic signals [  62].	transcription
60206	3	336032	5	NULL	NULL	0	NULL	phosphatidic acid phosphohydrolase	GP		breaks down					lyso-PA	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_130	10425402	Also, ceramide stimulates the phosphatidic acid phosphohydrolase which breaks down PA as well as lyso-PA, ceramide phosphate and sphingosine thereby ablating these antagonistic signals [  62].	transcription
60207	4	336032	5	NULL	NULL	0	NULL	phosphatidic acid phosphohydrolase	GP		breaks down					ceramide phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_130	10425402	Also, ceramide stimulates the phosphatidic acid phosphohydrolase which breaks down PA as well as lyso-PA, ceramide phosphate and sphingosine thereby ablating these antagonistic signals [  62].	transcription
60208	5	336032	5	NULL	NULL	0	NULL	phosphatidic acid phosphohydrolase	GP		breaks down					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_130	10425402	Also, ceramide stimulates the phosphatidic acid phosphohydrolase which breaks down PA as well as lyso-PA, ceramide phosphate and sphingosine thereby ablating these antagonistic signals [  62].	transcription
66724	1	336032	7	NULL	NULL	0	NULL	 ceramide	Chemical		stimulates					phosphatidic acid phosphohydrolase	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_130	10425402	Also, ceramide stimulates the phosphatidic acid phosphohydrolase which breaks down PA as well as lyso-PA, ceramide phosphate and sphingosine thereby ablating these antagonistic signals [  62].	transcription
66725	2	336032	7	NULL	NULL	0	NULL	phosphatidic acid phosphohydrolase	GP		breaksdown					PA	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_130	10425402	Also, ceramide stimulates the phosphatidic acid phosphohydrolase which breaks down PA as well as lyso-PA, ceramide phosphate and sphingosine thereby ablating these antagonistic signals [  62].	transcription
66726	3	336032	7	NULL	NULL	0	NULL	phosphatidic acid phosphohydrolase	GP		breaksdown					lyso-PA	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_130	10425402	Also, ceramide stimulates the phosphatidic acid phosphohydrolase which breaks down PA as well as lyso-PA, ceramide phosphate and sphingosine thereby ablating these antagonistic signals [  62].	transcription
66727	4	336032	7	NULL	NULL	0	NULL	phosphatidic acid phosphohydrolase	GP		breaksdown					ceramide phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_130	10425402	Also, ceramide stimulates the phosphatidic acid phosphohydrolase which breaks down PA as well as lyso-PA, ceramide phosphate and sphingosine thereby ablating these antagonistic signals [  62].	transcription
66728	5	336032	7	NULL	NULL	0	NULL	phosphatidic acid phosphohydrolase	GP		breaksdown					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_130	10425402	Also, ceramide stimulates the phosphatidic acid phosphohydrolase which breaks down PA as well as lyso-PA, ceramide phosphate and sphingosine thereby ablating these antagonistic signals [  62].	transcription
66729	6	336032	7	NULL	NULL	0	NULL	statement 2	Process		ablate					antagonistic signals	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_130	10425402	Also, ceramide stimulates the phosphatidic acid phosphohydrolase which breaks down PA as well as lyso-PA, ceramide phosphate and sphingosine thereby ablating these antagonistic signals [  62].	transcription
66730	7	336032	7	NULL	NULL	0	NULL	statement 3	Process		ablate					antagonistic signals	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_130	10425402	Also, ceramide stimulates the phosphatidic acid phosphohydrolase which breaks down PA as well as lyso-PA, ceramide phosphate and sphingosine thereby ablating these antagonistic signals [  62].	transcription
66731	8	336032	7	NULL	NULL	0	NULL	statement 4	Process		ablate					antagonistic signals	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_130	10425402	Also, ceramide stimulates the phosphatidic acid phosphohydrolase which breaks down PA as well as lyso-PA, ceramide phosphate and sphingosine thereby ablating these antagonistic signals [  62].	transcription
66732	9	336032	7	NULL	NULL	0	NULL	statement 5	Process		ablate					antagonistic signals	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_2_291_s_130	10425402	Also, ceramide stimulates the phosphatidic acid phosphohydrolase which breaks down PA as well as lyso-PA, ceramide phosphate and sphingosine thereby ablating these antagonistic signals [  62].	transcription
60209	1	336033	5	NULL	NULL	0	NULL	SPP	Chemical		is converted to					sphingosine	Chemical				NULL	human fibroblasts	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_1_17_s_112	10395962	Elegantly, Gomez-Munoz et al. [ 43] demonstrated that C2-Cer stimulates the conversion of SPP to sphingosine and ceramide in human fibroblasts, whereas Rani et al. [ 29] showed that C2-Cer is able to increase the endogenous ceramide content.	transcription
60210	2	336033	5	NULL	NULL	0	NULL	SPP	Chemical		is converted to					ceramide	Chemical				NULL	human fibroblasts	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_1_17_s_112	10395962	Elegantly, Gomez-Munoz et al. [ 43] demonstrated that C2-Cer stimulates the conversion of SPP to sphingosine and ceramide in human fibroblasts, whereas Rani et al. [ 29] showed that C2-Cer is able to increase the endogenous ceramide content.	transcription
60211	3	336033	5	NULL	NULL	0	NULL	C2-Cer	Chemical		stimulates					statement 1	Process				NULL	human fibroblasts	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_1_17_s_112	10395962	Elegantly, Gomez-Munoz et al. [ 43] demonstrated that C2-Cer stimulates the conversion of SPP to sphingosine and ceramide in human fibroblasts, whereas Rani et al. [ 29] showed that C2-Cer is able to increase the endogenous ceramide content.	transcription
60212	4	336033	5	NULL	NULL	0	NULL	C2-Cer	Chemical		stimulates					statement 2	Process				NULL	human fibroblasts	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_1_17_s_112	10395962	Elegantly, Gomez-Munoz et al. [ 43] demonstrated that C2-Cer stimulates the conversion of SPP to sphingosine and ceramide in human fibroblasts, whereas Rani et al. [ 29] showed that C2-Cer is able to increase the endogenous ceramide content.	transcription
60213	5	336033	5	NULL	NULL	0	NULL	C2-Cer	Chemical		increases					ceramide	Chemical	endogenous			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_1_17_s_112	10395962	Elegantly, Gomez-Munoz et al. [ 43] demonstrated that C2-Cer stimulates the conversion of SPP to sphingosine and ceramide in human fibroblasts, whereas Rani et al. [ 29] showed that C2-Cer is able to increase the endogenous ceramide content.	transcription
66733	1	336033	7	NULL	NULL	NULL	NULL	 SPP	Chemical		converted to					sphingosine	Chemical				NULL	human fibroblasts	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_1_17_s_112	10395962	Elegantly, Gomez-Munoz et al. [ 43] demonstrated that C2-Cer stimulates the conversion of SPP to sphingosine and ceramide in human fibroblasts, whereas Rani et al. [ 29] showed that C2-Cer is able to increase the endogenous ceramide content.	transcription
66734	2	336033	7	NULL	NULL	0	NULL	 SPP	Chemical		converted to					ceramide	Chemical				NULL	human fibroblasts	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_1_17_s_112	10395962	Elegantly, Gomez-Munoz et al. [ 43] demonstrated that C2-Cer stimulates the conversion of SPP to sphingosine and ceramide in human fibroblasts, whereas Rani et al. [ 29] showed that C2-Cer is able to increase the endogenous ceramide content.	transcription
66735	3	336033	7	NULL	NULL	NULL	NULL	C2-Cer	Chemical		stimulate					statement 1	Process				NULL	human fibroblasts	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_1_17_s_112	10395962	Elegantly, Gomez-Munoz et al. [ 43] demonstrated that C2-Cer stimulates the conversion of SPP to sphingosine and ceramide in human fibroblasts, whereas Rani et al. [ 29] showed that C2-Cer is able to increase the endogenous ceramide content.	transcription
66736	4	336033	7	NULL	NULL	NULL	NULL	C2-Cer	Chemical		stimulate					statement 2	Chemical				NULL	human fibroblasts	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_1_17_s_112	10395962	Elegantly, Gomez-Munoz et al. [ 43] demonstrated that C2-Cer stimulates the conversion of SPP to sphingosine and ceramide in human fibroblasts, whereas Rani et al. [ 29] showed that C2-Cer is able to increase the endogenous ceramide content.	transcription
66737	5	336033	7	NULL	NULL	0	NULL	C2-Cer	Chemical		increase					ceramide content	Process	endogenous			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_1_17_s_112	10395962	Elegantly, Gomez-Munoz et al. [ 43] demonstrated that C2-Cer stimulates the conversion of SPP to sphingosine and ceramide in human fibroblasts, whereas Rani et al. [ 29] showed that C2-Cer is able to increase the endogenous ceramide content.	transcription
66738	6	336033	7	NULL	NULL	0	NULL	C2-Cer	Chemical		increase					ceramide content	Process	endogenous			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1439_1_17_s_112	10395962	Elegantly, Gomez-Munoz et al. [ 43] demonstrated that C2-Cer stimulates the conversion of SPP to sphingosine and ceramide in human fibroblasts, whereas Rani et al. [ 29] showed that C2-Cer is able to increase the endogenous ceramide content.	transcription
60214	1	336034	5	NULL	NULL	0	NULL	ceramide	Chemical		is induced by					daunorubicin	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1488_3_219_s_221	11082532	To exclude the possibility that daunorubicin-induced ceramide was rapidly hydrolyzed to sphingosine by ceramidase and therefore its increase could not be detected, we measured the ceramide generation in A-431 cells treated with daunorubicin in the presence of  N-oleoylethanolamine, a ceramidase inhibitor.	transcription
60215	2	336034	5	NULL	NULL	0	NULL	statement 1	Chemical		is hydrolyzed to		rapidly			sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1488_3_219_s_221	11082532	To exclude the possibility that daunorubicin-induced ceramide was rapidly hydrolyzed to sphingosine by ceramidase and therefore its increase could not be detected, we measured the ceramide generation in A-431 cells treated with daunorubicin in the presence of  N-oleoylethanolamine, a ceramidase inhibitor.	transcription
60216	3	336034	5	NULL	NULL	0	NULL	ceramidase	GP		catalyzes					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1488_3_219_s_221	11082532	To exclude the possibility that daunorubicin-induced ceramide was rapidly hydrolyzed to sphingosine by ceramidase and therefore its increase could not be detected, we measured the ceramide generation in A-431 cells treated with daunorubicin in the presence of  N-oleoylethanolamine, a ceramidase inhibitor.	transcription
60217	4	336034	5	NULL	NULL	0	NULL	N-oleoylethanolamine	Chemical		is an inhibitor of					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1488_3_219_s_221	11082532	To exclude the possibility that daunorubicin-induced ceramide was rapidly hydrolyzed to sphingosine by ceramidase and therefore its increase could not be detected, we measured the ceramide generation in A-431 cells treated with daunorubicin in the presence of  N-oleoylethanolamine, a ceramidase inhibitor.	transcription
66746	1	336034	7	NULL	NULL	0	NULL	daunorubicin	Chemical		induce					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1488_3_219_s_221	11082532	To exclude the possibility that daunorubicin-induced ceramide was rapidly hydrolyzed to sphingosine by ceramidase and therefore its increase could not be detected, we measured the ceramide generation in A-431 cells treated with daunorubicin in the presence of  N-oleoylethanolamine, a ceramidase inhibitor.	transcription
66747	2	336034	7	NULL	NULL	0	NULL	statement 1	Process		hydrolyze to		rapidly			sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1488_3_219_s_221	11082532	To exclude the possibility that daunorubicin-induced ceramide was rapidly hydrolyzed to sphingosine by ceramidase and therefore its increase could not be detected, we measured the ceramide generation in A-431 cells treated with daunorubicin in the presence of  N-oleoylethanolamine, a ceramidase inhibitor.	transcription
66748	3	336034	7	NULL	NULL	0	NULL	ceramidase	GP		catalyze					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1488_3_219_s_221	11082532	To exclude the possibility that daunorubicin-induced ceramide was rapidly hydrolyzed to sphingosine by ceramidase and therefore its increase could not be detected, we measured the ceramide generation in A-431 cells treated with daunorubicin in the presence of  N-oleoylethanolamine, a ceramidase inhibitor.	transcription
66749	4	336034	7	NULL	NULL	0	NULL	N-oleoylethanolamine	Chemical		is an inhibitor of					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1488_3_219_s_221	11082532	To exclude the possibility that daunorubicin-induced ceramide was rapidly hydrolyzed to sphingosine by ceramidase and therefore its increase could not be detected, we measured the ceramide generation in A-431 cells treated with daunorubicin in the presence of  N-oleoylethanolamine, a ceramidase inhibitor.	transcription
60218	1	336035	5	NULL	NULL	0	NULL	FB1	Chemical		is an inhibitor of					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_187	12235122	Yet, FB1, an inhibitor of ceramide synthase, induced accumulation of sphingoid bases when cells were treated with either S1P or dihydro-S1P, suggesting that the sphingosine and sphinganine produced in these cells are indeed substrates for ceramide synthase.	transcription
60219	2	336035	5	NULL	NULL	0	NULL	FB1	Chemical		induce					sphingoid bases	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_187	12235122	Yet, FB1, an inhibitor of ceramide synthase, induced accumulation of sphingoid bases when cells were treated with either S1P or dihydro-S1P, suggesting that the sphingosine and sphinganine produced in these cells are indeed substrates for ceramide synthase.	transcription
60220	3	336035	5	NULL	NULL	0	NULL	statement 2	Process		occurs upon					S1P	Chemical	treatment			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_187	12235122	Yet, FB1, an inhibitor of ceramide synthase, induced accumulation of sphingoid bases when cells were treated with either S1P or dihydro-S1P, suggesting that the sphingosine and sphinganine produced in these cells are indeed substrates for ceramide synthase.	transcription
60221	4	336035	5	NULL	NULL	0	NULL	statement 2	Process		occurs upon					dihydro-S1P	Chemical	treatment			NULL		0	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_187	12235122	Yet, FB1, an inhibitor of ceramide synthase, induced accumulation of sphingoid bases when cells were treated with either S1P or dihydro-S1P, suggesting that the sphingosine and sphinganine produced in these cells are indeed substrates for ceramide synthase.	transcription
60222	5	336035	5	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_187	12235122	Yet, FB1, an inhibitor of ceramide synthase, induced accumulation of sphingoid bases when cells were treated with either S1P or dihydro-S1P, suggesting that the sphingosine and sphinganine produced in these cells are indeed substrates for ceramide synthase.	transcription
60223	6	336035	5	NULL	NULL	0	NULL	sphingosine	Chemical		is a substrate of					ceramide synthase	GP				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_187	12235122	Yet, FB1, an inhibitor of ceramide synthase, induced accumulation of sphingoid bases when cells were treated with either S1P or dihydro-S1P, suggesting that the sphingosine and sphinganine produced in these cells are indeed substrates for ceramide synthase.	transcription
60224	7	336035	5	NULL	NULL	0	NULL	sphinganine	Chemical		is a substrate of					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_187	12235122	Yet, FB1, an inhibitor of ceramide synthase, induced accumulation of sphingoid bases when cells were treated with either S1P or dihydro-S1P, suggesting that the sphingosine and sphinganine produced in these cells are indeed substrates for ceramide synthase.	transcription
66750	1	336035	7	NULL	NULL	0	NULL	FB1	Chemical		is an inhibitor of					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_187	12235122	Yet, FB1, an inhibitor of ceramide synthase, induced accumulation of sphingoid bases when cells were treated with either S1P or dihydro-S1P, suggesting that the sphingosine and sphinganine produced in these cells are indeed substrates for ceramide synthase.	transcription
66751	2	336035	7	NULL	NULL	0	NULL	FB1	Chemical		induce					sphingoid bases	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_187	12235122	Yet, FB1, an inhibitor of ceramide synthase, induced accumulation of sphingoid bases when cells were treated with either S1P or dihydro-S1P, suggesting that the sphingosine and sphinganine produced in these cells are indeed substrates for ceramide synthase.	transcription
66752	3	336035	7	NULL	NULL	0	NULL	statement 2	Process		occur upon					S1P	Chemical	treatment with			NULL		0	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_187	12235122	Yet, FB1, an inhibitor of ceramide synthase, induced accumulation of sphingoid bases when cells were treated with either S1P or dihydro-S1P, suggesting that the sphingosine and sphinganine produced in these cells are indeed substrates for ceramide synthase.	transcription
66753	4	336035	7	NULL	NULL	NULL	NULL	statement 2	Process		occur upon					dihydro-S1P	Chemical	treatment with			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_187	12235122	Yet, FB1, an inhibitor of ceramide synthase, induced accumulation of sphingoid bases when cells were treated with either S1P or dihydro-S1P, suggesting that the sphingosine and sphinganine produced in these cells are indeed substrates for ceramide synthase.	transcription
66754	5	336035	7	NULL	NULL	0	NULL	sphingosine	Chemical		substrate for					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_187	12235122	Yet, FB1, an inhibitor of ceramide synthase, induced accumulation of sphingoid bases when cells were treated with either S1P or dihydro-S1P, suggesting that the sphingosine and sphinganine produced in these cells are indeed substrates for ceramide synthase.	transcription
66755	6	336035	7	NULL	NULL	0	NULL	sphinganine 	Chemical		substrate for					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_187	12235122	Yet, FB1, an inhibitor of ceramide synthase, induced accumulation of sphingoid bases when cells were treated with either S1P or dihydro-S1P, suggesting that the sphingosine and sphinganine produced in these cells are indeed substrates for ceramide synthase.	transcription
60225	1	336036	5	NULL	NULL	0	NULL	1 ,25(OH)2D3	Chemical		activates					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_chembiol_7_3_173_s_236	10712934	It has been shown that 1 ,25(OH)2D3 activates sphingosine kinase, which in turn converts ceramide to sphingosin-1-phosphate (SPP) and prevents HL-60 cell ceramide-induced apoptosis  [50]  .	transcription
60226	2	336036	5	NULL	NULL	0	NULL	ceramide	Chemical		is converted to					SPP	Chemical				NULL		0	NULL	NULL	NULL	gw60_chembiol_7_3_173_s_236	10712934	It has been shown that 1 ,25(OH)2D3 activates sphingosine kinase, which in turn converts ceramide to sphingosin-1-phosphate (SPP) and prevents HL-60 cell ceramide-induced apoptosis  [50]  .	transcription
60227	3	336036	5	NULL	NULL	0	NULL	SPP	Chemical		is					sphingosin-1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_chembiol_7_3_173_s_236	10712934	It has been shown that 1 ,25(OH)2D3 activates sphingosine kinase, which in turn converts ceramide to sphingosin-1-phosphate (SPP) and prevents HL-60 cell ceramide-induced apoptosis  [50]  .	transcription
60228	4	336036	5	NULL	NULL	0	NULL	sphingosine kinase	GP	activated	catalyzes					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_chembiol_7_3_173_s_236	10712934	It has been shown that 1 ,25(OH)2D3 activates sphingosine kinase, which in turn converts ceramide to sphingosin-1-phosphate (SPP) and prevents HL-60 cell ceramide-induced apoptosis  [50]  .	transcription
60229	5	336036	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					ceramide	Chemical				NULL	HL-60 cell	0	NULL	NULL	NULL	gw60_chembiol_7_3_173_s_236	10712934	It has been shown that 1 ,25(OH)2D3 activates sphingosine kinase, which in turn converts ceramide to sphingosin-1-phosphate (SPP) and prevents HL-60 cell ceramide-induced apoptosis  [50]  .	transcription
60230	6	336036	5	NULL	NULL	0	NULL	statement 2	Process		prevents					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_chembiol_7_3_173_s_236	10712934	It has been shown that 1 ,25(OH)2D3 activates sphingosine kinase, which in turn converts ceramide to sphingosin-1-phosphate (SPP) and prevents HL-60 cell ceramide-induced apoptosis  [50]  .	transcription
66850	1	336036	7	NULL	NULL	0	NULL	1 ,25(OH)2D3	Chemical		activates					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_chembiol_7_3_173_s_236	10712934	It has been shown that 1 ,25(OH)2D3 activates sphingosine kinase, which in turn converts ceramide to sphingosin-1-phosphate (SPP) and prevents HL-60 cell ceramide-induced apoptosis  [50]  .	transcription
66851	2	336036	7	NULL	NULL	0	NULL	ceramide	Chemical		converted to					SPP	Chemical				NULL		0	NULL	NULL	NULL	gw60_chembiol_7_3_173_s_236	10712934	It has been shown that 1 ,25(OH)2D3 activates sphingosine kinase, which in turn converts ceramide to sphingosin-1-phosphate (SPP) and prevents HL-60 cell ceramide-induced apoptosis  [50]  .	transcription
66852	3	336036	7	NULL	NULL	NULL	NULL	sphingosine kinase	GP		catalyze					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_7_3_173_s_236	10712934	It has been shown that 1 ,25(OH)2D3 activates sphingosine kinase, which in turn converts ceramide to sphingosin-1-phosphate (SPP) and prevents HL-60 cell ceramide-induced apoptosis  [50]  .	transcription
66853	4	336036	7	NULL	NULL	NULL	NULL	ceramide	Chemical	HL-60 cell 	induce					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_chembiol_7_3_173_s_236	10712934	It has been shown that 1 ,25(OH)2D3 activates sphingosine kinase, which in turn converts ceramide to sphingosin-1-phosphate (SPP) and prevents HL-60 cell ceramide-induced apoptosis  [50]  .	transcription
66854	5	336036	7	NULL	NULL	0	NULL	sphingosine kinase	GP		prevents					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_chembiol_7_3_173_s_236	10712934	It has been shown that 1 ,25(OH)2D3 activates sphingosine kinase, which in turn converts ceramide to sphingosin-1-phosphate (SPP) and prevents HL-60 cell ceramide-induced apoptosis  [50]  .	transcription
66855	6	336036	7	NULL	NULL	0	NULL	SPP	Chemical		is					sphingosin-1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_chembiol_7_3_173_s_236	10712934	It has been shown that 1 ,25(OH)2D3 activates sphingosine kinase, which in turn converts ceramide to sphingosin-1-phosphate (SPP) and prevents HL-60 cell ceramide-induced apoptosis  [50]  .	transcription
60231	1	336037	5	NULL	NULL	0	NULL	ceramide	Chemical	levels of	is induced by					LPS	Chemical				NULL	mice	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_34_30784_s_242	12072440	First we showed that old MO have significantly higher LPS-induced ceramide levels compared with young mice, whereas there is no age difference in ceramide downstream metabolite sphingosine.	transcription
60232	2	336037	5	NULL	NULL	0	NULL	sphingosine	Chemical		is a metabolite of					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_34_30784_s_242	12072440	First we showed that old MO have significantly higher LPS-induced ceramide levels compared with young mice, whereas there is no age difference in ceramide downstream metabolite sphingosine.	transcription
66856	1	336037	7	NULL	NULL	0	NULL	 LPS	Chemical		induce					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_34_30784_s_242	12072440	First we showed that old MO have significantly higher LPS-induced ceramide levels compared with young mice, whereas there is no age difference in ceramide downstream metabolite sphingosine.	transcription
66857	2	336037	7	NULL	NULL	NULL	NULL	sphingosine	Chemical		is downstream metabolite of					ceramide	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_34_30784_s_242	12072440	First we showed that old MO have significantly higher LPS-induced ceramide levels compared with young mice, whereas there is no age difference in ceramide downstream metabolite sphingosine.	transcription
60245	1	336038	5	NULL	NULL	0	NULL	neurons	Cell	 death of	is induced by					NGF	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_9812_s_149	11777929	Ceramide Itself, and Not a Downstream Lipid Metabolite, Signals NGF-induced Neuronal Death-- Ceramide can be degraded by ceramidases to downstream metabolites such as sphingosine 1-phosphate, which has been shown to act as an extracellular initiator of apoptosis ( 47,  48).	transcription
60246	2	336038	5	NULL	NULL	0	NULL	ceramide	Chemical		signals					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_9812_s_149	11777929	Ceramide Itself, and Not a Downstream Lipid Metabolite, Signals NGF-induced Neuronal Death-- Ceramide can be degraded by ceramidases to downstream metabolites such as sphingosine 1-phosphate, which has been shown to act as an extracellular initiator of apoptosis ( 47,  48).	transcription
60247	3	336038	5	NULL	NULL	0	NULL	ceramide	Chemical		is degraded to					sphingosine 1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_9812_s_149	11777929	Ceramide Itself, and Not a Downstream Lipid Metabolite, Signals NGF-induced Neuronal Death-- Ceramide can be degraded by ceramidases to downstream metabolites such as sphingosine 1-phosphate, which has been shown to act as an extracellular initiator of apoptosis ( 47,  48).	transcription
60248	4	336038	5	NULL	NULL	0	NULL	ceramidases	GP		catalyzes					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_9812_s_149	11777929	Ceramide Itself, and Not a Downstream Lipid Metabolite, Signals NGF-induced Neuronal Death-- Ceramide can be degraded by ceramidases to downstream metabolites such as sphingosine 1-phosphate, which has been shown to act as an extracellular initiator of apoptosis ( 47,  48).	transcription
60249	5	336038	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		is an initiator of					apoptosis	Process				NULL	extracellularly	0	NULL	NULL	NULL	gw60_jbiolchem_277_12_9812_s_149	11777929	Ceramide Itself, and Not a Downstream Lipid Metabolite, Signals NGF-induced Neuronal Death-- Ceramide can be degraded by ceramidases to downstream metabolites such as sphingosine 1-phosphate, which has been shown to act as an extracellular initiator of apoptosis ( 47,  48).	transcription
66858	1	336038	7	NULL	NULL	0	NULL	NGF	GP		induce					Neuronal death	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_9812_s_149	11777929	Ceramide Itself, and Not a Downstream Lipid Metabolite, Signals NGF-induced Neuronal Death-- Ceramide can be degraded by ceramidases to downstream metabolites such as sphingosine 1-phosphate, which has been shown to act as an extracellular initiator of apoptosis ( 47,  48).	transcription
66859	2	336038	7	NULL	NULL	0	NULL	ceramide	Chemical		degraded to					sphingosine 1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_9812_s_149	11777929	Ceramide Itself, and Not a Downstream Lipid Metabolite, Signals NGF-induced Neuronal Death-- Ceramide can be degraded by ceramidases to downstream metabolites such as sphingosine 1-phosphate, which has been shown to act as an extracellular initiator of apoptosis ( 47,  48).	transcription
66860	3	336038	7	NULL	NULL	0	NULL	ceramidases	GP		catalyze					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_9812_s_149	11777929	Ceramide Itself, and Not a Downstream Lipid Metabolite, Signals NGF-induced Neuronal Death-- Ceramide can be degraded by ceramidases to downstream metabolites such as sphingosine 1-phosphate, which has been shown to act as an extracellular initiator of apoptosis ( 47,  48).	transcription
66861	4	336038	7	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		act as an					apoptosis	Process	extracellular initiator of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_9812_s_149	11777929	Ceramide Itself, and Not a Downstream Lipid Metabolite, Signals NGF-induced Neuronal Death-- Ceramide can be degraded by ceramidases to downstream metabolites such as sphingosine 1-phosphate, which has been shown to act as an extracellular initiator of apoptosis ( 47,  48).	transcription
60259	1	336039	5	NULL	NULL	0	NULL	ceramide	Chemical		is hydrolyzed to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_23	11956206	Although termination of the second messenger actions of ceramide is considered to be mediated by ceramidase, which hydrolyzes it to form sphingosine, it was suggested more than a decade ago that ceramide can also be phosphorylated to ceramide-1-phosphate ( 22).	transcription
60260	2	336039	5	NULL	NULL	0	NULL	ceramidase	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_23	11956206	Although termination of the second messenger actions of ceramide is considered to be mediated by ceramidase, which hydrolyzes it to form sphingosine, it was suggested more than a decade ago that ceramide can also be phosphorylated to ceramide-1-phosphate ( 22).	transcription
60261	3	336039	5	NULL	NULL	0	NULL	ceramide	Chemical		is phosphorylated to					ceramide-1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_23	11956206	Although termination of the second messenger actions of ceramide is considered to be mediated by ceramidase, which hydrolyzes it to form sphingosine, it was suggested more than a decade ago that ceramide can also be phosphorylated to ceramide-1-phosphate ( 22).	transcription
66866	1	336039	7	NULL	NULL	0	NULL	ceramide	Chemical		hydrolyzed to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_23	11956206	Although termination of the second messenger actions of ceramide is considered to be mediated by ceramidase, which hydrolyzes it to form sphingosine, it was suggested more than a decade ago that ceramide can also be phosphorylated to ceramide-1-phosphate ( 22).	transcription
66867	2	336039	7	NULL	NULL	0	NULL	ceramidase	GP		catalyze					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_23	11956206	Although termination of the second messenger actions of ceramide is considered to be mediated by ceramidase, which hydrolyzes it to form sphingosine, it was suggested more than a decade ago that ceramide can also be phosphorylated to ceramide-1-phosphate ( 22).	transcription
66868	3	336039	7	NULL	NULL	0	NULL	ceramidase	GP		mediates					second messenger actions	Process	termination of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_23	11956206	Although termination of the second messenger actions of ceramide is considered to be mediated by ceramidase, which hydrolyzes it to form sphingosine, it was suggested more than a decade ago that ceramide can also be phosphorylated to ceramide-1-phosphate ( 22).	transcription
66869	4	336039	7	NULL	NULL	NULL	NULL	statement 3	Process		occur through					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_23	11956206	Although termination of the second messenger actions of ceramide is considered to be mediated by ceramidase, which hydrolyzes it to form sphingosine, it was suggested more than a decade ago that ceramide can also be phosphorylated to ceramide-1-phosphate ( 22).	transcription
66871	5	336039	7	NULL	NULL	0	NULL	ceramide	Chemical		phosphorylated to					ceramide-1-phosphate 	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_23	11956206	Although termination of the second messenger actions of ceramide is considered to be mediated by ceramidase, which hydrolyzes it to form sphingosine, it was suggested more than a decade ago that ceramide can also be phosphorylated to ceramide-1-phosphate ( 22).	transcription
60262	1	336040	5	NULL	NULL	0	NULL	S1P	Chemical		is implicated in					cell growth	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_36_32947_s_21	12080051	In contrast to the growth inhibitory and pro-apoptotic effects of ceramide and sphingosine, a further metabolite, S1P, has been implicated in cell growth ( 7) and inhibition of ceramide-mediated apoptosis ( 8-13).	transcription
60264	2	336040	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_36_32947_s_21	12080051	In contrast to the growth inhibitory and pro-apoptotic effects of ceramide and sphingosine, a further metabolite, S1P, has been implicated in cell growth ( 7) and inhibition of ceramide-mediated apoptosis ( 8-13).	transcription
60265	3	336040	5	NULL	NULL	0	NULL	S1P	Chemical		inhibits					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_36_32947_s_21	12080051	In contrast to the growth inhibitory and pro-apoptotic effects of ceramide and sphingosine, a further metabolite, S1P, has been implicated in cell growth ( 7) and inhibition of ceramide-mediated apoptosis ( 8-13).	transcription
66874	1	336040	7	NULL	NULL	0	NULL	ceramide	Chemical		inhibits					growth	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_36_32947_s_21	12080051	In contrast to the growth inhibitory and pro-apoptotic effects of ceramide and sphingosine, a further metabolite, S1P, has been implicated in cell growth ( 7) and inhibition of ceramide-mediated apoptosis ( 8-13).	transcription
66882	2	336040	7	NULL	NULL	0	NULL	ceramide	Chemical		effect					pro-apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_36_32947_s_21	12080051	In contrast to the growth inhibitory and pro-apoptotic effects of ceramide and sphingosine, a further metabolite, S1P, has been implicated in cell growth ( 7) and inhibition of ceramide-mediated apoptosis ( 8-13).	transcription
66885	3	336040	7	NULL	NULL	0	NULL	sphingosine	Chemical		inhibits					growth	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_36_32947_s_21	12080051	In contrast to the growth inhibitory and pro-apoptotic effects of ceramide and sphingosine, a further metabolite, S1P, has been implicated in cell growth ( 7) and inhibition of ceramide-mediated apoptosis ( 8-13).	transcription
66886	4	336040	7	NULL	NULL	0	NULL	sphingosine	Chemical		effect					pro-apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_36_32947_s_21	12080051	In contrast to the growth inhibitory and pro-apoptotic effects of ceramide and sphingosine, a further metabolite, S1P, has been implicated in cell growth ( 7) and inhibition of ceramide-mediated apoptosis ( 8-13).	transcription
66887	5	336040	7	NULL	NULL	0	NULL	S1P	Chemical		implicated in					cell growth	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_36_32947_s_21	12080051	In contrast to the growth inhibitory and pro-apoptotic effects of ceramide and sphingosine, a further metabolite, S1P, has been implicated in cell growth ( 7) and inhibition of ceramide-mediated apoptosis ( 8-13).	transcription
66888	6	336040	7	NULL	NULL	0	NULL	ceramide	Chemical		mediate					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_36_32947_s_21	12080051	In contrast to the growth inhibitory and pro-apoptotic effects of ceramide and sphingosine, a further metabolite, S1P, has been implicated in cell growth ( 7) and inhibition of ceramide-mediated apoptosis ( 8-13).	transcription
66896	7	336040	7	NULL	NULL	0	NULL	S1P	Chemical		inhibit					statement 6					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_36_32947_s_21	12080051	In contrast to the growth inhibitory and pro-apoptotic effects of ceramide and sphingosine, a further metabolite, S1P, has been implicated in cell growth ( 7) and inhibition of ceramide-mediated apoptosis ( 8-13).	transcription
60266	1	336041	5	NULL	NULL	0	NULL	ceramidases	GP		regulates					ceramide	Chemical	level of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_25847_s_108	12011103	For example, ceramidases can regulate the levels of ceramide (substrate) and/or sphingosine and S1P (products), with S1P often exerting anti-apoptotic effects that antagonize ceramide-mediated responses (see minireview by Spiegel and Milstien ( 58)).	transcription
60267	2	336041	5	NULL	NULL	0	NULL	ceramidases	GP		regulates					sphingosine	Chemical	level of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_25847_s_108	12011103	For example, ceramidases can regulate the levels of ceramide (substrate) and/or sphingosine and S1P (products), with S1P often exerting anti-apoptotic effects that antagonize ceramide-mediated responses (see minireview by Spiegel and Milstien ( 58)).	transcription
60268	3	336041	5	NULL	NULL	0	NULL	ceramidases	GP		regulates					S1P	Chemical	level of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_25847_s_108	12011103	For example, ceramidases can regulate the levels of ceramide (substrate) and/or sphingosine and S1P (products), with S1P often exerting anti-apoptotic effects that antagonize ceramide-mediated responses (see minireview by Spiegel and Milstien ( 58)).	transcription
66897	1	336041	7	NULL	NULL	0	NULL	ceramidases	GP		regulate					ceramide	Chemical	levels of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_25847_s_108	12011103	For example, ceramidases can regulate the levels of ceramide (substrate) and/or sphingosine and S1P (products), with S1P often exerting anti-apoptotic effects that antagonize ceramide-mediated responses (see minireview by Spiegel and Milstien ( 58)).	transcription
66898	2	336041	7	NULL	NULL	0	NULL	ceramidases	GP		regulate					sphingosine	Chemical	levels of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_25847_s_108	12011103	For example, ceramidases can regulate the levels of ceramide (substrate) and/or sphingosine and S1P (products), with S1P often exerting anti-apoptotic effects that antagonize ceramide-mediated responses (see minireview by Spiegel and Milstien ( 58)).	transcription
66899	3	336041	7	NULL	NULL	0	NULL	ceramidases	GP		regulate					S1P	Chemical	levels of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_25847_s_108	12011103	For example, ceramidases can regulate the levels of ceramide (substrate) and/or sphingosine and S1P (products), with S1P often exerting anti-apoptotic effects that antagonize ceramide-mediated responses (see minireview by Spiegel and Milstien ( 58)).	transcription
66900	4	336041	7	NULL	NULL	0	NULL	S1P	Chemical		exerts					anti-apoptotic effects	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_25847_s_108	12011103	For example, ceramidases can regulate the levels of ceramide (substrate) and/or sphingosine and S1P (products), with S1P often exerting anti-apoptotic effects that antagonize ceramide-mediated responses (see minireview by Spiegel and Milstien ( 58)).	transcription
66901	5	336041	7	NULL	NULL	0	NULL	ceramide	Chemical		mediate					responses	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_25847_s_108	12011103	For example, ceramidases can regulate the levels of ceramide (substrate) and/or sphingosine and S1P (products), with S1P often exerting anti-apoptotic effects that antagonize ceramide-mediated responses (see minireview by Spiegel and Milstien ( 58)).	transcription
66902	6	336041	7	NULL	NULL	0	NULL	S1P	Chemical		antagonize					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_29_25847_s_108	12011103	For example, ceramidases can regulate the levels of ceramide (substrate) and/or sphingosine and S1P (products), with S1P often exerting anti-apoptotic effects that antagonize ceramide-mediated responses (see minireview by Spiegel and Milstien ( 58)).	transcription
60275	1	336042	5	NULL	NULL	0	NULL	PLA2	GP		does not induce		significantly			JNK	GP	activity of			NULL	MS1418 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_70	9346918	In contrast, PLA2 or PLC did not show significant induction of JNK activity, and C2-Dhc (an inactive form of ceramide) or sphingosine (a metabolic of ceramide) induces only very weak JNK activation in MS1418 cells (Fig.  6).	transcription
60276	2	336042	5	NULL	NULL	0	NULL	PLC	GP		does not induce		significantly			JNK	GP	activity of			NULL	MS1418 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_70	9346918	In contrast, PLA2 or PLC did not show significant induction of JNK activity, and C2-Dhc (an inactive form of ceramide) or sphingosine (a metabolic of ceramide) induces only very weak JNK activation in MS1418 cells (Fig.  6).	transcription
60277	3	336042	5	NULL	NULL	0	NULL	C2-Dhc	Chemical		is an inactive form of					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_70	9346918	In contrast, PLA2 or PLC did not show significant induction of JNK activity, and C2-Dhc (an inactive form of ceramide) or sphingosine (a metabolic of ceramide) induces only very weak JNK activation in MS1418 cells (Fig.  6).	transcription
60278	4	336042	5	NULL	NULL	0	NULL	C2-Dhc	Chemical		induce		weakly			JNK	GP	activation of			NULL	MS1418 cells	0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_70	9346918	In contrast, PLA2 or PLC did not show significant induction of JNK activity, and C2-Dhc (an inactive form of ceramide) or sphingosine (a metabolic of ceramide) induces only very weak JNK activation in MS1418 cells (Fig.  6).	transcription
60279	5	336042	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce		weakly			JNK	GP	activation of			NULL	MS1418 cells	0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_70	9346918	In contrast, PLA2 or PLC did not show significant induction of JNK activity, and C2-Dhc (an inactive form of ceramide) or sphingosine (a metabolic of ceramide) induces only very weak JNK activation in MS1418 cells (Fig.  6).	transcription
60281	6	336042	5	NULL	NULL	0	NULL	sphingosine	Chemical		is a metabolite of					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_70	9346918	In contrast, PLA2 or PLC did not show significant induction of JNK activity, and C2-Dhc (an inactive form of ceramide) or sphingosine (a metabolic of ceramide) induces only very weak JNK activation in MS1418 cells (Fig.  6).	transcription
66903	1	336042	7	NULL	NULL	0	NULL	PLA2	Chemical		does not induce		significantly			JNK activity	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_70	9346918	In contrast, PLA2 or PLC did not show significant induction of JNK activity, and C2-Dhc (an inactive form of ceramide) or sphingosine (a metabolic of ceramide) induces only very weak JNK activation in MS1418 cells (Fig.  6).	transcription
66904	2	336042	7	NULL	NULL	0	NULL	PLC 	Chemical		does not induce		significantly			JNK activity	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_70	9346918	In contrast, PLA2 or PLC did not show significant induction of JNK activity, and C2-Dhc (an inactive form of ceramide) or sphingosine (a metabolic of ceramide) induces only very weak JNK activation in MS1418 cells (Fig.  6).	transcription
66905	3	336042	7	NULL	NULL	0	NULL	C2-Dhc	Chemical		is inactive form of					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_70	9346918	In contrast, PLA2 or PLC did not show significant induction of JNK activity, and C2-Dhc (an inactive form of ceramide) or sphingosine (a metabolic of ceramide) induces only very weak JNK activation in MS1418 cells (Fig.  6).	transcription
66906	4	336042	7	NULL	NULL	0	NULL	C2-Dhc	Chemical		induce		weakly			JNK	GP	activation of			NULL	MS1418 cells	0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_70	9346918	In contrast, PLA2 or PLC did not show significant induction of JNK activity, and C2-Dhc (an inactive form of ceramide) or sphingosine (a metabolic of ceramide) induces only very weak JNK activation in MS1418 cells (Fig.  6).	transcription
66907	5	336042	7	NULL	NULL	0	NULL	sphingosine	Chemical		is a metabolite of					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_70	9346918	In contrast, PLA2 or PLC did not show significant induction of JNK activity, and C2-Dhc (an inactive form of ceramide) or sphingosine (a metabolic of ceramide) induces only very weak JNK activation in MS1418 cells (Fig.  6).	transcription
66908	6	336042	7	NULL	NULL	0	NULL	sphingosine	Chemical		induce		weakly			JNK	GP	activation of			NULL	MS1418 cells	0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_70	9346918	In contrast, PLA2 or PLC did not show significant induction of JNK activity, and C2-Dhc (an inactive form of ceramide) or sphingosine (a metabolic of ceramide) induces only very weak JNK activation in MS1418 cells (Fig.  6).	transcription
60282	1	336043	5	NULL	NULL	0	NULL	sphingosine	Chemical		is converted to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_79	10747891	To examine the possibility that sphingosine could induce apoptosis due to its conversion to ceramide, we investigated the effect of the mycotoxin fumonisin B1, a known inhibitor of ceramide synthase ( 39).	transcription
60284	2	336043	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce		possibly			apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_79	10747891	To examine the possibility that sphingosine could induce apoptosis due to its conversion to ceramide, we investigated the effect of the mycotoxin fumonisin B1, a known inhibitor of ceramide synthase ( 39).	transcription
60285	3	336043	5	NULL	NULL	0	NULL	statement 1	Process		leads to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_79	10747891	To examine the possibility that sphingosine could induce apoptosis due to its conversion to ceramide, we investigated the effect of the mycotoxin fumonisin B1, a known inhibitor of ceramide synthase ( 39).	transcription
60286	4	336043	5	NULL	NULL	0	NULL	fumonisin B1	Chemical		is a type of					mycotoxin	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_79	10747891	To examine the possibility that sphingosine could induce apoptosis due to its conversion to ceramide, we investigated the effect of the mycotoxin fumonisin B1, a known inhibitor of ceramide synthase ( 39).	transcription
60287	5	336043	5	NULL	NULL	0	NULL	fumonisin B1	Chemical		is an inhibitor of					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_79	10747891	To examine the possibility that sphingosine could induce apoptosis due to its conversion to ceramide, we investigated the effect of the mycotoxin fumonisin B1, a known inhibitor of ceramide synthase ( 39).	transcription
66909	1	336043	7	NULL	NULL	0	NULL	sphingosine	Chemical		converted to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_79	10747891	To examine the possibility that sphingosine could induce apoptosis due to its conversion to ceramide, we investigated the effect of the mycotoxin fumonisin B1, a known inhibitor of ceramide synthase ( 39).	transcription
66910	2	336043	7	NULL	NULL	0	NULL	fumonisin B1	Chemical		is an inhibitor of					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_79	10747891	To examine the possibility that sphingosine could induce apoptosis due to its conversion to ceramide, we investigated the effect of the mycotoxin fumonisin B1, a known inhibitor of ceramide synthase ( 39).	transcription
66911	3	336043	7	NULL	NULL	0	NULL	fumonisin B1	Chemical		is a type of					mycotoxin	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_79	10747891	To examine the possibility that sphingosine could induce apoptosis due to its conversion to ceramide, we investigated the effect of the mycotoxin fumonisin B1, a known inhibitor of ceramide synthase ( 39).	transcription
60326	1	336044	5	NULL	NULL	0	NULL	sphingosine	Chemical		is a metabolite of					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_245	10747891	Our study also suggests a potential role for sphingosine, a further metabolite of ceramide, in Fas-induced apoptosis of type II cells, and demonstrates that similar to ceramide it also mediates cyt  c release.	transcription
60327	2	336044	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					Fas	GP				NULL	type II cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_245	10747891	Our study also suggests a potential role for sphingosine, a further metabolite of ceramide, in Fas-induced apoptosis of type II cells, and demonstrates that similar to ceramide it also mediates cyt  c release.	transcription
60328	3	336044	5	NULL	NULL	0	NULL	sphingosine	Chemical		plays a role in		potentially			statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_245	10747891	Our study also suggests a potential role for sphingosine, a further metabolite of ceramide, in Fas-induced apoptosis of type II cells, and demonstrates that similar to ceramide it also mediates cyt  c release.	transcription
60329	4	336044	5	NULL	NULL	0	NULL	ceramide	Chemical		mediates					cyt c	GP	release of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_245	10747891	Our study also suggests a potential role for sphingosine, a further metabolite of ceramide, in Fas-induced apoptosis of type II cells, and demonstrates that similar to ceramide it also mediates cyt  c release.	transcription
60330	5	336044	5	NULL	NULL	0	NULL	sphingosine	Chemical		mediates					cyt c	GP	release of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_245	10747891	Our study also suggests a potential role for sphingosine, a further metabolite of ceramide, in Fas-induced apoptosis of type II cells, and demonstrates that similar to ceramide it also mediates cyt  c release.	transcription
67126	1	336044	7	NULL	NULL	0	NULL	sphingosine	Chemical		metabolite of					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_245	10747891	Our study also suggests a potential role for sphingosine, a further metabolite of ceramide, in Fas-induced apoptosis of type II cells, and demonstrates that similar to ceramide it also mediates cyt  c release.	transcription
67127	2	336044	7	NULL	NULL	NULL	NULL	sphingosine	Chemical		mediate					cyt c	GP	release of			NULL	Fas-induced apoptosis of type II cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_245	10747891	Our study also suggests a potential role for sphingosine, a further metabolite of ceramide, in Fas-induced apoptosis of type II cells, and demonstrates that similar to ceramide it also mediates cyt  c release.	transcription
67128	3	336044	7	NULL	NULL	NULL	NULL	ceramide	Chemical		mediate					cyt c	GP	release of			NULL	Fas-induced apoptosis of type II cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_245	10747891	Our study also suggests a potential role for sphingosine, a further metabolite of ceramide, in Fas-induced apoptosis of type II cells, and demonstrates that similar to ceramide it also mediates cyt  c release.	transcription
60331	1	336045	5	NULL	NULL	0	NULL	TPA	Chemical		activates					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_40_28286_s_244	10497185	Also TPA has been shown to activate sphingosine kinase, leading to increased concentrations of sphingosine-1-phosphate (SPP), which is a metabolite of ceramide and suppresses ceramide-mediated apoptosis ( 65,  77).	transcription
60332	2	336045	5	NULL	NULL	0	NULL	statement 1	Process		increases					SPP	Chemical	concentration of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_40_28286_s_244	10497185	Also TPA has been shown to activate sphingosine kinase, leading to increased concentrations of sphingosine-1-phosphate (SPP), which is a metabolite of ceramide and suppresses ceramide-mediated apoptosis ( 65,  77).	transcription
60333	3	336045	5	NULL	NULL	0	NULL	SPP	Chemical		is a metabolite of					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_40_28286_s_244	10497185	Also TPA has been shown to activate sphingosine kinase, leading to increased concentrations of sphingosine-1-phosphate (SPP), which is a metabolite of ceramide and suppresses ceramide-mediated apoptosis ( 65,  77).	transcription
60334	4	336045	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_40_28286_s_244	10497185	Also TPA has been shown to activate sphingosine kinase, leading to increased concentrations of sphingosine-1-phosphate (SPP), which is a metabolite of ceramide and suppresses ceramide-mediated apoptosis ( 65,  77).	transcription
60335	5	336045	5	NULL	NULL	0	NULL	SPP	Chemical		supress					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_40_28286_s_244	10497185	Also TPA has been shown to activate sphingosine kinase, leading to increased concentrations of sphingosine-1-phosphate (SPP), which is a metabolite of ceramide and suppresses ceramide-mediated apoptosis ( 65,  77).	transcription
60336	6	336045	5	NULL	NULL	0	NULL	SPP	Chemical		is					sphingosine 1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_40_28286_s_244	10497185	Also TPA has been shown to activate sphingosine kinase, leading to increased concentrations of sphingosine-1-phosphate (SPP), which is a metabolite of ceramide and suppresses ceramide-mediated apoptosis ( 65,  77).	transcription
67129	1	336045	7	NULL	NULL	0	NULL	TPA	Chemical		activate					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_40_28286_s_244	10497185	Also TPA has been shown to activate sphingosine kinase, leading to increased concentrations of sphingosine-1-phosphate (SPP), which is a metabolite of ceramide and suppresses ceramide-mediated apoptosis ( 65,  77).	transcription
67130	2	336045	7	NULL	NULL	0	NULL	statement 1	Process		leads to					SPP	Chemical	increased concentrations of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_40_28286_s_244	10497185	Also TPA has been shown to activate sphingosine kinase, leading to increased concentrations of sphingosine-1-phosphate (SPP), which is a metabolite of ceramide and suppresses ceramide-mediated apoptosis ( 65,  77).	transcription
67131	3	336045	7	NULL	NULL	NULL	NULL	SPP	Chemical		is a metabolite of					ceramide	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_40_28286_s_244	10497185	Also TPA has been shown to activate sphingosine kinase, leading to increased concentrations of sphingosine-1-phosphate (SPP), which is a metabolite of ceramide and suppresses ceramide-mediated apoptosis ( 65,  77).	transcription
67132	4	336045	7	NULL	NULL	0	NULL	ceramide	Chemical		mediate					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_40_28286_s_244	10497185	Also TPA has been shown to activate sphingosine kinase, leading to increased concentrations of sphingosine-1-phosphate (SPP), which is a metabolite of ceramide and suppresses ceramide-mediated apoptosis ( 65,  77).	transcription
67133	5	336045	7	NULL	NULL	0	NULL	SPP	Chemical		suppress					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_40_28286_s_244	10497185	Also TPA has been shown to activate sphingosine kinase, leading to increased concentrations of sphingosine-1-phosphate (SPP), which is a metabolite of ceramide and suppresses ceramide-mediated apoptosis ( 65,  77).	transcription
67134	6	336045	7	NULL	NULL	0	NULL	SPP	Chemical		is					sphingosine-1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_40_28286_s_244	10497185	Also TPA has been shown to activate sphingosine kinase, leading to increased concentrations of sphingosine-1-phosphate (SPP), which is a metabolite of ceramide and suppresses ceramide-mediated apoptosis ( 65,  77).	transcription
60337	1	336046	5	NULL	NULL	0	NULL	sphingosine	Chemical		is produced from					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_43_30580_s_207	10521441	Such pathways could produce sphingosine from ceramide through the action of a ceramidase or utilize ceramide for ganglioside synthesis because recent studies have indicated that ganglioside synthesis is necessary for Fas-induced apoptosis ( 28).	transcription
60338	2	336046	5	NULL	NULL	0	NULL	ceramidase	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_43_30580_s_207	10521441	Such pathways could produce sphingosine from ceramide through the action of a ceramidase or utilize ceramide for ganglioside synthesis because recent studies have indicated that ganglioside synthesis is necessary for Fas-induced apoptosis ( 28).	transcription
60339	3	336046	5	NULL	NULL	0	NULL	ganglioside	Chemical		is synthesized from					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_43_30580_s_207	10521441	Such pathways could produce sphingosine from ceramide through the action of a ceramidase or utilize ceramide for ganglioside synthesis because recent studies have indicated that ganglioside synthesis is necessary for Fas-induced apoptosis ( 28).	transcription
60340	4	336046	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					Fas	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_43_30580_s_207	10521441	Such pathways could produce sphingosine from ceramide through the action of a ceramidase or utilize ceramide for ganglioside synthesis because recent studies have indicated that ganglioside synthesis is necessary for Fas-induced apoptosis ( 28).	transcription
60341	5	336046	5	NULL	NULL	0	NULL	statement 3	Process		is required for					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_43_30580_s_207	10521441	Such pathways could produce sphingosine from ceramide through the action of a ceramidase or utilize ceramide for ganglioside synthesis because recent studies have indicated that ganglioside synthesis is necessary for Fas-induced apoptosis ( 28).	transcription
67135	1	336046	7	NULL	NULL	0	NULL	ceramide	Chemical		produced from					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_43_30580_s_207	10521441	Such pathways could produce sphingosine from ceramide through the action of a ceramidase or utilize ceramide for ganglioside synthesis because recent studies have indicated that ganglioside synthesis is necessary for Fas-induced apoptosis ( 28).	transcription
67136	2	336046	7	NULL	NULL	0	NULL	statement 1	Process		occur through					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_43_30580_s_207	10521441	Such pathways could produce sphingosine from ceramide through the action of a ceramidase or utilize ceramide for ganglioside synthesis because recent studies have indicated that ganglioside synthesis is necessary for Fas-induced apoptosis ( 28).	transcription
67137	3	336046	7	NULL	NULL	0	NULL	ceramide	Chemical		utilized for					ganglioside synthesis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_43_30580_s_207	10521441	Such pathways could produce sphingosine from ceramide through the action of a ceramidase or utilize ceramide for ganglioside synthesis because recent studies have indicated that ganglioside synthesis is necessary for Fas-induced apoptosis ( 28).	transcription
67138	4	336046	7	NULL	NULL	0	NULL	Fas	GP		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_43_30580_s_207	10521441	Such pathways could produce sphingosine from ceramide through the action of a ceramidase or utilize ceramide for ganglioside synthesis because recent studies have indicated that ganglioside synthesis is necessary for Fas-induced apoptosis ( 28).	transcription
67139	5	336046	7	NULL	NULL	0	NULL	ganglioside synthesis	Process		necessary for					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_43_30580_s_207	10521441	Such pathways could produce sphingosine from ceramide through the action of a ceramidase or utilize ceramide for ganglioside synthesis because recent studies have indicated that ganglioside synthesis is necessary for Fas-induced apoptosis ( 28).	transcription
60425	1	336047	5	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL	neonatal cells	0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_164	8981934	The lower effectiveness of ceramide in inducing neonatal cells into apoptosis is  in agreement with the comet data of Fig.  3 D, showing that in  adult cells, sphingosine produced a higher yield of apoptotic  type cells than did ceramide.	transcription
60427	2	336047	5	NULL	NULL	0	NULL	sphingosine	Chemical		produce					apoptotic type cells	Cell				NULL	adult cells	0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_164	8981934	The lower effectiveness of ceramide in inducing neonatal cells into apoptosis is  in agreement with the comet data of Fig.  3 D, showing that in  adult cells, sphingosine produced a higher yield of apoptotic  type cells than did ceramide.	transcription
60429	3	336047	5	NULL	NULL	0	NULL	ceramide	Chemical		produce					apoptotic type cells	Cell				NULL	adult cells	0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_164	8981934	The lower effectiveness of ceramide in inducing neonatal cells into apoptosis is  in agreement with the comet data of Fig.  3 D, showing that in  adult cells, sphingosine produced a higher yield of apoptotic  type cells than did ceramide.	transcription
60431	4	336047	5	NULL	NULL	0	NULL	statement 2	Process		higher yield than					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_164	8981934	The lower effectiveness of ceramide in inducing neonatal cells into apoptosis is  in agreement with the comet data of Fig.  3 D, showing that in  adult cells, sphingosine produced a higher yield of apoptotic  type cells than did ceramide.	transcription
67140	1	336047	7	NULL	NULL	0	NULL	neonatal cells	Cell		induced to					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_164	8981934	The lower effectiveness of ceramide in inducing neonatal cells into apoptosis is  in agreement with the comet data of Fig.  3 D, showing that in  adult cells, sphingosine produced a higher yield of apoptotic  type cells than did ceramide.	transcription
67141	2	336047	7	NULL	NULL	0	NULL	ceramide	Chemical		mediate					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_164	8981934	The lower effectiveness of ceramide in inducing neonatal cells into apoptosis is  in agreement with the comet data of Fig.  3 D, showing that in  adult cells, sphingosine produced a higher yield of apoptotic  type cells than did ceramide.	transcription
67142	3	336047	7	NULL	NULL	NULL	NULL	sphingosine	Chemical		produce					apoptotic type cells	Cell				NULL	adult cells	NULL	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_164	8981934	The lower effectiveness of ceramide in inducing neonatal cells into apoptosis is  in agreement with the comet data of Fig.  3 D, showing that in  adult cells, sphingosine produced a higher yield of apoptotic  type cells than did ceramide.	transcription
67143	4	336047	7	NULL	NULL	NULL	NULL	ceramide	Chemical		produce					apoptotic type cells	Cell				NULL	adult cells	NULL	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_164	8981934	The lower effectiveness of ceramide in inducing neonatal cells into apoptosis is  in agreement with the comet data of Fig.  3 D, showing that in  adult cells, sphingosine produced a higher yield of apoptotic  type cells than did ceramide.	transcription
67144	5	336047	7	NULL	NULL	NULL	NULL	statement 3	Process		 higher  than					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_164	8981934	The lower effectiveness of ceramide in inducing neonatal cells into apoptosis is  in agreement with the comet data of Fig.  3 D, showing that in  adult cells, sphingosine produced a higher yield of apoptotic  type cells than did ceramide.	transcription
60464	1	336048	5	NULL	NULL	0	NULL	apoptosis	Process		initiated by					TNF	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_1_1_s_90	9469581	In fact, the initiation of apoptosis by TNF in some cell types appears to derive not from N-SMase-mediated generation of ceramide, but rather from the subsequent deacylation of ceramide to sphingosine  ( 46) ( 47).	transcription
60465	2	336048	5	NULL	NULL	0	NULL	ceramide	Chemical	generation of	is mediated by					N-SMase	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_1_1_s_90	9469581	In fact, the initiation of apoptosis by TNF in some cell types appears to derive not from N-SMase-mediated generation of ceramide, but rather from the subsequent deacylation of ceramide to sphingosine  ( 46) ( 47).	transcription
60466	3	336048	5	NULL	NULL	0	NULL	statement 1	Process		not derived from					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_1_1_s_90	9469581	In fact, the initiation of apoptosis by TNF in some cell types appears to derive not from N-SMase-mediated generation of ceramide, but rather from the subsequent deacylation of ceramide to sphingosine  ( 46) ( 47).	transcription
60467	4	336048	5	NULL	NULL	0	NULL	ceramide	Chemical		deacetylated to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_1_1_s_90	9469581	In fact, the initiation of apoptosis by TNF in some cell types appears to derive not from N-SMase-mediated generation of ceramide, but rather from the subsequent deacylation of ceramide to sphingosine  ( 46) ( 47).	transcription
60468	5	336048	5	NULL	NULL	0	NULL	statement 2	Process		followed by					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_1_1_s_90	9469581	In fact, the initiation of apoptosis by TNF in some cell types appears to derive not from N-SMase-mediated generation of ceramide, but rather from the subsequent deacylation of ceramide to sphingosine  ( 46) ( 47).	transcription
60469	6	336048	5	NULL	NULL	0	NULL	statement 1	Process		is derived from					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_1_1_s_90	9469581	In fact, the initiation of apoptosis by TNF in some cell types appears to derive not from N-SMase-mediated generation of ceramide, but rather from the subsequent deacylation of ceramide to sphingosine  ( 46) ( 47).	transcription
67145	1	336048	7	NULL	NULL	0	NULL	TNF	GP		initiate					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_1_1_s_90	9469581	In fact, the initiation of apoptosis by TNF in some cell types appears to derive not from N-SMase-mediated generation of ceramide, but rather from the subsequent deacylation of ceramide to sphingosine  ( 46) ( 47).	transcription
67146	2	336048	7	NULL	NULL	0	NULL	N-SMase	GP		mediate					ceramide	Chemical	generation of			NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_1_1_s_90	9469581	In fact, the initiation of apoptosis by TNF in some cell types appears to derive not from N-SMase-mediated generation of ceramide, but rather from the subsequent deacylation of ceramide to sphingosine  ( 46) ( 47).	transcription
67147	3	336048	7	NULL	NULL	0	NULL	ceramide	Chemical		deacylated to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_1_1_s_90	9469581	In fact, the initiation of apoptosis by TNF in some cell types appears to derive not from N-SMase-mediated generation of ceramide, but rather from the subsequent deacylation of ceramide to sphingosine  ( 46) ( 47).	transcription
67148	4	336048	7	NULL	NULL	0	NULL	statement 1	Process		does not derive from					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_1_1_s_90	9469581	In fact, the initiation of apoptosis by TNF in some cell types appears to derive not from N-SMase-mediated generation of ceramide, but rather from the subsequent deacylation of ceramide to sphingosine  ( 46) ( 47).	transcription
67149	5	336048	7	NULL	NULL	0	NULL	statement 1	Process		derived from					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jlipidres_39_1_1_s_90	9469581	In fact, the initiation of apoptosis by TNF in some cell types appears to derive not from N-SMase-mediated generation of ceramide, but rather from the subsequent deacylation of ceramide to sphingosine  ( 46) ( 47).	transcription
60470	1	336049	5	NULL	NULL	0	NULL	sphingosine	Chemical		is converted to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_191	9278531	This effect may be mediated by conversion of sphingosine to ceramide, because elevation of ceramide levels by treatment of PC12 cells with sphingomyelinase suppresses neurite outgrowth induced by NGF via a PKC-independent pathway (Tamura et al., 1994  ).	transcription
60471	2	336049	5	NULL	NULL	0	NULL	PC12 cells	Cell		treated with					sphingomyelinase	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_191	9278531	This effect may be mediated by conversion of sphingosine to ceramide, because elevation of ceramide levels by treatment of PC12 cells with sphingomyelinase suppresses neurite outgrowth induced by NGF via a PKC-independent pathway (Tamura et al., 1994  ).	transcription
60472	3	336049	5	NULL	NULL	0	NULL	statement 2	Process		elevates					ceramide	Chemical	level of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_191	9278531	This effect may be mediated by conversion of sphingosine to ceramide, because elevation of ceramide levels by treatment of PC12 cells with sphingomyelinase suppresses neurite outgrowth induced by NGF via a PKC-independent pathway (Tamura et al., 1994  ).	transcription
60480	4	336049	5	NULL	NULL	0	NULL	neurite	CellComponent	outgrowth of	is induced by					NGF	GP				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_191	9278531	This effect may be mediated by conversion of sphingosine to ceramide, because elevation of ceramide levels by treatment of PC12 cells with sphingomyelinase suppresses neurite outgrowth induced by NGF via a PKC-independent pathway (Tamura et al., 1994  ).	transcription
60481	5	336049	5	NULL	NULL	0	NULL	statement 3	Process		supress					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_191	9278531	This effect may be mediated by conversion of sphingosine to ceramide, because elevation of ceramide levels by treatment of PC12 cells with sphingomyelinase suppresses neurite outgrowth induced by NGF via a PKC-independent pathway (Tamura et al., 1994  ).	transcription
60483	6	336049	5	NULL	NULL	0	NULL	statement 5	Process		via					PKC-independent pathway	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_191	9278531	This effect may be mediated by conversion of sphingosine to ceramide, because elevation of ceramide levels by treatment of PC12 cells with sphingomyelinase suppresses neurite outgrowth induced by NGF via a PKC-independent pathway (Tamura et al., 1994  ).	transcription
67150	1	336049	7	NULL	NULL	0	NULL	sphingosine	Chemical		converted to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_191	9278531	This effect may be mediated by conversion of sphingosine to ceramide, because elevation of ceramide levels by treatment of PC12 cells with sphingomyelinase suppresses neurite outgrowth induced by NGF via a PKC-independent pathway (Tamura et al., 1994  ).	transcription
67151	2	336049	7	NULL	NULL	0	NULL	PC12 cells 	Cell		treated with					sphingomyelinase	GP				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_191	9278531	This effect may be mediated by conversion of sphingosine to ceramide, because elevation of ceramide levels by treatment of PC12 cells with sphingomyelinase suppresses neurite outgrowth induced by NGF via a PKC-independent pathway (Tamura et al., 1994  ).	transcription
67152	3	336049	7	NULL	NULL	0	NULL	statement 2	Process		elevates					ceramide	Chemical	levels of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_191	9278531	This effect may be mediated by conversion of sphingosine to ceramide, because elevation of ceramide levels by treatment of PC12 cells with sphingomyelinase suppresses neurite outgrowth induced by NGF via a PKC-independent pathway (Tamura et al., 1994  ).	transcription
67153	4	336049	7	NULL	NULL	0	NULL	NGF	GP		induce					neurite outgrowth	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_191	9278531	This effect may be mediated by conversion of sphingosine to ceramide, because elevation of ceramide levels by treatment of PC12 cells with sphingomyelinase suppresses neurite outgrowth induced by NGF via a PKC-independent pathway (Tamura et al., 1994  ).	transcription
67154	5	336049	7	NULL	NULL	0	NULL	statement 3	Process		suppress					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_191	9278531	This effect may be mediated by conversion of sphingosine to ceramide, because elevation of ceramide levels by treatment of PC12 cells with sphingomyelinase suppresses neurite outgrowth induced by NGF via a PKC-independent pathway (Tamura et al., 1994  ).	transcription
67155	6	336049	7	NULL	NULL	0	NULL	statement 4	Process		via					PKC-independent pathway	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_191	9278531	This effect may be mediated by conversion of sphingosine to ceramide, because elevation of ceramide levels by treatment of PC12 cells with sphingomyelinase suppresses neurite outgrowth induced by NGF via a PKC-independent pathway (Tamura et al., 1994  ).	transcription
60484	1	336050	5	NULL	NULL	0	NULL	PKC	GP	activation of	is dependent on					DAG	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_221	9536027	Studies show that DAG-dependent PKC activation and ceramide production have an antagonistic relationship, and sphinganine and sphingosine inhibit PKC, thereby increasing the potency and efficacy of the ceramide in inducing apoptosis in cell lines (Jarvis  et al., 1996  ).	transcription
60485	2	336050	5	NULL	NULL	0	NULL	statement 1	Process		is antagonistic to					ceramide	Chemical	production of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_221	9536027	Studies show that DAG-dependent PKC activation and ceramide production have an antagonistic relationship, and sphinganine and sphingosine inhibit PKC, thereby increasing the potency and efficacy of the ceramide in inducing apoptosis in cell lines (Jarvis  et al., 1996  ).	transcription
60487	3	336050	5	NULL	NULL	0	NULL	sphinganine	Chemical		inhibits					PKC	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_221	9536027	Studies show that DAG-dependent PKC activation and ceramide production have an antagonistic relationship, and sphinganine and sphingosine inhibit PKC, thereby increasing the potency and efficacy of the ceramide in inducing apoptosis in cell lines (Jarvis  et al., 1996  ).	transcription
60488	4	336050	5	NULL	NULL	0	NULL	sphingosine	Chemical		inhibits					PKC	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_221	9536027	Studies show that DAG-dependent PKC activation and ceramide production have an antagonistic relationship, and sphinganine and sphingosine inhibit PKC, thereby increasing the potency and efficacy of the ceramide in inducing apoptosis in cell lines (Jarvis  et al., 1996  ).	transcription
60489	5	336050	5	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_221	9536027	Studies show that DAG-dependent PKC activation and ceramide production have an antagonistic relationship, and sphinganine and sphingosine inhibit PKC, thereby increasing the potency and efficacy of the ceramide in inducing apoptosis in cell lines (Jarvis  et al., 1996  ).	transcription
60491	6	336050	5	NULL	NULL	0	NULL	statement 3	Process		increases					statement 5	Process	potency of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_221	9536027	Studies show that DAG-dependent PKC activation and ceramide production have an antagonistic relationship, and sphinganine and sphingosine inhibit PKC, thereby increasing the potency and efficacy of the ceramide in inducing apoptosis in cell lines (Jarvis  et al., 1996  ).	transcription
60493	7	336050	5	NULL	NULL	0	NULL	statement 3	Process		increases					statement 5	Process	efficacy of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_221	9536027	Studies show that DAG-dependent PKC activation and ceramide production have an antagonistic relationship, and sphinganine and sphingosine inhibit PKC, thereby increasing the potency and efficacy of the ceramide in inducing apoptosis in cell lines (Jarvis  et al., 1996  ).	transcription
60494	8	336050	5	NULL	NULL	0	NULL	statement 4	Process		increases					statement 5	Process	potency of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_221	9536027	Studies show that DAG-dependent PKC activation and ceramide production have an antagonistic relationship, and sphinganine and sphingosine inhibit PKC, thereby increasing the potency and efficacy of the ceramide in inducing apoptosis in cell lines (Jarvis  et al., 1996  ).	transcription
60495	9	336050	5	NULL	NULL	0	NULL	statement 4	Process		increases					statement 5	Process	efficacy of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_221	9536027	Studies show that DAG-dependent PKC activation and ceramide production have an antagonistic relationship, and sphinganine and sphingosine inhibit PKC, thereby increasing the potency and efficacy of the ceramide in inducing apoptosis in cell lines (Jarvis  et al., 1996  ).	transcription
67156	1	336050	7	NULL	NULL	0	NULL	PKC	GP	activation of	depends on					DAG	Chemical				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_221	9536027	Studies show that DAG-dependent PKC activation and ceramide production have an antagonistic relationship, and sphinganine and sphingosine inhibit PKC, thereby increasing the potency and efficacy of the ceramide in inducing apoptosis in cell lines (Jarvis  et al., 1996  ).	transcription
67157	2	336050	7	NULL	NULL	0	NULL	ceramide	Chemical	production of	depends on					DAG	Chemical				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_221	9536027	Studies show that DAG-dependent PKC activation and ceramide production have an antagonistic relationship, and sphinganine and sphingosine inhibit PKC, thereby increasing the potency and efficacy of the ceramide in inducing apoptosis in cell lines (Jarvis  et al., 1996  ).	transcription
67158	3	336050	7	NULL	NULL	0	NULL	statement 1	Process		antagonizes with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_221	9536027	Studies show that DAG-dependent PKC activation and ceramide production have an antagonistic relationship, and sphinganine and sphingosine inhibit PKC, thereby increasing the potency and efficacy of the ceramide in inducing apoptosis in cell lines (Jarvis  et al., 1996  ).	transcription
67159	4	336050	7	NULL	NULL	0	NULL	sphinganine	Chemical		inhibit					PKC	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_221	9536027	Studies show that DAG-dependent PKC activation and ceramide production have an antagonistic relationship, and sphinganine and sphingosine inhibit PKC, thereby increasing the potency and efficacy of the ceramide in inducing apoptosis in cell lines (Jarvis  et al., 1996  ).	transcription
67160	5	336050	7	NULL	NULL	0	NULL	sphingosine	Chemical		inhibit					PKC	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_221	9536027	Studies show that DAG-dependent PKC activation and ceramide production have an antagonistic relationship, and sphinganine and sphingosine inhibit PKC, thereby increasing the potency and efficacy of the ceramide in inducing apoptosis in cell lines (Jarvis  et al., 1996  ).	transcription
67161	6	336050	7	NULL	NULL	NULL	NULL	statement 4	Process		increase					ceramide	Chemical	potency of;;efficacy of			NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_221	9536027	Studies show that DAG-dependent PKC activation and ceramide production have an antagonistic relationship, and sphinganine and sphingosine inhibit PKC, thereby increasing the potency and efficacy of the ceramide in inducing apoptosis in cell lines (Jarvis  et al., 1996  ).	transcription
67162	7	336050	7	NULL	NULL	NULL	NULL	statement 5	Process		increase					ceramide	Chemical	potency of;;efficacy of			NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_221	9536027	Studies show that DAG-dependent PKC activation and ceramide production have an antagonistic relationship, and sphinganine and sphingosine inhibit PKC, thereby increasing the potency and efficacy of the ceramide in inducing apoptosis in cell lines (Jarvis  et al., 1996  ).	transcription
67163	8	336050	7	NULL	NULL	0	NULL	statement 6	Process		induce					apoptosis	Process				NULL	cell lines	0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_221	9536027	Studies show that DAG-dependent PKC activation and ceramide production have an antagonistic relationship, and sphinganine and sphingosine inhibit PKC, thereby increasing the potency and efficacy of the ceramide in inducing apoptosis in cell lines (Jarvis  et al., 1996  ).	transcription
67164	9	336050	7	NULL	NULL	0	NULL	statement 7	Process		induce					apoptosis	Process				NULL	cell lines	0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_221	9536027	Studies show that DAG-dependent PKC activation and ceramide production have an antagonistic relationship, and sphinganine and sphingosine inhibit PKC, thereby increasing the potency and efficacy of the ceramide in inducing apoptosis in cell lines (Jarvis  et al., 1996  ).	transcription
60497	1	336051	5	NULL	NULL	0	NULL	inflammatory cytokines	GP		stimulates					sphingomyelinase	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_ann-n-y-acad-sci_845_1_9668339_s_5	9668339	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also leading to accumulation of ceramide, whereas growth signals  also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
60498	2	336051	5	NULL	NULL	0	NULL	inflammatory cytokines	GP		does not stimulate					ceramidase	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_ann-n-y-acad-sci_845_1_9668339_s_5	9668339	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also leading to accumulation of ceramide, whereas growth signals  also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
60499	3	336051	5	NULL	NULL	0	NULL	statement 2	Process		leads to					ceramide	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_ann-n-y-acad-sci_845_1_9668339_s_5	9668339	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also leading to accumulation of ceramide, whereas growth signals  also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
60657	4	336051	5	NULL	NULL	0	NULL	growth signals	GP		accumulates					ceramide	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_ann-n-y-acad-sci_845_1_9668339_s_5	9668339	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also leading to accumulation of ceramide, whereas growth signals  also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
60658	5	336051	5	NULL	NULL	0	NULL	growth signals	GP		stimulates					ceramidase	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_ann-n-y-acad-sci_845_1_9668339_s_5	9668339	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also leading to accumulation of ceramide, whereas growth signals  also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
60659	6	336051	5	NULL	NULL	0	NULL	growth signals	GP		stimulates					sphingosine kinase	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_ann-n-y-acad-sci_845_1_9668339_s_5	9668339	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also leading to accumulation of ceramide, whereas growth signals  also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
60660	7	336051	5	NULL	NULL	0	NULL	statement 5	Process		increases					SPP	Chemical	level of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_ann-n-y-acad-sci_845_1_9668339_s_5	9668339	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also leading to accumulation of ceramide, whereas growth signals  also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
60661	8	336051	5	NULL	NULL	0	NULL	statement 6	Process		increases					SPP	Chemical	level of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_ann-n-y-acad-sci_845_1_9668339_s_5	9668339	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also leading to accumulation of ceramide, whereas growth signals  also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
67165	1	336051	7	NULL	NULL	NULL	NULL	Inflammatory cytokines	GP		stimulate					sphingomyelinase	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_ann-n-y-acad-sci_845_1_9668339_s_5	9668339	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also leading to accumulation of ceramide, whereas growth signals  also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
67166	2	336051	7	NULL	NULL	0	NULL	Inflammatory cytokines 	GP		does not stimulate					ceramidase	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_ann-n-y-acad-sci_845_1_9668339_s_5	9668339	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also leading to accumulation of ceramide, whereas growth signals  also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
67167	3	336051	7	NULL	NULL	0	NULL	statement 2	Process		leads to					ceramide	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_ann-n-y-acad-sci_845_1_9668339_s_5	9668339	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also leading to accumulation of ceramide, whereas growth signals  also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
67168	4	336051	7	NULL	NULL	NULL	NULL	growth signals	GP		leads to					ceramide	Chemical	accumulation of			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_ann-n-y-acad-sci_845_1_9668339_s_5	9668339	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also leading to accumulation of ceramide, whereas growth signals  also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
67169	5	336051	7	NULL	NULL	0	NULL	growth signals	GP		stimulate					ceramidase	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_ann-n-y-acad-sci_845_1_9668339_s_5	9668339	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also leading to accumulation of ceramide, whereas growth signals  also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
67170	6	336051	7	NULL	NULL	NULL	NULL	growth signals	GP		stimulate					sphingosine kinase	GP				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_ann-n-y-acad-sci_845_1_9668339_s_5	9668339	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also leading to accumulation of ceramide, whereas growth signals  also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
67171	7	336051	7	NULL	NULL	0	NULL	statement 5	Process		leads to					SPP	Chemical	increased levels of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_ann-n-y-acad-sci_845_1_9668339_s_5	9668339	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also leading to accumulation of ceramide, whereas growth signals  also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
67172	8	336051	7	NULL	NULL	0	NULL	statement 6	Process		leads to					SPP	Chemical	increased levels of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_ann-n-y-acad-sci_845_1_9668339_s_5	9668339	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also leading to accumulation of ceramide, whereas growth signals  also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
60662	1	336052	5	NULL	NULL	0	NULL	HeLa cells	Cell		treated with					D-e-sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_3_1555_s_269	15647381	In contrast, treatment of HeLa cells with 2.5 muM D-e-sphingosine in the presence of 50 muM fumonisin B1 (FB1), which prevents sphingosine from being incorporated into ceramide by inhibiting ceramide synthase, rapidly induced the GC fragmentation ( Figure 9E).	transcription
60663	2	336052	5	NULL	NULL	0	NULL	statement 1	Process		in the presence of					FB1	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_3_1555_s_269	15647381	In contrast, treatment of HeLa cells with 2.5 muM D-e-sphingosine in the presence of 50 muM fumonisin B1 (FB1), which prevents sphingosine from being incorporated into ceramide by inhibiting ceramide synthase, rapidly induced the GC fragmentation ( Figure 9E).	transcription
60664	3	336052	5	NULL	NULL	0	NULL	FB1	Chemical		is					fumonisin B1	Chemical				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_3_1555_s_269	15647381	In contrast, treatment of HeLa cells with 2.5 muM D-e-sphingosine in the presence of 50 muM fumonisin B1 (FB1), which prevents sphingosine from being incorporated into ceramide by inhibiting ceramide synthase, rapidly induced the GC fragmentation ( Figure 9E).	transcription
60665	4	336052	5	NULL	NULL	0	NULL	sphingosine	Chemical		is incorporated into					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_3_1555_s_269	15647381	In contrast, treatment of HeLa cells with 2.5 muM D-e-sphingosine in the presence of 50 muM fumonisin B1 (FB1), which prevents sphingosine from being incorporated into ceramide by inhibiting ceramide synthase, rapidly induced the GC fragmentation ( Figure 9E).	transcription
60666	5	336052	5	NULL	NULL	0	NULL	ceramide synthase	GP		plays a role in					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_3_1555_s_269	15647381	In contrast, treatment of HeLa cells with 2.5 muM D-e-sphingosine in the presence of 50 muM fumonisin B1 (FB1), which prevents sphingosine from being incorporated into ceramide by inhibiting ceramide synthase, rapidly induced the GC fragmentation ( Figure 9E).	transcription
60667	6	336052	5	NULL	NULL	0	NULL	FB1	Chemical		inhibits					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_3_1555_s_269	15647381	In contrast, treatment of HeLa cells with 2.5 muM D-e-sphingosine in the presence of 50 muM fumonisin B1 (FB1), which prevents sphingosine from being incorporated into ceramide by inhibiting ceramide synthase, rapidly induced the GC fragmentation ( Figure 9E).	transcription
60668	7	336052	5	NULL	NULL	0	NULL	statement 6	Process		inhibits					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_3_1555_s_269	15647381	In contrast, treatment of HeLa cells with 2.5 muM D-e-sphingosine in the presence of 50 muM fumonisin B1 (FB1), which prevents sphingosine from being incorporated into ceramide by inhibiting ceramide synthase, rapidly induced the GC fragmentation ( Figure 9E).	transcription
60669	8	336052	5	NULL	NULL	0	NULL	statement 1	Process		induces					GC	CellComponent	fragmentation of			NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_3_1555_s_269	15647381	In contrast, treatment of HeLa cells with 2.5 muM D-e-sphingosine in the presence of 50 muM fumonisin B1 (FB1), which prevents sphingosine from being incorporated into ceramide by inhibiting ceramide synthase, rapidly induced the GC fragmentation ( Figure 9E).	transcription
67175	1	336052	7	NULL	NULL	NULL	NULL	FB1	Chemical		is					fumonisin B1	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_3_1555_s_269	15647381	In contrast, treatment of HeLa cells with 2.5 muM D-e-sphingosine in the presence of 50 muM fumonisin B1 (FB1), which prevents sphingosine from being incorporated into ceramide by inhibiting ceramide synthase, rapidly induced the GC fragmentation ( Figure 9E).	transcription
67176	2	336052	7	NULL	NULL	NULL	NULL	sphingosine	Chemical		incorporated into					ceramide	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_3_1555_s_269	15647381	In contrast, treatment of HeLa cells with 2.5 muM D-e-sphingosine in the presence of 50 muM fumonisin B1 (FB1), which prevents sphingosine from being incorporated into ceramide by inhibiting ceramide synthase, rapidly induced the GC fragmentation ( Figure 9E).	transcription
67177	3	336052	7	NULL	NULL	NULL	NULL	ceramide synthase	GP		mediate					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_3_1555_s_269	15647381	In contrast, treatment of HeLa cells with 2.5 muM D-e-sphingosine in the presence of 50 muM fumonisin B1 (FB1), which prevents sphingosine from being incorporated into ceramide by inhibiting ceramide synthase, rapidly induced the GC fragmentation ( Figure 9E).	transcription
67178	4	336052	7	NULL	NULL	NULL	NULL	FB1	Chemical		inhibit					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_3_1555_s_269	15647381	In contrast, treatment of HeLa cells with 2.5 muM D-e-sphingosine in the presence of 50 muM fumonisin B1 (FB1), which prevents sphingosine from being incorporated into ceramide by inhibiting ceramide synthase, rapidly induced the GC fragmentation ( Figure 9E).	transcription
67179	5	336052	7	NULL	NULL	0	NULL	FB1	Chemical		induce		rapidly			GC fragmentation	Process				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_3_1555_s_269	15647381	In contrast, treatment of HeLa cells with 2.5 muM D-e-sphingosine in the presence of 50 muM fumonisin B1 (FB1), which prevents sphingosine from being incorporated into ceramide by inhibiting ceramide synthase, rapidly induced the GC fragmentation ( Figure 9E).	transcription
60670	1	336053	5	NULL	NULL	0	NULL	CDase	GP	guinea pig;;epidermis	suppressed by					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_21_12677_s_151	7759519	The fact that two CDase species in guinea pig epidermis  were suppressed by the sphingosine ( Fig. 7) suggests that  ceramide hydrolysis liberating free sphingosine could also provide a  feedback mechanism for regulating ceramide breakdown, supporting the  notion that CDase activities are controlled by the balance of substrate  degradation and production.	transcription
60671	2	336053	5	NULL	NULL	0	NULL	ceramide	Chemical	hydrolysis of	liberates					sphingosine	Chemical	free			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_21_12677_s_151	7759519	The fact that two CDase species in guinea pig epidermis  were suppressed by the sphingosine ( Fig. 7) suggests that  ceramide hydrolysis liberating free sphingosine could also provide a  feedback mechanism for regulating ceramide breakdown, supporting the  notion that CDase activities are controlled by the balance of substrate  degradation and production.	transcription
60672	3	336053	5	NULL	NULL	0	NULL	statement 2	Process		regulates					ceramide	Chemical	breakdown of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_21_12677_s_151	7759519	The fact that two CDase species in guinea pig epidermis  were suppressed by the sphingosine ( Fig. 7) suggests that  ceramide hydrolysis liberating free sphingosine could also provide a  feedback mechanism for regulating ceramide breakdown, supporting the  notion that CDase activities are controlled by the balance of substrate  degradation and production.	transcription
60673	4	336053	5	NULL	NULL	0	NULL	statement 3	Process		is a type of					feedback mechanism	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_21_12677_s_151	7759519	The fact that two CDase species in guinea pig epidermis  were suppressed by the sphingosine ( Fig. 7) suggests that  ceramide hydrolysis liberating free sphingosine could also provide a  feedback mechanism for regulating ceramide breakdown, supporting the  notion that CDase activities are controlled by the balance of substrate  degradation and production.	transcription
67180	1	336053	7	NULL	NULL	0	NULL	sphingosine	Chemical		suppress					 CDase	GP	guinea pig epidermis			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_21_12677_s_151	7759519	The fact that two CDase species in guinea pig epidermis  were suppressed by the sphingosine ( Fig. 7) suggests that  ceramide hydrolysis liberating free sphingosine could also provide a  feedback mechanism for regulating ceramide breakdown, supporting the  notion that CDase activities are controlled by the balance of substrate  degradation and production.	transcription
67181	2	336053	7	NULL	NULL	0	NULL	ceramide	Chemical		hydrolyzed to					sphingosine	Chemical	liberate free			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_21_12677_s_151	7759519	The fact that two CDase species in guinea pig epidermis  were suppressed by the sphingosine ( Fig. 7) suggests that  ceramide hydrolysis liberating free sphingosine could also provide a  feedback mechanism for regulating ceramide breakdown, supporting the  notion that CDase activities are controlled by the balance of substrate  degradation and production.	transcription
67182	3	336053	7	NULL	NULL	0	NULL	statement 2	Process		regulate					ceramide	Chemical	breakdown of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_21_12677_s_151	7759519	The fact that two CDase species in guinea pig epidermis  were suppressed by the sphingosine ( Fig. 7) suggests that  ceramide hydrolysis liberating free sphingosine could also provide a  feedback mechanism for regulating ceramide breakdown, supporting the  notion that CDase activities are controlled by the balance of substrate  degradation and production.	transcription
60674	1	336054	5	NULL	NULL	0	NULL	N-SMase	GP		is					neutral sphingomyelinase	GP				NULL		0	NULL	NULL	NULL	gw70_circulation_109_3_406_s_21	14732751	7,8  We proposed that sphingosine was produced by downstream ceramide production after activation by arachidonic acid of the Mg-dependent neutral sphingomyelinase (N-SMase).	transcription
60675	2	336054	5	NULL	NULL	0	NULL	N-SMase	GP		is dependent on					Mg	Chemical				NULL		0	NULL	NULL	NULL	gw70_circulation_109_3_406_s_21	14732751	7,8  We proposed that sphingosine was produced by downstream ceramide production after activation by arachidonic acid of the Mg-dependent neutral sphingomyelinase (N-SMase).	transcription
60676	3	336054	5	NULL	NULL	0	NULL	arachidonic acid	Chemical		activates					statement 2	GP				NULL		0	NULL	NULL	NULL	gw70_circulation_109_3_406_s_21	14732751	7,8  We proposed that sphingosine was produced by downstream ceramide production after activation by arachidonic acid of the Mg-dependent neutral sphingomyelinase (N-SMase).	transcription
60677	4	336054	5	NULL	NULL	0	NULL	statement 3	Process		produce					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_circulation_109_3_406_s_21	14732751	7,8  We proposed that sphingosine was produced by downstream ceramide production after activation by arachidonic acid of the Mg-dependent neutral sphingomyelinase (N-SMase).	transcription
60678	5	336054	5	NULL	NULL	0	NULL	statement 4	Process		produce					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_circulation_109_3_406_s_21	14732751	7,8  We proposed that sphingosine was produced by downstream ceramide production after activation by arachidonic acid of the Mg-dependent neutral sphingomyelinase (N-SMase).	transcription
67183	1	336054	7	NULL	NULL	0	NULL	arachidonic acid	Chemical		activate					N-SMase	GP				NULL		0	NULL	NULL	NULL	gw70_circulation_109_3_406_s_21	14732751	7,8  We proposed that sphingosine was produced by downstream ceramide production after activation by arachidonic acid of the Mg-dependent neutral sphingomyelinase (N-SMase).	transcription
67184	2	336054	7	NULL	NULL	0	NULL	sphingosine 	Chemical		produced by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_circulation_109_3_406_s_21	14732751	7,8  We proposed that sphingosine was produced by downstream ceramide production after activation by arachidonic acid of the Mg-dependent neutral sphingomyelinase (N-SMase).	transcription
67185	3	336054	7	NULL	NULL	0	NULL	statement 2	Process		occur after					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_circulation_109_3_406_s_21	14732751	7,8  We proposed that sphingosine was produced by downstream ceramide production after activation by arachidonic acid of the Mg-dependent neutral sphingomyelinase (N-SMase).	transcription
67186	4	336054	7	NULL	NULL	0	NULL	N-SMase	GP		is					neutral sphingomyelinase	GP				NULL		0	NULL	NULL	NULL	gw70_circulation_109_3_406_s_21	14732751	7,8  We proposed that sphingosine was produced by downstream ceramide production after activation by arachidonic acid of the Mg-dependent neutral sphingomyelinase (N-SMase).	transcription
60679	1	336055	5	NULL	NULL	0	NULL	TNF-alpha	GP		is a type of					cytokine	GP				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_12_1140_s_103	15591236	Cytokines such as TNF-alpha also deplete GSH and activate membrane-associated neutral sphingomyelinase (NSM),  which in turn increases ceramide (C) and sphingosine levels.	transcription
60680	2	336055	5	NULL	NULL	0	NULL	TNF-alpha	GP		deplete					GSH	GP				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_12_1140_s_103	15591236	Cytokines such as TNF-alpha also deplete GSH and activate membrane-associated neutral sphingomyelinase (NSM),  which in turn increases ceramide (C) and sphingosine levels.	transcription
60681	3	336055	5	NULL	NULL	0	NULL	TNF-alpha	GP		activates					NSM	GP				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_12_1140_s_103	15591236	Cytokines such as TNF-alpha also deplete GSH and activate membrane-associated neutral sphingomyelinase (NSM),  which in turn increases ceramide (C) and sphingosine levels.	transcription
60682	4	336055	5	NULL	NULL	0	NULL	statement 3	Process		increases					ceramide	Chemical	level of			NULL		0	NULL	NULL	NULL	gw70_circulationres_95_12_1140_s_103	15591236	Cytokines such as TNF-alpha also deplete GSH and activate membrane-associated neutral sphingomyelinase (NSM),  which in turn increases ceramide (C) and sphingosine levels.	transcription
60683	5	336055	5	NULL	NULL	0	NULL	statement 3	Process		increases					sphingosine	Chemical	level of			NULL		0	NULL	NULL	NULL	gw70_circulationres_95_12_1140_s_103	15591236	Cytokines such as TNF-alpha also deplete GSH and activate membrane-associated neutral sphingomyelinase (NSM),  which in turn increases ceramide (C) and sphingosine levels.	transcription
60684	6	336055	5	NULL	NULL	0	NULL	NSM	GP		is					neutral sphingomyelinase	GP				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_12_1140_s_103	15591236	Cytokines such as TNF-alpha also deplete GSH and activate membrane-associated neutral sphingomyelinase (NSM),  which in turn increases ceramide (C) and sphingosine levels.	transcription
60685	7	336055	5	NULL	NULL	0	NULL	NSM	GP		is associated with					membrane	CellComponent				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_12_1140_s_103	15591236	Cytokines such as TNF-alpha also deplete GSH and activate membrane-associated neutral sphingomyelinase (NSM),  which in turn increases ceramide (C) and sphingosine levels.	transcription
67187	1	336055	7	NULL	NULL	0	NULL	TNF-alpha	GP		deplete					GSH	GP				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_12_1140_s_103	15591236	Cytokines such as TNF-alpha also deplete GSH and activate membrane-associated neutral sphingomyelinase (NSM),  which in turn increases ceramide (C) and sphingosine levels.	transcription
67188	2	336055	7	NULL	NULL	NULL	NULL	TNF-alpha	GP		activate					NSM	GP	membrane-associated			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_12_1140_s_103	15591236	Cytokines such as TNF-alpha also deplete GSH and activate membrane-associated neutral sphingomyelinase (NSM),  which in turn increases ceramide (C) and sphingosine levels.	transcription
67189	3	336055	7	NULL	NULL	0	NULL	statement 1	Process		leads to					ceramide	Chemical	increased levels of			NULL		0	NULL	NULL	NULL	gw70_circulationres_95_12_1140_s_103	15591236	Cytokines such as TNF-alpha also deplete GSH and activate membrane-associated neutral sphingomyelinase (NSM),  which in turn increases ceramide (C) and sphingosine levels.	transcription
67190	4	336055	7	NULL	NULL	0	NULL	statement 2	Process		leads to					ceramide	Chemical	increased levels of			NULL		0	NULL	NULL	NULL	gw70_circulationres_95_12_1140_s_103	15591236	Cytokines such as TNF-alpha also deplete GSH and activate membrane-associated neutral sphingomyelinase (NSM),  which in turn increases ceramide (C) and sphingosine levels.	transcription
67191	5	336055	7	NULL	NULL	NULL	NULL	statement 1	Process		leads to					sphingosine	Chemical	increased levels of			NULL		NULL	NULL	NULL	NULL	gw70_circulationres_95_12_1140_s_103	15591236	Cytokines such as TNF-alpha also deplete GSH and activate membrane-associated neutral sphingomyelinase (NSM),  which in turn increases ceramide (C) and sphingosine levels.	transcription
67192	6	336055	7	NULL	NULL	0	NULL	statement 2	Process		leads to					sphingosine	Chemical	increased levels of			NULL		0	NULL	NULL	NULL	gw70_circulationres_95_12_1140_s_103	15591236	Cytokines such as TNF-alpha also deplete GSH and activate membrane-associated neutral sphingomyelinase (NSM),  which in turn increases ceramide (C) and sphingosine levels.	transcription
67193	7	336055	7	NULL	NULL	0	NULL	NSM	GP		is					neutral sphingomyelinase	GP				NULL		0	NULL	NULL	NULL	gw70_circulationres_95_12_1140_s_103	15591236	Cytokines such as TNF-alpha also deplete GSH and activate membrane-associated neutral sphingomyelinase (NSM),  which in turn increases ceramide (C) and sphingosine levels.	transcription
60686	1	336056	5	NULL	NULL	0	NULL	ceramide	Chemical		induce					neuro-protection	Process				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_8_1130_s_300	14614956	We assessed the effects of the ceramidase  inhibitor NOE and the sphingosine kinase inhibitor DMS ( [  Edsall et al., 1998]) on ceramide-induced neuro-protection.	transcription
60687	2	336056	5	NULL	NULL	0	NULL	NOE	Chemical		is an inhibitor of					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_8_1130_s_300	14614956	We assessed the effects of the ceramidase  inhibitor NOE and the sphingosine kinase inhibitor DMS ( [  Edsall et al., 1998]) on ceramide-induced neuro-protection.	transcription
60688	3	336056	5	NULL	NULL	0	NULL	DMS	Chemical		is an inhibitor of					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_8_1130_s_300	14614956	We assessed the effects of the ceramidase  inhibitor NOE and the sphingosine kinase inhibitor DMS ( [  Edsall et al., 1998]) on ceramide-induced neuro-protection.	transcription
60689	4	336056	5	NULL	NULL	0	NULL	NOE	Chemical		effects		potentially			statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_8_1130_s_300	14614956	We assessed the effects of the ceramidase  inhibitor NOE and the sphingosine kinase inhibitor DMS ( [  Edsall et al., 1998]) on ceramide-induced neuro-protection.	transcription
60690	5	336056	5	NULL	NULL	0	NULL	DMS	Chemical		effects		potentially			statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_8_1130_s_300	14614956	We assessed the effects of the ceramidase  inhibitor NOE and the sphingosine kinase inhibitor DMS ( [  Edsall et al., 1998]) on ceramide-induced neuro-protection.	transcription
67408	1	336056	7	NULL	NULL	0	NULL	ceramide 	Chemical		induce					 neuro-protection	Process				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_8_1130_s_300	14614956	We assessed the effects of the ceramidase  inhibitor NOE and the sphingosine kinase inhibitor DMS ( [  Edsall et al., 1998]) on ceramide-induced neuro-protection.	transcription
67409	2	336056	7	NULL	NULL	0	NULL	NOE	Chemical		is a type of					ceramidase inhibitor	Chemical				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_8_1130_s_300	14614956	We assessed the effects of the ceramidase  inhibitor NOE and the sphingosine kinase inhibitor DMS ( [  Edsall et al., 1998]) on ceramide-induced neuro-protection.	transcription
67410	3	336056	7	NULL	NULL	0	NULL	DMS	Chemical		is a type of					sphingosine kinase inhibitor	Chemical				NULL		0	NULL	NULL	NULL	gw70_neuropharmacology_45_8_1130_s_300	14614956	We assessed the effects of the ceramidase  inhibitor NOE and the sphingosine kinase inhibitor DMS ( [  Edsall et al., 1998]) on ceramide-induced neuro-protection.	transcription
60691	1	336057	5	NULL	NULL	0	NULL	fumonisin B1	Chemical		block					ceramide	Chemical	production of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_6	15180992	Although fumonisin B1 blocked ceramide production and increased sphingosine, it did not reverse the negative effect of SPP-1 expression on EGF- or S1P-induced chemotaxis.	transcription
60692	2	336057	5	NULL	NULL	0	NULL	fumonisin B1	Chemical		increases					sphingosine	Chemical	production of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_6	15180992	Although fumonisin B1 blocked ceramide production and increased sphingosine, it did not reverse the negative effect of SPP-1 expression on EGF- or S1P-induced chemotaxis.	transcription
60693	3	336057	5	NULL	NULL	0	NULL	S1P	Chemical		induce					chemotaxis	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_6	15180992	Although fumonisin B1 blocked ceramide production and increased sphingosine, it did not reverse the negative effect of SPP-1 expression on EGF- or S1P-induced chemotaxis.	transcription
60694	4	336057	5	NULL	NULL	0	NULL	EGF	GP		induce					chemotaxis	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_6	15180992	Although fumonisin B1 blocked ceramide production and increased sphingosine, it did not reverse the negative effect of SPP-1 expression on EGF- or S1P-induced chemotaxis.	transcription
60695	5	336057	5	NULL	NULL	0	NULL	SPP-1	Chemical	expression of	effects		negatively			statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_6	15180992	Although fumonisin B1 blocked ceramide production and increased sphingosine, it did not reverse the negative effect of SPP-1 expression on EGF- or S1P-induced chemotaxis.	transcription
60696	6	336057	5	NULL	NULL	0	NULL	SPP-1	Chemical	expression of	effects		negatively			statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_6	15180992	Although fumonisin B1 blocked ceramide production and increased sphingosine, it did not reverse the negative effect of SPP-1 expression on EGF- or S1P-induced chemotaxis.	transcription
60697	7	336057	5	NULL	NULL	0	NULL	fumonisin B1	Chemical		does not reverse					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_6	15180992	Although fumonisin B1 blocked ceramide production and increased sphingosine, it did not reverse the negative effect of SPP-1 expression on EGF- or S1P-induced chemotaxis.	transcription
60698	8	336057	5	NULL	NULL	0	NULL	fumonisin B1	Chemical		does not reverse					statement 6	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_6	15180992	Although fumonisin B1 blocked ceramide production and increased sphingosine, it did not reverse the negative effect of SPP-1 expression on EGF- or S1P-induced chemotaxis.	transcription
67411	1	336057	7	NULL	NULL	0	NULL	fumonisin B1	Chemical		blocks					ceramide	Chemical	production of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_6	15180992	Although fumonisin B1 blocked ceramide production and increased sphingosine, it did not reverse the negative effect of SPP-1 expression on EGF- or S1P-induced chemotaxis.	transcription
67412	2	336057	7	NULL	NULL	0	NULL	fumonisin B1	Chemical		increase					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_6	15180992	Although fumonisin B1 blocked ceramide production and increased sphingosine, it did not reverse the negative effect of SPP-1 expression on EGF- or S1P-induced chemotaxis.	transcription
67413	3	336057	7	NULL	NULL	0	NULL	SPP-1	GP	expression of	effect		negatively			EGF	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_6	15180992	Although fumonisin B1 blocked ceramide production and increased sphingosine, it did not reverse the negative effect of SPP-1 expression on EGF- or S1P-induced chemotaxis.	transcription
67414	4	336057	7	NULL	NULL	0	NULL	S1P	Chemical		induce					chemotaxis	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_6	15180992	Although fumonisin B1 blocked ceramide production and increased sphingosine, it did not reverse the negative effect of SPP-1 expression on EGF- or S1P-induced chemotaxis.	transcription
67415	5	336057	7	NULL	NULL	0	NULL	SPP-1	GP	expression of	effect		negatively			statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_6	15180992	Although fumonisin B1 blocked ceramide production and increased sphingosine, it did not reverse the negative effect of SPP-1 expression on EGF- or S1P-induced chemotaxis.	transcription
67416	6	336057	7	NULL	NULL	0	NULL	fumonisin B1	Chemical		does not reverse					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_6	15180992	Although fumonisin B1 blocked ceramide production and increased sphingosine, it did not reverse the negative effect of SPP-1 expression on EGF- or S1P-induced chemotaxis.	transcription
67417	7	336057	7	NULL	NULL	0	NULL	fumonisin B1	Chemical		does not reverse					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_6	15180992	Although fumonisin B1 blocked ceramide production and increased sphingosine, it did not reverse the negative effect of SPP-1 expression on EGF- or S1P-induced chemotaxis.	transcription
67418	8	336057	7	NULL	NULL	0	NULL	statement 6	Process		is an alternative to					statement 7	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_33_34290_s_6	15180992	Although fumonisin B1 blocked ceramide production and increased sphingosine, it did not reverse the negative effect of SPP-1 expression on EGF- or S1P-induced chemotaxis.	transcription
60699	1	336058	5	NULL	NULL	0	NULL	L-Cycloserine	Chemical		inhibits					serine palmitoyltransferase	GP	activity of			NULL	in vitro and in vivo	0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_51	12424251	L-Cycloserine and beta-chloro-L-alanine block sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity both  in vitro and  in vivo ( ,  ).	transcription
60700	2	336058	5	NULL	NULL	0	NULL	statement 1	Process		blocks					sphingosine	Chemical	biosynthesis of			NULL	in vitro and in vivo	0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_51	12424251	L-Cycloserine and beta-chloro-L-alanine block sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity both  in vitro and  in vivo ( ,  ).	transcription
60701	3	336058	5	NULL	NULL	0	NULL	statement 1	Process		blocks					ceramide	Chemical	biosynthesis of			NULL	in vitro and in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_51	12424251	L-Cycloserine and beta-chloro-L-alanine block sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity both  in vitro and  in vivo ( ,  ).	transcription
60702	4	336058	5	NULL	NULL	0	NULL	beta-chloro-L-alanine	Chemical		inhibits					serine palmitoyltransferase	GP	activity of			NULL	in vitro and in vivo	0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_51	12424251	L-Cycloserine and beta-chloro-L-alanine block sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity both  in vitro and  in vivo ( ,  ).	transcription
60703	5	336058	5	NULL	NULL	0	NULL	statement 4	Process		blocks					sphingosine	Chemical	biosynthesis of			NULL	in vitro and in vivo	0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_51	12424251	L-Cycloserine and beta-chloro-L-alanine block sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity both  in vitro and  in vivo ( ,  ).	transcription
60704	6	336058	5	NULL	NULL	0	NULL	statement 4	Process		blocks					ceramide	Chemical	biosynthesis of			NULL	in vitro and in vivo	0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_51	12424251	L-Cycloserine and beta-chloro-L-alanine block sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity both  in vitro and  in vivo ( ,  ).	transcription
67419	1	336058	7	NULL	NULL	0	NULL	L-Cycloserine	AminoAcid		block					sphingosine	Chemical	biosynthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_51	12424251	L-Cycloserine and beta-chloro-L-alanine block sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity both  in vitro and  in vivo ( ,  ).	transcription
67420	2	336058	7	NULL	NULL	NULL	NULL	 beta-chloro-L-alanine	AminoAcid		block					sphingosine	Chemical	biosynthesis of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_51	12424251	L-Cycloserine and beta-chloro-L-alanine block sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity both  in vitro and  in vivo ( ,  ).	transcription
67421	3	336058	7	NULL	NULL	0	NULL	L-Cycloserine	AminoAcid		block					ceramide	Chemical	biosynthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_51	12424251	L-Cycloserine and beta-chloro-L-alanine block sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity both  in vitro and  in vivo ( ,  ).	transcription
67424	4	336058	7	NULL	NULL	0	NULL	beta-chloro-L-alanine	Chemical		block					ceramide	Chemical	biosynthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_51	12424251	L-Cycloserine and beta-chloro-L-alanine block sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity both  in vitro and  in vivo ( ,  ).	transcription
67439	5	336058	7	NULL	NULL	0	NULL	statement 1	Process		occur by					serine palmitoyltransferase activity	Process	inhibition of			NULL	in vitro	0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_51	12424251	L-Cycloserine and beta-chloro-L-alanine block sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity both  in vitro and  in vivo ( ,  ).	transcription
67440	6	336058	7	NULL	NULL	NULL	NULL	statement 1	Process		occur by					serine palmitoyltransferase activity	Process	inhibition of			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_51	12424251	L-Cycloserine and beta-chloro-L-alanine block sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity both  in vitro and  in vivo ( ,  ).	transcription
67441	7	336058	7	NULL	NULL	NULL	NULL	statement 2	Process		occur by					serine palmitoyltransferase activity	Process	inhibition of			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_51	12424251	L-Cycloserine and beta-chloro-L-alanine block sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity both  in vitro and  in vivo ( ,  ).	transcription
67442	8	336058	7	NULL	NULL	0	NULL	statement 2	Process		occur by					serine palmitoyltransferase activity	Process	inhibition of			NULL	in vivo	0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_51	12424251	L-Cycloserine and beta-chloro-L-alanine block sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity both  in vitro and  in vivo ( ,  ).	transcription
67443	9	336058	7	NULL	NULL	NULL	NULL	statement 3	Process		occur by					serine palmitoyltransferase activity	Process	inhibition of			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_51	12424251	L-Cycloserine and beta-chloro-L-alanine block sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity both  in vitro and  in vivo ( ,  ).	transcription
67444	10	336058	7	NULL	NULL	NULL	NULL	statement 3	Process		occur by					serine palmitoyltransferase activity	Process	inhibition of			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_51	12424251	L-Cycloserine and beta-chloro-L-alanine block sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity both  in vitro and  in vivo ( ,  ).	transcription
67445	11	336058	7	NULL	NULL	0	NULL	statement 4	Process		occur by					serine palmitoyltransferase activity	Process	inhibition of			NULL	in vitro	0	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_51	12424251	L-Cycloserine and beta-chloro-L-alanine block sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity both  in vitro and  in vivo ( ,  ).	transcription
67446	12	336058	7	NULL	NULL	NULL	NULL	statement 4	Process		occur by					serine palmitoyltransferase activity	Process	inhibition of			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_2_974_s_51	12424251	L-Cycloserine and beta-chloro-L-alanine block sphingosine and ceramide biosynthesis by inhibiting serine palmitoyltransferase activity both  in vitro and  in vivo ( ,  ).	transcription
60705	1	336059	5	NULL	NULL	0	NULL	sphingosine	Chemical		is phosphorylated to					S1P	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_52	12069805	S1P, produced by phosphorylation of sphingosine by SPHK ( Fig. 1 and  Fig. 2), suppresses ceramide-induced apoptosis and stimulates mitogenic pathways [ 1,  2,  3 and  6].	transcription
60706	2	336059	5	NULL	NULL	0	NULL	SPHK	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_52	12069805	S1P, produced by phosphorylation of sphingosine by SPHK ( Fig. 1 and  Fig. 2), suppresses ceramide-induced apoptosis and stimulates mitogenic pathways [ 1,  2,  3 and  6].	transcription
60707	3	336059	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_52	12069805	S1P, produced by phosphorylation of sphingosine by SPHK ( Fig. 1 and  Fig. 2), suppresses ceramide-induced apoptosis and stimulates mitogenic pathways [ 1,  2,  3 and  6].	transcription
60708	4	336059	5	NULL	NULL	0	NULL	S1P	Chemical		suppress					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_52	12069805	S1P, produced by phosphorylation of sphingosine by SPHK ( Fig. 1 and  Fig. 2), suppresses ceramide-induced apoptosis and stimulates mitogenic pathways [ 1,  2,  3 and  6].	transcription
60709	5	336059	5	NULL	NULL	0	NULL	S1P	Chemical		stimulates					mitogenic pathways	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_52	12069805	S1P, produced by phosphorylation of sphingosine by SPHK ( Fig. 1 and  Fig. 2), suppresses ceramide-induced apoptosis and stimulates mitogenic pathways [ 1,  2,  3 and  6].	transcription
67425	1	336059	7	NULL	NULL	0	NULL	S1P	Chemical		produced by					sphingosine	Chemical	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_52	12069805	S1P, produced by phosphorylation of sphingosine by SPHK ( Fig. 1 and  Fig. 2), suppresses ceramide-induced apoptosis and stimulates mitogenic pathways [ 1,  2,  3 and  6].	transcription
67426	2	336059	7	NULL	NULL	0	NULL	SPHK			catalyze					statement 1					NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_52	12069805	S1P, produced by phosphorylation of sphingosine by SPHK ( Fig. 1 and  Fig. 2), suppresses ceramide-induced apoptosis and stimulates mitogenic pathways [ 1,  2,  3 and  6].	transcription
67427	3	336059	7	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_52	12069805	S1P, produced by phosphorylation of sphingosine by SPHK ( Fig. 1 and  Fig. 2), suppresses ceramide-induced apoptosis and stimulates mitogenic pathways [ 1,  2,  3 and  6].	transcription
67428	4	336059	7	NULL	NULL	0	NULL	S1P	Chemical		suppress					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_52	12069805	S1P, produced by phosphorylation of sphingosine by SPHK ( Fig. 1 and  Fig. 2), suppresses ceramide-induced apoptosis and stimulates mitogenic pathways [ 1,  2,  3 and  6].	transcription
67429	5	336059	7	NULL	NULL	0	NULL	S1P	Chemical		stimulates					mitogenic pathways	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_8_s_52	12069805	S1P, produced by phosphorylation of sphingosine by SPHK ( Fig. 1 and  Fig. 2), suppresses ceramide-induced apoptosis and stimulates mitogenic pathways [ 1,  2,  3 and  6].	transcription
60710	1	336060	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		inhibits					caspases	GP	activation of			NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_currbiol_10_23_1527_s_121	11114522	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide- mediated apoptosis in Jurkat T lymphocytes.	transcription
60711	2	336060	5	NULL	NULL	0	NULL	caspases	GP		cleave					poly(ADP-ribose) polymerase	GP				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_currbiol_10_23_1527_s_121	11114522	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide- mediated apoptosis in Jurkat T lymphocytes.	transcription
60712	3	336060	5	NULL	NULL	0	NULL	caspases	GP		cleave					lamins	GP				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_currbiol_10_23_1527_s_121	11114522	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide- mediated apoptosis in Jurkat T lymphocytes.	transcription
60713	4	336060	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					Fas	GP				NULL	Jurkat T lymphocytes	NULL	NULL	NULL	NULL	gw60_currbiol_10_23_1527_s_121	11114522	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide- mediated apoptosis in Jurkat T lymphocytes.	transcription
60714	5	336060	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					ceramide	Chemical				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_currbiol_10_23_1527_s_121	11114522	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide- mediated apoptosis in Jurkat T lymphocytes.	transcription
60715	6	336060	5	NULL	NULL	0	NULL	statement 2	Process		occurs during					statement 4	Process				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_currbiol_10_23_1527_s_121	11114522	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide- mediated apoptosis in Jurkat T lymphocytes.	transcription
60716	7	336060	5	NULL	NULL	0	NULL	statement 2	Process		occurs during					statement 5	Process				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_currbiol_10_23_1527_s_121	11114522	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide- mediated apoptosis in Jurkat T lymphocytes.	transcription
60717	8	336060	5	NULL	NULL	0	NULL	statement 3	Process		occurs during					statement 4	Process				NULL	Jurkat T lymphocytes	NULL	NULL	NULL	NULL	gw60_currbiol_10_23_1527_s_121	11114522	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide- mediated apoptosis in Jurkat T lymphocytes.	transcription
60718	9	336060	5	NULL	NULL	0	NULL	statement 3	Process		occurs during					statement 5	Process				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_currbiol_10_23_1527_s_121	11114522	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide- mediated apoptosis in Jurkat T lymphocytes.	transcription
67430	1	336060	7	NULL	NULL	0	NULL	Sphingosine 1-phosphate	Chemical		inhibits					caspases	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_currbiol_10_23_1527_s_121	11114522	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide- mediated apoptosis in Jurkat T lymphocytes.	transcription
67431	2	336060	7	NULL	NULL	NULL	NULL	caspases	GP		cleave					poly(ADP-ribose) polymerase	GP				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_23_1527_s_121	11114522	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide- mediated apoptosis in Jurkat T lymphocytes.	transcription
67432	3	336060	7	NULL	NULL	0	NULL	caspases	GP		cleave					lamins	GP				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_23_1527_s_121	11114522	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide- mediated apoptosis in Jurkat T lymphocytes.	transcription
67433	4	336060	7	NULL	NULL	NULL	NULL	Fas	GP		mediates					apoptosis 	Process				NULL	Jurkat T lymphocytes	NULL	NULL	NULL	NULL	gw60_currbiol_10_23_1527_s_121	11114522	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide- mediated apoptosis in Jurkat T lymphocytes.	transcription
67434	5	336060	7	NULL	NULL	0	NULL	ceramide	Chemical		mediates					apoptosis	Process				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_currbiol_10_23_1527_s_121	11114522	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide- mediated apoptosis in Jurkat T lymphocytes.	transcription
67435	6	336060	7	NULL	NULL	NULL	NULL	statement 2	Process		occur during					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_currbiol_10_23_1527_s_121	11114522	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide- mediated apoptosis in Jurkat T lymphocytes.	transcription
67436	7	336060	7	NULL	NULL	0	NULL	statement 2	Process		occur during					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_23_1527_s_121	11114522	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide- mediated apoptosis in Jurkat T lymphocytes.	transcription
67437	8	336060	7	NULL	NULL	0	NULL	statement 3	Process		occur during					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_23_1527_s_121	11114522	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide- mediated apoptosis in Jurkat T lymphocytes.	transcription
67438	9	336060	7	NULL	NULL	0	NULL	statement 3	Process		occur during					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_currbiol_10_23_1527_s_121	11114522	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide- mediated apoptosis in Jurkat T lymphocytes.	transcription
60719	1	336061	5	NULL	NULL	0	NULL	C2-ceramide	Chemical	treatment;;exogenous	increases					ceramide	Chemical	endogenous			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_23_1_163_s_26	12482970	It was further shown that treatment of cells with exogenous C2-ceramide not only increases the level of endogenous ceramide but also leads to a marked increase in the level of cellular sphingosine ( 9).	transcription
60720	2	336061	5	NULL	NULL	0	NULL	C2-ceramide	Chemical	treatment;;exogenous	increases					sphingosine	Chemical	cellular levels of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_1_163_s_26	12482970	It was further shown that treatment of cells with exogenous C2-ceramide not only increases the level of endogenous ceramide but also leads to a marked increase in the level of cellular sphingosine ( 9).	transcription
67447	1	336061	7	NULL	NULL	0	NULL	C2-ceramide	Chemical	exogenous	increase					ceramide	Chemical	level of endogenous			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_1_163_s_26	12482970	It was further shown that treatment of cells with exogenous C2-ceramide not only increases the level of endogenous ceramide but also leads to a marked increase in the level of cellular sphingosine ( 9).	transcription
67448	2	336061	7	NULL	NULL	0	NULL	C2-ceramide	Chemical	exogenous	increase					cellular sphingosine	Chemical	levels of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_1_163_s_26	12482970	It was further shown that treatment of cells with exogenous C2-ceramide not only increases the level of endogenous ceramide but also leads to a marked increase in the level of cellular sphingosine ( 9).	transcription
60721	1	336063	5	NULL	NULL	0	NULL	CERK	GP		is homologous to					SPK	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_263	11956206	Although CERK is somewhat homologous to SPK, especially in the previously identified conserved domains ( 28), it is highly specific for ceramide as substrate and does not catalyze phosphorylation of sphingosine or diacylglycerol.	transcription
60722	2	336063	5	NULL	NULL	0	NULL	CERK	GP		is specific for		highly			ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_263	11956206	Although CERK is somewhat homologous to SPK, especially in the previously identified conserved domains ( 28), it is highly specific for ceramide as substrate and does not catalyze phosphorylation of sphingosine or diacylglycerol.	transcription
60723	3	336063	5	NULL	NULL	0	NULL	CERK	GP		does not catalyze					sphingosine	Chemical	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_263	11956206	Although CERK is somewhat homologous to SPK, especially in the previously identified conserved domains ( 28), it is highly specific for ceramide as substrate and does not catalyze phosphorylation of sphingosine or diacylglycerol.	transcription
60724	4	336063	5	NULL	NULL	0	NULL	CERK	GP		does not catalyze					diacylglycerol	Chemical	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_263	11956206	Although CERK is somewhat homologous to SPK, especially in the previously identified conserved domains ( 28), it is highly specific for ceramide as substrate and does not catalyze phosphorylation of sphingosine or diacylglycerol.	transcription
60725	5	336063	5	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_263	11956206	Although CERK is somewhat homologous to SPK, especially in the previously identified conserved domains ( 28), it is highly specific for ceramide as substrate and does not catalyze phosphorylation of sphingosine or diacylglycerol.	transcription
67449	1	336063	7	NULL	NULL	0	NULL	CERK	GP		homologous to					SPK	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_263	11956206	Although CERK is somewhat homologous to SPK, especially in the previously identified conserved domains ( 28), it is highly specific for ceramide as substrate and does not catalyze phosphorylation of sphingosine or diacylglycerol.	transcription
67450	2	336063	7	NULL	NULL	0	NULL	ceramide	Chemical		substrate for					CERK	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_263	11956206	Although CERK is somewhat homologous to SPK, especially in the previously identified conserved domains ( 28), it is highly specific for ceramide as substrate and does not catalyze phosphorylation of sphingosine or diacylglycerol.	transcription
67451	3	336063	7	NULL	NULL	0	NULL	CERK	GP		does not catalyze					sphingosine	Chemical	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_263	11956206	Although CERK is somewhat homologous to SPK, especially in the previously identified conserved domains ( 28), it is highly specific for ceramide as substrate and does not catalyze phosphorylation of sphingosine or diacylglycerol.	transcription
67452	4	336063	7	NULL	NULL	0	NULL	CERK	GP		does not catalyze					diacylglycerol	Chemical	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_263	11956206	Although CERK is somewhat homologous to SPK, especially in the previously identified conserved domains ( 28), it is highly specific for ceramide as substrate and does not catalyze phosphorylation of sphingosine or diacylglycerol.	transcription
60726	1	336064	5	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_193	10747891	Because ceramide and sphingosine induce apoptosis in a Bcl-xL-dependent manner, we determined whether they were also capable of mediating caspase-8 activation.	transcription
60727	2	336064	5	NULL	NULL	0	NULL	statement 1	Process		is dependent on					Bcl-xL	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_193	10747891	Because ceramide and sphingosine induce apoptosis in a Bcl-xL-dependent manner, we determined whether they were also capable of mediating caspase-8 activation.	transcription
60728	3	336064	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_193	10747891	Because ceramide and sphingosine induce apoptosis in a Bcl-xL-dependent manner, we determined whether they were also capable of mediating caspase-8 activation.	transcription
60729	4	336064	5	NULL	NULL	0	NULL	statement 3	Process		is dependent on					Bcl-xL	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_193	10747891	Because ceramide and sphingosine induce apoptosis in a Bcl-xL-dependent manner, we determined whether they were also capable of mediating caspase-8 activation.	transcription
67453	1	336064	7	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_193	10747891	Because ceramide and sphingosine induce apoptosis in a Bcl-xL-dependent manner, we determined whether they were also capable of mediating caspase-8 activation.	transcription
67454	2	336064	7	NULL	NULL	0	NULL	sphingosine	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_193	10747891	Because ceramide and sphingosine induce apoptosis in a Bcl-xL-dependent manner, we determined whether they were also capable of mediating caspase-8 activation.	transcription
67455	3	336064	7	NULL	NULL	0	NULL	statement 1	Process		depends on					Bcl-xL	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_193	10747891	Because ceramide and sphingosine induce apoptosis in a Bcl-xL-dependent manner, we determined whether they were also capable of mediating caspase-8 activation.	transcription
67456	4	336064	7	NULL	NULL	0	NULL	statement 2	Process		depends on					Bcl-xL	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_193	10747891	Because ceramide and sphingosine induce apoptosis in a Bcl-xL-dependent manner, we determined whether they were also capable of mediating caspase-8 activation.	transcription
60730	1	336065	5	NULL	NULL	0	NULL	ceramide	Chemical	apoptotic response to	is regulated by		indirectly			sphingosine & diglyceride	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_38	8626522	Thus, it  appears that the apoptotic response to ceramide is indirectly regulated  by the combined actions of sphingosine and diglyceride, which  respectively limit or extend the cytoprotective influence of PKC.	transcription
60731	2	336065	5	NULL	NULL	0	NULL	statement 1	Process		limits					PKC	GP	cytoprotective influence of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_38	8626522	Thus, it  appears that the apoptotic response to ceramide is indirectly regulated  by the combined actions of sphingosine and diglyceride, which  respectively limit or extend the cytoprotective influence of PKC.	transcription
60732	3	336065	5	NULL	NULL	0	NULL	statement 1	Process		extends					PKC	GP	cytoprotective influence of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_38	8626522	Thus, it  appears that the apoptotic response to ceramide is indirectly regulated  by the combined actions of sphingosine and diglyceride, which  respectively limit or extend the cytoprotective influence of PKC.	transcription
60733	4	336065	5	NULL	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_38	8626522	Thus, it  appears that the apoptotic response to ceramide is indirectly regulated  by the combined actions of sphingosine and diglyceride, which  respectively limit or extend the cytoprotective influence of PKC.	transcription
67457	1	336065	7	NULL	NULL	0	NULL	ceramide	Chemical		shows					apoptotic response	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_38	8626522	Thus, it  appears that the apoptotic response to ceramide is indirectly regulated  by the combined actions of sphingosine and diglyceride, which  respectively limit or extend the cytoprotective influence of PKC.	transcription
67458	2	336065	7	NULL	NULL	NULL	NULL	statement 1	Process		 regulated by		indirectly			sphingosine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_38	8626522	Thus, it  appears that the apoptotic response to ceramide is indirectly regulated  by the combined actions of sphingosine and diglyceride, which  respectively limit or extend the cytoprotective influence of PKC.	transcription
67459	3	336065	7	NULL	NULL	0	NULL	statement 1	Process		regulated by		indirectly			diglyceride	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_38	8626522	Thus, it  appears that the apoptotic response to ceramide is indirectly regulated  by the combined actions of sphingosine and diglyceride, which  respectively limit or extend the cytoprotective influence of PKC.	transcription
67460	4	336065	7	NULL	NULL	NULL	NULL	statement 2	Process		limit					PKC	GP	cytoprotective influence of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_38	8626522	Thus, it  appears that the apoptotic response to ceramide is indirectly regulated  by the combined actions of sphingosine and diglyceride, which  respectively limit or extend the cytoprotective influence of PKC.	transcription
67461	5	336065	7	NULL	NULL	0	NULL	statement 3	Process		extend					PKC	GP	cytoprotective influence of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_38	8626522	Thus, it  appears that the apoptotic response to ceramide is indirectly regulated  by the combined actions of sphingosine and diglyceride, which  respectively limit or extend the cytoprotective influence of PKC.	transcription
60734	1	336066	5	NULL	NULL	0	NULL	cell death	Process		is dependent on					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_263	8626522	First, as  already noted, sphingosine and sphinganine exhibited equivalent potency  and efficacy in both the direct induction of apoptosis and the  potentiation of ceramide-dependent cell death.	transcription
60735	2	336066	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce		directly			apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_263	8626522	First, as  already noted, sphingosine and sphinganine exhibited equivalent potency  and efficacy in both the direct induction of apoptosis and the  potentiation of ceramide-dependent cell death.	transcription
60736	3	336066	5	NULL	NULL	0	NULL	sphinganine	Chemical		induce		directly			apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_263	8626522	First, as  already noted, sphingosine and sphinganine exhibited equivalent potency  and efficacy in both the direct induction of apoptosis and the  potentiation of ceramide-dependent cell death.	transcription
60737	4	336066	5	NULL	NULL	0	NULL	sphingosine	Chemical		potentiate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_263	8626522	First, as  already noted, sphingosine and sphinganine exhibited equivalent potency  and efficacy in both the direct induction of apoptosis and the  potentiation of ceramide-dependent cell death.	transcription
60738	5	336066	5	NULL	NULL	0	NULL	sphinganine	Chemical		potentiate					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_263	8626522	First, as  already noted, sphingosine and sphinganine exhibited equivalent potency  and efficacy in both the direct induction of apoptosis and the  potentiation of ceramide-dependent cell death.	transcription
60739	6	336066	5	NULL	NULL	0	NULL	statement 2	Process	potency of	is equivalent to					statement 3	Process	potency of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_263	8626522	First, as  already noted, sphingosine and sphinganine exhibited equivalent potency  and efficacy in both the direct induction of apoptosis and the  potentiation of ceramide-dependent cell death.	transcription
60740	7	336066	5	NULL	NULL	0	NULL	statement 2	Process	efficacy of	is equivalent to					statement 3	Process	efficacy of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_263	8626522	First, as  already noted, sphingosine and sphinganine exhibited equivalent potency  and efficacy in both the direct induction of apoptosis and the  potentiation of ceramide-dependent cell death.	transcription
60741	8	336066	5	NULL	NULL	0	NULL	statement 4	Process	potency of	is equivalent to					statement 5	Process	potency of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_263	8626522	First, as  already noted, sphingosine and sphinganine exhibited equivalent potency  and efficacy in both the direct induction of apoptosis and the  potentiation of ceramide-dependent cell death.	transcription
60742	9	336066	5	NULL	NULL	0	NULL	statement 4	Process	efficacy of	is equivalent to					statement 5	Process	efficacy of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_263	8626522	First, as  already noted, sphingosine and sphinganine exhibited equivalent potency  and efficacy in both the direct induction of apoptosis and the  potentiation of ceramide-dependent cell death.	transcription
67462	1	336066	7	NULL	NULL	0	NULL	sphingosine	Chemical		induce		directly			apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_263	8626522	First, as  already noted, sphingosine and sphinganine exhibited equivalent potency  and efficacy in both the direct induction of apoptosis and the  potentiation of ceramide-dependent cell death.	transcription
67463	2	336066	7	NULL	NULL	NULL	NULL	sphinganine	Chemical		induce		directly			apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_263	8626522	First, as  already noted, sphingosine and sphinganine exhibited equivalent potency  and efficacy in both the direct induction of apoptosis and the  potentiation of ceramide-dependent cell death.	transcription
67464	3	336066	7	NULL	NULL	0	NULL	cell death	Process		depends on					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_263	8626522	First, as  already noted, sphingosine and sphinganine exhibited equivalent potency  and efficacy in both the direct induction of apoptosis and the  potentiation of ceramide-dependent cell death.	transcription
67465	4	336066	7	NULL	NULL	0	NULL	sphingosine	Chemical		potentiate					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_263	8626522	First, as  already noted, sphingosine and sphinganine exhibited equivalent potency  and efficacy in both the direct induction of apoptosis and the  potentiation of ceramide-dependent cell death.	transcription
67466	5	336066	7	NULL	NULL	0	NULL	sphinganine	Chemical		potentiate					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_263	8626522	First, as  already noted, sphingosine and sphinganine exhibited equivalent potency  and efficacy in both the direct induction of apoptosis and the  potentiation of ceramide-dependent cell death.	transcription
60743	1	336067	5	NULL	NULL	0	NULL	ceramide	Chemical		deacetylated to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_28_16506_s_25	8663293	Deacylation of ceramide produces sphingosine which inhibits protein kinase C ( 20) and Mg2+-dependent and -independent PAP activities ( 24,  25).	transcription
60744	2	336067	5	NULL	NULL	0	NULL	sphingosine	Chemical		inhibits					protein kinase C	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_28_16506_s_25	8663293	Deacylation of ceramide produces sphingosine which inhibits protein kinase C ( 20) and Mg2+-dependent and -independent PAP activities ( 24,  25).	transcription
60745	3	336067	5	NULL	NULL	0	NULL	PAP	GP	activity of	is dependent on					Mg2+	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_28_16506_s_25	8663293	Deacylation of ceramide produces sphingosine which inhibits protein kinase C ( 20) and Mg2+-dependent and -independent PAP activities ( 24,  25).	transcription
60746	4	336067	5	NULL	NULL	0	NULL	PAP	GP	activity of	is independent of					Mg2+	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_28_16506_s_25	8663293	Deacylation of ceramide produces sphingosine which inhibits protein kinase C ( 20) and Mg2+-dependent and -independent PAP activities ( 24,  25).	transcription
60747	5	336067	5	NULL	NULL	0	NULL	sphingosine	Chemical		inhibits					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_28_16506_s_25	8663293	Deacylation of ceramide produces sphingosine which inhibits protein kinase C ( 20) and Mg2+-dependent and -independent PAP activities ( 24,  25).	transcription
60748	6	336067	5	NULL	NULL	0	NULL	sphingosine	Chemical		inhibits					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_28_16506_s_25	8663293	Deacylation of ceramide produces sphingosine which inhibits protein kinase C ( 20) and Mg2+-dependent and -independent PAP activities ( 24,  25).	transcription
67467	1	336067	7	NULL	NULL	0	NULL	ceramide	Chemical	deacylation of	produce					sphingosine 	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_28_16506_s_25	8663293	Deacylation of ceramide produces sphingosine which inhibits protein kinase C ( 20) and Mg2+-dependent and -independent PAP activities ( 24,  25).	transcription
67468	2	336067	7	NULL	NULL	0	NULL	sphingosine	Chemical		inhibit					protein kinase C	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_28_16506_s_25	8663293	Deacylation of ceramide produces sphingosine which inhibits protein kinase C ( 20) and Mg2+-dependent and -independent PAP activities ( 24,  25).	transcription
67469	3	336067	7	NULL	NULL	0	NULL	PAP activities	Process		depend on					Mg2+	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_28_16506_s_25	8663293	Deacylation of ceramide produces sphingosine which inhibits protein kinase C ( 20) and Mg2+-dependent and -independent PAP activities ( 24,  25).	transcription
67470	4	336067	7	NULL	NULL	0	NULL	PAP activities	Process		independent of					Mg2+ 	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_28_16506_s_25	8663293	Deacylation of ceramide produces sphingosine which inhibits protein kinase C ( 20) and Mg2+-dependent and -independent PAP activities ( 24,  25).	transcription
67471	5	336067	7	NULL	NULL	0	NULL	sphingosine	Chemical		inhibit					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_28_16506_s_25	8663293	Deacylation of ceramide produces sphingosine which inhibits protein kinase C ( 20) and Mg2+-dependent and -independent PAP activities ( 24,  25).	transcription
67472	6	336067	7	NULL	NULL	0	NULL	sphingosine	Chemical		inhibit					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_28_16506_s_25	8663293	Deacylation of ceramide produces sphingosine which inhibits protein kinase C ( 20) and Mg2+-dependent and -independent PAP activities ( 24,  25).	transcription
60749	1	336068	5	NULL	NULL	0	NULL	DL- threo-dihydrosphingosine	Chemical		increases					c-jun	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_45_27326_s_203	7592995	We found that DL- threo-dihydrosphingosine rather increased  c- jun  expression,   suggesting that sphingosine  1-phosphate is not involved in c- jun  induction by ceramide.	transcription
60750	2	336068	5	NULL	NULL	0	NULL	c- jun	Chemical		is induced by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_45_27326_s_203	7592995	We found that DL- threo-dihydrosphingosine rather increased  c- jun  expression,   suggesting that sphingosine  1-phosphate is not involved in c- jun  induction by ceramide.	transcription
60751	3	336068	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		is not involved in					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_45_27326_s_203	7592995	We found that DL- threo-dihydrosphingosine rather increased  c- jun  expression,   suggesting that sphingosine  1-phosphate is not involved in c- jun  induction by ceramide.	transcription
60752	4	336068	5	NULL	NULL	0	NULL	statement 1	Process		suggest					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_45_27326_s_203	7592995	We found that DL- threo-dihydrosphingosine rather increased  c- jun  expression,   suggesting that sphingosine  1-phosphate is not involved in c- jun  induction by ceramide.	transcription
67473	1	336068	7	NULL	NULL	0	NULL	DL- threo-dihydrosphingosine	Chemical		increase					c-jun	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_45_27326_s_203	7592995	We found that DL- threo-dihydrosphingosine rather increased  c- jun  expression,   suggesting that sphingosine  1-phosphate is not involved in c- jun  induction by ceramide.	transcription
67474	2	336068	7	NULL	NULL	0	NULL	ceramide	Chemical		induce					c-jun	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_45_27326_s_203	7592995	We found that DL- threo-dihydrosphingosine rather increased  c- jun  expression,   suggesting that sphingosine  1-phosphate is not involved in c- jun  induction by ceramide.	transcription
67475	3	336068	7	NULL	NULL	0	NULL	sphingosine 1-phosphate	GP		is not involved in					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_45_27326_s_203	7592995	We found that DL- threo-dihydrosphingosine rather increased  c- jun  expression,   suggesting that sphingosine  1-phosphate is not involved in c- jun  induction by ceramide.	transcription
67476	4	336068	7	NULL	NULL	0	NULL	statement 1	Process		suggest					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_45_27326_s_203	7592995	We found that DL- threo-dihydrosphingosine rather increased  c- jun  expression,   suggesting that sphingosine  1-phosphate is not involved in c- jun  induction by ceramide.	transcription
60753	1	336069	5	NULL	NULL	0	NULL	SPP	Chemical		bind					Edg-3	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_8_4626_s_105	9988698	Sphingosine had a small but statistically significant effect on SPP binding to both Edg-3 and H218, while ceramide had a similarly small effect on binding to H218 only.	transcription
60754	2	336069	5	NULL	NULL	0	NULL	SPP	Chemical		bind					H218	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_8_4626_s_105	9988698	Sphingosine had a small but statistically significant effect on SPP binding to both Edg-3 and H218, while ceramide had a similarly small effect on binding to H218 only.	transcription
60755	3	336069	5	NULL	NULL	0	NULL	sphingosine	Chemical		effects		significantly			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_8_4626_s_105	9988698	Sphingosine had a small but statistically significant effect on SPP binding to both Edg-3 and H218, while ceramide had a similarly small effect on binding to H218 only.	transcription
60756	4	336069	5	NULL	NULL	0	NULL	sphingosine	Chemical		effects		significantly			statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_8_4626_s_105	9988698	Sphingosine had a small but statistically significant effect on SPP binding to both Edg-3 and H218, while ceramide had a similarly small effect on binding to H218 only.	transcription
60757	5	336069	5	NULL	NULL	0	NULL	ceramide	Chemical		effects					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_8_4626_s_105	9988698	Sphingosine had a small but statistically significant effect on SPP binding to both Edg-3 and H218, while ceramide had a similarly small effect on binding to H218 only.	transcription
67477	1	336069	7	NULL	NULL	0	NULL	SPP	Chemical		bind					Edg-3	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_8_4626_s_105	9988698	Sphingosine had a small but statistically significant effect on SPP binding to both Edg-3 and H218, while ceramide had a similarly small effect on binding to H218 only.	transcription
67478	2	336069	7	NULL	NULL	NULL	NULL	SPP	Chemical		bind					H218	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_8_4626_s_105	9988698	Sphingosine had a small but statistically significant effect on SPP binding to both Edg-3 and H218, while ceramide had a similarly small effect on binding to H218 only.	transcription
67479	3	336069	7	NULL	NULL	0	NULL	Sphingosine	Chemical		effect		significantly			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_8_4626_s_105	9988698	Sphingosine had a small but statistically significant effect on SPP binding to both Edg-3 and H218, while ceramide had a similarly small effect on binding to H218 only.	transcription
67480	4	336069	7	NULL	NULL	0	NULL	sphingosine	Chemical		effect		significantly			statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_8_4626_s_105	9988698	Sphingosine had a small but statistically significant effect on SPP binding to both Edg-3 and H218, while ceramide had a similarly small effect on binding to H218 only.	transcription
67481	5	336069	7	NULL	NULL	0	NULL	ceramide	Chemical		effect on		small			statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_8_4626_s_105	9988698	Sphingosine had a small but statistically significant effect on SPP binding to both Edg-3 and H218, while ceramide had a similarly small effect on binding to H218 only.	transcription
60765	1	336070	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					phorbol ester	Chemical				NULL	adherent HL-60 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_25_15345_s_25	9624115	The principal mediator of apoptosis in these cases is ceramide, not sphingosine, but SPP could be equally effective in the protection of adherent HL-60 cells from phorbol ester-induced apoptosis.	transcription
60768	2	336070	5	NULL	NULL	0	NULL	SPP	Chemical		protects					statement 1	Process				NULL	adherent HL-60 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_25_15345_s_25	9624115	The principal mediator of apoptosis in these cases is ceramide, not sphingosine, but SPP could be equally effective in the protection of adherent HL-60 cells from phorbol ester-induced apoptosis.	transcription
60787	3	336070	5	NULL	NULL	0	NULL	ceramide	Chemical		mediates					apoptosis	Process				NULL	adherent HL-60 cells	0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15345_s_25	9624115	The principal mediator of apoptosis in these cases is ceramide, not sphingosine, but SPP could be equally effective in the protection of adherent HL-60 cells from phorbol ester-induced apoptosis.	transcription
60788	4	336070	5	NULL	NULL	0	NULL	sphingosine	Chemical		does not mediate					apoptosis	Process				NULL	adherent HL-60 cells	0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15345_s_25	9624115	The principal mediator of apoptosis in these cases is ceramide, not sphingosine, but SPP could be equally effective in the protection of adherent HL-60 cells from phorbol ester-induced apoptosis.	transcription
67482	1	336070	7	NULL	NULL	0	NULL	 ceramide	Chemical		mediate					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15345_s_25	9624115	The principal mediator of apoptosis in these cases is ceramide, not sphingosine, but SPP could be equally effective in the protection of adherent HL-60 cells from phorbol ester-induced apoptosis.	transcription
67483	2	336070	7	NULL	NULL	0	NULL	sphingosine	Chemical		does not mediate					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15345_s_25	9624115	The principal mediator of apoptosis in these cases is ceramide, not sphingosine, but SPP could be equally effective in the protection of adherent HL-60 cells from phorbol ester-induced apoptosis.	transcription
67484	3	336070	7	NULL	NULL	0	NULL	phorbol ester	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15345_s_25	9624115	The principal mediator of apoptosis in these cases is ceramide, not sphingosine, but SPP could be equally effective in the protection of adherent HL-60 cells from phorbol ester-induced apoptosis.	transcription
67485	4	336070	7	NULL	NULL	0	NULL	SPP	Chemical		protect					adherent HL-60 cells	Cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15345_s_25	9624115	The principal mediator of apoptosis in these cases is ceramide, not sphingosine, but SPP could be equally effective in the protection of adherent HL-60 cells from phorbol ester-induced apoptosis.	transcription
67486	5	336070	7	NULL	NULL	0	NULL	statement 4	Process		protected from					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_25_15345_s_25	9624115	The principal mediator of apoptosis in these cases is ceramide, not sphingosine, but SPP could be equally effective in the protection of adherent HL-60 cells from phorbol ester-induced apoptosis.	transcription
60793	1	336071	5	NULL	NULL	0	NULL	ceramide	Chemical		is a metabolite of					sphingolipid	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_20_12558_s_22	9575216	The sphingolipid metabolite ceramide has been implicated as a stimulator of PKC-inactivating phosphatase catalysis ( 12), and the related metabolite sphingosine is a reversible inhibitor of PKC ( 13).	transcription
60794	2	336071	5	NULL	NULL	0	NULL	PKC	GP		inactivates					phosphatase	GP	catalysis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_20_12558_s_22	9575216	The sphingolipid metabolite ceramide has been implicated as a stimulator of PKC-inactivating phosphatase catalysis ( 12), and the related metabolite sphingosine is a reversible inhibitor of PKC ( 13).	transcription
60795	3	336071	5	NULL	NULL	0	NULL	ceramide	Chemical		stimulates					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_20_12558_s_22	9575216	The sphingolipid metabolite ceramide has been implicated as a stimulator of PKC-inactivating phosphatase catalysis ( 12), and the related metabolite sphingosine is a reversible inhibitor of PKC ( 13).	transcription
60796	4	336071	5	NULL	NULL	0	NULL	sphingosine	GP		is a reversible inhibitor of					PKC	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_20_12558_s_22	9575216	The sphingolipid metabolite ceramide has been implicated as a stimulator of PKC-inactivating phosphatase catalysis ( 12), and the related metabolite sphingosine is a reversible inhibitor of PKC ( 13).	transcription
67487	1	336071	7	NULL	NULL	0	NULL	ceramide	Chemical		stimulate					PKC-inactivating phosphatase catalysis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_20_12558_s_22	9575216	The sphingolipid metabolite ceramide has been implicated as a stimulator of PKC-inactivating phosphatase catalysis ( 12), and the related metabolite sphingosine is a reversible inhibitor of PKC ( 13).	transcription
67488	2	336071	7	NULL	NULL	0	NULL	sphingosine	Chemical		inhibit		reversibly			PKC	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_20_12558_s_22	9575216	The sphingolipid metabolite ceramide has been implicated as a stimulator of PKC-inactivating phosphatase catalysis ( 12), and the related metabolite sphingosine is a reversible inhibitor of PKC ( 13).	transcription
67489	3	336071	7	NULL	NULL	0	NULL	ceramide	Chemical		is a type of					sphingolipid metabolite	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_20_12558_s_22	9575216	The sphingolipid metabolite ceramide has been implicated as a stimulator of PKC-inactivating phosphatase catalysis ( 12), and the related metabolite sphingosine is a reversible inhibitor of PKC ( 13).	transcription
60797	1	336072	5	NULL	NULL	0	NULL	TNFalpha	GP		induce					apoptosis	Process				NULL	cardiomyocytes	0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_174	8981934	This study provides the first evidence that TNFalpha and its sphingolipid second messenger molecules, including ceramide, sphingosine, and sphingosine-1-phosphate, can induce apoptosis  in cardiomyocytes.	transcription
60798	2	336072	5	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL	cardiomyocytes	0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_174	8981934	This study provides the first evidence that TNFalpha and its sphingolipid second messenger molecules, including ceramide, sphingosine, and sphingosine-1-phosphate, can induce apoptosis  in cardiomyocytes.	transcription
60800	3	336072	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					apoptosis	Process				NULL	cardiomyocytes	0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_174	8981934	This study provides the first evidence that TNFalpha and its sphingolipid second messenger molecules, including ceramide, sphingosine, and sphingosine-1-phosphate, can induce apoptosis  in cardiomyocytes.	transcription
60801	4	336072	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		induce					apoptosis	Process				NULL	cardiomyocytes	0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_174	8981934	This study provides the first evidence that TNFalpha and its sphingolipid second messenger molecules, including ceramide, sphingosine, and sphingosine-1-phosphate, can induce apoptosis  in cardiomyocytes.	transcription
60802	5	336072	5	NULL	NULL	0	NULL	ceramide	Chemical		is a type of					sphingolipid second messenger molecule	Chemical				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_174	8981934	This study provides the first evidence that TNFalpha and its sphingolipid second messenger molecules, including ceramide, sphingosine, and sphingosine-1-phosphate, can induce apoptosis  in cardiomyocytes.	transcription
60803	6	336072	5	NULL	NULL	0	NULL	sphingosine	Chemical		is a type of					sphingolipid second messenger molecule	Chemical				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_174	8981934	This study provides the first evidence that TNFalpha and its sphingolipid second messenger molecules, including ceramide, sphingosine, and sphingosine-1-phosphate, can induce apoptosis  in cardiomyocytes.	transcription
60804	7	336072	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		is a type of					sphingolipid second messenger molecule	Chemical				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_174	8981934	This study provides the first evidence that TNFalpha and its sphingolipid second messenger molecules, including ceramide, sphingosine, and sphingosine-1-phosphate, can induce apoptosis  in cardiomyocytes.	transcription
67490	1	336072	7	NULL	NULL	0	NULL	TNFalpha	GP		induce					apoptosis	Process				NULL	cardiomyocytes	0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_174	8981934	This study provides the first evidence that TNFalpha and its sphingolipid second messenger molecules, including ceramide, sphingosine, and sphingosine-1-phosphate, can induce apoptosis  in cardiomyocytes.	transcription
67491	2	336072	7	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL	cardiomyocytes	0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_174	8981934	This study provides the first evidence that TNFalpha and its sphingolipid second messenger molecules, including ceramide, sphingosine, and sphingosine-1-phosphate, can induce apoptosis  in cardiomyocytes.	transcription
67492	3	336072	7	NULL	NULL	0	NULL	sphingosine	Chemical		induce					apoptosis	Process				NULL	cardiomyocytes	0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_174	8981934	This study provides the first evidence that TNFalpha and its sphingolipid second messenger molecules, including ceramide, sphingosine, and sphingosine-1-phosphate, can induce apoptosis  in cardiomyocytes.	transcription
67493	4	336072	7	NULL	NULL	NULL	NULL	sphingosine-1-phosphate	Chemical		induce					apoptosis	Process				NULL	cardiomyocytes	NULL	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_174	8981934	This study provides the first evidence that TNFalpha and its sphingolipid second messenger molecules, including ceramide, sphingosine, and sphingosine-1-phosphate, can induce apoptosis  in cardiomyocytes.	transcription
67494	5	336072	7	NULL	NULL	0	NULL	ceramide	Chemical		is a type of					sphingolipid second messenger molecule	Chemical				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_174	8981934	This study provides the first evidence that TNFalpha and its sphingolipid second messenger molecules, including ceramide, sphingosine, and sphingosine-1-phosphate, can induce apoptosis  in cardiomyocytes.	transcription
67495	6	336072	7	NULL	NULL	0	NULL	sphingosine	Chemical		is a type of					sphingolipid second messenger molecule	Chemical				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_174	8981934	This study provides the first evidence that TNFalpha and its sphingolipid second messenger molecules, including ceramide, sphingosine, and sphingosine-1-phosphate, can induce apoptosis  in cardiomyocytes.	transcription
67496	7	336072	7	NULL	NULL	0	NULL	sphingosine-1-phosphate	Chemical		is a type of					sphingolipid second messenger molecule	Chemical				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_174	8981934	This study provides the first evidence that TNFalpha and its sphingolipid second messenger molecules, including ceramide, sphingosine, and sphingosine-1-phosphate, can induce apoptosis  in cardiomyocytes.	transcription
60805	1	336073	5	NULL	NULL	0	NULL	apoptosis	Process		is dependent on					SAPK/AP1	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_8	10454518	In parallel trials, the lethal actions of ceramide (but not of sphingosine) were markedly diminished by pretreatment with diferuloylmethane or expression of TAM-67, confirming the effectiveness of these interventions in suppression of SAPK/AP1-dependent apoptosis.	transcription
60806	2	336073	5	NULL	NULL	0	NULL	diferuloylmethane	Chemical	pretreatment with	diminishes					ceramide	Chemical	lethal actions of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_8	10454518	In parallel trials, the lethal actions of ceramide (but not of sphingosine) were markedly diminished by pretreatment with diferuloylmethane or expression of TAM-67, confirming the effectiveness of these interventions in suppression of SAPK/AP1-dependent apoptosis.	transcription
60807	3	336073	5	NULL	NULL	0	NULL	TAM-67	GP	expression of	diminishes					ceramide	Chemical	lethal actions of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_8	10454518	In parallel trials, the lethal actions of ceramide (but not of sphingosine) were markedly diminished by pretreatment with diferuloylmethane or expression of TAM-67, confirming the effectiveness of these interventions in suppression of SAPK/AP1-dependent apoptosis.	transcription
60809	4	336073	5	NULL	NULL	0	NULL	statement 2	Process		suppress					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_8	10454518	In parallel trials, the lethal actions of ceramide (but not of sphingosine) were markedly diminished by pretreatment with diferuloylmethane or expression of TAM-67, confirming the effectiveness of these interventions in suppression of SAPK/AP1-dependent apoptosis.	transcription
60810	5	336073	5	NULL	NULL	0	NULL	statement 3	Process		suppress					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_8	10454518	In parallel trials, the lethal actions of ceramide (but not of sphingosine) were markedly diminished by pretreatment with diferuloylmethane or expression of TAM-67, confirming the effectiveness of these interventions in suppression of SAPK/AP1-dependent apoptosis.	transcription
67497	1	336073	7	NULL	NULL	0	NULL	diferuloylmethane	Chemical		diminish					ceramide	Chemical	lethal actions of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_8	10454518	In parallel trials, the lethal actions of ceramide (but not of sphingosine) were markedly diminished by pretreatment with diferuloylmethane or expression of TAM-67, confirming the effectiveness of these interventions in suppression of SAPK/AP1-dependent apoptosis.	transcription
67498	2	336073	7	NULL	NULL	NULL	NULL	TAM-67	GP	expression of	diminish					ceramide	Chemical	lethal actions of			NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_8	10454518	In parallel trials, the lethal actions of ceramide (but not of sphingosine) were markedly diminished by pretreatment with diferuloylmethane or expression of TAM-67, confirming the effectiveness of these interventions in suppression of SAPK/AP1-dependent apoptosis.	transcription
67499	3	336073	7	NULL	NULL	0	NULL	diferuloylmethane	Chemical		does not diminish					sphingosine	Chemical	lethal actions of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_8	10454518	In parallel trials, the lethal actions of ceramide (but not of sphingosine) were markedly diminished by pretreatment with diferuloylmethane or expression of TAM-67, confirming the effectiveness of these interventions in suppression of SAPK/AP1-dependent apoptosis.	transcription
67500	4	336073	7	NULL	NULL	0	NULL	TAM-67	GP	expression of	does not diminish					sphingosine	Chemical	lethal actions of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_8	10454518	In parallel trials, the lethal actions of ceramide (but not of sphingosine) were markedly diminished by pretreatment with diferuloylmethane or expression of TAM-67, confirming the effectiveness of these interventions in suppression of SAPK/AP1-dependent apoptosis.	transcription
67501	5	336073	7	NULL	NULL	0	NULL	apoptosis	Process		depends on					SAPK/AP1	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_8	10454518	In parallel trials, the lethal actions of ceramide (but not of sphingosine) were markedly diminished by pretreatment with diferuloylmethane or expression of TAM-67, confirming the effectiveness of these interventions in suppression of SAPK/AP1-dependent apoptosis.	transcription
67502	6	336073	7	NULL	NULL	0	NULL	diferuloylmethane	Chemical		suppress					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_8	10454518	In parallel trials, the lethal actions of ceramide (but not of sphingosine) were markedly diminished by pretreatment with diferuloylmethane or expression of TAM-67, confirming the effectiveness of these interventions in suppression of SAPK/AP1-dependent apoptosis.	transcription
67503	7	336073	7	NULL	NULL	0	NULL	 TAM-67	GP	expression of	suppress					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_8	10454518	In parallel trials, the lethal actions of ceramide (but not of sphingosine) were markedly diminished by pretreatment with diferuloylmethane or expression of TAM-67, confirming the effectiveness of these interventions in suppression of SAPK/AP1-dependent apoptosis.	transcription
60892	1	336074	5	NULL	NULL	0	NULL	sphingosine	Chemical		activates					PLD	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
60893	2	336074	5	NULL	NULL	0	NULL	statement 1	Process		increases					mitogenesis	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
60894	3	336074	5	NULL	NULL	0	NULL	sphingosine	Chemical		activates					phosphatidic acid	Chemical				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
60896	4	336074	5	NULL	NULL	0	NULL	statement 3	Process		increases					mitogenesis	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
60897	5	336074	5	NULL	NULL	0	NULL	S-1-P	Chemical		activates					PLD	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
60898	6	336074	5	NULL	NULL	0	NULL	statement 5	Process		increases					mitogenesis	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
60900	7	336074	5	NULL	NULL	0	NULL	S-1-P	Chemical		activates					phosphatidic acid	Chemical				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
60901	8	336074	5	NULL	NULL	0	NULL	statement 7	Process		increases					mitogenesis	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
60903	9	336074	5	NULL	NULL	0	NULL	ceramide	Chemical		inhibits					PLD	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
60904	10	336074	5	NULL	NULL	0	NULL	statement 9	Process		inhibits					mitogenesis	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
67504	1	336074	7	NULL	NULL	0	NULL	Sphingosine	Chemical		activate					PLD	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
67505	2	336074	7	NULL	NULL	0	NULL	S-1-P	Chemical		activate					PLD	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
67506	3	336074	7	NULL	NULL	0	NULL	Sphingosine 	Chemical		activate					phosphatidic acid	Chemical				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
67507	4	336074	7	NULL	NULL	0	NULL	S-1-P	Chemical		activate					phosphatidic acid	Chemical				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
67508	5	336074	7	NULL	NULL	0	NULL	statement 1	Process		increase					mitogenesis	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
67509	6	336074	7	NULL	NULL	0	NULL	statement 2	Process		increase					mitogenesis	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
67510	7	336074	7	NULL	NULL	0	NULL	statement 3	Process		increase					mitogenesis	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
67511	8	336074	7	NULL	NULL	0	NULL	statement 4	Process		increase					mitogenesis	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
67512	9	336074	7	NULL	NULL	0	NULL	ceramide	Chemical		inhibit					PLD	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
67513	10	336074	7	NULL	NULL	0	NULL	ceramide	Chemical		inhibit					mitogenesis	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_285_1_317_s_207	9536027	Sphingosine and S-1-P activate PLD and phosphatidic acid and increase mitogenesis, whereas ceramide inhibits PLD and mitogenesis (Yamada and Sakane, 1993  ; Gomez  et al., 1994  ).	transcription
60911	1	336075	5	NULL	NULL	0	NULL	inflammatory cytokines	GP		stimulates					sphingomyelinase	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochemistry-(mosc)_63_1_9526097_s_5	9526097	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
60912	2	336075	5	NULL	NULL	0	NULL	Inflammatory cytokines	GP		does not stimulate					ceramidase	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochemistry-(mosc)_63_1_9526097_s_5	9526097	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
60913	3	336075	5	NULL	NULL	0	NULL	statement 2	Process		accumulates					ceramide	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochemistry-(mosc)_63_1_9526097_s_5	9526097	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
60915	4	336075	5	NULL	NULL	0	NULL	growth signals	GP		stimulates					ceramidase	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochemistry-(mosc)_63_1_9526097_s_5	9526097	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
60916	5	336075	5	NULL	NULL	0	NULL	statement 4	Process		increases					SPP	Chemical	level of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochemistry-(mosc)_63_1_9526097_s_5	9526097	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
60917	6	336075	5	NULL	NULL	0	NULL	growth signals	GP		stimulates					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochemistry-(mosc)_63_1_9526097_s_5	9526097	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
60919	7	336075	5	NULL	NULL	0	NULL	statement 6	Process		increases					SPP	Chemical	level of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochemistry-(mosc)_63_1_9526097_s_5	9526097	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
67514	1	336075	7	NULL	NULL	0	NULL	Inflammatory cytokines 	GP		stimulate					sphingomyelinase	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochemistry-(mosc)_63_1_9526097_s_5	9526097	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
67515	2	336075	7	NULL	NULL	0	NULL	Inflammatory cytokines	GP		does not stimulate					ceramidase	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochemistry-(mosc)_63_1_9526097_s_5	9526097	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
67516	3	336075	7	NULL	NULL	0	NULL	statement 2	Process		leads to					ceramide	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochemistry-(mosc)_63_1_9526097_s_5	9526097	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
67517	4	336075	7	NULL	NULL	0	NULL	growth signals	GP		stimulate					ceramidase	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochemistry-(mosc)_63_1_9526097_s_5	9526097	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
67518	5	336075	7	NULL	NULL	0	NULL	growth signals	GP		stimulate					sphingosine kinase 	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochemistry-(mosc)_63_1_9526097_s_5	9526097	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
67519	6	336075	7	NULL	NULL	0	NULL	statement 4	Process		leads to					SPP	Chemical	increased levels of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochemistry-(mosc)_63_1_9526097_s_5	9526097	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
67520	7	336075	7	NULL	NULL	0	NULL	statement 5	Process		leads to					SPP	Chemical	increased levels of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochemistry-(mosc)_63_1_9526097_s_5	9526097	Inflammatory cytokines stimulate sphingomyelinase,  but not ceramidase, leading to accumulation of ceramide, whereas growth  signals also stimulate ceramidase and sphingosine kinase leading to increased  SPP levels.	transcription
61011	1	336076	5	NULL	NULL	0	NULL	lipid	Chemical		mediates					cytotoxicity	Process				NULL	U937 cells	0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_156	9415703	View this table:   [in this window]   [in a new window]     [[ TABLE 3        Selectivity ]] of lipid-mediated cytotoxicity in U937 cells    U937 cells were exposed to ceramide or sphingosine at equimolar levels (10 muM) in the presence of the ceramide acylhydrolase inhibitor oleoylethanolamine (100 muM) or the ceramide synthase inhibitor fumonisin B1 (100 muM).	transcription
61012	2	336076	5	NULL	NULL	0	NULL	oleoylethanolamine	Chemical		is an inhibitor of					ceramide acylhydrolase	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_156	9415703	View this table:   [in this window]   [in a new window]     [[ TABLE 3        Selectivity ]] of lipid-mediated cytotoxicity in U937 cells    U937 cells were exposed to ceramide or sphingosine at equimolar levels (10 muM) in the presence of the ceramide acylhydrolase inhibitor oleoylethanolamine (100 muM) or the ceramide synthase inhibitor fumonisin B1 (100 muM).	transcription
61013	3	336076	5	NULL	NULL	0	NULL	fumonisin B1	Chemical		is an inhibitor of					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_156	9415703	View this table:   [in this window]   [in a new window]     [[ TABLE 3        Selectivity ]] of lipid-mediated cytotoxicity in U937 cells    U937 cells were exposed to ceramide or sphingosine at equimolar levels (10 muM) in the presence of the ceramide acylhydrolase inhibitor oleoylethanolamine (100 muM) or the ceramide synthase inhibitor fumonisin B1 (100 muM).	transcription
67521	1	336076	7	NULL	NULL	0	NULL	lipid	Chemical		mediate					cytotoxicity	Process				NULL	U937 cells	0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_156	9415703	View this table:   [in this window]   [in a new window]     [[ TABLE 3        Selectivity ]] of lipid-mediated cytotoxicity in U937 cells    U937 cells were exposed to ceramide or sphingosine at equimolar levels (10 muM) in the presence of the ceramide acylhydrolase inhibitor oleoylethanolamine (100 muM) or the ceramide synthase inhibitor fumonisin B1 (100 muM).	transcription
67522	2	336076	7	NULL	NULL	0	NULL	oleoylethanolamine	Chemical		is a type of					ceramide acylhydrolase inhibitor	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_156	9415703	View this table:   [in this window]   [in a new window]     [[ TABLE 3        Selectivity ]] of lipid-mediated cytotoxicity in U937 cells    U937 cells were exposed to ceramide or sphingosine at equimolar levels (10 muM) in the presence of the ceramide acylhydrolase inhibitor oleoylethanolamine (100 muM) or the ceramide synthase inhibitor fumonisin B1 (100 muM).	transcription
67523	3	336076	7	NULL	NULL	0	NULL	fumonisin B1	Chemical		is a type of					 ceramide synthase inhibitor	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_156	9415703	View this table:   [in this window]   [in a new window]     [[ TABLE 3        Selectivity ]] of lipid-mediated cytotoxicity in U937 cells    U937 cells were exposed to ceramide or sphingosine at equimolar levels (10 muM) in the presence of the ceramide acylhydrolase inhibitor oleoylethanolamine (100 muM) or the ceramide synthase inhibitor fumonisin B1 (100 muM).	transcription
61014	1	336077	5	NULL	NULL	0	NULL	K562 cells	Cell	death of	is induced by					ceramide	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_38_22625_s_141	7545682	To test whether Abl could protect against  ceramide-induced death, K562 cells were exposed to various  concentrations of  N-hexanoyl sphingosine  (C -ceramide), a synthetic cell-permeable ceramide analogue,  and were assessed for apoptosis by flow cytometric analysis.	transcription
61015	2	336077	5	NULL	NULL	0	NULL	Abl	GP		protects against		potentially			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_38_22625_s_141	7545682	To test whether Abl could protect against  ceramide-induced death, K562 cells were exposed to various  concentrations of  N-hexanoyl sphingosine  (C -ceramide), a synthetic cell-permeable ceramide analogue,  and were assessed for apoptosis by flow cytometric analysis.	transcription
67524	1	336077	7	NULL	NULL	0	NULL	ceramide	Chemical		induce					death	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_38_22625_s_141	7545682	To test whether Abl could protect against  ceramide-induced death, K562 cells were exposed to various  concentrations of  N-hexanoyl sphingosine  (C -ceramide), a synthetic cell-permeable ceramide analogue,  and were assessed for apoptosis by flow cytometric analysis.	transcription
67525	2	336077	7	NULL	NULL	0	NULL	N-hexanoyl sphingosine	Chemical		is a type of					synthetic cell-permeable ceramide analogue	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_38_22625_s_141	7545682	To test whether Abl could protect against  ceramide-induced death, K562 cells were exposed to various  concentrations of  N-hexanoyl sphingosine  (C -ceramide), a synthetic cell-permeable ceramide analogue,  and were assessed for apoptosis by flow cytometric analysis.	transcription
67526	3	336077	7	NULL	NULL	0	NULL	N-hexanoyl sphingosine	Chemical		is					C -ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_38_22625_s_141	7545682	To test whether Abl could protect against  ceramide-induced death, K562 cells were exposed to various  concentrations of  N-hexanoyl sphingosine  (C -ceramide), a synthetic cell-permeable ceramide analogue,  and were assessed for apoptosis by flow cytometric analysis.	transcription
61016	1	336078	5	NULL	NULL	0	NULL	OE	Chemical		is					oleoylethanolamine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2591_s_155	9446561	After 24 h of incubation, concentration of nitrite was measured in the supernatants as mentioned under     Oleoylethanolamine (OE), an inhibitor of ceramidase, the enzyme responsible for the catabolism of ceramide to sphingosine and fatty acid, has been reported to induce apoptosis in neuroblastoma cells ( 23) because of the increased concentration of ceramide due to the inhibition of catabolism of ceramide ( 23).	transcription
61017	2	336078	5	NULL	NULL	0	NULL	oleoylethanolamine	Chemical		is an inhibitor of					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2591_s_155	9446561	After 24 h of incubation, concentration of nitrite was measured in the supernatants as mentioned under     Oleoylethanolamine (OE), an inhibitor of ceramidase, the enzyme responsible for the catabolism of ceramide to sphingosine and fatty acid, has been reported to induce apoptosis in neuroblastoma cells ( 23) because of the increased concentration of ceramide due to the inhibition of catabolism of ceramide ( 23).	transcription
61018	3	336078	5	NULL	NULL	0	NULL	ceramide	Chemical		is catabolised to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2591_s_155	9446561	After 24 h of incubation, concentration of nitrite was measured in the supernatants as mentioned under     Oleoylethanolamine (OE), an inhibitor of ceramidase, the enzyme responsible for the catabolism of ceramide to sphingosine and fatty acid, has been reported to induce apoptosis in neuroblastoma cells ( 23) because of the increased concentration of ceramide due to the inhibition of catabolism of ceramide ( 23).	transcription
61019	4	336078	5	NULL	NULL	0	NULL	ceramide	Chemical		is catabolised to					fatty acid	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2591_s_155	9446561	After 24 h of incubation, concentration of nitrite was measured in the supernatants as mentioned under     Oleoylethanolamine (OE), an inhibitor of ceramidase, the enzyme responsible for the catabolism of ceramide to sphingosine and fatty acid, has been reported to induce apoptosis in neuroblastoma cells ( 23) because of the increased concentration of ceramide due to the inhibition of catabolism of ceramide ( 23).	transcription
61020	5	336078	5	NULL	NULL	0	NULL	statement 3	Process		occurs along with					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2591_s_155	9446561	After 24 h of incubation, concentration of nitrite was measured in the supernatants as mentioned under     Oleoylethanolamine (OE), an inhibitor of ceramidase, the enzyme responsible for the catabolism of ceramide to sphingosine and fatty acid, has been reported to induce apoptosis in neuroblastoma cells ( 23) because of the increased concentration of ceramide due to the inhibition of catabolism of ceramide ( 23).	transcription
61021	6	336078	5	NULL	NULL	0	NULL	ceramidase	GP		catalyzes					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2591_s_155	9446561	After 24 h of incubation, concentration of nitrite was measured in the supernatants as mentioned under     Oleoylethanolamine (OE), an inhibitor of ceramidase, the enzyme responsible for the catabolism of ceramide to sphingosine and fatty acid, has been reported to induce apoptosis in neuroblastoma cells ( 23) because of the increased concentration of ceramide due to the inhibition of catabolism of ceramide ( 23).	transcription
61022	7	336078	5	NULL	NULL	0	NULL	oleoylethanolamine	Chemical		induce					apoptosis	Process				NULL	neuroblastoma cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2591_s_155	9446561	After 24 h of incubation, concentration of nitrite was measured in the supernatants as mentioned under     Oleoylethanolamine (OE), an inhibitor of ceramidase, the enzyme responsible for the catabolism of ceramide to sphingosine and fatty acid, has been reported to induce apoptosis in neuroblastoma cells ( 23) because of the increased concentration of ceramide due to the inhibition of catabolism of ceramide ( 23).	transcription
61023	8	336078	5	NULL	NULL	0	NULL	ceramide	Chemical	inhibition of;;catabolism of	increases					ceramide	Chemical	concentration of			NULL	neuroblastoma cells	0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2591_s_155	9446561	After 24 h of incubation, concentration of nitrite was measured in the supernatants as mentioned under     Oleoylethanolamine (OE), an inhibitor of ceramidase, the enzyme responsible for the catabolism of ceramide to sphingosine and fatty acid, has been reported to induce apoptosis in neuroblastoma cells ( 23) because of the increased concentration of ceramide due to the inhibition of catabolism of ceramide ( 23).	transcription
61024	9	336078	5	NULL	NULL	0	NULL	statement 8	Process		leads to					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2591_s_155	9446561	After 24 h of incubation, concentration of nitrite was measured in the supernatants as mentioned under     Oleoylethanolamine (OE), an inhibitor of ceramidase, the enzyme responsible for the catabolism of ceramide to sphingosine and fatty acid, has been reported to induce apoptosis in neuroblastoma cells ( 23) because of the increased concentration of ceramide due to the inhibition of catabolism of ceramide ( 23).	transcription
67527	1	336078	7	NULL	NULL	0	NULL	ceramide	Chemical		catabolized to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2591_s_155	9446561	After 24 h of incubation, concentration of nitrite was measured in the supernatants as mentioned under     Oleoylethanolamine (OE), an inhibitor of ceramidase, the enzyme responsible for the catabolism of ceramide to sphingosine and fatty acid, has been reported to induce apoptosis in neuroblastoma cells ( 23) because of the increased concentration of ceramide due to the inhibition of catabolism of ceramide ( 23).	transcription
67528	2	336078	7	NULL	NULL	0	NULL	ceramide	Chemical		catabolized to					fatty acid	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2591_s_155	9446561	After 24 h of incubation, concentration of nitrite was measured in the supernatants as mentioned under     Oleoylethanolamine (OE), an inhibitor of ceramidase, the enzyme responsible for the catabolism of ceramide to sphingosine and fatty acid, has been reported to induce apoptosis in neuroblastoma cells ( 23) because of the increased concentration of ceramide due to the inhibition of catabolism of ceramide ( 23).	transcription
67529	3	336078	7	NULL	NULL	0	NULL	statement 1	Process		occur along with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2591_s_155	9446561	After 24 h of incubation, concentration of nitrite was measured in the supernatants as mentioned under     Oleoylethanolamine (OE), an inhibitor of ceramidase, the enzyme responsible for the catabolism of ceramide to sphingosine and fatty acid, has been reported to induce apoptosis in neuroblastoma cells ( 23) because of the increased concentration of ceramide due to the inhibition of catabolism of ceramide ( 23).	transcription
67530	4	336078	7	NULL	NULL	0	NULL	ceramidase	GP		catalyze					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2591_s_155	9446561	After 24 h of incubation, concentration of nitrite was measured in the supernatants as mentioned under     Oleoylethanolamine (OE), an inhibitor of ceramidase, the enzyme responsible for the catabolism of ceramide to sphingosine and fatty acid, has been reported to induce apoptosis in neuroblastoma cells ( 23) because of the increased concentration of ceramide due to the inhibition of catabolism of ceramide ( 23).	transcription
67531	5	336078	7	NULL	NULL	0	NULL	OE	Chemical		is an inhibitor of					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2591_s_155	9446561	After 24 h of incubation, concentration of nitrite was measured in the supernatants as mentioned under     Oleoylethanolamine (OE), an inhibitor of ceramidase, the enzyme responsible for the catabolism of ceramide to sphingosine and fatty acid, has been reported to induce apoptosis in neuroblastoma cells ( 23) because of the increased concentration of ceramide due to the inhibition of catabolism of ceramide ( 23).	transcription
67532	6	336078	7	NULL	NULL	0	NULL	OE	Chemical		is					Oleoylethanolamine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2591_s_155	9446561	After 24 h of incubation, concentration of nitrite was measured in the supernatants as mentioned under     Oleoylethanolamine (OE), an inhibitor of ceramidase, the enzyme responsible for the catabolism of ceramide to sphingosine and fatty acid, has been reported to induce apoptosis in neuroblastoma cells ( 23) because of the increased concentration of ceramide due to the inhibition of catabolism of ceramide ( 23).	transcription
67533	7	336078	7	NULL	NULL	0	NULL	statement 3	Process		induce					apoptosis	Process				NULL	neuroblastoma cells	0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2591_s_155	9446561	After 24 h of incubation, concentration of nitrite was measured in the supernatants as mentioned under     Oleoylethanolamine (OE), an inhibitor of ceramidase, the enzyme responsible for the catabolism of ceramide to sphingosine and fatty acid, has been reported to induce apoptosis in neuroblastoma cells ( 23) because of the increased concentration of ceramide due to the inhibition of catabolism of ceramide ( 23).	transcription
67534	8	336078	7	NULL	NULL	0	NULL	statement 7	Process		because of					ceramide 	Chemical	increased concentration of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2591_s_155	9446561	After 24 h of incubation, concentration of nitrite was measured in the supernatants as mentioned under     Oleoylethanolamine (OE), an inhibitor of ceramidase, the enzyme responsible for the catabolism of ceramide to sphingosine and fatty acid, has been reported to induce apoptosis in neuroblastoma cells ( 23) because of the increased concentration of ceramide due to the inhibition of catabolism of ceramide ( 23).	transcription
61025	1	336079	5	NULL	NULL	0	NULL	SPP	Chemical		is					sphingosine 1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_3	9446602	A further metabolite of ceramide, sphingosine 1-phosphate (SPP), prevents ceramide-mediated apoptosis, and it has been suggested that the balance between intracellular ceramide and SPP levels may determine the cell fate (Cuvillier, O., Pirianov, G, Kleuser, B., Vanek, P. G., Coso, O.	transcription
61026	2	336079	5	NULL	NULL	0	NULL	SPP	Chemical		is a metabolite of					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_3	9446602	A further metabolite of ceramide, sphingosine 1-phosphate (SPP), prevents ceramide-mediated apoptosis, and it has been suggested that the balance between intracellular ceramide and SPP levels may determine the cell fate (Cuvillier, O., Pirianov, G, Kleuser, B., Vanek, P. G., Coso, O.	transcription
61027	3	336079	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_3	9446602	A further metabolite of ceramide, sphingosine 1-phosphate (SPP), prevents ceramide-mediated apoptosis, and it has been suggested that the balance between intracellular ceramide and SPP levels may determine the cell fate (Cuvillier, O., Pirianov, G, Kleuser, B., Vanek, P. G., Coso, O.	transcription
61028	4	336079	5	NULL	NULL	0	NULL	SPP	Chemical		prevents					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_3	9446602	A further metabolite of ceramide, sphingosine 1-phosphate (SPP), prevents ceramide-mediated apoptosis, and it has been suggested that the balance between intracellular ceramide and SPP levels may determine the cell fate (Cuvillier, O., Pirianov, G, Kleuser, B., Vanek, P. G., Coso, O.	transcription
61029	5	336079	5	NULL	NULL	0	NULL	ceramide	Chemical	intracellular levels of	is balanced with					SPP	Chemical	intracellular levels of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_3	9446602	A further metabolite of ceramide, sphingosine 1-phosphate (SPP), prevents ceramide-mediated apoptosis, and it has been suggested that the balance between intracellular ceramide and SPP levels may determine the cell fate (Cuvillier, O., Pirianov, G, Kleuser, B., Vanek, P. G., Coso, O.	transcription
61030	6	336079	5	NULL	NULL	0	NULL	statement 5	Process		determines		may			cell fate	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_3	9446602	A further metabolite of ceramide, sphingosine 1-phosphate (SPP), prevents ceramide-mediated apoptosis, and it has been suggested that the balance between intracellular ceramide and SPP levels may determine the cell fate (Cuvillier, O., Pirianov, G, Kleuser, B., Vanek, P. G., Coso, O.	transcription
67535	1	336079	7	NULL	NULL	0	NULL	ceramide	Chemical		mediate					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_3	9446602	A further metabolite of ceramide, sphingosine 1-phosphate (SPP), prevents ceramide-mediated apoptosis, and it has been suggested that the balance between intracellular ceramide and SPP levels may determine the cell fate (Cuvillier, O., Pirianov, G, Kleuser, B., Vanek, P. G., Coso, O.	transcription
67536	2	336079	7	NULL	NULL	0	NULL	SPP	Chemical		prevents					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_3	9446602	A further metabolite of ceramide, sphingosine 1-phosphate (SPP), prevents ceramide-mediated apoptosis, and it has been suggested that the balance between intracellular ceramide and SPP levels may determine the cell fate (Cuvillier, O., Pirianov, G, Kleuser, B., Vanek, P. G., Coso, O.	transcription
67537	3	336079	7	NULL	NULL	0	NULL	SPP	Chemical		is					sphingosine 1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_3	9446602	A further metabolite of ceramide, sphingosine 1-phosphate (SPP), prevents ceramide-mediated apoptosis, and it has been suggested that the balance between intracellular ceramide and SPP levels may determine the cell fate (Cuvillier, O., Pirianov, G, Kleuser, B., Vanek, P. G., Coso, O.	transcription
67538	4	336079	7	NULL	NULL	0	NULL	SPP	Chemical		is a metabolite of					ceramide 	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_3	9446602	A further metabolite of ceramide, sphingosine 1-phosphate (SPP), prevents ceramide-mediated apoptosis, and it has been suggested that the balance between intracellular ceramide and SPP levels may determine the cell fate (Cuvillier, O., Pirianov, G, Kleuser, B., Vanek, P. G., Coso, O.	transcription
67539	5	336079	7	NULL	NULL	0	NULL	ceramide	Chemical	intracellular	balanced with					SPP	Chemical	levels of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_3	9446602	A further metabolite of ceramide, sphingosine 1-phosphate (SPP), prevents ceramide-mediated apoptosis, and it has been suggested that the balance between intracellular ceramide and SPP levels may determine the cell fate (Cuvillier, O., Pirianov, G, Kleuser, B., Vanek, P. G., Coso, O.	transcription
67540	6	336079	7	NULL	NULL	0	NULL	statement 5	Process		determine					cell fate	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_3	9446602	A further metabolite of ceramide, sphingosine 1-phosphate (SPP), prevents ceramide-mediated apoptosis, and it has been suggested that the balance between intracellular ceramide and SPP levels may determine the cell fate (Cuvillier, O., Pirianov, G, Kleuser, B., Vanek, P. G., Coso, O.	transcription
61031	1	336080	5	NULL	NULL	0	NULL	progesterone	GP	production of	is induced by					LH	GP				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_153	9915989	Since exogenous SMase inhibited LH-induced progesterone production, the abilities of ceramides of different acyl chain length (C2-, C6-, and C8-ceramide) and of sphingosine to inhibit LH (10 ng/ml)-induced progesterone production were also assessed to confirm that the effects of SMase were mediated via ceramide and not through nonspecific actions of the enzyme ( Fig. 4).	transcription
61032	2	336080	5	NULL	NULL	0	NULL	SMase	GP		inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_153	9915989	Since exogenous SMase inhibited LH-induced progesterone production, the abilities of ceramides of different acyl chain length (C2-, C6-, and C8-ceramide) and of sphingosine to inhibit LH (10 ng/ml)-induced progesterone production were also assessed to confirm that the effects of SMase were mediated via ceramide and not through nonspecific actions of the enzyme ( Fig. 4).	transcription
61033	3	336080	5	NULL	NULL	0	NULL	sphingosine	Chemical		inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_153	9915989	Since exogenous SMase inhibited LH-induced progesterone production, the abilities of ceramides of different acyl chain length (C2-, C6-, and C8-ceramide) and of sphingosine to inhibit LH (10 ng/ml)-induced progesterone production were also assessed to confirm that the effects of SMase were mediated via ceramide and not through nonspecific actions of the enzyme ( Fig. 4).	transcription
61034	4	336080	5	NULL	NULL	0	NULL	C2-ceramide	Chemical		inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_153	9915989	Since exogenous SMase inhibited LH-induced progesterone production, the abilities of ceramides of different acyl chain length (C2-, C6-, and C8-ceramide) and of sphingosine to inhibit LH (10 ng/ml)-induced progesterone production were also assessed to confirm that the effects of SMase were mediated via ceramide and not through nonspecific actions of the enzyme ( Fig. 4).	transcription
61035	5	336080	5	NULL	NULL	0	NULL	C6-ceramide	Chemical		inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_153	9915989	Since exogenous SMase inhibited LH-induced progesterone production, the abilities of ceramides of different acyl chain length (C2-, C6-, and C8-ceramide) and of sphingosine to inhibit LH (10 ng/ml)-induced progesterone production were also assessed to confirm that the effects of SMase were mediated via ceramide and not through nonspecific actions of the enzyme ( Fig. 4).	transcription
61036	6	336080	5	NULL	NULL	0	NULL	C8-ceramide	Chemical		inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_153	9915989	Since exogenous SMase inhibited LH-induced progesterone production, the abilities of ceramides of different acyl chain length (C2-, C6-, and C8-ceramide) and of sphingosine to inhibit LH (10 ng/ml)-induced progesterone production were also assessed to confirm that the effects of SMase were mediated via ceramide and not through nonspecific actions of the enzyme ( Fig. 4).	transcription
61037	7	336080	5	NULL	NULL	0	NULL	statement 2	Process		via					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_153	9915989	Since exogenous SMase inhibited LH-induced progesterone production, the abilities of ceramides of different acyl chain length (C2-, C6-, and C8-ceramide) and of sphingosine to inhibit LH (10 ng/ml)-induced progesterone production were also assessed to confirm that the effects of SMase were mediated via ceramide and not through nonspecific actions of the enzyme ( Fig. 4).	transcription
67541	1	336080	7	NULL	NULL	0	NULL	 LH	GP		induce					progesterone	Chemical	production of			NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_153	9915989	Since exogenous SMase inhibited LH-induced progesterone production, the abilities of ceramides of different acyl chain length (C2-, C6-, and C8-ceramide) and of sphingosine to inhibit LH (10 ng/ml)-induced progesterone production were also assessed to confirm that the effects of SMase were mediated via ceramide and not through nonspecific actions of the enzyme ( Fig. 4).	transcription
67542	2	336080	7	NULL	NULL	0	NULL	SMase	GP		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_153	9915989	Since exogenous SMase inhibited LH-induced progesterone production, the abilities of ceramides of different acyl chain length (C2-, C6-, and C8-ceramide) and of sphingosine to inhibit LH (10 ng/ml)-induced progesterone production were also assessed to confirm that the effects of SMase were mediated via ceramide and not through nonspecific actions of the enzyme ( Fig. 4).	transcription
67543	3	336080	7	NULL	NULL	NULL	NULL	C2-ceramide	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_153	9915989	Since exogenous SMase inhibited LH-induced progesterone production, the abilities of ceramides of different acyl chain length (C2-, C6-, and C8-ceramide) and of sphingosine to inhibit LH (10 ng/ml)-induced progesterone production were also assessed to confirm that the effects of SMase were mediated via ceramide and not through nonspecific actions of the enzyme ( Fig. 4).	transcription
67544	4	336080	7	NULL	NULL	0	NULL	C6-ceramide	Chemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_153	9915989	Since exogenous SMase inhibited LH-induced progesterone production, the abilities of ceramides of different acyl chain length (C2-, C6-, and C8-ceramide) and of sphingosine to inhibit LH (10 ng/ml)-induced progesterone production were also assessed to confirm that the effects of SMase were mediated via ceramide and not through nonspecific actions of the enzyme ( Fig. 4).	transcription
67545	5	336080	7	NULL	NULL	0	NULL	C8-ceramide	Chemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_153	9915989	Since exogenous SMase inhibited LH-induced progesterone production, the abilities of ceramides of different acyl chain length (C2-, C6-, and C8-ceramide) and of sphingosine to inhibit LH (10 ng/ml)-induced progesterone production were also assessed to confirm that the effects of SMase were mediated via ceramide and not through nonspecific actions of the enzyme ( Fig. 4).	transcription
67546	6	336080	7	NULL	NULL	0	NULL	sphingosine	Chemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_153	9915989	Since exogenous SMase inhibited LH-induced progesterone production, the abilities of ceramides of different acyl chain length (C2-, C6-, and C8-ceramide) and of sphingosine to inhibit LH (10 ng/ml)-induced progesterone production were also assessed to confirm that the effects of SMase were mediated via ceramide and not through nonspecific actions of the enzyme ( Fig. 4).	transcription
67547	7	336080	7	NULL	NULL	0	NULL	SMase	GP	effects of	mediated via					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_153	9915989	Since exogenous SMase inhibited LH-induced progesterone production, the abilities of ceramides of different acyl chain length (C2-, C6-, and C8-ceramide) and of sphingosine to inhibit LH (10 ng/ml)-induced progesterone production were also assessed to confirm that the effects of SMase were mediated via ceramide and not through nonspecific actions of the enzyme ( Fig. 4).	transcription
67548	1	336081	7	NULL	NULL	0	NULL	ceramide 	Chemical	short acyl chain analogues of	metabolized to		mainly			GlcCer	Chemical				NULL	fibroblasts	0	NULL	NULL	NULL	gw60_jbiolchem_272_3_1558_s_99	8999828	Since in fibroblasts, short acyl chain analogues of ceramide are metabolized mainly to GlcCer and SM (not shown; see also Meivar-Levy  et al. ( 24)), and since sphinganine, sphingosine, and ceramides do not significantly affect cell morphology, these data together demonstrate that the ability of GM3 to restore cell morphology is due to depletion of an essential higher order glycosphingolipid, probably GM3, and not due to accumulation or depletion of bioactive intermediates.	transcription
67549	2	336081	7	NULL	NULL	0	NULL	ceramide	Chemical	short acyl chain analogues of	metabolized to		mainly			SM	Chemical				NULL	fibroblasts	0	NULL	NULL	NULL	gw60_jbiolchem_272_3_1558_s_99	8999828	Since in fibroblasts, short acyl chain analogues of ceramide are metabolized mainly to GlcCer and SM (not shown; see also Meivar-Levy  et al. ( 24)), and since sphinganine, sphingosine, and ceramides do not significantly affect cell morphology, these data together demonstrate that the ability of GM3 to restore cell morphology is due to depletion of an essential higher order glycosphingolipid, probably GM3, and not due to accumulation or depletion of bioactive intermediates.	transcription
67550	3	336081	7	NULL	NULL	0	NULL	statement 1	Process		occur along with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_3_1558_s_99	8999828	Since in fibroblasts, short acyl chain analogues of ceramide are metabolized mainly to GlcCer and SM (not shown; see also Meivar-Levy  et al. ( 24)), and since sphinganine, sphingosine, and ceramides do not significantly affect cell morphology, these data together demonstrate that the ability of GM3 to restore cell morphology is due to depletion of an essential higher order glycosphingolipid, probably GM3, and not due to accumulation or depletion of bioactive intermediates.	transcription
67551	4	336081	7	NULL	NULL	NULL	NULL	sphinganine	Chemical		does not affect		significantly			cell morphology	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_3_1558_s_99	8999828	Since in fibroblasts, short acyl chain analogues of ceramide are metabolized mainly to GlcCer and SM (not shown; see also Meivar-Levy  et al. ( 24)), and since sphinganine, sphingosine, and ceramides do not significantly affect cell morphology, these data together demonstrate that the ability of GM3 to restore cell morphology is due to depletion of an essential higher order glycosphingolipid, probably GM3, and not due to accumulation or depletion of bioactive intermediates.	transcription
67552	5	336081	7	NULL	NULL	0	NULL	sphingosine	Chemical		does not affect		significantly			cell morphology	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_3_1558_s_99	8999828	Since in fibroblasts, short acyl chain analogues of ceramide are metabolized mainly to GlcCer and SM (not shown; see also Meivar-Levy  et al. ( 24)), and since sphinganine, sphingosine, and ceramides do not significantly affect cell morphology, these data together demonstrate that the ability of GM3 to restore cell morphology is due to depletion of an essential higher order glycosphingolipid, probably GM3, and not due to accumulation or depletion of bioactive intermediates.	transcription
67553	6	336081	7	NULL	NULL	0	NULL	ceramides	Chemical		does not affect		significantly			cell morphology	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_3_1558_s_99	8999828	Since in fibroblasts, short acyl chain analogues of ceramide are metabolized mainly to GlcCer and SM (not shown; see also Meivar-Levy  et al. ( 24)), and since sphinganine, sphingosine, and ceramides do not significantly affect cell morphology, these data together demonstrate that the ability of GM3 to restore cell morphology is due to depletion of an essential higher order glycosphingolipid, probably GM3, and not due to accumulation or depletion of bioactive intermediates.	transcription
67554	7	336081	7	NULL	NULL	0	NULL	GM3	Chemical		restore					cell morphology	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_3_1558_s_99	8999828	Since in fibroblasts, short acyl chain analogues of ceramide are metabolized mainly to GlcCer and SM (not shown; see also Meivar-Levy  et al. ( 24)), and since sphinganine, sphingosine, and ceramides do not significantly affect cell morphology, these data together demonstrate that the ability of GM3 to restore cell morphology is due to depletion of an essential higher order glycosphingolipid, probably GM3, and not due to accumulation or depletion of bioactive intermediates.	transcription
67555	8	336081	7	NULL	NULL	0	NULL	statement 7	Process		due to					GM3	Chemical	depletion of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_3_1558_s_99	8999828	Since in fibroblasts, short acyl chain analogues of ceramide are metabolized mainly to GlcCer and SM (not shown; see also Meivar-Levy  et al. ( 24)), and since sphinganine, sphingosine, and ceramides do not significantly affect cell morphology, these data together demonstrate that the ability of GM3 to restore cell morphology is due to depletion of an essential higher order glycosphingolipid, probably GM3, and not due to accumulation or depletion of bioactive intermediates.	transcription
67556	9	336081	7	NULL	NULL	0	NULL	GM3	Chemical		is a type of					essential higher order glycosphingolipid	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_3_1558_s_99	8999828	Since in fibroblasts, short acyl chain analogues of ceramide are metabolized mainly to GlcCer and SM (not shown; see also Meivar-Levy  et al. ( 24)), and since sphinganine, sphingosine, and ceramides do not significantly affect cell morphology, these data together demonstrate that the ability of GM3 to restore cell morphology is due to depletion of an essential higher order glycosphingolipid, probably GM3, and not due to accumulation or depletion of bioactive intermediates.	transcription
67557	10	336081	7	NULL	NULL	0	NULL	statement 7	Process		not due to					bioactive intermediates	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_3_1558_s_99	8999828	Since in fibroblasts, short acyl chain analogues of ceramide are metabolized mainly to GlcCer and SM (not shown; see also Meivar-Levy  et al. ( 24)), and since sphinganine, sphingosine, and ceramides do not significantly affect cell morphology, these data together demonstrate that the ability of GM3 to restore cell morphology is due to depletion of an essential higher order glycosphingolipid, probably GM3, and not due to accumulation or depletion of bioactive intermediates.	transcription
67558	11	336081	7	NULL	NULL	0	NULL	statement 7	Process		not due to					bioactive intermediates	Chemical	depletion of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_3_1558_s_99	8999828	Since in fibroblasts, short acyl chain analogues of ceramide are metabolized mainly to GlcCer and SM (not shown; see also Meivar-Levy  et al. ( 24)), and since sphinganine, sphingosine, and ceramides do not significantly affect cell morphology, these data together demonstrate that the ability of GM3 to restore cell morphology is due to depletion of an essential higher order glycosphingolipid, probably GM3, and not due to accumulation or depletion of bioactive intermediates.	transcription
61130	1	336082	5	NULL	NULL	0	NULL	sphingosine burst	Process		arise from					complex sphingolipids	Chemical	turnover of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
61131	2	336082	5	NULL	NULL	0	NULL	[ H]serine	AminoAcid		not incorporated into					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
61132	3	336082	5	NULL	NULL	0	NULL	[ H]palmitate	Chemical		not incorporated into					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
61133	4	336082	5	NULL	NULL	0	NULL	sphingosine 	Chemical	mass of	is not affected by					beta-F-alanine	AminoAcid	concentration of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
61134	5	336082	5	NULL	NULL	0	NULL	sphingosine	Chemical	mass of	is not affected by					serine	AminoAcid	concentration of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
61135	6	336082	5	NULL	NULL	0	NULL	sphingosine	Chemical		is release from					sphingomyelin	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
61136	7	336082	5	NULL	NULL	0	NULL	ceramide	Chemical		is release from					sphingomyelin	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
61137	8	336082	5	NULL	NULL	0	NULL	sphingomyelin	Chemical		is a type of					complex sphingolipids	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
61138	9	336082	5	NULL	NULL	0	NULL	sphingosine burst	Process		followed by					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
61139	10	336082	5	NULL	NULL	0	NULL	sphingosine burst	Process		followed by					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
61140	11	336082	5	NULL	NULL	0	NULL	statement 9	Process		is inhibited by					NH Cl	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
61141	12	336082	5	NULL	NULL	0	NULL	statement 9	Process		is inhibited by					chloroquine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
61142	13	336082	5	NULL	NULL	0	NULL	statement 10	Process		is inhibited by					NH Cl	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
61143	14	336082	5	NULL	NULL	0	NULL	statement 10	Process		is inhibited by					chloroquine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
71927	1	336082	7	NULL	NULL	0	NULL	sphingosine	Chemical		released from					sphingomyelin	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
71928	2	336082	7	NULL	NULL	0	NULL	ceramide	Chemical		released from					sphingomyelin	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
71929	3	336082	7	NULL	NULL	0	NULL	NH Cl 	Chemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
71930	4	336082	7	NULL	NULL	0	NULL	chloroquine	Chemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
71931	5	336082	7	NULL	NULL	0	NULL	NH Cl 	Chemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
71932	6	336082	7	NULL	NULL	0	NULL	chloroquine	Chemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
71933	7	336082	7	NULL	NULL	0	NULL	sphingomyelin	Chemical		is a type of					complex sphingolipids	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_32_18749_s_6	7642524	In contrast, the sphingosine  burst arose mainly from turnover of complex sphingolipids because no  incorporation of [ H]serine or  [ H]palmitate into sphingosine was detected;  sphingosine mass was not affected by beta-F-alanine or the serine  concentration; and, the burst could be followed by the release of  sphingosine and ceramide from complex sphingolipids (especially  sphingomyelin) in a process that was inhibited by NH Cl and  chloroquine.	transcription
61144	1	336083	5	NULL	NULL	0	NULL	lung epithelia	OrganismPart		engage in					ceramide	Chemical	de novo synthesis of			NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_219	15772421	The new observations from these studies include the following:  i) that lung epithelia engage in high-level de novo ceramide synthesis using sphingoid bases;  ii) that D- erythro-[3-3H]sphingosine in lung cells is rapidly incorporated into ceramide, indicative of a robust  N-acyltransferase mechanism catalyzed by a ceramide synthase;  iii) that LASS5 is the predominant isoform conferring ceramide synthase activity that was developmentally regulated in the lung; and  iv) that PtdCho synthesis is dependently regulated with de novo ceramide synthesis.	transcription
61145	2	336083	5	NULL	NULL	0	NULL	statement 1	Process		uses					sphingoid bases	Chemical				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_219	15772421	The new observations from these studies include the following:  i) that lung epithelia engage in high-level de novo ceramide synthesis using sphingoid bases;  ii) that D- erythro-[3-3H]sphingosine in lung cells is rapidly incorporated into ceramide, indicative of a robust  N-acyltransferase mechanism catalyzed by a ceramide synthase;  iii) that LASS5 is the predominant isoform conferring ceramide synthase activity that was developmentally regulated in the lung; and  iv) that PtdCho synthesis is dependently regulated with de novo ceramide synthesis.	transcription
61146	3	336083	5	NULL	NULL	0	NULL	D- erythro-[3-3H]sphingosine	Chemical		incorporated into		rapidly			ceramide	Chemical				NULL	lung cells	0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_219	15772421	The new observations from these studies include the following:  i) that lung epithelia engage in high-level de novo ceramide synthesis using sphingoid bases;  ii) that D- erythro-[3-3H]sphingosine in lung cells is rapidly incorporated into ceramide, indicative of a robust  N-acyltransferase mechanism catalyzed by a ceramide synthase;  iii) that LASS5 is the predominant isoform conferring ceramide synthase activity that was developmentally regulated in the lung; and  iv) that PtdCho synthesis is dependently regulated with de novo ceramide synthesis.	transcription
61147	4	336083	5	NULL	NULL	0	NULL	N-acyltransferase mechanism	Process		is catalyzed by					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_219	15772421	The new observations from these studies include the following:  i) that lung epithelia engage in high-level de novo ceramide synthesis using sphingoid bases;  ii) that D- erythro-[3-3H]sphingosine in lung cells is rapidly incorporated into ceramide, indicative of a robust  N-acyltransferase mechanism catalyzed by a ceramide synthase;  iii) that LASS5 is the predominant isoform conferring ceramide synthase activity that was developmentally regulated in the lung; and  iv) that PtdCho synthesis is dependently regulated with de novo ceramide synthesis.	transcription
61148	5	336083	5	NULL	NULL	0	NULL	statement 3	Process		indicates					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_219	15772421	The new observations from these studies include the following:  i) that lung epithelia engage in high-level de novo ceramide synthesis using sphingoid bases;  ii) that D- erythro-[3-3H]sphingosine in lung cells is rapidly incorporated into ceramide, indicative of a robust  N-acyltransferase mechanism catalyzed by a ceramide synthase;  iii) that LASS5 is the predominant isoform conferring ceramide synthase activity that was developmentally regulated in the lung; and  iv) that PtdCho synthesis is dependently regulated with de novo ceramide synthesis.	transcription
61149	6	336083	5	NULL	NULL	0	NULL	LASS5	GP		is an isoform of					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_219	15772421	The new observations from these studies include the following:  i) that lung epithelia engage in high-level de novo ceramide synthesis using sphingoid bases;  ii) that D- erythro-[3-3H]sphingosine in lung cells is rapidly incorporated into ceramide, indicative of a robust  N-acyltransferase mechanism catalyzed by a ceramide synthase;  iii) that LASS5 is the predominant isoform conferring ceramide synthase activity that was developmentally regulated in the lung; and  iv) that PtdCho synthesis is dependently regulated with de novo ceramide synthesis.	transcription
61150	7	336083	5	NULL	NULL	0	NULL	LASS5	GP		is developmentally regulated in					lung	OrganismPart				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_219	15772421	The new observations from these studies include the following:  i) that lung epithelia engage in high-level de novo ceramide synthesis using sphingoid bases;  ii) that D- erythro-[3-3H]sphingosine in lung cells is rapidly incorporated into ceramide, indicative of a robust  N-acyltransferase mechanism catalyzed by a ceramide synthase;  iii) that LASS5 is the predominant isoform conferring ceramide synthase activity that was developmentally regulated in the lung; and  iv) that PtdCho synthesis is dependently regulated with de novo ceramide synthesis.	transcription
61151	8	336083	5	NULL	NULL	0	NULL	PtdCho	Chemical		is regulated in		dependently			ceramide	Chemical	de novo synthesis of			NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_219	15772421	The new observations from these studies include the following:  i) that lung epithelia engage in high-level de novo ceramide synthesis using sphingoid bases;  ii) that D- erythro-[3-3H]sphingosine in lung cells is rapidly incorporated into ceramide, indicative of a robust  N-acyltransferase mechanism catalyzed by a ceramide synthase;  iii) that LASS5 is the predominant isoform conferring ceramide synthase activity that was developmentally regulated in the lung; and  iv) that PtdCho synthesis is dependently regulated with de novo ceramide synthesis.	transcription
67559	1	336083	7	NULL	NULL	0	NULL	lung epithelia	Cell		engage in					de novo ceramide synthesis	Process	high-level of			NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_219	15772421	The new observations from these studies include the following:  i) that lung epithelia engage in high-level de novo ceramide synthesis using sphingoid bases;  ii) that D- erythro-[3-3H]sphingosine in lung cells is rapidly incorporated into ceramide, indicative of a robust  N-acyltransferase mechanism catalyzed by a ceramide synthase;  iii) that LASS5 is the predominant isoform conferring ceramide synthase activity that was developmentally regulated in the lung; and  iv) that PtdCho synthesis is dependently regulated with de novo ceramide synthesis.	transcription
67560	2	336083	7	NULL	NULL	0	NULL	statement 1	Process		use					sphingoid bases	Chemical				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_219	15772421	The new observations from these studies include the following:  i) that lung epithelia engage in high-level de novo ceramide synthesis using sphingoid bases;  ii) that D- erythro-[3-3H]sphingosine in lung cells is rapidly incorporated into ceramide, indicative of a robust  N-acyltransferase mechanism catalyzed by a ceramide synthase;  iii) that LASS5 is the predominant isoform conferring ceramide synthase activity that was developmentally regulated in the lung; and  iv) that PtdCho synthesis is dependently regulated with de novo ceramide synthesis.	transcription
67561	3	336083	7	NULL	NULL	0	NULL	D- erythro-[3-3H]sphingosine	Chemical	lung cells	incorporated into					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_219	15772421	The new observations from these studies include the following:  i) that lung epithelia engage in high-level de novo ceramide synthesis using sphingoid bases;  ii) that D- erythro-[3-3H]sphingosine in lung cells is rapidly incorporated into ceramide, indicative of a robust  N-acyltransferase mechanism catalyzed by a ceramide synthase;  iii) that LASS5 is the predominant isoform conferring ceramide synthase activity that was developmentally regulated in the lung; and  iv) that PtdCho synthesis is dependently regulated with de novo ceramide synthesis.	transcription
67562	4	336083	7	NULL	NULL	0	NULL	statement 3	Process		indicative of					N-acyltransferase mechanism	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_219	15772421	The new observations from these studies include the following:  i) that lung epithelia engage in high-level de novo ceramide synthesis using sphingoid bases;  ii) that D- erythro-[3-3H]sphingosine in lung cells is rapidly incorporated into ceramide, indicative of a robust  N-acyltransferase mechanism catalyzed by a ceramide synthase;  iii) that LASS5 is the predominant isoform conferring ceramide synthase activity that was developmentally regulated in the lung; and  iv) that PtdCho synthesis is dependently regulated with de novo ceramide synthesis.	transcription
67563	5	336083	7	NULL	NULL	0	NULL	statement 4	Process		catalyzed by					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_219	15772421	The new observations from these studies include the following:  i) that lung epithelia engage in high-level de novo ceramide synthesis using sphingoid bases;  ii) that D- erythro-[3-3H]sphingosine in lung cells is rapidly incorporated into ceramide, indicative of a robust  N-acyltransferase mechanism catalyzed by a ceramide synthase;  iii) that LASS5 is the predominant isoform conferring ceramide synthase activity that was developmentally regulated in the lung; and  iv) that PtdCho synthesis is dependently regulated with de novo ceramide synthesis.	transcription
67564	6	336083	7	NULL	NULL	NULL	NULL	LASS5	GP	predominant isoform	confer					ceramide synthase activity	Process				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_219	15772421	The new observations from these studies include the following:  i) that lung epithelia engage in high-level de novo ceramide synthesis using sphingoid bases;  ii) that D- erythro-[3-3H]sphingosine in lung cells is rapidly incorporated into ceramide, indicative of a robust  N-acyltransferase mechanism catalyzed by a ceramide synthase;  iii) that LASS5 is the predominant isoform conferring ceramide synthase activity that was developmentally regulated in the lung; and  iv) that PtdCho synthesis is dependently regulated with de novo ceramide synthesis.	transcription
67565	7	336083	7	NULL	NULL	NULL	NULL	 ceramide synthase activity	Process		regulated in the 		developmentally			lung	OrganismPart				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_219	15772421	The new observations from these studies include the following:  i) that lung epithelia engage in high-level de novo ceramide synthesis using sphingoid bases;  ii) that D- erythro-[3-3H]sphingosine in lung cells is rapidly incorporated into ceramide, indicative of a robust  N-acyltransferase mechanism catalyzed by a ceramide synthase;  iii) that LASS5 is the predominant isoform conferring ceramide synthase activity that was developmentally regulated in the lung; and  iv) that PtdCho synthesis is dependently regulated with de novo ceramide synthesis.	transcription
67566	8	336083	7	NULL	NULL	0	NULL	PtdCho synthesis	Process		regulated with		dependently			de novo ceramide synthesis	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_219	15772421	The new observations from these studies include the following:  i) that lung epithelia engage in high-level de novo ceramide synthesis using sphingoid bases;  ii) that D- erythro-[3-3H]sphingosine in lung cells is rapidly incorporated into ceramide, indicative of a robust  N-acyltransferase mechanism catalyzed by a ceramide synthase;  iii) that LASS5 is the predominant isoform conferring ceramide synthase activity that was developmentally regulated in the lung; and  iv) that PtdCho synthesis is dependently regulated with de novo ceramide synthesis.	transcription
61152	1	336084	5	NULL	NULL	0	NULL	ceramidase	GP	activated	removes					ceramide	Chemical	excess			NULL	human umbilical vein endothelial cells	0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
61153	2	336084	5	NULL	NULL	0	NULL	cell death	Process		is induced by					TNF-alpha	GP				NULL	human umbilical vein endothelial cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
61154	3	336084	5	NULL	NULL	0	NULL	statement 1	Process		prevents					statement 2	Process				NULL	human umbilical vein endothelial cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
61157	4	336084	5	NULL	NULL	0	NULL	statement 3	Process		results in					sphingosine	Process	accumulation of			NULL	human umbilical vein endothelial cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
61158	5	336084	5	NULL	NULL	0	NULL	statement 3	Process		results in					sphingosine phosphate	Chemical	accumulation of			NULL	human umbilical vein endothelial cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
61159	6	336084	5	NULL	NULL	0	NULL	statement 4	Process		induce					E-selectin	GP	expression of			NULL	human umbilical vein endothelial cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
61160	7	336084	5	NULL	NULL	0	NULL	statement 4	Process		induce					vascular cell adhesion molecule-1 	GP	expression of			NULL	human umbilical vein endothelial cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
61161	8	336084	5	NULL	NULL	0	NULL	statement 5	Process		induce					E-selectin	GP	expression of			NULL	human umbilical vein endothelial cells	NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
61162	9	336084	5	NULL	NULL	0	NULL	statement 4	Process		induce					vascular cell adhesion molecule-1 	GP	expression of			NULL	human umbilical vein endothelial cells	0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
61163	10	336084	5	NULL	NULL	0	NULL	E-selectin	GP		is a type of					adhesion molecule	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
61164	11	336084	5	NULL	NULL	0	NULL	vascular cell adhesion molecule-1	GP		is a type of					adhesion molecule	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
67567	1	336084	7	NULL	NULL	0	NULL	ceramidase	GP	activating	remove					ceramide	Chemical	excess of			NULL	human umbilical vein endothelial cells	0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
67568	2	336084	7	NULL	NULL	0	NULL	TNF-alpha	GP		induce					cell death	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
67569	3	336084	7	NULL	NULL	0	NULL	statement 1	Process		prevents					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
67570	4	336084	7	NULL	NULL	0	NULL	statement 3	Process		result in					sphingosine	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
67571	5	336084	7	NULL	NULL	0	NULL	statement 3	Process		result in					sphingosine phosphate	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
67572	6	336084	7	NULL	NULL	NULL	NULL	sphingosine	Chemical		induce					E-selectin	Chemical	expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
67573	7	336084	7	NULL	NULL	NULL	NULL	sphingosine phosphate	Chemical		induce					E-selectin	Chemical	expression of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
67574	8	336084	7	NULL	NULL	0	NULL	sphingosine	Chemical		induce					vascular cell adhesion molecule-1	Chemical	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
67575	9	336084	7	NULL	NULL	0	NULL	sphingosine phosphate	Chemical		induce					vascular cell adhesion molecule-1	Chemical	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
67576	10	336084	7	NULL	NULL	NULL	NULL	E-selectin	Chemical		is a type of					adhesion molecule	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
67577	11	336084	7	NULL	NULL	0	NULL	vascular cell adhesion molecule-1	Chemical		is a type of					adhesion molecule	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_29_26992_s_26	12721293	Also,  removal of excess ceramide in human umbilical vein endothelial cells by  activating ceramidase prevents TNF-alpha-induced cell death and the  resulting accumulation of sphingosine and sphingosine phosphate induces the  expression of the adhesion molecules E-selectin and vascular cell adhesion  molecule-1 ( ).	transcription
61165	1	336085	5	NULL	NULL	0	NULL	sphingosine	GP		activates					executioner caspases	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_92	10747891	Sphingosine Induces Apoptosis by Activation of Executioner Caspases in a Bcl-xL-inhibitable Fashion-- Because current evidence suggests that ceramide functions proximal to the executioner caspases ( 15,  37), we examined whether addition of sphingosine resulted in activation of caspase-3 and -7, which drive the effector phase of apoptosis.	transcription
61166	2	336085	5	NULL	NULL	0	NULL	statement 1	Process		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_92	10747891	Sphingosine Induces Apoptosis by Activation of Executioner Caspases in a Bcl-xL-inhibitable Fashion-- Because current evidence suggests that ceramide functions proximal to the executioner caspases ( 15,  37), we examined whether addition of sphingosine resulted in activation of caspase-3 and -7, which drive the effector phase of apoptosis.	transcription
61167	3	336085	5	NULL	NULL	0	NULL	statement 2	Process		is inhibited by					Bcl-xL	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_92	10747891	Sphingosine Induces Apoptosis by Activation of Executioner Caspases in a Bcl-xL-inhibitable Fashion-- Because current evidence suggests that ceramide functions proximal to the executioner caspases ( 15,  37), we examined whether addition of sphingosine resulted in activation of caspase-3 and -7, which drive the effector phase of apoptosis.	transcription
61168	4	336085	5	NULL	NULL	0	NULL	ceramide	Chemical	functional	is proximal to					executioner caspases	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_92	10747891	Sphingosine Induces Apoptosis by Activation of Executioner Caspases in a Bcl-xL-inhibitable Fashion-- Because current evidence suggests that ceramide functions proximal to the executioner caspases ( 15,  37), we examined whether addition of sphingosine resulted in activation of caspase-3 and -7, which drive the effector phase of apoptosis.	transcription
61169	5	336085	5	NULL	NULL	0	NULL	caspase-3	GP	activation of	drives					apoptosis	Process	effector phase of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_92	10747891	Sphingosine Induces Apoptosis by Activation of Executioner Caspases in a Bcl-xL-inhibitable Fashion-- Because current evidence suggests that ceramide functions proximal to the executioner caspases ( 15,  37), we examined whether addition of sphingosine resulted in activation of caspase-3 and -7, which drive the effector phase of apoptosis.	transcription
61170	6	336085	5	NULL	NULL	0	NULL	caspase-7	GP	activation of	drives					apoptosis	Process	effector phase of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_92	10747891	Sphingosine Induces Apoptosis by Activation of Executioner Caspases in a Bcl-xL-inhibitable Fashion-- Because current evidence suggests that ceramide functions proximal to the executioner caspases ( 15,  37), we examined whether addition of sphingosine resulted in activation of caspase-3 and -7, which drive the effector phase of apoptosis.	transcription
61171	7	336085	5	NULL	NULL	0	NULL	sphingosine	Chemical	addition of	activates		potentially			statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_92	10747891	Sphingosine Induces Apoptosis by Activation of Executioner Caspases in a Bcl-xL-inhibitable Fashion-- Because current evidence suggests that ceramide functions proximal to the executioner caspases ( 15,  37), we examined whether addition of sphingosine resulted in activation of caspase-3 and -7, which drive the effector phase of apoptosis.	transcription
61172	8	336085	5	NULL	NULL	0	NULL	sphingosine	Chemical	addition of	activates		potentially			statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_92	10747891	Sphingosine Induces Apoptosis by Activation of Executioner Caspases in a Bcl-xL-inhibitable Fashion-- Because current evidence suggests that ceramide functions proximal to the executioner caspases ( 15,  37), we examined whether addition of sphingosine resulted in activation of caspase-3 and -7, which drive the effector phase of apoptosis.	transcription
67578	1	336085	7	NULL	NULL	0	NULL	Sphingosine	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_92	10747891	Sphingosine Induces Apoptosis by Activation of Executioner Caspases in a Bcl-xL-inhibitable Fashion-- Because current evidence suggests that ceramide functions proximal to the executioner caspases ( 15,  37), we examined whether addition of sphingosine resulted in activation of caspase-3 and -7, which drive the effector phase of apoptosis.	transcription
67579	2	336085	7	NULL	NULL	0	NULL	statement 1	Process		occur by					Executioner Caspases	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_92	10747891	Sphingosine Induces Apoptosis by Activation of Executioner Caspases in a Bcl-xL-inhibitable Fashion-- Because current evidence suggests that ceramide functions proximal to the executioner caspases ( 15,  37), we examined whether addition of sphingosine resulted in activation of caspase-3 and -7, which drive the effector phase of apoptosis.	transcription
67580	3	336085	7	NULL	NULL	0	NULL	statement 2	Process		occur in a					Bcl-xL-inhibitable Fashion	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_92	10747891	Sphingosine Induces Apoptosis by Activation of Executioner Caspases in a Bcl-xL-inhibitable Fashion-- Because current evidence suggests that ceramide functions proximal to the executioner caspases ( 15,  37), we examined whether addition of sphingosine resulted in activation of caspase-3 and -7, which drive the effector phase of apoptosis.	transcription
67581	4	336085	7	NULL	NULL	0	NULL	ceramide	Chemical		functions					Executioner Caspases	GP	proximal to			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_92	10747891	Sphingosine Induces Apoptosis by Activation of Executioner Caspases in a Bcl-xL-inhibitable Fashion-- Because current evidence suggests that ceramide functions proximal to the executioner caspases ( 15,  37), we examined whether addition of sphingosine resulted in activation of caspase-3 and -7, which drive the effector phase of apoptosis.	transcription
67582	5	336085	7	NULL	NULL	0	NULL	caspase-3	GP		drive					apoptosis	Process	effector phase of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_92	10747891	Sphingosine Induces Apoptosis by Activation of Executioner Caspases in a Bcl-xL-inhibitable Fashion-- Because current evidence suggests that ceramide functions proximal to the executioner caspases ( 15,  37), we examined whether addition of sphingosine resulted in activation of caspase-3 and -7, which drive the effector phase of apoptosis.	transcription
67583	6	336085	7	NULL	NULL	0	NULL	caspase-7	GP		drive					apoptosis	Process	effector phase of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_92	10747891	Sphingosine Induces Apoptosis by Activation of Executioner Caspases in a Bcl-xL-inhibitable Fashion-- Because current evidence suggests that ceramide functions proximal to the executioner caspases ( 15,  37), we examined whether addition of sphingosine resulted in activation of caspase-3 and -7, which drive the effector phase of apoptosis.	transcription
61173	1	336087	5	NULL	NULL	0	NULL	3T3-L1 adipocytes	Cell		treated with					short-chain ceramide	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61174	2	336087	5	NULL	NULL	0	NULL	3T3-L1 adipocytes	Cell		treated with					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61175	3	336087	5	NULL	NULL	0	NULL	3T3-L1 adipocytes	Cell		treated with					S1P	Chemical				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61176	4	336087	5	NULL	NULL	0	NULL	statement 1	Process		induce					PAI-1	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61177	5	336087	5	NULL	NULL	0	NULL	statement 2	Process		induce					PAI-1	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61178	6	336087	5	NULL	NULL	0	NULL	statement 3	Process		induce					PAI-1	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61179	7	336087	5	NULL	NULL	0	NULL	PAI-1	GP		is a type of					prothrombotic molecule	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61180	8	336087	5	NULL	NULL	0	NULL	statement 1	Process		induce					TNF-alpha	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61181	9	336087	5	NULL	NULL	0	NULL	statement 2	Process		induce					TNF-alpha	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61182	10	336087	5	NULL	NULL	0	NULL	statement 3	Process		induce					TNF-alpha	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61183	11	336087	5	NULL	NULL	0	NULL	statement 1	Process		induce					IL-6	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61184	12	336087	5	NULL	NULL	0	NULL	statement 2	Process		induce					IL-6	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61185	13	336087	5	NULL	NULL	0	NULL	statement 3	Process		induce					IL-6	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61186	14	336087	5	NULL	NULL	0	NULL	statement 1	Process		induce					MCP-1	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61187	15	336087	5	NULL	NULL	0	NULL	statement 2	Process		induce					MCP-1	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61188	16	336087	5	NULL	NULL	0	NULL	statement 3	Process		induce					MCP-1	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61189	17	336087	5	NULL	NULL	0	NULL	statement 1	Process		induce					KC	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61190	18	336087	5	NULL	NULL	0	NULL	statement 2	Process		induce					KC	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61191	19	336087	5	NULL	NULL	0	NULL	statement 3	Process		induce					KC	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61192	20	336087	5	NULL	NULL	0	NULL	TNF-alpha	GP		is a type of					proinflammatory molecule	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61193	21	336087	5	NULL	NULL	0	NULL	IL-6	GP		is a type of					proinflammatory molecule	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61194	22	336087	5	NULL	NULL	0	NULL	MCP-1	GP		is a type of					proinflammatory molecule	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61195	23	336087	5	NULL	NULL	0	NULL	KC	GP		is a type of					proinflammatory molecule	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67584	1	336087	7	NULL	NULL	NULL	NULL	short-chain ceramide	Chemical		induce					PAI-1	GP	expression of			NULL	 3T3-L1 adipocytes	NULL	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67585	2	336087	7	NULL	NULL	NULL	NULL	sphingosine	Chemical		induce					PAI-1	GP	expression of			NULL	 3T3-L1 adipocytes	NULL	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67586	3	336087	7	NULL	NULL	NULL	NULL	 S1P	Chemical		induce					PAI-1	GP	expression of			NULL	 3T3-L1 adipocytes	NULL	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67587	4	336087	7	NULL	NULL	0	NULL	PAI-1	GP		is a type of					prothrombotic molecule	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67588	5	336087	7	NULL	NULL	0	NULL	short-chain ceramide	Chemical		induce					TNF-alpha	GP	expression of			NULL	3T3-L1 adipocytes	0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67589	6	336087	7	NULL	NULL	NULL	NULL	sphingosine	Chemical		induce					TNF-alpha	GP	expression of			NULL	3T3-L1 adipocytes	NULL	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67590	7	336087	7	NULL	NULL	NULL	NULL	S1P	Chemical		induce					TNF-alpha	GP	expression of			NULL	3T3-L1 adipocytes	NULL	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67591	8	336087	7	NULL	NULL	0	NULL	 short-chain ceramide	Chemical		induce					IL-6	GP	expression of			NULL	3T3-L1 adipocytes	0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67592	9	336087	7	NULL	NULL	0	NULL	sphingosine	Chemical		induce					IL-6	GP	expression of			NULL	3T3-L1 adipocytes	0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67593	10	336087	7	NULL	NULL	0	NULL	S1P	Chemical		induce					IL-6	GP	expression of			NULL	3T3-L1 adipocytes	0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67594	11	336087	7	NULL	NULL	NULL	NULL	short-chain ceramide	Chemical		induce					MCP-1	GP	expression of			NULL	3T3-L1 adipocytes	NULL	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67595	12	336087	7	NULL	NULL	NULL	NULL	sphingosine	Chemical		induce					MCP-1	GP	expression of			NULL	3T3-L1 adipocytes	NULL	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67596	13	336087	7	NULL	NULL	NULL	NULL	S1P	Chemical		induce					MCP-1	GP	expression of			NULL	3T3-L1 adipocytes	NULL	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67597	14	336087	7	NULL	NULL	0	NULL	short-chain ceramide	Chemical		induce					KC	GP	expression of			NULL	3T3-L1 adipocytes	0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67598	15	336087	7	NULL	NULL	0	NULL	sphingosine	Chemical		induce					KC	GP	expression of			NULL	3T3-L1 adipocytes	0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67599	16	336087	7	NULL	NULL	0	NULL	 S1P	Chemical		induce					KC	GP	expression of			NULL	3T3-L1 adipocytes	0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67600	17	336087	7	NULL	NULL	0	NULL	TNF-alpha	GP		is a type of					proinflammatory molecule	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67601	18	336087	7	NULL	NULL	0	NULL	IL-6	GP		is a type of					proinflammatory molecule	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67602	19	336087	7	NULL	NULL	0	NULL	MCP-1	GP		is a type of					proinflammatory molecule	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
67603	20	336087	7	NULL	NULL	0	NULL	KC	GP		is a type of					proinflammatory molecule	GP				NULL		0	NULL	NULL	NULL	gw70_diabetes_55_9_2579_s_191	16936207	We demonstrate that treatment of 3T3-L1 adipocytes with short-chain ceramide, sphingosine, or S1P induced the expression of the prothrombotic molecule PAI-1 and the expression of the proinflammatory molecules, TNF-alpha, IL-6, MCP-1, and KC ( Fig. 5) to various extents.	transcription
61196	1	336088	5	NULL	NULL	0	NULL	ceramide	Chemical		is converted to					sphingosine	Chemical				NULL	lysosome	0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_11	15774472	To determine the contribution of either sphingolipid in FFA-dependent inhibition of insulin action, we generated C2C12 myotubes that constitutively overexpress  acid  ceramidase (AC), an enzyme that catalyzes the lysosomal conversion of ceramide to sphingosine.	transcription
61197	2	336088	5	NULL	NULL	0	NULL	AC	GP		catalyzes					statement 1	Process				NULL	lysosome	0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_11	15774472	To determine the contribution of either sphingolipid in FFA-dependent inhibition of insulin action, we generated C2C12 myotubes that constitutively overexpress  acid  ceramidase (AC), an enzyme that catalyzes the lysosomal conversion of ceramide to sphingosine.	transcription
61198	3	336088	5	NULL	NULL	0	NULL	AC	GP		is					acid ceramidase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_11	15774472	To determine the contribution of either sphingolipid in FFA-dependent inhibition of insulin action, we generated C2C12 myotubes that constitutively overexpress  acid  ceramidase (AC), an enzyme that catalyzes the lysosomal conversion of ceramide to sphingosine.	transcription
61199	4	336088	5	NULL	NULL	0	NULL	insulin	GP	inhibition of;;action of	is dependent on					FFA	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_11	15774472	To determine the contribution of either sphingolipid in FFA-dependent inhibition of insulin action, we generated C2C12 myotubes that constitutively overexpress  acid  ceramidase (AC), an enzyme that catalyzes the lysosomal conversion of ceramide to sphingosine.	transcription
61200	5	336088	5	NULL	NULL	0	NULL	sphingolipid	Chemical		contribute to		potentially			statement 4					NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_11	15774472	To determine the contribution of either sphingolipid in FFA-dependent inhibition of insulin action, we generated C2C12 myotubes that constitutively overexpress  acid  ceramidase (AC), an enzyme that catalyzes the lysosomal conversion of ceramide to sphingosine.	transcription
67604	1	336088	7	NULL	NULL	0	NULL	 ceramide	Chemical		converted to					sphingosine	Chemical				NULL	lysosomes	0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_11	15774472	To determine the contribution of either sphingolipid in FFA-dependent inhibition of insulin action, we generated C2C12 myotubes that constitutively overexpress  acid  ceramidase (AC), an enzyme that catalyzes the lysosomal conversion of ceramide to sphingosine.	transcription
67605	2	336088	7	NULL	NULL	0	NULL	AC	GP		catalyze					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_11	15774472	To determine the contribution of either sphingolipid in FFA-dependent inhibition of insulin action, we generated C2C12 myotubes that constitutively overexpress  acid  ceramidase (AC), an enzyme that catalyzes the lysosomal conversion of ceramide to sphingosine.	transcription
67606	3	336088	7	NULL	NULL	0	NULL	AC	GP		is					acid ceramidase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_11	15774472	To determine the contribution of either sphingolipid in FFA-dependent inhibition of insulin action, we generated C2C12 myotubes that constitutively overexpress  acid  ceramidase (AC), an enzyme that catalyzes the lysosomal conversion of ceramide to sphingosine.	transcription
61201	1	336089	5	NULL	NULL	0	NULL	palmitate	Chemical		inhibits					Akt/PKB	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_76	15774472	Under conditions where palmitate inhibits Akt/PKB, it induces the accumulation of both ceramide and sphingosine ( Fig. 1), two lipid metabolites shown previously to inhibit insulin-stimulated glucose transport ( ,   -  ).	transcription
61202	2	336089	5	NULL	NULL	0	NULL	statement 1	Process		induce					ceramide	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_76	15774472	Under conditions where palmitate inhibits Akt/PKB, it induces the accumulation of both ceramide and sphingosine ( Fig. 1), two lipid metabolites shown previously to inhibit insulin-stimulated glucose transport ( ,   -  ).	transcription
61203	3	336089	5	NULL	NULL	0	NULL	statement 1	Process		induce					sphingosine	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_76	15774472	Under conditions where palmitate inhibits Akt/PKB, it induces the accumulation of both ceramide and sphingosine ( Fig. 1), two lipid metabolites shown previously to inhibit insulin-stimulated glucose transport ( ,   -  ).	transcription
61204	4	336089	5	NULL	NULL	0	NULL	ceramide	Chemical		is a metabolite of					lipid	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_76	15774472	Under conditions where palmitate inhibits Akt/PKB, it induces the accumulation of both ceramide and sphingosine ( Fig. 1), two lipid metabolites shown previously to inhibit insulin-stimulated glucose transport ( ,   -  ).	transcription
61205	5	336089	5	NULL	NULL	0	NULL	sphingosine	Chemical		is a metabolite of					lipid	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_76	15774472	Under conditions where palmitate inhibits Akt/PKB, it induces the accumulation of both ceramide and sphingosine ( Fig. 1), two lipid metabolites shown previously to inhibit insulin-stimulated glucose transport ( ,   -  ).	transcription
61206	6	336089	5	NULL	NULL	0	NULL	glucose	Chemical	transport of	is stimulated by					insulin	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_76	15774472	Under conditions where palmitate inhibits Akt/PKB, it induces the accumulation of both ceramide and sphingosine ( Fig. 1), two lipid metabolites shown previously to inhibit insulin-stimulated glucose transport ( ,   -  ).	transcription
61207	7	336089	5	NULL	NULL	0	NULL	ceramide	Chemical		inhibits					statement 6	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_76	15774472	Under conditions where palmitate inhibits Akt/PKB, it induces the accumulation of both ceramide and sphingosine ( Fig. 1), two lipid metabolites shown previously to inhibit insulin-stimulated glucose transport ( ,   -  ).	transcription
61208	8	336089	5	NULL	NULL	0	NULL	sphingosine	Chemical		inhibits					statement 6	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_76	15774472	Under conditions where palmitate inhibits Akt/PKB, it induces the accumulation of both ceramide and sphingosine ( Fig. 1), two lipid metabolites shown previously to inhibit insulin-stimulated glucose transport ( ,   -  ).	transcription
67607	1	336089	7	NULL	NULL	0	NULL	 palmitate	Chemical		inhibits					Akt/PKB	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_76	15774472	Under conditions where palmitate inhibits Akt/PKB, it induces the accumulation of both ceramide and sphingosine ( Fig. 1), two lipid metabolites shown previously to inhibit insulin-stimulated glucose transport ( ,   -  ).	transcription
67608	2	336089	7	NULL	NULL	0	NULL	statement 1	Process		induce					ceramide	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_76	15774472	Under conditions where palmitate inhibits Akt/PKB, it induces the accumulation of both ceramide and sphingosine ( Fig. 1), two lipid metabolites shown previously to inhibit insulin-stimulated glucose transport ( ,   -  ).	transcription
67609	3	336089	7	NULL	NULL	0	NULL	statement 1	Process		induce					sphingosine	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_76	15774472	Under conditions where palmitate inhibits Akt/PKB, it induces the accumulation of both ceramide and sphingosine ( Fig. 1), two lipid metabolites shown previously to inhibit insulin-stimulated glucose transport ( ,   -  ).	transcription
67610	4	336089	7	NULL	NULL	0	NULL	insulin	GP		stimulate					glucose transport	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_76	15774472	Under conditions where palmitate inhibits Akt/PKB, it induces the accumulation of both ceramide and sphingosine ( Fig. 1), two lipid metabolites shown previously to inhibit insulin-stimulated glucose transport ( ,   -  ).	transcription
67611	5	336089	7	NULL	NULL	NULL	NULL	ceramide	Chemical		inhibit					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_76	15774472	Under conditions where palmitate inhibits Akt/PKB, it induces the accumulation of both ceramide and sphingosine ( Fig. 1), two lipid metabolites shown previously to inhibit insulin-stimulated glucose transport ( ,   -  ).	transcription
67612	6	336089	7	NULL	NULL	0	NULL	sphingosine	Chemical		inhibit					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_76	15774472	Under conditions where palmitate inhibits Akt/PKB, it induces the accumulation of both ceramide and sphingosine ( Fig. 1), two lipid metabolites shown previously to inhibit insulin-stimulated glucose transport ( ,   -  ).	transcription
67613	7	336089	7	NULL	NULL	0	NULL	ceramide	Chemical		is a type of					lipid metabolite	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_76	15774472	Under conditions where palmitate inhibits Akt/PKB, it induces the accumulation of both ceramide and sphingosine ( Fig. 1), two lipid metabolites shown previously to inhibit insulin-stimulated glucose transport ( ,   -  ).	transcription
67614	8	336089	7	NULL	NULL	0	NULL	sphingosine	Chemical		is a type of					lipid metabolite	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20148_s_76	15774472	Under conditions where palmitate inhibits Akt/PKB, it induces the accumulation of both ceramide and sphingosine ( Fig. 1), two lipid metabolites shown previously to inhibit insulin-stimulated glucose transport ( ,   -  ).	transcription
61209	1	336090	5	NULL	NULL	0	NULL	PMA	Chemical		stimulates					sphingolipid	Chemical	turnover of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_161	15546881	On the other hand, if PMA stimulates turnover of sphingolipids resulting in the formation of sphingosine as a breakdown product which is then acylated back to ceramide, then PMA would not stimulate the acute incorporation of palmitate.	transcription
61210	2	336090	5	NULL	NULL	0	NULL	statement 1	Process		results in					sphingosine	Chemical	formation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_161	15546881	On the other hand, if PMA stimulates turnover of sphingolipids resulting in the formation of sphingosine as a breakdown product which is then acylated back to ceramide, then PMA would not stimulate the acute incorporation of palmitate.	transcription
61211	3	336090	5	NULL	NULL	0	NULL	sphingosine	Chemical		acylated to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_161	15546881	On the other hand, if PMA stimulates turnover of sphingolipids resulting in the formation of sphingosine as a breakdown product which is then acylated back to ceramide, then PMA would not stimulate the acute incorporation of palmitate.	transcription
61212	4	336090	5	NULL	NULL	0	NULL	PMA	Chemical		does not stimulate					palmitate	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_161	15546881	On the other hand, if PMA stimulates turnover of sphingolipids resulting in the formation of sphingosine as a breakdown product which is then acylated back to ceramide, then PMA would not stimulate the acute incorporation of palmitate.	transcription
67615	1	336090	7	NULL	NULL	0	NULL	PMA	Chemical		stimulate					sphingolipids	Chemical	turnover of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_161	15546881	On the other hand, if PMA stimulates turnover of sphingolipids resulting in the formation of sphingosine as a breakdown product which is then acylated back to ceramide, then PMA would not stimulate the acute incorporation of palmitate.	transcription
67616	2	336090	7	NULL	NULL	0	NULL	statement 1	Process		result in					sphingosine	Chemical	formation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_161	15546881	On the other hand, if PMA stimulates turnover of sphingolipids resulting in the formation of sphingosine as a breakdown product which is then acylated back to ceramide, then PMA would not stimulate the acute incorporation of palmitate.	transcription
67617	3	336090	7	NULL	NULL	0	NULL	sphingosine	Chemical		acylated to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_161	15546881	On the other hand, if PMA stimulates turnover of sphingolipids resulting in the formation of sphingosine as a breakdown product which is then acylated back to ceramide, then PMA would not stimulate the acute incorporation of palmitate.	transcription
67618	4	336090	7	NULL	NULL	0	NULL	sphingosine	Chemical		is a type of					breakdown product	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_161	15546881	On the other hand, if PMA stimulates turnover of sphingolipids resulting in the formation of sphingosine as a breakdown product which is then acylated back to ceramide, then PMA would not stimulate the acute incorporation of palmitate.	transcription
67619	5	336090	7	NULL	NULL	NULL	NULL	PMA	Chemical		does not stimulate					palmitate	Chemical	acute incorporation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_161	15546881	On the other hand, if PMA stimulates turnover of sphingolipids resulting in the formation of sphingosine as a breakdown product which is then acylated back to ceramide, then PMA would not stimulate the acute incorporation of palmitate.	transcription
61213	1	336091	5	NULL	NULL	0	NULL	Fumonisin B1	Chemical		inhibits					sphinganine/sphingosine fatty-acyl-CoA N-acyltransferase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_26680_s_143	15919667	Fumonisin B1 inhibits the sphinganine/sphingosine fatty-acyl-CoA  N-acyltransferase, blocking both ceramide synthesis  de novo and the salvage pathway ( ), whereas PPMP inhibits UDPG:CGT, the enzyme that catalyzes glucosylceramide synthesis ( ).	transcription
61214	2	336091	5	NULL	NULL	0	NULL	statement 1	Process		blocks					ceramide	Chemical	de novo synthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_26680_s_143	15919667	Fumonisin B1 inhibits the sphinganine/sphingosine fatty-acyl-CoA  N-acyltransferase, blocking both ceramide synthesis  de novo and the salvage pathway ( ), whereas PPMP inhibits UDPG:CGT, the enzyme that catalyzes glucosylceramide synthesis ( ).	transcription
61215	3	336091	5	NULL	NULL	0	NULL	statement 1	Process		blocks					salvage pathway	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_26680_s_143	15919667	Fumonisin B1 inhibits the sphinganine/sphingosine fatty-acyl-CoA  N-acyltransferase, blocking both ceramide synthesis  de novo and the salvage pathway ( ), whereas PPMP inhibits UDPG:CGT, the enzyme that catalyzes glucosylceramide synthesis ( ).	transcription
61216	4	336091	5	NULL	NULL	0	NULL	PPMP	Chemical		inhibits					UDPG:CGT	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_26680_s_143	15919667	Fumonisin B1 inhibits the sphinganine/sphingosine fatty-acyl-CoA  N-acyltransferase, blocking both ceramide synthesis  de novo and the salvage pathway ( ), whereas PPMP inhibits UDPG:CGT, the enzyme that catalyzes glucosylceramide synthesis ( ).	transcription
61217	5	336091	5	NULL	NULL	0	NULL	UDPG:CGT	GP		catalyzes					glucosylceramide	Chemical	synthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_26680_s_143	15919667	Fumonisin B1 inhibits the sphinganine/sphingosine fatty-acyl-CoA  N-acyltransferase, blocking both ceramide synthesis  de novo and the salvage pathway ( ), whereas PPMP inhibits UDPG:CGT, the enzyme that catalyzes glucosylceramide synthesis ( ).	transcription
67620	1	336091	7	NULL	NULL	0	NULL	Fumonisin B1	Chemical		inhibit					sphinganine fatty-acyl-CoA N-acyltransferase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_26680_s_143	15919667	Fumonisin B1 inhibits the sphinganine/sphingosine fatty-acyl-CoA  N-acyltransferase, blocking both ceramide synthesis  de novo and the salvage pathway ( ), whereas PPMP inhibits UDPG:CGT, the enzyme that catalyzes glucosylceramide synthesis ( ).	transcription
67621	2	336091	7	NULL	NULL	0	NULL	Fumonisin B1	Chemical		inhibit					sphingosine fatty-acyl-CoA N-acyltransferase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_26680_s_143	15919667	Fumonisin B1 inhibits the sphinganine/sphingosine fatty-acyl-CoA  N-acyltransferase, blocking both ceramide synthesis  de novo and the salvage pathway ( ), whereas PPMP inhibits UDPG:CGT, the enzyme that catalyzes glucosylceramide synthesis ( ).	transcription
67622	3	336091	7	NULL	NULL	0	NULL	statement 1	Process		block					ceramide synthesis	Process	de novo			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_26680_s_143	15919667	Fumonisin B1 inhibits the sphinganine/sphingosine fatty-acyl-CoA  N-acyltransferase, blocking both ceramide synthesis  de novo and the salvage pathway ( ), whereas PPMP inhibits UDPG:CGT, the enzyme that catalyzes glucosylceramide synthesis ( ).	transcription
67623	4	336091	7	NULL	NULL	0	NULL	statement 1	Process		block					ceramide synthesis	Process	salvage			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_26680_s_143	15919667	Fumonisin B1 inhibits the sphinganine/sphingosine fatty-acyl-CoA  N-acyltransferase, blocking both ceramide synthesis  de novo and the salvage pathway ( ), whereas PPMP inhibits UDPG:CGT, the enzyme that catalyzes glucosylceramide synthesis ( ).	transcription
67624	5	336091	7	NULL	NULL	0	NULL	statement 2	Process		block					ceramide synthesis	Process	de novo			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_26680_s_143	15919667	Fumonisin B1 inhibits the sphinganine/sphingosine fatty-acyl-CoA  N-acyltransferase, blocking both ceramide synthesis  de novo and the salvage pathway ( ), whereas PPMP inhibits UDPG:CGT, the enzyme that catalyzes glucosylceramide synthesis ( ).	transcription
67625	6	336091	7	NULL	NULL	0	NULL	statement 2	Process		block					ceramide synthesis	Process	salvage			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_26680_s_143	15919667	Fumonisin B1 inhibits the sphinganine/sphingosine fatty-acyl-CoA  N-acyltransferase, blocking both ceramide synthesis  de novo and the salvage pathway ( ), whereas PPMP inhibits UDPG:CGT, the enzyme that catalyzes glucosylceramide synthesis ( ).	transcription
67626	7	336091	7	NULL	NULL	0	NULL	PPMP	Chemical		inhibit					UDPG:CGT	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_26680_s_143	15919667	Fumonisin B1 inhibits the sphinganine/sphingosine fatty-acyl-CoA  N-acyltransferase, blocking both ceramide synthesis  de novo and the salvage pathway ( ), whereas PPMP inhibits UDPG:CGT, the enzyme that catalyzes glucosylceramide synthesis ( ).	transcription
67627	8	336091	7	NULL	NULL	0	NULL	UDPG:CGT	GP		catalyze					glucosylceramide synthesis	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_29_26680_s_143	15919667	Fumonisin B1 inhibits the sphinganine/sphingosine fatty-acyl-CoA  N-acyltransferase, blocking both ceramide synthesis  de novo and the salvage pathway ( ), whereas PPMP inhibits UDPG:CGT, the enzyme that catalyzes glucosylceramide synthesis ( ).	transcription
61218	1	336092	5	NULL	NULL	0	NULL	ceramide ( N-acyl sphingosine)	Chemical		is a metabolite of					sphingomyelin	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12036_s_18	14722105	For instance, one sphingomyelin metabolic product, ceramide ( N-acyl sphingosine) induces apoptosis, whereas another metabolic product, sphingosine-1-phosphate (S1P),  1 induces cell proliferation ( ,  ).	transcription
61219	2	336092	5	NULL	NULL	0	NULL	ceramide ( N-acyl sphingosine)	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12036_s_18	14722105	For instance, one sphingomyelin metabolic product, ceramide ( N-acyl sphingosine) induces apoptosis, whereas another metabolic product, sphingosine-1-phosphate (S1P),  1 induces cell proliferation ( ,  ).	transcription
61220	3	336092	5	NULL	NULL	0	NULL	S1P	Chemical		is					sphingosine-1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12036_s_18	14722105	For instance, one sphingomyelin metabolic product, ceramide ( N-acyl sphingosine) induces apoptosis, whereas another metabolic product, sphingosine-1-phosphate (S1P),  1 induces cell proliferation ( ,  ).	transcription
61221	4	336092	5	NULL	NULL	0	NULL	S1P	Chemical		is a metabolite of					sphingomyelin	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12036_s_18	14722105	For instance, one sphingomyelin metabolic product, ceramide ( N-acyl sphingosine) induces apoptosis, whereas another metabolic product, sphingosine-1-phosphate (S1P),  1 induces cell proliferation ( ,  ).	transcription
61222	5	336092	5	NULL	NULL	0	NULL	S1P	Chemical		induce					cell proliferation	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12036_s_18	14722105	For instance, one sphingomyelin metabolic product, ceramide ( N-acyl sphingosine) induces apoptosis, whereas another metabolic product, sphingosine-1-phosphate (S1P),  1 induces cell proliferation ( ,  ).	transcription
67628	1	336092	7	NULL	NULL	0	NULL	ceramide ( N-acyl sphingosine) 	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12036_s_18	14722105	For instance, one sphingomyelin metabolic product, ceramide ( N-acyl sphingosine) induces apoptosis, whereas another metabolic product, sphingosine-1-phosphate (S1P),  1 induces cell proliferation ( ,  ).	transcription
67629	2	336092	7	NULL	NULL	0	NULL	S1P	Chemical		induce					cell proliferation	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12036_s_18	14722105	For instance, one sphingomyelin metabolic product, ceramide ( N-acyl sphingosine) induces apoptosis, whereas another metabolic product, sphingosine-1-phosphate (S1P),  1 induces cell proliferation ( ,  ).	transcription
67630	3	336092	7	NULL	NULL	0	NULL	ceramide ( N-acyl sphingosine)	Chemical		is a metabolic product of					sphingomyelin	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12036_s_18	14722105	For instance, one sphingomyelin metabolic product, ceramide ( N-acyl sphingosine) induces apoptosis, whereas another metabolic product, sphingosine-1-phosphate (S1P),  1 induces cell proliferation ( ,  ).	transcription
67631	4	336092	7	NULL	NULL	0	NULL	S1P	Chemical		is a metabolic product of					sphingomyelin	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12036_s_18	14722105	For instance, one sphingomyelin metabolic product, ceramide ( N-acyl sphingosine) induces apoptosis, whereas another metabolic product, sphingosine-1-phosphate (S1P),  1 induces cell proliferation ( ,  ).	transcription
67632	5	336092	7	NULL	NULL	0	NULL	S1P	Chemical		is					sphingosine-1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_13_12036_s_18	14722105	For instance, one sphingomyelin metabolic product, ceramide ( N-acyl sphingosine) induces apoptosis, whereas another metabolic product, sphingosine-1-phosphate (S1P),  1 induces cell proliferation ( ,  ).	transcription
61223	1	336093	5	NULL	NULL	0	NULL	SK1	GP		plays a role in					S1P	Chemical	regulation of;;levels of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24695_s_20	16803890	Although SK1 plays a major role, regulation of S1P levels is a function of the net responses of enzymes of the sphingolipid network that influence the levels of ceramide and sphingosine (precursors for S1P synthesis).	transcription
67633	1	336093	7	NULL	NULL	0	NULL	 S1P 	Chemical	regulation of;;levels of	is a function of					sphingolipid network	Chemical	enzymes of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24695_s_20	16803890	Although SK1 plays a major role, regulation of S1P levels is a function of the net responses of enzymes of the sphingolipid network that influence the levels of ceramide and sphingosine (precursors for S1P synthesis).	transcription
67634	2	336093	7	NULL	NULL	0	NULL	ceramide	Chemical		is a precursor of					S1P synthesis	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24695_s_20	16803890	Although SK1 plays a major role, regulation of S1P levels is a function of the net responses of enzymes of the sphingolipid network that influence the levels of ceramide and sphingosine (precursors for S1P synthesis).	transcription
67635	3	336093	7	NULL	NULL	0	NULL	sphingosine	Chemical		is a precursor of					S1P synthesis	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_34_24695_s_20	16803890	Although SK1 plays a major role, regulation of S1P levels is a function of the net responses of enzymes of the sphingolipid network that influence the levels of ceramide and sphingosine (precursors for S1P synthesis).	transcription
61224	1	336094	5	NULL	NULL	0	NULL	AC	GP	purified;;recombinant;;human	catalyzes					ceramide	Chemical	synthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_273	12815059	We therefore decided to test whether our purified, recombinant human AC  could catalyze ceramide synthesis using 14C-labeled C12  fatty acid and sphingosine as substrates.	transcription
61225	2	336094	5	NULL	NULL	0	NULL	C12 fatty acid	Chemical	14C-labeled	is a substrate for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_273	12815059	We therefore decided to test whether our purified, recombinant human AC  could catalyze ceramide synthesis using 14C-labeled C12  fatty acid and sphingosine as substrates.	transcription
61226	3	336094	5	NULL	NULL	0	NULL	sphingosine	Chemical		is a substrate for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_273	12815059	We therefore decided to test whether our purified, recombinant human AC  could catalyze ceramide synthesis using 14C-labeled C12  fatty acid and sphingosine as substrates.	transcription
61227	1	336095	5	NULL	NULL	0	NULL	C/EBP	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_11_2497_s_138	16106045	To test whether other sphingolipids in addition to ceramide might induce C/EBP DNA binding, hepatocytes were treated with 30 muM C2-dihydroceramide, sphingosine, or dihydrosphingosine (sphinganine).	transcription
61228	2	336095	5	NULL	NULL	0	NULL	ceramide	Chemical		induce					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_11_2497_s_138	16106045	To test whether other sphingolipids in addition to ceramide might induce C/EBP DNA binding, hepatocytes were treated with 30 muM C2-dihydroceramide, sphingosine, or dihydrosphingosine (sphinganine).	transcription
61229	3	336095	5	NULL	NULL	0	NULL	sphingolipids	Chemical		induce		may			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_46_11_2497_s_138	16106045	To test whether other sphingolipids in addition to ceramide might induce C/EBP DNA binding, hepatocytes were treated with 30 muM C2-dihydroceramide, sphingosine, or dihydrosphingosine (sphinganine).	transcription
61230	1	336096	5	NULL	NULL	0	NULL	S1P	Chemical		is					sphingosine 1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_9_1772_s_21	12777464	In contrast, its catabolic intermediate sphingosine 1-phosphate (S1P) has been implicated as a second messenger in cellular proliferation and survival ( ), and also in protection against ceramide-mediated apoptosis ( ).	transcription
61231	2	336096	5	NULL	NULL	0	NULL	S1P	Chemical		is a type of					second messenger	Chemical				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_9_1772_s_21	12777464	In contrast, its catabolic intermediate sphingosine 1-phosphate (S1P) has been implicated as a second messenger in cellular proliferation and survival ( ), and also in protection against ceramide-mediated apoptosis ( ).	transcription
61232	3	336096	5	NULL	NULL	0	NULL	S1P	Chemical		plays a role in					cellular proliferation	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_9_1772_s_21	12777464	In contrast, its catabolic intermediate sphingosine 1-phosphate (S1P) has been implicated as a second messenger in cellular proliferation and survival ( ), and also in protection against ceramide-mediated apoptosis ( ).	transcription
61233	4	336096	5	NULL	NULL	0	NULL	S1P	Chemical		plays a role in					cell survival	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_9_1772_s_21	12777464	In contrast, its catabolic intermediate sphingosine 1-phosphate (S1P) has been implicated as a second messenger in cellular proliferation and survival ( ), and also in protection against ceramide-mediated apoptosis ( ).	transcription
61234	5	336096	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_9_1772_s_21	12777464	In contrast, its catabolic intermediate sphingosine 1-phosphate (S1P) has been implicated as a second messenger in cellular proliferation and survival ( ), and also in protection against ceramide-mediated apoptosis ( ).	transcription
61235	6	336096	5	NULL	NULL	0	NULL	S1P	Chemical		protects against					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_9_1772_s_21	12777464	In contrast, its catabolic intermediate sphingosine 1-phosphate (S1P) has been implicated as a second messenger in cellular proliferation and survival ( ), and also in protection against ceramide-mediated apoptosis ( ).	transcription
67637	1	336096	7	NULL	NULL	0	NULL	S1P	Chemical		implicated as					cellular proliferation	Process	second messenger in			NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_9_1772_s_21	12777464	In contrast, its catabolic intermediate sphingosine 1-phosphate (S1P) has been implicated as a second messenger in cellular proliferation and survival ( ), and also in protection against ceramide-mediated apoptosis ( ).	transcription
67638	2	336096	7	NULL	NULL	0	NULL	S1P	Chemical		implicated as					cellular survival	Process	second messenger in			NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_9_1772_s_21	12777464	In contrast, its catabolic intermediate sphingosine 1-phosphate (S1P) has been implicated as a second messenger in cellular proliferation and survival ( ), and also in protection against ceramide-mediated apoptosis ( ).	transcription
67639	3	336096	7	NULL	NULL	0	NULL	ceramide	Chemical		mediate					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_9_1772_s_21	12777464	In contrast, its catabolic intermediate sphingosine 1-phosphate (S1P) has been implicated as a second messenger in cellular proliferation and survival ( ), and also in protection against ceramide-mediated apoptosis ( ).	transcription
67640	4	336096	7	NULL	NULL	0	NULL	S1P	Chemical		protects from					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_9_1772_s_21	12777464	In contrast, its catabolic intermediate sphingosine 1-phosphate (S1P) has been implicated as a second messenger in cellular proliferation and survival ( ), and also in protection against ceramide-mediated apoptosis ( ).	transcription
67641	5	336096	7	NULL	NULL	0	NULL	S1P	Chemical		is					sphingosine 1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_9_1772_s_21	12777464	In contrast, its catabolic intermediate sphingosine 1-phosphate (S1P) has been implicated as a second messenger in cellular proliferation and survival ( ), and also in protection against ceramide-mediated apoptosis ( ).	transcription
61236	1	336097	5	NULL	NULL	0	NULL	FB1	Chemical		is an inhibitor of		potent			ceramide synthase	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_305_1_232_s_188	12649374	FB1 is a potent inhibitor of sphinganine (sphingosine)  N-acetyltransferase (ceramide synthase) in vivo, and it exhibits competitive-type inhibition with respect to both substrates of this enzyme (Wang et al., 1991 ).	transcription
61237	2	336097	5	NULL	NULL	0	NULL	ceramide synthase	GP		is					sphinganine (sphingosine) N-acetyltransferase	GP				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_305_1_232_s_188	12649374	FB1 is a potent inhibitor of sphinganine (sphingosine)  N-acetyltransferase (ceramide synthase) in vivo, and it exhibits competitive-type inhibition with respect to both substrates of this enzyme (Wang et al., 1991 ).	transcription
67642	1	336097	7	NULL	NULL	NULL	NULL	FB1	Chemical		is an inhibitor of		potent			sphinganine (sphingosine) N-acetyltransferase	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_305_1_232_s_188	12649374	FB1 is a potent inhibitor of sphinganine (sphingosine)  N-acetyltransferase (ceramide synthase) in vivo, and it exhibits competitive-type inhibition with respect to both substrates of this enzyme (Wang et al., 1991 ).	transcription
67643	2	336097	7	NULL	NULL	0	NULL	sphinganine (sphingosine) N-acetyltransferase	GP		is					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw70_jpharmacolexpther_305_1_232_s_188	12649374	FB1 is a potent inhibitor of sphinganine (sphingosine)  N-acetyltransferase (ceramide synthase) in vivo, and it exhibits competitive-type inhibition with respect to both substrates of this enzyme (Wang et al., 1991 ).	transcription
61238	1	336098	5	NULL	NULL	0	NULL	D- erythro- N-octanoyl-sphingosine	Chemical	alterations in degree and position of;;unsaturation of;;bonds in sphingoid backbone of 	affects					ceramide analogs		antiproliferative ability of 			NULL	breast cancer cells	NULL	NULL	NULL	NULL	gw70_jpharmacolexpther_309_2_523_s_3	14742741	This study demonstrates that alterations in the degree and position of unsaturation of bonds in the sphingoid backbone of D- erythro- N-octanoyl-sphingosine (Cer) affect the antiproliferative ability of ceramide analogs in breast cancer cells.	transcription
67644	1	336098	7	NULL	NULL	0	NULL	D- erythro- N-octanoyl-sphingosine (Cer)	Chemical	alterations in sphingoid backbone of	affect					ceramide analogs	Chemical	antiproliferative ability of			NULL	breast cancer cells	0	NULL	NULL	NULL	gw70_jpharmacolexpther_309_2_523_s_3	14742741	This study demonstrates that alterations in the degree and position of unsaturation of bonds in the sphingoid backbone of D- erythro- N-octanoyl-sphingosine (Cer) affect the antiproliferative ability of ceramide analogs in breast cancer cells.	transcription
67645	1	336099	7	NULL	NULL	0	NULL	Natural ceramide	Chemical		induce					c-jun	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_66	12135749	HL-60 cells were treated with the indicated concentrations of sphingosine for 1 h. C2, treated with 5  M C2-ceramide for 1 h. C: Natural ceramide-induced c-jun expression.	transcription
61239	1	336100	5	NULL	NULL	0	NULL	sphingosine	Chemical		increases					PA	Chemical	intracellular levels of			NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7356_s_213	11705908	Sphingosine and sphingosine-1-phosphate increase intracellular levels of PA, thereby stimulating mitogenesis, while ceramide inhibits phospholipase D activation, thereby decreasing PA levels and enhancing the apoptotic response ( 22).	transcription
61240	2	336100	5	NULL	NULL	0	NULL	sphingosine-1-phosphate	Chemical		increases					PA	Chemical	intracellular levels of			NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7356_s_213	11705908	Sphingosine and sphingosine-1-phosphate increase intracellular levels of PA, thereby stimulating mitogenesis, while ceramide inhibits phospholipase D activation, thereby decreasing PA levels and enhancing the apoptotic response ( 22).	transcription
61241	3	336100	5	NULL	NULL	0	NULL	statement 1	Process		stimulates					mitogenesis	Process				NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7356_s_213	11705908	Sphingosine and sphingosine-1-phosphate increase intracellular levels of PA, thereby stimulating mitogenesis, while ceramide inhibits phospholipase D activation, thereby decreasing PA levels and enhancing the apoptotic response ( 22).	transcription
61242	4	336100	5	NULL	NULL	0	NULL	statement 2	Process		stimulates					mitogenesis	Process				NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7356_s_213	11705908	Sphingosine and sphingosine-1-phosphate increase intracellular levels of PA, thereby stimulating mitogenesis, while ceramide inhibits phospholipase D activation, thereby decreasing PA levels and enhancing the apoptotic response ( 22).	transcription
61243	5	336100	5	NULL	NULL	0	NULL	ceramide	Chemical		inhibits					phospholipase D	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7356_s_213	11705908	Sphingosine and sphingosine-1-phosphate increase intracellular levels of PA, thereby stimulating mitogenesis, while ceramide inhibits phospholipase D activation, thereby decreasing PA levels and enhancing the apoptotic response ( 22).	transcription
61244	6	336100	5	NULL	NULL	0	NULL	statement 5	Process		decreases					PA	Chemical	level of			NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7356_s_213	11705908	Sphingosine and sphingosine-1-phosphate increase intracellular levels of PA, thereby stimulating mitogenesis, while ceramide inhibits phospholipase D activation, thereby decreasing PA levels and enhancing the apoptotic response ( 22).	transcription
61245	7	336100	5	NULL	NULL	0	NULL	statement 6	Process		enhances					apoptotic response	Process				NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7356_s_213	11705908	Sphingosine and sphingosine-1-phosphate increase intracellular levels of PA, thereby stimulating mitogenesis, while ceramide inhibits phospholipase D activation, thereby decreasing PA levels and enhancing the apoptotic response ( 22).	transcription
67646	1	336100	7	NULL	NULL	0	NULL	Sphingosine	Chemical		increase					PA	Chemical	 intracellular levels of 			NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7356_s_213	11705908	Sphingosine and sphingosine-1-phosphate increase intracellular levels of PA, thereby stimulating mitogenesis, while ceramide inhibits phospholipase D activation, thereby decreasing PA levels and enhancing the apoptotic response ( 22).	transcription
67647	2	336100	7	NULL	NULL	0	NULL	sphingosine-1-phosphate	Chemical		increase					PA	Chemical	intracellular levels of			NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7356_s_213	11705908	Sphingosine and sphingosine-1-phosphate increase intracellular levels of PA, thereby stimulating mitogenesis, while ceramide inhibits phospholipase D activation, thereby decreasing PA levels and enhancing the apoptotic response ( 22).	transcription
67648	3	336100	7	NULL	NULL	0	NULL	statement 1	Process		stimulate					mitogenesis	Process				NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7356_s_213	11705908	Sphingosine and sphingosine-1-phosphate increase intracellular levels of PA, thereby stimulating mitogenesis, while ceramide inhibits phospholipase D activation, thereby decreasing PA levels and enhancing the apoptotic response ( 22).	transcription
67649	4	336100	7	NULL	NULL	0	NULL	statement 2	Process		stimulate					mitogenesis	Process				NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7356_s_213	11705908	Sphingosine and sphingosine-1-phosphate increase intracellular levels of PA, thereby stimulating mitogenesis, while ceramide inhibits phospholipase D activation, thereby decreasing PA levels and enhancing the apoptotic response ( 22).	transcription
67650	5	336100	7	NULL	NULL	0	NULL	ceramide	Chemical		inhibit					phospholipase D	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7356_s_213	11705908	Sphingosine and sphingosine-1-phosphate increase intracellular levels of PA, thereby stimulating mitogenesis, while ceramide inhibits phospholipase D activation, thereby decreasing PA levels and enhancing the apoptotic response ( 22).	transcription
67651	6	336100	7	NULL	NULL	0	NULL	statement 5	Process		decrease					PA 	Chemical	levels of			NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7356_s_213	11705908	Sphingosine and sphingosine-1-phosphate increase intracellular levels of PA, thereby stimulating mitogenesis, while ceramide inhibits phospholipase D activation, thereby decreasing PA levels and enhancing the apoptotic response ( 22).	transcription
67652	7	336100	7	NULL	NULL	0	NULL	statement 5	Process		enhance					apoptotic response	Process				NULL		0	NULL	NULL	NULL	gw60_infectimmun_69_12_7356_s_213	11705908	Sphingosine and sphingosine-1-phosphate increase intracellular levels of PA, thereby stimulating mitogenesis, while ceramide inhibits phospholipase D activation, thereby decreasing PA levels and enhancing the apoptotic response ( 22).	transcription
61246	1	336101	5	NULL	NULL	0	NULL	caspases	GP	active	cleave					poly(ADP-ribose) polymerase	GP				NULL	Jurkat T lymphocytes	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_135_s_210	12531546	O. Cuvillier, D.S. Rosenthal, M.E. Smulson and S. Spiegel , Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
61247	2	336101	5	NULL	NULL	0	NULL	caspases	GP	active	cleave					lamins	GP				NULL	Jurkat T lymphocytes	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_135_s_210	12531546	O. Cuvillier, D.S. Rosenthal, M.E. Smulson and S. Spiegel , Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
61248	3	336101	5	NULL	NULL	0	NULL	Sphingosine 1-phosphate	Chemical		inhibits					caspases	GP	activation of			NULL	Jurkat T lymphocytes	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_135_s_210	12531546	O. Cuvillier, D.S. Rosenthal, M.E. Smulson and S. Spiegel , Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
61249	4	336101	5	NULL	NULL	0	NULL	Fas	GP		mediates					apoptosis	Process				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_135_s_210	12531546	O. Cuvillier, D.S. Rosenthal, M.E. Smulson and S. Spiegel , Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
61250	5	336101	5	NULL	NULL	0	NULL	ceramide	Chemical		mediates					apoptosis	Process				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_135_s_210	12531546	O. Cuvillier, D.S. Rosenthal, M.E. Smulson and S. Spiegel , Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
61251	6	336101	5	NULL	NULL	0	NULL	statement 3	Process		occurs during					statement 4	Process				NULL	Jurkat T lymphocytes	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_135_s_210	12531546	O. Cuvillier, D.S. Rosenthal, M.E. Smulson and S. Spiegel , Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
61252	7	336101	5	NULL	NULL	0	NULL	statement 3	Process		occurs during					statement 5	Process				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_135_s_210	12531546	O. Cuvillier, D.S. Rosenthal, M.E. Smulson and S. Spiegel , Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
67653	1	336101	7	NULL	NULL	0	NULL	Sphingosine 1-phosphate	Chemical		inhibit					caspases	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_135_s_210	12531546	O. Cuvillier, D.S. Rosenthal, M.E. Smulson and S. Spiegel , Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
67654	2	336101	7	NULL	NULL	0	NULL	caspases	GP		cleave					poly(ADP-ribose) polymerase	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_135_s_210	12531546	O. Cuvillier, D.S. Rosenthal, M.E. Smulson and S. Spiegel , Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
67655	3	336101	7	NULL	NULL	0	NULL	caspases	GP		cleave					lamins	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_135_s_210	12531546	O. Cuvillier, D.S. Rosenthal, M.E. Smulson and S. Spiegel , Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
67656	4	336101	7	NULL	NULL	0	NULL	Fas	GP		mediate					apoptosis	Process				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_135_s_210	12531546	O. Cuvillier, D.S. Rosenthal, M.E. Smulson and S. Spiegel , Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
67657	5	336101	7	NULL	NULL	0	NULL	ceramide	Chemical		mediate					apoptosis	Process				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_135_s_210	12531546	O. Cuvillier, D.S. Rosenthal, M.E. Smulson and S. Spiegel , Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
67658	6	336101	7	NULL	NULL	0	NULL	statement 2	Process		occur during					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_135_s_210	12531546	O. Cuvillier, D.S. Rosenthal, M.E. Smulson and S. Spiegel , Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
67659	7	336101	7	NULL	NULL	0	NULL	statement 2	Process		occur during					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_135_s_210	12531546	O. Cuvillier, D.S. Rosenthal, M.E. Smulson and S. Spiegel , Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
67660	8	336101	7	NULL	NULL	0	NULL	statement 3	Process		occur during					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_135_s_210	12531546	O. Cuvillier, D.S. Rosenthal, M.E. Smulson and S. Spiegel , Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
67661	9	336101	7	NULL	NULL	0	NULL	statement 3	Process		occur during					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_135_s_210	12531546	O. Cuvillier, D.S. Rosenthal, M.E. Smulson and S. Spiegel , Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
61253	1	336102	5	NULL	NULL	0	NULL	neutrophils	Cell	human	treated with					TNF 	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_26	12531549	Treatment of human neutrophils with tumor necrosis factor  (TNF ) induced elevation of both intracellular ceramide and sphingosine contents during the first 60 min prior to any apoptotic morphological changes [  5.	transcription
61254	2	336102	5	NULL	NULL	0	NULL	TNF 	GP		is					tumor necrosis factor	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_26	12531549	Treatment of human neutrophils with tumor necrosis factor  (TNF ) induced elevation of both intracellular ceramide and sphingosine contents during the first 60 min prior to any apoptotic morphological changes [  5.	transcription
61255	3	336102	5	NULL	NULL	0	NULL	statement 1	Process		induce					ceramide	Chemical	elevation of;;intracellular			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_26	12531549	Treatment of human neutrophils with tumor necrosis factor  (TNF ) induced elevation of both intracellular ceramide and sphingosine contents during the first 60 min prior to any apoptotic morphological changes [  5.	transcription
61256	4	336102	5	NULL	NULL	0	NULL	statement 1	Process		induce					sphingosine	Chemical	elevation of;;intracellular			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_26	12531549	Treatment of human neutrophils with tumor necrosis factor  (TNF ) induced elevation of both intracellular ceramide and sphingosine contents during the first 60 min prior to any apoptotic morphological changes [  5.	transcription
61257	5	336102	5	NULL	NULL	0	NULL	statement 3	Process		occurs prior to					apoptotic morphological changes	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_26	12531549	Treatment of human neutrophils with tumor necrosis factor  (TNF ) induced elevation of both intracellular ceramide and sphingosine contents during the first 60 min prior to any apoptotic morphological changes [  5.	transcription
61258	6	336102	5	NULL	NULL	0	NULL	statement 4	Process		occurs prior to					apoptotic morphological changes	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_26	12531549	Treatment of human neutrophils with tumor necrosis factor  (TNF ) induced elevation of both intracellular ceramide and sphingosine contents during the first 60 min prior to any apoptotic morphological changes [  5.	transcription
67662	1	336102	7	NULL	NULL	NULL	NULL	TNF	GP		induce					ceramide	Chemical	elevation of;;intracellular			NULL	human neutrophils	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_26	12531549	Treatment of human neutrophils with tumor necrosis factor  (TNF ) induced elevation of both intracellular ceramide and sphingosine contents during the first 60 min prior to any apoptotic morphological changes [  5.	transcription
67663	2	336102	7	NULL	NULL	NULL	NULL	TNF	GP		induce					sphingosine	Chemical	elevation of;;intracellular			NULL	human neutrophils	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_153_s_26	12531549	Treatment of human neutrophils with tumor necrosis factor  (TNF ) induced elevation of both intracellular ceramide and sphingosine contents during the first 60 min prior to any apoptotic morphological changes [  5.	transcription
61259	1	336103	5	NULL	NULL	0	NULL	sphingosine	Chemical	free	is synthesized by		only			ceramide	Chemical	hydrolysis of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1485_2_63_s_377	10832090	Because free sphingosine can only be produced by ceramide hydrolysis and not by de novo biosynthesis [ 167 and   191], AC may play a critical role in the production of these important compounds and thus in the regulation of cell growth and differentiation.	transcription
61260	2	336103	5	NULL	NULL	0	NULL	AC	GP		plays a role in		critical			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1485_2_63_s_377	10832090	Because free sphingosine can only be produced by ceramide hydrolysis and not by de novo biosynthesis [ 167 and   191], AC may play a critical role in the production of these important compounds and thus in the regulation of cell growth and differentiation.	transcription
61261	3	336103	5	NULL	NULL	0	NULL	AC	GP		plays a role in		critical			cell growth	Process	regulation of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1485_2_63_s_377	10832090	Because free sphingosine can only be produced by ceramide hydrolysis and not by de novo biosynthesis [ 167 and   191], AC may play a critical role in the production of these important compounds and thus in the regulation of cell growth and differentiation.	transcription
61262	4	336103	5	NULL	NULL	0	NULL	AC	GP		plays a role in		critical			cell differentiation	Process	regulation of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1485_2_63_s_377	10832090	Because free sphingosine can only be produced by ceramide hydrolysis and not by de novo biosynthesis [ 167 and   191], AC may play a critical role in the production of these important compounds and thus in the regulation of cell growth and differentiation.	transcription
61263	5	336103	5	NULL	NULL	0	NULL	statement 2	Process		leads to					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1485_2_63_s_377	10832090	Because free sphingosine can only be produced by ceramide hydrolysis and not by de novo biosynthesis [ 167 and   191], AC may play a critical role in the production of these important compounds and thus in the regulation of cell growth and differentiation.	transcription
61264	6	336103	5	NULL	NULL	0	NULL	statement 2	Process		leads to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1485_2_63_s_377	10832090	Because free sphingosine can only be produced by ceramide hydrolysis and not by de novo biosynthesis [ 167 and   191], AC may play a critical role in the production of these important compounds and thus in the regulation of cell growth and differentiation.	transcription
67664	1	336103	7	NULL	NULL	NULL	NULL	sphingosine	GP	free	produced by					ceramide	Chemical	hydrolysis of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1485_2_63_s_377	10832090	Because free sphingosine can only be produced by ceramide hydrolysis and not by de novo biosynthesis [ 167 and   191], AC may play a critical role in the production of these important compounds and thus in the regulation of cell growth and differentiation.	transcription
67665	2	336103	7	NULL	NULL	0	NULL	sphingosine	Chemical	free	is not produced by					de novo biosynthesis	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1485_2_63_s_377	10832090	Because free sphingosine can only be produced by ceramide hydrolysis and not by de novo biosynthesis [ 167 and   191], AC may play a critical role in the production of these important compounds and thus in the regulation of cell growth and differentiation.	transcription
67666	3	336103	7	NULL	NULL	0	NULL	AC	GP		play a critical role in					sphingosine	Chemical	production of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1485_2_63_s_377	10832090	Because free sphingosine can only be produced by ceramide hydrolysis and not by de novo biosynthesis [ 167 and   191], AC may play a critical role in the production of these important compounds and thus in the regulation of cell growth and differentiation.	transcription
67667	4	336103	7	NULL	NULL	0	NULL	statement 3	Process		play a role in					cell growth	Process	regulation of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1485_2_63_s_377	10832090	Because free sphingosine can only be produced by ceramide hydrolysis and not by de novo biosynthesis [ 167 and   191], AC may play a critical role in the production of these important compounds and thus in the regulation of cell growth and differentiation.	transcription
67668	5	336103	7	NULL	NULL	0	NULL	statement 3	Process		play a role in					cell differentiation	Process	regulation of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1485_2_63_s_377	10832090	Because free sphingosine can only be produced by ceramide hydrolysis and not by de novo biosynthesis [ 167 and   191], AC may play a critical role in the production of these important compounds and thus in the regulation of cell growth and differentiation.	transcription
61265	1	336104	5	NULL	NULL	0	NULL	cell death	Process		is induced by					TNF	GP				NULL	promyeloid U937 cells	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1485_2_63_s_496	10832090	Obeid et al. were the first to show that an exogenously added cell-permeable short-chain ceramide analog,  N-acetyl-sphingosine, mimicked TNF -induced cell death in promyeloid U937 cells [  270].	transcription
61266	2	336104	5	NULL	NULL	0	NULL	N-acetyl-sphingosine	Chemical	exogenously added;;cell-permeable	mimics					statement 1					NULL	promyeloid U937 cells	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1485_2_63_s_496	10832090	Obeid et al. were the first to show that an exogenously added cell-permeable short-chain ceramide analog,  N-acetyl-sphingosine, mimicked TNF -induced cell death in promyeloid U937 cells [  270].	transcription
61267	3	336104	5	NULL	NULL	0	NULL	N-acetyl-sphingosine	Chemical		is an analog of					short-chain ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1485_2_63_s_496	10832090	Obeid et al. were the first to show that an exogenously added cell-permeable short-chain ceramide analog,  N-acetyl-sphingosine, mimicked TNF -induced cell death in promyeloid U937 cells [  270].	transcription
67669	1	336104	7	NULL	NULL	0	NULL	 TNF	GP		induce					cell death	Process				NULL	promyeloid U937 cells	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1485_2_63_s_496	10832090	Obeid et al. were the first to show that an exogenously added cell-permeable short-chain ceramide analog,  N-acetyl-sphingosine, mimicked TNF -induced cell death in promyeloid U937 cells [  270].	transcription
67670	2	336104	7	NULL	NULL	0	NULL	N-acetyl-sphingosine	Chemical		mimick					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1485_2_63_s_496	10832090	Obeid et al. were the first to show that an exogenously added cell-permeable short-chain ceramide analog,  N-acetyl-sphingosine, mimicked TNF -induced cell death in promyeloid U937 cells [  270].	transcription
67671	3	336104	7	NULL	NULL	0	NULL	N-acetyl-sphingosine	Chemical		is a type of					cell-permeable short-chain ceramide analog	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1485_2_63_s_496	10832090	Obeid et al. were the first to show that an exogenously added cell-permeable short-chain ceramide analog,  N-acetyl-sphingosine, mimicked TNF -induced cell death in promyeloid U937 cells [  270].	transcription
61268	1	336105	5	NULL	NULL	0	NULL	S1P	Chemical		ligand for		high affinity			S1P2/EDG-5	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
61269	2	336105	5	NULL	NULL	0	NULL	S1P	Chemical		bind					S1P2/EDG-5	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
61270	3	336105	5	NULL	NULL	0	NULL	dihydro-S1P	Chemical		bind					S1P2/EDG-5	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
61271	4	336105	5	NULL	NULL	0	NULL	statement 3	Process		competes with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
61272	5	336105	5	NULL	NULL	0	NULL	sphingosine	Chemical		does not compete with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
61273	6	336105	5	NULL	NULL	0	NULL	sphingomyelin	Chemical		does not compete with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
61274	7	336105	5	NULL	NULL	0	NULL	homophosphonate S1P	Chemical		does not compete with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
61275	8	336105	5	NULL	NULL	0	NULL	ceramide	Process		does not compete with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
61276	9	336105	5	NULL	NULL	0	NULL	ceramide-1-phosphate	Chemical		does not compete with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
61277	10	336105	5	NULL	NULL	0	NULL	LPA	Chemical		does not compete with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
67672	1	336105	7	NULL	NULL	NULL	NULL	S1P	Chemical		ligand for		high affinity			S1P2/EDG-5	GP				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
67673	2	336105	7	NULL	NULL	0	NULL	S1P	Chemical		bind					S1P2/EDG-5	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
67674	3	336105	7	NULL	NULL	0	NULL	dihydro-S1P	Chemical		bind					S1P2/EDG-5	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
67675	4	336105	7	NULL	NULL	0	NULL	statement 3	Process		compete with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
67676	5	336105	7	NULL	NULL	0	NULL	sphingosine	Chemical		does not compete with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
67677	6	336105	7	NULL	NULL	0	NULL	sphingomyelin	Chemical		does not compete with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
67678	7	336105	7	NULL	NULL	0	NULL	homophosphonate S1P	Chemical		does not compete with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
67679	8	336105	7	NULL	NULL	0	NULL	ceramide	Chemical		does not compete with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
67680	9	336105	7	NULL	NULL	0	NULL	ceramide-1-phosphate	Chemical		does not compete with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
67681	10	336105	7	NULL	NULL	0	NULL	LPA	Chemical		does not compete with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_72_s_90	12069812	S1P is a high affinity ligand (Kd 16-27 nM) for S1P2/EDG-5 [ 7,  15,  19 and   43] and the binding of S1P to S1P2/EDG-5 can be competed by dihydro-S1P but not by sphingosine, sphingomyelin, homophosphonate S1P, ceramide, ceramide-1-phosphate or LPA [ 19 and  43].	transcription
66572	1	336106	5	NULL	NULL	NULL	NULL	SPP	Chemical		leads to					angiogenic responses	Process				NULL	cells treated with sphingolipids	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_228_s_56	12069833	Treatment of cells with related sphingolipids, including sphingosine, sphingomyelin, ceramide and ceramide-1-phosphate, or instillation of SPP into the cytoplasm by microinjection had no effect, demonstrating that the angiogenic responses to SPP resulted from ligation of specific cell surface receptors.	transcription
66573	2	336106	5	NULL	NULL	NULL	NULL	cell surface receptors	GP	ligation of;;specific	results in					statement 1	Process				NULL	cells treated with sphingolipids	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_228_s_56	12069833	Treatment of cells with related sphingolipids, including sphingosine, sphingomyelin, ceramide and ceramide-1-phosphate, or instillation of SPP into the cytoplasm by microinjection had no effect, demonstrating that the angiogenic responses to SPP resulted from ligation of specific cell surface receptors.	transcription
66574	3	336106	5	NULL	NULL	0	NULL	sphingosine	Chemical		is a type of					sphingolipid	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_228_s_56	12069833	Treatment of cells with related sphingolipids, including sphingosine, sphingomyelin, ceramide and ceramide-1-phosphate, or instillation of SPP into the cytoplasm by microinjection had no effect, demonstrating that the angiogenic responses to SPP resulted from ligation of specific cell surface receptors.	transcription
66575	4	336106	5	NULL	NULL	0	NULL	sphingomyelin	Chemical		is a type of					sphingolipid	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_228_s_56	12069833	Treatment of cells with related sphingolipids, including sphingosine, sphingomyelin, ceramide and ceramide-1-phosphate, or instillation of SPP into the cytoplasm by microinjection had no effect, demonstrating that the angiogenic responses to SPP resulted from ligation of specific cell surface receptors.	transcription
66576	5	336106	5	NULL	NULL	0	NULL	ceramide	Chemical		is a type of					sphingolipid	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_228_s_56	12069833	Treatment of cells with related sphingolipids, including sphingosine, sphingomyelin, ceramide and ceramide-1-phosphate, or instillation of SPP into the cytoplasm by microinjection had no effect, demonstrating that the angiogenic responses to SPP resulted from ligation of specific cell surface receptors.	transcription
66577	6	336106	5	NULL	NULL	0	NULL	ceramide-1-phosphate	Chemical		is a type of					sphingolipid	Chemical				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_228_s_56	12069833	Treatment of cells with related sphingolipids, including sphingosine, sphingomyelin, ceramide and ceramide-1-phosphate, or instillation of SPP into the cytoplasm by microinjection had no effect, demonstrating that the angiogenic responses to SPP resulted from ligation of specific cell surface receptors.	transcription
67682	1	336106	7	NULL	NULL	0	NULL	SPP	Chemical	angiogenic responses to	result from					cell surface receptors	GP	ligation of specific			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1582_1_228_s_56	12069833	Treatment of cells with related sphingolipids, including sphingosine, sphingomyelin, ceramide and ceramide-1-phosphate, or instillation of SPP into the cytoplasm by microinjection had no effect, demonstrating that the angiogenic responses to SPP resulted from ligation of specific cell surface receptors.	transcription
66578	1	336107	5	NULL	NULL	0	NULL	MAPP	Chemical		is an inhibitor of					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_2_417_s_145	11815377	This was further supported by experiments with the ceramidase inhibitor, MAPP (Bielawska  et al., 1996  ) which prevents formation of sphingosine and sphingosine-1-phosphate from ceramide and causes accumulation of the latter (Bielawska  et al., 1996  ; Hannun & Luberto, 2000  ).	transcription
66579	2	336107	5	NULL	NULL	0	NULL	sphingosine	Chemical		is formed from					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_2_417_s_145	11815377	This was further supported by experiments with the ceramidase inhibitor, MAPP (Bielawska  et al., 1996  ) which prevents formation of sphingosine and sphingosine-1-phosphate from ceramide and causes accumulation of the latter (Bielawska  et al., 1996  ; Hannun & Luberto, 2000  ).	transcription
66580	3	336107	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		is formed from					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_2_417_s_145	11815377	This was further supported by experiments with the ceramidase inhibitor, MAPP (Bielawska  et al., 1996  ) which prevents formation of sphingosine and sphingosine-1-phosphate from ceramide and causes accumulation of the latter (Bielawska  et al., 1996  ; Hannun & Luberto, 2000  ).	transcription
66581	4	336107	5	NULL	NULL	0	NULL	statement 2	Process		occurs along with					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_2_417_s_145	11815377	This was further supported by experiments with the ceramidase inhibitor, MAPP (Bielawska  et al., 1996  ) which prevents formation of sphingosine and sphingosine-1-phosphate from ceramide and causes accumulation of the latter (Bielawska  et al., 1996  ; Hannun & Luberto, 2000  ).	transcription
66583	5	336107	5	NULL	NULL	0	NULL	MAPP	Chemical		prevents					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_2_417_s_145	11815377	This was further supported by experiments with the ceramidase inhibitor, MAPP (Bielawska  et al., 1996  ) which prevents formation of sphingosine and sphingosine-1-phosphate from ceramide and causes accumulation of the latter (Bielawska  et al., 1996  ; Hannun & Luberto, 2000  ).	transcription
66584	6	336107	5	NULL	NULL	0	NULL	statement 5	Process		accumulates					sphingosine 1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_2_417_s_145	11815377	This was further supported by experiments with the ceramidase inhibitor, MAPP (Bielawska  et al., 1996  ) which prevents formation of sphingosine and sphingosine-1-phosphate from ceramide and causes accumulation of the latter (Bielawska  et al., 1996  ; Hannun & Luberto, 2000  ).	transcription
67684	1	336107	7	NULL	NULL	0	NULL	MAPP	Chemical		is a type of					ceramidase inhibitor	Chemical				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_2_417_s_145	11815377	This was further supported by experiments with the ceramidase inhibitor, MAPP (Bielawska  et al., 1996  ) which prevents formation of sphingosine and sphingosine-1-phosphate from ceramide and causes accumulation of the latter (Bielawska  et al., 1996  ; Hannun & Luberto, 2000  ).	transcription
67685	2	336107	7	NULL	NULL	0	NULL	sphingosine	Chemical		formed from					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_2_417_s_145	11815377	This was further supported by experiments with the ceramidase inhibitor, MAPP (Bielawska  et al., 1996  ) which prevents formation of sphingosine and sphingosine-1-phosphate from ceramide and causes accumulation of the latter (Bielawska  et al., 1996  ; Hannun & Luberto, 2000  ).	transcription
67686	3	336107	7	NULL	NULL	0	NULL	sphingosine-1-phosphate	Chemical		formed from					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_2_417_s_145	11815377	This was further supported by experiments with the ceramidase inhibitor, MAPP (Bielawska  et al., 1996  ) which prevents formation of sphingosine and sphingosine-1-phosphate from ceramide and causes accumulation of the latter (Bielawska  et al., 1996  ; Hannun & Luberto, 2000  ).	transcription
67687	4	336107	7	NULL	NULL	0	NULL	MAPP	Chemical		prevents					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_2_417_s_145	11815377	This was further supported by experiments with the ceramidase inhibitor, MAPP (Bielawska  et al., 1996  ) which prevents formation of sphingosine and sphingosine-1-phosphate from ceramide and causes accumulation of the latter (Bielawska  et al., 1996  ; Hannun & Luberto, 2000  ).	transcription
67688	5	336107	7	NULL	NULL	0	NULL	MAPP	Chemical		prevents					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_2_417_s_145	11815377	This was further supported by experiments with the ceramidase inhibitor, MAPP (Bielawska  et al., 1996  ) which prevents formation of sphingosine and sphingosine-1-phosphate from ceramide and causes accumulation of the latter (Bielawska  et al., 1996  ; Hannun & Luberto, 2000  ).	transcription
67709	6	336107	7	NULL	NULL	0	NULL	MAPP	Chemical		cause					ceramide	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_135_2_417_s_145	11815377	This was further supported by experiments with the ceramidase inhibitor, MAPP (Bielawska  et al., 1996  ) which prevents formation of sphingosine and sphingosine-1-phosphate from ceramide and causes accumulation of the latter (Bielawska  et al., 1996  ; Hannun & Luberto, 2000  ).	transcription
66596	1	336108	5	NULL	NULL	NULL	NULL	apoptosis	Process		is induced by					serum deprivation	Process				NULL	Jurkat T cells	NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_13	10545499	In Jurkat T cells, overexpression of sphingosine kinase also suppressed serum deprivation- and ceramide-induced apoptosis and, to a lesser extent, Fas-induced apoptosis, which correlated with inhibition of DEVDase activity, as well as inhibition of the executionary caspase-3.	transcription
66597	2	336108	5	NULL	NULL	NULL	NULL	apoptosis	Process		is induced by					ceramide	Chemical				NULL	Jurkat T cells	NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_13	10545499	In Jurkat T cells, overexpression of sphingosine kinase also suppressed serum deprivation- and ceramide-induced apoptosis and, to a lesser extent, Fas-induced apoptosis, which correlated with inhibition of DEVDase activity, as well as inhibition of the executionary caspase-3.	transcription
66598	3	336108	5	NULL	NULL	NULL	NULL	apoptosis	Process		is induced by					Fas	GP				NULL	Jurkat T cells	NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_13	10545499	In Jurkat T cells, overexpression of sphingosine kinase also suppressed serum deprivation- and ceramide-induced apoptosis and, to a lesser extent, Fas-induced apoptosis, which correlated with inhibition of DEVDase activity, as well as inhibition of the executionary caspase-3.	transcription
66599	4	336108	5	NULL	NULL	0	NULL	sphingosine kinase	GP	overexpression of	suppress					statement 1	Process				NULL	Jurkat T cells	0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_13	10545499	In Jurkat T cells, overexpression of sphingosine kinase also suppressed serum deprivation- and ceramide-induced apoptosis and, to a lesser extent, Fas-induced apoptosis, which correlated with inhibition of DEVDase activity, as well as inhibition of the executionary caspase-3.	transcription
66600	5	336108	5	NULL	NULL	0	NULL	sphingosine kinase	GP	overexpression of	suppress					statement 2	Process				NULL	Jurkat T cells	0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_13	10545499	In Jurkat T cells, overexpression of sphingosine kinase also suppressed serum deprivation- and ceramide-induced apoptosis and, to a lesser extent, Fas-induced apoptosis, which correlated with inhibition of DEVDase activity, as well as inhibition of the executionary caspase-3.	transcription
66601	6	336108	5	NULL	NULL	NULL	NULL	sphingosine kinase	GP	overexpression of	suppress					statement 3	Process				NULL	Jurkat T cells	NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_13	10545499	In Jurkat T cells, overexpression of sphingosine kinase also suppressed serum deprivation- and ceramide-induced apoptosis and, to a lesser extent, Fas-induced apoptosis, which correlated with inhibition of DEVDase activity, as well as inhibition of the executionary caspase-3.	transcription
66602	7	336108	5	NULL	NULL	0	NULL	statement 6	Process		lesser extent than					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_13	10545499	In Jurkat T cells, overexpression of sphingosine kinase also suppressed serum deprivation- and ceramide-induced apoptosis and, to a lesser extent, Fas-induced apoptosis, which correlated with inhibition of DEVDase activity, as well as inhibition of the executionary caspase-3.	transcription
66603	8	336108	5	NULL	NULL	0	NULL	statement 6	Process		lesser extent than					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_13	10545499	In Jurkat T cells, overexpression of sphingosine kinase also suppressed serum deprivation- and ceramide-induced apoptosis and, to a lesser extent, Fas-induced apoptosis, which correlated with inhibition of DEVDase activity, as well as inhibition of the executionary caspase-3.	transcription
66604	9	336108	5	NULL	NULL	NULL	NULL	statement 6	Process		corelates with					DEVDase	GP	inhibition of;;activity of			NULL	Jurkat T cells	NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_13	10545499	In Jurkat T cells, overexpression of sphingosine kinase also suppressed serum deprivation- and ceramide-induced apoptosis and, to a lesser extent, Fas-induced apoptosis, which correlated with inhibition of DEVDase activity, as well as inhibition of the executionary caspase-3.	transcription
66605	10	336108	5	NULL	NULL	NULL	NULL	statement 6	Process		corelates with					executionary caspase-3	GP	inhibition of			NULL	Jurkat T cells	NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_13	10545499	In Jurkat T cells, overexpression of sphingosine kinase also suppressed serum deprivation- and ceramide-induced apoptosis and, to a lesser extent, Fas-induced apoptosis, which correlated with inhibition of DEVDase activity, as well as inhibition of the executionary caspase-3.	transcription
67689	1	336108	7	NULL	NULL	NULL	NULL	sphingosine kinase	GP	overexpression of	suppress					serum deprivation	Process				NULL	Jurkat T cells	NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_13	10545499	In Jurkat T cells, overexpression of sphingosine kinase also suppressed serum deprivation- and ceramide-induced apoptosis and, to a lesser extent, Fas-induced apoptosis, which correlated with inhibition of DEVDase activity, as well as inhibition of the executionary caspase-3.	transcription
67690	2	336108	7	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_13	10545499	In Jurkat T cells, overexpression of sphingosine kinase also suppressed serum deprivation- and ceramide-induced apoptosis and, to a lesser extent, Fas-induced apoptosis, which correlated with inhibition of DEVDase activity, as well as inhibition of the executionary caspase-3.	transcription
67691	3	336108	7	NULL	NULL	NULL	NULL	sphingosine kinase	GP	overexpression of	suppress					statement 2	Process				NULL	Jurkat T cells	NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_13	10545499	In Jurkat T cells, overexpression of sphingosine kinase also suppressed serum deprivation- and ceramide-induced apoptosis and, to a lesser extent, Fas-induced apoptosis, which correlated with inhibition of DEVDase activity, as well as inhibition of the executionary caspase-3.	transcription
67692	4	336108	7	NULL	NULL	0	NULL	Fas	GP		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_13	10545499	In Jurkat T cells, overexpression of sphingosine kinase also suppressed serum deprivation- and ceramide-induced apoptosis and, to a lesser extent, Fas-induced apoptosis, which correlated with inhibition of DEVDase activity, as well as inhibition of the executionary caspase-3.	transcription
67693	5	336108	7	NULL	NULL	NULL	NULL	sphingosine kinase	GP	overexpression of	suppress					statement 4	Process				NULL	Jurkat T cells	NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_13	10545499	In Jurkat T cells, overexpression of sphingosine kinase also suppressed serum deprivation- and ceramide-induced apoptosis and, to a lesser extent, Fas-induced apoptosis, which correlated with inhibition of DEVDase activity, as well as inhibition of the executionary caspase-3.	transcription
67694	6	336108	7	NULL	NULL	0	NULL	statement 4	Process	suppression of	occur to a lesser extent than					statement 2	Process	suppression of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_13	10545499	In Jurkat T cells, overexpression of sphingosine kinase also suppressed serum deprivation- and ceramide-induced apoptosis and, to a lesser extent, Fas-induced apoptosis, which correlated with inhibition of DEVDase activity, as well as inhibition of the executionary caspase-3.	transcription
67695	7	336108	7	NULL	NULL	0	NULL	statement 6	Process		correlates with					DEVDase activity	Process	inhibition of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_13	10545499	In Jurkat T cells, overexpression of sphingosine kinase also suppressed serum deprivation- and ceramide-induced apoptosis and, to a lesser extent, Fas-induced apoptosis, which correlated with inhibition of DEVDase activity, as well as inhibition of the executionary caspase-3.	transcription
67696	8	336108	7	NULL	NULL	NULL	NULL	statement 6	Process		correlates with					caspase-3	GP	inhibition of;;executionary			NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_13	10545499	In Jurkat T cells, overexpression of sphingosine kinase also suppressed serum deprivation- and ceramide-induced apoptosis and, to a lesser extent, Fas-induced apoptosis, which correlated with inhibition of DEVDase activity, as well as inhibition of the executionary caspase-3.	transcription
66606	1	336109	5	NULL	NULL	0	NULL	sphingosine kinase	GP	overexpression of	increases					SPP	Chemical	levels of;;intracellular			NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_33	10545499	In this study, we demonstrate that overexpression of sphingosine kinase markedly increased intracellular mass levels of SPP, enhanced proliferation by promoting the G1 to S phase transition, and suppressed serum deprivation- and ceramide-induced apoptosis.	transcription
66607	2	336109	5	NULL	NULL	0	NULL	sphingosine kinase	GP	overexpression of	enhances					cellular proliferation	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_33	10545499	In this study, we demonstrate that overexpression of sphingosine kinase markedly increased intracellular mass levels of SPP, enhanced proliferation by promoting the G1 to S phase transition, and suppressed serum deprivation- and ceramide-induced apoptosis.	transcription
66608	3	336109	5	NULL	NULL	NULL	NULL	cell	Cell		undergoes transition from					G1 phase	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_33	10545499	In this study, we demonstrate that overexpression of sphingosine kinase markedly increased intracellular mass levels of SPP, enhanced proliferation by promoting the G1 to S phase transition, and suppressed serum deprivation- and ceramide-induced apoptosis.	transcription
66609	4	336109	5	NULL	NULL	NULL	NULL	cell	Cell		undergoes transition to					S phase	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_33	10545499	In this study, we demonstrate that overexpression of sphingosine kinase markedly increased intracellular mass levels of SPP, enhanced proliferation by promoting the G1 to S phase transition, and suppressed serum deprivation- and ceramide-induced apoptosis.	transcription
66610	5	336109	5	NULL	NULL	0	NULL	statement 3	Process		occurs along with					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_33	10545499	In this study, we demonstrate that overexpression of sphingosine kinase markedly increased intracellular mass levels of SPP, enhanced proliferation by promoting the G1 to S phase transition, and suppressed serum deprivation- and ceramide-induced apoptosis.	transcription
66611	6	336109	5	NULL	NULL	NULL	NULL	sphingosine kinase	GP	overexpression of	promotes					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_33	10545499	In this study, we demonstrate that overexpression of sphingosine kinase markedly increased intracellular mass levels of SPP, enhanced proliferation by promoting the G1 to S phase transition, and suppressed serum deprivation- and ceramide-induced apoptosis.	transcription
66612	7	336109	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					serum deprivation	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_33	10545499	In this study, we demonstrate that overexpression of sphingosine kinase markedly increased intracellular mass levels of SPP, enhanced proliferation by promoting the G1 to S phase transition, and suppressed serum deprivation- and ceramide-induced apoptosis.	transcription
66613	8	336109	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_33	10545499	In this study, we demonstrate that overexpression of sphingosine kinase markedly increased intracellular mass levels of SPP, enhanced proliferation by promoting the G1 to S phase transition, and suppressed serum deprivation- and ceramide-induced apoptosis.	transcription
66614	9	336109	5	NULL	NULL	0	NULL	sphingosine kinase	GP	overexpression of	suppress					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_33	10545499	In this study, we demonstrate that overexpression of sphingosine kinase markedly increased intracellular mass levels of SPP, enhanced proliferation by promoting the G1 to S phase transition, and suppressed serum deprivation- and ceramide-induced apoptosis.	transcription
66615	10	336109	5	NULL	NULL	0	NULL	sphingosine kinase	GP	overexpression of	suppress					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_33	10545499	In this study, we demonstrate that overexpression of sphingosine kinase markedly increased intracellular mass levels of SPP, enhanced proliferation by promoting the G1 to S phase transition, and suppressed serum deprivation- and ceramide-induced apoptosis.	transcription
66616	11	336109	5	NULL	NULL	0	NULL	statement 6	Process		leads to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_33	10545499	In this study, we demonstrate that overexpression of sphingosine kinase markedly increased intracellular mass levels of SPP, enhanced proliferation by promoting the G1 to S phase transition, and suppressed serum deprivation- and ceramide-induced apoptosis.	transcription
67697	1	336109	7	NULL	NULL	0	NULL	sphingosine kinase	GP	overexpression of	increase		markedly			SPP	Chemical	intracellular masslevels of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_33	10545499	In this study, we demonstrate that overexpression of sphingosine kinase markedly increased intracellular mass levels of SPP, enhanced proliferation by promoting the G1 to S phase transition, and suppressed serum deprivation- and ceramide-induced apoptosis.	transcription
67698	2	336109	7	NULL	NULL	0	NULL	G1 phase	Process		transition to					S phase	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_33	10545499	In this study, we demonstrate that overexpression of sphingosine kinase markedly increased intracellular mass levels of SPP, enhanced proliferation by promoting the G1 to S phase transition, and suppressed serum deprivation- and ceramide-induced apoptosis.	transcription
67699	3	336109	7	NULL	NULL	NULL	NULL	sphingosine kinase	GP		enhance					proliferation	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_33	10545499	In this study, we demonstrate that overexpression of sphingosine kinase markedly increased intracellular mass levels of SPP, enhanced proliferation by promoting the G1 to S phase transition, and suppressed serum deprivation- and ceramide-induced apoptosis.	transcription
67702	4	336109	7	NULL	NULL	0	NULL	statement 3	Process		occur by					statement 2	Process	promoting			NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_33	10545499	In this study, we demonstrate that overexpression of sphingosine kinase markedly increased intracellular mass levels of SPP, enhanced proliferation by promoting the G1 to S phase transition, and suppressed serum deprivation- and ceramide-induced apoptosis.	transcription
67706	5	336109	7	NULL	NULL	NULL	NULL	sphingosine kinase	GP		suppress					serum deprivation	Process				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_33	10545499	In this study, we demonstrate that overexpression of sphingosine kinase markedly increased intracellular mass levels of SPP, enhanced proliferation by promoting the G1 to S phase transition, and suppressed serum deprivation- and ceramide-induced apoptosis.	transcription
67707	6	336109	7	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_33	10545499	In this study, we demonstrate that overexpression of sphingosine kinase markedly increased intracellular mass levels of SPP, enhanced proliferation by promoting the G1 to S phase transition, and suppressed serum deprivation- and ceramide-induced apoptosis.	transcription
67708	7	336109	7	NULL	NULL	0	NULL	sphingosine kinase	GP		suppress					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_33	10545499	In this study, we demonstrate that overexpression of sphingosine kinase markedly increased intracellular mass levels of SPP, enhanced proliferation by promoting the G1 to S phase transition, and suppressed serum deprivation- and ceramide-induced apoptosis.	transcription
66617	2	336110	5	NULL	NULL	NULL	NULL	sphingosine kinase	GP	activation of	mediates					statement 1	Process				NULL	hippocampal neurons	NULL	NULL	NULL	NULL	gw60_neuroscience_115_4_1089_s_356	12453482	Overall, our findings provide strong evidence that activation of sphingosine kinase but not NSMase activation or enhanced ceramide synthesis mediated NGF-triggered survival signaling in hippocampal neurons.	transcription
66618	1	336110	5	NULL	NULL	NULL	NULL	survival signaling	Process		is triggerd by					NGF	GP				NULL	hippocampal neurons	NULL	NULL	NULL	NULL	gw60_neuroscience_115_4_1089_s_356	12453482	Overall, our findings provide strong evidence that activation of sphingosine kinase but not NSMase activation or enhanced ceramide synthesis mediated NGF-triggered survival signaling in hippocampal neurons.	transcription
66619	3	336110	5	NULL	NULL	0	NULL	NSMase	GP	activation of	does not mediate					statement 1	Process				NULL	hippocampal neurons	0	NULL	NULL	NULL	gw60_neuroscience_115_4_1089_s_356	12453482	Overall, our findings provide strong evidence that activation of sphingosine kinase but not NSMase activation or enhanced ceramide synthesis mediated NGF-triggered survival signaling in hippocampal neurons.	transcription
66620	4	336110	5	NULL	NULL	0	NULL	ceramide	Chemical	enhanced synthesis of	does not mediate					statement 1	Process				NULL	hippocampal neurons	0	NULL	NULL	NULL	gw60_neuroscience_115_4_1089_s_356	12453482	Overall, our findings provide strong evidence that activation of sphingosine kinase but not NSMase activation or enhanced ceramide synthesis mediated NGF-triggered survival signaling in hippocampal neurons.	transcription
67710	1	336110	7	NULL	NULL	0	NULL	NGF	GP		trigger					survival signaling	Process				NULL	hippocampal neurons	0	NULL	NULL	NULL	gw60_neuroscience_115_4_1089_s_356	12453482	Overall, our findings provide strong evidence that activation of sphingosine kinase but not NSMase activation or enhanced ceramide synthesis mediated NGF-triggered survival signaling in hippocampal neurons.	transcription
67711	2	336110	7	NULL	NULL	0	NULL	sphingosine kinase	GP	activation of	mediate					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_neuroscience_115_4_1089_s_356	12453482	Overall, our findings provide strong evidence that activation of sphingosine kinase but not NSMase activation or enhanced ceramide synthesis mediated NGF-triggered survival signaling in hippocampal neurons.	transcription
67712	3	336110	7	NULL	NULL	0	NULL	NSMase	GP	activation of	does not mediate					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_neuroscience_115_4_1089_s_356	12453482	Overall, our findings provide strong evidence that activation of sphingosine kinase but not NSMase activation or enhanced ceramide synthesis mediated NGF-triggered survival signaling in hippocampal neurons.	transcription
67713	4	336110	7	NULL	NULL	0	NULL	ceramide	Chemical	enhanced synthesis of	mediate					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_neuroscience_115_4_1089_s_356	12453482	Overall, our findings provide strong evidence that activation of sphingosine kinase but not NSMase activation or enhanced ceramide synthesis mediated NGF-triggered survival signaling in hippocampal neurons.	transcription
66621	1	336111	5	NULL	NULL	0	NULL	p42-ERK1/p44-ERK2	GP	basal activity of	is reduced by		gradually			ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_6	9415703	Characterization of the mitogen-activated protein kinase (MAPK) cascade in these responses revealed a further functional disparity between the two lipids: basal p42-ERK1/p44-ERK2 activity was gradually reduced by ceramide but immediately and completely suppressed by sphingosine.	transcription
66622	2	336111	5	NULL	NULL	0	NULL	p42-ERK1/p44-ERK2	GP	basal activity of	suppressed by		immediately;;completely			sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_6	9415703	Characterization of the mitogen-activated protein kinase (MAPK) cascade in these responses revealed a further functional disparity between the two lipids: basal p42-ERK1/p44-ERK2 activity was gradually reduced by ceramide but immediately and completely suppressed by sphingosine.	transcription
67714	1	336111	7	NULL	NULL	0	NULL	ceramide	Chemical		reduce					basal p42-ERK1/p44-ERK2 activity	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_6	9415703	Characterization of the mitogen-activated protein kinase (MAPK) cascade in these responses revealed a further functional disparity between the two lipids: basal p42-ERK1/p44-ERK2 activity was gradually reduced by ceramide but immediately and completely suppressed by sphingosine.	transcription
67715	2	336111	7	NULL	NULL	0	NULL	sphingosine	Chemical		suppress		completely			basal p42-ERK1/p44-ERK2 activity	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_6	9415703	Characterization of the mitogen-activated protein kinase (MAPK) cascade in these responses revealed a further functional disparity between the two lipids: basal p42-ERK1/p44-ERK2 activity was gradually reduced by ceramide but immediately and completely suppressed by sphingosine.	transcription
66623	1	336112	5	NULL	NULL	0	NULL	lipid	Chemical		increases		sharply			p38-RK	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_8	9415703	Both lipids sharply increased p38-RK activity; selective pharmacological inhibition of p38-RK by the pyridinyl imidazole SB-203580 failed to mitigate the cytotoxicity associated with either ceramide or sphingosine, suggesting that p38-RK is not essential for lipid-induced apoptosis.	transcription
66624	2	336112	5	NULL	NULL	NULL	NULL	p38-RK	GP		is inhibited by		selective;;pharmacological			pyridinyl imidazole SB-203580	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_8	9415703	Both lipids sharply increased p38-RK activity; selective pharmacological inhibition of p38-RK by the pyridinyl imidazole SB-203580 failed to mitigate the cytotoxicity associated with either ceramide or sphingosine, suggesting that p38-RK is not essential for lipid-induced apoptosis.	transcription
66627	3	336112	5	NULL	NULL	0	NULL	cytotoxicity	Process		is associated with					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_8	9415703	Both lipids sharply increased p38-RK activity; selective pharmacological inhibition of p38-RK by the pyridinyl imidazole SB-203580 failed to mitigate the cytotoxicity associated with either ceramide or sphingosine, suggesting that p38-RK is not essential for lipid-induced apoptosis.	transcription
66628	4	336112	5	NULL	NULL	0	NULL	cytotoxicity	Process		is associated with					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_8	9415703	Both lipids sharply increased p38-RK activity; selective pharmacological inhibition of p38-RK by the pyridinyl imidazole SB-203580 failed to mitigate the cytotoxicity associated with either ceramide or sphingosine, suggesting that p38-RK is not essential for lipid-induced apoptosis.	transcription
66629	5	336112	5	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_8	9415703	Both lipids sharply increased p38-RK activity; selective pharmacological inhibition of p38-RK by the pyridinyl imidazole SB-203580 failed to mitigate the cytotoxicity associated with either ceramide or sphingosine, suggesting that p38-RK is not essential for lipid-induced apoptosis.	transcription
66630	6	336112	5	NULL	NULL	0	NULL	statement 2	Process		fails to mitigate					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_8	9415703	Both lipids sharply increased p38-RK activity; selective pharmacological inhibition of p38-RK by the pyridinyl imidazole SB-203580 failed to mitigate the cytotoxicity associated with either ceramide or sphingosine, suggesting that p38-RK is not essential for lipid-induced apoptosis.	transcription
66631	7	336112	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					lipid	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_8	9415703	Both lipids sharply increased p38-RK activity; selective pharmacological inhibition of p38-RK by the pyridinyl imidazole SB-203580 failed to mitigate the cytotoxicity associated with either ceramide or sphingosine, suggesting that p38-RK is not essential for lipid-induced apoptosis.	transcription
66632	8	336112	5	NULL	NULL	0	NULL	p38-RK	GP		is not essential for					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_8	9415703	Both lipids sharply increased p38-RK activity; selective pharmacological inhibition of p38-RK by the pyridinyl imidazole SB-203580 failed to mitigate the cytotoxicity associated with either ceramide or sphingosine, suggesting that p38-RK is not essential for lipid-induced apoptosis.	transcription
66633	9	336112	5	NULL	NULL	NULL	NULL	statement 6	Process		suggest					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_8	9415703	Both lipids sharply increased p38-RK activity; selective pharmacological inhibition of p38-RK by the pyridinyl imidazole SB-203580 failed to mitigate the cytotoxicity associated with either ceramide or sphingosine, suggesting that p38-RK is not essential for lipid-induced apoptosis.	transcription
67716	1	336112	7	NULL	NULL	NULL	NULL	SB-203580	Chemical		inhibit		selectively;;pharmacological			p38-RK	GP				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_8	9415703	Both lipids sharply increased p38-RK activity; selective pharmacological inhibition of p38-RK by the pyridinyl imidazole SB-203580 failed to mitigate the cytotoxicity associated with either ceramide or sphingosine, suggesting that p38-RK is not essential for lipid-induced apoptosis.	transcription
67717	2	336112	7	NULL	NULL	0	NULL	cytotoxicity	Process		associated with					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_8	9415703	Both lipids sharply increased p38-RK activity; selective pharmacological inhibition of p38-RK by the pyridinyl imidazole SB-203580 failed to mitigate the cytotoxicity associated with either ceramide or sphingosine, suggesting that p38-RK is not essential for lipid-induced apoptosis.	transcription
67718	3	336112	7	NULL	NULL	0	NULL	cytotoxicity	Process		associated with					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_8	9415703	Both lipids sharply increased p38-RK activity; selective pharmacological inhibition of p38-RK by the pyridinyl imidazole SB-203580 failed to mitigate the cytotoxicity associated with either ceramide or sphingosine, suggesting that p38-RK is not essential for lipid-induced apoptosis.	transcription
67719	4	336112	7	NULL	NULL	0	NULL	statement 1	Process		failed to mitigate					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_8	9415703	Both lipids sharply increased p38-RK activity; selective pharmacological inhibition of p38-RK by the pyridinyl imidazole SB-203580 failed to mitigate the cytotoxicity associated with either ceramide or sphingosine, suggesting that p38-RK is not essential for lipid-induced apoptosis.	transcription
67720	5	336112	7	NULL	NULL	0	NULL	statement 1	Process		failed to mitigate					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_8	9415703	Both lipids sharply increased p38-RK activity; selective pharmacological inhibition of p38-RK by the pyridinyl imidazole SB-203580 failed to mitigate the cytotoxicity associated with either ceramide or sphingosine, suggesting that p38-RK is not essential for lipid-induced apoptosis.	transcription
67721	6	336112	7	NULL	NULL	0	NULL	lipid	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_8	9415703	Both lipids sharply increased p38-RK activity; selective pharmacological inhibition of p38-RK by the pyridinyl imidazole SB-203580 failed to mitigate the cytotoxicity associated with either ceramide or sphingosine, suggesting that p38-RK is not essential for lipid-induced apoptosis.	transcription
67722	7	336112	7	NULL	NULL	0	NULL	p38-RK	GP		is not essential for					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_8	9415703	Both lipids sharply increased p38-RK activity; selective pharmacological inhibition of p38-RK by the pyridinyl imidazole SB-203580 failed to mitigate the cytotoxicity associated with either ceramide or sphingosine, suggesting that p38-RK is not essential for lipid-induced apoptosis.	transcription
67723	8	336112	7	NULL	NULL	0	NULL	statement 4	Process		suggest					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_8	9415703	Both lipids sharply increased p38-RK activity; selective pharmacological inhibition of p38-RK by the pyridinyl imidazole SB-203580 failed to mitigate the cytotoxicity associated with either ceramide or sphingosine, suggesting that p38-RK is not essential for lipid-induced apoptosis.	transcription
67724	9	336112	7	NULL	NULL	0	NULL	statement 5	Process		suggest					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_8	9415703	Both lipids sharply increased p38-RK activity; selective pharmacological inhibition of p38-RK by the pyridinyl imidazole SB-203580 failed to mitigate the cytotoxicity associated with either ceramide or sphingosine, suggesting that p38-RK is not essential for lipid-induced apoptosis.	transcription
67726	10	336112	7	NULL	NULL	0	NULL	SB-203580	Chemical		is a type of					pyridinyl imidazole	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_8	9415703	Both lipids sharply increased p38-RK activity; selective pharmacological inhibition of p38-RK by the pyridinyl imidazole SB-203580 failed to mitigate the cytotoxicity associated with either ceramide or sphingosine, suggesting that p38-RK is not essential for lipid-induced apoptosis.	transcription
66635	1	336113	5	NULL	NULL	0	NULL	lipids	Chemical	lethal actions of	entail alterations in		reciprocal;;coordinated			SAPK	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_29	9415703	The results demonstrate that the lethal actions of these lipids entail reciprocal, but coordinated, alterations in SAPK and MAPK activities such that both ceramide and sphingosine stimulate p46-JNK1/p54-JNK2 but suppress p42-ERK1/p44-ERK2, albeit to varying degrees.	transcription
66636	2	336113	5	NULL	NULL	0	NULL	lipids	Chemical	lethal actions of	entail alterations in		reciprocal;;coordinated			MAPK	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_29	9415703	The results demonstrate that the lethal actions of these lipids entail reciprocal, but coordinated, alterations in SAPK and MAPK activities such that both ceramide and sphingosine stimulate p46-JNK1/p54-JNK2 but suppress p42-ERK1/p44-ERK2, albeit to varying degrees.	transcription
66637	3	336113	5	NULL	NULL	0	NULL	ceramide	Chemical		stimulates					p46-JNK1/p54-JNK2	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_29	9415703	The results demonstrate that the lethal actions of these lipids entail reciprocal, but coordinated, alterations in SAPK and MAPK activities such that both ceramide and sphingosine stimulate p46-JNK1/p54-JNK2 but suppress p42-ERK1/p44-ERK2, albeit to varying degrees.	transcription
66638	4	336113	5	NULL	NULL	0	NULL	sphingosine	Chemical		stimulates					p46-JNK1/p54-JNK2	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_29	9415703	The results demonstrate that the lethal actions of these lipids entail reciprocal, but coordinated, alterations in SAPK and MAPK activities such that both ceramide and sphingosine stimulate p46-JNK1/p54-JNK2 but suppress p42-ERK1/p44-ERK2, albeit to varying degrees.	transcription
66639	5	336113	5	NULL	NULL	0	NULL	ceramide	Chemical		suppress					p42-ERK1/p44-ERK2	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_29	9415703	The results demonstrate that the lethal actions of these lipids entail reciprocal, but coordinated, alterations in SAPK and MAPK activities such that both ceramide and sphingosine stimulate p46-JNK1/p54-JNK2 but suppress p42-ERK1/p44-ERK2, albeit to varying degrees.	transcription
66640	6	336113	5	NULL	NULL	0	NULL	sphingosine	Chemical		suppress					p42-ERK1/p44-ERK2	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_29	9415703	The results demonstrate that the lethal actions of these lipids entail reciprocal, but coordinated, alterations in SAPK and MAPK activities such that both ceramide and sphingosine stimulate p46-JNK1/p54-JNK2 but suppress p42-ERK1/p44-ERK2, albeit to varying degrees.	transcription
67725	1	336113	7	NULL	NULL	0	NULL	ceramide	Chemical		stimulate					p46-JNK1/p54-JNK2	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_29	9415703	The results demonstrate that the lethal actions of these lipids entail reciprocal, but coordinated, alterations in SAPK and MAPK activities such that both ceramide and sphingosine stimulate p46-JNK1/p54-JNK2 but suppress p42-ERK1/p44-ERK2, albeit to varying degrees.	transcription
67727	2	336113	7	NULL	NULL	0	NULL	sphingosine	Chemical		stimulate					p46-JNK1/p54-JNK2	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_29	9415703	The results demonstrate that the lethal actions of these lipids entail reciprocal, but coordinated, alterations in SAPK and MAPK activities such that both ceramide and sphingosine stimulate p46-JNK1/p54-JNK2 but suppress p42-ERK1/p44-ERK2, albeit to varying degrees.	transcription
67728	3	336113	7	NULL	NULL	0	NULL	ceramide	Chemical		suppress					p42-ERK1/p44-ERK2	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_29	9415703	The results demonstrate that the lethal actions of these lipids entail reciprocal, but coordinated, alterations in SAPK and MAPK activities such that both ceramide and sphingosine stimulate p46-JNK1/p54-JNK2 but suppress p42-ERK1/p44-ERK2, albeit to varying degrees.	transcription
67729	4	336113	7	NULL	NULL	0	NULL	sphingosine	Chemical		suppress					p42-ERK1/p44-ERK2	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_29	9415703	The results demonstrate that the lethal actions of these lipids entail reciprocal, but coordinated, alterations in SAPK and MAPK activities such that both ceramide and sphingosine stimulate p46-JNK1/p54-JNK2 but suppress p42-ERK1/p44-ERK2, albeit to varying degrees.	transcription
66641	1	336115	5	NULL	NULL	0	NULL	ceramide	Chemical		elicits					p38-RK	GP	complex activation of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_339	9415703	The complex activation of p38-RK elicited by ceramide and sphingosine may therefore represent a consequence, rather than a cause, of lipid-induced apoptosis and possibly constitutes a cytoprotective response to lethal insult.	transcription
66642	2	336115	5	NULL	NULL	0	NULL	sphingosine	Chemical		elicits					p38-RK	GP	complex activation of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_339	9415703	The complex activation of p38-RK elicited by ceramide and sphingosine may therefore represent a consequence, rather than a cause, of lipid-induced apoptosis and possibly constitutes a cytoprotective response to lethal insult.	transcription
66643	3	336115	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					lipid	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_339	9415703	The complex activation of p38-RK elicited by ceramide and sphingosine may therefore represent a consequence, rather than a cause, of lipid-induced apoptosis and possibly constitutes a cytoprotective response to lethal insult.	transcription
66644	4	336115	5	NULL	NULL	0	NULL	statement 3	Process		leads to					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_339	9415703	The complex activation of p38-RK elicited by ceramide and sphingosine may therefore represent a consequence, rather than a cause, of lipid-induced apoptosis and possibly constitutes a cytoprotective response to lethal insult.	transcription
66645	5	336115	5	NULL	NULL	0	NULL	statement 3	Process		leads to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_339	9415703	The complex activation of p38-RK elicited by ceramide and sphingosine may therefore represent a consequence, rather than a cause, of lipid-induced apoptosis and possibly constitutes a cytoprotective response to lethal insult.	transcription
67730	1	336115	7	NULL	NULL	NULL	NULL	ceramide	Chemical		elicit					p38-RK	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_339	9415703	The complex activation of p38-RK elicited by ceramide and sphingosine may therefore represent a consequence, rather than a cause, of lipid-induced apoptosis and possibly constitutes a cytoprotective response to lethal insult.	transcription
67731	2	336115	7	NULL	NULL	0	NULL	sphingosine	Chemical		elicit					p38-RK	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_339	9415703	The complex activation of p38-RK elicited by ceramide and sphingosine may therefore represent a consequence, rather than a cause, of lipid-induced apoptosis and possibly constitutes a cytoprotective response to lethal insult.	transcription
67732	3	336115	7	NULL	NULL	0	NULL	lipid	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_339	9415703	The complex activation of p38-RK elicited by ceramide and sphingosine may therefore represent a consequence, rather than a cause, of lipid-induced apoptosis and possibly constitutes a cytoprotective response to lethal insult.	transcription
67733	4	336115	7	NULL	NULL	0	NULL	statement 1	Process		represent					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_339	9415703	The complex activation of p38-RK elicited by ceramide and sphingosine may therefore represent a consequence, rather than a cause, of lipid-induced apoptosis and possibly constitutes a cytoprotective response to lethal insult.	transcription
67734	5	336115	7	NULL	NULL	0	NULL	statement 2	Process		represent					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_339	9415703	The complex activation of p38-RK elicited by ceramide and sphingosine may therefore represent a consequence, rather than a cause, of lipid-induced apoptosis and possibly constitutes a cytoprotective response to lethal insult.	transcription
66646	1	336116	5	NULL	NULL	0	NULL	ceramide	Chemical		stimulates		strongly			SAPK	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_346	9415703	In the primary induction of apoptosis, we found that (a) ceramide strongly stimulates SAPK and weakly inhibits MAPK, whereas (b) sphingosine weakly stimulates SAPK but strongly inhibits MAPK.	transcription
66647	2	336116	5	NULL	NULL	0	NULL	ceramide	Chemical		inhibits		weakly			MAPK	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_346	9415703	In the primary induction of apoptosis, we found that (a) ceramide strongly stimulates SAPK and weakly inhibits MAPK, whereas (b) sphingosine weakly stimulates SAPK but strongly inhibits MAPK.	transcription
66648	3	336116	5	NULL	NULL	0	NULL	sphingosine	Chemical		stimulates		weakly			SAPK	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_346	9415703	In the primary induction of apoptosis, we found that (a) ceramide strongly stimulates SAPK and weakly inhibits MAPK, whereas (b) sphingosine weakly stimulates SAPK but strongly inhibits MAPK.	transcription
66649	4	336116	5	NULL	NULL	0	NULL	sphingosine	Chemical		inhibits		strongly			MAPK	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_346	9415703	In the primary induction of apoptosis, we found that (a) ceramide strongly stimulates SAPK and weakly inhibits MAPK, whereas (b) sphingosine weakly stimulates SAPK but strongly inhibits MAPK.	transcription
66650	5	336116	5	NULL	NULL	0	NULL	statement 1	Process		occurs during					apoptosis	Process	primary induction of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_346	9415703	In the primary induction of apoptosis, we found that (a) ceramide strongly stimulates SAPK and weakly inhibits MAPK, whereas (b) sphingosine weakly stimulates SAPK but strongly inhibits MAPK.	transcription
66651	6	336116	5	NULL	NULL	0	NULL	statement 2	Process		occurs during					apoptosis	Process	primary induction of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_346	9415703	In the primary induction of apoptosis, we found that (a) ceramide strongly stimulates SAPK and weakly inhibits MAPK, whereas (b) sphingosine weakly stimulates SAPK but strongly inhibits MAPK.	transcription
66652	7	336116	5	NULL	NULL	0	NULL	statement 3	Process		occurs during					apoptosis	Process	primary induction of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_346	9415703	In the primary induction of apoptosis, we found that (a) ceramide strongly stimulates SAPK and weakly inhibits MAPK, whereas (b) sphingosine weakly stimulates SAPK but strongly inhibits MAPK.	transcription
66653	8	336116	5	NULL	NULL	0	NULL	statement 4	Process		occurs during					apoptosis	Process	primary induction of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_346	9415703	In the primary induction of apoptosis, we found that (a) ceramide strongly stimulates SAPK and weakly inhibits MAPK, whereas (b) sphingosine weakly stimulates SAPK but strongly inhibits MAPK.	transcription
67735	1	336116	7	NULL	NULL	0	NULL	ceramide	Chemical		stimulate		strongly			SAPK	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_346	9415703	In the primary induction of apoptosis, we found that (a) ceramide strongly stimulates SAPK and weakly inhibits MAPK, whereas (b) sphingosine weakly stimulates SAPK but strongly inhibits MAPK.	transcription
67736	2	336116	7	NULL	NULL	0	NULL	ceramide	Chemical		inhibit		weakly			MAPK	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_346	9415703	In the primary induction of apoptosis, we found that (a) ceramide strongly stimulates SAPK and weakly inhibits MAPK, whereas (b) sphingosine weakly stimulates SAPK but strongly inhibits MAPK.	transcription
67737	3	336116	7	NULL	NULL	0	NULL	sphingosine	Chemical		stimulate		weakly			MAPK	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_346	9415703	In the primary induction of apoptosis, we found that (a) ceramide strongly stimulates SAPK and weakly inhibits MAPK, whereas (b) sphingosine weakly stimulates SAPK but strongly inhibits MAPK.	transcription
67738	4	336116	7	NULL	NULL	0	NULL	sphingosine	Chemical		inhibit		strongly			MAPK	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_346	9415703	In the primary induction of apoptosis, we found that (a) ceramide strongly stimulates SAPK and weakly inhibits MAPK, whereas (b) sphingosine weakly stimulates SAPK but strongly inhibits MAPK.	transcription
67739	5	336116	7	NULL	NULL	0	NULL	statement 1	Process		occur during					apoptosis	Process	primary induction of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_346	9415703	In the primary induction of apoptosis, we found that (a) ceramide strongly stimulates SAPK and weakly inhibits MAPK, whereas (b) sphingosine weakly stimulates SAPK but strongly inhibits MAPK.	transcription
67740	6	336116	7	NULL	NULL	0	NULL	statement 2	Process		occur during					apoptosis	Process	primary induction of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_346	9415703	In the primary induction of apoptosis, we found that (a) ceramide strongly stimulates SAPK and weakly inhibits MAPK, whereas (b) sphingosine weakly stimulates SAPK but strongly inhibits MAPK.	transcription
67741	7	336116	7	NULL	NULL	0	NULL	statement 3	Process		occur during					apoptosis	Process	primary induction of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_346	9415703	In the primary induction of apoptosis, we found that (a) ceramide strongly stimulates SAPK and weakly inhibits MAPK, whereas (b) sphingosine weakly stimulates SAPK but strongly inhibits MAPK.	transcription
67742	8	336116	7	NULL	NULL	0	NULL	statement 4	Process		occur during					apoptosis	Process	primary induction of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_346	9415703	In the primary induction of apoptosis, we found that (a) ceramide strongly stimulates SAPK and weakly inhibits MAPK, whereas (b) sphingosine weakly stimulates SAPK but strongly inhibits MAPK.	transcription
66654	1	336117	5	NULL	NULL	0	NULL	LPS	Chemical		induce					ceramide	Chemical	level of			NULL	old mice	0	NULL	NULL	NULL	gw60_jbiolchem_277_34_30784_s_5	12072440	Furthermore, the results show that LPS-induced ceramide levels from the old mice are significantly higher than those of young mice, whereas there is no age-related difference in concentration of its down stream metabolite, sphingosine.	transcription
66655	2	336117	5	NULL	NULL	0	NULL	LPS	Chemical		induce					ceramide	Chemical	level of			NULL	young mice	0	NULL	NULL	NULL	gw60_jbiolchem_277_34_30784_s_5	12072440	Furthermore, the results show that LPS-induced ceramide levels from the old mice are significantly higher than those of young mice, whereas there is no age-related difference in concentration of its down stream metabolite, sphingosine.	transcription
66656	3	336117	5	NULL	NULL	0	NULL	statement 1	Process		is higher than		significantly			statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_34_30784_s_5	12072440	Furthermore, the results show that LPS-induced ceramide levels from the old mice are significantly higher than those of young mice, whereas there is no age-related difference in concentration of its down stream metabolite, sphingosine.	transcription
67743	1	336117	7	NULL	NULL	0	NULL	LPS	Chemical		induce					ceramide	Chemical	levels of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_34_30784_s_5	12072440	Furthermore, the results show that LPS-induced ceramide levels from the old mice are significantly higher than those of young mice, whereas there is no age-related difference in concentration of its down stream metabolite, sphingosine.	transcription
66739	1	336118	5	NULL	NULL	0	NULL	TNF-alpha	GP		stimulates					GTPCH	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_33	11815603	As TNF-alpha stimulates GTPCH expression via a ceramide-independent pathway ( 12) and increases SPP levels ( 17-19), it was of interest to investigate the role of sphingosine kinase and SPP in the regulation of GTPCH and BH4 biosynthesis.	transcription
66740	2	336118	5	NULL	NULL	0	NULL	statement 1	Process		via					ceramide-independent pathway	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_33	11815603	As TNF-alpha stimulates GTPCH expression via a ceramide-independent pathway ( 12) and increases SPP levels ( 17-19), it was of interest to investigate the role of sphingosine kinase and SPP in the regulation of GTPCH and BH4 biosynthesis.	transcription
66741	3	336118	5	NULL	NULL	0	NULL	statement 1	Process		increases					SPP	Chemical	level of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_33	11815603	As TNF-alpha stimulates GTPCH expression via a ceramide-independent pathway ( 12) and increases SPP levels ( 17-19), it was of interest to investigate the role of sphingosine kinase and SPP in the regulation of GTPCH and BH4 biosynthesis.	transcription
66742	4	336118	5	NULL	NULL	NULL	NULL	sphingosine kinase	GP		regulates		potentially			GTPCH	GP	biosynthesis of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_33	11815603	As TNF-alpha stimulates GTPCH expression via a ceramide-independent pathway ( 12) and increases SPP levels ( 17-19), it was of interest to investigate the role of sphingosine kinase and SPP in the regulation of GTPCH and BH4 biosynthesis.	transcription
66743	5	336118	5	NULL	NULL	NULL	NULL	sphingosine kinase	GP		regulates		potentially			BH4	Chemical	biosynthesis of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_33	11815603	As TNF-alpha stimulates GTPCH expression via a ceramide-independent pathway ( 12) and increases SPP levels ( 17-19), it was of interest to investigate the role of sphingosine kinase and SPP in the regulation of GTPCH and BH4 biosynthesis.	transcription
66744	6	336118	5	NULL	NULL	0	NULL	SPP	Chemical		regulates		potentially			GTPCH	GP	biosynthesis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_33	11815603	As TNF-alpha stimulates GTPCH expression via a ceramide-independent pathway ( 12) and increases SPP levels ( 17-19), it was of interest to investigate the role of sphingosine kinase and SPP in the regulation of GTPCH and BH4 biosynthesis.	transcription
66745	7	336118	5	NULL	NULL	0	NULL	SPP	Chemical		regulates		potentially			BH4	Chemical	biosynthesis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_33	11815603	As TNF-alpha stimulates GTPCH expression via a ceramide-independent pathway ( 12) and increases SPP levels ( 17-19), it was of interest to investigate the role of sphingosine kinase and SPP in the regulation of GTPCH and BH4 biosynthesis.	transcription
67744	1	336118	7	NULL	NULL	0	NULL	TNF-alpha	GP		stimulate					GTPCH	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_33	11815603	As TNF-alpha stimulates GTPCH expression via a ceramide-independent pathway ( 12) and increases SPP levels ( 17-19), it was of interest to investigate the role of sphingosine kinase and SPP in the regulation of GTPCH and BH4 biosynthesis.	transcription
67745	2	336118	7	NULL	NULL	0	NULL	statement 1	Process		via					ceramide-independent pathway	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_33	11815603	As TNF-alpha stimulates GTPCH expression via a ceramide-independent pathway ( 12) and increases SPP levels ( 17-19), it was of interest to investigate the role of sphingosine kinase and SPP in the regulation of GTPCH and BH4 biosynthesis.	transcription
67746	3	336118	7	NULL	NULL	0	NULL	statement 1	Process		increase					SPP 	Chemical	levels of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_33	11815603	As TNF-alpha stimulates GTPCH expression via a ceramide-independent pathway ( 12) and increases SPP levels ( 17-19), it was of interest to investigate the role of sphingosine kinase and SPP in the regulation of GTPCH and BH4 biosynthesis.	transcription
66756	1	336119	5	NULL	NULL	NULL	NULL	long chain ceramide	Chemical	generation of	in response to					C6-ceramide	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_163	11815611	Therefore, these results further demonstrate that the generation of endogenous long chain ceramide formation in response to C6-ceramide is not via the activation of the  de novo pathway but involves the recycling of the sphingosine backbone following deacylation and reacylation, a process inhibited by FB1.	transcription
66757	2	336119	5	NULL	NULL	NULL	NULL	statement 1	Process		is not via					de novo pathway	Process	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_163	11815611	Therefore, these results further demonstrate that the generation of endogenous long chain ceramide formation in response to C6-ceramide is not via the activation of the  de novo pathway but involves the recycling of the sphingosine backbone following deacylation and reacylation, a process inhibited by FB1.	transcription
66758	3	336119	5	NULL	NULL	0	NULL	statement 1	Process		involves					sphingosine backbone	Chemical	recycling of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_163	11815611	Therefore, these results further demonstrate that the generation of endogenous long chain ceramide formation in response to C6-ceramide is not via the activation of the  de novo pathway but involves the recycling of the sphingosine backbone following deacylation and reacylation, a process inhibited by FB1.	transcription
66759	4	336119	5	NULL	NULL	0	NULL	statement 3	Process		followed by					ceramide	Chemical	deacylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_163	11815611	Therefore, these results further demonstrate that the generation of endogenous long chain ceramide formation in response to C6-ceramide is not via the activation of the  de novo pathway but involves the recycling of the sphingosine backbone following deacylation and reacylation, a process inhibited by FB1.	transcription
66760	5	336119	5	NULL	NULL	0	NULL	statement 3	Process		followed by					ceramide	Chemical	reacylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_163	11815611	Therefore, these results further demonstrate that the generation of endogenous long chain ceramide formation in response to C6-ceramide is not via the activation of the  de novo pathway but involves the recycling of the sphingosine backbone following deacylation and reacylation, a process inhibited by FB1.	transcription
66761	6	336119	5	NULL	NULL	0	NULL	FB1	Chemical		inhibits					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_163	11815611	Therefore, these results further demonstrate that the generation of endogenous long chain ceramide formation in response to C6-ceramide is not via the activation of the  de novo pathway but involves the recycling of the sphingosine backbone following deacylation and reacylation, a process inhibited by FB1.	transcription
67747	1	336119	7	NULL	NULL	0	NULL	 long chain ceramide	Chemical	formation of;;endogenous	in response to					C6-ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_163	11815611	Therefore, these results further demonstrate that the generation of endogenous long chain ceramide formation in response to C6-ceramide is not via the activation of the  de novo pathway but involves the recycling of the sphingosine backbone following deacylation and reacylation, a process inhibited by FB1.	transcription
67748	2	336119	7	NULL	NULL	0	NULL	statement 1	Process		not via					de novo pathway	Process	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_163	11815611	Therefore, these results further demonstrate that the generation of endogenous long chain ceramide formation in response to C6-ceramide is not via the activation of the  de novo pathway but involves the recycling of the sphingosine backbone following deacylation and reacylation, a process inhibited by FB1.	transcription
67749	3	336119	7	NULL	NULL	NULL	NULL	statement 1	Process		involves					sphingosine backbone	Chemical	recycling of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_163	11815611	Therefore, these results further demonstrate that the generation of endogenous long chain ceramide formation in response to C6-ceramide is not via the activation of the  de novo pathway but involves the recycling of the sphingosine backbone following deacylation and reacylation, a process inhibited by FB1.	transcription
67750	4	336119	7	NULL	NULL	0	NULL	FB1	Chemical		inhibit					sphingosine backbone	Chemical	deacylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_163	11815611	Therefore, these results further demonstrate that the generation of endogenous long chain ceramide formation in response to C6-ceramide is not via the activation of the  de novo pathway but involves the recycling of the sphingosine backbone following deacylation and reacylation, a process inhibited by FB1.	transcription
67751	5	336119	7	NULL	NULL	0	NULL	FB1	Chemical		inhibit					sphingosine backbone	Chemical	reacylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_163	11815611	Therefore, these results further demonstrate that the generation of endogenous long chain ceramide formation in response to C6-ceramide is not via the activation of the  de novo pathway but involves the recycling of the sphingosine backbone following deacylation and reacylation, a process inhibited by FB1.	transcription
66762	1	336120	5	NULL	NULL	0	NULL	MFs	Cell	human	undergoes					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_117	12138095	Indeed, both ceramide and sphingosine induced apoptosis of human hMFs, as shown by increased nuclei fragmentation (Fig.  3 A), DNA laddering (Fig.  3 B), and decreased cell viability (Fig.  3 C).	transcription
66763	2	336120	5	NULL	NULL	0	NULL	ceramide	Chemical		induce					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_117	12138095	Indeed, both ceramide and sphingosine induced apoptosis of human hMFs, as shown by increased nuclei fragmentation (Fig.  3 A), DNA laddering (Fig.  3 B), and decreased cell viability (Fig.  3 C).	transcription
66764	3	336120	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_117	12138095	Indeed, both ceramide and sphingosine induced apoptosis of human hMFs, as shown by increased nuclei fragmentation (Fig.  3 A), DNA laddering (Fig.  3 B), and decreased cell viability (Fig.  3 C).	transcription
67752	1	336120	7	NULL	NULL	NULL	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL	human hMFs	NULL	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_117	12138095	Indeed, both ceramide and sphingosine induced apoptosis of human hMFs, as shown by increased nuclei fragmentation (Fig.  3 A), DNA laddering (Fig.  3 B), and decreased cell viability (Fig.  3 C).	transcription
67753	2	336120	7	NULL	NULL	0	NULL	sphingosine	Chemical		induce					apoptosis	Process				NULL	human hMFs	0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_117	12138095	Indeed, both ceramide and sphingosine induced apoptosis of human hMFs, as shown by increased nuclei fragmentation (Fig.  3 A), DNA laddering (Fig.  3 B), and decreased cell viability (Fig.  3 C).	transcription
66765	1	336121	5	NULL	NULL	0	NULL	ceramide	Chemical	apoptotic effects of	requires					S1P	Chemical	high micromolar concentrations of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_119	12138095	As shown in Fig.  3 C, apoptotic effects of ceramide and sphingosine required high micromolar concentrations like S1P, arguing against an apoptotic effect of S1P related to metabolite conversion.	transcription
66766	2	336121	5	NULL	NULL	0	NULL	sphingosine	Chemical	apoptotic effects of	requires					S1P	Chemical	high micromolar concentrations of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_119	12138095	As shown in Fig.  3 C, apoptotic effects of ceramide and sphingosine required high micromolar concentrations like S1P, arguing against an apoptotic effect of S1P related to metabolite conversion.	transcription
67754	1	336121	7	NULL	NULL	0	NULL	ceramide	Chemical	apoptotic effects of 	require					S1P	Chemical	high concentration of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_119	12138095	As shown in Fig.  3 C, apoptotic effects of ceramide and sphingosine required high micromolar concentrations like S1P, arguing against an apoptotic effect of S1P related to metabolite conversion.	transcription
67755	2	336121	7	NULL	NULL	0	NULL	sphingosine	Chemical	apoptotic effects of 	require					S1P	Chemical	high concentration of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_40_37323_s_119	12138095	As shown in Fig.  3 C, apoptotic effects of ceramide and sphingosine required high micromolar concentrations like S1P, arguing against an apoptotic effect of S1P related to metabolite conversion.	transcription
66767	1	336122	5	NULL	NULL	0	NULL	DGKgamma	GP	human	catalyzes					diacylglycerol	Chemical	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_126	11956206	In comparison with human DGKgamma, bacterial DGK, and human SPK1, these lysates were enriched in specific ATP-dependent ceramide-phosphorylating activity and did not significantly catalyze the phosphorylation of diacylglycerol or sphingosine (Fig.  2 A).	transcription
66768	2	336122	5	NULL	NULL	0	NULL	DGKgamma	GP	human	catalyzes					sphingosine	Chemical	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_126	11956206	In comparison with human DGKgamma, bacterial DGK, and human SPK1, these lysates were enriched in specific ATP-dependent ceramide-phosphorylating activity and did not significantly catalyze the phosphorylation of diacylglycerol or sphingosine (Fig.  2 A).	transcription
66769	3	336122	5	NULL	NULL	0	NULL	DGK	GP	bacterial	catalyzes					diacylglycerol	Chemical	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_126	11956206	In comparison with human DGKgamma, bacterial DGK, and human SPK1, these lysates were enriched in specific ATP-dependent ceramide-phosphorylating activity and did not significantly catalyze the phosphorylation of diacylglycerol or sphingosine (Fig.  2 A).	transcription
66770	4	336122	5	NULL	NULL	0	NULL	DGK	GP	bacterial	catalyzes					sphingosine	Chemical	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_126	11956206	In comparison with human DGKgamma, bacterial DGK, and human SPK1, these lysates were enriched in specific ATP-dependent ceramide-phosphorylating activity and did not significantly catalyze the phosphorylation of diacylglycerol or sphingosine (Fig.  2 A).	transcription
66771	5	336122	5	NULL	NULL	0	NULL	SPK1	GP	human	catalyzes					diacylglycerol	Chemical	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_126	11956206	In comparison with human DGKgamma, bacterial DGK, and human SPK1, these lysates were enriched in specific ATP-dependent ceramide-phosphorylating activity and did not significantly catalyze the phosphorylation of diacylglycerol or sphingosine (Fig.  2 A).	transcription
66772	6	336122	5	NULL	NULL	0	NULL	SPK1	GP	human	catalyzes					sphingosine	Chemical	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_26_23294_s_126	11956206	In comparison with human DGKgamma, bacterial DGK, and human SPK1, these lysates were enriched in specific ATP-dependent ceramide-phosphorylating activity and did not significantly catalyze the phosphorylation of diacylglycerol or sphingosine (Fig.  2 A).	transcription
66773	1	336123	5	NULL	NULL	0	NULL	(CHO)1 cells	Cell		is					Chinese hamster ovary 1 cells	Cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4046_s_24	11058589	Here we show that short chain ceramide analogs and sphingosine inhibit Na+/Ca2+ exchange activity in transfected Chinese hamster ovary (CHO)1 cells expressing the bovine or canine cardiac Na+/Ca2+ exchangers.	transcription
66776	2	336123	5	NULL	NULL	0	NULL	short chain ceramide analogs	Chemical		inhibits					Na+/Ca2+ exchange activity	Process				NULL	transfected Chinese hamster ovary (CHO)1 cells expressing bovine cardiac Na+/Ca2+ exchangers	0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4046_s_24	11058589	Here we show that short chain ceramide analogs and sphingosine inhibit Na+/Ca2+ exchange activity in transfected Chinese hamster ovary (CHO)1 cells expressing the bovine or canine cardiac Na+/Ca2+ exchangers.	transcription
66777	3	336123	5	NULL	NULL	0	NULL	short chain ceramide analogs	Chemical		inhibits					Na+/Ca2+ exchange activity	Process				NULL	transfected Chinese hamster ovary (CHO)1 cells expressing canine cardiac Na+/Ca2+ exchangers	0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4046_s_24	11058589	Here we show that short chain ceramide analogs and sphingosine inhibit Na+/Ca2+ exchange activity in transfected Chinese hamster ovary (CHO)1 cells expressing the bovine or canine cardiac Na+/Ca2+ exchangers.	transcription
66778	4	336123	5	NULL	NULL	0	NULL	sphingosine	Chemical		inhibits					Na+/Ca2+ exchange activity	Process				NULL	transfected Chinese hamster ovary (CHO)1 cells expressing bovine cardiac Na+/Ca2+ exchangers	0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4046_s_24	11058589	Here we show that short chain ceramide analogs and sphingosine inhibit Na+/Ca2+ exchange activity in transfected Chinese hamster ovary (CHO)1 cells expressing the bovine or canine cardiac Na+/Ca2+ exchangers.	transcription
66779	5	336123	5	NULL	NULL	0	NULL	sphingosine	Chemical		inhibits					Na+/Ca2+ exchange activity	Process				NULL	transfected Chinese hamster ovary (CHO)1 cells expressing canine cardiac Na+/Ca2+ exchangers	0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4046_s_24	11058589	Here we show that short chain ceramide analogs and sphingosine inhibit Na+/Ca2+ exchange activity in transfected Chinese hamster ovary (CHO)1 cells expressing the bovine or canine cardiac Na+/Ca2+ exchangers.	transcription
67759	1	336123	7	NULL	NULL	0	NULL	short chain ceramide analogs	Chemical		inhibit					Na+/Ca2+ exchange activity 	Process				NULL	(CHO)1 cells expressing the bovine cardiac Na+/Ca2+ exchangers	0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4046_s_24	11058589	Here we show that short chain ceramide analogs and sphingosine inhibit Na+/Ca2+ exchange activity in transfected Chinese hamster ovary (CHO)1 cells expressing the bovine or canine cardiac Na+/Ca2+ exchangers.	transcription
67760	2	336123	7	NULL	NULL	0	NULL	short chain ceramide analogs	Chemical		inhibit					Na+/Ca2+ exchange activity	Process				NULL	(CHO)1 cells expressing the canine cardiac Na+/Ca2+ exchangers	0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4046_s_24	11058589	Here we show that short chain ceramide analogs and sphingosine inhibit Na+/Ca2+ exchange activity in transfected Chinese hamster ovary (CHO)1 cells expressing the bovine or canine cardiac Na+/Ca2+ exchangers.	transcription
67761	3	336123	7	NULL	NULL	0	NULL	sphingosine	Chemical		inhibit					Na+/Ca2+ exchange activity	Process				NULL	(CHO)1 cells expressing the bovine cardiac Na+/Ca2+ exchangers	0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4046_s_24	11058589	Here we show that short chain ceramide analogs and sphingosine inhibit Na+/Ca2+ exchange activity in transfected Chinese hamster ovary (CHO)1 cells expressing the bovine or canine cardiac Na+/Ca2+ exchangers.	transcription
67762	4	336123	7	NULL	NULL	0	NULL	sphingosine	Chemical		inhibit					Na+/Ca2+ exchange activity 	Process				NULL	(CHO)1 cells expressing the canine cardiac Na+/Ca2+ exchangers	0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4046_s_24	11058589	Here we show that short chain ceramide analogs and sphingosine inhibit Na+/Ca2+ exchange activity in transfected Chinese hamster ovary (CHO)1 cells expressing the bovine or canine cardiac Na+/Ca2+ exchangers.	transcription
67763	5	336123	7	NULL	NULL	0	NULL	(CHO)1 cells	Cell		is					Chinese hamster ovary cells	Cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_6_4046_s_24	11058589	Here we show that short chain ceramide analogs and sphingosine inhibit Na+/Ca2+ exchange activity in transfected Chinese hamster ovary (CHO)1 cells expressing the bovine or canine cardiac Na+/Ca2+ exchangers.	transcription
66780	1	336124	5	NULL	NULL	0	NULL	C2-ceramide	Chemical	treatment;;exogenous	leads to					cell death	Process				NULL	LM cells	0	NULL	NULL	NULL	gw60_jbiolchem_276_29_27129_s_5	11369765	Treatment with exogenous C2-ceramide and sphingosine led to cell death in both LM and LME6, and treatment of the LME6 cells with MNNG resulted in a transient increase in intracellular ceramide of ~50% over a period of 3 h.	transcription
66781	2	336124	5	NULL	NULL	0	NULL	C2-ceramide	Chemical	treatment;;exogenous	leads to					cell death	Process				NULL	LME6 cells	0	NULL	NULL	NULL	gw60_jbiolchem_276_29_27129_s_5	11369765	Treatment with exogenous C2-ceramide and sphingosine led to cell death in both LM and LME6, and treatment of the LME6 cells with MNNG resulted in a transient increase in intracellular ceramide of ~50% over a period of 3 h.	transcription
66782	3	336124	5	NULL	NULL	0	NULL	sphingosine	Chemical	treatment	leads to					cell death	Process				NULL	LM cells	0	NULL	NULL	NULL	gw60_jbiolchem_276_29_27129_s_5	11369765	Treatment with exogenous C2-ceramide and sphingosine led to cell death in both LM and LME6, and treatment of the LME6 cells with MNNG resulted in a transient increase in intracellular ceramide of ~50% over a period of 3 h.	transcription
66783	4	336124	5	NULL	NULL	0	NULL	sphingosine	Chemical	treatment	leads to					cell death	Process				NULL	LME6 cells	0	NULL	NULL	NULL	gw60_jbiolchem_276_29_27129_s_5	11369765	Treatment with exogenous C2-ceramide and sphingosine led to cell death in both LM and LME6, and treatment of the LME6 cells with MNNG resulted in a transient increase in intracellular ceramide of ~50% over a period of 3 h.	transcription
66784	5	336124	5	NULL	NULL	0	NULL	MNNG	Chemical	treatment	results in					ceramide	Chemical	transient increase in;;intracellular			NULL	LME6 cells	0	NULL	NULL	NULL	gw60_jbiolchem_276_29_27129_s_5	11369765	Treatment with exogenous C2-ceramide and sphingosine led to cell death in both LM and LME6, and treatment of the LME6 cells with MNNG resulted in a transient increase in intracellular ceramide of ~50% over a period of 3 h.	transcription
67764	1	336124	7	NULL	NULL	NULL	NULL	C2-ceramide 	Chemical	exogenous	lead to					cell death	Process				NULL	LM 	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_27129_s_5	11369765	Treatment with exogenous C2-ceramide and sphingosine led to cell death in both LM and LME6, and treatment of the LME6 cells with MNNG resulted in a transient increase in intracellular ceramide of ~50% over a period of 3 h.	transcription
67765	2	336124	7	NULL	NULL	0	NULL	C2-ceramide	Chemical	exogenous	lead to					cell death	Process				NULL	LME6 cells	0	NULL	NULL	NULL	gw60_jbiolchem_276_29_27129_s_5	11369765	Treatment with exogenous C2-ceramide and sphingosine led to cell death in both LM and LME6, and treatment of the LME6 cells with MNNG resulted in a transient increase in intracellular ceramide of ~50% over a period of 3 h.	transcription
67766	3	336124	7	NULL	NULL	NULL	NULL	sphingosine	Chemical	exogenous	lead to					cell death	Process				NULL	LM	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_27129_s_5	11369765	Treatment with exogenous C2-ceramide and sphingosine led to cell death in both LM and LME6, and treatment of the LME6 cells with MNNG resulted in a transient increase in intracellular ceramide of ~50% over a period of 3 h.	transcription
67767	4	336124	7	NULL	NULL	0	NULL	sphingosine	Chemical	exogenous	lead to					cell death	Process				NULL	LME6 cells	0	NULL	NULL	NULL	gw60_jbiolchem_276_29_27129_s_5	11369765	Treatment with exogenous C2-ceramide and sphingosine led to cell death in both LM and LME6, and treatment of the LME6 cells with MNNG resulted in a transient increase in intracellular ceramide of ~50% over a period of 3 h.	transcription
67768	5	336124	7	NULL	NULL	NULL	NULL	MNNG	Chemical		increase					ceramide	Chemical	intracellular			NULL	LME6 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_276_29_27129_s_5	11369765	Treatment with exogenous C2-ceramide and sphingosine led to cell death in both LM and LME6, and treatment of the LME6 cells with MNNG resulted in a transient increase in intracellular ceramide of ~50% over a period of 3 h.	transcription
66785	1	336125	5	NULL	NULL	NULL	NULL	UV irradiation			activates		dose dependently			AP-1	GP	transactivation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_50	9346918	The results showed that, in addition to UV irradiation, both SMase and C2-ceramide induced the transactivation of AP-1 activity in a dose-dependent manner (Fig.  1), whereas sphingosine, a metabolite of ceramide, did not induce AP-1 activity (Fig.  1).	transcription
66786	2	336125	5	NULL	NULL	NULL	NULL	SMase	GP		activates		dose dependently			AP-1	GP	transactivation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_50	9346918	The results showed that, in addition to UV irradiation, both SMase and C2-ceramide induced the transactivation of AP-1 activity in a dose-dependent manner (Fig.  1), whereas sphingosine, a metabolite of ceramide, did not induce AP-1 activity (Fig.  1).	transcription
66787	3	336125	5	NULL	NULL	0	NULL	C2-ceramide	Chemical		activates		dose dependently			AP-1	GP	transactivation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_50	9346918	The results showed that, in addition to UV irradiation, both SMase and C2-ceramide induced the transactivation of AP-1 activity in a dose-dependent manner (Fig.  1), whereas sphingosine, a metabolite of ceramide, did not induce AP-1 activity (Fig.  1).	transcription
66788	4	336125	5	NULL	NULL	0	NULL	sphingosine	Chemical		is a metabolite of					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_50	9346918	The results showed that, in addition to UV irradiation, both SMase and C2-ceramide induced the transactivation of AP-1 activity in a dose-dependent manner (Fig.  1), whereas sphingosine, a metabolite of ceramide, did not induce AP-1 activity (Fig.  1).	transcription
66789	5	336125	5	NULL	NULL	0	NULL	sphingosine	Chemical		does not activate					AP-1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_50	9346918	The results showed that, in addition to UV irradiation, both SMase and C2-ceramide induced the transactivation of AP-1 activity in a dose-dependent manner (Fig.  1), whereas sphingosine, a metabolite of ceramide, did not induce AP-1 activity (Fig.  1).	transcription
67769	1	336125	7	NULL	NULL	0	NULL	SMase	GP		induce		dose-dependently			AP-1 activity 	Process	transactivation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_50	9346918	The results showed that, in addition to UV irradiation, both SMase and C2-ceramide induced the transactivation of AP-1 activity in a dose-dependent manner (Fig.  1), whereas sphingosine, a metabolite of ceramide, did not induce AP-1 activity (Fig.  1).	transcription
67770	2	336125	7	NULL	NULL	NULL	NULL	C2-ceramide	Chemical		induce		dose-dependently			AP-1 activity 	Process	transactivation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_50	9346918	The results showed that, in addition to UV irradiation, both SMase and C2-ceramide induced the transactivation of AP-1 activity in a dose-dependent manner (Fig.  1), whereas sphingosine, a metabolite of ceramide, did not induce AP-1 activity (Fig.  1).	transcription
67771	3	336125	7	NULL	NULL	0	NULL	sphingosine	Chemical		is a metabolite of					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_50	9346918	The results showed that, in addition to UV irradiation, both SMase and C2-ceramide induced the transactivation of AP-1 activity in a dose-dependent manner (Fig.  1), whereas sphingosine, a metabolite of ceramide, did not induce AP-1 activity (Fig.  1).	transcription
67772	4	336125	7	NULL	NULL	0	NULL	sphingosine	Chemical		does not induce					AP-1 activity 	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27753_s_50	9346918	The results showed that, in addition to UV irradiation, both SMase and C2-ceramide induced the transactivation of AP-1 activity in a dose-dependent manner (Fig.  1), whereas sphingosine, a metabolite of ceramide, did not induce AP-1 activity (Fig.  1).	transcription
66790	1	336126	5	NULL	NULL	0	NULL	ceramide	Chemical		is converted to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4836_s_133	9030540	Next, to determine whether blocking the conversion of ceramide to sphingosine would abrogate the negative inotropic effects of TNF-alpha, the cells were pretreated (60 min) with a specific inhibitor of ceramidase:  n-oleoylethanolamine (NOE) ( 28).	transcription
66791	2	336126	5	NULL	NULL	0	NULL	statement 1	Process	blocking of	abrogates		possibly			TNF-alpha	GP	negative inotropic effects of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4836_s_133	9030540	Next, to determine whether blocking the conversion of ceramide to sphingosine would abrogate the negative inotropic effects of TNF-alpha, the cells were pretreated (60 min) with a specific inhibitor of ceramidase:  n-oleoylethanolamine (NOE) ( 28).	transcription
66792	3	336126	5	NULL	NULL	NULL	NULL	NOE	Chemical		is					n-oleoylethanolamine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_8_4836_s_133	9030540	Next, to determine whether blocking the conversion of ceramide to sphingosine would abrogate the negative inotropic effects of TNF-alpha, the cells were pretreated (60 min) with a specific inhibitor of ceramidase:  n-oleoylethanolamine (NOE) ( 28).	transcription
66793	4	336126	5	NULL	NULL	0	NULL	NOE	Chemical		is an inhibitor of					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4836_s_133	9030540	Next, to determine whether blocking the conversion of ceramide to sphingosine would abrogate the negative inotropic effects of TNF-alpha, the cells were pretreated (60 min) with a specific inhibitor of ceramidase:  n-oleoylethanolamine (NOE) ( 28).	transcription
67773	1	336126	7	NULL	NULL	0	NULL	NOE	Chemical		is an inhibitor of					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4836_s_133	9030540	Next, to determine whether blocking the conversion of ceramide to sphingosine would abrogate the negative inotropic effects of TNF-alpha, the cells were pretreated (60 min) with a specific inhibitor of ceramidase:  n-oleoylethanolamine (NOE) ( 28).	transcription
67774	2	336126	7	NULL	NULL	0	NULL	NOE	Chemical		is dependent on					n-oleoylethanolamine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4836_s_133	9030540	Next, to determine whether blocking the conversion of ceramide to sphingosine would abrogate the negative inotropic effects of TNF-alpha, the cells were pretreated (60 min) with a specific inhibitor of ceramidase:  n-oleoylethanolamine (NOE) ( 28).	transcription
66794	1	336127	5	NULL	NULL	0	NULL	PAP2	GP	rat;;liver	is inhibited by					lyso-PA	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10361_s_9	9099673	Like rat liver PAP2, the Mg2+-independent PA phosphatase activity of DGPP phosphatase purified from  S. cerevisiae was inhibited by lyso-PA, sphingosine 1-phosphate, and ceramide 1-phosphate.	transcription
66795	2	336127	5	NULL	NULL	0	NULL	PAP2	GP	rat;;liver	is inhibited by					sphingosine 1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10361_s_9	9099673	Like rat liver PAP2, the Mg2+-independent PA phosphatase activity of DGPP phosphatase purified from  S. cerevisiae was inhibited by lyso-PA, sphingosine 1-phosphate, and ceramide 1-phosphate.	transcription
66796	3	336127	5	NULL	NULL	0	NULL	PAP2	GP	rat;;liver	is inhibited by					ceramide-1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10361_s_9	9099673	Like rat liver PAP2, the Mg2+-independent PA phosphatase activity of DGPP phosphatase purified from  S. cerevisiae was inhibited by lyso-PA, sphingosine 1-phosphate, and ceramide 1-phosphate.	transcription
66797	4	336127	5	NULL	NULL	0	NULL	DGPP phosphatase	GP	S. cerevisiae	activates					PA phosphatase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10361_s_9	9099673	Like rat liver PAP2, the Mg2+-independent PA phosphatase activity of DGPP phosphatase purified from  S. cerevisiae was inhibited by lyso-PA, sphingosine 1-phosphate, and ceramide 1-phosphate.	transcription
66798	5	336127	5	NULL	NULL	0	NULL	statement 4	Process		is independent of					Mg2+	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10361_s_9	9099673	Like rat liver PAP2, the Mg2+-independent PA phosphatase activity of DGPP phosphatase purified from  S. cerevisiae was inhibited by lyso-PA, sphingosine 1-phosphate, and ceramide 1-phosphate.	transcription
66799	6	336127	5	NULL	NULL	0	NULL	statement 4	Process		is inhibited by					lyso-PA	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10361_s_9	9099673	Like rat liver PAP2, the Mg2+-independent PA phosphatase activity of DGPP phosphatase purified from  S. cerevisiae was inhibited by lyso-PA, sphingosine 1-phosphate, and ceramide 1-phosphate.	transcription
66800	7	336127	5	NULL	NULL	0	NULL	statement 4	Process		is inhibited by					sphingosine 1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10361_s_9	9099673	Like rat liver PAP2, the Mg2+-independent PA phosphatase activity of DGPP phosphatase purified from  S. cerevisiae was inhibited by lyso-PA, sphingosine 1-phosphate, and ceramide 1-phosphate.	transcription
66801	8	336127	5	NULL	NULL	0	NULL	statement 4	Process		is inhibited by					ceramide-1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10361_s_9	9099673	Like rat liver PAP2, the Mg2+-independent PA phosphatase activity of DGPP phosphatase purified from  S. cerevisiae was inhibited by lyso-PA, sphingosine 1-phosphate, and ceramide 1-phosphate.	transcription
67775	1	336127	7	NULL	NULL	NULL	NULL	DGPP phosphatase	GP	Mg2+-independent PA phosphatase activity of;; purified from S. cerevisiae	is independent of					Mg2+	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_16_10361_s_9	9099673	Like rat liver PAP2, the Mg2+-independent PA phosphatase activity of DGPP phosphatase purified from  S. cerevisiae was inhibited by lyso-PA, sphingosine 1-phosphate, and ceramide 1-phosphate.	transcription
67776	2	336127	7	NULL	NULL	0	NULL	lyso-PA	Chemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10361_s_9	9099673	Like rat liver PAP2, the Mg2+-independent PA phosphatase activity of DGPP phosphatase purified from  S. cerevisiae was inhibited by lyso-PA, sphingosine 1-phosphate, and ceramide 1-phosphate.	transcription
67777	3	336127	7	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10361_s_9	9099673	Like rat liver PAP2, the Mg2+-independent PA phosphatase activity of DGPP phosphatase purified from  S. cerevisiae was inhibited by lyso-PA, sphingosine 1-phosphate, and ceramide 1-phosphate.	transcription
67778	4	336127	7	NULL	NULL	0	NULL	ceramide 1-phosphate	Chemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_16_10361_s_9	9099673	Like rat liver PAP2, the Mg2+-independent PA phosphatase activity of DGPP phosphatase purified from  S. cerevisiae was inhibited by lyso-PA, sphingosine 1-phosphate, and ceramide 1-phosphate.	transcription
66802	1	336128	5	NULL	NULL	0	NULL	sphingosine	Chemical	elevation of;;endogenous	is caused by					fumonisin B1	Chemical	addition of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_9_5640_s_8	9038174	Elevation of endogenous sphinganine by a second method (addition of fumonisin B1, an inhibitor of ceramide synthase) also reduced [3]PDBu binding; therefore, elevations in sphingosine and sphinganine can both affect PKC.	transcription
66803	2	336128	5	NULL	NULL	0	NULL	fumonisin B1	Chemical		is an inhibitor of					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_9_5640_s_8	9038174	Elevation of endogenous sphinganine by a second method (addition of fumonisin B1, an inhibitor of ceramide synthase) also reduced [3]PDBu binding; therefore, elevations in sphingosine and sphinganine can both affect PKC.	transcription
66804	3	336128	5	NULL	NULL	0	NULL	statement 1	Process		reduce					PDBu	Chemical	binding of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_9_5640_s_8	9038174	Elevation of endogenous sphinganine by a second method (addition of fumonisin B1, an inhibitor of ceramide synthase) also reduced [3]PDBu binding; therefore, elevations in sphingosine and sphinganine can both affect PKC.	transcription
66805	4	336128	5	NULL	NULL	0	NULL	sphingosine	Chemical	elevation of	affect					PKC	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_9_5640_s_8	9038174	Elevation of endogenous sphinganine by a second method (addition of fumonisin B1, an inhibitor of ceramide synthase) also reduced [3]PDBu binding; therefore, elevations in sphingosine and sphinganine can both affect PKC.	transcription
66806	5	336128	5	NULL	NULL	0	NULL	sphinganine	Chemical	elevation of	affects					PKC	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_9_5640_s_8	9038174	Elevation of endogenous sphinganine by a second method (addition of fumonisin B1, an inhibitor of ceramide synthase) also reduced [3]PDBu binding; therefore, elevations in sphingosine and sphinganine can both affect PKC.	transcription
67779	1	336128	7	NULL	NULL	0	NULL	fumonisin B1	Chemical		is an inhibitor of					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_9_5640_s_8	9038174	Elevation of endogenous sphinganine by a second method (addition of fumonisin B1, an inhibitor of ceramide synthase) also reduced [3]PDBu binding; therefore, elevations in sphingosine and sphinganine can both affect PKC.	transcription
67780	2	336128	7	NULL	NULL	NULL	NULL	sphinganine 	Chemical	elevation of endogenous	reduce					PDBu	Chemical	binding of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_9_5640_s_8	9038174	Elevation of endogenous sphinganine by a second method (addition of fumonisin B1, an inhibitor of ceramide synthase) also reduced [3]PDBu binding; therefore, elevations in sphingosine and sphinganine can both affect PKC.	transcription
67781	3	336128	7	NULL	NULL	0	NULL	sphingosine	Chemical	elevation in	affect					PKC	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_9_5640_s_8	9038174	Elevation of endogenous sphinganine by a second method (addition of fumonisin B1, an inhibitor of ceramide synthase) also reduced [3]PDBu binding; therefore, elevations in sphingosine and sphinganine can both affect PKC.	transcription
67782	4	336128	7	NULL	NULL	NULL	NULL	sphinganine	Chemical	elevation in	affect					PKC	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_9_5640_s_8	9038174	Elevation of endogenous sphinganine by a second method (addition of fumonisin B1, an inhibitor of ceramide synthase) also reduced [3]PDBu binding; therefore, elevations in sphingosine and sphinganine can both affect PKC.	transcription
66807	1	336129	5	NULL	NULL	0	NULL	COS-7 cells	Cell		treated with					sphingomyelinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41201_s_249	10995762	We next wanted to determine whether transfected PDK1 could become activated in COS-7 cells treated for 30 min with 1 unit/ml sphingomyelinase, which catalyzes the breakdown of sphingomyelin to form ceramide and subsequently sphingosine.	transcription
66808	2	336129	5	NULL	NULL	0	NULL	PDK1	GP	transfected	is activated in		possibly			statement 1	Cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41201_s_249	10995762	We next wanted to determine whether transfected PDK1 could become activated in COS-7 cells treated for 30 min with 1 unit/ml sphingomyelinase, which catalyzes the breakdown of sphingomyelin to form ceramide and subsequently sphingosine.	transcription
66809	3	336129	5	NULL	NULL	0	NULL	sphingomyelin	Chemical		broken down into					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41201_s_249	10995762	We next wanted to determine whether transfected PDK1 could become activated in COS-7 cells treated for 30 min with 1 unit/ml sphingomyelinase, which catalyzes the breakdown of sphingomyelin to form ceramide and subsequently sphingosine.	transcription
66810	4	336129	5	NULL	NULL	0	NULL	sphingomyelin	Chemical		broken down into					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41201_s_249	10995762	We next wanted to determine whether transfected PDK1 could become activated in COS-7 cells treated for 30 min with 1 unit/ml sphingomyelinase, which catalyzes the breakdown of sphingomyelin to form ceramide and subsequently sphingosine.	transcription
66811	5	336129	5	NULL	NULL	0	NULL	statement 3	Process		subsequent to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41201_s_249	10995762	We next wanted to determine whether transfected PDK1 could become activated in COS-7 cells treated for 30 min with 1 unit/ml sphingomyelinase, which catalyzes the breakdown of sphingomyelin to form ceramide and subsequently sphingosine.	transcription
66812	6	336129	5	NULL	NULL	NULL	NULL	sphingomyelinase	GP		catalyzes					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41201_s_249	10995762	We next wanted to determine whether transfected PDK1 could become activated in COS-7 cells treated for 30 min with 1 unit/ml sphingomyelinase, which catalyzes the breakdown of sphingomyelin to form ceramide and subsequently sphingosine.	transcription
67783	1	336129	7	NULL	NULL	NULL	NULL	sphingomyelin	Chemical		forms					ceramide	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_52_41201_s_249	10995762	We next wanted to determine whether transfected PDK1 could become activated in COS-7 cells treated for 30 min with 1 unit/ml sphingomyelinase, which catalyzes the breakdown of sphingomyelin to form ceramide and subsequently sphingosine.	transcription
67784	2	336129	7	NULL	NULL	0	NULL	ceramide	Chemical		 forms		subsequently			sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41201_s_249	10995762	We next wanted to determine whether transfected PDK1 could become activated in COS-7 cells treated for 30 min with 1 unit/ml sphingomyelinase, which catalyzes the breakdown of sphingomyelin to form ceramide and subsequently sphingosine.	transcription
67785	3	336129	7	NULL	NULL	0	NULL	sphingomyelinase	GP		catalyze					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41201_s_249	10995762	We next wanted to determine whether transfected PDK1 could become activated in COS-7 cells treated for 30 min with 1 unit/ml sphingomyelinase, which catalyzes the breakdown of sphingomyelin to form ceramide and subsequently sphingosine.	transcription
67786	4	336129	7	NULL	NULL	0	NULL	sphingomyelinase	GP		catalyze					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_52_41201_s_249	10995762	We next wanted to determine whether transfected PDK1 could become activated in COS-7 cells treated for 30 min with 1 unit/ml sphingomyelinase, which catalyzes the breakdown of sphingomyelin to form ceramide and subsequently sphingosine.	transcription
66813	1	336130	5	NULL	NULL	0	NULL	ceramide	Chemical		is hydrolyzed to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_70	10747891	Sphingosine, the product of ceramide hydrolysis catalyzed by ceramidases, has been shown to be rapidly produced during TNFalpha-mediated apoptosis in human neutrophils ( 28) and rat cardiomyocytes ( 32).	transcription
66814	2	336130	5	NULL	NULL	0	NULL	ceramidases	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_70	10747891	Sphingosine, the product of ceramide hydrolysis catalyzed by ceramidases, has been shown to be rapidly produced during TNFalpha-mediated apoptosis in human neutrophils ( 28) and rat cardiomyocytes ( 32).	transcription
66815	3	336130	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					TNFalpha	GP				NULL	human neutrophils	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_70	10747891	Sphingosine, the product of ceramide hydrolysis catalyzed by ceramidases, has been shown to be rapidly produced during TNFalpha-mediated apoptosis in human neutrophils ( 28) and rat cardiomyocytes ( 32).	transcription
66816	4	336130	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					TNFalpha	GP				NULL	rat cardiomyocytes	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_70	10747891	Sphingosine, the product of ceramide hydrolysis catalyzed by ceramidases, has been shown to be rapidly produced during TNFalpha-mediated apoptosis in human neutrophils ( 28) and rat cardiomyocytes ( 32).	transcription
66817	5	336130	5	NULL	NULL	0	NULL	statement 3	Process		produce		rapidly			sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_70	10747891	Sphingosine, the product of ceramide hydrolysis catalyzed by ceramidases, has been shown to be rapidly produced during TNFalpha-mediated apoptosis in human neutrophils ( 28) and rat cardiomyocytes ( 32).	transcription
66818	6	336130	5	NULL	NULL	0	NULL	statement 4	Process		produce		rapidly			sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_70	10747891	Sphingosine, the product of ceramide hydrolysis catalyzed by ceramidases, has been shown to be rapidly produced during TNFalpha-mediated apoptosis in human neutrophils ( 28) and rat cardiomyocytes ( 32).	transcription
67787	1	336130	7	NULL	NULL	0	NULL	ceramide	Chemical	hydrolysis of	produce					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_70	10747891	Sphingosine, the product of ceramide hydrolysis catalyzed by ceramidases, has been shown to be rapidly produced during TNFalpha-mediated apoptosis in human neutrophils ( 28) and rat cardiomyocytes ( 32).	transcription
67788	2	336130	7	NULL	NULL	0	NULL	ceramidases	GP		catalyze					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_70	10747891	Sphingosine, the product of ceramide hydrolysis catalyzed by ceramidases, has been shown to be rapidly produced during TNFalpha-mediated apoptosis in human neutrophils ( 28) and rat cardiomyocytes ( 32).	transcription
67789	3	336130	7	NULL	NULL	NULL	NULL	TNFalpha	GP		mediate					apoptosis	Process				NULL	human neutrophils	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_70	10747891	Sphingosine, the product of ceramide hydrolysis catalyzed by ceramidases, has been shown to be rapidly produced during TNFalpha-mediated apoptosis in human neutrophils ( 28) and rat cardiomyocytes ( 32).	transcription
67790	4	336130	7	NULL	NULL	0	NULL	TNFalpha	GP		mediate					apoptosis	Process				NULL	rat cardiomyocytes	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_70	10747891	Sphingosine, the product of ceramide hydrolysis catalyzed by ceramidases, has been shown to be rapidly produced during TNFalpha-mediated apoptosis in human neutrophils ( 28) and rat cardiomyocytes ( 32).	transcription
67791	5	336130	7	NULL	NULL	0	NULL	statement 1	Process		occur during		rapidly			statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_70	10747891	Sphingosine, the product of ceramide hydrolysis catalyzed by ceramidases, has been shown to be rapidly produced during TNFalpha-mediated apoptosis in human neutrophils ( 28) and rat cardiomyocytes ( 32).	transcription
67792	6	336130	7	NULL	NULL	0	NULL	statement 1	Process		occur during		rapidly			statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_70	10747891	Sphingosine, the product of ceramide hydrolysis catalyzed by ceramidases, has been shown to be rapidly produced during TNFalpha-mediated apoptosis in human neutrophils ( 28) and rat cardiomyocytes ( 32).	transcription
66819	1	336131	5	NULL	NULL	0	NULL	Bcl-2	GP	overexpression of	protects against					apoptotic stimuli		diverse			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_106	10747891	Because overexpression of Bcl-2 or Bcl-xL protects against diverse apoptotic stimuli, including ceramide-induced apoptosis ( 41-46), it was important to determine whether the effects of sphingosine were also blocked by these proteins.	transcription
66820	2	336131	5	NULL	NULL	0	NULL	Bcl-xL	GP	overexpression of	protects against					apoptotic stimuli		diverse			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_106	10747891	Because overexpression of Bcl-2 or Bcl-xL protects against diverse apoptotic stimuli, including ceramide-induced apoptosis ( 41-46), it was important to determine whether the effects of sphingosine were also blocked by these proteins.	transcription
66821	3	336131	5	NULL	NULL	NULL	NULL	apoptosis	Process		is induced by					ceramide	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_106	10747891	Because overexpression of Bcl-2 or Bcl-xL protects against diverse apoptotic stimuli, including ceramide-induced apoptosis ( 41-46), it was important to determine whether the effects of sphingosine were also blocked by these proteins.	transcription
66822	4	336131	5	NULL	NULL	0	NULL	statement 1	Process		includes					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_106	10747891	Because overexpression of Bcl-2 or Bcl-xL protects against diverse apoptotic stimuli, including ceramide-induced apoptosis ( 41-46), it was important to determine whether the effects of sphingosine were also blocked by these proteins.	transcription
66823	5	336131	5	NULL	NULL	0	NULL	statement 2	Process		includes					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_106	10747891	Because overexpression of Bcl-2 or Bcl-xL protects against diverse apoptotic stimuli, including ceramide-induced apoptosis ( 41-46), it was important to determine whether the effects of sphingosine were also blocked by these proteins.	transcription
66824	6	336131	5	NULL	NULL	0	NULL	Bcl-xL	GP		blocks		possibly			sphingosine	Chemical	effects of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_106	10747891	Because overexpression of Bcl-2 or Bcl-xL protects against diverse apoptotic stimuli, including ceramide-induced apoptosis ( 41-46), it was important to determine whether the effects of sphingosine were also blocked by these proteins.	transcription
66825	7	336131	5	NULL	NULL	NULL	NULL	Bcl-2	GP		blocks		possibly			sphingosine	Chemical	effects of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_106	10747891	Because overexpression of Bcl-2 or Bcl-xL protects against diverse apoptotic stimuli, including ceramide-induced apoptosis ( 41-46), it was important to determine whether the effects of sphingosine were also blocked by these proteins.	transcription
67808	1	336131	7	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_106	10747891	Because overexpression of Bcl-2 or Bcl-xL protects against diverse apoptotic stimuli, including ceramide-induced apoptosis ( 41-46), it was important to determine whether the effects of sphingosine were also blocked by these proteins.	transcription
67809	2	336131	7	NULL	NULL	0	NULL	Bcl-2	GP	overexpression of	protects					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_106	10747891	Because overexpression of Bcl-2 or Bcl-xL protects against diverse apoptotic stimuli, including ceramide-induced apoptosis ( 41-46), it was important to determine whether the effects of sphingosine were also blocked by these proteins.	transcription
67810	3	336131	7	NULL	NULL	0	NULL	Bcl-xL	GP	overexpression of	protects					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_106	10747891	Because overexpression of Bcl-2 or Bcl-xL protects against diverse apoptotic stimuli, including ceramide-induced apoptosis ( 41-46), it was important to determine whether the effects of sphingosine were also blocked by these proteins.	transcription
67811	4	336131	7	NULL	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_106	10747891	Because overexpression of Bcl-2 or Bcl-xL protects against diverse apoptotic stimuli, including ceramide-induced apoptosis ( 41-46), it was important to determine whether the effects of sphingosine were also blocked by these proteins.	transcription
66826	1	336132	5	NULL	NULL	0	NULL	caspase	GP	activation of	is required for		potentially			ceramide	Chemical	early generation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_132	10747891	To assess whether caspase activation was required for early ceramide and sphingosine generation triggered by anti-Fas mAb, we utilized the pharmacological peptide ZVAD-fmk, a competitive inhibitor of all caspases ( 50).	transcription
66827	2	336132	5	NULL	NULL	0	NULL	caspase	GP	activation of	is required for		potentially			sphingosine	Chemical	early generation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_132	10747891	To assess whether caspase activation was required for early ceramide and sphingosine generation triggered by anti-Fas mAb, we utilized the pharmacological peptide ZVAD-fmk, a competitive inhibitor of all caspases ( 50).	transcription
66828	3	336132	5	NULL	NULL	NULL	NULL	ZVAD-fmk 	AminoAcid		is an inhibitor of		competitive			caspases	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_132	10747891	To assess whether caspase activation was required for early ceramide and sphingosine generation triggered by anti-Fas mAb, we utilized the pharmacological peptide ZVAD-fmk, a competitive inhibitor of all caspases ( 50).	transcription
66829	4	336132	5	NULL	NULL	0	NULL	ZVAD-fmk	AminoAcid		is a type of					pharmacological peptide 	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_132	10747891	To assess whether caspase activation was required for early ceramide and sphingosine generation triggered by anti-Fas mAb, we utilized the pharmacological peptide ZVAD-fmk, a competitive inhibitor of all caspases ( 50).	transcription
67812	1	336132	7	NULL	NULL	0	NULL	anti-Fas mAb	GP		trigger					ceramide	Chemical	generation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_132	10747891	To assess whether caspase activation was required for early ceramide and sphingosine generation triggered by anti-Fas mAb, we utilized the pharmacological peptide ZVAD-fmk, a competitive inhibitor of all caspases ( 50).	transcription
67813	2	336132	7	NULL	NULL	0	NULL	anti-Fas mAb	GP		trigger					sphingosine	Chemical	generation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_132	10747891	To assess whether caspase activation was required for early ceramide and sphingosine generation triggered by anti-Fas mAb, we utilized the pharmacological peptide ZVAD-fmk, a competitive inhibitor of all caspases ( 50).	transcription
67814	3	336132	7	NULL	NULL	NULL	NULL	ZVAD-fmk	AminoAcid		 inhibitor of		competitive			caspases	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_132	10747891	To assess whether caspase activation was required for early ceramide and sphingosine generation triggered by anti-Fas mAb, we utilized the pharmacological peptide ZVAD-fmk, a competitive inhibitor of all caspases ( 50).	transcription
67815	4	336132	7	NULL	NULL	0	NULL	ZVAD-fmk	AminoAcid		is a type of					pharmacological peptide 	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_132	10747891	To assess whether caspase activation was required for early ceramide and sphingosine generation triggered by anti-Fas mAb, we utilized the pharmacological peptide ZVAD-fmk, a competitive inhibitor of all caspases ( 50).	transcription
66830	1	336133	5	NULL	NULL	0	NULL	Jurkat cells	Cell		prerteated with					ZVAD-fmk	AminoAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_133	10747891	Pretreatment of Jurkat cells with ZVAD-fmk (25 muM) inhibited early accumulation of ceramide (Fig.  6 B), similar to a previous report ( 20), and sphingosine (Fig.  6 B) induced by anti-Fas mAb.	transcription
66831	2	336133	5	NULL	NULL	0	NULL	statement 1	Process		inhibits					ceramide	Chemical	early accumulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_133	10747891	Pretreatment of Jurkat cells with ZVAD-fmk (25 muM) inhibited early accumulation of ceramide (Fig.  6 B), similar to a previous report ( 20), and sphingosine (Fig.  6 B) induced by anti-Fas mAb.	transcription
66832	3	336133	5	NULL	NULL	0	NULL	statement 1	Process		inhibits					sphingosine	Chemical	early accumulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_133	10747891	Pretreatment of Jurkat cells with ZVAD-fmk (25 muM) inhibited early accumulation of ceramide (Fig.  6 B), similar to a previous report ( 20), and sphingosine (Fig.  6 B) induced by anti-Fas mAb.	transcription
66833	4	336133	5	NULL	NULL	0	NULL	sphingosine	Chemical		is induced by					anti-Fas mAb	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_133	10747891	Pretreatment of Jurkat cells with ZVAD-fmk (25 muM) inhibited early accumulation of ceramide (Fig.  6 B), similar to a previous report ( 20), and sphingosine (Fig.  6 B) induced by anti-Fas mAb.	transcription
67816	1	336133	7	NULL	NULL	NULL	NULL	anti-Fas mAb	GP		induce					ceramide	Chemical	early accumulation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_133	10747891	Pretreatment of Jurkat cells with ZVAD-fmk (25 muM) inhibited early accumulation of ceramide (Fig.  6 B), similar to a previous report ( 20), and sphingosine (Fig.  6 B) induced by anti-Fas mAb.	transcription
67817	2	336133	7	NULL	NULL	NULL	NULL	anti-Fas mAb	GP		induce					sphingosine	Chemical	early accumulation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_133	10747891	Pretreatment of Jurkat cells with ZVAD-fmk (25 muM) inhibited early accumulation of ceramide (Fig.  6 B), similar to a previous report ( 20), and sphingosine (Fig.  6 B) induced by anti-Fas mAb.	transcription
67818	3	336133	7	NULL	NULL	0	NULL	ZVAD-fmk	AminoAcid		inhibit					statement 1	Process				NULL	Jurkat cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_133	10747891	Pretreatment of Jurkat cells with ZVAD-fmk (25 muM) inhibited early accumulation of ceramide (Fig.  6 B), similar to a previous report ( 20), and sphingosine (Fig.  6 B) induced by anti-Fas mAb.	transcription
67819	4	336133	7	NULL	NULL	0	NULL	ZVAD-fmk	AminoAcid		inhibit					statement 2	Process				NULL	Jurkat cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_133	10747891	Pretreatment of Jurkat cells with ZVAD-fmk (25 muM) inhibited early accumulation of ceramide (Fig.  6 B), similar to a previous report ( 20), and sphingosine (Fig.  6 B) induced by anti-Fas mAb.	transcription
66834	1	336134	5	NULL	NULL	0	NULL	executioner caspases	GP	activation of	is induced by					ceramide	Chemical	elevation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_167	10747891	Because Bcl-xL overexpression totally blocks activation of executioner caspases induced by ceramide and sphingosine elevations, it was of interest to determine whether these sphingolipid metabolites could also induce cyt  c release.	transcription
66835	2	336134	5	NULL	NULL	0	NULL	executioner caspases	GP	activation of	is induced by					sphingosine	Chemical	elevation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_167	10747891	Because Bcl-xL overexpression totally blocks activation of executioner caspases induced by ceramide and sphingosine elevations, it was of interest to determine whether these sphingolipid metabolites could also induce cyt  c release.	transcription
66836	3	336134	5	NULL	NULL	NULL	NULL	Bcl-xL	GP	overexpression of	blocks		totally			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_167	10747891	Because Bcl-xL overexpression totally blocks activation of executioner caspases induced by ceramide and sphingosine elevations, it was of interest to determine whether these sphingolipid metabolites could also induce cyt  c release.	transcription
66837	4	336134	5	NULL	NULL	0	NULL	Bcl-xL	GP	overexpression of	blocks		totally			statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_167	10747891	Because Bcl-xL overexpression totally blocks activation of executioner caspases induced by ceramide and sphingosine elevations, it was of interest to determine whether these sphingolipid metabolites could also induce cyt  c release.	transcription
66838	5	336134	5	NULL	NULL	0	NULL	ceramide	Chemical		induce		potentially			cyt c	GP	release of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_167	10747891	Because Bcl-xL overexpression totally blocks activation of executioner caspases induced by ceramide and sphingosine elevations, it was of interest to determine whether these sphingolipid metabolites could also induce cyt  c release.	transcription
66839	6	336134	5	NULL	NULL	0	NULL	sphingosine	Chemical		induce		potentially			cyt c	GP	release of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_167	10747891	Because Bcl-xL overexpression totally blocks activation of executioner caspases induced by ceramide and sphingosine elevations, it was of interest to determine whether these sphingolipid metabolites could also induce cyt  c release.	transcription
66840	7	336134	5	NULL	NULL	0	NULL	sphingosine	Chemical		is a type of					sphingolipid metabolite	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_167	10747891	Because Bcl-xL overexpression totally blocks activation of executioner caspases induced by ceramide and sphingosine elevations, it was of interest to determine whether these sphingolipid metabolites could also induce cyt  c release.	transcription
66841	8	336134	5	NULL	NULL	0	NULL	ceramide	Chemical		is a type of					sphingolipid metabolite	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_167	10747891	Because Bcl-xL overexpression totally blocks activation of executioner caspases induced by ceramide and sphingosine elevations, it was of interest to determine whether these sphingolipid metabolites could also induce cyt  c release.	transcription
67820	1	336134	7	NULL	NULL	NULL	NULL	ceramide	Chemical	elevation of	induce					executioner caspases	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_167	10747891	Because Bcl-xL overexpression totally blocks activation of executioner caspases induced by ceramide and sphingosine elevations, it was of interest to determine whether these sphingolipid metabolites could also induce cyt  c release.	transcription
67821	2	336134	7	NULL	NULL	NULL	NULL	sphingosine	Chemical	elevation of	induce					executioner caspases	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_167	10747891	Because Bcl-xL overexpression totally blocks activation of executioner caspases induced by ceramide and sphingosine elevations, it was of interest to determine whether these sphingolipid metabolites could also induce cyt  c release.	transcription
67822	3	336134	7	NULL	NULL	0	NULL	Bcl-xL 	GP	overexpression of	blocks					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_167	10747891	Because Bcl-xL overexpression totally blocks activation of executioner caspases induced by ceramide and sphingosine elevations, it was of interest to determine whether these sphingolipid metabolites could also induce cyt  c release.	transcription
67823	4	336134	7	NULL	NULL	0	NULL	Bcl-xL 	GP	overexpression of	blocks					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_167	10747891	Because Bcl-xL overexpression totally blocks activation of executioner caspases induced by ceramide and sphingosine elevations, it was of interest to determine whether these sphingolipid metabolites could also induce cyt  c release.	transcription
66842	1	336135	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_225	10747891	FasL/as Interaction Is Not Required for Apoptosis Induced by Sphingosine-- Up-regulation of Fas ligand (FasL) has been proposed as a mechanism of ceramide-mediated apoptosis induced by gamma-irradiation or doxorubicin ( 69).	transcription
66843	2	336135	5	NULL	NULL	0	NULL	FasL/Fas	GP	interactions of	is not required for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_225	10747891	FasL/as Interaction Is Not Required for Apoptosis Induced by Sphingosine-- Up-regulation of Fas ligand (FasL) has been proposed as a mechanism of ceramide-mediated apoptosis induced by gamma-irradiation or doxorubicin ( 69).	transcription
66844	3	336135	5	NULL	NULL	0	NULL	FasL	GP		is					Fas ligand	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_225	10747891	FasL/as Interaction Is Not Required for Apoptosis Induced by Sphingosine-- Up-regulation of Fas ligand (FasL) has been proposed as a mechanism of ceramide-mediated apoptosis induced by gamma-irradiation or doxorubicin ( 69).	transcription
66845	4	336135	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_225	10747891	FasL/as Interaction Is Not Required for Apoptosis Induced by Sphingosine-- Up-regulation of Fas ligand (FasL) has been proposed as a mechanism of ceramide-mediated apoptosis induced by gamma-irradiation or doxorubicin ( 69).	transcription
66846	5	336135	5	NULL	NULL	0	NULL	gamma-irradiation			induce					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_225	10747891	FasL/as Interaction Is Not Required for Apoptosis Induced by Sphingosine-- Up-regulation of Fas ligand (FasL) has been proposed as a mechanism of ceramide-mediated apoptosis induced by gamma-irradiation or doxorubicin ( 69).	transcription
66847	6	336135	5	NULL	NULL	0	NULL	doxorubicin	Chemical		induce					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_225	10747891	FasL/as Interaction Is Not Required for Apoptosis Induced by Sphingosine-- Up-regulation of Fas ligand (FasL) has been proposed as a mechanism of ceramide-mediated apoptosis induced by gamma-irradiation or doxorubicin ( 69).	transcription
66848	7	336135	5	NULL	NULL	0	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_225	10747891	FasL/as Interaction Is Not Required for Apoptosis Induced by Sphingosine-- Up-regulation of Fas ligand (FasL) has been proposed as a mechanism of ceramide-mediated apoptosis induced by gamma-irradiation or doxorubicin ( 69).	transcription
66849	8	336135	5	NULL	NULL	0	NULL	FasL	GP	upregulation of	plays a role in					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_225	10747891	FasL/as Interaction Is Not Required for Apoptosis Induced by Sphingosine-- Up-regulation of Fas ligand (FasL) has been proposed as a mechanism of ceramide-mediated apoptosis induced by gamma-irradiation or doxorubicin ( 69).	transcription
67824	1	336135	7	NULL	NULL	0	NULL	sphingosine	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_225	10747891	FasL/as Interaction Is Not Required for Apoptosis Induced by Sphingosine-- Up-regulation of Fas ligand (FasL) has been proposed as a mechanism of ceramide-mediated apoptosis induced by gamma-irradiation or doxorubicin ( 69).	transcription
67825	2	336135	7	NULL	NULL	0	NULL	FasL/as Interaction	Process		is not required for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_225	10747891	FasL/as Interaction Is Not Required for Apoptosis Induced by Sphingosine-- Up-regulation of Fas ligand (FasL) has been proposed as a mechanism of ceramide-mediated apoptosis induced by gamma-irradiation or doxorubicin ( 69).	transcription
67826	3	336135	7	NULL	NULL	0	NULL	ceramide	Chemical		mediate					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_225	10747891	FasL/as Interaction Is Not Required for Apoptosis Induced by Sphingosine-- Up-regulation of Fas ligand (FasL) has been proposed as a mechanism of ceramide-mediated apoptosis induced by gamma-irradiation or doxorubicin ( 69).	transcription
67827	4	336135	7	NULL	NULL	0	NULL	gamma-irradiation 			induce					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_225	10747891	FasL/as Interaction Is Not Required for Apoptosis Induced by Sphingosine-- Up-regulation of Fas ligand (FasL) has been proposed as a mechanism of ceramide-mediated apoptosis induced by gamma-irradiation or doxorubicin ( 69).	transcription
67828	5	336135	7	NULL	NULL	0	NULL	 doxorubicin	Chemical		induce					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_225	10747891	FasL/as Interaction Is Not Required for Apoptosis Induced by Sphingosine-- Up-regulation of Fas ligand (FasL) has been proposed as a mechanism of ceramide-mediated apoptosis induced by gamma-irradiation or doxorubicin ( 69).	transcription
66873	1	336136	5	NULL	NULL	NULL	NULL	caspase-8	GP		is activated					mitochondria	CellComponent	upstream of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_278	10747891	Hence, we infer that caspase-8 can be activated both upstream and downstream of mitochondria in Fas-induced apoptosis but only downstream of mitochondria in ceramide-and sphingosine-mediated cell death.	transcription
66875	2	336136	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					Fas					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_278	10747891	Hence, we infer that caspase-8 can be activated both upstream and downstream of mitochondria in Fas-induced apoptosis but only downstream of mitochondria in ceramide-and sphingosine-mediated cell death.	transcription
66876	3	336136	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_278	10747891	Hence, we infer that caspase-8 can be activated both upstream and downstream of mitochondria in Fas-induced apoptosis but only downstream of mitochondria in ceramide-and sphingosine-mediated cell death.	transcription
66877	4	336136	5	NULL	NULL	0	NULL	caspase-8	GP		is activated					mitochondria	CellComponent	downstream of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_278	10747891	Hence, we infer that caspase-8 can be activated both upstream and downstream of mitochondria in Fas-induced apoptosis but only downstream of mitochondria in ceramide-and sphingosine-mediated cell death.	transcription
66878	5	336136	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_278	10747891	Hence, we infer that caspase-8 can be activated both upstream and downstream of mitochondria in Fas-induced apoptosis but only downstream of mitochondria in ceramide-and sphingosine-mediated cell death.	transcription
66879	6	336136	5	NULL	NULL	0	NULL	cell death	Process		is mediated by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_278	10747891	Hence, we infer that caspase-8 can be activated both upstream and downstream of mitochondria in Fas-induced apoptosis but only downstream of mitochondria in ceramide-and sphingosine-mediated cell death.	transcription
66880	7	336136	5	NULL	NULL	0	NULL	cell death	Process		is mediated by					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_278	10747891	Hence, we infer that caspase-8 can be activated both upstream and downstream of mitochondria in Fas-induced apoptosis but only downstream of mitochondria in ceramide-and sphingosine-mediated cell death.	transcription
66881	8	336136	5	NULL	NULL	0	NULL	statement 4	Process		occurs in		only			statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_278	10747891	Hence, we infer that caspase-8 can be activated both upstream and downstream of mitochondria in Fas-induced apoptosis but only downstream of mitochondria in ceramide-and sphingosine-mediated cell death.	transcription
66883	9	336136	5	NULL	NULL	0	NULL	statement 4	Process		occurs in		only			statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_278	10747891	Hence, we infer that caspase-8 can be activated both upstream and downstream of mitochondria in Fas-induced apoptosis but only downstream of mitochondria in ceramide-and sphingosine-mediated cell death.	transcription
67829	1	336136	7	NULL	NULL	0	NULL	Fas	GP		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_278	10747891	Hence, we infer that caspase-8 can be activated both upstream and downstream of mitochondria in Fas-induced apoptosis but only downstream of mitochondria in ceramide-and sphingosine-mediated cell death.	transcription
67830	2	336136	7	NULL	NULL	0	NULL	caspase-8	GP	upstream of mitochondria	activated by					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_278	10747891	Hence, we infer that caspase-8 can be activated both upstream and downstream of mitochondria in Fas-induced apoptosis but only downstream of mitochondria in ceramide-and sphingosine-mediated cell death.	transcription
67831	3	336136	7	NULL	NULL	0	NULL	caspase-8	GP	downstream of mitochondria	activated by					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_278	10747891	Hence, we infer that caspase-8 can be activated both upstream and downstream of mitochondria in Fas-induced apoptosis but only downstream of mitochondria in ceramide-and sphingosine-mediated cell death.	transcription
67832	4	336136	7	NULL	NULL	0	NULL	ceramide	Chemical		mediate					cell death	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_278	10747891	Hence, we infer that caspase-8 can be activated both upstream and downstream of mitochondria in Fas-induced apoptosis but only downstream of mitochondria in ceramide-and sphingosine-mediated cell death.	transcription
67833	5	336136	7	NULL	NULL	0	NULL	sphingosine	Chemical		mediate					cell death	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_278	10747891	Hence, we infer that caspase-8 can be activated both upstream and downstream of mitochondria in Fas-induced apoptosis but only downstream of mitochondria in ceramide-and sphingosine-mediated cell death.	transcription
67834	6	336136	7	NULL	NULL	0	NULL	caspase-8	GP	downstream of mitochondria	activated by					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_278	10747891	Hence, we infer that caspase-8 can be activated both upstream and downstream of mitochondria in Fas-induced apoptosis but only downstream of mitochondria in ceramide-and sphingosine-mediated cell death.	transcription
67835	7	336136	7	NULL	NULL	0	NULL	caspase-8	GP	downstream of mitochondria	activated by					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_278	10747891	Hence, we infer that caspase-8 can be activated both upstream and downstream of mitochondria in Fas-induced apoptosis but only downstream of mitochondria in ceramide-and sphingosine-mediated cell death.	transcription
66862	1	336137	5	NULL	NULL	0	NULL	fatty acid	Chemical		is condensed to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3462_s_10	10652340	This study also clearly demonstrated that the purified 94-kDa ceramidase catalyzed the condensation of fatty acid to sphingosine to generate ceramide, but did not catalyze acyl-CoA-dependent acyl-transfer reaction.	transcription
66863	2	336137	5	NULL	NULL	0	NULL	sphingosine	Chemical		is converted to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3462_s_10	10652340	This study also clearly demonstrated that the purified 94-kDa ceramidase catalyzed the condensation of fatty acid to sphingosine to generate ceramide, but did not catalyze acyl-CoA-dependent acyl-transfer reaction.	transcription
66864	3	336137	5	NULL	NULL	0	NULL	94-kDa ceramidase	GP		catalyzes					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3462_s_10	10652340	This study also clearly demonstrated that the purified 94-kDa ceramidase catalyzed the condensation of fatty acid to sphingosine to generate ceramide, but did not catalyze acyl-CoA-dependent acyl-transfer reaction.	transcription
66865	4	336137	5	NULL	NULL	0	NULL	statement 1	Process		followed by					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3462_s_10	10652340	This study also clearly demonstrated that the purified 94-kDa ceramidase catalyzed the condensation of fatty acid to sphingosine to generate ceramide, but did not catalyze acyl-CoA-dependent acyl-transfer reaction.	transcription
66870	5	336137	5	NULL	NULL	0	NULL	acyl-transfer reaction	Process		is dependent on					acyl-CoA	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3462_s_10	10652340	This study also clearly demonstrated that the purified 94-kDa ceramidase catalyzed the condensation of fatty acid to sphingosine to generate ceramide, but did not catalyze acyl-CoA-dependent acyl-transfer reaction.	transcription
66872	6	336137	5	NULL	NULL	0	NULL	94-kDa ceramidase	GP		does not catalyze					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3462_s_10	10652340	This study also clearly demonstrated that the purified 94-kDa ceramidase catalyzed the condensation of fatty acid to sphingosine to generate ceramide, but did not catalyze acyl-CoA-dependent acyl-transfer reaction.	transcription
67836	1	336137	7	NULL	NULL	0	NULL	fatty acid	Chemical		condense to form					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3462_s_10	10652340	This study also clearly demonstrated that the purified 94-kDa ceramidase catalyzed the condensation of fatty acid to sphingosine to generate ceramide, but did not catalyze acyl-CoA-dependent acyl-transfer reaction.	transcription
67837	2	336137	7	NULL	NULL	0	NULL	statement 1	Process		generate					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_5_3462_s_10	10652340	This study also clearly demonstrated that the purified 94-kDa ceramidase catalyzed the condensation of fatty acid to sphingosine to generate ceramide, but did not catalyze acyl-CoA-dependent acyl-transfer reaction.	transcription
67838	3	336137	7	NULL	NULL	NULL	NULL	ceramidase	GP	purified	catalyze					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3462_s_10	10652340	This study also clearly demonstrated that the purified 94-kDa ceramidase catalyzed the condensation of fatty acid to sphingosine to generate ceramide, but did not catalyze acyl-CoA-dependent acyl-transfer reaction.	transcription
67839	4	336137	7	NULL	NULL	NULL	NULL	ceramidase	GP	purified	does not catalyze					acyl-CoA-dependent acyl-transfer reaction	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_5_3462_s_10	10652340	This study also clearly demonstrated that the purified 94-kDa ceramidase catalyzed the condensation of fatty acid to sphingosine to generate ceramide, but did not catalyze acyl-CoA-dependent acyl-transfer reaction.	transcription
66884	1	336138	5	NULL	NULL	0	NULL	DHS	Chemical		is an inhibitor of		potent			sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_41_32220_s_229	10915783	Therefore, using DHS, a potent inhibitor of sphingosine kinase, we explored whether the selective stimulation of ceramide for the expression of RAR-alpha and RXR-alpha genes in MC3T3-E1 cells was mediated by SPP.	transcription
66889	2	336138	5	NULL	NULL	NULL	NULL	ceramide	Chemical	selective stimulation of	express					RAR-alpha gene	GP				NULL	MC3T3-E1 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_32220_s_229	10915783	Therefore, using DHS, a potent inhibitor of sphingosine kinase, we explored whether the selective stimulation of ceramide for the expression of RAR-alpha and RXR-alpha genes in MC3T3-E1 cells was mediated by SPP.	transcription
66890	3	336138	5	NULL	NULL	NULL	NULL	SPP	Chemical		mediates		possibly			statement 2	Process				NULL	MC3T3-E1 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_32220_s_229	10915783	Therefore, using DHS, a potent inhibitor of sphingosine kinase, we explored whether the selective stimulation of ceramide for the expression of RAR-alpha and RXR-alpha genes in MC3T3-E1 cells was mediated by SPP.	transcription
66891	4	336138	5	NULL	NULL	0	NULL	ceramide	Chemical	selective stimulation of	express					RXR-alpha gene	GP				NULL	MC3T3-E1 cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_41_32220_s_229	10915783	Therefore, using DHS, a potent inhibitor of sphingosine kinase, we explored whether the selective stimulation of ceramide for the expression of RAR-alpha and RXR-alpha genes in MC3T3-E1 cells was mediated by SPP.	transcription
66892	5	336138	5	NULL	NULL	NULL	NULL	SPP	Chemical		mediates		possibly			statement 4	Process				NULL	MC3T3-E1 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_41_32220_s_229	10915783	Therefore, using DHS, a potent inhibitor of sphingosine kinase, we explored whether the selective stimulation of ceramide for the expression of RAR-alpha and RXR-alpha genes in MC3T3-E1 cells was mediated by SPP.	transcription
67840	1	336138	7	NULL	NULL	0	NULL	DHS	Chemical		potent inhibitor of					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_41_32220_s_229	10915783	Therefore, using DHS, a potent inhibitor of sphingosine kinase, we explored whether the selective stimulation of ceramide for the expression of RAR-alpha and RXR-alpha genes in MC3T3-E1 cells was mediated by SPP.	transcription
66893	1	336139	5	NULL	NULL	0	NULL	C -ceramide	Chemical		blocks		completely			SPP	Chemical	effects of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_159	7592842	Furthermore,  C -ceramide, which blocks the effect of SPP completely (  Fig. 1and  Fig. 2), had only a marginal effect on the  inhibition of DNA synthesis induced by sphingosine ( Fig. 3).	transcription
66894	2	336139	5	NULL	NULL	0	NULL	DNA	NucleicAcid	synthesis of	is induced by					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_159	7592842	Furthermore,  C -ceramide, which blocks the effect of SPP completely (  Fig. 1and  Fig. 2), had only a marginal effect on the  inhibition of DNA synthesis induced by sphingosine ( Fig. 3).	transcription
66895	3	336139	5	NULL	NULL	0	NULL	C -ceramide	Chemical		effects		marginal			statement 2	Process	inhibition of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_159	7592842	Furthermore,  C -ceramide, which blocks the effect of SPP completely (  Fig. 1and  Fig. 2), had only a marginal effect on the  inhibition of DNA synthesis induced by sphingosine ( Fig. 3).	transcription
67841	1	336139	7	NULL	NULL	0	NULL	 C -ceramide	Chemical		blocks		completely			SPP	Chemical	effect of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_159	7592842	Furthermore,  C -ceramide, which blocks the effect of SPP completely (  Fig. 1and  Fig. 2), had only a marginal effect on the  inhibition of DNA synthesis induced by sphingosine ( Fig. 3).	transcription
67842	2	336139	7	NULL	NULL	0	NULL	sphingosine	Chemical		induce					DNA synthesis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_159	7592842	Furthermore,  C -ceramide, which blocks the effect of SPP completely (  Fig. 1and  Fig. 2), had only a marginal effect on the  inhibition of DNA synthesis induced by sphingosine ( Fig. 3).	transcription
67843	3	336139	7	NULL	NULL	0	NULL	C -ceramide	Chemical		inhibit		marginally			statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_44_26318_s_159	7592842	Furthermore,  C -ceramide, which blocks the effect of SPP completely (  Fig. 1and  Fig. 2), had only a marginal effect on the  inhibition of DNA synthesis induced by sphingosine ( Fig. 3).	transcription
66912	1	336140	5	NULL	NULL	0	NULL	gangliosides	Chemical		incorporates					carbohydrate moiety	Chemical	homogeneous			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_50_30173_s_181	8530426	These molecular ions suggest the presence of  a series of gangliosides incorporating a homogeneous carbohydrate  moiety,  i.e.  a monoacetylated tetrasaccharide of the  composition AcNeuAc-NeuAc-Hex   linked to a heterogeneous  ceramide portion with C19-C24 fatty acids bound to a C18 sphingosine.	transcription
66913	2	336140	5	NULL	NULL	0	NULL	carbohydrate moiety	Chemical		is a type of					tetrasaccharide	Chemical	monoacetylated			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_50_30173_s_181	8530426	These molecular ions suggest the presence of  a series of gangliosides incorporating a homogeneous carbohydrate  moiety,  i.e.  a monoacetylated tetrasaccharide of the  composition AcNeuAc-NeuAc-Hex   linked to a heterogeneous  ceramide portion with C19-C24 fatty acids bound to a C18 sphingosine.	transcription
66914	3	336140	5	NULL	NULL	0	NULL	AcNeuAc-NeuAc-Hex	Chemical		is the composition of					tetrasaccharide	Chemical	monoacetylated			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_50_30173_s_181	8530426	These molecular ions suggest the presence of  a series of gangliosides incorporating a homogeneous carbohydrate  moiety,  i.e.  a monoacetylated tetrasaccharide of the  composition AcNeuAc-NeuAc-Hex   linked to a heterogeneous  ceramide portion with C19-C24 fatty acids bound to a C18 sphingosine.	transcription
66915	4	336140	5	NULL	NULL	0	NULL	tetrasaccharide	Chemical	monoacetylated	is linked to					ceramide portion	Chemical	heterogeneous			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_50_30173_s_181	8530426	These molecular ions suggest the presence of  a series of gangliosides incorporating a homogeneous carbohydrate  moiety,  i.e.  a monoacetylated tetrasaccharide of the  composition AcNeuAc-NeuAc-Hex   linked to a heterogeneous  ceramide portion with C19-C24 fatty acids bound to a C18 sphingosine.	transcription
66916	5	336140	5	NULL	NULL	0	NULL	C19-C24 fatty acids	Chemical		bind					C18 sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_50_30173_s_181	8530426	These molecular ions suggest the presence of  a series of gangliosides incorporating a homogeneous carbohydrate  moiety,  i.e.  a monoacetylated tetrasaccharide of the  composition AcNeuAc-NeuAc-Hex   linked to a heterogeneous  ceramide portion with C19-C24 fatty acids bound to a C18 sphingosine.	transcription
66917	6	336140	5	NULL	NULL	0	NULL	statement 4	Process		occurs with					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_50_30173_s_181	8530426	These molecular ions suggest the presence of  a series of gangliosides incorporating a homogeneous carbohydrate  moiety,  i.e.  a monoacetylated tetrasaccharide of the  composition AcNeuAc-NeuAc-Hex   linked to a heterogeneous  ceramide portion with C19-C24 fatty acids bound to a C18 sphingosine.	transcription
67844	1	336140	7	NULL	NULL	NULL	NULL	AcNeuAc-NeuAc-Hex 	Chemical		linked to					ceramide with C19-C24 fatty acids	Chemical	heterogeneous			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_50_30173_s_181	8530426	These molecular ions suggest the presence of  a series of gangliosides incorporating a homogeneous carbohydrate  moiety,  i.e.  a monoacetylated tetrasaccharide of the  composition AcNeuAc-NeuAc-Hex   linked to a heterogeneous  ceramide portion with C19-C24 fatty acids bound to a C18 sphingosine.	transcription
67845	2	336140	7	NULL	NULL	NULL	NULL	statement 1	Chemical		bind					C18 sphingosine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_270_50_30173_s_181	8530426	These molecular ions suggest the presence of  a series of gangliosides incorporating a homogeneous carbohydrate  moiety,  i.e.  a monoacetylated tetrasaccharide of the  composition AcNeuAc-NeuAc-Hex   linked to a heterogeneous  ceramide portion with C19-C24 fatty acids bound to a C18 sphingosine.	transcription
67846	3	336140	7	NULL	NULL	0	NULL	AcNeuAc-NeuAc-Hex	Chemical		is a type of					monoacetylated tetrasaccharide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_270_50_30173_s_181	8530426	These molecular ions suggest the presence of  a series of gangliosides incorporating a homogeneous carbohydrate  moiety,  i.e.  a monoacetylated tetrasaccharide of the  composition AcNeuAc-NeuAc-Hex   linked to a heterogeneous  ceramide portion with C19-C24 fatty acids bound to a C18 sphingosine.	transcription
66918	1	336141	5	NULL	NULL	0	NULL	FB1	Chemical		inhibits					sphingosine N-acyltransferase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_20763_s_128	10409615	FB1 inhibits sphingosine  N-acyltransferase (ceramide synthase) in a concentration-dependent manner and thereby interferes with the biosynthesis of all sphingolipids beyond the sphingoid base, in a variety of cells ( 57).	transcription
66919	2	336141	5	NULL	NULL	0	NULL	sphingosine N-acyltransferase	GP		is					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_20763_s_128	10409615	FB1 inhibits sphingosine  N-acyltransferase (ceramide synthase) in a concentration-dependent manner and thereby interferes with the biosynthesis of all sphingolipids beyond the sphingoid base, in a variety of cells ( 57).	transcription
66920	3	336141	5	NULL	NULL	0	NULL	statement 1	Process		is dependent on					concentration	QuantityOrMeasure				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_20763_s_128	10409615	FB1 inhibits sphingosine  N-acyltransferase (ceramide synthase) in a concentration-dependent manner and thereby interferes with the biosynthesis of all sphingolipids beyond the sphingoid base, in a variety of cells ( 57).	transcription
66921	4	336141	5	NULL	NULL	0	NULL	statement 1	Process		interfere with					sphingolipids	Chemical	biosynthesis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_20763_s_128	10409615	FB1 inhibits sphingosine  N-acyltransferase (ceramide synthase) in a concentration-dependent manner and thereby interferes with the biosynthesis of all sphingolipids beyond the sphingoid base, in a variety of cells ( 57).	transcription
67847	1	336141	7	NULL	NULL	NULL	NULL	FB1	Chemical		inhibit					sphingosine N-acyltransferase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_20763_s_128	10409615	FB1 inhibits sphingosine  N-acyltransferase (ceramide synthase) in a concentration-dependent manner and thereby interferes with the biosynthesis of all sphingolipids beyond the sphingoid base, in a variety of cells ( 57).	transcription
67848	2	336141	7	NULL	NULL	0	NULL	statement 1	Process		depends on					concentration	QuantityOrMeasure				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_20763_s_128	10409615	FB1 inhibits sphingosine  N-acyltransferase (ceramide synthase) in a concentration-dependent manner and thereby interferes with the biosynthesis of all sphingolipids beyond the sphingoid base, in a variety of cells ( 57).	transcription
67849	3	336141	7	NULL	NULL	NULL	NULL	statement 1	Process		interferes with					sphingolipids	Chemical	biosynthesis of			NULL	variety of cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_30_20763_s_128	10409615	FB1 inhibits sphingosine  N-acyltransferase (ceramide synthase) in a concentration-dependent manner and thereby interferes with the biosynthesis of all sphingolipids beyond the sphingoid base, in a variety of cells ( 57).	transcription
67850	4	336141	7	NULL	NULL	0	NULL	sphingosine N-acyltransferase	GP		is					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_30_20763_s_128	10409615	FB1 inhibits sphingosine  N-acyltransferase (ceramide synthase) in a concentration-dependent manner and thereby interferes with the biosynthesis of all sphingolipids beyond the sphingoid base, in a variety of cells ( 57).	transcription
66922	1	336142	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_37_23722_s_108	9726979	Interestingly, we previously demonstrated that inhibition of ceramide-induced apoptosis by protein kinase C activation results from stimulation of sphingosine kinase and concomitant increase in cellular SPP levels ( 3).	transcription
66923	2	336142	5	NULL	NULL	0	NULL	protein kinase C	GP	activated	inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_37_23722_s_108	9726979	Interestingly, we previously demonstrated that inhibition of ceramide-induced apoptosis by protein kinase C activation results from stimulation of sphingosine kinase and concomitant increase in cellular SPP levels ( 3).	transcription
66924	3	336142	5	NULL	NULL	0	NULL	sphingosine kinase	GP	stimulation of	results in					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_37_23722_s_108	9726979	Interestingly, we previously demonstrated that inhibition of ceramide-induced apoptosis by protein kinase C activation results from stimulation of sphingosine kinase and concomitant increase in cellular SPP levels ( 3).	transcription
66925	4	336142	5	NULL	NULL	0	NULL	SPP	Chemical	concomitant increase in;;cellular levels of	results in					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_37_23722_s_108	9726979	Interestingly, we previously demonstrated that inhibition of ceramide-induced apoptosis by protein kinase C activation results from stimulation of sphingosine kinase and concomitant increase in cellular SPP levels ( 3).	transcription
67851	1	336142	7	NULL	NULL	0	NULL	 ceramide	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_37_23722_s_108	9726979	Interestingly, we previously demonstrated that inhibition of ceramide-induced apoptosis by protein kinase C activation results from stimulation of sphingosine kinase and concomitant increase in cellular SPP levels ( 3).	transcription
67852	2	336142	7	NULL	NULL	0	NULL	 protein kinase C	GP	activation of	inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_37_23722_s_108	9726979	Interestingly, we previously demonstrated that inhibition of ceramide-induced apoptosis by protein kinase C activation results from stimulation of sphingosine kinase and concomitant increase in cellular SPP levels ( 3).	transcription
67853	3	336142	7	NULL	NULL	0	NULL	statement 2	Process		result from					sphingosine kinase	Chemical	stimulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_37_23722_s_108	9726979	Interestingly, we previously demonstrated that inhibition of ceramide-induced apoptosis by protein kinase C activation results from stimulation of sphingosine kinase and concomitant increase in cellular SPP levels ( 3).	transcription
67854	4	336142	7	NULL	NULL	0	NULL	statement 2	Process		result from					SPP	Chemical	concomitant increase in levels of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_37_23722_s_108	9726979	Interestingly, we previously demonstrated that inhibition of ceramide-induced apoptosis by protein kinase C activation results from stimulation of sphingosine kinase and concomitant increase in cellular SPP levels ( 3).	transcription
66926	1	336143	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					nerve growth factor	GP	withdrawal of			NULL	PC12 cells	0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2931_s_230	9446605	Conversely, MAPK activation prevented apoptosis induced by nerve growth factor withdrawal in PC12 cells ( 66) and was required for the suppression of ceramide-induced apoptosis by sphingosine 1-phosphate in HL-60 cells ( 67).	transcription
66927	2	336143	5	NULL	NULL	NULL	NULL	MAPK	GP	activation of	prevents					statement 1	Process				NULL	PC12 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2931_s_230	9446605	Conversely, MAPK activation prevented apoptosis induced by nerve growth factor withdrawal in PC12 cells ( 66) and was required for the suppression of ceramide-induced apoptosis by sphingosine 1-phosphate in HL-60 cells ( 67).	transcription
66928	3	336143	5	NULL	NULL	NULL	NULL	apoptosis	Process		is induced by					ceramide	Chemical				NULL	HL-60 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2931_s_230	9446605	Conversely, MAPK activation prevented apoptosis induced by nerve growth factor withdrawal in PC12 cells ( 66) and was required for the suppression of ceramide-induced apoptosis by sphingosine 1-phosphate in HL-60 cells ( 67).	transcription
66929	4	336143	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		suppress					statement 3	Process				NULL	HL-60 cells	0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2931_s_230	9446605	Conversely, MAPK activation prevented apoptosis induced by nerve growth factor withdrawal in PC12 cells ( 66) and was required for the suppression of ceramide-induced apoptosis by sphingosine 1-phosphate in HL-60 cells ( 67).	transcription
66930	5	336143	5	NULL	NULL	0	NULL	MAPK	GP	activation of	is required for					statement 4	Process				NULL	HL-60 cells	0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2931_s_230	9446605	Conversely, MAPK activation prevented apoptosis induced by nerve growth factor withdrawal in PC12 cells ( 66) and was required for the suppression of ceramide-induced apoptosis by sphingosine 1-phosphate in HL-60 cells ( 67).	transcription
67855	1	336143	7	NULL	NULL	0	NULL	nerve growth factor 	GP	withdrawal of	induce					apoptosis	Process				NULL	 PC12 cells 	0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2931_s_230	9446605	Conversely, MAPK activation prevented apoptosis induced by nerve growth factor withdrawal in PC12 cells ( 66) and was required for the suppression of ceramide-induced apoptosis by sphingosine 1-phosphate in HL-60 cells ( 67).	transcription
67856	2	336143	7	NULL	NULL	0	NULL	MAPK	GP	activation of	prevents					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2931_s_230	9446605	Conversely, MAPK activation prevented apoptosis induced by nerve growth factor withdrawal in PC12 cells ( 66) and was required for the suppression of ceramide-induced apoptosis by sphingosine 1-phosphate in HL-60 cells ( 67).	transcription
67857	3	336143	7	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL	HL-60 cells	0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2931_s_230	9446605	Conversely, MAPK activation prevented apoptosis induced by nerve growth factor withdrawal in PC12 cells ( 66) and was required for the suppression of ceramide-induced apoptosis by sphingosine 1-phosphate in HL-60 cells ( 67).	transcription
67858	4	336143	7	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		suppress					statement 3	Process				NULL	HL-60 cells	0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2931_s_230	9446605	Conversely, MAPK activation prevented apoptosis induced by nerve growth factor withdrawal in PC12 cells ( 66) and was required for the suppression of ceramide-induced apoptosis by sphingosine 1-phosphate in HL-60 cells ( 67).	transcription
67859	5	336143	7	NULL	NULL	NULL	NULL	MAPK	GP	activation of	is required for					statement 4	Process				NULL	HL-60 cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2931_s_230	9446605	Conversely, MAPK activation prevented apoptosis induced by nerve growth factor withdrawal in PC12 cells ( 66) and was required for the suppression of ceramide-induced apoptosis by sphingosine 1-phosphate in HL-60 cells ( 67).	transcription
66931	1	336144	5	NULL	NULL	NULL	NULL	PARP	GP	activation of;;cleavage of	is induced by					Fas	GP	ligation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_88	9446602	Sphingosine 1-Phosphate and TPA Inhibit Activation of PARP Cleavage Induced by Fas Ligation and Ceramide-- Because Fas ligation leads to proteolytic cleavage of PARP ( 12,  25-27), it was of interest to determine whether SPP and TPA could inhibit this cleavage.	transcription
66932	2	336144	5	NULL	NULL	NULL	NULL	PARP	GP	activation of;;cleavage of	is induced by					ceramide	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_88	9446602	Sphingosine 1-Phosphate and TPA Inhibit Activation of PARP Cleavage Induced by Fas Ligation and Ceramide-- Because Fas ligation leads to proteolytic cleavage of PARP ( 12,  25-27), it was of interest to determine whether SPP and TPA could inhibit this cleavage.	transcription
66933	3	336144	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_88	9446602	Sphingosine 1-Phosphate and TPA Inhibit Activation of PARP Cleavage Induced by Fas Ligation and Ceramide-- Because Fas ligation leads to proteolytic cleavage of PARP ( 12,  25-27), it was of interest to determine whether SPP and TPA could inhibit this cleavage.	transcription
66934	4	336144	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		inhibits					statement 2	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_88	9446602	Sphingosine 1-Phosphate and TPA Inhibit Activation of PARP Cleavage Induced by Fas Ligation and Ceramide-- Because Fas ligation leads to proteolytic cleavage of PARP ( 12,  25-27), it was of interest to determine whether SPP and TPA could inhibit this cleavage.	transcription
66935	5	336144	5	NULL	NULL	0	NULL	TPA	Chemical		inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_88	9446602	Sphingosine 1-Phosphate and TPA Inhibit Activation of PARP Cleavage Induced by Fas Ligation and Ceramide-- Because Fas ligation leads to proteolytic cleavage of PARP ( 12,  25-27), it was of interest to determine whether SPP and TPA could inhibit this cleavage.	transcription
66936	6	336144	5	NULL	NULL	0	NULL	TPA	Chemical		inhibits					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_88	9446602	Sphingosine 1-Phosphate and TPA Inhibit Activation of PARP Cleavage Induced by Fas Ligation and Ceramide-- Because Fas ligation leads to proteolytic cleavage of PARP ( 12,  25-27), it was of interest to determine whether SPP and TPA could inhibit this cleavage.	transcription
67860	3	336144	7	NULL	NULL	NULL	NULL	Sphingosine 1-Phosphate	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_88	9446602	Sphingosine 1-Phosphate and TPA Inhibit Activation of PARP Cleavage Induced by Fas Ligation and Ceramide-- Because Fas ligation leads to proteolytic cleavage of PARP ( 12,  25-27), it was of interest to determine whether SPP and TPA could inhibit this cleavage.	transcription
67861	4	336144	7	NULL	NULL	NULL	NULL	TPA	Chemical		inhibit					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_88	9446602	Sphingosine 1-Phosphate and TPA Inhibit Activation of PARP Cleavage Induced by Fas Ligation and Ceramide-- Because Fas ligation leads to proteolytic cleavage of PARP ( 12,  25-27), it was of interest to determine whether SPP and TPA could inhibit this cleavage.	transcription
67862	1	336144	7	NULL	NULL	0	NULL	Fas ligation	Process		induce					PARP	GP	activation of;;cleavage of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_88	9446602	Sphingosine 1-Phosphate and TPA Inhibit Activation of PARP Cleavage Induced by Fas Ligation and Ceramide-- Because Fas ligation leads to proteolytic cleavage of PARP ( 12,  25-27), it was of interest to determine whether SPP and TPA could inhibit this cleavage.	transcription
67863	2	336144	7	NULL	NULL	0	NULL	ceramide	Chemical		induce					PARP	GP	activation of;;cleavage of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_88	9446602	Sphingosine 1-Phosphate and TPA Inhibit Activation of PARP Cleavage Induced by Fas Ligation and Ceramide-- Because Fas ligation leads to proteolytic cleavage of PARP ( 12,  25-27), it was of interest to determine whether SPP and TPA could inhibit this cleavage.	transcription
67864	5	336144	7	NULL	NULL	0	NULL	Sphingosine 1-Phosphate	Chemical		inhibit					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_88	9446602	Sphingosine 1-Phosphate and TPA Inhibit Activation of PARP Cleavage Induced by Fas Ligation and Ceramide-- Because Fas ligation leads to proteolytic cleavage of PARP ( 12,  25-27), it was of interest to determine whether SPP and TPA could inhibit this cleavage.	transcription
67865	6	336144	7	NULL	NULL	0	NULL	TPA	Chemical		inhibit					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_88	9446602	Sphingosine 1-Phosphate and TPA Inhibit Activation of PARP Cleavage Induced by Fas Ligation and Ceramide-- Because Fas ligation leads to proteolytic cleavage of PARP ( 12,  25-27), it was of interest to determine whether SPP and TPA could inhibit this cleavage.	transcription
67866	7	336144	7	NULL	NULL	0	NULL	Fas ligation	Process		leads to					PARP	GP	proteolytic cleavage of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_88	9446602	Sphingosine 1-Phosphate and TPA Inhibit Activation of PARP Cleavage Induced by Fas Ligation and Ceramide-- Because Fas ligation leads to proteolytic cleavage of PARP ( 12,  25-27), it was of interest to determine whether SPP and TPA could inhibit this cleavage.	transcription
66937	1	336145	5	NULL	NULL	0	NULL	programmed cell death	Process		is mediated by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jclininvest_101_2_301_s_521	9435301	Cuvillier, O., G. Pirianov, B. Kleuser, P.G. Vanek, O.A. Coso, S. Gutkind, and S. Spiegel    (1996) Suppression of ceramide-mediated programmed cell  death by sphingosine-A-phosphate.	transcription
66938	2	336145	5	NULL	NULL	0	NULL	sphingosine-A-phosphate	Chemical		suppress					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jclininvest_101_2_301_s_521	9435301	Cuvillier, O., G. Pirianov, B. Kleuser, P.G. Vanek, O.A. Coso, S. Gutkind, and S. Spiegel    (1996) Suppression of ceramide-mediated programmed cell  death by sphingosine-A-phosphate.	transcription
67867	1	336145	7	NULL	NULL	0	NULL	ceramide	Chemical		mediate					programmed cell death	Process				NULL		0	NULL	NULL	NULL	gw60_jclininvest_101_2_301_s_521	9435301	Cuvillier, O., G. Pirianov, B. Kleuser, P.G. Vanek, O.A. Coso, S. Gutkind, and S. Spiegel    (1996) Suppression of ceramide-mediated programmed cell  death by sphingosine-A-phosphate.	transcription
67868	2	336145	7	NULL	NULL	0	NULL	sphingosine-A-phosphate	Chemical		suppress					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jclininvest_101_2_301_s_521	9435301	Cuvillier, O., G. Pirianov, B. Kleuser, P.G. Vanek, O.A. Coso, S. Gutkind, and S. Spiegel    (1996) Suppression of ceramide-mediated programmed cell  death by sphingosine-A-phosphate.	transcription
66939	1	336146	5	NULL	NULL	0	NULL	ceramide	Chemical		modulate					protein	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	gw60_jlipidres_42_2_301_s_18	11181761	For example, ceramide modulates protein phosphorylation, the activity of protein kinase C (PKC), and phospholipase A2, and mediates signal transduction  ( 2) ( 3), while sphingosine and psychosine are potent inhibitors of PKC  ( 4).	transcription
66940	2	336146	5	NULL	NULL	0	NULL	ceramide	Chemical		modulate					PKC	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_jlipidres_42_2_301_s_18	11181761	For example, ceramide modulates protein phosphorylation, the activity of protein kinase C (PKC), and phospholipase A2, and mediates signal transduction  ( 2) ( 3), while sphingosine and psychosine are potent inhibitors of PKC  ( 4).	transcription
66941	3	336146	5	NULL	NULL	0	NULL	PKC	GP		is					protein kinase C	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_42_2_301_s_18	11181761	For example, ceramide modulates protein phosphorylation, the activity of protein kinase C (PKC), and phospholipase A2, and mediates signal transduction  ( 2) ( 3), while sphingosine and psychosine are potent inhibitors of PKC  ( 4).	transcription
66942	4	336146	5	NULL	NULL	0	NULL	ceramide	Chemical		modulate					phospholipase A2	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_42_2_301_s_18	11181761	For example, ceramide modulates protein phosphorylation, the activity of protein kinase C (PKC), and phospholipase A2, and mediates signal transduction  ( 2) ( 3), while sphingosine and psychosine are potent inhibitors of PKC  ( 4).	transcription
66943	5	336146	5	NULL	NULL	0	NULL	ceramide	Chemical		mediates					signal transduction	Process				NULL		0	NULL	NULL	NULL	gw60_jlipidres_42_2_301_s_18	11181761	For example, ceramide modulates protein phosphorylation, the activity of protein kinase C (PKC), and phospholipase A2, and mediates signal transduction  ( 2) ( 3), while sphingosine and psychosine are potent inhibitors of PKC  ( 4).	transcription
66944	6	336146	5	NULL	NULL	0	NULL	sphingosine	Chemical		is an inhibitor of		potent			PKC	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_42_2_301_s_18	11181761	For example, ceramide modulates protein phosphorylation, the activity of protein kinase C (PKC), and phospholipase A2, and mediates signal transduction  ( 2) ( 3), while sphingosine and psychosine are potent inhibitors of PKC  ( 4).	transcription
66945	7	336146	5	NULL	NULL	0	NULL	psychosine	Chemical		is an inhibitor of		potent			PKC	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_42_2_301_s_18	11181761	For example, ceramide modulates protein phosphorylation, the activity of protein kinase C (PKC), and phospholipase A2, and mediates signal transduction  ( 2) ( 3), while sphingosine and psychosine are potent inhibitors of PKC  ( 4).	transcription
67869	1	336146	7	NULL	NULL	0	NULL	ceramide	Chemical		modulates					protein phosphorylation	Process				NULL		0	NULL	NULL	NULL	gw60_jlipidres_42_2_301_s_18	11181761	For example, ceramide modulates protein phosphorylation, the activity of protein kinase C (PKC), and phospholipase A2, and mediates signal transduction  ( 2) ( 3), while sphingosine and psychosine are potent inhibitors of PKC  ( 4).	transcription
67870	2	336146	7	NULL	NULL	0	NULL	ceramide	Chemical		modulates					PKC activity	Process				NULL		0	NULL	NULL	NULL	gw60_jlipidres_42_2_301_s_18	11181761	For example, ceramide modulates protein phosphorylation, the activity of protein kinase C (PKC), and phospholipase A2, and mediates signal transduction  ( 2) ( 3), while sphingosine and psychosine are potent inhibitors of PKC  ( 4).	transcription
67871	3	336146	7	NULL	NULL	0	NULL	ceramide	Chemical		modulates					phospholipase A2	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_42_2_301_s_18	11181761	For example, ceramide modulates protein phosphorylation, the activity of protein kinase C (PKC), and phospholipase A2, and mediates signal transduction  ( 2) ( 3), while sphingosine and psychosine are potent inhibitors of PKC  ( 4).	transcription
67872	4	336146	7	NULL	NULL	0	NULL	ceramide	Chemical		mediates					signal transduction	Process				NULL		0	NULL	NULL	NULL	gw60_jlipidres_42_2_301_s_18	11181761	For example, ceramide modulates protein phosphorylation, the activity of protein kinase C (PKC), and phospholipase A2, and mediates signal transduction  ( 2) ( 3), while sphingosine and psychosine are potent inhibitors of PKC  ( 4).	transcription
67873	5	336146	7	NULL	NULL	0	NULL	sphingosine	Chemical		potent inhibitor of					PKC	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_42_2_301_s_18	11181761	For example, ceramide modulates protein phosphorylation, the activity of protein kinase C (PKC), and phospholipase A2, and mediates signal transduction  ( 2) ( 3), while sphingosine and psychosine are potent inhibitors of PKC  ( 4).	transcription
67874	6	336146	7	NULL	NULL	0	NULL	psychosine	Chemical		potent inhibitor of					PKC	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_42_2_301_s_18	11181761	For example, ceramide modulates protein phosphorylation, the activity of protein kinase C (PKC), and phospholipase A2, and mediates signal transduction  ( 2) ( 3), while sphingosine and psychosine are potent inhibitors of PKC  ( 4).	transcription
67875	7	336146	7	NULL	NULL	0	NULL	PKC	GP		is					protein kinase C	GP				NULL		0	NULL	NULL	NULL	gw60_jlipidres_42_2_301_s_18	11181761	For example, ceramide modulates protein phosphorylation, the activity of protein kinase C (PKC), and phospholipase A2, and mediates signal transduction  ( 2) ( 3), while sphingosine and psychosine are potent inhibitors of PKC  ( 4).	transcription
66946	1	336147	5	NULL	NULL	0	NULL	sphingomyelinases	GP		is activated by					TNF-alpha	GP				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
66947	2	336147	5	NULL	NULL	0	NULL	sphingomyelinases	GP		is activated by					Fas ligand	GP				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
66948	3	336147	5	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
66949	4	336147	5	NULL	NULL	0	NULL	statement 1	Process		leads to					ceramide	Chemical	formation of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
66950	5	336147	5	NULL	NULL	0	NULL	statement 2	Process		leads to					ceramide	Chemical	formation of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
66951	6	336147	5	NULL	NULL	0	NULL	statement 1	Process		leads to					sphingosine	Chemical	formation of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
66952	7	336147	5	NULL	NULL	0	NULL	statement 2	Process		leads to					sphingosine	Chemical	formation of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
66953	8	336147	5	NULL	NULL	0	NULL	statement 1	Process		leads to					sphingosine 1-phosphate	Chemical	formation of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
66954	9	336147	5	NULL	NULL	0	NULL	statement 2	Process		leads to					sphingosine 1-phosphate	Chemical	formation of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
66955	10	336147	5	NULL	NULL	0	NULL	sphingomyelinases	GP		is					SMases	GP				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
66956	11	336147	5	NULL	NULL	0	NULL	TNF-alpha	GP		is					tumor necrosis factor-alpha	GP				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
66957	12	336147	5	NULL	NULL	0	NULL	ceramide	Chemical		is					cer	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
66958	13	336147	5	NULL	NULL	0	NULL	sphingosine	Chemical		is					sph	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
66959	14	336147	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		is					SPP	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
67876	1	336147	7	NULL	NULL	0	NULL	TNF-alpha	GP		activates					SMases	GP				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
67877	2	336147	7	NULL	NULL	NULL	NULL	Fas ligand	GP		leads to					cer	Chemical	formation of			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
67878	3	336147	7	NULL	NULL	NULL	NULL	Fas ligand	GP		leads to					sph	Chemical	formation of			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
67879	4	336147	7	NULL	NULL	0	NULL	Fas ligand	GP		leads to					SPP	Chemical	formation of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
67880	5	336147	7	NULL	NULL	0	NULL	SMases	GP		is					sphingomyelinases 	GP				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
67881	6	336147	7	NULL	NULL	0	NULL	TNF-alpha	GP		is					tumor necrosis factor-alpha	GP				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
67882	7	336147	7	NULL	NULL	0	NULL	cer	Chemical		is					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
67883	8	336147	7	NULL	NULL	0	NULL	sph	Chemical		is					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
67884	9	336147	7	NULL	NULL	0	NULL	SPP	Chemical		is					sphingosine-1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
67885	10	336147	7	NULL	NULL	0	NULL	TNF-alpha	GP		is a type of					extracellular factor	GP				NULL		0	NULL	NULL	NULL	gw60_jneurosci_19_17_7458_s_15	10460252	Activation of sphingomyelinases (SMases) by extracellular factors such as tumor necrosis factor-alpha (TNF-alpha) or Fas ligand leads to the formation of ceramide (cer), sphingosine (sph), and sphingosine-1-phosphate (SPP).	transcription
66960	1	336148	5	NULL	NULL	0	NULL	programmed cell death	Process		is mediated by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_236	9278531	Cuvillier O, Pirianov G, Kleuser B, Vanek P, Coso O, Gutkind J, Spiegel S    (1996) Sphingosine 1-phosphate inhibits ceramide mediated programmed cell death.	transcription
66961	2	336148	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_236	9278531	Cuvillier O, Pirianov G, Kleuser B, Vanek P, Coso O, Gutkind J, Spiegel S    (1996) Sphingosine 1-phosphate inhibits ceramide mediated programmed cell death.	transcription
67886	1	336148	7	NULL	NULL	0	NULL	ceramide	Chemical		mediates					programmed cell death	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_236	9278531	Cuvillier O, Pirianov G, Kleuser B, Vanek P, Coso O, Gutkind J, Spiegel S    (1996) Sphingosine 1-phosphate inhibits ceramide mediated programmed cell death.	transcription
67887	2	336148	7	NULL	NULL	0	NULL	Sphingosine 1-phosphate	Chemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_236	9278531	Cuvillier O, Pirianov G, Kleuser B, Vanek P, Coso O, Gutkind J, Spiegel S    (1996) Sphingosine 1-phosphate inhibits ceramide mediated programmed cell death.	transcription
66962	1	336149	5	NULL	NULL	0	NULL	programmed cell death	Process		is mediated by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_9_2929_s_339	11312276	Guvillier O, Pirianov G, Kleuser B, Vanek PG, Coso OA, Gutkind JS, Spiegel S   (1996) Suppression of ceramide-mediated programmed cell death by sphingosine-a-phosphate.	transcription
66963	2	336149	5	NULL	NULL	0	NULL	sphingosine-a-phosphate	Chemical		suppress					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_9_2929_s_339	11312276	Guvillier O, Pirianov G, Kleuser B, Vanek PG, Coso OA, Gutkind JS, Spiegel S   (1996) Suppression of ceramide-mediated programmed cell death by sphingosine-a-phosphate.	transcription
67888	1	336149	7	NULL	NULL	0	NULL	ceramide	Chemical		mediate					programmed cell death	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_9_2929_s_339	11312276	Guvillier O, Pirianov G, Kleuser B, Vanek PG, Coso OA, Gutkind JS, Spiegel S   (1996) Suppression of ceramide-mediated programmed cell death by sphingosine-a-phosphate.	transcription
67889	2	336149	7	NULL	NULL	0	NULL	sphingosine-a-phosphate	Chemical		suppress					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_21_9_2929_s_339	11312276	Guvillier O, Pirianov G, Kleuser B, Vanek PG, Coso OA, Gutkind JS, Spiegel S   (1996) Suppression of ceramide-mediated programmed cell death by sphingosine-a-phosphate.	transcription
66964	1	336150	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					tumor necrosis factor-alpha	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_184	10454518	For example, induction of apoptosis by tumor necrosis factor-alpha via activation of tumor necrosis factor R1 can involve acute generation of either ceramide (Jarvis et al., 1994a  ) or sphingosine (Ohta et al., 1994  ).	transcription
66965	2	336150	5	NULL	NULL	NULL	NULL	statement 1	Process		via					tumor necrosis factor R1	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_184	10454518	For example, induction of apoptosis by tumor necrosis factor-alpha via activation of tumor necrosis factor R1 can involve acute generation of either ceramide (Jarvis et al., 1994a  ) or sphingosine (Ohta et al., 1994  ).	transcription
66966	3	336150	5	NULL	NULL	0	NULL	statement 2	Process		involves					ceramide	Chemical	acute generation of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_184	10454518	For example, induction of apoptosis by tumor necrosis factor-alpha via activation of tumor necrosis factor R1 can involve acute generation of either ceramide (Jarvis et al., 1994a  ) or sphingosine (Ohta et al., 1994  ).	transcription
66967	4	336150	5	NULL	NULL	0	NULL	statement 2	Process		involves					sphingosine	Chemical	acute generation of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_184	10454518	For example, induction of apoptosis by tumor necrosis factor-alpha via activation of tumor necrosis factor R1 can involve acute generation of either ceramide (Jarvis et al., 1994a  ) or sphingosine (Ohta et al., 1994  ).	transcription
66968	5	336150	5	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_184	10454518	For example, induction of apoptosis by tumor necrosis factor-alpha via activation of tumor necrosis factor R1 can involve acute generation of either ceramide (Jarvis et al., 1994a  ) or sphingosine (Ohta et al., 1994  ).	transcription
67890	1	336150	7	NULL	NULL	0	NULL	tumor necrosis factor-alpha	GP		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_184	10454518	For example, induction of apoptosis by tumor necrosis factor-alpha via activation of tumor necrosis factor R1 can involve acute generation of either ceramide (Jarvis et al., 1994a  ) or sphingosine (Ohta et al., 1994  ).	transcription
67891	2	336150	7	NULL	NULL	0	NULL	statement 1	Process		via					R1	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_184	10454518	For example, induction of apoptosis by tumor necrosis factor-alpha via activation of tumor necrosis factor R1 can involve acute generation of either ceramide (Jarvis et al., 1994a  ) or sphingosine (Ohta et al., 1994  ).	transcription
67892	3	336150	7	NULL	NULL	0	NULL	statement 1	Process		involve					ceramide	Chemical	acute generation of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_184	10454518	For example, induction of apoptosis by tumor necrosis factor-alpha via activation of tumor necrosis factor R1 can involve acute generation of either ceramide (Jarvis et al., 1994a  ) or sphingosine (Ohta et al., 1994  ).	transcription
67893	4	336150	7	NULL	NULL	0	NULL	statement 1	Process		involve					sphingosine	Chemical	acute generation of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_184	10454518	For example, induction of apoptosis by tumor necrosis factor-alpha via activation of tumor necrosis factor R1 can involve acute generation of either ceramide (Jarvis et al., 1994a  ) or sphingosine (Ohta et al., 1994  ).	transcription
67894	5	336150	7	NULL	NULL	0	NULL	R1	GP		is a type of					tumor necrosis factor	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_184	10454518	For example, induction of apoptosis by tumor necrosis factor-alpha via activation of tumor necrosis factor R1 can involve acute generation of either ceramide (Jarvis et al., 1994a  ) or sphingosine (Ohta et al., 1994  ).	transcription
66969	1	336151	5	NULL	NULL	NULL	NULL	dihydro-C2-ceramide	Chemical		does not inhibit		significantly			n-K+ channels	GP				NULL	JCaM1.6 cells	NULL	NULL	NULL	NULL	gw60_pnas_94_14_7661_s_108	9207149	Furthermore, dihydro-C2-ceramide or sphingosine did not significantly inhibit n-K+ channels in JCaM1.6 or herbimycin A-treated cells, excluding a direct, structural inhibition of n-K+ channels by ceramide.	transcription
66970	2	336151	5	NULL	NULL	0	NULL	sphingosine	Chemical		does not inhibit		significantly			n-K+ channels	GP				NULL	JCaM1.6 cells	0	NULL	NULL	NULL	gw60_pnas_94_14_7661_s_108	9207149	Furthermore, dihydro-C2-ceramide or sphingosine did not significantly inhibit n-K+ channels in JCaM1.6 or herbimycin A-treated cells, excluding a direct, structural inhibition of n-K+ channels by ceramide.	transcription
66971	3	336151	5	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7661_s_108	9207149	Furthermore, dihydro-C2-ceramide or sphingosine did not significantly inhibit n-K+ channels in JCaM1.6 or herbimycin A-treated cells, excluding a direct, structural inhibition of n-K+ channels by ceramide.	transcription
66972	4	336151	5	NULL	NULL	0	NULL	dihydro-C2-ceramide	Chemical		does not inhibit		significantly			n-K+ channels	GP				NULL	herbimycin A-treated cells	0	NULL	NULL	NULL	gw60_pnas_94_14_7661_s_108	9207149	Furthermore, dihydro-C2-ceramide or sphingosine did not significantly inhibit n-K+ channels in JCaM1.6 or herbimycin A-treated cells, excluding a direct, structural inhibition of n-K+ channels by ceramide.	transcription
66973	5	336151	5	NULL	NULL	0	NULL	sphingosine	Chemical		does not inhibit		significantly			n-K+ channels	GP				NULL	herbimycin A-treated cells	0	NULL	NULL	NULL	gw60_pnas_94_14_7661_s_108	9207149	Furthermore, dihydro-C2-ceramide or sphingosine did not significantly inhibit n-K+ channels in JCaM1.6 or herbimycin A-treated cells, excluding a direct, structural inhibition of n-K+ channels by ceramide.	transcription
66974	6	336151	5	NULL	NULL	0	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7661_s_108	9207149	Furthermore, dihydro-C2-ceramide or sphingosine did not significantly inhibit n-K+ channels in JCaM1.6 or herbimycin A-treated cells, excluding a direct, structural inhibition of n-K+ channels by ceramide.	transcription
66975	7	336151	5	NULL	NULL	NULL	NULL	ceramide	Chemical		inhibits		direct;;structural			n-K+ channels	GP				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_14_7661_s_108	9207149	Furthermore, dihydro-C2-ceramide or sphingosine did not significantly inhibit n-K+ channels in JCaM1.6 or herbimycin A-treated cells, excluding a direct, structural inhibition of n-K+ channels by ceramide.	transcription
66976	8	336151	5	NULL	NULL	0	NULL	statement 1	Process		exclude					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7661_s_108	9207149	Furthermore, dihydro-C2-ceramide or sphingosine did not significantly inhibit n-K+ channels in JCaM1.6 or herbimycin A-treated cells, excluding a direct, structural inhibition of n-K+ channels by ceramide.	transcription
66977	9	336151	5	NULL	NULL	0	NULL	statement 2	Process		exclude					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7661_s_108	9207149	Furthermore, dihydro-C2-ceramide or sphingosine did not significantly inhibit n-K+ channels in JCaM1.6 or herbimycin A-treated cells, excluding a direct, structural inhibition of n-K+ channels by ceramide.	transcription
66978	10	336151	5	NULL	NULL	0	NULL	statement 4	Process		exclude					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7661_s_108	9207149	Furthermore, dihydro-C2-ceramide or sphingosine did not significantly inhibit n-K+ channels in JCaM1.6 or herbimycin A-treated cells, excluding a direct, structural inhibition of n-K+ channels by ceramide.	transcription
66979	11	336151	5	NULL	NULL	0	NULL	statement 5	Process		exclude					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7661_s_108	9207149	Furthermore, dihydro-C2-ceramide or sphingosine did not significantly inhibit n-K+ channels in JCaM1.6 or herbimycin A-treated cells, excluding a direct, structural inhibition of n-K+ channels by ceramide.	transcription
69437	1	336151	7	NULL	NULL	0	NULL	dihydro-C2-ceramide	Chemical		does not inhibit		significantly			n-K+ channels	Chemical				NULL	JCaM1.6 treated cells	0	NULL	NULL	NULL	gw60_pnas_94_14_7661_s_108	9207149	Furthermore, dihydro-C2-ceramide or sphingosine did not significantly inhibit n-K+ channels in JCaM1.6 or herbimycin A-treated cells, excluding a direct, structural inhibition of n-K+ channels by ceramide.	transcription
69438	2	336151	7	NULL	NULL	0	NULL	 dihydro-C2-ceramide	Chemical		does not inhibit		significantly			n-K+ channels	Chemical				NULL	herbimycin A-treated cells	0	NULL	NULL	NULL	gw60_pnas_94_14_7661_s_108	9207149	Furthermore, dihydro-C2-ceramide or sphingosine did not significantly inhibit n-K+ channels in JCaM1.6 or herbimycin A-treated cells, excluding a direct, structural inhibition of n-K+ channels by ceramide.	transcription
69439	3	336151	7	NULL	NULL	0	NULL	sphingosine	Chemical		does not inhibit		significantly			n-K+ channels	Chemical				NULL	JCaM1.6 treated cells	0	NULL	NULL	NULL	gw60_pnas_94_14_7661_s_108	9207149	Furthermore, dihydro-C2-ceramide or sphingosine did not significantly inhibit n-K+ channels in JCaM1.6 or herbimycin A-treated cells, excluding a direct, structural inhibition of n-K+ channels by ceramide.	transcription
69440	4	336151	7	NULL	NULL	0	NULL	sphingosine	Chemical		does not inhibit		significantly			n-K+ channels	Chemical				NULL	herbimycin A-treated cells	0	NULL	NULL	NULL	gw60_pnas_94_14_7661_s_108	9207149	Furthermore, dihydro-C2-ceramide or sphingosine did not significantly inhibit n-K+ channels in JCaM1.6 or herbimycin A-treated cells, excluding a direct, structural inhibition of n-K+ channels by ceramide.	transcription
69441	5	336151	7	NULL	NULL	0	NULL	ceramide	Chemical		inhibit		direct;;structurally			n-K+ channels 	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7661_s_108	9207149	Furthermore, dihydro-C2-ceramide or sphingosine did not significantly inhibit n-K+ channels in JCaM1.6 or herbimycin A-treated cells, excluding a direct, structural inhibition of n-K+ channels by ceramide.	transcription
66980	1	336152	5	NULL	NULL	0	NULL	sphingosine-recycling pathway	Process		generates					long-chain ceramide	Chemical	endogenous			NULL		0	NULL	NULL	NULL	abs-batch0550-0559_biochem-j_393_pt-2_16201965_s_10	16201965	These  data demonstrate that the sphingosine-recycling pathway for the generation  of endogenous long-chain ceramide in response to exogenous C(6)-cer is  regulated by ROS, and plays an important biological role in controlling  c-Myc function.	transcription
66981	2	336152	5	NULL	NULL	0	NULL	statement 1	Process		in response to					C(6)-cer	Chemical	exogenous			NULL		0	NULL	NULL	NULL	abs-batch0550-0559_biochem-j_393_pt-2_16201965_s_10	16201965	These  data demonstrate that the sphingosine-recycling pathway for the generation  of endogenous long-chain ceramide in response to exogenous C(6)-cer is  regulated by ROS, and plays an important biological role in controlling  c-Myc function.	transcription
66982	3	336152	5	NULL	NULL	0	NULL	statement 2	Process		is regulated by					ROS	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0550-0559_biochem-j_393_pt-2_16201965_s_10	16201965	These  data demonstrate that the sphingosine-recycling pathway for the generation  of endogenous long-chain ceramide in response to exogenous C(6)-cer is  regulated by ROS, and plays an important biological role in controlling  c-Myc function.	transcription
66983	4	336152	5	NULL	NULL	0	NULL	statement 1	Process		plays a role in		biological			c-Myc	GP	controlling;;function of			NULL		0	NULL	NULL	NULL	abs-batch0550-0559_biochem-j_393_pt-2_16201965_s_10	16201965	These  data demonstrate that the sphingosine-recycling pathway for the generation  of endogenous long-chain ceramide in response to exogenous C(6)-cer is  regulated by ROS, and plays an important biological role in controlling  c-Myc function.	transcription
69442	1	336152	7	NULL	NULL	0	NULL	 C(6)-cer	Chemical	exogenous	generate					long-chain ceramide	Chemical	endogenous			NULL		0	NULL	NULL	NULL	abs-batch0550-0559_biochem-j_393_pt-2_16201965_s_10	16201965	These  data demonstrate that the sphingosine-recycling pathway for the generation  of endogenous long-chain ceramide in response to exogenous C(6)-cer is  regulated by ROS, and plays an important biological role in controlling  c-Myc function.	transcription
69443	2	336152	7	NULL	NULL	0	NULL	ROS	Chemical		regulate					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0550-0559_biochem-j_393_pt-2_16201965_s_10	16201965	These  data demonstrate that the sphingosine-recycling pathway for the generation  of endogenous long-chain ceramide in response to exogenous C(6)-cer is  regulated by ROS, and plays an important biological role in controlling  c-Myc function.	transcription
69444	3	336152	7	NULL	NULL	0	NULL	statement 2	Process		play a role in		important			c-Myc	GP	function of			NULL		0	NULL	NULL	NULL	abs-batch0550-0559_biochem-j_393_pt-2_16201965_s_10	16201965	These  data demonstrate that the sphingosine-recycling pathway for the generation  of endogenous long-chain ceramide in response to exogenous C(6)-cer is  regulated by ROS, and plays an important biological role in controlling  c-Myc function.	transcription
69445	4	336152	7	NULL	NULL	0	NULL	statement 1	Process		is a type of					sphingosine-recycling pathway	Process				NULL		0	NULL	NULL	NULL	abs-batch0550-0559_biochem-j_393_pt-2_16201965_s_10	16201965	These  data demonstrate that the sphingosine-recycling pathway for the generation  of endogenous long-chain ceramide in response to exogenous C(6)-cer is  regulated by ROS, and plays an important biological role in controlling  c-Myc function.	transcription
66984	1	336153	5	NULL	NULL	0	NULL	ceramide	Chemical		causes					apoptosis	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-mol-biol_39_2_16584625_s_3	16584625	The balance between cellular levels of these  bioactive products is increasingly recognized to be critical to cell regulation;  whereby, ceramide and sphingosine cause apoptosis and growth arrest phenotypes,  and sphingosine-1-phosphate mediates proliferative and angiogenic responses.	transcription
66985	2	336153	5	NULL	NULL	0	NULL	sphingosine	Chemical		causes					apoptosis	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-mol-biol_39_2_16584625_s_3	16584625	The balance between cellular levels of these  bioactive products is increasingly recognized to be critical to cell regulation;  whereby, ceramide and sphingosine cause apoptosis and growth arrest phenotypes,  and sphingosine-1-phosphate mediates proliferative and angiogenic responses.	transcription
66986	3	336153	5	NULL	NULL	0	NULL	ceramide	Chemical		causes					growth arrest phenotypes					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-mol-biol_39_2_16584625_s_3	16584625	The balance between cellular levels of these  bioactive products is increasingly recognized to be critical to cell regulation;  whereby, ceramide and sphingosine cause apoptosis and growth arrest phenotypes,  and sphingosine-1-phosphate mediates proliferative and angiogenic responses.	transcription
66987	4	336153	5	NULL	NULL	0	NULL	sphingosine	Chemical		causes					growth arrest phenotypes					NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-mol-biol_39_2_16584625_s_3	16584625	The balance between cellular levels of these  bioactive products is increasingly recognized to be critical to cell regulation;  whereby, ceramide and sphingosine cause apoptosis and growth arrest phenotypes,  and sphingosine-1-phosphate mediates proliferative and angiogenic responses.	transcription
66988	5	336153	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		mediates					proliferative responses	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-mol-biol_39_2_16584625_s_3	16584625	The balance between cellular levels of these  bioactive products is increasingly recognized to be critical to cell regulation;  whereby, ceramide and sphingosine cause apoptosis and growth arrest phenotypes,  and sphingosine-1-phosphate mediates proliferative and angiogenic responses.	transcription
66989	6	336153	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		mediates					angiogenic responses	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-mol-biol_39_2_16584625_s_3	16584625	The balance between cellular levels of these  bioactive products is increasingly recognized to be critical to cell regulation;  whereby, ceramide and sphingosine cause apoptosis and growth arrest phenotypes,  and sphingosine-1-phosphate mediates proliferative and angiogenic responses.	transcription
69446	1	336153	7	NULL	NULL	0	NULL	ceramide	Chemical		cause					apoptosis	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-mol-biol_39_2_16584625_s_3	16584625	The balance between cellular levels of these  bioactive products is increasingly recognized to be critical to cell regulation;  whereby, ceramide and sphingosine cause apoptosis and growth arrest phenotypes,  and sphingosine-1-phosphate mediates proliferative and angiogenic responses.	transcription
69447	2	336153	7	NULL	NULL	0	NULL	sphingosine	Chemical		cause					apoptosis	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-mol-biol_39_2_16584625_s_3	16584625	The balance between cellular levels of these  bioactive products is increasingly recognized to be critical to cell regulation;  whereby, ceramide and sphingosine cause apoptosis and growth arrest phenotypes,  and sphingosine-1-phosphate mediates proliferative and angiogenic responses.	transcription
69448	3	336153	7	NULL	NULL	0	NULL	ceramide	Chemical		cause					growth arrest phenotypes	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-mol-biol_39_2_16584625_s_3	16584625	The balance between cellular levels of these  bioactive products is increasingly recognized to be critical to cell regulation;  whereby, ceramide and sphingosine cause apoptosis and growth arrest phenotypes,  and sphingosine-1-phosphate mediates proliferative and angiogenic responses.	transcription
69449	4	336153	7	NULL	NULL	0	NULL	sphingosine	Chemical		cause					growth arrest phenotypes	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-mol-biol_39_2_16584625_s_3	16584625	The balance between cellular levels of these  bioactive products is increasingly recognized to be critical to cell regulation;  whereby, ceramide and sphingosine cause apoptosis and growth arrest phenotypes,  and sphingosine-1-phosphate mediates proliferative and angiogenic responses.	transcription
69450	5	336153	7	NULL	NULL	0	NULL	sphingosine-1-phosphate	Chemical		mediates					proliferative response	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-mol-biol_39_2_16584625_s_3	16584625	The balance between cellular levels of these  bioactive products is increasingly recognized to be critical to cell regulation;  whereby, ceramide and sphingosine cause apoptosis and growth arrest phenotypes,  and sphingosine-1-phosphate mediates proliferative and angiogenic responses.	transcription
69451	6	336153	7	NULL	NULL	0	NULL	sphingosine-1-phosphate	Chemical		mediates					angiogenic response	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biochem-mol-biol_39_2_16584625_s_3	16584625	The balance between cellular levels of these  bioactive products is increasingly recognized to be critical to cell regulation;  whereby, ceramide and sphingosine cause apoptosis and growth arrest phenotypes,  and sphingosine-1-phosphate mediates proliferative and angiogenic responses.	transcription
66990	1	336154	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					TNF-alpha	GP				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_cytokine_34_1-2_16730193_s_3	16730193	Sphingosine/ceramide  and nitric oxide have been associated with apoptosis induced by TNF-alpha;  however, signaling mechanisms of TNF-alpha-induced apoptosis in cardiac  myocytes are not well defined.	transcription
66991	2	336154	5	NULL	NULL	0	NULL	sphingosine/ceramide	Chemical		is associated with					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_cytokine_34_1-2_16730193_s_3	16730193	Sphingosine/ceramide  and nitric oxide have been associated with apoptosis induced by TNF-alpha;  however, signaling mechanisms of TNF-alpha-induced apoptosis in cardiac  myocytes are not well defined.	transcription
66992	3	336154	5	NULL	NULL	0	NULL	nitric oxide	Chemical		is associated with					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_cytokine_34_1-2_16730193_s_3	16730193	Sphingosine/ceramide  and nitric oxide have been associated with apoptosis induced by TNF-alpha;  however, signaling mechanisms of TNF-alpha-induced apoptosis in cardiac  myocytes are not well defined.	transcription
66993	4	336154	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					TNF-alpha	GP				NULL	cardiac myocytes	0	NULL	NULL	NULL	abs-batch0700-0719_cytokine_34_1-2_16730193_s_3	16730193	Sphingosine/ceramide  and nitric oxide have been associated with apoptosis induced by TNF-alpha;  however, signaling mechanisms of TNF-alpha-induced apoptosis in cardiac  myocytes are not well defined.	transcription
69452	1	336154	7	NULL	NULL	0	NULL	TNF-alpha	GP		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_cytokine_34_1-2_16730193_s_3	16730193	Sphingosine/ceramide  and nitric oxide have been associated with apoptosis induced by TNF-alpha;  however, signaling mechanisms of TNF-alpha-induced apoptosis in cardiac  myocytes are not well defined.	transcription
69453	2	336154	7	NULL	NULL	0	NULL	Sphingosine	Chemical		associated with					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_cytokine_34_1-2_16730193_s_3	16730193	Sphingosine/ceramide  and nitric oxide have been associated with apoptosis induced by TNF-alpha;  however, signaling mechanisms of TNF-alpha-induced apoptosis in cardiac  myocytes are not well defined.	transcription
69454	3	336154	7	NULL	NULL	0	NULL	ceramide	Chemical		associated with					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_cytokine_34_1-2_16730193_s_3	16730193	Sphingosine/ceramide  and nitric oxide have been associated with apoptosis induced by TNF-alpha;  however, signaling mechanisms of TNF-alpha-induced apoptosis in cardiac  myocytes are not well defined.	transcription
69455	4	336154	7	NULL	NULL	0	NULL	 nitric oxide	Chemical		associated with					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0700-0719_cytokine_34_1-2_16730193_s_3	16730193	Sphingosine/ceramide  and nitric oxide have been associated with apoptosis induced by TNF-alpha;  however, signaling mechanisms of TNF-alpha-induced apoptosis in cardiac  myocytes are not well defined.	transcription
69456	5	336154	7	NULL	NULL	0	NULL	TNF-alpha	GP		induce					apoptosis	Process				NULL	cardiac myocytes	0	NULL	NULL	NULL	abs-batch0700-0719_cytokine_34_1-2_16730193_s_3	16730193	Sphingosine/ceramide  and nitric oxide have been associated with apoptosis induced by TNF-alpha;  however, signaling mechanisms of TNF-alpha-induced apoptosis in cardiac  myocytes are not well defined.	transcription
66994	1	336155	5	NULL	NULL	0	NULL	PLD	GP		is					phospholipase D	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochim-biophys-acta_1348_3_9366247_s_6	9366247	Moreover, in contrast to sphingosine which activates  phospholipase D (PLD) leading to an increase in phosphatidic acid levels,  sphingomyelinase, but not ceramide analogs, reduced TPA-stimulated PLD  activity.	transcription
66995	2	336155	5	NULL	NULL	0	NULL	sphingosine	Chemical		activates					PLD	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochim-biophys-acta_1348_3_9366247_s_6	9366247	Moreover, in contrast to sphingosine which activates  phospholipase D (PLD) leading to an increase in phosphatidic acid levels,  sphingomyelinase, but not ceramide analogs, reduced TPA-stimulated PLD  activity.	transcription
66999	4	336155	5	NULL	NULL	NULL	NULL	PLD	GP	activity of	is stimulated by					TPA	Chemical				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_biochim-biophys-acta_1348_3_9366247_s_6	9366247	Moreover, in contrast to sphingosine which activates  phospholipase D (PLD) leading to an increase in phosphatidic acid levels,  sphingomyelinase, but not ceramide analogs, reduced TPA-stimulated PLD  activity.	transcription
67001	3	336155	5	NULL	NULL	0	NULL	statement 2	Process		increases					phosphatidic acid	Chemical	level of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochim-biophys-acta_1348_3_9366247_s_6	9366247	Moreover, in contrast to sphingosine which activates  phospholipase D (PLD) leading to an increase in phosphatidic acid levels,  sphingomyelinase, but not ceramide analogs, reduced TPA-stimulated PLD  activity.	transcription
67002	5	336155	5	NULL	NULL	0	NULL	sphingomyelinase	GP		reduce					statement 4	Process				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochim-biophys-acta_1348_3_9366247_s_6	9366247	Moreover, in contrast to sphingosine which activates  phospholipase D (PLD) leading to an increase in phosphatidic acid levels,  sphingomyelinase, but not ceramide analogs, reduced TPA-stimulated PLD  activity.	transcription
67003	6	336155	5	NULL	NULL	0	NULL	ceramide analogs	Chemical		does not reduce					statement 4	Process				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochim-biophys-acta_1348_3_9366247_s_6	9366247	Moreover, in contrast to sphingosine which activates  phospholipase D (PLD) leading to an increase in phosphatidic acid levels,  sphingomyelinase, but not ceramide analogs, reduced TPA-stimulated PLD  activity.	transcription
69457	1	336155	7	NULL	NULL	0	NULL	sphingosine	Chemical		activates					PLD	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochim-biophys-acta_1348_3_9366247_s_6	9366247	Moreover, in contrast to sphingosine which activates  phospholipase D (PLD) leading to an increase in phosphatidic acid levels,  sphingomyelinase, but not ceramide analogs, reduced TPA-stimulated PLD  activity.	transcription
69458	2	336155	7	NULL	NULL	0	NULL	statement 1	Process		increase					phosphatidic acid 	Chemical	levels of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochim-biophys-acta_1348_3_9366247_s_6	9366247	Moreover, in contrast to sphingosine which activates  phospholipase D (PLD) leading to an increase in phosphatidic acid levels,  sphingomyelinase, but not ceramide analogs, reduced TPA-stimulated PLD  activity.	transcription
69459	3	336155	7	NULL	NULL	0	NULL	statement 1	Process		increase					sphingomyelinase	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochim-biophys-acta_1348_3_9366247_s_6	9366247	Moreover, in contrast to sphingosine which activates  phospholipase D (PLD) leading to an increase in phosphatidic acid levels,  sphingomyelinase, but not ceramide analogs, reduced TPA-stimulated PLD  activity.	transcription
69460	4	336155	7	NULL	NULL	0	NULL	statement 1	Process		does not increase					ceramide analogs	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochim-biophys-acta_1348_3_9366247_s_6	9366247	Moreover, in contrast to sphingosine which activates  phospholipase D (PLD) leading to an increase in phosphatidic acid levels,  sphingomyelinase, but not ceramide analogs, reduced TPA-stimulated PLD  activity.	transcription
69461	5	336155	7	NULL	NULL	0	NULL	TPA	Chemical		stimulates					PLD	GP	activity of			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochim-biophys-acta_1348_3_9366247_s_6	9366247	Moreover, in contrast to sphingosine which activates  phospholipase D (PLD) leading to an increase in phosphatidic acid levels,  sphingomyelinase, but not ceramide analogs, reduced TPA-stimulated PLD  activity.	transcription
69462	6	336155	7	NULL	NULL	0	NULL	statement 1	Process		reduce					statement 5	Process				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochim-biophys-acta_1348_3_9366247_s_6	9366247	Moreover, in contrast to sphingosine which activates  phospholipase D (PLD) leading to an increase in phosphatidic acid levels,  sphingomyelinase, but not ceramide analogs, reduced TPA-stimulated PLD  activity.	transcription
69463	7	336155	7	NULL	NULL	0	NULL	PLD	GP		is					phospholipase D	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_biochim-biophys-acta_1348_3_9366247_s_6	9366247	Moreover, in contrast to sphingosine which activates  phospholipase D (PLD) leading to an increase in phosphatidic acid levels,  sphingomyelinase, but not ceramide analogs, reduced TPA-stimulated PLD  activity.	transcription
67004	1	336156	5	NULL	NULL	0	NULL	phospholipase D	GP	stimulation of	increases					phosphatidic acid	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_chem-phys-lipids_80_1-2_8681426_s_6	8681426	Stimulation  of phospholipase D leading to an increase in phosphatidic acid, a positive  regulator of cell growth, by sphingosine and SPP, and its inhibition by  ceramide, might be related to their opposite effects on cell growth.	transcription
67005	2	336156	5	NULL	NULL	0	NULL	phosphatidic acid	Chemical		is a regulator of		positive			cell growth	Process				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_chem-phys-lipids_80_1-2_8681426_s_6	8681426	Stimulation  of phospholipase D leading to an increase in phosphatidic acid, a positive  regulator of cell growth, by sphingosine and SPP, and its inhibition by  ceramide, might be related to their opposite effects on cell growth.	transcription
67006	3	336156	5	NULL	NULL	0	NULL	sphingosine	Chemical		is required for					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_chem-phys-lipids_80_1-2_8681426_s_6	8681426	Stimulation  of phospholipase D leading to an increase in phosphatidic acid, a positive  regulator of cell growth, by sphingosine and SPP, and its inhibition by  ceramide, might be related to their opposite effects on cell growth.	transcription
67007	4	336156	5	NULL	NULL	0	NULL	SPP	Chemical		is required for					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_chem-phys-lipids_80_1-2_8681426_s_6	8681426	Stimulation  of phospholipase D leading to an increase in phosphatidic acid, a positive  regulator of cell growth, by sphingosine and SPP, and its inhibition by  ceramide, might be related to their opposite effects on cell growth.	transcription
67008	5	336156	5	NULL	NULL	0	NULL	ceramide	Chemical		inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_chem-phys-lipids_80_1-2_8681426_s_6	8681426	Stimulation  of phospholipase D leading to an increase in phosphatidic acid, a positive  regulator of cell growth, by sphingosine and SPP, and its inhibition by  ceramide, might be related to their opposite effects on cell growth.	transcription
71170	1	336156	7	NULL	NULL	NULL	NULL	phospholipase D	GP	stimulation of	leads to					phosphatidic acid	Chemical	increase in			NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_chem-phys-lipids_80_1-2_8681426_s_6	8681426	Stimulation  of phospholipase D leading to an increase in phosphatidic acid, a positive  regulator of cell growth, by sphingosine and SPP, and its inhibition by  ceramide, might be related to their opposite effects on cell growth.	transcription
71171	2	336156	7	NULL	NULL	NULL	NULL	phosphatidic acid	Chemical		 regulator of		 positive			cell growth	Process				NULL		NULL	NULL	NULL	NULL	abs-batch0720-0739_chem-phys-lipids_80_1-2_8681426_s_6	8681426	Stimulation  of phospholipase D leading to an increase in phosphatidic acid, a positive  regulator of cell growth, by sphingosine and SPP, and its inhibition by  ceramide, might be related to their opposite effects on cell growth.	transcription
71172	3	336156	7	NULL	NULL	0	NULL	sphingosine	Chemical		stimulate					phospholipase D	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_chem-phys-lipids_80_1-2_8681426_s_6	8681426	Stimulation  of phospholipase D leading to an increase in phosphatidic acid, a positive  regulator of cell growth, by sphingosine and SPP, and its inhibition by  ceramide, might be related to their opposite effects on cell growth.	transcription
71173	4	336156	7	NULL	NULL	0	NULL	SPP	Chemical		stimulate					phospholipase D	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_chem-phys-lipids_80_1-2_8681426_s_6	8681426	Stimulation  of phospholipase D leading to an increase in phosphatidic acid, a positive  regulator of cell growth, by sphingosine and SPP, and its inhibition by  ceramide, might be related to their opposite effects on cell growth.	transcription
71174	5	336156	7	NULL	NULL	0	NULL	ceramide	Chemical		inhibit					phospholipase D	GP				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_chem-phys-lipids_80_1-2_8681426_s_6	8681426	Stimulation  of phospholipase D leading to an increase in phosphatidic acid, a positive  regulator of cell growth, by sphingosine and SPP, and its inhibition by  ceramide, might be related to their opposite effects on cell growth.	transcription
71175	6	336156	7	NULL	NULL	0	NULL	statement 5	Process		cause					cell growth	Process	opposite effect on			NULL		0	NULL	NULL	NULL	abs-batch0720-0739_chem-phys-lipids_80_1-2_8681426_s_6	8681426	Stimulation  of phospholipase D leading to an increase in phosphatidic acid, a positive  regulator of cell growth, by sphingosine and SPP, and its inhibition by  ceramide, might be related to their opposite effects on cell growth.	transcription
67009	1	336157	5	NULL	NULL	NULL	NULL	promotive immune response	Process		is induced by					alpha-mannosyl ceramide analogues	Chemical				NULL	Valpha19 NKT cell	NULL	NULL	NULL	NULL	abs-batch0720-0739_eur-j-med-chem_41_5_16545892_s_1	16545892	Induction of promotive rather than suppressive immune responses from a novel NKT cell repertoire Valpha19 NKT cell with alpha-mannosyl ceramide analogues consisting of the immunosuppressant ISP-I as the sphingosine unit..	transcription
67010	2	336157	5	NULL	NULL	0	NULL	alpha-mannosyl ceramide analogues	Chemical		consists of					ISP-I	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_eur-j-med-chem_41_5_16545892_s_1	16545892	Induction of promotive rather than suppressive immune responses from a novel NKT cell repertoire Valpha19 NKT cell with alpha-mannosyl ceramide analogues consisting of the immunosuppressant ISP-I as the sphingosine unit..	transcription
67011	3	336157	5	NULL	NULL	0	NULL	ISP-I	Chemical		is a type of					immunosuppressant	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_eur-j-med-chem_41_5_16545892_s_1	16545892	Induction of promotive rather than suppressive immune responses from a novel NKT cell repertoire Valpha19 NKT cell with alpha-mannosyl ceramide analogues consisting of the immunosuppressant ISP-I as the sphingosine unit..	transcription
67012	4	336157	5	NULL	NULL	0	NULL	ISP-I	Chemical		is a unit of					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_eur-j-med-chem_41_5_16545892_s_1	16545892	Induction of promotive rather than suppressive immune responses from a novel NKT cell repertoire Valpha19 NKT cell with alpha-mannosyl ceramide analogues consisting of the immunosuppressant ISP-I as the sphingosine unit..	transcription
67013	5	336157	5	NULL	NULL	0	NULL	Valpha19 NKT cell	Cell		is repertoire of		novel			NKT cell	Cell				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_eur-j-med-chem_41_5_16545892_s_1	16545892	Induction of promotive rather than suppressive immune responses from a novel NKT cell repertoire Valpha19 NKT cell with alpha-mannosyl ceramide analogues consisting of the immunosuppressant ISP-I as the sphingosine unit..	transcription
67014	6	336157	5	NULL	NULL	NULL	NULL	suppressive immune response	Process		is not induced by					alpha-mannosyl ceramide analogues	Chemical				NULL	Valpha19 NKT cell	NULL	NULL	NULL	NULL	abs-batch0720-0739_eur-j-med-chem_41_5_16545892_s_1	16545892	Induction of promotive rather than suppressive immune responses from a novel NKT cell repertoire Valpha19 NKT cell with alpha-mannosyl ceramide analogues consisting of the immunosuppressant ISP-I as the sphingosine unit..	transcription
71176	1	336157	7	NULL	NULL	0	NULL	Valpha19 NKT cell 	Cell		consist of					alpha-mannosyl ceramide analogues	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_eur-j-med-chem_41_5_16545892_s_1	16545892	Induction of promotive rather than suppressive immune responses from a novel NKT cell repertoire Valpha19 NKT cell with alpha-mannosyl ceramide analogues consisting of the immunosuppressant ISP-I as the sphingosine unit..	transcription
71177	2	336157	7	NULL	NULL	0	NULL	alpha-mannosyl ceramide analogues	Chemical		consist of					ISP-I 	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_eur-j-med-chem_41_5_16545892_s_1	16545892	Induction of promotive rather than suppressive immune responses from a novel NKT cell repertoire Valpha19 NKT cell with alpha-mannosyl ceramide analogues consisting of the immunosuppressant ISP-I as the sphingosine unit..	transcription
71178	3	336157	7	NULL	NULL	0	NULL	ISP-I 	Chemical		is a type of					immunosuppressant	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_eur-j-med-chem_41_5_16545892_s_1	16545892	Induction of promotive rather than suppressive immune responses from a novel NKT cell repertoire Valpha19 NKT cell with alpha-mannosyl ceramide analogues consisting of the immunosuppressant ISP-I as the sphingosine unit..	transcription
71179	4	336157	7	NULL	NULL	0	NULL	ISP-I	Chemical		is a type of					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_eur-j-med-chem_41_5_16545892_s_1	16545892	Induction of promotive rather than suppressive immune responses from a novel NKT cell repertoire Valpha19 NKT cell with alpha-mannosyl ceramide analogues consisting of the immunosuppressant ISP-I as the sphingosine unit..	transcription
71180	5	336157	7	NULL	NULL	0	NULL	Valpha19 NKT cell	Cell		induce					promotive immune response	Process				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_eur-j-med-chem_41_5_16545892_s_1	16545892	Induction of promotive rather than suppressive immune responses from a novel NKT cell repertoire Valpha19 NKT cell with alpha-mannosyl ceramide analogues consisting of the immunosuppressant ISP-I as the sphingosine unit..	transcription
71181	6	336157	7	NULL	NULL	0	NULL	Valpha19 NKT cell	Cell		is a type of					novel NKT cell repertoire	Cell				NULL		0	NULL	NULL	NULL	abs-batch0720-0739_eur-j-med-chem_41_5_16545892_s_1	16545892	Induction of promotive rather than suppressive immune responses from a novel NKT cell repertoire Valpha19 NKT cell with alpha-mannosyl ceramide analogues consisting of the immunosuppressant ISP-I as the sphingosine unit..	transcription
67015	1	336158	5	NULL	NULL	0	NULL	sphingosine	Chemical	exogenous	increases					ceramide acyl chain species	Chemical	mass of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_249	16118219	Exogenous sphingosine increased the mass of all ceramide acyl chain species, most obviously enhancing the C16 and C18 species ( Fig. 9 A), and as suggested from the labeling experiments ( Fig. 8 B), expression of SphK1 reduced, whereas SphK2 increased all ceramide species ( Fig. 9 A).	transcription
67016	2	336158	5	NULL	NULL	NULL	NULL	sphingosine	Chemical	exogenous	enhances					C16 ceramide	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_249	16118219	Exogenous sphingosine increased the mass of all ceramide acyl chain species, most obviously enhancing the C16 and C18 species ( Fig. 9 A), and as suggested from the labeling experiments ( Fig. 8 B), expression of SphK1 reduced, whereas SphK2 increased all ceramide species ( Fig. 9 A).	transcription
67017	3	336158	5	NULL	NULL	0	NULL	sphingosine	Chemical	exogenous	enhances					C18 ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_249	16118219	Exogenous sphingosine increased the mass of all ceramide acyl chain species, most obviously enhancing the C16 and C18 species ( Fig. 9 A), and as suggested from the labeling experiments ( Fig. 8 B), expression of SphK1 reduced, whereas SphK2 increased all ceramide species ( Fig. 9 A).	transcription
67018	4	336158	5	NULL	NULL	NULL	NULL	SphK1	GP	expression of	reduce					ceramide species	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_249	16118219	Exogenous sphingosine increased the mass of all ceramide acyl chain species, most obviously enhancing the C16 and C18 species ( Fig. 9 A), and as suggested from the labeling experiments ( Fig. 8 B), expression of SphK1 reduced, whereas SphK2 increased all ceramide species ( Fig. 9 A).	transcription
67019	5	336158	5	NULL	NULL	0	NULL	SphK2	GP	expression of	increases					ceramide species	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_249	16118219	Exogenous sphingosine increased the mass of all ceramide acyl chain species, most obviously enhancing the C16 and C18 species ( Fig. 9 A), and as suggested from the labeling experiments ( Fig. 8 B), expression of SphK1 reduced, whereas SphK2 increased all ceramide species ( Fig. 9 A).	transcription
71184	1	336158	7	NULL	NULL	0	NULL	sphingosine	Chemical	exogenous	increase					ceramide acyl chain species	Chemical	mass of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_249	16118219	Exogenous sphingosine increased the mass of all ceramide acyl chain species, most obviously enhancing the C16 and C18 species ( Fig. 9 A), and as suggested from the labeling experiments ( Fig. 8 B), expression of SphK1 reduced, whereas SphK2 increased all ceramide species ( Fig. 9 A).	transcription
71185	2	336158	7	NULL	NULL	NULL	NULL	statement 1	Process		enhance					C16 species	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_249	16118219	Exogenous sphingosine increased the mass of all ceramide acyl chain species, most obviously enhancing the C16 and C18 species ( Fig. 9 A), and as suggested from the labeling experiments ( Fig. 8 B), expression of SphK1 reduced, whereas SphK2 increased all ceramide species ( Fig. 9 A).	transcription
71187	3	336158	7	NULL	NULL	0	NULL	statement 1	Process		enhance					C18 species	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_249	16118219	Exogenous sphingosine increased the mass of all ceramide acyl chain species, most obviously enhancing the C16 and C18 species ( Fig. 9 A), and as suggested from the labeling experiments ( Fig. 8 B), expression of SphK1 reduced, whereas SphK2 increased all ceramide species ( Fig. 9 A).	transcription
71191	4	336158	7	NULL	NULL	NULL	NULL	SphK1	GP	expression of	reduce					ceramide species	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_249	16118219	Exogenous sphingosine increased the mass of all ceramide acyl chain species, most obviously enhancing the C16 and C18 species ( Fig. 9 A), and as suggested from the labeling experiments ( Fig. 8 B), expression of SphK1 reduced, whereas SphK2 increased all ceramide species ( Fig. 9 A).	transcription
71193	5	336158	7	NULL	NULL	0	NULL	SphK2	GP		increase					ceramide species	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_44_37118_s_249	16118219	Exogenous sphingosine increased the mass of all ceramide acyl chain species, most obviously enhancing the C16 and C18 species ( Fig. 9 A), and as suggested from the labeling experiments ( Fig. 8 B), expression of SphK1 reduced, whereas SphK2 increased all ceramide species ( Fig. 9 A).	transcription
67020	1	336159	5	NULL	NULL	0	NULL	fumonisin B1	Chemical		inhibits					ceramide	Chemical	formation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_11	15546881	This conclusion was based on the following: 1) the ability of fumonisin B1 but not myriocin to inhibit ceramide formation, 2) the ability of PMA to induce increases in palmitate-labeled ceramide only under chase labeling but not acute pulse labeling, 3) the induction of the levels of sphingosine but not dihydrosphingosine in response to PMA, and 4) induction of sphingomyelin hydrolysis in response to PMA.	transcription
67021	2	336159	5	NULL	NULL	0	NULL	myriocin	Chemical		does not inhibit					ceramide	Chemical	formation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_11	15546881	This conclusion was based on the following: 1) the ability of fumonisin B1 but not myriocin to inhibit ceramide formation, 2) the ability of PMA to induce increases in palmitate-labeled ceramide only under chase labeling but not acute pulse labeling, 3) the induction of the levels of sphingosine but not dihydrosphingosine in response to PMA, and 4) induction of sphingomyelin hydrolysis in response to PMA.	transcription
67022	3	336159	5	NULL	NULL	0	NULL	PMA	Chemical		increases					ceramide	Chemical	palmitate-labeled			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_11	15546881	This conclusion was based on the following: 1) the ability of fumonisin B1 but not myriocin to inhibit ceramide formation, 2) the ability of PMA to induce increases in palmitate-labeled ceramide only under chase labeling but not acute pulse labeling, 3) the induction of the levels of sphingosine but not dihydrosphingosine in response to PMA, and 4) induction of sphingomyelin hydrolysis in response to PMA.	transcription
67023	4	336159	5	NULL	NULL	0	NULL	PMA	Chemical		induce					sphingosine	Chemical	level of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_11	15546881	This conclusion was based on the following: 1) the ability of fumonisin B1 but not myriocin to inhibit ceramide formation, 2) the ability of PMA to induce increases in palmitate-labeled ceramide only under chase labeling but not acute pulse labeling, 3) the induction of the levels of sphingosine but not dihydrosphingosine in response to PMA, and 4) induction of sphingomyelin hydrolysis in response to PMA.	transcription
67024	5	336159	5	NULL	NULL	0	NULL	PMA	Chemical		does not induce					dihydrosphingosine	Chemical	level of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_11	15546881	This conclusion was based on the following: 1) the ability of fumonisin B1 but not myriocin to inhibit ceramide formation, 2) the ability of PMA to induce increases in palmitate-labeled ceramide only under chase labeling but not acute pulse labeling, 3) the induction of the levels of sphingosine but not dihydrosphingosine in response to PMA, and 4) induction of sphingomyelin hydrolysis in response to PMA.	transcription
67025	6	336159	5	NULL	NULL	0	NULL	PMA	Chemical		induce					sphingomyelin	Chemical	hydrolysis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_11	15546881	This conclusion was based on the following: 1) the ability of fumonisin B1 but not myriocin to inhibit ceramide formation, 2) the ability of PMA to induce increases in palmitate-labeled ceramide only under chase labeling but not acute pulse labeling, 3) the induction of the levels of sphingosine but not dihydrosphingosine in response to PMA, and 4) induction of sphingomyelin hydrolysis in response to PMA.	transcription
71234	1	336159	7	NULL	NULL	0	NULL	fumonisin B1	Chemical		inhibit					ceramide	Chemical	formation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_11	15546881	This conclusion was based on the following: 1) the ability of fumonisin B1 but not myriocin to inhibit ceramide formation, 2) the ability of PMA to induce increases in palmitate-labeled ceramide only under chase labeling but not acute pulse labeling, 3) the induction of the levels of sphingosine but not dihydrosphingosine in response to PMA, and 4) induction of sphingomyelin hydrolysis in response to PMA.	transcription
71235	2	336159	7	NULL	NULL	0	NULL	myriocin	Chemical		does not inhibit					ceramide	Chemical	formation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_11	15546881	This conclusion was based on the following: 1) the ability of fumonisin B1 but not myriocin to inhibit ceramide formation, 2) the ability of PMA to induce increases in palmitate-labeled ceramide only under chase labeling but not acute pulse labeling, 3) the induction of the levels of sphingosine but not dihydrosphingosine in response to PMA, and 4) induction of sphingomyelin hydrolysis in response to PMA.	transcription
71236	3	336159	7	NULL	NULL	0	NULL	 PMA	Chemical		induce					ceramide	Chemical	increase in palmitate-labeled			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_11	15546881	This conclusion was based on the following: 1) the ability of fumonisin B1 but not myriocin to inhibit ceramide formation, 2) the ability of PMA to induce increases in palmitate-labeled ceramide only under chase labeling but not acute pulse labeling, 3) the induction of the levels of sphingosine but not dihydrosphingosine in response to PMA, and 4) induction of sphingomyelin hydrolysis in response to PMA.	transcription
71237	4	336159	7	NULL	NULL	0	NULL	PMA	Chemical		induce					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_11	15546881	This conclusion was based on the following: 1) the ability of fumonisin B1 but not myriocin to inhibit ceramide formation, 2) the ability of PMA to induce increases in palmitate-labeled ceramide only under chase labeling but not acute pulse labeling, 3) the induction of the levels of sphingosine but not dihydrosphingosine in response to PMA, and 4) induction of sphingomyelin hydrolysis in response to PMA.	transcription
71238	5	336159	7	NULL	NULL	0	NULL	PMA	Chemical		does not induce					dihydrosphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_11	15546881	This conclusion was based on the following: 1) the ability of fumonisin B1 but not myriocin to inhibit ceramide formation, 2) the ability of PMA to induce increases in palmitate-labeled ceramide only under chase labeling but not acute pulse labeling, 3) the induction of the levels of sphingosine but not dihydrosphingosine in response to PMA, and 4) induction of sphingomyelin hydrolysis in response to PMA.	transcription
71239	6	336159	7	NULL	NULL	0	NULL	PMA	Chemical		induce					sphingomyelin	Chemical	hydrolysis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_4_2606_s_11	15546881	This conclusion was based on the following: 1) the ability of fumonisin B1 but not myriocin to inhibit ceramide formation, 2) the ability of PMA to induce increases in palmitate-labeled ceramide only under chase labeling but not acute pulse labeling, 3) the induction of the levels of sphingosine but not dihydrosphingosine in response to PMA, and 4) induction of sphingomyelin hydrolysis in response to PMA.	transcription
67026	1	336160	5	NULL	NULL	0	NULL	AC	GP	recombinant	catalyzes					ceramide	Chemical	degradation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_34	12815059	We find that many properties of the recombinant enzyme are similar to  those reported previously for enzyme obtained from natural sources and that in  addition to ceramide degradation, recombinant AC could catalyze ceramide  synthesis using free fatty acid and sphingosine as substrates.	transcription
67027	2	336160	5	NULL	NULL	0	NULL	AC	GP	recombinant	catalyzes					ceramide	Chemical	synthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_34	12815059	We find that many properties of the recombinant enzyme are similar to  those reported previously for enzyme obtained from natural sources and that in  addition to ceramide degradation, recombinant AC could catalyze ceramide  synthesis using free fatty acid and sphingosine as substrates.	transcription
67028	3	336160	5	NULL	NULL	0	NULL	fatty acid	Chemical	free	is a substrate for					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_34	12815059	We find that many properties of the recombinant enzyme are similar to  those reported previously for enzyme obtained from natural sources and that in  addition to ceramide degradation, recombinant AC could catalyze ceramide  synthesis using free fatty acid and sphingosine as substrates.	transcription
67029	4	336160	5	NULL	NULL	0	NULL	sphingosine	Chemical		is a substrate for					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_34	12815059	We find that many properties of the recombinant enzyme are similar to  those reported previously for enzyme obtained from natural sources and that in  addition to ceramide degradation, recombinant AC could catalyze ceramide  synthesis using free fatty acid and sphingosine as substrates.	transcription
71240	1	336160	7	NULL	NULL	0	NULL	AC 	GP	recombinant	catalyze					 ceramide 	Chemical	synthesis of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_34	12815059	We find that many properties of the recombinant enzyme are similar to  those reported previously for enzyme obtained from natural sources and that in  addition to ceramide degradation, recombinant AC could catalyze ceramide  synthesis using free fatty acid and sphingosine as substrates.	transcription
71241	2	336160	7	NULL	NULL	0	NULL	sphingosine	Chemical		act as					substrate	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_34	12815059	We find that many properties of the recombinant enzyme are similar to  those reported previously for enzyme obtained from natural sources and that in  addition to ceramide degradation, recombinant AC could catalyze ceramide  synthesis using free fatty acid and sphingosine as substrates.	transcription
71242	3	336160	7	NULL	NULL	0	NULL	free fatty acid	Chemical		act as					substrate	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_34	12815059	We find that many properties of the recombinant enzyme are similar to  those reported previously for enzyme obtained from natural sources and that in  addition to ceramide degradation, recombinant AC could catalyze ceramide  synthesis using free fatty acid and sphingosine as substrates.	transcription
71243	4	336160	7	NULL	NULL	0	NULL	statement 2	Process		occur along with					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_34	12815059	We find that many properties of the recombinant enzyme are similar to  those reported previously for enzyme obtained from natural sources and that in  addition to ceramide degradation, recombinant AC could catalyze ceramide  synthesis using free fatty acid and sphingosine as substrates.	transcription
71244	5	336160	7	NULL	NULL	NULL	NULL	AC	Chemical	recombinant	catalyze					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_34	12815059	We find that many properties of the recombinant enzyme are similar to  those reported previously for enzyme obtained from natural sources and that in  addition to ceramide degradation, recombinant AC could catalyze ceramide  synthesis using free fatty acid and sphingosine as substrates.	transcription
71245	6	336160	7	NULL	NULL	0	NULL	AC	GP	recombinant	catalyze					ceramide	Chemical	degradation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_35_32978_s_34	12815059	We find that many properties of the recombinant enzyme are similar to  those reported previously for enzyme obtained from natural sources and that in  addition to ceramide degradation, recombinant AC could catalyze ceramide  synthesis using free fatty acid and sphingosine as substrates.	transcription
67030	1	336161	5	NULL	NULL	0	NULL	ceramide	Chemical	synthesis of	is involved in		potentially			PA	Chemical	growth-limiting properties of			NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_1_118_s_192	12518030	To further evaluate if ceramide synthesis could be involved in the growth-limiting properties of PA and TTA, we cultivated PA and TTA-treated D54Mg ( Fig. 7C) and BT4Cn ( Fig. 7D) cells in the absence or presence of sphingosine 1-phosphate, a compound that is known to prevent ceramide-mediated apoptosis ( ), and four different inhibitors of enzymes involved in sphingolipid metabolism.	transcription
67031	2	336161	5	NULL	NULL	0	NULL	ceramide	Chemical	synthesis of	is involved in		potentially			TTA	Chemical	growth-limiting properties of 			NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_1_118_s_192	12518030	To further evaluate if ceramide synthesis could be involved in the growth-limiting properties of PA and TTA, we cultivated PA and TTA-treated D54Mg ( Fig. 7C) and BT4Cn ( Fig. 7D) cells in the absence or presence of sphingosine 1-phosphate, a compound that is known to prevent ceramide-mediated apoptosis ( ), and four different inhibitors of enzymes involved in sphingolipid metabolism.	transcription
67032	3	336161	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_1_118_s_192	12518030	To further evaluate if ceramide synthesis could be involved in the growth-limiting properties of PA and TTA, we cultivated PA and TTA-treated D54Mg ( Fig. 7C) and BT4Cn ( Fig. 7D) cells in the absence or presence of sphingosine 1-phosphate, a compound that is known to prevent ceramide-mediated apoptosis ( ), and four different inhibitors of enzymes involved in sphingolipid metabolism.	transcription
67033	4	336161	5	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		prevents					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_1_118_s_192	12518030	To further evaluate if ceramide synthesis could be involved in the growth-limiting properties of PA and TTA, we cultivated PA and TTA-treated D54Mg ( Fig. 7C) and BT4Cn ( Fig. 7D) cells in the absence or presence of sphingosine 1-phosphate, a compound that is known to prevent ceramide-mediated apoptosis ( ), and four different inhibitors of enzymes involved in sphingolipid metabolism.	transcription
71272	1	336161	7	NULL	NULL	0	NULL	ceramide	Chemical		mediates					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_1_118_s_192	12518030	To further evaluate if ceramide synthesis could be involved in the growth-limiting properties of PA and TTA, we cultivated PA and TTA-treated D54Mg ( Fig. 7C) and BT4Cn ( Fig. 7D) cells in the absence or presence of sphingosine 1-phosphate, a compound that is known to prevent ceramide-mediated apoptosis ( ), and four different inhibitors of enzymes involved in sphingolipid metabolism.	transcription
71273	2	336161	7	NULL	NULL	0	NULL	sphingosine 1-phosphate	Chemical		prevent					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_1_118_s_192	12518030	To further evaluate if ceramide synthesis could be involved in the growth-limiting properties of PA and TTA, we cultivated PA and TTA-treated D54Mg ( Fig. 7C) and BT4Cn ( Fig. 7D) cells in the absence or presence of sphingosine 1-phosphate, a compound that is known to prevent ceramide-mediated apoptosis ( ), and four different inhibitors of enzymes involved in sphingolipid metabolism.	transcription
67034	1	336162	5	NULL	NULL	0	NULL	ceramide	Chemical	M. sexta	induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_45_7_1221_s_245	15102888	The results provided initial evidence suggesting that the ceramide mixture obtained from stage 12  M. sexta is more effective in inducing apoptosis than the commercial ceramide lacking extra unsaturation, supporting the hypothesis that the extra unsaturation at C-6 of the sphingosine enhances apoptosis.	transcription
67035	2	336162	5	NULL	NULL	0	NULL	ceramide	Chemical	commercial	induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_45_7_1221_s_245	15102888	The results provided initial evidence suggesting that the ceramide mixture obtained from stage 12  M. sexta is more effective in inducing apoptosis than the commercial ceramide lacking extra unsaturation, supporting the hypothesis that the extra unsaturation at C-6 of the sphingosine enhances apoptosis.	transcription
67036	3	336162	5	NULL	NULL	0	NULL	statement 1	Process		more effective than					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_45_7_1221_s_245	15102888	The results provided initial evidence suggesting that the ceramide mixture obtained from stage 12  M. sexta is more effective in inducing apoptosis than the commercial ceramide lacking extra unsaturation, supporting the hypothesis that the extra unsaturation at C-6 of the sphingosine enhances apoptosis.	transcription
67037	4	336162	5	NULL	NULL	0	NULL	sphingosine	Chemical	extra unsaturation at C-6 of	enhances					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_45_7_1221_s_245	15102888	The results provided initial evidence suggesting that the ceramide mixture obtained from stage 12  M. sexta is more effective in inducing apoptosis than the commercial ceramide lacking extra unsaturation, supporting the hypothesis that the extra unsaturation at C-6 of the sphingosine enhances apoptosis.	transcription
67038	5	336162	5	NULL	NULL	0	NULL	ceramide	Chemical	commercial	lacks					unsaturation	Process	extra			NULL		0	NULL	NULL	NULL	gw70_jlipidres_45_7_1221_s_245	15102888	The results provided initial evidence suggesting that the ceramide mixture obtained from stage 12  M. sexta is more effective in inducing apoptosis than the commercial ceramide lacking extra unsaturation, supporting the hypothesis that the extra unsaturation at C-6 of the sphingosine enhances apoptosis.	transcription
71274	1	336162	7	NULL	NULL	0	NULL	ceramide mixture	Chemical		obtained from					stage 12 M. sexta	Organism				NULL		0	NULL	NULL	NULL	gw70_jlipidres_45_7_1221_s_245	15102888	The results provided initial evidence suggesting that the ceramide mixture obtained from stage 12  M. sexta is more effective in inducing apoptosis than the commercial ceramide lacking extra unsaturation, supporting the hypothesis that the extra unsaturation at C-6 of the sphingosine enhances apoptosis.	transcription
71275	2	336162	7	NULL	NULL	0	NULL	statement 1	Process		induce		effectively			apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_45_7_1221_s_245	15102888	The results provided initial evidence suggesting that the ceramide mixture obtained from stage 12  M. sexta is more effective in inducing apoptosis than the commercial ceramide lacking extra unsaturation, supporting the hypothesis that the extra unsaturation at C-6 of the sphingosine enhances apoptosis.	transcription
71276	3	336162	7	NULL	NULL	NULL	NULL	sphingosine	Chemical	unsaturation at C-6	enhance					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_45_7_1221_s_245	15102888	The results provided initial evidence suggesting that the ceramide mixture obtained from stage 12  M. sexta is more effective in inducing apoptosis than the commercial ceramide lacking extra unsaturation, supporting the hypothesis that the extra unsaturation at C-6 of the sphingosine enhances apoptosis.	transcription
67039	1	336163	5	NULL	NULL	0	NULL	TID-ceramide	Chemical	radiolabelled	bind					CTSD	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_73	10508159	As shown in Figure  2A, D- erythro-C6-ceramide and D- erythro-sphingosine dose-dependently competed for binding of the radiolabeled [125]TID-ceramide, whereas the biologically inactive D- erythro-dihydroceramide and D- erythro-dihydrosphingosine were significantly less potent in competing for TID-ceramide binding to CTSD.	transcription
67040	2	336163	5	NULL	NULL	0	NULL	D- erythro-C6-ceramide	Chemical		bind					CTSD	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_73	10508159	As shown in Figure  2A, D- erythro-C6-ceramide and D- erythro-sphingosine dose-dependently competed for binding of the radiolabeled [125]TID-ceramide, whereas the biologically inactive D- erythro-dihydroceramide and D- erythro-dihydrosphingosine were significantly less potent in competing for TID-ceramide binding to CTSD.	transcription
67041	3	336163	5	NULL	NULL	0	NULL	D- erythro-sphingosine	Chemical		bind					CTSD	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_73	10508159	As shown in Figure  2A, D- erythro-C6-ceramide and D- erythro-sphingosine dose-dependently competed for binding of the radiolabeled [125]TID-ceramide, whereas the biologically inactive D- erythro-dihydroceramide and D- erythro-dihydrosphingosine were significantly less potent in competing for TID-ceramide binding to CTSD.	transcription
67042	4	336163	5	NULL	NULL	0	NULL	statement 2	Process		competes with		dose dependently			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_73	10508159	As shown in Figure  2A, D- erythro-C6-ceramide and D- erythro-sphingosine dose-dependently competed for binding of the radiolabeled [125]TID-ceramide, whereas the biologically inactive D- erythro-dihydroceramide and D- erythro-dihydrosphingosine were significantly less potent in competing for TID-ceramide binding to CTSD.	transcription
67043	5	336163	5	NULL	NULL	0	NULL	statement 3	Process		competes with		dose dependently			statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_73	10508159	As shown in Figure  2A, D- erythro-C6-ceramide and D- erythro-sphingosine dose-dependently competed for binding of the radiolabeled [125]TID-ceramide, whereas the biologically inactive D- erythro-dihydroceramide and D- erythro-dihydrosphingosine were significantly less potent in competing for TID-ceramide binding to CTSD.	transcription
67044	6	336163	5	NULL	NULL	0	NULL	D- erythro-dihydroceramide	Chemical	biologically inactive	bind					CTSD	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_73	10508159	As shown in Figure  2A, D- erythro-C6-ceramide and D- erythro-sphingosine dose-dependently competed for binding of the radiolabeled [125]TID-ceramide, whereas the biologically inactive D- erythro-dihydroceramide and D- erythro-dihydrosphingosine were significantly less potent in competing for TID-ceramide binding to CTSD.	transcription
67045	7	336163	5	NULL	NULL	0	NULL	D- erythro-dihydrosphingosine	Chemical		bind					CTSD	GP				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_73	10508159	As shown in Figure  2A, D- erythro-C6-ceramide and D- erythro-sphingosine dose-dependently competed for binding of the radiolabeled [125]TID-ceramide, whereas the biologically inactive D- erythro-dihydroceramide and D- erythro-dihydrosphingosine were significantly less potent in competing for TID-ceramide binding to CTSD.	transcription
67046	8	336163	5	NULL	NULL	NULL	NULL	statement 7	Process		competes with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_19_5252_s_73	10508159	As shown in Figure  2A, D- erythro-C6-ceramide and D- erythro-sphingosine dose-dependently competed for binding of the radiolabeled [125]TID-ceramide, whereas the biologically inactive D- erythro-dihydroceramide and D- erythro-dihydrosphingosine were significantly less potent in competing for TID-ceramide binding to CTSD.	transcription
67047	9	336163	5	NULL	NULL	NULL	NULL	statement 6	Process		competes with					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_19_5252_s_73	10508159	As shown in Figure  2A, D- erythro-C6-ceramide and D- erythro-sphingosine dose-dependently competed for binding of the radiolabeled [125]TID-ceramide, whereas the biologically inactive D- erythro-dihydroceramide and D- erythro-dihydrosphingosine were significantly less potent in competing for TID-ceramide binding to CTSD.	transcription
67048	10	336163	5	NULL	NULL	0	NULL	statement 8	Process		less potent than					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_73	10508159	As shown in Figure  2A, D- erythro-C6-ceramide and D- erythro-sphingosine dose-dependently competed for binding of the radiolabeled [125]TID-ceramide, whereas the biologically inactive D- erythro-dihydroceramide and D- erythro-dihydrosphingosine were significantly less potent in competing for TID-ceramide binding to CTSD.	transcription
67049	11	336163	5	NULL	NULL	NULL	NULL	statement 8	Process		less potent than					statement 5	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_19_5252_s_73	10508159	As shown in Figure  2A, D- erythro-C6-ceramide and D- erythro-sphingosine dose-dependently competed for binding of the radiolabeled [125]TID-ceramide, whereas the biologically inactive D- erythro-dihydroceramide and D- erythro-dihydrosphingosine were significantly less potent in competing for TID-ceramide binding to CTSD.	transcription
67050	12	336163	5	NULL	NULL	0	NULL	statement 9	Process		less potent than					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_73	10508159	As shown in Figure  2A, D- erythro-C6-ceramide and D- erythro-sphingosine dose-dependently competed for binding of the radiolabeled [125]TID-ceramide, whereas the biologically inactive D- erythro-dihydroceramide and D- erythro-dihydrosphingosine were significantly less potent in competing for TID-ceramide binding to CTSD.	transcription
67051	13	336163	5	NULL	NULL	0	NULL	statement 9	Process		less potent than					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_73	10508159	As shown in Figure  2A, D- erythro-C6-ceramide and D- erythro-sphingosine dose-dependently competed for binding of the radiolabeled [125]TID-ceramide, whereas the biologically inactive D- erythro-dihydroceramide and D- erythro-dihydrosphingosine were significantly less potent in competing for TID-ceramide binding to CTSD.	transcription
71277	2	336163	7	NULL	NULL	NULL	NULL	D- erythro-C6-ceramide	Chemical		compete with		dose-dependently			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_19_5252_s_73	10508159	As shown in Figure  2A, D- erythro-C6-ceramide and D- erythro-sphingosine dose-dependently competed for binding of the radiolabeled [125]TID-ceramide, whereas the biologically inactive D- erythro-dihydroceramide and D- erythro-dihydrosphingosine were significantly less potent in competing for TID-ceramide binding to CTSD.	transcription
71278	2	336163	7	NULL	NULL	NULL	NULL	D- erythro-sphingosine	Chemical		compete with		dose-dependently			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_19_5252_s_73	10508159	As shown in Figure  2A, D- erythro-C6-ceramide and D- erythro-sphingosine dose-dependently competed for binding of the radiolabeled [125]TID-ceramide, whereas the biologically inactive D- erythro-dihydroceramide and D- erythro-dihydrosphingosine were significantly less potent in competing for TID-ceramide binding to CTSD.	transcription
71279	1	336163	7	NULL	NULL	NULL	NULL	[125]TID-ceramide	Chemical	radiolabeled	bind					CTSD	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_19_5252_s_73	10508159	As shown in Figure  2A, D- erythro-C6-ceramide and D- erythro-sphingosine dose-dependently competed for binding of the radiolabeled [125]TID-ceramide, whereas the biologically inactive D- erythro-dihydroceramide and D- erythro-dihydrosphingosine were significantly less potent in competing for TID-ceramide binding to CTSD.	transcription
71280	4	336163	7	NULL	NULL	0	NULL	TID-ceramide	Chemical		bind					CTSD	Chemical				NULL		0	NULL	NULL	NULL	gw60_embo_18_19_5252_s_73	10508159	As shown in Figure  2A, D- erythro-C6-ceramide and D- erythro-sphingosine dose-dependently competed for binding of the radiolabeled [125]TID-ceramide, whereas the biologically inactive D- erythro-dihydroceramide and D- erythro-dihydrosphingosine were significantly less potent in competing for TID-ceramide binding to CTSD.	transcription
71281	5	336163	7	NULL	NULL	NULL	NULL	D- erythro-dihydroceramide	Chemical	biologically inactive	compete with		less potently			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_19_5252_s_73	10508159	As shown in Figure  2A, D- erythro-C6-ceramide and D- erythro-sphingosine dose-dependently competed for binding of the radiolabeled [125]TID-ceramide, whereas the biologically inactive D- erythro-dihydroceramide and D- erythro-dihydrosphingosine were significantly less potent in competing for TID-ceramide binding to CTSD.	transcription
71282	6	336163	7	NULL	NULL	NULL	NULL	D- erythro-dihydrosphingosine	Chemical	biologically inactive	compete with		less potently			statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_embo_18_19_5252_s_73	10508159	As shown in Figure  2A, D- erythro-C6-ceramide and D- erythro-sphingosine dose-dependently competed for binding of the radiolabeled [125]TID-ceramide, whereas the biologically inactive D- erythro-dihydroceramide and D- erythro-dihydrosphingosine were significantly less potent in competing for TID-ceramide binding to CTSD.	transcription
67052	1	336164	5	NULL	NULL	0	NULL	ceramide	Chemical	elevation of;;plasma	is induced by					LPS	Chemical				NULL		0	NULL	NULL	NULL	gw60_brainres_895_1_59_s_166	11259760	Evidence from experiments on macrophage cell lines, which have been shown to produce ceramide in response to LPS [ 23], and on human neutrophils, which upregulate sphingosine levels in response to various agonists [  47], suggests that blood cells could also contribute to LPS-induced plasma ceramide elevation.	transcription
67053	2	336164	5	NULL	NULL	0	NULL	blood cells	Cell		contribute to					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_brainres_895_1_59_s_166	11259760	Evidence from experiments on macrophage cell lines, which have been shown to produce ceramide in response to LPS [ 23], and on human neutrophils, which upregulate sphingosine levels in response to various agonists [  47], suggests that blood cells could also contribute to LPS-induced plasma ceramide elevation.	transcription
67054	3	336164	5	NULL	NULL	NULL	NULL	ceramide	Chemical		is produced					LPS	Chemical	in response to			NULL	macrophage cell lines	NULL	NULL	NULL	NULL	gw60_brainres_895_1_59_s_166	11259760	Evidence from experiments on macrophage cell lines, which have been shown to produce ceramide in response to LPS [ 23], and on human neutrophils, which upregulate sphingosine levels in response to various agonists [  47], suggests that blood cells could also contribute to LPS-induced plasma ceramide elevation.	transcription
67055	4	336164	5	NULL	NULL	0	NULL	agonists	Chemical		upregulates					sphingosine	Chemical	levels of			NULL	human neutrophils	0	NULL	NULL	NULL	gw60_brainres_895_1_59_s_166	11259760	Evidence from experiments on macrophage cell lines, which have been shown to produce ceramide in response to LPS [ 23], and on human neutrophils, which upregulate sphingosine levels in response to various agonists [  47], suggests that blood cells could also contribute to LPS-induced plasma ceramide elevation.	transcription
71283	1	336164	7	NULL	NULL	0	NULL	LPS	Chemical		produce					ceramide	Chemical				NULL	macrophage cell lines	0	NULL	NULL	NULL	gw60_brainres_895_1_59_s_166	11259760	Evidence from experiments on macrophage cell lines, which have been shown to produce ceramide in response to LPS [ 23], and on human neutrophils, which upregulate sphingosine levels in response to various agonists [  47], suggests that blood cells could also contribute to LPS-induced plasma ceramide elevation.	transcription
71284	2	336164	7	NULL	NULL	0	NULL	LPS	Chemical		induce					plasma ceramide	Chemical	elevation of			NULL		0	NULL	NULL	NULL	gw60_brainres_895_1_59_s_166	11259760	Evidence from experiments on macrophage cell lines, which have been shown to produce ceramide in response to LPS [ 23], and on human neutrophils, which upregulate sphingosine levels in response to various agonists [  47], suggests that blood cells could also contribute to LPS-induced plasma ceramide elevation.	transcription
71285	3	336164	7	NULL	NULL	0	NULL	blood cells	Cell		contribute to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_brainres_895_1_59_s_166	11259760	Evidence from experiments on macrophage cell lines, which have been shown to produce ceramide in response to LPS [ 23], and on human neutrophils, which upregulate sphingosine levels in response to various agonists [  47], suggests that blood cells could also contribute to LPS-induced plasma ceramide elevation.	transcription
67060	1	336165	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					serum deprivation	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
67061	2	336165	5	NULL	NULL	0	NULL	sphingosine kinase	GP		is expressed in					3T3 fibroblasts	Cell				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
67062	3	336165	5	NULL	NULL	0	NULL	sphingosine kinase	GP		is expressed in					HEK 293	Cell				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
67063	4	336165	5	NULL	NULL	0	NULL	sphingosine kinase	GP		is expressed in					Jurkat T cells	Cell				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
67064	5	336165	5	NULL	NULL	0	NULL	statement 2	Process		suppress					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
67065	6	336165	5	NULL	NULL	0	NULL	statement 3	Process		suppress					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
67066	7	336165	5	NULL	NULL	0	NULL	statement 4	Process		suppress					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
67067	8	336165	5	NULL	NULL	0	NULL	statement 1	Process		increases					ceramide	Chemical	level of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
67068	9	336165	5	NULL	NULL	NULL	NULL	C2-ceramide	Chemical		is an analogue of					ceramide	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
71286	1	336165	7	NULL	NULL	0	NULL	serum 	OrganismPart	deprivation of	induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
71287	2	336165	7	NULL	NULL	0	NULL	sphingosine kinase	GP		suppress					statement 1	Process				NULL	3T3 fibroblasts	0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
71288	3	336165	7	NULL	NULL	NULL	NULL	sphingosine kinase	GP		suppress					statement 1	Process				NULL	HEK 293 cells	NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
71289	4	336165	7	NULL	NULL	NULL	NULL	sphingosine kinase	GP		suppress					statement 1	Process				NULL	Jurkat T cells	NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
71290	5	336165	7	NULL	NULL	0	NULL	sphingosine kinase	GP		increase					ceramide	Chemical				NULL	3T3 fibroblasts	0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
71291	6	336165	7	NULL	NULL	0	NULL	sphingosine kinase	GP		increase					ceramide	Chemical				NULL	HEK 293 cells	0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
71292	7	336165	7	NULL	NULL	0	NULL	sphingosine kinase	GP		increase					ceramide	Chemical				NULL	Jurkat T cells	0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
71293	8	336165	7	NULL	NULL	0	NULL	sphingosine kinase	GP		increase					C2-ceramide	Chemical				NULL	3T3 fibroblasts	0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
71294	9	336165	7	NULL	NULL	0	NULL	sphingosine kinase	GP		increase					C2-ceramide	Chemical				NULL	HEK293 cells	0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
71295	10	336165	7	NULL	NULL	0	NULL	sphingosine kinase	GP		increase					C2-ceramide	Chemical				NULL	Jurkat T cells	0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
71296	11	336165	7	NULL	NULL	NULL	NULL	sphingosine kinase	GP		inhibit					caspase-3	GP	activation of executionary			NULL	3T3 fibroblasts	NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
71297	12	336165	7	NULL	NULL	0	NULL	sphingosine kinase	GP		inhibit					caspase-3	GP	activation of executionary			NULL	HEK293 cells	0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
71298	13	336165	7	NULL	NULL	NULL	NULL	sphingosine kinase	GP		inhibit					caspase-3	GP	activation of executionary			NULL	Jurkat T cells	NULL	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
71299	14	336165	7	NULL	NULL	0	NULL	C2-ceramide	Chemical		is a type of					ceramide analogue	Chemical				NULL		0	NULL	NULL	NULL	gw60_cellbiol_147_3_545_s_302	10545499	Our present results show that expression of sphingosine kinase in 3T3 fibroblasts, HEK 293, and Jurkat T cells suppressed apoptosis induced by serum deprivation, known to increase ceramide levels, or by the ceramide analogue, C2-ceramide, with concomitant inhibition of activation of the executionary caspase-3.	transcription
67069	1	336166	5	NULL	NULL	0	NULL	sphingosine	Chemical		is a metabolite of					sphingolipid	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13275_s_109	10788433	This appears to be a specific ceramide effect because other related sphingolipid metabolites, including sphingosine and the inactive ceramide analogue, C2-dihydroceramide, which has the same structure as C2-ceramide but lacks the double bond, did not replicate the effects of C2-ceramide or SMase (data not shown).	transcription
67070	2	336166	5	NULL	NULL	0	NULL	C2-dihydroceramide	Chemical		is an analogue of					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13275_s_109	10788433	This appears to be a specific ceramide effect because other related sphingolipid metabolites, including sphingosine and the inactive ceramide analogue, C2-dihydroceramide, which has the same structure as C2-ceramide but lacks the double bond, did not replicate the effects of C2-ceramide or SMase (data not shown).	transcription
67071	3	336166	5	NULL	NULL	0	NULL	C2-dihydroceramide	Chemical		is a metabolite of					sphingolipid	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13275_s_109	10788433	This appears to be a specific ceramide effect because other related sphingolipid metabolites, including sphingosine and the inactive ceramide analogue, C2-dihydroceramide, which has the same structure as C2-ceramide but lacks the double bond, did not replicate the effects of C2-ceramide or SMase (data not shown).	transcription
67072	4	336166	5	NULL	NULL	0	NULL	C2-dihydroceramide	Chemical	structure of	same as					C2-ceramide	Chemical	structure of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13275_s_109	10788433	This appears to be a specific ceramide effect because other related sphingolipid metabolites, including sphingosine and the inactive ceramide analogue, C2-dihydroceramide, which has the same structure as C2-ceramide but lacks the double bond, did not replicate the effects of C2-ceramide or SMase (data not shown).	transcription
67073	5	336166	5	NULL	NULL	NULL	NULL	C2-dihydroceramide	Chemical	inactive	does not replicate					C2-ceramide	Chemical	effects of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_18_13275_s_109	10788433	This appears to be a specific ceramide effect because other related sphingolipid metabolites, including sphingosine and the inactive ceramide analogue, C2-dihydroceramide, which has the same structure as C2-ceramide but lacks the double bond, did not replicate the effects of C2-ceramide or SMase (data not shown).	transcription
67074	6	336166	5	NULL	NULL	0	NULL	C2-dihydroceramide	Chemical	inactive	does not replicate					SMase	GP	effects of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13275_s_109	10788433	This appears to be a specific ceramide effect because other related sphingolipid metabolites, including sphingosine and the inactive ceramide analogue, C2-dihydroceramide, which has the same structure as C2-ceramide but lacks the double bond, did not replicate the effects of C2-ceramide or SMase (data not shown).	transcription
71300	1	336166	7	NULL	NULL	0	NULL	sphingosine	Chemical		is a type of					sphingolipid metabolite	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13275_s_109	10788433	This appears to be a specific ceramide effect because other related sphingolipid metabolites, including sphingosine and the inactive ceramide analogue, C2-dihydroceramide, which has the same structure as C2-ceramide but lacks the double bond, did not replicate the effects of C2-ceramide or SMase (data not shown).	transcription
71301	2	336166	7	NULL	NULL	0	NULL	C2-dihydroceramide	Chemical		is a type of					ceramide analogue	Chemical	inactive			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13275_s_109	10788433	This appears to be a specific ceramide effect because other related sphingolipid metabolites, including sphingosine and the inactive ceramide analogue, C2-dihydroceramide, which has the same structure as C2-ceramide but lacks the double bond, did not replicate the effects of C2-ceramide or SMase (data not shown).	transcription
71302	3	336166	7	NULL	NULL	0	NULL	C2-dihydroceramide	Chemical		lacks					C2-ceramide	Chemical	double bond of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13275_s_109	10788433	This appears to be a specific ceramide effect because other related sphingolipid metabolites, including sphingosine and the inactive ceramide analogue, C2-dihydroceramide, which has the same structure as C2-ceramide but lacks the double bond, did not replicate the effects of C2-ceramide or SMase (data not shown).	transcription
71303	4	336166	7	NULL	NULL	0	NULL	C2-dihydroceramide	Chemical		does not replicate					C2-ceramide	Chemical	effects of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_18_13275_s_109	10788433	This appears to be a specific ceramide effect because other related sphingolipid metabolites, including sphingosine and the inactive ceramide analogue, C2-dihydroceramide, which has the same structure as C2-ceramide but lacks the double bond, did not replicate the effects of C2-ceramide or SMase (data not shown).	transcription
71304	5	336166	7	NULL	NULL	NULL	NULL	C2-dihydroceramide	Chemical		does not replicate					SMase	GP	effects of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_18_13275_s_109	10788433	This appears to be a specific ceramide effect because other related sphingolipid metabolites, including sphingosine and the inactive ceramide analogue, C2-dihydroceramide, which has the same structure as C2-ceramide but lacks the double bond, did not replicate the effects of C2-ceramide or SMase (data not shown).	transcription
67075	1	336167	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					Fas	GP				NULL	Type II Cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_240	10747891	Potential Involvement of Ceramide and Sphingosine in Fas-induced Apoptosis of Type II Cells-- Abundant reports have suggested that ceramide may play a role in apoptotic signals initiated through the Fas system in various types of cells ( 10- 21, 27, 72).	transcription
67076	2	336167	5	NULL	NULL	0	NULL	ceramide	Chemical		is involved in		potentially			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_240	10747891	Potential Involvement of Ceramide and Sphingosine in Fas-induced Apoptosis of Type II Cells-- Abundant reports have suggested that ceramide may play a role in apoptotic signals initiated through the Fas system in various types of cells ( 10- 21, 27, 72).	transcription
67077	3	336167	5	NULL	NULL	0	NULL	sphingosine	Chemical		is involved in		potentially			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_240	10747891	Potential Involvement of Ceramide and Sphingosine in Fas-induced Apoptosis of Type II Cells-- Abundant reports have suggested that ceramide may play a role in apoptotic signals initiated through the Fas system in various types of cells ( 10- 21, 27, 72).	transcription
67078	4	336167	5	NULL	NULL	NULL	NULL	apoptotic signals	Process		initiated through					Fas system	GP				NULL	various types of cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_240	10747891	Potential Involvement of Ceramide and Sphingosine in Fas-induced Apoptosis of Type II Cells-- Abundant reports have suggested that ceramide may play a role in apoptotic signals initiated through the Fas system in various types of cells ( 10- 21, 27, 72).	transcription
67079	5	336167	5	NULL	NULL	0	NULL	ceramide	Chemical		plays a role in		may			statement 4	Process				NULL	various types of cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_240	10747891	Potential Involvement of Ceramide and Sphingosine in Fas-induced Apoptosis of Type II Cells-- Abundant reports have suggested that ceramide may play a role in apoptotic signals initiated through the Fas system in various types of cells ( 10- 21, 27, 72).	transcription
71305	1	336167	7	NULL	NULL	0	NULL	Fas	GP		induce					apoptosis	Process				NULL	Type II cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_240	10747891	Potential Involvement of Ceramide and Sphingosine in Fas-induced Apoptosis of Type II Cells-- Abundant reports have suggested that ceramide may play a role in apoptotic signals initiated through the Fas system in various types of cells ( 10- 21, 27, 72).	transcription
71306	2	336167	7	NULL	NULL	0	NULL	Ceramide	Chemical		play a role in		may			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_240	10747891	Potential Involvement of Ceramide and Sphingosine in Fas-induced Apoptosis of Type II Cells-- Abundant reports have suggested that ceramide may play a role in apoptotic signals initiated through the Fas system in various types of cells ( 10- 21, 27, 72).	transcription
71307	3	336167	7	NULL	NULL	0	NULL	Sphingosine	Chemical		play a role in		may			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_240	10747891	Potential Involvement of Ceramide and Sphingosine in Fas-induced Apoptosis of Type II Cells-- Abundant reports have suggested that ceramide may play a role in apoptotic signals initiated through the Fas system in various types of cells ( 10- 21, 27, 72).	transcription
67080	1	336168	5	NULL	NULL	0	NULL	TNF-alpha	GP		effects					PKCalpha	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29290_s_142	10887171	In an attempt to determine whether ceramide production is necessary for the observed effect of TNF-alpha on PKCalpha, we examined the effect of fumonisin B1, an inhibitor of sphingosine  N-acyltransferase or ceramide synthase ( 30), on PKC activity upon TNF-alpha treatment.	transcription
67081	2	336168	5	NULL	NULL	0	NULL	ceramide	Chemical	production of	is necessary for		potentially			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29290_s_142	10887171	In an attempt to determine whether ceramide production is necessary for the observed effect of TNF-alpha on PKCalpha, we examined the effect of fumonisin B1, an inhibitor of sphingosine  N-acyltransferase or ceramide synthase ( 30), on PKC activity upon TNF-alpha treatment.	transcription
67082	3	336168	5	NULL	NULL	0	NULL	fumonisin B1	Chemical		is an inhibitor of					sphingosine N-acyltransferase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29290_s_142	10887171	In an attempt to determine whether ceramide production is necessary for the observed effect of TNF-alpha on PKCalpha, we examined the effect of fumonisin B1, an inhibitor of sphingosine  N-acyltransferase or ceramide synthase ( 30), on PKC activity upon TNF-alpha treatment.	transcription
67083	4	336168	5	NULL	NULL	0	NULL	fumonisin B1	Chemical		effects		potentially			PKC	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29290_s_142	10887171	In an attempt to determine whether ceramide production is necessary for the observed effect of TNF-alpha on PKCalpha, we examined the effect of fumonisin B1, an inhibitor of sphingosine  N-acyltransferase or ceramide synthase ( 30), on PKC activity upon TNF-alpha treatment.	transcription
67084	5	336168	5	NULL	NULL	0	NULL	statement 4	Process		occurs upon					TNF-alpha	GP	treatment			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29290_s_142	10887171	In an attempt to determine whether ceramide production is necessary for the observed effect of TNF-alpha on PKCalpha, we examined the effect of fumonisin B1, an inhibitor of sphingosine  N-acyltransferase or ceramide synthase ( 30), on PKC activity upon TNF-alpha treatment.	transcription
67085	6	336168	5	NULL	NULL	0	NULL	ceramide synthase	GP		effects		potentially			PKC	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29290_s_142	10887171	In an attempt to determine whether ceramide production is necessary for the observed effect of TNF-alpha on PKCalpha, we examined the effect of fumonisin B1, an inhibitor of sphingosine  N-acyltransferase or ceramide synthase ( 30), on PKC activity upon TNF-alpha treatment.	transcription
67086	7	336168	5	NULL	NULL	0	NULL	statement 6	Process		occurs upon					TNF-alpha	GP	treatment			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29290_s_142	10887171	In an attempt to determine whether ceramide production is necessary for the observed effect of TNF-alpha on PKCalpha, we examined the effect of fumonisin B1, an inhibitor of sphingosine  N-acyltransferase or ceramide synthase ( 30), on PKC activity upon TNF-alpha treatment.	transcription
71308	1	336168	7	NULL	NULL	0	NULL	fumonisin B1	Chemical		inhibit					sphingosine N-acyltransferase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29290_s_142	10887171	In an attempt to determine whether ceramide production is necessary for the observed effect of TNF-alpha on PKCalpha, we examined the effect of fumonisin B1, an inhibitor of sphingosine  N-acyltransferase or ceramide synthase ( 30), on PKC activity upon TNF-alpha treatment.	transcription
71309	2	336168	7	NULL	NULL	0	NULL	fumonisin B1	Chemical		inhibit					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_38_29290_s_142	10887171	In an attempt to determine whether ceramide production is necessary for the observed effect of TNF-alpha on PKCalpha, we examined the effect of fumonisin B1, an inhibitor of sphingosine  N-acyltransferase or ceramide synthase ( 30), on PKC activity upon TNF-alpha treatment.	transcription
67087	1	336169	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_4_2502_s_217	9891021	Effects of Ceramide Analogs and AHR Ligands on Ceramide induced Apoptosis-- Dihydro- N-acetyl-D- erythro-sphingosine (DHC2-ceramide) differs from C2-ceramide in only one respect; it lacks the double bond between carbons 4 and 5 of the sphingoid backbone.	transcription
67088	2	336169	5	NULL	NULL	0	NULL	ceramide analogs	Chemical		effects					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_4_2502_s_217	9891021	Effects of Ceramide Analogs and AHR Ligands on Ceramide induced Apoptosis-- Dihydro- N-acetyl-D- erythro-sphingosine (DHC2-ceramide) differs from C2-ceramide in only one respect; it lacks the double bond between carbons 4 and 5 of the sphingoid backbone.	transcription
67089	3	336169	5	NULL	NULL	0	NULL	AHR Ligands	Chemical		effects					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_4_2502_s_217	9891021	Effects of Ceramide Analogs and AHR Ligands on Ceramide induced Apoptosis-- Dihydro- N-acetyl-D- erythro-sphingosine (DHC2-ceramide) differs from C2-ceramide in only one respect; it lacks the double bond between carbons 4 and 5 of the sphingoid backbone.	transcription
67090	4	336169	5	NULL	NULL	0	NULL	DHC2-ceramide	Chemical		is					Dihydro- N-acetyl-D- erythro-sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_4_2502_s_217	9891021	Effects of Ceramide Analogs and AHR Ligands on Ceramide induced Apoptosis-- Dihydro- N-acetyl-D- erythro-sphingosine (DHC2-ceramide) differs from C2-ceramide in only one respect; it lacks the double bond between carbons 4 and 5 of the sphingoid backbone.	transcription
71310	1	336169	7	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_4_2502_s_217	9891021	Effects of Ceramide Analogs and AHR Ligands on Ceramide induced Apoptosis-- Dihydro- N-acetyl-D- erythro-sphingosine (DHC2-ceramide) differs from C2-ceramide in only one respect; it lacks the double bond between carbons 4 and 5 of the sphingoid backbone.	transcription
71311	2	336169	7	NULL	NULL	0	NULL	DHC2-ceramide	Chemical		differs from					C2-ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_4_2502_s_217	9891021	Effects of Ceramide Analogs and AHR Ligands on Ceramide induced Apoptosis-- Dihydro- N-acetyl-D- erythro-sphingosine (DHC2-ceramide) differs from C2-ceramide in only one respect; it lacks the double bond between carbons 4 and 5 of the sphingoid backbone.	transcription
71312	3	336169	7	NULL	NULL	0	NULL	statement 2	Process		lacks 					sphingoid backbone	Chemical	double bond between carbons 4 and 5 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_4_2502_s_217	9891021	Effects of Ceramide Analogs and AHR Ligands on Ceramide induced Apoptosis-- Dihydro- N-acetyl-D- erythro-sphingosine (DHC2-ceramide) differs from C2-ceramide in only one respect; it lacks the double bond between carbons 4 and 5 of the sphingoid backbone.	transcription
71313	4	336169	7	NULL	NULL	0	NULL	DHC2-ceramide	Chemical		is					Dihydro- N-acetyl-D- erythro-sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_4_2502_s_217	9891021	Effects of Ceramide Analogs and AHR Ligands on Ceramide induced Apoptosis-- Dihydro- N-acetyl-D- erythro-sphingosine (DHC2-ceramide) differs from C2-ceramide in only one respect; it lacks the double bond between carbons 4 and 5 of the sphingoid backbone.	transcription
67091	1	336170	5	NULL	NULL	0	NULL	TNFalpha	GP		produce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_146	8981934	Because it has been demonstrated that TNFalpha may produce apoptosis in a variety of cell types, principally through  ceramide production ( 18,  19) or via ceramide's conversion  product, sphingosine ( 20), it is possible that TNFalpha-mediated  cardiac apoptosis may result from enhanced sphingolipid production.	transcription
67092	2	336170	5	NULL	NULL	0	NULL	statement 1	Process		through		principally			ceramide	Chemical	production of			NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_146	8981934	Because it has been demonstrated that TNFalpha may produce apoptosis in a variety of cell types, principally through  ceramide production ( 18,  19) or via ceramide's conversion  product, sphingosine ( 20), it is possible that TNFalpha-mediated  cardiac apoptosis may result from enhanced sphingolipid production.	transcription
67093	3	336170	5	NULL	NULL	0	NULL	statement 1	Process		via					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_146	8981934	Because it has been demonstrated that TNFalpha may produce apoptosis in a variety of cell types, principally through  ceramide production ( 18,  19) or via ceramide's conversion  product, sphingosine ( 20), it is possible that TNFalpha-mediated  cardiac apoptosis may result from enhanced sphingolipid production.	transcription
67094	4	336170	5	NULL	NULL	0	NULL	sphingosine	Chemical		is a conversion product of					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_146	8981934	Because it has been demonstrated that TNFalpha may produce apoptosis in a variety of cell types, principally through  ceramide production ( 18,  19) or via ceramide's conversion  product, sphingosine ( 20), it is possible that TNFalpha-mediated  cardiac apoptosis may result from enhanced sphingolipid production.	transcription
67095	5	336170	5	NULL	NULL	0	NULL	TNFalpha	GP		mediates					apoptosis	Process	cardiac			NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_146	8981934	Because it has been demonstrated that TNFalpha may produce apoptosis in a variety of cell types, principally through  ceramide production ( 18,  19) or via ceramide's conversion  product, sphingosine ( 20), it is possible that TNFalpha-mediated  cardiac apoptosis may result from enhanced sphingolipid production.	transcription
67096	6	336170	5	NULL	NULL	0	NULL	statement 5	Process		results from		may			sphingosine	Chemical	enhanced production of			NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_146	8981934	Because it has been demonstrated that TNFalpha may produce apoptosis in a variety of cell types, principally through  ceramide production ( 18,  19) or via ceramide's conversion  product, sphingosine ( 20), it is possible that TNFalpha-mediated  cardiac apoptosis may result from enhanced sphingolipid production.	transcription
71314	1	336170	7	NULL	NULL	0	NULL	TNFalpha	GP		produce		may			apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_146	8981934	Because it has been demonstrated that TNFalpha may produce apoptosis in a variety of cell types, principally through  ceramide production ( 18,  19) or via ceramide's conversion  product, sphingosine ( 20), it is possible that TNFalpha-mediated  cardiac apoptosis may result from enhanced sphingolipid production.	transcription
71315	2	336170	7	NULL	NULL	0	NULL	statement 1	Process		occur through					ceramide	Chemical	production of			NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_146	8981934	Because it has been demonstrated that TNFalpha may produce apoptosis in a variety of cell types, principally through  ceramide production ( 18,  19) or via ceramide's conversion  product, sphingosine ( 20), it is possible that TNFalpha-mediated  cardiac apoptosis may result from enhanced sphingolipid production.	transcription
71316	3	336170	7	NULL	NULL	0	NULL	statement 1	Process		occur through					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_146	8981934	Because it has been demonstrated that TNFalpha may produce apoptosis in a variety of cell types, principally through  ceramide production ( 18,  19) or via ceramide's conversion  product, sphingosine ( 20), it is possible that TNFalpha-mediated  cardiac apoptosis may result from enhanced sphingolipid production.	transcription
71317	4	336170	7	NULL	NULL	0	NULL	sphingosine	Chemical		is a type of					ceramide conversion product	Chemical				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_146	8981934	Because it has been demonstrated that TNFalpha may produce apoptosis in a variety of cell types, principally through  ceramide production ( 18,  19) or via ceramide's conversion  product, sphingosine ( 20), it is possible that TNFalpha-mediated  cardiac apoptosis may result from enhanced sphingolipid production.	transcription
71318	5	336170	7	NULL	NULL	0	NULL	TNFalpha	GP		mediates					cardiac apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_146	8981934	Because it has been demonstrated that TNFalpha may produce apoptosis in a variety of cell types, principally through  ceramide production ( 18,  19) or via ceramide's conversion  product, sphingosine ( 20), it is possible that TNFalpha-mediated  cardiac apoptosis may result from enhanced sphingolipid production.	transcription
71319	6	336170	7	NULL	NULL	0	NULL	statement 5	Process		result from		may			sphingolipid	Chemical	enhanced production of			NULL		0	NULL	NULL	NULL	gw60_jclininvest_98_12_2854_s_146	8981934	Because it has been demonstrated that TNFalpha may produce apoptosis in a variety of cell types, principally through  ceramide production ( 18,  19) or via ceramide's conversion  product, sphingosine ( 20), it is possible that TNFalpha-mediated  cardiac apoptosis may result from enhanced sphingolipid production.	transcription
67097	1	336171	5	NULL	NULL	0	NULL	SPHK1	GP	enforced expression of 	increases		significantly			SPHK1	GP	kinase activity of			NULL	PC12 cells	0	NULL	NULL	NULL	abs-batch0650-0679_j-neurochem_76_5_11238741_s_5	11238741	Enforced expression of SPHK1 in PC12  cells resulted in significant increases in kinase activity, with corresponding  increases in intracellular SPP levels and concomitant decreases in both  sphingosine and ceramide, and marked suppression of apoptosis induced  by trophic factor withdrawal or by C(2)-ceramide.	transcription
67098	2	336171	5	NULL	NULL	0	NULL	statement 1	Process		increases					SPP	Chemical	intracellular levels of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-neurochem_76_5_11238741_s_5	11238741	Enforced expression of SPHK1 in PC12  cells resulted in significant increases in kinase activity, with corresponding  increases in intracellular SPP levels and concomitant decreases in both  sphingosine and ceramide, and marked suppression of apoptosis induced  by trophic factor withdrawal or by C(2)-ceramide.	transcription
67099	3	336171	5	NULL	NULL	0	NULL	statement 1	Process		decreases					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-neurochem_76_5_11238741_s_5	11238741	Enforced expression of SPHK1 in PC12  cells resulted in significant increases in kinase activity, with corresponding  increases in intracellular SPP levels and concomitant decreases in both  sphingosine and ceramide, and marked suppression of apoptosis induced  by trophic factor withdrawal or by C(2)-ceramide.	transcription
67100	4	336171	5	NULL	NULL	0	NULL	statement 1	Process		decreases					ceramide	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-neurochem_76_5_11238741_s_5	11238741	Enforced expression of SPHK1 in PC12  cells resulted in significant increases in kinase activity, with corresponding  increases in intracellular SPP levels and concomitant decreases in both  sphingosine and ceramide, and marked suppression of apoptosis induced  by trophic factor withdrawal or by C(2)-ceramide.	transcription
67101	5	336171	5	NULL	NULL	0	NULL	statement 3	Process		is concomitant to					statement 2	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-neurochem_76_5_11238741_s_5	11238741	Enforced expression of SPHK1 in PC12  cells resulted in significant increases in kinase activity, with corresponding  increases in intracellular SPP levels and concomitant decreases in both  sphingosine and ceramide, and marked suppression of apoptosis induced  by trophic factor withdrawal or by C(2)-ceramide.	transcription
67102	6	336171	5	NULL	NULL	0	NULL	statement 4	Process		is concomitant to					statement 2	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-neurochem_76_5_11238741_s_5	11238741	Enforced expression of SPHK1 in PC12  cells resulted in significant increases in kinase activity, with corresponding  increases in intracellular SPP levels and concomitant decreases in both  sphingosine and ceramide, and marked suppression of apoptosis induced  by trophic factor withdrawal or by C(2)-ceramide.	transcription
67103	7	336171	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					trophic factor	GP	withdrawal of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-neurochem_76_5_11238741_s_5	11238741	Enforced expression of SPHK1 in PC12  cells resulted in significant increases in kinase activity, with corresponding  increases in intracellular SPP levels and concomitant decreases in both  sphingosine and ceramide, and marked suppression of apoptosis induced  by trophic factor withdrawal or by C(2)-ceramide.	transcription
67104	8	336171	5	NULL	NULL	0	NULL	apoptosis	Process		is induced by					C(2)-ceramide	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-neurochem_76_5_11238741_s_5	11238741	Enforced expression of SPHK1 in PC12  cells resulted in significant increases in kinase activity, with corresponding  increases in intracellular SPP levels and concomitant decreases in both  sphingosine and ceramide, and marked suppression of apoptosis induced  by trophic factor withdrawal or by C(2)-ceramide.	transcription
67105	9	336171	5	NULL	NULL	0	NULL	statement 7	Process		is an alternative to					statement 8	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-neurochem_76_5_11238741_s_5	11238741	Enforced expression of SPHK1 in PC12  cells resulted in significant increases in kinase activity, with corresponding  increases in intracellular SPP levels and concomitant decreases in both  sphingosine and ceramide, and marked suppression of apoptosis induced  by trophic factor withdrawal or by C(2)-ceramide.	transcription
67106	10	336171	5	NULL	NULL	0	NULL	statement 1	Process		suppress					statement 7	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-neurochem_76_5_11238741_s_5	11238741	Enforced expression of SPHK1 in PC12  cells resulted in significant increases in kinase activity, with corresponding  increases in intracellular SPP levels and concomitant decreases in both  sphingosine and ceramide, and marked suppression of apoptosis induced  by trophic factor withdrawal or by C(2)-ceramide.	transcription
67107	11	336171	5	NULL	NULL	0	NULL	statement 1	Process		suppress					statement 8	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-neurochem_76_5_11238741_s_5	11238741	Enforced expression of SPHK1 in PC12  cells resulted in significant increases in kinase activity, with corresponding  increases in intracellular SPP levels and concomitant decreases in both  sphingosine and ceramide, and marked suppression of apoptosis induced  by trophic factor withdrawal or by C(2)-ceramide.	transcription
71320	1	336171	7	NULL	NULL	0	NULL	SPHK1	GP		increase		significantly			kinase activity	Process				NULL	PC12 cells	0	NULL	NULL	NULL	abs-batch0650-0679_j-neurochem_76_5_11238741_s_5	11238741	Enforced expression of SPHK1 in PC12  cells resulted in significant increases in kinase activity, with corresponding  increases in intracellular SPP levels and concomitant decreases in both  sphingosine and ceramide, and marked suppression of apoptosis induced  by trophic factor withdrawal or by C(2)-ceramide.	transcription
71321	2	336171	7	NULL	NULL	NULL	NULL	statement 1	Process		increase		correspondingly			SPP	Chemical	intracellular			NULL	PC12 cells	NULL	NULL	NULL	NULL	abs-batch0650-0679_j-neurochem_76_5_11238741_s_5	11238741	Enforced expression of SPHK1 in PC12  cells resulted in significant increases in kinase activity, with corresponding  increases in intracellular SPP levels and concomitant decreases in both  sphingosine and ceramide, and marked suppression of apoptosis induced  by trophic factor withdrawal or by C(2)-ceramide.	transcription
71322	3	336171	7	NULL	NULL	NULL	NULL	statement 1	Process		decrease		concomitantly			sphingosine	Chemical				NULL	PC12 cells	NULL	NULL	NULL	NULL	abs-batch0650-0679_j-neurochem_76_5_11238741_s_5	11238741	Enforced expression of SPHK1 in PC12  cells resulted in significant increases in kinase activity, with corresponding  increases in intracellular SPP levels and concomitant decreases in both  sphingosine and ceramide, and marked suppression of apoptosis induced  by trophic factor withdrawal or by C(2)-ceramide.	transcription
71323	4	336171	7	NULL	NULL	NULL	NULL	statement 1	Process		decrease		concomitantly			ceramide	Chemical				NULL	PC12 cells	NULL	NULL	NULL	NULL	abs-batch0650-0679_j-neurochem_76_5_11238741_s_5	11238741	Enforced expression of SPHK1 in PC12  cells resulted in significant increases in kinase activity, with corresponding  increases in intracellular SPP levels and concomitant decreases in both  sphingosine and ceramide, and marked suppression of apoptosis induced  by trophic factor withdrawal or by C(2)-ceramide.	transcription
71324	5	336171	7	NULL	NULL	NULL	NULL	trophic factor	GP	withdrawal of	induce					apoptosis	Process				NULL	PC12 cells	NULL	NULL	NULL	NULL	abs-batch0650-0679_j-neurochem_76_5_11238741_s_5	11238741	Enforced expression of SPHK1 in PC12  cells resulted in significant increases in kinase activity, with corresponding  increases in intracellular SPP levels and concomitant decreases in both  sphingosine and ceramide, and marked suppression of apoptosis induced  by trophic factor withdrawal or by C(2)-ceramide.	transcription
71325	6	336171	7	NULL	NULL	NULL	NULL	C(2)-ceramide	Chemical		induce					apoptosis	Process				NULL	PC12 cells	NULL	NULL	NULL	NULL	abs-batch0650-0679_j-neurochem_76_5_11238741_s_5	11238741	Enforced expression of SPHK1 in PC12  cells resulted in significant increases in kinase activity, with corresponding  increases in intracellular SPP levels and concomitant decreases in both  sphingosine and ceramide, and marked suppression of apoptosis induced  by trophic factor withdrawal or by C(2)-ceramide.	transcription
71326	7	336171	7	NULL	NULL	NULL	NULL	SPHK1	GP		suppress		markedly			statement 5	Process				NULL	PC12 cells	NULL	NULL	NULL	NULL	abs-batch0650-0679_j-neurochem_76_5_11238741_s_5	11238741	Enforced expression of SPHK1 in PC12  cells resulted in significant increases in kinase activity, with corresponding  increases in intracellular SPP levels and concomitant decreases in both  sphingosine and ceramide, and marked suppression of apoptosis induced  by trophic factor withdrawal or by C(2)-ceramide.	transcription
71327	8	336171	7	NULL	NULL	NULL	NULL	SPHK1	GP		suppress		markedly			statement 6	Process				NULL	PC12 cells	NULL	NULL	NULL	NULL	abs-batch0650-0679_j-neurochem_76_5_11238741_s_5	11238741	Enforced expression of SPHK1 in PC12  cells resulted in significant increases in kinase activity, with corresponding  increases in intracellular SPP levels and concomitant decreases in both  sphingosine and ceramide, and marked suppression of apoptosis induced  by trophic factor withdrawal or by C(2)-ceramide.	transcription
67108	1	336172	5	NULL	NULL	0	NULL	long chain ceramide	Chemical	sustained generation of;;endogenous	requires					C6-ceramide	Chemical	biochemical recycling of;;sphingosine backbone of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_37	11815611	We show here, for the first time, that the sustained generation of long chain endogenous ceramide requires the biochemical recycling of the sphingosine backbone of C6-ceramide, which involves deacylation and reacylation of ceramide for the generation of endogenous long chain ceramide (mainly C16:0- and C24:1-ceramides), most likely by CoA-dependent ceramide synthase, which is inhibited by fumonisin B1.	transcription
67109	2	336172	5	NULL	NULL	0	NULL	C6-ceramide	Chemical	biochemical recycling of;;sphingosine backbone of	involves					ceramide	Chemical	deacylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_37	11815611	We show here, for the first time, that the sustained generation of long chain endogenous ceramide requires the biochemical recycling of the sphingosine backbone of C6-ceramide, which involves deacylation and reacylation of ceramide for the generation of endogenous long chain ceramide (mainly C16:0- and C24:1-ceramides), most likely by CoA-dependent ceramide synthase, which is inhibited by fumonisin B1.	transcription
67110	3	336172	5	NULL	NULL	0	NULL	C6-ceramide	Chemical	biochemical recycling of;;sphingosine backbone of	involves					ceramide	Chemical	reacylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_37	11815611	We show here, for the first time, that the sustained generation of long chain endogenous ceramide requires the biochemical recycling of the sphingosine backbone of C6-ceramide, which involves deacylation and reacylation of ceramide for the generation of endogenous long chain ceramide (mainly C16:0- and C24:1-ceramides), most likely by CoA-dependent ceramide synthase, which is inhibited by fumonisin B1.	transcription
67111	4	336172	5	NULL	NULL	0	NULL	statement 2	Process		occurs along with					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_37	11815611	We show here, for the first time, that the sustained generation of long chain endogenous ceramide requires the biochemical recycling of the sphingosine backbone of C6-ceramide, which involves deacylation and reacylation of ceramide for the generation of endogenous long chain ceramide (mainly C16:0- and C24:1-ceramides), most likely by CoA-dependent ceramide synthase, which is inhibited by fumonisin B1.	transcription
67112	5	336172	5	NULL	NULL	0	NULL	statement 4	Process		generates					long chain ceramide	Chemical	endogenous			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_37	11815611	We show here, for the first time, that the sustained generation of long chain endogenous ceramide requires the biochemical recycling of the sphingosine backbone of C6-ceramide, which involves deacylation and reacylation of ceramide for the generation of endogenous long chain ceramide (mainly C16:0- and C24:1-ceramides), most likely by CoA-dependent ceramide synthase, which is inhibited by fumonisin B1.	transcription
67113	6	336172	5	NULL	NULL	0	NULL	C24:1-ceramide	Chemical		is a type of					long chain ceramide					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_37	11815611	We show here, for the first time, that the sustained generation of long chain endogenous ceramide requires the biochemical recycling of the sphingosine backbone of C6-ceramide, which involves deacylation and reacylation of ceramide for the generation of endogenous long chain ceramide (mainly C16:0- and C24:1-ceramides), most likely by CoA-dependent ceramide synthase, which is inhibited by fumonisin B1.	transcription
67114	7	336172	5	NULL	NULL	0	NULL	C16:0-ceramide	Chemical		is a type of					long chain ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_37	11815611	We show here, for the first time, that the sustained generation of long chain endogenous ceramide requires the biochemical recycling of the sphingosine backbone of C6-ceramide, which involves deacylation and reacylation of ceramide for the generation of endogenous long chain ceramide (mainly C16:0- and C24:1-ceramides), most likely by CoA-dependent ceramide synthase, which is inhibited by fumonisin B1.	transcription
67115	8	336172	5	NULL	NULL	0	NULL	ceramide synthase	GP		is dependent on					CoA	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_37	11815611	We show here, for the first time, that the sustained generation of long chain endogenous ceramide requires the biochemical recycling of the sphingosine backbone of C6-ceramide, which involves deacylation and reacylation of ceramide for the generation of endogenous long chain ceramide (mainly C16:0- and C24:1-ceramides), most likely by CoA-dependent ceramide synthase, which is inhibited by fumonisin B1.	transcription
67116	9	336172	5	NULL	NULL	0	NULL	ceramide synthase	GP		catalyzes					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_37	11815611	We show here, for the first time, that the sustained generation of long chain endogenous ceramide requires the biochemical recycling of the sphingosine backbone of C6-ceramide, which involves deacylation and reacylation of ceramide for the generation of endogenous long chain ceramide (mainly C16:0- and C24:1-ceramides), most likely by CoA-dependent ceramide synthase, which is inhibited by fumonisin B1.	transcription
67117	10	336172	5	NULL	NULL	0	NULL	ceramide synthase	GP		catalyzes					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_37	11815611	We show here, for the first time, that the sustained generation of long chain endogenous ceramide requires the biochemical recycling of the sphingosine backbone of C6-ceramide, which involves deacylation and reacylation of ceramide for the generation of endogenous long chain ceramide (mainly C16:0- and C24:1-ceramides), most likely by CoA-dependent ceramide synthase, which is inhibited by fumonisin B1.	transcription
67118	11	336172	5	NULL	NULL	0	NULL	fumonisin B1	Chemical		inhibits					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_37	11815611	We show here, for the first time, that the sustained generation of long chain endogenous ceramide requires the biochemical recycling of the sphingosine backbone of C6-ceramide, which involves deacylation and reacylation of ceramide for the generation of endogenous long chain ceramide (mainly C16:0- and C24:1-ceramides), most likely by CoA-dependent ceramide synthase, which is inhibited by fumonisin B1.	transcription
71328	1	336172	7	NULL	NULL	0	NULL	long chain ceramide	Chemical	sustained generation of ;;endogenous 	requires					C6-ceramide	Chemical	biochemical recycling of;;sphingosine backbone of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_37	11815611	We show here, for the first time, that the sustained generation of long chain endogenous ceramide requires the biochemical recycling of the sphingosine backbone of C6-ceramide, which involves deacylation and reacylation of ceramide for the generation of endogenous long chain ceramide (mainly C16:0- and C24:1-ceramides), most likely by CoA-dependent ceramide synthase, which is inhibited by fumonisin B1.	transcription
71329	2	336172	7	NULL	NULL	NULL	NULL	C6-ceramide	Chemical	biochemical recycling of	involves					ceramide	Chemical	deacylation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_37	11815611	We show here, for the first time, that the sustained generation of long chain endogenous ceramide requires the biochemical recycling of the sphingosine backbone of C6-ceramide, which involves deacylation and reacylation of ceramide for the generation of endogenous long chain ceramide (mainly C16:0- and C24:1-ceramides), most likely by CoA-dependent ceramide synthase, which is inhibited by fumonisin B1.	transcription
71330	3	336172	7	NULL	NULL	0	NULL	C6-ceramide	Chemical	biochemical recycling of	involves					ceramide	Chemical	reacylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_37	11815611	We show here, for the first time, that the sustained generation of long chain endogenous ceramide requires the biochemical recycling of the sphingosine backbone of C6-ceramide, which involves deacylation and reacylation of ceramide for the generation of endogenous long chain ceramide (mainly C16:0- and C24:1-ceramides), most likely by CoA-dependent ceramide synthase, which is inhibited by fumonisin B1.	transcription
71331	4	336172	7	NULL	NULL	0	NULL	statement 2	Process		occur along with					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_37	11815611	We show here, for the first time, that the sustained generation of long chain endogenous ceramide requires the biochemical recycling of the sphingosine backbone of C6-ceramide, which involves deacylation and reacylation of ceramide for the generation of endogenous long chain ceramide (mainly C16:0- and C24:1-ceramides), most likely by CoA-dependent ceramide synthase, which is inhibited by fumonisin B1.	transcription
71332	5	336172	7	NULL	NULL	NULL	NULL	statement 4	Process		generate					C16:0 ceramide	Chemical	endogenous;;long chain			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_37	11815611	We show here, for the first time, that the sustained generation of long chain endogenous ceramide requires the biochemical recycling of the sphingosine backbone of C6-ceramide, which involves deacylation and reacylation of ceramide for the generation of endogenous long chain ceramide (mainly C16:0- and C24:1-ceramides), most likely by CoA-dependent ceramide synthase, which is inhibited by fumonisin B1.	transcription
71333	6	336172	7	NULL	NULL	NULL	NULL	statement 4	Process		generate					C24:1ceramide	Chemical	endogenous;;long chain			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_37	11815611	We show here, for the first time, that the sustained generation of long chain endogenous ceramide requires the biochemical recycling of the sphingosine backbone of C6-ceramide, which involves deacylation and reacylation of ceramide for the generation of endogenous long chain ceramide (mainly C16:0- and C24:1-ceramides), most likely by CoA-dependent ceramide synthase, which is inhibited by fumonisin B1.	transcription
71334	7	336172	7	NULL	NULL	0	NULL	CoA-dependent ceramide synthase	GP		catalyze					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_37	11815611	We show here, for the first time, that the sustained generation of long chain endogenous ceramide requires the biochemical recycling of the sphingosine backbone of C6-ceramide, which involves deacylation and reacylation of ceramide for the generation of endogenous long chain ceramide (mainly C16:0- and C24:1-ceramides), most likely by CoA-dependent ceramide synthase, which is inhibited by fumonisin B1.	transcription
71335	8	336172	7	NULL	NULL	0	NULL	fumonisin B1	Chemical		inhibit					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12960_s_37	11815611	We show here, for the first time, that the sustained generation of long chain endogenous ceramide requires the biochemical recycling of the sphingosine backbone of C6-ceramide, which involves deacylation and reacylation of ceramide for the generation of endogenous long chain ceramide (mainly C16:0- and C24:1-ceramides), most likely by CoA-dependent ceramide synthase, which is inhibited by fumonisin B1.	transcription
67198	1	336173	5	NULL	NULL	NULL	NULL	sphingomyelinase	GP	bacterial	generates					ceramide	Chemical				NULL	plasma membrane	NULL	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
67199	2	336173	5	NULL	NULL	0	NULL	PDMP3	Chemical		is					D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol	Chemical				NULL		0	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
67200	3	336173	5	NULL	NULL	0	NULL	ceramide	Chemical		is incorporated into					glycolipids	Chemical				NULL		0	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
67201	4	336173	5	NULL	NULL	0	NULL	PDMP	Chemical		inhibits					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
67202	5	336173	5	NULL	NULL	0	NULL	D-MAPP	Chemical		is					D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol	Chemical				NULL		0	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
67203	6	336173	5	NULL	NULL	0	NULL	ceramide	Chemical	metabolism of	occurs through					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
67204	7	336173	5	NULL	NULL	0	NULL	D-MAPP	Chemical		inhibits					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
67205	8	336173	5	NULL	NULL	0	NULL	ganglioside precursor	Chemical	addition of	results in					ceramide	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
67206	9	336173	5	NULL	NULL	0	NULL	sphingosine precursor	Chemical	addition of	results in					ceramide	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
67207	10	336173	5	NULL	NULL	0	NULL	sphingomyelinase	GP	addition of;;bacterial	results in					ceramide	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
67208	11	336173	5	NULL	NULL	0	NULL	PDMP	Chemical	addition of	results in					ceramide	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
67209	12	336173	5	NULL	NULL	0	NULL	D-MAPP	Chemical	addition of	results in					ceramide	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
71336	1	336173	7	NULL	NULL	NULL	NULL	precursor gangliosides	Chemical	addition of	results in					ceramide	Chemical	accumulation of			NULL	unstimulated cells	NULL	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
71337	2	336173	7	NULL	NULL	NULL	NULL	precursor sphingosine	Chemical	addition of	results in					ceramide	Chemical	accumulation of			NULL	unstimulated cells	NULL	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
71338	3	336173	7	NULL	NULL	0	NULL	sphingomyelinase	GP	bacterial	generates					ceramide	Chemical				NULL	plasma membrane	0	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
71339	4	336173	7	NULL	NULL	NULL	NULL	sphingomyelinase	GP	bacterial;addition of	results in					ceramide	Chemical	accumulation of			NULL	unstimulated cells	NULL	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
71340	5	336173	7	NULL	NULL	NULL	NULL	PDMP	Chemical	addition of	results in					ceramide	Chemical	accumulation of			NULL	unstimulated cells	NULL	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
71341	6	336173	7	NULL	NULL	0	NULL	ceramide	Chemical		incorporated into					glycolipids	Chemical				NULL		0	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
71342	7	336173	7	NULL	NULL	0	NULL	PDMP	Chemical		inhibit					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
71343	8	336173	7	NULL	NULL	0	NULL	PDMP	Chemical		is					D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol 	Chemical				NULL		0	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
71344	9	336173	7	NULL	NULL	NULL	NULL	D-MAPP	Chemical		results in					ceramide	Chemical	accumulation of			NULL	unstimulated cells	NULL	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
71345	10	336173	7	NULL	NULL	0	NULL	D-MAPP	Chemical		inhibit					ceramide metabolism	Process				NULL		0	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
71346	11	336173	7	NULL	NULL	0	NULL	statement 10	Process		occur through					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
71347	12	336173	7	NULL	NULL	0	NULL	D-MAPP	Chemical		is					D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol	Chemical				NULL		0	NULL	NULL	NULL	gw60_science_274_5294_1855_s_69	8943189	For example, the addition of precursor gangliosides, precursor sphingosine, bacterial sphingomyelinase (which generates ceramide at the plasma membrane), D- threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol (PDMP) (which inhibits further incorporation of ceramide into glycolipids), or D- erythro-2-( N-myristoylamino)-1-phenyl-1-propanol (D-MAPP) (which inhibits ceramide metabolism through ceramidase) results in accumulation of ceramide ranging from three to eight times the concentrations in unstimulated cells ( 19).	transcription
67210	1	336174	5	NULL	NULL	0	NULL	apoptosis	Process		induced through					Fas	GP	stimulation of			NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_9	9207084	Sphingosine-based ceramides have been strongly implicated in the process of apoptosis induced (among other methods) through stimulation of the Fas ( 1-8) and tumor necrosis factor (TNF) receptors ( 7,  9-11), by UV ( 3,  7,  12) and x-ray irradiation ( 12,  13), or through treatment with certain chemotherapy drugs (refs.	transcription
67211	2	336174	5	NULL	NULL	0	NULL	apoptosis	Process		induced through					TNF receptor	GP	stimulation of			NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_9	9207084	Sphingosine-based ceramides have been strongly implicated in the process of apoptosis induced (among other methods) through stimulation of the Fas ( 1-8) and tumor necrosis factor (TNF) receptors ( 7,  9-11), by UV ( 3,  7,  12) and x-ray irradiation ( 12,  13), or through treatment with certain chemotherapy drugs (refs.	transcription
67212	3	336174	5	NULL	NULL	0	NULL	apoptosis	Process		induced by					UV					NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_9	9207084	Sphingosine-based ceramides have been strongly implicated in the process of apoptosis induced (among other methods) through stimulation of the Fas ( 1-8) and tumor necrosis factor (TNF) receptors ( 7,  9-11), by UV ( 3,  7,  12) and x-ray irradiation ( 12,  13), or through treatment with certain chemotherapy drugs (refs.	transcription
67213	4	336174	5	NULL	NULL	0	NULL	apoptosis	Process		induced by					x-ray		irradiation of			NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_9	9207084	Sphingosine-based ceramides have been strongly implicated in the process of apoptosis induced (among other methods) through stimulation of the Fas ( 1-8) and tumor necrosis factor (TNF) receptors ( 7,  9-11), by UV ( 3,  7,  12) and x-ray irradiation ( 12,  13), or through treatment with certain chemotherapy drugs (refs.	transcription
67214	5	336174	5	NULL	NULL	0	NULL	apoptosis	Process		induced through					chemotherapy drugs	Chemical	treatment with			NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_9	9207084	Sphingosine-based ceramides have been strongly implicated in the process of apoptosis induced (among other methods) through stimulation of the Fas ( 1-8) and tumor necrosis factor (TNF) receptors ( 7,  9-11), by UV ( 3,  7,  12) and x-ray irradiation ( 12,  13), or through treatment with certain chemotherapy drugs (refs.	transcription
67215	6	336174	5	NULL	NULL	0	NULL	sphingosine-based ceramides	Chemical		implicated in		strongly			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_9	9207084	Sphingosine-based ceramides have been strongly implicated in the process of apoptosis induced (among other methods) through stimulation of the Fas ( 1-8) and tumor necrosis factor (TNF) receptors ( 7,  9-11), by UV ( 3,  7,  12) and x-ray irradiation ( 12,  13), or through treatment with certain chemotherapy drugs (refs.	transcription
67216	7	336174	5	NULL	NULL	0	NULL	sphingosine-based ceramides	Chemical		implicated in		strongly			statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_9	9207084	Sphingosine-based ceramides have been strongly implicated in the process of apoptosis induced (among other methods) through stimulation of the Fas ( 1-8) and tumor necrosis factor (TNF) receptors ( 7,  9-11), by UV ( 3,  7,  12) and x-ray irradiation ( 12,  13), or through treatment with certain chemotherapy drugs (refs.	transcription
67217	8	336174	5	NULL	NULL	0	NULL	Sphingosine-based ceramides	Chemical		implicated in		strongly			statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_9	9207084	Sphingosine-based ceramides have been strongly implicated in the process of apoptosis induced (among other methods) through stimulation of the Fas ( 1-8) and tumor necrosis factor (TNF) receptors ( 7,  9-11), by UV ( 3,  7,  12) and x-ray irradiation ( 12,  13), or through treatment with certain chemotherapy drugs (refs.	transcription
67218	9	336174	5	NULL	NULL	0	NULL	Sphingosine-based ceramides	Chemical		implicated in		strongly			statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_9	9207084	Sphingosine-based ceramides have been strongly implicated in the process of apoptosis induced (among other methods) through stimulation of the Fas ( 1-8) and tumor necrosis factor (TNF) receptors ( 7,  9-11), by UV ( 3,  7,  12) and x-ray irradiation ( 12,  13), or through treatment with certain chemotherapy drugs (refs.	transcription
67219	10	336174	5	NULL	NULL	0	NULL	sphingosine-based ceramides	Chemical		implicated in		strongly			statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_9	9207084	Sphingosine-based ceramides have been strongly implicated in the process of apoptosis induced (among other methods) through stimulation of the Fas ( 1-8) and tumor necrosis factor (TNF) receptors ( 7,  9-11), by UV ( 3,  7,  12) and x-ray irradiation ( 12,  13), or through treatment with certain chemotherapy drugs (refs.	transcription
71348	1	336174	7	NULL	NULL	0	NULL	Sphingosine-based ceramides	Chemical		is implicated in		strongly			apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_9	9207084	Sphingosine-based ceramides have been strongly implicated in the process of apoptosis induced (among other methods) through stimulation of the Fas ( 1-8) and tumor necrosis factor (TNF) receptors ( 7,  9-11), by UV ( 3,  7,  12) and x-ray irradiation ( 12,  13), or through treatment with certain chemotherapy drugs (refs.	transcription
71349	2	336174	7	NULL	NULL	NULL	NULL	Fas	GP	stimulation of	induce					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_9	9207084	Sphingosine-based ceramides have been strongly implicated in the process of apoptosis induced (among other methods) through stimulation of the Fas ( 1-8) and tumor necrosis factor (TNF) receptors ( 7,  9-11), by UV ( 3,  7,  12) and x-ray irradiation ( 12,  13), or through treatment with certain chemotherapy drugs (refs.	transcription
71350	3	336174	7	NULL	NULL	0	NULL	TNF receptor	GP	stimulation of	induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_9	9207084	Sphingosine-based ceramides have been strongly implicated in the process of apoptosis induced (among other methods) through stimulation of the Fas ( 1-8) and tumor necrosis factor (TNF) receptors ( 7,  9-11), by UV ( 3,  7,  12) and x-ray irradiation ( 12,  13), or through treatment with certain chemotherapy drugs (refs.	transcription
71351	4	336174	7	NULL	NULL	0	NULL	UV			induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_9	9207084	Sphingosine-based ceramides have been strongly implicated in the process of apoptosis induced (among other methods) through stimulation of the Fas ( 1-8) and tumor necrosis factor (TNF) receptors ( 7,  9-11), by UV ( 3,  7,  12) and x-ray irradiation ( 12,  13), or through treatment with certain chemotherapy drugs (refs.	transcription
71352	5	336174	7	NULL	NULL	0	NULL	x-ray irradiation			induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_9	9207084	Sphingosine-based ceramides have been strongly implicated in the process of apoptosis induced (among other methods) through stimulation of the Fas ( 1-8) and tumor necrosis factor (TNF) receptors ( 7,  9-11), by UV ( 3,  7,  12) and x-ray irradiation ( 12,  13), or through treatment with certain chemotherapy drugs (refs.	transcription
71353	6	336174	7	NULL	NULL	0	NULL	chemotherapy drugs	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_9	9207084	Sphingosine-based ceramides have been strongly implicated in the process of apoptosis induced (among other methods) through stimulation of the Fas ( 1-8) and tumor necrosis factor (TNF) receptors ( 7,  9-11), by UV ( 3,  7,  12) and x-ray irradiation ( 12,  13), or through treatment with certain chemotherapy drugs (refs.	transcription
67220	1	336175	5	NULL	NULL	0	NULL	apoptosis	Process		induced by					Fas	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_95	9207084	Thus, the use of a direct MS-based assay, which is highly selective and sensitive, clearly demonstrated that  in vivo generation of sphingosine-based ceramides does not occur during Fas-induced apoptosis, contrary to the many published reports mentioned above.	transcription
67221	2	336175	5	NULL	NULL	0	NULL	sphingosine-based ceramides	Chemical	in vivo generation of	does not occur during					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_95	9207084	Thus, the use of a direct MS-based assay, which is highly selective and sensitive, clearly demonstrated that  in vivo generation of sphingosine-based ceramides does not occur during Fas-induced apoptosis, contrary to the many published reports mentioned above.	transcription
71354	1	336175	7	NULL	NULL	0	NULL	Fas	GP		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_95	9207084	Thus, the use of a direct MS-based assay, which is highly selective and sensitive, clearly demonstrated that  in vivo generation of sphingosine-based ceramides does not occur during Fas-induced apoptosis, contrary to the many published reports mentioned above.	transcription
71355	2	336175	7	NULL	NULL	0	NULL	sphingosine-based ceramides 	Chemical	in vivo generation of	does not occur					statement 1	Process	during			NULL		0	NULL	NULL	NULL	gw60_pnas_94_14_7292_s_95	9207084	Thus, the use of a direct MS-based assay, which is highly selective and sensitive, clearly demonstrated that  in vivo generation of sphingosine-based ceramides does not occur during Fas-induced apoptosis, contrary to the many published reports mentioned above.	transcription
67222	1	336176	5	NULL	NULL	0	NULL	TAM-67	GP		is a deletion mutant of					c-Jun	GP		NH2-terminus		NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_5	9415703	Dominant-negative blockade of normal c-Jun activity by transfection with the TAM-67 c-Jun NH2-terminal deletion mutant abolished the lethal actions of ceramide but was without effect on those of sphingosine, indicating that ceramide-related apoptosis is directly dependent on activation of c-Jun, whereas sphingosine-induced cell death proceeds via an unrelated downstream mechanism.	transcription
67223	2	336176	5	NULL	NULL	0	NULL	statement 1	Process	transfection with	blocks		dominant-negative			c-Jun	GP	normal activity of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_5	9415703	Dominant-negative blockade of normal c-Jun activity by transfection with the TAM-67 c-Jun NH2-terminal deletion mutant abolished the lethal actions of ceramide but was without effect on those of sphingosine, indicating that ceramide-related apoptosis is directly dependent on activation of c-Jun, whereas sphingosine-induced cell death proceeds via an unrelated downstream mechanism.	transcription
67224	3	336176	5	NULL	NULL	0	NULL	statement 2	Process		abolishes					ceramide	Chemical	lethal actions of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_5	9415703	Dominant-negative blockade of normal c-Jun activity by transfection with the TAM-67 c-Jun NH2-terminal deletion mutant abolished the lethal actions of ceramide but was without effect on those of sphingosine, indicating that ceramide-related apoptosis is directly dependent on activation of c-Jun, whereas sphingosine-induced cell death proceeds via an unrelated downstream mechanism.	transcription
67225	4	336176	5	NULL	NULL	0	NULL	statement 2	Process		does not effect					sphingosine	Chemical	lethal actions of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_5	9415703	Dominant-negative blockade of normal c-Jun activity by transfection with the TAM-67 c-Jun NH2-terminal deletion mutant abolished the lethal actions of ceramide but was without effect on those of sphingosine, indicating that ceramide-related apoptosis is directly dependent on activation of c-Jun, whereas sphingosine-induced cell death proceeds via an unrelated downstream mechanism.	transcription
67226	5	336176	5	NULL	NULL	0	NULL	apoptosis	Process		is related to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_5	9415703	Dominant-negative blockade of normal c-Jun activity by transfection with the TAM-67 c-Jun NH2-terminal deletion mutant abolished the lethal actions of ceramide but was without effect on those of sphingosine, indicating that ceramide-related apoptosis is directly dependent on activation of c-Jun, whereas sphingosine-induced cell death proceeds via an unrelated downstream mechanism.	transcription
67227	6	336176	5	NULL	NULL	0	NULL	statement 5	Process		is dependent on		directly			c-Jun	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_5	9415703	Dominant-negative blockade of normal c-Jun activity by transfection with the TAM-67 c-Jun NH2-terminal deletion mutant abolished the lethal actions of ceramide but was without effect on those of sphingosine, indicating that ceramide-related apoptosis is directly dependent on activation of c-Jun, whereas sphingosine-induced cell death proceeds via an unrelated downstream mechanism.	transcription
67228	7	336176	5	NULL	NULL	0	NULL	cell death	Process		induced by					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_5	9415703	Dominant-negative blockade of normal c-Jun activity by transfection with the TAM-67 c-Jun NH2-terminal deletion mutant abolished the lethal actions of ceramide but was without effect on those of sphingosine, indicating that ceramide-related apoptosis is directly dependent on activation of c-Jun, whereas sphingosine-induced cell death proceeds via an unrelated downstream mechanism.	transcription
67229	8	336176	5	NULL	NULL	0	NULL	statement 7	Process		proceeds via					unrelated downstream mechanism					NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_5	9415703	Dominant-negative blockade of normal c-Jun activity by transfection with the TAM-67 c-Jun NH2-terminal deletion mutant abolished the lethal actions of ceramide but was without effect on those of sphingosine, indicating that ceramide-related apoptosis is directly dependent on activation of c-Jun, whereas sphingosine-induced cell death proceeds via an unrelated downstream mechanism.	transcription
71356	1	336176	7	NULL	NULL	0	NULL	TAM-67 c-Jun	GP	deletion mutant	abolish			NH2-terminal		ceramide	Chemical	lethal actions of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_5	9415703	Dominant-negative blockade of normal c-Jun activity by transfection with the TAM-67 c-Jun NH2-terminal deletion mutant abolished the lethal actions of ceramide but was without effect on those of sphingosine, indicating that ceramide-related apoptosis is directly dependent on activation of c-Jun, whereas sphingosine-induced cell death proceeds via an unrelated downstream mechanism.	transcription
71357	2	336176	7	NULL	NULL	0	NULL	TAM-67 c-Jun 	GP	deletion mutant	does not effect			NH2-terminal		sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_5	9415703	Dominant-negative blockade of normal c-Jun activity by transfection with the TAM-67 c-Jun NH2-terminal deletion mutant abolished the lethal actions of ceramide but was without effect on those of sphingosine, indicating that ceramide-related apoptosis is directly dependent on activation of c-Jun, whereas sphingosine-induced cell death proceeds via an unrelated downstream mechanism.	transcription
71358	3	336176	7	NULL	NULL	NULL	NULL	ceramide	Chemical		related to					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_5	9415703	Dominant-negative blockade of normal c-Jun activity by transfection with the TAM-67 c-Jun NH2-terminal deletion mutant abolished the lethal actions of ceramide but was without effect on those of sphingosine, indicating that ceramide-related apoptosis is directly dependent on activation of c-Jun, whereas sphingosine-induced cell death proceeds via an unrelated downstream mechanism.	transcription
71359	4	336176	7	NULL	NULL	0	NULL	statement3	Process		depends on		directly			c-Jun	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_5	9415703	Dominant-negative blockade of normal c-Jun activity by transfection with the TAM-67 c-Jun NH2-terminal deletion mutant abolished the lethal actions of ceramide but was without effect on those of sphingosine, indicating that ceramide-related apoptosis is directly dependent on activation of c-Jun, whereas sphingosine-induced cell death proceeds via an unrelated downstream mechanism.	transcription
71360	5	336176	7	NULL	NULL	0	NULL	sphingosine	Chemical		induce					cell death	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_5	9415703	Dominant-negative blockade of normal c-Jun activity by transfection with the TAM-67 c-Jun NH2-terminal deletion mutant abolished the lethal actions of ceramide but was without effect on those of sphingosine, indicating that ceramide-related apoptosis is directly dependent on activation of c-Jun, whereas sphingosine-induced cell death proceeds via an unrelated downstream mechanism.	transcription
71361	6	336176	7	NULL	NULL	0	NULL	statement 5	Process		proceed via					 unrelated downstream mechanism	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_5	9415703	Dominant-negative blockade of normal c-Jun activity by transfection with the TAM-67 c-Jun NH2-terminal deletion mutant abolished the lethal actions of ceramide but was without effect on those of sphingosine, indicating that ceramide-related apoptosis is directly dependent on activation of c-Jun, whereas sphingosine-induced cell death proceeds via an unrelated downstream mechanism.	transcription
67230	1	336177	5	NULL	NULL	0	NULL	apoptosis	Process		induced by					Fas	GP				NULL	Type II Cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
67231	2	336177	5	NULL	NULL	0	NULL	sphingosine	Chemical		plays a role in		potentially			statement 1	Process				NULL	Type II Cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
67232	3	336177	5	NULL	NULL	0	NULL	ceramide	Chemical		plays a role in		potentially			statement 1	Process				NULL	Type II Cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
67233	4	336177	5	NULL	NULL	0	NULL	Bcl-2	GP		inhibits					statement 1	Process				NULL	Type II Cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
67234	5	336177	5	NULL	NULL	0	NULL	Bcl-xL	GP		inhibits					statement 1	Process				NULL	Type II Cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
67235	6	336177	5	NULL	NULL	0	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
67236	7	336177	5	NULL	NULL	0	NULL	apoptosis	Process		induced by					Fas	GP				NULL	Jurkat cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
67237	8	336177	5	NULL	NULL	0	NULL	Bcl-xL	GP		inhibits					statement 7	Process				NULL	Jurkat cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
67238	9	336177	5	NULL	NULL	0	NULL	apoptosis	Process		induced by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
67239	10	336177	5	NULL	NULL	0	NULL	apoptosis	Process		induced by					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
67240	11	336177	5	NULL	NULL	0	NULL	Bcl-xL	GP		inhibits					statement 9	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
67241	12	336177	5	NULL	NULL	0	NULL	Bcl-xL	GP		inhibits					statement 10	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
67242	13	336177	5	NULL	NULL	0	NULL	statement 8	Process		lesser extent than					statement 11	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
67243	14	336177	5	NULL	NULL	0	NULL	statement 8	Process		lesser extent than					statement 12	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
71362	1	336177	7	NULL	NULL	0	NULL	Fas	GP		induce					apoptosis	Process				NULL	Jurkat cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
71363	2	336177	7	NULL	NULL	0	NULL	Bcl-xL	GP		inhibit					statement 1	Process				NULL	Jurkat cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
71364	3	336177	7	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
71365	4	336177	7	NULL	NULL	0	NULL	sphingosine	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
71366	5	336177	7	NULL	NULL	0	NULL	Bcl-xL	GP		inhibit					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
71367	6	336177	7	NULL	NULL	0	NULL	Bcl-xL	GP		inhibit					statement 4					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
71368	7	336177	7	NULL	NULL	0	NULL	statement 2	Process	inhibition of	is lesser than					statement 5	Process	inhibition of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
71369	8	336177	7	NULL	NULL	0	NULL	statement 2	Process	inhibition of	is lesser than					statement 6	Process	inhibition of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
71370	9	336177	7	NULL	NULL	NULL	NULL	Fas	GP		induce					apoptosis	Process				NULL	type II cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
71371	10	336177	7	NULL	NULL	0	NULL	Bcl-2	GP		inhibit					statement 9	Process				NULL	type II cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
71372	11	336177	7	NULL	NULL	NULL	NULL	Bcl-xL	GP		inhibit					statement 9	Process				NULL	type II cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_280	10747891	Proposed Role of Sphingosine and Ceramide in Fas-induced Apoptosis of Type II Cells-- Consistent with other studies on inhibition of Fas-induced apoptosis by Bcl-2 or Bcl-xL in type II cells ( 2,  55,  67,  87-89), we found that Bcl-xL inhibited Fas-induced apoptosis in Jurkat cells, albeit to a lesser extent than its effect on ceramide- and sphingosine-induced apoptosis.	transcription
67244	1	336178	5	NULL	NULL	0	NULL	fumonisin B	Chemical		is a type of					mycotoxin	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
67245	2	336178	5	NULL	NULL	0	NULL	fumonisin B	Chemical		inhibits					ceramide syhthase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
67246	3	336178	5	NULL	NULL	0	NULL	sphingosine	Chemical	acylation of	leads to					ceramide	Chemical	formation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
67247	4	336178	5	NULL	NULL	0	NULL	sphinganine	Chemical	acylation of	leads to					ceramide	Chemical	formation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
67248	5	336178	5	NULL	NULL	0	NULL	statement 2	Process		blocks					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
67249	6	336178	5	NULL	NULL	0	NULL	statement 2	Process		blocks					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
67250	7	336178	5	NULL	NULL	0	NULL	COS-7 cells	Cell		is treated with					fumonisin B	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
67251	8	336178	5	NULL	NULL	0	NULL	COS-7 cells	Cell		is treated with					sphingomyelinase	GP	Bacillus cereus			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
67252	9	336178	5	NULL	NULL	0	NULL	statement 7	Process		stimulates					~68-kDa kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
67253	10	336178	5	NULL	NULL	0	NULL	statement 8	Process		stimulates					~68-kDa kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
67254	11	336178	5	NULL	NULL	0	NULL	COS-7 cells	Cell		is treated with					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
67255	12	336178	5	NULL	NULL	0	NULL	statement 11	Process		stimulates					~68-kDa kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
67256	13	336178	5	NULL	NULL	0	NULL	statement 9	Process		greater magnitude than					statement 12	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
67257	14	336178	5	NULL	NULL	0	NULL	statement 10	Process		greater magnitude than					statement 12					NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
71373	1	336178	7	NULL	NULL	0	NULL	fumonisin B	Chemical		inhibit					ceramide synthase	GP				NULL	COS-7 cells	0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
71374	2	336178	7	NULL	NULL	0	NULL	statement 1	Process		blocks 					sphingosine	Chemical	acylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
71375	3	336178	7	NULL	NULL	0	NULL	statement 1	Process		blocks					sphinganine	Chemical	acylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
71376	4	336178	7	NULL	NULL	0	NULL	sphingosine	Chemical	acylation of	forms					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
71377	5	336178	7	NULL	NULL	0	NULL	sphinganine	Chemical	acylation of	forms					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
71378	6	336178	7	NULL	NULL	0	NULL	fumonisin B	Chemical		is a type of					mycotoxin	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_14_8137_s_157	9525917	Similarly, treatment of the COS-7 cells with 5-10 muM fumonisin B, a mycotoxin that inhibits ceramide synthase and thereby blocks the acylation of sphingosine and sphinganine to form ceramide, for 10 min or with 1 unit/ml sphingomyelinase from  Bacillus cereus for 30 min also caused a stimulation of this ~68-kDa kinase which was of even greater magnitude than was observed with exogenously added sphingosine.	transcription
67258	1	336179	5	NULL	NULL	0	NULL	ceramide	Chemical		induces		directly			apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67259	2	336179	5	NULL	NULL	0	NULL	ceramide	Chemical	elevations of	induced by					agonist	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67260	3	336179	5	NULL	NULL	0	NULL	statement 2	Process		precede					apoptosis	Process	biochemical manifestations of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67261	4	336179	5	NULL	NULL	0	NULL	statement 2	Process		precede					apoptosis	Process	morphological manifestations of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67262	5	336179	5	NULL	NULL	0	NULL	ceramide	Chemical	natural	elevates					ceramide	Chemical	cellular			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67263	6	336179	5	NULL	NULL	0	NULL	stress	Process		effects					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67264	7	336179	5	NULL	NULL	0	NULL	statement 5	Process		mimics					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67265	8	336179	5	NULL	NULL	0	NULL	ceramide analogs	Chemical		elevates					ceramide	Chemical	cellular			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67266	9	336179	5	NULL	NULL	0	NULL	statement 8	Process		mimics					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67267	10	336179	5	NULL	NULL	0	NULL	SMases	GP		elevates					ceramide	Chemical	cellular			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67268	11	336179	5	NULL	NULL	0	NULL	statement 10	Process		mimics					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67269	12	336179	5	NULL	NULL	0	NULL	pharmacological agents	Chemical		interfere with					ceramide metabolism enzymes	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67270	13	336179	5	NULL	NULL	0	NULL	statement 12	Process		elevates					ceramide	Chemical	cellular			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67271	14	336179	5	NULL	NULL	0	NULL	D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol	Chemical		is an inhibitor of					glucosylceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67272	15	336179	5	NULL	NULL	0	NULL	N-oleoylethanolamine	Chemical		is an inhibitor of					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67273	16	336179	5	NULL	NULL	0	NULL	D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol	Chemical		is a type of					pharmacological agent	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67274	17	336179	5	NULL	NULL	0	NULL	N-oleoylethanolamine			is a type of					pharmacological agents	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67275	18	336179	5	NULL	NULL	0	NULL	statement 13	Process		enhance					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67276	19	336179	5	NULL	NULL	0	NULL	fumonisin B1	Chemical		is an inhibitor of					ceramide syhthase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67277	20	336179	5	NULL	NULL	0	NULL	statement 19	Process		reduce					ceramide	Chemical	generation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67278	21	336179	5	NULL	NULL	0	NULL	statement 20	Process		prevent					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67279	22	336179	5	NULL	NULL	0	NULL	lipids	Chemical		fail to signal		consistently			apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67280	23	336179	5	NULL	NULL	0	NULL	sphingolipid metabolites	Chemical		fail to signal		consistently			apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67281	24	336179	5	NULL	NULL	0	NULL	sphingosine	Chemical		does not fail to signal					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71379	1	336179	7	NULL	NULL	0	NULL	 ceramide	Chemical		is involved in		directly			apoptosis	Process	induction of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71380	2	336179	7	NULL	NULL	0	NULL	agonist	Chemical		induce					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71381	3	336179	7	NULL	NULL	0	NULL	apoptosis	Process	biochemical manifestations of	precede					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71382	4	336179	7	NULL	NULL	0	NULL	apoptosis	Process	morphological manifestations of	precede					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71383	5	336179	7	NULL	NULL	0	NULL	natural ceramide	Chemical		elevates					cellular ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71384	6	336179	7	NULL	NULL	0	NULL	 ceramide analogs	Chemical		elevates					cellular ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71385	7	336179	7	NULL	NULL	0	NULL	 SMases	GP	exogenous	elevates					cellular ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71386	8	336179	7	NULL	NULL	0	NULL	statement 5	Process		mimic					apoptosis	Process	effects of stress on			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71387	9	336179	7	NULL	NULL	0	NULL	statement 6	Process		mimic					apoptosis	Process	effects of stress on			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71388	10	336179	7	NULL	NULL	0	NULL	statement 7	Process		mimic					apoptosis	Process	effects of stress on			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71389	11	336179	7	NULL	NULL	0	NULL	D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol 	Chemical		inhibit					glucosylceramide synthase	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71390	12	336179	7	NULL	NULL	0	NULL	D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol 	Chemical		interferes with					ceramide metabolism	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71391	13	336179	7	NULL	NULL	0	NULL	D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol 	Chemical		elevate					cellular ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71392	14	336179	7	NULL	NULL	0	NULL	N-oleoylethanolamine	Chemical		inhibit					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71393	15	336179	7	NULL	NULL	0	NULL	N-oleoylethanolamine	Chemical		interferes with					ceramide metabolism	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71394	16	336179	7	NULL	NULL	0	NULL	N-oleoylethanolamine	Chemical		elevate					cellular ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71395	17	336179	7	NULL	NULL	0	NULL	D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol	Chemical		enhance		uniformly			apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71396	18	336179	7	NULL	NULL	0	NULL	N-oleoylethanolamine	Chemical		enhance		uniformly			apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71397	19	336179	7	NULL	NULL	0	NULL	fumonisin B1	Chemical		inhibit					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71398	20	336179	7	NULL	NULL	0	NULL	fumonisin B1	Chemical		prevent					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71399	21	336179	7	NULL	NULL	0	NULL	fumonisin B1	Chemical		reduce					ceramide	Chemical	generation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71400	22	336179	7	NULL	NULL	0	NULL	sphingolipid metabolites	Chemical		fail to		consistently			apoptosis	Process	signal			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71401	23	336179	7	NULL	NULL	0	NULL	sphingosine	Chemical		signals					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71402	24	336179	7	NULL	NULL	0	NULL	statement 3	Process		support					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71403	25	336179	7	NULL	NULL	0	NULL	statement 4	Process		support					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71404	26	336179	7	NULL	NULL	0	NULL	statement 8	Process		support					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71405	27	336179	7	NULL	NULL	0	NULL	statement 9	Process		support					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71406	28	336179	7	NULL	NULL	0	NULL	statement 10	Process		support					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71407	29	336179	7	NULL	NULL	0	NULL	statement 17	Process		support					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71408	30	336179	7	NULL	NULL	0	NULL	statement 18	Process		support					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71409	31	336179	7	NULL	NULL	0	NULL	statement 20	Process		support					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
71410	32	336179	7	NULL	NULL	0	NULL	statement 22	Process		support					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_442_s_15	11031259	Evidence that ceramide is involved directly in the induction of apoptosis is summarized as follows: (i) agonist-induced ceramide elevations precede biochemical and morphological manifestations of apoptosis ( 4-7); (ii) elevation of cellular ceramide levels using natural ceramide ( 8-10), ceramide analogs, or exogenous SMases mimic the effects of stress on apoptosis ( 11-16); (iii) pharmacological agents which interfere with enzymes of ceramide metabolism and elevate cellular ceramide, such as the glucosylceramide synthase inhibitor D-threo-1-phenyl-decanoylamino-3-morpholino-1-propanol or the ceramidase inhibitor  N-oleoylethanolamine, uniformly enhance apoptosis ( 17-19), whereas agents that reduce ceramide generation, such as the ceramide synthase inhibitor fumonisin B1, prevent apoptosis ( 10,  20,  21); and (iv) other lipids, including other sphingolipid metabolites (except perhaps sphingosine), fail to consistently signal apoptosis ( 12,  13,  16).	transcription
67282	1	336180	5	NULL	NULL	0	NULL	sphingosine	Chemical		induces					c-Jun	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_135	12135749	Here we demonstrated that (i) sphingosine (as well as ceramide) induced c-jun expression, (ii) sphingosine-induced c-jun expression was stimulated by H-89, a PKA inhibitor, whereas C2-ceramide-induced c-jun expression was not affected by H-89, (iii) sphingosine-induced c-jun expression was only slightly affected by PKC inhibitors, whereas C2-ceramide-induced c-jun expression was strongly inhibited by PKC inhibitors.	transcription
67283	2	336180	5	NULL	NULL	0	NULL	ceramide	Chemical		induces					c-Jun	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_135	12135749	Here we demonstrated that (i) sphingosine (as well as ceramide) induced c-jun expression, (ii) sphingosine-induced c-jun expression was stimulated by H-89, a PKA inhibitor, whereas C2-ceramide-induced c-jun expression was not affected by H-89, (iii) sphingosine-induced c-jun expression was only slightly affected by PKC inhibitors, whereas C2-ceramide-induced c-jun expression was strongly inhibited by PKC inhibitors.	transcription
67284	3	336180	5	NULL	NULL	0	NULL	H-89	Chemical		is an inhibitor of					PKA	GP				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_135	12135749	Here we demonstrated that (i) sphingosine (as well as ceramide) induced c-jun expression, (ii) sphingosine-induced c-jun expression was stimulated by H-89, a PKA inhibitor, whereas C2-ceramide-induced c-jun expression was not affected by H-89, (iii) sphingosine-induced c-jun expression was only slightly affected by PKC inhibitors, whereas C2-ceramide-induced c-jun expression was strongly inhibited by PKC inhibitors.	transcription
67285	4	336180	5	NULL	NULL	0	NULL	H-89	Chemical		stimulates					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_135	12135749	Here we demonstrated that (i) sphingosine (as well as ceramide) induced c-jun expression, (ii) sphingosine-induced c-jun expression was stimulated by H-89, a PKA inhibitor, whereas C2-ceramide-induced c-jun expression was not affected by H-89, (iii) sphingosine-induced c-jun expression was only slightly affected by PKC inhibitors, whereas C2-ceramide-induced c-jun expression was strongly inhibited by PKC inhibitors.	transcription
67286	5	336180	5	NULL	NULL	0	NULL	C2-ceramide	Chemical		induces					c-Jun	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_135	12135749	Here we demonstrated that (i) sphingosine (as well as ceramide) induced c-jun expression, (ii) sphingosine-induced c-jun expression was stimulated by H-89, a PKA inhibitor, whereas C2-ceramide-induced c-jun expression was not affected by H-89, (iii) sphingosine-induced c-jun expression was only slightly affected by PKC inhibitors, whereas C2-ceramide-induced c-jun expression was strongly inhibited by PKC inhibitors.	transcription
67287	6	336180	5	NULL	NULL	0	NULL	H-89	Chemical		does not affect					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_135	12135749	Here we demonstrated that (i) sphingosine (as well as ceramide) induced c-jun expression, (ii) sphingosine-induced c-jun expression was stimulated by H-89, a PKA inhibitor, whereas C2-ceramide-induced c-jun expression was not affected by H-89, (iii) sphingosine-induced c-jun expression was only slightly affected by PKC inhibitors, whereas C2-ceramide-induced c-jun expression was strongly inhibited by PKC inhibitors.	transcription
67288	7	336180	5	NULL	NULL	0	NULL	PKC inhibitors	Chemical		affects		slightly			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_135	12135749	Here we demonstrated that (i) sphingosine (as well as ceramide) induced c-jun expression, (ii) sphingosine-induced c-jun expression was stimulated by H-89, a PKA inhibitor, whereas C2-ceramide-induced c-jun expression was not affected by H-89, (iii) sphingosine-induced c-jun expression was only slightly affected by PKC inhibitors, whereas C2-ceramide-induced c-jun expression was strongly inhibited by PKC inhibitors.	transcription
67289	8	336180	5	NULL	NULL	0	NULL	PKC inhibitors	Chemical		inhibits		strongly			statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_135	12135749	Here we demonstrated that (i) sphingosine (as well as ceramide) induced c-jun expression, (ii) sphingosine-induced c-jun expression was stimulated by H-89, a PKA inhibitor, whereas C2-ceramide-induced c-jun expression was not affected by H-89, (iii) sphingosine-induced c-jun expression was only slightly affected by PKC inhibitors, whereas C2-ceramide-induced c-jun expression was strongly inhibited by PKC inhibitors.	transcription
71411	1	336180	7	NULL	NULL	0	NULL	sphingosine	Chemical		induce					c-jun	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_135	12135749	Here we demonstrated that (i) sphingosine (as well as ceramide) induced c-jun expression, (ii) sphingosine-induced c-jun expression was stimulated by H-89, a PKA inhibitor, whereas C2-ceramide-induced c-jun expression was not affected by H-89, (iii) sphingosine-induced c-jun expression was only slightly affected by PKC inhibitors, whereas C2-ceramide-induced c-jun expression was strongly inhibited by PKC inhibitors.	transcription
71412	2	336180	7	NULL	NULL	0	NULL	ceramide	Chemical		induce					c-jun	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_135	12135749	Here we demonstrated that (i) sphingosine (as well as ceramide) induced c-jun expression, (ii) sphingosine-induced c-jun expression was stimulated by H-89, a PKA inhibitor, whereas C2-ceramide-induced c-jun expression was not affected by H-89, (iii) sphingosine-induced c-jun expression was only slightly affected by PKC inhibitors, whereas C2-ceramide-induced c-jun expression was strongly inhibited by PKC inhibitors.	transcription
71413	3	336180	7	NULL	NULL	0	NULL	H-89	Chemical		stimulate					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_135	12135749	Here we demonstrated that (i) sphingosine (as well as ceramide) induced c-jun expression, (ii) sphingosine-induced c-jun expression was stimulated by H-89, a PKA inhibitor, whereas C2-ceramide-induced c-jun expression was not affected by H-89, (iii) sphingosine-induced c-jun expression was only slightly affected by PKC inhibitors, whereas C2-ceramide-induced c-jun expression was strongly inhibited by PKC inhibitors.	transcription
71414	4	336180	7	NULL	NULL	0	NULL	H-89	Chemical		is a type of					PKA inhibitor	Chemical				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_135	12135749	Here we demonstrated that (i) sphingosine (as well as ceramide) induced c-jun expression, (ii) sphingosine-induced c-jun expression was stimulated by H-89, a PKA inhibitor, whereas C2-ceramide-induced c-jun expression was not affected by H-89, (iii) sphingosine-induced c-jun expression was only slightly affected by PKC inhibitors, whereas C2-ceramide-induced c-jun expression was strongly inhibited by PKC inhibitors.	transcription
71415	5	336180	7	NULL	NULL	0	NULL	C2-ceramide	Chemical		induce					c-jun	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_135	12135749	Here we demonstrated that (i) sphingosine (as well as ceramide) induced c-jun expression, (ii) sphingosine-induced c-jun expression was stimulated by H-89, a PKA inhibitor, whereas C2-ceramide-induced c-jun expression was not affected by H-89, (iii) sphingosine-induced c-jun expression was only slightly affected by PKC inhibitors, whereas C2-ceramide-induced c-jun expression was strongly inhibited by PKC inhibitors.	transcription
71416	6	336180	7	NULL	NULL	0	NULL	H-89	Chemical		does not affect					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_135	12135749	Here we demonstrated that (i) sphingosine (as well as ceramide) induced c-jun expression, (ii) sphingosine-induced c-jun expression was stimulated by H-89, a PKA inhibitor, whereas C2-ceramide-induced c-jun expression was not affected by H-89, (iii) sphingosine-induced c-jun expression was only slightly affected by PKC inhibitors, whereas C2-ceramide-induced c-jun expression was strongly inhibited by PKC inhibitors.	transcription
71417	7	336180	7	NULL	NULL	0	NULL	PKC inhibitors	Chemical		affect		slightly			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_135	12135749	Here we demonstrated that (i) sphingosine (as well as ceramide) induced c-jun expression, (ii) sphingosine-induced c-jun expression was stimulated by H-89, a PKA inhibitor, whereas C2-ceramide-induced c-jun expression was not affected by H-89, (iii) sphingosine-induced c-jun expression was only slightly affected by PKC inhibitors, whereas C2-ceramide-induced c-jun expression was strongly inhibited by PKC inhibitors.	transcription
71418	8	336180	7	NULL	NULL	0	NULL	PKC inhibitors	Chemical		inhibit		strongly			statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_febslett_524_1_103_s_135	12135749	Here we demonstrated that (i) sphingosine (as well as ceramide) induced c-jun expression, (ii) sphingosine-induced c-jun expression was stimulated by H-89, a PKA inhibitor, whereas C2-ceramide-induced c-jun expression was not affected by H-89, (iii) sphingosine-induced c-jun expression was only slightly affected by PKC inhibitors, whereas C2-ceramide-induced c-jun expression was strongly inhibited by PKC inhibitors.	transcription
67290	1	336181	5	NULL	NULL	0	NULL	apoptosis	Process		induced by					Fas	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_58	10747891	Early Transient Increases in Ceramide and Sphingosine during Fas-induced Apoptosis Precede Executioner Caspases Activation and Cell Death and Are Followed by a Sustained Accumulation of Ceramide-- As previously reported ( 10,  14,  20,  21), we found that treatment of Jurkat cells with 50 ng/ml anti-Fas antibody resulted in acute changes in ceramide levels within 30 min from a basal level of ~10 pmol/nmol total phospholipids (Fig.  1 A).	transcription
67291	2	336181	5	NULL	NULL	0	NULL	ceramide	Chemical	early;;transient increase of	occurs during					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_58	10747891	Early Transient Increases in Ceramide and Sphingosine during Fas-induced Apoptosis Precede Executioner Caspases Activation and Cell Death and Are Followed by a Sustained Accumulation of Ceramide-- As previously reported ( 10,  14,  20,  21), we found that treatment of Jurkat cells with 50 ng/ml anti-Fas antibody resulted in acute changes in ceramide levels within 30 min from a basal level of ~10 pmol/nmol total phospholipids (Fig.  1 A).	transcription
67292	3	336181	5	NULL	NULL	0	NULL	sphingosine	Chemical	early;;transient increase of	occurs during					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_58	10747891	Early Transient Increases in Ceramide and Sphingosine during Fas-induced Apoptosis Precede Executioner Caspases Activation and Cell Death and Are Followed by a Sustained Accumulation of Ceramide-- As previously reported ( 10,  14,  20,  21), we found that treatment of Jurkat cells with 50 ng/ml anti-Fas antibody resulted in acute changes in ceramide levels within 30 min from a basal level of ~10 pmol/nmol total phospholipids (Fig.  1 A).	transcription
67293	4	336181	5	NULL	NULL	0	NULL	statement 2	Process		precede					executioner caspases	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_58	10747891	Early Transient Increases in Ceramide and Sphingosine during Fas-induced Apoptosis Precede Executioner Caspases Activation and Cell Death and Are Followed by a Sustained Accumulation of Ceramide-- As previously reported ( 10,  14,  20,  21), we found that treatment of Jurkat cells with 50 ng/ml anti-Fas antibody resulted in acute changes in ceramide levels within 30 min from a basal level of ~10 pmol/nmol total phospholipids (Fig.  1 A).	transcription
67294	5	336181	5	NULL	NULL	0	NULL	statement 2	Process		precede					cell death	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_58	10747891	Early Transient Increases in Ceramide and Sphingosine during Fas-induced Apoptosis Precede Executioner Caspases Activation and Cell Death and Are Followed by a Sustained Accumulation of Ceramide-- As previously reported ( 10,  14,  20,  21), we found that treatment of Jurkat cells with 50 ng/ml anti-Fas antibody resulted in acute changes in ceramide levels within 30 min from a basal level of ~10 pmol/nmol total phospholipids (Fig.  1 A).	transcription
67295	6	336181	5	NULL	NULL	0	NULL	statement 3	Process		precede					executioner caspases	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_58	10747891	Early Transient Increases in Ceramide and Sphingosine during Fas-induced Apoptosis Precede Executioner Caspases Activation and Cell Death and Are Followed by a Sustained Accumulation of Ceramide-- As previously reported ( 10,  14,  20,  21), we found that treatment of Jurkat cells with 50 ng/ml anti-Fas antibody resulted in acute changes in ceramide levels within 30 min from a basal level of ~10 pmol/nmol total phospholipids (Fig.  1 A).	transcription
67296	7	336181	5	NULL	NULL	0	NULL	statement 3	Process		precede					cell death	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_58	10747891	Early Transient Increases in Ceramide and Sphingosine during Fas-induced Apoptosis Precede Executioner Caspases Activation and Cell Death and Are Followed by a Sustained Accumulation of Ceramide-- As previously reported ( 10,  14,  20,  21), we found that treatment of Jurkat cells with 50 ng/ml anti-Fas antibody resulted in acute changes in ceramide levels within 30 min from a basal level of ~10 pmol/nmol total phospholipids (Fig.  1 A).	transcription
67297	8	336181	5	NULL	NULL	0	NULL	statement 2	Process		followed by					ceramide	Chemical	sustained accumulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_58	10747891	Early Transient Increases in Ceramide and Sphingosine during Fas-induced Apoptosis Precede Executioner Caspases Activation and Cell Death and Are Followed by a Sustained Accumulation of Ceramide-- As previously reported ( 10,  14,  20,  21), we found that treatment of Jurkat cells with 50 ng/ml anti-Fas antibody resulted in acute changes in ceramide levels within 30 min from a basal level of ~10 pmol/nmol total phospholipids (Fig.  1 A).	transcription
67298	9	336181	5	NULL	NULL	0	NULL	statement 3	Process		followed by					ceramide	Chemical	sustained accumulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_58	10747891	Early Transient Increases in Ceramide and Sphingosine during Fas-induced Apoptosis Precede Executioner Caspases Activation and Cell Death and Are Followed by a Sustained Accumulation of Ceramide-- As previously reported ( 10,  14,  20,  21), we found that treatment of Jurkat cells with 50 ng/ml anti-Fas antibody resulted in acute changes in ceramide levels within 30 min from a basal level of ~10 pmol/nmol total phospholipids (Fig.  1 A).	transcription
67299	10	336181	5	NULL	NULL	NULL	NULL	anti-Fas antibody	GP	treatment	results in					ceramide	Chemical	acute change of;;level of			NULL	Jurkat cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_58	10747891	Early Transient Increases in Ceramide and Sphingosine during Fas-induced Apoptosis Precede Executioner Caspases Activation and Cell Death and Are Followed by a Sustained Accumulation of Ceramide-- As previously reported ( 10,  14,  20,  21), we found that treatment of Jurkat cells with 50 ng/ml anti-Fas antibody resulted in acute changes in ceramide levels within 30 min from a basal level of ~10 pmol/nmol total phospholipids (Fig.  1 A).	transcription
71419	1	336181	7	NULL	NULL	0	NULL	Fas	GP		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_58	10747891	Early Transient Increases in Ceramide and Sphingosine during Fas-induced Apoptosis Precede Executioner Caspases Activation and Cell Death and Are Followed by a Sustained Accumulation of Ceramide-- As previously reported ( 10,  14,  20,  21), we found that treatment of Jurkat cells with 50 ng/ml anti-Fas antibody resulted in acute changes in ceramide levels within 30 min from a basal level of ~10 pmol/nmol total phospholipids (Fig.  1 A).	transcription
71420	2	336181	7	NULL	NULL	0	NULL	ceramide	Chemical	Transient Increases in	occur during					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_58	10747891	Early Transient Increases in Ceramide and Sphingosine during Fas-induced Apoptosis Precede Executioner Caspases Activation and Cell Death and Are Followed by a Sustained Accumulation of Ceramide-- As previously reported ( 10,  14,  20,  21), we found that treatment of Jurkat cells with 50 ng/ml anti-Fas antibody resulted in acute changes in ceramide levels within 30 min from a basal level of ~10 pmol/nmol total phospholipids (Fig.  1 A).	transcription
71421	3	336181	7	NULL	NULL	0	NULL	sphingosine	Chemical	Transient Increases in	occur during					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_58	10747891	Early Transient Increases in Ceramide and Sphingosine during Fas-induced Apoptosis Precede Executioner Caspases Activation and Cell Death and Are Followed by a Sustained Accumulation of Ceramide-- As previously reported ( 10,  14,  20,  21), we found that treatment of Jurkat cells with 50 ng/ml anti-Fas antibody resulted in acute changes in ceramide levels within 30 min from a basal level of ~10 pmol/nmol total phospholipids (Fig.  1 A).	transcription
71422	4	336181	7	NULL	NULL	0	NULL	statement 2	Process		precede					executioner caspases	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_58	10747891	Early Transient Increases in Ceramide and Sphingosine during Fas-induced Apoptosis Precede Executioner Caspases Activation and Cell Death and Are Followed by a Sustained Accumulation of Ceramide-- As previously reported ( 10,  14,  20,  21), we found that treatment of Jurkat cells with 50 ng/ml anti-Fas antibody resulted in acute changes in ceramide levels within 30 min from a basal level of ~10 pmol/nmol total phospholipids (Fig.  1 A).	transcription
71423	5	336181	7	NULL	NULL	0	NULL	statement 2	Process		precede					cell death	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_58	10747891	Early Transient Increases in Ceramide and Sphingosine during Fas-induced Apoptosis Precede Executioner Caspases Activation and Cell Death and Are Followed by a Sustained Accumulation of Ceramide-- As previously reported ( 10,  14,  20,  21), we found that treatment of Jurkat cells with 50 ng/ml anti-Fas antibody resulted in acute changes in ceramide levels within 30 min from a basal level of ~10 pmol/nmol total phospholipids (Fig.  1 A).	transcription
71424	6	336181	7	NULL	NULL	0	NULL	statement 4	Process		followed by					ceramide	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_58	10747891	Early Transient Increases in Ceramide and Sphingosine during Fas-induced Apoptosis Precede Executioner Caspases Activation and Cell Death and Are Followed by a Sustained Accumulation of Ceramide-- As previously reported ( 10,  14,  20,  21), we found that treatment of Jurkat cells with 50 ng/ml anti-Fas antibody resulted in acute changes in ceramide levels within 30 min from a basal level of ~10 pmol/nmol total phospholipids (Fig.  1 A).	transcription
71425	7	336181	7	NULL	NULL	0	NULL	statement 5	Process		followed by					ceramide	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_58	10747891	Early Transient Increases in Ceramide and Sphingosine during Fas-induced Apoptosis Precede Executioner Caspases Activation and Cell Death and Are Followed by a Sustained Accumulation of Ceramide-- As previously reported ( 10,  14,  20,  21), we found that treatment of Jurkat cells with 50 ng/ml anti-Fas antibody resulted in acute changes in ceramide levels within 30 min from a basal level of ~10 pmol/nmol total phospholipids (Fig.  1 A).	transcription
67300	1	336182	5	NULL	NULL	NULL	NULL	sphingosine kinase gene	GP	temporal expression patterns of;;Drosophila	affects					long chain base	Chemical	metabolism of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
67301	2	336182	5	NULL	NULL	0	NULL	sphingosine kinase gene	GP	tissue-specific expression patterns of;;Drosophila	affects					long chain base	Chemical	metabolism of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
67302	3	336182	5	NULL	NULL	0	NULL	statement 1	Process		similar to					SPL	GP	temporal expression patterns of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
67303	4	336182	5	NULL	NULL	0	NULL	statement 2	Process		similar to					SPL	GP	tissue-specific expression patterns of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
67304	5	336182	5	NULL	NULL	0	NULL	ceramidase gene	GP	temporal expression patterns of;;Drosophila	affects					long chain base	Chemical	metabolism of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
67305	6	336182	5	NULL	NULL	0	NULL	ceramidase gene	GP	tissue-specific expression patterns of;;Drosophila	affects					long chain base	Chemical	metabolism of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
67306	7	336182	5	NULL	NULL	0	NULL	statement 5	Process		similar to					SPL	GP	temporal expression patterns of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
67307	8	336182	5	NULL	NULL	0	NULL	statement 6	Process		similar to					SPL	GP	tissue-specific expression patterns of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
67308	9	336182	5	NULL	NULL	0	NULL	ceramide kinase gene	GP	temporal expression patterns of;;Drosophila	affects					long chain base	Chemical	metabolism of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
67309	10	336182	5	NULL	NULL	0	NULL	ceramide kinase gene	GP	tissue-specific expression patterns of;;Drosophila	affects					long chain base	Chemical	metabolism of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
67310	11	336182	5	NULL	NULL	0	NULL	statement 9	Process		similar to					SPL	GP	temporal expression patterns of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
67311	12	336182	5	NULL	NULL	0	NULL	statement 10	Process		similar to					SPL	GP	tissue-specific expression patterns of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
71426	1	336182	7	NULL	NULL	0	NULL	Drosophila genes	GP	temporal specific expression patterns of	affect					long chain base metabolism	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
71427	2	336182	7	NULL	NULL	0	NULL	Drosophila genes	GP	tissue-specific expression patterns of	affect					long chain base metabolism	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
71428	3	336182	7	NULL	NULL	0	NULL	statement 1	Process		affect					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
71429	4	336182	7	NULL	NULL	0	NULL	statement 2	Process		affect					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
71430	5	336182	7	NULL	NULL	0	NULL	statement 1	Process		affect					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
71431	6	336182	7	NULL	NULL	0	NULL	statement 2	Process		affect					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
71432	7	336182	7	NULL	NULL	0	NULL	statement 1	Process		affect					ceramide kinase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
71433	8	336182	7	NULL	NULL	NULL	NULL	statement 2	Process		affect					ceramide kinase	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_18_18403_s_227	15734735	Furthermore, our results as well as recent work from the laboratory of Ruth Lehmann indicate that the temporal and tissue-specific expression patterns of additional  Drosophila genes affecting long chain base metabolism, including sphingosine kinase, ceramidase, and ceramide kinase, are similar to that of SPL ( ,  ).	transcription
67312	1	336183	5	NULL	NULL	0	NULL	sphingosine	Chemical		is phosphorylated to					S1-P	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_227	11102354	On the other hand, S1-P, which is formed by phosphorylation of sphingosine, has been implicated in a number of important cellular functions including promotion of cell proliferation and inhibition of cell motility, tumor cell invasiveness, ceramide-mediated apoptosis, and developmental processes.	transcription
67313	2	336183	5	NULL	NULL	0	NULL	S1-P	Chemical		promotes					cell proliferation	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_227	11102354	On the other hand, S1-P, which is formed by phosphorylation of sphingosine, has been implicated in a number of important cellular functions including promotion of cell proliferation and inhibition of cell motility, tumor cell invasiveness, ceramide-mediated apoptosis, and developmental processes.	transcription
67314	3	336183	5	NULL	NULL	0	NULL	S1-P	Chemical		inhibits					cell motility	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_227	11102354	On the other hand, S1-P, which is formed by phosphorylation of sphingosine, has been implicated in a number of important cellular functions including promotion of cell proliferation and inhibition of cell motility, tumor cell invasiveness, ceramide-mediated apoptosis, and developmental processes.	transcription
67315	4	336183	5	NULL	NULL	0	NULL	S1-P	Chemical		inhibits					tumor cell	Cell	invasiveness of			NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_227	11102354	On the other hand, S1-P, which is formed by phosphorylation of sphingosine, has been implicated in a number of important cellular functions including promotion of cell proliferation and inhibition of cell motility, tumor cell invasiveness, ceramide-mediated apoptosis, and developmental processes.	transcription
67316	5	336183	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_227	11102354	On the other hand, S1-P, which is formed by phosphorylation of sphingosine, has been implicated in a number of important cellular functions including promotion of cell proliferation and inhibition of cell motility, tumor cell invasiveness, ceramide-mediated apoptosis, and developmental processes.	transcription
67317	6	336183	5	NULL	NULL	0	NULL	S1-P	Chemical		inhibits					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_227	11102354	On the other hand, S1-P, which is formed by phosphorylation of sphingosine, has been implicated in a number of important cellular functions including promotion of cell proliferation and inhibition of cell motility, tumor cell invasiveness, ceramide-mediated apoptosis, and developmental processes.	transcription
67318	7	336183	5	NULL	NULL	0	NULL	S1-P	Chemical		inhibits					developmental processes	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_227	11102354	On the other hand, S1-P, which is formed by phosphorylation of sphingosine, has been implicated in a number of important cellular functions including promotion of cell proliferation and inhibition of cell motility, tumor cell invasiveness, ceramide-mediated apoptosis, and developmental processes.	transcription
71434	1	336183	7	NULL	NULL	0	NULL	sphingosine	Chemical	phosphorylation of	forms					S1-P	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_227	11102354	On the other hand, S1-P, which is formed by phosphorylation of sphingosine, has been implicated in a number of important cellular functions including promotion of cell proliferation and inhibition of cell motility, tumor cell invasiveness, ceramide-mediated apoptosis, and developmental processes.	transcription
71435	2	336183	7	NULL	NULL	NULL	NULL	S1-P	Chemical		promote					cell proliferation	Process				NULL		NULL	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_227	11102354	On the other hand, S1-P, which is formed by phosphorylation of sphingosine, has been implicated in a number of important cellular functions including promotion of cell proliferation and inhibition of cell motility, tumor cell invasiveness, ceramide-mediated apoptosis, and developmental processes.	transcription
71436	3	336183	7	NULL	NULL	0	NULL	S1-P	Chemical		inhibit					cell motility	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_227	11102354	On the other hand, S1-P, which is formed by phosphorylation of sphingosine, has been implicated in a number of important cellular functions including promotion of cell proliferation and inhibition of cell motility, tumor cell invasiveness, ceramide-mediated apoptosis, and developmental processes.	transcription
71437	4	336183	7	NULL	NULL	0	NULL	S1-P	Chemical		inhibit					tumor cell invasiveness	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_227	11102354	On the other hand, S1-P, which is formed by phosphorylation of sphingosine, has been implicated in a number of important cellular functions including promotion of cell proliferation and inhibition of cell motility, tumor cell invasiveness, ceramide-mediated apoptosis, and developmental processes.	transcription
71438	5	336183	7	NULL	NULL	0	NULL	ceramide	Chemical		mediates					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_227	11102354	On the other hand, S1-P, which is formed by phosphorylation of sphingosine, has been implicated in a number of important cellular functions including promotion of cell proliferation and inhibition of cell motility, tumor cell invasiveness, ceramide-mediated apoptosis, and developmental processes.	transcription
71439	6	336183	7	NULL	NULL	0	NULL	S1-P	Chemical		inhibit					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_227	11102354	On the other hand, S1-P, which is formed by phosphorylation of sphingosine, has been implicated in a number of important cellular functions including promotion of cell proliferation and inhibition of cell motility, tumor cell invasiveness, ceramide-mediated apoptosis, and developmental processes.	transcription
71440	7	336183	7	NULL	NULL	0	NULL	S1-P	Chemical		inhibit					developmental processes	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_227	11102354	On the other hand, S1-P, which is formed by phosphorylation of sphingosine, has been implicated in a number of important cellular functions including promotion of cell proliferation and inhibition of cell motility, tumor cell invasiveness, ceramide-mediated apoptosis, and developmental processes.	transcription
67319	1	336184	5	NULL	NULL	NULL	NULL	Sphingosine 1-phosphate	GP		inhibits					caspases	GP	activation of			NULL	Jurkat T lymphocytes	NULL	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_279	11102354	CUVILLIER, O., D. S. ROSENTHAL, M. E. SMULSON, and S. SPIEGEL, 1998  Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
67320	2	336184	5	NULL	NULL	0	NULL	caspases	GP		cleave					poly(ADP-ribose) polymerase	GP				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_279	11102354	CUVILLIER, O., D. S. ROSENTHAL, M. E. SMULSON, and S. SPIEGEL, 1998  Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
67321	3	336184	5	NULL	NULL	0	NULL	caspases	GP		cleave					lamins	GP				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_279	11102354	CUVILLIER, O., D. S. ROSENTHAL, M. E. SMULSON, and S. SPIEGEL, 1998  Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
67322	4	336184	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					Fas	GP				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_279	11102354	CUVILLIER, O., D. S. ROSENTHAL, M. E. SMULSON, and S. SPIEGEL, 1998  Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
67323	5	336184	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					ceramide	Chemical				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_279	11102354	CUVILLIER, O., D. S. ROSENTHAL, M. E. SMULSON, and S. SPIEGEL, 1998  Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
67324	6	336184	5	NULL	NULL	0	NULL	statement 2	Process		occurs during					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_279	11102354	CUVILLIER, O., D. S. ROSENTHAL, M. E. SMULSON, and S. SPIEGEL, 1998  Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
67325	7	336184	5	NULL	NULL	0	NULL	statement 2	Process		occurs during					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_279	11102354	CUVILLIER, O., D. S. ROSENTHAL, M. E. SMULSON, and S. SPIEGEL, 1998  Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
67326	8	336184	5	NULL	NULL	0	NULL	statement 3	Process		occurs during					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_279	11102354	CUVILLIER, O., D. S. ROSENTHAL, M. E. SMULSON, and S. SPIEGEL, 1998  Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
67327	9	336184	5	NULL	NULL	0	NULL	statement 3	Process		occurs during					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_279	11102354	CUVILLIER, O., D. S. ROSENTHAL, M. E. SMULSON, and S. SPIEGEL, 1998  Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
71441	1	336184	7	NULL	NULL	0	NULL	caspases	GP		cleave					poly(ADP-ribose) polymerase	GP				NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_279	11102354	CUVILLIER, O., D. S. ROSENTHAL, M. E. SMULSON, and S. SPIEGEL, 1998  Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
71442	2	336184	7	NULL	NULL	0	NULL	caspases	GP		cleave					lamins	Chemical				NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_279	11102354	CUVILLIER, O., D. S. ROSENTHAL, M. E. SMULSON, and S. SPIEGEL, 1998  Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
71444	3	336184	7	NULL	NULL	0	NULL	Fas	GP		mediates					apoptosis	Process				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_279	11102354	CUVILLIER, O., D. S. ROSENTHAL, M. E. SMULSON, and S. SPIEGEL, 1998  Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
71445	4	336184	7	NULL	NULL	0	NULL	ceramide	Chemical		mediates					apoptosis	Process				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_279	11102354	CUVILLIER, O., D. S. ROSENTHAL, M. E. SMULSON, and S. SPIEGEL, 1998  Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
71446	5	336184	7	NULL	NULL	0	NULL	Sphingosine 1-phosphate	Chemical		inhibit					caspases	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_genetics_156_4_1519_s_279	11102354	CUVILLIER, O., D. S. ROSENTHAL, M. E. SMULSON, and S. SPIEGEL, 1998  Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	transcription
67328	1	336185	5	NULL	NULL	0	NULL	NOE	Chemical		is an inhibitor of					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_185	10051135	The ceramidase inhibitor, NOE, which attenuated the depressant actions of TNF under constant flow and constant pressure conditions, disrupts signalling through sphingomyelin breakdown by inhibiting the conversion of ceramide to sphingosine (Sugita  et al., 1975  ), an action which appears to be specific for the SMase pathway (Coroneos  et al., 1995  ).	transcription
67329	2	336185	5	NULL	NULL	0	NULL	NOE	Chemical		attenuates					TNF	GP	depressant actions of			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_185	10051135	The ceramidase inhibitor, NOE, which attenuated the depressant actions of TNF under constant flow and constant pressure conditions, disrupts signalling through sphingomyelin breakdown by inhibiting the conversion of ceramide to sphingosine (Sugita  et al., 1975  ), an action which appears to be specific for the SMase pathway (Coroneos  et al., 1995  ).	transcription
67330	3	336185	5	NULL	NULL	0	NULL	statement 2	Process		under conditions of					flow	Process	constant			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_185	10051135	The ceramidase inhibitor, NOE, which attenuated the depressant actions of TNF under constant flow and constant pressure conditions, disrupts signalling through sphingomyelin breakdown by inhibiting the conversion of ceramide to sphingosine (Sugita  et al., 1975  ), an action which appears to be specific for the SMase pathway (Coroneos  et al., 1995  ).	transcription
67331	4	336185	5	NULL	NULL	NULL	NULL	statement 2	Process		under conditions of					pressure	PhysicalPhenomenon	constant			NULL		NULL	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_185	10051135	The ceramidase inhibitor, NOE, which attenuated the depressant actions of TNF under constant flow and constant pressure conditions, disrupts signalling through sphingomyelin breakdown by inhibiting the conversion of ceramide to sphingosine (Sugita  et al., 1975  ), an action which appears to be specific for the SMase pathway (Coroneos  et al., 1995  ).	transcription
67332	5	336185	5	NULL	NULL	0	NULL	statement 2	Process		disrupt					signalling	Process				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_185	10051135	The ceramidase inhibitor, NOE, which attenuated the depressant actions of TNF under constant flow and constant pressure conditions, disrupts signalling through sphingomyelin breakdown by inhibiting the conversion of ceramide to sphingosine (Sugita  et al., 1975  ), an action which appears to be specific for the SMase pathway (Coroneos  et al., 1995  ).	transcription
67333	6	336185	5	NULL	NULL	0	NULL	statement 5	Process		occurs through					sphingomyelin	Chemical	breakdown of			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_185	10051135	The ceramidase inhibitor, NOE, which attenuated the depressant actions of TNF under constant flow and constant pressure conditions, disrupts signalling through sphingomyelin breakdown by inhibiting the conversion of ceramide to sphingosine (Sugita  et al., 1975  ), an action which appears to be specific for the SMase pathway (Coroneos  et al., 1995  ).	transcription
67334	7	336185	5	NULL	NULL	0	NULL	ceramide	Chemical		converted to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_185	10051135	The ceramidase inhibitor, NOE, which attenuated the depressant actions of TNF under constant flow and constant pressure conditions, disrupts signalling through sphingomyelin breakdown by inhibiting the conversion of ceramide to sphingosine (Sugita  et al., 1975  ), an action which appears to be specific for the SMase pathway (Coroneos  et al., 1995  ).	transcription
67335	8	336185	5	NULL	NULL	0	NULL	statement 2	Process		inhibits					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_185	10051135	The ceramidase inhibitor, NOE, which attenuated the depressant actions of TNF under constant flow and constant pressure conditions, disrupts signalling through sphingomyelin breakdown by inhibiting the conversion of ceramide to sphingosine (Sugita  et al., 1975  ), an action which appears to be specific for the SMase pathway (Coroneos  et al., 1995  ).	transcription
67336	9	336185	5	NULL	NULL	0	NULL	statement 8	Process		leads to					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_185	10051135	The ceramidase inhibitor, NOE, which attenuated the depressant actions of TNF under constant flow and constant pressure conditions, disrupts signalling through sphingomyelin breakdown by inhibiting the conversion of ceramide to sphingosine (Sugita  et al., 1975  ), an action which appears to be specific for the SMase pathway (Coroneos  et al., 1995  ).	transcription
67337	10	336185	5	NULL	NULL	0	NULL	statement 7	Process		is specific to					SMase pathway	Process				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_185	10051135	The ceramidase inhibitor, NOE, which attenuated the depressant actions of TNF under constant flow and constant pressure conditions, disrupts signalling through sphingomyelin breakdown by inhibiting the conversion of ceramide to sphingosine (Sugita  et al., 1975  ), an action which appears to be specific for the SMase pathway (Coroneos  et al., 1995  ).	transcription
71447	1	336185	7	NULL	NULL	0	NULL	NOE	Chemical		attenuate					TNF	GP	depressant actions of			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_185	10051135	The ceramidase inhibitor, NOE, which attenuated the depressant actions of TNF under constant flow and constant pressure conditions, disrupts signalling through sphingomyelin breakdown by inhibiting the conversion of ceramide to sphingosine (Sugita  et al., 1975  ), an action which appears to be specific for the SMase pathway (Coroneos  et al., 1995  ).	transcription
71448	2	336185	7	NULL	NULL	0	NULL	NOE	Chemical		inhibit					ceramidase	GP				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_185	10051135	The ceramidase inhibitor, NOE, which attenuated the depressant actions of TNF under constant flow and constant pressure conditions, disrupts signalling through sphingomyelin breakdown by inhibiting the conversion of ceramide to sphingosine (Sugita  et al., 1975  ), an action which appears to be specific for the SMase pathway (Coroneos  et al., 1995  ).	transcription
71449	3	336185	7	NULL	NULL	0	NULL	ceramide	Chemical		converted to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_185	10051135	The ceramidase inhibitor, NOE, which attenuated the depressant actions of TNF under constant flow and constant pressure conditions, disrupts signalling through sphingomyelin breakdown by inhibiting the conversion of ceramide to sphingosine (Sugita  et al., 1975  ), an action which appears to be specific for the SMase pathway (Coroneos  et al., 1995  ).	transcription
71450	4	336185	7	NULL	NULL	0	NULL	NOE	Chemical		disrupt					signaling	Process				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_185	10051135	The ceramidase inhibitor, NOE, which attenuated the depressant actions of TNF under constant flow and constant pressure conditions, disrupts signalling through sphingomyelin breakdown by inhibiting the conversion of ceramide to sphingosine (Sugita  et al., 1975  ), an action which appears to be specific for the SMase pathway (Coroneos  et al., 1995  ).	transcription
71451	5	336185	7	NULL	NULL	0	NULL	statement 4	Process		occur through					sphingomyelin	Chemical	breakdown of			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_185	10051135	The ceramidase inhibitor, NOE, which attenuated the depressant actions of TNF under constant flow and constant pressure conditions, disrupts signalling through sphingomyelin breakdown by inhibiting the conversion of ceramide to sphingosine (Sugita  et al., 1975  ), an action which appears to be specific for the SMase pathway (Coroneos  et al., 1995  ).	transcription
71452	6	336185	7	NULL	NULL	0	NULL	statement 5	Process		occur by					statement 3	Process	inhibition of			NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_185	10051135	The ceramidase inhibitor, NOE, which attenuated the depressant actions of TNF under constant flow and constant pressure conditions, disrupts signalling through sphingomyelin breakdown by inhibiting the conversion of ceramide to sphingosine (Sugita  et al., 1975  ), an action which appears to be specific for the SMase pathway (Coroneos  et al., 1995  ).	transcription
71453	7	336185	7	NULL	NULL	0	NULL	statement 3	Process		specific for					SMase pathway	Process				NULL		0	NULL	NULL	NULL	gw60_brjpharmacol_126_1_189_s_185	10051135	The ceramidase inhibitor, NOE, which attenuated the depressant actions of TNF under constant flow and constant pressure conditions, disrupts signalling through sphingomyelin breakdown by inhibiting the conversion of ceramide to sphingosine (Sugita  et al., 1975  ), an action which appears to be specific for the SMase pathway (Coroneos  et al., 1995  ).	transcription
67338	1	336186	5	NULL	NULL	0	NULL	TNF-alpha	GP		activates					Ras	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67339	2	336186	5	NULL	NULL	0	NULL	TNF-alpha	GP		activates					PI 3-K	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67340	3	336186	5	NULL	NULL	0	NULL	TNF-alpha	GP		activates					SK	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67341	4	336186	5	NULL	NULL	0	NULL	TNF-alpha	GP		activates					Cdc42	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67342	5	336186	5	NULL	NULL	0	NULL	TNF-alpha	GP		activates					Rac	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67343	6	336186	5	NULL	NULL	0	NULL	TNF-alpha	GP		activates					Rho	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67344	7	336186	5	NULL	NULL	0	NULL	TNF-alpha	GP		activates					PAK	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67345	8	336186	5	NULL	NULL	NULL	NULL	statement 1	Process		phosphorylates					FAK	GP		tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67346	9	336186	5	NULL	NULL	NULL	NULL	statement 1	Process		phosphorylates					paxillin	GP		tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67347	10	336186	5	NULL	NULL	0	NULL	statement 2	Process		phosphorylates					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67348	11	336186	5	NULL	NULL	0	NULL	statement 2	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67349	12	336186	5	NULL	NULL	0	NULL	statement 3	Process		phosphorylates					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67350	13	336186	5	NULL	NULL	0	NULL	statement 3	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67351	14	336186	5	NULL	NULL	0	NULL	statement 4	Process		phosphorylates					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67352	15	336186	5	NULL	NULL	0	NULL	statement 4	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67353	16	336186	5	NULL	NULL	0	NULL	statement 5	Process		phosphorylates					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67354	17	336186	5	NULL	NULL	0	NULL	statement 5	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67355	18	336186	5	NULL	NULL	0	NULL	statement 6	Process		phosphorylates					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67356	19	336186	5	NULL	NULL	0	NULL	statement 6	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67357	20	336186	5	NULL	NULL	0	NULL	statement 7	Process		phosphorylates					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67358	21	336186	5	NULL	NULL	0	NULL	statement 7	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67359	22	336186	5	NULL	NULL	0	NULL	sphingomyelinase	GP		activates					Ras	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67360	23	336186	5	NULL	NULL	0	NULL	statement 22	Process		phosphorylates					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67361	24	336186	5	NULL	NULL	0	NULL	statement 22	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67362	25	336186	5	NULL	NULL	0	NULL	sphingomyelinase	GP		activates					PI 3-K	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67363	26	336186	5	NULL	NULL	0	NULL	statement 25	Process		phosphorylates					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67364	27	336186	5	NULL	NULL	0	NULL	statement 25	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67365	28	336186	5	NULL	NULL	0	NULL	sphingomyelinase	GP		activates					SK	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67366	29	336186	5	NULL	NULL	NULL	NULL	statement 28	Process		phosphorylates					FAK	GP		tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67367	30	336186	5	NULL	NULL	0	NULL	statement 28	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67368	31	336186	5	NULL	NULL	0	NULL	sphingomyelinase	GP		activates					Cdc42	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67369	32	336186	5	NULL	NULL	0	NULL	statement 31	Process		phosphorylates					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67370	33	336186	5	NULL	NULL	0	NULL	statement 31	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67371	34	336186	5	NULL	NULL	0	NULL	sphingomyelinase	GP		activates					Rac	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67372	35	336186	5	NULL	NULL	0	NULL	statement 34	Process		phosphorylates					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67373	36	336186	5	NULL	NULL	0	NULL	statement 34	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67374	37	336186	5	NULL	NULL	0	NULL	sphingomyelinase	GP		activates					Rho	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67376	38	336186	5	NULL	NULL	0	NULL	statement 37	Process		phosphorylates					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67379	39	336186	5	NULL	NULL	0	NULL	statement 37	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67380	40	336186	5	NULL	NULL	0	NULL	sphingomyelinase	GP		activates					PAK	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67381	41	336186	5	NULL	NULL	0	NULL	statement 40	Process		phosphorylates					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67382	42	336186	5	NULL	NULL	0	NULL	statement 40	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67383	43	336186	5	NULL	NULL	0	NULL	C2-ceramide	Chemical		activates					Ras	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67384	44	336186	5	NULL	NULL	0	NULL	statement 43	Process		phosphorylates					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67385	45	336186	5	NULL	NULL	0	NULL	statement 43	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67386	46	336186	5	NULL	NULL	0	NULL	C2-ceramide	Chemical		activates					PI 3-K	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67387	47	336186	5	NULL	NULL	0	NULL	statement 46	Process		phosphorylates					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67388	48	336186	5	NULL	NULL	0	NULL	statement 46	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67389	49	336186	5	NULL	NULL	0	NULL	C2-ceramide	Chemical		activates					SK	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67390	50	336186	5	NULL	NULL	0	NULL	statement 49	Process		phosphorylates					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67391	51	336186	5	NULL	NULL	0	NULL	statement 49	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67392	52	336186	5	NULL	NULL	0	NULL	C2-ceramide	Chemical		activates					Cdc42	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67393	53	336186	5	NULL	NULL	0	NULL	statement 52	Process		phosphorylates					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67394	54	336186	5	NULL	NULL	0	NULL	statement 52	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67395	55	336186	5	NULL	NULL	0	NULL	C2-ceramide	Chemical		activates					Rac	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67396	56	336186	5	NULL	NULL	0	NULL	statement 55	Process		phosphorylates					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67397	57	336186	5	NULL	NULL	0	NULL	statement 55	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67398	58	336186	5	NULL	NULL	0	NULL	C2-ceramide	Chemical		activates					Rho	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67399	59	336186	5	NULL	NULL	0	NULL	statement 58	Process		phosphorylates					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67400	60	336186	5	NULL	NULL	0	NULL	statement 58	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67401	61	336186	5	NULL	NULL	0	NULL	C2-ceramide	Chemical		activates					PAK	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67402	62	336186	5	NULL	NULL	0	NULL	statement 61	Process		phosphorylates					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67404	63	336186	5	NULL	NULL	0	NULL	statement 61	Process		phosphorylates					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67405	64	336186	5	NULL	NULL	0	NULL	C2-ceramide	Chemical		is a type of					cell-permeable ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67406	65	336186	5	NULL	NULL	0	NULL	SK	GP		is					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
67407	66	336186	5	NULL	NULL	0	NULL	PAK	GP		is					p21-activated protein kinase	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71454	1	336186	7	NULL	NULL	0	NULL	TNF-alpha	GP		activate					Ras	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71455	2	336186	7	NULL	NULL	0	NULL	TNF-alpha	GP		activate					PI 3-K	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71456	3	336186	7	NULL	NULL	0	NULL	TNF-alpha	GP		activate					SK	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71457	4	336186	7	NULL	NULL	0	NULL	TNF-alpha	GP		activate					Cdc42	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71458	5	336186	7	NULL	NULL	0	NULL	TNF-alpha	GP		activate					Rac	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71459	6	336186	7	NULL	NULL	0	NULL	TNF-alpha	GP		activate					Rho	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71460	7	336186	7	NULL	NULL	0	NULL	TNF-alpha	GP		activate					PAK	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71461	8	336186	7	NULL	NULL	0	NULL	TNF-alpha	GP		phosphorylate					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71462	9	336186	7	NULL	NULL	0	NULL	TNF-alpha	GP		phosphorylate					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71463	10	336186	7	NULL	NULL	0	NULL	sphingomyelinase	GP		activate					Ras	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71464	11	336186	7	NULL	NULL	0	NULL	sphingomyelinase	GP		activate					PI 3-K	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71465	12	336186	7	NULL	NULL	0	NULL	sphingomyelinase	GP		activate					SK	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71466	13	336186	7	NULL	NULL	0	NULL	sphingomyelinase	GP		activate					Cdc42	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71467	14	336186	7	NULL	NULL	0	NULL	sphingomyelinase	GP		activate					Rac	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71468	15	336186	7	NULL	NULL	0	NULL	sphingomyelinase	GP		activate					Rho	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71469	16	336186	7	NULL	NULL	0	NULL	sphingomyelinase	GP		activate					PAK	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71470	17	336186	7	NULL	NULL	0	NULL	sphingomyelinase	GP		phosphorylate					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71471	18	336186	7	NULL	NULL	0	NULL	sphingomyelinase	GP		phosphorylate					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71472	19	336186	7	NULL	NULL	0	NULL	C2-ceramide	Chemical		activate					Ras	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71473	20	336186	7	NULL	NULL	0	NULL	C2-ceramide	Chemical		activate					PI 3-K	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71474	21	336186	7	NULL	NULL	0	NULL	C2-ceramide	Chemical		activate					SK	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71475	22	336186	7	NULL	NULL	0	NULL	C2-ceramide	Chemical		activate					Cdc42	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71476	23	336186	7	NULL	NULL	0	NULL	C2-ceramide	Chemical		activate					Rac	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71477	24	336186	7	NULL	NULL	0	NULL	C2-ceramide	Chemical		activate					Rho	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71478	25	336186	7	NULL	NULL	0	NULL	C2-ceramide	Chemical		activate					PAK	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71479	26	336186	7	NULL	NULL	0	NULL	C2-ceramide	Chemical		phosphorylate					FAK	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71480	27	336186	7	NULL	NULL	0	NULL	C2-ceramide	Chemical		phosphorylate					paxillin	GP		tyrosine		NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71481	28	336186	7	NULL	NULL	0	NULL	C2-ceramide	Chemical		is a type of					cell-permeable ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71482	29	336186	7	NULL	NULL	0	NULL	SK	GP		is					 sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
71483	30	336186	7	NULL	NULL	0	NULL	PAK	GP		is					p21-activated protein kinase	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_12_11_3618_s_32	11694593	The present work shows that TNF-alpha, sphingomyelinase, and C2-ceramide (a cell-permeable ceramide) activate Ras, PI 3-K, sphingosine kinase (SK), Cdc42, Rac, Rho, and p21-activated protein kinase (PAK) and cause the tyrosine phosphorylation of FAK and paxillin.	transcription
69426	1	336187	5	NULL	NULL	0	NULL	p38-RK	GP	activation of	is associated with		closely			ceramide	Chemical	action of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_245	9415703	In the current study, the close association of p38-RK activation with the actions of both ceramide and sphingosine raised the possibility that this signaling element could represent a common or convergent element in the ultimate apoptotic processes initiated by the two lipids; this was of particular interest inasmuch as dominant-negative suppression of c-Jun by TAM-67 was not sufficient to rule out an essential involvement of p38-RK.	transcription
69427	2	336187	5	NULL	NULL	0	NULL	p38-RK	GP	activation of	is associated with		closely			sphingosine	Chemical	action of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_245	9415703	In the current study, the close association of p38-RK activation with the actions of both ceramide and sphingosine raised the possibility that this signaling element could represent a common or convergent element in the ultimate apoptotic processes initiated by the two lipids; this was of particular interest inasmuch as dominant-negative suppression of c-Jun by TAM-67 was not sufficient to rule out an essential involvement of p38-RK.	transcription
69428	3	336187	5	NULL	NULL	0	NULL	apoptosis	Process		initiated by					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_245	9415703	In the current study, the close association of p38-RK activation with the actions of both ceramide and sphingosine raised the possibility that this signaling element could represent a common or convergent element in the ultimate apoptotic processes initiated by the two lipids; this was of particular interest inasmuch as dominant-negative suppression of c-Jun by TAM-67 was not sufficient to rule out an essential involvement of p38-RK.	transcription
69429	4	336187	5	NULL	NULL	0	NULL	apoptosis	Process		initiated by					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_245	9415703	In the current study, the close association of p38-RK activation with the actions of both ceramide and sphingosine raised the possibility that this signaling element could represent a common or convergent element in the ultimate apoptotic processes initiated by the two lipids; this was of particular interest inasmuch as dominant-negative suppression of c-Jun by TAM-67 was not sufficient to rule out an essential involvement of p38-RK.	transcription
69430	5	336187	5	NULL	NULL	NULL	NULL	p38-RK	GP		represent		possibly			statement 3	Process	common element of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_245	9415703	In the current study, the close association of p38-RK activation with the actions of both ceramide and sphingosine raised the possibility that this signaling element could represent a common or convergent element in the ultimate apoptotic processes initiated by the two lipids; this was of particular interest inasmuch as dominant-negative suppression of c-Jun by TAM-67 was not sufficient to rule out an essential involvement of p38-RK.	transcription
69431	6	336187	5	NULL	NULL	NULL	NULL	p38-RK	GP		represent		possibly			statement 4	Process	common element of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_245	9415703	In the current study, the close association of p38-RK activation with the actions of both ceramide and sphingosine raised the possibility that this signaling element could represent a common or convergent element in the ultimate apoptotic processes initiated by the two lipids; this was of particular interest inasmuch as dominant-negative suppression of c-Jun by TAM-67 was not sufficient to rule out an essential involvement of p38-RK.	transcription
69432	7	336187	5	NULL	NULL	NULL	NULL	p38-RK	GP		represent		possibly			statement 3	Process	convergent element of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_245	9415703	In the current study, the close association of p38-RK activation with the actions of both ceramide and sphingosine raised the possibility that this signaling element could represent a common or convergent element in the ultimate apoptotic processes initiated by the two lipids; this was of particular interest inasmuch as dominant-negative suppression of c-Jun by TAM-67 was not sufficient to rule out an essential involvement of p38-RK.	transcription
69433	8	336187	5	NULL	NULL	NULL	NULL	p38-RK	GP		represent		possibly			statement 4	Process	convergent element of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_245	9415703	In the current study, the close association of p38-RK activation with the actions of both ceramide and sphingosine raised the possibility that this signaling element could represent a common or convergent element in the ultimate apoptotic processes initiated by the two lipids; this was of particular interest inasmuch as dominant-negative suppression of c-Jun by TAM-67 was not sufficient to rule out an essential involvement of p38-RK.	transcription
69434	9	336187	5	NULL	NULL	0	NULL	statement 5	Process		is an alternative to					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_245	9415703	In the current study, the close association of p38-RK activation with the actions of both ceramide and sphingosine raised the possibility that this signaling element could represent a common or convergent element in the ultimate apoptotic processes initiated by the two lipids; this was of particular interest inasmuch as dominant-negative suppression of c-Jun by TAM-67 was not sufficient to rule out an essential involvement of p38-RK.	transcription
69435	10	336187	5	NULL	NULL	0	NULL	statement 6	Process		is an alternative to					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_245	9415703	In the current study, the close association of p38-RK activation with the actions of both ceramide and sphingosine raised the possibility that this signaling element could represent a common or convergent element in the ultimate apoptotic processes initiated by the two lipids; this was of particular interest inasmuch as dominant-negative suppression of c-Jun by TAM-67 was not sufficient to rule out an essential involvement of p38-RK.	transcription
69436	11	336187	5	NULL	NULL	0	NULL	TAM-67	GP		suppress		dominant-negative			c-Jun	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_245	9415703	In the current study, the close association of p38-RK activation with the actions of both ceramide and sphingosine raised the possibility that this signaling element could represent a common or convergent element in the ultimate apoptotic processes initiated by the two lipids; this was of particular interest inasmuch as dominant-negative suppression of c-Jun by TAM-67 was not sufficient to rule out an essential involvement of p38-RK.	transcription
71484	1	336187	7	NULL	NULL	0	NULL	p38	GP		associate with					RK	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_245	9415703	In the current study, the close association of p38-RK activation with the actions of both ceramide and sphingosine raised the possibility that this signaling element could represent a common or convergent element in the ultimate apoptotic processes initiated by the two lipids; this was of particular interest inasmuch as dominant-negative suppression of c-Jun by TAM-67 was not sufficient to rule out an essential involvement of p38-RK.	transcription
71485	2	336187	7	NULL	NULL	0	NULL	p38-RK	GP	activation of	associated with					ceramide	Chemical	actions of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_245	9415703	In the current study, the close association of p38-RK activation with the actions of both ceramide and sphingosine raised the possibility that this signaling element could represent a common or convergent element in the ultimate apoptotic processes initiated by the two lipids; this was of particular interest inasmuch as dominant-negative suppression of c-Jun by TAM-67 was not sufficient to rule out an essential involvement of p38-RK.	transcription
71486	3	336187	7	NULL	NULL	0	NULL	p38-RK	GP	activation of	associate with					sphingosine	Chemical	actions of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_245	9415703	In the current study, the close association of p38-RK activation with the actions of both ceramide and sphingosine raised the possibility that this signaling element could represent a common or convergent element in the ultimate apoptotic processes initiated by the two lipids; this was of particular interest inasmuch as dominant-negative suppression of c-Jun by TAM-67 was not sufficient to rule out an essential involvement of p38-RK.	transcription
71487	4	336187	7	NULL	NULL	0	NULL	p38-RK	GP		participate in		could			apoptotic process	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_245	9415703	In the current study, the close association of p38-RK activation with the actions of both ceramide and sphingosine raised the possibility that this signaling element could represent a common or convergent element in the ultimate apoptotic processes initiated by the two lipids; this was of particular interest inasmuch as dominant-negative suppression of c-Jun by TAM-67 was not sufficient to rule out an essential involvement of p38-RK.	transcription
71488	5	336187	7	NULL	NULL	0	NULL	ceramide	Chemical		initiates					apoptotic process	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_245	9415703	In the current study, the close association of p38-RK activation with the actions of both ceramide and sphingosine raised the possibility that this signaling element could represent a common or convergent element in the ultimate apoptotic processes initiated by the two lipids; this was of particular interest inasmuch as dominant-negative suppression of c-Jun by TAM-67 was not sufficient to rule out an essential involvement of p38-RK.	transcription
71489	6	336187	7	NULL	NULL	0	NULL	sphingosine	Chemical		initiates					apoptotic process	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_52_6_935_s_245	9415703	In the current study, the close association of p38-RK activation with the actions of both ceramide and sphingosine raised the possibility that this signaling element could represent a common or convergent element in the ultimate apoptotic processes initiated by the two lipids; this was of particular interest inasmuch as dominant-negative suppression of c-Jun by TAM-67 was not sufficient to rule out an essential involvement of p38-RK.	transcription
69464	1	336188	5	NULL	NULL	0	NULL	sphingosine kinase	GP	overexpression of	increases					SPP	Chemical	level of			NULL	C6 Cells	0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_115	11815603	Overexpression of Sphingosine Kinase in C6 Cells Increases SPP Levels-- Previously, we found that, although TNF-alpha-induced expression of iNOS and subsequent NO production were mediated in part by increases in ceramide levels, GTPCH expression and activity and levels of the iNOS cofactor BH4 were not increased in parallel ( 12).	transcription
69465	2	336188	5	NULL	NULL	0	NULL	iNOS	GP	expression of	is induced by					TNF-alpha	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_115	11815603	Overexpression of Sphingosine Kinase in C6 Cells Increases SPP Levels-- Previously, we found that, although TNF-alpha-induced expression of iNOS and subsequent NO production were mediated in part by increases in ceramide levels, GTPCH expression and activity and levels of the iNOS cofactor BH4 were not increased in parallel ( 12).	transcription
69466	3	336188	5	NULL	NULL	0	NULL	statement 2	Process		leads to		subsequently			NO	Chemical	production of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_115	11815603	Overexpression of Sphingosine Kinase in C6 Cells Increases SPP Levels-- Previously, we found that, although TNF-alpha-induced expression of iNOS and subsequent NO production were mediated in part by increases in ceramide levels, GTPCH expression and activity and levels of the iNOS cofactor BH4 were not increased in parallel ( 12).	transcription
69467	4	336188	5	NULL	NULL	0	NULL	ceramide	Chemical	increase in;;levels of	mediates					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_115	11815603	Overexpression of Sphingosine Kinase in C6 Cells Increases SPP Levels-- Previously, we found that, although TNF-alpha-induced expression of iNOS and subsequent NO production were mediated in part by increases in ceramide levels, GTPCH expression and activity and levels of the iNOS cofactor BH4 were not increased in parallel ( 12).	transcription
69468	5	336188	5	NULL	NULL	0	NULL	BH4	Chemical		is a cofactor of					iNOS	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_115	11815603	Overexpression of Sphingosine Kinase in C6 Cells Increases SPP Levels-- Previously, we found that, although TNF-alpha-induced expression of iNOS and subsequent NO production were mediated in part by increases in ceramide levels, GTPCH expression and activity and levels of the iNOS cofactor BH4 were not increased in parallel ( 12).	transcription
69469	6	336188	5	NULL	NULL	0	NULL	statement 4	Process		does not increase		parallely			GTPCH	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_115	11815603	Overexpression of Sphingosine Kinase in C6 Cells Increases SPP Levels-- Previously, we found that, although TNF-alpha-induced expression of iNOS and subsequent NO production were mediated in part by increases in ceramide levels, GTPCH expression and activity and levels of the iNOS cofactor BH4 were not increased in parallel ( 12).	transcription
69470	7	336188	5	NULL	NULL	0	NULL	statement 4	Process		does not activate		parallely			GTPCH	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_115	11815603	Overexpression of Sphingosine Kinase in C6 Cells Increases SPP Levels-- Previously, we found that, although TNF-alpha-induced expression of iNOS and subsequent NO production were mediated in part by increases in ceramide levels, GTPCH expression and activity and levels of the iNOS cofactor BH4 were not increased in parallel ( 12).	transcription
69471	8	336188	5	NULL	NULL	0	NULL	statement 4	Process		does not increase		parallely			BH4	Chemical	level of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_115	11815603	Overexpression of Sphingosine Kinase in C6 Cells Increases SPP Levels-- Previously, we found that, although TNF-alpha-induced expression of iNOS and subsequent NO production were mediated in part by increases in ceramide levels, GTPCH expression and activity and levels of the iNOS cofactor BH4 were not increased in parallel ( 12).	transcription
71490	1	336188	7	NULL	NULL	0	NULL	Sphingosine Kinase	GP	overexpression of	increase					SPP 	Chemical	levels of			NULL	C6 cells	0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_115	11815603	Overexpression of Sphingosine Kinase in C6 Cells Increases SPP Levels-- Previously, we found that, although TNF-alpha-induced expression of iNOS and subsequent NO production were mediated in part by increases in ceramide levels, GTPCH expression and activity and levels of the iNOS cofactor BH4 were not increased in parallel ( 12).	transcription
71491	2	336188	7	NULL	NULL	NULL	NULL	TNF-alpha	GP		induce					iNOS	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_115	11815603	Overexpression of Sphingosine Kinase in C6 Cells Increases SPP Levels-- Previously, we found that, although TNF-alpha-induced expression of iNOS and subsequent NO production were mediated in part by increases in ceramide levels, GTPCH expression and activity and levels of the iNOS cofactor BH4 were not increased in parallel ( 12).	transcription
71492	3	336188	7	NULL	NULL	0	NULL	statement 2	Process		produce					NO	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_115	11815603	Overexpression of Sphingosine Kinase in C6 Cells Increases SPP Levels-- Previously, we found that, although TNF-alpha-induced expression of iNOS and subsequent NO production were mediated in part by increases in ceramide levels, GTPCH expression and activity and levels of the iNOS cofactor BH4 were not increased in parallel ( 12).	transcription
71493	4	336188	7	NULL	NULL	0	NULL	statement 3	Process		mediated by		partly			ceramide	Chemical	increase in			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_115	11815603	Overexpression of Sphingosine Kinase in C6 Cells Increases SPP Levels-- Previously, we found that, although TNF-alpha-induced expression of iNOS and subsequent NO production were mediated in part by increases in ceramide levels, GTPCH expression and activity and levels of the iNOS cofactor BH4 were not increased in parallel ( 12).	transcription
71494	5	336188	7	NULL	NULL	NULL	NULL	statement 3	Process		mediated by		partly			GTPCH	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_115	11815603	Overexpression of Sphingosine Kinase in C6 Cells Increases SPP Levels-- Previously, we found that, although TNF-alpha-induced expression of iNOS and subsequent NO production were mediated in part by increases in ceramide levels, GTPCH expression and activity and levels of the iNOS cofactor BH4 were not increased in parallel ( 12).	transcription
71495	6	336188	7	NULL	NULL	0	NULL	statement 3	Process		mediated by		partly			GTPCH	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_115	11815603	Overexpression of Sphingosine Kinase in C6 Cells Increases SPP Levels-- Previously, we found that, although TNF-alpha-induced expression of iNOS and subsequent NO production were mediated in part by increases in ceramide levels, GTPCH expression and activity and levels of the iNOS cofactor BH4 were not increased in parallel ( 12).	transcription
71496	7	336188	7	NULL	NULL	0	NULL	statement 3	Process		does not increase					BH4	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_115	11815603	Overexpression of Sphingosine Kinase in C6 Cells Increases SPP Levels-- Previously, we found that, although TNF-alpha-induced expression of iNOS and subsequent NO production were mediated in part by increases in ceramide levels, GTPCH expression and activity and levels of the iNOS cofactor BH4 were not increased in parallel ( 12).	transcription
71497	8	336188	7	NULL	NULL	0	NULL	BH4 	Chemical		is a type of					 iNOS cofactor	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_15_12649_s_115	11815603	Overexpression of Sphingosine Kinase in C6 Cells Increases SPP Levels-- Previously, we found that, although TNF-alpha-induced expression of iNOS and subsequent NO production were mediated in part by increases in ceramide levels, GTPCH expression and activity and levels of the iNOS cofactor BH4 were not increased in parallel ( 12).	transcription
69472	1	336189	5	NULL	NULL	0	NULL	ceramide	Chemical		is converted to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4836_s_69	9030540	First, to determine whether blocking the conversion of ceramide to sphingosine would abrogate the negative inotropic effects of TNF-alpha, freshly isolated feline cardiac myocytes were allowed to stabilize for 1 h and were then treated for 30 min at 37  degrees C with 200 units.	transcription
69473	2	336189	5	NULL	NULL	0	NULL	statement 1	Process	blocking of	abrogates		possibly			TNF-alpha	GP	negative inotropic effects of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4836_s_69	9030540	First, to determine whether blocking the conversion of ceramide to sphingosine would abrogate the negative inotropic effects of TNF-alpha, freshly isolated feline cardiac myocytes were allowed to stabilize for 1 h and were then treated for 30 min at 37  degrees C with 200 units.	transcription
71498	1	336189	7	NULL	NULL	0	NULL	ceramide	Chemical		converted to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_8_4836_s_69	9030540	First, to determine whether blocking the conversion of ceramide to sphingosine would abrogate the negative inotropic effects of TNF-alpha, freshly isolated feline cardiac myocytes were allowed to stabilize for 1 h and were then treated for 30 min at 37  degrees C with 200 units.	transcription
69474	1	336190	5	NULL	NULL	0	NULL	Jurkat cells	Cell		treated with					anti-Fas antibody	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
69475	2	336190	5	NULL	NULL	0	NULL	statement 1	Process		induce					ceramide	Chemical	rapid generation of 			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
69476	3	336190	5	NULL	NULL	0	NULL	statement 2	Process		followed by		immediately			sphingosine	Chemical	transient production of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
69477	4	336190	5	NULL	NULL	0	NULL	statement 2	Process		precede					cyt c	GP	release of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
69478	5	336190	5	NULL	NULL	0	NULL	statement 3	Process		preced					cyt c	GP	release of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
69479	6	336190	5	NULL	NULL	0	NULL	statement 2	Process		precede					caspase-3	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
69480	7	336190	5	NULL	NULL	0	NULL	statement 3	Process		precede					caspase-3	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
69481	8	336190	5	NULL	NULL	0	NULL	statement 2	Process		precede					caspase-6	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
69482	9	336190	5	NULL	NULL	0	NULL	statement 3	Process		precede					caspase-6	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
69483	10	336190	5	NULL	NULL	0	NULL	statement 2	Process		precede					caspase-7	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
69484	11	336190	5	NULL	NULL	0	NULL	statement 3	Process		precede					caspase-7	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
69485	12	336190	5	NULL	NULL	0	NULL	caspase-3	GP		is a type of					executioner caspase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
69486	13	336190	5	NULL	NULL	0	NULL	caspase-6	GP		is a type of					executioner caspase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
69487	14	336190	5	NULL	NULL	0	NULL	caspase-7	GP		is a type of					executioner caspase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
69488	15	336190	5	NULL	NULL	0	NULL	statement 2	Process		precede					caspase-8	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
69489	16	336190	5	NULL	NULL	0	NULL	statement 3	Process		precede					caspase-8	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
69490	17	336190	5	NULL	NULL	0	NULL	statement 2	Process		precede					Bid	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
69491	18	336190	5	NULL	NULL	0	NULL	statement 3	Process		precede					Bid	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
71499	1	336190	7	NULL	NULL	0	NULL	 Jurkat cells	Cell		treated with					anti-Fas antibody	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
71500	2	336190	7	NULL	NULL	0	NULL	statement 1	Process		induces					ceramide	Chemical	rapid generation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
71501	3	336190	7	NULL	NULL	0	NULL	statement 2	Process		followed by		immediately			sphingosine	Chemical	transient production of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
71502	4	336190	7	NULL	NULL	0	NULL	statement 3	Process		precede					cyt c	Chemical	release of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
71503	5	336190	7	NULL	NULL	0	NULL	statement 3	Process		precede					caspase-3	GP	activation of executioner			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
71504	6	336190	7	NULL	NULL	0	NULL	statement 3	Process		precede					caspase-6	GP	activation of executioner			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
71505	7	336190	7	NULL	NULL	0	NULL	statement 3	Process		precede					caspase-7	GP	activation of executioner			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
71506	8	336190	7	NULL	NULL	0	NULL	statement 3	Process		precede					caspase-8	GP	activation of executioner			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
71507	9	336190	7	NULL	NULL	0	NULL	statement 3	Process		precede					Bid	GP	activation of executioner			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_18	10747891	Herein, we report that treatment of Jurkat cells with anti-Fas antibody induces rapid generation of ceramide immediately followed by transient production of sphingosine, both preceding cyt  c release and activation of executioner caspase-3, -6, and -7 as well as caspase-8 and Bid activation.	transcription
69493	1	336191	5	NULL	NULL	0	NULL	Fas	GP	cross-linking of 	triggers		rapidly			ceramide	Chemical	generation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
69494	2	336191	5	NULL	NULL	0	NULL	statement 1	Process		is dependent on					caspase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
69495	3	336191	5	NULL	NULL	0	NULL	ceramide	Chemical		is converted to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
69496	4	336191	5	NULL	NULL	0	NULL	statement 1	Process		followed by					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
69497	5	336191	5	NULL	NULL	0	NULL	cyt c	GP		is translocated from					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
69498	6	336191	5	NULL	NULL	0	NULL	cyt c	GP		is translocated to					cytosol	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
69499	7	336191	5	NULL	NULL	0	NULL	statement 5	Process		occurs simultaneously with					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
69500	8	336191	5	NULL	NULL	0	NULL	statement 7	Process		is controlled by					Bcl-xL	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
69501	9	336191	5	NULL	NULL	0	NULL	sphingosine	Chemical		is involved in		may be			statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
69502	10	336191	5	NULL	NULL	0	NULL	ceramide	Chemical		is involved in		may be			statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
69503	11	336191	5	NULL	NULL	0	NULL	cyt c	GP		stimulates					executioner caspases	GP	proteolytic activation of			NULL	cytosol	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
69504	12	336191	5	NULL	NULL	0	NULL	statement 11	Process		occurs through					caspase-9	GP				NULL	cytosol	0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
71508	1	336191	7	NULL	NULL	0	NULL	Fas	GP	crosslinking of	trigger		could;;rapidly			ceramide	Chemical	generation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
71509	2	336191	7	NULL	NULL	0	NULL	statement 1	Process		depends on					caspase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
71510	3	336191	7	NULL	NULL	0	NULL	ceramide	Chemical		converted to					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
71511	4	336191	7	NULL	NULL	0	NULL	cyt c	GP		translocated from					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
71512	5	336191	7	NULL	NULL	NULL	NULL	cyt c	GP		translocated to					cytosol	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
71513	6	336191	7	NULL	NULL	0	NULL	statement 4	Process		occur along with					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
71514	7	336191	7	NULL	NULL	0	NULL	ceramide	Chemical		be involved in		may			statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
71515	8	336191	7	NULL	NULL	0	NULL	sphingosine	Chemical		be involved in		may			statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
71516	9	336191	7	NULL	NULL	0	NULL	statement 6	Process		stimulate					executioner caspases	GP	proteolytic activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
71517	10	336191	7	NULL	NULL	0	NULL	statement 9	Process		occur through					caspase-9	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_21_15691_s_282	10747891	Thus, cross-linking of Fas could rapidly trigger generation of ceramide, in a caspase-dependent manner, which is then converted to sphingosine, and both sphingolipid metabolites may be involved in the translocation of cyt  c from mitochondria to the cytosol (under the control of Bcl-xL), where it can stimulate proteolytic activation of executioner caspases through caspase-9.	transcription
69505	1	336192	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					Fas	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_71	9446602	Sphingosine 1-Phosphate and TPA Inhibit Fas- and C 2 -Ceramide-mediated Apoptosis--  s described previously ( 7,  18,  20), Jurkat cells treated with Fas antibody underwent extensive cell death within 3 h as measured by the quantitative DNA fragmentation assay (Fig.  1 A).	transcription
69506	2	336192	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					C 2 -Ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_71	9446602	Sphingosine 1-Phosphate and TPA Inhibit Fas- and C 2 -Ceramide-mediated Apoptosis--  s described previously ( 7,  18,  20), Jurkat cells treated with Fas antibody underwent extensive cell death within 3 h as measured by the quantitative DNA fragmentation assay (Fig.  1 A).	transcription
69507	3	336192	5	NULL	NULL	0	NULL	Sphingosine 1-Phosphate	Chemical		inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_71	9446602	Sphingosine 1-Phosphate and TPA Inhibit Fas- and C 2 -Ceramide-mediated Apoptosis--  s described previously ( 7,  18,  20), Jurkat cells treated with Fas antibody underwent extensive cell death within 3 h as measured by the quantitative DNA fragmentation assay (Fig.  1 A).	transcription
69508	4	336192	5	NULL	NULL	0	NULL	Sphingosine 1-Phosphate	Chemical		inhibits					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_71	9446602	Sphingosine 1-Phosphate and TPA Inhibit Fas- and C 2 -Ceramide-mediated Apoptosis--  s described previously ( 7,  18,  20), Jurkat cells treated with Fas antibody underwent extensive cell death within 3 h as measured by the quantitative DNA fragmentation assay (Fig.  1 A).	transcription
69509	5	336192	5	NULL	NULL	0	NULL	TPA	Chemical		inhibits					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_71	9446602	Sphingosine 1-Phosphate and TPA Inhibit Fas- and C 2 -Ceramide-mediated Apoptosis--  s described previously ( 7,  18,  20), Jurkat cells treated with Fas antibody underwent extensive cell death within 3 h as measured by the quantitative DNA fragmentation assay (Fig.  1 A).	transcription
69510	6	336192	5	NULL	NULL	0	NULL	TPA	Chemical		inhibits					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_71	9446602	Sphingosine 1-Phosphate and TPA Inhibit Fas- and C 2 -Ceramide-mediated Apoptosis--  s described previously ( 7,  18,  20), Jurkat cells treated with Fas antibody underwent extensive cell death within 3 h as measured by the quantitative DNA fragmentation assay (Fig.  1 A).	transcription
71518	1	336192	7	NULL	NULL	0	NULL	Fas	GP		mediates					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_71	9446602	Sphingosine 1-Phosphate and TPA Inhibit Fas- and C 2 -Ceramide-mediated Apoptosis--  s described previously ( 7,  18,  20), Jurkat cells treated with Fas antibody underwent extensive cell death within 3 h as measured by the quantitative DNA fragmentation assay (Fig.  1 A).	transcription
71519	2	336192	7	NULL	NULL	0	NULL	C 2 -Ceramide	Chemical		mediates					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_71	9446602	Sphingosine 1-Phosphate and TPA Inhibit Fas- and C 2 -Ceramide-mediated Apoptosis--  s described previously ( 7,  18,  20), Jurkat cells treated with Fas antibody underwent extensive cell death within 3 h as measured by the quantitative DNA fragmentation assay (Fig.  1 A).	transcription
71520	3	336192	7	NULL	NULL	0	NULL	Sphingosine 1-Phosphate	Chemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_71	9446602	Sphingosine 1-Phosphate and TPA Inhibit Fas- and C 2 -Ceramide-mediated Apoptosis--  s described previously ( 7,  18,  20), Jurkat cells treated with Fas antibody underwent extensive cell death within 3 h as measured by the quantitative DNA fragmentation assay (Fig.  1 A).	transcription
71521	4	336192	7	NULL	NULL	0	NULL	Sphingosine 1-Phosphate	Chemical		inhibit					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_71	9446602	Sphingosine 1-Phosphate and TPA Inhibit Fas- and C 2 -Ceramide-mediated Apoptosis--  s described previously ( 7,  18,  20), Jurkat cells treated with Fas antibody underwent extensive cell death within 3 h as measured by the quantitative DNA fragmentation assay (Fig.  1 A).	transcription
71522	5	336192	7	NULL	NULL	0	NULL	TPA	Chemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_71	9446602	Sphingosine 1-Phosphate and TPA Inhibit Fas- and C 2 -Ceramide-mediated Apoptosis--  s described previously ( 7,  18,  20), Jurkat cells treated with Fas antibody underwent extensive cell death within 3 h as measured by the quantitative DNA fragmentation assay (Fig.  1 A).	transcription
71523	6	336192	7	NULL	NULL	0	NULL	TPA	Chemical		inhibit					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_5_2910_s_71	9446602	Sphingosine 1-Phosphate and TPA Inhibit Fas- and C 2 -Ceramide-mediated Apoptosis--  s described previously ( 7,  18,  20), Jurkat cells treated with Fas antibody underwent extensive cell death within 3 h as measured by the quantitative DNA fragmentation assay (Fig.  1 A).	transcription
69511	1	336193	5	NULL	NULL	NULL	NULL	p125FAK	GP		undergoes					phosphorylation	Process		tyrosine		NULL	Swiss 3T3 cells	NULL	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
69512	2	336193	5	NULL	NULL	NULL	NULL	paxillin	GP		undergoes					phosphorylation	Process		tyrosine		NULL	Swiss 3T3 cells	NULL	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
69513	3	336193	5	NULL	NULL	0	NULL	sphingosine	Chemical		stimulates					actin stress fiber	CellComponent	formation of			NULL	Swiss 3T3 cells	0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
69514	4	336193	5	NULL	NULL	0	NULL	ceramide	Chemical		stimulates					actin stress fiber	CellComponent	formation of			NULL	Swiss 3T3 cells	0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
69515	5	336193	5	NULL	NULL	NULL	NULL	sphingosine	Chemical		stimulates					focal adhesion	CellComponent	assembly of			NULL	Swiss 3T3 cells	NULL	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
69517	6	336193	5	NULL	NULL	0	NULL	ceramide	Chemical		stimulates					focal adhesion	CellComponent	assembly of			NULL	Swiss 3T3 cells	0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
69518	7	336193	5	NULL	NULL	0	NULL	statement 1	Process		leads to					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
69519	8	336193	5	NULL	NULL	NULL	NULL	statement 1	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
69520	9	336193	5	NULL	NULL	0	NULL	statement 1	Process		leads to					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
69521	10	336193	5	NULL	NULL	0	NULL	statement 1	Process		leads to					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
69522	11	336193	5	NULL	NULL	0	NULL	statement 2	Process		leads to					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
69523	12	336193	5	NULL	NULL	0	NULL	statement 2	Process		leads to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
69524	13	336193	5	NULL	NULL	0	NULL	statement 2	Process		leads to					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
69525	14	336193	5	NULL	NULL	0	NULL	statement 2	Process		leads to					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
71524	1	336193	7	NULL	NULL	NULL	NULL	sphingosine	Chemical		stimulate					actin stress fiber	GP	formation of			NULL	Swiss 3T3 cells	NULL	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
71525	2	336193	7	NULL	NULL	0	NULL	ceramide	Chemical		stimulate					actin stress fiber	GP	formation of			NULL	Swiss 3T3 cells	0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
71526	3	336193	7	NULL	NULL	0	NULL	sphingosine	Chemical		stimulate					focal adhesion assembly	Process				NULL	Swiss 3T3 cells	0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
71527	4	336193	7	NULL	NULL	0	NULL	ceramide	Chemical		stimulate					focal adhesion assembly	Process				NULL	Swiss 3T3 cells	0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
71528	5	336193	7	NULL	NULL	0	NULL	statement 1	Process		as a result of					p125FAK	GP	phosphorylation of	tyrosine 		NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
71529	6	336193	7	NULL	NULL	NULL	NULL	statement 1	Process		as a result of					paxillin	GP	phosphorylation of	tyrosine		NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
71530	7	336193	7	NULL	NULL	0	NULL	statement 2	Process		as a result of					p125FAK	GP	phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
71531	8	336193	7	NULL	NULL	0	NULL	statement 2	Process		as a result of					paxillin	GP	phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
71532	9	336193	7	NULL	NULL	0	NULL	statement 3	Process		as a result of					p125FAK	GP	phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
71533	10	336193	7	NULL	NULL	0	NULL	statement 3	Process		as a result of					paxillin	GP	phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
71534	11	336193	7	NULL	NULL	0	NULL	statement 4	Process		as a result of					p125FAK	GP	phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
71535	12	336193	7	NULL	NULL	0	NULL	statement 4	Process		as a result of					paxillin	GP	phosphorylation of	tyrosine		NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
71536	13	336193	7	NULL	NULL	NULL	NULL	statement 1	Process		 events in the		early			signaling pathways	Process	action of diverse			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
71537	14	336193	7	NULL	NULL	0	NULL	statement 2	Process		events in the		early			signaling pathways	Process	action of diverse			NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
71538	15	336193	7	NULL	NULL	0	NULL	statement 13	Process		leads to					cytoskeletal organization	Process	alterations in			NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
71539	16	336193	7	NULL	NULL	0	NULL	statement 14	Process		leads to					cytoskeletal organization	Process	alterations in			NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_145	9096129	However, both sphingosine and ceramide stimulate actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells as a result of tyrosine phosphorylation of p125FAK and paxillin (Seufferlein and Rozengurt, 1994  ), which are early events in the action of diverse signaling pathways that lead to alterations in cytoskeletal organization.	transcription
69526	1	336194	5	NULL	NULL	0	NULL	SAPK	GP		induce					apoptosis	Process				NULL	U937 cells	0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_186	10454518	Direct comparison of SAPK and AP1 involvement in the induction of apoptosis in U937 cells by these cytotoxic messengers revealed that ceramide lethality is markedly attenuated by disruption of the SEK/JNK module or interference with AP1 (Jarvis et al., 1997  ), whereas sphingosine lethality is unaffected by such manipulations (Jarvis et al., 1997  ).	transcription
69527	2	336194	5	NULL	NULL	NULL	NULL	AP1	GP		is involved in					apoptosis	Process				NULL	U937 cells	NULL	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_186	10454518	Direct comparison of SAPK and AP1 involvement in the induction of apoptosis in U937 cells by these cytotoxic messengers revealed that ceramide lethality is markedly attenuated by disruption of the SEK/JNK module or interference with AP1 (Jarvis et al., 1997  ), whereas sphingosine lethality is unaffected by such manipulations (Jarvis et al., 1997  ).	transcription
69528	3	336194	5	NULL	NULL	0	NULL	ceramide lethality	Process		attenuated by		markedly			SEK/JNK module	Process	disruption of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_186	10454518	Direct comparison of SAPK and AP1 involvement in the induction of apoptosis in U937 cells by these cytotoxic messengers revealed that ceramide lethality is markedly attenuated by disruption of the SEK/JNK module or interference with AP1 (Jarvis et al., 1997  ), whereas sphingosine lethality is unaffected by such manipulations (Jarvis et al., 1997  ).	transcription
69529	4	336194	5	NULL	NULL	0	NULL	ceramide lethality	Process		attenuated by		markedly			AP1	GP	interference of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_186	10454518	Direct comparison of SAPK and AP1 involvement in the induction of apoptosis in U937 cells by these cytotoxic messengers revealed that ceramide lethality is markedly attenuated by disruption of the SEK/JNK module or interference with AP1 (Jarvis et al., 1997  ), whereas sphingosine lethality is unaffected by such manipulations (Jarvis et al., 1997  ).	transcription
71548	1	336194	7	NULL	NULL	0	NULL	SAPK	GP		is involved in					apoptosis	Process	induction of			NULL	U937 cells	0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_186	10454518	Direct comparison of SAPK and AP1 involvement in the induction of apoptosis in U937 cells by these cytotoxic messengers revealed that ceramide lethality is markedly attenuated by disruption of the SEK/JNK module or interference with AP1 (Jarvis et al., 1997  ), whereas sphingosine lethality is unaffected by such manipulations (Jarvis et al., 1997  ).	transcription
71549	2	336194	7	NULL	NULL	0	NULL	AP1	GP		is involved in					apoptosis	Process	induction of			NULL	U937 cells	0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_186	10454518	Direct comparison of SAPK and AP1 involvement in the induction of apoptosis in U937 cells by these cytotoxic messengers revealed that ceramide lethality is markedly attenuated by disruption of the SEK/JNK module or interference with AP1 (Jarvis et al., 1997  ), whereas sphingosine lethality is unaffected by such manipulations (Jarvis et al., 1997  ).	transcription
71550	3	336194	7	NULL	NULL	0	NULL	SAPK	GP		is a type of					cytotoxic messengers	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_186	10454518	Direct comparison of SAPK and AP1 involvement in the induction of apoptosis in U937 cells by these cytotoxic messengers revealed that ceramide lethality is markedly attenuated by disruption of the SEK/JNK module or interference with AP1 (Jarvis et al., 1997  ), whereas sphingosine lethality is unaffected by such manipulations (Jarvis et al., 1997  ).	transcription
71551	4	336194	7	NULL	NULL	0	NULL	AP1	GP		is a type of					cytotoxic messengers	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_186	10454518	Direct comparison of SAPK and AP1 involvement in the induction of apoptosis in U937 cells by these cytotoxic messengers revealed that ceramide lethality is markedly attenuated by disruption of the SEK/JNK module or interference with AP1 (Jarvis et al., 1997  ), whereas sphingosine lethality is unaffected by such manipulations (Jarvis et al., 1997  ).	transcription
71552	5	336194	7	NULL	NULL	0	NULL	 ceramide	Chemical	lethality of	attenuated by		markedly			SEK/JNK module	GP	disruption of			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_186	10454518	Direct comparison of SAPK and AP1 involvement in the induction of apoptosis in U937 cells by these cytotoxic messengers revealed that ceramide lethality is markedly attenuated by disruption of the SEK/JNK module or interference with AP1 (Jarvis et al., 1997  ), whereas sphingosine lethality is unaffected by such manipulations (Jarvis et al., 1997  ).	transcription
71553	6	336194	7	NULL	NULL	0	NULL	ceramide	Chemical	lethality of	attenuated by		markedly			AP1	GP	interference with			NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_186	10454518	Direct comparison of SAPK and AP1 involvement in the induction of apoptosis in U937 cells by these cytotoxic messengers revealed that ceramide lethality is markedly attenuated by disruption of the SEK/JNK module or interference with AP1 (Jarvis et al., 1997  ), whereas sphingosine lethality is unaffected by such manipulations (Jarvis et al., 1997  ).	transcription
71554	7	336194	7	NULL	NULL	0	NULL	sphingosine	Chemical	lethality of	does not affect					SEK/JNK module	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_186	10454518	Direct comparison of SAPK and AP1 involvement in the induction of apoptosis in U937 cells by these cytotoxic messengers revealed that ceramide lethality is markedly attenuated by disruption of the SEK/JNK module or interference with AP1 (Jarvis et al., 1997  ), whereas sphingosine lethality is unaffected by such manipulations (Jarvis et al., 1997  ).	transcription
71555	8	336194	7	NULL	NULL	0	NULL	sphingosine	Chemical	lethality of	does not affect					AP1	GP				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_186	10454518	Direct comparison of SAPK and AP1 involvement in the induction of apoptosis in U937 cells by these cytotoxic messengers revealed that ceramide lethality is markedly attenuated by disruption of the SEK/JNK module or interference with AP1 (Jarvis et al., 1997  ), whereas sphingosine lethality is unaffected by such manipulations (Jarvis et al., 1997  ).	transcription
71556	9	336194	7	NULL	NULL	0	NULL	statement 1	Process		reveals					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_186	10454518	Direct comparison of SAPK and AP1 involvement in the induction of apoptosis in U937 cells by these cytotoxic messengers revealed that ceramide lethality is markedly attenuated by disruption of the SEK/JNK module or interference with AP1 (Jarvis et al., 1997  ), whereas sphingosine lethality is unaffected by such manipulations (Jarvis et al., 1997  ).	transcription
71557	10	336194	7	NULL	NULL	0	NULL	statement 1	Process		reveals					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_186	10454518	Direct comparison of SAPK and AP1 involvement in the induction of apoptosis in U937 cells by these cytotoxic messengers revealed that ceramide lethality is markedly attenuated by disruption of the SEK/JNK module or interference with AP1 (Jarvis et al., 1997  ), whereas sphingosine lethality is unaffected by such manipulations (Jarvis et al., 1997  ).	transcription
71558	11	336194	7	NULL	NULL	0	NULL	statement 2	Process		reveals					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_186	10454518	Direct comparison of SAPK and AP1 involvement in the induction of apoptosis in U937 cells by these cytotoxic messengers revealed that ceramide lethality is markedly attenuated by disruption of the SEK/JNK module or interference with AP1 (Jarvis et al., 1997  ), whereas sphingosine lethality is unaffected by such manipulations (Jarvis et al., 1997  ).	transcription
71559	12	336194	7	NULL	NULL	0	NULL	statement 2	Process		reveals					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jpharmacolexpther_290_3_1384_s_186	10454518	Direct comparison of SAPK and AP1 involvement in the induction of apoptosis in U937 cells by these cytotoxic messengers revealed that ceramide lethality is markedly attenuated by disruption of the SEK/JNK module or interference with AP1 (Jarvis et al., 1997  ), whereas sphingosine lethality is unaffected by such manipulations (Jarvis et al., 1997  ).	transcription
69530	1	336196	5	NULL	NULL	0	NULL	arachidonic acid	Chemical		is the product of					PLA2	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
69531	2	336196	5	NULL	NULL	0	NULL	arachidonic acid	Chemical		hydrolyzes					SM	Chemical				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
69532	3	336196	5	NULL	NULL	0	NULL	PLA2	GP	cytosolic	is inhibited by					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
69533	4	336196	5	NULL	NULL	0	NULL	PLA2	GP	cytosolic	is inhibited by					SM	Chemical				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
69534	5	336196	5	NULL	NULL	0	NULL	sphingomyelinase	GP		removes					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
69535	6	336196	5	NULL	NULL	0	NULL	PLA2	GP	calcium-dependent	is translocated from					cytosol	CellComponent				NULL	platelets	0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
69536	7	336196	5	NULL	NULL	0	NULL	PLA2	GP	calcium-dependent	is translocated to					membranes	CellComponent				NULL	platelets	0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
69537	8	336196	5	NULL	NULL	0	NULL	statement 6	Process		occurs along with					statement 7	Process				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
69539	9	336196	5	NULL	NULL	0	NULL	ceramide	Chemical		accelerates					statement 6	Process				NULL	platelets	0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
69540	10	336196	5	NULL	NULL	0	NULL	ceramide	Chemical		accelerates					statement 7	Process				NULL	platelets	0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
69541	11	336196	5	NULL	NULL	0	NULL	sphingosine	Chemical		inhibits		directly			PLA2	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
69542	12	336196	5	NULL	NULL	0	NULL	sphinganine	Chemical		inhibits		directly			PLA2	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
71560	1	336196	7	NULL	NULL	0	NULL	arachidonic acid	Chemical		is the product of					PLA2	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
71561	2	336196	7	NULL	NULL	0	NULL	arachidonic acid	Chemical		induces					SM	Chemical	hydrolysis of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
71562	3	336196	7	NULL	NULL	0	NULL	sphingosine	Chemical		inhibit					PLA2	GP	cytosolic			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
71563	4	336196	7	NULL	NULL	0	NULL	SM	Chemical		inhibit					PLA2	GP	cytosolic			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
71564	5	336196	7	NULL	NULL	0	NULL	sphingomyelinase	GP		remove					statement 4	Process	inhibition of			NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
71565	6	336196	7	NULL	NULL	0	NULL	 PLA2	GP	calcium-dependent	translocated from					cytosol	CellComponent				NULL	platelets	0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
71566	7	336196	7	NULL	NULL	0	NULL	PLA2	GP	calcium-dependent	translocated to					membranes	CellComponent				NULL	platelets	0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
71567	8	336196	7	NULL	NULL	0	NULL	statement 6	Process		occur along with					statement 7	Process				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
71568	9	336196	7	NULL	NULL	0	NULL	ceramide	Chemical		accelerates					statement 8	Process				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
71569	10	336196	7	NULL	NULL	0	NULL	sphingosine	Chemical		inhibit		directly			PLA2	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
71570	11	336196	7	NULL	NULL	0	NULL	sphinganine	Chemical		inhibit		directly			PLA2	GP				NULL		0	NULL	NULL	NULL	gw70_biochimbiophysacta_1735_1_68_s_17	15950537	Thus, arachidonic acid, the product  of PLA2, induces SM hydrolysis   [16], the cytosolic PLA2 can be inhibited by sphingosine   [17] and by SM   [17] and   [18], the inhibition by SM can be removed by sphingomyelinase   [18], ceramide accelerates the translocation of calcium-dependent PLA2 from cytosol to membranes in platelets   [19], and sphingosine and sphinganine directly inhibit PLA2  [20].	transcription
69543	1	336197	5	NULL	NULL	0	NULL	PI-3K	GP	activation of	is induced by					oxLDL	Chemical				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
69544	2	336197	5	NULL	NULL	0	NULL	statement 1	Process		is dependent on					EGFR	GP				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
69545	3	336197	5	NULL	NULL	0	NULL	PI-3K	GP	activation of	is independent of					sphingomyelin/ceramide/sphingosine-1-phosphate pathway	Process				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
69546	4	336197	5	NULL	NULL	0	NULL	PI-3K	GP		is inhibited by					LY294002	Chemical				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
69547	5	336197	5	NULL	NULL	0	NULL	PI-3K	GP		is inhibited by					deltap85	GP	dominant-negative mutant			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
69548	6	336197	5	NULL	NULL	0	NULL	statement 4	Process		doe not abrogate					sphingomyelin	Chemical	hydrolysis of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
69549	7	336197	5	NULL	NULL	0	NULL	statement 5	Process		doe not abrogate					sphingomyelin	Chemical	hydrolysis of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
69550	8	336197	5	NULL	NULL	0	NULL	C2-ceramide	Chemical	permeant	does not alter					PI-3K	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
69551	9	336197	5	NULL	NULL	0	NULL	N,N-dimethyl-sphingosine	Chemical		does not alter					PI-3K	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
69552	10	336197	5	NULL	NULL	0	NULL	N,N-dimethyl-sphingosine	Chemical		is an inhibitor of					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
71571	1	336197	7	NULL	NULL	0	NULL	oxLDL	Chemical		induce					PI-3K	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
71572	2	336197	7	NULL	NULL	0	NULL	statement 1	Process		depends on					EGFR	GP				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
71573	3	336197	7	NULL	NULL	0	NULL	PI-3K	GP	activation of	is independent of					sphingomyelin pathway	Process				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
71575	4	336197	7	NULL	NULL	NULL	NULL	PI-3K	GP	activation of	is independent of					ceramide pathway	Process				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
71576	5	336197	7	NULL	NULL	0	NULL	PI-3K	GP	activation of	is independent of					sphingosine-1-phosphate pathway	Process				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
71577	6	336197	7	NULL	NULL	0	NULL	LY294002	Chemical		inhibit					PI-3K	GP				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
71578	7	336197	7	NULL	NULL	NULL	NULL	deltap85	GP	dominant-negative mutant	inhibit					PI 3-K	GP				NULL		NULL	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
71579	8	336197	7	NULL	NULL	0	NULL	statement 6	Process		does not abrogate					sphingomyelin	Chemical	hydrolysis of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
71580	9	336197	7	NULL	NULL	0	NULL	statement 7	Process		does not abrogate					sphingomyelin	Chemical	hydrolysis of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
71581	10	336197	7	NULL	NULL	0	NULL	statement 6	Process		is an alternative to					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
71582	11	336197	7	NULL	NULL	0	NULL	C2-ceramide	Chemical		does not alter					PI-3K 	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
71583	12	336197	7	NULL	NULL	0	NULL	N,N-dimethyl-sphingosine	Chemical		does not alter					PI-3K 	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
71584	13	336197	7	NULL	NULL	0	NULL	N,N-dimethyl-sphingosine	Chemical		inhibit					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_22_12_1990_s_5	12482824	Methods and Results --  Coimmunoprecipitation experiments and the use of inhibitors and dominant-negative mutant showed that oxLDL-induced PI-3K activation is dependent on EGFR. PI-3K activation is independent of the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, because PI-3K inhibition by LY294002 or dominant-negative deltap85 mutant does not abrogate sphingomyelin hydrolysis, and, conversely, the use of permeant C2-ceramide and of  N,N-dimethyl-sphingosine, a sphingosine kinase inhibitor, does not alter PI-3K activity.	transcription
71585	1	336200	7	NULL	NULL	NULL	NULL	PDMP	Chemical		inhibits		potently			glucosylceramide synthase	GP	activity of			NULL	in vitro	NULL	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_156	12235122	PDMP at 10 muM, a concentration that potently inhibits glucosylceramide synthase activity in vitro ( Shayman et al., 2000), increased ceramide by 2.5-fold over basal levels in untreated and dihydro-S1P - treated mSPP-1 - expressing cells, and markedly augmented the elevated ceramide accumulation induced by S1P ( Fig. 10 A) without significantly affecting sphingosine levels ( Fig. 10 B).	transcription
71586	2	336200	7	NULL	NULL	NULL	NULL	PDMP	Chemical		increase					ceramide	Chemical				NULL	untreated mSPP-1 - expressing cells	NULL	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_156	12235122	PDMP at 10 muM, a concentration that potently inhibits glucosylceramide synthase activity in vitro ( Shayman et al., 2000), increased ceramide by 2.5-fold over basal levels in untreated and dihydro-S1P - treated mSPP-1 - expressing cells, and markedly augmented the elevated ceramide accumulation induced by S1P ( Fig. 10 A) without significantly affecting sphingosine levels ( Fig. 10 B).	transcription
71587	3	336200	7	NULL	NULL	0	NULL	PDMP	Chemical		increase					ceramide	Chemical				NULL	dihydro-S1P - treated mSPP-1 - expressing cells	0	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_156	12235122	PDMP at 10 muM, a concentration that potently inhibits glucosylceramide synthase activity in vitro ( Shayman et al., 2000), increased ceramide by 2.5-fold over basal levels in untreated and dihydro-S1P - treated mSPP-1 - expressing cells, and markedly augmented the elevated ceramide accumulation induced by S1P ( Fig. 10 A) without significantly affecting sphingosine levels ( Fig. 10 B).	transcription
71588	4	336200	7	NULL	NULL	0	NULL	PDMP	Chemical		augments		markedly			ceramide	Chemical	elevated			NULL		0	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_156	12235122	PDMP at 10 muM, a concentration that potently inhibits glucosylceramide synthase activity in vitro ( Shayman et al., 2000), increased ceramide by 2.5-fold over basal levels in untreated and dihydro-S1P - treated mSPP-1 - expressing cells, and markedly augmented the elevated ceramide accumulation induced by S1P ( Fig. 10 A) without significantly affecting sphingosine levels ( Fig. 10 B).	transcription
71589	5	336200	7	NULL	NULL	0	NULL	S1P	Chemical		induce					ceramide	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_156	12235122	PDMP at 10 muM, a concentration that potently inhibits glucosylceramide synthase activity in vitro ( Shayman et al., 2000), increased ceramide by 2.5-fold over basal levels in untreated and dihydro-S1P - treated mSPP-1 - expressing cells, and markedly augmented the elevated ceramide accumulation induced by S1P ( Fig. 10 A) without significantly affecting sphingosine levels ( Fig. 10 B).	transcription
71590	6	336200	7	NULL	NULL	0	NULL	statement 4	Process		does not affect		significantly			sphingosine	Chemical	levels of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_158_6_1039_s_156	12235122	PDMP at 10 muM, a concentration that potently inhibits glucosylceramide synthase activity in vitro ( Shayman et al., 2000), increased ceramide by 2.5-fold over basal levels in untreated and dihydro-S1P - treated mSPP-1 - expressing cells, and markedly augmented the elevated ceramide accumulation induced by S1P ( Fig. 10 A) without significantly affecting sphingosine levels ( Fig. 10 B).	transcription
69554	1	336201	5	NULL	NULL	0	NULL	ceramide	Chemical	accumulation of	does not effect					6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine	Chemical	trafficking of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
69555	2	336201	5	NULL	NULL	0	NULL	ceramide	Chemical	accumulation of	does not effect					6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine	Chemical	metabolism of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
69556	3	336201	5	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
69557	4	336201	5	NULL	NULL	0	NULL	6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine	Chemical		labels		rapidly			Golgi	CellComponent				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
69559	5	336201	5	NULL	NULL	0	NULL	ts045 G protein	GP	vesicular stomatitis virus	is fused to					green fluorescent protein	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
69560	6	336201	5	NULL	NULL	NULL	NULL	statement 5	GP		trafficked from					ER	CellComponent				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
69561	7	336201	5	NULL	NULL	0	NULL	statement 5	GP		trafficked to					Golgi	CellComponent				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
69562	8	336201	5	NULL	NULL	0	NULL	statement 6	Process		occurs along with					statement 7	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
69563	9	336201	5	NULL	NULL	0	NULL	statement 6	Process		is inhibited in					S1P	Chemical	presence of			NULL	SPP-1-overexpressing cells	0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
69564	10	336201	5	NULL	NULL	0	NULL	statement 7	Process		is inhibited in					S1P	Chemical	presence of			NULL	SPP-1-overexpressing cells	0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
69565	12	336201	5	NULL	NULL	NULL	NULL	statement 7	Process		is not inhibited in					dihydro-S1P	Chemical	presence of			NULL	SPP-1-overexpressing cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
69566	11	336201	5	NULL	NULL	NULL	NULL	statement 6	Process		is not inhibited in					dihydro-S1P	Chemical	presence of			NULL	SPP-1-overexpressing cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
71591	1	336201	7	NULL	NULL	0	NULL	ceramide 	Chemical	accumulation of	no effect on					 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine	Chemical	trafficking of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
71592	2	336201	7	NULL	NULL	0	NULL	ceramide	Chemical	accumulation of	no effect on					 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine	Chemical	metabolism of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
71593	3	336201	7	NULL	NULL	0	NULL	 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine	Chemical		labels		rapidly			Golgi	CellComponent				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
71594	4	336201	7	NULL	NULL	0	NULL	protein	GP		trafficking from					ER	CellComponent				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
71595	5	336201	7	NULL	NULL	0	NULL	Protein	GP		trafficking to					Golgi	CellComponent				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
71596	6	336201	7	NULL	NULL	0	NULL	statement 4	Process		occur along with					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
71597	7	336201	7	NULL	NULL	NULL	NULL	statement 6	Process		inhibited					S1P	Chemical	in the presence of			NULL	SPP-1-overexpressing cells	NULL	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
71598	8	336201	7	NULL	NULL	0	NULL	statement 6	Process		is not inhibited					dihydro-S1P	Chemical	in the presence of			NULL	SPP-1-overexpressing cells	0	NULL	NULL	NULL	gw70_molcellbiol_26_13_5055_s_6	16782891	In contrast, ceramide accumulation had no effect on either the trafficking or the metabolism of 6-([ N-(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]hexanoyl)-sphingosine, which rapidly labels the Golgi even at 4 degrees C. Protein trafficking from the ER to the Golgi, determined with vesicular stomatitis virus ts045 G protein fused to green fluorescent protein, was also inhibited in SPP-1-overexpressing cells in the presence of S1P but not in the presence of dihydro-S1P.	transcription
69567	1	336202	5	NULL	NULL	0	NULL	Ca2+ transient	Process		is induced by					sphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_220	9915989	Nonetheless, although sphingosine-induced Ca2+ transients have been previously reported to occur via mobilization of Ca2+ from intracellular stores [ 33,  34], this study represents the first demonstration that ceramide regulates [Ca2+]i. Cch-induced Ca2+ transients occur via IP3-mediated mobilization of Ca2+ from intracellular stores and/or transmembrane influx of Ca2+ [ 22,  24].	transcription
69568	2	336202	5	NULL	NULL	0	NULL	Ca2+	Chemical		is mobilized from					intracellular stores	CellComponent				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_220	9915989	Nonetheless, although sphingosine-induced Ca2+ transients have been previously reported to occur via mobilization of Ca2+ from intracellular stores [ 33,  34], this study represents the first demonstration that ceramide regulates [Ca2+]i. Cch-induced Ca2+ transients occur via IP3-mediated mobilization of Ca2+ from intracellular stores and/or transmembrane influx of Ca2+ [ 22,  24].	transcription
69569	3	336202	5	NULL	NULL	0	NULL	statement 1	Process		via					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_220	9915989	Nonetheless, although sphingosine-induced Ca2+ transients have been previously reported to occur via mobilization of Ca2+ from intracellular stores [ 33,  34], this study represents the first demonstration that ceramide regulates [Ca2+]i. Cch-induced Ca2+ transients occur via IP3-mediated mobilization of Ca2+ from intracellular stores and/or transmembrane influx of Ca2+ [ 22,  24].	transcription
69570	4	336202	5	NULL	NULL	0	NULL	ceramide	Chemical		regulates					[Ca2+]i	Chemical				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_220	9915989	Nonetheless, although sphingosine-induced Ca2+ transients have been previously reported to occur via mobilization of Ca2+ from intracellular stores [ 33,  34], this study represents the first demonstration that ceramide regulates [Ca2+]i. Cch-induced Ca2+ transients occur via IP3-mediated mobilization of Ca2+ from intracellular stores and/or transmembrane influx of Ca2+ [ 22,  24].	transcription
69571	5	336202	5	NULL	NULL	0	NULL	Ca2+ transient	Process		is induced by					Cch	Chemical				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_220	9915989	Nonetheless, although sphingosine-induced Ca2+ transients have been previously reported to occur via mobilization of Ca2+ from intracellular stores [ 33,  34], this study represents the first demonstration that ceramide regulates [Ca2+]i. Cch-induced Ca2+ transients occur via IP3-mediated mobilization of Ca2+ from intracellular stores and/or transmembrane influx of Ca2+ [ 22,  24].	transcription
69572	6	336202	5	NULL	NULL	0	NULL	IP3	Chemical		mediates					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_220	9915989	Nonetheless, although sphingosine-induced Ca2+ transients have been previously reported to occur via mobilization of Ca2+ from intracellular stores [ 33,  34], this study represents the first demonstration that ceramide regulates [Ca2+]i. Cch-induced Ca2+ transients occur via IP3-mediated mobilization of Ca2+ from intracellular stores and/or transmembrane influx of Ca2+ [ 22,  24].	transcription
69573	7	336202	5	NULL	NULL	0	NULL	statement 5	Process		via					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_220	9915989	Nonetheless, although sphingosine-induced Ca2+ transients have been previously reported to occur via mobilization of Ca2+ from intracellular stores [ 33,  34], this study represents the first demonstration that ceramide regulates [Ca2+]i. Cch-induced Ca2+ transients occur via IP3-mediated mobilization of Ca2+ from intracellular stores and/or transmembrane influx of Ca2+ [ 22,  24].	transcription
69574	8	336202	5	NULL	NULL	0	NULL	statement 5	Process		via					Ca2+	Chemical	transmembrane influx of			NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_220	9915989	Nonetheless, although sphingosine-induced Ca2+ transients have been previously reported to occur via mobilization of Ca2+ from intracellular stores [ 33,  34], this study represents the first demonstration that ceramide regulates [Ca2+]i. Cch-induced Ca2+ transients occur via IP3-mediated mobilization of Ca2+ from intracellular stores and/or transmembrane influx of Ca2+ [ 22,  24].	transcription
71599	1	336202	7	NULL	NULL	0	NULL	sphingosine	Chemical		induce					Ca2+	Chemical	transient			NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_220	9915989	Nonetheless, although sphingosine-induced Ca2+ transients have been previously reported to occur via mobilization of Ca2+ from intracellular stores [ 33,  34], this study represents the first demonstration that ceramide regulates [Ca2+]i. Cch-induced Ca2+ transients occur via IP3-mediated mobilization of Ca2+ from intracellular stores and/or transmembrane influx of Ca2+ [ 22,  24].	transcription
71600	2	336202	7	NULL	NULL	NULL	NULL	Ca2+	Chemical		mobilized from					intracellular stores	CellComponent				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_220	9915989	Nonetheless, although sphingosine-induced Ca2+ transients have been previously reported to occur via mobilization of Ca2+ from intracellular stores [ 33,  34], this study represents the first demonstration that ceramide regulates [Ca2+]i. Cch-induced Ca2+ transients occur via IP3-mediated mobilization of Ca2+ from intracellular stores and/or transmembrane influx of Ca2+ [ 22,  24].	transcription
71601	3	336202	7	NULL	NULL	0	NULL	statement 1	Process		occur via					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_220	9915989	Nonetheless, although sphingosine-induced Ca2+ transients have been previously reported to occur via mobilization of Ca2+ from intracellular stores [ 33,  34], this study represents the first demonstration that ceramide regulates [Ca2+]i. Cch-induced Ca2+ transients occur via IP3-mediated mobilization of Ca2+ from intracellular stores and/or transmembrane influx of Ca2+ [ 22,  24].	transcription
71602	4	336202	7	NULL	NULL	0	NULL	ceramide	Chemical		regulates					[Ca2+]i	Chemical				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_220	9915989	Nonetheless, although sphingosine-induced Ca2+ transients have been previously reported to occur via mobilization of Ca2+ from intracellular stores [ 33,  34], this study represents the first demonstration that ceramide regulates [Ca2+]i. Cch-induced Ca2+ transients occur via IP3-mediated mobilization of Ca2+ from intracellular stores and/or transmembrane influx of Ca2+ [ 22,  24].	transcription
71603	5	336202	7	NULL	NULL	0	NULL	Cch	Chemical		induce					Ca2+	Chemical	transient			NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_220	9915989	Nonetheless, although sphingosine-induced Ca2+ transients have been previously reported to occur via mobilization of Ca2+ from intracellular stores [ 33,  34], this study represents the first demonstration that ceramide regulates [Ca2+]i. Cch-induced Ca2+ transients occur via IP3-mediated mobilization of Ca2+ from intracellular stores and/or transmembrane influx of Ca2+ [ 22,  24].	transcription
71604	6	336202	7	NULL	NULL	0	NULL	IP3	Chemical		mediates					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_220	9915989	Nonetheless, although sphingosine-induced Ca2+ transients have been previously reported to occur via mobilization of Ca2+ from intracellular stores [ 33,  34], this study represents the first demonstration that ceramide regulates [Ca2+]i. Cch-induced Ca2+ transients occur via IP3-mediated mobilization of Ca2+ from intracellular stores and/or transmembrane influx of Ca2+ [ 22,  24].	transcription
71605	7	336202	7	NULL	NULL	0	NULL	statement 5	Process		occur via					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_220	9915989	Nonetheless, although sphingosine-induced Ca2+ transients have been previously reported to occur via mobilization of Ca2+ from intracellular stores [ 33,  34], this study represents the first demonstration that ceramide regulates [Ca2+]i. Cch-induced Ca2+ transients occur via IP3-mediated mobilization of Ca2+ from intracellular stores and/or transmembrane influx of Ca2+ [ 22,  24].	transcription
71606	8	336202	7	NULL	NULL	0	NULL	Ca2+	Chemical		mobilized from					Ca2+	Chemical	transmembrane influx of			NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_220	9915989	Nonetheless, although sphingosine-induced Ca2+ transients have been previously reported to occur via mobilization of Ca2+ from intracellular stores [ 33,  34], this study represents the first demonstration that ceramide regulates [Ca2+]i. Cch-induced Ca2+ transients occur via IP3-mediated mobilization of Ca2+ from intracellular stores and/or transmembrane influx of Ca2+ [ 22,  24].	transcription
71607	9	336202	7	NULL	NULL	NULL	NULL	IP3	Chemical		mediates					statement 8	Process				NULL		NULL	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_220	9915989	Nonetheless, although sphingosine-induced Ca2+ transients have been previously reported to occur via mobilization of Ca2+ from intracellular stores [ 33,  34], this study represents the first demonstration that ceramide regulates [Ca2+]i. Cch-induced Ca2+ transients occur via IP3-mediated mobilization of Ca2+ from intracellular stores and/or transmembrane influx of Ca2+ [ 22,  24].	transcription
71608	10	336202	7	NULL	NULL	0	NULL	statement 5	Process		occur via					statement 9	Process				NULL		0	NULL	NULL	NULL	gw60_biolreprod_60_2_262_s_220	9915989	Nonetheless, although sphingosine-induced Ca2+ transients have been previously reported to occur via mobilization of Ca2+ from intracellular stores [ 33,  34], this study represents the first demonstration that ceramide regulates [Ca2+]i. Cch-induced Ca2+ transients occur via IP3-mediated mobilization of Ca2+ from intracellular stores and/or transmembrane influx of Ca2+ [ 22,  24].	transcription
69575	1	336203	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					Fas	GP				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_molpharmacol_61_3_486_s_178	11854428	In contrast, sphingosine 1-phosphate (S1P), which protects Jurkat T lymphocytes from Fas- and ceramide-mediated apoptosis (Cuvillier et al., 1996  ), had a significant protective effect against FCCP-induced cell death; the percentage of apoptotic cells measured after 3 h of FCCP treatment decreasing from about 50 to 27% in the presence of 10 muM S1P.	transcription
69576	2	336203	5	NULL	NULL	0	NULL	apoptosis	Process		is mediated by					ceramide	Chemical				NULL	Jurkat T lymphocytes	0	NULL	NULL	NULL	gw60_molpharmacol_61_3_486_s_178	11854428	In contrast, sphingosine 1-phosphate (S1P), which protects Jurkat T lymphocytes from Fas- and ceramide-mediated apoptosis (Cuvillier et al., 1996  ), had a significant protective effect against FCCP-induced cell death; the percentage of apoptotic cells measured after 3 h of FCCP treatment decreasing from about 50 to 27% in the presence of 10 muM S1P.	transcription
69577	3	336203	5	NULL	NULL	0	NULL	S1P	Chemical		is					sphingosine 1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_486_s_178	11854428	In contrast, sphingosine 1-phosphate (S1P), which protects Jurkat T lymphocytes from Fas- and ceramide-mediated apoptosis (Cuvillier et al., 1996  ), had a significant protective effect against FCCP-induced cell death; the percentage of apoptotic cells measured after 3 h of FCCP treatment decreasing from about 50 to 27% in the presence of 10 muM S1P.	transcription
69578	4	336203	5	NULL	NULL	0	NULL	S1P	Chemical		protects					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_486_s_178	11854428	In contrast, sphingosine 1-phosphate (S1P), which protects Jurkat T lymphocytes from Fas- and ceramide-mediated apoptosis (Cuvillier et al., 1996  ), had a significant protective effect against FCCP-induced cell death; the percentage of apoptotic cells measured after 3 h of FCCP treatment decreasing from about 50 to 27% in the presence of 10 muM S1P.	transcription
69579	5	336203	5	NULL	NULL	0	NULL	S1P	Chemical		protects					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_486_s_178	11854428	In contrast, sphingosine 1-phosphate (S1P), which protects Jurkat T lymphocytes from Fas- and ceramide-mediated apoptosis (Cuvillier et al., 1996  ), had a significant protective effect against FCCP-induced cell death; the percentage of apoptotic cells measured after 3 h of FCCP treatment decreasing from about 50 to 27% in the presence of 10 muM S1P.	transcription
69580	6	336203	5	NULL	NULL	0	NULL	cell death	Process		is induced by					FCCP	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_486_s_178	11854428	In contrast, sphingosine 1-phosphate (S1P), which protects Jurkat T lymphocytes from Fas- and ceramide-mediated apoptosis (Cuvillier et al., 1996  ), had a significant protective effect against FCCP-induced cell death; the percentage of apoptotic cells measured after 3 h of FCCP treatment decreasing from about 50 to 27% in the presence of 10 muM S1P.	transcription
69581	7	336203	5	NULL	NULL	0	NULL	S1P	Chemical		protects					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_486_s_178	11854428	In contrast, sphingosine 1-phosphate (S1P), which protects Jurkat T lymphocytes from Fas- and ceramide-mediated apoptosis (Cuvillier et al., 1996  ), had a significant protective effect against FCCP-induced cell death; the percentage of apoptotic cells measured after 3 h of FCCP treatment decreasing from about 50 to 27% in the presence of 10 muM S1P.	transcription
71609	1	336203	7	NULL	NULL	0	NULL	Fas	GP		mediates					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_486_s_178	11854428	In contrast, sphingosine 1-phosphate (S1P), which protects Jurkat T lymphocytes from Fas- and ceramide-mediated apoptosis (Cuvillier et al., 1996  ), had a significant protective effect against FCCP-induced cell death; the percentage of apoptotic cells measured after 3 h of FCCP treatment decreasing from about 50 to 27% in the presence of 10 muM S1P.	transcription
71610	2	336203	7	NULL	NULL	0	NULL	ceramide	Chemical		mediates					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_486_s_178	11854428	In contrast, sphingosine 1-phosphate (S1P), which protects Jurkat T lymphocytes from Fas- and ceramide-mediated apoptosis (Cuvillier et al., 1996  ), had a significant protective effect against FCCP-induced cell death; the percentage of apoptotic cells measured after 3 h of FCCP treatment decreasing from about 50 to 27% in the presence of 10 muM S1P.	transcription
71611	3	336203	7	NULL	NULL	0	NULL	S1P	Chemical		protects					Jurkat T lymphocytes	Cell				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_486_s_178	11854428	In contrast, sphingosine 1-phosphate (S1P), which protects Jurkat T lymphocytes from Fas- and ceramide-mediated apoptosis (Cuvillier et al., 1996  ), had a significant protective effect against FCCP-induced cell death; the percentage of apoptotic cells measured after 3 h of FCCP treatment decreasing from about 50 to 27% in the presence of 10 muM S1P.	transcription
71612	4	336203	7	NULL	NULL	0	NULL	Jurkat T lymphocytes	Cell		protected from					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_486_s_178	11854428	In contrast, sphingosine 1-phosphate (S1P), which protects Jurkat T lymphocytes from Fas- and ceramide-mediated apoptosis (Cuvillier et al., 1996  ), had a significant protective effect against FCCP-induced cell death; the percentage of apoptotic cells measured after 3 h of FCCP treatment decreasing from about 50 to 27% in the presence of 10 muM S1P.	transcription
71613	5	336203	7	NULL	NULL	0	NULL	Jurkat T lymphocytes	Cell		protected from					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_486_s_178	11854428	In contrast, sphingosine 1-phosphate (S1P), which protects Jurkat T lymphocytes from Fas- and ceramide-mediated apoptosis (Cuvillier et al., 1996  ), had a significant protective effect against FCCP-induced cell death; the percentage of apoptotic cells measured after 3 h of FCCP treatment decreasing from about 50 to 27% in the presence of 10 muM S1P.	transcription
71614	6	336203	7	NULL	NULL	0	NULL	FCCP	Chemical		induce					cell death	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_486_s_178	11854428	In contrast, sphingosine 1-phosphate (S1P), which protects Jurkat T lymphocytes from Fas- and ceramide-mediated apoptosis (Cuvillier et al., 1996  ), had a significant protective effect against FCCP-induced cell death; the percentage of apoptotic cells measured after 3 h of FCCP treatment decreasing from about 50 to 27% in the presence of 10 muM S1P.	transcription
71615	7	336203	7	NULL	NULL	0	NULL	S1P	Chemical		protect against		significantly			statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_486_s_178	11854428	In contrast, sphingosine 1-phosphate (S1P), which protects Jurkat T lymphocytes from Fas- and ceramide-mediated apoptosis (Cuvillier et al., 1996  ), had a significant protective effect against FCCP-induced cell death; the percentage of apoptotic cells measured after 3 h of FCCP treatment decreasing from about 50 to 27% in the presence of 10 muM S1P.	transcription
71616	8	336203	7	NULL	NULL	0	NULL	S1P	Chemical		is					sphingosine 1-phosphate	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_61_3_486_s_178	11854428	In contrast, sphingosine 1-phosphate (S1P), which protects Jurkat T lymphocytes from Fas- and ceramide-mediated apoptosis (Cuvillier et al., 1996  ), had a significant protective effect against FCCP-induced cell death; the percentage of apoptotic cells measured after 3 h of FCCP treatment decreasing from about 50 to 27% in the presence of 10 muM S1P.	transcription
69582	1	336204	5	NULL	NULL	0	NULL	cell death	Process		is related to					sphingoid base	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_140	8626522	There was no evidence of apoptotic DNA damage  following exposure of HL-60 cells to fumonisin B   (100  muM) for 6 h; moreover, the extent of DNA fragmentation  elicited by exposure to sphingosine (10 muM) or sphinganine  (10 muM) for 6 h was not attenuated in the presence of  fumonisin B   ( Table 1 ), confirming that sphingoid  base-related cell death was not mediated by ceramide.	transcription
69583	2	336204	5	NULL	NULL	0	NULL	ceramide	Chemical		does not mediate					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_140	8626522	There was no evidence of apoptotic DNA damage  following exposure of HL-60 cells to fumonisin B   (100  muM) for 6 h; moreover, the extent of DNA fragmentation  elicited by exposure to sphingosine (10 muM) or sphinganine  (10 muM) for 6 h was not attenuated in the presence of  fumonisin B   ( Table 1 ), confirming that sphingoid  base-related cell death was not mediated by ceramide.	transcription
71617	1	336204	7	NULL	NULL	0	NULL	fumonisin B	Chemical		does not cause					apoptotic DNA damage	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_140	8626522	There was no evidence of apoptotic DNA damage  following exposure of HL-60 cells to fumonisin B   (100  muM) for 6 h; moreover, the extent of DNA fragmentation  elicited by exposure to sphingosine (10 muM) or sphinganine  (10 muM) for 6 h was not attenuated in the presence of  fumonisin B   ( Table 1 ), confirming that sphingoid  base-related cell death was not mediated by ceramide.	transcription
71618	2	336204	7	NULL	NULL	0	NULL	statement 1	Process		occur in					HL-60 cells 	Cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_140	8626522	There was no evidence of apoptotic DNA damage  following exposure of HL-60 cells to fumonisin B   (100  muM) for 6 h; moreover, the extent of DNA fragmentation  elicited by exposure to sphingosine (10 muM) or sphinganine  (10 muM) for 6 h was not attenuated in the presence of  fumonisin B   ( Table 1 ), confirming that sphingoid  base-related cell death was not mediated by ceramide.	transcription
71619	3	336204	7	NULL	NULL	0	NULL	sphingosine	Chemical		elicit					DNA fragmentation	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_140	8626522	There was no evidence of apoptotic DNA damage  following exposure of HL-60 cells to fumonisin B   (100  muM) for 6 h; moreover, the extent of DNA fragmentation  elicited by exposure to sphingosine (10 muM) or sphinganine  (10 muM) for 6 h was not attenuated in the presence of  fumonisin B   ( Table 1 ), confirming that sphingoid  base-related cell death was not mediated by ceramide.	transcription
71620	4	336204	7	NULL	NULL	0	NULL	sphinganine	Chemical		elicit					DNA fragmentation	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_140	8626522	There was no evidence of apoptotic DNA damage  following exposure of HL-60 cells to fumonisin B   (100  muM) for 6 h; moreover, the extent of DNA fragmentation  elicited by exposure to sphingosine (10 muM) or sphinganine  (10 muM) for 6 h was not attenuated in the presence of  fumonisin B   ( Table 1 ), confirming that sphingoid  base-related cell death was not mediated by ceramide.	transcription
71621	5	336204	7	NULL	NULL	0	NULL	fumonisin B 	Chemical		does not attenuate					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_140	8626522	There was no evidence of apoptotic DNA damage  following exposure of HL-60 cells to fumonisin B   (100  muM) for 6 h; moreover, the extent of DNA fragmentation  elicited by exposure to sphingosine (10 muM) or sphinganine  (10 muM) for 6 h was not attenuated in the presence of  fumonisin B   ( Table 1 ), confirming that sphingoid  base-related cell death was not mediated by ceramide.	transcription
71622	6	336204	7	NULL	NULL	0	NULL	fumonisin B  	Chemical		does not attenuate					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_140	8626522	There was no evidence of apoptotic DNA damage  following exposure of HL-60 cells to fumonisin B   (100  muM) for 6 h; moreover, the extent of DNA fragmentation  elicited by exposure to sphingosine (10 muM) or sphinganine  (10 muM) for 6 h was not attenuated in the presence of  fumonisin B   ( Table 1 ), confirming that sphingoid  base-related cell death was not mediated by ceramide.	transcription
71623	7	336204	7	NULL	NULL	0	NULL	sphingoid base	Chemical		relates to					cell death	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_140	8626522	There was no evidence of apoptotic DNA damage  following exposure of HL-60 cells to fumonisin B   (100  muM) for 6 h; moreover, the extent of DNA fragmentation  elicited by exposure to sphingosine (10 muM) or sphinganine  (10 muM) for 6 h was not attenuated in the presence of  fumonisin B   ( Table 1 ), confirming that sphingoid  base-related cell death was not mediated by ceramide.	transcription
71624	8	336204	7	NULL	NULL	0	NULL	ceramide	Chemical		does not mediate					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_14_8275_s_140	8626522	There was no evidence of apoptotic DNA damage  following exposure of HL-60 cells to fumonisin B   (100  muM) for 6 h; moreover, the extent of DNA fragmentation  elicited by exposure to sphingosine (10 muM) or sphinganine  (10 muM) for 6 h was not attenuated in the presence of  fumonisin B   ( Table 1 ), confirming that sphingoid  base-related cell death was not mediated by ceramide.	transcription
69584	1	336205	5	NULL	NULL	0	NULL	trkA	GP	inhibition of	is required for		possibly			growth arrest	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
69585	2	336205	5	NULL	NULL	0	NULL	trkA	GP	inhibition of	is required for		possibly			neurite	Cell	 retraction of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
69586	3	336205	5	NULL	NULL	0	NULL	p75NGFR	GP	engagement of	activates		possibly			sphingomyelinase	GP				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
69587	4	336205	5	NULL	NULL	0	NULL	statement 3	Process		leads to		possibly			ceramide	Chemical	increase in;;levels of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
69588	5	336205	5	NULL	NULL	0	NULL	p75NGFR	GP		stimulates					sphingomyelinase	GP				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
69589	6	336205	5	NULL	NULL	0	NULL	trkA	GP		suppress					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
69591	7	336205	5	NULL	NULL	0	NULL	trkA	GP		stimulates					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
69592	8	336205	5	NULL	NULL	0	NULL	statement 7	Process		increases					SPP	Chemical	level of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
69593	9	336205	5	NULL	NULL	0	NULL	statement 6	Process		is required for		possibly			survival	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
69594	10	336205	5	NULL	NULL	0	NULL	statement 6	Process		is required for		possibly			neurite	Cell	extension of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
71625	1	336205	7	NULL	NULL	NULL	NULL	growth arrest	Process	requirement of	inhibit		may			trkA	GP	functions of			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
71626	2	336205	7	NULL	NULL	NULL	NULL	 neurite retraction 	Process	requirement of	inhibit		may			 trkA	GP	functions of			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
71627	3	336205	7	NULL	NULL	0	NULL	p75NGFR	GP		activate					sphingomyelinase	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
71628	4	336205	7	NULL	NULL	0	NULL	statement 3	Process		leads to					ceramide levels	Chemical	increased			NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
71629	5	336205	7	NULL	NULL	0	NULL	p75NGFR	GP		stimulate					sphingomyelinase	GP				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
71630	6	336205	7	NULL	NULL	0	NULL	 trkA	GP		suppress					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
71631	7	336205	7	NULL	NULL	0	NULL	trkA	GP		stimulate					sphingosine kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
71632	8	336205	7	NULL	NULL	0	NULL	trkA	GP		increase					SPP	Chemical	levels of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
71633	9	336205	7	NULL	NULL	0	NULL	statement 6	Process		occur upon					survival	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
71634	10	336205	7	NULL	NULL	0	NULL	statement 6	Process		occur upon					neurite extenstions	Process	requirement of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
71635	11	336205	7	NULL	NULL	0	NULL	statement 7	Process		occur upon					survival	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
71636	12	336205	7	NULL	NULL	0	NULL	statement 7	Process		occur upon					neurite extenstions	Process	requirement of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
71637	13	336205	7	NULL	NULL	0	NULL	statement 8	Process		occur upon					survival	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
71638	14	336205	7	NULL	NULL	NULL	NULL	statement 8	Process		occur upon					neurite extenstions	Process	requirement of			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_17_18_6952_s_213	9278531	As similarly speculated by Posse de Chaves et al. (1997)  , when growth arrest and neurite retraction are required, it is anticipated that trkA functions would be inhibited, and engagement of p75NGFR would activate sphingomyelinase activity, leading to increased ceramide levels, and conversely, when survival and neurite extensions are required, trkA would not only suppress the ability of p75NGFR to stimulate sphingomyelinase, it would also stimulate sphingosine kinase and increase SPP levels.	transcription
69595	1	336206	5	NULL	NULL	0	NULL	FB1	Chemical		is					fumonisin B1	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_22	9096129	We originally demonstrated that incubation with fumonisin B1 (FB1), a specific inhibitor of  N-acylation of the sphingoid long chain bases dihydrosphingosine (sphinganine) and sphingosine to dihydroceramide and ceramide, respectively (Merrill et al., 1996  ), disrupted axon growth during the early part of stage 3, between days 2 and 3 in culture (Harel and Futerman, 1993  ).	transcription
69596	2	336206	5	NULL	NULL	0	NULL	sphinganine	Chemical		is					dihydrosphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_22	9096129	We originally demonstrated that incubation with fumonisin B1 (FB1), a specific inhibitor of  N-acylation of the sphingoid long chain bases dihydrosphingosine (sphinganine) and sphingosine to dihydroceramide and ceramide, respectively (Merrill et al., 1996  ), disrupted axon growth during the early part of stage 3, between days 2 and 3 in culture (Harel and Futerman, 1993  ).	transcription
69597	3	336206	5	NULL	NULL	NULL	NULL	FB1	Chemical		is an inhibitor of		specific			dihydrosphingosine	Chemical	N-acylation of sphingoid long chain bases			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_22	9096129	We originally demonstrated that incubation with fumonisin B1 (FB1), a specific inhibitor of  N-acylation of the sphingoid long chain bases dihydrosphingosine (sphinganine) and sphingosine to dihydroceramide and ceramide, respectively (Merrill et al., 1996  ), disrupted axon growth during the early part of stage 3, between days 2 and 3 in culture (Harel and Futerman, 1993  ).	transcription
69598	4	336206	5	NULL	NULL	0	NULL	sphingosine	Chemical		is converted to					dihydroceramide 	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_22	9096129	We originally demonstrated that incubation with fumonisin B1 (FB1), a specific inhibitor of  N-acylation of the sphingoid long chain bases dihydrosphingosine (sphinganine) and sphingosine to dihydroceramide and ceramide, respectively (Merrill et al., 1996  ), disrupted axon growth during the early part of stage 3, between days 2 and 3 in culture (Harel and Futerman, 1993  ).	transcription
69599	5	336206	5	NULL	NULL	0	NULL	sphingosine	Chemical		is converted to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_22	9096129	We originally demonstrated that incubation with fumonisin B1 (FB1), a specific inhibitor of  N-acylation of the sphingoid long chain bases dihydrosphingosine (sphinganine) and sphingosine to dihydroceramide and ceramide, respectively (Merrill et al., 1996  ), disrupted axon growth during the early part of stage 3, between days 2 and 3 in culture (Harel and Futerman, 1993  ).	transcription
69600	6	336206	5	NULL	NULL	0	NULL	statement 4	Process		occurs along with					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_22	9096129	We originally demonstrated that incubation with fumonisin B1 (FB1), a specific inhibitor of  N-acylation of the sphingoid long chain bases dihydrosphingosine (sphinganine) and sphingosine to dihydroceramide and ceramide, respectively (Merrill et al., 1996  ), disrupted axon growth during the early part of stage 3, between days 2 and 3 in culture (Harel and Futerman, 1993  ).	transcription
69601	7	336206	5	NULL	NULL	0	NULL	FB1	Chemical		inhibits		specifically			statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_22	9096129	We originally demonstrated that incubation with fumonisin B1 (FB1), a specific inhibitor of  N-acylation of the sphingoid long chain bases dihydrosphingosine (sphinganine) and sphingosine to dihydroceramide and ceramide, respectively (Merrill et al., 1996  ), disrupted axon growth during the early part of stage 3, between days 2 and 3 in culture (Harel and Futerman, 1993  ).	transcription
69602	8	336206	5	NULL	NULL	0	NULL	FB1	Chemical		inhibits		specifically			statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_22	9096129	We originally demonstrated that incubation with fumonisin B1 (FB1), a specific inhibitor of  N-acylation of the sphingoid long chain bases dihydrosphingosine (sphinganine) and sphingosine to dihydroceramide and ceramide, respectively (Merrill et al., 1996  ), disrupted axon growth during the early part of stage 3, between days 2 and 3 in culture (Harel and Futerman, 1993  ).	transcription
69603	9	336206	5	NULL	NULL	NULL	NULL	FB1	Chemical		disrupts					axon	CellComponent	growth of			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_22	9096129	We originally demonstrated that incubation with fumonisin B1 (FB1), a specific inhibitor of  N-acylation of the sphingoid long chain bases dihydrosphingosine (sphinganine) and sphingosine to dihydroceramide and ceramide, respectively (Merrill et al., 1996  ), disrupted axon growth during the early part of stage 3, between days 2 and 3 in culture (Harel and Futerman, 1993  ).	transcription
71639	3	336206	7	NULL	NULL	NULL	NULL	FB1	Chemical		inhibit					statement 1	Process	 N-acylation of 			NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_22	9096129	We originally demonstrated that incubation with fumonisin B1 (FB1), a specific inhibitor of  N-acylation of the sphingoid long chain bases dihydrosphingosine (sphinganine) and sphingosine to dihydroceramide and ceramide, respectively (Merrill et al., 1996  ), disrupted axon growth during the early part of stage 3, between days 2 and 3 in culture (Harel and Futerman, 1993  ).	transcription
71640	1	336206	7	NULL	NULL	NULL	NULL	sphinganine	Chemical		acylated to					dihydroceramide	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_22	9096129	We originally demonstrated that incubation with fumonisin B1 (FB1), a specific inhibitor of  N-acylation of the sphingoid long chain bases dihydrosphingosine (sphinganine) and sphingosine to dihydroceramide and ceramide, respectively (Merrill et al., 1996  ), disrupted axon growth during the early part of stage 3, between days 2 and 3 in culture (Harel and Futerman, 1993  ).	transcription
71641	2	336206	7	NULL	NULL	NULL	NULL	 sphingosine 	Chemical		acylated to					ceramide	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_22	9096129	We originally demonstrated that incubation with fumonisin B1 (FB1), a specific inhibitor of  N-acylation of the sphingoid long chain bases dihydrosphingosine (sphinganine) and sphingosine to dihydroceramide and ceramide, respectively (Merrill et al., 1996  ), disrupted axon growth during the early part of stage 3, between days 2 and 3 in culture (Harel and Futerman, 1993  ).	transcription
71642	4	336206	7	NULL	NULL	0	NULL	FB1	Chemical		inhibit					statement 2	Process	N-acylation of			NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_22	9096129	We originally demonstrated that incubation with fumonisin B1 (FB1), a specific inhibitor of  N-acylation of the sphingoid long chain bases dihydrosphingosine (sphinganine) and sphingosine to dihydroceramide and ceramide, respectively (Merrill et al., 1996  ), disrupted axon growth during the early part of stage 3, between days 2 and 3 in culture (Harel and Futerman, 1993  ).	transcription
71643	5	336206	7	NULL	NULL	0	NULL	sphinganine	Chemical		is					dihydrosphingosine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_22	9096129	We originally demonstrated that incubation with fumonisin B1 (FB1), a specific inhibitor of  N-acylation of the sphingoid long chain bases dihydrosphingosine (sphinganine) and sphingosine to dihydroceramide and ceramide, respectively (Merrill et al., 1996  ), disrupted axon growth during the early part of stage 3, between days 2 and 3 in culture (Harel and Futerman, 1993  ).	transcription
71644	6	336206	7	NULL	NULL	0	NULL	dihydrosphingosine	Chemical		contains					sphingoid long chain bases	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_22	9096129	We originally demonstrated that incubation with fumonisin B1 (FB1), a specific inhibitor of  N-acylation of the sphingoid long chain bases dihydrosphingosine (sphinganine) and sphingosine to dihydroceramide and ceramide, respectively (Merrill et al., 1996  ), disrupted axon growth during the early part of stage 3, between days 2 and 3 in culture (Harel and Futerman, 1993  ).	transcription
71645	7	336206	7	NULL	NULL	0	NULL	FB1	Chemical		disrupts					axon growth	Process				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_22	9096129	We originally demonstrated that incubation with fumonisin B1 (FB1), a specific inhibitor of  N-acylation of the sphingoid long chain bases dihydrosphingosine (sphinganine) and sphingosine to dihydroceramide and ceramide, respectively (Merrill et al., 1996  ), disrupted axon growth during the early part of stage 3, between days 2 and 3 in culture (Harel and Futerman, 1993  ).	transcription
71646	8	336206	7	NULL	NULL	0	NULL	FB1	Chemical		is					fumonisin B1	Chemical				NULL		0	NULL	NULL	NULL	gw60_jneurosci_17_9_2929_s_22	9096129	We originally demonstrated that incubation with fumonisin B1 (FB1), a specific inhibitor of  N-acylation of the sphingoid long chain bases dihydrosphingosine (sphinganine) and sphingosine to dihydroceramide and ceramide, respectively (Merrill et al., 1996  ), disrupted axon growth during the early part of stage 3, between days 2 and 3 in culture (Harel and Futerman, 1993  ).	transcription
69605	1	336209	5	NULL	NULL	0	NULL	capsiate	Chemical	sweet peppers	inhibits					NF-kappaB	GP	activation of			NULL	in vivo	0	NULL	NULL	NULL	gw60_neuropharmacology_44_7_958_s_328	12726827	Immunosuppressive activity of capsaicinoids: capsiate derived from sweet peppers inhibits NF-kappaB activation and is a potent antiinflammatory compound in vivo.	transcription
69606	2	336209	5	NULL	NULL	0	NULL	capsiate	Chemical		is a type of					capsaicinoids	Chemical				NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_44_7_958_s_328	12726827	Immunosuppressive activity of capsaicinoids: capsiate derived from sweet peppers inhibits NF-kappaB activation and is a potent antiinflammatory compound in vivo.	transcription
69607	3	336209	5	NULL	NULL	0	NULL	capsiate	Chemical		is a type of					potent antiinflammatory compound 	Chemical				NULL	in vivo	0	NULL	NULL	NULL	gw60_neuropharmacology_44_7_958_s_328	12726827	Immunosuppressive activity of capsaicinoids: capsiate derived from sweet peppers inhibits NF-kappaB activation and is a potent antiinflammatory compound in vivo.	transcription
71647	1	336209	7	NULL	NULL	0	NULL	capsiate	Chemical		derived from					sweet peppers	Organism				NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_44_7_958_s_328	12726827	Immunosuppressive activity of capsaicinoids: capsiate derived from sweet peppers inhibits NF-kappaB activation and is a potent antiinflammatory compound in vivo.	transcription
71648	2	336209	7	NULL	NULL	0	NULL	statement 1	Process		inhibits					NF-kappaB	GP	activation of			NULL	in vivo	0	NULL	NULL	NULL	gw60_neuropharmacology_44_7_958_s_328	12726827	Immunosuppressive activity of capsaicinoids: capsiate derived from sweet peppers inhibits NF-kappaB activation and is a potent antiinflammatory compound in vivo.	transcription
71649	3	336209	7	NULL	NULL	0	NULL	capsiate	Chemical		is a type of					potent antiinflammatory compound	Chemical				NULL	in vivo	0	NULL	NULL	NULL	gw60_neuropharmacology_44_7_958_s_328	12726827	Immunosuppressive activity of capsaicinoids: capsiate derived from sweet peppers inhibits NF-kappaB activation and is a potent antiinflammatory compound in vivo.	transcription
71650	4	336209	7	NULL	NULL	0	NULL	capsaicinoids	Chemical		shows					Immunosuppressive activity	Process				NULL		0	NULL	NULL	NULL	gw60_neuropharmacology_44_7_958_s_328	12726827	Immunosuppressive activity of capsaicinoids: capsiate derived from sweet peppers inhibits NF-kappaB activation and is a potent antiinflammatory compound in vivo.	transcription
69608	1	336212	5	NULL	NULL	NULL	NULL	HDL-apoE	GP		is involved in					lipoprotein	GP	metabolism of;;plasma			NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
69609	2	336212	5	NULL	NULL	0	NULL	HDL cholesterol	Chemical		is delivered to					liver	OrganismPart				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
69610	3	336212	5	NULL	NULL	0	NULL	receptor	GP		mediates					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
69611	4	336212	5	NULL	NULL	0	NULL	lipase	GP	hepatic	catalyzes					HDL phospholipid	Chemical	hydrolysis of 			NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
69612	5	336212	5	NULL	NULL	NULL	NULL	statement 1	Process		includes					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
69614	6	336212	5	NULL	NULL	0	NULL	statement 1	Process		includes					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
69615	7	336212	5	NULL	NULL	NULL	NULL	HDL-apoE	GP		is involved in					cholesterol	Chemical	esterification of;;plasma 			NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
69616	8	336212	5	NULL	NULL	0	NULL	HDL-apoE	GP		is involved in					cholesteryl ester	Chemical	transfer of;;plasma			NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
69617	9	336212	5	NULL	NULL	0	NULL	HDL-apoE	GP		is involved in					cholesterol	Chemical	efflux of;;cell-derived			NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
69618	10	336212	5	NULL	NULL	0	NULL	HDL-apoE	GP		is involved in					heparin sulfate	Chemical	stimulation of;;endothelial production of 			NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
71651	1	336212	7	NULL	NULL	0	NULL	HDL-apoE	GP		is involved in					plasma lipoprotein metabolism	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
71652	2	336212	7	NULL	NULL	0	NULL	HDL cholesterol	Chemical		delivered to					liver	OrganismPart				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
71653	3	336212	7	NULL	NULL	0	NULL	receptor	GP		mediates					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
71654	4	336212	7	NULL	NULL	0	NULL	hepatic lipase	GP		catalyze					HDL phospholipid	Chemical	hydrolysis of			NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
71655	5	336212	7	NULL	NULL	NULL	NULL	HDL-apoE	GP		is involved in					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
71656	6	336212	7	NULL	NULL	NULL	NULL	HDL-apoE	GP		is involved in					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
71657	7	336212	7	NULL	NULL	0	NULL	HDL-apoE	GP		is involved in					plasma cholesterol	Chemical	esterification of			NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
71658	8	336212	7	NULL	NULL	0	NULL	HDL-apoE	GP		is involved in					plasma CE	Chemical	transfer of			NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
71659	9	336212	7	NULL	NULL	0	NULL	cholesterol	Chemical		derived from					Cell	Cell				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
71660	10	336212	7	NULL	NULL	0	NULL	HDL-apoE	GP		is involved in					statement 9	Process				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
71661	11	336212	7	NULL	NULL	0	NULL	HDL-apoE	GP		is involved in					heparin sulfate	Chemical	stimulation of endothelial production of 			NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
71662	12	336212	7	NULL	NULL	0	NULL	CE	Chemical		is					cholesteryl ester	Chemical				NULL		0	NULL	NULL	NULL	gw70_jlipidres_44_5_884_s_22	12611904	It has been suggested that HDL-apoE is involved in several aspects of plasma lipoprotein metabolism, including  1) receptor-mediated delivery of HDL cholesterol to the liver ( ),  2) hepatic lipase-catalyzed hydrolysis of HDL phospholipid ( ),  3) plasma cholesterol esterification ( ),  4) plasma cholesteryl ester (CE) transfer ( ),  5) efflux of cell-derived cholesterol ( ,  ), and  6) stimulation of endothelial production of heparin sulfate ( ).	transcription
71663	1	336213	7	NULL	NULL	0	NULL	smaller remnant particles	Chemical		diffuse into					arterial intima	OrganismPart				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71664	2	336213	7	NULL	NULL	0	NULL	TRL remnants	GP		retained within					arterial intima	OrganismPart				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71665	3	336213	7	NULL	NULL	0	NULL	TRL remnants	GP		retained by					heparan sulfate proteoglycans	Chemical				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71666	4	336213	7	NULL	NULL	0	NULL	TRL remnants	GP		are reduced in					size	Process				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71667	5	336213	7	NULL	NULL	0	NULL	statement 2	Process		due to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71668	6	336213	7	NULL	NULL	0	NULL	TRL remnants	GP		contains					apoE content	GP	increased 			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71670	7	336213	7	NULL	NULL	0	NULL	statement 2	Process		due to					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71671	8	336213	7	NULL	NULL	0	NULL	TRL remnants	GP		associate with					lipoprotein lipase	GP				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71672	9	336213	7	NULL	NULL	0	NULL	statement 2	Process		due to					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71673	10	336213	7	NULL	NULL	0	NULL	TRL	GP		induce					 cholesteryl ester	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71674	11	336213	7	NULL	NULL	0	NULL	statement 10	Process		occur by					macrophages	CellComponent				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71675	12	336213	7	NULL	NULL	0	NULL	statement 10	Process		is dependent on					apoE epitopes	GP	exposure of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71676	13	336213	7	NULL	NULL	0	NULL	statement 12	Process		occur through					TRL	GP	lipolysis of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71677	14	336213	7	NULL	NULL	0	NULL	lipoprotein lipase	GP		mediates					TRL remnants	GP	generation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71678	15	336213	7	NULL	NULL	0	NULL	statement 14	Process		results in					lipolytic products	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71679	16	336213	7	NULL	NULL	0	NULL	lipolytic products	Chemical		cytotoxic to					macrophages	CellComponent				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71680	17	336213	7	NULL	NULL	0	NULL	macrophages	CellComponent		increase					endothelial cell layer 	CellComponent	permeability of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71681	18	336213	7	NULL	NULL	0	NULL	coagulation factor XII	GP	increased activity of	is dependent on					TRL	GP	lipolysis of			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71682	19	336213	7	NULL	NULL	0	NULL	statement 18	Process		occur in					hypertriglyceridemia patients	Organism				NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71683	20	336213	7	NULL	NULL	0	NULL	 large chylomicrons 	Chemical		are excluded from					vessel wall	CellComponent	entering the			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71684	21	336213	7	NULL	NULL	0	NULL	VLDL	GP		are excluded from					vessel wall	CellComponent	entering the			NULL		0	NULL	NULL	NULL	gw60_arterthrombvascbiol_19_10_2474_s_27	10521378	This is supported by experimental data showing the following: (1) smaller remnant particles can diffuse into the arterial intima, whereas large chylomicrons and VLDL (diameter >75 nm) are excluded from entering the vessel wall 13 ; (2) due to their reduced size, increased apoE content, and association with lipoprotein lipase, TRL remnants are more likely to be retained by heparan sulfate proteoglycans within the arterial intima 14 ;(3) TRL-induced cholesteryl ester accumulation by macrophages is dependent on the exposure of apoE epitopes through lipolysis of TRL 15 ; (4) lipoprotein lipase - mediated generation of TRL remnants results in the formation of lipolytic products, which are cytotoxic to macrophages 16  and which can increase endothelial cell layer permeability 17 ; and (5) increased activity of coagulation factor XII in patients with hypertriglyceridemia is dependent on TRL lipolysis.	transcription
71685	1	336214	7	NULL	NULL	0	NULL	phosphatidylcholine	Chemical		synthesize					SM	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_24_14636_s_87	8662871	Previous studies have shown that SM is mainly synthesized by phosphatidylcholine:ceramide cholinephosphotransferase that catalyzes a base-exchange reaction between ceramide and phosphatidylcholine ( 18).	transcription
71686	2	336214	7	NULL	NULL	0	NULL	ceramide	Chemical		converted to					phosphatidylcholine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_24_14636_s_87	8662871	Previous studies have shown that SM is mainly synthesized by phosphatidylcholine:ceramide cholinephosphotransferase that catalyzes a base-exchange reaction between ceramide and phosphatidylcholine ( 18).	transcription
71687	3	336214	7	NULL	NULL	0	NULL	ceramide cholinephosphotransferase 	GP		catalyze					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_24_14636_s_87	8662871	Previous studies have shown that SM is mainly synthesized by phosphatidylcholine:ceramide cholinephosphotransferase that catalyzes a base-exchange reaction between ceramide and phosphatidylcholine ( 18).	transcription
71688	4	336214	7	NULL	NULL	0	NULL	statement 2	Process		is a type of					base-exchange reaction	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_271_24_14636_s_87	8662871	Previous studies have shown that SM is mainly synthesized by phosphatidylcholine:ceramide cholinephosphotransferase that catalyzes a base-exchange reaction between ceramide and phosphatidylcholine ( 18).	transcription
69620	1	336215	5	NULL	NULL	0	NULL	agonist	Chemical		induce					phosphatidylcholine	Chemical	hydrolysis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24090_s_35	11953426	Whereas the agonist-induced hydrolysis of phosphatidylcholine (PC) results in PA production, the cleavage of sphingomyelin (SM) leads to generation of ceramides.	transcription
69621	2	336215	5	NULL	NULL	0	NULL	statement 1	Process		results in					PA	Chemical	production of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24090_s_35	11953426	Whereas the agonist-induced hydrolysis of phosphatidylcholine (PC) results in PA production, the cleavage of sphingomyelin (SM) leads to generation of ceramides.	transcription
69622	3	336215	5	NULL	NULL	0	NULL	sphingomyelin	Chemical	cleavage of	generates					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24090_s_35	11953426	Whereas the agonist-induced hydrolysis of phosphatidylcholine (PC) results in PA production, the cleavage of sphingomyelin (SM) leads to generation of ceramides.	transcription
69623	4	336215	5	NULL	NULL	0	NULL	PC	Chemical		is					phosphatidylcholine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24090_s_35	11953426	Whereas the agonist-induced hydrolysis of phosphatidylcholine (PC) results in PA production, the cleavage of sphingomyelin (SM) leads to generation of ceramides.	transcription
69624	5	336215	5	NULL	NULL	0	NULL	SM	Chemical		is					sphingomyelin	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24090_s_35	11953426	Whereas the agonist-induced hydrolysis of phosphatidylcholine (PC) results in PA production, the cleavage of sphingomyelin (SM) leads to generation of ceramides.	transcription
71689	1	336215	7	NULL	NULL	0	NULL	agonist	Chemical		induce					PC	Chemical	hydrolysis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24090_s_35	11953426	Whereas the agonist-induced hydrolysis of phosphatidylcholine (PC) results in PA production, the cleavage of sphingomyelin (SM) leads to generation of ceramides.	transcription
71690	2	336215	7	NULL	NULL	0	NULL	PC	Chemical		is					phosphatidylcholine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24090_s_35	11953426	Whereas the agonist-induced hydrolysis of phosphatidylcholine (PC) results in PA production, the cleavage of sphingomyelin (SM) leads to generation of ceramides.	transcription
71691	3	336215	7	NULL	NULL	0	NULL	statement 1	Process		results in					PA	Chemical	production of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24090_s_35	11953426	Whereas the agonist-induced hydrolysis of phosphatidylcholine (PC) results in PA production, the cleavage of sphingomyelin (SM) leads to generation of ceramides.	transcription
71692	4	336215	7	NULL	NULL	0	NULL	SM	Chemical	cleavage of 	leads to					ceramide	Chemical	generation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24090_s_35	11953426	Whereas the agonist-induced hydrolysis of phosphatidylcholine (PC) results in PA production, the cleavage of sphingomyelin (SM) leads to generation of ceramides.	transcription
71693	5	336215	7	NULL	NULL	0	NULL	SM	Chemical		is					sphingomyelin	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_27_24090_s_35	11953426	Whereas the agonist-induced hydrolysis of phosphatidylcholine (PC) results in PA production, the cleavage of sphingomyelin (SM) leads to generation of ceramides.	transcription
69625	1	336216	5	NULL	NULL	NULL	NULL	SM	Chemical	synthesis of	is mediated by					phosphatidylcholine:ceramide cholinephosphotransferase	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
69637	2	336216	5	NULL	NULL	0	NULL	phosphorylcholine moiety	Chemical		is transfered from					phosphatidylcholine	Chemical				NULL		0	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
69638	3	336216	5	NULL	NULL	0	NULL	phosphorylcholine moiety	Chemical		is transfered onto					ceramide	Chemical	primary hydroxyl  of			NULL		0	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
69639	4	336216	5	NULL	NULL	0	NULL	statement 2	Process		occurs along with					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
69640	5	336216	5	NULL	NULL	NULL	NULL	phosphatidylcholine:ceramide cholinephosphotransferase	GP		is involved in					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
69641	6	336216	5	NULL	NULL	NULL	NULL	phosphatidylcholine:ceramide cholinephosphotransferase	GP		is involved in					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
69642	7	336216	5	NULL	NULL	NULL	NULL	SM synthase	GP		is a synonym of					phosphatidylcholine:ceramide cholinephosphotransferase	GP				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
69644	9	336216	5	NULL	NULL	0	NULL	statement 4	Process		generates					SM	Chemical				NULL		0	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
69645	10	336216	5	NULL	NULL	0	NULL	statement 4	Process		generates					DAG	Chemical				NULL		0	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
69646	11	336216	5	NULL	NULL	0	NULL	DAG	Chemical		is					diacylglycerol	Chemical				NULL		0	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
69647	8	336216	5	NULL	NULL	NULL	NULL	PC	Chemical		is					phosphatidylcholine	Chemical				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
71694	1	336216	7	NULL	NULL	0	NULL	SM	Chemical	synthesis of	mediated by					phosphatidylcholine	Chemical				NULL		0	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
71695	2	336216	7	NULL	NULL	NULL	NULL	PC	Chemical	phosphorylcholine moiety of	transferred to					ceramide	Chemical	primary hydroxyl of			NULL		NULL	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
71696	3	336216	7	NULL	NULL	NULL	NULL	ceramide cholinephosphotransferase	Chemical		catalyze					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
71697	4	336216	7	NULL	NULL	0	NULL	SM synthase	GP		catalyze					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
71698	5	336216	7	NULL	NULL	0	NULL	statement 2	Process		generate					SM	Chemical				NULL		0	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
71699	6	336216	7	NULL	NULL	0	NULL	statement 2	Process		generate					DAG					NULL		0	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
71700	7	336216	7	NULL	NULL	0	NULL	statement 5	Process		occur along with					statement 6	Process				NULL		0	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
71701	8	336216	7	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
71702	9	336216	7	NULL	NULL	0	NULL	PC	Chemical		is					phosphatidylcholine	Chemical				NULL		0	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
71703	10	336216	7	NULL	NULL	0	NULL	DAG	Chemical		is					diacylglycerol	Chemical				NULL		0	NULL	NULL	NULL	gw70_embo_23_1_33_s_16	14685263	SM synthesis is mediated by a phosphatidylcholine:ceramide cholinephosphotransferase,  or SM synthase, which transfers the phosphorylcholine moiety from phosphatidylcholine  (PC) onto the primary hydroxyl of ceramide, thus generating SM and diacylglycerol  (DAG;  ;  ;  ).	transcription
69648	1	336217	5	NULL	NULL	0	NULL	Bid	GP		is translocated to					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_10073_s_370	11790791	Translocation of Bid to the Mitochondria with Ceramide--  Upon activation the Fas receptor generated ceramide, as a consequence of the sequential involvement of phosphatidylcholine-specific phospholipase C and an acidic sphingomyelinase ( 42).	transcription
69649	2	336217	5	NULL	NULL	0	NULL	statement 1	Process		occurs along with					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_10073_s_370	11790791	Translocation of Bid to the Mitochondria with Ceramide--  Upon activation the Fas receptor generated ceramide, as a consequence of the sequential involvement of phosphatidylcholine-specific phospholipase C and an acidic sphingomyelinase ( 42).	transcription
69650	3	336217	5	NULL	NULL	NULL	NULL	ceramide	Chemical		is generated by					Fas receptor	GP	activated			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10073_s_370	11790791	Translocation of Bid to the Mitochondria with Ceramide--  Upon activation the Fas receptor generated ceramide, as a consequence of the sequential involvement of phosphatidylcholine-specific phospholipase C and an acidic sphingomyelinase ( 42).	transcription
69651	4	336217	5	NULL	NULL	0	NULL	phospholipase C	GP		is specific to					phosphatidylcholine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_10073_s_370	11790791	Translocation of Bid to the Mitochondria with Ceramide--  Upon activation the Fas receptor generated ceramide, as a consequence of the sequential involvement of phosphatidylcholine-specific phospholipase C and an acidic sphingomyelinase ( 42).	transcription
69653	5	336217	5	NULL	NULL	0	NULL	statement 4	GP		is involved in		sequential			statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_10073_s_370	11790791	Translocation of Bid to the Mitochondria with Ceramide--  Upon activation the Fas receptor generated ceramide, as a consequence of the sequential involvement of phosphatidylcholine-specific phospholipase C and an acidic sphingomyelinase ( 42).	transcription
69654	6	336217	5	NULL	NULL	0	NULL	sphingomyelinase	GP	acidic	is involved in		sequential			statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_10073_s_370	11790791	Translocation of Bid to the Mitochondria with Ceramide--  Upon activation the Fas receptor generated ceramide, as a consequence of the sequential involvement of phosphatidylcholine-specific phospholipase C and an acidic sphingomyelinase ( 42).	transcription
71704	1	336217	7	NULL	NULL	0	NULL	Bid	GP		translocated to					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_10073_s_370	11790791	Translocation of Bid to the Mitochondria with Ceramide--  Upon activation the Fas receptor generated ceramide, as a consequence of the sequential involvement of phosphatidylcholine-specific phospholipase C and an acidic sphingomyelinase ( 42).	transcription
71705	2	336217	7	NULL	NULL	0	NULL	ceramide	Chemical		translocated to					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_10073_s_370	11790791	Translocation of Bid to the Mitochondria with Ceramide--  Upon activation the Fas receptor generated ceramide, as a consequence of the sequential involvement of phosphatidylcholine-specific phospholipase C and an acidic sphingomyelinase ( 42).	transcription
71706	3	336217	7	NULL	NULL	0	NULL	statement 1	Process		occur along with					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_10073_s_370	11790791	Translocation of Bid to the Mitochondria with Ceramide--  Upon activation the Fas receptor generated ceramide, as a consequence of the sequential involvement of phosphatidylcholine-specific phospholipase C and an acidic sphingomyelinase ( 42).	transcription
71707	4	336217	7	NULL	NULL	0	NULL	 Fas receptor	GP	activation of	generates					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_10073_s_370	11790791	Translocation of Bid to the Mitochondria with Ceramide--  Upon activation the Fas receptor generated ceramide, as a consequence of the sequential involvement of phosphatidylcholine-specific phospholipase C and an acidic sphingomyelinase ( 42).	transcription
71708	5	336217	7	NULL	NULL	NULL	NULL	statement 4	Process		involves					phosphatidylcholine-specific phospholipase C	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10073_s_370	11790791	Translocation of Bid to the Mitochondria with Ceramide--  Upon activation the Fas receptor generated ceramide, as a consequence of the sequential involvement of phosphatidylcholine-specific phospholipase C and an acidic sphingomyelinase ( 42).	transcription
71709	6	336217	7	NULL	NULL	NULL	NULL	statement 4	Process		involves					acidic sphingomyelinase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_277_12_10073_s_370	11790791	Translocation of Bid to the Mitochondria with Ceramide--  Upon activation the Fas receptor generated ceramide, as a consequence of the sequential involvement of phosphatidylcholine-specific phospholipase C and an acidic sphingomyelinase ( 42).	transcription
71710	7	336217	7	NULL	NULL	0	NULL	statement 6	Process		occur after					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_12_10073_s_370	11790791	Translocation of Bid to the Mitochondria with Ceramide--  Upon activation the Fas receptor generated ceramide, as a consequence of the sequential involvement of phosphatidylcholine-specific phospholipase C and an acidic sphingomyelinase ( 42).	transcription
69655	1	336218	5	NULL	NULL	0	NULL	phosphatidylcholine:ceramide phosphocholine transferase	GP		regulates					ceramide	Chemical	level of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14550_s_35	9603970	One of the most intriguing enzymes that regulate ceramide levels is the phosphatidylcholine:ceramide phosphocholine transferase (sphingomyelin synthase; SMS), which transfers the phosphocholine group from PC to ceramide generating sphingomyelin (SM) and DAG ( 27-33).	transcription
69656	2	336218	5	NULL	NULL	0	NULL	phosphatidylcholine:ceramide phosphocholine transferase	GP		is a synonym of					sphingomyelin synthase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14550_s_35	9603970	One of the most intriguing enzymes that regulate ceramide levels is the phosphatidylcholine:ceramide phosphocholine transferase (sphingomyelin synthase; SMS), which transfers the phosphocholine group from PC to ceramide generating sphingomyelin (SM) and DAG ( 27-33).	transcription
69657	3	336218	5	NULL	NULL	0	NULL	sphingomyelin synthase	GP		is					SMS	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14550_s_35	9603970	One of the most intriguing enzymes that regulate ceramide levels is the phosphatidylcholine:ceramide phosphocholine transferase (sphingomyelin synthase; SMS), which transfers the phosphocholine group from PC to ceramide generating sphingomyelin (SM) and DAG ( 27-33).	transcription
69658	4	336218	5	NULL	NULL	NULL	NULL	phosphocholine group	Chemical		is transfered from					PC	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_23_14550_s_35	9603970	One of the most intriguing enzymes that regulate ceramide levels is the phosphatidylcholine:ceramide phosphocholine transferase (sphingomyelin synthase; SMS), which transfers the phosphocholine group from PC to ceramide generating sphingomyelin (SM) and DAG ( 27-33).	transcription
69659	5	336218	5	NULL	NULL	0	NULL	phosphocholine group	Chemical		is transfered to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14550_s_35	9603970	One of the most intriguing enzymes that regulate ceramide levels is the phosphatidylcholine:ceramide phosphocholine transferase (sphingomyelin synthase; SMS), which transfers the phosphocholine group from PC to ceramide generating sphingomyelin (SM) and DAG ( 27-33).	transcription
69660	6	336218	5	NULL	NULL	0	NULL	statement 4	Process		occurs along with					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14550_s_35	9603970	One of the most intriguing enzymes that regulate ceramide levels is the phosphatidylcholine:ceramide phosphocholine transferase (sphingomyelin synthase; SMS), which transfers the phosphocholine group from PC to ceramide generating sphingomyelin (SM) and DAG ( 27-33).	transcription
69661	7	336218	5	NULL	NULL	0	NULL	statement 6	Process		generates					SM	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14550_s_35	9603970	One of the most intriguing enzymes that regulate ceramide levels is the phosphatidylcholine:ceramide phosphocholine transferase (sphingomyelin synthase; SMS), which transfers the phosphocholine group from PC to ceramide generating sphingomyelin (SM) and DAG ( 27-33).	transcription
69662	8	336218	5	NULL	NULL	0	NULL	statement 6	Process		generates					DAG	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14550_s_35	9603970	One of the most intriguing enzymes that regulate ceramide levels is the phosphatidylcholine:ceramide phosphocholine transferase (sphingomyelin synthase; SMS), which transfers the phosphocholine group from PC to ceramide generating sphingomyelin (SM) and DAG ( 27-33).	transcription
69663	9	336218	5	NULL	NULL	0	NULL	SM	Chemical		is					sphingomyelin	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14550_s_35	9603970	One of the most intriguing enzymes that regulate ceramide levels is the phosphatidylcholine:ceramide phosphocholine transferase (sphingomyelin synthase; SMS), which transfers the phosphocholine group from PC to ceramide generating sphingomyelin (SM) and DAG ( 27-33).	transcription
71711	1	336218	7	NULL	NULL	0	NULL	 PC	Chemical	phosphocholine group from	transferred to					 ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14550_s_35	9603970	One of the most intriguing enzymes that regulate ceramide levels is the phosphatidylcholine:ceramide phosphocholine transferase (sphingomyelin synthase; SMS), which transfers the phosphocholine group from PC to ceramide generating sphingomyelin (SM) and DAG ( 27-33).	transcription
71712	2	336218	7	NULL	NULL	0	NULL	phosphatidylcholine:ceramide phosphocholine transferase	GP		catalyze					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14550_s_35	9603970	One of the most intriguing enzymes that regulate ceramide levels is the phosphatidylcholine:ceramide phosphocholine transferase (sphingomyelin synthase; SMS), which transfers the phosphocholine group from PC to ceramide generating sphingomyelin (SM) and DAG ( 27-33).	transcription
71713	3	336218	7	NULL	NULL	0	NULL	statement 1	Process		generate					SM	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14550_s_35	9603970	One of the most intriguing enzymes that regulate ceramide levels is the phosphatidylcholine:ceramide phosphocholine transferase (sphingomyelin synthase; SMS), which transfers the phosphocholine group from PC to ceramide generating sphingomyelin (SM) and DAG ( 27-33).	transcription
71714	4	336218	7	NULL	NULL	0	NULL	statement 1	Process		generate					DAG	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14550_s_35	9603970	One of the most intriguing enzymes that regulate ceramide levels is the phosphatidylcholine:ceramide phosphocholine transferase (sphingomyelin synthase; SMS), which transfers the phosphocholine group from PC to ceramide generating sphingomyelin (SM) and DAG ( 27-33).	transcription
71715	5	336218	7	NULL	NULL	0	NULL	SM	Chemical		is					sphingomyelin 	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14550_s_35	9603970	One of the most intriguing enzymes that regulate ceramide levels is the phosphatidylcholine:ceramide phosphocholine transferase (sphingomyelin synthase; SMS), which transfers the phosphocholine group from PC to ceramide generating sphingomyelin (SM) and DAG ( 27-33).	transcription
71716	6	336218	7	NULL	NULL	0	NULL	phosphatidylcholine:ceramide phosphocholine transferase	GP		is					SMS	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14550_s_35	9603970	One of the most intriguing enzymes that regulate ceramide levels is the phosphatidylcholine:ceramide phosphocholine transferase (sphingomyelin synthase; SMS), which transfers the phosphocholine group from PC to ceramide generating sphingomyelin (SM) and DAG ( 27-33).	transcription
71717	7	336218	7	NULL	NULL	0	NULL	SMS	GP		is					sphingomyelin synthase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_23_14550_s_35	9603970	One of the most intriguing enzymes that regulate ceramide levels is the phosphatidylcholine:ceramide phosphocholine transferase (sphingomyelin synthase; SMS), which transfers the phosphocholine group from PC to ceramide generating sphingomyelin (SM) and DAG ( 27-33).	transcription
71719	8	336218	7	NULL	NULL	NULL	NULL	SMS	GP		regulate					ceramide	Chemical	levels of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_23_14550_s_35	9603970	One of the most intriguing enzymes that regulate ceramide levels is the phosphatidylcholine:ceramide phosphocholine transferase (sphingomyelin synthase; SMS), which transfers the phosphocholine group from PC to ceramide generating sphingomyelin (SM) and DAG ( 27-33).	transcription
69665	1	336219	5	NULL	NULL	0	NULL	ceramide	Chemical		induce		potentially			programmed cell death	Process				NULL	lung cells	0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_15	15772421	Ceramide potently induces programmed cell death in lung cells and inhibits the biosynthesis of phosphatidylcholine (PtdCho), the predominant phospholipid of alveolar surfactant ( ,   -  ).	transcription
69666	2	336219	5	NULL	NULL	0	NULL	ceramide	Chemical		inhibits					PtdCho	Chemical	biosynthesis of			NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_15	15772421	Ceramide potently induces programmed cell death in lung cells and inhibits the biosynthesis of phosphatidylcholine (PtdCho), the predominant phospholipid of alveolar surfactant ( ,   -  ).	transcription
69667	3	336219	5	NULL	NULL	0	NULL	PtdCho	Chemical		is					phosphatidylcholine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_15	15772421	Ceramide potently induces programmed cell death in lung cells and inhibits the biosynthesis of phosphatidylcholine (PtdCho), the predominant phospholipid of alveolar surfactant ( ,   -  ).	transcription
69668	4	336219	5	NULL	NULL	0	NULL	PtdCho	Chemical		is a type of					phospholipid	Chemical				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_15	15772421	Ceramide potently induces programmed cell death in lung cells and inhibits the biosynthesis of phosphatidylcholine (PtdCho), the predominant phospholipid of alveolar surfactant ( ,   -  ).	transcription
69669	5	336219	5	NULL	NULL	0	NULL	PtdCho	Chemical		is predominant in					alveolar surfactant	Chemical				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_15	15772421	Ceramide potently induces programmed cell death in lung cells and inhibits the biosynthesis of phosphatidylcholine (PtdCho), the predominant phospholipid of alveolar surfactant ( ,   -  ).	transcription
71720	1	336219	7	NULL	NULL	0	NULL	Ceramide	Chemical		induce		potently			programmed cell death	Process				NULL	lung cells	0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_15	15772421	Ceramide potently induces programmed cell death in lung cells and inhibits the biosynthesis of phosphatidylcholine (PtdCho), the predominant phospholipid of alveolar surfactant ( ,   -  ).	transcription
71721	2	336219	7	NULL	NULL	0	NULL	ceramide	Chemical		inhibit					PtdCho	Chemical	biosynthesis of			NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_15	15772421	Ceramide potently induces programmed cell death in lung cells and inhibits the biosynthesis of phosphatidylcholine (PtdCho), the predominant phospholipid of alveolar surfactant ( ,   -  ).	transcription
71722	3	336219	7	NULL	NULL	0	NULL	PtdCho	Chemical		is					phosphatidylcholine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_15	15772421	Ceramide potently induces programmed cell death in lung cells and inhibits the biosynthesis of phosphatidylcholine (PtdCho), the predominant phospholipid of alveolar surfactant ( ,   -  ).	transcription
71723	4	336219	7	NULL	NULL	0	NULL	phosphatidylcholine	Chemical		phospholipid of		predominant			alveolar surfactant	Chemical				NULL		0	NULL	NULL	NULL	gw70_jlipidres_46_6_1229_s_15	15772421	Ceramide potently induces programmed cell death in lung cells and inhibits the biosynthesis of phosphatidylcholine (PtdCho), the predominant phospholipid of alveolar surfactant ( ,   -  ).	transcription
69670	1	336221	5	NULL	NULL	NULL	NULL	apoptosis	Process		is induced by					Choline	Chemical	deficiency of			NULL	PC12 cells	NULL	NULL	NULL	NULL	gw60_neuroscience_118_1_107_s_341	12676142	Choline deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase.	transcription
69671	2	336221	5	NULL	NULL	NULL	NULL	statement 1	Process		is associated with					phosphatidylcholine	Chemical	diminished;;membrane			NULL	PC12 cells	NULL	NULL	NULL	NULL	gw60_neuroscience_118_1_107_s_341	12676142	Choline deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase.	transcription
69672	3	336221	5	NULL	NULL	NULL	NULL	statement 1	Process		is associated with					sphingomyelin	Chemical	diminished;;membrane			NULL	PC12 cells	NULL	NULL	NULL	NULL	gw60_neuroscience_118_1_107_s_341	12676142	Choline deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase.	transcription
69673	4	336221	5	NULL	NULL	0	NULL	statement 1	Process		is associated with					ceramide	Chemical	accumulation of			NULL	PC12 cells	0	NULL	NULL	NULL	gw60_neuroscience_118_1_107_s_341	12676142	Choline deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase.	transcription
69674	5	336221	5	NULL	NULL	NULL	NULL	statement 1	Process		is associated with					diacylglycerol	Chemical	accumulation of			NULL	PC12 cells	NULL	NULL	NULL	NULL	gw60_neuroscience_118_1_107_s_341	12676142	Choline deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase.	transcription
69675	6	336221	5	NULL	NULL	0	NULL	statement 1	Process		is associated with					caspase	GP	activation of			NULL	PC12 cells	0	NULL	NULL	NULL	gw60_neuroscience_118_1_107_s_341	12676142	Choline deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase.	transcription
71724	1	336221	7	NULL	NULL	0	NULL	Choline	Chemical	deficiency of	induce					apoptosis	Process				NULL	PC12 cells	0	NULL	NULL	NULL	gw60_neuroscience_118_1_107_s_341	12676142	Choline deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase.	transcription
71725	2	336221	7	NULL	NULL	0	NULL	statement 1	Process		is associated with					phosphatidylcholine 	Chemical	diminished membrane			NULL		0	NULL	NULL	NULL	gw60_neuroscience_118_1_107_s_341	12676142	Choline deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase.	transcription
71726	3	336221	7	NULL	NULL	0	NULL	statement 1	Process		is associated with					 sphingomyelin	Chemical				NULL		0	NULL	NULL	NULL	gw60_neuroscience_118_1_107_s_341	12676142	Choline deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase.	transcription
71727	4	336221	7	NULL	NULL	0	NULL	statement 1	Process		is associated with					ceramide	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw60_neuroscience_118_1_107_s_341	12676142	Choline deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase.	transcription
71728	5	336221	7	NULL	NULL	NULL	NULL	statement 1	Process		associated with					diacylglycerol	Chemical	accumulation of			NULL		NULL	NULL	NULL	NULL	gw60_neuroscience_118_1_107_s_341	12676142	Choline deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase.	transcription
71729	6	336221	7	NULL	NULL	0	NULL	statement 1	Process		is associated with					caspase	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_neuroscience_118_1_107_s_341	12676142	Choline deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase.	transcription
69676	1	336222	5	NULL	NULL	0	NULL	sphingomyelin	Chemical	hydrolysis of	forms					ceramide	Chemical	biologically active;;intracellular			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_5_815_s_3	11971953	They catalyze the hydrolysis of sphingomyelin, giving rise to the intracellular formation of biologically active ceramide and phosphatidylcholine.	transcription
69677	2	336222	5	NULL	NULL	0	NULL	sphingomyelin	Chemical	hydrolysis of	forms					phosphatidylcholine	Chemical	biologically active;;intracellular			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_5_815_s_3	11971953	They catalyze the hydrolysis of sphingomyelin, giving rise to the intracellular formation of biologically active ceramide and phosphatidylcholine.	transcription
71730	1	336222	7	NULL	NULL	NULL	NULL	sphingomyelin	Chemical		hydrolyzed to					ceramide	Chemical	 intracellular formation of biologically active			NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_43_5_815_s_3	11971953	They catalyze the hydrolysis of sphingomyelin, giving rise to the intracellular formation of biologically active ceramide and phosphatidylcholine.	transcription
71731	2	336222	7	NULL	NULL	0	NULL	sphingomyelin	Chemical		hydrolyzed to					phosphatidylcholine	Chemical	 intracellular formation of biologically active			NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_5_815_s_3	11971953	They catalyze the hydrolysis of sphingomyelin, giving rise to the intracellular formation of biologically active ceramide and phosphatidylcholine.	transcription
71934	1	336223	7	NULL	NULL	NULL	NULL	sphingomyelinases	GP		hydrolyze					sphingomyelin	Chemical				NULL	intact cells	NULL	NULL	NULL	NULL	gw60_jlipidres_43_5_815_s_79	11971953	Determination of SMase-activity   phingomyelinases in intact cells hydrolyze sphingomyelin leading to the formation of ceramide and phosphatidylcholine ( 23).	transcription
71935	2	336223	7	NULL	NULL	0	NULL	statement 1	Process		forms					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jlipidres_43_5_815_s_79	11971953	Determination of SMase-activity   phingomyelinases in intact cells hydrolyze sphingomyelin leading to the formation of ceramide and phosphatidylcholine ( 23).	transcription
71936	3	336223	7	NULL	NULL	NULL	NULL	statement 1	Process		forms					phosphatidylcholine	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_jlipidres_43_5_815_s_79	11971953	Determination of SMase-activity   phingomyelinases in intact cells hydrolyze sphingomyelin leading to the formation of ceramide and phosphatidylcholine ( 23).	transcription
71937	1	336224	7	NULL	NULL	0	NULL	SMS	GP		catalyze					sphingomyelin	Chemical	production of			NULL		0	NULL	NULL	NULL	gw70_gene_363_0_123_s_173	16226406	SMS catalyzes the production of sphingomyelin and diacylglycerol (DAG) using ceramide  and phosphatidylcholine as substrates (  Hannun et al., 2001 and   Hannun and Luberto, 2004).	transcription
71938	2	336224	7	NULL	NULL	0	NULL	SMS	GP		catalyze					DAG	Chemical	production of			NULL		0	NULL	NULL	NULL	gw70_gene_363_0_123_s_173	16226406	SMS catalyzes the production of sphingomyelin and diacylglycerol (DAG) using ceramide  and phosphatidylcholine as substrates (  Hannun et al., 2001 and   Hannun and Luberto, 2004).	transcription
71939	3	336224	7	NULL	NULL	0	NULL	ceramide	Chemical		substrate for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_gene_363_0_123_s_173	16226406	SMS catalyzes the production of sphingomyelin and diacylglycerol (DAG) using ceramide  and phosphatidylcholine as substrates (  Hannun et al., 2001 and   Hannun and Luberto, 2004).	transcription
71940	4	336224	7	NULL	NULL	0	NULL	ceramide	Chemical		substrate for					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_gene_363_0_123_s_173	16226406	SMS catalyzes the production of sphingomyelin and diacylglycerol (DAG) using ceramide  and phosphatidylcholine as substrates (  Hannun et al., 2001 and   Hannun and Luberto, 2004).	transcription
71941	5	336224	7	NULL	NULL	0	NULL	phosphatidylcholine	Chemical		substrate for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_gene_363_0_123_s_173	16226406	SMS catalyzes the production of sphingomyelin and diacylglycerol (DAG) using ceramide  and phosphatidylcholine as substrates (  Hannun et al., 2001 and   Hannun and Luberto, 2004).	transcription
71942	6	336224	7	NULL	NULL	0	NULL	phosphatidylcholine	Chemical		substrate for					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_gene_363_0_123_s_173	16226406	SMS catalyzes the production of sphingomyelin and diacylglycerol (DAG) using ceramide  and phosphatidylcholine as substrates (  Hannun et al., 2001 and   Hannun and Luberto, 2004).	transcription
71943	7	336224	7	NULL	NULL	0	NULL	DAG	Chemical		is					diacylglycerol	Chemical				NULL		0	NULL	NULL	NULL	gw70_gene_363_0_123_s_173	16226406	SMS catalyzes the production of sphingomyelin and diacylglycerol (DAG) using ceramide  and phosphatidylcholine as substrates (  Hannun et al., 2001 and   Hannun and Luberto, 2004).	transcription
71944	1	336225	7	NULL	NULL	NULL	NULL	phospholipase C	GP		mediate					PC	Chemical	hydrolysis of;;membrane			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_43_27800_s_20	9774389	Second messengers such as diacylglycerol and ceramide are generated in part by phospholipase C- and sphingomyelinase-mediated hydrolysis of membrane phosphatidylcholine (PC) and sphingomyelin (SM), respectively.	transcription
71945	2	336225	7	NULL	NULL	0	NULL	sphingomyelinase	GP		mediate					SM	Chemical	hydrolysis of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_43_27800_s_20	9774389	Second messengers such as diacylglycerol and ceramide are generated in part by phospholipase C- and sphingomyelinase-mediated hydrolysis of membrane phosphatidylcholine (PC) and sphingomyelin (SM), respectively.	transcription
71946	3	336225	7	NULL	NULL	0	NULL	statement 1	Process		generate					diacylglycerol	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_43_27800_s_20	9774389	Second messengers such as diacylglycerol and ceramide are generated in part by phospholipase C- and sphingomyelinase-mediated hydrolysis of membrane phosphatidylcholine (PC) and sphingomyelin (SM), respectively.	transcription
71947	4	336225	7	NULL	NULL	0	NULL	statement 1	Process		generate					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_43_27800_s_20	9774389	Second messengers such as diacylglycerol and ceramide are generated in part by phospholipase C- and sphingomyelinase-mediated hydrolysis of membrane phosphatidylcholine (PC) and sphingomyelin (SM), respectively.	transcription
71948	5	336225	7	NULL	NULL	0	NULL	PC	Chemical		is					phosphatidylcholine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_43_27800_s_20	9774389	Second messengers such as diacylglycerol and ceramide are generated in part by phospholipase C- and sphingomyelinase-mediated hydrolysis of membrane phosphatidylcholine (PC) and sphingomyelin (SM), respectively.	transcription
71949	6	336225	7	NULL	NULL	0	NULL	SM	Chemical		is					sphingomyelin	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_43_27800_s_20	9774389	Second messengers such as diacylglycerol and ceramide are generated in part by phospholipase C- and sphingomyelinase-mediated hydrolysis of membrane phosphatidylcholine (PC) and sphingomyelin (SM), respectively.	transcription
71950	7	336225	7	NULL	NULL	0	NULL	diacylglycerol	Chemical		is a type of					secondary messenger	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_43_27800_s_20	9774389	Second messengers such as diacylglycerol and ceramide are generated in part by phospholipase C- and sphingomyelinase-mediated hydrolysis of membrane phosphatidylcholine (PC) and sphingomyelin (SM), respectively.	transcription
71951	1	336226	7	NULL	NULL	NULL	NULL	sphingomyelin	Chemical	appearance of	shows					serine ceramide pathway	Process	increase in synthetic activity of			NULL	fa/fa islets	NULL	NULL	NULL	NULL	gw60_jbiolchem_273_49_32487_s_81	9829981	The appearance of [3]sphingomyelin, [3]phosphatidylethanolamine, and [3]phosphatidylcholine were the same in  +/+ and  fa/fa islets, evidence that the increase in synthetic activity was limited to the serine   ceramide pathway.	transcription
71952	2	336226	7	NULL	NULL	0	NULL	phosphatidylethanolamine	Chemical	appearance of	shows					serine ceramide pathway	Process	increase in synthetic activity of			NULL	fa/fa islets	0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32487_s_81	9829981	The appearance of [3]sphingomyelin, [3]phosphatidylethanolamine, and [3]phosphatidylcholine were the same in  +/+ and  fa/fa islets, evidence that the increase in synthetic activity was limited to the serine   ceramide pathway.	transcription
71953	3	336226	7	NULL	NULL	0	NULL	phosphatidylcholine	Chemical	appearance of	shows					serine ceramide pathway	Process	increase in synthetic activity of			NULL	fa/fa islets	0	NULL	NULL	NULL	gw60_jbiolchem_273_49_32487_s_81	9829981	The appearance of [3]sphingomyelin, [3]phosphatidylethanolamine, and [3]phosphatidylcholine were the same in  +/+ and  fa/fa islets, evidence that the increase in synthetic activity was limited to the serine   ceramide pathway.	transcription
71954	1	336227	7	NULL	NULL	0	NULL	LPS	Chemical		induce					TLR4	GP	assembly of			NULL		0	NULL	NULL	NULL	abs-batch0740-0759_j-leukoc-biol_80_2_16754725_s_4	16754725	The purpose of this study is to determine if  LPS-induced TLR4 assembly and activation are dependent on the sphingolipid  metabolite ceramide produced by phosphatidylcholine-specific phospholipase  C (PC-PLC) or CD14.	transcription
71955	2	336227	7	NULL	NULL	0	NULL	LPS	Chemical		induce					TLR4	GP	activation of			NULL		0	NULL	NULL	NULL	abs-batch0740-0759_j-leukoc-biol_80_2_16754725_s_4	16754725	The purpose of this study is to determine if  LPS-induced TLR4 assembly and activation are dependent on the sphingolipid  metabolite ceramide produced by phosphatidylcholine-specific phospholipase  C (PC-PLC) or CD14.	transcription
72116	3	336227	7	NULL	NULL	0	NULL	PC-PLC	GP		produce					ceramide	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_j-leukoc-biol_80_2_16754725_s_4	16754725	The purpose of this study is to determine if  LPS-induced TLR4 assembly and activation are dependent on the sphingolipid  metabolite ceramide produced by phosphatidylcholine-specific phospholipase  C (PC-PLC) or CD14.	transcription
72117	4	336227	7	NULL	NULL	0	NULL	CD14	GP		produce					ceramide	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_j-leukoc-biol_80_2_16754725_s_4	16754725	The purpose of this study is to determine if  LPS-induced TLR4 assembly and activation are dependent on the sphingolipid  metabolite ceramide produced by phosphatidylcholine-specific phospholipase  C (PC-PLC) or CD14.	transcription
72118	5	336227	7	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_j-leukoc-biol_80_2_16754725_s_4	16754725	The purpose of this study is to determine if  LPS-induced TLR4 assembly and activation are dependent on the sphingolipid  metabolite ceramide produced by phosphatidylcholine-specific phospholipase  C (PC-PLC) or CD14.	transcription
72119	6	336227	7	NULL	NULL	0	NULL	PC-PLC	GP		is					phosphatidylcholine-specific phospholipase C	GP				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_j-leukoc-biol_80_2_16754725_s_4	16754725	The purpose of this study is to determine if  LPS-induced TLR4 assembly and activation are dependent on the sphingolipid  metabolite ceramide produced by phosphatidylcholine-specific phospholipase  C (PC-PLC) or CD14.	transcription
72120	7	336227	7	NULL	NULL	0	NULL	ceramide	Chemical		is a type of					sphingolipid metabolite	Chemical				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_j-leukoc-biol_80_2_16754725_s_4	16754725	The purpose of this study is to determine if  LPS-induced TLR4 assembly and activation are dependent on the sphingolipid  metabolite ceramide produced by phosphatidylcholine-specific phospholipase  C (PC-PLC) or CD14.	transcription
72121	1	336228	7	NULL	NULL	0	NULL	MAb90	GP		induce					ceramide	Chemical	production of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5060_s_79	9478956	MAb90 and YTH862 Induce Ceramide Production under the Control of a Phosphatidylcholine-specific Phospholipase C-- Okadaic acid has been reported to inhibit ceramide-induced apoptosis, possibly by blocking a ceramide-activated protein phosphatase which belongs to the heterodimeric subfamily of the phosphatases 2A group ( 40).	transcription
72122	2	336228	7	NULL	NULL	0	NULL	YTH862	GP		induce					ceramide	Chemical	production of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5060_s_79	9478956	MAb90 and YTH862 Induce Ceramide Production under the Control of a Phosphatidylcholine-specific Phospholipase C-- Okadaic acid has been reported to inhibit ceramide-induced apoptosis, possibly by blocking a ceramide-activated protein phosphatase which belongs to the heterodimeric subfamily of the phosphatases 2A group ( 40).	transcription
72123	3	336228	7	NULL	NULL	0	NULL	statement 1	Process		under the control of					Phosphatidylcholine-specific Phospholipase C	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5060_s_79	9478956	MAb90 and YTH862 Induce Ceramide Production under the Control of a Phosphatidylcholine-specific Phospholipase C-- Okadaic acid has been reported to inhibit ceramide-induced apoptosis, possibly by blocking a ceramide-activated protein phosphatase which belongs to the heterodimeric subfamily of the phosphatases 2A group ( 40).	transcription
72124	4	336228	7	NULL	NULL	0	NULL	statement 2	Process		under the control of					phosphatidylcholine-specific phospholipase C	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5060_s_79	9478956	MAb90 and YTH862 Induce Ceramide Production under the Control of a Phosphatidylcholine-specific Phospholipase C-- Okadaic acid has been reported to inhibit ceramide-induced apoptosis, possibly by blocking a ceramide-activated protein phosphatase which belongs to the heterodimeric subfamily of the phosphatases 2A group ( 40).	transcription
72125	5	336228	7	NULL	NULL	0	NULL	ceramide	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5060_s_79	9478956	MAb90 and YTH862 Induce Ceramide Production under the Control of a Phosphatidylcholine-specific Phospholipase C-- Okadaic acid has been reported to inhibit ceramide-induced apoptosis, possibly by blocking a ceramide-activated protein phosphatase which belongs to the heterodimeric subfamily of the phosphatases 2A group ( 40).	transcription
72126	6	336228	7	NULL	NULL	0	NULL	Okadaic acid	Chemical		inhibit					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5060_s_79	9478956	MAb90 and YTH862 Induce Ceramide Production under the Control of a Phosphatidylcholine-specific Phospholipase C-- Okadaic acid has been reported to inhibit ceramide-induced apoptosis, possibly by blocking a ceramide-activated protein phosphatase which belongs to the heterodimeric subfamily of the phosphatases 2A group ( 40).	transcription
72127	7	336228	7	NULL	NULL	0	NULL	statement 6	Process		occur		possibly			ceramide-activated protein phosphatase	GP	by blocking of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5060_s_79	9478956	MAb90 and YTH862 Induce Ceramide Production under the Control of a Phosphatidylcholine-specific Phospholipase C-- Okadaic acid has been reported to inhibit ceramide-induced apoptosis, possibly by blocking a ceramide-activated protein phosphatase which belongs to the heterodimeric subfamily of the phosphatases 2A group ( 40).	transcription
72128	8	336228	7	NULL	NULL	0	NULL	ceramide-activated protein phosphatase	GP		belongs to					phosphatases 2A group	GP	heterodimeric subfamily of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5060_s_79	9478956	MAb90 and YTH862 Induce Ceramide Production under the Control of a Phosphatidylcholine-specific Phospholipase C-- Okadaic acid has been reported to inhibit ceramide-induced apoptosis, possibly by blocking a ceramide-activated protein phosphatase which belongs to the heterodimeric subfamily of the phosphatases 2A group ( 40).	transcription
72129	1	336229	7	NULL	NULL	0	NULL	TNF 	GP		interacts with					TNF receptor	GP				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_14_0_649_s_387	8717528	According to the current model, the interaction of TNF with  the 55-kDa TNF receptor activates an acidic sphingomyelinase (Smase) through the  generation of diacylglycerol by a phosphatidylcholine-specific phospholipase C. Smase  leads to the production of ceramide.	transcription
72130	2	336229	7	NULL	NULL	0	NULL	statement 1	Process		activates an					Smase	GP	acidic			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_14_0_649_s_387	8717528	According to the current model, the interaction of TNF with  the 55-kDa TNF receptor activates an acidic sphingomyelinase (Smase) through the  generation of diacylglycerol by a phosphatidylcholine-specific phospholipase C. Smase  leads to the production of ceramide.	transcription
72131	3	336229	7	NULL	NULL	0	NULL	phosphatidylcholine-specific phospholipase C	GP		generates					diacylglycerol	Chemical				NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_14_0_649_s_387	8717528	According to the current model, the interaction of TNF with  the 55-kDa TNF receptor activates an acidic sphingomyelinase (Smase) through the  generation of diacylglycerol by a phosphatidylcholine-specific phospholipase C. Smase  leads to the production of ceramide.	transcription
72132	4	336229	7	NULL	NULL	0	NULL	statement 2	Process		occur through					diacylglycerol	Chemical	generation of			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_14_0_649_s_387	8717528	According to the current model, the interaction of TNF with  the 55-kDa TNF receptor activates an acidic sphingomyelinase (Smase) through the  generation of diacylglycerol by a phosphatidylcholine-specific phospholipase C. Smase  leads to the production of ceramide.	transcription
72133	5	336229	7	NULL	NULL	0	NULL	Smase	GP		leads to					ceramide	Chemical	production of			NULL		0	NULL	NULL	NULL	gw70_annurevimmunol_14_0_649_s_387	8717528	According to the current model, the interaction of TNF with  the 55-kDa TNF receptor activates an acidic sphingomyelinase (Smase) through the  generation of diacylglycerol by a phosphatidylcholine-specific phospholipase C. Smase  leads to the production of ceramide.	transcription
72134	1	336230	7	NULL	NULL	0	NULL	 Choline	Chemical	deficiency of	induce					apoptosis	Process				NULL	PC12 cells 	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_87_s_483	12531541	C.L. Yen, M.H. Mar and S.H. Zeisel , Choline deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase.	transcription
72135	2	336230	7	NULL	NULL	0	NULL	statement 1	Process		associated with					phosphatidylcholine	Chemical	diminished;; membrane			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_87_s_483	12531541	C.L. Yen, M.H. Mar and S.H. Zeisel , Choline deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase.	transcription
72136	3	336230	7	NULL	NULL	0	NULL	statement 1	Process		associated with					sphingomyelin	Chemical	diminished;; membrane			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_87_s_483	12531541	C.L. Yen, M.H. Mar and S.H. Zeisel , Choline deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase.	transcription
72137	4	336230	7	NULL	NULL	0	NULL	statement 1	Process		associated with					ceramide	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_87_s_483	12531541	C.L. Yen, M.H. Mar and S.H. Zeisel , Choline deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase.	transcription
72138	5	336230	7	NULL	NULL	0	NULL	statement 1	Process		associated with					diacylglycerol	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_87_s_483	12531541	C.L. Yen, M.H. Mar and S.H. Zeisel , Choline deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase.	transcription
72139	6	336230	7	NULL	NULL	0	NULL	statement 1	Process		associated with					caspase	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1585_2_87_s_483	12531541	C.L. Yen, M.H. Mar and S.H. Zeisel , Choline deficiency-induced apoptosis in PC12 cells is associated with diminished membrane phosphatidylcholine and sphingomyelin, accumulation of ceramide and diacylglycerol, and activation of a caspase.	transcription
72147	1	336231	7	NULL	NULL	NULL	NULL	N. gonorrhoeae	Organism		activates					PC-PLC	GP				NULL	 human epithelial cells	NULL	NULL	NULL	NULL	gw60_cell_91_5_605_s_3	9393854	Using different human  epithelial cells and primary fibroblasts, we show here an activation of the phosphatidylcholine-specific  phospholipase C (PC-PLC) and acidic sphingomyelinase (ASM) by N. gonorrhoeae, resulting in the release of diacylglycerol  and ceramide.	transcription
72148	2	336231	7	NULL	NULL	NULL	NULL	N. gonorrhoeae	Organism		activates 					ASM	GP				NULL	 human epithelial cells	NULL	NULL	NULL	NULL	gw60_cell_91_5_605_s_3	9393854	Using different human  epithelial cells and primary fibroblasts, we show here an activation of the phosphatidylcholine-specific  phospholipase C (PC-PLC) and acidic sphingomyelinase (ASM) by N. gonorrhoeae, resulting in the release of diacylglycerol  and ceramide.	transcription
72149	3	336231	7	NULL	NULL	0	NULL	N. gonorrhoeae	Organism		activates					PC-PLC	GP				NULL	primary fibroblasts	0	NULL	NULL	NULL	gw60_cell_91_5_605_s_3	9393854	Using different human  epithelial cells and primary fibroblasts, we show here an activation of the phosphatidylcholine-specific  phospholipase C (PC-PLC) and acidic sphingomyelinase (ASM) by N. gonorrhoeae, resulting in the release of diacylglycerol  and ceramide.	transcription
72150	4	336231	7	NULL	NULL	NULL	NULL	N. gonorrhoeae	Organism		activates					ASM	GP				NULL	primary fibroblasts	NULL	NULL	NULL	NULL	gw60_cell_91_5_605_s_3	9393854	Using different human  epithelial cells and primary fibroblasts, we show here an activation of the phosphatidylcholine-specific  phospholipase C (PC-PLC) and acidic sphingomyelinase (ASM) by N. gonorrhoeae, resulting in the release of diacylglycerol  and ceramide.	transcription
72151	5	336231	7	NULL	NULL	0	NULL	statement 1	Process		result in					diacylglycerol	Chemical	release of			NULL		0	NULL	NULL	NULL	gw60_cell_91_5_605_s_3	9393854	Using different human  epithelial cells and primary fibroblasts, we show here an activation of the phosphatidylcholine-specific  phospholipase C (PC-PLC) and acidic sphingomyelinase (ASM) by N. gonorrhoeae, resulting in the release of diacylglycerol  and ceramide.	transcription
72152	6	336231	7	NULL	NULL	0	NULL	statement 2	Process		result in					diacylglycerol	Chemical	release of			NULL		0	NULL	NULL	NULL	gw60_cell_91_5_605_s_3	9393854	Using different human  epithelial cells and primary fibroblasts, we show here an activation of the phosphatidylcholine-specific  phospholipase C (PC-PLC) and acidic sphingomyelinase (ASM) by N. gonorrhoeae, resulting in the release of diacylglycerol  and ceramide.	transcription
72153	7	336231	7	NULL	NULL	0	NULL	statement 3	Process		result in					diacylglycerol	Chemical	release of			NULL		0	NULL	NULL	NULL	gw60_cell_91_5_605_s_3	9393854	Using different human  epithelial cells and primary fibroblasts, we show here an activation of the phosphatidylcholine-specific  phospholipase C (PC-PLC) and acidic sphingomyelinase (ASM) by N. gonorrhoeae, resulting in the release of diacylglycerol  and ceramide.	transcription
72154	8	336231	7	NULL	NULL	0	NULL	statement 4	Process		result in					diacylglycerol	Chemical	release of			NULL		0	NULL	NULL	NULL	gw60_cell_91_5_605_s_3	9393854	Using different human  epithelial cells and primary fibroblasts, we show here an activation of the phosphatidylcholine-specific  phospholipase C (PC-PLC) and acidic sphingomyelinase (ASM) by N. gonorrhoeae, resulting in the release of diacylglycerol  and ceramide.	transcription
72155	9	336231	7	NULL	NULL	0	NULL	statement 1	Process		result in					ceramide	Chemical	release of			NULL		0	NULL	NULL	NULL	gw60_cell_91_5_605_s_3	9393854	Using different human  epithelial cells and primary fibroblasts, we show here an activation of the phosphatidylcholine-specific  phospholipase C (PC-PLC) and acidic sphingomyelinase (ASM) by N. gonorrhoeae, resulting in the release of diacylglycerol  and ceramide.	transcription
72156	10	336231	7	NULL	NULL	0	NULL	statement 2	Process		result in					ceramide	Chemical	release of			NULL		0	NULL	NULL	NULL	gw60_cell_91_5_605_s_3	9393854	Using different human  epithelial cells and primary fibroblasts, we show here an activation of the phosphatidylcholine-specific  phospholipase C (PC-PLC) and acidic sphingomyelinase (ASM) by N. gonorrhoeae, resulting in the release of diacylglycerol  and ceramide.	transcription
72157	11	336231	7	NULL	NULL	0	NULL	statement 3	Process		result in					ceramide	Chemical	release of			NULL		0	NULL	NULL	NULL	gw60_cell_91_5_605_s_3	9393854	Using different human  epithelial cells and primary fibroblasts, we show here an activation of the phosphatidylcholine-specific  phospholipase C (PC-PLC) and acidic sphingomyelinase (ASM) by N. gonorrhoeae, resulting in the release of diacylglycerol  and ceramide.	transcription
72158	12	336231	7	NULL	NULL	0	NULL	statement 4	Process		result in					ceramide	Chemical	release of			NULL		0	NULL	NULL	NULL	gw60_cell_91_5_605_s_3	9393854	Using different human  epithelial cells and primary fibroblasts, we show here an activation of the phosphatidylcholine-specific  phospholipase C (PC-PLC) and acidic sphingomyelinase (ASM) by N. gonorrhoeae, resulting in the release of diacylglycerol  and ceramide.	transcription
72159	13	336231	7	NULL	NULL	0	NULL	PC-PLC	GP		is					phosphatidylcholine-specific phospholipase C	GP				NULL		0	NULL	NULL	NULL	gw60_cell_91_5_605_s_3	9393854	Using different human  epithelial cells and primary fibroblasts, we show here an activation of the phosphatidylcholine-specific  phospholipase C (PC-PLC) and acidic sphingomyelinase (ASM) by N. gonorrhoeae, resulting in the release of diacylglycerol  and ceramide.	transcription
72160	14	336231	7	NULL	NULL	0	NULL	ASM	GP		is					acidic sphingomyelinase	GP				NULL		0	NULL	NULL	NULL	gw60_cell_91_5_605_s_3	9393854	Using different human  epithelial cells and primary fibroblasts, we show here an activation of the phosphatidylcholine-specific  phospholipase C (PC-PLC) and acidic sphingomyelinase (ASM) by N. gonorrhoeae, resulting in the release of diacylglycerol  and ceramide.	transcription
72161	1	336232	7	NULL	NULL	0	NULL	TNF-R55	GP		initiates		sequentially	C-terminal domain		phosphatidylcholine-specific phospholipase C	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_cell_86_6_937_s_12	8808629	Recent studies have identified a C-terminal domain  of TNF-R55 that sequentially initiates the activation of a phosphatidylcholine-specific phospholipase C  and an acidic sphingomyelinase (A-SMase), generating ceramide (Schutze et al., 1992   ;  Wiegmann  et al., 1994   ).	transcription
72162	2	336232	7	NULL	NULL	NULL	NULL	TNF-R55	GP		initiates		sequentially	C-terminal domain		ASMase	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_cell_86_6_937_s_12	8808629	Recent studies have identified a C-terminal domain  of TNF-R55 that sequentially initiates the activation of a phosphatidylcholine-specific phospholipase C  and an acidic sphingomyelinase (A-SMase), generating ceramide (Schutze et al., 1992   ;  Wiegmann  et al., 1994   ).	transcription
72163	3	336232	7	NULL	NULL	0	NULL	statement 1	Process		generate					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_cell_86_6_937_s_12	8808629	Recent studies have identified a C-terminal domain  of TNF-R55 that sequentially initiates the activation of a phosphatidylcholine-specific phospholipase C  and an acidic sphingomyelinase (A-SMase), generating ceramide (Schutze et al., 1992   ;  Wiegmann  et al., 1994   ).	transcription
72164	4	336232	7	NULL	NULL	0	NULL	statement 2	Process		generate					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_cell_86_6_937_s_12	8808629	Recent studies have identified a C-terminal domain  of TNF-R55 that sequentially initiates the activation of a phosphatidylcholine-specific phospholipase C  and an acidic sphingomyelinase (A-SMase), generating ceramide (Schutze et al., 1992   ;  Wiegmann  et al., 1994   ).	transcription
72165	5	336232	7	NULL	NULL	0	NULL	ASMase	GP		is					acidic sphingomyelinase	GP				NULL		0	NULL	NULL	NULL	gw60_cell_86_6_937_s_12	8808629	Recent studies have identified a C-terminal domain  of TNF-R55 that sequentially initiates the activation of a phosphatidylcholine-specific phospholipase C  and an acidic sphingomyelinase (A-SMase), generating ceramide (Schutze et al., 1992   ;  Wiegmann  et al., 1994   ).	transcription
72366	1	336234	7	NULL	NULL	NULL	NULL	phosphatidylcholine specific phospholipase	GP	stimulation of	results in					diacylglycerol	Chemical	generation of			NULL	epithelial cell lines	NULL	NULL	NULL	NULL	gw60_microbesinfect_2_7_821_s_27	10955963	Into some epithelial cell lines (e.g., Chang cells), this entry process involves a signaling pathway requiring stimulation of the phosphatidylcholine specific phospholipase and acidic sphingomyelinase which results in the generation of the second messagers diacylglycerol and ceramide, respectively [  8.	transcription
72367	2	336234	7	NULL	NULL	NULL	NULL	acidic sphingomyelinase	GP		results in					ceramide	Chemical	generation of			NULL	epithelial cell lines	NULL	NULL	NULL	NULL	gw60_microbesinfect_2_7_821_s_27	10955963	Into some epithelial cell lines (e.g., Chang cells), this entry process involves a signaling pathway requiring stimulation of the phosphatidylcholine specific phospholipase and acidic sphingomyelinase which results in the generation of the second messagers diacylglycerol and ceramide, respectively [  8.	transcription
72368	3	336234	7	NULL	NULL	NULL	NULL	diacylglycerol	Chemical		is a type of					second messagers	Chemical				NULL		NULL	NULL	NULL	NULL	gw60_microbesinfect_2_7_821_s_27	10955963	Into some epithelial cell lines (e.g., Chang cells), this entry process involves a signaling pathway requiring stimulation of the phosphatidylcholine specific phospholipase and acidic sphingomyelinase which results in the generation of the second messagers diacylglycerol and ceramide, respectively [  8.	transcription
72369	4	336234	7	NULL	NULL	0	NULL	ceramide	Chemical		is a type of					second messagers	Chemical				NULL		0	NULL	NULL	NULL	gw60_microbesinfect_2_7_821_s_27	10955963	Into some epithelial cell lines (e.g., Chang cells), this entry process involves a signaling pathway requiring stimulation of the phosphatidylcholine specific phospholipase and acidic sphingomyelinase which results in the generation of the second messagers diacylglycerol and ceramide, respectively [  8.	transcription
72370	1	336235	7	NULL	NULL	0	NULL	SM synthase	GP		catalyzes					SM biosynthesis	Process	main pathway of			NULL	mammalian cells	0	NULL	NULL	NULL	gw60_jbiolchem_276_16_12797_s_199	11278937	Since the main pathway of SM biosynthesis in mammalian cells is catalyzed by SM synthase, and this occurs primarily through the transfer of the phosphorylcholine group from phosphatidylcholine to ceramide, the reaction products are both SM and diacylglycerol ( 38,  45,  47,  64).	transcription
72371	2	336235	7	NULL	NULL	0	NULL	phosphatidylcholine	Chemical	  phosphorylcholine group	transferred to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_16_12797_s_199	11278937	Since the main pathway of SM biosynthesis in mammalian cells is catalyzed by SM synthase, and this occurs primarily through the transfer of the phosphorylcholine group from phosphatidylcholine to ceramide, the reaction products are both SM and diacylglycerol ( 38,  45,  47,  64).	transcription
72372	3	336235	7	NULL	NULL	0	NULL	statement 1	Process		occur through					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_16_12797_s_199	11278937	Since the main pathway of SM biosynthesis in mammalian cells is catalyzed by SM synthase, and this occurs primarily through the transfer of the phosphorylcholine group from phosphatidylcholine to ceramide, the reaction products are both SM and diacylglycerol ( 38,  45,  47,  64).	transcription
72373	4	336235	7	NULL	NULL	0	NULL	SM	Chemical		reaction product of					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_16_12797_s_199	11278937	Since the main pathway of SM biosynthesis in mammalian cells is catalyzed by SM synthase, and this occurs primarily through the transfer of the phosphorylcholine group from phosphatidylcholine to ceramide, the reaction products are both SM and diacylglycerol ( 38,  45,  47,  64).	transcription
72374	5	336235	7	NULL	NULL	0	NULL	diacylglycerol	Chemical		reaction product of					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_16_12797_s_199	11278937	Since the main pathway of SM biosynthesis in mammalian cells is catalyzed by SM synthase, and this occurs primarily through the transfer of the phosphorylcholine group from phosphatidylcholine to ceramide, the reaction products are both SM and diacylglycerol ( 38,  45,  47,  64).	transcription
72375	1	336236	7	NULL	NULL	0	NULL	DAG	Chemical		generated by					PC-PLC	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27730_s_24	9346915	Diacylglycerol (DAG) generated by a phosphatidylcholine-specific phospholipase C (PC-PLC) has been reported to serve as important factor of activation of A-SMase, which, through the generation of ceramide, is a co-factor for the activation of NFkappaB ( 27).	transcription
72376	2	336236	7	NULL	NULL	0	NULL	DAG	Chemical		important factor for					A-SMase	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27730_s_24	9346915	Diacylglycerol (DAG) generated by a phosphatidylcholine-specific phospholipase C (PC-PLC) has been reported to serve as important factor of activation of A-SMase, which, through the generation of ceramide, is a co-factor for the activation of NFkappaB ( 27).	transcription
72377	3	336236	7	NULL	NULL	0	NULL	 A-SMase	GP		generates					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27730_s_24	9346915	Diacylglycerol (DAG) generated by a phosphatidylcholine-specific phospholipase C (PC-PLC) has been reported to serve as important factor of activation of A-SMase, which, through the generation of ceramide, is a co-factor for the activation of NFkappaB ( 27).	transcription
72378	4	336236	7	NULL	NULL	0	NULL	ceramide	Chemical		cofactor for					NFkappaB	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27730_s_24	9346915	Diacylglycerol (DAG) generated by a phosphatidylcholine-specific phospholipase C (PC-PLC) has been reported to serve as important factor of activation of A-SMase, which, through the generation of ceramide, is a co-factor for the activation of NFkappaB ( 27).	transcription
72379	5	336236	7	NULL	NULL	0	NULL	DAG	Chemical		is					Diacylglycerol	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27730_s_24	9346915	Diacylglycerol (DAG) generated by a phosphatidylcholine-specific phospholipase C (PC-PLC) has been reported to serve as important factor of activation of A-SMase, which, through the generation of ceramide, is a co-factor for the activation of NFkappaB ( 27).	transcription
72380	6	336236	7	NULL	NULL	0	NULL	PC-PLC	GP		is					phosphatidylcholine-specific phospholipase C	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_44_27730_s_24	9346915	Diacylglycerol (DAG) generated by a phosphatidylcholine-specific phospholipase C (PC-PLC) has been reported to serve as important factor of activation of A-SMase, which, through the generation of ceramide, is a co-factor for the activation of NFkappaB ( 27).	transcription
72492	1	336237	7	NULL	NULL	0	NULL	TNF	GP		activates 					NF-kappaB	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_12_6607_s_18	9506955	For example, the phosphatidylcholine-specific phospholipase C (PC-PLC) as part of the sphingomyelin pathway upstream of the second messenger ceramide has been implicated in TNF activation of NF-kappaB ( 14).	transcription
72493	2	336237	7	NULL	NULL	0	NULL	PC-PLC	GP		implicated in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_12_6607_s_18	9506955	For example, the phosphatidylcholine-specific phospholipase C (PC-PLC) as part of the sphingomyelin pathway upstream of the second messenger ceramide has been implicated in TNF activation of NF-kappaB ( 14).	transcription
72503	3	336237	7	NULL	NULL	0	NULL	PC-PLC	GP		is part of					sphingomyelin pathway	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_12_6607_s_18	9506955	For example, the phosphatidylcholine-specific phospholipase C (PC-PLC) as part of the sphingomyelin pathway upstream of the second messenger ceramide has been implicated in TNF activation of NF-kappaB ( 14).	transcription
72504	4	336237	7	NULL	NULL	0	NULL	PC-PLC	GP		upstream of					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_12_6607_s_18	9506955	For example, the phosphatidylcholine-specific phospholipase C (PC-PLC) as part of the sphingomyelin pathway upstream of the second messenger ceramide has been implicated in TNF activation of NF-kappaB ( 14).	transcription
72505	5	336237	7	NULL	NULL	0	NULL	ceramide	Chemical		is a type of					second messenger	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_12_6607_s_18	9506955	For example, the phosphatidylcholine-specific phospholipase C (PC-PLC) as part of the sphingomyelin pathway upstream of the second messenger ceramide has been implicated in TNF activation of NF-kappaB ( 14).	transcription
72506	6	336237	7	NULL	NULL	0	NULL	PC-PLC	GP		is					phosphatidylcholine-specific phospholipase C	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_12_6607_s_18	9506955	For example, the phosphatidylcholine-specific phospholipase C (PC-PLC) as part of the sphingomyelin pathway upstream of the second messenger ceramide has been implicated in TNF activation of NF-kappaB ( 14).	transcription
72507	1	336238	7	NULL	NULL	NULL	NULL	mAb90 	GP	mouse	bind					HLA class I	GP	human	alpha 1 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_9_5060_s_4	9478956	The mouse mAb90 or the rat YTH862 monoclonal antibodies which bind the human HLA class I alpha1 domain induced the production of ceramide which was blocked by addition of the phosphatidylcholine-dependent phospholipase C inhibitor, D609.	transcription
72508	2	336238	7	NULL	NULL	NULL	NULL	YTH862	GP	rat	bind					HLA class I	Gp	human	alpha 1 domain		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_9_5060_s_4	9478956	The mouse mAb90 or the rat YTH862 monoclonal antibodies which bind the human HLA class I alpha1 domain induced the production of ceramide which was blocked by addition of the phosphatidylcholine-dependent phospholipase C inhibitor, D609.	transcription
72509	4	336238	7	NULL	NULL	NULL	NULL	statement 3	Process		induce					ceramide	Chemical	production of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_273_9_5060_s_4	9478956	The mouse mAb90 or the rat YTH862 monoclonal antibodies which bind the human HLA class I alpha1 domain induced the production of ceramide which was blocked by addition of the phosphatidylcholine-dependent phospholipase C inhibitor, D609.	transcription
72510	3	336238	7	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5060_s_4	9478956	The mouse mAb90 or the rat YTH862 monoclonal antibodies which bind the human HLA class I alpha1 domain induced the production of ceramide which was blocked by addition of the phosphatidylcholine-dependent phospholipase C inhibitor, D609.	transcription
72511	5	336238	7	NULL	NULL	0	NULL	D609	Chemical		block					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5060_s_4	9478956	The mouse mAb90 or the rat YTH862 monoclonal antibodies which bind the human HLA class I alpha1 domain induced the production of ceramide which was blocked by addition of the phosphatidylcholine-dependent phospholipase C inhibitor, D609.	transcription
72512	6	336238	7	NULL	NULL	0	NULL	D609	Chemical		is a inhibitor of					phosphatidylcholine-dependent phospholipase C	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5060_s_4	9478956	The mouse mAb90 or the rat YTH862 monoclonal antibodies which bind the human HLA class I alpha1 domain induced the production of ceramide which was blocked by addition of the phosphatidylcholine-dependent phospholipase C inhibitor, D609.	transcription
72513	7	336238	7	NULL	NULL	0	NULL	 mAb90	GP	mouse	is a type of					monoclonal antibody	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5060_s_4	9478956	The mouse mAb90 or the rat YTH862 monoclonal antibodies which bind the human HLA class I alpha1 domain induced the production of ceramide which was blocked by addition of the phosphatidylcholine-dependent phospholipase C inhibitor, D609.	transcription
72514	8	336238	7	NULL	NULL	0	NULL	YTH862	GP	rat	is a type of					monoclonal antibody	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_273_9_5060_s_4	9478956	The mouse mAb90 or the rat YTH862 monoclonal antibodies which bind the human HLA class I alpha1 domain induced the production of ceramide which was blocked by addition of the phosphatidylcholine-dependent phospholipase C inhibitor, D609.	transcription
72515	1	336239	7	NULL	NULL	0	NULL	rCTB	GP		inhibit					sphingomyelin	Chemical	synthesis of			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-immunol_175_9_16237053_s_5	16237053	First, rCTB inhibits sphingomyelin synthesis;  second, it enhances phosphatidylcholine synthesis; and third, it activates  a raft-resident neutral sphingomyelinase resembling to neutral sphingomyelinase  type 1, thus generating a transient ceramide production.	transcription
72516	2	336239	7	NULL	NULL	0	NULL	rCTB	GP		enhance					phosphatidylcholine	Chemical	synthesis of			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-immunol_175_9_16237053_s_5	16237053	First, rCTB inhibits sphingomyelin synthesis;  second, it enhances phosphatidylcholine synthesis; and third, it activates  a raft-resident neutral sphingomyelinase resembling to neutral sphingomyelinase  type 1, thus generating a transient ceramide production.	transcription
72517	3	336239	7	NULL	NULL	0	NULL	rCTB	GP		activates					sphingomyelinase	GP	raft-resident neutral 			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-immunol_175_9_16237053_s_5	16237053	First, rCTB inhibits sphingomyelin synthesis;  second, it enhances phosphatidylcholine synthesis; and third, it activates  a raft-resident neutral sphingomyelinase resembling to neutral sphingomyelinase  type 1, thus generating a transient ceramide production.	transcription
72518	4	336239	7	NULL	NULL	0	NULL	statement 3	Process		generate					ceramide	Chemical	transient production of			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-immunol_175_9_16237053_s_5	16237053	First, rCTB inhibits sphingomyelin synthesis;  second, it enhances phosphatidylcholine synthesis; and third, it activates  a raft-resident neutral sphingomyelinase resembling to neutral sphingomyelinase  type 1, thus generating a transient ceramide production.	transcription
72519	5	336239	7	NULL	NULL	0	NULL	sphingomyelinase	GP	raft-resident neutral	resemble					sphingomyelinase	GP	neutral			NULL		0	NULL	NULL	NULL	abs-batch0530-0539_j-immunol_175_9_16237053_s_5	16237053	First, rCTB inhibits sphingomyelin synthesis;  second, it enhances phosphatidylcholine synthesis; and third, it activates  a raft-resident neutral sphingomyelinase resembling to neutral sphingomyelinase  type 1, thus generating a transient ceramide production.	transcription
72520	1	336240	7	NULL	NULL	0	NULL	ceramide	Chemical		activates					intracellular pathways	Process				NULL		0	NULL	NULL	NULL	gw70_circulation_107_10_1418_s_134	12642364	Role of Sphingomyelin-Ceramide Signaling Pathway in TNF-alpha - induced Effects   To explore the potential involvement of the ceramide-activated intracellular pathways in TNF-alpha - induced ROS production and mtDNA damage, we used D609, an inhibitor of the phosphatidylcholine-specific phospholipase C pathway and hence an indirect inhibitor of acid sphingomyelinase.	transcription
72521	2	336240	7	NULL	NULL	0	NULL	TNF-alpha	GP		induce					ROS	Chemical	production of			NULL		0	NULL	NULL	NULL	gw70_circulation_107_10_1418_s_134	12642364	Role of Sphingomyelin-Ceramide Signaling Pathway in TNF-alpha - induced Effects   To explore the potential involvement of the ceramide-activated intracellular pathways in TNF-alpha - induced ROS production and mtDNA damage, we used D609, an inhibitor of the phosphatidylcholine-specific phospholipase C pathway and hence an indirect inhibitor of acid sphingomyelinase.	transcription
72522	3	336240	7	NULL	NULL	0	NULL	TNF-alpha	GP		induce					mtDNA	NucleicAcid	damage of			NULL		0	NULL	NULL	NULL	gw70_circulation_107_10_1418_s_134	12642364	Role of Sphingomyelin-Ceramide Signaling Pathway in TNF-alpha - induced Effects   To explore the potential involvement of the ceramide-activated intracellular pathways in TNF-alpha - induced ROS production and mtDNA damage, we used D609, an inhibitor of the phosphatidylcholine-specific phospholipase C pathway and hence an indirect inhibitor of acid sphingomyelinase.	transcription
72523	4	336240	7	NULL	NULL	0	NULL	D609	Chemical		is a inhibitor of					phosphatidylcholine-specific phospholipase C pathway 	Process				NULL		0	NULL	NULL	NULL	gw70_circulation_107_10_1418_s_134	12642364	Role of Sphingomyelin-Ceramide Signaling Pathway in TNF-alpha - induced Effects   To explore the potential involvement of the ceramide-activated intracellular pathways in TNF-alpha - induced ROS production and mtDNA damage, we used D609, an inhibitor of the phosphatidylcholine-specific phospholipase C pathway and hence an indirect inhibitor of acid sphingomyelinase.	transcription
72524	5	336240	7	NULL	NULL	0	NULL	D609	Chemical		inhibitor of		indirect			acid sphingomyelinase	GP				NULL		0	NULL	NULL	NULL	gw70_circulation_107_10_1418_s_134	12642364	Role of Sphingomyelin-Ceramide Signaling Pathway in TNF-alpha - induced Effects   To explore the potential involvement of the ceramide-activated intracellular pathways in TNF-alpha - induced ROS production and mtDNA damage, we used D609, an inhibitor of the phosphatidylcholine-specific phospholipase C pathway and hence an indirect inhibitor of acid sphingomyelinase.	transcription
72525	1	336241	7	NULL	NULL	0	NULL	HS	PhysicalPhenomenon		induce					ceramide	Chemical	generation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_11_7668_s_262	10713077	These results strongly suggested the involvement of sphingomyelinase activation in HS-induced ceramide generation, even though it is unable to eliminate completely the role of other enzymes including phospholipase D type of sphingomyelinase and ceramide:phosphatidylcholine phosphocholine transferase in HS-induced apoptosis.	transcription
72526	2	336241	7	NULL	NULL	0	NULL	sphingomyelinase	GP	activation of	occur in					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_11_7668_s_262	10713077	These results strongly suggested the involvement of sphingomyelinase activation in HS-induced ceramide generation, even though it is unable to eliminate completely the role of other enzymes including phospholipase D type of sphingomyelinase and ceramide:phosphatidylcholine phosphocholine transferase in HS-induced apoptosis.	transcription
72527	3	336241	7	NULL	NULL	0	NULL	HS	PhysicalPhenomenon		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_11_7668_s_262	10713077	These results strongly suggested the involvement of sphingomyelinase activation in HS-induced ceramide generation, even though it is unable to eliminate completely the role of other enzymes including phospholipase D type of sphingomyelinase and ceramide:phosphatidylcholine phosphocholine transferase in HS-induced apoptosis.	transcription
72528	4	336241	7	NULL	NULL	0	NULL	phospholipase D type of sphingomyelinase	GP		is involved in					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_11_7668_s_262	10713077	These results strongly suggested the involvement of sphingomyelinase activation in HS-induced ceramide generation, even though it is unable to eliminate completely the role of other enzymes including phospholipase D type of sphingomyelinase and ceramide:phosphatidylcholine phosphocholine transferase in HS-induced apoptosis.	transcription
72529	5	336241	7	NULL	NULL	0	NULL	ceramide:phosphatidylcholine phosphocholine transferase	GP		is involved in					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_11_7668_s_262	10713077	These results strongly suggested the involvement of sphingomyelinase activation in HS-induced ceramide generation, even though it is unable to eliminate completely the role of other enzymes including phospholipase D type of sphingomyelinase and ceramide:phosphatidylcholine phosphocholine transferase in HS-induced apoptosis.	transcription
72530	1	336242	7	NULL	NULL	0	NULL	Choline	Chemical	deficiency of	induce					apoptosis	Process				NULL	pc12 cells 	0	NULL	NULL	NULL	gw70_brainresmolbrainres_134_2_309_s_513	15836926	[75] C.L. Yen, M.H. Mar and S.H. Zeisel, Choline deficiency-induced apoptosis in pc12  cells is associated with diminished membrane phosphatidylcholine and sphingomyelin,  accumulation of ceramide and diacylglycerol, and activation of a caspase,  FASEB J. 13 (1999), pp. 135-142.	transcription
72531	2	336242	7	NULL	NULL	0	NULL	statement 1	Process		associated with					 phosphatidylcholine	Chemical	diminished;; membrane			NULL		0	NULL	NULL	NULL	gw70_brainresmolbrainres_134_2_309_s_513	15836926	[75] C.L. Yen, M.H. Mar and S.H. Zeisel, Choline deficiency-induced apoptosis in pc12  cells is associated with diminished membrane phosphatidylcholine and sphingomyelin,  accumulation of ceramide and diacylglycerol, and activation of a caspase,  FASEB J. 13 (1999), pp. 135-142.	transcription
72532	3	336242	7	NULL	NULL	0	NULL	statement 1	Process		associated with					sphingomyelin	Chemical	diminished;; membrane			NULL		0	NULL	NULL	NULL	gw70_brainresmolbrainres_134_2_309_s_513	15836926	[75] C.L. Yen, M.H. Mar and S.H. Zeisel, Choline deficiency-induced apoptosis in pc12  cells is associated with diminished membrane phosphatidylcholine and sphingomyelin,  accumulation of ceramide and diacylglycerol, and activation of a caspase,  FASEB J. 13 (1999), pp. 135-142.	transcription
72533	4	336242	7	NULL	NULL	0	NULL	statement 1	Process		associated with					ceramide	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw70_brainresmolbrainres_134_2_309_s_513	15836926	[75] C.L. Yen, M.H. Mar and S.H. Zeisel, Choline deficiency-induced apoptosis in pc12  cells is associated with diminished membrane phosphatidylcholine and sphingomyelin,  accumulation of ceramide and diacylglycerol, and activation of a caspase,  FASEB J. 13 (1999), pp. 135-142.	transcription
72534	5	336242	7	NULL	NULL	0	NULL	statement 1	Process		associated with					diacylglycerol	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	gw70_brainresmolbrainres_134_2_309_s_513	15836926	[75] C.L. Yen, M.H. Mar and S.H. Zeisel, Choline deficiency-induced apoptosis in pc12  cells is associated with diminished membrane phosphatidylcholine and sphingomyelin,  accumulation of ceramide and diacylglycerol, and activation of a caspase,  FASEB J. 13 (1999), pp. 135-142.	transcription
72535	6	336242	7	NULL	NULL	0	NULL	statement 1	Process		associated with					caspase	GP	activation of			NULL		0	NULL	NULL	NULL	gw70_brainresmolbrainres_134_2_309_s_513	15836926	[75] C.L. Yen, M.H. Mar and S.H. Zeisel, Choline deficiency-induced apoptosis in pc12  cells is associated with diminished membrane phosphatidylcholine and sphingomyelin,  accumulation of ceramide and diacylglycerol, and activation of a caspase,  FASEB J. 13 (1999), pp. 135-142.	transcription
72536	1	336243	7	NULL	NULL	0	NULL	CD1b 	GP		bind		strongly			phosphatidylcholine	Chemical	NBD-labeled			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_1_299_s_6	14551186	Whereas group 1 CD1 isoforms (CD1b and CD1c) show stronger binding of nitrobenzoxadiazole (NBD)-labeled dialkyl-based ligands (phosphatidylcholine, sphingomyelin, and ceramide), group 2 CD1 (CD1d) proteins were stronger binders of small hydrophobic probes such as 1-anilinonaphthalene-8-sulfonic acid and 4,4''-dianilino-1,1''-naphthyl-5,5''-disulfonic acid.	transcription
72537	2	336243	7	NULL	NULL	NULL	NULL	CD1b	GP		bind		strongly			sphingomyelin	Chemical	NBD-labeled			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_1_299_s_6	14551186	Whereas group 1 CD1 isoforms (CD1b and CD1c) show stronger binding of nitrobenzoxadiazole (NBD)-labeled dialkyl-based ligands (phosphatidylcholine, sphingomyelin, and ceramide), group 2 CD1 (CD1d) proteins were stronger binders of small hydrophobic probes such as 1-anilinonaphthalene-8-sulfonic acid and 4,4''-dianilino-1,1''-naphthyl-5,5''-disulfonic acid.	transcription
72538	3	336243	7	NULL	NULL	0	NULL	CD1b	GP		bind		strongly			ceramide	Chemical	NBD-labeled			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_1_299_s_6	14551186	Whereas group 1 CD1 isoforms (CD1b and CD1c) show stronger binding of nitrobenzoxadiazole (NBD)-labeled dialkyl-based ligands (phosphatidylcholine, sphingomyelin, and ceramide), group 2 CD1 (CD1d) proteins were stronger binders of small hydrophobic probes such as 1-anilinonaphthalene-8-sulfonic acid and 4,4''-dianilino-1,1''-naphthyl-5,5''-disulfonic acid.	transcription
72539	4	336243	7	NULL	NULL	0	NULL	NBD	Chemical		is					nitrobenzoxadiazole	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_1_299_s_6	14551186	Whereas group 1 CD1 isoforms (CD1b and CD1c) show stronger binding of nitrobenzoxadiazole (NBD)-labeled dialkyl-based ligands (phosphatidylcholine, sphingomyelin, and ceramide), group 2 CD1 (CD1d) proteins were stronger binders of small hydrophobic probes such as 1-anilinonaphthalene-8-sulfonic acid and 4,4''-dianilino-1,1''-naphthyl-5,5''-disulfonic acid.	transcription
72540	5	336243	7	NULL	NULL	0	NULL	CD1c	GP		bind		strongly			phosphatidylcholine	Chemical	NBD-labeled			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_1_299_s_6	14551186	Whereas group 1 CD1 isoforms (CD1b and CD1c) show stronger binding of nitrobenzoxadiazole (NBD)-labeled dialkyl-based ligands (phosphatidylcholine, sphingomyelin, and ceramide), group 2 CD1 (CD1d) proteins were stronger binders of small hydrophobic probes such as 1-anilinonaphthalene-8-sulfonic acid and 4,4''-dianilino-1,1''-naphthyl-5,5''-disulfonic acid.	transcription
72541	6	336243	7	NULL	NULL	0	NULL	CD1c	GP		bind		strongly			sphingomyelin	Chemical	NBD-labeled			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_1_299_s_6	14551186	Whereas group 1 CD1 isoforms (CD1b and CD1c) show stronger binding of nitrobenzoxadiazole (NBD)-labeled dialkyl-based ligands (phosphatidylcholine, sphingomyelin, and ceramide), group 2 CD1 (CD1d) proteins were stronger binders of small hydrophobic probes such as 1-anilinonaphthalene-8-sulfonic acid and 4,4''-dianilino-1,1''-naphthyl-5,5''-disulfonic acid.	transcription
72542	7	336243	7	NULL	NULL	0	NULL	CD1c	GP		bind		strongly			ceramide	Chemical	NBD-labeled			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_1_299_s_6	14551186	Whereas group 1 CD1 isoforms (CD1b and CD1c) show stronger binding of nitrobenzoxadiazole (NBD)-labeled dialkyl-based ligands (phosphatidylcholine, sphingomyelin, and ceramide), group 2 CD1 (CD1d) proteins were stronger binders of small hydrophobic probes such as 1-anilinonaphthalene-8-sulfonic acid and 4,4''-dianilino-1,1''-naphthyl-5,5''-disulfonic acid.	transcription
72543	8	336243	7	NULL	NULL	0	NULL	CD1d	GP		bind		strongly			1-anilinonaphthalene-8-sulfonic acid	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_1_299_s_6	14551186	Whereas group 1 CD1 isoforms (CD1b and CD1c) show stronger binding of nitrobenzoxadiazole (NBD)-labeled dialkyl-based ligands (phosphatidylcholine, sphingomyelin, and ceramide), group 2 CD1 (CD1d) proteins were stronger binders of small hydrophobic probes such as 1-anilinonaphthalene-8-sulfonic acid and 4,4''-dianilino-1,1''-naphthyl-5,5''-disulfonic acid.	transcription
72544	9	336243	7	NULL	NULL	0	NULL	CD1d	GP		bind		strongly			4,4''-dianilino-1,1''-naphthyl-5,5''-disulfonic acid	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_1_299_s_6	14551186	Whereas group 1 CD1 isoforms (CD1b and CD1c) show stronger binding of nitrobenzoxadiazole (NBD)-labeled dialkyl-based ligands (phosphatidylcholine, sphingomyelin, and ceramide), group 2 CD1 (CD1d) proteins were stronger binders of small hydrophobic probes such as 1-anilinonaphthalene-8-sulfonic acid and 4,4''-dianilino-1,1''-naphthyl-5,5''-disulfonic acid.	transcription
72545	10	336243	7	NULL	NULL	0	NULL	phosphatidylcholine	Chemical		is a type of					dialkyl-based ligands 	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_1_299_s_6	14551186	Whereas group 1 CD1 isoforms (CD1b and CD1c) show stronger binding of nitrobenzoxadiazole (NBD)-labeled dialkyl-based ligands (phosphatidylcholine, sphingomyelin, and ceramide), group 2 CD1 (CD1d) proteins were stronger binders of small hydrophobic probes such as 1-anilinonaphthalene-8-sulfonic acid and 4,4''-dianilino-1,1''-naphthyl-5,5''-disulfonic acid.	transcription
72546	11	336243	7	NULL	NULL	0	NULL	sphingomyelin	Chemical		is a type of					dialkyl-based ligands 	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_1_299_s_6	14551186	Whereas group 1 CD1 isoforms (CD1b and CD1c) show stronger binding of nitrobenzoxadiazole (NBD)-labeled dialkyl-based ligands (phosphatidylcholine, sphingomyelin, and ceramide), group 2 CD1 (CD1d) proteins were stronger binders of small hydrophobic probes such as 1-anilinonaphthalene-8-sulfonic acid and 4,4''-dianilino-1,1''-naphthyl-5,5''-disulfonic acid.	transcription
72547	12	336243	7	NULL	NULL	0	NULL	ceramide	Chemical		is a type of					dialkyl-based ligands 	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_1_299_s_6	14551186	Whereas group 1 CD1 isoforms (CD1b and CD1c) show stronger binding of nitrobenzoxadiazole (NBD)-labeled dialkyl-based ligands (phosphatidylcholine, sphingomyelin, and ceramide), group 2 CD1 (CD1d) proteins were stronger binders of small hydrophobic probes such as 1-anilinonaphthalene-8-sulfonic acid and 4,4''-dianilino-1,1''-naphthyl-5,5''-disulfonic acid.	transcription
72548	13	336243	7	NULL	NULL	0	NULL	1-anilinonaphthalene-8-sulfonic acid 	Chemical		is a type of					small hydrophobic probes	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_1_299_s_6	14551186	Whereas group 1 CD1 isoforms (CD1b and CD1c) show stronger binding of nitrobenzoxadiazole (NBD)-labeled dialkyl-based ligands (phosphatidylcholine, sphingomyelin, and ceramide), group 2 CD1 (CD1d) proteins were stronger binders of small hydrophobic probes such as 1-anilinonaphthalene-8-sulfonic acid and 4,4''-dianilino-1,1''-naphthyl-5,5''-disulfonic acid.	transcription
72549	14	336243	7	NULL	NULL	0	NULL	4,4''-dianilino-1,1''-naphthyl-5,5''-disulfonic acid	Chemical		is a type of					small hydrophobic probes	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_1_299_s_6	14551186	Whereas group 1 CD1 isoforms (CD1b and CD1c) show stronger binding of nitrobenzoxadiazole (NBD)-labeled dialkyl-based ligands (phosphatidylcholine, sphingomyelin, and ceramide), group 2 CD1 (CD1d) proteins were stronger binders of small hydrophobic probes such as 1-anilinonaphthalene-8-sulfonic acid and 4,4''-dianilino-1,1''-naphthyl-5,5''-disulfonic acid.	transcription
72550	15	336243	7	NULL	NULL	0	NULL	CD1b	GP		is a type of					CD1 isoform	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_1_299_s_6	14551186	Whereas group 1 CD1 isoforms (CD1b and CD1c) show stronger binding of nitrobenzoxadiazole (NBD)-labeled dialkyl-based ligands (phosphatidylcholine, sphingomyelin, and ceramide), group 2 CD1 (CD1d) proteins were stronger binders of small hydrophobic probes such as 1-anilinonaphthalene-8-sulfonic acid and 4,4''-dianilino-1,1''-naphthyl-5,5''-disulfonic acid.	transcription
72551	16	336243	7	NULL	NULL	0	NULL	CD1c	GP		is a type of					CD1 isoform	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_1_299_s_6	14551186	Whereas group 1 CD1 isoforms (CD1b and CD1c) show stronger binding of nitrobenzoxadiazole (NBD)-labeled dialkyl-based ligands (phosphatidylcholine, sphingomyelin, and ceramide), group 2 CD1 (CD1d) proteins were stronger binders of small hydrophobic probes such as 1-anilinonaphthalene-8-sulfonic acid and 4,4''-dianilino-1,1''-naphthyl-5,5''-disulfonic acid.	transcription
72552	1	336244	7	NULL	NULL	0	NULL	ceramide	Chemical	generation of	derived from					sphingomyelin	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_55_1_118_s_3	9882705	The present study demonstrates that clinically relevant concentrations of the chemotherapeutic drugs daunorubicin and mitoxantrone (0.2-1 muM) transiently stimulated concurrently with sphingomyelin-derived ceramide generation and diacylglycerol and phosphorylcholine production within 4 to 10 min via phospholipase C hydrolysis of phosphatidylcholine.	transcription
72553	2	336244	7	NULL	NULL	NULL	NULL	daunorubicin	Chemical		stimulate		transiently			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_55_1_118_s_3	9882705	The present study demonstrates that clinically relevant concentrations of the chemotherapeutic drugs daunorubicin and mitoxantrone (0.2-1 muM) transiently stimulated concurrently with sphingomyelin-derived ceramide generation and diacylglycerol and phosphorylcholine production within 4 to 10 min via phospholipase C hydrolysis of phosphatidylcholine.	transcription
72554	3	336244	7	NULL	NULL	0	NULL	mitoxantrone	Chemical		stimulate		transiently			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_55_1_118_s_3	9882705	The present study demonstrates that clinically relevant concentrations of the chemotherapeutic drugs daunorubicin and mitoxantrone (0.2-1 muM) transiently stimulated concurrently with sphingomyelin-derived ceramide generation and diacylglycerol and phosphorylcholine production within 4 to 10 min via phospholipase C hydrolysis of phosphatidylcholine.	transcription
72555	4	336244	7	NULL	NULL	0	NULL	daunorubicin	Chemical		stimulate		transiently			diacylglycerol	Chemical	production of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_55_1_118_s_3	9882705	The present study demonstrates that clinically relevant concentrations of the chemotherapeutic drugs daunorubicin and mitoxantrone (0.2-1 muM) transiently stimulated concurrently with sphingomyelin-derived ceramide generation and diacylglycerol and phosphorylcholine production within 4 to 10 min via phospholipase C hydrolysis of phosphatidylcholine.	transcription
72556	5	336244	7	NULL	NULL	NULL	NULL	mitoxantrone	Chemical		stimulate		transiently			diacylglycerol	Chemical	production of			NULL		NULL	NULL	NULL	NULL	gw60_molpharmacol_55_1_118_s_3	9882705	The present study demonstrates that clinically relevant concentrations of the chemotherapeutic drugs daunorubicin and mitoxantrone (0.2-1 muM) transiently stimulated concurrently with sphingomyelin-derived ceramide generation and diacylglycerol and phosphorylcholine production within 4 to 10 min via phospholipase C hydrolysis of phosphatidylcholine.	transcription
72557	6	336244	7	NULL	NULL	0	NULL	daunorubicin	Chemical		stimulate		transiently			phosphoryl choline	Chemical	production of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_55_1_118_s_3	9882705	The present study demonstrates that clinically relevant concentrations of the chemotherapeutic drugs daunorubicin and mitoxantrone (0.2-1 muM) transiently stimulated concurrently with sphingomyelin-derived ceramide generation and diacylglycerol and phosphorylcholine production within 4 to 10 min via phospholipase C hydrolysis of phosphatidylcholine.	transcription
72558	7	336244	7	NULL	NULL	0	NULL	mitoxantrone	Chemical		stimulate		transiently			phosphoryl choline	Chemical	production of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_55_1_118_s_3	9882705	The present study demonstrates that clinically relevant concentrations of the chemotherapeutic drugs daunorubicin and mitoxantrone (0.2-1 muM) transiently stimulated concurrently with sphingomyelin-derived ceramide generation and diacylglycerol and phosphorylcholine production within 4 to 10 min via phospholipase C hydrolysis of phosphatidylcholine.	transcription
72559	8	336244	7	NULL	NULL	0	NULL	 phospholipase C 	GP		hydrolyze					phosphatidylcholine	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_55_1_118_s_3	9882705	The present study demonstrates that clinically relevant concentrations of the chemotherapeutic drugs daunorubicin and mitoxantrone (0.2-1 muM) transiently stimulated concurrently with sphingomyelin-derived ceramide generation and diacylglycerol and phosphorylcholine production within 4 to 10 min via phospholipase C hydrolysis of phosphatidylcholine.	transcription
72560	9	336244	7	NULL	NULL	0	NULL	phosphoryl choline	Chemical	production of	occur via					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_55_1_118_s_3	9882705	The present study demonstrates that clinically relevant concentrations of the chemotherapeutic drugs daunorubicin and mitoxantrone (0.2-1 muM) transiently stimulated concurrently with sphingomyelin-derived ceramide generation and diacylglycerol and phosphorylcholine production within 4 to 10 min via phospholipase C hydrolysis of phosphatidylcholine.	transcription
72561	10	336244	7	NULL	NULL	0	NULL	daunorubicin 	Chemical		is a type of					chemotherapeutic drug	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_55_1_118_s_3	9882705	The present study demonstrates that clinically relevant concentrations of the chemotherapeutic drugs daunorubicin and mitoxantrone (0.2-1 muM) transiently stimulated concurrently with sphingomyelin-derived ceramide generation and diacylglycerol and phosphorylcholine production within 4 to 10 min via phospholipase C hydrolysis of phosphatidylcholine.	transcription
72562	11	336244	7	NULL	NULL	0	NULL	mitoxantrone	Chemical		is a type of					chemotherapeutic drug	Chemical				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_55_1_118_s_3	9882705	The present study demonstrates that clinically relevant concentrations of the chemotherapeutic drugs daunorubicin and mitoxantrone (0.2-1 muM) transiently stimulated concurrently with sphingomyelin-derived ceramide generation and diacylglycerol and phosphorylcholine production within 4 to 10 min via phospholipase C hydrolysis of phosphatidylcholine.	transcription
72563	1	336245	7	NULL	NULL	0	NULL	TNF-alpha	GP		induce					transduction pathway	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_32_30527_s_37	11390371	The TNF-alpha-induced transduction pathway leading to activation of NF-kappaB has also been proposed to involve phosphatidylcholine-specific phospholipase C ( 37), sphingomyelinase ( 38,  39), and protein kinase C zeta activated by ceramide ( 40).	transcription
72564	2	336245	7	NULL	NULL	0	NULL	statement 1	Process		leads to					NF-kappaB	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_32_30527_s_37	11390371	The TNF-alpha-induced transduction pathway leading to activation of NF-kappaB has also been proposed to involve phosphatidylcholine-specific phospholipase C ( 37), sphingomyelinase ( 38,  39), and protein kinase C zeta activated by ceramide ( 40).	transcription
72565	3	336245	7	NULL	NULL	0	NULL	statement 2	Process		involve					phosphatidylcholine-specific phospholipase C	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_32_30527_s_37	11390371	The TNF-alpha-induced transduction pathway leading to activation of NF-kappaB has also been proposed to involve phosphatidylcholine-specific phospholipase C ( 37), sphingomyelinase ( 38,  39), and protein kinase C zeta activated by ceramide ( 40).	transcription
72566	4	336245	7	NULL	NULL	0	NULL	statement 2	Process		involve					sphingomyelinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_32_30527_s_37	11390371	The TNF-alpha-induced transduction pathway leading to activation of NF-kappaB has also been proposed to involve phosphatidylcholine-specific phospholipase C ( 37), sphingomyelinase ( 38,  39), and protein kinase C zeta activated by ceramide ( 40).	transcription
72567	5	336245	7	NULL	NULL	0	NULL	ceramide	Chemical		activate					protein kinase C zeta 	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_32_30527_s_37	11390371	The TNF-alpha-induced transduction pathway leading to activation of NF-kappaB has also been proposed to involve phosphatidylcholine-specific phospholipase C ( 37), sphingomyelinase ( 38,  39), and protein kinase C zeta activated by ceramide ( 40).	transcription
72568	6	336245	7	NULL	NULL	0	NULL	statement 2	Process		involve					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_32_30527_s_37	11390371	The TNF-alpha-induced transduction pathway leading to activation of NF-kappaB has also been proposed to involve phosphatidylcholine-specific phospholipase C ( 37), sphingomyelinase ( 38,  39), and protein kinase C zeta activated by ceramide ( 40).	transcription
72569	1	336246	7	NULL	NULL	NULL	NULL	enzyme systems	GP	Membrane-associated	transmit					TR55 signals	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_15_10203_s_23	10187805	Membrane-associated enzyme systems transmitting TR55 signals include plasmamembrane-bound phospholipases such as phosphatidylcholine-specific phospholipase C ( 25), which generates the lipid second messenger molecule 1,2-diacylglycerol and a N-SMase ( 9), producing ceramide by sphingomyelin hydrolysis.	transcription
72570	2	336246	7	NULL	NULL	0	NULL	statement 1	Process		include					phosphatidylcholine-specific phospholipase C	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_15_10203_s_23	10187805	Membrane-associated enzyme systems transmitting TR55 signals include plasmamembrane-bound phospholipases such as phosphatidylcholine-specific phospholipase C ( 25), which generates the lipid second messenger molecule 1,2-diacylglycerol and a N-SMase ( 9), producing ceramide by sphingomyelin hydrolysis.	transcription
72571	3	336246	7	NULL	NULL	0	NULL	phosphatidylcholine-specific phospholipase C	GP		generate					1,2-diacylglycerol 	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_15_10203_s_23	10187805	Membrane-associated enzyme systems transmitting TR55 signals include plasmamembrane-bound phospholipases such as phosphatidylcholine-specific phospholipase C ( 25), which generates the lipid second messenger molecule 1,2-diacylglycerol and a N-SMase ( 9), producing ceramide by sphingomyelin hydrolysis.	transcription
72572	4	336246	7	NULL	NULL	0	NULL	phosphatidylcholine-specific phospholipase C 	GP		generates					N-SMase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_15_10203_s_23	10187805	Membrane-associated enzyme systems transmitting TR55 signals include plasmamembrane-bound phospholipases such as phosphatidylcholine-specific phospholipase C ( 25), which generates the lipid second messenger molecule 1,2-diacylglycerol and a N-SMase ( 9), producing ceramide by sphingomyelin hydrolysis.	transcription
72573	5	336246	7	NULL	NULL	0	NULL	sphingomyelin	Chemical		hydrolyzed to					ceramide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_15_10203_s_23	10187805	Membrane-associated enzyme systems transmitting TR55 signals include plasmamembrane-bound phospholipases such as phosphatidylcholine-specific phospholipase C ( 25), which generates the lipid second messenger molecule 1,2-diacylglycerol and a N-SMase ( 9), producing ceramide by sphingomyelin hydrolysis.	transcription
72574	6	336246	7	NULL	NULL	0	NULL	 N-SMase	GP		produce					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_15_10203_s_23	10187805	Membrane-associated enzyme systems transmitting TR55 signals include plasmamembrane-bound phospholipases such as phosphatidylcholine-specific phospholipase C ( 25), which generates the lipid second messenger molecule 1,2-diacylglycerol and a N-SMase ( 9), producing ceramide by sphingomyelin hydrolysis.	transcription
72575	7	336246	7	NULL	NULL	0	NULL	 phosphatidylcholine-specific phospholipase C	GP		is a type of					plasmamembrane-bound phospholipases 	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_15_10203_s_23	10187805	Membrane-associated enzyme systems transmitting TR55 signals include plasmamembrane-bound phospholipases such as phosphatidylcholine-specific phospholipase C ( 25), which generates the lipid second messenger molecule 1,2-diacylglycerol and a N-SMase ( 9), producing ceramide by sphingomyelin hydrolysis.	transcription
72576	8	336246	7	NULL	NULL	0	NULL	1,2-diacylglycerol	Chemical		is a type of					lipid second messenger molecule	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_15_10203_s_23	10187805	Membrane-associated enzyme systems transmitting TR55 signals include plasmamembrane-bound phospholipases such as phosphatidylcholine-specific phospholipase C ( 25), which generates the lipid second messenger molecule 1,2-diacylglycerol and a N-SMase ( 9), producing ceramide by sphingomyelin hydrolysis.	transcription
72577	1	336247	7	NULL	NULL	0	NULL	PDMP	Chemical		inhibitor of					 glucosylceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_10_5480_s_98	10792026	Cells were treated with PDMP (10 muM), an inhibitor of glucosylceramide synthase that leads to increased ceramide concentrations ( 19); D609 (25 mug/ml), which inhibits acidic sphingomyelinase activity via inhibition of the phosphatidylcholine-specific phospholipase C ( 20); or fumonisin B1 (3 muM), an inhibitor of ceramide synthase and TNF-alpha-induced apoptosis ( 21).	transcription
72578	2	336247	7	NULL	NULL	0	NULL	statement 1	Process		leads to					ceramide	Chemical	increased			NULL		0	NULL	NULL	NULL	gw60_pnas_97_10_5480_s_98	10792026	Cells were treated with PDMP (10 muM), an inhibitor of glucosylceramide synthase that leads to increased ceramide concentrations ( 19); D609 (25 mug/ml), which inhibits acidic sphingomyelinase activity via inhibition of the phosphatidylcholine-specific phospholipase C ( 20); or fumonisin B1 (3 muM), an inhibitor of ceramide synthase and TNF-alpha-induced apoptosis ( 21).	transcription
72579	3	336247	7	NULL	NULL	0	NULL	statement 2	Process		inhibit					acidic sphingomyelinase	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_pnas_97_10_5480_s_98	10792026	Cells were treated with PDMP (10 muM), an inhibitor of glucosylceramide synthase that leads to increased ceramide concentrations ( 19); D609 (25 mug/ml), which inhibits acidic sphingomyelinase activity via inhibition of the phosphatidylcholine-specific phospholipase C ( 20); or fumonisin B1 (3 muM), an inhibitor of ceramide synthase and TNF-alpha-induced apoptosis ( 21).	transcription
72580	4	336247	7	NULL	NULL	NULL	NULL	statement 3	Process		occur via 					phosphatidylcholine-specific phospholipase C 	GP	inhibition of			NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_10_5480_s_98	10792026	Cells were treated with PDMP (10 muM), an inhibitor of glucosylceramide synthase that leads to increased ceramide concentrations ( 19); D609 (25 mug/ml), which inhibits acidic sphingomyelinase activity via inhibition of the phosphatidylcholine-specific phospholipase C ( 20); or fumonisin B1 (3 muM), an inhibitor of ceramide synthase and TNF-alpha-induced apoptosis ( 21).	transcription
72581	5	336247	7	NULL	NULL	0	NULL	fumonisin B1	Chemical		is an inhibitor of					ceramide synthase	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_10_5480_s_98	10792026	Cells were treated with PDMP (10 muM), an inhibitor of glucosylceramide synthase that leads to increased ceramide concentrations ( 19); D609 (25 mug/ml), which inhibits acidic sphingomyelinase activity via inhibition of the phosphatidylcholine-specific phospholipase C ( 20); or fumonisin B1 (3 muM), an inhibitor of ceramide synthase and TNF-alpha-induced apoptosis ( 21).	transcription
72582	6	336247	7	NULL	NULL	0	NULL	TNF-alpha	GP		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_97_10_5480_s_98	10792026	Cells were treated with PDMP (10 muM), an inhibitor of glucosylceramide synthase that leads to increased ceramide concentrations ( 19); D609 (25 mug/ml), which inhibits acidic sphingomyelinase activity via inhibition of the phosphatidylcholine-specific phospholipase C ( 20); or fumonisin B1 (3 muM), an inhibitor of ceramide synthase and TNF-alpha-induced apoptosis ( 21).	transcription
72583	7	336247	7	NULL	NULL	0	NULL	fumonisin B1	Chemical		inhibitor of					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_97_10_5480_s_98	10792026	Cells were treated with PDMP (10 muM), an inhibitor of glucosylceramide synthase that leads to increased ceramide concentrations ( 19); D609 (25 mug/ml), which inhibits acidic sphingomyelinase activity via inhibition of the phosphatidylcholine-specific phospholipase C ( 20); or fumonisin B1 (3 muM), an inhibitor of ceramide synthase and TNF-alpha-induced apoptosis ( 21).	transcription
72584	8	336247	7	NULL	NULL	0	NULL	statement 3	Process		occur via					fumonisin B1	Chemical	inhibition of			NULL		0	NULL	NULL	NULL	gw60_pnas_97_10_5480_s_98	10792026	Cells were treated with PDMP (10 muM), an inhibitor of glucosylceramide synthase that leads to increased ceramide concentrations ( 19); D609 (25 mug/ml), which inhibits acidic sphingomyelinase activity via inhibition of the phosphatidylcholine-specific phospholipase C ( 20); or fumonisin B1 (3 muM), an inhibitor of ceramide synthase and TNF-alpha-induced apoptosis ( 21).	transcription
72585	9	336247	7	NULL	NULL	0	NULL	statement 4	Process		is an alternative to					statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_97_10_5480_s_98	10792026	Cells were treated with PDMP (10 muM), an inhibitor of glucosylceramide synthase that leads to increased ceramide concentrations ( 19); D609 (25 mug/ml), which inhibits acidic sphingomyelinase activity via inhibition of the phosphatidylcholine-specific phospholipase C ( 20); or fumonisin B1 (3 muM), an inhibitor of ceramide synthase and TNF-alpha-induced apoptosis ( 21).	transcription
72586	1	336248	7	NULL	NULL	0	NULL	HDL	GP		triggers					PI-PLC	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_16478_s_13	12637559	HDL triggers a variety of intracellular signaling events, including activation of phosphatidylinositol- and phosphatidylcholine-specific phospholipases C and D (PI-PLC, PC-PLC, and PC-PLD), protein kinase C (PKC), mitogen-activated protein kinase (MAPK), tyrosine kinase, and heterotrimeric G-proteins ( 6,  7) but also production of cyclic AMP (cAMP), nitric oxide (NO), and ceramide ( 4) and intracellular Ca2+ release.	transcription
72587	2	336248	7	NULL	NULL	0	NULL	HDL	GP		triggers					PC-PLC	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_16478_s_13	12637559	HDL triggers a variety of intracellular signaling events, including activation of phosphatidylinositol- and phosphatidylcholine-specific phospholipases C and D (PI-PLC, PC-PLC, and PC-PLD), protein kinase C (PKC), mitogen-activated protein kinase (MAPK), tyrosine kinase, and heterotrimeric G-proteins ( 6,  7) but also production of cyclic AMP (cAMP), nitric oxide (NO), and ceramide ( 4) and intracellular Ca2+ release.	transcription
72588	3	336248	7	NULL	NULL	0	NULL	HDL	GP		triggers					PC-PLD	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_16478_s_13	12637559	HDL triggers a variety of intracellular signaling events, including activation of phosphatidylinositol- and phosphatidylcholine-specific phospholipases C and D (PI-PLC, PC-PLC, and PC-PLD), protein kinase C (PKC), mitogen-activated protein kinase (MAPK), tyrosine kinase, and heterotrimeric G-proteins ( 6,  7) but also production of cyclic AMP (cAMP), nitric oxide (NO), and ceramide ( 4) and intracellular Ca2+ release.	transcription
72589	4	336248	7	NULL	NULL	0	NULL	HDL	GP		triggers					PKC	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_16478_s_13	12637559	HDL triggers a variety of intracellular signaling events, including activation of phosphatidylinositol- and phosphatidylcholine-specific phospholipases C and D (PI-PLC, PC-PLC, and PC-PLD), protein kinase C (PKC), mitogen-activated protein kinase (MAPK), tyrosine kinase, and heterotrimeric G-proteins ( 6,  7) but also production of cyclic AMP (cAMP), nitric oxide (NO), and ceramide ( 4) and intracellular Ca2+ release.	transcription
72590	5	336248	7	NULL	NULL	0	NULL	HDL	GP		triggers					MAPK	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_16478_s_13	12637559	HDL triggers a variety of intracellular signaling events, including activation of phosphatidylinositol- and phosphatidylcholine-specific phospholipases C and D (PI-PLC, PC-PLC, and PC-PLD), protein kinase C (PKC), mitogen-activated protein kinase (MAPK), tyrosine kinase, and heterotrimeric G-proteins ( 6,  7) but also production of cyclic AMP (cAMP), nitric oxide (NO), and ceramide ( 4) and intracellular Ca2+ release.	transcription
72591	6	336248	7	NULL	NULL	0	NULL	HDL	GP		triggers					tyrosine kinase	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_16478_s_13	12637559	HDL triggers a variety of intracellular signaling events, including activation of phosphatidylinositol- and phosphatidylcholine-specific phospholipases C and D (PI-PLC, PC-PLC, and PC-PLD), protein kinase C (PKC), mitogen-activated protein kinase (MAPK), tyrosine kinase, and heterotrimeric G-proteins ( 6,  7) but also production of cyclic AMP (cAMP), nitric oxide (NO), and ceramide ( 4) and intracellular Ca2+ release.	transcription
72592	7	336248	7	NULL	NULL	NULL	NULL	HDL	GP		triggers					G-proteins	GP	activation of;;heterotrimeric			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_19_16478_s_13	12637559	HDL triggers a variety of intracellular signaling events, including activation of phosphatidylinositol- and phosphatidylcholine-specific phospholipases C and D (PI-PLC, PC-PLC, and PC-PLD), protein kinase C (PKC), mitogen-activated protein kinase (MAPK), tyrosine kinase, and heterotrimeric G-proteins ( 6,  7) but also production of cyclic AMP (cAMP), nitric oxide (NO), and ceramide ( 4) and intracellular Ca2+ release.	transcription
72593	8	336248	7	NULL	NULL	0	NULL	HDL	GP		triggers					cAMP	Chemical	production of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_16478_s_13	12637559	HDL triggers a variety of intracellular signaling events, including activation of phosphatidylinositol- and phosphatidylcholine-specific phospholipases C and D (PI-PLC, PC-PLC, and PC-PLD), protein kinase C (PKC), mitogen-activated protein kinase (MAPK), tyrosine kinase, and heterotrimeric G-proteins ( 6,  7) but also production of cyclic AMP (cAMP), nitric oxide (NO), and ceramide ( 4) and intracellular Ca2+ release.	transcription
72594	9	336248	7	NULL	NULL	0	NULL	HDL	GP		triggers					NO	Chemical	production of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_16478_s_13	12637559	HDL triggers a variety of intracellular signaling events, including activation of phosphatidylinositol- and phosphatidylcholine-specific phospholipases C and D (PI-PLC, PC-PLC, and PC-PLD), protein kinase C (PKC), mitogen-activated protein kinase (MAPK), tyrosine kinase, and heterotrimeric G-proteins ( 6,  7) but also production of cyclic AMP (cAMP), nitric oxide (NO), and ceramide ( 4) and intracellular Ca2+ release.	transcription
72595	10	336248	7	NULL	NULL	0	NULL	HDL	GP		triggers					ceramide	Chemical	production of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_16478_s_13	12637559	HDL triggers a variety of intracellular signaling events, including activation of phosphatidylinositol- and phosphatidylcholine-specific phospholipases C and D (PI-PLC, PC-PLC, and PC-PLD), protein kinase C (PKC), mitogen-activated protein kinase (MAPK), tyrosine kinase, and heterotrimeric G-proteins ( 6,  7) but also production of cyclic AMP (cAMP), nitric oxide (NO), and ceramide ( 4) and intracellular Ca2+ release.	transcription
72596	11	336248	7	NULL	NULL	0	NULL	HDL	GP		triggers					Ca2+	Chemical	release of;;intracellular			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_16478_s_13	12637559	HDL triggers a variety of intracellular signaling events, including activation of phosphatidylinositol- and phosphatidylcholine-specific phospholipases C and D (PI-PLC, PC-PLC, and PC-PLD), protein kinase C (PKC), mitogen-activated protein kinase (MAPK), tyrosine kinase, and heterotrimeric G-proteins ( 6,  7) but also production of cyclic AMP (cAMP), nitric oxide (NO), and ceramide ( 4) and intracellular Ca2+ release.	transcription
72597	12	336248	7	NULL	NULL	NULL	NULL	PI-PLC	GP		is					 phosphatidylinositol-specific phospholipase C	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_19_16478_s_13	12637559	HDL triggers a variety of intracellular signaling events, including activation of phosphatidylinositol- and phosphatidylcholine-specific phospholipases C and D (PI-PLC, PC-PLC, and PC-PLD), protein kinase C (PKC), mitogen-activated protein kinase (MAPK), tyrosine kinase, and heterotrimeric G-proteins ( 6,  7) but also production of cyclic AMP (cAMP), nitric oxide (NO), and ceramide ( 4) and intracellular Ca2+ release.	transcription
72598	13	336248	7	NULL	NULL	0	NULL	PC-PLC	GP		is					phosphatidylcholine-specific phospholipase C 	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_16478_s_13	12637559	HDL triggers a variety of intracellular signaling events, including activation of phosphatidylinositol- and phosphatidylcholine-specific phospholipases C and D (PI-PLC, PC-PLC, and PC-PLD), protein kinase C (PKC), mitogen-activated protein kinase (MAPK), tyrosine kinase, and heterotrimeric G-proteins ( 6,  7) but also production of cyclic AMP (cAMP), nitric oxide (NO), and ceramide ( 4) and intracellular Ca2+ release.	transcription
72599	14	336248	7	NULL	NULL	NULL	NULL	PC-PLD	GP		is					phosphatidylcholine-specific phospholipase D	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_19_16478_s_13	12637559	HDL triggers a variety of intracellular signaling events, including activation of phosphatidylinositol- and phosphatidylcholine-specific phospholipases C and D (PI-PLC, PC-PLC, and PC-PLD), protein kinase C (PKC), mitogen-activated protein kinase (MAPK), tyrosine kinase, and heterotrimeric G-proteins ( 6,  7) but also production of cyclic AMP (cAMP), nitric oxide (NO), and ceramide ( 4) and intracellular Ca2+ release.	transcription
72600	15	336248	7	NULL	NULL	0	NULL	PKC	GP		is					protein kinase C	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_16478_s_13	12637559	HDL triggers a variety of intracellular signaling events, including activation of phosphatidylinositol- and phosphatidylcholine-specific phospholipases C and D (PI-PLC, PC-PLC, and PC-PLD), protein kinase C (PKC), mitogen-activated protein kinase (MAPK), tyrosine kinase, and heterotrimeric G-proteins ( 6,  7) but also production of cyclic AMP (cAMP), nitric oxide (NO), and ceramide ( 4) and intracellular Ca2+ release.	transcription
72601	16	336248	7	NULL	NULL	0	NULL	MAPK	GP		is					mitogen-activated protein kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_16478_s_13	12637559	HDL triggers a variety of intracellular signaling events, including activation of phosphatidylinositol- and phosphatidylcholine-specific phospholipases C and D (PI-PLC, PC-PLC, and PC-PLD), protein kinase C (PKC), mitogen-activated protein kinase (MAPK), tyrosine kinase, and heterotrimeric G-proteins ( 6,  7) but also production of cyclic AMP (cAMP), nitric oxide (NO), and ceramide ( 4) and intracellular Ca2+ release.	transcription
72602	17	336248	7	NULL	NULL	0	NULL	cAMP	Chemical		is					cyclic AMP	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_16478_s_13	12637559	HDL triggers a variety of intracellular signaling events, including activation of phosphatidylinositol- and phosphatidylcholine-specific phospholipases C and D (PI-PLC, PC-PLC, and PC-PLD), protein kinase C (PKC), mitogen-activated protein kinase (MAPK), tyrosine kinase, and heterotrimeric G-proteins ( 6,  7) but also production of cyclic AMP (cAMP), nitric oxide (NO), and ceramide ( 4) and intracellular Ca2+ release.	transcription
72603	18	336248	7	NULL	NULL	0	NULL	NO	Chemical		is					nitric oxide	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_19_16478_s_13	12637559	HDL triggers a variety of intracellular signaling events, including activation of phosphatidylinositol- and phosphatidylcholine-specific phospholipases C and D (PI-PLC, PC-PLC, and PC-PLD), protein kinase C (PKC), mitogen-activated protein kinase (MAPK), tyrosine kinase, and heterotrimeric G-proteins ( 6,  7) but also production of cyclic AMP (cAMP), nitric oxide (NO), and ceramide ( 4) and intracellular Ca2+ release.	transcription
72604	1	336249	7	NULL	NULL	0	NULL	p53 	GP		regulate					 p21 CIP1/WAF1	GP	transcription of			NULL		0	NULL	NULL	NULL	gw70_nature_438_7068_690_s_71	16319895	Crucially, however, the amount of p53 protein, before and after ionizing  radiation, was not dependent on APC5 and/or APC7 gene expression ( Fig. 2c, bottom), suggesting that APC5 and APC7 affect p53-regulated transcription of p21 CIP1/WAF1 directly.	transcription
72605	2	336249	7	NULL	NULL	0	NULL	APC5 	GP		affect		directly			statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_nature_438_7068_690_s_71	16319895	Crucially, however, the amount of p53 protein, before and after ionizing  radiation, was not dependent on APC5 and/or APC7 gene expression ( Fig. 2c, bottom), suggesting that APC5 and APC7 affect p53-regulated transcription of p21 CIP1/WAF1 directly.	transcription
72606	3	336249	7	NULL	NULL	0	NULL	APC7	GP		affect		directly			statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_nature_438_7068_690_s_71	16319895	Crucially, however, the amount of p53 protein, before and after ionizing  radiation, was not dependent on APC5 and/or APC7 gene expression ( Fig. 2c, bottom), suggesting that APC5 and APC7 affect p53-regulated transcription of p21 CIP1/WAF1 directly.	transcription
72607	1	336250	7	NULL	NULL	0	NULL	APC1	GP	loss of	induce					G2/M  arrest	Process				NULL		0	NULL	NULL	NULL	gw70_genesdev_18_16_1952_s_100	15314021	Loss of APC1 induces G2/M arrest and apoptosis in the absence of p53	transcription
72608	2	336250	7	NULL	NULL	0	NULL	APC1	GP	loss of	induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw70_genesdev_18_16_1952_s_100	15314021	Loss of APC1 induces G2/M arrest and apoptosis in the absence of p53	transcription
72609	3	336250	7	NULL	NULL	0	NULL	statement 2	Process		in the absence of					p53	GP				NULL		0	NULL	NULL	NULL	gw70_genesdev_18_16_1952_s_100	15314021	Loss of APC1 induces G2/M arrest and apoptosis in the absence of p53	transcription
72610	1	336251	7	NULL	NULL	0	NULL	 APC	GP		downregulates					p53	GP				NULL	TNFalpha-induced HUVECs	0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_161	15769747	PAR1-dependent Down-regulation of p53 and Thrombospondin-1 by APC but Not Thrombin in TNFalpha-induced HUVECs --	transcription
72611	2	336251	7	NULL	NULL	0	NULL	APC	GP		downregulates					Thrombospondin-1	GP				NULL	TNFalpha-induced HUVECs	0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_161	15769747	PAR1-dependent Down-regulation of p53 and Thrombospondin-1 by APC but Not Thrombin in TNFalpha-induced HUVECs --	transcription
72612	3	336251	7	NULL	NULL	NULL	NULL	statement 1	Process		depends on					PAR1	GP				NULL	TNFalpha-induced HUVECs	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_161	15769747	PAR1-dependent Down-regulation of p53 and Thrombospondin-1 by APC but Not Thrombin in TNFalpha-induced HUVECs --	transcription
72613	4	336251	7	NULL	NULL	NULL	NULL	statement 2	Process		depends on					PAR1	GP				NULL	TNFalpha-induced HUVECs	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_161	15769747	PAR1-dependent Down-regulation of p53 and Thrombospondin-1 by APC but Not Thrombin in TNFalpha-induced HUVECs --	transcription
72614	5	336251	7	NULL	NULL	NULL	NULL	APC	GP		does not downregulate					thrombin	GP				NULL	TNFalpha-induced HUVECs	NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_161	15769747	PAR1-dependent Down-regulation of p53 and Thrombospondin-1 by APC but Not Thrombin in TNFalpha-induced HUVECs --	transcription
72615	1	336252	7	NULL	NULL	0	NULL	APC-EPCR-PAR1 	GP	signaling of	downregulates					p53 protein	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_200	15769747	Down-regulation of p53 protein expression by APC-EPCR-PAR1 signaling.	transcription
72616	1	336253	7	NULL	NULL	0	NULL	53BP2	GP		interacts with					p53	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_60_1_10646860_s_8	10646860	Because  53BP2 also interacts with p53 and Bcl2 and regulates p53 function, our  results suggest that APCL might be involved in the p53/Bcl2-linked pathway  of cell-cycle progression and cell death.	transcription
72617	2	336253	7	NULL	NULL	0	NULL	53BP2	GP		interacts with					Bcl2	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_60_1_10646860_s_8	10646860	Because  53BP2 also interacts with p53 and Bcl2 and regulates p53 function, our  results suggest that APCL might be involved in the p53/Bcl2-linked pathway  of cell-cycle progression and cell death.	transcription
72618	3	336253	7	NULL	NULL	0	NULL	53BP2	GP		regulates					p53	GP	function of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_60_1_10646860_s_8	10646860	Because  53BP2 also interacts with p53 and Bcl2 and regulates p53 function, our  results suggest that APCL might be involved in the p53/Bcl2-linked pathway  of cell-cycle progression and cell death.	transcription
72619	4	336253	7	NULL	NULL	0	NULL	APCL	GP		be involved in		might			 cell-cycle progression	Process	p53/Bcl2-linked pathway of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_60_1_10646860_s_8	10646860	Because  53BP2 also interacts with p53 and Bcl2 and regulates p53 function, our  results suggest that APCL might be involved in the p53/Bcl2-linked pathway  of cell-cycle progression and cell death.	transcription
72620	5	336253	7	NULL	NULL	0	NULL	APCL	GP		be involved in		might 			cell death	Process	p53/Bcl2-linked pathway of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_60_1_10646860_s_8	10646860	Because  53BP2 also interacts with p53 and Bcl2 and regulates p53 function, our  results suggest that APCL might be involved in the p53/Bcl2-linked pathway  of cell-cycle progression and cell death.	transcription
72621	1	336254	7	NULL	NULL	0	NULL	DNA damage	Process		induce					APC	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_87	9388195	Thus, if p53 is required for DNA damage-induced expression of  APC, then cell lines defective in wild-type functional p53 should fail to up-regulate  APC.	transcription
72622	2	336254	7	NULL	NULL	0	NULL	p53	GP		is required for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_87	9388195	Thus, if p53 is required for DNA damage-induced expression of  APC, then cell lines defective in wild-type functional p53 should fail to up-regulate  APC.	transcription
72623	3	336254	7	NULL	NULL	NULL	NULL	p53	GP	wild-type;;functional;;defective	fails to					APC	GP	up-regulate			NULL	cell lines	NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_87	9388195	Thus, if p53 is required for DNA damage-induced expression of  APC, then cell lines defective in wild-type functional p53 should fail to up-regulate  APC.	transcription
72624	1	336255	7	NULL	NULL	0	NULL	p53 transcription factor	GP		is required for					Apc 	GP	expression of			NULL	in vitro	0	NULL	NULL	NULL	gw60_pnas_97_7_3461_s_173	10716720	The  p53 transcription factor is required for  Apc expression  in vitro ( 34), so a deficiency of  p53 may lead to silencing of  Apc expression ( 35) and enhanced adenoma formation.	transcription
72625	2	336255	7	NULL	NULL	0	NULL	p53	GP	deficiency of	leads to		may			Apc	GP	silencing of;;expression of			NULL		0	NULL	NULL	NULL	gw60_pnas_97_7_3461_s_173	10716720	The  p53 transcription factor is required for  Apc expression  in vitro ( 34), so a deficiency of  p53 may lead to silencing of  Apc expression ( 35) and enhanced adenoma formation.	transcription
72626	3	336255	7	NULL	NULL	0	NULL	p53	GP	silencing of	leads to		may			adenoma formation	Process	enhanced			NULL		0	NULL	NULL	NULL	gw60_pnas_97_7_3461_s_173	10716720	The  p53 transcription factor is required for  Apc expression  in vitro ( 34), so a deficiency of  p53 may lead to silencing of  Apc expression ( 35) and enhanced adenoma formation.	transcription
72627	1	336256	7	NULL	NULL	0	NULL	APC	GP		down-regulates					p53 transcript	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_9	15769747	APC down-regulated transcripts for proapoptotic proteins including p53 and thrombospondin-1, but p53 was unchanged, and thrombospondin was even up-regulated by thrombin.	transcription
72628	2	336256	7	NULL	NULL	NULL	NULL	APC	GP		down-regulates					thrombospondin-1 transcript	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_9	15769747	APC down-regulated transcripts for proapoptotic proteins including p53 and thrombospondin-1, but p53 was unchanged, and thrombospondin was even up-regulated by thrombin.	transcription
72629	3	336256	7	NULL	NULL	0	NULL	thrombin	GP		up-regulates					thrombospondin	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_9	15769747	APC down-regulated transcripts for proapoptotic proteins including p53 and thrombospondin-1, but p53 was unchanged, and thrombospondin was even up-regulated by thrombin.	transcription
72630	4	336256	7	NULL	NULL	0	NULL	thrombin	GP		does not upregulate					p53	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_9	15769747	APC down-regulated transcripts for proapoptotic proteins including p53 and thrombospondin-1, but p53 was unchanged, and thrombospondin was even up-regulated by thrombin.	transcription
72631	5	336256	7	NULL	NULL	0	NULL	p53	GP		is a type of					proapoptotic protein	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_9	15769747	APC down-regulated transcripts for proapoptotic proteins including p53 and thrombospondin-1, but p53 was unchanged, and thrombospondin was even up-regulated by thrombin.	transcription
72632	6	336256	7	NULL	NULL	0	NULL	thrombospondin-1	GP		is a type of					proapoptotic protein	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_9	15769747	APC down-regulated transcripts for proapoptotic proteins including p53 and thrombospondin-1, but p53 was unchanged, and thrombospondin was even up-regulated by thrombin.	transcription
72633	1	336257	7	NULL	NULL	0	NULL	doxorubicin 	Chemical		increase					p53 protein	GP	levels of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_163	15769747	To test whether APC regulates p53, cells were treated with doxorubicin to increase p53 protein levels.	transcription
72634	1	336258	7	NULL	NULL	0	NULL	p53	GP	levels of	is limiting in					HCT-116 cells	Cell				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_98	9388195	These results are consistent with the idea that p53 levels are limiting in HCT-116 cells, and the increased levels of p53 may be necessary for induced expression of APC.	transcription
72635	2	336258	7	NULL	NULL	0	NULL	p53	GP	increased levels of	is necessary for					APC	GP	induced expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_98	9388195	These results are consistent with the idea that p53 levels are limiting in HCT-116 cells, and the increased levels of p53 may be necessary for induced expression of APC.	transcription
72636	1	336259	7	NULL	NULL	0	NULL	fetal-brain cDNA library	GP	human	interacts with					APCL	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_60_1_10646860_s_4	10646860	Among 166 cDNA clones isolated from a human  fetal-brain cDNA library as candidates for interaction with APCL, 32 encoded  parts of p53-binding protein 2 (53BP2), a molecule that interacts with  p53 and Bcl2.	transcription
72637	2	336259	7	NULL	NULL	0	NULL	p53-binding protein 2	GP		interacts with			32 encoded parts of		p53	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_60_1_10646860_s_4	10646860	Among 166 cDNA clones isolated from a human  fetal-brain cDNA library as candidates for interaction with APCL, 32 encoded  parts of p53-binding protein 2 (53BP2), a molecule that interacts with  p53 and Bcl2.	transcription
72638	3	336259	7	NULL	NULL	0	NULL	p53-binding protein 2	GP		interacts with			32 encoded parts of		Bcl2	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_60_1_10646860_s_4	10646860	Among 166 cDNA clones isolated from a human  fetal-brain cDNA library as candidates for interaction with APCL, 32 encoded  parts of p53-binding protein 2 (53BP2), a molecule that interacts with  p53 and Bcl2.	transcription
72639	1	336261	7	NULL	NULL	NULL	NULL	p53	GP		required for		consistently			APC	GP	upregulation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_115	9388195	Since we observed a consistent requirement for p53 in APC up-regulation, it appears that a p53-mediated signaling pathway is required for APC regulation in response to DNA damage.	transcription
72640	2	336261	7	NULL	NULL	0	NULL	 p53	GP		mediates					signaling pathway	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_115	9388195	Since we observed a consistent requirement for p53 in APC up-regulation, it appears that a p53-mediated signaling pathway is required for APC regulation in response to DNA damage.	transcription
72641	3	336261	7	NULL	NULL	0	NULL	statement 2	Process		is required for					APC	GP	regulation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_115	9388195	Since we observed a consistent requirement for p53 in APC up-regulation, it appears that a p53-mediated signaling pathway is required for APC regulation in response to DNA damage.	transcription
72642	4	336261	7	NULL	NULL	0	NULL	statement 3	Process		in response to					DNA damage	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_115	9388195	Since we observed a consistent requirement for p53 in APC up-regulation, it appears that a p53-mediated signaling pathway is required for APC regulation in response to DNA damage.	transcription
72643	1	336262	7	NULL	NULL	0	NULL	APC signaling	Process		down-regulates		strongly;;specifically			Thrombospondin-1	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_222	15769747	Thrombospondin-1, which was also strongly down-regulated specifically by APC signaling, is a target for positive transcriptional regulation by p53 ( ), suggesting that p53 suppression may be an upstream effector mechanism for protective APC signaling.	transcription
72644	2	336262	7	NULL	NULL	0	NULL	Thrombospondin-1	GP		target for					p53	GP	positive transcriptional regulation by			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_222	15769747	Thrombospondin-1, which was also strongly down-regulated specifically by APC signaling, is a target for positive transcriptional regulation by p53 ( ), suggesting that p53 suppression may be an upstream effector mechanism for protective APC signaling.	transcription
72645	3	336262	7	NULL	NULL	0	NULL	p53	GP	suppression of	upstream effector		may be			APC signaling	Process	mechanism for protective			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_222	15769747	Thrombospondin-1, which was also strongly down-regulated specifically by APC signaling, is a target for positive transcriptional regulation by p53 ( ), suggesting that p53 suppression may be an upstream effector mechanism for protective APC signaling.	transcription
72646	1	336263	7	NULL	NULL	0	NULL	alkylation	Process		induce					DNA damage	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_9	9388195	These results support a model featuring a direct link between p53 and APC in response to alkylation-induced DNA damage and suggest a novel role for p53 in a stress-response pathway involving APC.	transcription
72647	2	336263	7	NULL	NULL	0	NULL	stress response pathway	Process		involves					APC	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_9	9388195	These results support a model featuring a direct link between p53 and APC in response to alkylation-induced DNA damage and suggest a novel role for p53 in a stress-response pathway involving APC.	transcription
72648	3	336263	7	NULL	NULL	0	NULL	p53	GP		play a role in					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_9	9388195	These results support a model featuring a direct link between p53 and APC in response to alkylation-induced DNA damage and suggest a novel role for p53 in a stress-response pathway involving APC.	transcription
72649	4	336263	7	NULL	NULL	0	NULL	p53	GP		linked to		directly			APC	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_9	9388195	These results support a model featuring a direct link between p53 and APC in response to alkylation-induced DNA damage and suggest a novel role for p53 in a stress-response pathway involving APC.	transcription
72650	5	336263	7	NULL	NULL	0	NULL	statement 4	Process		in response to					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_9	9388195	These results support a model featuring a direct link between p53 and APC in response to alkylation-induced DNA damage and suggest a novel role for p53 in a stress-response pathway involving APC.	transcription
72651	1	336264	7	NULL	NULL	0	NULL	APC	GP	induction of;;wildtype	reduce					DNMT1 message	Process				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_24_1_17_s_149	12538344	Further reduction of  DNMT1 message, to almost 34% of that with p53 expression alone, was effected by induction of wildtype APC (Figure 4B,D).	transcription
72652	2	336264	7	NULL	NULL	0	NULL	statement 1	Process		occur with					p53	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_24_1_17_s_149	12538344	Further reduction of  DNMT1 message, to almost 34% of that with p53 expression alone, was effected by induction of wildtype APC (Figure 4B,D).	transcription
72653	1	336265	7	NULL	NULL	NULL	NULL	RXR	GP		regulates					beta-Catenin pathway	GP	degradation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_32_29954_s_191	12771132	The RXR-regulatedbeta -Catenin Degradation Pathway Is  Independent of the p53/ Siah-1- and GSK3beta -regulated APC  Pathways --	transcription
72654	2	336265	7	NULL	NULL	0	NULL	p53/ Siah-1	GP		regulates					APC pathway	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_32_29954_s_191	12771132	The RXR-regulatedbeta -Catenin Degradation Pathway Is  Independent of the p53/ Siah-1- and GSK3beta -regulated APC  Pathways --	transcription
72655	3	336265	7	NULL	NULL	0	NULL	GSK3beta	GP		regulates					APC pathway	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_32_29954_s_191	12771132	The RXR-regulatedbeta -Catenin Degradation Pathway Is  Independent of the p53/ Siah-1- and GSK3beta -regulated APC  Pathways --	transcription
72656	4	336265	7	NULL	NULL	0	NULL	statement 1	Process		is independent of					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_32_29954_s_191	12771132	The RXR-regulatedbeta -Catenin Degradation Pathway Is  Independent of the p53/ Siah-1- and GSK3beta -regulated APC  Pathways --	transcription
72657	5	336265	7	NULL	NULL	0	NULL	statement 1	Process		is independent of					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_32_29954_s_191	12771132	The RXR-regulatedbeta -Catenin Degradation Pathway Is  Independent of the p53/ Siah-1- and GSK3beta -regulated APC  Pathways --	transcription
72658	1	336266	7	NULL	NULL	0	NULL	 p53	GP		regulates		positively			TSP-1	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_pnas_100_22_12718_s_17	14555767	It has been previously shown that TSP-1 expression is positively regulated by the p53, PTEN, Smad, and APC tumor suppressor proteins (  -  ).	transcription
72659	2	336266	7	NULL	NULL	0	NULL	PTEN	GP		regulates		positively			TSP-1	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_pnas_100_22_12718_s_17	14555767	It has been previously shown that TSP-1 expression is positively regulated by the p53, PTEN, Smad, and APC tumor suppressor proteins (  -  ).	transcription
72660	3	336266	7	NULL	NULL	0	NULL	 Smad	GP		regulates		positively			TSP-1	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_pnas_100_22_12718_s_17	14555767	It has been previously shown that TSP-1 expression is positively regulated by the p53, PTEN, Smad, and APC tumor suppressor proteins (  -  ).	transcription
72661	4	336266	7	NULL	NULL	0	NULL	APC tumor suppressor proteins	GP		regulates		positively			TSP-1	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_pnas_100_22_12718_s_17	14555767	It has been previously shown that TSP-1 expression is positively regulated by the p53, PTEN, Smad, and APC tumor suppressor proteins (  -  ).	transcription
72662	1	336267	7	NULL	NULL	0	NULL	 Apc	GP	mutation of	cause					apoptosis	Process	resistance to			NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_22_5_821_s_109	11323404	Curcumin treatment may inhibit apoptosis resistance associated with  Apc mutation through alteration of the equilibrium of NFkappaB and p53.	transcription
72663	2	336267	7	NULL	NULL	0	NULL	curcumin	Chemical		inhibit		may			statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_22_5_821_s_109	11323404	Curcumin treatment may inhibit apoptosis resistance associated with  Apc mutation through alteration of the equilibrium of NFkappaB and p53.	transcription
72664	3	336267	7	NULL	NULL	0	NULL	statement 1	Process		occur through					NFkappaB	GP	alteration of;;equilibrium of			NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_22_5_821_s_109	11323404	Curcumin treatment may inhibit apoptosis resistance associated with  Apc mutation through alteration of the equilibrium of NFkappaB and p53.	transcription
72665	4	336267	7	NULL	NULL	0	NULL	statement 1	Process		occur through					p53	GP	alteration of;;equilibrium of			NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_22_5_821_s_109	11323404	Curcumin treatment may inhibit apoptosis resistance associated with  Apc mutation through alteration of the equilibrium of NFkappaB and p53.	transcription
72666	1	336268	7	NULL	NULL	0	NULL	p53	GP		downregulates					beta-Catenin	GP				NULL		0	NULL	NULL	NULL	gw60_cell_105_5_563_s_68	11389825	Dominant negative versions  of SIP, Ebi, and the C-terminal fragment of APC  also inhibited the downregulation of beta-catenin by  p53.	transcription
72667	2	336268	7	NULL	NULL	0	NULL	SIP	GP	dominant negative versions of	inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cell_105_5_563_s_68	11389825	Dominant negative versions  of SIP, Ebi, and the C-terminal fragment of APC  also inhibited the downregulation of beta-catenin by  p53.	transcription
72668	3	336268	7	NULL	NULL	0	NULL	Ebi	GP	dominant negative versions of	inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cell_105_5_563_s_68	11389825	Dominant negative versions  of SIP, Ebi, and the C-terminal fragment of APC  also inhibited the downregulation of beta-catenin by  p53.	transcription
72669	4	336268	7	NULL	NULL	0	NULL	APC	GP	dominant negative versions of	inhibit			C-terminal fragment of		statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_cell_105_5_563_s_68	11389825	Dominant negative versions  of SIP, Ebi, and the C-terminal fragment of APC  also inhibited the downregulation of beta-catenin by  p53.	transcription
72670	1	336269	7	NULL	NULL	0	NULL	 Siah-1	GP		induces					beta-Catenin	GP	degradation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_11_3803_s_401	11997515	It has recently been reported that Siah-1 induces the degradation of beta-catenin through APC in response to p53 ( 36,  38).	transcription
72671	2	336269	7	NULL	NULL	0	NULL	statement 1	Process		occur through					APC	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_11_3803_s_401	11997515	It has recently been reported that Siah-1 induces the degradation of beta-catenin through APC in response to p53 ( 36,  38).	transcription
72672	3	336269	7	NULL	NULL	0	NULL	statement 1	Process		in response to					p53	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_22_11_3803_s_401	11997515	It has recently been reported that Siah-1 induces the degradation of beta-catenin through APC in response to p53 ( 36,  38).	transcription
72673	1	336270	7	NULL	NULL	0	NULL	p53 protein	GP	increase in levels of	required for					APC gene	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_102	9388195	These results demonstrate that an increase in p53 protein level is required for  APC gene expression after DNA damage.	transcription
72674	2	336270	7	NULL	NULL	0	NULL	statement 1	Process		occur after					DNA damage	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_102	9388195	These results demonstrate that an increase in p53 protein level is required for  APC gene expression after DNA damage.	transcription
72675	1	336271	7	NULL	NULL	0	NULL	Apc	GP		interacts with					p53	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_7_3461_s_19	10716720	Does an interaction between  Apc and  p53 affect intestinal neoplasia in experimental models of cancer ( 6)?	transcription
72676	1	336272	7	NULL	NULL	0	NULL	Apc	GP	loss of	induce					apoptosis	Process				NULL	 neural crest-derived cells	0	NULL	NULL	NULL	gw60_pnas_99_1_297_s_167	11756652	These data strongly indicate that the apoptosis of neural crest-derived cells induced by the loss of Apc was not mediated by p53.	transcription
72677	2	336272	7	NULL	NULL	0	NULL	statement 1	Process		is not mediated by					p53	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_99_1_297_s_167	11756652	These data strongly indicate that the apoptosis of neural crest-derived cells induced by the loss of Apc was not mediated by p53.	transcription
72678	1	336273	7	NULL	NULL	0	NULL	MTS-1	GP		encode					p16	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_94_3_952_s_17	9023363	They include  Rb,  p53,  WT1,  BRCA1,  BRCA2,  VHL,  APC,  NF-1,  NF-2, and  MTS-1 (encodes p16, a cell cycle inhibitor).	transcription
72679	2	336273	7	NULL	NULL	0	NULL	p16	GP		is a inhibitor of					cell cycle 	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_94_3_952_s_17	9023363	They include  Rb,  p53,  WT1,  BRCA1,  BRCA2,  VHL,  APC,  NF-1,  NF-2, and  MTS-1 (encodes p16, a cell cycle inhibitor).	transcription
72680	1	336274	7	NULL	NULL	NULL	NULL	DMH	Chemical		induce					CRC susceptibility loci	Chromosome				NULL	recombinant congenic mice	NULL	NULL	NULL	NULL	gw60_pnas_94_7_3308_s_29	9096389	In support of this, DMH-induced CRC susceptibility loci mapped in recombinant congenic mice do not appear to involve  Apc or  P53 ( 10).	transcription
72681	2	336274	7	NULL	NULL	0	NULL	statement 1	Process		does not involve					Apc	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_94_7_3308_s_29	9096389	In support of this, DMH-induced CRC susceptibility loci mapped in recombinant congenic mice do not appear to involve  Apc or  P53 ( 10).	transcription
72682	3	336274	7	NULL	NULL	0	NULL	statement 1	Process		does not involve					p53	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_94_7_3308_s_29	9096389	In support of this, DMH-induced CRC susceptibility loci mapped in recombinant congenic mice do not appear to involve  Apc or  P53 ( 10).	transcription
72683	1	336275	7	NULL	NULL	0	NULL	APC	GP	intact/functional	required for					beta-Catenin	GP	suppression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_34_35583_s_225	15190077	Because a recent report suggested that intact/functional APC was required for the suppression of beta-catenin levels and colon carcinogenesis following PPARgamma activation ( ), we determined whether PPARgamma-mediated suppression of beta-catenin involved APC and p53.	transcription
72684	2	336275	7	NULL	NULL	0	NULL	APC	GP	intact/functional	required for					colon carcinogenesis	Process	suppression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_34_35583_s_225	15190077	Because a recent report suggested that intact/functional APC was required for the suppression of beta-catenin levels and colon carcinogenesis following PPARgamma activation ( ), we determined whether PPARgamma-mediated suppression of beta-catenin involved APC and p53.	transcription
72685	3	336275	7	NULL	NULL	0	NULL	statement 1	Process		occur upon					PPARgamma	GP	activation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_34_35583_s_225	15190077	Because a recent report suggested that intact/functional APC was required for the suppression of beta-catenin levels and colon carcinogenesis following PPARgamma activation ( ), we determined whether PPARgamma-mediated suppression of beta-catenin involved APC and p53.	transcription
72686	4	336275	7	NULL	NULL	0	NULL	statement 1	Process		required for					colon carcinogenesis	Process	activation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_34_35583_s_225	15190077	Because a recent report suggested that intact/functional APC was required for the suppression of beta-catenin levels and colon carcinogenesis following PPARgamma activation ( ), we determined whether PPARgamma-mediated suppression of beta-catenin involved APC and p53.	transcription
72687	5	336275	7	NULL	NULL	0	NULL	PPARgamma	GP		mediate					beta-catenin	GP	suppression of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_34_35583_s_225	15190077	Because a recent report suggested that intact/functional APC was required for the suppression of beta-catenin levels and colon carcinogenesis following PPARgamma activation ( ), we determined whether PPARgamma-mediated suppression of beta-catenin involved APC and p53.	transcription
72688	1	336276	7	NULL	NULL	0	NULL	p53	GP	expression of	regulate					APC gene	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_109	9388195	The results show that  APC mRNA levels were increased in a dose-dependent manner in CMV-p53-transfected  versus untransfected K562 cells (Fig.  4 B), clearly indicating that p53 expression can regulate  APC gene expression.	transcription
72689	1	336277	7	NULL	NULL	0	NULL	APC/Apc	GP		is involved in					neoplasia	MedicalFinding	controlling			NULL		0	NULL	NULL	NULL	gw60_pnas_97_7_3461_s_176	10716720	Beyond the negative regulatory genes of neoplasia,  APC/Apc and  p53, the modifier gene  Mom1 encoding the secretory phospholipase Pla2g2a and the pharmacological agents piroxicam and DFMO must be placed in the network of interactions controlling neoplasia.	transcription
72690	2	336277	7	NULL	NULL	0	NULL	p53	GP		is involved in					neoplasia	MedicalFinding	controlling			NULL		0	NULL	NULL	NULL	gw60_pnas_97_7_3461_s_176	10716720	Beyond the negative regulatory genes of neoplasia,  APC/Apc and  p53, the modifier gene  Mom1 encoding the secretory phospholipase Pla2g2a and the pharmacological agents piroxicam and DFMO must be placed in the network of interactions controlling neoplasia.	transcription
72691	3	336277	7	NULL	NULL	0	NULL	Mom1	GP		encode					Pla2g2a	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_7_3461_s_176	10716720	Beyond the negative regulatory genes of neoplasia,  APC/Apc and  p53, the modifier gene  Mom1 encoding the secretory phospholipase Pla2g2a and the pharmacological agents piroxicam and DFMO must be placed in the network of interactions controlling neoplasia.	transcription
72692	4	336277	7	NULL	NULL	0	NULL	Mom1	GP		is involved in					neoplasia	MedicalFinding	controlling			NULL		0	NULL	NULL	NULL	gw60_pnas_97_7_3461_s_176	10716720	Beyond the negative regulatory genes of neoplasia,  APC/Apc and  p53, the modifier gene  Mom1 encoding the secretory phospholipase Pla2g2a and the pharmacological agents piroxicam and DFMO must be placed in the network of interactions controlling neoplasia.	transcription
72693	5	336277	7	NULL	NULL	0	NULL	piroxicam 	Chemical		is involved in					neoplasia	MedicalFinding	controlling			NULL		0	NULL	NULL	NULL	gw60_pnas_97_7_3461_s_176	10716720	Beyond the negative regulatory genes of neoplasia,  APC/Apc and  p53, the modifier gene  Mom1 encoding the secretory phospholipase Pla2g2a and the pharmacological agents piroxicam and DFMO must be placed in the network of interactions controlling neoplasia.	transcription
72694	6	336277	7	NULL	NULL	0	NULL	DFMO	Chemical		is involved in					neoplasia	MedicalFinding	controlling			NULL		0	NULL	NULL	NULL	gw60_pnas_97_7_3461_s_176	10716720	Beyond the negative regulatory genes of neoplasia,  APC/Apc and  p53, the modifier gene  Mom1 encoding the secretory phospholipase Pla2g2a and the pharmacological agents piroxicam and DFMO must be placed in the network of interactions controlling neoplasia.	transcription
72695	7	336277	7	NULL	NULL	0	NULL	 Mom1	GP		is a type of					modifier gene	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_7_3461_s_176	10716720	Beyond the negative regulatory genes of neoplasia,  APC/Apc and  p53, the modifier gene  Mom1 encoding the secretory phospholipase Pla2g2a and the pharmacological agents piroxicam and DFMO must be placed in the network of interactions controlling neoplasia.	transcription
72696	8	336277	7	NULL	NULL	0	NULL	Pla2g2a	GP		is a type of					secretory phospholipase	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_7_3461_s_176	10716720	Beyond the negative regulatory genes of neoplasia,  APC/Apc and  p53, the modifier gene  Mom1 encoding the secretory phospholipase Pla2g2a and the pharmacological agents piroxicam and DFMO must be placed in the network of interactions controlling neoplasia.	transcription
72697	9	336277	7	NULL	NULL	0	NULL	piroxicam	Chemical		is a type of					pharmacological agent	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_97_7_3461_s_176	10716720	Beyond the negative regulatory genes of neoplasia,  APC/Apc and  p53, the modifier gene  Mom1 encoding the secretory phospholipase Pla2g2a and the pharmacological agents piroxicam and DFMO must be placed in the network of interactions controlling neoplasia.	transcription
72698	10	336277	7	NULL	NULL	0	NULL	DFMO	Chemical		is a type of					pharmacological agent	Chemical				NULL		0	NULL	NULL	NULL	gw60_pnas_97_7_3461_s_176	10716720	Beyond the negative regulatory genes of neoplasia,  APC/Apc and  p53, the modifier gene  Mom1 encoding the secretory phospholipase Pla2g2a and the pharmacological agents piroxicam and DFMO must be placed in the network of interactions controlling neoplasia.	transcription
72699	1	336278	7	NULL	NULL	0	NULL	p53BP-2	GP		interact with					Bcl-2	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_14514_s_47	11278422	Like p53, p53BP-2 is part of a protein network since it has been shown that p53BP-2 can also interact with Bcl-2 (an anti-apoptotic protein), protein phosphatase-1gamma, NF-kappaB subunit p65 (a transcription factor), and APCL ( adenomatous  polyposis  coli- like) protein (a tumor suppressor-like protein) ( 19-22).	transcription
72700	2	336278	7	NULL	NULL	0	NULL	p53BP-2	GP		interacts with					protein phosphatase-1gamma	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_14514_s_47	11278422	Like p53, p53BP-2 is part of a protein network since it has been shown that p53BP-2 can also interact with Bcl-2 (an anti-apoptotic protein), protein phosphatase-1gamma, NF-kappaB subunit p65 (a transcription factor), and APCL ( adenomatous  polyposis  coli- like) protein (a tumor suppressor-like protein) ( 19-22).	transcription
72701	3	336278	7	NULL	NULL	0	NULL	p53BP-2	GP		interacts with					p65	GP		NF-kappaB subunit 		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_14514_s_47	11278422	Like p53, p53BP-2 is part of a protein network since it has been shown that p53BP-2 can also interact with Bcl-2 (an anti-apoptotic protein), protein phosphatase-1gamma, NF-kappaB subunit p65 (a transcription factor), and APCL ( adenomatous  polyposis  coli- like) protein (a tumor suppressor-like protein) ( 19-22).	transcription
72702	4	336278	7	NULL	NULL	NULL	NULL	p53BP-2	GP		interacts with					APCL	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_17_14514_s_47	11278422	Like p53, p53BP-2 is part of a protein network since it has been shown that p53BP-2 can also interact with Bcl-2 (an anti-apoptotic protein), protein phosphatase-1gamma, NF-kappaB subunit p65 (a transcription factor), and APCL ( adenomatous  polyposis  coli- like) protein (a tumor suppressor-like protein) ( 19-22).	transcription
72703	5	336278	7	NULL	NULL	0	NULL	Bcl-2	GP		is a type of					anti-apoptotic protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_14514_s_47	11278422	Like p53, p53BP-2 is part of a protein network since it has been shown that p53BP-2 can also interact with Bcl-2 (an anti-apoptotic protein), protein phosphatase-1gamma, NF-kappaB subunit p65 (a transcription factor), and APCL ( adenomatous  polyposis  coli- like) protein (a tumor suppressor-like protein) ( 19-22).	transcription
72704	6	336278	7	NULL	NULL	0	NULL	p65	GP		is a type of					transcription factor	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_14514_s_47	11278422	Like p53, p53BP-2 is part of a protein network since it has been shown that p53BP-2 can also interact with Bcl-2 (an anti-apoptotic protein), protein phosphatase-1gamma, NF-kappaB subunit p65 (a transcription factor), and APCL ( adenomatous  polyposis  coli- like) protein (a tumor suppressor-like protein) ( 19-22).	transcription
72705	7	336278	7	NULL	NULL	0	NULL	APCL	GP		is					adenomatous polyposis coli- like	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_14514_s_47	11278422	Like p53, p53BP-2 is part of a protein network since it has been shown that p53BP-2 can also interact with Bcl-2 (an anti-apoptotic protein), protein phosphatase-1gamma, NF-kappaB subunit p65 (a transcription factor), and APCL ( adenomatous  polyposis  coli- like) protein (a tumor suppressor-like protein) ( 19-22).	transcription
72706	8	336278	7	NULL	NULL	0	NULL	APCL	GP		is a type of					tumor suppressor-like protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_14514_s_47	11278422	Like p53, p53BP-2 is part of a protein network since it has been shown that p53BP-2 can also interact with Bcl-2 (an anti-apoptotic protein), protein phosphatase-1gamma, NF-kappaB subunit p65 (a transcription factor), and APCL ( adenomatous  polyposis  coli- like) protein (a tumor suppressor-like protein) ( 19-22).	transcription
72707	9	336278	7	NULL	NULL	0	NULL	p53BP-2	GP		is like					p53	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_14514_s_47	11278422	Like p53, p53BP-2 is part of a protein network since it has been shown that p53BP-2 can also interact with Bcl-2 (an anti-apoptotic protein), protein phosphatase-1gamma, NF-kappaB subunit p65 (a transcription factor), and APCL ( adenomatous  polyposis  coli- like) protein (a tumor suppressor-like protein) ( 19-22).	transcription
72708	1	336279	7	NULL	NULL	0	NULL	 APC	GP		consist of				 promoter	single SP1 consensus sequence	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_64_2_415_s_153	12869646	The APC promoter consists of a single SP1 consensus sequence, possibly  contributing to p53 gene modulation, yet its necessity for p53 stimulation is  undermined by the existing alternate mechanisms (i.e., direct interaction of  p53 with promoter and modulation by a p53 complex with TFIIH)  (Jaiswal and Narayan, 2001  ).	transcription
72709	2	336279	7	NULL	NULL	0	NULL	statement 1	Process		contribute to					p53 gene 	GP	modulation of			NULL		0	NULL	NULL	NULL	gw60_molpharmacol_64_2_415_s_153	12869646	The APC promoter consists of a single SP1 consensus sequence, possibly  contributing to p53 gene modulation, yet its necessity for p53 stimulation is  undermined by the existing alternate mechanisms (i.e., direct interaction of  p53 with promoter and modulation by a p53 complex with TFIIH)  (Jaiswal and Narayan, 2001  ).	transcription
72710	3	336279	7	NULL	NULL	0	NULL	p53	GP		interacts with		directly							promoter	NULL		0	NULL	NULL	NULL	gw60_molpharmacol_64_2_415_s_153	12869646	The APC promoter consists of a single SP1 consensus sequence, possibly  contributing to p53 gene modulation, yet its necessity for p53 stimulation is  undermined by the existing alternate mechanisms (i.e., direct interaction of  p53 with promoter and modulation by a p53 complex with TFIIH)  (Jaiswal and Narayan, 2001  ).	transcription
72711	4	336279	7	NULL	NULL	0	NULL	p53	GP		complex with					TFIIH	GP				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_64_2_415_s_153	12869646	The APC promoter consists of a single SP1 consensus sequence, possibly  contributing to p53 gene modulation, yet its necessity for p53 stimulation is  undermined by the existing alternate mechanisms (i.e., direct interaction of  p53 with promoter and modulation by a p53 complex with TFIIH)  (Jaiswal and Narayan, 2001  ).	transcription
72712	5	336279	7	NULL	NULL	0	NULL	statement 3	Process		modulated by					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_molpharmacol_64_2_415_s_153	12869646	The APC promoter consists of a single SP1 consensus sequence, possibly  contributing to p53 gene modulation, yet its necessity for p53 stimulation is  undermined by the existing alternate mechanisms (i.e., direct interaction of  p53 with promoter and modulation by a p53 complex with TFIIH)  (Jaiswal and Narayan, 2001  ).	transcription
72713	1	336280	7	NULL	NULL	NULL	NULL	Apoptin	GP		induce					G2/M arrest	Process				NULL	p53 null transformed cells	NULL	NULL	NULL	NULL	gw70_genesdev_18_16_1952_s_121	15314021	Our results suggest that Apoptin induces G2/M arrest and apoptosis in p53 null transformed cells through association with and inhibition of the APC/C.	transcription
72714	2	336280	7	NULL	NULL	0	NULL	Apoptin	GP		induce					apoptosis	Process				NULL	p53 null transformed cells	0	NULL	NULL	NULL	gw70_genesdev_18_16_1952_s_121	15314021	Our results suggest that Apoptin induces G2/M arrest and apoptosis in p53 null transformed cells through association with and inhibition of the APC/C.	transcription
72715	3	336280	7	NULL	NULL	0	NULL	statement 1	Process		occur through					APC/C	GP	association with			NULL		0	NULL	NULL	NULL	gw70_genesdev_18_16_1952_s_121	15314021	Our results suggest that Apoptin induces G2/M arrest and apoptosis in p53 null transformed cells through association with and inhibition of the APC/C.	transcription
72716	4	336280	7	NULL	NULL	0	NULL	statement 2	Process		occur through					APC/C	GP	association with			NULL		0	NULL	NULL	NULL	gw70_genesdev_18_16_1952_s_121	15314021	Our results suggest that Apoptin induces G2/M arrest and apoptosis in p53 null transformed cells through association with and inhibition of the APC/C.	transcription
72717	5	336280	7	NULL	NULL	0	NULL	statement 1	Process		occur through					APC/C	GP	inhibition of			NULL		0	NULL	NULL	NULL	gw70_genesdev_18_16_1952_s_121	15314021	Our results suggest that Apoptin induces G2/M arrest and apoptosis in p53 null transformed cells through association with and inhibition of the APC/C.	transcription
72718	6	336280	7	NULL	NULL	0	NULL	statement 2	Process		occur through					APC/C	GP	inhibition of			NULL		0	NULL	NULL	NULL	gw70_genesdev_18_16_1952_s_121	15314021	Our results suggest that Apoptin induces G2/M arrest and apoptosis in p53 null transformed cells through association with and inhibition of the APC/C.	transcription
72719	7	336280	7	NULL	NULL	0	NULL	statement 3	Process		occur along with					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_genesdev_18_16_1952_s_121	15314021	Our results suggest that Apoptin induces G2/M arrest and apoptosis in p53 null transformed cells through association with and inhibition of the APC/C.	transcription
72720	8	336280	7	NULL	NULL	0	NULL	statement 4	Process		occur along with					statement 6	Process				NULL		0	NULL	NULL	NULL	gw70_genesdev_18_16_1952_s_121	15314021	Our results suggest that Apoptin induces G2/M arrest and apoptosis in p53 null transformed cells through association with and inhibition of the APC/C.	transcription
72721	1	336281	7	NULL	NULL	0	NULL	 APC	GP		bind					EPCR	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_165	15769747	Antibody-blocking experiments demonstrate that this suppressive effect on p53 expression was dependent on APC binding to EPCR as well as PAR1 cleavage ( Fig. 5 B).	transcription
72722	2	336281	7	NULL	NULL	0	NULL	APC	GP		bind					PAR1 cleavage 	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_165	15769747	Antibody-blocking experiments demonstrate that this suppressive effect on p53 expression was dependent on APC binding to EPCR as well as PAR1 cleavage ( Fig. 5 B).	transcription
72723	3	336281	7	NULL	NULL	0	NULL	p53	GP	suppressive effect of	depends on					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_165	15769747	Antibody-blocking experiments demonstrate that this suppressive effect on p53 expression was dependent on APC binding to EPCR as well as PAR1 cleavage ( Fig. 5 B).	transcription
72724	4	336281	7	NULL	NULL	NULL	NULL	p53	GP	suppressive effect of	depends on					statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_280_20_19808_s_165	15769747	Antibody-blocking experiments demonstrate that this suppressive effect on p53 expression was dependent on APC binding to EPCR as well as PAR1 cleavage ( Fig. 5 B).	transcription
72725	1	336282	7	NULL	NULL	0	NULL	N-MethylN''-nitro-N-nitrosoguanidine 	Chemical		activates					APC gene	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_cellbiol_136_3_693_s_460	9024698	Activation of Adenomatous Polyposis Coli (APC) Gene Expression by the DNA-alkylating Agent N-MethylN''-nitro-N-nitrosoguanidine Requires p53.	transcription
72726	2	336282	7	NULL	NULL	0	NULL	statement 1	Process		requires					p53	GP				NULL		0	NULL	NULL	NULL	gw60_cellbiol_136_3_693_s_460	9024698	Activation of Adenomatous Polyposis Coli (APC) Gene Expression by the DNA-alkylating Agent N-MethylN''-nitro-N-nitrosoguanidine Requires p53.	transcription
72727	3	336282	7	NULL	NULL	0	NULL	APC	Organism		is					Adenomatous Polyposis Coli	Organism				NULL		0	NULL	NULL	NULL	gw60_cellbiol_136_3_693_s_460	9024698	Activation of Adenomatous Polyposis Coli (APC) Gene Expression by the DNA-alkylating Agent N-MethylN''-nitro-N-nitrosoguanidine Requires p53.	transcription
72728	4	336282	7	NULL	NULL	0	NULL	N-MethylN''-nitro-N-nitrosoguanidine	Chemical		is a type of					DNA-alkylating Agent	Chemical				NULL		0	NULL	NULL	NULL	gw60_cellbiol_136_3_693_s_460	9024698	Activation of Adenomatous Polyposis Coli (APC) Gene Expression by the DNA-alkylating Agent N-MethylN''-nitro-N-nitrosoguanidine Requires p53.	transcription
72729	1	336283	7	NULL	NULL	0	NULL	APC gene	GP	inactivation of	during					adenoma	MedicalFinding	development of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_306_4_799_s_66	12821112	In this sequence, the APC gene (5q) is inactivated  at an early stage, followed by activation of the K-ras gene during the development  of moderate to severe adenoma, and inactivation of the p53 gene (17p) at the stage  of conversion from adenoma to carcinoma.	transcription
72730	2	336283	7	NULL	NULL	0	NULL	statement 1	Process		followed by					K-ras gene	GP	activation of			NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_306_4_799_s_66	12821112	In this sequence, the APC gene (5q) is inactivated  at an early stage, followed by activation of the K-ras gene during the development  of moderate to severe adenoma, and inactivation of the p53 gene (17p) at the stage  of conversion from adenoma to carcinoma.	transcription
72731	3	336283	7	NULL	NULL	0	NULL	adenoma	MedicalFinding		converted to					carcinoma	MedicalFinding				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_306_4_799_s_66	12821112	In this sequence, the APC gene (5q) is inactivated  at an early stage, followed by activation of the K-ras gene during the development  of moderate to severe adenoma, and inactivation of the p53 gene (17p) at the stage  of conversion from adenoma to carcinoma.	transcription
72732	4	336283	7	NULL	NULL	0	NULL	p53 gene	GP	inactivation of	occur during					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_biochmbiophyrescomm_306_4_799_s_66	12821112	In this sequence, the APC gene (5q) is inactivated  at an early stage, followed by activation of the K-ras gene during the development  of moderate to severe adenoma, and inactivation of the p53 gene (17p) at the stage  of conversion from adenoma to carcinoma.	transcription
72733	1	336284	7	NULL	NULL	0	NULL	APC gene	GP		is					inducible	Process				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_2_252_s_31	16150893	We also found that the  APC gene is inducible, and its expression can be regulated by DNA-alkylating agent  N-methyl- N''-nitro- N-nitrosoguanidine (MNNG), which is mediated by p53 (   -  ).	transcription
72734	2	336284	7	NULL	NULL	NULL	NULL	MNNG	Chemical		regulates					APC gene	GP	expression of			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_2_252_s_31	16150893	We also found that the  APC gene is inducible, and its expression can be regulated by DNA-alkylating agent  N-methyl- N''-nitro- N-nitrosoguanidine (MNNG), which is mediated by p53 (   -  ).	transcription
72735	3	336284	7	NULL	NULL	0	NULL	statement 2	Process		mediated by					p53	GP				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_2_252_s_31	16150893	We also found that the  APC gene is inducible, and its expression can be regulated by DNA-alkylating agent  N-methyl- N''-nitro- N-nitrosoguanidine (MNNG), which is mediated by p53 (   -  ).	transcription
72736	4	336284	7	NULL	NULL	0	NULL	MNNG	Chemical		is					N-methyl- N''-nitro- N-nitrosoguanidine	Chemical				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_2_252_s_31	16150893	We also found that the  APC gene is inducible, and its expression can be regulated by DNA-alkylating agent  N-methyl- N''-nitro- N-nitrosoguanidine (MNNG), which is mediated by p53 (   -  ).	transcription
72737	5	336284	7	NULL	NULL	0	NULL	MNNG	Chemical		is a type of					DNA-alkylating agent	Chemical				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_2_252_s_31	16150893	We also found that the  APC gene is inducible, and its expression can be regulated by DNA-alkylating agent  N-methyl- N''-nitro- N-nitrosoguanidine (MNNG), which is mediated by p53 (   -  ).	transcription
72738	1	336285	7	NULL	NULL	0	NULL	Apc	GP		initiate					intestinal tumor formation	MedicalFinding				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_17_7598_s_339	15314168	The loss of a single allele of the cyclin-dependent kinase inhibitor p21CIP1 also promoted  Apc-initiated intestinal tumor formation ( ), and the loss of a single  p27KIP1 allele ( ), or  p53, which is a regulator of p21CIP1 expression, also promotes tumor formation ( ).	transcription
72739	2	336285	7	NULL	NULL	NULL	NULL	p21CIP1 allele	GP	loss of single 	promote					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_17_7598_s_339	15314168	The loss of a single allele of the cyclin-dependent kinase inhibitor p21CIP1 also promoted  Apc-initiated intestinal tumor formation ( ), and the loss of a single  p27KIP1 allele ( ), or  p53, which is a regulator of p21CIP1 expression, also promotes tumor formation ( ).	transcription
72740	3	336285	7	NULL	NULL	0	NULL	 p27KIP1 allele	GP	loss of single	promote					tumor formation	MedicalFinding				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_17_7598_s_339	15314168	The loss of a single allele of the cyclin-dependent kinase inhibitor p21CIP1 also promoted  Apc-initiated intestinal tumor formation ( ), and the loss of a single  p27KIP1 allele ( ), or  p53, which is a regulator of p21CIP1 expression, also promotes tumor formation ( ).	transcription
72741	4	336285	7	NULL	NULL	0	NULL	p53	GP		regulate					p21CIP1	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_17_7598_s_339	15314168	The loss of a single allele of the cyclin-dependent kinase inhibitor p21CIP1 also promoted  Apc-initiated intestinal tumor formation ( ), and the loss of a single  p27KIP1 allele ( ), or  p53, which is a regulator of p21CIP1 expression, also promotes tumor formation ( ).	transcription
72742	5	336285	7	NULL	NULL	0	NULL	p53	GP		promote					tumor formation	MedicalFinding				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_17_7598_s_339	15314168	The loss of a single allele of the cyclin-dependent kinase inhibitor p21CIP1 also promoted  Apc-initiated intestinal tumor formation ( ), and the loss of a single  p27KIP1 allele ( ), or  p53, which is a regulator of p21CIP1 expression, also promotes tumor formation ( ).	transcription
72743	6	336285	7	NULL	NULL	0	NULL	p21CIP1	GP		is a type of					cyclin-dependent kinase inhibitor	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_17_7598_s_339	15314168	The loss of a single allele of the cyclin-dependent kinase inhibitor p21CIP1 also promoted  Apc-initiated intestinal tumor formation ( ), and the loss of a single  p27KIP1 allele ( ), or  p53, which is a regulator of p21CIP1 expression, also promotes tumor formation ( ).	transcription
72744	7	336285	7	NULL	NULL	0	NULL	statement 2	Process		is an alternative to					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_17_7598_s_339	15314168	The loss of a single allele of the cyclin-dependent kinase inhibitor p21CIP1 also promoted  Apc-initiated intestinal tumor formation ( ), and the loss of a single  p27KIP1 allele ( ), or  p53, which is a regulator of p21CIP1 expression, also promotes tumor formation ( ).	transcription
72746	1	336286	7	NULL	NULL	0	NULL	Mdm2	GP		mediate					ubiquitin/proteasome mechanism	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_11_10615_s_170	14688278	To rule out the possibility that Z-LLal directly inhibits proteasome function, we examined the effect of Z-LLal on the stability of p53 protein, which is known to be degraded by an Mdm2-mediated ubiquitin/proteasome mechanism but not by the APC-dependent pathway.	transcription
72747	2	336286	7	NULL	NULL	0	NULL	p53 protein	GP		not degraded by					APC-dependent pathway	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_11_10615_s_170	14688278	To rule out the possibility that Z-LLal directly inhibits proteasome function, we examined the effect of Z-LLal on the stability of p53 protein, which is known to be degraded by an Mdm2-mediated ubiquitin/proteasome mechanism but not by the APC-dependent pathway.	transcription
72748	3	336286	7	NULL	NULL	0	NULL	p53 protein	GP		degraded by					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_11_10615_s_170	14688278	To rule out the possibility that Z-LLal directly inhibits proteasome function, we examined the effect of Z-LLal on the stability of p53 protein, which is known to be degraded by an Mdm2-mediated ubiquitin/proteasome mechanism but not by the APC-dependent pathway.	transcription
72749	1	336287	7	NULL	NULL	0	NULL	p53	GP		down-regulate					beta-catenin	GP	wt			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_20_6768_s_233	11564862	While p53 could down-regulate wt beta-catenin in the presence of wt or even mutant APC, it failed to affect mutants of beta-catenin that are resistant to the APC-GSK3beta-axin-mediated degradation.	transcription
72750	2	336287	7	NULL	NULL	0	NULL	statement 1	Process		in the presence of					APC	GP	wt			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_20_6768_s_233	11564862	While p53 could down-regulate wt beta-catenin in the presence of wt or even mutant APC, it failed to affect mutants of beta-catenin that are resistant to the APC-GSK3beta-axin-mediated degradation.	transcription
72751	3	336287	7	NULL	NULL	0	NULL	statement 1	Process		in the presence of					APC	GP	mutant			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_20_6768_s_233	11564862	While p53 could down-regulate wt beta-catenin in the presence of wt or even mutant APC, it failed to affect mutants of beta-catenin that are resistant to the APC-GSK3beta-axin-mediated degradation.	transcription
72752	4	336287	7	NULL	NULL	0	NULL	APC-GSK3beta-axin	Process		mediate					beta-catenin	GP	degradation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_20_6768_s_233	11564862	While p53 could down-regulate wt beta-catenin in the presence of wt or even mutant APC, it failed to affect mutants of beta-catenin that are resistant to the APC-GSK3beta-axin-mediated degradation.	transcription
72753	5	336287	7	NULL	NULL	NULL	NULL	beta-catenin	GP	mutant	resistant to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_20_6768_s_233	11564862	While p53 could down-regulate wt beta-catenin in the presence of wt or even mutant APC, it failed to affect mutants of beta-catenin that are resistant to the APC-GSK3beta-axin-mediated degradation.	transcription
72754	6	336287	7	NULL	NULL	0	NULL	p53	GP		failed to affect					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_20_6768_s_233	11564862	While p53 could down-regulate wt beta-catenin in the presence of wt or even mutant APC, it failed to affect mutants of beta-catenin that are resistant to the APC-GSK3beta-axin-mediated degradation.	transcription
72755	1	336288	7	NULL	NULL	0	NULL	BRCA1	GP		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_23_16582_s_323	10347224	Many well described tumor suppressor/growth arrest genes, such as  BRCA1 ( 55),  APC ( 56),  p53 ( 57),  p33 ING1 ( 58),  CHOP ( 59), and the cyclin-dependent kinase inhibitor  p27 ( 45), also induce apoptosis.	transcription
72756	2	336288	7	NULL	NULL	0	NULL	APC	GP		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_23_16582_s_323	10347224	Many well described tumor suppressor/growth arrest genes, such as  BRCA1 ( 55),  APC ( 56),  p53 ( 57),  p33 ING1 ( 58),  CHOP ( 59), and the cyclin-dependent kinase inhibitor  p27 ( 45), also induce apoptosis.	transcription
72757	3	336288	7	NULL	NULL	0	NULL	p53	GP		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_23_16582_s_323	10347224	Many well described tumor suppressor/growth arrest genes, such as  BRCA1 ( 55),  APC ( 56),  p53 ( 57),  p33 ING1 ( 58),  CHOP ( 59), and the cyclin-dependent kinase inhibitor  p27 ( 45), also induce apoptosis.	transcription
72758	4	336288	7	NULL	NULL	NULL	NULL	p33 ING1	GP		induce					apoptosis	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_23_16582_s_323	10347224	Many well described tumor suppressor/growth arrest genes, such as  BRCA1 ( 55),  APC ( 56),  p53 ( 57),  p33 ING1 ( 58),  CHOP ( 59), and the cyclin-dependent kinase inhibitor  p27 ( 45), also induce apoptosis.	transcription
72759	5	336288	7	NULL	NULL	0	NULL	CHOP	GP		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_23_16582_s_323	10347224	Many well described tumor suppressor/growth arrest genes, such as  BRCA1 ( 55),  APC ( 56),  p53 ( 57),  p33 ING1 ( 58),  CHOP ( 59), and the cyclin-dependent kinase inhibitor  p27 ( 45), also induce apoptosis.	transcription
72760	6	336288	7	NULL	NULL	0	NULL	p27	GP		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_23_16582_s_323	10347224	Many well described tumor suppressor/growth arrest genes, such as  BRCA1 ( 55),  APC ( 56),  p53 ( 57),  p33 ING1 ( 58),  CHOP ( 59), and the cyclin-dependent kinase inhibitor  p27 ( 45), also induce apoptosis.	transcription
72761	7	336288	7	NULL	NULL	0	NULL	BRCA1	GP		is a type of					 tumor suppressor/growth arrest genes	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_23_16582_s_323	10347224	Many well described tumor suppressor/growth arrest genes, such as  BRCA1 ( 55),  APC ( 56),  p53 ( 57),  p33 ING1 ( 58),  CHOP ( 59), and the cyclin-dependent kinase inhibitor  p27 ( 45), also induce apoptosis.	transcription
72762	8	336288	7	NULL	NULL	0	NULL	APC	GP		is a type of					tumor suppressor/growth arrest genes	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_23_16582_s_323	10347224	Many well described tumor suppressor/growth arrest genes, such as  BRCA1 ( 55),  APC ( 56),  p53 ( 57),  p33 ING1 ( 58),  CHOP ( 59), and the cyclin-dependent kinase inhibitor  p27 ( 45), also induce apoptosis.	transcription
72763	9	336288	7	NULL	NULL	0	NULL	p53	GP		is a type of					tumor suppressor/growth arrest genes	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_23_16582_s_323	10347224	Many well described tumor suppressor/growth arrest genes, such as  BRCA1 ( 55),  APC ( 56),  p53 ( 57),  p33 ING1 ( 58),  CHOP ( 59), and the cyclin-dependent kinase inhibitor  p27 ( 45), also induce apoptosis.	transcription
72764	10	336288	7	NULL	NULL	0	NULL	p33 ING1	GP		is a type of					tumor suppressor/growth arrest genes	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_23_16582_s_323	10347224	Many well described tumor suppressor/growth arrest genes, such as  BRCA1 ( 55),  APC ( 56),  p53 ( 57),  p33 ING1 ( 58),  CHOP ( 59), and the cyclin-dependent kinase inhibitor  p27 ( 45), also induce apoptosis.	transcription
72765	11	336288	7	NULL	NULL	0	NULL	CHOP	GP		is a type of					tumor suppressor/growth arrest genes	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_23_16582_s_323	10347224	Many well described tumor suppressor/growth arrest genes, such as  BRCA1 ( 55),  APC ( 56),  p53 ( 57),  p33 ING1 ( 58),  CHOP ( 59), and the cyclin-dependent kinase inhibitor  p27 ( 45), also induce apoptosis.	transcription
72766	12	336288	7	NULL	NULL	0	NULL	p27	GP		is a type of					tumor suppressor/growth arrest genes	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_23_16582_s_323	10347224	Many well described tumor suppressor/growth arrest genes, such as  BRCA1 ( 55),  APC ( 56),  p53 ( 57),  p33 ING1 ( 58),  CHOP ( 59), and the cyclin-dependent kinase inhibitor  p27 ( 45), also induce apoptosis.	transcription
72767	13	336288	7	NULL	NULL	0	NULL	p27	GP		is a inhibitor of					cyclin-dependent kinase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_23_16582_s_323	10347224	Many well described tumor suppressor/growth arrest genes, such as  BRCA1 ( 55),  APC ( 56),  p53 ( 57),  p33 ING1 ( 58),  CHOP ( 59), and the cyclin-dependent kinase inhibitor  p27 ( 45), also induce apoptosis.	transcription
72768	1	336289	7	NULL	NULL	0	NULL	p53 activity	GP 	lack of 	does not effect					neoplasia	MedicalFinding	intestine			NULL	Min mice heterozygous for the Min nonsense allele of Apc	0	NULL	NULL	NULL	gw60_pnas_97_7_3461_s_20	10716720	Preliminary studies tested whether a lack of  p53 activity affected neoplasia in the intestine of Min (multiple intestinal neoplasia) mice heterozygous for the  Min nonsense allele of  Apc, but no significant effect was observed ( 7-10).	transcription
72769	2	336289	7	NULL	NULL	0	NULL	Min	MedicalFinding		is					multiple intestinal neoplasia	MedicalFinding				NULL		0	NULL	NULL	NULL	gw60_pnas_97_7_3461_s_20	10716720	Preliminary studies tested whether a lack of  p53 activity affected neoplasia in the intestine of Min (multiple intestinal neoplasia) mice heterozygous for the  Min nonsense allele of  Apc, but no significant effect was observed ( 7-10).	transcription
72770	1	336290	7	NULL	NULL	0	NULL	E2F	GP		mediate					transcription	Process				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_cell-cycle_5_14_16861914_s_5	16861914	We propose that loss of  pRb repression of E2F-mediated transcription causing misregulation of  Emi1 and APC/C substrates results in the generation of tetraploidy and  proliferation of genomically unstable cells in the absence of normal p53  function.	transcription
72771	2	336290	7	NULL	NULL	0	NULL	pRb	GP		repress					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0740-0759_cell-cycle_5_14_16861914_s_5	16861914	We propose that loss of  pRb repression of E2F-mediated transcription causing misregulation of  Emi1 and APC/C substrates results in the generation of tetraploidy and  proliferation of genomically unstable cells in the absence of normal p53  function.	transcription
72772	3	336290	7	NULL	NULL	0	NULL	statement 2	Process	loss of	cause					Emi1 substrates	GP	misregulation of			NULL		0	NULL	NULL	NULL	abs-batch0740-0759_cell-cycle_5_14_16861914_s_5	16861914	We propose that loss of  pRb repression of E2F-mediated transcription causing misregulation of  Emi1 and APC/C substrates results in the generation of tetraploidy and  proliferation of genomically unstable cells in the absence of normal p53  function.	transcription
72773	4	336290	7	NULL	NULL	0	NULL	statement 2	Process	loss of	cause					APC/C substrates	GP	misregulation of			NULL		0	NULL	NULL	NULL	abs-batch0740-0759_cell-cycle_5_14_16861914_s_5	16861914	We propose that loss of  pRb repression of E2F-mediated transcription causing misregulation of  Emi1 and APC/C substrates results in the generation of tetraploidy and  proliferation of genomically unstable cells in the absence of normal p53  function.	transcription
72774	5	336290	7	NULL	NULL	0	NULL	statement 3	Process		results in					tetraploidy	Process	generation of			NULL		0	NULL	NULL	NULL	abs-batch0740-0759_cell-cycle_5_14_16861914_s_5	16861914	We propose that loss of  pRb repression of E2F-mediated transcription causing misregulation of  Emi1 and APC/C substrates results in the generation of tetraploidy and  proliferation of genomically unstable cells in the absence of normal p53  function.	transcription
72775	6	336290	7	NULL	NULL	0	NULL	statement 3	Process		results in					genomically unstable cells	Cell	proliferation of			NULL		0	NULL	NULL	NULL	abs-batch0740-0759_cell-cycle_5_14_16861914_s_5	16861914	We propose that loss of  pRb repression of E2F-mediated transcription causing misregulation of  Emi1 and APC/C substrates results in the generation of tetraploidy and  proliferation of genomically unstable cells in the absence of normal p53  function.	transcription
72776	7	336290	7	NULL	NULL	0	NULL	statement 4	Process		results in					tetraploidy	Process	generation of			NULL		0	NULL	NULL	NULL	abs-batch0740-0759_cell-cycle_5_14_16861914_s_5	16861914	We propose that loss of  pRb repression of E2F-mediated transcription causing misregulation of  Emi1 and APC/C substrates results in the generation of tetraploidy and  proliferation of genomically unstable cells in the absence of normal p53  function.	transcription
72777	8	336290	7	NULL	NULL	0	NULL	statement 4	Process		results in					genomically unstable cells	Cell	proliferation of			NULL		0	NULL	NULL	NULL	abs-batch0740-0759_cell-cycle_5_14_16861914_s_5	16861914	We propose that loss of  pRb repression of E2F-mediated transcription causing misregulation of  Emi1 and APC/C substrates results in the generation of tetraploidy and  proliferation of genomically unstable cells in the absence of normal p53  function.	transcription
72778	9	336290	7	NULL	NULL	0	NULL	statement 5	Process		in the absence of					p53 function	Process	normal			NULL		0	NULL	NULL	NULL	abs-batch0740-0759_cell-cycle_5_14_16861914_s_5	16861914	We propose that loss of  pRb repression of E2F-mediated transcription causing misregulation of  Emi1 and APC/C substrates results in the generation of tetraploidy and  proliferation of genomically unstable cells in the absence of normal p53  function.	transcription
72779	10	336290	7	NULL	NULL	0	NULL	statement 6	Process		in the absence of					p53 function	Process	normal			NULL		0	NULL	NULL	NULL	abs-batch0740-0759_cell-cycle_5_14_16861914_s_5	16861914	We propose that loss of  pRb repression of E2F-mediated transcription causing misregulation of  Emi1 and APC/C substrates results in the generation of tetraploidy and  proliferation of genomically unstable cells in the absence of normal p53  function.	transcription
72780	11	336290	7	NULL	NULL	0	NULL	statement 7	Process		in the absence of					p53 function	Process	normal			NULL		0	NULL	NULL	NULL	abs-batch0740-0759_cell-cycle_5_14_16861914_s_5	16861914	We propose that loss of  pRb repression of E2F-mediated transcription causing misregulation of  Emi1 and APC/C substrates results in the generation of tetraploidy and  proliferation of genomically unstable cells in the absence of normal p53  function.	transcription
72781	12	336290	7	NULL	NULL	0	NULL	statement 8	Process		in the absence of					p53 function	Process	normal			NULL		0	NULL	NULL	NULL	abs-batch0740-0759_cell-cycle_5_14_16861914_s_5	16861914	We propose that loss of  pRb repression of E2F-mediated transcription causing misregulation of  Emi1 and APC/C substrates results in the generation of tetraploidy and  proliferation of genomically unstable cells in the absence of normal p53  function.	transcription
72782	1	336291	7	NULL	NULL	0	NULL	DMH	Chemical		induce					Colon tumors	MedicalFinding				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_22_2_315_s_27	11181454	Colon tumors induced by DMH contain Ki- ras mutations but lack genetic changes in  p53 ( 26), whereas those induced by IQ lack mutations in Ki- ras and  p53 genes, and have few microsatellite or  Apc mutations ( 27).	transcription
72783	2	336291	7	NULL	NULL	0	NULL	Colon tumors	MedicalFinding		contain					Ki- ras mutations	Process				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_22_2_315_s_27	11181454	Colon tumors induced by DMH contain Ki- ras mutations but lack genetic changes in  p53 ( 26), whereas those induced by IQ lack mutations in Ki- ras and  p53 genes, and have few microsatellite or  Apc mutations ( 27).	transcription
72784	3	336291	7	NULL	NULL	0	NULL	statement 2	Process		lack					p53	GP	genetic changes in			NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_22_2_315_s_27	11181454	Colon tumors induced by DMH contain Ki- ras mutations but lack genetic changes in  p53 ( 26), whereas those induced by IQ lack mutations in Ki- ras and  p53 genes, and have few microsatellite or  Apc mutations ( 27).	transcription
72785	4	336291	7	NULL	NULL	0	NULL	IQ	Chemical		induce					Colon tumors	MedicalFinding				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_22_2_315_s_27	11181454	Colon tumors induced by DMH contain Ki- ras mutations but lack genetic changes in  p53 ( 26), whereas those induced by IQ lack mutations in Ki- ras and  p53 genes, and have few microsatellite or  Apc mutations ( 27).	transcription
72786	5	336291	7	NULL	NULL	NULL	NULL	statement 4	Process		lack					Ki-ras gene	GP	mutations in			NULL		NULL	NULL	NULL	NULL	gw60_carcinogenesis_22_2_315_s_27	11181454	Colon tumors induced by DMH contain Ki- ras mutations but lack genetic changes in  p53 ( 26), whereas those induced by IQ lack mutations in Ki- ras and  p53 genes, and have few microsatellite or  Apc mutations ( 27).	transcription
72787	6	336291	7	NULL	NULL	0	NULL	statement 4	Process		lack					p53 gene	GP	mutations in			NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_22_2_315_s_27	11181454	Colon tumors induced by DMH contain Ki- ras mutations but lack genetic changes in  p53 ( 26), whereas those induced by IQ lack mutations in Ki- ras and  p53 genes, and have few microsatellite or  Apc mutations ( 27).	transcription
72788	7	336291	7	NULL	NULL	0	NULL	statement 4	Process		contain					microsatellite mutations	Process				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_22_2_315_s_27	11181454	Colon tumors induced by DMH contain Ki- ras mutations but lack genetic changes in  p53 ( 26), whereas those induced by IQ lack mutations in Ki- ras and  p53 genes, and have few microsatellite or  Apc mutations ( 27).	transcription
72789	8	336291	7	NULL	NULL	0	NULL	statement 4	Process		contain					Apc mutations	Process				NULL		0	NULL	NULL	NULL	gw60_carcinogenesis_22_2_315_s_27	11181454	Colon tumors induced by DMH contain Ki- ras mutations but lack genetic changes in  p53 ( 26), whereas those induced by IQ lack mutations in Ki- ras and  p53 genes, and have few microsatellite or  Apc mutations ( 27).	transcription
72790	1	336292	7	NULL	NULL	0	NULL	cells	Cell		progressed to					Cell cycle	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_7_2844_s_317	12857869	Our present results support that in cell lines with normal  APC and p53 products, such as epidermal keratinocytes analyzed here, a tight  regulation of cytoplasmic beta-catenin (nonassociated to adhesion complexes)  during G2 to M transition is required to allow the correct progression of  cells into the cell cycle.	transcription
72791	2	336292	7	NULL	NULL	NULL	NULL	beta-catenin	GP	tight regulation of;;cytoplasmic	required for					statement 1	Process	correct progression of			NULL	epidermal keratinocytes  with normal APC products	NULL	NULL	NULL	NULL	gw60_molbiolcell_14_7_2844_s_317	12857869	Our present results support that in cell lines with normal  APC and p53 products, such as epidermal keratinocytes analyzed here, a tight  regulation of cytoplasmic beta-catenin (nonassociated to adhesion complexes)  during G2 to M transition is required to allow the correct progression of  cells into the cell cycle.	transcription
72792	3	336292	7	NULL	NULL	NULL	NULL	beta-catenin	GP	tight regulation of;;cytoplasmic	required for					statement 1	Process	correct progression of			NULL	epidermal keratinocytes  with normal p53 products	NULL	NULL	NULL	NULL	gw60_molbiolcell_14_7_2844_s_317	12857869	Our present results support that in cell lines with normal  APC and p53 products, such as epidermal keratinocytes analyzed here, a tight  regulation of cytoplasmic beta-catenin (nonassociated to adhesion complexes)  during G2 to M transition is required to allow the correct progression of  cells into the cell cycle.	transcription
72793	4	336292	7	NULL	NULL	0	NULL	G2	Process		transition to					M	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_7_2844_s_317	12857869	Our present results support that in cell lines with normal  APC and p53 products, such as epidermal keratinocytes analyzed here, a tight  regulation of cytoplasmic beta-catenin (nonassociated to adhesion complexes)  during G2 to M transition is required to allow the correct progression of  cells into the cell cycle.	transcription
72794	5	336292	7	NULL	NULL	0	NULL	statement 2	Process		occur during					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_7_2844_s_317	12857869	Our present results support that in cell lines with normal  APC and p53 products, such as epidermal keratinocytes analyzed here, a tight  regulation of cytoplasmic beta-catenin (nonassociated to adhesion complexes)  during G2 to M transition is required to allow the correct progression of  cells into the cell cycle.	transcription
72795	6	336292	7	NULL	NULL	0	NULL	statement 3	Process		occur during					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_7_2844_s_317	12857869	Our present results support that in cell lines with normal  APC and p53 products, such as epidermal keratinocytes analyzed here, a tight  regulation of cytoplasmic beta-catenin (nonassociated to adhesion complexes)  during G2 to M transition is required to allow the correct progression of  cells into the cell cycle.	transcription
72796	7	336292	7	NULL	NULL	0	NULL	beta-catenin	GP		nonassociated to					adhesion complex	GP				NULL		0	NULL	NULL	NULL	gw60_molbiolcell_14_7_2844_s_317	12857869	Our present results support that in cell lines with normal  APC and p53 products, such as epidermal keratinocytes analyzed here, a tight  regulation of cytoplasmic beta-catenin (nonassociated to adhesion complexes)  during G2 to M transition is required to allow the correct progression of  cells into the cell cycle.	transcription
72797	1	336293	7	NULL	NULL	0	NULL	MNNG	Chemical		cause					colon cancer	MedicalFinding				NULL	animals	0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_3	9388195	In this study we treated  the HCT-116 colon cancer cell line with alkylating agents including  N-methyl- N -nitro- N-nitrosoguanidine (MNNG),which is known to cause colon cancer in animals, and examined the expression of both  APC and  p53 genes.	transcription
72798	2	336293	7	NULL	NULL	0	NULL	MNNG	Chemical		is					N-methyl- N -nitro- N-nitrosoguanidine	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_3	9388195	In this study we treated  the HCT-116 colon cancer cell line with alkylating agents including  N-methyl- N -nitro- N-nitrosoguanidine (MNNG),which is known to cause colon cancer in animals, and examined the expression of both  APC and  p53 genes.	transcription
72799	3	336293	7	NULL	NULL	0	NULL	MNNG	Chemical		is a type of					alkylating agent	Chemical				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_272_49_30619_s_3	9388195	In this study we treated  the HCT-116 colon cancer cell line with alkylating agents including  N-methyl- N -nitro- N-nitrosoguanidine (MNNG),which is known to cause colon cancer in animals, and examined the expression of both  APC and  p53 genes.	transcription
72803	1	336295	7	NULL	NULL	0	NULL	K-ras	GP	mutation in	increased in					Dukes' C tumors	MedicalFinding				NULL		0	NULL	NULL	NULL	gw60_pnas_99_14_9433_s_125	12093899	Interestingly, analysis of the relative contribution of APC, K-ras, and p53 to the overall mutation burden in early and advanced tumors demonstrated a statistically significant increase in the K-ras mutation frequency in Dukes' C tumors (Fig.  4 B), suggesting that altered K-ras function is an important determinant of tumor progression.	transcription
72804	2	336295	7	NULL	NULL	0	NULL	K-ras	GP	altered function of	determinant of		important			tumor progression	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_99_14_9433_s_125	12093899	Interestingly, analysis of the relative contribution of APC, K-ras, and p53 to the overall mutation burden in early and advanced tumors demonstrated a statistically significant increase in the K-ras mutation frequency in Dukes' C tumors (Fig.  4 B), suggesting that altered K-ras function is an important determinant of tumor progression.	transcription
72805	1	336296	7	NULL	NULL	0	NULL	Mdm2	GP		catalyze					Mdm2	GP	ubiquitination of			NULL		0	NULL	NULL	NULL	gw60_pnas_96_20_11364_s_17	10500182	Other E3s include Mdm2, which catalyzes both its own ubiquitination and that of p53 ( 6); the anaphase-promoting complex (APC); and other F box and cullin-containing complexes whose substrates include Sic1p, G1 cyclins, IkappaB, and beta-catenin ( 7).	transcription
72806	2	336296	7	NULL	NULL	0	NULL	Mdm2	GP		catalyze					p53	GP	ubiquitination of			NULL		0	NULL	NULL	NULL	gw60_pnas_96_20_11364_s_17	10500182	Other E3s include Mdm2, which catalyzes both its own ubiquitination and that of p53 ( 6); the anaphase-promoting complex (APC); and other F box and cullin-containing complexes whose substrates include Sic1p, G1 cyclins, IkappaB, and beta-catenin ( 7).	transcription
72807	3	336296	7	NULL	NULL	0	NULL	E3	GP		include					Mdm2	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_20_11364_s_17	10500182	Other E3s include Mdm2, which catalyzes both its own ubiquitination and that of p53 ( 6); the anaphase-promoting complex (APC); and other F box and cullin-containing complexes whose substrates include Sic1p, G1 cyclins, IkappaB, and beta-catenin ( 7).	transcription
72808	4	336296	7	NULL	NULL	0	NULL	E3	GP		include					APC	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_20_11364_s_17	10500182	Other E3s include Mdm2, which catalyzes both its own ubiquitination and that of p53 ( 6); the anaphase-promoting complex (APC); and other F box and cullin-containing complexes whose substrates include Sic1p, G1 cyclins, IkappaB, and beta-catenin ( 7).	transcription
72809	5	336296	7	NULL	NULL	0	NULL	E3	GP		include					F box	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_20_11364_s_17	10500182	Other E3s include Mdm2, which catalyzes both its own ubiquitination and that of p53 ( 6); the anaphase-promoting complex (APC); and other F box and cullin-containing complexes whose substrates include Sic1p, G1 cyclins, IkappaB, and beta-catenin ( 7).	transcription
72810	6	336296	7	NULL	NULL	0	NULL	E3	GP		include					cullin-containing complex	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_20_11364_s_17	10500182	Other E3s include Mdm2, which catalyzes both its own ubiquitination and that of p53 ( 6); the anaphase-promoting complex (APC); and other F box and cullin-containing complexes whose substrates include Sic1p, G1 cyclins, IkappaB, and beta-catenin ( 7).	transcription
72811	7	336296	7	NULL	NULL	0	NULL	APC	GP		is					anaphase-promoting complex	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_20_11364_s_17	10500182	Other E3s include Mdm2, which catalyzes both its own ubiquitination and that of p53 ( 6); the anaphase-promoting complex (APC); and other F box and cullin-containing complexes whose substrates include Sic1p, G1 cyclins, IkappaB, and beta-catenin ( 7).	transcription
72812	8	336296	7	NULL	NULL	0	NULL	cullin-containing complex	GP	substrate of	include					Sic1p	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_20_11364_s_17	10500182	Other E3s include Mdm2, which catalyzes both its own ubiquitination and that of p53 ( 6); the anaphase-promoting complex (APC); and other F box and cullin-containing complexes whose substrates include Sic1p, G1 cyclins, IkappaB, and beta-catenin ( 7).	transcription
72813	9	336296	7	NULL	NULL	0	NULL	cullin-containing complex	GP	substrate of	include					G1 cyclins	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_20_11364_s_17	10500182	Other E3s include Mdm2, which catalyzes both its own ubiquitination and that of p53 ( 6); the anaphase-promoting complex (APC); and other F box and cullin-containing complexes whose substrates include Sic1p, G1 cyclins, IkappaB, and beta-catenin ( 7).	transcription
72814	10	336296	7	NULL	NULL	0	NULL	cullin-containing complex	GP	substrate of	include					 IkappaB	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_20_11364_s_17	10500182	Other E3s include Mdm2, which catalyzes both its own ubiquitination and that of p53 ( 6); the anaphase-promoting complex (APC); and other F box and cullin-containing complexes whose substrates include Sic1p, G1 cyclins, IkappaB, and beta-catenin ( 7).	transcription
72815	11	336296	7	NULL	NULL	0	NULL	cullin-containing complex	GP	substrate of	include					beta-catenin	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_96_20_11364_s_17	10500182	Other E3s include Mdm2, which catalyzes both its own ubiquitination and that of p53 ( 6); the anaphase-promoting complex (APC); and other F box and cullin-containing complexes whose substrates include Sic1p, G1 cyclins, IkappaB, and beta-catenin ( 7).	transcription
72816	1	336297	7	NULL	NULL	0	NULL	APC	GP		induced by					quercetin	Chemical				NULL		0	NULL	NULL	NULL	gw70_clindiagnlabimmun_11_1_63_s_94	14715546	Furthermore, the six tumor suppressor genes adenomatosis polyposis coli ( APC), transforming growth factor beta receptor 11 ( TGFbetaR2), tumor suppressor protein p53 (p53), retinoblastoma 1 ( Rb), cyclin-dependent kinase inhbitor 1C (p57Kip2), and tuberous sclerosis 2 ( TSC-2) were induced by quercetin, whereas undetectable levels of these genes were expressed by control, untreated PC-3 cells.	transcription
72817	2	336297	7	NULL	NULL	0	NULL	TGFbetaR2	GP		induced by					quercetin	Chemical				NULL		0	NULL	NULL	NULL	gw70_clindiagnlabimmun_11_1_63_s_94	14715546	Furthermore, the six tumor suppressor genes adenomatosis polyposis coli ( APC), transforming growth factor beta receptor 11 ( TGFbetaR2), tumor suppressor protein p53 (p53), retinoblastoma 1 ( Rb), cyclin-dependent kinase inhbitor 1C (p57Kip2), and tuberous sclerosis 2 ( TSC-2) were induced by quercetin, whereas undetectable levels of these genes were expressed by control, untreated PC-3 cells.	transcription
72818	3	336297	7	NULL	NULL	0	NULL	p53	GP		induced by					quercetin	Chemical				NULL		0	NULL	NULL	NULL	gw70_clindiagnlabimmun_11_1_63_s_94	14715546	Furthermore, the six tumor suppressor genes adenomatosis polyposis coli ( APC), transforming growth factor beta receptor 11 ( TGFbetaR2), tumor suppressor protein p53 (p53), retinoblastoma 1 ( Rb), cyclin-dependent kinase inhbitor 1C (p57Kip2), and tuberous sclerosis 2 ( TSC-2) were induced by quercetin, whereas undetectable levels of these genes were expressed by control, untreated PC-3 cells.	transcription
72819	4	336297	7	NULL	NULL	0	NULL	Rb	GP		induced by					quercetin	Chemical				NULL		0	NULL	NULL	NULL	gw70_clindiagnlabimmun_11_1_63_s_94	14715546	Furthermore, the six tumor suppressor genes adenomatosis polyposis coli ( APC), transforming growth factor beta receptor 11 ( TGFbetaR2), tumor suppressor protein p53 (p53), retinoblastoma 1 ( Rb), cyclin-dependent kinase inhbitor 1C (p57Kip2), and tuberous sclerosis 2 ( TSC-2) were induced by quercetin, whereas undetectable levels of these genes were expressed by control, untreated PC-3 cells.	transcription
72820	5	336297	7	NULL	NULL	0	NULL	p57Kip2	GP		induced by					quercetin	Chemical				NULL		0	NULL	NULL	NULL	gw70_clindiagnlabimmun_11_1_63_s_94	14715546	Furthermore, the six tumor suppressor genes adenomatosis polyposis coli ( APC), transforming growth factor beta receptor 11 ( TGFbetaR2), tumor suppressor protein p53 (p53), retinoblastoma 1 ( Rb), cyclin-dependent kinase inhbitor 1C (p57Kip2), and tuberous sclerosis 2 ( TSC-2) were induced by quercetin, whereas undetectable levels of these genes were expressed by control, untreated PC-3 cells.	transcription
72821	6	336297	7	NULL	NULL	0	NULL	TSC-2	GP		induced by					quercetin	Chemical				NULL		0	NULL	NULL	NULL	gw70_clindiagnlabimmun_11_1_63_s_94	14715546	Furthermore, the six tumor suppressor genes adenomatosis polyposis coli ( APC), transforming growth factor beta receptor 11 ( TGFbetaR2), tumor suppressor protein p53 (p53), retinoblastoma 1 ( Rb), cyclin-dependent kinase inhbitor 1C (p57Kip2), and tuberous sclerosis 2 ( TSC-2) were induced by quercetin, whereas undetectable levels of these genes were expressed by control, untreated PC-3 cells.	transcription
72822	7	336297	7	NULL	NULL	0	NULL	APC	GP		is					adenomatosis polyposis coli	GP				NULL		0	NULL	NULL	NULL	gw70_clindiagnlabimmun_11_1_63_s_94	14715546	Furthermore, the six tumor suppressor genes adenomatosis polyposis coli ( APC), transforming growth factor beta receptor 11 ( TGFbetaR2), tumor suppressor protein p53 (p53), retinoblastoma 1 ( Rb), cyclin-dependent kinase inhbitor 1C (p57Kip2), and tuberous sclerosis 2 ( TSC-2) were induced by quercetin, whereas undetectable levels of these genes were expressed by control, untreated PC-3 cells.	transcription
72823	8	336297	7	NULL	NULL	0	NULL	APC	GP		is a type of					tumor suppressor genes	GP				NULL		0	NULL	NULL	NULL	gw70_clindiagnlabimmun_11_1_63_s_94	14715546	Furthermore, the six tumor suppressor genes adenomatosis polyposis coli ( APC), transforming growth factor beta receptor 11 ( TGFbetaR2), tumor suppressor protein p53 (p53), retinoblastoma 1 ( Rb), cyclin-dependent kinase inhbitor 1C (p57Kip2), and tuberous sclerosis 2 ( TSC-2) were induced by quercetin, whereas undetectable levels of these genes were expressed by control, untreated PC-3 cells.	transcription
72824	9	336297	7	NULL	NULL	0	NULL	TGFbetaR2	GP		is					transforming growth factor beta receptor 11	GP				NULL		0	NULL	NULL	NULL	gw70_clindiagnlabimmun_11_1_63_s_94	14715546	Furthermore, the six tumor suppressor genes adenomatosis polyposis coli ( APC), transforming growth factor beta receptor 11 ( TGFbetaR2), tumor suppressor protein p53 (p53), retinoblastoma 1 ( Rb), cyclin-dependent kinase inhbitor 1C (p57Kip2), and tuberous sclerosis 2 ( TSC-2) were induced by quercetin, whereas undetectable levels of these genes were expressed by control, untreated PC-3 cells.	transcription
72825	10	336297	7	NULL	NULL	NULL	NULL	TGFbetaR2	GP		is a type of					tumor suppressor genes	GP				NULL		NULL	NULL	NULL	NULL	gw70_clindiagnlabimmun_11_1_63_s_94	14715546	Furthermore, the six tumor suppressor genes adenomatosis polyposis coli ( APC), transforming growth factor beta receptor 11 ( TGFbetaR2), tumor suppressor protein p53 (p53), retinoblastoma 1 ( Rb), cyclin-dependent kinase inhbitor 1C (p57Kip2), and tuberous sclerosis 2 ( TSC-2) were induced by quercetin, whereas undetectable levels of these genes were expressed by control, untreated PC-3 cells.	transcription
72826	11	336297	7	NULL	NULL	0	NULL	p53	GP		is a type of					tumor suppressor protein	GP				NULL		0	NULL	NULL	NULL	gw70_clindiagnlabimmun_11_1_63_s_94	14715546	Furthermore, the six tumor suppressor genes adenomatosis polyposis coli ( APC), transforming growth factor beta receptor 11 ( TGFbetaR2), tumor suppressor protein p53 (p53), retinoblastoma 1 ( Rb), cyclin-dependent kinase inhbitor 1C (p57Kip2), and tuberous sclerosis 2 ( TSC-2) were induced by quercetin, whereas undetectable levels of these genes were expressed by control, untreated PC-3 cells.	transcription
72827	12	336297	7	NULL	NULL	0	NULL	Rb	GP		is 					retinoblastoma 1	GP				NULL		0	NULL	NULL	NULL	gw70_clindiagnlabimmun_11_1_63_s_94	14715546	Furthermore, the six tumor suppressor genes adenomatosis polyposis coli ( APC), transforming growth factor beta receptor 11 ( TGFbetaR2), tumor suppressor protein p53 (p53), retinoblastoma 1 ( Rb), cyclin-dependent kinase inhbitor 1C (p57Kip2), and tuberous sclerosis 2 ( TSC-2) were induced by quercetin, whereas undetectable levels of these genes were expressed by control, untreated PC-3 cells.	transcription
72828	13	336297	7	NULL	NULL	0	NULL	Rb	GP		is a type of					tumor suppressor genes	GP				NULL		0	NULL	NULL	NULL	gw70_clindiagnlabimmun_11_1_63_s_94	14715546	Furthermore, the six tumor suppressor genes adenomatosis polyposis coli ( APC), transforming growth factor beta receptor 11 ( TGFbetaR2), tumor suppressor protein p53 (p53), retinoblastoma 1 ( Rb), cyclin-dependent kinase inhbitor 1C (p57Kip2), and tuberous sclerosis 2 ( TSC-2) were induced by quercetin, whereas undetectable levels of these genes were expressed by control, untreated PC-3 cells.	transcription
72829	14	336297	7	NULL	NULL	NULL	NULL	p57Kip2	GP		is a type of					cyclin-dependent kinase inhbitor 1C	GP				NULL		NULL	NULL	NULL	NULL	gw70_clindiagnlabimmun_11_1_63_s_94	14715546	Furthermore, the six tumor suppressor genes adenomatosis polyposis coli ( APC), transforming growth factor beta receptor 11 ( TGFbetaR2), tumor suppressor protein p53 (p53), retinoblastoma 1 ( Rb), cyclin-dependent kinase inhbitor 1C (p57Kip2), and tuberous sclerosis 2 ( TSC-2) were induced by quercetin, whereas undetectable levels of these genes were expressed by control, untreated PC-3 cells.	transcription
72830	15	336297	7	NULL	NULL	NULL	NULL	p57Kip2	GP		is a type of					tumor suppressor genes	GP				NULL		NULL	NULL	NULL	NULL	gw70_clindiagnlabimmun_11_1_63_s_94	14715546	Furthermore, the six tumor suppressor genes adenomatosis polyposis coli ( APC), transforming growth factor beta receptor 11 ( TGFbetaR2), tumor suppressor protein p53 (p53), retinoblastoma 1 ( Rb), cyclin-dependent kinase inhbitor 1C (p57Kip2), and tuberous sclerosis 2 ( TSC-2) were induced by quercetin, whereas undetectable levels of these genes were expressed by control, untreated PC-3 cells.	transcription
72831	16	336297	7	NULL	NULL	0	NULL	TSC-2	GP		is					tuberous sclerosis 2	GP				NULL		0	NULL	NULL	NULL	gw70_clindiagnlabimmun_11_1_63_s_94	14715546	Furthermore, the six tumor suppressor genes adenomatosis polyposis coli ( APC), transforming growth factor beta receptor 11 ( TGFbetaR2), tumor suppressor protein p53 (p53), retinoblastoma 1 ( Rb), cyclin-dependent kinase inhbitor 1C (p57Kip2), and tuberous sclerosis 2 ( TSC-2) were induced by quercetin, whereas undetectable levels of these genes were expressed by control, untreated PC-3 cells.	transcription
72832	17	336297	7	NULL	NULL	0	NULL	TSC-2	GP		is a type of					tumor suppressor genes	GP				NULL		0	NULL	NULL	NULL	gw70_clindiagnlabimmun_11_1_63_s_94	14715546	Furthermore, the six tumor suppressor genes adenomatosis polyposis coli ( APC), transforming growth factor beta receptor 11 ( TGFbetaR2), tumor suppressor protein p53 (p53), retinoblastoma 1 ( Rb), cyclin-dependent kinase inhbitor 1C (p57Kip2), and tuberous sclerosis 2 ( TSC-2) were induced by quercetin, whereas undetectable levels of these genes were expressed by control, untreated PC-3 cells.	transcription
72833	1	336298	7	NULL	NULL	0	NULL	IkappaB 	GP		is a type of					transcriptional regulator	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_6_2999_s_11	15814838	These motors transport mRNAs for cell fate and polarity determinations (reviewed in Saxton, 2001 ), transcriptional regulators, such as the NF kappa B inhibitor IkappaB (Crepieux  et al., 1997 ), the tumor suppressor protein p53 (Giannakakou  et al., 2000 ; Giannakakou  et al., 2002 ), the developmental factors beta-catenin or adenomatous poliposis coli protein (APC, reviewed in Bienz, 2002 ), the apoptosis effector bim (Puthalakath  et al., 1999 ), and stress-related signaling kinases of the ERK and JNK families (reviewed in Verhey and Rapoport, 2001 ).	transcription
72834	2	336298	7	NULL	NULL	0	NULL	IkappaB	GP		inhibit					NF kappa B	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_6_2999_s_11	15814838	These motors transport mRNAs for cell fate and polarity determinations (reviewed in Saxton, 2001 ), transcriptional regulators, such as the NF kappa B inhibitor IkappaB (Crepieux  et al., 1997 ), the tumor suppressor protein p53 (Giannakakou  et al., 2000 ; Giannakakou  et al., 2002 ), the developmental factors beta-catenin or adenomatous poliposis coli protein (APC, reviewed in Bienz, 2002 ), the apoptosis effector bim (Puthalakath  et al., 1999 ), and stress-related signaling kinases of the ERK and JNK families (reviewed in Verhey and Rapoport, 2001 ).	transcription
72835	3	336298	7	NULL	NULL	0	NULL	p53	GP		is a type of					tumor suppressor protein	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_6_2999_s_11	15814838	These motors transport mRNAs for cell fate and polarity determinations (reviewed in Saxton, 2001 ), transcriptional regulators, such as the NF kappa B inhibitor IkappaB (Crepieux  et al., 1997 ), the tumor suppressor protein p53 (Giannakakou  et al., 2000 ; Giannakakou  et al., 2002 ), the developmental factors beta-catenin or adenomatous poliposis coli protein (APC, reviewed in Bienz, 2002 ), the apoptosis effector bim (Puthalakath  et al., 1999 ), and stress-related signaling kinases of the ERK and JNK families (reviewed in Verhey and Rapoport, 2001 ).	transcription
72836	4	336298	7	NULL	NULL	0	NULL	p53	GP		is a type of					transcriptional regulator	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_6_2999_s_11	15814838	These motors transport mRNAs for cell fate and polarity determinations (reviewed in Saxton, 2001 ), transcriptional regulators, such as the NF kappa B inhibitor IkappaB (Crepieux  et al., 1997 ), the tumor suppressor protein p53 (Giannakakou  et al., 2000 ; Giannakakou  et al., 2002 ), the developmental factors beta-catenin or adenomatous poliposis coli protein (APC, reviewed in Bienz, 2002 ), the apoptosis effector bim (Puthalakath  et al., 1999 ), and stress-related signaling kinases of the ERK and JNK families (reviewed in Verhey and Rapoport, 2001 ).	transcription
72837	5	336298	7	NULL	NULL	0	NULL	 beta-catenin	GP		is a type of					developmental factor	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_6_2999_s_11	15814838	These motors transport mRNAs for cell fate and polarity determinations (reviewed in Saxton, 2001 ), transcriptional regulators, such as the NF kappa B inhibitor IkappaB (Crepieux  et al., 1997 ), the tumor suppressor protein p53 (Giannakakou  et al., 2000 ; Giannakakou  et al., 2002 ), the developmental factors beta-catenin or adenomatous poliposis coli protein (APC, reviewed in Bienz, 2002 ), the apoptosis effector bim (Puthalakath  et al., 1999 ), and stress-related signaling kinases of the ERK and JNK families (reviewed in Verhey and Rapoport, 2001 ).	transcription
72838	6	336298	7	NULL	NULL	0	NULL	APC	GP		is a type of					developmental factor	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_6_2999_s_11	15814838	These motors transport mRNAs for cell fate and polarity determinations (reviewed in Saxton, 2001 ), transcriptional regulators, such as the NF kappa B inhibitor IkappaB (Crepieux  et al., 1997 ), the tumor suppressor protein p53 (Giannakakou  et al., 2000 ; Giannakakou  et al., 2002 ), the developmental factors beta-catenin or adenomatous poliposis coli protein (APC, reviewed in Bienz, 2002 ), the apoptosis effector bim (Puthalakath  et al., 1999 ), and stress-related signaling kinases of the ERK and JNK families (reviewed in Verhey and Rapoport, 2001 ).	transcription
72839	7	336298	7	NULL	NULL	0	NULL	beta-catenin	GP		is a type of					transcriptional regulator	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_6_2999_s_11	15814838	These motors transport mRNAs for cell fate and polarity determinations (reviewed in Saxton, 2001 ), transcriptional regulators, such as the NF kappa B inhibitor IkappaB (Crepieux  et al., 1997 ), the tumor suppressor protein p53 (Giannakakou  et al., 2000 ; Giannakakou  et al., 2002 ), the developmental factors beta-catenin or adenomatous poliposis coli protein (APC, reviewed in Bienz, 2002 ), the apoptosis effector bim (Puthalakath  et al., 1999 ), and stress-related signaling kinases of the ERK and JNK families (reviewed in Verhey and Rapoport, 2001 ).	transcription
72840	8	336298	7	NULL	NULL	0	NULL	APC	GP		is a type of					adenomatous poliposis coli protein	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_6_2999_s_11	15814838	These motors transport mRNAs for cell fate and polarity determinations (reviewed in Saxton, 2001 ), transcriptional regulators, such as the NF kappa B inhibitor IkappaB (Crepieux  et al., 1997 ), the tumor suppressor protein p53 (Giannakakou  et al., 2000 ; Giannakakou  et al., 2002 ), the developmental factors beta-catenin or adenomatous poliposis coli protein (APC, reviewed in Bienz, 2002 ), the apoptosis effector bim (Puthalakath  et al., 1999 ), and stress-related signaling kinases of the ERK and JNK families (reviewed in Verhey and Rapoport, 2001 ).	transcription
72841	9	336298	7	NULL	NULL	NULL	NULL	APC	GP		is a type of					transcriptional regulator	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_6_2999_s_11	15814838	These motors transport mRNAs for cell fate and polarity determinations (reviewed in Saxton, 2001 ), transcriptional regulators, such as the NF kappa B inhibitor IkappaB (Crepieux  et al., 1997 ), the tumor suppressor protein p53 (Giannakakou  et al., 2000 ; Giannakakou  et al., 2002 ), the developmental factors beta-catenin or adenomatous poliposis coli protein (APC, reviewed in Bienz, 2002 ), the apoptosis effector bim (Puthalakath  et al., 1999 ), and stress-related signaling kinases of the ERK and JNK families (reviewed in Verhey and Rapoport, 2001 ).	transcription
72842	10	336298	7	NULL	NULL	NULL	NULL	bim	GP		is a type of					apoptosis effector	GP				NULL		NULL	NULL	NULL	NULL	gw70_molbiolcell_16_6_2999_s_11	15814838	These motors transport mRNAs for cell fate and polarity determinations (reviewed in Saxton, 2001 ), transcriptional regulators, such as the NF kappa B inhibitor IkappaB (Crepieux  et al., 1997 ), the tumor suppressor protein p53 (Giannakakou  et al., 2000 ; Giannakakou  et al., 2002 ), the developmental factors beta-catenin or adenomatous poliposis coli protein (APC, reviewed in Bienz, 2002 ), the apoptosis effector bim (Puthalakath  et al., 1999 ), and stress-related signaling kinases of the ERK and JNK families (reviewed in Verhey and Rapoport, 2001 ).	transcription
72843	11	336298	7	NULL	NULL	0	NULL	ERK family	GP		is a type of					stress-related signaling kinases	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_6_2999_s_11	15814838	These motors transport mRNAs for cell fate and polarity determinations (reviewed in Saxton, 2001 ), transcriptional regulators, such as the NF kappa B inhibitor IkappaB (Crepieux  et al., 1997 ), the tumor suppressor protein p53 (Giannakakou  et al., 2000 ; Giannakakou  et al., 2002 ), the developmental factors beta-catenin or adenomatous poliposis coli protein (APC, reviewed in Bienz, 2002 ), the apoptosis effector bim (Puthalakath  et al., 1999 ), and stress-related signaling kinases of the ERK and JNK families (reviewed in Verhey and Rapoport, 2001 ).	transcription
72844	12	336298	7	NULL	NULL	0	NULL	JNK family	GP		is a type of					stress-related signaling kinases	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_6_2999_s_11	15814838	These motors transport mRNAs for cell fate and polarity determinations (reviewed in Saxton, 2001 ), transcriptional regulators, such as the NF kappa B inhibitor IkappaB (Crepieux  et al., 1997 ), the tumor suppressor protein p53 (Giannakakou  et al., 2000 ; Giannakakou  et al., 2002 ), the developmental factors beta-catenin or adenomatous poliposis coli protein (APC, reviewed in Bienz, 2002 ), the apoptosis effector bim (Puthalakath  et al., 1999 ), and stress-related signaling kinases of the ERK and JNK families (reviewed in Verhey and Rapoport, 2001 ).	transcription
72845	13	336298	7	NULL	NULL	0	NULL	bim	GP		is a type of					transcriptional regulator	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_6_2999_s_11	15814838	These motors transport mRNAs for cell fate and polarity determinations (reviewed in Saxton, 2001 ), transcriptional regulators, such as the NF kappa B inhibitor IkappaB (Crepieux  et al., 1997 ), the tumor suppressor protein p53 (Giannakakou  et al., 2000 ; Giannakakou  et al., 2002 ), the developmental factors beta-catenin or adenomatous poliposis coli protein (APC, reviewed in Bienz, 2002 ), the apoptosis effector bim (Puthalakath  et al., 1999 ), and stress-related signaling kinases of the ERK and JNK families (reviewed in Verhey and Rapoport, 2001 ).	transcription
72846	14	336298	7	NULL	NULL	0	NULL	ERK family	GP		is a type of					transcriptional regulator	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_6_2999_s_11	15814838	These motors transport mRNAs for cell fate and polarity determinations (reviewed in Saxton, 2001 ), transcriptional regulators, such as the NF kappa B inhibitor IkappaB (Crepieux  et al., 1997 ), the tumor suppressor protein p53 (Giannakakou  et al., 2000 ; Giannakakou  et al., 2002 ), the developmental factors beta-catenin or adenomatous poliposis coli protein (APC, reviewed in Bienz, 2002 ), the apoptosis effector bim (Puthalakath  et al., 1999 ), and stress-related signaling kinases of the ERK and JNK families (reviewed in Verhey and Rapoport, 2001 ).	transcription
72847	15	336298	7	NULL	NULL	0	NULL	JNK family	GP		is a type of					transcriptional regulator	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_16_6_2999_s_11	15814838	These motors transport mRNAs for cell fate and polarity determinations (reviewed in Saxton, 2001 ), transcriptional regulators, such as the NF kappa B inhibitor IkappaB (Crepieux  et al., 1997 ), the tumor suppressor protein p53 (Giannakakou  et al., 2000 ; Giannakakou  et al., 2002 ), the developmental factors beta-catenin or adenomatous poliposis coli protein (APC, reviewed in Bienz, 2002 ), the apoptosis effector bim (Puthalakath  et al., 1999 ), and stress-related signaling kinases of the ERK and JNK families (reviewed in Verhey and Rapoport, 2001 ).	transcription
72848	1	336299	7	NULL	NULL	0	NULL	 proliferation	Process	increase in	associated with					 beta-cat	GP				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_5_1619_s_373	12414510	14, 20, 62  This beta-cat-associated increase in proliferation is tightly controlled by the following mechanisms: 1) nuclear sequestration 10, 11  and cytoplasmic degradation of beta-cat by APC; 2- 9  2) activation of p53, that accumulates in response to beta-cat signaling and triggers a cell growth arrest; 15- 17  and 3) p27KIP-dependent cell-cycle arrest that results from the interplay between activation of nuclear beta-cat transcriptional targets (eg, myc 76 ) and E-cad.	transcription
72849	2	336299	7	NULL	NULL	0	NULL	APC	GP		sequesters		nuclear			beta-cat	GP				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_5_1619_s_373	12414510	14, 20, 62  This beta-cat-associated increase in proliferation is tightly controlled by the following mechanisms: 1) nuclear sequestration 10, 11  and cytoplasmic degradation of beta-cat by APC; 2- 9  2) activation of p53, that accumulates in response to beta-cat signaling and triggers a cell growth arrest; 15- 17  and 3) p27KIP-dependent cell-cycle arrest that results from the interplay between activation of nuclear beta-cat transcriptional targets (eg, myc 76 ) and E-cad.	transcription
72850	3	336299	7	NULL	NULL	0	NULL	APC	GP		degrades					beta-cat	GP	cytoplasmic			NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_5_1619_s_373	12414510	14, 20, 62  This beta-cat-associated increase in proliferation is tightly controlled by the following mechanisms: 1) nuclear sequestration 10, 11  and cytoplasmic degradation of beta-cat by APC; 2- 9  2) activation of p53, that accumulates in response to beta-cat signaling and triggers a cell growth arrest; 15- 17  and 3) p27KIP-dependent cell-cycle arrest that results from the interplay between activation of nuclear beta-cat transcriptional targets (eg, myc 76 ) and E-cad.	transcription
72851	4	336299	7	NULL	NULL	0	NULL	p53	GP	activation of	accumulate					beta-cat signaling	Process	in response to			NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_5_1619_s_373	12414510	14, 20, 62  This beta-cat-associated increase in proliferation is tightly controlled by the following mechanisms: 1) nuclear sequestration 10, 11  and cytoplasmic degradation of beta-cat by APC; 2- 9  2) activation of p53, that accumulates in response to beta-cat signaling and triggers a cell growth arrest; 15- 17  and 3) p27KIP-dependent cell-cycle arrest that results from the interplay between activation of nuclear beta-cat transcriptional targets (eg, myc 76 ) and E-cad.	transcription
72852	5	336299	7	NULL	NULL	NULL	NULL	statement 4	Process		triggers					cell growth arrest	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_5_1619_s_373	12414510	14, 20, 62  This beta-cat-associated increase in proliferation is tightly controlled by the following mechanisms: 1) nuclear sequestration 10, 11  and cytoplasmic degradation of beta-cat by APC; 2- 9  2) activation of p53, that accumulates in response to beta-cat signaling and triggers a cell growth arrest; 15- 17  and 3) p27KIP-dependent cell-cycle arrest that results from the interplay between activation of nuclear beta-cat transcriptional targets (eg, myc 76 ) and E-cad.	transcription
72853	6	336299	7	NULL	NULL	0	NULL	cell-cycle arrest	Process		depends on					 p27KIP	GP				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_5_1619_s_373	12414510	14, 20, 62  This beta-cat-associated increase in proliferation is tightly controlled by the following mechanisms: 1) nuclear sequestration 10, 11  and cytoplasmic degradation of beta-cat by APC; 2- 9  2) activation of p53, that accumulates in response to beta-cat signaling and triggers a cell growth arrest; 15- 17  and 3) p27KIP-dependent cell-cycle arrest that results from the interplay between activation of nuclear beta-cat transcriptional targets (eg, myc 76 ) and E-cad.	transcription
72854	7	336299	7	NULL	NULL	NULL	NULL	beta-cat transcriptional targets 	GP	activation of;;nuclear	interplay with					E-cad	GP				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_5_1619_s_373	12414510	14, 20, 62  This beta-cat-associated increase in proliferation is tightly controlled by the following mechanisms: 1) nuclear sequestration 10, 11  and cytoplasmic degradation of beta-cat by APC; 2- 9  2) activation of p53, that accumulates in response to beta-cat signaling and triggers a cell growth arrest; 15- 17  and 3) p27KIP-dependent cell-cycle arrest that results from the interplay between activation of nuclear beta-cat transcriptional targets (eg, myc 76 ) and E-cad.	transcription
72855	8	336299	7	NULL	NULL	NULL	NULL	statement 6	Process		result from					statement 7	Process				NULL		NULL	NULL	NULL	NULL	gw60_amjpathol_161_5_1619_s_373	12414510	14, 20, 62  This beta-cat-associated increase in proliferation is tightly controlled by the following mechanisms: 1) nuclear sequestration 10, 11  and cytoplasmic degradation of beta-cat by APC; 2- 9  2) activation of p53, that accumulates in response to beta-cat signaling and triggers a cell growth arrest; 15- 17  and 3) p27KIP-dependent cell-cycle arrest that results from the interplay between activation of nuclear beta-cat transcriptional targets (eg, myc 76 ) and E-cad.	transcription
72856	9	336299	7	NULL	NULL	0	NULL	statement 1	Process		controlled by		tightly			statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_5_1619_s_373	12414510	14, 20, 62  This beta-cat-associated increase in proliferation is tightly controlled by the following mechanisms: 1) nuclear sequestration 10, 11  and cytoplasmic degradation of beta-cat by APC; 2- 9  2) activation of p53, that accumulates in response to beta-cat signaling and triggers a cell growth arrest; 15- 17  and 3) p27KIP-dependent cell-cycle arrest that results from the interplay between activation of nuclear beta-cat transcriptional targets (eg, myc 76 ) and E-cad.	transcription
72857	10	336299	7	NULL	NULL	0	NULL	statement 1	Process		controlled by		tightly			statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_5_1619_s_373	12414510	14, 20, 62  This beta-cat-associated increase in proliferation is tightly controlled by the following mechanisms: 1) nuclear sequestration 10, 11  and cytoplasmic degradation of beta-cat by APC; 2- 9  2) activation of p53, that accumulates in response to beta-cat signaling and triggers a cell growth arrest; 15- 17  and 3) p27KIP-dependent cell-cycle arrest that results from the interplay between activation of nuclear beta-cat transcriptional targets (eg, myc 76 ) and E-cad.	transcription
72858	11	336299	7	NULL	NULL	0	NULL	statement 1	Process		controlled by		tightly			statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_5_1619_s_373	12414510	14, 20, 62  This beta-cat-associated increase in proliferation is tightly controlled by the following mechanisms: 1) nuclear sequestration 10, 11  and cytoplasmic degradation of beta-cat by APC; 2- 9  2) activation of p53, that accumulates in response to beta-cat signaling and triggers a cell growth arrest; 15- 17  and 3) p27KIP-dependent cell-cycle arrest that results from the interplay between activation of nuclear beta-cat transcriptional targets (eg, myc 76 ) and E-cad.	transcription
72859	12	336299	7	NULL	NULL	0	NULL	statement 1	Process		controlled by		tightly			statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_5_1619_s_373	12414510	14, 20, 62  This beta-cat-associated increase in proliferation is tightly controlled by the following mechanisms: 1) nuclear sequestration 10, 11  and cytoplasmic degradation of beta-cat by APC; 2- 9  2) activation of p53, that accumulates in response to beta-cat signaling and triggers a cell growth arrest; 15- 17  and 3) p27KIP-dependent cell-cycle arrest that results from the interplay between activation of nuclear beta-cat transcriptional targets (eg, myc 76 ) and E-cad.	transcription
72860	13	336299	7	NULL	NULL	0	NULL	statement 1	Process		controlled by		tightly			statement 8	Process				NULL		0	NULL	NULL	NULL	gw60_amjpathol_161_5_1619_s_373	12414510	14, 20, 62  This beta-cat-associated increase in proliferation is tightly controlled by the following mechanisms: 1) nuclear sequestration 10, 11  and cytoplasmic degradation of beta-cat by APC; 2- 9  2) activation of p53, that accumulates in response to beta-cat signaling and triggers a cell growth arrest; 15- 17  and 3) p27KIP-dependent cell-cycle arrest that results from the interplay between activation of nuclear beta-cat transcriptional targets (eg, myc 76 ) and E-cad.	transcription
72861	1	336300	7	NULL	NULL	0	NULL	 TACC	GP		regulate					spindle structure	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_99_24_15440_s_193	12422018	It would not be surprising if future studies revealed an effect of p53 on the ability of Aur-A to associate with or regulate other interacting proteins, including the APC/C activator cdc20 ( 23), the translational regulator CPEB ( 24), the kinesin-like motor Eg5 ( 25), the transforming protein TACC that can regulate spindle structure ( 26), TPX2, which is required for targeting Aur-A to spindles ( 27), a newly identified protein called AIP that can promote Aur-A destruction ( 28), or others yet to be discovered.	transcription
72862	2	336300	7	NULL	NULL	0	NULL	TACC	GP		is a type of					transforming protein	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_99_24_15440_s_193	12422018	It would not be surprising if future studies revealed an effect of p53 on the ability of Aur-A to associate with or regulate other interacting proteins, including the APC/C activator cdc20 ( 23), the translational regulator CPEB ( 24), the kinesin-like motor Eg5 ( 25), the transforming protein TACC that can regulate spindle structure ( 26), TPX2, which is required for targeting Aur-A to spindles ( 27), a newly identified protein called AIP that can promote Aur-A destruction ( 28), or others yet to be discovered.	transcription
72863	3	336300	7	NULL	NULL	0	NULL	AurA	GP		targeted to					spindles	Chromosome				NULL		0	NULL	NULL	NULL	gw60_pnas_99_24_15440_s_193	12422018	It would not be surprising if future studies revealed an effect of p53 on the ability of Aur-A to associate with or regulate other interacting proteins, including the APC/C activator cdc20 ( 23), the translational regulator CPEB ( 24), the kinesin-like motor Eg5 ( 25), the transforming protein TACC that can regulate spindle structure ( 26), TPX2, which is required for targeting Aur-A to spindles ( 27), a newly identified protein called AIP that can promote Aur-A destruction ( 28), or others yet to be discovered.	transcription
72864	4	336300	7	NULL	NULL	0	NULL	TPX2	GP		is required for					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_99_24_15440_s_193	12422018	It would not be surprising if future studies revealed an effect of p53 on the ability of Aur-A to associate with or regulate other interacting proteins, including the APC/C activator cdc20 ( 23), the translational regulator CPEB ( 24), the kinesin-like motor Eg5 ( 25), the transforming protein TACC that can regulate spindle structure ( 26), TPX2, which is required for targeting Aur-A to spindles ( 27), a newly identified protein called AIP that can promote Aur-A destruction ( 28), or others yet to be discovered.	transcription
72865	5	336300	7	NULL	NULL	0	NULL	AIP	GP		promote					Aur-A	GP	destruction of			NULL		0	NULL	NULL	NULL	gw60_pnas_99_24_15440_s_193	12422018	It would not be surprising if future studies revealed an effect of p53 on the ability of Aur-A to associate with or regulate other interacting proteins, including the APC/C activator cdc20 ( 23), the translational regulator CPEB ( 24), the kinesin-like motor Eg5 ( 25), the transforming protein TACC that can regulate spindle structure ( 26), TPX2, which is required for targeting Aur-A to spindles ( 27), a newly identified protein called AIP that can promote Aur-A destruction ( 28), or others yet to be discovered.	transcription
72869	1	336301	7	NULL	NULL	NULL	NULL	reactions	Process		contains					p53	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_169	14612423	The addition of consensus site DNA to reactions containing p53, p300, and acetyl-coenzyme A (CoA) stimulates p53 acetylation ( ).	transcription
72870	2	336301	7	NULL	NULL	0	NULL	reactions	Process		contains					p300	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_169	14612423	The addition of consensus site DNA to reactions containing p53, p300, and acetyl-coenzyme A (CoA) stimulates p53 acetylation ( ).	transcription
72871	3	336301	7	NULL	NULL	0	NULL	reactions	Process		contains					CoA	Chemical				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_169	14612423	The addition of consensus site DNA to reactions containing p53, p300, and acetyl-coenzyme A (CoA) stimulates p53 acetylation ( ).	transcription
72872	4	336301	7	NULL	NULL	0	NULL	CoA	Chemical		is					acetyl-coenzyme A	Chemical				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_169	14612423	The addition of consensus site DNA to reactions containing p53, p300, and acetyl-coenzyme A (CoA) stimulates p53 acetylation ( ).	transcription
72873	5	336301	7	NULL	NULL	0	NULL	statement 1	Process		stimulate					p53	GP	acetylation of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_169	14612423	The addition of consensus site DNA to reactions containing p53, p300, and acetyl-coenzyme A (CoA) stimulates p53 acetylation ( ).	transcription
72874	6	336301	7	NULL	NULL	0	NULL	statement 1	Process		stimulate					p300	GP	acetylation of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_169	14612423	The addition of consensus site DNA to reactions containing p53, p300, and acetyl-coenzyme A (CoA) stimulates p53 acetylation ( ).	transcription
72877	7	336301	7	NULL	NULL	0	NULL	statement 1	Process		stimulate					CoA	Chemical	acetylation of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_169	14612423	The addition of consensus site DNA to reactions containing p53, p300, and acetyl-coenzyme A (CoA) stimulates p53 acetylation ( ).	transcription
72885	1	336302	7	NULL	NULL	0	NULL	 Sirt1	GP	human	homologous to					Sir2a	GP	yeast			NULL		0	NULL	NULL	NULL	gw70_annurevpharmacol_45_0_269_s_168	15822178	The human homologue of yeast Sir2a, Sirt1,  inhibits p53 by removing the acetyl group from Lys382 in the C-terminal tail of p53  ( 85).	transcription
72886	2	336302	7	NULL	NULL	0	NULL	Sirt1	GP		inhibits					p53	GP				NULL		0	NULL	NULL	NULL	gw70_annurevpharmacol_45_0_269_s_168	15822178	The human homologue of yeast Sir2a, Sirt1,  inhibits p53 by removing the acetyl group from Lys382 in the C-terminal tail of p53  ( 85).	transcription
72887	3	336302	7	NULL	NULL	0	NULL	statement 2	Process		occur by					p53	GP	removing	acetyl group from Lys382 in the C-terminal tail of		NULL		0	NULL	NULL	NULL	gw70_annurevpharmacol_45_0_269_s_168	15822178	The human homologue of yeast Sir2a, Sirt1,  inhibits p53 by removing the acetyl group from Lys382 in the C-terminal tail of p53  ( 85).	transcription
72903	1	336303	7	NULL	NULL	NULL	NULL	p29ING4	GP		enhance					p53	GP	acetylation of	Lys-382 residue		NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_63_10_12750254_s_6	12750254	p29ING4 and p28ING5 enhance p53 acetylation at Lys-382 residues, and physically  interact with p300, a member of histone acetyl transferase complexes,  and p53 in vivo.	transcription
72904	2	336303	7	NULL	NULL	0	NULL	p28ING5	GP		enhance					p53	GP	acetylation of	Lys-382 residue		NULL		0	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_63_10_12750254_s_6	12750254	p29ING4 and p28ING5 enhance p53 acetylation at Lys-382 residues, and physically  interact with p300, a member of histone acetyl transferase complexes,  and p53 in vivo.	transcription
72905	3	336303	7	NULL	NULL	NULL	NULL	p29ING4	GP		interacts with		physically			p300	GP				NULL	in vivo	NULL	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_63_10_12750254_s_6	12750254	p29ING4 and p28ING5 enhance p53 acetylation at Lys-382 residues, and physically  interact with p300, a member of histone acetyl transferase complexes,  and p53 in vivo.	transcription
72906	4	336303	7	NULL	NULL	NULL	NULL	p28ING5	GP		interacts with		physically			p300	GP				NULL	in vivo	NULL	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_63_10_12750254_s_6	12750254	p29ING4 and p28ING5 enhance p53 acetylation at Lys-382 residues, and physically  interact with p300, a member of histone acetyl transferase complexes,  and p53 in vivo.	transcription
72907	5	336303	7	NULL	NULL	0	NULL	p29ING4	GP		interacts with		physically			p53	GP				NULL	in vivo	0	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_63_10_12750254_s_6	12750254	p29ING4 and p28ING5 enhance p53 acetylation at Lys-382 residues, and physically  interact with p300, a member of histone acetyl transferase complexes,  and p53 in vivo.	transcription
72908	6	336303	7	NULL	NULL	0	NULL	p28ING5	GP		interacts with		physically			p53	GP				NULL	in vivo	0	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_63_10_12750254_s_6	12750254	p29ING4 and p28ING5 enhance p53 acetylation at Lys-382 residues, and physically  interact with p300, a member of histone acetyl transferase complexes,  and p53 in vivo.	transcription
72909	7	336303	7	NULL	NULL	0	NULL	p300	GP		is a type of					histone acetyl transferase complex	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_63_10_12750254_s_6	12750254	p29ING4 and p28ING5 enhance p53 acetylation at Lys-382 residues, and physically  interact with p300, a member of histone acetyl transferase complexes,  and p53 in vivo.	transcription
72910	1	336304	7	NULL	NULL	0	NULL	histone acetyl transferases	GP		recruited to					p53-dependent promoter	GP				NULL		0	NULL	NULL	NULL	gw70_molbiolcell_17_4_1583_s_283	16436515	This modification may contribute to p53 activation by increasing the recruitment of histone acetyl transferases to p53-dependent promoters (Barlev  et al., 2001 ).	transcription
72911	1	336305	7	NULL	NULL	NULL	NULL	p300	GP		bind		stable			p53	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_176	14612423	In the absence of both DNA and acetyl-CoA, the PXXP repeat peptide reduced the stable binding of p300 to p53 (Fig.  3E).	transcription
72912	2	336305	7	NULL	NULL	0	NULL	PXXP repeat peptide	AminoAcid		reduce					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_176	14612423	In the absence of both DNA and acetyl-CoA, the PXXP repeat peptide reduced the stable binding of p300 to p53 (Fig.  3E).	transcription
72913	3	336305	7	NULL	NULL	0	NULL	statement 2	Process		in the absence of					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_176	14612423	In the absence of both DNA and acetyl-CoA, the PXXP repeat peptide reduced the stable binding of p300 to p53 (Fig.  3E).	transcription
72914	4	336305	7	NULL	NULL	0	NULL	statement 2	Process		in the absence of					acetyl-CoA	Chemical				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_176	14612423	In the absence of both DNA and acetyl-CoA, the PXXP repeat peptide reduced the stable binding of p300 to p53 (Fig.  3E).	transcription
72915	1	336306	7	NULL	NULL	0	NULL	p300	GP	full-length	bind					p53	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_49395_s_132	15337767	In fact, sequence-specific DNA can stabilize full-length p300 binding to p53 in the absence of acetyl-CoA ( ).	transcription
72916	2	336306	7	NULL	NULL	0	NULL	 DNA	NucleicAcid	sequence-specific	stabilize					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_49395_s_132	15337767	In fact, sequence-specific DNA can stabilize full-length p300 binding to p53 in the absence of acetyl-CoA ( ).	transcription
72917	3	336306	7	NULL	NULL	0	NULL	statement 1	Process		in the absence of					acetyl-CoA	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_47_49395_s_132	15337767	In fact, sequence-specific DNA can stabilize full-length p300 binding to p53 in the absence of acetyl-CoA ( ).	transcription
72918	1	336307	7	NULL	NULL	0	NULL	 IFN-alpha	GP		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_13547_s_7	11278370	The ability of IFN-alpha and vanadate to induce apoptosis did not require expression of p53 and was blocked by  N-acetyl-L-cysteine.	transcription
72919	2	336307	7	NULL	NULL	0	NULL	vanadate	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_13547_s_7	11278370	The ability of IFN-alpha and vanadate to induce apoptosis did not require expression of p53 and was blocked by  N-acetyl-L-cysteine.	transcription
72920	3	336307	7	NULL	NULL	0	NULL	statement 1	Process		does not require					p53	GP	expression of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_13547_s_7	11278370	The ability of IFN-alpha and vanadate to induce apoptosis did not require expression of p53 and was blocked by  N-acetyl-L-cysteine.	transcription
72921	4	336307	7	NULL	NULL	0	NULL	N-acetyl-L-cysteine	Chemical		blocks					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_13547_s_7	11278370	The ability of IFN-alpha and vanadate to induce apoptosis did not require expression of p53 and was blocked by  N-acetyl-L-cysteine.	transcription
72922	5	336307	7	NULL	NULL	0	NULL	N-acetyl-L-cysteine	Chemical		blocks					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_17_13547_s_7	11278370	The ability of IFN-alpha and vanadate to induce apoptosis did not require expression of p53 and was blocked by  N-acetyl-L-cysteine.	transcription
72923	1	336308	7	NULL	NULL	0	NULL	p300/CBP	GP		recruited to					target gene promoter	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_19_7386_s_23	15123817	First, p300/CBP are recruited by p53 to target gene promoters where they acetylate histones ( ,  ).	transcription
72924	2	336308	7	NULL	NULL	0	NULL	statement 1	Process		recruited by					p53	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_19_7386_s_23	15123817	First, p300/CBP are recruited by p53 to target gene promoters where they acetylate histones ( ,  ).	transcription
72925	1	336309	7	NULL	NULL	0	NULL	PCAF	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_200_s_113	11036071	Likewise, PCAF has been shown to acetylate p53, which then increases the DNA binding affinity of p53 ( 36,  37).	transcription
72926	2	336309	7	NULL	NULL	0	NULL	statement 1	Process		increase					p53	GP	DNA binding affinity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_200_s_113	11036071	Likewise, PCAF has been shown to acetylate p53, which then increases the DNA binding affinity of p53 ( 36,  37).	transcription
72927	1	336310	7	NULL	NULL	0	NULL	p53	GP		interacts with					CBP/p300	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_166	11960694	The interactions between p53 and CBP/p300 have been associated with subsequent acetylation at the C-terminus of p53 [ 117 and  125], leading to a fairly straightforward model in which stress-induced phosphorylation at the N-terminus of p53 augments interaction with the acetyl-transferases that modify the C-terminus of p53 and activate DNA binding (  Fig. 2).	transcription
72928	2	336310	7	NULL	NULL	NULL	NULL	statement 1	Process		associated with					p53	GP	acetylation at 	C-terminus 		NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_166	11960694	The interactions between p53 and CBP/p300 have been associated with subsequent acetylation at the C-terminus of p53 [ 117 and  125], leading to a fairly straightforward model in which stress-induced phosphorylation at the N-terminus of p53 augments interaction with the acetyl-transferases that modify the C-terminus of p53 and activate DNA binding (  Fig. 2).	transcription
72929	3	336310	7	NULL	NULL	0	NULL	stress	Process		induce					p53	GP	phosphorylation of	N-terminus		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_166	11960694	The interactions between p53 and CBP/p300 have been associated with subsequent acetylation at the C-terminus of p53 [ 117 and  125], leading to a fairly straightforward model in which stress-induced phosphorylation at the N-terminus of p53 augments interaction with the acetyl-transferases that modify the C-terminus of p53 and activate DNA binding (  Fig. 2).	transcription
72930	4	336310	7	NULL	NULL	0	NULL	statement 3	Process		augments					acetyl-transferases	GP	interaction with			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_166	11960694	The interactions between p53 and CBP/p300 have been associated with subsequent acetylation at the C-terminus of p53 [ 117 and  125], leading to a fairly straightforward model in which stress-induced phosphorylation at the N-terminus of p53 augments interaction with the acetyl-transferases that modify the C-terminus of p53 and activate DNA binding (  Fig. 2).	transcription
72931	5	336310	7	NULL	NULL	0	NULL	statement 4	Process		modify					p53	GP		C-terminus		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_166	11960694	The interactions between p53 and CBP/p300 have been associated with subsequent acetylation at the C-terminus of p53 [ 117 and  125], leading to a fairly straightforward model in which stress-induced phosphorylation at the N-terminus of p53 augments interaction with the acetyl-transferases that modify the C-terminus of p53 and activate DNA binding (  Fig. 2).	transcription
72932	6	336310	7	NULL	NULL	0	NULL	statement 5	Process		activate					DNA binding	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_166	11960694	The interactions between p53 and CBP/p300 have been associated with subsequent acetylation at the C-terminus of p53 [ 117 and  125], leading to a fairly straightforward model in which stress-induced phosphorylation at the N-terminus of p53 augments interaction with the acetyl-transferases that modify the C-terminus of p53 and activate DNA binding (  Fig. 2).	transcription
72933	1	336311	7	NULL	NULL	0	NULL	HDAC5	GP		 target of		down-stream			p53	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_62_10_12019172_s_4	12019172	We tested a hypothesis that HDAC5 is a p53  down-stream target gene that on induction by p53 inactivates p53 by removal  of acetyl group in p53 molecule, thus functioning as an auto-regulatory  negative feedback loop in analogue to p53-murine double minute 2 interaction.	transcription
72934	2	336311	7	NULL	NULL	0	NULL	p53	GP		induce					HDAC5	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_62_10_12019172_s_4	12019172	We tested a hypothesis that HDAC5 is a p53  down-stream target gene that on induction by p53 inactivates p53 by removal  of acetyl group in p53 molecule, thus functioning as an auto-regulatory  negative feedback loop in analogue to p53-murine double minute 2 interaction.	transcription
72935	3	336311	7	NULL	NULL	0	NULL	HDAC5	GP		inactivates					p53	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_62_10_12019172_s_4	12019172	We tested a hypothesis that HDAC5 is a p53  down-stream target gene that on induction by p53 inactivates p53 by removal  of acetyl group in p53 molecule, thus functioning as an auto-regulatory  negative feedback loop in analogue to p53-murine double minute 2 interaction.	transcription
72936	4	336311	7	NULL	NULL	0	NULL	statement 3	Process		occur by					p53	GP	removal of	acetyl group		NULL		0	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_62_10_12019172_s_4	12019172	We tested a hypothesis that HDAC5 is a p53  down-stream target gene that on induction by p53 inactivates p53 by removal  of acetyl group in p53 molecule, thus functioning as an auto-regulatory  negative feedback loop in analogue to p53-murine double minute 2 interaction.	transcription
72937	5	336311	7	NULL	NULL	0	NULL	HDAC5	GP		function as					auto-regulatory negative feedback loop	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_62_10_12019172_s_4	12019172	We tested a hypothesis that HDAC5 is a p53  down-stream target gene that on induction by p53 inactivates p53 by removal  of acetyl group in p53 molecule, thus functioning as an auto-regulatory  negative feedback loop in analogue to p53-murine double minute 2 interaction.	transcription
72938	6	336311	7	NULL	NULL	0	NULL	p53	GP		interacts with					murine double minute 2	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_62_10_12019172_s_4	12019172	We tested a hypothesis that HDAC5 is a p53  down-stream target gene that on induction by p53 inactivates p53 by removal  of acetyl group in p53 molecule, thus functioning as an auto-regulatory  negative feedback loop in analogue to p53-murine double minute 2 interaction.	transcription
72939	7	336311	7	NULL	NULL	0	NULL	statement 5	Process		is analogue to					statement 6	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_cancer-res_62_10_12019172_s_4	12019172	We tested a hypothesis that HDAC5 is a p53  down-stream target gene that on induction by p53 inactivates p53 by removal  of acetyl group in p53 molecule, thus functioning as an auto-regulatory  negative feedback loop in analogue to p53-murine double minute 2 interaction.	transcription
72940	1	336312	7	NULL	NULL	0	NULL	 p300	GP		regulator of		important			p53	GP	transcriptional activity of			NULL		0	NULL	NULL	NULL	gw70_pnas_101_33_12165_s_220	15295102	The acetyl-transferase p300 is an important regulator of the transcriptional activity of p53, and disruption of the p300 gene in HCT116 cells demonstrated that p300 also plays important roles for the function of p53  in vivo ( ).	transcription
72941	2	336312	7	NULL	NULL	0	NULL	p300	GP		important role in					p53	GP	function of			NULL	HCT116 cells;;in vivo	0	NULL	NULL	NULL	gw70_pnas_101_33_12165_s_220	15295102	The acetyl-transferase p300 is an important regulator of the transcriptional activity of p53, and disruption of the p300 gene in HCT116 cells demonstrated that p300 also plays important roles for the function of p53  in vivo ( ).	transcription
72942	3	336312	7	NULL	NULL	0	NULL	p300	GP		is a type of					acetyl-transferase	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_33_12165_s_220	15295102	The acetyl-transferase p300 is an important regulator of the transcriptional activity of p53, and disruption of the p300 gene in HCT116 cells demonstrated that p300 also plays important roles for the function of p53  in vivo ( ).	transcription
72943	1	336313	7	NULL	NULL	NULL	NULL	LMB	Chemical		induce					p53	GP	accumulation of			NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1177_s_6	12807744	Caffeine inhibited the accumulation of p53 induced by leptomycin B (LMB), an inhibitor of CRM1, but not  N-acetyl-leu-leu-norleucinal, a proteasome inhibitor.	transcription
72944	2	336313	7	NULL	NULL	0	NULL	Caffeine	Chemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1177_s_6	12807744	Caffeine inhibited the accumulation of p53 induced by leptomycin B (LMB), an inhibitor of CRM1, but not  N-acetyl-leu-leu-norleucinal, a proteasome inhibitor.	transcription
72945	3	336313	7	NULL	NULL	0	NULL	LMB	Chemical		inhibitor of					CRM1	Chemical				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1177_s_6	12807744	Caffeine inhibited the accumulation of p53 induced by leptomycin B (LMB), an inhibitor of CRM1, but not  N-acetyl-leu-leu-norleucinal, a proteasome inhibitor.	transcription
72946	4	336313	7	NULL	NULL	0	NULL	N-acetyl-leu-leu-norleucinal	Chemical		induce					p53	GP	accumulation of			NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1177_s_6	12807744	Caffeine inhibited the accumulation of p53 induced by leptomycin B (LMB), an inhibitor of CRM1, but not  N-acetyl-leu-leu-norleucinal, a proteasome inhibitor.	transcription
72947	5	336313	7	NULL	NULL	NULL	NULL	Caffeine	Chemical		does not inhibit					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1177_s_6	12807744	Caffeine inhibited the accumulation of p53 induced by leptomycin B (LMB), an inhibitor of CRM1, but not  N-acetyl-leu-leu-norleucinal, a proteasome inhibitor.	transcription
72948	6	336313	7	NULL	NULL	0	NULL	N-acetyl-leu-leu-norleucinal	Chemical		is a inhibitor of					proteasome	CellComponent				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1177_s_6	12807744	Caffeine inhibited the accumulation of p53 induced by leptomycin B (LMB), an inhibitor of CRM1, but not  N-acetyl-leu-leu-norleucinal, a proteasome inhibitor.	transcription
72949	7	336313	7	NULL	NULL	0	NULL	LMB	Chemical		is					 leptomycin B	Chemical				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_24_7_1177_s_6	12807744	Caffeine inhibited the accumulation of p53 induced by leptomycin B (LMB), an inhibitor of CRM1, but not  N-acetyl-leu-leu-norleucinal, a proteasome inhibitor.	transcription
72950	1	336314	7	NULL	NULL	0	NULL	N-acetyl-L-cysteine	Chemical	dietary	modulates					benzo[apyrene-induced skin tumors	MedicalFinding				NULL	cancer-prone p53 haploinsufficient Tg.AC (v-Ha-ras) mice	0	NULL	NULL	NULL	gw70_annurevnutr_24_0_223_s_697	15189120	Dietary  N-acetyl-L-cysteine modulates benzo[apyrene-induced skin tumors in cancer-prone  p53 haploinsufficient Tg.AC (v-Ha-ras) mice.	transcription
72951	1	336315	7	NULL	NULL	NULL	NULL	CobB protein	GP	Salmonella	deacetylates					acetyl-coenzyme A synthetase	GP		active site of		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_3_1301_s_18	14729974	The CobB protein of  Salmonella deacetylates the active site of acetyl-coenzyme A synthetase ( ), mammalian SIRT1 deacetylates the p53 tumor suppressor protein ( ,  ,  ), and human SIRT2 deacetylates tubulin ( ).	transcription
72952	2	336315	7	NULL	NULL	0	NULL	SIRT1	GP	mammalian	deacetylates					p53	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1301_s_18	14729974	The CobB protein of  Salmonella deacetylates the active site of acetyl-coenzyme A synthetase ( ), mammalian SIRT1 deacetylates the p53 tumor suppressor protein ( ,  ,  ), and human SIRT2 deacetylates tubulin ( ).	transcription
72953	3	336315	7	NULL	NULL	0	NULL	 SIRT2 	GP	human	deacetylates					tubulin	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1301_s_18	14729974	The CobB protein of  Salmonella deacetylates the active site of acetyl-coenzyme A synthetase ( ), mammalian SIRT1 deacetylates the p53 tumor suppressor protein ( ,  ,  ), and human SIRT2 deacetylates tubulin ( ).	transcription
72954	4	336315	7	NULL	NULL	0	NULL	p53	GP		is a type of					tumor suppressor protein	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_3_1301_s_18	14729974	The CobB protein of  Salmonella deacetylates the active site of acetyl-coenzyme A synthetase ( ), mammalian SIRT1 deacetylates the p53 tumor suppressor protein ( ,  ,  ), and human SIRT2 deacetylates tubulin ( ).	transcription
72955	1	336316	7	NULL	NULL	0	NULL	BPDE	Chemical		induce					p53	GP	accumulation of			NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_3_631_s_152	16244358	Next, we examined whether p53 accumulation and phosphorylation are also induced by proteasomal inhibitor  N-Acetyl-Leu-Leu-Nle-CHO (ALLN) (Calbiochem) in order to compare with BPDE-induced p53 accumulation and phosphorylation, and whether TPA can attenuate ALLN-induced p53 accumulation and phosphorylation, if they occurred.	transcription
72956	2	336316	7	NULL	NULL	0	NULL	BPDE	Chemical		induce					p53	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_3_631_s_152	16244358	Next, we examined whether p53 accumulation and phosphorylation are also induced by proteasomal inhibitor  N-Acetyl-Leu-Leu-Nle-CHO (ALLN) (Calbiochem) in order to compare with BPDE-induced p53 accumulation and phosphorylation, and whether TPA can attenuate ALLN-induced p53 accumulation and phosphorylation, if they occurred.	transcription
72957	3	336316	7	NULL	NULL	0	NULL	ALLN	Chemical		induce					p53	GP	accumulation of			NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_3_631_s_152	16244358	Next, we examined whether p53 accumulation and phosphorylation are also induced by proteasomal inhibitor  N-Acetyl-Leu-Leu-Nle-CHO (ALLN) (Calbiochem) in order to compare with BPDE-induced p53 accumulation and phosphorylation, and whether TPA can attenuate ALLN-induced p53 accumulation and phosphorylation, if they occurred.	transcription
72958	4	336316	7	NULL	NULL	0	NULL	ALLN	Chemical		induce					p53	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_3_631_s_152	16244358	Next, we examined whether p53 accumulation and phosphorylation are also induced by proteasomal inhibitor  N-Acetyl-Leu-Leu-Nle-CHO (ALLN) (Calbiochem) in order to compare with BPDE-induced p53 accumulation and phosphorylation, and whether TPA can attenuate ALLN-induced p53 accumulation and phosphorylation, if they occurred.	transcription
72959	5	336316	7	NULL	NULL	0	NULL	ALLN	Chemical		is					N-Acetyl-Leu-Leu-Nle-CHO	Chemical				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_3_631_s_152	16244358	Next, we examined whether p53 accumulation and phosphorylation are also induced by proteasomal inhibitor  N-Acetyl-Leu-Leu-Nle-CHO (ALLN) (Calbiochem) in order to compare with BPDE-induced p53 accumulation and phosphorylation, and whether TPA can attenuate ALLN-induced p53 accumulation and phosphorylation, if they occurred.	transcription
72960	6	336316	7	NULL	NULL	0	NULL	ALLN	Chemical		is a type of					proteasomal inhibitor	Chemical				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_3_631_s_152	16244358	Next, we examined whether p53 accumulation and phosphorylation are also induced by proteasomal inhibitor  N-Acetyl-Leu-Leu-Nle-CHO (ALLN) (Calbiochem) in order to compare with BPDE-induced p53 accumulation and phosphorylation, and whether TPA can attenuate ALLN-induced p53 accumulation and phosphorylation, if they occurred.	transcription
72961	1	336317	7	NULL	NULL	NULL	NULL	p53	GP	phosphorylation within	stimulate			N-terminus		p53	GP	transcriptional activity of			NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_165	11960694	Phosphorylation within the N-terminus of p53 can stimulate p53's transcriptional activity without influencing MDM2 binding, and both serine 15 and serine 33 phosphorylation leads to enhanced binding between p53 and histone acetyl transferases such as p300/CBP or pCAF [  123,   124 and   125].	transcription
72962	2	336317	7	NULL	NULL	0	NULL	statement 1	Process		does not influence					MDM2	GP	binding of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_165	11960694	Phosphorylation within the N-terminus of p53 can stimulate p53's transcriptional activity without influencing MDM2 binding, and both serine 15 and serine 33 phosphorylation leads to enhanced binding between p53 and histone acetyl transferases such as p300/CBP or pCAF [  123,   124 and   125].	transcription
72963	3	336317	7	NULL	NULL	0	NULL	p53	GP		bind					p300/CBP	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_165	11960694	Phosphorylation within the N-terminus of p53 can stimulate p53's transcriptional activity without influencing MDM2 binding, and both serine 15 and serine 33 phosphorylation leads to enhanced binding between p53 and histone acetyl transferases such as p300/CBP or pCAF [  123,   124 and   125].	transcription
72964	4	336317	7	NULL	NULL	0	NULL	p53	GP		bind					pCAF	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_165	11960694	Phosphorylation within the N-terminus of p53 can stimulate p53's transcriptional activity without influencing MDM2 binding, and both serine 15 and serine 33 phosphorylation leads to enhanced binding between p53 and histone acetyl transferases such as p300/CBP or pCAF [  123,   124 and   125].	transcription
72965	5	336317	7	NULL	NULL	0	NULL	p53	GP	phosphorylation of	enhance			serine 15		statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_165	11960694	Phosphorylation within the N-terminus of p53 can stimulate p53's transcriptional activity without influencing MDM2 binding, and both serine 15 and serine 33 phosphorylation leads to enhanced binding between p53 and histone acetyl transferases such as p300/CBP or pCAF [  123,   124 and   125].	transcription
72966	6	336317	7	NULL	NULL	NULL	NULL	p53	GP	phosphorylation of	enhance			serine 33		statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_165	11960694	Phosphorylation within the N-terminus of p53 can stimulate p53's transcriptional activity without influencing MDM2 binding, and both serine 15 and serine 33 phosphorylation leads to enhanced binding between p53 and histone acetyl transferases such as p300/CBP or pCAF [  123,   124 and   125].	transcription
72967	7	336317	7	NULL	NULL	0	NULL	p53	GP	phosphorylation of	enhance			serine 15		statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_165	11960694	Phosphorylation within the N-terminus of p53 can stimulate p53's transcriptional activity without influencing MDM2 binding, and both serine 15 and serine 33 phosphorylation leads to enhanced binding between p53 and histone acetyl transferases such as p300/CBP or pCAF [  123,   124 and   125].	transcription
72968	8	336317	7	NULL	NULL	0	NULL	p53	GP	phosphorylation of	enhance			serine 33		statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_165	11960694	Phosphorylation within the N-terminus of p53 can stimulate p53's transcriptional activity without influencing MDM2 binding, and both serine 15 and serine 33 phosphorylation leads to enhanced binding between p53 and histone acetyl transferases such as p300/CBP or pCAF [  123,   124 and   125].	transcription
72969	9	336317	7	NULL	NULL	0	NULL	p300/CBP	GP		is a type of					histone acetyl transferases	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_165	11960694	Phosphorylation within the N-terminus of p53 can stimulate p53's transcriptional activity without influencing MDM2 binding, and both serine 15 and serine 33 phosphorylation leads to enhanced binding between p53 and histone acetyl transferases such as p300/CBP or pCAF [  123,   124 and   125].	transcription
72970	10	336317	7	NULL	NULL	0	NULL	pCAF	GP		is a type of					histone acetyl transferases	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_165	11960694	Phosphorylation within the N-terminus of p53 can stimulate p53's transcriptional activity without influencing MDM2 binding, and both serine 15 and serine 33 phosphorylation leads to enhanced binding between p53 and histone acetyl transferases such as p300/CBP or pCAF [  123,   124 and   125].	transcription
72971	1	336318	7	NULL	NULL	0	NULL	p300	GP		acetylates					p53	GP		C terminus		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_48_47853_s_265	14500729	p300 acetylates the C terminus of p53, leading to transcriptional activation of p53 function ( ,  ).	transcription
72972	2	336318	7	NULL	NULL	0	NULL	statement 1	Process		leads to					p53 function	Process	transcriptional activation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_48_47853_s_265	14500729	p300 acetylates the C terminus of p53, leading to transcriptional activation of p53 function ( ,  ).	transcription
72973	1	336319	7	NULL	NULL	0	NULL	IE2	GP		downregulate		could			p53 function	Process				NULL		0	NULL	NULL	NULL	gw70_embo_23_11_2269_s_211	15141169	Thus far, we had demonstrated that IE2 could downregulate p53 function and inhibit  the acetylase activity of the p53 coactivators, p300/CBP, both  in vitro and  in vivo.	transcription
72974	2	336319	7	NULL	NULL	NULL	NULL	statement 1	Process		inhibit					p53 coactivators	GP	acetylase activity of			NULL	in vitro	NULL	NULL	NULL	NULL	gw70_embo_23_11_2269_s_211	15141169	Thus far, we had demonstrated that IE2 could downregulate p53 function and inhibit  the acetylase activity of the p53 coactivators, p300/CBP, both  in vitro and  in vivo.	transcription
72975	3	336319	7	NULL	NULL	NULL	NULL	statement 1	Process		inhibit					p53 coactivators	GP	acetylase activity of			NULL	in vivo	NULL	NULL	NULL	NULL	gw70_embo_23_11_2269_s_211	15141169	Thus far, we had demonstrated that IE2 could downregulate p53 function and inhibit  the acetylase activity of the p53 coactivators, p300/CBP, both  in vitro and  in vivo.	transcription
72976	4	336319	7	NULL	NULL	0	NULL	statement 1	Process		inhibit					 p300/CBP	GP				NULL	in vitro	0	NULL	NULL	NULL	gw70_embo_23_11_2269_s_211	15141169	Thus far, we had demonstrated that IE2 could downregulate p53 function and inhibit  the acetylase activity of the p53 coactivators, p300/CBP, both  in vitro and  in vivo.	transcription
72977	5	336319	7	NULL	NULL	0	NULL	statement 1	Process		inhibit					p300/CBP	GP				NULL	in vivo	0	NULL	NULL	NULL	gw70_embo_23_11_2269_s_211	15141169	Thus far, we had demonstrated that IE2 could downregulate p53 function and inhibit  the acetylase activity of the p53 coactivators, p300/CBP, both  in vitro and  in vivo.	transcription
72978	1	336320	7	NULL	NULL	0	NULL				interacts with			Tat domain					HAT domain		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_9390_s_100	15611041	Since we have previously demonstrated that Tat-HAT domain interactions prevent coactivator-mediated acetylation of the tumor suppressor p53 ( ), we investigated whether Tat-coactivator binding might inhibit histone acetylation by p300 and PCAF in radioactive acetylation assays using [14]acetyl-coenzyme A (acetyl-CoA).	transcription
72979	2	336320	7	NULL	NULL	0	NULL	coactivator	GP		mediate					p53	GP	acetylation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_9390_s_100	15611041	Since we have previously demonstrated that Tat-HAT domain interactions prevent coactivator-mediated acetylation of the tumor suppressor p53 ( ), we investigated whether Tat-coactivator binding might inhibit histone acetylation by p300 and PCAF in radioactive acetylation assays using [14]acetyl-coenzyme A (acetyl-CoA).	transcription
72980	3	336320	7	NULL	NULL	0	NULL	p53	GP		is a type of					tumor suppressor	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_9390_s_100	15611041	Since we have previously demonstrated that Tat-HAT domain interactions prevent coactivator-mediated acetylation of the tumor suppressor p53 ( ), we investigated whether Tat-coactivator binding might inhibit histone acetylation by p300 and PCAF in radioactive acetylation assays using [14]acetyl-coenzyme A (acetyl-CoA).	transcription
72981	4	336320	7	NULL	NULL	0	NULL	statement 1	Process		prevent					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_10_9390_s_100	15611041	Since we have previously demonstrated that Tat-HAT domain interactions prevent coactivator-mediated acetylation of the tumor suppressor p53 ( ), we investigated whether Tat-coactivator binding might inhibit histone acetylation by p300 and PCAF in radioactive acetylation assays using [14]acetyl-coenzyme A (acetyl-CoA).	transcription
72982	1	336321	7	NULL	NULL	0	NULL	p300	GP		bind					p53	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_18_2831_s_94	9744860	Although a small amount of binding was observed either when acetyl-CoA was omitted or when it was replaced by unacetylated CoA (Fig.  5, lanes 7,8,11,12), this amount was substantially less than in the presence of acetyl-CoA, indicating that acetylation and not simply binding of either p300 or PCAF to p53 was necessary for the effect on DNA-binding.	transcription
72983	2	336321	7	NULL	NULL	0	NULL	PCAF	GP		bind					p53	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_18_2831_s_94	9744860	Although a small amount of binding was observed either when acetyl-CoA was omitted or when it was replaced by unacetylated CoA (Fig.  5, lanes 7,8,11,12), this amount was substantially less than in the presence of acetyl-CoA, indicating that acetylation and not simply binding of either p300 or PCAF to p53 was necessary for the effect on DNA-binding.	transcription
72984	3	336321	7	NULL	NULL	0	NULL	p53	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_18_2831_s_94	9744860	Although a small amount of binding was observed either when acetyl-CoA was omitted or when it was replaced by unacetylated CoA (Fig.  5, lanes 7,8,11,12), this amount was substantially less than in the presence of acetyl-CoA, indicating that acetylation and not simply binding of either p300 or PCAF to p53 was necessary for the effect on DNA-binding.	transcription
72985	4	336321	7	NULL	NULL	0	NULL	acetyl-CoA	Chemical	acetylation by	is necessary for					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_18_2831_s_94	9744860	Although a small amount of binding was observed either when acetyl-CoA was omitted or when it was replaced by unacetylated CoA (Fig.  5, lanes 7,8,11,12), this amount was substantially less than in the presence of acetyl-CoA, indicating that acetylation and not simply binding of either p300 or PCAF to p53 was necessary for the effect on DNA-binding.	transcription
72986	5	336321	7	NULL	NULL	NULL	NULL	statement 1	Process		not required for					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_12_18_2831_s_94	9744860	Although a small amount of binding was observed either when acetyl-CoA was omitted or when it was replaced by unacetylated CoA (Fig.  5, lanes 7,8,11,12), this amount was substantially less than in the presence of acetyl-CoA, indicating that acetylation and not simply binding of either p300 or PCAF to p53 was necessary for the effect on DNA-binding.	transcription
72987	6	336321	7	NULL	NULL	0	NULL	statement 2	Process		not required for					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_genesdev_12_18_2831_s_94	9744860	Although a small amount of binding was observed either when acetyl-CoA was omitted or when it was replaced by unacetylated CoA (Fig.  5, lanes 7,8,11,12), this amount was substantially less than in the presence of acetyl-CoA, indicating that acetylation and not simply binding of either p300 or PCAF to p53 was necessary for the effect on DNA-binding.	transcription
72988	1	336322	7	NULL	NULL	0	NULL	CBP/p300	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw70_annurevgenet_34_0_77_s_284	11092823	Acetylation by CBP/p300 and PCAF both enhance p53's DNA-binding activity even  though the two factors acetylate different sites on p53.	transcription
72989	2	336322	7	NULL	NULL	0	NULL	PCAF	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw70_annurevgenet_34_0_77_s_284	11092823	Acetylation by CBP/p300 and PCAF both enhance p53's DNA-binding activity even  though the two factors acetylate different sites on p53.	transcription
72990	3	336322	7	NULL	NULL	0	NULL	p53	GP		bind					DNA 	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_annurevgenet_34_0_77_s_284	11092823	Acetylation by CBP/p300 and PCAF both enhance p53's DNA-binding activity even  though the two factors acetylate different sites on p53.	transcription
72991	4	336322	7	NULL	NULL	0	NULL	statement 1	Process		enhance					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_annurevgenet_34_0_77_s_284	11092823	Acetylation by CBP/p300 and PCAF both enhance p53's DNA-binding activity even  though the two factors acetylate different sites on p53.	transcription
72992	5	336322	7	NULL	NULL	0	NULL	statement 2	Process		enhance					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_annurevgenet_34_0_77_s_284	11092823	Acetylation by CBP/p300 and PCAF both enhance p53's DNA-binding activity even  though the two factors acetylate different sites on p53.	transcription
72993	6	336322	7	NULL	NULL	0	NULL	statement 1	GP	acetylation site of	is different from					statement 2	GP	acetylation site of			NULL		0	NULL	NULL	NULL	gw70_annurevgenet_34_0_77_s_284	11092823	Acetylation by CBP/p300 and PCAF both enhance p53's DNA-binding activity even  though the two factors acetylate different sites on p53.	transcription
72994	1	336323	7	NULL	NULL	0	NULL	p300/CBP	GP		acetylate					p53	GP		lysine residues within C terminus		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20111_s_40	15769743	In addition, p300/CBP is found to acetylate several lysine residues within the p53 C terminus, which enhances the DNA binding and thereby the transcriptional activity of p53 ( ,  ,   -  ).	transcription
72995	2	336323	7	NULL	NULL	0	NULL	p53	GP		bind					DNA	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20111_s_40	15769743	In addition, p300/CBP is found to acetylate several lysine residues within the p53 C terminus, which enhances the DNA binding and thereby the transcriptional activity of p53 ( ,  ,   -  ).	transcription
72996	3	336323	7	NULL	NULL	0	NULL	statement 1	Process		enhance					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20111_s_40	15769743	In addition, p300/CBP is found to acetylate several lysine residues within the p53 C terminus, which enhances the DNA binding and thereby the transcriptional activity of p53 ( ,  ,   -  ).	transcription
72997	4	336323	7	NULL	NULL	0	NULL	statement 3	Process		enhance					p53	GP	transcriptional activity of 			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_20_20111_s_40	15769743	In addition, p300/CBP is found to acetylate several lysine residues within the p53 C terminus, which enhances the DNA binding and thereby the transcriptional activity of p53 ( ,  ,   -  ).	transcription
72998	1	336324	7	NULL	NULL	0	NULL	p53	GP		interacts with					p300	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39115_s_5	11495913	Furthermore, interaction of p53 with the transcriptional coactivator p300 was induced, and Lys382 of p53 was acetylated.	transcription
72999	2	336324	7	NULL	NULL	0	NULL	p300	GP		is a type of					transcriptional coactivator	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_42_39115_s_5	11495913	Furthermore, interaction of p53 with the transcriptional coactivator p300 was induced, and Lys382 of p53 was acetylated.	transcription
73000	1	336325	7	NULL	NULL	0	NULL	RA	Chemical		induce					p53	GP				NULL		0	NULL	NULL	NULL	gw70_embo_25_17_4084_s_120	16946709	Despite the lower p53 levels induced by RA, acetylation of K320 but not of K372  of p53 was markedly increased, and RA treatment also clearly induced the expression  levels of the acetyltransferase PCAF, which is known to acetylate p53 at K320 (  et al).	transcription
73001	2	336325	7	NULL	NULL	0	NULL	statement 1	Process		increase					p53	GP	acetylation of	K320		NULL		0	NULL	NULL	NULL	gw70_embo_25_17_4084_s_120	16946709	Despite the lower p53 levels induced by RA, acetylation of K320 but not of K372  of p53 was markedly increased, and RA treatment also clearly induced the expression  levels of the acetyltransferase PCAF, which is known to acetylate p53 at K320 (  et al).	transcription
73002	3	336325	7	NULL	NULL	0	NULL	statement 1	Process		does not increase					p53	GP		K372		NULL		0	NULL	NULL	NULL	gw70_embo_25_17_4084_s_120	16946709	Despite the lower p53 levels induced by RA, acetylation of K320 but not of K372  of p53 was markedly increased, and RA treatment also clearly induced the expression  levels of the acetyltransferase PCAF, which is known to acetylate p53 at K320 (  et al).	transcription
73003	4	336325	7	NULL	NULL	0	NULL	RA	Chemical		induce					 PCAF	GP	expression of			NULL		0	NULL	NULL	NULL	gw70_embo_25_17_4084_s_120	16946709	Despite the lower p53 levels induced by RA, acetylation of K320 but not of K372  of p53 was markedly increased, and RA treatment also clearly induced the expression  levels of the acetyltransferase PCAF, which is known to acetylate p53 at K320 (  et al).	transcription
73004	5	336325	7	NULL	NULL	0	NULL	PCAF	GP		acetylate					p53	GP		K320		NULL		0	NULL	NULL	NULL	gw70_embo_25_17_4084_s_120	16946709	Despite the lower p53 levels induced by RA, acetylation of K320 but not of K372  of p53 was markedly increased, and RA treatment also clearly induced the expression  levels of the acetyltransferase PCAF, which is known to acetylate p53 at K320 (  et al).	transcription
73005	6	336325	7	NULL	NULL	0	NULL	PCAF	GP		is a type of					acetyltransferase	GP				NULL		0	NULL	NULL	NULL	gw70_embo_25_17_4084_s_120	16946709	Despite the lower p53 levels induced by RA, acetylation of K320 but not of K372  of p53 was markedly increased, and RA treatment also clearly induced the expression  levels of the acetyltransferase PCAF, which is known to acetylate p53 at K320 (  et al).	transcription
73006	1	336326	7	NULL	NULL	0	NULL	p300	GP		bind					anti-p300 serum	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_22_10083_s_258	15509808	(C) Acetylation reactions were carried out as described above but in the absence  of acetyl-CoA; p300 binding was determined by ELISA with anti-p300 serum (N15) following  capture of p53 by using ICA-9.	transcription
73007	1	336327	7	NULL	NULL	0	NULL	 reoxygenation	Process		induce					p53	GP	phosphorylation of	serine 15		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_14_12207_s_9	12519769	The reoxygenation-induced p53 serine 15 phosphorylation was inhibited by the addition of  N-acetyl-L-cysteine (NAC), indicating that free radical-induced DNA damage was mediated by reactive oxygen species.	transcription
73008	2	336327	7	NULL	NULL	0	NULL	NAC	Chemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_14_12207_s_9	12519769	The reoxygenation-induced p53 serine 15 phosphorylation was inhibited by the addition of  N-acetyl-L-cysteine (NAC), indicating that free radical-induced DNA damage was mediated by reactive oxygen species.	transcription
73009	3	336327	7	NULL	NULL	0	NULL	free radical	Chemical		induce					DNA damage	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_14_12207_s_9	12519769	The reoxygenation-induced p53 serine 15 phosphorylation was inhibited by the addition of  N-acetyl-L-cysteine (NAC), indicating that free radical-induced DNA damage was mediated by reactive oxygen species.	transcription
73010	4	336327	7	NULL	NULL	0	NULL	reactive oxygen species	Chemical		mediate					statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_14_12207_s_9	12519769	The reoxygenation-induced p53 serine 15 phosphorylation was inhibited by the addition of  N-acetyl-L-cysteine (NAC), indicating that free radical-induced DNA damage was mediated by reactive oxygen species.	transcription
73011	5	336327	7	NULL	NULL	0	NULL	NAC	Chemical		is					N-acetyl-L-cysteine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_14_12207_s_9	12519769	The reoxygenation-induced p53 serine 15 phosphorylation was inhibited by the addition of  N-acetyl-L-cysteine (NAC), indicating that free radical-induced DNA damage was mediated by reactive oxygen species.	transcription
73012	6	336327	7	NULL	NULL	0	NULL	statement 2	Process		indicate					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_14_12207_s_9	12519769	The reoxygenation-induced p53 serine 15 phosphorylation was inhibited by the addition of  N-acetyl-L-cysteine (NAC), indicating that free radical-induced DNA damage was mediated by reactive oxygen species.	transcription
73013	1	336328	7	NULL	NULL	0	NULL	 N-acetyl-L-cysteine	GP		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_circulation_105_1_79_s_170	11772880	28 Interestingly, the induction of apoptosis by  N-acetyl-L-cysteine has also been linked to an increase in p53 expression, 29 suggesting that antioxidants stimulate apoptosis via a p53-dependent pathway.	transcription
73014	2	336328	7	NULL	NULL	0	NULL	statement 1	Process		linked to					p53	GP	increased expression of			NULL		0	NULL	NULL	NULL	gw60_circulation_105_1_79_s_170	11772880	28 Interestingly, the induction of apoptosis by  N-acetyl-L-cysteine has also been linked to an increase in p53 expression, 29 suggesting that antioxidants stimulate apoptosis via a p53-dependent pathway.	transcription
73015	3	336328	7	NULL	NULL	0	NULL	antioxidants	Process		stimulate					apoptosis	Process				NULL		0	NULL	NULL	NULL	gw60_circulation_105_1_79_s_170	11772880	28 Interestingly, the induction of apoptosis by  N-acetyl-L-cysteine has also been linked to an increase in p53 expression, 29 suggesting that antioxidants stimulate apoptosis via a p53-dependent pathway.	transcription
73016	4	336328	7	NULL	NULL	0	NULL	statement 2	Process		via					p53 dependent pathway	Process				NULL		0	NULL	NULL	NULL	gw60_circulation_105_1_79_s_170	11772880	28 Interestingly, the induction of apoptosis by  N-acetyl-L-cysteine has also been linked to an increase in p53 expression, 29 suggesting that antioxidants stimulate apoptosis via a p53-dependent pathway.	transcription
73017	5	336328	7	NULL	NULL	0	NULL	statement 2	Process		suggest					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_circulation_105_1_79_s_170	11772880	28 Interestingly, the induction of apoptosis by  N-acetyl-L-cysteine has also been linked to an increase in p53 expression, 29 suggesting that antioxidants stimulate apoptosis via a p53-dependent pathway.	transcription
73018	1	336329	7	NULL	NULL	0	NULL	acetyl-CoA	Chemical		stimulate		greatly			p53	GP	binding of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1202_s_155	9891054	The addition of acetyl-CoA and PCAF greatly stimulated the binding of p53, both in the presence and absence of PAb421 (Fig.  5, compare lanes 2 and 3 to lanes 9 and 10).	transcription
73019	2	336329	7	NULL	NULL	0	NULL	PCAF	GP		stimulate		greatly			p53	GP	binding of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1202_s_155	9891054	The addition of acetyl-CoA and PCAF greatly stimulated the binding of p53, both in the presence and absence of PAb421 (Fig.  5, compare lanes 2 and 3 to lanes 9 and 10).	transcription
73020	1	336330	7	NULL	NULL	0	NULL	p300	GP		complex with					p53	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_15_13431_s_261	12499368	The stability of the p300.p53 complex was therefore quantitated without or with acetyl-CoA using the ELISA solid phase assay to determine whether p300 dissociates from p53 after acetylation in the absence or presence of consensus site DNA.	transcription
73021	1	336331	7	NULL	NULL	0	NULL	p300	GP		bind					p53	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_15_13431_s_265	12499368	Furthermore, p300 binding to p53 (Fig.  9,  lane 5) was de-stabilized by acetyl-CoA in reactions with nonspecific DNA (Fig.  9,  A and  B,  lane 11 versus 5).	transcription
73022	2	336331	7	NULL	NULL	NULL	NULL	acetyl-CoA	Chemical		in reactions with					nonspecific DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_15_13431_s_265	12499368	Furthermore, p300 binding to p53 (Fig.  9,  lane 5) was de-stabilized by acetyl-CoA in reactions with nonspecific DNA (Fig.  9,  A and  B,  lane 11 versus 5).	transcription
73023	3	336331	7	NULL	NULL	0	NULL	statement 2	Process		destabilize					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_15_13431_s_265	12499368	Furthermore, p300 binding to p53 (Fig.  9,  lane 5) was de-stabilized by acetyl-CoA in reactions with nonspecific DNA (Fig.  9,  A and  B,  lane 11 versus 5).	transcription
73024	1	336333	7	NULL	NULL	0	NULL	E2F1	GP		interacts with					HBx	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_iubmb-life_53_6_12625370_s_2	12625370	The functional effect of the interaction of E2F1 and hepatitis B virus  X protein (HBx) on the promoter of human p53 gene was studied using chloramphenicol  acetyl transferase (CAT) assay.	transcription
73025	2	336333	7	NULL	NULL	0	NULL	HBx	GP		present on					p53 gene	GP	human		promoter	NULL		0	NULL	NULL	NULL	abs-batch0650-0679_iubmb-life_53_6_12625370_s_2	12625370	The functional effect of the interaction of E2F1 and hepatitis B virus  X protein (HBx) on the promoter of human p53 gene was studied using chloramphenicol  acetyl transferase (CAT) assay.	transcription
73026	3	336333	7	NULL	NULL	0	NULL	HBx	GP		is					hepatitis B virus X protein	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_iubmb-life_53_6_12625370_s_2	12625370	The functional effect of the interaction of E2F1 and hepatitis B virus  X protein (HBx) on the promoter of human p53 gene was studied using chloramphenicol  acetyl transferase (CAT) assay.	transcription
73027	1	336334	7	NULL	NULL	0	NULL	coactivator	GP	recruitment of	depends on					p53	GP	acetylation of			NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mol-cell_13_2_14759370_s_4	14759370	This bromodomain/acetyl-lysine binding  is responsible for p53 acetylation-dependent coactivator recruitment after  DNA damage, a step essential for p53-induced transcriptional activation  of the cyclin-dependent kinase inhibitor p21 in G1 cell cycle arrest.	transcription
73028	2	336334	7	NULL	NULL	0	NULL	statement 1	Process		occur after					DNA damage	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mol-cell_13_2_14759370_s_4	14759370	This bromodomain/acetyl-lysine binding  is responsible for p53 acetylation-dependent coactivator recruitment after  DNA damage, a step essential for p53-induced transcriptional activation  of the cyclin-dependent kinase inhibitor p21 in G1 cell cycle arrest.	transcription
73029	3	336334	7	NULL	NULL	0	NULL	bromodomain/acetyl-lysine	Chemical	binding of	is responsible for					statement 1	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mol-cell_13_2_14759370_s_4	14759370	This bromodomain/acetyl-lysine binding  is responsible for p53 acetylation-dependent coactivator recruitment after  DNA damage, a step essential for p53-induced transcriptional activation  of the cyclin-dependent kinase inhibitor p21 in G1 cell cycle arrest.	transcription
73030	4	336334	7	NULL	NULL	NULL	NULL	p53	GP		induce					p21	GP	transcriptional activation of			NULL		NULL	NULL	NULL	NULL	abs-batch0650-0679_mol-cell_13_2_14759370_s_4	14759370	This bromodomain/acetyl-lysine binding  is responsible for p53 acetylation-dependent coactivator recruitment after  DNA damage, a step essential for p53-induced transcriptional activation  of the cyclin-dependent kinase inhibitor p21 in G1 cell cycle arrest.	transcription
73031	5	336334	7	NULL	NULL	0	NULL	statement 4	Process		occur in					G1 cell cycle arrest	Process				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mol-cell_13_2_14759370_s_4	14759370	This bromodomain/acetyl-lysine binding  is responsible for p53 acetylation-dependent coactivator recruitment after  DNA damage, a step essential for p53-induced transcriptional activation  of the cyclin-dependent kinase inhibitor p21 in G1 cell cycle arrest.	transcription
73032	6	336334	7	NULL	NULL	0	NULL	p21	GP		is a type of					cyclin-dependent kinase inhibitor	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_mol-cell_13_2_14759370_s_4	14759370	This bromodomain/acetyl-lysine binding  is responsible for p53 acetylation-dependent coactivator recruitment after  DNA damage, a step essential for p53-induced transcriptional activation  of the cyclin-dependent kinase inhibitor p21 in G1 cell cycle arrest.	transcription
73033	1	336335	7	NULL	NULL	0	NULL	p53	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_1_118_s_36	12147236	By using a acetylase defective mutant of CBP (L1690K/C1691L), we have found that the acetylase activity of CBP is not required for stimulation of p53 DNA binding (unpublished data).	transcription
73034	2	336335	7	NULL	NULL	0	NULL	CBP 	GP	acetylase activity of	is not required for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_1_118_s_36	12147236	By using a acetylase defective mutant of CBP (L1690K/C1691L), we have found that the acetylase activity of CBP is not required for stimulation of p53 DNA binding (unpublished data).	transcription
73035	1	336336	7	NULL	NULL	0	NULL	p53	GP		associates with					chromatin	Chromosome				NULL		0	NULL	NULL	NULL	gw60_cell_107_7_815_s_49	11779456	Roles of Acetylation in Transcriptional Regulation  by p53 Association of p53 (blue spheres) with chromatin  is not affected by its state of  acetylation, but p53-dependent alterations in chromatin structure by  histone acetylation and subsequent recruitment of the  transcriptional machinery (general transcription factors, mediator and RNA  polymerase II) are facilitated by interactions with acetylases, and  possibly by acetylation of p53 itself (acetyl  groups on p53 and histones are indicated  by red circles).	transcription
73036	2	336336	7	NULL	NULL	0	NULL	statement 1	Process		is not affected by					p53	GP	acetylation of			NULL		0	NULL	NULL	NULL	gw60_cell_107_7_815_s_49	11779456	Roles of Acetylation in Transcriptional Regulation  by p53 Association of p53 (blue spheres) with chromatin  is not affected by its state of  acetylation, but p53-dependent alterations in chromatin structure by  histone acetylation and subsequent recruitment of the  transcriptional machinery (general transcription factors, mediator and RNA  polymerase II) are facilitated by interactions with acetylases, and  possibly by acetylation of p53 itself (acetyl  groups on p53 and histones are indicated  by red circles).	transcription
73037	3	336336	7	NULL	NULL	0	NULL	chromatin structure	Chromosome	alterations in	depends on					p53	GP				NULL		0	NULL	NULL	NULL	gw60_cell_107_7_815_s_49	11779456	Roles of Acetylation in Transcriptional Regulation  by p53 Association of p53 (blue spheres) with chromatin  is not affected by its state of  acetylation, but p53-dependent alterations in chromatin structure by  histone acetylation and subsequent recruitment of the  transcriptional machinery (general transcription factors, mediator and RNA  polymerase II) are facilitated by interactions with acetylases, and  possibly by acetylation of p53 itself (acetyl  groups on p53 and histones are indicated  by red circles).	transcription
73038	4	336336	7	NULL	NULL	0	NULL	statement 3	Process		occur by					histone	GP	acetylation of			NULL		0	NULL	NULL	NULL	gw60_cell_107_7_815_s_49	11779456	Roles of Acetylation in Transcriptional Regulation  by p53 Association of p53 (blue spheres) with chromatin  is not affected by its state of  acetylation, but p53-dependent alterations in chromatin structure by  histone acetylation and subsequent recruitment of the  transcriptional machinery (general transcription factors, mediator and RNA  polymerase II) are facilitated by interactions with acetylases, and  possibly by acetylation of p53 itself (acetyl  groups on p53 and histones are indicated  by red circles).	transcription
73039	5	336336	7	NULL	NULL	0	NULL	statement 4	Process		followed by					transcription factors	GP	subsequent recruitment of			NULL		0	NULL	NULL	NULL	gw60_cell_107_7_815_s_49	11779456	Roles of Acetylation in Transcriptional Regulation  by p53 Association of p53 (blue spheres) with chromatin  is not affected by its state of  acetylation, but p53-dependent alterations in chromatin structure by  histone acetylation and subsequent recruitment of the  transcriptional machinery (general transcription factors, mediator and RNA  polymerase II) are facilitated by interactions with acetylases, and  possibly by acetylation of p53 itself (acetyl  groups on p53 and histones are indicated  by red circles).	transcription
73040	6	336336	7	NULL	NULL	0	NULL	statement 4	Process		followed by					RNA polymerase II	GP	subsequent recruitment of			NULL		0	NULL	NULL	NULL	gw60_cell_107_7_815_s_49	11779456	Roles of Acetylation in Transcriptional Regulation  by p53 Association of p53 (blue spheres) with chromatin  is not affected by its state of  acetylation, but p53-dependent alterations in chromatin structure by  histone acetylation and subsequent recruitment of the  transcriptional machinery (general transcription factors, mediator and RNA  polymerase II) are facilitated by interactions with acetylases, and  possibly by acetylation of p53 itself (acetyl  groups on p53 and histones are indicated  by red circles).	transcription
73041	7	336336	7	NULL	NULL	0	NULL	statement 5	Process		facilitated by					acetylases	GP	interactions with			NULL		0	NULL	NULL	NULL	gw60_cell_107_7_815_s_49	11779456	Roles of Acetylation in Transcriptional Regulation  by p53 Association of p53 (blue spheres) with chromatin  is not affected by its state of  acetylation, but p53-dependent alterations in chromatin structure by  histone acetylation and subsequent recruitment of the  transcriptional machinery (general transcription factors, mediator and RNA  polymerase II) are facilitated by interactions with acetylases, and  possibly by acetylation of p53 itself (acetyl  groups on p53 and histones are indicated  by red circles).	transcription
73042	8	336336	7	NULL	NULL	0	NULL	statement 6	Process		facilitated by					acetylases	GP	interactions with			NULL		0	NULL	NULL	NULL	gw60_cell_107_7_815_s_49	11779456	Roles of Acetylation in Transcriptional Regulation  by p53 Association of p53 (blue spheres) with chromatin  is not affected by its state of  acetylation, but p53-dependent alterations in chromatin structure by  histone acetylation and subsequent recruitment of the  transcriptional machinery (general transcription factors, mediator and RNA  polymerase II) are facilitated by interactions with acetylases, and  possibly by acetylation of p53 itself (acetyl  groups on p53 and histones are indicated  by red circles).	transcription
73043	9	336336	7	NULL	NULL	0	NULL	statement 5	Process		facilitated by					p53	GP	acetylation of			NULL		0	NULL	NULL	NULL	gw60_cell_107_7_815_s_49	11779456	Roles of Acetylation in Transcriptional Regulation  by p53 Association of p53 (blue spheres) with chromatin  is not affected by its state of  acetylation, but p53-dependent alterations in chromatin structure by  histone acetylation and subsequent recruitment of the  transcriptional machinery (general transcription factors, mediator and RNA  polymerase II) are facilitated by interactions with acetylases, and  possibly by acetylation of p53 itself (acetyl  groups on p53 and histones are indicated  by red circles).	transcription
73044	10	336336	7	NULL	NULL	0	NULL	statement 6	Process		facilitated by					p53	GP	acetylation of			NULL		0	NULL	NULL	NULL	gw60_cell_107_7_815_s_49	11779456	Roles of Acetylation in Transcriptional Regulation  by p53 Association of p53 (blue spheres) with chromatin  is not affected by its state of  acetylation, but p53-dependent alterations in chromatin structure by  histone acetylation and subsequent recruitment of the  transcriptional machinery (general transcription factors, mediator and RNA  polymerase II) are facilitated by interactions with acetylases, and  possibly by acetylation of p53 itself (acetyl  groups on p53 and histones are indicated  by red circles).	transcription
73045	1	336337	7	NULL	NULL	NULL	NULL	MageA2	GP		down-regulate					p53	GP	mutant;;nonacetylable;;transcriptional activity of 	9KR		NULL		NULL	NULL	NULL	NULL	gw70_pnas_103_30_11160_s_110	16847267	In fact, MageA2 was able to down-regulate the transcriptional activity of the nonacetylable p53 mutant, p539KR ( ), both alone or when cotransfected with the histone acetyl transferase p300 (Fig. 7  C and  D), strongly suggesting that histone hypoacetylation could represent the main mechanism used by MageA2 for targeting p53 activity.	transcription
73046	2	336337	7	NULL	NULL	0	NULL	MageA2	GP		target					p53	GP	activity of			NULL		0	NULL	NULL	NULL	gw70_pnas_103_30_11160_s_110	16847267	In fact, MageA2 was able to down-regulate the transcriptional activity of the nonacetylable p53 mutant, p539KR ( ), both alone or when cotransfected with the histone acetyl transferase p300 (Fig. 7  C and  D), strongly suggesting that histone hypoacetylation could represent the main mechanism used by MageA2 for targeting p53 activity.	transcription
73047	3	336337	7	NULL	NULL	0	NULL	histone	GP	hypoacetylation of	mechanism for					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_103_30_11160_s_110	16847267	In fact, MageA2 was able to down-regulate the transcriptional activity of the nonacetylable p53 mutant, p539KR ( ), both alone or when cotransfected with the histone acetyl transferase p300 (Fig. 7  C and  D), strongly suggesting that histone hypoacetylation could represent the main mechanism used by MageA2 for targeting p53 activity.	transcription
73048	4	336337	7	NULL	NULL	0	NULL	statement 1	Process		suggest		strongly			statement 3	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_103_30_11160_s_110	16847267	In fact, MageA2 was able to down-regulate the transcriptional activity of the nonacetylable p53 mutant, p539KR ( ), both alone or when cotransfected with the histone acetyl transferase p300 (Fig. 7  C and  D), strongly suggesting that histone hypoacetylation could represent the main mechanism used by MageA2 for targeting p53 activity.	transcription
73050	1	336338	7	NULL	NULL	0	NULL	CBP/p300	GP		shows					FAT activity	Process				NULL		0	NULL	NULL	NULL	gw60_cell_107_2_137_s_16	11672522	Significantly, the  observation of functional synergism between p53 and  CBP/p300 together with its intrinsic HAT activity  led to the discovery of an FAT  (transcriptional  factor  acetyl- transferase) activity of CBP/p300 on p53; this  finding also predicted that acetylation may represent  a general functional modification for nonhistone proteins  in vivo (Gu and Roeder, 1997   ).	transcription
73051	2	336338	7	NULL	NULL	0	NULL	statement 1	Process		occur on					p53	GP				NULL		0	NULL	NULL	NULL	gw60_cell_107_2_137_s_16	11672522	Significantly, the  observation of functional synergism between p53 and  CBP/p300 together with its intrinsic HAT activity  led to the discovery of an FAT  (transcriptional  factor  acetyl- transferase) activity of CBP/p300 on p53; this  finding also predicted that acetylation may represent  a general functional modification for nonhistone proteins  in vivo (Gu and Roeder, 1997   ).	transcription
73052	3	336338	7	NULL	NULL	0	NULL	acetylation	Process		represent		may			nonhistone proteins	GP	functional modification for			NULL	in vivo	0	NULL	NULL	NULL	gw60_cell_107_2_137_s_16	11672522	Significantly, the  observation of functional synergism between p53 and  CBP/p300 together with its intrinsic HAT activity  led to the discovery of an FAT  (transcriptional  factor  acetyl- transferase) activity of CBP/p300 on p53; this  finding also predicted that acetylation may represent  a general functional modification for nonhistone proteins  in vivo (Gu and Roeder, 1997   ).	transcription
73053	4	336338	7	NULL	NULL	0	NULL	statement 2	Process		predicts					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_cell_107_2_137_s_16	11672522	Significantly, the  observation of functional synergism between p53 and  CBP/p300 together with its intrinsic HAT activity  led to the discovery of an FAT  (transcriptional  factor  acetyl- transferase) activity of CBP/p300 on p53; this  finding also predicted that acetylation may represent  a general functional modification for nonhistone proteins  in vivo (Gu and Roeder, 1997   ).	transcription
73054	5	336338	7	NULL	NULL	0	NULL	FAT	GP		is					transcriptional factor acetyl- transferase	GP				NULL		0	NULL	NULL	NULL	gw60_cell_107_2_137_s_16	11672522	Significantly, the  observation of functional synergism between p53 and  CBP/p300 together with its intrinsic HAT activity  led to the discovery of an FAT  (transcriptional  factor  acetyl- transferase) activity of CBP/p300 on p53; this  finding also predicted that acetylation may represent  a general functional modification for nonhistone proteins  in vivo (Gu and Roeder, 1997   ).	transcription
73055	1	336339	7	NULL	NULL	0	NULL	Acetyl-CoA	Chemical		stabilizes					p300.p53AC complex	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_15_13431_s_239	12499368	Acetyl-CoA Stabilizes the p300.p53AC Complex--  With the  DNA-dependent p53 acetylation assay biochemically characterized, we could finally access the role of the phospho-Ser20 peptide-binding domains of p300 to both DNA-dependent p53 acetylation and DNA-independent histone acetylation (Fig.  8).	transcription
73056	2	336339	7	NULL	NULL	0	NULL	p53	GP	acetylation of	depends on					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_15_13431_s_239	12499368	Acetyl-CoA Stabilizes the p300.p53AC Complex--  With the  DNA-dependent p53 acetylation assay biochemically characterized, we could finally access the role of the phospho-Ser20 peptide-binding domains of p300 to both DNA-dependent p53 acetylation and DNA-independent histone acetylation (Fig.  8).	transcription
73057	3	336339	7	NULL	NULL	0	NULL	histone	GP	acetylation of	independent of					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_15_13431_s_239	12499368	Acetyl-CoA Stabilizes the p300.p53AC Complex--  With the  DNA-dependent p53 acetylation assay biochemically characterized, we could finally access the role of the phospho-Ser20 peptide-binding domains of p300 to both DNA-dependent p53 acetylation and DNA-independent histone acetylation (Fig.  8).	transcription
73058	1	336340	7	NULL	NULL	0	NULL	 p300 protein	GP		bind		stably			p53 protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_15_13431_s_274	12499368	The amount of p300 protein stably bound to p53 protein: ( /+)-acetyl-CoA, ( /+)-NS-DNA, or  ( /+)-pG-DNA was determined using an antibody to p300 and quantitated as p300 bound/total p53 using enhanced chemiluminescence expressed as relative light units ( RLU).	transcription
73106	1	336342	7	NULL	NULL	0	NULL	MDM2	GP		degrade					p53	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_9_7453_s_28	12493762	However, it is unclear whether p300 requires its acetylase activity to assist MDM2 in degrading p53.	transcription
73107	2	336342	7	NULL	NULL	NULL	NULL	p300	GP		activates 					acetylase	GP				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_278_9_7453_s_28	12493762	However, it is unclear whether p300 requires its acetylase activity to assist MDM2 in degrading p53.	transcription
73108	1	336343	7	NULL	NULL	0	NULL	CBP/p300	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw70_embo_25_8_1680_s_251	16601686	Alternatively, Tip60 can affect  the function of other HATs, such as CBP/p300, which are known to acetylate p53 ( ).	transcription
73109	2	336343	7	NULL	NULL	0	NULL	Tip60	GP		affect					CBP/p300 	GP	function of			NULL		0	NULL	NULL	NULL	gw70_embo_25_8_1680_s_251	16601686	Alternatively, Tip60 can affect  the function of other HATs, such as CBP/p300, which are known to acetylate p53 ( ).	transcription
73110	3	336343	7	NULL	NULL	0	NULL	CBP/p300	GP		is a type of					HAT	GP				NULL		0	NULL	NULL	NULL	gw70_embo_25_8_1680_s_251	16601686	Alternatively, Tip60 can affect  the function of other HATs, such as CBP/p300, which are known to acetylate p53 ( ).	transcription
73111	1	336344	7	NULL	NULL	0	NULL	p53	GP		interacts with					p300/CBP	GP				NULL		0	NULL	NULL	NULL	gw70_embo_24_14_2634_s_198	16001085	Moreover,  like p53, Tip60 was found to interact with p300/CBP, which could also acetylate the  protein on two specific lysines.	transcription
73112	2	336344	7	NULL	NULL	0	NULL	 Tip60	GP		interacts with					p300/CBP	GP				NULL		0	NULL	NULL	NULL	gw70_embo_24_14_2634_s_198	16001085	Moreover,  like p53, Tip60 was found to interact with p300/CBP, which could also acetylate the  protein on two specific lysines.	transcription
73113	3	336344	7	NULL	NULL	0	NULL	p300/CBP	GP		acetylate					Tip60	GP		two specific lysine		NULL		0	NULL	NULL	NULL	gw70_embo_24_14_2634_s_198	16001085	Moreover,  like p53, Tip60 was found to interact with p300/CBP, which could also acetylate the  protein on two specific lysines.	transcription
73114	4	336344	7	NULL	NULL	0	NULL	statement 1	Process		is similar to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_embo_24_14_2634_s_198	16001085	Moreover,  like p53, Tip60 was found to interact with p300/CBP, which could also acetylate the  protein on two specific lysines.	transcription
73115	1	336345	7	NULL	NULL	0	NULL	p53	GP		bind					CBP	GP				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_4_673_s_77	16308315	It also enables the binding of p53 to CBP, p300 and p/CAF (   -  ), which acetylate it at certain specific lysine residues ( , ).	transcription
73116	2	336345	7	NULL	NULL	0	NULL	p53	GP		bind					p300	GP				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_4_673_s_77	16308315	It also enables the binding of p53 to CBP, p300 and p/CAF (   -  ), which acetylate it at certain specific lysine residues ( , ).	transcription
73117	3	336345	7	NULL	NULL	0	NULL	p53	GP		bind					p/CAF	GP				NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_4_673_s_77	16308315	It also enables the binding of p53 to CBP, p300 and p/CAF (   -  ), which acetylate it at certain specific lysine residues ( , ).	transcription
73118	4	336345	7	NULL	NULL	NULL	NULL	CBP	GP		acetylate					p53			lysine residue		NULL		NULL	NULL	NULL	NULL	gw70_carcinogenesis_27_4_673_s_77	16308315	It also enables the binding of p53 to CBP, p300 and p/CAF (   -  ), which acetylate it at certain specific lysine residues ( , ).	transcription
73119	5	336345	7	NULL	NULL	0	NULL	p300	GP		acetylate					p53	GP		lysine residue		NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_4_673_s_77	16308315	It also enables the binding of p53 to CBP, p300 and p/CAF (   -  ), which acetylate it at certain specific lysine residues ( , ).	transcription
73120	6	336345	7	NULL	NULL	0	NULL	p/CAF	GP		acetylate					p53	GP		lysine residue		NULL		0	NULL	NULL	NULL	gw70_carcinogenesis_27_4_673_s_77	16308315	It also enables the binding of p53 to CBP, p300 and p/CAF (   -  ), which acetylate it at certain specific lysine residues ( , ).	transcription
73159	1	336346	7	NULL	NULL	0	NULL	p300	GP		acetylate					histones	GP				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_67_0_545_s_310	9759497	For example, in addition to histones, p300 will acetylate the tumor suppressor  protein, p53, enhancing its in vitro DNA-binding activity ( 202).	transcription
73160	2	336346	7	NULL	NULL	0	NULL	p300	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_67_0_545_s_310	9759497	For example, in addition to histones, p300 will acetylate the tumor suppressor  protein, p53, enhancing its in vitro DNA-binding activity ( 202).	transcription
73161	3	336346	7	NULL	NULL	0	NULL	statement 2	Process		enhance					DNA-binding activity	Process				NULL	in vitro	0	NULL	NULL	NULL	gw70_annurevbiochem_67_0_545_s_310	9759497	For example, in addition to histones, p300 will acetylate the tumor suppressor  protein, p53, enhancing its in vitro DNA-binding activity ( 202).	transcription
73162	4	336346	7	NULL	NULL	0	NULL	p53	GP		is a type of					tumor suppressor protein	GP				NULL		0	NULL	NULL	NULL	gw70_annurevbiochem_67_0_545_s_310	9759497	For example, in addition to histones, p300 will acetylate the tumor suppressor  protein, p53, enhancing its in vitro DNA-binding activity ( 202).	transcription
73163	1	336347	7	NULL	NULL	0	NULL	p300-deficient cells	Cell		fails to		fully			p53	GP	acetylate			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_15_6639_s_316	16024799	Hence, p300-deficient cells fail to fully acetylate p53 and do not transactivate p21 or undergo G1/S arrest after UV irradiation ( ).	transcription
73164	2	336347	7	NULL	NULL	NULL	NULL	 p300-deficient cells	Cell		does not transactivate					p21	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_15_6639_s_316	16024799	Hence, p300-deficient cells fail to fully acetylate p53 and do not transactivate p21 or undergo G1/S arrest after UV irradiation ( ).	transcription
73165	3	336347	7	NULL	NULL	0	NULL	p300-deficient cells	Cell		does not undergo					G1/S arrest	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_15_6639_s_316	16024799	Hence, p300-deficient cells fail to fully acetylate p53 and do not transactivate p21 or undergo G1/S arrest after UV irradiation ( ).	transcription
73166	4	336347	7	NULL	NULL	0	NULL	statement 3	Process		occur after					UV irradiation	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_15_6639_s_316	16024799	Hence, p300-deficient cells fail to fully acetylate p53 and do not transactivate p21 or undergo G1/S arrest after UV irradiation ( ).	transcription
73167	1	336348	7	NULL	NULL	0	NULL	p300	GP		does not acetylate					p53 tetramers	GP	native			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_2	14612423	The transcription coactivator p300 cannot acetylate native p53 tetramers, thus revealing intrinsic conformational constraints on p300-catalyzed acetylation.	transcription
73168	2	336348	7	NULL	NULL	0	NULL	p300	GP		catalyze					acetylation	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_2	14612423	The transcription coactivator p300 cannot acetylate native p53 tetramers, thus revealing intrinsic conformational constraints on p300-catalyzed acetylation.	transcription
73169	3	336348	7	NULL	NULL	0	NULL	statement 1	Process		reveal					statement 2	Process	intrinsic conformational constraints			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_2	14612423	The transcription coactivator p300 cannot acetylate native p53 tetramers, thus revealing intrinsic conformational constraints on p300-catalyzed acetylation.	transcription
73170	4	336348	7	NULL	NULL	0	NULL	p300	GP		is a type of					 transcription coactivator	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_2	14612423	The transcription coactivator p300 cannot acetylate native p53 tetramers, thus revealing intrinsic conformational constraints on p300-catalyzed acetylation.	transcription
73171	1	336349	7	NULL	NULL	NULL	NULL	p53	GP		recruit					p300	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_1_57_s_237	11511360	Particularly whether p53 recruits p300 to acetylate nucleosomal histones within the p21 promoter.	transcription
73172	2	336349	7	NULL	NULL	0	NULL	statement 1	Process		acetylate					nucleosomal histones	GP				NULL		0	NULL	NULL	NULL	gw60_molcell_8_1_57_s_237	11511360	Particularly whether p53 recruits p300 to acetylate nucleosomal histones within the p21 promoter.	transcription
73173	3	336349	7	NULL	NULL	0	NULL	statement 2	Process		occur within					p21	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_molcell_8_1_57_s_237	11511360	Particularly whether p53 recruits p300 to acetylate nucleosomal histones within the p21 promoter.	transcription
73174	1	336350	7	NULL	NULL	0	NULL	PCAF 	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_12_8136_s_28	10567539	PCAF can also acetylate p53, but at a different site ( 45), and chromosomal protein HMG-17 ( 32).	transcription
73175	2	336350	7	NULL	NULL	0	NULL	PCAF	GP		acetylate					HMG-17	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_12_8136_s_28	10567539	PCAF can also acetylate p53, but at a different site ( 45), and chromosomal protein HMG-17 ( 32).	transcription
73176	3	336350	7	NULL	NULL	0	NULL	HMG-17	GP		is a type of					chromosomal protein	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_12_8136_s_28	10567539	PCAF can also acetylate p53, but at a different site ( 45), and chromosomal protein HMG-17 ( 32).	transcription
73177	4	336350	7	NULL	NULL	0	NULL	statement 1	Process	binding site of	is different from					statement 2	Process	binding site of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_12_8136_s_28	10567539	PCAF can also acetylate p53, but at a different site ( 45), and chromosomal protein HMG-17 ( 32).	transcription
73178	1	336351	7	NULL	NULL	0	NULL	p300	GP	HAT activity of	acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6367_s_359	10454583	The HAT activity of p300 can acetylate p53, increasing its sequence-specific DNA binding activity ( 13).	transcription
73179	2	336351	7	NULL	NULL	NULL	NULL	p53	GP		bind		sequence-specific			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_19_9_6367_s_359	10454583	The HAT activity of p300 can acetylate p53, increasing its sequence-specific DNA binding activity ( 13).	transcription
73180	3	336351	7	NULL	NULL	0	NULL	statement 1	Process		increase					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_9_6367_s_359	10454583	The HAT activity of p300 can acetylate p53, increasing its sequence-specific DNA binding activity ( 13).	transcription
73181	1	336352	7	NULL	NULL	0	NULL	CBP/p300	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_20_16804_s_26	11279157	For example, CBP/p300 can acetylate p53, resulting in an enhancement of its DNA binding activity.	transcription
73182	2	336352	7	NULL	NULL	0	NULL	p53	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_20_16804_s_26	11279157	For example, CBP/p300 can acetylate p53, resulting in an enhancement of its DNA binding activity.	transcription
73183	3	336352	7	NULL	NULL	0	NULL	statement 1	Process		enhance					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_20_16804_s_26	11279157	For example, CBP/p300 can acetylate p53, resulting in an enhancement of its DNA binding activity.	transcription
73184	1	336353	7	NULL	NULL	0	NULL	stress	Process		activate					p53	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_428	15364927	It is well known that various types of stress activate p53 through inducing phosphorylation of p53 by a number of kinases and acetylation of p53 by acetylases p300 and PCAF ( ).	transcription
73185	3	336353	7	NULL	NULL	NULL	NULL	statement 1	Process		through					statement 2	GP				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_428	15364927	It is well known that various types of stress activate p53 through inducing phosphorylation of p53 by a number of kinases and acetylation of p53 by acetylases p300 and PCAF ( ).	transcription
73186	2	336353	7	NULL	NULL	NULL	NULL	kinases	GP		induce					p53	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_428	15364927	It is well known that various types of stress activate p53 through inducing phosphorylation of p53 by a number of kinases and acetylation of p53 by acetylases p300 and PCAF ( ).	transcription
73187	4	336353	7	NULL	NULL	0	NULL	p300	GP		induce					p53	GP	acetylation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_428	15364927	It is well known that various types of stress activate p53 through inducing phosphorylation of p53 by a number of kinases and acetylation of p53 by acetylases p300 and PCAF ( ).	transcription
73188	5	336353	7	NULL	NULL	0	NULL	PCAF	GP		induce					p53	GP	acetylation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_428	15364927	It is well known that various types of stress activate p53 through inducing phosphorylation of p53 by a number of kinases and acetylation of p53 by acetylases p300 and PCAF ( ).	transcription
73189	6	336353	7	NULL	NULL	0	NULL	p300	GP		is a type of					acetylases	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_428	15364927	It is well known that various types of stress activate p53 through inducing phosphorylation of p53 by a number of kinases and acetylation of p53 by acetylases p300 and PCAF ( ).	transcription
73190	7	336353	7	NULL	NULL	0	NULL	PCAF	GP		is a type of					acetylases	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_428	15364927	It is well known that various types of stress activate p53 through inducing phosphorylation of p53 by a number of kinases and acetylation of p53 by acetylases p300 and PCAF ( ).	transcription
73191	8	336353	7	NULL	NULL	0	NULL	statement 1	Process		through					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_428	15364927	It is well known that various types of stress activate p53 through inducing phosphorylation of p53 by a number of kinases and acetylation of p53 by acetylases p300 and PCAF ( ).	transcription
73192	9	336353	7	NULL	NULL	0	NULL	statement 1	Process		through					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_428	15364927	It is well known that various types of stress activate p53 through inducing phosphorylation of p53 by a number of kinases and acetylation of p53 by acetylases p300 and PCAF ( ).	transcription
73193	1	336354	7	NULL	NULL	0	NULL	 p300	GP		acetylates					p53	GP				NULL	in vivo	0	NULL	NULL	NULL	gw60_embo_20_6_1331_s_50	11250899	We also establish that,  in vivo, p300 and CBP can function as p53 acetylases and positively regulate p53 acetylation status, while MDM2 suppresses p53 acetylation.	transcription
73194	2	336354	7	NULL	NULL	NULL	NULL	CBP 	GP		acetylates					p53	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_embo_20_6_1331_s_50	11250899	We also establish that,  in vivo, p300 and CBP can function as p53 acetylases and positively regulate p53 acetylation status, while MDM2 suppresses p53 acetylation.	transcription
73195	3	336354	7	NULL	NULL	0	NULL	statement 1	Process		regulates		positively			p53	GP				NULL		0	NULL	NULL	NULL	gw60_embo_20_6_1331_s_50	11250899	We also establish that,  in vivo, p300 and CBP can function as p53 acetylases and positively regulate p53 acetylation status, while MDM2 suppresses p53 acetylation.	transcription
73196	4	336354	7	NULL	NULL	0	NULL	statement 2	Process		regulates		positively			p53	GP				NULL		0	NULL	NULL	NULL	gw60_embo_20_6_1331_s_50	11250899	We also establish that,  in vivo, p300 and CBP can function as p53 acetylases and positively regulate p53 acetylation status, while MDM2 suppresses p53 acetylation.	transcription
73197	5	336354	7	NULL	NULL	0	NULL	MDM2	GP		suppress					p53	GP	acetylation of			NULL		0	NULL	NULL	NULL	gw60_embo_20_6_1331_s_50	11250899	We also establish that,  in vivo, p300 and CBP can function as p53 acetylases and positively regulate p53 acetylation status, while MDM2 suppresses p53 acetylation.	transcription
73198	1	336355	7	NULL	NULL	NULL	NULL	PCAF	GP		interacts with		physically			p53	GP				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_8	10891493	We further show that the E1B 55-kDa protein interferes with the physical interaction between PCAF and p53, suggesting that the E1B 55-kDa protein inhibits PCAF acetylase function on p53 by preventing enzyme-substrate interaction.	transcription
73199	2	336355	7	NULL	NULL	0	NULL	 E1B 55-kDa protein	GP		interferes with					statement 1	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_8	10891493	We further show that the E1B 55-kDa protein interferes with the physical interaction between PCAF and p53, suggesting that the E1B 55-kDa protein inhibits PCAF acetylase function on p53 by preventing enzyme-substrate interaction.	transcription
73200	3	336355	7	NULL	NULL	0	NULL	PCAF	GP		acetylates					p53	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_8	10891493	We further show that the E1B 55-kDa protein interferes with the physical interaction between PCAF and p53, suggesting that the E1B 55-kDa protein inhibits PCAF acetylase function on p53 by preventing enzyme-substrate interaction.	transcription
73201	4	336355	7	NULL	NULL	0	NULL	E1B 55-kDa protein 	GP		inhibits					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_8	10891493	We further show that the E1B 55-kDa protein interferes with the physical interaction between PCAF and p53, suggesting that the E1B 55-kDa protein inhibits PCAF acetylase function on p53 by preventing enzyme-substrate interaction.	transcription
73202	1	336356	7	NULL	NULL	0	NULL	p300	GP		activates					acetylase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_49_45928_s_138	11591713	Since the acetylase activity of p300 is required for its stabilization of MDM2 but not for stabilization of p53, one would predict that the p300DY mutant's ability to stabilize p53 would not be affected by MDM2 expression.	transcription
73203	2	336356	7	NULL	NULL	0	NULL	statement 1	Process		required for					MDM2	GP	stabilization of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_49_45928_s_138	11591713	Since the acetylase activity of p300 is required for its stabilization of MDM2 but not for stabilization of p53, one would predict that the p300DY mutant's ability to stabilize p53 would not be affected by MDM2 expression.	transcription
73204	3	336356	7	NULL	NULL	NULL	NULL	statement 1	Process		is not required for					p53	GP	stabilization of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_276_49_45928_s_138	11591713	Since the acetylase activity of p300 is required for its stabilization of MDM2 but not for stabilization of p53, one would predict that the p300DY mutant's ability to stabilize p53 would not be affected by MDM2 expression.	transcription
73205	4	336356	7	NULL	NULL	0	NULL	p300	GP	mutant	stabilize			DY		p53	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_49_45928_s_138	11591713	Since the acetylase activity of p300 is required for its stabilization of MDM2 but not for stabilization of p53, one would predict that the p300DY mutant's ability to stabilize p53 would not be affected by MDM2 expression.	transcription
73206	5	336356	7	NULL	NULL	0	NULL	MDM2	GP	expression of	does not affect					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_49_45928_s_138	11591713	Since the acetylase activity of p300 is required for its stabilization of MDM2 but not for stabilization of p53, one would predict that the p300DY mutant's ability to stabilize p53 would not be affected by MDM2 expression.	transcription
73207	1	336357	7	NULL	NULL	NULL	NULL	p300	GP		acetylates					p53	GP		N terminus		NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_24_23_10366_s_289	15542844	Other molecules that interact with the p53 N terminus, such as the transcriptional coactivator p300 that acetylates p53 ( ), and the MdmX protein ( ,  ) can also contribute to p53 stabilization.	transcription
73208	2	336357	7	NULL	NULL	0	NULL	p300	GP		acetylates					MdmX protein 	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_23_10366_s_289	15542844	Other molecules that interact with the p53 N terminus, such as the transcriptional coactivator p300 that acetylates p53 ( ), and the MdmX protein ( ,  ) can also contribute to p53 stabilization.	transcription
73209	3	336357	7	NULL	NULL	0	NULL	p300	GP		contribute to					p53	GP	stabilization of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_23_10366_s_289	15542844	Other molecules that interact with the p53 N terminus, such as the transcriptional coactivator p300 that acetylates p53 ( ), and the MdmX protein ( ,  ) can also contribute to p53 stabilization.	transcription
73210	4	336357	7	NULL	NULL	0	NULL	p300	GP		is a type of					transcriptional coactivator 	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_23_10366_s_289	15542844	Other molecules that interact with the p53 N terminus, such as the transcriptional coactivator p300 that acetylates p53 ( ), and the MdmX protein ( ,  ) can also contribute to p53 stabilization.	transcription
73211	1	336358	7	NULL	NULL	0	NULL	p53	GP		interacts with					p300/CBP	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_122	11960694	N-terminal phosphorylation also enhances interactions of p53 with transcriptional co-activators like p300/CBP, which can acetylate residues in the C-terminus and promote p53's transcriptional activity.	transcription
73212	2	336358	7	NULL	NULL	0	NULL	p300/CBP	GP		acetylate					p53	GP		C-terminus		NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_122	11960694	N-terminal phosphorylation also enhances interactions of p53 with transcriptional co-activators like p300/CBP, which can acetylate residues in the C-terminus and promote p53's transcriptional activity.	transcription
73213	3	336358	7	NULL	NULL	0	NULL	statement 2	Process		promote					p53	GP	transcriptional activity of			NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_122	11960694	N-terminal phosphorylation also enhances interactions of p53 with transcriptional co-activators like p300/CBP, which can acetylate residues in the C-terminus and promote p53's transcriptional activity.	transcription
73214	4	336358	7	NULL	NULL	NULL	NULL	p53		phosphorylation 	enhance			N-terminal		statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_122	11960694	N-terminal phosphorylation also enhances interactions of p53 with transcriptional co-activators like p300/CBP, which can acetylate residues in the C-terminus and promote p53's transcriptional activity.	transcription
73215	5	336358	7	NULL	NULL	0	NULL	p300/CBP	GP		is a type of					transcriptional co-activator	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1602_1_47_s_122	11960694	N-terminal phosphorylation also enhances interactions of p53 with transcriptional co-activators like p300/CBP, which can acetylate residues in the C-terminus and promote p53's transcriptional activity.	transcription
73216	1	336359	7	NULL	NULL	0	NULL	PCAF	GP		acetylate		specifically			p53	GP		lysine 320		NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_34_30838_s_17	12068014	Although less studied, the  p300/ CBP- associated  factor (PCAF) has also been shown to specifically acetylate the lysine 320 of p53, leading to the enhancement of the sequence-specific DNA binding activity of p53  in vitro ( 13).	transcription
73217	2	336359	7	NULL	NULL	0	NULL	p53	GP		bind		sequence-specific			DNA	NucleicAcid				NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_277_34_30838_s_17	12068014	Although less studied, the  p300/ CBP- associated  factor (PCAF) has also been shown to specifically acetylate the lysine 320 of p53, leading to the enhancement of the sequence-specific DNA binding activity of p53  in vitro ( 13).	transcription
73218	3	336359	7	NULL	NULL	0	NULL	statement 1	Process		enhance					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_34_30838_s_17	12068014	Although less studied, the  p300/ CBP- associated  factor (PCAF) has also been shown to specifically acetylate the lysine 320 of p53, leading to the enhancement of the sequence-specific DNA binding activity of p53  in vitro ( 13).	transcription
73219	4	336359	7	NULL	NULL	0	NULL	PCAF	GP		is					p300/ CBP- associated factor	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_277_34_30838_s_17	12068014	Although less studied, the  p300/ CBP- associated  factor (PCAF) has also been shown to specifically acetylate the lysine 320 of p53, leading to the enhancement of the sequence-specific DNA binding activity of p53  in vitro ( 13).	transcription
73220	1	336360	7	NULL	NULL	0	NULL	TRRAP	GP		bind					p53	GP	acetylated			NULL	in vitro	0	NULL	NULL	NULL	gw60_molcell_8_6_1243_s_241	11779500	Binding of TRRAP and hGcn5 to Acetylated p53 In Vitro	transcription
73221	2	336360	7	NULL	NULL	0	NULL	hGcn5	GP		bind					p53	GP	acetylated			NULL	in vitro	0	NULL	NULL	NULL	gw60_molcell_8_6_1243_s_241	11779500	Binding of TRRAP and hGcn5 to Acetylated p53 In Vitro	transcription
73222	1	336361	7	NULL	NULL	0	NULL	Sir2 enzyme 	GP		bind					p53 peptide	GP	acetylated			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_23_9_3173_s_447	12697818	Structure of a Sir2 enzyme bound to an acetylated p53 peptide.	transcription
73223	1	336362	7	NULL	NULL	0	NULL	p300	GP		activates					acetylase	GP				NULL	in vitro	0	NULL	NULL	NULL	gw60_jbiolchem_276_1_48_s_168	11076933	First of all, p73alpha was a considerably poor substrate for the acetylase activity of p300  in vitro, in contrast with p53, which is acetylated by p300 in response to DNA damage ( 12,  13).	transcription
73224	2	336362	7	NULL	NULL	0	NULL	p73alpha	GP		poor substrate for					statement 1	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_48_s_168	11076933	First of all, p73alpha was a considerably poor substrate for the acetylase activity of p300  in vitro, in contrast with p53, which is acetylated by p300 in response to DNA damage ( 12,  13).	transcription
73225	3	336362	7	NULL	NULL	0	NULL	p300	GP		acetylates					p53	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_48_s_168	11076933	First of all, p73alpha was a considerably poor substrate for the acetylase activity of p300  in vitro, in contrast with p53, which is acetylated by p300 in response to DNA damage ( 12,  13).	transcription
73226	4	336362	7	NULL	NULL	0	NULL	statement 3	Process		in response to					DNA damage	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_48_s_168	11076933	First of all, p73alpha was a considerably poor substrate for the acetylase activity of p300  in vitro, in contrast with p53, which is acetylated by p300 in response to DNA damage ( 12,  13).	transcription
73227	5	336362	7	NULL	NULL	0	NULL	statement 2	Process		in contrast with					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_276_1_48_s_168	11076933	First of all, p73alpha was a considerably poor substrate for the acetylase activity of p300  in vitro, in contrast with p53, which is acetylated by p300 in response to DNA damage ( 12,  13).	transcription
73234	1	336363	7	NULL	NULL	0	NULL	P/CAF	GP		does not acetylate					 GATA-1 	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20853_s_291	10779504	P/CAF does not acetylate GATA-1 ( 21), and the carboxyl-terminal acetylation site of p53 is preferentially acetylated by p300 compared with P/CAF ( 19).	transcription
73236	2	336363	7	NULL	NULL	NULL	NULL	p300	GP		acetylate		preferentially			p53	GP		carboxyl-terminal acetylation site		NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_275_27_20853_s_291	10779504	P/CAF does not acetylate GATA-1 ( 21), and the carboxyl-terminal acetylation site of p53 is preferentially acetylated by p300 compared with P/CAF ( 19).	transcription
73254	1	336364	7	NULL	NULL	0	NULL	small oligonucleotides	NucleicAcid		stabilize			p53 consensus site		p300.p53 complex	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_15_13431_s_263	12499368	Using purified p300 and p53 proteins, we show that small oligonucleotides containing the p53 consensus site (Fig.  9 A) or supercoiled plasmid DNA containing the p53 consensus site (Fig.  9 B), can promote a striking stabilization of the p300.p53 complex after the addition of acetyl-CoA (Fig.  9,  A and  B,  lane 12), relative to nonspecific DNA (Fig.  9,  A and  B,  lane 11 versus 12).	transcription
73255	2	336364	7	NULL	NULL	0	NULL	statement 1	Process		occur after					acetyl-CoA	Chemical	addition of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_15_13431_s_263	12499368	Using purified p300 and p53 proteins, we show that small oligonucleotides containing the p53 consensus site (Fig.  9 A) or supercoiled plasmid DNA containing the p53 consensus site (Fig.  9 B), can promote a striking stabilization of the p300.p53 complex after the addition of acetyl-CoA (Fig.  9,  A and  B,  lane 12), relative to nonspecific DNA (Fig.  9,  A and  B,  lane 11 versus 12).	transcription
73256	3	336364	7	NULL	NULL	0	NULL	supercoiled plasmid DNA	NucleicAcid		stabilize			p53 consensus site		p300.p53 complex	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_15_13431_s_263	12499368	Using purified p300 and p53 proteins, we show that small oligonucleotides containing the p53 consensus site (Fig.  9 A) or supercoiled plasmid DNA containing the p53 consensus site (Fig.  9 B), can promote a striking stabilization of the p300.p53 complex after the addition of acetyl-CoA (Fig.  9,  A and  B,  lane 12), relative to nonspecific DNA (Fig.  9,  A and  B,  lane 11 versus 12).	transcription
73258	4	336364	7	NULL	NULL	0	NULL	statement 3	Process		occur after					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_15_13431_s_263	12499368	Using purified p300 and p53 proteins, we show that small oligonucleotides containing the p53 consensus site (Fig.  9 A) or supercoiled plasmid DNA containing the p53 consensus site (Fig.  9 B), can promote a striking stabilization of the p300.p53 complex after the addition of acetyl-CoA (Fig.  9,  A and  B,  lane 12), relative to nonspecific DNA (Fig.  9,  A and  B,  lane 11 versus 12).	transcription
73259	1	336365	7	NULL	NULL	0	NULL	p53	GP		associate with					U6	GP			promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3247_s_179	15798209	Second, low levels of p53 associate with the U6 promoter prior to stress and UV light stimulates p53 promoter association, but this p53 is not acetylated to a significant degree.	transcription
73260	2	336365	7	NULL	NULL	0	NULL	statement 1	Process		occur prior to					stress	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3247_s_179	15798209	Second, low levels of p53 associate with the U6 promoter prior to stress and UV light stimulates p53 promoter association, but this p53 is not acetylated to a significant degree.	transcription
73261	3	336365	7	NULL	NULL	0	NULL	UVlight	PhysicalPhenomenon		stimulate					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3247_s_179	15798209	Second, low levels of p53 associate with the U6 promoter prior to stress and UV light stimulates p53 promoter association, but this p53 is not acetylated to a significant degree.	transcription
73262	4	336365	7	NULL	NULL	0	NULL	statement 3	Process		does not acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3247_s_179	15798209	Second, low levels of p53 associate with the U6 promoter prior to stress and UV light stimulates p53 promoter association, but this p53 is not acetylated to a significant degree.	transcription
73264	1	336366	7	NULL	NULL	0	NULL	p300	GP		clamped to					p53	GP	acetylated			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_22_10083_s_311	15509808	Thus, the observation that acetylation of p53 enhances its transcriptional activity can be explained in part by the clamping of p300 to acetylated p53 when p53 is DNA bound ( ).	transcription
73265	2	336366	7	NULL	NULL	0	NULL	p53	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_22_10083_s_311	15509808	Thus, the observation that acetylation of p53 enhances its transcriptional activity can be explained in part by the clamping of p300 to acetylated p53 when p53 is DNA bound ( ).	transcription
73268	3	336366	7	NULL	NULL	0	NULL	p53	GP	acetylation of	enhance					p53	GP	transcriptional activity of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_24_22_10083_s_311	15509808	Thus, the observation that acetylation of p53 enhances its transcriptional activity can be explained in part by the clamping of p300 to acetylated p53 when p53 is DNA bound ( ).	transcription
73271	1	336367	7	NULL	NULL	0	NULL	p53	GP		bind					Daxx	GP	yeast			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_204	15364927	We showed above that several p53 mutants that mimic acetylated or phosphorylated p53 abolished binding of p53 to Daxx in yeast ( Fig. 1 G).	transcription
73274	2	336367	7	NULL	NULL	0	NULL	p53	GP	mutant mimicking acetylated	abolish					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_204	15364927	We showed above that several p53 mutants that mimic acetylated or phosphorylated p53 abolished binding of p53 to Daxx in yeast ( Fig. 1 G).	transcription
73276	3	336367	7	NULL	NULL	NULL	NULL	p53	GP	mutant mimicking phosphorylated	abolish					statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_204	15364927	We showed above that several p53 mutants that mimic acetylated or phosphorylated p53 abolished binding of p53 to Daxx in yeast ( Fig. 1 G).	transcription
73277	1	336368	7	NULL	NULL	0	NULL	 p53	GP	acetylation of	is a type of					transient event	Process				NULL		0	NULL	NULL	NULL	gw60_embo_20_6_1331_s_69	11250899	As shown in Figure  1A, p53 acetylation is a transient event and, after an initial increase, the abundance of acetylated p53 decreased due to the activity of a putative p53 deacetylase.	transcription
73278	2	336368	7	NULL	NULL	0	NULL	p53	GP	acetylated	decrease					putative p53 deacetylase	GP	due to activity of			NULL		0	NULL	NULL	NULL	gw60_embo_20_6_1331_s_69	11250899	As shown in Figure  1A, p53 acetylation is a transient event and, after an initial increase, the abundance of acetylated p53 decreased due to the activity of a putative p53 deacetylase.	transcription
73280	3	336368	7	NULL	NULL	0	NULL	statement 2	Process		occur after					p53	GP	initial increase of acetylated			NULL		0	NULL	NULL	NULL	gw60_embo_20_6_1331_s_69	11250899	As shown in Figure  1A, p53 acetylation is a transient event and, after an initial increase, the abundance of acetylated p53 decreased due to the activity of a putative p53 deacetylase.	transcription
73282	1	336369	7	NULL	NULL	0	NULL	PCAF	GP		acetylates					p53	GP		lysine 320		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_19_20035_s_34	14769800	PCAF also acetylates p53 at lysine 320 in response to DNA damage signals and activates the activity of p53 ( ).	transcription
73283	2	336369	7	NULL	NULL	0	NULL	statement 1	Process		in response to					DNA damage signals	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_19_20035_s_34	14769800	PCAF also acetylates p53 at lysine 320 in response to DNA damage signals and activates the activity of p53 ( ).	transcription
73284	3	336369	7	NULL	NULL	0	NULL	statement 1	Process		activates 					p53	GP	activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_19_20035_s_34	14769800	PCAF also acetylates p53 at lysine 320 in response to DNA damage signals and activates the activity of p53 ( ).	transcription
73285	1	336370	7	NULL	NULL	0	NULL	PCAF	GP		acetylate		efficiently			p53	GP				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1202_s_78	9891054	This result indicated that PCAF efficiently acetylates p53 in vitro and that PCAF and p300 target distinct residues within p53.	transcription
73286	2	336370	7	NULL	NULL	0	NULL	PCAF	GP		target					p53	GP		distinct residues		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1202_s_78	9891054	This result indicated that PCAF efficiently acetylates p53 in vitro and that PCAF and p300 target distinct residues within p53.	transcription
73287	3	336370	7	NULL	NULL	0	NULL	p300	GP		target					p53	GP		distinct residues		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1202_s_78	9891054	This result indicated that PCAF efficiently acetylates p53 in vitro and that PCAF and p300 target distinct residues within p53.	transcription
73288	1	336371	7	NULL	NULL	0	NULL	ZBP-89	GP		bind		directly			p21waf1	GP			promoter	NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_14_4670_s_378	11416144	ZBP-89 binds directly to the p21waf1 promoter ( 5,  19), but, in the absence of p53, ZBP-89 requires recruitment of a histone acetylase and inhibition of deacetylase activity ( 5).	transcription
73289	2	336371	7	NULL	NULL	0	NULL	statement 1	Process		in the absence of					p53	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_14_4670_s_378	11416144	ZBP-89 binds directly to the p21waf1 promoter ( 5,  19), but, in the absence of p53, ZBP-89 requires recruitment of a histone acetylase and inhibition of deacetylase activity ( 5).	transcription
73290	3	336371	7	NULL	NULL	NULL	NULL	 ZBP-89 	GP		requires					histone acetylase	GP	recruitment of			NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_14_4670_s_378	11416144	ZBP-89 binds directly to the p21waf1 promoter ( 5,  19), but, in the absence of p53, ZBP-89 requires recruitment of a histone acetylase and inhibition of deacetylase activity ( 5).	transcription
73291	4	336371	7	NULL	NULL	0	NULL	ZBP-89			requires					deacetylase activity	Process	inhibition of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_14_4670_s_378	11416144	ZBP-89 binds directly to the p21waf1 promoter ( 5,  19), but, in the absence of p53, ZBP-89 requires recruitment of a histone acetylase and inhibition of deacetylase activity ( 5).	transcription
73292	1	336372	7	NULL	NULL	0	NULL	CBP	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw60_molcell_3_1_125_s_24	10024886	For example, CBP can acetylate the tumor suppressor protein p53, and this modification stimulates its DNA binding activity ( Gu and Roeder 1997  ).	transcription
73293	2	336372	7	NULL	NULL	0	NULL	p53	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_molcell_3_1_125_s_24	10024886	For example, CBP can acetylate the tumor suppressor protein p53, and this modification stimulates its DNA binding activity ( Gu and Roeder 1997  ).	transcription
73294	3	336372	7	NULL	NULL	0	NULL	statement 1	Process		stimulate					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_3_1_125_s_24	10024886	For example, CBP can acetylate the tumor suppressor protein p53, and this modification stimulates its DNA binding activity ( Gu and Roeder 1997  ).	transcription
73295	4	336372	7	NULL	NULL	0	NULL	p53	GP		is a type of					tumor suppressor protein	GP				NULL		0	NULL	NULL	NULL	gw60_molcell_3_1_125_s_24	10024886	For example, CBP can acetylate the tumor suppressor protein p53, and this modification stimulates its DNA binding activity ( Gu and Roeder 1997  ).	transcription
73297	1	336373	7	NULL	NULL	0	NULL	p300	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_95_22_12924_s_136	9789016	For example, in addition to histones, p300 will acetylate the tumor suppressor protein, p53, thereby enhancing its DNA-binding activity  in vitro ( 37).	transcription
73298	2	336373	7	NULL	NULL	0	NULL	p300	GP		acetylate					histones	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_95_22_12924_s_136	9789016	For example, in addition to histones, p300 will acetylate the tumor suppressor protein, p53, thereby enhancing its DNA-binding activity  in vitro ( 37).	transcription
73299	3	336373	7	NULL	NULL	NULL	NULL	p53	GP		bind					DNA	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_pnas_95_22_12924_s_136	9789016	For example, in addition to histones, p300 will acetylate the tumor suppressor protein, p53, thereby enhancing its DNA-binding activity  in vitro ( 37).	transcription
73300	4	336373	7	NULL	NULL	0	NULL	p53	GP		is a type of					tumor suppressor protein	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_95_22_12924_s_136	9789016	For example, in addition to histones, p300 will acetylate the tumor suppressor protein, p53, thereby enhancing its DNA-binding activity  in vitro ( 37).	transcription
73301	1	336374	7	NULL	NULL	0	NULL	HDIs	GP		is a type of					transcriptional activator	GP				NULL		0	NULL	NULL	NULL	gw70_febslett_570_1_37_s_5	15251435	Hypotheses have been generated which suggest that HDIs are transcriptional activators  that disrupt the balance between histone deacetylase (HDAC) and histone acetyl transferase  (HAT) activity resulting in hyperacetylation of nucleosomal histones and non-histone  proteins, such as the transcription factor p53 [  5 and   6].	transcription
73302	2	336374	7	NULL	NULL	0	NULL	HDAC	GP	activity of	is in balance with					HAT	GP	activity of			NULL		0	NULL	NULL	NULL	gw70_febslett_570_1_37_s_5	15251435	Hypotheses have been generated which suggest that HDIs are transcriptional activators  that disrupt the balance between histone deacetylase (HDAC) and histone acetyl transferase  (HAT) activity resulting in hyperacetylation of nucleosomal histones and non-histone  proteins, such as the transcription factor p53 [  5 and   6].	transcription
73303	3	336374	7	NULL	NULL	0	NULL	HDI	GP		disrupt					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_febslett_570_1_37_s_5	15251435	Hypotheses have been generated which suggest that HDIs are transcriptional activators  that disrupt the balance between histone deacetylase (HDAC) and histone acetyl transferase  (HAT) activity resulting in hyperacetylation of nucleosomal histones and non-histone  proteins, such as the transcription factor p53 [  5 and   6].	transcription
73304	4	336374	7	NULL	NULL	0	NULL	statement 3	Process		result in					nucleosomal histones	GP	hyperacetylation of			NULL		0	NULL	NULL	NULL	gw70_febslett_570_1_37_s_5	15251435	Hypotheses have been generated which suggest that HDIs are transcriptional activators  that disrupt the balance between histone deacetylase (HDAC) and histone acetyl transferase  (HAT) activity resulting in hyperacetylation of nucleosomal histones and non-histone  proteins, such as the transcription factor p53 [  5 and   6].	transcription
73305	5	336374	7	NULL	NULL	0	NULL	statement 3	Process		result in					p53	GP	hyperacetylation of			NULL		0	NULL	NULL	NULL	gw70_febslett_570_1_37_s_5	15251435	Hypotheses have been generated which suggest that HDIs are transcriptional activators  that disrupt the balance between histone deacetylase (HDAC) and histone acetyl transferase  (HAT) activity resulting in hyperacetylation of nucleosomal histones and non-histone  proteins, such as the transcription factor p53 [  5 and   6].	transcription
73306	6	336374	7	NULL	NULL	0	NULL	p53	GP		is a type of					transcription factor	GP				NULL		0	NULL	NULL	NULL	gw70_febslett_570_1_37_s_5	15251435	Hypotheses have been generated which suggest that HDIs are transcriptional activators  that disrupt the balance between histone deacetylase (HDAC) and histone acetyl transferase  (HAT) activity resulting in hyperacetylation of nucleosomal histones and non-histone  proteins, such as the transcription factor p53 [  5 and   6].	transcription
73307	7	336374	7	NULL	NULL	0	NULL	p53	GP		is a type of					non-histone proteins	GP				NULL		0	NULL	NULL	NULL	gw70_febslett_570_1_37_s_5	15251435	Hypotheses have been generated which suggest that HDIs are transcriptional activators  that disrupt the balance between histone deacetylase (HDAC) and histone acetyl transferase  (HAT) activity resulting in hyperacetylation of nucleosomal histones and non-histone  proteins, such as the transcription factor p53 [  5 and   6].	transcription
73308	8	336374	7	NULL	NULL	0	NULL	HDAC	GP		is					histone deacetylase	GP				NULL		0	NULL	NULL	NULL	gw70_febslett_570_1_37_s_5	15251435	Hypotheses have been generated which suggest that HDIs are transcriptional activators  that disrupt the balance between histone deacetylase (HDAC) and histone acetyl transferase  (HAT) activity resulting in hyperacetylation of nucleosomal histones and non-histone  proteins, such as the transcription factor p53 [  5 and   6].	transcription
73309	9	336374	7	NULL	NULL	0	NULL	HAT	GP		is					histone acetyl transferase	GP				NULL		0	NULL	NULL	NULL	gw70_febslett_570_1_37_s_5	15251435	Hypotheses have been generated which suggest that HDIs are transcriptional activators  that disrupt the balance between histone deacetylase (HDAC) and histone acetyl transferase  (HAT) activity resulting in hyperacetylation of nucleosomal histones and non-histone  proteins, such as the transcription factor p53 [  5 and   6].	transcription
73310	1	336375	7	NULL	NULL	0	NULL	Myc oncogene	GP		induce					p53	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	gw70_nature_434_7035_864_s_106	15829956	Furthermore, unlike phosphorylations of p53 and H2AX induced  by the Myc oncogene, which are a consequence of oxygen radical generation 11, the DNA damage response in our experiments was only marginally repressed by the  antioxidant  N-acetyl- l-cysteine (NAC;  Fig. 4a and  Supplementary Figs S4d, S5b, c).	transcription
73311	2	336375	7	NULL	NULL	NULL	NULL	Myc oncogene	GP		induce					H2AX	GP	phosphorylation of			NULL		NULL	NULL	NULL	NULL	gw70_nature_434_7035_864_s_106	15829956	Furthermore, unlike phosphorylations of p53 and H2AX induced  by the Myc oncogene, which are a consequence of oxygen radical generation 11, the DNA damage response in our experiments was only marginally repressed by the  antioxidant  N-acetyl- l-cysteine (NAC;  Fig. 4a and  Supplementary Figs S4d, S5b, c).	transcription
73312	3	336375	7	NULL	NULL	0	NULL	statement 1	Process		as a consequence of					oxygen radical generation	Process				NULL		0	NULL	NULL	NULL	gw70_nature_434_7035_864_s_106	15829956	Furthermore, unlike phosphorylations of p53 and H2AX induced  by the Myc oncogene, which are a consequence of oxygen radical generation 11, the DNA damage response in our experiments was only marginally repressed by the  antioxidant  N-acetyl- l-cysteine (NAC;  Fig. 4a and  Supplementary Figs S4d, S5b, c).	transcription
73313	4	336375	7	NULL	NULL	0	NULL	statement 2	Process		as a consequence of					oxygen radical generation	Process				NULL		0	NULL	NULL	NULL	gw70_nature_434_7035_864_s_106	15829956	Furthermore, unlike phosphorylations of p53 and H2AX induced  by the Myc oncogene, which are a consequence of oxygen radical generation 11, the DNA damage response in our experiments was only marginally repressed by the  antioxidant  N-acetyl- l-cysteine (NAC;  Fig. 4a and  Supplementary Figs S4d, S5b, c).	transcription
73314	5	336375	7	NULL	NULL	0	NULL	NAC	Chemical		repress		marginally			DNA damage response	Process				NULL		0	NULL	NULL	NULL	gw70_nature_434_7035_864_s_106	15829956	Furthermore, unlike phosphorylations of p53 and H2AX induced  by the Myc oncogene, which are a consequence of oxygen radical generation 11, the DNA damage response in our experiments was only marginally repressed by the  antioxidant  N-acetyl- l-cysteine (NAC;  Fig. 4a and  Supplementary Figs S4d, S5b, c).	transcription
73315	6	336375	7	NULL	NULL	0	NULL	NAC	Chemical		is					N-acetyl- l-cysteine	Chemical				NULL		0	NULL	NULL	NULL	gw70_nature_434_7035_864_s_106	15829956	Furthermore, unlike phosphorylations of p53 and H2AX induced  by the Myc oncogene, which are a consequence of oxygen radical generation 11, the DNA damage response in our experiments was only marginally repressed by the  antioxidant  N-acetyl- l-cysteine (NAC;  Fig. 4a and  Supplementary Figs S4d, S5b, c).	transcription
73316	7	336375	7	NULL	NULL	0	NULL	NAC	Chemical		is a type of					antioxidant	Chemical				NULL		0	NULL	NULL	NULL	gw70_nature_434_7035_864_s_106	15829956	Furthermore, unlike phosphorylations of p53 and H2AX induced  by the Myc oncogene, which are a consequence of oxygen radical generation 11, the DNA damage response in our experiments was only marginally repressed by the  antioxidant  N-acetyl- l-cysteine (NAC;  Fig. 4a and  Supplementary Figs S4d, S5b, c).	transcription
73317	1	336376	7	NULL	NULL	0	NULL	acetyl-CoA	Chemical		promote					p53	GP	acetylation of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_174	14612423	Using the p300 acetylation reaction where acetyl-CoA promotes p53 acetylation in a sequence-specific DNA-dependent manner (Fig.  3B, lane 2 versus lane 1), the PXXP repeat peptide was found to be a specific inhibitor of DNA-dependent acetylation (Fig.  3B, lanes 8 to 10 versus lanes 2 to 6).	transcription
73318	2	336376	7	NULL	NULL	0	NULL	statement 1	Process		depends on					DNA	NucleicAcid	sequence-specific			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_174	14612423	Using the p300 acetylation reaction where acetyl-CoA promotes p53 acetylation in a sequence-specific DNA-dependent manner (Fig.  3B, lane 2 versus lane 1), the PXXP repeat peptide was found to be a specific inhibitor of DNA-dependent acetylation (Fig.  3B, lanes 8 to 10 versus lanes 2 to 6).	transcription
73319	3	336376	7	NULL	NULL	0	NULL	acetylation	Process		depends on					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_174	14612423	Using the p300 acetylation reaction where acetyl-CoA promotes p53 acetylation in a sequence-specific DNA-dependent manner (Fig.  3B, lane 2 versus lane 1), the PXXP repeat peptide was found to be a specific inhibitor of DNA-dependent acetylation (Fig.  3B, lanes 8 to 10 versus lanes 2 to 6).	transcription
73320	4	336376	7	NULL	NULL	0	NULL	PXXP repeat peptide	AminoAcid		inhibitor of		specific			statement 3	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_23_23_8846_s_174	14612423	Using the p300 acetylation reaction where acetyl-CoA promotes p53 acetylation in a sequence-specific DNA-dependent manner (Fig.  3B, lane 2 versus lane 1), the PXXP repeat peptide was found to be a specific inhibitor of DNA-dependent acetylation (Fig.  3B, lanes 8 to 10 versus lanes 2 to 6).	transcription
73321	1	336377	7	NULL	NULL	0	NULL	p53	GP		induce					ROS	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_17_17765_s_92	14764594	To examine whether ROS induction by p53 is critical for senescence and Bcl-xL and E1B-19K inhibit p53-induced senescence by preventing ROS generation, we examined the effects of anti-oxidants,  N-acetyl-L-cysteine (NAC) and 1-pyrrolydine dithiocarbamate (PDTC).	transcription
73322	2	336377	7	NULL	NULL	0	NULL	statement 1	Process		critical for					senescence	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_17_17765_s_92	14764594	To examine whether ROS induction by p53 is critical for senescence and Bcl-xL and E1B-19K inhibit p53-induced senescence by preventing ROS generation, we examined the effects of anti-oxidants,  N-acetyl-L-cysteine (NAC) and 1-pyrrolydine dithiocarbamate (PDTC).	transcription
73323	3	336377	7	NULL	NULL	0	NULL	Bcl-xL	GP		inhibit					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_17_17765_s_92	14764594	To examine whether ROS induction by p53 is critical for senescence and Bcl-xL and E1B-19K inhibit p53-induced senescence by preventing ROS generation, we examined the effects of anti-oxidants,  N-acetyl-L-cysteine (NAC) and 1-pyrrolydine dithiocarbamate (PDTC).	transcription
73324	4	336377	7	NULL	NULL	0	NULL	E1B-19K	GP		inhibit					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_17_17765_s_92	14764594	To examine whether ROS induction by p53 is critical for senescence and Bcl-xL and E1B-19K inhibit p53-induced senescence by preventing ROS generation, we examined the effects of anti-oxidants,  N-acetyl-L-cysteine (NAC) and 1-pyrrolydine dithiocarbamate (PDTC).	transcription
73325	5	336377	7	NULL	NULL	0	NULL	statement 3	Process		occur by					ROS	Chemical	preventing generation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_17_17765_s_92	14764594	To examine whether ROS induction by p53 is critical for senescence and Bcl-xL and E1B-19K inhibit p53-induced senescence by preventing ROS generation, we examined the effects of anti-oxidants,  N-acetyl-L-cysteine (NAC) and 1-pyrrolydine dithiocarbamate (PDTC).	transcription
73326	6	336377	7	NULL	NULL	0	NULL	statement 4	Process		occur by					ROS	Chemical	preventing generation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_17_17765_s_92	14764594	To examine whether ROS induction by p53 is critical for senescence and Bcl-xL and E1B-19K inhibit p53-induced senescence by preventing ROS generation, we examined the effects of anti-oxidants,  N-acetyl-L-cysteine (NAC) and 1-pyrrolydine dithiocarbamate (PDTC).	transcription
73327	7	336377	7	NULL	NULL	0	NULL	NAC	Chemical		is					N-acetyl-L-cysteine	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_17_17765_s_92	14764594	To examine whether ROS induction by p53 is critical for senescence and Bcl-xL and E1B-19K inhibit p53-induced senescence by preventing ROS generation, we examined the effects of anti-oxidants,  N-acetyl-L-cysteine (NAC) and 1-pyrrolydine dithiocarbamate (PDTC).	transcription
73328	8	336377	7	NULL	NULL	0	NULL	PDTC	Chemical		is					1-pyrrolydine dithiocarbamate	Chemical				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_17_17765_s_92	14764594	To examine whether ROS induction by p53 is critical for senescence and Bcl-xL and E1B-19K inhibit p53-induced senescence by preventing ROS generation, we examined the effects of anti-oxidants,  N-acetyl-L-cysteine (NAC) and 1-pyrrolydine dithiocarbamate (PDTC).	transcription
73329	1	336378	7	NULL	NULL	NULL	NULL	E1A protein	GP	human adenovirus	bind					retinoblastoma tumor suppressor family 	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_23_3104_s_18	11731475	In the case of human adenoviruses, binding of the viral early region 1A (E1A) protein with either the retinoblastoma tumor suppressor family or p300/CBP/p400 histone acetyl transferases induces the activation, stabilization, and accumulation of p53 (Chiou and White 1997  ; Querido et al. 1997b  ; Samuelson and Lowe 1997  ).	transcription
73330	2	336378	7	NULL	NULL	NULL	NULL	E1A protein	GP	human adenovirus	bind					p300/CBP/p400 histone acetyl transferases 	GP				NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_23_3104_s_18	11731475	In the case of human adenoviruses, binding of the viral early region 1A (E1A) protein with either the retinoblastoma tumor suppressor family or p300/CBP/p400 histone acetyl transferases induces the activation, stabilization, and accumulation of p53 (Chiou and White 1997  ; Querido et al. 1997b  ; Samuelson and Lowe 1997  ).	transcription
73331	3	336378	7	NULL	NULL	0	NULL	statement 1	Process		induce					p53	GP	activation of			NULL		0	NULL	NULL	NULL	gw60_genesdev_15_23_3104_s_18	11731475	In the case of human adenoviruses, binding of the viral early region 1A (E1A) protein with either the retinoblastoma tumor suppressor family or p300/CBP/p400 histone acetyl transferases induces the activation, stabilization, and accumulation of p53 (Chiou and White 1997  ; Querido et al. 1997b  ; Samuelson and Lowe 1997  ).	transcription
73332	4	336378	7	NULL	NULL	0	NULL	statement 1	Process		induce					p53	GP	stabilization of			NULL		0	NULL	NULL	NULL	gw60_genesdev_15_23_3104_s_18	11731475	In the case of human adenoviruses, binding of the viral early region 1A (E1A) protein with either the retinoblastoma tumor suppressor family or p300/CBP/p400 histone acetyl transferases induces the activation, stabilization, and accumulation of p53 (Chiou and White 1997  ; Querido et al. 1997b  ; Samuelson and Lowe 1997  ).	transcription
73333	5	336378	7	NULL	NULL	0	NULL	statement 1	Process		induce					p53	GP	accumulation of			NULL		0	NULL	NULL	NULL	gw60_genesdev_15_23_3104_s_18	11731475	In the case of human adenoviruses, binding of the viral early region 1A (E1A) protein with either the retinoblastoma tumor suppressor family or p300/CBP/p400 histone acetyl transferases induces the activation, stabilization, and accumulation of p53 (Chiou and White 1997  ; Querido et al. 1997b  ; Samuelson and Lowe 1997  ).	transcription
73334	6	336378	7	NULL	NULL	NULL	NULL	statement 2	Process		induce					p53	GP	activation of			NULL		NULL	NULL	NULL	NULL	gw60_genesdev_15_23_3104_s_18	11731475	In the case of human adenoviruses, binding of the viral early region 1A (E1A) protein with either the retinoblastoma tumor suppressor family or p300/CBP/p400 histone acetyl transferases induces the activation, stabilization, and accumulation of p53 (Chiou and White 1997  ; Querido et al. 1997b  ; Samuelson and Lowe 1997  ).	transcription
73335	7	336378	7	NULL	NULL	0	NULL	statement 2	Process		induce					p53	GP	stabilization of			NULL		0	NULL	NULL	NULL	gw60_genesdev_15_23_3104_s_18	11731475	In the case of human adenoviruses, binding of the viral early region 1A (E1A) protein with either the retinoblastoma tumor suppressor family or p300/CBP/p400 histone acetyl transferases induces the activation, stabilization, and accumulation of p53 (Chiou and White 1997  ; Querido et al. 1997b  ; Samuelson and Lowe 1997  ).	transcription
73336	8	336378	7	NULL	NULL	0	NULL	statement 2	Process		induce					p53	GP	accumulation of			NULL		0	NULL	NULL	NULL	gw60_genesdev_15_23_3104_s_18	11731475	In the case of human adenoviruses, binding of the viral early region 1A (E1A) protein with either the retinoblastoma tumor suppressor family or p300/CBP/p400 histone acetyl transferases induces the activation, stabilization, and accumulation of p53 (Chiou and White 1997  ; Querido et al. 1997b  ; Samuelson and Lowe 1997  ).	transcription
73337	9	336378	7	NULL	NULL	0	NULL	E1A protein	GP		is					viral early region 1A protein	GP				NULL		0	NULL	NULL	NULL	gw60_genesdev_15_23_3104_s_18	11731475	In the case of human adenoviruses, binding of the viral early region 1A (E1A) protein with either the retinoblastoma tumor suppressor family or p300/CBP/p400 histone acetyl transferases induces the activation, stabilization, and accumulation of p53 (Chiou and White 1997  ; Querido et al. 1997b  ; Samuelson and Lowe 1997  ).	transcription
73338	10	336378	7	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_genesdev_15_23_3104_s_18	11731475	In the case of human adenoviruses, binding of the viral early region 1A (E1A) protein with either the retinoblastoma tumor suppressor family or p300/CBP/p400 histone acetyl transferases induces the activation, stabilization, and accumulation of p53 (Chiou and White 1997  ; Querido et al. 1997b  ; Samuelson and Lowe 1997  ).	transcription
73339	1	336379	7	NULL	NULL	0	NULL	CBP/p300	GP		acetylates					p53	GP				NULL		0	NULL	NULL	NULL	gw60_molcell_8_1_57_s_19	11511360	Acetylation of p53 by the histone acetyl transferases CBP/p300 and PCAF activates DNA binding in vitro and each HAT can coactivate p53-dependent transcription in transient expression experiments      (Gu and Roeder, 1997  ; Avantaggiati et al., 1997  ; Lill et al., 1997  ; Scolnick et al., 1997  ; Liu et al., 1999  ).	transcription
73340	2	336379	7	NULL	NULL	0	NULL	PCAF	GP		acetylates					p53	GP				NULL		0	NULL	NULL	NULL	gw60_molcell_8_1_57_s_19	11511360	Acetylation of p53 by the histone acetyl transferases CBP/p300 and PCAF activates DNA binding in vitro and each HAT can coactivate p53-dependent transcription in transient expression experiments      (Gu and Roeder, 1997  ; Avantaggiati et al., 1997  ; Lill et al., 1997  ; Scolnick et al., 1997  ; Liu et al., 1999  ).	transcription
73341	4	336379	7	NULL	NULL	NULL	NULL	statement 1	Process		activates					statement 3	Process				NULL		NULL	NULL	NULL	NULL	gw60_molcell_8_1_57_s_19	11511360	Acetylation of p53 by the histone acetyl transferases CBP/p300 and PCAF activates DNA binding in vitro and each HAT can coactivate p53-dependent transcription in transient expression experiments      (Gu and Roeder, 1997  ; Avantaggiati et al., 1997  ; Lill et al., 1997  ; Scolnick et al., 1997  ; Liu et al., 1999  ).	transcription
73342	3	336379	7	NULL	NULL	NULL	NULL	p53	GP		bind					DNA	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	gw60_molcell_8_1_57_s_19	11511360	Acetylation of p53 by the histone acetyl transferases CBP/p300 and PCAF activates DNA binding in vitro and each HAT can coactivate p53-dependent transcription in transient expression experiments      (Gu and Roeder, 1997  ; Avantaggiati et al., 1997  ; Lill et al., 1997  ; Scolnick et al., 1997  ; Liu et al., 1999  ).	transcription
73343	5	336379	7	NULL	NULL	0	NULL	statement 2	Process		activates					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_8_1_57_s_19	11511360	Acetylation of p53 by the histone acetyl transferases CBP/p300 and PCAF activates DNA binding in vitro and each HAT can coactivate p53-dependent transcription in transient expression experiments      (Gu and Roeder, 1997  ; Avantaggiati et al., 1997  ; Lill et al., 1997  ; Scolnick et al., 1997  ; Liu et al., 1999  ).	transcription
73344	6	336379	7	NULL	NULL	0	NULL	transcription	Process		depends on					p53	GP				NULL		0	NULL	NULL	NULL	gw60_molcell_8_1_57_s_19	11511360	Acetylation of p53 by the histone acetyl transferases CBP/p300 and PCAF activates DNA binding in vitro and each HAT can coactivate p53-dependent transcription in transient expression experiments      (Gu and Roeder, 1997  ; Avantaggiati et al., 1997  ; Lill et al., 1997  ; Scolnick et al., 1997  ; Liu et al., 1999  ).	transcription
73345	7	336379	7	NULL	NULL	0	NULL	HAT	GP		coactivate					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_8_1_57_s_19	11511360	Acetylation of p53 by the histone acetyl transferases CBP/p300 and PCAF activates DNA binding in vitro and each HAT can coactivate p53-dependent transcription in transient expression experiments      (Gu and Roeder, 1997  ; Avantaggiati et al., 1997  ; Lill et al., 1997  ; Scolnick et al., 1997  ; Liu et al., 1999  ).	transcription
73346	8	336379	7	NULL	NULL	0	NULL	CBP/p300	GP		is a type of					histone acetyl transferases	GP				NULL		0	NULL	NULL	NULL	gw60_molcell_8_1_57_s_19	11511360	Acetylation of p53 by the histone acetyl transferases CBP/p300 and PCAF activates DNA binding in vitro and each HAT can coactivate p53-dependent transcription in transient expression experiments      (Gu and Roeder, 1997  ; Avantaggiati et al., 1997  ; Lill et al., 1997  ; Scolnick et al., 1997  ; Liu et al., 1999  ).	transcription
73347	9	336379	7	NULL	NULL	0	NULL	PCAF	GP		is a type of					histone acetyl transferases	GP				NULL		0	NULL	NULL	NULL	gw60_molcell_8_1_57_s_19	11511360	Acetylation of p53 by the histone acetyl transferases CBP/p300 and PCAF activates DNA binding in vitro and each HAT can coactivate p53-dependent transcription in transient expression experiments      (Gu and Roeder, 1997  ; Avantaggiati et al., 1997  ; Lill et al., 1997  ; Scolnick et al., 1997  ; Liu et al., 1999  ).	transcription
73348	1	336380	7	NULL	NULL	NULL	NULL	staurosporine	Chemical		result in		effectively			apoptosis	Process				NULL	SH-SY5Y cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_18128_s_126	10364268	Indeed, treatment of SH-SY5Y cells with staurosporine,  N-acetyl-D- erythro-sphingosine, or menadione effectively resulted in apoptosis as demonstrated by DNA ladder assay (Fig.  2 A), and yet none of these paradigms induced nuclear accumulation of p53 under identical conditions (Fig.  2 B), confirming that their apoptotic effects are likely to involve p53-independent mechanisms.	transcription
73349	2	336380	7	NULL	NULL	0	NULL	N-acetyl-D- erythro-sphingosine	Chemical		result in		effectively			apoptosis	Process				NULL	SH-SY5Y cells	0	NULL	NULL	NULL	gw60_jbiolchem_274_25_18128_s_126	10364268	Indeed, treatment of SH-SY5Y cells with staurosporine,  N-acetyl-D- erythro-sphingosine, or menadione effectively resulted in apoptosis as demonstrated by DNA ladder assay (Fig.  2 A), and yet none of these paradigms induced nuclear accumulation of p53 under identical conditions (Fig.  2 B), confirming that their apoptotic effects are likely to involve p53-independent mechanisms.	transcription
73350	3	336380	7	NULL	NULL	NULL	NULL	menadione	Chemical		result in		effectively			apoptosis	Process				NULL	SH-SY5Y cells	NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_18128_s_126	10364268	Indeed, treatment of SH-SY5Y cells with staurosporine,  N-acetyl-D- erythro-sphingosine, or menadione effectively resulted in apoptosis as demonstrated by DNA ladder assay (Fig.  2 A), and yet none of these paradigms induced nuclear accumulation of p53 under identical conditions (Fig.  2 B), confirming that their apoptotic effects are likely to involve p53-independent mechanisms.	transcription
73351	7	336380	7	NULL	NULL	NULL	NULL	apoptotic effects	Process		involve					p53-independent mechanism	Process				NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_18128_s_126	10364268	Indeed, treatment of SH-SY5Y cells with staurosporine,  N-acetyl-D- erythro-sphingosine, or menadione effectively resulted in apoptosis as demonstrated by DNA ladder assay (Fig.  2 A), and yet none of these paradigms induced nuclear accumulation of p53 under identical conditions (Fig.  2 B), confirming that their apoptotic effects are likely to involve p53-independent mechanisms.	transcription
73352	4	336380	7	NULL	NULL	NULL	NULL	statement 1	Process		does not involve					p53	GP	nuclear accumulation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_18128_s_126	10364268	Indeed, treatment of SH-SY5Y cells with staurosporine,  N-acetyl-D- erythro-sphingosine, or menadione effectively resulted in apoptosis as demonstrated by DNA ladder assay (Fig.  2 A), and yet none of these paradigms induced nuclear accumulation of p53 under identical conditions (Fig.  2 B), confirming that their apoptotic effects are likely to involve p53-independent mechanisms.	transcription
73353	5	336380	7	NULL	NULL	NULL	NULL	statement 2	Process		does not involve					p53	GP	nuclear accumulation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_18128_s_126	10364268	Indeed, treatment of SH-SY5Y cells with staurosporine,  N-acetyl-D- erythro-sphingosine, or menadione effectively resulted in apoptosis as demonstrated by DNA ladder assay (Fig.  2 A), and yet none of these paradigms induced nuclear accumulation of p53 under identical conditions (Fig.  2 B), confirming that their apoptotic effects are likely to involve p53-independent mechanisms.	transcription
73354	6	336380	7	NULL	NULL	NULL	NULL	statement 3	Process		does not involve					p53	GP	nuclear accumulation of			NULL		NULL	NULL	NULL	NULL	gw60_jbiolchem_274_25_18128_s_126	10364268	Indeed, treatment of SH-SY5Y cells with staurosporine,  N-acetyl-D- erythro-sphingosine, or menadione effectively resulted in apoptosis as demonstrated by DNA ladder assay (Fig.  2 A), and yet none of these paradigms induced nuclear accumulation of p53 under identical conditions (Fig.  2 B), confirming that their apoptotic effects are likely to involve p53-independent mechanisms.	transcription
73355	8	336380	7	NULL	NULL	0	NULL	statement 4	Process		confirms					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_18128_s_126	10364268	Indeed, treatment of SH-SY5Y cells with staurosporine,  N-acetyl-D- erythro-sphingosine, or menadione effectively resulted in apoptosis as demonstrated by DNA ladder assay (Fig.  2 A), and yet none of these paradigms induced nuclear accumulation of p53 under identical conditions (Fig.  2 B), confirming that their apoptotic effects are likely to involve p53-independent mechanisms.	transcription
73356	9	336380	7	NULL	NULL	0	NULL	statement 5	Process		confirms					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_18128_s_126	10364268	Indeed, treatment of SH-SY5Y cells with staurosporine,  N-acetyl-D- erythro-sphingosine, or menadione effectively resulted in apoptosis as demonstrated by DNA ladder assay (Fig.  2 A), and yet none of these paradigms induced nuclear accumulation of p53 under identical conditions (Fig.  2 B), confirming that their apoptotic effects are likely to involve p53-independent mechanisms.	transcription
73357	10	336380	7	NULL	NULL	0	NULL	statement 6	Process		confirms					statement 7	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_25_18128_s_126	10364268	Indeed, treatment of SH-SY5Y cells with staurosporine,  N-acetyl-D- erythro-sphingosine, or menadione effectively resulted in apoptosis as demonstrated by DNA ladder assay (Fig.  2 A), and yet none of these paradigms induced nuclear accumulation of p53 under identical conditions (Fig.  2 B), confirming that their apoptotic effects are likely to involve p53-independent mechanisms.	transcription
73358	1	336381	7	NULL	NULL	0	NULL	PID	GP		interacts with		specifically			p53	GP				NULL	in vitro	0	NULL	NULL	NULL	gw60_nature_408_6810_377_s_13	11099047	PID specifically interacts with p53 both  in vitro and  in vivo, and its expression reduces significantly the steady-state levels of acetylated p53.	transcription
73359	2	336381	7	NULL	NULL	NULL	NULL	PID	GP		interacts with		specifically			p53	GP				NULL	in vivo	NULL	NULL	NULL	NULL	gw60_nature_408_6810_377_s_13	11099047	PID specifically interacts with p53 both  in vitro and  in vivo, and its expression reduces significantly the steady-state levels of acetylated p53.	transcription
73360	3	336381	7	NULL	NULL	0	NULL	statement 1	Process	expression of	reduces		significantly			p53	GP	acetylated			NULL		0	NULL	NULL	NULL	gw60_nature_408_6810_377_s_13	11099047	PID specifically interacts with p53 both  in vitro and  in vivo, and its expression reduces significantly the steady-state levels of acetylated p53.	transcription
73361	4	336381	7	NULL	NULL	0	NULL	statement 2	Process	expression of	reduces		significantly			p53	GP	acetylated			NULL		0	NULL	NULL	NULL	gw60_nature_408_6810_377_s_13	11099047	PID specifically interacts with p53 both  in vitro and  in vivo, and its expression reduces significantly the steady-state levels of acetylated p53.	transcription
73362	1	336382	7	NULL	NULL	0	NULL	p300	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23027_s_231	10438470	Recently, Gu and Roeder ( 59) reported that p53 is acetylated by p300, a known histone acetyltransferase and transcriptional coactivator that is physically associated with p53.	transcription
73363	2	336382	7	NULL	NULL	0	NULL	p300	GP		associate with		physically			p53	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23027_s_231	10438470	Recently, Gu and Roeder ( 59) reported that p53 is acetylated by p300, a known histone acetyltransferase and transcriptional coactivator that is physically associated with p53.	transcription
73364	3	336382	7	NULL	NULL	0	NULL	p300	GP		is a type of					histone acetyltransferase	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23027_s_231	10438470	Recently, Gu and Roeder ( 59) reported that p53 is acetylated by p300, a known histone acetyltransferase and transcriptional coactivator that is physically associated with p53.	transcription
73365	4	336382	7	NULL	NULL	0	NULL	p300	GP		is a type of					transcriptional coactivator	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_33_23027_s_231	10438470	Recently, Gu and Roeder ( 59) reported that p53 is acetylated by p300, a known histone acetyltransferase and transcriptional coactivator that is physically associated with p53.	transcription
73366	1	336383	7	NULL	NULL	0	NULL	p53	GP		interacts with					p300	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_276_42_11495913_s_5	11495913	Furthermore, interaction  of p53 with the transcriptional coactivator p300 was induced, and Lys(382)  of p53 was acetylated.	transcription
73367	2	336383	7	NULL	NULL	0	NULL	statement 1	Process		acetylate					p53	GP		Lys(382)		NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_276_42_11495913_s_5	11495913	Furthermore, interaction  of p53 with the transcriptional coactivator p300 was induced, and Lys(382)  of p53 was acetylated.	transcription
73368	3	336383	7	NULL	NULL	0	NULL	p300	GP		is a type of					transcriptional coactivator	GP				NULL		0	NULL	NULL	NULL	abs-batch0650-0679_j-biol-chem_276_42_11495913_s_5	11495913	Furthermore, interaction  of p53 with the transcriptional coactivator p300 was induced, and Lys(382)  of p53 was acetylated.	transcription
73369	1	336384	7	NULL	NULL	0	NULL	p53	GP	site-specific;;acetylation of	depends on					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_7_2782_s_29	16537920	Dornan et al. reported that site-specific acetylation of p53 was DNA dependent; deletion of the p53 proline repeat allows p53 to bind to  p21, but p53 was unable to be acetylated, indicating that proline-directed acetylation of p53 is a post-DNA binding event ( ,  ).	transcription
73370	2	336384	7	NULL	NULL	0	NULL	p53	GP		bind					p21	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_7_2782_s_29	16537920	Dornan et al. reported that site-specific acetylation of p53 was DNA dependent; deletion of the p53 proline repeat allows p53 to bind to  p21, but p53 was unable to be acetylated, indicating that proline-directed acetylation of p53 is a post-DNA binding event ( ,  ).	transcription
73371	3	336384	7	NULL	NULL	0	NULL	p53	GP	deletion of	allows			proline repeat		statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_7_2782_s_29	16537920	Dornan et al. reported that site-specific acetylation of p53 was DNA dependent; deletion of the p53 proline repeat allows p53 to bind to  p21, but p53 was unable to be acetylated, indicating that proline-directed acetylation of p53 is a post-DNA binding event ( ,  ).	transcription
73372	4	336384	7	NULL	NULL	0	NULL	p53	GP		unable to be					acetylated	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_7_2782_s_29	16537920	Dornan et al. reported that site-specific acetylation of p53 was DNA dependent; deletion of the p53 proline repeat allows p53 to bind to  p21, but p53 was unable to be acetylated, indicating that proline-directed acetylation of p53 is a post-DNA binding event ( ,  ).	transcription
73373	5	336384	7	NULL	NULL	0	NULL	proline	AminoAcid		directs					p53	GP	acetylation of			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_7_2782_s_29	16537920	Dornan et al. reported that site-specific acetylation of p53 was DNA dependent; deletion of the p53 proline repeat allows p53 to bind to  p21, but p53 was unable to be acetylated, indicating that proline-directed acetylation of p53 is a post-DNA binding event ( ,  ).	transcription
73374	6	336384	7	NULL	NULL	0	NULL	statement 5	Process		is a type of					post-DNA binding event	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_7_2782_s_29	16537920	Dornan et al. reported that site-specific acetylation of p53 was DNA dependent; deletion of the p53 proline repeat allows p53 to bind to  p21, but p53 was unable to be acetylated, indicating that proline-directed acetylation of p53 is a post-DNA binding event ( ,  ).	transcription
73375	7	336384	7	NULL	NULL	0	NULL	statement 4	Process		indicates					statement 6	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_7_2782_s_29	16537920	Dornan et al. reported that site-specific acetylation of p53 was DNA dependent; deletion of the p53 proline repeat allows p53 to bind to  p21, but p53 was unable to be acetylated, indicating that proline-directed acetylation of p53 is a post-DNA binding event ( ,  ).	transcription
73376	1	336385	7	NULL	NULL	NULL	NULL	antiacetylated p53 antibody	GP		bind					p53 protein	GP	crosslinked			NULL		NULL	NULL	NULL	NULL	gw70_pnas_101_8_2259_s_133	14982997	Interestingly, although the antiacetylated p53 antibody only immunoprecipitated a small fraction of the total crosslinked p53 protein ( Fig. 3 B, lane 8 vs. 7), the p53 bound to the p21 promoter was enriched about 3-fold in acetylated p53 relative to total p53 ( Fig. 3 C).	transcription
73377	2	336385	7	NULL	NULL	0	NULL	p53	GP		bind					p21	GP			promoter	NULL		0	NULL	NULL	NULL	gw70_pnas_101_8_2259_s_133	14982997	Interestingly, although the antiacetylated p53 antibody only immunoprecipitated a small fraction of the total crosslinked p53 protein ( Fig. 3 B, lane 8 vs. 7), the p53 bound to the p21 promoter was enriched about 3-fold in acetylated p53 relative to total p53 ( Fig. 3 C).	transcription
73378	1	336386	7	NULL	NULL	0	NULL	acetyl-CoA	Chemical		promotes					p53	GP	weak;;acetylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_15_13431_s_179	12499368	Using the basal p300-acetylation reaction where acetyl-CoA promotes weak p53 acetylation (Fig.  4 C,  lane 3 versus lane 2), experiments demonstrated a stimulation of p53 acetylation by p300 upon titration of an excess of consensus site oligonucleotide DNA ( pG DNA; Fig.  5 A,  lanes 5-8 versus lane 4).	transcription
73379	2	336386	7	NULL	NULL	0	NULL	p300	GP		stimulates					p53	GP	acetylation of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_278_15_13431_s_179	12499368	Using the basal p300-acetylation reaction where acetyl-CoA promotes weak p53 acetylation (Fig.  4 C,  lane 3 versus lane 2), experiments demonstrated a stimulation of p53 acetylation by p300 upon titration of an excess of consensus site oligonucleotide DNA ( pG DNA; Fig.  5 A,  lanes 5-8 versus lane 4).	transcription
73380	1	336387	7	NULL	NULL	0	NULL	histones	GP		substrate for					PCAF	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11303_s_13	11027331	Although histones are physiologically relevant substrates for PCAF, PCAF also acetylates transcriptional activators p53 ( 6,  7) and MyoD ( 8), as originally demonstrated by p300 acetylase ( 9), and stimulates DNA binding.	transcription
73381	2	336387	7	NULL	NULL	0	NULL	PCAF	GP		acetylates					p53	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11303_s_13	11027331	Although histones are physiologically relevant substrates for PCAF, PCAF also acetylates transcriptional activators p53 ( 6,  7) and MyoD ( 8), as originally demonstrated by p300 acetylase ( 9), and stimulates DNA binding.	transcription
73382	3	336387	7	NULL	NULL	0	NULL	PCAF	GP		acetylates					MyoD	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11303_s_13	11027331	Although histones are physiologically relevant substrates for PCAF, PCAF also acetylates transcriptional activators p53 ( 6,  7) and MyoD ( 8), as originally demonstrated by p300 acetylase ( 9), and stimulates DNA binding.	transcription
73383	4	336387	7	NULL	NULL	0	NULL	p53	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11303_s_13	11027331	Although histones are physiologically relevant substrates for PCAF, PCAF also acetylates transcriptional activators p53 ( 6,  7) and MyoD ( 8), as originally demonstrated by p300 acetylase ( 9), and stimulates DNA binding.	transcription
73384	5	336387	7	NULL	NULL	0	NULL	MyoD	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11303_s_13	11027331	Although histones are physiologically relevant substrates for PCAF, PCAF also acetylates transcriptional activators p53 ( 6,  7) and MyoD ( 8), as originally demonstrated by p300 acetylase ( 9), and stimulates DNA binding.	transcription
73385	6	336387	7	NULL	NULL	NULL	NULL	statement 2	Process		stimulate					statement 4	Process				NULL		NULL	NULL	NULL	NULL	gw60_pnas_97_21_11303_s_13	11027331	Although histones are physiologically relevant substrates for PCAF, PCAF also acetylates transcriptional activators p53 ( 6,  7) and MyoD ( 8), as originally demonstrated by p300 acetylase ( 9), and stimulates DNA binding.	transcription
73386	7	336387	7	NULL	NULL	0	NULL	statement 3	Process		stimulate					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11303_s_13	11027331	Although histones are physiologically relevant substrates for PCAF, PCAF also acetylates transcriptional activators p53 ( 6,  7) and MyoD ( 8), as originally demonstrated by p300 acetylase ( 9), and stimulates DNA binding.	transcription
73387	8	336387	7	NULL	NULL	0	NULL	p53	GP		is a type of					transcriptional activator	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11303_s_13	11027331	Although histones are physiologically relevant substrates for PCAF, PCAF also acetylates transcriptional activators p53 ( 6,  7) and MyoD ( 8), as originally demonstrated by p300 acetylase ( 9), and stimulates DNA binding.	transcription
73388	9	336387	7	NULL	NULL	0	NULL	MyoD	GP		is a type of					transcriptional coactivator	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_21_11303_s_13	11027331	Although histones are physiologically relevant substrates for PCAF, PCAF also acetylates transcriptional activators p53 ( 6,  7) and MyoD ( 8), as originally demonstrated by p300 acetylase ( 9), and stimulates DNA binding.	transcription
73389	1	336388	7	NULL	NULL	0	NULL	CBP/p300	GP		acetylates		directly			GATA-1	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7300_s_337	10982847	Moreover, CBP/p300 directly acetylates transcription factors such as GATA-1 ( 6) and p53 ( 21).	transcription
73390	2	336388	7	NULL	NULL	0	NULL	CBP/p300	GP		acetylates		directly			p53	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7300_s_337	10982847	Moreover, CBP/p300 directly acetylates transcription factors such as GATA-1 ( 6) and p53 ( 21).	transcription
73391	3	336388	7	NULL	NULL	0	NULL	GATA-1	GP		is a type of					transcription factor	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7300_s_337	10982847	Moreover, CBP/p300 directly acetylates transcription factors such as GATA-1 ( 6) and p53 ( 21).	transcription
73392	4	336388	7	NULL	NULL	0	NULL	p53	GP		is a type of					transcription factor	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_19_7300_s_337	10982847	Moreover, CBP/p300 directly acetylates transcription factors such as GATA-1 ( 6) and p53 ( 21).	transcription
73393	1	336389	7	NULL	NULL	0	NULL	p300	GP		acetylates					p53	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_23_12547_s_2	11070080	p300 acetylates and activates the tumor suppressor p53 after DNA damage.	transcription
73394	2	336389	7	NULL	NULL	0	NULL	statement 1	Process		activates					p53	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_23_12547_s_2	11070080	p300 acetylates and activates the tumor suppressor p53 after DNA damage.	transcription
73395	3	336389	7	NULL	NULL	0	NULL	statement 2	Process		occur after					DNA damage	Process				NULL		0	NULL	NULL	NULL	gw60_pnas_97_23_12547_s_2	11070080	p300 acetylates and activates the tumor suppressor p53 after DNA damage.	transcription
73396	4	336389	7	NULL	NULL	0	NULL	p53	GP		is a type of					tumor suppressor	GP				NULL		0	NULL	NULL	NULL	gw60_pnas_97_23_12547_s_2	11070080	p300 acetylates and activates the tumor suppressor p53 after DNA damage.	transcription
73397	1	336390	7	NULL	NULL	0	NULL	p300	GP		acetylates					p53	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_26_24315_s_77	15851483	Expression of MLL Fusions Decreases p53 Acetylation by p300 in Response to Ionizing Radiation -- p300 is an important co-activator of p53 transcriptional activity that acetylates several critical lysine residues on the p53 C terminus ( ).	transcription
73398	2	336390	7	NULL	NULL	0	NULL	MLL Fusions	GP	expression of	decrease					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_26_24315_s_77	15851483	Expression of MLL Fusions Decreases p53 Acetylation by p300 in Response to Ionizing Radiation -- p300 is an important co-activator of p53 transcriptional activity that acetylates several critical lysine residues on the p53 C terminus ( ).	transcription
73399	3	336390	7	NULL	NULL	0	NULL	statement 2	Process		in response to					ionizing radiation	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_26_24315_s_77	15851483	Expression of MLL Fusions Decreases p53 Acetylation by p300 in Response to Ionizing Radiation -- p300 is an important co-activator of p53 transcriptional activity that acetylates several critical lysine residues on the p53 C terminus ( ).	transcription
73400	4	336390	7	NULL	NULL	0	NULL	p300	GP		coactivator of					p53	GP	transcriptional activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_26_24315_s_77	15851483	Expression of MLL Fusions Decreases p53 Acetylation by p300 in Response to Ionizing Radiation -- p300 is an important co-activator of p53 transcriptional activity that acetylates several critical lysine residues on the p53 C terminus ( ).	transcription
73401	5	336390	7	NULL	NULL	0	NULL	p300	GP		acetylates					p53	GP		lysine residues on C terminus		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_280_26_24315_s_77	15851483	Expression of MLL Fusions Decreases p53 Acetylation by p300 in Response to Ionizing Radiation -- p300 is an important co-activator of p53 transcriptional activity that acetylates several critical lysine residues on the p53 C terminus ( ).	transcription
73402	1	336391	7	NULL	NULL	0	NULL	p53	GP	acetylated	bind					TRRAP	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_28_25401_s_250	12738767	In this context, Barlev  et al.  ( ) showed that acetylated  p53 binds more tightly to the transcriptional cofactors TRRAP and CBP than  nonacetylated p53, although acetylated and nonacetylated p53 bind to the p21  promoter in the same manner.	transcription
73403	2	336391	7	NULL	NULL	0	NULL	p53	GP	acetylated	bind					CBP	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_28_25401_s_250	12738767	In this context, Barlev  et al.  ( ) showed that acetylated  p53 binds more tightly to the transcriptional cofactors TRRAP and CBP than  nonacetylated p53, although acetylated and nonacetylated p53 bind to the p21  promoter in the same manner.	transcription
73404	3	336391	7	NULL	NULL	0	NULL	p53	GP	nonacetylated	bind					TRRAP	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_28_25401_s_250	12738767	In this context, Barlev  et al.  ( ) showed that acetylated  p53 binds more tightly to the transcriptional cofactors TRRAP and CBP than  nonacetylated p53, although acetylated and nonacetylated p53 bind to the p21  promoter in the same manner.	transcription
73405	4	336391	7	NULL	NULL	0	NULL	p53	GP	nonacetylated	bind					CBP	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_28_25401_s_250	12738767	In this context, Barlev  et al.  ( ) showed that acetylated  p53 binds more tightly to the transcriptional cofactors TRRAP and CBP than  nonacetylated p53, although acetylated and nonacetylated p53 bind to the p21  promoter in the same manner.	transcription
73406	5	336391	7	NULL	NULL	0	NULL	statement 1	Process	binding of	is tighter than					statement 3	Process	binding of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_28_25401_s_250	12738767	In this context, Barlev  et al.  ( ) showed that acetylated  p53 binds more tightly to the transcriptional cofactors TRRAP and CBP than  nonacetylated p53, although acetylated and nonacetylated p53 bind to the p21  promoter in the same manner.	transcription
73407	6	336391	7	NULL	NULL	0	NULL	statement 2	Process	binding of	is tighter than					statement 4	Process	binding of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_28_25401_s_250	12738767	In this context, Barlev  et al.  ( ) showed that acetylated  p53 binds more tightly to the transcriptional cofactors TRRAP and CBP than  nonacetylated p53, although acetylated and nonacetylated p53 bind to the p21  promoter in the same manner.	transcription
73408	7	336391	7	NULL	NULL	NULL	NULL	p53	GP	acetylated	bind					p21	GP			promoter	NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_278_28_25401_s_250	12738767	In this context, Barlev  et al.  ( ) showed that acetylated  p53 binds more tightly to the transcriptional cofactors TRRAP and CBP than  nonacetylated p53, although acetylated and nonacetylated p53 bind to the p21  promoter in the same manner.	transcription
73409	8	336391	7	NULL	NULL	0	NULL	p53	GP	nonacetylated	bind					p21	GP			promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_28_25401_s_250	12738767	In this context, Barlev  et al.  ( ) showed that acetylated  p53 binds more tightly to the transcriptional cofactors TRRAP and CBP than  nonacetylated p53, although acetylated and nonacetylated p53 bind to the p21  promoter in the same manner.	transcription
73410	1	336392	7	NULL	NULL	NULL	NULL	CBP		mutant;;purified	is defective in			acetylase domain;;L160K/C161L		acetyltransferase activity	Process				NULL		NULL	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_1_118_s_67	12147236	As purified CBP acetylase domain that contains point mutations (L160K/C161L) and is defective in acetyltransferase activity stimulated p53 DNA binding activity as well as the wild-type acetyltransferase domain (data not shown), we examined the effect of these domains on p53 DNA binding.	transcription
73411	2	336392	7	NULL	NULL	0	NULL	p53	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_1_118_s_67	12147236	As purified CBP acetylase domain that contains point mutations (L160K/C161L) and is defective in acetyltransferase activity stimulated p53 DNA binding activity as well as the wild-type acetyltransferase domain (data not shown), we examined the effect of these domains on p53 DNA binding.	transcription
73412	3	336392	7	NULL	NULL	0	NULL	statement 1	Process		stimulate					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_1_118_s_67	12147236	As purified CBP acetylase domain that contains point mutations (L160K/C161L) and is defective in acetyltransferase activity stimulated p53 DNA binding activity as well as the wild-type acetyltransferase domain (data not shown), we examined the effect of these domains on p53 DNA binding.	transcription
73413	4	336392	7	NULL	NULL	0	NULL	CBP	GP	wild-type	stimulate			acetyltransferase domain		statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_biochmbiophyrescomm_296_1_118_s_67	12147236	As purified CBP acetylase domain that contains point mutations (L160K/C161L) and is defective in acetyltransferase activity stimulated p53 DNA binding activity as well as the wild-type acetyltransferase domain (data not shown), we examined the effect of these domains on p53 DNA binding.	transcription
73414	1	336393	7	NULL	NULL	0	NULL	UV irradiation	PhysicalPhenomenon		acetylates					p53	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_27_24594_s_181	12716906	This pattern of changes  in p53 acetylation is different from that induced by UV irradiation, which  acetylates p53 at all three sites in ECs  ( Fig. 1 B).	transcription
73415	2	336393	7	NULL	NULL	0	NULL	statement 1	Process		occur in					ECs	Cell				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_27_24594_s_181	12716906	This pattern of changes  in p53 acetylation is different from that induced by UV irradiation, which  acetylates p53 at all three sites in ECs  ( Fig. 1 B).	transcription
73416	1	336394	7	NULL	NULL	0	NULL	p53	GP		interacts with		directly			p300	GP				NULL		0	NULL	NULL	NULL	gw60_molcell_10_5_1213_s_205	12453427	p53 interacts directly with p300 that acetylates two specific lysine residues within p53 (lysine residues 373 and 382)  (Gu and Roeder, 1997  ).	transcription
73417	2	336394	7	NULL	NULL	0	NULL	p300	GP		acetylates					p53	GP		lysine residues 373 and 382		NULL		0	NULL	NULL	NULL	gw60_molcell_10_5_1213_s_205	12453427	p53 interacts directly with p300 that acetylates two specific lysine residues within p53 (lysine residues 373 and 382)  (Gu and Roeder, 1997  ).	transcription
73418	1	336395	7	NULL	NULL	0	NULL	PCAF	GP		acetylates					p53	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1202_s_99	9891054	[[            Since PCAF acetylates p53 ]] within a specific domain, we wanted to determine whether a stable interaction could be detected between PCAF and p53.	transcription
73419	1	336396	7	NULL	NULL	0	NULL	p53	GP		associate with					U1 snRNA gene	GP	endogenous		promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3247_s_178	15798209	Together, these data indicate that p53 associates with the endogenous U1 and U2 snRNA gene promoters prior to genotypic stress and UV light stimulates p53 association with these promoters, although the apparent proportion of p53 that is acetylated decreases.	transcription
73420	2	336396	7	NULL	NULL	0	NULL	p53	GP		associate with					U2 snRNA gene	GP	endogenous		promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3247_s_178	15798209	Together, these data indicate that p53 associates with the endogenous U1 and U2 snRNA gene promoters prior to genotypic stress and UV light stimulates p53 association with these promoters, although the apparent proportion of p53 that is acetylated decreases.	transcription
73421	3	336396	7	NULL	NULL	0	NULL	statement 1	Process		prior to					genotypic stress	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3247_s_178	15798209	Together, these data indicate that p53 associates with the endogenous U1 and U2 snRNA gene promoters prior to genotypic stress and UV light stimulates p53 association with these promoters, although the apparent proportion of p53 that is acetylated decreases.	transcription
73422	4	336396	7	NULL	NULL	0	NULL	statement 2	Process		prior to					genotypic stress	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3247_s_178	15798209	Together, these data indicate that p53 associates with the endogenous U1 and U2 snRNA gene promoters prior to genotypic stress and UV light stimulates p53 association with these promoters, although the apparent proportion of p53 that is acetylated decreases.	transcription
73423	5	336396	7	NULL	NULL	0	NULL	UVlight	PhysicalPhenomenon		stimulate					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3247_s_178	15798209	Together, these data indicate that p53 associates with the endogenous U1 and U2 snRNA gene promoters prior to genotypic stress and UV light stimulates p53 association with these promoters, although the apparent proportion of p53 that is acetylated decreases.	transcription
73424	6	336396	7	NULL	NULL	0	NULL	UVlight	PhysicalPhenomenon		stimulate					statement 2	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3247_s_178	15798209	Together, these data indicate that p53 associates with the endogenous U1 and U2 snRNA gene promoters prior to genotypic stress and UV light stimulates p53 association with these promoters, although the apparent proportion of p53 that is acetylated decreases.	transcription
73425	7	336396	7	NULL	NULL	0	NULL	statement 1	Process		decrease					p53	GP	acetylated			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3247_s_178	15798209	Together, these data indicate that p53 associates with the endogenous U1 and U2 snRNA gene promoters prior to genotypic stress and UV light stimulates p53 association with these promoters, although the apparent proportion of p53 that is acetylated decreases.	transcription
73426	8	336396	7	NULL	NULL	0	NULL	statement 2	Process		decrease					p53	GP	acetylated			NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_8_3247_s_178	15798209	Together, these data indicate that p53 associates with the endogenous U1 and U2 snRNA gene promoters prior to genotypic stress and UV light stimulates p53 association with these promoters, although the apparent proportion of p53 that is acetylated decreases.	transcription
73427	1	336397	7	NULL	NULL	0	NULL	HDM2	GP		inhibit					p53	GP	acetylation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_16943_s_228	16624812	In contrast, HDM2 inhibits the acetylation of p53, and under-acetylated p53 displays altered cell cycle regulation, reduced apoptosis, and altered promoter selectivity without changing binding of p53 to the promoter regions that were examined.	transcription
73428	2	336397	7	NULL	NULL	0	NULL	p53	GP	under-acetylated	display					cell cycle regulation	Process	altered			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_16943_s_228	16624812	In contrast, HDM2 inhibits the acetylation of p53, and under-acetylated p53 displays altered cell cycle regulation, reduced apoptosis, and altered promoter selectivity without changing binding of p53 to the promoter regions that were examined.	transcription
73429	3	336397	7	NULL	NULL	0	NULL	p53	GP	under-acetylated	display					apoptosis	Process	reduced			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_16943_s_228	16624812	In contrast, HDM2 inhibits the acetylation of p53, and under-acetylated p53 displays altered cell cycle regulation, reduced apoptosis, and altered promoter selectivity without changing binding of p53 to the promoter regions that were examined.	transcription
73430	4	336397	7	NULL	NULL	0	NULL	p53	GP	under-acetylated	display							altered selectivity of		promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_16943_s_228	16624812	In contrast, HDM2 inhibits the acetylation of p53, and under-acetylated p53 displays altered cell cycle regulation, reduced apoptosis, and altered promoter selectivity without changing binding of p53 to the promoter regions that were examined.	transcription
73431	5	336397	7	NULL	NULL	0	NULL	p53	GP		bind									promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_16943_s_228	16624812	In contrast, HDM2 inhibits the acetylation of p53, and under-acetylated p53 displays altered cell cycle regulation, reduced apoptosis, and altered promoter selectivity without changing binding of p53 to the promoter regions that were examined.	transcription
73432	6	336397	7	NULL	NULL	0	NULL	statement 2	Process		without changing					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_16943_s_228	16624812	In contrast, HDM2 inhibits the acetylation of p53, and under-acetylated p53 displays altered cell cycle regulation, reduced apoptosis, and altered promoter selectivity without changing binding of p53 to the promoter regions that were examined.	transcription
73433	7	336397	7	NULL	NULL	0	NULL	statement 3	Process		without changing					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_16943_s_228	16624812	In contrast, HDM2 inhibits the acetylation of p53, and under-acetylated p53 displays altered cell cycle regulation, reduced apoptosis, and altered promoter selectivity without changing binding of p53 to the promoter regions that were examined.	transcription
73434	8	336397	7	NULL	NULL	0	NULL	statement 4	Process		without changing					statement 5	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_25_16943_s_228	16624812	In contrast, HDM2 inhibits the acetylation of p53, and under-acetylated p53 displays altered cell cycle regulation, reduced apoptosis, and altered promoter selectivity without changing binding of p53 to the promoter regions that were examined.	transcription
73435	1	336398	7	NULL	NULL	0	NULL	p53	GP		recruit					p300/CBP	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_19_17557_s_40	12609999	Therefore, our data suggest that the amount of p300/CBP recruited by p53 and the extent of acetylated histones bound to the proximal promoter can in part explain the differential transcriptional activity among wild-type p53 and various p53 mutants.	transcription
73436	2	336398	7	NULL	NULL	0	NULL	histones	GP	acetylated	bind									proximal promoter	NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_19_17557_s_40	12609999	Therefore, our data suggest that the amount of p300/CBP recruited by p53 and the extent of acetylated histones bound to the proximal promoter can in part explain the differential transcriptional activity among wild-type p53 and various p53 mutants.	transcription
73437	1	336399	7	NULL	NULL	0	NULL	SIRT1 	GP		deacetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_100_19_10794_s_155	12960381	However, p53 was still clearly more acetylated in SIRT1deltaex4/deltaex4, than in SIRT1+/+ and SIRT1+/deltaex4 MEFs ( Fig. 3 B), providing evidence that SIRT1 deacetylation of p53 is not fully redundant with HDAC-mediated p53 deacetylation.	transcription
73438	2	336399	7	NULL	NULL	0	NULL	HDAC	GP		mediate					p53	GP	deacetylation of			NULL		0	NULL	NULL	NULL	gw70_pnas_100_19_10794_s_155	12960381	However, p53 was still clearly more acetylated in SIRT1deltaex4/deltaex4, than in SIRT1+/+ and SIRT1+/deltaex4 MEFs ( Fig. 3 B), providing evidence that SIRT1 deacetylation of p53 is not fully redundant with HDAC-mediated p53 deacetylation.	transcription
73439	3	336399	7	NULL	NULL	0	NULL	p53	GP	acetylation of	occur in					SIRT1deltaex4/deltaex4 MEF	Cell				NULL		0	NULL	NULL	NULL	gw70_pnas_100_19_10794_s_155	12960381	However, p53 was still clearly more acetylated in SIRT1deltaex4/deltaex4, than in SIRT1+/+ and SIRT1+/deltaex4 MEFs ( Fig. 3 B), providing evidence that SIRT1 deacetylation of p53 is not fully redundant with HDAC-mediated p53 deacetylation.	transcription
73440	4	336399	7	NULL	NULL	0	NULL	p53	GP	acetylation of	occur in					SIRT1+/+ MEF	Cell				NULL		0	NULL	NULL	NULL	gw70_pnas_100_19_10794_s_155	12960381	However, p53 was still clearly more acetylated in SIRT1deltaex4/deltaex4, than in SIRT1+/+ and SIRT1+/deltaex4 MEFs ( Fig. 3 B), providing evidence that SIRT1 deacetylation of p53 is not fully redundant with HDAC-mediated p53 deacetylation.	transcription
73441	5	336399	7	NULL	NULL	NULL	NULL	p53	GP	acetylation of	occur in					SIRT1+/deltaex4 MEF	Cell				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_19_10794_s_155	12960381	However, p53 was still clearly more acetylated in SIRT1deltaex4/deltaex4, than in SIRT1+/+ and SIRT1+/deltaex4 MEFs ( Fig. 3 B), providing evidence that SIRT1 deacetylation of p53 is not fully redundant with HDAC-mediated p53 deacetylation.	transcription
73442	6	336399	7	NULL	NULL	NULL	NULL	statement 3	Process	acetylation of	is more than					statement 4	Process	acetylation of			NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_19_10794_s_155	12960381	However, p53 was still clearly more acetylated in SIRT1deltaex4/deltaex4, than in SIRT1+/+ and SIRT1+/deltaex4 MEFs ( Fig. 3 B), providing evidence that SIRT1 deacetylation of p53 is not fully redundant with HDAC-mediated p53 deacetylation.	transcription
73443	7	336399	7	NULL	NULL	0	NULL	statement 3	Process	acetylation of	is more than					statement 5	Process	acetylation of			NULL		0	NULL	NULL	NULL	gw70_pnas_100_19_10794_s_155	12960381	However, p53 was still clearly more acetylated in SIRT1deltaex4/deltaex4, than in SIRT1+/+ and SIRT1+/deltaex4 MEFs ( Fig. 3 B), providing evidence that SIRT1 deacetylation of p53 is not fully redundant with HDAC-mediated p53 deacetylation.	transcription
73444	8	336399	7	NULL	NULL	NULL	NULL	statement 1	Process		 not redundant with		fully			statement 2	Process				NULL		NULL	NULL	NULL	NULL	gw70_pnas_100_19_10794_s_155	12960381	However, p53 was still clearly more acetylated in SIRT1deltaex4/deltaex4, than in SIRT1+/+ and SIRT1+/deltaex4 MEFs ( Fig. 3 B), providing evidence that SIRT1 deacetylation of p53 is not fully redundant with HDAC-mediated p53 deacetylation.	transcription
73445	1	336400	7	NULL	NULL	NULL	NULL	p300	GP		acetylate					p53	GP		C terminus		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_21_17_5979_s_317	11486036	This finding is reminiscent of acetylation of p53 by p300, in which the N terminus of p53 interacts with CBP ( 19,  41) while the region acetylated by p300 is at the C terminus of p53 ( 18).	transcription
73446	2	336400	7	NULL	NULL	0	NULL	p53	GP		interacts with			N terminus		CBP	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_17_5979_s_317	11486036	This finding is reminiscent of acetylation of p53 by p300, in which the N terminus of p53 interacts with CBP ( 19,  41) while the region acetylated by p300 is at the C terminus of p53 ( 18).	transcription
73447	1	336401	7	NULL	NULL	0	NULL	p300	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_4	10891493	It was shown recently that p53 is acetylated by transcriptional coactivators p300, CREB bidning protein (CBP), and PCAF and that acetylation of p53 by these proteins enhances p53 sequence-specific DNA binding.	transcription
73448	2	336401	7	NULL	NULL	0	NULL	CBP	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_4	10891493	It was shown recently that p53 is acetylated by transcriptional coactivators p300, CREB bidning protein (CBP), and PCAF and that acetylation of p53 by these proteins enhances p53 sequence-specific DNA binding.	transcription
73449	3	336401	7	NULL	NULL	0	NULL	PCAF	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_4	10891493	It was shown recently that p53 is acetylated by transcriptional coactivators p300, CREB bidning protein (CBP), and PCAF and that acetylation of p53 by these proteins enhances p53 sequence-specific DNA binding.	transcription
73450	4	336401	7	NULL	NULL	NULL	NULL	p53	GP		bind		sequence-specific			DNA	NucleicAcid				NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_4	10891493	It was shown recently that p53 is acetylated by transcriptional coactivators p300, CREB bidning protein (CBP), and PCAF and that acetylation of p53 by these proteins enhances p53 sequence-specific DNA binding.	transcription
73451	5	336401	7	NULL	NULL	0	NULL	statement 1	Process		enhance					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_4	10891493	It was shown recently that p53 is acetylated by transcriptional coactivators p300, CREB bidning protein (CBP), and PCAF and that acetylation of p53 by these proteins enhances p53 sequence-specific DNA binding.	transcription
73452	6	336401	7	NULL	NULL	0	NULL	statement 2	Process		enhance					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_4	10891493	It was shown recently that p53 is acetylated by transcriptional coactivators p300, CREB bidning protein (CBP), and PCAF and that acetylation of p53 by these proteins enhances p53 sequence-specific DNA binding.	transcription
73453	7	336401	7	NULL	NULL	0	NULL	statement 3	Process		enhance					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_4	10891493	It was shown recently that p53 is acetylated by transcriptional coactivators p300, CREB bidning protein (CBP), and PCAF and that acetylation of p53 by these proteins enhances p53 sequence-specific DNA binding.	transcription
73454	8	336401	7	NULL	NULL	0	NULL	CBP	GP		is					CREB bidning protein	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_4	10891493	It was shown recently that p53 is acetylated by transcriptional coactivators p300, CREB bidning protein (CBP), and PCAF and that acetylation of p53 by these proteins enhances p53 sequence-specific DNA binding.	transcription
73455	9	336401	7	NULL	NULL	0	NULL	p300	GP		is a type of					transcriptional coactivator	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_4	10891493	It was shown recently that p53 is acetylated by transcriptional coactivators p300, CREB bidning protein (CBP), and PCAF and that acetylation of p53 by these proteins enhances p53 sequence-specific DNA binding.	transcription
73456	10	336401	7	NULL	NULL	0	NULL	CBP	GP		is a type of					transcriptional coactivator	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_4	10891493	It was shown recently that p53 is acetylated by transcriptional coactivators p300, CREB bidning protein (CBP), and PCAF and that acetylation of p53 by these proteins enhances p53 sequence-specific DNA binding.	transcription
73457	11	336401	7	NULL	NULL	0	NULL	PCAF	GP		is a type of					transcriptional coactivator	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_4	10891493	It was shown recently that p53 is acetylated by transcriptional coactivators p300, CREB bidning protein (CBP), and PCAF and that acetylation of p53 by these proteins enhances p53 sequence-specific DNA binding.	transcription
73458	1	336402	7	NULL	NULL	0	NULL	ATM	GP		detect					genotoxic stress	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1552_2_47_s_178	11825686	So-called stress kinases (e.g. ATM, ATR, Chk2) which detect genotoxic stress and initiate signal transduction are in vivo kinases for specific p53 serine residues, while the histone acetyltransferases p300/CBP and PCAF (which at the same time are transcriptional coactivators) acetylate p53.	transcription
73459	2	336402	7	NULL	NULL	0	NULL	ATR	GP		detect					genotoxic stress	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1552_2_47_s_178	11825686	So-called stress kinases (e.g. ATM, ATR, Chk2) which detect genotoxic stress and initiate signal transduction are in vivo kinases for specific p53 serine residues, while the histone acetyltransferases p300/CBP and PCAF (which at the same time are transcriptional coactivators) acetylate p53.	transcription
73460	3	336402	7	NULL	NULL	0	NULL	Chk2	GP		detect					genotoxic stress	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1552_2_47_s_178	11825686	So-called stress kinases (e.g. ATM, ATR, Chk2) which detect genotoxic stress and initiate signal transduction are in vivo kinases for specific p53 serine residues, while the histone acetyltransferases p300/CBP and PCAF (which at the same time are transcriptional coactivators) acetylate p53.	transcription
73461	4	336402	7	NULL	NULL	0	NULL	statement 1	Process		initiate					signal transduction	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1552_2_47_s_178	11825686	So-called stress kinases (e.g. ATM, ATR, Chk2) which detect genotoxic stress and initiate signal transduction are in vivo kinases for specific p53 serine residues, while the histone acetyltransferases p300/CBP and PCAF (which at the same time are transcriptional coactivators) acetylate p53.	transcription
73462	5	336402	7	NULL	NULL	0	NULL	statement 2	Process		initiate					signal transduction	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1552_2_47_s_178	11825686	So-called stress kinases (e.g. ATM, ATR, Chk2) which detect genotoxic stress and initiate signal transduction are in vivo kinases for specific p53 serine residues, while the histone acetyltransferases p300/CBP and PCAF (which at the same time are transcriptional coactivators) acetylate p53.	transcription
73463	6	336402	7	NULL	NULL	0	NULL	statement 3	Process		initiate					signal transduction	Process				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1552_2_47_s_178	11825686	So-called stress kinases (e.g. ATM, ATR, Chk2) which detect genotoxic stress and initiate signal transduction are in vivo kinases for specific p53 serine residues, while the histone acetyltransferases p300/CBP and PCAF (which at the same time are transcriptional coactivators) acetylate p53.	transcription
73464	7	336402	7	NULL	NULL	NULL	NULL	ATM	GP		kinase for					p53	GP		serine residue		NULL	in vivo	NULL	NULL	NULL	NULL	gw60_biochimbiophysacta_1552_2_47_s_178	11825686	So-called stress kinases (e.g. ATM, ATR, Chk2) which detect genotoxic stress and initiate signal transduction are in vivo kinases for specific p53 serine residues, while the histone acetyltransferases p300/CBP and PCAF (which at the same time are transcriptional coactivators) acetylate p53.	transcription
73465	8	336402	7	NULL	NULL	0	NULL	ATR	GP		kinase for					p53	GP		serine residue		NULL	in vivo	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1552_2_47_s_178	11825686	So-called stress kinases (e.g. ATM, ATR, Chk2) which detect genotoxic stress and initiate signal transduction are in vivo kinases for specific p53 serine residues, while the histone acetyltransferases p300/CBP and PCAF (which at the same time are transcriptional coactivators) acetylate p53.	transcription
73466	9	336402	7	NULL	NULL	0	NULL	Chk2	GP		kinase for					p53	GP		serine residue		NULL	in vivo	0	NULL	NULL	NULL	gw60_biochimbiophysacta_1552_2_47_s_178	11825686	So-called stress kinases (e.g. ATM, ATR, Chk2) which detect genotoxic stress and initiate signal transduction are in vivo kinases for specific p53 serine residues, while the histone acetyltransferases p300/CBP and PCAF (which at the same time are transcriptional coactivators) acetylate p53.	transcription
73467	10	336402	7	NULL	NULL	0	NULL	p300/CBP	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1552_2_47_s_178	11825686	So-called stress kinases (e.g. ATM, ATR, Chk2) which detect genotoxic stress and initiate signal transduction are in vivo kinases for specific p53 serine residues, while the histone acetyltransferases p300/CBP and PCAF (which at the same time are transcriptional coactivators) acetylate p53.	transcription
73468	11	336402	7	NULL	NULL	0	NULL	PCAF	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1552_2_47_s_178	11825686	So-called stress kinases (e.g. ATM, ATR, Chk2) which detect genotoxic stress and initiate signal transduction are in vivo kinases for specific p53 serine residues, while the histone acetyltransferases p300/CBP and PCAF (which at the same time are transcriptional coactivators) acetylate p53.	transcription
73469	12	336402	7	NULL	NULL	0	NULL	p300/CBP	GP		is a type of					histone acetyl transferases	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1552_2_47_s_178	11825686	So-called stress kinases (e.g. ATM, ATR, Chk2) which detect genotoxic stress and initiate signal transduction are in vivo kinases for specific p53 serine residues, while the histone acetyltransferases p300/CBP and PCAF (which at the same time are transcriptional coactivators) acetylate p53.	transcription
73470	13	336402	7	NULL	NULL	0	NULL	PCAF	GP		is a type of					histone acetyl transferases	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1552_2_47_s_178	11825686	So-called stress kinases (e.g. ATM, ATR, Chk2) which detect genotoxic stress and initiate signal transduction are in vivo kinases for specific p53 serine residues, while the histone acetyltransferases p300/CBP and PCAF (which at the same time are transcriptional coactivators) acetylate p53.	transcription
73471	14	336402	7	NULL	NULL	0	NULL	ATM	GP		is a type of					stress kinases	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1552_2_47_s_178	11825686	So-called stress kinases (e.g. ATM, ATR, Chk2) which detect genotoxic stress and initiate signal transduction are in vivo kinases for specific p53 serine residues, while the histone acetyltransferases p300/CBP and PCAF (which at the same time are transcriptional coactivators) acetylate p53.	transcription
73472	15	336402	7	NULL	NULL	0	NULL	ATR	GP		is a type of					stress kinases	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1552_2_47_s_178	11825686	So-called stress kinases (e.g. ATM, ATR, Chk2) which detect genotoxic stress and initiate signal transduction are in vivo kinases for specific p53 serine residues, while the histone acetyltransferases p300/CBP and PCAF (which at the same time are transcriptional coactivators) acetylate p53.	transcription
73473	16	336402	7	NULL	NULL	0	NULL	Chk2	GP		is a type of					stress kinases	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1552_2_47_s_178	11825686	So-called stress kinases (e.g. ATM, ATR, Chk2) which detect genotoxic stress and initiate signal transduction are in vivo kinases for specific p53 serine residues, while the histone acetyltransferases p300/CBP and PCAF (which at the same time are transcriptional coactivators) acetylate p53.	transcription
73474	17	336402	7	NULL	NULL	0	NULL	p300/CBP	GP		is a type of					transcriptional coactivators	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1552_2_47_s_178	11825686	So-called stress kinases (e.g. ATM, ATR, Chk2) which detect genotoxic stress and initiate signal transduction are in vivo kinases for specific p53 serine residues, while the histone acetyltransferases p300/CBP and PCAF (which at the same time are transcriptional coactivators) acetylate p53.	transcription
73475	18	336402	7	NULL	NULL	0	NULL	PCAF	GP		is a type of					transcriptional coactivator	GP				NULL		0	NULL	NULL	NULL	gw60_biochimbiophysacta_1552_2_47_s_178	11825686	So-called stress kinases (e.g. ATM, ATR, Chk2) which detect genotoxic stress and initiate signal transduction are in vivo kinases for specific p53 serine residues, while the histone acetyltransferases p300/CBP and PCAF (which at the same time are transcriptional coactivators) acetylate p53.	transcription
73476	1	336403	7	NULL	NULL	0	NULL	p300	GP		bind					p21	GP			promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_7_2782_s_225	16537920	p53 acetylated at K373/382 is required for recruitment of p300 to the  p21 promoter.	transcription
73477	2	336403	7	NULL	NULL	0	NULL	p53	GP	acetylated	required for			K373/382		statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_26_7_2782_s_225	16537920	p53 acetylated at K373/382 is required for recruitment of p300 to the  p21 promoter.	transcription
73478	1	336404	7	NULL	NULL	NULL	NULL	p300/CREB-binding protein	GP		acetylate					p53	GP		lysine		NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_3_1394_s_3	16291740	Upon p53 activation, however, these lysines become acetylated by p300/CREB-binding protein.	transcription
73479	2	336404	7	NULL	NULL	0	NULL	statement 1	Process		occur upon					p53	GP	activation of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1394_s_3	16291740	Upon p53 activation, however, these lysines become acetylated by p300/CREB-binding protein.	transcription
73480	1	336405	7	NULL	NULL	NULL	NULL	p300	GP		acetylate					p53	GP		Lys-373;;Lys-382		NULL		NULL	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_182	10891493	p53 is acetylated by transcriptional coactivator p300 at Lys-373 and Lys-382 and by PCAF at Lys-320.	transcription
73481	2	336405	7	NULL	NULL	0	NULL	PCAF	GP		acetylate					p53	GP		Lys-320		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_182	10891493	p53 is acetylated by transcriptional coactivator p300 at Lys-373 and Lys-382 and by PCAF at Lys-320.	transcription
73482	3	336405	7	NULL	NULL	0	NULL	p300	GP		is a type of					transcriptional coactivator	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_20_15_5540_s_182	10891493	p53 is acetylated by transcriptional coactivator p300 at Lys-373 and Lys-382 and by PCAF at Lys-320.	transcription
73483	1	336406	7	NULL	NULL	NULL	NULL	p53	GP		bind					p21	GP			 promoter	NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_2014_s_481	15713654	In support of our model, recent studies have demonstrated that p53 target gene expression requires more than just p53 binding: p53 first binds to the p21 promoter and recruits p300, which then acetylates the p21 proximal promoter and cooperates with p53 to induce p21 ( ,  ).	transcription
73484	2	336406	7	NULL	NULL	NULL	NULL	statement 1	GP		recruit					p300	GP				NULL		NULL	NULL	NULL	NULL	gw70_molcellbiol_25_5_2014_s_481	15713654	In support of our model, recent studies have demonstrated that p53 target gene expression requires more than just p53 binding: p53 first binds to the p21 promoter and recruits p300, which then acetylates the p21 proximal promoter and cooperates with p53 to induce p21 ( ,  ).	transcription
73485	3	336406	7	NULL	NULL	0	NULL	p300	GP		acetylate					p21	GP			proximal promoter	NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_5_2014_s_481	15713654	In support of our model, recent studies have demonstrated that p53 target gene expression requires more than just p53 binding: p53 first binds to the p21 promoter and recruits p300, which then acetylates the p21 proximal promoter and cooperates with p53 to induce p21 ( ,  ).	transcription
73486	4	336406	7	NULL	NULL	0	NULL	p53	GP		induce					p21	GP				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_5_2014_s_481	15713654	In support of our model, recent studies have demonstrated that p53 target gene expression requires more than just p53 binding: p53 first binds to the p21 promoter and recruits p300, which then acetylates the p21 proximal promoter and cooperates with p53 to induce p21 ( ,  ).	transcription
73487	5	336406	7	NULL	NULL	0	NULL	statement 3	Process		cooperates with					statement 4	Process				NULL		0	NULL	NULL	NULL	gw70_molcellbiol_25_5_2014_s_481	15713654	In support of our model, recent studies have demonstrated that p53 target gene expression requires more than just p53 binding: p53 first binds to the p21 promoter and recruits p300, which then acetylates the p21 proximal promoter and cooperates with p53 to induce p21 ( ,  ).	transcription
73488	1	336407	7	NULL	NULL	0	NULL	PCAF	GP		acetylates		specifically			p53	GP		K320		NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1202_s_169	9891054	Our observations that PCAF specifically acetylates p53 at K320, that this acetylation stimulates p53's DNA binding in vitro, and that alteration of this residue partially lowers p53 transcriptional activity in vivo raised the question of whether the acetylation occurs in vivo, and if so, whether it is regulated by previously known physiological stimuli of p53, such as DNA damage.	transcription
73489	2	336407	7	NULL	NULL	0	NULL	p53	GP		bind					DNA	NucleicAcid				NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1202_s_169	9891054	Our observations that PCAF specifically acetylates p53 at K320, that this acetylation stimulates p53's DNA binding in vitro, and that alteration of this residue partially lowers p53 transcriptional activity in vivo raised the question of whether the acetylation occurs in vivo, and if so, whether it is regulated by previously known physiological stimuli of p53, such as DNA damage.	transcription
73490	3	336407	7	NULL	NULL	0	NULL	statement 1	Process		stimulate					statement 2	Process				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1202_s_169	9891054	Our observations that PCAF specifically acetylates p53 at K320, that this acetylation stimulates p53's DNA binding in vitro, and that alteration of this residue partially lowers p53 transcriptional activity in vivo raised the question of whether the acetylation occurs in vivo, and if so, whether it is regulated by previously known physiological stimuli of p53, such as DNA damage.	transcription
73491	4	336407	7	NULL	NULL	0	NULL	p53	GP	alteration of	lowers		partially	K320		p53	GP	transcriptional activity of 			NULL	in vivo	0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1202_s_169	9891054	Our observations that PCAF specifically acetylates p53 at K320, that this acetylation stimulates p53's DNA binding in vitro, and that alteration of this residue partially lowers p53 transcriptional activity in vivo raised the question of whether the acetylation occurs in vivo, and if so, whether it is regulated by previously known physiological stimuli of p53, such as DNA damage.	transcription
73492	5	336407	7	NULL	NULL	0	NULL	DNA damage	Process		physiological stimuli of					p53	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1202_s_169	9891054	Our observations that PCAF specifically acetylates p53 at K320, that this acetylation stimulates p53's DNA binding in vitro, and that alteration of this residue partially lowers p53 transcriptional activity in vivo raised the question of whether the acetylation occurs in vivo, and if so, whether it is regulated by previously known physiological stimuli of p53, such as DNA damage.	transcription
73493	1	336408	7	NULL	NULL	NULL	NULL	UV irradiation	PhysicalPhenomenon		induce					p53	GP	cytoplasmic			NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_281_3_1394_s_85	16291740	Importantly, cytoplasmic p53 induced by UV irradiation is acetylated, as it can be recognized by an antibody specific for the acetylated p53 ( Fig. 1 F,  lane 3, upper panel).	transcription
73494	2	336408	7	NULL	NULL	0	NULL	statement 1	Process		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1394_s_85	16291740	Importantly, cytoplasmic p53 induced by UV irradiation is acetylated, as it can be recognized by an antibody specific for the acetylated p53 ( Fig. 1 F,  lane 3, upper panel).	transcription
73495	3	336408	7	NULL	NULL	0	NULL	p53 antibody	GP	acetylated	recognize					p53	GP	acetylated			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_281_3_1394_s_85	16291740	Importantly, cytoplasmic p53 induced by UV irradiation is acetylated, as it can be recognized by an antibody specific for the acetylated p53 ( Fig. 1 F,  lane 3, upper panel).	transcription
73496	1	336409	7	NULL	NULL	0	NULL	hGcn5	GP		interacts with		specifically			p53	GP	acetylated			NULL		0	NULL	NULL	NULL	gw60_molcell_8_6_1243_s_239	11779500	hGcn5 also interacted specifically with acetylated p53   (Figure 7A), indicating that TRRAP/hGcn5 complex  (Vassilev et al., 1998  ) binds to acetylated p53.	transcription
73497	2	336409	7	NULL	NULL	0	NULL	TRRAP/hGcn5 complex 	GP		bind					p53	GP	acetylated			NULL		0	NULL	NULL	NULL	gw60_molcell_8_6_1243_s_239	11779500	hGcn5 also interacted specifically with acetylated p53   (Figure 7A), indicating that TRRAP/hGcn5 complex  (Vassilev et al., 1998  ) binds to acetylated p53.	transcription
73498	1	336410	7	NULL	NULL	0	NULL	p300	GP		catalyze					p53	GP	acetylation of	lysine 382 residue		NULL		0	NULL	NULL	NULL	gw70_embo_24_13_2425_s_141	15933712	As expected, the acetylase/coactivator  p300 catalyzed the acetylation of p53 lysine 382 residue ( Figure 5E, lane 2), while coexpressing ATF3, if anything, augmented acetylation ( Figure 5E, lane 3).	transcription
73499	2	336410	7	NULL	NULL	0	NULL	p300	GP		is a type of					acetylase/coactivator	GP				NULL		0	NULL	NULL	NULL	gw70_embo_24_13_2425_s_141	15933712	As expected, the acetylase/coactivator  p300 catalyzed the acetylation of p53 lysine 382 residue ( Figure 5E, lane 2), while coexpressing ATF3, if anything, augmented acetylation ( Figure 5E, lane 3).	transcription
73500	3	336410	7	NULL	NULL	0	NULL	 ATF3	GP		augments					statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_embo_24_13_2425_s_141	15933712	As expected, the acetylase/coactivator  p300 catalyzed the acetylation of p53 lysine 382 residue ( Figure 5E, lane 2), while coexpressing ATF3, if anything, augmented acetylation ( Figure 5E, lane 3).	transcription
73501	1	336411	7	NULL	NULL	0	NULL	Daxx	GP		interacts with					p53	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_150	15364927	Because mutation of either PCAF or p300/CBP acetylation sites into alanine is sufficient to inhibit Daxx-p53 interaction, acetylation by either acetylase could potentially block the binding of Daxx to p53.	transcription
73502	2	336411	7	NULL	NULL	0	NULL	PCAF	GP	mutant	inhibit			acetylation site;;alanine		statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_150	15364927	Because mutation of either PCAF or p300/CBP acetylation sites into alanine is sufficient to inhibit Daxx-p53 interaction, acetylation by either acetylase could potentially block the binding of Daxx to p53.	transcription
73503	3	336411	7	NULL	NULL	0	NULL	p300/CBP	GP	mutant	inhibit			acetylation site;;alanine		statement 1	Process				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_150	15364927	Because mutation of either PCAF or p300/CBP acetylation sites into alanine is sufficient to inhibit Daxx-p53 interaction, acetylation by either acetylase could potentially block the binding of Daxx to p53.	transcription
73504	4	336411	7	NULL	NULL	0	NULL	PCAF	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_150	15364927	Because mutation of either PCAF or p300/CBP acetylation sites into alanine is sufficient to inhibit Daxx-p53 interaction, acetylation by either acetylase could potentially block the binding of Daxx to p53.	transcription
73505	5	336411	7	NULL	NULL	0	NULL	p300/CBP	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_150	15364927	Because mutation of either PCAF or p300/CBP acetylation sites into alanine is sufficient to inhibit Daxx-p53 interaction, acetylation by either acetylase could potentially block the binding of Daxx to p53.	transcription
73506	6	336411	7	NULL	NULL	NULL	NULL	statement 4	Process		block		potentially			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_150	15364927	Because mutation of either PCAF or p300/CBP acetylation sites into alanine is sufficient to inhibit Daxx-p53 interaction, acetylation by either acetylase could potentially block the binding of Daxx to p53.	transcription
73507	7	336411	7	NULL	NULL	NULL	NULL	statement 5	Process		block		potentially			statement 1	Process				NULL		NULL	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_150	15364927	Because mutation of either PCAF or p300/CBP acetylation sites into alanine is sufficient to inhibit Daxx-p53 interaction, acetylation by either acetylase could potentially block the binding of Daxx to p53.	transcription
73508	8	336411	7	NULL	NULL	0	NULL	PCAF	GP		is a type of					acetylase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_150	15364927	Because mutation of either PCAF or p300/CBP acetylation sites into alanine is sufficient to inhibit Daxx-p53 interaction, acetylation by either acetylase could potentially block the binding of Daxx to p53.	transcription
73509	9	336411	7	NULL	NULL	0	NULL	p300/CBP	GP		is a type of					acetylase	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_279_48_50566_s_150	15364927	Because mutation of either PCAF or p300/CBP acetylation sites into alanine is sufficient to inhibit Daxx-p53 interaction, acetylation by either acetylase could potentially block the binding of Daxx to p53.	transcription
73510	1	336412	7	NULL	NULL	0	NULL	Mdm2 protein	GP	endogenous	complex with					p300	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3704_s_35	10207094	In cells, most of the endogenous Mdm2 protein is complexed with the histone acetylase p300, and Grossman et al. have shown that the specific interaction between p300 and Mdm2 is required for the degradation of p53 ( 18).	transcription
73511	2	336412	7	NULL	NULL	0	NULL	statement 1	Process		required for					p53	GP	degradation of			NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3704_s_35	10207094	In cells, most of the endogenous Mdm2 protein is complexed with the histone acetylase p300, and Grossman et al. have shown that the specific interaction between p300 and Mdm2 is required for the degradation of p53 ( 18).	transcription
73512	3	336412	7	NULL	NULL	0	NULL	p300	GP		is a type of					histone acetylase	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_19_5_3704_s_35	10207094	In cells, most of the endogenous Mdm2 protein is complexed with the histone acetylase p300, and Grossman et al. have shown that the specific interaction between p300 and Mdm2 is required for the degradation of p53 ( 18).	transcription
73513	1	336413	7	NULL	NULL	0	NULL	p300	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw70_pnas_101_5_1273_s_7	14732695	p300 is known to acetylate p53 in response to DNA damage, and when MSI+ cells null for p300 activity are forced to reexpress exogenous  p300 cells show slower growth and a flatter morphology.	transcription
73514	2	336413	7	NULL	NULL	0	NULL	statement 1	Process		in response to					DNA damage	Process				NULL		0	NULL	NULL	NULL	gw70_pnas_101_5_1273_s_7	14732695	p300 is known to acetylate p53 in response to DNA damage, and when MSI+ cells null for p300 activity are forced to reexpress exogenous  p300 cells show slower growth and a flatter morphology.	transcription
73515	1	336414	7	NULL	NULL	0	NULL	CBP 	GP		acetylate					nonhistone proteins	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73516	2	336414	7	NULL	NULL	0	NULL	pCAF	GP		acetylate					nonhistone proteins	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73517	3	336414	7	NULL	NULL	0	NULL	CBP	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73518	4	336414	7	NULL	NULL	0	NULL	pCAF	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73519	5	336414	7	NULL	NULL	0	NULL	CBP	GP		acetylate					E2F1	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73520	6	336414	7	NULL	NULL	0	NULL	pCAF	GP		acetylate					E2F1	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73521	7	336414	7	NULL	NULL	0	NULL	CBP	GP		acetylate					ELKF	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73522	8	336414	7	NULL	NULL	0	NULL	pCAF	GP		acetylate					ELKF	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73523	9	336414	7	NULL	NULL	0	NULL	CBP	GP		acetylate					GATA 1	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73524	10	336414	7	NULL	NULL	0	NULL	pCAF	GP		acetylate					GATA 1	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73525	11	336414	7	NULL	NULL	0	NULL	CBP	GP		acetylate					TFIIF	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73526	12	336414	7	NULL	NULL	0	NULL	pCAF	GP		acetylate					TFIIF	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73527	13	336414	7	NULL	NULL	0	NULL	CBP	GP		acetylate					TFIIEbeta	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73528	14	336414	7	NULL	NULL	0	NULL	pCAF	GP		acetylate					TFIIEbeta	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73529	15	336414	7	NULL	NULL	0	NULL	CBP	GP		acetylate					ACTR	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73530	16	336414	7	NULL	NULL	0	NULL	pCAF	GP		acetylate					ACTR	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73531	17	336414	7	NULL	NULL	0	NULL	CBP	GP		is a type of					coactivator	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73532	18	336414	7	NULL	NULL	0	NULL	pCAF	GP		is a type of					coactivator	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73533	19	336414	7	NULL	NULL	0	NULL	p53	GP		is a type of					transcription factor	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73534	20	336414	7	NULL	NULL	0	NULL	 E2F1	GP		is a type of					transcription factor	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73535	21	336414	7	NULL	NULL	0	NULL	GATA 1	GP		is a type of					transcription factor	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73536	22	336414	7	NULL	NULL	0	NULL	TFIIF	GP		is a type of					transcription factor	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73537	23	336414	7	NULL	NULL	0	NULL	TFIIEbeta	GP		is a type of					transcription factor	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73538	24	336414	7	NULL	NULL	0	NULL	ACTR	GP		is a type of					nuclear receptor coactivator 	GP				NULL		0	NULL	NULL	NULL	gw60_molcellbiol_21_4_1404_s_23	11158325	The coactivators CBP and pCAF can also acetylate nonhistone proteins, including transcription factors p53, E2F1, ELKF, GATA 1, TFIIF, and TFIIEbeta and the nuclear receptor coactivator ACTR (reviewed in reference  29).	transcription
73539	1	336415	7	NULL	NULL	0	NULL	p300/CBP	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_48_34020_s_47	10567368	p300/CBP have also been shown to acetylate several transcription factors including p53 ( 69), NF-Y ( 70), and GATA-1 ( 71), which influences their binding to DNA.	transcription
73540	2	336415	7	NULL	NULL	0	NULL	p300/CBP	GP		acetylate					NF-Y 	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_48_34020_s_47	10567368	p300/CBP have also been shown to acetylate several transcription factors including p53 ( 69), NF-Y ( 70), and GATA-1 ( 71), which influences their binding to DNA.	transcription
73541	3	336415	7	NULL	NULL	0	NULL	p300/CBP	GP		acetylate					GATA-1	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_48_34020_s_47	10567368	p300/CBP have also been shown to acetylate several transcription factors including p53 ( 69), NF-Y ( 70), and GATA-1 ( 71), which influences their binding to DNA.	transcription
73542	4	336415	7	NULL	NULL	0	NULL	p53	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_48_34020_s_47	10567368	p300/CBP have also been shown to acetylate several transcription factors including p53 ( 69), NF-Y ( 70), and GATA-1 ( 71), which influences their binding to DNA.	transcription
73543	5	336415	7	NULL	NULL	0	NULL	NF-Y 	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_48_34020_s_47	10567368	p300/CBP have also been shown to acetylate several transcription factors including p53 ( 69), NF-Y ( 70), and GATA-1 ( 71), which influences their binding to DNA.	transcription
73544	6	336415	7	NULL	NULL	0	NULL	GATA-1	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_48_34020_s_47	10567368	p300/CBP have also been shown to acetylate several transcription factors including p53 ( 69), NF-Y ( 70), and GATA-1 ( 71), which influences their binding to DNA.	transcription
73545	7	336415	7	NULL	NULL	0	NULL	statement 1	Process		influence					statement 4	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_48_34020_s_47	10567368	p300/CBP have also been shown to acetylate several transcription factors including p53 ( 69), NF-Y ( 70), and GATA-1 ( 71), which influences their binding to DNA.	transcription
73546	8	336415	7	NULL	NULL	0	NULL	statement 2	Process		influence					statement 5	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_48_34020_s_47	10567368	p300/CBP have also been shown to acetylate several transcription factors including p53 ( 69), NF-Y ( 70), and GATA-1 ( 71), which influences their binding to DNA.	transcription
73547	9	336415	7	NULL	NULL	0	NULL	statement 3	Process		influence					statement 6	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_48_34020_s_47	10567368	p300/CBP have also been shown to acetylate several transcription factors including p53 ( 69), NF-Y ( 70), and GATA-1 ( 71), which influences their binding to DNA.	transcription
73548	10	336415	7	NULL	NULL	0	NULL	p53	GP		is a type of					transcription factor	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_48_34020_s_47	10567368	p300/CBP have also been shown to acetylate several transcription factors including p53 ( 69), NF-Y ( 70), and GATA-1 ( 71), which influences their binding to DNA.	transcription
73549	11	336415	7	NULL	NULL	0	NULL	 NF-Y	GP		is a type of					transcription factor	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_48_34020_s_47	10567368	p300/CBP have also been shown to acetylate several transcription factors including p53 ( 69), NF-Y ( 70), and GATA-1 ( 71), which influences their binding to DNA.	transcription
73550	12	336415	7	NULL	NULL	0	NULL	GATA-1	GP		is a type of					transcription factor	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_274_48_34020_s_47	10567368	p300/CBP have also been shown to acetylate several transcription factors including p53 ( 69), NF-Y ( 70), and GATA-1 ( 71), which influences their binding to DNA.	transcription
73551	1	336416	7	NULL	NULL	0	NULL	HDAC1	GP		deacetylate					histones	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_39_37439_s_383	12876282	In addition to deacetylating histones, HDAC1,-2, and-3 are able to deacetylate p53 at the C terminus that can be acetylated by p300/CBP  in vivo ( ,  ), resulting in suppression of the p53 transactivation activity.	transcription
73552	2	336416	7	NULL	NULL	0	NULL	HDAC2	GP		deacetylate					histones	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_39_37439_s_383	12876282	In addition to deacetylating histones, HDAC1,-2, and-3 are able to deacetylate p53 at the C terminus that can be acetylated by p300/CBP  in vivo ( ,  ), resulting in suppression of the p53 transactivation activity.	transcription
73553	3	336416	7	NULL	NULL	0	NULL	HDAC3	GP		deacetylate					histones	GP				NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_39_37439_s_383	12876282	In addition to deacetylating histones, HDAC1,-2, and-3 are able to deacetylate p53 at the C terminus that can be acetylated by p300/CBP  in vivo ( ,  ), resulting in suppression of the p53 transactivation activity.	transcription
73554	4	336416	7	NULL	NULL	0	NULL	HDAC1	GP		deacetylate					p53	GP		C terminus		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_39_37439_s_383	12876282	In addition to deacetylating histones, HDAC1,-2, and-3 are able to deacetylate p53 at the C terminus that can be acetylated by p300/CBP  in vivo ( ,  ), resulting in suppression of the p53 transactivation activity.	transcription
73555	5	336416	7	NULL	NULL	0	NULL	HDAC2	GP		deacetylate					p53	GP		C terminus		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_39_37439_s_383	12876282	In addition to deacetylating histones, HDAC1,-2, and-3 are able to deacetylate p53 at the C terminus that can be acetylated by p300/CBP  in vivo ( ,  ), resulting in suppression of the p53 transactivation activity.	transcription
73556	6	336416	7	NULL	NULL	0	NULL	HDAC3	GP		deacetylate					p53	GP		C terminus		NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_39_37439_s_383	12876282	In addition to deacetylating histones, HDAC1,-2, and-3 are able to deacetylate p53 at the C terminus that can be acetylated by p300/CBP  in vivo ( ,  ), resulting in suppression of the p53 transactivation activity.	transcription
73557	7	336416	7	NULL	NULL	0	NULL	p300/CBP	GP		acetylate					p53	GP				NULL	in vivo	0	NULL	NULL	NULL	gw70_jbiolchem_278_39_37439_s_383	12876282	In addition to deacetylating histones, HDAC1,-2, and-3 are able to deacetylate p53 at the C terminus that can be acetylated by p300/CBP  in vivo ( ,  ), resulting in suppression of the p53 transactivation activity.	transcription
73558	8	336416	7	NULL	NULL	0	NULL	statement 4	Process		suppress					p53	GP	transactivation activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_39_37439_s_383	12876282	In addition to deacetylating histones, HDAC1,-2, and-3 are able to deacetylate p53 at the C terminus that can be acetylated by p300/CBP  in vivo ( ,  ), resulting in suppression of the p53 transactivation activity.	transcription
73559	9	336416	7	NULL	NULL	0	NULL	statement 5	Process		suppress					p53	GP	transactivation activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_39_37439_s_383	12876282	In addition to deacetylating histones, HDAC1,-2, and-3 are able to deacetylate p53 at the C terminus that can be acetylated by p300/CBP  in vivo ( ,  ), resulting in suppression of the p53 transactivation activity.	transcription
73560	10	336416	7	NULL	NULL	0	NULL	statement 6	Process		suppress					p53	GP	transactivation activity of			NULL		0	NULL	NULL	NULL	gw70_jbiolchem_278_39_37439_s_383	12876282	In addition to deacetylating histones, HDAC1,-2, and-3 are able to deacetylate p53 at the C terminus that can be acetylated by p300/CBP  in vivo ( ,  ), resulting in suppression of the p53 transactivation activity.	transcription
73561	1	336417	7	NULL	NULL	NULL	NULL	TSA	Chemical		inhibit		effectively			p53 deacetylase	GP				NULL	A549 cells	NULL	NULL	NULL	NULL	gw60_embo_20_6_1331_s_187	11250899	As shown in Figure  6A (top panel), TSA treatment effectively inhibited the p53 deacetylase and increased the levels of acetylated p53 in A549 cells.	transcription
73562	2	336417	7	NULL	NULL	0	NULL	statement 1	Process		increase					p53	GP	acetylated			NULL	A549 cells	0	NULL	NULL	NULL	gw60_embo_20_6_1331_s_187	11250899	As shown in Figure  6A (top panel), TSA treatment effectively inhibited the p53 deacetylase and increased the levels of acetylated p53 in A549 cells.	transcription
73563	1	336418	7	NULL	NULL	NULL	NULL	CBP/p300	GP		mediate					p53	GP	acetylation of			NULL	in vivo	NULL	NULL	NULL	NULL	gw60_cell_107_2_137_s_17	11672522	By developing site-specific acetylated p53  antibodies, CBP/p300 mediated acetylation of p53 was further  confirmed in vivo by a number of  studies (reviewed in Appella and Anderson, 2000   ).	transcription
73564	1	336419	7	NULL	NULL	0	NULL	p53	GP	mutant	acteylated by			lysine residue		p300	GP				NULL		0	NULL	NULL	NULL	gw60_molcell_8_1_57_s_273	11511360	We find that p53 proteins containing mutations in lysine residues acetylated by p300 are as active as wild-type p53 in regulating p21 transcription in vitro.	transcription
73565	2	336419	7	NULL	NULL	0	NULL	p53	GP	wild-type	regulate					p21	GP	transcription of			NULL	in vitro	0	NULL	NULL	NULL	gw60_molcell_8_1_57_s_273	11511360	We find that p53 proteins containing mutations in lysine residues acetylated by p300 are as active as wild-type p53 in regulating p21 transcription in vitro.	transcription
73566	3	336419	7	NULL	NULL	0	NULL	p53	GP	mutant	regulate			lysine residue		p21	GP	transcription of			NULL	in vitro	0	NULL	NULL	NULL	gw60_molcell_8_1_57_s_273	11511360	We find that p53 proteins containing mutations in lysine residues acetylated by p300 are as active as wild-type p53 in regulating p21 transcription in vitro.	transcription
73567	4	336419	7	NULL	NULL	0	NULL	statement 2	Process		is as active as					statement 3	Process				NULL		0	NULL	NULL	NULL	gw60_molcell_8_1_57_s_273	11511360	We find that p53 proteins containing mutations in lysine residues acetylated by p300 are as active as wild-type p53 in regulating p21 transcription in vitro.	transcription
73568	1	336420	7	NULL	NULL	0	NULL	PCAF	GP		acetylate					p53	GP		lysine		NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1202_s_204	9891054	In particular, under in vivo conditions that cause DNA damage, which potentiate p53 activity, increased p53 acetylation is detected at lysines acetylated in vitro by PCAF and p300.	transcription
73569	2	336420	7	NULL	NULL	0	NULL	p300	GP		acetylate					p53	GP		lysine		NULL	in vitro	0	NULL	NULL	NULL	gw60_molcellbiol_19_2_1202_s_204	9891054	In particular, under in vivo conditions that cause DNA damage, which potentiate p53 activity, increased p53 acetylation is detected at lysines acetylated in vitro by PCAF and p300.	transcription
73570	1	336421	7	NULL	NULL	0	NULL	HDAC	GP		down-regulates					p53	GP	activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20436_s_5	10777477	Down-regulation of p53 activity by HDACs is HDAC dosage-dependent, requires the deacetylase activity of HDACs, and depends on the region of p53 that is acetylated by p300/CREB-binding protein (CBP).	transcription
73571	2	336421	7	NULL	NULL	0	NULL	statement 1	Process		depends on					HDAC	GP	dose of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20436_s_5	10777477	Down-regulation of p53 activity by HDACs is HDAC dosage-dependent, requires the deacetylase activity of HDACs, and depends on the region of p53 that is acetylated by p300/CREB-binding protein (CBP).	transcription
73572	3	336421	7	NULL	NULL	0	NULL	statement 1	Process		requires					HDAC	GP	deacetylase activity of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20436_s_5	10777477	Down-regulation of p53 activity by HDACs is HDAC dosage-dependent, requires the deacetylase activity of HDACs, and depends on the region of p53 that is acetylated by p300/CREB-binding protein (CBP).	transcription
73573	4	336421	7	NULL	NULL	0	NULL	p300/CREB-binding protein 	GP		acetylate					p53	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20436_s_5	10777477	Down-regulation of p53 activity by HDACs is HDAC dosage-dependent, requires the deacetylase activity of HDACs, and depends on the region of p53 that is acetylated by p300/CREB-binding protein (CBP).	transcription
73574	5	336421	7	NULL	NULL	0	NULL	statement 1	Process		depends on					p53	GP	acetylated region of			NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20436_s_5	10777477	Down-regulation of p53 activity by HDACs is HDAC dosage-dependent, requires the deacetylase activity of HDACs, and depends on the region of p53 that is acetylated by p300/CREB-binding protein (CBP).	transcription
73575	6	336421	7	NULL	NULL	0	NULL	CBP	GP		is					CREB-binding protein	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_27_20436_s_5	10777477	Down-regulation of p53 activity by HDACs is HDAC dosage-dependent, requires the deacetylase activity of HDACs, and depends on the region of p53 that is acetylated by p300/CREB-binding protein (CBP).	transcription
73576	1	336422	7	NULL	NULL	0	NULL	p53	GP	acetylation of	depends on					DNA damage	Process				NULL	cultured cells	0	NULL	NULL	NULL	gw60_jbiolchem_275_29_21953_s_251	10777508	As p53 is acetylated in a DNA damage-dependent manner in cultured cells ( 6), the binding mode of PCAF to p53 might be regulated via a signaling network.	transcription
73577	2	336422	7	NULL	NULL	0	NULL	PCAF	GP		bind					p53	GP				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_29_21953_s_251	10777508	As p53 is acetylated in a DNA damage-dependent manner in cultured cells ( 6), the binding mode of PCAF to p53 might be regulated via a signaling network.	transcription
73578	3	336422	7	NULL	NULL	0	NULL	statement 2	Process		regulated via					signaling network	Process				NULL		0	NULL	NULL	NULL	gw60_jbiolchem_275_29_21953_s_251	10777508	As p53 is acetylated in a DNA damage-dependent manner in cultured cells ( 6), the binding mode of PCAF to p53 might be regulated via a signaling network.	transcription
67794	1	346003	9	NULL	NULL	NULL	NULL	deletion experiments	ResearchActivity		identified					heat regulation regions	GP				NULL	several different heat shock genes	NULL	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_2	3146692	 Regions responsible for heat regulation have been identified previously by deletion experiments with several different heat shock genes .	tag10-1
67801	1	346007	9	NULL	NULL	NULL	NULL	nucleotides at two positions	NucleicAcid		upstream					GAA segments	NucleicAcid				NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_6	3146692	 Second , the nucleotides at the two positions immediately upstream from GAA segments played an important role in defining the competence of regulatory elements .	tag10-1
67802	2	346007	9	NULL	NULL	NULL	NULL	statement 1	NucleicAcid		plays a role in					heat shock regulatory elements	NucleicAcid	competence of			NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_6	3146692	 Second , the nucleotides at the two positions immediately upstream from GAA segments played an important role in defining the competence of regulatory elements .	tag10-1
67900	1	346010	9	NULL	NULL	0	NULL	hsp70 genes	GP		expression by					heat-regulation	ResearchActivity				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_9	3146692	 In most cell types , the genes were expressed in a heat-regulated fashion .	tag10-1
67909	1	346013	9	NULL	NULL	0	NULL	CNNGAANNTTCNNG	NucleicAcid		is					heat shock consensus sequence	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_12	3146692	 Comparison of the -45 to -65 sequence of Drosophila hsp70 genes and of analogous sequences in other hsp genes led to the establishment of a heat shock consensus sequence , CNNGAANNTTCNNG ,  ( 31  ) , where N is any nucleotide .	tag10-1
67910	2	346013	9	NULL	NULL	0	NULL	heat shock consensus sequence	NucleicAcid		analogous to					hsp genes	GP	other			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_12	3146692	 Comparison of the -45 to -65 sequence of Drosophila hsp70 genes and of analogous sequences in other hsp genes led to the establishment of a heat shock consensus sequence , CNNGAANNTTCNNG ,  ( 31  ) , where N is any nucleotide .	tag10-1
67911	1	346014	9	NULL	NULL	0	NULL	Heat Shock Factors			cause					hsp genes		Transcriptional activation of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_13	3146692	 Factors binding to this type of sequence have been identified  ( 17 , 28 , 37 , 45 , 47 , 48  ) , and two groups have purified such factors from Drosophila nuclear extracts and have shown that they are specifically involved in transcriptional activation of hsp genes ( 28 , 45 , 48  ) .	tag10-1
67912	1	346015	9	NULL	NULL	0	NULL	heat shock transcription elements	Process		important for					heat shock regulation	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_14	3146692	 Since the sequences described above are the only elements specifically required for heat regulation and are also binding sites for hsp gene-specific transcription factors , they are of central importance for the understanding of heat shock regulation .	tag10-1
67915	1	346019	9	NULL	NULL	NULL	NULL	Plasmids	NucleicAcid		derived from					D88 contruct	NucleicAcid				NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_18	3146692	 Plasmids  ( Fig . 1 and 2  ) were derived from constructs D88 and D50  ( 2  ) .	tag10-1
67916	2	346019	9	NULL	NULL	0	NULL	Plasmids	NucleicAcid		derived from					D50 contruct	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_18	3146692	 Plasmids  ( Fig . 1 and 2  ) were derived from constructs D88 and D50  ( 2  ) .	tag10-1
67934	1	346024	9	NULL	NULL	0	NULL	Synthetic linkers	NucleicAcid		obtained from					New England Biolabs	Facility				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_23	3146692	 Synthetic linkers ( XhoI , BamHI , EcoRI , and SmaI  ) were obtained from New England Biolabs or International Biochemical Co.	tag10-1
67935	2	346024	9	NULL	NULL	0	NULL	Synthetic linkers	NucleicAcid		obtained from					International Biochemical Co	Facility				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_23	3146692	 Synthetic linkers ( XhoI , BamHI , EcoRI , and SmaI  ) were obtained from New England Biolabs or International Biochemical Co.	tag10-1
67936	3	346024	9	NULL	NULL	0	NULL	XhoI	NucleicAcid		is a type of					Synthetic linkers	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_23	3146692	 Synthetic linkers ( XhoI , BamHI , EcoRI , and SmaI  ) were obtained from New England Biolabs or International Biochemical Co.	tag10-1
67937	4	346024	9	NULL	NULL	0	NULL	BamHI	NucleicAcid		is a type of					Synthetic linkers	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_23	3146692	 Synthetic linkers ( XhoI , BamHI , EcoRI , and SmaI  ) were obtained from New England Biolabs or International Biochemical Co.	tag10-1
67938	5	346024	9	NULL	NULL	0	NULL	EcoRI 	NucleicAcid		is a type of					Synthetic linkers	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_23	3146692	 Synthetic linkers ( XhoI , BamHI , EcoRI , and SmaI  ) were obtained from New England Biolabs or International Biochemical Co.	tag10-1
67939	5	346024	9	NULL	NULL	0	NULL	EcoRI 	NucleicAcid		is a type of					Synthetic linkers	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_23	3146692	 Synthetic linkers ( XhoI , BamHI , EcoRI , and SmaI  ) were obtained from New England Biolabs or International Biochemical Co.	tag10-1
67940	6	346024	9	NULL	NULL	0	NULL	SmaI	NucleicAcid		is a type of					Synthetic linkers	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_23	3146692	 Synthetic linkers ( XhoI , BamHI , EcoRI , and SmaI  ) were obtained from New England Biolabs or International Biochemical Co.	tag10-1
67941	1	346026	9	NULL	NULL	0	NULL	Complementary segments	NucleicAcid		treated with					T4 polynucleotide kinase	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_25	3146692	 Complementary segments were annealed and treated with T4 polynucleotide kinase .	tag10-1
67942	1	346027	9	NULL	NULL	0	NULL	BssHII-Xba I fragment	NucleicAcid		isolated from					clone 122	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_26	3146692	 To prepare XBA8 , a BssHII-Xba I fragment  ( hsp70 sequences from -67 to -244  ) was isolated from clone 122  ( 12  ) , blunted , and inserted into the unique XhoI site ( filled  ) of D50 .	tag10-1
67943	2	346027	9	NULL	NULL	NULL	NULL	BssHII-Xba I fragment	NucleicAcid		inserted into					XhoI site	NucleicAcid	unique			NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_26	3146692	 To prepare XBA8 , a BssHII-Xba I fragment  ( hsp70 sequences from -67 to -244  ) was isolated from clone 122  ( 12  ) , blunted , and inserted into the unique XhoI site ( filled  ) of D50 .	tag10-1
67944	3	346027	9	NULL	NULL	0	NULL	BssHII-Xba I fragment	NucleicAcid		undergo					Blunting	ResearchActivity				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_26	3146692	 To prepare XBA8 , a BssHII-Xba I fragment  ( hsp70 sequences from -67 to -244  ) was isolated from clone 122  ( 12  ) , blunted , and inserted into the unique XhoI site ( filled  ) of D50 .	tag10-1
67945	4	346027	9	NULL	NULL	0	NULL	Statement 1	ResearchActivity		prepare					XBA8	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_26	3146692	 To prepare XBA8 , a BssHII-Xba I fragment  ( hsp70 sequences from -67 to -244  ) was isolated from clone 122  ( 12  ) , blunted , and inserted into the unique XhoI site ( filled  ) of D50 .	tag10-1
67946	5	346027	9	NULL	NULL	0	NULL	Statement 2	ResearchActivity		prepare					XBA8	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_26	3146692	 To prepare XBA8 , a BssHII-Xba I fragment  ( hsp70 sequences from -67 to -244  ) was isolated from clone 122  ( 12  ) , blunted , and inserted into the unique XhoI site ( filled  ) of D50 .	tag10-1
67963	1	346032	9	NULL	NULL	0	NULL	Sequencing	ResearchActivity		performed by					chemical procedure	ResearchActivity				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_31	3146692	 Sequencing was performed by either the chemical procedure  ( 21  ) or the dideoxy method ( 35  ) .	tag10-1
67964	2	346032	9	NULL	NULL	0	NULL	Sequencing	ResearchActivity		performed by					dideoxy method	ResearchActivity				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_8_9_3761_s_31	3146692	 Sequencing was performed by either the chemical procedure  ( 21  ) or the dideoxy method ( 35  ) .	tag10-1
61278	1	346226	5	NULL	NULL	0	NULL	heat shock factor	GP		interacts with					hsp7O	GP				NULL	in vivo	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_1	7935376	Interaction between Heat Shock Factor and hsp7O Is Insufficient To Suppress Induction of DNA-Binding Activity In Vivo  The intracellular level of free heat shock proteins, in particular the 70-kDa stress protein family, has been suggested to be the basis of an autoregulatory mechanism by which the cell measures the level of thermal stress and regulates the synthesis of heat shock proteins.	tag10-2
61281	3	346226	5	NULL	NULL	0	NULL	hsp7O	GP		is a member of					stress protein family	GP				NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_1	7935376	Interaction between Heat Shock Factor and hsp7O Is Insufficient To Suppress Induction of DNA-Binding Activity In Vivo  The intracellular level of free heat shock proteins, in particular the 70-kDa stress protein family, has been suggested to be the basis of an autoregulatory mechanism by which the cell measures the level of thermal stress and regulates the synthesis of heat shock proteins.	tag10-2
61282	4	346226	5	NULL	NULL	0	NULL	hsp7O	GP	intracellular level of;;free	plays a role in					autoregulatory mechanism	Process				NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_1	7935376	Interaction between Heat Shock Factor and hsp7O Is Insufficient To Suppress Induction of DNA-Binding Activity In Vivo  The intracellular level of free heat shock proteins, in particular the 70-kDa stress protein family, has been suggested to be the basis of an autoregulatory mechanism by which the cell measures the level of thermal stress and regulates the synthesis of heat shock proteins.	tag10-2
61283	5	346226	5	NULL	NULL	0	NULL	cell	Cell		measures					thermal stress	Process	level of			NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_1	7935376	Interaction between Heat Shock Factor and hsp7O Is Insufficient To Suppress Induction of DNA-Binding Activity In Vivo  The intracellular level of free heat shock proteins, in particular the 70-kDa stress protein family, has been suggested to be the basis of an autoregulatory mechanism by which the cell measures the level of thermal stress and regulates the synthesis of heat shock proteins.	tag10-2
61284	6	346226	5	NULL	NULL	0	NULL	cell	Cell		regulates					heat shock proteins	GP	synthesis of			NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_1	7935376	Interaction between Heat Shock Factor and hsp7O Is Insufficient To Suppress Induction of DNA-Binding Activity In Vivo  The intracellular level of free heat shock proteins, in particular the 70-kDa stress protein family, has been suggested to be the basis of an autoregulatory mechanism by which the cell measures the level of thermal stress and regulates the synthesis of heat shock proteins.	tag10-2
61285	7	346226	5	NULL	NULL	0	NULL	statement 5	Process		followed by					statement 6	Process				NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_1	7935376	Interaction between Heat Shock Factor and hsp7O Is Insufficient To Suppress Induction of DNA-Binding Activity In Vivo  The intracellular level of free heat shock proteins, in particular the 70-kDa stress protein family, has been suggested to be the basis of an autoregulatory mechanism by which the cell measures the level of thermal stress and regulates the synthesis of heat shock proteins.	tag10-2
61286	1	346227	5	NULL	NULL	0	NULL	HSF	GP		is					heat shock transcription factor	GP				NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_2	7935376	It has been proposed that the DNA-binding and oligomeric state of the heat shock transcription factor (HSF) is a principal step in the induction pathway that is responsive to the level of 70-kDa stress protein.	tag10-2
61287	2	346227	5	NULL	NULL	0	NULL	HSF	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_2	7935376	It has been proposed that the DNA-binding and oligomeric state of the heat shock transcription factor (HSF) is a principal step in the induction pathway that is responsive to the level of 70-kDa stress protein.	tag10-2
61288	3	346227	5	NULL	NULL	0	NULL	induction pathway	Process		is responsive to					70-kDa stress protein	GP	level of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_2	7935376	It has been proposed that the DNA-binding and oligomeric state of the heat shock transcription factor (HSF) is a principal step in the induction pathway that is responsive to the level of 70-kDa stress protein.	tag10-2
61289	4	346227	5	NULL	NULL	0	NULL	statement 2	Process		is a principal step in					statement 3	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_2	7935376	It has been proposed that the DNA-binding and oligomeric state of the heat shock transcription factor (HSF) is a principal step in the induction pathway that is responsive to the level of 70-kDa stress protein.	tag10-2
61290	5	346227	5	NULL	NULL	0	NULL	HSF	GP	oligomeric state of	is a principal step in					statement 3	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_2	7935376	It has been proposed that the DNA-binding and oligomeric state of the heat shock transcription factor (HSF) is a principal step in the induction pathway that is responsive to the level of 70-kDa stress protein.	tag10-2
61291	1	346228	5	NULL	NULL	0	NULL	HSF	GP		is associated with		potentially			70-kDa stress protein	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_3	7935376	To test this hypothesis, we investigated the association between HSF and 70-kDa stress protein by means of a coimmunoprecipitation assay.	tag10-2
61292	1	346229	5	NULL	NULL	0	NULL	70-kDa stress proteins	GP		associate with					HSF	GP	latent			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_4	7935376	We found that 70-kDa stress proteins associate to similar extents with both latent and active fonns of HSF, although unlike other 70-kDa stress protein substrates, the association with HSF was not significantly disrupted in the presence of ATP.	tag10-2
61293	2	346229	5	NULL	NULL	0	NULL	70-kDa stress proteins	GP		associate with					HSF	GP	active			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_4	7935376	We found that 70-kDa stress proteins associate to similar extents with both latent and active fonns of HSF, although unlike other 70-kDa stress protein substrates, the association with HSF was not significantly disrupted in the presence of ATP.	tag10-2
61294	3	346229	5	NULL	NULL	0	NULL	statement 1	Process	affinity of	is similar to					statement 2	Process	affinity of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_4	7935376	We found that 70-kDa stress proteins associate to similar extents with both latent and active fonns of HSF, although unlike other 70-kDa stress protein substrates, the association with HSF was not significantly disrupted in the presence of ATP.	tag10-2
61295	4	346229	5	NULL	NULL	0	NULL	statement 1	Process		is not disrupted by		significantly			ATP	Chemical	presence of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_4	7935376	We found that 70-kDa stress proteins associate to similar extents with both latent and active fonns of HSF, although unlike other 70-kDa stress protein substrates, the association with HSF was not significantly disrupted in the presence of ATP.	tag10-2
61296	5	346229	5	NULL	NULL	0	NULL	statement 2	Process		is not disrupted by					ATP	Chemical	presence of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_4	7935376	We found that 70-kDa stress proteins associate to similar extents with both latent and active fonns of HSF, although unlike other 70-kDa stress protein substrates, the association with HSF was not significantly disrupted in the presence of ATP.	tag10-2
61297	1	346230	5	NULL	NULL	0	NULL	HSF trimer	GP	bacterially purified;;active	is not deactivated with		substantially			70-kDa stress protein	GP	purified			NULL	in vitro	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_5	7935376	Gel mobility shift assays indicated that active HSF trimers purified from a bacterial expression system could not be substantially deactivated in vitro with purified 70-kDa stress protein and ATP.	tag10-2
61298	2	346230	5	NULL	NULL	0	NULL	HSF trimer	GP	bacterially purified;;active	is not deactivated with		substantially			ATP	Chemical				NULL	in vitro	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_5	7935376	Gel mobility shift assays indicated that active HSF trimers purified from a bacterial expression system could not be substantially deactivated in vitro with purified 70-kDa stress protein and ATP.	tag10-2
61299	1	346231	5	NULL	NULL	0	NULL	HSF	GP		activates					DNA	NucleicAcid	binding of			NULL	cultured rat cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_6	7935376	In addition, elevated concentrations of hsp7O alone could not significantly inhibit induction of the DNA-binding activity of endogenous HSF in cultured rat cells, and the induction was also not inhibited in cultured rat cells or Drosophila cells containing elevated levels of all members of the heat shock protein family.	tag10-2
61300	2	346231	5	NULL	NULL	0	NULL	hsp7O	GP	elevated concentrations of	does not inhibit		significantly			statement 1	Process	induction of			NULL	cultured rat cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_6	7935376	In addition, elevated concentrations of hsp7O alone could not significantly inhibit induction of the DNA-binding activity of endogenous HSF in cultured rat cells, and the induction was also not inhibited in cultured rat cells or Drosophila cells containing elevated levels of all members of the heat shock protein family.	tag10-2
61301	3	346231	5	NULL	NULL	0	NULL	heat shock protein family	GP	elevated levels of;;all members of	does not inhibit					statement 1	Process	induction of			NULL	cultured rat cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_6	7935376	In addition, elevated concentrations of hsp7O alone could not significantly inhibit induction of the DNA-binding activity of endogenous HSF in cultured rat cells, and the induction was also not inhibited in cultured rat cells or Drosophila cells containing elevated levels of all members of the heat shock protein family.	tag10-2
61302	4	346231	5	NULL	NULL	NULL	NULL	heat shock protein family	GP	elevated levels of;;all members of	does not inhibit					statement 1	Process	induction of			NULL	Drosophila cells	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_6	7935376	In addition, elevated concentrations of hsp7O alone could not significantly inhibit induction of the DNA-binding activity of endogenous HSF in cultured rat cells, and the induction was also not inhibited in cultured rat cells or Drosophila cells containing elevated levels of all members of the heat shock protein family.	tag10-2
61303	1	346232	5	NULL	NULL	0	NULL	HSF	GP	active	is deactivated to					HSF	GP	non-DNA-bound			NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_7	7935376	However, the deactivation of HSF to the non-DNA-binding state after prolonged heat stress or during recovery could be accelerated by increased levels of heat shock proteins.	tag10-2
61304	2	346232	5	NULL	NULL	0	NULL	heat stress	Process	prolonged	leads to					statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_7	7935376	However, the deactivation of HSF to the non-DNA-binding state after prolonged heat stress or during recovery could be accelerated by increased levels of heat shock proteins.	tag10-2
61305	3	346232	5	NULL	NULL	0	NULL	heat shock proteins	GP	increased levels of	accelerates					HSF	GP	recovery of;;deactivated			NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_7	7935376	However, the deactivation of HSF to the non-DNA-binding state after prolonged heat stress or during recovery could be accelerated by increased levels of heat shock proteins.	tag10-2
61306	1	346233	5	NULL	NULL	0	NULL	heat shock proteins	GP	level of	affects		may			HSF trimers	GP	rate of;;disassembly of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_8	7935376	Hence, the level of heat shock proteins may affect the rate of disassembly of HSF trimers, but another mechanism, as yet undefined, appears to control the onset of the oligomeric transitions.	tag10-2
61307	1	346234	5	NULL	NULL	0	NULL	organisms	Organism		respond to					temperature		elevated			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_9	7935376	Organisms respond to elevated temperatures and to a variety of chemical inducers by rapidly inducing the synthesis of the heat shock proteins (26, 27, 33, 35).	tag10-2
61308	2	346234	5	NULL	NULL	0	NULL	organisms	Organism		induce		rapidly			heat shock proteins	GP	synthesis of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_9	7935376	Organisms respond to elevated temperatures and to a variety of chemical inducers by rapidly inducing the synthesis of the heat shock proteins (26, 27, 33, 35).	tag10-2
61309	3	346234	5	NULL	NULL	0	NULL	statement 1	Process		leads to					statement 2	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_9	7935376	Organisms respond to elevated temperatures and to a variety of chemical inducers by rapidly inducing the synthesis of the heat shock proteins (26, 27, 33, 35).	tag10-2
61310	4	346234	5	NULL	NULL	0	NULL	organisms	Organism		respond to					chemical inducers	Chemical				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_9	7935376	Organisms respond to elevated temperatures and to a variety of chemical inducers by rapidly inducing the synthesis of the heat shock proteins (26, 27, 33, 35).	tag10-2
61311	5	346234	5	NULL	NULL	0	NULL	statement 4	Process		leads to					statement 2	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_9	7935376	Organisms respond to elevated temperatures and to a variety of chemical inducers by rapidly inducing the synthesis of the heat shock proteins (26, 27, 33, 35).	tag10-2
61312	1	346235	5	NULL	NULL	0	NULL	HSF	GP		is					heat shock factor	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_10	7935376	The regulation of this response in eukaryotes is mediated at the transcriptional level by a preexisting transcriptional activator heat shock factor (HSF), which binds to regulatory heat shock elements (HSEs) present upstream of all heat shock genes (28, 29, 48).	tag10-2
61313	2	346235	5	NULL	NULL	0	NULL	HSEs	NucleicAcid		is					heat shock elements	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_10	7935376	The regulation of this response in eukaryotes is mediated at the transcriptional level by a preexisting transcriptional activator heat shock factor (HSF), which binds to regulatory heat shock elements (HSEs) present upstream of all heat shock genes (28, 29, 48).	tag10-2
61314	3	346235	5	NULL	NULL	0	NULL	HSF	GP		bind					HSEs	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_10	7935376	The regulation of this response in eukaryotes is mediated at the transcriptional level by a preexisting transcriptional activator heat shock factor (HSF), which binds to regulatory heat shock elements (HSEs) present upstream of all heat shock genes (28, 29, 48).	tag10-2
61315	4	346235	5	NULL	NULL	0	NULL	HSF	GP		is a type of					transcriptional activator	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_10	7935376	The regulation of this response in eukaryotes is mediated at the transcriptional level by a preexisting transcriptional activator heat shock factor (HSF), which binds to regulatory heat shock elements (HSEs) present upstream of all heat shock genes (28, 29, 48).	tag10-2
61316	5	346235	5	NULL	NULL	0	NULL	HSEs	NucleicAcid		is located					heat shock genes	GP	upstream of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_10	7935376	The regulation of this response in eukaryotes is mediated at the transcriptional level by a preexisting transcriptional activator heat shock factor (HSF), which binds to regulatory heat shock elements (HSEs) present upstream of all heat shock genes (28, 29, 48).	tag10-2
61317	1	346236	5	NULL	NULL	0	NULL	HSE	NucleicAcid		interacts with				NGAAN repeats	HSF	GP				NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_11	7935376	The HSE is composed of contiguous, alternating repeats of the 5-bp sequence NGAAN; three NGAAN repeats are required for high-affinity interaction with HSF (3, 13, 37, 38, 59).	tag10-2
61318	1	346237	5	NULL	NULL	0	NULL	HSF	GP		respond to					heat shock signal 	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_12	7935376	HSF responds to the heat shock signal by the induction of DNAbinding activity and transcriptional competence rather than by increasing its own synthesis (22, 28, 48, 57, 58, 60).	tag10-2
61319	2	346237	5	NULL	NULL	0	NULL	HSF	GP		activates					DNA	NucleicAcid	binding of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_12	7935376	HSF responds to the heat shock signal by the induction of DNAbinding activity and transcriptional competence rather than by increasing its own synthesis (22, 28, 48, 57, 58, 60).	tag10-2
61320	3	346237	5	NULL	NULL	0	NULL	statement 1	Process		leads to					statement 2	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_12	7935376	HSF responds to the heat shock signal by the induction of DNAbinding activity and transcriptional competence rather than by increasing its own synthesis (22, 28, 48, 57, 58, 60).	tag10-2
61321	4	346237	5	NULL	NULL	0	NULL	HSF	GP		induce					transcriptional competence	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_12	7935376	HSF responds to the heat shock signal by the induction of DNAbinding activity and transcriptional competence rather than by increasing its own synthesis (22, 28, 48, 57, 58, 60).	tag10-2
61322	5	346237	5	NULL	NULL	0	NULL	statement 1	Process		leads to					statement 4	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_12	7935376	HSF responds to the heat shock signal by the induction of DNAbinding activity and transcriptional competence rather than by increasing its own synthesis (22, 28, 48, 57, 58, 60).	tag10-2
61323	6	346237	5	NULL	NULL	0	NULL	HSF	GP		does not increase					HSF	GP	synthesis of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_12	7935376	HSF responds to the heat shock signal by the induction of DNAbinding activity and transcriptional competence rather than by increasing its own synthesis (22, 28, 48, 57, 58, 60).	tag10-2
61324	1	346238	5	NULL	NULL	NULL	NULL	HSF	GP		bind		high affinity			HSEs	NucleicAcid				NULL	Drosophila melanogaster	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_13	7935376	For multicellular eukaryotes such as Drosophila melanogaster, vertebrates, and plants, the first stage of HSF activation involves the acquisition of high-affinity binding to HSEs.	tag10-2
61325	2	346238	5	NULL	NULL	NULL	NULL	statement 1	Process		activates					HSF	GP				NULL	Drosophila melanogaster	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_13	7935376	For multicellular eukaryotes such as Drosophila melanogaster, vertebrates, and plants, the first stage of HSF activation involves the acquisition of high-affinity binding to HSEs.	tag10-2
67119	3	346238	5	NULL	NULL	0	NULL	HSF	GP		bind		high affinity			HSEs	NucleicAcid				NULL	vertebrates	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_13	7935376	For multicellular eukaryotes such as Drosophila melanogaster, vertebrates, and plants, the first stage of HSF activation involves the acquisition of high-affinity binding to HSEs.	tag10-2
67120	4	346238	5	NULL	NULL	NULL	NULL	statement 3	Process		activates					HSF	GP				NULL	vertebrates	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_13	7935376	For multicellular eukaryotes such as Drosophila melanogaster, vertebrates, and plants, the first stage of HSF activation involves the acquisition of high-affinity binding to HSEs.	tag10-2
67121	5	346238	5	NULL	NULL	0	NULL	HSF	GP		bind		high affinity			HSEs	NucleicAcid				NULL	plants	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_13	7935376	For multicellular eukaryotes such as Drosophila melanogaster, vertebrates, and plants, the first stage of HSF activation involves the acquisition of high-affinity binding to HSEs.	tag10-2
67122	6	346238	5	NULL	NULL	0	NULL	statement 5	Process		activates					HSF	GP				NULL	plants	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_13	7935376	For multicellular eukaryotes such as Drosophila melanogaster, vertebrates, and plants, the first stage of HSF activation involves the acquisition of high-affinity binding to HSEs.	tag10-2
67123	7	346238	5	NULL	NULL	0	NULL	Drosophila melanogaster	Organism		is a type of					multicellular eukaryote	Organism				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_13	7935376	For multicellular eukaryotes such as Drosophila melanogaster, vertebrates, and plants, the first stage of HSF activation involves the acquisition of high-affinity binding to HSEs.	tag10-2
67124	8	346238	5	NULL	NULL	0	NULL	vertebrates	Organism		is a type of					multicellular eukaryote	Organism				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_13	7935376	For multicellular eukaryotes such as Drosophila melanogaster, vertebrates, and plants, the first stage of HSF activation involves the acquisition of high-affinity binding to HSEs.	tag10-2
67125	9	346238	5	NULL	NULL	0	NULL	plants	Organism		is a type of					multicellular eukaryote	Organism				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_13	7935376	For multicellular eukaryotes such as Drosophila melanogaster, vertebrates, and plants, the first stage of HSF activation involves the acquisition of high-affinity binding to HSEs.	tag10-2
61326	1	346239	5	NULL	NULL	0	NULL	HSF	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_14	7935376	This stress-inducible binding of HSF to DNA is controlled by a monomer-to-trimer transition of HSF protein (4, 44, 55, 56).	tag10-2
61327	2	346239	5	NULL	NULL	0	NULL	stress	Process		induce					statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_14	7935376	This stress-inducible binding of HSF to DNA is controlled by a monomer-to-trimer transition of HSF protein (4, 44, 55, 56).	tag10-2
61328	3	346239	5	NULL	NULL	0	NULL	HSF monomer protein	GP		is converted to					HSF trimer protein	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_14	7935376	This stress-inducible binding of HSF to DNA is controlled by a monomer-to-trimer transition of HSF protein (4, 44, 55, 56).	tag10-2
61329	4	346239	5	NULL	NULL	0	NULL	statement 3	Process		controls					statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_14	7935376	This stress-inducible binding of HSF to DNA is controlled by a monomer-to-trimer transition of HSF protein (4, 44, 55, 56).	tag10-2
61330	1	346240	5	NULL	NULL	0	NULL	HSF monomer	GP	isolated	bind		specifically;;low affinity	DNA-binding domain						NGAAN box	NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_15	7935376	An isolated, monomeric HSF DNA-binding domain is capable of binding specifically to a single NGAAN box, but the affinity of this interaction is relatively low (Kd = 10-7 to 10-8 M) (21).	tag10-2
61331	1	346241	5	NULL	NULL	0	NULL	HSF	GP		undergoes					trimerization	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_16	7935376	Trimerization increases the affinity for the HSE by several orders of magnitude through the assembly of three DNAbinding domains of HSF in one complex, thereby allowing the potential for concurrent interactions with all three NGAAN boxes of the HSE.	tag10-2
61332	1	346242	5	NULL	NULL	0	NULL	HSF trimers	GP		bind					HSE	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_17	7935376	The binding of HSF trimers to the HSE is necessary but apparently not sufficient for transactivation of heat shock promoters.	tag10-2
61333	2	346242	5	NULL	NULL	0	NULL	statement 1	Process		is necessary for					heat shock proteins	GP	transactivation of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_17	7935376	The binding of HSF trimers to the HSE is necessary but apparently not sufficient for transactivation of heat shock promoters.	tag10-2
61334	3	346242	5	NULL	NULL	0	NULL	statement 1	Process		is not sufficient for					heat shock proteins	GP	transactivation of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_17	7935376	The binding of HSF trimers to the HSE is necessary but apparently not sufficient for transactivation of heat shock promoters.	tag10-2
61335	1	346243	5	NULL	NULL	0	NULL	HSF	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_18	7935376	Under certain conditions, binding of mammalian HSF to DNA can be uncoupled from the acquisition of transcriptional activity (17, 20).	tag10-2
61336	1	346244	5	NULL	NULL	0	NULL	HSFs	GP	metazoan	undergoes					secondary activation process	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_19	7935376	It is likely that metazoan HSFs undergo a secondary activation process in addition to the monomer-trimer transition to achieve full competence in transactivation.	tag10-2
61337	2	346244	5	NULL	NULL	0	NULL	HSFs mononer	GP	metazoan	is converted to					HSFs trimer	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_19	7935376	It is likely that metazoan HSFs undergo a secondary activation process in addition to the monomer-trimer transition to achieve full competence in transactivation.	tag10-2
61338	3	346244	5	NULL	NULL	0	NULL	statement 1	Process		is required to achieve					HSF	GP	full competence in transactivation of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_19	7935376	It is likely that metazoan HSFs undergo a secondary activation process in addition to the monomer-trimer transition to achieve full competence in transactivation.	tag10-2
61339	4	346244	5	NULL	NULL	0	NULL	statement 2	Process		is required to achieve					HSF	GP	full competence in transactivation of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_19	7935376	It is likely that metazoan HSFs undergo a secondary activation process in addition to the monomer-trimer transition to achieve full competence in transactivation.	tag10-2
61340	1	346245	5	NULL	NULL	0	NULL	trimeric HSF proteins	GP		bind									cognate sites	NULL	in vivo in Saccharomyces cerevisiae	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_20	7935376	Indeed, regulation at the level ofDNA binding is bypassed in the yeasts Saccharomyces cerevisiae and Kluyveromyces lactis, which possess constitutively trimeric HSF proteins bound to their cognate sites in vivo (16, 18, 49, 50).	tag10-2
61341	2	346245	5	NULL	NULL	0	NULL	trimeric HSF proteins	GP		bind									cognate sites	NULL	in vivo in Kluyveromyces lactis	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_20	7935376	Indeed, regulation at the level ofDNA binding is bypassed in the yeasts Saccharomyces cerevisiae and Kluyveromyces lactis, which possess constitutively trimeric HSF proteins bound to their cognate sites in vivo (16, 18, 49, 50).	tag10-2
61342	1	346246	5	NULL	NULL	0	NULL	heat stress	Process		induce					HSF trimers		transactivation function of;;bound			NULL	S. cerevisiae	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_21	7935376	For S. cerevisiae, it is the transactivation function of bound HSF trimers which is induced upon heat stress, and this activity is correlated with increased phosphorylation at multiple serine and threonine residues (36, 51).	tag10-2
61343	1	346247	5	NULL	NULL	0	NULL	HSF	GP	S. cerevisiae	is masked by			transactivation domain		HSF	GP	internal region of;;S. cerevisiae			NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_22	7935376	The transactivation domain of S. cerevisiae HSF and K lactis HSF is masked by an internal region of the protein that includes a conserved heptapeptide sequence; mutations in this sequence lead to constitutive activity (6, 19, 36, 47).	tag10-2
61344	2	346247	5	NULL	NULL	0	NULL	HSF	GP	internal region of;;S. cerevisiae	constitutes					heptapeptide sequence	AminoAcid	conserved			NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_22	7935376	The transactivation domain of S. cerevisiae HSF and K lactis HSF is masked by an internal region of the protein that includes a conserved heptapeptide sequence; mutations in this sequence lead to constitutive activity (6, 19, 36, 47).	tag10-2
61345	3	346247	5	NULL	NULL	0	NULL	statement 2	Process	mutation of	leads to					HSF	GP	constitutive activity of;;S. cerevisiae			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_22	7935376	The transactivation domain of S. cerevisiae HSF and K lactis HSF is masked by an internal region of the protein that includes a conserved heptapeptide sequence; mutations in this sequence lead to constitutive activity (6, 19, 36, 47).	tag10-2
61346	4	346247	5	NULL	NULL	0	NULL	HSF	GP	K lactis	is masked by			transactivation domain		HSF	GP	internal region of;;K lactis			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_22	7935376	The transactivation domain of S. cerevisiae HSF and K lactis HSF is masked by an internal region of the protein that includes a conserved heptapeptide sequence; mutations in this sequence lead to constitutive activity (6, 19, 36, 47).	tag10-2
61347	5	346247	5	NULL	NULL	0	NULL	HSF	GP	internal region of;;K lactis	constitutes					heptapeptide sequence	AminoAcid	conserved			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_22	7935376	The transactivation domain of S. cerevisiae HSF and K lactis HSF is masked by an internal region of the protein that includes a conserved heptapeptide sequence; mutations in this sequence lead to constitutive activity (6, 19, 36, 47).	tag10-2
61348	6	346247	5	NULL	NULL	0	NULL	statement 5	Process	mutation of	leads to					HSF	GP	constitutive activity of;;K lactis			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_22	7935376	The transactivation domain of S. cerevisiae HSF and K lactis HSF is masked by an internal region of the protein that includes a conserved heptapeptide sequence; mutations in this sequence lead to constitutive activity (6, 19, 36, 47).	tag10-2
61349	1	346249	5	NULL	NULL	0	NULL	HSF	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_24	7935376	The regulation of metazoan HSF binding to DNA is also under negative control.	tag10-2
61350	1	346251	5	NULL	NULL	0	NULL	cellular factors			dictates					HSF	GP	temperature response of 			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_26	7935376	The role of cellular factors in dictating the temperature response of HSF is underscored by the behavior of human HSF1 when the protein is expressed in Drosophila cells, tobacco protoplasts, and frog oocytes.	tag10-2
61351	1	346252	5	NULL	NULL	0	NULL	HSF1	GP	human	is activated at					host heat shock temperature	QuantityOrMeasure				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_27	7935376	In such heterologous cell environments, human HSF1 is activated at the host heat shock temperature, about 10  C below its induction temperature in human cells (4, 8, 53).	tag10-2
61352	1	346253	5	NULL	NULL	0	NULL	HSF monomer	GP	stability of;;latent	is dependent on					HSF	GP		leucine zipper motif;;C-terminal end		NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_28	7935376	These cellular factors may assist in constraining HSF in a latent, monomeric state whose stability is dependent on the integrity of a leucine zipper motif located in the C-terminal end of the protein (41).	tag10-2
61353	1	346254	5	NULL	NULL	0	NULL	HSF	GP		associate with					hsp7O protein	GP				NULL	in vitro	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_29	7935376	While the mechanism of suppression of HSF trimerization is poorly understood in vivo, recent studies have shown an association between HSF and the hsp7O protein in vitro (1, 5, 34, 46).	tag10-2
61354	1	346255	5	NULL	NULL	0	NULL	HSF	GP		activates					DNA	NucleicAcid	binding of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_30	7935376	This association has led to a model for the regulation of the DNA-binding activity of HSF that is principally related to heat shock-induced changes in the level of hsp7O proteins in the cell.	tag10-2
61355	2	346255	5	NULL	NULL	0	NULL	hsp7O proteins	GP	changes in level of	is induced by					heat shock	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_30	7935376	This association has led to a model for the regulation of the DNA-binding activity of HSF that is principally related to heat shock-induced changes in the level of hsp7O proteins in the cell.	tag10-2
61356	3	346255	5	NULL	NULL	0	NULL	statement 1	Process	regulation of	is related to					statement 2	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_30	7935376	This association has led to a model for the regulation of the DNA-binding activity of HSF that is principally related to heat shock-induced changes in the level of hsp7O proteins in the cell.	tag10-2
61357	1	346256	5	NULL	NULL	0	NULL	HSF	GP		associate with					heat shock proteins	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_31	7935376	In this report, we have investigated the association of HSF with heat shock proteins by means of coimmunoprecipitation experiments.	tag10-2
61358	1	346257	5	NULL	NULL	0	NULL	hsp7O	GP		associate with					HSF	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_32	7935376	We find that hsp7O can be associated with HSF, although the extent of the interaction is the same for both the heat-shocked and the unshocked forms of HSF.	tag10-2
61359	1	346258	5	NULL	NULL	0	NULL	HSF	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_33	7935376	We also find that neither transfected cells expressing increased levels of hsp70 nor cells previously induced to express the entire complement of heat shock proteins show significant effects on the induction of HSF binding to DNA.	tag10-2
61360	1	346259	5	NULL	NULL	0	NULL	HSF	GP		activates					DNA	NucleicAcid	binding of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_34	7935376	These results do not support a simple model for the DNA-binding activity of HSF solely controlled by changes in the levels of hsp70 or other heat shock proteins.	tag10-2
61361	2	346259	5	NULL	NULL	0	NULL	hsp70	GP	changes in levels of	controls					statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_34	7935376	These results do not support a simple model for the DNA-binding activity of HSF solely controlled by changes in the levels of hsp70 or other heat shock proteins.	tag10-2
61362	3	346259	5	NULL	NULL	0	NULL	heat shock proteins	GP	changes in level of	controls					statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_34	7935376	These results do not support a simple model for the DNA-binding activity of HSF solely controlled by changes in the levels of hsp70 or other heat shock proteins.	tag10-2
61363	1	346288	5	NULL	NULL	0	NULL	HSF1	GP		complex with					hsp7O					NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_63	7935376	Immunoprecipitation of HSF1-hsp7O complexes.	tag10-2
61364	1	346301	5	NULL	NULL	0	NULL	HSF1	GP	human	associate with					heat shock proteins					NULL	normal HeLa cells	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_76	7935376	Association of human HSF1 with heat shock proteins in normal and heat-shocked HeLa cells.	tag10-2
61365	2	346301	5	NULL	NULL	0	NULL	HSF1	GP	human	associate with					heat shock proteins	GP				NULL	heat-shocked HeLa cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_76	7935376	Association of human HSF1 with heat shock proteins in normal and heat-shocked HeLa cells.	tag10-2
61366	1	346307	5	NULL	NULL	0	NULL	heat shock			effects		potentially			HSF1	GP	phosphorylation state of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_82	7935376	(B) Effect of heat shock on the phosphorylation state of human HSF1.	tag10-2
61367	1	346310	5	NULL	NULL	0	NULL	cellular proteins	GP	radiolabelled	associate with					hHSF1	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_85	7935376	(C) Radiolabeled cellular proteins associating with human HSF1 (hHSF1).	tag10-2
61368	2	346310	5	NULL	NULL	0	NULL	hHSF1	GP		is					human HSF1	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_85	7935376	(C) Radiolabeled cellular proteins associating with human HSF1 (hHSF1).	tag10-2
61369	1	346324	5	NULL	NULL	0	NULL	HSF1	GP		associate with					70-kDa stress proteins	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_99	7935376	RESULTS  Association of HSF1 with 70-kDa stress proteins under normal and heat-shocked conditions.	tag10-2
61370	1	346325	5	NULL	NULL	0	NULL	70-kDa stress proteins	GP		associate with		may			HSF1	GP	human			NULL	HeLa cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_100	7935376	We analyzed the association of the 70-kDa stress proteins with human HSF1, the major heat shock-inducible HSF species in HeLa cells (40), using antiserum specific for human HSF1 in a coimmunoprecipitation assay.	tag10-2
61371	1	346328	5	NULL	NULL	0	NULL	HSF1	GP		undergoes					proteolysis	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_103	7935376	As previously reported (23), human HSF1 migrates as a tight cluster of bands whose mobility after heat shock is retarded (Fig. 1A; this sample shows some proteolysis of HSF1).	tag10-2
61372	1	346329	5	NULL	NULL	0	NULL	HSF	GP		undergoes					phosphorylation	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_104	7935376	This change in the electrophoretic mobility of HSF after heat stress is associated with an increase in phosphorylation of the protein (Fig. 1B).	tag10-2
61373	1	346330	5	NULL	NULL	0	NULL	hsc70	GP		bind					HSF1	GP	human			NULL	HeLa cells	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_105	7935376	We observed that both hsc70 and hsp7O from HeLa cells coimmunoprecipitated with human HSF1, as revealed by closely spaced doublet bands that react with the N27 antibody (Fig. 1A).	tag10-2
61374	2	346330	5	NULL	NULL	0	NULL	hsp7O	GP		bind					HSF1	GP	human			NULL	HeLa cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_105	7935376	We observed that both hsc70 and hsp7O from HeLa cells coimmunoprecipitated with human HSF1, as revealed by closely spaced doublet bands that react with the N27 antibody (Fig. 1A).	tag10-2
61375	1	346331	5	NULL	NULL	0	NULL	70-kDa isoform	GP		is expressed in		significantly			primate cells	Cell				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_106	7935376	hsp7O, the lower band of the doublet, was specifically revealed with the C92 antibody; this stress-inducible 70-kDa isoform is expressed at a significant level in primate cells independent of heat stress (32, 54).	tag10-2
61376	2	346331	5	NULL	NULL	0	NULL	statement 1	Process		is independent of					heat stress					NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_106	7935376	hsp7O, the lower band of the doublet, was specifically revealed with the C92 antibody; this stress-inducible 70-kDa isoform is expressed at a significant level in primate cells independent of heat stress (32, 54).	tag10-2
61377	1	346332	5	NULL	NULL	0	NULL	hsp9O	GP		does not bind					HSF1	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_107	7935376	Precipitation of hsp7O or hsc70 was not observed when preimmune serum was used, and another heat shock protein, hsp9O, was not observed to coimmunoprecipitate with HSF1.	tag10-2
61378	1	346333	5	NULL	NULL	0	NULL	70-kDa stress protein		constitutive;;inducible forms of	associate with		specifically			HSF1	GP				NULL	normal HeLa cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_108	7935376	The data indicate that both the constitutive and inducible forms of the 70-kDa stress protein associate specifically with HSF1 in normal and heat-treated HeLa cells.	tag10-2
61379	2	346333	5	NULL	NULL	0	NULL	70-kDa stress protein	GP	constitutive;;inducible forms of	associate with		specifically			HSF1	GP				NULL	heat-treated HeLa cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_108	7935376	The data indicate that both the constitutive and inducible forms of the 70-kDa stress protein associate specifically with HSF1 in normal and heat-treated HeLa cells.	tag10-2
61380	1	346334	5	NULL	NULL	0	NULL	70-kDa species	GP	32S-labeled	bind					HSF1	GP				NULL	unshocked HeLa cells labeled with [35S]methionine	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_109	7935376	Consistent with these findings, a 32S-labeled 70-kDa species was also found to coimmunoprecipitate with HSF1 when unshocked and heatshocked HeLa cells labeled with [35S]methionine were analyzed (Fig. 1C).	tag10-2
61381	2	346334	5	NULL	NULL	0	NULL	70-kDa species	GP	32S-labeled	bind					HSF1	GP				NULL	heatshocked HeLa cells labeled with [35S]methionine	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_109	7935376	Consistent with these findings, a 32S-labeled 70-kDa species was also found to coimmunoprecipitate with HSF1 when unshocked and heatshocked HeLa cells labeled with [35S]methionine were analyzed (Fig. 1C).	tag10-2
61382	1	346336	5	NULL	NULL	0	NULL	70-kDa stress protein	GP		associate with					HSF1	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_111	7935376	The association between 70-kDa stress protein and HSF1 could not be competed for with unlabeled, exogenous hsc70 protein (Fig. 1D).	tag10-2
61383	2	346336	5	NULL	NULL	0	NULL	hsc70 protein	GP	unlabeled;;exogenous	does not compete with					statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_111	7935376	The association between 70-kDa stress protein and HSF1 could not be competed for with unlabeled, exogenous hsc70 protein (Fig. 1D).	tag10-2
61384	1	346337	5	NULL	NULL	0	NULL	HSF1	GP		associate with					hsp7O	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_112	7935376	Effect of ATP treatment or prolonged heat shock on the association of HSF1 and hsp7O.	tag10-2
61385	2	346337	5	NULL	NULL	0	NULL	ATP	Chemical	treatment	effects		may			statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_112	7935376	Effect of ATP treatment or prolonged heat shock on the association of HSF1 and hsp7O.	tag10-2
61386	3	346337	5	NULL	NULL	0	NULL	heat shock		prolonged	effects		may			statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_112	7935376	Effect of ATP treatment or prolonged heat shock on the association of HSF1 and hsp7O.	tag10-2
61387	1	346338	5	NULL	NULL	0	NULL	HSF1	GP		interacts with		physical			hsp7O	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_113	7935376	To explore the functional significance of the physical interaction between HSF1 and hsp70, we investigated the effects of ATP on the coimmunoprecipitation of the two proteins.	tag10-2
61388	2	346338	5	NULL	NULL	0	NULL	ATP	Chemical		effects		may			statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_113	7935376	To explore the functional significance of the physical interaction between HSF1 and hsp70, we investigated the effects of ATP on the coimmunoprecipitation of the two proteins.	tag10-2
61389	1	346340	5	NULL	NULL	0	NULL	hsp7O	GP		associate with					HSF1	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_115	7935376	As shown in Fig. 2, the amount of hsp70 associated with HSF1 was not substantially decreased when extracts were treated with ATP.	tag10-2
61390	2	346340	5	NULL	NULL	0	NULL	ATP	Chemical	treatment	does not decrease		substantially			statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_115	7935376	As shown in Fig. 2, the amount of hsp70 associated with HSF1 was not substantially decreased when extracts were treated with ATP.	tag10-2
61391	1	346342	5	NULL	NULL	0	NULL	HSF1	GP		associate with					hsp7O	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_117	7935376	We also analyzed the possibility of an increased association between HSF1 and hsp70 during prolonged heat stress, which brings about an attenuation of the DNA-binding activity of HSF (2, 42).	tag10-2
61392	2	346342	5	NULL	NULL	0	NULL	heat stress		prolonged	increases		possibly			statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_117	7935376	We also analyzed the possibility of an increased association between HSF1 and hsp70 during prolonged heat stress, which brings about an attenuation of the DNA-binding activity of HSF (2, 42).	tag10-2
61393	3	346342	5	NULL	NULL	0	NULL	HSF	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_117	7935376	We also analyzed the possibility of an increased association between HSF1 and hsp70 during prolonged heat stress, which brings about an attenuation of the DNA-binding activity of HSF (2, 42).	tag10-2
61394	4	346342	5	NULL	NULL	0	NULL	statement 2	Process		attenuate					statement 3	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_117	7935376	We also analyzed the possibility of an increased association between HSF1 and hsp70 during prolonged heat stress, which brings about an attenuation of the DNA-binding activity of HSF (2, 42).	tag10-2
61395	1	346343	5	NULL	NULL	0	NULL	HSF1	GP		interacts with					hsp7O	GP				NULL	HeLa cells	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_118	7935376	When the interaction between HSF1 and hsp7O was analyzed by immunoprecipitation after a continuous heat shock of HeLa cells for 3 h at 42  C, no significant change in the level of association was observed (Fig. 2).	tag10-2
61396	2	346343	5	NULL	NULL	0	NULL	heat shock		continuous	does not change					statement 1	Process	level of			NULL	HeLa cells	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_118	7935376	When the interaction between HSF1 and hsp7O was analyzed by immunoprecipitation after a continuous heat shock of HeLa cells for 3 h at 42  C, no significant change in the level of association was observed (Fig. 2).	tag10-2
61397	1	346345	5	NULL	NULL	0	NULL	HSF1	GP		activates					DNA	NucleicAcid	binding of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_120	7935376	Hence, the attenuation of DNA-binding activity of HSF1 after prolonged heat shock is apparently not correlated with a measurable increase in the interaction with hsp70 under the conditions of the immunoprecipitation assay.	tag10-2
61398	2	346345	5	NULL	NULL	0	NULL	heat shock		prolonged	attenuate					statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_120	7935376	Hence, the attenuation of DNA-binding activity of HSF1 after prolonged heat shock is apparently not correlated with a measurable increase in the interaction with hsp70 under the conditions of the immunoprecipitation assay.	tag10-2
61399	3	346345	5	NULL	NULL	0	NULL	HSF1	GP		interacts with					hsp7O	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_120	7935376	Hence, the attenuation of DNA-binding activity of HSF1 after prolonged heat shock is apparently not correlated with a measurable increase in the interaction with hsp70 under the conditions of the immunoprecipitation assay.	tag10-2
61400	4	346345	5	NULL	NULL	0	NULL	statement 2	Process		is not corelated with					statement 3	Process	increase in			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_120	7935376	Hence, the attenuation of DNA-binding activity of HSF1 after prolonged heat shock is apparently not correlated with a measurable increase in the interaction with hsp70 under the conditions of the immunoprecipitation assay.	tag10-2
61401	1	346346	5	NULL	NULL	0	NULL	HSF1	GP		interacts with					70-kDa stress proteins	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_121	7935376	Interaction between HSF1 and 70-kDa stress proteins in vitro does not affect DNA-binding activity.	tag10-2
61402	1	346347	5	NULL	NULL	0	NULL	HSF1	GP	bacterially expressed;;purified	bind					DNA	NucleicAcid				NULL	in vitro	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_122	7935376	To assess the role of 70-kDa stress proteins on the DNA-binding activity of HSF1 in vitro, purified bovine hsc70 active as uncoating ATPase (15) was incubated with purified, bacterially expressed HSF1.	tag10-2
61403	2	346347	5	NULL	NULL	0	NULL	hsc70	GP	purified;;bovine	plays a role in		may			statement 1	Process				NULL	in vitro	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_122	7935376	To assess the role of 70-kDa stress proteins on the DNA-binding activity of HSF1 in vitro, purified bovine hsc70 active as uncoating ATPase (15) was incubated with purified, bacterially expressed HSF1.	tag10-2
61405	3	346347	5	NULL	NULL	0	NULL	hsc70	GP		is a type of					70-kDa stress proteins	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_122	7935376	To assess the role of 70-kDa stress proteins on the DNA-binding activity of HSF1 in vitro, purified bovine hsc70 active as uncoating ATPase (15) was incubated with purified, bacterially expressed HSF1.	tag10-2
61404	1	346348	5	NULL	NULL	0	NULL	hsc70	GP		associate with					HSF1- DNA complex	GP				NULL	in vitro	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_123	7935376	As shown by a gel mobility shift assay, the addition of hsc7O caused a retardation in the mobility of the HSF1-DNA complex, suggesting an association between hsc70 and the HSF1- DNA complex in vitro.	tag10-2
61406	1	346349	5	NULL	NULL	0	NULL	HSF1	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_124	7935376	However, this interaction did not lead to a change in the amount of HSF1 bound to DNA (Fig. 3).	tag10-2
61407	1	346352	5	NULL	NULL	0	NULL	HSF1	GP		interacts with					hsc70	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_127	7935376	The results indicate that there is an interaction between HSF1 and hsc70, but this interaction does not significantly affect the DNA-binding activity of HSF1.	tag10-2
61408	2	346352	5	NULL	NULL	0	NULL	HSF1	GP		activates					DNA	NucleicAcid	binding of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_127	7935376	The results indicate that there is an interaction between HSF1 and hsc70, but this interaction does not significantly affect the DNA-binding activity of HSF1.	tag10-2
61409	3	346352	5	NULL	NULL	0	NULL	statement 1	Process		does not affect		significantly			statement 2	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_127	7935376	The results indicate that there is an interaction between HSF1 and hsc70, but this interaction does not significantly affect the DNA-binding activity of HSF1.	tag10-2
61410	1	346354	5	NULL	NULL	0	NULL	HSF1	GP	human	interacts with					70-kDa stress proteins	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_129	7935376	Effect of ATP and prolonged heat shock on the interaction between human HSF1 and 70-kDa stress proteins.	tag10-2
61411	2	346354	5	NULL	NULL	0	NULL	ATP	Chemical		effects		possibly			statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_129	7935376	Effect of ATP and prolonged heat shock on the interaction between human HSF1 and 70-kDa stress proteins.	tag10-2
61412	3	346354	5	NULL	NULL	0	NULL	heat shock		prolonged	effects		possibly			statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_129	7935376	Effect of ATP and prolonged heat shock on the interaction between human HSF1 and 70-kDa stress proteins.	tag10-2
61413	1	346361	5	NULL	NULL	0	NULL	70-kDa stress protein	GP		effects					HSF1	GP	activity of			NULL	in vitro	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_136	7935376	Effect of 70-kDa stress protein on HSF1 activity in vitro.	tag10-2
61414	1	346366	5	NULL	NULL	0	NULL	HSF1	GP	induction of;;activity of	is not effected by					hsp7O	GP	elevated			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_141	7935376	No effect of elevated hsp7O and heat shock protein levels on induction of HSF1 activity.	tag10-2
61415	2	346366	5	NULL	NULL	0	NULL	HSF1	GP	induction of;;activity of	is not effected by					heat shock protein	GP	level of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_141	7935376	No effect of elevated hsp7O and heat shock protein levels on induction of HSF1 activity.	tag10-2
61416	1	346367	5	NULL	NULL	0	NULL	HSF1	GP	endogenous	activates					DNA	NucleicAcid	binding of			NULL	in vivo rat fibroblast cell line	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_142	7935376	To assess the role of hsp70 on the DNA-binding activity of HSF1 in vivo, we analyzed the induction of the DNA-binding activity of the endogenous HSF in a rat fibroblast cell line (Ratl) and in the same cell line stably transfected and constitutively expressing the human hsp7O protein (M21 cells [24]).	tag10-2
61417	2	346367	5	NULL	NULL	0	NULL	hsp70	GP	human	plays a role in		possibly			statement 1	Process				NULL	in vivo rat fibroblast cell line	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_142	7935376	To assess the role of hsp70 on the DNA-binding activity of HSF1 in vivo, we analyzed the induction of the DNA-binding activity of the endogenous HSF in a rat fibroblast cell line (Ratl) and in the same cell line stably transfected and constitutively expressing the human hsp7O protein (M21 cells [24]).	tag10-2
61418	3	346367	5	NULL	NULL	0	NULL	Ratl	Cell		is					rat fibroblast cell line	Cell				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_142	7935376	To assess the role of hsp70 on the DNA-binding activity of HSF1 in vivo, we analyzed the induction of the DNA-binding activity of the endogenous HSF in a rat fibroblast cell line (Ratl) and in the same cell line stably transfected and constitutively expressing the human hsp7O protein (M21 cells [24]).	tag10-2
61419	1	346368	5	NULL	NULL	0	NULL	HSF	GP		activates					DNA	NucleicAcid	binding of			NULL	Ratl cells	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_143	7935376	We also analyzed the DNA-binding activity of HSF in Ratl cells rendered thermotolerant by heat shock at 45  C for 15 min followed by recovery for 16 h at 37  C.	tag10-2
61420	2	346368	5	NULL	NULL	0	NULL	statement 1	Process		is rendered					thermotolerant	Process				NULL	Ratl cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_143	7935376	We also analyzed the DNA-binding activity of HSF in Ratl cells rendered thermotolerant by heat shock at 45  C for 15 min followed by recovery for 16 h at 37  C.	tag10-2
61421	3	346368	5	NULL	NULL	0	NULL	heat shock	QuantityOrMeasure		plays a role in					statement 2	Process				NULL	Ratl cells	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_143	7935376	We also analyzed the DNA-binding activity of HSF in Ratl cells rendered thermotolerant by heat shock at 45  C for 15 min followed by recovery for 16 h at 37  C.	tag10-2
61422	1	346369	5	NULL	NULL	0	NULL	lTRatl	Cell		is					thermotolerant Ratl cells	Cell				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_144	7935376	These thermotolerant Ratl (lTRatl) cells have elevated levels of the entire complement of heat shock proteins and allow an assessment of whether the increased levels affect the level of the DNA-binding activity in vivo (30).	tag10-2
61423	2	346369	5	NULL	NULL	0	NULL	lTRatl	Cell		contains					heat shock proteins	GP	elevated levels of;;entire complement of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_144	7935376	These thermotolerant Ratl (lTRatl) cells have elevated levels of the entire complement of heat shock proteins and allow an assessment of whether the increased levels affect the level of the DNA-binding activity in vivo (30).	tag10-2
61424	1	346370	5	NULL	NULL	0	NULL	HSF1	GP		activates					DNA	NucleicAcid	binding of			NULL	Ratl cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_145	7935376	As shown by the gel mobility shift assay in Fig. 4A, we did not observe significant differences in the levels of DNAbinding activity of HSF1 in extracts prepared from Ratl, TFRatl, or M21 cells after 30 min of heat shock at 42  C.	tag10-2
61425	2	346370	5	NULL	NULL	0	NULL	HSF1	GP		activates					DNA	NucleicAcid	binding of			NULL	TFRatl	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_145	7935376	As shown by the gel mobility shift assay in Fig. 4A, we did not observe significant differences in the levels of DNAbinding activity of HSF1 in extracts prepared from Ratl, TFRatl, or M21 cells after 30 min of heat shock at 42  C.	tag10-2
61426	3	346370	5	NULL	NULL	0	NULL	HSF1	GP		activates					DNA	NucleicAcid	binding of			NULL	M21 cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_145	7935376	As shown by the gel mobility shift assay in Fig. 4A, we did not observe significant differences in the levels of DNAbinding activity of HSF1 in extracts prepared from Ratl, TFRatl, or M21 cells after 30 min of heat shock at 42  C.	tag10-2
61427	1	346374	5	NULL	NULL	0	NULL	Ratl cells	Cell	unstressed	contains					hsc70 protein	GP	endogenous			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_149	7935376	As shown in this experiment, unstressed Ratl cells contain endogenous hsc70 protein, while TTRatl cells have the same amount of hsc70 and approximately half that of hsp70 (lower band) accumulated as a result of thermotolerance.	tag10-2
61428	2	346374	5	NULL	NULL	0	NULL	TTRatl cells	Cell		contains					hsc70	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_149	7935376	As shown in this experiment, unstressed Ratl cells contain endogenous hsc70 protein, while TTRatl cells have the same amount of hsc70 and approximately half that of hsp70 (lower band) accumulated as a result of thermotolerance.	tag10-2
61429	3	346374	5	NULL	NULL	0	NULL	TTRatl cells	Cell		contains					hsp70	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_149	7935376	As shown in this experiment, unstressed Ratl cells contain endogenous hsc70 protein, while TTRatl cells have the same amount of hsc70 and approximately half that of hsp70 (lower band) accumulated as a result of thermotolerance.	tag10-2
61430	4	346374	5	NULL	NULL	0	NULL	thermotolerance	Process		leads to					statement 3	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_149	7935376	As shown in this experiment, unstressed Ratl cells contain endogenous hsc70 protein, while TTRatl cells have the same amount of hsc70 and approximately half that of hsp70 (lower band) accumulated as a result of thermotolerance.	tag10-2
61431	1	346375	5	NULL	NULL	0	NULL	M21 cells	Cell		contains					hsc70	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_150	7935376	M21 cells contain a level of hsc70 similar to that of Ratl and lTRat 1 cells, along with a comparable amount of human hsp7o (lower band).	tag10-2
61432	2	346375	5	NULL	NULL	0	NULL	M21 cells	Cell		contains					hsp70	GP	human			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_150	7935376	M21 cells contain a level of hsc70 similar to that of Ratl and lTRat 1 cells, along with a comparable amount of human hsp7o (lower band).	tag10-2
61433	3	346375	5	NULL	NULL	0	NULL	Ratl cells	Cell		contains					hsc70	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_150	7935376	M21 cells contain a level of hsc70 similar to that of Ratl and lTRat 1 cells, along with a comparable amount of human hsp7o (lower band).	tag10-2
61434	4	346375	5	NULL	NULL	0	NULL	lTRat 1 cells	Cell		contains					hsc70	GP				NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_150	7935376	M21 cells contain a level of hsc70 similar to that of Ratl and lTRat 1 cells, along with a comparable amount of human hsp7o (lower band).	tag10-2
61435	1	346376	5	NULL	NULL	0	NULL	HSF	GP	endogenous	activates					DNA	NucleicAcid	binding of			NULL	M21 cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_151	7935376	Thus, an artificial increase in the level of hsp70 protein approximating that found physiologically after a heat stress does not lead to an inhibition of the DNA-binding activity of the endogenous HSF when the M21 cells were subjected to a heat stress.	tag10-2
61436	2	346376	5	NULL	NULL	0	NULL	hsp70 protein	GP	artificial increase in level of	does not inhibit					statement 1	Process				NULL	M21 cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_151	7935376	Thus, an artificial increase in the level of hsp70 protein approximating that found physiologically after a heat stress does not lead to an inhibition of the DNA-binding activity of the endogenous HSF when the M21 cells were subjected to a heat stress.	tag10-2
61437	3	346376	5	NULL	NULL	0	NULL	M21 cells	Cell		subjected to					heat stress					NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_151	7935376	Thus, an artificial increase in the level of hsp70 protein approximating that found physiologically after a heat stress does not lead to an inhibition of the DNA-binding activity of the endogenous HSF when the M21 cells were subjected to a heat stress.	tag10-2
61438	4	346376	5	NULL	NULL	0	NULL	statement 3	Process		leads to					statement 2	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_151	7935376	Thus, an artificial increase in the level of hsp70 protein approximating that found physiologically after a heat stress does not lead to an inhibition of the DNA-binding activity of the endogenous HSF when the M21 cells were subjected to a heat stress.	tag10-2
61439	1	346379	5	NULL	NULL	0	NULL	HSF1	GP		activates					DNA	NucleicAcid	binding of			NULL	lTRatl cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_154	7935376	The only detectable effect of increased heat shock protein levels on HSF1 activity was a modest decrease (about 30%) in the DNAbinding activity after prolonged heat shock oflTRatl cells for 90 min, while Ratl and M21 cells showed a 10% decrease in the DNA-binding activity of HSF (Fig. 4; also see below).	tag10-2
61440	2	346379	5	NULL	NULL	0	NULL	heat shock		prolonged	decreases		modest			statement 1	Process				NULL	lTRatl cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_154	7935376	The only detectable effect of increased heat shock protein levels on HSF1 activity was a modest decrease (about 30%) in the DNAbinding activity after prolonged heat shock oflTRatl cells for 90 min, while Ratl and M21 cells showed a 10% decrease in the DNA-binding activity of HSF (Fig. 4; also see below).	tag10-2
61441	3	346379	5	NULL	NULL	0	NULL	HSF	GP		activates					DNA	NucleicAcid	binding of			NULL	Ratl cells	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_154	7935376	The only detectable effect of increased heat shock protein levels on HSF1 activity was a modest decrease (about 30%) in the DNAbinding activity after prolonged heat shock oflTRatl cells for 90 min, while Ratl and M21 cells showed a 10% decrease in the DNA-binding activity of HSF (Fig. 4; also see below).	tag10-2
61442	4	346379	5	NULL	NULL	0	NULL	heat shock		prolonged	decreases					statement 3	Process				NULL	Ratl cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_154	7935376	The only detectable effect of increased heat shock protein levels on HSF1 activity was a modest decrease (about 30%) in the DNAbinding activity after prolonged heat shock oflTRatl cells for 90 min, while Ratl and M21 cells showed a 10% decrease in the DNA-binding activity of HSF (Fig. 4; also see below).	tag10-2
61443	5	346379	5	NULL	NULL	0	NULL	HSF	GP		activates					DNA	NucleicAcid	binding of			NULL	M21 cells	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_154	7935376	The only detectable effect of increased heat shock protein levels on HSF1 activity was a modest decrease (about 30%) in the DNAbinding activity after prolonged heat shock oflTRatl cells for 90 min, while Ratl and M21 cells showed a 10% decrease in the DNA-binding activity of HSF (Fig. 4; also see below).	tag10-2
61444	6	346379	5	NULL	NULL	0	NULL	heat shock		prolonged	decreases					statement 5	Process				NULL	M21 cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_154	7935376	The only detectable effect of increased heat shock protein levels on HSF1 activity was a modest decrease (about 30%) in the DNAbinding activity after prolonged heat shock oflTRatl cells for 90 min, while Ratl and M21 cells showed a 10% decrease in the DNA-binding activity of HSF (Fig. 4; also see below).	tag10-2
61445	2	346385	5	NULL	NULL	0	NULL	heat shock proteins	GP	elevated expression of	accelerates					statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_160	7935376	Elevated expression of heat shock proteins accelerates decrease of HSF1 DNA-binding activity during recovery.	tag10-2
61446	1	346385	5	NULL	NULL	0	NULL	HSF1	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_160	7935376	Elevated expression of heat shock proteins accelerates decrease of HSF1 DNA-binding activity during recovery.	tag10-2
61447	3	346385	5	NULL	NULL	0	NULL	statement 2	Process		occurs during					recovery	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_160	7935376	Elevated expression of heat shock proteins accelerates decrease of HSF1 DNA-binding activity during recovery.	tag10-2
61448	1	346386	5	NULL	NULL	0	NULL	HSF1	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_161	7935376	Although there was no detectable effect of increased hsp70 and heat shock protein levels on induction of the DNA-binding activity of HSF1, we did observe a reproducible effect of heat shock protein levels on the kinetics of recovery from heat shock.	tag10-2
61449	2	346386	5	NULL	NULL	0	NULL	hsp70	GP	increased levels of	does not effect					statement 1	Process	induction of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_161	7935376	Although there was no detectable effect of increased hsp70 and heat shock protein levels on induction of the DNA-binding activity of HSF1, we did observe a reproducible effect of heat shock protein levels on the kinetics of recovery from heat shock.	tag10-2
61450	3	346386	5	NULL	NULL	0	NULL	heat shock proteins	GP	increased levels of	does not effect					statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_161	7935376	Although there was no detectable effect of increased hsp70 and heat shock protein levels on induction of the DNA-binding activity of HSF1, we did observe a reproducible effect of heat shock protein levels on the kinetics of recovery from heat shock.	tag10-2
61451	4	346386	5	NULL	NULL	0	NULL	heat shock		recovery from	effects					heat shock proteins	GP	levels of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_161	7935376	Although there was no detectable effect of increased hsp70 and heat shock protein levels on induction of the DNA-binding activity of HSF1, we did observe a reproducible effect of heat shock protein levels on the kinetics of recovery from heat shock.	tag10-2
61452	1	346390	5	NULL	NULL	0	NULL	HSF1	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_165	7935376	As shown in Fig. 5A, the DNA-binding activity of HSF1 was induced to the same extent in all three cell types.	tag10-2
61453	1	346392	5	NULL	NULL	0	NULL	HSF1	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_167	7935376	The DNA-binding activities of HSF1 relative to the amount of HSF1 protein in the Ratl and M21 samples (Fig. 5B) were observed to decrease to 50 and 40%, respectively, of maximal levels at 4 h of recovery.	tag10-2
61454	1	346394	5	NULL	NULL	0	NULL	hsp70	GP	increased levels of	effects		modest			HSF	GP	kinetics of;;deactivation of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_169	7935376	These results show that increased levels of hsp70 alone have a modest effect on the kinetics of HSF deactivation, while a full complement of stress proteins can accelerate recovery to the inactive state (Fig. 5D).	tag10-2
61455	1	346395	5	NULL	NULL	0	NULL	PTRatl cells	Cell	increased rate of recovery in	correlates with					HSF1	GP	reversion to hypophosphorylated form of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_170	7935376	This increased rate of recovery in PTRatl cells is also correlated with a reversion to the hypophosphorylated form of HSF1, as shown by the change in SDS-gel mobility (Fig. SB).	tag10-2
61456	1	346396	5	NULL	NULL	0	NULL	HSF	GP		activates					DNA	NucleicAcid	binding of			NULL	Drosophila cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_171	7935376	Elevated heat shock protein levels accelerate attenuation but do not block induction of HSF DNA-binding activity in Drosophila cells.	tag10-2
61457	2	346396	5	NULL	NULL	0	NULL	heat shock proteins	GP	elevated levels of	accelerates					statement 1	Process	attenuation of			NULL	Drosophila cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_171	7935376	Elevated heat shock protein levels accelerate attenuation but do not block induction of HSF DNA-binding activity in Drosophila cells.	tag10-2
61458	3	346396	5	NULL	NULL	0	NULL	heat shock proteins	GP	elevated levels of	does not block					statement 1	Process	induction of			NULL	Drosophila cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_171	7935376	Elevated heat shock protein levels accelerate attenuation but do not block induction of HSF DNA-binding activity in Drosophila cells.	tag10-2
61459	1	346397	5	NULL	NULL	0	NULL	HSF	GP	endogenous	activates					DNA	NucleicAcid	binding of			NULL	Drosophila SL2 cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_172	7935376	Since the results presented above could be peculiar to Ratl cells, we analyzed the effects of elevated heat shock protein levels on the DNA-binding activity of the endogenous HSF in Drosophila SL2 cells.	tag10-2
61460	2	346397	5	NULL	NULL	0	NULL	heat shock proteins	GP	elevated levels of	effects		possibly			statement 1	Process				NULL	Drosophila SL2 cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_172	7935376	Since the results presented above could be peculiar to Ratl cells, we analyzed the effects of elevated heat shock protein levels on the DNA-binding activity of the endogenous HSF in Drosophila SL2 cells.	tag10-2
61461	1	346398	5	NULL	NULL	0	NULL	HSF	GP	Drosophila	activates					DNA	NucleicAcid	binding of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_173	7935376	We first investigated the effects of prolonged heat shock on the DNA-binding activity of Drosophila HSF.	tag10-2
61462	2	346398	5	NULL	NULL	0	NULL	heat shock		prolonged	effects		possibly			statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_173	7935376	We first investigated the effects of prolonged heat shock on the DNA-binding activity of Drosophila HSF.	tag10-2
61463	1	346402	5	NULL	NULL	0	NULL	heat shock proteins	GP	elevated levels of	effects		potentially			HSF	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_177	7935376	Thus, the potential effects of elevated heat shock protein levels are operative on HSF only under moderate heat stress.	tag10-2
61464	2	346402	5	NULL	NULL	0	NULL	statement 1	Process		occurs during		only			heat stress	Process	moderate			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_177	7935376	Thus, the potential effects of elevated heat shock protein levels are operative on HSF only under moderate heat stress.	tag10-2
61465	1	346403	5	NULL	NULL	0	NULL	HSF	GP	Drosophila	is deactivated under		possibly			stress conditions	Process	moderate			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_178	7935376	To further investigate the kinetics of Drosophila HSF deactivation under moderate stress conditions, we analyzed the DNA-binding activity of HSF in thermotolerant SL2 (TTSL2) cells (which were previously induced to express heat shock proteins with a 20-min incubation at 37.5  C and a 5-h recovery at 22  C).	tag10-2
61466	1	346404	5	NULL	NULL	0	NULL	cycloheximide	Chemical		prevents					heat shock proteins	GP	de novo synthesis of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_179	7935376	Cells were treated with cycloheximide 30 min before the start of the 34.5  C heat shock to prevent de novo synthesis of heat shock proteins in the course of the continuous heat stress.	tag10-2
61467	1	346405	5	NULL	NULL	0	NULL	HSF	GP	Drosophila	activates					DNA	NucleicAcid	binding of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_180	7935376	As shown by the gel shift assay and Western blotting, the DNA binding activity of Drosophila HSF relative to the amount of HSF protein was not significantly affected when TISL2 cells heat shocked for 15 min were compared with nonthermotolerant SL2 cells stressed similarly (Fig. 7A and B).	tag10-2
61468	2	346405	5	NULL	NULL	0	NULL	statement 1	Process		relative to					HSF protein	GP	amount of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_180	7935376	As shown by the gel shift assay and Western blotting, the DNA binding activity of Drosophila HSF relative to the amount of HSF protein was not significantly affected when TISL2 cells heat shocked for 15 min were compared with nonthermotolerant SL2 cells stressed similarly (Fig. 7A and B).	tag10-2
61469	3	346405	5	NULL	NULL	0	NULL	TISL2 cells	Cell	heat shocked	does not effect					statement 2	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_180	7935376	As shown by the gel shift assay and Western blotting, the DNA binding activity of Drosophila HSF relative to the amount of HSF protein was not significantly affected when TISL2 cells heat shocked for 15 min were compared with nonthermotolerant SL2 cells stressed similarly (Fig. 7A and B).	tag10-2
61470	2	346407	5	NULL	NULL	0	NULL	statement 1		faster decay of	in the absence of					cycloheximide	Chemical				NULL	1TSL2 cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_182	7935376	A faster decay of the DNA-binding activity of HSF was also observed when 1TSL2 cells were analyzed in the absence of cycloheximide (data not shown).	tag10-2
61471	1	346407	5	NULL	NULL	0	NULL	HSF	GP		activates					DNA	NucleicAcid	binding of			NULL	1TSL2 cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_182	7935376	A faster decay of the DNA-binding activity of HSF was also observed when 1TSL2 cells were analyzed in the absence of cycloheximide (data not shown).	tag10-2
61472	1	346408	5	NULL	NULL	0	NULL	HSF	GP	Drosophila	activates					DNA	NucleicAcid	binding of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_183	7935376	Hence, the presence of previously synthesized heat shock proteins is correlated with an increased rate of attenuation but not with an inhibition of the DNA-binding activity of Drosophila HSF.	tag10-2
61473	2	346408	5	NULL	NULL	0	NULL	heat shock proteins	GP	presence of;;previously synthesized	corelates with					statement 1	Process	increased rate of;;attenuation of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_183	7935376	Hence, the presence of previously synthesized heat shock proteins is correlated with an increased rate of attenuation but not with an inhibition of the DNA-binding activity of Drosophila HSF.	tag10-2
61474	3	346408	5	NULL	NULL	0	NULL	heat shock proteins	GP	presence of;;previously synthesized	doet not corelate with					statement 1	Process	inhibition of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_183	7935376	Hence, the presence of previously synthesized heat shock proteins is correlated with an increased rate of attenuation but not with an inhibition of the DNA-binding activity of Drosophila HSF.	tag10-2
61475	1	346410	5	NULL	NULL	0	NULL	HSF	GP		activates					DNA	NucleicAcid	binding of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_185	7935376	(A to C) Accelerated decrease of HSF DNA-binding activity during recovery from heat shock.	tag10-2
61476	2	346410	5	NULL	NULL	0	NULL	statement 1	Process	accelerated decrease of	occurs during					heat shock		recovery from			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_185	7935376	(A to C) Accelerated decrease of HSF DNA-binding activity during recovery from heat shock.	tag10-2
61477	1	346416	5	NULL	NULL	0	NULL	cell	Cell		measures					thermal stress		level of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_191	7935376	DISCUSSION  The intracellular level of free heat shock proteins in general, and the hsp70 protein family in particular, has been suggested to be part of an autoregulatory loop by which the cell measures the level of thermal stress (10, 11).	tag10-2
61478	2	346416	5	NULL	NULL	0	NULL	autoregulatory loop	Process		plays a role in					statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_191	7935376	DISCUSSION  The intracellular level of free heat shock proteins in general, and the hsp70 protein family in particular, has been suggested to be part of an autoregulatory loop by which the cell measures the level of thermal stress (10, 11).	tag10-2
61479	3	346416	5	NULL	NULL	0	NULL	heat shock proteins	GP	intracellular level of;;free	is a part of		potentially			statement 2	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_191	7935376	DISCUSSION  The intracellular level of free heat shock proteins in general, and the hsp70 protein family in particular, has been suggested to be part of an autoregulatory loop by which the cell measures the level of thermal stress (10, 11).	tag10-2
61480	4	346416	5	NULL	NULL	0	NULL	hsp70 protein family	GP		is a part of		potentially			statement 2	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_191	7935376	DISCUSSION  The intracellular level of free heat shock proteins in general, and the hsp70 protein family in particular, has been suggested to be part of an autoregulatory loop by which the cell measures the level of thermal stress (10, 11).	tag10-2
61481	1	346417	5	NULL	NULL	0	NULL	HSF	GP		bind					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_192	7935376	This autoregulatory loop has been proposed to affect the DNA-binding and trimerization of HSF.	tag10-2
61482	2	346417	5	NULL	NULL	0	NULL	HSF	GP		undergoes					trimerization	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_192	7935376	This autoregulatory loop has been proposed to affect the DNA-binding and trimerization of HSF.	tag10-2
61483	3	346417	5	NULL	NULL	0	NULL	autoregulatory loop	Process		affects		potentially			statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_192	7935376	This autoregulatory loop has been proposed to affect the DNA-binding and trimerization of HSF.	tag10-2
61484	4	346417	5	NULL	NULL	0	NULL	autoregulatory loop			affects		potentially			statement 2	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_192	7935376	This autoregulatory loop has been proposed to affect the DNA-binding and trimerization of HSF.	tag10-2
61485	1	346418	5	NULL	NULL	0	NULL	70-kDa stress protein	GP		stabilize					HSF monomer	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_193	7935376	Accordingly, the DNA-binding activity of HSF would be suppressed under normal conditions by the constitutive level of free 70-kDa stress protein, which stabilizes the latent HSF monomer.	tag10-2
61486	2	346418	5	NULL	NULL	0	NULL	HSF	GP		activates					DNA	NucleicAcid	binding of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_193	7935376	Accordingly, the DNA-binding activity of HSF would be suppressed under normal conditions by the constitutive level of free 70-kDa stress protein, which stabilizes the latent HSF monomer.	tag10-2
61487	3	346418	5	NULL	NULL	0	NULL	70-kDa stress protein	GP	constitutive level of;;free	suppress					statement 2	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_193	7935376	Accordingly, the DNA-binding activity of HSF would be suppressed under normal conditions by the constitutive level of free 70-kDa stress protein, which stabilizes the latent HSF monomer.	tag10-2
61488	1	346419	5	NULL	NULL	0	NULL	heat shock		onset of	decreases					70-kDa stress protein	GP	level of;;free			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_194	7935376	As a consequence of the decreased level of free 70-kDa stress protein at the onset of heat shock, the monomeric form of HSF is able to trimerize, leading to high-affinity binding to HSEs and the initiation of the pathway for heat shock protein synthesis.	tag10-2
61489	2	346419	5	NULL	NULL	0	NULL	HSF monomer	GP		undergoes					trimerization	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_194	7935376	As a consequence of the decreased level of free 70-kDa stress protein at the onset of heat shock, the monomeric form of HSF is able to trimerize, leading to high-affinity binding to HSEs and the initiation of the pathway for heat shock protein synthesis.	tag10-2
61490	3	346419	5	NULL	NULL	0	NULL	statement 1	Process		leads to					statement 2	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_194	7935376	As a consequence of the decreased level of free 70-kDa stress protein at the onset of heat shock, the monomeric form of HSF is able to trimerize, leading to high-affinity binding to HSEs and the initiation of the pathway for heat shock protein synthesis.	tag10-2
61491	4	346419	5	NULL	NULL	0	NULL	HSF trimer	GP		bind		high affinity			HSEs	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_194	7935376	As a consequence of the decreased level of free 70-kDa stress protein at the onset of heat shock, the monomeric form of HSF is able to trimerize, leading to high-affinity binding to HSEs and the initiation of the pathway for heat shock protein synthesis.	tag10-2
61492	5	346419	5	NULL	NULL	0	NULL	statement 2	Process		leads to					statement 4	Process				NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_194	7935376	As a consequence of the decreased level of free 70-kDa stress protein at the onset of heat shock, the monomeric form of HSF is able to trimerize, leading to high-affinity binding to HSEs and the initiation of the pathway for heat shock protein synthesis.	tag10-2
61493	6	346419	5	NULL	NULL	0	NULL	statement 4	Process		initiates					heat shock protein 	GP	pathway for;;synthesis of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_194	7935376	As a consequence of the decreased level of free 70-kDa stress protein at the onset of heat shock, the monomeric form of HSF is able to trimerize, leading to high-affinity binding to HSEs and the initiation of the pathway for heat shock protein synthesis.	tag10-2
61494	1	346420	5	NULL	NULL	0	NULL	HSF monomers	GP		is in equilibrium with					HSF trimers	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_195	7935376	The ensuing increase in heat shock protein levels drives the equilibrium between HSF monomers and trimers toward the monomeric species, thus reestablishing the inert form of the transcription factor (5, 9, 31, 34).	tag10-2
61495	2	346420	5	NULL	NULL	0	NULL	statement 1	Process		is driven towards					HSF monomers	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_195	7935376	The ensuing increase in heat shock protein levels drives the equilibrium between HSF monomers and trimers toward the monomeric species, thus reestablishing the inert form of the transcription factor (5, 9, 31, 34).	tag10-2
61496	3	346420	5	NULL	NULL	0	NULL	heat shock proteins	GP	increased levels of	is required for					statement 2	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_195	7935376	The ensuing increase in heat shock protein levels drives the equilibrium between HSF monomers and trimers toward the monomeric species, thus reestablishing the inert form of the transcription factor (5, 9, 31, 34).	tag10-2
61497	4	346420	5	NULL	NULL	0	NULL	statement 3			reestablishes					HSF	GP	inert form of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_195	7935376	The ensuing increase in heat shock protein levels drives the equilibrium between HSF monomers and trimers toward the monomeric species, thus reestablishing the inert form of the transcription factor (5, 9, 31, 34).	tag10-2
61498	5	346420	5	NULL	NULL	0	NULL	HSF	GP		is a type of					transcription factor					NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_195	7935376	The ensuing increase in heat shock protein levels drives the equilibrium between HSF monomers and trimers toward the monomeric species, thus reestablishing the inert form of the transcription factor (5, 9, 31, 34).	tag10-2
61499	1	346422	5	NULL	NULL	0	NULL	HSF	GP	Drosophila	activates					DNA	NucleicAcid	binding of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_197	7935376	DNA-binding activity of Drosophila HSF is attenuated during prolonged heat shock.	tag10-2
61500	2	346422	5	NULL	NULL	0	NULL	heat shock		prolonged	attenuate					statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_197	7935376	DNA-binding activity of Drosophila HSF is attenuated during prolonged heat shock.	tag10-2
61501	1	346425	5	NULL	NULL	0	NULL	HSF	GP		activates					DNA	NucleicAcid	binding of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_200	7935376	A prediction of this model is that an artificial elevation of heat shock proteins to the level observed after heat shock should inhibit induction of the DNA-binding activity of HSF.	tag10-2
61502	2	346425	5	NULL	NULL	0	NULL	heat shock proteins	GP	artificial elevation of	inhibits					statement 1	Process	induction of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_200	7935376	A prediction of this model is that an artificial elevation of heat shock proteins to the level observed after heat shock should inhibit induction of the DNA-binding activity of HSF.	tag10-2
61505	1	346426	5	NULL	NULL	0	NULL	HSF	GP	endogenous	activates					DNA	NucleicAcid	binding of			NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_201	7935376	Our test of this prediction with rat M21 cells constitutively expressing hsp70 at a level close to that found physiologically after heat shock and with ITRatl cells expressing a full complement of heat shock proteins indicates that elevated concentrations of hsp7O, alone or in combination with the other heat shock proteins, do not significantly block induction of the DNA-binding activity of the endogenous HSF.	tag10-2
61506	2	346426	5	NULL	NULL	0	NULL	hsp7O	GP	elevated concentrations of	does not block		significantly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_201	7935376	Our test of this prediction with rat M21 cells constitutively expressing hsp70 at a level close to that found physiologically after heat shock and with ITRatl cells expressing a full complement of heat shock proteins indicates that elevated concentrations of hsp7O, alone or in combination with the other heat shock proteins, do not significantly block induction of the DNA-binding activity of the endogenous HSF.	tag10-2
61507	3	346426	5	NULL	NULL	0	NULL	heat shock proteins	GP	full complement of	does not block		significantly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_201	7935376	Our test of this prediction with rat M21 cells constitutively expressing hsp70 at a level close to that found physiologically after heat shock and with ITRatl cells expressing a full complement of heat shock proteins indicates that elevated concentrations of hsp7O, alone or in combination with the other heat shock proteins, do not significantly block induction of the DNA-binding activity of the endogenous HSF.	tag10-2
61508	1	346427	5	NULL	NULL	0	NULL	HSF monomers	GP		is in equilibrium with					HSF trimers	GP				NULL	Drosophila TTSL2 cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_202	7935376	Similar findings with Drosophila TTSL2 cells suggest that in general,the equilibrium between HSF monomers and trimers is not solely sensitive to changes in the concentration of heat shock proteins and that some other mechanism for controlling trimerization and the DNA-binding activity of HSF must exist.	tag10-2
61509	2	346427	5	NULL	NULL	0	NULL	statement 1	Process		is not solely sensitive to					heat shock proteins	GP	changes in the concentration of			NULL	Drosophila TTSL2 cells	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_202	7935376	Similar findings with Drosophila TTSL2 cells suggest that in general,the equilibrium between HSF monomers and trimers is not solely sensitive to changes in the concentration of heat shock proteins and that some other mechanism for controlling trimerization and the DNA-binding activity of HSF must exist.	tag10-2
61510	1	346428	5	NULL	NULL	0	NULL	HSF	GP		is converted to					HSF	GP	non-DNA-bound;;inactive			NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_203	7935376	However, the inactivation of HSF to the non-DNA-binding state is indeed accelerated by the increased levels of heat shock proteins.	tag10-2
61511	2	346428	5	NULL	NULL	0	NULL	heat shock proteins	GP	increased levels of	accelerates					statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_203	7935376	However, the inactivation of HSF to the non-DNA-binding state is indeed accelerated by the increased levels of heat shock proteins.	tag10-2
61512	1	346429	5	NULL	NULL	0	NULL	heat shock proteins	GP		assist		directly			HSF trimer	GP	disassembly of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_204	7935376	This finding confirms previous reports (34, 39) and suggests that heat shock proteins do assist, directly or indirectly, in the disassembly of the HSF trimer.	tag10-2
61513	2	346429	5	NULL	NULL	0	NULL	heat shock proteins	GP		assist		indirectly			HSF trimer	GP	disassembly of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_204	7935376	This finding confirms previous reports (34, 39) and suggests that heat shock proteins do assist, directly or indirectly, in the disassembly of the HSF trimer.	tag10-2
61514	3	346429	5	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_204	7935376	This finding confirms previous reports (34, 39) and suggests that heat shock proteins do assist, directly or indirectly, in the disassembly of the HSF trimer.	tag10-2
61515	1	346430	5	NULL	NULL	0	NULL	hsp70	GP		is sequestered in					granules	CellComponent				NULL	Drosophila cells	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_205	7935376	It should be noted that in a previous study, constitutive overexpression of hsp7O in Drosophila cells led to the sequestration of the protein in granules, where it appears to be irreversibly inactivated and unable to contribute to thermoresistance (12).	tag10-2
61516	2	346430	5	NULL	NULL	0	NULL	hsp70	GP	constitutive overexpression of	leads to					statement 1	Process				NULL	Drosophila cells	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_205	7935376	It should be noted that in a previous study, constitutive overexpression of hsp7O in Drosophila cells led to the sequestration of the protein in granules, where it appears to be irreversibly inactivated and unable to contribute to thermoresistance (12).	tag10-2
61517	3	346430	5	NULL	NULL	0	NULL	hsp70	GP	sequestered	is inactivated in		irreversibly			granules	CellComponent				NULL	Drosophila cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_205	7935376	It should be noted that in a previous study, constitutive overexpression of hsp7O in Drosophila cells led to the sequestration of the protein in granules, where it appears to be irreversibly inactivated and unable to contribute to thermoresistance (12).	tag10-2
61518	4	346430	5	NULL	NULL	0	NULL	hsp70	GP	sequestered	does not contribute to					thermoresistance	Process				NULL	Drosophila cells	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_205	7935376	It should be noted that in a previous study, constitutive overexpression of hsp7O in Drosophila cells led to the sequestration of the protein in granules, where it appears to be irreversibly inactivated and unable to contribute to thermoresistance (12).	tag10-2
61519	1	346431	5	NULL	NULL	0	NULL	hsp70	GP	constitutively expressed	is inactivate in		possibly			M21 cells	Cell	rat			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_206	7935376	While it is plausible that some of the constitutively expressed hsp7O protein in our rat M21 cells is similarly inactivated, most of the protein appears not to be sequestered in granules (25, 42) and is functional in providing thermoresistance (24, 25, 30).	tag10-2
61520	2	346431	5	NULL	NULL	0	NULL	hsp70	GP	most of	is not sequestered in					granules					NULL	rat M21 cells	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_206	7935376	While it is plausible that some of the constitutively expressed hsp7O protein in our rat M21 cells is similarly inactivated, most of the protein appears not to be sequestered in granules (25, 42) and is functional in providing thermoresistance (24, 25, 30).	tag10-2
61521	3	346431	5	NULL	NULL	0	NULL	statement 2	GP		provides					thermoresistance	Process				NULL	rat M21 cells	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_206	7935376	While it is plausible that some of the constitutively expressed hsp7O protein in our rat M21 cells is similarly inactivated, most of the protein appears not to be sequestered in granules (25, 42) and is functional in providing thermoresistance (24, 25, 30).	tag10-2
61522	1	346433	5	NULL	NULL	0	NULL	HSF	GP	Drosophila	activates					DNA	NucleicAcid	binding of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_208	7935376	(A to D) Accelerated decrease of the DNA-binding activity of Drosophila HSF in cells containing accumulated heat shock proteins.	tag10-2
61523	2	346433	5	NULL	NULL	0	NULL	cells	Cell		contain					heat shock proteins	GP	accumulated			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_208	7935376	(A to D) Accelerated decrease of the DNA-binding activity of Drosophila HSF in cells containing accumulated heat shock proteins.	tag10-2
61524	3	346433	5	NULL	NULL	0	NULL	statement 1	Process	accelerated decrease of	occurs in					statement 2	Cell				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_208	7935376	(A to D) Accelerated decrease of the DNA-binding activity of Drosophila HSF in cells containing accumulated heat shock proteins.	tag10-2
61525	1	346438	5	NULL	NULL	0	NULL	HSF	GP		activates					DNA	NucleicAcid	binding of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_213	7935376	(E) Graph showing the relative DNAbinding activity of HSF during prolonged heat shock.	tag10-2
61526	2	346438	5	NULL	NULL	0	NULL	statement 1	Process		occurs during					heat shock		prolonged			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_213	7935376	(E) Graph showing the relative DNAbinding activity of HSF during prolonged heat shock.	tag10-2
61527	1	346440	5	NULL	NULL	0	NULL	HSF	GP		interacts with					hsp70	GP				NULL	in vitro	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_215	7935376	Previous studies detecting in vitro interactions between HSF and hsp7O were based on the electrophoretic retardation of HSF-HSE complexes with hsp70-specific antibodies in a gel shift assay and on the analysis of HSF-hsp7O comnplexes on nondenaturing pore gradient gels (1, 5, 34, 46).	tag10-2
61528	1	346441	5	NULL	NULL	0	NULL	HSF	GP		associate with					hsp70	GP				NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_216	7935376	The gel shift assay also revealed a greater association of HSF with hsp7O upon prolonged heat stress (1).	tag10-2
61529	2	346441	5	NULL	NULL	0	NULL	heat stress		prolonged	leads to					statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_216	7935376	The gel shift assay also revealed a greater association of HSF with hsp7O upon prolonged heat stress (1).	tag10-2
61530	1	346442	5	NULL	NULL	0	NULL	70-kDa stress protein	GP		coimmunoprecipitates with					HSF	GP				NULL	heat-shocked cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_217	7935376	The coimmunoprecipitation of the 70-kDa stress proteins and HSF that we observed in extracts prepared from heat-shocked cells generally confirms these findings and indicates further that the complexes between HSF and hsp70 or hsc7O are most likely formed in the cell prior to the preparation of cell extracts, since the interaction could not be displaced with an excess of (unlabeled) hsc70 protein.	tag10-2
61531	1	346443	5	NULL	NULL	0	NULL	heat stress		increased	does not lead to					HSF-hsp70	GP	increased interaction of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_218	7935376	However, an increased HSF-hsp70 interaction after prolonged heat stress was not observed in our coimmunoprecipitation studies.	tag10-2
61532	1	346444	5	NULL	NULL	0	NULL	HSF	GP		interacts with					hsp70	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_219	7935376	This difference may be related to the different assays used and may imply a separate mode of interaction between HSF and hsp7O that is detectable only by the gel shift assay after prolonged heat stress.	tag10-2
61533	2	346444	5	NULL	NULL	0	NULL	statement 1	Process		occurs after					heat stress	GP	prolonged			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_219	7935376	This difference may be related to the different assays used and may imply a separate mode of interaction between HSF and hsp7O that is detectable only by the gel shift assay after prolonged heat stress.	tag10-2
61534	1	346445	5	NULL	NULL	0	NULL	70-kDa stress protein	GP		interacts with					HSF monomer	GP	latent			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_220	7935376	The interaction observed between the 70-kDa stress proteins and the latent (monomeric) form of HSF is a new finding.	tag10-2
61535	1	346447	5	NULL	NULL	0	NULL	HSF	GP	latent	coimmunoprecipitates with					70-kDa stress protein	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_222	7935376	The coimmunoprecipitation of both latent and active forms of HSF with the 70-kDa stress proteins is not necessarily inconsistent with sedimentation and gel filtration studies from our laboratory suggesting that the two native forms of HSF are composed of solely one and three HSF subunits, respectively.	tag10-2
61536	2	346447	5	NULL	NULL	0	NULL	HSF	GP	active	coimmunoprecipitates with					70-kDa stress protein	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_222	7935376	The coimmunoprecipitation of both latent and active forms of HSF with the 70-kDa stress proteins is not necessarily inconsistent with sedimentation and gel filtration studies from our laboratory suggesting that the two native forms of HSF are composed of solely one and three HSF subunits, respectively.	tag10-2
61537	3	346447	5	NULL	NULL	0	NULL	HSF	GP	native forms of 	is composed of					HSF subunits	GP				NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_222	7935376	The coimmunoprecipitation of both latent and active forms of HSF with the 70-kDa stress proteins is not necessarily inconsistent with sedimentation and gel filtration studies from our laboratory suggesting that the two native forms of HSF are composed of solely one and three HSF subunits, respectively.	tag10-2
61538	1	346449	5	NULL	NULL	0	NULL	hsp70	GP		interacts with					HSF	GP	latent			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_224	7935376	As with the interaction observed for the activated HSF, the functional implications of the interactions of hsp7O and hsc70 with the latent HSF are unclear, but they might reflect the participation of molecular chaperones in both the assembly and disassembly of HSF trimers.	tag10-2
61539	2	346449	5	NULL	NULL	0	NULL	hsc70	GP		interacts with					HSF	GP	latent			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_224	7935376	As with the interaction observed for the activated HSF, the functional implications of the interactions of hsp7O and hsc70 with the latent HSF are unclear, but they might reflect the participation of molecular chaperones in both the assembly and disassembly of HSF trimers.	tag10-2
61540	3	346449	5	NULL	NULL	0	NULL	molecular chaperones	GP		participates in		might			HSF trimers	GP	assembly of			NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_224	7935376	As with the interaction observed for the activated HSF, the functional implications of the interactions of hsp7O and hsc70 with the latent HSF are unclear, but they might reflect the participation of molecular chaperones in both the assembly and disassembly of HSF trimers.	tag10-2
61541	4	346449	5	NULL	NULL	0	NULL	molecular chaperones	GP		participates in		might			HSF trimers	GP	disassembly of			NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_224	7935376	As with the interaction observed for the activated HSF, the functional implications of the interactions of hsp7O and hsc70 with the latent HSF are unclear, but they might reflect the participation of molecular chaperones in both the assembly and disassembly of HSF trimers.	tag10-2
61542	1	346450	5	NULL	NULL	0	NULL	HSF	GP		interacts with					hsp70	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_225	7935376	We detected only a limited effect of ATP on the interaction between HSF and hsp7O.	tag10-2
61543	2	346450	5	NULL	NULL	0	NULL	ATP	Chemical		effects		limited			statement 1	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_225	7935376	We detected only a limited effect of ATP on the interaction between HSF and hsp7O.	tag10-2
61544	1	346452	5	NULL	NULL	0	NULL	hsp70	GP	chaperone action of	utilizes					ATP	Chemical	hydrolysis of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_227	7935376	In contrast, the known chaperone action of hsp70 utilizes ATP hydrolysis to alter the folded state of proteins and to dissociate oligomeric complexes (43).	tag10-2
61545	2	346452	5	NULL	NULL	0	NULL	statement 1	Process		alter					proteins	GP	folded state of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_227	7935376	In contrast, the known chaperone action of hsp70 utilizes ATP hydrolysis to alter the folded state of proteins and to dissociate oligomeric complexes (43).	tag10-2
61546	3	346452	5	NULL	NULL	0	NULL	statement 2	Process		leads to					oligomeric complex	GP	dissociation of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_227	7935376	In contrast, the known chaperone action of hsp70 utilizes ATP hydrolysis to alter the folded state of proteins and to dissociate oligomeric complexes (43).	tag10-2
61547	1	346453	5	NULL	NULL	0	NULL	HSF	GP		interacts with					hsp70	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_228	7935376	Thus, the observed interaction between HSF and hsp70 may only be a relic of a larger chaperone complex that failed to survive cell extraction.	tag10-2
61548	2	346453	5	NULL	NULL	0	NULL	statement 1	Process		is a relic of		may be			chaperone complex	GP	larger			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_228	7935376	Thus, the observed interaction between HSF and hsp70 may only be a relic of a larger chaperone complex that failed to survive cell extraction.	tag10-2
61549	1	346454	5	NULL	NULL	0	NULL	70-kDa stress protein	GP	purified	does not deactivate					HSF	GP				NULL	in vitro	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_229	7935376	This possibility is reinforced by the inability to deactivate HSF in vitro by using purified 70-kDa stress protein, ATP, and HSF trimers purified from a bacterial expression system.	tag10-2
61550	2	346454	5	NULL	NULL	0	NULL	ATP	Chemical		does not deactivate					HSF	GP				NULL	in vitro	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_229	7935376	This possibility is reinforced by the inability to deactivate HSF in vitro by using purified 70-kDa stress protein, ATP, and HSF trimers purified from a bacterial expression system.	tag10-2
61551	3	346454	5	NULL	NULL	0	NULL	HSF trimers	GP	purified	does not deactivate					HSF	GP				NULL	in vitro	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_229	7935376	This possibility is reinforced by the inability to deactivate HSF in vitro by using purified 70-kDa stress protein, ATP, and HSF trimers purified from a bacterial expression system.	tag10-2
61552	1	346455	5	NULL	NULL	0	NULL	ATP	Chemical	presence of	does not dissociate					HSF-hsp7O complexes					NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_230	7935376	A similar resistance of HSF-hsp7O complexes to disassociation in the presence of ATP has been reported (1, 5).	tag10-2
61553	1	346456	5	NULL	NULL	0	NULL	HSF1	GP	endogenous	activates					DNA	NucleicAcid	binding of			NULL	rat M21 cells	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_231	7935376	Our finding that the induction of the DNA-binding activity of endogenous HSF1 is not inhibited in rat M21 cells constitutively expressing hsp7O is in conflict with a recent report that showed an inhibition of HSF1 in human PEER cells constitutively expressing hsp7O at a comparable level (34).	tag10-2
61554	2	346456	5	NULL	NULL	0	NULL	rat M21 cells	Cell		express		constitutively			hsp70	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_231	7935376	Our finding that the induction of the DNA-binding activity of endogenous HSF1 is not inhibited in rat M21 cells constitutively expressing hsp7O is in conflict with a recent report that showed an inhibition of HSF1 in human PEER cells constitutively expressing hsp7O at a comparable level (34).	tag10-2
61555	3	346456	5	NULL	NULL	0	NULL	statement 1	Process	induction of	is not inhibited in					statement 2	Process				NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_231	7935376	Our finding that the induction of the DNA-binding activity of endogenous HSF1 is not inhibited in rat M21 cells constitutively expressing hsp7O is in conflict with a recent report that showed an inhibition of HSF1 in human PEER cells constitutively expressing hsp7O at a comparable level (34).	tag10-2
61556	4	346456	5	NULL	NULL	0	NULL	PEER cells	Cell	human	express					hsp70	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_231	7935376	Our finding that the induction of the DNA-binding activity of endogenous HSF1 is not inhibited in rat M21 cells constitutively expressing hsp7O is in conflict with a recent report that showed an inhibition of HSF1 in human PEER cells constitutively expressing hsp7O at a comparable level (34).	tag10-2
61557	5	346456	5	NULL	NULL	0	NULL	HSF1	GP		is inhibited in					statement 4	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_231	7935376	Our finding that the induction of the DNA-binding activity of endogenous HSF1 is not inhibited in rat M21 cells constitutively expressing hsp7O is in conflict with a recent report that showed an inhibition of HSF1 in human PEER cells constitutively expressing hsp7O at a comparable level (34).	tag10-2
61558	1	346458	5	NULL	NULL	0	NULL	HSF1	GP		is induced by					heat stress					NULL	human PEER cells	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_233	7935376	However, in the absence of a direct measurement of HSF1 levels in the extracts of the human PEER cells that were induced by heat stress, it remains difficult to interpret the observed changes in DNAbinding activity (34).	tag10-2
61559	1	346459	5	NULL	NULL	0	NULL	HSF	GP	latent	is converted to					HSF	GP	active;;DNA-bound			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_234	7935376	These differences indicate the necessity for additional investigations to clarify the role of heat shock proteins in the cycling of HSF between latent and active DNA-binding forms.	tag10-2
61560	2	346459	5	NULL	NULL	0	NULL	heat shock proteins	GP		plays a role in		possibly			statement 1	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_234	7935376	These differences indicate the necessity for additional investigations to clarify the role of heat shock proteins in the cycling of HSF between latent and active DNA-binding forms.	tag10-2
61561	1	346460	5	NULL	NULL	0	NULL	70-kDa stress protein	GP		interacts with		functionally			HSF	GP				NULL	S. cerevisiae	0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_235	7935376	In this respect, it should be noted that there is clear genetic evidence for a functional interaction between the 70-kDa stress proteins and HSF in S. cerevisiae (7, 52).	tag10-2
61562	1	346461	5	NULL	NULL	0	NULL	70-kDa stress protein	GP		repress					heat shock promoters	NucleicAcid	activity of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_236	7935376	These studies indicate that the 70-kDa stress proteins are involved in repressing the activity of heat shock promoters by two different pathways.	tag10-2
66657	1	346462	5	NULL	NULL	0	NULL	one pathway	Process		is independent of					HSE	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_237	7935376	One pathway is independent of the HSE (and HSF) and involves an adjacent SRS1 (self-regulating sequence) element (52).	tag10-2
66658	2	346462	5	NULL	NULL	0	NULL	one pathway	Process		is independent of					HSF	GP				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_237	7935376	One pathway is independent of the HSE (and HSF) and involves an adjacent SRS1 (self-regulating sequence) element (52).	tag10-2
66659	3	346462	5	NULL	NULL	0	NULL	statement 1	Process		involves					SRS1 element	NucleicAcid	adjacent			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_237	7935376	One pathway is independent of the HSE (and HSF) and involves an adjacent SRS1 (self-regulating sequence) element (52).	tag10-2
66660	4	346462	5	NULL	NULL	0	NULL	SRS1	NucleicAcid		is					self-regulating sequence	NucleicAcid				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_237	7935376	One pathway is independent of the HSE (and HSF) and involves an adjacent SRS1 (self-regulating sequence) element (52).	tag10-2
61563	1	346463	5	NULL	NULL	0	NULL	HSF trimer	GP	yeast	activates					DNA	NucleicAcid	binding of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_238	7935376	The other pathway implicates HSF, but it involves repression of the transcriptional, not the DNA-binding activity of the constitutively trimeric yeast HSF (7).	tag10-2
66665	2	346463	5	NULL	NULL	0	NULL	HSF trimer	GP	yeast	activates					transcription	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_238	7935376	The other pathway implicates HSF, but it involves repression of the transcriptional, not the DNA-binding activity of the constitutively trimeric yeast HSF (7).	tag10-2
66666	3	346463	5	NULL	NULL	0	NULL	other pathway	Process		repress					statement 2	Process				NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_238	7935376	The other pathway implicates HSF, but it involves repression of the transcriptional, not the DNA-binding activity of the constitutively trimeric yeast HSF (7).	tag10-2
66668	4	346463	5	NULL	NULL	NULL	NULL	other pathway	Process		does not repress					statement 1	Process				NULL		NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_238	7935376	The other pathway implicates HSF, but it involves repression of the transcriptional, not the DNA-binding activity of the constitutively trimeric yeast HSF (7).	tag10-2
61564	1	346464	5	NULL	NULL	0	NULL	HSF	GP	activity of	is repressed by		potentially			hsp70	GP				NULL	yeast	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_239	7935376	Perhaps it is this repression of HSF activity by hsp7O that operates in yeast and multicellular eukaryotes.	tag10-2
61565	2	346464	5	NULL	NULL	0	NULL	HSF	GP	activity of	is repressed by		potentially			hsp70	GP				NULL	multicellular eukaryotes	NULL	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_239	7935376	Perhaps it is this repression of HSF activity by hsp7O that operates in yeast and multicellular eukaryotes.	tag10-2
61566	1	346465	5	NULL	NULL	0	NULL	HSF	GP		activates					DNA	NucleicAcid	binding of			NULL		0	NULL	NULL	NULL	tag10_molcellbiol_14_10_6552_s_240	7935376	A different mechanism may have evolved to control the oligomeric transition and DNA-binding activity of HSF.	tag10-2
73620	1	354663	7	NULL	NULL	0	NULL	Aripiprazole	Chemical		is used in the					schizophrenia	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Aripiprazole is used to treat schizophrenia, bipolar mania and mixed manic/depressive episodes (as sole or adjunctive therapy) and as adjunctive (add-on) therapy for major depressive disorder.	topic_bd
73621	2	354663	7	NULL	NULL	0	NULL	Aripiprazole	Chemical		is used in the					bipolar mania	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Aripiprazole is used to treat schizophrenia, bipolar mania and mixed manic/depressive episodes (as sole or adjunctive therapy) and as adjunctive (add-on) therapy for major depressive disorder.	topic_bd
73622	3	354663	7	NULL	NULL	0	NULL	Aripiprazole	Chemical		is used in the					mixed manic/depressive episodes	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Aripiprazole is used to treat schizophrenia, bipolar mania and mixed manic/depressive episodes (as sole or adjunctive therapy) and as adjunctive (add-on) therapy for major depressive disorder.	topic_bd
73623	4	354663	7	NULL	NULL	0	NULL	Aripiprazole	Chemical		is used as					major depressive disorder	MedicalFinding	adjunctive therapy for			NULL		0	NULL	NULL	NULL	NULL	NULL	Aripiprazole is used to treat schizophrenia, bipolar mania and mixed manic/depressive episodes (as sole or adjunctive therapy) and as adjunctive (add-on) therapy for major depressive disorder.	topic_bd
73624	1	354664	7	NULL	NULL	0	NULL	Abilify	Chemical		brand name for					 aripiprazole	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Abilify is a brand name for aripiprazole.	topic_bd
73625	1	354665	7	NULL	NULL	0	NULL	aripiprazole	Chemical		is not associated with					suicide events	MedicalFinding	increased risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	aripiprazole is not associated with an increased risk of suicide events in an inception cohort of patients with ICD-9/ICD-10 codes indicative of schizophrenia or bipolar disorder.	topic_bd
73626	2	354665	7	NULL	NULL	0	NULL	statement 1	Process		occur in					ICD-9/ICD-10 codes	MedicalFinding	inception cohort of patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	aripiprazole is not associated with an increased risk of suicide events in an inception cohort of patients with ICD-9/ICD-10 codes indicative of schizophrenia or bipolar disorder.	topic_bd
73627	3	354665	7	NULL	NULL	0	NULL	ICD-9/ICD-10 codes	MedicalFinding		indicative of					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	aripiprazole is not associated with an increased risk of suicide events in an inception cohort of patients with ICD-9/ICD-10 codes indicative of schizophrenia or bipolar disorder.	topic_bd
73628	4	354665	7	NULL	NULL	NULL	NULL	ICD-9/ICD-10 codes	MedicalFinding		 indicative of					bipolar disorder	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	aripiprazole is not associated with an increased risk of suicide events in an inception cohort of patients with ICD-9/ICD-10 codes indicative of schizophrenia or bipolar disorder.	topic_bd
73629	5	354665	7	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	aripiprazole is not associated with an increased risk of suicide events in an inception cohort of patients with ICD-9/ICD-10 codes indicative of schizophrenia or bipolar disorder.	topic_bd
73630	1	354666	7	NULL	NULL	0	NULL	 lithium	Chemical		is useful during					manic phase	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The literature suggests that lithium is useful during the acute manic and the maintenance phase.	topic_bd
73631	2	354666	7	NULL	NULL	NULL	NULL	lithium	Chemical		is useful during					maintenance phase	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The literature suggests that lithium is useful during the acute manic and the maintenance phase.	topic_bd
73632	1	354667	7	NULL	NULL	0	NULL	Depakote	Chemical		is a type of					antiseizure medication	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Depakote is a antiseizure medication which also works to level out moods.	topic_bd
73633	2	354667	7	NULL	NULL	0	NULL	statement 1	Process		works to					level out moods	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Depakote is a antiseizure medication which also works to level out moods.	topic_bd
73634	1	354668	7	NULL	NULL	0	NULL	ECT	Chemical		treatment for		effective			manic symptoms	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Despite its scary reputation, ECT is an effective treatment for manic symptoms.	topic_bd
73635	1	354669	7	NULL	NULL	0	NULL	hypomania	MedicalFinding		is a type of					less-severe mania	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	This less-severe mania is called hypomania, and is a symptom of bipolar ii disorder.	topic_bd
73636	2	354669	7	NULL	NULL	0	NULL	hypomania	MedicalFinding		symptom of					bipolar ii disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	This less-severe mania is called hypomania, and is a symptom of bipolar ii disorder.	topic_bd
73637	1	354670	7	NULL	NULL	0	NULL	IL-12	GP		promotes					cell-mediated immunity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-12 (IL-12) promotes cell-mediated immunity by inducing Th1 cell differentiation and activation of both T cells and NK cells.	topic_ccc
73638	2	354670	7	NULL	NULL	0	NULL	statement 1	Process		occur by					Th1 cell	Cell	inducing differentiation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-12 (IL-12) promotes cell-mediated immunity by inducing Th1 cell differentiation and activation of both T cells and NK cells.	topic_ccc
73639	3	354670	7	NULL	NULL	0	NULL	statement 1	Process		occur by					T cell	Cell	activation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-12 (IL-12) promotes cell-mediated immunity by inducing Th1 cell differentiation and activation of both T cells and NK cells.	topic_ccc
73640	4	354670	7	NULL	NULL	0	NULL	statement 1	Process		occur by					NK cells	Cell	activation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-12 (IL-12) promotes cell-mediated immunity by inducing Th1 cell differentiation and activation of both T cells and NK cells.	topic_ccc
73641	5	354670	7	NULL	NULL	0	NULL	statement 3	Process		occur along with					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-12 (IL-12) promotes cell-mediated immunity by inducing Th1 cell differentiation and activation of both T cells and NK cells.	topic_ccc
73642	6	354670	7	NULL	NULL	0	NULL	IL-12	GP		is					Interleukin-12	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-12 (IL-12) promotes cell-mediated immunity by inducing Th1 cell differentiation and activation of both T cells and NK cells.	topic_ccc
73643	1	354671	7	NULL	NULL	0	NULL	A20 cells 	Cell		impairs					CD4 T-cell 	Cell	function of			NULL		0	NULL	NULL	NULL	NULL	NULL	By contrast, CD4 T-cell function appeared impaired after immunization with A20 cells alone or mixed with B78H1 cells. Indeed, only CD4(+) T cells from IL-12-treated mice could be restimulated with anti-OX40 monoclonal antibody (mAb) in place of a fourth cellular boost.	topic_ccc
73644	2	354671	7	NULL	NULL	0	NULL	A20 cells mixed withB78H1 cells	Cell		impairs					CD4 T-cell 	Cell	function of			NULL		0	NULL	NULL	NULL	NULL	NULL	By contrast, CD4 T-cell function appeared impaired after immunization with A20 cells alone or mixed with B78H1 cells. Indeed, only CD4(+) T cells from IL-12-treated mice could be restimulated with anti-OX40 monoclonal antibody (mAb) in place of a fourth cellular boost.	topic_ccc
73645	3	354671	7	NULL	NULL	0	NULL	anti-OX40 mAb	GP		restimulate					CD4(+) T cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	By contrast, CD4 T-cell function appeared impaired after immunization with A20 cells alone or mixed with B78H1 cells. Indeed, only CD4(+) T cells from IL-12-treated mice could be restimulated with anti-OX40 monoclonal antibody (mAb) in place of a fourth cellular boost.	topic_ccc
73646	4	354671	7	NULL	NULL	0	NULL	CD4(+) T cells	Cell		is from					 mice	Organism	 IL-12-treated			NULL		0	NULL	NULL	NULL	NULL	NULL	By contrast, CD4 T-cell function appeared impaired after immunization with A20 cells alone or mixed with B78H1 cells. Indeed, only CD4(+) T cells from IL-12-treated mice could be restimulated with anti-OX40 monoclonal antibody (mAb) in place of a fourth cellular boost.	topic_ccc
73647	1	354672	7	NULL	NULL	NULL	NULL	CD8(+) T cells	Cell		produce					IFN-gamma	GP	 tumor-specific			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Moreover, the IL-12-based tumor vaccine induced expansion of tumor-specific interferon-gamma (IFN-gamma)-producing CD8(+) T cells	topic_ccc
73648	2	354672	7	NULL	NULL	0	NULL	IL-12-based tumor vaccine	GP		induce					CD8(+) T cells	Cell	expansion of			NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, the IL-12-based tumor vaccine induced expansion of tumor-specific interferon-gamma (IFN-gamma)-producing CD8(+) T cells	topic_ccc
73649	3	354672	7	NULL	NULL	0	NULL	IFN-gamma	GP		is					interferon-gamma	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, the IL-12-based tumor vaccine induced expansion of tumor-specific interferon-gamma (IFN-gamma)-producing CD8(+) T cells	topic_ccc
73650	1	354673	7	NULL	NULL	0	NULL	IL-12	GP		displays					antitumor properties	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. This review focuses on anticancer effects of the IL-12 family in preclinical and clinical studies with an emphasis on colorectal cancer.	topic_ccc
73651	2	354673	7	NULL	NULL	0	NULL	CD4+ T cells	Cell		secrete					(IFN)-γ	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. This review focuses on anticancer effects of the IL-12 family in preclinical and clinical studies with an emphasis on colorectal cancer.	topic_ccc
73652	3	354673	7	NULL	NULL	0	NULL	CD8+ T cells	Cell		secrete					(IFN)-γ	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. This review focuses on anticancer effects of the IL-12 family in preclinical and clinical studies with an emphasis on colorectal cancer.	topic_ccc
73653	4	354673	7	NULL	NULL	0	NULL	NK cells	Cell		secrete					(IFN)-γ	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. This review focuses on anticancer effects of the IL-12 family in preclinical and clinical studies with an emphasis on colorectal cancer.	topic_ccc
73654	5	354673	7	NULL	NULL	0	NULL	NK-T cells	Cell		secrete					(IFN)-γ	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. This review focuses on anticancer effects of the IL-12 family in preclinical and clinical studies with an emphasis on colorectal cancer.	topic_ccc
73655	6	354673	7	NULL	NULL	0	NULL	statement 1	Process		mediated by					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. This review focuses on anticancer effects of the IL-12 family in preclinical and clinical studies with an emphasis on colorectal cancer.	topic_ccc
73656	7	354673	7	NULL	NULL	0	NULL	statement 1	Process		mediated by					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. This review focuses on anticancer effects of the IL-12 family in preclinical and clinical studies with an emphasis on colorectal cancer.	topic_ccc
73657	8	354673	7	NULL	NULL	0	NULL	statement 1	Process		mediated by					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. This review focuses on anticancer effects of the IL-12 family in preclinical and clinical studies with an emphasis on colorectal cancer.	topic_ccc
73658	9	354673	7	NULL	NULL	0	NULL	statement 1	Process		mediated by					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. This review focuses on anticancer effects of the IL-12 family in preclinical and clinical studies with an emphasis on colorectal cancer.	topic_ccc
73659	10	354673	7	NULL	NULL	0	NULL	NK cells	cell		is					natural killer cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. This review focuses on anticancer effects of the IL-12 family in preclinical and clinical studies with an emphasis on colorectal cancer.	topic_ccc
73660	1	354674	7	NULL	NULL	NULL	NULL	IL-12	GP		contributes to					tumor eradication	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	 Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication.	topic_ccc
73661	2	354674	7	NULL	NULL	NULL	NULL	MIG	GP		is					monokine induced by gamma interferon	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	 Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication.	topic_ccc
73662	3	354674	7	NULL	NULL	0	NULL	 IFN- γ	GP		induce					IP10	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication.	topic_ccc
73663	4	354674	7	NULL	NULL	0	NULL	 IFN- γ	GP		induce					MIG	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication.	topic_ccc
73664	5	354674	7	NULL	NULL	NULL	NULL	statement 1	Process		act through					statement 3	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	 Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication.	topic_ccc
73665	6	354674	7	NULL	NULL	NULL	NULL	statement 1	Process		act through					statement 4	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	 Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication.	topic_ccc
73666	7	354674	7	NULL	NULL	0	NULL	IP 10	GP		is a type of					antiangiogenic factors	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication.	topic_ccc
73667	8	354674	7	NULL	NULL	0	NULL	MIG	GP		is a type of					antiangiogenic factors	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication.	topic_ccc
73668	9	354674	7	NULL	NULL	0	NULL	IP 10	GP		is a type of					 interferon-inducible protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication.	topic_ccc
73669	1	354675	7	NULL	NULL	0	NULL	IL-12	GP		displays					antitumor properties	Process				NULL	murine models of tumorigenesis	0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells.	topic_ccc
73670	2	354675	7	NULL	NULL	0	NULL	CD4+ T cells	Cell		secrete					(IFN)-γ	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells.	topic_ccc
73671	3	354675	7	NULL	NULL	0	NULL	CD8+ T cells	Cell		secrete					(IFN)-γ	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells.	topic_ccc
73672	4	354675	7	NULL	NULL	0	NULL	NK cells	Cell		secrete					(IFN)-γ	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells.	topic_ccc
73673	5	354675	7	NULL	NULL	0	NULL	NK-T cells	Cell		secrete					(IFN)-γ	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells.	topic_ccc
73674	6	354675	7	NULL	NULL	0	NULL	statement 1	Process		mediated by					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells.	topic_ccc
73675	7	354675	7	NULL	NULL	0	NULL	statement 1	Process		mediated by					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells.	topic_ccc
73676	8	354675	7	NULL	NULL	0	NULL	statement 1	Process		mediated by					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells.	topic_ccc
73677	9	354675	7	NULL	NULL	0	NULL	statement 1	Process		mediated by					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells.	topic_ccc
73678	10	354675	7	NULL	NULL	0	NULL	NK cells	Cell		is					natural killer cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells.	topic_ccc
73679	1	354676	7	NULL	NULL	NULL	NULL	IL12p70	GP	antitumor effects of	mediated via					IFN γ -IP10/MIG-axis	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Similarly to IL12p70, antitumor effects of IL-27 are mediated via the IFN γ -IP10/MIG-axis and tumor-specific increase of cytotoxic T-lymphocyte activity.	topic_ccc
73680	2	354676	7	NULL	NULL	0	NULL	IL-27	GP	antitumor effects of	mediated via					cytotoxic T-lymphocyte activity	Process	tumor-specific increase of			NULL		0	NULL	NULL	NULL	NULL	NULL	Similarly to IL12p70, antitumor effects of IL-27 are mediated via the IFN γ -IP10/MIG-axis and tumor-specific increase of cytotoxic T-lymphocyte activity.	topic_ccc
73681	3	354676	7	NULL	NULL	NULL	NULL	IL-27	GP	antitumor effects of	mediated via					IFN γ -IP10/MIG-axis	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Similarly to IL12p70, antitumor effects of IL-27 are mediated via the IFN γ -IP10/MIG-axis and tumor-specific increase of cytotoxic T-lymphocyte activity.	topic_ccc
73682	4	354676	7	NULL	NULL	0	NULL	IL12p70	GP	antitumor effects of	mediated via					cytotoxic T-lymphocyte activity	Process	tumor-specific increase of			NULL		0	NULL	NULL	NULL	NULL	NULL	Similarly to IL12p70, antitumor effects of IL-27 are mediated via the IFN γ -IP10/MIG-axis and tumor-specific increase of cytotoxic T-lymphocyte activity.	topic_ccc
73683	1	354677	7	NULL	NULL	0	NULL	 IL-27	GP		mimic					IFN- γ	GP	function of			NULL		0	NULL	NULL	NULL	NULL	NULL	 Additionally, IL-27 itself may mimic the function of IFN- γ due to the similarity in usage of JAK/STAT signalling molecules such as STAT1.	topic_ccc
73684	2	354677	7	NULL	NULL	0	NULL	statement 1	Process		due to					STAT1	GP	similarity in usage of			NULL		0	NULL	NULL	NULL	NULL	NULL	 Additionally, IL-27 itself may mimic the function of IFN- γ due to the similarity in usage of JAK/STAT signalling molecules such as STAT1.	topic_ccc
73685	3	354677	7	NULL	NULL	0	NULL	STAT1	GP		is a type of					JAK/STAT signalling molecules	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 Additionally, IL-27 itself may mimic the function of IFN- γ due to the similarity in usage of JAK/STAT signalling molecules such as STAT1.	topic_ccc
73686	1	354678	7	NULL	NULL	0	NULL	IL-23	GP		act as					procancerogenic	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Whether IL-23 acts pro- or anticancerogenic seems to depend on a critical balance of STAT3 signalling in both the tumor and the immune cellular microenvironment of the tumor.	topic_ccc
73687	2	354678	7	NULL	NULL	0	NULL	IL-23	GP		act as					anticancerogenic	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Whether IL-23 acts pro- or anticancerogenic seems to depend on a critical balance of STAT3 signalling in both the tumor and the immune cellular microenvironment of the tumor.	topic_ccc
73688	3	354678	7	NULL	NULL	NULL	NULL	STAT3 signalling	Process		occur in					tumor	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Whether IL-23 acts pro- or anticancerogenic seems to depend on a critical balance of STAT3 signalling in both the tumor and the immune cellular microenvironment of the tumor.	topic_ccc
73689	4	354678	7	NULL	NULL	NULL	NULL	STAT3 signalling	Process		occur in					tumor	MedicalFinding	 immune cellular microenvironment of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Whether IL-23 acts pro- or anticancerogenic seems to depend on a critical balance of STAT3 signalling in both the tumor and the immune cellular microenvironment of the tumor.	topic_ccc
73690	5	354678	7	NULL	NULL	0	NULL	statement 3	Process		is in balance with					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Whether IL-23 acts pro- or anticancerogenic seems to depend on a critical balance of STAT3 signalling in both the tumor and the immune cellular microenvironment of the tumor.	topic_ccc
73691	6	354678	7	NULL	NULL	0	NULL	statement 1	Process		depends on					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Whether IL-23 acts pro- or anticancerogenic seems to depend on a critical balance of STAT3 signalling in both the tumor and the immune cellular microenvironment of the tumor.	topic_ccc
73692	7	354678	7	NULL	NULL	0	NULL	statement 1	Process		depends on					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Whether IL-23 acts pro- or anticancerogenic seems to depend on a critical balance of STAT3 signalling in both the tumor and the immune cellular microenvironment of the tumor.	topic_ccc
73693	8	354678	7	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Whether IL-23 acts pro- or anticancerogenic seems to depend on a critical balance of STAT3 signalling in both the tumor and the immune cellular microenvironment of the tumor.	topic_ccc
73694	1	354679	7	NULL	NULL	NULL	NULL	IL-12	GP	Long-term controlled expression of	is effective against					hepatic colon cancer metastases	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Long-term controlled expression of IL-12 using an HC-Ad vector in combination with oxaliplatin is effective and clinically applicable against hepatic colon cancer metastases.	topic_ccc
73695	2	354679	7	NULL	NULL	0	NULL	IL-12	GP		in combination with					oxaliplatin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Long-term controlled expression of IL-12 using an HC-Ad vector in combination with oxaliplatin is effective and clinically applicable against hepatic colon cancer metastases.	topic_ccc
73696	3	354679	7	NULL	NULL	0	NULL	IL-12	GP	Long-term controlled expression of	clinically applicable against					hepatic colon cancer metastases	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Long-term controlled expression of IL-12 using an HC-Ad vector in combination with oxaliplatin is effective and clinically applicable against hepatic colon cancer metastases.	topic_ccc
73697	1	354680	7	NULL	NULL	NULL	NULL	MZF	Chemical		upregulate					CD80	Cell	expression of			NULL	DCs	NULL	NULL	NULL	NULL	NULL	NULL	 In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
73698	2	354680	7	NULL	NULL	NULL	NULL	MZF	Chemical		upregulate					CD86	Cell	expression of			NULL	DCs	NULL	NULL	NULL	NULL	NULL	NULL	 In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
73699	3	354680	7	NULL	NULL	NULL	NULL	MZF	Chemical		upregulate					CD83	Cell	expression of			NULL	Dcs	NULL	NULL	NULL	NULL	NULL	NULL	 In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
73700	4	354680	7	NULL	NULL	0	NULL	MZF	Chemical		upregulate					MHC II	GP	expression of			NULL	DCs	0	NULL	NULL	NULL	NULL	NULL	 In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
73701	5	354680	7	NULL	NULL	0	NULL	DCs	Cell		produce					IL-12	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
73702	6	354680	7	NULL	NULL	0	NULL	DCs	Cell		produce					tumor necrosis factor-alpha	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
73703	7	354680	7	NULL	NULL	0	NULL	MZF	Chemical		increase		significantly;;dose-dependently			statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
73704	8	354680	7	NULL	NULL	0	NULL	MZF	Chemical		increase		significantly;;dose-dependently			statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
73705	9	354680	7	NULL	NULL	0	NULL	DCs	Cell		is					bone marrow-derived dendritic cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	 In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
73706	10	354680	7	NULL	NULL	0	NULL	IL-12	GP		is					interleukin-12	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
73707	1	354681	5	NULL	NULL	0	NULL	SHANK3	GP		is a type of					synaptic scaffolding protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the gene encoding the synaptic scaffolding protein SHANK3 are associated with autism spectrum disorders	topic_aut
73708	2	354681	5	NULL	NULL	0	NULL	SHANK3	GP	mutation of	is associated with					autism spectrum disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the gene encoding the synaptic scaffolding protein SHANK3 are associated with autism spectrum disorders	topic_aut
73709	1	354682	5	NULL	NULL	0	NULL	NLGN4 Gene	GP		is a member of					Neuroligin family	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	X-Linked Mental Retardation and Autism Are Associated with a Mutation in the NLGN4 Gene, a Member of the Neuroligin Family	topic_aut
73710	2	354682	5	NULL	NULL	0	NULL	X-Linked Mental Retardation	MedicalFinding		is associated with					NLGN4 Gene	GP	mutation of			NULL		0	NULL	NULL	NULL	NULL	NULL	X-Linked Mental Retardation and Autism Are Associated with a Mutation in the NLGN4 Gene, a Member of the Neuroligin Family	topic_aut
73711	3	354682	5	NULL	NULL	0	NULL	autism	MedicalFinding		is associated with					NLGN4 Gene	GP	mutation of			NULL		0	NULL	NULL	NULL	NULL	NULL	X-Linked Mental Retardation and Autism Are Associated with a Mutation in the NLGN4 Gene, a Member of the Neuroligin Family	topic_aut
73712	1	354683	5	NULL	NULL	0	NULL	toxoplasmosis	MedicalFinding		is linked to		most likely			schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Dr. Milton H. McAllister, professor of pathobiology in the College of Veterinary Medicine at the University of Illinois at Urbana-Champaign, recently announced the strong likelihood of a link between toxoplasmosis and schizophrenia.	topic_sch
73713	1	354684	5	NULL	NULL	NULL	NULL	fra(X)	MedicalFinding		is associated with		significantly			autism	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	With an overall 7.7% frequency of fra(X) among autistic males and an estimated 12.3% of autism among fra(X) males, we conclude there is likely to be a significant association of fra(X) with autism	topic_aut
73715	1	354686	5	NULL	NULL	0	NULL	rs3943552 T allele	NucleicAcid		is a type of					SNP	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	Association of the SNP rs3943552 T allele in the GLI2 gene with TD was observed in a subsample of Ashkenazi Jewish patients (N = 96, P = 0.018; P = 6.2 × 10(-5) in the CATIE sample).	topic_sch
73716	2	354686	5	NULL	NULL	0	NULL	rs3943552 T allele	NucleicAcid		is present in					GLI2 gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Association of the SNP rs3943552 T allele in the GLI2 gene with TD was observed in a subsample of Ashkenazi Jewish patients (N = 96, P = 0.018; P = 6.2 × 10(-5) in the CATIE sample).	topic_sch
73717	3	354686	5	NULL	NULL	NULL	NULL	statement 2	NucleicAcid		is associated with					TD	MedicalFinding				NULL	Ashkenazi Jewish patients	NULL	NULL	NULL	NULL	NULL	NULL	Association of the SNP rs3943552 T allele in the GLI2 gene with TD was observed in a subsample of Ashkenazi Jewish patients (N = 96, P = 0.018; P = 6.2 × 10(-5) in the CATIE sample).	topic_sch
73718	1	354687	5	NULL	NULL	0	NULL	GLI2 gene	GP		encodes					transcription factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The GLI2 gene encodes a transcription factor that participates in the development of the dopaminergic system during embryogenesis.	topic_sch
73719	2	354687	5	NULL	NULL	0	NULL	GLI2 gene	GP		participates in					dopaminergic system	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The GLI2 gene encodes a transcription factor that participates in the development of the dopaminergic system during embryogenesis.	topic_sch
73720	3	354687	5	NULL	NULL	0	NULL	statement 2	Process		occurs during					embryogenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The GLI2 gene encodes a transcription factor that participates in the development of the dopaminergic system during embryogenesis.	topic_sch
73721	1	354688	5	NULL	NULL	0	NULL	central serotonergic transmission	Process	dysfunctions of	is involved in		may be			schizophrenia	MedicalFinding	development of			NULL		0	NULL	NULL	NULL	NULL	NULL	Based on the evidence from neurobiological and pharmacological research, dysfunctions in central serotonergic transmission may be involved in the development of schizophrenia. 	topic_sch
73722	1	354689	5	NULL	NULL	0	NULL	TPH2	GP		is					Tryptophan hydroxylase 2	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Tryptophan hydroxylase 2 (TPH2), a newly identified isoform of tryptophan hydroxylase (the rate limiting enzyme in the biosynthesis of serotonin), regulates the brain-specific serotonin synthesis.	topic_sch
73723	2	354689	5	NULL	NULL	0	NULL	TPH2	GP		is an isoform of					tryptophan hydroxylase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Tryptophan hydroxylase 2 (TPH2), a newly identified isoform of tryptophan hydroxylase (the rate limiting enzyme in the biosynthesis of serotonin), regulates the brain-specific serotonin synthesis.	topic_sch
73724	3	354689	5	NULL	NULL	0	NULL	tryptophan hydroxylase	GP		acts as					rate limiting enzyme	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Tryptophan hydroxylase 2 (TPH2), a newly identified isoform of tryptophan hydroxylase (the rate limiting enzyme in the biosynthesis of serotonin), regulates the brain-specific serotonin synthesis.	topic_sch
73725	4	354689	5	NULL	NULL	0	NULL	statement 3	Process		plays a role in					serotonin	Chemical	biosynthesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	Tryptophan hydroxylase 2 (TPH2), a newly identified isoform of tryptophan hydroxylase (the rate limiting enzyme in the biosynthesis of serotonin), regulates the brain-specific serotonin synthesis.	topic_sch
73726	5	354689	5	NULL	NULL	0	NULL	serotonin	Chemical	synthesis of	is specific to					brain	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Tryptophan hydroxylase 2 (TPH2), a newly identified isoform of tryptophan hydroxylase (the rate limiting enzyme in the biosynthesis of serotonin), regulates the brain-specific serotonin synthesis.	topic_sch
73727	6	354689	5	NULL	NULL	0	NULL	TPH2	GP		regulate					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Tryptophan hydroxylase 2 (TPH2), a newly identified isoform of tryptophan hydroxylase (the rate limiting enzyme in the biosynthesis of serotonin), regulates the brain-specific serotonin synthesis.	topic_sch
73728	1	354691	5	NULL	NULL	0	NULL	TPH2	GP		develops				rs4570625	positive symptoms	PhysicalPhenomenon				NULL	Han Chinese schizophrenic patients	0	NULL	NULL	NULL	NULL	NULL	These results suggest that rs4570625 of TPH2 may play an important role in the development of positive symptoms in Han Chinese schizophrenic patients.	topic_sch
73730	1	354694	5	NULL	NULL	0	NULL	schizophrenia 	MedicalFinding		is associated with					frontotemporal lobar degeneration	Process	behavioral variant of			NULL		0	NULL	NULL	NULL	NULL	NULL	Major psychiatric diseases such as schizophrenia and mood disorders have not been linked to a specific pathology, but their clinical features overlap with some aspects of the behavioral variant of frontotemporal lobar degeneration.	topic_sch
73731	2	354694	5	NULL	NULL	0	NULL	mood disorders	MedicalFinding		is associated with					frontotemporal lobar degeneration	Process	behavioral variant of			NULL		0	NULL	NULL	NULL	NULL	NULL	Major psychiatric diseases such as schizophrenia and mood disorders have not been linked to a specific pathology, but their clinical features overlap with some aspects of the behavioral variant of frontotemporal lobar degeneration.	topic_sch
73732	1	354695	5	NULL	NULL	NULL	NULL	TDP-43	GP	pathological	plays a role in		significant			frontotemporal lobar degeneration	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Although the significance of pathological 43-kDa (transactivation response) DNA-binding protein (TDP-43) for frontotemporal lobar degeneration was appreciated only recently, the prevalence of TDP-43 pathology in patients with severe mental illness vs controls has not been systematically addressed.	topic_sch
73733	2	354695	5	NULL	NULL	0	NULL	TDP-43	GP		is					 43-kDa transactivation response DNA-binding protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Although the significance of pathological 43-kDa (transactivation response) DNA-binding protein (TDP-43) for frontotemporal lobar degeneration was appreciated only recently, the prevalence of TDP-43 pathology in patients with severe mental illness vs controls has not been systematically addressed.	topic_sch
73734	2	354697	5	NULL	NULL	0	NULL	GRN variant	GP		is found in					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	A new GRN variant of unknown significance (c.620T>C, p.Met207Thr) was found in 1 patient with schizophrenia with TDP-43 pathology.	topic_sch
73735	1	354697	5	NULL	NULL	0	NULL	schizophrenia patient	GroupOfPeople		contains					TDP-43	GP	pathological			NULL		0	NULL	NULL	NULL	NULL	NULL	A new GRN variant of unknown significance (c.620T>C, p.Met207Thr) was found in 1 patient with schizophrenia with TDP-43 pathology.	topic_sch
73736	1	354698	5	NULL	NULL	NULL	NULL	psychiatric patients	GroupOfPeople		is prone to					vascular risk	PhysicalPhenomenon	increased			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Evidence suggests that psychiatric patients are at an increased vascular risk. 	topic_sch
73737	1	354699	5	NULL	NULL	NULL	NULL	sRAGE	GP		is associated with					atherothrombosis	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	In this exploratory pilot study, we hypothesized that low levels of the soluble receptor for advanced glycation endproducts (sRAGE) might be found in psychiatric patients due to its association with atherothrombosis.	topic_sch
73738	2	354699	5	NULL	NULL	0	NULL	sRAGE	GP		is					soluble receptor for advanced glycation endproducts	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	In this exploratory pilot study, we hypothesized that low levels of the soluble receptor for advanced glycation endproducts (sRAGE) might be found in psychiatric patients due to its association with atherothrombosis.	topic_sch
73739	3	354699	5	NULL	NULL	0	NULL	sRAGE	GP	low levels of	is found in		might be			psychiatric patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	In this exploratory pilot study, we hypothesized that low levels of the soluble receptor for advanced glycation endproducts (sRAGE) might be found in psychiatric patients due to its association with atherothrombosis.	topic_sch
73740	1	354701	5	NULL	NULL	0	NULL	sRAGE	GP	reduced serum	contribute to					cardiovascular risk	MedicalFinding	increased			NULL	schizophrenia	0	NULL	NULL	NULL	NULL	NULL	Although subject to future confirmation, our findings suggest that the reduced serum sRAGE may contribute to increased cardiovascular risk in schizophrenia and major depression.	topic_sch
73741	2	354701	5	NULL	NULL	0	NULL	sRAGE	GP	reduced serum	contribute to					cardiovascular risk	MedicalFinding	increased			NULL	major depression	0	NULL	NULL	NULL	NULL	NULL	Although subject to future confirmation, our findings suggest that the reduced serum sRAGE may contribute to increased cardiovascular risk in schizophrenia and major depression.	topic_sch
73742	1	354702	5	NULL	NULL	0	NULL	AZD2624	Chemical		is a antagonist of					NK3 receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	AZD2624 was pharmacologically characterized as a NK3 receptor antagonist intended for treatment of schizophrenia.	topic_sch
73743	2	354702	5	NULL	NULL	0	NULL	AZD2624	Chemical		is intended for					schizophrenia	MedicalFinding	treatment of 			NULL		0	NULL	NULL	NULL	NULL	NULL	AZD2624 was pharmacologically characterized as a NK3 receptor antagonist intended for treatment of schizophrenia.	topic_sch
73744	1	354703	5	NULL	NULL	NULL	NULL	tardive OGC	MedicalFinding		is related to					amisulpride	Chemical				NULL	young woman with schizophrenia	NULL	NULL	NULL	NULL	NULL	NULL	We report a case of a young woman with schizophrenia who presented with tardive OGC related to amisulpride.	topic_sch
73745	1	354704	5	NULL	NULL	0	NULL	ZNF804A	Chemical		delinates					schizophrenia subtype	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	These data are consistent with our earlier behavioral data and suggest that ZNF804A is delineating a schizophrenia subtype characterized by relatively intact brain volume. 	topic_sch
73746	2	354704	5	NULL	NULL	0	NULL	schizophrenia subtype	MedicalFinding		is characterized by					brain volume	PhysicalPhenomenon	relatively intact			NULL		0	NULL	NULL	NULL	NULL	NULL	These data are consistent with our earlier behavioral data and suggest that ZNF804A is delineating a schizophrenia subtype characterized by relatively intact brain volume. 	topic_sch
73747	1	354705	5	NULL	NULL	NULL	NULL	ZNF804A variants	GP		increases		weakly			schizophrenia	MedicalFinding	susceptibility to			NULL		NULL	NULL	NULL	NULL	NULL	NULL	These include ZNF804A, TCF4 and NRGN, which contain common variants that weakly increase schizophrenia susceptibility, and NRXN1, in which rare copy number variants have a greater impact on schizophrenia risk. 	topic_sch
73748	2	354705	5	NULL	NULL	0	NULL	TCF4 variants	GP		increases		weakly			schizophrenia	MedicalFinding	susceptibility to			NULL		0	NULL	NULL	NULL	NULL	NULL	These include ZNF804A, TCF4 and NRGN, which contain common variants that weakly increase schizophrenia susceptibility, and NRXN1, in which rare copy number variants have a greater impact on schizophrenia risk. 	topic_sch
73749	3	354705	5	NULL	NULL	0	NULL	NRGN variants	GP		increases		weakly			schizophrenia	MedicalFinding	susceptibility to			NULL		0	NULL	NULL	NULL	NULL	NULL	These include ZNF804A, TCF4 and NRGN, which contain common variants that weakly increase schizophrenia susceptibility, and NRXN1, in which rare copy number variants have a greater impact on schizophrenia risk. 	topic_sch
73750	4	354705	5	NULL	NULL	0	NULL	NRXN1 variant	GP		impacts		greatly			schizophrenia 	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	These include ZNF804A, TCF4 and NRGN, which contain common variants that weakly increase schizophrenia susceptibility, and NRXN1, in which rare copy number variants have a greater impact on schizophrenia risk. 	topic_sch
73751	1	354706	5	NULL	NULL	0	NULL	mGluRs	GP	activation of	plays a role in		important			schizophrenia	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	In the meantime, several novel pharmacological strategies, including activation of mGluRs, elevation of synaptic glycine and inhibition of phosphodiesterase 10A, have recently shown promise for the treatment of schizophrenia in clinical trials.	topic_sch
73752	2	354706	5	NULL	NULL	0	NULL	synaptic glycine	AminoAcid	elevation of	plays a role in		important			schizophrenia	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	In the meantime, several novel pharmacological strategies, including activation of mGluRs, elevation of synaptic glycine and inhibition of phosphodiesterase 10A, have recently shown promise for the treatment of schizophrenia in clinical trials.	topic_sch
73753	3	354706	5	NULL	NULL	0	NULL	phosphodiesterase 10A	GP	inhibition of	plays a role in		important			schizophrenia	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	In the meantime, several novel pharmacological strategies, including activation of mGluRs, elevation of synaptic glycine and inhibition of phosphodiesterase 10A, have recently shown promise for the treatment of schizophrenia in clinical trials.	topic_sch
73754	1	354707	5	NULL	NULL	0	NULL	COMT	GP		is					Catechol-O-methyl transferase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Catechol-O-methyl transferase (COMT) encodes an enzyme involved in the metabolism of dopamine and maps to a commonly deleted region that increases schizophrenia risk. 	topic_sch
73755	2	354707	5	NULL	NULL	0	NULL	COMT	GP		is involved in					dopamine	Chemical	metabolism of			NULL		0	NULL	NULL	NULL	NULL	NULL	Catechol-O-methyl transferase (COMT) encodes an enzyme involved in the metabolism of dopamine and maps to a commonly deleted region that increases schizophrenia risk. 	topic_sch
73756	3	354707	5	NULL	NULL	0	NULL	COMT	GP	deletion of	increases					schizophrenia	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Catechol-O-methyl transferase (COMT) encodes an enzyme involved in the metabolism of dopamine and maps to a commonly deleted region that increases schizophrenia risk. 	topic_sch
73757	1	354708	5	NULL	NULL	NULL	NULL	rs4680	NucleicAcid		is associated with		significantly			schizophrenia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Two polymorphisms including rs4680 and rs165774 were found to be significantly associated with schizophrenia. 	topic_sch
73758	2	354708	5	NULL	NULL	NULL	NULL	rs165774	NucleicAcid		is associated with		significantly			schizophrenia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Two polymorphisms including rs4680 and rs165774 were found to be significantly associated with schizophrenia. 	topic_sch
73759	3	354708	5	NULL	NULL	0	NULL	rs4680	NucleicAcid		is a type of					polymorphism	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Two polymorphisms including rs4680 and rs165774 were found to be significantly associated with schizophrenia. 	topic_sch
73760	4	354708	5	NULL	NULL	0	NULL	rs165774	NucleicAcid		is a type of					polymorphism	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Two polymorphisms including rs4680 and rs165774 were found to be significantly associated with schizophrenia. 	topic_sch
74508	1	354709	6	NULL	NULL	0	NULL	BRCA1	GP		regulates					cell division	Process	cycle of 			NULL		0	NULL	NULL	NULL	NULL	NULL	Like many other tumor suppressor genes, BRCA1 regulates the cycle of cell division by keeping cells from growing and dividing too rapidly	topic_bc
74509	2	354709	6	NULL	NULL	0	NULL	BRCA1	GP		regulates					cells	Cell	rapid;; growing of			NULL		0	NULL	NULL	NULL	NULL	NULL	Like many other tumor suppressor genes, BRCA1 regulates the cycle of cell division by keeping cells from growing and dividing too rapidly	topic_bc
74510	1	354710	6	NULL	NULL	0	NULL	BRCA2	GP		belongs to					tumor suppressor gene family	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	BRCA2 belongs to the tumor suppressor gene family	topic_bc
74511	1	354711	6	NULL	NULL	0	NULL	BRCA1	GP	mutation of	increases					breast cancer	MedicalFinding	risk of 			NULL		0	NULL	NULL	NULL	NULL	NULL	A woman's risk of developing breast and/or ovarian cancer is greatly increased if she inherits a deleterious (harmful) BRCA1 or BRCA2 mutation. Men with these mutations also have an increased risk of breast cancer. Both men and women who have harmful BRCA1 or BRCA2 mutations may be at increased risk of other cancer	topic_bc
74512	2	354711	6	NULL	NULL	0	NULL	BRCA2	GP	mutation of	increases					breast cancer	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	A woman's risk of developing breast and/or ovarian cancer is greatly increased if she inherits a deleterious (harmful) BRCA1 or BRCA2 mutation. Men with these mutations also have an increased risk of breast cancer. Both men and women who have harmful BRCA1 or BRCA2 mutations may be at increased risk of other cancer	topic_bc
74513	3	354711	6	NULL	NULL	NULL	NULL	BRCA1	GP	mutation of	increases					ovarian cancer	MedicalFinding	risk of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	A woman's risk of developing breast and/or ovarian cancer is greatly increased if she inherits a deleterious (harmful) BRCA1 or BRCA2 mutation. Men with these mutations also have an increased risk of breast cancer. Both men and women who have harmful BRCA1 or BRCA2 mutations may be at increased risk of other cancer	topic_bc
74514	4	354711	6	NULL	NULL	0	NULL	BRCA2	GP	mutation of	increases					ovarian cancer	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	A woman's risk of developing breast and/or ovarian cancer is greatly increased if she inherits a deleterious (harmful) BRCA1 or BRCA2 mutation. Men with these mutations also have an increased risk of breast cancer. Both men and women who have harmful BRCA1 or BRCA2 mutations may be at increased risk of other cancer	topic_bc
74515	1	354712	6	NULL	NULL	0	NULL	colon cancer	MedicalFinding		is linked to					aging	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	There are certain cancers, in particular, that are linked to aging. These include colon, rectal, prostate, pancreas, lung, bladder, stomach and breast cancers.	topic_bc
74516	2	354712	6	NULL	NULL	0	NULL	rectal cancer	MedicalFinding		is linked to					aging	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	There are certain cancers, in particular, that are linked to aging. These include colon, rectal, prostate, pancreas, lung, bladder, stomach and breast cancers.	topic_bc
74517	3	354712	6	NULL	NULL	0	NULL	prostate cancer	MedicalFinding		is linked to					aging	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	There are certain cancers, in particular, that are linked to aging. These include colon, rectal, prostate, pancreas, lung, bladder, stomach and breast cancers.	topic_bc
74518	4	354712	6	NULL	NULL	0	NULL	pancreatic cancer	MedicalFinding		is linked to					aging	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	There are certain cancers, in particular, that are linked to aging. These include colon, rectal, prostate, pancreas, lung, bladder, stomach and breast cancers.	topic_bc
74519	5	354712	6	NULL	NULL	0	NULL	lung cancer	MedicalFinding		is linked to					aging	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	There are certain cancers, in particular, that are linked to aging. These include colon, rectal, prostate, pancreas, lung, bladder, stomach and breast cancers.	topic_bc
74520	6	354712	6	NULL	NULL	0	NULL	Bladder cancer	MedicalFinding		is linked to					aging	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	There are certain cancers, in particular, that are linked to aging. These include colon, rectal, prostate, pancreas, lung, bladder, stomach and breast cancers.	topic_bc
74521	7	354712	6	NULL	NULL	0	NULL	stomach cancer	MedicalFinding		is linked to					aging	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	There are certain cancers, in particular, that are linked to aging. These include colon, rectal, prostate, pancreas, lung, bladder, stomach and breast cancers.	topic_bc
74522	8	354712	6	NULL	NULL	0	NULL	breast cancer	MedicalFinding		is linked to					aging	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	There are certain cancers, in particular, that are linked to aging. These include colon, rectal, prostate, pancreas, lung, bladder, stomach and breast cancers.	topic_bc
74523	1	354713	6	NULL	NULL	0	NULL	women	GroupOfPeople		have					breast	CellComponent	dense			NULL		0	NULL	NULL	NULL	NULL	NULL	Cancer turns up five times more often in women with extremely dense breasts than in those with the most fatty tissue	topic_bc
74524	2	354713	6	NULL	NULL	0	NULL	cancer	MedicalFinding		is more in					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Cancer turns up five times more often in women with extremely dense breasts than in those with the most fatty tissue	topic_bc
74525	1	354714	6	NULL	NULL	0	NULL	post-menopausal hormone therapy	MedicalProcedure		increases 					breast cancer	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Use of combined post-menopausal hormone therapy increases the risk of getting breast cancer	topic_bc
74526	1	354715	6	NULL	NULL	0	NULL	wine	Food		increases					breast cancer	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	drinking as little as half a glass of wine a day may raise a woman's risk of developing breast cancer	topic_bc
74527	1	354716	6	NULL	NULL	0	NULL	exercise	MentalProcess	vigrous	cuts					breast cancer	MedicalFinding	risk of			NULL	post-menopausal women	0	NULL	NULL	NULL	NULL	NULL	New research from the US suggests that vigorous exercise cuts the risk of breast cancer in post-menopausal women	topic_bc
74528	1	354717	6	NULL	NULL	0	NULL	oxidation	Process		causes					DNA	NucleicAcid	damage to			NULL		0	NULL	NULL	NULL	NULL	NULL	While the importance of ATM function to protect against oxidative DNA damage and during ageing is well described	topic_bc
74529	2	354717	6	NULL	NULL	0	NULL	ATM	GP		protects against					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	While the importance of ATM function to protect against oxidative DNA damage and during ageing is well described	topic_bc
74530	3	354717	6	NULL	NULL	0	NULL	ATM	GP		protects against					ageing	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	While the importance of ATM function to protect against oxidative DNA damage and during ageing is well described	topic_bc
74531	1	354718	6	NULL	NULL	0	NULL	ATM gene	GP	mutation of	increases					breast cancer	MedicalFinding	risk of;; developing			NULL		0	NULL	NULL	NULL	NULL	NULL	Researchers have found that having a mutation in one copy of the ATM gene in each cell (particularly in people who have at least one family member with ataxia-telangiectasia) is associated with an increased risk of developing breast cancer	topic_bc
74532	1	354719	6	NULL	NULL	0	NULL	p53	GP		is encoded by					TP53 gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	p53 (also known as protein 53 or tumor protein 53), is a tumor suppressor protein that in humans is encoded by the TP53 gene	topic_bc
74533	2	354719	6	NULL	NULL	0	NULL	p53	GP		is a type of					tumor suppressor protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	p53 (also known as protein 53 or tumor protein 53), is a tumor suppressor protein that in humans is encoded by the TP53 gene	topic_bc
74534	3	354719	6	NULL	NULL	0	NULL	p53	GP		is a type of					protein 53	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	p53 (also known as protein 53 or tumor protein 53), is a tumor suppressor protein that in humans is encoded by the TP53 gene	topic_bc
74535	4	354719	6	NULL	NULL	0	NULL	p53	GP		is a type of					tumor protein 53	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	p53 (also known as protein 53 or tumor protein 53), is a tumor suppressor protein that in humans is encoded by the TP53 gene	topic_bc
74536	1	354720	6	NULL	NULL	0	NULL	p53	GP	mutant	is associated with					breast cancer	MedicalFinding	aggresive			NULL		0	NULL	NULL	NULL	NULL	NULL	In breast cancer, p53 mutation is associated with more aggressive disease and worse overall survival	topic_bc
74537	2	354720	6	NULL	NULL	NULL	NULL	p53	GP	mutant	is associated with					worse overall survival	Process				NULL	breast cancer	NULL	NULL	NULL	NULL	NULL	NULL	In breast cancer, p53 mutation is associated with more aggressive disease and worse overall survival	topic_bc
74538	1	354722	6	NULL	NULL	0	NULL	CHEK2	GP	abnormal variant of 	develops					breast cancer	MedicalFinding				NULL	women	0	NULL	NULL	NULL	NULL	NULL	Women who carry an abnormal variant of a gene known as CHEK2 are three times more likely to develop breast cancer than women who do not have	topic_bc
74539	1	354724	6	NULL	NULL	0	NULL	PTEN gene	GP	mutant	leads to					breast cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Approximately 50 percent of patients with breast cancer have a mutation in or loss of at least one copy of the PTEN gene	topic_bc
74540	1	354725	6	NULL	NULL	0	NULL	CDH1 gene	GP		encodes					Cadherin-1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Cadherin-1 is a protein that in humans is encoded by the CDH1 gene.	topic_bc
74541	1	354726	6	NULL	NULL	0	NULL	E-cadherin gene	GP	mutation of	increases					breast cancer	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	a mutation of the E-cadherin gene, puts the person at a 40% risk of breast cancer	topic_bc
74542	1	354727	6	NULL	NULL	0	NULL	Sixteen-carbon metabolites	Chemical		are toxic to					cellular DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	Sixteen-carbon metabolites are also toxic to cellular DNA. Synthetic xenoestrogens apparently block the 2-carbon pathway and promote 16-carbon metabolism	topic_bc
73761	1	354728	5	NULL	NULL	0	NULL	cerebellum	OrganismPart		plays a role in		may			pain perception	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The roles of the cerebellum in pain perception, attention deficit disorder, autism, dementia, and schizophrenia are discussed. 	topic_sch
73762	2	354728	5	NULL	NULL	0	NULL	cerebellum	OrganismPart		plays a role in		may			attention deficit disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The roles of the cerebellum in pain perception, attention deficit disorder, autism, dementia, and schizophrenia are discussed. 	topic_sch
73763	3	354728	5	NULL	NULL	0	NULL	cerebellum	OrganismPart		plays a role in		may			autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The roles of the cerebellum in pain perception, attention deficit disorder, autism, dementia, and schizophrenia are discussed. 	topic_sch
73764	4	354728	5	NULL	NULL	0	NULL	cerebellum	OrganismPart		plays a role in		may			dementia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The roles of the cerebellum in pain perception, attention deficit disorder, autism, dementia, and schizophrenia are discussed. 	topic_sch
73765	5	354728	5	NULL	NULL	0	NULL	cerebellum	OrganismPart		plays a role in		may			schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The roles of the cerebellum in pain perception, attention deficit disorder, autism, dementia, and schizophrenia are discussed. 	topic_sch
74543	1	354729	6	NULL	NULL	0	NULL	Obesity	PhysicalPhenomenon		risks					breast cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Obesity is a well-known risk factor for breast cancer after menopause	topic_bc
73766	1	354730	5	NULL	NULL	0	NULL	DNA viruses	Organism		infects					mother	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Maternal infection during pregnancy with a wide range of RNA and DNA viruses is associated with increased risk for schizophrenia and autism in their offspring.	topic_sch
73767	2	354730	5	NULL	NULL	0	NULL	statement 1	Process		occurs during					pregnancy	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Maternal infection during pregnancy with a wide range of RNA and DNA viruses is associated with increased risk for schizophrenia and autism in their offspring.	topic_sch
73768	3	354730	5	NULL	NULL	0	NULL	RNA viruses	Organism		infects					mother	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Maternal infection during pregnancy with a wide range of RNA and DNA viruses is associated with increased risk for schizophrenia and autism in their offspring.	topic_sch
73769	4	354730	5	NULL	NULL	0	NULL	statement 3	Process		occurs during					pregnancy	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Maternal infection during pregnancy with a wide range of RNA and DNA viruses is associated with increased risk for schizophrenia and autism in their offspring.	topic_sch
73770	5	354730	5	NULL	NULL	0	NULL	statement 2	Process		is associated with					schizophrenia	MedicalFinding	increased risk for			NULL	offspring	0	NULL	NULL	NULL	NULL	NULL	Maternal infection during pregnancy with a wide range of RNA and DNA viruses is associated with increased risk for schizophrenia and autism in their offspring.	topic_sch
73771	6	354730	5	NULL	NULL	0	NULL	statement 2	Process		is associated with					autism	MedicalFinding	increased risk for			NULL	offspring	0	NULL	NULL	NULL	NULL	NULL	Maternal infection during pregnancy with a wide range of RNA and DNA viruses is associated with increased risk for schizophrenia and autism in their offspring.	topic_sch
73772	7	354730	5	NULL	NULL	0	NULL	statement 4	Process		is associated with					schizophrenia	MedicalFinding	increased risk for			NULL	offspring	0	NULL	NULL	NULL	NULL	NULL	Maternal infection during pregnancy with a wide range of RNA and DNA viruses is associated with increased risk for schizophrenia and autism in their offspring.	topic_sch
73773	8	354730	5	NULL	NULL	0	NULL	statement 4	Process		is associated with					autism	MedicalFinding	increased risk for			NULL	offspring	0	NULL	NULL	NULL	NULL	NULL	Maternal infection during pregnancy with a wide range of RNA and DNA viruses is associated with increased risk for schizophrenia and autism in their offspring.	topic_sch
73778	1	354731	5	NULL	NULL	0	NULL	ASD patients	GroupOfPeople		shows					schizophrenia spectrum traits	MedicalFinding				NULL	adolescence	0	NULL	NULL	NULL	NULL	NULL	These findings indicate that patients diagnosed with an ASD show schizophrenia spectrum traits in adolescence. 	topic_sch
73779	1	354732	5	NULL	NULL	0	NULL	birth weight	PhysicalPhenomenon	low 	increases					schizophrenia	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Both low (OR 2.5; 95% CI 1.2-5.1) and high birth weight (OR 2.4; 95% CI 1.1-4.9) increased the risk of later schizophrenia. 	topic_sch
73780	2	354732	5	NULL	NULL	0	NULL	birth weight	PhysicalPhenomenon	high	increases					schizophrenia	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Both low (OR 2.5; 95% CI 1.2-5.1) and high birth weight (OR 2.4; 95% CI 1.1-4.9) increased the risk of later schizophrenia. 	topic_sch
73781	1	354733	5	NULL	NULL	NULL	NULL	babies	Organism	short	is at risk of		elevated			schizophrenia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	In addition, short (OR 2.6; 95% CI 1.1-5.9) and long babies had an elevated risk of schizophrenia as adults (OR 1.8; 95% CI 1.0-3.5).	topic_sch
73782	2	354733	5	NULL	NULL	NULL	NULL	babies	Organism	long	is at risk of		elevated			schizophrenia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	In addition, short (OR 2.6; 95% CI 1.1-5.9) and long babies had an elevated risk of schizophrenia as adults (OR 1.8; 95% CI 1.0-3.5).	topic_sch
73783	1	354734	5	NULL	NULL	0	NULL	potassium channel genes	GP		is a type of					candidate genes	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Previous studies have reported that some potassium channel genes might be candidate genes for susceptibility to schizophrenia.	topic_sch
73784	2	354734	5	NULL	NULL	0	NULL	statement 1	GP		is susceptible to					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Previous studies have reported that some potassium channel genes might be candidate genes for susceptibility to schizophrenia.	topic_sch
73785	1	354735	5	NULL	NULL	0	NULL	KCNH1	GP		is a type of					potassium channel gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	In the present study, we chose three potassium channel genes, KCNH1, KCNJ10, KCNN3 to investigate the role of potassium channels in schizophrenia by genotyping 23 SNPs (9 in KCNH1, 5 in KCNJ10 and 9 in KCNN3) in a Han Chinese sample consisting of 893 schizophrenia patients and 611 healthy controls. No significant difference in allelic or genotypic frequency was revealed between schizophrenia patients and healthy individuals. Nor was a significant difference in haplotypic distribution detected. MDR analysis revealed no gene-gene interaction within the three potassium channel genes. Our study suggests that the 23 SNPs within the three potassium genes we examined do not play a major role in schizophrenia in the Han Chinese population.	topic_sch
73786	2	354735	5	NULL	NULL	0	NULL	KCNJ10	GP		is a type of					potassium channel gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	In the present study, we chose three potassium channel genes, KCNH1, KCNJ10, KCNN3 to investigate the role of potassium channels in schizophrenia by genotyping 23 SNPs (9 in KCNH1, 5 in KCNJ10 and 9 in KCNN3) in a Han Chinese sample consisting of 893 schizophrenia patients and 611 healthy controls. No significant difference in allelic or genotypic frequency was revealed between schizophrenia patients and healthy individuals. Nor was a significant difference in haplotypic distribution detected. MDR analysis revealed no gene-gene interaction within the three potassium channel genes. Our study suggests that the 23 SNPs within the three potassium genes we examined do not play a major role in schizophrenia in the Han Chinese population.	topic_sch
73787	3	354735	5	NULL	NULL	0	NULL	KCNN3	GP		is a type of					potassium channel gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	In the present study, we chose three potassium channel genes, KCNH1, KCNJ10, KCNN3 to investigate the role of potassium channels in schizophrenia by genotyping 23 SNPs (9 in KCNH1, 5 in KCNJ10 and 9 in KCNN3) in a Han Chinese sample consisting of 893 schizophrenia patients and 611 healthy controls. No significant difference in allelic or genotypic frequency was revealed between schizophrenia patients and healthy individuals. Nor was a significant difference in haplotypic distribution detected. MDR analysis revealed no gene-gene interaction within the three potassium channel genes. Our study suggests that the 23 SNPs within the three potassium genes we examined do not play a major role in schizophrenia in the Han Chinese population.	topic_sch
73788	4	354735	5	NULL	NULL	0	NULL	KCNH1 SNPs	GP		does not play a role in		major			schizophrenia	MedicalFinding				NULL	Han Chinese population	0	NULL	NULL	NULL	NULL	NULL	In the present study, we chose three potassium channel genes, KCNH1, KCNJ10, KCNN3 to investigate the role of potassium channels in schizophrenia by genotyping 23 SNPs (9 in KCNH1, 5 in KCNJ10 and 9 in KCNN3) in a Han Chinese sample consisting of 893 schizophrenia patients and 611 healthy controls. No significant difference in allelic or genotypic frequency was revealed between schizophrenia patients and healthy individuals. Nor was a significant difference in haplotypic distribution detected. MDR analysis revealed no gene-gene interaction within the three potassium channel genes. Our study suggests that the 23 SNPs within the three potassium genes we examined do not play a major role in schizophrenia in the Han Chinese population.	topic_sch
73789	5	354735	5	NULL	NULL	0	NULL	KCNJ10 SNPs	GP		does not play a role in		major			schizophrenia	MedicalFinding				NULL	Han Chinese population	0	NULL	NULL	NULL	NULL	NULL	In the present study, we chose three potassium channel genes, KCNH1, KCNJ10, KCNN3 to investigate the role of potassium channels in schizophrenia by genotyping 23 SNPs (9 in KCNH1, 5 in KCNJ10 and 9 in KCNN3) in a Han Chinese sample consisting of 893 schizophrenia patients and 611 healthy controls. No significant difference in allelic or genotypic frequency was revealed between schizophrenia patients and healthy individuals. Nor was a significant difference in haplotypic distribution detected. MDR analysis revealed no gene-gene interaction within the three potassium channel genes. Our study suggests that the 23 SNPs within the three potassium genes we examined do not play a major role in schizophrenia in the Han Chinese population.	topic_sch
73790	6	354735	5	NULL	NULL	0	NULL	KCNN3 SNPs	GP		does not play a role in		major			schizophrenia	MedicalFinding				NULL	Han Chinese population	0	NULL	NULL	NULL	NULL	NULL	In the present study, we chose three potassium channel genes, KCNH1, KCNJ10, KCNN3 to investigate the role of potassium channels in schizophrenia by genotyping 23 SNPs (9 in KCNH1, 5 in KCNJ10 and 9 in KCNN3) in a Han Chinese sample consisting of 893 schizophrenia patients and 611 healthy controls. No significant difference in allelic or genotypic frequency was revealed between schizophrenia patients and healthy individuals. Nor was a significant difference in haplotypic distribution detected. MDR analysis revealed no gene-gene interaction within the three potassium channel genes. Our study suggests that the 23 SNPs within the three potassium genes we examined do not play a major role in schizophrenia in the Han Chinese population.	topic_sch
73791	1	354736	5	NULL	NULL	0	NULL	DAO	GP		is					D-amino acid oxidase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	D-amino acid oxidase (DAO), an enzyme that degrades D-serine, has been suggested as a susceptibility factor for schizophrenia.	topic_sch
73792	2	354736	5	NULL	NULL	0	NULL	DAO	GP		is a type of					enzyme	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	D-amino acid oxidase (DAO), an enzyme that degrades D-serine, has been suggested as a susceptibility factor for schizophrenia.	topic_sch
73793	3	354736	5	NULL	NULL	0	NULL	DAO	GP		degrades					D-serine	AminoAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	D-amino acid oxidase (DAO), an enzyme that degrades D-serine, has been suggested as a susceptibility factor for schizophrenia.	topic_sch
73794	4	354736	5	NULL	NULL	0	NULL	DAO	GP		is a susceptibility factor for					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	D-amino acid oxidase (DAO), an enzyme that degrades D-serine, has been suggested as a susceptibility factor for schizophrenia.	topic_sch
73795	1	354737	5	NULL	NULL	0	NULL	delusions			enhance					self-esteem					NULL		0	NULL	NULL	NULL	NULL	NULL	Although these findings do not support the hypothesis that delusions serve to enhance self-esteem, they underline the relevance of low self-esteem in patients with persecutory delusions and point to the necessity of enhancing self-esteem in therapy.	topic_sch
73796	1	354738	5	NULL	NULL	0	NULL	subjective experiences	Process		is associated with					schizophrenia	MedicalFinding	positive symptomatology in			NULL		0	NULL	NULL	NULL	NULL	NULL	The results of our study suggest that subjective experiences are significantly associated with positive symptomatology in schizophrenia, suggesting that they may share a common underlying neural basis.	topic_sch
73797	1	354739	5	NULL	NULL	0	NULL	estrogen	GP	oral	reduce		might			schizophrenia	MedicalFinding	symptom severity in			NULL		0	NULL	NULL	NULL	NULL	NULL	Emerging evidence from clinical trials suggests that oral estrogen and intranasal oxytocin might reduce symptom severity in schizophrenia. 	topic_sch
73798	2	354739	5	NULL	NULL	0	NULL	oxytocin	GP	intranasal	reduce		might			schizophrenia	MedicalFinding	symptom severity in			NULL		0	NULL	NULL	NULL	NULL	NULL	Emerging evidence from clinical trials suggests that oral estrogen and intranasal oxytocin might reduce symptom severity in schizophrenia. 	topic_sch
73799	1	354740	5	NULL	NULL	0	NULL	environmental stressors	PhysicalPhenomenon		exerts					brain	OrganismPart	major impact on;;development of			NULL		0	NULL	NULL	NULL	NULL	NULL	Environmental stressors during gestation can exert a major impact on brain development and thereby contribute to the pathogenesis of neuropsychiatric illnesses, such as depression and psychotic disorders including schizophrenia.	topic_sch
73800	2	354740	5	NULL	NULL	0	NULL	statement 1	Process		occurs during					gestation	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Environmental stressors during gestation can exert a major impact on brain development and thereby contribute to the pathogenesis of neuropsychiatric illnesses, such as depression and psychotic disorders including schizophrenia.	topic_sch
73801	3	354740	5	NULL	NULL	0	NULL	statement 1	Process		contribute to					depression	MedicalFinding	pathogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	Environmental stressors during gestation can exert a major impact on brain development and thereby contribute to the pathogenesis of neuropsychiatric illnesses, such as depression and psychotic disorders including schizophrenia.	topic_sch
73802	4	354740	5	NULL	NULL	0	NULL	depression	MedicalFinding		is a type of					neuropsychiatric illness	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Environmental stressors during gestation can exert a major impact on brain development and thereby contribute to the pathogenesis of neuropsychiatric illnesses, such as depression and psychotic disorders including schizophrenia.	topic_sch
73803	5	354740	5	NULL	NULL	0	NULL	statement 1	Process		contribute to					schizophrenia	MedicalFinding	pathogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	Environmental stressors during gestation can exert a major impact on brain development and thereby contribute to the pathogenesis of neuropsychiatric illnesses, such as depression and psychotic disorders including schizophrenia.	topic_sch
73804	6	354740	5	NULL	NULL	0	NULL	schizophrenia	MedicalFinding		is a type of					psychotic disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Environmental stressors during gestation can exert a major impact on brain development and thereby contribute to the pathogenesis of neuropsychiatric illnesses, such as depression and psychotic disorders including schizophrenia.	topic_sch
73805	1	354741	5	NULL	NULL	0	NULL	sildenafil 	Chemical		is adjunctive treatment strategy for		potential			schizophrenia	MedicalFinding	treatment of;;negative symptoms of			NULL		0	NULL	NULL	NULL	NULL	NULL	The present study indicates sildenafil as a potential adjunctive treatment strategy for treatment of negative symptoms of schizophrenia	topic_sch
73806	1	354742	5	NULL	NULL	0	NULL	mGluR2/3 agonist	Chemical		is effective in					anxiety	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Clinical trials have demonstrated positive proof of efficacy of dual metabotropic glutamate receptor 2/3 (mGluR2/3) agonists in both anxiety and schizophrenia.	topic_sch
73807	2	354742	5	NULL	NULL	0	NULL	mGluR2/3 agonist	Chemical		is effective in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Clinical trials have demonstrated positive proof of efficacy of dual metabotropic glutamate receptor 2/3 (mGluR2/3) agonists in both anxiety and schizophrenia.	topic_sch
73808	3	354742	5	NULL	NULL	0	NULL	mGluR2/3	GP		is					metabotropic glutamate receptor 2/3	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Clinical trials have demonstrated positive proof of efficacy of dual metabotropic glutamate receptor 2/3 (mGluR2/3) agonists in both anxiety and schizophrenia.	topic_sch
73809	1	354743	5	NULL	NULL	0	NULL	MONW individuals	GroupOfPeople		is present in					non-diabetic schizophrenia patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	The MONW individuals in non-diabetic schizophrenia patients seem to have an unfavorable metabolic profile and significant atherogenecity. 	topic_sch
73810	2	354743	5	NULL	NULL	NULL	NULL	statement 1	GroupOfPeople		possess					unfavorable metabolic profile	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The MONW individuals in non-diabetic schizophrenia patients seem to have an unfavorable metabolic profile and significant atherogenecity. 	topic_sch
73811	3	354743	5	NULL	NULL	0	NULL	statement 1	GroupOfPeople		possess					atherogenecity	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The MONW individuals in non-diabetic schizophrenia patients seem to have an unfavorable metabolic profile and significant atherogenecity. 	topic_sch
73812	1	354744	5	NULL	NULL	NULL	NULL	negative symptoms	MedicalFinding		is associated with					mental state concept	MentalProcess	lack of			NULL	schizophrenic patients	NULL	NULL	NULL	NULL	NULL	NULL	In schizophrenic patients, negative symptoms were associated with a lack of a mental state concept, while positive symptoms like delusions were associated with 'overmentalizing', supporting respective etiological concepts of delusions	topic_sch
73813	2	354744	5	NULL	NULL	0	NULL	delusion	MedicalFinding		is a type of					positive symptom	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In schizophrenic patients, negative symptoms were associated with a lack of a mental state concept, while positive symptoms like delusions were associated with 'overmentalizing', supporting respective etiological concepts of delusions	topic_sch
73814	3	354744	5	NULL	NULL	0	NULL	delusion	MedicalFinding		is associated with					overmentalizing	MedicalFinding				NULL	schizophrenic patients	0	NULL	NULL	NULL	NULL	NULL	In schizophrenic patients, negative symptoms were associated with a lack of a mental state concept, while positive symptoms like delusions were associated with 'overmentalizing', supporting respective etiological concepts of delusions	topic_sch
73815	1	354745	5	NULL	NULL	0	NULL	ketamine	Chemical		is a type of					noncompetitive N-methyl-D-aspartate antagonist	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Given the evidence that ketamine, a noncompetitive N-methyl-D-aspartate antagonist reproduces symptoms of schizophrenia, we sought to determine whether the rubber-hand illusion is augmented by ketamine.	topic_sch
73816	2	354745	5	NULL	NULL	0	NULL	ketamine	Chemical		reproduces					schizophrenia	MedicalFinding	symptoms of			NULL		0	NULL	NULL	NULL	NULL	NULL	Given the evidence that ketamine, a noncompetitive N-methyl-D-aspartate antagonist reproduces symptoms of schizophrenia, we sought to determine whether the rubber-hand illusion is augmented by ketamine.	topic_sch
73817	3	354745	5	NULL	NULL	0	NULL	rubber-hand illusion	Process		is augmented by		may be			ketamine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Given the evidence that ketamine, a noncompetitive N-methyl-D-aspartate antagonist reproduces symptoms of schizophrenia, we sought to determine whether the rubber-hand illusion is augmented by ketamine.	topic_sch
73818	1	354747	5	NULL	NULL	0	NULL	serotonin	Chemical		plays a role in					depression	MedicalFinding	etiology of			NULL		0	NULL	NULL	NULL	NULL	NULL	The profusion of 5-HT receptors should eventually allow a better understanding of the different and complex processes in which serotonin is involved. Its role is expected in the ethiology of several diseases, including depression, schizophrenia, anxiety and panic disorders, migraine, hypertension, pulmonary hypertension, eating disorders, vomiting and irritable bowel syndromes	topic_sch
73819	2	354747	5	NULL	NULL	0	NULL	serotonin	Chemical		plays a role in					schizophrenia	MedicalFinding	etiology of			NULL		0	NULL	NULL	NULL	NULL	NULL	The profusion of 5-HT receptors should eventually allow a better understanding of the different and complex processes in which serotonin is involved. Its role is expected in the ethiology of several diseases, including depression, schizophrenia, anxiety and panic disorders, migraine, hypertension, pulmonary hypertension, eating disorders, vomiting and irritable bowel syndromes	topic_sch
73820	3	354747	5	NULL	NULL	0	NULL	serotonin	Chemical		plays a role in					anxiety and panic disorders	MedicalFinding	etiology of			NULL		0	NULL	NULL	NULL	NULL	NULL	The profusion of 5-HT receptors should eventually allow a better understanding of the different and complex processes in which serotonin is involved. Its role is expected in the ethiology of several diseases, including depression, schizophrenia, anxiety and panic disorders, migraine, hypertension, pulmonary hypertension, eating disorders, vomiting and irritable bowel syndromes	topic_sch
73821	4	354747	5	NULL	NULL	0	NULL	serotonin	Chemical		plays a role in					migraine	MedicalFinding	etiology of			NULL		0	NULL	NULL	NULL	NULL	NULL	The profusion of 5-HT receptors should eventually allow a better understanding of the different and complex processes in which serotonin is involved. Its role is expected in the ethiology of several diseases, including depression, schizophrenia, anxiety and panic disorders, migraine, hypertension, pulmonary hypertension, eating disorders, vomiting and irritable bowel syndromes	topic_sch
73822	5	354747	5	NULL	NULL	0	NULL	serotonin	Chemical		plays a role in					hypertension	MedicalFinding	etiology of			NULL		0	NULL	NULL	NULL	NULL	NULL	The profusion of 5-HT receptors should eventually allow a better understanding of the different and complex processes in which serotonin is involved. Its role is expected in the ethiology of several diseases, including depression, schizophrenia, anxiety and panic disorders, migraine, hypertension, pulmonary hypertension, eating disorders, vomiting and irritable bowel syndromes	topic_sch
73823	6	354747	5	NULL	NULL	0	NULL	serotonin	Chemical		plays a role in					pulmonary hypertension	MedicalFinding	etiology of			NULL		0	NULL	NULL	NULL	NULL	NULL	The profusion of 5-HT receptors should eventually allow a better understanding of the different and complex processes in which serotonin is involved. Its role is expected in the ethiology of several diseases, including depression, schizophrenia, anxiety and panic disorders, migraine, hypertension, pulmonary hypertension, eating disorders, vomiting and irritable bowel syndromes	topic_sch
73824	7	354747	5	NULL	NULL	0	NULL	serotonin	Chemical		plays a role in					eating disorders	MedicalFinding	etiology of			NULL		0	NULL	NULL	NULL	NULL	NULL	The profusion of 5-HT receptors should eventually allow a better understanding of the different and complex processes in which serotonin is involved. Its role is expected in the ethiology of several diseases, including depression, schizophrenia, anxiety and panic disorders, migraine, hypertension, pulmonary hypertension, eating disorders, vomiting and irritable bowel syndromes	topic_sch
73825	8	354747	5	NULL	NULL	0	NULL	serotonin	Chemical		plays a role in					vomiting and irritable bowel syndromes	MedicalFinding	etiology of			NULL		0	NULL	NULL	NULL	NULL	NULL	The profusion of 5-HT receptors should eventually allow a better understanding of the different and complex processes in which serotonin is involved. Its role is expected in the ethiology of several diseases, including depression, schizophrenia, anxiety and panic disorders, migraine, hypertension, pulmonary hypertension, eating disorders, vomiting and irritable bowel syndromes	topic_sch
73826	1	354748	5	NULL	NULL	0	NULL	CB1 receptor	GP	alternation of;;function of	implicated in					depression	MedicalFinding				NULL	human	0	NULL	NULL	NULL	NULL	NULL	Alternation of CB1 receptor function has been implicated in a number of human diseases such as depression, schizophrenia, and obesity (4-6). 	topic_sch
73827	2	354748	5	NULL	NULL	0	NULL	CB1 receptor	GP	alternation of;;function of	implicated in					schizophrenia	MedicalFinding				NULL	human	0	NULL	NULL	NULL	NULL	NULL	Alternation of CB1 receptor function has been implicated in a number of human diseases such as depression, schizophrenia, and obesity (4-6). 	topic_sch
73828	3	354748	5	NULL	NULL	0	NULL	CB1 receptor	GP	alternation of;;function of	implicated in					obesity	MedicalFinding				NULL	human	0	NULL	NULL	NULL	NULL	NULL	Alternation of CB1 receptor function has been implicated in a number of human diseases such as depression, schizophrenia, and obesity (4-6). 	topic_sch
73829	1	354749	5	NULL	NULL	0	NULL	phenotypic defects	PhysicalPhenomenon		overlap		partly			schizophrenia	MedicalFinding	defects of			NULL	mice	0	NULL	NULL	NULL	NULL	NULL	In mice, the deletion of the LPA1 receptor causes some phenotypic defects partly overlapping with those found in schizophrenia.	topic_sch
73830	2	354749	5	NULL	NULL	NULL	NULL	LPA1 receptor	GP	deletion of	causes					statement 1	Process				NULL	mice	NULL	NULL	NULL	NULL	NULL	NULL	In mice, the deletion of the LPA1 receptor causes some phenotypic defects partly overlapping with those found in schizophrenia.	topic_sch
73831	1	354750	5	NULL	NULL	0	NULL	CaMKII	GP		plays a role in		important			neurons	Cell	maturation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in LPA1 KO mice the α/β isoform ratio of CaMKII, which plays a key role in neuronal maturation during development, was markedly decreased, as found previously in schizophrenia patients.	topic_sch
73832	2	354750	5	NULL	NULL	0	NULL	statement 1	Process		occurs during					development	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in LPA1 KO mice the α/β isoform ratio of CaMKII, which plays a key role in neuronal maturation during development, was markedly decreased, as found previously in schizophrenia patients.	topic_sch
73833	3	354750	5	NULL	NULL	0	NULL	CaMKII	GP	isoform ratio of	is decreased in		markedly			LPA1 KO mice	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in LPA1 KO mice the α/β isoform ratio of CaMKII, which plays a key role in neuronal maturation during development, was markedly decreased, as found previously in schizophrenia patients.	topic_sch
73834	4	354750	5	NULL	NULL	0	NULL	CaMKII	GP	isoform ratio of	is decreased in		markedly			schizophrenia patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in LPA1 KO mice the α/β isoform ratio of CaMKII, which plays a key role in neuronal maturation during development, was markedly decreased, as found previously in schizophrenia patients.	topic_sch
73835	1	354751	5	NULL	NULL	NULL	NULL	neurodevelopment disorder	MedicalFinding	primary	affect					cerebral cortex	OrganismPart	normal			NULL	schizophrenia	NULL	NULL	NULL	NULL	NULL	NULL	These findings support a primary neurodevelopment disorder affecting the normal cerebral cortex development in schizophrenia.	topic_sch
73836	1	354752	5	NULL	NULL	0	NULL	relatives of schizophrenia patients	GroupOfPeople		demonstrate					prefrontal cortex	OrganismPart	abnormalities in;;activation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Relatives of schizophrenia patients demonstrate abnormalities in prefrontal cortical activation during executive processing as measured by functional neuroimaging, albeit not consistently. 	topic_sch
73837	2	354752	5	NULL	NULL	0	NULL	statement 1	Process		occurs during					executive processing	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Relatives of schizophrenia patients demonstrate abnormalities in prefrontal cortical activation during executive processing as measured by functional neuroimaging, albeit not consistently. 	topic_sch
73838	1	354753	5	NULL	NULL	0	NULL	DUI	Time	prolonged	represents					prognostic factor		negative			NULL		0	NULL	NULL	NULL	NULL	NULL	A significant body of evidence shows that a prolonged DUI represents a negative prognostic factor particularly in schizophrenia.	topic_sch
73839	2	354753	5	NULL	NULL	0	NULL	statement 1	Process		occurs in		particularly			schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	A significant body of evidence shows that a prolonged DUI represents a negative prognostic factor particularly in schizophrenia.	topic_sch
73840	1	354754	5	NULL	NULL	0	NULL	Schizophrenic patients	GroupOfPeople		experience					HPA axis	OrganismPart	hyper function of			NULL		0	NULL	NULL	NULL	NULL	NULL	In summary, the evidence suggests people with schizophrenia can experience both hyper- and hypo-function of the HPA axis. 	topic_sch
73841	2	354754	5	NULL	NULL	0	NULL	Schizophrenic patients	GroupOfPeople		experience					HPA axis	OrganismPart	hypo function of			NULL		0	NULL	NULL	NULL	NULL	NULL	In summary, the evidence suggests people with schizophrenia can experience both hyper- and hypo-function of the HPA axis. 	topic_sch
73842	1	354755	5	NULL	NULL	NULL	NULL	Schizophrenic patients	GroupOfPeople		suffer					mortality		premature 			NULL		NULL	NULL	NULL	NULL	NULL	NULL	It is likely that this contributes to the pattern of poor physical health and premature mortality suffered by people with schizophrenia, in particular the high rates of cardiovascular and metabolic disturbance.	topic_sch
73843	2	354755	5	NULL	NULL	0	NULL	Schizophrenic patients	GroupOfPeople		suffer					physical health	PhysicalPhenomenon	poor			NULL		0	NULL	NULL	NULL	NULL	NULL	It is likely that this contributes to the pattern of poor physical health and premature mortality suffered by people with schizophrenia, in particular the high rates of cardiovascular and metabolic disturbance.	topic_sch
73844	3	354755	5	NULL	NULL	0	NULL	Schizophrenic patients	GroupOfPeople		suffer					cardiovascular disturbance	MedicalFinding	high rates of			NULL		0	NULL	NULL	NULL	NULL	NULL	It is likely that this contributes to the pattern of poor physical health and premature mortality suffered by people with schizophrenia, in particular the high rates of cardiovascular and metabolic disturbance.	topic_sch
73845	4	354755	5	NULL	NULL	0	NULL	Schizophrenic patients	GroupOfPeople		suffer					metabolic disturbance	MedicalFinding	high rates of			NULL		0	NULL	NULL	NULL	NULL	NULL	It is likely that this contributes to the pattern of poor physical health and premature mortality suffered by people with schizophrenia, in particular the high rates of cardiovascular and metabolic disturbance.	topic_sch
73846	1	354758	5	NULL	NULL	0	NULL	maternal schizophrenia	MedicalFinding		is predictive to					postpartum psychosis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	After adjusting for age, parity, unhealthy behaviors, length of antipsychotic treatment, and maternal-fetal attachment, maternal schizophrenia remains predictive to prematurity and postpartum psychosis.	topic_sch
73847	1	354759	5	NULL	NULL	0	NULL	Quetiapine	Chemical		is a type of					atypical antipsychotic agent	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Quetiapine is an atypical antipsychotic agent increasingly used to treat schizophrenia and bipolar disorder in pediatric patients.	topic_sch
73848	2	354759	5	NULL	NULL	0	NULL	Quetiapine	Chemical		treats					schizophrenia	MedicalFinding				NULL	pediatric patients	0	NULL	NULL	NULL	NULL	NULL	Quetiapine is an atypical antipsychotic agent increasingly used to treat schizophrenia and bipolar disorder in pediatric patients.	topic_sch
73849	3	354759	5	NULL	NULL	0	NULL	Quetiapine	Chemical		treats					bipolar disorder	MedicalFinding				NULL	pediatric patients	0	NULL	NULL	NULL	NULL	NULL	Quetiapine is an atypical antipsychotic agent increasingly used to treat schizophrenia and bipolar disorder in pediatric patients.	topic_sch
73850	1	354760	5	NULL	NULL	0	NULL	galantamine	Chemical		is an inhibitor of		weak			acetylcholine esterase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Clinical studies show that galantamine, a weak acetylcholine (ACh) esterase inhibitor and allosteric potentiator of nicotinic ACh receptors (nAChRs), improves negative and cognitive symptoms in schizophrenia, while donepezil, a potent ACh esterase inhibitor, does not. 	topic_sch
73851	2	354760	5	NULL	NULL	0	NULL	ACh	Chemical		is					acetylcholine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Clinical studies show that galantamine, a weak acetylcholine (ACh) esterase inhibitor and allosteric potentiator of nicotinic ACh receptors (nAChRs), improves negative and cognitive symptoms in schizophrenia, while donepezil, a potent ACh esterase inhibitor, does not. 	topic_sch
73852	3	354760	5	NULL	NULL	0	NULL	galantamine	Chemical		allosteric potentiator of					nAChRs	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Clinical studies show that galantamine, a weak acetylcholine (ACh) esterase inhibitor and allosteric potentiator of nicotinic ACh receptors (nAChRs), improves negative and cognitive symptoms in schizophrenia, while donepezil, a potent ACh esterase inhibitor, does not. 	topic_sch
73853	4	354760	5	NULL	NULL	0	NULL	nAChRs	GP		is					nicotinic ACh receptors	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Clinical studies show that galantamine, a weak acetylcholine (ACh) esterase inhibitor and allosteric potentiator of nicotinic ACh receptors (nAChRs), improves negative and cognitive symptoms in schizophrenia, while donepezil, a potent ACh esterase inhibitor, does not. 	topic_sch
73854	5	354760	5	NULL	NULL	0	NULL	galantamine	Chemical		improves					schizophrenia	MedicalFinding	negative symptoms of			NULL		0	NULL	NULL	NULL	NULL	NULL	Clinical studies show that galantamine, a weak acetylcholine (ACh) esterase inhibitor and allosteric potentiator of nicotinic ACh receptors (nAChRs), improves negative and cognitive symptoms in schizophrenia, while donepezil, a potent ACh esterase inhibitor, does not. 	topic_sch
73855	6	354760	5	NULL	NULL	0	NULL	galantamine	Chemical		improves					schizophrenia	MedicalFinding	cognitive symptoms of			NULL		0	NULL	NULL	NULL	NULL	NULL	Clinical studies show that galantamine, a weak acetylcholine (ACh) esterase inhibitor and allosteric potentiator of nicotinic ACh receptors (nAChRs), improves negative and cognitive symptoms in schizophrenia, while donepezil, a potent ACh esterase inhibitor, does not. 	topic_sch
73856	7	354760	5	NULL	NULL	0	NULL	donepezil	Chemical		is an inhibitor of		potent			ACh esterase	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Clinical studies show that galantamine, a weak acetylcholine (ACh) esterase inhibitor and allosteric potentiator of nicotinic ACh receptors (nAChRs), improves negative and cognitive symptoms in schizophrenia, while donepezil, a potent ACh esterase inhibitor, does not. 	topic_sch
73857	8	354760	5	NULL	NULL	0	NULL	donepezil	Chemical		does not improve					schizophrenia	MedicalFinding	negative symptoms of			NULL		0	NULL	NULL	NULL	NULL	NULL	Clinical studies show that galantamine, a weak acetylcholine (ACh) esterase inhibitor and allosteric potentiator of nicotinic ACh receptors (nAChRs), improves negative and cognitive symptoms in schizophrenia, while donepezil, a potent ACh esterase inhibitor, does not. 	topic_sch
73858	9	354760	5	NULL	NULL	0	NULL	donepezil	Chemical		does not improve					schizophrenia	MedicalFinding	cognitive symptoms of			NULL		0	NULL	NULL	NULL	NULL	NULL	Clinical studies show that galantamine, a weak acetylcholine (ACh) esterase inhibitor and allosteric potentiator of nicotinic ACh receptors (nAChRs), improves negative and cognitive symptoms in schizophrenia, while donepezil, a potent ACh esterase inhibitor, does not. 	topic_sch
73859	1	354761	5	NULL	NULL	0	NULL	QKI gene	GP	human	is a synonym of					quaking homolog, KH domain RNA binding (mouse)	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The human QKI gene, called quaking homolog, KH domain RNA binding (mouse), is a candidate gene for schizophrenia encoding an RNA-binding protein.	topic_sch
73860	2	354761	5	NULL	NULL	0	NULL	QKI gene	GP	human	is a candidate gene for					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The human QKI gene, called quaking homolog, KH domain RNA binding (mouse), is a candidate gene for schizophrenia encoding an RNA-binding protein.	topic_sch
73861	3	354761	5	NULL	NULL	0	NULL	QKI gene	GP		encodes					RNA-binding protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The human QKI gene, called quaking homolog, KH domain RNA binding (mouse), is a candidate gene for schizophrenia encoding an RNA-binding protein.	topic_sch
73862	1	354762	5	NULL	NULL	0	NULL	CHRNA7	GP		is a candidate gene for					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	CHRNA7 has been shown to be a strong candidate gene for schizophrenia and bipolar disorder.	topic_sch
73863	2	354762	5	NULL	NULL	0	NULL	CHRNA7	GP		is a candidate gene for					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	CHRNA7 has been shown to be a strong candidate gene for schizophrenia and bipolar disorder.	topic_sch
73864	1	354763	5	NULL	NULL	0	NULL	CHRNA7	GP		is a candidate gene for		strong			schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	CHRNA7 has been shown to be a strong candidate gene for schizophrenia and bipolar disorder. It is located on chromosome 15q13-q14, which is one of the replicated linkage spots for schizophrenia and bipolar disorder.	topic_sch
73865	2	354763	5	NULL	NULL	0	NULL	CHRNA7	GP		is a candidate gene for		strong			bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	CHRNA7 has been shown to be a strong candidate gene for schizophrenia and bipolar disorder. It is located on chromosome 15q13-q14, which is one of the replicated linkage spots for schizophrenia and bipolar disorder.	topic_sch
73866	3	354763	5	NULL	NULL	0	NULL	CHRNA7	GP		is located on					chromosome 15q13-q14	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	CHRNA7 has been shown to be a strong candidate gene for schizophrenia and bipolar disorder. It is located on chromosome 15q13-q14, which is one of the replicated linkage spots for schizophrenia and bipolar disorder.	topic_sch
73867	4	354763	5	NULL	NULL	0	NULL	chromosome 15q13-q14	Chromosome		is a linkage spot for					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	CHRNA7 has been shown to be a strong candidate gene for schizophrenia and bipolar disorder. It is located on chromosome 15q13-q14, which is one of the replicated linkage spots for schizophrenia and bipolar disorder.	topic_sch
73868	5	354763	5	NULL	NULL	0	NULL	chromosome 15q13-q14	Chromosome		is a linkage spot for					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	CHRNA7 has been shown to be a strong candidate gene for schizophrenia and bipolar disorder. It is located on chromosome 15q13-q14, which is one of the replicated linkage spots for schizophrenia and bipolar disorder.	topic_sch
73869	1	354764	5	NULL	NULL	0	NULL	schizophrenia outpatients	GroupOfPeople	clinically stable	maintains					remission states					NULL		0	NULL	NULL	NULL	NULL	NULL	This study suggested that most clinically stable outpatients with schizophrenia maintain their remission states after being switched to aripiprazole, without serious symptom aggravation and adverse events over a course of 26 weeks.	topic_sch
73870	2	354764	5	NULL	NULL	0	NULL	aripiprazole	Chemical	switching to	leads to					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	This study suggested that most clinically stable outpatients with schizophrenia maintain their remission states after being switched to aripiprazole, without serious symptom aggravation and adverse events over a course of 26 weeks.	topic_sch
73871	1	354765	5	NULL	NULL	0	NULL	Nrg1	GP		is					Neuregulin 1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Neuregulin 1 (Nrg1), a schizophrenia susceptibility gene, is involved in fundamental aspects of neurodevelopment. 	topic_sch
73872	2	354765	5	NULL	NULL	0	NULL	Neuregulin 1	GP		is a type of					schizophrenia susceptibility gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Neuregulin 1 (Nrg1), a schizophrenia susceptibility gene, is involved in fundamental aspects of neurodevelopment. 	topic_sch
73873	3	354765	5	NULL	NULL	0	NULL	Neuregulin 1	GP		is involved in					neurodevelopment	Process	fundamental aspects of			NULL		0	NULL	NULL	NULL	NULL	NULL	Neuregulin 1 (Nrg1), a schizophrenia susceptibility gene, is involved in fundamental aspects of neurodevelopment. 	topic_sch
73874	1	354768	5	NULL	NULL	0	NULL	CHRM1	GP		is decreased in		selectively			MRDS patients	GroupOfPeople	frontal cortex regions of			NULL		0	NULL	NULL	NULL	NULL	NULL	Having recently shown that CHRM1 levels are decreased selectively in frontal cortex regions of a subpopulation of schizophrenic patients (muscarinic receptor deficit schizophrenia, MRDS) we aimed to compare the protein expression of BACE1 and NRG1 in the agranular frontal cortex Brodmann's area 6 of SCZ subjects with normal levels of CHRM1 (N=19), MRDS (N=20), and age/gender-matched non-psychiatric (healthy) controls (HC; N=20).	topic_sch
73875	2	354768	5	NULL	NULL	0	NULL	MRDS	MedicalFinding		is					muscarinic receptor deficit schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Having recently shown that CHRM1 levels are decreased selectively in frontal cortex regions of a subpopulation of schizophrenic patients (muscarinic receptor deficit schizophrenia, MRDS) we aimed to compare the protein expression of BACE1 and NRG1 in the agranular frontal cortex Brodmann's area 6 of SCZ subjects with normal levels of CHRM1 (N=19), MRDS (N=20), and age/gender-matched non-psychiatric (healthy) controls (HC; N=20).	topic_sch
73876	3	354768	5	NULL	NULL	0	NULL	MRDS	MedicalFinding		is a subpopulation of					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Having recently shown that CHRM1 levels are decreased selectively in frontal cortex regions of a subpopulation of schizophrenic patients (muscarinic receptor deficit schizophrenia, MRDS) we aimed to compare the protein expression of BACE1 and NRG1 in the agranular frontal cortex Brodmann's area 6 of SCZ subjects with normal levels of CHRM1 (N=19), MRDS (N=20), and age/gender-matched non-psychiatric (healthy) controls (HC; N=20).	topic_sch
73877	1	354769	5	NULL	NULL	0	NULL	NRG1	GP	proteolytic processing of 	is impaired in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	These data suggest that the proteolytic processing of NRG1 is impaired in schizophrenia.	topic_sch
73774	1	354770	7	NULL	NULL	0	NULL	Bipolar I disorder	MedicalFinding		is a type of					mood disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar I disorder is a mood disorder that is characterized by at least one manic or mixed episode.	topic_bd
73775	2	354770	7	NULL	NULL	0	NULL	statement 1	Process		characterized by					manic episode	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar I disorder is a mood disorder that is characterized by at least one manic or mixed episode.	topic_bd
73776	3	354770	7	NULL	NULL	0	NULL	statement 1	Process		characterized by					mixed eposode	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar I disorder is a mood disorder that is characterized by at least one manic or mixed episode.	topic_bd
73777	1	354771	7	NULL	NULL	0	NULL	Bipolar II disorder	MedicalFinding		is a type of					bipolar spectrum disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar II disorder is a bipolar spectrum disorder characterized by at least one hypomanic episode and at least one major depressive episode; with this disorder, depressive episodes are more frequent and more intense than manic episodes.	topic_bd
73989	2	354771	7	NULL	NULL	0	NULL	statement 1	Process		characterized by					 hypomanic episode	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar II disorder is a bipolar spectrum disorder characterized by at least one hypomanic episode and at least one major depressive episode; with this disorder, depressive episodes are more frequent and more intense than manic episodes.	topic_bd
73990	3	354771	7	NULL	NULL	NULL	NULL	statement 1	Process		characterized by					major depressive episode	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Bipolar II disorder is a bipolar spectrum disorder characterized by at least one hypomanic episode and at least one major depressive episode; with this disorder, depressive episodes are more frequent and more intense than manic episodes.	topic_bd
73991	4	354771	7	NULL	NULL	NULL	NULL	depressive episodes 	MedicalFinding	frequency of	is more than					manic episodes	MedicalFinding	frequency of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Bipolar II disorder is a bipolar spectrum disorder characterized by at least one hypomanic episode and at least one major depressive episode; with this disorder, depressive episodes are more frequent and more intense than manic episodes.	topic_bd
73992	5	354771	7	NULL	NULL	0	NULL	depressive episodes 	MedicalFinding		more intense than					manic episodes	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar II disorder is a bipolar spectrum disorder characterized by at least one hypomanic episode and at least one major depressive episode; with this disorder, depressive episodes are more frequent and more intense than manic episodes.	topic_bd
73993	1	354772	7	NULL	NULL	0	NULL	Bipolar disorder	MedicalFinding		is a type of					mental illness	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar disorder is a serious mental illness that is characterized by extreme changes in mood, from mania to depression.	topic_bd
73994	2	354772	7	NULL	NULL	0	NULL	mania	MedicalFinding		changed to					depression	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar disorder is a serious mental illness that is characterized by extreme changes in mood, from mania to depression.	topic_bd
73995	3	354772	7	NULL	NULL	NULL	NULL	statement 1	Process		characterized by					statement 2	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Bipolar disorder is a serious mental illness that is characterized by extreme changes in mood, from mania to depression.	topic_bd
73996	1	354773	7	NULL	NULL	0	NULL	Women	GroupOfPeople		have more					mood episode	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Women are also at higher risk for rapid cycling, which means having four or more mood episodes in one year.	topic_bd
74001	1	354774	7	NULL	NULL	0	NULL	 bipolar disorder	MedicalFinding		involves					genetic component	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Experts do believe that bipolar disorder often runs in families, and there is a genetic component to this mood disorder.	topic_bd
73997	1	354775	7	NULL	NULL	0	NULL	bipolar disorder	MedicalFinding	treatment of	more difficult with					alcohol	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Stressful life events -- or alcohol or drug abuse -- can make bipolar disorder more difficult to treat.	topic_bd
73998	2	354775	7	NULL	NULL	NULL	NULL	bipolar disorder	MedicalFinding	treatment of	more difficult with					drug abuse	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Stressful life events -- or alcohol or drug abuse -- can make bipolar disorder more difficult to treat.	topic_bd
73999	1	354776	7	NULL	NULL	0	NULL	bipolar disorder	MedicalFinding		caused by		partly			neurotransmitter	Chemical	underlying problem with the balance of			NULL		0	NULL	NULL	NULL	NULL	NULL	Experts believe bipolar disorder is partly caused by an underlying problem with the balance of brain chemicals called neurotransmitters.	topic_bd
74000	2	354776	7	NULL	NULL	0	NULL	neurotransmitter	Chemical		is a type of					brain chemical	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Experts believe bipolar disorder is partly caused by an underlying problem with the balance of brain chemicals called neurotransmitters.	topic_bd
74002	1	354777	7	NULL	NULL	0	NULL	noradrenaline	Chemical		involved in					brain function	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Three brain chemicals -- noradrenaline (norepinephrine), serotonin, and dopamine -- are involved in both brain and bodily functions. 	topic_bd
74003	2	354777	7	NULL	NULL	0	NULL	serotonin	Chemical		involved in					brain function	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Three brain chemicals -- noradrenaline (norepinephrine), serotonin, and dopamine -- are involved in both brain and bodily functions. 	topic_bd
74004	3	354777	7	NULL	NULL	0	NULL	dopamine	Chemical		involved in					brain function	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Three brain chemicals -- noradrenaline (norepinephrine), serotonin, and dopamine -- are involved in both brain and bodily functions. 	topic_bd
74005	4	354777	7	NULL	NULL	0	NULL	noradrenaline	Chemical		involved in					body function	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Three brain chemicals -- noradrenaline (norepinephrine), serotonin, and dopamine -- are involved in both brain and bodily functions. 	topic_bd
74006	5	354777	7	NULL	NULL	0	NULL	serotonin	Chemical		involved in					body function	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Three brain chemicals -- noradrenaline (norepinephrine), serotonin, and dopamine -- are involved in both brain and bodily functions. 	topic_bd
74007	6	354777	7	NULL	NULL	0	NULL	dopamine	Chemical		involved in					body function	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Three brain chemicals -- noradrenaline (norepinephrine), serotonin, and dopamine -- are involved in both brain and bodily functions. 	topic_bd
74008	7	354777	7	NULL	NULL	0	NULL	 noradrenaline	Chemical		is					norepinephrine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Three brain chemicals -- noradrenaline (norepinephrine), serotonin, and dopamine -- are involved in both brain and bodily functions. 	topic_bd
74009	8	354777	7	NULL	NULL	0	NULL	noradrenaline	Chemical		is a type of					brain chemical	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Three brain chemicals -- noradrenaline (norepinephrine), serotonin, and dopamine -- are involved in both brain and bodily functions. 	topic_bd
74010	9	354777	7	NULL	NULL	0	NULL	serotonin	Chemical		is a type of					brain chemical	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Three brain chemicals -- noradrenaline (norepinephrine), serotonin, and dopamine -- are involved in both brain and bodily functions. 	topic_bd
74011	10	354777	7	NULL	NULL	0	NULL	dopamine	Chemical		is a type of					brain chemical	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Three brain chemicals -- noradrenaline (norepinephrine), serotonin, and dopamine -- are involved in both brain and bodily functions. 	topic_bd
74012	1	354778	7	NULL	NULL	0	NULL	Noradrenaline	Chemical		linked to					depression	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Noradrenaline and serotonin have been consistently linked to psychiatric mood disorders such as depression and bipolar disorder.	topic_bd
74013	2	354778	7	NULL	NULL	0	NULL	Noradrenaline	Chemical		linked to					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Noradrenaline and serotonin have been consistently linked to psychiatric mood disorders such as depression and bipolar disorder.	topic_bd
74014	3	354778	7	NULL	NULL	0	NULL	serotonin	Chemical		linked to					depression	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Noradrenaline and serotonin have been consistently linked to psychiatric mood disorders such as depression and bipolar disorder.	topic_bd
74015	4	354778	7	NULL	NULL	0	NULL	serotonin	Chemical		linked to					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Noradrenaline and serotonin have been consistently linked to psychiatric mood disorders such as depression and bipolar disorder.	topic_bd
74016	5	354778	7	NULL	NULL	0	NULL	depression	MedicalFinding		is a type of					psychiatric mood disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Noradrenaline and serotonin have been consistently linked to psychiatric mood disorders such as depression and bipolar disorder.	topic_bd
74017	6	354778	7	NULL	NULL	0	NULL	bipolar disorder	MedicalFinding		is a type of					 psychiatric mood disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Noradrenaline and serotonin have been consistently linked to psychiatric mood disorders such as depression and bipolar disorder.	topic_bd
74018	1	354779	7	NULL	NULL	0	NULL	bipolar II	MedicalFinding		diagnosis of		prevalent			bipolar I family	MedicalFinding	relatives in			NULL		0	NULL	NULL	NULL	NULL	NULL	However, among patients with bipolar II, researchers found onlyone relative with bipolar I disorder. They concluded that bipolar II is the most prevalent diagnosis of relatives in both bipolar I and bipolar II families.	topic_bd
74019	2	354779	7	NULL	NULL	0	NULL	 bipolar II	MedicalFinding		diagnosis of		prevalent			bipolar II family	MedicalFinding	relatives in			NULL		0	NULL	NULL	NULL	NULL	NULL	However, among patients with bipolar II, researchers found onlyone relative with bipolar I disorder. They concluded that bipolar II is the most prevalent diagnosis of relatives in both bipolar I and bipolar II families.	topic_bd
74020	1	354780	7	NULL	NULL	0	NULL	 bipolar disorder	MedicalFinding		have 					sleep-wake cycle	Process	genetic predisposition to abnormalities in			NULL		0	NULL	NULL	NULL	NULL	NULL	Some findings show that people with bipolar disorder have a genetic predisposition to sleep-wake cycle abnormalities that may be responsible for triggering the symptoms of depression and mania.	topic_bd
74021	2	354780	7	NULL	NULL	0	NULL	statement 1	Process		responsible for		may be			depression	MedicalFinding	triggering the symptoms of			NULL		0	NULL	NULL	NULL	NULL	NULL	Some findings show that people with bipolar disorder have a genetic predisposition to sleep-wake cycle abnormalities that may be responsible for triggering the symptoms of depression and mania.	topic_bd
74022	3	354780	7	NULL	NULL	NULL	NULL	statement 1	Process		responsible for		may be			mania	MedicalFinding	triggering the symptoms of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Some findings show that people with bipolar disorder have a genetic predisposition to sleep-wake cycle abnormalities that may be responsible for triggering the symptoms of depression and mania.	topic_bd
74023	1	354782	7	NULL	NULL	NULL	NULL	Fish	Organism		help with					 depression	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Fish may have earned its reputation as “brain food” because some people eat fish to help with depression, psychosis, attention deficit-hyperactivity disorder (ADHD), Alzheimer’s disease, and other thinking disorders.	topic_bd
74024	2	354782	7	NULL	NULL	NULL	NULL	Fish	Organism		help with					psychosis	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Fish may have earned its reputation as “brain food” because some people eat fish to help with depression, psychosis, attention deficit-hyperactivity disorder (ADHD), Alzheimer’s disease, and other thinking disorders.	topic_bd
74025	3	354782	7	NULL	NULL	0	NULL	Fish	Organism		help with					ADHD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Fish may have earned its reputation as “brain food” because some people eat fish to help with depression, psychosis, attention deficit-hyperactivity disorder (ADHD), Alzheimer’s disease, and other thinking disorders.	topic_bd
74026	4	354782	7	NULL	NULL	0	NULL	Fish	Organism		help with					Alzheimer disease	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Fish may have earned its reputation as “brain food” because some people eat fish to help with depression, psychosis, attention deficit-hyperactivity disorder (ADHD), Alzheimer’s disease, and other thinking disorders.	topic_bd
74027	5	354782	7	NULL	NULL	0	NULL	Fish	Organism		help with					thinking disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Fish may have earned its reputation as “brain food” because some people eat fish to help with depression, psychosis, attention deficit-hyperactivity disorder (ADHD), Alzheimer’s disease, and other thinking disorders.	topic_bd
74028	6	354782	7	NULL	NULL	0	NULL	ADHD	MedicalFinding		is					attention deficit-hyperactivity disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Fish may have earned its reputation as “brain food” because some people eat fish to help with depression, psychosis, attention deficit-hyperactivity disorder (ADHD), Alzheimer’s disease, and other thinking disorders.	topic_bd
74029	1	354784	7	NULL	NULL	NULL	NULL	Early onset bipolar disorder	MedicalFinding	symptoms of	 similar to		very			ADHD	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Early onset, or juvenile, bipolar disorder has symptoms very similar to ADHD (attention deficit hyperactivity disorder).	topic_bd
74030	2	354784	7	NULL	NULL	NULL	NULL	 juvenile bipolar disorder	MedicalFinding	symptoms of	similar to		very			ADHD	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Early onset, or juvenile, bipolar disorder has symptoms very similar to ADHD (attention deficit hyperactivity disorder).	topic_bd
74031	3	354784	7	NULL	NULL	0	NULL	ADHD	MedicalFinding		is					attention deficit hyperactivity disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Early onset, or juvenile, bipolar disorder has symptoms very similar to ADHD (attention deficit hyperactivity disorder).	topic_bd
73878	1	354786	5	NULL	NULL	0	NULL	TGM2	GP		is involved in					schizophrenia	MedicalFinding	dysfunction of;;immune system in			NULL		0	NULL	NULL	NULL	NULL	NULL	TGM2 may be involved in dysfunction of the immune system in schizophrenia.	topic_sch
74544	1	354787	6	NULL	NULL	0	NULL	Papillomatosis	MedicalFinding		is caused by					hyperplasia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Papillomatosis is skin surface elevation caused by hyperplasia	topic_bc
74545	2	354787	6	NULL	NULL	0	NULL	Papillomatosis	MedicalFinding		causes					skin surface	OrganismPart	elevation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Papillomatosis is skin surface elevation caused by hyperplasia	topic_bc
73879	1	354798	5	NULL	NULL	0	NULL	family income	PhysicalPhenomenon		does not affect					autism	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Family income, education, and lifestyle do not seem to affect the risk of autism.	topic_aut
73880	2	354798	5	NULL	NULL	0	NULL	education	Process		does not affect					autism	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Family income, education, and lifestyle do not seem to affect the risk of autism.	topic_aut
73881	3	354798	5	NULL	NULL	0	NULL	lifestyle	AbstractConcept		does not affect					autism	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Family income, education, and lifestyle do not seem to affect the risk of autism.	topic_aut
73882	1	354799	5	NULL	NULL	NULL	NULL	autism	MedicalFinding		is not linked to					MMR vaccine	MedicalProcedure				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The American Academy of Pediatrics and the Center for Disease Control and Prevention report that there is no proven link between autism and the MMR vaccine, or any other vaccine.	topic_aut
73883	1	354800	5	NULL	NULL	0	NULL	Asperger syndrome	MedicalFinding		similar to					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Asperger syndrome (like autism, but with normal language development)	topic_aut
73884	1	354801	5	NULL	NULL	0	NULL	PDD-NOS	MedicalFinding		is					Pervasive developmental disorder - not otherwise specified	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Pervasive developmental disorder - not otherwise specified (PDD-NOS), also called atypical autism.	topic_aut
73885	2	354801	5	NULL	NULL	0	NULL	PDD-NOS	MedicalFinding		is a synonym of					atypical autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Pervasive developmental disorder - not otherwise specified (PDD-NOS), also called atypical autism.	topic_aut
73886	1	354803	5	NULL	NULL	0	NULL	autism	MedicalFinding		is associated with		may be			Fragile X syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Autism can be associated with other disorders that affect the brain, such as: * Fragile X syndrome * Mental retardation * Tuberous sclerosis	topic_aut
73887	2	354803	5	NULL	NULL	0	NULL	autism	MedicalFinding		is associated with		may be			Mental retardation	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Autism can be associated with other disorders that affect the brain, such as: * Fragile X syndrome * Mental retardation * Tuberous sclerosis	topic_aut
73888	3	354803	5	NULL	NULL	0	NULL	autism	MedicalFinding		is associated with		may be			Mental retardation	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Autism can be associated with other disorders that affect the brain, such as: * Fragile X syndrome * Mental retardation * Tuberous sclerosis	topic_aut
73889	4	354803	5	NULL	NULL	0	NULL	Mental retardation	MedicalFinding		affect					brain	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Autism can be associated with other disorders that affect the brain, such as: * Fragile X syndrome * Mental retardation * Tuberous sclerosis	topic_aut
73890	5	354803	5	NULL	NULL	0	NULL	Fragile X syndrome	MedicalFinding		affect					brain	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Autism can be associated with other disorders that affect the brain, such as: * Fragile X syndrome * Mental retardation * Tuberous sclerosis	topic_aut
73891	6	354803	5	NULL	NULL	0	NULL	Mental retardation	MedicalFinding		affect					brain	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Autism can be associated with other disorders that affect the brain, such as: * Fragile X syndrome * Mental retardation * Tuberous sclerosis	topic_aut
73892	1	354804	5	NULL	NULL	0	NULL	autism	MedicalFinding		develops					seizures	MedicalFinding				NULL	few people	0	NULL	NULL	NULL	NULL	NULL	Some people with autism will develop seizures	topic_aut
74032	1	354806	7	NULL	NULL	0	NULL	bipolar disorder	MedicalFinding	people with	have					heart disease	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	People diagnosed with bipolar disorder are more likely to have certain other health problems, including heart disease, thyroid problems and obesity.	topic_bd
74033	2	354806	7	NULL	NULL	0	NULL	bipolar disorder	MedicalFinding	people with	have					thyroid problems	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	People diagnosed with bipolar disorder are more likely to have certain other health problems, including heart disease, thyroid problems and obesity.	topic_bd
74034	3	354806	7	NULL	NULL	0	NULL	bipolar disorder	MedicalFinding	people with	have					obesity	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	People diagnosed with bipolar disorder are more likely to have certain other health problems, including heart disease, thyroid problems and obesity.	topic_bd
74035	1	354807	7	NULL	NULL	0	NULL	Lithium	Chemical		effective at					stabilizing mood	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Lithium (Lithobid, others) is effective at stabilizing mood and preventing the extreme highs and lows of certain categories of bipolar disorder and has been used for many years. 	topic_bd
74036	2	354807	7	NULL	NULL	0	NULL	Lithium	Chemical		prevent					bipolar disorder	MedicalFinding	extreme high of			NULL		0	NULL	NULL	NULL	NULL	NULL	Lithium (Lithobid, others) is effective at stabilizing mood and preventing the extreme highs and lows of certain categories of bipolar disorder and has been used for many years. 	topic_bd
74037	3	354807	7	NULL	NULL	0	NULL	Lithium	Chemical		prevent					bipolar disorder	MedicalFinding	extreme lows of			NULL		0	NULL	NULL	NULL	NULL	NULL	Lithium (Lithobid, others) is effective at stabilizing mood and preventing the extreme highs and lows of certain categories of bipolar disorder and has been used for many years. 	topic_bd
74038	1	354808	7	NULL	NULL	0	NULL	 valproic acid 	Chemical		is a type of					mood stabilizing medications	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	•\tAnticonvulsants. These mood stabilizing medications include valproic acid (Depakene), divalproex (Depakote) and lamotrigine (Lamictal). 	topic_bd
74039	2	354808	7	NULL	NULL	0	NULL	divalproex	Chemical		is a type of					mood stabilizing medications	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	•\tAnticonvulsants. These mood stabilizing medications include valproic acid (Depakene), divalproex (Depakote) and lamotrigine (Lamictal). 	topic_bd
74040	3	354808	7	NULL	NULL	0	NULL	lamotrigine	Chemical		is a type of					mood stabilizing medications	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	•\tAnticonvulsants. These mood stabilizing medications include valproic acid (Depakene), divalproex (Depakote) and lamotrigine (Lamictal). 	topic_bd
74041	4	354808	7	NULL	NULL	0	NULL	valproic acid	Chemical		is					Depakene	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	•\tAnticonvulsants. These mood stabilizing medications include valproic acid (Depakene), divalproex (Depakote) and lamotrigine (Lamictal). 	topic_bd
74042	5	354808	7	NULL	NULL	0	NULL	divalproex 	Chemical		is					Depakote	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	•\tAnticonvulsants. These mood stabilizing medications include valproic acid (Depakene), divalproex (Depakote) and lamotrigine (Lamictal). 	topic_bd
74043	6	354808	7	NULL	NULL	0	NULL	lamotrigine	Chemical		is					Lamictal	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	•\tAnticonvulsants. These mood stabilizing medications include valproic acid (Depakene), divalproex (Depakote) and lamotrigine (Lamictal). 	topic_bd
74044	1	354810	7	NULL	NULL	0	NULL	antidepressants	Chemical		trigger					manic episodes	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In some people with bipolar disorder, antidepressants can trigger manic episodes, but may be OK if taken along with a mood stabilizer.	topic_bd
74045	2	354810	7	NULL	NULL	0	NULL	statement 1	Process		occur in					bipolar disorder	MedicalFinding	people with			NULL		0	NULL	NULL	NULL	NULL	NULL	In some people with bipolar disorder, antidepressants can trigger manic episodes, but may be OK if taken along with a mood stabilizer.	topic_bd
74046	3	354810	7	NULL	NULL	NULL	NULL	statement 1	Process		does not occur					mood stabilizer	Chemical	along with			NULL		NULL	NULL	NULL	NULL	NULL	NULL	In some people with bipolar disorder, antidepressants can trigger manic episodes, but may be OK if taken along with a mood stabilizer.	topic_bd
74047	1	354811	7	NULL	NULL	0	NULL	olanzapine	Chemical		is a type of					antipsychotic medication	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Certain antipsychotic medications, such as olanzapine (Zyprexa), risperidone (Risperdal) and quetiapine (Seroquel), may help people who don't gain benefits from anticonvulsants.	topic_bd
74048	2	354811	7	NULL	NULL	0	NULL	risperidone	Chemical		is a type of					antipsychotic medication	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Certain antipsychotic medications, such as olanzapine (Zyprexa), risperidone (Risperdal) and quetiapine (Seroquel), may help people who don't gain benefits from anticonvulsants.	topic_bd
74049	3	354811	7	NULL	NULL	0	NULL	quetiapine	Chemical		is a type of					antipsychotic medication	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Certain antipsychotic medications, such as olanzapine (Zyprexa), risperidone (Risperdal) and quetiapine (Seroquel), may help people who don't gain benefits from anticonvulsants.	topic_bd
74050	4	354811	7	NULL	NULL	0	NULL	olanzapine 	Chemical		is					Zyprexa	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Certain antipsychotic medications, such as olanzapine (Zyprexa), risperidone (Risperdal) and quetiapine (Seroquel), may help people who don't gain benefits from anticonvulsants.	topic_bd
74051	5	354811	7	NULL	NULL	0	NULL	 risperidone	Chemical		is					Risperdal	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Certain antipsychotic medications, such as olanzapine (Zyprexa), risperidone (Risperdal) and quetiapine (Seroquel), may help people who don't gain benefits from anticonvulsants.	topic_bd
74052	6	354811	7	NULL	NULL	0	NULL	quetiapine	Chemical		is					Seroquel	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Certain antipsychotic medications, such as olanzapine (Zyprexa), risperidone (Risperdal) and quetiapine (Seroquel), may help people who don't gain benefits from anticonvulsants.	topic_bd
74053	1	354812	7	NULL	NULL	0	NULL	anti-anxiety medications	Chemical		help with		may			anxiety	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	•\tBenzodiazepines. These anti-anxiety medications may help with anxiety and improve sleep. Examples include clonazepam (Klonopin), lorazepam (Ativan), diazepam (Valium), chlordiazepoxide (Librium) and alprazolam (Xanax).	topic_bd
74054	2	354812	7	NULL	NULL	NULL	NULL	anti-anxiety medications	Chemical		improve		may			sleep	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	•\tBenzodiazepines. These anti-anxiety medications may help with anxiety and improve sleep. Examples include clonazepam (Klonopin), lorazepam (Ativan), diazepam (Valium), chlordiazepoxide (Librium) and alprazolam (Xanax).	topic_bd
74055	3	354812	7	NULL	NULL	0	NULL	clonazepam	Chemical		is a type of					anti-anxiety medications	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	•\tBenzodiazepines. These anti-anxiety medications may help with anxiety and improve sleep. Examples include clonazepam (Klonopin), lorazepam (Ativan), diazepam (Valium), chlordiazepoxide (Librium) and alprazolam (Xanax).	topic_bd
74056	4	354812	7	NULL	NULL	0	NULL	lorazepam	Chemical		is a type of					anti-anxiety medications	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	•\tBenzodiazepines. These anti-anxiety medications may help with anxiety and improve sleep. Examples include clonazepam (Klonopin), lorazepam (Ativan), diazepam (Valium), chlordiazepoxide (Librium) and alprazolam (Xanax).	topic_bd
74057	5	354812	7	NULL	NULL	0	NULL	diazepam	Chemical		is a type of					anti-anxiety medications	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	•\tBenzodiazepines. These anti-anxiety medications may help with anxiety and improve sleep. Examples include clonazepam (Klonopin), lorazepam (Ativan), diazepam (Valium), chlordiazepoxide (Librium) and alprazolam (Xanax).	topic_bd
74058	6	354812	7	NULL	NULL	0	NULL	chlordiazepoxide	Chemical		is a type of					anti-anxiety medications	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	•\tBenzodiazepines. These anti-anxiety medications may help with anxiety and improve sleep. Examples include clonazepam (Klonopin), lorazepam (Ativan), diazepam (Valium), chlordiazepoxide (Librium) and alprazolam (Xanax).	topic_bd
74059	7	354812	7	NULL	NULL	0	NULL	alprazolam	Chemical		is a type of					anti-anxiety medications	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	•\tBenzodiazepines. These anti-anxiety medications may help with anxiety and improve sleep. Examples include clonazepam (Klonopin), lorazepam (Ativan), diazepam (Valium), chlordiazepoxide (Librium) and alprazolam (Xanax).	topic_bd
74060	8	354812	7	NULL	NULL	0	NULL	 clonazepam	Chemical		is					Klonopin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	•\tBenzodiazepines. These anti-anxiety medications may help with anxiety and improve sleep. Examples include clonazepam (Klonopin), lorazepam (Ativan), diazepam (Valium), chlordiazepoxide (Librium) and alprazolam (Xanax).	topic_bd
74061	9	354812	7	NULL	NULL	0	NULL	lorazepam	Chemical		is					Ativan	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	•\tBenzodiazepines. These anti-anxiety medications may help with anxiety and improve sleep. Examples include clonazepam (Klonopin), lorazepam (Ativan), diazepam (Valium), chlordiazepoxide (Librium) and alprazolam (Xanax).	topic_bd
74062	10	354812	7	NULL	NULL	0	NULL	diazepam	Chemical		is					Valium	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	•\tBenzodiazepines. These anti-anxiety medications may help with anxiety and improve sleep. Examples include clonazepam (Klonopin), lorazepam (Ativan), diazepam (Valium), chlordiazepoxide (Librium) and alprazolam (Xanax).	topic_bd
74063	11	354812	7	NULL	NULL	0	NULL	chlordiazepoxide	Chemical		is					Librium	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	•\tBenzodiazepines. These anti-anxiety medications may help with anxiety and improve sleep. Examples include clonazepam (Klonopin), lorazepam (Ativan), diazepam (Valium), chlordiazepoxide (Librium) and alprazolam (Xanax).	topic_bd
74064	12	354812	7	NULL	NULL	0	NULL	alprazolam	Chemical		is					Xanax	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	•\tBenzodiazepines. These anti-anxiety medications may help with anxiety and improve sleep. Examples include clonazepam (Klonopin), lorazepam (Ativan), diazepam (Valium), chlordiazepoxide (Librium) and alprazolam (Xanax).	topic_bd
74065	1	354814	7	NULL	NULL	0	NULL	Cyclothymia	MedicalFinding		is a mild form of					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Cyclothymia is a mild form of bipolar disorder. With cyclothymia, hypomania and depression can be disruptive, but the highs and lows are not as severe as they are with other types of bipolar disorder.	topic_bd
74066	2	354814	7	NULL	NULL	0	NULL	hypomania	MedicalFinding		can be					disruptive	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Cyclothymia is a mild form of bipolar disorder. With cyclothymia, hypomania and depression can be disruptive, but the highs and lows are not as severe as they are with other types of bipolar disorder.	topic_bd
74067	3	354814	7	NULL	NULL	0	NULL	depression	MedicalFinding		can be					disruptive	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Cyclothymia is a mild form of bipolar disorder. With cyclothymia, hypomania and depression can be disruptive, but the highs and lows are not as severe as they are with other types of bipolar disorder.	topic_bd
74068	4	354814	7	NULL	NULL	0	NULL	statement 2	Process		along with					cyclothymia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Cyclothymia is a mild form of bipolar disorder. With cyclothymia, hypomania and depression can be disruptive, but the highs and lows are not as severe as they are with other types of bipolar disorder.	topic_bd
74069	5	354814	7	NULL	NULL	0	NULL	statement 3	Process		along with					cyclothymia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Cyclothymia is a mild form of bipolar disorder. With cyclothymia, hypomania and depression can be disruptive, but the highs and lows are not as severe as they are with other types of bipolar disorder.	topic_bd
74070	6	354814	7	NULL	NULL	0	NULL	Cyclothymia	MedicalFinding	highs of	is not as severe as					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Cyclothymia is a mild form of bipolar disorder. With cyclothymia, hypomania and depression can be disruptive, but the highs and lows are not as severe as they are with other types of bipolar disorder.	topic_bd
74071	7	354814	7	NULL	NULL	0	NULL	Cyclothymia	MedicalFinding	lows of	is not as severe as					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Cyclothymia is a mild form of bipolar disorder. With cyclothymia, hypomania and depression can be disruptive, but the highs and lows are not as severe as they are with other types of bipolar disorder.	topic_bd
74086	1	354816	7	NULL	NULL	NULL	NULL	bipolar disorder	MedicalFinding	people with	have					brain	OrganismPart	physical changes in			NULL		NULL	NULL	NULL	NULL	NULL	NULL	People with bipolar disorder appear to have physical changes in their brains.	topic_bd
74087	1	354817	7	NULL	NULL	NULL	NULL	Imbalanced hormones	GP		involved in		may be			bipolar disorder	MedicalFinding	triggering			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imbalanced hormones may be involved in causing or triggering bipolar disorder.	topic_bd
74088	2	354817	7	NULL	NULL	0	NULL	Imbalanced hormones	GP		involved in		may be			bipolar disorder	MedicalFinding	causing			NULL		0	NULL	NULL	NULL	NULL	NULL	Imbalanced hormones may be involved in causing or triggering bipolar disorder.	topic_bd
74089	1	354818	7	NULL	NULL	NULL	NULL	Stress	Process		play a role in		may			bipolar disorder	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Stress, abuse, significant loss or other traumatic experiences may play a role in bipolar disorder.	topic_bd
74090	2	354818	7	NULL	NULL	0	NULL	abuse	Process		play a role in		may			bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Stress, abuse, significant loss or other traumatic experiences may play a role in bipolar disorder.	topic_bd
74091	3	354818	7	NULL	NULL	NULL	NULL	traumatic experiences 	Process		play a role in		may			bipolar disorder	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Stress, abuse, significant loss or other traumatic experiences may play a role in bipolar disorder.	topic_bd
74092	1	354819	7	NULL	NULL	0	NULL	monoamines	Chemical		involved in		may be			BPD	MedicalFinding	pathophysiology of			NULL		0	NULL	NULL	NULL	NULL	NULL	Current data suggest that monoamines, acetylcholine, amino acids, cortisol, thyroid hormones, and melatonin may be involved in the pathophysiology of bipolar disorder (BPD).	topic_bd
74093	2	354819	7	NULL	NULL	0	NULL	acetylcholine	Chemical		involved in		may be			BPD	MedicalFinding	pathophysiology of			NULL		0	NULL	NULL	NULL	NULL	NULL	Current data suggest that monoamines, acetylcholine, amino acids, cortisol, thyroid hormones, and melatonin may be involved in the pathophysiology of bipolar disorder (BPD).	topic_bd
74094	3	354819	7	NULL	NULL	0	NULL	 amino acids	AminoAcid		involved in		may be			BPD	MedicalFinding	pathophysiology of			NULL		0	NULL	NULL	NULL	NULL	NULL	Current data suggest that monoamines, acetylcholine, amino acids, cortisol, thyroid hormones, and melatonin may be involved in the pathophysiology of bipolar disorder (BPD).	topic_bd
74095	4	354819	7	NULL	NULL	NULL	NULL	cortisol	Chemical		 involved in		may be			BPD	MedicalFinding	pathophysiology of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Current data suggest that monoamines, acetylcholine, amino acids, cortisol, thyroid hormones, and melatonin may be involved in the pathophysiology of bipolar disorder (BPD).	topic_bd
74096	5	354819	7	NULL	NULL	NULL	NULL	thyroid hormones	Chemical		 involved in		may be			BPD	MedicalFinding	pathophysiology of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Current data suggest that monoamines, acetylcholine, amino acids, cortisol, thyroid hormones, and melatonin may be involved in the pathophysiology of bipolar disorder (BPD).	topic_bd
74097	6	354819	7	NULL	NULL	0	NULL	melatonin	Chemical		involved in		may be			BPD	MedicalFinding	pathophysiology of			NULL		0	NULL	NULL	NULL	NULL	NULL	Current data suggest that monoamines, acetylcholine, amino acids, cortisol, thyroid hormones, and melatonin may be involved in the pathophysiology of bipolar disorder (BPD).	topic_bd
74098	7	354819	7	NULL	NULL	0	NULL	BPD	MedicalFinding		is					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Current data suggest that monoamines, acetylcholine, amino acids, cortisol, thyroid hormones, and melatonin may be involved in the pathophysiology of bipolar disorder (BPD).	topic_bd
74099	1	354820	7	NULL	NULL	0	NULL	acetylcholine	Chemical		is a type of					neurotransmitter	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The chemical compound acetylcholine (often abbreviated ACh) is a neurotransmitter	topic_bd
74100	2	354820	7	NULL	NULL	0	NULL	ACh	Chemical		is					acetylcholine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The chemical compound acetylcholine (often abbreviated ACh) is a neurotransmitter	topic_bd
74101	3	354820	7	NULL	NULL	0	NULL	acetylcholine	Chemical		is a type of					chemical compound	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The chemical compound acetylcholine (often abbreviated ACh) is a neurotransmitter	topic_bd
74102	1	354821	7	NULL	NULL	0	NULL	Melatonin	GP		made by					pineal gland	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Melatonin is a hormone made by the pineal gland , a small gland in the brain. 	topic_bd
74103	2	354821	7	NULL	NULL	0	NULL	pineal gland	OrganismPart		is a type of					small gland	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Melatonin is a hormone made by the pineal gland , a small gland in the brain. 	topic_bd
74104	3	354821	7	NULL	NULL	0	NULL	Melatonin	GP		is a type of					hormone	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Melatonin is a hormone made by the pineal gland , a small gland in the brain. 	topic_bd
74105	1	354822	7	NULL	NULL	0	NULL	Antidepressants	Chemical		cause					TEM	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Antidepressants, stimulants, anticholinergics, steroids, and thyroid hormone have been reported to cause treatment-emergent mania (TEM) in BPD	topic_bd
74106	2	354822	7	NULL	NULL	0	NULL	stimulants	Chemical		cause					TEM	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Antidepressants, stimulants, anticholinergics, steroids, and thyroid hormone have been reported to cause treatment-emergent mania (TEM) in BPD	topic_bd
74107	3	354822	7	NULL	NULL	0	NULL	anticholinergics	Chemical		cause					TEM	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Antidepressants, stimulants, anticholinergics, steroids, and thyroid hormone have been reported to cause treatment-emergent mania (TEM) in BPD	topic_bd
74108	4	354822	7	NULL	NULL	0	NULL	steroids	Chemical		cause					TEM	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Antidepressants, stimulants, anticholinergics, steroids, and thyroid hormone have been reported to cause treatment-emergent mania (TEM) in BPD	topic_bd
74109	5	354822	7	NULL	NULL	0	NULL	 thyroid hormone	GP		cause					TEM	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Antidepressants, stimulants, anticholinergics, steroids, and thyroid hormone have been reported to cause treatment-emergent mania (TEM) in BPD	topic_bd
74110	6	354822	7	NULL	NULL	0	NULL	statement 1	Process		occur in					BPD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Antidepressants, stimulants, anticholinergics, steroids, and thyroid hormone have been reported to cause treatment-emergent mania (TEM) in BPD	topic_bd
74111	7	354822	7	NULL	NULL	0	NULL	statement 2	Process		occur in					BPD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Antidepressants, stimulants, anticholinergics, steroids, and thyroid hormone have been reported to cause treatment-emergent mania (TEM) in BPD	topic_bd
74112	8	354822	7	NULL	NULL	0	NULL	statement 3	Process		occur in					BPD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Antidepressants, stimulants, anticholinergics, steroids, and thyroid hormone have been reported to cause treatment-emergent mania (TEM) in BPD	topic_bd
74113	9	354822	7	NULL	NULL	0	NULL	statement 4	Process		occur in					BPD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Antidepressants, stimulants, anticholinergics, steroids, and thyroid hormone have been reported to cause treatment-emergent mania (TEM) in BPD	topic_bd
74114	10	354822	7	NULL	NULL	0	NULL	statement 5	Process		occur in					BPD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Antidepressants, stimulants, anticholinergics, steroids, and thyroid hormone have been reported to cause treatment-emergent mania (TEM) in BPD	topic_bd
74115	11	354822	7	NULL	NULL	0	NULL	TEM	MedicalFinding		is					 treatment-emergent mania	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Antidepressants, stimulants, anticholinergics, steroids, and thyroid hormone have been reported to cause treatment-emergent mania (TEM) in BPD	topic_bd
74116	1	354823	7	NULL	NULL	0	NULL	 anticholinergic agent 	Chemical		blocks					acetylcholine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	An anticholinergic agent is a substance that blocks the neurotransmitter acetylcholine in the central and the peripheral nervous system.	topic_bd
74117	2	354823	7	NULL	NULL	0	NULL	statement 1	Process		occur in					central nervous system	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	An anticholinergic agent is a substance that blocks the neurotransmitter acetylcholine in the central and the peripheral nervous system.	topic_bd
74118	3	354823	7	NULL	NULL	0	NULL	statement 1	Process		occur in					peripheral nervous system	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	An anticholinergic agent is a substance that blocks the neurotransmitter acetylcholine in the central and the peripheral nervous system.	topic_bd
74119	4	354823	7	NULL	NULL	0	NULL	acetylcholine	Chemical		is a type of					neurotransmitter	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	An anticholinergic agent is a substance that blocks the neurotransmitter acetylcholine in the central and the peripheral nervous system.	topic_bd
74120	1	354825	7	NULL	NULL	NULL	NULL	HNF6	GP		function as					key regulators	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	HNF6 and FOXA2 function as key regulators in human colorectal liver metastases.	topic_ccc
74121	2	354825	7	NULL	NULL	0	NULL	FOXA2	GP		function as					key regulators	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	HNF6 and FOXA2 function as key regulators in human colorectal liver metastases.	topic_ccc
74122	3	354825	7	NULL	NULL	0	NULL	statement 1	Process		occur in					 colorectal liver metastases	Process	human			NULL		0	NULL	NULL	NULL	NULL	NULL	HNF6 and FOXA2 function as key regulators in human colorectal liver metastases.	topic_ccc
74123	4	354825	7	NULL	NULL	NULL	NULL	statement 2	Process		occur in 					 colorectal liver metastases	Process	human			NULL		NULL	NULL	NULL	NULL	NULL	NULL	HNF6 and FOXA2 function as key regulators in human colorectal liver metastases.	topic_ccc
74124	1	354826	7	NULL	NULL	0	NULL	HNF6	GP		inhibit					cell cycle progression	Process				NULL	Caco-2 cell line	0	NULL	NULL	NULL	NULL	NULL	HNF6 inhibited cell cycle progression in the G2/M and G1 phase in Caco-2 and HepG2 cell lines	topic_ccc
74125	2	354826	7	NULL	NULL	0	NULL	HNF6	GP		inhibit					cell cycle progression	Process				NULL	HepG2 cell line	0	NULL	NULL	NULL	NULL	NULL	HNF6 inhibited cell cycle progression in the G2/M and G1 phase in Caco-2 and HepG2 cell lines	topic_ccc
74126	3	354826	7	NULL	NULL	0	NULL	statement 1	Process		occur in					G2/M phase	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	HNF6 inhibited cell cycle progression in the G2/M and G1 phase in Caco-2 and HepG2 cell lines	topic_ccc
74127	4	354826	7	NULL	NULL	0	NULL	statement 1	Process		occur in					G1 phase	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	HNF6 inhibited cell cycle progression in the G2/M and G1 phase in Caco-2 and HepG2 cell lines	topic_ccc
74128	5	354826	7	NULL	NULL	0	NULL	statement 2	Process		occur in					G2/M  phase	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	HNF6 inhibited cell cycle progression in the G2/M and G1 phase in Caco-2 and HepG2 cell lines	topic_ccc
74129	6	354826	7	NULL	NULL	0	NULL	statement 2	Process		occur in					G1 phase	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	HNF6 inhibited cell cycle progression in the G2/M and G1 phase in Caco-2 and HepG2 cell lines	topic_ccc
74130	1	354827	7	NULL	NULL	0	NULL	FOXA2	GP	functional knockdown of	recovered					HNF6 activity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Therefore functional knockdown of FOXA2 recovered HNF6 activity and inhibited growth of tumor-cells and may possibly represent a novel therapeutic target in primary and secondary liver malignancies.	topic_ccc
74131	2	354827	7	NULL	NULL	0	NULL	statement 1	Process		inhibit					tumor cells	Cell	growth of			NULL		0	NULL	NULL	NULL	NULL	NULL	Therefore functional knockdown of FOXA2 recovered HNF6 activity and inhibited growth of tumor-cells and may possibly represent a novel therapeutic target in primary and secondary liver malignancies.	topic_ccc
74132	3	354827	7	NULL	NULL	0	NULL	FOXA2	GP		therapeutic target in		novel			primary liver malignancy	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Therefore functional knockdown of FOXA2 recovered HNF6 activity and inhibited growth of tumor-cells and may possibly represent a novel therapeutic target in primary and secondary liver malignancies.	topic_ccc
74133	4	354827	7	NULL	NULL	0	NULL	FOXA2	GP		therapeutic target in 		novel			secondary liver malignancy	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Therefore functional knockdown of FOXA2 recovered HNF6 activity and inhibited growth of tumor-cells and may possibly represent a novel therapeutic target in primary and secondary liver malignancies.	topic_ccc
74134	1	354828	7	NULL	NULL	NULL	NULL	FOXA2	GP	functional knockdown of	recovered					HNF6 activity	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Thus, functional knockdown of FOXA2 recovered HNF6 activity.	topic_ccc
74135	1	354830	7	NULL	NULL	0	NULL	Programmed cell death	Process		is called					apoptosis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Programmed cell death is also called apoptosis.	topic_ccc
74136	1	354831	7	NULL	NULL	0	NULL	TNF�	Chemical	high dosage of	increase		significantly			apoptosis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	TNFα at a high dosage, a significant increase in the apoptosis rate was observed after 6 h and after 12 h in all dosage groups.	topic_ccc
74137	1	354832	7	NULL	NULL	0	NULL	CD95	Cell		induce					apoptosis	Process				NULL	liver metastases of colorectal carcinoma	0	NULL	NULL	NULL	NULL	NULL	CD95 and TNFα-induced apoptosis in liver metastases of colorectal carcinoma.As apoptosis contributes to the overall sensitivity to radiotherapy or chemotherapy, a better understanding of the apoptotic process in metastatic tumour tissues is necessary.	topic_ccc
74138	2	354832	7	NULL	NULL	0	NULL	TNF�	Chemical		induce 					apoptosis	Process				NULL	liver metastases of colorectal carcinoma	0	NULL	NULL	NULL	NULL	NULL	CD95 and TNFα-induced apoptosis in liver metastases of colorectal carcinoma.As apoptosis contributes to the overall sensitivity to radiotherapy or chemotherapy, a better understanding of the apoptotic process in metastatic tumour tissues is necessary.	topic_ccc
74139	1	354836	7	NULL	NULL	0	NULL	 P-LVD	OrganismPart	high expression of	associated with					stage I colorectal cancer	MedicalFinding	shorter disease-free interval in			NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, high P-LVD and high VEGF expression were significant negative prognostic parameters associated with a shorter disease-free interval in stage I colorectal cancer	topic_ccc
74140	2	354836	7	NULL	NULL	NULL	NULL	VEGF	GP	high expression of	associated with					stage I colorectal cancer	MedicalFinding	shorter disease-free interval in			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Moreover, high P-LVD and high VEGF expression were significant negative prognostic parameters associated with a shorter disease-free interval in stage I colorectal cancer	topic_ccc
74141	3	354836	7	NULL	NULL	0	NULL	P-LVD	OrganismPart		is a type of					negative prognostic parameters	QuantityOrMeasure				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, high P-LVD and high VEGF expression were significant negative prognostic parameters associated with a shorter disease-free interval in stage I colorectal cancer	topic_ccc
74142	4	354836	7	NULL	NULL	0	NULL	VEGF	GP		is a type of					negative prognostic parameters	QuantityOrMeasure				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, high P-LVD and high VEGF expression were significant negative prognostic parameters associated with a shorter disease-free interval in stage I colorectal cancer	topic_ccc
74143	1	354837	7	NULL	NULL	0	NULL	P-LVD	OrganismPart		used as a tool 					stage I colorectal cancer	MedicalFinding	to identify			NULL		0	NULL	NULL	NULL	NULL	NULL	Conclusions If our findings are further confirmed in other studies, the assessment of P-LVD on surgical specimens might be used as a tool to identify patients with stage I colorectal cancer 	topic_ccc
74276	1	354838	7	NULL	NULL	0	NULL	VEGF	GP	high expression of	associate with					stage I colorectal cancer	MedicalFinding	shorter disease-free interval in			NULL		0	NULL	NULL	NULL	NULL	NULL	 high VEGF expression were significant negative prognostic parameters associated with a shorter disease-free interval in stage I colorectal cancer.	topic_ccc
74277	2	354838	7	NULL	NULL	NULL	NULL	VEGF	GP	high expression of	is a type of					negative prognostic parameters	QuantityOrMeasure				NULL		NULL	NULL	NULL	NULL	NULL	NULL	 high VEGF expression were significant negative prognostic parameters associated with a shorter disease-free interval in stage I colorectal cancer.	topic_ccc
73893	1	354839	5	NULL	NULL	0	NULL	delusions	MedicalFinding		is a symptom of					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Over two-thirds of patients with NMDAR antibody encephalitis, and some with potassium channel antibody-associated limbic encephalitis, have prominent psychiatric symptoms, or may present to psychiatric services in the first instance. The psychiatric symptoms are those seen in schizophrenia including delusions, hallucinations, and catatonic movement disorder.	topic_sch
73894	2	354839	5	NULL	NULL	0	NULL	hallucinations	MedicalFinding		is a symptom of					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Over two-thirds of patients with NMDAR antibody encephalitis, and some with potassium channel antibody-associated limbic encephalitis, have prominent psychiatric symptoms, or may present to psychiatric services in the first instance. The psychiatric symptoms are those seen in schizophrenia including delusions, hallucinations, and catatonic movement disorder.	topic_sch
73895	3	354839	5	NULL	NULL	0	NULL	catatonic movement disorder	MedicalFinding		is a symptom of					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Over two-thirds of patients with NMDAR antibody encephalitis, and some with potassium channel antibody-associated limbic encephalitis, have prominent psychiatric symptoms, or may present to psychiatric services in the first instance. The psychiatric symptoms are those seen in schizophrenia including delusions, hallucinations, and catatonic movement disorder.	topic_sch
73896	1	354840	5	NULL	NULL	0	NULL	NDUFV2	GP		is					NADH dehydrogenase ubiquinone flavoprotein 2	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	NADH dehydrogenase ubiquinone flavoprotein 2 (NDUFV2), encoding a subunit of mitochondrial complex I, is a candidate gene for several neuronal diseases; schizophrenia, bipolar disorder and Parkinson disease (PD). 	topic_sch
73897	2	354840	5	NULL	NULL	0	NULL	NDUFV2	GP		encodes					mitochondrial complex I	GP	subunit of			NULL		0	NULL	NULL	NULL	NULL	NULL	NADH dehydrogenase ubiquinone flavoprotein 2 (NDUFV2), encoding a subunit of mitochondrial complex I, is a candidate gene for several neuronal diseases; schizophrenia, bipolar disorder and Parkinson disease (PD). 	topic_sch
73898	3	354840	5	NULL	NULL	0	NULL	NDUFV2	GP		is a candidate gene for					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	NADH dehydrogenase ubiquinone flavoprotein 2 (NDUFV2), encoding a subunit of mitochondrial complex I, is a candidate gene for several neuronal diseases; schizophrenia, bipolar disorder and Parkinson disease (PD). 	topic_sch
73899	4	354840	5	NULL	NULL	0	NULL	NDUFV2	GP		is a candidate gene for					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	NADH dehydrogenase ubiquinone flavoprotein 2 (NDUFV2), encoding a subunit of mitochondrial complex I, is a candidate gene for several neuronal diseases; schizophrenia, bipolar disorder and Parkinson disease (PD). 	topic_sch
73900	5	354840	5	NULL	NULL	0	NULL	NDUFV2	GP		is a candidate gene for					Parkinson disease	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	NADH dehydrogenase ubiquinone flavoprotein 2 (NDUFV2), encoding a subunit of mitochondrial complex I, is a candidate gene for several neuronal diseases; schizophrenia, bipolar disorder and Parkinson disease (PD). 	topic_sch
73901	6	354840	5	NULL	NULL	0	NULL	PD	MedicalFinding		is					Parkinson disease	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	NADH dehydrogenase ubiquinone flavoprotein 2 (NDUFV2), encoding a subunit of mitochondrial complex I, is a candidate gene for several neuronal diseases; schizophrenia, bipolar disorder and Parkinson disease (PD). 	topic_sch
73902	7	354840	5	NULL	NULL	0	NULL	schizophrenia	MedicalFinding		is a type of					neuronal disease	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	NADH dehydrogenase ubiquinone flavoprotein 2 (NDUFV2), encoding a subunit of mitochondrial complex I, is a candidate gene for several neuronal diseases; schizophrenia, bipolar disorder and Parkinson disease (PD). 	topic_sch
73903	8	354840	5	NULL	NULL	0	NULL	bipolar disorder	MedicalFinding		is a type of					neuronal disease	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	NADH dehydrogenase ubiquinone flavoprotein 2 (NDUFV2), encoding a subunit of mitochondrial complex I, is a candidate gene for several neuronal diseases; schizophrenia, bipolar disorder and Parkinson disease (PD). 	topic_sch
73904	9	354840	5	NULL	NULL	0	NULL	Parkinson disease	MedicalFinding		is a type of					neuronal disease	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	NADH dehydrogenase ubiquinone flavoprotein 2 (NDUFV2), encoding a subunit of mitochondrial complex I, is a candidate gene for several neuronal diseases; schizophrenia, bipolar disorder and Parkinson disease (PD). 	topic_sch
73905	1	354842	5	NULL	NULL	0	NULL	improper inhibitory control	MedicalFinding		is involved in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	To explore this issue, we examined visual and visuomotor processing in schizophrenia, utilizing an illusion known as the Roelofs effect. These results provide evidence for a hypothesis of improper inhibitory control as a common mechanism underpinning abnormal visual and visuomotor processes in this mental disorder.	topic_sch
73906	1	354844	5	NULL	NULL	0	NULL	physical capacity	Process		is lower in					schizophrenic patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	The (schizophrenic) patients exhibited significantly higher RQ on submaximal workloads and lower physical capacity. A significant lower calculated VO(2-max) remained after correction for body weight and fat free mass (FFM). Energy expenditure did not differ on fixed workloads.	topic_sch
73907	2	354844	5	NULL	NULL	0	NULL	RQ	QuantityOrMeasure		is higher in		significantly			schizophrenic patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	The (schizophrenic) patients exhibited significantly higher RQ on submaximal workloads and lower physical capacity. A significant lower calculated VO(2-max) remained after correction for body weight and fat free mass (FFM). Energy expenditure did not differ on fixed workloads.	topic_sch
73908	1	354845	5	NULL	NULL	0	NULL	hippocampal atrophy	MedicalFinding		is a type of					morphological manifestation	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	One morphological manifestation of schizophrenia is hippocampal atrophy.	topic_sch
73909	2	354845	5	NULL	NULL	0	NULL	hippocampal atrophy	MedicalFinding		occurs in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	One morphological manifestation of schizophrenia is hippocampal atrophy.	topic_sch
74191	1	354846	11	NULL	NULL	0	NULL	Staphylococcus aureus	Organism	Methicillin-resistant	is responsible for					 infections	Process	 humans			NULL		0	NULL	NULL	NULL	NULL	NULL	Methicillin-resistant Staphylococcus aureus (MRSA) is a bacterium responsible for several difficult-to-treat infections in humans	topic_mrs
74192	2	354846	11	NULL	NULL	0	NULL	Staphylococcus aureus	Organism	Methicillin-resistant	is a					bacterium	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Methicillin-resistant Staphylococcus aureus (MRSA) is a bacterium responsible for several difficult-to-treat infections in humans	topic_mrs
73911	1	354847	5	NULL	NULL	NULL	NULL	Glx	Chemical	lower levels of	corelates with					impaired cognition	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Although not reduced in schizophrenia as a group, lower Glx levels correlates with impaired cognition in the illness. 	topic_sch
74193	1	354847	5	11	NULL	NULL	NULL	Glx	Chemical	lower levels of	correlates with					impaired cognition	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Although not reduced in schizophrenia as a group, lower Glx levels correlates with impaired cognition in the illness. 	topic_sch
74197	1	354847	5	11	NULL	0	NULL	 Glx	Chemical	lower levels of	occurs in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Although not reduced in schizophrenia as a group, lower Glx levels correlates with impaired cognition in the illness. 	topic_sch
73912	1	354849	5	NULL	NULL	0	NULL	D-serine	AminoAcid		is a coagonist of					NMDA receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The NMDA receptor coagonist D-serine is important in a number of different processes in the central nervous system, ranging from synaptic plasticity to disease states, including schizophrenia. 	topic_sch
73913	2	354849	5	11	NULL	NULL	NULL	D-serine	AminoAcid		plays a role in		different processes of			central nervous system	OrganismPart				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The NMDA receptor coagonist D-serine is important in a number of different processes in the central nervous system, ranging from synaptic plasticity to disease states, including schizophrenia. 	topic_sch
73914	3	354849	5	NULL	NULL	0	NULL	D-serine	AminoAcid		plays a role in		important			synaptic plasticity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The NMDA receptor coagonist D-serine is important in a number of different processes in the central nervous system, ranging from synaptic plasticity to disease states, including schizophrenia. 	topic_sch
73915	4	354849	5	NULL	NULL	0	NULL	D-serine	AminoAcid		plays a role in		important			schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The NMDA receptor coagonist D-serine is important in a number of different processes in the central nervous system, ranging from synaptic plasticity to disease states, including schizophrenia. 	topic_sch
74205	1	354849	5	11	NULL	0	NULL	 D-serine	AminoAcid		is a coagonist of 					NMDA receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The NMDA receptor coagonist D-serine is important in a number of different processes in the central nervous system, ranging from synaptic plasticity to disease states, including schizophrenia. 	topic_sch
74214	1	354849	5	11	NULL	NULL	NULL	D-serine	AminoAcid		plays a role in		important			central nervous system	OrganismPart	different processes in			NULL		NULL	NULL	NULL	NULL	NULL	NULL	The NMDA receptor coagonist D-serine is important in a number of different processes in the central nervous system, ranging from synaptic plasticity to disease states, including schizophrenia. 	topic_sch
74223	1	354849	5	11	NULL	0	NULL	D-serine	AminoAcid		plays a role in					synaptic plasticity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The NMDA receptor coagonist D-serine is important in a number of different processes in the central nervous system, ranging from synaptic plasticity to disease states, including schizophrenia. 	topic_sch
74224	1	354849	5	11	NULL	0	NULL	D-serine	AminoAcid		plays a role in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The NMDA receptor coagonist D-serine is important in a number of different processes in the central nervous system, ranging from synaptic plasticity to disease states, including schizophrenia. 	topic_sch
76328	1	354850	11	NULL	NULL	0	NULL	Meticillin	Chemical		is also known as					methicillin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Meticillin  or methicillin  is a narrow-spectrum beta-lactam antibiotic of the penicillin class. 	topic_mrs
76329	2	354850	11	NULL	NULL	0	NULL	Meticillin	Chemical		is a type of 					 narrow-spectrum beta-lactam antibiotic 	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Meticillin  or methicillin  is a narrow-spectrum beta-lactam antibiotic of the penicillin class. 	topic_mrs
76330	3	354850	11	NULL	NULL	0	NULL	Meticillin	Chemical		is a class of					penicillin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Meticillin  or methicillin  is a narrow-spectrum beta-lactam antibiotic of the penicillin class. 	topic_mrs
74225	1	354851	11	NULL	NULL	0	NULL	Nafcillin sodium	Chemical		is a type of 					beta-lactam antibiotic	Chemical	narrow-spectrum			NULL		0	NULL	NULL	NULL	NULL	NULL	Nafcillin sodium is a narrow-spectrum beta-lactam antibiotic of the penicillin class. As a beta-lactamase-resistant penicillin, it is used to treat infections caused by Gram-positive bacteria, in particular, species of staphylococci that are resistant to other penicillins.	topic_mrs
74226	2	354851	11	NULL	NULL	0	NULL	Nafcillin sodium	Chemical		is a type of 					penicillin	Chemical	beta-lactamase-resistant 			NULL		0	NULL	NULL	NULL	NULL	NULL	Nafcillin sodium is a narrow-spectrum beta-lactam antibiotic of the penicillin class. As a beta-lactamase-resistant penicillin, it is used to treat infections caused by Gram-positive bacteria, in particular, species of staphylococci that are resistant to other penicillins.	topic_mrs
74227	3	354851	11	NULL	NULL	0	NULL	Nafcillin sodium	Chemical		 is used to treat					infections	Process	caused by staphylococci			NULL		0	NULL	NULL	NULL	NULL	NULL	Nafcillin sodium is a narrow-spectrum beta-lactam antibiotic of the penicillin class. As a beta-lactamase-resistant penicillin, it is used to treat infections caused by Gram-positive bacteria, in particular, species of staphylococci that are resistant to other penicillins.	topic_mrs
76331	1	354852	11	NULL	NULL	0	NULL	Clindamycin	Chemical		is a type of 					lincosamide antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Clindamycin  is a lincosamide antibiotic.	topic_mrs
76332	1	354853	11	NULL	NULL	0	NULL	Dicloxacillin	Chemical		is a type of 					 narrow spectrum beta-lactam antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Dicloxacillin  is a narrow spectrum beta-lactam antibiotic of the penicillin class	topic_mrs
76333	2	354853	11	NULL	NULL	0	NULL	Dicloxacillin	Chemical		is a class of					penicillin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Dicloxacillin  is a narrow spectrum beta-lactam antibiotic of the penicillin class	topic_mrs
76334	1	354854	11	NULL	NULL	0	NULL	β-Lactam antibiotics	Chemical		contains					β-lactam nucleus	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	β-Lactam antibiotics are a broad class of antibiotics, consisting of all antibiotic agents that contains a β-lactam nucleus in its molecular structure	topic_mrs
76335	1	354855	11	NULL	NULL	0	NULL	Penicillin	Chemical		is a group of					antibiotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Penicillin is a group of antibiotics derived from Penicillium fungi.	topic_mrs
76336	2	354855	11	NULL	NULL	0	NULL	Penicillin	Chemical		is derived from					Penicillium fungi	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Penicillin is a group of antibiotics derived from Penicillium fungi.	topic_mrs
73916	1	354856	5	NULL	NULL	0	NULL	Amphetamine	Chemical		improve					cognition	Process				NULL	schizophrenia patients	0	NULL	NULL	NULL	NULL	NULL	Amphetamine can improve cognition in healthy subjects and patients with schizophrenia, attention-deficit hyperactivity disorder (ADHD), and other neuropsychiatric diseases; higher doses, however, can impair cognitive function, especially those mediated by the prefrontal cortex (PFC). 	topic_sch
73917	2	354856	5	NULL	NULL	0	NULL	Amphetamine	Chemical		improve					cognition	Process				NULL	healthy subjects	0	NULL	NULL	NULL	NULL	NULL	Amphetamine can improve cognition in healthy subjects and patients with schizophrenia, attention-deficit hyperactivity disorder (ADHD), and other neuropsychiatric diseases; higher doses, however, can impair cognitive function, especially those mediated by the prefrontal cortex (PFC). 	topic_sch
73918	3	354856	5	NULL	NULL	0	NULL	Amphetamine	Chemical		improve					cognition	Process				NULL	ADHD patients	0	NULL	NULL	NULL	NULL	NULL	Amphetamine can improve cognition in healthy subjects and patients with schizophrenia, attention-deficit hyperactivity disorder (ADHD), and other neuropsychiatric diseases; higher doses, however, can impair cognitive function, especially those mediated by the prefrontal cortex (PFC). 	topic_sch
73919	4	354856	5	NULL	NULL	0	NULL	ADHD	MedicalFinding		is					attention-deficit hyperactivity disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Amphetamine can improve cognition in healthy subjects and patients with schizophrenia, attention-deficit hyperactivity disorder (ADHD), and other neuropsychiatric diseases; higher doses, however, can impair cognitive function, especially those mediated by the prefrontal cortex (PFC). 	topic_sch
73920	5	354856	5	NULL	NULL	0	NULL	Amphetamine	Chemical	higher doses of	impair					cognitive function	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Amphetamine can improve cognition in healthy subjects and patients with schizophrenia, attention-deficit hyperactivity disorder (ADHD), and other neuropsychiatric diseases; higher doses, however, can impair cognitive function, especially those mediated by the prefrontal cortex (PFC). 	topic_sch
73921	6	354856	5	NULL	NULL	0	NULL	cognitive function	Process		is mediated by					prefrontal cortex	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Amphetamine can improve cognition in healthy subjects and patients with schizophrenia, attention-deficit hyperactivity disorder (ADHD), and other neuropsychiatric diseases; higher doses, however, can impair cognitive function, especially those mediated by the prefrontal cortex (PFC). 	topic_sch
73922	7	354856	5	NULL	NULL	0	NULL	Amphetamine	Chemical	higher doses of	impair					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Amphetamine can improve cognition in healthy subjects and patients with schizophrenia, attention-deficit hyperactivity disorder (ADHD), and other neuropsychiatric diseases; higher doses, however, can impair cognitive function, especially those mediated by the prefrontal cortex (PFC). 	topic_sch
73923	8	354856	5	NULL	NULL	0	NULL	PFC	OrganismPart		is					prefrontal cortex	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Amphetamine can improve cognition in healthy subjects and patients with schizophrenia, attention-deficit hyperactivity disorder (ADHD), and other neuropsychiatric diseases; higher doses, however, can impair cognitive function, especially those mediated by the prefrontal cortex (PFC). 	topic_sch
73924	1	354858	5	NULL	NULL	0	NULL	Glutamate	Chemical		is present in					prefrontal cortex	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate in the prefrontal cortex (PFC) plays a significant role in several mental illnesses, including schizophrenia, addiction and anxiety. 	topic_sch
73925	2	354858	5	NULL	NULL	0	NULL	PFC	OrganismPart		is					prefrontal cortex	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate in the prefrontal cortex (PFC) plays a significant role in several mental illnesses, including schizophrenia, addiction and anxiety. 	topic_sch
73926	3	354858	5	NULL	NULL	0	NULL	Glutamate	Chemical		plays a role in		important			schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate in the prefrontal cortex (PFC) plays a significant role in several mental illnesses, including schizophrenia, addiction and anxiety. 	topic_sch
73927	4	354858	5	NULL	NULL	0	NULL	Glutamate	Chemical		plays a role in		important			addiction	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate in the prefrontal cortex (PFC) plays a significant role in several mental illnesses, including schizophrenia, addiction and anxiety. 	topic_sch
73928	5	354858	5	NULL	NULL	0	NULL	Glutamate	Chemical		plays a role in		important			anxiety	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate in the prefrontal cortex (PFC) plays a significant role in several mental illnesses, including schizophrenia, addiction and anxiety. 	topic_sch
76337	1	354859	11	NULL	NULL	0	NULL	β-Lactam antibiotics	Chemical		contains					 β-lactam nucleus	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	β-Lactam antibiotics are a broad class of antibiotics, consisting of all antibiotic agents that contains a β-lactam nucleus in its molecular structure. This includes penicillin derivatives (penams)  cephalosporins (cephems)	topic_mrs
76338	2	354859	11	NULL	NULL	0	NULL	β-Lactam antibiotics	Chemical		includes					cephalosporins 	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	β-Lactam antibiotics are a broad class of antibiotics, consisting of all antibiotic agents that contains a β-lactam nucleus in its molecular structure. This includes penicillin derivatives (penams)  cephalosporins (cephems)	topic_mrs
76339	3	354859	11	NULL	NULL	0	NULL	penams	Chemical		is a derivative of					penicillin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	β-Lactam antibiotics are a broad class of antibiotics, consisting of all antibiotic agents that contains a β-lactam nucleus in its molecular structure. This includes penicillin derivatives (penams)  cephalosporins (cephems)	topic_mrs
76340	4	354859	11	NULL	NULL	0	NULL	cephalosporins 	Chemical		is also known as					cephems	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	β-Lactam antibiotics are a broad class of antibiotics, consisting of all antibiotic agents that contains a β-lactam nucleus in its molecular structure. This includes penicillin derivatives (penams)  cephalosporins (cephems)	topic_mrs
73929	1	354860	5	NULL	NULL	0	NULL	STOP	GP		is a type of					microtubule-associated protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The deletion of microtubule-associated protein STOP leads to neuroanatomical, biochemical and severe behavioral alterations in mice, partly alleviated by antipsychotics. Therefore, STOP knockout (KO) mice have been proposed as a model of some schizophrenia-like symptoms. 	topic_sch
73930	2	354860	5	NULL	NULL	0	NULL	STOP	GP	deletion of	leads to					neuroanatomical alterations	MedicalFinding				NULL	mice	0	NULL	NULL	NULL	NULL	NULL	The deletion of microtubule-associated protein STOP leads to neuroanatomical, biochemical and severe behavioral alterations in mice, partly alleviated by antipsychotics. Therefore, STOP knockout (KO) mice have been proposed as a model of some schizophrenia-like symptoms. 	topic_sch
73931	3	354860	5	NULL	NULL	0	NULL	STOP	GP	deletion of	leads to					biochemical alterations	MedicalFinding				NULL	mice	0	NULL	NULL	NULL	NULL	NULL	The deletion of microtubule-associated protein STOP leads to neuroanatomical, biochemical and severe behavioral alterations in mice, partly alleviated by antipsychotics. Therefore, STOP knockout (KO) mice have been proposed as a model of some schizophrenia-like symptoms. 	topic_sch
73932	4	354860	5	NULL	NULL	0	NULL	STOP	GP	deletion of	leads to					bihavioral alterations	MedicalFinding	severe			NULL	mice	0	NULL	NULL	NULL	NULL	NULL	The deletion of microtubule-associated protein STOP leads to neuroanatomical, biochemical and severe behavioral alterations in mice, partly alleviated by antipsychotics. Therefore, STOP knockout (KO) mice have been proposed as a model of some schizophrenia-like symptoms. 	topic_sch
73934	5	354860	5	NULL	NULL	0	NULL	statement 2	Process		is alleviated by		partly			antipsychotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The deletion of microtubule-associated protein STOP leads to neuroanatomical, biochemical and severe behavioral alterations in mice, partly alleviated by antipsychotics. Therefore, STOP knockout (KO) mice have been proposed as a model of some schizophrenia-like symptoms. 	topic_sch
73935	6	354860	5	NULL	NULL	0	NULL	statement 3	Process		is alleviated by		partly			antipsychotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The deletion of microtubule-associated protein STOP leads to neuroanatomical, biochemical and severe behavioral alterations in mice, partly alleviated by antipsychotics. Therefore, STOP knockout (KO) mice have been proposed as a model of some schizophrenia-like symptoms. 	topic_sch
73936	7	354860	5	NULL	NULL	0	NULL	statement 4	Process		is alleviated by		partly			antipsychotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The deletion of microtubule-associated protein STOP leads to neuroanatomical, biochemical and severe behavioral alterations in mice, partly alleviated by antipsychotics. Therefore, STOP knockout (KO) mice have been proposed as a model of some schizophrenia-like symptoms. 	topic_sch
74931	1	354861	11	NULL	NULL	NULL	NULL	Vancomycin	Chemical		is a type of 					glycopeptide antibiotic	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Vancomycin is a glycopeptide antibiotic used in the prophylaxis and treatment of infections caused by Gram-positive bacteria	topic_mrs
74932	2	354861	11	NULL	NULL	NULL	NULL	Vancomycin	Chemical		is used in					prophylaxis	MedicalProcedure				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Vancomycin is a glycopeptide antibiotic used in the prophylaxis and treatment of infections caused by Gram-positive bacteria	topic_mrs
74933	3	354861	11	NULL	NULL	NULL	NULL	infections	MedicalFinding		is caused by					Gram-positive bacteria	Organism				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Vancomycin is a glycopeptide antibiotic used in the prophylaxis and treatment of infections caused by Gram-positive bacteria	topic_mrs
74934	4	354861	11	NULL	NULL	0	NULL	Vancomycin	Chemical		treats					 infections	Medical Finding				NULL		0	NULL	NULL	NULL	NULL	NULL	Vancomycin is a glycopeptide antibiotic used in the prophylaxis and treatment of infections caused by Gram-positive bacteria	topic_mrs
74935	1	354862	11	NULL	NULL	NULL	NULL	Glycopeptide  antibiotics	Chemical		is composed of					glycosylated cyclic nonribosomal peptides	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glycopeptide antibiotics are a class of antibiotic drugs. The class is composed of glycosylated cyclic or polycyclic nonribosomal peptides. Significant glycopeptide antibiotics include vancomycin, teicoplanin, telavancin, bleomycin, ramoplanin, and decaplanin.	topic_mrs
74936	2	354862	11	NULL	NULL	0	NULL	Glycopeptide antibiotics	Chemical		is composed of					glycosylated polycyclic nonribosomal peptides	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Glycopeptide antibiotics are a class of antibiotic drugs. The class is composed of glycosylated cyclic or polycyclic nonribosomal peptides. Significant glycopeptide antibiotics include vancomycin, teicoplanin, telavancin, bleomycin, ramoplanin, and decaplanin.	topic_mrs
74937	3	354862	11	NULL	NULL	NULL	NULL	statement 1	Process		is an alternative to 					statement 2	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glycopeptide antibiotics are a class of antibiotic drugs. The class is composed of glycosylated cyclic or polycyclic nonribosomal peptides. Significant glycopeptide antibiotics include vancomycin, teicoplanin, telavancin, bleomycin, ramoplanin, and decaplanin.	topic_mrs
75202	4	354862	11	NULL	NULL	0	NULL	Glycopeptide antibiotics	Chemical		is a class of					antibiotic drugs	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Glycopeptide antibiotics are a class of antibiotic drugs. The class is composed of glycosylated cyclic or polycyclic nonribosomal peptides. Significant glycopeptide antibiotics include vancomycin, teicoplanin, telavancin, bleomycin, ramoplanin, and decaplanin.	topic_mrs
75203	5	354862	11	NULL	NULL	0	NULL	vancomycin	Chemical		is a type of					glycopeptide antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Glycopeptide antibiotics are a class of antibiotic drugs. The class is composed of glycosylated cyclic or polycyclic nonribosomal peptides. Significant glycopeptide antibiotics include vancomycin, teicoplanin, telavancin, bleomycin, ramoplanin, and decaplanin.	topic_mrs
75204	6	354862	11	NULL	NULL	0	NULL	teicoplanin	Chemical		is a type of 					glycopeptide antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Glycopeptide antibiotics are a class of antibiotic drugs. The class is composed of glycosylated cyclic or polycyclic nonribosomal peptides. Significant glycopeptide antibiotics include vancomycin, teicoplanin, telavancin, bleomycin, ramoplanin, and decaplanin.	topic_mrs
75205	7	354862	11	NULL	NULL	0	NULL	telavancin	Chemical		is a type of 					glycopeptide antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Glycopeptide antibiotics are a class of antibiotic drugs. The class is composed of glycosylated cyclic or polycyclic nonribosomal peptides. Significant glycopeptide antibiotics include vancomycin, teicoplanin, telavancin, bleomycin, ramoplanin, and decaplanin.	topic_mrs
75206	8	354862	11	NULL	NULL	0	NULL	bleomycin	Chemical		is a type of 					glycopeptide antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Glycopeptide antibiotics are a class of antibiotic drugs. The class is composed of glycosylated cyclic or polycyclic nonribosomal peptides. Significant glycopeptide antibiotics include vancomycin, teicoplanin, telavancin, bleomycin, ramoplanin, and decaplanin.	topic_mrs
75207	9	354862	11	NULL	NULL	0	NULL	ramoplanin	Chemical		is a type of 					glycopeptide antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Glycopeptide antibiotics are a class of antibiotic drugs. The class is composed of glycosylated cyclic or polycyclic nonribosomal peptides. Significant glycopeptide antibiotics include vancomycin, teicoplanin, telavancin, bleomycin, ramoplanin, and decaplanin.	topic_mrs
75208	10	354862	11	NULL	NULL	0	NULL	decaplanin	Chemical		is a type of 					glycopeptide antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Glycopeptide antibiotics are a class of antibiotic drugs. The class is composed of glycosylated cyclic or polycyclic nonribosomal peptides. Significant glycopeptide antibiotics include vancomycin, teicoplanin, telavancin, bleomycin, ramoplanin, and decaplanin.	topic_mrs
75209	1	354863	11	NULL	NULL	0	NULL	Teicoplanin	Chemical		is a type of 					antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Teicoplanin is an antibiotic used in the prophylaxis and treatment of serious infections caused by Gram-positive bacteria, including methicillin-resistant Staphylococcus aureus	topic_mrs
75211	2	354863	11	NULL	NULL	0	NULL	Teicoplanin	Chemical		used in					prophylaxis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Teicoplanin is an antibiotic used in the prophylaxis and treatment of serious infections caused by Gram-positive bacteria, including methicillin-resistant Staphylococcus aureus	topic_mrs
75217	3	354863	11	NULL	NULL	0	NULL	infections	MedicalFinding		caused by					Gram-positive bacteria	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Teicoplanin is an antibiotic used in the prophylaxis and treatment of serious infections caused by Gram-positive bacteria, including methicillin-resistant Staphylococcus aureus	topic_mrs
75218	4	354863	11	NULL	NULL	0	NULL	Teicoplanin	Chemical		treats					infections	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Teicoplanin is an antibiotic used in the prophylaxis and treatment of serious infections caused by Gram-positive bacteria, including methicillin-resistant Staphylococcus aureus	topic_mrs
74984	1	354864	11	NULL	NULL	0	NULL	fibrinogen	GP		is converted to 					fibrin	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Coagulase is a protein produced by several microorganisms, which enables the conversion of fibrinogen to fibrin	topic_mrs
74985	2	354864	11	NULL	NULL	0	NULL	Coagulase	GP		enables					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Coagulase is a protein produced by several microorganisms, which enables the conversion of fibrinogen to fibrin	topic_mrs
74986	3	354864	11	NULL	NULL	0	NULL	Coagulase	GP		produced by					microorganisms	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Coagulase is a protein produced by several microorganisms, which enables the conversion of fibrinogen to fibrin	topic_mrs
75210	4	354864	11	NULL	NULL	0	NULL	Coagulase	GP		is a type of 					protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Coagulase is a protein produced by several microorganisms, which enables the conversion of fibrinogen to fibrin	topic_mrs
74987	1	354865	11	NULL	NULL	NULL	NULL	Coagulase	GP		complex with					prothrombin	GP	in the blood			NULL		NULL	NULL	NULL	NULL	NULL	NULL	If negative, the plasma remains liquid....If positive (i.e., the suspect colony is S. aureus), the serum will coagulate...Coagulase reacts with prothrombin in the blood. The resulting complex is called staphylothrombin, which enables the enzyme protease to convert fibrinogen to fibrin. This results in clotting of the blood. 	topic_mrs
74988	2	354865	11	NULL	NULL	0	NULL	statement 1	Process		produces					staphylothrombin	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	If negative, the plasma remains liquid....If positive (i.e., the suspect colony is S. aureus), the serum will coagulate...Coagulase reacts with prothrombin in the blood. The resulting complex is called staphylothrombin, which enables the enzyme protease to convert fibrinogen to fibrin. This results in clotting of the blood. 	topic_mrs
74989	3	354865	11	NULL	NULL	0	NULL	fibrinogen	GP		convert to					fibrin	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	If negative, the plasma remains liquid....If positive (i.e., the suspect colony is S. aureus), the serum will coagulate...Coagulase reacts with prothrombin in the blood. The resulting complex is called staphylothrombin, which enables the enzyme protease to convert fibrinogen to fibrin. This results in clotting of the blood. 	topic_mrs
74990	4	354865	11	NULL	NULL	0	NULL	protease	GP		enables					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	If negative, the plasma remains liquid....If positive (i.e., the suspect colony is S. aureus), the serum will coagulate...Coagulase reacts with prothrombin in the blood. The resulting complex is called staphylothrombin, which enables the enzyme protease to convert fibrinogen to fibrin. This results in clotting of the blood. 	topic_mrs
74991	5	354865	11	NULL	NULL	0	NULL	staphylothrombin	GP		enables					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	If negative, the plasma remains liquid....If positive (i.e., the suspect colony is S. aureus), the serum will coagulate...Coagulase reacts with prothrombin in the blood. The resulting complex is called staphylothrombin, which enables the enzyme protease to convert fibrinogen to fibrin. This results in clotting of the blood. 	topic_mrs
74992	6	354865	11	NULL	NULL	0	NULL	statement 3	Process		resulted in					blood clotting	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	If negative, the plasma remains liquid....If positive (i.e., the suspect colony is S. aureus), the serum will coagulate...Coagulase reacts with prothrombin in the blood. The resulting complex is called staphylothrombin, which enables the enzyme protease to convert fibrinogen to fibrin. This results in clotting of the blood. 	topic_mrs
75212	7	354865	11	NULL	NULL	0	NULL	protease	GP		is a type of 					enzyme	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	If negative, the plasma remains liquid....If positive (i.e., the suspect colony is S. aureus), the serum will coagulate...Coagulase reacts with prothrombin in the blood. The resulting complex is called staphylothrombin, which enables the enzyme protease to convert fibrinogen to fibrin. This results in clotting of the blood. 	topic_mrs
74993	1	354868	11	NULL	NULL	NULL	NULL	Peptidoglycan	Chemical		is also known as					murein	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Peptidoglycan, also known as murein, is a polymer consisting of sugars and amino acids 	topic_mrs
74994	2	354868	11	NULL	NULL	0	NULL	Peptidoglycan	Chemical		is a type of 					polymer	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Peptidoglycan, also known as murein, is a polymer consisting of sugars and amino acids 	topic_mrs
74995	3	354868	11	NULL	NULL	0	NULL	Peptidoglycan	Chemical		consisting of					sugars	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Peptidoglycan, also known as murein, is a polymer consisting of sugars and amino acids 	topic_mrs
74996	4	354868	11	NULL	NULL	0	NULL	Peptidoglycan	Chemical		consisting of					amino acids	amino acid				NULL		0	NULL	NULL	NULL	NULL	NULL	Peptidoglycan, also known as murein, is a polymer consisting of sugars and amino acids 	topic_mrs
75000	5	354868	11	NULL	NULL	NULL	NULL	statement 3	Process		occurs along with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Peptidoglycan, also known as murein, is a polymer consisting of sugars and amino acids 	topic_mrs
75001	1	354869	11	NULL	NULL	NULL	NULL	mesh-like layer	CellComponent		is formed					bacteria	Organism	ouside;;plasma membrane of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Peptidoglycan, also known as murein, is a polymer consisting of sugars and amino acids that forms a mesh-like layer outside the plasma membrane of bacteria (but not Archaea), forming the cell wall	topic_mrs
75213	2	354869	11	NULL	NULL	0	NULL	Peptidoglycan	Chemical		is a synonym of					 murein	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Peptidoglycan, also known as murein, is a polymer consisting of sugars and amino acids that forms a mesh-like layer outside the plasma membrane of bacteria (but not Archaea), forming the cell wall	topic_mrs
75214	3	354869	11	NULL	NULL	0	NULL	Peptidoglycan	Chemical		is a type of 					 polymer	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Peptidoglycan, also known as murein, is a polymer consisting of sugars and amino acids that forms a mesh-like layer outside the plasma membrane of bacteria (but not Archaea), forming the cell wall	topic_mrs
75219	4	354869	11	NULL	NULL	0	NULL	Peptidoglycan	Chemical		consisting of					sugars	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Peptidoglycan, also known as murein, is a polymer consisting of sugars and amino acids that forms a mesh-like layer outside the plasma membrane of bacteria (but not Archaea), forming the cell wall	topic_mrs
75220	5	354869	11	NULL	NULL	0	NULL	Peptidoglycan	Chemical		consisting of					amino acids	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Peptidoglycan, also known as murein, is a polymer consisting of sugars and amino acids that forms a mesh-like layer outside the plasma membrane of bacteria (but not Archaea), forming the cell wall	topic_mrs
75221	6	354869	11	NULL	NULL	0	NULL	statement 4	Process		occurs along with					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Peptidoglycan, also known as murein, is a polymer consisting of sugars and amino acids that forms a mesh-like layer outside the plasma membrane of bacteria (but not Archaea), forming the cell wall	topic_mrs
75222	7	354869	11	NULL	NULL	0	NULL	statement 6	Process		forms					cell wall	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	Peptidoglycan, also known as murein, is a polymer consisting of sugars and amino acids that forms a mesh-like layer outside the plasma membrane of bacteria (but not Archaea), forming the cell wall	topic_mrs
75223	8	354869	11	NULL	NULL	0	NULL	mesh-like layer	CellComponent		is not formed					Archaea	Organism	ouside;;plasma membrane of			NULL		0	NULL	NULL	NULL	NULL	NULL	Peptidoglycan, also known as murein, is a polymer consisting of sugars and amino acids that forms a mesh-like layer outside the plasma membrane of bacteria (but not Archaea), forming the cell wall	topic_mrs
75019	1	354870	11	NULL	NULL	0	NULL	Meticillin-resistant S. aureus	Organism		is					 MRSA	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Meticillin-resistant S. aureus or MRSA, is resistant to virtually all available beta-lactam antimicrobials. This resistance is mediated by the chromosomally located mecA gene.	topic_mrs
75020	2	354870	11	NULL	NULL	0	NULL	Meticillin-resistant S. aureus	Organism		is resistant to					beta-lactam antimicrobials	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Meticillin-resistant S. aureus or MRSA, is resistant to virtually all available beta-lactam antimicrobials. This resistance is mediated by the chromosomally located mecA gene.	topic_mrs
75021	3	354870	11	NULL	NULL	0	NULL	statement 2	Process		is mediated by					mecA gene	GP	chromosomal			NULL		0	NULL	NULL	NULL	NULL	NULL	Meticillin-resistant S. aureus or MRSA, is resistant to virtually all available beta-lactam antimicrobials. This resistance is mediated by the chromosomally located mecA gene.	topic_mrs
75022	1	354871	11	NULL	NULL	0	NULL	CC398	Organism		is a lineage of					MRSA	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	CC398 is the MRSA lineage most often associated with asymptomatic carriage in intensively reared food-producing animals.	topic_mrs
75215	2	354871	11	NULL	NULL	0	NULL	statement 1	Organism		is associated with					asymptomatic carriage	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	CC398 is the MRSA lineage most often associated with asymptomatic carriage in intensively reared food-producing animals.	topic_mrs
75216	3	354871	11	NULL	NULL	0	NULL	statement 2	Process		occurs in					food-producing animals	Organism	intensively reared			NULL		0	NULL	NULL	NULL	NULL	NULL	CC398 is the MRSA lineage most often associated with asymptomatic carriage in intensively reared food-producing animals.	topic_mrs
76341	1	354874	11	NULL	NULL	0	NULL	Healthcare-acquired methicillin-resistant Staphylococcus aureus	Organism		is					HA-MRSA	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Healthcare-acquired methicillin-resistant Staphylococcus aureus, or HA-MRSA, is a potentially deadly strain of Staph aureus that is resistant to several antibiotics. 	topic_mrs
76342	2	354874	11	NULL	NULL	0	NULL	HA-MRSA	Organism		is resistant to					antibiotics		several 			NULL		0	NULL	NULL	NULL	NULL	NULL	Healthcare-acquired methicillin-resistant Staphylococcus aureus, or HA-MRSA, is a potentially deadly strain of Staph aureus that is resistant to several antibiotics. 	topic_mrs
76343	1	354875	11	NULL	NULL	0	NULL	Staphylococcus aureus	Organism		is also known as					staph	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Staphylococcus aureus (staph) is a type of bacteria 	topic_mrs
76344	2	354875	11	NULL	NULL	0	NULL	Staphylococcus aureus	Organism		is a type of 					bacteria	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Staphylococcus aureus (staph) is a type of bacteria 	topic_mrs
75234	1	354876	11	NULL	NULL	0	NULL	MRSA	Organism		is a strain of					Staphylococcus aureus bacteria	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA is, by definition, any strain of Staphylococcus aureus bacteria that has developed resistance to beta-lactam antibiotics which include the penicillins (methicillin, dicloxacillin, nafcillin, oxacillin, etc.) and the cephalosporins.	topic_mrs
75236	2	354876	11	NULL	NULL	0	NULL	statement 1	Organism		has resistance to					beta-lactam antibiotics					NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA is, by definition, any strain of Staphylococcus aureus bacteria that has developed resistance to beta-lactam antibiotics which include the penicillins (methicillin, dicloxacillin, nafcillin, oxacillin, etc.) and the cephalosporins.	topic_mrs
75237	3	354876	11	NULL	NULL	NULL	NULL	methicillin	Chemical		is a type of 					penicillin	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	MRSA is, by definition, any strain of Staphylococcus aureus bacteria that has developed resistance to beta-lactam antibiotics which include the penicillins (methicillin, dicloxacillin, nafcillin, oxacillin, etc.) and the cephalosporins.	topic_mrs
75238	4	354876	11	NULL	NULL	NULL	NULL	dicloxacillin	Chemical		is a type of 					penicillin	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	MRSA is, by definition, any strain of Staphylococcus aureus bacteria that has developed resistance to beta-lactam antibiotics which include the penicillins (methicillin, dicloxacillin, nafcillin, oxacillin, etc.) and the cephalosporins.	topic_mrs
75285	5	354876	11	NULL	NULL	0	NULL	nafcillin	Chemical		is a type of 					penicillin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA is, by definition, any strain of Staphylococcus aureus bacteria that has developed resistance to beta-lactam antibiotics which include the penicillins (methicillin, dicloxacillin, nafcillin, oxacillin, etc.) and the cephalosporins.	topic_mrs
75286	6	354876	11	NULL	NULL	0	NULL	oxacillin	Chemical		is a type of 					penicillin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA is, by definition, any strain of Staphylococcus aureus bacteria that has developed resistance to beta-lactam antibiotics which include the penicillins (methicillin, dicloxacillin, nafcillin, oxacillin, etc.) and the cephalosporins.	topic_mrs
75289	7	354876	11	NULL	NULL	0	NULL	penicillins	Chemical		are a group of					beta-lactam antibiotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA is, by definition, any strain of Staphylococcus aureus bacteria that has developed resistance to beta-lactam antibiotics which include the penicillins (methicillin, dicloxacillin, nafcillin, oxacillin, etc.) and the cephalosporins.	topic_mrs
75290	8	354876	11	NULL	NULL	0	NULL	cephalosporins	Chemical		are a group of					beta-lactam antibiotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA is, by definition, any strain of Staphylococcus aureus bacteria that has developed resistance to beta-lactam antibiotics which include the penicillins (methicillin, dicloxacillin, nafcillin, oxacillin, etc.) and the cephalosporins.	topic_mrs
75294	9	354876	11	NULL	NULL	0	NULL	MRSA	Organism		has resistance to					methicillin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA is, by definition, any strain of Staphylococcus aureus bacteria that has developed resistance to beta-lactam antibiotics which include the penicillins (methicillin, dicloxacillin, nafcillin, oxacillin, etc.) and the cephalosporins.	topic_mrs
75296	10	354876	11	NULL	NULL	0	NULL	MRSA	Organism		has resistance to					dicloxacillin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA is, by definition, any strain of Staphylococcus aureus bacteria that has developed resistance to beta-lactam antibiotics which include the penicillins (methicillin, dicloxacillin, nafcillin, oxacillin, etc.) and the cephalosporins.	topic_mrs
75297	11	354876	11	NULL	NULL	0	NULL	MRSA	Organism		has resistance to					nafcillin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA is, by definition, any strain of Staphylococcus aureus bacteria that has developed resistance to beta-lactam antibiotics which include the penicillins (methicillin, dicloxacillin, nafcillin, oxacillin, etc.) and the cephalosporins.	topic_mrs
75298	12	354876	11	NULL	NULL	0	NULL	MRSA	Organism		has resistance to					oxacillin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA is, by definition, any strain of Staphylococcus aureus bacteria that has developed resistance to beta-lactam antibiotics which include the penicillins (methicillin, dicloxacillin, nafcillin, oxacillin, etc.) and the cephalosporins.	topic_mrs
75302	13	354876	11	NULL	NULL	0	NULL	MRSA	Organism		has resistance to					cephalosporins	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA is, by definition, any strain of Staphylococcus aureus bacteria that has developed resistance to beta-lactam antibiotics which include the penicillins (methicillin, dicloxacillin, nafcillin, oxacillin, etc.) and the cephalosporins.	topic_mrs
75303	1	354877	11	NULL	NULL	0	NULL	vanH gene	GP		code for					protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The vanH, vanA, and vanX genes code for proteins that are necessary for the expression of resistance	topic_mrs
75304	2	354877	11	NULL	NULL	0	NULL	vanA gene	GP		code for					proteins	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The vanH, vanA, and vanX genes code for proteins that are necessary for the expression of resistance	topic_mrs
75305	3	354877	11	NULL	NULL	0	NULL	vanX gene	GP		code for					protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The vanH, vanA, and vanX genes code for proteins that are necessary for the expression of resistance	topic_mrs
75306	4	354877	11	NULL	NULL	0	NULL	statement 1	GP		express					resistance	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The vanH, vanA, and vanX genes code for proteins that are necessary for the expression of resistance	topic_mrs
75307	5	354877	11	NULL	NULL	0	NULL	statement 2	GP		express					resistance	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The vanH, vanA, and vanX genes code for proteins that are necessary for the expression of resistance	topic_mrs
75308	6	354877	11	NULL	NULL	0	NULL	statement 3	GP		express					resistance	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The vanH, vanA, and vanX genes code for proteins that are necessary for the expression of resistance	topic_mrs
75309	1	354878	11	NULL	NULL	0	NULL	VanA-type resistance	Process		is inducible resistance to		high-level			vancomycin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	VanA-type resistance is characterized by high-level inducible resistance to both vancomycin and teicoplanin	topic_mrs
75310	2	354878	11	NULL	NULL	0	NULL	VanA-type resistance	Process		is inducible resistance to		high-level			teicoplanin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	VanA-type resistance is characterized by high-level inducible resistance to both vancomycin and teicoplanin	topic_mrs
75311	1	354879	11	NULL	NULL	0	NULL	Mupirocin	Chemical		is a type of 					antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Mupirocin (Bactroban or Centany) is an antibiotic originally isolated from Pseudomonas fluorescens	topic_mrs
75312	2	354879	11	NULL	NULL	0	NULL	Mupirocin	Chemical		is also known as					Bactroban	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Mupirocin (Bactroban or Centany) is an antibiotic originally isolated from Pseudomonas fluorescens	topic_mrs
75313	3	354879	11	NULL	NULL	0	NULL	Mupirocin	Chemical		is also known as					Centany	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Mupirocin (Bactroban or Centany) is an antibiotic originally isolated from Pseudomonas fluorescens	topic_mrs
75314	4	354879	11	NULL	NULL	0	NULL	Mupirocin	Chemical		isolates from					Pseudomonas fluorescens	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Mupirocin (Bactroban or Centany) is an antibiotic originally isolated from Pseudomonas fluorescens	topic_mrs
73937	1	354881	5	NULL	NULL	0	NULL	drugs	Chemical		dose not cure					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Drugs don't cure autism, but many autistic suffer from multiple problems such as depression or seizures, and the drugs can help with those secondary problems.	topic_aut
73938	2	354881	5	NULL	NULL	0	NULL	autistic	GroupOfPeople		suffer from					depression	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Drugs don't cure autism, but many autistic suffer from multiple problems such as depression or seizures, and the drugs can help with those secondary problems.	topic_aut
73939	3	354881	5	NULL	NULL	0	NULL	autistic	GroupOfPeople		suffer from					seizures	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Drugs don't cure autism, but many autistic suffer from multiple problems such as depression or seizures, and the drugs can help with those secondary problems.	topic_aut
75315	1	354881	5	11	NULL	0	NULL	depression	MedicalFinding		is a secondary problem of					 autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Drugs don't cure autism, but many autistic suffer from multiple problems such as depression or seizures, and the drugs can help with those secondary problems.	topic_aut
75316	1	354881	5	11	NULL	0	NULL	seizures	MedicalFinding		is a secondary problem of					 autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Drugs don't cure autism, but many autistic suffer from multiple problems such as depression or seizures, and the drugs can help with those secondary problems.	topic_aut
73940	1	354882	5	NULL	NULL	0	NULL	Mellaril	Chemical		is a type of					antipsychotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti psychotics (Mellaril, Haldol, Thorazine) - used to treat severe aggression, self-injurous behavior, agitation or insomnia	topic_aut
73941	2	354882	5	NULL	NULL	0	NULL	Haldol	Chemical		is a type of					antipsychotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti psychotics (Mellaril, Haldol, Thorazine) - used to treat severe aggression, self-injurous behavior, agitation or insomnia	topic_aut
73942	3	354882	5	NULL	NULL	0	NULL	Thorazine	Chemical		is a type of					antipsychotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti psychotics (Mellaril, Haldol, Thorazine) - used to treat severe aggression, self-injurous behavior, agitation or insomnia	topic_aut
73943	4	354882	5	NULL	NULL	0	NULL	aggression	MedicalFinding	severe	is treated with					Mellaril	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti psychotics (Mellaril, Haldol, Thorazine) - used to treat severe aggression, self-injurous behavior, agitation or insomnia	topic_aut
73944	5	354882	5	NULL	NULL	0	NULL	aggression	MedicalFinding	severe	is treated with					Haldol	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti psychotics (Mellaril, Haldol, Thorazine) - used to treat severe aggression, self-injurous behavior, agitation or insomnia	topic_aut
73945	6	354882	5	NULL	NULL	0	NULL	aggression	MedicalFinding	severe	is treated with					Thorazine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti psychotics (Mellaril, Haldol, Thorazine) - used to treat severe aggression, self-injurous behavior, agitation or insomnia	topic_aut
73946	7	354882	5	NULL	NULL	0	NULL	self-injurous behavior	MedicalFinding		is treated with					Mellaril	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti psychotics (Mellaril, Haldol, Thorazine) - used to treat severe aggression, self-injurous behavior, agitation or insomnia	topic_aut
73947	8	354882	5	NULL	NULL	0	NULL	self-injurous behavior	MedicalFinding		is treated with					Haldol	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti psychotics (Mellaril, Haldol, Thorazine) - used to treat severe aggression, self-injurous behavior, agitation or insomnia	topic_aut
73948	9	354882	5	NULL	NULL	0	NULL	self-injurous behavior	MedicalFinding		is treated with					Thorazine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti psychotics (Mellaril, Haldol, Thorazine) - used to treat severe aggression, self-injurous behavior, agitation or insomnia	topic_aut
73949	10	354882	5	NULL	NULL	0	NULL	agitation	MedicalFinding		is treated with					Mellaril	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti psychotics (Mellaril, Haldol, Thorazine) - used to treat severe aggression, self-injurous behavior, agitation or insomnia	topic_aut
73950	11	354882	5	NULL	NULL	0	NULL	agitation	MedicalFinding		is treated with					Haldol	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti psychotics (Mellaril, Haldol, Thorazine) - used to treat severe aggression, self-injurous behavior, agitation or insomnia	topic_aut
73951	12	354882	5	NULL	NULL	0	NULL	agitation	MedicalFinding		is treated with					Thorazine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti psychotics (Mellaril, Haldol, Thorazine) - used to treat severe aggression, self-injurous behavior, agitation or insomnia	topic_aut
73952	13	354882	5	NULL	NULL	0	NULL	insomnia	MedicalFinding		is treated with					Mellaril	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti psychotics (Mellaril, Haldol, Thorazine) - used to treat severe aggression, self-injurous behavior, agitation or insomnia	topic_aut
73953	14	354882	5	NULL	NULL	0	NULL	insomnia	MedicalFinding		is treated with					Haldol	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti psychotics (Mellaril, Haldol, Thorazine) - used to treat severe aggression, self-injurous behavior, agitation or insomnia	topic_aut
73954	15	354882	5	NULL	NULL	0	NULL	insomnia	MedicalFinding		is treated with					Thorazine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti psychotics (Mellaril, Haldol, Thorazine) - used to treat severe aggression, self-injurous behavior, agitation or insomnia	topic_aut
73955	1	354883	5	NULL	NULL	0	NULL	Tegretol	Chemical		is a type of					Anticonvulsants 	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anticonvulsants (Tegretol, Depakote, Dilantin) - used to control seizures	topic_aut
73956	2	354883	5	NULL	NULL	0	NULL	Depakote	Chemical		is a type of					Anticonvulsants	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anticonvulsants (Tegretol, Depakote, Dilantin) - used to control seizures	topic_aut
73957	3	354883	5	NULL	NULL	0	NULL	Dilantin	Chemical		is a type of					Anticonvulsants	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anticonvulsants (Tegretol, Depakote, Dilantin) - used to control seizures	topic_aut
73958	4	354883	5	NULL	NULL	0	NULL	seizures	MedicalFinding		is controlled by					Tegretol	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anticonvulsants (Tegretol, Depakote, Dilantin) - used to control seizures	topic_aut
73959	5	354883	5	NULL	NULL	0	NULL	seizures	MedicalFinding		is controlled by					Depakote	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anticonvulsants (Tegretol, Depakote, Dilantin) - used to control seizures	topic_aut
73960	6	354883	5	NULL	NULL	0	NULL	seizures	MedicalFinding		is controlled by					Dilantin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anticonvulsants (Tegretol, Depakote, Dilantin) - used to control seizures	topic_aut
73961	1	354884	5	NULL	NULL	0	NULL	Lithium	Chemical		is a type of					anti depressant	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti depression (Lithium, Depakote) - used for bipolar manic depression	topic_aut
73962	2	354884	5	NULL	NULL	0	NULL	Depakote	Chemical		is a type of					anti depressant	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti depression (Lithium, Depakote) - used for bipolar manic depression	topic_aut
73963	3	354884	5	NULL	NULL	0	NULL	bipolar manic depression	MedicalFinding		is treated with					Lithium	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti depression (Lithium, Depakote) - used for bipolar manic depression	topic_aut
73964	4	354884	5	NULL	NULL	0	NULL	bipolar manic depression	MedicalFinding		is treated with					Depakote	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti depression (Lithium, Depakote) - used for bipolar manic depression	topic_aut
73965	1	354885	5	NULL	NULL	0	NULL	Valium	Chemical		is a type of					Anti anxiety drug	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti anxiety (Valium, Librium) 	topic_aut
73966	2	354885	5	NULL	NULL	0	NULL	Librium	Chemical		is a type of					Anti anxiety drug	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Anti anxiety (Valium, Librium) 	topic_aut
73967	1	354886	5	NULL	NULL	0	NULL	Nadolol	Chemical		is a type of					beta blocker	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta Blockers (Nadolol, Buspirone)-used to decrease aggression or hyperactivity	topic_aut
73968	2	354886	5	NULL	NULL	0	NULL	Buspirone	Chemical		is a type of					beta blocker	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta Blockers (Nadolol, Buspirone)-used to decrease aggression or hyperactivity	topic_aut
73969	3	354886	5	NULL	NULL	0	NULL	Nadolol	Chemical		decreases					aggression	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta Blockers (Nadolol, Buspirone)-used to decrease aggression or hyperactivity	topic_aut
73970	4	354886	5	NULL	NULL	0	NULL	Nadolol	Chemical		decreases					hyperactivity	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta Blockers (Nadolol, Buspirone)-used to decrease aggression or hyperactivity	topic_aut
73971	5	354886	5	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta Blockers (Nadolol, Buspirone)-used to decrease aggression or hyperactivity	topic_aut
73972	6	354886	5	NULL	NULL	0	NULL	Buspirone	Chemical		decreases					aggression	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta Blockers (Nadolol, Buspirone)-used to decrease aggression or hyperactivity	topic_aut
73973	7	354886	5	NULL	NULL	0	NULL	Buspirone	Chemical		decreases					hyperactivity	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta Blockers (Nadolol, Buspirone)-used to decrease aggression or hyperactivity	topic_aut
73974	8	354886	5	NULL	NULL	0	NULL	statement 6	Process		is an alternative to					statement 7	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta Blockers (Nadolol, Buspirone)-used to decrease aggression or hyperactivity	topic_aut
73975	1	354887	5	NULL	NULL	NULL	NULL	Naltrexone/Trexan	Chemical		is a type of					opiate blocker	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Opiate Blockers (Naltrexone/Trexan) - control self injurious behaviors	topic_aut
73976	2	354887	5	NULL	NULL	NULL	NULL	Naltrexone/Trexan	Chemical		controls					self injurious behaviors	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Opiate Blockers (Naltrexone/Trexan) - control self injurious behaviors	topic_aut
73977	1	354888	5	NULL	NULL	0	NULL	Chloral Hydrate	Chemical		is a type of					sedative	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Sedatives (Chloral Hydrate, Noctec, and Benadryl) - for difficulty sleeping	topic_aut
73978	2	354888	5	NULL	NULL	0	NULL	Noctec	Chemical		is a type of					sedative	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Sedatives (Chloral Hydrate, Noctec, and Benadryl) - for difficulty sleeping	topic_aut
73979	3	354888	5	NULL	NULL	0	NULL	Benadryl	Chemical		is a type of					sedative	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Sedatives (Chloral Hydrate, Noctec, and Benadryl) - for difficulty sleeping	topic_aut
73980	4	354888	5	NULL	NULL	0	NULL	Chloral Hydrate	Chemical		treats					sleeping difficulty	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Sedatives (Chloral Hydrate, Noctec, and Benadryl) - for difficulty sleeping	topic_aut
73981	5	354888	5	NULL	NULL	0	NULL	Noctec	Chemical		treats					sleeping difficulty	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Sedatives (Chloral Hydrate, Noctec, and Benadryl) - for difficulty sleeping	topic_aut
73982	6	354888	5	NULL	NULL	0	NULL	Benadryl	Chemical		treats					sleeping difficulty	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Sedatives (Chloral Hydrate, Noctec, and Benadryl) - for difficulty sleeping	topic_aut
73983	1	354889	5	NULL	NULL	0	NULL	Ritalin	Chemical		is a type of					stimulant	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Stimulants (Ritalin, Dexedrine)-for hyperactivity and attention or concentration problems	topic_aut
73984	2	354889	5	NULL	NULL	0	NULL	Dexedrine	Chemical		is a type of					stimulant	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Stimulants (Ritalin, Dexedrine)-for hyperactivity and attention or concentration problems	topic_aut
73985	3	354889	5	NULL	NULL	0	NULL	hyperactivity	MedicalFinding		is treated with					Ritalin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Stimulants (Ritalin, Dexedrine)-for hyperactivity and attention or concentration problems	topic_aut
73986	4	354889	5	NULL	NULL	0	NULL	hyperactivity	MedicalFinding		is treated with					Dexedrine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Stimulants (Ritalin, Dexedrine)-for hyperactivity and attention or concentration problems	topic_aut
73987	5	354889	5	NULL	NULL	0	NULL	attention or concentration problems	MedicalFinding		is treated with					Ritalin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Stimulants (Ritalin, Dexedrine)-for hyperactivity and attention or concentration problems	topic_aut
73988	6	354889	5	NULL	NULL	0	NULL	attention or concentration problems	MedicalFinding		is treated with					Dexedrine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Stimulants (Ritalin, Dexedrine)-for hyperactivity and attention or concentration problems	topic_aut
74072	1	354890	5	NULL	NULL	0	NULL	candida albicans	Organism		is a synonym of					yeast	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	There are some evidence that candida albicans (yeast) may cause or exacerbate behavior and health problems in autistic individuals. The only physical symptoms are vaginal yeast infections and thrush (white patches in mouth). Candida overgrowth is often attributed to long term antibiotic treatments. It has been reported that some children whose autistic tendencies surfaced at 18- 24 months had been continuously treated with antibiotics to control chronic ear infections. The treatment doesn't cure autism, but is helpful for some autistic children.	topic_aut
74073	2	354890	5	NULL	NULL	0	NULL	candida albicans	Organism		cause		may			behavior problems	MedicalFinding				NULL	autistic individulas	0	NULL	NULL	NULL	NULL	NULL	There are some evidence that candida albicans (yeast) may cause or exacerbate behavior and health problems in autistic individuals. The only physical symptoms are vaginal yeast infections and thrush (white patches in mouth). Candida overgrowth is often attributed to long term antibiotic treatments. It has been reported that some children whose autistic tendencies surfaced at 18- 24 months had been continuously treated with antibiotics to control chronic ear infections. The treatment doesn't cure autism, but is helpful for some autistic children.	topic_aut
74074	3	354890	5	NULL	NULL	0	NULL	candida albicans	Organism		cause		may			health problems	MedicalFinding				NULL	autistic individulas	0	NULL	NULL	NULL	NULL	NULL	There are some evidence that candida albicans (yeast) may cause or exacerbate behavior and health problems in autistic individuals. The only physical symptoms are vaginal yeast infections and thrush (white patches in mouth). Candida overgrowth is often attributed to long term antibiotic treatments. It has been reported that some children whose autistic tendencies surfaced at 18- 24 months had been continuously treated with antibiotics to control chronic ear infections. The treatment doesn't cure autism, but is helpful for some autistic children.	topic_aut
74075	4	354890	5	NULL	NULL	0	NULL	vagina	OrganismPart	infection of	is a symptom of		physical			candida outgrowth	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	There are some evidence that candida albicans (yeast) may cause or exacerbate behavior and health problems in autistic individuals. The only physical symptoms are vaginal yeast infections and thrush (white patches in mouth). Candida overgrowth is often attributed to long term antibiotic treatments. It has been reported that some children whose autistic tendencies surfaced at 18- 24 months had been continuously treated with antibiotics to control chronic ear infections. The treatment doesn't cure autism, but is helpful for some autistic children.	topic_aut
74076	5	354890	5	NULL	NULL	0	NULL	thrush	MedicalFinding		is a symptom of		physical			candida outgrowth	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	There are some evidence that candida albicans (yeast) may cause or exacerbate behavior and health problems in autistic individuals. The only physical symptoms are vaginal yeast infections and thrush (white patches in mouth). Candida overgrowth is often attributed to long term antibiotic treatments. It has been reported that some children whose autistic tendencies surfaced at 18- 24 months had been continuously treated with antibiotics to control chronic ear infections. The treatment doesn't cure autism, but is helpful for some autistic children.	topic_aut
74077	6	354890	5	NULL	NULL	0	NULL	thrush	MedicalFinding		is a type of					white patches in mouth	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	There are some evidence that candida albicans (yeast) may cause or exacerbate behavior and health problems in autistic individuals. The only physical symptoms are vaginal yeast infections and thrush (white patches in mouth). Candida overgrowth is often attributed to long term antibiotic treatments. It has been reported that some children whose autistic tendencies surfaced at 18- 24 months had been continuously treated with antibiotics to control chronic ear infections. The treatment doesn't cure autism, but is helpful for some autistic children.	topic_aut
74082	1	354892	5	NULL	NULL	0	NULL	autistic individuals	GroupOfPeople		experience					sensory dysfunction	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Auditory training can be considered a form of sensory integration in which stimulation  may sensitize or desensitize one or more senses. Theoretically speaking, if one or more  senses are impaired in an individual, he or she may develop a distorted perception of the   environment. There has been much research in the past 15 years to indicate that many  autistic individuals have sensory dysfunction in one or more areas	topic_aut
74083	2	354892	5	NULL	NULL	0	NULL	senses	PhysicalPhenomenon	impaired	develops					environment	PhysicalPhenomenon	distorted perception of			NULL		0	NULL	NULL	NULL	NULL	NULL	Auditory training can be considered a form of sensory integration in which stimulation  may sensitize or desensitize one or more senses. Theoretically speaking, if one or more  senses are impaired in an individual, he or she may develop a distorted perception of the   environment. There has been much research in the past 15 years to indicate that many  autistic individuals have sensory dysfunction in one or more areas	topic_aut
76345	1	354894	11	NULL	NULL	0	NULL	antibacterial	Chemical		kills					bacteria	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	An antibacterial is a substance that kills bacteria or slows their growth. The term 'antibiotic' was coined by Selman Waksman in 1942 to describe any substance produced by a microorganism that is antagonistic to the growth of other microorganisms in high dilution.	topic_mrs
76346	2	354894	11	NULL	NULL	0	NULL	antibacterial	Chemical		slows					Bacterial growth	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	An antibacterial is a substance that kills bacteria or slows their growth. The term 'antibiotic' was coined by Selman Waksman in 1942 to describe any substance produced by a microorganism that is antagonistic to the growth of other microorganisms in high dilution.	topic_mrs
76347	3	354894	11	NULL	NULL	0	NULL	statement 1	Process		is an alternative to 					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	An antibacterial is a substance that kills bacteria or slows their growth. The term 'antibiotic' was coined by Selman Waksman in 1942 to describe any substance produced by a microorganism that is antagonistic to the growth of other microorganisms in high dilution.	topic_mrs
75408	1	354895	11	NULL	NULL	0	NULL	Bactroban	Chemical		contains					mupirocin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Bactroban contains mupirocin, an antibiotic. Mupirocin prevents bacteria from growing on your skin.	topic_mrs
75409	2	354895	11	NULL	NULL	0	NULL	mupirocin	Chemical		is a type of 					antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Bactroban contains mupirocin, an antibiotic. Mupirocin prevents bacteria from growing on your skin.	topic_mrs
75410	3	354895	11	NULL	NULL	0	NULL	Mupirocin	Chemical		prevents					Bacterial growth	Process	skin			NULL		0	NULL	NULL	NULL	NULL	NULL	Bactroban contains mupirocin, an antibiotic. Mupirocin prevents bacteria from growing on your skin.	topic_mrs
75411	1	354896	11	NULL	NULL	0	NULL	Mupirocin	Chemical		is a type of 					antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Mupirocin  is an antibiotic originally isolated from Pseudomonas fluorescens 	topic_mrs
75412	2	354896	11	NULL	NULL	0	NULL	Mupirocin	Chemical		isolated from					Pseudomonas fluorescens	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Mupirocin  is an antibiotic originally isolated from Pseudomonas fluorescens 	topic_mrs
74278	1	354897	7	NULL	NULL	0	NULL	HNPCC	MedicalFinding		is a type of					genetically heterogeneous disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary non-polyposis colorectal cancer (HNPCC or Lynch syndrome), is a genetically heterogeneous disorder that is believed to account for 2-10 per cent of all the colorectal cancer cases. The disease follows autosomal dominant inheritance pattern with high penetrance (85%) and younger age of onset when compared to patients with sporadic tumours.	topic_ccc
74279	2	354897	7	NULL	NULL	0	NULL	HNPCC	MedicalFinding		is 					Lynch syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary non-polyposis colorectal cancer (HNPCC or Lynch syndrome), is a genetically heterogeneous disorder that is believed to account for 2-10 per cent of all the colorectal cancer cases. The disease follows autosomal dominant inheritance pattern with high penetrance (85%) and younger age of onset when compared to patients with sporadic tumours.	topic_ccc
74280	3	354897	7	NULL	NULL	0	NULL	HNPCC	MedicalFinding		is					Hereditary non-polyposis colorectal cancer					NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary non-polyposis colorectal cancer (HNPCC or Lynch syndrome), is a genetically heterogeneous disorder that is believed to account for 2-10 per cent of all the colorectal cancer cases. The disease follows autosomal dominant inheritance pattern with high penetrance (85%) and younger age of onset when compared to patients with sporadic tumours.	topic_ccc
74281	4	354897	7	NULL	NULL	0	NULL	HNPCC	MedicalFinding		follows					autosomal dominant inheritance pattern	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary non-polyposis colorectal cancer (HNPCC or Lynch syndrome), is a genetically heterogeneous disorder that is believed to account for 2-10 per cent of all the colorectal cancer cases. The disease follows autosomal dominant inheritance pattern with high penetrance (85%) and younger age of onset when compared to patients with sporadic tumours.	topic_ccc
74282	1	354899	7	NULL	NULL	0	NULL	colorectal cancer	MedicalFinding		predisposition with		genetic			autosomal dominant of pattern of inheritance	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	1-5% of all patients presenting with colorectal cancer, have an underlying genetic predisposition with an autosomal dominant of pattern of inheritance. However, endometrial cancer, stomach cancer, small bowel cancer, urinary tract cancer and skin cancer among others are also inherent to the syndrome.	topic_ccc
74283	1	354900	7	NULL	NULL	0	NULL	hMSH2 genes	GP		located at					chromosome 2p21	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	The genomic loci for the mismatch repair genes hMSH2 and hMSH6 were mapped by fluorescence in situ hybridization, analysis of radiation hybrid panel markers, and linkage analysis of syntenic chromosome regions between human and mouse. Both genes were localized to chromosome 2p21	topic_ccc
74284	2	354900	7	NULL	NULL	0	NULL	hMSH6 genes	GP		located at					chromosome 2p21	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	The genomic loci for the mismatch repair genes hMSH2 and hMSH6 were mapped by fluorescence in situ hybridization, analysis of radiation hybrid panel markers, and linkage analysis of syntenic chromosome regions between human and mouse. Both genes were localized to chromosome 2p21	topic_ccc
74285	1	354902	7	NULL	NULL	0	NULL	VEGF	GP		expressed in					metastatic neoplasm	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation, whereas expression of bFGF, flt-1, bek, and flg did not differ among tumor types. Vessel counts were greater in metastatic tumors than in nonmetastatic tumors.	topic_ccc
74286	2	354902	7	NULL	NULL	0	NULL	VEGF	GP		expressed in					nonmetastatic neoplasm	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation, whereas expression of bFGF, flt-1, bek, and flg did not differ among tumor types. Vessel counts were greater in metastatic tumors than in nonmetastatic tumors.	topic_ccc
74287	3	354902	7	NULL	NULL	0	NULL	statement 1	Process		is higher than					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation, whereas expression of bFGF, flt-1, bek, and flg did not differ among tumor types. Vessel counts were greater in metastatic tumors than in nonmetastatic tumors.	topic_ccc
74288	4	354902	7	NULL	NULL	0	NULL	KDR	GP		expressed in					metastatic neoplasm	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation, whereas expression of bFGF, flt-1, bek, and flg did not differ among tumor types. Vessel counts were greater in metastatic tumors than in nonmetastatic tumors.	topic_ccc
74289	5	354902	7	NULL	NULL	0	NULL	KDR	GP		expressed in					nonmetastatic neoplasm	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation, whereas expression of bFGF, flt-1, bek, and flg did not differ among tumor types. Vessel counts were greater in metastatic tumors than in nonmetastatic tumors.	topic_ccc
74290	6	354902	7	NULL	NULL	0	NULL	statement 4	Process		is higher than					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation, whereas expression of bFGF, flt-1, bek, and flg did not differ among tumor types. Vessel counts were greater in metastatic tumors than in nonmetastatic tumors.	topic_ccc
74291	7	354902	7	NULL	NULL	0	NULL	statement 3	Process		correlates with					neovascularization	Process	extent of			NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation, whereas expression of bFGF, flt-1, bek, and flg did not differ among tumor types. Vessel counts were greater in metastatic tumors than in nonmetastatic tumors.	topic_ccc
74292	8	354902	7	NULL	NULL	0	NULL	statement 6	Process		correlates with					neovascularization	Process	extent of			NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation, whereas expression of bFGF, flt-1, bek, and flg did not differ among tumor types. Vessel counts were greater in metastatic tumors than in nonmetastatic tumors.	topic_ccc
74293	9	354902	7	NULL	NULL	0	NULL	statement 3	Process		correlates with					proliferation	Process	degree of			NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation, whereas expression of bFGF, flt-1, bek, and flg did not differ among tumor types. Vessel counts were greater in metastatic tumors than in nonmetastatic tumors.	topic_ccc
74294	10	354902	7	NULL	NULL	0	NULL	statement 6	Process		correlates with					proliferation	Process	degree of			NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation, whereas expression of bFGF, flt-1, bek, and flg did not differ among tumor types. Vessel counts were greater in metastatic tumors than in nonmetastatic tumors.	topic_ccc
74295	11	354902	7	NULL	NULL	0	NULL	bFGF	GP	expression of	does not differ among					tumor types	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation, whereas expression of bFGF, flt-1, bek, and flg did not differ among tumor types. Vessel counts were greater in metastatic tumors than in nonmetastatic tumors.	topic_ccc
74296	12	354902	7	NULL	NULL	NULL	NULL	flt-1	GP	expression of	does not differ among					tumor types	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation, whereas expression of bFGF, flt-1, bek, and flg did not differ among tumor types. Vessel counts were greater in metastatic tumors than in nonmetastatic tumors.	topic_ccc
74297	13	354902	7	NULL	NULL	0	NULL	 bek	GP	expression of	does not differ among					tumor types	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation, whereas expression of bFGF, flt-1, bek, and flg did not differ among tumor types. Vessel counts were greater in metastatic tumors than in nonmetastatic tumors.	topic_ccc
74298	14	354902	7	NULL	NULL	0	NULL	 flg	GP	expression of	does not differ among					tumor types	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation, whereas expression of bFGF, flt-1, bek, and flg did not differ among tumor types. Vessel counts were greater in metastatic tumors than in nonmetastatic tumors.	topic_ccc
74299	15	354902	7	NULL	NULL	0	NULL	metastatic tumor	MedicalFinding	vessel counts in	is greater than					nonmetastatic tumors	MedicalFinding	vessel counts in			NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation, whereas expression of bFGF, flt-1, bek, and flg did not differ among tumor types. Vessel counts were greater in metastatic tumors than in nonmetastatic tumors.	topic_ccc
74300	16	354902	7	NULL	NULL	0	NULL	VEGF	GP		is					vascular endothelial growth factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation, whereas expression of bFGF, flt-1, bek, and flg did not differ among tumor types. Vessel counts were greater in metastatic tumors than in nonmetastatic tumors.	topic_ccc
74301	17	354902	7	NULL	NULL	0	NULL	bFGF	GP		is					basic fibroblast growth factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation, whereas expression of bFGF, flt-1, bek, and flg did not differ among tumor types. Vessel counts were greater in metastatic tumors than in nonmetastatic tumors.	topic_ccc
74302	1	354903	7	NULL	NULL	0	NULL	VEGF	GP		expressed in					metastatic neoplasm	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation	topic_ccc
74303	2	354903	7	NULL	NULL	0	NULL	VEGF	GP		expressed in					nonmetastatic neoplasm	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation	topic_ccc
74304	3	354903	7	NULL	NULL	0	NULL	statement 1	Process		is higher than					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation	topic_ccc
74305	4	354903	7	NULL	NULL	0	NULL	KDR	GP		expressed in					metastatic neoplasm	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation	topic_ccc
74306	5	354903	7	NULL	NULL	0	NULL	KDR	GP		expressed in					nonmetastatic neoplasm	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation	topic_ccc
74307	6	354903	7	NULL	NULL	NULL	NULL	statement 4	Process		is higher than					statement 5	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation	topic_ccc
74308	7	354903	7	NULL	NULL	0	NULL	statement 3	Process		correlates with		directly			neovascularization	Process	extent of			NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation	topic_ccc
74309	8	354903	7	NULL	NULL	0	NULL	statement 6	Process		correlates with		directly			neovascularization	Process	extent of			NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation	topic_ccc
74310	9	354903	7	NULL	NULL	0	NULL	statement 3	Process		correlates with		directly			proliferation	Process	degree of			NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation	topic_ccc
74311	10	354903	7	NULL	NULL	0	NULL	statement 6	Process		correlates with		directly			proliferation	Process	degree of			NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation	topic_ccc
74312	11	354903	7	NULL	NULL	0	NULL	VEGF	GP		is					vascular endothelial growth factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation	topic_ccc
74313	12	354903	7	NULL	NULL	0	NULL	bFGF	GP		is					basic fibroblast growth factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	We studied the correlation between expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors with vascularity, metastasis, and proliferative index of human colon cancers.Expression of VEGF and KDR was higher in metastatic than in nonmetastatic neoplasms and directly correlated with the extent of neovascularization and the degree of proliferation	topic_ccc
74314	1	354905	7	NULL	NULL	0	NULL	Microsatellite instability	NucleicAcid		is associated with					patient survival	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Microsatellite instability is an important factor associated with patient survival in Chinese sporadic colorectal cancer.\t	topic_ccc
74315	2	354905	7	NULL	NULL	0	NULL	statement 1	Process		occur in					Chinese sporadic colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Microsatellite instability is an important factor associated with patient survival in Chinese sporadic colorectal cancer.\t	topic_ccc
74334	1	354906	7	NULL	NULL	0	NULL	VEGF	GP		is an important					angiogenic factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	hese findings support the hypothesis that VEGF is an important angiogenic factor in primary and metastatic human colon cancer.	topic_ccc
74335	2	354906	7	NULL	NULL	0	NULL	statement 1	Process		occur in 					primary human colon cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	hese findings support the hypothesis that VEGF is an important angiogenic factor in primary and metastatic human colon cancer.	topic_ccc
74336	3	354906	7	NULL	NULL	0	NULL	statement 1	Process		occur in					metastatic human colon cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	hese findings support the hypothesis that VEGF is an important angiogenic factor in primary and metastatic human colon cancer.	topic_ccc
74438	1	354908	7	NULL	NULL	0	NULL	CIMP	PhysicalPhenomenon		characterized by					p16	GP	abnormal methylation of		multiple CpG islands	NULL		0	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. \t	topic_ccc
74439	2	354908	7	NULL	NULL	0	NULL	CIMP	PhysicalPhenomenon		characterized by					hMLH1	GP	abnormal methylation of		multiple CpG islands	NULL		0	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. \t	topic_ccc
74440	3	354908	7	NULL	NULL	NULL	NULL	CIMP	PhysicalPhenomenon		characterized by					THBS1	GP	abnormal methylation of		multiple CpG islands	NULL		NULL	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. \t	topic_ccc
74441	4	354908	7	NULL	NULL	0	NULL	statement 1	Process		occur in					colorectal cancers	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. \t	topic_ccc
74442	5	354908	7	NULL	NULL	0	NULL	statement 2	Process		occur in					colorectal cancers	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. \t	topic_ccc
74443	6	354908	7	NULL	NULL	0	NULL	statement 3	Process		occur in					colorectal cancers	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. \t	topic_ccc
74444	7	354908	7	NULL	NULL	0	NULL	CIMP	PhysicalPhenomenon		is					CpG island methylator phenotype	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. \t	topic_ccc
74445	8	354908	7	NULL	NULL	0	NULL	p16	GP		is a type of					tumor suppressor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. \t	topic_ccc
74446	9	354908	7	NULL	NULL	0	NULL	hMLH1	GP		is a type of					tumor suppressor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. \t	topic_ccc
74447	10	354908	7	NULL	NULL	0	NULL	THBS1	GP		is a type of					tumor suppressor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. \t	topic_ccc
74448	1	354910	7	NULL	NULL	0	NULL	Oxygen	Chemical		associated with					genomic instability	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Oxygen is further shown to be associated with genomic instability in two additional cancer models involving the APC tumor suppressor gene and chemical carcinogenesis. 	topic_ccc
74449	2	354910	7	NULL	NULL	0	NULL	statement 1	Process		occur in					cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Oxygen is further shown to be associated with genomic instability in two additional cancer models involving the APC tumor suppressor gene and chemical carcinogenesis. 	topic_ccc
74450	3	354910	7	NULL	NULL	0	NULL	statement 2	Process		involves					APC tumor suppressor gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Oxygen is further shown to be associated with genomic instability in two additional cancer models involving the APC tumor suppressor gene and chemical carcinogenesis. 	topic_ccc
74451	4	354910	7	NULL	NULL	0	NULL	statement 2	Process		involves					chemical carcinogenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Oxygen is further shown to be associated with genomic instability in two additional cancer models involving the APC tumor suppressor gene and chemical carcinogenesis. 	topic_ccc
74452	1	354913	7	NULL	NULL	0	NULL	MMR genes 	GP	defects in	involved in					 renal carcinogenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	he complete absence of both hMLH1 and hMSH2 immunohistochemical expressions was observed only in the 3 cases with a high level of MSI. This study showed that defects in MMR genes are involved in renal carcinogenesis and correlate with the occurrence of 	topic_ccc
74453	1	354914	7	NULL	NULL	0	NULL	microsatellite loci 	NucleicAcid	instability at	attributed to					mismatch repair errors	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Instability at microsatellite loci is widely attributed to mismatch repair errors due to epigenetic alterations. Using three dinucleotide markers, D3S1313, D9S171, D17S250 and two mononucleotide markers BAT25, BATRII, we evaluated MSI in 97 cases enrolled for endoscopy of upper GI tract with symptoms of dyspepsia, reflux or dysphagia. We aimed at evaluating markers that reflect instability in esophageal malignancies, examine the prevalence of MSI in cancers and other pathologies of the esophagus, and determine the methylation status of hMLH1 gene in relation to MSI. 42% (21/50) cancers and 15.4%(2/13) precancers exhibited MSI where 85.7% cancers and 50% precancers with MSI, showed a hypermethylated hMLH1 promoter.	topic_ccc
74454	2	354914	7	NULL	NULL	0	NULL	statement 1	Process		due to					epigenetic alterations	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Instability at microsatellite loci is widely attributed to mismatch repair errors due to epigenetic alterations. Using three dinucleotide markers, D3S1313, D9S171, D17S250 and two mononucleotide markers BAT25, BATRII, we evaluated MSI in 97 cases enrolled for endoscopy of upper GI tract with symptoms of dyspepsia, reflux or dysphagia. We aimed at evaluating markers that reflect instability in esophageal malignancies, examine the prevalence of MSI in cancers and other pathologies of the esophagus, and determine the methylation status of hMLH1 gene in relation to MSI. 42% (21/50) cancers and 15.4%(2/13) precancers exhibited MSI where 85.7% cancers and 50% precancers with MSI, showed a hypermethylated hMLH1 promoter.	topic_ccc
74455	3	354914	7	NULL	NULL	0	NULL	cancers	MedicalFinding		shows					MSI	NucleicAcid	prevalence of			NULL		0	NULL	NULL	NULL	NULL	NULL	Instability at microsatellite loci is widely attributed to mismatch repair errors due to epigenetic alterations. Using three dinucleotide markers, D3S1313, D9S171, D17S250 and two mononucleotide markers BAT25, BATRII, we evaluated MSI in 97 cases enrolled for endoscopy of upper GI tract with symptoms of dyspepsia, reflux or dysphagia. We aimed at evaluating markers that reflect instability in esophageal malignancies, examine the prevalence of MSI in cancers and other pathologies of the esophagus, and determine the methylation status of hMLH1 gene in relation to MSI. 42% (21/50) cancers and 15.4%(2/13) precancers exhibited MSI where 85.7% cancers and 50% precancers with MSI, showed a hypermethylated hMLH1 promoter.	topic_ccc
74456	4	354914	7	NULL	NULL	0	NULL	precancers	MedicalFinding		shows					MSI	NucleicAcid	prevalence of			NULL		0	NULL	NULL	NULL	NULL	NULL	Instability at microsatellite loci is widely attributed to mismatch repair errors due to epigenetic alterations. Using three dinucleotide markers, D3S1313, D9S171, D17S250 and two mononucleotide markers BAT25, BATRII, we evaluated MSI in 97 cases enrolled for endoscopy of upper GI tract with symptoms of dyspepsia, reflux or dysphagia. We aimed at evaluating markers that reflect instability in esophageal malignancies, examine the prevalence of MSI in cancers and other pathologies of the esophagus, and determine the methylation status of hMLH1 gene in relation to MSI. 42% (21/50) cancers and 15.4%(2/13) precancers exhibited MSI where 85.7% cancers and 50% precancers with MSI, showed a hypermethylated hMLH1 promoter.	topic_ccc
74457	5	354914	7	NULL	NULL	NULL	NULL	statement 3	Process		involves					 hMLH1 	GP	hypermethylated		promoter	NULL		NULL	NULL	NULL	NULL	NULL	NULL	Instability at microsatellite loci is widely attributed to mismatch repair errors due to epigenetic alterations. Using three dinucleotide markers, D3S1313, D9S171, D17S250 and two mononucleotide markers BAT25, BATRII, we evaluated MSI in 97 cases enrolled for endoscopy of upper GI tract with symptoms of dyspepsia, reflux or dysphagia. We aimed at evaluating markers that reflect instability in esophageal malignancies, examine the prevalence of MSI in cancers and other pathologies of the esophagus, and determine the methylation status of hMLH1 gene in relation to MSI. 42% (21/50) cancers and 15.4%(2/13) precancers exhibited MSI where 85.7% cancers and 50% precancers with MSI, showed a hypermethylated hMLH1 promoter.	topic_ccc
74458	6	354914	7	NULL	NULL	NULL	NULL	statement 4	Process		involves					hMLH1	GP	hypermethylated		promoter	NULL		NULL	NULL	NULL	NULL	NULL	NULL	Instability at microsatellite loci is widely attributed to mismatch repair errors due to epigenetic alterations. Using three dinucleotide markers, D3S1313, D9S171, D17S250 and two mononucleotide markers BAT25, BATRII, we evaluated MSI in 97 cases enrolled for endoscopy of upper GI tract with symptoms of dyspepsia, reflux or dysphagia. We aimed at evaluating markers that reflect instability in esophageal malignancies, examine the prevalence of MSI in cancers and other pathologies of the esophagus, and determine the methylation status of hMLH1 gene in relation to MSI. 42% (21/50) cancers and 15.4%(2/13) precancers exhibited MSI where 85.7% cancers and 50% precancers with MSI, showed a hypermethylated hMLH1 promoter.	topic_ccc
74459	1	354916	7	NULL	NULL	0	NULL	hMLH1	GP	methylation of	correlated with		significantly			p53	GP	high level expression of			NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore, methylation of hMLH1 significantly correlated with high level of P53 expression (P = .006) and with overall survival (P = .015) suggesting that silencing of hMLH1 through aberrant promoter methylation could be used as a poor prognosis indicator in breast cancer.	topic_ccc
74460	2	354916	7	NULL	NULL	0	NULL	hMLH1	GP		silenced through							methylation of		aberrant promoter	NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore, methylation of hMLH1 significantly correlated with high level of P53 expression (P = .006) and with overall survival (P = .015) suggesting that silencing of hMLH1 through aberrant promoter methylation could be used as a poor prognosis indicator in breast cancer.	topic_ccc
74461	3	354916	7	NULL	NULL	0	NULL	statement 2	Process		used as					breast cancer	MedicalFinding	poor prognosis indicator in			NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore, methylation of hMLH1 significantly correlated with high level of P53 expression (P = .006) and with overall survival (P = .015) suggesting that silencing of hMLH1 through aberrant promoter methylation could be used as a poor prognosis indicator in breast cancer.	topic_ccc
74462	1	354917	7	NULL	NULL	0	NULL	hMLH1	GP	hypermethylation of 	is found in				promoter	MSI-H gastric carcinomas	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Promoter hypermethylation of hMLH1, E-cadherin, and p16(INK4A) was found in 89%, 78%, and 33% of MSI-H gastric carcinomas and in 16%, 32%, and 11% of MSS carcinomas, respectively (p = 0.01).	topic_ccc
74463	2	354917	7	NULL	NULL	0	NULL	E-cadheriny	GP	hypermethylation of 	is found in				promoter	MSI-H gastric carcinomas	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Promoter hypermethylation of hMLH1, E-cadherin, and p16(INK4A) was found in 89%, 78%, and 33% of MSI-H gastric carcinomas and in 16%, 32%, and 11% of MSS carcinomas, respectively (p = 0.01).	topic_ccc
74464	3	354917	7	NULL	NULL	0	NULL	p16(INK4A)	GP	hypermethylation of 	is found in				promoter	MSI-H gastric carcinomas	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Promoter hypermethylation of hMLH1, E-cadherin, and p16(INK4A) was found in 89%, 78%, and 33% of MSI-H gastric carcinomas and in 16%, 32%, and 11% of MSS carcinomas, respectively (p = 0.01).	topic_ccc
74465	4	354917	7	NULL	NULL	0	NULL	hMLH1	GP	hypermethylation of 	is found in				promoter	MSS carcinomas	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Promoter hypermethylation of hMLH1, E-cadherin, and p16(INK4A) was found in 89%, 78%, and 33% of MSI-H gastric carcinomas and in 16%, 32%, and 11% of MSS carcinomas, respectively (p = 0.01).	topic_ccc
74466	5	354917	7	NULL	NULL	0	NULL	E-cadherin	GP	hypermethylation of 	is found in				promoter	MSS carcinomas	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Promoter hypermethylation of hMLH1, E-cadherin, and p16(INK4A) was found in 89%, 78%, and 33% of MSI-H gastric carcinomas and in 16%, 32%, and 11% of MSS carcinomas, respectively (p = 0.01).	topic_ccc
74467	6	354917	7	NULL	NULL	0	NULL	p16(INK4A)	GP	hypermethylation of 	is found in				promoter	MSS carcinomas	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Promoter hypermethylation of hMLH1, E-cadherin, and p16(INK4A) was found in 89%, 78%, and 33% of MSI-H gastric carcinomas and in 16%, 32%, and 11% of MSS carcinomas, respectively (p = 0.01).	topic_ccc
74468	1	354918	7	NULL	NULL	0	NULL	BRCA1	GP	methylation of	correlated with					disease free survival	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	BRCA1 methylation correlated with age at diagnosis (P = .015) and 5-years disease free survival (P = .016) while hMLH1 methylation was more frequent in larger tumors (P = .002) and in presence of distant metastasis (P = .004).	topic_ccc
74469	2	354918	7	NULL	NULL	0	NULL	hMLH1	GP	methylation of	is more frequent in					larger tumors	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	BRCA1 methylation correlated with age at diagnosis (P = .015) and 5-years disease free survival (P = .016) while hMLH1 methylation was more frequent in larger tumors (P = .002) and in presence of distant metastasis (P = .004).	topic_ccc
74470	3	354918	7	NULL	NULL	0	NULL	hMLH1	GP	methylation of	is more frequent in					distant metastasis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	BRCA1 methylation correlated with age at diagnosis (P = .015) and 5-years disease free survival (P = .016) while hMLH1 methylation was more frequent in larger tumors (P = .002) and in presence of distant metastasis (P = .004).	topic_ccc
74471	1	354919	7	NULL	NULL	0	NULL	CTCF	GP		contributes to					Rb gene	GP	epigenetic regulation of;;human		promoter	NULL	tumoral cell lines	0	NULL	NULL	NULL	NULL	NULL	Here we addressed the contribution of the multifunctional nuclear factor CTCF to the epigenetic regulation of the human retinoblastoma (Rb) gene promoter in different tumoral cell lines.	topic_ccc
74472	2	354919	7	NULL	NULL	0	NULL	CTCF	GP		is a type of					multifunctional nuclear factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Here we addressed the contribution of the multifunctional nuclear factor CTCF to the epigenetic regulation of the human retinoblastoma (Rb) gene promoter in different tumoral cell lines.	topic_ccc
74473	3	354919	7	NULL	NULL	0	NULL	Rb	GP		is					retinoblastoma 	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Here we addressed the contribution of the multifunctional nuclear factor CTCF to the epigenetic regulation of the human retinoblastoma (Rb) gene promoter in different tumoral cell lines.	topic_ccc
74474	1	354920	7	NULL	NULL	0	NULL	LW6	Chemical		promotes					HIF-1alpha	GP	proteasomal degradation of			NULL	colon cancer cell line	0	NULL	NULL	NULL	NULL	NULL	LW6, a novel HIF-1 inhibitor, promotes proteasomal degradation of HIF-1alpha via upregulation of VHL in a colon cancer cell line.	topic_ccc
74475	2	354920	7	NULL	NULL	0	NULL	statement 1	Process		via					VHL	GP	upregulation of			NULL	colon cancer cell line	0	NULL	NULL	NULL	NULL	NULL	LW6, a novel HIF-1 inhibitor, promotes proteasomal degradation of HIF-1alpha via upregulation of VHL in a colon cancer cell line.	topic_ccc
74476	3	354920	7	NULL	NULL	0	NULL	LW6	Chemical		is a type of					HIF-1 inhibitor	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	LW6, a novel HIF-1 inhibitor, promotes proteasomal degradation of HIF-1alpha via upregulation of VHL in a colon cancer cell line.	topic_ccc
74478	1	354921	7	NULL	NULL	NULL	NULL	p16INK4A	GP	downregulation of	marker to		possible			retinoblastoma	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Downregulation and aberrant promoter methylation of p16INK4A: a possible novel heritable susceptibility marker to retinoblastoma.	topic_ccc
74479	2	354921	7	NULL	NULL	NULL	NULL	p16INK4A	GP	aberrant methylation of	marker to		possible		promoter	retinoblastoma	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Downregulation and aberrant promoter methylation of p16INK4A: a possible novel heritable susceptibility marker to retinoblastoma.	topic_ccc
74480	3	354921	7	NULL	NULL	0	NULL	p16INK4A	GP		is a type of					novel heritable susceptibility marker	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Downregulation and aberrant promoter methylation of p16INK4A: a possible novel heritable susceptibility marker to retinoblastoma.	topic_ccc
74482	1	354922	7	NULL	NULL	0	NULL	hMLH1 	GP		is involved in					DNA repair	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 In the current study, we aimed to assess by MSP, the methylation pattern of two cancer-related genes involved in DNA repair: hMLH1 (mutL homolog 1, colon cancer, nonpolyposis type 2 (E. coli) and BRCA1 (breast cancer 1, early onset) in 78 primary breast cancers from Tunisian patients.	topic_ccc
74484	2	354922	7	NULL	NULL	0	NULL	BRCA1	GP		is involved in					DNA repair	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 In the current study, we aimed to assess by MSP, the methylation pattern of two cancer-related genes involved in DNA repair: hMLH1 (mutL homolog 1, colon cancer, nonpolyposis type 2 (E. coli) and BRCA1 (breast cancer 1, early onset) in 78 primary breast cancers from Tunisian patients.	topic_ccc
74486	3	354922	7	NULL	NULL	0	NULL	 hMLH1	GP		is					mutL homolog 1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 In the current study, we aimed to assess by MSP, the methylation pattern of two cancer-related genes involved in DNA repair: hMLH1 (mutL homolog 1, colon cancer, nonpolyposis type 2 (E. coli) and BRCA1 (breast cancer 1, early onset) in 78 primary breast cancers from Tunisian patients.	topic_ccc
74487	4	354922	7	NULL	NULL	0	NULL	BRCA1	GP		is					breast cancer 1, early onset	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 In the current study, we aimed to assess by MSP, the methylation pattern of two cancer-related genes involved in DNA repair: hMLH1 (mutL homolog 1, colon cancer, nonpolyposis type 2 (E. coli) and BRCA1 (breast cancer 1, early onset) in 78 primary breast cancers from Tunisian patients.	topic_ccc
74500	1	354924	7	NULL	NULL	0	NULL	aspirin chemoprevention	Chemical		prevent		maybe;;effective 			colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Studies have indicated that aspirin chemoprevention may be effective in preventing colorectal cancer within the general population, and aspirin, celecoxib, and calcium may be effective in preventing adenomas within those people who have previously undergone polypectomy.	topic_ccc
74501	2	354924	7	NULL	NULL	NULL	NULL	aspirin	Chemical		prevent		may be;;effective			adenomas	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Studies have indicated that aspirin chemoprevention may be effective in preventing colorectal cancer within the general population, and aspirin, celecoxib, and calcium may be effective in preventing adenomas within those people who have previously undergone polypectomy.	topic_ccc
74502	3	354924	7	NULL	NULL	0	NULL	celecoxib	Chemical		prevent		maybe;;effective			adenomas	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Studies have indicated that aspirin chemoprevention may be effective in preventing colorectal cancer within the general population, and aspirin, celecoxib, and calcium may be effective in preventing adenomas within those people who have previously undergone polypectomy.	topic_ccc
74503	4	354924	7	NULL	NULL	0	NULL	calcium	Chemical		prevent		maybe;;effective			adenomas	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Studies have indicated that aspirin chemoprevention may be effective in preventing colorectal cancer within the general population, and aspirin, celecoxib, and calcium may be effective in preventing adenomas within those people who have previously undergone polypectomy.	topic_ccc
74504	5	354924	7	NULL	NULL	0	NULL	statement 2	Process		occur in					polypectomy people	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Studies have indicated that aspirin chemoprevention may be effective in preventing colorectal cancer within the general population, and aspirin, celecoxib, and calcium may be effective in preventing adenomas within those people who have previously undergone polypectomy.	topic_ccc
74505	6	354924	7	NULL	NULL	0	NULL	statement 3	Process		occur in					polypectomy people	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Studies have indicated that aspirin chemoprevention may be effective in preventing colorectal cancer within the general population, and aspirin, celecoxib, and calcium may be effective in preventing adenomas within those people who have previously undergone polypectomy.	topic_ccc
74506	7	354924	7	NULL	NULL	0	NULL	statement 4	Process		occur in					polypectomy people	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Studies have indicated that aspirin chemoprevention may be effective in preventing colorectal cancer within the general population, and aspirin, celecoxib, and calcium may be effective in preventing adenomas within those people who have previously undergone polypectomy.	topic_ccc
74507	8	354924	7	NULL	NULL	0	NULL	statement 1	Process		occur in					general population	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Studies have indicated that aspirin chemoprevention may be effective in preventing colorectal cancer within the general population, and aspirin, celecoxib, and calcium may be effective in preventing adenomas within those people who have previously undergone polypectomy.	topic_ccc
74549	1	354925	7	NULL	NULL	0	NULL	folate	Chemical	low level of	associated with		may be			CIMP-low/0 colon tumors	MedicalFinding	increased risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	This molecular pathological epidemiology study suggests that low level intake of folate may be associated with an increased risk of CIMP-low/0 colon tumors, but not that of CIMP-high tumors. 	topic_ccc
74550	2	354925	7	NULL	NULL	0	NULL	folate	Chemical	low level of	is not associated with					CIMP-high tumors	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	This molecular pathological epidemiology study suggests that low level intake of folate may be associated with an increased risk of CIMP-low/0 colon tumors, but not that of CIMP-high tumors. 	topic_ccc
74551	1	354926	7	NULL	NULL	0	NULL	 alcohol	Chemical	frequent consumption of	is associated with					distal colon cancer	MedicalFinding	elevated risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Frequent alcohol consumption and consuming high amounts of alcohol were associated with elevated risk for distal colon cancer in men and higher risk for rectal cancer in women.	topic_ccc
74552	2	354926	7	NULL	NULL	0	NULL	alcohol	Chemical	consuming high amounts of	is associated with					distal colon cancer	MedicalFinding	elevated risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Frequent alcohol consumption and consuming high amounts of alcohol were associated with elevated risk for distal colon cancer in men and higher risk for rectal cancer in women.	topic_ccc
74553	3	354926	7	NULL	NULL	0	NULL	statement 1	Process		occur in					men	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Frequent alcohol consumption and consuming high amounts of alcohol were associated with elevated risk for distal colon cancer in men and higher risk for rectal cancer in women.	topic_ccc
74554	4	354926	7	NULL	NULL	0	NULL	statement 2	Process		occur in 					men	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Frequent alcohol consumption and consuming high amounts of alcohol were associated with elevated risk for distal colon cancer in men and higher risk for rectal cancer in women.	topic_ccc
74555	5	354926	7	NULL	NULL	0	NULL	alcohol	Chemical	frequent consumption of	is associated with					rectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Frequent alcohol consumption and consuming high amounts of alcohol were associated with elevated risk for distal colon cancer in men and higher risk for rectal cancer in women.	topic_ccc
74556	6	354926	7	NULL	NULL	0	NULL	alcohol	Chemical	consuming high amounts of	is associated with					rectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Frequent alcohol consumption and consuming high amounts of alcohol were associated with elevated risk for distal colon cancer in men and higher risk for rectal cancer in women.	topic_ccc
74557	7	354926	7	NULL	NULL	0	NULL	statement 5	Process		occur in					women	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Frequent alcohol consumption and consuming high amounts of alcohol were associated with elevated risk for distal colon cancer in men and higher risk for rectal cancer in women.	topic_ccc
74558	8	354926	7	NULL	NULL	0	NULL	statement 6	Process		occur in					women	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Frequent alcohol consumption and consuming high amounts of alcohol were associated with elevated risk for distal colon cancer in men and higher risk for rectal cancer in women.	topic_ccc
74569	1	354927	7	NULL	NULL	NULL	NULL	MTHFR 677C/T genotype	Chromosome	distribution of	present in					cancer group	GroupOfPeople				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Distributions of MTHFR 677C/T genotype and allele frequencies in the individuals with and without metabolic syndrome in the cancer group showed no differences.	topic_ccc
74570	2	354927	7	NULL	NULL	NULL	NULL	statement 1	Process		occur with					metabolic syndrome	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Distributions of MTHFR 677C/T genotype and allele frequencies in the individuals with and without metabolic syndrome in the cancer group showed no differences.	topic_ccc
74571	3	354927	7	NULL	NULL	0	NULL	statement 1	Process		occur without					metabolic syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Distributions of MTHFR 677C/T genotype and allele frequencies in the individuals with and without metabolic syndrome in the cancer group showed no differences.	topic_ccc
74572	4	354927	7	NULL	NULL	NULL	NULL	MTHFR 677C/T genotype	Chromosome	distribution of;;allele frequencies of	present in					cancer group	GroupOfPeople				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Distributions of MTHFR 677C/T genotype and allele frequencies in the individuals with and without metabolic syndrome in the cancer group showed no differences.	topic_ccc
74573	5	354927	7	NULL	NULL	0	NULL	statement 4	Process		occur with					metabolic syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Distributions of MTHFR 677C/T genotype and allele frequencies in the individuals with and without metabolic syndrome in the cancer group showed no differences.	topic_ccc
74574	6	354927	7	NULL	NULL	0	NULL	statement 4	Process		occur without					metabolic syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Distributions of MTHFR 677C/T genotype and allele frequencies in the individuals with and without metabolic syndrome in the cancer group showed no differences.	topic_ccc
74575	7	354927	7	NULL	NULL	0	NULL	statement 2	Process		does not differ from					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Distributions of MTHFR 677C/T genotype and allele frequencies in the individuals with and without metabolic syndrome in the cancer group showed no differences.	topic_ccc
74576	8	354927	7	NULL	NULL	0	NULL	statement 5	Process		does not differ from					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Distributions of MTHFR 677C/T genotype and allele frequencies in the individuals with and without metabolic syndrome in the cancer group showed no differences.	topic_ccc
74577	1	354928	7	NULL	NULL	0	NULL	IGF	GP		is required for					carcinogenicity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Insulin-like growth factor (IGF)-I receptor (IGF-IR) signaling is required for carcinogenicity and proliferation of gastrointestinal cancers. 	topic_ccc
74578	2	354928	7	NULL	NULL	0	NULL	statement 1	Process		required for					gastrointestinal cancers	MedicalFinding	proliferation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Insulin-like growth factor (IGF)-I receptor (IGF-IR) signaling is required for carcinogenicity and proliferation of gastrointestinal cancers. 	topic_ccc
74579	3	354928	7	NULL	NULL	0	NULL	IGF-IR	GP		is required for					carcinogenicity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Insulin-like growth factor (IGF)-I receptor (IGF-IR) signaling is required for carcinogenicity and proliferation of gastrointestinal cancers. 	topic_ccc
74580	4	354928	7	NULL	NULL	0	NULL	statement 3	Process		required for					gastrointestinal cancers	MedicalFinding	proliferation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Insulin-like growth factor (IGF)-I receptor (IGF-IR) signaling is required for carcinogenicity and proliferation of gastrointestinal cancers. 	topic_ccc
74582	5	354928	7	NULL	NULL	0	NULL	IGF	GP		is					Insulin-like growth factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Insulin-like growth factor (IGF)-I receptor (IGF-IR) signaling is required for carcinogenicity and proliferation of gastrointestinal cancers. 	topic_ccc
74583	6	354928	7	NULL	NULL	0	NULL	IGF-IR	GP		is					IGF-I receptor 	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Insulin-like growth factor (IGF)-I receptor (IGF-IR) signaling is required for carcinogenicity and proliferation of gastrointestinal cancers. 	topic_ccc
74585	1	354929	7	NULL	NULL	0	NULL	Vitamin D	Chemical	intake of	inversely associated with					colorectal cancer	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Vitamin D intake and blood 25(OH)D levels were inversely associated with the risk of colorectal cancer in this meta-analysis.	topic_ccc
74586	2	354929	7	NULL	NULL	0	NULL	25(OH)D	Chemical		inversely associated with					colorectal cancer	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Vitamin D intake and blood 25(OH)D levels were inversely associated with the risk of colorectal cancer in this meta-analysis.	topic_ccc
74587	1	354930	7	NULL	NULL	0	NULL	calcium	Chemical		protective against					 colorectal neoplasia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion, a high calcium intake and the use of calcium supplements may be protective against colorectal neoplasia, although a greater sample may be required to observe significant associations in a multivariate model.	topic_ccc
74588	2	354930	7	NULL	NULL	0	NULL	calcium supplement	Chemical		protective against					colorectal neoplasia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion, a high calcium intake and the use of calcium supplements may be protective against colorectal neoplasia, although a greater sample may be required to observe significant associations in a multivariate model.	topic_ccc
74590	1	354931	7	NULL	NULL	0	NULL	combination chemotherapy	MedicalProcedure		applied in					mCRC	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Several randomized trials have indicated that combination chemotherapy applied in metastatic colorectal cancer (mCRC) does not significantly improve overall survival when compared to the sequential use of cytotoxic agents (CAIRO, MRC Focus, FFCD 2000-05).	topic_ccc
74591	2	354931	7	NULL	NULL	0	NULL	statement 1	Process		does not improve		significantly			survival	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Several randomized trials have indicated that combination chemotherapy applied in metastatic colorectal cancer (mCRC) does not significantly improve overall survival when compared to the sequential use of cytotoxic agents (CAIRO, MRC Focus, FFCD 2000-05).	topic_ccc
74592	3	354931	7	NULL	NULL	0	NULL	mCRC	MedicalFinding		is					metastatic colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Several randomized trials have indicated that combination chemotherapy applied in metastatic colorectal cancer (mCRC) does not significantly improve overall survival when compared to the sequential use of cytotoxic agents (CAIRO, MRC Focus, FFCD 2000-05).	topic_ccc
74597	1	354933	7	NULL	NULL	0	NULL	RUNX3	GP	methylation of	occur in				promoter	colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	RUNX3 promoter methylation in colorectal cancer: its relationship with microsatellite instability and its suitability as a novel serum tumor marker.	topic_ccc
74598	2	354933	7	NULL	NULL	NULL	NULL	RUNX3	GP	methylation of	is in relation with				promoter	microsatellite instability	Chromosome				NULL		NULL	NULL	NULL	NULL	NULL	NULL	RUNX3 promoter methylation in colorectal cancer: its relationship with microsatellite instability and its suitability as a novel serum tumor marker.	topic_ccc
74599	3	354933	7	NULL	NULL	0	NULL	RUNX3	GP	methylation of	acts as a				promoter	novel serum tumor marker	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	RUNX3 promoter methylation in colorectal cancer: its relationship with microsatellite instability and its suitability as a novel serum tumor marker.	topic_ccc
74600	1	354934	7	NULL	NULL	0	NULL	Epigenetic Gene	GP	methylation of	is associated with				promoter	Child's Later Adiposity	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	 Epigenetic Gene Promoter Methylation at Birth Is Associated With Child's Later Adiposity.	topic_ccc
74601	1	354935	7	NULL	NULL	0	NULL	adenosine A2A receptor	GP	genetic inactivation of	attenuates					pathologic angiogenesis	Process				NULL	mouse retina	0	NULL	NULL	NULL	NULL	NULL	Genetic inactivation of the adenosine A2A receptor attenuates pathologic but not developmental angiogenesis in the mouse retina.	topic_ccc
74602	2	354935	7	NULL	NULL	0	NULL	adenosine A2A receptor	GP	genetic inactivation of	does not attenuate					developmental angiogenesis	Process				NULL	mouse retina	0	NULL	NULL	NULL	NULL	NULL	Genetic inactivation of the adenosine A2A receptor attenuates pathologic but not developmental angiogenesis in the mouse retina.	topic_ccc
74603	1	354936	7	NULL	NULL	NULL	NULL	 MTHFR C677T 	Chemical	Functional polymorphisms of	affect					toxicity	Process	outcome of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Functional polymorphisms of MTHFR C677T and MTR A2756G can affect outcome and risk of toxicity during adjuvant chemotherapy in stage III colorectal cancer.	topic_ccc
74604	2	354936	7	NULL	NULL	0	NULL	MTR A2756G	Chemical	Functional polymorphisms of	affect					toxicity	Process	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Functional polymorphisms of MTHFR C677T and MTR A2756G can affect outcome and risk of toxicity during adjuvant chemotherapy in stage III colorectal cancer.	topic_ccc
74605	3	354936	7	NULL	NULL	0	NULL	statement 1	Process		occur during					stage III colorectal cancer	MedicalFinding	adjuvant chemotherapy in			NULL		0	NULL	NULL	NULL	NULL	NULL	Functional polymorphisms of MTHFR C677T and MTR A2756G can affect outcome and risk of toxicity during adjuvant chemotherapy in stage III colorectal cancer.	topic_ccc
74606	4	354936	7	NULL	NULL	0	NULL	statement 2	Process		occur during					stage III colorectal cancer	MedicalFinding	adjuvant chemotherapy in			NULL		0	NULL	NULL	NULL	NULL	NULL	Functional polymorphisms of MTHFR C677T and MTR A2756G can affect outcome and risk of toxicity during adjuvant chemotherapy in stage III colorectal cancer.	topic_ccc
74721	1	354937	7	NULL	NULL	0	NULL	MDR1 gene	GP		transcriptional target of 		direct			CDX2	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Evidence that the MDR1 gene was a direct transcriptional target of CDX2 was obtained, including analyses with MDR1 reporter gene constructs and chromatin immunoprecipitation assays.	topic_ccc
74722	1	354938	7	NULL	NULL	0	NULL	Bcl-2	GP		hypomethlated in				promoter	colorectal cancer tissue	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Bcl-2 promoter is hypomethylated in colorectal cancer tissue, and there is a significant correlation between MTHFR 677 TT or CT/TT genotypes and CRC or Bcl-2 promoter CGI methylation/oncoprotein expression in CRC.	topic_ccc
74723	2	354938	7	NULL	NULL	NULL	NULL	MTHFR 677 TT genotype	PhysicalPhenomenon		correlates with		significantly			CRC 	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Bcl-2 promoter is hypomethylated in colorectal cancer tissue, and there is a significant correlation between MTHFR 677 TT or CT/TT genotypes and CRC or Bcl-2 promoter CGI methylation/oncoprotein expression in CRC.	topic_ccc
74724	3	354938	7	NULL	NULL	NULL	NULL	CT/TT genotype	PhysicalPhenomenon		correlates with		significantly			CRC	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Bcl-2 promoter is hypomethylated in colorectal cancer tissue, and there is a significant correlation between MTHFR 677 TT or CT/TT genotypes and CRC or Bcl-2 promoter CGI methylation/oncoprotein expression in CRC.	topic_ccc
74725	4	354938	7	NULL	NULL	NULL	NULL	MTHFR 677 TT genotype	PhysicalPhenomenon		correlates with		significantly			Bcl-2	GP			promoter CGI methylation	NULL		NULL	NULL	NULL	NULL	NULL	NULL	Bcl-2 promoter is hypomethylated in colorectal cancer tissue, and there is a significant correlation between MTHFR 677 TT or CT/TT genotypes and CRC or Bcl-2 promoter CGI methylation/oncoprotein expression in CRC.	topic_ccc
74726	5	354938	7	NULL	NULL	NULL	NULL	CT/TT genotype	PhysicalPhenomenon		correlates with		significantly			Bcl2	GP			promoter CGI methylation	NULL		NULL	NULL	NULL	NULL	NULL	NULL	Bcl-2 promoter is hypomethylated in colorectal cancer tissue, and there is a significant correlation between MTHFR 677 TT or CT/TT genotypes and CRC or Bcl-2 promoter CGI methylation/oncoprotein expression in CRC.	topic_ccc
74727	6	354938	7	NULL	NULL	0	NULL	statement 4	Process		occur in					CRC	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bcl-2 promoter is hypomethylated in colorectal cancer tissue, and there is a significant correlation between MTHFR 677 TT or CT/TT genotypes and CRC or Bcl-2 promoter CGI methylation/oncoprotein expression in CRC.	topic_ccc
74728	7	354938	7	NULL	NULL	0	NULL	statement 5	Process		occur in					CRC	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bcl-2 promoter is hypomethylated in colorectal cancer tissue, and there is a significant correlation between MTHFR 677 TT or CT/TT genotypes and CRC or Bcl-2 promoter CGI methylation/oncoprotein expression in CRC.	topic_ccc
74729	8	354938	7	NULL	NULL	0	NULL	MTHFR 677 TT genotype	PhysicalPhenomenon		correlates with		significantly			Bcl-2	GP	oncoprotein expression		promoter 	NULL		0	NULL	NULL	NULL	NULL	NULL	Bcl-2 promoter is hypomethylated in colorectal cancer tissue, and there is a significant correlation between MTHFR 677 TT or CT/TT genotypes and CRC or Bcl-2 promoter CGI methylation/oncoprotein expression in CRC.	topic_ccc
74730	9	354938	7	NULL	NULL	0	NULL	CT/TT genotype	PhysicalPhenomenon		correlates with		significantly			Bcl-2	GP	oncoprotein expression		promoter	NULL		0	NULL	NULL	NULL	NULL	NULL	Bcl-2 promoter is hypomethylated in colorectal cancer tissue, and there is a significant correlation between MTHFR 677 TT or CT/TT genotypes and CRC or Bcl-2 promoter CGI methylation/oncoprotein expression in CRC.	topic_ccc
74731	10	354938	7	NULL	NULL	0	NULL	statement 8	Process		occur in					CRC	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bcl-2 promoter is hypomethylated in colorectal cancer tissue, and there is a significant correlation between MTHFR 677 TT or CT/TT genotypes and CRC or Bcl-2 promoter CGI methylation/oncoprotein expression in CRC.	topic_ccc
74732	11	354938	7	NULL	NULL	0	NULL	statement 9	Process		occur in					CRC 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bcl-2 promoter is hypomethylated in colorectal cancer tissue, and there is a significant correlation between MTHFR 677 TT or CT/TT genotypes and CRC or Bcl-2 promoter CGI methylation/oncoprotein expression in CRC.	topic_ccc
74733	1	354939	7	NULL	NULL	0	NULL	Fluoropyrimidine-based combination chemotherapy	MedicalProcedure		has efficacy in					ACC	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Fluoropyrimidine-based combination chemotherapy, in combination with either oxaliplatin or irinotecan, has demonstrated efficacy and tolerability in treatment of advanced colorectal cancer (ACC).	topic_ccc
74734	2	354939	7	NULL	NULL	NULL	NULL	Fluoropyrimidine-based combination chemotherapy	MedicalProcedure		has  tolerability in					ACC	MedicalFinding	treatment of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Fluoropyrimidine-based combination chemotherapy, in combination with either oxaliplatin or irinotecan, has demonstrated efficacy and tolerability in treatment of advanced colorectal cancer (ACC).	topic_ccc
74735	3	354939	7	NULL	NULL	0	NULL	ACC	MedicalFinding		is					advanced colorectal cancer 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Fluoropyrimidine-based combination chemotherapy, in combination with either oxaliplatin or irinotecan, has demonstrated efficacy and tolerability in treatment of advanced colorectal cancer (ACC).	topic_ccc
74736	4	354939	7	NULL	NULL	0	NULL	statement 1	Process		in combination with					oxaliplatin 	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Fluoropyrimidine-based combination chemotherapy, in combination with either oxaliplatin or irinotecan, has demonstrated efficacy and tolerability in treatment of advanced colorectal cancer (ACC).	topic_ccc
74737	5	354939	7	NULL	NULL	NULL	NULL	statement 1	Process		in combination with					irinotecan	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Fluoropyrimidine-based combination chemotherapy, in combination with either oxaliplatin or irinotecan, has demonstrated efficacy and tolerability in treatment of advanced colorectal cancer (ACC).	topic_ccc
74738	6	354939	7	NULL	NULL	0	NULL	statement 2	Process		in combination with					oxaliplatin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Fluoropyrimidine-based combination chemotherapy, in combination with either oxaliplatin or irinotecan, has demonstrated efficacy and tolerability in treatment of advanced colorectal cancer (ACC).	topic_ccc
74739	7	354939	7	NULL	NULL	0	NULL	statement 2	Process		in combination with					 irinotecan	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Fluoropyrimidine-based combination chemotherapy, in combination with either oxaliplatin or irinotecan, has demonstrated efficacy and tolerability in treatment of advanced colorectal cancer (ACC).	topic_ccc
74740	1	354940	7	NULL	NULL	NULL	NULL	APC	GP	epigenetic gene silencing of	play a role in					CRC	MedicalFinding	development of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	We examined the paired tumour and normal-tissue specimens of 86 CRC patients for the occurrence of aberrations in the mutation cluster region (MCR) of the APC gene and exon 3 of the β-catenin gene by polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) and/or PCR-direct sequencing. Although the number of mutations in the APC and β-catenin genes in our CRC cases was very low, the study confirms the role of epigenetic gene silencing of the pivotal molecular gladiator, APC, of the Wnt pathway in the development of CRC in the Kashmiri population.	topic_ccc
74741	2	354940	7	NULL	NULL	0	NULL	APC	GP		is a type of					pivotal molecular gladiator	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	We examined the paired tumour and normal-tissue specimens of 86 CRC patients for the occurrence of aberrations in the mutation cluster region (MCR) of the APC gene and exon 3 of the β-catenin gene by polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) and/or PCR-direct sequencing. Although the number of mutations in the APC and β-catenin genes in our CRC cases was very low, the study confirms the role of epigenetic gene silencing of the pivotal molecular gladiator, APC, of the Wnt pathway in the development of CRC in the Kashmiri population.	topic_ccc
74742	3	354940	7	NULL	NULL	0	NULL	APC	GP		belongs to					Wnt pathway	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	We examined the paired tumour and normal-tissue specimens of 86 CRC patients for the occurrence of aberrations in the mutation cluster region (MCR) of the APC gene and exon 3 of the β-catenin gene by polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) and/or PCR-direct sequencing. Although the number of mutations in the APC and β-catenin genes in our CRC cases was very low, the study confirms the role of epigenetic gene silencing of the pivotal molecular gladiator, APC, of the Wnt pathway in the development of CRC in the Kashmiri population.	topic_ccc
74743	4	354940	7	NULL	NULL	0	NULL	statement 1	Process		occur in					Kashmiri population	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	We examined the paired tumour and normal-tissue specimens of 86 CRC patients for the occurrence of aberrations in the mutation cluster region (MCR) of the APC gene and exon 3 of the β-catenin gene by polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) and/or PCR-direct sequencing. Although the number of mutations in the APC and β-catenin genes in our CRC cases was very low, the study confirms the role of epigenetic gene silencing of the pivotal molecular gladiator, APC, of the Wnt pathway in the development of CRC in the Kashmiri population.	topic_ccc
74744	1	354941	7	NULL	NULL	0	NULL	COX-1	GP		expressed in		constitutively 			normal tissue	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	COX-1 is constitutively expressed in normal tissue, serving an important role in tissue homeostasis, whereas COX-2 is an inducible enzyme, which is markedly overexpressed at sites of inflammation and colorectal neoplasms\t	topic_ccc
74745	2	354941	7	NULL	NULL	0	NULL	statement 1	Process		important role in					tissue homeostasis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	COX-1 is constitutively expressed in normal tissue, serving an important role in tissue homeostasis, whereas COX-2 is an inducible enzyme, which is markedly overexpressed at sites of inflammation and colorectal neoplasms\t	topic_ccc
74746	3	354941	7	NULL	NULL	0	NULL	 COX-2 	GP		is a type of					inducible enzyme	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	COX-1 is constitutively expressed in normal tissue, serving an important role in tissue homeostasis, whereas COX-2 is an inducible enzyme, which is markedly overexpressed at sites of inflammation and colorectal neoplasms\t	topic_ccc
74747	4	354941	7	NULL	NULL	0	NULL	COX-2	GP		overexpressed at		markedly			sites of inflammation	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	COX-1 is constitutively expressed in normal tissue, serving an important role in tissue homeostasis, whereas COX-2 is an inducible enzyme, which is markedly overexpressed at sites of inflammation and colorectal neoplasms\t	topic_ccc
74748	5	354941	7	NULL	NULL	0	NULL	COX-2	GP		overexpressed at		markedly			colorectal neoplasms	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	COX-1 is constitutively expressed in normal tissue, serving an important role in tissue homeostasis, whereas COX-2 is an inducible enzyme, which is markedly overexpressed at sites of inflammation and colorectal neoplasms\t	topic_ccc
74749	1	354942	7	NULL	NULL	0	NULL	sulindac 	Chemical		exert their		may			anti-neoplastic role	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	It may be stated that sulindac and celecoxib, the two NSAIDs may exert their anti-neoplastic role in colorectal cancer via modifying the physicochemical properties of the membranes. http://www.ncbi.nlm.nih.gov/pubmed/21725642	topic_ccc
74750	2	354942	7	NULL	NULL	0	NULL	celecoxib	Chemical		exert their		may			anti-neoplastic role	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	It may be stated that sulindac and celecoxib, the two NSAIDs may exert their anti-neoplastic role in colorectal cancer via modifying the physicochemical properties of the membranes. http://www.ncbi.nlm.nih.gov/pubmed/21725642	topic_ccc
74751	3	354942	7	NULL	NULL	0	NULL	statement 1	Process		occur in					colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	It may be stated that sulindac and celecoxib, the two NSAIDs may exert their anti-neoplastic role in colorectal cancer via modifying the physicochemical properties of the membranes. http://www.ncbi.nlm.nih.gov/pubmed/21725642	topic_ccc
74752	4	354942	7	NULL	NULL	0	NULL	statement 2	Process		occur in					colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	It may be stated that sulindac and celecoxib, the two NSAIDs may exert their anti-neoplastic role in colorectal cancer via modifying the physicochemical properties of the membranes. http://www.ncbi.nlm.nih.gov/pubmed/21725642	topic_ccc
74753	5	354942	7	NULL	NULL	0	NULL	statement 1	Process		occur via					membrane	CellComponent	modifying the physicochemical properties of			NULL		0	NULL	NULL	NULL	NULL	NULL	It may be stated that sulindac and celecoxib, the two NSAIDs may exert their anti-neoplastic role in colorectal cancer via modifying the physicochemical properties of the membranes. http://www.ncbi.nlm.nih.gov/pubmed/21725642	topic_ccc
74754	6	354942	7	NULL	NULL	0	NULL	statement 2	Process		occur via					membrane	CellComponent	modifying the physicochemical properties of 			NULL		0	NULL	NULL	NULL	NULL	NULL	It may be stated that sulindac and celecoxib, the two NSAIDs may exert their anti-neoplastic role in colorectal cancer via modifying the physicochemical properties of the membranes. http://www.ncbi.nlm.nih.gov/pubmed/21725642	topic_ccc
74755	7	354942	7	NULL	NULL	0	NULL	sulindac	Chemical		is a type of					NSAID	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	It may be stated that sulindac and celecoxib, the two NSAIDs may exert their anti-neoplastic role in colorectal cancer via modifying the physicochemical properties of the membranes. http://www.ncbi.nlm.nih.gov/pubmed/21725642	topic_ccc
74756	8	354942	7	NULL	NULL	0	NULL	celecoxib	Chemical		is a type of					NSAID	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	It may be stated that sulindac and celecoxib, the two NSAIDs may exert their anti-neoplastic role in colorectal cancer via modifying the physicochemical properties of the membranes. http://www.ncbi.nlm.nih.gov/pubmed/21725642	topic_ccc
74757	1	354943	7	NULL	NULL	0	NULL	Energy consumption	Process		influence					colorectal cancer	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Energy consumption also influences colorectal cancer risk, with obesity increasing risk and exercise reducing risk. 	topic_ccc
74758	2	354943	7	NULL	NULL	0	NULL	Energy consumption	Process		influence					obesity	MedicalFinding	increasing risk of 			NULL		0	NULL	NULL	NULL	NULL	NULL	Energy consumption also influences colorectal cancer risk, with obesity increasing risk and exercise reducing risk. 	topic_ccc
74759	3	354943	7	NULL	NULL	0	NULL	Energy consumption	Process		influence					exercise	Process	reducing risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Energy consumption also influences colorectal cancer risk, with obesity increasing risk and exercise reducing risk. 	topic_ccc
74760	1	354944	7	NULL	NULL	0	NULL	S100A4 	GP		target gene of					Wnt/β-catenin pathway	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	S100A4 is a target gene of the Wnt/β-catenin pathway, which is constitutively active in the majority of colon cancers.	topic_ccc
74761	2	354944	7	NULL	NULL	0	NULL	statement 1	Process		active in		constitutively 			colon cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	S100A4 is a target gene of the Wnt/β-catenin pathway, which is constitutively active in the majority of colon cancers.	topic_ccc
74762	1	354945	7	NULL	NULL	0	NULL	Obesity	MedicalFinding		influence					colorectal cancer	MedicalFinding	risk of developing			NULL		0	NULL	NULL	NULL	NULL	NULL	Obesity, consumption of red meat, a Western pattern diet, alcohol, and smoking influence one's risk of developing colorectal cancer while physical activity, vitamin D, postmenopausal estrogen use, aspirin, and nonsteroidal anti-inflammatory drugs (NSAIDs) decrease one's risk. 	topic_ccc
74763	2	354945	7	NULL	NULL	0	NULL	red meat	Food		influence					colorectal cancer	MedicalFinding	risk of developing			NULL		0	NULL	NULL	NULL	NULL	NULL	Obesity, consumption of red meat, a Western pattern diet, alcohol, and smoking influence one's risk of developing colorectal cancer while physical activity, vitamin D, postmenopausal estrogen use, aspirin, and nonsteroidal anti-inflammatory drugs (NSAIDs) decrease one's risk. 	topic_ccc
74764	3	354945	7	NULL	NULL	0	NULL	Western pattern diet	Food		influence					colorectal cancer	MedicalFinding	risk of developing			NULL		0	NULL	NULL	NULL	NULL	NULL	Obesity, consumption of red meat, a Western pattern diet, alcohol, and smoking influence one's risk of developing colorectal cancer while physical activity, vitamin D, postmenopausal estrogen use, aspirin, and nonsteroidal anti-inflammatory drugs (NSAIDs) decrease one's risk. 	topic_ccc
74765	4	354945	7	NULL	NULL	0	NULL	alcohol	Chemical		influence					colorectal cancer	MedicalFinding	risk of developing			NULL		0	NULL	NULL	NULL	NULL	NULL	Obesity, consumption of red meat, a Western pattern diet, alcohol, and smoking influence one's risk of developing colorectal cancer while physical activity, vitamin D, postmenopausal estrogen use, aspirin, and nonsteroidal anti-inflammatory drugs (NSAIDs) decrease one's risk. 	topic_ccc
74766	5	354945	7	NULL	NULL	0	NULL	smoking	Chemical		influence					colorectal cancer	MedicalFinding	risk of developing			NULL		0	NULL	NULL	NULL	NULL	NULL	Obesity, consumption of red meat, a Western pattern diet, alcohol, and smoking influence one's risk of developing colorectal cancer while physical activity, vitamin D, postmenopausal estrogen use, aspirin, and nonsteroidal anti-inflammatory drugs (NSAIDs) decrease one's risk. 	topic_ccc
74767	6	354945	7	NULL	NULL	0	NULL	physical activity	Process		decrease					colorectal cancer	MedicalFinding	risk of developing			NULL		0	NULL	NULL	NULL	NULL	NULL	Obesity, consumption of red meat, a Western pattern diet, alcohol, and smoking influence one's risk of developing colorectal cancer while physical activity, vitamin D, postmenopausal estrogen use, aspirin, and nonsteroidal anti-inflammatory drugs (NSAIDs) decrease one's risk. 	topic_ccc
74768	7	354945	7	NULL	NULL	0	NULL	Vitamin D	Chemical		decrease					colorectal cancer	MedicalFinding	risk of developing			NULL		0	NULL	NULL	NULL	NULL	NULL	Obesity, consumption of red meat, a Western pattern diet, alcohol, and smoking influence one's risk of developing colorectal cancer while physical activity, vitamin D, postmenopausal estrogen use, aspirin, and nonsteroidal anti-inflammatory drugs (NSAIDs) decrease one's risk. 	topic_ccc
74769	8	354945	7	NULL	NULL	0	NULL	postmenopausal estrogen use	Chemical		decrease					colorectal cancer	MedicalFinding	risk of developing			NULL		0	NULL	NULL	NULL	NULL	NULL	Obesity, consumption of red meat, a Western pattern diet, alcohol, and smoking influence one's risk of developing colorectal cancer while physical activity, vitamin D, postmenopausal estrogen use, aspirin, and nonsteroidal anti-inflammatory drugs (NSAIDs) decrease one's risk. 	topic_ccc
74770	9	354945	7	NULL	NULL	0	NULL	aspirin	Chemical		decrease					colorectal cancer	MedicalFinding	risk of developing			NULL		0	NULL	NULL	NULL	NULL	NULL	Obesity, consumption of red meat, a Western pattern diet, alcohol, and smoking influence one's risk of developing colorectal cancer while physical activity, vitamin D, postmenopausal estrogen use, aspirin, and nonsteroidal anti-inflammatory drugs (NSAIDs) decrease one's risk. 	topic_ccc
74771	10	354945	7	NULL	NULL	0	NULL	NSAIDs	Chemical		decrease					colorectal cancer	MedicalFinding	risk of developing			NULL		0	NULL	NULL	NULL	NULL	NULL	Obesity, consumption of red meat, a Western pattern diet, alcohol, and smoking influence one's risk of developing colorectal cancer while physical activity, vitamin D, postmenopausal estrogen use, aspirin, and nonsteroidal anti-inflammatory drugs (NSAIDs) decrease one's risk. 	topic_ccc
74772	11	354945	7	NULL	NULL	0	NULL	NSAIDs	Chemical		is					nonsteroidal anti-inflammatory drugs	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Obesity, consumption of red meat, a Western pattern diet, alcohol, and smoking influence one's risk of developing colorectal cancer while physical activity, vitamin D, postmenopausal estrogen use, aspirin, and nonsteroidal anti-inflammatory drugs (NSAIDs) decrease one's risk. 	topic_ccc
74773	1	354946	7	NULL	NULL	0	NULL	colorectal cancer patients 	GroupOfPeople		benefit from					bevacizumab therapy	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	vascular endothelial growth factor-A, thymidylate synthase, and tissue inhibitor of metalloproteinase 3 may enable selection of colorectal cancer patients who would benefit from bevacizumab therapy.	topic_ccc
74774	2	354946	7	NULL	NULL	0	NULL	vascular endothelial growth factor-A	GP		enable		may			statement 1	Process	selection of			NULL		0	NULL	NULL	NULL	NULL	NULL	vascular endothelial growth factor-A, thymidylate synthase, and tissue inhibitor of metalloproteinase 3 may enable selection of colorectal cancer patients who would benefit from bevacizumab therapy.	topic_ccc
74775	3	354946	7	NULL	NULL	0	NULL	thymidylate synthase	GP		enable		may			statement 1	Process	selection of			NULL		0	NULL	NULL	NULL	NULL	NULL	vascular endothelial growth factor-A, thymidylate synthase, and tissue inhibitor of metalloproteinase 3 may enable selection of colorectal cancer patients who would benefit from bevacizumab therapy.	topic_ccc
74776	4	354946	7	NULL	NULL	NULL	NULL	tissue inhibitor of metalloproteinase 3	GP		enable		may			statement 1	Process	selection of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	vascular endothelial growth factor-A, thymidylate synthase, and tissue inhibitor of metalloproteinase 3 may enable selection of colorectal cancer patients who would benefit from bevacizumab therapy.	topic_ccc
74777	1	354947	7	NULL	NULL	NULL	NULL	Microsatellite instability 	NucleicAcid		important factor 					patient survival	Process	associated with			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Microsatellite instability is an important factor associated with patient survival in Chinese sporadic colorectal cancer.	topic_ccc
74790	2	354947	7	NULL	NULL	0	NULL	statement 1	Process		occur in					Chinese sporadic colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Microsatellite instability is an important factor associated with patient survival in Chinese sporadic colorectal cancer.	topic_ccc
74793	1	354948	7	NULL	NULL	0	NULL	MGMT	GP	aberrant methylation of	correlates with					MGMT	GP	loss of expression of			NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis revealed abnormal hMLH1 (14, 12.5%), hMSH2 (11, 9.8%), and MGMT (53, 47.3%) expression with a significant correlation between aberrant MGMT methylation and a loss of MGMT expression.	topic_ccc
74794	2	354948	7	NULL	NULL	0	NULL	hMLH1	GP	abnormal expression of	correlates with		significantly			statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis revealed abnormal hMLH1 (14, 12.5%), hMSH2 (11, 9.8%), and MGMT (53, 47.3%) expression with a significant correlation between aberrant MGMT methylation and a loss of MGMT expression.	topic_ccc
74795	3	354948	7	NULL	NULL	NULL	NULL	hMSH2	GP	abnormal expression of	correlates with		significantly			statement 1	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis revealed abnormal hMLH1 (14, 12.5%), hMSH2 (11, 9.8%), and MGMT (53, 47.3%) expression with a significant correlation between aberrant MGMT methylation and a loss of MGMT expression.	topic_ccc
74796	4	354948	7	NULL	NULL	0	NULL	MGMT	GP	abnormal expression of	correlates with		significantly			statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis revealed abnormal hMLH1 (14, 12.5%), hMSH2 (11, 9.8%), and MGMT (53, 47.3%) expression with a significant correlation between aberrant MGMT methylation and a loss of MGMT expression.	topic_ccc
74797	1	354949	7	NULL	NULL	NULL	NULL	CIMP	PhysicalPhenomenon		characterized by					p16	GP	abnormal methylation of		multiple CpG islands	NULL		NULL	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. 	topic_ccc
74798	4	354949	7	NULL	NULL	NULL	NULL	statement 1	Process		occur in					colorectal cancer	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. 	topic_ccc
74799	2	354949	7	NULL	NULL	NULL	NULL	CIMP	PhysicalPhenomenon		characterized by					hMLH1	GP	abnormal methylation of		multiple CpG islands	NULL		NULL	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. 	topic_ccc
74800	3	354949	7	NULL	NULL	0	NULL	CIMP	PhysicalPhenomenon		characterized by					THBS1	GP	abnormal methylation of		multiple CpG islands	NULL		0	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. 	topic_ccc
74801	5	354949	7	NULL	NULL	0	NULL	statement 2	Process		occur in					colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. 	topic_ccc
74802	6	354949	7	NULL	NULL	0	NULL	statement 3	Process		occur in					colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. 	topic_ccc
74803	7	354949	7	NULL	NULL	0	NULL	CIMP	PhysicalPhenomenon		is					CpG island methylator phenotype	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. 	topic_ccc
74804	8	354949	7	NULL	NULL	0	NULL	p16	GP		is a type of					tumor suppressor gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. 	topic_ccc
74805	9	354949	7	NULL	NULL	0	NULL	hMLH1	GP		is a type of					tumor suppressor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. 	topic_ccc
74806	10	354949	7	NULL	NULL	0	NULL	THBS1	GP		is a type of					tumor suppressor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	CpG island methylator phenotype (CIMP) in colorectal cancers is characterized by abnormal methylation of multiple CpG islands including those in several tumor suppressor genes such as p16, hMLH1, and THBS1. 	topic_ccc
74807	1	354950	7	NULL	NULL	0	NULL	THBSI	GP		methylated in		frequently			adenomas	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	 THBSI was the most frequently methylated locus in both adenomas (n = 19, 47.5%) and carcinomas (n = 16, 44.4%).	topic_ccc
74808	1	354951	7	NULL	NULL	NULL	NULL	FAK activity	Process	induction of	occur					Wnt	GP	downstream of			NULL	mouse intestine	NULL	NULL	NULL	NULL	NULL	NULL	In contrast, in the mouse intestine, FAK activity was induced downstream of Wnt to promote intestinal regeneration and was also essential for tumorigenesis in an APC deletion model of colorectal cancer. Adding to this complexity, in human cell lines, FAK induced a context-dependent modulation of Wnt signaling to activate target-gene expression.	topic_ccc
74809	2	354951	7	NULL	NULL	NULL	NULL	statement 1	Process		promote					intestinal regeneration	Process				NULL	mouse intestine	NULL	NULL	NULL	NULL	NULL	NULL	In contrast, in the mouse intestine, FAK activity was induced downstream of Wnt to promote intestinal regeneration and was also essential for tumorigenesis in an APC deletion model of colorectal cancer. Adding to this complexity, in human cell lines, FAK induced a context-dependent modulation of Wnt signaling to activate target-gene expression.	topic_ccc
74810	3	354951	7	NULL	NULL	0	NULL	statement 1	Process		essential for					tumorigenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In contrast, in the mouse intestine, FAK activity was induced downstream of Wnt to promote intestinal regeneration and was also essential for tumorigenesis in an APC deletion model of colorectal cancer. Adding to this complexity, in human cell lines, FAK induced a context-dependent modulation of Wnt signaling to activate target-gene expression.	topic_ccc
74811	4	354951	7	NULL	NULL	0	NULL	statement 1	Process		occur in					colorectal cancer	MedicalFinding	APC deletion model of 			NULL		0	NULL	NULL	NULL	NULL	NULL	In contrast, in the mouse intestine, FAK activity was induced downstream of Wnt to promote intestinal regeneration and was also essential for tumorigenesis in an APC deletion model of colorectal cancer. Adding to this complexity, in human cell lines, FAK induced a context-dependent modulation of Wnt signaling to activate target-gene expression.	topic_ccc
74812	5	354951	7	NULL	NULL	0	NULL	FAK	GP		induce					Wnt signaling	Process	context-dependent modulation of			NULL	human cell lines	0	NULL	NULL	NULL	NULL	NULL	In contrast, in the mouse intestine, FAK activity was induced downstream of Wnt to promote intestinal regeneration and was also essential for tumorigenesis in an APC deletion model of colorectal cancer. Adding to this complexity, in human cell lines, FAK induced a context-dependent modulation of Wnt signaling to activate target-gene expression.	topic_ccc
74813	6	354951	7	NULL	NULL	0	NULL	statement 5	Process		activate					target-gene 	GP	expression of			NULL		0	NULL	NULL	NULL	NULL	NULL	In contrast, in the mouse intestine, FAK activity was induced downstream of Wnt to promote intestinal regeneration and was also essential for tumorigenesis in an APC deletion model of colorectal cancer. Adding to this complexity, in human cell lines, FAK induced a context-dependent modulation of Wnt signaling to activate target-gene expression.	topic_ccc
74814	1	354952	7	NULL	NULL	0	NULL	PGE2	GP		activate					p38MAPK	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 In addition, PGE2 is able to activate p38 MAPK and the inhibition of p38 MAPK	topic_ccc
74815	1	354953	7	NULL	NULL	0	NULL	17beta-estradiol	Chemical		inhibit					PGE2	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	However, it is unknown if 17beta-estradiol treatment is sufficient to inhibit prostaglandin E2 (PGE2)	topic_ccc
74816	2	354953	7	NULL	NULL	0	NULL	PGE2	Chemical		is					prostaglandin E2	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	However, it is unknown if 17beta-estradiol treatment is sufficient to inhibit prostaglandin E2 (PGE2)	topic_ccc
74817	1	354954	7	NULL	NULL	0	NULL	MapK	GP	activation of	occur in					large intestinal adenomas	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The large intestinal adenomas showed immunohistochemical evidence of activation of MapK	topic_ccc
74818	1	354955	7	NULL	NULL	0	NULL	 SDF-1	GP		induce					uPA	GP	expression of			NULL		0	NULL	NULL	NULL	NULL	NULL	xperiments involving specific inhibitors and small interfering RNA demonstrated that the activation of p38 mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K)/Akt pathways are critical for SDF-1-induced uPA expression.	topic_ccc
74819	2	354955	7	NULL	NULL	0	NULL	p38 mitogen-activated protein kinase	GP	activation of	critical for					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	xperiments involving specific inhibitors and small interfering RNA demonstrated that the activation of p38 mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K)/Akt pathways are critical for SDF-1-induced uPA expression.	topic_ccc
74825	3	354955	7	NULL	NULL	0	NULL	PI3K/Akt pathways	Process	activation of	critical for					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	xperiments involving specific inhibitors and small interfering RNA demonstrated that the activation of p38 mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K)/Akt pathways are critical for SDF-1-induced uPA expression.	topic_ccc
74826	4	354955	7	NULL	NULL	0	NULL	MAPK	GP		is					mitogen-activated protein kinase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	xperiments involving specific inhibitors and small interfering RNA demonstrated that the activation of p38 mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K)/Akt pathways are critical for SDF-1-induced uPA expression.	topic_ccc
74827	5	354955	7	NULL	NULL	0	NULL	PI3K	GP		is					phosphatidylinositol 3-kinase 	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	xperiments involving specific inhibitors and small interfering RNA demonstrated that the activation of p38 mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K)/Akt pathways are critical for SDF-1-induced uPA expression.	topic_ccc
74828	1	354956	7	NULL	NULL	0	NULL	DNA mismatch repair	Process		execute					5-fluorouracil	Chemical	cytotoxicity of			NULL	colorectal cancer cells	0	NULL	NULL	NULL	NULL	NULL	DNA mismatch repair proficiency executing 5-fluorouracil cytotoxicity in colorectal cancer cells.	topic_ccc
74829	1	354957	7	NULL	NULL	0	NULL	COX2 inhibitors	Chemical		widely used as					analgesics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Selective cyclooxygenase-2 (COX2) inhibitors are widely used as analgesics and it is unclear whether its long-term use affects cancer risk	topic_ccc
74830	2	354957	7	NULL	NULL	0	NULL	COX2	GP		is					cyclooxygenase-2	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Selective cyclooxygenase-2 (COX2) inhibitors are widely used as analgesics and it is unclear whether its long-term use affects cancer risk	topic_ccc
74831	1	354958	7	NULL	NULL	0	NULL	SCN5A gene	GP		encode		specifically			VGSC isotype Na(v)1.5	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Specifically, the SCN5A gene encoding the VGSC isotype Na(v)1.5 has been defined as a key driver of human cancer cell invasion.	topic_ccc
74832	2	354958	7	NULL	NULL	0	NULL	VGSC isotype Na(v)1.5	GP		key driver of					cancer cell 	cell	human;;invasion of			NULL		0	NULL	NULL	NULL	NULL	NULL	Specifically, the SCN5A gene encoding the VGSC isotype Na(v)1.5 has been defined as a key driver of human cancer cell invasion.	topic_ccc
74833	1	354959	7	NULL	NULL	0	NULL	 COX2 inhibitors	Chemical	prolonged use of	increase					breast cancer	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Prolonged use of COX2 inhibitors was associated with an increased risk of breast and haematological cancers and decreased risk of colorectal cancer.	topic_ccc
74834	2	354959	7	NULL	NULL	NULL	NULL	COX2 inhibitors	Chemical	prolonged use of	increase					haematological cancers 	MedicalFinding	risk of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Prolonged use of COX2 inhibitors was associated with an increased risk of breast and haematological cancers and decreased risk of colorectal cancer.	topic_ccc
74835	3	354959	7	NULL	NULL	0	NULL	COX2 inhibitors	Chemical	prolonged use of	decrease					colorectal cancer	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Prolonged use of COX2 inhibitors was associated with an increased risk of breast and haematological cancers and decreased risk of colorectal cancer.	topic_ccc
74836	1	354961	7	NULL	NULL	0	NULL	fibroblast	Cell		synthesizes					extracellular matrix	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	A fibroblast is a type of cell that synthesizes the extracellular matrix and collagen,[1] the structural framework (stroma) for animal tissues, and plays a critical role in wound healing. 	topic_ccc
74837	2	354961	7	NULL	NULL	0	NULL	fibroblast	Cell		synthesizes					collagen	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	A fibroblast is a type of cell that synthesizes the extracellular matrix and collagen,[1] the structural framework (stroma) for animal tissues, and plays a critical role in wound healing. 	topic_ccc
74838	3	354961	7	NULL	NULL	NULL	NULL	collagen	GP		stroma for					animal tissues	OrganismPart				NULL		NULL	NULL	NULL	NULL	NULL	NULL	A fibroblast is a type of cell that synthesizes the extracellular matrix and collagen,[1] the structural framework (stroma) for animal tissues, and plays a critical role in wound healing. 	topic_ccc
74839	4	354961	7	NULL	NULL	0	NULL	collagen	GP		play a critical role in					wound healing	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	A fibroblast is a type of cell that synthesizes the extracellular matrix and collagen,[1] the structural framework (stroma) for animal tissues, and plays a critical role in wound healing. 	topic_ccc
74845	5	354961	7	NULL	NULL	0	NULL	stroma	GP		is					structural framework	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	A fibroblast is a type of cell that synthesizes the extracellular matrix and collagen,[1] the structural framework (stroma) for animal tissues, and plays a critical role in wound healing. 	topic_ccc
74840	1	354962	7	NULL	NULL	0	NULL	sporadic colorectal cancer	MedicalFinding		characterized by					microsatellite sequences	NucleicAcid	mutations in			NULL		0	NULL	NULL	NULL	NULL	NULL	This pathway is present in nearly 15% of all cases of sporadic colorectal cancer. It is characterized by the presence of mutations in the microsatellite sequences caused by a defect in the DNA mismatch repair genes, mostly in hMLH1 or hMSH2.	topic_ccc
74841	2	354962	7	NULL	NULL	0	NULL	microsatellite sequences	NucleicAcid	mutations in	caused by					hMLH1	GP	defect in			NULL		0	NULL	NULL	NULL	NULL	NULL	This pathway is present in nearly 15% of all cases of sporadic colorectal cancer. It is characterized by the presence of mutations in the microsatellite sequences caused by a defect in the DNA mismatch repair genes, mostly in hMLH1 or hMSH2.	topic_ccc
74842	3	354962	7	NULL	NULL	0	NULL	 microsatellite sequences	NucleicAcid	mutations in	caused by					hMSH2	GP	defect in			NULL		0	NULL	NULL	NULL	NULL	NULL	This pathway is present in nearly 15% of all cases of sporadic colorectal cancer. It is characterized by the presence of mutations in the microsatellite sequences caused by a defect in the DNA mismatch repair genes, mostly in hMLH1 or hMSH2.	topic_ccc
74843	4	354962	7	NULL	NULL	0	NULL	hMLH1	GP		is a type of					DNA mismatch repair genes	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	This pathway is present in nearly 15% of all cases of sporadic colorectal cancer. It is characterized by the presence of mutations in the microsatellite sequences caused by a defect in the DNA mismatch repair genes, mostly in hMLH1 or hMSH2.	topic_ccc
74844	5	354962	7	NULL	NULL	0	NULL	hMSH2	GP		is a type of					DNA mismatch repair genes	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	This pathway is present in nearly 15% of all cases of sporadic colorectal cancer. It is characterized by the presence of mutations in the microsatellite sequences caused by a defect in the DNA mismatch repair genes, mostly in hMLH1 or hMSH2.	topic_ccc
74846	1	354963	7	NULL	NULL	0	NULL	LS	MedicalFinding		caused by					MSH2	GP	germline mutations in			NULL		0	NULL	NULL	NULL	NULL	NULL	Lynch syndrome (LS) is caused by germline mutations in MSH2, MLH1, MSH6, and PMS2 mismatch-repair genes and leads to a high risk of colorectal and endometrial cancer.	topic_ccc
74847	2	354963	7	NULL	NULL	0	NULL	LS	MedicalFinding		caused by					MLH1	GP	germline mutations in			NULL		0	NULL	NULL	NULL	NULL	NULL	Lynch syndrome (LS) is caused by germline mutations in MSH2, MLH1, MSH6, and PMS2 mismatch-repair genes and leads to a high risk of colorectal and endometrial cancer.	topic_ccc
74848	3	354963	7	NULL	NULL	0	NULL	LS	MedicalFinding		caused by					PMS2 mismatch-repair genes	GP	germline mutations in			NULL		0	NULL	NULL	NULL	NULL	NULL	Lynch syndrome (LS) is caused by germline mutations in MSH2, MLH1, MSH6, and PMS2 mismatch-repair genes and leads to a high risk of colorectal and endometrial cancer.	topic_ccc
74849	4	354963	7	NULL	NULL	0	NULL	LS	MedicalFinding		leads to					colorectal cancer	MedicalFinding	high risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Lynch syndrome (LS) is caused by germline mutations in MSH2, MLH1, MSH6, and PMS2 mismatch-repair genes and leads to a high risk of colorectal and endometrial cancer.	topic_ccc
74850	5	354963	7	NULL	NULL	NULL	NULL	LS	MedicalFinding		leads to					endometrial cancer	MedicalFinding	high risk of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Lynch syndrome (LS) is caused by germline mutations in MSH2, MLH1, MSH6, and PMS2 mismatch-repair genes and leads to a high risk of colorectal and endometrial cancer.	topic_ccc
74851	7	354963	7	NULL	NULL	NULL	NULL	LS	MedicalFinding		is					Lynch syndrome	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Lynch syndrome (LS) is caused by germline mutations in MSH2, MLH1, MSH6, and PMS2 mismatch-repair genes and leads to a high risk of colorectal and endometrial cancer.	topic_ccc
74852	8	354963	7	NULL	NULL	0	NULL	LS	MedicalFinding		caused by					MSH6	GP	germline mutations in			NULL		0	NULL	NULL	NULL	NULL	NULL	Lynch syndrome (LS) is caused by germline mutations in MSH2, MLH1, MSH6, and PMS2 mismatch-repair genes and leads to a high risk of colorectal and endometrial cancer.	topic_ccc
74854	1	354966	7	NULL	NULL	0	NULL	MMR	Process		due to					hMLH-1	GP	hypermethylation of		promoter	NULL		0	NULL	NULL	NULL	NULL	NULL	In sporadic CRCs, MMR is usually due to hypermethylation of the hMLH-1 promoter. 	topic_ccc
74855	2	354966	7	NULL	NULL	0	NULL	statement 1	Process		occur in					sporadic CRCs	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In sporadic CRCs, MMR is usually due to hypermethylation of the hMLH-1 promoter. 	topic_ccc
74876	1	354967	7	NULL	NULL	0	NULL	APC gene	GP	mutation of	congenital in					FAP syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The APC gene can be mutated in several ways during the colonic oncogenesis: congenital in the FAP syndrome, somatic in sporadic colorectal cancers and secondary to the MYH gene inactivation in MAP syndrome.	topic_ccc
74877	2	354967	7	NULL	NULL	0	NULL	APC gene	GP	somatic mutation of	occur in					sporadic colorectal cancers	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The APC gene can be mutated in several ways during the colonic oncogenesis: congenital in the FAP syndrome, somatic in sporadic colorectal cancers and secondary to the MYH gene inactivation in MAP syndrome.	topic_ccc
74878	3	354967	7	NULL	NULL	NULL	NULL	APC gene	GP	mutation of	occur 					MYH gene	GP	secondary to inactivation of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	The APC gene can be mutated in several ways during the colonic oncogenesis: congenital in the FAP syndrome, somatic in sporadic colorectal cancers and secondary to the MYH gene inactivation in MAP syndrome.	topic_ccc
74879	4	354967	7	NULL	NULL	0	NULL	statement 3	Process		occur in					MAP syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The APC gene can be mutated in several ways during the colonic oncogenesis: congenital in the FAP syndrome, somatic in sporadic colorectal cancers and secondary to the MYH gene inactivation in MAP syndrome.	topic_ccc
74880	1	354969	7	NULL	NULL	0	NULL	MMR	Process	inactivation of	result in					RER+ phenotype	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	These changes result in MMR inactivation, which causes RER+ phenotype. Our results suggest a connection between alteration in some tumor suppressor genes and MSI phenotype of sporadic colorectal cancer in Bosnian population.	topic_ccc
74881	2	354969	7	NULL	NULL	0	NULL	tumor suppressor genes	GP	alteration in	connected to					MSI phenotype 	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	These changes result in MMR inactivation, which causes RER+ phenotype. Our results suggest a connection between alteration in some tumor suppressor genes and MSI phenotype of sporadic colorectal cancer in Bosnian population.	topic_ccc
74882	3	354969	7	NULL	NULL	0	NULL	statement 2	Process		occur in					sporadic colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	These changes result in MMR inactivation, which causes RER+ phenotype. Our results suggest a connection between alteration in some tumor suppressor genes and MSI phenotype of sporadic colorectal cancer in Bosnian population.	topic_ccc
74883	4	354969	7	NULL	NULL	0	NULL	statement 2	Process		occur in					Bosnian population	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	These changes result in MMR inactivation, which causes RER+ phenotype. Our results suggest a connection between alteration in some tumor suppressor genes and MSI phenotype of sporadic colorectal cancer in Bosnian population.	topic_ccc
74924	1	354970	7	NULL	NULL	0	NULL	IL-8	GP	overexpression of	promotes					tumor growth	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Together, these findings indicate that overexpression of IL-8 promotes tumor growth, metastasis, chemoresistance and angiogenesis, implying IL-8 to be an important therapeutic target in CRC.	topic_ccc
74925	2	354970	7	NULL	NULL	0	NULL	IL-8	GP	overexpression of	promotes					metastasis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Together, these findings indicate that overexpression of IL-8 promotes tumor growth, metastasis, chemoresistance and angiogenesis, implying IL-8 to be an important therapeutic target in CRC.	topic_ccc
74926	3	354970	7	NULL	NULL	0	NULL	IL-8	GP	overexpression of	promotes					chemoresistance	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Together, these findings indicate that overexpression of IL-8 promotes tumor growth, metastasis, chemoresistance and angiogenesis, implying IL-8 to be an important therapeutic target in CRC.	topic_ccc
74927	4	354970	7	NULL	NULL	0	NULL	 IL-8	GP	overexpression of	promotes					angiogenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Together, these findings indicate that overexpression of IL-8 promotes tumor growth, metastasis, chemoresistance and angiogenesis, implying IL-8 to be an important therapeutic target in CRC.	topic_ccc
74928	5	354970	7	NULL	NULL	0	NULL	IL-8	GP		therapeutic target in					CRC	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Together, these findings indicate that overexpression of IL-8 promotes tumor growth, metastasis, chemoresistance and angiogenesis, implying IL-8 to be an important therapeutic target in CRC.	topic_ccc
74929	6	354970	7	NULL	NULL	0	NULL	statement 1	Process		implies					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Together, these findings indicate that overexpression of IL-8 promotes tumor growth, metastasis, chemoresistance and angiogenesis, implying IL-8 to be an important therapeutic target in CRC.	topic_ccc
74930	7	354970	7	NULL	NULL	0	NULL	statement 2	Process		implies					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Together, these findings indicate that overexpression of IL-8 promotes tumor growth, metastasis, chemoresistance and angiogenesis, implying IL-8 to be an important therapeutic target in CRC.	topic_ccc
74938	8	354970	7	NULL	NULL	0	NULL	statement 3	Process		implies					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Together, these findings indicate that overexpression of IL-8 promotes tumor growth, metastasis, chemoresistance and angiogenesis, implying IL-8 to be an important therapeutic target in CRC.	topic_ccc
74939	9	354970	7	NULL	NULL	0	NULL	statement 4	Process		implies					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Together, these findings indicate that overexpression of IL-8 promotes tumor growth, metastasis, chemoresistance and angiogenesis, implying IL-8 to be an important therapeutic target in CRC.	topic_ccc
74940	1	354972	7	NULL	NULL	0	NULL	IL-8	GP		is a type of					chemokine	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-8 (IL-8), a chemokine with a defining CXC amino acid motif, is known to possess tumorigenic and proangiogenic properties. Overexpression of IL-8 has been detected in many human tumors, including colorectal cancer (CRC), and is associated with poor prognosis.	topic_ccc
74941	2	354972	7	NULL	NULL	0	NULL	IL-8	GP		possess			CXC amino acid motif		tumorigenic properties	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-8 (IL-8), a chemokine with a defining CXC amino acid motif, is known to possess tumorigenic and proangiogenic properties. Overexpression of IL-8 has been detected in many human tumors, including colorectal cancer (CRC), and is associated with poor prognosis.	topic_ccc
74942	3	354972	7	NULL	NULL	0	NULL	IL-8	GP		possess			CXC amino acid motif		proangiogenic properties	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-8 (IL-8), a chemokine with a defining CXC amino acid motif, is known to possess tumorigenic and proangiogenic properties. Overexpression of IL-8 has been detected in many human tumors, including colorectal cancer (CRC), and is associated with poor prognosis.	topic_ccc
74943	4	354972	7	NULL	NULL	0	NULL	IL-8	GP	overexpression of	is detected in					CRC	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-8 (IL-8), a chemokine with a defining CXC amino acid motif, is known to possess tumorigenic and proangiogenic properties. Overexpression of IL-8 has been detected in many human tumors, including colorectal cancer (CRC), and is associated with poor prognosis.	topic_ccc
74944	5	354972	7	NULL	NULL	0	NULL	IL-8	GP	overexpression of	is associated with					CRC	MedicalFinding	poor prognosis of			NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-8 (IL-8), a chemokine with a defining CXC amino acid motif, is known to possess tumorigenic and proangiogenic properties. Overexpression of IL-8 has been detected in many human tumors, including colorectal cancer (CRC), and is associated with poor prognosis.	topic_ccc
74945	6	354972	7	NULL	NULL	0	NULL	CRC	MedicalFinding		is					colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-8 (IL-8), a chemokine with a defining CXC amino acid motif, is known to possess tumorigenic and proangiogenic properties. Overexpression of IL-8 has been detected in many human tumors, including colorectal cancer (CRC), and is associated with poor prognosis.	topic_ccc
74946	7	354972	7	NULL	NULL	0	NULL	CRC	MedicalFinding		is a type of					human tumor	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-8 (IL-8), a chemokine with a defining CXC amino acid motif, is known to possess tumorigenic and proangiogenic properties. Overexpression of IL-8 has been detected in many human tumors, including colorectal cancer (CRC), and is associated with poor prognosis.	topic_ccc
74947	8	354972	7	NULL	NULL	0	NULL	IL-8	GP		is					Interleukin-8	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-8 (IL-8), a chemokine with a defining CXC amino acid motif, is known to possess tumorigenic and proangiogenic properties. Overexpression of IL-8 has been detected in many human tumors, including colorectal cancer (CRC), and is associated with poor prognosis.	topic_ccc
74948	1	354973	7	NULL	NULL	0	NULL	 IL-8	GP	overexpression of	is detected in					CRC	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Overexpression of IL-8 has been detected in many human tumors, including colorectal cancer (CRC), and is associated with poor prognosis.	topic_ccc
74949	2	354973	7	NULL	NULL	0	NULL	CRC	MedicalFinding		is					colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Overexpression of IL-8 has been detected in many human tumors, including colorectal cancer (CRC), and is associated with poor prognosis.	topic_ccc
74950	3	354973	7	NULL	NULL	0	NULL	CRC	MedicalFinding		is a type of					human tumor	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Overexpression of IL-8 has been detected in many human tumors, including colorectal cancer (CRC), and is associated with poor prognosis.	topic_ccc
74951	4	354973	7	NULL	NULL	0	NULL	IL-8	GP	overexpression of	is associated with					CRC	MedicalFinding	poor prognosis of			NULL		0	NULL	NULL	NULL	NULL	NULL	Overexpression of IL-8 has been detected in many human tumors, including colorectal cancer (CRC), and is associated with poor prognosis.	topic_ccc
74952	1	354974	7	NULL	NULL	0	NULL	IL-8	GP		is a type of					chemokine	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-8 (IL-8), a chemokine with a defining CXC amino acid motif, is known to possess tumorigenic and proangiogenic properties.	topic_ccc
74953	2	354974	7	NULL	NULL	0	NULL	IL-8	GP		possess			CXC amino acid motif		tumorigenic properties	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-8 (IL-8), a chemokine with a defining CXC amino acid motif, is known to possess tumorigenic and proangiogenic properties.	topic_ccc
74954	3	354974	7	NULL	NULL	0	NULL	IL-8	GP		possess			CXC amino acid motif		proangiogenic properties	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-8 (IL-8), a chemokine with a defining CXC amino acid motif, is known to possess tumorigenic and proangiogenic properties.	topic_ccc
74955	4	354974	7	NULL	NULL	0	NULL	IL-8	GP		is					Interleukin-8	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-8 (IL-8), a chemokine with a defining CXC amino acid motif, is known to possess tumorigenic and proangiogenic properties.	topic_ccc
74956	1	354975	7	NULL	NULL	0	NULL	 IL-8	GP	overexpression of	is detected in					CRC	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Overexpression of IL-8 has been detected in many human tumors, including colorectal cancer (CRC). The IL-8 transfectants demonstrated increased cellular proliferation.	topic_ccc
74957	2	354975	7	NULL	NULL	0	NULL	CRC	MedicalFinding		is a type of					human tumor	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Overexpression of IL-8 has been detected in many human tumors, including colorectal cancer (CRC). The IL-8 transfectants demonstrated increased cellular proliferation.	topic_ccc
74958	3	354975	7	NULL	NULL	0	NULL	CRC	MedicalFinding		is					 colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Overexpression of IL-8 has been detected in many human tumors, including colorectal cancer (CRC). The IL-8 transfectants demonstrated increased cellular proliferation.	topic_ccc
74959	1	354976	7	NULL	NULL	0	NULL	VGSC SCN5A	GP		 regulator of		high level			colon cancer invasion network	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Probabilistic modeling of loss-of-function screens and microarray data established an unequivocal role of VGSC SCN5A as a high level regulator of a colon cancer invasion network, involving genes that encompass Wnt signaling, cell migration, ectoderm development, response to biotic stimulus, steroid metabolic process, and cell cycle control.	topic_ccc
74960	2	354976	7	NULL	NULL	0	NULL	statement 1	Process		encompass					Wnt signaling	Process	genes involved in			NULL		0	NULL	NULL	NULL	NULL	NULL	Probabilistic modeling of loss-of-function screens and microarray data established an unequivocal role of VGSC SCN5A as a high level regulator of a colon cancer invasion network, involving genes that encompass Wnt signaling, cell migration, ectoderm development, response to biotic stimulus, steroid metabolic process, and cell cycle control.	topic_ccc
74961	3	354976	7	NULL	NULL	0	NULL	statement 1	Process		encompass					cell migration	Process	genes involved in			NULL		0	NULL	NULL	NULL	NULL	NULL	Probabilistic modeling of loss-of-function screens and microarray data established an unequivocal role of VGSC SCN5A as a high level regulator of a colon cancer invasion network, involving genes that encompass Wnt signaling, cell migration, ectoderm development, response to biotic stimulus, steroid metabolic process, and cell cycle control.	topic_ccc
74962	4	354976	7	NULL	NULL	0	NULL	statement 1	Process		encompass					ectoderm development	Process	genes involved in			NULL		0	NULL	NULL	NULL	NULL	NULL	Probabilistic modeling of loss-of-function screens and microarray data established an unequivocal role of VGSC SCN5A as a high level regulator of a colon cancer invasion network, involving genes that encompass Wnt signaling, cell migration, ectoderm development, response to biotic stimulus, steroid metabolic process, and cell cycle control.	topic_ccc
74963	5	354976	7	NULL	NULL	0	NULL	statement 1	Process		encompass					biotic stimulus	GP	genes involved in response to			NULL		0	NULL	NULL	NULL	NULL	NULL	Probabilistic modeling of loss-of-function screens and microarray data established an unequivocal role of VGSC SCN5A as a high level regulator of a colon cancer invasion network, involving genes that encompass Wnt signaling, cell migration, ectoderm development, response to biotic stimulus, steroid metabolic process, and cell cycle control.	topic_ccc
74964	6	354976	7	NULL	NULL	0	NULL	statement 1	Process		encompass					steroid metabolic process	Process	genes involved in			NULL		0	NULL	NULL	NULL	NULL	NULL	Probabilistic modeling of loss-of-function screens and microarray data established an unequivocal role of VGSC SCN5A as a high level regulator of a colon cancer invasion network, involving genes that encompass Wnt signaling, cell migration, ectoderm development, response to biotic stimulus, steroid metabolic process, and cell cycle control.	topic_ccc
74965	7	354976	7	NULL	NULL	0	NULL	statement 1	Process		encompass					cell cycle control	Process	genes involved in			NULL		0	NULL	NULL	NULL	NULL	NULL	Probabilistic modeling of loss-of-function screens and microarray data established an unequivocal role of VGSC SCN5A as a high level regulator of a colon cancer invasion network, involving genes that encompass Wnt signaling, cell migration, ectoderm development, response to biotic stimulus, steroid metabolic process, and cell cycle control.	topic_ccc
74999	1	354977	7	NULL	NULL	0	NULL	 network connectivity	Process		drives					colon cancer invasion	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	siRNA-mediated knockdown of predicted downstream network components caused a loss of invasive behavior, demonstrating network connectivity and its function in driving colon cancer invasion.	topic_ccc
75010	1	354979	7	NULL	NULL	0	NULL	VGSC	GP		mediates					invasive potential	QuantityOrMeasure				NULL		0	NULL	NULL	NULL	NULL	NULL	We explored the mechanism of VGSC-mediated invasive potential on the basis of reported links between VGSC activity and gene expression in excitable cells.	topic_ccc
75011	2	354979	7	NULL	NULL	0	NULL	VGSC activity	Process		linked to					gene expression	GP				NULL	excitable cells	0	NULL	NULL	NULL	NULL	NULL	We explored the mechanism of VGSC-mediated invasive potential on the basis of reported links between VGSC activity and gene expression in excitable cells.	topic_ccc
75012	1	354980	7	NULL	NULL	0	NULL	sulindac	Chemical		chemopreventive agent in					sporadic colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The non-steroidal anti-inflammatory drug sulindac is an effective chemopreventive agent in sporadic colorectal cancer but its potential benefit in mismatch repair deficient cancers remains to be defined.	topic_ccc
75013	2	354980	7	NULL	NULL	0	NULL	sulindac	Chemical		is a type of					non-steroidal anti-inflammatory drug	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The non-steroidal anti-inflammatory drug sulindac is an effective chemopreventive agent in sporadic colorectal cancer but its potential benefit in mismatch repair deficient cancers remains to be defined.	topic_ccc
75051	1	354981	7	NULL	NULL	0	NULL	SOX17	GP	restoration of	inhibit					HepG2 colony formation	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 Restoration of SOX17 inhibits HepG2 colony formation and β-catenin/TCF-dependent transcription with the presence of HMG box in SOX17.	topic_ccc
75052	2	354981	7	NULL	NULL	0	NULL	 transcription	Process		depends on					 β-catenin	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 Restoration of SOX17 inhibits HepG2 colony formation and β-catenin/TCF-dependent transcription with the presence of HMG box in SOX17.	topic_ccc
75053	3	354981	7	NULL	NULL	0	NULL	transcription	Process		depends on					TCF	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 Restoration of SOX17 inhibits HepG2 colony formation and β-catenin/TCF-dependent transcription with the presence of HMG box in SOX17.	topic_ccc
75054	4	354981	7	NULL	NULL	0	NULL	SOX17	GP	restoration of	inhibit					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 Restoration of SOX17 inhibits HepG2 colony formation and β-catenin/TCF-dependent transcription with the presence of HMG box in SOX17.	topic_ccc
75055	5	354981	7	NULL	NULL	0	NULL	SOX17	GP	restoration of	inhibit					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 Restoration of SOX17 inhibits HepG2 colony formation and β-catenin/TCF-dependent transcription with the presence of HMG box in SOX17.	topic_ccc
75056	6	354981	7	NULL	NULL	NULL	NULL	statement 4	Process		in the presence of					SOX17	GP		HMG box		NULL		NULL	NULL	NULL	NULL	NULL	NULL	 Restoration of SOX17 inhibits HepG2 colony formation and β-catenin/TCF-dependent transcription with the presence of HMG box in SOX17.	topic_ccc
75057	7	354981	7	NULL	NULL	NULL	NULL	statement 5	Process		in the presence of					SOX17	GP		HMG box		NULL		NULL	NULL	NULL	NULL	NULL	NULL	 Restoration of SOX17 inhibits HepG2 colony formation and β-catenin/TCF-dependent transcription with the presence of HMG box in SOX17.	topic_ccc
75059	1	354982	7	NULL	NULL	0	NULL	IL-12 	GP		displays					antitumor properties	Process				NULL	murine models of tumorigenesis	0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication. 	topic_ccc
75060	2	354982	7	NULL	NULL	0	NULL	CD4+ cells	Cell		secrete					(IFN)-γ 	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication. 	topic_ccc
75061	3	354982	7	NULL	NULL	0	NULL	CD8+ T cells	Cell		secrete					(IFN)-γ	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication. 	topic_ccc
75062	4	354982	7	NULL	NULL	0	NULL	NK cells	Cell		secrete					(IFN)-γ	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication. 	topic_ccc
75063	5	354982	7	NULL	NULL	0	NULL	NK-T cells	Cell		secrete					(IFN)-γ	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication. 	topic_ccc
75064	6	354982	7	NULL	NULL	0	NULL	statement 1	Process		mediated by		mainly			statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication. 	topic_ccc
75065	7	354982	7	NULL	NULL	0	NULL	statement 1	Process		mediated by		mainly			statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication. 	topic_ccc
75066	8	354982	7	NULL	NULL	NULL	NULL	statement 1	Process		mediated by		mainly			statement 4	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication. 	topic_ccc
75067	9	354982	7	NULL	NULL	0	NULL	statement 1	Process		mediated by		mainly			statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication. 	topic_ccc
75068	10	354982	7	NULL	NULL	0	NULL	NK cells	cell		is					natural killer cells	cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication. 	topic_ccc
75069	11	354982	7	NULL	NULL	0	NULL	 IL-12	GP		contributes to					tumor eradication	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication. 	topic_ccc
75070	12	354982	7	NULL	NULL	0	NULL	IP 10	GP	induction of	depends on					IFN- γ	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication. 	topic_ccc
75071	13	354982	7	NULL	NULL	0	NULL	gamma interferon 	GP		induce					monokine	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication. 	topic_ccc
75072	14	354982	7	NULL	NULL	NULL	NULL	statement 11	Process		occur through					statement 12	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication. 	topic_ccc
75073	15	354982	7	NULL	NULL	0	NULL	statement 11	Process		occur through					statement 13	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication. 	topic_ccc
75074	16	354982	7	NULL	NULL	0	NULL	IP 10	GP		is a type of					 interferon-inducible protein 	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication. 	topic_ccc
75075	17	354982	7	NULL	NULL	0	NULL	IP 10	GP		is a type of					antiangiogenic factors	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication. 	topic_ccc
75076	18	354982	7	NULL	NULL	0	NULL	MIG	GP		is					monokine induced by gamma interferon 	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, in murine models of tumorigenesis, IL-12 displays remarkable antitumor properties that are mainly mediated by interferon (IFN)-γ secretion by CD4+, CD8+ T cells, natural killer (NK) or NK-T cells. Importantly, IL-12 through IFN- γ -dependent induction of the antiangiogenic factors interferon-inducible protein (IP) 10 and monokine induced by gamma interferon (MIG) contributes to tumor eradication. 	topic_ccc
75077	1	354983	7	NULL	NULL	NULL	NULL	S100A4 immunoreactivity protein	GP		absent in					cytoplasm	CellComponent				NULL	normal colorectal mucosa	NULL	NULL	NULL	NULL	NULL	NULL	In normal colorectal mucosa, protein S100A4 immunoreactivity was clearly absent in both cytoplasm and nucleus.	topic_ccc
75078	2	354983	7	NULL	NULL	0	NULL	S100A4 immunoreactivity protein	GP		absent in					nucleus	CellComponent				NULL	normal colorectal mucosa	0	NULL	NULL	NULL	NULL	NULL	In normal colorectal mucosa, protein S100A4 immunoreactivity was clearly absent in both cytoplasm and nucleus.	topic_ccc
75079	1	354985	7	NULL	NULL	0	NULL	Vitamin D	Chemical		is a group of					fat-soluble secosteroids	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Vitamin D is a group of fat-soluble secosteroids.	topic_ccc
75081	1	354987	7	NULL	NULL	NULL	NULL	Calcium 	Chemical		protect					polyps	MedicalFinding	high-risk people from developing			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Calcium seems to protect high-risk people from developing the polyps that can lead to colorectal cancer	topic_ccc
75082	2	354987	7	NULL	NULL	0	NULL	polyps	MedicalFinding		 lead to		could			colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Calcium seems to protect high-risk people from developing the polyps that can lead to colorectal cancer	topic_ccc
75083	1	354988	7	NULL	NULL	0	NULL	cigarette smoking 	PhysicalPhenomenon		play roles in					colorectal carcinogenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion, cigarette smoking and alcohol consumption play roles in colorectal carcinogenesis, and the association differs by the clinical features of the adenomas.	topic_ccc
75084	2	354988	7	NULL	NULL	0	NULL	alcohol consumption	PhysicalPhenomenon		play roles in					colorectal carcinogenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion, cigarette smoking and alcohol consumption play roles in colorectal carcinogenesis, and the association differs by the clinical features of the adenomas.	topic_ccc
75085	1	354989	7	NULL	NULL	0	NULL	bFGF	GP		mitogen for					endothelial cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Basic fibroblast growth factor (bFGF) is a mitogen for endothelial cells, which participates in tumor angiogenesis. In vitro, a CTL assay revealed that bFGF-specific cytotoxic T lymphocytes (CTL) resulted in the lysis of mouse microvascular endothelial cells (MS1) rather than that of the CT26 colorectal cancer cells.	topic_ccc
75086	2	354989	7	NULL	NULL	0	NULL	statement 1	Process		participates in					tumor angiogenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Basic fibroblast growth factor (bFGF) is a mitogen for endothelial cells, which participates in tumor angiogenesis. In vitro, a CTL assay revealed that bFGF-specific cytotoxic T lymphocytes (CTL) resulted in the lysis of mouse microvascular endothelial cells (MS1) rather than that of the CT26 colorectal cancer cells.	topic_ccc
75087	3	354989	7	NULL	NULL	NULL	NULL	bFGF-specific CTL	Cell		lyse					MS1	Cell	mouse			NULL	in vitro	NULL	NULL	NULL	NULL	NULL	NULL	Basic fibroblast growth factor (bFGF) is a mitogen for endothelial cells, which participates in tumor angiogenesis. In vitro, a CTL assay revealed that bFGF-specific cytotoxic T lymphocytes (CTL) resulted in the lysis of mouse microvascular endothelial cells (MS1) rather than that of the CT26 colorectal cancer cells.	topic_ccc
75088	4	354989	7	NULL	NULL	NULL	NULL	bFGF-specific CTL	Cell		does not lyse					CT26 colorectal cancer cells	Cell				NULL	in vitro	NULL	NULL	NULL	NULL	NULL	NULL	Basic fibroblast growth factor (bFGF) is a mitogen for endothelial cells, which participates in tumor angiogenesis. In vitro, a CTL assay revealed that bFGF-specific cytotoxic T lymphocytes (CTL) resulted in the lysis of mouse microvascular endothelial cells (MS1) rather than that of the CT26 colorectal cancer cells.	topic_ccc
75089	5	354989	7	NULL	NULL	0	NULL	bFGF	GP		is					Basic fibroblast growth factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Basic fibroblast growth factor (bFGF) is a mitogen for endothelial cells, which participates in tumor angiogenesis. In vitro, a CTL assay revealed that bFGF-specific cytotoxic T lymphocytes (CTL) resulted in the lysis of mouse microvascular endothelial cells (MS1) rather than that of the CT26 colorectal cancer cells.	topic_ccc
75090	6	354989	7	NULL	NULL	0	NULL	CTL	Cell		is					cytotoxic T lymphocytes 	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Basic fibroblast growth factor (bFGF) is a mitogen for endothelial cells, which participates in tumor angiogenesis. In vitro, a CTL assay revealed that bFGF-specific cytotoxic T lymphocytes (CTL) resulted in the lysis of mouse microvascular endothelial cells (MS1) rather than that of the CT26 colorectal cancer cells.	topic_ccc
75091	7	354989	7	NULL	NULL	0	NULL	MS1	Cell		is					microvascular endothelial cells 	Cell	mouse			NULL		0	NULL	NULL	NULL	NULL	NULL	Basic fibroblast growth factor (bFGF) is a mitogen for endothelial cells, which participates in tumor angiogenesis. In vitro, a CTL assay revealed that bFGF-specific cytotoxic T lymphocytes (CTL) resulted in the lysis of mouse microvascular endothelial cells (MS1) rather than that of the CT26 colorectal cancer cells.	topic_ccc
75092	1	354994	7	NULL	NULL	0	NULL	VEGF	GP		possess					angiogenic mechanism	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	To investigate the association of serum levels of proangiogenic cytokines with different indices of social support and loneliness by measuring the levels of expression of two important proangiogenic cytokines, vascular endothelial growth factor (VEGF), and interleukin-6 in tumors of colon and rectum.The results of this study suggest VEGF to be an angiogenic mechanism through which loneliness may lead to worse cancer-related outcomes.	topic_ccc
75093	2	354994	7	NULL	NULL	0	NULL	VEGF	GP		is					vascular endothelial growth factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	To investigate the association of serum levels of proangiogenic cytokines with different indices of social support and loneliness by measuring the levels of expression of two important proangiogenic cytokines, vascular endothelial growth factor (VEGF), and interleukin-6 in tumors of colon and rectum.The results of this study suggest VEGF to be an angiogenic mechanism through which loneliness may lead to worse cancer-related outcomes.	topic_ccc
75094	3	354994	7	NULL	NULL	0	NULL	loneliness	MentalProcess		leads to					cancer-related outcomes	MedicalFinding	worse			NULL		0	NULL	NULL	NULL	NULL	NULL	To investigate the association of serum levels of proangiogenic cytokines with different indices of social support and loneliness by measuring the levels of expression of two important proangiogenic cytokines, vascular endothelial growth factor (VEGF), and interleukin-6 in tumors of colon and rectum.The results of this study suggest VEGF to be an angiogenic mechanism through which loneliness may lead to worse cancer-related outcomes.	topic_ccc
75095	4	354994	7	NULL	NULL	0	NULL	VEGF	GP		is a type of					proangiogenic cytokines	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	To investigate the association of serum levels of proangiogenic cytokines with different indices of social support and loneliness by measuring the levels of expression of two important proangiogenic cytokines, vascular endothelial growth factor (VEGF), and interleukin-6 in tumors of colon and rectum.The results of this study suggest VEGF to be an angiogenic mechanism through which loneliness may lead to worse cancer-related outcomes.	topic_ccc
75096	5	354994	7	NULL	NULL	0	NULL	interleukin-6	GP		is a type of					proangiogenic cytokines	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	To investigate the association of serum levels of proangiogenic cytokines with different indices of social support and loneliness by measuring the levels of expression of two important proangiogenic cytokines, vascular endothelial growth factor (VEGF), and interleukin-6 in tumors of colon and rectum.The results of this study suggest VEGF to be an angiogenic mechanism through which loneliness may lead to worse cancer-related outcomes.	topic_ccc
75097	1	354995	7	NULL	NULL	0	NULL	CRC tumors	MedicalFinding		negative for					VEGFR2	GP	expression of			NULL		0	NULL	NULL	NULL	NULL	NULL	The authors have previously observed that up to 40% of vessels in colorectal carcinoma (CRC) tumors are negative for VEGF receptor 2 (VEGFR2) expression. Differential activity of transforming growth factor beta (TGF-β) is a potential contributor to this receptor heterogeneity because TGF-β contributes to both angiogenesis and CRC tumor progression.	topic_ccc
75098	2	354995	7	NULL	NULL	0	NULL	TGF-β	GP		potential contributor to					receptor heterogeneity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The authors have previously observed that up to 40% of vessels in colorectal carcinoma (CRC) tumors are negative for VEGF receptor 2 (VEGFR2) expression. Differential activity of transforming growth factor beta (TGF-β) is a potential contributor to this receptor heterogeneity because TGF-β contributes to both angiogenesis and CRC tumor progression.	topic_ccc
75099	3	354995	7	NULL	NULL	0	NULL	TGF-β	GP		contributes to					angiogenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The authors have previously observed that up to 40% of vessels in colorectal carcinoma (CRC) tumors are negative for VEGF receptor 2 (VEGFR2) expression. Differential activity of transforming growth factor beta (TGF-β) is a potential contributor to this receptor heterogeneity because TGF-β contributes to both angiogenesis and CRC tumor progression.	topic_ccc
75100	4	354995	7	NULL	NULL	0	NULL	TGF-β	GP		contributes to					CRC tumor	MedicalFinding	progression of			NULL		0	NULL	NULL	NULL	NULL	NULL	The authors have previously observed that up to 40% of vessels in colorectal carcinoma (CRC) tumors are negative for VEGF receptor 2 (VEGFR2) expression. Differential activity of transforming growth factor beta (TGF-β) is a potential contributor to this receptor heterogeneity because TGF-β contributes to both angiogenesis and CRC tumor progression.	topic_ccc
75101	5	354995	7	NULL	NULL	0	NULL	CRC	MedicalFinding		is					 colorectal carcinoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The authors have previously observed that up to 40% of vessels in colorectal carcinoma (CRC) tumors are negative for VEGF receptor 2 (VEGFR2) expression. Differential activity of transforming growth factor beta (TGF-β) is a potential contributor to this receptor heterogeneity because TGF-β contributes to both angiogenesis and CRC tumor progression.	topic_ccc
75102	6	354995	7	NULL	NULL	0	NULL	VEGFR2	GP		is					VEGF receptor 2	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The authors have previously observed that up to 40% of vessels in colorectal carcinoma (CRC) tumors are negative for VEGF receptor 2 (VEGFR2) expression. Differential activity of transforming growth factor beta (TGF-β) is a potential contributor to this receptor heterogeneity because TGF-β contributes to both angiogenesis and CRC tumor progression.	topic_ccc
75103	1	354996	7	NULL	NULL	0	NULL	Peritoneal elastic laminal invasion 	Process		associated with					colon cancer	MedicalFinding	recurrence in			NULL		0	NULL	NULL	NULL	NULL	NULL	Peritoneal elastic laminal invasion was associated with recurrence and prognosis in colon cancer and was an independent risk factor for the recurrence of stage II colon cancer.	topic_ccc
75104	2	354996	7	NULL	NULL	0	NULL	Peritoneal elastic laminal invasion 	Process		associated with					colon cancer	MedicalFinding	prognosis in			NULL		0	NULL	NULL	NULL	NULL	NULL	Peritoneal elastic laminal invasion was associated with recurrence and prognosis in colon cancer and was an independent risk factor for the recurrence of stage II colon cancer.	topic_ccc
75105	3	354996	7	NULL	NULL	NULL	NULL	Peritoneal elastic laminal invasion 	Process		 risk factor for		independent			stage II colon cancer	MedicalFinding	recurrence of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Peritoneal elastic laminal invasion was associated with recurrence and prognosis in colon cancer and was an independent risk factor for the recurrence of stage II colon cancer.	topic_ccc
75106	1	354997	7	NULL	NULL	0	NULL	folate 	Chemical	low dietary	associated with					colorectal cancer	MedicalFinding	increased risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Low dietary folate is associated with increased risk of colorectal cancer.	topic_ccc
75107	1	354998	7	NULL	NULL	0	NULL	Irinotecan	Chemical		used for					cancer	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Irinotecan (Camptosar, Pfizer; Campto, Yakult Honsha) is a drug used for the treatment of cancer.Its main use is in colon cancer, in particular, in combination with other chemotherapy agents. Irinotecan is activated by hydrolysis to SN-38, an inhibitor of topoisomerase I.	topic_ccc
75108	2	354998	7	NULL	NULL	0	NULL	Irinotecan	Chemical		is used in the					colon cancer	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Irinotecan (Camptosar, Pfizer; Campto, Yakult Honsha) is a drug used for the treatment of cancer.Its main use is in colon cancer, in particular, in combination with other chemotherapy agents. Irinotecan is activated by hydrolysis to SN-38, an inhibitor of topoisomerase I.	topic_ccc
75109	3	354998	7	NULL	NULL	0	NULL	Irinotecan	Chemical		hydrolyzed to					SN-38	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Irinotecan (Camptosar, Pfizer; Campto, Yakult Honsha) is a drug used for the treatment of cancer.Its main use is in colon cancer, in particular, in combination with other chemotherapy agents. Irinotecan is activated by hydrolysis to SN-38, an inhibitor of topoisomerase I.	topic_ccc
75110	4	354998	7	NULL	NULL	0	NULL	statement 3	Process		activates					Irinotecan	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Irinotecan (Camptosar, Pfizer; Campto, Yakult Honsha) is a drug used for the treatment of cancer.Its main use is in colon cancer, in particular, in combination with other chemotherapy agents. Irinotecan is activated by hydrolysis to SN-38, an inhibitor of topoisomerase I.	topic_ccc
75111	5	354998	7	NULL	NULL	0	NULL	SN-38	Chemical		inhibitor of					topoisomerase I	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Irinotecan (Camptosar, Pfizer; Campto, Yakult Honsha) is a drug used for the treatment of cancer.Its main use is in colon cancer, in particular, in combination with other chemotherapy agents. Irinotecan is activated by hydrolysis to SN-38, an inhibitor of topoisomerase I.	topic_ccc
75112	1	354999	7	NULL	NULL	0	NULL	Small bowel adenocarcinoma	MedicalFinding		diagnosed by					double balloon enteroscopy	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Small bowel adenocarcinoma diagnosed by double balloon enteroscopy in a patient with nonpolyposis colorectal cancer.	topic_ccc
75113	2	354999	7	NULL	NULL	0	NULL	statement 1	Process		done in					nonpolyposis colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Small bowel adenocarcinoma diagnosed by double balloon enteroscopy in a patient with nonpolyposis colorectal cancer.	topic_ccc
75114	1	355000	7	NULL	NULL	0	NULL	CRC	MedicalFinding		deadly form of		second most			cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Colorectal Cancer (CRC) is the second most deadly form of cancer among men and women, second to lung cancer.	topic_ccc
75115	2	355000	7	NULL	NULL	0	NULL	CRC	MedicalFinding		occur second to					lung cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Colorectal Cancer (CRC) is the second most deadly form of cancer among men and women, second to lung cancer.	topic_ccc
75116	3	355000	7	NULL	NULL	NULL	NULL	CRC	MedicalFinding		occur among					men	GroupOfPeople				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Colorectal Cancer (CRC) is the second most deadly form of cancer among men and women, second to lung cancer.	topic_ccc
75117	4	355000	7	NULL	NULL	0	NULL	CRC	MedicalFinding		occur among					women	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Colorectal Cancer (CRC) is the second most deadly form of cancer among men and women, second to lung cancer.	topic_ccc
75118	5	355000	7	NULL	NULL	0	NULL	CRC	MedicalFinding		is					Colorectal Cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Colorectal Cancer (CRC) is the second most deadly form of cancer among men and women, second to lung cancer.	topic_ccc
75119	1	355001	7	NULL	NULL	0	NULL	resected polyps 	MedicalFinding		is a type of					adenomatous	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	According to autopsy studies, colonic polyps occur in more than 30% of people over the age of 60. Approximately 70-80% of resected polyps are adenomatous. Adenomatous lesions have a well-documented relationship to colorectal cancer.	topic_ccc
75120	2	355001	7	NULL	NULL	0	NULL	Adenomatous lesions	MedicalFinding		relationship to					colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	According to autopsy studies, colonic polyps occur in more than 30% of people over the age of 60. Approximately 70-80% of resected polyps are adenomatous. Adenomatous lesions have a well-documented relationship to colorectal cancer.	topic_ccc
75121	1	355002	7	NULL	NULL	0	NULL	sulindac	Chemical		exert their		may			anti-neoplastic role	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 It may be stated that sulindac and celecoxib, the two NSAIDs may exert their anti-neoplastic role in colorectal cancer via modifying the physicochemical properties of the membranes.	topic_ccc
75122	2	355002	7	NULL	NULL	0	NULL	statement 1	Process		occur in					colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	 It may be stated that sulindac and celecoxib, the two NSAIDs may exert their anti-neoplastic role in colorectal cancer via modifying the physicochemical properties of the membranes.	topic_ccc
75123	3	355002	7	NULL	NULL	0	NULL	celecoxib	Chemical		exert their		may			anti-neoplastic role	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 It may be stated that sulindac and celecoxib, the two NSAIDs may exert their anti-neoplastic role in colorectal cancer via modifying the physicochemical properties of the membranes.	topic_ccc
75124	4	355002	7	NULL	NULL	0	NULL	statement 3	Process		occur in					colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	 It may be stated that sulindac and celecoxib, the two NSAIDs may exert their anti-neoplastic role in colorectal cancer via modifying the physicochemical properties of the membranes.	topic_ccc
75125	5	355002	7	NULL	NULL	0	NULL	statement 1	Process		via					membrane	CellComponent	modifying the physicochemical properties of			NULL		0	NULL	NULL	NULL	NULL	NULL	 It may be stated that sulindac and celecoxib, the two NSAIDs may exert their anti-neoplastic role in colorectal cancer via modifying the physicochemical properties of the membranes.	topic_ccc
75126	6	355002	7	NULL	NULL	0	NULL	statement 3	Process		via					membrane	CellComponent	modifying the physicochemical properties of			NULL		0	NULL	NULL	NULL	NULL	NULL	 It may be stated that sulindac and celecoxib, the two NSAIDs may exert their anti-neoplastic role in colorectal cancer via modifying the physicochemical properties of the membranes.	topic_ccc
75127	7	355002	7	NULL	NULL	0	NULL	sulindac	Chemical		is a type of					NSAID	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	 It may be stated that sulindac and celecoxib, the two NSAIDs may exert their anti-neoplastic role in colorectal cancer via modifying the physicochemical properties of the membranes.	topic_ccc
75128	8	355002	7	NULL	NULL	0	NULL	celecoxib	Chemical		is a type of					NSAID	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	 It may be stated that sulindac and celecoxib, the two NSAIDs may exert their anti-neoplastic role in colorectal cancer via modifying the physicochemical properties of the membranes.	topic_ccc
75129	1	355003	7	NULL	NULL	0	NULL	HIF-1α	GP		overexpressed in					human cancers	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Numerous studies have shown that hypoxia-inducible factor 1α (HIF-1α) is overexpressed in many human cancers and up-regulates a host of hypoxia-responsive genes for cancer growth and survival.	topic_ccc
75130	2	355003	7	NULL	NULL	0	NULL	HIF-1α	GP		upregulate					hypoxia-responsive genes	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Numerous studies have shown that hypoxia-inducible factor 1α (HIF-1α) is overexpressed in many human cancers and up-regulates a host of hypoxia-responsive genes for cancer growth and survival.	topic_ccc
75131	3	355003	7	NULL	NULL	0	NULL	hypoxia-responsive genes	GP		required for					cancer growth	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Numerous studies have shown that hypoxia-inducible factor 1α (HIF-1α) is overexpressed in many human cancers and up-regulates a host of hypoxia-responsive genes for cancer growth and survival.	topic_ccc
75132	4	355003	7	NULL	NULL	0	NULL	hypoxia-responsive genes	GP		required for					cancer survival	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Numerous studies have shown that hypoxia-inducible factor 1α (HIF-1α) is overexpressed in many human cancers and up-regulates a host of hypoxia-responsive genes for cancer growth and survival.	topic_ccc
75133	5	355003	7	NULL	NULL	0	NULL	HIF-1α	GP		is					 hypoxia-inducible factor 1α	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Numerous studies have shown that hypoxia-inducible factor 1α (HIF-1α) is overexpressed in many human cancers and up-regulates a host of hypoxia-responsive genes for cancer growth and survival.	topic_ccc
75134	1	355004	7	NULL	NULL	0	NULL	HIF-1α			is linked to					angiogenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Expression of hypoxia-inducible factor 1-alpha (HIF-1α), an important transcriptional factor linked with angiogenesis, was significantly down-regulated post 24 h hypoxia, HIF-1α expression could be significantly up-regulated and HIF-1α nuclear translocation significantly enhanced by pretreatment with GDF-15 in hypoxic HUVECs.	topic_ccc
75135	2	355004	7	NULL	NULL	0	NULL	statement 1	Process		down-regulated in		significantly			hypoxia	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Expression of hypoxia-inducible factor 1-alpha (HIF-1α), an important transcriptional factor linked with angiogenesis, was significantly down-regulated post 24 h hypoxia, HIF-1α expression could be significantly up-regulated and HIF-1α nuclear translocation significantly enhanced by pretreatment with GDF-15 in hypoxic HUVECs.	topic_ccc
75136	3	355004	7	NULL	NULL	NULL	NULL	HIF-1α	GP	expression of	up-regulated by		significantly			GDF-15	Chemical	pretreatment with			NULL	hypoxic HUVECs	NULL	NULL	NULL	NULL	NULL	NULL	Expression of hypoxia-inducible factor 1-alpha (HIF-1α), an important transcriptional factor linked with angiogenesis, was significantly down-regulated post 24 h hypoxia, HIF-1α expression could be significantly up-regulated and HIF-1α nuclear translocation significantly enhanced by pretreatment with GDF-15 in hypoxic HUVECs.	topic_ccc
75137	4	355004	7	NULL	NULL	0	NULL	HIF-1α	GP	nuclear translocation of	enhanced by		significantly			GDF-15	Chemical	pretreatment with			NULL	hypoxic HUVECs	0	NULL	NULL	NULL	NULL	NULL	Expression of hypoxia-inducible factor 1-alpha (HIF-1α), an important transcriptional factor linked with angiogenesis, was significantly down-regulated post 24 h hypoxia, HIF-1α expression could be significantly up-regulated and HIF-1α nuclear translocation significantly enhanced by pretreatment with GDF-15 in hypoxic HUVECs.	topic_ccc
75138	5	355004	7	NULL	NULL	0	NULL	HIF-1α	GP		is					hypoxia-inducible factor 1-alpha	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Expression of hypoxia-inducible factor 1-alpha (HIF-1α), an important transcriptional factor linked with angiogenesis, was significantly down-regulated post 24 h hypoxia, HIF-1α expression could be significantly up-regulated and HIF-1α nuclear translocation significantly enhanced by pretreatment with GDF-15 in hypoxic HUVECs.	topic_ccc
75139	6	355004	7	NULL	NULL	0	NULL	HIF-1α	GP		is a type of					transcriptional factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Expression of hypoxia-inducible factor 1-alpha (HIF-1α), an important transcriptional factor linked with angiogenesis, was significantly down-regulated post 24 h hypoxia, HIF-1α expression could be significantly up-regulated and HIF-1α nuclear translocation significantly enhanced by pretreatment with GDF-15 in hypoxic HUVECs.	topic_ccc
75140	1	355005	7	NULL	NULL	0	NULL	hepatic resection 	MedicalFinding	complications of extensive	encountered in					liver metastases 	Process	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	More and more complications of extensive hepatic resection are being encountered in patients treated for liver metastases from colorectal cancer.	topic_ccc
75141	2	355005	7	NULL	NULL	0	NULL	statement 1	Process		occur in					colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	More and more complications of extensive hepatic resection are being encountered in patients treated for liver metastases from colorectal cancer.	topic_ccc
75142	1	355006	7	NULL	NULL	0	NULL	COX-1	GP		expressed in		constitutively 			normal tissue	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	COX-1 is constitutively expressed in normal tissue, serving an important role in tissue homeostasis, whereas COX-2 is an inducible enzyme, which is markedly overexpressed at sites of inflammation and colorectal neoplasms	topic_ccc
75143	2	355006	7	NULL	NULL	0	NULL	statement 1	Process		important role in					tissue homeostasis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	COX-1 is constitutively expressed in normal tissue, serving an important role in tissue homeostasis, whereas COX-2 is an inducible enzyme, which is markedly overexpressed at sites of inflammation and colorectal neoplasms	topic_ccc
75144	3	355006	7	NULL	NULL	0	NULL	COX-2	GP		is a type of					inducible enzyme	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	COX-1 is constitutively expressed in normal tissue, serving an important role in tissue homeostasis, whereas COX-2 is an inducible enzyme, which is markedly overexpressed at sites of inflammation and colorectal neoplasms	topic_ccc
75145	4	355006	7	NULL	NULL	0	NULL	COX-2	GP		overexpressed at		markedly			inflammation sites	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	COX-1 is constitutively expressed in normal tissue, serving an important role in tissue homeostasis, whereas COX-2 is an inducible enzyme, which is markedly overexpressed at sites of inflammation and colorectal neoplasms	topic_ccc
75146	5	355006	7	NULL	NULL	0	NULL	COX-2	GP		overexpressed at		markedly			colorectal neoplasms	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	COX-1 is constitutively expressed in normal tissue, serving an important role in tissue homeostasis, whereas COX-2 is an inducible enzyme, which is markedly overexpressed at sites of inflammation and colorectal neoplasms	topic_ccc
75147	1	355008	7	NULL	NULL	0	NULL	FOLFIRI plus BV	Chemical		treatment for					mCRC refractory 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The results of this study suggest that FOLFIRI plus BV is a viable option in second-line treatment for mCRC refractory to first-line FOLFOX (5-fluorouracil, leucovorin, oxaliplatin) alone, and indicate that CA125 might be a predictive biomarker for the outcome.	topic_ccc
75148	1	355010	7	NULL	NULL	0	NULL	CRF	MedicalFinding		is a type of					 disabling symptom	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Cancer-related fatigue (CRF) is a disabling and distressing symptom that is highly prevalent across the cancer continuum from a patient's diagnosis and treatment through survivorship and end of life. 	topic_ccc
75149	2	355010	7	NULL	NULL	0	NULL	CRF	MedicalFinding		is a type of					distressing symptom 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Cancer-related fatigue (CRF) is a disabling and distressing symptom that is highly prevalent across the cancer continuum from a patient's diagnosis and treatment through survivorship and end of life. 	topic_ccc
75150	3	355010	7	NULL	NULL	0	NULL	CRF	MedicalFinding		is					Cancer-related fatigue	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Cancer-related fatigue (CRF) is a disabling and distressing symptom that is highly prevalent across the cancer continuum from a patient's diagnosis and treatment through survivorship and end of life. 	topic_ccc
75151	1	355011	7	NULL	NULL	0	NULL	CC	MedicalFinding		 cancer in		common			women	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Cervical cancer (CC) is the third most common cancer in women worldwide; however, CC is a preventable disease, and much effort should be done to prevent it. Persistence of high-risk HPV infection is the strongest epidemiologic risk factor for CC, however it is not sufficient for development of the disease it cofactors should be present.	topic_ccc
75152	2	355011	7	NULL	NULL	0	NULL	CC	MedicalFinding		is a type of					preventable disease	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Cervical cancer (CC) is the third most common cancer in women worldwide; however, CC is a preventable disease, and much effort should be done to prevent it. Persistence of high-risk HPV infection is the strongest epidemiologic risk factor for CC, however it is not sufficient for development of the disease it cofactors should be present.	topic_ccc
75153	3	355011	7	NULL	NULL	0	NULL	HPV infection	MedicalFinding	Persistence of high-risk	epidemiologic risk factor		strongest			CC	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Cervical cancer (CC) is the third most common cancer in women worldwide; however, CC is a preventable disease, and much effort should be done to prevent it. Persistence of high-risk HPV infection is the strongest epidemiologic risk factor for CC, however it is not sufficient for development of the disease it cofactors should be present.	topic_ccc
75154	4	355011	7	NULL	NULL	0	NULL	CC	MedicalFinding		is					cervical cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Cervical cancer (CC) is the third most common cancer in women worldwide; however, CC is a preventable disease, and much effort should be done to prevent it. Persistence of high-risk HPV infection is the strongest epidemiologic risk factor for CC, however it is not sufficient for development of the disease it cofactors should be present.	topic_ccc
75155	1	355012	7	NULL	NULL	0	NULL	HPV	MedicalFinding		is a member of					Viruses	Organism	papillomavirus family of 			NULL		0	NULL	NULL	NULL	NULL	NULL	Human papillomavirus (HPV) is a member of the papillomavirus family of viruses that is capable of infecting humans.	topic_ccc
75156	2	355012	7	NULL	NULL	0	NULL	HPV	Organism		infect					humans	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Human papillomavirus (HPV) is a member of the papillomavirus family of viruses that is capable of infecting humans.	topic_ccc
75157	3	355012	7	NULL	NULL	0	NULL	HPV	Organism		is					Human papillomavirus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Human papillomavirus (HPV) is a member of the papillomavirus family of viruses that is capable of infecting humans.	topic_ccc
75158	1	355013	7	NULL	NULL	0	NULL	abdominal obesity	MedicalFinding		is associated with					colon cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Among individual components, abdominal obesity (RR=1.51;95%CI:1.16-1.96) was associated with colon cancer	topic_ccc
75159	1	355014	7	NULL	NULL	0	NULL	HPV types 6	Organism		cause					genital warts	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	HPV types 6 and 11, which cause 90% of genital warts.	topic_ccc
75160	2	355014	7	NULL	NULL	0	NULL	HPV types 11	Organism		is a type of					genital warts	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	HPV types 6 and 11, which cause 90% of genital warts.	topic_ccc
75161	1	355015	7	NULL	NULL	0	NULL	HPV genome	Organism		is composed of					early E1 protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The HPV genome is composed of six early (E1, E2, E3, E4, E6, and E7) and two late (L1 and L2) proteins.	topic_ccc
75162	2	355015	7	NULL	NULL	0	NULL	HPV genome	Organism		is composed of					early E2 protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The HPV genome is composed of six early (E1, E2, E3, E4, E6, and E7) and two late (L1 and L2) proteins.	topic_ccc
75163	3	355015	7	NULL	NULL	NULL	NULL	HPV genome	Organism		is composed of					early E3 protein	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The HPV genome is composed of six early (E1, E2, E3, E4, E6, and E7) and two late (L1 and L2) proteins.	topic_ccc
75164	4	355015	7	NULL	NULL	0	NULL	HPV genome	Organism		is composed of					early E4 protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The HPV genome is composed of six early (E1, E2, E3, E4, E6, and E7) and two late (L1 and L2) proteins.	topic_ccc
75165	5	355015	7	NULL	NULL	0	NULL	HPV genome	Organism		is composed of					early E6 protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The HPV genome is composed of six early (E1, E2, E3, E4, E6, and E7) and two late (L1 and L2) proteins.	topic_ccc
75166	6	355015	7	NULL	NULL	0	NULL	HPV genome	Organism		is composed of					early E7 protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The HPV genome is composed of six early (E1, E2, E3, E4, E6, and E7) and two late (L1 and L2) proteins.	topic_ccc
75167	7	355015	7	NULL	NULL	0	NULL	HPV genome	Organism		is composed of					Late L1 protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The HPV genome is composed of six early (E1, E2, E3, E4, E6, and E7) and two late (L1 and L2) proteins.	topic_ccc
75168	8	355015	7	NULL	NULL	0	NULL	HPV genome	Organism		is composed of					Late L2 protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The HPV genome is composed of six early (E1, E2, E3, E4, E6, and E7) and two late (L1 and L2) proteins.	topic_ccc
75169	1	355016	7	NULL	NULL	0	NULL	E6 protein	GP		inactivates					p53	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	inactivation of tumor suppressor genes like p53 and pRB by HPV oncoproteins particularly E6 and E7	topic_ccc
75170	2	355016	7	NULL	NULL	0	NULL	E7 protein	GP		inactivates					pRB	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	inactivation of tumor suppressor genes like p53 and pRB by HPV oncoproteins particularly E6 and E7	topic_ccc
75171	3	355016	7	NULL	NULL	0	NULL	p53	GP		is a type of					tumor suppressor gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	inactivation of tumor suppressor genes like p53 and pRB by HPV oncoproteins particularly E6 and E7	topic_ccc
75172	4	355016	7	NULL	NULL	0	NULL	pRB	GP		is a type of					tumor suppressor gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	inactivation of tumor suppressor genes like p53 and pRB by HPV oncoproteins particularly E6 and E7	topic_ccc
75173	5	355016	7	NULL	NULL	NULL	NULL	E6 protein	GP		is a type of					HPV oncoprotein	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	inactivation of tumor suppressor genes like p53 and pRB by HPV oncoproteins particularly E6 and E7	topic_ccc
75174	6	355016	7	NULL	NULL	0	NULL	E7 protein	GP		is a type of					HPV oncoprotein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	inactivation of tumor suppressor genes like p53 and pRB by HPV oncoproteins particularly E6 and E7	topic_ccc
75241	1	355018	7	NULL	NULL	0	NULL	HPV16 E6	GP		induce					p53	GP	ubiquitinated degradation of			NULL		0	NULL	NULL	NULL	NULL	NULL	The ubiquitinated degradation of p53 can be induced by human papillomavirus type 16 (HPV16) early gene 6 (E6); the phosphorylated inactivation of pRb can be induced by HPV16 E7.	topic_ccc
75242	2	355018	7	NULL	NULL	0	NULL	HPV16 E7	GP		induce					pRb	GP	phosphorylated inactivation of			NULL		0	NULL	NULL	NULL	NULL	NULL	The ubiquitinated degradation of p53 can be induced by human papillomavirus type 16 (HPV16) early gene 6 (E6); the phosphorylated inactivation of pRb can be induced by HPV16 E7.	topic_ccc
75243	3	355018	7	NULL	NULL	0	NULL	HPV16	Organism		is					human papillomavirus type 16	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	The ubiquitinated degradation of p53 can be induced by human papillomavirus type 16 (HPV16) early gene 6 (E6); the phosphorylated inactivation of pRb can be induced by HPV16 E7.	topic_ccc
75244	4	355018	7	NULL	NULL	0	NULL	E6	GP		is					early gene 6	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The ubiquitinated degradation of p53 can be induced by human papillomavirus type 16 (HPV16) early gene 6 (E6); the phosphorylated inactivation of pRb can be induced by HPV16 E7.	topic_ccc
75245	1	355019	7	NULL	NULL	NULL	NULL	E6	GP		is involved in					beta-catenin	GP	nuclear accumulation of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Thus, E6 and E7 are involved in beta-catenin nuclear accumulation and activation of Wnt signaling in HPV-induced cancers.	topic_ccc
75246	2	355019	7	NULL	NULL	0	NULL	E7	GP		is involved in					beta-catenin	GP	nuclear accumulation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Thus, E6 and E7 are involved in beta-catenin nuclear accumulation and activation of Wnt signaling in HPV-induced cancers.	topic_ccc
75247	3	355019	7	NULL	NULL	NULL	NULL	E6	GP		is involved in					Wnt signaling	Process	activation of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Thus, E6 and E7 are involved in beta-catenin nuclear accumulation and activation of Wnt signaling in HPV-induced cancers.	topic_ccc
75248	4	355019	7	NULL	NULL	NULL	NULL	E7	GP		is involved in					Wnt signaling	Process	activation of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Thus, E6 and E7 are involved in beta-catenin nuclear accumulation and activation of Wnt signaling in HPV-induced cancers.	topic_ccc
75249	5	355019	7	NULL	NULL	0	NULL	statement 1	Process		occur in					HPV-induced cancers	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Thus, E6 and E7 are involved in beta-catenin nuclear accumulation and activation of Wnt signaling in HPV-induced cancers.	topic_ccc
75250	6	355019	7	NULL	NULL	NULL	NULL	statement 2	Process		occur in					HPV-induced cancers	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Thus, E6 and E7 are involved in beta-catenin nuclear accumulation and activation of Wnt signaling in HPV-induced cancers.	topic_ccc
75251	7	355019	7	NULL	NULL	0	NULL	statement 3	Process		occur in					HPV-induced cancers	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Thus, E6 and E7 are involved in beta-catenin nuclear accumulation and activation of Wnt signaling in HPV-induced cancers.	topic_ccc
75252	8	355019	7	NULL	NULL	0	NULL	statement 4	Process		occur in					HPV-induced cancers	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Thus, E6 and E7 are involved in beta-catenin nuclear accumulation and activation of Wnt signaling in HPV-induced cancers.	topic_ccc
75253	1	355020	7	NULL	NULL	0	NULL	HPV16 E6	GP		induce					p53	GP	ubiquitinated degradation of			NULL		0	NULL	NULL	NULL	NULL	NULL	The ubiquitinated degradation of p53 can be induced by human papillomavirus type 16 (HPV16) early gene 6 (E6); the phosphorylated inactivation of pRb can be induced by HPV16 E7. They are closely associated with the carcinogenesis and progression of cervical cancer.	topic_ccc
75254	2	355020	7	NULL	NULL	0	NULL	HPV16 E7	GP		induce					pRb	GP	phosphorylated inactivation of			NULL		0	NULL	NULL	NULL	NULL	NULL	The ubiquitinated degradation of p53 can be induced by human papillomavirus type 16 (HPV16) early gene 6 (E6); the phosphorylated inactivation of pRb can be induced by HPV16 E7. They are closely associated with the carcinogenesis and progression of cervical cancer.	topic_ccc
75255	3	355020	7	NULL	NULL	0	NULL	HPV16 	Organism		is					human papillomavirus type 16	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	The ubiquitinated degradation of p53 can be induced by human papillomavirus type 16 (HPV16) early gene 6 (E6); the phosphorylated inactivation of pRb can be induced by HPV16 E7. They are closely associated with the carcinogenesis and progression of cervical cancer.	topic_ccc
75256	4	355020	7	NULL	NULL	0	NULL	E6	GP		is 					early gene 6	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The ubiquitinated degradation of p53 can be induced by human papillomavirus type 16 (HPV16) early gene 6 (E6); the phosphorylated inactivation of pRb can be induced by HPV16 E7. They are closely associated with the carcinogenesis and progression of cervical cancer.	topic_ccc
75257	5	355020	7	NULL	NULL	NULL	NULL	statement 1	Process		associated with		closely			cervical cancer	MedicalFinding	carcinogenesis of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	The ubiquitinated degradation of p53 can be induced by human papillomavirus type 16 (HPV16) early gene 6 (E6); the phosphorylated inactivation of pRb can be induced by HPV16 E7. They are closely associated with the carcinogenesis and progression of cervical cancer.	topic_ccc
75258	6	355020	7	NULL	NULL	0	NULL	statement 1	Process		is associated with		closely			cervical cancer	MedicalFinding	progression of			NULL		0	NULL	NULL	NULL	NULL	NULL	The ubiquitinated degradation of p53 can be induced by human papillomavirus type 16 (HPV16) early gene 6 (E6); the phosphorylated inactivation of pRb can be induced by HPV16 E7. They are closely associated with the carcinogenesis and progression of cervical cancer.	topic_ccc
75259	7	355020	7	NULL	NULL	0	NULL	statement 5	Process		occur simultaneously with					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The ubiquitinated degradation of p53 can be induced by human papillomavirus type 16 (HPV16) early gene 6 (E6); the phosphorylated inactivation of pRb can be induced by HPV16 E7. They are closely associated with the carcinogenesis and progression of cervical cancer.	topic_ccc
75260	8	355020	7	NULL	NULL	0	NULL	statement 2	Process		associated with		closely			cervical cancer	MedicalFinding	carcinogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	The ubiquitinated degradation of p53 can be induced by human papillomavirus type 16 (HPV16) early gene 6 (E6); the phosphorylated inactivation of pRb can be induced by HPV16 E7. They are closely associated with the carcinogenesis and progression of cervical cancer.	topic_ccc
75261	9	355020	7	NULL	NULL	0	NULL	statement 2	Process		associated with		closely			cervical cancer	MedicalFinding	progression of			NULL		0	NULL	NULL	NULL	NULL	NULL	The ubiquitinated degradation of p53 can be induced by human papillomavirus type 16 (HPV16) early gene 6 (E6); the phosphorylated inactivation of pRb can be induced by HPV16 E7. They are closely associated with the carcinogenesis and progression of cervical cancer.	topic_ccc
75262	10	355020	7	NULL	NULL	0	NULL	statement 8	Process		occur simultaneously with					statement 9	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The ubiquitinated degradation of p53 can be induced by human papillomavirus type 16 (HPV16) early gene 6 (E6); the phosphorylated inactivation of pRb can be induced by HPV16 E7. They are closely associated with the carcinogenesis and progression of cervical cancer.	topic_ccc
75263	1	355022	7	NULL	NULL	0	NULL	E2F	GP	transcription activities of	suppressed by					peptide	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Luciferase reporter assay verified that transcription activities of E2F were suppressed by the peptide through restoration of pRb.	topic_ccc
75264	2	355022	7	NULL	NULL	0	NULL	statement 1	Process		occur through					pRb	GP	restoration of			NULL		0	NULL	NULL	NULL	NULL	NULL	Luciferase reporter assay verified that transcription activities of E2F were suppressed by the peptide through restoration of pRb.	topic_ccc
75265	1	355024	7	NULL	NULL	NULL	NULL	HPV	Organism	High-risk;;oncogenic type	cause					cervical cancer	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	High-risk or oncogenic types of HPV cause cervical, vaginal, and vulvar cancer in women.	topic_ccc
75266	2	355024	7	NULL	NULL	0	NULL	HPV	Organism	High-risk;;oncogenic type	cause					vaginal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	High-risk or oncogenic types of HPV cause cervical, vaginal, and vulvar cancer in women.	topic_ccc
75267	3	355024	7	NULL	NULL	0	NULL	HPV	Organism	High-risk;;oncogenic type	cause					vulvar cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	High-risk or oncogenic types of HPV cause cervical, vaginal, and vulvar cancer in women.	topic_ccc
75268	4	355024	7	NULL	NULL	0	NULL	statement 1	Process		occur in					women	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	High-risk or oncogenic types of HPV cause cervical, vaginal, and vulvar cancer in women.	topic_ccc
75269	5	355024	7	NULL	NULL	0	NULL	statement 2	Process		occur in					women	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	High-risk or oncogenic types of HPV cause cervical, vaginal, and vulvar cancer in women.	topic_ccc
75270	6	355024	7	NULL	NULL	0	NULL	statement 3	Process		occur in					women	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	High-risk or oncogenic types of HPV cause cervical, vaginal, and vulvar cancer in women.	topic_ccc
75271	1	355025	7	NULL	NULL	0	NULL	primary oropharyngeal cancers	MedicalFinding		is related to					HR-HPV	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	The association between squamous cell carcinoma of the head and neck (HNSCC) and infection with human papilloma viruses (HPV) has created considerable interest. Rates of primary oropharyngeal cancers have shown increasing incidence and declining age at presentation over the last decade, believed to relate to infection with oncogenic or high-risk subtypes of HPV (HR-HPV).	topic_ccc
75272	2	355025	7	NULL	NULL	NULL	NULL	HR-HPV	Organism		is 					high-risk HPV	Organism				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The association between squamous cell carcinoma of the head and neck (HNSCC) and infection with human papilloma viruses (HPV) has created considerable interest. Rates of primary oropharyngeal cancers have shown increasing incidence and declining age at presentation over the last decade, believed to relate to infection with oncogenic or high-risk subtypes of HPV (HR-HPV).	topic_ccc
75273	3	355025	7	NULL	NULL	0	NULL	HR-HPV	Organism		is					oncogenic HPV	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	The association between squamous cell carcinoma of the head and neck (HNSCC) and infection with human papilloma viruses (HPV) has created considerable interest. Rates of primary oropharyngeal cancers have shown increasing incidence and declining age at presentation over the last decade, believed to relate to infection with oncogenic or high-risk subtypes of HPV (HR-HPV).	topic_ccc
75274	4	355025	7	NULL	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The association between squamous cell carcinoma of the head and neck (HNSCC) and infection with human papilloma viruses (HPV) has created considerable interest. Rates of primary oropharyngeal cancers have shown increasing incidence and declining age at presentation over the last decade, believed to relate to infection with oncogenic or high-risk subtypes of HPV (HR-HPV).	topic_ccc
75275	1	355026	7	NULL	NULL	0	NULL	Aberrant DNA methylation	Process		molecular features of					CRCs	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Aberrant DNA methylation, Microsatellite Instability (MSI) and Chromosomal Instability (CIN) are well-characterised molecular features of sporadic colorectal cancers (CRCs). In addition to CpG island methylator phenotype (CIMP) associated with MSI, an intermediate methylation subgroup is also a feature of non-MSI cancers.	topic_ccc
75276	2	355026	7	NULL	NULL	0	NULL	MSI	Process		molecular features of					CRCs	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Aberrant DNA methylation, Microsatellite Instability (MSI) and Chromosomal Instability (CIN) are well-characterised molecular features of sporadic colorectal cancers (CRCs). In addition to CpG island methylator phenotype (CIMP) associated with MSI, an intermediate methylation subgroup is also a feature of non-MSI cancers.	topic_ccc
75277	3	355026	7	NULL	NULL	0	NULL	CIN	Process		molecular features of					CRCs	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Aberrant DNA methylation, Microsatellite Instability (MSI) and Chromosomal Instability (CIN) are well-characterised molecular features of sporadic colorectal cancers (CRCs). In addition to CpG island methylator phenotype (CIMP) associated with MSI, an intermediate methylation subgroup is also a feature of non-MSI cancers.	topic_ccc
75278	4	355026	7	NULL	NULL	0	NULL	CIMP	PhysicalPhenomenon		associated with					MSI	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Aberrant DNA methylation, Microsatellite Instability (MSI) and Chromosomal Instability (CIN) are well-characterised molecular features of sporadic colorectal cancers (CRCs). In addition to CpG island methylator phenotype (CIMP) associated with MSI, an intermediate methylation subgroup is also a feature of non-MSI cancers.	topic_ccc
75279	6	355026	7	NULL	NULL	NULL	NULL	statement 4	Process		feature of					non-MSI cancer	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Aberrant DNA methylation, Microsatellite Instability (MSI) and Chromosomal Instability (CIN) are well-characterised molecular features of sporadic colorectal cancers (CRCs). In addition to CpG island methylator phenotype (CIMP) associated with MSI, an intermediate methylation subgroup is also a feature of non-MSI cancers.	topic_ccc
75280	7	355026	7	NULL	NULL	NULL	NULL	 intermediate methylation subgroup	Chemical		is a feature of					non-MSI cancer	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Aberrant DNA methylation, Microsatellite Instability (MSI) and Chromosomal Instability (CIN) are well-characterised molecular features of sporadic colorectal cancers (CRCs). In addition to CpG island methylator phenotype (CIMP) associated with MSI, an intermediate methylation subgroup is also a feature of non-MSI cancers.	topic_ccc
75281	8	355026	7	NULL	NULL	0	NULL	MSI	Process		is					Microsatellite Instability	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Aberrant DNA methylation, Microsatellite Instability (MSI) and Chromosomal Instability (CIN) are well-characterised molecular features of sporadic colorectal cancers (CRCs). In addition to CpG island methylator phenotype (CIMP) associated with MSI, an intermediate methylation subgroup is also a feature of non-MSI cancers.	topic_ccc
75282	9	355026	7	NULL	NULL	0	NULL	CIN	Process		is					Chromosomal Instability	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Aberrant DNA methylation, Microsatellite Instability (MSI) and Chromosomal Instability (CIN) are well-characterised molecular features of sporadic colorectal cancers (CRCs). In addition to CpG island methylator phenotype (CIMP) associated with MSI, an intermediate methylation subgroup is also a feature of non-MSI cancers.	topic_ccc
75283	10	355026	7	NULL	NULL	0	NULL	CRCs	MedicalFinding		is					sporadic colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Aberrant DNA methylation, Microsatellite Instability (MSI) and Chromosomal Instability (CIN) are well-characterised molecular features of sporadic colorectal cancers (CRCs). In addition to CpG island methylator phenotype (CIMP) associated with MSI, an intermediate methylation subgroup is also a feature of non-MSI cancers.	topic_ccc
75284	11	355026	7	NULL	NULL	0	NULL	CIMP	PhysicalPhenomenon		is					CpG island methylator phenotype	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	Aberrant DNA methylation, Microsatellite Instability (MSI) and Chromosomal Instability (CIN) are well-characterised molecular features of sporadic colorectal cancers (CRCs). In addition to CpG island methylator phenotype (CIMP) associated with MSI, an intermediate methylation subgroup is also a feature of non-MSI cancers.	topic_ccc
75287	1	355027	7	NULL	NULL	0	NULL	hMLH1	GP		shows					tubular adenomas	MedicalFinding	specific methylation profiles for			NULL		0	NULL	NULL	NULL	NULL	NULL	Methylation analysis of hMLH1, CDKN2A/p16, and MGMT revealed specific methylation profiles for tubular adenomas, tubulovillous/villous adenomas, and colorectal cancers, supporting the use of these alterations in assessment of colorectal tumorigenesis.	topic_ccc
75288	2	355027	7	NULL	NULL	NULL	NULL	CDKN2A/p16	GP		shows					tubular adenomas	MedicalFinding	specific methylation profiles for			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Methylation analysis of hMLH1, CDKN2A/p16, and MGMT revealed specific methylation profiles for tubular adenomas, tubulovillous/villous adenomas, and colorectal cancers, supporting the use of these alterations in assessment of colorectal tumorigenesis.	topic_ccc
75291	3	355027	7	NULL	NULL	0	NULL	MGMT	GP		shows					tubular adenomas	MedicalFinding	specific methylation profiles for			NULL		0	NULL	NULL	NULL	NULL	NULL	Methylation analysis of hMLH1, CDKN2A/p16, and MGMT revealed specific methylation profiles for tubular adenomas, tubulovillous/villous adenomas, and colorectal cancers, supporting the use of these alterations in assessment of colorectal tumorigenesis.	topic_ccc
75292	4	355027	7	NULL	NULL	0	NULL	hMLH1	GP		shows					tubulovillous/villous adenomas	MedicalFinding	specific methylation profiles for			NULL		0	NULL	NULL	NULL	NULL	NULL	Methylation analysis of hMLH1, CDKN2A/p16, and MGMT revealed specific methylation profiles for tubular adenomas, tubulovillous/villous adenomas, and colorectal cancers, supporting the use of these alterations in assessment of colorectal tumorigenesis.	topic_ccc
75293	5	355027	7	NULL	NULL	0	NULL	CDKN2A/p16	GP		shows					tubulovillous/villous adenomas	MedicalFinding	specific methylation profiles for			NULL		0	NULL	NULL	NULL	NULL	NULL	Methylation analysis of hMLH1, CDKN2A/p16, and MGMT revealed specific methylation profiles for tubular adenomas, tubulovillous/villous adenomas, and colorectal cancers, supporting the use of these alterations in assessment of colorectal tumorigenesis.	topic_ccc
75295	6	355027	7	NULL	NULL	0	NULL	MGMT	GP		shows					tubulovillous/villous adenomas	MedicalFinding	specific methylation profiles for			NULL		0	NULL	NULL	NULL	NULL	NULL	Methylation analysis of hMLH1, CDKN2A/p16, and MGMT revealed specific methylation profiles for tubular adenomas, tubulovillous/villous adenomas, and colorectal cancers, supporting the use of these alterations in assessment of colorectal tumorigenesis.	topic_ccc
75299	7	355027	7	NULL	NULL	NULL	NULL	hMLH1	GP		shows					colorectal cancers	MedicalFinding	specific methylation profiles for			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Methylation analysis of hMLH1, CDKN2A/p16, and MGMT revealed specific methylation profiles for tubular adenomas, tubulovillous/villous adenomas, and colorectal cancers, supporting the use of these alterations in assessment of colorectal tumorigenesis.	topic_ccc
75300	8	355027	7	NULL	NULL	0	NULL	CDKN2A/p16	GP		shows					colorectal cancers	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Methylation analysis of hMLH1, CDKN2A/p16, and MGMT revealed specific methylation profiles for tubular adenomas, tubulovillous/villous adenomas, and colorectal cancers, supporting the use of these alterations in assessment of colorectal tumorigenesis.	topic_ccc
75301	9	355027	7	NULL	NULL	0	NULL	MGMT	GP		shows					colorectal cancers	MedicalFinding	specific methylation profiles for			NULL		0	NULL	NULL	NULL	NULL	NULL	Methylation analysis of hMLH1, CDKN2A/p16, and MGMT revealed specific methylation profiles for tubular adenomas, tubulovillous/villous adenomas, and colorectal cancers, supporting the use of these alterations in assessment of colorectal tumorigenesis.	topic_ccc
75317	1	355029	7	NULL	NULL	NULL	NULL	DNA methylation 	Process	anomalies in	include					CIMP1	PhysicalPhenomenon				NULL		NULL	NULL	NULL	NULL	NULL	NULL	In colorectal cancer (CRC), DNA methylation anomalies define distinct subgroups termed CpG island methylator phenotype 1 (CIMP1), CIMP2, and CIMP-negative.	topic_ccc
75318	2	355029	7	NULL	NULL	NULL	NULL	DNA methylation 	Process	anomalies in	include					CIMP2	PhysicalPhenomenon				NULL		NULL	NULL	NULL	NULL	NULL	NULL	In colorectal cancer (CRC), DNA methylation anomalies define distinct subgroups termed CpG island methylator phenotype 1 (CIMP1), CIMP2, and CIMP-negative.	topic_ccc
75319	3	355029	7	NULL	NULL	NULL	NULL	DNA methylation 	Process	anomalies in	include					CIMP-negative	PhysicalPhenomenon				NULL		NULL	NULL	NULL	NULL	NULL	NULL	In colorectal cancer (CRC), DNA methylation anomalies define distinct subgroups termed CpG island methylator phenotype 1 (CIMP1), CIMP2, and CIMP-negative.	topic_ccc
75320	4	355029	7	NULL	NULL	0	NULL	statement 1	Process		occur in					CRC	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In colorectal cancer (CRC), DNA methylation anomalies define distinct subgroups termed CpG island methylator phenotype 1 (CIMP1), CIMP2, and CIMP-negative.	topic_ccc
75321	5	355029	7	NULL	NULL	0	NULL	statement 2	Process		occur in					CRC	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In colorectal cancer (CRC), DNA methylation anomalies define distinct subgroups termed CpG island methylator phenotype 1 (CIMP1), CIMP2, and CIMP-negative.	topic_ccc
75322	6	355029	7	NULL	NULL	0	NULL	statement 3	Process		occur in					CRC	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In colorectal cancer (CRC), DNA methylation anomalies define distinct subgroups termed CpG island methylator phenotype 1 (CIMP1), CIMP2, and CIMP-negative.	topic_ccc
75323	7	355029	7	NULL	NULL	0	NULL	CRC	MedicalFinding		is					colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In colorectal cancer (CRC), DNA methylation anomalies define distinct subgroups termed CpG island methylator phenotype 1 (CIMP1), CIMP2, and CIMP-negative.	topic_ccc
75324	8	355029	7	NULL	NULL	0	NULL	CIMP1	PhysicalPhenomenon		is					CpG island methylator phenotype 1	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	In colorectal cancer (CRC), DNA methylation anomalies define distinct subgroups termed CpG island methylator phenotype 1 (CIMP1), CIMP2, and CIMP-negative.	topic_ccc
75325	1	355030	7	NULL	NULL	NULL	NULL	AMPK	GP	activation of	suppress		strongly			cell proliferation	Process				NULL	nonmalignant cells	NULL	NULL	NULL	NULL	NULL	NULL	Activation of AMP-activated protein kinase (AMPK), a physiological cellular energy sensor, strongly suppresses cell proliferation in both nonmalignant and tumor cells. 	topic_ccc
75326	2	355030	7	NULL	NULL	NULL	NULL	AMPK	GP	activation of	suppress		strongly			cell proliferation	Process				NULL	tumor cells	NULL	NULL	NULL	NULL	NULL	NULL	Activation of AMP-activated protein kinase (AMPK), a physiological cellular energy sensor, strongly suppresses cell proliferation in both nonmalignant and tumor cells. 	topic_ccc
75327	3	355030	7	NULL	NULL	0	NULL	AMPK	GP		is					AMP-activated protein kinase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Activation of AMP-activated protein kinase (AMPK), a physiological cellular energy sensor, strongly suppresses cell proliferation in both nonmalignant and tumor cells. 	topic_ccc
75328	4	355030	7	NULL	NULL	0	NULL	AMPK	GP		is a type of					physiological cellular energy sensor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Activation of AMP-activated protein kinase (AMPK), a physiological cellular energy sensor, strongly suppresses cell proliferation in both nonmalignant and tumor cells. 	topic_ccc
75329	1	355032	7	NULL	NULL	0	NULL	ras p21 Oncoprotein	GP	expression of	is related to					K-ras Gene	GP	mutation status of			NULL		0	NULL	NULL	NULL	NULL	NULL	Relationship Between Expression of ras p21 Oncoprotein and Mutation Status of the K-ras Gene in Sporadic Colorectal Cancer Patients in Tunisia.	topic_ccc
75330	2	355032	7	NULL	NULL	0	NULL	statement 1	Process		occur in					Sporadic Colorectal Cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Relationship Between Expression of ras p21 Oncoprotein and Mutation Status of the K-ras Gene in Sporadic Colorectal Cancer Patients in Tunisia.	topic_ccc
75331	1	355033	7	NULL	NULL	0	NULL	quercetin 	Chemical		induce					apoptosis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	All of these results indicate that quercetin induces apoptosis via AMPK activation and p53-dependent apoptotic cell death in HT-29 colon cancer cells and that it may be a potential chemopreventive or therapeutic agent against HT-29 colon cancer.	topic_ccc
75332	2	355033	7	NULL	NULL	0	NULL	statement 1	Process		via					AMPK	GP	activation of			NULL		0	NULL	NULL	NULL	NULL	NULL	All of these results indicate that quercetin induces apoptosis via AMPK activation and p53-dependent apoptotic cell death in HT-29 colon cancer cells and that it may be a potential chemopreventive or therapeutic agent against HT-29 colon cancer.	topic_ccc
75333	3	355033	7	NULL	NULL	0	NULL	apoptotic cell death	Process		depends on					p53	GP				NULL	HT-29 colon cancer cells	0	NULL	NULL	NULL	NULL	NULL	All of these results indicate that quercetin induces apoptosis via AMPK activation and p53-dependent apoptotic cell death in HT-29 colon cancer cells and that it may be a potential chemopreventive or therapeutic agent against HT-29 colon cancer.	topic_ccc
75334	4	355033	7	NULL	NULL	0	NULL	statement 1	Process		via					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	All of these results indicate that quercetin induces apoptosis via AMPK activation and p53-dependent apoptotic cell death in HT-29 colon cancer cells and that it may be a potential chemopreventive or therapeutic agent against HT-29 colon cancer.	topic_ccc
75335	5	355033	7	NULL	NULL	0	NULL	statement 2	Process		occur along with					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	All of these results indicate that quercetin induces apoptosis via AMPK activation and p53-dependent apoptotic cell death in HT-29 colon cancer cells and that it may be a potential chemopreventive or therapeutic agent against HT-29 colon cancer.	topic_ccc
75336	6	355033	7	NULL	NULL	NULL	NULL	quercetin 	Chemical		chemopreventive agent against		potential			HT-29 colon cancer	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	All of these results indicate that quercetin induces apoptosis via AMPK activation and p53-dependent apoptotic cell death in HT-29 colon cancer cells and that it may be a potential chemopreventive or therapeutic agent against HT-29 colon cancer.	topic_ccc
75337	7	355033	7	NULL	NULL	NULL	NULL	quercetin 	Chemical		therapeutic agent against		potential			HT-29 colon cancer	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	All of these results indicate that quercetin induces apoptosis via AMPK activation and p53-dependent apoptotic cell death in HT-29 colon cancer cells and that it may be a potential chemopreventive or therapeutic agent against HT-29 colon cancer.	topic_ccc
75338	8	355033	7	NULL	NULL	0	NULL	statement 6	Process		is an alternative to					statement 7	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	All of these results indicate that quercetin induces apoptosis via AMPK activation and p53-dependent apoptotic cell death in HT-29 colon cancer cells and that it may be a potential chemopreventive or therapeutic agent against HT-29 colon cancer.	topic_ccc
75339	1	355034	7	NULL	NULL	NULL	NULL	silibinin	Chemical	antitumor efficacy of	against					CRC	MedicalFinding				NULL	in vivo	NULL	NULL	NULL	NULL	NULL	NULL	These findings suggest in vivo antitumor efficacy of silibinin against CRC involving its antiproliferative, proapoptotic, and antiangiogenic activities.	topic_ccc
75340	2	355034	7	NULL	NULL	0	NULL	statement 1	Process		involves					antiproliferative activities	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	These findings suggest in vivo antitumor efficacy of silibinin against CRC involving its antiproliferative, proapoptotic, and antiangiogenic activities.	topic_ccc
75341	3	355034	7	NULL	NULL	0	NULL	statement 1	Process		involves					proapoptotic activities	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	These findings suggest in vivo antitumor efficacy of silibinin against CRC involving its antiproliferative, proapoptotic, and antiangiogenic activities.	topic_ccc
75342	4	355034	7	NULL	NULL	0	NULL	statement 1	Process		involves					antiangiogenic activities	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	These findings suggest in vivo antitumor efficacy of silibinin against CRC involving its antiproliferative, proapoptotic, and antiangiogenic activities.	topic_ccc
75343	1	355035	7	NULL	NULL	NULL	NULL	silibinin	Chemical		inhibits					cell proliferation	Process				NULL	tissue samples	NULL	NULL	NULL	NULL	NULL	NULL	Mechanistic studies in tissue samples showed that silibinin inhibits cell proliferation as evident by a decrease (P < 0.001) in proliferating cell nuclear antigen and cyclin D1, and increased Cip1/p21 levels.	topic_ccc
75344	2	355035	7	NULL	NULL	NULL	NULL	silibinin	Chemical		decrease					proliferating cell nuclear antigen	GP	levels of			NULL	tissue samples	NULL	NULL	NULL	NULL	NULL	NULL	Mechanistic studies in tissue samples showed that silibinin inhibits cell proliferation as evident by a decrease (P < 0.001) in proliferating cell nuclear antigen and cyclin D1, and increased Cip1/p21 levels.	topic_ccc
75345	3	355035	7	NULL	NULL	NULL	NULL	silibinin	Chemical		decrease					cyclin D1	GP	levels of			NULL	tissue samples	NULL	NULL	NULL	NULL	NULL	NULL	Mechanistic studies in tissue samples showed that silibinin inhibits cell proliferation as evident by a decrease (P < 0.001) in proliferating cell nuclear antigen and cyclin D1, and increased Cip1/p21 levels.	topic_ccc
75346	4	355035	7	NULL	NULL	NULL	NULL	silibinin	Chemical		increase					Cip1/p21	GP	levels of			NULL	tissue samples	NULL	NULL	NULL	NULL	NULL	NULL	Mechanistic studies in tissue samples showed that silibinin inhibits cell proliferation as evident by a decrease (P < 0.001) in proliferating cell nuclear antigen and cyclin D1, and increased Cip1/p21 levels.	topic_ccc
75347	1	355036	7	NULL	NULL	NULL	NULL	 silibinin	Chemical		chemopreventive agent against					CRC HT29 xenograft growth	MedicalFinding	human			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Herein, for the first time, we investigated in vivo efficacy and associated molecular biomarkers and mechanisms of a chemopreventive agent, silibinin, against human colorectal carcinoma (CRC) HT29 xenograft growth.	topic_ccc
75348	2	355036	7	NULL	NULL	0	NULL	CRC	MedicalFinding		is					colorectal carcinoma 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Herein, for the first time, we investigated in vivo efficacy and associated molecular biomarkers and mechanisms of a chemopreventive agent, silibinin, against human colorectal carcinoma (CRC) HT29 xenograft growth.	topic_ccc
75349	1	355037	7	NULL	NULL	0	NULL	silibinin	Chemical	Antiangiogenic effect of 	coupled with					inducible NOS	GP	strong decrease in			NULL		0	NULL	NULL	NULL	NULL	NULL	 Antiangiogenic effect of silibinin was coupled with a strong decrease in inducible nitric oxide synthase (NOS) and NOS3, cyclooxygenase-1 (COX-1) and COX-2, and hypoxia-inducing factor-1 alpha (HIF-1 alpha) and vascular endothelial growth factor (VEGF).	topic_ccc
75350	2	355037	7	NULL	NULL	0	NULL	silibinin	Chemical	Antiangiogenic effect of 	coupled with					NOS3	GP	strong decrease in			NULL		0	NULL	NULL	NULL	NULL	NULL	 Antiangiogenic effect of silibinin was coupled with a strong decrease in inducible nitric oxide synthase (NOS) and NOS3, cyclooxygenase-1 (COX-1) and COX-2, and hypoxia-inducing factor-1 alpha (HIF-1 alpha) and vascular endothelial growth factor (VEGF).	topic_ccc
75351	3	355037	7	NULL	NULL	0	NULL	silibinin	Chemical	Antiangiogenic effect of 	coupled with					COX-1	GP	strong decrease in			NULL		0	NULL	NULL	NULL	NULL	NULL	 Antiangiogenic effect of silibinin was coupled with a strong decrease in inducible nitric oxide synthase (NOS) and NOS3, cyclooxygenase-1 (COX-1) and COX-2, and hypoxia-inducing factor-1 alpha (HIF-1 alpha) and vascular endothelial growth factor (VEGF).	topic_ccc
75352	4	355037	7	NULL	NULL	0	NULL	silibinin	Chemical	Antiangiogenic effect of 	coupled with					COX-2	GP	strong decrease in			NULL		0	NULL	NULL	NULL	NULL	NULL	 Antiangiogenic effect of silibinin was coupled with a strong decrease in inducible nitric oxide synthase (NOS) and NOS3, cyclooxygenase-1 (COX-1) and COX-2, and hypoxia-inducing factor-1 alpha (HIF-1 alpha) and vascular endothelial growth factor (VEGF).	topic_ccc
75353	5	355037	7	NULL	NULL	NULL	NULL	silibinin	Chemical	Antiangiogenic effect of 	coupled with					HIF-1 alpha	GP	strong decrease in			NULL		NULL	NULL	NULL	NULL	NULL	NULL	 Antiangiogenic effect of silibinin was coupled with a strong decrease in inducible nitric oxide synthase (NOS) and NOS3, cyclooxygenase-1 (COX-1) and COX-2, and hypoxia-inducing factor-1 alpha (HIF-1 alpha) and vascular endothelial growth factor (VEGF).	topic_ccc
75354	6	355037	7	NULL	NULL	0	NULL	silibinin	Chemical	Antiangiogenic effect of 	coupled with					VEGF	GP	strong decrease in			NULL		0	NULL	NULL	NULL	NULL	NULL	 Antiangiogenic effect of silibinin was coupled with a strong decrease in inducible nitric oxide synthase (NOS) and NOS3, cyclooxygenase-1 (COX-1) and COX-2, and hypoxia-inducing factor-1 alpha (HIF-1 alpha) and vascular endothelial growth factor (VEGF).	topic_ccc
75355	7	355037	7	NULL	NULL	0	NULL	NOS	GP		is					nitric oxide synthase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 Antiangiogenic effect of silibinin was coupled with a strong decrease in inducible nitric oxide synthase (NOS) and NOS3, cyclooxygenase-1 (COX-1) and COX-2, and hypoxia-inducing factor-1 alpha (HIF-1 alpha) and vascular endothelial growth factor (VEGF).	topic_ccc
75356	8	355037	7	NULL	NULL	0	NULL	COX-1	GP		is					cyclooxygenase-1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 Antiangiogenic effect of silibinin was coupled with a strong decrease in inducible nitric oxide synthase (NOS) and NOS3, cyclooxygenase-1 (COX-1) and COX-2, and hypoxia-inducing factor-1 alpha (HIF-1 alpha) and vascular endothelial growth factor (VEGF).	topic_ccc
75357	9	355037	7	NULL	NULL	0	NULL	HIF-1 alpha	GP		is					hypoxia-inducing factor-1 alpha	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 Antiangiogenic effect of silibinin was coupled with a strong decrease in inducible nitric oxide synthase (NOS) and NOS3, cyclooxygenase-1 (COX-1) and COX-2, and hypoxia-inducing factor-1 alpha (HIF-1 alpha) and vascular endothelial growth factor (VEGF).	topic_ccc
75358	10	355037	7	NULL	NULL	0	NULL	VEGF	GP		is					vascular endothelial growth factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 Antiangiogenic effect of silibinin was coupled with a strong decrease in inducible nitric oxide synthase (NOS) and NOS3, cyclooxygenase-1 (COX-1) and COX-2, and hypoxia-inducing factor-1 alpha (HIF-1 alpha) and vascular endothelial growth factor (VEGF).	topic_ccc
75359	1	355038	7	NULL	NULL	0	NULL	Pak1	GP		overexpressed in					colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Pak1 has been reported to be overexpressed in colorectal cancer, but the role of Pak1 in colorectal cancer remains unclear.	topic_ccc
75360	1	355039	7	NULL	NULL	0	NULL	Pak1	GP	overexpression of	increase					cell motility	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 Overexpression of Pak1 increased colorectal cancer cell motility and invasion, whereas down-regulation of Pak1 expression or activity reduced colorectal cancer cell migration and invasion.	topic_ccc
75361	2	355039	7	NULL	NULL	0	NULL	Pak1	GP	overexpression of	increase					cell invasion	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 Overexpression of Pak1 increased colorectal cancer cell motility and invasion, whereas down-regulation of Pak1 expression or activity reduced colorectal cancer cell migration and invasion.	topic_ccc
75362	3	355039	7	NULL	NULL	0	NULL	statement 1	Process		occur in					colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	 Overexpression of Pak1 increased colorectal cancer cell motility and invasion, whereas down-regulation of Pak1 expression or activity reduced colorectal cancer cell migration and invasion.	topic_ccc
75363	4	355039	7	NULL	NULL	0	NULL	statement 2	Process		occur in					colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	 Overexpression of Pak1 increased colorectal cancer cell motility and invasion, whereas down-regulation of Pak1 expression or activity reduced colorectal cancer cell migration and invasion.	topic_ccc
75364	5	355039	7	NULL	NULL	0	NULL	Pak1	GP	down-regulation of ;;expression of	reduce					colorectal cancer cell migration 	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 Overexpression of Pak1 increased colorectal cancer cell motility and invasion, whereas down-regulation of Pak1 expression or activity reduced colorectal cancer cell migration and invasion.	topic_ccc
75365	6	355039	7	NULL	NULL	0	NULL	Pak1	GP	down-regulation of ;;expression of	reduce					colorectal cell invasion	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 Overexpression of Pak1 increased colorectal cancer cell motility and invasion, whereas down-regulation of Pak1 expression or activity reduced colorectal cancer cell migration and invasion.	topic_ccc
75366	1	355040	7	NULL	NULL	0	NULL	Chk1	GP	initial	involved in					G(2) arrest	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 We revealed subtle differences in the initial Chk1-involved G(2) arrest with respect to p53/p21(WAF1) : absence of either protein led to late G(2) arrest instead of the classic G(2) arrest during checkpoint initiation, and this impacted the release back into the cell cycle.	topic_ccc
75367	2	355040	7	NULL	NULL	0	NULL	statement 1	Process		difference 		subtle			p53/p21(WAF1)	GP	with respect to			NULL		0	NULL	NULL	NULL	NULL	NULL	 We revealed subtle differences in the initial Chk1-involved G(2) arrest with respect to p53/p21(WAF1) : absence of either protein led to late G(2) arrest instead of the classic G(2) arrest during checkpoint initiation, and this impacted the release back into the cell cycle.	topic_ccc
75368	3	355040	7	NULL	NULL	0	NULL	Chk1	GP	absence of	leads to					late G(2) arrest	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 We revealed subtle differences in the initial Chk1-involved G(2) arrest with respect to p53/p21(WAF1) : absence of either protein led to late G(2) arrest instead of the classic G(2) arrest during checkpoint initiation, and this impacted the release back into the cell cycle.	topic_ccc
75369	4	355040	7	NULL	NULL	0	NULL	p53/p21(WAF1)	GP	absence of	leads to					late G(2) arrest	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 We revealed subtle differences in the initial Chk1-involved G(2) arrest with respect to p53/p21(WAF1) : absence of either protein led to late G(2) arrest instead of the classic G(2) arrest during checkpoint initiation, and this impacted the release back into the cell cycle.	topic_ccc
75370	5	355040	7	NULL	NULL	0	NULL	Chk1	GP	absence of	does not lead to					classic G(2) arrest	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 We revealed subtle differences in the initial Chk1-involved G(2) arrest with respect to p53/p21(WAF1) : absence of either protein led to late G(2) arrest instead of the classic G(2) arrest during checkpoint initiation, and this impacted the release back into the cell cycle.	topic_ccc
75371	6	355040	7	NULL	NULL	0	NULL	p53/p21(WAF1)	GP	absence of	does not lead to					classic G(2) arrest	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 We revealed subtle differences in the initial Chk1-involved G(2) arrest with respect to p53/p21(WAF1) : absence of either protein led to late G(2) arrest instead of the classic G(2) arrest during checkpoint initiation, and this impacted the release back into the cell cycle.	topic_ccc
75372	7	355040	7	NULL	NULL	0	NULL	statement 3	Process		occur during					checkpoint initiation	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 We revealed subtle differences in the initial Chk1-involved G(2) arrest with respect to p53/p21(WAF1) : absence of either protein led to late G(2) arrest instead of the classic G(2) arrest during checkpoint initiation, and this impacted the release back into the cell cycle.	topic_ccc
75373	8	355040	7	NULL	NULL	0	NULL	statement 4	Process		occur during					checkpoint initiation	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 We revealed subtle differences in the initial Chk1-involved G(2) arrest with respect to p53/p21(WAF1) : absence of either protein led to late G(2) arrest instead of the classic G(2) arrest during checkpoint initiation, and this impacted the release back into the cell cycle.	topic_ccc
75374	9	355040	7	NULL	NULL	0	NULL	statement 3	Process		impacts					cell cycle	Process	release back into the			NULL		0	NULL	NULL	NULL	NULL	NULL	 We revealed subtle differences in the initial Chk1-involved G(2) arrest with respect to p53/p21(WAF1) : absence of either protein led to late G(2) arrest instead of the classic G(2) arrest during checkpoint initiation, and this impacted the release back into the cell cycle.	topic_ccc
75375	10	355040	7	NULL	NULL	0	NULL	statement 4	Process		impacts					Cell cycle	Process	release back into the			NULL		0	NULL	NULL	NULL	NULL	NULL	 We revealed subtle differences in the initial Chk1-involved G(2) arrest with respect to p53/p21(WAF1) : absence of either protein led to late G(2) arrest instead of the classic G(2) arrest during checkpoint initiation, and this impacted the release back into the cell cycle.	topic_ccc
75518	1	355042	7	NULL	NULL	0	NULL	colorectal adenomas	MedicalFinding	reduced risk of	associated with					GH1	GP	homozygous variant genotype			NULL		0	NULL	NULL	NULL	NULL	NULL	There was a reduced risk of colorectal adenomas (OR=0.63, 95% CI 0.42-0.94) and hyperplastic polyps (OR=0.7, 95% CI 0.5-0.9) associated with the homozygous variant genotype for GH1.	topic_ccc
75519	2	355042	7	NULL	NULL	0	NULL	hyperplastic polyps	MedicalFinding	reduced risk of	associated with					GH1	GP	homozygous variant genotype			NULL		0	NULL	NULL	NULL	NULL	NULL	There was a reduced risk of colorectal adenomas (OR=0.63, 95% CI 0.42-0.94) and hyperplastic polyps (OR=0.7, 95% CI 0.5-0.9) associated with the homozygous variant genotype for GH1.	topic_ccc
75520	1	355043	7	NULL	NULL	0	NULL	Colon cancer	MedicalFinding		is a common type of					cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Colon cancer is a common type of cancer. A number of risk factors increase the likelihood of developing colon cancer. A risk factor is something that increases your likelihood of developing cancer.	topic_ccc
75521	1	355044	7	NULL	NULL	0	NULL	sweetened beverages	Food		concern in		potential			obesity	MedicalFinding	relation to risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Some studies, specifically on sweetened beverages, highlighted a potential concern in relation to obesity risk, although these were limited by important methodological issues.	topic_ccc
75522	1	355045	7	NULL	NULL	0	NULL	HIF1A	GP	overexpression of	associated with		significantly			colorectal cancer-specific mortality 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	 HIF1A overexpression was significantly associated with higher colorectal cancer-specific mortality in Kaplan-Meier analysis (log-rank test, P < 0.0001), univariate Cox regression (hazard ratio = 1.84; 95% confidence interval, 1.37 to 2.47; P < 0.0001) and multivariate analysis (adjusted hazard ratio = 1.72; 95% confidence interval, 1.26 to 2.36; P = 0.0007) that adjusted for clinical and tumoral features, including microsatellite instability, TP53 (p53), PTGS2 (cyclooxygenase-2), CpG island methylator phenotype, and KRAS, BRAF, PIK3CA, and LINE-1 methylation.	topic_ccc
75523	1	355046	7	NULL	NULL	0	NULL	HIF-1	GP		mediators of		essential			cellular response	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia- inducible factor (HIF)-1 and HIF-2, which are essential mediators of cellular response to hypoxia, regulate gene expression for tumor angiogenesis, glucose metabolism, and resistance to oxidative stress. Their key regulatory subunits, HIF1A (HIF-1alpha) and endothelial PAS domain protein 1 (EPAS1; HIF-2alpha), are overexpressed and associated with patient prognosis in a variety of cancers.	topic_ccc
75524	2	355046	7	NULL	NULL	0	NULL	statement 1	Process		in response to					hypoxia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia- inducible factor (HIF)-1 and HIF-2, which are essential mediators of cellular response to hypoxia, regulate gene expression for tumor angiogenesis, glucose metabolism, and resistance to oxidative stress. Their key regulatory subunits, HIF1A (HIF-1alpha) and endothelial PAS domain protein 1 (EPAS1; HIF-2alpha), are overexpressed and associated with patient prognosis in a variety of cancers.	topic_ccc
75525	3	355046	7	NULL	NULL	NULL	NULL	HIF-2	GP		mediators of		essential			 cellular response	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hypoxia- inducible factor (HIF)-1 and HIF-2, which are essential mediators of cellular response to hypoxia, regulate gene expression for tumor angiogenesis, glucose metabolism, and resistance to oxidative stress. Their key regulatory subunits, HIF1A (HIF-1alpha) and endothelial PAS domain protein 1 (EPAS1; HIF-2alpha), are overexpressed and associated with patient prognosis in a variety of cancers.	topic_ccc
75526	4	355046	7	NULL	NULL	0	NULL	statement 3	Process		in response to					hypoxia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia- inducible factor (HIF)-1 and HIF-2, which are essential mediators of cellular response to hypoxia, regulate gene expression for tumor angiogenesis, glucose metabolism, and resistance to oxidative stress. Their key regulatory subunits, HIF1A (HIF-1alpha) and endothelial PAS domain protein 1 (EPAS1; HIF-2alpha), are overexpressed and associated with patient prognosis in a variety of cancers.	topic_ccc
75527	5	355046	7	NULL	NULL	0	NULL	HIF-1	GP		regulate					gene expression	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia- inducible factor (HIF)-1 and HIF-2, which are essential mediators of cellular response to hypoxia, regulate gene expression for tumor angiogenesis, glucose metabolism, and resistance to oxidative stress. Their key regulatory subunits, HIF1A (HIF-1alpha) and endothelial PAS domain protein 1 (EPAS1; HIF-2alpha), are overexpressed and associated with patient prognosis in a variety of cancers.	topic_ccc
75528	6	355046	7	NULL	NULL	0	NULL	HIF-2	GP		regulate					gene expression	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia- inducible factor (HIF)-1 and HIF-2, which are essential mediators of cellular response to hypoxia, regulate gene expression for tumor angiogenesis, glucose metabolism, and resistance to oxidative stress. Their key regulatory subunits, HIF1A (HIF-1alpha) and endothelial PAS domain protein 1 (EPAS1; HIF-2alpha), are overexpressed and associated with patient prognosis in a variety of cancers.	topic_ccc
75529	7	355046	7	NULL	NULL	0	NULL	statement 5	Process		occur for					tumor angiogenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia- inducible factor (HIF)-1 and HIF-2, which are essential mediators of cellular response to hypoxia, regulate gene expression for tumor angiogenesis, glucose metabolism, and resistance to oxidative stress. Their key regulatory subunits, HIF1A (HIF-1alpha) and endothelial PAS domain protein 1 (EPAS1; HIF-2alpha), are overexpressed and associated with patient prognosis in a variety of cancers.	topic_ccc
75530	8	355046	7	NULL	NULL	0	NULL	statement 6	Process		occur for					tumor angiogenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia- inducible factor (HIF)-1 and HIF-2, which are essential mediators of cellular response to hypoxia, regulate gene expression for tumor angiogenesis, glucose metabolism, and resistance to oxidative stress. Their key regulatory subunits, HIF1A (HIF-1alpha) and endothelial PAS domain protein 1 (EPAS1; HIF-2alpha), are overexpressed and associated with patient prognosis in a variety of cancers.	topic_ccc
75531	9	355046	7	NULL	NULL	0	NULL	statement 5	Process		occur for					glucose metabolism	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia- inducible factor (HIF)-1 and HIF-2, which are essential mediators of cellular response to hypoxia, regulate gene expression for tumor angiogenesis, glucose metabolism, and resistance to oxidative stress. Their key regulatory subunits, HIF1A (HIF-1alpha) and endothelial PAS domain protein 1 (EPAS1; HIF-2alpha), are overexpressed and associated with patient prognosis in a variety of cancers.	topic_ccc
75532	10	355046	7	NULL	NULL	0	NULL	statement 6	Process		occur for					glucose metabolism	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia- inducible factor (HIF)-1 and HIF-2, which are essential mediators of cellular response to hypoxia, regulate gene expression for tumor angiogenesis, glucose metabolism, and resistance to oxidative stress. Their key regulatory subunits, HIF1A (HIF-1alpha) and endothelial PAS domain protein 1 (EPAS1; HIF-2alpha), are overexpressed and associated with patient prognosis in a variety of cancers.	topic_ccc
75533	11	355046	7	NULL	NULL	0	NULL	statement 5	Process		occur for					oxidative stress	Process	resistance to			NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia- inducible factor (HIF)-1 and HIF-2, which are essential mediators of cellular response to hypoxia, regulate gene expression for tumor angiogenesis, glucose metabolism, and resistance to oxidative stress. Their key regulatory subunits, HIF1A (HIF-1alpha) and endothelial PAS domain protein 1 (EPAS1; HIF-2alpha), are overexpressed and associated with patient prognosis in a variety of cancers.	topic_ccc
75534	12	355046	7	NULL	NULL	0	NULL	statement 6	Process		occur for					oxidative stress	Process	resistance to			NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia- inducible factor (HIF)-1 and HIF-2, which are essential mediators of cellular response to hypoxia, regulate gene expression for tumor angiogenesis, glucose metabolism, and resistance to oxidative stress. Their key regulatory subunits, HIF1A (HIF-1alpha) and endothelial PAS domain protein 1 (EPAS1; HIF-2alpha), are overexpressed and associated with patient prognosis in a variety of cancers.	topic_ccc
75535	13	355046	7	NULL	NULL	NULL	NULL	HIF1A	GP		 subunit of		regulatory			HIF-1	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hypoxia- inducible factor (HIF)-1 and HIF-2, which are essential mediators of cellular response to hypoxia, regulate gene expression for tumor angiogenesis, glucose metabolism, and resistance to oxidative stress. Their key regulatory subunits, HIF1A (HIF-1alpha) and endothelial PAS domain protein 1 (EPAS1; HIF-2alpha), are overexpressed and associated with patient prognosis in a variety of cancers.	topic_ccc
75536	14	355046	7	NULL	NULL	0	NULL	HIF1A	GP	overexpression of	associated with					cancers	MedicalFinding	prognosis in			NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia- inducible factor (HIF)-1 and HIF-2, which are essential mediators of cellular response to hypoxia, regulate gene expression for tumor angiogenesis, glucose metabolism, and resistance to oxidative stress. Their key regulatory subunits, HIF1A (HIF-1alpha) and endothelial PAS domain protein 1 (EPAS1; HIF-2alpha), are overexpressed and associated with patient prognosis in a variety of cancers.	topic_ccc
75537	15	355046	7	NULL	NULL	NULL	NULL	EPAS1	GP		subunit of		regulatory			HIF-2	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hypoxia- inducible factor (HIF)-1 and HIF-2, which are essential mediators of cellular response to hypoxia, regulate gene expression for tumor angiogenesis, glucose metabolism, and resistance to oxidative stress. Their key regulatory subunits, HIF1A (HIF-1alpha) and endothelial PAS domain protein 1 (EPAS1; HIF-2alpha), are overexpressed and associated with patient prognosis in a variety of cancers.	topic_ccc
75538	16	355046	7	NULL	NULL	0	NULL	EPAS1	GP	overexpression of	associated with					cancers	MedicalFinding	prognosis in			NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia- inducible factor (HIF)-1 and HIF-2, which are essential mediators of cellular response to hypoxia, regulate gene expression for tumor angiogenesis, glucose metabolism, and resistance to oxidative stress. Their key regulatory subunits, HIF1A (HIF-1alpha) and endothelial PAS domain protein 1 (EPAS1; HIF-2alpha), are overexpressed and associated with patient prognosis in a variety of cancers.	topic_ccc
75539	17	355046	7	NULL	NULL	0	NULL	HIF1A	GP		is					HIF-1alpha	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia- inducible factor (HIF)-1 and HIF-2, which are essential mediators of cellular response to hypoxia, regulate gene expression for tumor angiogenesis, glucose metabolism, and resistance to oxidative stress. Their key regulatory subunits, HIF1A (HIF-1alpha) and endothelial PAS domain protein 1 (EPAS1; HIF-2alpha), are overexpressed and associated with patient prognosis in a variety of cancers.	topic_ccc
75540	18	355046	7	NULL	NULL	0	NULL	EPAS1	GP		is					endothelial PAS domain protein 1 	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia- inducible factor (HIF)-1 and HIF-2, which are essential mediators of cellular response to hypoxia, regulate gene expression for tumor angiogenesis, glucose metabolism, and resistance to oxidative stress. Their key regulatory subunits, HIF1A (HIF-1alpha) and endothelial PAS domain protein 1 (EPAS1; HIF-2alpha), are overexpressed and associated with patient prognosis in a variety of cancers.	topic_ccc
75541	1	355047	7	NULL	NULL	NULL	NULL	HIF1A 	GP	expression of	associated with		independently			colorectal cancer	MedicalFinding	poor prognosis in			NULL		NULL	NULL	NULL	NULL	NULL	NULL	 In conclusion, HIF1A expression is independently associated with poor prognosis in colorectal cancer, suggesting HIF1A as a biomarker with potentially important therapeutic implications.	topic_ccc
75542	2	355047	7	NULL	NULL	0	NULL	HIF1A	GP		biomarker with		potential			therapeutic implications	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	 In conclusion, HIF1A expression is independently associated with poor prognosis in colorectal cancer, suggesting HIF1A as a biomarker with potentially important therapeutic implications.	topic_ccc
75543	3	355047	7	NULL	NULL	0	NULL	statement 1	Process		suggest					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 In conclusion, HIF1A expression is independently associated with poor prognosis in colorectal cancer, suggesting HIF1A as a biomarker with potentially important therapeutic implications.	topic_ccc
75544	1	355048	7	NULL	NULL	0	NULL	IGF-IR	GP	signaling of	is required for					carcinogenicity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Insulin-like growth factor (IGF)-I receptor (IGF-IR) signaling is required for carcinogenicity and proliferation of gastrointestinal cancers.	topic_ccc
75545	2	355048	7	NULL	NULL	0	NULL	IGF-IR	GP	signaling of	is required for					gastrointestinal cancers	MedicalFinding	proliferation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Insulin-like growth factor (IGF)-I receptor (IGF-IR) signaling is required for carcinogenicity and proliferation of gastrointestinal cancers.	topic_ccc
75546	3	355048	7	NULL	NULL	0	NULL	IGF-IR	GP		is					Insulin-like growth factor-I receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Insulin-like growth factor (IGF)-I receptor (IGF-IR) signaling is required for carcinogenicity and proliferation of gastrointestinal cancers.	topic_ccc
75547	1	355049	7	NULL	NULL	0	NULL	IGF-1	GP		is critical to					inflammatory response	MedicalFinding	activate			NULL	liver	0	NULL	NULL	NULL	NULL	NULL	In the setting of obesity, our findings imply that IGF-1 is critical to activate and sustain an inflammatory response in the liver that is needed for hepatic metastasis, not only through direct, paracrine effect on tumor cell growth, but also through indirect effects involving the tumor microenvironment.	topic_ccc
75548	2	355049	7	NULL	NULL	0	NULL	IGF-1	GP		is critical to					inflammatory response	MedicalFinding	sustain			NULL	liver	0	NULL	NULL	NULL	NULL	NULL	In the setting of obesity, our findings imply that IGF-1 is critical to activate and sustain an inflammatory response in the liver that is needed for hepatic metastasis, not only through direct, paracrine effect on tumor cell growth, but also through indirect effects involving the tumor microenvironment.	topic_ccc
75549	3	355049	7	NULL	NULL	0	NULL	statement 1	Process		occur along with					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In the setting of obesity, our findings imply that IGF-1 is critical to activate and sustain an inflammatory response in the liver that is needed for hepatic metastasis, not only through direct, paracrine effect on tumor cell growth, but also through indirect effects involving the tumor microenvironment.	topic_ccc
75550	4	355049	7	NULL	NULL	0	NULL	statement 3	Process		required for					hepatic metastasis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In the setting of obesity, our findings imply that IGF-1 is critical to activate and sustain an inflammatory response in the liver that is needed for hepatic metastasis, not only through direct, paracrine effect on tumor cell growth, but also through indirect effects involving the tumor microenvironment.	topic_ccc
75551	5	355049	7	NULL	NULL	NULL	NULL	statement 4	Process		occur through		directly			tumor cell growth	Process	paracrine effect on			NULL		NULL	NULL	NULL	NULL	NULL	NULL	In the setting of obesity, our findings imply that IGF-1 is critical to activate and sustain an inflammatory response in the liver that is needed for hepatic metastasis, not only through direct, paracrine effect on tumor cell growth, but also through indirect effects involving the tumor microenvironment.	topic_ccc
75552	6	355049	7	NULL	NULL	0	NULL	statement 4	Process		occur through		indirectly			tumor microenvironment	Process	effects involving			NULL		0	NULL	NULL	NULL	NULL	NULL	In the setting of obesity, our findings imply that IGF-1 is critical to activate and sustain an inflammatory response in the liver that is needed for hepatic metastasis, not only through direct, paracrine effect on tumor cell growth, but also through indirect effects involving the tumor microenvironment.	topic_ccc
75553	1	355050	7	NULL	NULL	0	NULL	IL-12	GP		role in		prominent			TH1 T cell differentiation	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The prominent role of interleukin (IL)-12 in inflammatory responses, especially in TH1 T cell differentiation, is well established.	topic_ccc
75554	2	355050	7	NULL	NULL	0	NULL	TH1 T cell differentiation	Process		is a type of					 inflammatory response	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The prominent role of interleukin (IL)-12 in inflammatory responses, especially in TH1 T cell differentiation, is well established.	topic_ccc
75555	3	355050	7	NULL	NULL	0	NULL	IL-12	GP		is					Interleukin-12	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The prominent role of interleukin (IL)-12 in inflammatory responses, especially in TH1 T cell differentiation, is well established.	topic_ccc
74084	1	355052	5	NULL	NULL	0	NULL	siblings of schizophrenia patients	GroupOfPeople		experience					impaired cognition	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Siblings of patients with schizophrenia show impaired cognition and an increased prevalence of depression history.	topic_sch
74085	2	355052	5	NULL	NULL	0	NULL	siblings of schizophrenia patients	GroupOfPeople		experience					depression	MedicalFinding	increased prevalence of;;history of			NULL		0	NULL	NULL	NULL	NULL	NULL	Siblings of patients with schizophrenia show impaired cognition and an increased prevalence of depression history.	topic_sch
74144	1	355053	5	NULL	NULL	0	NULL	KYNA	Chemical		is					kynurenic acid	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Kynurenic acid (KYNA) is an endogenous tryptophan-metabolite found to be increased in the brain of patients with schizophrenia ([Erhardt et al., 2009] and [Wonodi and Schwarcz, 2010])	topic_sch
74145	2	355053	5	NULL	NULL	0	NULL	Kynurenic acid	Chemical		is a type of					endogenous tryptophan-metabolite 	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Kynurenic acid (KYNA) is an endogenous tryptophan-metabolite found to be increased in the brain of patients with schizophrenia ([Erhardt et al., 2009] and [Wonodi and Schwarcz, 2010])	topic_sch
74146	3	355053	5	NULL	NULL	0	NULL	Kynurenic acid	Chemical		is increased in					schizophrenia patients	GroupOfPeople	brain of			NULL		0	NULL	NULL	NULL	NULL	NULL	Kynurenic acid (KYNA) is an endogenous tryptophan-metabolite found to be increased in the brain of patients with schizophrenia ([Erhardt et al., 2009] and [Wonodi and Schwarcz, 2010])	topic_sch
74147	1	355054	5	NULL	NULL	0	NULL	hypoglutamatergia	MedicalFinding		is implicated in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	This unique receptor profile may account for both hypoglutamatergia and impairment in cholinergic signaling, conditions that are implicated in schizophrenia (Wonodi and Schwarcz, 2010).	topic_sch
74148	2	355054	5	NULL	NULL	0	NULL	cholinergic signaling	Process	impairment of	is implicated in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	This unique receptor profile may account for both hypoglutamatergia and impairment in cholinergic signaling, conditions that are implicated in schizophrenia (Wonodi and Schwarcz, 2010).	topic_sch
74149	1	355055	5	NULL	NULL	0	NULL	KMO gene	GP		is located on					1q42	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably, the KMO gene is located on 1q42, a chromosome region associated with schizophrenia ([Ekelund et al., 2004] and [Hamshere et al., 2005]).	topic_sch
74150	2	355055	5	NULL	NULL	0	NULL	1q42	Chromosome		is associated with					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably, the KMO gene is located on 1q42, a chromosome region associated with schizophrenia ([Ekelund et al., 2004] and [Hamshere et al., 2005]).	topic_sch
74151	1	355056	5	NULL	NULL	0	NULL	KMO variations	GP		is associated with		may be			schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Here, we investigate a possible association between KMO variations and schizophrenia.	topic_sch
74152	1	355057	5	NULL	NULL	0	NULL	KYNA	GP	synthesis of;;brain	is dependent on					kynurenine	GP	availability of			NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore, beyond the activity of KMO, the synthesis of brain KYNA is also highly dependent on the availability of kynurenine, the immediate precursor of KYNA. As recent studies show that also kynurenine is elevated in patients with schizophrenia ([Linderholm et al., in press] and [Wonodi and Schwarcz, 2010]), one may speculate that polymorphisms in genes encoding indoleamine 2,3-dioxygenase (IDO) and/or tryptophan 2,3-dioxygenase (TDO), enzymes converting tryptophan to kynurenine, may partly account for the elevated levels of KYNA in schizophrenia.	topic_sch
74153	2	355057	5	NULL	NULL	0	NULL	kynurenine	GP		is an immediate precursor of					KYNA	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore, beyond the activity of KMO, the synthesis of brain KYNA is also highly dependent on the availability of kynurenine, the immediate precursor of KYNA. As recent studies show that also kynurenine is elevated in patients with schizophrenia ([Linderholm et al., in press] and [Wonodi and Schwarcz, 2010]), one may speculate that polymorphisms in genes encoding indoleamine 2,3-dioxygenase (IDO) and/or tryptophan 2,3-dioxygenase (TDO), enzymes converting tryptophan to kynurenine, may partly account for the elevated levels of KYNA in schizophrenia.	topic_sch
74154	3	355057	5	NULL	NULL	0	NULL	kynurenine	GP		is elevated in					schizophrenic patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore, beyond the activity of KMO, the synthesis of brain KYNA is also highly dependent on the availability of kynurenine, the immediate precursor of KYNA. As recent studies show that also kynurenine is elevated in patients with schizophrenia ([Linderholm et al., in press] and [Wonodi and Schwarcz, 2010]), one may speculate that polymorphisms in genes encoding indoleamine 2,3-dioxygenase (IDO) and/or tryptophan 2,3-dioxygenase (TDO), enzymes converting tryptophan to kynurenine, may partly account for the elevated levels of KYNA in schizophrenia.	topic_sch
74155	4	355057	5	NULL	NULL	0	NULL	tryptophan	AminoAcid		is converted to					kynurenine	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore, beyond the activity of KMO, the synthesis of brain KYNA is also highly dependent on the availability of kynurenine, the immediate precursor of KYNA. As recent studies show that also kynurenine is elevated in patients with schizophrenia ([Linderholm et al., in press] and [Wonodi and Schwarcz, 2010]), one may speculate that polymorphisms in genes encoding indoleamine 2,3-dioxygenase (IDO) and/or tryptophan 2,3-dioxygenase (TDO), enzymes converting tryptophan to kynurenine, may partly account for the elevated levels of KYNA in schizophrenia.	topic_sch
74156	5	355057	5	NULL	NULL	0	NULL	enzymes	GP		is required for					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore, beyond the activity of KMO, the synthesis of brain KYNA is also highly dependent on the availability of kynurenine, the immediate precursor of KYNA. As recent studies show that also kynurenine is elevated in patients with schizophrenia ([Linderholm et al., in press] and [Wonodi and Schwarcz, 2010]), one may speculate that polymorphisms in genes encoding indoleamine 2,3-dioxygenase (IDO) and/or tryptophan 2,3-dioxygenase (TDO), enzymes converting tryptophan to kynurenine, may partly account for the elevated levels of KYNA in schizophrenia.	topic_sch
74157	6	355057	5	NULL	NULL	0	NULL	statement 5	Process		accounts for		partly			statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore, beyond the activity of KMO, the synthesis of brain KYNA is also highly dependent on the availability of kynurenine, the immediate precursor of KYNA. As recent studies show that also kynurenine is elevated in patients with schizophrenia ([Linderholm et al., in press] and [Wonodi and Schwarcz, 2010]), one may speculate that polymorphisms in genes encoding indoleamine 2,3-dioxygenase (IDO) and/or tryptophan 2,3-dioxygenase (TDO), enzymes converting tryptophan to kynurenine, may partly account for the elevated levels of KYNA in schizophrenia.	topic_sch
74158	7	355057	5	NULL	NULL	0	NULL	IDO	GP		is					indoleamine 2,3-dioxygenase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore, beyond the activity of KMO, the synthesis of brain KYNA is also highly dependent on the availability of kynurenine, the immediate precursor of KYNA. As recent studies show that also kynurenine is elevated in patients with schizophrenia ([Linderholm et al., in press] and [Wonodi and Schwarcz, 2010]), one may speculate that polymorphisms in genes encoding indoleamine 2,3-dioxygenase (IDO) and/or tryptophan 2,3-dioxygenase (TDO), enzymes converting tryptophan to kynurenine, may partly account for the elevated levels of KYNA in schizophrenia.	topic_sch
74159	8	355057	5	NULL	NULL	0	NULL	TDO	GP		is					tryptophan 2,3-dioxygenase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore, beyond the activity of KMO, the synthesis of brain KYNA is also highly dependent on the availability of kynurenine, the immediate precursor of KYNA. As recent studies show that also kynurenine is elevated in patients with schizophrenia ([Linderholm et al., in press] and [Wonodi and Schwarcz, 2010]), one may speculate that polymorphisms in genes encoding indoleamine 2,3-dioxygenase (IDO) and/or tryptophan 2,3-dioxygenase (TDO), enzymes converting tryptophan to kynurenine, may partly account for the elevated levels of KYNA in schizophrenia.	topic_sch
74160	9	355057	5	NULL	NULL	0	NULL	IDO gene	GP	polymorphism of	accounts for		partly			statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore, beyond the activity of KMO, the synthesis of brain KYNA is also highly dependent on the availability of kynurenine, the immediate precursor of KYNA. As recent studies show that also kynurenine is elevated in patients with schizophrenia ([Linderholm et al., in press] and [Wonodi and Schwarcz, 2010]), one may speculate that polymorphisms in genes encoding indoleamine 2,3-dioxygenase (IDO) and/or tryptophan 2,3-dioxygenase (TDO), enzymes converting tryptophan to kynurenine, may partly account for the elevated levels of KYNA in schizophrenia.	topic_sch
74161	10	355057	5	NULL	NULL	0	NULL	TDO gene	GP	polymorphism of	accounts for		partly			statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore, beyond the activity of KMO, the synthesis of brain KYNA is also highly dependent on the availability of kynurenine, the immediate precursor of KYNA. As recent studies show that also kynurenine is elevated in patients with schizophrenia ([Linderholm et al., in press] and [Wonodi and Schwarcz, 2010]), one may speculate that polymorphisms in genes encoding indoleamine 2,3-dioxygenase (IDO) and/or tryptophan 2,3-dioxygenase (TDO), enzymes converting tryptophan to kynurenine, may partly account for the elevated levels of KYNA in schizophrenia.	topic_sch
74162	1	355058	5	NULL	NULL	0	NULL	cannabis abuse	MedicalFinding	prevalence of	is increased in					schizophrenic patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Patients with schizophrenia show increased prevalence of cannabis abuse and this has been linked to severity of EPS.	topic_sch
74163	2	355058	5	NULL	NULL	0	NULL	statement 1	Process		is linked to					EPS	MedicalFinding	severity of			NULL		0	NULL	NULL	NULL	NULL	NULL	Patients with schizophrenia show increased prevalence of cannabis abuse and this has been linked to severity of EPS.	topic_sch
74164	1	355059	5	NULL	NULL	0	NULL	mitochondrial dysfunction	MedicalFinding		occurs in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Alterations in mitochondrial morphometry, brain energy metabolism, and enzymatic activity in the mitochondrial respiratory chain suggest a mitochondrial dysfunction in schizophrenia that could be related to the genetic characteristics of mtDNA. 	topic_sch
74165	2	355059	5	NULL	NULL	0	NULL	statement 1	Process		is related to					mtDNA	NucleicAcid	genetic characteristics of			NULL		0	NULL	NULL	NULL	NULL	NULL	Alterations in mitochondrial morphometry, brain energy metabolism, and enzymatic activity in the mitochondrial respiratory chain suggest a mitochondrial dysfunction in schizophrenia that could be related to the genetic characteristics of mtDNA. 	topic_sch
74166	3	355059	5	NULL	NULL	NULL	NULL	mitochondrial morphometry	QuantityOrMeasure	alterations in	suggest					statement 1	Process				NULL	mitochondrial respiratory chain	NULL	NULL	NULL	NULL	NULL	NULL	Alterations in mitochondrial morphometry, brain energy metabolism, and enzymatic activity in the mitochondrial respiratory chain suggest a mitochondrial dysfunction in schizophrenia that could be related to the genetic characteristics of mtDNA. 	topic_sch
74167	4	355059	5	NULL	NULL	NULL	NULL	brain energy metabolism	Process	alterations in	suggest					statement 1	Process				NULL	mitochondrial respiratory chain	NULL	NULL	NULL	NULL	NULL	NULL	Alterations in mitochondrial morphometry, brain energy metabolism, and enzymatic activity in the mitochondrial respiratory chain suggest a mitochondrial dysfunction in schizophrenia that could be related to the genetic characteristics of mtDNA. 	topic_sch
74168	5	355059	5	NULL	NULL	NULL	NULL	enzymatic activity	Process	alterations in	suggest					statement 1	Process				NULL	mitochondrial respiratory chain	NULL	NULL	NULL	NULL	NULL	NULL	Alterations in mitochondrial morphometry, brain energy metabolism, and enzymatic activity in the mitochondrial respiratory chain suggest a mitochondrial dysfunction in schizophrenia that could be related to the genetic characteristics of mtDNA. 	topic_sch
74169	1	355060	5	NULL	NULL	0	NULL	mtDNA	NucleicAcid		is involved in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, evidence of maternal inheritance and the presence of schizophrenia symptoms in patients suffering from a mitochondrial disorder related to an mtDNA mutation suggest that mtDNA is involved in schizophrenia	topic_sch
74170	2	355060	5	NULL	NULL	0	NULL	mitochondrial disorder	MedicalFinding		is related to					mtDNA	NucleicAcid	mutation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, evidence of maternal inheritance and the presence of schizophrenia symptoms in patients suffering from a mitochondrial disorder related to an mtDNA mutation suggest that mtDNA is involved in schizophrenia	topic_sch
74171	3	355060	5	NULL	NULL	NULL	NULL	maternal inheritance	Process		is evident in					mitochondrial disorder	MedicalFinding	patients of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Moreover, evidence of maternal inheritance and the presence of schizophrenia symptoms in patients suffering from a mitochondrial disorder related to an mtDNA mutation suggest that mtDNA is involved in schizophrenia	topic_sch
74172	4	355060	5	NULL	NULL	0	NULL	schizophrenia	MedicalFinding	presence of;;symptoms of	is present in					mitochondrial disorder	MedicalFinding	patients of			NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, evidence of maternal inheritance and the presence of schizophrenia symptoms in patients suffering from a mitochondrial disorder related to an mtDNA mutation suggest that mtDNA is involved in schizophrenia	topic_sch
75556	1	355062	7	NULL	NULL	0	NULL	Bipolar I disorder	MedicalFinding		sub-diagnosis of					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar I disorder is a sub-diagnosis of bipolar disorder that is characterized by at least one manic or mixed episode.	topic_bd
75557	2	355062	7	NULL	NULL	0	NULL	Bipolar I disorder	MedicalFinding		is characterized by					manic episode	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar I disorder is a sub-diagnosis of bipolar disorder that is characterized by at least one manic or mixed episode.	topic_bd
75558	3	355062	7	NULL	NULL	0	NULL	Bipolar I disorder	MedicalFinding		is characterized by					mixed episode	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar I disorder is a sub-diagnosis of bipolar disorder that is characterized by at least one manic or mixed episode.	topic_bd
75559	4	355062	7	NULL	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar I disorder is a sub-diagnosis of bipolar disorder that is characterized by at least one manic or mixed episode.	topic_bd
75413	1	355063	11	NULL	NULL	0	NULL	hlorhexidine	Chemical		is a type of 					chemical antiseptic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	hlorhexidine is a chemical antiseptic. It is effective on both Gram-positive and Gram-negative bacteria, although it is less effective with some Gram-negative bacteria. It has both bactericidal as well as bacteriostatic mechanisms of action,	topic_mrs
75414	2	355063	11	NULL	NULL	0	NULL	hlorhexidine	Chemical		is effective on					Gram-positive bacteria	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	hlorhexidine is a chemical antiseptic. It is effective on both Gram-positive and Gram-negative bacteria, although it is less effective with some Gram-negative bacteria. It has both bactericidal as well as bacteriostatic mechanisms of action,	topic_mrs
75415	3	355063	11	NULL	NULL	0	NULL	hlorhexidine	Chemical		is effective on		may			Gram-negative bacteria	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	hlorhexidine is a chemical antiseptic. It is effective on both Gram-positive and Gram-negative bacteria, although it is less effective with some Gram-negative bacteria. It has both bactericidal as well as bacteriostatic mechanisms of action,	topic_mrs
75416	4	355063	11	NULL	NULL	0	NULL	hlorhexidine	Chemical		acts as					bactericidal 	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	hlorhexidine is a chemical antiseptic. It is effective on both Gram-positive and Gram-negative bacteria, although it is less effective with some Gram-negative bacteria. It has both bactericidal as well as bacteriostatic mechanisms of action,	topic_mrs
75417	5	355063	11	NULL	NULL	0	NULL	hlorhexidine	Chemical		acts as					bacteriostatic	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	hlorhexidine is a chemical antiseptic. It is effective on both Gram-positive and Gram-negative bacteria, although it is less effective with some Gram-negative bacteria. It has both bactericidal as well as bacteriostatic mechanisms of action,	topic_mrs
75418	1	355065	11	NULL	NULL	0	NULL	 tea tree oil	Chemical		is a type of 					 antiseptic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Proponents believe tea tree oil is an antiseptic and use it to fight germs. It has been used to treat cuts, minor burns, athlete's foot, and insect bites. Some claim it can treat bacterial and fungal skin infections, wound infections, gum infections, acne, head lice, eczema, vaginal yeast infections, colds, pneumonia, and other respiratory illnesses.	topic_mrs
75419	2	355065	11	NULL	NULL	0	NULL	tea tree oil	Chemical		use to 					fight germs	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Proponents believe tea tree oil is an antiseptic and use it to fight germs. It has been used to treat cuts, minor burns, athlete's foot, and insect bites. Some claim it can treat bacterial and fungal skin infections, wound infections, gum infections, acne, head lice, eczema, vaginal yeast infections, colds, pneumonia, and other respiratory illnesses.	topic_mrs
75420	3	355065	11	NULL	NULL	0	NULL	tea tree oil	Chemical		 treat					cuts	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Proponents believe tea tree oil is an antiseptic and use it to fight germs. It has been used to treat cuts, minor burns, athlete's foot, and insect bites. Some claim it can treat bacterial and fungal skin infections, wound infections, gum infections, acne, head lice, eczema, vaginal yeast infections, colds, pneumonia, and other respiratory illnesses.	topic_mrs
75421	4	355065	11	NULL	NULL	0	NULL	tea tree oil	Chemical		treats					minor burns	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Proponents believe tea tree oil is an antiseptic and use it to fight germs. It has been used to treat cuts, minor burns, athlete's foot, and insect bites. Some claim it can treat bacterial and fungal skin infections, wound infections, gum infections, acne, head lice, eczema, vaginal yeast infections, colds, pneumonia, and other respiratory illnesses.	topic_mrs
75422	5	355065	11	NULL	NULL	0	NULL	tea tree oil	Chemical		treats					athlete's foot	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Proponents believe tea tree oil is an antiseptic and use it to fight germs. It has been used to treat cuts, minor burns, athlete's foot, and insect bites. Some claim it can treat bacterial and fungal skin infections, wound infections, gum infections, acne, head lice, eczema, vaginal yeast infections, colds, pneumonia, and other respiratory illnesses.	topic_mrs
75423	6	355065	11	NULL	NULL	0	NULL	tea tree oil	Chemical		treats					insect bites	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Proponents believe tea tree oil is an antiseptic and use it to fight germs. It has been used to treat cuts, minor burns, athlete's foot, and insect bites. Some claim it can treat bacterial and fungal skin infections, wound infections, gum infections, acne, head lice, eczema, vaginal yeast infections, colds, pneumonia, and other respiratory illnesses.	topic_mrs
75424	7	355065	11	NULL	NULL	0	NULL	tea tree oil	Chemical		treat		may			skin infections	Process	bacterial;;fungal 			NULL		0	NULL	NULL	NULL	NULL	NULL	Proponents believe tea tree oil is an antiseptic and use it to fight germs. It has been used to treat cuts, minor burns, athlete's foot, and insect bites. Some claim it can treat bacterial and fungal skin infections, wound infections, gum infections, acne, head lice, eczema, vaginal yeast infections, colds, pneumonia, and other respiratory illnesses.	topic_mrs
75425	8	355065	11	NULL	NULL	0	NULL	tea tree oil	Chemical		treats		may			wound infections	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Proponents believe tea tree oil is an antiseptic and use it to fight germs. It has been used to treat cuts, minor burns, athlete's foot, and insect bites. Some claim it can treat bacterial and fungal skin infections, wound infections, gum infections, acne, head lice, eczema, vaginal yeast infections, colds, pneumonia, and other respiratory illnesses.	topic_mrs
75426	9	355065	11	NULL	NULL	0	NULL	tea tree oil	Chemical		treats		may			 gum infections	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Proponents believe tea tree oil is an antiseptic and use it to fight germs. It has been used to treat cuts, minor burns, athlete's foot, and insect bites. Some claim it can treat bacterial and fungal skin infections, wound infections, gum infections, acne, head lice, eczema, vaginal yeast infections, colds, pneumonia, and other respiratory illnesses.	topic_mrs
75427	10	355065	11	NULL	NULL	0	NULL	tea tree oil	Chemical		treats		may			 acne	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Proponents believe tea tree oil is an antiseptic and use it to fight germs. It has been used to treat cuts, minor burns, athlete's foot, and insect bites. Some claim it can treat bacterial and fungal skin infections, wound infections, gum infections, acne, head lice, eczema, vaginal yeast infections, colds, pneumonia, and other respiratory illnesses.	topic_mrs
75428	11	355065	11	NULL	NULL	0	NULL	tea tree oil	Chemical		treats		may			head lice	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Proponents believe tea tree oil is an antiseptic and use it to fight germs. It has been used to treat cuts, minor burns, athlete's foot, and insect bites. Some claim it can treat bacterial and fungal skin infections, wound infections, gum infections, acne, head lice, eczema, vaginal yeast infections, colds, pneumonia, and other respiratory illnesses.	topic_mrs
75429	12	355065	11	NULL	NULL	0	NULL	tea tree oil	Chemical		treats		may			eczema	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Proponents believe tea tree oil is an antiseptic and use it to fight germs. It has been used to treat cuts, minor burns, athlete's foot, and insect bites. Some claim it can treat bacterial and fungal skin infections, wound infections, gum infections, acne, head lice, eczema, vaginal yeast infections, colds, pneumonia, and other respiratory illnesses.	topic_mrs
75430	13	355065	11	NULL	NULL	0	NULL	tea tree oil	Chemical		treats		may			vaginal infections	Process	 yeast 			NULL		0	NULL	NULL	NULL	NULL	NULL	Proponents believe tea tree oil is an antiseptic and use it to fight germs. It has been used to treat cuts, minor burns, athlete's foot, and insect bites. Some claim it can treat bacterial and fungal skin infections, wound infections, gum infections, acne, head lice, eczema, vaginal yeast infections, colds, pneumonia, and other respiratory illnesses.	topic_mrs
75431	14	355065	11	NULL	NULL	0	NULL	tea tree oil	Chemical		treats		may			colds	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Proponents believe tea tree oil is an antiseptic and use it to fight germs. It has been used to treat cuts, minor burns, athlete's foot, and insect bites. Some claim it can treat bacterial and fungal skin infections, wound infections, gum infections, acne, head lice, eczema, vaginal yeast infections, colds, pneumonia, and other respiratory illnesses.	topic_mrs
75432	15	355065	11	NULL	NULL	0	NULL	tea tree oil	Chemical		treats		may			pneumonia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Proponents believe tea tree oil is an antiseptic and use it to fight germs. It has been used to treat cuts, minor burns, athlete's foot, and insect bites. Some claim it can treat bacterial and fungal skin infections, wound infections, gum infections, acne, head lice, eczema, vaginal yeast infections, colds, pneumonia, and other respiratory illnesses.	topic_mrs
75433	16	355065	11	NULL	NULL	0	NULL	tea tree oil	Chemical		treats		may			respiratory illnesses	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Proponents believe tea tree oil is an antiseptic and use it to fight germs. It has been used to treat cuts, minor burns, athlete's foot, and insect bites. Some claim it can treat bacterial and fungal skin infections, wound infections, gum infections, acne, head lice, eczema, vaginal yeast infections, colds, pneumonia, and other respiratory illnesses.	topic_mrs
74173	1	355066	5	NULL	NULL	0	NULL	savantism	MedicalFinding		is a form of					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	People with a form of autism, called savantism, have exceptional skills in specific areas such as music, art, and numbers. People with savantism are able to perform these skills without lessons or practice	topic_aut
74174	2	355066	5	NULL	NULL	0	NULL	savants	GroupOfPeople		is skilled in		exceptionally			music	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	People with a form of autism, called savantism, have exceptional skills in specific areas such as music, art, and numbers. People with savantism are able to perform these skills without lessons or practice	topic_aut
74175	3	355066	5	NULL	NULL	0	NULL	savants	GroupOfPeople		is skilled in		exceptionally			art	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	People with a form of autism, called savantism, have exceptional skills in specific areas such as music, art, and numbers. People with savantism are able to perform these skills without lessons or practice	topic_aut
74176	4	355066	5	NULL	NULL	0	NULL	savants	GroupOfPeople		is skilled in		exceptionally			numbers	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	People with a form of autism, called savantism, have exceptional skills in specific areas such as music, art, and numbers. People with savantism are able to perform these skills without lessons or practice	topic_aut
75434	1	355068	11	NULL	NULL	0	NULL	Panton-Valentine leukocidin	Chemical		is					PVL	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Panton-Valentine leukocidin (PVL) is a cytotoxin—one of the β-pore-forming toxins. The presence of PVL is associated with increased virulence of certain strains (isolates) of Staphylococcus aureus. 	topic_mrs
75435	2	355068	11	NULL	NULL	NULL	NULL	Panton-Valentine leukocidin	Chemical		is a type of 					 cytotoxin	Chemical	β-pore-forming			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Panton-Valentine leukocidin (PVL) is a cytotoxin—one of the β-pore-forming toxins. The presence of PVL is associated with increased virulence of certain strains (isolates) of Staphylococcus aureus. 	topic_mrs
75436	3	355068	11	NULL	NULL	0	NULL	Panton-Valentine leukocidin	Chemical		increased		may			virulence	PhysicalPhenomenon	Staphylococcus aureus			NULL		0	NULL	NULL	NULL	NULL	NULL	Panton-Valentine leukocidin (PVL) is a cytotoxin—one of the β-pore-forming toxins. The presence of PVL is associated with increased virulence of certain strains (isolates) of Staphylococcus aureus. 	topic_mrs
75437	1	355069	11	NULL	NULL	0	NULL	community-associated Methicillin-resistant Staphylococcus aureus	Organism		is					CA-MRSA	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	It is present in the majority of community-associated Methicillin-resistant Staphylococcus aureus (CA-MRSA) isolates studied and is the cause of necrotic lesions involving the skin or mucosa, including necrotic hemorrhagic pneumonia. 	topic_mrs
75438	2	355069	11	NULL	NULL	0	NULL	community-associated Methicillin-resistant Staphylococcus aureus	Organism		cause					necrotic lesions	Process	skin;;mucosa			NULL		0	NULL	NULL	NULL	NULL	NULL	It is present in the majority of community-associated Methicillin-resistant Staphylococcus aureus (CA-MRSA) isolates studied and is the cause of necrotic lesions involving the skin or mucosa, including necrotic hemorrhagic pneumonia. 	topic_mrs
75439	3	355069	11	NULL	NULL	0	NULL	community-associated Methicillin-resistant Staphylococcus aureus	Organism		cause					necrotic hemorrhagic pneumonia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	It is present in the majority of community-associated Methicillin-resistant Staphylococcus aureus (CA-MRSA) isolates studied and is the cause of necrotic lesions involving the skin or mucosa, including necrotic hemorrhagic pneumonia. 	topic_mrs
76352	1	355070	11	NULL	NULL	0	NULL	Tea tree oil	Chemical		is also known as					melaleuca oil	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Tea tree oil, or melaleuca oil, is a pale yellow colour to nearly clear essential oil with a fresh camphoraceous odor.[	topic_mrs
76353	2	355070	11	NULL	NULL	0	NULL	Tea tree oil	Chemical		colored 					pale yellow	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Tea tree oil, or melaleuca oil, is a pale yellow colour to nearly clear essential oil with a fresh camphoraceous odor.[	topic_mrs
76354	3	355070	11	NULL	NULL	0	NULL	Tea tree oil	Chemical		is a type of 					essential oil 	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Tea tree oil, or melaleuca oil, is a pale yellow colour to nearly clear essential oil with a fresh camphoraceous odor.[	topic_mrs
76355	4	355070	11	NULL	NULL	0	NULL	Tea tree oil	Chemical		has a					fresh camphoraceous odor	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Tea tree oil, or melaleuca oil, is a pale yellow colour to nearly clear essential oil with a fresh camphoraceous odor.[	topic_mrs
75440	1	355071	11	NULL	NULL	0	NULL	Lemongrass oil	Chemical		is a type of 					pesticide	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Lemongrass oil is used as a pesticide and a preservative. Research shows that lemongrass oil has anti-fungal properties	topic_mrs
75441	2	355071	11	NULL	NULL	0	NULL	Lemongrass oil	Chemical		is a type of 					preservative	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Lemongrass oil is used as a pesticide and a preservative. Research shows that lemongrass oil has anti-fungal properties	topic_mrs
75442	3	355071	11	NULL	NULL	NULL	NULL	lemongrass oil 	Chemical		act as					anti-fungal	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Lemongrass oil is used as a pesticide and a preservative. Research shows that lemongrass oil has anti-fungal properties	topic_mrs
76358	1	355073	11	NULL	NULL	0	NULL	Lincosamides	Chemical		are a class of					antibiotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Lincosamides (eg. lincomycin, clindamycin) are a class of antibiotics. NULL	topic_mrs
76359	2	355073	11	NULL	NULL	0	NULL	lincomycin	Chemical		is a type of 					Lincosamides	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Lincosamides (eg. lincomycin, clindamycin) are a class of antibiotics. NULL	topic_mrs
76360	3	355073	11	NULL	NULL	0	NULL	clindamycin	Chemical		is a type of 					Lincosamides	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Lincosamides (eg. lincomycin, clindamycin) are a class of antibiotics. NULL	topic_mrs
74177	1	355074	5	NULL	NULL	NULL	NULL	fT	GP		is implicated in					social development	MentalProcess				NULL		NULL	NULL	NULL	NULL	NULL	NULL	fT was also positively correlated with restricted interests in boys. CONCLUSIONS: These findings implicate fT in both social development and attentional focus. They may also have implications for understanding the sex ratio in autism	topic_aut
74178	2	355074	5	NULL	NULL	0	NULL	fT	GP		is implicated in					attentional focus	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	fT was also positively correlated with restricted interests in boys. CONCLUSIONS: These findings implicate fT in both social development and attentional focus. They may also have implications for understanding the sex ratio in autism	topic_aut
74179	3	355074	5	NULL	NULL	0	NULL	fT	GP		is implicated in					autism	MedicalFinding	understanding of;;sex ratio in			NULL		0	NULL	NULL	NULL	NULL	NULL	fT was also positively correlated with restricted interests in boys. CONCLUSIONS: These findings implicate fT in both social development and attentional focus. They may also have implications for understanding the sex ratio in autism	topic_aut
74180	2	355075	5	NULL	NULL	0	NULL	fT	GP		correlates with		positively			statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	fT was also positively correlated with restricted interests in boys. 	topic_aut
74181	1	355075	5	NULL	NULL	NULL	NULL	restricted interests	MentalProcess		is observed in					boys	Organism				NULL		NULL	NULL	NULL	NULL	NULL	NULL	fT was also positively correlated with restricted interests in boys. 	topic_aut
74182	1	355076	5	NULL	NULL	NULL	NULL	ASD children	GroupOfPeople		engage in					rocking	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Many children with ASD engage in repetitive movements such as rocking and twirling, or in self-abusive behavior such as biting or head-banging	topic_aut
74183	2	355076	5	NULL	NULL	0	NULL	ASD children	GroupOfPeople		engage in					twirling	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Many children with ASD engage in repetitive movements such as rocking and twirling, or in self-abusive behavior such as biting or head-banging	topic_aut
74184	3	355076	5	NULL	NULL	0	NULL	rocking	MedicalFinding		is a type of					repetitive movement	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Many children with ASD engage in repetitive movements such as rocking and twirling, or in self-abusive behavior such as biting or head-banging	topic_aut
74185	4	355076	5	NULL	NULL	0	NULL	twirling	MedicalFinding		is a type of					repetitive movement	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Many children with ASD engage in repetitive movements such as rocking and twirling, or in self-abusive behavior such as biting or head-banging	topic_aut
74186	5	355076	5	NULL	NULL	0	NULL	ASD children	GroupOfPeople		engage in					biting	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Many children with ASD engage in repetitive movements such as rocking and twirling, or in self-abusive behavior such as biting or head-banging	topic_aut
74187	6	355076	5	NULL	NULL	0	NULL	ASD children	GroupOfPeople		engage in					head-banging	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Many children with ASD engage in repetitive movements such as rocking and twirling, or in self-abusive behavior such as biting or head-banging	topic_aut
74188	7	355076	5	NULL	NULL	0	NULL	biting	MedicalFinding		is a type of					self-abusive behaviour	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Many children with ASD engage in repetitive movements such as rocking and twirling, or in self-abusive behavior such as biting or head-banging	topic_aut
74189	8	355076	5	NULL	NULL	0	NULL	head-banging	MedicalFinding		is a type of					self-abusive behaviour	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Many children with ASD engage in repetitive movements such as rocking and twirling, or in self-abusive behavior such as biting or head-banging	topic_aut
74190	9	355076	5	NULL	NULL	0	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Many children with ASD engage in repetitive movements such as rocking and twirling, or in self-abusive behavior such as biting or head-banging	topic_aut
74194	1	355078	5	NULL	NULL	0	NULL	ASD children	GroupOfPeople		is at risk of		higher			Fragile X syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Children with ASD appear to have a higher than normal risk for certain co-occurring conditions, including Fragile X syndrome (which causes mental retardation), tuberous sclerosis (in which tumors grow on the brain), epileptic seizures, Tourette syndrome, learning disabilities, and attention deficit disorder.  About 20 to 30 percent of children with ASD develop epilepsy by the time they reach adulthood	topic_aut
74195	2	355078	5	NULL	NULL	0	NULL	Fragile X syndrome	MedicalFinding		causes					mental retardation	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Children with ASD appear to have a higher than normal risk for certain co-occurring conditions, including Fragile X syndrome (which causes mental retardation), tuberous sclerosis (in which tumors grow on the brain), epileptic seizures, Tourette syndrome, learning disabilities, and attention deficit disorder.  About 20 to 30 percent of children with ASD develop epilepsy by the time they reach adulthood	topic_aut
74196	3	355078	5	NULL	NULL	0	NULL	ASD children	GroupOfPeople		is at risk of		higher			tuberous sclerosis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Children with ASD appear to have a higher than normal risk for certain co-occurring conditions, including Fragile X syndrome (which causes mental retardation), tuberous sclerosis (in which tumors grow on the brain), epileptic seizures, Tourette syndrome, learning disabilities, and attention deficit disorder.  About 20 to 30 percent of children with ASD develop epilepsy by the time they reach adulthood	topic_aut
74198	4	355078	5	NULL	NULL	0	NULL	tuberous sclerosis	MedicalFinding		causes					tumors	MedicalFinding	growth of			NULL	brain	0	NULL	NULL	NULL	NULL	NULL	Children with ASD appear to have a higher than normal risk for certain co-occurring conditions, including Fragile X syndrome (which causes mental retardation), tuberous sclerosis (in which tumors grow on the brain), epileptic seizures, Tourette syndrome, learning disabilities, and attention deficit disorder.  About 20 to 30 percent of children with ASD develop epilepsy by the time they reach adulthood	topic_aut
74199	5	355078	5	NULL	NULL	0	NULL	ASD children	GroupOfPeople		is at risk of		higher			epileptic seizures	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Children with ASD appear to have a higher than normal risk for certain co-occurring conditions, including Fragile X syndrome (which causes mental retardation), tuberous sclerosis (in which tumors grow on the brain), epileptic seizures, Tourette syndrome, learning disabilities, and attention deficit disorder.  About 20 to 30 percent of children with ASD develop epilepsy by the time they reach adulthood	topic_aut
74200	6	355078	5	NULL	NULL	0	NULL	ASD children	GroupOfPeople		is at risk of		higher			Tourette syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Children with ASD appear to have a higher than normal risk for certain co-occurring conditions, including Fragile X syndrome (which causes mental retardation), tuberous sclerosis (in which tumors grow on the brain), epileptic seizures, Tourette syndrome, learning disabilities, and attention deficit disorder.  About 20 to 30 percent of children with ASD develop epilepsy by the time they reach adulthood	topic_aut
74201	7	355078	5	NULL	NULL	0	NULL	ASD children	GroupOfPeople		is at risk of		higher			learning disabilities	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Children with ASD appear to have a higher than normal risk for certain co-occurring conditions, including Fragile X syndrome (which causes mental retardation), tuberous sclerosis (in which tumors grow on the brain), epileptic seizures, Tourette syndrome, learning disabilities, and attention deficit disorder.  About 20 to 30 percent of children with ASD develop epilepsy by the time they reach adulthood	topic_aut
74202	8	355078	5	NULL	NULL	0	NULL	ASD children	GroupOfPeople		is at risk of		higher			attention deficit disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Children with ASD appear to have a higher than normal risk for certain co-occurring conditions, including Fragile X syndrome (which causes mental retardation), tuberous sclerosis (in which tumors grow on the brain), epileptic seizures, Tourette syndrome, learning disabilities, and attention deficit disorder.  About 20 to 30 percent of children with ASD develop epilepsy by the time they reach adulthood	topic_aut
74203	9	355078	5	NULL	NULL	0	NULL	ASD children	GroupOfPeople		develops					epilepsy	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Children with ASD appear to have a higher than normal risk for certain co-occurring conditions, including Fragile X syndrome (which causes mental retardation), tuberous sclerosis (in which tumors grow on the brain), epileptic seizures, Tourette syndrome, learning disabilities, and attention deficit disorder.  About 20 to 30 percent of children with ASD develop epilepsy by the time they reach adulthood	topic_aut
74204	10	355078	5	NULL	NULL	0	NULL	statement 9	Process		occurs before					adulthood	Time				NULL		0	NULL	NULL	NULL	NULL	NULL	Children with ASD appear to have a higher than normal risk for certain co-occurring conditions, including Fragile X syndrome (which causes mental retardation), tuberous sclerosis (in which tumors grow on the brain), epileptic seizures, Tourette syndrome, learning disabilities, and attention deficit disorder.  About 20 to 30 percent of children with ASD develop epilepsy by the time they reach adulthood	topic_aut
74206	1	355079	5	NULL	NULL	0	NULL	serotonin	Chemical	abnormal levels of 	is present in					ASD patients	GroupOfPeople	brain of			NULL		0	NULL	NULL	NULL	NULL	NULL	Other studies suggest that people with ASD have abnormal levels of serotonin or other neurotransmitters in the brain	topic_aut
74207	2	355079	5	NULL	NULL	0	NULL	neurotransmitters	Chemical	abnormal levels of	is present in					ASD patients	GroupOfPeople	brain of			NULL		0	NULL	NULL	NULL	NULL	NULL	Other studies suggest that people with ASD have abnormal levels of serotonin or other neurotransmitters in the brain	topic_aut
74208	3	355079	5	NULL	NULL	0	NULL	serotonin	Chemical		is a type of					neurotransmitter	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Other studies suggest that people with ASD have abnormal levels of serotonin or other neurotransmitters in the brain	topic_aut
74209	1	355080	5	NULL	NULL	0	NULL	parental practices	AbstractConcept		not responsible for					ASD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The theory that parental practices are responsible for ASD has long been disproved. 	topic_aut
74210	1	355082	5	NULL	NULL	0	NULL	manic depression	MedicalFinding		is a type of					emotional disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Evidence also suggests that some emotional disorders, such as manic depression, occur more frequently than average in the families of people with ASD.	topic_aut
74211	2	355082	5	NULL	NULL	0	NULL	manic depression	MedicalFinding		occurs in		frequently			ASD people	GroupOfPeople	families of			NULL		0	NULL	NULL	NULL	NULL	NULL	Evidence also suggests that some emotional disorders, such as manic depression, occur more frequently than average in the families of people with ASD.	topic_aut
74212	1	355083	5	NULL	NULL	0	NULL	MET gene	GP		is involved in					brain	OrganismPart	development of			NULL		0	NULL	NULL	NULL	NULL	NULL	They found a single mutation in a gene called MET, which is known to be involved in brain development, regulation of the immune system and repair of the gastrointestinal system. All of these systems can be affected in children with autism.	topic_aut
74213	2	355083	5	NULL	NULL	0	NULL	MET gene	GP		is involved in					immune system	OrganismPart	regulation of			NULL		0	NULL	NULL	NULL	NULL	NULL	They found a single mutation in a gene called MET, which is known to be involved in brain development, regulation of the immune system and repair of the gastrointestinal system. All of these systems can be affected in children with autism.	topic_aut
74215	3	355083	5	NULL	NULL	0	NULL	MET gene	GP		is involved in					gastrointestinal system	OrganismPart	repair of			NULL		0	NULL	NULL	NULL	NULL	NULL	They found a single mutation in a gene called MET, which is known to be involved in brain development, regulation of the immune system and repair of the gastrointestinal system. All of these systems can be affected in children with autism.	topic_aut
74216	4	355083	5	NULL	NULL	0	NULL	brain	OrganismPart		is affected in					autistic children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	They found a single mutation in a gene called MET, which is known to be involved in brain development, regulation of the immune system and repair of the gastrointestinal system. All of these systems can be affected in children with autism.	topic_aut
74217	5	355083	5	NULL	NULL	0	NULL	immune system	OrganismPart		is affected in					autistic children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	They found a single mutation in a gene called MET, which is known to be involved in brain development, regulation of the immune system and repair of the gastrointestinal system. All of these systems can be affected in children with autism.	topic_aut
74218	6	355083	5	NULL	NULL	0	NULL	gastrointestinal system	OrganismPart		is affected in					autistic children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	They found a single mutation in a gene called MET, which is known to be involved in brain development, regulation of the immune system and repair of the gastrointestinal system. All of these systems can be affected in children with autism.	topic_aut
74219	1	355084	5	NULL	NULL	0	NULL	MET	GP		is					Mesenchymal epithelial transition factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	    MET (Mesenchymal epithelial transition factor), also known as hepatocyte growth factor receptor (HGFR) is a proto-oncogenic receptor tyrosine kinase	topic_aut
74220	2	355084	5	NULL	NULL	0	NULL	HGFR	GP		is					hepatocyte growth factor receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	    MET (Mesenchymal epithelial transition factor), also known as hepatocyte growth factor receptor (HGFR) is a proto-oncogenic receptor tyrosine kinase	topic_aut
74221	3	355084	5	NULL	NULL	0	NULL	MET	GP		is a synonym of					hepatocyte growth factor receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	    MET (Mesenchymal epithelial transition factor), also known as hepatocyte growth factor receptor (HGFR) is a proto-oncogenic receptor tyrosine kinase	topic_aut
74222	4	355084	5	NULL	NULL	0	NULL	MET	GP		is a type of					proto-oncogenic receptor tyrosine kinase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	    MET (Mesenchymal epithelial transition factor), also known as hepatocyte growth factor receptor (HGFR) is a proto-oncogenic receptor tyrosine kinase	topic_aut
74228	1	355086	5	NULL	NULL	NULL	NULL	television viewing	Process	early childhood	triggers		potentially			autism	MedicalFinding	onset of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	“The analysis shows that early childhood television viewing could be an environmental trigger for the onset of autism and strongly points to the need for more research by experts in the field of autism	topic_aut
74229	1	355087	5	NULL	NULL	0	NULL	autistic children	GroupOfPeople		is prone to					spontaneous mutations	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	It turned out that children with autism were much more likely than other kids to have these 'spontaneous' mutations	topic_aut
74230	2	355087	5	NULL	NULL	0	NULL	normal children	GroupOfPeople		is prone to					spontaneous mutations	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	It turned out that children with autism were much more likely than other kids to have these 'spontaneous' mutations	topic_aut
74231	3	355087	5	NULL	NULL	0	NULL	statement 1	Process		is more likely than					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	It turned out that children with autism were much more likely than other kids to have these 'spontaneous' mutations	topic_aut
74232	1	355088	5	NULL	NULL	0	NULL	oxytocin	GP		is a type of					hormone	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	For example, Sebat says one child in the study was missing a copy of the gene for oxytocin – a hormone that seems to influence social behavior.	topic_aut
74233	2	355088	5	NULL	NULL	0	NULL	oxytocin gene	GP		influence					social behavior	AbstractConcept				NULL		0	NULL	NULL	NULL	NULL	NULL	For example, Sebat says one child in the study was missing a copy of the gene for oxytocin – a hormone that seems to influence social behavior.	topic_aut
74234	1	355091	5	NULL	NULL	0	NULL	chromosome 16	Chromosome	variation of	is present in					autistic people	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	On Thursday, scientists reported that 1 percent of people with autism share a variation on chromosome 16	topic_aut
74235	1	355093	5	NULL	NULL	0	NULL	CNVs	Chromosome		over-represented in		heavily			autistic people	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	In the article the group reveals that a survey of 1,000 individuals with autism and 1,300 without showed that Copy Number Variants (CNVs) - sub-microscopic abnormalities in the chromosomes - are heavily over-represented in autistic people	topic_aut
74236	2	355093	5	NULL	NULL	0	NULL	CNVs	Chromosome		is					Copy Number Variants	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	In the article the group reveals that a survey of 1,000 individuals with autism and 1,300 without showed that Copy Number Variants (CNVs) - sub-microscopic abnormalities in the chromosomes - are heavily over-represented in autistic people	topic_aut
74237	3	355093	5	NULL	NULL	0	NULL	chromosomes	Chromosome	sub-microscopic abnormalities of	is known as					Copy Number Variants	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	In the article the group reveals that a survey of 1,000 individuals with autism and 1,300 without showed that Copy Number Variants (CNVs) - sub-microscopic abnormalities in the chromosomes - are heavily over-represented in autistic people	topic_aut
75443	1	355095	11	NULL	NULL	0	NULL	Linezolid	Chemical		is a type of 					synthetic antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Linezolid is a synthetic antibiotic used for the treatment of serious infections caused by Gram-positive bacteria that are resistant to several other antibiotics	topic_mrs
75444	2	355095	11	NULL	NULL	0	NULL	Gram-positive bacteria	Organism		cause					infections	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Linezolid is a synthetic antibiotic used for the treatment of serious infections caused by Gram-positive bacteria that are resistant to several other antibiotics	topic_mrs
75445	3	355095	11	NULL	NULL	0	NULL	Linezolid	Chemical		treats					statement 2					NULL		0	NULL	NULL	NULL	NULL	NULL	Linezolid is a synthetic antibiotic used for the treatment of serious infections caused by Gram-positive bacteria that are resistant to several other antibiotics	topic_mrs
75446	1	355096	11	NULL	NULL	0	NULL	S. aureus	Organism		colonizes					anterior nares	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	S. aureus most commonly colonizes the anterior nares (the nostrils), although the rest of the respiratory tract, opened wounds, intravenous catheters, and urinary tract are also potential sites for infection. Healthy individuals may carry MRSA asymptomatically for periods ranging from a few weeks to many years.	topic_mrs
75447	2	355096	11	NULL	NULL	0	NULL	anterior nares	OrganismPart		is					nostrils	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	S. aureus most commonly colonizes the anterior nares (the nostrils), although the rest of the respiratory tract, opened wounds, intravenous catheters, and urinary tract are also potential sites for infection. Healthy individuals may carry MRSA asymptomatically for periods ranging from a few weeks to many years.	topic_mrs
75448	3	355096	11	NULL	NULL	NULL	NULL	S. aureus	OrganismPart		infects					respiratory tract	OrganismPart				NULL		NULL	NULL	NULL	NULL	NULL	NULL	S. aureus most commonly colonizes the anterior nares (the nostrils), although the rest of the respiratory tract, opened wounds, intravenous catheters, and urinary tract are also potential sites for infection. Healthy individuals may carry MRSA asymptomatically for periods ranging from a few weeks to many years.	topic_mrs
75449	4	355096	11	NULL	NULL	NULL	NULL	S. aureus	Organism		infects					opened wounds	OrganismPart				NULL		NULL	NULL	NULL	NULL	NULL	NULL	S. aureus most commonly colonizes the anterior nares (the nostrils), although the rest of the respiratory tract, opened wounds, intravenous catheters, and urinary tract are also potential sites for infection. Healthy individuals may carry MRSA asymptomatically for periods ranging from a few weeks to many years.	topic_mrs
75450	5	355096	11	NULL	NULL	NULL	NULL	S. aureus	Organism		infects					intravenous catheters	MedicalProcedure				NULL		NULL	NULL	NULL	NULL	NULL	NULL	S. aureus most commonly colonizes the anterior nares (the nostrils), although the rest of the respiratory tract, opened wounds, intravenous catheters, and urinary tract are also potential sites for infection. Healthy individuals may carry MRSA asymptomatically for periods ranging from a few weeks to many years.	topic_mrs
75451	6	355096	11	NULL	NULL	NULL	NULL	S. aureus	Organism		infects					urinary tract	OrganismPart				NULL		NULL	NULL	NULL	NULL	NULL	NULL	S. aureus most commonly colonizes the anterior nares (the nostrils), although the rest of the respiratory tract, opened wounds, intravenous catheters, and urinary tract are also potential sites for infection. Healthy individuals may carry MRSA asymptomatically for periods ranging from a few weeks to many years.	topic_mrs
75452	7	355096	11	NULL	NULL	0	NULL	MRSA	Organism		colonizes		may			asymptomatically	Process	in Healthy individuals			NULL		0	NULL	NULL	NULL	NULL	NULL	S. aureus most commonly colonizes the anterior nares (the nostrils), although the rest of the respiratory tract, opened wounds, intravenous catheters, and urinary tract are also potential sites for infection. Healthy individuals may carry MRSA asymptomatically for periods ranging from a few weeks to many years.	topic_mrs
75453	1	355097	11	NULL	NULL	0	NULL	MRSA	Organism		progress to		may			topical symptoms	Process	initial			NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA may progress substantially within 24–48 hours of initial topical symptoms. After 72 hours MRSA can take hold in human tissues and eventually become resistant to treatment. The initial presentation of MRSA is small red bumps that resemble pimples, spider bites, or boils that may be accompanied by fever and occasionally rashes. 	topic_mrs
75454	2	355097	11	NULL	NULL	0	NULL	MRSA	Organism		presents					small red bumps	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA may progress substantially within 24–48 hours of initial topical symptoms. After 72 hours MRSA can take hold in human tissues and eventually become resistant to treatment. The initial presentation of MRSA is small red bumps that resemble pimples, spider bites, or boils that may be accompanied by fever and occasionally rashes. 	topic_mrs
75455	3	355097	11	NULL	NULL	0	NULL	statement 2	Process		accompanies					fever	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA may progress substantially within 24–48 hours of initial topical symptoms. After 72 hours MRSA can take hold in human tissues and eventually become resistant to treatment. The initial presentation of MRSA is small red bumps that resemble pimples, spider bites, or boils that may be accompanied by fever and occasionally rashes. 	topic_mrs
75456	4	355097	11	NULL	NULL	0	NULL	statement 2	Process		accompanies					 rashes	Process	occasionally			NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA may progress substantially within 24–48 hours of initial topical symptoms. After 72 hours MRSA can take hold in human tissues and eventually become resistant to treatment. The initial presentation of MRSA is small red bumps that resemble pimples, spider bites, or boils that may be accompanied by fever and occasionally rashes. 	topic_mrs
75457	1	355098	11	NULL	NULL	0	NULL	Gram-positive organism	Organism		causes					infections	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Daptomycin is a novel lipopeptide antibiotic used in the treatment of certain infections caused by Gram-positive organisms. 	topic_mrs
75458	2	355098	11	NULL	NULL	0	NULL	Daptomycin	Chemical		is a type of 					lipopeptide antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Daptomycin is a novel lipopeptide antibiotic used in the treatment of certain infections caused by Gram-positive organisms. 	topic_mrs
75459	3	355098	11	NULL	NULL	0	NULL	Daptomycin	Chemical		treats					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Daptomycin is a novel lipopeptide antibiotic used in the treatment of certain infections caused by Gram-positive organisms. 	topic_mrs
76361	1	355099	11	NULL	NULL	0	NULL	lipopeptide	Chemical		 consisting of					lipid	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	A lipopeptide is a molecule consisting of a lipid connected to a peptide. Certain lipopeptides are used as antibiotics.	topic_mrs
76362	2	355099	11	NULL	NULL	0	NULL	lipopeptide	Chemical		consisting of					peptide	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	A lipopeptide is a molecule consisting of a lipid connected to a peptide. Certain lipopeptides are used as antibiotics.	topic_mrs
76363	3	355099	11	NULL	NULL	0	NULL	statement 1	Chemical		connected to 					statement 2	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	A lipopeptide is a molecule consisting of a lipid connected to a peptide. Certain lipopeptides are used as antibiotics.	topic_mrs
76364	4	355099	11	NULL	NULL	0	NULL	lipopeptides	Chemical	Certain	are used as					antibiotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	A lipopeptide is a molecule consisting of a lipid connected to a peptide. Certain lipopeptides are used as antibiotics.	topic_mrs
75460	1	355100	11	NULL	NULL	NULL	NULL	bone	Organism part	infection of	is known as					Osteomyelitis	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Osteomyelitis simply means an infection of the bone or bone marrow.	topic_mrs
76622	2	355100	11	NULL	NULL	0	NULL	bone marrow	Organism part	infection of	is known as					osteomyelitis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Osteomyelitis simply means an infection of the bone or bone marrow.	topic_mrs
75575	1	355101	7	NULL	NULL	NULL	NULL	bipolar II/hypomania	MedicalFinding	rapid cycling	 increased risk in					Women	GroupOfPeople				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Most studies, but not all, report an almost equal gender ratio in the prevalence of bipolar disorder but the majority of studies do report an increased risk in women of bipolar II/hypomania, rapid cycling and mixed episodes.	topic_bd
75576	2	355101	7	NULL	NULL	NULL	NULL	bipolar II/hypomania	MedicalFinding	mixed episodes of	increased risk in					Women	GroupOfPeople				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Most studies, but not all, report an almost equal gender ratio in the prevalence of bipolar disorder but the majority of studies do report an increased risk in women of bipolar II/hypomania, rapid cycling and mixed episodes.	topic_bd
75577	1	355102	7	NULL	NULL	0	NULL	bipolar disorder	MedicalFinding		impacts					reproductive life events	MedicalFinding				NULL	Women	0	NULL	NULL	NULL	NULL	NULL	Unsurprisingly, however, perhaps the major distinction between men and women with bipolar disorder is the impact that reproductive life events, particularly childbirth, have on women with this diagnosis.	topic_bd
75578	1	355109	7	NULL	NULL	0	NULL	Geodon	Chemical		is a type of					antipsychotic medication	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Geodon (ziprasidone) is an antipsychotic medication. 	topic_bd
75579	2	355109	7	NULL	NULL	0	NULL	Geodon 	Chemical		is					ziprasidone	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Geodon (ziprasidone) is an antipsychotic medication. 	topic_bd
75580	1	355110	7	NULL	NULL	NULL	NULL	Geodon	Chemical		is used to treat					schizophrenia	MedicalFinding				NULL	adults	NULL	NULL	NULL	NULL	NULL	NULL	Geodon is used to treat schizophrenia and the manic symptoms of bipolar disorder (manic depression) in adults and children who are at least 10 years old.	topic_bd
75581	2	355110	7	NULL	NULL	0	NULL	Geodon	Chemical		is used to treat					bipolar disorder	MedicalFinding	manic symptoms of			NULL	adults	0	NULL	NULL	NULL	NULL	NULL	Geodon is used to treat schizophrenia and the manic symptoms of bipolar disorder (manic depression) in adults and children who are at least 10 years old.	topic_bd
75582	3	355110	7	NULL	NULL	NULL	NULL	Geodon	Chemical		is used to treat					schizophrenia	MedicalFinding				NULL	children	NULL	NULL	NULL	NULL	NULL	NULL	Geodon is used to treat schizophrenia and the manic symptoms of bipolar disorder (manic depression) in adults and children who are at least 10 years old.	topic_bd
75583	4	355110	7	NULL	NULL	NULL	NULL	Geodon	Chemical		is used to treat					bipolar disorder	MedicalFinding	manic symptoms of			NULL	children	NULL	NULL	NULL	NULL	NULL	NULL	Geodon is used to treat schizophrenia and the manic symptoms of bipolar disorder (manic depression) in adults and children who are at least 10 years old.	topic_bd
75584	5	355110	7	NULL	NULL	0	NULL	bipolar disorder	MedicalFinding		is a type of					manic depression	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Geodon is used to treat schizophrenia and the manic symptoms of bipolar disorder (manic depression) in adults and children who are at least 10 years old.	topic_bd
75585	1	355111	7	NULL	NULL	0	NULL	dysphoria	MedicalFinding		is a state of					feeling unhappy	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	dysphoria is actually very straightforward - a state of feeling unwell or unhappy.	topic_bd
75586	2	355111	7	NULL	NULL	0	NULL	dysphoria	MedicalFinding		is a state of					feeling unwell	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	dysphoria is actually very straightforward - a state of feeling unwell or unhappy.	topic_bd
75587	3	355111	7	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	dysphoria is actually very straightforward - a state of feeling unwell or unhappy.	topic_bd
75588	1	355112	7	NULL	NULL	0	NULL	Dysphoric depression	MedicalFinding		is a type of					mixed episode	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Dysphoric depression, which many people think of as a mixed episode, consists of "intrusions of hypomanic symptoms or hyperthymic traits into a retarded major depressive episode" (Merck). 	topic_bd
75589	2	355112	7	NULL	NULL	0	NULL	Dysphoric depression	MedicalFinding		consist of					hypomanic symptoms	MedicalFinding	intrusions of			NULL		0	NULL	NULL	NULL	NULL	NULL	Dysphoric depression, which many people think of as a mixed episode, consists of "intrusions of hypomanic symptoms or hyperthymic traits into a retarded major depressive episode" (Merck). 	topic_bd
75590	3	355112	7	NULL	NULL	0	NULL	Dysphoric depression	MedicalFinding		consist of					retarded major depressive episode	MedicalFinding	hyperthymic traits into 			NULL		0	NULL	NULL	NULL	NULL	NULL	Dysphoric depression, which many people think of as a mixed episode, consists of "intrusions of hypomanic symptoms or hyperthymic traits into a retarded major depressive episode" (Merck). 	topic_bd
75591	1	355115	7	NULL	NULL	0	NULL	Lithium	Chemical		cause					Thyroid Goiters	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	You need to know that Lithium can cause Thyroid Goiters. 	topic_bd
75592	1	355116	7	NULL	NULL	0	NULL	BP'ers	GroupOfPeople		have					trauma issues	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Since many BP'ers have trauma issues EDMR is helpful for resolving trauma and another common type is Dialectal Behavior Therapy.	topic_bd
75593	2	355116	7	NULL	NULL	0	NULL	EDMR	MedicalProcedure		is helpful for					trauma	MedicalFinding	resolving			NULL		0	NULL	NULL	NULL	NULL	NULL	Since many BP'ers have trauma issues EDMR is helpful for resolving trauma and another common type is Dialectal Behavior Therapy.	topic_bd
75594	3	355116	7	NULL	NULL	0	NULL	Dialectal Behavior Therapy	MedicalProcedure		is helpful for					trauma	MedicalFinding	resolving			NULL		0	NULL	NULL	NULL	NULL	NULL	Since many BP'ers have trauma issues EDMR is helpful for resolving trauma and another common type is Dialectal Behavior Therapy.	topic_bd
74238	1	355117	5	NULL	NULL	NULL	NULL	 D(2) receptor (D(2)R)	GP		is a subtype of					dopamine receptor	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Among the characterized dopamine receptor subtypes, D(2) receptor (D(2)R) and D(3) receptor (D(3)R) are the main targets of neuroleptics that are currently in use. In particular, D(3)R is closely related to the etiology of schizophrenia and drug addiction. 	topic_sch
74240	2	355117	5	NULL	NULL	0	NULL	D(3) receptor (D(3)R)	GP		is a subtype of					dopamine receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Among the characterized dopamine receptor subtypes, D(2) receptor (D(2)R) and D(3) receptor (D(3)R) are the main targets of neuroleptics that are currently in use. In particular, D(3)R is closely related to the etiology of schizophrenia and drug addiction. 	topic_sch
74241	3	355117	5	NULL	NULL	0	NULL	D(2) receptor (D(2)R)	GP		is a target of		main			neuroleptics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Among the characterized dopamine receptor subtypes, D(2) receptor (D(2)R) and D(3) receptor (D(3)R) are the main targets of neuroleptics that are currently in use. In particular, D(3)R is closely related to the etiology of schizophrenia and drug addiction. 	topic_sch
74242	4	355117	5	NULL	NULL	0	NULL	D(3) receptor (D(3)R)	GP		is a target of		main			neuroleptics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Among the characterized dopamine receptor subtypes, D(2) receptor (D(2)R) and D(3) receptor (D(3)R) are the main targets of neuroleptics that are currently in use. In particular, D(3)R is closely related to the etiology of schizophrenia and drug addiction. 	topic_sch
74243	5	355117	5	NULL	NULL	NULL	NULL	 D(3)R	GP		is related to		closely			schizophrenia	MedicalFinding	etiology of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Among the characterized dopamine receptor subtypes, D(2) receptor (D(2)R) and D(3) receptor (D(3)R) are the main targets of neuroleptics that are currently in use. In particular, D(3)R is closely related to the etiology of schizophrenia and drug addiction. 	topic_sch
74244	6	355117	5	NULL	NULL	NULL	NULL	 D(3)R	GP		is related to		closely			drug addiction	MentalProcess	etiology of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Among the characterized dopamine receptor subtypes, D(2) receptor (D(2)R) and D(3) receptor (D(3)R) are the main targets of neuroleptics that are currently in use. In particular, D(3)R is closely related to the etiology of schizophrenia and drug addiction. 	topic_sch
74245	1	355118	5	NULL	NULL	0	NULL	Clozapine	Chemical		delays					treatment resistant schizophrenia patients	GroupOfPeople	hospitalization of			NULL		0	NULL	NULL	NULL	NULL	NULL	Clozapine delays hospitalization in patients with treatment resistant schizophrenia if they are started on clozapine in the community or successfully discharged from hospital following their index admission.	topic_sch
74246	1	355119	5	NULL	NULL	0	NULL	Risperidone	Chemical		is a type of					antipsychotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Results demonstrated that antipsychotic treatment with Risperidone, Olanzapine or Aripiprazole in adolescents affected by Schizophrenia led to significant improvements in symptomatology.	topic_sch
74247	2	355119	5	NULL	NULL	0	NULL	Olanzapine	Chemical		is a type of					antipsychotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Results demonstrated that antipsychotic treatment with Risperidone, Olanzapine or Aripiprazole in adolescents affected by Schizophrenia led to significant improvements in symptomatology.	topic_sch
74248	3	355119	5	NULL	NULL	0	NULL	Aripiprazole	Chemical		is a type of					antipsychotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Results demonstrated that antipsychotic treatment with Risperidone, Olanzapine or Aripiprazole in adolescents affected by Schizophrenia led to significant improvements in symptomatology.	topic_sch
74249	5	355119	5	NULL	NULL	0	NULL	Risperidone	Chemical	treatment	leads to					statement 4	Process	significant improvements in;;symptomatology of			NULL		0	NULL	NULL	NULL	NULL	NULL	Results demonstrated that antipsychotic treatment with Risperidone, Olanzapine or Aripiprazole in adolescents affected by Schizophrenia led to significant improvements in symptomatology.	topic_sch
74250	4	355119	5	NULL	NULL	0	NULL	adolescents	GroupOfPeople		is affected by					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Results demonstrated that antipsychotic treatment with Risperidone, Olanzapine or Aripiprazole in adolescents affected by Schizophrenia led to significant improvements in symptomatology.	topic_sch
74251	6	355119	5	NULL	NULL	0	NULL	Olanzapine	Chemical	treatment	leads to					statement 4	Process	significant improvements in;;symptomatology of			NULL		0	NULL	NULL	NULL	NULL	NULL	Results demonstrated that antipsychotic treatment with Risperidone, Olanzapine or Aripiprazole in adolescents affected by Schizophrenia led to significant improvements in symptomatology.	topic_sch
74252	7	355119	5	NULL	NULL	0	NULL	Aripiprazole	Chemical	treatment	leads to					statement 4	Process	significant improvements in;;symptomatology of			NULL		0	NULL	NULL	NULL	NULL	NULL	Results demonstrated that antipsychotic treatment with Risperidone, Olanzapine or Aripiprazole in adolescents affected by Schizophrenia led to significant improvements in symptomatology.	topic_sch
74253	1	355120	5	NULL	NULL	0	NULL	schizophrenia people	GroupOfPeople		is at risk of					death	AbstractConcept	premature			NULL		0	NULL	NULL	NULL	NULL	NULL	People with schizophrenia show a two to threefold increased risk to die prematurely than those without schizophrenia. 	topic_sch
74254	2	355120	5	NULL	NULL	0	NULL	non-schizophrenia people	GroupOfPeople		is at risk of					death	AbstractConcept	premature			NULL		0	NULL	NULL	NULL	NULL	NULL	People with schizophrenia show a two to threefold increased risk to die prematurely than those without schizophrenia. 	topic_sch
74255	3	355120	5	NULL	NULL	0	NULL	statement 1	Process		is more likely than					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	People with schizophrenia show a two to threefold increased risk to die prematurely than those without schizophrenia. 	topic_sch
74256	1	355121	5	NULL	NULL	0	NULL	cardiac arrhythmia	MedicalFinding		plays a role in		potentially			schizophrenic patients	GroupOfPeople	sudden death of			NULL		0	NULL	NULL	NULL	NULL	NULL	The exact pathophysiological cause of sudden death in schizophrenia is unknown, but it is likely that cardiac arrhythmia and respiratory abnormalities play potential role.	topic_sch
74257	2	355121	5	NULL	NULL	0	NULL	respiratory abnormalities	MedicalFinding		plays a role in		potentially			schizophrenic patients	GroupOfPeople	sudden death of			NULL		0	NULL	NULL	NULL	NULL	NULL	The exact pathophysiological cause of sudden death in schizophrenia is unknown, but it is likely that cardiac arrhythmia and respiratory abnormalities play potential role.	topic_sch
74316	1	355122	5	NULL	NULL	0	NULL	hyperthyroidism	MedicalFinding	subclinical	is linked to					cardiovascular disease	MedicalFinding	increased risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	As subclinical hyperthyroidism has been linked with increased risk of cardiovascular disease and cerebella progressive atrophy has been observed in patients with schizophrenia, we propose in this paper that subclinical thyroid dysfunction and cerebella volume loss could be considered as new risk factor for sudden cardiac death in schizophrenia.	topic_sch
74317	2	355122	5	NULL	NULL	0	NULL	cerebella progressive atrophy	MedicalFinding		is observed in					schizophrenia patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	As subclinical hyperthyroidism has been linked with increased risk of cardiovascular disease and cerebella progressive atrophy has been observed in patients with schizophrenia, we propose in this paper that subclinical thyroid dysfunction and cerebella volume loss could be considered as new risk factor for sudden cardiac death in schizophrenia.	topic_sch
74318	3	355122	5	NULL	NULL	0	NULL	cardiac death	AbstractConcept	sudden	is observed in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	As subclinical hyperthyroidism has been linked with increased risk of cardiovascular disease and cerebella progressive atrophy has been observed in patients with schizophrenia, we propose in this paper that subclinical thyroid dysfunction and cerebella volume loss could be considered as new risk factor for sudden cardiac death in schizophrenia.	topic_sch
74319	4	355122	5	NULL	NULL	0	NULL	thyroid dysfunction	MedicalFinding	subclinical	is a risk factor for		possibly			statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	As subclinical hyperthyroidism has been linked with increased risk of cardiovascular disease and cerebella progressive atrophy has been observed in patients with schizophrenia, we propose in this paper that subclinical thyroid dysfunction and cerebella volume loss could be considered as new risk factor for sudden cardiac death in schizophrenia.	topic_sch
74320	5	355122	5	NULL	NULL	0	NULL	cerebella volume loss	MedicalFinding		is a risk factor for		possibly			statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	As subclinical hyperthyroidism has been linked with increased risk of cardiovascular disease and cerebella progressive atrophy has been observed in patients with schizophrenia, we propose in this paper that subclinical thyroid dysfunction and cerebella volume loss could be considered as new risk factor for sudden cardiac death in schizophrenia.	topic_sch
74258	1	355123	5	NULL	NULL	0	NULL	ADNP/ADNP2	GP	imbalance of;;expression of	impacts		may			schizophrenia	MedicalFinding	progression of			NULL		0	NULL	NULL	NULL	NULL	NULL	Imbalance in ADNP/ADNP2 expression in the schizophrenia brain may impact disease progression.	topic_sch
74259	1	355124	5	NULL	NULL	0	NULL	Akt1 isoform	GP		regulates					hippocampus	OrganismPart	 neuroplasticity of			NULL		0	NULL	NULL	NULL	NULL	NULL	Taken together, these results implicate the Akt1 isoform in regulating hippocampal neuroplasticity and cognition and in contributing to the etiology of schizophrenia.	topic_sch
74260	2	355124	5	NULL	NULL	0	NULL	Akt1 isoform	GP		regulates					cognition	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Taken together, these results implicate the Akt1 isoform in regulating hippocampal neuroplasticity and cognition and in contributing to the etiology of schizophrenia.	topic_sch
74261	3	355124	5	NULL	NULL	0	NULL	Akt1 isoform	GP		contribute to					schizophrenia	MedicalFinding	etiology of			NULL		0	NULL	NULL	NULL	NULL	NULL	Taken together, these results implicate the Akt1 isoform in regulating hippocampal neuroplasticity and cognition and in contributing to the etiology of schizophrenia.	topic_sch
74262	1	355126	5	NULL	NULL	0	NULL	drugs	Chemical	novel	counteracts					schizophrenia	MedicalFinding	cognitive deficits of 			NULL		0	NULL	NULL	NULL	NULL	NULL	This supports the proposal that suppression in GLU release might be a target for the development of novel drugs aimed at counteracting some aspects of cognitive deficits of schizophrenia.	topic_sch
74263	2	355126	5	NULL	NULL	0	NULL	GLU	GP	suppression of;;release of	is a target for		might be			statement 1	Process	development of			NULL		0	NULL	NULL	NULL	NULL	NULL	This supports the proposal that suppression in GLU release might be a target for the development of novel drugs aimed at counteracting some aspects of cognitive deficits of schizophrenia.	topic_sch
74264	1	355127	5	NULL	NULL	0	NULL	SLC6A3 A1343G polymorphism	AbstractConcept		is associated with					SCZ phenotype	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	Thus the SLC6A3 A1343G polymorphism was associated to the SCZ phenotype in the investigated sample.	topic_sch
74265	1	355128	5	NULL	NULL	0	NULL	depression	MedicalFinding		is associated with		significantly			schizophrenic persons	GroupOfPeople	nonadherence of			NULL		0	NULL	NULL	NULL	NULL	NULL	Depression and social support deficits were significantly associated with nonadherence in persons with schizophrenia.	topic_sch
74266	2	355128	5	NULL	NULL	0	NULL	social support	AbstractConcept	deficits of	is associated with		significantly			schizophrenic persons	GroupOfPeople	nonadherence of			NULL		0	NULL	NULL	NULL	NULL	NULL	Depression and social support deficits were significantly associated with nonadherence in persons with schizophrenia.	topic_sch
74267	1	355129	5	NULL	NULL	0	NULL	eye gaze	AbstractConcept	deficits of	occurs during					negative social interactions	AbstractConcept				NULL		0	NULL	NULL	NULL	NULL	NULL	Deficits in eye gaze during negative social interactions in patients with schizophrenia.	topic_sch
74268	2	355129	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					schizophrenic patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Deficits in eye gaze during negative social interactions in patients with schizophrenia.	topic_sch
74269	1	355130	5	NULL	NULL	0	NULL	Gsk-3	GP	altered activity of	is implicated in					diabetes	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Underscoring their biological significance, altered Gsk-3 activity has been implicated in diabetes, Alzheimers disease, schizophrenia, and bipolar disorder.	topic_sch
74270	2	355130	5	NULL	NULL	0	NULL	Gsk-3	GP	altered activity of	is implicated in					Alzheimers disease	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Underscoring their biological significance, altered Gsk-3 activity has been implicated in diabetes, Alzheimers disease, schizophrenia, and bipolar disorder.	topic_sch
74271	3	355130	5	NULL	NULL	0	NULL	Gsk-3	GP	altered activity of	is implicated in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Underscoring their biological significance, altered Gsk-3 activity has been implicated in diabetes, Alzheimers disease, schizophrenia, and bipolar disorder.	topic_sch
74272	4	355130	5	NULL	NULL	0	NULL	Gsk-3	GP	altered activity of	is implicated in					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Underscoring their biological significance, altered Gsk-3 activity has been implicated in diabetes, Alzheimers disease, schizophrenia, and bipolar disorder.	topic_sch
76365	1	355133	11	NULL	NULL	0	NULL	community-associated MRSA	Organism		causes					 infections	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Most infections caused by these community-associated (CA) MRSA appear to involve the skin	topic_mrs
76366	2	355133	11	NULL	NULL	0	NULL	statement 1	Process		involves					skin	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Most infections caused by these community-associated (CA) MRSA appear to involve the skin	topic_mrs
76367	1	355136	11	NULL	NULL	0	NULL	Alcohol	Chemical		is a type of 					surface sanitizer	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	alcohol-based hand sanitizers were placed in involved areas, Alcohol has been proven to be an effective surface sanitizer against MRSA	topic_mrs
76368	2	355136	11	NULL	NULL	0	NULL	Alcohol	Chemical		is effective against					MRSA	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	alcohol-based hand sanitizers were placed in involved areas, Alcohol has been proven to be an effective surface sanitizer against MRSA	topic_mrs
76369	1	355138	11	NULL	NULL	0	NULL	 MRSA	Organism		is a type of 					bacterium	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	These new evolutions of the MRSA bacterium have been dubbed Vancomycin intermediate-resistant Staphylococcus aureus (VISA).	topic_mrs
76370	2	355138	11	NULL	NULL	0	NULL	MRSA bacterium	Organism		is also known as					Vancomycin intermediate-resistant Staphylococcus aureus 	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	These new evolutions of the MRSA bacterium have been dubbed Vancomycin intermediate-resistant Staphylococcus aureus (VISA).	topic_mrs
76371	3	355138	11	NULL	NULL	0	NULL	Vancomycin intermediate-resistant Staphylococcus aureus 	Organism		is					VISA	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	These new evolutions of the MRSA bacterium have been dubbed Vancomycin intermediate-resistant Staphylococcus aureus (VISA).	topic_mrs
76372	1	355139	11	NULL	NULL	NULL	NULL	Staphylococcus aureus	Organism		cause					staph infections	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Staphylococcus aureus is a facultatively anaerobic, Gram-positive coccus and is the most common cause of staph infections. It is frequently part of the skin flora found in the nose and on skin. About 20% of the human population are long-term carriers of S. aureus.	topic_mrs
76373	2	355139	11	NULL	NULL	0	NULL	Staphylococcus aureus	Organism		is a part of					 skin flora	Organism	nose ;; skin			NULL		0	NULL	NULL	NULL	NULL	NULL	Staphylococcus aureus is a facultatively anaerobic, Gram-positive coccus and is the most common cause of staph infections. It is frequently part of the skin flora found in the nose and on skin. About 20% of the human population are long-term carriers of S. aureus.	topic_mrs
75595	1	355141	7	NULL	NULL	0	NULL	Seroquel	Chemical		is a type of					antipsychotic medication	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Seroquel (quetiapine) is an antipsychotic medication.	topic_bd
75596	2	355141	7	NULL	NULL	0	NULL	Seroquel	Chemical		is					quetiapine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Seroquel (quetiapine) is an antipsychotic medication.	topic_bd
75597	1	355142	7	NULL	NULL	NULL	NULL	quetiapine	Chemical		inhibits					brain nerves	Process	communication between			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Although the mechanism of action of quetiapine is unknown, like other anti-psychotics, it inhibits communication between nerves of the brain. It does this by blocking receptors on the nerves for several neurotransmitters, the chemicals that nerves use to communicate with each other. It is thought that its beneficial effect is due to blocking of the dopamine type 2 (D2) and serotonin type 2 (5-HT2) receptors. 	topic_bd
75598	2	355142	7	NULL	NULL	0	NULL	statement 1	Process		occur by					neurotransmitters	Chemical	blocking receptors of			NULL	nerves	0	NULL	NULL	NULL	NULL	NULL	Although the mechanism of action of quetiapine is unknown, like other anti-psychotics, it inhibits communication between nerves of the brain. It does this by blocking receptors on the nerves for several neurotransmitters, the chemicals that nerves use to communicate with each other. It is thought that its beneficial effect is due to blocking of the dopamine type 2 (D2) and serotonin type 2 (5-HT2) receptors. 	topic_bd
75599	3	355142	7	NULL	NULL	0	NULL	neurotransmitters	Chemical		helps in					nerves	OrganismPart	communication between			NULL		0	NULL	NULL	NULL	NULL	NULL	Although the mechanism of action of quetiapine is unknown, like other anti-psychotics, it inhibits communication between nerves of the brain. It does this by blocking receptors on the nerves for several neurotransmitters, the chemicals that nerves use to communicate with each other. It is thought that its beneficial effect is due to blocking of the dopamine type 2 (D2) and serotonin type 2 (5-HT2) receptors. 	topic_bd
75600	4	355142	7	NULL	NULL	0	NULL	quetiapine	Chemical		blocks					D2 receptors	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Although the mechanism of action of quetiapine is unknown, like other anti-psychotics, it inhibits communication between nerves of the brain. It does this by blocking receptors on the nerves for several neurotransmitters, the chemicals that nerves use to communicate with each other. It is thought that its beneficial effect is due to blocking of the dopamine type 2 (D2) and serotonin type 2 (5-HT2) receptors. 	topic_bd
75601	5	355142	7	NULL	NULL	0	NULL	quetiapine	Chemical		blocks					5-HT2 receptor	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Although the mechanism of action of quetiapine is unknown, like other anti-psychotics, it inhibits communication between nerves of the brain. It does this by blocking receptors on the nerves for several neurotransmitters, the chemicals that nerves use to communicate with each other. It is thought that its beneficial effect is due to blocking of the dopamine type 2 (D2) and serotonin type 2 (5-HT2) receptors. 	topic_bd
75602	6	355142	7	NULL	NULL	0	NULL	D2 receptor	GP		is					dopamine type 2 receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Although the mechanism of action of quetiapine is unknown, like other anti-psychotics, it inhibits communication between nerves of the brain. It does this by blocking receptors on the nerves for several neurotransmitters, the chemicals that nerves use to communicate with each other. It is thought that its beneficial effect is due to blocking of the dopamine type 2 (D2) and serotonin type 2 (5-HT2) receptors. 	topic_bd
75603	7	355142	7	NULL	NULL	NULL	NULL	5-HT2 receptor	GP		is					serotonin type 2 receptor	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Although the mechanism of action of quetiapine is unknown, like other anti-psychotics, it inhibits communication between nerves of the brain. It does this by blocking receptors on the nerves for several neurotransmitters, the chemicals that nerves use to communicate with each other. It is thought that its beneficial effect is due to blocking of the dopamine type 2 (D2) and serotonin type 2 (5-HT2) receptors. 	topic_bd
75604	8	355142	7	NULL	NULL	0	NULL	quetiapine	Chemical	beneficial effect of	is due to					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Although the mechanism of action of quetiapine is unknown, like other anti-psychotics, it inhibits communication between nerves of the brain. It does this by blocking receptors on the nerves for several neurotransmitters, the chemicals that nerves use to communicate with each other. It is thought that its beneficial effect is due to blocking of the dopamine type 2 (D2) and serotonin type 2 (5-HT2) receptors. 	topic_bd
75605	9	355142	7	NULL	NULL	0	NULL	quetiapine	Chemical	beneficial effect of	is due to					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Although the mechanism of action of quetiapine is unknown, like other anti-psychotics, it inhibits communication between nerves of the brain. It does this by blocking receptors on the nerves for several neurotransmitters, the chemicals that nerves use to communicate with each other. It is thought that its beneficial effect is due to blocking of the dopamine type 2 (D2) and serotonin type 2 (5-HT2) receptors. 	topic_bd
75606	1	355145	7	NULL	NULL	0	NULL	HIF-1α	GP	expression of	is associated with					VEGF	GP	expression of			NULL		0	NULL	NULL	NULL	NULL	NULL	HIF-1α expression is associated with VEGF expression and angiogenesis in colorectal carcinoma.	topic_ccc
75607	2	355145	7	NULL	NULL	0	NULL	HIF-1α	GP	expression of	is associated with					angiogenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	HIF-1α expression is associated with VEGF expression and angiogenesis in colorectal carcinoma.	topic_ccc
75608	3	355145	7	NULL	NULL	0	NULL	statement 1	Process		occur in					colorectal carcinoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	HIF-1α expression is associated with VEGF expression and angiogenesis in colorectal carcinoma.	topic_ccc
75609	4	355145	7	NULL	NULL	0	NULL	statement 2	Process		occur in					colorectal carcinoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	HIF-1α expression is associated with VEGF expression and angiogenesis in colorectal carcinoma.	topic_ccc
75633	1	355146	7	NULL	NULL	0	NULL	Neuroleptic	Chemical		refers to					antipsychotic drugs	Chemical	effects of			NULL		0	NULL	NULL	NULL	NULL	NULL	Neuroleptic: A term that refers to the effects of antipsychotic drugs on a patient, especially on his or her cognition and behavior.	topic_bd
75634	2	355146	7	NULL	NULL	0	NULL	statement 1	Process		effect					patients cognition	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Neuroleptic: A term that refers to the effects of antipsychotic drugs on a patient, especially on his or her cognition and behavior.	topic_bd
75635	3	355146	7	NULL	NULL	0	NULL	statement 1	Process		effect					patient behavior	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Neuroleptic: A term that refers to the effects of antipsychotic drugs on a patient, especially on his or her cognition and behavior.	topic_bd
75636	1	355147	7	NULL	NULL	0	NULL	TD	MedicalFinding	persistent	is seen among					neuroleptic-treated bipolar patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	There appears to be a significant risk of persistent TD among neuroleptic-treated bipolar patients	topic_bd
75637	1	355149	7	NULL	NULL	0	NULL	HIF-1α 	GP	expression of	is associated with					angiogenesis	Process				NULL	tumor tissue	0	NULL	NULL	NULL	NULL	NULL	 the expression of HIF-1α in tumor tissue is associated with angiogenesis and poor overall survival in patients with colorectal cancer	topic_ccc
75638	2	355149	7	NULL	NULL	0	NULL	HIF-1α 	GP	expression of	is associated with					poor survival	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 the expression of HIF-1α in tumor tissue is associated with angiogenesis and poor overall survival in patients with colorectal cancer	topic_ccc
75639	3	355149	7	NULL	NULL	0	NULL	statement 2	Process		occur in					colorectal cancer patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	 the expression of HIF-1α in tumor tissue is associated with angiogenesis and poor overall survival in patients with colorectal cancer	topic_ccc
75640	1	355150	7	NULL	NULL	0	NULL	 smokers	GroupOfPeople		increased risk of					colon cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Ever smokers have an increased risk of colon cancer, which appeared to be more pronounced in the proximal than the distal colon location.	topic_ccc
75641	2	355150	7	NULL	NULL	0	NULL	statement 1	Process		occur in the					proximal colon	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Ever smokers have an increased risk of colon cancer, which appeared to be more pronounced in the proximal than the distal colon location.	topic_ccc
75642	1	355151	7	NULL	NULL	0	NULL	euthymic	MedicalFinding		pertains to					normal mood	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	euthymic, pertaining to a normal mood in which the range of emotions is neither depressed nor highly elevated. NULL	topic_bd
75643	2	355151	7	NULL	NULL	NULL	NULL	euthymic	MedicalFinding		pertains to					depressed	MedicalFinding	emotions which is not			NULL		NULL	NULL	NULL	NULL	NULL	NULL	euthymic, pertaining to a normal mood in which the range of emotions is neither depressed nor highly elevated. NULL	topic_bd
75644	3	355151	7	NULL	NULL	0	NULL	euthymic	MedicalFinding		pertains to					highly elevated	Process	emotions which is not			NULL		0	NULL	NULL	NULL	NULL	NULL	euthymic, pertaining to a normal mood in which the range of emotions is neither depressed nor highly elevated. NULL	topic_bd
75645	4	355151	7	NULL	NULL	0	NULL	statement 2	Process		occur along with					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	euthymic, pertaining to a normal mood in which the range of emotions is neither depressed nor highly elevated. NULL	topic_bd
75646	1	355152	7	NULL	NULL	NULL	NULL	bipolar patients	GroupOfPeople		show					cognitive deficits 	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Previous studies have reported cognitive deficits on tasks of declarative memory in bipolar patients in the euthymic state.	topic_bd
75647	2	355152	7	NULL	NULL	0	NULL	statement 1	Process		occur in					euthymic state	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Previous studies have reported cognitive deficits on tasks of declarative memory in bipolar patients in the euthymic state.	topic_bd
75648	1	355153	7	NULL	NULL	0	NULL	Bipolar patients	MedicalFinding		does not perform for					declarative memory	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar patients performed worse than control subjects on a measure of declarative memory (California Verbal Learning Test) but did not differ from the performance of control subjects on either of the two procedural learning tasks (Pursuit Rotor Task and Star Mirror Task).	topic_bd
75649	1	355154	7	NULL	NULL	0	NULL	bipolar disorder persons	GroupOfPeople		has disturbed 					temporal lobe	OrganismPart	function of			NULL		0	NULL	NULL	NULL	NULL	NULL	These results suggest disturbed function of temporal lobe, but not basal ganglia, structures in persons with bipolar disorder.	topic_bd
75650	2	355154	7	NULL	NULL	0	NULL	bipolar disorder persons	GroupOfPeople		does not have					basal ganglia	MedicalFinding	disturbance function in			NULL		0	NULL	NULL	NULL	NULL	NULL	These results suggest disturbed function of temporal lobe, but not basal ganglia, structures in persons with bipolar disorder.	topic_bd
75651	1	355155	7	NULL	NULL	0	NULL	Physical exercise	PhysicalPhenomenon		maintains					cardiovascular function	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Physical exercise which maintains cardiovascular function can keep the endocrine system in "balance" and is imperative for people with bipolar expression.	topic_bd
75652	2	355155	7	NULL	NULL	0	NULL	statement 1	Process		balance					endocrine system	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Physical exercise which maintains cardiovascular function can keep the endocrine system in "balance" and is imperative for people with bipolar expression.	topic_bd
75653	3	355155	7	NULL	NULL	0	NULL	statement 1	Process		imperative for					bipolar expression 	MedicalFinding	people with			NULL		0	NULL	NULL	NULL	NULL	NULL	Physical exercise which maintains cardiovascular function can keep the endocrine system in "balance" and is imperative for people with bipolar expression.	topic_bd
75654	1	355156	7	NULL	NULL	NULL	NULL	PAPST1 transcripts	GP	 amounts of	is higher than					PAPST2 transcripts	GP	amounts of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	 The relative amount of PAPST1 transcripts was found to be higher than those of PAPST2 in colorectal cancerous tissues.	topic_ccc
75655	2	355156	7	NULL	NULL	0	NULL	statement 1	Process		occur in					colorectal cancerous tissues	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	 The relative amount of PAPST1 transcripts was found to be higher than those of PAPST2 in colorectal cancerous tissues.	topic_ccc
75656	1	355157	7	NULL	NULL	NULL	NULL	PAPS transporter genes	GP		reduce					cellular proteins	GP	extent of sulfation of			NULL	human colorectal carcinoma cells	NULL	NULL	NULL	NULL	NULL	NULL	RNA interference of either of the 2 PAPS transporter genes reduced the extent of sulfation of cellular proteins and cellular proliferation of DLD-1 human colorectal carcinoma cells.	topic_ccc
75657	2	355157	7	NULL	NULL	NULL	NULL	PAPS transporter genes	GP		reduce					DLD-1	Cell	extent of cellular proliferation of			NULL	human colorectal carcinoma cells	NULL	NULL	NULL	NULL	NULL	NULL	RNA interference of either of the 2 PAPS transporter genes reduced the extent of sulfation of cellular proteins and cellular proliferation of DLD-1 human colorectal carcinoma cells.	topic_ccc
74273	1	355158	5	NULL	NULL	0	NULL	pregnancy infection	MedicalFinding	early	confers risk of					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Recent epidemiological studies find that early rather than late pregnancy infection confers the greater risk of schizophrenia.	topic_sch
74274	2	355158	5	NULL	NULL	0	NULL	pregnancy infection	MedicalFinding	late	confers risk of					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Recent epidemiological studies find that early rather than late pregnancy infection confers the greater risk of schizophrenia.	topic_sch
74275	3	355158	5	NULL	NULL	0	NULL	statement 1	Process		is more likely than					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Recent epidemiological studies find that early rather than late pregnancy infection confers the greater risk of schizophrenia.	topic_sch
74321	1	355159	5	NULL	NULL	NULL	NULL	type-1 immune response	AbstractConcept	blunted	is associated with		may			IDO	GP	dysbalance of;;activation of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	In schizophrenia a blunted type-1 immune response seems to be associated with a dysbalance in the activation of the enzyme indoleamine 2,3-dioxygenase (IDO) and in the tryptophan - kynurenine metabolism resulting in increased production of kynurenic acid in schizophrenia.	topic_sch
74322	2	355159	5	NULL	NULL	0	NULL	IDO	GP		is					indoleamine 2,3-dioxygenase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	In schizophrenia a blunted type-1 immune response seems to be associated with a dysbalance in the activation of the enzyme indoleamine 2,3-dioxygenase (IDO) and in the tryptophan - kynurenine metabolism resulting in increased production of kynurenic acid in schizophrenia.	topic_sch
74323	3	355159	5	NULL	NULL	0	NULL	IDO	GP		is a type of					enzyme	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	In schizophrenia a blunted type-1 immune response seems to be associated with a dysbalance in the activation of the enzyme indoleamine 2,3-dioxygenase (IDO) and in the tryptophan - kynurenine metabolism resulting in increased production of kynurenic acid in schizophrenia.	topic_sch
74324	4	355159	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In schizophrenia a blunted type-1 immune response seems to be associated with a dysbalance in the activation of the enzyme indoleamine 2,3-dioxygenase (IDO) and in the tryptophan - kynurenine metabolism resulting in increased production of kynurenic acid in schizophrenia.	topic_sch
74325	5	355159	5	NULL	NULL	0	NULL	type-1 immune response	AbstractConcept	blunted	is associated with		may			tryptophan - kynurenine metabolism	Process	dysfunction of			NULL		0	NULL	NULL	NULL	NULL	NULL	In schizophrenia a blunted type-1 immune response seems to be associated with a dysbalance in the activation of the enzyme indoleamine 2,3-dioxygenase (IDO) and in the tryptophan - kynurenine metabolism resulting in increased production of kynurenic acid in schizophrenia.	topic_sch
74326	6	355159	5	NULL	NULL	0	NULL	statement 5	Process		occurs in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In schizophrenia a blunted type-1 immune response seems to be associated with a dysbalance in the activation of the enzyme indoleamine 2,3-dioxygenase (IDO) and in the tryptophan - kynurenine metabolism resulting in increased production of kynurenic acid in schizophrenia.	topic_sch
74327	7	355159	5	NULL	NULL	0	NULL	kynurenic acid	Chemical		is produced in		increased			schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In schizophrenia a blunted type-1 immune response seems to be associated with a dysbalance in the activation of the enzyme indoleamine 2,3-dioxygenase (IDO) and in the tryptophan - kynurenine metabolism resulting in increased production of kynurenic acid in schizophrenia.	topic_sch
74328	8	355159	5	NULL	NULL	0	NULL	statement 1	Process		results in					statement 7	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In schizophrenia a blunted type-1 immune response seems to be associated with a dysbalance in the activation of the enzyme indoleamine 2,3-dioxygenase (IDO) and in the tryptophan - kynurenine metabolism resulting in increased production of kynurenic acid in schizophrenia.	topic_sch
74329	9	355159	5	NULL	NULL	0	NULL	statement 5	Process		results in					statement 7	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In schizophrenia a blunted type-1 immune response seems to be associated with a dysbalance in the activation of the enzyme indoleamine 2,3-dioxygenase (IDO) and in the tryptophan - kynurenine metabolism resulting in increased production of kynurenic acid in schizophrenia.	topic_sch
74330	1	355163	5	NULL	NULL	0	NULL	COX-2 inhibitors	Chemical		effects		favourable			schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	COX-2 inhibitors have been tested in clinical trials, pointing to favourable effects in schizophrenia.	topic_sch
74331	1	355165	5	NULL	NULL	NULL	NULL	CB1 receptor	GP	alternation of;;function of	is implicated in					depression	MedicalFinding				NULL	human	NULL	NULL	NULL	NULL	NULL	NULL	Alteration of CB1 receptor function has been implicated in a number of human diseases such as depression, schizophrenia, and obesity (4-6). 	topic_sch
74332	2	355165	5	NULL	NULL	0	NULL	CB1 receptor	GP	alternation of;;function of	is implicated in					schizophrenia	MedicalFinding				NULL	human	0	NULL	NULL	NULL	NULL	NULL	Alteration of CB1 receptor function has been implicated in a number of human diseases such as depression, schizophrenia, and obesity (4-6). 	topic_sch
74333	3	355165	5	NULL	NULL	0	NULL	CB1 receptor	GP	alternation of;;function of	is implicated in					obesity	MedicalFinding				NULL	human	0	NULL	NULL	NULL	NULL	NULL	Alteration of CB1 receptor function has been implicated in a number of human diseases such as depression, schizophrenia, and obesity (4-6). 	topic_sch
74337	1	355166	5	NULL	NULL	0	NULL	PCP	Chemical		is					Phencyclidine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Phencyclidine (PCP), a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, increases locomotor activity in rodents and causes schizophrenia-like symptoms in humans. 	topic_sch
74338	2	355166	5	NULL	NULL	0	NULL	NMDA	Chemical		is					N-methyl-D-aspartate	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Phencyclidine (PCP), a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, increases locomotor activity in rodents and causes schizophrenia-like symptoms in humans. 	topic_sch
74339	3	355166	5	NULL	NULL	0	NULL	PCP	Chemical		is an antagonist of					NMDA receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Phencyclidine (PCP), a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, increases locomotor activity in rodents and causes schizophrenia-like symptoms in humans. 	topic_sch
74340	4	355166	5	NULL	NULL	0	NULL	PCP	Chemical		increases					locomotor activity	Process				NULL	rodents	0	NULL	NULL	NULL	NULL	NULL	Phencyclidine (PCP), a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, increases locomotor activity in rodents and causes schizophrenia-like symptoms in humans. 	topic_sch
74341	5	355166	5	NULL	NULL	0	NULL	PCP	Chemical		causes					schizophrenia-like symptoms	MedicalFinding				NULL	human	0	NULL	NULL	NULL	NULL	NULL	Phencyclidine (PCP), a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, increases locomotor activity in rodents and causes schizophrenia-like symptoms in humans. 	topic_sch
74342	1	355167	5	NULL	NULL	0	NULL	weight	QuantityOrMeasure	gain of	induced by					antipsychotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The study findings suggest a potential role for leptin to mediate the link between antipsychotic-induced weight gain and beneficial therapeutic response in schizophrenia.	topic_sch
74343	2	355167	5	NULL	NULL	0	NULL	statement 1	QuantityOrMeasure		is linked to					schizophrenia	MedicalFinding	beneficial therapeutic response of			NULL		0	NULL	NULL	NULL	NULL	NULL	The study findings suggest a potential role for leptin to mediate the link between antipsychotic-induced weight gain and beneficial therapeutic response in schizophrenia.	topic_sch
74344	3	355167	5	NULL	NULL	0	NULL	leptin	GP		mediates		may			statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The study findings suggest a potential role for leptin to mediate the link between antipsychotic-induced weight gain and beneficial therapeutic response in schizophrenia.	topic_sch
74345	1	355168	5	NULL	NULL	0	NULL	ADNP	GP		is essential for					brain	OrganismPart	formation of			NULL		0	NULL	NULL	NULL	NULL	NULL	ADNP is essential for brain formation, proper development and neuronal plasticity, all reported to be impaired in schizophrenia. 	topic_sch
74346	2	355168	5	NULL	NULL	0	NULL	ADNP	GP		is essential for					development	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	ADNP is essential for brain formation, proper development and neuronal plasticity, all reported to be impaired in schizophrenia. 	topic_sch
74347	3	355168	5	NULL	NULL	0	NULL	ADNP	GP		is essential for					neuronal plasticity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	ADNP is essential for brain formation, proper development and neuronal plasticity, all reported to be impaired in schizophrenia. 	topic_sch
74348	4	355168	5	NULL	NULL	0	NULL	brain	OrganismPart	development of	is impaired in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	ADNP is essential for brain formation, proper development and neuronal plasticity, all reported to be impaired in schizophrenia. 	topic_sch
74349	5	355168	5	NULL	NULL	0	NULL	development	Process		is impaired in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	ADNP is essential for brain formation, proper development and neuronal plasticity, all reported to be impaired in schizophrenia. 	topic_sch
74350	6	355168	5	NULL	NULL	0	NULL	neuronal plasticity	Process		is impaired in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	ADNP is essential for brain formation, proper development and neuronal plasticity, all reported to be impaired in schizophrenia. 	topic_sch
74351	1	355169	5	NULL	NULL	0	NULL	ADNP haploinsufficiency	MedicalFinding		inhibits					social function	AbstractConcept				NULL		0	NULL	NULL	NULL	NULL	NULL	ADNP haploinsufficiency inhibits social and cognitive functions, major hallmarks in schizophrenia.	topic_sch
74352	2	355169	5	NULL	NULL	0	NULL	ADNP haploinsufficiency	MedicalFinding		inhibits					cognitive functions	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	ADNP haploinsufficiency inhibits social and cognitive functions, major hallmarks in schizophrenia.	topic_sch
74353	3	355169	5	NULL	NULL	0	NULL	social functions	AbstractConcept	impaired	is a hallmark of					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	ADNP haploinsufficiency inhibits social and cognitive functions, major hallmarks in schizophrenia.	topic_sch
74354	4	355169	5	NULL	NULL	0	NULL	cognitive functions	MentalProcess	impaired	is a hallmark of					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	ADNP haploinsufficiency inhibits social and cognitive functions, major hallmarks in schizophrenia.	topic_sch
74355	1	355171	5	NULL	NULL	0	NULL	ADNP/ADNP2	GP	expression of	is not balanced in					schizophrenia brain	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Imbalance in ADNP/ADNP2 expression in the schizophrenia brain may impact disease progression. 	topic_sch
74356	2	355171	5	NULL	NULL	0	NULL	statement 1	Process		impact		may			schizophrenia spectrum traits	MedicalFinding	progression of			NULL		0	NULL	NULL	NULL	NULL	NULL	Imbalance in ADNP/ADNP2 expression in the schizophrenia brain may impact disease progression. 	topic_sch
74357	1	355174	5	NULL	NULL	0	NULL	serotonin biochemistry regulating gene	GP		cause		may			autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The most likely genes to be candidates for causing autism are those that regulate serotonin biochemistry	topic_aut
74358	1	355176	5	NULL	NULL	0	NULL	serotonin transporter gene	GP		cause		may			autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The serotonin transporter gene has been implicated as a candidate gene in autism owing to the effectiveness of specific drugs that inhibit serotonin transport to minimize some characteristic autistic behaviors.	topic_aut
74359	1	355177	5	NULL	NULL	0	NULL	autism	MedicalFinding		is associated with					serotonin transporter gene	GP	polymorphisms of			NULL		0	NULL	NULL	NULL	NULL	NULL	Cook et al. (1997) reported an association between autism and two distinct polymorphisms of the serotonin transporter gene (HTT)	topic_aut
74360	2	355177	5	NULL	NULL	0	NULL	HTT	GP		is					serotonin transporter gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Cook et al. (1997) reported an association between autism and two distinct polymorphisms of the serotonin transporter gene (HTT)	topic_aut
74361	1	355179	5	NULL	NULL	0	NULL	serotonin	Chemical		is implicated in					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In addition to serotonin, the catecholaminergic neurotransmitters have been implicated in autism.	topic_aut
74362	2	355179	5	NULL	NULL	0	NULL	catecholaminergic neurotransmitters	Chemical		is implicated in					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In addition to serotonin, the catecholaminergic neurotransmitters have been implicated in autism.	topic_aut
74363	1	355180	5	NULL	NULL	NULL	NULL	autism	MedicalFinding		is associated with					HRAS gene marker	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	An association has also been found between autism and a marker in the c-harvey ras (HRAS) gene, located on chromosome 11 (Herault et al., 1995).	topic_aut
74364	2	355180	5	NULL	NULL	NULL	NULL	HRAS gene marker	GP		is located on					chromosome 11	Chromosome				NULL		NULL	NULL	NULL	NULL	NULL	NULL	An association has also been found between autism and a marker in the c-harvey ras (HRAS) gene, located on chromosome 11 (Herault et al., 1995).	topic_aut
74365	3	355180	5	NULL	NULL	0	NULL	HRAS gene	GP		is					c-harvey ras gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	An association has also been found between autism and a marker in the c-harvey ras (HRAS) gene, located on chromosome 11 (Herault et al., 1995).	topic_aut
74366	1	355181	5	NULL	NULL	NULL	NULL	HRAS markers	NucleicAcid	region including	confers					autism	MedicalFinding	 susceptibility of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Although this association suggests that the region including the HRAS markers confers susceptibility to autism, it is unclear whether the HRAS gene itself, or a gene nearby, is contributing to the autism syndrome (Herault et al., 1995).	topic_aut
74367	1	355182	5	NULL	NULL	0	NULL	15qll-13	Chromosome	duplications of;;small parts of;;the long arm of	plays a role in					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	A number of duplications of small parts of the long arm of chromosome 15 (15qll-13) have been reported in individuals with autism (Baker, Piven, Schwartz, & Patil, 1994), suggesting that a gene may lie in that area.	topic_aut
74368	2	355182	5	NULL	NULL	0	NULL	15qll-13	Chromosome		is present in					chromosome 15	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	A number of duplications of small parts of the long arm of chromosome 15 (15qll-13) have been reported in individuals with autism (Baker, Piven, Schwartz, & Patil, 1994), suggesting that a gene may lie in that area.	topic_aut
76374	1	355183	11	NULL	NULL	0	NULL	Diabetes mellitus	MedicalFinding		is also known as					diabetes	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Diabetes mellitus, often simply referred to as diabetes	topic_mrs
76544	1	355187	11	NULL	NULL	0	NULL	wound	MedicalFinding	open	is at risk of					MRSA infection	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA is especially troublesome in hospitals where patients with open wounds, invasive devices and weakened immune systems are at greater risk of infection than the general public.	topic_mrs
76545	2	355187	11	NULL	NULL	0	NULL	patient with  invasive devices	GroupOfPeople		is at risk of					MRSA infection	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA is especially troublesome in hospitals where patients with open wounds, invasive devices and weakened immune systems are at greater risk of infection than the general public.	topic_mrs
76546	3	355187	11	NULL	NULL	0	NULL	immune system	OrganismPart		is weak in					patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA is especially troublesome in hospitals where patients with open wounds, invasive devices and weakened immune systems are at greater risk of infection than the general public.	topic_mrs
76547	4	355187	11	NULL	NULL	0	NULL	statement 3	Process		is at risk of					MRSA infection	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA is especially troublesome in hospitals where patients with open wounds, invasive devices and weakened immune systems are at greater risk of infection than the general public.	topic_mrs
75461	1	355188	11	NULL	NULL	0	NULL	Vancomycin	Chemical		is a type of 					glycopeptide antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Vancomycin  is a glycopeptide antibiotic used in the prophylaxis and treatment of infections caused by Gram-positive bacteria. It has traditionally been reserved as a drug of 'last resort', used only after treatment with other antibiotics had failed	topic_mrs
75462	2	355188	11	NULL	NULL	0	NULL	Gram-positive bacteria	Organism		cause					 infections	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Vancomycin  is a glycopeptide antibiotic used in the prophylaxis and treatment of infections caused by Gram-positive bacteria. It has traditionally been reserved as a drug of 'last resort', used only after treatment with other antibiotics had failed	topic_mrs
75463	3	355188	11	NULL	NULL	0	NULL	Vancomycin	Chemical		used in					 prophylaxis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Vancomycin  is a glycopeptide antibiotic used in the prophylaxis and treatment of infections caused by Gram-positive bacteria. It has traditionally been reserved as a drug of 'last resort', used only after treatment with other antibiotics had failed	topic_mrs
75464	4	355188	11	NULL	NULL	0	NULL	Vancomycin	Chemical		treats					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Vancomycin  is a glycopeptide antibiotic used in the prophylaxis and treatment of infections caused by Gram-positive bacteria. It has traditionally been reserved as a drug of 'last resort', used only after treatment with other antibiotics had failed	topic_mrs
76376	1	355189	11	NULL	NULL	0	NULL	vancomycin	Chemical		is a type of 					 glycopeptide	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	 Linezolid, quinupristin/dalfopristin (synercid), daptomycin, and tigecycline are used to treat more severe infections that do not respond to glycopeptides such as vancomycin.	topic_mrs
76377	2	355189	11	NULL	NULL	0	NULL	severe infections	Process		do not respond to					glycopeptides	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	 Linezolid, quinupristin/dalfopristin (synercid), daptomycin, and tigecycline are used to treat more severe infections that do not respond to glycopeptides such as vancomycin.	topic_mrs
76378	3	355189	11	NULL	NULL	0	NULL	Linezolid	Chemical		treat					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 Linezolid, quinupristin/dalfopristin (synercid), daptomycin, and tigecycline are used to treat more severe infections that do not respond to glycopeptides such as vancomycin.	topic_mrs
76379	4	355189	11	NULL	NULL	0	NULL	quinupristin/dalfopristin	Chemical		treats					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 Linezolid, quinupristin/dalfopristin (synercid), daptomycin, and tigecycline are used to treat more severe infections that do not respond to glycopeptides such as vancomycin.	topic_mrs
76380	5	355189	11	NULL	NULL	0	NULL	daptomycin	Chemical		treats					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 Linezolid, quinupristin/dalfopristin (synercid), daptomycin, and tigecycline are used to treat more severe infections that do not respond to glycopeptides such as vancomycin.	topic_mrs
76381	6	355189	11	NULL	NULL	0	NULL	tigecycline	Chemical		treats					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 Linezolid, quinupristin/dalfopristin (synercid), daptomycin, and tigecycline are used to treat more severe infections that do not respond to glycopeptides such as vancomycin.	topic_mrs
76382	7	355189	11	NULL	NULL	0	NULL	quinupristin/dalfopristin	Chemical		is also known as					synercid	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	 Linezolid, quinupristin/dalfopristin (synercid), daptomycin, and tigecycline are used to treat more severe infections that do not respond to glycopeptides such as vancomycin.	topic_mrs
75465	1	355190	11	NULL	NULL	0	NULL	Gram-positive organisms	Organism		causes					 infections	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Daptomycin is a novel lipopeptide antibiotic used in the treatment of certain infections caused by Gram-positive organisms.	topic_mrs
75466	2	355190	11	NULL	NULL	0	NULL	Daptomycin	Chemical		is a type of 					lipopeptide antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Daptomycin is a novel lipopeptide antibiotic used in the treatment of certain infections caused by Gram-positive organisms.	topic_mrs
75467	3	355190	11	NULL	NULL	0	NULL	Daptomycin	Chemical		treats					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Daptomycin is a novel lipopeptide antibiotic used in the treatment of certain infections caused by Gram-positive organisms.	topic_mrs
76383	1	355191	11	NULL	NULL	0	NULL	methicillin-resistant Staphylococcus aureus 	Organism		is					MRSA	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Rifampicin also has a role in the treatment of methicillin-resistant Staphylococcus aureus (MRSA) in combination with fusidic acid, although recent inquiries have raised questions over the lack of studies into the efficacy of this treatment.	topic_mrs
76384	2	355191	11	NULL	NULL	0	NULL	Rifampicin	Chemical		treats					methicillin-resistant Staphylococcus aureus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Rifampicin also has a role in the treatment of methicillin-resistant Staphylococcus aureus (MRSA) in combination with fusidic acid, although recent inquiries have raised questions over the lack of studies into the efficacy of this treatment.	topic_mrs
76385	3	355191	11	NULL	NULL	0	NULL	fusidic acid	Chemical		treats					methicillin-resistant Staphylococcus aureus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Rifampicin also has a role in the treatment of methicillin-resistant Staphylococcus aureus (MRSA) in combination with fusidic acid, although recent inquiries have raised questions over the lack of studies into the efficacy of this treatment.	topic_mrs
76386	4	355191	11	NULL	NULL	0	NULL	statement 2	Chemical		combines with					statement 3	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Rifampicin also has a role in the treatment of methicillin-resistant Staphylococcus aureus (MRSA) in combination with fusidic acid, although recent inquiries have raised questions over the lack of studies into the efficacy of this treatment.	topic_mrs
76387	1	355192	11	NULL	NULL	0	NULL	Community-Acquired MRSA	Organism		is					CA-MRSA	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Community-Acquired MRSA ( CA-MRSA) is a rapidly emerging public health problem. CA-MRSA strains are generally susceptible to a wider range of antibiotics (e.g., usually susceptible to fluoroquinolones and trimethoprim/sulfamethoxazole [TMP/SMX])	topic_mrs
76388	2	355192	11	NULL	NULL	0	NULL	CA-MRSA	Organism		susceptible to		generally			 antibiotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Community-Acquired MRSA ( CA-MRSA) is a rapidly emerging public health problem. CA-MRSA strains are generally susceptible to a wider range of antibiotics (e.g., usually susceptible to fluoroquinolones and trimethoprim/sulfamethoxazole [TMP/SMX])	topic_mrs
76389	3	355192	11	NULL	NULL	0	NULL	Community-Acquired MRSA	Organism		susceptible to 					fluoroquinolones	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Community-Acquired MRSA ( CA-MRSA) is a rapidly emerging public health problem. CA-MRSA strains are generally susceptible to a wider range of antibiotics (e.g., usually susceptible to fluoroquinolones and trimethoprim/sulfamethoxazole [TMP/SMX])	topic_mrs
76390	4	355192	11	NULL	NULL	0	NULL	Community-Acquired MRSA	Organism		susceptible to 					trimethoprim/sulfamethoxazole	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Community-Acquired MRSA ( CA-MRSA) is a rapidly emerging public health problem. CA-MRSA strains are generally susceptible to a wider range of antibiotics (e.g., usually susceptible to fluoroquinolones and trimethoprim/sulfamethoxazole [TMP/SMX])	topic_mrs
76391	5	355192	11	NULL	NULL	0	NULL	trimethoprim/sulfamethoxazole	Chemical		is					TMP/SMX	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Community-Acquired MRSA ( CA-MRSA) is a rapidly emerging public health problem. CA-MRSA strains are generally susceptible to a wider range of antibiotics (e.g., usually susceptible to fluoroquinolones and trimethoprim/sulfamethoxazole [TMP/SMX])	topic_mrs
75468	1	355193	11	NULL	NULL	0	NULL	Cellulitis	MedicalFinding		is a type of 					diffuse inflammation	Process	connective tissue			NULL		0	NULL	NULL	NULL	NULL	NULL	Cellulitis is a diffuse inflammation of connective tissue with severe inflammation of dermal and subcutaneous layers of the skin. Cellulitis can be caused by normal skin flora or by exogenous bacteria,	topic_mrs
75469	2	355193	11	NULL	NULL	0	NULL	Cellulitis	MedicalFinding		causes					inflammation	Process	 skin			NULL		0	NULL	NULL	NULL	NULL	NULL	Cellulitis is a diffuse inflammation of connective tissue with severe inflammation of dermal and subcutaneous layers of the skin. Cellulitis can be caused by normal skin flora or by exogenous bacteria,	topic_mrs
75472	3	355193	11	NULL	NULL	0	NULL	Cellulitis	MedicalFinding		caused by		may			normal skin flora	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Cellulitis is a diffuse inflammation of connective tissue with severe inflammation of dermal and subcutaneous layers of the skin. Cellulitis can be caused by normal skin flora or by exogenous bacteria,	topic_mrs
75483	4	355193	11	NULL	NULL	0	NULL	Cellulitis	MedicalFinding		caused by		may			exogenous bacteria	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Cellulitis is a diffuse inflammation of connective tissue with severe inflammation of dermal and subcutaneous layers of the skin. Cellulitis can be caused by normal skin flora or by exogenous bacteria,	topic_mrs
75487	1	355194	11	NULL	NULL	0	NULL	furuncles	MedicalFinding		caused by					S. aureus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Cellulitis may be caused by numerous organisms that are indigenous to the skin or to particular environmental niches. Cellulitis associated with furuncles, carbuncles, or abscesses is usually caused by S. aureus	topic_mrs
75489	2	355194	11	NULL	NULL	0	NULL	carbuncles	MedicalFinding		caused by					S. aureus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Cellulitis may be caused by numerous organisms that are indigenous to the skin or to particular environmental niches. Cellulitis associated with furuncles, carbuncles, or abscesses is usually caused by S. aureus	topic_mrs
75490	3	355194	11	NULL	NULL	0	NULL	abscesses	MedicalFinding		caused by					S. aureus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Cellulitis may be caused by numerous organisms that are indigenous to the skin or to particular environmental niches. Cellulitis associated with furuncles, carbuncles, or abscesses is usually caused by S. aureus	topic_mrs
75491	4	355194	11	NULL	NULL	0	NULL	Cellulitis	MedicalFinding		associated with					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Cellulitis may be caused by numerous organisms that are indigenous to the skin or to particular environmental niches. Cellulitis associated with furuncles, carbuncles, or abscesses is usually caused by S. aureus	topic_mrs
75492	5	355194	11	NULL	NULL	0	NULL	Cellulitis	MedicalFinding		associated with					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Cellulitis may be caused by numerous organisms that are indigenous to the skin or to particular environmental niches. Cellulitis associated with furuncles, carbuncles, or abscesses is usually caused by S. aureus	topic_mrs
75494	6	355194	11	NULL	NULL	0	NULL	Cellulitis	MedicalFinding		associates with					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Cellulitis may be caused by numerous organisms that are indigenous to the skin or to particular environmental niches. Cellulitis associated with furuncles, carbuncles, or abscesses is usually caused by S. aureus	topic_mrs
75498	1	355195	11	NULL	NULL	0	NULL	Impetigo	MedicalFinding		is a type of 					skin infection	Process	 bacterial			NULL		0	NULL	NULL	NULL	NULL	NULL	Impetigo is a highly contagious bacterial skin infection most common among pre-school children	topic_mrs
76623	2	355195	11	NULL	NULL	0	NULL	Impetigo	MedicalFinding		is common among					pre-school children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Impetigo is a highly contagious bacterial skin infection most common among pre-school children	topic_mrs
76392	1	355200	11	NULL	NULL	0	NULL	Impetigo	MedicalFinding		occurs in		frequently			children	GroupOfPeople	economically disadvantaged			NULL		0	NULL	NULL	NULL	NULL	NULL	Impetigo occurs most frequently among economically disadvantaged children	topic_mrs
76393	1	355201	11	NULL	NULL	0	NULL	streptococcus	Organism		is responsible for					impetigo	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Prospective studies of streptococcal impetigo have demonstrated that the responsible microorganisms initially colonize the unbroken skin, an observation that probably explains the influence of personal hygiene on disease incidence	topic_mrs
76394	2	355201	11	NULL	NULL	0	NULL	streptococcus	Organism		colonizes		initially			unbroken skin	Organism part				NULL		0	NULL	NULL	NULL	NULL	NULL	Prospective studies of streptococcal impetigo have demonstrated that the responsible microorganisms initially colonize the unbroken skin, an observation that probably explains the influence of personal hygiene on disease incidence	topic_mrs
75510	1	355204	11	NULL	NULL	NULL	NULL	Ecthyma	MedicalFinding		is a form of		serious			impetigo	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Ecthyma is a more serious form of impetigo in which the infection penetrates deeper into the skin's second layer, the dermis. 	topic_mrs
75511	2	355204	11	NULL	NULL	0	NULL	Ecthyma	MedicalFinding		 infects					 dermis	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Ecthyma is a more serious form of impetigo in which the infection penetrates deeper into the skin's second layer, the dermis. 	topic_mrs
76395	1	355205	11	NULL	NULL	0	NULL	Crystal violet	Chemical		is also known as					Gentian violet	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Crystal violet or Gentian violet (also hexamethyl pararosaniline chloride) is a triarylmethane dye... and was formerly important as a topical antiseptic.	topic_mrs
76396	2	355205	11	NULL	NULL	0	NULL	Crystal violet	Chemical		is a type of 					triarylmethane dye	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Crystal violet or Gentian violet (also hexamethyl pararosaniline chloride) is a triarylmethane dye... and was formerly important as a topical antiseptic.	topic_mrs
76397	3	355205	11	NULL	NULL	0	NULL	hexamethyl pararosaniline chloride	Chemical		is a type of 					triarylmethane dye	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Crystal violet or Gentian violet (also hexamethyl pararosaniline chloride) is a triarylmethane dye... and was formerly important as a topical antiseptic.	topic_mrs
76398	4	355205	11	NULL	NULL	0	NULL	Crystal violet	Chemical		used as		formerly			topical antiseptic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Crystal violet or Gentian violet (also hexamethyl pararosaniline chloride) is a triarylmethane dye... and was formerly important as a topical antiseptic.	topic_mrs
76399	5	355205	11	NULL	NULL	0	NULL	hexamethyl pararosaniline chloride	Chemical		used as		formerly			topical antiseptic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Crystal violet or Gentian violet (also hexamethyl pararosaniline chloride) is a triarylmethane dye... and was formerly important as a topical antiseptic.	topic_mrs
75512	1	355207	11	NULL	NULL	0	NULL	Fusidic acid	Chemical		is a type of 					antibiotic	Chemical	bacteriostatic			NULL		0	NULL	NULL	NULL	NULL	NULL	Fusidic acid is a bacteriostatic antibiotic that is often used topically in creams and eyedrops, but may also be given systemically as tablets or injections	topic_mrs
75513	2	355207	11	NULL	NULL	0	NULL	Fusidic acid	Chemical		is used in					creams	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Fusidic acid is a bacteriostatic antibiotic that is often used topically in creams and eyedrops, but may also be given systemically as tablets or injections	topic_mrs
75514	3	355207	11	NULL	NULL	0	NULL	Fusidic acid	Chemical		is used in					eyedrops	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Fusidic acid is a bacteriostatic antibiotic that is often used topically in creams and eyedrops, but may also be given systemically as tablets or injections	topic_mrs
75515	4	355207	11	NULL	NULL	0	NULL	Fusidic acid	Chemical		is used in		may			 tablets	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Fusidic acid is a bacteriostatic antibiotic that is often used topically in creams and eyedrops, but may also be given systemically as tablets or injections	topic_mrs
75516	5	355207	11	NULL	NULL	0	NULL	Fusidic acid	Chemical		is used in					injection	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Fusidic acid is a bacteriostatic antibiotic that is often used topically in creams and eyedrops, but may also be given systemically as tablets or injections	topic_mrs
76400	1	355208	11	NULL	NULL	0	NULL	fusidic acid	Chemical		is a type of 					bactericidal ointment	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Mild cases may be treated with bactericidal ointment, such as fusidic acid, mupirocin, chloramphenicol or neosporin, which in some countries may be available over-the-counter.	topic_mrs
76401	2	355208	11	NULL	NULL	0	NULL	mupirocin	Chemical		is a type of 					bactericidal ointment	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Mild cases may be treated with bactericidal ointment, such as fusidic acid, mupirocin, chloramphenicol or neosporin, which in some countries may be available over-the-counter.	topic_mrs
76402	3	355208	11	NULL	NULL	0	NULL	chloramphenicol	Chemical		is a type of 					bactericidal ointment	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Mild cases may be treated with bactericidal ointment, such as fusidic acid, mupirocin, chloramphenicol or neosporin, which in some countries may be available over-the-counter.	topic_mrs
76403	4	355208	11	NULL	NULL	0	NULL	neosporin	Chemical		is a type of 					bactericidal ointment	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Mild cases may be treated with bactericidal ointment, such as fusidic acid, mupirocin, chloramphenicol or neosporin, which in some countries may be available over-the-counter.	topic_mrs
76404	1	355209	11	NULL	NULL	0	NULL	Neosporin	Chemical		prevents					 infection	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Neosporin is the product name of an antibiotic ointment produced by Pfizer used in the prevention of infection and speeding the healing of wounds. The original ointment contains three different antibiotics: bacitracin, neomycin, and polymyxin B, in a petroleum jelly base. Other brand names for this mixture include Mycitracin and Topisporin.	topic_mrs
76405	2	355209	11	NULL	NULL	0	NULL	Neosporin	Chemical		heals					wounds	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Neosporin is the product name of an antibiotic ointment produced by Pfizer used in the prevention of infection and speeding the healing of wounds. The original ointment contains three different antibiotics: bacitracin, neomycin, and polymyxin B, in a petroleum jelly base. Other brand names for this mixture include Mycitracin and Topisporin.	topic_mrs
76406	3	355209	11	NULL	NULL	0	NULL	Neosporin	Chemical		contains					bacitracin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Neosporin is the product name of an antibiotic ointment produced by Pfizer used in the prevention of infection and speeding the healing of wounds. The original ointment contains three different antibiotics: bacitracin, neomycin, and polymyxin B, in a petroleum jelly base. Other brand names for this mixture include Mycitracin and Topisporin.	topic_mrs
76407	4	355209	11	NULL	NULL	0	NULL	Neosporin	Chemical		contains					neomycin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Neosporin is the product name of an antibiotic ointment produced by Pfizer used in the prevention of infection and speeding the healing of wounds. The original ointment contains three different antibiotics: bacitracin, neomycin, and polymyxin B, in a petroleum jelly base. Other brand names for this mixture include Mycitracin and Topisporin.	topic_mrs
76408	5	355209	11	NULL	NULL	0	NULL	Neosporin	Chemical		contains					polymyxin B	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Neosporin is the product name of an antibiotic ointment produced by Pfizer used in the prevention of infection and speeding the healing of wounds. The original ointment contains three different antibiotics: bacitracin, neomycin, and polymyxin B, in a petroleum jelly base. Other brand names for this mixture include Mycitracin and Topisporin.	topic_mrs
76409	6	355209	11	NULL	NULL	0	NULL	Neosporin	Chemical		contains					petroleum jelly base	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Neosporin is the product name of an antibiotic ointment produced by Pfizer used in the prevention of infection and speeding the healing of wounds. The original ointment contains three different antibiotics: bacitracin, neomycin, and polymyxin B, in a petroleum jelly base. Other brand names for this mixture include Mycitracin and Topisporin.	topic_mrs
76410	7	355209	11	NULL	NULL	0	NULL	bacitracin	Chemical		is a type of 					antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Neosporin is the product name of an antibiotic ointment produced by Pfizer used in the prevention of infection and speeding the healing of wounds. The original ointment contains three different antibiotics: bacitracin, neomycin, and polymyxin B, in a petroleum jelly base. Other brand names for this mixture include Mycitracin and Topisporin.	topic_mrs
76411	8	355209	11	NULL	NULL	0	NULL	 neomycin	Chemical		is a type of 					antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Neosporin is the product name of an antibiotic ointment produced by Pfizer used in the prevention of infection and speeding the healing of wounds. The original ointment contains three different antibiotics: bacitracin, neomycin, and polymyxin B, in a petroleum jelly base. Other brand names for this mixture include Mycitracin and Topisporin.	topic_mrs
76412	9	355209	11	NULL	NULL	0	NULL	polymyxin B	Chemical		is a type of 					antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Neosporin is the product name of an antibiotic ointment produced by Pfizer used in the prevention of infection and speeding the healing of wounds. The original ointment contains three different antibiotics: bacitracin, neomycin, and polymyxin B, in a petroleum jelly base. Other brand names for this mixture include Mycitracin and Topisporin.	topic_mrs
76413	10	355209	11	NULL	NULL	0	NULL	statement 3	Chemical		mixtured with					statement 4	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Neosporin is the product name of an antibiotic ointment produced by Pfizer used in the prevention of infection and speeding the healing of wounds. The original ointment contains three different antibiotics: bacitracin, neomycin, and polymyxin B, in a petroleum jelly base. Other brand names for this mixture include Mycitracin and Topisporin.	topic_mrs
76414	11	355209	11	NULL	NULL	0	NULL	statement 10	Chemical		mixtured with					statement 5	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Neosporin is the product name of an antibiotic ointment produced by Pfizer used in the prevention of infection and speeding the healing of wounds. The original ointment contains three different antibiotics: bacitracin, neomycin, and polymyxin B, in a petroleum jelly base. Other brand names for this mixture include Mycitracin and Topisporin.	topic_mrs
76415	12	355209	11	NULL	NULL	0	NULL	statement 11	Chemical		mixtured with					statement 6	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Neosporin is the product name of an antibiotic ointment produced by Pfizer used in the prevention of infection and speeding the healing of wounds. The original ointment contains three different antibiotics: bacitracin, neomycin, and polymyxin B, in a petroleum jelly base. Other brand names for this mixture include Mycitracin and Topisporin.	topic_mrs
76416	13	355209	11	NULL	NULL	0	NULL	statement 12	Chemical		also known as					Mycitracin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Neosporin is the product name of an antibiotic ointment produced by Pfizer used in the prevention of infection and speeding the healing of wounds. The original ointment contains three different antibiotics: bacitracin, neomycin, and polymyxin B, in a petroleum jelly base. Other brand names for this mixture include Mycitracin and Topisporin.	topic_mrs
76417	14	355209	11	NULL	NULL	0	NULL	statement 12	Chemical		is also known as					Topisporin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Neosporin is the product name of an antibiotic ointment produced by Pfizer used in the prevention of infection and speeding the healing of wounds. The original ointment contains three different antibiotics: bacitracin, neomycin, and polymyxin B, in a petroleum jelly base. Other brand names for this mixture include Mycitracin and Topisporin.	topic_mrs
76418	1	355211	11	NULL	NULL	0	NULL	Hydrogen peroxide	Chemical		is viscous than		slightly			water	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen peroxide is a clear liquid, slightly more viscous than water, that appears colorless in dilute solution. It is used as a disinfectant, antiseptic	topic_mrs
76419	2	355211	11	NULL	NULL	0	NULL	Hydrogen peroxide	Chemical		is used as					disinfectant	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen peroxide is a clear liquid, slightly more viscous than water, that appears colorless in dilute solution. It is used as a disinfectant, antiseptic	topic_mrs
76420	3	355211	11	NULL	NULL	0	NULL	Hydrogen peroxide	Chemical		is used as					antiseptic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen peroxide is a clear liquid, slightly more viscous than water, that appears colorless in dilute solution. It is used as a disinfectant, antiseptic	topic_mrs
75517	1	355212	11	NULL	NULL	NULL	NULL	Hydrogen peroxide	Chemical		treats					Impetigo Contagiosa	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hydrogen peroxide is an alternative to topical antibiotics in the treatment of Impetigo. In a cream formulation hydrogen peroxide 1% is stabilized, thereby avoiding fast degradation with the result of prolonged antimicrobial effect and effective treatment. Hydrogen peroxide has been shown to be as effective as antibiotics in the treatment of Impetigo Contagiosa.	topic_mrs
76624	2	355212	11	NULL	NULL	0	NULL	Hydrogen peroxide	Chemical		is an alternative to					topical antibiotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen peroxide is an alternative to topical antibiotics in the treatment of Impetigo. In a cream formulation hydrogen peroxide 1% is stabilized, thereby avoiding fast degradation with the result of prolonged antimicrobial effect and effective treatment. Hydrogen peroxide has been shown to be as effective as antibiotics in the treatment of Impetigo Contagiosa.	topic_mrs
74546	1	355213	6	NULL	NULL	0	NULL	HER2 protein	GP		is a type of					HER2 receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The HER2 protein, also called the HER2 receptor	topic_bc
74547	1	355214	6	NULL	NULL	0	NULL	Herceptin	Chemical		is a type of					trastuzumab	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Herceptin (trastuzumab) is part of a treatment plan for the adjuvant treatment of patients with HER2 overexpressing, node-positive HER2+ breast cancer	topic_bc
74548	2	355214	6	NULL	NULL	NULL	NULL	Herceptin	Chemical		is a treatment for					HER2+ breast cancer	MedicalFinding				NULL	patients	NULL	NULL	NULL	NULL	NULL	NULL	Herceptin (trastuzumab) is part of a treatment plan for the adjuvant treatment of patients with HER2 overexpressing, node-positive HER2+ breast cancer	topic_bc
74559	1	355215	6	NULL	NULL	0	NULL	anthracyclines	Chemical		is used as a treatment for					breast cancer	MedicalFinding				NULL	women	0	NULL	NULL	NULL	NULL	NULL	For decades, anthracyclines have been the gold standard of treatment for women with breast cancer, but that could be changing.	topic_bc
74560	1	355216	6	NULL	NULL	NULL	NULL	HER2/ER	GP		cross talk with					lapatinib	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Interruption of HER2/ER cross-talk with lapatinib can restore sensitivity to anti-estrogens	topic_bc
74561	2	355216	6	NULL	NULL	0	NULL	statement 1	Process	interruption of	restore					anti-estrogens	Chemical	sensitivity to			NULL		0	NULL	NULL	NULL	NULL	NULL	Interruption of HER2/ER cross-talk with lapatinib can restore sensitivity to anti-estrogens	topic_bc
74562	1	355217	6	NULL	NULL	0	NULL	radiotherapy	MedicalProcedure		prevents					breast cancer	MedicalFinding	recurrence of			NULL	patients	0	NULL	NULL	NULL	NULL	NULL	 After surgery and standard radiotherapy, an extra boost of radiotherapy can help prevent the recurrence of early breast cancer for patients	topic_bc
74563	1	355218	6	NULL	NULL	0	NULL	CtBP1	GP	stablization of 	is dependent on					Bcl3	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Bcl3-dependent stabilization of CtBP1 is crucial for the inhibition of apoptosis and tumor progression in breast cancer.	topic_bc
74564	2	355218	6	NULL	NULL	0	NULL	statement 1	Process		is crucial for					apoptosis	Process				NULL	breast cancer	0	NULL	NULL	NULL	NULL	NULL	Bcl3-dependent stabilization of CtBP1 is crucial for the inhibition of apoptosis and tumor progression in breast cancer.	topic_bc
74565	3	355218	6	NULL	NULL	0	NULL	statement 1	Process		is crucial for					tumor	Cell	progression of 			NULL	breast cancer	0	NULL	NULL	NULL	NULL	NULL	Bcl3-dependent stabilization of CtBP1 is crucial for the inhibition of apoptosis and tumor progression in breast cancer.	topic_bc
74566	1	355219	6	NULL	NULL	0	NULL	quercetin	Chemical		help in					cancer	MedicalFinding	prevention of			NULL		0	NULL	NULL	NULL	NULL	NULL	Research has shown quercetin may help to prevent cancer	topic_bc
74567	1	355220	6	NULL	NULL	NULL	NULL	mucinous carcinoma	MedicalFinding		is a type of		rare			breast cancer	MedicalFinding	invasive			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Mucinous (colloid) carcinoma is a rare type of invasive breast cancer that is formed when cancer cells within your breast produce mucous	topic_bc
74568	2	355220	6	NULL	NULL	0	NULL	mucinous carcinoma	MedicalFinding		is a type of					colloid carcinoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mucinous (colloid) carcinoma is a rare type of invasive breast cancer that is formed when cancer cells within your breast produce mucous	topic_bc
74581	3	355220	6	NULL	NULL	0	NULL	breast	CellComponent		produce					mucosa	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Mucinous (colloid) carcinoma is a rare type of invasive breast cancer that is formed when cancer cells within your breast produce mucous	topic_bc
74584	4	355220	6	NULL	NULL	0	NULL	statement 1	Process		is due to					statement 3	process				NULL		0	NULL	NULL	NULL	NULL	NULL	Mucinous (colloid) carcinoma is a rare type of invasive breast cancer that is formed when cancer cells within your breast produce mucous	topic_bc
74589	1	355221	6	NULL	NULL	NULL	NULL	TNC	GP		is involved in					breast cancer	MedicalFinding	metastatic			NULL		NULL	NULL	NULL	NULL	NULL	NULL	TNC is just one gene involved in metastatic breast cancer	topic_bc
74594	1	355222	6	NULL	NULL	0	NULL	IBC			is					Inflammatory breast cancer					NULL		0	NULL	NULL	NULL	NULL	NULL	Inflammatory breast cancer (IBC) is rare	topic_bc
76548	1	355223	11	NULL	NULL	0	NULL	nose	Organism part	skin of	is infected by		actively			MRSA	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Often, MRSA will live somewhat harmlessly in the nasal passages of people who have had previous infections or who work in hospital environments. Less commonly, MRSA will cause active infections in the skin of the nose.	topic_mrs
75560	1	355224	11	NULL	NULL	NULL	NULL	Cutaneous abscesses	MedicalFinding		are collections of					pus	AbstractConcept	dermis;;deeper skin tissues			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Cutaneous abscesses are collections of pus within the dermis and deeper skin tissues.S. aureus is present, usually as a single pathogen, in only ∼25% of cutaneous abscesses overall.	topic_mrs
75561	2	355224	11	NULL	NULL	0	NULL	S. aureus	Organism		causes		possibly			statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Cutaneous abscesses are collections of pus within the dermis and deeper skin tissues.S. aureus is present, usually as a single pathogen, in only ∼25% of cutaneous abscesses overall.	topic_mrs
75562	1	355226	11	NULL	NULL	0	NULL	Furuncles	MedicalFinding		infects					hair follicle	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Furuncles (or “boils”) are infections of the hair follicle, usually caused by S. aureus, in which suppuration extends through the dermis into the subcutaneous tissue, where a small abscess forms	topic_mrs
75563	2	355226	11	NULL	NULL	0	NULL	 S. aureus	Organism		causes					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Furuncles (or “boils”) are infections of the hair follicle, usually caused by S. aureus, in which suppuration extends through the dermis into the subcutaneous tissue, where a small abscess forms	topic_mrs
75564	3	355226	11	NULL	NULL	0	NULL	Furuncles	MedicalFinding		associates with					suppuration	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Furuncles (or “boils”) are infections of the hair follicle, usually caused by S. aureus, in which suppuration extends through the dermis into the subcutaneous tissue, where a small abscess forms	topic_mrs
76421	1	355227	11	NULL	NULL	0	NULL	furuncles	MedicalFinding		promotes					drainage	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	For small furuncles, moist heat, which seems to promote drainage, is satisfactory	topic_mrs
76422	1	355228	11	NULL	NULL	0	NULL	Larger furuncles	MedicalFinding		require					 incision	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Larger furuncles and all carbuncles require incision and drainage	topic_mrs
76423	2	355228	11	NULL	NULL	0	NULL	Larger furuncles	MedicalFinding		require					drainage	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Larger furuncles and all carbuncles require incision and drainage	topic_mrs
76424	3	355228	11	NULL	NULL	0	NULL	statement 1	Process		occurs along with					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Larger furuncles and all carbuncles require incision and drainage	topic_mrs
76425	4	355228	11	NULL	NULL	0	NULL	carbuncles	MedicalFinding		require					incision	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Larger furuncles and all carbuncles require incision and drainage	topic_mrs
76426	5	355228	11	NULL	NULL	0	NULL	carbuncles	MedicalFinding		require					drainage	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Larger furuncles and all carbuncles require incision and drainage	topic_mrs
76427	6	355228	11	NULL	NULL	0	NULL	statement 4	Process		occurs along with					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Larger furuncles and all carbuncles require incision and drainage	topic_mrs
75565	1	355229	11	NULL	NULL	NULL	NULL	Carbuncles	MedicalFinding		develop on		tend to			neck	OrganismPart	back of 			NULL		NULL	NULL	NULL	NULL	NULL	NULL	a coalescent inflammatory mass with pus draining from multiple follicular orifices, the lesion is called a carbuncle. Carbuncles tend to develop on the back of the neck and are especially likely to occur in diabetic persons.	topic_mrs
75566	2	355229	11	NULL	NULL	0	NULL	statement 1	Process		occur in		likely 			diabetic persons	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	a coalescent inflammatory mass with pus draining from multiple follicular orifices, the lesion is called a carbuncle. Carbuncles tend to develop on the back of the neck and are especially likely to occur in diabetic persons.	topic_mrs
75567	3	355229	11	NULL	NULL	0	NULL	carbuncle	MedicalFinding		is a type of 					 lesion	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	a coalescent inflammatory mass with pus draining from multiple follicular orifices, the lesion is called a carbuncle. Carbuncles tend to develop on the back of the neck and are especially likely to occur in diabetic persons.	topic_mrs
76428	1	355232	11	NULL	NULL	0	NULL	fomite	Chemical		carries					infectious organisms	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	A fomite is any inanimate object or substance capable of carrying infectious organisms (such as germs or parasites) and hence transferring them from one individual to another. A fomite can be anything (such as a cloth or mop head), so when cleaning, it is important to remember that such items could aid the spread of pathogenic organisms. Skin cells, hair, clothing, and bedding are common hospital sources of contamination.	topic_mrs
76429	2	355232	11	NULL	NULL	0	NULL	germs	Organism		is a type of 					 infectious organisms	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	A fomite is any inanimate object or substance capable of carrying infectious organisms (such as germs or parasites) and hence transferring them from one individual to another. A fomite can be anything (such as a cloth or mop head), so when cleaning, it is important to remember that such items could aid the spread of pathogenic organisms. Skin cells, hair, clothing, and bedding are common hospital sources of contamination.	topic_mrs
76430	3	355232	11	NULL	NULL	0	NULL	parasites	Organism		is a type of 					infectious organisms	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	A fomite is any inanimate object or substance capable of carrying infectious organisms (such as germs or parasites) and hence transferring them from one individual to another. A fomite can be anything (such as a cloth or mop head), so when cleaning, it is important to remember that such items could aid the spread of pathogenic organisms. Skin cells, hair, clothing, and bedding are common hospital sources of contamination.	topic_mrs
76431	4	355232	11	NULL	NULL	0	NULL	cloth	Chemical		is a type of 					fomite	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	A fomite is any inanimate object or substance capable of carrying infectious organisms (such as germs or parasites) and hence transferring them from one individual to another. A fomite can be anything (such as a cloth or mop head), so when cleaning, it is important to remember that such items could aid the spread of pathogenic organisms. Skin cells, hair, clothing, and bedding are common hospital sources of contamination.	topic_mrs
76432	5	355232	11	NULL	NULL	0	NULL	mop head	Chemical		is a type of 					fomite	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	A fomite is any inanimate object or substance capable of carrying infectious organisms (such as germs or parasites) and hence transferring them from one individual to another. A fomite can be anything (such as a cloth or mop head), so when cleaning, it is important to remember that such items could aid the spread of pathogenic organisms. Skin cells, hair, clothing, and bedding are common hospital sources of contamination.	topic_mrs
76433	6	355232	11	NULL	NULL	0	NULL	Skin cells	Cell		are source of 		common			hospital contamination	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	A fomite is any inanimate object or substance capable of carrying infectious organisms (such as germs or parasites) and hence transferring them from one individual to another. A fomite can be anything (such as a cloth or mop head), so when cleaning, it is important to remember that such items could aid the spread of pathogenic organisms. Skin cells, hair, clothing, and bedding are common hospital sources of contamination.	topic_mrs
76434	7	355232	11	NULL	NULL	0	NULL	hair	OrganismPart		are source of		common			hospital contamination					NULL		0	NULL	NULL	NULL	NULL	NULL	A fomite is any inanimate object or substance capable of carrying infectious organisms (such as germs or parasites) and hence transferring them from one individual to another. A fomite can be anything (such as a cloth or mop head), so when cleaning, it is important to remember that such items could aid the spread of pathogenic organisms. Skin cells, hair, clothing, and bedding are common hospital sources of contamination.	topic_mrs
76435	8	355232	11	NULL	NULL	0	NULL	clothing	Chemical		are source of		common			hospital contamination	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	A fomite is any inanimate object or substance capable of carrying infectious organisms (such as germs or parasites) and hence transferring them from one individual to another. A fomite can be anything (such as a cloth or mop head), so when cleaning, it is important to remember that such items could aid the spread of pathogenic organisms. Skin cells, hair, clothing, and bedding are common hospital sources of contamination.	topic_mrs
76436	9	355232	11	NULL	NULL	0	NULL	bedding	Chemical		are source of		common			hospital contamination	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	A fomite is any inanimate object or substance capable of carrying infectious organisms (such as germs or parasites) and hence transferring them from one individual to another. A fomite can be anything (such as a cloth or mop head), so when cleaning, it is important to remember that such items could aid the spread of pathogenic organisms. Skin cells, hair, clothing, and bedding are common hospital sources of contamination.	topic_mrs
76437	1	355233	11	NULL	NULL	0	NULL	chlorhexidine	Chemical		is a type of 					 antibacterial soaps	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	In some cases, fomites may harbor the organism and facilitate transmission of the infection. Depending on the individual circumstances, control of outbreaks may require bathing with antibacterial soaps, such as chlorhexidine; thorough laundering of clothing, towels, and bed wear; separate use of towels and washcloths; and attempted eradication of staphylococcal carriage among colonized persons.	topic_mrs
76438	2	355233	11	NULL	NULL	0	NULL	fomites	Chemical		harbor		may			organism 	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	In some cases, fomites may harbor the organism and facilitate transmission of the infection. Depending on the individual circumstances, control of outbreaks may require bathing with antibacterial soaps, such as chlorhexidine; thorough laundering of clothing, towels, and bed wear; separate use of towels and washcloths; and attempted eradication of staphylococcal carriage among colonized persons.	topic_mrs
76439	3	355233	11	NULL	NULL	0	NULL	fomites	Chemical		transmit					infection	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In some cases, fomites may harbor the organism and facilitate transmission of the infection. Depending on the individual circumstances, control of outbreaks may require bathing with antibacterial soaps, such as chlorhexidine; thorough laundering of clothing, towels, and bed wear; separate use of towels and washcloths; and attempted eradication of staphylococcal carriage among colonized persons.	topic_mrs
76440	1	355235	11	NULL	NULL	0	NULL	mupirocin ointment	Chemical		treats					nasal colonization	Process	anterior nares			NULL		0	NULL	NULL	NULL	NULL	NULL	For persons with nasal colonization, one approach is the application of mupirocin ointment twice daily in the anterior nares for the first 5 days each month. This regimen reduces recurrences by ∼50%.	topic_mrs
76441	2	355235	11	NULL	NULL	0	NULL	statement 1	Process		reduces					recurrence	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	For persons with nasal colonization, one approach is the application of mupirocin ointment twice daily in the anterior nares for the first 5 days each month. This regimen reduces recurrences by ∼50%.	topic_mrs
75568	1	355236	11	NULL	NULL	0	NULL	S. aureus	Organism		causes					furunculosis	MedicalFinding	recurrent			NULL		0	NULL	NULL	NULL	NULL	NULL	Clindamycin is an exception, and probably the best program for recurrent furunculosis caused by susceptible S. aureus is a single oral daily dose of 150 mg of this agent for 3 months, which decreases subsequent infections by ∼80%.	topic_mrs
75569	2	355236	11	NULL	NULL	0	NULL	Clindamycin	Chemical		treats		probably			statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Clindamycin is an exception, and probably the best program for recurrent furunculosis caused by susceptible S. aureus is a single oral daily dose of 150 mg of this agent for 3 months, which decreases subsequent infections by ∼80%.	topic_mrs
76442	1	355237	11	NULL	NULL	0	NULL	Erysipelas	MedicalFinding		is a type of 					cutaneous infection	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Erysipelas is distinguished clinically from other forms of cutaneous infection by the following 2 features: the lesions are raised above the level of the surrounding skin, and there is a clear line of demarcation between involved and uninvolved tissue...Rarely, group B streptococci or S. aureus may be involved.	topic_mrs
76443	2	355237	11	NULL	NULL	0	NULL	B streptococci	Organism		involved in		may			Erysipelas	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Erysipelas is distinguished clinically from other forms of cutaneous infection by the following 2 features: the lesions are raised above the level of the surrounding skin, and there is a clear line of demarcation between involved and uninvolved tissue...Rarely, group B streptococci or S. aureus may be involved.	topic_mrs
76444	3	355237	11	NULL	NULL	0	NULL	S. aureus	Organism		involved in		may			Erysipelas	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Erysipelas is distinguished clinically from other forms of cutaneous infection by the following 2 features: the lesions are raised above the level of the surrounding skin, and there is a clear line of demarcation between involved and uninvolved tissue...Rarely, group B streptococci or S. aureus may be involved.	topic_mrs
75570	1	355238	11	NULL	NULL	0	NULL	erysipelas	MedicalFinding		is also known as					Holy Fire	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	erysipelas is an acute streptococcus bacterial infection of the dermis, resulting in inflammation. It is also known as Holy Fire 	topic_mrs
75573	2	355238	11	NULL	NULL	NULL	NULL	erysipelas	MedicalFinding		is a type of 					acute streptococcus bacterial infection	MedicalFinding	of dermis			NULL		NULL	NULL	NULL	NULL	NULL	NULL	erysipelas is an acute streptococcus bacterial infection of the dermis, resulting in inflammation. It is also known as Holy Fire 	topic_mrs
75574	3	355238	11	NULL	NULL	0	NULL	statement 2	Process		resulting in					inflammation	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	erysipelas is an acute streptococcus bacterial infection of the dermis, resulting in inflammation. It is also known as Holy Fire 	topic_mrs
76445	1	355241	11	NULL	NULL	0	NULL	saphenous venectomy	MedicalProcedure		is a type of 					Surgical procedure	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Surgical procedures that increase the risk for cellulitis, presumably due to disruption of lymphatic drainage, include saphenous venectomy, axillary node dissection for breast cancer, and operations for gynecologic malignancies that involve lymph node dissection, especially when followed by radiation therapy, such as radical vulvectomy and radical hysterectomy	topic_mrs
76446	2	355241	11	NULL	NULL	0	NULL	axillary node dissection	MedicalFinding	for breast cancer	is a type of 					Surgical procedure	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Surgical procedures that increase the risk for cellulitis, presumably due to disruption of lymphatic drainage, include saphenous venectomy, axillary node dissection for breast cancer, and operations for gynecologic malignancies that involve lymph node dissection, especially when followed by radiation therapy, such as radical vulvectomy and radical hysterectomy	topic_mrs
76447	3	355241	11	NULL	NULL	0	NULL	lymph node dissection	MedicalFinding		is a type of 					Surgical procedure	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Surgical procedures that increase the risk for cellulitis, presumably due to disruption of lymphatic drainage, include saphenous venectomy, axillary node dissection for breast cancer, and operations for gynecologic malignancies that involve lymph node dissection, especially when followed by radiation therapy, such as radical vulvectomy and radical hysterectomy	topic_mrs
76448	4	355241	11	NULL	NULL	0	NULL	radical vulvectomy	MedicalFinding		is a type of 					radiation therapy	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Surgical procedures that increase the risk for cellulitis, presumably due to disruption of lymphatic drainage, include saphenous venectomy, axillary node dissection for breast cancer, and operations for gynecologic malignancies that involve lymph node dissection, especially when followed by radiation therapy, such as radical vulvectomy and radical hysterectomy	topic_mrs
76449	5	355241	11	NULL	NULL	0	NULL	radical hysterectomy	MedicalFinding		is a type of 					radiation therapy	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Surgical procedures that increase the risk for cellulitis, presumably due to disruption of lymphatic drainage, include saphenous venectomy, axillary node dissection for breast cancer, and operations for gynecologic malignancies that involve lymph node dissection, especially when followed by radiation therapy, such as radical vulvectomy and radical hysterectomy	topic_mrs
76450	6	355241	11	NULL	NULL	0	NULL	saphenous venectomy	MedicalFinding		 increase					cellulitis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Surgical procedures that increase the risk for cellulitis, presumably due to disruption of lymphatic drainage, include saphenous venectomy, axillary node dissection for breast cancer, and operations for gynecologic malignancies that involve lymph node dissection, especially when followed by radiation therapy, such as radical vulvectomy and radical hysterectomy	topic_mrs
76451	7	355241	11	NULL	NULL	0	NULL	axillary node dissection	MedicalFinding		increases					 cellulitis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Surgical procedures that increase the risk for cellulitis, presumably due to disruption of lymphatic drainage, include saphenous venectomy, axillary node dissection for breast cancer, and operations for gynecologic malignancies that involve lymph node dissection, especially when followed by radiation therapy, such as radical vulvectomy and radical hysterectomy	topic_mrs
76452	8	355241	11	NULL	NULL	0	NULL	lymph node dissection	MedicalFinding		increases					cellulitis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Surgical procedures that increase the risk for cellulitis, presumably due to disruption of lymphatic drainage, include saphenous venectomy, axillary node dissection for breast cancer, and operations for gynecologic malignancies that involve lymph node dissection, especially when followed by radiation therapy, such as radical vulvectomy and radical hysterectomy	topic_mrs
76453	9	355241	11	NULL	NULL	0	NULL	radical vulvectomy	MedicalFinding		increases					cellulitis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Surgical procedures that increase the risk for cellulitis, presumably due to disruption of lymphatic drainage, include saphenous venectomy, axillary node dissection for breast cancer, and operations for gynecologic malignancies that involve lymph node dissection, especially when followed by radiation therapy, such as radical vulvectomy and radical hysterectomy	topic_mrs
76454	10	355241	11	NULL	NULL	0	NULL	radical hysterectomy	MedicalFinding		increases					cellulitis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Surgical procedures that increase the risk for cellulitis, presumably due to disruption of lymphatic drainage, include saphenous venectomy, axillary node dissection for breast cancer, and operations for gynecologic malignancies that involve lymph node dissection, especially when followed by radiation therapy, such as radical vulvectomy and radical hysterectomy	topic_mrs
75610	1	355243	11	NULL	NULL	0	NULL	Necrosis	MedicalFinding		means					 premature death	Process	cells;;living tissue			NULL		0	NULL	NULL	NULL	NULL	NULL	Necrosis is the premature death of cells and living tissue. Necrosis is caused by factors external to the cell or tissue, such as infection, toxins, or trauma. 	topic_mrs
75611	2	355243	11	NULL	NULL	0	NULL	Necrosis	MedicalFinding		caused by					infection	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Necrosis is the premature death of cells and living tissue. Necrosis is caused by factors external to the cell or tissue, such as infection, toxins, or trauma. 	topic_mrs
75612	3	355243	11	NULL	NULL	0	NULL	Necrosis	MedicalFinding		caused by					toxins	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Necrosis is the premature death of cells and living tissue. Necrosis is caused by factors external to the cell or tissue, such as infection, toxins, or trauma. 	topic_mrs
75613	4	355243	11	NULL	NULL	0	NULL	Necrosis	MedicalFinding		caused by					trauma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Necrosis is the premature death of cells and living tissue. Necrosis is caused by factors external to the cell or tissue, such as infection, toxins, or trauma. 	topic_mrs
76455	1	355244	11	NULL	NULL	NULL	NULL	Debridement	MedicalProcedure		is removal of 		 medical 			dead tissues	OrganismPart				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Debridement is the medical removal of a patient's dead, damaged, or infected tissue to improve the healing potential of the remaining healthy tissue	topic_mrs
76456	2	355244	11	NULL	NULL	NULL	NULL	Debridement	MedicalProcedure		is removal of 					dead tissues	Organism part				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Debridement is the medical removal of a patient's dead, damaged, or infected tissue to improve the healing potential of the remaining healthy tissue	topic_mrs
76457	3	355244	11	NULL	NULL	NULL	NULL	Debridement	MedicalProcedure		is removal of					dead tissues	Organism part				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Debridement is the medical removal of a patient's dead, damaged, or infected tissue to improve the healing potential of the remaining healthy tissue	topic_mrs
76458	4	355244	11	NULL	NULL	NULL	NULL	statement 1	Process		improve					healthy tissues	OrganismPart	healing potential of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Debridement is the medical removal of a patient's dead, damaged, or infected tissue to improve the healing potential of the remaining healthy tissue	topic_mrs
76459	5	355244	11	NULL	NULL	NULL	NULL	statement 2	Process		improve					healthy tissue	OrganismPart	healing potential of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Debridement is the medical removal of a patient's dead, damaged, or infected tissue to improve the healing potential of the remaining healthy tissue	topic_mrs
76460	6	355244	11	NULL	NULL	NULL	NULL	statement 3	Process		improve					healthy tissue	OrganismPart	healing potential of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Debridement is the medical removal of a patient's dead, damaged, or infected tissue to improve the healing potential of the remaining healthy tissue	topic_mrs
76461	1	355245	11	NULL	NULL	0	NULL	cefazolin	Chemical		is also known as					cefazoline	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	cefazolin, also known as cefazoline or cephazolin, is a first-generation cephalosporin antibiotic.	topic_mrs
76462	2	355245	11	NULL	NULL	0	NULL	cefazolin	Chemical		is also known as					cephazolin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	cefazolin, also known as cefazoline or cephazolin, is a first-generation cephalosporin antibiotic.	topic_mrs
76463	3	355245	11	NULL	NULL	0	NULL	cefazolin	Chemical		is a type of 					first-generation cephalosporin antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	cefazolin, also known as cefazoline or cephazolin, is a first-generation cephalosporin antibiotic.	topic_mrs
76464	1	355248	11	NULL	NULL	NULL	NULL	Elevation	MedicalProcedure		drains					swollen fluids	Cell Component				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Elevation leads to drainage of swollen fluids, leading to a faster recovery time	topic_mrs
76465	2	355248	11	NULL	NULL	NULL	NULL	statement 1	Process		leading to					recovery	Process	faster			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Elevation leads to drainage of swollen fluids, leading to a faster recovery time	topic_mrs
76466	1	355250	11	NULL	NULL	NULL	NULL	antibiotic solution	Chemical		decrease					wound	MedicalFinding	infection of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	 Irrigation of wounds with antibiotic solutions is associated with decreased rate of wound infection. 	topic_mrs
76467	1	355253	11	NULL	NULL	NULL	NULL	surgical site infection	MedicalFinding		occurs after					surgery	MedicalProcedure				NULL		NULL	NULL	NULL	NULL	NULL	NULL	A surgical site infection is an infection that occurs after surgery in the part of the body where the surgery took place. Most patients who have surgery do not develop an infection. However, infections develop in about 1 to 3 out of every 100 patients who have surgery.	topic_mrs
76549	1	355254	11	NULL	NULL	0	NULL	SSI	medical finding	therapy for	include					incision	medical finding	opening of			NULL		0	NULL	NULL	NULL	NULL	NULL	The primary, and most important, therapy for SSI is to open the incision, evacuate the infected material, and continue dressing changes until the wound heals by secondary intention.	topic_mrs
76550	2	355254	11	NULL	NULL	0	NULL	statement 1	Process		is followed by					infected material	AbstractConcept	evacuation of			NULL		0	NULL	NULL	NULL	NULL	NULL	The primary, and most important, therapy for SSI is to open the incision, evacuate the infected material, and continue dressing changes until the wound heals by secondary intention.	topic_mrs
76551	3	355254	11	NULL	NULL	0	NULL	statement 2	Process		is followed by					dressing	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	The primary, and most important, therapy for SSI is to open the incision, evacuate the infected material, and continue dressing changes until the wound heals by secondary intention.	topic_mrs
76552	4	355254	11	NULL	NULL	0	NULL	wound	MedicalFinding		heals by					secondary intention	medical procedure				NULL		0	NULL	NULL	NULL	NULL	NULL	The primary, and most important, therapy for SSI is to open the incision, evacuate the infected material, and continue dressing changes until the wound heals by secondary intention.	topic_mrs
76553	5	355254	11	NULL	NULL	0	NULL	statement 3	Process		is continued untill					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The primary, and most important, therapy for SSI is to open the incision, evacuate the infected material, and continue dressing changes until the wound heals by secondary intention.	topic_mrs
74369	1	355255	5	NULL	NULL	0	NULL	Rs9722	Chromosome		is a type of					SNP	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	Rs9722 and rs1051169 have been reported as affecting the levels of S100B in the serum or the brain, and haplotypes containing these two SNPs have been associated with schizophrenia.	topic_sch
74370	2	355255	5	NULL	NULL	0	NULL	rs1051169	Chromosome		is a type of					SNP	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	Rs9722 and rs1051169 have been reported as affecting the levels of S100B in the serum or the brain, and haplotypes containing these two SNPs have been associated with schizophrenia.	topic_sch
74371	3	355255	5	NULL	NULL	0	NULL	Rs9722	Chromosome		affects					S100B	GP	level of			NULL	serum	0	NULL	NULL	NULL	NULL	NULL	Rs9722 and rs1051169 have been reported as affecting the levels of S100B in the serum or the brain, and haplotypes containing these two SNPs have been associated with schizophrenia.	topic_sch
74372	4	355255	5	NULL	NULL	0	NULL	Rs9722	Chromosome		affects					S100B	GP	level of			NULL	brain	0	NULL	NULL	NULL	NULL	NULL	Rs9722 and rs1051169 have been reported as affecting the levels of S100B in the serum or the brain, and haplotypes containing these two SNPs have been associated with schizophrenia.	topic_sch
74373	5	355255	5	NULL	NULL	0	NULL	rs1051169	Chromosome		affects					S100B	GP	level of			NULL	serum	0	NULL	NULL	NULL	NULL	NULL	Rs9722 and rs1051169 have been reported as affecting the levels of S100B in the serum or the brain, and haplotypes containing these two SNPs have been associated with schizophrenia.	topic_sch
74374	6	355255	5	NULL	NULL	0	NULL	rs1051169	Chromosome		affects					S100B	GP	level of			NULL	brain	0	NULL	NULL	NULL	NULL	NULL	Rs9722 and rs1051169 have been reported as affecting the levels of S100B in the serum or the brain, and haplotypes containing these two SNPs have been associated with schizophrenia.	topic_sch
74375	7	355255	5	NULL	NULL	0	NULL	haplotype	Chromosome		contains					Rs9722	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	Rs9722 and rs1051169 have been reported as affecting the levels of S100B in the serum or the brain, and haplotypes containing these two SNPs have been associated with schizophrenia.	topic_sch
74376	8	355255	5	NULL	NULL	0	NULL	haplotype	Chromosome		contains					rs1051169	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	Rs9722 and rs1051169 have been reported as affecting the levels of S100B in the serum or the brain, and haplotypes containing these two SNPs have been associated with schizophrenia.	topic_sch
74377	9	355255	5	NULL	NULL	0	NULL	statement 7	Process		occurs along with					statement 8	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Rs9722 and rs1051169 have been reported as affecting the levels of S100B in the serum or the brain, and haplotypes containing these two SNPs have been associated with schizophrenia.	topic_sch
74378	10	355255	5	NULL	NULL	0	NULL	statement 7	Process		is associated with					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Rs9722 and rs1051169 have been reported as affecting the levels of S100B in the serum or the brain, and haplotypes containing these two SNPs have been associated with schizophrenia.	topic_sch
74379	11	355255	5	NULL	NULL	0	NULL	statement 8	Process		is associated with					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Rs9722 and rs1051169 have been reported as affecting the levels of S100B in the serum or the brain, and haplotypes containing these two SNPs have been associated with schizophrenia.	topic_sch
74380	1	355256	5	NULL	NULL	NULL	NULL	S100B gene polymorphism	AbstractConcept		plays a role in					schizophrenia patients	GroupOfPeople	cognitive functions of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	These results implicate a role for S100B gene polymorphisms in the cognitive functions of schizophrenia patients and encourage further investigation into spatial disability as an endophenotype of schizophrenia.	topic_sch
74381	2	355256	5	NULL	NULL	0	NULL	spatial disability	MedicalFinding		is an endophenotype of					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	These results implicate a role for S100B gene polymorphisms in the cognitive functions of schizophrenia patients and encourage further investigation into spatial disability as an endophenotype of schizophrenia.	topic_sch
75658	1	355257	7	NULL	NULL	0	NULL	mitochondrial respiration	Process	decreased	indicates					mitochondria	CellComponent	dysfunction of			NULL		0	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial previous termdisorders.next term	topic_bd
75659	2	355257	7	NULL	NULL	0	NULL	mitochondrial morphology	CellComponent	changes in	indicates					mitochondria	CellComponent	dysfunction of			NULL		0	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial previous termdisorders.next term	topic_bd
75660	3	355257	7	NULL	NULL	0	NULL	mtDNA polymorphisms	NucleicAcid	increase in	indicates					mitochondria	CellComponent	dysfunction of			NULL		0	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial previous termdisorders.next term	topic_bd
75661	4	355257	7	NULL	NULL	NULL	NULL	mtDNA 	NucleicAcid	increase in;;mutations in	indicates					mitochondria	CellComponent	dysfunction of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial previous termdisorders.next term	topic_bd
75662	5	355257	7	NULL	NULL	NULL	NULL	nuclear mRNA molecules 	NucleicAcid	downregulation of	indicates					mitochondria	CellComponent	dysfunction of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial previous termdisorders.next term	topic_bd
75663	6	355257	7	NULL	NULL	NULL	NULL	nuclear proteins	GP	downregulation of	indicates					mitochondria	CellComponent	dysfunction of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial previous termdisorders.next term	topic_bd
75664	7	355257	7	NULL	NULL	0	NULL	nuclear mRNA molecules 	GP		involved in					mitochondrial respiration	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial previous termdisorders.next term	topic_bd
75665	8	355257	7	NULL	NULL	0	NULL	nuclear proteins	GP		involved in					mitochondrial respiration	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial previous termdisorders.next term	topic_bd
75666	9	355257	7	NULL	NULL	NULL	NULL	high energy phosphates	Chemical	decrease of;;brain	indicates					mitochondria	CellComponent	dysfunction of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial previous termdisorders.next term	topic_bd
75667	10	355257	7	NULL	NULL	0	NULL	pH	PhysicalPhenomenon	decrease of;;brain	indicates					mitochondria	CellComponent	dysfunction of			NULL		0	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial previous termdisorders.next term	topic_bd
75668	1	355259	7	NULL	NULL	0	NULL	Schizophrenia	MedicalFinding	phenotype of	share with					BPD-I	MedicalFinding	phenotype of			NULL		0	NULL	NULL	NULL	NULL	NULL	Schizophrenia and BPD-I share many overlapping phenotypes ([Lin and Mitchell, 2008] and [Thaker, 2008]). Evidence for shared genetic factors derives from pharmacology, pathology, family studies and DNA linkage analysis 	topic_bd
75669	1	355260	7	NULL	NULL	0	NULL	mtDNA	NucleicAcid	mutation of	 cause					mitochondrial disorders	MedicalFinding	primary disease in			NULL		0	NULL	NULL	NULL	NULL	NULL	the primary disease-causing event in mitochondrial disorders is the mtDNA mutation.	topic_bd
75670	1	355261	7	NULL	NULL	0	NULL	mitochondrial diseases	MedicalFinding		comorbid with					psychotic symptoms	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Conversely, bona fide mitochondrial diseases are frequently comorbid with psychotic symptoms and misdiagnosed as SZ or BPD	topic_bd
75671	2	355261	7	NULL	NULL	0	NULL	mitochondrial diseases	MedicalFinding		misdiagnosed as					SZ	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Conversely, bona fide mitochondrial diseases are frequently comorbid with psychotic symptoms and misdiagnosed as SZ or BPD	topic_bd
75672	3	355261	7	NULL	NULL	0	NULL	mitochondrial diseases	MedicalFinding		misdiagnosed as					BPD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Conversely, bona fide mitochondrial diseases are frequently comorbid with psychotic symptoms and misdiagnosed as SZ or BPD	topic_bd
75673	1	355262	7	NULL	NULL	0	NULL	Mood stabilizers	Chemical		protect against		partial			mitochondrial toxicity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Mood stabilizers provide partial protection against mitochondrial toxicity, whereas first-generation antipsychotic drugs might have adverse effects on mitochondrial respiration	topic_bd
75674	2	355262	7	NULL	NULL	0	NULL	antipsychotic drugs	Chemical		adverse effects on					mitochondrial respiration	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Mood stabilizers provide partial protection against mitochondrial toxicity, whereas first-generation antipsychotic drugs might have adverse effects on mitochondrial respiration	topic_bd
75675	1	355263	7	NULL	NULL	NULL	NULL	Mitochondrial pathology	MedicalFinding		consequence of		could be			genetic susceptibility	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Mitochondrial pathology could be the consequence of genetic susceptibility secondary to dysregulation of other neurotransmitter systems 	topic_bd
75676	2	355263	7	NULL	NULL	NULL	NULL	statement 1	Process		secondary to					neurotransmitter system	Chemical	dysregulation of 			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Mitochondrial pathology could be the consequence of genetic susceptibility secondary to dysregulation of other neurotransmitter systems 	topic_bd
75677	1	355264	7	NULL	NULL	0	NULL	Mitochondrial pathology	MedicalFinding		consequence of		could be			genetic susceptibility	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mitochondrial pathology could be the consequence of genetic susceptibility secondary to dysregulation of other neurotransmitter systems or the results of environmental impacts such as exposure to toxins, famine, infections and substance abuse all of which are known risk factors for BPD and SZ.	topic_bd
75678	2	355264	7	NULL	NULL	0	NULL	statement 1	Process		secondary to					neurotransmitter system	Chemical	dysregulation of 			NULL		0	NULL	NULL	NULL	NULL	NULL	Mitochondrial pathology could be the consequence of genetic susceptibility secondary to dysregulation of other neurotransmitter systems or the results of environmental impacts such as exposure to toxins, famine, infections and substance abuse all of which are known risk factors for BPD and SZ.	topic_bd
75679	3	355264	7	NULL	NULL	0	NULL	 toxins	Chemical	exposure to	risk factor of					BPD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mitochondrial pathology could be the consequence of genetic susceptibility secondary to dysregulation of other neurotransmitter systems or the results of environmental impacts such as exposure to toxins, famine, infections and substance abuse all of which are known risk factors for BPD and SZ.	topic_bd
75680	4	355264	7	NULL	NULL	0	NULL	famine	PhysicalPhenomenon		risk factor of					BPD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mitochondrial pathology could be the consequence of genetic susceptibility secondary to dysregulation of other neurotransmitter systems or the results of environmental impacts such as exposure to toxins, famine, infections and substance abuse all of which are known risk factors for BPD and SZ.	topic_bd
75681	5	355264	7	NULL	NULL	0	NULL	infection	MedicalFinding		risk factor of					BPD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mitochondrial pathology could be the consequence of genetic susceptibility secondary to dysregulation of other neurotransmitter systems or the results of environmental impacts such as exposure to toxins, famine, infections and substance abuse all of which are known risk factors for BPD and SZ.	topic_bd
75682	6	355264	7	NULL	NULL	0	NULL	substance abuse	Chemical		risk factor of					BPD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mitochondrial pathology could be the consequence of genetic susceptibility secondary to dysregulation of other neurotransmitter systems or the results of environmental impacts such as exposure to toxins, famine, infections and substance abuse all of which are known risk factors for BPD and SZ.	topic_bd
75683	7	355264	7	NULL	NULL	0	NULL	toxins	Chemical	exposure to	risk factor of					SZ	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mitochondrial pathology could be the consequence of genetic susceptibility secondary to dysregulation of other neurotransmitter systems or the results of environmental impacts such as exposure to toxins, famine, infections and substance abuse all of which are known risk factors for BPD and SZ.	topic_bd
75684	8	355264	7	NULL	NULL	0	NULL	famine	PhysicalPhenomenon		risk factor of					SZ	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mitochondrial pathology could be the consequence of genetic susceptibility secondary to dysregulation of other neurotransmitter systems or the results of environmental impacts such as exposure to toxins, famine, infections and substance abuse all of which are known risk factors for BPD and SZ.	topic_bd
75685	9	355264	7	NULL	NULL	0	NULL	infection	MedicalFinding		risk factor of					SZ	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mitochondrial pathology could be the consequence of genetic susceptibility secondary to dysregulation of other neurotransmitter systems or the results of environmental impacts such as exposure to toxins, famine, infections and substance abuse all of which are known risk factors for BPD and SZ.	topic_bd
75686	10	355264	7	NULL	NULL	0	NULL	substance abuse	Chemical		risk factor of					SZ	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mitochondrial pathology could be the consequence of genetic susceptibility secondary to dysregulation of other neurotransmitter systems or the results of environmental impacts such as exposure to toxins, famine, infections and substance abuse all of which are known risk factors for BPD and SZ.	topic_bd
75687	1	355265	7	NULL	NULL	0	NULL	Mitochondria	CellComponent		smaller in		significantly			PFC	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	Mitochondria were significantly smaller in the prefrontal cortex (PFC) of BPD patients compared to normal controls 	topic_bd
75688	2	355265	7	NULL	NULL	0	NULL	statement 1	Process		occur in					BPD	MedicalFinding	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	Mitochondria were significantly smaller in the prefrontal cortex (PFC) of BPD patients compared to normal controls 	topic_bd
75689	3	355265	7	NULL	NULL	0	NULL	PFC	CellComponent		is					prefrontal cortex	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	Mitochondria were significantly smaller in the prefrontal cortex (PFC) of BPD patients compared to normal controls 	topic_bd
75690	1	355266	7	NULL	NULL	0	NULL	mitochondria	CellComponent	cellular location of	altered in					lymphoblastoid cell line	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	The cellular location of mitochondria was altered in lymphoblastoid and fibroblast cell lines of BPD patients	topic_bd
75691	2	355266	7	NULL	NULL	NULL	NULL	mitochondria	CellComponent	cellular location of	altered in					 fibroblast cell lines	Cell				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The cellular location of mitochondria was altered in lymphoblastoid and fibroblast cell lines of BPD patients	topic_bd
75692	3	355266	7	NULL	NULL	0	NULL	statement 1	Process		occur in					BPD	MedicalFinding	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	The cellular location of mitochondria was altered in lymphoblastoid and fibroblast cell lines of BPD patients	topic_bd
75693	4	355266	7	NULL	NULL	0	NULL	statement 2	Process		occur in					BPD	MedicalFinding	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	The cellular location of mitochondria was altered in lymphoblastoid and fibroblast cell lines of BPD patients	topic_bd
75694	1	355267	7	NULL	NULL	NULL	NULL	BPD	MedicalFinding	lymphocytes of patients of	does not respond to 					glucose	Chemical	deprivation of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Lymphocytes of BPD patients failed to respond to glucose deprivation while lymphocytes of normal controls responded with an upregulation of the elements of the electron transport chain	topic_bd
75695	2	355267	7	NULL	NULL	0	NULL	normal lymphocytes	cell		respond to					glucose 	Chemical	deprivation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Lymphocytes of BPD patients failed to respond to glucose deprivation while lymphocytes of normal controls responded with an upregulation of the elements of the electron transport chain	topic_bd
75696	3	355267	7	NULL	NULL	0	NULL	statement 2	Process		upregulate					electron transport chain	Process	elements of			NULL		0	NULL	NULL	NULL	NULL	NULL	Lymphocytes of BPD patients failed to respond to glucose deprivation while lymphocytes of normal controls responded with an upregulation of the elements of the electron transport chain	topic_bd
74595	1	355271	6	NULL	NULL	0	NULL	SERM	Chemical		act on					estrogen receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Selective Estrogen Receptor Modulators (SERMs) are a class of compounds that act on the estrogen receptor.	topic_bc
74596	1	355272	6	NULL	NULL	NULL	NULL	raloxifene hydrochloride	Chemical		reduces					breast cancer	MedicalFinding	risk of;; invasive			NULL	post-menopausal women with Osteoporosis	NULL	NULL	NULL	NULL	NULL	NULL	On September 13, 2007, the U. S. Food and Drug Administration approved raloxifene hydrochloride tablets (Evista® tablets, made by Eli Lilly and Company) for reduction in the risk of invasive breast cancer in postmenopausal women with osteoporosis and in postmenopausal women at high risk for invasive breast cancer.	topic_bc
74607	2	355272	6	NULL	NULL	0	NULL	post-menopausal women	Person		is at					breast cancer	MedicalFinding	high risk;; invasive			NULL		0	NULL	NULL	NULL	NULL	NULL	On September 13, 2007, the U. S. Food and Drug Administration approved raloxifene hydrochloride tablets (Evista® tablets, made by Eli Lilly and Company) for reduction in the risk of invasive breast cancer in postmenopausal women with osteoporosis and in postmenopausal women at high risk for invasive breast cancer.	topic_bc
74608	3	355272	6	NULL	NULL	0	NULL	raloxifene hydrochloride	Chemical		reduces					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	On September 13, 2007, the U. S. Food and Drug Administration approved raloxifene hydrochloride tablets (Evista® tablets, made by Eli Lilly and Company) for reduction in the risk of invasive breast cancer in postmenopausal women with osteoporosis and in postmenopausal women at high risk for invasive breast cancer.	topic_bc
74382	1	355273	5	NULL	NULL	0	NULL	Asenapine	Chemical		is a type of					atypical antipsychotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Asenapine is an atypical antipsychotic approved by the US Food and Drug Administration in adults for treatment of schizophrenia or acute treatment, as monotherapy or adjunct therapy to lithium or valproate, of manic or mixed episodes of bipolar I disorder.	topic_sch
74383	2	355273	5	NULL	NULL	0	NULL	Asenapine	Chemical		is approved by					US Food and Drug Administration	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Asenapine is an atypical antipsychotic approved by the US Food and Drug Administration in adults for treatment of schizophrenia or acute treatment, as monotherapy or adjunct therapy to lithium or valproate, of manic or mixed episodes of bipolar I disorder.	topic_sch
74384	3	355273	5	NULL	NULL	0	NULL	Asenapine	Chemical		treats					schizophrenia	MedicalFinding				NULL	adults	0	NULL	NULL	NULL	NULL	NULL	Asenapine is an atypical antipsychotic approved by the US Food and Drug Administration in adults for treatment of schizophrenia or acute treatment, as monotherapy or adjunct therapy to lithium or valproate, of manic or mixed episodes of bipolar I disorder.	topic_sch
74385	4	355273	5	NULL	NULL	0	NULL	Lithium	Chemical		treats					bipolar I disorder	MedicalFinding	 manic episodes of;;mixed episodes of			NULL		0	NULL	NULL	NULL	NULL	NULL	Asenapine is an atypical antipsychotic approved by the US Food and Drug Administration in adults for treatment of schizophrenia or acute treatment, as monotherapy or adjunct therapy to lithium or valproate, of manic or mixed episodes of bipolar I disorder.	topic_sch
74386	5	355273	5	NULL	NULL	0	NULL	valproate	Chemical		treats					bipolar I disorder	MedicalFinding	manic episodes of;;mixed episodes of			NULL		0	NULL	NULL	NULL	NULL	NULL	Asenapine is an atypical antipsychotic approved by the US Food and Drug Administration in adults for treatment of schizophrenia or acute treatment, as monotherapy or adjunct therapy to lithium or valproate, of manic or mixed episodes of bipolar I disorder.	topic_sch
74387	6	355273	5	NULL	NULL	0	NULL	Asenapine	Chemical		is an adjunct therapy to					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Asenapine is an atypical antipsychotic approved by the US Food and Drug Administration in adults for treatment of schizophrenia or acute treatment, as monotherapy or adjunct therapy to lithium or valproate, of manic or mixed episodes of bipolar I disorder.	topic_sch
74388	7	355273	5	NULL	NULL	0	NULL	Asenapine	Chemical		is an adjunct therapy to					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Asenapine is an atypical antipsychotic approved by the US Food and Drug Administration in adults for treatment of schizophrenia or acute treatment, as monotherapy or adjunct therapy to lithium or valproate, of manic or mixed episodes of bipolar I disorder.	topic_sch
74389	1	355275	5	NULL	NULL	0	NULL	major histocompatability complex	GP		is present in					chromosome 6p	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	The major histocompatability complex on chromosome 6p has often been identified as containing potential risk factors for schizophrenia.	topic_sch
74390	2	355275	5	NULL	NULL	0	NULL	major histocompatability complex	GP		plays a role in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The major histocompatability complex on chromosome 6p has often been identified as containing potential risk factors for schizophrenia.	topic_sch
74391	1	355276	5	NULL	NULL	0	NULL	NOTCH4 gene	GP		is located in					6p21.3	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	The NOTCH4 gene is located within this region (6p21.3) and sequence variants have previously shown association to the disease.	topic_sch
74392	1	355277	5	NULL	NULL	0	NULL	 NOTCH4 gene	GP		is located in					6p21.3	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	The NOTCH4 gene is located within this region (6p21.3) and sequence variants have previously shown association to the disease. It is further implicated from a functional standpoint as it plays a critical role during the neurodevelopmental process.	topic_sch
74393	2	355277	5	NULL	NULL	0	NULL	 NOTCH4 gene	GP		plays a role in					neurodevelopment	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The NOTCH4 gene is located within this region (6p21.3) and sequence variants have previously shown association to the disease. It is further implicated from a functional standpoint as it plays a critical role during the neurodevelopmental process.	topic_sch
74394	1	355278	5	NULL	NULL	0	NULL	25 C/T polymorphism	Process		is not associated with					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	It also established that the -25 C/T polymorphism was not associated to schizophrenia.	topic_sch
74395	1	355279	5	NULL	NULL	0	NULL	autism	MedicalFinding		is a type of					PDDs	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The term pervasive developmental disorders (PDDs) refers to a group of developmental conditions that involve delayed or impaired communication and social skills, behaviors, and cognitive skills (learning). autism is the best-known of the PDDs	topic_aut
74396	2	355279	5	NULL	NULL	0	NULL	PDDs	MedicalFinding		is					pervasive developmental disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The term pervasive developmental disorders (PDDs) refers to a group of developmental conditions that involve delayed or impaired communication and social skills, behaviors, and cognitive skills (learning). autism is the best-known of the PDDs	topic_aut
74397	3	355279	5	NULL	NULL	0	NULL	PDDs	MedicalFinding		involves					communication	AbstractConcept	delayed			NULL		0	NULL	NULL	NULL	NULL	NULL	The term pervasive developmental disorders (PDDs) refers to a group of developmental conditions that involve delayed or impaired communication and social skills, behaviors, and cognitive skills (learning). autism is the best-known of the PDDs	topic_aut
74398	4	355279	5	NULL	NULL	0	NULL	PDDs	MedicalFinding		involves					communication	AbstractConcept	impaired			NULL		0	NULL	NULL	NULL	NULL	NULL	The term pervasive developmental disorders (PDDs) refers to a group of developmental conditions that involve delayed or impaired communication and social skills, behaviors, and cognitive skills (learning). autism is the best-known of the PDDs	topic_aut
74399	5	355279	5	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The term pervasive developmental disorders (PDDs) refers to a group of developmental conditions that involve delayed or impaired communication and social skills, behaviors, and cognitive skills (learning). autism is the best-known of the PDDs	topic_aut
74400	6	355279	5	NULL	NULL	0	NULL	PDDs	MedicalFinding		involves					social skills	AbstractConcept	delayed			NULL		0	NULL	NULL	NULL	NULL	NULL	The term pervasive developmental disorders (PDDs) refers to a group of developmental conditions that involve delayed or impaired communication and social skills, behaviors, and cognitive skills (learning). autism is the best-known of the PDDs	topic_aut
74401	7	355279	5	NULL	NULL	0	NULL	PDDs	MedicalFinding		involves					social skills	AbstractConcept	impaired			NULL		0	NULL	NULL	NULL	NULL	NULL	The term pervasive developmental disorders (PDDs) refers to a group of developmental conditions that involve delayed or impaired communication and social skills, behaviors, and cognitive skills (learning). autism is the best-known of the PDDs	topic_aut
74402	8	355279	5	NULL	NULL	0	NULL	statement 6	Process		is an alternative to					statement 7	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The term pervasive developmental disorders (PDDs) refers to a group of developmental conditions that involve delayed or impaired communication and social skills, behaviors, and cognitive skills (learning). autism is the best-known of the PDDs	topic_aut
74403	9	355279	5	NULL	NULL	0	NULL	PDDs	MedicalFinding		involves					behavior	AbstractConcept	delayed			NULL		0	NULL	NULL	NULL	NULL	NULL	The term pervasive developmental disorders (PDDs) refers to a group of developmental conditions that involve delayed or impaired communication and social skills, behaviors, and cognitive skills (learning). autism is the best-known of the PDDs	topic_aut
74404	10	355279	5	NULL	NULL	0	NULL	PDDs	MedicalFinding		involves					behavior	AbstractConcept	impaired			NULL		0	NULL	NULL	NULL	NULL	NULL	The term pervasive developmental disorders (PDDs) refers to a group of developmental conditions that involve delayed or impaired communication and social skills, behaviors, and cognitive skills (learning). autism is the best-known of the PDDs	topic_aut
74405	11	355279	5	NULL	NULL	0	NULL	statement 9	Process		is an alternative to					statement 10	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The term pervasive developmental disorders (PDDs) refers to a group of developmental conditions that involve delayed or impaired communication and social skills, behaviors, and cognitive skills (learning). autism is the best-known of the PDDs	topic_aut
74406	12	355279	5	NULL	NULL	0	NULL	PDDs	MedicalFinding		involves					cognitive skills	MentalProcess	delayed			NULL		0	NULL	NULL	NULL	NULL	NULL	The term pervasive developmental disorders (PDDs) refers to a group of developmental conditions that involve delayed or impaired communication and social skills, behaviors, and cognitive skills (learning). autism is the best-known of the PDDs	topic_aut
74407	13	355279	5	NULL	NULL	0	NULL	PDDs	MedicalFinding		involves					cognitive skills	MentalProcess	impaired			NULL		0	NULL	NULL	NULL	NULL	NULL	The term pervasive developmental disorders (PDDs) refers to a group of developmental conditions that involve delayed or impaired communication and social skills, behaviors, and cognitive skills (learning). autism is the best-known of the PDDs	topic_aut
74408	14	355279	5	NULL	NULL	0	NULL	statement 12	Process		is an alternative to					statement 13	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The term pervasive developmental disorders (PDDs) refers to a group of developmental conditions that involve delayed or impaired communication and social skills, behaviors, and cognitive skills (learning). autism is the best-known of the PDDs	topic_aut
75697	1	355280	7	NULL	NULL	0	NULL	VPA	Chemical		is metabolized in					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	The mood stabilizer VPA is metabolized in mitochondria, and many antipsychotic drugs or their metabolites are taken up into mitochondria	topic_bd
75698	2	355280	7	NULL	NULL	0	NULL	antipsychotic drugs	Chemical		taken up in					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	The mood stabilizer VPA is metabolized in mitochondria, and many antipsychotic drugs or their metabolites are taken up into mitochondria	topic_bd
75699	3	355280	7	NULL	NULL	0	NULL	antipsychotic drugs	Chemical	metabolites of	taken up in					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	The mood stabilizer VPA is metabolized in mitochondria, and many antipsychotic drugs or their metabolites are taken up into mitochondria	topic_bd
75705	4	355280	7	NULL	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The mood stabilizer VPA is metabolized in mitochondria, and many antipsychotic drugs or their metabolites are taken up into mitochondria	topic_bd
75700	1	355281	7	NULL	NULL	0	NULL	VPA	Chemical		is metabolized in					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	The mood stabilizer VPA is metabolized in mitochondria, and many antipsychotic drugs or their metabolites are taken up into mitochondria 	topic_bd
75701	2	355281	7	NULL	NULL	0	NULL	VPA	Chemical		is a type of					mood stabilizer	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The mood stabilizer VPA is metabolized in mitochondria, and many antipsychotic drugs or their metabolites are taken up into mitochondria 	topic_bd
75702	3	355281	7	NULL	NULL	0	NULL	antipsychotic drugs	Chemical		taken up in					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	The mood stabilizer VPA is metabolized in mitochondria, and many antipsychotic drugs or their metabolites are taken up into mitochondria 	topic_bd
75703	4	355281	7	NULL	NULL	0	NULL	antipsychotic drugs	Chemical	metabolites of	taken up in					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	The mood stabilizer VPA is metabolized in mitochondria, and many antipsychotic drugs or their metabolites are taken up into mitochondria 	topic_bd
75704	5	355281	7	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The mood stabilizer VPA is metabolized in mitochondria, and many antipsychotic drugs or their metabolites are taken up into mitochondria 	topic_bd
75706	1	355282	7	NULL	NULL	0	NULL	VPA	Chemical		increase					 oxygen consumption	Process	mitochondrial			NULL		0	NULL	NULL	NULL	NULL	NULL	VPA and lithium induced increases in mitochondrial oxygen consumption and mitochondrial membrane potential	topic_bd
75707	2	355282	7	NULL	NULL	0	NULL	VPA	Chemical		increase					membrane potential	QuantityOrMeasure	mitochondrial			NULL		0	NULL	NULL	NULL	NULL	NULL	VPA and lithium induced increases in mitochondrial oxygen consumption and mitochondrial membrane potential	topic_bd
75708	3	355282	7	NULL	NULL	0	NULL	lithium	Chemical		increase					oxygen consumption	Process	mitochondrial			NULL		0	NULL	NULL	NULL	NULL	NULL	VPA and lithium induced increases in mitochondrial oxygen consumption and mitochondrial membrane potential	topic_bd
75709	4	355282	7	NULL	NULL	0	NULL	lithium	Chemical		increase					membrane potential	QuantityOrMeasure	mitochondrial			NULL		0	NULL	NULL	NULL	NULL	NULL	VPA and lithium induced increases in mitochondrial oxygen consumption and mitochondrial membrane potential	topic_bd
75710	1	355283	7	NULL	NULL	0	NULL	 mood stabilizers	Chemical		alleviate					BPD	MedicalFinding	symptoms of			NULL		0	NULL	NULL	NULL	NULL	NULL	This indicates that mood stabilizers may alleviate some of the symptoms of BPD by improving mitochondrial function	topic_bd
75711	2	355283	7	NULL	NULL	0	NULL	statement 1	Process		improve					mitochondrial function	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	This indicates that mood stabilizers may alleviate some of the symptoms of BPD by improving mitochondrial function	topic_bd
75712	1	355284	7	NULL	NULL	0	NULL	lithium	Chemical		shows					antiapoptotic effects	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Both drugs [lithium and VPA] also have antiapoptotic effects. They are known to inhibit cytochrome c release from mitochondria and to increase expression of the anti-apoptotic gene Bcl-2.	topic_bd
75713	2	355284	7	NULL	NULL	0	NULL	VPA	Chemical		shows					antiapoptotic effects	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Both drugs [lithium and VPA] also have antiapoptotic effects. They are known to inhibit cytochrome c release from mitochondria and to increase expression of the anti-apoptotic gene Bcl-2.	topic_bd
75714	3	355284	7	NULL	NULL	0	NULL	lithium	Chemical		inhibit					cytochrome c	GP	release of			NULL		0	NULL	NULL	NULL	NULL	NULL	Both drugs [lithium and VPA] also have antiapoptotic effects. They are known to inhibit cytochrome c release from mitochondria and to increase expression of the anti-apoptotic gene Bcl-2.	topic_bd
75715	4	355284	7	NULL	NULL	0	NULL	statement 3	Process		occur from					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	Both drugs [lithium and VPA] also have antiapoptotic effects. They are known to inhibit cytochrome c release from mitochondria and to increase expression of the anti-apoptotic gene Bcl-2.	topic_bd
75716	5	355284	7	NULL	NULL	0	NULL	lithium	Chemical		increase					Bcl-2	GP	expression of			NULL		0	NULL	NULL	NULL	NULL	NULL	Both drugs [lithium and VPA] also have antiapoptotic effects. They are known to inhibit cytochrome c release from mitochondria and to increase expression of the anti-apoptotic gene Bcl-2.	topic_bd
75717	6	355284	7	NULL	NULL	0	NULL	Bcl-2	GP		is a type of					anti-apoptotic gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Both drugs [lithium and VPA] also have antiapoptotic effects. They are known to inhibit cytochrome c release from mitochondria and to increase expression of the anti-apoptotic gene Bcl-2.	topic_bd
75718	7	355284	7	NULL	NULL	0	NULL	VPA	Chemical		inhibit					cytochrome c	GP	release of			NULL		0	NULL	NULL	NULL	NULL	NULL	Both drugs [lithium and VPA] also have antiapoptotic effects. They are known to inhibit cytochrome c release from mitochondria and to increase expression of the anti-apoptotic gene Bcl-2.	topic_bd
75719	8	355284	7	NULL	NULL	0	NULL	statement 7	Process		occur from					mitochondria	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	Both drugs [lithium and VPA] also have antiapoptotic effects. They are known to inhibit cytochrome c release from mitochondria and to increase expression of the anti-apoptotic gene Bcl-2.	topic_bd
75720	9	355284	7	NULL	NULL	0	NULL	VPA	Chemical		increase					Bcl-2	GP	expression of			NULL		0	NULL	NULL	NULL	NULL	NULL	Both drugs [lithium and VPA] also have antiapoptotic effects. They are known to inhibit cytochrome c release from mitochondria and to increase expression of the anti-apoptotic gene Bcl-2.	topic_bd
75721	1	355286	7	NULL	NULL	0	NULL	VPA	Chemical		is a inhibitor of					histone deacetylase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	VPA is a histone deacetylase inhibitor and facilitates gene expression via this epigenetic mechanism	topic_bd
75722	2	355286	7	NULL	NULL	0	NULL	VPA	Chemical		facilitate					gene expression	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	VPA is a histone deacetylase inhibitor and facilitates gene expression via this epigenetic mechanism	topic_bd
75723	3	355286	7	NULL	NULL	0	NULL	statement 2	Process		occur via					epigenetic mechanism	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	VPA is a histone deacetylase inhibitor and facilitates gene expression via this epigenetic mechanism	topic_bd
75724	1	355287	7	NULL	NULL	0	NULL	conventional antipsychotics	Chemical		inhibitors of					dopamine D2 receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The first generation of antipsychotic drugs, “conventional antipsychotics”, are potent inhibitors of the dopamine D2 receptor	topic_bd
75725	2	355287	7	NULL	NULL	0	NULL	conventional antipsychotics	Chemical		belongs to					antipsychotic drugs	Chemical	first generation of			NULL		0	NULL	NULL	NULL	NULL	NULL	The first generation of antipsychotic drugs, “conventional antipsychotics”, are potent inhibitors of the dopamine D2 receptor	topic_bd
75726	1	355288	7	NULL	NULL	0	NULL	Atypical antipsychotic drugs	Chemical		target					serotonin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	“Atypical antipsychotic drugs” target other neurotransmitter systems, including serotonin, norepinephrine, and cannabinoids, and produce fewer extrapyramidal side effects	topic_bd
75727	2	355288	7	NULL	NULL	0	NULL	Atypical antipsychotic drugs	Chemical		target					norepinephrine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	“Atypical antipsychotic drugs” target other neurotransmitter systems, including serotonin, norepinephrine, and cannabinoids, and produce fewer extrapyramidal side effects	topic_bd
75728	3	355288	7	NULL	NULL	0	NULL	Atypical antipsychotic drugs	Chemical		target					cannabinoids	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	“Atypical antipsychotic drugs” target other neurotransmitter systems, including serotonin, norepinephrine, and cannabinoids, and produce fewer extrapyramidal side effects	topic_bd
75729	4	355288	7	NULL	NULL	NULL	NULL	statement 1	Process		produce					extrapyramidal side effects	MedicalFinding	fewer			NULL		NULL	NULL	NULL	NULL	NULL	NULL	“Atypical antipsychotic drugs” target other neurotransmitter systems, including serotonin, norepinephrine, and cannabinoids, and produce fewer extrapyramidal side effects	topic_bd
75730	5	355288	7	NULL	NULL	NULL	NULL	statement 2	Process		produce					extrapyramidal side effects	MedicalFinding	fewer			NULL		NULL	NULL	NULL	NULL	NULL	NULL	“Atypical antipsychotic drugs” target other neurotransmitter systems, including serotonin, norepinephrine, and cannabinoids, and produce fewer extrapyramidal side effects	topic_bd
75731	6	355288	7	NULL	NULL	0	NULL	statement 3	Process		produce					extrapyramidal side effects	MedicalFinding	fewer			NULL		0	NULL	NULL	NULL	NULL	NULL	“Atypical antipsychotic drugs” target other neurotransmitter systems, including serotonin, norepinephrine, and cannabinoids, and produce fewer extrapyramidal side effects	topic_bd
75732	7	355288	7	NULL	NULL	0	NULL	serotonin	Chemical		is a type of					neurotransmitter	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	“Atypical antipsychotic drugs” target other neurotransmitter systems, including serotonin, norepinephrine, and cannabinoids, and produce fewer extrapyramidal side effects	topic_bd
75733	8	355288	7	NULL	NULL	0	NULL	norepinephrine	Chemical		is a type of					neurotransmitter	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	“Atypical antipsychotic drugs” target other neurotransmitter systems, including serotonin, norepinephrine, and cannabinoids, and produce fewer extrapyramidal side effects	topic_bd
75734	9	355288	7	NULL	NULL	0	NULL	cannabinoids	Chemical		is a type of					neurotransmitter	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	“Atypical antipsychotic drugs” target other neurotransmitter systems, including serotonin, norepinephrine, and cannabinoids, and produce fewer extrapyramidal side effects	topic_bd
75735	1	355289	7	NULL	NULL	0	NULL	complex I 	GP	inhibition of	results in					maximal oxygen consumption rate	QuantityOrMeasure	inhibition of			NULL		0	NULL	NULL	NULL	NULL	NULL	Despite the increased complex IV activity seen with many antipsychotics, it appears that their inhibition of complex I results in an overall inhibition of maximal oxygen consumption rate after uncoupling and, more importantly, might reduce the ability to produce ATP. This suggests that antipsychotics might contribute to mitochondrial instability.	topic_bd
75736	2	355289	7	NULL	NULL	0	NULL	statement 1	Process		occur after					uncoupling	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Despite the increased complex IV activity seen with many antipsychotics, it appears that their inhibition of complex I results in an overall inhibition of maximal oxygen consumption rate after uncoupling and, more importantly, might reduce the ability to produce ATP. This suggests that antipsychotics might contribute to mitochondrial instability.	topic_bd
75737	3	355289	7	NULL	NULL	0	NULL	statement 1	Process		reduce		might			ATP	Chemical	ability to produce			NULL		0	NULL	NULL	NULL	NULL	NULL	Despite the increased complex IV activity seen with many antipsychotics, it appears that their inhibition of complex I results in an overall inhibition of maximal oxygen consumption rate after uncoupling and, more importantly, might reduce the ability to produce ATP. This suggests that antipsychotics might contribute to mitochondrial instability.	topic_bd
75738	4	355289	7	NULL	NULL	0	NULL	antipsychotics	Chemical		increase					complex IV activity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Despite the increased complex IV activity seen with many antipsychotics, it appears that their inhibition of complex I results in an overall inhibition of maximal oxygen consumption rate after uncoupling and, more importantly, might reduce the ability to produce ATP. This suggests that antipsychotics might contribute to mitochondrial instability.	topic_bd
75739	5	355289	7	NULL	NULL	0	NULL	antipsychotics 	Chemical		contribute to		might			mitochondrial instability	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Despite the increased complex IV activity seen with many antipsychotics, it appears that their inhibition of complex I results in an overall inhibition of maximal oxygen consumption rate after uncoupling and, more importantly, might reduce the ability to produce ATP. This suggests that antipsychotics might contribute to mitochondrial instability.	topic_bd
75740	6	355289	7	NULL	NULL	0	NULL	statement 3	Process		suggest					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Despite the increased complex IV activity seen with many antipsychotics, it appears that their inhibition of complex I results in an overall inhibition of maximal oxygen consumption rate after uncoupling and, more importantly, might reduce the ability to produce ATP. This suggests that antipsychotics might contribute to mitochondrial instability.	topic_bd
75741	1	355290	7	NULL	NULL	NULL	NULL	mitochondria	CellComponent	overall stability of 	affected in					BPD	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	A large number of studies have shown that the overall stability of mitochondria, the efficiency of OXPHOS, and the ability to buffer Ca2+ and neutralize ROS, are affected in BPD and SZ. 	topic_bd
75742	2	355290	7	NULL	NULL	0	NULL	mitochondria	CellComponent	overall stability of 	affected in					SZ	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	A large number of studies have shown that the overall stability of mitochondria, the efficiency of OXPHOS, and the ability to buffer Ca2+ and neutralize ROS, are affected in BPD and SZ. 	topic_bd
75743	3	355290	7	NULL	NULL	0	NULL	OXPHOS	Chemical	efficiency of	affected in					BPD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	A large number of studies have shown that the overall stability of mitochondria, the efficiency of OXPHOS, and the ability to buffer Ca2+ and neutralize ROS, are affected in BPD and SZ. 	topic_bd
75744	4	355290	7	NULL	NULL	0	NULL	OXPHOS	Chemical	efficiency of	affected in					SZ	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	A large number of studies have shown that the overall stability of mitochondria, the efficiency of OXPHOS, and the ability to buffer Ca2+ and neutralize ROS, are affected in BPD and SZ. 	topic_bd
75745	5	355290	7	NULL	NULL	0	NULL	Ca2+	Chemical	ability to buffer	affected in					BPD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	A large number of studies have shown that the overall stability of mitochondria, the efficiency of OXPHOS, and the ability to buffer Ca2+ and neutralize ROS, are affected in BPD and SZ. 	topic_bd
75746	6	355290	7	NULL	NULL	0	NULL	Ca2+	Chemical	ability to buffer	affected in					SZ	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	A large number of studies have shown that the overall stability of mitochondria, the efficiency of OXPHOS, and the ability to buffer Ca2+ and neutralize ROS, are affected in BPD and SZ. 	topic_bd
75747	7	355290	7	NULL	NULL	0	NULL	ROS	Chemical	ability to neutralize	affected in					BPD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	A large number of studies have shown that the overall stability of mitochondria, the efficiency of OXPHOS, and the ability to buffer Ca2+ and neutralize ROS, are affected in BPD and SZ. 	topic_bd
75748	8	355290	7	NULL	NULL	0	NULL	ROS	Chemical	ability to neutralize	affected in					SZ	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	A large number of studies have shown that the overall stability of mitochondria, the efficiency of OXPHOS, and the ability to buffer Ca2+ and neutralize ROS, are affected in BPD and SZ. 	topic_bd
75749	1	355291	7	NULL	NULL	NULL	NULL	ROS	Chemical		is a type of					oxygen-containing free radicals	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Reactive oxygen species (ROS) are oxygen-containing free radicals created as byproducts of both physiological and abnormal electron transport. 	topic_bd
75750	2	355291	7	NULL	NULL	0	NULL	ROS	Chemical		byproducts of					electron transport	Process	physiological			NULL		0	NULL	NULL	NULL	NULL	NULL	Reactive oxygen species (ROS) are oxygen-containing free radicals created as byproducts of both physiological and abnormal electron transport. 	topic_bd
75751	3	355291	7	NULL	NULL	0	NULL	ROS	Chemical		byproducts of					electron transport	Process	abnormal			NULL		0	NULL	NULL	NULL	NULL	NULL	Reactive oxygen species (ROS) are oxygen-containing free radicals created as byproducts of both physiological and abnormal electron transport. 	topic_bd
75752	4	355291	7	NULL	NULL	0	NULL	ROS	Chemical		is					Reactive oxygen species 	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Reactive oxygen species (ROS) are oxygen-containing free radicals created as byproducts of both physiological and abnormal electron transport. 	topic_bd
75753	1	355293	7	NULL	NULL	NULL	NULL	mitochondrial viability	Process	reduced	decrease					ATP	Chemical	production of;;reserves of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Reduced mitochondrial viability and function causes decreased ATP production and reserves. Ion pumps need ATP to maintain the membrane potential in neurons. Proper information processing depends on the ability of the neuron to maintain a solid membrane potential with minimal leakage. One could imagine how a flaccid membrane potential could lead to (a) diminished information processing, i.e. not all information gets adequately propagated, or (b) chance depolarization leading to an erroneous signal.	topic_bd
75754	2	355293	7	NULL	NULL	NULL	NULL	mitochondrial function	Process	reduced	decrease					ATP	Chemical	production of;;reserves of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Reduced mitochondrial viability and function causes decreased ATP production and reserves. Ion pumps need ATP to maintain the membrane potential in neurons. Proper information processing depends on the ability of the neuron to maintain a solid membrane potential with minimal leakage. One could imagine how a flaccid membrane potential could lead to (a) diminished information processing, i.e. not all information gets adequately propagated, or (b) chance depolarization leading to an erroneous signal.	topic_bd
75755	3	355293	7	NULL	NULL	0	NULL	Ion pumps	CellComponent		need					ATP	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Reduced mitochondrial viability and function causes decreased ATP production and reserves. Ion pumps need ATP to maintain the membrane potential in neurons. Proper information processing depends on the ability of the neuron to maintain a solid membrane potential with minimal leakage. One could imagine how a flaccid membrane potential could lead to (a) diminished information processing, i.e. not all information gets adequately propagated, or (b) chance depolarization leading to an erroneous signal.	topic_bd
75756	4	355293	7	NULL	NULL	NULL	NULL	statement 3	Process		maintain					membrane potential	QuantityOrMeasure				NULL	neurons	NULL	NULL	NULL	NULL	NULL	NULL	Reduced mitochondrial viability and function causes decreased ATP production and reserves. Ion pumps need ATP to maintain the membrane potential in neurons. Proper information processing depends on the ability of the neuron to maintain a solid membrane potential with minimal leakage. One could imagine how a flaccid membrane potential could lead to (a) diminished information processing, i.e. not all information gets adequately propagated, or (b) chance depolarization leading to an erroneous signal.	topic_bd
75757	5	355293	7	NULL	NULL	NULL	NULL	neurons	OrganismPart		maintain					solid membrane potential	QuantityOrMeasure				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Reduced mitochondrial viability and function causes decreased ATP production and reserves. Ion pumps need ATP to maintain the membrane potential in neurons. Proper information processing depends on the ability of the neuron to maintain a solid membrane potential with minimal leakage. One could imagine how a flaccid membrane potential could lead to (a) diminished information processing, i.e. not all information gets adequately propagated, or (b) chance depolarization leading to an erroneous signal.	topic_bd
75758	6	355293	7	NULL	NULL	0	NULL	statement 5	Process		occur with					minimal leakage	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Reduced mitochondrial viability and function causes decreased ATP production and reserves. Ion pumps need ATP to maintain the membrane potential in neurons. Proper information processing depends on the ability of the neuron to maintain a solid membrane potential with minimal leakage. One could imagine how a flaccid membrane potential could lead to (a) diminished information processing, i.e. not all information gets adequately propagated, or (b) chance depolarization leading to an erroneous signal.	topic_bd
75759	7	355293	7	NULL	NULL	NULL	NULL	flaccid membrane potential	QuantityOrMeasure		leads to					diminished information processing	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Reduced mitochondrial viability and function causes decreased ATP production and reserves. Ion pumps need ATP to maintain the membrane potential in neurons. Proper information processing depends on the ability of the neuron to maintain a solid membrane potential with minimal leakage. One could imagine how a flaccid membrane potential could lead to (a) diminished information processing, i.e. not all information gets adequately propagated, or (b) chance depolarization leading to an erroneous signal.	topic_bd
75760	8	355293	7	NULL	NULL	0	NULL	chance depolarization	Process		leads to					erroneous signal	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Reduced mitochondrial viability and function causes decreased ATP production and reserves. Ion pumps need ATP to maintain the membrane potential in neurons. Proper information processing depends on the ability of the neuron to maintain a solid membrane potential with minimal leakage. One could imagine how a flaccid membrane potential could lead to (a) diminished information processing, i.e. not all information gets adequately propagated, or (b) chance depolarization leading to an erroneous signal.	topic_bd
75761	9	355293	7	NULL	NULL	0	NULL	 flaccid membrane potential	QuantityOrMeasure		leads to					statement 8	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Reduced mitochondrial viability and function causes decreased ATP production and reserves. Ion pumps need ATP to maintain the membrane potential in neurons. Proper information processing depends on the ability of the neuron to maintain a solid membrane potential with minimal leakage. One could imagine how a flaccid membrane potential could lead to (a) diminished information processing, i.e. not all information gets adequately propagated, or (b) chance depolarization leading to an erroneous signal.	topic_bd
75762	10	355293	7	NULL	NULL	0	NULL	diminished information processing	Process		is					adequately propagated	Process	not all information gets			NULL		0	NULL	NULL	NULL	NULL	NULL	Reduced mitochondrial viability and function causes decreased ATP production and reserves. Ion pumps need ATP to maintain the membrane potential in neurons. Proper information processing depends on the ability of the neuron to maintain a solid membrane potential with minimal leakage. One could imagine how a flaccid membrane potential could lead to (a) diminished information processing, i.e. not all information gets adequately propagated, or (b) chance depolarization leading to an erroneous signal.	topic_bd
75763	11	355293	7	NULL	NULL	0	NULL	 Proper information processing	Process		depends on					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Reduced mitochondrial viability and function causes decreased ATP production and reserves. Ion pumps need ATP to maintain the membrane potential in neurons. Proper information processing depends on the ability of the neuron to maintain a solid membrane potential with minimal leakage. One could imagine how a flaccid membrane potential could lead to (a) diminished information processing, i.e. not all information gets adequately propagated, or (b) chance depolarization leading to an erroneous signal.	topic_bd
75764	1	355294	7	NULL	NULL	0	NULL	neuronal types 	OrganismPart	energy demands of	responsible for					 vulnerability	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	First, the energy demands of particular neuronal types might be responsible for their vulnerability. For example, in the hippocampus certain populations of GABA interneurons have higher activities of cytochrome c, indicating higher energy demands in these cells (Gulyas et al., 2006). Interestingly, markers for GABA neurons are dramatically reduced in the hippocampus in SZ and BPD (Benes et al., 1998 F.M. Benes, E.W. Kwok, S.L. Vincent and M.S. Todtenkopf, A reduction of nonpyramidal cells in sector CA2 of schizophrenics and manic depressives, Biol. Psychiatry 44 (1998), pp. 88–97. Article | PDF (335 K) | View Record in Scopus | Cited By in Scopus (210)[Benes et al., 1998] and [Heckers et al., 2002]), and in BPD are correlated with a reduction in nuclear genes coding for the mitochondrial electron transport chain (Konradi et al., 2004). Thus, neurons with the highest energy demands are abnormal in BPD and SZ. Other neurons might have lower energy demands and less vulnerability to subtle mitochondrial abnormalities.	topic_bd
75765	2	355294	7	NULL	NULL	0	NULL	GABA interneurons 	OrganismPart		shows					cytochrome c	GP	higher activities of			NULL	 hippocampus	0	NULL	NULL	NULL	NULL	NULL	First, the energy demands of particular neuronal types might be responsible for their vulnerability. For example, in the hippocampus certain populations of GABA interneurons have higher activities of cytochrome c, indicating higher energy demands in these cells (Gulyas et al., 2006). Interestingly, markers for GABA neurons are dramatically reduced in the hippocampus in SZ and BPD (Benes et al., 1998 F.M. Benes, E.W. Kwok, S.L. Vincent and M.S. Todtenkopf, A reduction of nonpyramidal cells in sector CA2 of schizophrenics and manic depressives, Biol. Psychiatry 44 (1998), pp. 88–97. Article | PDF (335 K) | View Record in Scopus | Cited By in Scopus (210)[Benes et al., 1998] and [Heckers et al., 2002]), and in BPD are correlated with a reduction in nuclear genes coding for the mitochondrial electron transport chain (Konradi et al., 2004). Thus, neurons with the highest energy demands are abnormal in BPD and SZ. Other neurons might have lower energy demands and less vulnerability to subtle mitochondrial abnormalities.	topic_bd
75766	3	355294	7	NULL	NULL	0	NULL	statement 2	Process		indicates					hippocampus	OrganismPart	higher energy demands in			NULL		0	NULL	NULL	NULL	NULL	NULL	First, the energy demands of particular neuronal types might be responsible for their vulnerability. For example, in the hippocampus certain populations of GABA interneurons have higher activities of cytochrome c, indicating higher energy demands in these cells (Gulyas et al., 2006). Interestingly, markers for GABA neurons are dramatically reduced in the hippocampus in SZ and BPD (Benes et al., 1998 F.M. Benes, E.W. Kwok, S.L. Vincent and M.S. Todtenkopf, A reduction of nonpyramidal cells in sector CA2 of schizophrenics and manic depressives, Biol. Psychiatry 44 (1998), pp. 88–97. Article | PDF (335 K) | View Record in Scopus | Cited By in Scopus (210)[Benes et al., 1998] and [Heckers et al., 2002]), and in BPD are correlated with a reduction in nuclear genes coding for the mitochondrial electron transport chain (Konradi et al., 2004). Thus, neurons with the highest energy demands are abnormal in BPD and SZ. Other neurons might have lower energy demands and less vulnerability to subtle mitochondrial abnormalities.	topic_bd
75767	4	355294	7	NULL	NULL	NULL	NULL	GABA neurons	OrganismPart		reduced in		dramatically			hippocampus	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	First, the energy demands of particular neuronal types might be responsible for their vulnerability. For example, in the hippocampus certain populations of GABA interneurons have higher activities of cytochrome c, indicating higher energy demands in these cells (Gulyas et al., 2006). Interestingly, markers for GABA neurons are dramatically reduced in the hippocampus in SZ and BPD (Benes et al., 1998 F.M. Benes, E.W. Kwok, S.L. Vincent and M.S. Todtenkopf, A reduction of nonpyramidal cells in sector CA2 of schizophrenics and manic depressives, Biol. Psychiatry 44 (1998), pp. 88–97. Article | PDF (335 K) | View Record in Scopus | Cited By in Scopus (210)[Benes et al., 1998] and [Heckers et al., 2002]), and in BPD are correlated with a reduction in nuclear genes coding for the mitochondrial electron transport chain (Konradi et al., 2004). Thus, neurons with the highest energy demands are abnormal in BPD and SZ. Other neurons might have lower energy demands and less vulnerability to subtle mitochondrial abnormalities.	topic_bd
75768	5	355294	7	NULL	NULL	0	NULL	statement 4	Process		occur in					SZ	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	First, the energy demands of particular neuronal types might be responsible for their vulnerability. For example, in the hippocampus certain populations of GABA interneurons have higher activities of cytochrome c, indicating higher energy demands in these cells (Gulyas et al., 2006). Interestingly, markers for GABA neurons are dramatically reduced in the hippocampus in SZ and BPD (Benes et al., 1998 F.M. Benes, E.W. Kwok, S.L. Vincent and M.S. Todtenkopf, A reduction of nonpyramidal cells in sector CA2 of schizophrenics and manic depressives, Biol. Psychiatry 44 (1998), pp. 88–97. Article | PDF (335 K) | View Record in Scopus | Cited By in Scopus (210)[Benes et al., 1998] and [Heckers et al., 2002]), and in BPD are correlated with a reduction in nuclear genes coding for the mitochondrial electron transport chain (Konradi et al., 2004). Thus, neurons with the highest energy demands are abnormal in BPD and SZ. Other neurons might have lower energy demands and less vulnerability to subtle mitochondrial abnormalities.	topic_bd
75769	6	355294	7	NULL	NULL	0	NULL	statement 4	Process		occur in					BPD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	First, the energy demands of particular neuronal types might be responsible for their vulnerability. For example, in the hippocampus certain populations of GABA interneurons have higher activities of cytochrome c, indicating higher energy demands in these cells (Gulyas et al., 2006). Interestingly, markers for GABA neurons are dramatically reduced in the hippocampus in SZ and BPD (Benes et al., 1998 F.M. Benes, E.W. Kwok, S.L. Vincent and M.S. Todtenkopf, A reduction of nonpyramidal cells in sector CA2 of schizophrenics and manic depressives, Biol. Psychiatry 44 (1998), pp. 88–97. Article | PDF (335 K) | View Record in Scopus | Cited By in Scopus (210)[Benes et al., 1998] and [Heckers et al., 2002]), and in BPD are correlated with a reduction in nuclear genes coding for the mitochondrial electron transport chain (Konradi et al., 2004). Thus, neurons with the highest energy demands are abnormal in BPD and SZ. Other neurons might have lower energy demands and less vulnerability to subtle mitochondrial abnormalities.	topic_bd
75770	7	355294	7	NULL	NULL	0	NULL	nuclear genes	GP		code					electron transport chain	Process	mitochondrial			NULL		0	NULL	NULL	NULL	NULL	NULL	First, the energy demands of particular neuronal types might be responsible for their vulnerability. For example, in the hippocampus certain populations of GABA interneurons have higher activities of cytochrome c, indicating higher energy demands in these cells (Gulyas et al., 2006). Interestingly, markers for GABA neurons are dramatically reduced in the hippocampus in SZ and BPD (Benes et al., 1998 F.M. Benes, E.W. Kwok, S.L. Vincent and M.S. Todtenkopf, A reduction of nonpyramidal cells in sector CA2 of schizophrenics and manic depressives, Biol. Psychiatry 44 (1998), pp. 88–97. Article | PDF (335 K) | View Record in Scopus | Cited By in Scopus (210)[Benes et al., 1998] and [Heckers et al., 2002]), and in BPD are correlated with a reduction in nuclear genes coding for the mitochondrial electron transport chain (Konradi et al., 2004). Thus, neurons with the highest energy demands are abnormal in BPD and SZ. Other neurons might have lower energy demands and less vulnerability to subtle mitochondrial abnormalities.	topic_bd
75771	8	355294	7	NULL	NULL	0	NULL	BPD	MedicalFinding		correlated with					statement 7	Process	reduction in			NULL		0	NULL	NULL	NULL	NULL	NULL	First, the energy demands of particular neuronal types might be responsible for their vulnerability. For example, in the hippocampus certain populations of GABA interneurons have higher activities of cytochrome c, indicating higher energy demands in these cells (Gulyas et al., 2006). Interestingly, markers for GABA neurons are dramatically reduced in the hippocampus in SZ and BPD (Benes et al., 1998 F.M. Benes, E.W. Kwok, S.L. Vincent and M.S. Todtenkopf, A reduction of nonpyramidal cells in sector CA2 of schizophrenics and manic depressives, Biol. Psychiatry 44 (1998), pp. 88–97. Article | PDF (335 K) | View Record in Scopus | Cited By in Scopus (210)[Benes et al., 1998] and [Heckers et al., 2002]), and in BPD are correlated with a reduction in nuclear genes coding for the mitochondrial electron transport chain (Konradi et al., 2004). Thus, neurons with the highest energy demands are abnormal in BPD and SZ. Other neurons might have lower energy demands and less vulnerability to subtle mitochondrial abnormalities.	topic_bd
75772	9	355294	7	NULL	NULL	0	NULL	neurons 	OrganismPart	highest energy demands in	abnormal in					BPD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	First, the energy demands of particular neuronal types might be responsible for their vulnerability. For example, in the hippocampus certain populations of GABA interneurons have higher activities of cytochrome c, indicating higher energy demands in these cells (Gulyas et al., 2006). Interestingly, markers for GABA neurons are dramatically reduced in the hippocampus in SZ and BPD (Benes et al., 1998 F.M. Benes, E.W. Kwok, S.L. Vincent and M.S. Todtenkopf, A reduction of nonpyramidal cells in sector CA2 of schizophrenics and manic depressives, Biol. Psychiatry 44 (1998), pp. 88–97. Article | PDF (335 K) | View Record in Scopus | Cited By in Scopus (210)[Benes et al., 1998] and [Heckers et al., 2002]), and in BPD are correlated with a reduction in nuclear genes coding for the mitochondrial electron transport chain (Konradi et al., 2004). Thus, neurons with the highest energy demands are abnormal in BPD and SZ. Other neurons might have lower energy demands and less vulnerability to subtle mitochondrial abnormalities.	topic_bd
75773	10	355294	7	NULL	NULL	0	NULL	neurons	OrganismPart	highest energy demands in	abnormal in					SZ	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	First, the energy demands of particular neuronal types might be responsible for their vulnerability. For example, in the hippocampus certain populations of GABA interneurons have higher activities of cytochrome c, indicating higher energy demands in these cells (Gulyas et al., 2006). Interestingly, markers for GABA neurons are dramatically reduced in the hippocampus in SZ and BPD (Benes et al., 1998 F.M. Benes, E.W. Kwok, S.L. Vincent and M.S. Todtenkopf, A reduction of nonpyramidal cells in sector CA2 of schizophrenics and manic depressives, Biol. Psychiatry 44 (1998), pp. 88–97. Article | PDF (335 K) | View Record in Scopus | Cited By in Scopus (210)[Benes et al., 1998] and [Heckers et al., 2002]), and in BPD are correlated with a reduction in nuclear genes coding for the mitochondrial electron transport chain (Konradi et al., 2004). Thus, neurons with the highest energy demands are abnormal in BPD and SZ. Other neurons might have lower energy demands and less vulnerability to subtle mitochondrial abnormalities.	topic_bd
74609	1	355301	6	NULL	NULL	NULL	NULL	DES	Chemical		is involved in					breast cancer	MedicalFinding	treatment of 			NULL	post-menopausal women	NULL	NULL	NULL	NULL	NULL	NULL	In 1960, DES was found to be more effective than androgens in the treatment of advanced breast cancer in postmenopausal women.  DES was the hormonal treatment of choice for advanced breast cancer in postmenopausal women until 1977	topic_bc
74610	2	355301	6	NULL	NULL	NULL	NULL	androgens	Chemical		is involved in					breast cancer	MedicalFinding	treatment of			NULL	post-menopausal women	NULL	NULL	NULL	NULL	NULL	NULL	In 1960, DES was found to be more effective than androgens in the treatment of advanced breast cancer in postmenopausal women.  DES was the hormonal treatment of choice for advanced breast cancer in postmenopausal women until 1977	topic_bc
74611	3	355301	6	NULL	NULL	0	NULL	statement 1			is more than					statement 2					NULL		0	NULL	NULL	NULL	NULL	NULL	In 1960, DES was found to be more effective than androgens in the treatment of advanced breast cancer in postmenopausal women.  DES was the hormonal treatment of choice for advanced breast cancer in postmenopausal women until 1977	topic_bc
74612	1	355302	6	NULL	NULL	0	NULL	fibroadenoma patients	GroupOfPeople		have					breast cancer	MedicalFinding	increased risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	patients with fibroadenoma have a slightly higher risk of breast cancer later in life	topic_bc
74613	1	355303	6	NULL	NULL	0	NULL	Sixteen-carbon metabolites	Chemical		are toxic to					cellular DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	 Sixteen-carbon metabolites are also toxic to cellular DNA. Synthetic xenoestrogens apparently block the 2-carbon pathway and promote 16-carbon metabolism	topic_bc
74614	2	355303	6	NULL	NULL	0	NULL	xenoestrogens	Chemical		block					2-carbon pathway 	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	 Sixteen-carbon metabolites are also toxic to cellular DNA. Synthetic xenoestrogens apparently block the 2-carbon pathway and promote 16-carbon metabolism	topic_bc
74615	3	355303	6	NULL	NULL	0	NULL	xenoestrogens	Chemical		promote					16-carbon metabolism	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 Sixteen-carbon metabolites are also toxic to cellular DNA. Synthetic xenoestrogens apparently block the 2-carbon pathway and promote 16-carbon metabolism	topic_bc
74645	1	355304	6	NULL	NULL	NULL	NULL	Bras			obstruct					lymph	CellComponent	flow of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	have suggested that bras cause breast cancer by obstructing lymph flow	topic_bc
74646	2	355304	6	NULL	NULL	0	NULL	statement 1	Process		leads to					breast cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	have suggested that bras cause breast cancer by obstructing lymph flow	topic_bc
74648	1	355305	6	NULL	NULL	0	NULL	alcohol		use of	is linked to					breast cancer	MedicalFinding	increased risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	The use of alcohol is clearly linked to an increased risk of developing breast cancer.	topic_bc
75571	1	355306	6	NULL	NULL	0	NULL	Premenopausal women	Person		exposed to					smoke	Chemical	secondhand			NULL		0	NULL	NULL	NULL	NULL	NULL	Premenopausal women who are exposed to secondhand smoke on a regular basis have an increased risk of breast cancer	topic_bc
75572	2	355306	6	NULL	NULL	0	NULL	statement 1	Process		increases					breast cancer	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Premenopausal women who are exposed to secondhand smoke on a regular basis have an increased risk of breast cancer	topic_bc
77450	1	355307	6	NULL	NULL	0	NULL	Honey	Chemical		is abundant in					phenol	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Further, honey samples with richly abundant phenolic content were found to limit oxidant-induced cell death more effectively. Cytotoxic studies of a selected sample on a breast cancer cell displayed growth inhibition, depending on the concentration used	topic_bc
77632	2	355307	6	NULL	NULL	0	NULL	oxidant	Chemical		induces					cell death	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Further, honey samples with richly abundant phenolic content were found to limit oxidant-induced cell death more effectively. Cytotoxic studies of a selected sample on a breast cancer cell displayed growth inhibition, depending on the concentration used	topic_bc
77633	3	355307	6	NULL	NULL	0	NULL	statement 1	Process		inhibits					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Further, honey samples with richly abundant phenolic content were found to limit oxidant-induced cell death more effectively. Cytotoxic studies of a selected sample on a breast cancer cell displayed growth inhibition, depending on the concentration used	topic_bc
75774	1	355308	7	NULL	NULL	0	NULL	alpha-defensin	GP	expression of	enhanced in					colon cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	It is known that alpha-defensin expression is enhanced in colon cancer.	topic_ccc
75775	1	355309	7	NULL	NULL	0	NULL	DEFA 6	GP	expression of	marker for		potential			adenoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We suggest that the expression of DEFA 6 preferably can be used as a potential diagnostic marker for adenoma and not as a marker for fully blown carcinoma.	topic_ccc
75776	2	355309	7	NULL	NULL	0	NULL	DEFA 6	GP	expression of	not as marker for					fully blown carcinoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We suggest that the expression of DEFA 6 preferably can be used as a potential diagnostic marker for adenoma and not as a marker for fully blown carcinoma.	topic_ccc
75777	1	355310	7	NULL	NULL	NULL	NULL	DEFA 6	GP	gene expression of	increased in		moderately			tumor samples	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The median gene expression of human defensin alpha 6 (DEFA 6) has been found to be moderately increased (~ 5 fold) in tumor samples derived from individuals with colorectal cancer (CRC) when compared to their normal counterparts.	topic_ccc
75778	2	355310	7	NULL	NULL	0	NULL	statement 1	Process		occur in					CRC	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The median gene expression of human defensin alpha 6 (DEFA 6) has been found to be moderately increased (~ 5 fold) in tumor samples derived from individuals with colorectal cancer (CRC) when compared to their normal counterparts.	topic_ccc
75779	3	355310	7	NULL	NULL	0	NULL	CRC	MedicalFinding		is					colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The median gene expression of human defensin alpha 6 (DEFA 6) has been found to be moderately increased (~ 5 fold) in tumor samples derived from individuals with colorectal cancer (CRC) when compared to their normal counterparts.	topic_ccc
75780	4	355310	7	NULL	NULL	0	NULL	DEFA 6	GP		is					human defensin alpha 6 	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The median gene expression of human defensin alpha 6 (DEFA 6) has been found to be moderately increased (~ 5 fold) in tumor samples derived from individuals with colorectal cancer (CRC) when compared to their normal counterparts.	topic_ccc
75781	1	355311	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		expressed in		strongly			low grade colorectal carcinoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	 IGFBP-rP1 strongly expressed in low grade colorectal carcinoma and weakly expressed in high grade colorectal carcinoma. 	topic_ccc
75782	2	355311	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		expressed in		weakly			high grade colorectal carcinoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	 IGFBP-rP1 strongly expressed in low grade colorectal carcinoma and weakly expressed in high grade colorectal carcinoma. 	topic_ccc
75783	1	355312	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		upregulate					TAGLN	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 IGFBP-rP1 could upregulate Transgelin (TAGLN)	topic_ccc
75784	2	355312	7	NULL	NULL	0	NULL	TAGLN	GP		is					Transgelin 	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 IGFBP-rP1 could upregulate Transgelin (TAGLN)	topic_ccc
75785	1	355313	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		upregulate					TAGLN	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY	topic_ccc
75786	2	355313	7	NULL	NULL	0	NULL	TAGLN	GP		is involved in					Transgelin	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY	topic_ccc
75787	3	355313	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		downregulate					SRY	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY	topic_ccc
75788	1	355314	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		upregulate					TAGLN	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1)	topic_ccc
75789	2	355314	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		downregulate					SRY-box9	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1)	topic_ccc
75790	3	355314	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		downregulate					SOX9	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1)	topic_ccc
75791	4	355314	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		downregulate					IRS1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1)	topic_ccc
75792	5	355314	7	NULL	NULL	0	NULL	TAGLN	GP		is					Transgelin	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1)	topic_ccc
75793	6	355314	7	NULL	NULL	0	NULL	SRY	GP		is					sex determining region Y	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1)	topic_ccc
75794	7	355314	7	NULL	NULL	0	NULL	IRS1	GP		is					insulin receptor substrate 1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1)	topic_ccc
75795	1	355315	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		upregulate					TAGLN	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B),	topic_ccc
75796	2	355315	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		downregulate					SRY-box 9	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B),	topic_ccc
75797	3	355315	7	NULL	NULL	0	NULL	IGFBP-rP1 	GP		downregulate					IRS1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B),	topic_ccc
75798	4	355315	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		downregulate					CDKN2B	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B),	topic_ccc
75799	5	355315	7	NULL	NULL	0	NULL	p15	GP		inhibits					CDK4	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B),	topic_ccc
75800	6	355315	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		downregulate					SOX9	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B),	topic_ccc
75801	7	355315	7	NULL	NULL	0	NULL	TAGLN	GP		is					Transgelin	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B),	topic_ccc
75802	8	355315	7	NULL	NULL	0	NULL	IRS1	GP		is					 insulin receptor substrate 1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B),	topic_ccc
75803	9	355315	7	NULL	NULL	0	NULL	CDKN2B	GP		is					cyclin-dependent kinase inhibitor 2B	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B),	topic_ccc
75804	10	355315	7	NULL	NULL	0	NULL	SRY	GP		is					sex determining region Y	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B),	topic_ccc
75805	1	355316	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		upregulate					TAGLN	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	. IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG)	topic_ccc
75806	2	355316	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		downregulate					SRY-box 9	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	. IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG)	topic_ccc
75807	3	355316	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		downregulate					SOX9	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	. IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG)	topic_ccc
75808	4	355316	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		downregulate					IRS1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	. IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG)	topic_ccc
75809	5	355316	7	NULL	NULL	0	NULL	IGFBP-rP1 	GP		downregulate					CDKN2B	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	. IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG)	topic_ccc
75810	6	355316	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		downregulate					AREG	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	. IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG)	topic_ccc
75811	7	355316	7	NULL	NULL	0	NULL	TAGLN	GP		is					Transgelin	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	. IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG)	topic_ccc
75812	8	355316	7	NULL	NULL	0	NULL	SRY	GP		is					sex determining region Y	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	. IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG)	topic_ccc
75813	9	355316	7	NULL	NULL	NULL	NULL	IRS1	GP		is					insulin receptor substrate 1	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	. IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG)	topic_ccc
75814	10	355316	7	NULL	NULL	0	NULL	CDKN2B	GP		is 					cyclin-dependent kinase inhibitor 2B	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	. IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG)	topic_ccc
75815	11	355316	7	NULL	NULL	0	NULL	p15	GP		inhibit					CDK4	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	. IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG)	topic_ccc
75816	12	355316	7	NULL	NULL	0	NULL	AREG	GP		is					 amphiregulin	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	. IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG)	topic_ccc
75817	13	355316	7	NULL	NULL	0	NULL	AREG	GP		is a type of					schwannoma-derived growth factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	. IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG)	topic_ccc
75818	1	355317	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		upregulate					TAGLN	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG) and immediate early response 5-like(IER5L)	topic_ccc
75819	2	355317	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		downregulate					SRY-box 9	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG) and immediate early response 5-like(IER5L)	topic_ccc
75820	3	355317	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		downregulate					SOX9	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG) and immediate early response 5-like(IER5L)	topic_ccc
75821	4	355317	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		downregulate					IRS1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG) and immediate early response 5-like(IER5L)	topic_ccc
75822	5	355317	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		downregulate					CDKN2B	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG) and immediate early response 5-like(IER5L)	topic_ccc
75823	6	355317	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		downregulate					AREG	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG) and immediate early response 5-like(IER5L)	topic_ccc
75824	7	355317	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		downregulate					IER5L	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG) and immediate early response 5-like(IER5L)	topic_ccc
75825	8	355317	7	NULL	NULL	0	NULL	p15	GP		inhibit					CDK4	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG) and immediate early response 5-like(IER5L)	topic_ccc
75826	9	355317	7	NULL	NULL	0	NULL	TAGLN	GP		is					Transgelin	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG) and immediate early response 5-like(IER5L)	topic_ccc
75827	10	355317	7	NULL	NULL	0	NULL	SRY	GP		is involved in					sex determining region Y	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG) and immediate early response 5-like(IER5L)	topic_ccc
75828	11	355317	7	NULL	NULL	0	NULL	IRS1	GP		is involved in					insulin receptor substrate 1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG) and immediate early response 5-like(IER5L)	topic_ccc
75829	12	355317	7	NULL	NULL	0	NULL	CDKN2B	GP		is involved in					cyclin-dependent kinase inhibitor 2B	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG) and immediate early response 5-like(IER5L)	topic_ccc
75830	13	355317	7	NULL	NULL	0	NULL	AREG	GP		is					amphiregulin	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG) and immediate early response 5-like(IER5L)	topic_ccc
75831	14	355317	7	NULL	NULL	0	NULL	IER5L	GP		is					immediate early response 5-like	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 could upreguate Transgelin (TAGLN), downregulate SRY (sex determining region Y)-box 9(campomelic dysplasia, autosomal sex-reversal) (SOX9), insulin receptor substrate 1(IRS1), cyclin-dependent kinase inhibitor 2B (p15, inhibits CDK4) (CDKN2B), amphiregulin(schwannoma-derived growth factor) (AREG) and immediate early response 5-like(IER5L)	topic_ccc
75832	1	355318	7	NULL	NULL	0	NULL	sodium butyrate	Chemical		induce					Caco2 cell	Cell	differentiation of			NULL		0	NULL	NULL	NULL	NULL	NULL	During sodium butyrate-induced Caco2 cell differentiation, IGFBP-rP1 was upregulated 	topic_ccc
75833	1	355319	7	NULL	NULL	0	NULL	IGFBP-rP1	GP	 upregulation of	correlates with					AKP activity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 was upregulated and the expression showed significant correlation with the AKP activity	topic_ccc
75834	1	355320	7	NULL	NULL	0	NULL	IGFBP-rP1	GP		associated with					colon cancer	MedicalFinding	differentiation of			NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 was a potential key molecule associated with colon cancer differentiation. Downregulation of IRS1 and SOX9 may the possible key downstream genes involved in the process.	topic_ccc
75835	2	355320	7	NULL	NULL	0	NULL	IRS1	GP	downregulation of	downstream		possible			gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 was a potential key molecule associated with colon cancer differentiation. Downregulation of IRS1 and SOX9 may the possible key downstream genes involved in the process.	topic_ccc
75836	3	355320	7	NULL	NULL	0	NULL	SOX9 	GP	downregulation of	downstream		possible			gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-rP1 was a potential key molecule associated with colon cancer differentiation. Downregulation of IRS1 and SOX9 may the possible key downstream genes involved in the process.	topic_ccc
75837	1	355321	7	NULL	NULL	0	NULL	5T4	GP		expressed in					human adenocarcinomas	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The oncofetal antigen, 5T4, is a surface glycoprotein that is expressed on a variety of human adenocarcinomas but rarely on normal tissue. 	topic_ccc
75838	2	355321	7	NULL	NULL	0	NULL	5T4	GP		is a type of					oncofetal antigen	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The oncofetal antigen, 5T4, is a surface glycoprotein that is expressed on a variety of human adenocarcinomas but rarely on normal tissue. 	topic_ccc
75839	3	355321	7	NULL	NULL	0	NULL	5T4	GP		is a type of					surface glycoprotein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The oncofetal antigen, 5T4, is a surface glycoprotein that is expressed on a variety of human adenocarcinomas but rarely on normal tissue. 	topic_ccc
75840	4	355321	7	NULL	NULL	0	NULL	5T4	GP		expressed in		rarely			normal tissue	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The oncofetal antigen, 5T4, is a surface glycoprotein that is expressed on a variety of human adenocarcinomas but rarely on normal tissue. 	topic_ccc
75841	1	355323	7	NULL	NULL	NULL	NULL	GIV-fl	GP	expression of;;tumor epithelium	correlated with					shortened metastasis-free survival	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	A prospective, exploratory biomarker study conducted on a cohort of 56 patients with stage II colorectal cancer revealed a significant correlation between GIV-fl expression in tumor epithelium and shortened metastasis-free survival.	topic_ccc
75842	2	355323	7	NULL	NULL	0	NULL	statement 1	Process		occur in					stage II colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	A prospective, exploratory biomarker study conducted on a cohort of 56 patients with stage II colorectal cancer revealed a significant correlation between GIV-fl expression in tumor epithelium and shortened metastasis-free survival.	topic_ccc
75843	1	355324	7	NULL	NULL	0	NULL	GIV/Girdin	GP	expression of	predicts					patient survival	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Expression of GIV/Girdin, a metastasis-related protein, predicts patient survival in colon cancer.	topic_ccc
75844	2	355324	7	NULL	NULL	0	NULL	statement 1	Process		occur in					colon cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Expression of GIV/Girdin, a metastasis-related protein, predicts patient survival in colon cancer.	topic_ccc
75845	3	355324	7	NULL	NULL	0	NULL	GIV/Girdin	GP		is a type of					metastasis-related protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Expression of GIV/Girdin, a metastasis-related protein, predicts patient survival in colon cancer.	topic_ccc
74409	1	355325	5	NULL	NULL	0	NULL	schizophrenia	OrganismPart		involves					brain	OrganismPart	aberrant topology of;;structural infrastructure of;;network of			NULL		0	NULL	NULL	NULL	NULL	NULL	Here, we demonstrate that schizophrenia involves an aberrant topology of the structural infrastructure of the brain network.	topic_sch
75846	1	355327	7	NULL	NULL	0	NULL	Senescence	Process		implicated as					tumor suppression	Process	mechanism of			NULL		0	NULL	NULL	NULL	NULL	NULL	Senescence has been implicated as an important mechanism of tumour suppression in a number of human malignancies, including colorectal cancer (CRC).	topic_ccc
75847	2	355327	7	NULL	NULL	0	NULL	statement 1	Process		occur in					CRC	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Senescence has been implicated as an important mechanism of tumour suppression in a number of human malignancies, including colorectal cancer (CRC).	topic_ccc
75848	3	355327	7	NULL	NULL	0	NULL	CRC	MedicalFinding		is a type of					human malignancy	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Senescence has been implicated as an important mechanism of tumour suppression in a number of human malignancies, including colorectal cancer (CRC).	topic_ccc
75849	1	355328	7	NULL	NULL	0	NULL	Apc	GP	loss of	induce					senescence	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	n this study we have examined the capacity of Apc loss to induce senescence in the intestinal epithelium compared to the renal epithelium. 	topic_ccc
75850	2	355328	7	NULL	NULL	0	NULL	statement 1	Process		occur in					intestinal epithelium	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	n this study we have examined the capacity of Apc loss to induce senescence in the intestinal epithelium compared to the renal epithelium. 	topic_ccc
75862	1	355330	7	NULL	NULL	0	NULL	 Apc function	Process	loss of	leads to					senescence	Process	induction of			NULL		0	NULL	NULL	NULL	NULL	NULL	Within the renal epithelium, loss of Apc function led to an induction of senescence, however, bypassing senescence through combined Apc and p21 or Ink4A gene deletion rapidly initiated renal carcinoma. 	topic_ccc
75863	2	355330	7	NULL	NULL	0	NULL	statement 1	Process		occur in					renal epithelium	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Within the renal epithelium, loss of Apc function led to an induction of senescence, however, bypassing senescence through combined Apc and p21 or Ink4A gene deletion rapidly initiated renal carcinoma. 	topic_ccc
75864	3	355330	7	NULL	NULL	0	NULL	Apc	GP		combined with					p21	GP	gene deletion of			NULL		0	NULL	NULL	NULL	NULL	NULL	Within the renal epithelium, loss of Apc function led to an induction of senescence, however, bypassing senescence through combined Apc and p21 or Ink4A gene deletion rapidly initiated renal carcinoma. 	topic_ccc
75865	4	355330	7	NULL	NULL	0	NULL	Apc	GP		combined with					Ink4A	GP	gene deletion of			NULL		0	NULL	NULL	NULL	NULL	NULL	Within the renal epithelium, loss of Apc function led to an induction of senescence, however, bypassing senescence through combined Apc and p21 or Ink4A gene deletion rapidly initiated renal carcinoma. 	topic_ccc
75866	5	355330	7	NULL	NULL	0	NULL	statement 3	Process		initiate		rapidly			renal carcinoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Within the renal epithelium, loss of Apc function led to an induction of senescence, however, bypassing senescence through combined Apc and p21 or Ink4A gene deletion rapidly initiated renal carcinoma. 	topic_ccc
75867	6	355330	7	NULL	NULL	0	NULL	statement 4	Process		initiate		rapidly			renal carcinoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Within the renal epithelium, loss of Apc function led to an induction of senescence, however, bypassing senescence through combined Apc and p21 or Ink4A gene deletion rapidly initiated renal carcinoma. 	topic_ccc
75868	7	355330	7	NULL	NULL	0	NULL	senescence 	Process	bypassing	leads to					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Within the renal epithelium, loss of Apc function led to an induction of senescence, however, bypassing senescence through combined Apc and p21 or Ink4A gene deletion rapidly initiated renal carcinoma. 	topic_ccc
75869	8	355330	7	NULL	NULL	0	NULL	senescence 	Process	bypassing	leads to					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Within the renal epithelium, loss of Apc function led to an induction of senescence, however, bypassing senescence through combined Apc and p21 or Ink4A gene deletion rapidly initiated renal carcinoma. 	topic_ccc
75870	1	355331	7	NULL	NULL	0	NULL	cancer stem cells	Cell		limitation for 		severe			cancer	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	cancer stem or tumor-initiating cells (TICs) are a severe limitation for the treatment of cancer by conventional therapies.	topic_ccc
75871	2	355331	7	NULL	NULL	NULL	NULL	TICs	Cell		limitation for 		severe			cancer	MedicalFinding	treatment of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	cancer stem or tumor-initiating cells (TICs) are a severe limitation for the treatment of cancer by conventional therapies.	topic_ccc
75872	3	355331	7	NULL	NULL	0	NULL	TICs	Cell		is					tumor-initiating cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	cancer stem or tumor-initiating cells (TICs) are a severe limitation for the treatment of cancer by conventional therapies.	topic_ccc
75873	1	355332	7	NULL	NULL	0	NULL	MT110	Chemical		recognizes					EpCAM	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	MT110 recognizes EpCAM, a cell adhesion molecule expressed on TICs from diverse human carcinoma	topic_ccc
75874	2	355332	7	NULL	NULL	0	NULL	EpCAM	GP		is a type of					cell adhesion molecule	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	MT110 recognizes EpCAM, a cell adhesion molecule expressed on TICs from diverse human carcinoma	topic_ccc
75875	3	355332	7	NULL	NULL	0	NULL	EpCAM	GP		expressed on					TICs	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	MT110 recognizes EpCAM, a cell adhesion molecule expressed on TICs from diverse human carcinoma	topic_ccc
75876	4	355332	7	NULL	NULL	0	NULL	statement 3	Process		occur in					diverse human carcinoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	MT110 recognizes EpCAM, a cell adhesion molecule expressed on TICs from diverse human carcinoma	topic_ccc
75877	1	355334	7	NULL	NULL	0	NULL	MT110	Chemical		mediates		highly;;potent			 KRAS	GP	complete redirected lysis of			NULL		0	NULL	NULL	NULL	NULL	NULL	 MT110 was highly potent in mediating complete redirected lysis of KRAS-, PI3 kinase- and BRAF-mutated colorectal TICs, as demonstrated in a soft agar assay	topic_ccc
75878	2	355334	7	NULL	NULL	0	NULL	MT110	Chemical		mediates		highly;;potent			PI3 kinase	GP	complete redirected lysis of			NULL		0	NULL	NULL	NULL	NULL	NULL	 MT110 was highly potent in mediating complete redirected lysis of KRAS-, PI3 kinase- and BRAF-mutated colorectal TICs, as demonstrated in a soft agar assay	topic_ccc
75879	3	355334	7	NULL	NULL	NULL	NULL	MT110	Chemical		mediates		highly;;potent			colorectal TICs	Cell	complete redirected lysis of;;BRAF-mutated 			NULL		NULL	NULL	NULL	NULL	NULL	NULL	 MT110 was highly potent in mediating complete redirected lysis of KRAS-, PI3 kinase- and BRAF-mutated colorectal TICs, as demonstrated in a soft agar assay	topic_ccc
75880	1	355335	7	NULL	NULL	NULL	NULL	neoadjuvant chemoradiotherapy 	MedicalProcedure		improve					rectal carcinoma	MedicalFinding	local recurrence rates of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	There is substantial evidence for neoadjuvant chemoradiotherapy and extended abdominoperineal excision (APE) for improving local recurrence rates and overall survival for rectal carcinoma	topic_ccc
75881	2	355335	7	NULL	NULL	0	NULL	APE	MedicalProcedure		improve					rectal carcinoma	MedicalFinding	local recurrence rates of			NULL		0	NULL	NULL	NULL	NULL	NULL	There is substantial evidence for neoadjuvant chemoradiotherapy and extended abdominoperineal excision (APE) for improving local recurrence rates and overall survival for rectal carcinoma	topic_ccc
75882	3	355335	7	NULL	NULL	0	NULL	neoadjuvant chemoradiotherapy	MedicalProcedure		improve					rectal carcinoma	MedicalFinding	overall survival for			NULL		0	NULL	NULL	NULL	NULL	NULL	There is substantial evidence for neoadjuvant chemoradiotherapy and extended abdominoperineal excision (APE) for improving local recurrence rates and overall survival for rectal carcinoma	topic_ccc
75883	4	355335	7	NULL	NULL	0	NULL	APE	MedicalProcedure		improve					rectal carcinoma	MedicalFinding	overall survival for			NULL		0	NULL	NULL	NULL	NULL	NULL	There is substantial evidence for neoadjuvant chemoradiotherapy and extended abdominoperineal excision (APE) for improving local recurrence rates and overall survival for rectal carcinoma	topic_ccc
75884	5	355335	7	NULL	NULL	0	NULL	APE	MedicalProcedure		is					abdominoperineal excision	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	There is substantial evidence for neoadjuvant chemoradiotherapy and extended abdominoperineal excision (APE) for improving local recurrence rates and overall survival for rectal carcinoma	topic_ccc
75885	1	355336	7	NULL	NULL	NULL	NULL	bipolar disorder	MedicalFinding		have					small amygdalae	OrganismPart				NULL		NULL	NULL	NULL	NULL	NULL	NULL	There are a number of studies that show that children with bipolar disorder have small amygdalae compared to controls. There’s also evidence that their amygdalae, although small, may also be overactive. NULL	topic_bd
75886	2	355336	7	NULL	NULL	NULL	NULL	small amygdalae	OrganismPart		may be					overactive	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	There are a number of studies that show that children with bipolar disorder have small amygdalae compared to controls. There’s also evidence that their amygdalae, although small, may also be overactive. NULL	topic_bd
75887	1	355338	7	NULL	NULL	0	NULL	right amygdala	OrganismPart		located inside					brain	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	There’s a right and left amygdala, and they’re located deep inside the brain roughly on a line from your temples. They are one of the parts of the brain that govern emotions.	topic_bd
75888	2	355338	7	NULL	NULL	0	NULL	left amygdala	OrganismPart		located inside					brain	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	There’s a right and left amygdala, and they’re located deep inside the brain roughly on a line from your temples. They are one of the parts of the brain that govern emotions.	topic_bd
75889	3	355338	7	NULL	NULL	0	NULL	statement 1	Process		govern					emotions	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	There’s a right and left amygdala, and they’re located deep inside the brain roughly on a line from your temples. They are one of the parts of the brain that govern emotions.	topic_bd
75890	4	355338	7	NULL	NULL	0	NULL	statement 2	Process		govern					emotions	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	There’s a right and left amygdala, and they’re located deep inside the brain roughly on a line from your temples. They are one of the parts of the brain that govern emotions.	topic_bd
75891	1	355339	7	NULL	NULL	0	NULL	dangerous things	MentalProcess		capture					amygdalae	OrganismPart	attention of			NULL		0	NULL	NULL	NULL	NULL	NULL	Things that are really dangerous or really rewarding capture the attention of the amygdalae. 	topic_bd
75892	2	355339	7	NULL	NULL	0	NULL	rewarding things	MentalProcess		capture					amygdalae	OrganismPart	attention of			NULL		0	NULL	NULL	NULL	NULL	NULL	Things that are really dangerous or really rewarding capture the attention of the amygdalae. 	topic_bd
75893	1	355340	7	NULL	NULL	0	NULL	ADHD	MedicalFinding	children with	similar to					bipolar disorder	MedicalFinding	children with			NULL		0	NULL	NULL	NULL	NULL	NULL	What we’re finding is that these very irritable children with ADHD share some characteristics with children with bipolar disorder, but also have significant differences.	topic_bd
75894	2	355340	7	NULL	NULL	NULL	NULL	ADHD	MedicalFinding	children with	differ in		significantly			bipolar disorder	MedicalFinding	children with			NULL		NULL	NULL	NULL	NULL	NULL	NULL	What we’re finding is that these very irritable children with ADHD share some characteristics with children with bipolar disorder, but also have significant differences.	topic_bd
75895	1	355342	7	NULL	NULL	0	NULL	Classic bipolar disorder	MedicalFinding		characterized by					episodes	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Classic bipolar disorder is characterized by episodes.	topic_bd
75896	1	355343	7	NULL	NULL	0	NULL	bipolar	MedicalFinding		severely					mood dysregulated	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	One term being applied to these children who don’t quite fit the definition of bipolar is severely mood dysregulated, or S.M.D.	topic_bd
75897	2	355343	7	NULL	NULL	0	NULL	SMD	MedicalFinding		is					severely mood dysregulated	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	One term being applied to these children who don’t quite fit the definition of bipolar is severely mood dysregulated, or S.M.D.	topic_bd
75898	1	355344	7	NULL	NULL	0	NULL	prefrontal cortex	OrganismPart		damp down					amygdalae	OrganismPart	activity of			NULL		0	NULL	NULL	NULL	NULL	NULL	For example, we know that one action of the prefrontal cortex is to damp down the activity of the amygdalae. So in terms of treatment of bipolar disorder, where the amygdalae may be overactive, we’re thinking about whether we might be able to teach or stimulate the prefrontal cortex to damp down the amygdalae more. 	topic_bd
75899	1	355345	7	NULL	NULL	NULL	NULL	family-focused therapy	MedicalProcedure		help in					patient illness	MedicalFinding	managing			NULL		NULL	NULL	NULL	NULL	NULL	NULL	family-focused therapy the point is not to treat relatives, but to enlist their help in managing the patient’s illness.	topic_bd
75900	1	355346	7	NULL	NULL	0	NULL	 family-focused therapy	MedicalFinding		help in					episodes	MedicalFinding	quicker recoveries from			NULL		0	NULL	NULL	NULL	NULL	NULL	consistently find that if you combine medication and family-focused therapy, you get quicker recoveries from episodes and longer intervals of wellness	topic_bd
75901	2	355346	7	NULL	NULL	0	NULL	medication	MedicalProcedure		help in					episodes	MedicalFinding	quicker recoveries from			NULL		0	NULL	NULL	NULL	NULL	NULL	consistently find that if you combine medication and family-focused therapy, you get quicker recoveries from episodes and longer intervals of wellness	topic_bd
75902	1	355347	7	NULL	NULL	0	NULL	Cep55/c10orf3 	GP	expression of	collated with					CRC	MedicalFinding	high histological grade of 			NULL		0	NULL	NULL	NULL	NULL	NULL	Sixty-three percent cases showed weak positive for Cep55/c10orf3 in total 70 CRC cases. The Cep55/c10orf3 expression intention was collated with high histological grade of CRC.	topic_ccc
75903	1	355348	7	NULL	NULL	0	NULL	Cep55/c10orf3 	GP	peptide from	targeted by					CTLs					NULL	PBMCs	0	NULL	NULL	NULL	NULL	NULL	In our previous study, we demonstrated that a peptide derived from the novel centrosome residing protein Cep55/c10orf3 can be targeted by the cytotoxic T lymphocytes (CTLs) in peripheral blood mononuclear cells (PBMCs) of breast carcinoma patients.	topic_ccc
75904	2	355348	7	NULL	NULL	0	NULL	statement 1	Process		occur in					breast carcinoma patients	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In our previous study, we demonstrated that a peptide derived from the novel centrosome residing protein Cep55/c10orf3 can be targeted by the cytotoxic T lymphocytes (CTLs) in peripheral blood mononuclear cells (PBMCs) of breast carcinoma patients.	topic_ccc
75905	3	355348	7	NULL	NULL	0	NULL	CTLs	Cell		is					cytotoxic T lymphocytes	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	In our previous study, we demonstrated that a peptide derived from the novel centrosome residing protein Cep55/c10orf3 can be targeted by the cytotoxic T lymphocytes (CTLs) in peripheral blood mononuclear cells (PBMCs) of breast carcinoma patients.	topic_ccc
75906	4	355348	7	NULL	NULL	0	NULL	PBMCs	Cell		is					peripheral blood mononuclear cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	In our previous study, we demonstrated that a peptide derived from the novel centrosome residing protein Cep55/c10orf3 can be targeted by the cytotoxic T lymphocytes (CTLs) in peripheral blood mononuclear cells (PBMCs) of breast carcinoma patients.	topic_ccc
75907	5	355348	7	NULL	NULL	0	NULL	Cep55/c10orf3	GP		is a type of					novel centrosome residing protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	In our previous study, we demonstrated that a peptide derived from the novel centrosome residing protein Cep55/c10orf3 can be targeted by the cytotoxic T lymphocytes (CTLs) in peripheral blood mononuclear cells (PBMCs) of breast carcinoma patients.	topic_ccc
75908	1	355349	7	NULL	NULL	NULL	NULL	Methylation	Process	 tolerance of	occur due to					MGMT	GP	field defect in			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Methylation tolerance due to an O6-methylguanine DNA methyltransferase (MGMT) field defect in the colonic mucosa: an initiating step in the development of mismatch repair-deficient colorectal cancers.	topic_ccc
75909	2	355349	7	NULL	NULL	0	NULL	statement 1	Process		occur in					colonic mucosa	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Methylation tolerance due to an O6-methylguanine DNA methyltransferase (MGMT) field defect in the colonic mucosa: an initiating step in the development of mismatch repair-deficient colorectal cancers.	topic_ccc
75910	3	355349	7	NULL	NULL	NULL	NULL	MGMT	GP		is					O6-methylguanine DNA methyltransferase	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Methylation tolerance due to an O6-methylguanine DNA methyltransferase (MGMT) field defect in the colonic mucosa: an initiating step in the development of mismatch repair-deficient colorectal cancers.	topic_ccc
75911	4	355349	7	NULL	NULL	0	NULL	Methylation	Process	tolerance in	initiating step in					mismatch repair-deficient colorectal cancers	MedicalFinding	development of			NULL		0	NULL	NULL	NULL	NULL	NULL	Methylation tolerance due to an O6-methylguanine DNA methyltransferase (MGMT) field defect in the colonic mucosa: an initiating step in the development of mismatch repair-deficient colorectal cancers.	topic_ccc
75912	1	355350	7	NULL	NULL	0	NULL	HSP27	GP		prognostic indicator in					rectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Low molecular weight heat shock protein HSP27 is a prognostic indicator in rectal cancer but not colon cancer.	topic_ccc
75913	2	355350	7	NULL	NULL	0	NULL	HSP27	GP		is not a prognostic indicator in					colon cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Low molecular weight heat shock protein HSP27 is a prognostic indicator in rectal cancer but not colon cancer.	topic_ccc
75914	3	355350	7	NULL	NULL	0	NULL	HSP27	GP		is a type of					Low molecular weight heat shock protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Low molecular weight heat shock protein HSP27 is a prognostic indicator in rectal cancer but not colon cancer.	topic_ccc
75915	1	355351	7	NULL	NULL	NULL	NULL	P-LVD	OrganismPart	high density of	associated with					VEGF	GP	high expression of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	 Results A high density of peritumoural lymphatics (P-LVD) was significantly associated with high VEGF expression and disease progression.	topic_ccc
75916	2	355351	7	NULL	NULL	NULL	NULL	P-LVD	OrganismPart	high density of	associated with					disease progression	Process	high			NULL		NULL	NULL	NULL	NULL	NULL	NULL	 Results A high density of peritumoural lymphatics (P-LVD) was significantly associated with high VEGF expression and disease progression.	topic_ccc
75917	3	355351	7	NULL	NULL	0	NULL	P-LVD	OrganismPart		is					 peritumoural lymphatics	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	 Results A high density of peritumoural lymphatics (P-LVD) was significantly associated with high VEGF expression and disease progression.	topic_ccc
74411	1	355353	5	NULL	NULL	0	NULL	VENTX	GP		is					Vent-like homeobox gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Vent-like homeobox gene VENTX, a putative homolog of the Xenopus xvent2 gene, 	topic_ll
74412	2	355353	5	NULL	NULL	0	NULL	VENTX	GP		is a homolog of		putative			xvent2 gene	GP	Xenopus			NULL		0	NULL	NULL	NULL	NULL	NULL	Vent-like homeobox gene VENTX, a putative homolog of the Xenopus xvent2 gene, 	topic_ll
74413	1	355354	5	NULL	NULL	0	NULL	VENTX	GP		is					Vent-like homeobox gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The vent-like homeobox gene VENTX promotes human myeloid differentiation 	topic_ll
74414	2	355354	5	NULL	NULL	0	NULL	VENTX	GP		promotes					myeloid differentiation	Process	human			NULL		0	NULL	NULL	NULL	NULL	NULL	The vent-like homeobox gene VENTX promotes human myeloid differentiation 	topic_ll
74415	1	355356	5	NULL	NULL	0	NULL	RIZ1 gene	GP		is inactivated in		partly			MDS	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	RIZ1 gene is inactivated in MDS and AML in part by methylation, 	topic_ll
74416	2	355356	5	NULL	NULL	0	NULL	RIZ1 gene	GP		is inactivated in		partly			AML	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	RIZ1 gene is inactivated in MDS and AML in part by methylation, 	topic_ll
74417	3	355356	5	NULL	NULL	0	NULL	methylation	Process		plays a role in					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	RIZ1 gene is inactivated in MDS and AML in part by methylation, 	topic_ll
74418	4	355356	5	NULL	NULL	0	NULL	methylation	Process		plays a role in					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	RIZ1 gene is inactivated in MDS and AML in part by methylation, 	topic_ll
74419	1	355359	5	NULL	NULL	0	NULL	FOXM1	GP	aberrant expression of	induce					AML cell	Cell	 proliferation of			NULL		0	NULL	NULL	NULL	NULL	NULL	aberrant expression of FOXM1 induces AML cell proliferation through modulation of cell cycle progression.	topic_ll
74420	2	355359	5	NULL	NULL	0	NULL	statement 1	Process		occurs through					cell cycle progression	Process	modulation of			NULL		0	NULL	NULL	NULL	NULL	NULL	aberrant expression of FOXM1 induces AML cell proliferation through modulation of cell cycle progression.	topic_ll
74421	1	355361	5	NULL	NULL	0	NULL	amplicons	Chromosome		is expressed in					breast cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Retinoic acid receptor alpha (RARA) and other target sequences at 17p11.2 often represent the amplicons expressed in breast cancer, not in AML	topic_ll
74422	2	355361	5	NULL	NULL	0	NULL	RARA	GP		is					retinoic acid receptor alpha	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Retinoic acid receptor alpha (RARA) and other target sequences at 17p11.2 often represent the amplicons expressed in breast cancer, not in AML	topic_ll
74423	3	355361	5	NULL	NULL	0	NULL	RARA	GP		represent					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Retinoic acid receptor alpha (RARA) and other target sequences at 17p11.2 often represent the amplicons expressed in breast cancer, not in AML	topic_ll
74424	4	355361	5	NULL	NULL	0	NULL	target sequences	NucleicAcid		is present in					17p11.2	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	Retinoic acid receptor alpha (RARA) and other target sequences at 17p11.2 often represent the amplicons expressed in breast cancer, not in AML	topic_ll
74425	5	355361	5	NULL	NULL	0	NULL	statement 4	NucleicAcid		represent					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Retinoic acid receptor alpha (RARA) and other target sequences at 17p11.2 often represent the amplicons expressed in breast cancer, not in AML	topic_ll
74426	6	355361	5	NULL	NULL	0	NULL	amplicons	Chromosome		is not expressed in					AML	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Retinoic acid receptor alpha (RARA) and other target sequences at 17p11.2 often represent the amplicons expressed in breast cancer, not in AML	topic_ll
74427	1	355363	5	NULL	NULL	0	NULL	AML cells	Cell		is differentiated into					dendritic cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	AML cells can be differentiated into dendritic cells (AML-DCs), which have increased immunogenicity and have been proposed as vaccines against leukemia. 	topic_ll
74428	2	355363	5	NULL	NULL	0	NULL	statement 1	Cell		is					AML-DCs	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	AML cells can be differentiated into dendritic cells (AML-DCs), which have increased immunogenicity and have been proposed as vaccines against leukemia. 	topic_ll
74429	3	355363	5	NULL	NULL	0	NULL	AML-DCs	Cell		contains					immunogenicity	AbstractConcept	increased			NULL		0	NULL	NULL	NULL	NULL	NULL	AML cells can be differentiated into dendritic cells (AML-DCs), which have increased immunogenicity and have been proposed as vaccines against leukemia. 	topic_ll
74430	4	355363	5	NULL	NULL	0	NULL	AML-DCs	Cell		is a type of					vaccine	AbstractConcept				NULL		0	NULL	NULL	NULL	NULL	NULL	AML cells can be differentiated into dendritic cells (AML-DCs), which have increased immunogenicity and have been proposed as vaccines against leukemia. 	topic_ll
74431	5	355363	5	NULL	NULL	0	NULL	AML-DCs	Cell		acts against					leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	AML cells can be differentiated into dendritic cells (AML-DCs), which have increased immunogenicity and have been proposed as vaccines against leukemia. 	topic_ll
74432	1	355365	5	NULL	NULL	0	NULL	FLT3	GP		is					 fms-like receptor tyrosine kinase-3	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	ms-like receptor tyrosine kinase-3 (FLT3), which is important for the normal development of hematopoietic stem cells and cells of the immune system, is frequently mutated in patients with acute myeloid leukemia (AML). 	topic_ll
74433	2	355365	5	NULL	NULL	0	NULL	FLT3	GP		is important for					hematopoietic stem cells	Cell	normal development of			NULL		0	NULL	NULL	NULL	NULL	NULL	ms-like receptor tyrosine kinase-3 (FLT3), which is important for the normal development of hematopoietic stem cells and cells of the immune system, is frequently mutated in patients with acute myeloid leukemia (AML). 	topic_ll
74434	3	355365	5	NULL	NULL	0	NULL	FLT3	GP		is important for					immune system	OrganismPart	normal development of;;cells of			NULL		0	NULL	NULL	NULL	NULL	NULL	ms-like receptor tyrosine kinase-3 (FLT3), which is important for the normal development of hematopoietic stem cells and cells of the immune system, is frequently mutated in patients with acute myeloid leukemia (AML). 	topic_ll
74435	4	355365	5	NULL	NULL	NULL	NULL	FLT3	GP		is mutated in		frequently			AML patients	GroupOfPeople				NULL		NULL	NULL	NULL	NULL	NULL	NULL	ms-like receptor tyrosine kinase-3 (FLT3), which is important for the normal development of hematopoietic stem cells and cells of the immune system, is frequently mutated in patients with acute myeloid leukemia (AML). 	topic_ll
74436	5	355365	5	NULL	NULL	0	NULL	AML	MedicalFinding		is					acute myeloid leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	ms-like receptor tyrosine kinase-3 (FLT3), which is important for the normal development of hematopoietic stem cells and cells of the immune system, is frequently mutated in patients with acute myeloid leukemia (AML). 	topic_ll
74477	1	355366	5	NULL	NULL	NULL	NULL	FLT3	GP		is mutated in					AML patients	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	FLT3 inhibitors have shown therapeutic activity in AML patients with FLT3 mutations. Sorafenib and sunitinib were the first FLT3 inhibitors to be studied in the clinic and have the most clinically relevant data.	topic_ll
74481	2	355366	5	NULL	NULL	NULL	NULL	FLT3 inhibitors	Chemical		is therapeutically active in					AML patients	GroupOfPeople				NULL		NULL	NULL	NULL	NULL	NULL	NULL	FLT3 inhibitors have shown therapeutic activity in AML patients with FLT3 mutations. Sorafenib and sunitinib were the first FLT3 inhibitors to be studied in the clinic and have the most clinically relevant data.	topic_ll
74483	3	355366	5	NULL	NULL	0	NULL	sunitinib	Chemical		is an inhibitor of					FLT3	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	FLT3 inhibitors have shown therapeutic activity in AML patients with FLT3 mutations. Sorafenib and sunitinib were the first FLT3 inhibitors to be studied in the clinic and have the most clinically relevant data.	topic_ll
74485	4	355366	5	NULL	NULL	0	NULL	sorafenib	Chemical		is an inhibitor of					FLT3	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	FLT3 inhibitors have shown therapeutic activity in AML patients with FLT3 mutations. Sorafenib and sunitinib were the first FLT3 inhibitors to be studied in the clinic and have the most clinically relevant data.	topic_ll
74488	1	355368	5	NULL	NULL	0	NULL	FLT3 inhibitors	Chemical		is therapeutically active in					AML patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	FLT3 inhibitors have shown therapeutic activity in AML patients with FLT3 mutations.	topic_ll
74489	2	355368	5	NULL	NULL	0	NULL	FLT3	GP		is mutated in					AML patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	FLT3 inhibitors have shown therapeutic activity in AML patients with FLT3 mutations.	topic_ll
74490	1	355369	5	NULL	NULL	0	NULL	formaldehyde	Chemical		cause		potentially			leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Hematological and toxicological evaluation of formaldehyde as a potential cause of human leukemia.	topic_ll
74491	1	355370	5	NULL	NULL	0	NULL	formaldehyde	Chemical	exposure	is associated with					AML	MedicalFinding	higher risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	formaldehyde exposure is associated with a higher risk of acute myelogenous leukemia (AML)	topic_ll
74492	2	355370	5	NULL	NULL	0	NULL	AML	MedicalFinding		is					acute myelogenous leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	formaldehyde exposure is associated with a higher risk of acute myelogenous leukemia (AML)	topic_ll
74493	1	355373	5	NULL	NULL	0	NULL	transplantation	Process	allogeneic	salvage					chemotherapy	MedicalProcedure	failures of			NULL		0	NULL	NULL	NULL	NULL	NULL	Allogeneic transplantation can act as a salvage for chemotherapy failures	topic_ll
74494	1	355376	5	NULL	NULL	0	NULL	SMT-A07	Chemical		induces					leukemia cells	Cell	apoptosis of			NULL	in vitro	0	NULL	NULL	NULL	NULL	NULL	SMT-A07, a 3-(Indol-2-yl) indazole derivative, induces apoptosis of leukemia cells in vitro.	topic_ll
74495	2	355376	5	NULL	NULL	0	NULL	SMT-A07	Chemical		is a derivative of					3-(Indol-2-yl) indazole	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	SMT-A07, a 3-(Indol-2-yl) indazole derivative, induces apoptosis of leukemia cells in vitro.	topic_ll
74496	1	355377	5	NULL	NULL	NULL	NULL	IL-24	GP		induces					chronic lymphocytic leukemia B cells	Cell	apoptosis of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	IL-24 Induces Apoptosis of Chronic Lymphocytic Leukemia B Cells Engaged into the Cell Cycle through Dephosphorylation of STAT3 and Stabilization of p53 Expression	topic_ll
74497	2	355377	5	NULL	NULL	0	NULL	chronic lymphocytic leukemia B cells\t	Cell		engaged in					cell cycle	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	IL-24 Induces Apoptosis of Chronic Lymphocytic Leukemia B Cells Engaged into the Cell Cycle through Dephosphorylation of STAT3 and Stabilization of p53 Expression	topic_ll
74498	3	355377	5	NULL	NULL	0	NULL	statement 1	Process		occurs through					STAT3	GP	dephosphoylation of			NULL		0	NULL	NULL	NULL	NULL	NULL	IL-24 Induces Apoptosis of Chronic Lymphocytic Leukemia B Cells Engaged into the Cell Cycle through Dephosphorylation of STAT3 and Stabilization of p53 Expression	topic_ll
74499	4	355377	5	NULL	NULL	0	NULL	statement 1	Process		occurs through					p53	GP	stabilization of;;expression of			NULL		0	NULL	NULL	NULL	NULL	NULL	IL-24 Induces Apoptosis of Chronic Lymphocytic Leukemia B Cells Engaged into the Cell Cycle through Dephosphorylation of STAT3 and Stabilization of p53 Expression	topic_ll
74616	1	355378	5	NULL	NULL	0	NULL	curcumin	Chemical		downregulates					egr-1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Curcumin causes the growth arrest and apoptosis of B cell lymphoma by downregulation of egr-1, c-myc, bcl-XL, NF-kappa B, and p53.	topic_ll
74617	2	355378	5	NULL	NULL	0	NULL	statement 1	Process		cause					growth arrest	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Curcumin causes the growth arrest and apoptosis of B cell lymphoma by downregulation of egr-1, c-myc, bcl-XL, NF-kappa B, and p53.	topic_ll
74618	3	355378	5	NULL	NULL	NULL	NULL	statement 1	Process		cause					B cell lymphoma	Cell	apoptosis of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Curcumin causes the growth arrest and apoptosis of B cell lymphoma by downregulation of egr-1, c-myc, bcl-XL, NF-kappa B, and p53.	topic_ll
74619	4	355378	5	NULL	NULL	0	NULL	curcumin	Chemical		downregulates					c-myc	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Curcumin causes the growth arrest and apoptosis of B cell lymphoma by downregulation of egr-1, c-myc, bcl-XL, NF-kappa B, and p53.	topic_ll
74620	5	355378	5	NULL	NULL	0	NULL	statement 4	Process		cause					growth arrest	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Curcumin causes the growth arrest and apoptosis of B cell lymphoma by downregulation of egr-1, c-myc, bcl-XL, NF-kappa B, and p53.	topic_ll
74621	6	355378	5	NULL	NULL	0	NULL	statement 4	Process		cause					B cell lymphoma	Cell	apoptosis of			NULL		0	NULL	NULL	NULL	NULL	NULL	Curcumin causes the growth arrest and apoptosis of B cell lymphoma by downregulation of egr-1, c-myc, bcl-XL, NF-kappa B, and p53.	topic_ll
74622	7	355378	5	NULL	NULL	0	NULL	curcumin	Chemical		downregulates					bcl-XL	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Curcumin causes the growth arrest and apoptosis of B cell lymphoma by downregulation of egr-1, c-myc, bcl-XL, NF-kappa B, and p53.	topic_ll
74623	8	355378	5	NULL	NULL	0	NULL	statement 7	Process		cause					growth arrest	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Curcumin causes the growth arrest and apoptosis of B cell lymphoma by downregulation of egr-1, c-myc, bcl-XL, NF-kappa B, and p53.	topic_ll
74624	9	355378	5	NULL	NULL	0	NULL	statement 7	Process		cause					B cell lymphoma	Cell	apoptosis of			NULL		0	NULL	NULL	NULL	NULL	NULL	Curcumin causes the growth arrest and apoptosis of B cell lymphoma by downregulation of egr-1, c-myc, bcl-XL, NF-kappa B, and p53.	topic_ll
74625	10	355378	5	NULL	NULL	0	NULL	curcumin	Chemical		downregulates					NF-kappa B	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Curcumin causes the growth arrest and apoptosis of B cell lymphoma by downregulation of egr-1, c-myc, bcl-XL, NF-kappa B, and p53.	topic_ll
74626	11	355378	5	NULL	NULL	0	NULL	statement 10	Process		cause					growth arrest	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Curcumin causes the growth arrest and apoptosis of B cell lymphoma by downregulation of egr-1, c-myc, bcl-XL, NF-kappa B, and p53.	topic_ll
74627	12	355378	5	NULL	NULL	0	NULL	statement 10	Process		cause					B cell lymphoma	Cell	apoptosis of			NULL		0	NULL	NULL	NULL	NULL	NULL	Curcumin causes the growth arrest and apoptosis of B cell lymphoma by downregulation of egr-1, c-myc, bcl-XL, NF-kappa B, and p53.	topic_ll
74628	13	355378	5	NULL	NULL	0	NULL	curcumin	Chemical		downregulates					p53	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Curcumin causes the growth arrest and apoptosis of B cell lymphoma by downregulation of egr-1, c-myc, bcl-XL, NF-kappa B, and p53.	topic_ll
74629	14	355378	5	NULL	NULL	0	NULL	statement 13	Process		cause					growth arrest	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Curcumin causes the growth arrest and apoptosis of B cell lymphoma by downregulation of egr-1, c-myc, bcl-XL, NF-kappa B, and p53.	topic_ll
74630	15	355378	5	NULL	NULL	0	NULL	statement 13	Process		cause					B cell lymphoma	Cell	apoptosis of			NULL		0	NULL	NULL	NULL	NULL	NULL	Curcumin causes the growth arrest and apoptosis of B cell lymphoma by downregulation of egr-1, c-myc, bcl-XL, NF-kappa B, and p53.	topic_ll
77680	1	355385	6	NULL	NULL	0	NULL	EGF receptor	GP		plays a role in					Breast cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	at least two of these receptors, the EGF receptor and HER2, play a role in breast cancer	topic_bc
77681	2	355385	6	NULL	NULL	0	NULL	HER2	GP		plays a role in					Breast cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	at least two of these receptors, the EGF receptor and HER2, play a role in breast cancer	topic_bc
77682	1	355386	6	NULL	NULL	0	NULL	Tenascin-C	Chemical		stimulates					cell proliferation	Process				NULL	cancer	0	NULL	NULL	NULL	NULL	NULL	Tenascin-C stimulates cancer cell proliferation. 	topic_bc
77683	1	355387	6	NULL	NULL	0	NULL	Breast cancer	MedicalFinding		causes 					TNC	GP	upregulation of			NULL		0	NULL	NULL	NULL	NULL	NULL	The ECM protein tenascin-C (TNC) is frequently up-regulated in breast cancer	topic_bc
77684	2	355387	6	NULL	NULL	0	NULL	Tenascin-C	GP		is a type of					ECM protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The ECM protein tenascin-C (TNC) is frequently up-regulated in breast cancer	topic_bc
77685	3	355387	6	NULL	NULL	0	NULL	TNC	GP		is					tenascin-C	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The ECM protein tenascin-C (TNC) is frequently up-regulated in breast cancer	topic_bc
77686	1	355388	6	NULL	NULL	NULL	NULL	Estradiol	GP		plays a role in		critical			breast cancer 	MedicalFinding	sporadic;; progression of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Estradiol (E2) play a critical role in sporadic breast cancer progression and decrease apoptosis in breast cancer cells	topic_bc
77687	2	355388	6	NULL	NULL	0	NULL	Estradiol	GP		decrease					apoptosis	Process				NULL	breast cancer cells	0	NULL	NULL	NULL	NULL	NULL	Estradiol (E2) play a critical role in sporadic breast cancer progression and decrease apoptosis in breast cancer cells	topic_bc
77735	3	355388	6	NULL	NULL	0	NULL	Estradiol	GP		is					E2	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Estradiol (E2) play a critical role in sporadic breast cancer progression and decrease apoptosis in breast cancer cells	topic_bc
77736	1	355389	6	NULL	NULL	0	NULL	tamoxifen	Chemical		acts as					Breast cancer 	MedicalFinding	drug for			NULL		0	NULL	NULL	NULL	NULL	NULL	The widely used breast cancer drug tamoxifen (Nolvadex®), which can become less effective over time, might retain its full strength indefinitely if used along with a second drug	topic_bc
77737	2	355389	6	NULL	NULL	0	NULL	tamoxifen	Chemical		is					Nolvadex�	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The widely used breast cancer drug tamoxifen (Nolvadex®), which can become less effective over time, might retain its full strength indefinitely if used along with a second drug	topic_bc
77738	1	355390	6	NULL	NULL	0	NULL	tumor	Cell	growth of	is a result of					proliferation	Process	uncontrolled			NULL		0	NULL	NULL	NULL	NULL	NULL	 tumour growth is not just a result of uncontrolled proliferation but also of reduced apoptosis.	topic_bc
77739	2	355390	6	NULL	NULL	0	NULL	tumor	Cell	growth of	is a result of					apoptosis	Process	reduction of 			NULL		0	NULL	NULL	NULL	NULL	NULL	 tumour growth is not just a result of uncontrolled proliferation but also of reduced apoptosis.	topic_bc
77740	1	355391	6	NULL	NULL	0	NULL	Nitric oxide	Chemical		increases					glucose	Chemical	transport of			NULL	breast cancer cells	0	NULL	NULL	NULL	NULL	NULL	Nitric oxide will increase glucose transport in breast cancer cells more than in normal breast cells	topic_bc
77741	2	355391	6	NULL	NULL	0	NULL	Nitric oxide	Chemical		increases					glucose	Chemical	transport of			NULL	normal breast cells	0	NULL	NULL	NULL	NULL	NULL	Nitric oxide will increase glucose transport in breast cancer cells more than in normal breast cells	topic_bc
77742	3	355391	6	NULL	NULL	NULL	NULL	statement 1	Process		is more as compared to					statement 2	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nitric oxide will increase glucose transport in breast cancer cells more than in normal breast cells	topic_bc
77743	2	355392	6	NULL	NULL	NULL	NULL	Breast cancer cell	Cell		uses 					statement 1	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The ability of a cancer cell to grow ultimately depends on its ability to take up and metabolize fuel. The primary fuel that is used by the breast cancer cell is carbohydrate. Nitric oxide may regulate the uptake of carbohydrate ultimately affecting its ability to cause hypertrophy in tissues such as skeletal muscle. 	topic_bc
77744	1	355392	6	NULL	NULL	0	NULL	Carbohydrate	Chemical		is used as					primary fuel					NULL		0	NULL	NULL	NULL	NULL	NULL	The ability of a cancer cell to grow ultimately depends on its ability to take up and metabolize fuel. The primary fuel that is used by the breast cancer cell is carbohydrate. Nitric oxide may regulate the uptake of carbohydrate ultimately affecting its ability to cause hypertrophy in tissues such as skeletal muscle. 	topic_bc
77745	3	355392	6	NULL	NULL	0	NULL	Nitric oxide	Chemical		regulate		may			carbohydrate	Chemical	uptake of 			NULL		0	NULL	NULL	NULL	NULL	NULL	The ability of a cancer cell to grow ultimately depends on its ability to take up and metabolize fuel. The primary fuel that is used by the breast cancer cell is carbohydrate. Nitric oxide may regulate the uptake of carbohydrate ultimately affecting its ability to cause hypertrophy in tissues such as skeletal muscle. 	topic_bc
77746	4	355392	6	NULL	NULL	0	NULL	hypertrophy	MedicalFinding		is caused in 					skeletal muscle	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The ability of a cancer cell to grow ultimately depends on its ability to take up and metabolize fuel. The primary fuel that is used by the breast cancer cell is carbohydrate. Nitric oxide may regulate the uptake of carbohydrate ultimately affecting its ability to cause hypertrophy in tissues such as skeletal muscle. 	topic_bc
77747	5	355392	6	NULL	NULL	0	NULL	statement 3	Process		affects					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The ability of a cancer cell to grow ultimately depends on its ability to take up and metabolize fuel. The primary fuel that is used by the breast cancer cell is carbohydrate. Nitric oxide may regulate the uptake of carbohydrate ultimately affecting its ability to cause hypertrophy in tissues such as skeletal muscle. 	topic_bc
77748	1	355394	6	NULL	NULL	0	NULL	estrogen	GP		increases					Breast cancer	MedicalFinding	occurrence of 			NULL		0	NULL	NULL	NULL	NULL	NULL	Some kinds of breast cancer are fueled by high amounts of estrogen. That's the reason that estrogen suppression medications are an important part of treatment that prevents recurrence	topic_bc
77749	1	355395	6	NULL	NULL	0	NULL	Breast cancer	MedicalFinding		spreads beyond the					breast	cell				NULL		0	NULL	NULL	NULL	NULL	NULL	When breast cancer spreads beyond the breast, it is said to be metastatic	topic_bc
77750	2	355395	6	NULL	NULL	0	NULL	statement 1	Process		is 					metastatic	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	When breast cancer spreads beyond the breast, it is said to be metastatic	topic_bc
77751	1	355396	6	NULL	NULL	0	NULL	estrogen	Chemical	higher levels of	leads to					Breast cancer	MedicalFinding	reoccurence of 			NULL		0	NULL	NULL	NULL	NULL	NULL	It appears that the higher a breast cancer survivor's level of estrogen is the greater is her risk of developing breast cancer again	topic_bc
77752	1	355397	6	NULL	NULL	0	NULL	DLC-1	GP		acts as 					metastasis-suppressor gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The finding that DLC-1 can act as a metastasis-suppressor gene	topic_bc
77753	1	355401	6	NULL	NULL	NULL	NULL	Capecitabine	Chemical		is used in					breast cancer	MedicalFinding	metastatic;; treatment of 			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Capecitabine (INN Xeloda, Roche) is an orally-administered chemotherapeutic agent used in the treatment of metastatic breast and colorectal cancers	topic_bc
77754	2	355401	6	NULL	NULL	0	NULL	Capecitabine	Chemical		is used in					colorectal cancer	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Capecitabine (INN Xeloda, Roche) is an orally-administered chemotherapeutic agent used in the treatment of metastatic breast and colorectal cancers	topic_bc
74634	1	355404	5	NULL	NULL	0	NULL	JMML	MedicalFinding		is					Juvenile Myelomonocytic Leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Juvenile Myelomonocytic Leukemia (JMML) is a rare form of leukemia which affects young children, generally under the age of five.	topic_ll
74635	2	355404	5	NULL	NULL	0	NULL	JMML	MedicalFinding		is a form of		rare			leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Juvenile Myelomonocytic Leukemia (JMML) is a rare form of leukemia which affects young children, generally under the age of five.	topic_ll
74636	3	355404	5	NULL	NULL	0	NULL	JMML	MedicalFinding		affect					children	GroupOfPeople	young			NULL		0	NULL	NULL	NULL	NULL	NULL	Juvenile Myelomonocytic Leukemia (JMML) is a rare form of leukemia which affects young children, generally under the age of five.	topic_ll
74637	1	355405	5	NULL	NULL	0	NULL	CLL	MedicalFinding		is					Chronic lymphocytic leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Chronic lymphocytic leukemia (CLL) is one of four main types of leukemia. 	topic_ll
74638	2	355405	5	NULL	NULL	0	NULL	CLL	MedicalFinding		is a type of					leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Chronic lymphocytic leukemia (CLL) is one of four main types of leukemia. 	topic_ll
74639	1	355406	5	NULL	NULL	0	NULL	CLL	MedicalFinding		is					Chronic lymphocytic leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Chronic lymphocytic leukemia (chronic lymphoid leukemia, CLL) is a monoclonal disorder	topic_ll
74640	2	355406	5	NULL	NULL	0	NULL	CLL	MedicalFinding		is					chronic lymphoid leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Chronic lymphocytic leukemia (chronic lymphoid leukemia, CLL) is a monoclonal disorder	topic_ll
74641	3	355406	5	NULL	NULL	0	NULL	CLL	MedicalFinding		is a type of					monoclonal disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Chronic lymphocytic leukemia (chronic lymphoid leukemia, CLL) is a monoclonal disorder	topic_ll
77755	1	355407	6	NULL	NULL	0	NULL	Breast carcinoma	MedicalFinding	human	co-express					EGF receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Human breast carcinomas frequently co-express the epidermal growth factor (EGF) receptor and the other three members of the EGF receptor family (HER2, -3 and -4).	topic_bc
77756	2	355407	6	NULL	NULL	0	NULL	Breast carcinoma	MedicalFinding	human	co-express					HER2	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Human breast carcinomas frequently co-express the epidermal growth factor (EGF) receptor and the other three members of the EGF receptor family (HER2, -3 and -4).	topic_bc
77757	3	355407	6	NULL	NULL	0	NULL	Breast carcinoma	MedicalFinding	human	co-express					HER3	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Human breast carcinomas frequently co-express the epidermal growth factor (EGF) receptor and the other three members of the EGF receptor family (HER2, -3 and -4).	topic_bc
77758	4	355407	6	NULL	NULL	0	NULL	Breast carcinoma	MedicalFinding	human	co-express					HER4	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Human breast carcinomas frequently co-express the epidermal growth factor (EGF) receptor and the other three members of the EGF receptor family (HER2, -3 and -4).	topic_bc
77759	5	355407	6	NULL	NULL	0	NULL	HER2	GP		is a type of					EGF receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Human breast carcinomas frequently co-express the epidermal growth factor (EGF) receptor and the other three members of the EGF receptor family (HER2, -3 and -4).	topic_bc
77760	6	355407	6	NULL	NULL	0	NULL	HER3	GP		is a type of					EGF receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Human breast carcinomas frequently co-express the epidermal growth factor (EGF) receptor and the other three members of the EGF receptor family (HER2, -3 and -4).	topic_bc
77761	7	355407	6	NULL	NULL	0	NULL	HER4	GP		is a type of					EGF receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Human breast carcinomas frequently co-express the epidermal growth factor (EGF) receptor and the other three members of the EGF receptor family (HER2, -3 and -4).	topic_bc
78028	1	355410	6	NULL	NULL	0	NULL	fat	Chemical	intake of	is associated with					Breast cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	a positive association between high dietary fat intake and breast cancer	topic_bc
78029	1	355412	6	NULL	NULL	0	NULL	progesterone	Chemical		decreases					Breast cancer	MedicalFinding	risk of 			NULL		0	NULL	NULL	NULL	NULL	NULL	progesterone may actually decrease a woman's risk of breast cancer	topic_bc
78030	1	355413	6	NULL	NULL	0	NULL	early pregnancy	PhysicalPhenomenon		prevents		may			Breast cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	early pregnancy, prolonged lactation, chemical or surgical sterilization, exercise, abstinence from alcohol, and a low-fat diet may help prevent breast cancer	topic_bc
78031	2	355413	6	NULL	NULL	0	NULL	lactation	PhysicalPhenomenon	prolonged	prevents					Breast cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	early pregnancy, prolonged lactation, chemical or surgical sterilization, exercise, abstinence from alcohol, and a low-fat diet may help prevent breast cancer	topic_bc
78032	3	355413	6	NULL	NULL	0	NULL	chemical sterilization	MedicalProcedure		prevents					Breast cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	early pregnancy, prolonged lactation, chemical or surgical sterilization, exercise, abstinence from alcohol, and a low-fat diet may help prevent breast cancer	topic_bc
78033	4	355413	6	NULL	NULL	0	NULL	excercise	PhysicalPhenomenon		prevents					Breast cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	early pregnancy, prolonged lactation, chemical or surgical sterilization, exercise, abstinence from alcohol, and a low-fat diet may help prevent breast cancer	topic_bc
78034	5	355413	6	NULL	NULL	0	NULL	alcohol	Chemical	abstinence from	prevents					Breast cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	early pregnancy, prolonged lactation, chemical or surgical sterilization, exercise, abstinence from alcohol, and a low-fat diet may help prevent breast cancer	topic_bc
78035	6	355413	6	NULL	NULL	0	NULL	low-fat diet			prevents					Breast cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	early pregnancy, prolonged lactation, chemical or surgical sterilization, exercise, abstinence from alcohol, and a low-fat diet may help prevent breast cancer	topic_bc
78036	1	355414	6	NULL	NULL	0	NULL	sterilization	MedicalProcedure		reduce		may			Breast cancer	MedicalFinding	risk of 			NULL		0	NULL	NULL	NULL	NULL	NULL	sterilization may reduce the risk of breast cancer	topic_bc
78037	1	355415	6	NULL	NULL	0	NULL	tamoxifen	Chemical		is used for					Breast cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	tamoxifen is currently used widely in patients with early stage, surgically treated breast cancer and has been shown to decrease contralateral breast cancer by 40%	topic_bc
78038	2	355415	6	NULL	NULL	0	NULL	tamoxifen	Chemical		decrease					contralateral cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	tamoxifen is currently used widely in patients with early stage, surgically treated breast cancer and has been shown to decrease contralateral breast cancer by 40%	topic_bc
78039	1	355416	6	NULL	NULL	0	NULL	skin	OrganismPart	dimpling of	occur due to					Cooper ligament	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	skin dimpling can occur due to tethering of Cooper ligaments from the mass underneath	topic_bc
78040	1	355417	6	NULL	NULL	0	NULL	CHEK2	GP		is					 CHK2 checkpoint homolog	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	CHEK2 is the official symbol for the human gene CHK2 checkpoint homolog.	topic_bc
78042	1	355420	6	NULL	NULL	NULL	NULL	parabens	Chemical		have					estrogen	Chemical	properties of;; weak			NULL	breast cancer tumor	NULL	NULL	NULL	NULL	NULL	NULL	One small study has found trace levels of parabens (used as preservatives in antiperspirants and other products), which have weak estrogen-like properties, in a small sample of breast cancer tumors	topic_bc
78043	1	355421	6	NULL	NULL	0	NULL	Breast cancer	MedicalFinding		have					melatonin	Chemical	low levels of			NULL		0	NULL	NULL	NULL	NULL	NULL	 Many women with breast cancer have lower levels of melatonin than those without	topic_bc
75918	1	355423	7	NULL	NULL	0	NULL	Dopamine	Chemical		is a type of					catecholamine neurotransmitter	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Dopamine is a catecholamine neurotransmitter present in a wide variety of animals	topic_bd
75919	2	355423	7	NULL	NULL	0	NULL	statement 1	Process		occur in					animals	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Dopamine is a catecholamine neurotransmitter present in a wide variety of animals	topic_bd
78044	1	355424	6	NULL	NULL	0	NULL	Rb gene	GP		is located on					chromosome 13q14	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	The Rb gene is located on chromosome 13q14, and loss of this region has been implicated in breast cancer progression.  Structural abnormalities including chromo-somal loss and mutation of the Rb gene have been reported in approximately 20-30% of breast cancers	topic_bc
78045	2	355424	6	NULL	NULL	0	NULL	Rb gene	GP	loss of	leads to					Breast cancer	MedicalFinding	progression of			NULL		0	NULL	NULL	NULL	NULL	NULL	The Rb gene is located on chromosome 13q14, and loss of this region has been implicated in breast cancer progression.  Structural abnormalities including chromo-somal loss and mutation of the Rb gene have been reported in approximately 20-30% of breast cancers	topic_bc
78046	3	355424	6	NULL	NULL	0	NULL	Rb gene	GP	mutation of	leads to					Breast cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The Rb gene is located on chromosome 13q14, and loss of this region has been implicated in breast cancer progression.  Structural abnormalities including chromo-somal loss and mutation of the Rb gene have been reported in approximately 20-30% of breast cancers	topic_bc
78047	1	355426	6	NULL	NULL	0	NULL	BRCA3	GP		is linked to					Breast cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	There is evidence for an additional breast cancer suscep- tibility gene (BRCA3) in families at high risk for breast cancer which do not have linkage to either BRCA1 or BRCA2.	topic_bc
78048	2	355426	6	NULL	NULL	0	NULL	BRCA3			is					breast cancer susceptibility gene					NULL		0	NULL	NULL	NULL	NULL	NULL	There is evidence for an additional breast cancer suscep- tibility gene (BRCA3) in families at high risk for breast cancer which do not have linkage to either BRCA1 or BRCA2.	topic_bc
78049	1	355427	6	NULL	NULL	0	NULL	ATM	GP		is located on					chromosome 11q23	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	ATM is located on 11q23 	topic_bc
78050	1	355428	6	NULL	NULL	0	NULL	PTEN	GP		is mapped to					chromosome 10q23	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	PTEN is a protein phosphatase with homology to tensin, which has been mapped to 10q23	topic_bc
78051	2	355428	6	NULL	NULL	0	NULL	PTEN	GP		is homologous to					tensin	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	PTEN is a protein phosphatase with homology to tensin, which has been mapped to 10q23	topic_bc
78052	3	355428	6	NULL	NULL	0	NULL	PTEN	GP		is a type of					protein phosphatase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	PTEN is a protein phosphatase with homology to tensin, which has been mapped to 10q23	topic_bc
75920	1	355429	7	NULL	NULL	0	NULL	Estrogen	Chemical		is a type of					female hormone	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Estrogen and progesterone are female hormones that regulate the menstrual cycle and likely serve an important role in the regulation of mood.	topic_bd
75921	2	355429	7	NULL	NULL	0	NULL	Estrogen	Chemical		regulate					menstrual cycle	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Estrogen and progesterone are female hormones that regulate the menstrual cycle and likely serve an important role in the regulation of mood.	topic_bd
75922	3	355429	7	NULL	NULL	0	NULL	Estrogen	Chemical		important role in					mood	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Estrogen and progesterone are female hormones that regulate the menstrual cycle and likely serve an important role in the regulation of mood.	topic_bd
75923	4	355429	7	NULL	NULL	0	NULL	progesterone	Chemical		is a type of					female hormone	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Estrogen and progesterone are female hormones that regulate the menstrual cycle and likely serve an important role in the regulation of mood.	topic_bd
75924	5	355429	7	NULL	NULL	0	NULL	progesterone	Chemical		regulate					menstrual cycle	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Estrogen and progesterone are female hormones that regulate the menstrual cycle and likely serve an important role in the regulation of mood.	topic_bd
75925	6	355429	7	NULL	NULL	0	NULL	progesterone	Chemical		important role in					mood	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Estrogen and progesterone are female hormones that regulate the menstrual cycle and likely serve an important role in the regulation of mood.	topic_bd
75926	1	355430	7	NULL	NULL	0	NULL	menstrual cycle	Process	hormonal shifts of	influence					bipolar symptoms	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	the hormonal shifts of the menstrual cycle likely influence bipolar symptoms, but confirmatory research is lacking. NULL	topic_bd
74642	1	355433	5	NULL	NULL	0	NULL	Philadelphia Chromosome	Chromosome		is					Ph chromosome	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	CML patients have what is called the "Philadelphia Chromosome" (Ph chromosome).	topic_ll
74643	2	355433	5	NULL	NULL	0	NULL	Ph chromosome	Chromosome		is present in					CML patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	CML patients have what is called the "Philadelphia Chromosome" (Ph chromosome).	topic_ll
74644	1	355434	5	NULL	NULL	0	NULL	Bcr-Abl cancer gene	GP		cause					CML	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The Bcr and Abl genes combine to make the CML-causing gene called the Bcr-Abl cancer gene. 	topic_ll
74647	1	355435	5	NULL	NULL	0	NULL	SLL	MedicalFinding		is					Small lymphocytic lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Small lymphocytic lymphoma (SLL) A disease with identical physical changes in lymph nodes as CLL. 	topic_ll
74649	2	355435	5	NULL	NULL	0	NULL	lymph nodes	OrganismPart		undergo					physical changes	PhysicalPhenomenon	identical			NULL		0	NULL	NULL	NULL	NULL	NULL	Small lymphocytic lymphoma (SLL) A disease with identical physical changes in lymph nodes as CLL. 	topic_ll
74650	3	355435	5	NULL	NULL	NULL	NULL	statement 2	Process		is a symptom of					SLL	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Small lymphocytic lymphoma (SLL) A disease with identical physical changes in lymph nodes as CLL. 	topic_ll
74651	4	355435	5	NULL	NULL	0	NULL	SLL	MedicalFinding		is similar to					CLL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Small lymphocytic lymphoma (SLL) A disease with identical physical changes in lymph nodes as CLL. 	topic_ll
74652	1	355436	5	NULL	NULL	0	NULL	sprycel	Chemical		is the brand name of					dasatinib	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Sprycel The brand name for dasatinib	topic_ll
74653	1	355437	5	NULL	NULL	0	NULL	Tasigna	Chemical		is the brand name of					nilotinib	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Tasigna The brand name for nilotinib	topic_ll
74654	1	355439	5	NULL	NULL	0	NULL	benzene	Chemical	long-term exposure	cause		may			AML	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The Environmental Protection Agency (EPA) has determined that long-term exposure to benzene may cause acute myelogenous leukemia (AML).	topic_ll
74655	2	355439	5	NULL	NULL	0	NULL	AML	MedicalFinding		is					acute myelogenous leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The Environmental Protection Agency (EPA) has determined that long-term exposure to benzene may cause acute myelogenous leukemia (AML).	topic_ll
74656	3	355439	5	NULL	NULL	0	NULL	EPA	GroupOfPeople		is					Environmental Protection Agency	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	The Environmental Protection Agency (EPA) has determined that long-term exposure to benzene may cause acute myelogenous leukemia (AML).	topic_ll
74657	4	355439	5	NULL	NULL	0	NULL	EPA	GroupOfPeople		determine					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The Environmental Protection Agency (EPA) has determined that long-term exposure to benzene may cause acute myelogenous leukemia (AML).	topic_ll
74658	1	355441	5	NULL	NULL	0	NULL	HTLV	Organism		is					human T-cell lymphocytotropic virus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	People infected with human T-cell lymphocytotropic virus (HTLV) or human immunodeficiency virus (HIV) also have an increased probability of developing Hodgkin lymphoma.	topic_ll
74659	2	355441	5	NULL	NULL	0	NULL	HIV	Organism		is					human immunodeficiency virus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	People infected with human T-cell lymphocytotropic virus (HTLV) or human immunodeficiency virus (HIV) also have an increased probability of developing Hodgkin lymphoma.	topic_ll
74660	3	355441	5	NULL	NULL	NULL	NULL	HIV patients	GroupOfPeople		develops		most likely			Hodgkin lymphoma	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	People infected with human T-cell lymphocytotropic virus (HTLV) or human immunodeficiency virus (HIV) also have an increased probability of developing Hodgkin lymphoma.	topic_ll
74661	4	355441	5	NULL	NULL	0	NULL	HTLV patients	GroupOfPeople		develops		most likely			Hodgkin lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	People infected with human T-cell lymphocytotropic virus (HTLV) or human immunodeficiency virus (HIV) also have an increased probability of developing Hodgkin lymphoma.	topic_ll
74662	1	355443	5	NULL	NULL	0	NULL	immune suppression	Process		plays a role in		may			NHL	MedicalFinding	development of			NULL		0	NULL	NULL	NULL	NULL	NULL	The reasons for the development of NHL are not known. Immune suppression plays a role in certain cases.	topic_ll
74663	1	355445	5	NULL	NULL	0	NULL	farming communities	GroupOfPeople		have high incidence of					NHL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	There is a higher incidence of NHL in farming communities. Studies suggest that specific ingredients in herbicides and pesticides such as organochlorine, organophosphate and phenoxyacid compounds are linked to lymphoma. 	topic_ll
74664	2	355445	5	NULL	NULL	0	NULL	organochlorine	Chemical		plays a role in					lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	There is a higher incidence of NHL in farming communities. Studies suggest that specific ingredients in herbicides and pesticides such as organochlorine, organophosphate and phenoxyacid compounds are linked to lymphoma. 	topic_ll
74665	3	355445	5	NULL	NULL	0	NULL	organophosphate	Chemical		is linked to					lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	There is a higher incidence of NHL in farming communities. Studies suggest that specific ingredients in herbicides and pesticides such as organochlorine, organophosphate and phenoxyacid compounds are linked to lymphoma. 	topic_ll
74666	4	355445	5	NULL	NULL	0	NULL	phenoxyacid compounds	Chemical		is linked to					lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	There is a higher incidence of NHL in farming communities. Studies suggest that specific ingredients in herbicides and pesticides such as organochlorine, organophosphate and phenoxyacid compounds are linked to lymphoma. 	topic_ll
74667	5	355445	5	NULL	NULL	0	NULL	organochlorine	Chemical		is an ingredient of					herbicides	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	There is a higher incidence of NHL in farming communities. Studies suggest that specific ingredients in herbicides and pesticides such as organochlorine, organophosphate and phenoxyacid compounds are linked to lymphoma. 	topic_ll
74668	6	355445	5	NULL	NULL	0	NULL	organochlorine	Chemical		is an ingredient of					pesticides	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	There is a higher incidence of NHL in farming communities. Studies suggest that specific ingredients in herbicides and pesticides such as organochlorine, organophosphate and phenoxyacid compounds are linked to lymphoma. 	topic_ll
74669	7	355445	5	NULL	NULL	0	NULL	organophosphate	Chemical		is an ingredient of					herbicides	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	There is a higher incidence of NHL in farming communities. Studies suggest that specific ingredients in herbicides and pesticides such as organochlorine, organophosphate and phenoxyacid compounds are linked to lymphoma. 	topic_ll
74670	8	355445	5	NULL	NULL	0	NULL	organophosphate	Chemical		is an ingredient of					pesticides	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	There is a higher incidence of NHL in farming communities. Studies suggest that specific ingredients in herbicides and pesticides such as organochlorine, organophosphate and phenoxyacid compounds are linked to lymphoma. 	topic_ll
74671	9	355445	5	NULL	NULL	0	NULL	phenoxyacid compounds	Chemical		is an ingredient of					herbicides	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	There is a higher incidence of NHL in farming communities. Studies suggest that specific ingredients in herbicides and pesticides such as organochlorine, organophosphate and phenoxyacid compounds are linked to lymphoma. 	topic_ll
74672	10	355445	5	NULL	NULL	0	NULL	phenoxyacid compounds	Chemical		is an ingredient of					pesticides	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	There is a higher incidence of NHL in farming communities. Studies suggest that specific ingredients in herbicides and pesticides such as organochlorine, organophosphate and phenoxyacid compounds are linked to lymphoma. 	topic_ll
74673	1	355449	5	NULL	NULL	0	NULL	EBV	Organism		is					Epstein-Barr virus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Epstein-Barr virus (EBV) infection—in patients from specific geographical regions—is strongly associated with African Burkitt lymphoma.	topic_ll
74674	2	355449	5	NULL	NULL	NULL	NULL	EBV	Organism		infects					specific geographical region	GeographicNotProper	patients of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Epstein-Barr virus (EBV) infection—in patients from specific geographical regions—is strongly associated with African Burkitt lymphoma.	topic_ll
74675	3	355449	5	NULL	NULL	0	NULL	statement 2	Process		is associated with		strongly			African Burkitt lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Epstein-Barr virus (EBV) infection—in patients from specific geographical regions—is strongly associated with African Burkitt lymphoma.	topic_ll
74676	1	355450	5	NULL	NULL	0	NULL	immune systems	OrganismPart		suppressed in					NHL patients	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Epstein-Barr virus infection may play a role in the increased risk of NHL in persons whose immune systems are suppressed as a result of organ transplantation and its associated therapy.	topic_ll
74677	2	355450	5	NULL	NULL	0	NULL	statement 1	Process		is a result of					organ transplantation	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Epstein-Barr virus infection may play a role in the increased risk of NHL in persons whose immune systems are suppressed as a result of organ transplantation and its associated therapy.	topic_ll
74678	3	355450	5	NULL	NULL	0	NULL	Epstein-Barr virus	Organism	infection of	plays a role in					statement 1	Process	increased risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Epstein-Barr virus infection may play a role in the increased risk of NHL in persons whose immune systems are suppressed as a result of organ transplantation and its associated therapy.	topic_ll
74679	1	355451	5	NULL	NULL	0	NULL	Nodular Sclerosis	MedicalFinding		is a subtype of		most common			Hodgkin lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Nodular Sclerosis is the most common subtype of Hodgkin lymphoma	topic_ll
74680	1	355452	5	NULL	NULL	NULL	NULL	Mixed Cellularity	MedicalFinding		is present in					Hodgkin lymphoma	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Mixed Cellularity accounts for about 15 percent to 30 percent of all cases of Hodgkin lymphoma and is found more com­monly in men than women.	topic_ll
74681	2	355452	5	NULL	NULL	0	NULL	statement 1	MedicalFinding		is present in					men	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Mixed Cellularity accounts for about 15 percent to 30 percent of all cases of Hodgkin lymphoma and is found more com­monly in men than women.	topic_ll
74682	3	355452	5	NULL	NULL	0	NULL	statement 1	MedicalFinding		is present in					women	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Mixed Cellularity accounts for about 15 percent to 30 percent of all cases of Hodgkin lymphoma and is found more com­monly in men than women.	topic_ll
74683	4	355452	5	NULL	NULL	0	NULL	statement 2	Process		more common than					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Mixed Cellularity accounts for about 15 percent to 30 percent of all cases of Hodgkin lymphoma and is found more com­monly in men than women.	topic_ll
74684	1	355453	5	NULL	NULL	0	NULL	lymphocyte 	Cell	depletion of	is present in					Hodgkin cases	GroupOfPeople	few			NULL		0	NULL	NULL	NULL	NULL	NULL	Lymphocyte Depletion accounts for fewer than 5 percent of all Hodgkin cases.	topic_ll
74685	1	355456	5	NULL	NULL	0	NULL	diffuse lymphocyte predominant	MedicalFinding		is rare than					nodular lymphocyte predominant Hodgkin lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Diffuse Lymphocyte Predominant is extremely rare. The existence of this subtype has been questioned. Most cases are in fact nodular lymphocyte predominant Hodgkin lymphoma with an ill-defined nodular pattern.	topic_ll
74686	1	355457	5	NULL	NULL	0	NULL	monoclonal antibodies	GP		is used to treat		possibly			Hodgkin lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Many promising therapies are currently under investigation in clinical trials for Hodgkin lymphoma. Types of therapy under investigation include: •      Monoclonal antibodies (e.g., SGN-35, which targets the CD30 antigen found on the surface of some Hodgkin lymphoma cells) •      Histone deacetylase inhibitors (e.g., panobinostat or vorinostat, also known as Zolinza) •      Proteasome inhibitors (e.g., bortezomib, also known as Velcade) •      Alkylating agents (e.g., bendamustine, also known as Treanda)	topic_ll
74687	2	355457	5	NULL	NULL	0	NULL	SGN-35	GP		is a type of					monoclonal antibody	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Many promising therapies are currently under investigation in clinical trials for Hodgkin lymphoma. Types of therapy under investigation include: •      Monoclonal antibodies (e.g., SGN-35, which targets the CD30 antigen found on the surface of some Hodgkin lymphoma cells) •      Histone deacetylase inhibitors (e.g., panobinostat or vorinostat, also known as Zolinza) •      Proteasome inhibitors (e.g., bortezomib, also known as Velcade) •      Alkylating agents (e.g., bendamustine, also known as Treanda)	topic_ll
74688	3	355457	5	NULL	NULL	0	NULL	SGN-35	GP		targets					CD30 antigen	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Many promising therapies are currently under investigation in clinical trials for Hodgkin lymphoma. Types of therapy under investigation include: •      Monoclonal antibodies (e.g., SGN-35, which targets the CD30 antigen found on the surface of some Hodgkin lymphoma cells) •      Histone deacetylase inhibitors (e.g., panobinostat or vorinostat, also known as Zolinza) •      Proteasome inhibitors (e.g., bortezomib, also known as Velcade) •      Alkylating agents (e.g., bendamustine, also known as Treanda)	topic_ll
74689	4	355457	5	NULL	NULL	0	NULL	CD30 antigen	GP		is present in					Hodgkin lymphoma cells	Cell	surface of			NULL		0	NULL	NULL	NULL	NULL	NULL	Many promising therapies are currently under investigation in clinical trials for Hodgkin lymphoma. Types of therapy under investigation include: •      Monoclonal antibodies (e.g., SGN-35, which targets the CD30 antigen found on the surface of some Hodgkin lymphoma cells) •      Histone deacetylase inhibitors (e.g., panobinostat or vorinostat, also known as Zolinza) •      Proteasome inhibitors (e.g., bortezomib, also known as Velcade) •      Alkylating agents (e.g., bendamustine, also known as Treanda)	topic_ll
74690	5	355457	5	NULL	NULL	0	NULL	histone deacetylase inhibitors	Chemical		is used to treat		possibly			Hodgkin lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Many promising therapies are currently under investigation in clinical trials for Hodgkin lymphoma. Types of therapy under investigation include: •      Monoclonal antibodies (e.g., SGN-35, which targets the CD30 antigen found on the surface of some Hodgkin lymphoma cells) •      Histone deacetylase inhibitors (e.g., panobinostat or vorinostat, also known as Zolinza) •      Proteasome inhibitors (e.g., bortezomib, also known as Velcade) •      Alkylating agents (e.g., bendamustine, also known as Treanda)	topic_ll
74691	6	355457	5	NULL	NULL	0	NULL	panobinostat	Chemical		is a type of					histone deacetylase inhibitor	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Many promising therapies are currently under investigation in clinical trials for Hodgkin lymphoma. Types of therapy under investigation include: •      Monoclonal antibodies (e.g., SGN-35, which targets the CD30 antigen found on the surface of some Hodgkin lymphoma cells) •      Histone deacetylase inhibitors (e.g., panobinostat or vorinostat, also known as Zolinza) •      Proteasome inhibitors (e.g., bortezomib, also known as Velcade) •      Alkylating agents (e.g., bendamustine, also known as Treanda)	topic_ll
74692	7	355457	5	NULL	NULL	0	NULL	vorinostat	Chemical		is a type of					histone deacetylase inhibitor	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Many promising therapies are currently under investigation in clinical trials for Hodgkin lymphoma. Types of therapy under investigation include: •      Monoclonal antibodies (e.g., SGN-35, which targets the CD30 antigen found on the surface of some Hodgkin lymphoma cells) •      Histone deacetylase inhibitors (e.g., panobinostat or vorinostat, also known as Zolinza) •      Proteasome inhibitors (e.g., bortezomib, also known as Velcade) •      Alkylating agents (e.g., bendamustine, also known as Treanda)	topic_ll
74693	8	355457	5	NULL	NULL	0	NULL	vorinostat	Chemical		is known as					Zolinza	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Many promising therapies are currently under investigation in clinical trials for Hodgkin lymphoma. Types of therapy under investigation include: •      Monoclonal antibodies (e.g., SGN-35, which targets the CD30 antigen found on the surface of some Hodgkin lymphoma cells) •      Histone deacetylase inhibitors (e.g., panobinostat or vorinostat, also known as Zolinza) •      Proteasome inhibitors (e.g., bortezomib, also known as Velcade) •      Alkylating agents (e.g., bendamustine, also known as Treanda)	topic_ll
74694	9	355457	5	NULL	NULL	0	NULL	proteasome inhibitors	Chemical		is used to treat		possibly			Hodgkin lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Many promising therapies are currently under investigation in clinical trials for Hodgkin lymphoma. Types of therapy under investigation include: •      Monoclonal antibodies (e.g., SGN-35, which targets the CD30 antigen found on the surface of some Hodgkin lymphoma cells) •      Histone deacetylase inhibitors (e.g., panobinostat or vorinostat, also known as Zolinza) •      Proteasome inhibitors (e.g., bortezomib, also known as Velcade) •      Alkylating agents (e.g., bendamustine, also known as Treanda)	topic_ll
74695	10	355457	5	NULL	NULL	0	NULL	bortezomib	Chemical		is a type of					proteasome inhibitors	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Many promising therapies are currently under investigation in clinical trials for Hodgkin lymphoma. Types of therapy under investigation include: •      Monoclonal antibodies (e.g., SGN-35, which targets the CD30 antigen found on the surface of some Hodgkin lymphoma cells) •      Histone deacetylase inhibitors (e.g., panobinostat or vorinostat, also known as Zolinza) •      Proteasome inhibitors (e.g., bortezomib, also known as Velcade) •      Alkylating agents (e.g., bendamustine, also known as Treanda)	topic_ll
74696	11	355457	5	NULL	NULL	0	NULL	bortezomib	Chemical		is known as					Velcade	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Many promising therapies are currently under investigation in clinical trials for Hodgkin lymphoma. Types of therapy under investigation include: •      Monoclonal antibodies (e.g., SGN-35, which targets the CD30 antigen found on the surface of some Hodgkin lymphoma cells) •      Histone deacetylase inhibitors (e.g., panobinostat or vorinostat, also known as Zolinza) •      Proteasome inhibitors (e.g., bortezomib, also known as Velcade) •      Alkylating agents (e.g., bendamustine, also known as Treanda)	topic_ll
74697	12	355457	5	NULL	NULL	0	NULL	alkylating agents	Chemical		is used to treat		possibly			Hodgkin lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Many promising therapies are currently under investigation in clinical trials for Hodgkin lymphoma. Types of therapy under investigation include: •      Monoclonal antibodies (e.g., SGN-35, which targets the CD30 antigen found on the surface of some Hodgkin lymphoma cells) •      Histone deacetylase inhibitors (e.g., panobinostat or vorinostat, also known as Zolinza) •      Proteasome inhibitors (e.g., bortezomib, also known as Velcade) •      Alkylating agents (e.g., bendamustine, also known as Treanda)	topic_ll
74698	13	355457	5	NULL	NULL	0	NULL	bendamustine	Chemical		is a type of					alkylating agents	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Many promising therapies are currently under investigation in clinical trials for Hodgkin lymphoma. Types of therapy under investigation include: •      Monoclonal antibodies (e.g., SGN-35, which targets the CD30 antigen found on the surface of some Hodgkin lymphoma cells) •      Histone deacetylase inhibitors (e.g., panobinostat or vorinostat, also known as Zolinza) •      Proteasome inhibitors (e.g., bortezomib, also known as Velcade) •      Alkylating agents (e.g., bendamustine, also known as Treanda)	topic_ll
74699	14	355457	5	NULL	NULL	0	NULL	bendamustine	Chemical		is known as					Treanda	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Many promising therapies are currently under investigation in clinical trials for Hodgkin lymphoma. Types of therapy under investigation include: •      Monoclonal antibodies (e.g., SGN-35, which targets the CD30 antigen found on the surface of some Hodgkin lymphoma cells) •      Histone deacetylase inhibitors (e.g., panobinostat or vorinostat, also known as Zolinza) •      Proteasome inhibitors (e.g., bortezomib, also known as Velcade) •      Alkylating agents (e.g., bendamustine, also known as Treanda)	topic_ll
74700	1	355458	5	NULL	NULL	0	NULL	alkylating agents	Chemical		is used to treat		possibly			Hodgkin lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Many promising therapies are currently under investigation in clinical trials for Hodgkin lymphoma. Types of therapy under investigation include: •      Alkylating agents (e.g., bendamustine, also known as Treanda)	topic_ll
74701	2	355458	5	NULL	NULL	0	NULL	bendamustine	Chemical		is a type of					alkylating agents	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Many promising therapies are currently under investigation in clinical trials for Hodgkin lymphoma. Types of therapy under investigation include: •      Alkylating agents (e.g., bendamustine, also known as Treanda)	topic_ll
74702	3	355458	5	NULL	NULL	0	NULL	bendamustine	Chemical		is known as					Treanda	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Many promising therapies are currently under investigation in clinical trials for Hodgkin lymphoma. Types of therapy under investigation include: •      Alkylating agents (e.g., bendamustine, also known as Treanda)	topic_ll
74703	1	355459	5	NULL	NULL	0	NULL	HIV/AIDS	MedicalFinding		compromise on					immune system	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Having a compromised immune system, such as from HIV/AIDS or from having an organ transplant requiring medications to suppress your immune response, also appears to put you at a greater risk of Hodgkin's lymphoma	topic_ll
74704	2	355459	5	NULL	NULL	0	NULL	medications	Chemical		suppress					immune system	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Having a compromised immune system, such as from HIV/AIDS or from having an organ transplant requiring medications to suppress your immune response, also appears to put you at a greater risk of Hodgkin's lymphoma	topic_ll
74705	3	355459	5	NULL	NULL	0	NULL	organ transplant	MedicalProcedure		requires					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Having a compromised immune system, such as from HIV/AIDS or from having an organ transplant requiring medications to suppress your immune response, also appears to put you at a greater risk of Hodgkin's lymphoma	topic_ll
74706	4	355459	5	NULL	NULL	NULL	NULL	statement 1	Process		is at risk of		greater			Hodgkin lymphoma	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Having a compromised immune system, such as from HIV/AIDS or from having an organ transplant requiring medications to suppress your immune response, also appears to put you at a greater risk of Hodgkin's lymphoma	topic_ll
74707	5	355459	5	NULL	NULL	NULL	NULL	statement 3	Process		is at risk of		greater			Hodgkin lymphoma	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Having a compromised immune system, such as from HIV/AIDS or from having an organ transplant requiring medications to suppress your immune response, also appears to put you at a greater risk of Hodgkin's lymphoma	topic_ll
74708	1	355460	5	NULL	NULL	0	NULL	follicular lymphoma	MedicalFinding		is slow-growing		most common			NHL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Slow-Growing or Indolent NHL * Follicular lymphoma - the most common slow-growing NHL * Chronic lymphocytic leukemia * Cutaneous T-cell lymphoma * Lymphoplasmacytic lymphoma * Marginal zone lymphoma * Mucosa-associated lymphoid tissue (MALT) lymphoma * Small cell lymphocytic lymphoma * Waldenström macroglobulinemia	topic_ll
74709	1	355461	5	NULL	NULL	NULL	NULL	Rituxan®	Chemical		is also known as					rituximab	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Rituxan® (rituximab) and certain other drugs are used to treat some types of NHL	topic_ll
74710	2	355461	5	NULL	NULL	0	NULL	Rituxan®	Chemical		is used to treat					NHL	MedicalFinding	some types of			NULL		0	NULL	NULL	NULL	NULL	NULL	Rituxan® (rituximab) and certain other drugs are used to treat some types of NHL	topic_ll
74711	1	355464	5	NULL	NULL	0	NULL	Aranesp®	Chemical		increases					red cell	Cell	count of			NULL		0	NULL	NULL	NULL	NULL	NULL	Aranesp® (darbepoetin alfa) and Procrit® (epoetin alfa) - these can increase the red cell count 	topic_ll
74712	2	355464	5	NULL	NULL	0	NULL	Procrit®	Chemical		increases					red cell	Cell	count of			NULL		0	NULL	NULL	NULL	NULL	NULL	Aranesp® (darbepoetin alfa) and Procrit® (epoetin alfa) - these can increase the red cell count 	topic_ll
74713	3	355464	5	NULL	NULL	0	NULL	Procrit®	Chemical		is also known as					epoetin alfa	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Aranesp® (darbepoetin alfa) and Procrit® (epoetin alfa) - these can increase the red cell count 	topic_ll
74714	4	355464	5	NULL	NULL	0	NULL	Aranesp®	Chemical		is also known as					darbepoetin alfa	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Aranesp® (darbepoetin alfa) and Procrit® (epoetin alfa) - these can increase the red cell count 	topic_ll
74715	1	355465	5	NULL	NULL	0	NULL	Neupogen®	Chemical		is a synonym of					Neulasta®	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Neupogen® or Neulasta®(also called G-CSF ) and Leukine®(also called GM-CSF) - these can increase the number of neutrophils (white cells).	topic_ll
74716	2	355465	5	NULL	NULL	0	NULL	Neulasta®	Chemical		is also known as					G-CSF	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Neupogen® or Neulasta®(also called G-CSF ) and Leukine®(also called GM-CSF) - these can increase the number of neutrophils (white cells).	topic_ll
74717	3	355465	5	NULL	NULL	0	NULL	Leukine®	Chemical		is also known as					GM-CSF	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Neupogen® or Neulasta®(also called G-CSF ) and Leukine®(also called GM-CSF) - these can increase the number of neutrophils (white cells).	topic_ll
74718	4	355465	5	NULL	NULL	0	NULL	Leukine®	Chemical		increases					neutrophils	Cell	number of			NULL		0	NULL	NULL	NULL	NULL	NULL	Neupogen® or Neulasta®(also called G-CSF ) and Leukine®(also called GM-CSF) - these can increase the number of neutrophils (white cells).	topic_ll
74719	5	355465	5	NULL	NULL	0	NULL	Neulasta®	Chemical		increases					neutrophils	Cell	number of			NULL		0	NULL	NULL	NULL	NULL	NULL	Neupogen® or Neulasta®(also called G-CSF ) and Leukine®(also called GM-CSF) - these can increase the number of neutrophils (white cells).	topic_ll
74720	6	355465	5	NULL	NULL	0	NULL	neutrophils	Cell		is a type of					white cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Neupogen® or Neulasta®(also called G-CSF ) and Leukine®(also called GM-CSF) - these can increase the number of neutrophils (white cells).	topic_ll
74778	1	355466	5	NULL	NULL	0	NULL	Neupogen®	Chemical		is a synonym of					Neulasta®	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	A red cell transfusion or drugs called blood cell growth factors may be needed until the side effects of chemotherapy wear off. Neupogen® or Neulasta®(also called G-CSF ) and Leukine®(also called GM-CSF) - these can increase the number of neutrophils (white cells).	topic_ll
74779	2	355466	5	NULL	NULL	0	NULL	Neulasta®	Chemical		is also known as					G-CSF	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	A red cell transfusion or drugs called blood cell growth factors may be needed until the side effects of chemotherapy wear off. Neupogen® or Neulasta®(also called G-CSF ) and Leukine®(also called GM-CSF) - these can increase the number of neutrophils (white cells).	topic_ll
74780	3	355466	5	NULL	NULL	0	NULL	Leukine®	Chemical		is also known as					GM-CSF	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	A red cell transfusion or drugs called blood cell growth factors may be needed until the side effects of chemotherapy wear off. Neupogen® or Neulasta®(also called G-CSF ) and Leukine®(also called GM-CSF) - these can increase the number of neutrophils (white cells).	topic_ll
74781	4	355466	5	NULL	NULL	NULL	NULL	Neulasta®	Chemical		increases					neutrophils	Cell	number of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	A red cell transfusion or drugs called blood cell growth factors may be needed until the side effects of chemotherapy wear off. Neupogen® or Neulasta®(also called G-CSF ) and Leukine®(also called GM-CSF) - these can increase the number of neutrophils (white cells).	topic_ll
74782	5	355466	5	NULL	NULL	NULL	NULL	Leukine®	Chemical		increases					neutrophils	Cell	number of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	A red cell transfusion or drugs called blood cell growth factors may be needed until the side effects of chemotherapy wear off. Neupogen® or Neulasta®(also called G-CSF ) and Leukine®(also called GM-CSF) - these can increase the number of neutrophils (white cells).	topic_ll
74783	6	355466	5	NULL	NULL	0	NULL	neutrophils	Cell		is a type of					white cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	A red cell transfusion or drugs called blood cell growth factors may be needed until the side effects of chemotherapy wear off. Neupogen® or Neulasta®(also called G-CSF ) and Leukine®(also called GM-CSF) - these can increase the number of neutrophils (white cells).	topic_ll
74784	1	355467	5	NULL	NULL	0	NULL	Aranesp®	Chemical		is also known as					Darbepoetin alfa	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	A red cell transfusion or drugs called blood cell growth factors may be needed until the side effects of chemotherapy wear off. Aranesp® (Darbepoetin alfa) and Procrit® (epoetin alfa) - these can increase the red cell count 	topic_ll
74785	2	355467	5	NULL	NULL	0	NULL	Procrit®	Chemical		is also known as					epoetin alfa	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	A red cell transfusion or drugs called blood cell growth factors may be needed until the side effects of chemotherapy wear off. Aranesp® (Darbepoetin alfa) and Procrit® (epoetin alfa) - these can increase the red cell count 	topic_ll
74786	3	355467	5	NULL	NULL	0	NULL	Procrit®	Chemical		induce					red cell	Cell	count of			NULL		0	NULL	NULL	NULL	NULL	NULL	A red cell transfusion or drugs called blood cell growth factors may be needed until the side effects of chemotherapy wear off. Aranesp® (Darbepoetin alfa) and Procrit® (epoetin alfa) - these can increase the red cell count 	topic_ll
74787	4	355467	5	NULL	NULL	0	NULL	Aranesp®	Chemical		increases					red cell	Cell	count of			NULL		0	NULL	NULL	NULL	NULL	NULL	A red cell transfusion or drugs called blood cell growth factors may be needed until the side effects of chemotherapy wear off. Aranesp® (Darbepoetin alfa) and Procrit® (epoetin alfa) - these can increase the red cell count 	topic_ll
75927	1	355468	7	NULL	NULL	0	NULL	pregnant women	GroupOfPeople		likely to have					depression	MedicalFinding	diagnosis of			NULL		0	NULL	NULL	NULL	NULL	NULL	this cohort study of more than 43,000 women from the Veterans Health Administration system found that those who were pregnant were twice as likely to have a diagnosis of depression, anxiety, posttraumatic stress disorder (PTSD), bipolar disorder, or schizophrenia as their counterparts who were not pregnant.	topic_bd
75928	2	355468	7	NULL	NULL	0	NULL	pregnant women	GroupOfPeople		likely to have					anxiety	MedicalFinding	diagnosis of			NULL		0	NULL	NULL	NULL	NULL	NULL	this cohort study of more than 43,000 women from the Veterans Health Administration system found that those who were pregnant were twice as likely to have a diagnosis of depression, anxiety, posttraumatic stress disorder (PTSD), bipolar disorder, or schizophrenia as their counterparts who were not pregnant.	topic_bd
75929	3	355468	7	NULL	NULL	0	NULL	pregnant women	GroupOfPeople		likely to have					PTSD	MedicalFinding	diagnosis of			NULL		0	NULL	NULL	NULL	NULL	NULL	this cohort study of more than 43,000 women from the Veterans Health Administration system found that those who were pregnant were twice as likely to have a diagnosis of depression, anxiety, posttraumatic stress disorder (PTSD), bipolar disorder, or schizophrenia as their counterparts who were not pregnant.	topic_bd
75930	4	355468	7	NULL	NULL	0	NULL	pregnant women	GroupOfPeople		likely to have					bipolar disorder	MedicalFinding	diagnosis of			NULL		0	NULL	NULL	NULL	NULL	NULL	this cohort study of more than 43,000 women from the Veterans Health Administration system found that those who were pregnant were twice as likely to have a diagnosis of depression, anxiety, posttraumatic stress disorder (PTSD), bipolar disorder, or schizophrenia as their counterparts who were not pregnant.	topic_bd
75931	5	355468	7	NULL	NULL	0	NULL	pregnant women	GroupOfPeople		likely to have					schizophrenia	MedicalFinding	diagnosis of			NULL		0	NULL	NULL	NULL	NULL	NULL	this cohort study of more than 43,000 women from the Veterans Health Administration system found that those who were pregnant were twice as likely to have a diagnosis of depression, anxiety, posttraumatic stress disorder (PTSD), bipolar disorder, or schizophrenia as their counterparts who were not pregnant.	topic_bd
75932	6	355468	7	NULL	NULL	0	NULL	PTSD	MedicalFinding		is					posttraumatic stress disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	this cohort study of more than 43,000 women from the Veterans Health Administration system found that those who were pregnant were twice as likely to have a diagnosis of depression, anxiety, posttraumatic stress disorder (PTSD), bipolar disorder, or schizophrenia as their counterparts who were not pregnant.	topic_bd
75933	7	355468	7	NULL	NULL	0	NULL	nonpregnant women	GroupOfPeople		likely to have					depression	MedicalFinding	diagnosis of			NULL		0	NULL	NULL	NULL	NULL	NULL	this cohort study of more than 43,000 women from the Veterans Health Administration system found that those who were pregnant were twice as likely to have a diagnosis of depression, anxiety, posttraumatic stress disorder (PTSD), bipolar disorder, or schizophrenia as their counterparts who were not pregnant.	topic_bd
75934	8	355468	7	NULL	NULL	0	NULL	nonpregnant women	GroupOfPeople		likely to have					anxiety	MedicalFinding	diagnosis of			NULL		0	NULL	NULL	NULL	NULL	NULL	this cohort study of more than 43,000 women from the Veterans Health Administration system found that those who were pregnant were twice as likely to have a diagnosis of depression, anxiety, posttraumatic stress disorder (PTSD), bipolar disorder, or schizophrenia as their counterparts who were not pregnant.	topic_bd
75935	9	355468	7	NULL	NULL	0	NULL	nonpregnant women	GroupOfPeople		likely to have					PTSD	MedicalFinding	diagnosis of			NULL		0	NULL	NULL	NULL	NULL	NULL	this cohort study of more than 43,000 women from the Veterans Health Administration system found that those who were pregnant were twice as likely to have a diagnosis of depression, anxiety, posttraumatic stress disorder (PTSD), bipolar disorder, or schizophrenia as their counterparts who were not pregnant.	topic_bd
75936	10	355468	7	NULL	NULL	0	NULL	nonpregnant women	GroupOfPeople		likely to have					bipolar disorder	MedicalFinding	diagnosis of			NULL		0	NULL	NULL	NULL	NULL	NULL	this cohort study of more than 43,000 women from the Veterans Health Administration system found that those who were pregnant were twice as likely to have a diagnosis of depression, anxiety, posttraumatic stress disorder (PTSD), bipolar disorder, or schizophrenia as their counterparts who were not pregnant.	topic_bd
75937	11	355468	7	NULL	NULL	0	NULL	nonpregnant women	GroupOfPeople		likely to have					schizophrenia	MedicalFinding	diagnosis of			NULL		0	NULL	NULL	NULL	NULL	NULL	this cohort study of more than 43,000 women from the Veterans Health Administration system found that those who were pregnant were twice as likely to have a diagnosis of depression, anxiety, posttraumatic stress disorder (PTSD), bipolar disorder, or schizophrenia as their counterparts who were not pregnant.	topic_bd
75938	12	355468	7	NULL	NULL	0	NULL	statement 1	Process	occurence in	is more than					statement 7	Process	occurence in			NULL		0	NULL	NULL	NULL	NULL	NULL	this cohort study of more than 43,000 women from the Veterans Health Administration system found that those who were pregnant were twice as likely to have a diagnosis of depression, anxiety, posttraumatic stress disorder (PTSD), bipolar disorder, or schizophrenia as their counterparts who were not pregnant.	topic_bd
75939	13	355468	7	NULL	NULL	0	NULL	statement 2	Process	occurence in	is more than					statement 8	Process	occurence in			NULL		0	NULL	NULL	NULL	NULL	NULL	this cohort study of more than 43,000 women from the Veterans Health Administration system found that those who were pregnant were twice as likely to have a diagnosis of depression, anxiety, posttraumatic stress disorder (PTSD), bipolar disorder, or schizophrenia as their counterparts who were not pregnant.	topic_bd
75940	14	355468	7	NULL	NULL	0	NULL	statement 3	Process	occurence in	is more than					statement 9	Process	occurence in			NULL		0	NULL	NULL	NULL	NULL	NULL	this cohort study of more than 43,000 women from the Veterans Health Administration system found that those who were pregnant were twice as likely to have a diagnosis of depression, anxiety, posttraumatic stress disorder (PTSD), bipolar disorder, or schizophrenia as their counterparts who were not pregnant.	topic_bd
75941	15	355468	7	NULL	NULL	0	NULL	statement 4	Process	occurence in	is more than					statement 10	Process	occurence in			NULL		0	NULL	NULL	NULL	NULL	NULL	this cohort study of more than 43,000 women from the Veterans Health Administration system found that those who were pregnant were twice as likely to have a diagnosis of depression, anxiety, posttraumatic stress disorder (PTSD), bipolar disorder, or schizophrenia as their counterparts who were not pregnant.	topic_bd
75942	16	355468	7	NULL	NULL	0	NULL	statement 5	Process	occurence in	is more than					statement 11	Process	occurence in			NULL		0	NULL	NULL	NULL	NULL	NULL	this cohort study of more than 43,000 women from the Veterans Health Administration system found that those who were pregnant were twice as likely to have a diagnosis of depression, anxiety, posttraumatic stress disorder (PTSD), bipolar disorder, or schizophrenia as their counterparts who were not pregnant.	topic_bd
75943	1	355472	7	NULL	NULL	0	NULL	scholastic achievement	MentalProcess		is in relation with					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	the relationship between scholastic achievement and bipolar disorder appeared to be stronger in boys than girls.	topic_bd
75944	2	355472	7	NULL	NULL	0	NULL	statement 1	Process		appear in					boys	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	the relationship between scholastic achievement and bipolar disorder appeared to be stronger in boys than girls.	topic_bd
75945	3	355472	7	NULL	NULL	0	NULL	statement 2	Process		appear in					girls	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	the relationship between scholastic achievement and bipolar disorder appeared to be stronger in boys than girls.	topic_bd
75946	4	355472	7	NULL	NULL	0	NULL	statement 2	Process		more stronger than					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	the relationship between scholastic achievement and bipolar disorder appeared to be stronger in boys than girls.	topic_bd
75947	1	355473	7	NULL	NULL	0	NULL	creative people	GroupOfPeople		more susceptible to					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The study gives credence to the idea that creative people are more susceptible to bipolar disorder.	topic_bd
75948	1	355474	7	NULL	NULL	0	NULL	higher academic marks 	QuantityOrMeasure		associated with					schizophrenia	MedicalFinding	decreased risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	higher academic marks are associated with decreased risk for schizophrenia, the study authors noted.	topic_bd
75949	1	355475	7	NULL	NULL	0	NULL	schizophrenia 	MedicalFinding		genetically linked to		closely			bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	That’s "very striking" in light of a recent theory that schizophrenia and bipolar disorder are more closely genetically linked than previously believed, commented Dr. MacCabe. 	topic_bd
75950	1	355476	7	NULL	NULL	0	NULL	autoimmune thyroiditis	MedicalFinding		related to					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In a study of twins, autoimmune thyroiditis was related to bipolar disorder and the genetic tendency to develop bipolar disorder.	topic_bd
75951	2	355476	7	NULL	NULL	0	NULL	statement 1	Process		occur in					twins	Person				NULL		0	NULL	NULL	NULL	NULL	NULL	In a study of twins, autoimmune thyroiditis was related to bipolar disorder and the genetic tendency to develop bipolar disorder.	topic_bd
75952	3	355476	7	NULL	NULL	0	NULL	twins	Person		genetic tendency					bipolar disorder	MedicalFinding	to develop			NULL		0	NULL	NULL	NULL	NULL	NULL	In a study of twins, autoimmune thyroiditis was related to bipolar disorder and the genetic tendency to develop bipolar disorder.	topic_bd
75969	1	355477	7	NULL	NULL	NULL	NULL	Thyroid dysfunction	MedicalFinding		occur in					rapid cycling bipolar disorder	MedicalFinding	patients with			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Thyroid dysfunction is more common in patients with rapid cycling bipolar disorder (ie, having 4 or more mood swings or episodes in a 12-month period) or mixed states (ie, an episode that simultaneously presents symptoms of both depression and mania) than in patients with classic mania	topic_bd
75970	2	355477	7	NULL	NULL	0	NULL	Thyroid dysfunction	MedicalFinding		occur in					mixed state	MedicalFinding	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	Thyroid dysfunction is more common in patients with rapid cycling bipolar disorder (ie, having 4 or more mood swings or episodes in a 12-month period) or mixed states (ie, an episode that simultaneously presents symptoms of both depression and mania) than in patients with classic mania	topic_bd
75971	3	355477	7	NULL	NULL	0	NULL	Thyroid dysfunction	MedicalFinding		occur in					classic mania	MedicalFinding	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	Thyroid dysfunction is more common in patients with rapid cycling bipolar disorder (ie, having 4 or more mood swings or episodes in a 12-month period) or mixed states (ie, an episode that simultaneously presents symptoms of both depression and mania) than in patients with classic mania	topic_bd
75972	1	355478	7	NULL	NULL	0	NULL	Levothyroxine 	GP		decrease		may			manic episodes	MedicalFinding	severity of			NULL		0	NULL	NULL	NULL	NULL	NULL	Levothyroxine may decrease the severity and frequency of manic and depressive episodes.	topic_bd
75973	2	355478	7	NULL	NULL	NULL	NULL	Levothyroxine	GP		decrease		may			depressive episodes	MedicalFinding	severity of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Levothyroxine may decrease the severity and frequency of manic and depressive episodes.	topic_bd
75974	3	355478	7	NULL	NULL	0	NULL	Levothyroxine	GP		decrease		may			manic episodes	MedicalFinding	frequency of			NULL		0	NULL	NULL	NULL	NULL	NULL	Levothyroxine may decrease the severity and frequency of manic and depressive episodes.	topic_bd
75975	4	355478	7	NULL	NULL	NULL	NULL	Levothyroxine	GP		decrease		may			depressive episodes	MedicalFinding	frequency of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Levothyroxine may decrease the severity and frequency of manic and depressive episodes.	topic_bd
75976	1	355479	7	NULL	NULL	0	NULL	Levothyroxine	GP		is a synthetic form of					thyroxine	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Levothyroxine, also L-thyroxine, synthetic T4, or 3,5,3',5'-tetraiodo-L-thyronine, is a synthetic form of thyroxine (thyroid hormone), used as a hormone replacement for patients with thyroid problems.	topic_bd
75977	2	355479	7	NULL	NULL	0	NULL	L-thyroxine	GP		is a synthetic form of					thyroxine	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Levothyroxine, also L-thyroxine, synthetic T4, or 3,5,3',5'-tetraiodo-L-thyronine, is a synthetic form of thyroxine (thyroid hormone), used as a hormone replacement for patients with thyroid problems.	topic_bd
75978	3	355479	7	NULL	NULL	NULL	NULL	synthetic T4	GP		is a synthetic form of					thyroxine	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Levothyroxine, also L-thyroxine, synthetic T4, or 3,5,3',5'-tetraiodo-L-thyronine, is a synthetic form of thyroxine (thyroid hormone), used as a hormone replacement for patients with thyroid problems.	topic_bd
75979	4	355479	7	NULL	NULL	0	NULL	3,5,3',5'-tetraiodo-L-thyronine	GP		is a synthetic form of					thyroxine	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Levothyroxine, also L-thyroxine, synthetic T4, or 3,5,3',5'-tetraiodo-L-thyronine, is a synthetic form of thyroxine (thyroid hormone), used as a hormone replacement for patients with thyroid problems.	topic_bd
75980	5	355479	7	NULL	NULL	0	NULL	statement 1	Process		used as					hormone	GP	replacement of			NULL		0	NULL	NULL	NULL	NULL	NULL	Levothyroxine, also L-thyroxine, synthetic T4, or 3,5,3',5'-tetraiodo-L-thyronine, is a synthetic form of thyroxine (thyroid hormone), used as a hormone replacement for patients with thyroid problems.	topic_bd
75981	6	355479	7	NULL	NULL	0	NULL	statement 2	Process		used as					hormone	GP	replacement of			NULL		0	NULL	NULL	NULL	NULL	NULL	Levothyroxine, also L-thyroxine, synthetic T4, or 3,5,3',5'-tetraiodo-L-thyronine, is a synthetic form of thyroxine (thyroid hormone), used as a hormone replacement for patients with thyroid problems.	topic_bd
75982	7	355479	7	NULL	NULL	0	NULL	statement 3	Process		used as					hormone	GP	replacement of			NULL		0	NULL	NULL	NULL	NULL	NULL	Levothyroxine, also L-thyroxine, synthetic T4, or 3,5,3',5'-tetraiodo-L-thyronine, is a synthetic form of thyroxine (thyroid hormone), used as a hormone replacement for patients with thyroid problems.	topic_bd
75983	8	355479	7	NULL	NULL	0	NULL	statement 4	Process		used as					hormone	GP	replacement of			NULL		0	NULL	NULL	NULL	NULL	NULL	Levothyroxine, also L-thyroxine, synthetic T4, or 3,5,3',5'-tetraiodo-L-thyronine, is a synthetic form of thyroxine (thyroid hormone), used as a hormone replacement for patients with thyroid problems.	topic_bd
75984	9	355479	7	NULL	NULL	0	NULL	thyroxine	GP		is					thyroid hormone	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Levothyroxine, also L-thyroxine, synthetic T4, or 3,5,3',5'-tetraiodo-L-thyronine, is a synthetic form of thyroxine (thyroid hormone), used as a hormone replacement for patients with thyroid problems.	topic_bd
75985	10	355479	7	NULL	NULL	0	NULL	statement 5	Process		occur in					thyroid patients	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Levothyroxine, also L-thyroxine, synthetic T4, or 3,5,3',5'-tetraiodo-L-thyronine, is a synthetic form of thyroxine (thyroid hormone), used as a hormone replacement for patients with thyroid problems.	topic_bd
75986	11	355479	7	NULL	NULL	0	NULL	statement 6	Process		occur in					thyroid patients	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Levothyroxine, also L-thyroxine, synthetic T4, or 3,5,3',5'-tetraiodo-L-thyronine, is a synthetic form of thyroxine (thyroid hormone), used as a hormone replacement for patients with thyroid problems.	topic_bd
75987	12	355479	7	NULL	NULL	0	NULL	statement 7	Process		occur in					thyroid patients	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Levothyroxine, also L-thyroxine, synthetic T4, or 3,5,3',5'-tetraiodo-L-thyronine, is a synthetic form of thyroxine (thyroid hormone), used as a hormone replacement for patients with thyroid problems.	topic_bd
75988	13	355479	7	NULL	NULL	0	NULL	statement 8	Process		occur in					thyroid patients	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Levothyroxine, also L-thyroxine, synthetic T4, or 3,5,3',5'-tetraiodo-L-thyronine, is a synthetic form of thyroxine (thyroid hormone), used as a hormone replacement for patients with thyroid problems.	topic_bd
75989	1	355480	7	NULL	NULL	0	NULL	triiodothyronine	GP		used as		effectively			augmentation agent	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	In addition, triiodothyronine has been effectively used as an augmentation agent in treatment-resistant bipolar depression.	topic_bd
75990	2	355480	7	NULL	NULL	0	NULL	statement 1	Process		is used in					treatment-resistant bipolar depression	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In addition, triiodothyronine has been effectively used as an augmentation agent in treatment-resistant bipolar depression.	topic_bd
75991	1	355481	7	NULL	NULL	NULL	NULL	Triiodothyronine	AminoAcid		also known as					T3	AminoAcid				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Triiodothyronine, C15H12I3NO4, also known as T3, is a thyroid hormone	topic_bd
75992	2	355481	7	NULL	NULL	0	NULL	T3	AminoAcid		is a type of					thyroid hormone	AminoAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	Triiodothyronine, C15H12I3NO4, also known as T3, is a thyroid hormone	topic_bd
75993	3	355481	7	NULL	NULL	0	NULL	C15H12I3NO4	AminoAcid		also known as					T3	AminoAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	Triiodothyronine, C15H12I3NO4, also known as T3, is a thyroid hormone	topic_bd
75994	1	355482	7	NULL	NULL	0	NULL	bipolar disorder patients	MedicalFinding		greater risk for					hyperthyroidism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In a Danish registry study,[7] patients hospitalized with bipolar disorder were at greater risk for readmission with hyperthyroidism compared with control patients. 	topic_bd
75995	1	355483	7	NULL	NULL	0	NULL	 mania	MedicalFinding		associated with					hypothyroidism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	there are case reports of mania or hypomania associated with hypothyroidism. 	topic_bd
75996	2	355483	7	NULL	NULL	0	NULL	hypomania	MedicalFinding		associated with					hypothyroidism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	there are case reports of mania or hypomania associated with hypothyroidism. 	topic_bd
75997	3	355483	7	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	there are case reports of mania or hypomania associated with hypothyroidism. 	topic_bd
76042	1	355484	7	NULL	NULL	NULL	NULL	free thyroxine index 	GP	lower values of	associated with					bipolar depression	MedicalFinding	longer time to remission in patients with			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Cole and colleagues[9] evaluated free thyroxine index and thyroid-stimulating hormone (TSH) levels in 65 patients with bipolar depression. A longer time to remission was significantly associated with both lower values of free thyroxine index and higher values of TSH.	topic_bd
76043	2	355484	7	NULL	NULL	0	NULL	TSH	GP	higher values of	associated with					bipolar depression	MedicalFinding	longer time to remission in patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	Cole and colleagues[9] evaluated free thyroxine index and thyroid-stimulating hormone (TSH) levels in 65 patients with bipolar depression. A longer time to remission was significantly associated with both lower values of free thyroxine index and higher values of TSH.	topic_bd
76044	1	355485	7	NULL	NULL	0	NULL	Hypothyroidism 	MedicalFinding		occur upon		may			lithium	Chemical	use of			NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothyroidism may occur in the early years of lithium use, in middle-aged women, and when thyroid autoimmunity is present;	topic_bd
76045	2	355485	7	NULL	NULL	0	NULL	statement 1	Process		occur in					middle-aged women	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothyroidism may occur in the early years of lithium use, in middle-aged women, and when thyroid autoimmunity is present;	topic_bd
76046	3	355485	7	NULL	NULL	0	NULL	statement 1	Process		occur upon					thyroid autoimmunity	MedicalFinding	presence of			NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothyroidism may occur in the early years of lithium use, in middle-aged women, and when thyroid autoimmunity is present;	topic_bd
76047	1	355486	7	NULL	NULL	0	NULL	Hyperthyroidism	MedicalFinding		uncommon during					lithium	Chemical	treatment with			NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperthyroidism and thyroid cancer are uncommon during treatment with lithium.	topic_bd
76048	2	355486	7	NULL	NULL	0	NULL	thyroid cancer	MedicalFinding		uncommon during					lithium	Chemical	treatment with			NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperthyroidism and thyroid cancer are uncommon during treatment with lithium.	topic_bd
76049	1	355487	7	NULL	NULL	0	NULL	thyroid dysfunction 	MedicalFinding	lithium treated	is not different from					general population	GroupOfPeople	observed in			NULL		0	NULL	NULL	NULL	NULL	NULL	The outcome of thyroid dysfunction in patients who have been on lithium for many years is not greatly different from that observed in the general population	topic_bd
76050	1	355488	7	NULL	NULL	0	NULL	Classic bipolar disorder	MedicalFinding		have difficulty					face emotions	MentalProcess	labeling			NULL		0	NULL	NULL	NULL	NULL	NULL	Earlier research had shown that both youth with classic, episodic bipolar and those with nonepisodic irritability have difficulty labeling face emotions.	topic_bd
76051	2	355488	7	NULL	NULL	0	NULL	episodic bipolar disorder	MedicalFinding		have difficulty					face emotions	MentalProcess	labeling			NULL		0	NULL	NULL	NULL	NULL	NULL	Earlier research had shown that both youth with classic, episodic bipolar and those with nonepisodic irritability have difficulty labeling face emotions.	topic_bd
76052	3	355488	7	NULL	NULL	0	NULL	nonepisodic irritability 	MedicalFinding		have difficulty					face emotions	MentalProcess	labeling			NULL		0	NULL	NULL	NULL	NULL	NULL	Earlier research had shown that both youth with classic, episodic bipolar and those with nonepisodic irritability have difficulty labeling face emotions.	topic_bd
76248	1	355489	7	NULL	NULL	0	NULL	healthy subjects	GroupOfPeople	amygdala activation  in	does not differ from		significantly			bipolar disorder	MedicalFinding	amygdala activation in patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	, the study shows that patients with bipolar disorder did not differ significantly from healthy comparison subjects in amygdala activation. 	topic_bd
76249	1	355518	7	NULL	NULL	0	NULL	Alcohol 	Chemical	misuse of	associated with					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Alcohol misuse is associated with bipolar disorder.	topic_bd
76250	1	355519	7	NULL	NULL	0	NULL	circadian clockwork	Process	abnormalities in	play a role in					bipolar disorder	MedicalFinding	pathogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	Abnormalities in the circadian clockwork play a role in the pathogenesis of bipolar disorder	topic_bd
76251	1	355520	7	NULL	NULL	0	NULL	Alcohol 	Chemical	intake of	affect		likely			circadian phenotype	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	Alcohol intake is likely to affect the circadian phenotype.	topic_bd
76252	1	355521	7	NULL	NULL	NULL	NULL	co-morbid alcohol use disorder patients	GroupOfPeople		were more of					morning type	Time				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Patients with the co-morbid alcohol use disorder were more of the morning type as compared with patients with bipolar disorder only.	topic_bd
76253	2	355521	7	NULL	NULL	0	NULL	statement 1	Process		in comparison with					bipolar disorder patients	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Patients with the co-morbid alcohol use disorder were more of the morning type as compared with patients with bipolar disorder only.	topic_bd
76254	1	355522	7	NULL	NULL	0	NULL	Co-morbid patients	GroupOfPeople		prefers					daily activities	Process	morning hours			NULL		0	NULL	NULL	NULL	NULL	NULL	Co-morbid patients preferred more the morning hours for their daily activities, indicative of alcohol consumption having an effect on the circadian clock.	topic_bd
76255	2	355522	7	NULL	NULL	NULL	NULL	statement 1	Process		indicates					alcohol 	Process	consumption of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Co-morbid patients preferred more the morning hours for their daily activities, indicative of alcohol consumption having an effect on the circadian clock.	topic_bd
76256	3	355522	7	NULL	NULL	0	NULL	statement 2	Process		effect					circadian clock	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Co-morbid patients preferred more the morning hours for their daily activities, indicative of alcohol consumption having an effect on the circadian clock.	topic_bd
76257	1	355523	7	NULL	NULL	NULL	NULL	sleep deprivation	MedicalFinding		alleviate					depression	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	sleep deprivation tends to alleviate depression in patients with bipolar disorder 	topic_bd
76258	2	355523	7	NULL	NULL	0	NULL	statement 1	Process		in patients with					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	sleep deprivation tends to alleviate depression in patients with bipolar disorder 	topic_bd
76259	1	355524	7	NULL	NULL	0	NULL	Lithium	Chemical		acts on		directly			circadian pacemaker cells 	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Lithium acts directly on the circadian pacemaker cells and lengthens the period of circadian rhythms	topic_bd
76260	2	355524	7	NULL	NULL	0	NULL	statement 1	Process		lengthens					circadian rhythms	Process	period of			NULL		0	NULL	NULL	NULL	NULL	NULL	Lithium acts directly on the circadian pacemaker cells and lengthens the period of circadian rhythms	topic_bd
76261	1	355525	7	NULL	NULL	NULL	NULL	bipolar disorder	MedicalFinding	Preschool children of parents with	is in the risk of					ADHD	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Preschool children of parents with bipolar disorder have more than an 8-fold higher risk for attention-deficit/hyperactivity disorder (ADHD) than offspring of parents without this disorder	topic_bd
76262	2	355525	7	NULL	NULL	NULL	NULL	bipolar disorder	MedicalFinding	Preschool children of parents without	is in the risk of					ADHD	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Preschool children of parents with bipolar disorder have more than an 8-fold higher risk for attention-deficit/hyperactivity disorder (ADHD) than offspring of parents without this disorder	topic_bd
76263	3	355525	7	NULL	NULL	NULL	NULL	statement 1	Process	risk of	is higher than					statement 2	Process	risk of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Preschool children of parents with bipolar disorder have more than an 8-fold higher risk for attention-deficit/hyperactivity disorder (ADHD) than offspring of parents without this disorder	topic_bd
76268	4	355525	7	NULL	NULL	0	NULL	ADHD	MedicalFinding		is					attention-deficit/hyperactivity disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Preschool children of parents with bipolar disorder have more than an 8-fold higher risk for attention-deficit/hyperactivity disorder (ADHD) than offspring of parents without this disorder	topic_bd
76264	1	355526	7	NULL	NULL	0	NULL	suicide	MentalProcess	 risk of	is increased in					bipolar disorder	MedicalFinding	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	Clinicians should know that, on average in the United States, 1 suicide occurs for every 30 attempts. In bipolar patients, it's 1 suicide for every 3 attempts,[1] which confirms the increased risk of suicide in patients with bipolar disorder: their attempts are 10 times more lethal.	topic_bd
76265	1	355527	7	NULL	NULL	0	NULL	Suicide	MentalProcess		outcome of		devastating			depression	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Suicide is a devastating outcome of depression, and patients with bipolar disorder spend more time depressed than manic.	topic_bd
76266	2	355527	7	NULL	NULL	NULL	NULL	bipolar disorder	MedicalFinding	depression in patients with	is more than					bipolar disorder	MedicalFinding	manic in patients with			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Suicide is a devastating outcome of depression, and patients with bipolar disorder spend more time depressed than manic.	topic_bd
76267	1	355528	7	NULL	NULL	0	NULL	Bipolar patients	MedicalFinding		have					mixed mood states	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar patients sometimes have mixed mood states, in which they're both depressed and manic at the same time. In other words, they're not euphoric like most manic patients, they're irritable and they have increased energy. That's a particularly risky situation for a bipolar patient.	topic_bd
76269	2	355528	7	NULL	NULL	NULL	NULL	depression	MedicalFinding		occur at the same time as					manic	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Bipolar patients sometimes have mixed mood states, in which they're both depressed and manic at the same time. In other words, they're not euphoric like most manic patients, they're irritable and they have increased energy. That's a particularly risky situation for a bipolar patient.	topic_bd
76270	3	355528	7	NULL	NULL	0	NULL	statement 2	Process		occur in					bipolar patients	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar patients sometimes have mixed mood states, in which they're both depressed and manic at the same time. In other words, they're not euphoric like most manic patients, they're irritable and they have increased energy. That's a particularly risky situation for a bipolar patient.	topic_bd
76271	4	355528	7	NULL	NULL	0	NULL	Bipolar patients	MedicalFinding		are not					euphoric	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar patients sometimes have mixed mood states, in which they're both depressed and manic at the same time. In other words, they're not euphoric like most manic patients, they're irritable and they have increased energy. That's a particularly risky situation for a bipolar patient.	topic_bd
76272	5	355528	7	NULL	NULL	0	NULL	manic patients	MedicalFinding		are					euphoric	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar patients sometimes have mixed mood states, in which they're both depressed and manic at the same time. In other words, they're not euphoric like most manic patients, they're irritable and they have increased energy. That's a particularly risky situation for a bipolar patient.	topic_bd
76273	6	355528	7	NULL	NULL	0	NULL	Bipolar patients	MedicalFinding		are					irritable	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar patients sometimes have mixed mood states, in which they're both depressed and manic at the same time. In other words, they're not euphoric like most manic patients, they're irritable and they have increased energy. That's a particularly risky situation for a bipolar patient.	topic_bd
76274	7	355528	7	NULL	NULL	0	NULL	Bipolar patients	MedicalFinding		have increased					energy	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar patients sometimes have mixed mood states, in which they're both depressed and manic at the same time. In other words, they're not euphoric like most manic patients, they're irritable and they have increased energy. That's a particularly risky situation for a bipolar patient.	topic_bd
76275	8	355528	7	NULL	NULL	0	NULL	statement 1	Process		risky situation for					bipolar patient	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar patients sometimes have mixed mood states, in which they're both depressed and manic at the same time. In other words, they're not euphoric like most manic patients, they're irritable and they have increased energy. That's a particularly risky situation for a bipolar patient.	topic_bd
76327	1	355529	7	NULL	NULL	NULL	NULL	severe anxiety	MedicalFinding		risk factor for					suicide	MentalProcess				NULL		NULL	NULL	NULL	NULL	NULL	NULL	if the patient is experiencing severe anxiety, such as anxious thoughts the patient can't stop. This could be a serious risk factor for suicide	topic_bd
76669	1	355530	7	NULL	NULL	NULL	NULL	bipolar patients	MedicalFinding		 risk factor for		highest			suicide	MentalProcess				NULL		NULL	NULL	NULL	NULL	NULL	NULL	In a recent study of 32,000 bipolar patients' records,[2] the highest risk factor for suicide was being male and having a comorbid anxiety disorder, compared with being young and having a substance-use disorder, which predicted attempts but not necessarily suicide.	topic_bd
76670	2	355530	7	NULL	NULL	0	NULL	statement 1	Process		occur in					comorbid anxiety disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In a recent study of 32,000 bipolar patients' records,[2] the highest risk factor for suicide was being male and having a comorbid anxiety disorder, compared with being young and having a substance-use disorder, which predicted attempts but not necessarily suicide.	topic_bd
76671	3	355530	7	NULL	NULL	0	NULL	statement 1	Process		occur in					substance-use disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In a recent study of 32,000 bipolar patients' records,[2] the highest risk factor for suicide was being male and having a comorbid anxiety disorder, compared with being young and having a substance-use disorder, which predicted attempts but not necessarily suicide.	topic_bd
76672	4	355530	7	NULL	NULL	0	NULL	statement 2	Process		is higher than					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In a recent study of 32,000 bipolar patients' records,[2] the highest risk factor for suicide was being male and having a comorbid anxiety disorder, compared with being young and having a substance-use disorder, which predicted attempts but not necessarily suicide.	topic_bd
76468	1	355531	7	NULL	NULL	NULL	NULL	Fluoxetine	Chemical		prevents					bipolar type II	MedicalFinding	major depressive episodes in patients with			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Fluoxetine appears superior to lithium in preventing recurrence of major depressive episodes in patients with bipolar type II, according to new research.	topic_bd
76469	2	355531	7	NULL	NULL	0	NULL	 lithium	Chemical		prevents					bipolar type II	MedicalFinding	major depressive episodes in patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	Fluoxetine appears superior to lithium in preventing recurrence of major depressive episodes in patients with bipolar type II, according to new research.	topic_bd
76470	3	355531	7	NULL	NULL	0	NULL	statement 1	Process		is superior than					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Fluoxetine appears superior to lithium in preventing recurrence of major depressive episodes in patients with bipolar type II, according to new research.	topic_bd
76471	1	355532	7	NULL	NULL	0	NULL	lithium	Chemical	patients taking	suffer 					relapse	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Patients taking lithium were at risk of suffering a relapse much sooner than those on fluoxetine (Prozac),	topic_bd
76472	2	355532	7	NULL	NULL	NULL	NULL	fluoxetine	Chemical	patients taking	suffer					relapse	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Patients taking lithium were at risk of suffering a relapse much sooner than those on fluoxetine (Prozac),	topic_bd
76473	3	355532	7	NULL	NULL	0	NULL	statement 1	Process	relapse of	sooner than					statement 2	Process	relapse of			NULL		0	NULL	NULL	NULL	NULL	NULL	Patients taking lithium were at risk of suffering a relapse much sooner than those on fluoxetine (Prozac),	topic_bd
76474	1	355535	7	NULL	NULL	0	NULL	 alcohol 	Chemical		does not worsen					mood symptoms	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Among people with bipolar disorder who strictly followed their medication plan, drinking alcohol did not appear to worsen their mood symptoms, hint findings of a small study from The Netherlands.	topic_bd
76475	2	355535	7	NULL	NULL	0	NULL	statement 1	Process		occur in					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Among people with bipolar disorder who strictly followed their medication plan, drinking alcohol did not appear to worsen their mood symptoms, hint findings of a small study from The Netherlands.	topic_bd
76477	1	355538	7	NULL	NULL	0	NULL	bipolar spectrum	MedicalFinding		embraces					mania	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	there is ample evidence to support the hypothesis that a wide bipolar spectrum exists in clinical samples...This spectrum embraces mania, hypomania, recurrent brief hypomania, sporadic brief hypomania and cyclothymia.	topic_bd
76478	2	355538	7	NULL	NULL	0	NULL	bipolar spectrum	MedicalFinding		embraces					hypomania	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	there is ample evidence to support the hypothesis that a wide bipolar spectrum exists in clinical samples...This spectrum embraces mania, hypomania, recurrent brief hypomania, sporadic brief hypomania and cyclothymia.	topic_bd
76479	3	355538	7	NULL	NULL	0	NULL	bipolar spectrum	MedicalFinding		embraces					hypomania	MedicalFinding	recurrent brief 			NULL		0	NULL	NULL	NULL	NULL	NULL	there is ample evidence to support the hypothesis that a wide bipolar spectrum exists in clinical samples...This spectrum embraces mania, hypomania, recurrent brief hypomania, sporadic brief hypomania and cyclothymia.	topic_bd
76480	4	355538	7	NULL	NULL	0	NULL	bipolar spectrum	MedicalFinding		embraces					hypomania	MedicalFinding	sporadic brief 			NULL		0	NULL	NULL	NULL	NULL	NULL	there is ample evidence to support the hypothesis that a wide bipolar spectrum exists in clinical samples...This spectrum embraces mania, hypomania, recurrent brief hypomania, sporadic brief hypomania and cyclothymia.	topic_bd
76481	5	355538	7	NULL	NULL	0	NULL	bipolar spectrum	MedicalFinding		embraces					cyclothymia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	there is ample evidence to support the hypothesis that a wide bipolar spectrum exists in clinical samples...This spectrum embraces mania, hypomania, recurrent brief hypomania, sporadic brief hypomania and cyclothymia.	topic_bd
74788	1	355539	5	NULL	NULL	0	NULL	splenectomy	MedicalProcedure		is a type of					surgical procedure	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	There are different types of treatment for patients with hairy cell leukemia. : splenectomy is a surgical procedure to remove the spleen. 	topic_ll
74789	2	355539	5	NULL	NULL	0	NULL	splenectomy	MedicalFinding		removes					spleen	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	There are different types of treatment for patients with hairy cell leukemia. : splenectomy is a surgical procedure to remove the spleen. 	topic_ll
74791	1	355540	5	NULL	NULL	0	NULL	monoclonal antibody therapy	MedicalProcedure		is a type of					targeted therapy	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Monoclonal antibody therapy is a type of targeted therapy being studied in the treatment of hairy cell leukemia.	topic_ll
74792	2	355540	5	NULL	NULL	0	NULL	monoclonal antibody therapy	MedicalProcedure		is used to treat		may be			hairy cell leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Monoclonal antibody therapy is a type of targeted therapy being studied in the treatment of hairy cell leukemia.	topic_ll
74820	1	355542	5	NULL	NULL	0	NULL	Hairy (leukemia) cells	Cell		is present in					blood	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The hairy cell leukemia is newly diagnosed and has not been treated except to relieve symptoms such as weight loss and infections. In untreated hairy cell leukemia, some or all of the following conditions occur: * Hairy (leukemia) cells are found in the blood and bone marrow. * The number of red blood cells, white blood cells, or platelets may be lower than normal. * The spleen may be larger than normal. NULL	topic_ll
74821	2	355542	5	NULL	NULL	0	NULL	Hairy (leukemia) cells	Cell		is present in					bone marrow	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The hairy cell leukemia is newly diagnosed and has not been treated except to relieve symptoms such as weight loss and infections. In untreated hairy cell leukemia, some or all of the following conditions occur: * Hairy (leukemia) cells are found in the blood and bone marrow. * The number of red blood cells, white blood cells, or platelets may be lower than normal. * The spleen may be larger than normal. NULL	topic_ll
74822	3	355542	5	NULL	NULL	0	NULL	treatment	Process		is not available for					hairy cell leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The hairy cell leukemia is newly diagnosed and has not been treated except to relieve symptoms such as weight loss and infections. In untreated hairy cell leukemia, some or all of the following conditions occur: * Hairy (leukemia) cells are found in the blood and bone marrow. * The number of red blood cells, white blood cells, or platelets may be lower than normal. * The spleen may be larger than normal. NULL	topic_ll
74823	4	355542	5	NULL	NULL	0	NULL	hairy cell leukemia	MedicalFinding	treatment	relieves					weight loss	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The hairy cell leukemia is newly diagnosed and has not been treated except to relieve symptoms such as weight loss and infections. In untreated hairy cell leukemia, some or all of the following conditions occur: * Hairy (leukemia) cells are found in the blood and bone marrow. * The number of red blood cells, white blood cells, or platelets may be lower than normal. * The spleen may be larger than normal. NULL	topic_ll
74824	5	355542	5	NULL	NULL	0	NULL	hairy cell leukemia	MedicalFinding	treatment	relieves					infections	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The hairy cell leukemia is newly diagnosed and has not been treated except to relieve symptoms such as weight loss and infections. In untreated hairy cell leukemia, some or all of the following conditions occur: * Hairy (leukemia) cells are found in the blood and bone marrow. * The number of red blood cells, white blood cells, or platelets may be lower than normal. * The spleen may be larger than normal. NULL	topic_ll
74856	1	355543	5	NULL	NULL	0	NULL	Btk	GP		is					Bruton's tyrosine kinase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	I found another one -- a Btk (Bruton's tyrosine kinase) Inhibitor, PCI-32765, that is currently in Phase I clinical trials in patients with B cell malignancies (specifically Non-Hodgkin's Lymphoma).  Btk is an essential signalling factor needed for the development of  B-cells.  By inhibiting it, the Btk protein production is blocked and B-cells can't develop.	topic_ll
74857	2	355543	5	NULL	NULL	0	NULL	Btk	GP		is a type of					signalling factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	I found another one -- a Btk (Bruton's tyrosine kinase) Inhibitor, PCI-32765, that is currently in Phase I clinical trials in patients with B cell malignancies (specifically Non-Hodgkin's Lymphoma).  Btk is an essential signalling factor needed for the development of  B-cells.  By inhibiting it, the Btk protein production is blocked and B-cells can't develop.	topic_ll
74858	3	355543	5	NULL	NULL	0	NULL	Btk	GP		is needed for					B-cells	Cell	development of			NULL		0	NULL	NULL	NULL	NULL	NULL	I found another one -- a Btk (Bruton's tyrosine kinase) Inhibitor, PCI-32765, that is currently in Phase I clinical trials in patients with B cell malignancies (specifically Non-Hodgkin's Lymphoma).  Btk is an essential signalling factor needed for the development of  B-cells.  By inhibiting it, the Btk protein production is blocked and B-cells can't develop.	topic_ll
74859	4	355543	5	NULL	NULL	0	NULL	Btk	GP	inhibition of	blocks					Btk protein	GP	production of			NULL		0	NULL	NULL	NULL	NULL	NULL	I found another one -- a Btk (Bruton's tyrosine kinase) Inhibitor, PCI-32765, that is currently in Phase I clinical trials in patients with B cell malignancies (specifically Non-Hodgkin's Lymphoma).  Btk is an essential signalling factor needed for the development of  B-cells.  By inhibiting it, the Btk protein production is blocked and B-cells can't develop.	topic_ll
74860	5	355543	5	NULL	NULL	0	NULL	statement 4	Process		blocks					B-cells	Cell	development of			NULL		0	NULL	NULL	NULL	NULL	NULL	I found another one -- a Btk (Bruton's tyrosine kinase) Inhibitor, PCI-32765, that is currently in Phase I clinical trials in patients with B cell malignancies (specifically Non-Hodgkin's Lymphoma).  Btk is an essential signalling factor needed for the development of  B-cells.  By inhibiting it, the Btk protein production is blocked and B-cells can't develop.	topic_ll
74861	6	355543	5	NULL	NULL	0	NULL	PCI-32765	Chemical		is an inhibitor of					Btk	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	I found another one -- a Btk (Bruton's tyrosine kinase) Inhibitor, PCI-32765, that is currently in Phase I clinical trials in patients with B cell malignancies (specifically Non-Hodgkin's Lymphoma).  Btk is an essential signalling factor needed for the development of  B-cells.  By inhibiting it, the Btk protein production is blocked and B-cells can't develop.	topic_ll
74862	7	355543	5	NULL	NULL	0	NULL	Non-Hodgkin's Lymphoma	MedicalFinding		is a type of					B cell malignancies	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	I found another one -- a Btk (Bruton's tyrosine kinase) Inhibitor, PCI-32765, that is currently in Phase I clinical trials in patients with B cell malignancies (specifically Non-Hodgkin's Lymphoma).  Btk is an essential signalling factor needed for the development of  B-cells.  By inhibiting it, the Btk protein production is blocked and B-cells can't develop.	topic_ll
74863	8	355543	5	NULL	NULL	0	NULL	PCI-32765	Chemical		treats		potentially			Non-Hodgkin's Lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	I found another one -- a Btk (Bruton's tyrosine kinase) Inhibitor, PCI-32765, that is currently in Phase I clinical trials in patients with B cell malignancies (specifically Non-Hodgkin's Lymphoma).  Btk is an essential signalling factor needed for the development of  B-cells.  By inhibiting it, the Btk protein production is blocked and B-cells can't develop.	topic_ll
74864	1	355544	5	NULL	NULL	0	NULL	leukemia cells	Cell		is addicted to					glucose	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Leukemia cells, like most cancers, are addicted to glucose to generate their energy, but new research shows for the first time that these cells also rely on fatty acid metabolism to grow and to evade cell death.	topic_ll
74865	2	355544	5	NULL	NULL	NULL	NULL	glucose	Chemical		generates					energy	AbstractConcept				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Leukemia cells, like most cancers, are addicted to glucose to generate their energy, but new research shows for the first time that these cells also rely on fatty acid metabolism to grow and to evade cell death.	topic_ll
74866	3	355544	5	NULL	NULL	0	NULL	leukemia cells	Cell		rely on					fatty acid	Chemical	metabolism of			NULL		0	NULL	NULL	NULL	NULL	NULL	Leukemia cells, like most cancers, are addicted to glucose to generate their energy, but new research shows for the first time that these cells also rely on fatty acid metabolism to grow and to evade cell death.	topic_ll
74867	4	355544	5	NULL	NULL	0	NULL	statement 3	Process		is required for					growth	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Leukemia cells, like most cancers, are addicted to glucose to generate their energy, but new research shows for the first time that these cells also rely on fatty acid metabolism to grow and to evade cell death.	topic_ll
74868	5	355544	5	NULL	NULL	0	NULL	leukemia cells	Cell		evade					cell death	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Leukemia cells, like most cancers, are addicted to glucose to generate their energy, but new research shows for the first time that these cells also rely on fatty acid metabolism to grow and to evade cell death.	topic_ll
74869	6	355544	5	NULL	NULL	0	NULL	statement 3	Process		is required for					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Leukemia cells, like most cancers, are addicted to glucose to generate their energy, but new research shows for the first time that these cells also rely on fatty acid metabolism to grow and to evade cell death.	topic_ll
74870	1	355545	5	NULL	NULL	0	NULL	fat oxidation	Process		promote		seems to			leukemia cell	Cell	survival of			NULL		0	NULL	NULL	NULL	NULL	NULL	"More importantly, fat oxidation seems to promote leukemia cell survival. Conversely, shutting off fat oxidation makes the cells vulnerable to self-destruction. If these initial results hold up, inhibitors of fat oxidation may become a new way to treat leukemia patients."	topic_ll
74871	3	355545	5	NULL	NULL	0	NULL	fat oxidation	Process	shutting off	leads to					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	"More importantly, fat oxidation seems to promote leukemia cell survival. Conversely, shutting off fat oxidation makes the cells vulnerable to self-destruction. If these initial results hold up, inhibitors of fat oxidation may become a new way to treat leukemia patients."	topic_ll
74872	2	355545	5	NULL	NULL	0	NULL	leukemia cells	Cell		is vulnerable to					self-destruction	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	"More importantly, fat oxidation seems to promote leukemia cell survival. Conversely, shutting off fat oxidation makes the cells vulnerable to self-destruction. If these initial results hold up, inhibitors of fat oxidation may become a new way to treat leukemia patients."	topic_ll
74873	4	355545	5	NULL	NULL	0	NULL	fat oxidation inhibitors	AbstractConcept		treats		potentially			leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	"More importantly, fat oxidation seems to promote leukemia cell survival. Conversely, shutting off fat oxidation makes the cells vulnerable to self-destruction. If these initial results hold up, inhibitors of fat oxidation may become a new way to treat leukemia patients."	topic_ll
74874	1	355546	5	NULL	NULL	0	NULL	etomoxir	Chemical		inhibits					fatty acid	Chemical	oxidation of			NULL		0	NULL	NULL	NULL	NULL	NULL	The team, led by Michael Andreeff and Heinrich Taegtmeyer, found that inhibition of fatty acid oxidation with either etomoxir, a drug that was tested in clinical trials for the treatment of heart disease but never made it to market due to unacceptable toxicities, or ranolazine, a drug approved for the treatment of chronic angina, inhibited human leukemic cell proliferation in vitro.	topic_ll
74884	2	355546	5	NULL	NULL	0	NULL	ranolazine	Chemical		inhibits					fatty acid\t\t	Chemical	oxidation of			NULL		0	NULL	NULL	NULL	NULL	NULL	The team, led by Michael Andreeff and Heinrich Taegtmeyer, found that inhibition of fatty acid oxidation with either etomoxir, a drug that was tested in clinical trials for the treatment of heart disease but never made it to market due to unacceptable toxicities, or ranolazine, a drug approved for the treatment of chronic angina, inhibited human leukemic cell proliferation in vitro.	topic_ll
74885	3	355546	5	NULL	NULL	NULL	NULL	statement 1	Process		inhibits					leukemic cell	Cell	proliferation of;;human			NULL	in vitro	NULL	NULL	NULL	NULL	NULL	NULL	The team, led by Michael Andreeff and Heinrich Taegtmeyer, found that inhibition of fatty acid oxidation with either etomoxir, a drug that was tested in clinical trials for the treatment of heart disease but never made it to market due to unacceptable toxicities, or ranolazine, a drug approved for the treatment of chronic angina, inhibited human leukemic cell proliferation in vitro.	topic_ll
74886	4	355546	5	NULL	NULL	NULL	NULL	statement 2	Process		inhibits					leukemic cell	Cell	proliferation of;;human			NULL	in vitro	NULL	NULL	NULL	NULL	NULL	NULL	The team, led by Michael Andreeff and Heinrich Taegtmeyer, found that inhibition of fatty acid oxidation with either etomoxir, a drug that was tested in clinical trials for the treatment of heart disease but never made it to market due to unacceptable toxicities, or ranolazine, a drug approved for the treatment of chronic angina, inhibited human leukemic cell proliferation in vitro.	topic_ll
74887	5	355546	5	NULL	NULL	0	NULL	ranolazine	Chemical		is a type of					drug	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The team, led by Michael Andreeff and Heinrich Taegtmeyer, found that inhibition of fatty acid oxidation with either etomoxir, a drug that was tested in clinical trials for the treatment of heart disease but never made it to market due to unacceptable toxicities, or ranolazine, a drug approved for the treatment of chronic angina, inhibited human leukemic cell proliferation in vitro.	topic_ll
74888	6	355546	5	NULL	NULL	0	NULL	ranolazine	Chemical		is approved for					chronic angina	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	The team, led by Michael Andreeff and Heinrich Taegtmeyer, found that inhibition of fatty acid oxidation with either etomoxir, a drug that was tested in clinical trials for the treatment of heart disease but never made it to market due to unacceptable toxicities, or ranolazine, a drug approved for the treatment of chronic angina, inhibited human leukemic cell proliferation in vitro.	topic_ll
74889	7	355546	5	NULL	NULL	0	NULL	etomoxir	Chemical		is a type of					drug	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The team, led by Michael Andreeff and Heinrich Taegtmeyer, found that inhibition of fatty acid oxidation with either etomoxir, a drug that was tested in clinical trials for the treatment of heart disease but never made it to market due to unacceptable toxicities, or ranolazine, a drug approved for the treatment of chronic angina, inhibited human leukemic cell proliferation in vitro.	topic_ll
74890	8	355546	5	NULL	NULL	0	NULL	etomoxir	Chemical		is not approved for					heart disease	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	The team, led by Michael Andreeff and Heinrich Taegtmeyer, found that inhibition of fatty acid oxidation with either etomoxir, a drug that was tested in clinical trials for the treatment of heart disease but never made it to market due to unacceptable toxicities, or ranolazine, a drug approved for the treatment of chronic angina, inhibited human leukemic cell proliferation in vitro.	topic_ll
74891	9	355546	5	NULL	NULL	0	NULL	toxicities	AbstractConcept	unacceptable	leads to					statement 8	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The team, led by Michael Andreeff and Heinrich Taegtmeyer, found that inhibition of fatty acid oxidation with either etomoxir, a drug that was tested in clinical trials for the treatment of heart disease but never made it to market due to unacceptable toxicities, or ranolazine, a drug approved for the treatment of chronic angina, inhibited human leukemic cell proliferation in vitro.	topic_ll
74892	1	355548	5	NULL	NULL	0	NULL	Gfi1b	GP		is inactivated in					stem cells	Cell	transplanted			NULL		0	NULL	NULL	NULL	NULL	NULL	inactivation of Gfi1b in the transplanted stem cells could accelerate the production of new blood cells, thus making stem cell therapy more efficient and less dangerous for the patient.	topic_ll
74893	2	355548	5	NULL	NULL	0	NULL	statement 1	Process		accelerates					blood cells	Cell	production of;;new			NULL		0	NULL	NULL	NULL	NULL	NULL	inactivation of Gfi1b in the transplanted stem cells could accelerate the production of new blood cells, thus making stem cell therapy more efficient and less dangerous for the patient.	topic_ll
74894	3	355548	5	NULL	NULL	0	NULL	stem cell therapy	MedicalProcedure		is more efficient for					patient	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	inactivation of Gfi1b in the transplanted stem cells could accelerate the production of new blood cells, thus making stem cell therapy more efficient and less dangerous for the patient.	topic_ll
74895	4	355548	5	NULL	NULL	0	NULL	stem cell therapy	MedicalProcedure		is less dangerous for					patient	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	inactivation of Gfi1b in the transplanted stem cells could accelerate the production of new blood cells, thus making stem cell therapy more efficient and less dangerous for the patient.	topic_ll
74896	1	355549	5	NULL	NULL	0	NULL	AHI-1 protein	GP		is present in					leukemia cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	The team found that a protein called AHI-1, which has been found in leukemia cells in the past, is highly expressed in CML stem cells.	topic_ll
74897	2	355549	5	NULL	NULL	0	NULL	AHI-1 protein	GP		is expressed in		highly			CML stem cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	The team found that a protein called AHI-1, which has been found in leukemia cells in the past, is highly expressed in CML stem cells.	topic_ll
74898	1	355551	5	NULL	NULL	0	NULL	RRLON	MedicalFinding		is a side-effect of					Rituxan	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	but after some more investigation, my best guess is that I've experienced a side-effect of Rituxan known as Rituxan related late onset  neutropenia  (RRLON).  	topic_ll
74899	2	355551	5	NULL	NULL	0	NULL	RRLON	MedicalFinding		is					Rituxan related late onset neutropenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	but after some more investigation, my best guess is that I've experienced a side-effect of Rituxan known as Rituxan related late onset  neutropenia  (RRLON).  	topic_ll
74900	1	355552	5	NULL	NULL	0	NULL	HCL	MedicalFinding		is a disorder of		uncommon;;chronic;;neoplastic 			B lymphocytes	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	HCL is an uncommon, chronic, neoplastic (malignant) disorder of B lymphocytes (a type of white blood cell) that afflicts middle-aged men. The patient usually presents with pancytopenia (broad spectrum reduction in blood counts -- low platelets, low white blood cells, low red blood cells).	topic_ll
74901	2	355552	5	NULL	NULL	0	NULL	B lymphocytes	Cell		is a type of					white blood cell	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	HCL is an uncommon, chronic, neoplastic (malignant) disorder of B lymphocytes (a type of white blood cell) that afflicts middle-aged men. The patient usually presents with pancytopenia (broad spectrum reduction in blood counts -- low platelets, low white blood cells, low red blood cells).	topic_ll
74902	3	355552	5	NULL	NULL	NULL	NULL	HCL	MedicalFinding		afflicts					men	GroupOfPeople	middle-aged			NULL		NULL	NULL	NULL	NULL	NULL	NULL	HCL is an uncommon, chronic, neoplastic (malignant) disorder of B lymphocytes (a type of white blood cell) that afflicts middle-aged men. The patient usually presents with pancytopenia (broad spectrum reduction in blood counts -- low platelets, low white blood cells, low red blood cells).	topic_ll
74903	4	355552	5	NULL	NULL	0	NULL	HCL patients	GroupOfPeople		presents with					pancytopenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	HCL is an uncommon, chronic, neoplastic (malignant) disorder of B lymphocytes (a type of white blood cell) that afflicts middle-aged men. The patient usually presents with pancytopenia (broad spectrum reduction in blood counts -- low platelets, low white blood cells, low red blood cells).	topic_ll
74904	5	355552	5	NULL	NULL	0	NULL	blood counts	AbstractConcept	reduction of	is known as					pancytopenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	HCL is an uncommon, chronic, neoplastic (malignant) disorder of B lymphocytes (a type of white blood cell) that afflicts middle-aged men. The patient usually presents with pancytopenia (broad spectrum reduction in blood counts -- low platelets, low white blood cells, low red blood cells).	topic_ll
74905	6	355552	5	NULL	NULL	0	NULL	platelets	Cell		is a type of					blood cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	HCL is an uncommon, chronic, neoplastic (malignant) disorder of B lymphocytes (a type of white blood cell) that afflicts middle-aged men. The patient usually presents with pancytopenia (broad spectrum reduction in blood counts -- low platelets, low white blood cells, low red blood cells).	topic_ll
74906	7	355552	5	NULL	NULL	0	NULL	white blood cells	Cell		is a type of					blood cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	HCL is an uncommon, chronic, neoplastic (malignant) disorder of B lymphocytes (a type of white blood cell) that afflicts middle-aged men. The patient usually presents with pancytopenia (broad spectrum reduction in blood counts -- low platelets, low white blood cells, low red blood cells).	topic_ll
74907	8	355552	5	NULL	NULL	0	NULL	 red blood cells	Cell		is a type of					blood cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	HCL is an uncommon, chronic, neoplastic (malignant) disorder of B lymphocytes (a type of white blood cell) that afflicts middle-aged men. The patient usually presents with pancytopenia (broad spectrum reduction in blood counts -- low platelets, low white blood cells, low red blood cells).	topic_ll
74908	1	355554	5	NULL	NULL	0	NULL	caffeine	Chemical		lowers					TNFa	GP	levels of			NULL		0	NULL	NULL	NULL	NULL	NULL	After my testing in August, I blogged about some research which indicated that caffeine can lower TNFa levels and hypothesized that since some research indicates that HCL apparently thrives on TNFa, maybe drinking coffee and consuming other TNFa lowering foods may improve or sustain my response.	topic_ll
74909	2	355554	5	NULL	NULL	0	NULL	HCL	MedicalFinding		thrives on		apparently			TNFa	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	After my testing in August, I blogged about some research which indicated that caffeine can lower TNFa levels and hypothesized that since some research indicates that HCL apparently thrives on TNFa, maybe drinking coffee and consuming other TNFa lowering foods may improve or sustain my response.	topic_ll
74910	1	355555	5	NULL	NULL	0	NULL	HCL	MedicalFinding	risk of	is concentrated in					males	GroupOfPeople	white			NULL		0	NULL	NULL	NULL	NULL	NULL	HCL risk was concentrated in white males; there were few black and Asian patients for analysis.	topic_ll
74911	1	355556	5	NULL	NULL	0	NULL	HCL	MedicalFinding	risk of	is concentrated in					males	GroupOfPeople	white			NULL		0	NULL	NULL	NULL	NULL	NULL	HCL risk was concentrated in white males; there were few black and Asian patients for analysis. Using data from all cancer patients diagnosed during the study period, Jewish men had significantly greater risk of HCL than Protestant men.	topic_ll
74912	2	355556	5	NULL	NULL	0	NULL	men	GroupOfPeople	Jewish	is at risk of					HCL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	HCL risk was concentrated in white males; there were few black and Asian patients for analysis. Using data from all cancer patients diagnosed during the study period, Jewish men had significantly greater risk of HCL than Protestant men.	topic_ll
74913	3	355556	5	NULL	NULL	0	NULL	men	GroupOfPeople	Protestant	is at risk of					HCL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	HCL risk was concentrated in white males; there were few black and Asian patients for analysis. Using data from all cancer patients diagnosed during the study period, Jewish men had significantly greater risk of HCL than Protestant men.	topic_ll
74914	4	355556	5	NULL	NULL	0	NULL	statement 2	Process		greater than		significantly			statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	HCL risk was concentrated in white males; there were few black and Asian patients for analysis. Using data from all cancer patients diagnosed during the study period, Jewish men had significantly greater risk of HCL than Protestant men.	topic_ll
74915	1	355558	5	NULL	NULL	0	NULL	GSE	CellComponent		is					grape seed extract	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	cell death effects of Grape Seed Extract (GSE) on Jurkat cells through increased activation of JNK enzymes in these leukemic T-cells. Prior studies of GSE in Jurkat cells as well as prostate cancer show that GSE is highly effective in activating JNK enzymes and inducing apoptosis in those cell lines.	topic_ll
74916	2	355558	5	NULL	NULL	NULL	NULL	GSE	CellComponent		activates		effectively			JNK enzymes	GP				NULL	Jurkat cells	NULL	NULL	NULL	NULL	NULL	NULL	cell death effects of Grape Seed Extract (GSE) on Jurkat cells through increased activation of JNK enzymes in these leukemic T-cells. Prior studies of GSE in Jurkat cells as well as prostate cancer show that GSE is highly effective in activating JNK enzymes and inducing apoptosis in those cell lines.	topic_ll
74917	3	355558	5	NULL	NULL	NULL	NULL	statement 2	Process		induce					apoptosis	Process				NULL	Jurkat cells	NULL	NULL	NULL	NULL	NULL	NULL	cell death effects of Grape Seed Extract (GSE) on Jurkat cells through increased activation of JNK enzymes in these leukemic T-cells. Prior studies of GSE in Jurkat cells as well as prostate cancer show that GSE is highly effective in activating JNK enzymes and inducing apoptosis in those cell lines.	topic_ll
74922	4	355558	5	NULL	NULL	NULL	NULL	GSE	CellComponent		activates		effectively			JNK enzymes	GP				NULL	prostate cancer	NULL	NULL	NULL	NULL	NULL	NULL	cell death effects of Grape Seed Extract (GSE) on Jurkat cells through increased activation of JNK enzymes in these leukemic T-cells. Prior studies of GSE in Jurkat cells as well as prostate cancer show that GSE is highly effective in activating JNK enzymes and inducing apoptosis in those cell lines.	topic_ll
74923	5	355558	5	NULL	NULL	0	NULL	statement 4	Process		induce					apoptosis	Process				NULL	prostate cancer	0	NULL	NULL	NULL	NULL	NULL	cell death effects of Grape Seed Extract (GSE) on Jurkat cells through increased activation of JNK enzymes in these leukemic T-cells. Prior studies of GSE in Jurkat cells as well as prostate cancer show that GSE is highly effective in activating JNK enzymes and inducing apoptosis in those cell lines.	topic_ll
74966	6	355558	5	NULL	NULL	NULL	NULL	GSE	CellComponent		effects					cell death	Process				NULL	Jurkat cells	NULL	NULL	NULL	NULL	NULL	NULL	cell death effects of Grape Seed Extract (GSE) on Jurkat cells through increased activation of JNK enzymes in these leukemic T-cells. Prior studies of GSE in Jurkat cells as well as prostate cancer show that GSE is highly effective in activating JNK enzymes and inducing apoptosis in those cell lines.	topic_ll
74967	7	355558	5	NULL	NULL	0	NULL	statement 6	Process		occurs through					JNK enzymes	GP	increased activation of			NULL	leukemic T-cells	0	NULL	NULL	NULL	NULL	NULL	cell death effects of Grape Seed Extract (GSE) on Jurkat cells through increased activation of JNK enzymes in these leukemic T-cells. Prior studies of GSE in Jurkat cells as well as prostate cancer show that GSE is highly effective in activating JNK enzymes and inducing apoptosis in those cell lines.	topic_ll
74918	1	355559	5	NULL	NULL	NULL	NULL	GSE	CellComponent		activates		effectively			JNK enzymes	GP				NULL	Jurkat cells	NULL	NULL	NULL	NULL	NULL	NULL	Prior studies of GSE in Jurkat cells as well as prostate cancer show that GSE is highly effective in activating JNK enzymes and inducing apoptosis in those cell lines. 	topic_ll
74919	2	355559	5	NULL	NULL	0	NULL	GSE	CellComponent		activates		effectively			JNK enzymes	GP				NULL	prostate cancer	0	NULL	NULL	NULL	NULL	NULL	Prior studies of GSE in Jurkat cells as well as prostate cancer show that GSE is highly effective in activating JNK enzymes and inducing apoptosis in those cell lines. 	topic_ll
74920	3	355559	5	NULL	NULL	0	NULL	statement 1	Process		induce					apoptosis	Process				NULL	Jurkat cells	0	NULL	NULL	NULL	NULL	NULL	Prior studies of GSE in Jurkat cells as well as prostate cancer show that GSE is highly effective in activating JNK enzymes and inducing apoptosis in those cell lines. 	topic_ll
74921	4	355559	5	NULL	NULL	NULL	NULL	statement 2	Process		induce					apoptosis	Process				NULL	prostate cancer	NULL	NULL	NULL	NULL	NULL	NULL	Prior studies of GSE in Jurkat cells as well as prostate cancer show that GSE is highly effective in activating JNK enzymes and inducing apoptosis in those cell lines. 	topic_ll
74968	1	355561	5	NULL	NULL	0	NULL	Aloe-Emodin	Chemical		is present in					Rhubarb	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Aloe-Emodin, found in Rhubarb and Aloe, is also a pronounced JNK activator and apoptosis agent. Rhubarb is also a known blood thinner which could cause spontaneous bleeding in individuals with Thrombocytopenia or clinical HCL.	topic_ll
74969	2	355561	5	NULL	NULL	0	NULL	Aloe-Emodin	Chemical		is present in					Aloe	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Aloe-Emodin, found in Rhubarb and Aloe, is also a pronounced JNK activator and apoptosis agent. Rhubarb is also a known blood thinner which could cause spontaneous bleeding in individuals with Thrombocytopenia or clinical HCL.	topic_ll
74970	3	355561	5	NULL	NULL	0	NULL	Aloe-Emodin	Chemical		is an activator of		pronounced			JNK	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Aloe-Emodin, found in Rhubarb and Aloe, is also a pronounced JNK activator and apoptosis agent. Rhubarb is also a known blood thinner which could cause spontaneous bleeding in individuals with Thrombocytopenia or clinical HCL.	topic_ll
74971	4	355561	5	NULL	NULL	0	NULL	Aloe-Emodin	Chemical		is a type of					apoptosis agent	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Aloe-Emodin, found in Rhubarb and Aloe, is also a pronounced JNK activator and apoptosis agent. Rhubarb is also a known blood thinner which could cause spontaneous bleeding in individuals with Thrombocytopenia or clinical HCL.	topic_ll
74972	5	355561	5	NULL	NULL	0	NULL	Rhubarb	Chemical		is a type of					blood thinner	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Aloe-Emodin, found in Rhubarb and Aloe, is also a pronounced JNK activator and apoptosis agent. Rhubarb is also a known blood thinner which could cause spontaneous bleeding in individuals with Thrombocytopenia or clinical HCL.	topic_ll
74973	6	355561	5	NULL	NULL	0	NULL	Rhubarb	Chemical		cause					spontaneous bleeding	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Aloe-Emodin, found in Rhubarb and Aloe, is also a pronounced JNK activator and apoptosis agent. Rhubarb is also a known blood thinner which could cause spontaneous bleeding in individuals with Thrombocytopenia or clinical HCL.	topic_ll
74974	7	355561	5	NULL	NULL	0	NULL	statement 6	Process		occurs in					Thrombocytopenia individuals	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Aloe-Emodin, found in Rhubarb and Aloe, is also a pronounced JNK activator and apoptosis agent. Rhubarb is also a known blood thinner which could cause spontaneous bleeding in individuals with Thrombocytopenia or clinical HCL.	topic_ll
74975	8	355561	5	NULL	NULL	0	NULL	statement 6	Process		occurs in					clinical HCL individuals	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Aloe-Emodin, found in Rhubarb and Aloe, is also a pronounced JNK activator and apoptosis agent. Rhubarb is also a known blood thinner which could cause spontaneous bleeding in individuals with Thrombocytopenia or clinical HCL.	topic_ll
74976	1	355562	5	NULL	NULL	0	NULL	decoy IL-1 receptor	GP		is present in					hairy cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	This same research indicates that hairy cells may have a decoy IL-1 (interleukin) receptor 	topic_ll
74977	2	355562	5	NULL	NULL	0	NULL	IL	GP		is					interleukin	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	This same research indicates that hairy cells may have a decoy IL-1 (interleukin) receptor 	topic_ll
74978	1	355563	5	NULL	NULL	0	NULL	hairy cell leukemia	MedicalFinding		consumes					cholesterol	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	hairy cell leukemia also consumes cholesterol. Several studies have shown that hairy cells contain more cholesterol than their normal B-cell counterparts. Likewise, patients with hairy cell leukemia typically have low levels of both LDL (bad) and HDL (good) cholesterol.	topic_ll
74979	2	355563	5	NULL	NULL	0	NULL	hairy cells	Cell		contains					cholesterol	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	hairy cell leukemia also consumes cholesterol. Several studies have shown that hairy cells contain more cholesterol than their normal B-cell counterparts. Likewise, patients with hairy cell leukemia typically have low levels of both LDL (bad) and HDL (good) cholesterol.	topic_ll
74980	3	355563	5	NULL	NULL	0	NULL	B-cell counterparts	Cell	normal	contains					cholesterol	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	hairy cell leukemia also consumes cholesterol. Several studies have shown that hairy cells contain more cholesterol than their normal B-cell counterparts. Likewise, patients with hairy cell leukemia typically have low levels of both LDL (bad) and HDL (good) cholesterol.	topic_ll
74981	4	355563	5	NULL	NULL	0	NULL	statement 2	Process		is more than					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	hairy cell leukemia also consumes cholesterol. Several studies have shown that hairy cells contain more cholesterol than their normal B-cell counterparts. Likewise, patients with hairy cell leukemia typically have low levels of both LDL (bad) and HDL (good) cholesterol.	topic_ll
74982	5	355563	5	NULL	NULL	0	NULL	LDL Cholestrol	Chemical	level of	is low in					hairy cell leukemia pateints	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	hairy cell leukemia also consumes cholesterol. Several studies have shown that hairy cells contain more cholesterol than their normal B-cell counterparts. Likewise, patients with hairy cell leukemia typically have low levels of both LDL (bad) and HDL (good) cholesterol.	topic_ll
74983	6	355563	5	NULL	NULL	0	NULL	HDL Cholestrol	Chemical	level of	is low in					hairy cell leukemia pateints	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	hairy cell leukemia also consumes cholesterol. Several studies have shown that hairy cells contain more cholesterol than their normal B-cell counterparts. Likewise, patients with hairy cell leukemia typically have low levels of both LDL (bad) and HDL (good) cholesterol.	topic_ll
74997	1	355564	5	NULL	NULL	0	NULL	LDL cholesterol	Chemical	level of	is low in					 hairy cell leukemia patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Likewise, patients with hairy cell leukemia typically have low levels of both LDL (bad) and HDL (good) cholesterol.	topic_ll
74998	2	355564	5	NULL	NULL	0	NULL	HDL cholesterol	Chemical	level of	is low in					hairy cell leukemia patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Likewise, patients with hairy cell leukemia typically have low levels of both LDL (bad) and HDL (good) cholesterol.	topic_ll
75002	1	355565	5	NULL	NULL	0	NULL	Theory of Mind deficit	MedicalFinding		is observed in					autistic individuals	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	It is now widely accepted that individuals with autism have a Theory of Mind (ToM) or mentalizing deficit	topic_aut
75003	2	355565	5	NULL	NULL	0	NULL	Theory of Mind	MentalProcess		is also known as					mentalizing	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	It is now widely accepted that individuals with autism have a Theory of Mind (ToM) or mentalizing deficit	topic_aut
76482	1	355580	7	NULL	NULL	0	NULL	migraine	MedicalFinding		associated with					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	There would also be a trend towards an association of migraine with bipolar disorder, but not with substance abuse/dependence.	topic_bd
76483	2	355580	7	NULL	NULL	0	NULL	migraine	MedicalFinding		not associated with					substance abuse/dependence	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	There would also be a trend towards an association of migraine with bipolar disorder, but not with substance abuse/dependence.	topic_bd
75004	1	355589	5	NULL	NULL	0	NULL	PBSCs	Cell		is					peripheral blood stem cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	These multipotent peripheral blood stem cells, or PBSCs, can be used just like bone marrow stem cells to treat leukemia, other cancers and various blood disorders. 	topic_ll
75005	2	355589	5	NULL	NULL	0	NULL	bone marrow stem cells	Cell		is used to treat					leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	These multipotent peripheral blood stem cells, or PBSCs, can be used just like bone marrow stem cells to treat leukemia, other cancers and various blood disorders. 	topic_ll
75006	3	355589	5	NULL	NULL	0	NULL	PBSCs	Cell	multipotent 	is used to treat					leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	These multipotent peripheral blood stem cells, or PBSCs, can be used just like bone marrow stem cells to treat leukemia, other cancers and various blood disorders. 	topic_ll
75007	4	355589	5	NULL	NULL	NULL	NULL	PBSCs	Cell	multipotent	is used to treat					cancer	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	These multipotent peripheral blood stem cells, or PBSCs, can be used just like bone marrow stem cells to treat leukemia, other cancers and various blood disorders. 	topic_ll
75008	5	355589	5	NULL	NULL	0	NULL	PBSCs	Cell	multipotent	is used to treat					 blood disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	These multipotent peripheral blood stem cells, or PBSCs, can be used just like bone marrow stem cells to treat leukemia, other cancers and various blood disorders. 	topic_ll
75009	1	355590	5	NULL	NULL	0	NULL	stem-cell-rich blood	OrganismPart	multipotent	is present in					umbilical cord	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	the multipotent-stem-cell-rich blood found in the umbilical cord has proven useful in treating the same types of health problems as those treated using bone marrow stem cells and PBSCs. Umbilical cord blood stem cell transplants are less prone to rejection than either bone marrow or peripheral blood stem cells.	topic_ll
75014	2	355590	5	NULL	NULL	NULL	NULL	stem cell transplants	Cell	umbilical cord blood 	is prone to					rejection	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	the multipotent-stem-cell-rich blood found in the umbilical cord has proven useful in treating the same types of health problems as those treated using bone marrow stem cells and PBSCs. Umbilical cord blood stem cell transplants are less prone to rejection than either bone marrow or peripheral blood stem cells.	topic_ll
75015	3	355590	5	NULL	NULL	0	NULL	bone marrow	OrganismPart		is prone to					rejection	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	the multipotent-stem-cell-rich blood found in the umbilical cord has proven useful in treating the same types of health problems as those treated using bone marrow stem cells and PBSCs. Umbilical cord blood stem cell transplants are less prone to rejection than either bone marrow or peripheral blood stem cells.	topic_ll
75016	4	355590	5	NULL	NULL	0	NULL	peripheral blood stem cells	Cell		is prone to					rejection	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	the multipotent-stem-cell-rich blood found in the umbilical cord has proven useful in treating the same types of health problems as those treated using bone marrow stem cells and PBSCs. Umbilical cord blood stem cell transplants are less prone to rejection than either bone marrow or peripheral blood stem cells.	topic_ll
75017	5	355590	5	NULL	NULL	0	NULL	statement 2	Process		lesser than					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	the multipotent-stem-cell-rich blood found in the umbilical cord has proven useful in treating the same types of health problems as those treated using bone marrow stem cells and PBSCs. Umbilical cord blood stem cell transplants are less prone to rejection than either bone marrow or peripheral blood stem cells.	topic_ll
75018	6	355590	5	NULL	NULL	0	NULL	statement 2	Process		lesser than					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	the multipotent-stem-cell-rich blood found in the umbilical cord has proven useful in treating the same types of health problems as those treated using bone marrow stem cells and PBSCs. Umbilical cord blood stem cell transplants are less prone to rejection than either bone marrow or peripheral blood stem cells.	topic_ll
75023	1	355591	5	NULL	NULL	0	NULL	HyperCVAD	Chemical		is a type of					chemotherapy regimen	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	HyperCVAD is a chemotherapy regimen used to treat some forms of leukemia, non-Hodgkin lymphoma (high grade) and lymphoblastic lymphoma.	topic_ll
75024	2	355591	5	NULL	NULL	0	NULL	HyperCVAD	Chemical		is used to treat					leukemia	MedicalFinding	some forms of			NULL		0	NULL	NULL	NULL	NULL	NULL	HyperCVAD is a chemotherapy regimen used to treat some forms of leukemia, non-Hodgkin lymphoma (high grade) and lymphoblastic lymphoma.	topic_ll
75025	3	355591	5	NULL	NULL	0	NULL	HyperCVAD	Chemical		is used to treat					non-Hodgkin lymphoma (high grade)	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	HyperCVAD is a chemotherapy regimen used to treat some forms of leukemia, non-Hodgkin lymphoma (high grade) and lymphoblastic lymphoma.	topic_ll
75026	4	355591	5	NULL	NULL	0	NULL	HyperCVAD	Chemical		is used to treat					lymphoblastic lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	HyperCVAD is a chemotherapy regimen used to treat some forms of leukemia, non-Hodgkin lymphoma (high grade) and lymphoblastic lymphoma.	topic_ll
75029	1	355593	5	NULL	NULL	NULL	NULL	vegetables	Organism	consumption of	reduce					leukemia	MedicalFinding	risk of;;adult			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Diet and Adult Leukemia Risk: The findings of this study indicate that people eating at least three to four servings of vegetables per day appear to have 44% lower risk when compared to people eating less vegetables. 	topic_ll
75031	1	355594	5	NULL	NULL	0	NULL	fruit	OrganismPart		rich in					vitamin C	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Overall, the study results suggest that during the first two years of life, regular consumption of fruits and fruit juices high in vitamin C and or potassium may reduce the risk of childhood leukemia	topic_ll
75033	2	355594	5	NULL	NULL	0	NULL	fruit juice	AbstractConcept		rich in					vitamin C	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Overall, the study results suggest that during the first two years of life, regular consumption of fruits and fruit juices high in vitamin C and or potassium may reduce the risk of childhood leukemia	topic_ll
75034	3	355594	5	NULL	NULL	0	NULL	fruit	OrganismPart		rich in					potassium	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Overall, the study results suggest that during the first two years of life, regular consumption of fruits and fruit juices high in vitamin C and or potassium may reduce the risk of childhood leukemia	topic_ll
75035	4	355594	5	NULL	NULL	0	NULL	fruit juice	AbstractConcept		rich in					potassium	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Overall, the study results suggest that during the first two years of life, regular consumption of fruits and fruit juices high in vitamin C and or potassium may reduce the risk of childhood leukemia	topic_ll
75037	5	355594	5	NULL	NULL	0	NULL	statement 1	Process	regular consumption of	reduce					leukemia	MedicalFinding	risk of;;childhood			NULL		0	NULL	NULL	NULL	NULL	NULL	Overall, the study results suggest that during the first two years of life, regular consumption of fruits and fruit juices high in vitamin C and or potassium may reduce the risk of childhood leukemia	topic_ll
75038	6	355594	5	NULL	NULL	0	NULL	statement 2	Process	regular consumption of	reduce					leukemia	MedicalFinding	risk of;;childhood			NULL		0	NULL	NULL	NULL	NULL	NULL	Overall, the study results suggest that during the first two years of life, regular consumption of fruits and fruit juices high in vitamin C and or potassium may reduce the risk of childhood leukemia	topic_ll
75040	7	355594	5	NULL	NULL	0	NULL	statement 3	Process	regular consumption of	reduce					leukemia	MedicalFinding	risk of;;childhood			NULL		0	NULL	NULL	NULL	NULL	NULL	Overall, the study results suggest that during the first two years of life, regular consumption of fruits and fruit juices high in vitamin C and or potassium may reduce the risk of childhood leukemia	topic_ll
75042	8	355594	5	NULL	NULL	0	NULL	statement 4	Process	regular consumption of	reduce					leukemia	MedicalFinding	risk of;;childhood			NULL		0	NULL	NULL	NULL	NULL	NULL	Overall, the study results suggest that during the first two years of life, regular consumption of fruits and fruit juices high in vitamin C and or potassium may reduce the risk of childhood leukemia	topic_ll
75043	1	355595	5	NULL	NULL	0	NULL	bioflavonoids	Chemical		breaks					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientists from the University of Chicago Medical Center have found molecular evidence that bioflavonoids, which are ordinarily considered quite beneficial, can cause breaks in DNA that could trigger the development of infant leukemias.	topic_ll
75044	2	355595	5	NULL	NULL	0	NULL	statement 1	Process		triggers					leukemia	MedicalFinding	development of;;infant			NULL		0	NULL	NULL	NULL	NULL	NULL	Scientists from the University of Chicago Medical Center have found molecular evidence that bioflavonoids, which are ordinarily considered quite beneficial, can cause breaks in DNA that could trigger the development of infant leukemias.	topic_ll
75045	1	355596	5	NULL	NULL	0	NULL	bioflavonoids	Chemical		breaks					DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientists from the University of Chicago Medical Center have found molecular evidence that bioflavonoids, which are ordinarily considered quite beneficial, can cause breaks in DNA that could trigger the development of infant leukemias. Certain types of bioflavonoids, especially the flavonols, were more powerful topo-II inhibitors than others. For example, two different forms of quercetin, a dietary supplement, and fisetin, which is derived from herbs, were equal to VP16 in triggering MLL cleavage. 	topic_ll
75046	2	355596	5	NULL	NULL	0	NULL	statement 1	Process		triggers					leukemia	MedicalFinding	development of;;infant			NULL		0	NULL	NULL	NULL	NULL	NULL	Scientists from the University of Chicago Medical Center have found molecular evidence that bioflavonoids, which are ordinarily considered quite beneficial, can cause breaks in DNA that could trigger the development of infant leukemias. Certain types of bioflavonoids, especially the flavonols, were more powerful topo-II inhibitors than others. For example, two different forms of quercetin, a dietary supplement, and fisetin, which is derived from herbs, were equal to VP16 in triggering MLL cleavage. 	topic_ll
75047	3	355596	5	NULL	NULL	0	NULL	flavonols	Chemical		is a type of					bioflavonoids	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientists from the University of Chicago Medical Center have found molecular evidence that bioflavonoids, which are ordinarily considered quite beneficial, can cause breaks in DNA that could trigger the development of infant leukemias. Certain types of bioflavonoids, especially the flavonols, were more powerful topo-II inhibitors than others. For example, two different forms of quercetin, a dietary supplement, and fisetin, which is derived from herbs, were equal to VP16 in triggering MLL cleavage. 	topic_ll
75048	4	355596	5	NULL	NULL	0	NULL	flavonols	Chemical		is an inhibitor of		powerful			topo-II	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientists from the University of Chicago Medical Center have found molecular evidence that bioflavonoids, which are ordinarily considered quite beneficial, can cause breaks in DNA that could trigger the development of infant leukemias. Certain types of bioflavonoids, especially the flavonols, were more powerful topo-II inhibitors than others. For example, two different forms of quercetin, a dietary supplement, and fisetin, which is derived from herbs, were equal to VP16 in triggering MLL cleavage. 	topic_ll
75049	5	355596	5	NULL	NULL	0	NULL	VP16	Chemical		triggers					MLL	GP	cleavage of			NULL		0	NULL	NULL	NULL	NULL	NULL	Scientists from the University of Chicago Medical Center have found molecular evidence that bioflavonoids, which are ordinarily considered quite beneficial, can cause breaks in DNA that could trigger the development of infant leukemias. Certain types of bioflavonoids, especially the flavonols, were more powerful topo-II inhibitors than others. For example, two different forms of quercetin, a dietary supplement, and fisetin, which is derived from herbs, were equal to VP16 in triggering MLL cleavage. 	topic_ll
75050	6	355596	5	NULL	NULL	0	NULL	quercetin	Chemical		is a type of					dietary supplement	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientists from the University of Chicago Medical Center have found molecular evidence that bioflavonoids, which are ordinarily considered quite beneficial, can cause breaks in DNA that could trigger the development of infant leukemias. Certain types of bioflavonoids, especially the flavonols, were more powerful topo-II inhibitors than others. For example, two different forms of quercetin, a dietary supplement, and fisetin, which is derived from herbs, were equal to VP16 in triggering MLL cleavage. 	topic_ll
75177	7	355596	5	NULL	NULL	0	NULL	fisetin	Chemical		is derived from					herbs	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientists from the University of Chicago Medical Center have found molecular evidence that bioflavonoids, which are ordinarily considered quite beneficial, can cause breaks in DNA that could trigger the development of infant leukemias. Certain types of bioflavonoids, especially the flavonols, were more powerful topo-II inhibitors than others. For example, two different forms of quercetin, a dietary supplement, and fisetin, which is derived from herbs, were equal to VP16 in triggering MLL cleavage. 	topic_ll
75178	8	355596	5	NULL	NULL	0	NULL	fisetin	Chemical		trigger					MLL	GP	cleavage of			NULL		0	NULL	NULL	NULL	NULL	NULL	Scientists from the University of Chicago Medical Center have found molecular evidence that bioflavonoids, which are ordinarily considered quite beneficial, can cause breaks in DNA that could trigger the development of infant leukemias. Certain types of bioflavonoids, especially the flavonols, were more powerful topo-II inhibitors than others. For example, two different forms of quercetin, a dietary supplement, and fisetin, which is derived from herbs, were equal to VP16 in triggering MLL cleavage. 	topic_ll
75179	9	355596	5	NULL	NULL	0	NULL	quercetin	Chemical		trigger					MLL	GP	cleavage of			NULL		0	NULL	NULL	NULL	NULL	NULL	Scientists from the University of Chicago Medical Center have found molecular evidence that bioflavonoids, which are ordinarily considered quite beneficial, can cause breaks in DNA that could trigger the development of infant leukemias. Certain types of bioflavonoids, especially the flavonols, were more powerful topo-II inhibitors than others. For example, two different forms of quercetin, a dietary supplement, and fisetin, which is derived from herbs, were equal to VP16 in triggering MLL cleavage. 	topic_ll
75180	10	355596	5	NULL	NULL	0	NULL	statement 8	Process		is equal to					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientists from the University of Chicago Medical Center have found molecular evidence that bioflavonoids, which are ordinarily considered quite beneficial, can cause breaks in DNA that could trigger the development of infant leukemias. Certain types of bioflavonoids, especially the flavonols, were more powerful topo-II inhibitors than others. For example, two different forms of quercetin, a dietary supplement, and fisetin, which is derived from herbs, were equal to VP16 in triggering MLL cleavage. 	topic_ll
75181	11	355596	5	NULL	NULL	0	NULL	statement 9	Process		is equal to					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientists from the University of Chicago Medical Center have found molecular evidence that bioflavonoids, which are ordinarily considered quite beneficial, can cause breaks in DNA that could trigger the development of infant leukemias. Certain types of bioflavonoids, especially the flavonols, were more powerful topo-II inhibitors than others. For example, two different forms of quercetin, a dietary supplement, and fisetin, which is derived from herbs, were equal to VP16 in triggering MLL cleavage. 	topic_ll
75182	1	355599	5	NULL	NULL	0	NULL	MLL	GP		is a type of					promiscuous gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	MLL is a promiscuous gene. Once broken, it can reconnect with any of more than 40 other genes in a translocation, a process that involves an exchange of DNA between two chromosomes. Extensive recombinations usually cause cell death; but subtle translocations involving MLL can result in the rapid, uncontrolled cell division seen in leukemia.	topic_ll
75183	2	355599	5	NULL	NULL	0	NULL	MLL gene	GP	broken	reconnect with					gene	GP	any			NULL		0	NULL	NULL	NULL	NULL	NULL	MLL is a promiscuous gene. Once broken, it can reconnect with any of more than 40 other genes in a translocation, a process that involves an exchange of DNA between two chromosomes. Extensive recombinations usually cause cell death; but subtle translocations involving MLL can result in the rapid, uncontrolled cell division seen in leukemia.	topic_ll
75184	3	355599	5	NULL	NULL	0	NULL	statement 2	Process		occurs during					translocation	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	MLL is a promiscuous gene. Once broken, it can reconnect with any of more than 40 other genes in a translocation, a process that involves an exchange of DNA between two chromosomes. Extensive recombinations usually cause cell death; but subtle translocations involving MLL can result in the rapid, uncontrolled cell division seen in leukemia.	topic_ll
75185	4	355599	5	NULL	NULL	0	NULL	DNA	NucleicAcid		is exchanged between					chromosomes	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	MLL is a promiscuous gene. Once broken, it can reconnect with any of more than 40 other genes in a translocation, a process that involves an exchange of DNA between two chromosomes. Extensive recombinations usually cause cell death; but subtle translocations involving MLL can result in the rapid, uncontrolled cell division seen in leukemia.	topic_ll
75186	5	355599	5	NULL	NULL	0	NULL	translocation	Process		involves					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	MLL is a promiscuous gene. Once broken, it can reconnect with any of more than 40 other genes in a translocation, a process that involves an exchange of DNA between two chromosomes. Extensive recombinations usually cause cell death; but subtle translocations involving MLL can result in the rapid, uncontrolled cell division seen in leukemia.	topic_ll
75187	6	355599	5	NULL	NULL	0	NULL	recombinations	Process	extensive	cause		usually			cell death	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	MLL is a promiscuous gene. Once broken, it can reconnect with any of more than 40 other genes in a translocation, a process that involves an exchange of DNA between two chromosomes. Extensive recombinations usually cause cell death; but subtle translocations involving MLL can result in the rapid, uncontrolled cell division seen in leukemia.	topic_ll
75188	7	355599	5	NULL	NULL	0	NULL	translocation	Process	subtle	involve					MLL	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	MLL is a promiscuous gene. Once broken, it can reconnect with any of more than 40 other genes in a translocation, a process that involves an exchange of DNA between two chromosomes. Extensive recombinations usually cause cell death; but subtle translocations involving MLL can result in the rapid, uncontrolled cell division seen in leukemia.	topic_ll
75189	8	355599	5	NULL	NULL	0	NULL	statement 7	Process		results in					cell division	Process	repid;;uncontrolled			NULL		0	NULL	NULL	NULL	NULL	NULL	MLL is a promiscuous gene. Once broken, it can reconnect with any of more than 40 other genes in a translocation, a process that involves an exchange of DNA between two chromosomes. Extensive recombinations usually cause cell death; but subtle translocations involving MLL can result in the rapid, uncontrolled cell division seen in leukemia.	topic_ll
75190	9	355599	5	NULL	NULL	0	NULL	statement 8	Process		is seen in					leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	MLL is a promiscuous gene. Once broken, it can reconnect with any of more than 40 other genes in a translocation, a process that involves an exchange of DNA between two chromosomes. Extensive recombinations usually cause cell death; but subtle translocations involving MLL can result in the rapid, uncontrolled cell division seen in leukemia.	topic_ll
75191	1	355600	5	NULL	NULL	0	NULL	VP16	Chemical		is a type of					anti-cancer drug	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The DNA damage seen after exposure to either bioflavonoids or to anti-cancer drugs VP16 or doxorubicin (Dox) was identical, affecting one small region of the MLL gene. Although most adult leukemias involving MLL affect a different part of the gene, the breakpoints found in infant leukemias and secondary leukemias occur predominantly in the small region altered by the bioflavonoids.	topic_ll
75192	2	355600	5	NULL	NULL	0	NULL	Dox	Chemical		is					doxorubicin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The DNA damage seen after exposure to either bioflavonoids or to anti-cancer drugs VP16 or doxorubicin (Dox) was identical, affecting one small region of the MLL gene. Although most adult leukemias involving MLL affect a different part of the gene, the breakpoints found in infant leukemias and secondary leukemias occur predominantly in the small region altered by the bioflavonoids.	topic_ll
75193	3	355600	5	NULL	NULL	0	NULL	doxorubicin	Chemical		is a type of					anti-cancer drug	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The DNA damage seen after exposure to either bioflavonoids or to anti-cancer drugs VP16 or doxorubicin (Dox) was identical, affecting one small region of the MLL gene. Although most adult leukemias involving MLL affect a different part of the gene, the breakpoints found in infant leukemias and secondary leukemias occur predominantly in the small region altered by the bioflavonoids.	topic_ll
75194	4	355600	5	NULL	NULL	0	NULL	bioflavonoids	Chemical	exposure	leads to					DNA damage	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The DNA damage seen after exposure to either bioflavonoids or to anti-cancer drugs VP16 or doxorubicin (Dox) was identical, affecting one small region of the MLL gene. Although most adult leukemias involving MLL affect a different part of the gene, the breakpoints found in infant leukemias and secondary leukemias occur predominantly in the small region altered by the bioflavonoids.	topic_ll
75195	5	355600	5	NULL	NULL	0	NULL	VP16	Chemical	exposure	leads to					DNA damage	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The DNA damage seen after exposure to either bioflavonoids or to anti-cancer drugs VP16 or doxorubicin (Dox) was identical, affecting one small region of the MLL gene. Although most adult leukemias involving MLL affect a different part of the gene, the breakpoints found in infant leukemias and secondary leukemias occur predominantly in the small region altered by the bioflavonoids.	topic_ll
75196	6	355600	5	NULL	NULL	0	NULL	doxorubicin	Chemical	exposure	leads to					DNA damage	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The DNA damage seen after exposure to either bioflavonoids or to anti-cancer drugs VP16 or doxorubicin (Dox) was identical, affecting one small region of the MLL gene. Although most adult leukemias involving MLL affect a different part of the gene, the breakpoints found in infant leukemias and secondary leukemias occur predominantly in the small region altered by the bioflavonoids.	topic_ll
75197	7	355600	5	NULL	NULL	0	NULL	statement 4	Process		identical to					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The DNA damage seen after exposure to either bioflavonoids or to anti-cancer drugs VP16 or doxorubicin (Dox) was identical, affecting one small region of the MLL gene. Although most adult leukemias involving MLL affect a different part of the gene, the breakpoints found in infant leukemias and secondary leukemias occur predominantly in the small region altered by the bioflavonoids.	topic_ll
75198	8	355600	5	NULL	NULL	0	NULL	statement 5	Process		identical to					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The DNA damage seen after exposure to either bioflavonoids or to anti-cancer drugs VP16 or doxorubicin (Dox) was identical, affecting one small region of the MLL gene. Although most adult leukemias involving MLL affect a different part of the gene, the breakpoints found in infant leukemias and secondary leukemias occur predominantly in the small region altered by the bioflavonoids.	topic_ll
75199	9	355600	5	NULL	NULL	0	NULL	statement 4	Process		affect					MLL gene	GP	small region of			NULL		0	NULL	NULL	NULL	NULL	NULL	The DNA damage seen after exposure to either bioflavonoids or to anti-cancer drugs VP16 or doxorubicin (Dox) was identical, affecting one small region of the MLL gene. Although most adult leukemias involving MLL affect a different part of the gene, the breakpoints found in infant leukemias and secondary leukemias occur predominantly in the small region altered by the bioflavonoids.	topic_ll
75200	10	355600	5	NULL	NULL	0	NULL	statement 5	Process		affect					MLL gene	GP	small region of			NULL		0	NULL	NULL	NULL	NULL	NULL	The DNA damage seen after exposure to either bioflavonoids or to anti-cancer drugs VP16 or doxorubicin (Dox) was identical, affecting one small region of the MLL gene. Although most adult leukemias involving MLL affect a different part of the gene, the breakpoints found in infant leukemias and secondary leukemias occur predominantly in the small region altered by the bioflavonoids.	topic_ll
75201	11	355600	5	NULL	NULL	0	NULL	statement 6	Process		affect					MLL gene	GP	small region of			NULL		0	NULL	NULL	NULL	NULL	NULL	The DNA damage seen after exposure to either bioflavonoids or to anti-cancer drugs VP16 or doxorubicin (Dox) was identical, affecting one small region of the MLL gene. Although most adult leukemias involving MLL affect a different part of the gene, the breakpoints found in infant leukemias and secondary leukemias occur predominantly in the small region altered by the bioflavonoids.	topic_ll
75224	12	355600	5	NULL	NULL	NULL	NULL	leukemia	MedicalFinding	adult	involve					MLL gene	GP	damage of;;different part of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	The DNA damage seen after exposure to either bioflavonoids or to anti-cancer drugs VP16 or doxorubicin (Dox) was identical, affecting one small region of the MLL gene. Although most adult leukemias involving MLL affect a different part of the gene, the breakpoints found in infant leukemias and secondary leukemias occur predominantly in the small region altered by the bioflavonoids.	topic_ll
75225	13	355600	5	NULL	NULL	0	NULL	statement 9	Process		leads to					leukemia	MedicalFinding	infant			NULL		0	NULL	NULL	NULL	NULL	NULL	The DNA damage seen after exposure to either bioflavonoids or to anti-cancer drugs VP16 or doxorubicin (Dox) was identical, affecting one small region of the MLL gene. Although most adult leukemias involving MLL affect a different part of the gene, the breakpoints found in infant leukemias and secondary leukemias occur predominantly in the small region altered by the bioflavonoids.	topic_ll
75226	14	355600	5	NULL	NULL	0	NULL	statement 9	Process		leads to					leukemia	MedicalFinding	secondary			NULL		0	NULL	NULL	NULL	NULL	NULL	The DNA damage seen after exposure to either bioflavonoids or to anti-cancer drugs VP16 or doxorubicin (Dox) was identical, affecting one small region of the MLL gene. Although most adult leukemias involving MLL affect a different part of the gene, the breakpoints found in infant leukemias and secondary leukemias occur predominantly in the small region altered by the bioflavonoids.	topic_ll
75227	1	355601	5	NULL	NULL	0	NULL	bioflavonoids	Chemical		cause					DNA damage	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Some bioflavonoids were as active in causing DNA damage as the powerful anti-cancer drug etoposide (VP16), which has been tied to secondary leukemias--cancers of the bone marrow that result from previous anti-cancer therapy.	topic_ll
75228	2	355601	5	NULL	NULL	0	NULL	VP16	Chemical		cause					DNA damage	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Some bioflavonoids were as active in causing DNA damage as the powerful anti-cancer drug etoposide (VP16), which has been tied to secondary leukemias--cancers of the bone marrow that result from previous anti-cancer therapy.	topic_ll
75229	3	355601	5	NULL	NULL	0	NULL	bioflavonoids	Chemical		is as active as					VP16	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Some bioflavonoids were as active in causing DNA damage as the powerful anti-cancer drug etoposide (VP16), which has been tied to secondary leukemias--cancers of the bone marrow that result from previous anti-cancer therapy.	topic_ll
75230	4	355601	5	NULL	NULL	0	NULL	VP16	Chemical		is also known as					etoposide	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Some bioflavonoids were as active in causing DNA damage as the powerful anti-cancer drug etoposide (VP16), which has been tied to secondary leukemias--cancers of the bone marrow that result from previous anti-cancer therapy.	topic_ll
75231	5	355601	5	NULL	NULL	0	NULL	etoposide	Chemical		is a type of					anti-cancer drug	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Some bioflavonoids were as active in causing DNA damage as the powerful anti-cancer drug etoposide (VP16), which has been tied to secondary leukemias--cancers of the bone marrow that result from previous anti-cancer therapy.	topic_ll
75232	6	355601	5	NULL	NULL	0	NULL	VP16	Chemical		is associated with					leukemia	MedicalFinding	secondary			NULL		0	NULL	NULL	NULL	NULL	NULL	Some bioflavonoids were as active in causing DNA damage as the powerful anti-cancer drug etoposide (VP16), which has been tied to secondary leukemias--cancers of the bone marrow that result from previous anti-cancer therapy.	topic_ll
75233	7	355601	5	NULL	NULL	0	NULL	bone marrow cancer	MedicalFinding		results from					anti-cancer therapy	MedicalProcedure	previous			NULL		0	NULL	NULL	NULL	NULL	NULL	Some bioflavonoids were as active in causing DNA damage as the powerful anti-cancer drug etoposide (VP16), which has been tied to secondary leukemias--cancers of the bone marrow that result from previous anti-cancer therapy.	topic_ll
75235	8	355601	5	NULL	NULL	0	NULL	statement 7	Process		is a type of					leukemia	MedicalFinding	secondary			NULL		0	NULL	NULL	NULL	NULL	NULL	Some bioflavonoids were as active in causing DNA damage as the powerful anti-cancer drug etoposide (VP16), which has been tied to secondary leukemias--cancers of the bone marrow that result from previous anti-cancer therapy.	topic_ll
75239	1	355602	5	NULL	NULL	0	NULL	leukemia	MedicalFinding	childhood	is a type of					cancer	MedicalFinding	childhood			NULL		0	NULL	NULL	NULL	NULL	NULL	A new study led by researchers at the University of California, Berkeley, suggests that women who eat more vegetables, fruit and foods containing protein before pregnancy may have a lower risk of having a child who develops leukemia, the most common childhood cancer in the United States. 	topic_ll
75240	2	355602	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					United States	GeographicLocation				NULL		0	NULL	NULL	NULL	NULL	NULL	A new study led by researchers at the University of California, Berkeley, suggests that women who eat more vegetables, fruit and foods containing protein before pregnancy may have a lower risk of having a child who develops leukemia, the most common childhood cancer in the United States. 	topic_ll
75376	1	355603	5	NULL	NULL	0	NULL	MLL	GP		is translocated in					ALL infants	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	The results show that 74% of infants with ALL had an MLL translocation; the most common partner genes were AF4, ENL, and AF9. Both AF4 (located on chromosome 4) and ENL (located on chromosome 19) negatively affected patient survival, whereas AF9 (located on chromosome 9) was associated with better survival.	topic_ll
75377	2	355603	5	NULL	NULL	0	NULL	AF4	GP		is a partner of					MLL	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The results show that 74% of infants with ALL had an MLL translocation; the most common partner genes were AF4, ENL, and AF9. Both AF4 (located on chromosome 4) and ENL (located on chromosome 19) negatively affected patient survival, whereas AF9 (located on chromosome 9) was associated with better survival.	topic_ll
75378	3	355603	5	NULL	NULL	0	NULL	ENL	GP		is a partner of					MLL	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The results show that 74% of infants with ALL had an MLL translocation; the most common partner genes were AF4, ENL, and AF9. Both AF4 (located on chromosome 4) and ENL (located on chromosome 19) negatively affected patient survival, whereas AF9 (located on chromosome 9) was associated with better survival.	topic_ll
75379	4	355603	5	NULL	NULL	0	NULL	AF9	GP		is a partner of					MLL	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The results show that 74% of infants with ALL had an MLL translocation; the most common partner genes were AF4, ENL, and AF9. Both AF4 (located on chromosome 4) and ENL (located on chromosome 19) negatively affected patient survival, whereas AF9 (located on chromosome 9) was associated with better survival.	topic_ll
75380	5	355603	5	NULL	NULL	0	NULL	AF4	GP		is located on					chromosome 4	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	The results show that 74% of infants with ALL had an MLL translocation; the most common partner genes were AF4, ENL, and AF9. Both AF4 (located on chromosome 4) and ENL (located on chromosome 19) negatively affected patient survival, whereas AF9 (located on chromosome 9) was associated with better survival.	topic_ll
75381	6	355603	5	NULL	NULL	0	NULL	ENL	GP		is located on					chromosome 19	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	The results show that 74% of infants with ALL had an MLL translocation; the most common partner genes were AF4, ENL, and AF9. Both AF4 (located on chromosome 4) and ENL (located on chromosome 19) negatively affected patient survival, whereas AF9 (located on chromosome 9) was associated with better survival.	topic_ll
75382	7	355603	5	NULL	NULL	0	NULL	AF4	GP		affects		negatively			ALL infants	GroupOfPeople	survival of			NULL		0	NULL	NULL	NULL	NULL	NULL	The results show that 74% of infants with ALL had an MLL translocation; the most common partner genes were AF4, ENL, and AF9. Both AF4 (located on chromosome 4) and ENL (located on chromosome 19) negatively affected patient survival, whereas AF9 (located on chromosome 9) was associated with better survival.	topic_ll
75383	8	355603	5	NULL	NULL	0	NULL	ENL	GP		affects		negatively			ALL infants	GroupOfPeople	survival of			NULL		0	NULL	NULL	NULL	NULL	NULL	The results show that 74% of infants with ALL had an MLL translocation; the most common partner genes were AF4, ENL, and AF9. Both AF4 (located on chromosome 4) and ENL (located on chromosome 19) negatively affected patient survival, whereas AF9 (located on chromosome 9) was associated with better survival.	topic_ll
75384	9	355603	5	NULL	NULL	0	NULL	AF9	GP		is located on					chromosome 9	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	The results show that 74% of infants with ALL had an MLL translocation; the most common partner genes were AF4, ENL, and AF9. Both AF4 (located on chromosome 4) and ENL (located on chromosome 19) negatively affected patient survival, whereas AF9 (located on chromosome 9) was associated with better survival.	topic_ll
75385	10	355603	5	NULL	NULL	0	NULL	AF9	GP		is associated with					ALL infants	GroupOfPeople	better survival of			NULL		0	NULL	NULL	NULL	NULL	NULL	The results show that 74% of infants with ALL had an MLL translocation; the most common partner genes were AF4, ENL, and AF9. Both AF4 (located on chromosome 4) and ENL (located on chromosome 19) negatively affected patient survival, whereas AF9 (located on chromosome 9) was associated with better survival.	topic_ll
75386	1	355604	5	NULL	NULL	0	NULL	MLL	GP		fuse with					AF4	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	that the less favorable fusion of MLL with AF4 was associated with a higher white count, and that the fusion of MLL with AF9 was associated with a lower white blood cell count.	topic_ll
75387	2	355604	5	NULL	NULL	NULL	NULL	statement 1	Process		is associated with					white blood cell count	MedicalProcedure	higher			NULL		NULL	NULL	NULL	NULL	NULL	NULL	that the less favorable fusion of MLL with AF4 was associated with a higher white count, and that the fusion of MLL with AF9 was associated with a lower white blood cell count.	topic_ll
75388	3	355604	5	NULL	NULL	0	NULL	MLL	GP		fuse with					AF9	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	that the less favorable fusion of MLL with AF4 was associated with a higher white count, and that the fusion of MLL with AF9 was associated with a lower white blood cell count.	topic_ll
75389	4	355604	5	NULL	NULL	0	NULL	statement 3	Process		is associated with					white blood cell count	MedicalProcedure	lower			NULL		0	NULL	NULL	NULL	NULL	NULL	that the less favorable fusion of MLL with AF4 was associated with a higher white count, and that the fusion of MLL with AF9 was associated with a lower white blood cell count.	topic_ll
75390	1	355606	5	NULL	NULL	0	NULL	MLL	GP		is translocated in					ALL infants	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	The results show that 74% of infants with ALL had an MLL translocation -  the most common partner genes were AF4, ENL, and AF9.	topic_ll
75391	2	355606	5	NULL	NULL	0	NULL	AF4	GP		is a partner of					MLL	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The results show that 74% of infants with ALL had an MLL translocation -  the most common partner genes were AF4, ENL, and AF9.	topic_ll
75392	3	355606	5	NULL	NULL	0	NULL	ENL	GP		is a partner of					MLL	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The results show that 74% of infants with ALL had an MLL translocation -  the most common partner genes were AF4, ENL, and AF9.	topic_ll
75393	4	355606	5	NULL	NULL	0	NULL	AF9	GP		is a partner of					MLL	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The results show that 74% of infants with ALL had an MLL translocation -  the most common partner genes were AF4, ENL, and AF9.	topic_ll
75394	1	355607	5	NULL	NULL	0	NULL	acute lymphoblastic leukemia	MedicalFinding	few cases of	is associated with					Down syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia: Although a few cases are associated with inherited genetic syndromes (ie, Down syndrome, Bloom syndrome, Fanconi anemia), the cause remains largely unknown. Many environmental factors (ie, exposure to ionizing radiation and electromagnetic fields, parental use of alcohol and tobacco) have been investigated as potential risk factors, but none has been definitively shown to cause acute lymphoblastic leukemia. 	topic_ll
75395	2	355607	5	NULL	NULL	0	NULL	acute lymphoblastic leukemia	MedicalFinding	few cases of	is associated with					Bloom syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia: Although a few cases are associated with inherited genetic syndromes (ie, Down syndrome, Bloom syndrome, Fanconi anemia), the cause remains largely unknown. Many environmental factors (ie, exposure to ionizing radiation and electromagnetic fields, parental use of alcohol and tobacco) have been investigated as potential risk factors, but none has been definitively shown to cause acute lymphoblastic leukemia. 	topic_ll
75396	3	355607	5	NULL	NULL	0	NULL	acute lymphoblastic leukemia	MedicalFinding		is associated with					Fanconi anemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia: Although a few cases are associated with inherited genetic syndromes (ie, Down syndrome, Bloom syndrome, Fanconi anemia), the cause remains largely unknown. Many environmental factors (ie, exposure to ionizing radiation and electromagnetic fields, parental use of alcohol and tobacco) have been investigated as potential risk factors, but none has been definitively shown to cause acute lymphoblastic leukemia. 	topic_ll
75397	4	355607	5	NULL	NULL	0	NULL	Down syndrome	MedicalFinding		is a type of					inherited genetic syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia: Although a few cases are associated with inherited genetic syndromes (ie, Down syndrome, Bloom syndrome, Fanconi anemia), the cause remains largely unknown. Many environmental factors (ie, exposure to ionizing radiation and electromagnetic fields, parental use of alcohol and tobacco) have been investigated as potential risk factors, but none has been definitively shown to cause acute lymphoblastic leukemia. 	topic_ll
75398	5	355607	5	NULL	NULL	0	NULL	Bloom syndrome	MedicalFinding		is a type of					inherited genetic syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia: Although a few cases are associated with inherited genetic syndromes (ie, Down syndrome, Bloom syndrome, Fanconi anemia), the cause remains largely unknown. Many environmental factors (ie, exposure to ionizing radiation and electromagnetic fields, parental use of alcohol and tobacco) have been investigated as potential risk factors, but none has been definitively shown to cause acute lymphoblastic leukemia. 	topic_ll
75399	6	355607	5	NULL	NULL	0	NULL	Fanconi anemia	MedicalFinding		is a type of					inherited genetic syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia: Although a few cases are associated with inherited genetic syndromes (ie, Down syndrome, Bloom syndrome, Fanconi anemia), the cause remains largely unknown. Many environmental factors (ie, exposure to ionizing radiation and electromagnetic fields, parental use of alcohol and tobacco) have been investigated as potential risk factors, but none has been definitively shown to cause acute lymphoblastic leukemia. 	topic_ll
75400	7	355607	5	NULL	NULL	0	NULL	ionizing radiation	PhysicalPhenomenon	exposure to	does not cause					acute lymphoblastic leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia: Although a few cases are associated with inherited genetic syndromes (ie, Down syndrome, Bloom syndrome, Fanconi anemia), the cause remains largely unknown. Many environmental factors (ie, exposure to ionizing radiation and electromagnetic fields, parental use of alcohol and tobacco) have been investigated as potential risk factors, but none has been definitively shown to cause acute lymphoblastic leukemia. 	topic_ll
75401	8	355607	5	NULL	NULL	0	NULL	electromagnetic fields	PhysicalPhenomenon	exposure to	does not cause					acute lymphoblastic leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia: Although a few cases are associated with inherited genetic syndromes (ie, Down syndrome, Bloom syndrome, Fanconi anemia), the cause remains largely unknown. Many environmental factors (ie, exposure to ionizing radiation and electromagnetic fields, parental use of alcohol and tobacco) have been investigated as potential risk factors, but none has been definitively shown to cause acute lymphoblastic leukemia. 	topic_ll
75402	9	355607	5	NULL	NULL	0	NULL	alcohol	Chemical	parental use of	does not cause					acute lymphoblastic leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia: Although a few cases are associated with inherited genetic syndromes (ie, Down syndrome, Bloom syndrome, Fanconi anemia), the cause remains largely unknown. Many environmental factors (ie, exposure to ionizing radiation and electromagnetic fields, parental use of alcohol and tobacco) have been investigated as potential risk factors, but none has been definitively shown to cause acute lymphoblastic leukemia. 	topic_ll
75403	10	355607	5	NULL	NULL	0	NULL	tobacco	Chemical	parental use of	does not cause					acute lymphoblastic leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia: Although a few cases are associated with inherited genetic syndromes (ie, Down syndrome, Bloom syndrome, Fanconi anemia), the cause remains largely unknown. Many environmental factors (ie, exposure to ionizing radiation and electromagnetic fields, parental use of alcohol and tobacco) have been investigated as potential risk factors, but none has been definitively shown to cause acute lymphoblastic leukemia. 	topic_ll
75404	11	355607	5	NULL	NULL	0	NULL	ionizing radiation	PhysicalPhenomenon		is a type of					environmental factor	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia: Although a few cases are associated with inherited genetic syndromes (ie, Down syndrome, Bloom syndrome, Fanconi anemia), the cause remains largely unknown. Many environmental factors (ie, exposure to ionizing radiation and electromagnetic fields, parental use of alcohol and tobacco) have been investigated as potential risk factors, but none has been definitively shown to cause acute lymphoblastic leukemia. 	topic_ll
75405	12	355607	5	NULL	NULL	0	NULL	electromagnetic fields	PhysicalPhenomenon		is a type of					environmental factor	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia: Although a few cases are associated with inherited genetic syndromes (ie, Down syndrome, Bloom syndrome, Fanconi anemia), the cause remains largely unknown. Many environmental factors (ie, exposure to ionizing radiation and electromagnetic fields, parental use of alcohol and tobacco) have been investigated as potential risk factors, but none has been definitively shown to cause acute lymphoblastic leukemia. 	topic_ll
75406	13	355607	5	NULL	NULL	0	NULL	alcohol	Chemical		is a type of					environmental factor	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia: Although a few cases are associated with inherited genetic syndromes (ie, Down syndrome, Bloom syndrome, Fanconi anemia), the cause remains largely unknown. Many environmental factors (ie, exposure to ionizing radiation and electromagnetic fields, parental use of alcohol and tobacco) have been investigated as potential risk factors, but none has been definitively shown to cause acute lymphoblastic leukemia. 	topic_ll
75407	14	355607	5	NULL	NULL	0	NULL	tobacco	Chemical		is a type of					environmental factor	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia: Although a few cases are associated with inherited genetic syndromes (ie, Down syndrome, Bloom syndrome, Fanconi anemia), the cause remains largely unknown. Many environmental factors (ie, exposure to ionizing radiation and electromagnetic fields, parental use of alcohol and tobacco) have been investigated as potential risk factors, but none has been definitively shown to cause acute lymphoblastic leukemia. 	topic_ll
75470	1	355608	5	NULL	NULL	0	NULL	Wiskott-Aldrich syndrome	MedicalFinding		is a type of					congenital immunodeficiencies	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia may also occur in children with various congenital immunodeficiencies (ie, Wiskott-Aldrich syndrome, congenital hypogammaglobulinemia, ataxia-telangiectasia) that have an increased predisposition to develop lymphoid malignancies.	topic_ll
75471	2	355608	5	NULL	NULL	0	NULL	congenital hypogammaglobulinemia	MedicalFinding		is a type of					congenital immunodeficiencies	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia may also occur in children with various congenital immunodeficiencies (ie, Wiskott-Aldrich syndrome, congenital hypogammaglobulinemia, ataxia-telangiectasia) that have an increased predisposition to develop lymphoid malignancies.	topic_ll
75473	3	355608	5	NULL	NULL	0	NULL	ataxia-telangiectasia	MedicalFinding		is a type of					congenital immunodeficiencies	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia may also occur in children with various congenital immunodeficiencies (ie, Wiskott-Aldrich syndrome, congenital hypogammaglobulinemia, ataxia-telangiectasia) that have an increased predisposition to develop lymphoid malignancies.	topic_ll
75474	4	355608	5	NULL	NULL	0	NULL	children	GroupOfPeople		suffer from					statement 1	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia may also occur in children with various congenital immunodeficiencies (ie, Wiskott-Aldrich syndrome, congenital hypogammaglobulinemia, ataxia-telangiectasia) that have an increased predisposition to develop lymphoid malignancies.	topic_ll
75475	5	355608	5	NULL	NULL	NULL	NULL	children	GroupOfPeople		suffer from					statement 2	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia may also occur in children with various congenital immunodeficiencies (ie, Wiskott-Aldrich syndrome, congenital hypogammaglobulinemia, ataxia-telangiectasia) that have an increased predisposition to develop lymphoid malignancies.	topic_ll
75476	6	355608	5	NULL	NULL	0	NULL	children	GroupOfPeople		suffer from					statement 3	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia may also occur in children with various congenital immunodeficiencies (ie, Wiskott-Aldrich syndrome, congenital hypogammaglobulinemia, ataxia-telangiectasia) that have an increased predisposition to develop lymphoid malignancies.	topic_ll
75477	7	355608	5	NULL	NULL	0	NULL	acute lymphoblastic leukemia	MedicalFinding		occurs in		may			statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia may also occur in children with various congenital immunodeficiencies (ie, Wiskott-Aldrich syndrome, congenital hypogammaglobulinemia, ataxia-telangiectasia) that have an increased predisposition to develop lymphoid malignancies.	topic_ll
75478	8	355608	5	NULL	NULL	0	NULL	acute lymphoblastic leukemia	MedicalFinding		occurs in		may			statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia may also occur in children with various congenital immunodeficiencies (ie, Wiskott-Aldrich syndrome, congenital hypogammaglobulinemia, ataxia-telangiectasia) that have an increased predisposition to develop lymphoid malignancies.	topic_ll
75479	9	355608	5	NULL	NULL	0	NULL	acute lymphoblastic leukemia	MedicalFinding		occurs in		may			statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia may also occur in children with various congenital immunodeficiencies (ie, Wiskott-Aldrich syndrome, congenital hypogammaglobulinemia, ataxia-telangiectasia) that have an increased predisposition to develop lymphoid malignancies.	topic_ll
75480	10	355608	5	NULL	NULL	0	NULL	statement 1	MedicalFinding		predisposed to develop		increase			lymphoid malignancies	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia may also occur in children with various congenital immunodeficiencies (ie, Wiskott-Aldrich syndrome, congenital hypogammaglobulinemia, ataxia-telangiectasia) that have an increased predisposition to develop lymphoid malignancies.	topic_ll
75481	11	355608	5	NULL	NULL	NULL	NULL	statement 2	MedicalFinding		predisposed to develop		increase			lymphoid malignancies	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia may also occur in children with various congenital immunodeficiencies (ie, Wiskott-Aldrich syndrome, congenital hypogammaglobulinemia, ataxia-telangiectasia) that have an increased predisposition to develop lymphoid malignancies.	topic_ll
75482	12	355608	5	NULL	NULL	0	NULL	statement 3	MedicalFinding		predisposed to develop		increase			lymphoid malignancies	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute lymphoblastic leukemia may also occur in children with various congenital immunodeficiencies (ie, Wiskott-Aldrich syndrome, congenital hypogammaglobulinemia, ataxia-telangiectasia) that have an increased predisposition to develop lymphoid malignancies.	topic_ll
75484	1	355609	5	NULL	NULL	0	NULL	virus	Organism		is linked to		may be			leukemia	MedicalFinding	development of			NULL		0	NULL	NULL	NULL	NULL	NULL	Various viruses may be linked to the development of leukemia, particularly when prenatal viral exposure occurs in mothers recently infected with influenza or varicella. 	topic_ll
75485	2	355609	5	NULL	NULL	0	NULL	mothers	GroupOfPeople		infected with		recently			influenza	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Various viruses may be linked to the development of leukemia, particularly when prenatal viral exposure occurs in mothers recently infected with influenza or varicella. 	topic_ll
75486	3	355609	5	NULL	NULL	0	NULL	mothers	GroupOfPeople		infected with		recently			varicella	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Various viruses may be linked to the development of leukemia, particularly when prenatal viral exposure occurs in mothers recently infected with influenza or varicella. 	topic_ll
75488	4	355609	5	NULL	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Various viruses may be linked to the development of leukemia, particularly when prenatal viral exposure occurs in mothers recently infected with influenza or varicella. 	topic_ll
75493	5	355609	5	NULL	NULL	0	NULL	statement 2	Process		is exposed to		prenatally			virus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Various viruses may be linked to the development of leukemia, particularly when prenatal viral exposure occurs in mothers recently infected with influenza or varicella. 	topic_ll
75495	6	355609	5	NULL	NULL	0	NULL	statement 5	Process		is associated with					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Various viruses may be linked to the development of leukemia, particularly when prenatal viral exposure occurs in mothers recently infected with influenza or varicella. 	topic_ll
75496	7	355609	5	NULL	NULL	0	NULL	statement 3	Process		is exposed to		prenatally			virus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Various viruses may be linked to the development of leukemia, particularly when prenatal viral exposure occurs in mothers recently infected with influenza or varicella. 	topic_ll
75497	8	355609	5	NULL	NULL	0	NULL	statement 7	Process		is associated with					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Various viruses may be linked to the development of leukemia, particularly when prenatal viral exposure occurs in mothers recently infected with influenza or varicella. 	topic_ll
76484	1	355610	11	NULL	NULL	0	NULL	Sulfonamide	Chemical		is also known as					sulfa drugs	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Sulfonamide is the basis of several groups of drugs. The original antibacterial sulfonamides (sometimes called simply sulfa drugs) are synthetic antimicrobial agents that contain the sulfonamide group	topic_mrs
76485	2	355610	11	NULL	NULL	0	NULL	Sulfonamide	Chemical		is a type of 					 synthetic antimicrobial agent	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Sulfonamide is the basis of several groups of drugs. The original antibacterial sulfonamides (sometimes called simply sulfa drugs) are synthetic antimicrobial agents that contain the sulfonamide group	topic_mrs
75614	1	355611	11	NULL	NULL	0	NULL	Staphylococcus aureus 	Organism		causes					skin and soft tissue infections	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Staphylococcus aureus skin and soft tissue infections (SSTI) in outpatients in Illinois, in the setting of increasing levels of community-associated methicillin resistant S. aureus (CA-MRSA).	topic_mrs
75615	2	355611	11	NULL	NULL	0	NULL	skin and soft tissue infections	MedicalFinding		is					SSTI	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Staphylococcus aureus skin and soft tissue infections (SSTI) in outpatients in Illinois, in the setting of increasing levels of community-associated methicillin resistant S. aureus (CA-MRSA).	topic_mrs
76486	1	355612	11	NULL	NULL	0	NULL	cutaneous abscess	MedicalFinding		treats by 					 incision	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	For a cutaneous abscess, incision and drainage is the primary treatment. For simple abscesses or boils, incision and drainage alone is likely to be adequate, but additional data are needed to further deﬁne the role of antibiotics, if any, in this setting.	topic_mrs
76487	2	355612	11	NULL	NULL	0	NULL	cutaneous abscess	MedicalFinding		treats by 					drainage	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	For a cutaneous abscess, incision and drainage is the primary treatment. For simple abscesses or boils, incision and drainage alone is likely to be adequate, but additional data are needed to further deﬁne the role of antibiotics, if any, in this setting.	topic_mrs
76488	3	355612	11	NULL	NULL	0	NULL	statement 1	Process		occurs along with					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	For a cutaneous abscess, incision and drainage is the primary treatment. For simple abscesses or boils, incision and drainage alone is likely to be adequate, but additional data are needed to further deﬁne the role of antibiotics, if any, in this setting.	topic_mrs
76489	4	355612	11	NULL	NULL	0	NULL	 simple abscesses	MedicalFinding		treats by 					incision	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	For a cutaneous abscess, incision and drainage is the primary treatment. For simple abscesses or boils, incision and drainage alone is likely to be adequate, but additional data are needed to further deﬁne the role of antibiotics, if any, in this setting.	topic_mrs
76490	5	355612	11	NULL	NULL	0	NULL	 simple abscesses	MedicalFinding		treats by 					drainage	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	For a cutaneous abscess, incision and drainage is the primary treatment. For simple abscesses or boils, incision and drainage alone is likely to be adequate, but additional data are needed to further deﬁne the role of antibiotics, if any, in this setting.	topic_mrs
76491	6	355612	11	NULL	NULL	0	NULL	statement 4	Process		occurs along with					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	For a cutaneous abscess, incision and drainage is the primary treatment. For simple abscesses or boils, incision and drainage alone is likely to be adequate, but additional data are needed to further deﬁne the role of antibiotics, if any, in this setting.	topic_mrs
76492	7	355612	11	NULL	NULL	0	NULL	boils	MedicalFinding		treats by 					incision	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	For a cutaneous abscess, incision and drainage is the primary treatment. For simple abscesses or boils, incision and drainage alone is likely to be adequate, but additional data are needed to further deﬁne the role of antibiotics, if any, in this setting.	topic_mrs
76493	8	355612	11	NULL	NULL	0	NULL	boils	MedicalFinding		treats by 					drainage	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	For a cutaneous abscess, incision and drainage is the primary treatment. For simple abscesses or boils, incision and drainage alone is likely to be adequate, but additional data are needed to further deﬁne the role of antibiotics, if any, in this setting.	topic_mrs
76494	9	355612	11	NULL	NULL	0	NULL	statement 7	Process		occurs along with					statement 8	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	For a cutaneous abscess, incision and drainage is the primary treatment. For simple abscesses or boils, incision and drainage alone is likely to be adequate, but additional data are needed to further deﬁne the role of antibiotics, if any, in this setting.	topic_mrs
76495	1	355614	11	NULL	NULL	0	NULL	mupirocin	Chemical		treats					Nasal decolonization	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nasal decolonization with mupirocin twice daily for 5–10 days	topic_mrs
76496	1	355615	11	NULL	NULL	0	NULL	mupirocin	Chemical		treats					Nasal decolonization	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nasal decolonization with mupirocin twice daily for 5–10 days and topical body decolonization regimens with a skin antiseptic solution (eg, chlorhexidine) for 5–14 days or dilute bleach baths.	topic_mrs
76497	2	355615	11	NULL	NULL	0	NULL	chlorhexidine	Chemical		is a type of 					skin antiseptic solution	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Nasal decolonization with mupirocin twice daily for 5–10 days and topical body decolonization regimens with a skin antiseptic solution (eg, chlorhexidine) for 5–14 days or dilute bleach baths.	topic_mrs
76498	1	355616	11	NULL	NULL	0	NULL	recurrent skin infections	Process		treats by 					Dilute bleach baths	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Dilute bleach baths have long been recommended to help children with recurrent skin infections, especially those with hard to control eczema and/or MRSA (Methicillin resistant Staphylococcus aureus) infections.	topic_mrs
76499	2	355616	11	NULL	NULL	0	NULL	Methicillin resistant Staphylococcus aureus	Organism		is					MRSA	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Dilute bleach baths have long been recommended to help children with recurrent skin infections, especially those with hard to control eczema and/or MRSA (Methicillin resistant Staphylococcus aureus) infections.	topic_mrs
76500	3	355616	11	NULL	NULL	0	NULL	eczema	MedicalFinding		is a type of 					recurrent skin infections	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Dilute bleach baths have long been recommended to help children with recurrent skin infections, especially those with hard to control eczema and/or MRSA (Methicillin resistant Staphylococcus aureus) infections.	topic_mrs
76501	4	355616	11	NULL	NULL	0	NULL	MRSA infection	Process		is a type of 					recurrent skin infections	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Dilute bleach baths have long been recommended to help children with recurrent skin infections, especially those with hard to control eczema and/or MRSA (Methicillin resistant Staphylococcus aureus) infections.	topic_mrs
76502	5	355616	11	NULL	NULL	0	NULL	eczema	MedicalFinding		treats by 					Dilute bleach baths	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Dilute bleach baths have long been recommended to help children with recurrent skin infections, especially those with hard to control eczema and/or MRSA (Methicillin resistant Staphylococcus aureus) infections.	topic_mrs
76503	6	355616	11	NULL	NULL	0	NULL	MRSA infection	Process		treats by 					Dilute bleach baths	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Dilute bleach baths have long been recommended to help children with recurrent skin infections, especially those with hard to control eczema and/or MRSA (Methicillin resistant Staphylococcus aureus) infections.	topic_mrs
75616	1	355618	11	NULL	NULL	0	NULL	Pleural empyema	MedicalFinding		also known as					pyothorax	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Pleural empyema (also known as a pyothorax or purulent pleuritis) is an accumulation of pus in the pleural cavity. Most pleural empyemas arise from an infection within the lung (pneumonia), often associated with parapneumonic effusions	topic_mrs
75617	2	355618	11	NULL	NULL	0	NULL	Pleural empyema	MedicalFinding		also known as					purulent pleuritis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Pleural empyema (also known as a pyothorax or purulent pleuritis) is an accumulation of pus in the pleural cavity. Most pleural empyemas arise from an infection within the lung (pneumonia), often associated with parapneumonic effusions	topic_mrs
75618	3	355618	11	NULL	NULL	0	NULL	Pleural empyema	MedicalFinding		accumulates					pus	CellComponent	pleural cavity			NULL		0	NULL	NULL	NULL	NULL	NULL	Pleural empyema (also known as a pyothorax or purulent pleuritis) is an accumulation of pus in the pleural cavity. Most pleural empyemas arise from an infection within the lung (pneumonia), often associated with parapneumonic effusions	topic_mrs
75619	4	355618	11	NULL	NULL	0	NULL	pleural empyemas	MedicalFinding		arise from					pneumonia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Pleural empyema (also known as a pyothorax or purulent pleuritis) is an accumulation of pus in the pleural cavity. Most pleural empyemas arise from an infection within the lung (pneumonia), often associated with parapneumonic effusions	topic_mrs
75620	5	355618	11	NULL	NULL	0	NULL	pneumonia	MedicalFinding		infects					lung 	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Pleural empyema (also known as a pyothorax or purulent pleuritis) is an accumulation of pus in the pleural cavity. Most pleural empyemas arise from an infection within the lung (pneumonia), often associated with parapneumonic effusions	topic_mrs
75621	6	355618	11	NULL	NULL	0	NULL	Pleural empyema	MedicalFinding		associates with		may			parapneumonic effusions	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Pleural empyema (also known as a pyothorax or purulent pleuritis) is an accumulation of pus in the pleural cavity. Most pleural empyemas arise from an infection within the lung (pneumonia), often associated with parapneumonic effusions	topic_mrs
77239	1	355620	11	NULL	NULL	0	NULL	fluids	Chemical		is withdrawn from		systematically			wound	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Drainage is the systematic withdrawal of fluids and discharges from a wound, sore, or cavity.	topic_mrs
77240	2	355620	11	NULL	NULL	0	NULL	statement 1	MedicalFinding		is known as					drainage	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Drainage is the systematic withdrawal of fluids and discharges from a wound, sore, or cavity.	topic_mrs
77241	3	355620	11	NULL	NULL	0	NULL	fluids	Chemical		is withdrawn from		systematically			sore	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Drainage is the systematic withdrawal of fluids and discharges from a wound, sore, or cavity.	topic_mrs
77242	4	355620	11	NULL	NULL	0	NULL	statement 3	MedicalProcedure		is known as					drainage	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Drainage is the systematic withdrawal of fluids and discharges from a wound, sore, or cavity.	topic_mrs
77243	5	355620	11	NULL	NULL	0	NULL	fluids	Chemical		is withdrawn from		systematically			cavity	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Drainage is the systematic withdrawal of fluids and discharges from a wound, sore, or cavity.	topic_mrs
77244	6	355620	11	NULL	NULL	0	NULL	statement 5	MedicalProcedure		is known as					drainage	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Drainage is the systematic withdrawal of fluids and discharges from a wound, sore, or cavity.	topic_mrs
77245	7	355620	11	NULL	NULL	0	NULL	discharge	Chemical		is withdrawn from		systematically\t			wound	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Drainage is the systematic withdrawal of fluids and discharges from a wound, sore, or cavity.	topic_mrs
77246	8	355620	11	NULL	NULL	NULL	NULL	statement 7	MedicalFinding		is known as					drainage	MedicalProcedure				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Drainage is the systematic withdrawal of fluids and discharges from a wound, sore, or cavity.	topic_mrs
77247	9	355620	11	NULL	NULL	0	NULL	discharge	Chemical		is withdrawn from		systematically			sore	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Drainage is the systematic withdrawal of fluids and discharges from a wound, sore, or cavity.	topic_mrs
77248	10	355620	11	NULL	NULL	0	NULL	statement 9	MedicalProcedure\t		is known as					drainage	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Drainage is the systematic withdrawal of fluids and discharges from a wound, sore, or cavity.	topic_mrs
77249	11	355620	11	NULL	NULL	0	NULL	discharge	Chemical		is withdrawn from		systematically			cavity	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Drainage is the systematic withdrawal of fluids and discharges from a wound, sore, or cavity.	topic_mrs
77250	12	355620	11	NULL	NULL	0	NULL	statement 11	MedicalProcedure		is known as					drainage	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Drainage is the systematic withdrawal of fluids and discharges from a wound, sore, or cavity.	topic_mrs
76504	1	355621	11	NULL	NULL	0	NULL	MRSA pneumonia	MedicalFinding		treats by 					antimicrobial therapy	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In patients with MRSA pneumonia complicated by empyema, antimicrobial therapy against MRSA should be used in conjunction with drainage procedures	topic_mrs
75622	1	355623	11	NULL	NULL	0	NULL	Trimethoprim-sulfamethoxazole	Chemical		is a synonym of					Co-trimoxazole	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Trimethoprim-sulfamethoxazole or Co-trimoxazole (abbreviated SXT, TMP-SMX, TMP-SMZ or TMP-sulfa) is a sulfonamide antibiotic combination of trimethoprim and sulfamethoxazole, in the ratio of 1 to 5, used in the treatment of a variety of bacterial infections. 	topic_mrs
75623	2	355623	11	NULL	NULL	0	NULL	Trimethoprim-sulfamethoxazole	Chemical		is					SXT	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Trimethoprim-sulfamethoxazole or Co-trimoxazole (abbreviated SXT, TMP-SMX, TMP-SMZ or TMP-sulfa) is a sulfonamide antibiotic combination of trimethoprim and sulfamethoxazole, in the ratio of 1 to 5, used in the treatment of a variety of bacterial infections. 	topic_mrs
75624	3	355623	11	NULL	NULL	0	NULL	Trimethoprim-sulfamethoxazole	Chemical		is					TMP-SMX	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Trimethoprim-sulfamethoxazole or Co-trimoxazole (abbreviated SXT, TMP-SMX, TMP-SMZ or TMP-sulfa) is a sulfonamide antibiotic combination of trimethoprim and sulfamethoxazole, in the ratio of 1 to 5, used in the treatment of a variety of bacterial infections. 	topic_mrs
75625	4	355623	11	NULL	NULL	0	NULL	Trimethoprim-sulfamethoxazole	Chemical		is					TMP-SMZ	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Trimethoprim-sulfamethoxazole or Co-trimoxazole (abbreviated SXT, TMP-SMX, TMP-SMZ or TMP-sulfa) is a sulfonamide antibiotic combination of trimethoprim and sulfamethoxazole, in the ratio of 1 to 5, used in the treatment of a variety of bacterial infections. 	topic_mrs
75626	5	355623	11	NULL	NULL	0	NULL	Trimethoprim-sulfamethoxazole	Chemical		is					TMP-sulfa	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Trimethoprim-sulfamethoxazole or Co-trimoxazole (abbreviated SXT, TMP-SMX, TMP-SMZ or TMP-sulfa) is a sulfonamide antibiotic combination of trimethoprim and sulfamethoxazole, in the ratio of 1 to 5, used in the treatment of a variety of bacterial infections. 	topic_mrs
75627	6	355623	11	NULL	NULL	0	NULL	Trimethoprim-sulfamethoxazole	Chemical		is a type of 					 sulfonamide antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Trimethoprim-sulfamethoxazole or Co-trimoxazole (abbreviated SXT, TMP-SMX, TMP-SMZ or TMP-sulfa) is a sulfonamide antibiotic combination of trimethoprim and sulfamethoxazole, in the ratio of 1 to 5, used in the treatment of a variety of bacterial infections. 	topic_mrs
75628	7	355623	11	NULL	NULL	0	NULL	Trimethoprim-sulfamethoxazole	Chemical		treats					bacterial infections	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Trimethoprim-sulfamethoxazole or Co-trimoxazole (abbreviated SXT, TMP-SMX, TMP-SMZ or TMP-sulfa) is a sulfonamide antibiotic combination of trimethoprim and sulfamethoxazole, in the ratio of 1 to 5, used in the treatment of a variety of bacterial infections. 	topic_mrs
76514	1	355624	11	NULL	NULL	0	NULL	TMP-SMX	Chemical		is a type of 					antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Some antibiotic options with parenteral and oral routes of administration include the following: TMP-SMX 4 mg/kg/dose (TMP component) twice daily	topic_mrs
76505	1	355625	11	NULL	NULL	0	NULL	Magnetic resonance imaging	Process		is a type of 					medical imaging technique	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Magnetic resonance imaging (MRI), nuclear magnetic resonance imaging (NMRI), or magnetic resonance tomography (MRT) is a medical imaging technique used in radiology to visualize detailed internal structures. 	topic_mrs
76506	2	355625	11	NULL	NULL	0	NULL	nuclear magnetic resonance imaging	Process		is a type of 					 medical imaging technique	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Magnetic resonance imaging (MRI), nuclear magnetic resonance imaging (NMRI), or magnetic resonance tomography (MRT) is a medical imaging technique used in radiology to visualize detailed internal structures. 	topic_mrs
76507	3	355625	11	NULL	NULL	0	NULL	magnetic resonance tomography	Process		is a type of 					medical imaging technique	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Magnetic resonance imaging (MRI), nuclear magnetic resonance imaging (NMRI), or magnetic resonance tomography (MRT) is a medical imaging technique used in radiology to visualize detailed internal structures. 	topic_mrs
76508	4	355625	11	NULL	NULL	0	NULL	Magnetic resonance imaging	Process		is					MRI	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Magnetic resonance imaging (MRI), nuclear magnetic resonance imaging (NMRI), or magnetic resonance tomography (MRT) is a medical imaging technique used in radiology to visualize detailed internal structures. 	topic_mrs
76509	5	355625	11	NULL	NULL	0	NULL	nuclear magnetic resonance imaging	Process		is					NMRI	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Magnetic resonance imaging (MRI), nuclear magnetic resonance imaging (NMRI), or magnetic resonance tomography (MRT) is a medical imaging technique used in radiology to visualize detailed internal structures. 	topic_mrs
76510	6	355625	11	NULL	NULL	0	NULL	magnetic resonance tomography	Process		is					MRT	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Magnetic resonance imaging (MRI), nuclear magnetic resonance imaging (NMRI), or magnetic resonance tomography (MRT) is a medical imaging technique used in radiology to visualize detailed internal structures. 	topic_mrs
76511	1	355626	11	NULL	NULL	0	NULL	Magnetic resonance imaging	Process		is					MRI	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 Magnetic resonance imaging (MRI) with gadolinium is the imaging modality of choice, particularly for detection of early osteomyelitis and associated soft-tissue diseas	topic_mrs
76512	2	355626	11	NULL	NULL	0	NULL	Magnetic resonance imaging	Process		detects					osteomyelitis	MedicalFinding	early			NULL		0	NULL	NULL	NULL	NULL	NULL	 Magnetic resonance imaging (MRI) with gadolinium is the imaging modality of choice, particularly for detection of early osteomyelitis and associated soft-tissue diseas	topic_mrs
76513	3	355626	11	NULL	NULL	0	NULL	Magnetic resonance imaging	Process		detects					soft-tissue diseas	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	 Magnetic resonance imaging (MRI) with gadolinium is the imaging modality of choice, particularly for detection of early osteomyelitis and associated soft-tissue diseas	topic_mrs
76515	1	355628	11	NULL	NULL	0	NULL	linezolid	Chemical		is an alternative to 					IV vancomycin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	IV vancomycin for 2 weeks is recommended. Alternatives include the following: linezolid 600 mg PO/IV twice daily or TMP-SMX 5 mg/kg/dose IV every 8–12 h	topic_mrs
76516	2	355628	11	NULL	NULL	0	NULL	TMP-SMX	Chemical		is an alternative to 					IV vancomycin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	IV vancomycin for 2 weeks is recommended. Alternatives include the following: linezolid 600 mg PO/IV twice daily or TMP-SMX 5 mg/kg/dose IV every 8–12 h	topic_mrs
76517	1	355629	11	NULL	NULL	0	NULL	Vancomycin	Chemical		administered in		slowly			 dilute solution	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Vancomycin must be administered in a dilute solution slowly, over at least 60 minutes (maximum rate of 10 mg/minute for doses >500 mg). This is due to the high incidence of pain and thrombophlebitis and to avoid an infusion reaction known as the red man syndrome or red neck syndrome.	topic_mrs
76518	2	355629	11	NULL	NULL	0	NULL	statement 1	Process		avoid					pain	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Vancomycin must be administered in a dilute solution slowly, over at least 60 minutes (maximum rate of 10 mg/minute for doses >500 mg). This is due to the high incidence of pain and thrombophlebitis and to avoid an infusion reaction known as the red man syndrome or red neck syndrome.	topic_mrs
76519	3	355629	11	NULL	NULL	0	NULL	statement 1	Process		avoid					thrombophlebitis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Vancomycin must be administered in a dilute solution slowly, over at least 60 minutes (maximum rate of 10 mg/minute for doses >500 mg). This is due to the high incidence of pain and thrombophlebitis and to avoid an infusion reaction known as the red man syndrome or red neck syndrome.	topic_mrs
76520	4	355629	11	NULL	NULL	0	NULL	statement 1	Process		avoid					red man syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Vancomycin must be administered in a dilute solution slowly, over at least 60 minutes (maximum rate of 10 mg/minute for doses >500 mg). This is due to the high incidence of pain and thrombophlebitis and to avoid an infusion reaction known as the red man syndrome or red neck syndrome.	topic_mrs
76521	5	355629	11	NULL	NULL	NULL	NULL	red man syndrome	MedicalFinding		is also known as					red neck syndrome	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Vancomycin must be administered in a dilute solution slowly, over at least 60 minutes (maximum rate of 10 mg/minute for doses >500 mg). This is due to the high incidence of pain and thrombophlebitis and to avoid an infusion reaction known as the red man syndrome or red neck syndrome.	topic_mrs
76522	6	355629	11	NULL	NULL	NULL	NULL	red man syndrome	MedicalFinding		is a type of 					infusion reaction	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Vancomycin must be administered in a dilute solution slowly, over at least 60 minutes (maximum rate of 10 mg/minute for doses >500 mg). This is due to the high incidence of pain and thrombophlebitis and to avoid an infusion reaction known as the red man syndrome or red neck syndrome.	topic_mrs
76523	1	355630	11	NULL	NULL	0	NULL	osteomyelitis	MedicalFinding		is a type of 					CA-MRSA infections	Process	invasive susceptible			NULL		0	NULL	NULL	NULL	NULL	NULL	Although not speciﬁcally approved for treatment of MRSA infection, it has become widely used for treatment of SSTI and has been successfully used for treatment of invasive susceptible CA-MRSA infections in children, including osteomyelitis, septic arthritis, pneumonia, and lymphadenitis	topic_mrs
76524	2	355630	11	NULL	NULL	0	NULL	septic arthritis	MedicalFinding		is a type of 					CA-MRSA infections	Process	invasive susceptible			NULL		0	NULL	NULL	NULL	NULL	NULL	Although not speciﬁcally approved for treatment of MRSA infection, it has become widely used for treatment of SSTI and has been successfully used for treatment of invasive susceptible CA-MRSA infections in children, including osteomyelitis, septic arthritis, pneumonia, and lymphadenitis	topic_mrs
76525	3	355630	11	NULL	NULL	0	NULL	 pneumonia	MedicalFinding		is a type of 					CA-MRSA infections	Process	invasive susceptible			NULL		0	NULL	NULL	NULL	NULL	NULL	Although not speciﬁcally approved for treatment of MRSA infection, it has become widely used for treatment of SSTI and has been successfully used for treatment of invasive susceptible CA-MRSA infections in children, including osteomyelitis, septic arthritis, pneumonia, and lymphadenitis	topic_mrs
76526	4	355630	11	NULL	NULL	0	NULL	 lymphadenitis	MedicalFinding		is a type of 					CA-MRSA infection	Process	invasive susceptible			NULL		0	NULL	NULL	NULL	NULL	NULL	Although not speciﬁcally approved for treatment of MRSA infection, it has become widely used for treatment of SSTI and has been successfully used for treatment of invasive susceptible CA-MRSA infections in children, including osteomyelitis, septic arthritis, pneumonia, and lymphadenitis	topic_mrs
76527	1	355631	11	NULL	NULL	NULL	NULL	infective endocarditis	MedicalFinding		is a type of 					 endovascular infections	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Because it is bacteriostatic, it is not recommended for endovascular infections, such as infective endocarditis or septic thrombophlebitis.	topic_mrs
76528	2	355631	11	NULL	NULL	NULL	NULL	 septic thrombophlebitis	MedicalFinding		is a type of 					endovascular infections	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Because it is bacteriostatic, it is not recommended for endovascular infections, such as infective endocarditis or septic thrombophlebitis.	topic_mrs
75499	1	355632	5	NULL	NULL	0	NULL	MALT lymphoma patients	GroupOfPeople		infected with					H pylori	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	It has been seen that in those patients with MALT lymphoma who also test positive for H pylori, antibiotics for H pylori may actually control the cancer.	topic_ll
75500	2	355632	5	NULL	NULL	0	NULL	H pylori antibiotics	Chemical		control					MALT lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	It has been seen that in those patients with MALT lymphoma who also test positive for H pylori, antibiotics for H pylori may actually control the cancer.	topic_ll
75501	1	355633	5	NULL	NULL	0	NULL	MALT lymphoma	MedicalFinding		affects		most commonly			stomach	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The most commonly affected organ is the stomach, which accounts for nearly 2 out of every 3 cases. But other organs are also affected by MALT lymphoma.	topic_ll
75502	1	355634	5	NULL	NULL	0	NULL	MALT lymphoma	MedicalFinding		affects					stomach	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The symptoms of MALT lymphoma depend on the organ affected. When MALT lymphoma affects the stomach, you may feel indigestion, weight loss and black stools because of bleeding into the stomach. Some people may feel a vague pain in the abdomen.	topic_ll
75503	2	355634	5	NULL	NULL	0	NULL	indigestion	MedicalFinding		is a symptom of					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The symptoms of MALT lymphoma depend on the organ affected. When MALT lymphoma affects the stomach, you may feel indigestion, weight loss and black stools because of bleeding into the stomach. Some people may feel a vague pain in the abdomen.	topic_ll
75504	3	355634	5	NULL	NULL	0	NULL	weight loss	MedicalFinding		is a symptom of					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The symptoms of MALT lymphoma depend on the organ affected. When MALT lymphoma affects the stomach, you may feel indigestion, weight loss and black stools because of bleeding into the stomach. Some people may feel a vague pain in the abdomen.	topic_ll
75505	4	355634	5	NULL	NULL	0	NULL	black stools	MedicalFinding		is a symptom of					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The symptoms of MALT lymphoma depend on the organ affected. When MALT lymphoma affects the stomach, you may feel indigestion, weight loss and black stools because of bleeding into the stomach. Some people may feel a vague pain in the abdomen.	topic_ll
75506	5	355634	5	NULL	NULL	0	NULL	stomach	OrganismPart	bleeding of	causes					black stools	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The symptoms of MALT lymphoma depend on the organ affected. When MALT lymphoma affects the stomach, you may feel indigestion, weight loss and black stools because of bleeding into the stomach. Some people may feel a vague pain in the abdomen.	topic_ll
75507	6	355634	5	NULL	NULL	0	NULL	abdominal pain	MedicalFinding	vague	is a symptom of					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The symptoms of MALT lymphoma depend on the organ affected. When MALT lymphoma affects the stomach, you may feel indigestion, weight loss and black stools because of bleeding into the stomach. Some people may feel a vague pain in the abdomen.	topic_ll
75963	1	355635	11	NULL	NULL	0	NULL	Beta-lactamase	GP		is					enzyme	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta-lactamases are enzymes produced by some bacteria and are responsible for their resistance to beta-lactam antibiotics like penicillins, cephamycins, and carbapenems (ertapenem).	topic_mrs
75964	2	355635	11	NULL	NULL	0	NULL	Beta-lactamases	GP		produced by					bacteria	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta-lactamases are enzymes produced by some bacteria and are responsible for their resistance to beta-lactam antibiotics like penicillins, cephamycins, and carbapenems (ertapenem).	topic_mrs
75965	3	355635	11	NULL	NULL	0	NULL	penicillins	Chemical		is a type of 					beta-lactam antibiotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta-lactamases are enzymes produced by some bacteria and are responsible for their resistance to beta-lactam antibiotics like penicillins, cephamycins, and carbapenems (ertapenem).	topic_mrs
75966	4	355635	11	NULL	NULL	0	NULL	cephamycins	Chemical		is a type of 					beta-lactam antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta-lactamases are enzymes produced by some bacteria and are responsible for their resistance to beta-lactam antibiotics like penicillins, cephamycins, and carbapenems (ertapenem).	topic_mrs
75967	5	355635	11	NULL	NULL	0	NULL	carbapenems	Chemical		is a type of 					beta-lactam antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta-lactamases are enzymes produced by some bacteria and are responsible for their resistance to beta-lactam antibiotics like penicillins, cephamycins, and carbapenems (ertapenem).	topic_mrs
75968	6	355635	11	NULL	NULL	0	NULL	carbapenems	Chemical		is a synonym of					ertapenem	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta-lactamases are enzymes produced by some bacteria and are responsible for their resistance to beta-lactam antibiotics like penicillins, cephamycins, and carbapenems (ertapenem).	topic_mrs
75508	1	355636	5	NULL	NULL	0	NULL	follicular lymphoma	MedicalFinding	risk of	is associated with		possibly			diet	Food				NULL		0	NULL	NULL	NULL	NULL	NULL	Studies suggest risk of follicular lymphoma is associated with a person's diet to say the least.  A new study linked nitrite intake with increased risk of follicular lymphoma.	topic_ll
75509	2	355636	5	NULL	NULL	0	NULL	nitrite	Chemical	intake of	increases					follicular lymphoma	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Studies suggest risk of follicular lymphoma is associated with a person's diet to say the least.  A new study linked nitrite intake with increased risk of follicular lymphoma.	topic_ll
76129	1	355638	11	NULL	NULL	0	NULL	Bacteremia	MedicalFinding		is the presence of					bacteria	Organism	in the blood			NULL		0	NULL	NULL	NULL	NULL	NULL	Bacteremia (also Bacteraemia or Bacteræmia) is the presence of bacteria in the blood. The blood is normally a sterile environment, so the detection of bacteria in the blood (most commonly with blood cultures) is always abnormal.	topic_mrs
76130	2	355638	11	NULL	NULL	0	NULL	Bacteremia	MedicalFinding		is a synonym of					Bacteraemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bacteremia (also Bacteraemia or Bacteræmia) is the presence of bacteria in the blood. The blood is normally a sterile environment, so the detection of bacteria in the blood (most commonly with blood cultures) is always abnormal.	topic_mrs
76131	3	355638	11	NULL	NULL	0	NULL	 blood	OrganismPart		is		normally			sterile	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Bacteremia (also Bacteraemia or Bacteræmia) is the presence of bacteria in the blood. The blood is normally a sterile environment, so the detection of bacteria in the blood (most commonly with blood cultures) is always abnormal.	topic_mrs
76166	4	355638	11	NULL	NULL	0	NULL	Bacteremia	MedicalFinding		is always					abnormal	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Bacteremia (also Bacteraemia or Bacteræmia) is the presence of bacteria in the blood. The blood is normally a sterile environment, so the detection of bacteria in the blood (most commonly with blood cultures) is always abnormal.	topic_mrs
75953	1	355639	5	NULL	NULL	0	NULL	Resveratrol	Chemical		induces					apoptosis	process				NULL	OCI-LY8 cells	0	NULL	NULL	NULL	NULL	NULL	Resveratrol induces apoptosis in transformed follicular lymphoma OCI-LY8 cells: Evidence for a novel mechanism involving inhibition of BCL6 signaling	topic_ll
75954	2	355639	5	NULL	NULL	0	NULL	OCI-LY8	Cell		is a type of					transformed follicular lymphoma cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Resveratrol induces apoptosis in transformed follicular lymphoma OCI-LY8 cells: Evidence for a novel mechanism involving inhibition of BCL6 signaling	topic_ll
75955	3	355639	5	NULL	NULL	0	NULL	statement 1	Process		inhibits					BCL6 signaling	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Resveratrol induces apoptosis in transformed follicular lymphoma OCI-LY8 cells: Evidence for a novel mechanism involving inhibition of BCL6 signaling	topic_ll
76529	1	355641	11	NULL	NULL	NULL	NULL	echocardiogram	MedicalProcedure		is also known as					 cardiac ECHO 	MedicalProcedure				NULL		NULL	NULL	NULL	NULL	NULL	NULL	An echocardiogram, often referred to in the medical community as a cardiac ECHO or simply an ECHO, is a sonogram of the heart...an echocardiogram can also produce accurate assessment of the velocity of blood and cardiac tissue	topic_mrs
76530	2	355641	11	NULL	NULL	NULL	NULL	echocardiogram	MedicalProcedure		is also known as					ECHO	MedicalProcedure				NULL		NULL	NULL	NULL	NULL	NULL	NULL	An echocardiogram, often referred to in the medical community as a cardiac ECHO or simply an ECHO, is a sonogram of the heart...an echocardiogram can also produce accurate assessment of the velocity of blood and cardiac tissue	topic_mrs
76531	3	355641	11	NULL	NULL	NULL	NULL	 echocardiogram	MedicalProcedure		is a type of 					sonogram	MedicalProcedure	heart			NULL		NULL	NULL	NULL	NULL	NULL	NULL	An echocardiogram, often referred to in the medical community as a cardiac ECHO or simply an ECHO, is a sonogram of the heart...an echocardiogram can also produce accurate assessment of the velocity of blood and cardiac tissue	topic_mrs
76532	4	355641	11	NULL	NULL	NULL	NULL	echocardiogram	MedicalProcedure		 assess 					blood	OrganismPart	velocity of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	An echocardiogram, often referred to in the medical community as a cardiac ECHO or simply an ECHO, is a sonogram of the heart...an echocardiogram can also produce accurate assessment of the velocity of blood and cardiac tissue	topic_mrs
76533	5	355641	11	NULL	NULL	0	NULL	echocardiogram	MedicalProcedure		assess					cardiac tissue	Organism part				NULL		0	NULL	NULL	NULL	NULL	NULL	An echocardiogram, often referred to in the medical community as a cardiac ECHO or simply an ECHO, is a sonogram of the heart...an echocardiogram can also produce accurate assessment of the velocity of blood and cardiac tissue	topic_mrs
75956	1	355642	5	NULL	NULL	0	NULL	dust	Chemical	exposure to	is not linked to					cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	As if being involved in the 9/11 attack on the World Trade Centers wasn't horrific enough, it's now appearing as if people present at the WTC on that world-changing day have higher than normal rates of lymphatic and blood cancers. While New York city's health commissioner has said there is no evidence linking dust exposure to cancer, the Medical Monitoring Program reports a "handful of cases of multiple myeloma in very young individuals." They add, "multiple myeloma is a condition that ... almost aways presents later in life." NULL	topic_ll
76172	1	355643	11	NULL	NULL	0	NULL	Echocardiography	MedicalProcedure		is recommended for					bacteremia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Echocardiography is recommended for all adult patients with bacteremia	topic_mrs
75957	1	355644	5	NULL	NULL	0	NULL	uranium miners	GroupOfPeople		prone to					leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Leukemia among uranium miners--late effects of exposure to uranium dust?	topic_ll
75958	1	355645	5	NULL	NULL	0	NULL	miners	GroupOfPeople	underground	is at risk of					leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Radon and leukemia risk in underground miners: are working level months the most appropriate exposure parameter?	topic_ll
75959	2	355645	5	NULL	NULL	0	NULL	radon	Chemical		plays a role in		possibly			statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Radon and leukemia risk in underground miners: are working level months the most appropriate exposure parameter?	topic_ll
76174	1	355646	11	NULL	NULL	0	NULL	Daptomycin	Chemical		is a type of 					lipopeptide class antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Daptomycin is a lipopeptide class antibiotic that disrupts cell membrane function via calcium-dependent binding, resulting in bactericidal activity in a concentration-dependent fashion	topic_mrs
76176	2	355646	11	NULL	NULL	0	NULL	Daptomycin	Chemical		disrupts					cell membrane	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	Daptomycin is a lipopeptide class antibiotic that disrupts cell membrane function via calcium-dependent binding, resulting in bactericidal activity in a concentration-dependent fashion	topic_mrs
76178	3	355646	11	NULL	NULL	0	NULL	calcium-dependent binding	Process		disrupts in 					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Daptomycin is a lipopeptide class antibiotic that disrupts cell membrane function via calcium-dependent binding, resulting in bactericidal activity in a concentration-dependent fashion	topic_mrs
76179	4	355646	11	NULL	NULL	0	NULL	statement 2	Process		resulted in					 bactericidal activity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Daptomycin is a lipopeptide class antibiotic that disrupts cell membrane function via calcium-dependent binding, resulting in bactericidal activity in a concentration-dependent fashion	topic_mrs
76181	5	355646	11	NULL	NULL	0	NULL	statement 4	Process		is in a					concentration-dependent fashion	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Daptomycin is a lipopeptide class antibiotic that disrupts cell membrane function via calcium-dependent binding, resulting in bactericidal activity in a concentration-dependent fashion	topic_mrs
76184	1	355647	11	NULL	NULL	0	NULL	Daptomycin	Chemical		not treat					non-hematogenous MRSA pneumonia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Daptomycin should not be used for the treatment of non-hematogenous MRSA pneumonia, because its activity is inhibited by pulmonary surfactant.	topic_mrs
76185	2	355647	11	NULL	NULL	0	NULL	Daptomycin	Chemical		inhibited by					pulmonary surfactant	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Daptomycin should not be used for the treatment of non-hematogenous MRSA pneumonia, because its activity is inhibited by pulmonary surfactant.	topic_mrs
76192	1	355650	11	NULL	NULL	0	NULL	vancomycin 	Chemical		 cross-resist with		possibly			daptomycin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Prior exposure to vancomycin and elevated vancomycin MICs have been associated with increases in daptomycin MICs, suggesting possible cross-resistance	topic_mrs
76201	1	355651	11	NULL	NULL	0	NULL	Quinupristin	Chemical		is a type of 					streptogramin antibiotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Quinupristin-dalfopristin is a combination of 2 streptogramin antibiotics and inhibits protein synthesis	topic_mrs
76202	2	355651	11	NULL	NULL	0	NULL	dalfopristin	Chemical		is a type of 					streptogramin antibiotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Quinupristin-dalfopristin is a combination of 2 streptogramin antibiotics and inhibits protein synthesis	topic_mrs
76204	3	355651	11	NULL	NULL	0	NULL	Quinupristin	Chemical		combines with					dalfopristin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Quinupristin-dalfopristin is a combination of 2 streptogramin antibiotics and inhibits protein synthesis	topic_mrs
76206	4	355651	11	NULL	NULL	0	NULL	statement 3	Process		inhibits					protein synthesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Quinupristin-dalfopristin is a combination of 2 streptogramin antibiotics and inhibits protein synthesis	topic_mrs
76209	1	355653	11	NULL	NULL	0	NULL	Quinupristin-Dalfopristin	Chemical		is approved for		 FDA			cSSTI	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Quinupristin-Dalfopristin  is FDA-approved for cSSTI in adults and children greater than 16 years of age.	topic_mrs
76212	1	355654	11	NULL	NULL	0	NULL	Rifampin	Chemical		has					bactericidal activity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Rifampin has bactericidal activity against S. aureus and achieves high intracellular levels, in addition to penetrating bioﬁlms	topic_mrs
76213	2	355654	11	NULL	NULL	0	NULL	statement 1	Process		is against					S. aureus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Rifampin has bactericidal activity against S. aureus and achieves high intracellular levels, in addition to penetrating bioﬁlms	topic_mrs
76214	3	355654	11	NULL	NULL	0	NULL	Rifampin	Chemical		 achieves					high intracellular levels	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Rifampin has bactericidal activity against S. aureus and achieves high intracellular levels, in addition to penetrating bioﬁlms	topic_mrs
76215	4	355654	11	NULL	NULL	0	NULL	Rifampin	Chemical		penetrate					biofilms	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Rifampin has bactericidal activity against S. aureus and achieves high intracellular levels, in addition to penetrating bioﬁlms	topic_mrs
76216	1	355655	11	NULL	NULL	0	NULL	biofilm	Organism		is an aggregate of					microorganisms	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	A biofilm is an aggregate of microorganisms in which cells adhere to each other and/or to a surface. These adherent cells are frequently embedded within a self-produced matrix of extracellular polymeric substance (EPS)	topic_mrs
76217	2	355655	11	NULL	NULL	0	NULL	statement 1	Process		are embedded within		frequently			extracellular polymeric substance	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	A biofilm is an aggregate of microorganisms in which cells adhere to each other and/or to a surface. These adherent cells are frequently embedded within a self-produced matrix of extracellular polymeric substance (EPS)	topic_mrs
76218	3	355655	11	NULL	NULL	0	NULL	extracellular polymeric substance	Chemical		is					EPS	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	A biofilm is an aggregate of microorganisms in which cells adhere to each other and/or to a surface. These adherent cells are frequently embedded within a self-produced matrix of extracellular polymeric substance (EPS)	topic_mrs
76219	4	355655	11	NULL	NULL	0	NULL	extracellular polymeric substance	Chemical		is a product of					biofilm	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	A biofilm is an aggregate of microorganisms in which cells adhere to each other and/or to a surface. These adherent cells are frequently embedded within a self-produced matrix of extracellular polymeric substance (EPS)	topic_mrs
76220	1	355656	11	NULL	NULL	0	NULL	 biofilm	Organism		is held together by					 EPS	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The biofilm is held together and protected by a matrix of excreted polymeric compounds called EPS. EPS is an abbreviation for either extracellular polymeric substance or exopolysaccharide. This matrix protects the cells within it and facilitates communication among them through biochemical signals.	topic_mrs
76221	2	355656	11	NULL	NULL	0	NULL	 EPS	Chemical		is					extracellular polymeric substance	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The biofilm is held together and protected by a matrix of excreted polymeric compounds called EPS. EPS is an abbreviation for either extracellular polymeric substance or exopolysaccharide. This matrix protects the cells within it and facilitates communication among them through biochemical signals.	topic_mrs
76222	3	355656	11	NULL	NULL	0	NULL	EPS	Chemical		is a type of 					exopolysaccharide	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The biofilm is held together and protected by a matrix of excreted polymeric compounds called EPS. EPS is an abbreviation for either extracellular polymeric substance or exopolysaccharide. This matrix protects the cells within it and facilitates communication among them through biochemical signals.	topic_mrs
76223	4	355656	11	NULL	NULL	0	NULL	EPS	Chemical		protects					cells	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	The biofilm is held together and protected by a matrix of excreted polymeric compounds called EPS. EPS is an abbreviation for either extracellular polymeric substance or exopolysaccharide. This matrix protects the cells within it and facilitates communication among them through biochemical signals.	topic_mrs
76224	5	355656	11	NULL	NULL	0	NULL	EPS	Chemical		facilitates					communication	Process	 by biochemical signals			NULL		0	NULL	NULL	NULL	NULL	NULL	The biofilm is held together and protected by a matrix of excreted polymeric compounds called EPS. EPS is an abbreviation for either extracellular polymeric substance or exopolysaccharide. This matrix protects the cells within it and facilitates communication among them through biochemical signals.	topic_mrs
76227	1	355657	7	NULL	NULL	NULL	NULL	methylation	Process		crucial role in					polyp/adenoma	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	These findings suggest a potentially crucial role for methylation in the polyp/adenoma to cancer progression in colorectal carcinogenesis	topic_ccc
76228	2	355657	7	NULL	NULL	NULL	NULL	polyp/adenoma	MedicalFinding		progressed to					cancer	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	These findings suggest a potentially crucial role for methylation in the polyp/adenoma to cancer progression in colorectal carcinogenesis	topic_ccc
76554	3	355657	7	NULL	NULL	0	NULL	statement 2	Process		occur in					colorectal carcinogenesis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	These findings suggest a potentially crucial role for methylation in the polyp/adenoma to cancer progression in colorectal carcinogenesis	topic_ccc
76534	1	355658	7	11	NULL	0	NULL	Stage 2 colon cancer	MedicalFinding		is also known as					Duke's B colon cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Stage 2 colon cancer used to be called Duke's B colon cancer.	topic_ccc
76556	1	355661	7	NULL	NULL	0	NULL	RASSF1A	GP		methylated in		frequently			 mucosae	OrganismPart	distal normal-appearing			NULL		0	NULL	NULL	NULL	NULL	NULL	Along with RASSF1A and SFRP1, two identified genes, HOXA5 and PDE10A, were also frequently methylated in distal normal-appearing mucosae and CRCs. 	topic_ccc
76557	2	355661	7	NULL	NULL	NULL	NULL	RASSF1A	GP		methylated in		frequently			CRC	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Along with RASSF1A and SFRP1, two identified genes, HOXA5 and PDE10A, were also frequently methylated in distal normal-appearing mucosae and CRCs. 	topic_ccc
76558	3	355661	7	NULL	NULL	NULL	NULL	SFRP1	GP		methylated in		frequently			mucosae 	OrganismPart	distal normal-appearing			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Along with RASSF1A and SFRP1, two identified genes, HOXA5 and PDE10A, were also frequently methylated in distal normal-appearing mucosae and CRCs. 	topic_ccc
76559	4	355661	7	NULL	NULL	NULL	NULL	SFRP1	GP		methylated in		frequently			CRC	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Along with RASSF1A and SFRP1, two identified genes, HOXA5 and PDE10A, were also frequently methylated in distal normal-appearing mucosae and CRCs. 	topic_ccc
76560	5	355661	7	NULL	NULL	0	NULL	HOXA5 	GP		methylated in		frequently			mucosae 	OrganismPart	distal normal-appearing			NULL		0	NULL	NULL	NULL	NULL	NULL	Along with RASSF1A and SFRP1, two identified genes, HOXA5 and PDE10A, were also frequently methylated in distal normal-appearing mucosae and CRCs. 	topic_ccc
76561	6	355661	7	NULL	NULL	NULL	NULL	HOXA5 	GP		methylated in		frequently			CRC	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Along with RASSF1A and SFRP1, two identified genes, HOXA5 and PDE10A, were also frequently methylated in distal normal-appearing mucosae and CRCs. 	topic_ccc
76562	7	355661	7	NULL	NULL	0	NULL	PDE10A	GP		methylated in		frequently			mucosae 	OrganismPart	distal normal-appearing			NULL		0	NULL	NULL	NULL	NULL	NULL	Along with RASSF1A and SFRP1, two identified genes, HOXA5 and PDE10A, were also frequently methylated in distal normal-appearing mucosae and CRCs. 	topic_ccc
76563	8	355661	7	NULL	NULL	0	NULL	PDE10A	GP		methylated in		frequently			CRC	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Along with RASSF1A and SFRP1, two identified genes, HOXA5 and PDE10A, were also frequently methylated in distal normal-appearing mucosae and CRCs. 	topic_ccc
76564	1	355663	7	NULL	NULL	0	NULL	A(3) receptor	GP		subtype of		abundant			cancer tissues	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	 At a protein levels low amount of A(1), A(2A), and A(2B) receptors were detected, whilst the A(3) was the most abundant subtype in both cancer tissues and cells, with a pharmacological profile typical of the A(3) subtype.	topic_ccc
76565	2	355663	7	NULL	NULL	0	NULL	A(3) receptor	GP		subtype of		abundant			cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	 At a protein levels low amount of A(1), A(2A), and A(2B) receptors were detected, whilst the A(3) was the most abundant subtype in both cancer tissues and cells, with a pharmacological profile typical of the A(3) subtype.	topic_ccc
76566	1	355664	7	NULL	NULL	0	NULL	Adenosine 	Chemical		interacts with					A(1) receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Adenosine may affect several pathophysiological processes, including cellular proliferation, through interaction with A(1), A(2A), A(2B), and A(3) receptors. In this study we characterized adenosine receptors in human colon cancer tissues and in colon cancer cell lines Caco2, DLD1, HT29. mRNA of all adenosine subtypes was detected in cancer tissues and cell lines. 	topic_ccc
76567	2	355664	7	NULL	NULL	0	NULL	Adenosine	Chemical		interacts with					A(2A) receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Adenosine may affect several pathophysiological processes, including cellular proliferation, through interaction with A(1), A(2A), A(2B), and A(3) receptors. In this study we characterized adenosine receptors in human colon cancer tissues and in colon cancer cell lines Caco2, DLD1, HT29. mRNA of all adenosine subtypes was detected in cancer tissues and cell lines. 	topic_ccc
76568	3	355664	7	NULL	NULL	0	NULL	Adenosine	Chemical		interacts with					A(2B) receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Adenosine may affect several pathophysiological processes, including cellular proliferation, through interaction with A(1), A(2A), A(2B), and A(3) receptors. In this study we characterized adenosine receptors in human colon cancer tissues and in colon cancer cell lines Caco2, DLD1, HT29. mRNA of all adenosine subtypes was detected in cancer tissues and cell lines. 	topic_ccc
76569	4	355664	7	NULL	NULL	0	NULL	Adenosine	Chemical		interacts with					A(3) receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Adenosine may affect several pathophysiological processes, including cellular proliferation, through interaction with A(1), A(2A), A(2B), and A(3) receptors. In this study we characterized adenosine receptors in human colon cancer tissues and in colon cancer cell lines Caco2, DLD1, HT29. mRNA of all adenosine subtypes was detected in cancer tissues and cell lines. 	topic_ccc
76570	5	355664	7	NULL	NULL	NULL	NULL	Adenosine	Chemical		affect		may			cellular proliferation	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Adenosine may affect several pathophysiological processes, including cellular proliferation, through interaction with A(1), A(2A), A(2B), and A(3) receptors. In this study we characterized adenosine receptors in human colon cancer tissues and in colon cancer cell lines Caco2, DLD1, HT29. mRNA of all adenosine subtypes was detected in cancer tissues and cell lines. 	topic_ccc
76571	6	355664	7	NULL	NULL	0	NULL	cellular proliferation	Process		is a type of					pathophysiological process	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Adenosine may affect several pathophysiological processes, including cellular proliferation, through interaction with A(1), A(2A), A(2B), and A(3) receptors. In this study we characterized adenosine receptors in human colon cancer tissues and in colon cancer cell lines Caco2, DLD1, HT29. mRNA of all adenosine subtypes was detected in cancer tissues and cell lines. 	topic_ccc
76572	7	355664	7	NULL	NULL	0	NULL	adenosine receptor	GP		characterized in					colon cancer tissues	OrganismPart	human			NULL		0	NULL	NULL	NULL	NULL	NULL	Adenosine may affect several pathophysiological processes, including cellular proliferation, through interaction with A(1), A(2A), A(2B), and A(3) receptors. In this study we characterized adenosine receptors in human colon cancer tissues and in colon cancer cell lines Caco2, DLD1, HT29. mRNA of all adenosine subtypes was detected in cancer tissues and cell lines. 	topic_ccc
76573	8	355664	7	NULL	NULL	0	NULL	adenosine receptor	GP		characterized in					Caco2	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Adenosine may affect several pathophysiological processes, including cellular proliferation, through interaction with A(1), A(2A), A(2B), and A(3) receptors. In this study we characterized adenosine receptors in human colon cancer tissues and in colon cancer cell lines Caco2, DLD1, HT29. mRNA of all adenosine subtypes was detected in cancer tissues and cell lines. 	topic_ccc
76574	9	355664	7	NULL	NULL	0	NULL	adenosine receptor	GP		characterized in					DLD1	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Adenosine may affect several pathophysiological processes, including cellular proliferation, through interaction with A(1), A(2A), A(2B), and A(3) receptors. In this study we characterized adenosine receptors in human colon cancer tissues and in colon cancer cell lines Caco2, DLD1, HT29. mRNA of all adenosine subtypes was detected in cancer tissues and cell lines. 	topic_ccc
76575	10	355664	7	NULL	NULL	0	NULL	adenosine receptor	GP		characterized in					HT29	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Adenosine may affect several pathophysiological processes, including cellular proliferation, through interaction with A(1), A(2A), A(2B), and A(3) receptors. In this study we characterized adenosine receptors in human colon cancer tissues and in colon cancer cell lines Caco2, DLD1, HT29. mRNA of all adenosine subtypes was detected in cancer tissues and cell lines. 	topic_ccc
76576	11	355664	7	NULL	NULL	0	NULL	Caco2	Cell		is a type of					 colon cancer cell line	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Adenosine may affect several pathophysiological processes, including cellular proliferation, through interaction with A(1), A(2A), A(2B), and A(3) receptors. In this study we characterized adenosine receptors in human colon cancer tissues and in colon cancer cell lines Caco2, DLD1, HT29. mRNA of all adenosine subtypes was detected in cancer tissues and cell lines. 	topic_ccc
76577	12	355664	7	NULL	NULL	0	NULL	DLD1	Cell		is a type of					colon cancer cell line	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Adenosine may affect several pathophysiological processes, including cellular proliferation, through interaction with A(1), A(2A), A(2B), and A(3) receptors. In this study we characterized adenosine receptors in human colon cancer tissues and in colon cancer cell lines Caco2, DLD1, HT29. mRNA of all adenosine subtypes was detected in cancer tissues and cell lines. 	topic_ccc
76578	13	355664	7	NULL	NULL	0	NULL	HT29	Cell		is a type of					colon cancer cell line	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Adenosine may affect several pathophysiological processes, including cellular proliferation, through interaction with A(1), A(2A), A(2B), and A(3) receptors. In this study we characterized adenosine receptors in human colon cancer tissues and in colon cancer cell lines Caco2, DLD1, HT29. mRNA of all adenosine subtypes was detected in cancer tissues and cell lines. 	topic_ccc
76579	1	355665	7	NULL	NULL	NULL	NULL	 sleep latency	MedicalFinding	Prolonged	polysomnographic features in 					bipolar disorder	MedicalFinding	patients with			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Prolonged sleep latency, reduced sleep efficiency, increased number and duration of awakenings, reduced delta sleep, shortened REM sleep latency, and increased REM density are common polysomnographic features in patients with bipolar disorder.	topic_bd
76580	2	355665	7	NULL	NULL	NULL	NULL	 sleep efficiency	MedicalFinding	reduced	polysomnographic features in					bipolar disorder	MedicalFinding	patients with			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Prolonged sleep latency, reduced sleep efficiency, increased number and duration of awakenings, reduced delta sleep, shortened REM sleep latency, and increased REM density are common polysomnographic features in patients with bipolar disorder.	topic_bd
76581	3	355665	7	NULL	NULL	NULL	NULL	awakenings	MedicalFinding	increased number and duration of 	polysomnographic features in					bipolar disorder	MedicalFinding	patients with			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Prolonged sleep latency, reduced sleep efficiency, increased number and duration of awakenings, reduced delta sleep, shortened REM sleep latency, and increased REM density are common polysomnographic features in patients with bipolar disorder.	topic_bd
76582	4	355665	7	NULL	NULL	NULL	NULL	delta sleep	MedicalFinding	reduced	polysomnographic features in					bipolar disorder	MedicalFinding	patients with			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Prolonged sleep latency, reduced sleep efficiency, increased number and duration of awakenings, reduced delta sleep, shortened REM sleep latency, and increased REM density are common polysomnographic features in patients with bipolar disorder.	topic_bd
76583	5	355665	7	NULL	NULL	0	NULL	REM sleep latency	MedicalFinding	shortened	polysomnographic features in					bipolar disorder	MedicalFinding	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	Prolonged sleep latency, reduced sleep efficiency, increased number and duration of awakenings, reduced delta sleep, shortened REM sleep latency, and increased REM density are common polysomnographic features in patients with bipolar disorder.	topic_bd
76584	6	355665	7	NULL	NULL	0	NULL	REM density 	MedicalFinding	increased	polysomnographic features in					bipolar disorder	MedicalFinding	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	Prolonged sleep latency, reduced sleep efficiency, increased number and duration of awakenings, reduced delta sleep, shortened REM sleep latency, and increased REM density are common polysomnographic features in patients with bipolar disorder.	topic_bd
76625	1	355666	7	NULL	NULL	NULL	NULL	S100A4 protein	GP	expression of	predictor of					colorectal cancer	MedicalFinding	recurrence in			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Expression of protein S100A4 is a predictor of recurrence in colorectal cancer.	topic_ccc
76626	1	355667	7	NULL	NULL	0	NULL	Luvox	Chemical		is a type of					antidepressant 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Luvox - Generic Fluvoxamine - which is a prescription antidepressant of the SSRI classification that may be used in the treatment of bipolar bipolar disorder and other mental illnesses.	topic_bd
76627	2	355667	7	NULL	NULL	0	NULL	Luvox	Chemical		is used in the					bipolar disorder	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Luvox - Generic Fluvoxamine - which is a prescription antidepressant of the SSRI classification that may be used in the treatment of bipolar bipolar disorder and other mental illnesses.	topic_bd
76628	3	355667	7	NULL	NULL	NULL	NULL	Luvox	Chemical		belongs to					SSRI 	Chemical	classification of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Luvox - Generic Fluvoxamine - which is a prescription antidepressant of the SSRI classification that may be used in the treatment of bipolar bipolar disorder and other mental illnesses.	topic_bd
76629	4	355667	7	NULL	NULL	NULL	NULL	Luvox	Chemical	generic name of	 is					Fluvoxamine	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Luvox - Generic Fluvoxamine - which is a prescription antidepressant of the SSRI classification that may be used in the treatment of bipolar bipolar disorder and other mental illnesses.	topic_bd
76630	5	355667	7	NULL	NULL	0	NULL	Luvox	Chemical		is used in the					mental illness	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Luvox - Generic Fluvoxamine - which is a prescription antidepressant of the SSRI classification that may be used in the treatment of bipolar bipolar disorder and other mental illnesses.	topic_bd
76631	1	355668	7	NULL	NULL	0	NULL	adenoma	MedicalFinding		distinguished from					fully blown colon carcinoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Defensin alpha 6 (DEFA 6) overexpression threshold of over 60 fold can distinguish between adenoma and fully blown colon carcinoma in individual patients.	topic_ccc
76632	2	355668	7	NULL	NULL	0	NULL	DEFA 6	GP	overexpression of	helps in					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Defensin alpha 6 (DEFA 6) overexpression threshold of over 60 fold can distinguish between adenoma and fully blown colon carcinoma in individual patients.	topic_ccc
76633	3	355668	7	NULL	NULL	0	NULL	DEFA 6	GP		is					Defensin alpha 6	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Defensin alpha 6 (DEFA 6) overexpression threshold of over 60 fold can distinguish between adenoma and fully blown colon carcinoma in individual patients.	topic_ccc
76634	1	355669	7	NULL	NULL	NULL	NULL	SSRI	Chemical		used as					antidepressant 	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Selective serotonin reuptake inhibitors or serotonin-specific reuptake inhibitor[1] (SSRIs) are a class of compounds typically used as antidepressants in the treatment of depression, anxiety disorders, and some personality disorders.	topic_bd
76636	2	355669	7	NULL	NULL	NULL	NULL	SSRI	Chemical		used in the 					depression	MedicalFinding	treatment of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Selective serotonin reuptake inhibitors or serotonin-specific reuptake inhibitor[1] (SSRIs) are a class of compounds typically used as antidepressants in the treatment of depression, anxiety disorders, and some personality disorders.	topic_bd
76637	3	355669	7	NULL	NULL	NULL	NULL	SSRI	Chemical		used in the 					anxiety disorders	MedicalFinding	treatment of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Selective serotonin reuptake inhibitors or serotonin-specific reuptake inhibitor[1] (SSRIs) are a class of compounds typically used as antidepressants in the treatment of depression, anxiety disorders, and some personality disorders.	topic_bd
76638	4	355669	7	NULL	NULL	NULL	NULL	SSRI	Chemical		used in the					personality disorders	MedicalFinding	treatment of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Selective serotonin reuptake inhibitors or serotonin-specific reuptake inhibitor[1] (SSRIs) are a class of compounds typically used as antidepressants in the treatment of depression, anxiety disorders, and some personality disorders.	topic_bd
76642	5	355669	7	NULL	NULL	NULL	NULL	SSRI	Chemical		is					serotonin-specific reuptake inhibitor	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Selective serotonin reuptake inhibitors or serotonin-specific reuptake inhibitor[1] (SSRIs) are a class of compounds typically used as antidepressants in the treatment of depression, anxiety disorders, and some personality disorders.	topic_bd
76643	6	355669	7	NULL	NULL	0	NULL	SSRI	Chemical		is					Selective serotonin reuptake inhibitors	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Selective serotonin reuptake inhibitors or serotonin-specific reuptake inhibitor[1] (SSRIs) are a class of compounds typically used as antidepressants in the treatment of depression, anxiety disorders, and some personality disorders.	topic_bd
76644	7	355669	7	NULL	NULL	0	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Selective serotonin reuptake inhibitors or serotonin-specific reuptake inhibitor[1] (SSRIs) are a class of compounds typically used as antidepressants in the treatment of depression, anxiety disorders, and some personality disorders.	topic_bd
76645	1	355671	7	NULL	NULL	0	NULL	SSRI	Chemical		first-line choice					bipolar disease	MedicalFinding	for the depressed phase of			NULL		0	NULL	NULL	NULL	NULL	NULL	Selective serotonin reuptake inhibitors (SSRIs) and other new antidepressants, such as buproprion and venlafaxine, are generally considered to be the first-line choices for the depressed phase of bipolar disease.	topic_bd
76646	2	355671	7	NULL	NULL	0	NULL	buproprion	Chemical		is a type of					new antidepressant	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Selective serotonin reuptake inhibitors (SSRIs) and other new antidepressants, such as buproprion and venlafaxine, are generally considered to be the first-line choices for the depressed phase of bipolar disease.	topic_bd
76647	3	355671	7	NULL	NULL	0	NULL	venlafaxine	Chemical		is a type of					new antidepressant 	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Selective serotonin reuptake inhibitors (SSRIs) and other new antidepressants, such as buproprion and venlafaxine, are generally considered to be the first-line choices for the depressed phase of bipolar disease.	topic_bd
76648	4	355671	7	NULL	NULL	0	NULL	buproprion	Chemical		first-line choice					bipolar disease	MedicalFinding	for the depressed phase of			NULL		0	NULL	NULL	NULL	NULL	NULL	Selective serotonin reuptake inhibitors (SSRIs) and other new antidepressants, such as buproprion and venlafaxine, are generally considered to be the first-line choices for the depressed phase of bipolar disease.	topic_bd
76649	5	355671	7	NULL	NULL	0	NULL	venlafaxine	Chemical		first-line choice					bipolar disease	MedicalFinding	for the depressed phase of			NULL		0	NULL	NULL	NULL	NULL	NULL	Selective serotonin reuptake inhibitors (SSRIs) and other new antidepressants, such as buproprion and venlafaxine, are generally considered to be the first-line choices for the depressed phase of bipolar disease.	topic_bd
76650	6	355671	7	NULL	NULL	0	NULL	SSRI	Chemical		is					Selective serotonin reuptake inhibitors	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Selective serotonin reuptake inhibitors (SSRIs) and other new antidepressants, such as buproprion and venlafaxine, are generally considered to be the first-line choices for the depressed phase of bipolar disease.	topic_bd
76651	1	355672	7	NULL	NULL	0	NULL	SSRI	Chemical		induce					mania	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mania or hypomania is a possible side effect. Users with some type of bipolar disorder are at a much higher risk, however SSRI-induced mania in patients previously diagnosed with unipolar depression can trigger a bipolar diagnosis.	topic_bd
76652	2	355672	7	NULL	NULL	0	NULL	statement 1	Process		occur in					unipolar depression	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mania or hypomania is a possible side effect. Users with some type of bipolar disorder are at a much higher risk, however SSRI-induced mania in patients previously diagnosed with unipolar depression can trigger a bipolar diagnosis.	topic_bd
76653	3	355672	7	NULL	NULL	0	NULL	statement 1	Process		trigger		could			bipolar depression	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mania or hypomania is a possible side effect. Users with some type of bipolar disorder are at a much higher risk, however SSRI-induced mania in patients previously diagnosed with unipolar depression can trigger a bipolar diagnosis.	topic_bd
76654	1	355673	7	NULL	NULL	0	NULL	lithium	Chemical		act through		potentially			GSK3	GP	inhibition of			NULL		0	NULL	NULL	NULL	NULL	NULL	Since lithium has been shown to potentially act through glycogen synthase kinase-3 (GSK3) inhibition, we evaluated the efficacy of selective GSK3 inhibitors in this model.	topic_bd
76655	2	355673	7	NULL	NULL	NULL	NULL	GSK3	GP		is					glycogen synthase kinase-3	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Since lithium has been shown to potentially act through glycogen synthase kinase-3 (GSK3) inhibition, we evaluated the efficacy of selective GSK3 inhibitors in this model.	topic_bd
76656	1	355674	7	NULL	NULL	0	NULL	DISC1gene	GP		associated with					schizophrenia	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	The Disrupted in Schizophrenia 1 (DISC1) gene has been associated with the risk of schizophrenia, schizoaffective disorder, bipolar disorder, major depression, autism, and Asperger syndrome in different populations.	topic_bd
76657	2	355674	7	NULL	NULL	0	NULL	DISC1gene	GP		associated with					schizoaffective disorder	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	The Disrupted in Schizophrenia 1 (DISC1) gene has been associated with the risk of schizophrenia, schizoaffective disorder, bipolar disorder, major depression, autism, and Asperger syndrome in different populations.	topic_bd
76658	3	355674	7	NULL	NULL	0	NULL	DISC1gene	GP		associated with					bipolar disorder	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	The Disrupted in Schizophrenia 1 (DISC1) gene has been associated with the risk of schizophrenia, schizoaffective disorder, bipolar disorder, major depression, autism, and Asperger syndrome in different populations.	topic_bd
76659	4	355674	7	NULL	NULL	0	NULL	DISC1gene	GP		associated with					major depression	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	The Disrupted in Schizophrenia 1 (DISC1) gene has been associated with the risk of schizophrenia, schizoaffective disorder, bipolar disorder, major depression, autism, and Asperger syndrome in different populations.	topic_bd
76660	5	355674	7	NULL	NULL	0	NULL	DISC1gene	GP		associated with					autism	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	The Disrupted in Schizophrenia 1 (DISC1) gene has been associated with the risk of schizophrenia, schizoaffective disorder, bipolar disorder, major depression, autism, and Asperger syndrome in different populations.	topic_bd
76661	6	355674	7	NULL	NULL	0	NULL	DISC1gene	GP		associated with					Asperger syndrome	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	The Disrupted in Schizophrenia 1 (DISC1) gene has been associated with the risk of schizophrenia, schizoaffective disorder, bipolar disorder, major depression, autism, and Asperger syndrome in different populations.	topic_bd
76662	7	355674	7	NULL	NULL	0	NULL	DISC1gene	GP		is					Disrupted in Schizophrenia 1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The Disrupted in Schizophrenia 1 (DISC1) gene has been associated with the risk of schizophrenia, schizoaffective disorder, bipolar disorder, major depression, autism, and Asperger syndrome in different populations.	topic_bd
76663	1	355675	7	NULL	NULL	0	NULL	MDR1 gene	GP	Polymorphism in the	occur in					colon cancer 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Polymorphism in the P-glycoprotein drug transporter MDR1 gene in colon cancer patients. 	topic_ccc
76664	2	355675	7	NULL	NULL	0	NULL	MDR1 gene	GP		is a type of					P-glycoprotein drug transporter	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Polymorphism in the P-glycoprotein drug transporter MDR1 gene in colon cancer patients. 	topic_ccc
76665	1	355677	7	NULL	NULL	NULL	NULL	MDR1 gene	GP	polymorphism of	associated with					colon cancer	MedicalFinding	occurence of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	 In the present study, an association of MDR1 gene polymorphism and the occurrence of colon cancer were evaluated.	topic_ccc
76666	1	355678	7	NULL	NULL	0	NULL	SN-38 	Chemical		active metabolite of					irinotecan	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	SN-38 is an active metabolite of the topoisomerase I inhibitor irinotecan. The mechanism behind its antitumor effect in colorectal cancer is not fully understood. 	topic_ccc
76667	2	355678	7	NULL	NULL	0	NULL	irinotecan	Chemical		is a type of					topoisomerase I inhibitor	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	SN-38 is an active metabolite of the topoisomerase I inhibitor irinotecan. The mechanism behind its antitumor effect in colorectal cancer is not fully understood. 	topic_ccc
76668	3	355678	7	NULL	NULL	0	NULL	SN-38	Chemical		possess					colorectal cancer	MedicalFinding	antitumor effect in			NULL		0	NULL	NULL	NULL	NULL	NULL	SN-38 is an active metabolite of the topoisomerase I inhibitor irinotecan. The mechanism behind its antitumor effect in colorectal cancer is not fully understood. 	topic_ccc
75960	1	355679	5	NULL	NULL	0	NULL	macrocephaly	MedicalFinding		is present in					autistic children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Research indicates the presence of macrocephaly or abnormally large head circumferences in children with autism and spectrum-related disorders, compared with their typically developing peers	topic_aut
75961	2	355679	5	NULL	NULL	0	NULL	macrocephaly	MedicalFinding		is present in					spectrum-related disorder children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Research indicates the presence of macrocephaly or abnormally large head circumferences in children with autism and spectrum-related disorders, compared with their typically developing peers	topic_aut
75962	3	355679	5	NULL	NULL	0	NULL	macrocephaly	MedicalFinding		is a synonym of					abnormally large head circumference	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Research indicates the presence of macrocephaly or abnormally large head circumferences in children with autism and spectrum-related disorders, compared with their typically developing peers	topic_aut
75998	1	355680	5	NULL	NULL	0	NULL	synaptic genes	GP	alternation of	plays a role in		important			ASD	MedicalFinding	pathogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	Recent genetic studies demonstrate that alterations in synaptic genes including those encoding cell adhesion molecules and their interaction partners play important roles in the pathogenesis of ASD	topic_aut
75999	2	355680	5	NULL	NULL	0	NULL	synaptic genes	GP		include					cell adhesion molecules	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Recent genetic studies demonstrate that alterations in synaptic genes including those encoding cell adhesion molecules and their interaction partners play important roles in the pathogenesis of ASD	topic_aut
76000	1	355681	5	NULL	NULL	0	NULL	autistic individuals	GroupOfPeople		use					emotion processing	Process	multiple routes of 			NULL		0	NULL	NULL	NULL	NULL	NULL	I elaborate on this model by discussing recent research on emotional recognition in individuals with autism, who can use multiple routes of emotion processing, and consequently can show atypical and typical patterns of embodied simulation and mimicry.	topic_aut
76001	2	355681	5	NULL	NULL	0	NULL	statement 1	Process		leads to		consequetly			embodied simulation	Process	atypical patterns of			NULL		0	NULL	NULL	NULL	NULL	NULL	I elaborate on this model by discussing recent research on emotional recognition in individuals with autism, who can use multiple routes of emotion processing, and consequently can show atypical and typical patterns of embodied simulation and mimicry.	topic_aut
76002	3	355681	5	NULL	NULL	0	NULL	statement 1	Process		leads to		consequetly			mimicry	Process	atypical patterns of			NULL		0	NULL	NULL	NULL	NULL	NULL	I elaborate on this model by discussing recent research on emotional recognition in individuals with autism, who can use multiple routes of emotion processing, and consequently can show atypical and typical patterns of embodied simulation and mimicry.	topic_aut
76003	4	355681	5	NULL	NULL	0	NULL	statement 1	Process		leads to		consequetly			embodied simulation	Process	typical patterns of			NULL		0	NULL	NULL	NULL	NULL	NULL	I elaborate on this model by discussing recent research on emotional recognition in individuals with autism, who can use multiple routes of emotion processing, and consequently can show atypical and typical patterns of embodied simulation and mimicry.	topic_aut
76004	5	355681	5	NULL	NULL	0	NULL	statement 1	Process		leads to		consequetly			mimicry	Process	typical patterns of			NULL		0	NULL	NULL	NULL	NULL	NULL	I elaborate on this model by discussing recent research on emotional recognition in individuals with autism, who can use multiple routes of emotion processing, and consequently can show atypical and typical patterns of embodied simulation and mimicry.	topic_aut
76005	1	355682	5	NULL	NULL	0	NULL	pregnancy	MedicalFinding	complications of 	implicate					fetal hypoxia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Autism spectrum disorders (ASD) are associated with complications of pregnancy that implicate fetal hypoxia (FH)	topic_aut
76006	2	355682	5	NULL	NULL	0	NULL	FH	MedicalFinding		is					fetal hypoxia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Autism spectrum disorders (ASD) are associated with complications of pregnancy that implicate fetal hypoxia (FH)	topic_aut
76007	3	355682	5	NULL	NULL	0	NULL	ASD	MedicalFinding		is					autism spectrum disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Autism spectrum disorders (ASD) are associated with complications of pregnancy that implicate fetal hypoxia (FH)	topic_aut
76008	4	355682	5	NULL	NULL	0	NULL	ASD	MedicalFinding		is associated with					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Autism spectrum disorders (ASD) are associated with complications of pregnancy that implicate fetal hypoxia (FH)	topic_aut
76009	1	355684	5	NULL	NULL	0	NULL	thimerosal	Chemical		is a type of					mercurial	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	These findings document neurotoxic effects of thimerosal, at doses equivalent to those used in infant vaccines or higher, in developing rat brain, suggesting likely involvement of this mercurial in neurodevelopmental disorders	topic_aut
76010	2	355684	5	NULL	NULL	0	NULL	thimerosal	Chemical		is involved in					neurodevelopmental disorders	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	These findings document neurotoxic effects of thimerosal, at doses equivalent to those used in infant vaccines or higher, in developing rat brain, suggesting likely involvement of this mercurial in neurodevelopmental disorders	topic_aut
76011	1	355686	5	NULL	NULL	0	NULL	porphyrin	Chemical	disordered metabolism of	is a characteristic of		salient			autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	These findings identify disordered porphyrin metabolism as a salient characteristic of autism.	topic_aut
76012	1	355687	5	NULL	NULL	0	NULL	familial platelet disorder 	MedicalFinding		confers susceptibility to					acute myelogenous leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Gilliland and his colleagues have identified genetic mutations that cause a familial platelet disorder that confers susceptibility to acute myelogenous leukemia (AML).	topic_ll
76013	2	355687	5	NULL	NULL	0	NULL	acute myelogenous leukemia	MedicalFinding		is					AML	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Gilliland and his colleagues have identified genetic mutations that cause a familial platelet disorder that confers susceptibility to acute myelogenous leukemia (AML).	topic_ll
76014	1	355688	5	NULL	NULL	0	NULL	CBFA2 protein	GP		activates					blood cell	Cell	development of			NULL		0	NULL	NULL	NULL	NULL	NULL	Looking more closely at that region of chromosome 21, the researchers found a mutation in the gene, CBFA2, which produces a protein that activates blood cell development.	topic_ll
76015	2	355688	5	NULL	NULL	0	NULL	CBFA2 gene	GP		is present in					chromosome 21	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	Looking more closely at that region of chromosome 21, the researchers found a mutation in the gene, CBFA2, which produces a protein that activates blood cell development.	topic_ll
76016	1	355689	5	NULL	NULL	0	NULL	chromosomes	Chromosome		swap		inappropriately			genetic material	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	Leukemias and lymphomas can arise when chromosomes inappropriately swap genetic material.	topic_ll
76017	2	355689	5	NULL	NULL	0	NULL	statement 1	Process		leads to					leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Leukemias and lymphomas can arise when chromosomes inappropriately swap genetic material.	topic_ll
76018	3	355689	5	NULL	NULL	0	NULL	statement 1	Process		leads to					lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Leukemias and lymphomas can arise when chromosomes inappropriately swap genetic material.	topic_ll
76019	1	355691	5	NULL	NULL	0	NULL	gene	GP	complex translocation of	leads to					genome	Chromosome	amplification of;;large regions of 			NULL		0	NULL	NULL	NULL	NULL	NULL	In some cases, more complex gene translocations (as opposed to swapping one gene for another) lead to amplification of large regions of the genome. Alt and his colleagues coined the term complicon—derived from complex translocation—to describe this phenomenon. 	topic_ll
76020	2	355691	5	NULL	NULL	0	NULL	statement 1	Process		is termed					complicon	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In some cases, more complex gene translocations (as opposed to swapping one gene for another) lead to amplification of large regions of the genome. Alt and his colleagues coined the term complicon—derived from complex translocation—to describe this phenomenon. 	topic_ll
76021	1	355693	5	NULL	NULL	0	NULL	lymphoma	MedicalFinding		is a type of					blood cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In the 1970s, clinicians noted that the blood cancer lymphoma was also very common in boys with XLP. “	topic_ll
76022	2	355693	5	NULL	NULL	0	NULL	lymphoma	MedicalFinding		is common in					XLP boys	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	In the 1970s, clinicians noted that the blood cancer lymphoma was also very common in boys with XLP. “	topic_ll
76023	1	355694	5	NULL	NULL	0	NULL	XLP	MedicalFinding		is					X-linked lymphoproliferative disease	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The findings, published on August 2, 2009 in Nature Immunology, may also lead to better understanding of a rare genetic disorder called X-linked lymphoproliferative disease (XLP), which causes the immune system to go into overdrive. 	topic_ll
76024	2	355694	5	NULL	NULL	0	NULL	XLP	MedicalFinding		is a type of					rare genetic disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The findings, published on August 2, 2009 in Nature Immunology, may also lead to better understanding of a rare genetic disorder called X-linked lymphoproliferative disease (XLP), which causes the immune system to go into overdrive. 	topic_ll
76025	3	355694	5	NULL	NULL	0	NULL	XLP	MedicalFinding		overdrives					immune system	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The findings, published on August 2, 2009 in Nature Immunology, may also lead to better understanding of a rare genetic disorder called X-linked lymphoproliferative disease (XLP), which causes the immune system to go into overdrive. 	topic_ll
76026	1	355695	5	NULL	NULL	0	NULL	natural killer cells	Cell		lacks					SAP-related molecules	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Further experiments in live mice confirmed that the natural killer cells lacking the SAP-related molecules were unable to kill lymphoma cells. 	topic_ll
76027	2	355695	5	NULL	NULL	0	NULL	statement 1	Process		unable to kill					lymphoma cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Further experiments in live mice confirmed that the natural killer cells lacking the SAP-related molecules were unable to kill lymphoma cells. 	topic_ll
76028	1	355696	5	NULL	NULL	0	NULL	SAP	GP		is					SLAM-Associated Protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	molecules interact with SAP (which stands for SLAM-Associated Protein), but no one understood what role SAP played in commanding the immune system’s assassins to attack. 	topic_ll
76029	2	355696	5	NULL	NULL	0	NULL	immune system assassins	GP		is commanded to					attack	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	molecules interact with SAP (which stands for SLAM-Associated Protein), but no one understood what role SAP played in commanding the immune system’s assassins to attack. 	topic_ll
76030	3	355696	5	NULL	NULL	0	NULL	SAP	GP		plays a role in		possibly			statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	molecules interact with SAP (which stands for SLAM-Associated Protein), but no one understood what role SAP played in commanding the immune system’s assassins to attack. 	topic_ll
76031	1	355697	5	NULL	NULL	0	NULL	mycosis fungoides	MedicalFinding		is also known as					Alibert-Bazin syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mycosis fungoides (also known as Alibert-Bazin syndrome or granuloma fungoides), is the most common form of cutaneous T-cell lymphoma.	topic_ll
76032	2	355697	5	NULL	NULL	0	NULL	mycosis fungoides	MedicalFinding		is also known as					granuloma fungoides	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mycosis fungoides (also known as Alibert-Bazin syndrome or granuloma fungoides), is the most common form of cutaneous T-cell lymphoma.	topic_ll
76033	3	355697	5	NULL	NULL	0	NULL	mycosis fungoides	MedicalFinding		is a form of		most common			cutaneous T-cell lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mycosis fungoides (also known as Alibert-Bazin syndrome or granuloma fungoides), is the most common form of cutaneous T-cell lymphoma.	topic_ll
76034	1	355699	5	NULL	NULL	0	NULL	lymphocyte	Cell		is a type of					white blood cell	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Mycosis fungoides and the Sézary syndrome are diseases in which lymphocytes (a type of white blood cell) become malignant (cancerous) and affect the skin.	topic_ll
76035	2	355699	5	NULL	NULL	0	NULL	 lymphocyte	Cell		become					malignant	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mycosis fungoides and the Sézary syndrome are diseases in which lymphocytes (a type of white blood cell) become malignant (cancerous) and affect the skin.	topic_ll
76036	3	355699	5	NULL	NULL	0	NULL	statement 2	Process		affects					skin	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Mycosis fungoides and the Sézary syndrome are diseases in which lymphocytes (a type of white blood cell) become malignant (cancerous) and affect the skin.	topic_ll
76037	4	355699	5	NULL	NULL	0	NULL	malignant	MedicalFinding		is also known as					cancerous	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mycosis fungoides and the Sézary syndrome are diseases in which lymphocytes (a type of white blood cell) become malignant (cancerous) and affect the skin.	topic_ll
76038	5	355699	5	NULL	NULL	0	NULL	mycosis fungoides	MedicalFinding		leads to					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Mycosis fungoides and the Sézary syndrome are diseases in which lymphocytes (a type of white blood cell) become malignant (cancerous) and affect the skin.	topic_ll
76039	6	355699	5	NULL	NULL	0	NULL	Sézary syndrome	MedicalFinding		leads to					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Mycosis fungoides and the Sézary syndrome are diseases in which lymphocytes (a type of white blood cell) become malignant (cancerous) and affect the skin.	topic_ll
76040	1	355700	5	NULL	NULL	0	NULL	Pagetoid reticulosis of Woringer-Kolopp	MedicalFinding		is a form of		rare			cutaneous T-cell lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Pagetoid reticulosis of Woringer-Kolopp is a rare form of cutaneous T-cell lymphoma that primarily affects middle-aged males.	topic_ll
76041	2	355700	5	NULL	NULL	0	NULL	cutaneous T-cell lymphoma	MedicalFinding		affects		primarily			middle-aged males	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Pagetoid reticulosis of Woringer-Kolopp is a rare form of cutaneous T-cell lymphoma that primarily affects middle-aged males.	topic_ll
76053	1	355701	5	NULL	NULL	0	NULL	Pagetoid reticulosis of Woringer-Kolopp	MedicalFinding		is a form of		rare			cutaneous T-cell lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Pagetoid reticulosis of Woringer-Kolopp is a rare form of cutaneous T-cell lymphoma that primarily affects middle-aged males. It is characterized by the presence of one or several scaly patches and plaques with an acral distribution.	topic_ll
76054	2	355701	5	NULL	NULL	0	NULL	statement 1	MedicalFinding		affects		primarily			middle-aged males	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Pagetoid reticulosis of Woringer-Kolopp is a rare form of cutaneous T-cell lymphoma that primarily affects middle-aged males. It is characterized by the presence of one or several scaly patches and plaques with an acral distribution.	topic_ll
76055	3	355701	5	NULL	NULL	0	NULL	statement 1	MedicalFinding		is characterized by					scaly patches	MedicalFinding	presence of			NULL		0	NULL	NULL	NULL	NULL	NULL	Pagetoid reticulosis of Woringer-Kolopp is a rare form of cutaneous T-cell lymphoma that primarily affects middle-aged males. It is characterized by the presence of one or several scaly patches and plaques with an acral distribution.	topic_ll
76056	4	355701	5	NULL	NULL	0	NULL	statement 1	MedicalFinding		is characterized by					plaques	MedicalFinding	presence of			NULL		0	NULL	NULL	NULL	NULL	NULL	Pagetoid reticulosis of Woringer-Kolopp is a rare form of cutaneous T-cell lymphoma that primarily affects middle-aged males. It is characterized by the presence of one or several scaly patches and plaques with an acral distribution.	topic_ll
76057	5	355701	5	NULL	NULL	0	NULL	scaly patches	MedicalFinding		is distributed					acrally	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Pagetoid reticulosis of Woringer-Kolopp is a rare form of cutaneous T-cell lymphoma that primarily affects middle-aged males. It is characterized by the presence of one or several scaly patches and plaques with an acral distribution.	topic_ll
76058	6	355701	5	NULL	NULL	0	NULL	plaques	MedicalFinding		is distributed					acrally	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Pagetoid reticulosis of Woringer-Kolopp is a rare form of cutaneous T-cell lymphoma that primarily affects middle-aged males. It is characterized by the presence of one or several scaly patches and plaques with an acral distribution.	topic_ll
76059	1	355702	5	NULL	NULL	0	NULL	pagetoid reticulosis	MedicalFinding	localized	is a type of					polycyclic erythematous scaly lesions	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Localized pagetoid reticulosis is an uncommon disease described by Woringer and Kolopp in 1939 as "polycyclic erythematous scaly lesions with 6-year evolution on the forearm of 13-year-old boy" [1]. 	topic_ll
76060	2	355702	5	NULL	NULL	0	NULL	pagetoid reticulosis	MedicalFinding	localized	identified by					Woringer and Kolopp	Person				NULL		0	NULL	NULL	NULL	NULL	NULL	Localized pagetoid reticulosis is an uncommon disease described by Woringer and Kolopp in 1939 as "polycyclic erythematous scaly lesions with 6-year evolution on the forearm of 13-year-old boy" [1]. 	topic_ll
76061	1	355703	5	NULL	NULL	0	NULL	Pagetoid reticulosis	MedicalFinding		features					lesions	MedicalFinding	acral distribution of			NULL		0	NULL	NULL	NULL	NULL	NULL	Pagetoid reticulosis features acral distribution of lesions, pronounced hyperkeratosis and acanthosis, prominent epidermotropism, and expression of a cutaneous lymphocyte antigen 	topic_ll
76062	2	355703	5	NULL	NULL	0	NULL	Pagetoid reticulosis	MedicalFinding		features					hyperkeratosis	MedicalFinding	pronounced			NULL		0	NULL	NULL	NULL	NULL	NULL	Pagetoid reticulosis features acral distribution of lesions, pronounced hyperkeratosis and acanthosis, prominent epidermotropism, and expression of a cutaneous lymphocyte antigen 	topic_ll
76063	3	355703	5	NULL	NULL	0	NULL	Pagetoid reticulosis	MedicalFinding		features					acanthosis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Pagetoid reticulosis features acral distribution of lesions, pronounced hyperkeratosis and acanthosis, prominent epidermotropism, and expression of a cutaneous lymphocyte antigen 	topic_ll
76064	4	355703	5	NULL	NULL	0	NULL	Pagetoid reticulosis	MedicalFinding		features					epidermotropism	MedicalFinding	prominent			NULL		0	NULL	NULL	NULL	NULL	NULL	Pagetoid reticulosis features acral distribution of lesions, pronounced hyperkeratosis and acanthosis, prominent epidermotropism, and expression of a cutaneous lymphocyte antigen 	topic_ll
76065	5	355703	5	NULL	NULL	0	NULL	Pagetoid reticulosis	MedicalFinding		features					cutaneous lymphocyte antigen	GP	 expression of			NULL		0	NULL	NULL	NULL	NULL	NULL	Pagetoid reticulosis features acral distribution of lesions, pronounced hyperkeratosis and acanthosis, prominent epidermotropism, and expression of a cutaneous lymphocyte antigen 	topic_ll
76066	1	355704	5	NULL	NULL	0	NULL	GSS	MedicalFinding		is					granulomatous slack skin	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Granulomatous slack skin (GSS) is a rare cutaneous disorder characterized clinically by the evolution of circumscribed erythematous lax skin masses, especially in the body folds, and histologically by a granulomatous T-cell infiltrate and loss of elastic fibers.	topic_ll
76067	2	355704	5	NULL	NULL	0	NULL	granulomatous slack skin\t\t	MedicalFinding		is a type of					rare cutaneous disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Granulomatous slack skin (GSS) is a rare cutaneous disorder characterized clinically by the evolution of circumscribed erythematous lax skin masses, especially in the body folds, and histologically by a granulomatous T-cell infiltrate and loss of elastic fibers.	topic_ll
76068	3	355704	5	NULL	NULL	NULL	NULL	GSS	MedicalFinding		is characterized by		clinically			erythematous lax skin masses	MedicalFinding	evolution of;;circumscribed			NULL	body folds	NULL	NULL	NULL	NULL	NULL	NULL	Granulomatous slack skin (GSS) is a rare cutaneous disorder characterized clinically by the evolution of circumscribed erythematous lax skin masses, especially in the body folds, and histologically by a granulomatous T-cell infiltrate and loss of elastic fibers.	topic_ll
76069	4	355704	5	NULL	NULL	0	NULL	GSS	MedicalFinding		is characterized by		histologically			granulomatous T-cell infiltrate	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Granulomatous slack skin (GSS) is a rare cutaneous disorder characterized clinically by the evolution of circumscribed erythematous lax skin masses, especially in the body folds, and histologically by a granulomatous T-cell infiltrate and loss of elastic fibers.	topic_ll
76070	5	355704	5	NULL	NULL	NULL	NULL	GSS	MedicalFinding		is characterized by					elastic fibers	CellComponent	loss of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Granulomatous slack skin (GSS) is a rare cutaneous disorder characterized clinically by the evolution of circumscribed erythematous lax skin masses, especially in the body folds, and histologically by a granulomatous T-cell infiltrate and loss of elastic fibers.	topic_ll
76071	1	355705	5	NULL	NULL	0	NULL	GSS	MedicalFinding		is associated with					lymphoproliferative malignancies	MedicalFinding	preceding			NULL		0	NULL	NULL	NULL	NULL	NULL	GSS is often associated with preceding or subsequent lymphoproliferative malignancies, especially mycosis fungoides (MF) and Hodgkin's disease (HD). 	topic_ll
76072	2	355705	5	NULL	NULL	0	NULL	GSS	MedicalFinding		is associated with					lymphoproliferative malignancies	MedicalFinding	subsequent			NULL		0	NULL	NULL	NULL	NULL	NULL	GSS is often associated with preceding or subsequent lymphoproliferative malignancies, especially mycosis fungoides (MF) and Hodgkin's disease (HD). 	topic_ll
76073	3	355705	5	NULL	NULL	0	NULL	MF	MedicalFinding		is					mycosis fungoides	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	GSS is often associated with preceding or subsequent lymphoproliferative malignancies, especially mycosis fungoides (MF) and Hodgkin's disease (HD). 	topic_ll
76074	4	355705	5	NULL	NULL	0	NULL	HD	MedicalFinding		is					Hodgkin's disease	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	GSS is often associated with preceding or subsequent lymphoproliferative malignancies, especially mycosis fungoides (MF) and Hodgkin's disease (HD). 	topic_ll
76075	5	355705	5	NULL	NULL	0	NULL	MF	MedicalFinding		is a type of					lymphoproliferative malignancies	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	GSS is often associated with preceding or subsequent lymphoproliferative malignancies, especially mycosis fungoides (MF) and Hodgkin's disease (HD). 	topic_ll
76076	6	355705	5	NULL	NULL	0	NULL	HD	MedicalFinding		is a type of					lymphoproliferative malignancies	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	GSS is often associated with preceding or subsequent lymphoproliferative malignancies, especially mycosis fungoides (MF) and Hodgkin's disease (HD). 	topic_ll
76089	7	355705	5	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	GSS is often associated with preceding or subsequent lymphoproliferative malignancies, especially mycosis fungoides (MF) and Hodgkin's disease (HD). 	topic_ll
76077	1	355706	5	NULL	NULL	0	NULL	elastic fibers	CellComponent	disappearance of	results in					lax skin	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Apparently, the disease is associated with a peculiar immune response, characterized by granuloma formation and disappearance of elastic fibers resulting in the lax skin. 	topic_ll
76078	1	355708	5	NULL	NULL	0	NULL	Bexarotene capsules	Chemical		slow					CTCL tumors	MedicalFinding	growth of;;large			NULL		0	NULL	NULL	NULL	NULL	NULL	Bexarotene capsules Bexarotene in capsule form can slow or stall the growth of large CTCL tumors. The patient ingests the pill with food daily.	topic_ll
76079	2	355708	5	NULL	NULL	0	NULL	Bexarotene capsules	Chemical		stall					CTCL tumors	MedicalFinding	growth of;;large			NULL		0	NULL	NULL	NULL	NULL	NULL	Bexarotene capsules Bexarotene in capsule form can slow or stall the growth of large CTCL tumors. The patient ingests the pill with food daily.	topic_ll
76080	3	355708	5	NULL	NULL	0	NULL	Bexarotene capsules	Chemical		is ingested with					food	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Bexarotene capsules Bexarotene in capsule form can slow or stall the growth of large CTCL tumors. The patient ingests the pill with food daily.	topic_ll
76081	1	355709	5	NULL	NULL	0	NULL	PUVA treatment	MedicalProcedure		is also known as					photochemotherapy	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Also known as photochemotherapy, PUVA treatment is successful in treating CTCL where large areas of the skin are affected.	topic_ll
76082	2	355709	5	NULL	NULL	0	NULL	PUVA treatment	MedicalProcedure		is used to treat		successfully			CTCL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Also known as photochemotherapy, PUVA treatment is successful in treating CTCL where large areas of the skin are affected.	topic_ll
76083	3	355709	5	NULL	NULL	0	NULL	CTCL	MedicalFinding		affects					skin	OrganismPart	large areas of			NULL		0	NULL	NULL	NULL	NULL	NULL	Also known as photochemotherapy, PUVA treatment is successful in treating CTCL where large areas of the skin are affected.	topic_ll
76084	1	355710	5	NULL	NULL	0	NULL	psoralen	Chemical		is a type of					drug	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The patient takes a drug called psoralen (P), which makes the skin sensitive to Ultraviolet A light rays. The UVA then attacks cancerous cells.	topic_ll
76085	2	355710	5	NULL	NULL	0	NULL	skin	OrganismPart		is made sensitive to					Ultraviolet A light rays	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	The patient takes a drug called psoralen (P), which makes the skin sensitive to Ultraviolet A light rays. The UVA then attacks cancerous cells.	topic_ll
76086	3	355710	5	NULL	NULL	0	NULL	psoralen	Chemical		plays a role in					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The patient takes a drug called psoralen (P), which makes the skin sensitive to Ultraviolet A light rays. The UVA then attacks cancerous cells.	topic_ll
76087	4	355710	5	NULL	NULL	0	NULL	UVA	PhysicalPhenomenon		attacks					cancerous cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	The patient takes a drug called psoralen (P), which makes the skin sensitive to Ultraviolet A light rays. The UVA then attacks cancerous cells.	topic_ll
76088	5	355710	5	NULL	NULL	0	NULL	statement 2	Process		is followed by					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The patient takes a drug called psoralen (P), which makes the skin sensitive to Ultraviolet A light rays. The UVA then attacks cancerous cells.	topic_ll
76090	1	355712	5	NULL	NULL	0	NULL	blood	OrganismPart		is removed from 					patient	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76091	2	355712	5	NULL	NULL	0	NULL	blood	OrganismPart		is cycled through					machine	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76092	3	355712	5	NULL	NULL	0	NULL	statement 1	Process		is followed by					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76093	13	355712	5	NULL	NULL	NULL	NULL	Pheresis treatment	MedicalProcedure		involves					statement 1	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76094	14	355712	5	NULL	NULL	NULL	NULL	Pheresis treatment	MedicalProcedure		involves					statement 2	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76095	4	355712	5	NULL	NULL	0	NULL	statement 2	Process		cleans					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76096	5	355712	5	NULL	NULL	NULL	NULL	statement 2	Process		treats					statement 1	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76097	6	355712	5	NULL	NULL	0	NULL	statement 4	Process		is an alternative to					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76098	7	355712	5	NULL	NULL	0	NULL	blood	OrganismPart	cleaned	returned to					patient	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76099	8	355712	5	NULL	NULL	0	NULL	blood	OrganismPart	treated	returned to					patient	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76100	9	355712	5	NULL	NULL	0	NULL	statement 2	Process		is followed by					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76101	10	355712	5	NULL	NULL	0	NULL	statement 2	Process		is followed by					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76102	11	355712	5	NULL	NULL	0	NULL	statement 9	Process		is followed by					statement 7	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76103	12	355712	5	NULL	NULL	0	NULL	statement 10	Process		is followed by					statement 8	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76104	15	355712	5	NULL	NULL	0	NULL	Pheresis treatment	MedicalProcedure		involves					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76105	16	355712	5	NULL	NULL	0	NULL	Pheresis treatment	MedicalProcedure		involves					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76106	17	355712	5	NULL	NULL	0	NULL	Pheresis treatment	MedicalProcedure		involves					statement 7	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76107	18	355712	5	NULL	NULL	0	NULL	Pheresis treatment	MedicalProcedure		involves					statement 8	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76108	19	355712	5	NULL	NULL	NULL	NULL	blood	OrganismPart		is exposed to					UV light	PhysicalPhenomenon				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76109	20	355712	5	NULL	NULL	0	NULL	statement 19	Process		before returning to					Sézary Syndrome patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76110	21	355712	5	NULL	NULL	0	NULL	T-cells	Cell	affected	is removed from					blood	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76111	22	355712	5	NULL	NULL	NULL	NULL	statement 19	Process		leads to					statement 21	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Photopheresis Pheresis treatments involve removing blood from a patient, cycling it through a machine to clean or treat it, and then returning it to the patient. For Sézary Syndrome patients, the blood is exposed to UV light before it is returned to the body. This helps remove affected T-cells from the blood.	topic_ll
76112	1	355713	5	NULL	NULL	NULL	NULL	Zevalin®	Chemical		is a form of					radioimmunotherapy	MedicalProcedure				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Zevalin® (ibritumomab tiuxetan) is a form of radioimmunotherapy (a radiolabeled monoclonal antibody) indicated for treatment of patients with relapsed or refractory, low grade or follicular B-cell non-Hodgkin's lymphoma (NHL) or for patients with previously untreated follicular NHL who achieve a partial or complete response to first-line chemotherapy.	topic_ll
76113	2	355713	5	NULL	NULL	NULL	NULL	Zevalin®	Chemical		is a type of					radiolabeled monoclonal antibody	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Zevalin® (ibritumomab tiuxetan) is a form of radioimmunotherapy (a radiolabeled monoclonal antibody) indicated for treatment of patients with relapsed or refractory, low grade or follicular B-cell non-Hodgkin's lymphoma (NHL) or for patients with previously untreated follicular NHL who achieve a partial or complete response to first-line chemotherapy.	topic_ll
76114	3	355713	5	NULL	NULL	0	NULL	Zevalin® 	Chemical		is also known as					ibritumomab tiuxetan	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Zevalin® (ibritumomab tiuxetan) is a form of radioimmunotherapy (a radiolabeled monoclonal antibody) indicated for treatment of patients with relapsed or refractory, low grade or follicular B-cell non-Hodgkin's lymphoma (NHL) or for patients with previously untreated follicular NHL who achieve a partial or complete response to first-line chemotherapy.	topic_ll
76115	4	355713	5	NULL	NULL	0	NULL	Zevalin®	Chemical		is used to treat					NHL	MedicalFinding	relapsed or refractory;;low grade or follicular B-cell			NULL		0	NULL	NULL	NULL	NULL	NULL	Zevalin® (ibritumomab tiuxetan) is a form of radioimmunotherapy (a radiolabeled monoclonal antibody) indicated for treatment of patients with relapsed or refractory, low grade or follicular B-cell non-Hodgkin's lymphoma (NHL) or for patients with previously untreated follicular NHL who achieve a partial or complete response to first-line chemotherapy.	topic_ll
76116	5	355713	5	NULL	NULL	0	NULL	NHL	MedicalFinding		is					non-Hodgkin's lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Zevalin® (ibritumomab tiuxetan) is a form of radioimmunotherapy (a radiolabeled monoclonal antibody) indicated for treatment of patients with relapsed or refractory, low grade or follicular B-cell non-Hodgkin's lymphoma (NHL) or for patients with previously untreated follicular NHL who achieve a partial or complete response to first-line chemotherapy.	topic_ll
76117	8	355713	5	NULL	NULL	NULL	NULL	Zevalin®	Chemical		is used to treat					statement 6	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Zevalin® (ibritumomab tiuxetan) is a form of radioimmunotherapy (a radiolabeled monoclonal antibody) indicated for treatment of patients with relapsed or refractory, low grade or follicular B-cell non-Hodgkin's lymphoma (NHL) or for patients with previously untreated follicular NHL who achieve a partial or complete response to first-line chemotherapy.	topic_ll
76118	6	355713	5	NULL	NULL	NULL	NULL	follicular NHL patients	GroupOfPeople	untreated	respond to		partially			first-line chemotherapy	MedicalProcedure				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Zevalin® (ibritumomab tiuxetan) is a form of radioimmunotherapy (a radiolabeled monoclonal antibody) indicated for treatment of patients with relapsed or refractory, low grade or follicular B-cell non-Hodgkin's lymphoma (NHL) or for patients with previously untreated follicular NHL who achieve a partial or complete response to first-line chemotherapy.	topic_ll
76119	7	355713	5	NULL	NULL	0	NULL	follicular NHL patients	GroupOfPeople	untreated	respond to		completely			first-line chemotherapy	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Zevalin® (ibritumomab tiuxetan) is a form of radioimmunotherapy (a radiolabeled monoclonal antibody) indicated for treatment of patients with relapsed or refractory, low grade or follicular B-cell non-Hodgkin's lymphoma (NHL) or for patients with previously untreated follicular NHL who achieve a partial or complete response to first-line chemotherapy.	topic_ll
76120	9	355713	5	NULL	NULL	0	NULL	Zevalin®	Chemical		is used to treat					statement 7	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Zevalin® (ibritumomab tiuxetan) is a form of radioimmunotherapy (a radiolabeled monoclonal antibody) indicated for treatment of patients with relapsed or refractory, low grade or follicular B-cell non-Hodgkin's lymphoma (NHL) or for patients with previously untreated follicular NHL who achieve a partial or complete response to first-line chemotherapy.	topic_ll
76121	1	355714	5	NULL	NULL	0	NULL	lymphoma	MedicalFinding		causes		may			lymph nodes	OrganismPart	swelling of			NULL	neck	0	NULL	NULL	NULL	NULL	NULL	Lymphoma may cause swelling of lymph nodes in the neck, chest, abdomen and on the skin.	topic_ll
76122	2	355714	5	NULL	NULL	0	NULL	lymphoma	MedicalFinding		causes		may			lymph nodes	OrganismPart	swelling of			NULL	chest	0	NULL	NULL	NULL	NULL	NULL	Lymphoma may cause swelling of lymph nodes in the neck, chest, abdomen and on the skin.	topic_ll
76123	3	355714	5	NULL	NULL	0	NULL	lymphoma	MedicalFinding		causes		may			lymph nodes	OrganismPart	swelling of			NULL	abdomen	0	NULL	NULL	NULL	NULL	NULL	Lymphoma may cause swelling of lymph nodes in the neck, chest, abdomen and on the skin.	topic_ll
76124	4	355714	5	NULL	NULL	NULL	NULL	lymphoma	MedicalFinding		causes		may			lymph nodes	OrganismPart	swelling of			NULL	skin	NULL	NULL	NULL	NULL	NULL	NULL	Lymphoma may cause swelling of lymph nodes in the neck, chest, abdomen and on the skin.	topic_ll
76125	1	355715	5	NULL	NULL	0	NULL	lymphoma	MedicalFinding		affects					thymus	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Chest pain Chest pain may occur if the lymphoma affects the thymus	topic_ll
76126	2	355715	5	NULL	NULL	0	NULL	statement 1	Process		causes					Chest pain	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Chest pain Chest pain may occur if the lymphoma affects the thymus	topic_ll
76127	1	355716	5	NULL	NULL	0	NULL	fever	MedicalFinding		recurs					other symptoms	MedicalFinding	 in comjuction with			NULL		0	NULL	NULL	NULL	NULL	NULL	Recurring Fevers Obviously, fever can be a sign of just about anything. When fever recurs for no apparent reason, especially in conjunction with other symptoms, it could be a sign of lymphoma.	topic_ll
76128	2	355716	5	NULL	NULL	0	NULL	statement 1	Process		is a sign of					lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Recurring Fevers Obviously, fever can be a sign of just about anything. When fever recurs for no apparent reason, especially in conjunction with other symptoms, it could be a sign of lymphoma.	topic_ll
76132	1	355717	5	NULL	NULL	0	NULL	pruritis	MedicalFinding		is a synonym of					Itchy skin	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Rashes Itchy skin (pruritis), rashes and lesions can be a sign of lymphoma, particularly cutaneous lymphoma	topic_ll
76133	2	355717	5	NULL	NULL	0	NULL	pruritis	MedicalFinding		is a sign of					cutaneous lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Rashes Itchy skin (pruritis), rashes and lesions can be a sign of lymphoma, particularly cutaneous lymphoma	topic_ll
76134	3	355717	5	NULL	NULL	0	NULL	rashes 	MedicalFinding		is a sign of					cutaneous lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Rashes Itchy skin (pruritis), rashes and lesions can be a sign of lymphoma, particularly cutaneous lymphoma	topic_ll
76135	4	355717	5	NULL	NULL	0	NULL	lesions	MedicalFinding		is a sign of					cutaneous lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Rashes Itchy skin (pruritis), rashes and lesions can be a sign of lymphoma, particularly cutaneous lymphoma	topic_ll
76136	1	355719	5	NULL	NULL	0	NULL	alcohol	Chemical	consumption of	puts stress on					lymphatic system	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Sore lymph nodes after drinking Alchohol consumption puts stress on the lymphatic system which, along with the liver and kidneys, is part of the body's blood cleansing apparatus. If the lymph system is weakened by lymphoma, drinking may cause pain in the affected areas.Lymph nodes are possibly painful after alcohol consumption. 	topic_ll
76137	2	355719	5	NULL	NULL	0	NULL	lymphatic system	OrganismPart		is a part of					blood cleansing apparatus	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Sore lymph nodes after drinking Alchohol consumption puts stress on the lymphatic system which, along with the liver and kidneys, is part of the body's blood cleansing apparatus. If the lymph system is weakened by lymphoma, drinking may cause pain in the affected areas.Lymph nodes are possibly painful after alcohol consumption. 	topic_ll
76138	3	355719	5	NULL	NULL	0	NULL	liver	OrganismPart		is a part of					blood cleansing apparatus	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Sore lymph nodes after drinking Alchohol consumption puts stress on the lymphatic system which, along with the liver and kidneys, is part of the body's blood cleansing apparatus. If the lymph system is weakened by lymphoma, drinking may cause pain in the affected areas.Lymph nodes are possibly painful after alcohol consumption. 	topic_ll
76139	4	355719	5	NULL	NULL	0	NULL	kidneys	OrganismPart		is a part of					blood cleansing apparatus	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Sore lymph nodes after drinking Alchohol consumption puts stress on the lymphatic system which, along with the liver and kidneys, is part of the body's blood cleansing apparatus. If the lymph system is weakened by lymphoma, drinking may cause pain in the affected areas.Lymph nodes are possibly painful after alcohol consumption. 	topic_ll
76140	5	355719	5	NULL	NULL	0	NULL	 lymph system	OrganismPart		is weakened by					lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Sore lymph nodes after drinking Alchohol consumption puts stress on the lymphatic system which, along with the liver and kidneys, is part of the body's blood cleansing apparatus. If the lymph system is weakened by lymphoma, drinking may cause pain in the affected areas.Lymph nodes are possibly painful after alcohol consumption. 	topic_ll
76141	6	355719	5	NULL	NULL	0	NULL	drinking	Process		causes					affected areas	OrganismPart	pain of			NULL		0	NULL	NULL	NULL	NULL	NULL	Sore lymph nodes after drinking Alchohol consumption puts stress on the lymphatic system which, along with the liver and kidneys, is part of the body's blood cleansing apparatus. If the lymph system is weakened by lymphoma, drinking may cause pain in the affected areas.Lymph nodes are possibly painful after alcohol consumption. 	topic_ll
76142	7	355719	5	NULL	NULL	0	NULL	statement 5	Process		leads to					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Sore lymph nodes after drinking Alchohol consumption puts stress on the lymphatic system which, along with the liver and kidneys, is part of the body's blood cleansing apparatus. If the lymph system is weakened by lymphoma, drinking may cause pain in the affected areas.Lymph nodes are possibly painful after alcohol consumption. 	topic_ll
76143	8	355719	5	NULL	NULL	NULL	NULL	alcohol	Chemical	consumption of	leads to					painful lymph nodes	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Sore lymph nodes after drinking Alchohol consumption puts stress on the lymphatic system which, along with the liver and kidneys, is part of the body's blood cleansing apparatus. If the lymph system is weakened by lymphoma, drinking may cause pain in the affected areas.Lymph nodes are possibly painful after alcohol consumption. 	topic_ll
76144	1	355720	5	NULL	NULL	0	NULL	AILT	MedicalFinding		is					Angioimmunoblastic T-cell Lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Angioimmunoblastic T-cell Lymphoma (AILT), aka immunoblastic lymphadenopathy, is an aggressive cancer that originates in the T-cells. It accounts for 1% of all Non-Hodgkin’s Lymphomas (NHL) and is found mostly in the elderly. Males have a higher incidence than females.	topic_ll
76145	2	355720	5	NULL	NULL	0	NULL	Angioimmunoblastic T-cell Lymphoma	MedicalFinding		is also known as					immunoblastic lymphadenopathy	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Angioimmunoblastic T-cell Lymphoma (AILT), aka immunoblastic lymphadenopathy, is an aggressive cancer that originates in the T-cells. It accounts for 1% of all Non-Hodgkin’s Lymphomas (NHL) and is found mostly in the elderly. Males have a higher incidence than females.	topic_ll
76146	3	355720	5	NULL	NULL	0	NULL	AILT	MedicalFinding		is a type of					aggressive cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Angioimmunoblastic T-cell Lymphoma (AILT), aka immunoblastic lymphadenopathy, is an aggressive cancer that originates in the T-cells. It accounts for 1% of all Non-Hodgkin’s Lymphomas (NHL) and is found mostly in the elderly. Males have a higher incidence than females.	topic_ll
76147	4	355720	5	NULL	NULL	0	NULL	AILT	MedicalFinding		originates in					T-cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Angioimmunoblastic T-cell Lymphoma (AILT), aka immunoblastic lymphadenopathy, is an aggressive cancer that originates in the T-cells. It accounts for 1% of all Non-Hodgkin’s Lymphomas (NHL) and is found mostly in the elderly. Males have a higher incidence than females.	topic_ll
76148	5	355720	5	NULL	NULL	0	NULL	T-cells	MedicalFinding		found in		mostly			elderly	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Angioimmunoblastic T-cell Lymphoma (AILT), aka immunoblastic lymphadenopathy, is an aggressive cancer that originates in the T-cells. It accounts for 1% of all Non-Hodgkin’s Lymphomas (NHL) and is found mostly in the elderly. Males have a higher incidence than females.	topic_ll
76149	6	355720	5	NULL	NULL	0	NULL	males	GroupOfPeople		higher incidence than					females	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Angioimmunoblastic T-cell Lymphoma (AILT), aka immunoblastic lymphadenopathy, is an aggressive cancer that originates in the T-cells. It accounts for 1% of all Non-Hodgkin’s Lymphomas (NHL) and is found mostly in the elderly. Males have a higher incidence than females.	topic_ll
76150	7	355720	5	NULL	NULL	0	NULL	statement 6	Process		for					AILT	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Angioimmunoblastic T-cell Lymphoma (AILT), aka immunoblastic lymphadenopathy, is an aggressive cancer that originates in the T-cells. It accounts for 1% of all Non-Hodgkin’s Lymphomas (NHL) and is found mostly in the elderly. Males have a higher incidence than females.	topic_ll
76151	1	355721	5	NULL	NULL	0	NULL	Angio	AbstractConcept		refers to					blood	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	"Angio" is a term that refers to the blood vessels. This cancer is marked by the presence of abnormal blood vessels in affected body parts.	topic_ll
76152	2	355721	5	NULL	NULL	0	NULL	blood cancer	MedicalFinding		leads to					blood vessels	OrganismPart	abnormal			NULL	affected body parts	0	NULL	NULL	NULL	NULL	NULL	"Angio" is a term that refers to the blood vessels. This cancer is marked by the presence of abnormal blood vessels in affected body parts.	topic_ll
76153	1	355722	5	NULL	NULL	0	NULL	CHOP 	MedicalProcedure		is a type of					chemotherapy regimen	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	CHOP is one of the most common chemotherapy regimens for treating Non-Hodgkin's lymphoma. Regimen Drugs.	topic_ll
76154	2	355722	5	NULL	NULL	0	NULL	CHOP	MedicalProcedure		is used to treat					Non-Hodgkin's lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	CHOP is one of the most common chemotherapy regimens for treating Non-Hodgkin's lymphoma. Regimen Drugs.	topic_ll
76155	1	355723	5	NULL	NULL	0	NULL	cytoxan	Chemical		is the brand name of					Cyclophosphamide	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The following are the drugs used in the regimen. Select a drug to see a page and pertinent information. * Cyclophosphamide (brand names cytoxan, neosar) * Adriamycin (doxorubicin / hydroxydoxorubicin) * Vincristine (Oncovin) * Prednisone (sometimes called Deltasone or Orasone)	topic_ll
76156	2	355723	5	NULL	NULL	0	NULL	neosar	Chemical		is the brand name of					Cyclophosphamide	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The following are the drugs used in the regimen. Select a drug to see a page and pertinent information. * Cyclophosphamide (brand names cytoxan, neosar) * Adriamycin (doxorubicin / hydroxydoxorubicin) * Vincristine (Oncovin) * Prednisone (sometimes called Deltasone or Orasone)	topic_ll
76160	1	355724	5	NULL	NULL	0	NULL	alopecia	MedicalFinding		is a synonym of					Hair loss	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Hair loss (alopecia) may occur. People have many ways of dealing with hair loss including hats and scarves. 	topic_ll
76161	1	355726	5	NULL	NULL	0	NULL	Non Hodgkin's lymphoma	MedicalFinding		starts in					eye	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Non Hodgkin's lymphoma can start in the eye. It is called ocular lymphoma when it did not start elsewhere including the central nervous system (CNS) (brain etc.) 	topic_ll
76162	2	355726	5	NULL	NULL	0	NULL	statement 1	Process		is called					ocular lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Non Hodgkin's lymphoma can start in the eye. It is called ocular lymphoma when it did not start elsewhere including the central nervous system (CNS) (brain etc.) 	topic_ll
76163	3	355726	5	NULL	NULL	0	NULL	ocular lymphoma	MedicalFinding		does not start in					CNS	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Non Hodgkin's lymphoma can start in the eye. It is called ocular lymphoma when it did not start elsewhere including the central nervous system (CNS) (brain etc.) 	topic_ll
76164	4	355726	5	NULL	NULL	0	NULL	CNS	OrganismPart		is					central nervous system	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Non Hodgkin's lymphoma can start in the eye. It is called ocular lymphoma when it did not start elsewhere including the central nervous system (CNS) (brain etc.) 	topic_ll
76165	1	355731	5	NULL	NULL	0	NULL	hair dye	Chemical		is linked to					lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	There has been a lot of press over the years linking hair dye to lymphoma and other cancers	topic_ll
76167	1	355732	5	NULL	NULL	0	NULL	Henna tattoos	Chemical		is linked to					leukemia	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Henna tattoos linked to leukaemia risk Researchers believe that certain compounds used with Henna products are causing instances of leukemia. 	topic_ll
76168	1	355733	5	NULL	NULL	0	NULL	Henna tattoos	Chemical		is linked to					leukemia	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Henna tattoos linked to leukaemia risk 	topic_ll
76169	1	355734	5	NULL	NULL	0	NULL	Benzene	Chemical		used as					solvent	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	They believe that it is not the henna itself that is the problem, but the compounds used as a solvent for the henna powder. Benzene, which is known to cause cancer, is banned for this purpose in many countries, but is still widely employed.	topic_ll
76170	2	355734	5	NULL	NULL	0	NULL	statement 1	Process		is used in					henna powder	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	They believe that it is not the henna itself that is the problem, but the compounds used as a solvent for the henna powder. Benzene, which is known to cause cancer, is banned for this purpose in many countries, but is still widely employed.	topic_ll
76171	3	355734	5	NULL	NULL	0	NULL	Benzene	Chemical		causes					cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	They believe that it is not the henna itself that is the problem, but the compounds used as a solvent for the henna powder. Benzene, which is known to cause cancer, is banned for this purpose in many countries, but is still widely employed.	topic_ll
76173	1	355735	5	NULL	NULL	0	NULL	vitamin K	Chemical	dietary 	is linked to					lymphoma	MedicalFinding	decreased risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Dietary vitamin K linked to decreased lymphoma risk	topic_ll
76175	1	355736	5	NULL	NULL	NULL	NULL	red blood cell transfusion	MedicalProcedure	receiving of	increases					non-Hodgkin's lymphoma	MedicalFinding	risk of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Findings from a meta-study presented at the American Society of Hematology meeting suggest that receiving a red blood cell transfusion increases one's risk of developing a non-Hodgkin's lymphoma. 	topic_ll
76177	1	355737	5	NULL	NULL	0	NULL	red blood cell transfusion	MedicalProcedure		causes					immunosuppression	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Immunosuppression. A red blood cell transfusion causes immunosuppression, which by itself could promote a preexisting NHL to develop.	topic_ll
76180	2	355737	5	NULL	NULL	0	NULL	NHL	MedicalFinding	preexisting	is promoted to					develop	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Immunosuppression. A red blood cell transfusion causes immunosuppression, which by itself could promote a preexisting NHL to develop.	topic_ll
76182	3	355737	5	NULL	NULL	0	NULL	statement 1	Process		leads to					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Immunosuppression. A red blood cell transfusion causes immunosuppression, which by itself could promote a preexisting NHL to develop.	topic_ll
76183	1	355738	5	NULL	NULL	0	NULL	Humira drug	Chemical	consumption of	causes					lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	"Abbott Laboratories was sued by a Texas rheumatoid arthritis sufferer who claims she developed lymphoma after taking its drug Humira in a company-sponsored clinical trial in 2005.	topic_ll
76186	1	355740	5	NULL	NULL	0	NULL	Vitamin C	Chemical	intravenous 	kills		may			lymphoma cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Intravenous Vitamin C may Kill Lymphoma Cells	topic_ll
76187	1	355741	5	NULL	NULL	NULL	NULL	malt whisky	Chemical	drinking of	prevents		may			cancer	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Drinking malt whisky may help prevent cancer, a scientific conference has been told. The medicinal properties of antioxidants in red wine are well known, but delegates at a biochemistry conference were told that whisky offered 'even greater health benefits'.	topic_ll
76188	1	355742	5	NULL	NULL	0	NULL	malt whisky	Chemical	drinking of	prevents		may			cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Drinking malt whisky may help prevent cancer, a scientific conference has been told. The medicinal properties of antioxidants in red wine are well known, but delegates at a biochemistry conference were told that whisky offered "even greater health benefits". "However, research has shown that there are even greater health benefits to people who drink single malt whiskies. Why? Single malt whiskies have more ellagic acid than red wine." 	topic_ll
76189	2	355742	5	NULL	NULL	0	NULL	Single malt whiskies	Chemical		contains					ellagic acid	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Drinking malt whisky may help prevent cancer, a scientific conference has been told. The medicinal properties of antioxidants in red wine are well known, but delegates at a biochemistry conference were told that whisky offered "even greater health benefits". "However, research has shown that there are even greater health benefits to people who drink single malt whiskies. Why? Single malt whiskies have more ellagic acid than red wine." 	topic_ll
76190	3	355742	5	NULL	NULL	0	NULL	red wine	Chemical		contains					ellagic acid	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Drinking malt whisky may help prevent cancer, a scientific conference has been told. The medicinal properties of antioxidants in red wine are well known, but delegates at a biochemistry conference were told that whisky offered "even greater health benefits". "However, research has shown that there are even greater health benefits to people who drink single malt whiskies. Why? Single malt whiskies have more ellagic acid than red wine." 	topic_ll
76191	4	355742	5	NULL	NULL	0	NULL	statement 2	Process		is more than					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Drinking malt whisky may help prevent cancer, a scientific conference has been told. The medicinal properties of antioxidants in red wine are well known, but delegates at a biochemistry conference were told that whisky offered "even greater health benefits". "However, research has shown that there are even greater health benefits to people who drink single malt whiskies. Why? Single malt whiskies have more ellagic acid than red wine." 	topic_ll
76193	1	355743	5	NULL	NULL	0	NULL	Single malt whiskies	Chemical		contains					ellagic acid	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	"However, research has shown that there are even greater health benefits to people who drink single malt whiskies. Why? Single malt whiskies have more ellagic acid than red wine." 	topic_ll
76194	2	355743	5	NULL	NULL	0	NULL	red wine	Chemical		contains					ellagic acid	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	"However, research has shown that there are even greater health benefits to people who drink single malt whiskies. Why? Single malt whiskies have more ellagic acid than red wine." 	topic_ll
76195	3	355743	5	NULL	NULL	0	NULL	statement 1	Process		is more than					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	"However, research has shown that there are even greater health benefits to people who drink single malt whiskies. Why? Single malt whiskies have more ellagic acid than red wine." 	topic_ll
76196	1	355744	5	NULL	NULL	0	NULL	autism	MedicalFinding		is associated with					 ITGA4 gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	We recently published evidence of an association between autism and the ITGA4 gene	topic_aut
76197	1	355745	5	NULL	NULL	0	NULL	ITGA3	GP		is not associated with					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	No markers in ITGA3, ITGA6, ITGAV and ITGB3 were found to be associated with autism	topic_aut
76198	2	355745	5	NULL	NULL	0	NULL	ITGA6	GP		is not associated with					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	No markers in ITGA3, ITGA6, ITGAV and ITGB3 were found to be associated with autism	topic_aut
76199	3	355745	5	NULL	NULL	0	NULL	ITGAV	GP		is not associated with					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	No markers in ITGA3, ITGA6, ITGAV and ITGB3 were found to be associated with autism	topic_aut
76200	4	355745	5	NULL	NULL	0	NULL	ITGB3	GP		is not associated with					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	No markers in ITGA3, ITGA6, ITGAV and ITGB3 were found to be associated with autism	topic_aut
76203	1	355746	5	NULL	NULL	NULL	NULL	CD38	GP	low expression of	is associated with					autism	MedicalFinding				NULL	lymphoblastoid cells	NULL	NULL	NULL	NULL	NULL	NULL	Low CD38 expression in lymphoblastoid cells and haplotypes are both associated with autism in a family-based study.	topic_aut
76205	2	355746	5	NULL	NULL	0	NULL	CD38	GP	low expression of	is associated with					autism	MedicalFinding				NULL	haplotypes	0	NULL	NULL	NULL	NULL	NULL	Low CD38 expression in lymphoblastoid cells and haplotypes are both associated with autism in a family-based study.	topic_aut
76207	1	355747	5	NULL	NULL	0	NULL	freeway	GeographicNotProper	living near	is associated with					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Living near a freeway was associated with autism. Examination of associations with measured air pollutants is needed	topic_aut
76208	1	355748	5	NULL	NULL	0	NULL	uridine phosphorylase 2	GP		is associated with					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	uridine phosphorylase 2, with a joint P-value of 2.3E-9, has been previously linked and associated with Autism in independent samples	topic_aut
76210	1	355749	5	NULL	NULL	0	NULL	Calcium channel defects	MedicalFinding		is connected to					ASD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Calcium channel defects have been connected to Autism spectrum disorder (ASD) by Timothy Syndrome, which is Mendelian, and a previous targeted sex-specific association analysis of idiopathic Autism	topic_aut
76211	2	355749	5	NULL	NULL	0	NULL	ASD	MedicalFinding		is					Autism spectrum disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Calcium channel defects have been connected to Autism spectrum disorder (ASD) by Timothy Syndrome, which is Mendelian, and a previous targeted sex-specific association analysis of idiopathic Autism	topic_aut
76225	3	355749	5	NULL	NULL	0	NULL	Timothy Syndrome	MedicalFinding		plays a role in					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Calcium channel defects have been connected to Autism spectrum disorder (ASD) by Timothy Syndrome, which is Mendelian, and a previous targeted sex-specific association analysis of idiopathic Autism	topic_aut
76276	1	355750	5	NULL	NULL	NULL	NULL	autistic children	GroupOfPeople		more likely to have					mitochondrial dysfunction	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	In this exploratory study, children with autism were more likely to have mitochondrial dysfunction, mtDNA overreplication, and mtDNA deletions than typically developing children	topic_aut
76277	2	355750	5	NULL	NULL	NULL	NULL	autistic children	GroupOfPeople		more likely to have					mtDNA overreplication	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	In this exploratory study, children with autism were more likely to have mitochondrial dysfunction, mtDNA overreplication, and mtDNA deletions than typically developing children	topic_aut
76278	3	355750	5	NULL	NULL	NULL	NULL	autistic children	GroupOfPeople		more likely to have					mtDNA deletions	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	In this exploratory study, children with autism were more likely to have mitochondrial dysfunction, mtDNA overreplication, and mtDNA deletions than typically developing children	topic_aut
76279	1	355751	5	NULL	NULL	NULL	NULL	ITGB3	GP		is					integrin-beta 3 gene	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The integrin-β 3 gene (ITGB3), located on human chromosome 17q21.3, was previously identified as a quantitative trait locus (QTL) for 5-HT blood levels and has been implicated as a candidate gene for autism spectrum disorder (ASD)	topic_aut
76280	2	355751	5	NULL	NULL	0	NULL	ITGB3	GP		is located on					chromosome 17q21.3	Chromosome	human			NULL		0	NULL	NULL	NULL	NULL	NULL	The integrin-β 3 gene (ITGB3), located on human chromosome 17q21.3, was previously identified as a quantitative trait locus (QTL) for 5-HT blood levels and has been implicated as a candidate gene for autism spectrum disorder (ASD)	topic_aut
76281	3	355751	5	NULL	NULL	0	NULL	ITGB3	GP		is a type of					QTL	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	The integrin-β 3 gene (ITGB3), located on human chromosome 17q21.3, was previously identified as a quantitative trait locus (QTL) for 5-HT blood levels and has been implicated as a candidate gene for autism spectrum disorder (ASD)	topic_aut
76282	4	355751	5	NULL	NULL	0	NULL	QTL	Chromosome		is					quantitative trait locus	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	The integrin-β 3 gene (ITGB3), located on human chromosome 17q21.3, was previously identified as a quantitative trait locus (QTL) for 5-HT blood levels and has been implicated as a candidate gene for autism spectrum disorder (ASD)	topic_aut
76283	5	355751	5	NULL	NULL	0	NULL	statement 4	Process		for					5-HT	GP	levels of;;blood			NULL		0	NULL	NULL	NULL	NULL	NULL	The integrin-β 3 gene (ITGB3), located on human chromosome 17q21.3, was previously identified as a quantitative trait locus (QTL) for 5-HT blood levels and has been implicated as a candidate gene for autism spectrum disorder (ASD)	topic_aut
76284	6	355751	5	NULL	NULL	0	NULL	ITGB3	GP		is a candidate gene for					ASD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The integrin-β 3 gene (ITGB3), located on human chromosome 17q21.3, was previously identified as a quantitative trait locus (QTL) for 5-HT blood levels and has been implicated as a candidate gene for autism spectrum disorder (ASD)	topic_aut
76285	7	355751	5	NULL	NULL	0	NULL	ASD	MedicalFinding		is					autism spectrum disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The integrin-β 3 gene (ITGB3), located on human chromosome 17q21.3, was previously identified as a quantitative trait locus (QTL) for 5-HT blood levels and has been implicated as a candidate gene for autism spectrum disorder (ASD)	topic_aut
76286	1	355752	5	NULL	NULL	0	NULL	RTT	MedicalFinding		is					Rett syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Rett syndrome (RTT) as an ASD genetic model	topic_aut
76287	2	355752	5	NULL	NULL	0	NULL	Rett syndrome	MedicalFinding		is a genetic model of					ASD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Rett syndrome (RTT) as an ASD genetic model	topic_aut
76288	1	355754	5	NULL	NULL	0	NULL	early alterations	Process		is present in					RTT neurons	OrganismPart	developing;;human			NULL		0	NULL	NULL	NULL	NULL	NULL	Our data uncovered early alterations in developing human RTT neurons	topic_aut
76289	1	355755	5	NULL	NULL	0	NULL	MECP2 gene	GP		is a type of					X-linked gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the X-linked MECP2 gene, which encodes the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2), cause Rett syndrome and several neurodevelopmental disorders including cognitive disorders, autism, juvenile-onset schizophrenia and encephalopathy with early lethality	topic_aut
76290	2	355755	5	NULL	NULL	0	NULL	MECP2 gene	GP		encodes					methyl-CpG-binding protein 2	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the X-linked MECP2 gene, which encodes the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2), cause Rett syndrome and several neurodevelopmental disorders including cognitive disorders, autism, juvenile-onset schizophrenia and encephalopathy with early lethality	topic_aut
76291	3	355755	5	NULL	NULL	0	NULL	methyl-CpG-binding protein 2	GP		is					MeCP2	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the X-linked MECP2 gene, which encodes the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2), cause Rett syndrome and several neurodevelopmental disorders including cognitive disorders, autism, juvenile-onset schizophrenia and encephalopathy with early lethality	topic_aut
76292	4	355755	5	NULL	NULL	0	NULL	MeCP2	GP		is a type of					transcriptional regulator	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the X-linked MECP2 gene, which encodes the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2), cause Rett syndrome and several neurodevelopmental disorders including cognitive disorders, autism, juvenile-onset schizophrenia and encephalopathy with early lethality	topic_aut
76293	5	355755	5	NULL	NULL	0	NULL	MECP2 gene	GP	mutation of	cause					Rett syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the X-linked MECP2 gene, which encodes the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2), cause Rett syndrome and several neurodevelopmental disorders including cognitive disorders, autism, juvenile-onset schizophrenia and encephalopathy with early lethality	topic_aut
76294	6	355755	5	NULL	NULL	0	NULL	MECP2 gene	GP		cause					cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the X-linked MECP2 gene, which encodes the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2), cause Rett syndrome and several neurodevelopmental disorders including cognitive disorders, autism, juvenile-onset schizophrenia and encephalopathy with early lethality	topic_aut
76295	7	355755	5	NULL	NULL	0	NULL	MECP2 gene	GP	mutation of	cause					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the X-linked MECP2 gene, which encodes the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2), cause Rett syndrome and several neurodevelopmental disorders including cognitive disorders, autism, juvenile-onset schizophrenia and encephalopathy with early lethality	topic_aut
76296	8	355755	5	NULL	NULL	0	NULL	MECP2 gene	GP	mutation of	cause					juvenile-onset schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the X-linked MECP2 gene, which encodes the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2), cause Rett syndrome and several neurodevelopmental disorders including cognitive disorders, autism, juvenile-onset schizophrenia and encephalopathy with early lethality	topic_aut
76297	9	355755	5	NULL	NULL	0	NULL	MECP2 gene	GP	mutation of	cause					encephalopathy	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the X-linked MECP2 gene, which encodes the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2), cause Rett syndrome and several neurodevelopmental disorders including cognitive disorders, autism, juvenile-onset schizophrenia and encephalopathy with early lethality	topic_aut
76298	10	355755	5	NULL	NULL	0	NULL	cognitive disorders	MedicalFinding		is a type of					neurodevelopmental disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the X-linked MECP2 gene, which encodes the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2), cause Rett syndrome and several neurodevelopmental disorders including cognitive disorders, autism, juvenile-onset schizophrenia and encephalopathy with early lethality	topic_aut
76299	11	355755	5	NULL	NULL	0	NULL	autism	MedicalFinding		is a type of					neurodevelopmental disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the X-linked MECP2 gene, which encodes the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2), cause Rett syndrome and several neurodevelopmental disorders including cognitive disorders, autism, juvenile-onset schizophrenia and encephalopathy with early lethality	topic_aut
76300	12	355755	5	NULL	NULL	0	NULL	juvenile-onset schizophrenia	MedicalFinding		is a type of					neurodevelopmental disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the X-linked MECP2 gene, which encodes the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2), cause Rett syndrome and several neurodevelopmental disorders including cognitive disorders, autism, juvenile-onset schizophrenia and encephalopathy with early lethality	topic_aut
76301	13	355755	5	NULL	NULL	0	NULL	encephalopathy	MedicalFinding		is a type of					neurodevelopmental disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the X-linked MECP2 gene, which encodes the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2), cause Rett syndrome and several neurodevelopmental disorders including cognitive disorders, autism, juvenile-onset schizophrenia and encephalopathy with early lethality	topic_aut
76535	1	355756	11	NULL	NULL	0	NULL	Empirical therapy	MedicalProcedure		 is recommended for					Beta-hemolytic streptococci	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Empirical therapy for Beta-hemolytic streptococci is recommended. Empirical coverage for CA-MRSA is recommended in patients who do not respond to Beta-lactam therapy and may be considered in those with systemic toxicity. 	topic_mrs
76536	2	355756	11	NULL	NULL	0	NULL	Empirical coverage	MedicalProcedure		is recommended for					CA-MRSA	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Empirical therapy for Beta-hemolytic streptococci is recommended. Empirical coverage for CA-MRSA is recommended in patients who do not respond to Beta-lactam therapy and may be considered in those with systemic toxicity. 	topic_mrs
76537	1	355757	11	NULL	NULL	NULL	NULL	Nonpurulent cellulitis	MedicalFinding		have no					purulent drainage	BiologicalProcess				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nonpurulent cellulitis is defined as cellulitis with no purulent drainage or exudate and no associated abscess.	topic_mrs
76538	2	355757	11	NULL	NULL	NULL	NULL	Nonpurulent cellulitis	MedicalFinding		have no					exudate	BiologicalProcess				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nonpurulent cellulitis is defined as cellulitis with no purulent drainage or exudate and no associated abscess.	topic_mrs
76539	3	355757	11	NULL	NULL	0	NULL	Nonpurulent cellulitis	MedicalFinding		have no					abscess	MedicalFinding	associated			NULL		0	NULL	NULL	NULL	NULL	NULL	Nonpurulent cellulitis is defined as cellulitis with no purulent drainage or exudate and no associated abscess.	topic_mrs
77235	1	355758	11	NULL	NULL	NULL	NULL	cellulitis	MedicalFinding		is associated with					purulent drainage	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Purulent cellulitis is cellulitis associated with purulent drainage or exudate in the absence of a drainable abscess	topic_mrs
77236	2	355758	11	NULL	NULL	0	NULL	statement 1	Process		is known as					Purulent cellulitis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Purulent cellulitis is cellulitis associated with purulent drainage or exudate in the absence of a drainable abscess	topic_mrs
77237	3	355758	11	NULL	NULL	0	NULL	exudate	MedicalFinding		in the absence of					abscess	MedicalFinding	drainable			NULL		0	NULL	NULL	NULL	NULL	NULL	Purulent cellulitis is cellulitis associated with purulent drainage or exudate in the absence of a drainable abscess	topic_mrs
77238	4	355758	11	NULL	NULL	0	NULL	statement 3	Process		is known as					Purulent cellulitis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Purulent cellulitis is cellulitis associated with purulent drainage or exudate in the absence of a drainable abscess	topic_mrs
76239	1	355759	11	NULL	NULL	0	NULL	Telavancin	Chemical		is a type of 					bactericidal lipoglycopeptide	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Telavancin (trade name Vibativ) is a bactericidal lipoglycopeptide for use in MRSA or other Gram-positive infections. Telavancin is a synthetic derivative of vancomycin.	topic_mrs
76240	2	355759	11	NULL	NULL	0	NULL	Telavancin	Chemical		is a synonym of					Vibativ	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Telavancin (trade name Vibativ) is a bactericidal lipoglycopeptide for use in MRSA or other Gram-positive infections. Telavancin is a synthetic derivative of vancomycin.	topic_mrs
76241	3	355759	11	NULL	NULL	NULL	NULL	Telavancin	Chemical		used in					 infections	BiologicalProcess	MRSA ;; Gram-positive			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Telavancin (trade name Vibativ) is a bactericidal lipoglycopeptide for use in MRSA or other Gram-positive infections. Telavancin is a synthetic derivative of vancomycin.	topic_mrs
76242	4	355759	11	NULL	NULL	NULL	NULL	Telavancin	Chemical		is a derivative of		synthetic 			vancomycin	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Telavancin (trade name Vibativ) is a bactericidal lipoglycopeptide for use in MRSA or other Gram-positive infections. Telavancin is a synthetic derivative of vancomycin.	topic_mrs
76540	1	355760	11	NULL	NULL	0	NULL	lipoglycopeptides	Chemical		are a class of 					antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	lipoglycopeptides are a class of antibiotic that have lipophilic side-chains linked to glycopeptides. The class includes oritavancin, telavancin and dalbavancin.	topic_mrs
76541	2	355760	11	NULL	NULL	0	NULL	lipoglycopeptides	Chemical		includes					oritavancin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	lipoglycopeptides are a class of antibiotic that have lipophilic side-chains linked to glycopeptides. The class includes oritavancin, telavancin and dalbavancin.	topic_mrs
76542	3	355760	11	NULL	NULL	0	NULL	lipoglycopeptide	Chemical		includes					telavancin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	lipoglycopeptides are a class of antibiotic that have lipophilic side-chains linked to glycopeptides. The class includes oritavancin, telavancin and dalbavancin.	topic_mrs
76543	4	355760	11	NULL	NULL	0	NULL	lipoglycopeptides	Chemical		includes					dalbavancin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	lipoglycopeptides are a class of antibiotic that have lipophilic side-chains linked to glycopeptides. The class includes oritavancin, telavancin and dalbavancin.	topic_mrs
76243	1	355761	11	NULL	NULL	0	NULL	Telavancin	Chemical		approved for		FDA			 cSSTI	MedicalFinding	in adults			NULL		0	NULL	NULL	NULL	NULL	NULL	Telavancin is FDA-approved for cSSTI in adults	topic_mrs
76244	1	355762	11	NULL	NULL	0	NULL	Tetracycline	Chemical		is a type of 					polyketide antibiotic	Chemical	broad-spectrum			NULL		0	NULL	NULL	NULL	NULL	NULL	Tetracycline is a broad-spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria, indicated for use against many bacterial infections. 	topic_mrs
76245	2	355762	11	NULL	NULL	0	NULL	Streptomyces	Organism		is a genus of					Actinobacteria	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Tetracycline is a broad-spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria, indicated for use against many bacterial infections. 	topic_mrs
76246	3	355762	11	NULL	NULL	0	NULL	Tetracycline	Chemical		is produced by 					Streptomyces	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Tetracycline is a broad-spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria, indicated for use against many bacterial infections. 	topic_mrs
76247	4	355762	11	NULL	NULL	NULL	NULL	Tetracycline	Chemical		used against		can be			infections	BiologicalProcess	 bacterial 			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Tetracycline is a broad-spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria, indicated for use against many bacterial infections. 	topic_mrs
76935	1	355763	11	NULL	NULL	0	NULL	S. aureus	Organism		causes					SSTI	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Doxycycline is FDA-approved for the treatment of SSTI due to S. aureus, although not speciﬁcally for those caused by MRSA	topic_mrs
76936	2	355763	11	NULL	NULL	0	NULL	MRSA	Organism		causes					SSTI	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Doxycycline is FDA-approved for the treatment of SSTI due to S. aureus, although not speciﬁcally for those caused by MRSA	topic_mrs
76937	3	355763	11	NULL	NULL	0	NULL	Doxycycline	Chemical		treats					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Doxycycline is FDA-approved for the treatment of SSTI due to S. aureus, although not speciﬁcally for those caused by MRSA	topic_mrs
76938	1	355764	11	NULL	NULL	0	NULL	murein	Chemical		is a type of 					polymer	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	murein is a polymer consisting of sugars and amino acids that forms a mesh-like layer outside the plasma membrane of bacteria 	topic_mrs
76939	2	355764	11	NULL	NULL	0	NULL	murein	Chemical		consisting of					sugars	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	murein is a polymer consisting of sugars and amino acids that forms a mesh-like layer outside the plasma membrane of bacteria 	topic_mrs
76940	3	355764	11	NULL	NULL	0	NULL	murein	Chemical		consisting of					 amino acids	amino acid				NULL		0	NULL	NULL	NULL	NULL	NULL	murein is a polymer consisting of sugars and amino acids that forms a mesh-like layer outside the plasma membrane of bacteria 	topic_mrs
76941	4	355764	11	NULL	NULL	0	NULL	statement 2	Process		occurs along with					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	murein is a polymer consisting of sugars and amino acids that forms a mesh-like layer outside the plasma membrane of bacteria 	topic_mrs
76942	5	355764	11	NULL	NULL	0	NULL	murein	Chemical		forms a					mesh-like layer	CellComponent	outside the plasma membrane			NULL	 bacteria	0	NULL	NULL	NULL	NULL	NULL	murein is a polymer consisting of sugars and amino acids that forms a mesh-like layer outside the plasma membrane of bacteria 	topic_mrs
76943	1	355765	11	NULL	NULL	NULL	NULL	Penicillin	Chemical		impaires					cell wall synthesis	BiologicalProcess	bacteria			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Penicillin kills bacteria by interfering with the ability to synthesize cell wall.	topic_mrs
76944	2	355765	11	NULL	NULL	0	NULL	statement 1	Process		kills					bacteria	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Penicillin kills bacteria by interfering with the ability to synthesize cell wall.	topic_mrs
76945	1	355766	11	NULL	NULL	0	NULL	MRSA	Organism		is a strain of					Staphylococcus aureus bacteria	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA is, by definition, any strain of Staphylococcus aureus bacteria that has developed resistance to beta-lactam antibiotics which include the penicillins 	topic_mrs
76946	2	355766	11	NULL	NULL	0	NULL	MRSA	Organism		has resistance to					beta-lactam antibiotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA is, by definition, any strain of Staphylococcus aureus bacteria that has developed resistance to beta-lactam antibiotics which include the penicillins 	topic_mrs
76947	3	355766	11	NULL	NULL	0	NULL	 penicillins	Chemical		is a type of 					 beta-lactam antibiotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA is, by definition, any strain of Staphylococcus aureus bacteria that has developed resistance to beta-lactam antibiotics which include the penicillins 	topic_mrs
76948	4	355766	11	NULL	NULL	0	NULL	MRSA	Organism		has resistance to					penicillins	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	MRSA is, by definition, any strain of Staphylococcus aureus bacteria that has developed resistance to beta-lactam antibiotics which include the penicillins 	topic_mrs
76949	1	355767	11	NULL	NULL	NULL	NULL	 community-associated MRSA	Organism		causes		possibly			 infections	MedicalFinding	skin;; soft tissue			NULL		NULL	NULL	NULL	NULL	NULL	NULL	About 75 percent of community-associated (CA-) MRSA infections are localized to skin and soft tissue and usually can be treated effectively. However, some CA-MRSA strains display enhanced virulence, spreading more rapidly and causing illness much more severe than traditional healthcare-associated (HA-) MRSA infections, and they can affect vital organs and lead to widespread infection	topic_mrs
76950	2	355767	11	NULL	NULL	0	NULL	CA-MRSA	Organism		is					community-associated MRSA	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	About 75 percent of community-associated (CA-) MRSA infections are localized to skin and soft tissue and usually can be treated effectively. However, some CA-MRSA strains display enhanced virulence, spreading more rapidly and causing illness much more severe than traditional healthcare-associated (HA-) MRSA infections, and they can affect vital organs and lead to widespread infection	topic_mrs
76951	3	355767	11	NULL	NULL	NULL	NULL	CA-MRSA	Organism		causes		can			widespread infection	MedicalFinding	vital organs			NULL		NULL	NULL	NULL	NULL	NULL	NULL	About 75 percent of community-associated (CA-) MRSA infections are localized to skin and soft tissue and usually can be treated effectively. However, some CA-MRSA strains display enhanced virulence, spreading more rapidly and causing illness much more severe than traditional healthcare-associated (HA-) MRSA infections, and they can affect vital organs and lead to widespread infection	topic_mrs
76952	1	355768	11	NULL	NULL	0	NULL	PVL	Chemical		is a type of 					CA-MRSA toxin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	and they can affect vital organs and lead to widespread infection (sepsis), toxic shock syndrome and necrotizing ('flesh-eating') pneumonia. This is thought to be due to toxins carried by CA-MRSA strains, such as PVL and PSM	topic_mrs
76953	2	355768	11	NULL	NULL	0	NULL	PSM	Chemical		is a type of 					CA-MRSA toxin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	and they can affect vital organs and lead to widespread infection (sepsis), toxic shock syndrome and necrotizing ('flesh-eating') pneumonia. This is thought to be due to toxins carried by CA-MRSA strains, such as PVL and PSM	topic_mrs
76954	3	355768	11	NULL	NULL	0	NULL	CA-MRSA strain	Organism		produces					toxins	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	and they can affect vital organs and lead to widespread infection (sepsis), toxic shock syndrome and necrotizing ('flesh-eating') pneumonia. This is thought to be due to toxins carried by CA-MRSA strains, such as PVL and PSM	topic_mrs
76955	4	355768	11	NULL	NULL	NULL	NULL	CA-MRSA strain	Organism		causes					widespread infection	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	and they can affect vital organs and lead to widespread infection (sepsis), toxic shock syndrome and necrotizing ('flesh-eating') pneumonia. This is thought to be due to toxins carried by CA-MRSA strains, such as PVL and PSM	topic_mrs
76956	5	355768	11	NULL	NULL	0	NULL	CA-MRSA strain	Organism		causes					toxic shock syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	and they can affect vital organs and lead to widespread infection (sepsis), toxic shock syndrome and necrotizing ('flesh-eating') pneumonia. This is thought to be due to toxins carried by CA-MRSA strains, such as PVL and PSM	topic_mrs
76957	6	355768	11	NULL	NULL	0	NULL	CA-MRSA strain	Organism		causes					necrotizing pneumonia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	and they can affect vital organs and lead to widespread infection (sepsis), toxic shock syndrome and necrotizing ('flesh-eating') pneumonia. This is thought to be due to toxins carried by CA-MRSA strains, such as PVL and PSM	topic_mrs
76958	7	355768	11	NULL	NULL	NULL	NULL	sepsis	MedicalFinding		is also known as					infection	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	and they can affect vital organs and lead to widespread infection (sepsis), toxic shock syndrome and necrotizing ('flesh-eating') pneumonia. This is thought to be due to toxins carried by CA-MRSA strains, such as PVL and PSM	topic_mrs
76979	1	355769	11	NULL	NULL	0	NULL	Bacteria	Organism		express					lipopeptide	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	A lipopeptide is a molecule consisting of a lipid connected to a peptide. Bacteria express these molecules. They are bound by TLR 1, and other, Toll-like receptors. Certain lipopeptides are used as antibiotics.	topic_mrs
76980	2	355769	11	NULL	NULL	0	NULL	TLR 1	GP		is a type of 					Toll-like receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	A lipopeptide is a molecule consisting of a lipid connected to a peptide. Bacteria express these molecules. They are bound by TLR 1, and other, Toll-like receptors. Certain lipopeptides are used as antibiotics.	topic_mrs
76981	3	355769	11	NULL	NULL	0	NULL	 lipopeptide	Chemical		bounds by					Toll-like receptors	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	A lipopeptide is a molecule consisting of a lipid connected to a peptide. Bacteria express these molecules. They are bound by TLR 1, and other, Toll-like receptors. Certain lipopeptides are used as antibiotics.	topic_mrs
76982	4	355769	11	NULL	NULL	0	NULL	 lipopeptide	Chemical		bounds by					TLR 1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	A lipopeptide is a molecule consisting of a lipid connected to a peptide. Bacteria express these molecules. They are bound by TLR 1, and other, Toll-like receptors. Certain lipopeptides are used as antibiotics.	topic_mrs
76983	5	355769	11	NULL	NULL	0	NULL	lipopeptides	Chemical		are used as		possibly			antibiotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	A lipopeptide is a molecule consisting of a lipid connected to a peptide. Bacteria express these molecules. They are bound by TLR 1, and other, Toll-like receptors. Certain lipopeptides are used as antibiotics.	topic_mrs
76985	1	355770	11	NULL	NULL	NULL	NULL	Endocarditis	MedicalFinding		is a type of 					inflammation	MedicalFinding	endocardium;;heart valves			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Endocarditis is an inflammation of the inner layer of the heart, the endocardium. It usually involves the heart valves	topic_mrs
76986	2	355770	11	NULL	NULL	0	NULL	endocardium	OrganismPart		is a type of 					inner layer of the heart	Organism part				NULL		0	NULL	NULL	NULL	NULL	NULL	Endocarditis is an inflammation of the inner layer of the heart, the endocardium. It usually involves the heart valves	topic_mrs
76987	1	355771	11	NULL	NULL	0	NULL	ORSA	Organism		is					Oxacillin Resistant Staph aureus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	ORSA stands for Oxacillin Resistant Staph aureus. MRSA stands for Methicillin Resistant Staph aureus. ORSA and MRSA are different names for the same bacteria. Oxacillin and Methicillin are in the penicillin drug family, and some strains of Staph have become resistant to both of these antibiotics as well as other related antibiotics. Other drugs can be used to treat infections caused by this bacteria.	topic_mrs
76988	2	355771	11	NULL	NULL	0	NULL	MRSA	Organism		is					Methicillin Resistant Staph aureus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	ORSA stands for Oxacillin Resistant Staph aureus. MRSA stands for Methicillin Resistant Staph aureus. ORSA and MRSA are different names for the same bacteria. Oxacillin and Methicillin are in the penicillin drug family, and some strains of Staph have become resistant to both of these antibiotics as well as other related antibiotics. Other drugs can be used to treat infections caused by this bacteria.	topic_mrs
76989	3	355771	11	NULL	NULL	0	NULL	ORSA	Organism		is also known as					 MRSA 	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	ORSA stands for Oxacillin Resistant Staph aureus. MRSA stands for Methicillin Resistant Staph aureus. ORSA and MRSA are different names for the same bacteria. Oxacillin and Methicillin are in the penicillin drug family, and some strains of Staph have become resistant to both of these antibiotics as well as other related antibiotics. Other drugs can be used to treat infections caused by this bacteria.	topic_mrs
76990	4	355771	11	NULL	NULL	0	NULL	Oxacillin	Chemical		is a type of 					penicillin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	ORSA stands for Oxacillin Resistant Staph aureus. MRSA stands for Methicillin Resistant Staph aureus. ORSA and MRSA are different names for the same bacteria. Oxacillin and Methicillin are in the penicillin drug family, and some strains of Staph have become resistant to both of these antibiotics as well as other related antibiotics. Other drugs can be used to treat infections caused by this bacteria.	topic_mrs
76991	5	355771	11	NULL	NULL	0	NULL	Methicillin	Chemical		is a type of 					penicillin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	ORSA stands for Oxacillin Resistant Staph aureus. MRSA stands for Methicillin Resistant Staph aureus. ORSA and MRSA are different names for the same bacteria. Oxacillin and Methicillin are in the penicillin drug family, and some strains of Staph have become resistant to both of these antibiotics as well as other related antibiotics. Other drugs can be used to treat infections caused by this bacteria.	topic_mrs
76992	6	355771	11	NULL	NULL	0	NULL	Staph strains	Organism		become resistant to		may			Oxacillin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	ORSA stands for Oxacillin Resistant Staph aureus. MRSA stands for Methicillin Resistant Staph aureus. ORSA and MRSA are different names for the same bacteria. Oxacillin and Methicillin are in the penicillin drug family, and some strains of Staph have become resistant to both of these antibiotics as well as other related antibiotics. Other drugs can be used to treat infections caused by this bacteria.	topic_mrs
76993	7	355771	11	NULL	NULL	0	NULL	Staph strains	Organism		become resistant to		may			methicillin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	ORSA stands for Oxacillin Resistant Staph aureus. MRSA stands for Methicillin Resistant Staph aureus. ORSA and MRSA are different names for the same bacteria. Oxacillin and Methicillin are in the penicillin drug family, and some strains of Staph have become resistant to both of these antibiotics as well as other related antibiotics. Other drugs can be used to treat infections caused by this bacteria.	topic_mrs
76994	1	355772	11	NULL	NULL	0	NULL	clonal complex 398	Organism		is a subtype of					methicillin-resistant Staphylococcus aureus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	n emerging subtype of methicillin-resistant Staphylococcus aureus (MRSA), clonal complex (CC) 398, is associated with animals, particularly pigs.	topic_mrs
76995	2	355772	11	NULL	NULL	0	NULL	methicillin-resistant Staphylococcus aureus	Organism		is					MRSA	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	n emerging subtype of methicillin-resistant Staphylococcus aureus (MRSA), clonal complex (CC) 398, is associated with animals, particularly pigs.	topic_mrs
76996	3	355772	11	NULL	NULL	0	NULL	clonal complex 398	Organism		is associated with					 pigs	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	n emerging subtype of methicillin-resistant Staphylococcus aureus (MRSA), clonal complex (CC) 398, is associated with animals, particularly pigs.	topic_mrs
76997	4	355772	11	NULL	NULL	0	NULL	clonal complex 398	Organism		 is associated with					animals	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	n emerging subtype of methicillin-resistant Staphylococcus aureus (MRSA), clonal complex (CC) 398, is associated with animals, particularly pigs.	topic_mrs
76302	1	355774	5	NULL	NULL	0	NULL	BCL6	GP		is a type of					oncogene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Here's what we know: The oncogene known as BCL6 is generally associated with diffuse large B-cell lymphoma (DLBCL).	topic_ll
76303	2	355774	5	NULL	NULL	0	NULL	BCL6	GP		is associated with					DLBCL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Here's what we know: The oncogene known as BCL6 is generally associated with diffuse large B-cell lymphoma (DLBCL).	topic_ll
76304	3	355774	5	NULL	NULL	0	NULL	DLBCL	MedicalFinding		is					diffuse large B-cell lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Here's what we know: The oncogene known as BCL6 is generally associated with diffuse large B-cell lymphoma (DLBCL).	topic_ll
76305	1	355775	5	NULL	NULL	0	NULL	79-6	Chemical		is an inhibitor of					BCL6	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	So researchers have gone looking for the right BCL6 inhibitor, and they may have found it in a compound known as 79-6, which has proven effective in killing the DLBCL cell lines.	topic_ll
76306	2	355775	5	NULL	NULL	0	NULL	79-6	Chemical		kills		effectively			DLBCL cell lines	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	So researchers have gone looking for the right BCL6 inhibitor, and they may have found it in a compound known as 79-6, which has proven effective in killing the DLBCL cell lines.	topic_ll
76307	1	355778	5	NULL	NULL	0	NULL	BEACOPP regimen	MedicalProcedure		is used to treat					HL	MedicalFinding	late-stage;;unfavorable			NULL		0	NULL	NULL	NULL	NULL	NULL	The BEACOPP regimen was established by the GHSG in 1989 for the treatment of late-stage, unfavorable HL. 	topic_ll
76308	2	355778	5	NULL	NULL	0	NULL	BEACOPP regimen	MedicalProcedure		established by					GHSG	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	The BEACOPP regimen was established by the GHSG in 1989 for the treatment of late-stage, unfavorable HL. 	topic_ll
76309	1	355779	5	NULL	NULL	0	NULL	Pralatrexate	Chemical		is a type of					orphan drug	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Pralatrexate given orphan drug status for CTCL in Europe	topic_ll
76310	2	355779	5	NULL	NULL	0	NULL	Pralatrexate	Chemical		is used to treat					CTCL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Pralatrexate given orphan drug status for CTCL in Europe	topic_ll
77045	1	355782	11	NULL	NULL	0	NULL	Silver	Chemical		purify					water	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Silver has been used since antiquity to purify water.  While silver's importance as a bactericide has only been documented since the late 1800s, its use in purification has been known throughout the ages.	topic_mrs
77046	2	355782	11	NULL	NULL	0	NULL	Silver	Chemical		is a type of 					bactericide	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Silver has been used since antiquity to purify water.  While silver's importance as a bactericide has only been documented since the late 1800s, its use in purification has been known throughout the ages.	topic_mrs
77047	1	355783	11	NULL	NULL	0	NULL	Colloidal Silver	Chemical		kill					organisms	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Colloidal Silver is thought to kill an average of 650 different organisms, compared to the 6 of a standard antibiotic.  It is safe for adults, children, animals and pregnant and nursing women. It can be applied topically and used internally and has no reaction with other medications.	topic_mrs
77125	2	355783	11	NULL	NULL	0	NULL	Colloidal Silver\t	Chemical		has no reaction with					medications	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Colloidal Silver is thought to kill an average of 650 different organisms, compared to the 6 of a standard antibiotic.  It is safe for adults, children, animals and pregnant and nursing women. It can be applied topically and used internally and has no reaction with other medications.	topic_mrs
77126	3	355783	11	NULL	NULL	0	NULL	Colloidal Silver	Chemical		can be applied 					topically	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Colloidal Silver is thought to kill an average of 650 different organisms, compared to the 6 of a standard antibiotic.  It is safe for adults, children, animals and pregnant and nursing women. It can be applied topically and used internally and has no reaction with other medications.	topic_mrs
77127	4	355783	11	NULL	NULL	0	NULL	Colloidal Silver	Chemical		can be used					internally	Organism part				NULL		0	NULL	NULL	NULL	NULL	NULL	Colloidal Silver is thought to kill an average of 650 different organisms, compared to the 6 of a standard antibiotic.  It is safe for adults, children, animals and pregnant and nursing women. It can be applied topically and used internally and has no reaction with other medications.	topic_mrs
77128	5	355783	11	NULL	NULL	0	NULL	Colloidal Silver	Chemical		is safe for					adults	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Colloidal Silver is thought to kill an average of 650 different organisms, compared to the 6 of a standard antibiotic.  It is safe for adults, children, animals and pregnant and nursing women. It can be applied topically and used internally and has no reaction with other medications.	topic_mrs
77129	6	355783	11	NULL	NULL	0	NULL	Colloidal Silver	Chemical		is safe for					children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Colloidal Silver is thought to kill an average of 650 different organisms, compared to the 6 of a standard antibiotic.  It is safe for adults, children, animals and pregnant and nursing women. It can be applied topically and used internally and has no reaction with other medications.	topic_mrs
77130	7	355783	11	NULL	NULL	0	NULL	Colloidal Silver 	Chemical		is safe for					animals	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Colloidal Silver is thought to kill an average of 650 different organisms, compared to the 6 of a standard antibiotic.  It is safe for adults, children, animals and pregnant and nursing women. It can be applied topically and used internally and has no reaction with other medications.	topic_mrs
77131	8	355783	11	NULL	NULL	0	NULL	Colloidal Silver	Chemical		is safe for					pregnant women	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Colloidal Silver is thought to kill an average of 650 different organisms, compared to the 6 of a standard antibiotic.  It is safe for adults, children, animals and pregnant and nursing women. It can be applied topically and used internally and has no reaction with other medications.	topic_mrs
77132	9	355783	11	NULL	NULL	0	NULL	Colloidal Silver	Chemical		is safe for					nursing women	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Colloidal Silver is thought to kill an average of 650 different organisms, compared to the 6 of a standard antibiotic.  It is safe for adults, children, animals and pregnant and nursing women. It can be applied topically and used internally and has no reaction with other medications.	topic_mrs
77133	1	355784	11	NULL	NULL	0	NULL	Oleuropein	Chemical		is an ingredient in					Olive Leaf Extract	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientific research has shown that the active ingredient in Olive Leaf Extract - Oleuropein, has powerful healing properties that fights the bacteria, viruses, fungi and parasites that cause infection and disease.	topic_mrs
77134	2	355784	11	NULL	NULL	0	NULL	Oleuropein	Chemical		has					healing properties	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientific research has shown that the active ingredient in Olive Leaf Extract - Oleuropein, has powerful healing properties that fights the bacteria, viruses, fungi and parasites that cause infection and disease.	topic_mrs
77135	3	355784	11	NULL	NULL	0	NULL	Oleuropein	Chemical		fights with 					bacteria	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientific research has shown that the active ingredient in Olive Leaf Extract - Oleuropein, has powerful healing properties that fights the bacteria, viruses, fungi and parasites that cause infection and disease.	topic_mrs
77136	4	355784	11	NULL	NULL	0	NULL	Oleuropein	Chemical		fights with 					viruses	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientific research has shown that the active ingredient in Olive Leaf Extract - Oleuropein, has powerful healing properties that fights the bacteria, viruses, fungi and parasites that cause infection and disease.	topic_mrs
77137	5	355784	11	NULL	NULL	0	NULL	Oleuropein	Chemical		fights with 					fungi	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientific research has shown that the active ingredient in Olive Leaf Extract - Oleuropein, has powerful healing properties that fights the bacteria, viruses, fungi and parasites that cause infection and disease.	topic_mrs
77138	6	355784	11	NULL	NULL	0	NULL	Oleuropein	Chemical		fights with 					parasites	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientific research has shown that the active ingredient in Olive Leaf Extract - Oleuropein, has powerful healing properties that fights the bacteria, viruses, fungi and parasites that cause infection and disease.	topic_mrs
77139	7	355784	11	NULL	NULL	0	NULL	bacteria	Organism		causes					infection	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientific research has shown that the active ingredient in Olive Leaf Extract - Oleuropein, has powerful healing properties that fights the bacteria, viruses, fungi and parasites that cause infection and disease.	topic_mrs
77140	8	355784	11	NULL	NULL	0	NULL	Bacteria	Organism		causes					disease	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientific research has shown that the active ingredient in Olive Leaf Extract - Oleuropein, has powerful healing properties that fights the bacteria, viruses, fungi and parasites that cause infection and disease.	topic_mrs
77141	9	355784	11	NULL	NULL	0	NULL	viruses	Organism		causes					infection	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientific research has shown that the active ingredient in Olive Leaf Extract - Oleuropein, has powerful healing properties that fights the bacteria, viruses, fungi and parasites that cause infection and disease.	topic_mrs
77142	10	355784	11	NULL	NULL	0	NULL	viruses	Organism		causes					disease	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientific research has shown that the active ingredient in Olive Leaf Extract - Oleuropein, has powerful healing properties that fights the bacteria, viruses, fungi and parasites that cause infection and disease.	topic_mrs
77143	11	355784	11	NULL	NULL	0	NULL	 fungi	Organism		causes					infection	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientific research has shown that the active ingredient in Olive Leaf Extract - Oleuropein, has powerful healing properties that fights the bacteria, viruses, fungi and parasites that cause infection and disease.	topic_mrs
77144	12	355784	11	NULL	NULL	0	NULL	fungi	Organism		causes					disease	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientific research has shown that the active ingredient in Olive Leaf Extract - Oleuropein, has powerful healing properties that fights the bacteria, viruses, fungi and parasites that cause infection and disease.	topic_mrs
77145	13	355784	11	NULL	NULL	0	NULL	parasites	Organism		causes					infection	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientific research has shown that the active ingredient in Olive Leaf Extract - Oleuropein, has powerful healing properties that fights the bacteria, viruses, fungi and parasites that cause infection and disease.	topic_mrs
77146	14	355784	11	NULL	NULL	0	NULL	parasites	Organism		causes					disease	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Scientific research has shown that the active ingredient in Olive Leaf Extract - Oleuropein, has powerful healing properties that fights the bacteria, viruses, fungi and parasites that cause infection and disease.	topic_mrs
77147	1	355785	11	NULL	NULL	0	NULL	Garlic	Chemical		is a type of 					natural antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Garlic has been scientifically proven to be a powerful natural antibiotic, antiviral and antifungal agent. Garlic has also been shown to kill highly resistant MRSA infections in human clinical studies	topic_mrs
77148	2	355785	11	NULL	NULL	0	NULL	Garlic	Chemical		is a type of 					antiviral agent	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Garlic has been scientifically proven to be a powerful natural antibiotic, antiviral and antifungal agent. Garlic has also been shown to kill highly resistant MRSA infections in human clinical studies	topic_mrs
77149	3	355785	11	NULL	NULL	0	NULL	Garlic	Chemical		is a type of 					 antifungal agent	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Garlic has been scientifically proven to be a powerful natural antibiotic, antiviral and antifungal agent. Garlic has also been shown to kill highly resistant MRSA infections in human clinical studies	topic_mrs
77150	4	355785	11	NULL	NULL	0	NULL	Garlic	Chemical		kills					 MRSA infections	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Garlic has been scientifically proven to be a powerful natural antibiotic, antiviral and antifungal agent. Garlic has also been shown to kill highly resistant MRSA infections in human clinical studies	topic_mrs
77151	1	355786	11	NULL	NULL	NULL	NULL	allicin	Chemical	stabilized 	treats					MRSA infection	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	In 2008, Dr. Ron Cutler and the University of East London  released the results from a human clinical study performed on 52 patients with hospital acquired HA-MRSA. All 52 patients were treated with a form of stabilized allicin and recovered fully from their MRSA infections.	topic_mrs
77152	1	355787	11	NULL	NULL	0	NULL	Manuka honey	Chemical		is a type of 					honey	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Manuka honey is a special medicinal honey that is one of the best natural remedies for Staph and MRSA and has been used for treating infections for over 200 years	topic_mrs
77153	2	355787	11	NULL	NULL	0	NULL	Manuka honey	Chemical		has the property of					medicine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Manuka honey is a special medicinal honey that is one of the best natural remedies for Staph and MRSA and has been used for treating infections for over 200 years	topic_mrs
77154	3	355787	11	NULL	NULL	0	NULL	Manuka honey	Chemical		treats					staph infections	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Manuka honey is a special medicinal honey that is one of the best natural remedies for Staph and MRSA and has been used for treating infections for over 200 years	topic_mrs
77155	4	355787	11	NULL	NULL	0	NULL	Manuka honey	Chemical		treats					MRSA infection	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Manuka honey is a special medicinal honey that is one of the best natural remedies for Staph and MRSA and has been used for treating infections for over 200 years	topic_mrs
77156	1	355788	11	NULL	NULL	0	NULL	MRSA	Organism		is a type of 					bacterial infections	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Phage Therapy is the therapeutic use of these bacteriophages to treat pathogenic bacterial infections like MRSA. 	topic_mrs
77157	2	355788	11	NULL	NULL	NULL	NULL	Phage Therapy	MedicalProcedure		used in					therapeutic	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Phage Therapy is the therapeutic use of these bacteriophages to treat pathogenic bacterial infections like MRSA. 	topic_mrs
77158	3	355788	11	NULL	NULL	0	NULL	Phage Therapy	MedicalProcedure		treats					bacterial infections	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Phage Therapy is the therapeutic use of these bacteriophages to treat pathogenic bacterial infections like MRSA. 	topic_mrs
77159	1	355789	11	NULL	NULL	0	NULL	Turmeric	Organism		is a type of 					herb	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Turmeric is an herb that contains antibacterial as well as anti-inflammatory properties and has been used to treat boils and other staph infections of the skin, including MRSA, with much success.	topic_mrs
77160	2	355789	11	NULL	NULL	0	NULL	Turmeric	Chemical		has					antibacterial properties	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Turmeric is an herb that contains antibacterial as well as anti-inflammatory properties and has been used to treat boils and other staph infections of the skin, including MRSA, with much success.	topic_mrs
77161	3	355789	11	NULL	NULL	0	NULL	Turmeric	Chemical		has					anti-inflammatory property	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Turmeric is an herb that contains antibacterial as well as anti-inflammatory properties and has been used to treat boils and other staph infections of the skin, including MRSA, with much success.	topic_mrs
77162	4	355789	11	NULL	NULL	0	NULL	Turmeric	Chemical		 treat					boils	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Turmeric is an herb that contains antibacterial as well as anti-inflammatory properties and has been used to treat boils and other staph infections of the skin, including MRSA, with much success.	topic_mrs
77163	5	355789	11	NULL	NULL	0	NULL	Turmeric	Chemical		treats					staph infection	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Turmeric is an herb that contains antibacterial as well as anti-inflammatory properties and has been used to treat boils and other staph infections of the skin, including MRSA, with much success.	topic_mrs
77164	6	355789	11	NULL	NULL	0	NULL	Turmeric	Chemical		treats					MRSA infection	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Turmeric is an herb that contains antibacterial as well as anti-inflammatory properties and has been used to treat boils and other staph infections of the skin, including MRSA, with much success.	topic_mrs
77165	1	355791	11	NULL	NULL	0	NULL	Co-trimoxazole	Chemical		contains					trimethoprim	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Co-trimoxazole is a combination of trimethoprim and sulfamethoxazole, a sulfa drug. It eliminates bacteria that cause various infections, including infections of the urinary tract, lungs (pneumonia), ears, and intestines	topic_mrs
77166	2	355791	11	NULL	NULL	0	NULL	Co-trimoxazole	Chemical		contains					sulfamethoxazole	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Co-trimoxazole is a combination of trimethoprim and sulfamethoxazole, a sulfa drug. It eliminates bacteria that cause various infections, including infections of the urinary tract, lungs (pneumonia), ears, and intestines	topic_mrs
77167	3	355791	11	NULL	NULL	0	NULL	statement 1	Chemical		occurs along with					statement 2	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Co-trimoxazole is a combination of trimethoprim and sulfamethoxazole, a sulfa drug. It eliminates bacteria that cause various infections, including infections of the urinary tract, lungs (pneumonia), ears, and intestines	topic_mrs
77168	4	355791	11	NULL	NULL	0	NULL	sulfamethoxazole	Chemical		is a type of 					sulfa drug	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Co-trimoxazole is a combination of trimethoprim and sulfamethoxazole, a sulfa drug. It eliminates bacteria that cause various infections, including infections of the urinary tract, lungs (pneumonia), ears, and intestines	topic_mrs
77169	5	355791	11	NULL	NULL	0	NULL	bacteria	Organism		infects					urinary tract	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Co-trimoxazole is a combination of trimethoprim and sulfamethoxazole, a sulfa drug. It eliminates bacteria that cause various infections, including infections of the urinary tract, lungs (pneumonia), ears, and intestines	topic_mrs
77170	6	355791	11	NULL	NULL	NULL	NULL	bacteria	Organism		infects					lungs	Organism part				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Co-trimoxazole is a combination of trimethoprim and sulfamethoxazole, a sulfa drug. It eliminates bacteria that cause various infections, including infections of the urinary tract, lungs (pneumonia), ears, and intestines	topic_mrs
77171	7	355791	11	NULL	NULL	0	NULL	pneumonia	MedicalFinding		infects					lungs	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Co-trimoxazole is a combination of trimethoprim and sulfamethoxazole, a sulfa drug. It eliminates bacteria that cause various infections, including infections of the urinary tract, lungs (pneumonia), ears, and intestines	topic_mrs
77172	8	355791	11	NULL	NULL	0	NULL	bacteria	Organism		infects					ears	Organism part				NULL		0	NULL	NULL	NULL	NULL	NULL	Co-trimoxazole is a combination of trimethoprim and sulfamethoxazole, a sulfa drug. It eliminates bacteria that cause various infections, including infections of the urinary tract, lungs (pneumonia), ears, and intestines	topic_mrs
77173	9	355791	11	NULL	NULL	0	NULL	bacteria	Organism		infects					intestines	Organism part				NULL		0	NULL	NULL	NULL	NULL	NULL	Co-trimoxazole is a combination of trimethoprim and sulfamethoxazole, a sulfa drug. It eliminates bacteria that cause various infections, including infections of the urinary tract, lungs (pneumonia), ears, and intestines	topic_mrs
77174	10	355791	11	NULL	NULL	0	NULL	Co-trimoxazole	Chemical		treats					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Co-trimoxazole is a combination of trimethoprim and sulfamethoxazole, a sulfa drug. It eliminates bacteria that cause various infections, including infections of the urinary tract, lungs (pneumonia), ears, and intestines	topic_mrs
77175	11	355791	11	NULL	NULL	0	NULL	Co-trimoxazole	Chemical		treats					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Co-trimoxazole is a combination of trimethoprim and sulfamethoxazole, a sulfa drug. It eliminates bacteria that cause various infections, including infections of the urinary tract, lungs (pneumonia), ears, and intestines	topic_mrs
77176	12	355791	11	NULL	NULL	0	NULL	Co-trimoxazole	Chemical		treats					statement 8	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Co-trimoxazole is a combination of trimethoprim and sulfamethoxazole, a sulfa drug. It eliminates bacteria that cause various infections, including infections of the urinary tract, lungs (pneumonia), ears, and intestines	topic_mrs
77177	13	355791	11	NULL	NULL	0	NULL	Co-trimoxazole	Chemical		treats					statement 9	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Co-trimoxazole is a combination of trimethoprim and sulfamethoxazole, a sulfa drug. It eliminates bacteria that cause various infections, including infections of the urinary tract, lungs (pneumonia), ears, and intestines	topic_mrs
77178	1	355792	11	NULL	NULL	0	NULL	Bactrim	Chemical		is a type of 					antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Bactrim (sulfamethoxazole and trimethoprim) is an antibiotic used to treat ear infections, urinary tract and other infections.	topic_mrs
77179	2	355792	11	NULL	NULL	0	NULL	Bactrim	Chemical		contains					sulfamethoxazole	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Bactrim (sulfamethoxazole and trimethoprim) is an antibiotic used to treat ear infections, urinary tract and other infections.	topic_mrs
77180	3	355792	11	NULL	NULL	0	NULL	Bactrim	Chemical		contains					trimethoprim	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Bactrim (sulfamethoxazole and trimethoprim) is an antibiotic used to treat ear infections, urinary tract and other infections.	topic_mrs
77181	4	355792	11	NULL	NULL	0	NULL	statement 2	Chemical		occurs along with					statement 3	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Bactrim (sulfamethoxazole and trimethoprim) is an antibiotic used to treat ear infections, urinary tract and other infections.	topic_mrs
77182	5	355792	11	NULL	NULL	NULL	NULL	Bactrim	Chemical		treats					ear infections	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Bactrim (sulfamethoxazole and trimethoprim) is an antibiotic used to treat ear infections, urinary tract and other infections.	topic_mrs
77234	6	355792	11	NULL	NULL	0	NULL	Bactrim	Chemical		treats					urinary tract infections	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bactrim (sulfamethoxazole and trimethoprim) is an antibiotic used to treat ear infections, urinary tract and other infections.	topic_mrs
77183	1	355793	11	NULL	NULL	0	NULL	Sepsis	MedicalFinding		is a type of 					 illness	Process	 severe			NULL		0	NULL	NULL	NULL	NULL	NULL	Sepsis is a severe illness in which the bloodstream is overwhelmed by bacteria. Sepsis in its most severe form, septic shock, can carry mortality rates well above 50%, even with optimal sepsis treatment.	topic_mrs
77184	2	355793	11	NULL	NULL	0	NULL	sepsis	MedicalFinding	severe	is also known as					 septic shock	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Sepsis is a severe illness in which the bloodstream is overwhelmed by bacteria. Sepsis in its most severe form, septic shock, can carry mortality rates well above 50%, even with optimal sepsis treatment.	topic_mrs
77185	3	355793	11	NULL	NULL	NULL	NULL	 septic shock	MedicalFinding		increases		possibly			mortality	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Sepsis is a severe illness in which the bloodstream is overwhelmed by bacteria. Sepsis in its most severe form, septic shock, can carry mortality rates well above 50%, even with optimal sepsis treatment.	topic_mrs
77186	1	355794	11	NULL	NULL	0	NULL	Antibiotic	Chemical		may cause					diarrhea	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Antibiotic-associated diarrhea describes frequent, watery bowel movements (diarrhea) that occur in response to medications used to treat bacterial infections (antibiotics)	topic_mrs
77187	2	355794	11	NULL	NULL	0	NULL	diarrhea	MedicalFinding		describes					bowel movements	Process	frequent;;watery			NULL		0	NULL	NULL	NULL	NULL	NULL	Antibiotic-associated diarrhea describes frequent, watery bowel movements (diarrhea) that occur in response to medications used to treat bacterial infections (antibiotics)	topic_mrs
77188	1	355795	11	NULL	NULL	0	NULL	C. difficile	Organism		is a type of 					bacterium	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	C. difficile is a bacterium that is normally found, along with hundreds of thousands of other bacteria, in the intestines of healthy people.	topic_mrs
77189	2	355795	11	NULL	NULL	0	NULL	C. difficile	Organism		found in					intestines	Organism part	 healthy people			NULL		0	NULL	NULL	NULL	NULL	NULL	C. difficile is a bacterium that is normally found, along with hundreds of thousands of other bacteria, in the intestines of healthy people.	topic_mrs
77190	1	355796	11	NULL	NULL	0	NULL	Clostridium difficile	Organism		is					C. difficile	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	One of the most common causes of antibiotic-associated diarrhea is infection with a bacterium, Clostridium difficile (C. difficile). C. difficile infections are most common in people who are hospitalized, affecting more than 60 hospitalized patients per 100,000 (0.06 percent) in the United States	topic_mrs
77191	2	355796	11	NULL	NULL	0	NULL	Clostridium difficile	Organism		is a type of 					bacterium	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	One of the most common causes of antibiotic-associated diarrhea is infection with a bacterium, Clostridium difficile (C. difficile). C. difficile infections are most common in people who are hospitalized, affecting more than 60 hospitalized patients per 100,000 (0.06 percent) in the United States	topic_mrs
77192	3	355796	11	NULL	NULL	0	NULL	Clostridium difficile	Organism		causes					antibiotic-associated diarrhea	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	One of the most common causes of antibiotic-associated diarrhea is infection with a bacterium, Clostridium difficile (C. difficile). C. difficile infections are most common in people who are hospitalized, affecting more than 60 hospitalized patients per 100,000 (0.06 percent) in the United States	topic_mrs
77193	1	355798	11	NULL	NULL	0	NULL	oral antibiotic	Chemical		treats					C. difficile	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	An oral antibiotic is usually recommended to treat people who are infected with C. difficile.	topic_mrs
78363	1	355800	11	NULL	NULL	0	NULL	antibiotics	Chemical		 related to		possibly			diarrhea	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Some studies have found that probiotics modestly shortened the duration of diarrhea related to antibiotics, but not all patients in these studies had C. difficile	topic_mrs
78364	2	355800	11	NULL	NULL	0	NULL	probiotics	Organism		shortened		modestly			diarrhea	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Some studies have found that probiotics modestly shortened the duration of diarrhea related to antibiotics, but not all patients in these studies had C. difficile	topic_mrs
78365	1	355801	11	NULL	NULL	0	NULL	Hand 	Organism part	washing	prevents					C. difficile	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Hand washing is an effective way to prevent the spread of C. difficile. Hands should be washed after using the bathroom and before eating. 	topic_mrs
78366	1	355802	11	NULL	NULL	0	NULL	Fatigue	MedicalFinding		is also known as					exhaustion	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Fatigue (also called exhaustion, lethargy, languidness, languor, lassitude, and listlessness) is a state of awareness describing a range of afflictions, usually associated with physical and/or mental weakness, though varying from a general state of lethargy to a specific work-induced burning sensation within one's muscles. 	topic_mrs
78367	2	355802	11	NULL	NULL	0	NULL	Fatigue	MedicalFinding		is also known as					 lethargy	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Fatigue (also called exhaustion, lethargy, languidness, languor, lassitude, and listlessness) is a state of awareness describing a range of afflictions, usually associated with physical and/or mental weakness, though varying from a general state of lethargy to a specific work-induced burning sensation within one's muscles. 	topic_mrs
78368	3	355802	11	NULL	NULL	0	NULL	Fatigue	MedicalFinding		is also known as					languidness	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Fatigue (also called exhaustion, lethargy, languidness, languor, lassitude, and listlessness) is a state of awareness describing a range of afflictions, usually associated with physical and/or mental weakness, though varying from a general state of lethargy to a specific work-induced burning sensation within one's muscles. 	topic_mrs
78369	4	355802	11	NULL	NULL	0	NULL	Fatigue	MedicalFinding		is also known as					languor	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Fatigue (also called exhaustion, lethargy, languidness, languor, lassitude, and listlessness) is a state of awareness describing a range of afflictions, usually associated with physical and/or mental weakness, though varying from a general state of lethargy to a specific work-induced burning sensation within one's muscles. 	topic_mrs
78370	5	355802	11	NULL	NULL	0	NULL	Fatigue	MedicalFinding		is also known as					listlessness	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Fatigue (also called exhaustion, lethargy, languidness, languor, lassitude, and listlessness) is a state of awareness describing a range of afflictions, usually associated with physical and/or mental weakness, though varying from a general state of lethargy to a specific work-induced burning sensation within one's muscles. 	topic_mrs
78371	6	355802	11	NULL	NULL	0	NULL	Fatigue 	MedicalFinding		is also known as					lassitude	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Fatigue (also called exhaustion, lethargy, languidness, languor, lassitude, and listlessness) is a state of awareness describing a range of afflictions, usually associated with physical and/or mental weakness, though varying from a general state of lethargy to a specific work-induced burning sensation within one's muscles. 	topic_mrs
78372	7	355802	11	NULL	NULL	0	NULL	Fatigue	MedicalFinding		associated with					weakness	PhysicalPhenomenon	physical;;mental			NULL		0	NULL	NULL	NULL	NULL	NULL	Fatigue (also called exhaustion, lethargy, languidness, languor, lassitude, and listlessness) is a state of awareness describing a range of afflictions, usually associated with physical and/or mental weakness, though varying from a general state of lethargy to a specific work-induced burning sensation within one's muscles. 	topic_mrs
78373	8	355802	11	NULL	NULL	0	NULL	Fatigue	MedicalFinding		 is a state of					awareness	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Fatigue (also called exhaustion, lethargy, languidness, languor, lassitude, and listlessness) is a state of awareness describing a range of afflictions, usually associated with physical and/or mental weakness, though varying from a general state of lethargy to a specific work-induced burning sensation within one's muscles. 	topic_mrs
78374	9	355802	11	NULL	NULL	0	NULL	statement 8	Process		is a range of					afflictions	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Fatigue (also called exhaustion, lethargy, languidness, languor, lassitude, and listlessness) is a state of awareness describing a range of afflictions, usually associated with physical and/or mental weakness, though varying from a general state of lethargy to a specific work-induced burning sensation within one's muscles. 	topic_mrs
78375	10	355802	11	NULL	NULL	0	NULL	work	Process		induced					burning sensation	Process	muscles			NULL		0	NULL	NULL	NULL	NULL	NULL	Fatigue (also called exhaustion, lethargy, languidness, languor, lassitude, and listlessness) is a state of awareness describing a range of afflictions, usually associated with physical and/or mental weakness, though varying from a general state of lethargy to a specific work-induced burning sensation within one's muscles. 	topic_mrs
78376	11	355802	11	NULL	NULL	0	NULL	Fatigue	MedicalFinding		leads to		may			statement 10	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Fatigue (also called exhaustion, lethargy, languidness, languor, lassitude, and listlessness) is a state of awareness describing a range of afflictions, usually associated with physical and/or mental weakness, though varying from a general state of lethargy to a specific work-induced burning sensation within one's muscles. 	topic_mrs
78658	1	355803	11	NULL	NULL	0	NULL	antibiotic	Chemical	short-term	had no effect on		deleterious			aerobic capacity	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We concluded that in healthy individuals, a short-term antibiotic treatment had no deleterious effect on aerobic capacity or on muscle strength and was not associated with subjective side effects	topic_mrs
78659	2	355803	11	NULL	NULL	0	NULL	Antibiotic	Chemical	short-term	had no effect on		deleterious			muscle strength	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We concluded that in healthy individuals, a short-term antibiotic treatment had no deleterious effect on aerobic capacity or on muscle strength and was not associated with subjective side effects	topic_mrs
78660	3	355803	11	NULL	NULL	0	NULL	Antibiotic	Chemical	short-term	was not associated with					side effects	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We concluded that in healthy individuals, a short-term antibiotic treatment had no deleterious effect on aerobic capacity or on muscle strength and was not associated with subjective side effects	topic_mrs
78663	1	355805	11	NULL	NULL	0	NULL	Marijuana	Chemical		is					Cannabis satiVa	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Marijuana (Cannabis satiVa) has long been known to contain antibacterial cannabinoids	topic_mrs
78664	2	355805	11	NULL	NULL	0	NULL	cannabinoids	Chemical		is a type of 					antibacterial	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Marijuana (Cannabis satiVa) has long been known to contain antibacterial cannabinoids	topic_mrs
78665	3	355805	11	NULL	NULL	0	NULL	Marijuana	Chemical		contain					cannabinoids	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Marijuana (Cannabis satiVa) has long been known to contain antibacterial cannabinoids	topic_mrs
76311	1	355807	5	11	NULL	NULL	NULL	DNMT3A gene	GP	mutation of	is associated with					AML	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	According to research published in the November 11 issue of the New England Journal of Medicine, researchers sequenced the genome of a patient who died of AML, then compared that genome to those of 281 other patients, and found that over 20% of them shared this mutation, at a gene known as DNMT3A, 	topic_ll
78666	1	355807	5	11	NULL	0	NULL	DNMT3A	GP	mutation of	published in					New England Journal of Medicine	Journal				NULL		0	NULL	NULL	NULL	NULL	NULL	According to research published in the November 11 issue of the New England Journal of Medicine, researchers sequenced the genome of a patient who died of AML, then compared that genome to those of 281 other patients, and found that over 20% of them shared this mutation, at a gene known as DNMT3A, 	topic_ll
78667	1	355808	5	11	NULL	0	NULL	glands	Organism part		produces					saliva	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Biopsying the glands that produce saliva to test for germinal center-like formation when someone is diagnosed with primary Sjögren’s Syndrome can predict later development of non-Hodgkin’s lymphoma, according to research presented this week at the American College of Rheumatology Annual Scientific Meeting in Atlanta.	topic_ll
76312	1	355809	5	NULL	NULL	0	NULL	NHL	MedicalFinding		is					non-Hodgkin lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	"Some patients with non-Hodgkin lymphoma (NHL) - a cancer of B cells - harbor a particular mutation in the gene encoding the receptor for B cell activating factor (BAFF), 	topic_ll
76313	2	355809	5	NULL	NULL	0	NULL	BAFF	GP		is					B cell activating factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	"Some patients with non-Hodgkin lymphoma (NHL) - a cancer of B cells - harbor a particular mutation in the gene encoding the receptor for B cell activating factor (BAFF), 	topic_ll
76314	3	355809	5	NULL	NULL	0	NULL	NHL	MedicalFinding		is a type of					cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	"Some patients with non-Hodgkin lymphoma (NHL) - a cancer of B cells - harbor a particular mutation in the gene encoding the receptor for B cell activating factor (BAFF), 	topic_ll
76315	4	355809	5	11	NULL	NULL	NULL	NHL	MedicalFinding		affects					B cells	Cell				NULL		NULL	NULL	NULL	NULL	NULL	NULL	"Some patients with non-Hodgkin lymphoma (NHL) - a cancer of B cells - harbor a particular mutation in the gene encoding the receptor for B cell activating factor (BAFF), 	topic_ll
76316	5	355809	5	11	NULL	NULL	NULL	BAFF receptor	GP	mutation of	leads to					NHL	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	"Some patients with non-Hodgkin lymphoma (NHL) - a cancer of B cells - harbor a particular mutation in the gene encoding the receptor for B cell activating factor (BAFF), 	topic_ll
78668	1	355809	5	11	NULL	0	NULL	non-Hodgkin lymphoma	MedicalFinding		is					NHL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	"Some patients with non-Hodgkin lymphoma (NHL) - a cancer of B cells - harbor a particular mutation in the gene encoding the receptor for B cell activating factor (BAFF), 	topic_ll
78669	1	355809	5	11	NULL	NULL	NULL	non-Hodgkin lymphoma	MedicalFinding		is a type of 					cancer	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	"Some patients with non-Hodgkin lymphoma (NHL) - a cancer of B cells - harbor a particular mutation in the gene encoding the receptor for B cell activating factor (BAFF), 	topic_ll
78670	1	355809	5	11	NULL	0	NULL	 B cell activating factor	GP		is					BAFF	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	"Some patients with non-Hodgkin lymphoma (NHL) - a cancer of B cells - harbor a particular mutation in the gene encoding the receptor for B cell activating factor (BAFF), 	topic_ll
76317	1	355810	5	11	NULL	NULL	NULL	sun tanning	Process		is linked to		may be			lymphomas	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Over the years, several peer-reviewed medical studies have attempted to establish a link between sun tanning and lymphomas, with the verdict closely split down the middle.	topic_ll
76318	1	355812	5	NULL	NULL	0	NULL	DHA	Chemical		is a type of					cosmetic ingredient	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The FDA approves DHA as a cosmetic ingredient, and it has no known direct connection to causing lymphomas or any other type of disease.	topic_ll
76319	2	355812	5	NULL	NULL	0	NULL	FDA	GroupOfPeople		approves					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The FDA approves DHA as a cosmetic ingredient, and it has no known direct connection to causing lymphomas or any other type of disease.	topic_ll
76320	3	355812	5	NULL	NULL	0	NULL	DHA	Chemical		does not cause					lymphomas	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The FDA approves DHA as a cosmetic ingredient, and it has no known direct connection to causing lymphomas or any other type of disease.	topic_ll
76321	1	355814	5	NULL	NULL	0	NULL	DHA	Chemical		is					Dihydroxyacetone	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	they usually contain a substance called DHA (Dihydroxyacetone), which stains the outer layer of dead skin cells a darker color.	topic_ll
76322	2	355814	5	NULL	NULL	0	NULL	skin	OrganismPart	outer layer of;;dead	is stained					darker color	AbstractConcept				NULL		0	NULL	NULL	NULL	NULL	NULL	they usually contain a substance called DHA (Dihydroxyacetone), which stains the outer layer of dead skin cells a darker color.	topic_ll
76323	3	355814	5	NULL	NULL	0	NULL	DHA	Chemical		is required for					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	they usually contain a substance called DHA (Dihydroxyacetone), which stains the outer layer of dead skin cells a darker color.	topic_ll
76324	1	355815	5	NULL	NULL	0	NULL	HHV6	GP	presence of	indicator of		predicting			cellular immunosuppression	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The presence of HHV6 can be considered as a predicting indicator of cellular immunosuppression preceding the onset of CMV infection which may result in a severe outcome among pediatric lymphoma patients.	topic_ll
76325	2	355815	5	NULL	NULL	0	NULL	cellular immunosuppression	MedicalFinding		precedes					CMV infection	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The presence of HHV6 can be considered as a predicting indicator of cellular immunosuppression preceding the onset of CMV infection which may result in a severe outcome among pediatric lymphoma patients.	topic_ll
76326	3	355815	5	NULL	NULL	0	NULL	statement 2	Process		results in		may			pediatric lymphoma patients	GroupOfPeople	severe outcome of			NULL		0	NULL	NULL	NULL	NULL	NULL	The presence of HHV6 can be considered as a predicting indicator of cellular immunosuppression preceding the onset of CMV infection which may result in a severe outcome among pediatric lymphoma patients.	topic_ll
76585	1	355817	5	NULL	NULL	0	NULL	cancers	MedicalFinding	secondary	is not uncommon for					Hodgkin's patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Since secondary cancers are not uncommon for Hodgkin's patients anywhere from 5-25 years down the road due to exposure to chemo and radiation, this study suggests that many patients are being overtreated at the current guidelines and that the lower chemo and radiation levels should be considered. 	topic_ll
76586	2	355817	5	NULL	NULL	0	NULL	chemo	MedicalProcedure	exposure to	causes					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Since secondary cancers are not uncommon for Hodgkin's patients anywhere from 5-25 years down the road due to exposure to chemo and radiation, this study suggests that many patients are being overtreated at the current guidelines and that the lower chemo and radiation levels should be considered. 	topic_ll
76587	3	355817	5	NULL	NULL	0	NULL	radiation	PhysicalPhenomenon	exposure to	causes					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Since secondary cancers are not uncommon for Hodgkin's patients anywhere from 5-25 years down the road due to exposure to chemo and radiation, this study suggests that many patients are being overtreated at the current guidelines and that the lower chemo and radiation levels should be considered. 	topic_ll
76588	1	355818	5	NULL	NULL	0	NULL	FDG	Chemical	high rates of	exists in					T-cell lymphomas	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	They determined that high rates of FDG positivity did indeed exist in T-cell lymphomas and "given the propensity for disease involvement outside the normal scan range of diagnostic CT, we recommend that patients with T-cell lymphoma be scanned from vertex to feet by use of PET/CT.	topic_ll
76589	2	355818	5	NULL	NULL	0	NULL	T-cell lymphoma patients	GroupOfPeople		scanned from					vertex	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	They determined that high rates of FDG positivity did indeed exist in T-cell lymphomas and "given the propensity for disease involvement outside the normal scan range of diagnostic CT, we recommend that patients with T-cell lymphoma be scanned from vertex to feet by use of PET/CT.	topic_ll
76590	3	355818	5	NULL	NULL	0	NULL	T-cell lymphoma patients	GroupOfPeople		scanned to					feet	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	They determined that high rates of FDG positivity did indeed exist in T-cell lymphomas and "given the propensity for disease involvement outside the normal scan range of diagnostic CT, we recommend that patients with T-cell lymphoma be scanned from vertex to feet by use of PET/CT.	topic_ll
76591	4	355818	5	NULL	NULL	0	NULL	statement 2	Process		occurs along with					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	They determined that high rates of FDG positivity did indeed exist in T-cell lymphomas and "given the propensity for disease involvement outside the normal scan range of diagnostic CT, we recommend that patients with T-cell lymphoma be scanned from vertex to feet by use of PET/CT.	topic_ll
76592	5	355818	5	NULL	NULL	0	NULL	PET/CT	MedicalProcedure		is used for					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	They determined that high rates of FDG positivity did indeed exist in T-cell lymphomas and "given the propensity for disease involvement outside the normal scan range of diagnostic CT, we recommend that patients with T-cell lymphoma be scanned from vertex to feet by use of PET/CT.	topic_ll
76593	6	355818	5	NULL	NULL	0	NULL	PET/CT	MedicalProcedure		is used for					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	They determined that high rates of FDG positivity did indeed exist in T-cell lymphomas and "given the propensity for disease involvement outside the normal scan range of diagnostic CT, we recommend that patients with T-cell lymphoma be scanned from vertex to feet by use of PET/CT.	topic_ll
76594	1	355819	5	NULL	NULL	0	NULL	PET-CT	MedicalProcedure	extended	is recommended for					T-cell lymphomas	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Extended PET-CT recommended for T-cell lymphomas 	topic_ll
76673	1	355820	7	NULL	NULL	0	NULL	FDG	Chemical		used during					 PET-CT scan	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	FDG (fluorodeoxyglucose) is the radiopharmaceutical agent used during a PET-CT scan 	topic_ll
76674	2	355820	7	NULL	NULL	0	NULL	FDG	Chemical		is a type of					radiopharmaceutical agent	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	FDG (fluorodeoxyglucose) is the radiopharmaceutical agent used during a PET-CT scan 	topic_ll
76675	3	355820	7	NULL	NULL	0	NULL	FDG	Chemical		is					fluorodeoxyglucose	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	FDG (fluorodeoxyglucose) is the radiopharmaceutical agent used during a PET-CT scan 	topic_ll
76676	1	355821	7	NULL	NULL	0	NULL	social rhythm therapy	MedicalProcedure		added to					interpersonal psychotherapy	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Addition of social rhythm therapy to interpersonal psychotherapy leads to create a new psychotherapy adaptated to bipolar disorders: InterPersonal and Social Rhythm Therapy (IPSRT).	topic_bd
76677	2	355821	7	NULL	NULL	NULL	NULL	statement 1	Process		leads to					IPSRT	MedicalProcedure				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Addition of social rhythm therapy to interpersonal psychotherapy leads to create a new psychotherapy adaptated to bipolar disorders: InterPersonal and Social Rhythm Therapy (IPSRT).	topic_bd
76678	3	355821	7	NULL	NULL	0	NULL	statement 2	Process		adaptated to					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Addition of social rhythm therapy to interpersonal psychotherapy leads to create a new psychotherapy adaptated to bipolar disorders: InterPersonal and Social Rhythm Therapy (IPSRT).	topic_bd
76679	4	355821	7	NULL	NULL	0	NULL	IPSRT	MedicalProcedure		is a type of					new psychotherapy	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Addition of social rhythm therapy to interpersonal psychotherapy leads to create a new psychotherapy adaptated to bipolar disorders: InterPersonal and Social Rhythm Therapy (IPSRT).	topic_bd
76680	5	355821	7	NULL	NULL	0	NULL	IPSRT	MedicalProcedure		is					InterPersonal and Social Rhythm Therapy	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Addition of social rhythm therapy to interpersonal psychotherapy leads to create a new psychotherapy adaptated to bipolar disorders: InterPersonal and Social Rhythm Therapy (IPSRT).	topic_bd
76688	1	355822	7	NULL	NULL	0	NULL	rTMS	MedicalProcedure		used in the 					mood episodes	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Thus, treating mood episodes and fighting against resistant and residual symptoms or chronicity of the disorders constitute major clinical issues and economic challenges. They have generated great interest in finding new non-pharmacological approaches such as repetitive transcranial magnetic stimulation (rTMS).	topic_bd
76689	2	355822	7	NULL	NULL	0	NULL	rTMS	MedicalProcedure		is					repetitive transcranial magnetic stimulation	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Thus, treating mood episodes and fighting against resistant and residual symptoms or chronicity of the disorders constitute major clinical issues and economic challenges. They have generated great interest in finding new non-pharmacological approaches such as repetitive transcranial magnetic stimulation (rTMS).	topic_bd
76690	3	355822	7	NULL	NULL	0	NULL	rTMS	MedicalProcedure		is a type of					non-pharmacological approach	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Thus, treating mood episodes and fighting against resistant and residual symptoms or chronicity of the disorders constitute major clinical issues and economic challenges. They have generated great interest in finding new non-pharmacological approaches such as repetitive transcranial magnetic stimulation (rTMS).	topic_bd
76681	1	355824	7	NULL	NULL	0	NULL	dorsolateral prefrontal cortex	OrganismPart	left side of	have effect in					mood control	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Given the hypothesis that the right and left sides of the dorsolateral prefrontal cortex have opposing effects in mood control, high-frequency rTMS activates the left side and low-frequency to inhibit the right side in the treatment of depression.	topic_bd
76682	2	355824	7	NULL	NULL	NULL	NULL	dorsolateral prefrontal cortex	OrganismPart	right side of	have effect in					mood control	MentalProcess				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given the hypothesis that the right and left sides of the dorsolateral prefrontal cortex have opposing effects in mood control, high-frequency rTMS activates the left side and low-frequency to inhibit the right side in the treatment of depression.	topic_bd
76683	3	355824	7	NULL	NULL	0	NULL	statement 1	Process		opposing effect to					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Given the hypothesis that the right and left sides of the dorsolateral prefrontal cortex have opposing effects in mood control, high-frequency rTMS activates the left side and low-frequency to inhibit the right side in the treatment of depression.	topic_bd
76684	4	355824	7	NULL	NULL	NULL	NULL	rTMS	MedicalProcedure	high-frequency	activates 					dorsolateral prefrontal cortex	OrganismPart	left side of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given the hypothesis that the right and left sides of the dorsolateral prefrontal cortex have opposing effects in mood control, high-frequency rTMS activates the left side and low-frequency to inhibit the right side in the treatment of depression.	topic_bd
76685	5	355824	7	NULL	NULL	0	NULL	rTMS	MedicalProcedure	low-frequency	inhibit					dorsolateral prefrontal cortex	OrganismPart	right side of			NULL		0	NULL	NULL	NULL	NULL	NULL	Given the hypothesis that the right and left sides of the dorsolateral prefrontal cortex have opposing effects in mood control, high-frequency rTMS activates the left side and low-frequency to inhibit the right side in the treatment of depression.	topic_bd
76686	6	355824	7	NULL	NULL	0	NULL	statement 4	Process		in the treatment of					depression	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Given the hypothesis that the right and left sides of the dorsolateral prefrontal cortex have opposing effects in mood control, high-frequency rTMS activates the left side and low-frequency to inhibit the right side in the treatment of depression.	topic_bd
76687	7	355824	7	NULL	NULL	0	NULL	statement 5	Process		in the treatment of					depression	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Given the hypothesis that the right and left sides of the dorsolateral prefrontal cortex have opposing effects in mood control, high-frequency rTMS activates the left side and low-frequency to inhibit the right side in the treatment of depression.	topic_bd
76862	1	355825	7	NULL	NULL	0	NULL	rTMS 	MedicalProcedure		effective in the					bipolar depression	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Overall, rTMS seems to be effective in the treatment of bipolar depression but further trials with larger cohorts should determine optimal parameters of stimulation.	topic_bd
76863	1	355826	7	NULL	NULL	0	NULL	vVBM	MedicalProcedure	optimized	shows					bipolar I disorder	MedicalFinding	smaller volumes in the left inferior parietal lobule			NULL		0	NULL	NULL	NULL	NULL	NULL	There was no difference in whole-brain gray matter volume between the two groups. Optimized vVBM showed that subjects with bipolar I disorder had smaller volumes in the left inferior parietal lobule, right superior temporal gyrus, right middle frontal gyrus and left caudate	topic_bd
76864	2	355826	7	NULL	NULL	0	NULL	 vVBM	MedicalProcedure	optimized	shows					bipolar I disorder	MedicalFinding	smaller volumes in right superior temporal gyrus			NULL		0	NULL	NULL	NULL	NULL	NULL	There was no difference in whole-brain gray matter volume between the two groups. Optimized vVBM showed that subjects with bipolar I disorder had smaller volumes in the left inferior parietal lobule, right superior temporal gyrus, right middle frontal gyrus and left caudate	topic_bd
76865	3	355826	7	NULL	NULL	NULL	NULL	vVBM	MedicalProcedure	optimized	shows					bipolar I disorder	MedicalFinding	small volumes in right  middle frontal gyrus			NULL		NULL	NULL	NULL	NULL	NULL	NULL	There was no difference in whole-brain gray matter volume between the two groups. Optimized vVBM showed that subjects with bipolar I disorder had smaller volumes in the left inferior parietal lobule, right superior temporal gyrus, right middle frontal gyrus and left caudate	topic_bd
76866	4	355826	7	NULL	NULL	0	NULL	vVBM	MedicalProcedure	optimized	shows					bipolar I disorder	MedicalFinding	smaller volumes in left caudate			NULL		0	NULL	NULL	NULL	NULL	NULL	There was no difference in whole-brain gray matter volume between the two groups. Optimized vVBM showed that subjects with bipolar I disorder had smaller volumes in the left inferior parietal lobule, right superior temporal gyrus, right middle frontal gyrus and left caudate	topic_bd
76867	1	355827	7	NULL	NULL	0	NULL	gray matter defects	OrganismPart		seen in					bipolar I disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	These results suggest widespread gray matter defects in bipolar I disorder, which may play an important role in onset of the illness.	topic_bd
76868	2	355827	7	NULL	NULL	0	NULL	statement 1	Process		important role in					illness	MedicalFinding	onset of			NULL		0	NULL	NULL	NULL	NULL	NULL	These results suggest widespread gray matter defects in bipolar I disorder, which may play an important role in onset of the illness.	topic_bd
76869	1	355830	7	NULL	NULL	0	NULL	lintuzumab	Chemical		failed to 					survival	Process	demonstrate overall			NULL		0	NULL	NULL	NULL	NULL	NULL	A Phase IIb study of the monoclonal antibody lintuzumab, also known as SGN33, failed to demonstrate an improvement in overall survival compared to current chemotherapy	topic_ll
76870	2	355830	7	NULL	NULL	0	NULL	lintuzumab	Chemical		is known as					SGN33	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	A Phase IIb study of the monoclonal antibody lintuzumab, also known as SGN33, failed to demonstrate an improvement in overall survival compared to current chemotherapy	topic_ll
76871	3	355830	7	NULL	NULL	0	NULL	lintuzumab	Chemical		is a type of					monoclonal antibody	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	A Phase IIb study of the monoclonal antibody lintuzumab, also known as SGN33, failed to demonstrate an improvement in overall survival compared to current chemotherapy	topic_ll
76872	1	355831	7	NULL	NULL	0	NULL	children	GroupOfPeople	older father	risk of					NHLs	MedicalFinding	developing			NULL		0	NULL	NULL	NULL	NULL	NULL	Now a new and possibly unique study out of City of Hope Hospital in southern California suggests kids of born of older fathers are at an increased risk of developing NHLs.	topic_ll
76873	1	355832	7	NULL	NULL	0	NULL	Shark cartilage extract	GP		does not produce					anti-cancer effects	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Shark cartilage extract produces no anti-cancer effects in latest study	topic_ll
76874	1	355833	7	NULL	NULL	0	NULL	brentuximab vedotin	Chemical		is a type of					anti-cancer drug	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Seattle Genetics is reporting positive preliminary results from a phase II trial of its promising anti-cancer drug brentuximab vedotin (SGN-35) against patients with anaplastic large cell lymphoma, (ALCL)	topic_ll
76875	2	355833	7	NULL	NULL	0	NULL	brentuximab vedotin	Chemical		against					ALCL	MedicalFinding	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	Seattle Genetics is reporting positive preliminary results from a phase II trial of its promising anti-cancer drug brentuximab vedotin (SGN-35) against patients with anaplastic large cell lymphoma, (ALCL)	topic_ll
76876	3	355833	7	NULL	NULL	0	NULL	ALCL	MedicalFinding		is					anaplastic large cell lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Seattle Genetics is reporting positive preliminary results from a phase II trial of its promising anti-cancer drug brentuximab vedotin (SGN-35) against patients with anaplastic large cell lymphoma, (ALCL)	topic_ll
76877	4	355833	7	NULL	NULL	0	NULL	 brentuximab vedotin 	Chemical		is known as					SGN-35	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Seattle Genetics is reporting positive preliminary results from a phase II trial of its promising anti-cancer drug brentuximab vedotin (SGN-35) against patients with anaplastic large cell lymphoma, (ALCL)	topic_ll
76878	1	355834	7	NULL	NULL	0	NULL	brentuximab vedotin	Chemical		is used for					relapsed Hodgkin's lymphoma	MedicalFinding	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	Seattle Genetics has announced top-line results from a phase II trial of its antibody-drug conjugate (ADC) brentuximab vedotin (SGN-35) for patients with relapsed or refractory Hodgkin's lymphoma	topic_ll
76879	2	355834	7	NULL	NULL	NULL	NULL	brentuximab vedotin	Chemical		is used for					refractory Hodgkin's lymphoma	MedicalFinding	patients with			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Seattle Genetics has announced top-line results from a phase II trial of its antibody-drug conjugate (ADC) brentuximab vedotin (SGN-35) for patients with relapsed or refractory Hodgkin's lymphoma	topic_ll
76880	3	355834	7	NULL	NULL	0	NULL	brentuximab vedotin 	Chemical		is a type of					ADC	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Seattle Genetics has announced top-line results from a phase II trial of its antibody-drug conjugate (ADC) brentuximab vedotin (SGN-35) for patients with relapsed or refractory Hodgkin's lymphoma	topic_ll
76881	4	355834	7	NULL	NULL	0	NULL	ADC	Chemical		is					antibody-drug conjugate	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Seattle Genetics has announced top-line results from a phase II trial of its antibody-drug conjugate (ADC) brentuximab vedotin (SGN-35) for patients with relapsed or refractory Hodgkin's lymphoma	topic_ll
76882	5	355834	7	NULL	NULL	0	NULL	brentuximab vedotin	Chemical		is known as					SGN-35	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Seattle Genetics has announced top-line results from a phase II trial of its antibody-drug conjugate (ADC) brentuximab vedotin (SGN-35) for patients with relapsed or refractory Hodgkin's lymphoma	topic_ll
76883	1	355835	7	NULL	NULL	0	NULL	Personalized Lymphoma Vaccine	Chemical		prevent					follicular lymphoma patients	MedicalFinding	recurrence among			NULL		0	NULL	NULL	NULL	NULL	NULL	Personalized Lymphoma Vaccine Increases Survival by Two Years A personalized vaccine is a powerful therapy to prevent recurrence among certain follicular lymphoma patients, according to the latest results of ongoing research led by the University of Pennsylvania School of Medicine.	topic_ll
76884	2	355835	7	NULL	NULL	0	NULL	Personalized Lymphoma Vaccine	MedicalFinding		increase					follicular lymphoma patients	MedicalFinding	survival of			NULL		0	NULL	NULL	NULL	NULL	NULL	Personalized Lymphoma Vaccine Increases Survival by Two Years A personalized vaccine is a powerful therapy to prevent recurrence among certain follicular lymphoma patients, according to the latest results of ongoing research led by the University of Pennsylvania School of Medicine.	topic_ll
76885	1	355837	7	NULL	NULL	0	NULL	Omapro	Chemical		used for					CML	MedicalFinding	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	a diagnostic test to identify patients with the T3151 genetic mutation prior to giving approval to ChemGenex Pharmaceuticals' Omapro (omacetaxine) as a treatment for patients with chronic myeloid leukemia (CML) who did not respond to initial treatment with Gleevec (imatinib).	topic_ll
76886	2	355837	7	NULL	NULL	0	NULL	Omapro	Chemical		is					omacetaxine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	a diagnostic test to identify patients with the T3151 genetic mutation prior to giving approval to ChemGenex Pharmaceuticals' Omapro (omacetaxine) as a treatment for patients with chronic myeloid leukemia (CML) who did not respond to initial treatment with Gleevec (imatinib).	topic_ll
76887	3	355837	7	NULL	NULL	NULL	NULL	CML patients	MedicalFinding		did not respond to					Gleevec	Chemical	initial treatment with			NULL		NULL	NULL	NULL	NULL	NULL	NULL	a diagnostic test to identify patients with the T3151 genetic mutation prior to giving approval to ChemGenex Pharmaceuticals' Omapro (omacetaxine) as a treatment for patients with chronic myeloid leukemia (CML) who did not respond to initial treatment with Gleevec (imatinib).	topic_ll
76888	4	355837	7	NULL	NULL	0	NULL	Omapro	Chemical		is used in					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	a diagnostic test to identify patients with the T3151 genetic mutation prior to giving approval to ChemGenex Pharmaceuticals' Omapro (omacetaxine) as a treatment for patients with chronic myeloid leukemia (CML) who did not respond to initial treatment with Gleevec (imatinib).	topic_ll
76889	5	355837	7	NULL	NULL	0	NULL	CML	MedicalFinding		is					chronic myeloid leukemia 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	a diagnostic test to identify patients with the T3151 genetic mutation prior to giving approval to ChemGenex Pharmaceuticals' Omapro (omacetaxine) as a treatment for patients with chronic myeloid leukemia (CML) who did not respond to initial treatment with Gleevec (imatinib).	topic_ll
76896	6	355837	7	NULL	NULL	0	NULL	Gleevec	Chemical		is					imatinib	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	a diagnostic test to identify patients with the T3151 genetic mutation prior to giving approval to ChemGenex Pharmaceuticals' Omapro (omacetaxine) as a treatment for patients with chronic myeloid leukemia (CML) who did not respond to initial treatment with Gleevec (imatinib).	topic_ll
76890	1	355838	7	NULL	NULL	0	NULL	GVAX Leukemia Vaccine	Chemical		reduces		severly			cancer cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	GVAX Leukemia Vaccine either severely reduces or completely eliminates cancer cells remaining in some patients with chronic myeloid leukemia (CML) who have been on Gleevec for a year or longer.	topic_ll
76891	2	355838	7	NULL	NULL	0	NULL	GVAX Leukemia Vaccine	Chemical		eliminates		completely			cancer cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	GVAX Leukemia Vaccine either severely reduces or completely eliminates cancer cells remaining in some patients with chronic myeloid leukemia (CML) who have been on Gleevec for a year or longer.	topic_ll
76892	3	355838	7	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	GVAX Leukemia Vaccine either severely reduces or completely eliminates cancer cells remaining in some patients with chronic myeloid leukemia (CML) who have been on Gleevec for a year or longer.	topic_ll
76893	5	355838	7	NULL	NULL	NULL	NULL	statement 3	Process		in patients with					statement 4	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	GVAX Leukemia Vaccine either severely reduces or completely eliminates cancer cells remaining in some patients with chronic myeloid leukemia (CML) who have been on Gleevec for a year or longer.	topic_ll
76894	4	355838	7	NULL	NULL	NULL	NULL	Gleevec	Chemical		used in the					CML	MedicalFinding	treatment of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	GVAX Leukemia Vaccine either severely reduces or completely eliminates cancer cells remaining in some patients with chronic myeloid leukemia (CML) who have been on Gleevec for a year or longer.	topic_ll
76895	6	355838	7	NULL	NULL	0	NULL	CML	MedicalFinding		is					chronic myeloid leukemia 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	GVAX Leukemia Vaccine either severely reduces or completely eliminates cancer cells remaining in some patients with chronic myeloid leukemia (CML) who have been on Gleevec for a year or longer.	topic_ll
76897	1	355840	7	NULL	NULL	0	NULL	tumors	Cell		have					CD68-positive macrophages	Cell	high number of			NULL		0	NULL	NULL	NULL	NULL	NULL	The minority of patients who relapse and sometimes die if they don't receive more aggressive therapy appear to have something in their tumors the others don't: a high number of white cells called CD68-positive macrophages (scavenger cells). It appears that the more of these cells in the tumor, the shorter the 10-year survival rate, the more aggressive the secondary treatment required. 	topic_ll
76898	2	355840	7	NULL	NULL	0	NULL	statement 1	Process		leads to					 survival rate	Process	shorter			NULL		0	NULL	NULL	NULL	NULL	NULL	The minority of patients who relapse and sometimes die if they don't receive more aggressive therapy appear to have something in their tumors the others don't: a high number of white cells called CD68-positive macrophages (scavenger cells). It appears that the more of these cells in the tumor, the shorter the 10-year survival rate, the more aggressive the secondary treatment required. 	topic_ll
76899	3	355840	7	NULL	NULL	0	NULL	statement 1	Process		requires					secondary treatment 	MedicalProcedure	aggressive			NULL		0	NULL	NULL	NULL	NULL	NULL	The minority of patients who relapse and sometimes die if they don't receive more aggressive therapy appear to have something in their tumors the others don't: a high number of white cells called CD68-positive macrophages (scavenger cells). It appears that the more of these cells in the tumor, the shorter the 10-year survival rate, the more aggressive the secondary treatment required. 	topic_ll
76900	4	355840	7	NULL	NULL	0	NULL	CD68-positive macrophages	Cell		is a type of					white cells 	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	The minority of patients who relapse and sometimes die if they don't receive more aggressive therapy appear to have something in their tumors the others don't: a high number of white cells called CD68-positive macrophages (scavenger cells). It appears that the more of these cells in the tumor, the shorter the 10-year survival rate, the more aggressive the secondary treatment required. 	topic_ll
76901	5	355840	7	NULL	NULL	0	NULL	CD68-positive macrophages	Cell		is a type of					scavenger cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	The minority of patients who relapse and sometimes die if they don't receive more aggressive therapy appear to have something in their tumors the others don't: a high number of white cells called CD68-positive macrophages (scavenger cells). It appears that the more of these cells in the tumor, the shorter the 10-year survival rate, the more aggressive the secondary treatment required. 	topic_ll
76902	1	355841	7	NULL	NULL	0	NULL	natural sunlight	Chemical		produce					vitamin D	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Research conducted in this area reveals the fact that exposure to natural sunlight produces vitamin D that helps fight against symptoms of non-Hodgkin's lymphoma.	topic_ll
76903	2	355841	7	NULL	NULL	0	NULL	statement 1	Process		helps in					non-Hodgkin's lymphoma	MedicalFinding	fight against symptoms of			NULL		0	NULL	NULL	NULL	NULL	NULL	Research conducted in this area reveals the fact that exposure to natural sunlight produces vitamin D that helps fight against symptoms of non-Hodgkin's lymphoma.	topic_ll
76904	1	355842	7	NULL	NULL	NULL	NULL	Non-Hodgkins lymphoma	MedicalFinding	treatment of	include		may			Reishi mushroom	Organism	use of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Non-Hodgkin’s lymphoma and Hodgkin’s lymphoma treatments may include the use of Reishi mushroom, green tea, olive leaf, milk thistle, and standardized extract.	topic_ll
76905	2	355842	7	NULL	NULL	NULL	NULL	Non-Hodgkins lymphoma	MedicalFinding	treatment of	include		may			green tea	Organism	use of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Non-Hodgkin’s lymphoma and Hodgkin’s lymphoma treatments may include the use of Reishi mushroom, green tea, olive leaf, milk thistle, and standardized extract.	topic_ll
76906	3	355842	7	NULL	NULL	NULL	NULL	Non-Hodgkins lymphoma	MedicalFinding	treatment of	include		may			milk thistle	Organism	use of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Non-Hodgkin’s lymphoma and Hodgkin’s lymphoma treatments may include the use of Reishi mushroom, green tea, olive leaf, milk thistle, and standardized extract.	topic_ll
76907	5	355842	7	NULL	NULL	NULL	NULL	Hodgkins lymphoma	MedicalFinding	treatment of	include		may			Reishi mushroom	Organism	use of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Non-Hodgkin’s lymphoma and Hodgkin’s lymphoma treatments may include the use of Reishi mushroom, green tea, olive leaf, milk thistle, and standardized extract.	topic_ll
76908	4	355842	7	NULL	NULL	NULL	NULL	Non-Hodgkins lymphoma 	MedicalFinding	treatment of	include		may			olive leaf	OrganismPart	use of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Non-Hodgkin’s lymphoma and Hodgkin’s lymphoma treatments may include the use of Reishi mushroom, green tea, olive leaf, milk thistle, and standardized extract.	topic_ll
76909	6	355842	7	NULL	NULL	0	NULL	Hodgkins lymphoma	MedicalFinding	treatment of	include		may			green tea	Organism	use of			NULL		0	NULL	NULL	NULL	NULL	NULL	Non-Hodgkin’s lymphoma and Hodgkin’s lymphoma treatments may include the use of Reishi mushroom, green tea, olive leaf, milk thistle, and standardized extract.	topic_ll
76910	7	355842	7	NULL	NULL	0	NULL	Hodgkins lymphoma	MedicalFinding	treatment of	include		may			olive leaf	OrganismPart	use of			NULL		0	NULL	NULL	NULL	NULL	NULL	Non-Hodgkin’s lymphoma and Hodgkin’s lymphoma treatments may include the use of Reishi mushroom, green tea, olive leaf, milk thistle, and standardized extract.	topic_ll
76911	8	355842	7	NULL	NULL	0	NULL	Hodgkins lymphoma	MedicalFinding		include		may			milk thistle	Organism	use of			NULL		0	NULL	NULL	NULL	NULL	NULL	Non-Hodgkin’s lymphoma and Hodgkin’s lymphoma treatments may include the use of Reishi mushroom, green tea, olive leaf, milk thistle, and standardized extract.	topic_ll
76912	1	355846	7	NULL	NULL	0	NULL	SHIP	GP		suppress					B cell lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Protein ID'ed May Help with Lymphoma Therapies SHIP and PTEN act cooperatively to suppress B cell lymphoma.	topic_ll
76913	2	355846	7	NULL	NULL	NULL	NULL	PTEN	GP		suppress					B cell lymphoma	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Protein ID'ed May Help with Lymphoma Therapies SHIP and PTEN act cooperatively to suppress B cell lymphoma.	topic_ll
76914	3	355846	7	NULL	NULL	0	NULL	statement 1	Process		in cooperation with					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Protein ID'ed May Help with Lymphoma Therapies SHIP and PTEN act cooperatively to suppress B cell lymphoma.	topic_ll
77048	1	355847	7	NULL	NULL	0	NULL	SHIP	GP		act in cooperation with					PTEN	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Inflammatory Diseases Program at Sanford-Burnham Medical Research Institute (Sanford-Burnham), explores the roles of two enzymes, called SHIP and PTEN, in B cell growth and proliferation.Protein ID'ed May Help with Lymphoma Therapies SHIP and PTEN act cooperatively to suppress B cell lymphoma. 	topic_ll
77049	2	355847	7	NULL	NULL	0	NULL	statement 1	Process		suppress					B cell lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Inflammatory Diseases Program at Sanford-Burnham Medical Research Institute (Sanford-Burnham), explores the roles of two enzymes, called SHIP and PTEN, in B cell growth and proliferation.Protein ID'ed May Help with Lymphoma Therapies SHIP and PTEN act cooperatively to suppress B cell lymphoma. 	topic_ll
77050	3	355847	7	NULL	NULL	0	NULL	SHIP	GP		is a type of					enzyme	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Inflammatory Diseases Program at Sanford-Burnham Medical Research Institute (Sanford-Burnham), explores the roles of two enzymes, called SHIP and PTEN, in B cell growth and proliferation.Protein ID'ed May Help with Lymphoma Therapies SHIP and PTEN act cooperatively to suppress B cell lymphoma. 	topic_ll
77051	4	355847	7	NULL	NULL	0	NULL	PTEN	GP		is a type of					enzyme	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Inflammatory Diseases Program at Sanford-Burnham Medical Research Institute (Sanford-Burnham), explores the roles of two enzymes, called SHIP and PTEN, in B cell growth and proliferation.Protein ID'ed May Help with Lymphoma Therapies SHIP and PTEN act cooperatively to suppress B cell lymphoma. 	topic_ll
77052	1	355850	7	NULL	NULL	0	NULL	 primary central nervous system lymphoma	MedicalFinding	prognosis of	poor					therapy	MedicalProcedure	regardless of			NULL		0	NULL	NULL	NULL	NULL	NULL	Noting that the prognosis for most patients with primary central nervous system lymphoma is poor regardless of therapy and that only a minority of patients achieve a complete response to current chemotherapy regimens, Mayo Clinic researchers carried out a randomized phase II clinical trial in which high-dose cytarabine was added to high-dose methotrexate . 	topic_ll
77053	1	355853	7	NULL	NULL	0	NULL	ENMD-2076	Chemical		used to					AML	MedicalFinding	treat			NULL		0	NULL	NULL	NULL	NULL	NULL	The US FDA has granted orphan-drug status to EntreMed's ENMD-2076, the company's lead cancer drug candidate designed to treat acute myeloid leukemia (AML). 	topic_ll
77054	2	355853	7	NULL	NULL	0	NULL	AML	MedicalFinding		is					acute myeloid leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The US FDA has granted orphan-drug status to EntreMed's ENMD-2076, the company's lead cancer drug candidate designed to treat acute myeloid leukemia (AML). 	topic_ll
77090	1	355855	7	NULL	NULL	0	NULL	British garden rhubarb 	Organism	baking of	raise					polyphenols	Chemical	levels of			NULL		0	NULL	NULL	NULL	NULL	NULL	Findings published in the journal Food Chemistry suggest that baking a specific variety of British garden rhubarb grown in South Yorkshire for just 20 minutes raises the level of anti-cancerous chemicals known as polyphenols found in the plant.	topic_ll
77091	2	355855	7	NULL	NULL	0	NULL	polyphenols	Chemical		is a type of					anti-cancerous chemicals	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Findings published in the journal Food Chemistry suggest that baking a specific variety of British garden rhubarb grown in South Yorkshire for just 20 minutes raises the level of anti-cancerous chemicals known as polyphenols found in the plant.	topic_ll
77092	1	355857	7	NULL	NULL	0	NULL	Polyphenols	Chemical		kills					cancer cells	Cell	active			NULL		0	NULL	NULL	NULL	NULL	NULL	Polyphenols have been shown in the past to be active cancer cell killers and researchers from the Biomedical Research Centre of Sheffield Hallam University believe there may be some potential benefit to applying these findings to a less toxic treatment for certain leukemias, even those proven to be resistant to current treatment	topic_ll
77093	1	355860	7	NULL	NULL	0	NULL	yellow/orange fruits	Food		associated with					NHL	MedicalFinding	lower risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Greater intake of total fruits and vegetables, yellow/orange and cruciferous vegetables, broccoli and apple juice/cider are associated with a lower NHL risk, although this was only observed for follicular lymphoma, not in DLBCL.	topic_ll
77094	2	355860	7	NULL	NULL	NULL	NULL	cruciferous vegetables	Food		associated with					NHL	MedicalFinding	lower risk of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Greater intake of total fruits and vegetables, yellow/orange and cruciferous vegetables, broccoli and apple juice/cider are associated with a lower NHL risk, although this was only observed for follicular lymphoma, not in DLBCL.	topic_ll
77095	3	355860	7	NULL	NULL	0	NULL	broccoli 	Food		associated with					NHL	MedicalFinding	lower risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Greater intake of total fruits and vegetables, yellow/orange and cruciferous vegetables, broccoli and apple juice/cider are associated with a lower NHL risk, although this was only observed for follicular lymphoma, not in DLBCL.	topic_ll
77096	4	355860	7	NULL	NULL	0	NULL	apple juice/cider	Food		associated with					NHL	MedicalFinding	lower risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Greater intake of total fruits and vegetables, yellow/orange and cruciferous vegetables, broccoli and apple juice/cider are associated with a lower NHL risk, although this was only observed for follicular lymphoma, not in DLBCL.	topic_ll
77097	5	355860	7	NULL	NULL	0	NULL	statement 1	Process		observed in					follicular lymphoma 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Greater intake of total fruits and vegetables, yellow/orange and cruciferous vegetables, broccoli and apple juice/cider are associated with a lower NHL risk, although this was only observed for follicular lymphoma, not in DLBCL.	topic_ll
77098	6	355860	7	NULL	NULL	NULL	NULL	statement 2	Process		observed in					follicular lymphoma 	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Greater intake of total fruits and vegetables, yellow/orange and cruciferous vegetables, broccoli and apple juice/cider are associated with a lower NHL risk, although this was only observed for follicular lymphoma, not in DLBCL.	topic_ll
77099	7	355860	7	NULL	NULL	0	NULL	statement 3	Process		observed in					follicular lymphoma 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Greater intake of total fruits and vegetables, yellow/orange and cruciferous vegetables, broccoli and apple juice/cider are associated with a lower NHL risk, although this was only observed for follicular lymphoma, not in DLBCL.	topic_ll
77100	8	355860	7	NULL	NULL	0	NULL	statement 4	Process		observed in					follicular lymphoma 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Greater intake of total fruits and vegetables, yellow/orange and cruciferous vegetables, broccoli and apple juice/cider are associated with a lower NHL risk, although this was only observed for follicular lymphoma, not in DLBCL.	topic_ll
77101	9	355860	7	NULL	NULL	0	NULL	statement 1	Process		not observed in					DLBCL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Greater intake of total fruits and vegetables, yellow/orange and cruciferous vegetables, broccoli and apple juice/cider are associated with a lower NHL risk, although this was only observed for follicular lymphoma, not in DLBCL.	topic_ll
77102	10	355860	7	NULL	NULL	0	NULL	statement 2	Process		not observed in					DLBCL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Greater intake of total fruits and vegetables, yellow/orange and cruciferous vegetables, broccoli and apple juice/cider are associated with a lower NHL risk, although this was only observed for follicular lymphoma, not in DLBCL.	topic_ll
77103	11	355860	7	NULL	NULL	0	NULL	statement 3	Process		not observed in					DLBCL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Greater intake of total fruits and vegetables, yellow/orange and cruciferous vegetables, broccoli and apple juice/cider are associated with a lower NHL risk, although this was only observed for follicular lymphoma, not in DLBCL.	topic_ll
77104	12	355860	7	NULL	NULL	0	NULL	statement 4	Process		not observed in					DLBCL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Greater intake of total fruits and vegetables, yellow/orange and cruciferous vegetables, broccoli and apple juice/cider are associated with a lower NHL risk, although this was only observed for follicular lymphoma, not in DLBCL.	topic_ll
77105	1	355864	7	NULL	NULL	0	NULL	B cells	Cell	desensitization of	occur by					antigen receptors	GP	inactivating			NULL		0	NULL	NULL	NULL	NULL	NULL	National Jewish Health has been issued a US patent claiming a method to desensitize B cells by inactivating antigen receptors on their surfaces. The method, discovered by John Cambier, PhD, Chairman of the Integrated Department of Immunology at National Jewish Health, holds promise for treatment of B-cell mediated diseases, such as lymphoma and leukemia	topic_ll
77106	2	355864	7	NULL	NULL	0	NULL	antigen receptors 	GP		present on					B cells	Cell	surface of			NULL		0	NULL	NULL	NULL	NULL	NULL	National Jewish Health has been issued a US patent claiming a method to desensitize B cells by inactivating antigen receptors on their surfaces. The method, discovered by John Cambier, PhD, Chairman of the Integrated Department of Immunology at National Jewish Health, holds promise for treatment of B-cell mediated diseases, such as lymphoma and leukemia	topic_ll
77107	3	355864	7	NULL	NULL	0	NULL	statement 1	Process		used in the					lymphoma	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	National Jewish Health has been issued a US patent claiming a method to desensitize B cells by inactivating antigen receptors on their surfaces. The method, discovered by John Cambier, PhD, Chairman of the Integrated Department of Immunology at National Jewish Health, holds promise for treatment of B-cell mediated diseases, such as lymphoma and leukemia	topic_ll
77108	4	355864	7	NULL	NULL	0	NULL	statement 1	Process		used in the					leukemia	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	National Jewish Health has been issued a US patent claiming a method to desensitize B cells by inactivating antigen receptors on their surfaces. The method, discovered by John Cambier, PhD, Chairman of the Integrated Department of Immunology at National Jewish Health, holds promise for treatment of B-cell mediated diseases, such as lymphoma and leukemia	topic_ll
77109	5	355864	7	NULL	NULL	0	NULL	lymphoma	MedicalFinding		is a type of					B-cell mediated diseases	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	National Jewish Health has been issued a US patent claiming a method to desensitize B cells by inactivating antigen receptors on their surfaces. The method, discovered by John Cambier, PhD, Chairman of the Integrated Department of Immunology at National Jewish Health, holds promise for treatment of B-cell mediated diseases, such as lymphoma and leukemia	topic_ll
77110	6	355864	7	NULL	NULL	0	NULL	leukemia	MedicalFinding		is a type of					B-cell mediated diseases	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	National Jewish Health has been issued a US patent claiming a method to desensitize B cells by inactivating antigen receptors on their surfaces. The method, discovered by John Cambier, PhD, Chairman of the Integrated Department of Immunology at National Jewish Health, holds promise for treatment of B-cell mediated diseases, such as lymphoma and leukemia	topic_ll
77111	1	355865	7	NULL	NULL	NULL	NULL	MALT1	GP		boost 					 DLBCL	MedicalFinding	effectiveness of treatment against			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Working independently of one another, two groups of researchers have uncovered a possible strategy involving a protease enzyme known as MALT1 to boost the effectiveness of treatment against diffuse large B-cell lymphoma (DLBCL), 	topic_ll
77112	2	355865	7	NULL	NULL	0	NULL	DLBCL	MedicalFinding		is					diffuse large B-cell lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Working independently of one another, two groups of researchers have uncovered a possible strategy involving a protease enzyme known as MALT1 to boost the effectiveness of treatment against diffuse large B-cell lymphoma (DLBCL), 	topic_ll
77113	3	355865	7	NULL	NULL	0	NULL	MALT1	GP		is a type of					protease enzyme	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Working independently of one another, two groups of researchers have uncovered a possible strategy involving a protease enzyme known as MALT1 to boost the effectiveness of treatment against diffuse large B-cell lymphoma (DLBCL), 	topic_ll
77114	1	355867	7	NULL	NULL	0	NULL	romidepsin	Chemical		used in the					CTCL	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Earlier this month, the US FDA approved the antibiotic histone deacetylase inhibitor romidepsin (marketed as Istodax injection) for treating patients with cutaneous T-cell lymphoma (CTCL) who have undergone at least one prior systemic therapy. 	topic_ll
77115	2	355867	7	NULL	NULL	0	NULL	CTCL	MedicalFinding		is					cutaneous T-cell lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Earlier this month, the US FDA approved the antibiotic histone deacetylase inhibitor romidepsin (marketed as Istodax injection) for treating patients with cutaneous T-cell lymphoma (CTCL) who have undergone at least one prior systemic therapy. 	topic_ll
77116	3	355867	7	NULL	NULL	0	NULL	romidepsin	Chemical		is a type of					histone deacetylase inhibitor	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Earlier this month, the US FDA approved the antibiotic histone deacetylase inhibitor romidepsin (marketed as Istodax injection) for treating patients with cutaneous T-cell lymphoma (CTCL) who have undergone at least one prior systemic therapy. 	topic_ll
77117	4	355867	7	NULL	NULL	0	NULL	romidepsin	Chemical		is a type of					antibiotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Earlier this month, the US FDA approved the antibiotic histone deacetylase inhibitor romidepsin (marketed as Istodax injection) for treating patients with cutaneous T-cell lymphoma (CTCL) who have undergone at least one prior systemic therapy. 	topic_ll
77118	1	355869	7	NULL	NULL	0	NULL	Bendamustine	Chemical		used to treat					iNHL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Results from a study published in the journal Cancer suggest that patients with indolent B-cell non-Hodgkin’s lymphoma (iNHL) are responding well to Bendamustine, a chemo drug generally used to treat chronic lymphocytocic leukemia and some NHLs. 	topic_ll
77119	2	355869	7	NULL	NULL	0	NULL	Bendamustine	Chemical		used to treat					chronic lymphocytocic leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Results from a study published in the journal Cancer suggest that patients with indolent B-cell non-Hodgkin’s lymphoma (iNHL) are responding well to Bendamustine, a chemo drug generally used to treat chronic lymphocytocic leukemia and some NHLs. 	topic_ll
77120	3	355869	7	NULL	NULL	0	NULL	Bendamustine	Chemical		used to treat					NHL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Results from a study published in the journal Cancer suggest that patients with indolent B-cell non-Hodgkin’s lymphoma (iNHL) are responding well to Bendamustine, a chemo drug generally used to treat chronic lymphocytocic leukemia and some NHLs. 	topic_ll
77121	4	355869	7	NULL	NULL	NULL	NULL	iNHL	MedicalFinding		is 					indolent B-cell non-Hodgkins lymphoma	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Results from a study published in the journal Cancer suggest that patients with indolent B-cell non-Hodgkin’s lymphoma (iNHL) are responding well to Bendamustine, a chemo drug generally used to treat chronic lymphocytocic leukemia and some NHLs. 	topic_ll
77122	5	355869	7	NULL	NULL	0	NULL	Bendamustine	Chemical		is a type of					chemodrug	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Results from a study published in the journal Cancer suggest that patients with indolent B-cell non-Hodgkin’s lymphoma (iNHL) are responding well to Bendamustine, a chemo drug generally used to treat chronic lymphocytocic leukemia and some NHLs. 	topic_ll
77123	1	355871	7	NULL	NULL	0	NULL	X-rays 	MedicalProcedure	exposure to	associated with					ALL	MedicalFinding	children with			NULL		0	NULL	NULL	NULL	NULL	NULL	Specifically, the researchers found that children with acute lymphoid leukemia (ALL) had almost twice the chance of having been exposed to three or more X-rays compared with children who did not have leukemia.	topic_ll
77124	2	355871	7	NULL	NULL	0	NULL	ALL	MedicalFinding		is					acute lymphoid leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Specifically, the researchers found that children with acute lymphoid leukemia (ALL) had almost twice the chance of having been exposed to three or more X-rays compared with children who did not have leukemia.	topic_ll
77194	1	355872	7	NULL	NULL	NULL	NULL	X-rays	MedicalProcedure		increase					ALL	MedicalFinding	risk for			NULL		NULL	NULL	NULL	NULL	NULL	NULL	The study found an increased risk from X-rays for ALL, but not for AML or T-cell leukemia, and there was no association with age at first exposure.	topic_ll
77195	2	355872	7	NULL	NULL	0	NULL	X-rays	MedicalProcedure		does not increase					AML	MedicalFinding	risk for			NULL		0	NULL	NULL	NULL	NULL	NULL	The study found an increased risk from X-rays for ALL, but not for AML or T-cell leukemia, and there was no association with age at first exposure.	topic_ll
77196	3	355872	7	NULL	NULL	NULL	NULL	X-rays	MedicalProcedure		does not increase					T-cell leukemia	MedicalFinding	risk for			NULL		NULL	NULL	NULL	NULL	NULL	NULL	The study found an increased risk from X-rays for ALL, but not for AML or T-cell leukemia, and there was no association with age at first exposure.	topic_ll
77197	1	355873	7	NULL	NULL	0	NULL	Fmn2 gene	GP	excessive synthesis of	associated with					B-cell lymphocytic leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Charfi first compared the transcriptome (the set of active genes in a cell) of leukemic and healthy mice. From this analysis, she was able to isolate groups of genes with abnormal activity in the leukemic mice. This led to the discovery that excessive synthesis of the Fmn2 gene and protein is associated with B-cell lymphocytic leukemia.	topic_ll
77198	2	355873	7	NULL	NULL	0	NULL	Fmn2 protein	GP	excessive synthesis of	associated with					B-cell lymphocytic leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Charfi first compared the transcriptome (the set of active genes in a cell) of leukemic and healthy mice. From this analysis, she was able to isolate groups of genes with abnormal activity in the leukemic mice. This led to the discovery that excessive synthesis of the Fmn2 gene and protein is associated with B-cell lymphocytic leukemia.	topic_ll
77199	1	355875	7	NULL	NULL	0	NULL	IL-7 	GP		trigger					B cells	Cell	maturation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Upon closer evaluation, the research team found that Miz-1 has a very particular function: it is required for IL-7 to effectively trigger the maturation of B cells in the bone marrow. 	topic_ll
77200	2	355875	7	NULL	NULL	0	NULL	statement 1	Process		occur in					bone marrow	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Upon closer evaluation, the research team found that Miz-1 has a very particular function: it is required for IL-7 to effectively trigger the maturation of B cells in the bone marrow. 	topic_ll
77201	3	355875	7	NULL	NULL	0	NULL	Miz-1	GP		required for					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Upon closer evaluation, the research team found that Miz-1 has a very particular function: it is required for IL-7 to effectively trigger the maturation of B cells in the bone marrow. 	topic_ll
77202	1	355877	7	NULL	NULL	0	NULL	brain tumors 	MedicalFinding	low-grade	have					IDH gene	GP	mutated version of			NULL		0	NULL	NULL	NULL	NULL	NULL	About 75 percent of people with low-grade brain tumors and 20 percent of people with acute myeloid leukemia have a mutated version of a gene known as IDH.	topic_ll
77203	2	355877	7	NULL	NULL	0	NULL	acute myeloid leukemia	MedicalFinding		have					IDH gene	GP	mutated version of			NULL		0	NULL	NULL	NULL	NULL	NULL	About 75 percent of people with low-grade brain tumors and 20 percent of people with acute myeloid leukemia have a mutated version of a gene known as IDH.	topic_ll
77204	1	355878	7	NULL	NULL	NULL	NULL	IDH	GP	cells with mutation of	produce					α-KG	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The researchers discovered that cells with the IDH mutation produce less α-KG and more 2-HG than normal cells. 2-HG then outcompetes α-KG, disabling a whole family of enzymes that depend on α-KG to do their jobs in the cell. Normal cell functions break down, contributing to the development of cancer.	topic_ll
77205	2	355878	7	NULL	NULL	NULL	NULL	IDH	GP	cells with mutation of	produce					 2-HG	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The researchers discovered that cells with the IDH mutation produce less α-KG and more 2-HG than normal cells. 2-HG then outcompetes α-KG, disabling a whole family of enzymes that depend on α-KG to do their jobs in the cell. Normal cell functions break down, contributing to the development of cancer.	topic_ll
77206	3	355878	7	NULL	NULL	NULL	NULL	normal cells	Cell		produce					α-KG 	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The researchers discovered that cells with the IDH mutation produce less α-KG and more 2-HG than normal cells. 2-HG then outcompetes α-KG, disabling a whole family of enzymes that depend on α-KG to do their jobs in the cell. Normal cell functions break down, contributing to the development of cancer.	topic_ll
77207	4	355878	7	NULL	NULL	0	NULL	normal cells	Cell		produce					 2-HG 	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The researchers discovered that cells with the IDH mutation produce less α-KG and more 2-HG than normal cells. 2-HG then outcompetes α-KG, disabling a whole family of enzymes that depend on α-KG to do their jobs in the cell. Normal cell functions break down, contributing to the development of cancer.	topic_ll
77208	5	355878	7	NULL	NULL	0	NULL	statement 1	Process		is less compared to					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The researchers discovered that cells with the IDH mutation produce less α-KG and more 2-HG than normal cells. 2-HG then outcompetes α-KG, disabling a whole family of enzymes that depend on α-KG to do their jobs in the cell. Normal cell functions break down, contributing to the development of cancer.	topic_ll
77209	6	355878	7	NULL	NULL	0	NULL	statement 2	Process		is more compared to					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The researchers discovered that cells with the IDH mutation produce less α-KG and more 2-HG than normal cells. 2-HG then outcompetes α-KG, disabling a whole family of enzymes that depend on α-KG to do their jobs in the cell. Normal cell functions break down, contributing to the development of cancer.	topic_ll
77210	7	355878	7	NULL	NULL	0	NULL	Normal cell	Cell		functions					breakdown	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The researchers discovered that cells with the IDH mutation produce less α-KG and more 2-HG than normal cells. 2-HG then outcompetes α-KG, disabling a whole family of enzymes that depend on α-KG to do their jobs in the cell. Normal cell functions break down, contributing to the development of cancer.	topic_ll
77211	8	355878	7	NULL	NULL	0	NULL	statement 7	Process		contributes to					cancer	MedicalFinding	development of			NULL		0	NULL	NULL	NULL	NULL	NULL	The researchers discovered that cells with the IDH mutation produce less α-KG and more 2-HG than normal cells. 2-HG then outcompetes α-KG, disabling a whole family of enzymes that depend on α-KG to do their jobs in the cell. Normal cell functions break down, contributing to the development of cancer.	topic_ll
77212	1	355879	7	NULL	NULL	0	NULL	RG7112	Chemical		used to treat					refractory acute leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Patients with relapsed or refractory acute or chronic leukemia were given RG7112 orally each day for 10 days, followed by 18 days of rest. Forty-seven patients, including 27 with acute myeloid leukemia (AML), have been treated to date.	topic_ll
77213	2	355879	7	NULL	NULL	0	NULL	RG7112	Chemical		used to treat					refractory chronic leukemia 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Patients with relapsed or refractory acute or chronic leukemia were given RG7112 orally each day for 10 days, followed by 18 days of rest. Forty-seven patients, including 27 with acute myeloid leukemia (AML), have been treated to date.	topic_ll
77214	3	355879	7	NULL	NULL	0	NULL	AML	MedicalFinding		is					acute myeloid leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Patients with relapsed or refractory acute or chronic leukemia were given RG7112 orally each day for 10 days, followed by 18 days of rest. Forty-seven patients, including 27 with acute myeloid leukemia (AML), have been treated to date.	topic_ll
77215	4	355879	7	NULL	NULL	0	NULL	RG7112 	Chemical		used to treat					relapsed acute leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Patients with relapsed or refractory acute or chronic leukemia were given RG7112 orally each day for 10 days, followed by 18 days of rest. Forty-seven patients, including 27 with acute myeloid leukemia (AML), have been treated to date.	topic_ll
77216	5	355879	7	NULL	NULL	0	NULL	RG7112	Chemical		used to treat					relapsed chronic leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Patients with relapsed or refractory acute or chronic leukemia were given RG7112 orally each day for 10 days, followed by 18 days of rest. Forty-seven patients, including 27 with acute myeloid leukemia (AML), have been treated to date.	topic_ll
77217	1	355880	7	NULL	NULL	0	NULL	RG7112	Chemical		used to treat					relapsed acute leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Patients with relapsed or refractory acute or chronic leukemia were given RG7112 orally each day for 10 days, followed by 18 days of rest. Forty-seven patients, including 27 with acute myeloid leukemia (AML), have been treated to date. The drug used in this study, RG7112, a novel small molecule being developed by Roche, is a member of the Nutlin family.	topic_ll
77218	2	355880	7	NULL	NULL	0	NULL	RG7112	Chemical		used to treat					relapsed chronic leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Patients with relapsed or refractory acute or chronic leukemia were given RG7112 orally each day for 10 days, followed by 18 days of rest. Forty-seven patients, including 27 with acute myeloid leukemia (AML), have been treated to date. The drug used in this study, RG7112, a novel small molecule being developed by Roche, is a member of the Nutlin family.	topic_ll
77219	3	355880	7	NULL	NULL	0	NULL	RG7112	Chemical		used to treat					refractory acute leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Patients with relapsed or refractory acute or chronic leukemia were given RG7112 orally each day for 10 days, followed by 18 days of rest. Forty-seven patients, including 27 with acute myeloid leukemia (AML), have been treated to date. The drug used in this study, RG7112, a novel small molecule being developed by Roche, is a member of the Nutlin family.	topic_ll
77220	4	355880	7	NULL	NULL	0	NULL	RG7112	Chemical		used to treat					refractory chronic leukemia 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Patients with relapsed or refractory acute or chronic leukemia were given RG7112 orally each day for 10 days, followed by 18 days of rest. Forty-seven patients, including 27 with acute myeloid leukemia (AML), have been treated to date. The drug used in this study, RG7112, a novel small molecule being developed by Roche, is a member of the Nutlin family.	topic_ll
77221	5	355880	7	NULL	NULL	0	NULL	AML	MedicalFinding		is					acute myeloid leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Patients with relapsed or refractory acute or chronic leukemia were given RG7112 orally each day for 10 days, followed by 18 days of rest. Forty-seven patients, including 27 with acute myeloid leukemia (AML), have been treated to date. The drug used in this study, RG7112, a novel small molecule being developed by Roche, is a member of the Nutlin family.	topic_ll
77222	6	355880	7	NULL	NULL	0	NULL	RG7112	Chemical		is a member of					Nutlin family	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Patients with relapsed or refractory acute or chronic leukemia were given RG7112 orally each day for 10 days, followed by 18 days of rest. Forty-seven patients, including 27 with acute myeloid leukemia (AML), have been treated to date. The drug used in this study, RG7112, a novel small molecule being developed by Roche, is a member of the Nutlin family.	topic_ll
77223	1	355881	7	NULL	NULL	0	NULL	TP53 gene 	GP	mutations of	rare in					blood	OrganismPart	cancers of			NULL		0	NULL	NULL	NULL	NULL	NULL	While mutations of the TP53 gene are rare in cancers of the blood, the p53 protein may be degraded by other factors, including high levels of MDM2, which binds to p53 and orchestrates its degradation.	topic_ll
77224	2	355881	7	NULL	NULL	0	NULL	MDM2	GP	high levels of	degrade		may 			p53 protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	While mutations of the TP53 gene are rare in cancers of the blood, the p53 protein may be degraded by other factors, including high levels of MDM2, which binds to p53 and orchestrates its degradation.	topic_ll
77225	3	355881	7	NULL	NULL	0	NULL	MDM2	GP		bind					p53	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	While mutations of the TP53 gene are rare in cancers of the blood, the p53 protein may be degraded by other factors, including high levels of MDM2, which binds to p53 and orchestrates its degradation.	topic_ll
77226	4	355881	7	NULL	NULL	0	NULL	statement 3	Process		orchestrates					p53	GP	degradation of			NULL		0	NULL	NULL	NULL	NULL	NULL	While mutations of the TP53 gene are rare in cancers of the blood, the p53 protein may be degraded by other factors, including high levels of MDM2, which binds to p53 and orchestrates its degradation.	topic_ll
77227	1	355882	7	NULL	NULL	0	NULL	Small Molecule	Chemical		disarm		may			Cancer-Fighting P53	GP	 Enemy of			NULL		0	NULL	NULL	NULL	NULL	NULL	Small Molecule May Disarm Enemy of Cancer-Fighting P53	topic_ll
77228	1	355883	7	NULL	NULL	0	NULL	Nutlins	Chemical		effective in					leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In preclinical studies, small-molecule MDM2 antagonists called Nutlins were found to be effective in solid tumors, leukemia and lymphoma.	topic_ll
77229	2	355883	7	NULL	NULL	0	NULL	Nutlins	Chemical		effective in					lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In preclinical studies, small-molecule MDM2 antagonists called Nutlins were found to be effective in solid tumors, leukemia and lymphoma.	topic_ll
77230	3	355883	7	NULL	NULL	0	NULL	Nutlins	Chemical		is a type of					MDM2 antagonists	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	In preclinical studies, small-molecule MDM2 antagonists called Nutlins were found to be effective in solid tumors, leukemia and lymphoma.	topic_ll
77231	4	355883	7	NULL	NULL	0	NULL	Nutlins	Chemical		is a type of					small molecule	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	In preclinical studies, small-molecule MDM2 antagonists called Nutlins were found to be effective in solid tumors, leukemia and lymphoma.	topic_ll
77232	5	355883	7	NULL	NULL	0	NULL	leukemia	MedicalFinding		is a type of					solid tumor	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In preclinical studies, small-molecule MDM2 antagonists called Nutlins were found to be effective in solid tumors, leukemia and lymphoma.	topic_ll
77233	6	355883	7	NULL	NULL	0	NULL	lymphoma	MedicalFinding		is a type of					solid tumor	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In preclinical studies, small-molecule MDM2 antagonists called Nutlins were found to be effective in solid tumors, leukemia and lymphoma.	topic_ll
77255	1	355884	7	NULL	NULL	0	NULL	RG7112	Chemical		is a type of					novel small molecule	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The drug used in this study, RG7112, a novel small molecule being developed by Roche, is a member of the Nutlin family.	topic_ll
77256	2	355884	7	NULL	NULL	0	NULL	RG7112	Chemical		is a member of					Nutlin family	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The drug used in this study, RG7112, a novel small molecule being developed by Roche, is a member of the Nutlin family.	topic_ll
77257	1	355885	7	NULL	NULL	NULL	NULL	lymph node	OrganismPart	Reduction in	seen in					CLL	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Reductions in lymph node and spleen size, as well as in circulating leukemia cells, were seen in chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL).	topic_ll
77258	2	355885	7	NULL	NULL	NULL	NULL	spleen	OrganismPart	reduction in size of	seen in					CLL	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Reductions in lymph node and spleen size, as well as in circulating leukemia cells, were seen in chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL).	topic_ll
77259	3	355885	7	NULL	NULL	0	NULL	circulating leukemia cells	Cell	reduction in	seen in					CLL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Reductions in lymph node and spleen size, as well as in circulating leukemia cells, were seen in chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL).	topic_ll
77260	4	355885	7	NULL	NULL	0	NULL	lymph node	OrganismPart	reduction in	seen in					SLL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Reductions in lymph node and spleen size, as well as in circulating leukemia cells, were seen in chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL).	topic_ll
77261	5	355885	7	NULL	NULL	0	NULL	spleen	OrganismPart	reduction in size of	seen in					SLL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Reductions in lymph node and spleen size, as well as in circulating leukemia cells, were seen in chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL).	topic_ll
77262	6	355885	7	NULL	NULL	0	NULL	circulating leukemia cells	Cell	reduction in	seen in					SLL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Reductions in lymph node and spleen size, as well as in circulating leukemia cells, were seen in chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL).	topic_ll
77263	7	355885	7	NULL	NULL	0	NULL	CLL	MedicalFinding		is					chronic lymphocytic leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Reductions in lymph node and spleen size, as well as in circulating leukemia cells, were seen in chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL).	topic_ll
77264	8	355885	7	NULL	NULL	0	NULL	SLL	MedicalFinding		is					small lymphocytic lymphoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Reductions in lymph node and spleen size, as well as in circulating leukemia cells, were seen in chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL).	topic_ll
77265	1	355886	7	NULL	NULL	0	NULL	AAK	GP		essential for					cell division	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	AAK is essential for cell division (mitotic progression) and is amplified or overexpressed in AML and other blood cancers.	topic_ll
77266	2	355886	7	NULL	NULL	0	NULL	cell division 	Process		is					mitotic progression	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	AAK is essential for cell division (mitotic progression) and is amplified or overexpressed in AML and other blood cancers.	topic_ll
77267	3	355886	7	NULL	NULL	0	NULL	AAK	GP		overexpressed in					AML	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	AAK is essential for cell division (mitotic progression) and is amplified or overexpressed in AML and other blood cancers.	topic_ll
77268	4	355886	7	NULL	NULL	0	NULL	AAK	GP		overexpressed in					blood cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	AAK is essential for cell division (mitotic progression) and is amplified or overexpressed in AML and other blood cancers.	topic_ll
77269	5	355886	7	NULL	NULL	0	NULL	AAK	GP		amplified in					AML	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	AAK is essential for cell division (mitotic progression) and is amplified or overexpressed in AML and other blood cancers.	topic_ll
77270	6	355886	7	NULL	NULL	0	NULL	AAK	GP		amplified in					blood cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	AAK is essential for cell division (mitotic progression) and is amplified or overexpressed in AML and other blood cancers.	topic_ll
77271	7	355886	7	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	AAK is essential for cell division (mitotic progression) and is amplified or overexpressed in AML and other blood cancers.	topic_ll
77272	8	355886	7	NULL	NULL	0	NULL	statement 4	Process		is an alternative to					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	AAK is essential for cell division (mitotic progression) and is amplified or overexpressed in AML and other blood cancers.	topic_ll
77273	1	355887	7	NULL	NULL	NULL	NULL	MLN8237 	Chemical		inhibitor of		potent;;selective			AAK	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	An investigational drug, MLN8237 is an orally available, potent, and selective AAK inhibitor. It has shown preclinical activity against leukemia, lymphoma,	topic_ll
77274	2	355887	7	NULL	NULL	0	NULL	statement 1	Process		shows					leukemia	MedicalFinding	preclinical activity against			NULL		0	NULL	NULL	NULL	NULL	NULL	An investigational drug, MLN8237 is an orally available, potent, and selective AAK inhibitor. It has shown preclinical activity against leukemia, lymphoma,	topic_ll
77275	3	355887	7	NULL	NULL	0	NULL	statement 1	Process		shows 					lymphoma	MedicalFinding	preclinical activity against			NULL		0	NULL	NULL	NULL	NULL	NULL	An investigational drug, MLN8237 is an orally available, potent, and selective AAK inhibitor. It has shown preclinical activity against leukemia, lymphoma,	topic_ll
77276	4	355887	7	NULL	NULL	0	NULL	MLN8237	Chemical		is a type of					orally available drug	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	An investigational drug, MLN8237 is an orally available, potent, and selective AAK inhibitor. It has shown preclinical activity against leukemia, lymphoma,	topic_ll
77277	1	355888	7	NULL	NULL	0	NULL	T-rapa cell	Cell		is a type of					white blood cell	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	The T-rapa cell is a type of white blood cell that is cultured with rapamycin, co-stimulation and interleukin-4. These cells express a balanced Th2/Th1 effector phenotype -- a T-cell profile that is thought to protect against transplant rejection and improve the outcome of patients by reducing graft versus host disease and improving graft versus tumor effect.	topic_ll
77278	2	355888	7	NULL	NULL	0	NULL	T-rapa cell	Cell		express					Th2/Th1 effector phenotype	PhysicalPhenomenon	balanced			NULL		0	NULL	NULL	NULL	NULL	NULL	The T-rapa cell is a type of white blood cell that is cultured with rapamycin, co-stimulation and interleukin-4. These cells express a balanced Th2/Th1 effector phenotype -- a T-cell profile that is thought to protect against transplant rejection and improve the outcome of patients by reducing graft versus host disease and improving graft versus tumor effect.	topic_ll
77279	3	355888	7	NULL	NULL	0	NULL	Th2/Th1 effector phenotype	PhysicalPhenomenon		is a type of					T-cell profile	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The T-rapa cell is a type of white blood cell that is cultured with rapamycin, co-stimulation and interleukin-4. These cells express a balanced Th2/Th1 effector phenotype -- a T-cell profile that is thought to protect against transplant rejection and improve the outcome of patients by reducing graft versus host disease and improving graft versus tumor effect.	topic_ll
77280	4	355888	7	NULL	NULL	0	NULL	Th2/Th1 effector phenotype	PhysicalPhenomenon		protect against					transplant rejection	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The T-rapa cell is a type of white blood cell that is cultured with rapamycin, co-stimulation and interleukin-4. These cells express a balanced Th2/Th1 effector phenotype -- a T-cell profile that is thought to protect against transplant rejection and improve the outcome of patients by reducing graft versus host disease and improving graft versus tumor effect.	topic_ll
77281	5	355888	7	NULL	NULL	0	NULL	Th2/Th1 effector phenotype	PhysicalPhenomenon		reduce					graft versus host disease	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The T-rapa cell is a type of white blood cell that is cultured with rapamycin, co-stimulation and interleukin-4. These cells express a balanced Th2/Th1 effector phenotype -- a T-cell profile that is thought to protect against transplant rejection and improve the outcome of patients by reducing graft versus host disease and improving graft versus tumor effect.	topic_ll
77282	6	355888	7	NULL	NULL	0	NULL	Th2/Th1 effector phenotype	PhysicalPhenomenon		improve					graft versus tumor effect	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The T-rapa cell is a type of white blood cell that is cultured with rapamycin, co-stimulation and interleukin-4. These cells express a balanced Th2/Th1 effector phenotype -- a T-cell profile that is thought to protect against transplant rejection and improve the outcome of patients by reducing graft versus host disease and improving graft versus tumor effect.	topic_ll
77283	7	355888	7	NULL	NULL	0	NULL	Th2/Th1 effector phenotype	PhysicalPhenomenon		improve					patients	GroupOfPeople	outcome of			NULL		0	NULL	NULL	NULL	NULL	NULL	The T-rapa cell is a type of white blood cell that is cultured with rapamycin, co-stimulation and interleukin-4. These cells express a balanced Th2/Th1 effector phenotype -- a T-cell profile that is thought to protect against transplant rejection and improve the outcome of patients by reducing graft versus host disease and improving graft versus tumor effect.	topic_ll
77284	8	355888	7	NULL	NULL	0	NULL	statement 7	Process		occur by					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The T-rapa cell is a type of white blood cell that is cultured with rapamycin, co-stimulation and interleukin-4. These cells express a balanced Th2/Th1 effector phenotype -- a T-cell profile that is thought to protect against transplant rejection and improve the outcome of patients by reducing graft versus host disease and improving graft versus tumor effect.	topic_ll
77285	9	355888	7	NULL	NULL	0	NULL	statement 7	Process		occur by					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The T-rapa cell is a type of white blood cell that is cultured with rapamycin, co-stimulation and interleukin-4. These cells express a balanced Th2/Th1 effector phenotype -- a T-cell profile that is thought to protect against transplant rejection and improve the outcome of patients by reducing graft versus host disease and improving graft versus tumor effect.	topic_ll
77286	1	355889	7	NULL	NULL	0	NULL	IDH1	GP	mutation of	generate					poison	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	They went on to show that IDH1 and IDH2 mutations generate a 'poison' that blocks the ability of a protective factor called TET2 to remove the methylation from the genome. Interestingly, the researchers also showed that many AML patients have mutations that inactivate TET2, and this causes the same abnormal DNA methylation effect as IDH1 and IDH2 mutations.	topic_ll
77287	3	355889	7	NULL	NULL	NULL	NULL	statement 1	Process		blocks					statement 2	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	They went on to show that IDH1 and IDH2 mutations generate a 'poison' that blocks the ability of a protective factor called TET2 to remove the methylation from the genome. Interestingly, the researchers also showed that many AML patients have mutations that inactivate TET2, and this causes the same abnormal DNA methylation effect as IDH1 and IDH2 mutations.	topic_ll
77288	2	355889	7	NULL	NULL	0	NULL	TET2	GP		remove					genome	Organism	methylation from			NULL		0	NULL	NULL	NULL	NULL	NULL	They went on to show that IDH1 and IDH2 mutations generate a 'poison' that blocks the ability of a protective factor called TET2 to remove the methylation from the genome. Interestingly, the researchers also showed that many AML patients have mutations that inactivate TET2, and this causes the same abnormal DNA methylation effect as IDH1 and IDH2 mutations.	topic_ll
77289	4	355889	7	NULL	NULL	NULL	NULL	AML patients	GroupOfPeople	mutations of	inactivate					TET2	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	They went on to show that IDH1 and IDH2 mutations generate a 'poison' that blocks the ability of a protective factor called TET2 to remove the methylation from the genome. Interestingly, the researchers also showed that many AML patients have mutations that inactivate TET2, and this causes the same abnormal DNA methylation effect as IDH1 and IDH2 mutations.	topic_ll
77290	5	355889	7	NULL	NULL	0	NULL	statement 4	Process		cause					IDH1	GP	mutations of			NULL		0	NULL	NULL	NULL	NULL	NULL	They went on to show that IDH1 and IDH2 mutations generate a 'poison' that blocks the ability of a protective factor called TET2 to remove the methylation from the genome. Interestingly, the researchers also showed that many AML patients have mutations that inactivate TET2, and this causes the same abnormal DNA methylation effect as IDH1 and IDH2 mutations.	topic_ll
77291	6	355889	7	NULL	NULL	0	NULL	statement 4	Process		cause					IDH2	GP	mutations of			NULL		0	NULL	NULL	NULL	NULL	NULL	They went on to show that IDH1 and IDH2 mutations generate a 'poison' that blocks the ability of a protective factor called TET2 to remove the methylation from the genome. Interestingly, the researchers also showed that many AML patients have mutations that inactivate TET2, and this causes the same abnormal DNA methylation effect as IDH1 and IDH2 mutations.	topic_ll
77292	7	355889	7	NULL	NULL	0	NULL	IDH1	GP	mutations of	is a type of					abnormal DNA methylation effect	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	They went on to show that IDH1 and IDH2 mutations generate a 'poison' that blocks the ability of a protective factor called TET2 to remove the methylation from the genome. Interestingly, the researchers also showed that many AML patients have mutations that inactivate TET2, and this causes the same abnormal DNA methylation effect as IDH1 and IDH2 mutations.	topic_ll
77293	8	355889	7	NULL	NULL	0	NULL	IDH2	GP	mutations of	generate					poison	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	They went on to show that IDH1 and IDH2 mutations generate a 'poison' that blocks the ability of a protective factor called TET2 to remove the methylation from the genome. Interestingly, the researchers also showed that many AML patients have mutations that inactivate TET2, and this causes the same abnormal DNA methylation effect as IDH1 and IDH2 mutations.	topic_ll
77294	9	355889	7	NULL	NULL	0	NULL	statement 8	Process		blocks					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	They went on to show that IDH1 and IDH2 mutations generate a 'poison' that blocks the ability of a protective factor called TET2 to remove the methylation from the genome. Interestingly, the researchers also showed that many AML patients have mutations that inactivate TET2, and this causes the same abnormal DNA methylation effect as IDH1 and IDH2 mutations.	topic_ll
77295	10	355889	7	NULL	NULL	0	NULL	IDH2	GP	mutations of	is a type of					abnormal DNA methylation effect	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	They went on to show that IDH1 and IDH2 mutations generate a 'poison' that blocks the ability of a protective factor called TET2 to remove the methylation from the genome. Interestingly, the researchers also showed that many AML patients have mutations that inactivate TET2, and this causes the same abnormal DNA methylation effect as IDH1 and IDH2 mutations.	topic_ll
77324	11	355889	7	NULL	NULL	0	NULL	TET2	GP		is a type of					protective factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	They went on to show that IDH1 and IDH2 mutations generate a 'poison' that blocks the ability of a protective factor called TET2 to remove the methylation from the genome. Interestingly, the researchers also showed that many AML patients have mutations that inactivate TET2, and this causes the same abnormal DNA methylation effect as IDH1 and IDH2 mutations.	topic_ll
77296	1	355891	7	NULL	NULL	0	NULL	AML patients	MedicalFinding	mutations of	inactivate					TET2	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	many AML patients have mutations that inactivate TET2, 	topic_ll
77297	1	355892	7	NULL	NULL	0	NULL	miR-125b	GP	overexpression of	cause		independently			leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Whitehead Institute researchers have shown in mouse models that overexpression of the microRNA 125b (miR-125b) can independently cause leukemia and accelerate the disease's progression.	topic_ll
77298	2	355892	7	NULL	NULL	0	NULL	statement 1	Process		accelerate					disease progression	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Whitehead Institute researchers have shown in mouse models that overexpression of the microRNA 125b (miR-125b) can independently cause leukemia and accelerate the disease's progression.	topic_ll
77299	3	355892	7	NULL	NULL	0	NULL	miR-125b	GP		is					microRNA 125b	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Whitehead Institute researchers have shown in mouse models that overexpression of the microRNA 125b (miR-125b) can independently cause leukemia and accelerate the disease's progression.	topic_ll
77300	1	355893	7	NULL	NULL	NULL	NULL	 ponatinib	Chemical		produce					 hematologic response	Process	complete			NULL		NULL	NULL	NULL	NULL	NULL	NULL	n a Phase I clinical trial, the drug ponatinib produced major or complete hematologic responses (absence of CML cells in the blood) and cytogenetic responses (absence of leukemia cells in the bone marrow) among two groups of patients:	topic_ll
77301	2	355893	7	NULL	NULL	0	NULL	 ponatinib 	Chemical		produce					cytogenetic response	Process	complete			NULL		0	NULL	NULL	NULL	NULL	NULL	n a Phase I clinical trial, the drug ponatinib produced major or complete hematologic responses (absence of CML cells in the blood) and cytogenetic responses (absence of leukemia cells in the bone marrow) among two groups of patients:	topic_ll
77302	3	355893	7	NULL	NULL	0	NULL	hematologic response	Process		is					CML cells	Cell	absence of			NULL		0	NULL	NULL	NULL	NULL	NULL	n a Phase I clinical trial, the drug ponatinib produced major or complete hematologic responses (absence of CML cells in the blood) and cytogenetic responses (absence of leukemia cells in the bone marrow) among two groups of patients:	topic_ll
77303	4	355893	7	NULL	NULL	0	NULL	statement 3	Process		occur in					blood	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	n a Phase I clinical trial, the drug ponatinib produced major or complete hematologic responses (absence of CML cells in the blood) and cytogenetic responses (absence of leukemia cells in the bone marrow) among two groups of patients:	topic_ll
77304	5	355893	7	NULL	NULL	0	NULL	cytogenetic response	Process		is					leukemia cells	Cell	absence of			NULL		0	NULL	NULL	NULL	NULL	NULL	n a Phase I clinical trial, the drug ponatinib produced major or complete hematologic responses (absence of CML cells in the blood) and cytogenetic responses (absence of leukemia cells in the bone marrow) among two groups of patients:	topic_ll
77305	6	355893	7	NULL	NULL	0	NULL	statement 5	Process		occur in					bone marrow	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	n a Phase I clinical trial, the drug ponatinib produced major or complete hematologic responses (absence of CML cells in the blood) and cytogenetic responses (absence of leukemia cells in the bone marrow) among two groups of patients:	topic_ll
77306	1	355894	7	NULL	NULL	0	NULL	ponatinib	Chemical		produce					hematologic response	Process	complete			NULL		0	NULL	NULL	NULL	NULL	NULL	n a Phase I clinical trial, the drug ponatinib produced major or complete hematologic responses (absence of CML cells in the blood) and cytogenetic responses (absence of leukemia cells in the bone marrow) among two groups of patients: And those whose leukemia cells carry the T315I mutation, which resists all current therapies.	topic_ll
77307	2	355894	7	NULL	NULL	NULL	NULL	ponatinib	Chemical		produce					cytogenetic response	Process	complete			NULL		NULL	NULL	NULL	NULL	NULL	NULL	n a Phase I clinical trial, the drug ponatinib produced major or complete hematologic responses (absence of CML cells in the blood) and cytogenetic responses (absence of leukemia cells in the bone marrow) among two groups of patients: And those whose leukemia cells carry the T315I mutation, which resists all current therapies.	topic_ll
77308	3	355894	7	NULL	NULL	0	NULL	hematologic response	Process		is					CML cells	Cell	absence of			NULL		0	NULL	NULL	NULL	NULL	NULL	n a Phase I clinical trial, the drug ponatinib produced major or complete hematologic responses (absence of CML cells in the blood) and cytogenetic responses (absence of leukemia cells in the bone marrow) among two groups of patients: And those whose leukemia cells carry the T315I mutation, which resists all current therapies.	topic_ll
77309	4	355894	7	NULL	NULL	0	NULL	statement 3	Process		occur in					blood	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	n a Phase I clinical trial, the drug ponatinib produced major or complete hematologic responses (absence of CML cells in the blood) and cytogenetic responses (absence of leukemia cells in the bone marrow) among two groups of patients: And those whose leukemia cells carry the T315I mutation, which resists all current therapies.	topic_ll
77310	5	355894	7	NULL	NULL	0	NULL	cytogenetic response	Process		is					leukemia cells	Cell	absence of			NULL		0	NULL	NULL	NULL	NULL	NULL	n a Phase I clinical trial, the drug ponatinib produced major or complete hematologic responses (absence of CML cells in the blood) and cytogenetic responses (absence of leukemia cells in the bone marrow) among two groups of patients: And those whose leukemia cells carry the T315I mutation, which resists all current therapies.	topic_ll
77311	6	355894	7	NULL	NULL	0	NULL	statement 5	Process		occur in					bone marrow	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	n a Phase I clinical trial, the drug ponatinib produced major or complete hematologic responses (absence of CML cells in the blood) and cytogenetic responses (absence of leukemia cells in the bone marrow) among two groups of patients: And those whose leukemia cells carry the T315I mutation, which resists all current therapies.	topic_ll
77312	7	355894	7	NULL	NULL	0	NULL	 leukemia cells	Cell		carry							mutations of	T315I		NULL		0	NULL	NULL	NULL	NULL	NULL	n a Phase I clinical trial, the drug ponatinib produced major or complete hematologic responses (absence of CML cells in the blood) and cytogenetic responses (absence of leukemia cells in the bone marrow) among two groups of patients: And those whose leukemia cells carry the T315I mutation, which resists all current therapies.	topic_ll
77313	8	355894	7	NULL	NULL	0	NULL	statement 7	Process		resist					 therapies	MedicalProcedure	current			NULL		0	NULL	NULL	NULL	NULL	NULL	n a Phase I clinical trial, the drug ponatinib produced major or complete hematologic responses (absence of CML cells in the blood) and cytogenetic responses (absence of leukemia cells in the bone marrow) among two groups of patients: And those whose leukemia cells carry the T315I mutation, which resists all current therapies.	topic_ll
77314	1	355895	7	NULL	NULL	0	NULL	leukemia cells	Cell		carry							mutations of	T315I		NULL		0	NULL	NULL	NULL	NULL	NULL	And those whose leukemia cells carry the T315I mutation, which resists all current therapies.	topic_ll
77315	1	355896	7	NULL	NULL	0	NULL	 leukemia cells	Cell		trigger					protective response	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Massey researchers have uncovered the mechanism by which leukemia cells trigger a protective response when exposed to a class of cancer-killing agents known as histone deacetylase inhibitors (HDACIs). Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. 	topic_ll
77316	2	355896	7	NULL	NULL	0	NULL	statement 1	Process		occur when					HDACIs	Chemical	exposed to			NULL		0	NULL	NULL	NULL	NULL	NULL	Massey researchers have uncovered the mechanism by which leukemia cells trigger a protective response when exposed to a class of cancer-killing agents known as histone deacetylase inhibitors (HDACIs). Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. 	topic_ll
77317	3	355896	7	NULL	NULL	0	NULL	HDACIs	Chemical		is					 histone deacetylase inhibitors	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Massey researchers have uncovered the mechanism by which leukemia cells trigger a protective response when exposed to a class of cancer-killing agents known as histone deacetylase inhibitors (HDACIs). Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. 	topic_ll
77318	4	355896	7	NULL	NULL	0	NULL	HDACIs	Chemical		is a type of					cancer-killing agents	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Massey researchers have uncovered the mechanism by which leukemia cells trigger a protective response when exposed to a class of cancer-killing agents known as histone deacetylase inhibitors (HDACIs). Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. 	topic_ll
77319	5	355896	7	NULL	NULL	0	NULL	HDACIs	Chemical		induce		initially			DNA damage	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Massey researchers have uncovered the mechanism by which leukemia cells trigger a protective response when exposed to a class of cancer-killing agents known as histone deacetylase inhibitors (HDACIs). Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. 	topic_ll
77320	6	355896	7	NULL	NULL	0	NULL	statement 5	Process		occur within					cell nucleus	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	Massey researchers have uncovered the mechanism by which leukemia cells trigger a protective response when exposed to a class of cancer-killing agents known as histone deacetylase inhibitors (HDACIs). Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. 	topic_ll
77321	7	355896	7	NULL	NULL	0	NULL	statement 5	Process		leads to					NEMO protein	GP	modification of			NULL		0	NULL	NULL	NULL	NULL	NULL	Massey researchers have uncovered the mechanism by which leukemia cells trigger a protective response when exposed to a class of cancer-killing agents known as histone deacetylase inhibitors (HDACIs). Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. 	topic_ll
77322	8	355896	7	NULL	NULL	0	NULL	NEMO protein	GP		triggers					 NF-κB pathway	Process	cytoprotective			NULL		0	NULL	NULL	NULL	NULL	NULL	Massey researchers have uncovered the mechanism by which leukemia cells trigger a protective response when exposed to a class of cancer-killing agents known as histone deacetylase inhibitors (HDACIs). Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. 	topic_ll
77325	1	355897	7	NULL	NULL	0	NULL	leukemia cells	Cell		trigger					 protective response	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Massey researchers have uncovered the mechanism by which leukemia cells trigger a protective response when exposed to a class of cancer-killing agents known as histone deacetylase inhibitors (HDACIs).	topic_ll
77326	2	355897	7	NULL	NULL	0	NULL	statement 1	Process		occur when					HDACIs	Chemical	exposed to			NULL		0	NULL	NULL	NULL	NULL	NULL	Massey researchers have uncovered the mechanism by which leukemia cells trigger a protective response when exposed to a class of cancer-killing agents known as histone deacetylase inhibitors (HDACIs).	topic_ll
77327	3	355897	7	NULL	NULL	0	NULL	HDACIs	Chemical		is					histone deacetylase inhibitors	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Massey researchers have uncovered the mechanism by which leukemia cells trigger a protective response when exposed to a class of cancer-killing agents known as histone deacetylase inhibitors (HDACIs).	topic_ll
77328	4	355897	7	NULL	NULL	0	NULL	HDACIs	Chemical		is a type of					cancer-killing agents	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Massey researchers have uncovered the mechanism by which leukemia cells trigger a protective response when exposed to a class of cancer-killing agents known as histone deacetylase inhibitors (HDACIs).	topic_ll
77329	1	355898	7	NULL	NULL	0	NULL	HDACIs	Chemical		induce		initially			DNA damage	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	What VCU Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. By disrupting modifications of the NEMO protein, NF-κB activation can be prevented, and as a consequence, the cancer-killing capacity of HDACIs increases dramatically. NULL	topic_ll
77330	2	355898	7	NULL	NULL	0	NULL	statement 1	Process		occur within					cell nucleus	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	What VCU Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. By disrupting modifications of the NEMO protein, NF-κB activation can be prevented, and as a consequence, the cancer-killing capacity of HDACIs increases dramatically. NULL	topic_ll
77331	3	355898	7	NULL	NULL	0	NULL	statement 1	Process		leads to					NEMO protein	GP	modification of			NULL		0	NULL	NULL	NULL	NULL	NULL	What VCU Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. By disrupting modifications of the NEMO protein, NF-κB activation can be prevented, and as a consequence, the cancer-killing capacity of HDACIs increases dramatically. NULL	topic_ll
77332	4	355898	7	NULL	NULL	0	NULL	NEMO protein	GP		trigger					NF-κB pathway	Process	cytoprotective			NULL		0	NULL	NULL	NULL	NULL	NULL	What VCU Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. By disrupting modifications of the NEMO protein, NF-κB activation can be prevented, and as a consequence, the cancer-killing capacity of HDACIs increases dramatically. NULL	topic_ll
77333	5	355898	7	NULL	NULL	0	NULL	NEMO protein	GP	disrupting modifications of	prevent					NF-κB	GP	activation of			NULL		0	NULL	NULL	NULL	NULL	NULL	What VCU Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. By disrupting modifications of the NEMO protein, NF-κB activation can be prevented, and as a consequence, the cancer-killing capacity of HDACIs increases dramatically. NULL	topic_ll
77334	6	355898	7	NULL	NULL	0	NULL	HDACIs 	Chemical		kills					cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	What VCU Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. By disrupting modifications of the NEMO protein, NF-κB activation can be prevented, and as a consequence, the cancer-killing capacity of HDACIs increases dramatically. NULL	topic_ll
77335	7	355898	7	NULL	NULL	0	NULL	statement 5	Process		increase		dramatically			statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	What VCU Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. By disrupting modifications of the NEMO protein, NF-κB activation can be prevented, and as a consequence, the cancer-killing capacity of HDACIs increases dramatically. NULL	topic_ll
77336	1	355899	7	NULL	NULL	0	NULL	HDACIs	Chemical		induce		initially			DNA damage	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	What VCU Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. By disrupting modifications of the NEMO protein, NF-κB activation can be prevented, and as a consequence, the cancer-killing capacity of HDACIs increases dramatically. Grant's team is now focusing on ways to capitalize on this discovery by designing strategies that interrupt NEMO modifications through the use of pharmacologic agents and other means. NULL	topic_ll
77337	2	355899	7	NULL	NULL	0	NULL	statement 1	Process		occur within					cell nucleus	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	What VCU Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. By disrupting modifications of the NEMO protein, NF-κB activation can be prevented, and as a consequence, the cancer-killing capacity of HDACIs increases dramatically. Grant's team is now focusing on ways to capitalize on this discovery by designing strategies that interrupt NEMO modifications through the use of pharmacologic agents and other means. NULL	topic_ll
77338	3	355899	7	NULL	NULL	0	NULL	statement 2	Process		leads to					NEMO protein	GP	modification of			NULL		0	NULL	NULL	NULL	NULL	NULL	What VCU Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. By disrupting modifications of the NEMO protein, NF-κB activation can be prevented, and as a consequence, the cancer-killing capacity of HDACIs increases dramatically. Grant's team is now focusing on ways to capitalize on this discovery by designing strategies that interrupt NEMO modifications through the use of pharmacologic agents and other means. NULL	topic_ll
77339	4	355899	7	NULL	NULL	0	NULL	statement 3	Process		trigger					NF-κB pathway	Process	cytoprotective			NULL		0	NULL	NULL	NULL	NULL	NULL	What VCU Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. By disrupting modifications of the NEMO protein, NF-κB activation can be prevented, and as a consequence, the cancer-killing capacity of HDACIs increases dramatically. Grant's team is now focusing on ways to capitalize on this discovery by designing strategies that interrupt NEMO modifications through the use of pharmacologic agents and other means. NULL	topic_ll
77340	5	355899	7	NULL	NULL	0	NULL	NEMO protein	GP	disrupting modifications of	prevents					NF-κB	GP	activation of			NULL		0	NULL	NULL	NULL	NULL	NULL	What VCU Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. By disrupting modifications of the NEMO protein, NF-κB activation can be prevented, and as a consequence, the cancer-killing capacity of HDACIs increases dramatically. Grant's team is now focusing on ways to capitalize on this discovery by designing strategies that interrupt NEMO modifications through the use of pharmacologic agents and other means. NULL	topic_ll
77341	6	355899	7	NULL	NULL	0	NULL	HDACIs 	Chemical		kills					cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	What VCU Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. By disrupting modifications of the NEMO protein, NF-κB activation can be prevented, and as a consequence, the cancer-killing capacity of HDACIs increases dramatically. Grant's team is now focusing on ways to capitalize on this discovery by designing strategies that interrupt NEMO modifications through the use of pharmacologic agents and other means. NULL	topic_ll
77342	7	355899	7	NULL	NULL	0	NULL	statement 5	Process		increase		dramatically			statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	What VCU Massey researchers discovered was that HDACIs initially induce DNA damage within the cell nucleus, leading to modification of the NEMO protein, which then triggers the cytoprotective NF-κB pathway. By disrupting modifications of the NEMO protein, NF-κB activation can be prevented, and as a consequence, the cancer-killing capacity of HDACIs increases dramatically. Grant's team is now focusing on ways to capitalize on this discovery by designing strategies that interrupt NEMO modifications through the use of pharmacologic agents and other means. NULL	topic_ll
76595	1	355909	5	NULL	NULL	0	NULL	GABAergic system	OrganismPart	hypofunction of	plays a causal role in					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The hypofunction of GABAergic system and glutamate toxicity are generally believed to have a causal role for autism.	topic_aut
76596	2	355909	5	NULL	NULL	0	NULL	glutamate toxicity	MedicalFinding		plays a causal role in					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The hypofunction of GABAergic system and glutamate toxicity are generally believed to have a causal role for autism.	topic_aut
76597	1	355910	5	NULL	NULL	0	NULL	NMDA	Chemical		is					N-methyl-D: -aspartic acid	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The antagonist of the N-methyl-D: -aspartic acid (NMDA) glutamate receptor improves autism. Glycine is required for the activation of NMDA receptor. The antagonist of glycine site decreases NMDA receptor conductance. It is hypothesis that glycine site antagonists can be tested as a new strategy for the management of autism.	topic_aut
76598	2	355910	5	NULL	NULL	0	NULL	(NMDA glutamate receptor antagonist	Chemical		improves					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The antagonist of the N-methyl-D: -aspartic acid (NMDA) glutamate receptor improves autism. Glycine is required for the activation of NMDA receptor. The antagonist of glycine site decreases NMDA receptor conductance. It is hypothesis that glycine site antagonists can be tested as a new strategy for the management of autism.	topic_aut
76599	3	355910	5	NULL	NULL	0	NULL	Glycine	Chemical		activates					NMDA receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The antagonist of the N-methyl-D: -aspartic acid (NMDA) glutamate receptor improves autism. Glycine is required for the activation of NMDA receptor. The antagonist of glycine site decreases NMDA receptor conductance. It is hypothesis that glycine site antagonists can be tested as a new strategy for the management of autism.	topic_aut
76600	4	355910	5	NULL	NULL	0	NULL	glycine site antagonist	Chemical		decreases					NMDA receptor 	GP	conductance of			NULL		0	NULL	NULL	NULL	NULL	NULL	The antagonist of the N-methyl-D: -aspartic acid (NMDA) glutamate receptor improves autism. Glycine is required for the activation of NMDA receptor. The antagonist of glycine site decreases NMDA receptor conductance. It is hypothesis that glycine site antagonists can be tested as a new strategy for the management of autism.	topic_aut
76601	5	355910	5	NULL	NULL	0	NULL	glycine site antagonists	Chemical		plays a role in					autism	MedicalFinding	management of			NULL		0	NULL	NULL	NULL	NULL	NULL	The antagonist of the N-methyl-D: -aspartic acid (NMDA) glutamate receptor improves autism. Glycine is required for the activation of NMDA receptor. The antagonist of glycine site decreases NMDA receptor conductance. It is hypothesis that glycine site antagonists can be tested as a new strategy for the management of autism.	topic_aut
76602	1	355911	5	NULL	NULL	0	NULL	brain membranes	OrganismPart		undergoes					degradation	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The degradation of brain membranes in autism (2) and the role of phospholipases (3) in autism has been reported for many years	topic_aut
76603	2	355911	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The degradation of brain membranes in autism (2) and the role of phospholipases (3) in autism has been reported for many years	topic_aut
76604	3	355911	5	NULL	NULL	0	NULL	phospholipases	GP		plays a role in					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The degradation of brain membranes in autism (2) and the role of phospholipases (3) in autism has been reported for many years	topic_aut
76605	1	355914	5	NULL	NULL	0	NULL	memantine	Chemical		is a antagonist of					Glutamate	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate antagonists (7) such as memantine, an antagonist of the N-methyl-D-aspartic acid (NMDA) glutamate receptor, have shown a significant improvement in open-label use for autism	topic_aut
76606	2	355914	5	NULL	NULL	0	NULL	NMDA	Chemical		is					N-methyl-D-aspartic acid	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate antagonists (7) such as memantine, an antagonist of the N-methyl-D-aspartic acid (NMDA) glutamate receptor, have shown a significant improvement in open-label use for autism	topic_aut
76607	3	355914	5	NULL	NULL	0	NULL	NMDA glutamate receptor antagonist	Chemical		is used to treat					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate antagonists (7) such as memantine, an antagonist of the N-methyl-D-aspartic acid (NMDA) glutamate receptor, have shown a significant improvement in open-label use for autism	topic_aut
76608	4	355914	5	NULL	NULL	0	NULL	NMDA glutamate receptor antagonist	Process		is used in					open-label trial	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate antagonists (7) such as memantine, an antagonist of the N-methyl-D-aspartic acid (NMDA) glutamate receptor, have shown a significant improvement in open-label use for autism	topic_aut
76609	5	355914	5	NULL	NULL	0	NULL	memantine	Chemical		is used to treat					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate antagonists (7) such as memantine, an antagonist of the N-methyl-D-aspartic acid (NMDA) glutamate receptor, have shown a significant improvement in open-label use for autism	topic_aut
76610	6	355914	5	NULL	NULL	0	NULL	memantine	Chemical		is used in					open-label trial	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate antagonists (7) such as memantine, an antagonist of the N-methyl-D-aspartic acid (NMDA) glutamate receptor, have shown a significant improvement in open-label use for autism	topic_aut
76611	1	355915	5	NULL	NULL	0	NULL	proinflammatory cytokines	GP	enhanced	is observed in					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Enhanced proinflammatory cytokines and activation of microglia and astrocytes are observed in autism	topic_aut
76612	2	355915	5	NULL	NULL	0	NULL	microglia	Cell		is activated in					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Enhanced proinflammatory cytokines and activation of microglia and astrocytes are observed in autism	topic_aut
76613	3	355915	5	NULL	NULL	0	NULL	astrocytes	Cell		is activated in					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Enhanced proinflammatory cytokines and activation of microglia and astrocytes are observed in autism	topic_aut
76614	1	355916	5	NULL	NULL	0	NULL	inflammation	MedicalFinding	active	is observed in					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In addition, active inflammation has been noted in autism	topic_aut
76615	1	355917	5	NULL	NULL	0	NULL	IL-1β	GP	enhanced activity of	is associated with					neuroinflammation	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Enhanced IL-1β activity is associated with neuroinflammation	topic_aut
76616	1	355919	5	NULL	NULL	0	NULL	TNF-α	GP		induce					nitric oxide	Chemical				NULL	brain	0	NULL	NULL	NULL	NULL	NULL	TNF-α is neurotoxic and induces nitric oxide and free radicals in the brain. Enhanced IL-1β activity is associated with neuroinflammation (16). Therefore, excessive glutamate enhances proinflammatory activities and induces neurotoxicity.	topic_aut
76617	2	355919	5	NULL	NULL	0	NULL	TNF-α	GP		induce					free radicals	Chemical				NULL	brain	0	NULL	NULL	NULL	NULL	NULL	TNF-α is neurotoxic and induces nitric oxide and free radicals in the brain. Enhanced IL-1β activity is associated with neuroinflammation (16). Therefore, excessive glutamate enhances proinflammatory activities and induces neurotoxicity.	topic_aut
76618	3	355919	5	NULL	NULL	0	NULL	TNF-α	GP		is a type of					neurotoxic	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	TNF-α is neurotoxic and induces nitric oxide and free radicals in the brain. Enhanced IL-1β activity is associated with neuroinflammation (16). Therefore, excessive glutamate enhances proinflammatory activities and induces neurotoxicity.	topic_aut
76619	4	355919	5	NULL	NULL	0	NULL	IL-1β 	GP	enhanced activity of	is associated with					neuroinflammation	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	TNF-α is neurotoxic and induces nitric oxide and free radicals in the brain. Enhanced IL-1β activity is associated with neuroinflammation (16). Therefore, excessive glutamate enhances proinflammatory activities and induces neurotoxicity.	topic_aut
76620	5	355919	5	NULL	NULL	0	NULL	glutamate	Chemical	excessive	enhances					proinflammatory activities	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	TNF-α is neurotoxic and induces nitric oxide and free radicals in the brain. Enhanced IL-1β activity is associated with neuroinflammation (16). Therefore, excessive glutamate enhances proinflammatory activities and induces neurotoxicity.	topic_aut
76621	6	355919	5	NULL	NULL	0	NULL	statement 5	Process		induce					neurotoxicity	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	TNF-α is neurotoxic and induces nitric oxide and free radicals in the brain. Enhanced IL-1β activity is associated with neuroinflammation (16). Therefore, excessive glutamate enhances proinflammatory activities and induces neurotoxicity.	topic_aut
76691	1	355921	5	NULL	NULL	NULL	NULL	glutamate stress	PhysicalPhenomenon		is associated with					phospholipid biomarkers	AbstractConcept	plasma			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Considering that glutamate stress is associated with plasma phospholipid biomarkers	topic_aut
76692	1	355922	5	NULL	NULL	0	NULL	MSO	Chemical		is					methionine sulfoximine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	It is interesting that another recently published study introduced methionine sulfoximine (MSO) as an inhibitor of glutamine synthetase (17). MSO decreases the glutamate level in the brains of animal models (17). Therefore, MSO may play a role in lowering the level of plasma phospholipid biomarkers in autism.	topic_aut
76693	2	355922	5	NULL	NULL	0	NULL	MSO	Chemical		is an inhibitor of					glutamine synthetase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	It is interesting that another recently published study introduced methionine sulfoximine (MSO) as an inhibitor of glutamine synthetase (17). MSO decreases the glutamate level in the brains of animal models (17). Therefore, MSO may play a role in lowering the level of plasma phospholipid biomarkers in autism.	topic_aut
76694	3	355922	5	NULL	NULL	0	NULL	MSO	Chemical		decrease					glutamate	Chemical	levels of			NULL		0	NULL	NULL	NULL	NULL	NULL	It is interesting that another recently published study introduced methionine sulfoximine (MSO) as an inhibitor of glutamine synthetase (17). MSO decreases the glutamate level in the brains of animal models (17). Therefore, MSO may play a role in lowering the level of plasma phospholipid biomarkers in autism.	topic_aut
76695	4	355922	5	NULL	NULL	0	NULL	statement 3	Process		occurs in					brain	OrganismPart				NULL	animal models	0	NULL	NULL	NULL	NULL	NULL	It is interesting that another recently published study introduced methionine sulfoximine (MSO) as an inhibitor of glutamine synthetase (17). MSO decreases the glutamate level in the brains of animal models (17). Therefore, MSO may play a role in lowering the level of plasma phospholipid biomarkers in autism.	topic_aut
76696	5	355922	5	NULL	NULL	0	NULL	MSO	Chemical		lowers		possibly			phospholipid biomarkers	AbstractConcept	plasma			NULL		0	NULL	NULL	NULL	NULL	NULL	It is interesting that another recently published study introduced methionine sulfoximine (MSO) as an inhibitor of glutamine synthetase (17). MSO decreases the glutamate level in the brains of animal models (17). Therefore, MSO may play a role in lowering the level of plasma phospholipid biomarkers in autism.	topic_aut
76697	6	355922	5	NULL	NULL	0	NULL	statement 5	Process		occurs in					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	It is interesting that another recently published study introduced methionine sulfoximine (MSO) as an inhibitor of glutamine synthetase (17). MSO decreases the glutamate level in the brains of animal models (17). Therefore, MSO may play a role in lowering the level of plasma phospholipid biomarkers in autism.	topic_aut
76698	1	355924	5	NULL	NULL	0	NULL	Tumor necrosis factor	GP		is a type of					cytokine	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Tumor necrosis factor is a cytokine involved in systemic inflammation	topic_aut
76699	2	355924	5	NULL	NULL	0	NULL	Tumor necrosis factor	GP		is involved in					systemic inflammation	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Tumor necrosis factor is a cytokine involved in systemic inflammation	topic_aut
76700	1	355925	5	NULL	NULL	0	NULL	IL-1β	GP		is					Interleukin-1 beta	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-1 beta (IL-1β) also known as catabolin, is a cytokine protein	topic_aut
76701	2	355925	5	NULL	NULL	0	NULL	Interleukin-1 beta	GP		is also known as					catabolin	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-1 beta (IL-1β) also known as catabolin, is a cytokine protein	topic_aut
76702	3	355925	5	NULL	NULL	0	NULL	Interleukin-1 beta	GP		is a type of					cytokine protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-1 beta (IL-1β) also known as catabolin, is a cytokine protein	topic_aut
76703	1	355926	5	NULL	NULL	0	NULL	PBDE	Chemical		is					Polybrominated diphenyl ethers	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Polybrominated diphenyl ethers or PBDE, are organobromine compounds that are used as flame retardants	topic_aut
76704	2	355926	5	NULL	NULL	0	NULL	PBDE	Chemical		is a type of					organobromine compounds	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Polybrominated diphenyl ethers or PBDE, are organobromine compounds that are used as flame retardants	topic_aut
76705	3	355926	5	NULL	NULL	0	NULL	PBDE	Chemical		is used as					flame retardants	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Polybrominated diphenyl ethers or PBDE, are organobromine compounds that are used as flame retardants	topic_aut
76706	1	355927	5	NULL	NULL	0	NULL	environmental trigger	PhysicalPhenomenon		activates					mast cell	Cell	non-allergic			NULL		0	NULL	NULL	NULL	NULL	NULL	These findings suggest non-allergic mast cell activation, probably in response to environmental and stress triggers that could contribute to inflammation	topic_aut
76707	2	355927	5	NULL	NULL	0	NULL	stress trigger	PhysicalPhenomenon		activates					mast cell	Cell	non-allergic			NULL		0	NULL	NULL	NULL	NULL	NULL	These findings suggest non-allergic mast cell activation, probably in response to environmental and stress triggers that could contribute to inflammation	topic_aut
76708	3	355927	5	NULL	NULL	0	NULL	statement 1	Process		contribute to					inflammation	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	These findings suggest non-allergic mast cell activation, probably in response to environmental and stress triggers that could contribute to inflammation	topic_aut
76709	4	355927	5	NULL	NULL	0	NULL	statement 2	Process		contribute to					inflammation	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	These findings suggest non-allergic mast cell activation, probably in response to environmental and stress triggers that could contribute to inflammation	topic_aut
76710	1	355928	5	NULL	NULL	0	NULL	utero	OrganismPart	inflammation of	leads to					labor	PhysicalPhenomenon	preterm			NULL		0	NULL	NULL	NULL	NULL	NULL	In utero inflammation can lead to preterm labor and has itself been strongly associated with adverse neurodevelopmental outcomes.	topic_aut
76711	2	355928	5	NULL	NULL	0	NULL	statement 2			is associated with		strongly			neurodevelopmental outcomes	MedicalFinding	adverse			NULL		0	NULL	NULL	NULL	NULL	NULL	In utero inflammation can lead to preterm labor and has itself been strongly associated with adverse neurodevelopmental outcomes.	topic_aut
76712	1	355929	5	NULL	NULL	0	NULL	SERT	GP		is					serotonin transporter	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The known Gly56Ala mutation in the serotonin transporter SERT (or 5-HTT), encoded by the SLC6A4 gene, causes increased serotonin reuptake and has been associated with autism and rigid-compulsive behavior	topic_aut
76713	2	355929	5	NULL	NULL	0	NULL	SERT	GP		is also known as					5-HTT	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The known Gly56Ala mutation in the serotonin transporter SERT (or 5-HTT), encoded by the SLC6A4 gene, causes increased serotonin reuptake and has been associated with autism and rigid-compulsive behavior	topic_aut
76714	3	355929	5	NULL	NULL	0	NULL	SERT	GP		is encoded by					SLC6A4 gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The known Gly56Ala mutation in the serotonin transporter SERT (or 5-HTT), encoded by the SLC6A4 gene, causes increased serotonin reuptake and has been associated with autism and rigid-compulsive behavior	topic_aut
76715	4	355929	5	NULL	NULL	0	NULL	SERT	GP	mutant	increases			Gly56Ala		serotonin	Chemical	uptake of			NULL		0	NULL	NULL	NULL	NULL	NULL	The known Gly56Ala mutation in the serotonin transporter SERT (or 5-HTT), encoded by the SLC6A4 gene, causes increased serotonin reuptake and has been associated with autism and rigid-compulsive behavior	topic_aut
76716	5	355929	5	NULL	NULL	0	NULL	SERT	GP	mutant	is associated with			Gly56Ala		autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The known Gly56Ala mutation in the serotonin transporter SERT (or 5-HTT), encoded by the SLC6A4 gene, causes increased serotonin reuptake and has been associated with autism and rigid-compulsive behavior	topic_aut
76717	6	355929	5	NULL	NULL	0	NULL	SERT	GP	mutant	is associated with			Gly56Ala		rigid-compulsive behavior	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The known Gly56Ala mutation in the serotonin transporter SERT (or 5-HTT), encoded by the SLC6A4 gene, causes increased serotonin reuptake and has been associated with autism and rigid-compulsive behavior	topic_aut
76718	1	355930	5	NULL	NULL	0	NULL	SERT	GP		is					serotonin transporter	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The serotonin transporter (SERT) is a monoamine transporter protein.	topic_aut
76719	2	355930	5	NULL	NULL	0	NULL	SERT	GP		is a type of					monoamine transporter protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The serotonin transporter (SERT) is a monoamine transporter protein.	topic_aut
76720	1	355931	5	NULL	NULL	0	NULL	5HIAA	Chemical		is					5-hydroxyindolacetic acid	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Low levels of the serotonin end-metabolite 5-hydroxyindolacetic acid (5HIAA) in CSF were detected	topic_aut
76721	2	355931	5	NULL	NULL	0	NULL	5HIAA	Chemical		is an end-metabolite of					serotonin	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Low levels of the serotonin end-metabolite 5-hydroxyindolacetic acid (5HIAA) in CSF were detected	topic_aut
76722	3	355931	5	NULL	NULL	0	NULL	CSF	OrganismPart		contains					5HIAA	Chemical	low levels of			NULL		0	NULL	NULL	NULL	NULL	NULL	Low levels of the serotonin end-metabolite 5-hydroxyindolacetic acid (5HIAA) in CSF were detected	topic_aut
76723	1	355933	5	NULL	NULL	0	NULL	MAO	GP		is					Monoamine oxidases	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Monoamine oxidases (MAO) (EC 1.4.3.4) are a family of enzymes that catalyze the oxidation of monoamines	topic_aut
76724	2	355933	5	NULL	NULL	0	NULL	MAO	GP		is a family of					enzymes	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Monoamine oxidases (MAO) (EC 1.4.3.4) are a family of enzymes that catalyze the oxidation of monoamines	topic_aut
76725	3	355933	5	NULL	NULL	0	NULL	MAO	GP		oxidize					monoamines	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Monoamine oxidases (MAO) (EC 1.4.3.4) are a family of enzymes that catalyze the oxidation of monoamines	topic_aut
76726	1	355934	5	NULL	NULL	0	NULL	Shank3	GP		plays a role in		important			synaptic function	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 Our results are consistent with altered synaptic development and function in Shank3 haploinsufficiency, highlighting the importance of Shank3 in synaptic function and supporting a link between deficits in synapse function and neurodevelopmental disorders	topic_aut
76727	2	355934	5	NULL	NULL	0	NULL	synapse function	Process	deficits of	is linked to					neurodevelopmental disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	 Our results are consistent with altered synaptic development and function in Shank3 haploinsufficiency, highlighting the importance of Shank3 in synaptic function and supporting a link between deficits in synapse function and neurodevelopmental disorders	topic_aut
76728	3	355934	5	NULL	NULL	0	NULL	Shank3	GP		plays a role in		important			statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 Our results are consistent with altered synaptic development and function in Shank3 haploinsufficiency, highlighting the importance of Shank3 in synaptic function and supporting a link between deficits in synapse function and neurodevelopmental disorders	topic_aut
76729	1	355935	5	NULL	NULL	0	NULL	IBI	MedicalProcedure		is					Intensive Behavioural Intervention	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Evidence-based treatments such as behavioural therapies, have come to the forefront of autism literature Smith (1999), in his review of outcome studies, recognized Intensive Behavioural Intervention (IBI) as the most effective treatment for autism	topic_aut
76730	2	355935	5	NULL	NULL	0	NULL	Intensive Behavioural Intervention	MedicalProcedure		is treatment for		most effective			autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Evidence-based treatments such as behavioural therapies, have come to the forefront of autism literature Smith (1999), in his review of outcome studies, recognized Intensive Behavioural Intervention (IBI) as the most effective treatment for autism	topic_aut
76731	1	355936	5	NULL	NULL	0	NULL	Secretin	GP		does not play a role in					ASD	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Secretin was an unstudied treatment that gained widespread popularity and use through anecdotal reports before scientific investigation failed to find any evidence of efficacy for treating ASD	topic_aut
76732	1	355937	5	NULL	NULL	0	NULL	Secretin	GP		is a type of					gastrointestinal hormone	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Secretin is a gastrointestinal hormone that stimulates the secretion of bile from the liver, as well as acts as a stress regulatory hormone that impacts GABA levels	topic_aut
76733	2	355937	5	NULL	NULL	0	NULL	bile	OrganismPart		is secreted from					liver	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Secretin is a gastrointestinal hormone that stimulates the secretion of bile from the liver, as well as acts as a stress regulatory hormone that impacts GABA levels	topic_aut
76734	3	355937	5	NULL	NULL	0	NULL	Secretin	GP		stimulates					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Secretin is a gastrointestinal hormone that stimulates the secretion of bile from the liver, as well as acts as a stress regulatory hormone that impacts GABA levels	topic_aut
76735	4	355937	5	NULL	NULL	0	NULL	Secretin	GP		act as					stress regulatory hormone	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Secretin is a gastrointestinal hormone that stimulates the secretion of bile from the liver, as well as acts as a stress regulatory hormone that impacts GABA levels	topic_aut
76736	5	355937	5	NULL	NULL	0	NULL	statement 4	Process		impacts					GABA	Chemical	level of			NULL		0	NULL	NULL	NULL	NULL	NULL	Secretin is a gastrointestinal hormone that stimulates the secretion of bile from the liver, as well as acts as a stress regulatory hormone that impacts GABA levels	topic_aut
76737	1	355938	5	NULL	NULL	0	NULL	GABA receptors	GP		is a class of					receptors	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The GABA receptors are a class of receptors that respond to the neurotransmitter gamma-aminobutyric acid (GABA)	topic_aut
76738	2	355938	5	NULL	NULL	NULL	NULL	GABA receptors	GP		respond to					GABA	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The GABA receptors are a class of receptors that respond to the neurotransmitter gamma-aminobutyric acid (GABA)	topic_aut
76739	3	355938	5	NULL	NULL	0	NULL	GABA	Chemical		is					gamma-aminobutyric acid	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The GABA receptors are a class of receptors that respond to the neurotransmitter gamma-aminobutyric acid (GABA)	topic_aut
76740	4	355938	5	NULL	NULL	0	NULL	GABA	Chemical		is a type of					neurotransmitter	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The GABA receptors are a class of receptors that respond to the neurotransmitter gamma-aminobutyric acid (GABA)	topic_aut
76741	1	355939	5	NULL	NULL	0	NULL	alternative diets	Food		does not play a role in					ASD	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	There is little to no empirical support for alternative diets in treating ASD	topic_aut
76742	1	355941	5	NULL	NULL	0	NULL	Martin�??Bell syndrome	MedicalFinding		is also known as					Fragile X syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Fragile X syndrome or Martin–Bell syndrome, is a genetic syndrome	topic_aut
76743	2	355941	5	NULL	NULL	0	NULL	Martin�??Bell syndrome	MedicalFinding		is a type of					genetic syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Fragile X syndrome or Martin–Bell syndrome, is a genetic syndrome	topic_aut
76744	1	355942	5	NULL	NULL	0	NULL	INN	Chemical		is					Thiomersal	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Thiomersal (INN) and commonly known in the US as thimerosal, is an organomercury compound.	topic_aut
76745	2	355942	5	NULL	NULL	0	NULL	Thiomersal	Chemical		is commonly known as					thimerosal	Chemical				NULL	US	0	NULL	NULL	NULL	NULL	NULL	Thiomersal (INN) and commonly known in the US as thimerosal, is an organomercury compound.	topic_aut
76746	3	355942	5	NULL	NULL	0	NULL	INN	Chemical		is a type of					organomercury compound	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Thiomersal (INN) and commonly known in the US as thimerosal, is an organomercury compound.	topic_aut
76747	1	355943	5	NULL	NULL	0	NULL	CD38	GP		is					cluster of differentiation 38	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	CD38 (cluster of differentiation 38), also known as cyclic ADP ribose hydrolase is a glycoprotein[1] found on the surface of many immune cells 	topic_aut
76748	2	355943	5	NULL	NULL	0	NULL	CD38	GP		is also known as					cyclic ADP ribose hydrolase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	CD38 (cluster of differentiation 38), also known as cyclic ADP ribose hydrolase is a glycoprotein[1] found on the surface of many immune cells 	topic_aut
76749	3	355943	5	NULL	NULL	0	NULL	CD38	GP		is a type of					glycoprotein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	CD38 (cluster of differentiation 38), also known as cyclic ADP ribose hydrolase is a glycoprotein[1] found on the surface of many immune cells 	topic_aut
76750	4	355943	5	NULL	NULL	0	NULL	CD38	GP		is found on					immune cells	Cell	surface of			NULL		0	NULL	NULL	NULL	NULL	NULL	CD38 (cluster of differentiation 38), also known as cyclic ADP ribose hydrolase is a glycoprotein[1] found on the surface of many immune cells 	topic_aut
76751	1	355944	5	NULL	NULL	0	NULL	uridine phosphorylase	GP		is a type of					enzyme	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	In enzymology, an uridine phosphorylase (EC 2.4.2.3) is an enzyme	topic_aut
76752	1	355945	5	NULL	NULL	0	NULL	5-HIAA	Chemical		is					5-Hydroxyindoleacetic acid	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	5-Hydroxyindoleacetic acid (5-HIAA) is the main metabolite of serotonin in the human body	topic_aut
76753	2	355945	5	NULL	NULL	0	NULL	5-HIAA	Chemical		is a metabolite of					serotonin	Chemical				NULL	human body	0	NULL	NULL	NULL	NULL	NULL	5-Hydroxyindoleacetic acid (5-HIAA) is the main metabolite of serotonin in the human body	topic_aut
76754	1	355946	5	NULL	NULL	0	NULL	VNTR	Chromosome		is					Variable Number Tandem Repeat	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	A Variable Number Tandem Repeat (or VNTR) is a location in a genome where a short nucleotide sequence is organized as a tandem repeat	topic_aut
76755	2	355946	5	NULL	NULL	0	NULL	VNTR	Chromosome		is located on					genome	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	A Variable Number Tandem Repeat (or VNTR) is a location in a genome where a short nucleotide sequence is organized as a tandem repeat	topic_aut
76756	3	355946	5	NULL	NULL	0	NULL	nucleotide sequence	NucleicAcid	short	is organized as					tandem repeat	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	A Variable Number Tandem Repeat (or VNTR) is a location in a genome where a short nucleotide sequence is organized as a tandem repeat	topic_aut
76757	4	355946	5	NULL	NULL	0	NULL	statement 3	Process		forms					VNTR	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	A Variable Number Tandem Repeat (or VNTR) is a location in a genome where a short nucleotide sequence is organized as a tandem repeat	topic_aut
76758	1	355947	5	NULL	NULL	0	NULL	β-blockers	Chemical		is					Beta blockers	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta blockers (sometimes written as β-blockers) or beta-adrenergic blocking agents, beta-adrenergic antagonists, or beta antagonists, are a class of drugs used for various indications, but particularly for the management of cardiac arrhythmias, cardioprotection after myocardial infarction	topic_aut
76759	2	355947	5	NULL	NULL	0	NULL	Beta blockers	Chemical		is also known as					 beta-adrenergic blocking agents	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta blockers (sometimes written as β-blockers) or beta-adrenergic blocking agents, beta-adrenergic antagonists, or beta antagonists, are a class of drugs used for various indications, but particularly for the management of cardiac arrhythmias, cardioprotection after myocardial infarction	topic_aut
76760	3	355947	5	NULL	NULL	0	NULL	Beta blockers	Chemical		is also known as					beta-adrenergic antagonists	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta blockers (sometimes written as β-blockers) or beta-adrenergic blocking agents, beta-adrenergic antagonists, or beta antagonists, are a class of drugs used for various indications, but particularly for the management of cardiac arrhythmias, cardioprotection after myocardial infarction	topic_aut
76761	4	355947	5	NULL	NULL	0	NULL	Beta blockers	Chemical		is also known as					beta antagonists	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta blockers (sometimes written as β-blockers) or beta-adrenergic blocking agents, beta-adrenergic antagonists, or beta antagonists, are a class of drugs used for various indications, but particularly for the management of cardiac arrhythmias, cardioprotection after myocardial infarction	topic_aut
76762	5	355947	5	NULL	NULL	0	NULL	Beta blockers	Chemical		is a class of					drugs	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta blockers (sometimes written as β-blockers) or beta-adrenergic blocking agents, beta-adrenergic antagonists, or beta antagonists, are a class of drugs used for various indications, but particularly for the management of cardiac arrhythmias, cardioprotection after myocardial infarction	topic_aut
76763	6	355947	5	NULL	NULL	0	NULL	Beta blockers	Chemical		is used in					cardiac arrhythmias	MedicalFinding	management of			NULL		0	NULL	NULL	NULL	NULL	NULL	Beta blockers (sometimes written as β-blockers) or beta-adrenergic blocking agents, beta-adrenergic antagonists, or beta antagonists, are a class of drugs used for various indications, but particularly for the management of cardiac arrhythmias, cardioprotection after myocardial infarction	topic_aut
76764	7	355947	5	NULL	NULL	0	NULL	Beta blockers	Chemical		is used in					cardioprotection	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta blockers (sometimes written as β-blockers) or beta-adrenergic blocking agents, beta-adrenergic antagonists, or beta antagonists, are a class of drugs used for various indications, but particularly for the management of cardiac arrhythmias, cardioprotection after myocardial infarction	topic_aut
76765	8	355947	5	NULL	NULL	0	NULL	statement 7	Process		occurs after					myocardial infarction	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Beta blockers (sometimes written as β-blockers) or beta-adrenergic blocking agents, beta-adrenergic antagonists, or beta antagonists, are a class of drugs used for various indications, but particularly for the management of cardiac arrhythmias, cardioprotection after myocardial infarction	topic_aut
76766	1	355948	5	NULL	NULL	0	NULL	Catecholamines	GP		is a type of					"fight-or-flight" hormones	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Catecholamines are "fight-or-flight" hormones	topic_aut
76767	1	355949	5	NULL	NULL	0	NULL	genomic DNA	NucleicAcid	alterations of	is known as					Copy-number variations	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	Copy-number variations are alterations of genomic DNA that correspond to relatively large regions of the genome that have been deleted or amplified on certain chromosomes	topic_aut
76768	1	355950	5	NULL	NULL	0	NULL	Cytokines	GP		is a type of					small cell-signaling protein molecules	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Cytokines (Greek cyto-, cell; and -kinos, movement) are small cell-signaling protein molecules	topic_aut
76769	1	355951	5	NULL	NULL	0	NULL	GABA	Chemical		is					γ-Aminobutyric acid	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	γ-Aminobutyric acid (GABA) is the chief inhibitory neurotransmitter in the mammalian central nervous system	topic_aut
76770	2	355951	5	NULL	NULL	0	NULL	GABA	Chemical		is a type of					 inhibitory neurotransmitter	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	γ-Aminobutyric acid (GABA) is the chief inhibitory neurotransmitter in the mammalian central nervous system	topic_aut
76771	3	355951	5	NULL	NULL	0	NULL	GABA	Chemical		is present in					central nervous system	OrganismPart	mammalian			NULL		0	NULL	NULL	NULL	NULL	NULL	γ-Aminobutyric acid (GABA) is the chief inhibitory neurotransmitter in the mammalian central nervous system	topic_aut
78672	1	355952	11	NULL	NULL	0	NULL	Staphylococcus aureus skin and soft tissue infections	MedicalFinding		is					SSTI	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	This document is intended to provide interim clinical guidance for management of Staphylococcus aureus skin and soft tissue infections (SSTI) in outpatients in Illinois	topic_mrs
78673	1	355953	11	NULL	NULL	NULL	NULL	Erysipelas	MedicalFinding		is caused by		often			β-hemolytic streptococci	Organism	 group A			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Erysipelas is most often caused by group A (or rarely group C or G) β-hemolytic streptococci and occurs most frequently on the legs and face. However, other causes have been reported, including Staphylococcus aureus (including methicillin-resistant S. aureus [MRSA])	topic_mrs
78674	2	355953	11	NULL	NULL	0	NULL	Erysipelas	MedicalFinding		is caused by		rarely			β-hemolytic streptococci	Organism	group C or G			NULL		0	NULL	NULL	NULL	NULL	NULL	Erysipelas is most often caused by group A (or rarely group C or G) β-hemolytic streptococci and occurs most frequently on the legs and face. However, other causes have been reported, including Staphylococcus aureus (including methicillin-resistant S. aureus [MRSA])	topic_mrs
78675	3	355953	11	NULL	NULL	0	NULL	Erysipelas	MedicalFinding		occurs on		frequently			legs	Organism part				NULL		0	NULL	NULL	NULL	NULL	NULL	Erysipelas is most often caused by group A (or rarely group C or G) β-hemolytic streptococci and occurs most frequently on the legs and face. However, other causes have been reported, including Staphylococcus aureus (including methicillin-resistant S. aureus [MRSA])	topic_mrs
78676	4	355953	11	NULL	NULL	0	NULL	Erysipelas	MedicalFinding		occurs on					face	Organism part				NULL		0	NULL	NULL	NULL	NULL	NULL	Erysipelas is most often caused by group A (or rarely group C or G) β-hemolytic streptococci and occurs most frequently on the legs and face. However, other causes have been reported, including Staphylococcus aureus (including methicillin-resistant S. aureus [MRSA])	topic_mrs
78677	5	355953	11	NULL	NULL	0	NULL	statement 3	Process		occurs along with					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Erysipelas is most often caused by group A (or rarely group C or G) β-hemolytic streptococci and occurs most frequently on the legs and face. However, other causes have been reported, including Staphylococcus aureus (including methicillin-resistant S. aureus [MRSA])	topic_mrs
78678	6	355953	11	NULL	NULL	0	NULL	methicillin-resistant S. aureus	Organism		is					MRSA	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Erysipelas is most often caused by group A (or rarely group C or G) β-hemolytic streptococci and occurs most frequently on the legs and face. However, other causes have been reported, including Staphylococcus aureus (including methicillin-resistant S. aureus [MRSA])	topic_mrs
78679	7	355953	11	NULL	NULL	0	NULL	MRSA	Organism		is a type of 					Staphylococcus aureus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Erysipelas is most often caused by group A (or rarely group C or G) β-hemolytic streptococci and occurs most frequently on the legs and face. However, other causes have been reported, including Staphylococcus aureus (including methicillin-resistant S. aureus [MRSA])	topic_mrs
78680	8	355953	11	NULL	NULL	0	NULL	MRSA	Organism		causes					Erysipelas	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Erysipelas is most often caused by group A (or rarely group C or G) β-hemolytic streptococci and occurs most frequently on the legs and face. However, other causes have been reported, including Staphylococcus aureus (including methicillin-resistant S. aureus [MRSA])	topic_mrs
76772	1	355954	5	NULL	NULL	0	NULL	Interleukin-1 alpha	GP		is a type of					protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-1 alpha (IL-1α) is a protein	topic_aut
76773	2	355954	5	NULL	NULL	0	NULL	Interleukin-1 alpha	GP		is					IL-1α	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Interleukin-1 alpha (IL-1α) is a protein	topic_aut
76774	1	355955	5	NULL	NULL	0	NULL	c-Met	GP		is					Mesenchymal�??epithelial transition factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Mesenchymal−epithelial transition factor (c-Met) is a receptor tyrosine kinase	topic_aut
76775	2	355955	5	NULL	NULL	0	NULL	c-Met	GP		is a type of					receptor tyrosine kinase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Mesenchymal−epithelial transition factor (c-Met) is a receptor tyrosine kinase	topic_aut
76776	1	355956	5	NULL	NULL	0	NULL	MAO	GP		is					Monoamine oxidases	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Monoamine oxidases (MAO) (EC 1.4.3.4) are a family of enzymes	topic_aut
76777	2	355956	5	NULL	NULL	0	NULL	Monoamine oxidases	GP		is a family of					enzymes	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Monoamine oxidases (MAO) (EC 1.4.3.4) are a family of enzymes	topic_aut
76778	1	355957	5	NULL	NULL	0	NULL	proinflammatory cytokine	GP		is a type of					cytokine	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 A proinflammatory cytokine is a cytokine which promotes systemic inflammation	topic_aut
76779	2	355957	5	NULL	NULL	0	NULL	proinflammatory cytokine	GP		promotes					systemic inflammation	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	 A proinflammatory cytokine is a cytokine which promotes systemic inflammation	topic_aut
76780	1	355958	5	NULL	NULL	0	NULL	RTK	GP		is					proto-oncogenic receptor tyrosine kinases	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	proto-oncogenic receptor tyrosine kinases (RTK)s are the high-affinity cell surface receptors 	topic_aut
76781	2	355958	5	NULL	NULL	0	NULL	RTK	GP		is a type of					cell surface receptors	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	proto-oncogenic receptor tyrosine kinases (RTK)s are the high-affinity cell surface receptors 	topic_aut
76782	1	355959	5	NULL	NULL	0	NULL	Sensory integration	Process		is a type of					neurological process	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Sensory integration is defined as the neurological process that organizes sensation from one's own body and the environment	topic_aut
76783	2	355959	5	NULL	NULL	0	NULL	neurological process	Process		organizes					sensation	Process				NULL	body	0	NULL	NULL	NULL	NULL	NULL	Sensory integration is defined as the neurological process that organizes sensation from one's own body and the environment	topic_aut
76784	3	355959	5	NULL	NULL	0	NULL	neurological process	Process		organizes					environment	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	Sensory integration is defined as the neurological process that organizes sensation from one's own body and the environment	topic_aut
76785	4	355959	5	NULL	NULL	0	NULL	statement 2	Process		occurs simultaneously with					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Sensory integration is defined as the neurological process that organizes sensation from one's own body and the environment	topic_aut
76786	1	355960	5	NULL	NULL	0	NULL	AD	MedicalFinding		is					autistic disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	patient who was diagnosed with autistic disorder (AD) and responded positively to buspirone, demonstrated by a reduction in target behaviors of self-injury, property destruction, and physical aggression	topic_aut
76787	2	355960	5	NULL	NULL	0	NULL	AD patients	GroupOfPeople		responds to		positively			buspirone	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	patient who was diagnosed with autistic disorder (AD) and responded positively to buspirone, demonstrated by a reduction in target behaviors of self-injury, property destruction, and physical aggression	topic_aut
76788	3	355960	5	NULL	NULL	0	NULL	AD patients	GroupOfPeople		is prone to					self-injury	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	patient who was diagnosed with autistic disorder (AD) and responded positively to buspirone, demonstrated by a reduction in target behaviors of self-injury, property destruction, and physical aggression	topic_aut
76789	4	355960	5	NULL	NULL	0	NULL	AD patients	GroupOfPeople		is prone to					property destruction	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	patient who was diagnosed with autistic disorder (AD) and responded positively to buspirone, demonstrated by a reduction in target behaviors of self-injury, property destruction, and physical aggression	topic_aut
76790	5	355960	5	NULL	NULL	0	NULL	AD patients	GroupOfPeople		is prone to					 physical aggression	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	patient who was diagnosed with autistic disorder (AD) and responded positively to buspirone, demonstrated by a reduction in target behaviors of self-injury, property destruction, and physical aggression	topic_aut
76791	6	355960	5	NULL	NULL	0	NULL	statement 2	Process		reduce					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	patient who was diagnosed with autistic disorder (AD) and responded positively to buspirone, demonstrated by a reduction in target behaviors of self-injury, property destruction, and physical aggression	topic_aut
76792	7	355960	5	NULL	NULL	0	NULL	statement 2	Process		reduce					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	patient who was diagnosed with autistic disorder (AD) and responded positively to buspirone, demonstrated by a reduction in target behaviors of self-injury, property destruction, and physical aggression	topic_aut
76793	8	355960	5	NULL	NULL	0	NULL	statement 2	Process		reduce					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	patient who was diagnosed with autistic disorder (AD) and responded positively to buspirone, demonstrated by a reduction in target behaviors of self-injury, property destruction, and physical aggression	topic_aut
76794	1	355961	5	NULL	NULL	0	NULL	risperidone	Chemical		is a type of					atypical antipsychotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Investigations to date suggest that the atypical antipsychotics such as risperidone have efficacy for certain symptoms of autistic disorder and may be better tolerated than typical antipsychotics	topic_aut
76795	2	355961	5	NULL	NULL	0	NULL	risperidone	Chemical		have efficacy for					autistic disorder	MedicalFinding	certain symptoms of			NULL		0	NULL	NULL	NULL	NULL	NULL	Investigations to date suggest that the atypical antipsychotics such as risperidone have efficacy for certain symptoms of autistic disorder and may be better tolerated than typical antipsychotics	topic_aut
76796	3	355961	5	NULL	NULL	0	NULL	atypical antipsychotics	Chemical		better tolerated than		may be			typical antipsychotics	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Investigations to date suggest that the atypical antipsychotics such as risperidone have efficacy for certain symptoms of autistic disorder and may be better tolerated than typical antipsychotics	topic_aut
76797	1	355962	5	NULL	NULL	0	NULL	haloperidol	Chemical		is a type of					antipsychotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The typical antipsychotic haloperidol is the best-studied medication in autistic disorder but is associated with a high rate of dyskinesias	topic_aut
76798	2	355962	5	NULL	NULL	0	NULL	haloperidol	Chemical		is used to treat					autistic disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The typical antipsychotic haloperidol is the best-studied medication in autistic disorder but is associated with a high rate of dyskinesias	topic_aut
76799	3	355962	5	NULL	NULL	0	NULL	haloperidol	Chemical		is associated with					dyskinesias	MedicalFinding	high rate of			NULL		0	NULL	NULL	NULL	NULL	NULL	The typical antipsychotic haloperidol is the best-studied medication in autistic disorder but is associated with a high rate of dyskinesias	topic_aut
76800	1	355963	5	NULL	NULL	0	NULL	Dyskinesia	MedicalFinding		is a type of					movement disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Dyskinesia is a movement disorder which consists of effects including diminished voluntary movements[1] and the presence of involuntary movements, similar to tics or chorea	topic_aut
76801	2	355963	5	NULL	NULL	0	NULL	voluntary movements	PhysicalPhenomenon		is diminished in					Dyskinesia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Dyskinesia is a movement disorder which consists of effects including diminished voluntary movements[1] and the presence of involuntary movements, similar to tics or chorea	topic_aut
76802	3	355963	5	NULL	NULL	0	NULL	involuntary movements	PhysicalPhenomenon		is present in					Dyskinesia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Dyskinesia is a movement disorder which consists of effects including diminished voluntary movements[1] and the presence of involuntary movements, similar to tics or chorea	topic_aut
76803	4	355963	5	NULL	NULL	0	NULL	tics	MedicalFinding		is a type of					involuntary movement	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	Dyskinesia is a movement disorder which consists of effects including diminished voluntary movements[1] and the presence of involuntary movements, similar to tics or chorea	topic_aut
76804	5	355963	5	NULL	NULL	0	NULL	chorea	MedicalFinding		is a type of					involuntary movement	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	Dyskinesia is a movement disorder which consists of effects including diminished voluntary movements[1] and the presence of involuntary movements, similar to tics or chorea	topic_aut
76805	1	355964	5	NULL	NULL	NULL	NULL	hyperactivity	MedicalFinding		is observed in					autistic children	GroupOfPeople				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Psychostimulants reduced hyperactivity and irritability in one small double-blind crossover study in children with autistic disorder, although these agents are frequently reported to exacerbate irritability, insomnia, and aggression in clinical populations	topic_aut
76806	2	355964	5	NULL	NULL	0	NULL	irritability	MedicalFinding		is observed in					autistic children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Psychostimulants reduced hyperactivity and irritability in one small double-blind crossover study in children with autistic disorder, although these agents are frequently reported to exacerbate irritability, insomnia, and aggression in clinical populations	topic_aut
76807	3	355964	5	NULL	NULL	0	NULL	Psychostimulants	Chemical		reduce					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Psychostimulants reduced hyperactivity and irritability in one small double-blind crossover study in children with autistic disorder, although these agents are frequently reported to exacerbate irritability, insomnia, and aggression in clinical populations	topic_aut
76808	4	355964	5	NULL	NULL	0	NULL	Psychostimulants	Chemical		reduce					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Psychostimulants reduced hyperactivity and irritability in one small double-blind crossover study in children with autistic disorder, although these agents are frequently reported to exacerbate irritability, insomnia, and aggression in clinical populations	topic_aut
76809	5	355964	5	NULL	NULL	0	NULL	Psychostimulants	Chemical		exacerbate					irritability	MedicalFinding				NULL	clinical populations	0	NULL	NULL	NULL	NULL	NULL	Psychostimulants reduced hyperactivity and irritability in one small double-blind crossover study in children with autistic disorder, although these agents are frequently reported to exacerbate irritability, insomnia, and aggression in clinical populations	topic_aut
76810	6	355964	5	NULL	NULL	0	NULL	Psychostimulants	Chemical		exacerbate					insomnia	MedicalFinding				NULL	clinical populations	0	NULL	NULL	NULL	NULL	NULL	Psychostimulants reduced hyperactivity and irritability in one small double-blind crossover study in children with autistic disorder, although these agents are frequently reported to exacerbate irritability, insomnia, and aggression in clinical populations	topic_aut
76811	7	355964	5	NULL	NULL	0	NULL	Psychostimulants	Chemical		exacerbate					aggression	MedicalFinding				NULL	clinical populations	0	NULL	NULL	NULL	NULL	NULL	Psychostimulants reduced hyperactivity and irritability in one small double-blind crossover study in children with autistic disorder, although these agents are frequently reported to exacerbate irritability, insomnia, and aggression in clinical populations	topic_aut
76812	1	355965	5	NULL	NULL	NULL	NULL	sertraline	Chemical	small doses of	is effective in		may be			anxiety	MedicalFinding	treatment of;;symptoms of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Our experience suggests that small doses of sertraline may be effective for treating symptoms of anxiety and agitation	topic_aut
76813	2	355965	5	NULL	NULL	NULL	NULL	sertraline	Chemical	small doses of	is effective in		may be			agitation	MedicalFinding	treatment of;;symptoms of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Our experience suggests that small doses of sertraline may be effective for treating symptoms of anxiety and agitation	topic_aut
76814	1	355966	5	NULL	NULL	NULL	NULL	Sertraline hydrochloride	Chemical		is a type of					generic antidepressant	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Sertraline hydrochloride (trade names Zoloft and Lustral) is a generic antidepressant	topic_aut
76815	2	355966	5	NULL	NULL	0	NULL	Zoloft	Chemical		is the trade name of					Sertraline hydrochloride	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Sertraline hydrochloride (trade names Zoloft and Lustral) is a generic antidepressant	topic_aut
76816	3	355966	5	NULL	NULL	0	NULL	Lustral	Chemical		is the trade name of					Sertraline hydrochloride	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Sertraline hydrochloride (trade names Zoloft and Lustral) is a generic antidepressant	topic_aut
76817	1	355967	5	NULL	NULL	0	NULL	irritability	MedicalFinding	high rate of	is observed in					autistic children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Children with autism and autism spectrum disorders have a high rate of irritability and aggressive symptoms	topic_aut
76818	2	355967	5	NULL	NULL	0	NULL	irritability	MedicalFinding	high rate of	is observed in					autism spectrum disorder children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Children with autism and autism spectrum disorders have a high rate of irritability and aggressive symptoms	topic_aut
76819	3	355967	5	NULL	NULL	0	NULL	aggressive symptoms	MedicalFinding	high rate of	is observed in					autistic children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Children with autism and autism spectrum disorders have a high rate of irritability and aggressive symptoms	topic_aut
76820	4	355967	5	NULL	NULL	NULL	NULL	aggressive symptoms	MedicalFinding	high rate of	is observed in					autism spectrum disorder children	GroupOfPeople				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Children with autism and autism spectrum disorders have a high rate of irritability and aggressive symptoms	topic_aut
76821	1	355968	5	NULL	NULL	0	NULL	irritability	MedicalFinding		is a symptom of					autistic children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	children with autism have symptoms of irritability and aggression including aggression, severe tantrums, and deliberate self injurious behavior	topic_aut
76822	2	355968	5	NULL	NULL	0	NULL	aggression	MedicalFinding		is a symptom of					autistic children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	children with autism have symptoms of irritability and aggression including aggression, severe tantrums, and deliberate self injurious behavior	topic_aut
76823	3	355968	5	NULL	NULL	0	NULL	tantrums	MedicalFinding	severe	is a symptom of					autistic children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	children with autism have symptoms of irritability and aggression including aggression, severe tantrums, and deliberate self injurious behavior	topic_aut
76824	4	355968	5	NULL	NULL	0	NULL	self injurious behavior	MedicalFinding	delibrate	is a symptom of					autistic children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	children with autism have symptoms of irritability and aggression including aggression, severe tantrums, and deliberate self injurious behavior	topic_aut
76825	1	355969	5	NULL	NULL	0	NULL	Aripiprazole	Chemical		is a type of					atypical antipsychotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Aripiprazole is an atypical or newer generation antipsychotic with a unique mechanism of action impacting dopaminergic and serotonergic neurotransmission. The drug has been found efficacious for several indications, including most recently for use targeting irritability associated with autistic disorder	topic_aut
76826	2	355969	5	NULL	NULL	0	NULL	Aripiprazole	Chemical		is a type of					newer generation antipsychotic	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Aripiprazole is an atypical or newer generation antipsychotic with a unique mechanism of action impacting dopaminergic and serotonergic neurotransmission. The drug has been found efficacious for several indications, including most recently for use targeting irritability associated with autistic disorder	topic_aut
76827	3	355969	5	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Aripiprazole is an atypical or newer generation antipsychotic with a unique mechanism of action impacting dopaminergic and serotonergic neurotransmission. The drug has been found efficacious for several indications, including most recently for use targeting irritability associated with autistic disorder	topic_aut
76828	4	355969	5	NULL	NULL	0	NULL	Aripiprazole	Chemical		impact					dopaminergic neurotransmission	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Aripiprazole is an atypical or newer generation antipsychotic with a unique mechanism of action impacting dopaminergic and serotonergic neurotransmission. The drug has been found efficacious for several indications, including most recently for use targeting irritability associated with autistic disorder	topic_aut
76829	5	355969	5	NULL	NULL	0	NULL	Aripiprazole	Chemical		impact					serotonergic neurotransmission	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Aripiprazole is an atypical or newer generation antipsychotic with a unique mechanism of action impacting dopaminergic and serotonergic neurotransmission. The drug has been found efficacious for several indications, including most recently for use targeting irritability associated with autistic disorder	topic_aut
76830	6	355969	5	NULL	NULL	0	NULL	irritability	MedicalFinding		is associated with					autistic disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Aripiprazole is an atypical or newer generation antipsychotic with a unique mechanism of action impacting dopaminergic and serotonergic neurotransmission. The drug has been found efficacious for several indications, including most recently for use targeting irritability associated with autistic disorder	topic_aut
76831	7	355969	5	NULL	NULL	0	NULL	Aripiprazole	Chemical		is efficacious for					statement 6	Process	targeting			NULL		0	NULL	NULL	NULL	NULL	NULL	Aripiprazole is an atypical or newer generation antipsychotic with a unique mechanism of action impacting dopaminergic and serotonergic neurotransmission. The drug has been found efficacious for several indications, including most recently for use targeting irritability associated with autistic disorder	topic_aut
77390	1	355970	7	NULL	NULL	0	NULL	PKCβ1 isoform	GP		expressed in					B-ALL cell line	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Expression of PKCβ1 and PKCβ2 isoforms was demonstrated in five B-ALL cell lines characterized by distinctive chromosomal translocations	topic_ll
77391	2	355970	7	NULL	NULL	0	NULL	PKCβ2 isoform	GP		expressed in					B-ALL cell line	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Expression of PKCβ1 and PKCβ2 isoforms was demonstrated in five B-ALL cell lines characterized by distinctive chromosomal translocations	topic_ll
77394	1	355972	7	NULL	NULL	NULL	NULL	B-ALL cell lines	Cell		express					PKCβ1 isoform	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Expression of PKCβ1 and PKCβ2 isoforms was demonstrated in five B-ALL cell lines characterized by distinctive chromosomal translocations, and sensitivity to PKCβ-selective inhibition was examined. Inhibitor treatment resulted in a dose-dependent reduction in viability in all cell lines, although pro-B ALL with t(4;11)(q21;q23) was most sensitive.	topic_ll
77395	2	355972	7	NULL	NULL	0	NULL	B-ALL cell lines	Cell		express					PKCβ2 isoform	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Expression of PKCβ1 and PKCβ2 isoforms was demonstrated in five B-ALL cell lines characterized by distinctive chromosomal translocations, and sensitivity to PKCβ-selective inhibition was examined. Inhibitor treatment resulted in a dose-dependent reduction in viability in all cell lines, although pro-B ALL with t(4;11)(q21;q23) was most sensitive.	topic_ll
77396	3	355972	7	NULL	NULL	NULL	NULL	Inhibitor	Chemical	treatment 	reduce		dose-dependently			viability	Process				NULL	cell lines	NULL	NULL	NULL	NULL	NULL	NULL	Expression of PKCβ1 and PKCβ2 isoforms was demonstrated in five B-ALL cell lines characterized by distinctive chromosomal translocations, and sensitivity to PKCβ-selective inhibition was examined. Inhibitor treatment resulted in a dose-dependent reduction in viability in all cell lines, although pro-B ALL with t(4;11)(q21;q23) was most sensitive.	topic_ll
77397	4	355972	7	NULL	NULL	0	NULL	 pro-B ALL	MedicalFinding		contains									t(4;11)(q21;q23)	NULL		0	NULL	NULL	NULL	NULL	NULL	Expression of PKCβ1 and PKCβ2 isoforms was demonstrated in five B-ALL cell lines characterized by distinctive chromosomal translocations, and sensitivity to PKCβ-selective inhibition was examined. Inhibitor treatment resulted in a dose-dependent reduction in viability in all cell lines, although pro-B ALL with t(4;11)(q21;q23) was most sensitive.	topic_ll
77398	5	355972	7	NULL	NULL	0	NULL	 pro-B ALL 	MedicalFinding		is sensitive to					inhibitor	Chemical	treatment with			NULL		0	NULL	NULL	NULL	NULL	NULL	Expression of PKCβ1 and PKCβ2 isoforms was demonstrated in five B-ALL cell lines characterized by distinctive chromosomal translocations, and sensitivity to PKCβ-selective inhibition was examined. Inhibitor treatment resulted in a dose-dependent reduction in viability in all cell lines, although pro-B ALL with t(4;11)(q21;q23) was most sensitive.	topic_ll
77399	1	355973	7	NULL	NULL	0	NULL	PKCβ	GP	targeting	treatment for					B-ALL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	These results indicate that PKCβ targeting should be considered as a potential treatment option in B-ALL. NULL	topic_ll
77400	1	355975	7	NULL	NULL	0	NULL	oxidative stress	Process	increased	occur in					acute lymphoblastic leukemia	MedicalFinding	childhood			NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of anti-oxidant status and apoptosis on the induction phase of chemotherapy in childhood acute lymphoblastic leukemia.Our study showed that there was increased oxidative stress at diagnosis and after treatment with chemotherapy. 	topic_ll
77401	2	355975	7	NULL	NULL	0	NULL	statement 1	Process		occur during					diagnosis	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of anti-oxidant status and apoptosis on the induction phase of chemotherapy in childhood acute lymphoblastic leukemia.Our study showed that there was increased oxidative stress at diagnosis and after treatment with chemotherapy. 	topic_ll
77402	3	355975	7	NULL	NULL	0	NULL	statement 1	Process		occur after					chemotherapy	MedicalProcedure	treatment with			NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of anti-oxidant status and apoptosis on the induction phase of chemotherapy in childhood acute lymphoblastic leukemia.Our study showed that there was increased oxidative stress at diagnosis and after treatment with chemotherapy. 	topic_ll
77403	4	355975	7	NULL	NULL	0	NULL	statement 2	Process		occur along with					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of anti-oxidant status and apoptosis on the induction phase of chemotherapy in childhood acute lymphoblastic leukemia.Our study showed that there was increased oxidative stress at diagnosis and after treatment with chemotherapy. 	topic_ll
78053	1	355976	6	NULL	NULL	0	NULL	Mucinous carcinomas	MedicalFinding		accounts for					Breast cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mucinous carcinomas are a rare entity accounting for up to 2% of all breast cancers, which have been shown to display a gene expression profile distinct from that of invasive ductal carcinomas of no special type (IDC-NSTs)	topic_bc
78054	1	355977	6	NULL	NULL	0	NULL	PTEN gene	GP	mutation of	is found in					breast carcinoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Loss of heterozygosity (LOH) in loci of the 10q23 region that harbor the PTEN gene and mutations in the sequence of this gene have been found in several primary human tumors including breast carcinomas	topic_bc
78055	2	355977	6	NULL	NULL	0	NULL	PTEN	GP		is located on					chromosome 10q23					NULL		0	NULL	NULL	NULL	NULL	NULL	Loss of heterozygosity (LOH) in loci of the 10q23 region that harbor the PTEN gene and mutations in the sequence of this gene have been found in several primary human tumors including breast carcinomas	topic_bc
78056	1	355978	6	NULL	NULL	0	NULL	CDK inhibitors	Chemical		serve as					Breast cancer	MedicalFinding	therapeutics for			NULL		0	NULL	NULL	NULL	NULL	NULL	CDK inhibitors as potential breast cancer therapeutics: new evidence for enhanced efficacy in ER+ disease	topic_bc
78057	1	355979	6	NULL	NULL	0	NULL	CDK inhibitor	Chemical		inhibits					CDK	GP	function of 			NULL		0	NULL	NULL	NULL	NULL	NULL	A CDK (Cyclin-dependent kinase) inhibitor is a chemical that inhibits the function of CDKs	topic_bc
78058	2	355979	6	NULL	NULL	0	NULL	CDK	GP		is					Cyclin-dependent kinase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	A CDK (Cyclin-dependent kinase) inhibitor is a chemical that inhibits the function of CDKs	topic_bc
77404	1	355980	7	NULL	NULL	NULL	NULL	BD	MedicalFinding		associated with					neurocognitive deficits	MedicalFinding	significant			NULL		NULL	NULL	NULL	NULL	NULL	NULL	There is evidence that bipolar disorder (BD) is associated with significant neurocognitive deficits and this occurs in individuals with BD type I (BD I) and with BD type II (BD II). 	topic_bd
77405	2	355980	7	NULL	NULL	NULL	NULL	neurocognitive deficits	MedicalFinding	significant	occur in					BD I	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	There is evidence that bipolar disorder (BD) is associated with significant neurocognitive deficits and this occurs in individuals with BD type I (BD I) and with BD type II (BD II). 	topic_bd
77406	3	355980	7	NULL	NULL	NULL	NULL	neurocognitive deficits	MedicalFinding	significant	occur in					BD II	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	There is evidence that bipolar disorder (BD) is associated with significant neurocognitive deficits and this occurs in individuals with BD type I (BD I) and with BD type II (BD II). 	topic_bd
77407	4	355980	7	NULL	NULL	NULL	NULL	BD	MedicalFinding		is					bipolar disorder	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	There is evidence that bipolar disorder (BD) is associated with significant neurocognitive deficits and this occurs in individuals with BD type I (BD I) and with BD type II (BD II). 	topic_bd
77408	5	355980	7	NULL	NULL	0	NULL	BD I	MedicalFinding		is					BD type I	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	There is evidence that bipolar disorder (BD) is associated with significant neurocognitive deficits and this occurs in individuals with BD type I (BD I) and with BD type II (BD II). 	topic_bd
77409	6	355980	7	NULL	NULL	0	NULL	BD II	MedicalFinding		is					BD type II	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	There is evidence that bipolar disorder (BD) is associated with significant neurocognitive deficits and this occurs in individuals with BD type I (BD I) and with BD type II (BD II). 	topic_bd
77410	1	355981	7	NULL	NULL	0	NULL	Main cognitive deficits	MedicalFinding		observed in					BD II	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Main cognitive deficits found in BD II include working memory and some measures of executive functions (inhibitory control) and approximately half of the studies also detected verbal memory impairment.	topic_bd
77411	2	355981	7	NULL	NULL	0	NULL	statement 1	Process		include					working memory	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Main cognitive deficits found in BD II include working memory and some measures of executive functions (inhibitory control) and approximately half of the studies also detected verbal memory impairment.	topic_bd
77412	3	355981	7	NULL	NULL	0	NULL	statement 1	Process		include					verbal memory impairment	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Main cognitive deficits found in BD II include working memory and some measures of executive functions (inhibitory control) and approximately half of the studies also detected verbal memory impairment.	topic_bd
76832	1	355982	5	NULL	NULL	0	NULL	CNTNAP2 protein	GP		is active in					brain	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	CNTNAP2 encodes a protein active in the brain during development. One particular variant in the gene was first linked to autism in 2006. Later studies have also implicated CNTNAP2 variants in specific language impairment, ADHD, Tourette syndrome, and schizophrenia.	topic_aut
76833	2	355982	5	NULL	NULL	0	NULL	statement 1	Process		occurs during					development	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	CNTNAP2 encodes a protein active in the brain during development. One particular variant in the gene was first linked to autism in 2006. Later studies have also implicated CNTNAP2 variants in specific language impairment, ADHD, Tourette syndrome, and schizophrenia.	topic_aut
76834	3	355982	5	NULL	NULL	0	NULL	CNTNAP2 variant	GP		is linked to					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	CNTNAP2 encodes a protein active in the brain during development. One particular variant in the gene was first linked to autism in 2006. Later studies have also implicated CNTNAP2 variants in specific language impairment, ADHD, Tourette syndrome, and schizophrenia.	topic_aut
76835	4	355982	5	NULL	NULL	NULL	NULL	CNTNAP2 variant	GP		is implicated in					language impairment	MedicalFinding	specific			NULL		NULL	NULL	NULL	NULL	NULL	NULL	CNTNAP2 encodes a protein active in the brain during development. One particular variant in the gene was first linked to autism in 2006. Later studies have also implicated CNTNAP2 variants in specific language impairment, ADHD, Tourette syndrome, and schizophrenia.	topic_aut
76836	5	355982	5	NULL	NULL	0	NULL	CNTNAP2 variant	GP		is implicated in					ADHD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	CNTNAP2 encodes a protein active in the brain during development. One particular variant in the gene was first linked to autism in 2006. Later studies have also implicated CNTNAP2 variants in specific language impairment, ADHD, Tourette syndrome, and schizophrenia.	topic_aut
76837	6	355982	5	NULL	NULL	0	NULL	CNTNAP2 variant	GP		is implicated in					Tourette syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	CNTNAP2 encodes a protein active in the brain during development. One particular variant in the gene was first linked to autism in 2006. Later studies have also implicated CNTNAP2 variants in specific language impairment, ADHD, Tourette syndrome, and schizophrenia.	topic_aut
76838	7	355982	5	NULL	NULL	0	NULL	CNTNAP2 variant	GP		is implicated in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	CNTNAP2 encodes a protein active in the brain during development. One particular variant in the gene was first linked to autism in 2006. Later studies have also implicated CNTNAP2 variants in specific language impairment, ADHD, Tourette syndrome, and schizophrenia.	topic_aut
76839	1	355983	5	NULL	NULL	0	NULL	neuroligin-3 protein	GP		is involved in					autism	MedicalFinding	gene mutation of			NULL		0	NULL	NULL	NULL	NULL	NULL	At U.C. San Diego, lead researcher Dr. Palmer Taylor says autism’s gene mutation involves a protein called neuroligin-3, which appears to prevent normal communication between the nerves.	topic_aut
76840	2	355983	5	NULL	NULL	NULL	NULL	communication	Process	normal	is present between					nerves	OrganismPart				NULL		NULL	NULL	NULL	NULL	NULL	NULL	At U.C. San Diego, lead researcher Dr. Palmer Taylor says autism’s gene mutation involves a protein called neuroligin-3, which appears to prevent normal communication between the nerves.	topic_aut
76841	3	355983	5	NULL	NULL	0	NULL	neuroligin-3 protein	GP		prevent					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	At U.C. San Diego, lead researcher Dr. Palmer Taylor says autism’s gene mutation involves a protein called neuroligin-3, which appears to prevent normal communication between the nerves.	topic_aut
76842	1	355984	5	NULL	NULL	0	NULL	PTCHD1 gene	GP		is present in					X chromosome	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	The research data found that 1% of boys affected with ASD had mutations that are linked with the PTCHD1 gene on the X chromosome.	topic_aut
76843	2	355984	5	NULL	NULL	0	NULL	PTCHD1 gene	GP	mutation of	is linked to					ASD	MedicalFinding				NULL	boys	0	NULL	NULL	NULL	NULL	NULL	The research data found that 1% of boys affected with ASD had mutations that are linked with the PTCHD1 gene on the X chromosome.	topic_aut
77413	1	355985	7	NULL	NULL	0	NULL	 hypovitaminosis D	MedicalFinding		associated with					basic cognitive functions	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Several studies suggest an association between hypovitaminosis D and basic and executive cognitive functions, depression, bipolar disorder, and schizophrenia.	topic_bd
77414	2	355985	7	NULL	NULL	0	NULL	hypovitaminosis D	MedicalFinding		associated with					executive cognitive functions	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Several studies suggest an association between hypovitaminosis D and basic and executive cognitive functions, depression, bipolar disorder, and schizophrenia.	topic_bd
77415	3	355985	7	NULL	NULL	0	NULL	hypovitaminosis D	MedicalFinding		associated with					depression	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Several studies suggest an association between hypovitaminosis D and basic and executive cognitive functions, depression, bipolar disorder, and schizophrenia.	topic_bd
77416	4	355985	7	NULL	NULL	0	NULL	hypovitaminosis D	MedicalFinding		associated with					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Several studies suggest an association between hypovitaminosis D and basic and executive cognitive functions, depression, bipolar disorder, and schizophrenia.	topic_bd
77417	5	355985	7	NULL	NULL	0	NULL	hypovitaminosis D	MedicalFinding		associated with					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Several studies suggest an association between hypovitaminosis D and basic and executive cognitive functions, depression, bipolar disorder, and schizophrenia.	topic_bd
76844	1	355986	5	NULL	NULL	0	NULL	gene	GP	certain versions of	is present in					chromosome 7	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	In the inherited form of risk, people with autism were more prone than healthy controls to have certain versions of a gene on Chromosome 7	topic_aut
76845	2	355986	5	NULL	NULL	NULL	NULL	healthy control	Organism		contains					statement 1	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	In the inherited form of risk, people with autism were more prone than healthy controls to have certain versions of a gene on Chromosome 7	topic_aut
76846	3	355986	5	NULL	NULL	NULL	NULL	autistic people	GroupOfPeople		contains					statement 1	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	In the inherited form of risk, people with autism were more prone than healthy controls to have certain versions of a gene on Chromosome 7	topic_aut
76847	4	355986	5	NULL	NULL	0	NULL	statement 3	Process		more prone than					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In the inherited form of risk, people with autism were more prone than healthy controls to have certain versions of a gene on Chromosome 7	topic_aut
76848	1	355987	5	NULL	NULL	0	NULL	gene	GP		is missing on					chromosome 16	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	In the spontaneous form, one percent of autism was traced to a conspicuous 'hot spot' of missing or duplicated genes on Chromosome 16.	topic_aut
76849	2	355987	5	NULL	NULL	0	NULL	gene	GP		is duplicated on					chromosome 16	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	In the spontaneous form, one percent of autism was traced to a conspicuous 'hot spot' of missing or duplicated genes on Chromosome 16.	topic_aut
76850	3	355987	5	NULL	NULL	0	NULL	autism	MedicalFinding	one percent of	is traced to					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In the spontaneous form, one percent of autism was traced to a conspicuous 'hot spot' of missing or duplicated genes on Chromosome 16.	topic_aut
76851	4	355987	5	NULL	NULL	0	NULL	autism	MedicalFinding	one percent of	is traced to					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In the spontaneous form, one percent of autism was traced to a conspicuous 'hot spot' of missing or duplicated genes on Chromosome 16.	topic_aut
76852	5	355987	5	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In the spontaneous form, one percent of autism was traced to a conspicuous 'hot spot' of missing or duplicated genes on Chromosome 16.	topic_aut
76853	1	355989	5	NULL	NULL	0	NULL	CNTNAP2	GP		is present in					chromosome 7	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	Also drawing upon the AGRE resource, three other teams of researchers independently linked inherited variation in a gene on Chromosome 7, called CNTNAP2, with autism. 	topic_aut
76854	2	355989	5	NULL	NULL	0	NULL	CNTNAP2	GP		is linked to					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Also drawing upon the AGRE resource, three other teams of researchers independently linked inherited variation in a gene on Chromosome 7, called CNTNAP2, with autism. 	topic_aut
77418	1	355990	7	NULL	NULL	0	NULL	Ion dysregulation	Process		involved in		may be			bipolar illness	MedicalFinding	pathophysiology of			NULL		0	NULL	NULL	NULL	NULL	NULL	Ion dysregulation is thought to be involved in the pathophysiology of bipolar illness, suggesting that memantine may be effective in treating bipolar manic and/or depressive episodes. 	topic_bd
77419	2	355990	7	NULL	NULL	0	NULL	memantine	Chemical		effective in		may be			bipolar manic episode	MedicalFinding	treating			NULL		0	NULL	NULL	NULL	NULL	NULL	Ion dysregulation is thought to be involved in the pathophysiology of bipolar illness, suggesting that memantine may be effective in treating bipolar manic and/or depressive episodes. 	topic_bd
77420	3	355990	7	NULL	NULL	0	NULL	memantine	Chemical		effective in		may be			bipolar depressive episodes	MedicalFinding	treating			NULL		0	NULL	NULL	NULL	NULL	NULL	Ion dysregulation is thought to be involved in the pathophysiology of bipolar illness, suggesting that memantine may be effective in treating bipolar manic and/or depressive episodes. 	topic_bd
77421	4	355990	7	NULL	NULL	0	NULL	statement 1	Process		suggest					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Ion dysregulation is thought to be involved in the pathophysiology of bipolar illness, suggesting that memantine may be effective in treating bipolar manic and/or depressive episodes. 	topic_bd
77422	5	355990	7	NULL	NULL	0	NULL	statement 1	Process		suggest					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Ion dysregulation is thought to be involved in the pathophysiology of bipolar illness, suggesting that memantine may be effective in treating bipolar manic and/or depressive episodes. 	topic_bd
76855	1	355991	5	NULL	NULL	0	NULL	NCAM2	GP		is					neural cell adhesion molecule 2	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	One of the new genes identified was neural cell adhesion molecule 2 (NCAM2). NCAM2 is expressed in the hippocampus of the human brain -- a region previously associated with autism.	topic_aut
76856	3	355991	5	NULL	NULL	NULL	NULL	NCAM2	GP		expressed in					statement 2	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	One of the new genes identified was neural cell adhesion molecule 2 (NCAM2). NCAM2 is expressed in the hippocampus of the human brain -- a region previously associated with autism.	topic_aut
76857	2	355991	5	NULL	NULL	0	NULL	hippocampus	OrganismPart	human	is present in					brain	OrganismPart	human			NULL		0	NULL	NULL	NULL	NULL	NULL	One of the new genes identified was neural cell adhesion molecule 2 (NCAM2). NCAM2 is expressed in the hippocampus of the human brain -- a region previously associated with autism.	topic_aut
76858	4	355991	5	NULL	NULL	0	NULL	statement 2	Process		is associated with		previously			autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	One of the new genes identified was neural cell adhesion molecule 2 (NCAM2). NCAM2 is expressed in the hippocampus of the human brain -- a region previously associated with autism.	topic_aut
77423	1	355992	7	NULL	NULL	0	NULL	 hippocampal slices	OrganismPart	rat	treated with					ouabain 	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	In a second model of bipolar disorder, cycling between population spikes and epileptiform bursts was investigated in rat hippocampal slices treated with ouabain (3.3μM) alone or in combination with memantine (0.5, 1.0, and 5.0μM). Ouabain-induced hyperlocomotion was normalized with acute and chronic lithium and chronic use of memantine. Memantine delayed the onset of ouabain-induced-cycling in hippocampal slices. Memantine may have antimanic properties.	topic_bd
77424	2	355992	7	NULL	NULL	0	NULL	population spikes 	MedicalFinding		cycle between					epileptiform bursts	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In a second model of bipolar disorder, cycling between population spikes and epileptiform bursts was investigated in rat hippocampal slices treated with ouabain (3.3μM) alone or in combination with memantine (0.5, 1.0, and 5.0μM). Ouabain-induced hyperlocomotion was normalized with acute and chronic lithium and chronic use of memantine. Memantine delayed the onset of ouabain-induced-cycling in hippocampal slices. Memantine may have antimanic properties.	topic_bd
77425	3	355992	7	NULL	NULL	0	NULL	statement 2	Process		occur upon					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In a second model of bipolar disorder, cycling between population spikes and epileptiform bursts was investigated in rat hippocampal slices treated with ouabain (3.3μM) alone or in combination with memantine (0.5, 1.0, and 5.0μM). Ouabain-induced hyperlocomotion was normalized with acute and chronic lithium and chronic use of memantine. Memantine delayed the onset of ouabain-induced-cycling in hippocampal slices. Memantine may have antimanic properties.	topic_bd
77426	4	355992	7	NULL	NULL	0	NULL	statement 1	Process		treated with					memantine 	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	In a second model of bipolar disorder, cycling between population spikes and epileptiform bursts was investigated in rat hippocampal slices treated with ouabain (3.3μM) alone or in combination with memantine (0.5, 1.0, and 5.0μM). Ouabain-induced hyperlocomotion was normalized with acute and chronic lithium and chronic use of memantine. Memantine delayed the onset of ouabain-induced-cycling in hippocampal slices. Memantine may have antimanic properties.	topic_bd
77427	5	355992	7	NULL	NULL	0	NULL	statement 2	Process		occur upon					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In a second model of bipolar disorder, cycling between population spikes and epileptiform bursts was investigated in rat hippocampal slices treated with ouabain (3.3μM) alone or in combination with memantine (0.5, 1.0, and 5.0μM). Ouabain-induced hyperlocomotion was normalized with acute and chronic lithium and chronic use of memantine. Memantine delayed the onset of ouabain-induced-cycling in hippocampal slices. Memantine may have antimanic properties.	topic_bd
77428	6	355992	7	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In a second model of bipolar disorder, cycling between population spikes and epileptiform bursts was investigated in rat hippocampal slices treated with ouabain (3.3μM) alone or in combination with memantine (0.5, 1.0, and 5.0μM). Ouabain-induced hyperlocomotion was normalized with acute and chronic lithium and chronic use of memantine. Memantine delayed the onset of ouabain-induced-cycling in hippocampal slices. Memantine may have antimanic properties.	topic_bd
77429	7	355992	7	NULL	NULL	0	NULL	Ouabain	GP		induce					hyperlocomotion	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In a second model of bipolar disorder, cycling between population spikes and epileptiform bursts was investigated in rat hippocampal slices treated with ouabain (3.3μM) alone or in combination with memantine (0.5, 1.0, and 5.0μM). Ouabain-induced hyperlocomotion was normalized with acute and chronic lithium and chronic use of memantine. Memantine delayed the onset of ouabain-induced-cycling in hippocampal slices. Memantine may have antimanic properties.	topic_bd
77430	8	355992	7	NULL	NULL	0	NULL	statement 7	Process		normalized with					acute lithium	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	In a second model of bipolar disorder, cycling between population spikes and epileptiform bursts was investigated in rat hippocampal slices treated with ouabain (3.3μM) alone or in combination with memantine (0.5, 1.0, and 5.0μM). Ouabain-induced hyperlocomotion was normalized with acute and chronic lithium and chronic use of memantine. Memantine delayed the onset of ouabain-induced-cycling in hippocampal slices. Memantine may have antimanic properties.	topic_bd
77431	9	355992	7	NULL	NULL	0	NULL	statement 7	Process		normalized with					chronic lithium	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	In a second model of bipolar disorder, cycling between population spikes and epileptiform bursts was investigated in rat hippocampal slices treated with ouabain (3.3μM) alone or in combination with memantine (0.5, 1.0, and 5.0μM). Ouabain-induced hyperlocomotion was normalized with acute and chronic lithium and chronic use of memantine. Memantine delayed the onset of ouabain-induced-cycling in hippocampal slices. Memantine may have antimanic properties.	topic_bd
77432	10	355992	7	NULL	NULL	0	NULL	statement 7	Process		normalized with					memantine 	Chemical	chronic use of			NULL		0	NULL	NULL	NULL	NULL	NULL	In a second model of bipolar disorder, cycling between population spikes and epileptiform bursts was investigated in rat hippocampal slices treated with ouabain (3.3μM) alone or in combination with memantine (0.5, 1.0, and 5.0μM). Ouabain-induced hyperlocomotion was normalized with acute and chronic lithium and chronic use of memantine. Memantine delayed the onset of ouabain-induced-cycling in hippocampal slices. Memantine may have antimanic properties.	topic_bd
77433	11	355992	7	NULL	NULL	0	NULL	ouabain	GP		induce					cycling	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In a second model of bipolar disorder, cycling between population spikes and epileptiform bursts was investigated in rat hippocampal slices treated with ouabain (3.3μM) alone or in combination with memantine (0.5, 1.0, and 5.0μM). Ouabain-induced hyperlocomotion was normalized with acute and chronic lithium and chronic use of memantine. Memantine delayed the onset of ouabain-induced-cycling in hippocampal slices. Memantine may have antimanic properties.	topic_bd
77434	12	355992	7	NULL	NULL	0	NULL	statement 11	Process		occur in					hippocampal slices	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	In a second model of bipolar disorder, cycling between population spikes and epileptiform bursts was investigated in rat hippocampal slices treated with ouabain (3.3μM) alone or in combination with memantine (0.5, 1.0, and 5.0μM). Ouabain-induced hyperlocomotion was normalized with acute and chronic lithium and chronic use of memantine. Memantine delayed the onset of ouabain-induced-cycling in hippocampal slices. Memantine may have antimanic properties.	topic_bd
77435	13	355992	7	NULL	NULL	0	NULL	Memantine 	Chemical		delays					statement 11	Process	onset of			NULL		0	NULL	NULL	NULL	NULL	NULL	In a second model of bipolar disorder, cycling between population spikes and epileptiform bursts was investigated in rat hippocampal slices treated with ouabain (3.3μM) alone or in combination with memantine (0.5, 1.0, and 5.0μM). Ouabain-induced hyperlocomotion was normalized with acute and chronic lithium and chronic use of memantine. Memantine delayed the onset of ouabain-induced-cycling in hippocampal slices. Memantine may have antimanic properties.	topic_bd
77436	14	355992	7	NULL	NULL	0	NULL	Memantine	Chemical		have		may			antimanic properties	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In a second model of bipolar disorder, cycling between population spikes and epileptiform bursts was investigated in rat hippocampal slices treated with ouabain (3.3μM) alone or in combination with memantine (0.5, 1.0, and 5.0μM). Ouabain-induced hyperlocomotion was normalized with acute and chronic lithium and chronic use of memantine. Memantine delayed the onset of ouabain-induced-cycling in hippocampal slices. Memantine may have antimanic properties.	topic_bd
77437	1	355993	7	NULL	NULL	0	NULL	cannabis 	Organism	excessive	associated with					bipolar disorder	MedicalFinding	earlier age at onset			NULL		0	NULL	NULL	NULL	NULL	NULL	Excessive cannabis use is associated with earlier age at onset in bipolar disorder.	topic_bd
76859	1	355994	5	NULL	NULL	0	NULL	chemical fingerprint	Chemical		is present in					autistic children	GroupOfPeople				NULL	urine	0	NULL	NULL	NULL	NULL	NULL	Children with autism have a different chemical fingerprint in their urine than non-autistic children, according to new research published tomorrow in the print edition of the Journal of Proteome Research	topic_aut
76860	2	355994	5	NULL	NULL	0	NULL	chemical fingerprint	Chemical		is present in					non-autistic children	GroupOfPeople				NULL	urine	0	NULL	NULL	NULL	NULL	NULL	Children with autism have a different chemical fingerprint in their urine than non-autistic children, according to new research published tomorrow in the print edition of the Journal of Proteome Research	topic_aut
76861	3	355994	5	NULL	NULL	0	NULL	statement 1	Process		different from					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Children with autism have a different chemical fingerprint in their urine than non-autistic children, according to new research published tomorrow in the print edition of the Journal of Proteome Research	topic_aut
77438	1	355995	7	NULL	NULL	0	NULL	bipolar disorder	MedicalFinding	early onset of	increase		may			cannabis	Organism	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	This indicates that an early onset may increase the risk of cannabis use and that cannabis use may trigger bipolar disorder in vulnerable individuals.	topic_bd
77439	2	355995	7	NULL	NULL	0	NULL	cannabis	Organism		trigger		may			bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	This indicates that an early onset may increase the risk of cannabis use and that cannabis use may trigger bipolar disorder in vulnerable individuals.	topic_bd
76915	1	355996	5	NULL	NULL	NULL	NULL	diarrhea	MedicalFinding		is not associated with					ASDs	MedicalFinding				NULL	children	NULL	NULL	NULL	NULL	NULL	NULL	Parents of children and adolescents with autism spectrum disorders (ASDs) sometimes report that their children suffer from gastrointestinal (GI) symptoms, such as diarrhea and constipation. However, studies on how prevalent these symptoms are have had conflicting results.	topic_aut
76916	2	355996	5	NULL	NULL	NULL	NULL	diarrhea	MedicalFinding		is not associated with					ASDs	MedicalFinding				NULL	adolescents	NULL	NULL	NULL	NULL	NULL	NULL	Parents of children and adolescents with autism spectrum disorders (ASDs) sometimes report that their children suffer from gastrointestinal (GI) symptoms, such as diarrhea and constipation. However, studies on how prevalent these symptoms are have had conflicting results.	topic_aut
76917	3	355996	5	NULL	NULL	NULL	NULL	constipation	MedicalFinding		is not associated with					ASDs	MedicalFinding				NULL	children	NULL	NULL	NULL	NULL	NULL	NULL	Parents of children and adolescents with autism spectrum disorders (ASDs) sometimes report that their children suffer from gastrointestinal (GI) symptoms, such as diarrhea and constipation. However, studies on how prevalent these symptoms are have had conflicting results.	topic_aut
76918	4	355996	5	NULL	NULL	NULL	NULL	constipation	MedicalFinding		is not associated with					ASDs	MedicalFinding				NULL	adolescents	NULL	NULL	NULL	NULL	NULL	NULL	Parents of children and adolescents with autism spectrum disorders (ASDs) sometimes report that their children suffer from gastrointestinal (GI) symptoms, such as diarrhea and constipation. However, studies on how prevalent these symptoms are have had conflicting results.	topic_aut
76919	5	355996	5	NULL	NULL	0	NULL	ASDs	MedicalFinding		is					autism spectrum disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Parents of children and adolescents with autism spectrum disorders (ASDs) sometimes report that their children suffer from gastrointestinal (GI) symptoms, such as diarrhea and constipation. However, studies on how prevalent these symptoms are have had conflicting results.	topic_aut
76920	6	355996	5	NULL	NULL	0	NULL	GI	OrganismPart		is					gastrointestinal	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Parents of children and adolescents with autism spectrum disorders (ASDs) sometimes report that their children suffer from gastrointestinal (GI) symptoms, such as diarrhea and constipation. However, studies on how prevalent these symptoms are have had conflicting results.	topic_aut
76921	7	355996	5	NULL	NULL	0	NULL	diarrhea	MedicalFinding		is a type of					GI symptom	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Parents of children and adolescents with autism spectrum disorders (ASDs) sometimes report that their children suffer from gastrointestinal (GI) symptoms, such as diarrhea and constipation. However, studies on how prevalent these symptoms are have had conflicting results.	topic_aut
76922	8	355996	5	NULL	NULL	0	NULL	constipation	MedicalFinding		is a type of					GI symptom	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Parents of children and adolescents with autism spectrum disorders (ASDs) sometimes report that their children suffer from gastrointestinal (GI) symptoms, such as diarrhea and constipation. However, studies on how prevalent these symptoms are have had conflicting results.	topic_aut
76923	1	355997	5	NULL	NULL	0	NULL	ASDs	MedicalFinding		is					autism spectrum disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Reports have suggested that sleep problems in children and adolescents with autism spectrum disorders (ASDs) are associated with challenging daytime behaviors.	topic_aut
76924	2	355997	5	NULL	NULL	0	NULL	ASDs children	GroupOfPeople		suffer from					sleep problems	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Reports have suggested that sleep problems in children and adolescents with autism spectrum disorders (ASDs) are associated with challenging daytime behaviors.	topic_aut
76925	3	355997	5	NULL	NULL	0	NULL	statement 2	Process		is associated with					daytime behaviors	MentalProcess	challenging			NULL		0	NULL	NULL	NULL	NULL	NULL	Reports have suggested that sleep problems in children and adolescents with autism spectrum disorders (ASDs) are associated with challenging daytime behaviors.	topic_aut
76926	4	355997	5	NULL	NULL	0	NULL	ASDs adolescents	GroupOfPeople		suffer from					sleep problems	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Reports have suggested that sleep problems in children and adolescents with autism spectrum disorders (ASDs) are associated with challenging daytime behaviors.	topic_aut
76927	5	355997	5	NULL	NULL	0	NULL	statement 4	Process		is associated with					daytime behaviors	MentalProcess	challenging			NULL		0	NULL	NULL	NULL	NULL	NULL	Reports have suggested that sleep problems in children and adolescents with autism spectrum disorders (ASDs) are associated with challenging daytime behaviors.	topic_aut
77440	1	355998	7	NULL	NULL	0	NULL	neuroplasticity	MedicalFinding	changes in	neuropathological findings in					BD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Recent data suggest that changes in neuroplasticity, cell resilience and connectivity are the main neuropathological findings in BD.	topic_bd
77441	2	355998	7	NULL	NULL	0	NULL	cell resilience	Process	changes in	neuropathological findings in					BD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Recent data suggest that changes in neuroplasticity, cell resilience and connectivity are the main neuropathological findings in BD.	topic_bd
77442	3	355998	7	NULL	NULL	NULL	NULL	cell connectivity 	Process	changes in	neuropathological findings in					BD	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Recent data suggest that changes in neuroplasticity, cell resilience and connectivity are the main neuropathological findings in BD.	topic_bd
77443	1	355999	7	NULL	NULL	0	NULL	nephrotic syndrome	MedicalFinding		occur during					 induction chemotherapy	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	This report is the first to document minimal change nephrotic syndrome occurring during induction chemotherapy for childhood acute lymphoblastic leukemia (ALL). 	topic_ll
77444	2	355999	7	NULL	NULL	0	NULL	statement 1	Process		occur upon					ALL	MedicalFinding	childhood			NULL		0	NULL	NULL	NULL	NULL	NULL	This report is the first to document minimal change nephrotic syndrome occurring during induction chemotherapy for childhood acute lymphoblastic leukemia (ALL). 	topic_ll
77445	3	355999	7	NULL	NULL	0	NULL	ALL	MedicalFinding		is					acute lymphoblastic leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	This report is the first to document minimal change nephrotic syndrome occurring during induction chemotherapy for childhood acute lymphoblastic leukemia (ALL). 	topic_ll
77446	1	356001	7	NULL	NULL	0	NULL	immune cell dysregulation	Process		central to					nephrotic syndrome	MedicalFinding	pathogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	This occurrence lends further support to the theory of immune cell dysregulation being central to the pathogenesis of nephrotic syndrome in ALL	topic_ll
77447	2	356001	7	NULL	NULL	0	NULL	statement 1	Process		occur in					ALL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	This occurrence lends further support to the theory of immune cell dysregulation being central to the pathogenesis of nephrotic syndrome in ALL	topic_ll
77448	1	356002	7	NULL	NULL	0	NULL	GSK-3	GP		helps in					apoptosis	Process	regulating			NULL		0	NULL	NULL	NULL	NULL	NULL	Among many other things, GSK-3 helps regulate programmed cell death (apoptosis).	topic_bd
77449	2	356002	7	NULL	NULL	0	NULL	apoptosis	Process		is					programmed cell death	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Among many other things, GSK-3 helps regulate programmed cell death (apoptosis).	topic_bd
76928	1	356003	5	NULL	NULL	0	NULL	healthy children	GroupOfPeople		deficient in					tryptophan	AminoAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	This method is precise and sensitive for the detection of low concentrations of tryptophan and can be applicable to monitoring its level in human urine. Children with autism have a higher deficiency of tryptophan than the control group of healthy children	topic_aut
76929	2	356003	5	NULL	NULL	0	NULL	autistic children	GroupOfPeople		deficient in					tryptophan	AminoAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	This method is precise and sensitive for the detection of low concentrations of tryptophan and can be applicable to monitoring its level in human urine. Children with autism have a higher deficiency of tryptophan than the control group of healthy children	topic_aut
76930	3	356003	5	NULL	NULL	0	NULL	statement 2	Process		is higher than					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	This method is precise and sensitive for the detection of low concentrations of tryptophan and can be applicable to monitoring its level in human urine. Children with autism have a higher deficiency of tryptophan than the control group of healthy children	topic_aut
76931	1	356004	5	NULL	NULL	0	NULL	depression	MedicalFinding	mild	is a symptom of					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Lower levels of tryptophan may lead to the worsening of autistic symptoms such as mild depression and increased irritability.	topic_aut
76932	2	356004	5	NULL	NULL	0	NULL	irritability	MedicalFinding	increased	is a symptom of					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Lower levels of tryptophan may lead to the worsening of autistic symptoms such as mild depression and increased irritability.	topic_aut
76933	3	356004	5	NULL	NULL	0	NULL	tryptophan	AminoAcid	lower levels of	worsens					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Lower levels of tryptophan may lead to the worsening of autistic symptoms such as mild depression and increased irritability.	topic_aut
76934	4	356004	5	NULL	NULL	0	NULL	tryptophan	AminoAcid	lower levels of	worsens					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Lower levels of tryptophan may lead to the worsening of autistic symptoms such as mild depression and increased irritability.	topic_aut
76959	1	356005	5	NULL	NULL	0	NULL	HVA	Chemical		is present in					autistic children	GroupOfPeople	urine of			NULL		0	NULL	NULL	NULL	NULL	NULL	The levels of HVA and VMA were higher in the urine of autistic children (28.8+/-15.5 micromol/mmol creatinine and 22.2+/-13.0 micromol/mmol creatinine, respectively) compared with those of the generally healthy children (4.6+/-0.7 micromol/mmol creatinine for HVA and 3.8+/-0.6 micromol/mmol creatinine for VMA).	topic_aut
76960	2	356005	5	NULL	NULL	0	NULL	HVA	Chemical		is present in					healthy children	GroupOfPeople	urine of			NULL		0	NULL	NULL	NULL	NULL	NULL	The levels of HVA and VMA were higher in the urine of autistic children (28.8+/-15.5 micromol/mmol creatinine and 22.2+/-13.0 micromol/mmol creatinine, respectively) compared with those of the generally healthy children (4.6+/-0.7 micromol/mmol creatinine for HVA and 3.8+/-0.6 micromol/mmol creatinine for VMA).	topic_aut
76961	3	356005	5	NULL	NULL	0	NULL	statement 1	Process	level of	is higher than					statement 2	Process	levels of			NULL		0	NULL	NULL	NULL	NULL	NULL	The levels of HVA and VMA were higher in the urine of autistic children (28.8+/-15.5 micromol/mmol creatinine and 22.2+/-13.0 micromol/mmol creatinine, respectively) compared with those of the generally healthy children (4.6+/-0.7 micromol/mmol creatinine for HVA and 3.8+/-0.6 micromol/mmol creatinine for VMA).	topic_aut
76962	4	356005	5	NULL	NULL	0	NULL	VMA	Chemical		is present in					autistic children	GroupOfPeople	urine of			NULL		0	NULL	NULL	NULL	NULL	NULL	The levels of HVA and VMA were higher in the urine of autistic children (28.8+/-15.5 micromol/mmol creatinine and 22.2+/-13.0 micromol/mmol creatinine, respectively) compared with those of the generally healthy children (4.6+/-0.7 micromol/mmol creatinine for HVA and 3.8+/-0.6 micromol/mmol creatinine for VMA).	topic_aut
76963	5	356005	5	NULL	NULL	0	NULL	VMA	Chemical		is present in					healthy children	GroupOfPeople	urine of			NULL		0	NULL	NULL	NULL	NULL	NULL	The levels of HVA and VMA were higher in the urine of autistic children (28.8+/-15.5 micromol/mmol creatinine and 22.2+/-13.0 micromol/mmol creatinine, respectively) compared with those of the generally healthy children (4.6+/-0.7 micromol/mmol creatinine for HVA and 3.8+/-0.6 micromol/mmol creatinine for VMA).	topic_aut
76964	6	356005	5	NULL	NULL	0	NULL	statement 4	Process	level of	is higher than					statement 5	Process	level of			NULL		0	NULL	NULL	NULL	NULL	NULL	The levels of HVA and VMA were higher in the urine of autistic children (28.8+/-15.5 micromol/mmol creatinine and 22.2+/-13.0 micromol/mmol creatinine, respectively) compared with those of the generally healthy children (4.6+/-0.7 micromol/mmol creatinine for HVA and 3.8+/-0.6 micromol/mmol creatinine for VMA).	topic_aut
76965	1	356006	5	NULL	NULL	0	NULL	dopamine metabolism disorder	MedicalFinding		is present in					autistic children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Quantification of urinary homovanillic acid (HVA) and vanillylmandelic acid (VMA) can be a very important tool in the study of disorders of dopamine metabolism in autistic children	topic_aut
76966	2	356006	5	NULL	NULL	NULL	NULL	HVA	Chemical	quantification of;;urinary	plays a role in		may			statement 1	Process	study of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Quantification of urinary homovanillic acid (HVA) and vanillylmandelic acid (VMA) can be a very important tool in the study of disorders of dopamine metabolism in autistic children	topic_aut
76967	3	356006	5	NULL	NULL	NULL	NULL	VMA	Chemical	quantification of;;urinary	plays a role in		may			statement 1	Process	study of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Quantification of urinary homovanillic acid (HVA) and vanillylmandelic acid (VMA) can be a very important tool in the study of disorders of dopamine metabolism in autistic children	topic_aut
76968	4	356006	5	NULL	NULL	0	NULL	VMA	Chemical		is					vanillylmandelic acid	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Quantification of urinary homovanillic acid (HVA) and vanillylmandelic acid (VMA) can be a very important tool in the study of disorders of dopamine metabolism in autistic children	topic_aut
76969	5	356006	5	NULL	NULL	0	NULL	HVA	Chemical		is					homovanillic acid	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Quantification of urinary homovanillic acid (HVA) and vanillylmandelic acid (VMA) can be a very important tool in the study of disorders of dopamine metabolism in autistic children	topic_aut
76970	1	356007	5	NULL	NULL	0	NULL	VMA	Chemical		is					Vanillyl mandelic acid	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Vanillyl mandelic acid (VMA) is an end-stage metabolite of the catecholamines epinephrine and norepinephrine. It is produced via intermediary metabolites	topic_aut
76971	2	356007	5	NULL	NULL	0	NULL	epinephrine	Chemical		is a type of					catecholamines	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Vanillyl mandelic acid (VMA) is an end-stage metabolite of the catecholamines epinephrine and norepinephrine. It is produced via intermediary metabolites	topic_aut
76972	3	356007	5	NULL	NULL	0	NULL	norepinephrine	Chemical		is a type of					catecholamines	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Vanillyl mandelic acid (VMA) is an end-stage metabolite of the catecholamines epinephrine and norepinephrine. It is produced via intermediary metabolites	topic_aut
76973	4	356007	5	NULL	NULL	0	NULL	VMA	Chemical		is an end-stage metabolite of					epinephrine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Vanillyl mandelic acid (VMA) is an end-stage metabolite of the catecholamines epinephrine and norepinephrine. It is produced via intermediary metabolites	topic_aut
76974	5	356007	5	NULL	NULL	0	NULL	VMA	Chemical		is an end-stage metabolite of					norepinephrine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Vanillyl mandelic acid (VMA) is an end-stage metabolite of the catecholamines epinephrine and norepinephrine. It is produced via intermediary metabolites	topic_aut
76975	1	356008	5	NULL	NULL	0	NULL	(HOC6H3(OCH3)CH2COOH	Chemical		is					Homovanillic acid	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Homovanillic acid (HOC6H3(OCH3)CH2COOH;  is a major catecholamine metabolite.	topic_aut
76976	2	356008	5	NULL	NULL	0	NULL	Homovanillic acid	Chemical		is a metabolite of					catecholamine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Homovanillic acid (HOC6H3(OCH3)CH2COOH;  is a major catecholamine metabolite.	topic_aut
76977	1	356009	5	NULL	NULL	0	NULL	ASD	MedicalFinding		is					autistic spectrum disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Insomnia is the predominant sleep concern in children with autistic spectrum disorder (ASD)	topic_aut
76978	2	356009	5	NULL	NULL	0	NULL	Insomnia	MedicalFinding		is a symptom of					ASD children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Insomnia is the predominant sleep concern in children with autistic spectrum disorder (ASD)	topic_aut
76984	1	356010	5	NULL	NULL	NULL	NULL	melatonin	GP	low concentration of	is caused by					acetylserotonin methyltransferase activity	Process	primary deficit in			NULL		NULL	NULL	NULL	NULL	NULL	NULL	A recent study using a combination of genetic and functional experimental techniques reported evidence that low melatonin concentration caused by a primary deficit in acetylserotonin methyltransferase activity is a risk factor for ASD	topic_aut
76998	2	356010	5	NULL	NULL	0	NULL	statement 1	Process		is a risk factor for					ASD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	A recent study using a combination of genetic and functional experimental techniques reported evidence that low melatonin concentration caused by a primary deficit in acetylserotonin methyltransferase activity is a risk factor for ASD	topic_aut
76999	1	356011	5	NULL	NULL	NULL	NULL	repetitive behavior	MedicalFinding		is a symptom of					autism spectrum disorders	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Results of this trial do not support the use of citalopram for the treatment of repetitive behavior in children and adolescents with autism spectrum disorders	topic_aut
77000	2	356011	5	NULL	NULL	NULL	NULL	citalopram	Chemical		does not treat					statement 1	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Results of this trial do not support the use of citalopram for the treatment of repetitive behavior in children and adolescents with autism spectrum disorders	topic_aut
77001	3	356011	5	NULL	NULL	0	NULL	statement 1	MedicalFinding		occurs in					children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Results of this trial do not support the use of citalopram for the treatment of repetitive behavior in children and adolescents with autism spectrum disorders	topic_aut
77002	4	356011	5	NULL	NULL	0	NULL	statement 2	MedicalFinding		occurs in					adolescents	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Results of this trial do not support the use of citalopram for the treatment of repetitive behavior in children and adolescents with autism spectrum disorders	topic_aut
77451	1	356012	7	NULL	NULL	0	NULL	memantine	Chemical		have		may			antimanic properties	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Memantine may have antimanic properties.	topic_bd
78059	1	356015	6	NULL	NULL	NULL	NULL	 zoledronic acid	Chemical		improves					premenopausal patients	Person	survival of 			NULL		NULL	NULL	NULL	NULL	NULL	NULL	The addition of zoledronic acid to adjuvant endocrine therapy improves disease-free survival in premenopausal patients with estrogen-responsive early breast cancer.	topic_bc
78181	1	356016	6	NULL	NULL	0	NULL	tamoxifen	Chemical		decrease					Breast cancer	MedicalFinding	mortality from			NULL		0	NULL	NULL	NULL	NULL	NULL	Endocrine therapies targeting oestrogen action (anti-oestrogens, such as tamoxifen, and aromatase inhibitors) decrease mortality from breast cancer, but their efficacy is limited by intrinsic and acquired therapeutic resistance.	topic_bc
78182	2	356016	6	NULL	NULL	0	NULL	aromatase inhibitor	Chemical		decrease					Breast cancer	MedicalFinding	mortality from			NULL		0	NULL	NULL	NULL	NULL	NULL	Endocrine therapies targeting oestrogen action (anti-oestrogens, such as tamoxifen, and aromatase inhibitors) decrease mortality from breast cancer, but their efficacy is limited by intrinsic and acquired therapeutic resistance.	topic_bc
78183	3	356016	6	NULL	NULL	0	NULL	tamoxifen	Chemical		is a type of					anti-estrogen	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Endocrine therapies targeting oestrogen action (anti-oestrogens, such as tamoxifen, and aromatase inhibitors) decrease mortality from breast cancer, but their efficacy is limited by intrinsic and acquired therapeutic resistance.	topic_bc
78184	4	356016	6	NULL	NULL	0	NULL	aromatase inhibitor	Chemical		is a type of					anti-oestrogen	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Endocrine therapies targeting oestrogen action (anti-oestrogens, such as tamoxifen, and aromatase inhibitors) decrease mortality from breast cancer, but their efficacy is limited by intrinsic and acquired therapeutic resistance.	topic_bc
78060	1	356017	6	NULL	NULL	0	NULL	Oestrogen	Chemical		causes					epithelium	OrganismPart	hyperproliferation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Oestrogen predominance over progesterone may cause hyperproliferation of mammary epithelium and thus promote breast carcinogenesis.	topic_bc
78061	2	356017	6	NULL	NULL	0	NULL	statement 1	process		promotes					breast carcinoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Oestrogen predominance over progesterone may cause hyperproliferation of mammary epithelium and thus promote breast carcinogenesis.	topic_bc
77452	1	356019	7	NULL	NULL	0	NULL	RUNX1	GP		known as					CBFA2 	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	RUNX1, also known as CBFA2 (core binding factor A2)	topic_ll
77453	2	356019	7	NULL	NULL	0	NULL	CBFA2	GP		is					core binding factor A2	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	RUNX1, also known as CBFA2 (core binding factor A2)	topic_ll
77003	1	356020	5	NULL	NULL	0	NULL	gene loci	Chromosome	different	is located on					6p22.1	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	Recently, genetic data from multiple large cohorts of patients were published in ‘Nature’ showing that different gene loci located on chromosome 6p22.1 are the most probable susceptibility genes for schizophrenia (Shi et al., 2009; Stefansson et al., 2009; Purcell et al., 2009). NULL	topic_sch
77004	2	356020	5	NULL	NULL	NULL	NULL	statement 1	Chromosome		susceptibile to		most probable			schizophrenia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Recently, genetic data from multiple large cohorts of patients were published in ‘Nature’ showing that different gene loci located on chromosome 6p22.1 are the most probable susceptibility genes for schizophrenia (Shi et al., 2009; Stefansson et al., 2009; Purcell et al., 2009). NULL	topic_sch
77005	1	356022	5	NULL	NULL	0	NULL	genes	GP		is present in					HLA complex	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, several genes of the HLA complex, which regulate the immune function and already earlier have been discussed to be involved in schizophrenia, are located in these regions (Fellerhoff et al., 2007). 	topic_sch
77006	2	356022	5	NULL	NULL	0	NULL	statement 1	GP		regulates					immune function	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, several genes of the HLA complex, which regulate the immune function and already earlier have been discussed to be involved in schizophrenia, are located in these regions (Fellerhoff et al., 2007). 	topic_sch
77007	3	356022	5	NULL	NULL	0	NULL	statement 1	GP		is involved in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, several genes of the HLA complex, which regulate the immune function and already earlier have been discussed to be involved in schizophrenia, are located in these regions (Fellerhoff et al., 2007). 	topic_sch
77008	1	356024	5	NULL	NULL	0	NULL	IL-8	GP		is					Interleukin-8	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	In humans it could be shown that increased maternal levels of the pro-inflammatory cytokine Interleukin-8 (IL-8) during pregnancy are associated with an increased risk for schizophrenia in the offspring – whatever the reason for increased IL-8 was (Brown, 2006).	topic_sch
77009	2	356024	5	NULL	NULL	0	NULL	IL-8	GP		is a type of					pro-inflammatory cytokine	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	In humans it could be shown that increased maternal levels of the pro-inflammatory cytokine Interleukin-8 (IL-8) during pregnancy are associated with an increased risk for schizophrenia in the offspring – whatever the reason for increased IL-8 was (Brown, 2006).	topic_sch
77010	3	356024	5	NULL	NULL	0	NULL	IL-8	GP	increase in;;levels of;;maternal	occurs during					pregnancy	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In humans it could be shown that increased maternal levels of the pro-inflammatory cytokine Interleukin-8 (IL-8) during pregnancy are associated with an increased risk for schizophrenia in the offspring – whatever the reason for increased IL-8 was (Brown, 2006).	topic_sch
77011	4	356024	5	NULL	NULL	0	NULL	statement 3	Process		is associated with					schizophrenia	MedicalFinding	increased risk for			NULL		0	NULL	NULL	NULL	NULL	NULL	In humans it could be shown that increased maternal levels of the pro-inflammatory cytokine Interleukin-8 (IL-8) during pregnancy are associated with an increased risk for schizophrenia in the offspring – whatever the reason for increased IL-8 was (Brown, 2006).	topic_sch
77012	5	356024	5	NULL	NULL	0	NULL	statement 4	Process		occurs in					offspring	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	In humans it could be shown that increased maternal levels of the pro-inflammatory cytokine Interleukin-8 (IL-8) during pregnancy are associated with an increased risk for schizophrenia in the offspring – whatever the reason for increased IL-8 was (Brown, 2006).	topic_sch
77013	1	356025	5	NULL	NULL	0	NULL	mother	GroupOfPeople	immune response of	is related to		may be			schizophrenia	MedicalFinding	increased risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	As opposed to any single pathogen, the immune response, itself, of the mother may be related to the increased risk for schizophrenia in the offspring (Zuckerman and Weiner, 2005).	topic_sch
77014	2	356025	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					offspring	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	As opposed to any single pathogen, the immune response, itself, of the mother may be related to the increased risk for schizophrenia in the offspring (Zuckerman and Weiner, 2005).	topic_sch
77015	1	356026	5	NULL	NULL	NULL	NULL	CNS	OrganismPart		infected during					childhood	Time	early			NULL		NULL	NULL	NULL	NULL	NULL	NULL	A five-fold increased risk for developing psychoses later on, however, was detected after infection of the CNS in early childhood (Brown et al., 2004; Gattaz et al., 2004).	topic_sch
77016	2	356026	5	NULL	NULL	0	NULL	statement 1	Process		increases					psychoses	MedicalFinding	risk of;;development of			NULL		0	NULL	NULL	NULL	NULL	NULL	A five-fold increased risk for developing psychoses later on, however, was detected after infection of the CNS in early childhood (Brown et al., 2004; Gattaz et al., 2004).	topic_sch
77017	1	356027	5	NULL	NULL	0	NULL	inflammation	MedicalFinding	signs of	is present in					brain	OrganismPart	schizophrenic			NULL		0	NULL	NULL	NULL	NULL	NULL	Signs of inflammation were found in schizophrenic brains (Körschenhausen et al., 1996), and the term ‘mild localized chronic encephalitis’ to describe a slight but chronic inflammatory process in schizophrenia was proposed (Bechter, 2001). 	topic_sch
77018	2	356027	5	NULL	NULL	0	NULL	inflammatory process	MedicalFinding	slight;;chronic	is observed in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Signs of inflammation were found in schizophrenic brains (Körschenhausen et al., 1996), and the term ‘mild localized chronic encephalitis’ to describe a slight but chronic inflammatory process in schizophrenia was proposed (Bechter, 2001). 	topic_sch
77019	3	356027	5	NULL	NULL	0	NULL	statement 2	Process		is termed as					mild localized chronic encephalitis�	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Signs of inflammation were found in schizophrenic brains (Körschenhausen et al., 1996), and the term ‘mild localized chronic encephalitis’ to describe a slight but chronic inflammatory process in schizophrenia was proposed (Bechter, 2001). 	topic_sch
77020	1	356028	5	NULL	NULL	NULL	NULL	IL-2	GP	decreased;;production of	reflects					type-1 cytokines	GP	blunted production of			NULL	in vitro	NULL	NULL	NULL	NULL	NULL	NULL	A well established finding in schizophrenia is the decreased in vitro production of IL-2 and IFN-! (Wilke et al., 1996; Müller et al., 2000), reflecting a blunted production of type-1 cytokines	topic_sch
77021	2	356028	5	NULL	NULL	NULL	NULL	IFN-gamma	GP	decreased;;production of	reflects					type-1 cytokines	GP	blunted production of			NULL	in vitro	NULL	NULL	NULL	NULL	NULL	NULL	A well established finding in schizophrenia is the decreased in vitro production of IL-2 and IFN-! (Wilke et al., 1996; Müller et al., 2000), reflecting a blunted production of type-1 cytokines	topic_sch
77022	3	356028	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	A well established finding in schizophrenia is the decreased in vitro production of IL-2 and IFN-! (Wilke et al., 1996; Müller et al., 2000), reflecting a blunted production of type-1 cytokines	topic_sch
77023	4	356028	5	NULL	NULL	0	NULL	statement 2	Process		occurs in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	A well established finding in schizophrenia is the decreased in vitro production of IL-2 and IFN-! (Wilke et al., 1996; Müller et al., 2000), reflecting a blunted production of type-1 cytokines	topic_sch
77454	1	356029	7	NULL	NULL	0	NULL	p-STAT3	GP	overexpression of	associated with		significantly			colorectal cancer-specific mortality	Process	higher			NULL		0	NULL	NULL	NULL	NULL	NULL	 p-STAT3 overexpression was associated with significantly higher colorectal cancer-specific mortality	topic_ccc
77455	1	356030	7	NULL	NULL	0	NULL	Preoperative serum p53 Abs 	GP		not marker for					tumor 	MedicalFinding	progression of			NULL		0	NULL	NULL	NULL	NULL	NULL	Preoperative serum p53 Abs do not seem to be a marker of tumor progression but may be a useful marker for detecting high risk of lymph node metastasis in T1 colorectal cancer.	topic_ccc
77456	2	356030	7	NULL	NULL	0	NULL	Preoperative serum p53 Abs 	GP		marker for		useful			lymph node metastasis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Preoperative serum p53 Abs do not seem to be a marker of tumor progression but may be a useful marker for detecting high risk of lymph node metastasis in T1 colorectal cancer.	topic_ccc
77457	3	356030	7	NULL	NULL	0	NULL	statement 2	Process		occur in					T1 colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Preoperative serum p53 Abs do not seem to be a marker of tumor progression but may be a useful marker for detecting high risk of lymph node metastasis in T1 colorectal cancer.	topic_ccc
77458	1	356031	7	NULL	NULL	0	NULL	MSH2 	GP	mutations of	underlie					hereditary non-polyposis colorectal cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the mismatch repair gene MSH2 underlie hereditary non-polyposis colorectal cancer (Lynch syndrome)	topic_ccc
77459	2	356031	7	NULL	NULL	0	NULL	MSH2	GP		is a type of					mismatch repair gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the mismatch repair gene MSH2 underlie hereditary non-polyposis colorectal cancer (Lynch syndrome)	topic_ccc
77460	3	356031	7	NULL	NULL	0	NULL	hereditary non-polyposis colorectal cancer	MedicalFinding		is					Lynch syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the mismatch repair gene MSH2 underlie hereditary non-polyposis colorectal cancer (Lynch syndrome)	topic_ccc
77461	1	356032	7	NULL	NULL	0	NULL	MSH2	GP	mutations of	underlie					hereditary non-polyposis colorectal cancer 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the mismatch repair gene MSH2 underlie hereditary non-polyposis colorectal cancer (Lynch syndrome). While disruptive mutations are overtly pathogenic, the implications of missense mutations found in sporadic colorectal cancer patients or in suspected Lynch syndrome families are often unknown.	topic_ccc
77462	2	356032	7	NULL	NULL	0	NULL	hereditary non-polyposis colorectal cancer 	MedicalFinding		is					Lynch syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the mismatch repair gene MSH2 underlie hereditary non-polyposis colorectal cancer (Lynch syndrome). While disruptive mutations are overtly pathogenic, the implications of missense mutations found in sporadic colorectal cancer patients or in suspected Lynch syndrome families are often unknown.	topic_ccc
77463	3	356032	7	NULL	NULL	0	NULL	MSH2	GP	disruptive mutations of	are					pathogenic	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the mismatch repair gene MSH2 underlie hereditary non-polyposis colorectal cancer (Lynch syndrome). While disruptive mutations are overtly pathogenic, the implications of missense mutations found in sporadic colorectal cancer patients or in suspected Lynch syndrome families are often unknown.	topic_ccc
77464	4	356032	7	NULL	NULL	0	NULL	missense mutations 	Process		found in					sporadic colorectal cancer 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the mismatch repair gene MSH2 underlie hereditary non-polyposis colorectal cancer (Lynch syndrome). While disruptive mutations are overtly pathogenic, the implications of missense mutations found in sporadic colorectal cancer patients or in suspected Lynch syndrome families are often unknown.	topic_ccc
77465	5	356032	7	NULL	NULL	0	NULL	missense mutations	Process		found in					suspected Lynch syndrome families	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the mismatch repair gene MSH2 underlie hereditary non-polyposis colorectal cancer (Lynch syndrome). While disruptive mutations are overtly pathogenic, the implications of missense mutations found in sporadic colorectal cancer patients or in suspected Lynch syndrome families are often unknown.	topic_ccc
77484	6	356032	7	NULL	NULL	0	NULL	MSH2	GP		is a type of					mismatch repair gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Mutations in the mismatch repair gene MSH2 underlie hereditary non-polyposis colorectal cancer (Lynch syndrome). While disruptive mutations are overtly pathogenic, the implications of missense mutations found in sporadic colorectal cancer patients or in suspected Lynch syndrome families are often unknown.	topic_ccc
77024	1	356033	5	NULL	NULL	0	NULL	autism	MedicalFinding		is characterized by					social relatedness	MentalProcess	core impairments of			NULL		0	NULL	NULL	NULL	NULL	NULL	Autism is characterized by core impairments in social relatedness and communication and interfering repetitive behaviors	topic_aut
77025	2	356033	5	NULL	NULL	0	NULL	autism	MedicalFinding		is characterized by					communication	MentalProcess	core impairments of			NULL		0	NULL	NULL	NULL	NULL	NULL	Autism is characterized by core impairments in social relatedness and communication and interfering repetitive behaviors	topic_aut
77026	3	356033	5	NULL	NULL	0	NULL	autism	MedicalFinding		is characterized by					interfering repetitive behaviors	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Autism is characterized by core impairments in social relatedness and communication and interfering repetitive behaviors	topic_aut
77027	1	356035	5	NULL	NULL	0	NULL	5-hydroxytryptophan	Chemical	daily treatment with	clinically improves					5HIAA	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	Daily treatment with 5-hydroxytryptophan (and carbidopa) led to clinical improvement and normalization of 5HIAA, implying that brain serotonin turnover normalized	topic_aut
77028	2	356035	5	NULL	NULL	0	NULL	5-hydroxytryptophan	Chemical	daily treatment with	normalize					5HIAA	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Daily treatment with 5-hydroxytryptophan (and carbidopa) led to clinical improvement and normalization of 5HIAA, implying that brain serotonin turnover normalized	topic_aut
77029	3	356035	5	NULL	NULL	NULL	NULL	carbidopa	Chemical	daily treatment with	clinically improves					5HIAA	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Daily treatment with 5-hydroxytryptophan (and carbidopa) led to clinical improvement and normalization of 5HIAA, implying that brain serotonin turnover normalized	topic_aut
77030	4	356035	5	NULL	NULL	0	NULL	carbidopa	Chemical	daily treatment with	normalize					5HIAA	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Daily treatment with 5-hydroxytryptophan (and carbidopa) led to clinical improvement and normalization of 5HIAA, implying that brain serotonin turnover normalized	topic_aut
77031	5	356035	5	NULL	NULL	0	NULL	statement 1	Process		imply					serotonin	GP	normalized turnover of;;brain			NULL		0	NULL	NULL	NULL	NULL	NULL	Daily treatment with 5-hydroxytryptophan (and carbidopa) led to clinical improvement and normalization of 5HIAA, implying that brain serotonin turnover normalized	topic_aut
77032	6	356035	5	NULL	NULL	0	NULL	statement 2	Process		imply					serotonin	GP	normalized turnover of;;brain			NULL		0	NULL	NULL	NULL	NULL	NULL	Daily treatment with 5-hydroxytryptophan (and carbidopa) led to clinical improvement and normalization of 5HIAA, implying that brain serotonin turnover normalized	topic_aut
77033	7	356035	5	NULL	NULL	0	NULL	statement 3	Process		imply					serotonin	GP	normalized turnover of;;brain			NULL		0	NULL	NULL	NULL	NULL	NULL	Daily treatment with 5-hydroxytryptophan (and carbidopa) led to clinical improvement and normalization of 5HIAA, implying that brain serotonin turnover normalized	topic_aut
77034	8	356035	5	NULL	NULL	0	NULL	statement 4	Process		imply					serotonin	GP	normalized turnover of;;brain			NULL		0	NULL	NULL	NULL	NULL	NULL	Daily treatment with 5-hydroxytryptophan (and carbidopa) led to clinical improvement and normalization of 5HIAA, implying that brain serotonin turnover normalized	topic_aut
77466	1	356036	7	NULL	NULL	0	NULL	IDH2	GP	overexpression of;;wild-type	increase		significantly			 5-methylcytosine 	Chemical	levels of			NULL		0	NULL	NULL	NULL	NULL	NULL	Overexpression of wild-type IDH2 also led to a small but significant increase in 5-methylcytosine levels compared to vector control, consistent with the small 2HG elevation observed in these cells.	topic_ll
77467	2	356036	7	NULL	NULL	0	NULL	IDH2	GP	overexpression of;;wild-type	elevates					2HG	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Overexpression of wild-type IDH2 also led to a small but significant increase in 5-methylcytosine levels compared to vector control, consistent with the small 2HG elevation observed in these cells.	topic_ll
77468	1	356037	7	NULL	NULL	NULL	NULL	GATA1 	GP		hypermethylated in		aberrantly			IDH1-mutant AMLs	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	GATA1 was aberrantly hypermethylated and silenced specifically in IDH1-mutant AMLs 	topic_ll
77469	2	356037	7	NULL	NULL	0	NULL	GATA1	GP		silenced in		specifically			IDH1-mutant AMLs	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	GATA1 was aberrantly hypermethylated and silenced specifically in IDH1-mutant AMLs 	topic_ll
77470	1	356038	7	NULL	NULL	0	NULL	TET2	GP	mutations in	constitute					AML	MedicalFinding	distinct mutational class in			NULL		0	NULL	NULL	NULL	NULL	NULL	These data suggest that TET2 and IDH1/2 mutations constitute a distinct mutational class in AML which affects the epigenetic state	topic_ll
77471	2	356038	7	NULL	NULL	0	NULL	statement 1	Process		affects					epigenetic state	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	These data suggest that TET2 and IDH1/2 mutations constitute a distinct mutational class in AML which affects the epigenetic state	topic_ll
77472	3	356038	7	NULL	NULL	0	NULL	IDH1/2 	GP	mutations in	constitute					AML	MedicalFinding	distinct mutational class in			NULL		0	NULL	NULL	NULL	NULL	NULL	These data suggest that TET2 and IDH1/2 mutations constitute a distinct mutational class in AML which affects the epigenetic state	topic_ll
77473	4	356038	7	NULL	NULL	0	NULL	statement 3			affects					epigenetic state	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	These data suggest that TET2 and IDH1/2 mutations constitute a distinct mutational class in AML which affects the epigenetic state	topic_ll
77474	1	356039	7	NULL	NULL	NULL	NULL	IDH1/ 2 	GP	expression of;;mutant	induce					DNA hypermethylation	Process	increase in;;global			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Most importantly, expression of IDH1/ 2 mutants induced an increase in global DNA hypermethylation, and inhibited TET2-induced cytosine 5-hydroxymethylation.	topic_ll
77475	2	356039	7	NULL	NULL	0	NULL	TET2	GP		induce					cytosine 5-hydroxymethylation	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Most importantly, expression of IDH1/ 2 mutants induced an increase in global DNA hypermethylation, and inhibited TET2-induced cytosine 5-hydroxymethylation.	topic_ll
77476	3	356039	7	NULL	NULL	0	NULL	IDH1/ 2	GP	expression of;;mutant	inhibit					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Most importantly, expression of IDH1/ 2 mutants induced an increase in global DNA hypermethylation, and inhibited TET2-induced cytosine 5-hydroxymethylation.	topic_ll
77477	1	356040	7	NULL	NULL	0	NULL	TET2	GP		hydroxylates					5-methylcytosine 	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	expression of mutant IDH is able to inhibit the hydroxylation of 5-methylcytosine by TET2 and subsequent DNA demethylation.	topic_ll
77478	2	356040	7	NULL	NULL	0	NULL	IDH	GP	expression of;;mutant	inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	expression of mutant IDH is able to inhibit the hydroxylation of 5-methylcytosine by TET2 and subsequent DNA demethylation.	topic_ll
77479	3	356040	7	NULL	NULL	0	NULL	statement 2	Process		demethylates		subsequently			DNA	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	expression of mutant IDH is able to inhibit the hydroxylation of 5-methylcytosine by TET2 and subsequent DNA demethylation.	topic_ll
77480	1	356042	7	NULL	NULL	NULL	NULL	Down syndrome	MedicalFinding	children with	risk of		increased			AMKL	MedicalFinding	developing			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Children with constitutional trisomy 21 (Down syndrome) have an approximately 500-fold increased risk of developing acute megakaryoblastic leukemia (AMKL), a form of acute myeloid leukemia.	topic_ll
77481	2	356042	7	NULL	NULL	0	NULL	AMKL	MedicalFinding		is					acute megakaryoblastic leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Children with constitutional trisomy 21 (Down syndrome) have an approximately 500-fold increased risk of developing acute megakaryoblastic leukemia (AMKL), a form of acute myeloid leukemia.	topic_ll
77482	3	356042	7	NULL	NULL	0	NULL	AMKL	MedicalFinding		is a type of					acute myeloid leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Children with constitutional trisomy 21 (Down syndrome) have an approximately 500-fold increased risk of developing acute megakaryoblastic leukemia (AMKL), a form of acute myeloid leukemia.	topic_ll
77483	4	356042	7	NULL	NULL	0	NULL	Down syndrome	MedicalFinding		is					constitutional trisomy 21	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Children with constitutional trisomy 21 (Down syndrome) have an approximately 500-fold increased risk of developing acute megakaryoblastic leukemia (AMKL), a form of acute myeloid leukemia.	topic_ll
77485	1	356043	7	NULL	NULL	0	NULL	Down syndrome	MedicalFinding	newborn infants with	have					TL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Unique to newborn infants with Down syndrome is a transient leukemia (TL), also referred to as transient myeloproliferative syn- drome, that undergoes spontaneous re-mission in the majority of cases but in approximately 20% is followed by AMKL later in life.	topic_ll
77486	2	356043	7	NULL	NULL	0	NULL	TL	MedicalFinding		is					transient leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Unique to newborn infants with Down syndrome is a transient leukemia (TL), also referred to as transient myeloproliferative syn- drome, that undergoes spontaneous re-mission in the majority of cases but in approximately 20% is followed by AMKL later in life.	topic_ll
77487	3	356043	7	NULL	NULL	0	NULL	TL	MedicalFinding		also referred as					transient myeloproliferative syn- drome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Unique to newborn infants with Down syndrome is a transient leukemia (TL), also referred to as transient myeloproliferative syn- drome, that undergoes spontaneous re-mission in the majority of cases but in approximately 20% is followed by AMKL later in life.	topic_ll
77488	4	356043	7	NULL	NULL	NULL	NULL	TL	MedicalFinding		undergoes					 AMKL	MedicalFinding	spontaneous re-mission to form			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Unique to newborn infants with Down syndrome is a transient leukemia (TL), also referred to as transient myeloproliferative syn- drome, that undergoes spontaneous re-mission in the majority of cases but in approximately 20% is followed by AMKL later in life.	topic_ll
77489	5	356043	7	NULL	NULL	0	NULL	statement 4	Process		follows					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Unique to newborn infants with Down syndrome is a transient leukemia (TL), also referred to as transient myeloproliferative syn- drome, that undergoes spontaneous re-mission in the majority of cases but in approximately 20% is followed by AMKL later in life.	topic_ll
77490	1	356044	7	NULL	NULL	NULL	NULL	GATA1	GP	mutations of 	specific for					AMKL	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Recently mutations of the gene encoding the hematopoietic tran- scription factor GATA1 were shown to be specific for AMKL of Down syndrome.	topic_ll
77491	2	356044	7	NULL	NULL	0	NULL	statement 1	Process		occur in					Down syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Recently mutations of the gene encoding the hematopoietic tran- scription factor GATA1 were shown to be specific for AMKL of Down syndrome.	topic_ll
77492	3	356044	7	NULL	NULL	0	NULL	GATA1	GP		is a type of					hematopoietic tran- scription factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Recently mutations of the gene encoding the hematopoietic tran- scription factor GATA1 were shown to be specific for AMKL of Down syndrome.	topic_ll
77493	1	356045	7	NULL	NULL	0	NULL	 GATA1 	GP	mutations of	present in					TL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	we hypothesized that GATA1 mutations are present in TL of Down syndrome	topic_ll
77494	2	356045	7	NULL	NULL	0	NULL	statement 1	Process		occur in					Down syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	we hypothesized that GATA1 mutations are present in TL of Down syndrome	topic_ll
77495	1	356046	7	NULL	NULL	NULL	NULL	GATA1 function	Process	lack of	result in					megakaryocytes	Cell	accumulation of abnormally differentiated			NULL	hematopoietic cells	NULL	NULL	NULL	NULL	NULL	NULL	Lack of GATA1 function in hematopoietic cells had previously been shown to result in the accumulation of abnormally differentiated megakaryocytes and thrombocytopenia without leukemic transformation.	topic_ll
77496	2	356046	7	NULL	NULL	0	NULL	GATA1 function	Process	lack of	result in					thrombocytopenia	MedicalFinding				NULL	hematopoietic cells	0	NULL	NULL	NULL	NULL	NULL	Lack of GATA1 function in hematopoietic cells had previously been shown to result in the accumulation of abnormally differentiated megakaryocytes and thrombocytopenia without leukemic transformation.	topic_ll
77497	3	356046	7	NULL	NULL	0	NULL	statement 2	Process		occur without					leukemic transformation	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Lack of GATA1 function in hematopoietic cells had previously been shown to result in the accumulation of abnormally differentiated megakaryocytes and thrombocytopenia without leukemic transformation.	topic_ll
77035	1	356048	5	NULL	NULL	0	NULL	ICAM-1	GP		is					inter-cellular adhesion molecule-1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Decreased levels of the soluble (s) inter-cellular adhesion molecule-1 (ICAM-1), as found in schizophrenia, also represent an under-activation of the type-1 immune system (Schwarz et al., 2000).	topic_sch
77036	2	356048	5	NULL	NULL	0	NULL	ICAM-1	GP	level of;;soluble	decreased in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Decreased levels of the soluble (s) inter-cellular adhesion molecule-1 (ICAM-1), as found in schizophrenia, also represent an under-activation of the type-1 immune system (Schwarz et al., 2000).	topic_sch
77037	3	356048	5	NULL	NULL	NULL	NULL	ICAM-1	GP	decreased level of;;soluble	represent					type-1 immune system	OrganismPart	under-activation of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Decreased levels of the soluble (s) inter-cellular adhesion molecule-1 (ICAM-1), as found in schizophrenia, also represent an under-activation of the type-1 immune system (Schwarz et al., 2000).	topic_sch
77038	1	356049	5	NULL	NULL	0	NULL	p55	GP		is a type of					TNF-receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Decreased levels of the soluble TNF-receptor p55 – mostly decreased when TNF-" is decreased – were observed, too (Haack et al., 1999).	topic_sch
77039	2	356049	5	NULL	NULL	0	NULL	TNF	GP	decrease in	decreases					p55	GP	level of;;soluble			NULL		0	NULL	NULL	NULL	NULL	NULL	Decreased levels of the soluble TNF-receptor p55 – mostly decreased when TNF-" is decreased – were observed, too (Haack et al., 1999).	topic_sch
77040	1	356050	5	NULL	NULL	0	NULL	antipsychotic medication	Chemical		is a type of					confounding factor	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The results of this meta-analysis support the view, that antipsychotic medication is a confounding factor in the analysis of the immune system in schizophrenia, upregulating type-1 immune markers.	topic_sch
77041	2	356050	5	NULL	NULL	0	NULL	statement 1	Process		in analysis of					immune system	OrganismPart	schizophrenic			NULL		0	NULL	NULL	NULL	NULL	NULL	The results of this meta-analysis support the view, that antipsychotic medication is a confounding factor in the analysis of the immune system in schizophrenia, upregulating type-1 immune markers.	topic_sch
77042	3	356050	5	NULL	NULL	0	NULL	antipsychotic medication	Chemical		upregulates					type-1 immune markers	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The results of this meta-analysis support the view, that antipsychotic medication is a confounding factor in the analysis of the immune system in schizophrenia, upregulating type-1 immune markers.	topic_sch
77055	1	356052	5	NULL	NULL	0	NULL	type-2 immune response	Process		is activated in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, several other signs of activation of the type-2 immune response are described in schizophrenia, including the increased Th2 type of lymphocytes in the blood (Sperner- Unterweger et al., 1999b), the increased production of Immunoglobulin E (IgE) and an increase of IL-10 serum levels (Schwarz et al., 2001; van Kammen et al., 1997).	topic_sch
77056	2	356052	5	NULL	NULL	0	NULL	Th2 lymphocytes	Cell		is present in					blood	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, several other signs of activation of the type-2 immune response are described in schizophrenia, including the increased Th2 type of lymphocytes in the blood (Sperner- Unterweger et al., 1999b), the increased production of Immunoglobulin E (IgE) and an increase of IL-10 serum levels (Schwarz et al., 2001; van Kammen et al., 1997).	topic_sch
77057	3	356052	5	NULL	NULL	0	NULL	statement 1	Process		is increased in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, several other signs of activation of the type-2 immune response are described in schizophrenia, including the increased Th2 type of lymphocytes in the blood (Sperner- Unterweger et al., 1999b), the increased production of Immunoglobulin E (IgE) and an increase of IL-10 serum levels (Schwarz et al., 2001; van Kammen et al., 1997).	topic_sch
77058	4	356052	5	NULL	NULL	0	NULL	IgE	GP		is					Immunoglobulin E	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, several other signs of activation of the type-2 immune response are described in schizophrenia, including the increased Th2 type of lymphocytes in the blood (Sperner- Unterweger et al., 1999b), the increased production of Immunoglobulin E (IgE) and an increase of IL-10 serum levels (Schwarz et al., 2001; van Kammen et al., 1997).	topic_sch
77059	5	356052	5	NULL	NULL	0	NULL	IgE	GP	production of	is increased in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, several other signs of activation of the type-2 immune response are described in schizophrenia, including the increased Th2 type of lymphocytes in the blood (Sperner- Unterweger et al., 1999b), the increased production of Immunoglobulin E (IgE) and an increase of IL-10 serum levels (Schwarz et al., 2001; van Kammen et al., 1997).	topic_sch
77060	6	356052	5	NULL	NULL	0	NULL	IL-10	GP	levels of;;serum	is increased in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Moreover, several other signs of activation of the type-2 immune response are described in schizophrenia, including the increased Th2 type of lymphocytes in the blood (Sperner- Unterweger et al., 1999b), the increased production of Immunoglobulin E (IgE) and an increase of IL-10 serum levels (Schwarz et al., 2001; van Kammen et al., 1997).	topic_sch
77061	1	356053	5	NULL	NULL	0	NULL	IL-4	GP	levels of	is increased in					schizophrenic patients	GroupOfPeople	juvenile			NULL		0	NULL	NULL	NULL	NULL	NULL	Increased levels of IL-4 in the CSF of juvenile schizophrenic patients have been reported (Mittleman et al., 1997), which indicates that the increased type-2 response in schizophrenia is not only a phenomenon of the peripheral immune response.	topic_sch
77062	2	356053	5	NULL	NULL	0	NULL	type-2 response	Process		is increased in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Increased levels of IL-4 in the CSF of juvenile schizophrenic patients have been reported (Mittleman et al., 1997), which indicates that the increased type-2 response in schizophrenia is not only a phenomenon of the peripheral immune response.	topic_sch
77063	3	356053	5	NULL	NULL	0	NULL	statement 2	Process		is a type of					peripheral immune response	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Increased levels of IL-4 in the CSF of juvenile schizophrenic patients have been reported (Mittleman et al., 1997), which indicates that the increased type-2 response in schizophrenia is not only a phenomenon of the peripheral immune response.	topic_sch
77498	1	356054	7	NULL	NULL	0	NULL	GSK3	GP		therapeutic target in		potential			bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Preclinical studies have suggested that glycogen synthase kinase-3 (GSK3) is a potential therapeutic target in bipolar disorder, but evidence of abnormal GSK3 in human bipolar disorder and its response to treatment is still lacking.	topic_bd
77499	2	356054	7	NULL	NULL	0	NULL	GSK3	GP		is					glycogen synthase kinase-3	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Preclinical studies have suggested that glycogen synthase kinase-3 (GSK3) is a potential therapeutic target in bipolar disorder, but evidence of abnormal GSK3 in human bipolar disorder and its response to treatment is still lacking.	topic_bd
77500	1	356055	7	NULL	NULL	0	NULL	CCNH	GP	genetic variants in	associated with		strongly			CLL 	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	After adjustment for multiple testing, strong associations were identified between CLL risk and genetic variants in CCNH, APAF1, IL16, CASP8, NOS2A, and CCR7. 	topic_ll
77501	2	356055	7	NULL	NULL	0	NULL	APAF1	GP	genetic variants in	associated with		strongly			CLL	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	After adjustment for multiple testing, strong associations were identified between CLL risk and genetic variants in CCNH, APAF1, IL16, CASP8, NOS2A, and CCR7. 	topic_ll
77502	3	356055	7	NULL	NULL	0	NULL	IL16	GP	genetic variants in	associated with		strongly			CLL	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	After adjustment for multiple testing, strong associations were identified between CLL risk and genetic variants in CCNH, APAF1, IL16, CASP8, NOS2A, and CCR7. 	topic_ll
77503	4	356055	7	NULL	NULL	0	NULL	CASP8	GP	genetic variants in	associated with		strongly			CLL	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	After adjustment for multiple testing, strong associations were identified between CLL risk and genetic variants in CCNH, APAF1, IL16, CASP8, NOS2A, and CCR7. 	topic_ll
77504	5	356055	7	NULL	NULL	0	NULL	NOS2A	GP	genetic variants in	associated with		strongly			CLL	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	After adjustment for multiple testing, strong associations were identified between CLL risk and genetic variants in CCNH, APAF1, IL16, CASP8, NOS2A, and CCR7. 	topic_ll
77505	6	356055	7	NULL	NULL	0	NULL	CCR7	GP	genetic variants in	associated with		strongly			CLL	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	After adjustment for multiple testing, strong associations were identified between CLL risk and genetic variants in CCNH, APAF1, IL16, CASP8, NOS2A, and CCR7. 	topic_ll
77506	1	356056	7	NULL	NULL	NULL	NULL	CCNH gene	GP	humans	encode					Cyclin-H protein	GP	humans			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Cyclin-H is a protein that in humans is encoded by the CCNH gene.	topic_ll
77507	1	356057	7	NULL	NULL	0	NULL	PI3 kinase	GP		promotes					CLL B cells	Cell	survival of			NULL		0	NULL	NULL	NULL	NULL	NULL	PI3 kinase promotes survival of chronic lymphocytic leukemia (CLL) B cells by preventing caspase-8 activation.	topic_ll
77508	2	356057	7	NULL	NULL	0	NULL	statement 1	Process		prevent					caspase-8	GP	activation of			NULL		0	NULL	NULL	NULL	NULL	NULL	PI3 kinase promotes survival of chronic lymphocytic leukemia (CLL) B cells by preventing caspase-8 activation.	topic_ll
77509	3	356057	7	NULL	NULL	0	NULL	CLL	MedicalFinding		is					chronic lymphocytic leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	PI3 kinase promotes survival of chronic lymphocytic leukemia (CLL) B cells by preventing caspase-8 activation.	topic_ll
77510	1	356058	7	NULL	NULL	0	NULL	Fas-L	GP		ligates					Fas molecule	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Ligation of the cell-surface Fas molecule by its ligand (Fas-L) or agonistic anti-Fas monoclonal antibodies results in the cleavage and activation of the cysteine protease procaspase 8 followed by the activation of procaspase 3 and by apoptosis.	topic_ll
77511	2	356058	7	NULL	NULL	0	NULL	anti-Fas monoclonal antibodies	GP		ligates					Fas molecule	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Ligation of the cell-surface Fas molecule by its ligand (Fas-L) or agonistic anti-Fas monoclonal antibodies results in the cleavage and activation of the cysteine protease procaspase 8 followed by the activation of procaspase 3 and by apoptosis.	topic_ll
77512	3	356058	7	NULL	NULL	NULL	NULL	statement 1	Process		results in					procaspase 8	GP	cleavage of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Ligation of the cell-surface Fas molecule by its ligand (Fas-L) or agonistic anti-Fas monoclonal antibodies results in the cleavage and activation of the cysteine protease procaspase 8 followed by the activation of procaspase 3 and by apoptosis.	topic_ll
77513	4	356058	7	NULL	NULL	NULL	NULL	statement 2	Process		results in					procaspase 8	GP	cleavage of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Ligation of the cell-surface Fas molecule by its ligand (Fas-L) or agonistic anti-Fas monoclonal antibodies results in the cleavage and activation of the cysteine protease procaspase 8 followed by the activation of procaspase 3 and by apoptosis.	topic_ll
77514	5	356058	7	NULL	NULL	0	NULL	statement 1	Process		results in					procaspase 8	GP	activation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Ligation of the cell-surface Fas molecule by its ligand (Fas-L) or agonistic anti-Fas monoclonal antibodies results in the cleavage and activation of the cysteine protease procaspase 8 followed by the activation of procaspase 3 and by apoptosis.	topic_ll
77515	6	356058	7	NULL	NULL	0	NULL	statement 2	Process		results in					procaspase 8	GP	activation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Ligation of the cell-surface Fas molecule by its ligand (Fas-L) or agonistic anti-Fas monoclonal antibodies results in the cleavage and activation of the cysteine protease procaspase 8 followed by the activation of procaspase 3 and by apoptosis.	topic_ll
77516	7	356058	7	NULL	NULL	0	NULL	statement 3	Process		occur with					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Ligation of the cell-surface Fas molecule by its ligand (Fas-L) or agonistic anti-Fas monoclonal antibodies results in the cleavage and activation of the cysteine protease procaspase 8 followed by the activation of procaspase 3 and by apoptosis.	topic_ll
77517	8	356058	7	NULL	NULL	0	NULL	statement 4	Process		occur with					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Ligation of the cell-surface Fas molecule by its ligand (Fas-L) or agonistic anti-Fas monoclonal antibodies results in the cleavage and activation of the cysteine protease procaspase 8 followed by the activation of procaspase 3 and by apoptosis.	topic_ll
77518	9	356058	7	NULL	NULL	0	NULL	statement 7	Process		followed by					procaspase 3	GP	activation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Ligation of the cell-surface Fas molecule by its ligand (Fas-L) or agonistic anti-Fas monoclonal antibodies results in the cleavage and activation of the cysteine protease procaspase 8 followed by the activation of procaspase 3 and by apoptosis.	topic_ll
77519	10	356058	7	NULL	NULL	0	NULL	statement 8	Process		followed by					procaspase 3	GP	activation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Ligation of the cell-surface Fas molecule by its ligand (Fas-L) or agonistic anti-Fas monoclonal antibodies results in the cleavage and activation of the cysteine protease procaspase 8 followed by the activation of procaspase 3 and by apoptosis.	topic_ll
77520	11	356058	7	NULL	NULL	0	NULL	statement 7	Process		followed by					apoptosis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Ligation of the cell-surface Fas molecule by its ligand (Fas-L) or agonistic anti-Fas monoclonal antibodies results in the cleavage and activation of the cysteine protease procaspase 8 followed by the activation of procaspase 3 and by apoptosis.	topic_ll
77521	12	356058	7	NULL	NULL	0	NULL	statement 8	Process		followed by					apoptosis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Ligation of the cell-surface Fas molecule by its ligand (Fas-L) or agonistic anti-Fas monoclonal antibodies results in the cleavage and activation of the cysteine protease procaspase 8 followed by the activation of procaspase 3 and by apoptosis.	topic_ll
77522	13	356058	7	NULL	NULL	0	NULL	Fas molecule 	GP		is a type of					cell-surface molecule	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Ligation of the cell-surface Fas molecule by its ligand (Fas-L) or agonistic anti-Fas monoclonal antibodies results in the cleavage and activation of the cysteine protease procaspase 8 followed by the activation of procaspase 3 and by apoptosis.	topic_ll
77523	14	356058	7	NULL	NULL	0	NULL	procaspase 8	GP		is a type of					cysteine protease	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Ligation of the cell-surface Fas molecule by its ligand (Fas-L) or agonistic anti-Fas monoclonal antibodies results in the cleavage and activation of the cysteine protease procaspase 8 followed by the activation of procaspase 3 and by apoptosis.	topic_ll
77524	1	356059	7	NULL	NULL	0	NULL	cytotoxic drugs	Chemical		induce					Fas-L	GP	expression of			NULL	leukemia cell lines	0	NULL	NULL	NULL	NULL	NULL	In some leukemia cell lines, cytotoxic drugs induce expression of Fas-L, which may contribute to cell killing through the ligation of Fas. These data suggest that the Fas/Fas-L signaling system does not play a major role in the induction of apoptosis in B-CLL cells treated with cytotoxic drugs or radiation. However, Fas-independent activation of caspase 8 may play a crucial role in the regulation of apoptosis in these cells.	topic_ll
77525	2	356059	7	NULL	NULL	NULL	NULL	statement 1	Process		contribute to		may			cell 	Cell	killing of			NULL	leukemia cell lines	NULL	NULL	NULL	NULL	NULL	NULL	In some leukemia cell lines, cytotoxic drugs induce expression of Fas-L, which may contribute to cell killing through the ligation of Fas. These data suggest that the Fas/Fas-L signaling system does not play a major role in the induction of apoptosis in B-CLL cells treated with cytotoxic drugs or radiation. However, Fas-independent activation of caspase 8 may play a crucial role in the regulation of apoptosis in these cells.	topic_ll
77526	3	356059	7	NULL	NULL	NULL	NULL	statement 2	Process		occur through					Fas	GP	ligation of			NULL	leukemia cell lines	NULL	NULL	NULL	NULL	NULL	NULL	In some leukemia cell lines, cytotoxic drugs induce expression of Fas-L, which may contribute to cell killing through the ligation of Fas. These data suggest that the Fas/Fas-L signaling system does not play a major role in the induction of apoptosis in B-CLL cells treated with cytotoxic drugs or radiation. However, Fas-independent activation of caspase 8 may play a crucial role in the regulation of apoptosis in these cells.	topic_ll
77527	4	356059	7	NULL	NULL	0	NULL	Fas/Fas-L signaling	Process		does not play					apoptosis	Process	major role in induction of			NULL		0	NULL	NULL	NULL	NULL	NULL	In some leukemia cell lines, cytotoxic drugs induce expression of Fas-L, which may contribute to cell killing through the ligation of Fas. These data suggest that the Fas/Fas-L signaling system does not play a major role in the induction of apoptosis in B-CLL cells treated with cytotoxic drugs or radiation. However, Fas-independent activation of caspase 8 may play a crucial role in the regulation of apoptosis in these cells.	topic_ll
77528	5	356059	7	NULL	NULL	0	NULL	B-CLL cells	Cell		treated with					cytotoxic drugs	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	In some leukemia cell lines, cytotoxic drugs induce expression of Fas-L, which may contribute to cell killing through the ligation of Fas. These data suggest that the Fas/Fas-L signaling system does not play a major role in the induction of apoptosis in B-CLL cells treated with cytotoxic drugs or radiation. However, Fas-independent activation of caspase 8 may play a crucial role in the regulation of apoptosis in these cells.	topic_ll
77529	6	356059	7	NULL	NULL	0	NULL	B-CLL cells	Cell		treated with					radiation	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	In some leukemia cell lines, cytotoxic drugs induce expression of Fas-L, which may contribute to cell killing through the ligation of Fas. These data suggest that the Fas/Fas-L signaling system does not play a major role in the induction of apoptosis in B-CLL cells treated with cytotoxic drugs or radiation. However, Fas-independent activation of caspase 8 may play a crucial role in the regulation of apoptosis in these cells.	topic_ll
77530	7	356059	7	NULL	NULL	0	NULL	statement 4	Process		occur in					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In some leukemia cell lines, cytotoxic drugs induce expression of Fas-L, which may contribute to cell killing through the ligation of Fas. These data suggest that the Fas/Fas-L signaling system does not play a major role in the induction of apoptosis in B-CLL cells treated with cytotoxic drugs or radiation. However, Fas-independent activation of caspase 8 may play a crucial role in the regulation of apoptosis in these cells.	topic_ll
77531	8	356059	7	NULL	NULL	0	NULL	statement 4	Process		occur in					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In some leukemia cell lines, cytotoxic drugs induce expression of Fas-L, which may contribute to cell killing through the ligation of Fas. These data suggest that the Fas/Fas-L signaling system does not play a major role in the induction of apoptosis in B-CLL cells treated with cytotoxic drugs or radiation. However, Fas-independent activation of caspase 8 may play a crucial role in the regulation of apoptosis in these cells.	topic_ll
77532	9	356059	7	NULL	NULL	0	NULL	statement 7	Process		is an alternative to					statement 8	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In some leukemia cell lines, cytotoxic drugs induce expression of Fas-L, which may contribute to cell killing through the ligation of Fas. These data suggest that the Fas/Fas-L signaling system does not play a major role in the induction of apoptosis in B-CLL cells treated with cytotoxic drugs or radiation. However, Fas-independent activation of caspase 8 may play a crucial role in the regulation of apoptosis in these cells.	topic_ll
77533	10	356059	7	NULL	NULL	NULL	NULL	caspase 8	GP	activation of	is independent of					Fas	GP				NULL	leukemia cell lines	NULL	NULL	NULL	NULL	NULL	NULL	In some leukemia cell lines, cytotoxic drugs induce expression of Fas-L, which may contribute to cell killing through the ligation of Fas. These data suggest that the Fas/Fas-L signaling system does not play a major role in the induction of apoptosis in B-CLL cells treated with cytotoxic drugs or radiation. However, Fas-independent activation of caspase 8 may play a crucial role in the regulation of apoptosis in these cells.	topic_ll
77534	11	356059	7	NULL	NULL	NULL	NULL	statement 10	Process		play crucial role in		may			apoptosis	Process	regulation of			NULL	leukemia cell lines	NULL	NULL	NULL	NULL	NULL	NULL	In some leukemia cell lines, cytotoxic drugs induce expression of Fas-L, which may contribute to cell killing through the ligation of Fas. These data suggest that the Fas/Fas-L signaling system does not play a major role in the induction of apoptosis in B-CLL cells treated with cytotoxic drugs or radiation. However, Fas-independent activation of caspase 8 may play a crucial role in the regulation of apoptosis in these cells.	topic_ll
77535	1	356061	7	NULL	NULL	0	NULL	CLL risk loci	Chromosome		identified at					6p25.3 (IRF4)	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	Six previously unreported CLL risk loci were identified at 6p25.3 (IRF4), 19q13.32 (PRKD2), 2q37.1 (SP140), 2q13, 11q24.1, and 15q23 for which there was statistically significant evidence for an association on a genome-wide basis (i.e. p<10–7).	topic_ll
77536	2	356061	7	NULL	NULL	0	NULL	CLL risk loci	Chromosome		identified at					19q13.32 (PRKD2)	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	Six previously unreported CLL risk loci were identified at 6p25.3 (IRF4), 19q13.32 (PRKD2), 2q37.1 (SP140), 2q13, 11q24.1, and 15q23 for which there was statistically significant evidence for an association on a genome-wide basis (i.e. p<10–7).	topic_ll
77537	3	356061	7	NULL	NULL	0	NULL	CLL risk loci	Chromosome		identified at					2q37.1 (SP140)	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	Six previously unreported CLL risk loci were identified at 6p25.3 (IRF4), 19q13.32 (PRKD2), 2q37.1 (SP140), 2q13, 11q24.1, and 15q23 for which there was statistically significant evidence for an association on a genome-wide basis (i.e. p<10–7).	topic_ll
77538	4	356061	7	NULL	NULL	0	NULL	CLL risk loci 	Chromosome		identified at					2q13	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	Six previously unreported CLL risk loci were identified at 6p25.3 (IRF4), 19q13.32 (PRKD2), 2q37.1 (SP140), 2q13, 11q24.1, and 15q23 for which there was statistically significant evidence for an association on a genome-wide basis (i.e. p<10–7).	topic_ll
77539	5	356061	7	NULL	NULL	0	NULL	CLL risk loci	Chromosome		identified at					11q24.1	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	Six previously unreported CLL risk loci were identified at 6p25.3 (IRF4), 19q13.32 (PRKD2), 2q37.1 (SP140), 2q13, 11q24.1, and 15q23 for which there was statistically significant evidence for an association on a genome-wide basis (i.e. p<10–7).	topic_ll
77540	6	356061	7	NULL	NULL	NULL	NULL	CLL risk loci	Chromosome		identified at					15q23	Chromosome				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Six previously unreported CLL risk loci were identified at 6p25.3 (IRF4), 19q13.32 (PRKD2), 2q37.1 (SP140), 2q13, 11q24.1, and 15q23 for which there was statistically significant evidence for an association on a genome-wide basis (i.e. p<10–7).	topic_ll
77541	1	356062	7	NULL	NULL	0	NULL	SP140	GP		lymphoid-restricted homolog of					SP100	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	SP140 is the lymphoid-restricted homolog of SP100, expressed in all mature B cells and plasma cell lines, as well as some T cells. SP100 is a major mediator of EBNA-LP (Epstein- Barr virus (EBV) encoded nuclear antigen leader protein), whose co-activation is important for establishing latent viral infections and EBV-mediated B-cell immortalization. A significant dose relationship between rs13397985 genotype and SP140 expression in lymphocytes was demonstrable, with risk alleles being associated with reduced levels of mRNA. SP140 expression has been implicated in innate response to immunodeficiency virus type 1; hence, although speculative, it is possible that genetic variation in SP140 influences the risk of developing CLL through differing response to antigenic challenge.	topic_ll
77542	2	356062	7	NULL	NULL	0	NULL	SP140	GP		expressed in					mature B cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	SP140 is the lymphoid-restricted homolog of SP100, expressed in all mature B cells and plasma cell lines, as well as some T cells. SP100 is a major mediator of EBNA-LP (Epstein- Barr virus (EBV) encoded nuclear antigen leader protein), whose co-activation is important for establishing latent viral infections and EBV-mediated B-cell immortalization. A significant dose relationship between rs13397985 genotype and SP140 expression in lymphocytes was demonstrable, with risk alleles being associated with reduced levels of mRNA. SP140 expression has been implicated in innate response to immunodeficiency virus type 1; hence, although speculative, it is possible that genetic variation in SP140 influences the risk of developing CLL through differing response to antigenic challenge.	topic_ll
77543	3	356062	7	NULL	NULL	0	NULL	SP140	GP		expressed in					plasma cell lines	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	SP140 is the lymphoid-restricted homolog of SP100, expressed in all mature B cells and plasma cell lines, as well as some T cells. SP100 is a major mediator of EBNA-LP (Epstein- Barr virus (EBV) encoded nuclear antigen leader protein), whose co-activation is important for establishing latent viral infections and EBV-mediated B-cell immortalization. A significant dose relationship between rs13397985 genotype and SP140 expression in lymphocytes was demonstrable, with risk alleles being associated with reduced levels of mRNA. SP140 expression has been implicated in innate response to immunodeficiency virus type 1; hence, although speculative, it is possible that genetic variation in SP140 influences the risk of developing CLL through differing response to antigenic challenge.	topic_ll
77544	4	356062	7	NULL	NULL	0	NULL	SP140	GP		expressed in					T cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	SP140 is the lymphoid-restricted homolog of SP100, expressed in all mature B cells and plasma cell lines, as well as some T cells. SP100 is a major mediator of EBNA-LP (Epstein- Barr virus (EBV) encoded nuclear antigen leader protein), whose co-activation is important for establishing latent viral infections and EBV-mediated B-cell immortalization. A significant dose relationship between rs13397985 genotype and SP140 expression in lymphocytes was demonstrable, with risk alleles being associated with reduced levels of mRNA. SP140 expression has been implicated in innate response to immunodeficiency virus type 1; hence, although speculative, it is possible that genetic variation in SP140 influences the risk of developing CLL through differing response to antigenic challenge.	topic_ll
77545	5	356062	7	NULL	NULL	0	NULL	SP100	GP		mediator of		major			EBNA-LP	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	SP140 is the lymphoid-restricted homolog of SP100, expressed in all mature B cells and plasma cell lines, as well as some T cells. SP100 is a major mediator of EBNA-LP (Epstein- Barr virus (EBV) encoded nuclear antigen leader protein), whose co-activation is important for establishing latent viral infections and EBV-mediated B-cell immortalization. A significant dose relationship between rs13397985 genotype and SP140 expression in lymphocytes was demonstrable, with risk alleles being associated with reduced levels of mRNA. SP140 expression has been implicated in innate response to immunodeficiency virus type 1; hence, although speculative, it is possible that genetic variation in SP140 influences the risk of developing CLL through differing response to antigenic challenge.	topic_ll
77546	6	356062	7	NULL	NULL	0	NULL	EBNA-LP	GP		is					Epstein- Barr virus encoded nuclear antigen leader protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	SP140 is the lymphoid-restricted homolog of SP100, expressed in all mature B cells and plasma cell lines, as well as some T cells. SP100 is a major mediator of EBNA-LP (Epstein- Barr virus (EBV) encoded nuclear antigen leader protein), whose co-activation is important for establishing latent viral infections and EBV-mediated B-cell immortalization. A significant dose relationship between rs13397985 genotype and SP140 expression in lymphocytes was demonstrable, with risk alleles being associated with reduced levels of mRNA. SP140 expression has been implicated in innate response to immunodeficiency virus type 1; hence, although speculative, it is possible that genetic variation in SP140 influences the risk of developing CLL through differing response to antigenic challenge.	topic_ll
77547	7	356062	7	NULL	NULL	0	NULL	EBNA-LP	GP	coactivation of	is important for					latent viral infections	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	SP140 is the lymphoid-restricted homolog of SP100, expressed in all mature B cells and plasma cell lines, as well as some T cells. SP100 is a major mediator of EBNA-LP (Epstein- Barr virus (EBV) encoded nuclear antigen leader protein), whose co-activation is important for establishing latent viral infections and EBV-mediated B-cell immortalization. A significant dose relationship between rs13397985 genotype and SP140 expression in lymphocytes was demonstrable, with risk alleles being associated with reduced levels of mRNA. SP140 expression has been implicated in innate response to immunodeficiency virus type 1; hence, although speculative, it is possible that genetic variation in SP140 influences the risk of developing CLL through differing response to antigenic challenge.	topic_ll
77548	8	356062	7	NULL	NULL	0	NULL	EBV	Organism		mediates					B-cell immortalization	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	SP140 is the lymphoid-restricted homolog of SP100, expressed in all mature B cells and plasma cell lines, as well as some T cells. SP100 is a major mediator of EBNA-LP (Epstein- Barr virus (EBV) encoded nuclear antigen leader protein), whose co-activation is important for establishing latent viral infections and EBV-mediated B-cell immortalization. A significant dose relationship between rs13397985 genotype and SP140 expression in lymphocytes was demonstrable, with risk alleles being associated with reduced levels of mRNA. SP140 expression has been implicated in innate response to immunodeficiency virus type 1; hence, although speculative, it is possible that genetic variation in SP140 influences the risk of developing CLL through differing response to antigenic challenge.	topic_ll
77549	9	356062	7	NULL	NULL	0	NULL	EBNA-LP	GP	coactivation of	is important for					statement 8	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	SP140 is the lymphoid-restricted homolog of SP100, expressed in all mature B cells and plasma cell lines, as well as some T cells. SP100 is a major mediator of EBNA-LP (Epstein- Barr virus (EBV) encoded nuclear antigen leader protein), whose co-activation is important for establishing latent viral infections and EBV-mediated B-cell immortalization. A significant dose relationship between rs13397985 genotype and SP140 expression in lymphocytes was demonstrable, with risk alleles being associated with reduced levels of mRNA. SP140 expression has been implicated in innate response to immunodeficiency virus type 1; hence, although speculative, it is possible that genetic variation in SP140 influences the risk of developing CLL through differing response to antigenic challenge.	topic_ll
77550	10	356062	7	NULL	NULL	NULL	NULL	rs13397985 genotype	GP		exist in 					SP140	GP	relationship with expression of			NULL	lymphocytes	NULL	NULL	NULL	NULL	NULL	NULL	SP140 is the lymphoid-restricted homolog of SP100, expressed in all mature B cells and plasma cell lines, as well as some T cells. SP100 is a major mediator of EBNA-LP (Epstein- Barr virus (EBV) encoded nuclear antigen leader protein), whose co-activation is important for establishing latent viral infections and EBV-mediated B-cell immortalization. A significant dose relationship between rs13397985 genotype and SP140 expression in lymphocytes was demonstrable, with risk alleles being associated with reduced levels of mRNA. SP140 expression has been implicated in innate response to immunodeficiency virus type 1; hence, although speculative, it is possible that genetic variation in SP140 influences the risk of developing CLL through differing response to antigenic challenge.	topic_ll
77551	11	356062	7	NULL	NULL	0	NULL	SP140 	GP	expression of	has been implicated in					 immunodeficiency virus type 1	Organism	innate response to			NULL		0	NULL	NULL	NULL	NULL	NULL	SP140 is the lymphoid-restricted homolog of SP100, expressed in all mature B cells and plasma cell lines, as well as some T cells. SP100 is a major mediator of EBNA-LP (Epstein- Barr virus (EBV) encoded nuclear antigen leader protein), whose co-activation is important for establishing latent viral infections and EBV-mediated B-cell immortalization. A significant dose relationship between rs13397985 genotype and SP140 expression in lymphocytes was demonstrable, with risk alleles being associated with reduced levels of mRNA. SP140 expression has been implicated in innate response to immunodeficiency virus type 1; hence, although speculative, it is possible that genetic variation in SP140 influences the risk of developing CLL through differing response to antigenic challenge.	topic_ll
77552	12	356062	7	NULL	NULL	NULL	NULL	SP140	GP	genetic variation in	influence					CLL	MedicalFinding	risk of developing			NULL		NULL	NULL	NULL	NULL	NULL	NULL	SP140 is the lymphoid-restricted homolog of SP100, expressed in all mature B cells and plasma cell lines, as well as some T cells. SP100 is a major mediator of EBNA-LP (Epstein- Barr virus (EBV) encoded nuclear antigen leader protein), whose co-activation is important for establishing latent viral infections and EBV-mediated B-cell immortalization. A significant dose relationship between rs13397985 genotype and SP140 expression in lymphocytes was demonstrable, with risk alleles being associated with reduced levels of mRNA. SP140 expression has been implicated in innate response to immunodeficiency virus type 1; hence, although speculative, it is possible that genetic variation in SP140 influences the risk of developing CLL through differing response to antigenic challenge.	topic_ll
77553	13	356062	7	NULL	NULL	0	NULL	statement 12	Process		occur through					antigenic challenge	Process	response to			NULL		0	NULL	NULL	NULL	NULL	NULL	SP140 is the lymphoid-restricted homolog of SP100, expressed in all mature B cells and plasma cell lines, as well as some T cells. SP100 is a major mediator of EBNA-LP (Epstein- Barr virus (EBV) encoded nuclear antigen leader protein), whose co-activation is important for establishing latent viral infections and EBV-mediated B-cell immortalization. A significant dose relationship between rs13397985 genotype and SP140 expression in lymphocytes was demonstrable, with risk alleles being associated with reduced levels of mRNA. SP140 expression has been implicated in innate response to immunodeficiency virus type 1; hence, although speculative, it is possible that genetic variation in SP140 influences the risk of developing CLL through differing response to antigenic challenge.	topic_ll
77554	1	356063	7	NULL	NULL	0	NULL	MBL	MedicalFinding		develops into					CLL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Intriguingly this assertion is supported by the observation that CLL-phenotype B cells (CD5+, CD23+, CD20low, sIgMlow) of monoclonal B-cell lymphocytosis (MBL) are detectable in ~ 3% of adults in the general population26 and that they are essentially indistinguishable from CLL B cells in terms of chromosomal abnormalities and IgVH mutation status. The recent report that MBL develops into CLL at a rate of 1.1% per year provides direct evidence that MBL is a precursor lesion for CLL. 	topic_ll
77555	2	356063	7	NULL	NULL	0	NULL	MBL	MedicalFinding		is a precursor lesion for					CLL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Intriguingly this assertion is supported by the observation that CLL-phenotype B cells (CD5+, CD23+, CD20low, sIgMlow) of monoclonal B-cell lymphocytosis (MBL) are detectable in ~ 3% of adults in the general population26 and that they are essentially indistinguishable from CLL B cells in terms of chromosomal abnormalities and IgVH mutation status. The recent report that MBL develops into CLL at a rate of 1.1% per year provides direct evidence that MBL is a precursor lesion for CLL. 	topic_ll
77556	3	356063	7	NULL	NULL	0	NULL	MBL	MedicalFinding		is					monoclonal B-cell lymphocytosis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Intriguingly this assertion is supported by the observation that CLL-phenotype B cells (CD5+, CD23+, CD20low, sIgMlow) of monoclonal B-cell lymphocytosis (MBL) are detectable in ~ 3% of adults in the general population26 and that they are essentially indistinguishable from CLL B cells in terms of chromosomal abnormalities and IgVH mutation status. The recent report that MBL develops into CLL at a rate of 1.1% per year provides direct evidence that MBL is a precursor lesion for CLL. 	topic_ll
77557	4	356063	7	NULL	NULL	0	NULL	CLL-phenotype B cells 	Cell		indistinguishable from		essentially			CLL B cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Intriguingly this assertion is supported by the observation that CLL-phenotype B cells (CD5+, CD23+, CD20low, sIgMlow) of monoclonal B-cell lymphocytosis (MBL) are detectable in ~ 3% of adults in the general population26 and that they are essentially indistinguishable from CLL B cells in terms of chromosomal abnormalities and IgVH mutation status. The recent report that MBL develops into CLL at a rate of 1.1% per year provides direct evidence that MBL is a precursor lesion for CLL. 	topic_ll
77558	5	356063	7	NULL	NULL	0	NULL	statement 4	Process		in terms of					chromosomal abnormalities	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Intriguingly this assertion is supported by the observation that CLL-phenotype B cells (CD5+, CD23+, CD20low, sIgMlow) of monoclonal B-cell lymphocytosis (MBL) are detectable in ~ 3% of adults in the general population26 and that they are essentially indistinguishable from CLL B cells in terms of chromosomal abnormalities and IgVH mutation status. The recent report that MBL develops into CLL at a rate of 1.1% per year provides direct evidence that MBL is a precursor lesion for CLL. 	topic_ll
77559	6	356063	7	NULL	NULL	0	NULL	statement 4	Process		in terms of					IgVH mutation status	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Intriguingly this assertion is supported by the observation that CLL-phenotype B cells (CD5+, CD23+, CD20low, sIgMlow) of monoclonal B-cell lymphocytosis (MBL) are detectable in ~ 3% of adults in the general population26 and that they are essentially indistinguishable from CLL B cells in terms of chromosomal abnormalities and IgVH mutation status. The recent report that MBL develops into CLL at a rate of 1.1% per year provides direct evidence that MBL is a precursor lesion for CLL. 	topic_ll
77560	7	356063	7	NULL	NULL	0	NULL	statement 1	Process		evidence for		direct			statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Intriguingly this assertion is supported by the observation that CLL-phenotype B cells (CD5+, CD23+, CD20low, sIgMlow) of monoclonal B-cell lymphocytosis (MBL) are detectable in ~ 3% of adults in the general population26 and that they are essentially indistinguishable from CLL B cells in terms of chromosomal abnormalities and IgVH mutation status. The recent report that MBL develops into CLL at a rate of 1.1% per year provides direct evidence that MBL is a precursor lesion for CLL. 	topic_ll
77561	1	356064	7	NULL	NULL	0	NULL	IgVH	GP	mutation status of	prognostic marker in					CLL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	IgVH mutation status is a well accepted prognostic marker in chronic lymphocytic leukemia (CLL). 	topic_ll
77562	2	356064	7	NULL	NULL	0	NULL	CLL	MedicalFinding		is					chronic lymphocytic leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	IgVH mutation status is a well accepted prognostic marker in chronic lymphocytic leukemia (CLL). 	topic_ll
77563	1	356065	7	NULL	NULL	NULL	NULL	CLL	MedicalFinding	development of	influenced by					antigenic recognition	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Evidence suggests that the development of CLL might be influenced by antigenic recognition or selection through the B-cell receptor (BCR).	topic_ll
77564	2	356065	7	NULL	NULL	NULL	NULL	CLL	MedicalFinding	development of	influenced by					antigenic selection	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Evidence suggests that the development of CLL might be influenced by antigenic recognition or selection through the B-cell receptor (BCR).	topic_ll
77565	3	356065	7	NULL	NULL	0	NULL	statement 1	Process		occur through					BCR	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Evidence suggests that the development of CLL might be influenced by antigenic recognition or selection through the B-cell receptor (BCR).	topic_ll
77566	4	356065	7	NULL	NULL	0	NULL	statement 2	Process		occur through					BCR	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Evidence suggests that the development of CLL might be influenced by antigenic recognition or selection through the B-cell receptor (BCR).	topic_ll
77567	5	356065	7	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Evidence suggests that the development of CLL might be influenced by antigenic recognition or selection through the B-cell receptor (BCR).	topic_ll
77568	6	356065	7	NULL	NULL	0	NULL	BCR	GP		is					B-cell receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Evidence suggests that the development of CLL might be influenced by antigenic recognition or selection through the B-cell receptor (BCR).	topic_ll
77569	1	356066	7	NULL	NULL	0	NULL	IGHV1-69	GP	Asymmetric usage of	characterized in					CLL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Asymmetric usage of the immunoglobulin genes have been well characterized in CLL, with notable overrepresentation of various genes, including IGHV1-69 and IGHV4-34.	topic_ll
77570	2	356066	7	NULL	NULL	0	NULL	IGHV4-34	GP	Asymmetric usage of	characterized in					CLL	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Asymmetric usage of the immunoglobulin genes have been well characterized in CLL, with notable overrepresentation of various genes, including IGHV1-69 and IGHV4-34.	topic_ll
77571	1	356067	7	NULL	NULL	0	NULL	B cells	Cell	Preferential stimulation of	express					IGHV4-34 gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Preferential stimulation of B cells expressing the IGHV4-34 gene occurs in a number of infections, including those caused by Epstein-Barr virus (EBV) and cytomegalovirus (CMV).	topic_ll
77572	2	356067	7	NULL	NULL	0	NULL	EBV	Organism	infection of	cause					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Preferential stimulation of B cells expressing the IGHV4-34 gene occurs in a number of infections, including those caused by Epstein-Barr virus (EBV) and cytomegalovirus (CMV).	topic_ll
77573	3	356067	7	NULL	NULL	0	NULL	CMV	Organism	infection of	cause					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Preferential stimulation of B cells expressing the IGHV4-34 gene occurs in a number of infections, including those caused by Epstein-Barr virus (EBV) and cytomegalovirus (CMV).	topic_ll
77574	4	356067	7	NULL	NULL	0	NULL	EBV	Organism		is involved in					Epstein-Barr virus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Preferential stimulation of B cells expressing the IGHV4-34 gene occurs in a number of infections, including those caused by Epstein-Barr virus (EBV) and cytomegalovirus (CMV).	topic_ll
77575	5	356067	7	NULL	NULL	0	NULL	CMV	Organism		is					cytomegalovirus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Preferential stimulation of B cells expressing the IGHV4-34 gene occurs in a number of infections, including those caused by Epstein-Barr virus (EBV) and cytomegalovirus (CMV).	topic_ll
77576	1	356068	7	NULL	NULL	0	NULL	Resveratrol	Chemical		blocks					cancer promoting genes	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Resveratrol: This phytochemical blocks the actions of a number of a number of cancer promoting genes thereby causing cancer cells to enter into apoptosis (cell death) and is included in the treatment of all cancers.	topic_ll
77577	2	356068	7	NULL	NULL	0	NULL	cancer cells	Cell		enter into					apoptosis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Resveratrol: This phytochemical blocks the actions of a number of a number of cancer promoting genes thereby causing cancer cells to enter into apoptosis (cell death) and is included in the treatment of all cancers.	topic_ll
77578	3	356068	7	NULL	NULL	0	NULL	statement 1	Process		cause					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Resveratrol: This phytochemical blocks the actions of a number of a number of cancer promoting genes thereby causing cancer cells to enter into apoptosis (cell death) and is included in the treatment of all cancers.	topic_ll
77579	4	356068	7	NULL	NULL	0	NULL	Resveratrol	Chemical		is used in the					cancer	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Resveratrol: This phytochemical blocks the actions of a number of a number of cancer promoting genes thereby causing cancer cells to enter into apoptosis (cell death) and is included in the treatment of all cancers.	topic_ll
77580	5	356068	7	NULL	NULL	0	NULL	Resveratrol	Chemical		is a type of					phytochemical	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Resveratrol: This phytochemical blocks the actions of a number of a number of cancer promoting genes thereby causing cancer cells to enter into apoptosis (cell death) and is included in the treatment of all cancers.	topic_ll
77581	1	356069	7	NULL	NULL	0	NULL	MP	Chemical		role in		significant			AML	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	The results of the present study, together with our previous clinical experience, suggest that MP, especially at high doses, could have a significant role in the treatment of some AML patients by inducing apoptosis and differentiation of leukemic cells.	topic_ll
77582	2	356069	7	NULL	NULL	0	NULL	statement 1	Process		occur by					apoptosis	Process	inducing			NULL		0	NULL	NULL	NULL	NULL	NULL	The results of the present study, together with our previous clinical experience, suggest that MP, especially at high doses, could have a significant role in the treatment of some AML patients by inducing apoptosis and differentiation of leukemic cells.	topic_ll
77583	3	356069	7	NULL	NULL	0	NULL	statement 1	Process		occur by					leukemic cells	Cell	differentiation of			NULL		0	NULL	NULL	NULL	NULL	NULL	The results of the present study, together with our previous clinical experience, suggest that MP, especially at high doses, could have a significant role in the treatment of some AML patients by inducing apoptosis and differentiation of leukemic cells.	topic_ll
77584	1	356070	7	NULL	NULL	0	NULL	Resveratrol	Chemical		is a type of					natural phytochemical	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Resveratrol (trans-3,5,4′-trihydroxystilbene) is a natural phytochemical found in grapes and wine. Numerous biological effects of resveratrol have been reported in the last 10 years. In this paper, the competitive inhibition of intracellular uptake of glucose and dehydroascorbic acid in U937 and HL-60 cells by resveratrol is reported.	topic_ll
77585	2	356070	7	NULL	NULL	0	NULL	statement 1	Process		found in					grapes	Food				NULL		0	NULL	NULL	NULL	NULL	NULL	Resveratrol (trans-3,5,4′-trihydroxystilbene) is a natural phytochemical found in grapes and wine. Numerous biological effects of resveratrol have been reported in the last 10 years. In this paper, the competitive inhibition of intracellular uptake of glucose and dehydroascorbic acid in U937 and HL-60 cells by resveratrol is reported.	topic_ll
77586	3	356070	7	NULL	NULL	0	NULL	statement 1	Process		found in					wine	Food				NULL		0	NULL	NULL	NULL	NULL	NULL	Resveratrol (trans-3,5,4′-trihydroxystilbene) is a natural phytochemical found in grapes and wine. Numerous biological effects of resveratrol have been reported in the last 10 years. In this paper, the competitive inhibition of intracellular uptake of glucose and dehydroascorbic acid in U937 and HL-60 cells by resveratrol is reported.	topic_ll
77587	4	356070	7	NULL	NULL	NULL	NULL	resveratrol 	Chemical		inhibits		competitively			glucose	Chemical	intracellular uptake of			NULL	U937 cells	NULL	NULL	NULL	NULL	NULL	NULL	Resveratrol (trans-3,5,4′-trihydroxystilbene) is a natural phytochemical found in grapes and wine. Numerous biological effects of resveratrol have been reported in the last 10 years. In this paper, the competitive inhibition of intracellular uptake of glucose and dehydroascorbic acid in U937 and HL-60 cells by resveratrol is reported.	topic_ll
77588	5	356070	7	NULL	NULL	NULL	NULL	resveratrol	Chemical		inhibits		competitively			dehydroascorbic acid	Chemical	intracellular uptake of			NULL	U937 cells	NULL	NULL	NULL	NULL	NULL	NULL	Resveratrol (trans-3,5,4′-trihydroxystilbene) is a natural phytochemical found in grapes and wine. Numerous biological effects of resveratrol have been reported in the last 10 years. In this paper, the competitive inhibition of intracellular uptake of glucose and dehydroascorbic acid in U937 and HL-60 cells by resveratrol is reported.	topic_ll
77589	6	356070	7	NULL	NULL	0	NULL	resveratrol	Chemical		inhibits		competitively			glucose	Chemical	intracellular uptake of			NULL	HL-60 cells	0	NULL	NULL	NULL	NULL	NULL	Resveratrol (trans-3,5,4′-trihydroxystilbene) is a natural phytochemical found in grapes and wine. Numerous biological effects of resveratrol have been reported in the last 10 years. In this paper, the competitive inhibition of intracellular uptake of glucose and dehydroascorbic acid in U937 and HL-60 cells by resveratrol is reported.	topic_ll
77590	7	356070	7	NULL	NULL	NULL	NULL	resveratrol	Chemical		inhibits		competitively			dehydroascorbic acid	Chemical	intracellular uptake of			NULL	HL-60 cells	NULL	NULL	NULL	NULL	NULL	NULL	Resveratrol (trans-3,5,4′-trihydroxystilbene) is a natural phytochemical found in grapes and wine. Numerous biological effects of resveratrol have been reported in the last 10 years. In this paper, the competitive inhibition of intracellular uptake of glucose and dehydroascorbic acid in U937 and HL-60 cells by resveratrol is reported.	topic_ll
77591	8	356070	7	NULL	NULL	0	NULL	resveratrol	Chemical		is					trans-3,5,4�?�-trihydroxystilbene	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Resveratrol (trans-3,5,4′-trihydroxystilbene) is a natural phytochemical found in grapes and wine. Numerous biological effects of resveratrol have been reported in the last 10 years. In this paper, the competitive inhibition of intracellular uptake of glucose and dehydroascorbic acid in U937 and HL-60 cells by resveratrol is reported.	topic_ll
77592	1	356071	7	NULL	NULL	NULL	NULL	mitochondrial respiration	Process	decreased	point to					mitochondria	CellComponent	underlying dysfunction of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial disorders. 	topic_bd
77593	2	356071	7	NULL	NULL	0	NULL	mitochondrial morphology	PhysicalPhenomenon	changes in	point to					mitochondria	CellComponent	underlying dysfunction of			NULL		0	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial disorders. 	topic_bd
77594	3	356071	7	NULL	NULL	0	NULL	mtDNA	NucleicAcid	increase in	point to					mitochondria	CellComponent	underlying dysfunction of			NULL		0	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial disorders. 	topic_bd
77595	4	356071	7	NULL	NULL	0	NULL	mtDNA	NucleicAcid	increase in levels of mutation of	point to					mitochondria	CellComponent	underlying dysfunction of			NULL		0	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial disorders. 	topic_bd
77596	5	356071	7	NULL	NULL	NULL	NULL	 nuclear mRNA molecule	GP		involved in					mitochondrial respiration	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial disorders. 	topic_bd
77597	6	356071	7	NULL	NULL	NULL	NULL	nuclear proteins	GP		involved in					mitochondrial respiration	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial disorders. 	topic_bd
77598	7	356071	7	NULL	NULL	0	NULL	nuclear mRNA molecule	GP	downregulation of	point to					mitochondria	CellComponent	underlying dysfunction of			NULL		0	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial disorders. 	topic_bd
77599	8	356071	7	NULL	NULL	0	NULL	nuclear proteins	GP	downregulation of	point to					mitochondria	CellComponent	underlying dysfunction of			NULL		0	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial disorders. 	topic_bd
77600	9	356071	7	NULL	NULL	NULL	NULL	high energy phosphates	Chemical	decreased	point to					mitochondria	CellComponent	underlying dysfunction of			NULL	brain	NULL	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial disorders. 	topic_bd
77601	10	356071	7	NULL	NULL	NULL	NULL	pH	QuantityOrMeasure	decreased	point to					mitochondria	CellComponent	underlying dysfunction of			NULL	brain	NULL	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial disorders. 	topic_bd
77602	11	356071	7	NULL	NULL	0	NULL	mitochondrial disorder	MedicalFinding	psychotic symptoms in	point to					mitochondria	CellComponent	underlying dysfunction of			NULL		0	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial disorders. 	topic_bd
77603	12	356071	7	NULL	NULL	0	NULL	mitochondrial disorder	MedicalFinding	affective symptoms in	point to					mitochondria	CellComponent	underlying dysfunction of			NULL		0	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial disorders. 	topic_bd
77604	13	356071	7	NULL	NULL	0	NULL	mitochondrial disorder	MedicalFinding	cognitive decline in	point to					mitochondria	CellComponent	underlying dysfunction of			NULL		0	NULL	NULL	NULL	NULL	NULL	Several pieces of evidence point to an underlying dysfunction of mitochondria: (i) decreased mitochondrial respiration; (ii) changes in mitochondrial morphology; (iii) increases in mitochondrial DNA (mtDNA) polymorphisms and in levels of mtDNA mutations; (iv) downregulation of nuclear mRNA molecules and proteins involved in mitochondrial respiration; (v) decreased high-energy phosphates and decreased pH in the brain; and (vi) psychotic and affective symptoms, and cognitive decline in mitochondrial disorders. 	topic_bd
78062	1	356072	6	NULL	NULL	0	NULL	age	AbstractConcept		increases					Breast cancer	MedicalFinding	development of			NULL		0	NULL	NULL	NULL	NULL	NULL	Your risk of developing breast cancer increases as you get older. About 1 out of 8 invasive breast cancers are found in women younger than 45, while about 2 out of 3 invasive breast cancers are found in women age 55 or older.	topic_bc
78063	1	356072	6	NULL	NULL	0	NULL	age	AbstractConcept		increases					Breast cancer	MedicalFinding	development of			NULL		0	NULL	NULL	NULL	NULL	NULL	Your risk of developing breast cancer increases as you get older. About 1 out of 8 invasive breast cancers are found in women younger than 45, while about 2 out of 3 invasive breast cancers are found in women age 55 or older.	topic_bc
77605	1	356073	7	NULL	NULL	0	NULL	BPD susceptibility region	Chromosome		located at					3q29	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	We identified a bipolar disorder (BPD) susceptibility region on chromosome 3q29 in a genome-wide linkage scan ( Bailer et al. 2002 (Biol Psychiatry 52: 40), NPL-score 4.09) and follow-up linkage analysis ( Schosser et al. 2004 (J Psychiatr Res 38(3): 357), NPL-scores >3 with five markers). 	topic_bd
77606	2	356073	7	NULL	NULL	0	NULL	BPD	MedicalFinding		is					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We identified a bipolar disorder (BPD) susceptibility region on chromosome 3q29 in a genome-wide linkage scan ( Bailer et al. 2002 (Biol Psychiatry 52: 40), NPL-score 4.09) and follow-up linkage analysis ( Schosser et al. 2004 (J Psychiatr Res 38(3): 357), NPL-scores >3 with five markers). 	topic_bd
77607	1	356074	7	NULL	NULL	0	NULL	BPD susceptibility region	Chromosome		located at					3q29 	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	We identified a bipolar disorder (BPD) susceptibility region on chromosome 3q29 in a genome-wide linkage scan ( Bailer et al. 2002 (Biol Psychiatry 52: 40), NPL-score 4.09) and follow-up linkage analysis ( Schosser et al. 2004 (J Psychiatr Res 38(3): 357), NPL-scores >3 with five markers). These findings were supported by further fine-mapping of this region ( Schosser et al. 2007 (Eur Neuropsychopharmacol 17(6-7): 501)), finding NPL-scores >3.9 with SNPs (single nucleotide polymorphisms) spanning a region of 3.46 Mbp in BPD families. Since genetic association studies are more powerful than linkage studies for detecting susceptibility genes of small effect size, we aimed to replicate these findings in an independent case-control sample collected in London (UK) and Vienna (Austria). Methods. A total of 51 SNPs were genotyped using Sequenom MassARRAY(®) iPLEX Gold and tested for association in a sample of 526 cases suffering from DSM-IV and/or ICD-10 diagnosis of BPD and 691 controls. Results. No genotypic and/or allelic association, as well as no haplotypic association, was found for any SNP after multiple testing correction. Conclusions. However, we cannot exclude the possibility that our sample might not have the power to detect rare variants associated with susceptibility to BPD.	topic_bd
77608	2	356074	7	NULL	NULL	0	NULL	BPD	MedicalFinding		is					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We identified a bipolar disorder (BPD) susceptibility region on chromosome 3q29 in a genome-wide linkage scan ( Bailer et al. 2002 (Biol Psychiatry 52: 40), NPL-score 4.09) and follow-up linkage analysis ( Schosser et al. 2004 (J Psychiatr Res 38(3): 357), NPL-scores >3 with five markers). These findings were supported by further fine-mapping of this region ( Schosser et al. 2007 (Eur Neuropsychopharmacol 17(6-7): 501)), finding NPL-scores >3.9 with SNPs (single nucleotide polymorphisms) spanning a region of 3.46 Mbp in BPD families. Since genetic association studies are more powerful than linkage studies for detecting susceptibility genes of small effect size, we aimed to replicate these findings in an independent case-control sample collected in London (UK) and Vienna (Austria). Methods. A total of 51 SNPs were genotyped using Sequenom MassARRAY(®) iPLEX Gold and tested for association in a sample of 526 cases suffering from DSM-IV and/or ICD-10 diagnosis of BPD and 691 controls. Results. No genotypic and/or allelic association, as well as no haplotypic association, was found for any SNP after multiple testing correction. Conclusions. However, we cannot exclude the possibility that our sample might not have the power to detect rare variants associated with susceptibility to BPD.	topic_bd
77609	1	356075	7	NULL	NULL	0	NULL	 transcriptome	NucleicAcid		is the set of					RNA molecules	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	The transcriptome is the set of all RNA molecules, including mRNA, rRNA, tRNA, and other non-coding RNA produced in one or a population of cells.	topic_bd
77610	2	356075	7	NULL	NULL	0	NULL	RNA molecules	NucleicAcid		include					mRNA	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	The transcriptome is the set of all RNA molecules, including mRNA, rRNA, tRNA, and other non-coding RNA produced in one or a population of cells.	topic_bd
77611	3	356075	7	NULL	NULL	0	NULL	RNA molecules	NucleicAcid		include					rRNA	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	The transcriptome is the set of all RNA molecules, including mRNA, rRNA, tRNA, and other non-coding RNA produced in one or a population of cells.	topic_bd
77612	4	356075	7	NULL	NULL	0	NULL	RNA molecules	NucleicAcid		include					tRNA	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	The transcriptome is the set of all RNA molecules, including mRNA, rRNA, tRNA, and other non-coding RNA produced in one or a population of cells.	topic_bd
77613	5	356075	7	NULL	NULL	0	NULL	RNA molecules	NucleicAcid		include					non-coding RNA	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	The transcriptome is the set of all RNA molecules, including mRNA, rRNA, tRNA, and other non-coding RNA produced in one or a population of cells.	topic_bd
77614	6	356075	7	NULL	NULL	NULL	NULL	statement 1	NucleicAcid		occur in					cells	Cell	population of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	The transcriptome is the set of all RNA molecules, including mRNA, rRNA, tRNA, and other non-coding RNA produced in one or a population of cells.	topic_bd
77615	7	356075	7	NULL	NULL	NULL	NULL	statement 1	NucleicAcid		occur in					one cell	Cell				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The transcriptome is the set of all RNA molecules, including mRNA, rRNA, tRNA, and other non-coding RNA produced in one or a population of cells.	topic_bd
77616	8	356075	7	NULL	NULL	0	NULL	statement 6	Process		is an alternative to					statement 7	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The transcriptome is the set of all RNA molecules, including mRNA, rRNA, tRNA, and other non-coding RNA produced in one or a population of cells.	topic_bd
77617	1	356076	7	NULL	NULL	0	NULL	Transcriptome	NucleicAcid		refers to					mRNAs	NucleicAcid	entirety of			NULL		0	NULL	NULL	NULL	NULL	NULL	‘Transcriptome’ refers to the entirety of messenger ribonucleic acids (mRNAs) in a particular tissue. It is assumed that an altered expression level of an mRNA in a disease is an indication for an abnormality in either the encoded protein, or a biologically connected structure or function. I	topic_bd
77618	2	356076	7	NULL	NULL	0	NULL	statement 1	NucleicAcid		occur in					tissue	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	‘Transcriptome’ refers to the entirety of messenger ribonucleic acids (mRNAs) in a particular tissue. It is assumed that an altered expression level of an mRNA in a disease is an indication for an abnormality in either the encoded protein, or a biologically connected structure or function. I	topic_bd
77619	3	356076	7	NULL	NULL	NULL	NULL	mRNA	NucleicAcid	altered expression level of 	indicate					encoded protein	GP	abnormality in			NULL		NULL	NULL	NULL	NULL	NULL	NULL	‘Transcriptome’ refers to the entirety of messenger ribonucleic acids (mRNAs) in a particular tissue. It is assumed that an altered expression level of an mRNA in a disease is an indication for an abnormality in either the encoded protein, or a biologically connected structure or function. I	topic_bd
77620	4	356076	7	NULL	NULL	0	NULL	statement 3	Process		occur in a					disease	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	‘Transcriptome’ refers to the entirety of messenger ribonucleic acids (mRNAs) in a particular tissue. It is assumed that an altered expression level of an mRNA in a disease is an indication for an abnormality in either the encoded protein, or a biologically connected structure or function. I	topic_bd
77621	5	356076	7	NULL	NULL	0	NULL	mRNA	NucleicAcid	altered expression level of 	indicate					biologically connected structure	CellComponent	abnormality in			NULL		0	NULL	NULL	NULL	NULL	NULL	‘Transcriptome’ refers to the entirety of messenger ribonucleic acids (mRNAs) in a particular tissue. It is assumed that an altered expression level of an mRNA in a disease is an indication for an abnormality in either the encoded protein, or a biologically connected structure or function. I	topic_bd
77622	6	356076	7	NULL	NULL	0	NULL	mRNA	NucleicAcid	altered expression level of 	indicate					biological function	Process	abnormality in			NULL		0	NULL	NULL	NULL	NULL	NULL	‘Transcriptome’ refers to the entirety of messenger ribonucleic acids (mRNAs) in a particular tissue. It is assumed that an altered expression level of an mRNA in a disease is an indication for an abnormality in either the encoded protein, or a biologically connected structure or function. I	topic_bd
77623	7	356076	7	NULL	NULL	0	NULL	statement 5	Process		occur in a					disease	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	‘Transcriptome’ refers to the entirety of messenger ribonucleic acids (mRNAs) in a particular tissue. It is assumed that an altered expression level of an mRNA in a disease is an indication for an abnormality in either the encoded protein, or a biologically connected structure or function. I	topic_bd
77624	8	356076	7	NULL	NULL	0	NULL	statement 6	Process		occur in a					disease	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	‘Transcriptome’ refers to the entirety of messenger ribonucleic acids (mRNAs) in a particular tissue. It is assumed that an altered expression level of an mRNA in a disease is an indication for an abnormality in either the encoded protein, or a biologically connected structure or function. I	topic_bd
77625	9	356076	7	NULL	NULL	0	NULL	mRNA	NucleicAcid		is					messenger ribonucleic acids	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	‘Transcriptome’ refers to the entirety of messenger ribonucleic acids (mRNAs) in a particular tissue. It is assumed that an altered expression level of an mRNA in a disease is an indication for an abnormality in either the encoded protein, or a biologically connected structure or function. I	topic_bd
78176	1	356077	6	NULL	NULL	0	NULL	miR-126	NucleicAcid	restoration of	reduces					tumour growth	process				NULL		0	NULL	NULL	NULL	NULL	NULL	A search for general regulators of cancer metastasis has yielded a set of microRNAs for which expression is specifically lost as human breast cancer cells develop metastatic potential. Here we show that restoring the expression of these microRNAs in malignant cells suppresses lung and bone metastasis by human cancer cells in vivo. Of these microRNAs, miR-126 restoration reduces overall tumour growth and proliferation, whereas miR-335 inhibits metastatic cell invasion. miR-335 regulates a set of genes whose collective expression in a large cohort of human tumours is associated with risk of distal metastasis. miR-335 suppresses metastasis and migration through targeting of the progenitor cell transcription factor SOX4 and extracellular matrix component tenascin C. Expression of miR-126 and miR-335 is lost in the majority of primary breast tumours from patients who relapse, and the loss of expression of either microRNA is associated with poor distal metastasis-free survival. miR-335 and miR-126 are thus identified as metastasis suppressor microRNAs in human breast cancer.	topic_bc
78177	2	356077	6	NULL	NULL	0	NULL	miR-126	NucleicAcid		reduces					tumour proliferation	process				NULL		0	NULL	NULL	NULL	NULL	NULL	A search for general regulators of cancer metastasis has yielded a set of microRNAs for which expression is specifically lost as human breast cancer cells develop metastatic potential. Here we show that restoring the expression of these microRNAs in malignant cells suppresses lung and bone metastasis by human cancer cells in vivo. Of these microRNAs, miR-126 restoration reduces overall tumour growth and proliferation, whereas miR-335 inhibits metastatic cell invasion. miR-335 regulates a set of genes whose collective expression in a large cohort of human tumours is associated with risk of distal metastasis. miR-335 suppresses metastasis and migration through targeting of the progenitor cell transcription factor SOX4 and extracellular matrix component tenascin C. Expression of miR-126 and miR-335 is lost in the majority of primary breast tumours from patients who relapse, and the loss of expression of either microRNA is associated with poor distal metastasis-free survival. miR-335 and miR-126 are thus identified as metastasis suppressor microRNAs in human breast cancer.	topic_bc
78178	3	356077	6	NULL	NULL	0	NULL	miR-335	NucleicAcid		inhibits					metastatic cell	cell	invasion of 			NULL		0	NULL	NULL	NULL	NULL	NULL	A search for general regulators of cancer metastasis has yielded a set of microRNAs for which expression is specifically lost as human breast cancer cells develop metastatic potential. Here we show that restoring the expression of these microRNAs in malignant cells suppresses lung and bone metastasis by human cancer cells in vivo. Of these microRNAs, miR-126 restoration reduces overall tumour growth and proliferation, whereas miR-335 inhibits metastatic cell invasion. miR-335 regulates a set of genes whose collective expression in a large cohort of human tumours is associated with risk of distal metastasis. miR-335 suppresses metastasis and migration through targeting of the progenitor cell transcription factor SOX4 and extracellular matrix component tenascin C. Expression of miR-126 and miR-335 is lost in the majority of primary breast tumours from patients who relapse, and the loss of expression of either microRNA is associated with poor distal metastasis-free survival. miR-335 and miR-126 are thus identified as metastasis suppressor microRNAs in human breast cancer.	topic_bc
78179	4	356077	6	NULL	NULL	0	NULL	SOX4	GP		is a type of					progenitor cell transcription factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	A search for general regulators of cancer metastasis has yielded a set of microRNAs for which expression is specifically lost as human breast cancer cells develop metastatic potential. Here we show that restoring the expression of these microRNAs in malignant cells suppresses lung and bone metastasis by human cancer cells in vivo. Of these microRNAs, miR-126 restoration reduces overall tumour growth and proliferation, whereas miR-335 inhibits metastatic cell invasion. miR-335 regulates a set of genes whose collective expression in a large cohort of human tumours is associated with risk of distal metastasis. miR-335 suppresses metastasis and migration through targeting of the progenitor cell transcription factor SOX4 and extracellular matrix component tenascin C. Expression of miR-126 and miR-335 is lost in the majority of primary breast tumours from patients who relapse, and the loss of expression of either microRNA is associated with poor distal metastasis-free survival. miR-335 and miR-126 are thus identified as metastasis suppressor microRNAs in human breast cancer.	topic_bc
78180	5	356077	6	NULL	NULL	0	NULL	 tenascin C	GP		is a type of					 extracellular matrix component	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	A search for general regulators of cancer metastasis has yielded a set of microRNAs for which expression is specifically lost as human breast cancer cells develop metastatic potential. Here we show that restoring the expression of these microRNAs in malignant cells suppresses lung and bone metastasis by human cancer cells in vivo. Of these microRNAs, miR-126 restoration reduces overall tumour growth and proliferation, whereas miR-335 inhibits metastatic cell invasion. miR-335 regulates a set of genes whose collective expression in a large cohort of human tumours is associated with risk of distal metastasis. miR-335 suppresses metastasis and migration through targeting of the progenitor cell transcription factor SOX4 and extracellular matrix component tenascin C. Expression of miR-126 and miR-335 is lost in the majority of primary breast tumours from patients who relapse, and the loss of expression of either microRNA is associated with poor distal metastasis-free survival. miR-335 and miR-126 are thus identified as metastasis suppressor microRNAs in human breast cancer.	topic_bc
78171	1	356080	6	NULL	NULL	0	NULL	rs4415084	NucleicAcid		is located on					chromosome 5p12	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	We carried out a genome-wide association study of breast cancer predisposition with replication and refinement studies involving 6,145 cases and 33,016 controls and identified two SNPs (rs4415084 and rs10941679) on 5p12 that confer risk, preferentially for estrogen receptor (ER)-positive tumors (OR = 1.27, P = 2.5 × 10−12 for rs10941679). The nearest gene, MRPS30, was previously implicated in apoptosis, ER-positive tumors and favorable prognosis. A recently reported signal in FGFR2 was also found to associate specifically with ER-positive breast cancer. http://www.nature.com/ng/journal/v40/n6/full/ng.131.html	topic_bc
78172	2	356080	6	NULL	NULL	0	NULL	rs10941679	NucleicAcid		is located on					chromosome 5p12	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	We carried out a genome-wide association study of breast cancer predisposition with replication and refinement studies involving 6,145 cases and 33,016 controls and identified two SNPs (rs4415084 and rs10941679) on 5p12 that confer risk, preferentially for estrogen receptor (ER)-positive tumors (OR = 1.27, P = 2.5 × 10−12 for rs10941679). The nearest gene, MRPS30, was previously implicated in apoptosis, ER-positive tumors and favorable prognosis. A recently reported signal in FGFR2 was also found to associate specifically with ER-positive breast cancer. http://www.nature.com/ng/journal/v40/n6/full/ng.131.html	topic_bc
78173	3	356080	6	NULL	NULL	0	NULL	statement 1	process		poses risk for					ER positive tumors	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We carried out a genome-wide association study of breast cancer predisposition with replication and refinement studies involving 6,145 cases and 33,016 controls and identified two SNPs (rs4415084 and rs10941679) on 5p12 that confer risk, preferentially for estrogen receptor (ER)-positive tumors (OR = 1.27, P = 2.5 × 10−12 for rs10941679). The nearest gene, MRPS30, was previously implicated in apoptosis, ER-positive tumors and favorable prognosis. A recently reported signal in FGFR2 was also found to associate specifically with ER-positive breast cancer. http://www.nature.com/ng/journal/v40/n6/full/ng.131.html	topic_bc
78174	4	356080	6	NULL	NULL	0	NULL	statement 2	process		poses risk for					ER positive tumors	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We carried out a genome-wide association study of breast cancer predisposition with replication and refinement studies involving 6,145 cases and 33,016 controls and identified two SNPs (rs4415084 and rs10941679) on 5p12 that confer risk, preferentially for estrogen receptor (ER)-positive tumors (OR = 1.27, P = 2.5 × 10−12 for rs10941679). The nearest gene, MRPS30, was previously implicated in apoptosis, ER-positive tumors and favorable prognosis. A recently reported signal in FGFR2 was also found to associate specifically with ER-positive breast cancer. http://www.nature.com/ng/journal/v40/n6/full/ng.131.html	topic_bc
78175	5	356080	6	NULL	NULL	0	NULL	MRPS30	GP		is implicated in					apoptosis	process				NULL		0	NULL	NULL	NULL	NULL	NULL	We carried out a genome-wide association study of breast cancer predisposition with replication and refinement studies involving 6,145 cases and 33,016 controls and identified two SNPs (rs4415084 and rs10941679) on 5p12 that confer risk, preferentially for estrogen receptor (ER)-positive tumors (OR = 1.27, P = 2.5 × 10−12 for rs10941679). The nearest gene, MRPS30, was previously implicated in apoptosis, ER-positive tumors and favorable prognosis. A recently reported signal in FGFR2 was also found to associate specifically with ER-positive breast cancer. http://www.nature.com/ng/journal/v40/n6/full/ng.131.html	topic_bc
78167	1	356081	6	NULL	NULL	0	NULL	Mesenchymal stem cells	Cell		localize					breast carcinoma	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Mesenchymal stem cells have been recently described to localize to breast carcinomas, where they integrate into the tumour-associated stroma. However, the involvement of mesenchymal stem cells (or their derivatives) in tumour pathophysiology has not been addressed. Here, we demonstrate that bone-marrow-derived human mesenchymal stem cells, when mixed with otherwise weakly metastatic human breast carcinoma cells, cause the cancer cells to increase their metastatic potency greatly when this cell mixture is introduced into a subcutaneous site and allowed to form a tumour xenograft. The breast cancer cells stimulate de novo secretion of the chemokine CCL5 (also called RANTES) from mesenchymal stem cells, which then acts in a paracrine fashion on the cancer cells to enhance their motility, invasion and metastasis. This enhanced metastatic ability is reversible and is dependent on CCL5 signalling through the chemokine receptor CCR5. Collectively, these data demonstrate that the tumour microenvironment facilitates metastatic spread by eliciting reversible changes in the phenotype of cancer cells.	topic_bc
78168	2	356081	6	NULL	NULL	0	NULL	breast cancer cell	Cell		stimulate					CCL5	Chemical	secretion of			NULL	de novo	0	NULL	NULL	NULL	NULL	NULL	Mesenchymal stem cells have been recently described to localize to breast carcinomas, where they integrate into the tumour-associated stroma. However, the involvement of mesenchymal stem cells (or their derivatives) in tumour pathophysiology has not been addressed. Here, we demonstrate that bone-marrow-derived human mesenchymal stem cells, when mixed with otherwise weakly metastatic human breast carcinoma cells, cause the cancer cells to increase their metastatic potency greatly when this cell mixture is introduced into a subcutaneous site and allowed to form a tumour xenograft. The breast cancer cells stimulate de novo secretion of the chemokine CCL5 (also called RANTES) from mesenchymal stem cells, which then acts in a paracrine fashion on the cancer cells to enhance their motility, invasion and metastasis. This enhanced metastatic ability is reversible and is dependent on CCL5 signalling through the chemokine receptor CCR5. Collectively, these data demonstrate that the tumour microenvironment facilitates metastatic spread by eliciting reversible changes in the phenotype of cancer cells.	topic_bc
78169	3	356081	6	NULL	NULL	0	NULL	CCL5	Chemical		is a type of					chemokine	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Mesenchymal stem cells have been recently described to localize to breast carcinomas, where they integrate into the tumour-associated stroma. However, the involvement of mesenchymal stem cells (or their derivatives) in tumour pathophysiology has not been addressed. Here, we demonstrate that bone-marrow-derived human mesenchymal stem cells, when mixed with otherwise weakly metastatic human breast carcinoma cells, cause the cancer cells to increase their metastatic potency greatly when this cell mixture is introduced into a subcutaneous site and allowed to form a tumour xenograft. The breast cancer cells stimulate de novo secretion of the chemokine CCL5 (also called RANTES) from mesenchymal stem cells, which then acts in a paracrine fashion on the cancer cells to enhance their motility, invasion and metastasis. This enhanced metastatic ability is reversible and is dependent on CCL5 signalling through the chemokine receptor CCR5. Collectively, these data demonstrate that the tumour microenvironment facilitates metastatic spread by eliciting reversible changes in the phenotype of cancer cells.	topic_bc
78170	4	356081	6	NULL	NULL	0	NULL	CCL5	Chemical		is					RANTES	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Mesenchymal stem cells have been recently described to localize to breast carcinomas, where they integrate into the tumour-associated stroma. However, the involvement of mesenchymal stem cells (or their derivatives) in tumour pathophysiology has not been addressed. Here, we demonstrate that bone-marrow-derived human mesenchymal stem cells, when mixed with otherwise weakly metastatic human breast carcinoma cells, cause the cancer cells to increase their metastatic potency greatly when this cell mixture is introduced into a subcutaneous site and allowed to form a tumour xenograft. The breast cancer cells stimulate de novo secretion of the chemokine CCL5 (also called RANTES) from mesenchymal stem cells, which then acts in a paracrine fashion on the cancer cells to enhance their motility, invasion and metastasis. This enhanced metastatic ability is reversible and is dependent on CCL5 signalling through the chemokine receptor CCR5. Collectively, these data demonstrate that the tumour microenvironment facilitates metastatic spread by eliciting reversible changes in the phenotype of cancer cells.	topic_bc
78122	1	356084	6	NULL	NULL	0	NULL	VEGF	GP		is					vascular endothelial growth factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78123	2	356084	6	NULL	NULL	0	NULL	VEGF	GP		plays a role in					angiogenesis	process				NULL		0	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78124	3	356084	6	NULL	NULL	0	NULL	VEGF	GP		plays a role in					tumor	MedicalFinding	progression of			NULL		0	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78125	4	356084	6	NULL	NULL	0	NULL	VEGF	GP		is regulated by					estrogen	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78127	5	356084	6	NULL	NULL	0	NULL	Genistein	Chemical		increase					VEGF	GP	secretion of			NULL	MELN cells	0	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78129	6	356084	6	NULL	NULL	NULL	NULL	BPA	Chemical		increases					VEGF	GP	secretion of			NULL	MELN cells	NULL	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78130	7	356084	6	NULL	NULL	NULL	NULL	OP	Chemical		increases					VEGF	GP	secretion of			NULL	MELN cells	NULL	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78132	8	356084	6	NULL	NULL	0	NULL	OP	GP		is					 4-(tert-octyl)phenol	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78133	9	356084	6	NULL	NULL	NULL	NULL	dieldrin	Chemical		increases					VEGF	GP	secretion of			NULL	MELN cells	NULL	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78134	10	356084	6	NULL	NULL	NULL	NULL	BBP	Chemical		increases					VEGF	GP	secretion of			NULL	MELN cells	NULL	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78137	11	356084	6	NULL	NULL	0	NULL	BBP			is					benzyl butyl phthalate					NULL		0	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78140	12	356084	6	NULL	NULL	0	NULL	di-ethyl-2-hexyle phthalate	Chemical		is					DEHP	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78142	13	356084	6	NULL	NULL	NULL	NULL	DEHP	Chemical		increases					VEGF	GP	secretion of			NULL	MELN cells	NULL	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78144	14	356084	6	NULL	NULL	0	NULL	Genistein	Chemical		increases					VEGF	GP	secretion of			NULL	MCF-7 cells	0	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78145	15	356084	6	NULL	NULL	0	NULL	BPA	Chemical		increases					VEGF	GP	secretion of			NULL	MCF-7 cells	0	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78146	16	356084	6	NULL	NULL	0	NULL	OP	Chemical		increases					VEGF	GP	secretion of			NULL	MCF-7 cells	0	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78147	17	356084	6	NULL	NULL	0	NULL	dieldrin	Chemical		increases					VEGF	GP	secretion of			NULL	MCF-7 cells	0	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78148	18	356084	6	NULL	NULL	NULL	NULL	DEHP	Chemical		increases					VEGF	GP	secretion of			NULL	MCF-7 cells	NULL	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78155	19	356084	6	NULL	NULL	0	NULL	BBP	Chemical		increases					VEGF	GP	secretion of			NULL		0	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78157	20	356084	6	NULL	NULL	0	NULL	BPA	Chemical		is a type of					xenoestrogen	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78160	21	356084	6	NULL	NULL	0	NULL	OP	Chemical		is a type of					xenoestrogen	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78161	22	356084	6	NULL	NULL	0	NULL	dieldrin	Chemical		is a type of					xenoestrogen	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78162	23	356084	6	NULL	NULL	0	NULL	BBP	Chemical		is a type of					xenoestrogen	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78163	24	356084	6	NULL	NULL	0	NULL	DEHP	Chemical		is a type of					xenoestrogen	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78164	25	356084	6	NULL	NULL	NULL	NULL	VEGF	GP		increases					capillary	OrganismPart	permeability of 			NULL	in vivo	NULL	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78165	26	356084	6	NULL	NULL	NULL	NULL	VEGF	GP		increases					angiogenesis	process				NULL	in vivo	NULL	NULL	NULL	NULL	NULL	NULL	nvironmental chemicals may affect human health by disrupting endocrine function. Their possible role in the mammary gland and breast tumors is still unknown. Previous studies have demonstrated that vascular endothelial growth factor (VEGF), a key factor in angiogenesis and tumor progression, is an estrogen-regulated gene. We analyzed whether VEGF expression is regulated by different xenoestrogens in several breast cancer cells, MELN (derived from MCF-7) and MELP (derived from MDA-MB-231) and stably expressing estrogen receptor  (ER); these cell lines stably express estrogen response element (β-globin)-luciferase. Genistein, bisphenol A (BPA), 4-(tert-octyl)phenol (OP), dieldrin, and several phthalates, including benzyl butyl phthalate (BBP) and di-ethyl-2-hexyle phthalate (DEHP), were first shown to be estrogenic. These compounds induced a dose-dependent increase of VEGF secretion in MELN and MCF-7 cells; maximal effect was observed at 1–10 µM non-cytotoxic concentrations and was inhibited by the antiestrogen ICI 182 780. VEGF increase was not observed in ER-negative MDA-MB-231 cells. Most substances increased VEGF transcript levels in MELN cells. In contrast, -hexachlorocyclohexane, vinclozolin, and the phthalates (mono-n-butyl ester phthalic acid, di-isononyle phthalate, and di-isodecyle phthalate) were ineffective on both VEGF secretion and estrogenic luciferase induction in these cell lines. Specific kinase inhibitors PD98059, SB203580, or LY294002 suppressed the xenoestrogen-induced VEGF response, suggesting activation of MEK, p38 kinase, and phosphatidylinositol-3-kinase pathways. Our in vitro results show for the first time that genistein and xenoestrogens (BPA, OP, dieldrin, BBP, and DEHP at high concentrations) up-regulate VEGF expression in MELN cells by an ER-dependent mechanism. Since VEGF increases capillary permeability and breast tumor angiogenesis in vivo, the physiological relevance of these findings is discussed. http://joe.endocrinology-journals.org/cgi/content/abstract/196/2/399	topic_bc
78090	1	356085	6	NULL	NULL	0	NULL	estrogen	Chemical	deprivation of	causes					Breast cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78091	2	356085	6	NULL	NULL	0	NULL	oophorectomy	MedicalProcedure		is used for					Breast cancer	MedicalFinding	treatment of 			NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78092	3	356085	6	NULL	NULL	0	NULL	oophorectomy	MedicalProcedure		lowers					estradiol	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78093	4	356085	6	NULL	NULL	0	NULL	LTED	process		is					Long Term Estradiol Deprivation	process				NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78094	5	356085	6	NULL	NULL	0	NULL	LTED	process		causes					estradiol	Chemical	hypersensitivity to			NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78095	6	356085	6	NULL	NULL	0	NULL	statement 5	process		leads to					ER1	GP	upregulation of 			NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78096	7	356085	6	NULL	NULL	0	NULL	statement 5	process		leads to					MAP kinase	GP	upregulation of 			NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78097	8	356085	6	NULL	NULL	0	NULL	statement 5	process		leads to					PI-3 kinase pathway	process	upregulation of 			NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78098	9	356085	6	NULL	NULL	0	NULL	C promoter	GP	demethylation of	leads to					ER1	GP	upregulation of 			NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78099	10	356085	6	NULL	NULL	0	NULL	SHC	GP		bind					Grb-2	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78100	11	356085	6	NULL	NULL	0	NULL	SHC	GP		bind					Sos	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78101	12	356085	6	NULL	NULL	0	NULL	statement 10	process		leads to					MAP kinase	GP	activation of 			NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78102	13	356085	6	NULL	NULL	0	NULL	ER1	GP		bind					IGF-1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78103	14	356085	6	NULL	NULL	0	NULL	ER1	GP		bind					EGF receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78104	15	356085	6	NULL	NULL	0	NULL	statement 13	process		is induced by					estradiol	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78105	16	356085	6	NULL	NULL	0	NULL	statement 14	process		is induced by					estradiol	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78106	17	356085	6	NULL	NULL	0	NULL	statement 13	process		activates					PI-3-kinase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78107	18	356085	6	NULL	NULL	0	NULL	statement 13	process		activates					mTOR pathway	process				NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78108	19	356085	6	NULL	NULL	0	NULL	statement 14	process		activates					PI-3 kinase pathway	process				NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78109	20	356085	6	NULL	NULL	0	NULL	statement 14	process		activates					mTOR pathway	process				NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78110	21	356085	6	NULL	NULL	0	NULL	ER1	GP		is localized to					plasma membrane	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78111	22	356085	6	NULL	NULL	0	NULL	estradiol	Chemical		causes					SHC	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78112	23	356085	6	NULL	NULL	0	NULL	estradiol	Chemical		causes					IGF-1	GP	phosphorylation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78113	24	356085	6	NULL	NULL	0	NULL	SHC	GP		is a type of					adaptor protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78114	25	356085	6	NULL	NULL	0	NULL	IGF-1	GP		is a type of					adaptor protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby Long Term Estradiol Deprivation (LTED) causes cells to adapts and develop hypersensitivity to estradiol. Several mechanisms are associated with this response including up-regulation of ERα and the MAP kinase, PI-3-kinase and mTOR growth factor pathways. ERα is 4–10 fold up-regulated as a result of demethylation of its C promoter, This nuclear receptor then co-opts a classical growth factor pathway using SHC, Grb-2 and Sos. This induces rapid nongenomic effects which are enhanced in LTED cells. The molecules involved in the nongenomic signaling process have been identified. Estradiol binds to cell membrance-associated ERα which physically associates with the adaptor protein SHC and induces its phosphorylation. In turn, SHC binds Grb-2 and Sos which results in the rapid activation of MAP kinase. These nongenomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membrances. Additional effects include activation of the PI-3-kinase and mTOR pathways through estradiol-induced binding of ERα to the IGF-1 and EGF receptors. A major question is how ERα locates in the plasma membrance since it does not contain an inherent membrance localization signal. We have provided evidence that the IGF-1 receptor serves as an anchor for ERα in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, SHC and the IGF-1 receptor itself. SHC, after binding to ERα, serves as the “glue” which tethers ERα to SHC binding sites on the activated IFG-1 receptors. Use of siRNA methodology to knock down SHC allows the conclusion that SHC is needed for ERα to localize in the plasma membrane.	topic_bc
78086	1	356086	6	NULL	NULL	0	NULL	 rs13387042			is located on					chromosome 2q35	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	Familial clustering studies indicate that breast cancer risk has a substantial genetic component1, 2, 3. To identify new breast cancer risk variants, we genotyped approximately 300,000 SNPs in 1,600 Icelandic individuals with breast cancer and 11,563 controls using the Illumina Hap300 platform. We then tested selected SNPs in five replication sample sets. Overall, we studied 4,554 affected individuals and 17,577 controls. Two SNPs consistently associated with breast cancer: 25% of individuals of European descent are homozygous for allele A of rs13387042 on chromosome 2q35 and have an estimated 1.44-fold greater risk than noncarriers, and for allele T of rs3803662 on 16q12, about 7% are homozygous and have a 1.64-fold greater risk. Risk from both alleles was confined to estrogen receptor–positive tumors. At present, no genes have been identified in the linkage disequilibrium block containing rs13387042. rs3803662 is near the 5' end of TNRC9, a high mobility group chromatin–associated protein whose expression is implicated in breast cancer metastasis to bone4.	topic_bc
78087	2	356086	6	NULL	NULL	NULL	NULL	 rs3803662			is located on					Chromosome 16q12	Chromosome				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Familial clustering studies indicate that breast cancer risk has a substantial genetic component1, 2, 3. To identify new breast cancer risk variants, we genotyped approximately 300,000 SNPs in 1,600 Icelandic individuals with breast cancer and 11,563 controls using the Illumina Hap300 platform. We then tested selected SNPs in five replication sample sets. Overall, we studied 4,554 affected individuals and 17,577 controls. Two SNPs consistently associated with breast cancer: 25% of individuals of European descent are homozygous for allele A of rs13387042 on chromosome 2q35 and have an estimated 1.44-fold greater risk than noncarriers, and for allele T of rs3803662 on 16q12, about 7% are homozygous and have a 1.64-fold greater risk. Risk from both alleles was confined to estrogen receptor–positive tumors. At present, no genes have been identified in the linkage disequilibrium block containing rs13387042. rs3803662 is near the 5' end of TNRC9, a high mobility group chromatin–associated protein whose expression is implicated in breast cancer metastasis to bone4.	topic_bc
78088	3	356086	6	NULL	NULL	0	NULL	statement 1	process		leads to					 estrogen receptor positive tumor	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Familial clustering studies indicate that breast cancer risk has a substantial genetic component1, 2, 3. To identify new breast cancer risk variants, we genotyped approximately 300,000 SNPs in 1,600 Icelandic individuals with breast cancer and 11,563 controls using the Illumina Hap300 platform. We then tested selected SNPs in five replication sample sets. Overall, we studied 4,554 affected individuals and 17,577 controls. Two SNPs consistently associated with breast cancer: 25% of individuals of European descent are homozygous for allele A of rs13387042 on chromosome 2q35 and have an estimated 1.44-fold greater risk than noncarriers, and for allele T of rs3803662 on 16q12, about 7% are homozygous and have a 1.64-fold greater risk. Risk from both alleles was confined to estrogen receptor–positive tumors. At present, no genes have been identified in the linkage disequilibrium block containing rs13387042. rs3803662 is near the 5' end of TNRC9, a high mobility group chromatin–associated protein whose expression is implicated in breast cancer metastasis to bone4.	topic_bc
78089	4	356086	6	NULL	NULL	0	NULL	statement 2	process		leads to					 estrogen receptor positive tumor	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Familial clustering studies indicate that breast cancer risk has a substantial genetic component1, 2, 3. To identify new breast cancer risk variants, we genotyped approximately 300,000 SNPs in 1,600 Icelandic individuals with breast cancer and 11,563 controls using the Illumina Hap300 platform. We then tested selected SNPs in five replication sample sets. Overall, we studied 4,554 affected individuals and 17,577 controls. Two SNPs consistently associated with breast cancer: 25% of individuals of European descent are homozygous for allele A of rs13387042 on chromosome 2q35 and have an estimated 1.44-fold greater risk than noncarriers, and for allele T of rs3803662 on 16q12, about 7% are homozygous and have a 1.64-fold greater risk. Risk from both alleles was confined to estrogen receptor–positive tumors. At present, no genes have been identified in the linkage disequilibrium block containing rs13387042. rs3803662 is near the 5' end of TNRC9, a high mobility group chromatin–associated protein whose expression is implicated in breast cancer metastasis to bone4.	topic_bc
77064	1	356087	5	NULL	NULL	0	NULL	IL-6	GP	levels of;;serum	is increased in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Several reports described increased serum IL-6 levels in schizophrenia (Cazzullo et al., 1998). IL-6 serum levels might be especially high in patients with an unfavourable course of the disease (Lin et al., 1998) and in patients with a long duration of the disease (Ganguli et al., 1994).	topic_sch
77065	2	356087	5	NULL	NULL	0	NULL	IL-6	GP	levels of;;serum	is higher in					schizophrenia	MedicalFinding	patients of;;unfavourable course of			NULL		0	NULL	NULL	NULL	NULL	NULL	Several reports described increased serum IL-6 levels in schizophrenia (Cazzullo et al., 1998). IL-6 serum levels might be especially high in patients with an unfavourable course of the disease (Lin et al., 1998) and in patients with a long duration of the disease (Ganguli et al., 1994).	topic_sch
77066	3	356087	5	NULL	NULL	0	NULL	IL-6	GP	levels of;;serum	is higher in					schizophrenia	MedicalFinding	patients of;;long duration of			NULL		0	NULL	NULL	NULL	NULL	NULL	Several reports described increased serum IL-6 levels in schizophrenia (Cazzullo et al., 1998). IL-6 serum levels might be especially high in patients with an unfavourable course of the disease (Lin et al., 1998) and in patients with a long duration of the disease (Ganguli et al., 1994).	topic_sch
77067	1	356088	5	NULL	NULL	0	NULL	IL-6R	GP	level of;;soluble;;CSF	is related to					paranoid-hallucinatory symptoms	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	On the other hand, a significant relationship between the soluble IL-6R levels in the CSF and the paranoid-hallucinatory symptoms in schizophrenia have been reported (Müller et al., 1997a).	topic_sch
77068	2	356088	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	On the other hand, a significant relationship between the soluble IL-6R levels in the CSF and the paranoid-hallucinatory symptoms in schizophrenia have been reported (Müller et al., 1997a).	topic_sch
77069	1	356089	5	NULL	NULL	0	NULL	IL-6	GP		is a product of					monocytes	Cell	active			NULL		0	NULL	NULL	NULL	NULL	NULL	IL-6 is a product of activated monocytes and some authors refer it as a marker of the type-2 immune response, although it is acting as a pro-inflammatory cytokine, too.	topic_sch
77070	2	356089	5	NULL	NULL	0	NULL	IL-6	GP		is a marker of					type-2 immune response	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	IL-6 is a product of activated monocytes and some authors refer it as a marker of the type-2 immune response, although it is acting as a pro-inflammatory cytokine, too.	topic_sch
77071	3	356089	5	NULL	NULL	0	NULL	IL-6	GP		act as					pro-inflammatory cytokine	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	IL-6 is a product of activated monocytes and some authors refer it as a marker of the type-2 immune response, although it is acting as a pro-inflammatory cytokine, too.	topic_sch
77072	1	356090	5	NULL	NULL	0	NULL	type-1 response	Process		is found in		primarily			schizophrenia	MedicalFinding	early stages of			NULL		0	NULL	NULL	NULL	NULL	NULL	It can be hypothesized that the blunted type-1 response is found primarily in early stages of schizophrenia, while a chronic pro-inflammatory stage with an overweight of the type-2 response including high IL-6 levels may predominate in later stages.	topic_sch
77073	2	356090	5	NULL	NULL	0	NULL	pro-inflammatory stage	Time	chronic	occurs along with					type-2 response	Process	overweight of			NULL		0	NULL	NULL	NULL	NULL	NULL	It can be hypothesized that the blunted type-1 response is found primarily in early stages of schizophrenia, while a chronic pro-inflammatory stage with an overweight of the type-2 response including high IL-6 levels may predominate in later stages.	topic_sch
77074	3	356090	5	NULL	NULL	0	NULL	statement 2	Process		includes					IL-6	GP	high levels of			NULL		0	NULL	NULL	NULL	NULL	NULL	It can be hypothesized that the blunted type-1 response is found primarily in early stages of schizophrenia, while a chronic pro-inflammatory stage with an overweight of the type-2 response including high IL-6 levels may predominate in later stages.	topic_sch
77075	4	356090	5	NULL	NULL	0	NULL	statement 3	Process		predominate in					schizophrenia	MedicalFinding	later stages of			NULL		0	NULL	NULL	NULL	NULL	NULL	It can be hypothesized that the blunted type-1 response is found primarily in early stages of schizophrenia, while a chronic pro-inflammatory stage with an overweight of the type-2 response including high IL-6 levels may predominate in later stages.	topic_sch
77076	1	356092	5	NULL	NULL	0	NULL	cyclo-oxygenase-2 inhibitors	Chemical		have therapeutic effects in					schizophrenia	MedicalFinding	early stages of			NULL		0	NULL	NULL	NULL	NULL	NULL	The view of different immune stages can also be underlined from the view of therapeutic studies: as it is discussed later, cyclo-oxygenase-2 inhibitors have therapeutic effects in early stages of schizophrenia, but seemingly only marginal effects in late stages.	topic_sch
77077	2	356092	5	NULL	NULL	0	NULL	cyclo-oxygenase-2 inhibitors	Chemical		effects		marginal			schizophrenia	MedicalFinding	later stages of			NULL		0	NULL	NULL	NULL	NULL	NULL	The view of different immune stages can also be underlined from the view of therapeutic studies: as it is discussed later, cyclo-oxygenase-2 inhibitors have therapeutic effects in early stages of schizophrenia, but seemingly only marginal effects in late stages.	topic_sch
77078	1	356093	5	NULL	NULL	NULL	NULL	 IL-18	GP	levels of;;serum	is elevated in					schizophrenics	GroupOfPeople	medicated			NULL		NULL	NULL	NULL	NULL	NULL	NULL	An elevation of IL-18 serum levels was described in medicated schizophrenics (Tanaka et al., 2000). Since IL-18 plays a pivotal role in the type-1 immune response, this finding is consistent with other descriptions of type-1 activation during antipsychotic treatment.	topic_sch
77079	2	356093	5	NULL	NULL	0	NULL	IL-18	GP		plays a role in		pivotal			type-1 immune response	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	An elevation of IL-18 serum levels was described in medicated schizophrenics (Tanaka et al., 2000). Since IL-18 plays a pivotal role in the type-1 immune response, this finding is consistent with other descriptions of type-1 activation during antipsychotic treatment.	topic_sch
77080	3	356093	5	NULL	NULL	0	NULL	type-1 response	Process		is activated during					antipsychotic treatment	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	An elevation of IL-18 serum levels was described in medicated schizophrenics (Tanaka et al., 2000). Since IL-18 plays a pivotal role in the type-1 immune response, this finding is consistent with other descriptions of type-1 activation during antipsychotic treatment.	topic_sch
77081	1	356094	5	NULL	NULL	NULL	NULL	memory cells	Cell	increase of	is a source of		main			IFN-gamma	GP	production of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	An increase of ‘memory cells’ (CD4+CD45RO+ cells) - one of the main sources of IFN-gamma production - during anti-psychotic therapy with neuroleptics was observed by different groups (Müller et al., 1997c).	topic_sch
77082	2	356094	5	NULL	NULL	0	NULL	neuroleptics	Chemical		is used in					anti-psychotic therapy	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	An increase of ‘memory cells’ (CD4+CD45RO+ cells) - one of the main sources of IFN-gamma production - during anti-psychotic therapy with neuroleptics was observed by different groups (Müller et al., 1997c).	topic_sch
77083	3	356094	5	NULL	NULL	NULL	NULL	memory cells	Cell	increase of	occurs during					statement 2	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	An increase of ‘memory cells’ (CD4+CD45RO+ cells) - one of the main sources of IFN-gamma production - during anti-psychotic therapy with neuroleptics was observed by different groups (Müller et al., 1997c).	topic_sch
77084	1	356095	5	NULL	NULL	0	NULL	sIL-2R	GP	increase in	reflects					IL-2 bearing T-cells	Cell	 increase of;;activated			NULL		0	NULL	NULL	NULL	NULL	NULL	Additionally, an increase of sIL-2R - the increase reflects an increase of activated, IL-2 bearing T-cells - during anti-psychotic treatment was described (Müller et al., 1997b).	topic_sch
77085	2	356095	5	NULL	NULL	0	NULL	statement 1	Process		occurs during					anti-psychotic treatment	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Additionally, an increase of sIL-2R - the increase reflects an increase of activated, IL-2 bearing T-cells - during anti-psychotic treatment was described (Müller et al., 1997b).	topic_sch
77086	1	356096	5	NULL	NULL	0	NULL	sICAM-1	GP	reduced	is increased during		significantly			anti-psychotic therapy	MedicalProcedure	short term			NULL		0	NULL	NULL	NULL	NULL	NULL	The reduced sICAM-1 levels show a significant increase during short term anti-psychotic therapy (Schwarz et al., 2000) and the ICAM-1 ligand leucocyte function antigen-1 (LFA-1) shows a significantly increased expression during antipsychotic therapy (Müller et al., 1999).	topic_sch
77087	2	356096	5	NULL	NULL	0	NULL	ICAM-1 ligand leucocyte function antigen-1	GP	expression of	is increased during		significantly			antipsychotic therapy	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	The reduced sICAM-1 levels show a significant increase during short term anti-psychotic therapy (Schwarz et al., 2000) and the ICAM-1 ligand leucocyte function antigen-1 (LFA-1) shows a significantly increased expression during antipsychotic therapy (Müller et al., 1999).	topic_sch
77088	1	356097	5	NULL	NULL	0	NULL	clozapine tharapy	MedicalProcedure		increases		repeatedly			TNF-alpha	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The increase of TNF-alpha and TNF-alpha receptors during therapy with clozapine was observed repeatedly (Pollmächer et al., 2001).	topic_sch
77089	2	356097	5	NULL	NULL	0	NULL	clozapine tharapy	MedicalProcedure		increases		repeatedly			TNF-alpha receptors	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The increase of TNF-alpha and TNF-alpha receptors during therapy with clozapine was observed repeatedly (Pollmächer et al., 2001).	topic_sch
77343	1	356099	5	NULL	NULL	0	NULL	anti-psychotic therapy	MedicalProcedure		is accompanied by					IL-6	GP	functional decrease of			NULL		0	NULL	NULL	NULL	NULL	NULL	Regarding the type-2 response, several studies point out that anti-psychotic therapy is accompanied by a functional decrease of the IL-6 system (Maes et al., 1997; Müller et al., 2000). These findings provide further evidence that antipsychotics have a ‘balancing’ effect on cytokines.	topic_sch
77344	2	356099	5	NULL	NULL	0	NULL	antipsychotics	Chemical		balancing effect on					cytokines	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Regarding the type-2 response, several studies point out that anti-psychotic therapy is accompanied by a functional decrease of the IL-6 system (Maes et al., 1997; Müller et al., 2000). These findings provide further evidence that antipsychotics have a ‘balancing’ effect on cytokines.	topic_sch
77345	1	356100	5	NULL	NULL	0	NULL	chromosome 7q	Chromosome		undergo					duplication	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Among the discoveries was a duplication in the tip of chromosome 7q. This duplication was found in people with schizophrenia at a rate 14 times that of healthy people. The duplication affects a particular gene called the vasoactive intestinal peptide receptor 2 gene, which is known to play a role in behavior and learning. In people with schizophrenia, the expression of this gene is much higher, the researchers found. The VIPR2 gene mutation, therefore, will be an important target in developing medications that might alter the symptoms of the illness.	topic_sch
77346	2	356100	5	NULL	NULL	0	NULL	statement 1	Process		is found in					people	GroupOfPeople	healthy			NULL		0	NULL	NULL	NULL	NULL	NULL	Among the discoveries was a duplication in the tip of chromosome 7q. This duplication was found in people with schizophrenia at a rate 14 times that of healthy people. The duplication affects a particular gene called the vasoactive intestinal peptide receptor 2 gene, which is known to play a role in behavior and learning. In people with schizophrenia, the expression of this gene is much higher, the researchers found. The VIPR2 gene mutation, therefore, will be an important target in developing medications that might alter the symptoms of the illness.	topic_sch
77347	3	356100	5	NULL	NULL	NULL	NULL	statement 1	Process		is found in					schizophrenic	GroupOfPeople				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Among the discoveries was a duplication in the tip of chromosome 7q. This duplication was found in people with schizophrenia at a rate 14 times that of healthy people. The duplication affects a particular gene called the vasoactive intestinal peptide receptor 2 gene, which is known to play a role in behavior and learning. In people with schizophrenia, the expression of this gene is much higher, the researchers found. The VIPR2 gene mutation, therefore, will be an important target in developing medications that might alter the symptoms of the illness.	topic_sch
77348	4	356100	5	NULL	NULL	0	NULL	statement 3	Process	rate of	is more than					statement 2	Process	rate of			NULL		0	NULL	NULL	NULL	NULL	NULL	Among the discoveries was a duplication in the tip of chromosome 7q. This duplication was found in people with schizophrenia at a rate 14 times that of healthy people. The duplication affects a particular gene called the vasoactive intestinal peptide receptor 2 gene, which is known to play a role in behavior and learning. In people with schizophrenia, the expression of this gene is much higher, the researchers found. The VIPR2 gene mutation, therefore, will be an important target in developing medications that might alter the symptoms of the illness.	topic_sch
77349	5	356100	5	NULL	NULL	0	NULL	statement 1	Process		affects					vasoactive intestinal peptide receptor 2 gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Among the discoveries was a duplication in the tip of chromosome 7q. This duplication was found in people with schizophrenia at a rate 14 times that of healthy people. The duplication affects a particular gene called the vasoactive intestinal peptide receptor 2 gene, which is known to play a role in behavior and learning. In people with schizophrenia, the expression of this gene is much higher, the researchers found. The VIPR2 gene mutation, therefore, will be an important target in developing medications that might alter the symptoms of the illness.	topic_sch
77350	6	356100	5	NULL	NULL	0	NULL	vasoactive intestinal peptide receptor 2 gene	GP		plays a role in					behavior	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Among the discoveries was a duplication in the tip of chromosome 7q. This duplication was found in people with schizophrenia at a rate 14 times that of healthy people. The duplication affects a particular gene called the vasoactive intestinal peptide receptor 2 gene, which is known to play a role in behavior and learning. In people with schizophrenia, the expression of this gene is much higher, the researchers found. The VIPR2 gene mutation, therefore, will be an important target in developing medications that might alter the symptoms of the illness.	topic_sch
77351	7	356100	5	NULL	NULL	0	NULL	vasoactive intestinal peptide receptor 2 gene	GP		plays a role in					learning	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Among the discoveries was a duplication in the tip of chromosome 7q. This duplication was found in people with schizophrenia at a rate 14 times that of healthy people. The duplication affects a particular gene called the vasoactive intestinal peptide receptor 2 gene, which is known to play a role in behavior and learning. In people with schizophrenia, the expression of this gene is much higher, the researchers found. The VIPR2 gene mutation, therefore, will be an important target in developing medications that might alter the symptoms of the illness.	topic_sch
77352	8	356100	5	NULL	NULL	0	NULL	vasoactive intestinal peptide receptor 2 gene	GP		expressed in		highly			schizophrenic	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Among the discoveries was a duplication in the tip of chromosome 7q. This duplication was found in people with schizophrenia at a rate 14 times that of healthy people. The duplication affects a particular gene called the vasoactive intestinal peptide receptor 2 gene, which is known to play a role in behavior and learning. In people with schizophrenia, the expression of this gene is much higher, the researchers found. The VIPR2 gene mutation, therefore, will be an important target in developing medications that might alter the symptoms of the illness.	topic_sch
77353	9	356100	5	NULL	NULL	0	NULL	VIPR2 gene	GP	mutation of	is targeted for					medications	MedicalProcedure	development of			NULL		0	NULL	NULL	NULL	NULL	NULL	Among the discoveries was a duplication in the tip of chromosome 7q. This duplication was found in people with schizophrenia at a rate 14 times that of healthy people. The duplication affects a particular gene called the vasoactive intestinal peptide receptor 2 gene, which is known to play a role in behavior and learning. In people with schizophrenia, the expression of this gene is much higher, the researchers found. The VIPR2 gene mutation, therefore, will be an important target in developing medications that might alter the symptoms of the illness.	topic_sch
77354	10	356100	5	NULL	NULL	0	NULL	statement 9	Process		alter		might			schizophrenia	MedicalFinding	symptoms of			NULL		0	NULL	NULL	NULL	NULL	NULL	Among the discoveries was a duplication in the tip of chromosome 7q. This duplication was found in people with schizophrenia at a rate 14 times that of healthy people. The duplication affects a particular gene called the vasoactive intestinal peptide receptor 2 gene, which is known to play a role in behavior and learning. In people with schizophrenia, the expression of this gene is much higher, the researchers found. The VIPR2 gene mutation, therefore, will be an important target in developing medications that might alter the symptoms of the illness.	topic_sch
77355	1	356101	5	NULL	NULL	0	NULL	energy drinks	Food	caffeinated	trigger					psychotic episode	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Caffeinated energy drinks may trigger a psychotic episode in people with mental illness, an expert has warned after documenting the case of a young man with schizophrenia.	topic_sch
77356	2	356101	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Caffeinated energy drinks may trigger a psychotic episode in people with mental illness, an expert has warned after documenting the case of a young man with schizophrenia.	topic_sch
77357	1	356102	5	NULL	NULL	0	NULL	antipsychotic drugs	Chemical	use of	treats					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The use of antipsychotic drugs to treat schizophrenia is associated with the loss of a small but measurable amount of brain tissue, a new study finds.	topic_sch
77358	2	356102	5	NULL	NULL	0	NULL	statement 1	Process		is associated with					brain tissue	OrganismPart	loss of;;small;;measurable amount of			NULL		0	NULL	NULL	NULL	NULL	NULL	The use of antipsychotic drugs to treat schizophrenia is associated with the loss of a small but measurable amount of brain tissue, a new study finds.	topic_sch
77359	1	356103	5	NULL	NULL	0	NULL	Creative folks	GroupOfPeople		tend to have					default network	OrganismPart	overactive			NULL		0	NULL	NULL	NULL	NULL	NULL	Creative folks and those with schizophrenia tend to have an overactive default network. 	topic_sch
77360	2	356103	5	NULL	NULL	NULL	NULL	Schizophrenic people	GroupOfPeople		tend to have					default network	OrganismPart	overactive			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Creative folks and those with schizophrenia tend to have an overactive default network. 	topic_sch
77361	1	356104	5	NULL	NULL	NULL	NULL	brain network	OrganismPart		involves					working memory network	OrganismPart				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77362	2	356104	5	NULL	NULL	0	NULL	brain network	OrganismPart		involves					default brain network	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77363	3	356104	5	NULL	NULL	0	NULL	statement 1	Process		occurs along with					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77364	4	356104	5	NULL	NULL	0	NULL	world	GeographicNotProper	attention to;;outside	is known as					 working memory network	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77365	5	356104	5	NULL	NULL	0	NULL	working memory network	OrganismPart		consists of		primarily			lateral cortex	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77366	6	356104	5	NULL	NULL	0	NULL	working memory network	OrganismPart		consists of		primarily			frontal cortex	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77367	7	356104	5	NULL	NULL	0	NULL	working memory network	OrganismPart		consists of		primarily			parietal cortex	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77368	8	356104	5	NULL	NULL	0	NULL	default brain network	OrganismPart		consists of					medial prefrontal cortex	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77369	9	356104	5	NULL	NULL	0	NULL	default brain network	OrganismPart		consists of					posterior cingulate cortex	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77370	10	356104	5	NULL	NULL	0	NULL	working memory network	OrganismPart	deactivation of	is followed by					default network	OrganismPart	taking over of			NULL		0	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77371	11	356104	5	NULL	NULL	0	NULL	statement 10	Process		occurs during					sleep	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77372	12	356104	5	NULL	NULL	0	NULL	default brain network	OrganismPart		involves					self-representations	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77373	13	356104	5	NULL	NULL	0	NULL	default brain network	OrganismPart		involves					dreams	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77374	14	356104	5	NULL	NULL	0	NULL	default brain network	OrganismPart		involves					imagination	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77375	15	356104	5	NULL	NULL	0	NULL	default brain network	OrganismPart		involves					current concerns	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77376	16	356104	5	NULL	NULL	0	NULL	default brain network	OrganismPart		involves					autobiographical memory	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77377	17	356104	5	NULL	NULL	0	NULL	default brain network	OrganismPart		involves					perspective-taking ability	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77378	18	356104	5	NULL	NULL	0	NULL	people	GroupOfPeople		have					default network activity	Process	higher			NULL		0	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77379	19	356104	5	NULL	NULL	0	NULL	statement 18	Process		occurs during					rest	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77380	20	356104	5	NULL	NULL	NULL	NULL	statement 18	Process		tendency to		frequently			daydream	MentalProcess				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77381	21	356104	5	NULL	NULL	0	NULL	default network	OrganismPart		involves					consciousness	MentalProcess	inner stream of			NULL		0	NULL	NULL	NULL	NULL	NULL	Research shows that when most of us fall asleep, the brain network that involves attention to the outside world (the working memory network consisting primarily of the lateral frontal and parietal cortices) deactivates and our default brain network (medial prefrontal and posterior cingulate cortices) takes over. The discovery of the default brain network is important, as it involves various aspects of our self, such as our self-representations, dreams, imagination, current concerns, autobiographical memory and perspective-taking ability. Those with higher default network activity during rest have a tendency to daydream more frequently, which makes sense if one thinks of the default network as involving our inner stream of consciousness.	topic_sch
77634	1	356107	7	NULL	NULL	0	NULL	valproic acid	Chemical		role for					BPD	MedicalFinding	epigenetic mechanism in			NULL		0	NULL	NULL	NULL	NULL	NULL	valproic acid introduced a role for epigenetic mechanisms in BPD	topic_bd
77635	1	356108	7	NULL	NULL	0	NULL	lithium 	Chemical	studies with	led to the					glycogen synthase kinase 3 beta pathway	Process	hypothesis of a role of			NULL		0	NULL	NULL	NULL	NULL	NULL	Discovery-driven studies and novel technologies changed that picture and created interesting new models. Initial studies focused on known neurotransmitter systems such as biogenic amines ([Cousins et al., 2009], [Manji and Lenox, 2000] and [Schildkraut, 1974]), glutamate, and GABA ([Krystal et al., 2002] and Post, 1990 R.M. Post, Non-lithium treatment for bipolar disorder, J. Clin. Psychiatry 51 (Suppl) (1990), pp. 9–16 discussion 17–9. View Record in Scopus | Cited By in Scopus (37)[Post, 1990]), and on altered regulation of glucocorticoids ([Daban et al., 2005] and [Watson et al., 2004]), with implications of an involvement of each system. Studies with lithium led to the hypothesis of a role of the glycogen synthase kinase 3 beta pathway ([Ikonomov and Manji, 1999] and [Klein and Melton, 1996]), while studies with valproic acid introduced a role for epigenetic mechanisms in BPD (Phiel et al., 2001). Serotonin and norepinephrine became a focus because of their involvement in the mechanism of action of antidepressants (Owens, 2004). Overall, many different systems seemed to be implicated in BPD, with supportive evidence for each one.	topic_bd
77636	2	356108	7	NULL	NULL	0	NULL	statement 1	Process		occur in					BPD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Discovery-driven studies and novel technologies changed that picture and created interesting new models. Initial studies focused on known neurotransmitter systems such as biogenic amines ([Cousins et al., 2009], [Manji and Lenox, 2000] and [Schildkraut, 1974]), glutamate, and GABA ([Krystal et al., 2002] and Post, 1990 R.M. Post, Non-lithium treatment for bipolar disorder, J. Clin. Psychiatry 51 (Suppl) (1990), pp. 9–16 discussion 17–9. View Record in Scopus | Cited By in Scopus (37)[Post, 1990]), and on altered regulation of glucocorticoids ([Daban et al., 2005] and [Watson et al., 2004]), with implications of an involvement of each system. Studies with lithium led to the hypothesis of a role of the glycogen synthase kinase 3 beta pathway ([Ikonomov and Manji, 1999] and [Klein and Melton, 1996]), while studies with valproic acid introduced a role for epigenetic mechanisms in BPD (Phiel et al., 2001). Serotonin and norepinephrine became a focus because of their involvement in the mechanism of action of antidepressants (Owens, 2004). Overall, many different systems seemed to be implicated in BPD, with supportive evidence for each one.	topic_bd
77637	3	356108	7	NULL	NULL	0	NULL	 valproic acid	Chemical	studies with	introduced a					epigenetic mechanism	Process	role for			NULL		0	NULL	NULL	NULL	NULL	NULL	Discovery-driven studies and novel technologies changed that picture and created interesting new models. Initial studies focused on known neurotransmitter systems such as biogenic amines ([Cousins et al., 2009], [Manji and Lenox, 2000] and [Schildkraut, 1974]), glutamate, and GABA ([Krystal et al., 2002] and Post, 1990 R.M. Post, Non-lithium treatment for bipolar disorder, J. Clin. Psychiatry 51 (Suppl) (1990), pp. 9–16 discussion 17–9. View Record in Scopus | Cited By in Scopus (37)[Post, 1990]), and on altered regulation of glucocorticoids ([Daban et al., 2005] and [Watson et al., 2004]), with implications of an involvement of each system. Studies with lithium led to the hypothesis of a role of the glycogen synthase kinase 3 beta pathway ([Ikonomov and Manji, 1999] and [Klein and Melton, 1996]), while studies with valproic acid introduced a role for epigenetic mechanisms in BPD (Phiel et al., 2001). Serotonin and norepinephrine became a focus because of their involvement in the mechanism of action of antidepressants (Owens, 2004). Overall, many different systems seemed to be implicated in BPD, with supportive evidence for each one.	topic_bd
77638	4	356108	7	NULL	NULL	0	NULL	statement 3	Process		occur in					BPD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Discovery-driven studies and novel technologies changed that picture and created interesting new models. Initial studies focused on known neurotransmitter systems such as biogenic amines ([Cousins et al., 2009], [Manji and Lenox, 2000] and [Schildkraut, 1974]), glutamate, and GABA ([Krystal et al., 2002] and Post, 1990 R.M. Post, Non-lithium treatment for bipolar disorder, J. Clin. Psychiatry 51 (Suppl) (1990), pp. 9–16 discussion 17–9. View Record in Scopus | Cited By in Scopus (37)[Post, 1990]), and on altered regulation of glucocorticoids ([Daban et al., 2005] and [Watson et al., 2004]), with implications of an involvement of each system. Studies with lithium led to the hypothesis of a role of the glycogen synthase kinase 3 beta pathway ([Ikonomov and Manji, 1999] and [Klein and Melton, 1996]), while studies with valproic acid introduced a role for epigenetic mechanisms in BPD (Phiel et al., 2001). Serotonin and norepinephrine became a focus because of their involvement in the mechanism of action of antidepressants (Owens, 2004). Overall, many different systems seemed to be implicated in BPD, with supportive evidence for each one.	topic_bd
77639	5	356108	7	NULL	NULL	0	NULL	serotonin	Chemical		is involved in					antidepressant 	Chemical	mechanism of;;action of			NULL		0	NULL	NULL	NULL	NULL	NULL	Discovery-driven studies and novel technologies changed that picture and created interesting new models. Initial studies focused on known neurotransmitter systems such as biogenic amines ([Cousins et al., 2009], [Manji and Lenox, 2000] and [Schildkraut, 1974]), glutamate, and GABA ([Krystal et al., 2002] and Post, 1990 R.M. Post, Non-lithium treatment for bipolar disorder, J. Clin. Psychiatry 51 (Suppl) (1990), pp. 9–16 discussion 17–9. View Record in Scopus | Cited By in Scopus (37)[Post, 1990]), and on altered regulation of glucocorticoids ([Daban et al., 2005] and [Watson et al., 2004]), with implications of an involvement of each system. Studies with lithium led to the hypothesis of a role of the glycogen synthase kinase 3 beta pathway ([Ikonomov and Manji, 1999] and [Klein and Melton, 1996]), while studies with valproic acid introduced a role for epigenetic mechanisms in BPD (Phiel et al., 2001). Serotonin and norepinephrine became a focus because of their involvement in the mechanism of action of antidepressants (Owens, 2004). Overall, many different systems seemed to be implicated in BPD, with supportive evidence for each one.	topic_bd
77640	6	356108	7	NULL	NULL	0	NULL	norepinephrine	Chemical		is involved in					antidepressant 	Chemical	mechanism of;;action of			NULL		0	NULL	NULL	NULL	NULL	NULL	Discovery-driven studies and novel technologies changed that picture and created interesting new models. Initial studies focused on known neurotransmitter systems such as biogenic amines ([Cousins et al., 2009], [Manji and Lenox, 2000] and [Schildkraut, 1974]), glutamate, and GABA ([Krystal et al., 2002] and Post, 1990 R.M. Post, Non-lithium treatment for bipolar disorder, J. Clin. Psychiatry 51 (Suppl) (1990), pp. 9–16 discussion 17–9. View Record in Scopus | Cited By in Scopus (37)[Post, 1990]), and on altered regulation of glucocorticoids ([Daban et al., 2005] and [Watson et al., 2004]), with implications of an involvement of each system. Studies with lithium led to the hypothesis of a role of the glycogen synthase kinase 3 beta pathway ([Ikonomov and Manji, 1999] and [Klein and Melton, 1996]), while studies with valproic acid introduced a role for epigenetic mechanisms in BPD (Phiel et al., 2001). Serotonin and norepinephrine became a focus because of their involvement in the mechanism of action of antidepressants (Owens, 2004). Overall, many different systems seemed to be implicated in BPD, with supportive evidence for each one.	topic_bd
77641	1	356109	7	NULL	NULL	0	NULL	GC	Chemical		bind					GR	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Glucocorticoids (GC) are a class of steroid hormones that bind to the glucocorticoid receptor (GR), which is present in almost every vertebrate animal cell	topic_bd
77642	2	356109	7	NULL	NULL	0	NULL	GC	Chemical		is a type of					steroid hormones	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Glucocorticoids (GC) are a class of steroid hormones that bind to the glucocorticoid receptor (GR), which is present in almost every vertebrate animal cell	topic_bd
77643	3	356109	7	NULL	NULL	0	NULL	GR	GP		is					glucocorticoid receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Glucocorticoids (GC) are a class of steroid hormones that bind to the glucocorticoid receptor (GR), which is present in almost every vertebrate animal cell	topic_bd
77644	4	356109	7	NULL	NULL	0	NULL	GR	GP		is present in					vertebrate animal cell	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Glucocorticoids (GC) are a class of steroid hormones that bind to the glucocorticoid receptor (GR), which is present in almost every vertebrate animal cell	topic_bd
77645	1	356110	7	NULL	NULL	0	NULL	Gene expression profile	GP		shows					mRNA	NucleicAcid	decrease of			NULL		0	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS)	topic_bd
77646	2	356110	7	NULL	NULL	0	NULL	mRNA	NucleicAcid		involved in					OXPHOS	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS)	topic_bd
77647	3	356110	7	NULL	NULL	0	NULL	protein expression profile	GP		shows					proteins	GP	decrease of			NULL		0	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS)	topic_bd
77648	4	356110	7	NULL	NULL	0	NULL	proteins	GP		involved in					OXPHOS	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS)	topic_bd
77649	5	356110	7	NULL	NULL	0	NULL	OXPHOS	Process		is					oxidative phosphorylation	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS)	topic_bd
77650	6	356110	7	NULL	NULL	0	NULL	OXPHOS	Process		is a type of					mitochondrial function	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS)	topic_bd
77651	1	356111	7	NULL	NULL	0	NULL	Gene expression profile	GP		shows 					mRNA	NucleicAcid	decrease of			NULL		0	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS) (Iwamoto et al., 2005 K. Iwamoto, M. Bundo and T. Kato, Altered expression of mitochondria-related genes in postmortem brains of patients with bipolar disorder or schizophrenia, as revealed by large-scale DNA microarray analysis, Hum. Mol. Genet. 14 (2005), pp. 241–253. View Record in Scopus | Cited By in Scopus (130)[Iwamoto et al., 2005], [Konradi et al., 2004], [Pennington et al., 2008] and [Washizuka et al., 2005]). Downregulations were observed in the prefrontal cortex (PFC; Brodmann areas 9 and 46, Table 1), ([Iwamoto et al., 2005], [Pennington et al., 2008] and [Sun et al., 2006]), hippocampus (Konradi et al., 2004) and in lymphoblastoid cell lines (Table 2), (Washizuka et al., 2005). Under compromised OXPHOS, ATP levels decrease and the activity of ATP-dependent ion pumps such as the Na+/K+-ATPase is slowed down, causing the membrane potential to shift toward hypopolarization. Neurotransmitters are released, and their uptake is delayed.	topic_bd
77652	2	356111	7	NULL	NULL	0	NULL	mRNA	NucleicAcid		involved in					OXPHOS	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS) (Iwamoto et al., 2005 K. Iwamoto, M. Bundo and T. Kato, Altered expression of mitochondria-related genes in postmortem brains of patients with bipolar disorder or schizophrenia, as revealed by large-scale DNA microarray analysis, Hum. Mol. Genet. 14 (2005), pp. 241–253. View Record in Scopus | Cited By in Scopus (130)[Iwamoto et al., 2005], [Konradi et al., 2004], [Pennington et al., 2008] and [Washizuka et al., 2005]). Downregulations were observed in the prefrontal cortex (PFC; Brodmann areas 9 and 46, Table 1), ([Iwamoto et al., 2005], [Pennington et al., 2008] and [Sun et al., 2006]), hippocampus (Konradi et al., 2004) and in lymphoblastoid cell lines (Table 2), (Washizuka et al., 2005). Under compromised OXPHOS, ATP levels decrease and the activity of ATP-dependent ion pumps such as the Na+/K+-ATPase is slowed down, causing the membrane potential to shift toward hypopolarization. Neurotransmitters are released, and their uptake is delayed.	topic_bd
77653	3	356111	7	NULL	NULL	0	NULL	protein expression profile	GP		shows					proteins	GP	decrease of			NULL		0	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS) (Iwamoto et al., 2005 K. Iwamoto, M. Bundo and T. Kato, Altered expression of mitochondria-related genes in postmortem brains of patients with bipolar disorder or schizophrenia, as revealed by large-scale DNA microarray analysis, Hum. Mol. Genet. 14 (2005), pp. 241–253. View Record in Scopus | Cited By in Scopus (130)[Iwamoto et al., 2005], [Konradi et al., 2004], [Pennington et al., 2008] and [Washizuka et al., 2005]). Downregulations were observed in the prefrontal cortex (PFC; Brodmann areas 9 and 46, Table 1), ([Iwamoto et al., 2005], [Pennington et al., 2008] and [Sun et al., 2006]), hippocampus (Konradi et al., 2004) and in lymphoblastoid cell lines (Table 2), (Washizuka et al., 2005). Under compromised OXPHOS, ATP levels decrease and the activity of ATP-dependent ion pumps such as the Na+/K+-ATPase is slowed down, causing the membrane potential to shift toward hypopolarization. Neurotransmitters are released, and their uptake is delayed.	topic_bd
77654	4	356111	7	NULL	NULL	0	NULL	proteins	GP		involved in					OXPHOS	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS) (Iwamoto et al., 2005 K. Iwamoto, M. Bundo and T. Kato, Altered expression of mitochondria-related genes in postmortem brains of patients with bipolar disorder or schizophrenia, as revealed by large-scale DNA microarray analysis, Hum. Mol. Genet. 14 (2005), pp. 241–253. View Record in Scopus | Cited By in Scopus (130)[Iwamoto et al., 2005], [Konradi et al., 2004], [Pennington et al., 2008] and [Washizuka et al., 2005]). Downregulations were observed in the prefrontal cortex (PFC; Brodmann areas 9 and 46, Table 1), ([Iwamoto et al., 2005], [Pennington et al., 2008] and [Sun et al., 2006]), hippocampus (Konradi et al., 2004) and in lymphoblastoid cell lines (Table 2), (Washizuka et al., 2005). Under compromised OXPHOS, ATP levels decrease and the activity of ATP-dependent ion pumps such as the Na+/K+-ATPase is slowed down, causing the membrane potential to shift toward hypopolarization. Neurotransmitters are released, and their uptake is delayed.	topic_bd
77655	5	356111	7	NULL	NULL	0	NULL	OXPHOS	Process		is					oxidative phosphorylation	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS) (Iwamoto et al., 2005 K. Iwamoto, M. Bundo and T. Kato, Altered expression of mitochondria-related genes in postmortem brains of patients with bipolar disorder or schizophrenia, as revealed by large-scale DNA microarray analysis, Hum. Mol. Genet. 14 (2005), pp. 241–253. View Record in Scopus | Cited By in Scopus (130)[Iwamoto et al., 2005], [Konradi et al., 2004], [Pennington et al., 2008] and [Washizuka et al., 2005]). Downregulations were observed in the prefrontal cortex (PFC; Brodmann areas 9 and 46, Table 1), ([Iwamoto et al., 2005], [Pennington et al., 2008] and [Sun et al., 2006]), hippocampus (Konradi et al., 2004) and in lymphoblastoid cell lines (Table 2), (Washizuka et al., 2005). Under compromised OXPHOS, ATP levels decrease and the activity of ATP-dependent ion pumps such as the Na+/K+-ATPase is slowed down, causing the membrane potential to shift toward hypopolarization. Neurotransmitters are released, and their uptake is delayed.	topic_bd
77656	6	356111	7	NULL	NULL	0	NULL	OXPHOS	Process		is a type of					mitochondrial function	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS) (Iwamoto et al., 2005 K. Iwamoto, M. Bundo and T. Kato, Altered expression of mitochondria-related genes in postmortem brains of patients with bipolar disorder or schizophrenia, as revealed by large-scale DNA microarray analysis, Hum. Mol. Genet. 14 (2005), pp. 241–253. View Record in Scopus | Cited By in Scopus (130)[Iwamoto et al., 2005], [Konradi et al., 2004], [Pennington et al., 2008] and [Washizuka et al., 2005]). Downregulations were observed in the prefrontal cortex (PFC; Brodmann areas 9 and 46, Table 1), ([Iwamoto et al., 2005], [Pennington et al., 2008] and [Sun et al., 2006]), hippocampus (Konradi et al., 2004) and in lymphoblastoid cell lines (Table 2), (Washizuka et al., 2005). Under compromised OXPHOS, ATP levels decrease and the activity of ATP-dependent ion pumps such as the Na+/K+-ATPase is slowed down, causing the membrane potential to shift toward hypopolarization. Neurotransmitters are released, and their uptake is delayed.	topic_bd
77657	7	356111	7	NULL	NULL	NULL	NULL	mitochondria-related genes	GP	altered expression of	occur in					bipolar disorder	MedicalFinding				NULL	postmortem brains of patients	NULL	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS) (Iwamoto et al., 2005 K. Iwamoto, M. Bundo and T. Kato, Altered expression of mitochondria-related genes in postmortem brains of patients with bipolar disorder or schizophrenia, as revealed by large-scale DNA microarray analysis, Hum. Mol. Genet. 14 (2005), pp. 241–253. View Record in Scopus | Cited By in Scopus (130)[Iwamoto et al., 2005], [Konradi et al., 2004], [Pennington et al., 2008] and [Washizuka et al., 2005]). Downregulations were observed in the prefrontal cortex (PFC; Brodmann areas 9 and 46, Table 1), ([Iwamoto et al., 2005], [Pennington et al., 2008] and [Sun et al., 2006]), hippocampus (Konradi et al., 2004) and in lymphoblastoid cell lines (Table 2), (Washizuka et al., 2005). Under compromised OXPHOS, ATP levels decrease and the activity of ATP-dependent ion pumps such as the Na+/K+-ATPase is slowed down, causing the membrane potential to shift toward hypopolarization. Neurotransmitters are released, and their uptake is delayed.	topic_bd
77658	8	356111	7	NULL	NULL	NULL	NULL	mitochondria-related genes	GP	altered expression of	occur in					schizophrenia	MedicalFinding				NULL	postmortem brains of patients	NULL	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS) (Iwamoto et al., 2005 K. Iwamoto, M. Bundo and T. Kato, Altered expression of mitochondria-related genes in postmortem brains of patients with bipolar disorder or schizophrenia, as revealed by large-scale DNA microarray analysis, Hum. Mol. Genet. 14 (2005), pp. 241–253. View Record in Scopus | Cited By in Scopus (130)[Iwamoto et al., 2005], [Konradi et al., 2004], [Pennington et al., 2008] and [Washizuka et al., 2005]). Downregulations were observed in the prefrontal cortex (PFC; Brodmann areas 9 and 46, Table 1), ([Iwamoto et al., 2005], [Pennington et al., 2008] and [Sun et al., 2006]), hippocampus (Konradi et al., 2004) and in lymphoblastoid cell lines (Table 2), (Washizuka et al., 2005). Under compromised OXPHOS, ATP levels decrease and the activity of ATP-dependent ion pumps such as the Na+/K+-ATPase is slowed down, causing the membrane potential to shift toward hypopolarization. Neurotransmitters are released, and their uptake is delayed.	topic_bd
77659	9	356111	7	NULL	NULL	0	NULL	ATP	Chemical	levels of	decrease					OXPHOS	Process	under compromised			NULL		0	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS) (Iwamoto et al., 2005 K. Iwamoto, M. Bundo and T. Kato, Altered expression of mitochondria-related genes in postmortem brains of patients with bipolar disorder or schizophrenia, as revealed by large-scale DNA microarray analysis, Hum. Mol. Genet. 14 (2005), pp. 241–253. View Record in Scopus | Cited By in Scopus (130)[Iwamoto et al., 2005], [Konradi et al., 2004], [Pennington et al., 2008] and [Washizuka et al., 2005]). Downregulations were observed in the prefrontal cortex (PFC; Brodmann areas 9 and 46, Table 1), ([Iwamoto et al., 2005], [Pennington et al., 2008] and [Sun et al., 2006]), hippocampus (Konradi et al., 2004) and in lymphoblastoid cell lines (Table 2), (Washizuka et al., 2005). Under compromised OXPHOS, ATP levels decrease and the activity of ATP-dependent ion pumps such as the Na+/K+-ATPase is slowed down, causing the membrane potential to shift toward hypopolarization. Neurotransmitters are released, and their uptake is delayed.	topic_bd
77660	10	356111	7	NULL	NULL	0	NULL	Na+/K+-ATPase	GP	activity of	slowed down					OXPHOS	Process	under compromised			NULL		0	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS) (Iwamoto et al., 2005 K. Iwamoto, M. Bundo and T. Kato, Altered expression of mitochondria-related genes in postmortem brains of patients with bipolar disorder or schizophrenia, as revealed by large-scale DNA microarray analysis, Hum. Mol. Genet. 14 (2005), pp. 241–253. View Record in Scopus | Cited By in Scopus (130)[Iwamoto et al., 2005], [Konradi et al., 2004], [Pennington et al., 2008] and [Washizuka et al., 2005]). Downregulations were observed in the prefrontal cortex (PFC; Brodmann areas 9 and 46, Table 1), ([Iwamoto et al., 2005], [Pennington et al., 2008] and [Sun et al., 2006]), hippocampus (Konradi et al., 2004) and in lymphoblastoid cell lines (Table 2), (Washizuka et al., 2005). Under compromised OXPHOS, ATP levels decrease and the activity of ATP-dependent ion pumps such as the Na+/K+-ATPase is slowed down, causing the membrane potential to shift toward hypopolarization. Neurotransmitters are released, and their uptake is delayed.	topic_bd
77661	11	356111	7	NULL	NULL	0	NULL	membrane potential	Process		shift toward					hypopolarization	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS) (Iwamoto et al., 2005 K. Iwamoto, M. Bundo and T. Kato, Altered expression of mitochondria-related genes in postmortem brains of patients with bipolar disorder or schizophrenia, as revealed by large-scale DNA microarray analysis, Hum. Mol. Genet. 14 (2005), pp. 241–253. View Record in Scopus | Cited By in Scopus (130)[Iwamoto et al., 2005], [Konradi et al., 2004], [Pennington et al., 2008] and [Washizuka et al., 2005]). Downregulations were observed in the prefrontal cortex (PFC; Brodmann areas 9 and 46, Table 1), ([Iwamoto et al., 2005], [Pennington et al., 2008] and [Sun et al., 2006]), hippocampus (Konradi et al., 2004) and in lymphoblastoid cell lines (Table 2), (Washizuka et al., 2005). Under compromised OXPHOS, ATP levels decrease and the activity of ATP-dependent ion pumps such as the Na+/K+-ATPase is slowed down, causing the membrane potential to shift toward hypopolarization. Neurotransmitters are released, and their uptake is delayed.	topic_bd
77663	12	356111	7	NULL	NULL	NULL	NULL	statement 10	Process		cause					statement 11	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS) (Iwamoto et al., 2005 K. Iwamoto, M. Bundo and T. Kato, Altered expression of mitochondria-related genes in postmortem brains of patients with bipolar disorder or schizophrenia, as revealed by large-scale DNA microarray analysis, Hum. Mol. Genet. 14 (2005), pp. 241–253. View Record in Scopus | Cited By in Scopus (130)[Iwamoto et al., 2005], [Konradi et al., 2004], [Pennington et al., 2008] and [Washizuka et al., 2005]). Downregulations were observed in the prefrontal cortex (PFC; Brodmann areas 9 and 46, Table 1), ([Iwamoto et al., 2005], [Pennington et al., 2008] and [Sun et al., 2006]), hippocampus (Konradi et al., 2004) and in lymphoblastoid cell lines (Table 2), (Washizuka et al., 2005). Under compromised OXPHOS, ATP levels decrease and the activity of ATP-dependent ion pumps such as the Na+/K+-ATPase is slowed down, causing the membrane potential to shift toward hypopolarization. Neurotransmitters are released, and their uptake is delayed.	topic_bd
77664	13	356111	7	NULL	NULL	NULL	NULL	neurotransmitters	Chemical		are					released	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS) (Iwamoto et al., 2005 K. Iwamoto, M. Bundo and T. Kato, Altered expression of mitochondria-related genes in postmortem brains of patients with bipolar disorder or schizophrenia, as revealed by large-scale DNA microarray analysis, Hum. Mol. Genet. 14 (2005), pp. 241–253. View Record in Scopus | Cited By in Scopus (130)[Iwamoto et al., 2005], [Konradi et al., 2004], [Pennington et al., 2008] and [Washizuka et al., 2005]). Downregulations were observed in the prefrontal cortex (PFC; Brodmann areas 9 and 46, Table 1), ([Iwamoto et al., 2005], [Pennington et al., 2008] and [Sun et al., 2006]), hippocampus (Konradi et al., 2004) and in lymphoblastoid cell lines (Table 2), (Washizuka et al., 2005). Under compromised OXPHOS, ATP levels decrease and the activity of ATP-dependent ion pumps such as the Na+/K+-ATPase is slowed down, causing the membrane potential to shift toward hypopolarization. Neurotransmitters are released, and their uptake is delayed.	topic_bd
77665	14	356111	7	NULL	NULL	NULL	NULL	neurotransmitter	Chemical	uptake of	is					delayed	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS) (Iwamoto et al., 2005 K. Iwamoto, M. Bundo and T. Kato, Altered expression of mitochondria-related genes in postmortem brains of patients with bipolar disorder or schizophrenia, as revealed by large-scale DNA microarray analysis, Hum. Mol. Genet. 14 (2005), pp. 241–253. View Record in Scopus | Cited By in Scopus (130)[Iwamoto et al., 2005], [Konradi et al., 2004], [Pennington et al., 2008] and [Washizuka et al., 2005]). Downregulations were observed in the prefrontal cortex (PFC; Brodmann areas 9 and 46, Table 1), ([Iwamoto et al., 2005], [Pennington et al., 2008] and [Sun et al., 2006]), hippocampus (Konradi et al., 2004) and in lymphoblastoid cell lines (Table 2), (Washizuka et al., 2005). Under compromised OXPHOS, ATP levels decrease and the activity of ATP-dependent ion pumps such as the Na+/K+-ATPase is slowed down, causing the membrane potential to shift toward hypopolarization. Neurotransmitters are released, and their uptake is delayed.	topic_bd
77666	15	356111	7	NULL	NULL	0	NULL	statement 10	Process		cause					statement 14	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Gene and protein expression profiles in BPD show a decrease of mRNA and proteins involved in mitochondrial functions such as oxidative phosphorylation (OXPHOS) (Iwamoto et al., 2005 K. Iwamoto, M. Bundo and T. Kato, Altered expression of mitochondria-related genes in postmortem brains of patients with bipolar disorder or schizophrenia, as revealed by large-scale DNA microarray analysis, Hum. Mol. Genet. 14 (2005), pp. 241–253. View Record in Scopus | Cited By in Scopus (130)[Iwamoto et al., 2005], [Konradi et al., 2004], [Pennington et al., 2008] and [Washizuka et al., 2005]). Downregulations were observed in the prefrontal cortex (PFC; Brodmann areas 9 and 46, Table 1), ([Iwamoto et al., 2005], [Pennington et al., 2008] and [Sun et al., 2006]), hippocampus (Konradi et al., 2004) and in lymphoblastoid cell lines (Table 2), (Washizuka et al., 2005). Under compromised OXPHOS, ATP levels decrease and the activity of ATP-dependent ion pumps such as the Na+/K+-ATPase is slowed down, causing the membrane potential to shift toward hypopolarization. Neurotransmitters are released, and their uptake is delayed.	topic_bd
77667	1	356112	7	NULL	NULL	0	NULL	pH	QuantityOrMeasure	reduced frontal lobe	occur in					BPD patients	MedicalFinding	medicated			NULL		0	NULL	NULL	NULL	NULL	NULL	Kato et al. found reduced frontal lobe pH in medicated and unmedicated BPD patients ([Kato et al., 1998] and [Kato et al., 1993]), and two-dimensional proton echo-planar spectroscopic imaging of medication-free BPD patients showed a shift from OXPHOS to glycolysis (Dager et al., 2004 S.R. Dager et al., Brain metabolic alterations in medication-free patients with bipolar disorder, Arch. Gen. Psychiatry 61 (2004), pp. 450–458. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (137)Dager et al., 2004), (Fig. 1).	topic_bd
77668	2	356112	7	NULL	NULL	0	NULL	pH	QuantityOrMeasure	reduced frontal lobe	occur in					BPD patients	MedicalFinding	unmedicated			NULL		0	NULL	NULL	NULL	NULL	NULL	Kato et al. found reduced frontal lobe pH in medicated and unmedicated BPD patients ([Kato et al., 1998] and [Kato et al., 1993]), and two-dimensional proton echo-planar spectroscopic imaging of medication-free BPD patients showed a shift from OXPHOS to glycolysis (Dager et al., 2004 S.R. Dager et al., Brain metabolic alterations in medication-free patients with bipolar disorder, Arch. Gen. Psychiatry 61 (2004), pp. 450–458. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (137)Dager et al., 2004), (Fig. 1).	topic_bd
77669	3	356112	7	NULL	NULL	0	NULL	OXPHOS	Process		shifted to					glycolysis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Kato et al. found reduced frontal lobe pH in medicated and unmedicated BPD patients ([Kato et al., 1998] and [Kato et al., 1993]), and two-dimensional proton echo-planar spectroscopic imaging of medication-free BPD patients showed a shift from OXPHOS to glycolysis (Dager et al., 2004 S.R. Dager et al., Brain metabolic alterations in medication-free patients with bipolar disorder, Arch. Gen. Psychiatry 61 (2004), pp. 450–458. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (137)Dager et al., 2004), (Fig. 1).	topic_bd
77670	4	356112	7	NULL	NULL	0	NULL	statement 3	Process		occur in					BPD patients	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Kato et al. found reduced frontal lobe pH in medicated and unmedicated BPD patients ([Kato et al., 1998] and [Kato et al., 1993]), and two-dimensional proton echo-planar spectroscopic imaging of medication-free BPD patients showed a shift from OXPHOS to glycolysis (Dager et al., 2004 S.R. Dager et al., Brain metabolic alterations in medication-free patients with bipolar disorder, Arch. Gen. Psychiatry 61 (2004), pp. 450–458. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (137)Dager et al., 2004), (Fig. 1).	topic_bd
77671	1	356113	7	NULL	NULL	NULL	NULL	mRNA	NucleicAcid	lower levels of	occur in the					electron transfer chain	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Specifically, lower mRNA and protein levels of the electron transfer chain cause a shift from OXPHOS to glycolysis to retain ATP production, which leads to the accumulation of lactic acid, the acidification of tissue, and a decrease in pH 	topic_bd
77672	2	356113	7	NULL	NULL	0	NULL	protein	GP	lower levels of	occur in the					electron transfer chain	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Specifically, lower mRNA and protein levels of the electron transfer chain cause a shift from OXPHOS to glycolysis to retain ATP production, which leads to the accumulation of lactic acid, the acidification of tissue, and a decrease in pH 	topic_bd
77673	3	356113	7	NULL	NULL	0	NULL	OXPHOS	Process		shifted to					glycolysis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Specifically, lower mRNA and protein levels of the electron transfer chain cause a shift from OXPHOS to glycolysis to retain ATP production, which leads to the accumulation of lactic acid, the acidification of tissue, and a decrease in pH 	topic_bd
77674	4	356113	7	NULL	NULL	0	NULL	statement 3	Process		retain					ATP	Chemical	production of			NULL		0	NULL	NULL	NULL	NULL	NULL	Specifically, lower mRNA and protein levels of the electron transfer chain cause a shift from OXPHOS to glycolysis to retain ATP production, which leads to the accumulation of lactic acid, the acidification of tissue, and a decrease in pH 	topic_bd
77675	5	356113	7	NULL	NULL	0	NULL	statement 1	Process		cause					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Specifically, lower mRNA and protein levels of the electron transfer chain cause a shift from OXPHOS to glycolysis to retain ATP production, which leads to the accumulation of lactic acid, the acidification of tissue, and a decrease in pH 	topic_bd
77676	6	356113	7	NULL	NULL	0	NULL	statement 2	Process		cause					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Specifically, lower mRNA and protein levels of the electron transfer chain cause a shift from OXPHOS to glycolysis to retain ATP production, which leads to the accumulation of lactic acid, the acidification of tissue, and a decrease in pH 	topic_bd
77677	7	356113	7	NULL	NULL	0	NULL	statement 4	Process		leads to					lactic acid	Chemical	accumulation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Specifically, lower mRNA and protein levels of the electron transfer chain cause a shift from OXPHOS to glycolysis to retain ATP production, which leads to the accumulation of lactic acid, the acidification of tissue, and a decrease in pH 	topic_bd
77678	8	356113	7	NULL	NULL	0	NULL	statement 7	Process		leads to					tissue	OrganismPart	acidification of			NULL		0	NULL	NULL	NULL	NULL	NULL	Specifically, lower mRNA and protein levels of the electron transfer chain cause a shift from OXPHOS to glycolysis to retain ATP production, which leads to the accumulation of lactic acid, the acidification of tissue, and a decrease in pH 	topic_bd
77679	9	356113	7	NULL	NULL	0	NULL	statement 8	Process		leads to					pH	QuantityOrMeasure	decrease of			NULL		0	NULL	NULL	NULL	NULL	NULL	Specifically, lower mRNA and protein levels of the electron transfer chain cause a shift from OXPHOS to glycolysis to retain ATP production, which leads to the accumulation of lactic acid, the acidification of tissue, and a decrease in pH 	topic_bd
77382	1	356114	5	NULL	NULL	0	NULL	synaptic maturation	Process	delayed	is linked to					FXS	MedicalFinding	pathogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	In particular, delayed synaptic maturation, abnormal synaptic structure and/or function and alterations in intracellular signaling pathways have been linked to the pathogenesis of FXS and ASD	topic_aut
77383	2	356114	5	NULL	NULL	0	NULL	synaptic maturation	Process	delayed	is linked to					ASD	MedicalFinding	pathogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	In particular, delayed synaptic maturation, abnormal synaptic structure and/or function and alterations in intracellular signaling pathways have been linked to the pathogenesis of FXS and ASD	topic_aut
77384	3	356114	5	NULL	NULL	0	NULL	synapse	OrganismPart	abnormal;;structure of	is linked to					FXS	MedicalFinding	pathogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	In particular, delayed synaptic maturation, abnormal synaptic structure and/or function and alterations in intracellular signaling pathways have been linked to the pathogenesis of FXS and ASD	topic_aut
77385	4	356114	5	NULL	NULL	0	NULL	synapse	OrganismPart	abnormal;;structure of	is linked to					ASD	MedicalFinding	pathogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	In particular, delayed synaptic maturation, abnormal synaptic structure and/or function and alterations in intracellular signaling pathways have been linked to the pathogenesis of FXS and ASD	topic_aut
77386	5	356114	5	NULL	NULL	0	NULL	signaling pathways	Process	function of ;;intracellular	is linked to					FXS	MedicalFinding	pathogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	In particular, delayed synaptic maturation, abnormal synaptic structure and/or function and alterations in intracellular signaling pathways have been linked to the pathogenesis of FXS and ASD	topic_aut
77387	6	356114	5	NULL	NULL	0	NULL	signaling pathways	Process	function of ;;intracellular	is linked to					ASD	MedicalFinding	pathogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	In particular, delayed synaptic maturation, abnormal synaptic structure and/or function and alterations in intracellular signaling pathways have been linked to the pathogenesis of FXS and ASD	topic_aut
77388	7	356114	5	NULL	NULL	0	NULL	signaling pathways	Process	alterations of;;intracellular	is linked to					FXS	MedicalFinding	pathogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	In particular, delayed synaptic maturation, abnormal synaptic structure and/or function and alterations in intracellular signaling pathways have been linked to the pathogenesis of FXS and ASD	topic_aut
77389	8	356114	5	NULL	NULL	0	NULL	signaling pathways	Process	alterations of;;intracellular	is linked to					ASD	MedicalFinding	pathogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	In particular, delayed synaptic maturation, abnormal synaptic structure and/or function and alterations in intracellular signaling pathways have been linked to the pathogenesis of FXS and ASD	topic_aut
78064	1	356115	5	NULL	NULL	0	NULL	GABA(A) receptor	GP		is a type of					ion channel	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Aberrations in GABA(A) receptor ion channels and the G-protein coupled metabotropic glutamate and GABA(B) transmitter systems are also linked to both disorders and these receptors are currently at the forefront of preclinical and clinical research into treatments for both autism and Fragile X Syndrome.	topic_aut
78065	2	356115	5	NULL	NULL	0	NULL	GABA(A) receptor	GP	aberrations of	is linked to					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Aberrations in GABA(A) receptor ion channels and the G-protein coupled metabotropic glutamate and GABA(B) transmitter systems are also linked to both disorders and these receptors are currently at the forefront of preclinical and clinical research into treatments for both autism and Fragile X Syndrome.	topic_aut
78066	3	356115	5	NULL	NULL	0	NULL	GABA(A) receptor	GP	aberrations of	is linked to					Fragile X Syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Aberrations in GABA(A) receptor ion channels and the G-protein coupled metabotropic glutamate and GABA(B) transmitter systems are also linked to both disorders and these receptors are currently at the forefront of preclinical and clinical research into treatments for both autism and Fragile X Syndrome.	topic_aut
78071	4	356115	5	NULL	NULL	0	NULL	G-protein coupled metabotropic glutamate	GP	aberrations of	is linked to					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Aberrations in GABA(A) receptor ion channels and the G-protein coupled metabotropic glutamate and GABA(B) transmitter systems are also linked to both disorders and these receptors are currently at the forefront of preclinical and clinical research into treatments for both autism and Fragile X Syndrome.	topic_aut
78072	5	356115	5	NULL	NULL	0	NULL	G-protein coupled metabotropic glutamate	GP	aberrations of	is linked to					Fragile X Syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Aberrations in GABA(A) receptor ion channels and the G-protein coupled metabotropic glutamate and GABA(B) transmitter systems are also linked to both disorders and these receptors are currently at the forefront of preclinical and clinical research into treatments for both autism and Fragile X Syndrome.	topic_aut
78073	6	356115	5	NULL	NULL	0	NULL	G-protein coupled GABA(B) transmitter systems	GP	aberrations of	is linked to					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Aberrations in GABA(A) receptor ion channels and the G-protein coupled metabotropic glutamate and GABA(B) transmitter systems are also linked to both disorders and these receptors are currently at the forefront of preclinical and clinical research into treatments for both autism and Fragile X Syndrome.	topic_aut
78074	7	356115	5	NULL	NULL	0	NULL	G-protein coupled GABA(B) transmitter systems	GP	aberrations of	is linked to					Fragile X Syndrome	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Aberrations in GABA(A) receptor ion channels and the G-protein coupled metabotropic glutamate and GABA(B) transmitter systems are also linked to both disorders and these receptors are currently at the forefront of preclinical and clinical research into treatments for both autism and Fragile X Syndrome.	topic_aut
78075	1	356116	5	NULL	NULL	NULL	NULL	GAD1 gene	GP	common genetic variation of	unlikely to play a role in		critical			ASD	MedicalFinding	susceptibility of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Our observations, when taken together with previous findings, suggest that common genetic variation in the GAD1 and DLX genes is unlikely to play a critical role in ASD susceptibility	topic_aut
78076	2	356116	5	NULL	NULL	0	NULL	DLX gene	GP	common genetic variation of	unlikely to play a role in		critical			ASD	MedicalFinding	susceptibility of			NULL		0	NULL	NULL	NULL	NULL	NULL	Our observations, when taken together with previous findings, suggest that common genetic variation in the GAD1 and DLX genes is unlikely to play a critical role in ASD susceptibility	topic_aut
78077	1	356117	5	NULL	NULL	0	NULL	GAD67	GP		is also known as					GAD1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate decarboxylase 1 (brain, 67kDa) (GAD67), also known as GAD1, is a human gene.[1] This gene encodes one of several forms of glutamic acid decarboxylase, identified as a major autoantigen in insulin-dependent diabetes	topic_aut
78078	2	356117	5	NULL	NULL	0	NULL	GAD67	GP		is					Glutamate decarboxylase 1 (brain, 67kDa) 	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate decarboxylase 1 (brain, 67kDa) (GAD67), also known as GAD1, is a human gene.[1] This gene encodes one of several forms of glutamic acid decarboxylase, identified as a major autoantigen in insulin-dependent diabetes	topic_aut
78079	3	356117	5	NULL	NULL	0	NULL	GAD1	GP	human	encodes					glutamic acid decarboxylase	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate decarboxylase 1 (brain, 67kDa) (GAD67), also known as GAD1, is a human gene.[1] This gene encodes one of several forms of glutamic acid decarboxylase, identified as a major autoantigen in insulin-dependent diabetes	topic_aut
78080	4	356117	5	NULL	NULL	0	NULL	glutamic acid decarboxylase	GP		is a type of					autoantigen	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate decarboxylase 1 (brain, 67kDa) (GAD67), also known as GAD1, is a human gene.[1] This gene encodes one of several forms of glutamic acid decarboxylase, identified as a major autoantigen in insulin-dependent diabetes	topic_aut
78081	5	356117	5	NULL	NULL	0	NULL	statement 4	GP		is present in					 insulin-dependent diabetes	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate decarboxylase 1 (brain, 67kDa) (GAD67), also known as GAD1, is a human gene.[1] This gene encodes one of several forms of glutamic acid decarboxylase, identified as a major autoantigen in insulin-dependent diabetes	topic_aut
78082	1	356118	5	NULL	NULL	0	NULL	Dlx	GP		is a family of					homeodomain transcription factors	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Dlx is a family of homeodomain transcription factors which are related to the Drosophila distal-less (Dll) gene [1]. The family has been related to a number of developmental features. The family seems to be well preserved across species[2].	topic_aut
78083	2	356118	5	NULL	NULL	0	NULL	Dlx	GP		is related to					Dll gene	GP	Drosophila			NULL		0	NULL	NULL	NULL	NULL	NULL	Dlx is a family of homeodomain transcription factors which are related to the Drosophila distal-less (Dll) gene [1]. The family has been related to a number of developmental features. The family seems to be well preserved across species[2].	topic_aut
78084	3	356118	5	NULL	NULL	0	NULL	Dll gene	GP		is					distal-less gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Dlx is a family of homeodomain transcription factors which are related to the Drosophila distal-less (Dll) gene [1]. The family has been related to a number of developmental features. The family seems to be well preserved across species[2].	topic_aut
78085	4	356118	5	NULL	NULL	0	NULL	Dlx	GP		is related to					developmental features	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Dlx is a family of homeodomain transcription factors which are related to the Drosophila distal-less (Dll) gene [1]. The family has been related to a number of developmental features. The family seems to be well preserved across species[2].	topic_aut
78115	1	356119	5	NULL	NULL	0	NULL	CNVs	NucleicAcid	rare	encompass					ASDs	MedicalFinding	potential;;candidate regions for			NULL		0	NULL	NULL	NULL	NULL	NULL	We conclude that rare CNVs, encompassing potential candidate regions for ASDs, increase the susceptibility for the development of ASDs and related neuropsychiatric disorders giving us further insight into the complex genetics underlying ASDs.	topic_aut
78116	2	356119	5	NULL	NULL	0	NULL	CNVs	NucleicAcid	rare	increases					ASDs	MedicalFinding	susceptibility of;;development of			NULL		0	NULL	NULL	NULL	NULL	NULL	We conclude that rare CNVs, encompassing potential candidate regions for ASDs, increase the susceptibility for the development of ASDs and related neuropsychiatric disorders giving us further insight into the complex genetics underlying ASDs.	topic_aut
78117	3	356119	5	NULL	NULL	0	NULL	CNVs	NucleicAcid	rare	increases					neuropsychiatric disorders	MedicalFinding	susceptibility of;;development of			NULL		0	NULL	NULL	NULL	NULL	NULL	We conclude that rare CNVs, encompassing potential candidate regions for ASDs, increase the susceptibility for the development of ASDs and related neuropsychiatric disorders giving us further insight into the complex genetics underlying ASDs.	topic_aut
78118	1	356120	5	NULL	NULL	0	NULL	SCARB2 gene	GP		is linked to					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The following candidate genes were identified in children with autism by in silico analysis: SCARB2, TPPP, PDCD6, SEPT5, GP1BB, PI4KA, NPTX1, STCH, NRIP1, and CXADR	topic_aut
78119	2	356120	5	NULL	NULL	0	NULL	TPPP gene	GP		is linked to					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The following candidate genes were identified in children with autism by in silico analysis: SCARB2, TPPP, PDCD6, SEPT5, GP1BB, PI4KA, NPTX1, STCH, NRIP1, and CXADR	topic_aut
78120	3	356120	5	NULL	NULL	0	NULL	PDCD6 gene	GP		is linked to					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The following candidate genes were identified in children with autism by in silico analysis: SCARB2, TPPP, PDCD6, SEPT5, GP1BB, PI4KA, NPTX1, STCH, NRIP1, and CXADR	topic_aut
78121	4	356120	5	NULL	NULL	0	NULL	SEPT5 gene	GP		is linked to					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The following candidate genes were identified in children with autism by in silico analysis: SCARB2, TPPP, PDCD6, SEPT5, GP1BB, PI4KA, NPTX1, STCH, NRIP1, and CXADR	topic_aut
78126	5	356120	5	NULL	NULL	0	NULL	GP1BB gene	GP		is linked to					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The following candidate genes were identified in children with autism by in silico analysis: SCARB2, TPPP, PDCD6, SEPT5, GP1BB, PI4KA, NPTX1, STCH, NRIP1, and CXADR	topic_aut
78128	6	356120	5	NULL	NULL	0	NULL	PI4KA gene	GP		is linked to					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The following candidate genes were identified in children with autism by in silico analysis: SCARB2, TPPP, PDCD6, SEPT5, GP1BB, PI4KA, NPTX1, STCH, NRIP1, and CXADR	topic_aut
78131	7	356120	5	NULL	NULL	0	NULL	NPTX1 gene	GP		is linked to					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The following candidate genes were identified in children with autism by in silico analysis: SCARB2, TPPP, PDCD6, SEPT5, GP1BB, PI4KA, NPTX1, STCH, NRIP1, and CXADR	topic_aut
78135	8	356120	5	NULL	NULL	0	NULL	STCH gene	GP		is linked to					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The following candidate genes were identified in children with autism by in silico analysis: SCARB2, TPPP, PDCD6, SEPT5, GP1BB, PI4KA, NPTX1, STCH, NRIP1, and CXADR	topic_aut
78136	9	356120	5	NULL	NULL	0	NULL	NRIP1 gene	GP		is linked to					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The following candidate genes were identified in children with autism by in silico analysis: SCARB2, TPPP, PDCD6, SEPT5, GP1BB, PI4KA, NPTX1, STCH, NRIP1, and CXADR	topic_aut
78138	10	356120	5	NULL	NULL	0	NULL	CXADR gene	GP		is linked to					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The following candidate genes were identified in children with autism by in silico analysis: SCARB2, TPPP, PDCD6, SEPT5, GP1BB, PI4KA, NPTX1, STCH, NRIP1, and CXADR	topic_aut
78139	1	356121	5	NULL	NULL	0	NULL	Lysosome membrane protein 2	GP	human	is encoded by					SCARB2 gene	GP	human			NULL		0	NULL	NULL	NULL	NULL	NULL	Lysosome membrane protein 2 is a protein that in humans is encoded by the SCARB2 gene	topic_aut
78141	1	356122	5	NULL	NULL	0	NULL	Tubulin polymerization-promoting protein	GP	human	is encoded by					TPPP gene	GP	human			NULL		0	NULL	NULL	NULL	NULL	NULL	Tubulin polymerization-promoting protein is a protein that in humans is encoded by the TPPP gene.	topic_aut
78143	1	356123	5	NULL	NULL	0	NULL	Programmed cell death protein 6	GP	human	is encoded by					PDCD6 gene	GP	human			NULL		0	NULL	NULL	NULL	NULL	NULL	Programmed cell death protein 6 is a protein that in humans is encoded by the PDCD6 gene	topic_aut
78149	1	356124	5	NULL	NULL	0	NULL	Septin-5 protein	GP	human	is encoded by					SEPT5 gene	GP	human			NULL		0	NULL	NULL	NULL	NULL	NULL	Septin-5 is a protein that in humans is encoded by the SEPT5 gene	topic_aut
78150	1	356126	5	NULL	NULL	0	NULL	Phosphatidylinositol 4-kinase alpha	GP	human	is a type of					enzyme	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Phosphatidylinositol 4-kinase alpha is an enzyme that in humans is encoded by the PI4KA gene	topic_aut
78151	2	356126	5	NULL	NULL	0	NULL	Phosphatidylinositol 4-kinase alpha	GP	human	is encoded by					PI4KA gene	GP	human			NULL		0	NULL	NULL	NULL	NULL	NULL	Phosphatidylinositol 4-kinase alpha is an enzyme that in humans is encoded by the PI4KA gene	topic_aut
78152	1	356127	5	NULL	NULL	0	NULL	NP1	GP		is					Neuronal pentraxin-1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Neuronal pentraxin-1 (NP1) is a protein that in humans is encoded by the NPTX1 gene	topic_aut
78153	2	356127	5	NULL	NULL	0	NULL	NP1 protein	GP	human	is encoded by					NPTX1 gene	GP	human			NULL		0	NULL	NULL	NULL	NULL	NULL	Neuronal pentraxin-1 (NP1) is a protein that in humans is encoded by the NPTX1 gene	topic_aut
78154	1	356128	5	NULL	NULL	0	NULL	Heat shock 70 kDa protein 13	GP	human	is encoded by					HSPA13 gene	GP	human			NULL		0	NULL	NULL	NULL	NULL	NULL	Heat shock 70 kDa protein 13 is a protein that in humans is encoded by the HSPA13 gene.	topic_aut
78156	1	356129	5	NULL	NULL	0	NULL	Nuclear receptor-interacting protein 1	GP	human	is encoded by					NRIP1 gene	GP	human			NULL		0	NULL	NULL	NULL	NULL	NULL	Nuclear receptor-interacting protein 1 is a protein that in humans is encoded by the NRIP1 gene	topic_aut
78158	1	356130	5	NULL	NULL	0	NULL	CAR	GP		is					coxsackievirus and adenovirus receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Coxsackievirus and adenovirus receptor (CAR) is a protein that in humans is encoded by the CXADR gene	topic_aut
78159	2	356130	5	NULL	NULL	0	NULL	CAR gene	GP	human	is encoded by					CXADR gene	GP	human			NULL		0	NULL	NULL	NULL	NULL	NULL	Coxsackievirus and adenovirus receptor (CAR) is a protein that in humans is encoded by the CXADR gene	topic_aut
78166	1	356131	5	NULL	NULL	0	NULL	schizophrenia	MedicalFinding		is associated with					white matter	OrganismPart	widespread changes in;;structure of			NULL		0	NULL	NULL	NULL	NULL	NULL	Schizophrenia is associated with often widespread changes in white matter structure.	topic_sch
78242	1	356133	5	NULL	NULL	0	NULL	 frontostriatocingulate network	OrganismPart	decreased activation of	is associated with					decision making	MentalProcess	uncertinity of			NULL		0	NULL	NULL	NULL	NULL	NULL	Decision-making under uncertainty was associated with a significantly decreased activation in a frontostriatocingulate network in the schizophrenia group. Structurally, they exhibited increased radial diffusivity in temporal white matter that was negatively correlated with activation in parts of the frontostriatocingulate network.	topic_sch
78243	2	356133	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					schizophrenia group	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Decision-making under uncertainty was associated with a significantly decreased activation in a frontostriatocingulate network in the schizophrenia group. Structurally, they exhibited increased radial diffusivity in temporal white matter that was negatively correlated with activation in parts of the frontostriatocingulate network.	topic_sch
78244	3	356133	5	NULL	NULL	0	NULL	radial diffusivity	AbstractConcept		is increased in					temporal white matter	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Decision-making under uncertainty was associated with a significantly decreased activation in a frontostriatocingulate network in the schizophrenia group. Structurally, they exhibited increased radial diffusivity in temporal white matter that was negatively correlated with activation in parts of the frontostriatocingulate network.	topic_sch
78245	4	356133	5	NULL	NULL	0	NULL	statement 3	Process		correlates with		negatively			frontostriatocingulate network	OrganismPart	activation of;;parts of			NULL		0	NULL	NULL	NULL	NULL	NULL	Decision-making under uncertainty was associated with a significantly decreased activation in a frontostriatocingulate network in the schizophrenia group. Structurally, they exhibited increased radial diffusivity in temporal white matter that was negatively correlated with activation in parts of the frontostriatocingulate network.	topic_sch
78246	1	356134	5	NULL	NULL	NULL	NULL	diffusivity	AbstractConcept		altered in					white matter networks	OrganismPart	relevant			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Present data indicate that altered diffusivity within relevant white matter networks may be closely linked to abnormal neural activation in schizophrenia.	topic_sch
78247	2	356134	5	NULL	NULL	0	NULL	statement 1	Process		is linked to		closely			neural activation	Process	abnormal			NULL		0	NULL	NULL	NULL	NULL	NULL	Present data indicate that altered diffusivity within relevant white matter networks may be closely linked to abnormal neural activation in schizophrenia.	topic_sch
78248	3	356134	5	NULL	NULL	0	NULL	statement 2	Process		occurs in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Present data indicate that altered diffusivity within relevant white matter networks may be closely linked to abnormal neural activation in schizophrenia.	topic_sch
77688	1	356135	7	NULL	NULL	NULL	NULL	bipolar disorder	MedicalFinding	patients with	impaired					social competence	MentalProcess				NULL		NULL	NULL	NULL	NULL	NULL	NULL	A subgroup of outpatients with bipolar disorder has impaired social competence, which, when present, worsened the impact of depression and cognitive impairment on social functioning.	topic_bd
77689	2	356135	7	NULL	NULL	0	NULL	statement 1	Process		worsens					depression	MedicalFinding	impact of			NULL		0	NULL	NULL	NULL	NULL	NULL	A subgroup of outpatients with bipolar disorder has impaired social competence, which, when present, worsened the impact of depression and cognitive impairment on social functioning.	topic_bd
77690	3	356135	7	NULL	NULL	0	NULL	statement 1	Process		worsens					social functioning	MentalProcess	cognitive impairment on			NULL		0	NULL	NULL	NULL	NULL	NULL	A subgroup of outpatients with bipolar disorder has impaired social competence, which, when present, worsened the impact of depression and cognitive impairment on social functioning.	topic_bd
77691	1	356136	7	NULL	NULL	0	NULL	Prodromal clinical phenomenology	MedicalProcedure		nonspecific to					FMAE	MedicalFinding	predict the occurrence of			NULL		0	NULL	NULL	NULL	NULL	NULL	Prodromal clinical phenomenology is too nonspecific to predict the occurrence of the FMAE of BD-II. However, identifiable subgroups may exist. We hypothesize that neurocognitive deficits together with pronounced irritability and aggressiveness may constitute a vulnerability marker for a subgroup of individuals who subsequently develop BD-II. This subgroup may be of potential interest for early identification.	topic_bd
77692	2	356136	7	NULL	NULL	0	NULL	statement 1	Process		occur in					BD-II	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Prodromal clinical phenomenology is too nonspecific to predict the occurrence of the FMAE of BD-II. However, identifiable subgroups may exist. We hypothesize that neurocognitive deficits together with pronounced irritability and aggressiveness may constitute a vulnerability marker for a subgroup of individuals who subsequently develop BD-II. This subgroup may be of potential interest for early identification.	topic_bd
77693	3	356136	7	NULL	NULL	0	NULL	neurocognitive deficits 	MedicalFinding		vulnerability marker for		may be			BD-II	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Prodromal clinical phenomenology is too nonspecific to predict the occurrence of the FMAE of BD-II. However, identifiable subgroups may exist. We hypothesize that neurocognitive deficits together with pronounced irritability and aggressiveness may constitute a vulnerability marker for a subgroup of individuals who subsequently develop BD-II. This subgroup may be of potential interest for early identification.	topic_bd
77694	4	356136	7	NULL	NULL	0	NULL	statement 3	Process		occur with					irritability	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Prodromal clinical phenomenology is too nonspecific to predict the occurrence of the FMAE of BD-II. However, identifiable subgroups may exist. We hypothesize that neurocognitive deficits together with pronounced irritability and aggressiveness may constitute a vulnerability marker for a subgroup of individuals who subsequently develop BD-II. This subgroup may be of potential interest for early identification.	topic_bd
77695	5	356136	7	NULL	NULL	0	NULL	statement 3	Process		occur with					aggressiveness	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Prodromal clinical phenomenology is too nonspecific to predict the occurrence of the FMAE of BD-II. However, identifiable subgroups may exist. We hypothesize that neurocognitive deficits together with pronounced irritability and aggressiveness may constitute a vulnerability marker for a subgroup of individuals who subsequently develop BD-II. This subgroup may be of potential interest for early identification.	topic_bd
78249	1	356137	5	NULL	NULL	0	NULL	autistic people	GroupOfPeople		cannot eaisly recognize					faces	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Researchers have long known, for example, that people with autism have difficulty recognizing faces.	topic_aut
78250	1	356138	5	NULL	NULL	0	NULL	people	GroupOfPeople		recognize		better			right-side up faces	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	While most people are better at recognizing images of faces when they are right-side up, autistic subjects identify them faster when they are upside-down	topic_aut
78251	2	356138	5	NULL	NULL	0	NULL	autistic subjects	GroupOfPeople		identify		faster			upsie-down faces	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	While most people are better at recognizing images of faces when they are right-side up, autistic subjects identify them faster when they are upside-down	topic_aut
78252	1	356139	5	NULL	NULL	0	NULL	brain area	OrganismPart		is involved with					object recognition	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	when autistic adolescents and adults were shown pictures of faces, another brain area involved with object recognition was activated, while the fusiform gyrus remained quiet.	topic_aut
78253	2	356139	5	NULL	NULL	0	NULL	statement 1	Process		is activated in					autistic adolescents	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	when autistic adolescents and adults were shown pictures of faces, another brain area involved with object recognition was activated, while the fusiform gyrus remained quiet.	topic_aut
78254	3	356139	5	NULL	NULL	0	NULL	faces	OrganismPart	seeing	leads to					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	when autistic adolescents and adults were shown pictures of faces, another brain area involved with object recognition was activated, while the fusiform gyrus remained quiet.	topic_aut
78255	4	356139	5	NULL	NULL	0	NULL	statement 1	Process		is activated in					autistic adults	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	when autistic adolescents and adults were shown pictures of faces, another brain area involved with object recognition was activated, while the fusiform gyrus remained quiet.	topic_aut
78256	5	356139	5	NULL	NULL	0	NULL	faces	OrganismPart	seeing	leads to					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	when autistic adolescents and adults were shown pictures of faces, another brain area involved with object recognition was activated, while the fusiform gyrus remained quiet.	topic_aut
78257	6	356139	5	NULL	NULL	0	NULL	fusiform gyrus	OrganismPart		is not active in					autistic adolescents	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	when autistic adolescents and adults were shown pictures of faces, another brain area involved with object recognition was activated, while the fusiform gyrus remained quiet.	topic_aut
78258	7	356139	5	NULL	NULL	0	NULL	fusiform gyrus	OrganismPart		is not active in					autistic adults	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	when autistic adolescents and adults were shown pictures of faces, another brain area involved with object recognition was activated, while the fusiform gyrus remained quiet.	topic_aut
78259	8	356139	5	NULL	NULL	0	NULL	faces	OrganismPart	seeing	leads to					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	when autistic adolescents and adults were shown pictures of faces, another brain area involved with object recognition was activated, while the fusiform gyrus remained quiet.	topic_aut
78260	9	356139	5	NULL	NULL	0	NULL	faces	OrganismPart		leads to					statement 7	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	when autistic adolescents and adults were shown pictures of faces, another brain area involved with object recognition was activated, while the fusiform gyrus remained quiet.	topic_aut
78261	1	356140	5	NULL	NULL	0	NULL	fusiform gyrus	OrganismPart		is a component of					social brain	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	the fusiform gyrus may be a component of the social brain, intimately tied up with basic emotional responses like fear, anxiety and love.	topic_aut
78262	2	356140	5	NULL	NULL	0	NULL	fusiform gyrus	OrganismPart		is tied up with		intimately			fear	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	the fusiform gyrus may be a component of the social brain, intimately tied up with basic emotional responses like fear, anxiety and love.	topic_aut
78263	3	356140	5	NULL	NULL	0	NULL	fusiform gyrus	OrganismPart		is tied up with		intimately			anxiety	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	the fusiform gyrus may be a component of the social brain, intimately tied up with basic emotional responses like fear, anxiety and love.	topic_aut
78264	4	356140	5	NULL	NULL	0	NULL	fusiform gyrus	OrganismPart		is tied up with		intimately			love	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	the fusiform gyrus may be a component of the social brain, intimately tied up with basic emotional responses like fear, anxiety and love.	topic_aut
78265	5	356140	5	NULL	NULL	0	NULL	fear	MentalProcess		is a type of					emotional response	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	the fusiform gyrus may be a component of the social brain, intimately tied up with basic emotional responses like fear, anxiety and love.	topic_aut
78266	6	356140	5	NULL	NULL	0	NULL	anxiety	MentalProcess		is a type of					emotional response	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	the fusiform gyrus may be a component of the social brain, intimately tied up with basic emotional responses like fear, anxiety and love.	topic_aut
78267	7	356140	5	NULL	NULL	0	NULL	love	MentalProcess		is a type of					emotional response	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	the fusiform gyrus may be a component of the social brain, intimately tied up with basic emotional responses like fear, anxiety and love.	topic_aut
78648	1	356141	5	NULL	NULL	0	NULL	neurons	Cell	stacks of	is known as					mini-columns	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	an increase in autistic brains in the stacks of neurons known as mini-columns that extend through the layers of the neocortex. The brains of people with autism not only had more mini-columns, Dr. Casanova found, but the neurons that made up the columns were less variable in size than in normal brains	topic_aut
78649	2	356141	5	NULL	NULL	NULL	NULL	mini-columns	OrganismPart		extend through					neocortex	OrganismPart	layers of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	an increase in autistic brains in the stacks of neurons known as mini-columns that extend through the layers of the neocortex. The brains of people with autism not only had more mini-columns, Dr. Casanova found, but the neurons that made up the columns were less variable in size than in normal brains	topic_aut
78650	3	356141	5	NULL	NULL	0	NULL	mini-columns	OrganismPart	more	is present in					autistic people	GroupOfPeople	brains of			NULL		0	NULL	NULL	NULL	NULL	NULL	an increase in autistic brains in the stacks of neurons known as mini-columns that extend through the layers of the neocortex. The brains of people with autism not only had more mini-columns, Dr. Casanova found, but the neurons that made up the columns were less variable in size than in normal brains	topic_aut
78651	4	356141	5	NULL	NULL	0	NULL	neurons	Cell	size of	is variable in					brain	OrganismPart	autistic			NULL		0	NULL	NULL	NULL	NULL	NULL	an increase in autistic brains in the stacks of neurons known as mini-columns that extend through the layers of the neocortex. The brains of people with autism not only had more mini-columns, Dr. Casanova found, but the neurons that made up the columns were less variable in size than in normal brains	topic_aut
78652	5	356141	5	NULL	NULL	0	NULL	neurons	Cell	size of	is variable in					brain	OrganismPart	normal			NULL		0	NULL	NULL	NULL	NULL	NULL	an increase in autistic brains in the stacks of neurons known as mini-columns that extend through the layers of the neocortex. The brains of people with autism not only had more mini-columns, Dr. Casanova found, but the neurons that made up the columns were less variable in size than in normal brains	topic_aut
78653	6	356141	5	NULL	NULL	0	NULL	statement 4	Process		lesser than					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	an increase in autistic brains in the stacks of neurons known as mini-columns that extend through the layers of the neocortex. The brains of people with autism not only had more mini-columns, Dr. Casanova found, but the neurons that made up the columns were less variable in size than in normal brains	topic_aut
78268	1	356142	5	NULL	NULL	0	NULL	mini-columns	OrganismPart	proliferation of	results in		might			stimulation	Process	deluge of			NULL		0	NULL	NULL	NULL	NULL	NULL	Dr. Casanova, for his part, theorizes that the proliferation of mini-columns might result in a deluge of stimulation, or as he puts it, ''way too much information.'	topic_aut
78269	1	356143	5	NULL	NULL	0	NULL	infants	GroupOfPeople	male	is genetically vulnerable to					stresses	PhysicalPhenomenon	early			NULL		0	NULL	NULL	NULL	NULL	NULL	We postulate that higher TST levels and, therefore, higher amounts of arousal-related inputs to the amygdala sensitize these genetically vulnerable male infants to very early stresses	topic_aut
78270	2	356143	5	NULL	NULL	0	NULL	TST	GP	higher levels of	leads to					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	We postulate that higher TST levels and, therefore, higher amounts of arousal-related inputs to the amygdala sensitize these genetically vulnerable male infants to very early stresses	topic_aut
78271	3	356143	5	NULL	NULL	0	NULL	TST	GP	higher levels of	leads to					arousal-related inputs	AbstractConcept	higher amounts of			NULL	amygdala	0	NULL	NULL	NULL	NULL	NULL	We postulate that higher TST levels and, therefore, higher amounts of arousal-related inputs to the amygdala sensitize these genetically vulnerable male infants to very early stresses	topic_aut
78272	4	356143	5	NULL	NULL	0	NULL	statement 3	Process		leads to					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	We postulate that higher TST levels and, therefore, higher amounts of arousal-related inputs to the amygdala sensitize these genetically vulnerable male infants to very early stresses	topic_aut
78273	1	356145	5	NULL	NULL	0	NULL	oxidative stress	PhysicalPhenomenon		is implicated in					autism	MedicalFinding	pathophysiology of			NULL		0	NULL	NULL	NULL	NULL	NULL	Oxidative stress and abnormal DNA methylation have been implicated in the pathophysiology of autism	topic_aut
78274	2	356145	5	NULL	NULL	0	NULL	DNA	NucleicAcid	abnormal methylation of	is implicated in					autism	MedicalFinding	pathophysiology of			NULL		0	NULL	NULL	NULL	NULL	NULL	Oxidative stress and abnormal DNA methylation have been implicated in the pathophysiology of autism	topic_aut
78275	1	356146	5	NULL	NULL	0	NULL	antioxidant	Chemical	deficit in	is specific for					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	These data indicate that the deficit in antioxidant and methylation capacity is specific for autism and may promote cellular damage and altered epigenetic gene expression	topic_aut
78276	2	356146	5	NULL	NULL	0	NULL	antioxidant	Chemical	deficit in	promote		may			cellular damage	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	These data indicate that the deficit in antioxidant and methylation capacity is specific for autism and may promote cellular damage and altered epigenetic gene expression	topic_aut
78277	3	356146	5	NULL	NULL	NULL	NULL	antioxidant	Chemical	deficit in	promote		may			gene expression	Process	altered;;epigenetic			NULL		NULL	NULL	NULL	NULL	NULL	NULL	These data indicate that the deficit in antioxidant and methylation capacity is specific for autism and may promote cellular damage and altered epigenetic gene expression	topic_aut
78278	4	356146	5	NULL	NULL	0	NULL	methylation capacity	Process		is specific for					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	These data indicate that the deficit in antioxidant and methylation capacity is specific for autism and may promote cellular damage and altered epigenetic gene expression	topic_aut
78290	1	356147	5	NULL	NULL	NULL	NULL	communication	MentalProcess	problems of	is a symptom of		prevalent			ASDs	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Communication problems and language delay are a prevalent symptom of autism spectrum disorders (ASDs)	topic_aut
78291	2	356147	5	NULL	NULL	0	NULL	language	MentalProcess	delay of	is a symptom of		prevalent			ASDs	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Communication problems and language delay are a prevalent symptom of autism spectrum disorders (ASDs)	topic_aut
78292	3	356147	5	NULL	NULL	0	NULL	ASDs	MedicalFinding		is					autism spectrum disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Communication problems and language delay are a prevalent symptom of autism spectrum disorders (ASDs)	topic_aut
78293	1	356148	5	NULL	NULL	0	NULL	language	MentalProcess	delay of	is a symptom of					ASD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We detected candidate single-nucleotide polymorphisms (SNPs) in chromosome 11, rs11212733 (p-value=9.76×10(-6)) and rs7125479 (p-value=1.48×10(-4)), as a marker of language delay in ASD using the transmission disequilibrium test and multifactor dimensionality reduction test	topic_aut
78294	2	356148	5	NULL	NULL	0	NULL	SNPs	NucleicAcid		is					single-nucleotide polymorphisms	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	We detected candidate single-nucleotide polymorphisms (SNPs) in chromosome 11, rs11212733 (p-value=9.76×10(-6)) and rs7125479 (p-value=1.48×10(-4)), as a marker of language delay in ASD using the transmission disequilibrium test and multifactor dimensionality reduction test	topic_aut
78295	3	356148	5	NULL	NULL	0	NULL	rs11212733	NucleicAcid		is a type of					SNPs	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	We detected candidate single-nucleotide polymorphisms (SNPs) in chromosome 11, rs11212733 (p-value=9.76×10(-6)) and rs7125479 (p-value=1.48×10(-4)), as a marker of language delay in ASD using the transmission disequilibrium test and multifactor dimensionality reduction test	topic_aut
78296	4	356148	5	NULL	NULL	0	NULL	rs11212733	NucleicAcid		is present in					chromosome 11	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	We detected candidate single-nucleotide polymorphisms (SNPs) in chromosome 11, rs11212733 (p-value=9.76×10(-6)) and rs7125479 (p-value=1.48×10(-4)), as a marker of language delay in ASD using the transmission disequilibrium test and multifactor dimensionality reduction test	topic_aut
78297	5	356148	5	NULL	NULL	0	NULL	rs11212733	NucleicAcid		is a marker of					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	We detected candidate single-nucleotide polymorphisms (SNPs) in chromosome 11, rs11212733 (p-value=9.76×10(-6)) and rs7125479 (p-value=1.48×10(-4)), as a marker of language delay in ASD using the transmission disequilibrium test and multifactor dimensionality reduction test	topic_aut
78298	6	356148	5	NULL	NULL	0	NULL	rs7125479	NucleicAcid		is a type of					SNPs	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	We detected candidate single-nucleotide polymorphisms (SNPs) in chromosome 11, rs11212733 (p-value=9.76×10(-6)) and rs7125479 (p-value=1.48×10(-4)), as a marker of language delay in ASD using the transmission disequilibrium test and multifactor dimensionality reduction test	topic_aut
78299	7	356148	5	NULL	NULL	0	NULL	rs7125479	NucleicAcid		is present in					chromosome 11	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	We detected candidate single-nucleotide polymorphisms (SNPs) in chromosome 11, rs11212733 (p-value=9.76×10(-6)) and rs7125479 (p-value=1.48×10(-4)), as a marker of language delay in ASD using the transmission disequilibrium test and multifactor dimensionality reduction test	topic_aut
78300	8	356148	5	NULL	NULL	0	NULL	rs7125479	NucleicAcid		is a marker of					ASD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We detected candidate single-nucleotide polymorphisms (SNPs) in chromosome 11, rs11212733 (p-value=9.76×10(-6)) and rs7125479 (p-value=1.48×10(-4)), as a marker of language delay in ASD using the transmission disequilibrium test and multifactor dimensionality reduction test	topic_aut
78301	1	356149	5	NULL	NULL	0	NULL	Melatonin	GP	administration of	is associated with					sleep	Process	improved parameters of			NULL		0	NULL	NULL	NULL	NULL	NULL	Melatonin administration in ASD is associated with improved sleep parameters, better daytime behavior, and minimal side effects	topic_aut
78302	2	356149	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					ASD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Melatonin administration in ASD is associated with improved sleep parameters, better daytime behavior, and minimal side effects	topic_aut
78303	3	356149	5	NULL	NULL	0	NULL	Melatonin	GP	administration of	is associated with					daytime behavior	MentalProcess	better			NULL		0	NULL	NULL	NULL	NULL	NULL	Melatonin administration in ASD is associated with improved sleep parameters, better daytime behavior, and minimal side effects	topic_aut
78304	4	356149	5	NULL	NULL	0	NULL	statement 3	Process		occurs in					ASD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Melatonin administration in ASD is associated with improved sleep parameters, better daytime behavior, and minimal side effects	topic_aut
78305	5	356149	5	NULL	NULL	0	NULL	Melatonin	GP	administration of	is associated with					side effects	AbstractConcept	minimal			NULL		0	NULL	NULL	NULL	NULL	NULL	Melatonin administration in ASD is associated with improved sleep parameters, better daytime behavior, and minimal side effects	topic_aut
78306	6	356149	5	NULL	NULL	0	NULL	statement 5	Process		occurs in					ASD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Melatonin administration in ASD is associated with improved sleep parameters, better daytime behavior, and minimal side effects	topic_aut
78307	1	356150	5	NULL	NULL	0	NULL	SNAP-25 gene	GP		is involved in					neurotransmission	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The finding that polymorphisms of the SNAP-25 gene, a gene involved in neurotransmission and regulation of calcium homeostasis, are associated with the degree of hyperactivity in children with ASD, reinforces the hypothesis that alterations of these mechanisms play a pivotal role in the events leading to ASD-associated behavioral impairment	topic_aut
78308	2	356150	5	NULL	NULL	0	NULL	SNAP-25 gene	GP		regulates					calcium homeostasis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The finding that polymorphisms of the SNAP-25 gene, a gene involved in neurotransmission and regulation of calcium homeostasis, are associated with the degree of hyperactivity in children with ASD, reinforces the hypothesis that alterations of these mechanisms play a pivotal role in the events leading to ASD-associated behavioral impairment	topic_aut
78309	3	356150	5	NULL	NULL	0	NULL	hyperactivity	MedicalFinding		is a symptom of					ASD children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	The finding that polymorphisms of the SNAP-25 gene, a gene involved in neurotransmission and regulation of calcium homeostasis, are associated with the degree of hyperactivity in children with ASD, reinforces the hypothesis that alterations of these mechanisms play a pivotal role in the events leading to ASD-associated behavioral impairment	topic_aut
78310	4	356150	5	NULL	NULL	0	NULL	SNAP-25 gene	GP	polymorphism of	is associated with					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The finding that polymorphisms of the SNAP-25 gene, a gene involved in neurotransmission and regulation of calcium homeostasis, are associated with the degree of hyperactivity in children with ASD, reinforces the hypothesis that alterations of these mechanisms play a pivotal role in the events leading to ASD-associated behavioral impairment	topic_aut
78311	1	356151	5	NULL	NULL	0	NULL	GLOI	GP		is					glyoxalase I gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	We have shown that a non-conservative, non-synonymous SNP in the glyoxalase I gene, GLOI, may be an autism susceptibility factor. The GLOI rs2736654 SNP is a C→A change that causes an Ala111Glu change in the Glo1 enzyme.	topic_aut
78312	2	356151	5	NULL	NULL	NULL	NULL	SNP	NucleicAcid	non-conservative;;non-synonymous	occurs in					GLOI	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	We have shown that a non-conservative, non-synonymous SNP in the glyoxalase I gene, GLOI, may be an autism susceptibility factor. The GLOI rs2736654 SNP is a C→A change that causes an Ala111Glu change in the Glo1 enzyme.	topic_aut
78313	3	356151	5	NULL	NULL	0	NULL	statement 2	Process		is a type of					autism susceptibility factor	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	We have shown that a non-conservative, non-synonymous SNP in the glyoxalase I gene, GLOI, may be an autism susceptibility factor. The GLOI rs2736654 SNP is a C→A change that causes an Ala111Glu change in the Glo1 enzyme.	topic_aut
78314	4	356151	5	NULL	NULL	0	NULL	GLOI rs2736654 SNP	NucleicAcid		is					C�??A change	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	We have shown that a non-conservative, non-synonymous SNP in the glyoxalase I gene, GLOI, may be an autism susceptibility factor. The GLOI rs2736654 SNP is a C→A change that causes an Ala111Glu change in the Glo1 enzyme.	topic_aut
78315	5	356151	5	NULL	NULL	0	NULL	statement 4	Process		causes					Ala111Glu change	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	We have shown that a non-conservative, non-synonymous SNP in the glyoxalase I gene, GLOI, may be an autism susceptibility factor. The GLOI rs2736654 SNP is a C→A change that causes an Ala111Glu change in the Glo1 enzyme.	topic_aut
78316	6	356151	5	NULL	NULL	0	NULL	statement 5	Process		occurs in					Glo1 enzyme	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	We have shown that a non-conservative, non-synonymous SNP in the glyoxalase I gene, GLOI, may be an autism susceptibility factor. The GLOI rs2736654 SNP is a C→A change that causes an Ala111Glu change in the Glo1 enzyme.	topic_aut
77696	1	356154	7	NULL	NULL	0	NULL	childhood abuse	MentalProcess		is linked to					psychosis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	A high prevalence of childhood abuse has been reported in patients with severe mental illness. We conducted a cross-sectional study of 102 patients with schizophrenia, bipolar disorder, or schizoaffective disorder. Social, demographic, and clinical data were obtained. Patients were evaluated using Brief Psychotic Relative Scale, and Traumatic Life Events and Distressing Event questionnaires. Almost half (47.5%) of these patients had suffered some kind of child abuse, and our results confirmed a relationship between a history of childhood abuse and more severe psychosis. Diagnosis of schizophrenia was determined 4.1 years earlier in victims of childhood abuse. Hospital admissions were twice as high in victims of psychological abuse. Patients with a history of sexual abuse were more than twice as likely to attempt suicide (68% vs. 28.9%).	topic_bd
77697	2	356154	7	NULL	NULL	0	NULL	childhood abuse	MentalProcess		reported in					mental illness	MedicalFinding	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	A high prevalence of childhood abuse has been reported in patients with severe mental illness. We conducted a cross-sectional study of 102 patients with schizophrenia, bipolar disorder, or schizoaffective disorder. Social, demographic, and clinical data were obtained. Patients were evaluated using Brief Psychotic Relative Scale, and Traumatic Life Events and Distressing Event questionnaires. Almost half (47.5%) of these patients had suffered some kind of child abuse, and our results confirmed a relationship between a history of childhood abuse and more severe psychosis. Diagnosis of schizophrenia was determined 4.1 years earlier in victims of childhood abuse. Hospital admissions were twice as high in victims of psychological abuse. Patients with a history of sexual abuse were more than twice as likely to attempt suicide (68% vs. 28.9%).	topic_bd
77698	1	356155	7	NULL	NULL	NULL	NULL	sexual abuse	MentalProcess	patients with history of	more likely to					suicide	MentalProcess	attempt			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Patients with a history of sexual abuse were more than twice as likely to attempt suicide (68% vs. 28.9%).	topic_bd
77699	1	356156	7	NULL	NULL	NULL	NULL	GDs	MedicalFinding		found in					bipolar disorder	MedicalFinding	patients with			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Grandiose delusions (GDs) are found across a wide range of psychiatric conditions, including in around two-thirds of patients diagnosed with bipolar disorder, half of patients diagnosed with schizophrenia, as well as in a substantial proportion of patients with substance abuse disorders.	topic_bd
77700	2	356156	7	NULL	NULL	NULL	NULL	GDs	MedicalFinding		found in					schizophrenia	MedicalFinding	patients with			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Grandiose delusions (GDs) are found across a wide range of psychiatric conditions, including in around two-thirds of patients diagnosed with bipolar disorder, half of patients diagnosed with schizophrenia, as well as in a substantial proportion of patients with substance abuse disorders.	topic_bd
77701	3	356156	7	NULL	NULL	NULL	NULL	GDs	MedicalFinding		found in					substance abuse disorders	MedicalFinding	patients with			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Grandiose delusions (GDs) are found across a wide range of psychiatric conditions, including in around two-thirds of patients diagnosed with bipolar disorder, half of patients diagnosed with schizophrenia, as well as in a substantial proportion of patients with substance abuse disorders.	topic_bd
77702	4	356156	7	NULL	NULL	0	NULL	GDs	MedicalFinding		is					Grandiose delusions	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Grandiose delusions (GDs) are found across a wide range of psychiatric conditions, including in around two-thirds of patients diagnosed with bipolar disorder, half of patients diagnosed with schizophrenia, as well as in a substantial proportion of patients with substance abuse disorders.	topic_bd
77703	1	356157	7	NULL	NULL	0	NULL	mood symptoms	MentalProcess		associated with					 self-perceived stigma	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Objective The aim of this study was to investigate the impact of self-rated stigma and functioning in patients with previous termbipolar disordernext term in Latin-America. Methods Two-hundred and forty-one participants with previous termbipolar disordernext term were recruited from three Latin American countries (Argentina, Brazil, and Colombia). Functional impairment was assessed with the Functioning Assessment Short Test (FAST) and experiences with and impact of perceived stigma was evaluated using the Inventory of Stigmatizing Experiences (ISE). Results Higher scores of self-perceived stigma were correlated with lower scores of functioning. After multiple regression analysis, being on disability benefit, current mood symptoms and functioning were associated with self-perceived stigma. Conclusions This is the first study to demonstrate an association between stigma and poor functioning in previous termbipolar disorder.next term Possible implications of such findings for practitioners are discussed.	topic_bd
77704	2	356157	7	NULL	NULL	0	NULL	 self-perceived stigma	MentalProcess		associated with					previous termbipolar disorder	MedicalFinding	poor functioning in 			NULL		0	NULL	NULL	NULL	NULL	NULL	Objective The aim of this study was to investigate the impact of self-rated stigma and functioning in patients with previous termbipolar disordernext term in Latin-America. Methods Two-hundred and forty-one participants with previous termbipolar disordernext term were recruited from three Latin American countries (Argentina, Brazil, and Colombia). Functional impairment was assessed with the Functioning Assessment Short Test (FAST) and experiences with and impact of perceived stigma was evaluated using the Inventory of Stigmatizing Experiences (ISE). Results Higher scores of self-perceived stigma were correlated with lower scores of functioning. After multiple regression analysis, being on disability benefit, current mood symptoms and functioning were associated with self-perceived stigma. Conclusions This is the first study to demonstrate an association between stigma and poor functioning in previous termbipolar disorder.next term Possible implications of such findings for practitioners are discussed.	topic_bd
78070	1	356161	6	NULL	NULL	0	NULL	antimitotic drugs	Chemical		kill		may			tumor cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	How do antimitotic drugs kill cells in tumors? Timothy J. Mitchison, Harvard Medical School	topic_bc
78068	1	356164	6	NULL	NULL	0	NULL	metformin	Chemical		kills		selectively			cancer cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	an epigenetic switch linking inflammation to cancer and selective killing of cancer stem cells by metformin kevin struhl, harvard medical school	topic_bc
78069	2	356164	6	NULL	NULL	0	NULL	inflammation	MedicalFinding		is linked to					cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	an epigenetic switch linking inflammation to cancer and selective killing of cancer stem cells by metformin kevin struhl, harvard medical school	topic_bc
78067	1	356167	6	NULL	NULL	0	NULL	 jorge s reis-filno	MedicalFinding		is a type of					Breast cancer	MedicalFinding	metastatic			NULL		0	NULL	NULL	NULL	NULL	NULL	the molecular pathology of metaplastic breast cancer jorge s reis-filno	topic_bc
77705	1	356169	7	NULL	NULL	0	NULL	ECT	MedicalProcedure		is used in the					psychiatric disorders	MedicalFinding	somatic treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Until recently, a review of nonpharmacological, somatic treatments of psychiatric disorders would have included only electroconvulsive therapy (ECT). This situation is now changing very substantially. Although ECT remains the only modality in widespread clinical use, several new techniques are under investigation. Their principal indication in the psychiatric context is the treatment of major depression, but other applications are also being studied. All the novel treatments involve brain stimulation, which is achieved by different technological methods. The treatment closest to the threshold of clinical acceptability is transcranial magnetic stimulation (TMS). Although TMS is safe and relatively easy to administer, its efficacy has still to be definitively established. Other modalities, at various stages of research development, include magnetic seizure therapy (MST), deep brain stimulation (DBS), and vagus nerve stimulation (VNS). We briefly review the development and technical aspects of these treatments, their potential role in the treatment of major depression, adverse effects, and putative mechanism of action. As the only one of these treatment modalities that is in widespread clinical use, more extended consideration is given to ECT Although more than half a century has elapsed since ECT was first introduced, it remains the most effective treatment for major depression, with efficacy in patients refractory to antidepressant drugs and an acceptable safety profile. Although they hold considerable promise, the novel brain stimulation techniques reviewed here will be need to be further developed before they achieve clinical acceptability.	topic_bd
77706	2	356169	7	NULL	NULL	0	NULL	ECT	MedicalProcedure		is					electroconvulsive therapy	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Until recently, a review of nonpharmacological, somatic treatments of psychiatric disorders would have included only electroconvulsive therapy (ECT). This situation is now changing very substantially. Although ECT remains the only modality in widespread clinical use, several new techniques are under investigation. Their principal indication in the psychiatric context is the treatment of major depression, but other applications are also being studied. All the novel treatments involve brain stimulation, which is achieved by different technological methods. The treatment closest to the threshold of clinical acceptability is transcranial magnetic stimulation (TMS). Although TMS is safe and relatively easy to administer, its efficacy has still to be definitively established. Other modalities, at various stages of research development, include magnetic seizure therapy (MST), deep brain stimulation (DBS), and vagus nerve stimulation (VNS). We briefly review the development and technical aspects of these treatments, their potential role in the treatment of major depression, adverse effects, and putative mechanism of action. As the only one of these treatment modalities that is in widespread clinical use, more extended consideration is given to ECT Although more than half a century has elapsed since ECT was first introduced, it remains the most effective treatment for major depression, with efficacy in patients refractory to antidepressant drugs and an acceptable safety profile. Although they hold considerable promise, the novel brain stimulation techniques reviewed here will be need to be further developed before they achieve clinical acceptability.	topic_bd
77707	3	356169	7	NULL	NULL	0	NULL	TMS	MedicalProcedure		is used in the					major depression	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Until recently, a review of nonpharmacological, somatic treatments of psychiatric disorders would have included only electroconvulsive therapy (ECT). This situation is now changing very substantially. Although ECT remains the only modality in widespread clinical use, several new techniques are under investigation. Their principal indication in the psychiatric context is the treatment of major depression, but other applications are also being studied. All the novel treatments involve brain stimulation, which is achieved by different technological methods. The treatment closest to the threshold of clinical acceptability is transcranial magnetic stimulation (TMS). Although TMS is safe and relatively easy to administer, its efficacy has still to be definitively established. Other modalities, at various stages of research development, include magnetic seizure therapy (MST), deep brain stimulation (DBS), and vagus nerve stimulation (VNS). We briefly review the development and technical aspects of these treatments, their potential role in the treatment of major depression, adverse effects, and putative mechanism of action. As the only one of these treatment modalities that is in widespread clinical use, more extended consideration is given to ECT Although more than half a century has elapsed since ECT was first introduced, it remains the most effective treatment for major depression, with efficacy in patients refractory to antidepressant drugs and an acceptable safety profile. Although they hold considerable promise, the novel brain stimulation techniques reviewed here will be need to be further developed before they achieve clinical acceptability.	topic_bd
77708	4	356169	7	NULL	NULL	0	NULL	TMS	MedicalProcedure		is					transcranial magnetic stimulation 	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Until recently, a review of nonpharmacological, somatic treatments of psychiatric disorders would have included only electroconvulsive therapy (ECT). This situation is now changing very substantially. Although ECT remains the only modality in widespread clinical use, several new techniques are under investigation. Their principal indication in the psychiatric context is the treatment of major depression, but other applications are also being studied. All the novel treatments involve brain stimulation, which is achieved by different technological methods. The treatment closest to the threshold of clinical acceptability is transcranial magnetic stimulation (TMS). Although TMS is safe and relatively easy to administer, its efficacy has still to be definitively established. Other modalities, at various stages of research development, include magnetic seizure therapy (MST), deep brain stimulation (DBS), and vagus nerve stimulation (VNS). We briefly review the development and technical aspects of these treatments, their potential role in the treatment of major depression, adverse effects, and putative mechanism of action. As the only one of these treatment modalities that is in widespread clinical use, more extended consideration is given to ECT Although more than half a century has elapsed since ECT was first introduced, it remains the most effective treatment for major depression, with efficacy in patients refractory to antidepressant drugs and an acceptable safety profile. Although they hold considerable promise, the novel brain stimulation techniques reviewed here will be need to be further developed before they achieve clinical acceptability.	topic_bd
77709	5	356169	7	NULL	NULL	0	NULL	MST	MedicalProcedure		is used in the					major depression	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Until recently, a review of nonpharmacological, somatic treatments of psychiatric disorders would have included only electroconvulsive therapy (ECT). This situation is now changing very substantially. Although ECT remains the only modality in widespread clinical use, several new techniques are under investigation. Their principal indication in the psychiatric context is the treatment of major depression, but other applications are also being studied. All the novel treatments involve brain stimulation, which is achieved by different technological methods. The treatment closest to the threshold of clinical acceptability is transcranial magnetic stimulation (TMS). Although TMS is safe and relatively easy to administer, its efficacy has still to be definitively established. Other modalities, at various stages of research development, include magnetic seizure therapy (MST), deep brain stimulation (DBS), and vagus nerve stimulation (VNS). We briefly review the development and technical aspects of these treatments, their potential role in the treatment of major depression, adverse effects, and putative mechanism of action. As the only one of these treatment modalities that is in widespread clinical use, more extended consideration is given to ECT Although more than half a century has elapsed since ECT was first introduced, it remains the most effective treatment for major depression, with efficacy in patients refractory to antidepressant drugs and an acceptable safety profile. Although they hold considerable promise, the novel brain stimulation techniques reviewed here will be need to be further developed before they achieve clinical acceptability.	topic_bd
77710	6	356169	7	NULL	NULL	0	NULL	MST	MedicalProcedure		is					magnetic seizure therapy	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Until recently, a review of nonpharmacological, somatic treatments of psychiatric disorders would have included only electroconvulsive therapy (ECT). This situation is now changing very substantially. Although ECT remains the only modality in widespread clinical use, several new techniques are under investigation. Their principal indication in the psychiatric context is the treatment of major depression, but other applications are also being studied. All the novel treatments involve brain stimulation, which is achieved by different technological methods. The treatment closest to the threshold of clinical acceptability is transcranial magnetic stimulation (TMS). Although TMS is safe and relatively easy to administer, its efficacy has still to be definitively established. Other modalities, at various stages of research development, include magnetic seizure therapy (MST), deep brain stimulation (DBS), and vagus nerve stimulation (VNS). We briefly review the development and technical aspects of these treatments, their potential role in the treatment of major depression, adverse effects, and putative mechanism of action. As the only one of these treatment modalities that is in widespread clinical use, more extended consideration is given to ECT Although more than half a century has elapsed since ECT was first introduced, it remains the most effective treatment for major depression, with efficacy in patients refractory to antidepressant drugs and an acceptable safety profile. Although they hold considerable promise, the novel brain stimulation techniques reviewed here will be need to be further developed before they achieve clinical acceptability.	topic_bd
77711	7	356169	7	NULL	NULL	0	NULL	DBS	MedicalProcedure		is used in the					major depression	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Until recently, a review of nonpharmacological, somatic treatments of psychiatric disorders would have included only electroconvulsive therapy (ECT). This situation is now changing very substantially. Although ECT remains the only modality in widespread clinical use, several new techniques are under investigation. Their principal indication in the psychiatric context is the treatment of major depression, but other applications are also being studied. All the novel treatments involve brain stimulation, which is achieved by different technological methods. The treatment closest to the threshold of clinical acceptability is transcranial magnetic stimulation (TMS). Although TMS is safe and relatively easy to administer, its efficacy has still to be definitively established. Other modalities, at various stages of research development, include magnetic seizure therapy (MST), deep brain stimulation (DBS), and vagus nerve stimulation (VNS). We briefly review the development and technical aspects of these treatments, their potential role in the treatment of major depression, adverse effects, and putative mechanism of action. As the only one of these treatment modalities that is in widespread clinical use, more extended consideration is given to ECT Although more than half a century has elapsed since ECT was first introduced, it remains the most effective treatment for major depression, with efficacy in patients refractory to antidepressant drugs and an acceptable safety profile. Although they hold considerable promise, the novel brain stimulation techniques reviewed here will be need to be further developed before they achieve clinical acceptability.	topic_bd
77712	8	356169	7	NULL	NULL	0	NULL	DBS	MedicalProcedure		is					deep brain stimulation	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Until recently, a review of nonpharmacological, somatic treatments of psychiatric disorders would have included only electroconvulsive therapy (ECT). This situation is now changing very substantially. Although ECT remains the only modality in widespread clinical use, several new techniques are under investigation. Their principal indication in the psychiatric context is the treatment of major depression, but other applications are also being studied. All the novel treatments involve brain stimulation, which is achieved by different technological methods. The treatment closest to the threshold of clinical acceptability is transcranial magnetic stimulation (TMS). Although TMS is safe and relatively easy to administer, its efficacy has still to be definitively established. Other modalities, at various stages of research development, include magnetic seizure therapy (MST), deep brain stimulation (DBS), and vagus nerve stimulation (VNS). We briefly review the development and technical aspects of these treatments, their potential role in the treatment of major depression, adverse effects, and putative mechanism of action. As the only one of these treatment modalities that is in widespread clinical use, more extended consideration is given to ECT Although more than half a century has elapsed since ECT was first introduced, it remains the most effective treatment for major depression, with efficacy in patients refractory to antidepressant drugs and an acceptable safety profile. Although they hold considerable promise, the novel brain stimulation techniques reviewed here will be need to be further developed before they achieve clinical acceptability.	topic_bd
77713	9	356169	7	NULL	NULL	0	NULL	VNS	MedicalProcedure		is used in the					major depression	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Until recently, a review of nonpharmacological, somatic treatments of psychiatric disorders would have included only electroconvulsive therapy (ECT). This situation is now changing very substantially. Although ECT remains the only modality in widespread clinical use, several new techniques are under investigation. Their principal indication in the psychiatric context is the treatment of major depression, but other applications are also being studied. All the novel treatments involve brain stimulation, which is achieved by different technological methods. The treatment closest to the threshold of clinical acceptability is transcranial magnetic stimulation (TMS). Although TMS is safe and relatively easy to administer, its efficacy has still to be definitively established. Other modalities, at various stages of research development, include magnetic seizure therapy (MST), deep brain stimulation (DBS), and vagus nerve stimulation (VNS). We briefly review the development and technical aspects of these treatments, their potential role in the treatment of major depression, adverse effects, and putative mechanism of action. As the only one of these treatment modalities that is in widespread clinical use, more extended consideration is given to ECT Although more than half a century has elapsed since ECT was first introduced, it remains the most effective treatment for major depression, with efficacy in patients refractory to antidepressant drugs and an acceptable safety profile. Although they hold considerable promise, the novel brain stimulation techniques reviewed here will be need to be further developed before they achieve clinical acceptability.	topic_bd
77714	10	356169	7	NULL	NULL	0	NULL	VNS	MedicalProcedure		is					vagus nerve stimulation 	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Until recently, a review of nonpharmacological, somatic treatments of psychiatric disorders would have included only electroconvulsive therapy (ECT). This situation is now changing very substantially. Although ECT remains the only modality in widespread clinical use, several new techniques are under investigation. Their principal indication in the psychiatric context is the treatment of major depression, but other applications are also being studied. All the novel treatments involve brain stimulation, which is achieved by different technological methods. The treatment closest to the threshold of clinical acceptability is transcranial magnetic stimulation (TMS). Although TMS is safe and relatively easy to administer, its efficacy has still to be definitively established. Other modalities, at various stages of research development, include magnetic seizure therapy (MST), deep brain stimulation (DBS), and vagus nerve stimulation (VNS). We briefly review the development and technical aspects of these treatments, their potential role in the treatment of major depression, adverse effects, and putative mechanism of action. As the only one of these treatment modalities that is in widespread clinical use, more extended consideration is given to ECT Although more than half a century has elapsed since ECT was first introduced, it remains the most effective treatment for major depression, with efficacy in patients refractory to antidepressant drugs and an acceptable safety profile. Although they hold considerable promise, the novel brain stimulation techniques reviewed here will be need to be further developed before they achieve clinical acceptability.	topic_bd
78317	1	356197	5	NULL	NULL	0	NULL	microglia	Cell	stimulation of	leads to					positive-feedback loop	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Microglia and astrocyte stimulation lead to a positive-feedback loop that also facilitates the development of a chronic inflammatory environment within the fetus, pre-disposing it to lifelong comorbid psychiatric and systemic pathologies	topic_aut
78318	2	356197	5	NULL	NULL	NULL	NULL	statement 1	Process		facilitates					chronic inflammatory environment	AbstractConcept	development of			NULL	within fetus	NULL	NULL	NULL	NULL	NULL	NULL	Microglia and astrocyte stimulation lead to a positive-feedback loop that also facilitates the development of a chronic inflammatory environment within the fetus, pre-disposing it to lifelong comorbid psychiatric and systemic pathologies	topic_aut
78319	3	356197	5	NULL	NULL	0	NULL	fetus	OrganismPart		is pre-disposed to					comorbid psychiatric pathologies	MedicalFinding	lifelong			NULL		0	NULL	NULL	NULL	NULL	NULL	Microglia and astrocyte stimulation lead to a positive-feedback loop that also facilitates the development of a chronic inflammatory environment within the fetus, pre-disposing it to lifelong comorbid psychiatric and systemic pathologies	topic_aut
78320	4	356197	5	NULL	NULL	0	NULL	statement 2	Process		leads to					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Microglia and astrocyte stimulation lead to a positive-feedback loop that also facilitates the development of a chronic inflammatory environment within the fetus, pre-disposing it to lifelong comorbid psychiatric and systemic pathologies	topic_aut
78321	5	356197	5	NULL	NULL	0	NULL	fetus	OrganismPart		is pre-disposed to					systemic pathologies	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Microglia and astrocyte stimulation lead to a positive-feedback loop that also facilitates the development of a chronic inflammatory environment within the fetus, pre-disposing it to lifelong comorbid psychiatric and systemic pathologies	topic_aut
78322	6	356197	5	NULL	NULL	0	NULL	statement 2	Process		leads to					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Microglia and astrocyte stimulation lead to a positive-feedback loop that also facilitates the development of a chronic inflammatory environment within the fetus, pre-disposing it to lifelong comorbid psychiatric and systemic pathologies	topic_aut
78323	7	356197	5	NULL	NULL	0	NULL	astrocyte	Cell	stimulation of	leads to					positive-feedback loop	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Microglia and astrocyte stimulation lead to a positive-feedback loop that also facilitates the development of a chronic inflammatory environment within the fetus, pre-disposing it to lifelong comorbid psychiatric and systemic pathologies	topic_aut
78324	8	356197	5	NULL	NULL	0	NULL	statement 7	Process		leads to					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Microglia and astrocyte stimulation lead to a positive-feedback loop that also facilitates the development of a chronic inflammatory environment within the fetus, pre-disposing it to lifelong comorbid psychiatric and systemic pathologies	topic_aut
78325	9	356197	5	NULL	NULL	0	NULL	statement 7	Process		leads to					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Microglia and astrocyte stimulation lead to a positive-feedback loop that also facilitates the development of a chronic inflammatory environment within the fetus, pre-disposing it to lifelong comorbid psychiatric and systemic pathologies	topic_aut
78326	1	356198	5	NULL	NULL	0	NULL	autistic individuals	GroupOfPeople		is hyper-sensite to					environmental stimuli	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	Such a mechanism could account for many of the observed symptoms and behaviors of autistic individuals such as hyper-sensitivity to environmental stimuli, object fixation, echolalia, repetitive physical behaviors, chronic enterocolitis, autoimmune disease, and, at the extreme, savantism	topic_aut
78327	2	356198	5	NULL	NULL	0	NULL	object fixation	MedicalFinding		is a symptom of					autistic individuals	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Such a mechanism could account for many of the observed symptoms and behaviors of autistic individuals such as hyper-sensitivity to environmental stimuli, object fixation, echolalia, repetitive physical behaviors, chronic enterocolitis, autoimmune disease, and, at the extreme, savantism	topic_aut
78328	3	356198	5	NULL	NULL	0	NULL	echolalia	MedicalFinding		is a symptom of					autistic individuals	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Such a mechanism could account for many of the observed symptoms and behaviors of autistic individuals such as hyper-sensitivity to environmental stimuli, object fixation, echolalia, repetitive physical behaviors, chronic enterocolitis, autoimmune disease, and, at the extreme, savantism	topic_aut
78329	4	356198	5	NULL	NULL	0	NULL	repetitive physical behaviors	MedicalFinding		is a symptom of					autistic individuals	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Such a mechanism could account for many of the observed symptoms and behaviors of autistic individuals such as hyper-sensitivity to environmental stimuli, object fixation, echolalia, repetitive physical behaviors, chronic enterocolitis, autoimmune disease, and, at the extreme, savantism	topic_aut
78330	5	356198	5	NULL	NULL	0	NULL	chronic enterocolitis	MedicalFinding		is a symptom of					autistic individuals	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Such a mechanism could account for many of the observed symptoms and behaviors of autistic individuals such as hyper-sensitivity to environmental stimuli, object fixation, echolalia, repetitive physical behaviors, chronic enterocolitis, autoimmune disease, and, at the extreme, savantism	topic_aut
78331	6	356198	5	NULL	NULL	0	NULL	autoimmune disease	MedicalFinding		is a symptom of					autistic individuals	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Such a mechanism could account for many of the observed symptoms and behaviors of autistic individuals such as hyper-sensitivity to environmental stimuli, object fixation, echolalia, repetitive physical behaviors, chronic enterocolitis, autoimmune disease, and, at the extreme, savantism	topic_aut
78332	7	356198	5	NULL	NULL	0	NULL	savantism	MedicalFinding		is a symptom of					autistic individuals	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Such a mechanism could account for many of the observed symptoms and behaviors of autistic individuals such as hyper-sensitivity to environmental stimuli, object fixation, echolalia, repetitive physical behaviors, chronic enterocolitis, autoimmune disease, and, at the extreme, savantism	topic_aut
78333	1	356199	5	NULL	NULL	NULL	NULL	vocalizations	Process		repeated by		automatically			another person	GroupOfPeople				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Echolalia is the automatic repetition of vocalizations made by another person. It is closely related to echopraxia, the automatic repetition of movements made by another person.	topic_aut
78334	2	356199	5	NULL	NULL	NULL	NULL	statement 1	Process		is termed as					Echolalia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Echolalia is the automatic repetition of vocalizations made by another person. It is closely related to echopraxia, the automatic repetition of movements made by another person.	topic_aut
78335	3	356199	5	NULL	NULL	NULL	NULL	echolalia	MedicalFinding		is related to		closely			echopraxia	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Echolalia is the automatic repetition of vocalizations made by another person. It is closely related to echopraxia, the automatic repetition of movements made by another person.	topic_aut
78336	4	356199	5	NULL	NULL	0	NULL	movements	PhysicalPhenomenon		repeated by		automatically			another person	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Echolalia is the automatic repetition of vocalizations made by another person. It is closely related to echopraxia, the automatic repetition of movements made by another person.	topic_aut
78337	5	356199	5	NULL	NULL	0	NULL	statement 4	Process		is termed as					echopraxia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Echolalia is the automatic repetition of vocalizations made by another person. It is closely related to echopraxia, the automatic repetition of movements made by another person.	topic_aut
78338	1	356200	5	NULL	NULL	0	NULL	colon	OrganismPart	inflammation of	is known as					enterocolitis 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Enterocolitis (or 'coloenteritis') is an inflammation of the colon and small intestine.[1] However, most conditions are categorized as one or the other of the following:	topic_aut
78339	2	356200	5	NULL	NULL	0	NULL	small intestine	OrganismPart	inflammation of	is known as					enterocolitis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Enterocolitis (or 'coloenteritis') is an inflammation of the colon and small intestine.[1] However, most conditions are categorized as one or the other of the following:	topic_aut
78340	3	356200	5	NULL	NULL	0	NULL	coloenteritis	MedicalFinding		is also known as					enterocolitis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Enterocolitis (or 'coloenteritis') is an inflammation of the colon and small intestine.[1] However, most conditions are categorized as one or the other of the following:	topic_aut
78348	1	356202	5	NULL	NULL	0	NULL	pathogens	Organism	prenatal exposure to	corelates with		significantly			ASD	MedicalFinding	occurence of			NULL		0	NULL	NULL	NULL	NULL	NULL	Epidemiological data has highlighted this relationship showing significant correlations between prenatal exposure to pathogens, including influenza, and the occurrence of ASD	topic_aut
78349	1	356203	5	NULL	NULL	0	NULL	MIA	Process		is					maternal immune activation	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Several groups utilizing these animal models have found that activation of the maternal immune system, termed maternal immune activation (MIA), and more specifically the exposure of the developing fetus to maternal cytokines precipitate the neurological, immunological and behavioral abnormalities observed in the offspring of these animals	topic_aut
78350	2	356203	5	NULL	NULL	0	NULL	maternal immune system	Process	activated	is termed as					MIA	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Several groups utilizing these animal models have found that activation of the maternal immune system, termed maternal immune activation (MIA), and more specifically the exposure of the developing fetus to maternal cytokines precipitate the neurological, immunological and behavioral abnormalities observed in the offspring of these animals	topic_aut
78351	3	356203	5	NULL	NULL	0	NULL	statement 2	Process		precipitate					neurological abnormalities	MedicalFinding				NULL	animal offsprings	0	NULL	NULL	NULL	NULL	NULL	Several groups utilizing these animal models have found that activation of the maternal immune system, termed maternal immune activation (MIA), and more specifically the exposure of the developing fetus to maternal cytokines precipitate the neurological, immunological and behavioral abnormalities observed in the offspring of these animals	topic_aut
78352	4	356203	5	NULL	NULL	0	NULL	statement 2	Process		precipitate					immunological abnormalities	MedicalFinding				NULL	animal offsprings	0	NULL	NULL	NULL	NULL	NULL	Several groups utilizing these animal models have found that activation of the maternal immune system, termed maternal immune activation (MIA), and more specifically the exposure of the developing fetus to maternal cytokines precipitate the neurological, immunological and behavioral abnormalities observed in the offspring of these animals	topic_aut
78353	5	356203	5	NULL	NULL	0	NULL	statement 2	Process		precipitate					behavioral abnormalities	MedicalFinding				NULL	animal offsprings	0	NULL	NULL	NULL	NULL	NULL	Several groups utilizing these animal models have found that activation of the maternal immune system, termed maternal immune activation (MIA), and more specifically the exposure of the developing fetus to maternal cytokines precipitate the neurological, immunological and behavioral abnormalities observed in the offspring of these animals	topic_aut
78354	6	356203	5	NULL	NULL	0	NULL	fetus	OrganismPart	developing	is exposed to					cytokines	GP	maternal			NULL		0	NULL	NULL	NULL	NULL	NULL	Several groups utilizing these animal models have found that activation of the maternal immune system, termed maternal immune activation (MIA), and more specifically the exposure of the developing fetus to maternal cytokines precipitate the neurological, immunological and behavioral abnormalities observed in the offspring of these animals	topic_aut
78355	7	356203	5	NULL	NULL	0	NULL	statement 6	Process		precipitate					neurological abnormalities	MedicalFinding				NULL	animal offsprings	0	NULL	NULL	NULL	NULL	NULL	Several groups utilizing these animal models have found that activation of the maternal immune system, termed maternal immune activation (MIA), and more specifically the exposure of the developing fetus to maternal cytokines precipitate the neurological, immunological and behavioral abnormalities observed in the offspring of these animals	topic_aut
78356	8	356203	5	NULL	NULL	0	NULL	statement 6	Process		precipitate					immunological abnormalities	MedicalFinding				NULL	animal offsprings	0	NULL	NULL	NULL	NULL	NULL	Several groups utilizing these animal models have found that activation of the maternal immune system, termed maternal immune activation (MIA), and more specifically the exposure of the developing fetus to maternal cytokines precipitate the neurological, immunological and behavioral abnormalities observed in the offspring of these animals	topic_aut
78357	9	356203	5	NULL	NULL	0	NULL	statement 6	Process		precipitate					behavioral abnormalities	MedicalFinding				NULL	animal offsprings	0	NULL	NULL	NULL	NULL	NULL	Several groups utilizing these animal models have found that activation of the maternal immune system, termed maternal immune activation (MIA), and more specifically the exposure of the developing fetus to maternal cytokines precipitate the neurological, immunological and behavioral abnormalities observed in the offspring of these animals	topic_aut
78358	1	356204	5	NULL	NULL	NULL	NULL	autism spectrum conditions	MedicalFinding		is an exaggeration of					low-empathizing behaviors	MedicalFinding	normal;;male			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Autism spectrum conditions have been hypothesized to be an exaggeration of normal male low-empathizing and high-systemizing behaviors.	topic_aut
78359	2	356204	5	NULL	NULL	0	NULL	autism spectrum conditions	MedicalFinding		is an exaggeration of					high-systemizing behavior	MedicalFinding	normal;;male			NULL		0	NULL	NULL	NULL	NULL	NULL	Autism spectrum conditions have been hypothesized to be an exaggeration of normal male low-empathizing and high-systemizing behaviors.	topic_aut
78360	1	356206	5	NULL	NULL	0	NULL	cytokines	GP	levels of	is increased in					AS	MedicalFinding	male			NULL		0	NULL	NULL	NULL	NULL	NULL	Males with AS showed altered levels of 24 biomarkers including increased levels of cytokines and other inflammatory molecules	topic_aut
78361	2	356206	5	NULL	NULL	0	NULL	inflammatory molecules	GP	levels of	is increased in					AS	MedicalFinding	male			NULL		0	NULL	NULL	NULL	NULL	NULL	Males with AS showed altered levels of 24 biomarkers including increased levels of cytokines and other inflammatory molecules	topic_aut
78362	1	356207	5	NULL	NULL	0	NULL	testosterone	GP		is elevated in					AS	MedicalFinding	females			NULL		0	NULL	NULL	NULL	NULL	NULL	The finding of elevated testosterone in AS females confirmed predictions from the 'extreme male brain' and androgen theories of autism spectrum conditions	topic_aut
78377	1	356208	5	NULL	NULL	0	NULL	cellular immune function	Process	altered;;adaptive	is present in					ASD children	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Overall these data indicate significantly altered adaptive cellular immune function in children with ASD that may reflect dysfunctional immune activation, along with evidence that these perturbations may be linked to disturbances in behavior and developmental functioning	topic_aut
78378	2	356208	5	NULL	NULL	0	NULL	statement 1	Process		reflects		may			immune activation	Process	dysfunctional			NULL		0	NULL	NULL	NULL	NULL	NULL	Overall these data indicate significantly altered adaptive cellular immune function in children with ASD that may reflect dysfunctional immune activation, along with evidence that these perturbations may be linked to disturbances in behavior and developmental functioning	topic_aut
78379	3	356208	5	NULL	NULL	0	NULL	statement 1	Process		is linked to					behavior	MentalProcess	disturbances in			NULL		0	NULL	NULL	NULL	NULL	NULL	Overall these data indicate significantly altered adaptive cellular immune function in children with ASD that may reflect dysfunctional immune activation, along with evidence that these perturbations may be linked to disturbances in behavior and developmental functioning	topic_aut
78380	4	356208	5	NULL	NULL	0	NULL	statement 1	Process		is linked to					developmental functioning	Process	disturbances in			NULL		0	NULL	NULL	NULL	NULL	NULL	Overall these data indicate significantly altered adaptive cellular immune function in children with ASD that may reflect dysfunctional immune activation, along with evidence that these perturbations may be linked to disturbances in behavior and developmental functioning	topic_aut
78381	1	356209	5	NULL	NULL	0	NULL	TNF-�	GP		is a type of					pro-inflammatory cytokines	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	We found increased expression levels of pro-inflammatory cytokines TNF-α and IL-6, but decreased Bcl2 expression in lymphoblasts of autistic subjects.	topic_aut
78382	2	356209	5	NULL	NULL	0	NULL	IL-6	GP		is a type of					pro-inflammatory cytokines	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	We found increased expression levels of pro-inflammatory cytokines TNF-α and IL-6, but decreased Bcl2 expression in lymphoblasts of autistic subjects.	topic_aut
78383	3	356209	5	NULL	NULL	0	NULL	TNF-�	GP	expression of	is increased in					autistic subjects	GroupOfPeople	lymphoblasts of			NULL		0	NULL	NULL	NULL	NULL	NULL	We found increased expression levels of pro-inflammatory cytokines TNF-α and IL-6, but decreased Bcl2 expression in lymphoblasts of autistic subjects.	topic_aut
78384	4	356209	5	NULL	NULL	0	NULL	IL-6	GP	expression of	is increased in					autistic subjects	GroupOfPeople	lymphoblasts of			NULL		0	NULL	NULL	NULL	NULL	NULL	We found increased expression levels of pro-inflammatory cytokines TNF-α and IL-6, but decreased Bcl2 expression in lymphoblasts of autistic subjects.	topic_aut
78385	5	356209	5	NULL	NULL	0	NULL	Bcl2	GP	expression of	decreased in					autistic subjects	GroupOfPeople	lymphoblasts of			NULL		0	NULL	NULL	NULL	NULL	NULL	We found increased expression levels of pro-inflammatory cytokines TNF-α and IL-6, but decreased Bcl2 expression in lymphoblasts of autistic subjects.	topic_aut
78386	1	356210	5	NULL	NULL	NULL	NULL	maternal infection	MedicalFinding	human	occurs during					pregnancy	Process	human			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Epidemiological studies with human populations indicate associations between maternal infection during pregnancy and increased risk in offspring for central nervous system (CNS) disorders including schizophrenia, autism and cerebral palsy.	topic_aut
78387	2	356210	5	NULL	NULL	0	NULL	statement 1	Process		increases					schizophrenia	MedicalFinding	risk of;;offspring			NULL		0	NULL	NULL	NULL	NULL	NULL	Epidemiological studies with human populations indicate associations between maternal infection during pregnancy and increased risk in offspring for central nervous system (CNS) disorders including schizophrenia, autism and cerebral palsy.	topic_aut
78388	3	356210	5	NULL	NULL	0	NULL	statement 1	Process		increases					autism	MedicalFinding	risk of;;offspring			NULL		0	NULL	NULL	NULL	NULL	NULL	Epidemiological studies with human populations indicate associations between maternal infection during pregnancy and increased risk in offspring for central nervous system (CNS) disorders including schizophrenia, autism and cerebral palsy.	topic_aut
78389	4	356210	5	NULL	NULL	0	NULL	statement 1	Process		increases					cerebral palsy	MedicalFinding	risk of;;childhood			NULL		0	NULL	NULL	NULL	NULL	NULL	Epidemiological studies with human populations indicate associations between maternal infection during pregnancy and increased risk in offspring for central nervous system (CNS) disorders including schizophrenia, autism and cerebral palsy.	topic_aut
78390	5	356210	5	NULL	NULL	0	NULL	schizophrenia	MedicalFinding		is a type of					CNS disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Epidemiological studies with human populations indicate associations between maternal infection during pregnancy and increased risk in offspring for central nervous system (CNS) disorders including schizophrenia, autism and cerebral palsy.	topic_aut
78391	6	356210	5	NULL	NULL	0	NULL	autism	MedicalFinding		is a type of					CNS disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Epidemiological studies with human populations indicate associations between maternal infection during pregnancy and increased risk in offspring for central nervous system (CNS) disorders including schizophrenia, autism and cerebral palsy.	topic_aut
78392	7	356210	5	NULL	NULL	0	NULL	cerebral palsy	MedicalFinding		is a type of					CNS disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Epidemiological studies with human populations indicate associations between maternal infection during pregnancy and increased risk in offspring for central nervous system (CNS) disorders including schizophrenia, autism and cerebral palsy.	topic_aut
78393	8	356210	5	NULL	NULL	0	NULL	CNS disorder	MedicalFinding		is					central nervous system disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Epidemiological studies with human populations indicate associations between maternal infection during pregnancy and increased risk in offspring for central nervous system (CNS) disorders including schizophrenia, autism and cerebral palsy.	topic_aut
78394	1	356212	5	NULL	NULL	0	NULL	ASD	MedicalFinding		is					autism spectrum disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Many patients with Autism Spectrum Disorders (ASD) have "allergic" symptoms; moreover, the prevalence of ASD in patients with mastocytosis, characterized by numerous hyperactive mast cells in most tissues, is 10-fold higher than the general population suggesting mast cell involvement	topic_aut
78395	2	356212	5	NULL	NULL	0	NULL	ASD patients	GroupOfPeople		is prevalent in					mastocytosis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Many patients with Autism Spectrum Disorders (ASD) have "allergic" symptoms; moreover, the prevalence of ASD in patients with mastocytosis, characterized by numerous hyperactive mast cells in most tissues, is 10-fold higher than the general population suggesting mast cell involvement	topic_aut
78396	3	356212	5	NULL	NULL	0	NULL	mastocytosis	MedicalFinding		is characterized by					mast cells	Cell	numerous;;hyperactive			NULL	most tissues	0	NULL	NULL	NULL	NULL	NULL	Many patients with Autism Spectrum Disorders (ASD) have "allergic" symptoms; moreover, the prevalence of ASD in patients with mastocytosis, characterized by numerous hyperactive mast cells in most tissues, is 10-fold higher than the general population suggesting mast cell involvement	topic_aut
78397	1	356213	5	NULL	NULL	NULL	NULL	blood-brain-barrier	PhysicalPhenomenon	disruption of	permit					brain inflammation	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	This phenomenon could disrupt the blood-brain-barrier and permit brain inflammation	topic_aut
78398	1	356214	5	NULL	NULL	0	NULL	VEGF	GP		is released from					mast cells	Cell	human			NULL		0	NULL	NULL	NULL	NULL	NULL	HgCl2 stimulates VEGF and IL-6 release from human mast cells. This phenomenon could disrupt the blood-brain-barrier and permit brain inflammation.	topic_aut
78399	2	356214	5	NULL	NULL	0	NULL	IL-6	GP		is released from					mast cells	Cell	human			NULL		0	NULL	NULL	NULL	NULL	NULL	HgCl2 stimulates VEGF and IL-6 release from human mast cells. This phenomenon could disrupt the blood-brain-barrier and permit brain inflammation.	topic_aut
78400	3	356214	5	NULL	NULL	0	NULL	HgCl2	Chemical		stimulates					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	HgCl2 stimulates VEGF and IL-6 release from human mast cells. This phenomenon could disrupt the blood-brain-barrier and permit brain inflammation.	topic_aut
78401	4	356214	5	NULL	NULL	0	NULL	HgCl2	Chemical		stimulates					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	HgCl2 stimulates VEGF and IL-6 release from human mast cells. This phenomenon could disrupt the blood-brain-barrier and permit brain inflammation.	topic_aut
78402	5	356214	5	NULL	NULL	0	NULL	statement 3	Process		disrupt					blood-brain-barrier	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	HgCl2 stimulates VEGF and IL-6 release from human mast cells. This phenomenon could disrupt the blood-brain-barrier and permit brain inflammation.	topic_aut
78403	6	356214	5	NULL	NULL	0	NULL	statement 5	Process		permit					brain inflammation	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	HgCl2 stimulates VEGF and IL-6 release from human mast cells. This phenomenon could disrupt the blood-brain-barrier and permit brain inflammation.	topic_aut
78404	7	356214	5	NULL	NULL	0	NULL	statement 4	Process		disrupt					blood-brain-barrier	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	HgCl2 stimulates VEGF and IL-6 release from human mast cells. This phenomenon could disrupt the blood-brain-barrier and permit brain inflammation.	topic_aut
78405	8	356214	5	NULL	NULL	0	NULL	statement 7	Process		permit					brain inflammation	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	HgCl2 stimulates VEGF and IL-6 release from human mast cells. This phenomenon could disrupt the blood-brain-barrier and permit brain inflammation.	topic_aut
78406	1	356215	5	NULL	NULL	0	NULL	IL-1	GP		mediates					placental damage	MedicalFinding				NULL	offspring	0	NULL	NULL	NULL	NULL	NULL	In this study, we demonstrate that IL-1 plays a key role in mediating severe placental damage and neurodevelopmental anomalies in offspring.	topic_aut
78407	2	356215	5	NULL	NULL	0	NULL	IL-1	GP		mediates					neurodevelopmental anomalies	MedicalFinding				NULL	offspring	0	NULL	NULL	NULL	NULL	NULL	In this study, we demonstrate that IL-1 plays a key role in mediating severe placental damage and neurodevelopmental anomalies in offspring.	topic_aut
78408	1	356216	5	NULL	NULL	0	NULL	rats	Organism	gestation exposure of;;pregnant	exposed to					LPS	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Our results show that end of gestation exposure of pregnant rats to systemic microbial product (LPS) triggers placental inflammation and massive cell death, fetal mortality, and both forebrain white matter and motor behavioral alterations in the offspring	topic_aut
78409	2	356216	5	NULL	NULL	0	NULL	LPS	Chemical		is a type of					systemic microbial product	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Our results show that end of gestation exposure of pregnant rats to systemic microbial product (LPS) triggers placental inflammation and massive cell death, fetal mortality, and both forebrain white matter and motor behavioral alterations in the offspring	topic_aut
78410	3	356216	5	NULL	NULL	0	NULL	statement 1	Process		trigger					placental inflammation	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Our results show that end of gestation exposure of pregnant rats to systemic microbial product (LPS) triggers placental inflammation and massive cell death, fetal mortality, and both forebrain white matter and motor behavioral alterations in the offspring	topic_aut
78411	4	356216	5	NULL	NULL	0	NULL	statement 1	Process		trigger					cell death	MedicalFinding	massive			NULL		0	NULL	NULL	NULL	NULL	NULL	Our results show that end of gestation exposure of pregnant rats to systemic microbial product (LPS) triggers placental inflammation and massive cell death, fetal mortality, and both forebrain white matter and motor behavioral alterations in the offspring	topic_aut
78412	5	356216	5	NULL	NULL	0	NULL	statement 1	Process		trigger					fetal mortality	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Our results show that end of gestation exposure of pregnant rats to systemic microbial product (LPS) triggers placental inflammation and massive cell death, fetal mortality, and both forebrain white matter and motor behavioral alterations in the offspring	topic_aut
78413	6	356216	5	NULL	NULL	0	NULL	statement 1	Process		trigger					behavioral alterations	MedicalFinding	forebrain white matter			NULL	offspring	0	NULL	NULL	NULL	NULL	NULL	Our results show that end of gestation exposure of pregnant rats to systemic microbial product (LPS) triggers placental inflammation and massive cell death, fetal mortality, and both forebrain white matter and motor behavioral alterations in the offspring	topic_aut
78414	7	356216	5	NULL	NULL	0	NULL	statement 1	Process		trigger					behavioral alterations	MedicalFinding	motor			NULL	offspring	0	NULL	NULL	NULL	NULL	NULL	Our results show that end of gestation exposure of pregnant rats to systemic microbial product (LPS) triggers placental inflammation and massive cell death, fetal mortality, and both forebrain white matter and motor behavioral alterations in the offspring	topic_aut
77715	1	356218	7	NULL	NULL	0	NULL	GIV 	GP		is a type of					metastasis-related protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Here we identify GIV as a metastasis-related protein whose full-length transcript (GIV-fl) is expressed exclusively in highly invasive colon, breast, and pancreatic carcinoma cells and not in their poorly invasive counterparts.	topic_ccc
77716	2	356218	7	NULL	NULL	NULL	NULL	GIV-fl	GP		expressed in		exclusively			colon carcinoma cells	Cell	highly invasive			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we identify GIV as a metastasis-related protein whose full-length transcript (GIV-fl) is expressed exclusively in highly invasive colon, breast, and pancreatic carcinoma cells and not in their poorly invasive counterparts.	topic_ccc
77717	3	356218	7	NULL	NULL	0	NULL	GIV-fl	GP		expressed in		exclusively			breast carcinoma cells	Cell	highly invasive			NULL		0	NULL	NULL	NULL	NULL	NULL	Here we identify GIV as a metastasis-related protein whose full-length transcript (GIV-fl) is expressed exclusively in highly invasive colon, breast, and pancreatic carcinoma cells and not in their poorly invasive counterparts.	topic_ccc
77718	4	356218	7	NULL	NULL	NULL	NULL	GIV-fl	GP		expressed in		exclusively			pancreatic carcinoma cells	Cell	highly invasive			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we identify GIV as a metastasis-related protein whose full-length transcript (GIV-fl) is expressed exclusively in highly invasive colon, breast, and pancreatic carcinoma cells and not in their poorly invasive counterparts.	topic_ccc
77719	5	356218	7	NULL	NULL	0	NULL	GIV-fl	GP		not expressed in					poorly invasive cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Here we identify GIV as a metastasis-related protein whose full-length transcript (GIV-fl) is expressed exclusively in highly invasive colon, breast, and pancreatic carcinoma cells and not in their poorly invasive counterparts.	topic_ccc
77720	6	356218	7	NULL	NULL	0	NULL	GIV-fl	GP		is					GIV full-length transcript	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Here we identify GIV as a metastasis-related protein whose full-length transcript (GIV-fl) is expressed exclusively in highly invasive colon, breast, and pancreatic carcinoma cells and not in their poorly invasive counterparts.	topic_ccc
77721	1	356219	7	NULL	NULL	0	NULL	serotonin signaling	Process	dysfunction of	involved in					SCZ	MedicalFinding	pathogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	Several lines of evidence indicate that dysfunction of serotonin signaling and HTR2A receptor are involved in the pathogenesis of schizophrenia (SCZ) and bipolar disorder (BD). DNA methylation of HTR2A at T102C polymorphic site influences HTR2A expression and aberrant DNA methylation of HTR2A promoter was reported in postmortem brain of patients with SCZ and BD. Hypothesizing that the brain's epigenetic alteration of HTR2A may also exist in peripheral tissues that can be used as a diagnostic/therapeutic biomarker, we analyzed HTR2A promoter DNA methylation in DNA extracted from the saliva of patients with SCZ and BD, and their first degree relatives versus normal controls. Bisulfite sequencing was used to screen DNA methylation status of the HTR2A promoter CpGs and qMSP was used to quantify the degree of cytosine methylation at differentially methylated sites. Most of the cytosines of the HTR2A promoter were unmethylated. However, CpGs of the -1438A/G polymorphism site, -1420 and -1223 were >95% methylated. The CpG at T102C polymorphic site and neighboring CpGs were ∼70% methylated both in the patients and controls. qMSP analysis revealed that the cytosine of the T102C polymorphic site was significantly hypo-methylated in SCZ, BD, and their first degree relatives compared to the controls. Cytosine methylation of HTR2A at T102C polymorphic site in DNA derived from the saliva can potentially be used as a diagnostic, prognostic, and/or therapeutic biomarker in SCZ and BD. However, these preliminary observations need to be replicated in other populations with a larger sample size to be considered for clinical applications. © 2011 Wiley-Liss, Inc.	topic_bd
77722	2	356219	7	NULL	NULL	NULL	NULL	HTR2A receptor	GP	dysfunction of	involved in					SCZ	MedicalFinding	pathogenesis of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Several lines of evidence indicate that dysfunction of serotonin signaling and HTR2A receptor are involved in the pathogenesis of schizophrenia (SCZ) and bipolar disorder (BD). DNA methylation of HTR2A at T102C polymorphic site influences HTR2A expression and aberrant DNA methylation of HTR2A promoter was reported in postmortem brain of patients with SCZ and BD. Hypothesizing that the brain's epigenetic alteration of HTR2A may also exist in peripheral tissues that can be used as a diagnostic/therapeutic biomarker, we analyzed HTR2A promoter DNA methylation in DNA extracted from the saliva of patients with SCZ and BD, and their first degree relatives versus normal controls. Bisulfite sequencing was used to screen DNA methylation status of the HTR2A promoter CpGs and qMSP was used to quantify the degree of cytosine methylation at differentially methylated sites. Most of the cytosines of the HTR2A promoter were unmethylated. However, CpGs of the -1438A/G polymorphism site, -1420 and -1223 were >95% methylated. The CpG at T102C polymorphic site and neighboring CpGs were ∼70% methylated both in the patients and controls. qMSP analysis revealed that the cytosine of the T102C polymorphic site was significantly hypo-methylated in SCZ, BD, and their first degree relatives compared to the controls. Cytosine methylation of HTR2A at T102C polymorphic site in DNA derived from the saliva can potentially be used as a diagnostic, prognostic, and/or therapeutic biomarker in SCZ and BD. However, these preliminary observations need to be replicated in other populations with a larger sample size to be considered for clinical applications. © 2011 Wiley-Liss, Inc.	topic_bd
77723	3	356219	7	NULL	NULL	NULL	NULL	serotonin signaling	Process	dysfunction of	involved in					BD	MedicalFinding	pathogenesis of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Several lines of evidence indicate that dysfunction of serotonin signaling and HTR2A receptor are involved in the pathogenesis of schizophrenia (SCZ) and bipolar disorder (BD). DNA methylation of HTR2A at T102C polymorphic site influences HTR2A expression and aberrant DNA methylation of HTR2A promoter was reported in postmortem brain of patients with SCZ and BD. Hypothesizing that the brain's epigenetic alteration of HTR2A may also exist in peripheral tissues that can be used as a diagnostic/therapeutic biomarker, we analyzed HTR2A promoter DNA methylation in DNA extracted from the saliva of patients with SCZ and BD, and their first degree relatives versus normal controls. Bisulfite sequencing was used to screen DNA methylation status of the HTR2A promoter CpGs and qMSP was used to quantify the degree of cytosine methylation at differentially methylated sites. Most of the cytosines of the HTR2A promoter were unmethylated. However, CpGs of the -1438A/G polymorphism site, -1420 and -1223 were >95% methylated. The CpG at T102C polymorphic site and neighboring CpGs were ∼70% methylated both in the patients and controls. qMSP analysis revealed that the cytosine of the T102C polymorphic site was significantly hypo-methylated in SCZ, BD, and their first degree relatives compared to the controls. Cytosine methylation of HTR2A at T102C polymorphic site in DNA derived from the saliva can potentially be used as a diagnostic, prognostic, and/or therapeutic biomarker in SCZ and BD. However, these preliminary observations need to be replicated in other populations with a larger sample size to be considered for clinical applications. © 2011 Wiley-Liss, Inc.	topic_bd
77724	4	356219	7	NULL	NULL	0	NULL	HTR2A receptor	GP	dysfunction of	involved in					BD	MedicalFinding	pathogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	Several lines of evidence indicate that dysfunction of serotonin signaling and HTR2A receptor are involved in the pathogenesis of schizophrenia (SCZ) and bipolar disorder (BD). DNA methylation of HTR2A at T102C polymorphic site influences HTR2A expression and aberrant DNA methylation of HTR2A promoter was reported in postmortem brain of patients with SCZ and BD. Hypothesizing that the brain's epigenetic alteration of HTR2A may also exist in peripheral tissues that can be used as a diagnostic/therapeutic biomarker, we analyzed HTR2A promoter DNA methylation in DNA extracted from the saliva of patients with SCZ and BD, and their first degree relatives versus normal controls. Bisulfite sequencing was used to screen DNA methylation status of the HTR2A promoter CpGs and qMSP was used to quantify the degree of cytosine methylation at differentially methylated sites. Most of the cytosines of the HTR2A promoter were unmethylated. However, CpGs of the -1438A/G polymorphism site, -1420 and -1223 were >95% methylated. The CpG at T102C polymorphic site and neighboring CpGs were ∼70% methylated both in the patients and controls. qMSP analysis revealed that the cytosine of the T102C polymorphic site was significantly hypo-methylated in SCZ, BD, and their first degree relatives compared to the controls. Cytosine methylation of HTR2A at T102C polymorphic site in DNA derived from the saliva can potentially be used as a diagnostic, prognostic, and/or therapeutic biomarker in SCZ and BD. However, these preliminary observations need to be replicated in other populations with a larger sample size to be considered for clinical applications. © 2011 Wiley-Liss, Inc.	topic_bd
77725	5	356219	7	NULL	NULL	0	NULL	HTR2A	GP	DNA methylation of	occur at									T102C polymorphic site 	NULL		0	NULL	NULL	NULL	NULL	NULL	Several lines of evidence indicate that dysfunction of serotonin signaling and HTR2A receptor are involved in the pathogenesis of schizophrenia (SCZ) and bipolar disorder (BD). DNA methylation of HTR2A at T102C polymorphic site influences HTR2A expression and aberrant DNA methylation of HTR2A promoter was reported in postmortem brain of patients with SCZ and BD. Hypothesizing that the brain's epigenetic alteration of HTR2A may also exist in peripheral tissues that can be used as a diagnostic/therapeutic biomarker, we analyzed HTR2A promoter DNA methylation in DNA extracted from the saliva of patients with SCZ and BD, and their first degree relatives versus normal controls. Bisulfite sequencing was used to screen DNA methylation status of the HTR2A promoter CpGs and qMSP was used to quantify the degree of cytosine methylation at differentially methylated sites. Most of the cytosines of the HTR2A promoter were unmethylated. However, CpGs of the -1438A/G polymorphism site, -1420 and -1223 were >95% methylated. The CpG at T102C polymorphic site and neighboring CpGs were ∼70% methylated both in the patients and controls. qMSP analysis revealed that the cytosine of the T102C polymorphic site was significantly hypo-methylated in SCZ, BD, and their first degree relatives compared to the controls. Cytosine methylation of HTR2A at T102C polymorphic site in DNA derived from the saliva can potentially be used as a diagnostic, prognostic, and/or therapeutic biomarker in SCZ and BD. However, these preliminary observations need to be replicated in other populations with a larger sample size to be considered for clinical applications. © 2011 Wiley-Liss, Inc.	topic_bd
77726	6	356219	7	NULL	NULL	0	NULL	statement 5	Process		influences					HTR2A	GP	expression of			NULL		0	NULL	NULL	NULL	NULL	NULL	Several lines of evidence indicate that dysfunction of serotonin signaling and HTR2A receptor are involved in the pathogenesis of schizophrenia (SCZ) and bipolar disorder (BD). DNA methylation of HTR2A at T102C polymorphic site influences HTR2A expression and aberrant DNA methylation of HTR2A promoter was reported in postmortem brain of patients with SCZ and BD. Hypothesizing that the brain's epigenetic alteration of HTR2A may also exist in peripheral tissues that can be used as a diagnostic/therapeutic biomarker, we analyzed HTR2A promoter DNA methylation in DNA extracted from the saliva of patients with SCZ and BD, and their first degree relatives versus normal controls. Bisulfite sequencing was used to screen DNA methylation status of the HTR2A promoter CpGs and qMSP was used to quantify the degree of cytosine methylation at differentially methylated sites. Most of the cytosines of the HTR2A promoter were unmethylated. However, CpGs of the -1438A/G polymorphism site, -1420 and -1223 were >95% methylated. The CpG at T102C polymorphic site and neighboring CpGs were ∼70% methylated both in the patients and controls. qMSP analysis revealed that the cytosine of the T102C polymorphic site was significantly hypo-methylated in SCZ, BD, and their first degree relatives compared to the controls. Cytosine methylation of HTR2A at T102C polymorphic site in DNA derived from the saliva can potentially be used as a diagnostic, prognostic, and/or therapeutic biomarker in SCZ and BD. However, these preliminary observations need to be replicated in other populations with a larger sample size to be considered for clinical applications. © 2011 Wiley-Liss, Inc.	topic_bd
77727	7	356219	7	NULL	NULL	0	NULL	HTR2A	GP	aberrant DNA methylation of 	reported in				promoter	brain	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Several lines of evidence indicate that dysfunction of serotonin signaling and HTR2A receptor are involved in the pathogenesis of schizophrenia (SCZ) and bipolar disorder (BD). DNA methylation of HTR2A at T102C polymorphic site influences HTR2A expression and aberrant DNA methylation of HTR2A promoter was reported in postmortem brain of patients with SCZ and BD. Hypothesizing that the brain's epigenetic alteration of HTR2A may also exist in peripheral tissues that can be used as a diagnostic/therapeutic biomarker, we analyzed HTR2A promoter DNA methylation in DNA extracted from the saliva of patients with SCZ and BD, and their first degree relatives versus normal controls. Bisulfite sequencing was used to screen DNA methylation status of the HTR2A promoter CpGs and qMSP was used to quantify the degree of cytosine methylation at differentially methylated sites. Most of the cytosines of the HTR2A promoter were unmethylated. However, CpGs of the -1438A/G polymorphism site, -1420 and -1223 were >95% methylated. The CpG at T102C polymorphic site and neighboring CpGs were ∼70% methylated both in the patients and controls. qMSP analysis revealed that the cytosine of the T102C polymorphic site was significantly hypo-methylated in SCZ, BD, and their first degree relatives compared to the controls. Cytosine methylation of HTR2A at T102C polymorphic site in DNA derived from the saliva can potentially be used as a diagnostic, prognostic, and/or therapeutic biomarker in SCZ and BD. However, these preliminary observations need to be replicated in other populations with a larger sample size to be considered for clinical applications. © 2011 Wiley-Liss, Inc.	topic_bd
77728	8	356219	7	NULL	NULL	0	NULL	statement 7	Process		occur in					SCZ	MedicalFinding	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	Several lines of evidence indicate that dysfunction of serotonin signaling and HTR2A receptor are involved in the pathogenesis of schizophrenia (SCZ) and bipolar disorder (BD). DNA methylation of HTR2A at T102C polymorphic site influences HTR2A expression and aberrant DNA methylation of HTR2A promoter was reported in postmortem brain of patients with SCZ and BD. Hypothesizing that the brain's epigenetic alteration of HTR2A may also exist in peripheral tissues that can be used as a diagnostic/therapeutic biomarker, we analyzed HTR2A promoter DNA methylation in DNA extracted from the saliva of patients with SCZ and BD, and their first degree relatives versus normal controls. Bisulfite sequencing was used to screen DNA methylation status of the HTR2A promoter CpGs and qMSP was used to quantify the degree of cytosine methylation at differentially methylated sites. Most of the cytosines of the HTR2A promoter were unmethylated. However, CpGs of the -1438A/G polymorphism site, -1420 and -1223 were >95% methylated. The CpG at T102C polymorphic site and neighboring CpGs were ∼70% methylated both in the patients and controls. qMSP analysis revealed that the cytosine of the T102C polymorphic site was significantly hypo-methylated in SCZ, BD, and their first degree relatives compared to the controls. Cytosine methylation of HTR2A at T102C polymorphic site in DNA derived from the saliva can potentially be used as a diagnostic, prognostic, and/or therapeutic biomarker in SCZ and BD. However, these preliminary observations need to be replicated in other populations with a larger sample size to be considered for clinical applications. © 2011 Wiley-Liss, Inc.	topic_bd
77729	9	356219	7	NULL	NULL	0	NULL	statement 7	Process		occur in					BD	MedicalFinding	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	Several lines of evidence indicate that dysfunction of serotonin signaling and HTR2A receptor are involved in the pathogenesis of schizophrenia (SCZ) and bipolar disorder (BD). DNA methylation of HTR2A at T102C polymorphic site influences HTR2A expression and aberrant DNA methylation of HTR2A promoter was reported in postmortem brain of patients with SCZ and BD. Hypothesizing that the brain's epigenetic alteration of HTR2A may also exist in peripheral tissues that can be used as a diagnostic/therapeutic biomarker, we analyzed HTR2A promoter DNA methylation in DNA extracted from the saliva of patients with SCZ and BD, and their first degree relatives versus normal controls. Bisulfite sequencing was used to screen DNA methylation status of the HTR2A promoter CpGs and qMSP was used to quantify the degree of cytosine methylation at differentially methylated sites. Most of the cytosines of the HTR2A promoter were unmethylated. However, CpGs of the -1438A/G polymorphism site, -1420 and -1223 were >95% methylated. The CpG at T102C polymorphic site and neighboring CpGs were ∼70% methylated both in the patients and controls. qMSP analysis revealed that the cytosine of the T102C polymorphic site was significantly hypo-methylated in SCZ, BD, and their first degree relatives compared to the controls. Cytosine methylation of HTR2A at T102C polymorphic site in DNA derived from the saliva can potentially be used as a diagnostic, prognostic, and/or therapeutic biomarker in SCZ and BD. However, these preliminary observations need to be replicated in other populations with a larger sample size to be considered for clinical applications. © 2011 Wiley-Liss, Inc.	topic_bd
77731	10	356219	7	NULL	NULL	NULL	NULL	HTR2A	GP	cytosine of	hypo-methylated in				T102C polymorphic site	SCZ	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Several lines of evidence indicate that dysfunction of serotonin signaling and HTR2A receptor are involved in the pathogenesis of schizophrenia (SCZ) and bipolar disorder (BD). DNA methylation of HTR2A at T102C polymorphic site influences HTR2A expression and aberrant DNA methylation of HTR2A promoter was reported in postmortem brain of patients with SCZ and BD. Hypothesizing that the brain's epigenetic alteration of HTR2A may also exist in peripheral tissues that can be used as a diagnostic/therapeutic biomarker, we analyzed HTR2A promoter DNA methylation in DNA extracted from the saliva of patients with SCZ and BD, and their first degree relatives versus normal controls. Bisulfite sequencing was used to screen DNA methylation status of the HTR2A promoter CpGs and qMSP was used to quantify the degree of cytosine methylation at differentially methylated sites. Most of the cytosines of the HTR2A promoter were unmethylated. However, CpGs of the -1438A/G polymorphism site, -1420 and -1223 were >95% methylated. The CpG at T102C polymorphic site and neighboring CpGs were ∼70% methylated both in the patients and controls. qMSP analysis revealed that the cytosine of the T102C polymorphic site was significantly hypo-methylated in SCZ, BD, and their first degree relatives compared to the controls. Cytosine methylation of HTR2A at T102C polymorphic site in DNA derived from the saliva can potentially be used as a diagnostic, prognostic, and/or therapeutic biomarker in SCZ and BD. However, these preliminary observations need to be replicated in other populations with a larger sample size to be considered for clinical applications. © 2011 Wiley-Liss, Inc.	topic_bd
77732	11	356219	7	NULL	NULL	NULL	NULL	HTR2A	GP	cytosine of	hypo-methylated in				T102C polymorphic site	BD	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Several lines of evidence indicate that dysfunction of serotonin signaling and HTR2A receptor are involved in the pathogenesis of schizophrenia (SCZ) and bipolar disorder (BD). DNA methylation of HTR2A at T102C polymorphic site influences HTR2A expression and aberrant DNA methylation of HTR2A promoter was reported in postmortem brain of patients with SCZ and BD. Hypothesizing that the brain's epigenetic alteration of HTR2A may also exist in peripheral tissues that can be used as a diagnostic/therapeutic biomarker, we analyzed HTR2A promoter DNA methylation in DNA extracted from the saliva of patients with SCZ and BD, and their first degree relatives versus normal controls. Bisulfite sequencing was used to screen DNA methylation status of the HTR2A promoter CpGs and qMSP was used to quantify the degree of cytosine methylation at differentially methylated sites. Most of the cytosines of the HTR2A promoter were unmethylated. However, CpGs of the -1438A/G polymorphism site, -1420 and -1223 were >95% methylated. The CpG at T102C polymorphic site and neighboring CpGs were ∼70% methylated both in the patients and controls. qMSP analysis revealed that the cytosine of the T102C polymorphic site was significantly hypo-methylated in SCZ, BD, and their first degree relatives compared to the controls. Cytosine methylation of HTR2A at T102C polymorphic site in DNA derived from the saliva can potentially be used as a diagnostic, prognostic, and/or therapeutic biomarker in SCZ and BD. However, these preliminary observations need to be replicated in other populations with a larger sample size to be considered for clinical applications. © 2011 Wiley-Liss, Inc.	topic_bd
77733	12	356219	7	NULL	NULL	0	NULL	HTR2A	GP	Cytosine methylation of	used as a		potentially		T102C polymorphic site 	SCZ	MedicalFinding	diagnostic marker in			NULL		0	NULL	NULL	NULL	NULL	NULL	Several lines of evidence indicate that dysfunction of serotonin signaling and HTR2A receptor are involved in the pathogenesis of schizophrenia (SCZ) and bipolar disorder (BD). DNA methylation of HTR2A at T102C polymorphic site influences HTR2A expression and aberrant DNA methylation of HTR2A promoter was reported in postmortem brain of patients with SCZ and BD. Hypothesizing that the brain's epigenetic alteration of HTR2A may also exist in peripheral tissues that can be used as a diagnostic/therapeutic biomarker, we analyzed HTR2A promoter DNA methylation in DNA extracted from the saliva of patients with SCZ and BD, and their first degree relatives versus normal controls. Bisulfite sequencing was used to screen DNA methylation status of the HTR2A promoter CpGs and qMSP was used to quantify the degree of cytosine methylation at differentially methylated sites. Most of the cytosines of the HTR2A promoter were unmethylated. However, CpGs of the -1438A/G polymorphism site, -1420 and -1223 were >95% methylated. The CpG at T102C polymorphic site and neighboring CpGs were ∼70% methylated both in the patients and controls. qMSP analysis revealed that the cytosine of the T102C polymorphic site was significantly hypo-methylated in SCZ, BD, and their first degree relatives compared to the controls. Cytosine methylation of HTR2A at T102C polymorphic site in DNA derived from the saliva can potentially be used as a diagnostic, prognostic, and/or therapeutic biomarker in SCZ and BD. However, these preliminary observations need to be replicated in other populations with a larger sample size to be considered for clinical applications. © 2011 Wiley-Liss, Inc.	topic_bd
77734	13	356219	7	NULL	NULL	NULL	NULL	HTR2A	GP	Cytosine methylation of	used as a 		potentially		T102C polymorphic site	SCZ	MedicalFinding	prognostic marker in			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Several lines of evidence indicate that dysfunction of serotonin signaling and HTR2A receptor are involved in the pathogenesis of schizophrenia (SCZ) and bipolar disorder (BD). DNA methylation of HTR2A at T102C polymorphic site influences HTR2A expression and aberrant DNA methylation of HTR2A promoter was reported in postmortem brain of patients with SCZ and BD. Hypothesizing that the brain's epigenetic alteration of HTR2A may also exist in peripheral tissues that can be used as a diagnostic/therapeutic biomarker, we analyzed HTR2A promoter DNA methylation in DNA extracted from the saliva of patients with SCZ and BD, and their first degree relatives versus normal controls. Bisulfite sequencing was used to screen DNA methylation status of the HTR2A promoter CpGs and qMSP was used to quantify the degree of cytosine methylation at differentially methylated sites. Most of the cytosines of the HTR2A promoter were unmethylated. However, CpGs of the -1438A/G polymorphism site, -1420 and -1223 were >95% methylated. The CpG at T102C polymorphic site and neighboring CpGs were ∼70% methylated both in the patients and controls. qMSP analysis revealed that the cytosine of the T102C polymorphic site was significantly hypo-methylated in SCZ, BD, and their first degree relatives compared to the controls. Cytosine methylation of HTR2A at T102C polymorphic site in DNA derived from the saliva can potentially be used as a diagnostic, prognostic, and/or therapeutic biomarker in SCZ and BD. However, these preliminary observations need to be replicated in other populations with a larger sample size to be considered for clinical applications. © 2011 Wiley-Liss, Inc.	topic_bd
77762	14	356219	7	NULL	NULL	0	NULL	HTR2A	GP	Cytosine methylation of	used as a		potentially		T102C polymorphic site	SCZ	MedicalFinding	therapeutic biomarker in			NULL		0	NULL	NULL	NULL	NULL	NULL	Several lines of evidence indicate that dysfunction of serotonin signaling and HTR2A receptor are involved in the pathogenesis of schizophrenia (SCZ) and bipolar disorder (BD). DNA methylation of HTR2A at T102C polymorphic site influences HTR2A expression and aberrant DNA methylation of HTR2A promoter was reported in postmortem brain of patients with SCZ and BD. Hypothesizing that the brain's epigenetic alteration of HTR2A may also exist in peripheral tissues that can be used as a diagnostic/therapeutic biomarker, we analyzed HTR2A promoter DNA methylation in DNA extracted from the saliva of patients with SCZ and BD, and their first degree relatives versus normal controls. Bisulfite sequencing was used to screen DNA methylation status of the HTR2A promoter CpGs and qMSP was used to quantify the degree of cytosine methylation at differentially methylated sites. Most of the cytosines of the HTR2A promoter were unmethylated. However, CpGs of the -1438A/G polymorphism site, -1420 and -1223 were >95% methylated. The CpG at T102C polymorphic site and neighboring CpGs were ∼70% methylated both in the patients and controls. qMSP analysis revealed that the cytosine of the T102C polymorphic site was significantly hypo-methylated in SCZ, BD, and their first degree relatives compared to the controls. Cytosine methylation of HTR2A at T102C polymorphic site in DNA derived from the saliva can potentially be used as a diagnostic, prognostic, and/or therapeutic biomarker in SCZ and BD. However, these preliminary observations need to be replicated in other populations with a larger sample size to be considered for clinical applications. © 2011 Wiley-Liss, Inc.	topic_bd
77763	15	356219	7	NULL	NULL	NULL	NULL	HTR2A	GP	Cytosine methylation of	used as a		potentially		T102C polymorphic site	BD	MedicalFinding	diagnostic marker in			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Several lines of evidence indicate that dysfunction of serotonin signaling and HTR2A receptor are involved in the pathogenesis of schizophrenia (SCZ) and bipolar disorder (BD). DNA methylation of HTR2A at T102C polymorphic site influences HTR2A expression and aberrant DNA methylation of HTR2A promoter was reported in postmortem brain of patients with SCZ and BD. Hypothesizing that the brain's epigenetic alteration of HTR2A may also exist in peripheral tissues that can be used as a diagnostic/therapeutic biomarker, we analyzed HTR2A promoter DNA methylation in DNA extracted from the saliva of patients with SCZ and BD, and their first degree relatives versus normal controls. Bisulfite sequencing was used to screen DNA methylation status of the HTR2A promoter CpGs and qMSP was used to quantify the degree of cytosine methylation at differentially methylated sites. Most of the cytosines of the HTR2A promoter were unmethylated. However, CpGs of the -1438A/G polymorphism site, -1420 and -1223 were >95% methylated. The CpG at T102C polymorphic site and neighboring CpGs were ∼70% methylated both in the patients and controls. qMSP analysis revealed that the cytosine of the T102C polymorphic site was significantly hypo-methylated in SCZ, BD, and their first degree relatives compared to the controls. Cytosine methylation of HTR2A at T102C polymorphic site in DNA derived from the saliva can potentially be used as a diagnostic, prognostic, and/or therapeutic biomarker in SCZ and BD. However, these preliminary observations need to be replicated in other populations with a larger sample size to be considered for clinical applications. © 2011 Wiley-Liss, Inc.	topic_bd
77764	16	356219	7	NULL	NULL	NULL	NULL	HTR2A	GP	Cytosine methylation of	used as a		potentially		T102C polymorphic site	BD	MedicalFinding	prognostic marker in			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Several lines of evidence indicate that dysfunction of serotonin signaling and HTR2A receptor are involved in the pathogenesis of schizophrenia (SCZ) and bipolar disorder (BD). DNA methylation of HTR2A at T102C polymorphic site influences HTR2A expression and aberrant DNA methylation of HTR2A promoter was reported in postmortem brain of patients with SCZ and BD. Hypothesizing that the brain's epigenetic alteration of HTR2A may also exist in peripheral tissues that can be used as a diagnostic/therapeutic biomarker, we analyzed HTR2A promoter DNA methylation in DNA extracted from the saliva of patients with SCZ and BD, and their first degree relatives versus normal controls. Bisulfite sequencing was used to screen DNA methylation status of the HTR2A promoter CpGs and qMSP was used to quantify the degree of cytosine methylation at differentially methylated sites. Most of the cytosines of the HTR2A promoter were unmethylated. However, CpGs of the -1438A/G polymorphism site, -1420 and -1223 were >95% methylated. The CpG at T102C polymorphic site and neighboring CpGs were ∼70% methylated both in the patients and controls. qMSP analysis revealed that the cytosine of the T102C polymorphic site was significantly hypo-methylated in SCZ, BD, and their first degree relatives compared to the controls. Cytosine methylation of HTR2A at T102C polymorphic site in DNA derived from the saliva can potentially be used as a diagnostic, prognostic, and/or therapeutic biomarker in SCZ and BD. However, these preliminary observations need to be replicated in other populations with a larger sample size to be considered for clinical applications. © 2011 Wiley-Liss, Inc.	topic_bd
77765	17	356219	7	NULL	NULL	0	NULL	HTR2A	GP	Cytosine methylation of	used as a		potentially		T102C polymorphic site	BD	MedicalFinding	therapeutic biomarker in			NULL		0	NULL	NULL	NULL	NULL	NULL	Several lines of evidence indicate that dysfunction of serotonin signaling and HTR2A receptor are involved in the pathogenesis of schizophrenia (SCZ) and bipolar disorder (BD). DNA methylation of HTR2A at T102C polymorphic site influences HTR2A expression and aberrant DNA methylation of HTR2A promoter was reported in postmortem brain of patients with SCZ and BD. Hypothesizing that the brain's epigenetic alteration of HTR2A may also exist in peripheral tissues that can be used as a diagnostic/therapeutic biomarker, we analyzed HTR2A promoter DNA methylation in DNA extracted from the saliva of patients with SCZ and BD, and their first degree relatives versus normal controls. Bisulfite sequencing was used to screen DNA methylation status of the HTR2A promoter CpGs and qMSP was used to quantify the degree of cytosine methylation at differentially methylated sites. Most of the cytosines of the HTR2A promoter were unmethylated. However, CpGs of the -1438A/G polymorphism site, -1420 and -1223 were >95% methylated. The CpG at T102C polymorphic site and neighboring CpGs were ∼70% methylated both in the patients and controls. qMSP analysis revealed that the cytosine of the T102C polymorphic site was significantly hypo-methylated in SCZ, BD, and their first degree relatives compared to the controls. Cytosine methylation of HTR2A at T102C polymorphic site in DNA derived from the saliva can potentially be used as a diagnostic, prognostic, and/or therapeutic biomarker in SCZ and BD. However, these preliminary observations need to be replicated in other populations with a larger sample size to be considered for clinical applications. © 2011 Wiley-Liss, Inc.	topic_bd
77767	18	356219	7	NULL	NULL	0	NULL	SCZ	MedicalFinding		is					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Several lines of evidence indicate that dysfunction of serotonin signaling and HTR2A receptor are involved in the pathogenesis of schizophrenia (SCZ) and bipolar disorder (BD). DNA methylation of HTR2A at T102C polymorphic site influences HTR2A expression and aberrant DNA methylation of HTR2A promoter was reported in postmortem brain of patients with SCZ and BD. Hypothesizing that the brain's epigenetic alteration of HTR2A may also exist in peripheral tissues that can be used as a diagnostic/therapeutic biomarker, we analyzed HTR2A promoter DNA methylation in DNA extracted from the saliva of patients with SCZ and BD, and their first degree relatives versus normal controls. Bisulfite sequencing was used to screen DNA methylation status of the HTR2A promoter CpGs and qMSP was used to quantify the degree of cytosine methylation at differentially methylated sites. Most of the cytosines of the HTR2A promoter were unmethylated. However, CpGs of the -1438A/G polymorphism site, -1420 and -1223 were >95% methylated. The CpG at T102C polymorphic site and neighboring CpGs were ∼70% methylated both in the patients and controls. qMSP analysis revealed that the cytosine of the T102C polymorphic site was significantly hypo-methylated in SCZ, BD, and their first degree relatives compared to the controls. Cytosine methylation of HTR2A at T102C polymorphic site in DNA derived from the saliva can potentially be used as a diagnostic, prognostic, and/or therapeutic biomarker in SCZ and BD. However, these preliminary observations need to be replicated in other populations with a larger sample size to be considered for clinical applications. © 2011 Wiley-Liss, Inc.	topic_bd
77768	19	356219	7	NULL	NULL	0	NULL	BD	MedicalFinding		is					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Several lines of evidence indicate that dysfunction of serotonin signaling and HTR2A receptor are involved in the pathogenesis of schizophrenia (SCZ) and bipolar disorder (BD). DNA methylation of HTR2A at T102C polymorphic site influences HTR2A expression and aberrant DNA methylation of HTR2A promoter was reported in postmortem brain of patients with SCZ and BD. Hypothesizing that the brain's epigenetic alteration of HTR2A may also exist in peripheral tissues that can be used as a diagnostic/therapeutic biomarker, we analyzed HTR2A promoter DNA methylation in DNA extracted from the saliva of patients with SCZ and BD, and their first degree relatives versus normal controls. Bisulfite sequencing was used to screen DNA methylation status of the HTR2A promoter CpGs and qMSP was used to quantify the degree of cytosine methylation at differentially methylated sites. Most of the cytosines of the HTR2A promoter were unmethylated. However, CpGs of the -1438A/G polymorphism site, -1420 and -1223 were >95% methylated. The CpG at T102C polymorphic site and neighboring CpGs were ∼70% methylated both in the patients and controls. qMSP analysis revealed that the cytosine of the T102C polymorphic site was significantly hypo-methylated in SCZ, BD, and their first degree relatives compared to the controls. Cytosine methylation of HTR2A at T102C polymorphic site in DNA derived from the saliva can potentially be used as a diagnostic, prognostic, and/or therapeutic biomarker in SCZ and BD. However, these preliminary observations need to be replicated in other populations with a larger sample size to be considered for clinical applications. © 2011 Wiley-Liss, Inc.	topic_bd
77766	1	356220	7	NULL	NULL	0	NULL	HPA axis	OrganismPart		dysregulated in					BD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract INTRODUCTION: The hypothalamus-pituitary-adrenal (HPA)-axis is often found to be dysregulated in bipolar disorder (BD) while stress and changes in day-night rhythms can trigger a new mood episode. Genetic variants of the glucocorticoid receptor (GR)- and mineralocorticoid receptor (MR)-gene influence both the reactivity of the stress-response and associate with changes in mood. In this study we tested the hypothesis that these polymorphisms associate with different clinical characteristics of BD. METHODS: We studied 326 outpatients with BD and performed GR genotyping of the TthIIII, ER22/23EK, N363S, BclI, and 9β polymorphisms, as well as MR genotyping of the 2G/C and I180V variants. All patients were interviewed for clinical characteristics. RESULTS: Seasonal patterns of hypomania are related to the BclI haplotype and the TthIIII+9β haplotype of the GR gene (respectively, crude p=.007 and crude p=.005). Carriers of the ER22/23EK polymorphism had an almost 8 years earlier onset of their first (hypo)manic episode than non-carriers (crude p=.004, after adjustment p=.016). No evidence for a role of the MR in modifying clinical manifestations was found. CONCLUSION: Polymorphisms of the GR-gene are factors which influence some clinical manifestations of BD, with respect to seasonal pattern of (hypo)mania and age of onset.	topic_bd
77769	2	356220	7	NULL	NULL	0	NULL	stress	MentalProcess		triggers					new mood episode	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract INTRODUCTION: The hypothalamus-pituitary-adrenal (HPA)-axis is often found to be dysregulated in bipolar disorder (BD) while stress and changes in day-night rhythms can trigger a new mood episode. Genetic variants of the glucocorticoid receptor (GR)- and mineralocorticoid receptor (MR)-gene influence both the reactivity of the stress-response and associate with changes in mood. In this study we tested the hypothesis that these polymorphisms associate with different clinical characteristics of BD. METHODS: We studied 326 outpatients with BD and performed GR genotyping of the TthIIII, ER22/23EK, N363S, BclI, and 9β polymorphisms, as well as MR genotyping of the 2G/C and I180V variants. All patients were interviewed for clinical characteristics. RESULTS: Seasonal patterns of hypomania are related to the BclI haplotype and the TthIIII+9β haplotype of the GR gene (respectively, crude p=.007 and crude p=.005). Carriers of the ER22/23EK polymorphism had an almost 8 years earlier onset of their first (hypo)manic episode than non-carriers (crude p=.004, after adjustment p=.016). No evidence for a role of the MR in modifying clinical manifestations was found. CONCLUSION: Polymorphisms of the GR-gene are factors which influence some clinical manifestations of BD, with respect to seasonal pattern of (hypo)mania and age of onset.	topic_bd
77770	3	356220	7	NULL	NULL	0	NULL	day-night rhythms	MentalProcess		trigger					new mood episode	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract INTRODUCTION: The hypothalamus-pituitary-adrenal (HPA)-axis is often found to be dysregulated in bipolar disorder (BD) while stress and changes in day-night rhythms can trigger a new mood episode. Genetic variants of the glucocorticoid receptor (GR)- and mineralocorticoid receptor (MR)-gene influence both the reactivity of the stress-response and associate with changes in mood. In this study we tested the hypothesis that these polymorphisms associate with different clinical characteristics of BD. METHODS: We studied 326 outpatients with BD and performed GR genotyping of the TthIIII, ER22/23EK, N363S, BclI, and 9β polymorphisms, as well as MR genotyping of the 2G/C and I180V variants. All patients were interviewed for clinical characteristics. RESULTS: Seasonal patterns of hypomania are related to the BclI haplotype and the TthIIII+9β haplotype of the GR gene (respectively, crude p=.007 and crude p=.005). Carriers of the ER22/23EK polymorphism had an almost 8 years earlier onset of their first (hypo)manic episode than non-carriers (crude p=.004, after adjustment p=.016). No evidence for a role of the MR in modifying clinical manifestations was found. CONCLUSION: Polymorphisms of the GR-gene are factors which influence some clinical manifestations of BD, with respect to seasonal pattern of (hypo)mania and age of onset.	topic_bd
77771	4	356220	7	NULL	NULL	0	NULL	GR gene	GP	genetic variants of	influence					stress-response	MentalProcess	reactivity of			NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract INTRODUCTION: The hypothalamus-pituitary-adrenal (HPA)-axis is often found to be dysregulated in bipolar disorder (BD) while stress and changes in day-night rhythms can trigger a new mood episode. Genetic variants of the glucocorticoid receptor (GR)- and mineralocorticoid receptor (MR)-gene influence both the reactivity of the stress-response and associate with changes in mood. In this study we tested the hypothesis that these polymorphisms associate with different clinical characteristics of BD. METHODS: We studied 326 outpatients with BD and performed GR genotyping of the TthIIII, ER22/23EK, N363S, BclI, and 9β polymorphisms, as well as MR genotyping of the 2G/C and I180V variants. All patients were interviewed for clinical characteristics. RESULTS: Seasonal patterns of hypomania are related to the BclI haplotype and the TthIIII+9β haplotype of the GR gene (respectively, crude p=.007 and crude p=.005). Carriers of the ER22/23EK polymorphism had an almost 8 years earlier onset of their first (hypo)manic episode than non-carriers (crude p=.004, after adjustment p=.016). No evidence for a role of the MR in modifying clinical manifestations was found. CONCLUSION: Polymorphisms of the GR-gene are factors which influence some clinical manifestations of BD, with respect to seasonal pattern of (hypo)mania and age of onset.	topic_bd
77772	5	356220	7	NULL	NULL	0	NULL	MR gene	GP	genetic variants of	influence					stress-response	MentalProcess	reactivity of			NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract INTRODUCTION: The hypothalamus-pituitary-adrenal (HPA)-axis is often found to be dysregulated in bipolar disorder (BD) while stress and changes in day-night rhythms can trigger a new mood episode. Genetic variants of the glucocorticoid receptor (GR)- and mineralocorticoid receptor (MR)-gene influence both the reactivity of the stress-response and associate with changes in mood. In this study we tested the hypothesis that these polymorphisms associate with different clinical characteristics of BD. METHODS: We studied 326 outpatients with BD and performed GR genotyping of the TthIIII, ER22/23EK, N363S, BclI, and 9β polymorphisms, as well as MR genotyping of the 2G/C and I180V variants. All patients were interviewed for clinical characteristics. RESULTS: Seasonal patterns of hypomania are related to the BclI haplotype and the TthIIII+9β haplotype of the GR gene (respectively, crude p=.007 and crude p=.005). Carriers of the ER22/23EK polymorphism had an almost 8 years earlier onset of their first (hypo)manic episode than non-carriers (crude p=.004, after adjustment p=.016). No evidence for a role of the MR in modifying clinical manifestations was found. CONCLUSION: Polymorphisms of the GR-gene are factors which influence some clinical manifestations of BD, with respect to seasonal pattern of (hypo)mania and age of onset.	topic_bd
77773	6	356220	7	NULL	NULL	0	NULL	GR gene	GP	genetic variants of	associate with					mood	MentalProcess	changes in			NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract INTRODUCTION: The hypothalamus-pituitary-adrenal (HPA)-axis is often found to be dysregulated in bipolar disorder (BD) while stress and changes in day-night rhythms can trigger a new mood episode. Genetic variants of the glucocorticoid receptor (GR)- and mineralocorticoid receptor (MR)-gene influence both the reactivity of the stress-response and associate with changes in mood. In this study we tested the hypothesis that these polymorphisms associate with different clinical characteristics of BD. METHODS: We studied 326 outpatients with BD and performed GR genotyping of the TthIIII, ER22/23EK, N363S, BclI, and 9β polymorphisms, as well as MR genotyping of the 2G/C and I180V variants. All patients were interviewed for clinical characteristics. RESULTS: Seasonal patterns of hypomania are related to the BclI haplotype and the TthIIII+9β haplotype of the GR gene (respectively, crude p=.007 and crude p=.005). Carriers of the ER22/23EK polymorphism had an almost 8 years earlier onset of their first (hypo)manic episode than non-carriers (crude p=.004, after adjustment p=.016). No evidence for a role of the MR in modifying clinical manifestations was found. CONCLUSION: Polymorphisms of the GR-gene are factors which influence some clinical manifestations of BD, with respect to seasonal pattern of (hypo)mania and age of onset.	topic_bd
77774	7	356220	7	NULL	NULL	0	NULL	MR gene	GP	genetic variants of	associate with					mood	MentalProcess	changes in			NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract INTRODUCTION: The hypothalamus-pituitary-adrenal (HPA)-axis is often found to be dysregulated in bipolar disorder (BD) while stress and changes in day-night rhythms can trigger a new mood episode. Genetic variants of the glucocorticoid receptor (GR)- and mineralocorticoid receptor (MR)-gene influence both the reactivity of the stress-response and associate with changes in mood. In this study we tested the hypothesis that these polymorphisms associate with different clinical characteristics of BD. METHODS: We studied 326 outpatients with BD and performed GR genotyping of the TthIIII, ER22/23EK, N363S, BclI, and 9β polymorphisms, as well as MR genotyping of the 2G/C and I180V variants. All patients were interviewed for clinical characteristics. RESULTS: Seasonal patterns of hypomania are related to the BclI haplotype and the TthIIII+9β haplotype of the GR gene (respectively, crude p=.007 and crude p=.005). Carriers of the ER22/23EK polymorphism had an almost 8 years earlier onset of their first (hypo)manic episode than non-carriers (crude p=.004, after adjustment p=.016). No evidence for a role of the MR in modifying clinical manifestations was found. CONCLUSION: Polymorphisms of the GR-gene are factors which influence some clinical manifestations of BD, with respect to seasonal pattern of (hypo)mania and age of onset.	topic_bd
77775	8	356220	7	NULL	NULL	0	NULL	GR-gene	GP	Polymorphisms of	influence					BD	MedicalFinding	clinical manifestations of 			NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract INTRODUCTION: The hypothalamus-pituitary-adrenal (HPA)-axis is often found to be dysregulated in bipolar disorder (BD) while stress and changes in day-night rhythms can trigger a new mood episode. Genetic variants of the glucocorticoid receptor (GR)- and mineralocorticoid receptor (MR)-gene influence both the reactivity of the stress-response and associate with changes in mood. In this study we tested the hypothesis that these polymorphisms associate with different clinical characteristics of BD. METHODS: We studied 326 outpatients with BD and performed GR genotyping of the TthIIII, ER22/23EK, N363S, BclI, and 9β polymorphisms, as well as MR genotyping of the 2G/C and I180V variants. All patients were interviewed for clinical characteristics. RESULTS: Seasonal patterns of hypomania are related to the BclI haplotype and the TthIIII+9β haplotype of the GR gene (respectively, crude p=.007 and crude p=.005). Carriers of the ER22/23EK polymorphism had an almost 8 years earlier onset of their first (hypo)manic episode than non-carriers (crude p=.004, after adjustment p=.016). No evidence for a role of the MR in modifying clinical manifestations was found. CONCLUSION: Polymorphisms of the GR-gene are factors which influence some clinical manifestations of BD, with respect to seasonal pattern of (hypo)mania and age of onset.	topic_bd
77776	9	356220	7	NULL	NULL	0	NULL	HPA axis	OrganismPart		is					hypothalamus-pituitary-adrenal -axis					NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract INTRODUCTION: The hypothalamus-pituitary-adrenal (HPA)-axis is often found to be dysregulated in bipolar disorder (BD) while stress and changes in day-night rhythms can trigger a new mood episode. Genetic variants of the glucocorticoid receptor (GR)- and mineralocorticoid receptor (MR)-gene influence both the reactivity of the stress-response and associate with changes in mood. In this study we tested the hypothesis that these polymorphisms associate with different clinical characteristics of BD. METHODS: We studied 326 outpatients with BD and performed GR genotyping of the TthIIII, ER22/23EK, N363S, BclI, and 9β polymorphisms, as well as MR genotyping of the 2G/C and I180V variants. All patients were interviewed for clinical characteristics. RESULTS: Seasonal patterns of hypomania are related to the BclI haplotype and the TthIIII+9β haplotype of the GR gene (respectively, crude p=.007 and crude p=.005). Carriers of the ER22/23EK polymorphism had an almost 8 years earlier onset of their first (hypo)manic episode than non-carriers (crude p=.004, after adjustment p=.016). No evidence for a role of the MR in modifying clinical manifestations was found. CONCLUSION: Polymorphisms of the GR-gene are factors which influence some clinical manifestations of BD, with respect to seasonal pattern of (hypo)mania and age of onset.	topic_bd
77777	10	356220	7	NULL	NULL	0	NULL	GR	GP		is					glucocorticoid receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract INTRODUCTION: The hypothalamus-pituitary-adrenal (HPA)-axis is often found to be dysregulated in bipolar disorder (BD) while stress and changes in day-night rhythms can trigger a new mood episode. Genetic variants of the glucocorticoid receptor (GR)- and mineralocorticoid receptor (MR)-gene influence both the reactivity of the stress-response and associate with changes in mood. In this study we tested the hypothesis that these polymorphisms associate with different clinical characteristics of BD. METHODS: We studied 326 outpatients with BD and performed GR genotyping of the TthIIII, ER22/23EK, N363S, BclI, and 9β polymorphisms, as well as MR genotyping of the 2G/C and I180V variants. All patients were interviewed for clinical characteristics. RESULTS: Seasonal patterns of hypomania are related to the BclI haplotype and the TthIIII+9β haplotype of the GR gene (respectively, crude p=.007 and crude p=.005). Carriers of the ER22/23EK polymorphism had an almost 8 years earlier onset of their first (hypo)manic episode than non-carriers (crude p=.004, after adjustment p=.016). No evidence for a role of the MR in modifying clinical manifestations was found. CONCLUSION: Polymorphisms of the GR-gene are factors which influence some clinical manifestations of BD, with respect to seasonal pattern of (hypo)mania and age of onset.	topic_bd
77778	11	356220	7	NULL	NULL	0	NULL	MR	GP		is					mineralocorticoid receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract INTRODUCTION: The hypothalamus-pituitary-adrenal (HPA)-axis is often found to be dysregulated in bipolar disorder (BD) while stress and changes in day-night rhythms can trigger a new mood episode. Genetic variants of the glucocorticoid receptor (GR)- and mineralocorticoid receptor (MR)-gene influence both the reactivity of the stress-response and associate with changes in mood. In this study we tested the hypothesis that these polymorphisms associate with different clinical characteristics of BD. METHODS: We studied 326 outpatients with BD and performed GR genotyping of the TthIIII, ER22/23EK, N363S, BclI, and 9β polymorphisms, as well as MR genotyping of the 2G/C and I180V variants. All patients were interviewed for clinical characteristics. RESULTS: Seasonal patterns of hypomania are related to the BclI haplotype and the TthIIII+9β haplotype of the GR gene (respectively, crude p=.007 and crude p=.005). Carriers of the ER22/23EK polymorphism had an almost 8 years earlier onset of their first (hypo)manic episode than non-carriers (crude p=.004, after adjustment p=.016). No evidence for a role of the MR in modifying clinical manifestations was found. CONCLUSION: Polymorphisms of the GR-gene are factors which influence some clinical manifestations of BD, with respect to seasonal pattern of (hypo)mania and age of onset.	topic_bd
77781	12	356220	7	NULL	NULL	0	NULL	BD	MedicalFinding		is					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract INTRODUCTION: The hypothalamus-pituitary-adrenal (HPA)-axis is often found to be dysregulated in bipolar disorder (BD) while stress and changes in day-night rhythms can trigger a new mood episode. Genetic variants of the glucocorticoid receptor (GR)- and mineralocorticoid receptor (MR)-gene influence both the reactivity of the stress-response and associate with changes in mood. In this study we tested the hypothesis that these polymorphisms associate with different clinical characteristics of BD. METHODS: We studied 326 outpatients with BD and performed GR genotyping of the TthIIII, ER22/23EK, N363S, BclI, and 9β polymorphisms, as well as MR genotyping of the 2G/C and I180V variants. All patients were interviewed for clinical characteristics. RESULTS: Seasonal patterns of hypomania are related to the BclI haplotype and the TthIIII+9β haplotype of the GR gene (respectively, crude p=.007 and crude p=.005). Carriers of the ER22/23EK polymorphism had an almost 8 years earlier onset of their first (hypo)manic episode than non-carriers (crude p=.004, after adjustment p=.016). No evidence for a role of the MR in modifying clinical manifestations was found. CONCLUSION: Polymorphisms of the GR-gene are factors which influence some clinical manifestations of BD, with respect to seasonal pattern of (hypo)mania and age of onset.	topic_bd
77779	1	356222	7	NULL	NULL	0	NULL	Psychotic features	MedicalFinding		defined as					delusions	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract Psychotic features, defined as delusions or hallucinations, commonly occur in bipolar disorder (BP) and may be indicative of a more homogeneous form of the illness, with possible etiologic ties to schizophrenia. Several studies have shown that psychotic features aggregate in bipolar families, and increased interest in the molecular genetics of psychotic BP is emerging. Although preliminary, linkage studies of psychotic BP show replicated evidence for suggestive genome-wide linkage to chromosomes 8p and 13q, which have been implicated in prior linkage studies of schizophrenia and BP. Association studies of psychotic BP and subtypes such as mood-incongruent psychotic BP have uncovered modest positive results for several candidate schizophrenia susceptibility genes, including dysbindin, DAOA/G30, Disrupted-in-Schizophrenia-1, and neuregulin 1. These tentative results are consistent with the hypothesis that the subphenotype of psychotic BP may represent a clinical manifestation of 'overlap' genes between schizophrenia and mood disorder syndromes.	topic_bd
77780	2	356222	7	NULL	NULL	0	NULL	Psychotic features	MedicalFinding		defined as					hallucinations	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract Psychotic features, defined as delusions or hallucinations, commonly occur in bipolar disorder (BP) and may be indicative of a more homogeneous form of the illness, with possible etiologic ties to schizophrenia. Several studies have shown that psychotic features aggregate in bipolar families, and increased interest in the molecular genetics of psychotic BP is emerging. Although preliminary, linkage studies of psychotic BP show replicated evidence for suggestive genome-wide linkage to chromosomes 8p and 13q, which have been implicated in prior linkage studies of schizophrenia and BP. Association studies of psychotic BP and subtypes such as mood-incongruent psychotic BP have uncovered modest positive results for several candidate schizophrenia susceptibility genes, including dysbindin, DAOA/G30, Disrupted-in-Schizophrenia-1, and neuregulin 1. These tentative results are consistent with the hypothesis that the subphenotype of psychotic BP may represent a clinical manifestation of 'overlap' genes between schizophrenia and mood disorder syndromes.	topic_bd
78015	3	356222	7	NULL	NULL	0	NULL	statement 1	Process		occur in		commonly			BP	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract Psychotic features, defined as delusions or hallucinations, commonly occur in bipolar disorder (BP) and may be indicative of a more homogeneous form of the illness, with possible etiologic ties to schizophrenia. Several studies have shown that psychotic features aggregate in bipolar families, and increased interest in the molecular genetics of psychotic BP is emerging. Although preliminary, linkage studies of psychotic BP show replicated evidence for suggestive genome-wide linkage to chromosomes 8p and 13q, which have been implicated in prior linkage studies of schizophrenia and BP. Association studies of psychotic BP and subtypes such as mood-incongruent psychotic BP have uncovered modest positive results for several candidate schizophrenia susceptibility genes, including dysbindin, DAOA/G30, Disrupted-in-Schizophrenia-1, and neuregulin 1. These tentative results are consistent with the hypothesis that the subphenotype of psychotic BP may represent a clinical manifestation of 'overlap' genes between schizophrenia and mood disorder syndromes.	topic_bd
78016	4	356222	7	NULL	NULL	0	NULL	statement 2	Process		occur in		commonly			BP	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract Psychotic features, defined as delusions or hallucinations, commonly occur in bipolar disorder (BP) and may be indicative of a more homogeneous form of the illness, with possible etiologic ties to schizophrenia. Several studies have shown that psychotic features aggregate in bipolar families, and increased interest in the molecular genetics of psychotic BP is emerging. Although preliminary, linkage studies of psychotic BP show replicated evidence for suggestive genome-wide linkage to chromosomes 8p and 13q, which have been implicated in prior linkage studies of schizophrenia and BP. Association studies of psychotic BP and subtypes such as mood-incongruent psychotic BP have uncovered modest positive results for several candidate schizophrenia susceptibility genes, including dysbindin, DAOA/G30, Disrupted-in-Schizophrenia-1, and neuregulin 1. These tentative results are consistent with the hypothesis that the subphenotype of psychotic BP may represent a clinical manifestation of 'overlap' genes between schizophrenia and mood disorder syndromes.	topic_bd
78017	5	356222	7	NULL	NULL	0	NULL	BP	MedicalFinding		is					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract Psychotic features, defined as delusions or hallucinations, commonly occur in bipolar disorder (BP) and may be indicative of a more homogeneous form of the illness, with possible etiologic ties to schizophrenia. Several studies have shown that psychotic features aggregate in bipolar families, and increased interest in the molecular genetics of psychotic BP is emerging. Although preliminary, linkage studies of psychotic BP show replicated evidence for suggestive genome-wide linkage to chromosomes 8p and 13q, which have been implicated in prior linkage studies of schizophrenia and BP. Association studies of psychotic BP and subtypes such as mood-incongruent psychotic BP have uncovered modest positive results for several candidate schizophrenia susceptibility genes, including dysbindin, DAOA/G30, Disrupted-in-Schizophrenia-1, and neuregulin 1. These tentative results are consistent with the hypothesis that the subphenotype of psychotic BP may represent a clinical manifestation of 'overlap' genes between schizophrenia and mood disorder syndromes.	topic_bd
78018	6	356222	7	NULL	NULL	0	NULL	statement 3	Process		indicative of					illness	MedicalFinding	homogeneous form of			NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract Psychotic features, defined as delusions or hallucinations, commonly occur in bipolar disorder (BP) and may be indicative of a more homogeneous form of the illness, with possible etiologic ties to schizophrenia. Several studies have shown that psychotic features aggregate in bipolar families, and increased interest in the molecular genetics of psychotic BP is emerging. Although preliminary, linkage studies of psychotic BP show replicated evidence for suggestive genome-wide linkage to chromosomes 8p and 13q, which have been implicated in prior linkage studies of schizophrenia and BP. Association studies of psychotic BP and subtypes such as mood-incongruent psychotic BP have uncovered modest positive results for several candidate schizophrenia susceptibility genes, including dysbindin, DAOA/G30, Disrupted-in-Schizophrenia-1, and neuregulin 1. These tentative results are consistent with the hypothesis that the subphenotype of psychotic BP may represent a clinical manifestation of 'overlap' genes between schizophrenia and mood disorder syndromes.	topic_bd
78019	7	356222	7	NULL	NULL	0	NULL	statement 4	Process		indicative of					illness	MedicalFinding	homogeneous form of			NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract Psychotic features, defined as delusions or hallucinations, commonly occur in bipolar disorder (BP) and may be indicative of a more homogeneous form of the illness, with possible etiologic ties to schizophrenia. Several studies have shown that psychotic features aggregate in bipolar families, and increased interest in the molecular genetics of psychotic BP is emerging. Although preliminary, linkage studies of psychotic BP show replicated evidence for suggestive genome-wide linkage to chromosomes 8p and 13q, which have been implicated in prior linkage studies of schizophrenia and BP. Association studies of psychotic BP and subtypes such as mood-incongruent psychotic BP have uncovered modest positive results for several candidate schizophrenia susceptibility genes, including dysbindin, DAOA/G30, Disrupted-in-Schizophrenia-1, and neuregulin 1. These tentative results are consistent with the hypothesis that the subphenotype of psychotic BP may represent a clinical manifestation of 'overlap' genes between schizophrenia and mood disorder syndromes.	topic_bd
78020	8	356222	7	NULL	NULL	0	NULL	statement 3	Process		etiologic ties to		possible			schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract Psychotic features, defined as delusions or hallucinations, commonly occur in bipolar disorder (BP) and may be indicative of a more homogeneous form of the illness, with possible etiologic ties to schizophrenia. Several studies have shown that psychotic features aggregate in bipolar families, and increased interest in the molecular genetics of psychotic BP is emerging. Although preliminary, linkage studies of psychotic BP show replicated evidence for suggestive genome-wide linkage to chromosomes 8p and 13q, which have been implicated in prior linkage studies of schizophrenia and BP. Association studies of psychotic BP and subtypes such as mood-incongruent psychotic BP have uncovered modest positive results for several candidate schizophrenia susceptibility genes, including dysbindin, DAOA/G30, Disrupted-in-Schizophrenia-1, and neuregulin 1. These tentative results are consistent with the hypothesis that the subphenotype of psychotic BP may represent a clinical manifestation of 'overlap' genes between schizophrenia and mood disorder syndromes.	topic_bd
78021	9	356222	7	NULL	NULL	0	NULL	statement 4	Process		etiologic ties to		possible			schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract Psychotic features, defined as delusions or hallucinations, commonly occur in bipolar disorder (BP) and may be indicative of a more homogeneous form of the illness, with possible etiologic ties to schizophrenia. Several studies have shown that psychotic features aggregate in bipolar families, and increased interest in the molecular genetics of psychotic BP is emerging. Although preliminary, linkage studies of psychotic BP show replicated evidence for suggestive genome-wide linkage to chromosomes 8p and 13q, which have been implicated in prior linkage studies of schizophrenia and BP. Association studies of psychotic BP and subtypes such as mood-incongruent psychotic BP have uncovered modest positive results for several candidate schizophrenia susceptibility genes, including dysbindin, DAOA/G30, Disrupted-in-Schizophrenia-1, and neuregulin 1. These tentative results are consistent with the hypothesis that the subphenotype of psychotic BP may represent a clinical manifestation of 'overlap' genes between schizophrenia and mood disorder syndromes.	topic_bd
78022	10	356222	7	NULL	NULL	NULL	NULL	psychotic BP	MedicalFinding		show					chromosome 8p	Chromosome	evidence for suggestive genome-wide linkage to			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Abstract Psychotic features, defined as delusions or hallucinations, commonly occur in bipolar disorder (BP) and may be indicative of a more homogeneous form of the illness, with possible etiologic ties to schizophrenia. Several studies have shown that psychotic features aggregate in bipolar families, and increased interest in the molecular genetics of psychotic BP is emerging. Although preliminary, linkage studies of psychotic BP show replicated evidence for suggestive genome-wide linkage to chromosomes 8p and 13q, which have been implicated in prior linkage studies of schizophrenia and BP. Association studies of psychotic BP and subtypes such as mood-incongruent psychotic BP have uncovered modest positive results for several candidate schizophrenia susceptibility genes, including dysbindin, DAOA/G30, Disrupted-in-Schizophrenia-1, and neuregulin 1. These tentative results are consistent with the hypothesis that the subphenotype of psychotic BP may represent a clinical manifestation of 'overlap' genes between schizophrenia and mood disorder syndromes.	topic_bd
78023	11	356222	7	NULL	NULL	NULL	NULL	psychotic BP	MedicalFinding		show					chromosome 13q	Chromosome	evidence for suggestive genome-wide linkage to			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Abstract Psychotic features, defined as delusions or hallucinations, commonly occur in bipolar disorder (BP) and may be indicative of a more homogeneous form of the illness, with possible etiologic ties to schizophrenia. Several studies have shown that psychotic features aggregate in bipolar families, and increased interest in the molecular genetics of psychotic BP is emerging. Although preliminary, linkage studies of psychotic BP show replicated evidence for suggestive genome-wide linkage to chromosomes 8p and 13q, which have been implicated in prior linkage studies of schizophrenia and BP. Association studies of psychotic BP and subtypes such as mood-incongruent psychotic BP have uncovered modest positive results for several candidate schizophrenia susceptibility genes, including dysbindin, DAOA/G30, Disrupted-in-Schizophrenia-1, and neuregulin 1. These tentative results are consistent with the hypothesis that the subphenotype of psychotic BP may represent a clinical manifestation of 'overlap' genes between schizophrenia and mood disorder syndromes.	topic_bd
78024	12	356222	7	NULL	NULL	0	NULL	dysbindin	GP		is a type of					schizophrenia susceptibility genes	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract Psychotic features, defined as delusions or hallucinations, commonly occur in bipolar disorder (BP) and may be indicative of a more homogeneous form of the illness, with possible etiologic ties to schizophrenia. Several studies have shown that psychotic features aggregate in bipolar families, and increased interest in the molecular genetics of psychotic BP is emerging. Although preliminary, linkage studies of psychotic BP show replicated evidence for suggestive genome-wide linkage to chromosomes 8p and 13q, which have been implicated in prior linkage studies of schizophrenia and BP. Association studies of psychotic BP and subtypes such as mood-incongruent psychotic BP have uncovered modest positive results for several candidate schizophrenia susceptibility genes, including dysbindin, DAOA/G30, Disrupted-in-Schizophrenia-1, and neuregulin 1. These tentative results are consistent with the hypothesis that the subphenotype of psychotic BP may represent a clinical manifestation of 'overlap' genes between schizophrenia and mood disorder syndromes.	topic_bd
78025	13	356222	7	NULL	NULL	0	NULL	DAOA/G30	GP		is a type of					schizophrenia susceptibility genes	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract Psychotic features, defined as delusions or hallucinations, commonly occur in bipolar disorder (BP) and may be indicative of a more homogeneous form of the illness, with possible etiologic ties to schizophrenia. Several studies have shown that psychotic features aggregate in bipolar families, and increased interest in the molecular genetics of psychotic BP is emerging. Although preliminary, linkage studies of psychotic BP show replicated evidence for suggestive genome-wide linkage to chromosomes 8p and 13q, which have been implicated in prior linkage studies of schizophrenia and BP. Association studies of psychotic BP and subtypes such as mood-incongruent psychotic BP have uncovered modest positive results for several candidate schizophrenia susceptibility genes, including dysbindin, DAOA/G30, Disrupted-in-Schizophrenia-1, and neuregulin 1. These tentative results are consistent with the hypothesis that the subphenotype of psychotic BP may represent a clinical manifestation of 'overlap' genes between schizophrenia and mood disorder syndromes.	topic_bd
78026	14	356222	7	NULL	NULL	0	NULL	Disrupted-in-Schizophrenia-1	GP		is a type of					schizophrenia susceptibility genes	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract Psychotic features, defined as delusions or hallucinations, commonly occur in bipolar disorder (BP) and may be indicative of a more homogeneous form of the illness, with possible etiologic ties to schizophrenia. Several studies have shown that psychotic features aggregate in bipolar families, and increased interest in the molecular genetics of psychotic BP is emerging. Although preliminary, linkage studies of psychotic BP show replicated evidence for suggestive genome-wide linkage to chromosomes 8p and 13q, which have been implicated in prior linkage studies of schizophrenia and BP. Association studies of psychotic BP and subtypes such as mood-incongruent psychotic BP have uncovered modest positive results for several candidate schizophrenia susceptibility genes, including dysbindin, DAOA/G30, Disrupted-in-Schizophrenia-1, and neuregulin 1. These tentative results are consistent with the hypothesis that the subphenotype of psychotic BP may represent a clinical manifestation of 'overlap' genes between schizophrenia and mood disorder syndromes.	topic_bd
78027	15	356222	7	NULL	NULL	0	NULL	neuregulin 1	GP		is a type of					schizophrenia susceptibility genes	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Abstract Psychotic features, defined as delusions or hallucinations, commonly occur in bipolar disorder (BP) and may be indicative of a more homogeneous form of the illness, with possible etiologic ties to schizophrenia. Several studies have shown that psychotic features aggregate in bipolar families, and increased interest in the molecular genetics of psychotic BP is emerging. Although preliminary, linkage studies of psychotic BP show replicated evidence for suggestive genome-wide linkage to chromosomes 8p and 13q, which have been implicated in prior linkage studies of schizophrenia and BP. Association studies of psychotic BP and subtypes such as mood-incongruent psychotic BP have uncovered modest positive results for several candidate schizophrenia susceptibility genes, including dysbindin, DAOA/G30, Disrupted-in-Schizophrenia-1, and neuregulin 1. These tentative results are consistent with the hypothesis that the subphenotype of psychotic BP may represent a clinical manifestation of 'overlap' genes between schizophrenia and mood disorder syndromes.	topic_bd
77782	1	356223	7	NULL	NULL	0	NULL	SIAT4A	GP		associated with					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	RESULTS: No genes specifically chosen to probe the action of lithium were associated with bipolar disorder. However, gene-based analysis of sialyltransferase 4A (SIAT4A), tachykinin receptor 1 (TACR1), and gamma-aminobutyric acid(A) beta2 receptor subunit (GABRB2) yielded evidence of association (empirical P value, <.005). Among 3 genes associated with schizophrenia or bipolar disorder in multiple previous studies, including dysbindin (DTNBP1), neuregulin (NRG1), and disrupted-in-schizophrenia 1 (DISC1), only DISC1 showed evidence of association in this cohort. In a secondary analysis of these 6 genes among parent-proband trios with a history of psychosis, evidence of the association with SIAT4A was strengthened.	topic_bd
77783	2	356223	7	NULL	NULL	0	NULL	TACR1	GP		associated with					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	RESULTS: No genes specifically chosen to probe the action of lithium were associated with bipolar disorder. However, gene-based analysis of sialyltransferase 4A (SIAT4A), tachykinin receptor 1 (TACR1), and gamma-aminobutyric acid(A) beta2 receptor subunit (GABRB2) yielded evidence of association (empirical P value, <.005). Among 3 genes associated with schizophrenia or bipolar disorder in multiple previous studies, including dysbindin (DTNBP1), neuregulin (NRG1), and disrupted-in-schizophrenia 1 (DISC1), only DISC1 showed evidence of association in this cohort. In a secondary analysis of these 6 genes among parent-proband trios with a history of psychosis, evidence of the association with SIAT4A was strengthened.	topic_bd
77784	3	356223	7	NULL	NULL	0	NULL	GABRB2	GP		associated with					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	RESULTS: No genes specifically chosen to probe the action of lithium were associated with bipolar disorder. However, gene-based analysis of sialyltransferase 4A (SIAT4A), tachykinin receptor 1 (TACR1), and gamma-aminobutyric acid(A) beta2 receptor subunit (GABRB2) yielded evidence of association (empirical P value, <.005). Among 3 genes associated with schizophrenia or bipolar disorder in multiple previous studies, including dysbindin (DTNBP1), neuregulin (NRG1), and disrupted-in-schizophrenia 1 (DISC1), only DISC1 showed evidence of association in this cohort. In a secondary analysis of these 6 genes among parent-proband trios with a history of psychosis, evidence of the association with SIAT4A was strengthened.	topic_bd
77785	4	356223	7	NULL	NULL	0	NULL	DISC1	GP		associated with					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	RESULTS: No genes specifically chosen to probe the action of lithium were associated with bipolar disorder. However, gene-based analysis of sialyltransferase 4A (SIAT4A), tachykinin receptor 1 (TACR1), and gamma-aminobutyric acid(A) beta2 receptor subunit (GABRB2) yielded evidence of association (empirical P value, <.005). Among 3 genes associated with schizophrenia or bipolar disorder in multiple previous studies, including dysbindin (DTNBP1), neuregulin (NRG1), and disrupted-in-schizophrenia 1 (DISC1), only DISC1 showed evidence of association in this cohort. In a secondary analysis of these 6 genes among parent-proband trios with a history of psychosis, evidence of the association with SIAT4A was strengthened.	topic_bd
77786	5	356223	7	NULL	NULL	0	NULL	DISC1	GP		associated with					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	RESULTS: No genes specifically chosen to probe the action of lithium were associated with bipolar disorder. However, gene-based analysis of sialyltransferase 4A (SIAT4A), tachykinin receptor 1 (TACR1), and gamma-aminobutyric acid(A) beta2 receptor subunit (GABRB2) yielded evidence of association (empirical P value, <.005). Among 3 genes associated with schizophrenia or bipolar disorder in multiple previous studies, including dysbindin (DTNBP1), neuregulin (NRG1), and disrupted-in-schizophrenia 1 (DISC1), only DISC1 showed evidence of association in this cohort. In a secondary analysis of these 6 genes among parent-proband trios with a history of psychosis, evidence of the association with SIAT4A was strengthened.	topic_bd
77787	6	356223	7	NULL	NULL	0	NULL	SIAT4A	GP		is					sialyltransferase 4A	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	RESULTS: No genes specifically chosen to probe the action of lithium were associated with bipolar disorder. However, gene-based analysis of sialyltransferase 4A (SIAT4A), tachykinin receptor 1 (TACR1), and gamma-aminobutyric acid(A) beta2 receptor subunit (GABRB2) yielded evidence of association (empirical P value, <.005). Among 3 genes associated with schizophrenia or bipolar disorder in multiple previous studies, including dysbindin (DTNBP1), neuregulin (NRG1), and disrupted-in-schizophrenia 1 (DISC1), only DISC1 showed evidence of association in this cohort. In a secondary analysis of these 6 genes among parent-proband trios with a history of psychosis, evidence of the association with SIAT4A was strengthened.	topic_bd
77788	7	356223	7	NULL	NULL	0	NULL	TACR1	GP		is					tachykinin receptor 1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	RESULTS: No genes specifically chosen to probe the action of lithium were associated with bipolar disorder. However, gene-based analysis of sialyltransferase 4A (SIAT4A), tachykinin receptor 1 (TACR1), and gamma-aminobutyric acid(A) beta2 receptor subunit (GABRB2) yielded evidence of association (empirical P value, <.005). Among 3 genes associated with schizophrenia or bipolar disorder in multiple previous studies, including dysbindin (DTNBP1), neuregulin (NRG1), and disrupted-in-schizophrenia 1 (DISC1), only DISC1 showed evidence of association in this cohort. In a secondary analysis of these 6 genes among parent-proband trios with a history of psychosis, evidence of the association with SIAT4A was strengthened.	topic_bd
77789	8	356223	7	NULL	NULL	0	NULL	GABRB2	GP		is					gamma-aminobutyric acid(A) beta2 receptor subunit 	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	RESULTS: No genes specifically chosen to probe the action of lithium were associated with bipolar disorder. However, gene-based analysis of sialyltransferase 4A (SIAT4A), tachykinin receptor 1 (TACR1), and gamma-aminobutyric acid(A) beta2 receptor subunit (GABRB2) yielded evidence of association (empirical P value, <.005). Among 3 genes associated with schizophrenia or bipolar disorder in multiple previous studies, including dysbindin (DTNBP1), neuregulin (NRG1), and disrupted-in-schizophrenia 1 (DISC1), only DISC1 showed evidence of association in this cohort. In a secondary analysis of these 6 genes among parent-proband trios with a history of psychosis, evidence of the association with SIAT4A was strengthened.	topic_bd
77790	9	356223	7	NULL	NULL	0	NULL	DISC1	GP		is					disrupted-in-schizophrenia 1	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	RESULTS: No genes specifically chosen to probe the action of lithium were associated with bipolar disorder. However, gene-based analysis of sialyltransferase 4A (SIAT4A), tachykinin receptor 1 (TACR1), and gamma-aminobutyric acid(A) beta2 receptor subunit (GABRB2) yielded evidence of association (empirical P value, <.005). Among 3 genes associated with schizophrenia or bipolar disorder in multiple previous studies, including dysbindin (DTNBP1), neuregulin (NRG1), and disrupted-in-schizophrenia 1 (DISC1), only DISC1 showed evidence of association in this cohort. In a secondary analysis of these 6 genes among parent-proband trios with a history of psychosis, evidence of the association with SIAT4A was strengthened.	topic_bd
78415	1	356224	5	NULL	NULL	0	NULL	gray matter	OrganismPart	volume of	reduced in					pars opercularis	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	A significant gray matter volume reduction of both the pars opercularis and triangularis was found bilaterally in the subjects with ASD compared with the typical control subjects	topic_aut
78416	2	356224	5	NULL	NULL	0	NULL	gray matter	OrganismPart	volume of	reduced in					triangularis	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	A significant gray matter volume reduction of both the pars opercularis and triangularis was found bilaterally in the subjects with ASD compared with the typical control subjects	topic_aut
78417	3	356224	5	NULL	NULL	0	NULL	statement 1	Process		is present in					ASD subjects	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	A significant gray matter volume reduction of both the pars opercularis and triangularis was found bilaterally in the subjects with ASD compared with the typical control subjects	topic_aut
78418	4	356224	5	NULL	NULL	0	NULL	statement 2	Process		is present in					ASD subjects	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	A significant gray matter volume reduction of both the pars opercularis and triangularis was found bilaterally in the subjects with ASD compared with the typical control subjects	topic_aut
78419	1	356225	5	NULL	NULL	0	NULL	social communication	Process	severity of;;problems of	is increased in					ASD group	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	The reduced volume of right as well as total pars opercularis showed a significant association with the increased severity of social communication problems in the ASD group	topic_aut
78420	2	356225	5	NULL	NULL	0	NULL	pars opercularis	OrganismPart	reduced volume of;;right	is associated with		significantly			statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The reduced volume of right as well as total pars opercularis showed a significant association with the increased severity of social communication problems in the ASD group	topic_aut
78421	3	356225	5	NULL	NULL	0	NULL	pars opercularis	OrganismPart	reduced volume of;;total	is associated with		significantly			statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The reduced volume of right as well as total pars opercularis showed a significant association with the increased severity of social communication problems in the ASD group	topic_aut
78422	1	356226	5	NULL	NULL	0	NULL	imitation	Process		is a type of					MN related function	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Promising research has identified that interventions targeting MN related functions such as imitation can improve social functioning in ASDs	topic_aut
78423	2	356226	5	NULL	NULL	0	NULL	interventions	Process		target					MN related function	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Promising research has identified that interventions targeting MN related functions such as imitation can improve social functioning in ASDs	topic_aut
78424	3	356226	5	NULL	NULL	0	NULL	statement 2	Process		improves					social functioning	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Promising research has identified that interventions targeting MN related functions such as imitation can improve social functioning in ASDs	topic_aut
78425	4	356226	5	NULL	NULL	0	NULL	statement 3	Process		occurs in					ASDs	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Promising research has identified that interventions targeting MN related functions such as imitation can improve social functioning in ASDs	topic_aut
77791	1	356230	7	NULL	NULL	0	NULL	bipolar disorder	MedicalFinding		risky combination with					cardiometabolic diseases	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	'Bipolar disorder and cardiometabolic diseases- a risky combination' F. Laghrissi-Thode 9th International Conference on Bipolar Disorder	topic_bd
77792	1	356231	7	NULL	NULL	NULL	NULL	Obesity	MedicalFinding		involves					body fat	PhysicalPhenomenon	accumulation of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Obesity is a medical condition in which excess body fat has accumulated to the extent that it may have an adverse effect on health. It is defined by body mass index (BMI) and further evaluated in terms of fat distribution via the waist–hip ratio and total cardiovascular risk factors.	topic_bd
77793	2	356231	7	NULL	NULL	0	NULL	statement 1	Process		adverse effect on		may have			health	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	Obesity is a medical condition in which excess body fat has accumulated to the extent that it may have an adverse effect on health. It is defined by body mass index (BMI) and further evaluated in terms of fat distribution via the waist–hip ratio and total cardiovascular risk factors.	topic_bd
77794	3	356231	7	NULL	NULL	0	NULL	Obesity	MedicalFinding		is defined by					BMI	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	Obesity is a medical condition in which excess body fat has accumulated to the extent that it may have an adverse effect on health. It is defined by body mass index (BMI) and further evaluated in terms of fat distribution via the waist–hip ratio and total cardiovascular risk factors.	topic_bd
77795	4	356231	7	NULL	NULL	0	NULL	BMI	PhysicalPhenomenon		is					body mass index	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	Obesity is a medical condition in which excess body fat has accumulated to the extent that it may have an adverse effect on health. It is defined by body mass index (BMI) and further evaluated in terms of fat distribution via the waist–hip ratio and total cardiovascular risk factors.	topic_bd
77796	1	356234	7	NULL	NULL	NULL	NULL	immunoglobulin	GP		is a type of					large Y-shaped protein	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	An antibody, also known as an immunoglobulin, is a large Y-shaped protein used by the immune system to identify and neutralize foreign objects such as bacteria and viruses.	topic_bd
77797	2	356234	7	NULL	NULL	0	NULL	Antibody	GP		also known as					immunoglobulin	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	An antibody, also known as an immunoglobulin, is a large Y-shaped protein used by the immune system to identify and neutralize foreign objects such as bacteria and viruses.	topic_bd
77798	3	356234	7	NULL	NULL	0	NULL	immunoglobulin	GP		used by					immune system	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	An antibody, also known as an immunoglobulin, is a large Y-shaped protein used by the immune system to identify and neutralize foreign objects such as bacteria and viruses.	topic_bd
77799	4	356234	7	NULL	NULL	0	NULL	immunoglobulin	GP		identify					bacteria	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	An antibody, also known as an immunoglobulin, is a large Y-shaped protein used by the immune system to identify and neutralize foreign objects such as bacteria and viruses.	topic_bd
77800	5	356234	7	NULL	NULL	0	NULL	immunoglobulin	GP		identify					virus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	An antibody, also known as an immunoglobulin, is a large Y-shaped protein used by the immune system to identify and neutralize foreign objects such as bacteria and viruses.	topic_bd
77801	6	356234	7	NULL	NULL	NULL	NULL	immunoglobulin	GP		neutralize					bacteria	Organism				NULL		NULL	NULL	NULL	NULL	NULL	NULL	An antibody, also known as an immunoglobulin, is a large Y-shaped protein used by the immune system to identify and neutralize foreign objects such as bacteria and viruses.	topic_bd
77802	7	356234	7	NULL	NULL	0	NULL	statement 4	Process		occur with					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	An antibody, also known as an immunoglobulin, is a large Y-shaped protein used by the immune system to identify and neutralize foreign objects such as bacteria and viruses.	topic_bd
77803	8	356234	7	NULL	NULL	0	NULL	immunoglobulin	GP		neutralize					virus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	An antibody, also known as an immunoglobulin, is a large Y-shaped protein used by the immune system to identify and neutralize foreign objects such as bacteria and viruses.	topic_bd
77804	9	356234	7	NULL	NULL	0	NULL	statement 5	Process		occur with					statement 8	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	An antibody, also known as an immunoglobulin, is a large Y-shaped protein used by the immune system to identify and neutralize foreign objects such as bacteria and viruses.	topic_bd
77805	10	356234	7	NULL	NULL	0	NULL	bacteria	Organism		is a type of					foreign object	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	An antibody, also known as an immunoglobulin, is a large Y-shaped protein used by the immune system to identify and neutralize foreign objects such as bacteria and viruses.	topic_bd
77806	11	356234	7	NULL	NULL	0	NULL	virus	Organism		is a type of					foreign object	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	An antibody, also known as an immunoglobulin, is a large Y-shaped protein used by the immune system to identify and neutralize foreign objects such as bacteria and viruses.	topic_bd
77807	1	356235	7	NULL	NULL	0	NULL	NMDAR	GP		is a type of					glutamate receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The NMDA receptor (NMDAR), a glutamate receptor, is the predominant molecular device for controlling synaptic plasticity and memory function.	topic_bd
77808	2	356235	7	NULL	NULL	0	NULL	NMDAR	GP		predominant					synaptic plasticity 	Process	molecular device for controlling			NULL		0	NULL	NULL	NULL	NULL	NULL	The NMDA receptor (NMDAR), a glutamate receptor, is the predominant molecular device for controlling synaptic plasticity and memory function.	topic_bd
77809	3	356235	7	NULL	NULL	0	NULL	NMDAR	GP		predominant					memory function	Process	molecular device for controlling			NULL		0	NULL	NULL	NULL	NULL	NULL	The NMDA receptor (NMDAR), a glutamate receptor, is the predominant molecular device for controlling synaptic plasticity and memory function.	topic_bd
77810	4	356235	7	NULL	NULL	0	NULL	NMDAR	GP		is					NMDA receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The NMDA receptor (NMDAR), a glutamate receptor, is the predominant molecular device for controlling synaptic plasticity and memory function.	topic_bd
77811	1	356236	7	NULL	NULL	0	NULL	Glutamic acid	AminoAcid		is a type of					 20 proteinogenic amino acids	AminoAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamic acid (abbreviated as Glu or E) is one of the 20 proteinogenic amino acids, and its codons are GAA and GAG. It is a non-essential amino acid. The carboxylate anions and salts of glutamic acid are known as glutamates. In neuroscience, glutamate is an important neurotransmitter that plays a key role in long-term potentiation and is important for learning and memory.	topic_bd
77812	2	356236	7	NULL	NULL	0	NULL	GAA	GP		codon for					Glutamic acid	AminoAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamic acid (abbreviated as Glu or E) is one of the 20 proteinogenic amino acids, and its codons are GAA and GAG. It is a non-essential amino acid. The carboxylate anions and salts of glutamic acid are known as glutamates. In neuroscience, glutamate is an important neurotransmitter that plays a key role in long-term potentiation and is important for learning and memory.	topic_bd
77813	3	356236	7	NULL	NULL	0	NULL	GAG	GP		codon for					Glutamic acid	AminoAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamic acid (abbreviated as Glu or E) is one of the 20 proteinogenic amino acids, and its codons are GAA and GAG. It is a non-essential amino acid. The carboxylate anions and salts of glutamic acid are known as glutamates. In neuroscience, glutamate is an important neurotransmitter that plays a key role in long-term potentiation and is important for learning and memory.	topic_bd
77814	4	356236	7	NULL	NULL	0	NULL	Glutamic acid	AminoAcid		abbreviated as					Glu	AminoAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamic acid (abbreviated as Glu or E) is one of the 20 proteinogenic amino acids, and its codons are GAA and GAG. It is a non-essential amino acid. The carboxylate anions and salts of glutamic acid are known as glutamates. In neuroscience, glutamate is an important neurotransmitter that plays a key role in long-term potentiation and is important for learning and memory.	topic_bd
77815	5	356236	7	NULL	NULL	0	NULL	Glutamic acid	AminoAcid		abbreviated as					E	AminoAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamic acid (abbreviated as Glu or E) is one of the 20 proteinogenic amino acids, and its codons are GAA and GAG. It is a non-essential amino acid. The carboxylate anions and salts of glutamic acid are known as glutamates. In neuroscience, glutamate is an important neurotransmitter that plays a key role in long-term potentiation and is important for learning and memory.	topic_bd
77816	6	356236	7	NULL	NULL	0	NULL	Glu	AminoAcid		is a type of					non-essential amino acid	AminoAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamic acid (abbreviated as Glu or E) is one of the 20 proteinogenic amino acids, and its codons are GAA and GAG. It is a non-essential amino acid. The carboxylate anions and salts of glutamic acid are known as glutamates. In neuroscience, glutamate is an important neurotransmitter that plays a key role in long-term potentiation and is important for learning and memory.	topic_bd
77817	7	356236	7	NULL	NULL	NULL	NULL	Glutamic acid	AminoAcid	carboxylate anions of	known as					glutamates	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glutamic acid (abbreviated as Glu or E) is one of the 20 proteinogenic amino acids, and its codons are GAA and GAG. It is a non-essential amino acid. The carboxylate anions and salts of glutamic acid are known as glutamates. In neuroscience, glutamate is an important neurotransmitter that plays a key role in long-term potentiation and is important for learning and memory.	topic_bd
77818	8	356236	7	NULL	NULL	NULL	NULL	Glutamic acid	AminoAcid	salts of	known as					glutamates	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glutamic acid (abbreviated as Glu or E) is one of the 20 proteinogenic amino acids, and its codons are GAA and GAG. It is a non-essential amino acid. The carboxylate anions and salts of glutamic acid are known as glutamates. In neuroscience, glutamate is an important neurotransmitter that plays a key role in long-term potentiation and is important for learning and memory.	topic_bd
77819	9	356236	7	NULL	NULL	0	NULL	glutamate	Chemical		is an important					neurotransmitter	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamic acid (abbreviated as Glu or E) is one of the 20 proteinogenic amino acids, and its codons are GAA and GAG. It is a non-essential amino acid. The carboxylate anions and salts of glutamic acid are known as glutamates. In neuroscience, glutamate is an important neurotransmitter that plays a key role in long-term potentiation and is important for learning and memory.	topic_bd
77820	10	356236	7	NULL	NULL	0	NULL	glutamate	Chemical		play					long-term potentiation	Process	key role in			NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamic acid (abbreviated as Glu or E) is one of the 20 proteinogenic amino acids, and its codons are GAA and GAG. It is a non-essential amino acid. The carboxylate anions and salts of glutamic acid are known as glutamates. In neuroscience, glutamate is an important neurotransmitter that plays a key role in long-term potentiation and is important for learning and memory.	topic_bd
77821	11	356236	7	NULL	NULL	0	NULL	glutamate	Chemical		is important for					learning	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamic acid (abbreviated as Glu or E) is one of the 20 proteinogenic amino acids, and its codons are GAA and GAG. It is a non-essential amino acid. The carboxylate anions and salts of glutamic acid are known as glutamates. In neuroscience, glutamate is an important neurotransmitter that plays a key role in long-term potentiation and is important for learning and memory.	topic_bd
77822	12	356236	7	NULL	NULL	0	NULL	glutamate	Chemical		is important for					memory	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamic acid (abbreviated as Glu or E) is one of the 20 proteinogenic amino acids, and its codons are GAA and GAG. It is a non-essential amino acid. The carboxylate anions and salts of glutamic acid are known as glutamates. In neuroscience, glutamate is an important neurotransmitter that plays a key role in long-term potentiation and is important for learning and memory.	topic_bd
77823	1	356237	7	NULL	NULL	0	NULL	Mitochondrial dysfunction	Process		occur in					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	"Mitochondrial dysfunction and oxidative stress in bipolar disorder" LT Young 9th International Conference on Bipolar Disorder	topic_bd
77824	2	356237	7	NULL	NULL	0	NULL	oxidative stress	Process		occur in					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	"Mitochondrial dysfunction and oxidative stress in bipolar disorder" LT Young 9th International Conference on Bipolar Disorder	topic_bd
77825	1	356238	7	NULL	NULL	0	NULL	reactive oxygen species	Chemical	production of	imbalance with					Reactive oxygen species 	Chemical	manifestation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Oxidative stress represents an imbalance between the production and manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage.	topic_bd
77826	2	356238	7	NULL	NULL	0	NULL	oxidative stress	Process		represents					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Oxidative stress represents an imbalance between the production and manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage.	topic_bd
77827	3	356238	7	NULL	NULL	0	NULL	biological system	Process		detoxify		readily			reactive intermediates	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Oxidative stress represents an imbalance between the production and manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage.	topic_bd
77828	4	356238	7	NULL	NULL	NULL	NULL	oxidative stress	Process		represents					statement 3	Process	ability of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Oxidative stress represents an imbalance between the production and manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage.	topic_bd
77829	5	356238	7	NULL	NULL	0	NULL	biological system	Process		repair					 damage	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Oxidative stress represents an imbalance between the production and manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage.	topic_bd
77830	6	356238	7	NULL	NULL	0	NULL	oxidative stress	Process		represents					statement 5	Process	ability of			NULL		0	NULL	NULL	NULL	NULL	NULL	Oxidative stress represents an imbalance between the production and manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage.	topic_bd
77831	7	356238	7	NULL	NULL	0	NULL	statement 4	Process		is an alternative to					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Oxidative stress represents an imbalance between the production and manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage.	topic_bd
77832	1	356239	7	NULL	NULL	0	NULL	Radicals	Chemical		referred to as					free radicals	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Radicals (often referred to as free radicals) are atoms, molecules, or ions with unpaired electrons on an open shell configuration. Free radicals may have positive, negative, or zero charge. With some exceptions, the unpaired electrons cause radicals to be highly chemically reactive. Radicals, if allowed to run free in the body, are believed to be involved in degenerative diseases and cancers.	topic_bd
77833	2	356239	7	NULL	NULL	0	NULL	Radicals	Chemical		is a type of					atoms	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Radicals (often referred to as free radicals) are atoms, molecules, or ions with unpaired electrons on an open shell configuration. Free radicals may have positive, negative, or zero charge. With some exceptions, the unpaired electrons cause radicals to be highly chemically reactive. Radicals, if allowed to run free in the body, are believed to be involved in degenerative diseases and cancers.	topic_bd
77834	3	356239	7	NULL	NULL	0	NULL	Radicals	Chemical		is a type of					molecule	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Radicals (often referred to as free radicals) are atoms, molecules, or ions with unpaired electrons on an open shell configuration. Free radicals may have positive, negative, or zero charge. With some exceptions, the unpaired electrons cause radicals to be highly chemically reactive. Radicals, if allowed to run free in the body, are believed to be involved in degenerative diseases and cancers.	topic_bd
77835	5	356239	7	NULL	NULL	NULL	NULL	Radicals	Chemical		is a type of					statement 4	Chemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Radicals (often referred to as free radicals) are atoms, molecules, or ions with unpaired electrons on an open shell configuration. Free radicals may have positive, negative, or zero charge. With some exceptions, the unpaired electrons cause radicals to be highly chemically reactive. Radicals, if allowed to run free in the body, are believed to be involved in degenerative diseases and cancers.	topic_bd
77836	4	356239	7	NULL	NULL	NULL	NULL	ions	Chemical		contain					unpaired electron	Chemical	an open shell configuration			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Radicals (often referred to as free radicals) are atoms, molecules, or ions with unpaired electrons on an open shell configuration. Free radicals may have positive, negative, or zero charge. With some exceptions, the unpaired electrons cause radicals to be highly chemically reactive. Radicals, if allowed to run free in the body, are believed to be involved in degenerative diseases and cancers.	topic_bd
77837	6	356239	7	NULL	NULL	0	NULL	free radicals	Chemical		have		may			positive charge	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Radicals (often referred to as free radicals) are atoms, molecules, or ions with unpaired electrons on an open shell configuration. Free radicals may have positive, negative, or zero charge. With some exceptions, the unpaired electrons cause radicals to be highly chemically reactive. Radicals, if allowed to run free in the body, are believed to be involved in degenerative diseases and cancers.	topic_bd
77838	7	356239	7	NULL	NULL	0	NULL	free radicals	Chemical		have		may			negative charge	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Radicals (often referred to as free radicals) are atoms, molecules, or ions with unpaired electrons on an open shell configuration. Free radicals may have positive, negative, or zero charge. With some exceptions, the unpaired electrons cause radicals to be highly chemically reactive. Radicals, if allowed to run free in the body, are believed to be involved in degenerative diseases and cancers.	topic_bd
77839	8	356239	7	NULL	NULL	0	NULL	free radicals	Chemical		have		may			zero charge	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Radicals (often referred to as free radicals) are atoms, molecules, or ions with unpaired electrons on an open shell configuration. Free radicals may have positive, negative, or zero charge. With some exceptions, the unpaired electrons cause radicals to be highly chemically reactive. Radicals, if allowed to run free in the body, are believed to be involved in degenerative diseases and cancers.	topic_bd
77840	9	356239	7	NULL	NULL	0	NULL	radicals	Chemical		chemically		highly			reactive	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Radicals (often referred to as free radicals) are atoms, molecules, or ions with unpaired electrons on an open shell configuration. Free radicals may have positive, negative, or zero charge. With some exceptions, the unpaired electrons cause radicals to be highly chemically reactive. Radicals, if allowed to run free in the body, are believed to be involved in degenerative diseases and cancers.	topic_bd
77841	10	356239	7	NULL	NULL	0	NULL	unpaired electrons	Chemical		cause					statement 9	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Radicals (often referred to as free radicals) are atoms, molecules, or ions with unpaired electrons on an open shell configuration. Free radicals may have positive, negative, or zero charge. With some exceptions, the unpaired electrons cause radicals to be highly chemically reactive. Radicals, if allowed to run free in the body, are believed to be involved in degenerative diseases and cancers.	topic_bd
77842	11	356239	7	NULL	NULL	0	NULL	radicals	Chemical		involved in					 degenerative diseases 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Radicals (often referred to as free radicals) are atoms, molecules, or ions with unpaired electrons on an open shell configuration. Free radicals may have positive, negative, or zero charge. With some exceptions, the unpaired electrons cause radicals to be highly chemically reactive. Radicals, if allowed to run free in the body, are believed to be involved in degenerative diseases and cancers.	topic_bd
77843	12	356239	7	NULL	NULL	0	NULL	radicals	Chemical		involved in					cancers	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Radicals (often referred to as free radicals) are atoms, molecules, or ions with unpaired electrons on an open shell configuration. Free radicals may have positive, negative, or zero charge. With some exceptions, the unpaired electrons cause radicals to be highly chemically reactive. Radicals, if allowed to run free in the body, are believed to be involved in degenerative diseases and cancers.	topic_bd
77844	13	356239	7	NULL	NULL	0	NULL	statement 6	Process		is an alternative to					statement 7	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Radicals (often referred to as free radicals) are atoms, molecules, or ions with unpaired electrons on an open shell configuration. Free radicals may have positive, negative, or zero charge. With some exceptions, the unpaired electrons cause radicals to be highly chemically reactive. Radicals, if allowed to run free in the body, are believed to be involved in degenerative diseases and cancers.	topic_bd
77845	14	356239	7	NULL	NULL	0	NULL	statement 6	Process		is an alternative to					statement 8	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Radicals (often referred to as free radicals) are atoms, molecules, or ions with unpaired electrons on an open shell configuration. Free radicals may have positive, negative, or zero charge. With some exceptions, the unpaired electrons cause radicals to be highly chemically reactive. Radicals, if allowed to run free in the body, are believed to be involved in degenerative diseases and cancers.	topic_bd
77846	1	356241	7	NULL	NULL	0	NULL	glutamate	Chemical		is involved in					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The neurotransmitter glutamate is thought to be involved in bipolar disorder.	topic_bd
77847	2	356241	7	NULL	NULL	0	NULL	glutamate	Chemical		is a type of					neurotransmitter	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The neurotransmitter glutamate is thought to be involved in bipolar disorder.	topic_bd
77848	1	356242	7	NULL	NULL	0	NULL	Body mass index	PhysicalPhenomenon		associated with		positively			CRC	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	Body mass index in early adulthood is positively associated with risk of CRC for MMR gene mutation carriers and non-carriers.British Journal of Cancer advance online publication	topic_ccc
77849	2	356242	7	NULL	NULL	0	NULL	statement 1	Process		occur in					MMR gene mutation carriers	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Body mass index in early adulthood is positively associated with risk of CRC for MMR gene mutation carriers and non-carriers.British Journal of Cancer advance online publication	topic_ccc
77850	3	356242	7	NULL	NULL	0	NULL	statement 1	Process		occur in					MMR gene mutation non-carriers	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Body mass index in early adulthood is positively associated with risk of CRC for MMR gene mutation carriers and non-carriers.British Journal of Cancer advance online publication	topic_ccc
77851	4	356242	7	NULL	NULL	0	NULL	statement 1	Process		occur in					early adulthood	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	Body mass index in early adulthood is positively associated with risk of CRC for MMR gene mutation carriers and non-carriers.British Journal of Cancer advance online publication	topic_ccc
78001	1	356245	7	NULL	NULL	NULL	NULL	cytokines	Chemical		is a type of					cell-signaling protein molecules	GP	small			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Cytokines (Greek cyto-, cell; and -kinos, movement) are small cell-signaling protein molecules that are secreted by the glial cells of the nervous system and by numerous cells of the immune system and are a category of signaling molecules used extensively in intercellular communication. Cytokines can be classified as proteins, peptides, or glycoproteins; the term "cytokine" encompasses a large and diverse family of regulators produced throughout the body by cells of diverse embryological origin.[1]	topic_bd
78002	2	356245	7	NULL	NULL	0	NULL	statement 1	Process		secreted by					nervous system	OrganismPart	glial cells of			NULL		0	NULL	NULL	NULL	NULL	NULL	Cytokines (Greek cyto-, cell; and -kinos, movement) are small cell-signaling protein molecules that are secreted by the glial cells of the nervous system and by numerous cells of the immune system and are a category of signaling molecules used extensively in intercellular communication. Cytokines can be classified as proteins, peptides, or glycoproteins; the term "cytokine" encompasses a large and diverse family of regulators produced throughout the body by cells of diverse embryological origin.[1]	topic_bd
78003	3	356245	7	NULL	NULL	NULL	NULL	statement 1	Process		secreted by					immune system	OrganismPart	cells of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Cytokines (Greek cyto-, cell; and -kinos, movement) are small cell-signaling protein molecules that are secreted by the glial cells of the nervous system and by numerous cells of the immune system and are a category of signaling molecules used extensively in intercellular communication. Cytokines can be classified as proteins, peptides, or glycoproteins; the term "cytokine" encompasses a large and diverse family of regulators produced throughout the body by cells of diverse embryological origin.[1]	topic_bd
78004	4	356245	7	NULL	NULL	0	NULL	cytokines	Chemical		used in		extensively			intercellular communication	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Cytokines (Greek cyto-, cell; and -kinos, movement) are small cell-signaling protein molecules that are secreted by the glial cells of the nervous system and by numerous cells of the immune system and are a category of signaling molecules used extensively in intercellular communication. Cytokines can be classified as proteins, peptides, or glycoproteins; the term "cytokine" encompasses a large and diverse family of regulators produced throughout the body by cells of diverse embryological origin.[1]	topic_bd
78005	5	356245	7	NULL	NULL	0	NULL	cytokines	Chemical		classified  as					proteins	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Cytokines (Greek cyto-, cell; and -kinos, movement) are small cell-signaling protein molecules that are secreted by the glial cells of the nervous system and by numerous cells of the immune system and are a category of signaling molecules used extensively in intercellular communication. Cytokines can be classified as proteins, peptides, or glycoproteins; the term "cytokine" encompasses a large and diverse family of regulators produced throughout the body by cells of diverse embryological origin.[1]	topic_bd
78006	6	356245	7	NULL	NULL	0	NULL	cytokines	Chemical		classified  as					peptides	AminoAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	Cytokines (Greek cyto-, cell; and -kinos, movement) are small cell-signaling protein molecules that are secreted by the glial cells of the nervous system and by numerous cells of the immune system and are a category of signaling molecules used extensively in intercellular communication. Cytokines can be classified as proteins, peptides, or glycoproteins; the term "cytokine" encompasses a large and diverse family of regulators produced throughout the body by cells of diverse embryological origin.[1]	topic_bd
78007	7	356245	7	NULL	NULL	0	NULL	cytokines	Chemical		classified  as					glycoproteins	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Cytokines (Greek cyto-, cell; and -kinos, movement) are small cell-signaling protein molecules that are secreted by the glial cells of the nervous system and by numerous cells of the immune system and are a category of signaling molecules used extensively in intercellular communication. Cytokines can be classified as proteins, peptides, or glycoproteins; the term "cytokine" encompasses a large and diverse family of regulators produced throughout the body by cells of diverse embryological origin.[1]	topic_bd
78008	8	356245	7	NULL	NULL	NULL	NULL	cytokines	Chemical		encompasses					regulators	Chemical	large and diverse family of 			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Cytokines (Greek cyto-, cell; and -kinos, movement) are small cell-signaling protein molecules that are secreted by the glial cells of the nervous system and by numerous cells of the immune system and are a category of signaling molecules used extensively in intercellular communication. Cytokines can be classified as proteins, peptides, or glycoproteins; the term "cytokine" encompasses a large and diverse family of regulators produced throughout the body by cells of diverse embryological origin.[1]	topic_bd
78009	9	356245	7	NULL	NULL	0	NULL	cytokines	Chemical		produced					embryological origin	OrganismPart	throughout the body cells of diverse			NULL		0	NULL	NULL	NULL	NULL	NULL	Cytokines (Greek cyto-, cell; and -kinos, movement) are small cell-signaling protein molecules that are secreted by the glial cells of the nervous system and by numerous cells of the immune system and are a category of signaling molecules used extensively in intercellular communication. Cytokines can be classified as proteins, peptides, or glycoproteins; the term "cytokine" encompasses a large and diverse family of regulators produced throughout the body by cells of diverse embryological origin.[1]	topic_bd
78010	1	356246	7	NULL	NULL	0	NULL	Somatic treatment	MedicalProcedure		treatment of					physical means	MedicalProcedure	mental illness by			NULL		0	NULL	NULL	NULL	NULL	NULL	Somatic treatment is the treatment of mental illness by physical means (such as medication, electroconvulsive therapy, or psychosurgery) rather than psychotherapy.	topic_bd
78011	2	356246	7	NULL	NULL	0	NULL	physical means	MedicalProcedure		include					medication	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Somatic treatment is the treatment of mental illness by physical means (such as medication, electroconvulsive therapy, or psychosurgery) rather than psychotherapy.	topic_bd
78012	3	356246	7	NULL	NULL	0	NULL	physical means	MedicalProcedure		include					electroconvulsive therapy	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Somatic treatment is the treatment of mental illness by physical means (such as medication, electroconvulsive therapy, or psychosurgery) rather than psychotherapy.	topic_bd
78013	4	356246	7	NULL	NULL	0	NULL	physical means	MedicalProcedure		include					 psychosurgery	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Somatic treatment is the treatment of mental illness by physical means (such as medication, electroconvulsive therapy, or psychosurgery) rather than psychotherapy.	topic_bd
78014	5	356246	7	NULL	NULL	0	NULL	physical means	MedicalProcedure		does not mean					psychotherapy	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Somatic treatment is the treatment of mental illness by physical means (such as medication, electroconvulsive therapy, or psychosurgery) rather than psychotherapy.	topic_bd
77852	1	356247	7	NULL	NULL	0	NULL	cerebral cortex	OrganismPart	 temporal lobe of	located beneath					Sylvian fissure	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The temporal lobe is a region of the cerebral cortex that is located beneath the Sylvian fissure on both cerebral hemispheres of the mammalian brain.	topic_bd
77853	2	356247	7	NULL	NULL	0	NULL	statement 1	Process		present on					mammalian brain	OrganismPart	cerebral hemispheres of			NULL		0	NULL	NULL	NULL	NULL	NULL	The temporal lobe is a region of the cerebral cortex that is located beneath the Sylvian fissure on both cerebral hemispheres of the mammalian brain.	topic_bd
77854	1	356248	7	NULL	NULL	NULL	NULL	basal ganglia	OrganismPart		group of					nuclei	CellComponent				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The basal ganglia (or basal nuclei) are a group of nuclei of varied origin (mostly telencephalic embryonal origin, with some diencephalic and mesencephalic elements) in the brains of vertebrates that act as a cohesive functional unit.	topic_bd
77855	2	356248	7	NULL	NULL	0	NULL	statement 1	Process		belongs to					telencephalic embryonal origin	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	The basal ganglia (or basal nuclei) are a group of nuclei of varied origin (mostly telencephalic embryonal origin, with some diencephalic and mesencephalic elements) in the brains of vertebrates that act as a cohesive functional unit.	topic_bd
77856	3	356248	7	NULL	NULL	0	NULL	statement 1	Process		belongs to					diencephalic element	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The basal ganglia (or basal nuclei) are a group of nuclei of varied origin (mostly telencephalic embryonal origin, with some diencephalic and mesencephalic elements) in the brains of vertebrates that act as a cohesive functional unit.	topic_bd
77857	4	356248	7	NULL	NULL	0	NULL	statement 1	Process		belongs to					mesencephalic elements	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The basal ganglia (or basal nuclei) are a group of nuclei of varied origin (mostly telencephalic embryonal origin, with some diencephalic and mesencephalic elements) in the brains of vertebrates that act as a cohesive functional unit.	topic_bd
77858	5	356248	7	NULL	NULL	0	NULL	basal ganglia	CellComponent		present in					vertebrates	Organism	brains of			NULL		0	NULL	NULL	NULL	NULL	NULL	The basal ganglia (or basal nuclei) are a group of nuclei of varied origin (mostly telencephalic embryonal origin, with some diencephalic and mesencephalic elements) in the brains of vertebrates that act as a cohesive functional unit.	topic_bd
77859	6	356248	7	NULL	NULL	0	NULL	basal ganglia	OrganismPart		act as a					cohesive functional unit	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The basal ganglia (or basal nuclei) are a group of nuclei of varied origin (mostly telencephalic embryonal origin, with some diencephalic and mesencephalic elements) in the brains of vertebrates that act as a cohesive functional unit.	topic_bd
77860	1	356249	7	NULL	NULL	0	NULL	Thyroid disorders	MedicalFinding		include					hyperthyroidism 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Thyroid disorders include hyperthyroidism (abnormally increased activity), hypothyroidism (abnormally decreased activity) and thyroid nodules, which are generally benign thyroid neoplasms, but may be thyroid cancers.	topic_bd
77861	2	356249	7	NULL	NULL	0	NULL	Thyroid disorders	MedicalFinding		include					hypothyroidism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Thyroid disorders include hyperthyroidism (abnormally increased activity), hypothyroidism (abnormally decreased activity) and thyroid nodules, which are generally benign thyroid neoplasms, but may be thyroid cancers.	topic_bd
77862	3	356249	7	NULL	NULL	0	NULL	Thyroid disorders	MedicalFinding		include					thyroid nodules	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Thyroid disorders include hyperthyroidism (abnormally increased activity), hypothyroidism (abnormally decreased activity) and thyroid nodules, which are generally benign thyroid neoplasms, but may be thyroid cancers.	topic_bd
77863	4	356249	7	NULL	NULL	0	NULL	thyroid nodules	OrganismPart		benign		generally			thyroid neoplasms	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Thyroid disorders include hyperthyroidism (abnormally increased activity), hypothyroidism (abnormally decreased activity) and thyroid nodules, which are generally benign thyroid neoplasms, but may be thyroid cancers.	topic_bd
77864	5	356249	7	NULL	NULL	0	NULL	thyroid neoplasms	OrganismPart		may be					thyroid cancers	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Thyroid disorders include hyperthyroidism (abnormally increased activity), hypothyroidism (abnormally decreased activity) and thyroid nodules, which are generally benign thyroid neoplasms, but may be thyroid cancers.	topic_bd
77865	6	356249	7	NULL	NULL	0	NULL	Hyperthyroidism	MedicalFinding		shows					abnormal increased activity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Thyroid disorders include hyperthyroidism (abnormally increased activity), hypothyroidism (abnormally decreased activity) and thyroid nodules, which are generally benign thyroid neoplasms, but may be thyroid cancers.	topic_bd
77866	7	356249	7	NULL	NULL	0	NULL	Hypothyroidism 	MedicalFinding		shows					abnormal decreased activity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Thyroid disorders include hyperthyroidism (abnormally increased activity), hypothyroidism (abnormally decreased activity) and thyroid nodules, which are generally benign thyroid neoplasms, but may be thyroid cancers.	topic_bd
77867	1	356250	7	NULL	NULL	0	NULL	thyroid gland	OrganismPart		is found in					neck	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The thyroid gland is found in the neck, below (inferior to) the thyroid cartilage (which forms the laryngeal prominence, or 'Adam's Apple').	topic_bd
77868	2	356250	7	NULL	NULL	0	NULL	thyroid gland	OrganismPart		is found below					thyroid cartilage	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The thyroid gland is found in the neck, below (inferior to) the thyroid cartilage (which forms the laryngeal prominence, or 'Adam's Apple').	topic_bd
77869	3	356250	7	NULL	NULL	0	NULL	thryoid cartilage	OrganismPart		forms					laryngeal prominence	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The thyroid gland is found in the neck, below (inferior to) the thyroid cartilage (which forms the laryngeal prominence, or 'Adam's Apple').	topic_bd
77870	4	356250	7	NULL	NULL	0	NULL	laryngeal prominence	OrganismPart		is known as					Adam's apple	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The thyroid gland is found in the neck, below (inferior to) the thyroid cartilage (which forms the laryngeal prominence, or 'Adam's Apple').	topic_bd
77871	1	356251	7	NULL	NULL	0	NULL	hypothalamus	OrganismPart		is a portion of					brain	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The Hypothalamus  is a portion of the brain that contains a number of small nuclei with a variety of functions.	topic_bd
77872	2	356251	7	NULL	NULL	0	NULL	hypothalamus	OrganismPart		contains					small nuclei	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	The Hypothalamus  is a portion of the brain that contains a number of small nuclei with a variety of functions.	topic_bd
77873	1	356252	7	NULL	NULL	0	NULL	abnormal gene expression	Process		is defined as					gene	GP	transcription of below normal levels of			NULL		0	NULL	NULL	NULL	NULL	NULL	Abnormal gene expression is the transcription of a gene above or below normal levels.	topic_bd
77874	2	356252	7	NULL	NULL	NULL	NULL	abnormal gene expression	Process		is defined as					gene	GP	transcription of above normal levels of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Abnormal gene expression is the transcription of a gene above or below normal levels.	topic_bd
77875	1	356253	7	NULL	NULL	0	NULL	Bipolar disorder	MedicalFinding		referred to as					bipolar affective disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar disorder or manic–depressive disorder, also referred to as bipolar affective disorder or manic depression, is a psychiatric diagnosis that describes a category of mood disorders defined by the presence of one or more episodes of abnormally elevated energy levels, cognition, and mood with or without one or more depressive episodes.	topic_bd
77876	2	356253	7	NULL	NULL	0	NULL	manic depressive disorder	MedicalFinding		referred to as					manic depression 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar disorder or manic–depressive disorder, also referred to as bipolar affective disorder or manic depression, is a psychiatric diagnosis that describes a category of mood disorders defined by the presence of one or more episodes of abnormally elevated energy levels, cognition, and mood with or without one or more depressive episodes.	topic_bd
77877	3	356253	7	NULL	NULL	0	NULL	bipolar disorder	MedicalFinding		is a type of					psychiatric diagnosis	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar disorder or manic–depressive disorder, also referred to as bipolar affective disorder or manic depression, is a psychiatric diagnosis that describes a category of mood disorders defined by the presence of one or more episodes of abnormally elevated energy levels, cognition, and mood with or without one or more depressive episodes.	topic_bd
77878	4	356253	7	NULL	NULL	0	NULL	manic depressive disorder	MedicalFinding		is a type of					psychiatric diagnosis	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar disorder or manic–depressive disorder, also referred to as bipolar affective disorder or manic depression, is a psychiatric diagnosis that describes a category of mood disorders defined by the presence of one or more episodes of abnormally elevated energy levels, cognition, and mood with or without one or more depressive episodes.	topic_bd
77879	5	356253	7	NULL	NULL	0	NULL	bipolar disorder	MedicalFinding		describes					mood disorders	MedicalFinding	category of			NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar disorder or manic–depressive disorder, also referred to as bipolar affective disorder or manic depression, is a psychiatric diagnosis that describes a category of mood disorders defined by the presence of one or more episodes of abnormally elevated energy levels, cognition, and mood with or without one or more depressive episodes.	topic_bd
77880	6	356253	7	NULL	NULL	0	NULL	mood disorders	MedicalFinding		defined by					energy levels	MentalProcess	episodes of abnormally elevated			NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar disorder or manic–depressive disorder, also referred to as bipolar affective disorder or manic depression, is a psychiatric diagnosis that describes a category of mood disorders defined by the presence of one or more episodes of abnormally elevated energy levels, cognition, and mood with or without one or more depressive episodes.	topic_bd
77881	7	356253	7	NULL	NULL	0	NULL	mood disorders	MedicalFinding		defined by					cognition	MentalProcess	presence of			NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar disorder or manic–depressive disorder, also referred to as bipolar affective disorder or manic depression, is a psychiatric diagnosis that describes a category of mood disorders defined by the presence of one or more episodes of abnormally elevated energy levels, cognition, and mood with or without one or more depressive episodes.	topic_bd
77882	8	356253	7	NULL	NULL	0	NULL	mood disorders	MedicalFinding		defined by					depressive episodes	MentalProcess	mood with			NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar disorder or manic–depressive disorder, also referred to as bipolar affective disorder or manic depression, is a psychiatric diagnosis that describes a category of mood disorders defined by the presence of one or more episodes of abnormally elevated energy levels, cognition, and mood with or without one or more depressive episodes.	topic_bd
77883	9	356253	7	NULL	NULL	0	NULL	mood disorders	MedicalFinding		defined by					depressive episodes	MedicalFinding	mood without			NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar disorder or manic–depressive disorder, also referred to as bipolar affective disorder or manic depression, is a psychiatric diagnosis that describes a category of mood disorders defined by the presence of one or more episodes of abnormally elevated energy levels, cognition, and mood with or without one or more depressive episodes.	topic_bd
77884	10	356253	7	NULL	NULL	0	NULL	statement 8	Process		is an alternative to					statement 9	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar disorder or manic–depressive disorder, also referred to as bipolar affective disorder or manic depression, is a psychiatric diagnosis that describes a category of mood disorders defined by the presence of one or more episodes of abnormally elevated energy levels, cognition, and mood with or without one or more depressive episodes.	topic_bd
77885	11	356253	7	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Bipolar disorder or manic–depressive disorder, also referred to as bipolar affective disorder or manic depression, is a psychiatric diagnosis that describes a category of mood disorders defined by the presence of one or more episodes of abnormally elevated energy levels, cognition, and mood with or without one or more depressive episodes.	topic_bd
77886	1	356254	7	NULL	NULL	0	NULL	Neurotransmitters	Chemical		is a type of					endogenous chemicals	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Neurotransmitters are endogenous chemicals that transmit signals from a neuron to a target cell across a synapse, and their dysfunction is associated with neurotransmitter diseases such as bipolar disorder.	topic_bd
77887	2	356254	7	NULL	NULL	NULL	NULL	neuron	Cell	signal from	transmitted to					target cell	Cell				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Neurotransmitters are endogenous chemicals that transmit signals from a neuron to a target cell across a synapse, and their dysfunction is associated with neurotransmitter diseases such as bipolar disorder.	topic_bd
77888	3	356254	7	NULL	NULL	0	NULL	statement 2	Process		via					synapse	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	Neurotransmitters are endogenous chemicals that transmit signals from a neuron to a target cell across a synapse, and their dysfunction is associated with neurotransmitter diseases such as bipolar disorder.	topic_bd
77889	4	356254	7	NULL	NULL	NULL	NULL	statement 3	Chemical	dysfunction of	associated with					bipolar disorder	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Neurotransmitters are endogenous chemicals that transmit signals from a neuron to a target cell across a synapse, and their dysfunction is associated with neurotransmitter diseases such as bipolar disorder.	topic_bd
77890	5	356254	7	NULL	NULL	0	NULL	bipolar disorder	MedicalFinding		is a type of					neurotransmitter disease	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Neurotransmitters are endogenous chemicals that transmit signals from a neuron to a target cell across a synapse, and their dysfunction is associated with neurotransmitter diseases such as bipolar disorder.	topic_bd
77891	1	356255	7	NULL	NULL	NULL	NULL	amygdala activation	Process	abnormal	is a state of					amygdala	OrganismPart	activity of above normal levels of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Abnormal amygdala activation is a state of activity of the amygdala above or below normal levels.	topic_bd
77892	2	356255	7	NULL	NULL	0	NULL	amygdala activation	Process	abnormal	is a state of					amygdala	OrganismPart	activity of below normal levels of			NULL		0	NULL	NULL	NULL	NULL	NULL	Abnormal amygdala activation is a state of activity of the amygdala above or below normal levels.	topic_bd
77893	1	356256	7	NULL	NULL	NULL	NULL	Memory loss	MentalProcess		decrease in					remember	MentalProcess	ability to			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Memory loss is the decrease in the ability to remember.	topic_bd
77894	1	356257	7	NULL	NULL	0	NULL	hypomania	MedicalFinding		is a type of					mood state	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Hypomania is a mood state characterized by persistent and pervasive elevated (euphoric) or irritable mood, as well as thoughts and behaviors that are consistent with such a mood state.	topic_bd
77895	2	356257	7	NULL	NULL	0	NULL	hypomania	MedicalFinding		characterized by					elevated mood	MentalProcess	persistent			NULL		0	NULL	NULL	NULL	NULL	NULL	Hypomania is a mood state characterized by persistent and pervasive elevated (euphoric) or irritable mood, as well as thoughts and behaviors that are consistent with such a mood state.	topic_bd
77896	3	356257	7	NULL	NULL	0	NULL	hypomania	MedicalFinding		characterized by					irritable mood	MentalProcess	persistent 			NULL		0	NULL	NULL	NULL	NULL	NULL	Hypomania is a mood state characterized by persistent and pervasive elevated (euphoric) or irritable mood, as well as thoughts and behaviors that are consistent with such a mood state.	topic_bd
77897	4	356257	7	NULL	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Hypomania is a mood state characterized by persistent and pervasive elevated (euphoric) or irritable mood, as well as thoughts and behaviors that are consistent with such a mood state.	topic_bd
77898	5	356257	7	NULL	NULL	0	NULL	hypomania	MedicalFinding		characterized by					elevated mood	MentalProcess	pervasive			NULL		0	NULL	NULL	NULL	NULL	NULL	Hypomania is a mood state characterized by persistent and pervasive elevated (euphoric) or irritable mood, as well as thoughts and behaviors that are consistent with such a mood state.	topic_bd
77899	6	356257	7	NULL	NULL	0	NULL	hypomania	MedicalFinding		characterized by					irritable mood	MentalProcess	pervasive			NULL		0	NULL	NULL	NULL	NULL	NULL	Hypomania is a mood state characterized by persistent and pervasive elevated (euphoric) or irritable mood, as well as thoughts and behaviors that are consistent with such a mood state.	topic_bd
77900	7	356257	7	NULL	NULL	0	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Hypomania is a mood state characterized by persistent and pervasive elevated (euphoric) or irritable mood, as well as thoughts and behaviors that are consistent with such a mood state.	topic_bd
77901	1	356258	7	NULL	NULL	0	NULL	abnormal brain structure	OrganismPart		deviates from					brain structure	OrganismPart	norm			NULL		0	NULL	NULL	NULL	NULL	NULL	An abnormal brain structure is a brain structure which deviates from the norm.	topic_bd
78426	1	356259	5	NULL	NULL	0	NULL	low-line animals	Organism		treated with					GLYX-13	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Treatment of low-line animals with the NMDAR glycine site partial agonist GLYX-13 rescued the deficits in play-induced pro-social 50-kHz and reduced monotonous USVs.	topic_aut
78427	2	356259	5	NULL	NULL	0	NULL	GLYX-13	Chemical		is a partial agonist of					NMDAR 	GP		glycine site		NULL		0	NULL	NULL	NULL	NULL	NULL	Treatment of low-line animals with the NMDAR glycine site partial agonist GLYX-13 rescued the deficits in play-induced pro-social 50-kHz and reduced monotonous USVs.	topic_aut
78428	3	356259	5	NULL	NULL	0	NULL	statement 1	Process		reduce					USVs	Process	monotonous			NULL		0	NULL	NULL	NULL	NULL	NULL	Treatment of low-line animals with the NMDAR glycine site partial agonist GLYX-13 rescued the deficits in play-induced pro-social 50-kHz and reduced monotonous USVs.	topic_aut
78429	1	356260	5	NULL	NULL	0	NULL	CNVs	NucleicAcid	multiple;;recurrent;; de novo	is associated with		strongly			autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Multiple Recurrent De Novo CNVs, Including Duplications of the 7q11.23 Williams Syndrome Region, Are Strongly Associated with Autism.	topic_aut
78430	2	356260	5	NULL	NULL	0	NULL	CNVs	NucleicAcid	multiple;;recurrent;; de novo	include					7q11.23	Chromosome	duplications of			NULL		0	NULL	NULL	NULL	NULL	NULL	Multiple Recurrent De Novo CNVs, Including Duplications of the 7q11.23 Williams Syndrome Region, Are Strongly Associated with Autism.	topic_aut
78431	3	356260	5	NULL	NULL	0	NULL	7q11.23	Chromosome		is					Williams Syndrome region	Chromosome				NULL		0	NULL	NULL	NULL	NULL	NULL	Multiple Recurrent De Novo CNVs, Including Duplications of the 7q11.23 Williams Syndrome Region, Are Strongly Associated with Autism.	topic_aut
78432	1	356262	5	NULL	NULL	0	NULL	ARX gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78433	2	356262	5	NULL	NULL	0	NULL	ARX gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78434	3	356262	5	NULL	NULL	0	NULL	ATRX gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78435	4	356262	5	NULL	NULL	0	NULL	ATRX gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78436	5	356262	5	NULL	NULL	NULL	NULL	CACNA1C gene	GP		cause					syndromic autism	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78437	6	356262	5	NULL	NULL	0	NULL	CACNA1C gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78438	7	356262	5	NULL	NULL	0	NULL	CDKL5 gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78439	8	356262	5	NULL	NULL	0	NULL	CDKL5 gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78440	9	356262	5	NULL	NULL	0	NULL	EML1 gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78441	10	356262	5	NULL	NULL	0	NULL	EML1 gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78442	11	356262	5	NULL	NULL	0	NULL	FMR1 gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78443	12	356262	5	NULL	NULL	0	NULL	FMR1 gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78444	13	356262	5	NULL	NULL	0	NULL	FOXP2 gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78445	14	356262	5	NULL	NULL	0	NULL	FOXP2 gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78446	15	356262	5	NULL	NULL	0	NULL	GRID2 gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78447	16	356262	5	NULL	NULL	0	NULL	GRID2 gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78448	17	356262	5	NULL	NULL	0	NULL	HOXA1 gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78449	18	356262	5	NULL	NULL	0	NULL	HOXA1 gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78450	19	356262	5	NULL	NULL	0	NULL	KCTD13 gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78451	20	356262	5	NULL	NULL	0	NULL	KCTD13 gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78452	21	356262	5	NULL	NULL	0	NULL	MAPK3 gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78453	2	356262	5	NULL	NULL	NULL	NULL	MAPK3 gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78454	22	356262	5	NULL	NULL	0	NULL	MAPK3 gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78455	23	356262	5	NULL	NULL	0	NULL	MECP2 gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78456	24	356262	5	NULL	NULL	0	NULL	MECP2 gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78457	25	356262	5	NULL	NULL	0	NULL	NLGN3 gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78458	26	356262	5	NULL	NULL	0	NULL	NLGN3 gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78459	27	356262	5	NULL	NULL	0	NULL	NLGN4X gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78460	28	356262	5	NULL	NULL	0	NULL	NLGN4X gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78461	29	356262	5	NULL	NULL	0	NULL	PTEN gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78462	30	356262	5	NULL	NULL	0	NULL	PTEN gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78463	31	356262	5	NULL	NULL	0	NULL	RS1 gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78464	32	356262	5	NULL	NULL	0	NULL	RS1 gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78465	33	356262	5	NULL	NULL	0	NULL	SHANK3 gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78466	34	356262	5	NULL	NULL	0	NULL	SHANK3 gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78467	35	356262	5	NULL	NULL	0	NULL	SLC25A12 gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78468	36	356262	5	NULL	NULL	0	NULL	SLC25A12 gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78469	37	356262	5	NULL	NULL	0	NULL	TSC1 gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78470	38	356262	5	NULL	NULL	0	NULL	TSC1 gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78471	39	356262	5	NULL	NULL	0	NULL	TSC2 gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78472	40	356262	5	NULL	NULL	0	NULL	TSC2 gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78473	41	356262	5	NULL	NULL	0	NULL	UBE3A gene	GP		cause					syndromic autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
78474	42	356262	5	NULL	NULL	0	NULL	UBE3A gene	GP		cause					other cognitive disorders	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	We sequenced a total of 21 genes (ARX, ATRX, CACNA1C, CDKL5, EML1, FMR1, FOXP2, GRID2, HOXA1, KCTD13, MAPK3, MECP2, NLGN3, NLGN4X, PTEN, RS1, SHANK3, SLC25A12, TSC1, TSC2 and UBE3A) known to cause syndromic autism and other cognitive disorders	topic_aut
77902	1	356263	7	NULL	NULL	0	NULL	copper-64-diacetyl-bis (N4-methylthiosemicarbazone)	Chemical		reduces					tumorigenic cells	Cell	CD133+ highly			NULL		0	NULL	NULL	NULL	NULL	NULL	Internal radiotherapy with copper-64-diacetyl-bis (N4-methylthiosemicarbazone) reduces CD133+ highly tumorigenic cells and metastatic ability of mouse colon carcinoma.	topic_ccc
77903	2	356263	7	NULL	NULL	NULL	NULL	copper-64-diacetyl-bis (N4-methylthiosemicarbazone)	Chemical		reduces					 colon carcinoma	MedicalFinding	metastatic ability of mouse			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Internal radiotherapy with copper-64-diacetyl-bis (N4-methylthiosemicarbazone) reduces CD133+ highly tumorigenic cells and metastatic ability of mouse colon carcinoma.	topic_ccc
77904	1	356264	7	NULL	NULL	0	NULL	transgelin	GP		associate with					lymph node metastasis	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Association of the actin-binding protein transgelin with lymph node metastasis in human colorectal cancer.	topic_ccc
77905	2	356264	7	NULL	NULL	0	NULL	statement 1	Process		occur in					colorectal cancer	MedicalFinding	human			NULL		0	NULL	NULL	NULL	NULL	NULL	Association of the actin-binding protein transgelin with lymph node metastasis in human colorectal cancer.	topic_ccc
77906	3	356264	7	NULL	NULL	0	NULL	transgelin	GP		is a type of					actin-binding protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Association of the actin-binding protein transgelin with lymph node metastasis in human colorectal cancer.	topic_ccc
77907	1	356265	7	NULL	NULL	NULL	NULL	total dietary fat 	Food	intake of	associated with					colon cancer	MedicalFinding	risk of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	As with breast cancer, international comparisons initially suggested an association between total dietary fat intake and colon cancer risk.	topic_ccc
77908	1	356266	7	NULL	NULL	NULL	NULL	intratumoral regions	OrganismPart		shows					CD133(+) cells	Cell	high density of			NULL	mouse colon carcinoma (Colon-26) model	NULL	NULL	NULL	NULL	NULL	NULL	 In a mouse colon carcinoma (Colon-26) model, we have shown that (64)Cu-ATSM preferentially localizes in intratumoral regions with a high density of CD133(+) cells, which show characteristics of cancer stem cells or cancer stem cell-like cells (collectively referred here as CSCs).	topic_ccc
77909	2	356266	7	NULL	NULL	NULL	NULL	(64)Cu-ATSM	Chemical		localizes in		preferentially			statement 1	Process				NULL	mouse colon carcinoma (Colon-26) model	NULL	NULL	NULL	NULL	NULL	NULL	 In a mouse colon carcinoma (Colon-26) model, we have shown that (64)Cu-ATSM preferentially localizes in intratumoral regions with a high density of CD133(+) cells, which show characteristics of cancer stem cells or cancer stem cell-like cells (collectively referred here as CSCs).	topic_ccc
77910	3	356266	7	NULL	NULL	NULL	NULL	CD133(+) cells	Cell		shows					cancer stem cells	Cell	characteristics of			NULL	mouse colon carcinoma (Colon-26) model	NULL	NULL	NULL	NULL	NULL	NULL	 In a mouse colon carcinoma (Colon-26) model, we have shown that (64)Cu-ATSM preferentially localizes in intratumoral regions with a high density of CD133(+) cells, which show characteristics of cancer stem cells or cancer stem cell-like cells (collectively referred here as CSCs).	topic_ccc
77911	4	356266	7	NULL	NULL	NULL	NULL	CD133(+) cells	Cell		shows					CSCs	Cell	characteristics of			NULL	mouse colon carcinoma (Colon-26) model	NULL	NULL	NULL	NULL	NULL	NULL	 In a mouse colon carcinoma (Colon-26) model, we have shown that (64)Cu-ATSM preferentially localizes in intratumoral regions with a high density of CD133(+) cells, which show characteristics of cancer stem cells or cancer stem cell-like cells (collectively referred here as CSCs).	topic_ccc
77912	5	356266	7	NULL	NULL	NULL	NULL	CSCs	Cell		is					cancer stem cell-like cells 	Cell				NULL	mouse colon carcinoma (Colon-26) model	NULL	NULL	NULL	NULL	NULL	NULL	 In a mouse colon carcinoma (Colon-26) model, we have shown that (64)Cu-ATSM preferentially localizes in intratumoral regions with a high density of CD133(+) cells, which show characteristics of cancer stem cells or cancer stem cell-like cells (collectively referred here as CSCs).	topic_ccc
77913	1	356268	7	NULL	NULL	0	NULL	64)Cu-ATSM	Chemical		inhibit					tumor growth	Process				NULL	in vivo	0	NULL	NULL	NULL	NULL	NULL	In vivo studies showed that (64)Cu-ATSM treatment inhibited tumor growth. The percentage of CD133(+) cells and metastatic ability in (64)Cu-ATSM treated tumors was decreased compared with that in control animals.	topic_ccc
77914	1	356269	7	NULL	NULL	NULL	NULL	(64)Cu-ATSM	Chemical		accumulates in					cells	Cell				NULL	in vitro	NULL	NULL	NULL	NULL	NULL	NULL	 In vitro studies demonstrated that (64)Cu-ATSM accumulated in cells under hypoxic conditions and incorporation of (64)Cu-ATSM under hypoxia caused cell death in both CD133(+) and CD133(-) cells in a similar extent.	topic_ccc
77915	2	356269	7	NULL	NULL	0	NULL	statement 1	Process		occur under					hypoxic condition	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 In vitro studies demonstrated that (64)Cu-ATSM accumulated in cells under hypoxic conditions and incorporation of (64)Cu-ATSM under hypoxia caused cell death in both CD133(+) and CD133(-) cells in a similar extent.	topic_ccc
77916	3	356269	7	NULL	NULL	NULL	NULL	statement 2	Process		cause					 CD133(+) cells	Cell	cell death of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	 In vitro studies demonstrated that (64)Cu-ATSM accumulated in cells under hypoxic conditions and incorporation of (64)Cu-ATSM under hypoxia caused cell death in both CD133(+) and CD133(-) cells in a similar extent.	topic_ccc
77917	4	356269	7	NULL	NULL	0	NULL	statement 2	Process		cause					CD133(-) cells	Cell	cell death of			NULL		0	NULL	NULL	NULL	NULL	NULL	 In vitro studies demonstrated that (64)Cu-ATSM accumulated in cells under hypoxic conditions and incorporation of (64)Cu-ATSM under hypoxia caused cell death in both CD133(+) and CD133(-) cells in a similar extent.	topic_ccc
77918	5	356269	7	NULL	NULL	0	NULL	statement 3	Process		is similar to					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 In vitro studies demonstrated that (64)Cu-ATSM accumulated in cells under hypoxic conditions and incorporation of (64)Cu-ATSM under hypoxia caused cell death in both CD133(+) and CD133(-) cells in a similar extent.	topic_ccc
77919	1	356270	7	NULL	NULL	0	NULL	Cu-ATSM	Chemical		reduce					tumor	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Cu-ATSM administration reduced tumor volume as well as the percentage of CD133(+) cells and the metastatic ability of Colon-26 tumors.	topic_ccc
77920	2	356270	7	NULL	NULL	0	NULL	Cu-ATSM	Chemical		reduce					CD133(+) cells	Cell	percentage of			NULL		0	NULL	NULL	NULL	NULL	NULL	Cu-ATSM administration reduced tumor volume as well as the percentage of CD133(+) cells and the metastatic ability of Colon-26 tumors.	topic_ccc
77921	3	356270	7	NULL	NULL	0	NULL	Cu-ATSM	Chemical		reduce					Colon-26 tumors	MedicalFinding	metastatic ability of			NULL		0	NULL	NULL	NULL	NULL	NULL	Cu-ATSM administration reduced tumor volume as well as the percentage of CD133(+) cells and the metastatic ability of Colon-26 tumors.	topic_ccc
77922	1	356271	7	NULL	NULL	NULL	NULL	MZF	Chemical		upregulate					CD80	Cell	expression of			NULL	bone marrow DCs	NULL	NULL	NULL	NULL	NULL	NULL	In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
77923	2	356271	7	NULL	NULL	NULL	NULL	MZF	Chemical		upregulate					CD86	Cell	expression of			NULL	bone marrow DCs	NULL	NULL	NULL	NULL	NULL	NULL	In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
77924	3	356271	7	NULL	NULL	NULL	NULL	MZF	Chemical		upregulate					CD83	Cell	expression of			NULL	bone marrow DCs	NULL	NULL	NULL	NULL	NULL	NULL	In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
77925	4	356271	7	NULL	NULL	NULL	NULL	MZF	Chemical		upregulate					MHC II	Cell	expression of			NULL	bone marrow DCs	NULL	NULL	NULL	NULL	NULL	NULL	In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
77926	5	356271	7	NULL	NULL	0	NULL	bone marrow DCs	Cell		is					bone marrow-derived dendritic cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
77927	6	356271	7	NULL	NULL	0	NULL	DCs	Cell		produce					IL-12	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
77928	7	356271	7	NULL	NULL	NULL	NULL	DCs	Cell		produce					tumor necrosis factor-alpha	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
77929	8	356271	7	NULL	NULL	0	NULL	MZF	Chemical		increase		dose-dependently;;significantly			statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
77930	9	356271	7	NULL	NULL	0	NULL	MZF	Chemical		increase		dose-dependently;;significantly			statement 7	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
77931	10	356271	7	NULL	NULL	0	NULL	IL-12	GP		is					interleukin-12	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	In this study, we demonstrated that MZF upregulated the expression of CD80, CD86, CD83, and MHC II on bone marrow-derived dendritic cells (DCs) and significantly increased interleukin-12 (IL-12) and tumor necrosis factor-alpha production by DCs in a dose-dependent manner.	topic_ccc
77932	1	356273	7	NULL	NULL	0	NULL	GH1 gene	GP		encode					somatotropin	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Somatotropin is a protein that in humans is encoded by the GH1 gene.	topic_ccc
77933	2	356273	7	NULL	NULL	0	NULL	statement 1	Process		occur in					human	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Somatotropin is a protein that in humans is encoded by the GH1 gene.	topic_ccc
77934	1	356274	7	NULL	NULL	0	NULL	Growth Factor	GP		functions to					cell division	Process	regulate			NULL		0	NULL	NULL	NULL	NULL	NULL	Growth Factor is a protein molecule made by the body; it functions to regulate cell division & cell survival.	topic_ccc
77935	2	356274	7	NULL	NULL	0	NULL	Growth Factor	GP		functions to					cell survival	Process	regulate			NULL		0	NULL	NULL	NULL	NULL	NULL	Growth Factor is a protein molecule made by the body; it functions to regulate cell division & cell survival.	topic_ccc
77936	3	356274	7	NULL	NULL	0	NULL	Growth Factor	GP		is a type of					protein molecule	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Growth Factor is a protein molecule made by the body; it functions to regulate cell division & cell survival.	topic_ccc
77937	1	356275	7	NULL	NULL	0	NULL	alpha-defensin	GP	expression of	is enhanced in					colon cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	It is known that alpha-defensin expression is enhanced in colon cancer. 	topic_ccc
77938	1	356276	7	NULL	NULL	0	NULL	MZF	Chemical		inhibit		significantly			tumor growth	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	We previously isolated the novel heteropolysaccharide maitake Z-fraction (MZF) from the maitake mushroom (Grifola frondosa), and demonstrated that MZF significantly inhibited tumor growth by inducing cell-mediated immunity.	topic_ccc
77939	2	356276	7	NULL	NULL	0	NULL	statement 1	Process		occur by					cell-mediated immunity	Process	inducing			NULL		0	NULL	NULL	NULL	NULL	NULL	We previously isolated the novel heteropolysaccharide maitake Z-fraction (MZF) from the maitake mushroom (Grifola frondosa), and demonstrated that MZF significantly inhibited tumor growth by inducing cell-mediated immunity.	topic_ccc
77940	3	356276	7	NULL	NULL	0	NULL	MZF	Chemical		is					maitake Z-fraction	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	We previously isolated the novel heteropolysaccharide maitake Z-fraction (MZF) from the maitake mushroom (Grifola frondosa), and demonstrated that MZF significantly inhibited tumor growth by inducing cell-mediated immunity.	topic_ccc
77941	4	356276	7	NULL	NULL	0	NULL	MZF	Chemical		is a type of					novel heteropolysaccharide	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	We previously isolated the novel heteropolysaccharide maitake Z-fraction (MZF) from the maitake mushroom (Grifola frondosa), and demonstrated that MZF significantly inhibited tumor growth by inducing cell-mediated immunity.	topic_ccc
77942	5	356276	7	NULL	NULL	0	NULL	MZF	Chemical		obtained from					maitake mushroom 	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	We previously isolated the novel heteropolysaccharide maitake Z-fraction (MZF) from the maitake mushroom (Grifola frondosa), and demonstrated that MZF significantly inhibited tumor growth by inducing cell-mediated immunity.	topic_ccc
77944	6	356276	7	NULL	NULL	0	NULL	maitake mushroom	Organism		is					Grifola frondosa	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	We previously isolated the novel heteropolysaccharide maitake Z-fraction (MZF) from the maitake mushroom (Grifola frondosa), and demonstrated that MZF significantly inhibited tumor growth by inducing cell-mediated immunity.	topic_ccc
78504	1	356277	5	NULL	NULL	0	NULL	FC	GroupOfPeople		is predisposed to					autism spectrum disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Our initial analysis revealed the presence of association at two loci: DXS6789 (P=0.026) and DXS8043 (P=0.0101). In a second step, we added support to the association at DXS8043 using additional markers, additional subjects and a haplotype-based analysis (best obtained P-value=0.00001). These results provide support for the existence of a locus on the X chromosome that predisposes the FC to autism spectrum disorders.	topic_aut
78508	2	356277	5	NULL	NULL	0	NULL	X chromosome	Chromosome		plays a role in					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Our initial analysis revealed the presence of association at two loci: DXS6789 (P=0.026) and DXS8043 (P=0.0101). In a second step, we added support to the association at DXS8043 using additional markers, additional subjects and a haplotype-based analysis (best obtained P-value=0.00001). These results provide support for the existence of a locus on the X chromosome that predisposes the FC to autism spectrum disorders.	topic_aut
78510	1	356278	5	NULL	NULL	0	NULL	ARX	GP		is					Aristaless related homeobox	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Aristaless related homeobox (ARX) is a paired-type homeobox gene	topic_aut
78511	2	356278	5	NULL	NULL	0	NULL	ARX gene	GP		is a type of					paired-type homeobox gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Aristaless related homeobox (ARX) is a paired-type homeobox gene	topic_aut
78518	1	356280	5	NULL	NULL	0	NULL	cyclin-dependent kinase-like 5	GP		is also known as					STK9	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	CDKL5 is a gene that provides instructions for making a protein called cyclin-dependent kinase-like 5 also known as serine/threonine kinase 9 (STK9)	topic_aut
78519	2	356280	5	NULL	NULL	0	NULL	STK9	GP		is					serine/threonine kinase 9	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	CDKL5 is a gene that provides instructions for making a protein called cyclin-dependent kinase-like 5 also known as serine/threonine kinase 9 (STK9)	topic_aut
78520	3	356280	5	NULL	NULL	0	NULL	CDKL5 gene	GP		encodes for					cyclin-dependent kinase-like 5 protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	CDKL5 is a gene that provides instructions for making a protein called cyclin-dependent kinase-like 5 also known as serine/threonine kinase 9 (STK9)	topic_aut
78521	1	356281	5	NULL	NULL	NULL	NULL	Echinoderm microtubule-associated protein-like 1 protein	GP	human	is encoded by					EML1 gene	GP	human			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Echinoderm microtubule-associated protein-like 1 is a protein that in humans is encoded by the EML1 gene	topic_aut
78522	1	356283	5	NULL	NULL	0	NULL	Forkhead box protein P2	GP		is also known as					FOXP2	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Forkhead box protein P2 also known as FOXP2 is a protein that in humans is encoded by the FOXP2 gene	topic_aut
78523	2	356283	5	NULL	NULL	0	NULL	FOXP2 protein	GP	human	is encoded by					FOXP2 gene	GP	human			NULL		0	NULL	NULL	NULL	NULL	NULL	Forkhead box protein P2 also known as FOXP2 is a protein that in humans is encoded by the FOXP2 gene	topic_aut
78524	1	356288	5	NULL	NULL	0	NULL	PTEN	GP		is					Phosphatase and tensin homolog	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Phosphatase and tensin homolog (PTEN) is a protein that, in humans, is encoded by the PTEN gene	topic_aut
78525	2	356288	5	NULL	NULL	0	NULL	PTEN protein	GP	human	is encoded by					PTEN gene	GP	human			NULL		0	NULL	NULL	NULL	NULL	NULL	Phosphatase and tensin homolog (PTEN) is a protein that, in humans, is encoded by the PTEN gene	topic_aut
78526	1	356289	5	NULL	NULL	0	NULL	Retinoschisin	GP		is also known as					X-linked juvenile retinoschisis protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Retinoschisin also known as X-linked juvenile retinoschisis protein is a protein that in humans is encoded by the RS1 gene	topic_aut
78527	2	356289	5	NULL	NULL	0	NULL	X-linked juvenile retinoschisis protein	GP	human	is encoded by					RS1 gene	GP	human			NULL		0	NULL	NULL	NULL	NULL	NULL	Retinoschisin also known as X-linked juvenile retinoschisis protein is a protein that in humans is encoded by the RS1 gene	topic_aut
78528	1	356294	5	NULL	NULL	0	NULL	homocysteine	AminoAcid	plasma	elevated in		significantly			autism mothers	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Metabolic profiling indicated that plasma homocysteine, adenosine, and S-adenosylhomocyteine were significantly elevated among autism mothers consistent with reduced methylation capacity and DNA hypomethylation. Together, these results suggest that the maternal genetics/epigenetics may influence fetal predisposition to autism.	topic_aut
78529	2	356294	5	NULL	NULL	0	NULL	adenosine	NucleicAcid		elevated in		significantly			autism mothers	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Metabolic profiling indicated that plasma homocysteine, adenosine, and S-adenosylhomocyteine were significantly elevated among autism mothers consistent with reduced methylation capacity and DNA hypomethylation. Together, these results suggest that the maternal genetics/epigenetics may influence fetal predisposition to autism.	topic_aut
78530	3	356294	5	NULL	NULL	0	NULL	S-adenosylhomocyteine	AminoAcid		elevated in		significantly			autism mothers	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Metabolic profiling indicated that plasma homocysteine, adenosine, and S-adenosylhomocyteine were significantly elevated among autism mothers consistent with reduced methylation capacity and DNA hypomethylation. Together, these results suggest that the maternal genetics/epigenetics may influence fetal predisposition to autism.	topic_aut
78531	4	356294	5	NULL	NULL	0	NULL	methylation capacity	Process		reduced in					autism mothers	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Metabolic profiling indicated that plasma homocysteine, adenosine, and S-adenosylhomocyteine were significantly elevated among autism mothers consistent with reduced methylation capacity and DNA hypomethylation. Together, these results suggest that the maternal genetics/epigenetics may influence fetal predisposition to autism.	topic_aut
78532	5	356294	5	NULL	NULL	0	NULL	DNA hypomethylation	Process		reduced in					autism mothers	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	Metabolic profiling indicated that plasma homocysteine, adenosine, and S-adenosylhomocyteine were significantly elevated among autism mothers consistent with reduced methylation capacity and DNA hypomethylation. Together, these results suggest that the maternal genetics/epigenetics may influence fetal predisposition to autism.	topic_aut
78533	6	356294	5	NULL	NULL	0	NULL	maternal genetics	Process		is also known as					epigenetics	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Metabolic profiling indicated that plasma homocysteine, adenosine, and S-adenosylhomocyteine were significantly elevated among autism mothers consistent with reduced methylation capacity and DNA hypomethylation. Together, these results suggest that the maternal genetics/epigenetics may influence fetal predisposition to autism.	topic_aut
78534	7	356294	5	NULL	NULL	0	NULL	epigenetics	Process		influence					autism	MedicalFinding	predisposition of;;fetal			NULL		0	NULL	NULL	NULL	NULL	NULL	Metabolic profiling indicated that plasma homocysteine, adenosine, and S-adenosylhomocyteine were significantly elevated among autism mothers consistent with reduced methylation capacity and DNA hypomethylation. Together, these results suggest that the maternal genetics/epigenetics may influence fetal predisposition to autism.	topic_aut
78535	1	356295	5	NULL	NULL	NULL	NULL	MECP2	GP		methylated in				promoter	autism male	GroupOfPeople	frontal cortex of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	A more frequent occurrence was significantly increased MECP2 promoter methylation in autism male frontal cortex compared to controls.	topic_aut
78536	2	356295	5	NULL	NULL	NULL	NULL	MECP2	GP		methylated in				promoter	controls	GroupOfPeople				NULL		NULL	NULL	NULL	NULL	NULL	NULL	A more frequent occurrence was significantly increased MECP2 promoter methylation in autism male frontal cortex compared to controls.	topic_aut
78537	3	356295	5	NULL	NULL	0	NULL	statement 1	Process		is increased than		significantly			statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	A more frequent occurrence was significantly increased MECP2 promoter methylation in autism male frontal cortex compared to controls.	topic_aut
78538	1	356296	5	NULL	NULL	0	NULL	genetic defects	MedicalFinding		reduce					MeCP2	GP	expression of			NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore, percent promoter methylation of MECP2 significantly correlated with reduced MeCP2 protein expression. These results suggest that both genetic and epigenetic defects lead to reduced MeCP2 expression and may be important in the complex etiology of autism.	topic_aut
78539	2	356296	5	NULL	NULL	0	NULL	epigenetic defects	MedicalFinding		reduce					MeCP2	GP	expression of			NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore, percent promoter methylation of MECP2 significantly correlated with reduced MeCP2 protein expression. These results suggest that both genetic and epigenetic defects lead to reduced MeCP2 expression and may be important in the complex etiology of autism.	topic_aut
78540	3	356296	5	NULL	NULL	0	NULL	statement 1	Process		plays a role in		may;;important			autism	MedicalFinding	complex etiology of			NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore, percent promoter methylation of MECP2 significantly correlated with reduced MeCP2 protein expression. These results suggest that both genetic and epigenetic defects lead to reduced MeCP2 expression and may be important in the complex etiology of autism.	topic_aut
78541	4	356296	5	NULL	NULL	0	NULL	statement 2	Process		plays a role in					autism	MedicalFinding	complex etiology of			NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore, percent promoter methylation of MECP2 significantly correlated with reduced MeCP2 protein expression. These results suggest that both genetic and epigenetic defects lead to reduced MeCP2 expression and may be important in the complex etiology of autism.	topic_aut
78542	1	356298	5	NULL	NULL	0	NULL	NRXN1 gene	GP		is vulnerable to					SCZ	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Our findings demonstrate that the NRXN1 gene, a vulnerability gene for SCZ and ASD, influences brain structure and cognitive function susceptible in both disorders	topic_aut
78543	2	356298	5	NULL	NULL	0	NULL	NRXN1 gene	GP		is vulnerable to					ASD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Our findings demonstrate that the NRXN1 gene, a vulnerability gene for SCZ and ASD, influences brain structure and cognitive function susceptible in both disorders	topic_aut
78544	3	356298	5	NULL	NULL	0	NULL	NRXN1 gene	GP		influence					brain structure	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	Our findings demonstrate that the NRXN1 gene, a vulnerability gene for SCZ and ASD, influences brain structure and cognitive function susceptible in both disorders	topic_aut
78545	4	356298	5	NULL	NULL	0	NULL	statement 2	Process		influence					cognitive functions	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Our findings demonstrate that the NRXN1 gene, a vulnerability gene for SCZ and ASD, influences brain structure and cognitive function susceptible in both disorders	topic_aut
80654	1	356299	5	NULL	NULL	0	NULL	DRB1	Gene	allelic variation of	modulates		pleiotropically			rheumatoid arthritis	Disease	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	These data allow robust testing of the hypotheses that allelic variation at DRB1 pleiotropically modulates risk of rheumatoid arthritis, autism and schizophrenia. Systematic review of the literature indicates that reported associations of DRB1 variants with these three conditions are congruent with a pleiotropic model: DRB1*04 alleles have been associated with increased risk of rheumatoid arthritis and autism but decreased risk of schizophrenia, and DRB1*13 alleles have been associated with protection from rheumatoid arthritis and autism but higher risk of schizophrenia.	topic_aut
80655	2	356299	5	NULL	NULL	0	NULL	DRB1	Gene	allelic variation of	modulates		pleiotropically			autism	Disease	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	These data allow robust testing of the hypotheses that allelic variation at DRB1 pleiotropically modulates risk of rheumatoid arthritis, autism and schizophrenia. Systematic review of the literature indicates that reported associations of DRB1 variants with these three conditions are congruent with a pleiotropic model: DRB1*04 alleles have been associated with increased risk of rheumatoid arthritis and autism but decreased risk of schizophrenia, and DRB1*13 alleles have been associated with protection from rheumatoid arthritis and autism but higher risk of schizophrenia.	topic_aut
80656	3	356299	5	NULL	NULL	NULL	NULL	DRB1	Gene	allelic variation of	modulates		pleiotropically			schizophrenia	Disease	risk of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	These data allow robust testing of the hypotheses that allelic variation at DRB1 pleiotropically modulates risk of rheumatoid arthritis, autism and schizophrenia. Systematic review of the literature indicates that reported associations of DRB1 variants with these three conditions are congruent with a pleiotropic model: DRB1*04 alleles have been associated with increased risk of rheumatoid arthritis and autism but decreased risk of schizophrenia, and DRB1*13 alleles have been associated with protection from rheumatoid arthritis and autism but higher risk of schizophrenia.	topic_aut
80657	4	356299	5	NULL	NULL	0	NULL	DRB1*04 alleles	Gene		is associated with					rheumatoid arthritis	Disease	increased risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	These data allow robust testing of the hypotheses that allelic variation at DRB1 pleiotropically modulates risk of rheumatoid arthritis, autism and schizophrenia. Systematic review of the literature indicates that reported associations of DRB1 variants with these three conditions are congruent with a pleiotropic model: DRB1*04 alleles have been associated with increased risk of rheumatoid arthritis and autism but decreased risk of schizophrenia, and DRB1*13 alleles have been associated with protection from rheumatoid arthritis and autism but higher risk of schizophrenia.	topic_aut
80658	5	356299	5	NULL	NULL	0	NULL	DRB1*04 alleles	Gene		is associated with					autism	Disease	increased risk for			NULL		0	NULL	NULL	NULL	NULL	NULL	These data allow robust testing of the hypotheses that allelic variation at DRB1 pleiotropically modulates risk of rheumatoid arthritis, autism and schizophrenia. Systematic review of the literature indicates that reported associations of DRB1 variants with these three conditions are congruent with a pleiotropic model: DRB1*04 alleles have been associated with increased risk of rheumatoid arthritis and autism but decreased risk of schizophrenia, and DRB1*13 alleles have been associated with protection from rheumatoid arthritis and autism but higher risk of schizophrenia.	topic_aut
80659	6	356299	5	NULL	NULL	0	NULL	DRB1*04 alleles	Gene		is associated with					schizophrenia	Disease	decreased risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	These data allow robust testing of the hypotheses that allelic variation at DRB1 pleiotropically modulates risk of rheumatoid arthritis, autism and schizophrenia. Systematic review of the literature indicates that reported associations of DRB1 variants with these three conditions are congruent with a pleiotropic model: DRB1*04 alleles have been associated with increased risk of rheumatoid arthritis and autism but decreased risk of schizophrenia, and DRB1*13 alleles have been associated with protection from rheumatoid arthritis and autism but higher risk of schizophrenia.	topic_aut
80660	7	356299	5	NULL	NULL	0	NULL	DRB1*13 alleles	Gene		is associated with					rheumatoid arthritis	Disease	protection from			NULL		0	NULL	NULL	NULL	NULL	NULL	These data allow robust testing of the hypotheses that allelic variation at DRB1 pleiotropically modulates risk of rheumatoid arthritis, autism and schizophrenia. Systematic review of the literature indicates that reported associations of DRB1 variants with these three conditions are congruent with a pleiotropic model: DRB1*04 alleles have been associated with increased risk of rheumatoid arthritis and autism but decreased risk of schizophrenia, and DRB1*13 alleles have been associated with protection from rheumatoid arthritis and autism but higher risk of schizophrenia.	topic_aut
80661	8	356299	5	NULL	NULL	0	NULL	DRB1*13 alleles	Gene		is associated with					autism	Disease	protection from			NULL		0	NULL	NULL	NULL	NULL	NULL	These data allow robust testing of the hypotheses that allelic variation at DRB1 pleiotropically modulates risk of rheumatoid arthritis, autism and schizophrenia. Systematic review of the literature indicates that reported associations of DRB1 variants with these three conditions are congruent with a pleiotropic model: DRB1*04 alleles have been associated with increased risk of rheumatoid arthritis and autism but decreased risk of schizophrenia, and DRB1*13 alleles have been associated with protection from rheumatoid arthritis and autism but higher risk of schizophrenia.	topic_aut
80663	9	356299	5	NULL	NULL	0	NULL	DRB1*13 alleles	Gene		is associated with					schizophrenia	Disease	higher risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	These data allow robust testing of the hypotheses that allelic variation at DRB1 pleiotropically modulates risk of rheumatoid arthritis, autism and schizophrenia. Systematic review of the literature indicates that reported associations of DRB1 variants with these three conditions are congruent with a pleiotropic model: DRB1*04 alleles have been associated with increased risk of rheumatoid arthritis and autism but decreased risk of schizophrenia, and DRB1*13 alleles have been associated with protection from rheumatoid arthritis and autism but higher risk of schizophrenia.	topic_aut
78546	1	356302	5	NULL	NULL	0	NULL	SHANK3	GP		is mutated in					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	SHANK3 mutations identified in autism lead to modification of dendritic spine morphology via an actin-dependent mechanism.	topic_aut
78547	2	356302	5	NULL	NULL	0	NULL	SHANK3	GP	mutation of	modifies					dendritic spine morphology	PhysicalPhenomenon				NULL		0	NULL	NULL	NULL	NULL	NULL	SHANK3 mutations identified in autism lead to modification of dendritic spine morphology via an actin-dependent mechanism.	topic_aut
78548	3	356302	5	NULL	NULL	0	NULL	statement 2	Process		via					actin-dependent mechanism	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	SHANK3 mutations identified in autism lead to modification of dendritic spine morphology via an actin-dependent mechanism.	topic_aut
78639	1	356303	5	NULL	NULL	NULL	NULL	Shank3	Protein		plays a role in					spine induction	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The de novo mutation in the ankyrin domain (Q321R) modifies the roles of Shank3 in spine induction and morphology, and actin accumulation in spines and affects growth cone motility. Finally, the two inherited mutations (R12C and R300C) have intermediate effects on spine density and synaptic transmission. Therefore, although inherited by healthy parents, the functional effects of these mutations strongly suggest that they could represent risk factors for ASD	topic_aut
78640	2	356303	5	NULL	NULL	NULL	NULL	Shank3	Protein		plays a role in					morphology	PhysicalPhenomenon				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The de novo mutation in the ankyrin domain (Q321R) modifies the roles of Shank3 in spine induction and morphology, and actin accumulation in spines and affects growth cone motility. Finally, the two inherited mutations (R12C and R300C) have intermediate effects on spine density and synaptic transmission. Therefore, although inherited by healthy parents, the functional effects of these mutations strongly suggest that they could represent risk factors for ASD	topic_aut
80665	3	356303	5	NULL	NULL	0	NULL	actin	Protein		accumulates in					spine	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The de novo mutation in the ankyrin domain (Q321R) modifies the roles of Shank3 in spine induction and morphology, and actin accumulation in spines and affects growth cone motility. Finally, the two inherited mutations (R12C and R300C) have intermediate effects on spine density and synaptic transmission. Therefore, although inherited by healthy parents, the functional effects of these mutations strongly suggest that they could represent risk factors for ASD	topic_aut
80669	4	356303	5	NULL	NULL	0	NULL	Shank3	Protein	de novo mutation of	modifies			ankyrin domain (Q321R)		statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The de novo mutation in the ankyrin domain (Q321R) modifies the roles of Shank3 in spine induction and morphology, and actin accumulation in spines and affects growth cone motility. Finally, the two inherited mutations (R12C and R300C) have intermediate effects on spine density and synaptic transmission. Therefore, although inherited by healthy parents, the functional effects of these mutations strongly suggest that they could represent risk factors for ASD	topic_aut
80670	5	356303	5	NULL	NULL	0	NULL	Shank3	Protein	de novo mutation of	modifies			ankyrin domain (Q321R)		statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The de novo mutation in the ankyrin domain (Q321R) modifies the roles of Shank3 in spine induction and morphology, and actin accumulation in spines and affects growth cone motility. Finally, the two inherited mutations (R12C and R300C) have intermediate effects on spine density and synaptic transmission. Therefore, although inherited by healthy parents, the functional effects of these mutations strongly suggest that they could represent risk factors for ASD	topic_aut
80672	6	356303	5	NULL	NULL	0	NULL	Shank3	Protein	de novo mutation of	modifies			ankyrin domain (Q321R)		statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The de novo mutation in the ankyrin domain (Q321R) modifies the roles of Shank3 in spine induction and morphology, and actin accumulation in spines and affects growth cone motility. Finally, the two inherited mutations (R12C and R300C) have intermediate effects on spine density and synaptic transmission. Therefore, although inherited by healthy parents, the functional effects of these mutations strongly suggest that they could represent risk factors for ASD	topic_aut
80673	6	356303	5	NULL	NULL	0	NULL	Shank3	Protein	de novo mutation of	modifies			ankyrin domain (Q321R)		statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The de novo mutation in the ankyrin domain (Q321R) modifies the roles of Shank3 in spine induction and morphology, and actin accumulation in spines and affects growth cone motility. Finally, the two inherited mutations (R12C and R300C) have intermediate effects on spine density and synaptic transmission. Therefore, although inherited by healthy parents, the functional effects of these mutations strongly suggest that they could represent risk factors for ASD	topic_aut
80676	7	356303	5	NULL	NULL	0	NULL	Shank3	Protein	de novo mutation of	affects			ankyrin domain (Q321R)		growth cone motility	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	The de novo mutation in the ankyrin domain (Q321R) modifies the roles of Shank3 in spine induction and morphology, and actin accumulation in spines and affects growth cone motility. Finally, the two inherited mutations (R12C and R300C) have intermediate effects on spine density and synaptic transmission. Therefore, although inherited by healthy parents, the functional effects of these mutations strongly suggest that they could represent risk factors for ASD	topic_aut
80679	8	356303	5	NULL	NULL	0	NULL	R12C	AminoAcid		is a type of					inherited mutations	AminoAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	The de novo mutation in the ankyrin domain (Q321R) modifies the roles of Shank3 in spine induction and morphology, and actin accumulation in spines and affects growth cone motility. Finally, the two inherited mutations (R12C and R300C) have intermediate effects on spine density and synaptic transmission. Therefore, although inherited by healthy parents, the functional effects of these mutations strongly suggest that they could represent risk factors for ASD	topic_aut
80680	9	356303	5	NULL	NULL	0	NULL	R300C	AminoAcid		is a type of					inherited mutations	AminoAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	The de novo mutation in the ankyrin domain (Q321R) modifies the roles of Shank3 in spine induction and morphology, and actin accumulation in spines and affects growth cone motility. Finally, the two inherited mutations (R12C and R300C) have intermediate effects on spine density and synaptic transmission. Therefore, although inherited by healthy parents, the functional effects of these mutations strongly suggest that they could represent risk factors for ASD	topic_aut
78549	1	356304	5	NULL	NULL	0	NULL	DISC1	GP		plays a role in		may			autism	MedicalFinding	pathogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	Our study provided evidence that the DISC1 may be the susceptibility gene of autism. It suggested DISC1 might play a role in the pathogenesis of autism.	topic_aut
78550	1	356306	5	NULL	NULL	0	NULL	Clozapine	Chemical		is a type of					second-generation antipsychotic drug	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Clozapine, a second-generation antipsychotic drug known to be effective in the treatment of aggression associated with schizophrenia, has received little attention in ASD.We conducted a retrospective analysis of the changes in disruptive behaviors for all patients with ASD treated with clozapine from 2002 to 2010	topic_aut
78551	3	356306	5	NULL	NULL	NULL	NULL	Clozapine	Chemical		treats		effectively			statement 2	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Clozapine, a second-generation antipsychotic drug known to be effective in the treatment of aggression associated with schizophrenia, has received little attention in ASD.We conducted a retrospective analysis of the changes in disruptive behaviors for all patients with ASD treated with clozapine from 2002 to 2010	topic_aut
78552	2	356306	5	NULL	NULL	0	NULL	aggression	MedicalFinding		is associated with					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Clozapine, a second-generation antipsychotic drug known to be effective in the treatment of aggression associated with schizophrenia, has received little attention in ASD.We conducted a retrospective analysis of the changes in disruptive behaviors for all patients with ASD treated with clozapine from 2002 to 2010	topic_aut
78553	4	356306	5	NULL	NULL	0	NULL	Clozapine	Chemical		is not effective		may			ASD	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Clozapine, a second-generation antipsychotic drug known to be effective in the treatment of aggression associated with schizophrenia, has received little attention in ASD.We conducted a retrospective analysis of the changes in disruptive behaviors for all patients with ASD treated with clozapine from 2002 to 2010	topic_aut
78554	1	356308	5	NULL	NULL	NULL	NULL	NRXN2	GP	disruption of	is linked to					ASD	MedicalFinding	pathogenesis of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Our findings link NRXN2 disruption to the pathogenesis of ASD for the first time and further strengthen the involvement of NRXN1 in SCZ, supporting the notion of a common genetic mechanism in these disorders.	topic_aut
78555	2	356308	5	NULL	NULL	0	NULL	NRXN2	GP		is involved in					SCZ	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Our findings link NRXN2 disruption to the pathogenesis of ASD for the first time and further strengthen the involvement of NRXN1 in SCZ, supporting the notion of a common genetic mechanism in these disorders.	topic_aut
77945	1	356309	7	NULL	NULL	0	NULL	Frequent binge drinking	Chemical		classed as					alcohol misuse	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Frequent binge drinking or getting severely drunk more than twice is classed as alcohol misuse.	topic_bd
78556	1	356310	5	NULL	NULL	0	NULL	autism	MedicalFinding		is associated with					immune dysfunction	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Evidence suggests an association between autism and immune dysfunction. The associations between human lymphocyte antigen (HLA)-A2, B44, DRβ1*04 (DR4), C4B, and haplotype B44-SC30-DR4 and autism have been reported in western countries	topic_aut
78557	2	356310	5	NULL	NULL	0	NULL	(HLA)-A2	GP		is a type of					human lymphocyte antigen	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Evidence suggests an association between autism and immune dysfunction. The associations between human lymphocyte antigen (HLA)-A2, B44, DRβ1*04 (DR4), C4B, and haplotype B44-SC30-DR4 and autism have been reported in western countries	topic_aut
78558	3	356310	5	NULL	NULL	0	NULL	(HLA)-B44	GP		is a type of					human lymphocyte antigen	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Evidence suggests an association between autism and immune dysfunction. The associations between human lymphocyte antigen (HLA)-A2, B44, DRβ1*04 (DR4), C4B, and haplotype B44-SC30-DR4 and autism have been reported in western countries	topic_aut
78559	4	356310	5	NULL	NULL	0	NULL	(HLA)-DR4	GP		is a type of					human lymphocyte antigen	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Evidence suggests an association between autism and immune dysfunction. The associations between human lymphocyte antigen (HLA)-A2, B44, DRβ1*04 (DR4), C4B, and haplotype B44-SC30-DR4 and autism have been reported in western countries	topic_aut
78560	5	356310	5	NULL	NULL	0	NULL	(HLA)-A2	GP		is associated with					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Evidence suggests an association between autism and immune dysfunction. The associations between human lymphocyte antigen (HLA)-A2, B44, DRβ1*04 (DR4), C4B, and haplotype B44-SC30-DR4 and autism have been reported in western countries	topic_aut
78561	6	356310	5	NULL	NULL	0	NULL	(HLA)-B44	GP		is associated with					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Evidence suggests an association between autism and immune dysfunction. The associations between human lymphocyte antigen (HLA)-A2, B44, DRβ1*04 (DR4), C4B, and haplotype B44-SC30-DR4 and autism have been reported in western countries	topic_aut
78562	7	356310	5	NULL	NULL	0	NULL	(HLA)-DR4	GP		is associated with					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Evidence suggests an association between autism and immune dysfunction. The associations between human lymphocyte antigen (HLA)-A2, B44, DRβ1*04 (DR4), C4B, and haplotype B44-SC30-DR4 and autism have been reported in western countries	topic_aut
78563	8	356310	5	NULL	NULL	0	NULL	B44-SC30-DR4	GP		is associated with					autism	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Evidence suggests an association between autism and immune dysfunction. The associations between human lymphocyte antigen (HLA)-A2, B44, DRβ1*04 (DR4), C4B, and haplotype B44-SC30-DR4 and autism have been reported in western countries	topic_aut
78564	1	356311	5	NULL	NULL	0	NULL	L-carnitine	Chemical		improves					mitochondrial dysfunction	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	L-carnitine was proposed as a potential treatment for patients diagnosed with an autism spectrum disorder to improve mitochondrial dysfunction	topic_aut
78565	2	356311	5	NULL	NULL	0	NULL	L-carnitine	Chemical		is a treatment for		potential			autism spectrum disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	L-carnitine was proposed as a potential treatment for patients diagnosed with an autism spectrum disorder to improve mitochondrial dysfunction	topic_aut
78566	1	356312	5	NULL	NULL	NULL	NULL	Desulfovibrio	Organism		is present in					autistic subjects	GroupOfPeople				NULL		NULL	NULL	NULL	NULL	NULL	NULL	However, a recent study of ours employing the powerful pyrosequencing technique on stools of subjects with regressive autism showed that Desulfovibrio was more common in autistic subjects than in controls.	topic_aut
78567	2	356312	5	NULL	NULL	0	NULL	Desulfovibrio	Organism		is present in					controls	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	However, a recent study of ours employing the powerful pyrosequencing technique on stools of subjects with regressive autism showed that Desulfovibrio was more common in autistic subjects than in controls.	topic_aut
78568	3	356312	5	NULL	NULL	0	NULL	statement 1	Process		more common than					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	However, a recent study of ours employing the powerful pyrosequencing technique on stools of subjects with regressive autism showed that Desulfovibrio was more common in autistic subjects than in controls.	topic_aut
78569	1	356313	5	NULL	NULL	0	NULL	ASD	MedicalFinding		is					autism spectrum disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Children with autism spectrum disorders (ASD) are at high risk for oral disease.	topic_aut
78570	2	356313	5	NULL	NULL	0	NULL	ASD children	GroupOfPeople		is at risk of		high			oral disesae	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Children with autism spectrum disorders (ASD) are at high risk for oral disease.	topic_aut
78571	1	356314	5	NULL	NULL	0	NULL	RRBs	MedicalFinding		is					restricted and repetitive behaviors	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Restricted and repetitive behaviors (RRBs) are a core symptom of autism spectrum disorders (ASD).	topic_aut
78572	2	356314	5	NULL	NULL	0	NULL	RRBs	MedicalFinding		is a core symptom of					ASD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Restricted and repetitive behaviors (RRBs) are a core symptom of autism spectrum disorders (ASD).	topic_aut
78573	3	356314	5	NULL	NULL	0	NULL	ASD	MedicalFinding		is					autism spectrum disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Restricted and repetitive behaviors (RRBs) are a core symptom of autism spectrum disorders (ASD).	topic_aut
78574	1	356315	5	NULL	NULL	NULL	NULL	white-matter abnormalities	MedicalFinding		is a key factor in					autism	MedicalFinding	 physiopathology of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Recent evidence points to white-matter abnormalities as a key factor in autism physiopathology	topic_aut
78575	1	356316	5	NULL	NULL	0	NULL	eyeblink synchronization	Process		is absent in					ASD individuals	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	By contrast, the ASD participants did not show any eyeblink synchronization with the speaker, even when viewing the speaker's eyes and mouth simultaneously. The lack of eyeblink entrainment to the speaker in individuals with ASD suggests that they are not able to temporally attune themselves to others' behaviors.	topic_aut
78577	1	356317	5	NULL	NULL	NULL	NULL	High-Functioning Autism individulas	GroupOfPeople		less able to differentiate					language dialects	MentalProcess				NULL		NULL	NULL	NULL	NULL	NULL	NULL	However, the participants with High-Functioning Autism were less able to differentiate among the dialects in a language attitudes task, suggesting that they do not share social stereotypes related to dialect variation with the typically developing comparison group.	topic_aut
77946	1	356318	7	NULL	NULL	0	NULL	Irinotecan	Chemical		activated by					SN-38	Chemical	hydrolysis to			NULL		0	NULL	NULL	NULL	NULL	NULL	Irinotecan is activated by hydrolysis to SN-38, an inhibitor of topoisomerase I.	topic_ccc
77947	2	356318	7	NULL	NULL	0	NULL	SN-38	Chemical		inhibitor of					topoisomerase I	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	Irinotecan is activated by hydrolysis to SN-38, an inhibitor of topoisomerase I.	topic_ccc
77948	1	356320	7	NULL	NULL	NULL	NULL	BAECs	Cell		repress		significantly;;time-dependently			VEGFR2 protein	GP				NULL		NULL	NULL	NULL	NULL	NULL	NULL	In bovine aortic endothelial cells (BAECs), TGF-β1 significantly repressed VEGFR2 protein in a time-dependent and dose-dependent fashion (P < .05).	topic_ccc
77949	2	356320	7	NULL	NULL	0	NULL	BAECs	Cell		repress		significantly;;dose-dependently			VEGFR2 protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	In bovine aortic endothelial cells (BAECs), TGF-β1 significantly repressed VEGFR2 protein in a time-dependent and dose-dependent fashion (P < .05).	topic_ccc
77950	3	356320	7	NULL	NULL	0	NULL	TGF-β1	GP		repress		significantly;;time-dependently			VEGFR2 protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	In bovine aortic endothelial cells (BAECs), TGF-β1 significantly repressed VEGFR2 protein in a time-dependent and dose-dependent fashion (P < .05).	topic_ccc
77951	4	356320	7	NULL	NULL	0	NULL	TGF-β1	GP		repress		significantly;;dose-dependently			VEGFR2 protein	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	In bovine aortic endothelial cells (BAECs), TGF-β1 significantly repressed VEGFR2 protein in a time-dependent and dose-dependent fashion (P < .05).	topic_ccc
77952	5	356320	7	NULL	NULL	0	NULL	BAECs	Cell		is					bovine aortic endothelial cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	In bovine aortic endothelial cells (BAECs), TGF-β1 significantly repressed VEGFR2 protein in a time-dependent and dose-dependent fashion (P < .05).	topic_ccc
77953	1	356323	7	NULL	NULL	0	NULL	bFGF	GP		mitogen for					endothelial cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	 Basic fibroblast growth factor (bFGF) is a mitogen for endothelial cells, which participates in tumor angiogenesis. In vitro, a CTL assay revealed that bFGF-specific cytotoxic T lymphocytes (CTL) resulted in the lysis of mouse microvascular endothelial cells (MS1) rather than that of the CT26 colorectal cancer cells.	topic_ccc
77954	2	356323	7	NULL	NULL	0	NULL	statement 1	Process		participates in					tumor angiogenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	 Basic fibroblast growth factor (bFGF) is a mitogen for endothelial cells, which participates in tumor angiogenesis. In vitro, a CTL assay revealed that bFGF-specific cytotoxic T lymphocytes (CTL) resulted in the lysis of mouse microvascular endothelial cells (MS1) rather than that of the CT26 colorectal cancer cells.	topic_ccc
77955	3	356323	7	NULL	NULL	0	NULL	bFGF-specific CTL	Cell		lyse					MS1	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	 Basic fibroblast growth factor (bFGF) is a mitogen for endothelial cells, which participates in tumor angiogenesis. In vitro, a CTL assay revealed that bFGF-specific cytotoxic T lymphocytes (CTL) resulted in the lysis of mouse microvascular endothelial cells (MS1) rather than that of the CT26 colorectal cancer cells.	topic_ccc
77956	4	356323	7	NULL	NULL	0	NULL	bFGF-specific CTL	Cell		does not lyse					CT26 colorectal cancer cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	 Basic fibroblast growth factor (bFGF) is a mitogen for endothelial cells, which participates in tumor angiogenesis. In vitro, a CTL assay revealed that bFGF-specific cytotoxic T lymphocytes (CTL) resulted in the lysis of mouse microvascular endothelial cells (MS1) rather than that of the CT26 colorectal cancer cells.	topic_ccc
77957	5	356323	7	NULL	NULL	0	NULL	bFGF	GP		is					Basic fibroblast growth factor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	 Basic fibroblast growth factor (bFGF) is a mitogen for endothelial cells, which participates in tumor angiogenesis. In vitro, a CTL assay revealed that bFGF-specific cytotoxic T lymphocytes (CTL) resulted in the lysis of mouse microvascular endothelial cells (MS1) rather than that of the CT26 colorectal cancer cells.	topic_ccc
77958	6	356323	7	NULL	NULL	0	NULL	CTL	Cell		is					cytotoxic T lymphocytes 	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	 Basic fibroblast growth factor (bFGF) is a mitogen for endothelial cells, which participates in tumor angiogenesis. In vitro, a CTL assay revealed that bFGF-specific cytotoxic T lymphocytes (CTL) resulted in the lysis of mouse microvascular endothelial cells (MS1) rather than that of the CT26 colorectal cancer cells.	topic_ccc
77959	1	356324	7	NULL	NULL	NULL	NULL	IGF1	GP	SNP rs6214 of	impact on		could			colorectal cancer	MedicalFinding	developing			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Our results suggest that the SNP rs6214 of IGF1 could have an impact on developing colorectal cancer and colorectal polyps with villous elements.	topic_ccc
77960	2	356324	7	NULL	NULL	NULL	NULL	IGF1	GP	SNP rs6214 of	impact on		could			colorectal polyps with villous elements	OrganismPart				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Our results suggest that the SNP rs6214 of IGF1 could have an impact on developing colorectal cancer and colorectal polyps with villous elements.	topic_ccc
77961	1	356325	7	NULL	NULL	0	NULL	Callosal volume 	OrganismPart	reduction in	observed in					bipolar disorder	MedicalFinding	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	Callosal volume reduction has been observed in patients with bipolar disorder, but whether these deficits reflect genetic vulnerability to the illness remains unresolved. 	topic_bd
77962	1	356326	7	NULL	NULL	0	NULL	corpus callosum	OrganismPart		is known as					colossal commissure	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The corpus callosum, also known as the colossal commissure, is a wide, flat bundle of neural fibers beneath the cortex in the eutherian brain at the longitudinal fissure. 	topic_bd
77963	2	356326	7	NULL	NULL	0	NULL	corpus callosum	OrganismPart		is a type of					neural fibers	OrganismPart	wide, flat bundle of 			NULL		0	NULL	NULL	NULL	NULL	NULL	The corpus callosum, also known as the colossal commissure, is a wide, flat bundle of neural fibers beneath the cortex in the eutherian brain at the longitudinal fissure. 	topic_bd
77964	3	356326	7	NULL	NULL	0	NULL	corpus callosum	OrganismPart		located beneath					eutherian brain 	OrganismPart	the cortex in			NULL		0	NULL	NULL	NULL	NULL	NULL	The corpus callosum, also known as the colossal commissure, is a wide, flat bundle of neural fibers beneath the cortex in the eutherian brain at the longitudinal fissure. 	topic_bd
77965	4	356326	7	NULL	NULL	0	NULL	eutherian brain	OrganismPart		occur at					longitudinal fissure	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The corpus callosum, also known as the colossal commissure, is a wide, flat bundle of neural fibers beneath the cortex in the eutherian brain at the longitudinal fissure. 	topic_bd
77966	1	356327	7	NULL	NULL	NULL	NULL	corpus collosum	OrganismPart	reduction of genu areas of	correlated with		significantly			verbal processing	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	In bipolar probands and co-twins, reduction of genu and splenium midsagittal areas  of the corpus collosum were significantly correlated with verbal processing speed and response inhibition. 	topic_bd
77967	2	356327	7	NULL	NULL	0	NULL	corpus callosum	OrganismPart	reduction of splenium midsagittal areas of	correlated with		significantly			response inhibition	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In bipolar probands and co-twins, reduction of genu and splenium midsagittal areas  of the corpus collosum were significantly correlated with verbal processing speed and response inhibition. 	topic_bd
77968	3	356327	7	NULL	NULL	0	NULL	statement 1	Process		occur in					bipolar probands	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In bipolar probands and co-twins, reduction of genu and splenium midsagittal areas  of the corpus collosum were significantly correlated with verbal processing speed and response inhibition. 	topic_bd
77969	4	356327	7	NULL	NULL	0	NULL	statement 1	Process		occur in					co-twins	Person				NULL		0	NULL	NULL	NULL	NULL	NULL	In bipolar probands and co-twins, reduction of genu and splenium midsagittal areas  of the corpus collosum were significantly correlated with verbal processing speed and response inhibition. 	topic_bd
77970	5	356327	7	NULL	NULL	0	NULL	statement 2	Process		occur in					bipolar probands	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In bipolar probands and co-twins, reduction of genu and splenium midsagittal areas  of the corpus collosum were significantly correlated with verbal processing speed and response inhibition. 	topic_bd
77971	6	356327	7	NULL	NULL	0	NULL	statement 2	Process		occur in					co-twins	Person				NULL		0	NULL	NULL	NULL	NULL	NULL	In bipolar probands and co-twins, reduction of genu and splenium midsagittal areas  of the corpus collosum were significantly correlated with verbal processing speed and response inhibition. 	topic_bd
77972	1	356328	7	NULL	NULL	0	NULL	callosal thinning	OrganismPart		appear to be					disease 	MedicalFinding	related to			NULL		0	NULL	NULL	NULL	NULL	NULL	However, findings of callosal thinning appear to be disease related, rather than reflecting genetic vulnerability to bipolar illness. 	topic_bd
77973	2	356328	7	NULL	NULL	NULL	NULL	callosal thinning	Process		does not reflect					bipolar illness	MedicalFinding	genetic vulnerability to			NULL		NULL	NULL	NULL	NULL	NULL	NULL	However, findings of callosal thinning appear to be disease related, rather than reflecting genetic vulnerability to bipolar illness. 	topic_bd
77974	1	356329	7	NULL	NULL	0	NULL	pineal gland	OrganismPart	putative dysfunction of 	not related to		directly			pineal gland	OrganismPart	abnormal volume of			NULL		0	NULL	NULL	NULL	NULL	NULL	These results indicate that the putative dysfunction of the pineal gland in bipolar disorder could be not directly related to an abnormal volume of the pineal gland.	topic_bd
77975	2	356329	7	NULL	NULL	0	NULL	statement 1	Process		occur in					bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	These results indicate that the putative dysfunction of the pineal gland in bipolar disorder could be not directly related to an abnormal volume of the pineal gland.	topic_bd
77976	1	356330	7	NULL	NULL	0	NULL	SNP (rs13438494)	NucleicAcid		intron of					PCLO gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	One SNP (rs13438494), in an intron of the piccolo (PCLO) gene, was significantly associated with bipolar disorder  in the meta-analysis of GWAS.	topic_bd
77977	2	356330	7	NULL	NULL	0	NULL	SNP (rs13438494)	NucleicAcid		associated with		significantly			bipolar disorder	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	One SNP (rs13438494), in an intron of the piccolo (PCLO) gene, was significantly associated with bipolar disorder  in the meta-analysis of GWAS.	topic_bd
77978	3	356330	7	NULL	NULL	0	NULL	PCLO gene	GP		is					piccolo gene	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	One SNP (rs13438494), in an intron of the piccolo (PCLO) gene, was significantly associated with bipolar disorder  in the meta-analysis of GWAS.	topic_bd
77979	1	356331	7	NULL	NULL	0	NULL	SNP	NucleicAcid		is a type of					DNA sequence	NucleicAcid	variation in			NULL		0	NULL	NULL	NULL	NULL	NULL	A single-nucleotide polymorphism (SNP, pronounced snip) is a DNA sequence variation occurring when a single nucleotide in the genome (or other shared sequence) differs between members of a biological species or paired chromosomes in an individual.	topic_bd
77980	2	356331	7	NULL	NULL	0	NULL	statement 1	Process		occur upon 					genome	GP	variation of single nucleotide			NULL		0	NULL	NULL	NULL	NULL	NULL	A single-nucleotide polymorphism (SNP, pronounced snip) is a DNA sequence variation occurring when a single nucleotide in the genome (or other shared sequence) differs between members of a biological species or paired chromosomes in an individual.	topic_bd
77981	3	356331	7	NULL	NULL	0	NULL	statement 2	Process		occur between					biological species	Organism	members of			NULL		0	NULL	NULL	NULL	NULL	NULL	A single-nucleotide polymorphism (SNP, pronounced snip) is a DNA sequence variation occurring when a single nucleotide in the genome (or other shared sequence) differs between members of a biological species or paired chromosomes in an individual.	topic_bd
77982	4	356331	7	NULL	NULL	0	NULL	statement 2	Process		occur between					individual	Person	paired chromosomes in			NULL		0	NULL	NULL	NULL	NULL	NULL	A single-nucleotide polymorphism (SNP, pronounced snip) is a DNA sequence variation occurring when a single nucleotide in the genome (or other shared sequence) differs between members of a biological species or paired chromosomes in an individual.	topic_bd
77983	5	356331	7	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	A single-nucleotide polymorphism (SNP, pronounced snip) is a DNA sequence variation occurring when a single nucleotide in the genome (or other shared sequence) differs between members of a biological species or paired chromosomes in an individual.	topic_bd
77984	6	356331	7	NULL	NULL	0	NULL	SNP	Process		is					single-nucleotide polymorphism	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	A single-nucleotide polymorphism (SNP, pronounced snip) is a DNA sequence variation occurring when a single nucleotide in the genome (or other shared sequence) differs between members of a biological species or paired chromosomes in an individual.	topic_bd
78578	1	356333	5	NULL	NULL	NULL	NULL	DUI	MedicalFinding		is not correlated to		significantly			brain	OrganismPart	change in volume of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	We found no significant correlation between DUI and brain volume (change) in schizophrenia patients.	topic_sch
78579	2	356333	5	NULL	NULL	NULL	NULL	statement 1	Process		occurs in					schizophrenia patients	GroupOfPeople				NULL		NULL	NULL	NULL	NULL	NULL	NULL	We found no significant correlation between DUI and brain volume (change) in schizophrenia patients.	topic_sch
78580	1	356334	5	NULL	NULL	0	NULL	Schizophrenic patients	GroupOfPeople		identify					emotions	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	In the first experiment, we found that patients with schizophrenia were less accurate at identifying emotions than a group of matched controls.	topic_sch
78581	2	356334	5	NULL	NULL	0	NULL	controls	GroupOfPeople		identify					emotions	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	In the first experiment, we found that patients with schizophrenia were less accurate at identifying emotions than a group of matched controls.	topic_sch
78582	3	356334	5	NULL	NULL	0	NULL	statement 1	Process		less accurate than					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	In the first experiment, we found that patients with schizophrenia were less accurate at identifying emotions than a group of matched controls.	topic_sch
78583	1	356335	5	NULL	NULL	0	NULL	oxytocin	GP	administration of	improves					schizophrenia	MedicalFinding	clinical symptoms of			NULL		0	NULL	NULL	NULL	NULL	NULL	nterest in oxytocin in schizophrenia is just beginning to emerge. Recent studies have shown improvements in clinical symptoms, including both positive and negative symptoms, with oxytocin administration (Feifel et al. 2010; Rubin et al. 2010). 	topic_sch
78584	1	356337	5	NULL	NULL	0	NULL	oxytocin	GP		effects		beneficial			emotion recognition	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Complementing this, our results suggest that oxytocin can have beneficial effects on emotion recognition, a well-documented deficit in this clinical population, which may have an impact on symptoms in the longer term, as differences were only evident after 3 weeks of treatment (Feifel et al. 2010), as well as contributing to better social functioning in the patients. Our study also demonstrates acute improvements in emotion recognition. This offers the potential in the future of integrating oxytocin treatment with psychological therapy using the window of opportunity created by the acute oxytocin effects.	topic_sch
78585	2	356337	5	NULL	NULL	0	NULL	statement 1	Process		contribute to					social functioning	Process	better			NULL		0	NULL	NULL	NULL	NULL	NULL	Complementing this, our results suggest that oxytocin can have beneficial effects on emotion recognition, a well-documented deficit in this clinical population, which may have an impact on symptoms in the longer term, as differences were only evident after 3 weeks of treatment (Feifel et al. 2010), as well as contributing to better social functioning in the patients. Our study also demonstrates acute improvements in emotion recognition. This offers the potential in the future of integrating oxytocin treatment with psychological therapy using the window of opportunity created by the acute oxytocin effects.	topic_sch
78586	1	356338	5	NULL	NULL	0	NULL	rs3016384	NucleicAcid		is a type of					SNP	NucleicAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	The previously discovered SNP associated with schizophrenia in Europeans, rs3016384, also showed significant association with schizophrenia in the Thai population [P = 0.01; odds ratio of the minor T allele, 0.59 (0.44-0.79)]. Therefore, the OPCML gene is considered to be a schizophrenia-susceptible gene in the Thai population.	topic_sch
78587	2	356338	5	NULL	NULL	0	NULL	rs3016384	NucleicAcid		is associated with					schizophrenia	MedicalFinding				NULL	Europeans	0	NULL	NULL	NULL	NULL	NULL	The previously discovered SNP associated with schizophrenia in Europeans, rs3016384, also showed significant association with schizophrenia in the Thai population [P = 0.01; odds ratio of the minor T allele, 0.59 (0.44-0.79)]. Therefore, the OPCML gene is considered to be a schizophrenia-susceptible gene in the Thai population.	topic_sch
78588	3	356338	5	NULL	NULL	0	NULL	statement 2	Process		is associated with					schizophrenia	MedicalFinding				NULL	Thai population	0	NULL	NULL	NULL	NULL	NULL	The previously discovered SNP associated with schizophrenia in Europeans, rs3016384, also showed significant association with schizophrenia in the Thai population [P = 0.01; odds ratio of the minor T allele, 0.59 (0.44-0.79)]. Therefore, the OPCML gene is considered to be a schizophrenia-susceptible gene in the Thai population.	topic_sch
78589	4	356338	5	NULL	NULL	0	NULL	OPCML gene	GP		 is considered to be					schizophrenia-susceptible gene	GP				NULL	Thai population	0	NULL	NULL	NULL	NULL	NULL	The previously discovered SNP associated with schizophrenia in Europeans, rs3016384, also showed significant association with schizophrenia in the Thai population [P = 0.01; odds ratio of the minor T allele, 0.59 (0.44-0.79)]. Therefore, the OPCML gene is considered to be a schizophrenia-susceptible gene in the Thai population.	topic_sch
78590	1	356339	5	NULL	NULL	0	NULL	cortical-striatal disconnection	Process		occurs within					CON	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Our findings suggest that schizophrenia is associated with cortical-striatal disconnection within the CON. The result provides a network basis for the cortico-striatal disconnection hypothesis of schizophrenia.	topic_sch
78591	2	356339	5	NULL	NULL	0	NULL	schizophrenia	MedicalFinding		is associated with					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Our findings suggest that schizophrenia is associated with cortical-striatal disconnection within the CON. The result provides a network basis for the cortico-striatal disconnection hypothesis of schizophrenia.	topic_sch
78592	1	356340	5	NULL	NULL	0	NULL	gamma oscillations	PhysicalPhenomenon	abnormal	reported in					SCZ patients	GroupOfPeople				NULL		0	NULL	NULL	NULL	NULL	NULL	For patients with schizophrenia (SCZ), a disease associated with poor cognition, abnormal gamma oscillations have been reported in many experimental paradigms. 	topic_sch
78593	2	356340	5	NULL	NULL	0	NULL	SCZ	MedicalFinding		is associated with					poor cognition	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	For patients with schizophrenia (SCZ), a disease associated with poor cognition, abnormal gamma oscillations have been reported in many experimental paradigms. 	topic_sch
78594	3	356340	5	NULL	NULL	0	NULL	SCZ	MedicalFinding		is					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	For patients with schizophrenia (SCZ), a disease associated with poor cognition, abnormal gamma oscillations have been reported in many experimental paradigms. 	topic_sch
78595	1	356341	5	NULL	NULL	0	NULL	γ oscillations	PhysicalPhenomenon	irregular	serve as		may			schizophrenia	MedicalFinding	endophenotypes of			NULL		0	NULL	NULL	NULL	NULL	NULL	Irregular γ oscillations may serve as endophenotypes for schizophrenia. 	topic_sch
78596	1	356342	5	NULL	NULL	0	NULL	schizophrenia	MedicalFinding		is associated with					DLPFC	GP	neurobiological abnormalities of			NULL		0	NULL	NULL	NULL	NULL	NULL	Schizophrenia is associated with neurobiological abnormalities in the DLPFC. 	topic_sch
78597	1	356344	5	NULL	NULL	0	NULL	oxytocin	GP	intranasal	reduce					schizophrenia	MedicalFinding	psychotic symptoms of			NULL		0	NULL	NULL	NULL	NULL	NULL	Intranasal oxytocin reduces psychotic symptoms and improves Theory of Mind and social perception in schizophrenia.	topic_sch
78598	2	356344	5	NULL	NULL	0	NULL	oxytocin	GP	intranasal	improves					schizophrenic	GroupOfPeople	social perception of			NULL		0	NULL	NULL	NULL	NULL	NULL	Intranasal oxytocin reduces psychotic symptoms and improves Theory of Mind and social perception in schizophrenia.	topic_sch
78599	3	356344	5	NULL	NULL	0	NULL	oxytocin	GP	intranasal	improves					schizophrenic	GroupOfPeople	Theory of Mind of			NULL		0	NULL	NULL	NULL	NULL	NULL	Intranasal oxytocin reduces psychotic symptoms and improves Theory of Mind and social perception in schizophrenia.	topic_sch
77985	1	356345	7	NULL	NULL	0	NULL	APL	MedicalFinding		subtype of					AML	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute promyelocytic leukemia (APL) is a subtype of the cancer acute myeloid leukemia (AML).	topic_ll
77986	2	356345	7	NULL	NULL	0	NULL	APL	MedicalFinding		is					Acute promyelocytic leukemia 	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute promyelocytic leukemia (APL) is a subtype of the cancer acute myeloid leukemia (AML).	topic_ll
77987	3	356345	7	NULL	NULL	0	NULL	AML	MedicalFinding		is					acute myeloid leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute promyelocytic leukemia (APL) is a subtype of the cancer acute myeloid leukemia (AML).	topic_ll
77988	4	356345	7	NULL	NULL	0	NULL	APL	MedicalFinding		subtype of					cancer	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Acute promyelocytic leukemia (APL) is a subtype of the cancer acute myeloid leukemia (AML).	topic_ll
77989	1	356346	7	NULL	NULL	NULL	NULL	Tumor vascularization	Process		occur in					lymphoma tissues	OrganismPart				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Tumor vascularization is higher in lymphoma tissue than in reactive lymph nodes and increases in step with clinically more aggressive lymphoma subtypes and advanced-stage disease.	topic_ll
77990	2	356346	7	NULL	NULL	0	NULL	Tumor vascularization	Process		occur in					reactive lymph nodes	OrganismPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Tumor vascularization is higher in lymphoma tissue than in reactive lymph nodes and increases in step with clinically more aggressive lymphoma subtypes and advanced-stage disease.	topic_ll
77991	3	356346	7	NULL	NULL	0	NULL	statement 1	Process		is higher than					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Tumor vascularization is higher in lymphoma tissue than in reactive lymph nodes and increases in step with clinically more aggressive lymphoma subtypes and advanced-stage disease.	topic_ll
77992	4	356346	7	NULL	NULL	0	NULL	Tumor vascularization	Process		increases					lymphoma subtypes	MedicalFinding	in step with more aggressive			NULL		0	NULL	NULL	NULL	NULL	NULL	Tumor vascularization is higher in lymphoma tissue than in reactive lymph nodes and increases in step with clinically more aggressive lymphoma subtypes and advanced-stage disease.	topic_ll
77993	1	356347	7	NULL	NULL	0	NULL	gene transfer therapy 	MedicalProcedure		create					"serial killer" T cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	The findings, published simultaneously in the New England Journal of Medicine and Science Translational Medicine on August 10, are the first demonstration of the use of gene transfer therapy to create "serial killer" T cells aimed at cancerous tumors.	topic_ll
77994	2	356347	7	NULL	NULL	0	NULL	"serial killer" T cells	Cell		aimed at					cancerous tumors	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The findings, published simultaneously in the New England Journal of Medicine and Science Translational Medicine on August 10, are the first demonstration of the use of gene transfer therapy to create "serial killer" T cells aimed at cancerous tumors.	topic_ll
77995	1	356348	7	NULL	NULL	0	NULL	CLL	MedicalFinding		treated with					T cells	Cell	genetically engineered versions of their own			NULL		0	NULL	NULL	NULL	NULL	NULL	In a cancer treatment breakthrough 20 years in the making, researchers from the University of Pennsylvania's Abramson Cancer Center and Perelman School of Medicine have shown sustained remissions of up to a year among a small group of advanced chronic lymphocytic leukemia (CLL) patients treated with genetically engineered versions of their own T cells.	topic_ll
77996	2	356348	7	NULL	NULL	0	NULL	CLL	MedicalFinding		is					chronic lymphocytic leukemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	In a cancer treatment breakthrough 20 years in the making, researchers from the University of Pennsylvania's Abramson Cancer Center and Perelman School of Medicine have shown sustained remissions of up to a year among a small group of advanced chronic lymphocytic leukemia (CLL) patients treated with genetically engineered versions of their own T cells.	topic_ll
77997	1	356349	7	NULL	NULL	0	NULL	NOC intake	Chemical	human	associated with					leukemia	MedicalFinding	risk of			NULL		0	NULL	NULL	NULL	NULL	NULL	While these results are compatible with the experimental animal literature and the hypothesis that human NOC intake is associated with leukemia risk, given potential biases in the data, further study of this hypothesis with more focused and comprehensive epidemiologic studies is warranted.	topic_ll
77998	1	356351	7	NULL	NULL	0	NULL	ISCs	Cell	gene signature specific for adult	predicts					disease relapse	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Here, we report that a gene signature specific for adult intestinal stem cells (ISCs) predicts disease relapse in CRC patients.	topic_ccc
77999	2	356351	7	NULL	NULL	0	NULL	statement 1	Process		occur in					CRC	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Here, we report that a gene signature specific for adult intestinal stem cells (ISCs) predicts disease relapse in CRC patients.	topic_ccc
78000	3	356351	7	NULL	NULL	0	NULL	ISCs	Cell		is					intestinal stem cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Here, we report that a gene signature specific for adult intestinal stem cells (ISCs) predicts disease relapse in CRC patients.	topic_ccc
78600	1	356352	5	NULL	NULL	0	NULL	D-serine	AminoAcid		is a coagonist of					NMDA receptor	GP				NULL		0	NULL	NULL	NULL	NULL	NULL	The NMDA receptor coagonist D-serine is important in a number of different processes in the central nervous system, ranging from synaptic plasticity to disease states, including schizophrenia.	topic_sch
78601	2	356352	5	NULL	NULL	0	NULL	D-serine	AminoAcid		is important in					central nervous system	OrganismPart	different processes of			NULL		0	NULL	NULL	NULL	NULL	NULL	The NMDA receptor coagonist D-serine is important in a number of different processes in the central nervous system, ranging from synaptic plasticity to disease states, including schizophrenia.	topic_sch
78602	3	356352	5	NULL	NULL	0	NULL	central nervous system	OrganismPart	different processes of	range from					synaptic plasticity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The NMDA receptor coagonist D-serine is important in a number of different processes in the central nervous system, ranging from synaptic plasticity to disease states, including schizophrenia.	topic_sch
78603	4	356352	5	NULL	NULL	0	NULL	central nervous system	OrganismPart	different processes of	range to					disease states	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The NMDA receptor coagonist D-serine is important in a number of different processes in the central nervous system, ranging from synaptic plasticity to disease states, including schizophrenia.	topic_sch
78604	5	356352	5	NULL	NULL	0	NULL	statement 3	Process		occurs along with					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The NMDA receptor coagonist D-serine is important in a number of different processes in the central nervous system, ranging from synaptic plasticity to disease states, including schizophrenia.	topic_sch
78605	6	356352	5	NULL	NULL	0	NULL	disease states	MedicalFinding		include					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The NMDA receptor coagonist D-serine is important in a number of different processes in the central nervous system, ranging from synaptic plasticity to disease states, including schizophrenia.	topic_sch
78606	1	356354	5	NULL	NULL	0	NULL	type-1 immune response	Process	capacity of	reduced in					schizophrenia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The decreased response of lymphocytes after stimulation with specific antigens reflects a reduced capacity for a type-1 immune response in schizophrenia, as well (Müller et al., 1991).	topic_sch
79630	1	356557	5	NULL	NULL	0	NULL	Bazedoxifene	NonProteinOrNucleicAcidChemical		is a type of					SERM	NonProteinOrNucleicAcidChemical	new-generation			NULL		0	NULL	NULL	NULL	NULL	NULL	( Bazedoxifene as a new-generation SERM ) .	manualset1
79631	1	356563	5	NULL	NULL	0	NULL	Biatrial re-synchronization	MedicalProcedure		is used to treat					Biatrial re-synchronization	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Biatrial re-synchronization in the treatment of paroxysmal atrial fibrillation .	manualset1
79632	1	356590	5	NULL	NULL	0	NULL	dead fetus	BodyPart	retension of	causes					coagulation disorder	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( COAGULATION DISORDERS CAUSED BY RETENTION OF A DEAD FETUS AND THEIR MANAGEMENT ) .	manualset1
79638	1	356592	5	NULL	NULL	0	NULL	Haurydrin	NonProteinOrNucleicAcidChemical		effects		may			Diuresis	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( CONTRIBUTION ON THE EFFECT OF HAURYDRIN ON DIURESIS AND ON THE ELECTROLYTE BALANCE ) .	manualset1
79639	2	356592	5	NULL	NULL	NULL	NULL	Haurydrin	NonProteinOrNucleicAcidChemical		effects		may			Electrolyte balance	BiologicalProcess				NULL		NULL	NULL	NULL	NULL	NULL	NULL	( CONTRIBUTION ON THE EFFECT OF HAURYDRIN ON DIURESIS AND ON THE ELECTROLYTE BALANCE ) .	manualset1
79640	1	356605	5	NULL	NULL	0	NULL	Capillary sprouting	Process		is a type of					reparation	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	( Capillary sprouting as a reparation principle in local radiation injuries ) .	manualset1
79641	2	356605	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					radiation injuries	MedicalFinding	local			NULL		0	NULL	NULL	NULL	NULL	NULL	( Capillary sprouting as a reparation principle in local radiation injuries ) .	manualset1
79642	1	356607	5	NULL	NULL	0	NULL	pneumatic dilatation	MedicalFinding		occurs in					achalasia	Disease				NULL	esophagus	0	NULL	NULL	NULL	NULL	NULL	( Cardiac arrhythmia during pneumatic dilatation of achalasia of the esophagus ( author 's transl ) ) .	manualset1
79643	2	356607	5	NULL	NULL	0	NULL	statement 1	Process		leads to					Cardiac arrhythmia	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Cardiac arrhythmia during pneumatic dilatation of achalasia of the esophagus ( author 's transl ) ) .	manualset1
79644	1	356608	5	NULL	NULL	0	NULL	cigarette smoking	Process		leads to					Cardiac responses	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Cardiac responses to cigarette smoking in healthy young male adults ( author 's transl ) ) .	manualset1
79645	2	356608	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					male adults	PersonGroup	healthy;;young			NULL		0	NULL	NULL	NULL	NULL	NULL	( Cardiac responses to cigarette smoking in healthy young male adults ( author 's transl ) ) .	manualset1
79646	1	356616	5	NULL	NULL	0	NULL	neuromyelitis optica	Disease		suspected to be					toxoplasmosis	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Case of neuromyelitis optica suspected to be toxoplasmosis ) .	manualset1
79647	1	356618	5	NULL	NULL	0	NULL	septicemia	Disease		is caused by					Clostridium perfringens	Organism	infection of;;postabortal			NULL		0	NULL	NULL	NULL	NULL	NULL	( Case of septicemia caused by postabortal Clostridium perfringens infection with anuria treated by exchange transfusion and tifomycin ) .	manualset1
79648	1	356621	5	NULL	NULL	0	NULL	all-trans retinoic acid	NonProteinOrNucleicAcidChemical		is used to treat					leukemia	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Central nervous system relapse with multiple brain masses in an acute promyelocytic leukemia patient treated with all-trans retinoic acid ) .	manualset1
79649	1	356626	5	NULL	NULL	0	NULL	Cerebral aneurysm	Disease		is associated with					persistent trigeminal artery	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	( Cerebral aneurysm associated with persistent trigeminal artery and occlusion of the subclavian artery .	manualset1
79650	2	356626	5	NULL	NULL	0	NULL	Cerebral aneurysm	Disease		is associated with					subclavian artery	BodyPart	occlusion of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Cerebral aneurysm associated with persistent trigeminal artery and occlusion of the subclavian artery .	manualset1
79651	1	356628	5	NULL	NULL	0	NULL	intracranial tumors	Disease	unsuspected	leads to					Cerebral hemorrhage	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Cerebral hemorrhage from unsuspected intracranial tumors ) .	manualset1
79652	1	356631	5	NULL	NULL	0	NULL	Cervical lymph node	BodyPart		metastases from					primary tumor	Disease	unknown			NULL		0	NULL	NULL	NULL	NULL	NULL	( Cervical lymph node metastases from an unknown primary tumor ) .	manualset1
79653	1	356636	5	NULL	NULL	0	NULL	erthrocytes	Cell	acidic resistance of	changes in		may			psychiatric disorders	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Changes in the acidic resistance of erythrocytes in psychiatric disorders ( author 's transl ) ) .	manualset1
79654	1	356637	5	NULL	NULL	0	NULL	chromatin	Chromosome	compactness of;;nucleosome	changes during					aging	BiologicalProcess				NULL	bovine liver	0	NULL	NULL	NULL	NULL	NULL	( Changes in the compactness of nucleosome chromatin from the bovine liver during aging ) .	manualset1
79655	1	356643	5	NULL	NULL	0	NULL	TNF-alpha	Protein		changes in					silicosis patients	PersonGroup				NULL		0	NULL	NULL	NULL	NULL	NULL	( Changes of TNF-alpha and C ( 3 ) complements in patients with silicosis ) .	manualset1
79656	2	356643	5	NULL	NULL	0	NULL	C ( 3 ) complements	Protein		changes in					silicosis patients	PersonGroup				NULL		0	NULL	NULL	NULL	NULL	NULL	( Changes of TNF-alpha and C ( 3 ) complements in patients with silicosis ) .	manualset1
79657	1	356654	5	NULL	NULL	0	NULL	Chlormezanone	NonProteinOrNucleicAcidChemical		is a type of					Chlormezanone	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	( Chlormezanone : muscle relaxant and neuropsychic normalizer .	manualset1
79658	2	356654	5	NULL	NULL	0	NULL	Chlormezanone	NonProteinOrNucleicAcidChemical		is a type of					neuropsychic normalizer	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	( Chlormezanone : muscle relaxant and neuropsychic normalizer .	manualset1
79659	1	356661	5	NULL	NULL	0	NULL	Toxocara canis	Organism		causes					Chronic endophthalmitis	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Chronic endophthalmitis due to Toxocara canis ) .	manualset1
79660	1	356685	5	NULL	NULL	0	NULL	radiation synovectomy	MedicalProcedure		treats					chronic synovitis					NULL	knee joint	0	NULL	NULL	NULL	NULL	NULL	( Clinical experience with radiation synovectomy in the treatment of chronic synovitis of the knee joint -- long-term investigation ( author 's transl ) ) .	manualset1
79670	1	356764	5	NULL	NULL	0	NULL	ventricular tachycardia	Disease		is controlled by					ventricle	BodyPart	rapid electric stimulation of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Control of ventricular tachycardia by rapid electric stimulation of the ventricle ) .	manualset1
79671	1	356765	5	NULL	NULL	0	NULL	Conus venoms	Protein		is a source of					toxins	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	( Conus venoms : a source of toxins which interact with membrane - potential-dependent sodium channels ) .	manualset1
79672	2	356765	5	NULL	NULL	0	NULL	Conus venoms	Protein		interacts with					membrane - potential-dependent sodium channels	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	( Conus venoms : a source of toxins which interact with membrane - potential-dependent sodium channels ) .	manualset1
79673	1	356790	5	NULL	NULL	0	NULL	Cutaneous giant cell tubercle	Disease		is induced by					tuberculin	Organism	desensitization with			NULL		0	NULL	NULL	NULL	NULL	NULL	( Cutaneous giant cell tubercle induced by desensitization with old tuberculin ( Koch ) ) .	manualset1
79674	1	356794	5	NULL	NULL	0	NULL	Cystic pulmonary metastasis	Disease		stimulates					histiocytosis X	Disease	diagnosis of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Cystic pulmonary metastasis simulating a diagnosis of histiocytosis X ) .	manualset1
79675	1	356805	5	NULL	NULL	NULL	NULL	macular ganglion cell complex	AnatomicalPart		is damaged in					multiple sclerosis	Disease				NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Damage of macular ganglion cell complex and peripapillary retinal nerve fiber layer in multiple sclerosis ) .	manualset1
79676	2	356805	5	NULL	NULL	0	NULL	peripapillary retinal nerve fiber layer	AnatomicalPart		is damaged in					multiple sclerosis	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Damage of macular ganglion cell complex and peripapillary retinal nerve fiber layer in multiple sclerosis ) .	manualset1
79677	1	356809	5	NULL	NULL	0	NULL	Vim nucleus	BodyPart	stimulation of	plays a role in					parkinsonian tremor	Disease	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Deep brain stimulation of the Vim nucleus of the thalamus in the treatment of parkinsonian tremor ) .	manualset1
79678	2	356809	5	NULL	NULL	0	NULL	Vim nucleus	BodyPart		is present in					thalamus	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	( Deep brain stimulation of the Vim nucleus of the thalamus in the treatment of parkinsonian tremor ) .	manualset1
79679	3	356809	5	NULL	NULL	0	NULL	statement 2	BodyPart		is a part of					deep brain	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	( Deep brain stimulation of the Vim nucleus of the thalamus in the treatment of parkinsonian tremor ) .	manualset1
80647	1	356855	5	NULL	NULL	0	NULL	imatinib mesylate	NonProteinOrNucleicAcidChemical		treats					Philadelphia chromosome-positive chronic myelogenous leukemia patients	PersonGroup				NULL		0	NULL	NULL	NULL	NULL	NULL	( Disease transformation in imatinib mesylate treated Philadelphia chromosome-positive chronic myelogenous leukemia patients achieved cytogenetic remissions ) .	manualset1
80648	2	356855	5	NULL	NULL	0	NULL	statement 1	Process	disease transformation of	achieved					cytogenetic remissions	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	( Disease transformation in imatinib mesylate treated Philadelphia chromosome-positive chronic myelogenous leukemia patients achieved cytogenetic remissions ) .	manualset1
79680	1	356890	5	NULL	NULL	0	NULL	1,3 butylene glycol	NonProteinOrNucleicAcidChemical		effects		may			reproduction	BiologicalProcess				NULL	rat	0	NULL	NULL	NULL	NULL	NULL	( Effect of 1,3 butylene glycol on reproduction in rats ) .	manualset1
79681	1	356891	5	NULL	NULL	0	NULL	ACTH	GeneOrProtein		effects		may			mortality	BiologicalProcess				NULL	irradiated mice	0	NULL	NULL	NULL	NULL	NULL	( Effect of ACTH on mortality of irradiated mice ) .	manualset1
79682	1	356892	5	NULL	NULL	0	NULL	BAL	Chemical		effects		may			pencillin	NonProteinOrNucleicAcidChemical	inhibitory property of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of BAL on the inhibitory property of penicillin and streptomycin ) .	manualset1
79683	2	356892	5	NULL	NULL	0	NULL	BAL	Chemical		effects		may			streptomycin	NonProteinOrNucleicAcidChemical	inhibitory property of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of BAL on the inhibitory property of penicillin and streptomycin ) .	manualset1
79684	1	356897	5	NULL	NULL	0	NULL	dexamethasone	NonProteinOrNucleicAcidChemical		effects		may			phospholipid spectrum	NonProteinOrNucleicAcidChemical	skin			NULL	laboratory animals	0	NULL	NULL	NULL	NULL	NULL	( Effect of dexamethasone on skin phospholipid spectrum in laboratory animals ) .	manualset1
79685	1	356898	5	NULL	NULL	0	NULL	olive oil	NonProteinOrNucleicAcidChemical	dietary	effects		may			high density lipoproteins	NonProteinOrNucleicAcidChemical	plasma			NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of dietary olive oil on plasma high density lipoproteins ) .	manualset1
79686	1	356899	5	NULL	NULL	0	NULL	diet	Food		contains					caloric levels	Measurement	different			NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of diets with different caloric levels on blood protein turnover ) .	manualset1
79687	2	356899	5	NULL	NULL	0	NULL	statement 1	Process		effects		may			protein	Protein	turnover of;;blood			NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of diets with different caloric levels on blood protein turnover ) .	manualset1
79693	1	356901	5	NULL	NULL	0	NULL	erythromycin	NonProteinOrNucleicAcidChemical		effects		may			polymorphonuclear leukocyte	Cell	ingestion of;;human			NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of erythromycin and phosphomycin on the ingestion and destruction capacity of the human polymorphonuclear leukocyte ) .	manualset1
79694	3	356901	5	NULL	NULL	0	NULL	erythromycin	NonProteinOrNucleicAcidChemical		effects		may			statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of erythromycin and phosphomycin on the ingestion and destruction capacity of the human polymorphonuclear leukocyte ) .	manualset1
79695	2	356901	5	NULL	NULL	0	NULL	polymorphonuclear leukocyte	Cell	human	is involved in					destruction	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of erythromycin and phosphomycin on the ingestion and destruction capacity of the human polymorphonuclear leukocyte ) .	manualset1
79696	4	356901	5	NULL	NULL	0	NULL	phosphomycin	NonProteinOrNucleicAcidChemical		effects		may			polymorphonuclear leukocyte	Cell	ingestion of;;human			NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of erythromycin and phosphomycin on the ingestion and destruction capacity of the human polymorphonuclear leukocyte ) .	manualset1
79697	5	356901	5	NULL	NULL	0	NULL	phosphomycin	NonProteinOrNucleicAcidChemical		effects		may			statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of erythromycin and phosphomycin on the ingestion and destruction capacity of the human polymorphonuclear leukocyte ) .	manualset1
79698	1	356902	5	NULL	NULL	NULL	NULL	gestrinone	NonProteinOrNucleicAcidChemical		effects		may			lipid	NonProteinOrNucleicAcidChemical	metabolic parameters of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Effect of gestrinone on the lipid metabolic parameters and bone mineral density in patients with endometriosis ) .	manualset1
79699	2	356902	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					endometriosis patients	PersonGroup				NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of gestrinone on the lipid metabolic parameters and bone mineral density in patients with endometriosis ) .	manualset1
79700	3	356902	5	NULL	NULL	0	NULL	gestrinone	NonProteinOrNucleicAcidChemical		effects		may			bone	BodyPart	mineral density of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of gestrinone on the lipid metabolic parameters and bone mineral density in patients with endometriosis ) .	manualset1
79701	4	356902	5	NULL	NULL	0	NULL	statement 3	Process		occurs in					endometriosis patients	PersonGroup				NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of gestrinone on the lipid metabolic parameters and bone mineral density in patients with endometriosis ) .	manualset1
79702	1	356903	5	NULL	NULL	0	NULL	glycosylation	MolecularProcess		effects		may			collagen type I fibrillogenesis	MolecularProcess				NULL	connective tissue	0	NULL	NULL	NULL	NULL	NULL	( Effect of glycosylation on collagen type I fibrillogenesis in a model of connective tissue ) .	manualset1
79703	1	356905	5	NULL	NULL	0	NULL	phenol	NonProteinOrNucleicAcidChemical		effects		may			V79 cells	Cell	cultured			NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of phenol on cultured V79 cells ) .	manualset1
79704	1	356906	5	NULL	NULL	0	NULL	physical exercise	Process		effects		may			bone tissue	BodyPart	calcified			NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of physical exercise on calcified bone tissue ) .	manualset1
79705	1	356907	5	NULL	NULL	NULL	NULL	lactose	NonProteinOrNucleicAcidChemical		is present in					rabbits	Organism	milk of;;lactating			NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Effect of reserpine on the lactose , iron and lactoferrin content of the milk of lactating rabbits ) .	manualset1
79706	2	356907	5	NULL	NULL	0	NULL	reserpine	NonProteinOrNucleicAcidChemical		effects		may			statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of reserpine on the lactose , iron and lactoferrin content of the milk of lactating rabbits ) .	manualset1
79707	3	356907	5	NULL	NULL	NULL	NULL	iron	NonProteinOrNucleicAcidChemical		is present in					rabbits	Organism	milk of;;lactating			NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Effect of reserpine on the lactose , iron and lactoferrin content of the milk of lactating rabbits ) .	manualset1
79708	4	356907	5	NULL	NULL	0	NULL	reserpine	NonProteinOrNucleicAcidChemical		effects		may			statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of reserpine on the lactose , iron and lactoferrin content of the milk of lactating rabbits ) .	manualset1
79709	5	356907	5	NULL	NULL	0	NULL	lactoferrin	NonProteinOrNucleicAcidChemical		is present in					rabbits	Organism	milk of;;lactating			NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of reserpine on the lactose , iron and lactoferrin content of the milk of lactating rabbits ) .	manualset1
79710	6	356907	5	NULL	NULL	0	NULL	reserpine	NonProteinOrNucleicAcidChemical		effects		may			statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of reserpine on the lactose , iron and lactoferrin content of the milk of lactating rabbits ) .	manualset1
79711	1	356909	5	NULL	NULL	0	NULL	siRNA	NucleicAcid	transfection of	targets					VEGF gene	Gene				NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of siRNA transfection targeting VEGF gene on proliferation and apoptosis of human breast cancer cells ) .	manualset1
79712	2	356909	5	NULL	NULL	0	NULL	statement 1	Process		effects		may			breast cancer cells	Cell	proliferation of;;human			NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of siRNA transfection targeting VEGF gene on proliferation and apoptosis of human breast cancer cells ) .	manualset1
79713	3	356909	5	NULL	NULL	0	NULL	statement 1	Process		effects		may			breast cancer cells	Cell	apoptosis of;;human			NULL		0	NULL	NULL	NULL	NULL	NULL	( Effect of siRNA transfection targeting VEGF gene on proliferation and apoptosis of human breast cancer cells ) .	manualset1
79714	1	356911	5	NULL	NULL	0	NULL	starvation	Process		effects		may			respiratory reactivity	Process				NULL	inbred rats	0	NULL	NULL	NULL	NULL	NULL	( Effect of starvation on respiratory reactivity in inbred rats ) .	manualset1
79722	1	356934	5	NULL	NULL	0	NULL	agents	Chemical		stimulates					histamine H1 receptor	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	( Electrophysiological changes in the state of uterine muscles under the action of agents stimulating histamine H1 and H2 receptors ) .	manualset1
79723	2	356934	5	NULL	NULL	0	NULL	agents	Chemical		stimulates					histamine H2 receptor	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	( Electrophysiological changes in the state of uterine muscles under the action of agents stimulating histamine H1 and H2 receptors ) .	manualset1
79724	3	356934	5	NULL	NULL	0	NULL	statement 1	Process		changes					uterine muscles	BodyPart	state of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Electrophysiological changes in the state of uterine muscles under the action of agents stimulating histamine H1 and H2 receptors ) .	manualset1
79725	4	356934	5	NULL	NULL	0	NULL	statement 2	Process		changes					uterine muscles	BodyPart	state of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Electrophysiological changes in the state of uterine muscles under the action of agents stimulating histamine H1 and H2 receptors ) .	manualset1
79726	1	357033	5	NULL	NULL	0	NULL	pancreatic islets	BodyPart		altered by					autoimmune system	AnatomicalPart				NULL	 diabetic subjects	0	NULL	NULL	NULL	NULL	NULL	( Functional study of pancreatic islets altered by the autoimmune system in diabetic and non-diabetic subjects ) .	manualset1
79727	2	357033	5	NULL	NULL	0	NULL	pancreatic islets	BodyPart		altered by					autoimmune system	AnatomicalPart				NULL	non-diabetic subjects	0	NULL	NULL	NULL	NULL	NULL	( Functional study of pancreatic islets altered by the autoimmune system in diabetic and non-diabetic subjects ) .	manualset1
79728	1	357062	5	NULL	NULL	0	NULL	myocardial calcification	MedicalFinding	severe	leads to					heart failure	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Heart failure due to severe myocardial calcification -- a rare complication after irradiation on the chest wall ) .	manualset1
79729	2	357062	5	NULL	NULL	0	NULL	statement 1	Process		is a type of					rare complication	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	( Heart failure due to severe myocardial calcification -- a rare complication after irradiation on the chest wall ) .	manualset1
79730	3	357062	5	NULL	NULL	0	NULL	statement 1	Process		occurs after					chest wall	BodyPart	irradiation of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Heart failure due to severe myocardial calcification -- a rare complication after irradiation on the chest wall ) .	manualset1
79731	1	357066	5	NULL	NULL	0	NULL	Hemosorption	NonProteinOrNucleicAcidChemical		treats					occlusive arterial diseases	Disease				NULL	legs	0	NULL	NULL	NULL	NULL	NULL	( Hemosorption in the treatment of occlusive arterial diseases of the legs ) .	manualset1
79732	1	357067	5	NULL	NULL	0	NULL	mexamine	NonProteinOrNucleicAcidChemical	hemostatic action of 	plays a role in					acute radiation sickness	Disease	experimental			NULL		0	NULL	NULL	NULL	NULL	NULL	( Hemostatic action of serotonin and mexamine in experimental acute radiation sickness ) .	manualset1
79733	2	357067	5	NULL	NULL	0	NULL	serotonin	Protein	hemostatic action of	plays a role in					acute radiation sickness	Disease	experimental			NULL		0	NULL	NULL	NULL	NULL	NULL	( Hemostatic action of serotonin and mexamine in experimental acute radiation sickness ) .	manualset1
79734	1	357069	5	NULL	NULL	0	NULL	pneumonia	Disease		causes					hepatocellular damage	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	( Hepatocellular damage during pneumonia ) .	manualset1
79735	1	357075	5	NULL	NULL	0	NULL	heparin	NonProteinOrNucleicAcidChemical		release					Histaminase	Protein				NULL	guinea pigs	0	NULL	NULL	NULL	NULL	NULL	( Histaminase release by heparin and protamine in guinea pigs ) .	manualset1
79736	2	357075	5	NULL	NULL	0	NULL	protamine	Protein		release					Histaminase	Protein				NULL	guinea pigs	0	NULL	NULL	NULL	NULL	NULL	( Histaminase release by heparin and protamine in guinea pigs ) .	manualset1
79737	1	357100	5	NULL	NULL	0	NULL	granulocytes	Cell	increase of	leads to					Hyperleukocytosis	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Hyperleukocytosis due to an increase in granulocytes ) .	manualset1
79738	1	357104	5	NULL	NULL	0	NULL	Hypoxidosis	MedicalFinding		causal factor in					skin diseases	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Hypoxidosis as causal factor in skin diseases ) .	manualset1
79826	1	357114	5	NULL	NULL	0	NULL	ICAM-1	Protein		is					intercellular cell adhesion molecule 1	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	( Immunohistologic study of the localization of ICAM-1 ( intercellular cell adhesion molecule 1 ) in alveolar epithelium in the human lung ) .	manualset1
79827	2	357114	5	NULL	NULL	NULL	NULL	ICAM-1	Protein		is localized in					alveolar epithelium	BodyPart				NULL	human lung	NULL	NULL	NULL	NULL	NULL	NULL	( Immunohistologic study of the localization of ICAM-1 ( intercellular cell adhesion molecule 1 ) in alveolar epithelium in the human lung ) .	manualset1
79828	1	357119	5	NULL	NULL	0	NULL	celioscopy	MedicalProcedure		is important for		may be			conjugal sterility	Process	involuntary			NULL		0	NULL	NULL	NULL	NULL	NULL	( Importance of celioscopy in involuntary conjugal sterility ) .	manualset1
79829	1	357120	5	NULL	NULL	0	NULL	intracardiac phonocardiography	MedicalProcedure		is important for		may be			tricuspid insufficiency	Disease	diagnosis of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Importance of intracardiac phonocardiography in the diagnosis of tricuspid insufficiency ) .	manualset1
79830	1	357121	5	NULL	NULL	0	NULL	isoimmunization	MedicalProcedure		is important for		may be			mongoloid idiocy	Disease	pathogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Importance of isoimmunization in pathogenesis of mongoloid idiocy ) .	manualset1
79875	1	357122	5	NULL	NULL	0	NULL	artificial respiration	MedicalProcedure	prolonged	is important for		may be			closed chest injuries	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Importance of prolonged artificial respiration in the treatment of closed chest injuries ) .	manualset1
79880	1	357124	5	NULL	NULL	0	NULL	surfactant system	Chemical		is important for		may be			hyaline membrane	BodyPart	pathogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Importance of the `` surfactant system '' in the pathogenesis of hyaline membrane in the newborn ) .	manualset1
79887	1	357142	5	NULL	NULL	0	NULL	mammary carcinomas	Disease		increases during					pregnancy	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	( Increase of mammary carcinomas during pregnancy and in the lactation period ) .	manualset1
79888	2	357142	5	NULL	NULL	0	NULL	mammary carcinomas	Disease		increases during					lactation period	Time				NULL		0	NULL	NULL	NULL	NULL	NULL	( Increase of mammary carcinomas during pregnancy and in the lactation period ) .	manualset1
79909	1	357147	5	NULL	NULL	NULL	NULL	antigens	Chemical	Individual	serological cause of					fetal injury	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Individual antigens as serological cause of fetal injury and their role in blood transfusion ) .	manualset1
79914	1	357155	5	NULL	NULL	NULL	NULL	dl-propranolol	NonProteinOrNucleicAcidChemical		inhibits					sperm capacitation	BiologicalProcess	guinea pig			NULL	in vitro	NULL	NULL	NULL	NULL	NULL	NULL	( Inhibition of guinea pig sperm capacitation , the acrosome reaction and sperm-egg fusion by dl-propranolol in vitro ) .	manualset1
79915	2	357155	5	NULL	NULL	0	NULL	dl-propranolol	NonProteinOrNucleicAcidChemical		inhibits					acrosome reaction	BiologicalProcess	guinea pig			NULL	in vitro	0	NULL	NULL	NULL	NULL	NULL	( Inhibition of guinea pig sperm capacitation , the acrosome reaction and sperm-egg fusion by dl-propranolol in vitro ) .	manualset1
79916	3	357155	5	NULL	NULL	0	NULL	dl-propranolol	NonProteinOrNucleicAcidChemical		inhibits					sperm-egg fusion	BiologicalProcess	guinea pig			NULL	in vitro	0	NULL	NULL	NULL	NULL	NULL	( Inhibition of guinea pig sperm capacitation , the acrosome reaction and sperm-egg fusion by dl-propranolol in vitro ) .	manualset1
79921	1	357163	5	NULL	NULL	0	NULL	14-3-3beta	GeneOrProtein	segments of	interacts with					PrP	GeneOrProtein				NULL	in vitro	0	NULL	NULL	NULL	NULL	NULL	( Interaction between various 14-3-3beta segments and PrP in vitro ) .	manualset1
79922	1	357165	5	NULL	NULL	0	NULL	androgen	GeneOrProtein		deprived in		intermittently			prostate cancer	Disease	advanced			NULL		0	NULL	NULL	NULL	NULL	NULL	( Intermittent androgen deprivation in advanced prostate cancer : a review ) .	manualset1
79923	1	357171	5	NULL	NULL	0	NULL	Intestinal occlusion	Disease		is caused by					retroperitoneal cysts	MedicalFinding	wolffian			NULL		0	NULL	NULL	NULL	NULL	NULL	( Intestinal occlusion caused by retroperitoneal cysts of wolffian origin ) .	manualset1
79924	1	357173	5	NULL	NULL	0	NULL	Intra uterine asphyxia	MedicalFinding		leads to					stillbirth					NULL		0	NULL	NULL	NULL	NULL	NULL	( Intra uterine asphyxia as a main factor of stillbirth ) .	manualset1
79925	1	357175	5	NULL	NULL	0	NULL	hyaluronic acid	NonProteinOrNucleicAcidChemical	Intra-articular injections of	plays a role in		may			knee osteoarthritis	Disease	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Intra-articular injections of hyaluronic acid in the treatment of knee osteoarthritis ) .	manualset1
79926	1	357185	5	NULL	NULL	0	NULL	H1 histone	Protein	phosphorylation of	is involved in					chromosome condensation	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	( Involvement of H1 histone phosphorylation in chromosome condensation at mitosis ) .	manualset1
79927	2	357185	5	NULL	NULL	0	NULL	statement 1	Process		occurs during					mitosis	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	( Involvement of H1 histone phosphorylation in chromosome condensation at mitosis ) .	manualset1
79928	1	357196	5	NULL	NULL	0	NULL	methotrexate	NonProteinOrNucleicAcidChemical		treats					rheumatic diseases	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Italian consensus on the recommendations about the use of methotrexate for the treatment of rheumatic diseases with a focus on rheumatoid arthritis : results from the `` 3E initiative '' ) .	manualset1
79929	1	357201	5	NULL	NULL	0	NULL	Klimovan injection	MedicalProcedure		is a diagnostic method in					pregnancy	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	( KLIMOVAN INJECTION AS A DIAGNOSTIC METHOD IN PREGNANCY ) .	manualset1
79930	1	357202	5	NULL	NULL	0	NULL	Ketamine	NonProteinOrNucleicAcidChemical		is used to treat		may be			status asthmaticus	Disease	severe;;therapy-resistant			NULL		0	NULL	NULL	NULL	NULL	NULL	( Ketamine in the treatment of severe therapy-resistant status asthmaticus ) .	manualset1
79931	1	357209	5	NULL	NULL	0	NULL	prednisone	NonProteinOrNucleicAcidChemical	imbalance of;;dosages of	influence		may			kidney	BodyPart	rejection of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Late kidney rejection : influence of imbalance in prednisone and azathioprine dosages ) .	manualset1
79932	2	357209	5	NULL	NULL	0	NULL	azathioprine	NonProteinOrNucleicAcidChemical	imbalance of;;dosages of	influence		may			kidney	BodyPart	rejection of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Late kidney rejection : influence of imbalance in prednisone and azathioprine dosages ) .	manualset1
79934	1	357221	5	NULL	NULL	0	NULL	PLAC 1	NonProteinOrNucleicAcidChemical		is					pravastatin	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	( Limitation of atherosclerosis in coronary arteries with pravastatin ( PLAC 1 ) ) .	manualset1
79935	2	357221	5	NULL	NULL	0	NULL	pravastatin	NonProteinOrNucleicAcidChemical		limits					atherosclerosis	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Limitation of atherosclerosis in coronary arteries with pravastatin ( PLAC 1 ) ) .	manualset1
79936	3	357221	5	NULL	NULL	0	NULL	statement 2	Process		occurs in					coronary arteries	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	( Limitation of atherosclerosis in coronary arteries with pravastatin ( PLAC 1 ) ) .	manualset1
79937	1	357222	5	NULL	NULL	0	NULL	noradrenaline	NonProteinOrNucleicAcidChemical		limits					noradrenaline	NonProteinOrNucleicAcidChemical	vascular effects of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Limitation of the vascular effects of noradrenaline using noradrenaline itself ) .	manualset1
79938	1	357226	5	NULL	NULL	NULL	NULL	Lipoprotein ( a )	Chemical		is a marker for					coronary disease	Disease	presence of;;severity of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Lipoprotein ( a ) , D-Dimer and apolipoprotein A1 as markers of presence and severity of coronary disease ) .	manualset1
79941	2	357226	5	NULL	NULL	0	NULL	D-Dimer	Chemical		is a marker for					coronary disease	Disease	presence of;;severity of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Lipoprotein ( a ) , D-Dimer and apolipoprotein A1 as markers of presence and severity of coronary disease ) .	manualset1
79943	3	357226	5	NULL	NULL	0	NULL	apolipoprotein A1	Protein		is a marker for					coronary disease	Disease	presence of;;severity of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Lipoprotein ( a ) , D-Dimer and apolipoprotein A1 as markers of presence and severity of coronary disease ) .	manualset1
79990	1	357251	5	NULL	NULL	0	NULL	hemoptysis	Disease		is caused by					bronchial aneurysm	MedicalFinding	disruption of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Massive hemoptysis caused by disruption of a bronchial aneurysm diagnosed by microscopic examination of the resected lung ) .	manualset1
79991	1	357260	5	NULL	NULL	0	NULL	enterotoxic staphylococci	Organism		causes					food poisoning	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Medico-legal considerations on a case of food poisoning due to enterotoxic staphylococci ) .	manualset1
79992	1	357268	5	NULL	NULL	0	NULL	Micafungin	NonProteinOrNucleicAcidChemical		is used to treat					invasive mycoses	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Micafungin , a new candin for the treatment of invasive mycoses ) .	manualset1
79993	1	357390	5	NULL	NULL	0	NULL	injuries	MedicalFinding	indirect	causes					Optic atrophy	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Optic atrophy caused by indirect injuries ) .	manualset1
79994	1	357424	5	NULL	NULL	0	NULL	Ca2 +	Chemical		influx into		passively			sarcoplasmic reticulum	BodyPart	vesicles of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Passive Ca2 + influx into vesicles of the sarcoplasmic reticulum , modified by succinic anhydride ) .	manualset1
79995	2	357424	5	NULL	NULL	0	NULL	succinic anhydride	NonProteinOrNucleicAcidChemical		modifies					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	( Passive Ca2 + influx into vesicles of the sarcoplasmic reticulum , modified by succinic anhydride ) .	manualset1
80080	1	357454	5	NULL	NULL	0	NULL	aldosterone	NonProteinOrNucleicAcidChemical		is a type of					Plasma mineralocorticoids	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	( Plasma mineralocorticoids -- aldosterone and desoxycorticosterone -- in patients with `` low-renin `` arterial hypertension ) .	manualset1
80081	2	357454	5	NULL	NULL	0	NULL	desoxycorticosterone	NonProteinOrNucleicAcidChemical		is a type of					Plasma mineralocorticoids	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	( Plasma mineralocorticoids -- aldosterone and desoxycorticosterone -- in patients with `` low-renin `` arterial hypertension ) .	manualset1
80082	1	357458	5	NULL	NULL	0	NULL	Pneumocystis carinii pneumopathy	Disease		occurs in					rheumatoid polyarthritis	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Pneumocystis carinii pneumopathy in rheumatoid polyarthritis treated by methotrexate in a patient with pulmonary asbestosis ) .	manualset1
80083	2	357458	5	NULL	NULL	0	NULL	methotrexate	NonProteinOrNucleicAcidChemical		treats					statement 1	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Pneumocystis carinii pneumopathy in rheumatoid polyarthritis treated by methotrexate in a patient with pulmonary asbestosis ) .	manualset1
80084	3	357458	5	NULL	NULL	0	NULL	statement 2	Process		occurs in					pulmonary asbestosis patient					NULL		0	NULL	NULL	NULL	NULL	NULL	( Pneumocystis carinii pneumopathy in rheumatoid polyarthritis treated by methotrexate in a patient with pulmonary asbestosis ) .	manualset1
80085	1	357556	5	NULL	NULL	0	NULL	radiation	EnvironmentalFactor		induce					injuries	MedicalFinding				NULL	children	0	NULL	NULL	NULL	NULL	NULL	( Radiation-induced injuries following roentgenotherapy of angiomas in children depending on the technic of radiation use ) .	manualset1
80086	2	357556	5	NULL	NULL	0	NULL	statement 1	Process		follows					angiomas	Disease	roentgenotherapy of			NULL	children	0	NULL	NULL	NULL	NULL	NULL	( Radiation-induced injuries following roentgenotherapy of angiomas in children depending on the technic of radiation use ) .	manualset1
80087	3	357556	5	NULL	NULL	NULL	NULL	statement 1	Process		depends on					raditaion	LaboratoryExperimentalFactor	technic of;;use of			NULL	children	NULL	NULL	NULL	NULL	NULL	NULL	( Radiation-induced injuries following roentgenotherapy of angiomas in children depending on the technic of radiation use ) .	manualset1
80088	1	357557	5	NULL	NULL	0	NULL	 Radioactive iodine treatment 	MedicalProcedure		is used to treat					hyperthyroidism	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Radioactive iodine treatment of hyperthyroidism associated with diabetes ) .	manualset1
80089	2	357557	5	NULL	NULL	0	NULL	statement 1	Process		is associated with					diabetes	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Radioactive iodine treatment of hyperthyroidism associated with diabetes ) .	manualset1
80090	1	357562	5	NULL	NULL	0	NULL	Raloxifene	NonProteinOrNucleicAcidChemical		is a modulator of		selective			estrogen receptors	GeneOrProtein				NULL		0	NULL	NULL	NULL	NULL	NULL	( Raloxifene : a selective modulator of estrogen receptors ) .	manualset1
80091	1	357575	5	NULL	NULL	0	NULL	hypotensive medication	MedicalProcedure		reduces the risk of					stroke	Disease	recurrence of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Reduced risk of stroke recurrence due to hypotensive medication , irrespective of the initial blood pressure ) .	manualset1
80092	2	357575	5	NULL	NULL	0	NULL	statement 1	Process		irrespective of					blood pressure	EnvironmentalFactor	initial			NULL		0	NULL	NULL	NULL	NULL	NULL	( Reduced risk of stroke recurrence due to hypotensive medication , irrespective of the initial blood pressure ) .	manualset1
80093	2	357576	5	NULL	NULL	NULL	NULL	statement 1	Process		undergoes					reduction	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Reduction of the functional activity of the calcium pump of the sarcoplasmic reticulum of skeletal muscles in response to cold ) .	manualset1
80094	3	357576	5	NULL	NULL	NULL	NULL	statement 2	Process		in response to					cold	EnvironmentalFactor				NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Reduction of the functional activity of the calcium pump of the sarcoplasmic reticulum of skeletal muscles in response to cold ) .	manualset1
80095	1	357576	5	NULL	NULL	0	NULL	calcium pump	BiologicalProcess		is active in		functionally			sarcoplasmic reticulum	BodyPart				NULL	skeletal muscles	0	NULL	NULL	NULL	NULL	NULL	( Reduction of the functional activity of the calcium pump of the sarcoplasmic reticulum of skeletal muscles in response to cold ) .	manualset1
80096	1	357590	5	NULL	NULL	0	NULL	 vincaleukoblastine	NonProteinOrNucleicAcidChemical		treats					malignant cutaneous reticulosis	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Remarkable action of vincaleukoblastine in the treatment of a case of malignant cutaneous reticulosis ) .	manualset1
80097	1	357595	5	NULL	NULL	0	NULL	angioplasty	MedicalProcedure		is not essential for					Renovascular hypertension	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Renovascular hypertension : angioplasty need not be essential ) .	manualset1
80098	1	357598	5	NULL	NULL	0	NULL	mandibular condyle	BodyPart	high fractures of;;neck of	leads to					mandibular condyle	BodyPart	dislocation of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Replantation as a method of treating high fractures of the neck of the mandibular condyle with dislocation of the articular head ) .	manualset1
80099	2	357598	5	NULL	NULL	0	NULL	Replantation	MedicalProcedure		is used to treat					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	( Replantation as a method of treating high fractures of the neck of the mandibular condyle with dislocation of the articular head ) .	manualset1
80100	1	357604	5	NULL	NULL	0	NULL	Cd2 +	Chemical	soil	is absorbed by					perennial ryegrass	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	( Research on the relevance of earthworms inducing soil Cd2 + absorbed by perennial ryegrass ) .	manualset1
80101	1	357626	5	NULL	NULL	NULL	NULL	apoptosis	BiologicalProcess	renal tubular cells	is induced by					post asphyxial serum	CellComponent	neonate			NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Role of Omi/HtrA2 in renal tubular cells apoptosis induced by post asphyxial serum of neonate ) .	manualset1
80102	1	357630	5	NULL	NULL	NULL	NULL	epithelium	BodyPart		transition to					mesenchyma	BodyPart				NULL	human peritoneal mesothelial cells	NULL	NULL	NULL	NULL	NULL	NULL	( Role of galectin-1 on epithelial-to-mesenchymal transition induced by high glucose peritoneal dialysate in human peritoneal mesothelial cells ) .	manualset1
80104	2	357630	5	NULL	NULL	0	NULL	glucose peritoneal dialysate	NonProteinOrNucleicAcidChemical	high	induce					statement 1					NULL	human peritoneal mesothelial cells	0	NULL	NULL	NULL	NULL	NULL	( Role of galectin-1 on epithelial-to-mesenchymal transition induced by high glucose peritoneal dialysate in human peritoneal mesothelial cells ) .	manualset1
80105	1	357639	5	NULL	NULL	0	NULL	Rubiaceae	Organism		is an important component of					medicine	Chemical	ayurvedic system of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Rubiaceae ) is an important component of the ayurvedic system of medicine .	manualset1
80106	1	357643	5	NULL	NULL	0	NULL	abdominal wall	BodyPart	Sarcoma of	is ruptured during					labor	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	( Sarcoma of the abdominal wall ruptured during labor ) .	manualset1
80107	1	357650	5	NULL	NULL	0	NULL	Neisseria gonorrhoeae	Organism		is sensitive to					spectinomycin	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	( Sensitivity of Neisseria gonorrhoeae to spectinomycin ) .	manualset1
80108	1	357651	5	NULL	NULL	0	NULL	ectoparasites	Organism	chicken	is sensitive to					methylbromfenvinphos	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	( Sensitivity of ectoparasites of chickens to methylbromfenvinphos ( Polwet 5 and Polwet 20 ) .	manualset1
80109	1	357659	5	NULL	NULL	NULL	NULL	encysted purulent pleurisy	Disease		leads to					pulmonary tuberculosis	Disease	severe			NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Severe pulmonary tuberculosis after encysted purulent pleurisy ) .	manualset1
80110	1	357666	5	NULL	NULL	0	NULL	fibrosis	MedicalFinding		is developed in					systemic scleroderma	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Significance of estradiol in the development of fibrosis in systemic scleroderma ( bases of sexual predisposition to the disease ) ) .	manualset1
80136	1	357679	5	NULL	NULL	0	NULL	Soft-tissue	BodyPart		changes in					metacarpal area	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	( Soft-tissue changes in the metacarpal area in chronic polyarthritis ) .	manualset1
80137	2	357679	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					chronic polyarthritis	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Soft-tissue changes in the metacarpal area in chronic polyarthritis ) .	manualset1
80138	1	357682	5	NULL	NULL	0	NULL	streptomycin	NonProteinOrNucleicAcidChemical		changes					antigenic complex	Chemical	Bacillus anthracis			NULL		0	NULL	NULL	NULL	NULL	NULL	( Some changes in the antigenic complex of Bacillus anthracis under the action of streptomycin ) .	manualset1
80139	1	357693	5	NULL	NULL	0	NULL	granuloma 	MedicalFinding	spermatozoal	causes		possibly			hydrocele	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Spermatozoal granuloma as a possible cause of hydrocele ) .	manualset1
80140	1	357695	5	NULL	NULL	NULL	NULL	ureteric tumor	Disease	metastatic 	ruptures		spontaneously			ureter	BodyPart				NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Spontaneous rupture of the ureter caused by metastatic ureteric tumor : a case report ) .	manualset1
80141	1	357696	5	NULL	NULL	NULL	NULL	excitation	BiologicalProcess		spreads from					ventromedial hypothalamus	BodyPart	brain			NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Spread of excitation from the ventromedial hypothalamus to the limbic-reticular structure of the brain ) .	manualset1
80142	2	357696	5	NULL	NULL	0	NULL	excitation	BiologicalProcess		spreads to					limbic-reticular structure	BodyPart	brain			NULL		0	NULL	NULL	NULL	NULL	NULL	( Spread of excitation from the ventromedial hypothalamus to the limbic-reticular structure of the brain ) .	manualset1
80143	3	357696	5	NULL	NULL	0	NULL	statement 1	Process		occurs simultaneously with					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	( Spread of excitation from the ventromedial hypothalamus to the limbic-reticular structure of the brain ) .	manualset1
80144	1	357709	5	NULL	NULL	0	NULL	Stiff man syndrome	Disease		is also known as					Moersch and Woltman syndrome	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Stiff man syndrome ( Moersch and Woltman syndrome ) .	manualset1
80145	1	357712	5	NULL	NULL	0	NULL	( Strept ) avidins	Protein		is a type of					exceptionally stable proteins	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	( Strept ) avidins are also exceptionally stable proteins .	manualset1
80146	1	357718	5	NULL	NULL	0	NULL	baicalin	NonProteinOrNucleicAcidChemical	metabolites of	is present in					urine	Chemical	human			NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on metabolites of baicalin in human urine ) .	manualset1
80823	1	357734	5	NULL	NULL	0	NULL	LDL receptors	Protein		is present in					non-parenchymal cells	Cell	liver			NULL		0	NULL	NULL	NULL	NULL	NULL	( Study on LDL receptors of liver non-parenchymal cells in hypertriglyceridemic rats induced by high carbohydrate diet ) .	manualset1
80824	2	357734	5	NULL	NULL	0	NULL	statement 1	Process		is present in					rat	Organism	hypertriglyceridemic			NULL		0	NULL	NULL	NULL	NULL	NULL	( Study on LDL receptors of liver non-parenchymal cells in hypertriglyceridemic rats induced by high carbohydrate diet ) .	manualset1
80825	3	357734	5	NULL	NULL	0	NULL	high carbohydrate diet	Food		induce					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	( Study on LDL receptors of liver non-parenchymal cells in hypertriglyceridemic rats induced by high carbohydrate diet ) .	manualset1
80826	1	357735	5	NULL	NULL	0	NULL	572 C/G	Gene		is a type of					interleukin 6 gene	Gene				NULL		0	NULL	NULL	NULL	NULL	NULL	( Study on linkage between polymorphism of interleukin 6 gene -572 C/G and susceptibility to myocardial infarction ) .	manualset1
80827	2	357735	5	NULL	NULL	NULL	NULL	572 C/G	Gene	polymorphism of	is linked to		may be			myocardial infarction	Process	susceptibility of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Study on linkage between polymorphism of interleukin 6 gene -572 C/G and susceptibility to myocardial infarction ) .	manualset1
80829	1	357737	5	NULL	NULL	0	NULL	Subacute septic endocarditis	Disease		is complicated by					vessels	OrganismPart	aneurysm of;;major			NULL		0	NULL	NULL	NULL	NULL	NULL	( Subacute septic endocarditis complicated by an aneurysm of the major vessels ) .	manualset1
80830	1	357738	5	NULL	NULL	0	NULL	Subclinical pulmonary dysfunction	MedicalFinding		is a complication of		probably			diabetes	Disease	unrecognized			NULL		0	NULL	NULL	NULL	NULL	NULL	( Subclinical pulmonary dysfunction : an unrecognized diabetes complication ? ) .	manualset1
80831	1	357742	5	NULL	NULL	NULL	NULL	cystoid macular edema	Disease		is treated with		successfully			etanercept	NonProteinOrNucleicAcidChemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Successful treatment of cystoid macular edema with etanercept in a patient with rheumatoid arthritis associated panuveitis ) .	manualset1
80832	2	357742	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					panuveitis patients	PersonGroup				NULL		0	NULL	NULL	NULL	NULL	NULL	( Successful treatment of cystoid macular edema with etanercept in a patient with rheumatoid arthritis associated panuveitis ) .	manualset1
80833	3	357742	5	NULL	NULL	0	NULL	panuveitis	Disease		is associated with					rheumatoid arthritis	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Successful treatment of cystoid macular edema with etanercept in a patient with rheumatoid arthritis associated panuveitis ) .	manualset1
80838	1	357743	5	NULL	NULL	0	NULL	pituitary-adrenal axis	Process		is suppressed by					triamcinolone acetonide	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	( Suppression of pituitary-adrenal axis by triamcinolone acetonide in asthmatics ) .	manualset1
80839	2	357743	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					asthmatics	PersonGroup				NULL		0	NULL	NULL	NULL	NULL	NULL	( Suppression of pituitary-adrenal axis by triamcinolone acetonide in asthmatics ) .	manualset1
80844	1	357750	5	NULL	NULL	0	NULL	intrahepatic biliary stones	MedicalFinding		is treated with					surgery	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgical treatment of intrahepatic biliary stones ) .	manualset1
80850	1	357751	5	NULL	NULL	0	NULL	malignant neoplasms	Disease		occurs in					pancreatoduodenal zone	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgical treatment of malignant neoplasms of the pancreatoduodenal zone ) .	manualset1
80851	2	357751	5	NULL	NULL	0	NULL	statement 1	Process		is treated with					surgery	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgical treatment of malignant neoplasms of the pancreatoduodenal zone ) .	manualset1
80852	1	357752	5	NULL	NULL	0	NULL	myocardial infarct	Disease		is treated with					surgery	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgical treatment of myocardial infarct in complications .	manualset1
80853	1	357753	5	NULL	NULL	0	NULL	intramedullary tumors	Disease		occurs in					neck	BodyPart	upper			NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgically treated case of intramedullary tumors of the upper neck witn an interesting postoperative course ) .	manualset1
80854	2	357753	5	NULL	NULL	0	NULL	statement 1	Process		is treated with					surgery	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgically treated case of intramedullary tumors of the upper neck witn an interesting postoperative course ) .	manualset1
80855	1	357756	5	NULL	NULL	0	NULL	Legionella pneumonia	Disease		shows					KL-6	Protein	high level of;;serum			NULL		0	NULL	NULL	NULL	NULL	NULL	( Surviving case of Legionella pneumonia showing a high level of serum KL-6 and complicated with rhabdomyolysis ) .	manualset1
80856	1	357757	5	NULL	NULL	0	NULL	Pseudomonas species	Organism		susceptibile to					aminoglycosides	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	( Susceptibilities of Pseudomonas species to aminoglycosides and tetracyclines ) .	manualset1
80857	2	357757	5	NULL	NULL	0	NULL	Pseudomonas species	Organism		susceptibile to					tetracyclines	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	( Susceptibilities of Pseudomonas species to aminoglycosides and tetracyclines ) .	manualset1
80858	1	357760	5	NULL	NULL	0	NULL	THAM citrate	NonProteinOrNucleicAcidChemical	oral administration of	treats					renal acidosis	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Symptomatic treatment of renal acidosis by oral administration of THAM citrate ) .	manualset1
80859	1	357762	5	NULL	NULL	0	NULL	testicular cells	Cell		express					Fas ligand	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	( Synergistic protective effect of testicular cells expressing Fas ligand and cyclosporine A on the survival of islet allografts ) .	manualset1
80860	2	357762	5	NULL	NULL	0	NULL	statement 1	Process		effects		protective			islet allografts	BodyPart	survival of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Synergistic protective effect of testicular cells expressing Fas ligand and cyclosporine A on the survival of islet allografts ) .	manualset1
80861	3	357762	5	NULL	NULL	0	NULL	cyclosporine A	NonProteinOrNucleicAcidChemical		effects		protective			islet allografts	BodyPart	survival of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Synergistic protective effect of testicular cells expressing Fas ligand and cyclosporine A on the survival of islet allografts ) .	manualset1
80862	4	357762	5	NULL	NULL	0	NULL	statement 2	Process		synergistic to					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	( Synergistic protective effect of testicular cells expressing Fas ligand and cyclosporine A on the survival of islet allografts ) .	manualset1
80863	1	357765	5	NULL	NULL	0	NULL	quinolines	NonProteinOrNucleicAcidChemical		is synthesised from					safrole	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	( Synthesis of quinolines from safrole ) .	manualset1
81122	1	357771	5	NULL	NULL	NULL	NULL	Chondroitin Sulphuric Acid	NonProteinOrNucleicAcidChemical		protective agent for					corneal transparency	BiologicalProcess				NULL		NULL	NULL	NULL	NULL	NULL	NULL	( THE EFFECT OF CHONDROITIN SULFURIC ACID USED AS PROTECTIVE AGENT FOR CORNEAL TRANSPARENCY DURING THE OPERATION OF RETINAL DETACHMENT ) .	manualset1
81123	2	357771	5	NULL	NULL	0	NULL	statement 1	Process		during					retinal detachment	Disease	operation of			NULL		0	NULL	NULL	NULL	NULL	NULL	( THE EFFECT OF CHONDROITIN SULFURIC ACID USED AS PROTECTIVE AGENT FOR CORNEAL TRANSPARENCY DURING THE OPERATION OF RETINAL DETACHMENT ) .	manualset1
81124	1	357777	5	NULL	NULL	0	NULL	TachoSil	Chemical		is used in					urologic surgery	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	( TachoSil : the value of its use in urologic surgery .	manualset1
81125	1	357792	5	NULL	NULL	0	NULL	A771726	NonProteinOrNucleicAcidChemical		is a metabolite of		active			leflunomide	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	( The active metabolite of leflunomide A771726 inhibits proliferation and collagen synthesis of hepatic stellate cell ) .	manualset1
81126	2	357792	5	NULL	NULL	0	NULL	A771726	NonProteinOrNucleicAcidChemical		inhibits					hepatic stellate cell	Cell	proliferation of			NULL		0	NULL	NULL	NULL	NULL	NULL	( The active metabolite of leflunomide A771726 inhibits proliferation and collagen synthesis of hepatic stellate cell ) .	manualset1
81127	3	357792	5	NULL	NULL	0	NULL	collagen	Protein		is synthesised by					hepatic stellate cell	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	( The active metabolite of leflunomide A771726 inhibits proliferation and collagen synthesis of hepatic stellate cell ) .	manualset1
81128	4	357792	5	NULL	NULL	0	NULL	A771726	NonProteinOrNucleicAcidChemical		inhibits					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	( The active metabolite of leflunomide A771726 inhibits proliferation and collagen synthesis of hepatic stellate cell ) .	manualset1
81130	1	357793	5	NULL	NULL	0	NULL	lipid peroxidation	BiologicalProcess		is active in					small intestine	BodyPart	mucosa of;;rat			NULL		0	NULL	NULL	NULL	NULL	NULL	( The activity of the lipid peroxidation processes in the mucosa of the rat small intestine and its morphofunctional state under acute irradiation and the administration of combined preparations created on a base of highly dispersed silica ) .	manualset1
81137	1	357795	5	NULL	NULL	0	NULL	hyaluronidase	Protein		is a type of					antialgesic	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	( The antialgesic action of hyaluronidase in the treatment of medicinal apical parodontitis after filling of the canal ) .	manualset1
81138	2	357795	5	NULL	NULL	0	NULL	statement 1	Protein		is used to treat					medicinal apical parodontitis	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( The antialgesic action of hyaluronidase in the treatment of medicinal apical parodontitis after filling of the canal ) .	manualset1
81139	1	357839	5	NULL	NULL	0	NULL	cefozopran	NonProteinOrNucleicAcidChemical		is a type of					antibacterial	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	( The in vitro antibacterial activity of cefozopran against clinically isolated bacteria ) .	manualset1
81140	2	357839	5	NULL	NULL	0	NULL	cefozopran	NonProteinOrNucleicAcidChemical		acts against					bacteria	Organism	clinically isolated			NULL	in vitro	0	NULL	NULL	NULL	NULL	NULL	( The in vitro antibacterial activity of cefozopran against clinically isolated bacteria ) .	manualset1
81143	1	357843	5	NULL	NULL	0	NULL	enteral feeding	MedicalProcedure	early postoperative	performed through		possibly			 jejunal tube	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	( The jejunal tube : a possibility for early postoperative enteral feeding ) .	manualset1
81144	2	357846	5	NULL	NULL	0	NULL	glucan	NonProteinOrNucleicAcidChemical		induce					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	( The mechanism of glucan-induced agglutination of Actinomyces viscosus ( author 's transl ) ) .	manualset1
81145	1	357846	5	NULL	NULL	NULL	NULL	Actinomyces viscosus	Organism		undergoes					agglutination	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The mechanism of glucan-induced agglutination of Actinomyces viscosus ( author 's transl ) ) .	manualset1
81147	1	357857	5	NULL	NULL	0	NULL	phosphoenolpyruvate	NonProteinOrNucleicAcidChemical		is present in					milk	Food				NULL		0	NULL	NULL	NULL	NULL	NULL	( The phosphoenolpyruvate content of milk as an indicator of the energy balance of the dairy cow ( short communication ) ) .	manualset1
81148	2	357857	5	NULL	NULL	0	NULL	phosphoenolpyruvate	NonProteinOrNucleicAcidChemical		is an indicator of					energy balance	Process				NULL	dairy cow	0	NULL	NULL	NULL	NULL	NULL	( The phosphoenolpyruvate content of milk as an indicator of the energy balance of the dairy cow ( short communication ) ) .	manualset1
81149	1	357870	5	NULL	NULL	0	NULL	nitric oxide	NonProteinOrNucleicAcidChemical		released from					nitroso compounds	NonProteinOrNucleicAcidChemical	organic			NULL	body of animals	0	NULL	NULL	NULL	NULL	NULL	( The release of nitric oxide from organic nitroso compounds in the body of animals ) .	manualset1
81150	1	357882	5	NULL	NULL	0	NULL	Nassarius sp	Organism		causes					poisoning	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	( The study of poisoning caused by Nassa ( Nassarius sp . )	manualset1
81254	1	357910	5	NULL	NULL	0	NULL	Thoracic pain	MedicalFinding		is caused by					coronary insufficiency	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Thoracic pain caused by coronary insufficiency ) .	manualset1
81255	1	357915	5	NULL	NULL	0	NULL	Thrombendarterectomy	MedicalProcedure		prevents		possibly			cerebrovascular insult	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombendarterectomy of the carotid artery in the prevention of cerebrovascular insult ) .	manualset1
81256	2	357915	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					carotid artery	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombendarterectomy of the carotid artery in the prevention of cerebrovascular insult ) .	manualset1
81259	1	357918	5	NULL	NULL	0	NULL	Thrombosis	Disease		occurs at 					aortic aneurysm	MedicalFinding	abdominal			NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombosis at the site of abdominal aortic aneurysm with repeated myocardial infarction ) .	manualset1
81260	2	357918	5	NULL	NULL	0	NULL	statement 1	Process		occurs with					myocardial infarction	Disease	repeated			NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombosis at the site of abdominal aortic aneurysm with repeated myocardial infarction ) .	manualset1
81261	1	357919	5	NULL	NULL	0	NULL	Thrombotic changes	BiologicalProcess		occurs in					hemostasis	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombotic changes in hemostasis following streptokinase therapy in myocardial infarct ) .	manualset1
81262	2	357919	5	NULL	NULL	0	NULL	statement 1	Process		occurs following					streptokinase therapy	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombotic changes in hemostasis following streptokinase therapy in myocardial infarct ) .	manualset1
81263	3	357919	5	NULL	NULL	0	NULL	statement 2	Process		occurs in					myocardial infarct	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombotic changes in hemostasis following streptokinase therapy in myocardial infarct ) .	manualset1
81264	1	357947	5	NULL	NULL	0	NULL	mithramycin	NonProteinOrNucleicAcidChemical		treats					hypercalcemia	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Treatment of hypercalcemia with mithramycin ) .	manualset1
81265	1	357949	5	NULL	NULL	0	NULL	varicose ulcers	Disease	leg	is treated with					dura mater	BodyPart	xenogenic			NULL		0	NULL	NULL	NULL	NULL	NULL	( Treatment of varicose ulcers of the leg with xenogenic dura mater of the animal ) .	manualset1
81266	1	357955	5	NULL	NULL	0	NULL	streptococcal endocarditis lenta	Disease		is treated by					penicillin V	NonProteinOrNucleicAcidChemical	oral			NULL		0	NULL	NULL	NULL	NULL	NULL	( Two cases of streptococcal endocarditis lenta treated by oral penicillin V ) .	manualset1
81267	1	357959	5	NULL	NULL	0	NULL	unilateral nerve lesion	MedicalFinding	surgical;;recurrent	is an indication for					tracheotomy	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	( UNILATERAL SURGICAL RECURRENT NERVE LESION AS AN INDICATION FOR TRACHEOTOMY ) .	manualset1
81269	1	357968	5	NULL	NULL	0	NULL	adrenergic beta blockaders	NonProteinOrNucleicAcidChemical		is used in					thyrotoxicosis	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Use of adrenergic beta blockaders in thyrotoxicosis and hypothyroidism ) .	manualset1
81270	2	357968	5	NULL	NULL	0	NULL	adrenergic beta blockaders	NonProteinOrNucleicAcidChemical		is used in					hypothyroidism	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Use of adrenergic beta blockaders in thyrotoxicosis and hypothyroidism ) .	manualset1
81268	1	357969	5	NULL	NULL	0	NULL	immunoglobulin	Protein	high dose;;intravenous	is used in					neurologic disease	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	( Use of high dose intravenous immunoglobulin in neurologic disease ) .	manualset1
81280	1	357975	5	NULL	NULL	0	NULL	arterial infusion chemotherapy	MedicalProcedure	continuous	useful for					residual hepatocellular carcinoma	Disease	post operative;;multiple recurrence			NULL		0	NULL	NULL	NULL	NULL	NULL	( Usefulness of continuous arterial infusion chemotherapy for post operative multiple recurrence and residual hepatocellular carcinoma ) .	manualset1
81496	1	357979	5	NULL	NULL	0	NULL	V-osteotomy	MedicalProcedure		corrects					popliteal fossa contractures	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	( V-osteotomy for the correction of popliteal fossa contractures in spina bifida children ) .	manualset1
81497	2	357979	5	NULL	NULL	0	NULL	popliteal fossa contractures	MedicalFinding		occurs in					spina bifida children	PersonGroup				NULL		0	NULL	NULL	NULL	NULL	NULL	( V-osteotomy for the correction of popliteal fossa contractures in spina bifida children ) .	manualset1
81499	1	357983	5	NULL	NULL	0	NULL	multidetector computed tomography	MedicalProcedureOrDevice		is used in					arterio-venous fistula	Disease	assessment of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Value of multidetector computed tomography and digital subtraction angiography in assessment of arterio-venous fistula for hemodialysis -- own experiences ) .	manualset1
81500	2	357983	5	NULL	NULL	0	NULL	digital subtraction angiography	MedicalProcedureOrDevice		is used in					arterio-venous fistula	Disease	assessment of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Value of multidetector computed tomography and digital subtraction angiography in assessment of arterio-venous fistula for hemodialysis -- own experiences ) .	manualset1
81501	3	357983	5	NULL	NULL	0	NULL	statement 1	Process		is required for					hemodialysis	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	( Value of multidetector computed tomography and digital subtraction angiography in assessment of arterio-venous fistula for hemodialysis -- own experiences ) .	manualset1
81502	4	357983	5	NULL	NULL	0	NULL	statement 2	Process		is required for					hemodialysis	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	( Value of multidetector computed tomography and digital subtraction angiography in assessment of arterio-venous fistula for hemodialysis -- own experiences ) .	manualset1
81498	1	357984	5	NULL	NULL	0	NULL	nuclear magnetic resonance tomography	MedicalProcedureOrDevice		is used in					infrarenal abdominal aortic aneurysms	Disease	diagnosis of			NULL		0	NULL	NULL	NULL	NULL	NULL	( Value of nuclear magnetic resonance tomography in diagnosis of infrarenal abdominal aortic aneurysms .	manualset1
81505	1	357996	5	NULL	NULL	0	NULL	Vesicostomy	MedicalProcedure		is a type of					temporary urinary diversion	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	( Vesicostomy : a temporary urinary diversion in childhood ) .	manualset1
81511	2	357996	5	NULL	NULL	0	NULL	statement 1	Process		is performed during					childhood	Time				NULL		0	NULL	NULL	NULL	NULL	NULL	( Vesicostomy : a temporary urinary diversion in childhood ) .	manualset1
81520	1	358000	5	NULL	NULL	0	NULL	Visceral leishmaniasis	Disease		is associated with					cutaneous lesions	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	( Visceral leishmaniasis associated with cutaneous lesions ) .	manualset1
81527	2	358001	5	NULL	NULL	0	NULL	Voluminous solitary non-parasitic cyst	MedicalFinding	liver	is treated with					statement 1	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	( Voluminous solitary non-parasitic cyst of the liver treated with marsupialization and following fistulo-entero-anastomosis ) .	manualset1
81528	1	358001	5	NULL	NULL	0	NULL	marsupialization	MedicalProcedure		is followed by					fistulo-entero-anastomosis	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	( Voluminous solitary non-parasitic cyst of the liver treated with marsupialization and following fistulo-entero-anastomosis ) .	manualset1
81565	1	358030	5	NULL	NULL	NULL	NULL	gI	Protein	deletion of	does not affect			cytoplasmic tail		gE	Protein	intracellular transport of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	( i ) Deletion of the cytoplasmic tail , the transmembrane region plus the C-terminal half of the ectodomain of gI , does not affect intracellular transport of gE .	manualset1
81567	2	358030	5	NULL	NULL	NULL	NULL	gI	Protein	deletion of	does not affect			transmembrane region		gE	Protein	intracellular transport of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	( i ) Deletion of the cytoplasmic tail , the transmembrane region plus the C-terminal half of the ectodomain of gI , does not affect intracellular transport of gE .	manualset1
81569	3	358030	5	NULL	NULL	0	NULL	gI	Protein		is deleted from			C-terminal half		gI	Protein		ectodomain		NULL		0	NULL	NULL	NULL	NULL	NULL	( i ) Deletion of the cytoplasmic tail , the transmembrane region plus the C-terminal half of the ectodomain of gI , does not affect intracellular transport of gE .	manualset1
81570	4	358030	5	NULL	NULL	0	NULL	statement 3	Process		does not affect					gE	Protein	intracellular transport of			NULL		0	NULL	NULL	NULL	NULL	NULL	( i ) Deletion of the cytoplasmic tail , the transmembrane region plus the C-terminal half of the ectodomain of gI , does not affect intracellular transport of gE .	manualset1
81571	1	358031	5	NULL	NULL	0	NULL	virus	Organism	initial;;asymptomatic;;reversible activation of	is judged by					inclusion bearing cells	Cell	presence of			NULL	urine	0	NULL	NULL	NULL	NULL	NULL	( i ) Initial , asymptomatic and reversible activation of the virus , judged by the presence of inclusion bearing cells in the urine .	manualset1
81583	1	358032	5	NULL	NULL	0	NULL	L-NAME	NonProteinOrNucleicAcidChemical		is					 N omega-nitro-L-arginine methyl ester	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	( ii ) The nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester ( L-NAME , 100 microM ) did not modulate 5-HT-initiated contractions at either level of PO2 .	manualset1
81584	2	358032	5	NULL	NULL	0	NULL	L-NAME	NonProteinOrNucleicAcidChemical		is an inhibitor of					nitric oxide synthase	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	( ii ) The nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester ( L-NAME , 100 microM ) did not modulate 5-HT-initiated contractions at either level of PO2 .	manualset1
81585	3	358032	5	NULL	NULL	0	NULL	contractions	Process		initiated by					5-HT	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	( ii ) The nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester ( L-NAME , 100 microM ) did not modulate 5-HT-initiated contractions at either level of PO2 .	manualset1
81586	4	358032	5	NULL	NULL	0	NULL	serotonin 	NonProteinOrNucleicAcidChemical		does not modulate					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	( ii ) The nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester ( L-NAME , 100 microM ) did not modulate 5-HT-initiated contractions at either level of PO2 .	manualset1
81587	1	358037	5	NULL	NULL	0	NULL	Placental implantation site	AnatomicalPart		is not related to					labor	BiologicalProcess	duration of			NULL		0	NULL	NULL	NULL	NULL	NULL	( p less than 0.05 ) 4 ) Placental implantation site had no relation with labor duration , fetal weight , placental weight , amount of hemorrhage during labor and cord-coiling .	manualset1
81588	2	358037	5	NULL	NULL	0	NULL	Placental implantation site	AnatomicalPart		is not related to					fetal weight	QuantityOrMeasure				NULL		0	NULL	NULL	NULL	NULL	NULL	( p less than 0.05 ) 4 ) Placental implantation site had no relation with labor duration , fetal weight , placental weight , amount of hemorrhage during labor and cord-coiling .	manualset1
81589	3	358037	5	NULL	NULL	0	NULL	Placental implantation site	AnatomicalPart		is not related to					placental weight	QuantityOrMeasure				NULL		0	NULL	NULL	NULL	NULL	NULL	( p less than 0.05 ) 4 ) Placental implantation site had no relation with labor duration , fetal weight , placental weight , amount of hemorrhage during labor and cord-coiling .	manualset1
81590	5	358037	5	NULL	NULL	0	NULL	Placental implantation site	AnatomicalPart		is not related to					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	( p less than 0.05 ) 4 ) Placental implantation site had no relation with labor duration , fetal weight , placental weight , amount of hemorrhage during labor and cord-coiling .	manualset1
81591	4	358037	5	NULL	NULL	0	NULL	hemorrhage	MedicalFinding		occurs during					labor	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	( p less than 0.05 ) 4 ) Placental implantation site had no relation with labor duration , fetal weight , placental weight , amount of hemorrhage during labor and cord-coiling .	manualset1
81592	6	358037	5	NULL	NULL	0	NULL	Placental implantation site	AnatomicalPart		is not related to					cord-coiling	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	( p less than 0.05 ) 4 ) Placental implantation site had no relation with labor duration , fetal weight , placental weight , amount of hemorrhage during labor and cord-coiling .	manualset1
81593	1	358054	5	NULL	NULL	0	NULL	endosome	CellComponent		is regulated to					Golgi pathway	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	- arrestins therefore seem to regulate an endosome to Golgi pathway used by multiple cargo proteins .	manualset1
81594	2	358054	5	NULL	NULL	0	NULL	arrestins	Protein		plays a role in					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	- arrestins therefore seem to regulate an endosome to Golgi pathway used by multiple cargo proteins .	manualset1
81595	1	358055	5	NULL	NULL	0	NULL	cell-cell adhesion	BiologicalProcess		is followed by					fusion	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	- catenin is a molecular switch that regulates transition of cell-cell adhesion to fusion .	manualset1
81596	2	358055	5	NULL	NULL	0	NULL	catenin	Protein		is a type of					molecular switch	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	- catenin is a molecular switch that regulates transition of cell-cell adhesion to fusion .	manualset1
81597	3	358055	5	NULL	NULL	0	NULL	catenin	Protein		regulate					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	- catenin is a molecular switch that regulates transition of cell-cell adhesion to fusion .	manualset1
81598	1	358057	5	NULL	NULL	0	NULL	immunological phenomena	Process		located in					epidermis	AnatomicalPart	psoriatic 			NULL		0	NULL	NULL	NULL	NULL	NULL	- this alteration in cell membranes results from immunological phenomena located in psoriatic epidermis .	manualset1
81599	2	358057	5	NULL	NULL	0	NULL	statement 1	Process		alters					cell membrane	AnatomicalPart				NULL		0	NULL	NULL	NULL	NULL	NULL	- this alteration in cell membranes results from immunological phenomena located in psoriatic epidermis .	manualset1
81812	1	358065	5	NULL	NULL	0	NULL	Leukotrienes	NonProteinOrNucleicAcidChemical		constitutes					bioactive mediators	NonProteinOrNucleicAcidChemical	class of;;potent			NULL		0	NULL	NULL	NULL	NULL	NULL	1 Leukotrienes constitute a class of potent bioactive mediators known to play a pivotal role in inflammation .	manualset1
81813	2	358065	5	NULL	NULL	0	NULL	statement 1	NonProteinOrNucleicAcidChemical		plays a role in		pivotal			inflammation	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	1 Leukotrienes constitute a class of potent bioactive mediators known to play a pivotal role in inflammation .	manualset1
81815	1	358077	5	NULL	NULL	0	NULL	1,7-Azulenequinones	NonProteinOrNucleicAcidChemical		shows					cytotoxicity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	1,5 - and 1,7-Azulenequinones generally showed higher cytotoxicity , as compared with tropolones and azulene derivatives .	manualset1
81817	2	358077	5	NULL	NULL	0	NULL	1,5-Azulenequinones	NonProteinOrNucleicAcidChemical		shows					cytotoxicity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	1,5 - and 1,7-Azulenequinones generally showed higher cytotoxicity , as compared with tropolones and azulene derivatives .	manualset1
81818	3	358077	5	NULL	NULL	0	NULL	tropolones	NonProteinOrNucleicAcidChemical		shows					cytotoxicity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	1,5 - and 1,7-Azulenequinones generally showed higher cytotoxicity , as compared with tropolones and azulene derivatives .	manualset1
81819	4	358077	5	NULL	NULL	0	NULL	azulene derivatives	NonProteinOrNucleicAcidChemical		shows					cytotoxicity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	1,5 - and 1,7-Azulenequinones generally showed higher cytotoxicity , as compared with tropolones and azulene derivatives .	manualset1
81820	5	358077	5	NULL	NULL	0	NULL	statement 1	Process		is higher in					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	1,5 - and 1,7-Azulenequinones generally showed higher cytotoxicity , as compared with tropolones and azulene derivatives .	manualset1
81821	6	358077	5	NULL	NULL	0	NULL	statement 1	Process		is higher than					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	1,5 - and 1,7-Azulenequinones generally showed higher cytotoxicity , as compared with tropolones and azulene derivatives .	manualset1
81822	7	358077	5	NULL	NULL	0	NULL	statement 2	Process		is higher than					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	1,5 - and 1,7-Azulenequinones generally showed higher cytotoxicity , as compared with tropolones and azulene derivatives .	manualset1
81823	8	358077	5	NULL	NULL	0	NULL	statement 2	Process		is higher than					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	1,5 - and 1,7-Azulenequinones generally showed higher cytotoxicity , as compared with tropolones and azulene derivatives .	manualset1
81824	1	358080	5	NULL	NULL	0	NULL	1-Carboxymethyl-3-hydroxy-2-methyl-4-pyridone	NonProteinOrNucleicAcidChemical		is obtained from					isomaltol	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	1-Carboxymethyl-3-hydroxy-2-methyl-4-pyridone is obtained from isomaltol and glycine .	manualset1
81825	2	358080	5	NULL	NULL	0	NULL	1-Carboxymethyl-3-hydroxy-2-methyl-4-pyridone	NonProteinOrNucleicAcidChemical		is obtained from					glycine	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	1-Carboxymethyl-3-hydroxy-2-methyl-4-pyridone is obtained from isomaltol and glycine .	manualset1
81826	1	358081	5	NULL	NULL	0	NULL	MPTP 	NonProteinOrNucleicAcidChemical		is					1-Methyl-4-phenyl-1 ,2,3,6 - tetrahydropyridine	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	1-Methyl-4-phenyl-1 ,2,3,6 - tetrahydropyridine ( MPTP ) - induced neurotoxicity is the most common experimental model used to investigate the pathogenesis of PD .	manualset1
81827	2	358081	5	NULL	NULL	0	NULL	MPTP 	NonProteinOrNucleicAcidChemical		induce					neurotoxicity	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	1-Methyl-4-phenyl-1 ,2,3,6 - tetrahydropyridine ( MPTP ) - induced neurotoxicity is the most common experimental model used to investigate the pathogenesis of PD .	manualset1
81828	3	358081	5	NULL	NULL	0	NULL	MPTP	NonProteinOrNucleicAcidChemical		is used to 					PD	Disease	investigate;;pathogenesis of			NULL		0	NULL	NULL	NULL	NULL	NULL	1-Methyl-4-phenyl-1 ,2,3,6 - tetrahydropyridine ( MPTP ) - induced neurotoxicity is the most common experimental model used to investigate the pathogenesis of PD .	manualset1
81829	1	358085	5	NULL	NULL	0	NULL	IKCa	NonProteinOrNucleicAcidChemical		is					non-inactivating current	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	10 % of cells ) showed only a non-inactivating current ( IKCa ) which was blocked by 2 mM TEA .	manualset1
81830	2	358085	5	NULL	NULL	0	NULL	IKCa	NonProteinOrNucleicAcidChemical		is blocked by					TEA	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	10 % of cells ) showed only a non-inactivating current ( IKCa ) which was blocked by 2 mM TEA .	manualset1
81831	1	358093	5	NULL	NULL	NULL	NULL	10-23 type deoxyribozymes	Protein		more active than					8-17 type deoxyribozymes	Protein				NULL		NULL	NULL	NULL	NULL	NULL	NULL	10-23 type deoxyribozymes generally appeared more active than 8-17 type and it was possible to predict deoxyribozymes with high cleavage efficiency using scanning array hybridization and computational analysis as guides .	manualset1
81832	1	358100	5	NULL	NULL	0	NULL	11 beta-HSD	Protein		is					11 beta-hydroxysteroid dehydrogenase	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	11 beta-hydroxysteroid dehydrogenase ( 11 beta-HSD ) catalyzes the interconversion of cortisol ( F ) to inactive cortisone ( E ) in man ( corticosterone ( B ) to 11-dehydrocorticosterone ( A ) in rodents ) and plays a crucial role in regulating corticosteroid hormone action .	manualset1
81833	2	358100	5	NULL	NULL	0	NULL	cortisol	Chemical		is interconverted to					cortisone	Chemical				NULL	man	0	NULL	NULL	NULL	NULL	NULL	11 beta-hydroxysteroid dehydrogenase ( 11 beta-HSD ) catalyzes the interconversion of cortisol ( F ) to inactive cortisone ( E ) in man ( corticosterone ( B ) to 11-dehydrocorticosterone ( A ) in rodents ) and plays a crucial role in regulating corticosteroid hormone action .	manualset1
81834	3	358100	5	NULL	NULL	NULL	NULL	corticosterone ( B )	Chemical		is interconverted to					1-dehydrocorticosterone ( A )	Chemical				NULL	rodents	NULL	NULL	NULL	NULL	NULL	NULL	11 beta-hydroxysteroid dehydrogenase ( 11 beta-HSD ) catalyzes the interconversion of cortisol ( F ) to inactive cortisone ( E ) in man ( corticosterone ( B ) to 11-dehydrocorticosterone ( A ) in rodents ) and plays a crucial role in regulating corticosteroid hormone action .	manualset1
81835	4	358100	5	NULL	NULL	0	NULL	11 beta-HSD	Protein		catalyzes					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	11 beta-hydroxysteroid dehydrogenase ( 11 beta-HSD ) catalyzes the interconversion of cortisol ( F ) to inactive cortisone ( E ) in man ( corticosterone ( B ) to 11-dehydrocorticosterone ( A ) in rodents ) and plays a crucial role in regulating corticosteroid hormone action .	manualset1
81836	5	358100	5	NULL	NULL	0	NULL	11 beta-HSD	Protein		catalyzes					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	11 beta-hydroxysteroid dehydrogenase ( 11 beta-HSD ) catalyzes the interconversion of cortisol ( F ) to inactive cortisone ( E ) in man ( corticosterone ( B ) to 11-dehydrocorticosterone ( A ) in rodents ) and plays a crucial role in regulating corticosteroid hormone action .	manualset1
81837	6	358100	5	NULL	NULL	0	NULL	11 beta-HSD	Protein		regulates					corticosteroid hormone 	Chemical	action of			NULL		0	NULL	NULL	NULL	NULL	NULL	11 beta-hydroxysteroid dehydrogenase ( 11 beta-HSD ) catalyzes the interconversion of cortisol ( F ) to inactive cortisone ( E ) in man ( corticosterone ( B ) to 11-dehydrocorticosterone ( A ) in rodents ) and plays a crucial role in regulating corticosteroid hormone action .	manualset1
81838	1	358106	5	NULL	NULL	0	NULL	125I-Antisauvagine-30	PartOfProtein		is a type of					novel and specific high-affinity radioligand	PartOfProtein				NULL		0	NULL	NULL	NULL	NULL	NULL	125I-Antisauvagine-30 : a novel and specific high-affinity radioligand for the characterization of corticotropin-releasing factor type 2 receptors .	manualset1
81839	2	358106	5	NULL	NULL	0	NULL	125I-Antisauvagine-30	PartOfProtein		is used in					corticotropin-releasing factor type 2 receptors	Protein	characterization of			NULL		0	NULL	NULL	NULL	NULL	NULL	125I-Antisauvagine-30 : a novel and specific high-affinity radioligand for the characterization of corticotropin-releasing factor type 2 receptors .	manualset1
81840	1	358107	5	NULL	NULL	0	NULL	125I-BoNT type B	Protein		interacts with					motor nerve terminal	BodyPart				NULL	 in vitro	0	NULL	NULL	NULL	NULL	NULL	125I-BoNT type B , applied in vitro to the murine neuromuscular junction , interacts likewise with the motor nerve terminal except that a lower proportion of internalized radioactivity is seen .	manualset1
81841	2	358107	5	NULL	NULL	0	NULL	statement 1	Process		occurs in					neuromuscular junction	BodyPart	murine			NULL	in vitro	0	NULL	NULL	NULL	NULL	NULL	125I-BoNT type B , applied in vitro to the murine neuromuscular junction , interacts likewise with the motor nerve terminal except that a lower proportion of internalized radioactivity is seen .	manualset1
81842	1	358123	5	NULL	NULL	0	NULL	16S rDNA	NucleicAcidSubstance		is not present in					Setaria equina	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	16S rDNA was not found in the equine filarial nematode Setaria equina , using either polymerase chain reaction ( PCR ) or DNA hybridization .	manualset1
81843	2	358123	5	NULL	NULL	0	NULL	Setaria equina	Organism		is a type of					equine filarial nematode	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	16S rDNA was not found in the equine filarial nematode Setaria equina , using either polymerase chain reaction ( PCR ) or DNA hybridization .	manualset1
81844	1	358140	5	NULL	NULL	NULL	NULL	2 ' ( 3 ' ) - O-L-Aminoacyl derivatives of `` bridged '' adenine ribonucleosides	Chemical		is a substrate for					fibosomal peptidyltransferase	Protein				NULL		NULL	NULL	NULL	NULL	NULL	NULL	2 ' ( 3 ' ) - O-L-Aminoacyl derivatives of `` bridged '' adenine ribonucleosides as substrates for fibosomal peptidyltransferase .	manualset1
81845	1	358145	5	NULL	NULL	0	NULL	 intravascular pressure	BiologicalProcess	elevation of	reduce		significantly			G-actin	GeneOrProtein	cytosolic concentration of			NULL		0	NULL	NULL	NULL	NULL	NULL	2 ) The cytosolic concentration of G-actin is significantly reduced by an elevation in intravascular pressure , demonstrating the dynamic nature of actin within VSM and implying a shift in the F : G equilibrium in favor of F-actin .	manualset1
81846	2	358145	5	NULL	NULL	0	NULL	 F : G equilibrium	BiologicalProcess		shifted					F-actin	GeneOrProtein	in favor of			NULL		0	NULL	NULL	NULL	NULL	NULL	2 ) The cytosolic concentration of G-actin is significantly reduced by an elevation in intravascular pressure , demonstrating the dynamic nature of actin within VSM and implying a shift in the F : G equilibrium in favor of F-actin .	manualset1
81847	3	358145	5	NULL	NULL	0	NULL	statement 1	Process		implies					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	2 ) The cytosolic concentration of G-actin is significantly reduced by an elevation in intravascular pressure , demonstrating the dynamic nature of actin within VSM and implying a shift in the F : G equilibrium in favor of F-actin .	manualset1
81848	4	358145	5	NULL	NULL	0	NULL	actin	GeneOrProtein		is dynamic within					VSM	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	2 ) The cytosolic concentration of G-actin is significantly reduced by an elevation in intravascular pressure , demonstrating the dynamic nature of actin within VSM and implying a shift in the F : G equilibrium in favor of F-actin .	manualset1
81849	5	358145	5	NULL	NULL	0	NULL	statement 1	Process		demonstrates					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	2 ) The cytosolic concentration of G-actin is significantly reduced by an elevation in intravascular pressure , demonstrating the dynamic nature of actin within VSM and implying a shift in the F : G equilibrium in favor of F-actin .	manualset1
81872	1	358154	5	NULL	NULL	0	NULL	Digitoxin	NonProteinOrNucleicAcidChemical		produce					inotropic responses	BiologicalProcess	greatest			NULL		0	NULL	NULL	NULL	NULL	NULL	2 Digitoxin produced the greatest inotropic responses in this series , while the sequence of cleavage products produced progressively smaller responses .	manualset1
81884	1	358160	5	NULL	NULL	0	NULL	2,3-butanediol	NonProteinOrNucleicAcidChemical		produced by					acetogenic bacteria	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	2,3-butanediol production by acetogenic bacteria , an alternative route to chemical synthesis , using industrial waste gas .	manualset1
81885	2	358160	5	NULL	NULL	0	NULL	statement 1	Process		uses					waste gas	NonProteinOrNucleicAcidChemical	industrial			NULL		0	NULL	NULL	NULL	NULL	NULL	2,3-butanediol production by acetogenic bacteria , an alternative route to chemical synthesis , using industrial waste gas .	manualset1
81886	3	358160	5	NULL	NULL	0	NULL	statement 1	Process		is an alternative route to					chemical synthesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	2,3-butanediol production by acetogenic bacteria , an alternative route to chemical synthesis , using industrial waste gas .	manualset1
81888	1	358161	5	NULL	NULL	0	NULL	2,4-Diamino-5 - ( 5 ' - ( 5-carboxypentyl ) -2 ' - methoxybenzyl ) pyrimidine	Chemical		is more potent than					TMP	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	2,4-Diamino-5 - ( 5 ' - ( 5-carboxypentyl ) -2 ' - methoxybenzyl ) pyrimidine ( 6 ) had a selectivity index of 490 against Tg DHFR and was 320 times more potent than TMP .	manualset1
81107	1	366696	6	NULL	NULL	0	NULL	bisacodyl	Chemical		decreases					ATPase	Protein	activity of			NULL	colonic	0	NULL	NULL	NULL	NULL	NULL	Eighteen hours after its intragastric administration , bisacodyl ( 5.9 mg/kg body wt ) decreased significantly jejunal and colonic ( Na + K ) ATPase activity : 36.4 + / - 1.4 ( SE ) and 28.3 + / - 1.4 , respectively , as compared to 42.1 + / - 1.6 and 37.0 + / - 2.9 mumol/mg protein/hr in saline-treated rats .	manualset1
81129	1	366706	6	NULL	NULL	NULL	NULL	interleukin 1-receptor	GP	elaboration of 	is not attenuated by					glucocorticoids	NonProteinOrNucleicAcidChemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Elaboration of interleukin 1-receptor antagonist is not attenuated by glucocorticoids after endotoxemia .	manualset1
81131	2	366706	6	NULL	NULL	0	NULL	statement 1	Process		occurs after					endotoxemia	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Elaboration of interleukin 1-receptor antagonist is not attenuated by glucocorticoids after endotoxemia .	manualset1
81132	1	366707	6	NULL	NULL	0	NULL	Elastic fibers	AnatomicalPart		are fragmented in					arterial walls	BodyPart	pulmonary			NULL		0	NULL	NULL	NULL	NULL	NULL	Elastic fibers in E18 .5 Lox ( - / - ) lungs were markedly less intensely stained and more disperse than in the wild type , especially in the mesenchyme surrounding the distal airways , bronchioles , bronchi , and trachea , and were fragmented in pulmonary arterial walls .	manualset1
81133	1	366708	6	NULL	NULL	0	NULL	Elastin peptides	Protein		are present in					serum	Protein	human			NULL		0	NULL	NULL	NULL	NULL	NULL	Elastin peptides derived from the degradation are present in human sera .	manualset1
81134	2	366708	6	NULL	NULL	0	NULL	Elastin peptides	Protein		is derived from					degradation	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Elastin peptides derived from the degradation are present in human sera .	manualset1
81135	1	366709	6	NULL	NULL	0	NULL	Elastosis	Disease		deposits					elastin	Protein	large amounts of 			NULL		0	NULL	NULL	NULL	NULL	NULL	Elastosis , the deposition of large amounts of elastin , is characteristic of the desmoplastic reaction to human breast carcinoma .	manualset1
81136	2	366709	6	NULL	NULL	NULL	NULL	Elastosis	Disease		is characteristic of 					Breast Carcinoma	Disease	human;; desmoplastic reaction to 			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Elastosis , the deposition of large amounts of elastin , is characteristic of the desmoplastic reaction to human breast carcinoma .	manualset1
81141	1	366720	6	NULL	NULL	0	NULL	S3	SmallMolecule	electrical stimulation of	results in					sphincter component	CellComponent	visible contraction of;; striated;; muscular;; anal			NULL		0	NULL	NULL	NULL	NULL	NULL	Electrical stimulation of S3 and S4 results in visible contraction of the different striated muscular anal sphincter components and in an increase of anal canal closure pressure .	manualset1
81142	2	366720	6	NULL	NULL	0	NULL	S4	SmallMolecule	electrical stimulation of	results in					sphincter component	CellComponent	visible contraction of;; striated;; muscular;; anal			NULL		0	NULL	NULL	NULL	NULL	NULL	Electrical stimulation of S3 and S4 results in visible contraction of the different striated muscular anal sphincter components and in an increase of anal canal closure pressure .	manualset1
81146	1	366723	6	NULL	NULL	0	NULL	dorsal raphe 	BodyPart	stimulation of 	inhibits					DA neurons	CellComponent	firing rate of 			NULL		0	NULL	NULL	NULL	NULL	NULL	Electrical stimulation of the dorsal raphe selectively inhibited the firing rate of slowly firing ( less than 4 spikes/sec ) DA neurons .	manualset1
81160	1	366734	6	NULL	NULL	NULL	NULL	electrolyte	Chemical	leakage of	is indicative of					membrane	CellComponent	perturbation of 			NULL	C. herbarum	NULL	NULL	NULL	NULL	NULL	NULL	Electrolyte leakage , indicative of membrane perturbation , was evident in both C. herbarum and B. cinerea exposed to 4-octyl cyclopentenone .	manualset1
81162	2	366734	6	NULL	NULL	0	NULL	electrolyte	Chemical	leakage of	is indicative of					membrane	CellComponent	perturbation of 			NULL	B. cinerea	0	NULL	NULL	NULL	NULL	NULL	Electrolyte leakage , indicative of membrane perturbation , was evident in both C. herbarum and B. cinerea exposed to 4-octyl cyclopentenone .	manualset1
81163	3	366734	6	NULL	NULL	0	NULL	statement 1	Process		occurs after					4-octyl cyclopentenone	NonProteinOrNucleicAcidChemical	exposure to			NULL		0	NULL	NULL	NULL	NULL	NULL	Electrolyte leakage , indicative of membrane perturbation , was evident in both C. herbarum and B. cinerea exposed to 4-octyl cyclopentenone .	manualset1
81164	4	366734	6	NULL	NULL	0	NULL	statement 2	Process		occurs after					4-octyl cyclopentenone	NonProteinOrNucleicAcidChemical	exposure to			NULL		0	NULL	NULL	NULL	NULL	NULL	Electrolyte leakage , indicative of membrane perturbation , was evident in both C. herbarum and B. cinerea exposed to 4-octyl cyclopentenone .	manualset1
81168	1	366738	6	NULL	NULL	0	NULL	orbicularis oris muscles	BodyPart	upper	produces					speech	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Electromyographic analysis of the upper and lower orbicularis oris muscles in the production of speech .	manualset1
81170	2	366738	6	NULL	NULL	0	NULL	orbicularis oris muscles	BodyPart	lower	produces					speech	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Electromyographic analysis of the upper and lower orbicularis oris muscles in the production of speech .	manualset1
81176	1	366739	6	NULL	NULL	0	NULL	depressor labii inferior muscle	BodyPart	right	does not have					voluntary activity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Electromyographic examination showed absent voluntary activity of the right depressor labii inferior muscle .	manualset1
81179	1	366746	6	NULL	NULL	0	NULL	epithelial autograft	MedicalProcedure	cultured;; healed	lacks					dermal attachments	AnatomicalPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Electron microscopic examination of a biopsy specimen of the healed cultured epithelial autograft ( 80 days after placement ) revealed a lack of dermal attachments of the anchoring fibrils .	manualset1
81181	2	366746	6	NULL	NULL	0	NULL	statement 1	Process		occurs in					fibrils	CellComponent	anchoring			NULL		0	NULL	NULL	NULL	NULL	NULL	Electron microscopic examination of a biopsy specimen of the healed cultured epithelial autograft ( 80 days after placement ) revealed a lack of dermal attachments of the anchoring fibrils .	manualset1
81197	1	366747	6	NULL	NULL	0	NULL	microtubular deposits	CellComponent		are present in					glomeruli	CellComponent	subendothelial space of			NULL		0	NULL	NULL	NULL	NULL	NULL	Electron microscopic examination revealed microtubular and fibrillary deposits with diameters of 80-100 and 9-16 nm , respectively , in the subendothelial space of the glomeruli .	manualset1
81198	1	366754	6	NULL	NULL	0	NULL	microfibrils	CellComponent	exposed appearance of	decreases					elastin	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Electron microscopy of dermal elastic fibers showed a decreased amount of elastin with an exposed appearance of microfibrils .	manualset1
81199	1	366758	6	NULL	NULL	0	NULL	DMPO	Chemical		is					5 , 5-dimethyl-1-pyrroline-N-oxide	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Electron spin resonance spectroscopy studies using 5 , 5-dimethyl-1-pyrroline-N-oxide ( DMPO ) as a spin trap indicate a complete inhibition of hydroxyl radical formation via the iron-catalyzed Fenton reaction at molar phytic acid/iron ratios ) 5 .	manualset1
81200	2	366758	6	NULL	NULL	0	NULL	DMPO	Chemical		inhibits					hydroxyl radical	Chemical	formation of 			NULL		0	NULL	NULL	NULL	NULL	NULL	Electron spin resonance spectroscopy studies using 5 , 5-dimethyl-1-pyrroline-N-oxide ( DMPO ) as a spin trap indicate a complete inhibition of hydroxyl radical formation via the iron-catalyzed Fenton reaction at molar phytic acid/iron ratios ) 5 .	manualset1
81203	1	366764	6	NULL	NULL	0	NULL	ouabain	Chemical		induces					ventricular dysrhythmias	Disease				NULL	rabbit	0	NULL	NULL	NULL	NULL	NULL	Electrophysiologic effects of potassium canrenoate on ouabain-induced ventricular dysrhythmias in rabbits .	manualset1
81333	1	366768	6	NULL	NULL	0	NULL	ultrafine fibers	AnatomicalPart	electrospun	increases					dissolution	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Electrospun ultrafine fibers increased the dissolution more effectively , owing to the formed solid solution and huge surface .	manualset1
81210	1	366773	6	NULL	NULL	0	NULL	antiganglioside antibodies 	Protein	elevated	is secondary to					axons	CellComponent	damage to			NULL		0	NULL	NULL	NULL	NULL	NULL	Elevated antiganglioside antibodies may be secondary to axonal damage or may be a cause of axonal damage and accumulating disability in progressive MS. In either case , they may serve as a marker of axonal damage in MS.	manualset1
81211	2	366773	6	NULL	NULL	0	NULL	antiganglioside antibodies 	Protein		may cause					MS	Disease	progressive;; disability in 			NULL		0	NULL	NULL	NULL	NULL	NULL	Elevated antiganglioside antibodies may be secondary to axonal damage or may be a cause of axonal damage and accumulating disability in progressive MS. In either case , they may serve as a marker of axonal damage in MS.	manualset1
81212	1	366775	6	NULL	NULL	0	NULL	SHBG-cholesterol	NonProteinOrNucleicAcidChemical	concentration of 	increases					luteal phase	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Elevated concentrations of SHBG and HDL-cholesterol and a suppression of LDL-cholesterol were found during the luteal compared to the follicular phase and these findings were interpreted as an estrogenic influence .	manualset1
81213	2	366775	6	NULL	NULL	0	NULL	HDL-cholesterol	NonProteinOrNucleicAcidChemical	concentration of 	increases during					luteal phase	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Elevated concentrations of SHBG and HDL-cholesterol and a suppression of LDL-cholesterol were found during the luteal compared to the follicular phase and these findings were interpreted as an estrogenic influence .	manualset1
81214	1	366776	6	NULL	NULL	0	NULL	corticosterone	NonProteinOrNucleicAcidChemical	elevated	affects					body size					NULL		0	NULL	NULL	NULL	NULL	NULL	Elevated corticosterone levels during embryonic development affected body size , growth rates , and sex ratios of the resultant offspring , but the direction and magnitude of these effects differed between the species .	manualset1
81215	2	366776	6	NULL	NULL	0	NULL	corticosterone	NonProteinOrNucleicAcidChemical	elevated	affects					growth rate	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Elevated corticosterone levels during embryonic development affected body size , growth rates , and sex ratios of the resultant offspring , but the direction and magnitude of these effects differed between the species .	manualset1
81216	3	366776	6	NULL	NULL	0	NULL	corticosterone	NonProteinOrNucleicAcidChemical	elevated	affects					sex ratios					NULL		0	NULL	NULL	NULL	NULL	NULL	Elevated corticosterone levels during embryonic development affected body size , growth rates , and sex ratios of the resultant offspring , but the direction and magnitude of these effects differed between the species .	manualset1
81336	1	366777	6	NULL	NULL	NULL	NULL	T-bet	GeneOrProtein	elevated expression of 	increases					Th1 cell 	cell	differentiation of			NULL	T-EP67-vaccinated mice	NULL	NULL	NULL	NULL	NULL	NULL	Elevated expression of T-bet and RORc transcription factors in T-EP67-vaccinated mice indicated the promotion of Th1 and Th17 cell differentiation .	manualset1
81342	2	366777	6	NULL	NULL	NULL	NULL	RORc	GeneOrProtein	elevated expression of 	increases					Th17 cell	cell	differentiation of			NULL	T-EP67-vaccinated mice	NULL	NULL	NULL	NULL	NULL	NULL	Elevated expression of T-bet and RORc transcription factors in T-EP67-vaccinated mice indicated the promotion of Th1 and Th17 cell differentiation .	manualset1
81358	1	366778	6	NULL	NULL	0	NULL	testosterone	Protein	maternal;; elevated levels of 	results in					2D:4D 	Protein	lower			NULL		0	NULL	NULL	NULL	NULL	NULL	Elevated levels of maternal testosterone resulted in lower 2D :4 D ratios and an elongated 4D on the left and right forepaws in both males and females .	manualset1
81362	1	366779	6	NULL	NULL	0	NULL	testosterone	Protein	elevated levels of 	results in					2D:4D 	Protein	lower			NULL		0	NULL	NULL	NULL	NULL	NULL	Elevated proline aminopeptidase activity has been identified as a reliable marker enzyme for bacterial vaginosis .	manualset1
81582	1	366780	6	NULL	NULL	0	NULL	serum IgE	Protein	elevated	reflects					immune regulation	BiologicalProcess	defective			NULL		0	NULL	NULL	NULL	NULL	NULL	Elevated serum IgE probably reflects defective immune regulation .	manualset1
79102	1	376994	7	NULL	NULL	NULL	NULL	Nevirapine nanosuspensions	NonProteinOrNucleicAcidChemical		target					HIV reservoir	organism				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nevirapine nanosuspensions for HIV reservoir targeting .	manualset1
79633	1	377001	7	NULL	NULL	0	NULL	Mycobacterium avium complex 	Organism	agents active against	selected										NULL		0	NULL	NULL	NULL	NULL	NULL	New agents active against Mycobacterium avium complex selected by molecular topology : a virtual screening method .	manualset1
79634	1	377002	7	NULL	NULL	0	NULL	curcumin	NonProteinOrNucleicAcidChemical	New analogs of	required for					therapeutics	MedicalProcedureOrDevice				NULL		0	NULL	NULL	NULL	NULL	NULL	New analogs of curcumin with improved properties are needed to meet therapeutic requirements .	manualset1
79635	1	377004	7	NULL	NULL	0	NULL	anemia	MedicalFinding		occur during					preconception	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	New chapters are added concerning anemia during preconception and the puerperium .	manualset1
79636	2	377004	7	NULL	NULL	0	NULL	anemia	MedicalFinding		occur during					puerperium	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	New chapters are added concerning anemia during preconception and the puerperium .	manualset1
79637	1	377011	7	NULL	NULL	0	NULL	cisplatin	NonProteinOrNucleicAcidChemical		shows					extracellular resistance mechanism	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	New extracellular resistance mechanism for cisplatin .	manualset1
79661	1	377014	7	NULL	NULL	0	NULL	archaeosomes	NonProteinOrNucleicAcidChemical		belongs to					liposomes	NonProteinOrNucleicAcidChemical	new generation of			NULL		0	NULL	NULL	NULL	NULL	NULL	New generation of liposomes called archaeosomes based on natural or synthetic archaeal lipids as innovative formulations for drug delivery .	manualset1
79662	2	377014	7	NULL	NULL	NULL	NULL	archaeosomes	NonProteinOrNucleicAcidChemical		based on					natural archaeal lipids	NonProteinOrNucleicAcidChemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	New generation of liposomes called archaeosomes based on natural or synthetic archaeal lipids as innovative formulations for drug delivery .	manualset1
79663	3	377014	7	NULL	NULL	0	NULL	archaeosomes	NonProteinOrNucleicAcidChemical		based on					synthetic archaeal lipids	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	New generation of liposomes called archaeosomes based on natural or synthetic archaeal lipids as innovative formulations for drug delivery .	manualset1
79664	4	377014	7	NULL	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	New generation of liposomes called archaeosomes based on natural or synthetic archaeal lipids as innovative formulations for drug delivery .	manualset1
79665	5	377014	7	NULL	NULL	0	NULL	archaeosomes	NonProteinOrNucleicAcidChemical		formulations for		innovative			drug delivery	MedicalProcedureOrDevice				NULL		0	NULL	NULL	NULL	NULL	NULL	New generation of liposomes called archaeosomes based on natural or synthetic archaeal lipids as innovative formulations for drug delivery .	manualset1
79666	1	377015	7	NULL	NULL	0	NULL	TPO	Protein		is involved in					ET	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	New insights are emerging into the role of the megakaryocytopoiesis regulator thrombopoietin ( TPO ) and its receptor , c-Mpl , in ET and related disorders , but TPO-Mpl dynamics appear to be complex .	manualset1
79667	2	377015	7	NULL	NULL	0	NULL	c-Mpl	GeneOrProtein		is involved in					ET	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	New insights are emerging into the role of the megakaryocytopoiesis regulator thrombopoietin ( TPO ) and its receptor , c-Mpl , in ET and related disorders , but TPO-Mpl dynamics appear to be complex .	manualset1
79668	3	377015	7	NULL	NULL	0	NULL	TPO	Protein		is					 thrombopoietin	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	New insights are emerging into the role of the megakaryocytopoiesis regulator thrombopoietin ( TPO ) and its receptor , c-Mpl , in ET and related disorders , but TPO-Mpl dynamics appear to be complex .	manualset1
79669	4	377015	7	NULL	NULL	0	NULL	TPO	Protein		is a type of					megakaryocytopoiesis regulator	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	New insights are emerging into the role of the megakaryocytopoiesis regulator thrombopoietin ( TPO ) and its receptor , c-Mpl , in ET and related disorders , but TPO-Mpl dynamics appear to be complex .	manualset1
79688	1	377022	7	NULL	NULL	0	NULL	psychotropic drugs	NonProteinOrNucleicAcidChemical		cure					plasmids	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	NULL	NULL	New mechanism of plasmid curing by psychotropic drugs .	manualset1
79689	1	377025	7	NULL	NULL	0	NULL	New oscillometric method	MedicalProcedureOrDevice		measures		indirectly			systolic arterial pressure	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	New oscillometric method for indirect measurement of systolic and mean arterial pressure in the human finger .	manualset1
79690	2	377025	7	NULL	NULL	0	NULL	New oscillometric method	MedicalProcedureOrDevice		measures		indirectly			mean arterial pressure	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	New oscillometric method for indirect measurement of systolic and mean arterial pressure in the human finger .	manualset1
79691	3	377025	7	NULL	NULL	0	NULL	statement 1	Process		occur in					 finger	BodyPart	human			NULL		0	NULL	NULL	NULL	NULL	NULL	New oscillometric method for indirect measurement of systolic and mean arterial pressure in the human finger .	manualset1
79692	4	377025	7	NULL	NULL	0	NULL	statement 2	Process		occur in					finger	BodyPart	human			NULL		0	NULL	NULL	NULL	NULL	NULL	New oscillometric method for indirect measurement of systolic and mean arterial pressure in the human finger .	manualset1
79739	1	377027	7	NULL	NULL	NULL	NULL	receptor-linked phospholipase D	Protein	coupling of	occur in					neutrophils	Cell	primed			NULL		NULL	NULL	NULL	NULL	NULL	NULL	New pathways of phagocyte activation : the coupling of receptor-linked phospholipase D and the role of tyrosine kinase in primed neutrophils .	manualset1
79740	2	377027	7	NULL	NULL	0	NULL	tyrosine kinase	Protein		participate in					phagocyte	Cell	activation of			NULL		0	NULL	NULL	NULL	NULL	NULL	New pathways of phagocyte activation : the coupling of receptor-linked phospholipase D and the role of tyrosine kinase in primed neutrophils .	manualset1
79741	3	377027	7	NULL	NULL	NULL	NULL	statement 1	Process		participate in					phagocyte	Cell	activation of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	New pathways of phagocyte activation : the coupling of receptor-linked phospholipase D and the role of tyrosine kinase in primed neutrophils .	manualset1
79742	4	377027	7	NULL	NULL	0	NULL	statement 1	Process		occur in					neutrophils	Cell	primed			NULL		0	NULL	NULL	NULL	NULL	NULL	New pathways of phagocyte activation : the coupling of receptor-linked phospholipase D and the role of tyrosine kinase in primed neutrophils .	manualset1
79743	1	377028	7	NULL	NULL	0	NULL	 mucAB	GeneOrProtein		associated with					new phenotype	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	New phenotypes associated with mucAB : alteration of a MucA sequence homologous to the LexA cleavage site .	manualset1
79744	2	377030	7	NULL	NULL	NULL	NULL	Fas2 gene	Gene	site-directed mutagenesis of;;synthetic	designed to					statement 1	Process	delineate the individual contributions of 			NULL		NULL	NULL	NULL	NULL	NULL	NULL	New probes , designed to delineate the individual contributions of the fasciculin residues to the complex formation and conformation , were generated by site-directed mutagenesis of a synthetic Fas2 gene .	manualset1
79745	1	377030	7	NULL	NULL	0	NULL	fasciculin residues	AminoAcid		forms					complex	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	New probes , designed to delineate the individual contributions of the fasciculin residues to the complex formation and conformation , were generated by site-directed mutagenesis of a synthetic Fas2 gene .	manualset1
79746	1	377033	7	NULL	NULL	0	NULL	rifampin	NonProteinOrNucleicAcidChemical	resistance to	detected in					Mycobacterium tuberculosis	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	New rapid phenotypic assays for the detection of rifampin resistance in Mycobacterium tuberculosis have recently been described , but most of these require liquid cultures , which reduces the utility of many tests in terms of turnaround times .	manualset1
79747	1	377039	7	NULL	NULL	0	NULL	New therapeutic approaches	MedicalProcedureOrDevice		based on					antimicrotubules agents	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	New therapeutic approaches are now based on antimicrotubules agents but it is difficult to evaluate their efficacity .	manualset1
79748	1	377040	7	NULL	NULL	0	NULL	New vascular graft	BodyPart		simplifies					aortic valve reimplantation technique	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	New vascular graft for simplification of the aortic valve reimplantation technique .	manualset1
79749	1	377041	7	NULL	NULL	0	NULL	New vesicular ampicillin-loaded delivery systems 	MedicalProcedureOrDevice		used for					topical application	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	New vesicular ampicillin-loaded delivery systems for topical application : characterization , in vitro permeation experiments and antimicrobial activity .	manualset1
79750	1	377044	7	NULL	NULL	NULL	NULL	Newer fluoroquinolones	NonProteinOrNucleicAcidChemical		activity against		increased;;in vitro			anaerobes	Organism				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Newer fluoroquinolones with increased in vitro activity against anaerobes are under development and include levofloxacin , clinafloxacin , sparfloxacin , trovafloxacin , grepafloxacin , and DU-6859a .	manualset1
79751	2	377044	7	NULL	NULL	0	NULL	levofloxacin	NonProteinOrNucleicAcidChemical		is a type of					Newer fluoroquinolones	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Newer fluoroquinolones with increased in vitro activity against anaerobes are under development and include levofloxacin , clinafloxacin , sparfloxacin , trovafloxacin , grepafloxacin , and DU-6859a .	manualset1
79752	3	377044	7	NULL	NULL	0	NULL	 clinafloxacin	NonProteinOrNucleicAcidChemical		is a type of					Newer fluoroquinolones	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Newer fluoroquinolones with increased in vitro activity against anaerobes are under development and include levofloxacin , clinafloxacin , sparfloxacin , trovafloxacin , grepafloxacin , and DU-6859a .	manualset1
79753	4	377044	7	NULL	NULL	0	NULL	sparfloxacin	NonProteinOrNucleicAcidChemical		is a type of					Newer fluoroquinolones	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Newer fluoroquinolones with increased in vitro activity against anaerobes are under development and include levofloxacin , clinafloxacin , sparfloxacin , trovafloxacin , grepafloxacin , and DU-6859a .	manualset1
79754	5	377044	7	NULL	NULL	0	NULL	trovafloxacin	NonProteinOrNucleicAcidChemical		is a type of					Newer fluoroquinolones	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Newer fluoroquinolones with increased in vitro activity against anaerobes are under development and include levofloxacin , clinafloxacin , sparfloxacin , trovafloxacin , grepafloxacin , and DU-6859a .	manualset1
79755	6	377044	7	NULL	NULL	0	NULL	grepafloxacin	NonProteinOrNucleicAcidChemical		is a type of					Newer fluoroquinolones	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Newer fluoroquinolones with increased in vitro activity against anaerobes are under development and include levofloxacin , clinafloxacin , sparfloxacin , trovafloxacin , grepafloxacin , and DU-6859a .	manualset1
79756	7	377044	7	NULL	NULL	0	NULL	DU-6859a	NonProteinOrNucleicAcidChemical		is a type of					Newer fluoroquinolones	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Newer fluoroquinolones with increased in vitro activity against anaerobes are under development and include levofloxacin , clinafloxacin , sparfloxacin , trovafloxacin , grepafloxacin , and DU-6859a .	manualset1
79761	1	377045	7	NULL	NULL	NULL	NULL	pancreatic inflammatory disease	Disease	complications of 	include					 pseudocysts	MedicalFinding	percutaneous drainage of 			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Newer management strategies for these complications of pancreatic inflammatory disease are discussed , including percutaneous drainage of pseudocysts and the use of octreotide in the management of pancreatic ascites and pancreatic fistulas .	manualset1
79762	2	377045	7	NULL	NULL	NULL	NULL	octreotide	NonProteinOrNucleicAcidChemical		used in the					pancreatic ascites 	MedicalFinding	management of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Newer management strategies for these complications of pancreatic inflammatory disease are discussed , including percutaneous drainage of pseudocysts and the use of octreotide in the management of pancreatic ascites and pancreatic fistulas .	manualset1
79763	3	377045	7	NULL	NULL	0	NULL	octreotide	NonProteinOrNucleicAcidChemical		used in the					pancreatic fistulas	MedicalFinding	management of			NULL		0	NULL	NULL	NULL	NULL	NULL	Newer management strategies for these complications of pancreatic inflammatory disease are discussed , including percutaneous drainage of pseudocysts and the use of octreotide in the management of pancreatic ascites and pancreatic fistulas .	manualset1
79765	1	377047	7	NULL	NULL	0	NULL	L-3 ,4 - dihydroxyphenylalanine	NonProteinOrNucleicAcidChemical		converted to					DA	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Next , AtT-20 neuroendocrine cells were transfected with wild-type and mutated TH genes because these cells were earlier shown to be capable of fully converting L-3 ,4 - dihydroxyphenylalanine into DA , whereby the catalytic activity of TH would be expected to be inhibited by the end product DA accumulating in the cells .	manualset1
79766	2	377047	7	NULL	NULL	NULL	NULL	AtT-20 neuroendocrine cells	Cell		transfected with					TH genes	Gene	wildtype			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Next , AtT-20 neuroendocrine cells were transfected with wild-type and mutated TH genes because these cells were earlier shown to be capable of fully converting L-3 ,4 - dihydroxyphenylalanine into DA , whereby the catalytic activity of TH would be expected to be inhibited by the end product DA accumulating in the cells .	manualset1
79767	3	377047	7	NULL	NULL	NULL	NULL	AtT-20 neuroendocrine cells 	Cell		transfected with					TH genes	Gene	mutated			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Next , AtT-20 neuroendocrine cells were transfected with wild-type and mutated TH genes because these cells were earlier shown to be capable of fully converting L-3 ,4 - dihydroxyphenylalanine into DA , whereby the catalytic activity of TH would be expected to be inhibited by the end product DA accumulating in the cells .	manualset1
79768	4	377047	7	NULL	NULL	NULL	NULL	statement 1	Process		occur in					statement 2	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Next , AtT-20 neuroendocrine cells were transfected with wild-type and mutated TH genes because these cells were earlier shown to be capable of fully converting L-3 ,4 - dihydroxyphenylalanine into DA , whereby the catalytic activity of TH would be expected to be inhibited by the end product DA accumulating in the cells .	manualset1
79769	5	377047	7	NULL	NULL	0	NULL	statement 1	Process		occur in					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Next , AtT-20 neuroendocrine cells were transfected with wild-type and mutated TH genes because these cells were earlier shown to be capable of fully converting L-3 ,4 - dihydroxyphenylalanine into DA , whereby the catalytic activity of TH would be expected to be inhibited by the end product DA accumulating in the cells .	manualset1
79770	6	377047	7	NULL	NULL	NULL	NULL	DA	NonProteinOrNucleicAcidChemical		accumulate in					AtT-20 neuroendocrine cells 	Cell				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Next , AtT-20 neuroendocrine cells were transfected with wild-type and mutated TH genes because these cells were earlier shown to be capable of fully converting L-3 ,4 - dihydroxyphenylalanine into DA , whereby the catalytic activity of TH would be expected to be inhibited by the end product DA accumulating in the cells .	manualset1
79771	7	377047	7	NULL	NULL	0	NULL	statement 6	Process		inhibit		may			TH	GeneOrProtein	catalytic activity of			NULL		0	NULL	NULL	NULL	NULL	NULL	Next , AtT-20 neuroendocrine cells were transfected with wild-type and mutated TH genes because these cells were earlier shown to be capable of fully converting L-3 ,4 - dihydroxyphenylalanine into DA , whereby the catalytic activity of TH would be expected to be inhibited by the end product DA accumulating in the cells .	manualset1
79772	8	377047	7	NULL	NULL	0	NULL	statement 2	Process		occur along with					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Next , AtT-20 neuroendocrine cells were transfected with wild-type and mutated TH genes because these cells were earlier shown to be capable of fully converting L-3 ,4 - dihydroxyphenylalanine into DA , whereby the catalytic activity of TH would be expected to be inhibited by the end product DA accumulating in the cells .	manualset1
79773	1	377048	7	NULL	NULL	NULL	NULL	VEGFR2 + cells	Cell	FACS-sorted	express					SMC-specific marker	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Next , FACS-sorted VEGFR2 + cells expressed highest and lowest levels of SMC - and fibroblast-specific markers , respectively , at days 7-14 after retinoic acid ( RA ) as compared with VEGFR2 + / PDGFR + cells .	manualset1
79774	2	377048	7	NULL	NULL	NULL	NULL	VEGFR2 + cells	Cell	FACS-sorted	express					fibroblast-specific marker	GeneOrProtein				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Next , FACS-sorted VEGFR2 + cells expressed highest and lowest levels of SMC - and fibroblast-specific markers , respectively , at days 7-14 after retinoic acid ( RA ) as compared with VEGFR2 + / PDGFR + cells .	manualset1
79775	3	377048	7	NULL	NULL	0	NULL	VEGFR2 + / PDGFR + cells	Cell		express					SMC-specific marker	GeneOrProtein				NULL		0	NULL	NULL	NULL	NULL	NULL	Next , FACS-sorted VEGFR2 + cells expressed highest and lowest levels of SMC - and fibroblast-specific markers , respectively , at days 7-14 after retinoic acid ( RA ) as compared with VEGFR2 + / PDGFR + cells .	manualset1
79776	4	377048	7	NULL	NULL	0	NULL	VEGFR2 + / PDGFR + cells	Cell		express					fibroblast-specific marker	GeneOrProtein				NULL		0	NULL	NULL	NULL	NULL	NULL	Next , FACS-sorted VEGFR2 + cells expressed highest and lowest levels of SMC - and fibroblast-specific markers , respectively , at days 7-14 after retinoic acid ( RA ) as compared with VEGFR2 + / PDGFR + cells .	manualset1
79777	5	377048	7	NULL	NULL	0	NULL	statement 1	Process		is higher than					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Next , FACS-sorted VEGFR2 + cells expressed highest and lowest levels of SMC - and fibroblast-specific markers , respectively , at days 7-14 after retinoic acid ( RA ) as compared with VEGFR2 + / PDGFR + cells .	manualset1
79778	6	377048	7	NULL	NULL	0	NULL	statement 2	Process		is higher than					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Next , FACS-sorted VEGFR2 + cells expressed highest and lowest levels of SMC - and fibroblast-specific markers , respectively , at days 7-14 after retinoic acid ( RA ) as compared with VEGFR2 + / PDGFR + cells .	manualset1
79781	1	377052	7	NULL	NULL	0	NULL	pWEE1B	GeneOrProtein		localize in					nucleus	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	Next , the localization of pWEE1B was examined by immunohistochemistry , and exclusive nuclear localization was revealed in the fully grown oocytes .	manualset1
79782	2	377052	7	NULL	NULL	0	NULL	statement 1	Process		occur in					oocytes	Cell	fully grown			NULL		0	NULL	NULL	NULL	NULL	NULL	Next , the localization of pWEE1B was examined by immunohistochemistry , and exclusive nuclear localization was revealed in the fully grown oocytes .	manualset1
79783	1	377055	7	NULL	NULL	0	NULL	UFH	NonProteinOrNucleicAcidChemical		is a type of		well-established			 intravenous therapy	MedicalProcedure	concomitant			NULL		0	NULL	NULL	NULL	NULL	NULL	Next to antiplatelet therapy , unfractionated heparin ( UFH ) is a well-established concomitant intravenous therapy during PCI .	manualset1
79784	2	377055	7	NULL	NULL	0	NULL	statement 1	Process		occur during					PCI	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Next to antiplatelet therapy , unfractionated heparin ( UFH ) is a well-established concomitant intravenous therapy during PCI .	manualset1
79785	3	377055	7	NULL	NULL	0	NULL	UFH	NonProteinOrNucleicAcidChemical		is 					unfractionated heparin	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Next to antiplatelet therapy , unfractionated heparin ( UFH ) is a well-established concomitant intravenous therapy during PCI .	manualset1
79786	4	377055	7	NULL	NULL	0	NULL	statement 1	Process		is used					antiplatelet therapy	MedicalProcedure	next to			NULL		0	NULL	NULL	NULL	NULL	NULL	Next to antiplatelet therapy , unfractionated heparin ( UFH ) is a well-established concomitant intravenous therapy during PCI .	manualset1
79787	1	377056	7	NULL	NULL	0	NULL	Nicergoline	NonProteinOrNucleicAcidChemical		enhances					glutamate 	AminoAcid	re-uptake of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nicergoline enhances glutamate re-uptake and protects against brain damage in rat global brain ischemia .	manualset1
79788	2	377056	7	NULL	NULL	0	NULL	statement 1	Process		protects against					brain 	BodyPart	damage of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nicergoline enhances glutamate re-uptake and protects against brain damage in rat global brain ischemia .	manualset1
79789	3	377056	7	NULL	NULL	NULL	NULL	statement 2	Process		occur in					global brain ischemia	Disease	rat			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nicergoline enhances glutamate re-uptake and protects against brain damage in rat global brain ischemia .	manualset1
79791	1	377057	7	NULL	NULL	NULL	NULL	Nickel	Chemical		catalyze					vinyl epoxides	NonProteinOrNucleicAcidChemical	borylative ring opening of 			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nickel-catalyzed borylative ring opening of vinyl epoxides and aziridines .	manualset1
79792	2	377057	7	NULL	NULL	NULL	NULL	Nickel	Chemical		catalyze					aziridines	NonProteinOrNucleicAcidChemical	borylative ring opening of 			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nickel-catalyzed borylative ring opening of vinyl epoxides and aziridines .	manualset1
79793	1	377058	7	NULL	NULL	NULL	NULL	Nicotinamide	NonProteinOrNucleicAcidChemical		decreases					nitric oxide	NonProteinOrNucleicAcidChemical	production of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nicotinamide decreases nitric oxide production and partially protects human pancreatic islets against the suppressive effects of combinations of cytokines .	manualset1
79794	2	377058	7	NULL	NULL	0	NULL	statement 1	Process		protects		partially			pancreatic islets	BodyPart	human			NULL		0	NULL	NULL	NULL	NULL	NULL	Nicotinamide decreases nitric oxide production and partially protects human pancreatic islets against the suppressive effects of combinations of cytokines .	manualset1
79795	3	377058	7	NULL	NULL	0	NULL	statement 2	Process		against					cytokines	NonProteinOrNucleicAcidChemical	 suppressive effects of combinations of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nicotinamide decreases nitric oxide production and partially protects human pancreatic islets against the suppressive effects of combinations of cytokines .	manualset1
79796	1	377059	7	NULL	NULL	NULL	NULL	Nicotine	NonProteinOrNucleicAcidChemical		interacts with					opioid 	NonProteinOrNucleicAcidChemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nicotine 's opioid and anti-opioid interactions : proposed role in smoking behavior .	manualset1
79797	2	377059	7	NULL	NULL	NULL	NULL	Nicotine	NonProteinOrNucleicAcidChemical		interacts with					anti-opioid	NonProteinOrNucleicAcidChemical				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nicotine 's opioid and anti-opioid interactions : proposed role in smoking behavior .	manualset1
79798	1	377062	7	NULL	NULL	NULL	NULL	array CGH	MedicalProcedureOrDevice		used to					chromosome 18	Chromosome	 illustrate the aberrations of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nine cases of aberrations involving chromosome 18 are used to illustrate the use and clinical potential of array CGH .	manualset1
79799	1	377064	7	NULL	NULL	0	NULL	 moss species 	Organism		shows					antibacterial activity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nine moss species showed antibacterial activity against Gram ( + ) bacteria , in particular H. splendens and its ethyl acetate fractions showed stronger activity .	manualset1
79800	2	377064	7	NULL	NULL	0	NULL	statement 1	Process		against					 H. splendens	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Nine moss species showed antibacterial activity against Gram ( + ) bacteria , in particular H. splendens and its ethyl acetate fractions showed stronger activity .	manualset1
79801	3	377064	7	NULL	NULL	0	NULL	 H. splendens	Organism		is a type of					Gram ( + ) bacteria	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Nine moss species showed antibacterial activity against Gram ( + ) bacteria , in particular H. splendens and its ethyl acetate fractions showed stronger activity .	manualset1
79802	1	377067	7	NULL	NULL	NULL	NULL	hypothyroidism	Disease		occur due to					thyroid ectopia	Disease				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nine patients suffering from hypothyroidism due to thyroid ectopia or hypogenesis , with a large sella turcica , were examined at adolescence or during adult life .	manualset1
79803	2	377067	7	NULL	NULL	NULL	NULL	hypothyroidism	Disease		occur due to					large sella turcica	BodyPart	hypogenesis with			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nine patients suffering from hypothyroidism due to thyroid ectopia or hypogenesis , with a large sella turcica , were examined at adolescence or during adult life .	manualset1
79804	1	377070	7	NULL	NULL	0	NULL	ATIII	Protein		used in the					 venous thrombosis	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nine subjects with acquired ATIII deficiency also received ATIII treatment for venous or arterial thrombosis or disseminated intravascular coagulation , all with low plasma ATIII levels .	manualset1
79805	2	377070	7	NULL	NULL	0	NULL	ATIII	Protein		used in the					arterial thrombosis	MedicalFinding	treatment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nine subjects with acquired ATIII deficiency also received ATIII treatment for venous or arterial thrombosis or disseminated intravascular coagulation , all with low plasma ATIII levels .	manualset1
79806	3	377070	7	NULL	NULL	NULL	NULL	ATIII	Protein		used in the					disseminated intravascular coagulation	BiologicalProcess	treatment of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nine subjects with acquired ATIII deficiency also received ATIII treatment for venous or arterial thrombosis or disseminated intravascular coagulation , all with low plasma ATIII levels .	manualset1
79807	4	377070	7	NULL	NULL	0	NULL	venous thrombosis	MedicalFinding		occur due to					ATIII	Protein	deficiency of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nine subjects with acquired ATIII deficiency also received ATIII treatment for venous or arterial thrombosis or disseminated intravascular coagulation , all with low plasma ATIII levels .	manualset1
79808	5	377070	7	NULL	NULL	0	NULL	arterial thrombosis	MedicalFinding		occur due to					ATIII	Protein	deficiency of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nine subjects with acquired ATIII deficiency also received ATIII treatment for venous or arterial thrombosis or disseminated intravascular coagulation , all with low plasma ATIII levels .	manualset1
79809	6	377070	7	NULL	NULL	0	NULL	disseminated intravascular coagulation	BiologicalProcess		occur due to					ATIII	Protein	deficiency of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nine subjects with acquired ATIII deficiency also received ATIII treatment for venous or arterial thrombosis or disseminated intravascular coagulation , all with low plasma ATIII levels .	manualset1
79810	1	377074	7	NULL	NULL	NULL	NULL	PAG 	BodyPart	stimulation of	relieves					back pain	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nineteen patients with both leg and back pain received electrodes in the PAG and the somatosensory regions ; whereas back pain was relieved by PAG stimulation , dysesthetic leg pain was controlled more effectively by somatosensory region stimulation .	manualset1
79811	2	377074	7	NULL	NULL	0	NULL	somatosensory region	BodyPart	stimulation of	controls		effectively			dysesthetic leg pain	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Nineteen patients with both leg and back pain received electrodes in the PAG and the somatosensory regions ; whereas back pain was relieved by PAG stimulation , dysesthetic leg pain was controlled more effectively by somatosensory region stimulation .	manualset1
79812	1	377077	7	NULL	NULL	0	NULL	dichloromethane	Chemical	crude extracts with	used in the					Yemeni ethnomedicine	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Ninety crude extracts , including dichloromethane , methanol and aqueous extracts from 30 medicinal plants used in the Yemeni ethnomedicine to treat common infections , were screened in vitro for antimicrobial activities against three Gram-positive bacteria and two Gram-negative bacteria , Candida maltosa and five opportunistic human fungal pathogens ( two yeasts , three hyphomycetes ) .	manualset1
79813	2	377077	7	NULL	NULL	0	NULL	methanol	Chemical	crude extracts with	used in the					Yemeni ethnomedicine	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Ninety crude extracts , including dichloromethane , methanol and aqueous extracts from 30 medicinal plants used in the Yemeni ethnomedicine to treat common infections , were screened in vitro for antimicrobial activities against three Gram-positive bacteria and two Gram-negative bacteria , Candida maltosa and five opportunistic human fungal pathogens ( two yeasts , three hyphomycetes ) .	manualset1
79814	1	377078	7	NULL	NULL	0	NULL	male F344 rats	Organism	tumors induced in	harbor					mutations	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Ninety percent ( 18 of 20 ) of the tumors induced in male F344 rats harbored mutations , which were detected in three of four adenomas ( 75 % ) and 15 of 16 adenocarcinomas ( 94 % ) .	manualset1
79816	1	377089	7	NULL	NULL	0	NULL	NitR	GeneOrProtein		regulator of					hmgA	GeneOrProtein	S. meliloti;;expression of			NULL		0	NULL	NULL	NULL	NULL	NULL	NitR was found to be a regulator of S. meliloti hmgA expression under nitrogen deprivation conditions , suggesting the presence of a ntr-independent nitrogen deprivation regulatory system .	manualset1
79817	2	377089	7	NULL	NULL	0	NULL	statement 1	Process		under					nitrogen	Chemical	deprivation condition of			NULL		0	NULL	NULL	NULL	NULL	NULL	NitR was found to be a regulator of S. meliloti hmgA expression under nitrogen deprivation conditions , suggesting the presence of a ntr-independent nitrogen deprivation regulatory system .	manualset1
79818	3	377089	7	NULL	NULL	0	NULL	statement 1	Process		suggest					ntr-independent nitrogen deprivation regulatory system	BiologicalProcess	presence of			NULL		0	NULL	NULL	NULL	NULL	NULL	NitR was found to be a regulator of S. meliloti hmgA expression under nitrogen deprivation conditions , suggesting the presence of a ntr-independent nitrogen deprivation regulatory system .	manualset1
79819	1	377090	7	NULL	NULL	0	NULL	Nitrates	Chemical		likely to be					active substances	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitrates are very likely to be active substances on Holter recorded angina but no controlled studies have been performed to really demonstrate it .	manualset1
79820	2	377090	7	NULL	NULL	0	NULL	statement 1	Process		occur on					Holter recorded angina	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitrates are very likely to be active substances on Holter recorded angina but no controlled studies have been performed to really demonstrate it .	manualset1
79821	1	377091	7	NULL	NULL	NULL	NULL	NO	NonProteinOrNucleicAcidChemical		play a role in					sensory activity	BiologicalProcess				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nitric oxide ( NO ) in the spinal cord plays a role in sensory and autonomic activity .	manualset1
79822	2	377091	7	NULL	NULL	NULL	NULL	NO	NonProteinOrNucleicAcidChemical		play a role in					autonomic activity	BiologicalProcess				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nitric oxide ( NO ) in the spinal cord plays a role in sensory and autonomic activity .	manualset1
79823	3	377091	7	NULL	NULL	0	NULL	statement 1	Process		occur in the					spinal cord	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitric oxide ( NO ) in the spinal cord plays a role in sensory and autonomic activity .	manualset1
79824	4	377091	7	NULL	NULL	NULL	NULL	statement 2	Process		occur in the					spinal cord	BodyPart				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nitric oxide ( NO ) in the spinal cord plays a role in sensory and autonomic activity .	manualset1
79825	5	377091	7	NULL	NULL	0	NULL	NO	Chemical		is					Nitric oxide	Chemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitric oxide ( NO ) in the spinal cord plays a role in sensory and autonomic activity .	manualset1
79848	1	377092	7	NULL	NULL	NULL	NULL	NO	NonProteinOrNucleicAcidChemical	production of	enhanced in					active ulcerative colitis	Disease				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nitric oxide ( NO ) production , as detectable by indirect and direct methods , as well as the expression of inducible nitric oxide synthase ( iNOS ) in the intestinal mucosa appear to be enhanced in active ulcerative colitis and , when in excess , to play a proinflammatory role in the disease .	manualset1
79850	2	377092	7	NULL	NULL	0	NULL	iNOS	Protein	expression of	enhanced in					active ulcerative colitis	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitric oxide ( NO ) production , as detectable by indirect and direct methods , as well as the expression of inducible nitric oxide synthase ( iNOS ) in the intestinal mucosa appear to be enhanced in active ulcerative colitis and , when in excess , to play a proinflammatory role in the disease .	manualset1
79851	3	377092	7	NULL	NULL	0	NULL	statement 1	Process		occur in					intestinal mucosa	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitric oxide ( NO ) production , as detectable by indirect and direct methods , as well as the expression of inducible nitric oxide synthase ( iNOS ) in the intestinal mucosa appear to be enhanced in active ulcerative colitis and , when in excess , to play a proinflammatory role in the disease .	manualset1
79852	4	377092	7	NULL	NULL	0	NULL	statement 2	Process		occur in					intestinal mucosa	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitric oxide ( NO ) production , as detectable by indirect and direct methods , as well as the expression of inducible nitric oxide synthase ( iNOS ) in the intestinal mucosa appear to be enhanced in active ulcerative colitis and , when in excess , to play a proinflammatory role in the disease .	manualset1
79854	5	377092	7	NULL	NULL	NULL	NULL	NO	NonProteinOrNucleicAcidChemical	excess of	proinflammatory role in					active ulcerative colitis	Disease				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nitric oxide ( NO ) production , as detectable by indirect and direct methods , as well as the expression of inducible nitric oxide synthase ( iNOS ) in the intestinal mucosa appear to be enhanced in active ulcerative colitis and , when in excess , to play a proinflammatory role in the disease .	manualset1
79860	6	377092	7	NULL	NULL	0	NULL	iNOS	Protein	excess of	proinflammatory role in					active ulcerative colitis	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitric oxide ( NO ) production , as detectable by indirect and direct methods , as well as the expression of inducible nitric oxide synthase ( iNOS ) in the intestinal mucosa appear to be enhanced in active ulcerative colitis and , when in excess , to play a proinflammatory role in the disease .	manualset1
79861	7	377092	7	NULL	NULL	0	NULL	NO	NonProteinOrNucleicAcidChemical		is					Nitric oxide	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitric oxide ( NO ) production , as detectable by indirect and direct methods , as well as the expression of inducible nitric oxide synthase ( iNOS ) in the intestinal mucosa appear to be enhanced in active ulcerative colitis and , when in excess , to play a proinflammatory role in the disease .	manualset1
79862	8	377092	7	NULL	NULL	0	NULL	iNOS	Protein		is					inducible nitric oxide synthase 	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitric oxide ( NO ) production , as detectable by indirect and direct methods , as well as the expression of inducible nitric oxide synthase ( iNOS ) in the intestinal mucosa appear to be enhanced in active ulcerative colitis and , when in excess , to play a proinflammatory role in the disease .	manualset1
79898	1	377095	7	NULL	NULL	0	NULL	NO donors 	NonProteinOrNucleicAcidChemical		produce		exogenously			Nitric oxide	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitric oxide produced exogenously by the addition of NO donors was able to delay or inhibit apoptosis induced by a combination of tumor necrosis factor alpha and actinomycin D and to suppress the activity of caspase 3 .	manualset1
79899	2	377095	7	NULL	NULL	0	NULL	tumor necrosis factor alpha	Protein		induce					apoptosis	MolecularProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitric oxide produced exogenously by the addition of NO donors was able to delay or inhibit apoptosis induced by a combination of tumor necrosis factor alpha and actinomycin D and to suppress the activity of caspase 3 .	manualset1
79900	3	377095	7	NULL	NULL	0	NULL	actinomycin D	NonProteinOrNucleicAcidChemical		induce					apoptosis	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitric oxide produced exogenously by the addition of NO donors was able to delay or inhibit apoptosis induced by a combination of tumor necrosis factor alpha and actinomycin D and to suppress the activity of caspase 3 .	manualset1
79901	4	377095	7	NULL	NULL	0	NULL	statement 2	Process		in combination with					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitric oxide produced exogenously by the addition of NO donors was able to delay or inhibit apoptosis induced by a combination of tumor necrosis factor alpha and actinomycin D and to suppress the activity of caspase 3 .	manualset1
79902	5	377095	7	NULL	NULL	0	NULL	Nitric oxide	NonProteinOrNucleicAcidChemical		delay					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitric oxide produced exogenously by the addition of NO donors was able to delay or inhibit apoptosis induced by a combination of tumor necrosis factor alpha and actinomycin D and to suppress the activity of caspase 3 .	manualset1
79903	6	377095	7	NULL	NULL	0	NULL	Nitric oxide	NonProteinOrNucleicAcidChemical		inhibit					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitric oxide produced exogenously by the addition of NO donors was able to delay or inhibit apoptosis induced by a combination of tumor necrosis factor alpha and actinomycin D and to suppress the activity of caspase 3 .	manualset1
79904	7	377095	7	NULL	NULL	0	NULL	statement 5	Process		is an alternative to					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitric oxide produced exogenously by the addition of NO donors was able to delay or inhibit apoptosis induced by a combination of tumor necrosis factor alpha and actinomycin D and to suppress the activity of caspase 3 .	manualset1
79905	8	377095	7	NULL	NULL	0	NULL	Nitric oxide	NonProteinOrNucleicAcidChemical		suppress					caspase 3	Protein	activity of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nitric oxide produced exogenously by the addition of NO donors was able to delay or inhibit apoptosis induced by a combination of tumor necrosis factor alpha and actinomycin D and to suppress the activity of caspase 3 .	manualset1
79906	1	377096	7	NULL	NULL	0	NULL	Nitric oxide	NonProteinOrNucleicAcidChemical	release of	reduce					psoriasis	Disease	incidence of cutaneous infections in			NULL		0	NULL	NULL	NULL	NULL	NULL	Nitric oxide release accounts for the reduced incidence of cutaneous infections in psoriasis .	manualset1
79907	1	377097	7	NULL	NULL	0	NULL	aminoguanidine	NonProteinOrNucleicAcidChemical	pentacycloundecane conjugates of	inhibit					Nitric oxide synthase	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitric oxide synthase inhibition by pentacycloundecane conjugates of aminoguanidine and tryptamine .	manualset1
79908	2	377097	7	NULL	NULL	NULL	NULL	tryptamine	NonProteinOrNucleicAcidChemical	pentacycloundecane conjugates of	inhibit					Nitric oxide synthase	Protein				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nitric oxide synthase inhibition by pentacycloundecane conjugates of aminoguanidine and tryptamine .	manualset1
79910	1	377100	7	NULL	NULL	0	NULL	risedronate	NonProteinOrNucleicAcidChemical		inhibit					farnesyl diphosphate synthase	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitrogen-containing bisphosphonate drugs such as risedronate act by inhibiting farnesyl diphosphate synthase , thereby disrupting protein prenylation in osteoclasts .	manualset1
79911	2	377100	7	NULL	NULL	NULL	NULL	statement 1	Process		disrupt					protein prenylation	MolecularProcess				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nitrogen-containing bisphosphonate drugs such as risedronate act by inhibiting farnesyl diphosphate synthase , thereby disrupting protein prenylation in osteoclasts .	manualset1
79912	3	377100	7	NULL	NULL	0	NULL	statement 1	Process		occur in					osteoclasts	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitrogen-containing bisphosphonate drugs such as risedronate act by inhibiting farnesyl diphosphate synthase , thereby disrupting protein prenylation in osteoclasts .	manualset1
79913	4	377100	7	NULL	NULL	0	NULL	risedronate	NonProteinOrNucleicAcidChemical		is a type of					Nitrogen-containing bisphosphonate drugs	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitrogen-containing bisphosphonate drugs such as risedronate act by inhibiting farnesyl diphosphate synthase , thereby disrupting protein prenylation in osteoclasts .	manualset1
79917	1	377101	7	NULL	NULL	NULL	NULL	Nitroglycerin	NonProteinOrNucleicAcidChemical		decrease					t-PA	Protein	thrombolytic effect of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nitroglycerin given with tissue-type plasminogen activator ( t-PA ) has been shown to decrease the thrombolytic effect of t-PA in animal models of coronary artery thrombosis .	manualset1
79918	2	377101	7	NULL	NULL	0	NULL	statement 1	Process		occur in					coronary artery thrombosis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitroglycerin given with tissue-type plasminogen activator ( t-PA ) has been shown to decrease the thrombolytic effect of t-PA in animal models of coronary artery thrombosis .	manualset1
79919	3	377101	7	NULL	NULL	0	NULL	statement 1	Process		along with					t-PA	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitroglycerin given with tissue-type plasminogen activator ( t-PA ) has been shown to decrease the thrombolytic effect of t-PA in animal models of coronary artery thrombosis .	manualset1
79920	4	377101	7	NULL	NULL	0	NULL	t-PA	Protein		is					tissue-type plasminogen activator	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitroglycerin given with tissue-type plasminogen activator ( t-PA ) has been shown to decrease the thrombolytic effect of t-PA in animal models of coronary artery thrombosis .	manualset1
79933	1	377103	7	NULL	NULL	0	NULL	Nitromethane	NonProteinOrNucleicAcidChemical		is used as					methyl 	Chemical	suitable photolytic precursor of 			NULL		0	NULL	NULL	NULL	NULL	NULL	Nitromethane was identified as a particularly suitable photolytic precursor of methyl for studies by photoionization and threshold photoelectron spectroscopy .	manualset1
79939	2	377103	7	NULL	NULL	0	NULL	statement 1	Process		is used in					photoionization studies	ResearchActivity				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitromethane was identified as a particularly suitable photolytic precursor of methyl for studies by photoionization and threshold photoelectron spectroscopy .	manualset1
79940	3	377103	7	NULL	NULL	0	NULL	statement 1	Process		is used in					threshold photoelectron spectroscopy	ResearchActivity				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitromethane was identified as a particularly suitable photolytic precursor of methyl for studies by photoionization and threshold photoelectron spectroscopy .	manualset1
79942	1	377104	7	NULL	NULL	0	NULL	 peroxynitrite	NonProteinOrNucleicAcidChemical		mediate					damage	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitrotyrosine detection in plasma and tissues may be a useful method to demonstrate peroxynitrite-mediated damage .	manualset1
79944	2	377104	7	NULL	NULL	NULL	NULL	Nitrotyrosine 	NonProteinOrNucleicAcidChemical	detection of	demonstrate					statement 1	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nitrotyrosine detection in plasma and tissues may be a useful method to demonstrate peroxynitrite-mediated damage .	manualset1
79945	3	377104	7	NULL	NULL	0	NULL	statement 1	Process		occur in					plasma	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitrotyrosine detection in plasma and tissues may be a useful method to demonstrate peroxynitrite-mediated damage .	manualset1
79946	4	377104	7	NULL	NULL	0	NULL	statement 1	Process		occur in					tissues	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Nitrotyrosine detection in plasma and tissues may be a useful method to demonstrate peroxynitrite-mediated damage .	manualset1
79947	1	377105	7	NULL	NULL	0	NULL	Nitrous oxide	NonProteinOrNucleicAcidChemical		becomes					dentists	PersonGroup	vice of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nitrous oxide becomes the vice of dentists .	manualset1
79948	1	377106	7	NULL	NULL	0	NULL	Nm23	GeneOrProtein		expressed in					tissue specimens	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Nm23 was found to be expressed in all the tissue specimens .	manualset1
79949	1	377109	7	NULL	NULL	0	NULL	Gs protein 	Protein		not detected in					CT1-producing cultures	LaboratoryExperimentalFactor				NULL		0	NULL	NULL	NULL	NULL	NULL	No Gs protein could be detected in the CT1-producing cultures .	manualset1
79988	1	377118	7	NULL	NULL	0	NULL	IL-6	Protein	levels of	not associated with					knee extensor muscle 	BodyPart	strength of			NULL		0	NULL	NULL	NULL	NULL	NULL	No association was found between IL-6 levels and knee extensor muscle ( r = 0.087 , P = 0.306 ) or flexor ( r = -0.011 , P = 0.894 ) strength .	manualset1
80011	1	377126	7	NULL	NULL	0	NULL	 light heteropaenia	Disease		detected in					chicks	Organism	CIAV-vaccinated			NULL		0	NULL	NULL	NULL	NULL	NULL	No clinical signs were observed but light heteropaenia was detected in CIAV-vaccinated chicks .	manualset1
80024	1	377128	7	NULL	NULL	0	NULL	anti-LPS antibody	Protein	regulation of	different with					anti-Ipa antibody	Protein	regulation of			NULL		0	NULL	NULL	NULL	NULL	NULL	No close correlations between the anti-LPS and anti-Ipa antibody responses were observed indicating that they may be differently regulated .	manualset1
80025	1	377134	7	NULL	NULL	NULL	NULL	deformability	BiologicalProcess	decrease in	not correlated with					extracorporeal circulation procedure	MedicalProcedure	duration of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	No correlation was found between decrease in deformability and duration of the extracorporeal circulation procedure .	manualset1
80260	1	377144	7	NULL	NULL	NULL	NULL	PPMS	Disease	 QoL of	does not differ with					progressive MS	Disease	QoL of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	No difference in QoL was found between patients with PPMS and those with secondary progressive MS. The Italian FAMS questionnaire is a valid measure to assess the QoL concerns of patients with MS. FAMS is also easy to administer and is well accepted by patients .	manualset1
80261	1	377145	7	NULL	NULL	0	NULL	sLepR mRNA	Gene	 level of brain;;fish fed reduced	does not differ with					sLepR mRNA	Gene	level of brain;;fish full feeded			NULL		0	NULL	NULL	NULL	NULL	NULL	No difference in brain sLepR mRNA levels was observed between fish fed reduced and full feeding regimes .	manualset1
80262	1	377159	7	NULL	NULL	NULL	NULL	clinical toxicity	MedicalFinding		not found in					plasma aluminium	Chemical	patients with maintained			NULL		NULL	NULL	NULL	NULL	NULL	NULL	No evidence of clinical toxicity was found in patients in whom the plasma aluminum was maintained up to 5 mumol/l .	manualset1
80263	1	377160	7	NULL	NULL	0	NULL	renal parenchymal pathologies	MedicalFinding	evidence of	is not implicated in					systemic hypertension 	MedicalFinding	etiology of			NULL		0	NULL	NULL	NULL	NULL	NULL	No evidence of renal parenchymal pathologies implicated in the etiology of systemic hypertension was observed , therefore , these animals would seem to be suitable models for human essential hypertension .	manualset1
80264	1	377163	7	NULL	NULL	0	NULL	NirBD	GeneOrProtein		required for		exclusively			assimilatory nitrite 	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	No functional redundancy between the genes was observed and we demonstrate that NirBD is exclusively required for assimilatory nitrite ( it does not detoxify nitrite ) and SirA exclusively for assimilatory sulfite reduction .	manualset1
80265	2	377163	7	NULL	NULL	0	NULL	NirBD	GeneOrProtein		does not detoxify					nitrite	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	No functional redundancy between the genes was observed and we demonstrate that NirBD is exclusively required for assimilatory nitrite ( it does not detoxify nitrite ) and SirA exclusively for assimilatory sulfite reduction .	manualset1
80266	3	377163	7	NULL	NULL	0	NULL	SirA	GeneOrProtein		reduce		exclusively			assimilatory sulfite	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	No functional redundancy between the genes was observed and we demonstrate that NirBD is exclusively required for assimilatory nitrite ( it does not detoxify nitrite ) and SirA exclusively for assimilatory sulfite reduction .	manualset1
80277	1	377175	7	NULL	NULL	0	NULL	primary tumor	MedicalFinding	morphology of	not different from					metastatic tumor	MedicalFinding	morphology of			NULL		0	NULL	NULL	NULL	NULL	NULL	No morphological differences could be observed between the primary and the metastatic tumors .	manualset1
80278	1	377180	7	NULL	NULL	NULL	NULL	thoracotomy	MedicalProcedureOrDevice	 technique of	does not reduce					chronic postthoracotomy pain	MedicalFinding	incidence of 			NULL		NULL	NULL	NULL	NULL	NULL	NULL	No one technique of thoracotomy has been shown to reduce the incidence of chronic postthoracotomy pain .	manualset1
80279	1	377185	7	NULL	NULL	0	NULL	 pathological tracer uptake	MedicalProcedureOrDevice		is not seen					gastric NHL	Disease	in patient with low-grade			NULL		0	NULL	NULL	NULL	NULL	NULL	No pathological tracer uptake was seen in the patient with low-grade gastric NHL of the MALT type .	manualset1
80280	2	377185	7	NULL	NULL	0	NULL	gastric NHL	Disease		is of					MALT type	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	No pathological tracer uptake was seen in the patient with low-grade gastric NHL of the MALT type .	manualset1
80307	1	377186	7	NULL	NULL	0	NULL	CHT	MedicalProcedure		does not cause					gastric perforation	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	No patient experienced gastric perforation or bleeding during CHT .	manualset1
80308	2	377186	7	NULL	NULL	0	NULL	CHT	MedicalProcedure		does not cause					bleeding	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	No patient experienced gastric perforation or bleeding during CHT .	manualset1
80309	1	377211	7	NULL	NULL	NULL	NULL	thiamine 	NonProteinOrNucleicAcidChemical	early stages of deficiency of	does not alter		significantly			M1 muscarinic binding sites	GeneOrProtein	densities of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	No significant alterations in densities of M1 , M2 or total muscarinic binding sites were observed in any brain structure evaluated at either early or late stages of thiamine deficiency .	manualset1
80310	2	377211	7	NULL	NULL	0	NULL	thiamine 	NonProteinOrNucleicAcidChemical	early stages of deficiency of	does not alter		significantly			M2 muscarinic binding sites	GeneOrProtein	densities of			NULL		0	NULL	NULL	NULL	NULL	NULL	No significant alterations in densities of M1 , M2 or total muscarinic binding sites were observed in any brain structure evaluated at either early or late stages of thiamine deficiency .	manualset1
80311	3	377211	7	NULL	NULL	NULL	NULL	thiamine 	NonProteinOrNucleicAcidChemical	early stages of deficiency of	does not alter		significantly			total muscarinic binding sites	GeneOrProtein	densities of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	No significant alterations in densities of M1 , M2 or total muscarinic binding sites were observed in any brain structure evaluated at either early or late stages of thiamine deficiency .	manualset1
80312	4	377211	7	NULL	NULL	0	NULL	thiamine 	NonProteinOrNucleicAcidChemical	late stages of deficiency of	does not alter		significantly			M1 muscarinic binding sites	GeneOrProtein	densities of			NULL		0	NULL	NULL	NULL	NULL	NULL	No significant alterations in densities of M1 , M2 or total muscarinic binding sites were observed in any brain structure evaluated at either early or late stages of thiamine deficiency .	manualset1
80313	5	377211	7	NULL	NULL	0	NULL	thiamine 	NonProteinOrNucleicAcidChemical	late stages of deficiency of	does not alter		significantly			M2 muscarinic binding sites	GeneOrProtein	densities of			NULL		0	NULL	NULL	NULL	NULL	NULL	No significant alterations in densities of M1 , M2 or total muscarinic binding sites were observed in any brain structure evaluated at either early or late stages of thiamine deficiency .	manualset1
80314	6	377211	7	NULL	NULL	0	NULL	thiamine 	NonProteinOrNucleicAcidChemical	late stages of deficiency of	does not alter		significantly			total muscarinic binding sites	GeneOrProtein	densities of			NULL		0	NULL	NULL	NULL	NULL	NULL	No significant alterations in densities of M1 , M2 or total muscarinic binding sites were observed in any brain structure evaluated at either early or late stages of thiamine deficiency .	manualset1
80315	7	377211	7	NULL	NULL	0	NULL	statement 1	Process		occur in					brain	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	No significant alterations in densities of M1 , M2 or total muscarinic binding sites were observed in any brain structure evaluated at either early or late stages of thiamine deficiency .	manualset1
80316	8	377211	7	NULL	NULL	0	NULL	statement 2	Process		occur in					brain	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	No significant alterations in densities of M1 , M2 or total muscarinic binding sites were observed in any brain structure evaluated at either early or late stages of thiamine deficiency .	manualset1
80317	9	377211	7	NULL	NULL	0	NULL	statement 3	Process		occur in					brain	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	No significant alterations in densities of M1 , M2 or total muscarinic binding sites were observed in any brain structure evaluated at either early or late stages of thiamine deficiency .	manualset1
80318	10	377211	7	NULL	NULL	0	NULL	statement 4	Process		occur in					brain	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	No significant alterations in densities of M1 , M2 or total muscarinic binding sites were observed in any brain structure evaluated at either early or late stages of thiamine deficiency .	manualset1
80319	11	377211	7	NULL	NULL	0	NULL	statement 5	Process		occur in					brain	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	No significant alterations in densities of M1 , M2 or total muscarinic binding sites were observed in any brain structure evaluated at either early or late stages of thiamine deficiency .	manualset1
80320	12	377211	7	NULL	NULL	0	NULL	statement 6	Process		occur in					brain	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	No significant alterations in densities of M1 , M2 or total muscarinic binding sites were observed in any brain structure evaluated at either early or late stages of thiamine deficiency .	manualset1
80321	13	377211	7	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	No significant alterations in densities of M1 , M2 or total muscarinic binding sites were observed in any brain structure evaluated at either early or late stages of thiamine deficiency .	manualset1
80322	14	377211	7	NULL	NULL	0	NULL	statement 2	Process		is an alternative to					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	No significant alterations in densities of M1 , M2 or total muscarinic binding sites were observed in any brain structure evaluated at either early or late stages of thiamine deficiency .	manualset1
80323	15	377211	7	NULL	NULL	0	NULL	statement 3	Process		is an alternative to					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	No significant alterations in densities of M1 , M2 or total muscarinic binding sites were observed in any brain structure evaluated at either early or late stages of thiamine deficiency .	manualset1
80324	1	377212	7	NULL	NULL	0	NULL	MMP-9	Protein	expression of	not associated with					herniation grade	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	No significant association was found between MMP-9 expression and herniation grade in patients who were 30-60 years or over 60 years of age .	manualset1
80325	1	377213	7	NULL	NULL	0	NULL	maternal smoking	Process		not associated with		significantly			IgE 	Protein	cord plasma levels of			NULL		0	NULL	NULL	NULL	NULL	NULL	No significant association was observed between maternal smoking and cord plasma IgE levels .	manualset1
80326	1	377216	7	NULL	NULL	0	NULL	Pkcd	Protein		substrate for					caspase 3	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	No significant cleavage of protein kinase C delta ( Pkcd ) in vivo , which is a substrate for caspase 3 , was detected , and intact Pkcd was retained in both cell lines for at least 72 h after irradiation .	manualset1
80327	2	377216	7	NULL	NULL	0	NULL	Pkcd	Protein		is					protein kinase C delta	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	No significant cleavage of protein kinase C delta ( Pkcd ) in vivo , which is a substrate for caspase 3 , was detected , and intact Pkcd was retained in both cell lines for at least 72 h after irradiation .	manualset1
80328	1	377220	7	NULL	NULL	0	NULL	RA1	GeneOrProtein		not different from					RA2	GeneOrProtein				NULL		0	NULL	NULL	NULL	NULL	NULL	No significant difference was observed between RA1 and RA2 .	manualset1
80329	1	377222	7	NULL	NULL	0	NULL	IgG antibody	Protein	levels of;;atopic recruits	does not differ with		significantly			IgG antibody	Protein	levels of;;non-atopic recruits			NULL		0	NULL	NULL	NULL	NULL	NULL	No significant difference was observed in IgG antibody levels to pneumococcal polysaccharides between atopic and non-atopic recruits , whereas seropositivity to T. gondii was found to be less frequent among the atopic recruits ( odds ratio , 0.37 ; 95 % CI , 0.17-0 .81 ; P = 0.01 ) .	manualset1
80330	2	377222	7	NULL	NULL	0	NULL	IgG antibody	Protein		in response to					pneumococcal polysaccharides	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	No significant difference was observed in IgG antibody levels to pneumococcal polysaccharides between atopic and non-atopic recruits , whereas seropositivity to T. gondii was found to be less frequent among the atopic recruits ( odds ratio , 0.37 ; 95 % CI , 0.17-0 .81 ; P = 0.01 ) .	manualset1
80331	3	377222	7	NULL	NULL	0	NULL	T. gondii	Organism	seropositivity to	less frequent among					atopic recruits	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	No significant difference was observed in IgG antibody levels to pneumococcal polysaccharides between atopic and non-atopic recruits , whereas seropositivity to T. gondii was found to be less frequent among the atopic recruits ( odds ratio , 0.37 ; 95 % CI , 0.17-0 .81 ; P = 0.01 ) .	manualset1
80332	1	377229	7	NULL	NULL	0	NULL	2-DG	NonProteinOrNucleicAcidChemical		substrate for					hexokinase	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	No significant differences were observed in the Km for hexokinase with 2-DG as the substrate in the glioma and normal brain tissue .	manualset1
80333	2	377229	7	NULL	NULL	0	NULL	statement 1	Process		occur in					glioma	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	No significant differences were observed in the Km for hexokinase with 2-DG as the substrate in the glioma and normal brain tissue .	manualset1
80334	3	377229	7	NULL	NULL	0	NULL	statement 1	Process		occur in					normal brain tissue	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	No significant differences were observed in the Km for hexokinase with 2-DG as the substrate in the glioma and normal brain tissue .	manualset1
80335	1	377231	7	NULL	NULL	0	NULL	XbaI genotype	Gene		does not effect		significantly			BMD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	No significant effect of the XbaI genotype on BMD was found at any site .	manualset1
80336	1	377237	7	NULL	NULL	0	NULL	spontaneous bleedings	MedicalFinding		does not occur at					birth	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	No spontaneous bleedings usually occur at birth in severe type 3 VWD .	manualset1
80337	2	377237	7	NULL	NULL	0	NULL	statement 1	Process		occur in					type 3 VWD	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	No spontaneous bleedings usually occur at birth in severe type 3 VWD .	manualset1
80427	1	377242	7	NULL	NULL	0	NULL	gastrin	Protein		does not stimulate					guanylate cyclase activity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	No stimulation of guanylate cyclase activity by gastrin was detected in the dispersed gastric corporal mucosal cells .	manualset1
80428	2	377242	7	NULL	NULL	0	NULL	statement 1	Process		occur in					gastric corporal mucosal cells	Cell	dispersed			NULL		0	NULL	NULL	NULL	NULL	NULL	No stimulation of guanylate cyclase activity by gastrin was detected in the dispersed gastric corporal mucosal cells .	manualset1
80429	1	377251	7	NULL	NULL	0	NULL	bcl-1	Gene		involved in					translocations	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	No translocations involving bcl-2 and the immunoglobulin heavy chain gene were identified ; two cases had translocations involving the bcl-1 and the immunoglobulin heavy chain genes .	manualset1
80430	2	377251	7	NULL	NULL	0	NULL	immunoglobulin heavy chain genes	Gene		involved in					translocations	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	No translocations involving bcl-2 and the immunoglobulin heavy chain gene were identified ; two cases had translocations involving the bcl-1 and the immunoglobulin heavy chain genes .	manualset1
80433	1	377258	7	NULL	NULL	0	NULL	Nocardia brain abscess	MedicalFinding		mimick					necrotic tumor 	Disease	high-grade			NULL		0	NULL	NULL	NULL	NULL	NULL	Nocardia brain abscess mimicking high-grade necrotic tumor on perfusion MRI .	manualset1
80436	1	377259	7	NULL	NULL	0	NULL	Nocturia	Disease		common symptom in 					elderly	PersonGroup				NULL		0	NULL	NULL	NULL	NULL	NULL	Nocturia is a common symptom in the elderly , which profoundly influences general health and quality of life .	manualset1
80437	2	377259	7	NULL	NULL	NULL	NULL	statement 1	Process		influences		profoundly			general health	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nocturia is a common symptom in the elderly , which profoundly influences general health and quality of life .	manualset1
80438	3	377259	7	NULL	NULL	0	NULL	statement 1	Process		influences		profoundly			quality of life	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nocturia is a common symptom in the elderly , which profoundly influences general health and quality of life .	manualset1
80441	1	377260	7	NULL	NULL	0	NULL	Noggin 	Protein		recruits					mesoderm progenitors	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Noggin recruits mesoderm progenitors from the dorsal aorta to a skeletal myogenic fate .	manualset1
80444	2	377260	7	NULL	NULL	0	NULL	statement 1	Process		occur from					dorsal aorta	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Noggin recruits mesoderm progenitors from the dorsal aorta to a skeletal myogenic fate .	manualset1
80445	3	377260	7	NULL	NULL	0	NULL	statement 1	Process		occur to					skeletal myogenic fate	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Noggin recruits mesoderm progenitors from the dorsal aorta to a skeletal myogenic fate .	manualset1
80446	4	377260	7	NULL	NULL	0	NULL	statement 2	Process		occur along with					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Noggin recruits mesoderm progenitors from the dorsal aorta to a skeletal myogenic fate .	manualset1
80447	1	377261	7	NULL	NULL	0	NULL	Nogo-B 	Protein		phosphorylated by			Ser107		MAPKAP-K2	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Nogo-B is phosphorylated at Ser107 in vitro by MAPKAP-K2 ( MAPK ( mitogen-activated protein kinase ) - activated protein kinase-2 ) or MAPKAP-K3 , but not by other protein kinases that are known to be activated by SAPK2a/p38a .	manualset1
80448	2	377261	7	NULL	NULL	0	NULL	Nogo-B 	Protein		phosphorylated by			Ser107		MAPKAP-K3	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Nogo-B is phosphorylated at Ser107 in vitro by MAPKAP-K2 ( MAPK ( mitogen-activated protein kinase ) - activated protein kinase-2 ) or MAPKAP-K3 , but not by other protein kinases that are known to be activated by SAPK2a/p38a .	manualset1
80449	3	377261	7	NULL	NULL	0	NULL	MAPKAP-K2	Protein		is					( MAPK ( mitogen-activated protein kinase ) - activated protein kinase-2 )	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Nogo-B is phosphorylated at Ser107 in vitro by MAPKAP-K2 ( MAPK ( mitogen-activated protein kinase ) - activated protein kinase-2 ) or MAPKAP-K3 , but not by other protein kinases that are known to be activated by SAPK2a/p38a .	manualset1
80450	4	377261	7	NULL	NULL	0	NULL	SAPK2a/p38a	Protein		activate					protein kinases	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Nogo-B is phosphorylated at Ser107 in vitro by MAPKAP-K2 ( MAPK ( mitogen-activated protein kinase ) - activated protein kinase-2 ) or MAPKAP-K3 , but not by other protein kinases that are known to be activated by SAPK2a/p38a .	manualset1
80451	5	377261	7	NULL	NULL	0	NULL	statement 4	Process		does not phosphorylate					Nogo-B	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Nogo-B is phosphorylated at Ser107 in vitro by MAPKAP-K2 ( MAPK ( mitogen-activated protein kinase ) - activated protein kinase-2 ) or MAPKAP-K3 , but not by other protein kinases that are known to be activated by SAPK2a/p38a .	manualset1
80452	6	377261	7	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nogo-B is phosphorylated at Ser107 in vitro by MAPKAP-K2 ( MAPK ( mitogen-activated protein kinase ) - activated protein kinase-2 ) or MAPKAP-K3 , but not by other protein kinases that are known to be activated by SAPK2a/p38a .	manualset1
80455	1	377264	7	NULL	NULL	0	NULL	( 3H ) dopamine	NonProteinOrNucleicAcidChemical		displaced by					( 1H ) dopamine	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Nomifensine , benztropine , PCP and amphetamine also inhibited the displacement of ( 3H ) dopamine by ( 1H ) dopamine at concentrations which have been shown previously to inhibit the uptake of ( 3H ) dopamine , suggesting that the mechanism behind displacement and uptake are very similar .	manualset1
80456	2	377264	7	NULL	NULL	0	NULL	Nomifensine	NonProteinOrNucleicAcidChemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nomifensine , benztropine , PCP and amphetamine also inhibited the displacement of ( 3H ) dopamine by ( 1H ) dopamine at concentrations which have been shown previously to inhibit the uptake of ( 3H ) dopamine , suggesting that the mechanism behind displacement and uptake are very similar .	manualset1
80457	3	377264	7	NULL	NULL	0	NULL	benztropine	NonProteinOrNucleicAcidChemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nomifensine , benztropine , PCP and amphetamine also inhibited the displacement of ( 3H ) dopamine by ( 1H ) dopamine at concentrations which have been shown previously to inhibit the uptake of ( 3H ) dopamine , suggesting that the mechanism behind displacement and uptake are very similar .	manualset1
80458	4	377264	7	NULL	NULL	0	NULL	PCP	NonProteinOrNucleicAcidChemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nomifensine , benztropine , PCP and amphetamine also inhibited the displacement of ( 3H ) dopamine by ( 1H ) dopamine at concentrations which have been shown previously to inhibit the uptake of ( 3H ) dopamine , suggesting that the mechanism behind displacement and uptake are very similar .	manualset1
80459	5	377264	7	NULL	NULL	0	NULL	amphetamine	NonProteinOrNucleicAcidChemical		inhibit					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nomifensine , benztropine , PCP and amphetamine also inhibited the displacement of ( 3H ) dopamine by ( 1H ) dopamine at concentrations which have been shown previously to inhibit the uptake of ( 3H ) dopamine , suggesting that the mechanism behind displacement and uptake are very similar .	manualset1
80460	6	377264	7	NULL	NULL	0	NULL	Nomifensine	NonProteinOrNucleicAcidChemical		inhibit					( 3H ) dopamine	NonProteinOrNucleicAcidChemical	uptake of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nomifensine , benztropine , PCP and amphetamine also inhibited the displacement of ( 3H ) dopamine by ( 1H ) dopamine at concentrations which have been shown previously to inhibit the uptake of ( 3H ) dopamine , suggesting that the mechanism behind displacement and uptake are very similar .	manualset1
80461	7	377264	7	NULL	NULL	0	NULL	benztropine	NonProteinOrNucleicAcidChemical		inhibit					( 3H ) dopamine	NonProteinOrNucleicAcidChemical	uptake of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nomifensine , benztropine , PCP and amphetamine also inhibited the displacement of ( 3H ) dopamine by ( 1H ) dopamine at concentrations which have been shown previously to inhibit the uptake of ( 3H ) dopamine , suggesting that the mechanism behind displacement and uptake are very similar .	manualset1
80462	8	377264	7	NULL	NULL	0	NULL	PCP	NonProteinOrNucleicAcidChemical		inhibit					( 3H ) dopamine	NonProteinOrNucleicAcidChemical	uptake of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nomifensine , benztropine , PCP and amphetamine also inhibited the displacement of ( 3H ) dopamine by ( 1H ) dopamine at concentrations which have been shown previously to inhibit the uptake of ( 3H ) dopamine , suggesting that the mechanism behind displacement and uptake are very similar .	manualset1
80463	9	377264	7	NULL	NULL	NULL	NULL	amphetamine	NonProteinOrNucleicAcidChemical		inhibit					( 3H ) dopamine	NonProteinOrNucleicAcidChemical	uptake of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nomifensine , benztropine , PCP and amphetamine also inhibited the displacement of ( 3H ) dopamine by ( 1H ) dopamine at concentrations which have been shown previously to inhibit the uptake of ( 3H ) dopamine , suggesting that the mechanism behind displacement and uptake are very similar .	manualset1
80464	10	377264	7	NULL	NULL	0	NULL	statement 2	Process		is similar to					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nomifensine , benztropine , PCP and amphetamine also inhibited the displacement of ( 3H ) dopamine by ( 1H ) dopamine at concentrations which have been shown previously to inhibit the uptake of ( 3H ) dopamine , suggesting that the mechanism behind displacement and uptake are very similar .	manualset1
80465	11	377264	7	NULL	NULL	0	NULL	statement 3	Process		is similar to					statement 7	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nomifensine , benztropine , PCP and amphetamine also inhibited the displacement of ( 3H ) dopamine by ( 1H ) dopamine at concentrations which have been shown previously to inhibit the uptake of ( 3H ) dopamine , suggesting that the mechanism behind displacement and uptake are very similar .	manualset1
80466	12	377264	7	NULL	NULL	0	NULL	statement 4	Process		is similar to					statement 8	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nomifensine , benztropine , PCP and amphetamine also inhibited the displacement of ( 3H ) dopamine by ( 1H ) dopamine at concentrations which have been shown previously to inhibit the uptake of ( 3H ) dopamine , suggesting that the mechanism behind displacement and uptake are very similar .	manualset1
80467	13	377264	7	NULL	NULL	0	NULL	statement 5	Process		is similar to					statement 9	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nomifensine , benztropine , PCP and amphetamine also inhibited the displacement of ( 3H ) dopamine by ( 1H ) dopamine at concentrations which have been shown previously to inhibit the uptake of ( 3H ) dopamine , suggesting that the mechanism behind displacement and uptake are very similar .	manualset1
80468	1	377268	7	NULL	NULL	0	NULL	2-deoxy-D-glucose	NonProteinOrNucleicAcidChemical		induce		Non-hypoxic			HIF-3alpha	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Non-hypoxic induction of HIF-3alpha by 2-deoxy-D-glucose and insulin .	manualset1
80469	2	377268	7	NULL	NULL	0	NULL	insulin	Protein		induce		Non-hypoxic			HIF-3alpha	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Non-hypoxic induction of HIF-3alpha by 2-deoxy-D-glucose and insulin .	manualset1
80470	1	377270	7	NULL	NULL	NULL	NULL	Non-invasive liver iron	NonProteinOrNucleicAcidChemical	quantification of	diagnostic parameter for		new			hereditary hemochromatosis	Disease				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Non-invasive liver iron quantification by SQUID-biosusceptometry and serum ferritin iron as new diagnostic parameters in hereditary hemochromatosis .	manualset1
80471	2	377270	7	NULL	NULL	0	NULL	serum ferritin iron	NonProteinOrNucleicAcidChemical		diagnostic parameter for					hereditary hemochromatosis	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	Non-invasive liver iron quantification by SQUID-biosusceptometry and serum ferritin iron as new diagnostic parameters in hereditary hemochromatosis .	manualset1
80472	1	377271	7	NULL	NULL	0	NULL	Non-invasive ventilation	MedicalProcedure		given in					amyotrophic lateral sclerosis	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	Non-invasive ventilation in amyotrophic lateral sclerosis : a 10 year population based study .	manualset1
80473	1	377272	7	NULL	NULL	0	NULL	Non-necrotizing heparin	Protein		induce					skin lesions	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Non-necrotizing heparin-induced skin lesions and the 4T 's score .	manualset1
80474	1	377273	7	NULL	NULL	0	NULL	Non-nucleoside reverse transcriptase inhibitors	NonProteinOrNucleicAcidChemical		used in					new therapeutic regimens	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Non-nucleoside reverse transcriptase inhibitors can be used in new therapeutic regimens .	manualset1
80475	1	377276	7	NULL	NULL	0	NULL	Non-steroid anti-inflammatory drug therapy	MedicalProcedure		used in					orthopedics	MedicalProcedureOrDevice				NULL		0	NULL	NULL	NULL	NULL	NULL	Non-steroid anti-inflammatory drug therapy in various fields -- orthopedics ) .	manualset1
80476	1	377277	7	NULL	NULL	NULL	NULL	ibuprofen	NonProteinOrNucleicAcidChemical		induce					apoptosis	Process				NULL	human leukemic cells in vitro	NULL	NULL	NULL	NULL	NULL	NULL	Non-steroidal anti-inflammatory agent ibuprofen-induced apoptosis , cell necrosis and cell cycle alterations in human leukemic cells in vitro .	manualset1
80477	2	377277	7	NULL	NULL	NULL	NULL	ibuprofen	NonProteinOrNucleicAcidChemical		induce					cell necrosis	Process				NULL	human leukemic cells in vitro	NULL	NULL	NULL	NULL	NULL	NULL	Non-steroidal anti-inflammatory agent ibuprofen-induced apoptosis , cell necrosis and cell cycle alterations in human leukemic cells in vitro .	manualset1
80478	3	377277	7	NULL	NULL	NULL	NULL	ibuprofen	NonProteinOrNucleicAcidChemical		induce					cell cycle alterations	Process				NULL	human leukemic cells in vitro	NULL	NULL	NULL	NULL	NULL	NULL	Non-steroidal anti-inflammatory agent ibuprofen-induced apoptosis , cell necrosis and cell cycle alterations in human leukemic cells in vitro .	manualset1
80479	4	377277	7	NULL	NULL	0	NULL	ibuprofen	NonProteinOrNucleicAcidChemical		is a type of					Non-steroidal anti-inflammatory agent	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Non-steroidal anti-inflammatory agent ibuprofen-induced apoptosis , cell necrosis and cell cycle alterations in human leukemic cells in vitro .	manualset1
80480	1	377280	7	NULL	NULL	0	NULL	Nonablative skin remodeling	MedicalProcedure		option for					skin rejuvenation	MedicalProcedure	patients who demand a noninvasive approach			NULL		0	NULL	NULL	NULL	NULL	NULL	Nonablative skin remodeling has become an attractive option for patients whose lifestyles demand a noninvasive approach to skin rejuvenation .	manualset1
80595	1	377282	7	NULL	NULL	NULL	NULL	NANC	Process		demonstrated in					animal urinary bladder	BodyPart				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nonadrenergic , noncholinergic ( NANC ) contraction has been demonstrated in animal urinary bladder .	manualset1
80597	2	377282	7	NULL	NULL	0	NULL	NANC	Process		is					Nonadrenergic , noncholinergic contraction	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonadrenergic , noncholinergic ( NANC ) contraction has been demonstrated in animal urinary bladder .	manualset1
80598	1	377284	7	NULL	NULL	0	NULL	benzoyl-CoA	NonProteinOrNucleicAcidChemical		converted to		anoxic			Nonaromatic products 	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonaromatic products from anoxic conversion of benzoyl-CoA with benzoyl-CoA reductase and cyclohexa-1 ,5 - diene-1-carbonyl-CoA hydratase .	manualset1
80599	2	377284	7	NULL	NULL	0	NULL	statement 1	Process		in presence with					benzoyl-CoA reductase	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonaromatic products from anoxic conversion of benzoyl-CoA with benzoyl-CoA reductase and cyclohexa-1 ,5 - diene-1-carbonyl-CoA hydratase .	manualset1
80600	3	377284	7	NULL	NULL	NULL	NULL	statement 1	Process		in presence with					cyclohexa-1 ,5 - diene-1-carbonyl-CoA hydratase	Protein				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nonaromatic products from anoxic conversion of benzoyl-CoA with benzoyl-CoA reductase and cyclohexa-1 ,5 - diene-1-carbonyl-CoA hydratase .	manualset1
80601	1	377285	7	NULL	NULL	0	NULL	Nonbacterial meningitis	Disease		not detected		readily			clinically	MedicalProcedure				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonbacterial meningitis can not be as readily detected clinically .	manualset1
80613	1	377286	7	NULL	NULL	0	NULL	Nonbacterial thrombotic endocarditis	Disease		occur with					malignant neoplastic diseases	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonbacterial thrombotic endocarditis in patients with malignant neoplastic diseases .	manualset1
80614	1	377292	7	NULL	NULL	NULL	NULL	`` C. upsaliensis '' strains	Organism		not agglutinated with					 C. jejuni	Organism	antisera against heat-labile antigens from			NULL		NULL	NULL	NULL	NULL	NULL	NULL	None of the `` C. upsaliensis '' strains could be agglutinated with antisera against heat-labile antigens from C. jejuni , C. coli , or C. laridis .	manualset1
80615	2	377292	7	NULL	NULL	NULL	NULL	`` C. upsaliensis '' strains	Organism		not agglutinated with					 C. coli	Organism	antisera against heat-labile antigens from			NULL		NULL	NULL	NULL	NULL	NULL	NULL	None of the `` C. upsaliensis '' strains could be agglutinated with antisera against heat-labile antigens from C. jejuni , C. coli , or C. laridis .	manualset1
80616	3	377292	7	NULL	NULL	0	NULL	`` C. upsaliensis '' strains	Organism		not agglutinated with					 C. laridis	Organism	antisera against heat-labile antigens from			NULL		0	NULL	NULL	NULL	NULL	NULL	None of the `` C. upsaliensis '' strains could be agglutinated with antisera against heat-labile antigens from C. jejuni , C. coli , or C. laridis .	manualset1
80617	1	377296	7	NULL	NULL	NULL	NULL	lymphoma	Disease	mice without	shows					sIL-2R	Protein	detectable human			NULL		NULL	NULL	NULL	NULL	NULL	NULL	None of the control mice without lymphoma or with human nonlymphoid tumors ( prostatic carcinoma , ovarian carcinoma , and glioblastoma multiforme ) showed detectable human sIL-2R .	manualset1
80618	2	377296	7	NULL	NULL	0	NULL	prostatic carcinoma	Disease	mice with human	shows					sIL-2R	Protein	detectable human			NULL		0	NULL	NULL	NULL	NULL	NULL	None of the control mice without lymphoma or with human nonlymphoid tumors ( prostatic carcinoma , ovarian carcinoma , and glioblastoma multiforme ) showed detectable human sIL-2R .	manualset1
80619	3	377296	7	NULL	NULL	0	NULL	ovarian carcinoma	Disease	mice with human	shows					sIL-2R	Protein	detectable human			NULL		0	NULL	NULL	NULL	NULL	NULL	None of the control mice without lymphoma or with human nonlymphoid tumors ( prostatic carcinoma , ovarian carcinoma , and glioblastoma multiforme ) showed detectable human sIL-2R .	manualset1
80620	4	377296	7	NULL	NULL	NULL	NULL	glioblastoma multiforme	Disease	mice with human	shows					sIL-2R	Protein	detectable human			NULL		NULL	NULL	NULL	NULL	NULL	NULL	None of the control mice without lymphoma or with human nonlymphoid tumors ( prostatic carcinoma , ovarian carcinoma , and glioblastoma multiforme ) showed detectable human sIL-2R .	manualset1
80621	5	377296	7	NULL	NULL	0	NULL	prostatic carcinoma	Disease		is a type of					nonlymphoid tumors	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	None of the control mice without lymphoma or with human nonlymphoid tumors ( prostatic carcinoma , ovarian carcinoma , and glioblastoma multiforme ) showed detectable human sIL-2R .	manualset1
80622	6	377296	7	NULL	NULL	0	NULL	ovarian carcinoma	Disease		is a type of					nonlymphoid tumors	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	None of the control mice without lymphoma or with human nonlymphoid tumors ( prostatic carcinoma , ovarian carcinoma , and glioblastoma multiforme ) showed detectable human sIL-2R .	manualset1
80623	7	377296	7	NULL	NULL	NULL	NULL	glioblastoma multiforme	Disease		is a type of					nonlymphoid tumors	Protein				NULL		NULL	NULL	NULL	NULL	NULL	NULL	None of the control mice without lymphoma or with human nonlymphoid tumors ( prostatic carcinoma , ovarian carcinoma , and glioblastoma multiforme ) showed detectable human sIL-2R .	manualset1
80624	1	377301	7	NULL	NULL	0	NULL	pFSH-PVP treatments 	MedicalProcedure		not effective in					superovulation	Process	inducing			NULL		0	NULL	NULL	NULL	NULL	NULL	None of the pFSH-PVP treatments were effective in inducing superovulation .	manualset1
80626	1	377307	7	NULL	NULL	0	NULL	endogenous compounds	NonProteinOrNucleicAcidChemical		bind					Na + , K + - ATPase	Protein		cardiac glycoside binding site		NULL		0	NULL	NULL	NULL	NULL	NULL	None of these endogenous compounds has been shown conclusively to modulate sodium pump activity by binding to the cardiac glycoside binding site on Na + , K + - ATPase .	manualset1
80628	2	377307	7	NULL	NULL	0	NULL	statement 1	Process		does not modulate					sodium pump activity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	None of these endogenous compounds has been shown conclusively to modulate sodium pump activity by binding to the cardiac glycoside binding site on Na + , K + - ATPase .	manualset1
80638	1	377312	7	NULL	NULL	0	NULL	protein C	Protein	Ser360Ala-activated 	shows					Nonenzymatic anticoagulant activity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonenzymatic anticoagulant activity of the mutant serine protease Ser360Ala-activated protein C mediated by factor Va.	manualset1
80639	2	377312	7	NULL	NULL	0	NULL	statement 1	Process		mediated by					factor Va	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonenzymatic anticoagulant activity of the mutant serine protease Ser360Ala-activated protein C mediated by factor Va.	manualset1
80640	3	377312	7	NULL	NULL	0	NULL	 protein C	Protein	Ser360Ala-activated 	is a type of					mutant serine protease	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonenzymatic anticoagulant activity of the mutant serine protease Ser360Ala-activated protein C mediated by factor Va.	manualset1
80641	1	377313	7	NULL	NULL	0	NULL	oxygen derivatives 	NonProteinOrNucleicAcidChemical	reduced	hydroxylation of		nonenzymatic			proline	AminoAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonenzymatic hydroxylations of proline and lysine by reduced oxygen derivatives .	manualset1
80642	2	377313	7	NULL	NULL	0	NULL	oxygen derivatives 	NonProteinOrNucleicAcidChemical	reduced	hydroxylation of		nonenzymatic			lysine	AminoAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonenzymatic hydroxylations of proline and lysine by reduced oxygen derivatives .	manualset1
80643	1	377314	7	NULL	NULL	0	NULL	short-chain phospholipids	NonProteinOrNucleicAcidChemical		activate		Nonessentially			phosphatidylinositol-specific phospholipase C	Protein	bacterial			NULL		0	NULL	NULL	NULL	NULL	NULL	Nonessential activation and competitive inhibition of bacterial phosphatidylinositol-specific phospholipase C by short-chain phospholipids and analogs .	manualset1
80644	2	377314	7	NULL	NULL	0	NULL	short-chain phospholipids	NonProteinOrNucleicAcidChemical		inhibit		competitively			phosphatidylinositol-specific phospholipase C	Protein	bacterial			NULL		0	NULL	NULL	NULL	NULL	NULL	Nonessential activation and competitive inhibition of bacterial phosphatidylinositol-specific phospholipase C by short-chain phospholipids and analogs .	manualset1
80645	3	377314	7	NULL	NULL	NULL	NULL	short-chain phospholipids	NonProteinOrNucleicAcidChemical	analogs of	activate		Nonessentially			phosphatidylinositol-specific phospholipase C	Protein	bacterial			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nonessential activation and competitive inhibition of bacterial phosphatidylinositol-specific phospholipase C by short-chain phospholipids and analogs .	manualset1
80646	4	377314	7	NULL	NULL	NULL	NULL	short-chain phospholipids	NonProteinOrNucleicAcidChemical	analogs of	inhibit		competitively			phosphatidylinositol-specific phospholipase C	Protein	bacterial			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nonessential activation and competitive inhibition of bacterial phosphatidylinositol-specific phospholipase C by short-chain phospholipids and analogs .	manualset1
80702	1	377321	7	NULL	NULL	0	NULL	Escherichia coli 	Organism	Nongrowing	produce					peptidoglycan	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Nongrowing Escherichia coli deprived of an essential amino acid continued to produce peptidoglycan at a rate approximately 30 % of that of growing cells .	manualset1
80703	2	377321	7	NULL	NULL	0	NULL	Escherichia coli 	Organism	Nongrowing	deprived of an					essential amino acid	AminoAcid				NULL		0	NULL	NULL	NULL	NULL	NULL	Nongrowing Escherichia coli deprived of an essential amino acid continued to produce peptidoglycan at a rate approximately 30 % of that of growing cells .	manualset1
80704	1	377322	7	NULL	NULL	0	NULL	Mre11 complex	Protein		mediate			globular domain		Nonhomologous end joining	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonhomologous end joining , which is probably mediated by the globular domain of the Mre11 complex , was also severely impaired by alteration of the coiled-coil and hook domains , providing the first evidence of their influence on this process .	manualset1
80705	2	377322	7	NULL	NULL	0	NULL			alteration of	impair		severely	coiled-coil		statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonhomologous end joining , which is probably mediated by the globular domain of the Mre11 complex , was also severely impaired by alteration of the coiled-coil and hook domains , providing the first evidence of their influence on this process .	manualset1
80707	3	377322	7	NULL	NULL	0	NULL			alteration of	impair		severely	hook domain		statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonhomologous end joining , which is probably mediated by the globular domain of the Mre11 complex , was also severely impaired by alteration of the coiled-coil and hook domains , providing the first evidence of their influence on this process .	manualset1
80718	1	377325	7	NULL	NULL	NULL	NULL	Noninvasive genetic sampling	ResearchActivity		important to					wildlife populations	Organism	study			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Noninvasive genetic sampling approaches are becoming increasingly important to study wildlife populations .	manualset1
80864	1	377331	7	NULL	NULL	0	NULL	Nonneoplastic mucocutaneous lesions	MedicalFinding		occur in					organ transplant recipients	PersonGroup				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonneoplastic mucocutaneous lesions in organ transplant recipients .	manualset1
80865	1	377335	7	NULL	NULL	0	NULL	sqt-1	Gene	Nonsense mutations of	cause					wild-type phenotypes	BiologicalProcess	not totally			NULL		0	NULL	NULL	NULL	NULL	NULL	Nonsense mutations of both sqt-1 and rol-6 cause nearly , but not totally , wild-type phenotypes .	manualset1
80866	2	377335	7	NULL	NULL	0	NULL	rol-6	Gene	Nonsense mutations of	cause					wild-type phenotypes	BiologicalProcess	not totally			NULL		0	NULL	NULL	NULL	NULL	NULL	Nonsense mutations of both sqt-1 and rol-6 cause nearly , but not totally , wild-type phenotypes .	manualset1
80867	1	377336	7	NULL	NULL	0	NULL	ketoconazole	NonProteinOrNucleicAcidChemical		inhibit		significantly			FK 506 metabolism	MolecularProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonspecific inhibitors of cytochrome P-450 , such as ketoconazole , itraconazole , fluconazole and SKF 525 A , and most of the cytochrome P-450 IIIA specific substrates used in this study significantly inhibited FK 506 metabolism .	manualset1
80868	2	377336	7	NULL	NULL	0	NULL	itraconazole	NonProteinOrNucleicAcidChemical		inhibit		significantly			FK 506 metabolism	MolecularProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonspecific inhibitors of cytochrome P-450 , such as ketoconazole , itraconazole , fluconazole and SKF 525 A , and most of the cytochrome P-450 IIIA specific substrates used in this study significantly inhibited FK 506 metabolism .	manualset1
80869	3	377336	7	NULL	NULL	0	NULL	fluconazole	NonProteinOrNucleicAcidChemical		inhibit		significantly			FK 506 metabolism	MolecularProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonspecific inhibitors of cytochrome P-450 , such as ketoconazole , itraconazole , fluconazole and SKF 525 A , and most of the cytochrome P-450 IIIA specific substrates used in this study significantly inhibited FK 506 metabolism .	manualset1
80870	4	377336	7	NULL	NULL	0	NULL	SKF 525 A	NonProteinOrNucleicAcidChemical		inhibit		significantly			FK 506 metabolism	MolecularProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonspecific inhibitors of cytochrome P-450 , such as ketoconazole , itraconazole , fluconazole and SKF 525 A , and most of the cytochrome P-450 IIIA specific substrates used in this study significantly inhibited FK 506 metabolism .	manualset1
80871	5	377336	7	NULL	NULL	0	NULL	cytochrome P-450 IIIA specific substrates	NonProteinOrNucleicAcidChemical		inhibit		significantly			FK 506 metabolism	MolecularProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonspecific inhibitors of cytochrome P-450 , such as ketoconazole , itraconazole , fluconazole and SKF 525 A , and most of the cytochrome P-450 IIIA specific substrates used in this study significantly inhibited FK 506 metabolism .	manualset1
80872	6	377336	7	NULL	NULL	0	NULL	ketoconazole	NonProteinOrNucleicAcidChemical		is a type of					cytochrome P-450	Protein	Nonspecific inhibitors of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nonspecific inhibitors of cytochrome P-450 , such as ketoconazole , itraconazole , fluconazole and SKF 525 A , and most of the cytochrome P-450 IIIA specific substrates used in this study significantly inhibited FK 506 metabolism .	manualset1
80900	7	377336	7	NULL	NULL	0	NULL	itraconazole	NonProteinOrNucleicAcidChemical		is a type of					cytochrome P-450	Protein	Nonspecific inhibitors of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nonspecific inhibitors of cytochrome P-450 , such as ketoconazole , itraconazole , fluconazole and SKF 525 A , and most of the cytochrome P-450 IIIA specific substrates used in this study significantly inhibited FK 506 metabolism .	manualset1
80901	8	377336	7	NULL	NULL	NULL	NULL	fluconazole	NonProteinOrNucleicAcidChemical		is a type of					cytochrome P-450	Protein	Nonspecific inhibitors of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nonspecific inhibitors of cytochrome P-450 , such as ketoconazole , itraconazole , fluconazole and SKF 525 A , and most of the cytochrome P-450 IIIA specific substrates used in this study significantly inhibited FK 506 metabolism .	manualset1
80902	9	377336	7	NULL	NULL	0	NULL	SKF 525 A	NonProteinOrNucleicAcidChemical		is a type of					cytochrome P-450	Protein	Nonspecific inhibitors of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nonspecific inhibitors of cytochrome P-450 , such as ketoconazole , itraconazole , fluconazole and SKF 525 A , and most of the cytochrome P-450 IIIA specific substrates used in this study significantly inhibited FK 506 metabolism .	manualset1
80965	1	377338	7	NULL	NULL	0	NULL	NSAIDs	NonProteinOrNucleicAcidChemical		cause					acute diffuse injury	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonsteroidal anti-inflammatory drugs ( NSAIDs ) cause acute diffuse injury to the gastroduodenal mucosa , and also cause chronic focal ulcers that may bleed or perforate without warning symptoms .	manualset1
80966	2	377338	7	NULL	NULL	0	NULL	statement 1	Process		occur in					gastroduodenal mucosa	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonsteroidal anti-inflammatory drugs ( NSAIDs ) cause acute diffuse injury to the gastroduodenal mucosa , and also cause chronic focal ulcers that may bleed or perforate without warning symptoms .	manualset1
80967	3	377338	7	NULL	NULL	0	NULL	NSAIDs	NonProteinOrNucleicAcidChemical		cause					chronic focal ulcers	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonsteroidal anti-inflammatory drugs ( NSAIDs ) cause acute diffuse injury to the gastroduodenal mucosa , and also cause chronic focal ulcers that may bleed or perforate without warning symptoms .	manualset1
80968	4	377338	7	NULL	NULL	0	NULL	chronic focal ulcers	MedicalFinding		may					bleed	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonsteroidal anti-inflammatory drugs ( NSAIDs ) cause acute diffuse injury to the gastroduodenal mucosa , and also cause chronic focal ulcers that may bleed or perforate without warning symptoms .	manualset1
80969	5	377338	7	NULL	NULL	NULL	NULL	chronic focal ulcers	MedicalFinding		may					perforate	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nonsteroidal anti-inflammatory drugs ( NSAIDs ) cause acute diffuse injury to the gastroduodenal mucosa , and also cause chronic focal ulcers that may bleed or perforate without warning symptoms .	manualset1
80970	6	377338	7	NULL	NULL	NULL	NULL	statement 4	Process		occur without					warning symptoms	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nonsteroidal anti-inflammatory drugs ( NSAIDs ) cause acute diffuse injury to the gastroduodenal mucosa , and also cause chronic focal ulcers that may bleed or perforate without warning symptoms .	manualset1
80971	7	377338	7	NULL	NULL	0	NULL	statement 5	Process		occur without					warning symptoms	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonsteroidal anti-inflammatory drugs ( NSAIDs ) cause acute diffuse injury to the gastroduodenal mucosa , and also cause chronic focal ulcers that may bleed or perforate without warning symptoms .	manualset1
80972	8	377338	7	NULL	NULL	0	NULL	NSAIDs	NonProteinOrNucleicAcidChemical		is					Nonsteroidal anti-inflammatory drugs	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonsteroidal anti-inflammatory drugs ( NSAIDs ) cause acute diffuse injury to the gastroduodenal mucosa , and also cause chronic focal ulcers that may bleed or perforate without warning symptoms .	manualset1
80973	1	377339	7	NULL	NULL	0	NULL	Nonsteroidal anti-inflammatory drugs	NonProteinOrNucleicAcidChemical		associated with					hepatotoxicity	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonsteroidal anti-inflammatory drugs have been associated with hepatotoxicity in susceptible patients .	manualset1
80974	2	377339	7	NULL	NULL	0	NULL	statement 1	Process		occur in					susceptible patients	PersonGroup				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonsteroidal anti-inflammatory drugs have been associated with hepatotoxicity in susceptible patients .	manualset1
80975	1	377342	7	NULL	NULL	0	NULL	1-stearoyllysophosphatidylcholine	NonProteinOrNucleicAcidChemical		dispersed in					water	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Nonsynchronicity phenomenon observed during the lamellar-micellar phase transitions of 1-stearoyllysophosphatidylcholine dispersed in water .	manualset1
80976	2	377342	7	NULL	NULL	0	NULL	Nonsynchronicity phenomenon	Process		observed during					statement 1	Process	lamellar-micellar phase transitions of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nonsynchronicity phenomenon observed during the lamellar-micellar phase transitions of 1-stearoyllysophosphatidylcholine dispersed in water .	manualset1
80977	1	377344	7	NULL	NULL	0	NULL	SHP-2 phosphatase	Protein	Noonan syndrome/leukemia-associated gain-of-function mutations in	enhance					cell migration	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Noonan syndrome/leukemia-associated gain-of-function mutations in SHP-2 phosphatase ( PTPN11 ) enhance cell migration and angiogenesis .	manualset1
80978	2	377344	7	NULL	NULL	0	NULL	SHP-2 phosphatase	Protein	Noonan syndrome/leukemia-associated gain-of-function mutations in	enhance					angiogenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Noonan syndrome/leukemia-associated gain-of-function mutations in SHP-2 phosphatase ( PTPN11 ) enhance cell migration and angiogenesis .	manualset1
80979	3	377344	7	NULL	NULL	0	NULL	SHP-2 phosphatase	Protein		is					PTPN11	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Noonan syndrome/leukemia-associated gain-of-function mutations in SHP-2 phosphatase ( PTPN11 ) enhance cell migration and angiogenesis .	manualset1
80980	1	377346	7	NULL	NULL	0	NULL	integrin	Protein		mediate					cell adhesiveness	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nor was the soluble peptide able to restore the loss of integrin-mediated cell adhesiveness to mini-laminin-332 after deletion of the gamma 2 chain C-terminus .	manualset1
80981	2	377346	7	NULL	NULL	NULL	NULL	soluble peptide	PartOfProtein		does not restore					statement 1	Process	loss of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nor was the soluble peptide able to restore the loss of integrin-mediated cell adhesiveness to mini-laminin-332 after deletion of the gamma 2 chain C-terminus .	manualset1
80982	3	377346	7	NULL	NULL	0	NULL	soluble peptide	PartOfProtein		does not restore					mini-laminin-332	Protein	loss of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nor was the soluble peptide able to restore the loss of integrin-mediated cell adhesiveness to mini-laminin-332 after deletion of the gamma 2 chain C-terminus .	manualset1
80983	4	377346	7	NULL	NULL	0	NULL	statement 3	Process		occur after					mini-laminin-332	Protein	deletion of	gamma 2 chain C-terminus		NULL		0	NULL	NULL	NULL	NULL	NULL	Nor was the soluble peptide able to restore the loss of integrin-mediated cell adhesiveness to mini-laminin-332 after deletion of the gamma 2 chain C-terminus .	manualset1
80984	1	377347	7	NULL	NULL	0	NULL	BNI	NonProteinOrNucleicAcidChemical		does not block					dynorphin A	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Nor-BNI ( 4.9 nmol/mouse , i.c.v. ) did not block the effects of dynorphin A - ( 2-13 ) on the CO-induced impairment of learning and/or memory .	manualset1
80985	2	377347	7	NULL	NULL	0	NULL	CO	NonProteinOrNucleicAcidChemical		induce					learning	MentalProcess	impairment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nor-BNI ( 4.9 nmol/mouse , i.c.v. ) did not block the effects of dynorphin A - ( 2-13 ) on the CO-induced impairment of learning and/or memory .	manualset1
80986	3	377347	7	NULL	NULL	0	NULL	CO	NonProteinOrNucleicAcidChemical		induce					memory	MentalProcess	impairment of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nor-BNI ( 4.9 nmol/mouse , i.c.v. ) did not block the effects of dynorphin A - ( 2-13 ) on the CO-induced impairment of learning and/or memory .	manualset1
80987	4	377347	7	NULL	NULL	0	NULL	statement 2	Process		is an alternative to					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nor-BNI ( 4.9 nmol/mouse , i.c.v. ) did not block the effects of dynorphin A - ( 2-13 ) on the CO-induced impairment of learning and/or memory .	manualset1
80988	5	377347	7	NULL	NULL	NULL	NULL	statement 1	Process		occur on					statement 2	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nor-BNI ( 4.9 nmol/mouse , i.c.v. ) did not block the effects of dynorphin A - ( 2-13 ) on the CO-induced impairment of learning and/or memory .	manualset1
80989	6	377347	7	NULL	NULL	0	NULL	statement 1	Process		occur on					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nor-BNI ( 4.9 nmol/mouse , i.c.v. ) did not block the effects of dynorphin A - ( 2-13 ) on the CO-induced impairment of learning and/or memory .	manualset1
80990	1	377348	7	NULL	NULL	0	NULL	Noradrenaline	NonProteinOrNucleicAcidChemical		release					Ca2+	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Noradrenaline and caffeine released 45Ca2 + from a cellular site in the aorta .	manualset1
80991	2	377348	7	NULL	NULL	0	NULL	caffeine	NonProteinOrNucleicAcidChemical		release					Ca2+	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Noradrenaline and caffeine released 45Ca2 + from a cellular site in the aorta .	manualset1
80992	3	377348	7	NULL	NULL	0	NULL	statement 1	Process		occur in					aorta	BodyPart	cellular site of			NULL		0	NULL	NULL	NULL	NULL	NULL	Noradrenaline and caffeine released 45Ca2 + from a cellular site in the aorta .	manualset1
80993	4	377348	7	NULL	NULL	0	NULL	statement 2	Process		occur in					aorta	BodyPart	cellular site of			NULL		0	NULL	NULL	NULL	NULL	NULL	Noradrenaline and caffeine released 45Ca2 + from a cellular site in the aorta .	manualset1
80994	1	377349	7	NULL	NULL	0	NULL	Norepinephrine	NonProteinOrNucleicAcidChemical		does not decrease					( methyl-14C ) choline	NonProteinOrNucleicAcidChemical	phosphorylation rate of			NULL		0	NULL	NULL	NULL	NULL	NULL	Norepinephrine ( plus propranolol ) does not decrease the uptake or phosphorylation rate of ( methyl-14C ) choline .	manualset1
80995	2	377349	7	NULL	NULL	NULL	NULL	Norepinephrine ( plus propranolol )	NonProteinOrNucleicAcidChemical		does not decrease					 ( methyl-14C ) choline	NonProteinOrNucleicAcidChemical	uptake of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Norepinephrine ( plus propranolol ) does not decrease the uptake or phosphorylation rate of ( methyl-14C ) choline .	manualset1
80996	1	377350	7	NULL	NULL	0	NULL	Norepinephrine	NonProteinOrNucleicAcidChemical		released from					sympathetic neurons	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Norepinephrine , released from sympathetic neurons , and epinephrine , released from the adrenal medulla , participate in a number of physiological processes including those that facilitate adaptation to stressful conditions .	manualset1
80997	2	377350	7	NULL	NULL	0	NULL	epinephrine	NonProteinOrNucleicAcidChemical		released from					adrenal medulla	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Norepinephrine , released from sympathetic neurons , and epinephrine , released from the adrenal medulla , participate in a number of physiological processes including those that facilitate adaptation to stressful conditions .	manualset1
80998	3	377350	7	NULL	NULL	NULL	NULL	statement 1	Process		participate in					physiological processes	BiologicalProcess				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Norepinephrine , released from sympathetic neurons , and epinephrine , released from the adrenal medulla , participate in a number of physiological processes including those that facilitate adaptation to stressful conditions .	manualset1
80999	4	377350	7	NULL	NULL	NULL	NULL	statement 2	Process		participate in					physiological processes	BiologicalProcess				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Norepinephrine , released from sympathetic neurons , and epinephrine , released from the adrenal medulla , participate in a number of physiological processes including those that facilitate adaptation to stressful conditions .	manualset1
81000	5	377350	7	NULL	NULL	NULL	NULL	physiological processes	BiologicalProcess		include					adaptation	BiologicalProcess				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Norepinephrine , released from sympathetic neurons , and epinephrine , released from the adrenal medulla , participate in a number of physiological processes including those that facilitate adaptation to stressful conditions .	manualset1
81001	6	377350	7	NULL	NULL	NULL	NULL	physiological processes	BiologicalProcess		include					stressful condition	BiologicalProcess				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Norepinephrine , released from sympathetic neurons , and epinephrine , released from the adrenal medulla , participate in a number of physiological processes including those that facilitate adaptation to stressful conditions .	manualset1
81002	7	377350	7	NULL	NULL	0	NULL	statement 1	Process		facilitate					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Norepinephrine , released from sympathetic neurons , and epinephrine , released from the adrenal medulla , participate in a number of physiological processes including those that facilitate adaptation to stressful conditions .	manualset1
81003	8	377350	7	NULL	NULL	0	NULL	statement 1	Process		facilitate					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Norepinephrine , released from sympathetic neurons , and epinephrine , released from the adrenal medulla , participate in a number of physiological processes including those that facilitate adaptation to stressful conditions .	manualset1
81004	9	377350	7	NULL	NULL	0	NULL	statement 2	Process		facilitate					statement 5	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Norepinephrine , released from sympathetic neurons , and epinephrine , released from the adrenal medulla , participate in a number of physiological processes including those that facilitate adaptation to stressful conditions .	manualset1
81005	10	377350	7	NULL	NULL	0	NULL	statement 2	Process		facilitate					statement 6	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Norepinephrine , released from sympathetic neurons , and epinephrine , released from the adrenal medulla , participate in a number of physiological processes including those that facilitate adaptation to stressful conditions .	manualset1
81006	1	377351	7	NULL	NULL	0	NULL	Norepinephrine	NonProteinOrNucleicAcidChemical		induces					VEGF	Protein	expression of			NULL		0	NULL	NULL	NULL	NULL	NULL	Norepinephrine induces VEGF expression and angiogenesis by a hypoxia-inducible factor-1 protein-dependent mechanism .	manualset1
81007	2	377351	7	NULL	NULL	0	NULL	statement 1	Process		occur by					 hypoxia-inducible factor-1 protein-dependent mechanism	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Norepinephrine induces VEGF expression and angiogenesis by a hypoxia-inducible factor-1 protein-dependent mechanism .	manualset1
81008	3	377351	7	NULL	NULL	0	NULL	Norepinephrine	NonProteinOrNucleicAcidChemical		induces					angiogenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Norepinephrine induces VEGF expression and angiogenesis by a hypoxia-inducible factor-1 protein-dependent mechanism .	manualset1
81151	4	377351	7	NULL	NULL	0	NULL	statement 3	Process		occur by					hypoxia-inducible factor-1 protein-dependent mechanism	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Norepinephrine induces VEGF expression and angiogenesis by a hypoxia-inducible factor-1 protein-dependent mechanism .	manualset1
81152	1	377353	7	NULL	NULL	0	NULL	trisomy 8	Chromosome		sole abnormality of					 trisomy	MedicalFinding	frequent			NULL		0	NULL	NULL	NULL	NULL	NULL	Normal cytogenetics ( CN ) constitutes the single largest group , while trisomy 8 ( +8 ) as a sole abnormality is the most frequent trisomy .	manualset1
81153	1	377354	7	NULL	NULL	0	NULL	gastrin	Protein	normal fasting levels of	occur in					Zollinger-Ellison syndrome	MedicalFinding	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	Normal fasting gastrin levels do occur in patients with overt Zollinger-Ellison syndrome and should not deter further investigation if clinical suspicion of this syndrome is high .	manualset1
81154	1	377356	7	NULL	NULL	0	NULL	2 , 3-diphosphoglycerate	NonProteinOrNucleicAcidChemical	normal levels of	occur despite					chronic lung disease	MedicalFinding	severe hypoxemia of			NULL		0	NULL	NULL	NULL	NULL	NULL	Normal levels of 2 , 3-diphosphoglycerate in red cells despite severe hypoxemia of chronic lung disease .	manualset1
81155	2	377356	7	NULL	NULL	0	NULL	statement 1	Process		occur in					red cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Normal levels of 2 , 3-diphosphoglycerate in red cells despite severe hypoxemia of chronic lung disease .	manualset1
81156	1	377357	7	NULL	NULL	0	NULL	brain	BodyPart	normal maturation of mammalian	characterized by					glucose transport	Process	periods of limitation in			NULL		0	NULL	NULL	NULL	NULL	NULL	Normal maturation of the mammalian brain is characterized by periods of limitations in glucose transport capacity and increased use of alternative cerebral metabolic fuels such as lactate and ketone bodies , all of which are important during H/I and influence the development of energy failure .	manualset1
81157	2	377357	7	NULL	NULL	0	NULL	brain	BodyPart	normal maturation of mammalian	characterized by					lactate	NonProteinOrNucleicAcidChemical	increased use of			NULL		0	NULL	NULL	NULL	NULL	NULL	Normal maturation of the mammalian brain is characterized by periods of limitations in glucose transport capacity and increased use of alternative cerebral metabolic fuels such as lactate and ketone bodies , all of which are important during H/I and influence the development of energy failure .	manualset1
81158	3	377357	7	NULL	NULL	0	NULL	brain	BodyPart	normal maturation of mammalian	characterized by					ketone bodies	NonProteinOrNucleicAcidChemical	increased use of			NULL		0	NULL	NULL	NULL	NULL	NULL	Normal maturation of the mammalian brain is characterized by periods of limitations in glucose transport capacity and increased use of alternative cerebral metabolic fuels such as lactate and ketone bodies , all of which are important during H/I and influence the development of energy failure .	manualset1
81159	4	377357	7	NULL	NULL	0	NULL	lactate	NonProteinOrNucleicAcidChemical		is a type of					alternative cerebral metabolic fuel	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Normal maturation of the mammalian brain is characterized by periods of limitations in glucose transport capacity and increased use of alternative cerebral metabolic fuels such as lactate and ketone bodies , all of which are important during H/I and influence the development of energy failure .	manualset1
81161	5	377357	7	NULL	NULL	0	NULL	Ketone bodies	NonProteinOrNucleicAcidChemical		is a type of					alternative cerebral metabolic fuel	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Normal maturation of the mammalian brain is characterized by periods of limitations in glucose transport capacity and increased use of alternative cerebral metabolic fuels such as lactate and ketone bodies , all of which are important during H/I and influence the development of energy failure .	manualset1
81165	6	377357	7	NULL	NULL	0	NULL	lactate	NonProteinOrNucleicAcidChemical		important during					H/I	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Normal maturation of the mammalian brain is characterized by periods of limitations in glucose transport capacity and increased use of alternative cerebral metabolic fuels such as lactate and ketone bodies , all of which are important during H/I and influence the development of energy failure .	manualset1
81166	7	377357	7	NULL	NULL	0	NULL	ketone bodies	NonProteinOrNucleicAcidChemical		important during					H/I	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Normal maturation of the mammalian brain is characterized by periods of limitations in glucose transport capacity and increased use of alternative cerebral metabolic fuels such as lactate and ketone bodies , all of which are important during H/I and influence the development of energy failure .	manualset1
81167	8	377357	7	NULL	NULL	0	NULL	lactate	NonProteinOrNucleicAcidChemical		influence					energy failure	Process	development of			NULL		0	NULL	NULL	NULL	NULL	NULL	Normal maturation of the mammalian brain is characterized by periods of limitations in glucose transport capacity and increased use of alternative cerebral metabolic fuels such as lactate and ketone bodies , all of which are important during H/I and influence the development of energy failure .	manualset1
81169	9	377357	7	NULL	NULL	0	NULL	ketone bodies	NonProteinOrNucleicAcidChemical		influence					energy failure	Process	development of			NULL		0	NULL	NULL	NULL	NULL	NULL	Normal maturation of the mammalian brain is characterized by periods of limitations in glucose transport capacity and increased use of alternative cerebral metabolic fuels such as lactate and ketone bodies , all of which are important during H/I and influence the development of energy failure .	manualset1
81171	1	377359	7	NULL	NULL	0	NULL	cerebral blood flow 	BiologicalProcess		low in					newborn	PersonGroup	normal			NULL		0	NULL	NULL	NULL	NULL	NULL	Normal newborn cerebral blood flow is low ; fetal asphyxia at birth causes delayed cerebral hyperperfusion in the neonate .	manualset1
81172	2	377359	7	NULL	NULL	0	NULL	fetal asphyxia	MedicalFinding		cause					cerebral hyperperfusion	BiologicalProcess	delayed			NULL		0	NULL	NULL	NULL	NULL	NULL	Normal newborn cerebral blood flow is low ; fetal asphyxia at birth causes delayed cerebral hyperperfusion in the neonate .	manualset1
81173	3	377359	7	NULL	NULL	0	NULL	statement 2	Process		occur at					birth	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Normal newborn cerebral blood flow is low ; fetal asphyxia at birth causes delayed cerebral hyperperfusion in the neonate .	manualset1
81174	4	377359	7	NULL	NULL	0	NULL	statement 2	Process		occur in the					neonate	PersonGroup				NULL		0	NULL	NULL	NULL	NULL	NULL	Normal newborn cerebral blood flow is low ; fetal asphyxia at birth causes delayed cerebral hyperperfusion in the neonate .	manualset1
81175	1	377360	7	NULL	NULL	0	NULL	 platelets	BodyPart	Normal	have					NOS activity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Normal platelets are known to have NOS activity , but little is known about NOS expression and NO production by platelets in patients with IPAH .	manualset1
81177	1	377361	7	NULL	NULL	0	NULL	left ventricle	BodyPart	Normal size	occur in					lethal hypoplastic left heart syndrome	MedicalFinding	antenatal scan			NULL		0	NULL	NULL	NULL	NULL	NULL	Normal size left ventricle on antenatal scan in lethal hypoplastic left heart syndrome .	manualset1
81178	1	377365	7	NULL	NULL	0	NULL	hemoglobin 	BodyPart	normalization of	does not have					cardiac structure	BodyPart	effect on			NULL		0	NULL	NULL	NULL	NULL	NULL	Normalization of hemoglobin in incident hemodialysis patients does not have a beneficial effect on cardiac structure , compared with partial correction .	manualset1
81180	2	377365	7	NULL	NULL	0	NULL	statement 1	Process		occur in					incident hemodialysis patients	PersonGroup				NULL		0	NULL	NULL	NULL	NULL	NULL	Normalization of hemoglobin in incident hemodialysis patients does not have a beneficial effect on cardiac structure , compared with partial correction .	manualset1
81182	1	377370	7	NULL	NULL	NULL	NULL	opioid receptor clones	Protein		expressed at			delta		low levels	Quantity				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Northern analyses with riboprobes derived from the delta and kappa opioid receptor clones indicate these sequences are expressed at low levels in human peripheral blood lymphocytes and in several human lymphoid cell lines .	manualset1
81183	2	377370	7	NULL	NULL	0	NULL	opioid receptor clones	Protein		expressed at			kappa		low levels	Quantity				NULL		0	NULL	NULL	NULL	NULL	NULL	Northern analyses with riboprobes derived from the delta and kappa opioid receptor clones indicate these sequences are expressed at low levels in human peripheral blood lymphocytes and in several human lymphoid cell lines .	manualset1
81184	3	377370	7	NULL	NULL	0	NULL	statement 1	Process		occur in					 peripheral blood lymphocytes	Cell	human			NULL		0	NULL	NULL	NULL	NULL	NULL	Northern analyses with riboprobes derived from the delta and kappa opioid receptor clones indicate these sequences are expressed at low levels in human peripheral blood lymphocytes and in several human lymphoid cell lines .	manualset1
81185	4	377370	7	NULL	NULL	0	NULL	statement 2	Process		occur in					peripheral blood lymphocytes	Cell	human			NULL		0	NULL	NULL	NULL	NULL	NULL	Northern analyses with riboprobes derived from the delta and kappa opioid receptor clones indicate these sequences are expressed at low levels in human peripheral blood lymphocytes and in several human lymphoid cell lines .	manualset1
81186	5	377370	7	NULL	NULL	NULL	NULL	statement 1	Process		occur in					lymphoid cell lines	Cell	human			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Northern analyses with riboprobes derived from the delta and kappa opioid receptor clones indicate these sequences are expressed at low levels in human peripheral blood lymphocytes and in several human lymphoid cell lines .	manualset1
81187	6	377370	7	NULL	NULL	0	NULL	statement 2	Process		occur in					lymphoid cell lines	Cell	human			NULL		0	NULL	NULL	NULL	NULL	NULL	Northern analyses with riboprobes derived from the delta and kappa opioid receptor clones indicate these sequences are expressed at low levels in human peripheral blood lymphocytes and in several human lymphoid cell lines .	manualset1
81188	1	377371	7	NULL	NULL	0	NULL	neugrin	Protein		expressed in		strongly			heart	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Northern analysis revealed that neugrin was strongly expressed in the heart , brain , and skeletal muscle , and m-neugrin in the liver , kidney , and brain .	manualset1
81189	2	377371	7	NULL	NULL	0	NULL	neugrin	Protein		expressed in		strongly			brain	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Northern analysis revealed that neugrin was strongly expressed in the heart , brain , and skeletal muscle , and m-neugrin in the liver , kidney , and brain .	manualset1
81190	3	377371	7	NULL	NULL	0	NULL	neugrin	Protein		expressed in		strongly			skeletal muscle	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Northern analysis revealed that neugrin was strongly expressed in the heart , brain , and skeletal muscle , and m-neugrin in the liver , kidney , and brain .	manualset1
81191	4	377371	7	NULL	NULL	0	NULL	 m-neugrin	Protein		expressed in					liver	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Northern analysis revealed that neugrin was strongly expressed in the heart , brain , and skeletal muscle , and m-neugrin in the liver , kidney , and brain .	manualset1
81192	5	377371	7	NULL	NULL	0	NULL	m-neugrin	Protein		expressed in					kidney	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Northern analysis revealed that neugrin was strongly expressed in the heart , brain , and skeletal muscle , and m-neugrin in the liver , kidney , and brain .	manualset1
81193	6	377371	7	NULL	NULL	0	NULL	m-neugrin	Protein		expressed in					brain	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Northern analysis revealed that neugrin was strongly expressed in the heart , brain , and skeletal muscle , and m-neugrin in the liver , kidney , and brain .	manualset1
81194	1	377372	7	NULL	NULL	NULL	NULL	Nogo-A	Protein		expressed in		predominantly			nervous system	BodyPart				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Northern and Western blot analysis indicated that Nogo-A is predominantly expressed in the nervous system with lower levels also present in testis and heart .	manualset1
81195	2	377372	7	NULL	NULL	0	NULL	Nogo-A	Protein		expressed in					testis	BodyPart	lower levels in			NULL		0	NULL	NULL	NULL	NULL	NULL	Northern and Western blot analysis indicated that Nogo-A is predominantly expressed in the nervous system with lower levels also present in testis and heart .	manualset1
81196	3	377372	7	NULL	NULL	0	NULL	Nogo-A	Protein		expressed in					heart	BodyPart	lower levels in			NULL		0	NULL	NULL	NULL	NULL	NULL	Northern and Western blot analysis indicated that Nogo-A is predominantly expressed in the nervous system with lower levels also present in testis and heart .	manualset1
81202	1	377377	7	NULL	NULL	0	NULL	11-9-1-4	Cell		express					galectin-3	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Not only did 11-9-1-4 express galectin-3 in the usual punctate pattern on its cell surface , it demonstrated a higher surface expression of alpha 6 beta 1 integrin compared to BT-549 .	manualset1
81204	2	377377	7	NULL	NULL	NULL	NULL	statement 1	Process		occur in the					cell surface	Cell	punctate pattern on			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Not only did 11-9-1-4 express galectin-3 in the usual punctate pattern on its cell surface , it demonstrated a higher surface expression of alpha 6 beta 1 integrin compared to BT-549 .	manualset1
81205	3	377377	7	NULL	NULL	0	NULL	11-9-1-4 	Cell		express					alpha 6 beta 1 integrin	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Not only did 11-9-1-4 express galectin-3 in the usual punctate pattern on its cell surface , it demonstrated a higher surface expression of alpha 6 beta 1 integrin compared to BT-549 .	manualset1
81206	4	377377	7	NULL	NULL	0	NULL	BT-549	Cell		express					alpha 6 beta 1 integrin	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Not only did 11-9-1-4 express galectin-3 in the usual punctate pattern on its cell surface , it demonstrated a higher surface expression of alpha 6 beta 1 integrin compared to BT-549 .	manualset1
81207	5	377377	7	NULL	NULL	0	NULL	statement 3	Process	expression of	is higher than					statement 4	Process	expression of			NULL		0	NULL	NULL	NULL	NULL	NULL	Not only did 11-9-1-4 express galectin-3 in the usual punctate pattern on its cell surface , it demonstrated a higher surface expression of alpha 6 beta 1 integrin compared to BT-549 .	manualset1
81201	1	377378	7	NULL	NULL	0	NULL	adult neurogenesis	Process		respond to					hippocampal damage 	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Not surprising , investigators of Alzheimer 's disease have also evaluated adult neurogenesis due to its responsiveness to hippocampal damage .	manualset1
81208	1	377379	7	NULL	NULL	0	NULL	ARD1	Protein		critical for					AR target genes	Gene	transcriptionally regulating			NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , ARD1 was critical for transcriptionally regulating a number of AR target genes that are involved in prostate tumorigenesis .	manualset1
81209	2	377379	7	NULL	NULL	0	NULL	AR target genes	Gene		involved in					prostate tumorigenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , ARD1 was critical for transcriptionally regulating a number of AR target genes that are involved in prostate tumorigenesis .	manualset1
81271	1	377381	7	NULL	NULL	NULL	NULL	HCV-JFH1 	Organism	 infection of	redistribute					G3BP1	Protein				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Notably , HCV-JFH1 infection also redistributed the stress granule components GTPase-activating protein ( SH3 domain ) - binding protein 1 ( G3BP1 ) , ataxin-2 ( ATX2 ) , and poly ( A ) - binding protein 1 ( PABP1 ) to the HCV production factory .	manualset1
81272	2	377381	7	NULL	NULL	0	NULL	HCV-JFH1 	Organism	infection of	redistribute					ATX2	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , HCV-JFH1 infection also redistributed the stress granule components GTPase-activating protein ( SH3 domain ) - binding protein 1 ( G3BP1 ) , ataxin-2 ( ATX2 ) , and poly ( A ) - binding protein 1 ( PABP1 ) to the HCV production factory .	manualset1
81273	3	377381	7	NULL	NULL	0	NULL	HCV-JFH1 	Organism	infection of	redistribute					PABP1	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , HCV-JFH1 infection also redistributed the stress granule components GTPase-activating protein ( SH3 domain ) - binding protein 1 ( G3BP1 ) , ataxin-2 ( ATX2 ) , and poly ( A ) - binding protein 1 ( PABP1 ) to the HCV production factory .	manualset1
81274	4	377381	7	NULL	NULL	0	NULL	statement 1	Process		redistribute to					HCV production factory	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , HCV-JFH1 infection also redistributed the stress granule components GTPase-activating protein ( SH3 domain ) - binding protein 1 ( G3BP1 ) , ataxin-2 ( ATX2 ) , and poly ( A ) - binding protein 1 ( PABP1 ) to the HCV production factory .	manualset1
81275	5	377381	7	NULL	NULL	0	NULL	statement 2	Process		redistribute to					HCV production factory	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , HCV-JFH1 infection also redistributed the stress granule components GTPase-activating protein ( SH3 domain ) - binding protein 1 ( G3BP1 ) , ataxin-2 ( ATX2 ) , and poly ( A ) - binding protein 1 ( PABP1 ) to the HCV production factory .	manualset1
81276	6	377381	7	NULL	NULL	0	NULL	statement 3	Process		redistribute to					HCV production factory	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , HCV-JFH1 infection also redistributed the stress granule components GTPase-activating protein ( SH3 domain ) - binding protein 1 ( G3BP1 ) , ataxin-2 ( ATX2 ) , and poly ( A ) - binding protein 1 ( PABP1 ) to the HCV production factory .	manualset1
81277	7	377381	7	NULL	NULL	0	NULL	G3BP1	Protein		is a type of					stress granule component	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , HCV-JFH1 infection also redistributed the stress granule components GTPase-activating protein ( SH3 domain ) - binding protein 1 ( G3BP1 ) , ataxin-2 ( ATX2 ) , and poly ( A ) - binding protein 1 ( PABP1 ) to the HCV production factory .	manualset1
81278	8	377381	7	NULL	NULL	0	NULL	ATX2	Protein		is a type of					stress granule component	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , HCV-JFH1 infection also redistributed the stress granule components GTPase-activating protein ( SH3 domain ) - binding protein 1 ( G3BP1 ) , ataxin-2 ( ATX2 ) , and poly ( A ) - binding protein 1 ( PABP1 ) to the HCV production factory .	manualset1
81279	9	377381	7	NULL	NULL	0	NULL	PABP1	Protein		is a type of					stress granule component	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , HCV-JFH1 infection also redistributed the stress granule components GTPase-activating protein ( SH3 domain ) - binding protein 1 ( G3BP1 ) , ataxin-2 ( ATX2 ) , and poly ( A ) - binding protein 1 ( PABP1 ) to the HCV production factory .	manualset1
81281	10	377381	7	NULL	NULL	0	NULL	G3BP1	Protein		is					GTPase-activating protein ( SH3 domain ) - binding protein 1	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , HCV-JFH1 infection also redistributed the stress granule components GTPase-activating protein ( SH3 domain ) - binding protein 1 ( G3BP1 ) , ataxin-2 ( ATX2 ) , and poly ( A ) - binding protein 1 ( PABP1 ) to the HCV production factory .	manualset1
81282	11	377381	7	NULL	NULL	0	NULL	ATX2	Protein		is					ataxin-2	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , HCV-JFH1 infection also redistributed the stress granule components GTPase-activating protein ( SH3 domain ) - binding protein 1 ( G3BP1 ) , ataxin-2 ( ATX2 ) , and poly ( A ) - binding protein 1 ( PABP1 ) to the HCV production factory .	manualset1
81283	12	377381	7	NULL	NULL	0	NULL	PABP1	Protein		is					poly ( A ) - binding protein 1	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , HCV-JFH1 infection also redistributed the stress granule components GTPase-activating protein ( SH3 domain ) - binding protein 1 ( G3BP1 ) , ataxin-2 ( ATX2 ) , and poly ( A ) - binding protein 1 ( PABP1 ) to the HCV production factory .	manualset1
81284	1	377382	7	NULL	NULL	0	NULL	HDAC inhibitors	NonProteinOrNucleicAcidChemical		led to					HDAC4	Protein	degradation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , HDAC inhibitors led to noticeable HDAC4 degradation , which was effectively prevented by MG132 .	manualset1
81285	2	377382	7	NULL	NULL	0	NULL	MG132	NonProteinOrNucleicAcidChemical		prevent		effectively			statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , HDAC inhibitors led to noticeable HDAC4 degradation , which was effectively prevented by MG132 .	manualset1
81286	1	377386	7	NULL	NULL	0	NULL	heparanase	Protein		stimulate					macrophage	Cell	activation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , heparanase stimulates macrophage activation , while macrophages induce production and activation of latent heparanase contributed by the colon epithelium , together generating a vicious cycle that powers colitis and the associated tumorigenesis .	manualset1
81287	2	377386	7	NULL	NULL	0	NULL	macrophages 	Cell		induce					latent heparanase	Protein	production of			NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , heparanase stimulates macrophage activation , while macrophages induce production and activation of latent heparanase contributed by the colon epithelium , together generating a vicious cycle that powers colitis and the associated tumorigenesis .	manualset1
81288	3	377386	7	NULL	NULL	0	NULL	macrophages 	Cell		induce					latent heparanase	Protein	activation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , heparanase stimulates macrophage activation , while macrophages induce production and activation of latent heparanase contributed by the colon epithelium , together generating a vicious cycle that powers colitis and the associated tumorigenesis .	manualset1
81289	4	377386	7	NULL	NULL	0	NULL	statement 2	Process		contributed by					colon epithelium	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , heparanase stimulates macrophage activation , while macrophages induce production and activation of latent heparanase contributed by the colon epithelium , together generating a vicious cycle that powers colitis and the associated tumorigenesis .	manualset1
81290	5	377386	7	NULL	NULL	0	NULL	statement 3	Process		contributed by					colon epithelium	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , heparanase stimulates macrophage activation , while macrophages induce production and activation of latent heparanase contributed by the colon epithelium , together generating a vicious cycle that powers colitis and the associated tumorigenesis .	manualset1
81291	6	377386	7	NULL	NULL	0	NULL	statement 4	Process		generate					vicious cycle	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , heparanase stimulates macrophage activation , while macrophages induce production and activation of latent heparanase contributed by the colon epithelium , together generating a vicious cycle that powers colitis and the associated tumorigenesis .	manualset1
81292	7	377386	7	NULL	NULL	0	NULL	statement 5	Process		generate					vicious cycle	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , heparanase stimulates macrophage activation , while macrophages induce production and activation of latent heparanase contributed by the colon epithelium , together generating a vicious cycle that powers colitis and the associated tumorigenesis .	manualset1
81293	8	377386	7	NULL	NULL	0	NULL	statement 6	Process		powers					colitis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , heparanase stimulates macrophage activation , while macrophages induce production and activation of latent heparanase contributed by the colon epithelium , together generating a vicious cycle that powers colitis and the associated tumorigenesis .	manualset1
81294	9	377386	7	NULL	NULL	0	NULL	statement 7	Process		powers					colitis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , heparanase stimulates macrophage activation , while macrophages induce production and activation of latent heparanase contributed by the colon epithelium , together generating a vicious cycle that powers colitis and the associated tumorigenesis .	manualset1
81295	10	377386	7	NULL	NULL	0	NULL	statement 6	Process		powers					tumorigenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , heparanase stimulates macrophage activation , while macrophages induce production and activation of latent heparanase contributed by the colon epithelium , together generating a vicious cycle that powers colitis and the associated tumorigenesis .	manualset1
81296	11	377386	7	NULL	NULL	0	NULL	statement 7	Process		powers					tumorigenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , heparanase stimulates macrophage activation , while macrophages induce production and activation of latent heparanase contributed by the colon epithelium , together generating a vicious cycle that powers colitis and the associated tumorigenesis .	manualset1
81297	1	377388	7	NULL	NULL	0	NULL	neuronal protein	Protein		aggregates					huntingtin	Protein	mutated			NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , neuronal protein aggregates of mutated huntingtin , which is typical HD neuropathology , were not found within the transplanted fetal tissue .	manualset1
81298	2	377388	7	NULL	NULL	0	NULL	statement 1	Process		is a type of					typical HD neuropathology	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , neuronal protein aggregates of mutated huntingtin , which is typical HD neuropathology , were not found within the transplanted fetal tissue .	manualset1
81299	3	377388	7	NULL	NULL	0	NULL	statement 1	Process		not found within					 fetal tissue	BodyPart	transplanted			NULL		0	NULL	NULL	NULL	NULL	NULL	Notably , neuronal protein aggregates of mutated huntingtin , which is typical HD neuropathology , were not found within the transplanted fetal tissue .	manualset1
81300	1	377391	7	NULL	NULL	0	NULL	Notch 	Protein		does not affect		overtly			cell cycle	Process	entry of			NULL		0	NULL	NULL	NULL	NULL	NULL	Notch does not overtly affect cell cycle entry or progression of CD4 ( + ) T cells .	manualset1
81301	2	377391	7	NULL	NULL	0	NULL	Notch	Protein		does not affect		overtly			CD4 ( + ) T cells	Cell	progression of			NULL		0	NULL	NULL	NULL	NULL	NULL	Notch does not overtly affect cell cycle entry or progression of CD4 ( + ) T cells .	manualset1
81366	1	377392	7	NULL	NULL	0	NULL	Notch	Protein		implicated as					myogenesis	Process	regulator of			NULL		0	NULL	NULL	NULL	NULL	NULL	Notch has also been implicated as a regulator of myogenesis , although its precise function there has remained controversial .	manualset1
81302	1	377393	7	NULL	NULL	0	NULL	Notch signaling	Process		is involved in					cell differentiation	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Notch signaling is involved in cell differentiation and patterning during morphogenesis .	manualset1
81303	2	377393	7	NULL	NULL	0	NULL	Notch signaling	Process		is involved in					patterning	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Notch signaling is involved in cell differentiation and patterning during morphogenesis .	manualset1
81304	3	377393	7	NULL	NULL	0	NULL	statement 1	Process		occur during					morphogenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Notch signaling is involved in cell differentiation and patterning during morphogenesis .	manualset1
81305	4	377393	7	NULL	NULL	0	NULL	statement 2	Process		occur during					morphogenesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Notch signaling is involved in cell differentiation and patterning during morphogenesis .	manualset1
81306	3	377398	7	NULL	NULL	NULL	NULL	chronic stress	MentalProcess		impair					statement 1	BodyPart	development of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Noting that chronic stress or abuse in childhood can impair development of the brain region involved in learning and memory , the authors show how the extreme stress of being placed in an orphanage leads to abnormal brain development and decreased cognitive functioning .	manualset1
81307	5	377398	7	NULL	NULL	NULL	NULL	statement 3	Process		during					childhood	Duration				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Noting that chronic stress or abuse in childhood can impair development of the brain region involved in learning and memory , the authors show how the extreme stress of being placed in an orphanage leads to abnormal brain development and decreased cognitive functioning .	manualset1
81308	1	377398	7	NULL	NULL	0	NULL	brain region	BodyPart		involved in					learning	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Noting that chronic stress or abuse in childhood can impair development of the brain region involved in learning and memory , the authors show how the extreme stress of being placed in an orphanage leads to abnormal brain development and decreased cognitive functioning .	manualset1
81309	2	377398	7	NULL	NULL	0	NULL	brain region	BodyPart		involved in					memory	MentalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	Noting that chronic stress or abuse in childhood can impair development of the brain region involved in learning and memory , the authors show how the extreme stress of being placed in an orphanage leads to abnormal brain development and decreased cognitive functioning .	manualset1
81310	4	377398	7	NULL	NULL	0	NULL	chronic stress	MentalProcess		impair					statement 2	Protein	development of			NULL		0	NULL	NULL	NULL	NULL	NULL	Noting that chronic stress or abuse in childhood can impair development of the brain region involved in learning and memory , the authors show how the extreme stress of being placed in an orphanage leads to abnormal brain development and decreased cognitive functioning .	manualset1
81311	6	377398	7	NULL	NULL	NULL	NULL	statement 4	Process		during					childhood	Duration				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Noting that chronic stress or abuse in childhood can impair development of the brain region involved in learning and memory , the authors show how the extreme stress of being placed in an orphanage leads to abnormal brain development and decreased cognitive functioning .	manualset1
81312	1	377401	7	NULL	NULL	0	NULL	Novel 5 ' - norcarbocyclic adenine analogs	NonProteinOrNucleicAcidChemical		synthesized from					epichlorohydrin 5	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Novel 5 ' - norcarbocyclic adenine and guanine phosphonic acid analogs with 6 ' ,6 ' - difluorine moiety were designed and synthesized from commercially available epichlorohydrin 5 .	manualset1
81313	2	377401	7	NULL	NULL	0	NULL	guanine phosphonic acid analogs with 6 ' ,6 ' - difluorine moiety	NonProteinOrNucleicAcidChemical		synthesized from					epichlorohydrin 5	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Novel 5 ' - norcarbocyclic adenine and guanine phosphonic acid analogs with 6 ' ,6 ' - difluorine moiety were designed and synthesized from commercially available epichlorohydrin 5 .	manualset1
81314	1	377404	7	NULL	NULL	0	NULL	Novel calpain inhibitors	NonProteinOrNucleicAcidChemical		derived from					phenyl alanine aldehydes	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Novel calpain inhibitors derived from phenyl alanine aldehydes or ketoamides carrying a benzoyl residue were prepared and evaluated for their biological potency .	manualset1
81315	2	377404	7	NULL	NULL	0	NULL	Novel calpain inhibitors	NonProteinOrNucleicAcidChemical		derived from					phenyl alanine ketoamides	NonProteinOrNucleicAcidChemical	carrying benzoyl residue			NULL		0	NULL	NULL	NULL	NULL	NULL	Novel calpain inhibitors derived from phenyl alanine aldehydes or ketoamides carrying a benzoyl residue were prepared and evaluated for their biological potency .	manualset1
81316	1	377405	7	NULL	NULL	0	NULL	Novel chitosan-polycaprolactone 	NonProteinOrNucleicAcidChemical		blends as					potential scaffold	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Novel chitosan-polycaprolactone blends as potential scaffold and carrier for corneal endothelial transplantation .	manualset1
81317	2	377405	7	NULL	NULL	0	NULL	Novel chitosan-polycaprolactone 	NonProteinOrNucleicAcidChemical		carrier for					corneal endothelial transplantation	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Novel chitosan-polycaprolactone blends as potential scaffold and carrier for corneal endothelial transplantation .	manualset1
81318	3	377405	7	NULL	NULL	0	NULL	statement 1	Process		for					corneal endothelial transplantation	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Novel chitosan-polycaprolactone blends as potential scaffold and carrier for corneal endothelial transplantation .	manualset1
81319	1	377406	7	NULL	NULL	0	NULL	Novel combination neo-adjuvant chemotherapy	MedicalProcedure		introduced for					T3 gastric cancer patients	PersonGroup				NULL		0	NULL	NULL	NULL	NULL	NULL	Novel combination neo-adjuvant chemotherapy has been introduced for T3 gastric cancer patients .	manualset1
81320	1	377407	7	NULL	NULL	0	NULL	proximal tubule cell line	Cell	Novel conditionally immortalized human	express					functional influx transporter	GeneOrProtein				NULL		0	NULL	NULL	NULL	NULL	NULL	Novel conditionally immortalized human proximal tubule cell line expressing functional influx and efflux transporters .	manualset1
81321	2	377407	7	NULL	NULL	0	NULL	proximal tubule cell line	Cell	Novel conditionally immortalized human	express					functional efflux transporter	GeneOrProtein				NULL		0	NULL	NULL	NULL	NULL	NULL	Novel conditionally immortalized human proximal tubule cell line expressing functional influx and efflux transporters .	manualset1
81322	1	377408	7	NULL	NULL	NULL	NULL	hnRNP G/RBMX protein	Protein	novel domains in	distinct role in					RNA	NucleicAcidSubstance	binding of			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Novel domains in the hnRNP G/RBMX protein with distinct roles in RNA binding and targeting nascent transcripts .	manualset1
81323	2	377408	7	NULL	NULL	NULL	NULL	hnRNP G/RBMX protein	Protein	novel domains in	distinct role in					nascent transcripts	NucleicAcidSubstance	targeting			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Novel domains in the hnRNP G/RBMX protein with distinct roles in RNA binding and targeting nascent transcripts .	manualset1
81324	1	377410	7	NULL	NULL	0	NULL	nitric oxide synthase	Protein	novel inhibitors of	shows					antioxidant properties	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Novel inhibitors of nitric oxide synthase with antioxidant properties .	manualset1
81325	1	377412	7	NULL	NULL	0	NULL	PKD1 gene	Gene	novel mutations in	occur with					autosomal dominant polycystic kidney disease	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	Novel mutations of PKD1 gene in Chinese patients with autosomal dominant polycystic kidney disease .	manualset1
81326	1	377414	7	NULL	NULL	0	NULL	toluene catabolism	Process	novel pathway of	occur in					bacterium g4	Organism	trichloroethylene-degrading			NULL		0	NULL	NULL	NULL	NULL	NULL	Novel pathway of toluene catabolism in the trichloroethylene-degrading bacterium g4 .	manualset1
81327	1	377416	7	NULL	NULL	0	NULL	Novel polyurethanes	NonProteinOrNucleicAcidChemical		induce					tissue remodeling	Process				NULL	in vivo	0	NULL	NULL	NULL	NULL	NULL	Novel polyurethanes with interconnected porous structure induce in vivo tissue remodeling and accompanied vascularization .	manualset1
81328	2	377416	7	NULL	NULL	0	NULL	Novel polyurethanes	NonProteinOrNucleicAcidChemical		induce					vascularization	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Novel polyurethanes with interconnected porous structure induce in vivo tissue remodeling and accompanied vascularization .	manualset1
81329	3	377416	7	NULL	NULL	0	NULL	Novel polyurethanes	NonProteinOrNucleicAcidChemical		have					 interconnected porous structure	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Novel polyurethanes with interconnected porous structure induce in vivo tissue remodeling and accompanied vascularization .	manualset1
81330	1	377418	7	NULL	NULL	NULL	NULL	serum proteomics	MedicalProcedureOrDevice		predict		may			prostate cancer	Disease	outcome in advanced			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Novel techniques such as serum proteomics , microarrays , and metastatic cell isolation methods may better predict outcome in advanced prostate cancer .	manualset1
81331	2	377418	7	NULL	NULL	0	NULL	microarrays	MedicalProcedureOrDevice		predict		may			prostate cancer	Disease	outcome in advanced			NULL		0	NULL	NULL	NULL	NULL	NULL	Novel techniques such as serum proteomics , microarrays , and metastatic cell isolation methods may better predict outcome in advanced prostate cancer .	manualset1
81332	3	377418	7	NULL	NULL	NULL	NULL	metastatic cell isolation	MedicalProcedureOrDevice		predict		may			prostate cancer	Disease	outcome in advanced			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Novel techniques such as serum proteomics , microarrays , and metastatic cell isolation methods may better predict outcome in advanced prostate cancer .	manualset1
81335	1	377427	7	NULL	NULL	0	NULL	Noxious mechanical stimuli	ExperimentalFactor		increase					iSP	GeneOrProtein	release of			NULL		0	NULL	NULL	NULL	NULL	NULL	Noxious mechanical stimuli , but not thermal stimuli , increased the release of immunoreactive substance P ( iSP ) .	manualset1
81337	2	377427	7	NULL	NULL	0	NULL	thermal stimuli	ExperimentalFactor		does not increase					iSP	GeneOrProtein				NULL		0	NULL	NULL	NULL	NULL	NULL	Noxious mechanical stimuli , but not thermal stimuli , increased the release of immunoreactive substance P ( iSP ) .	manualset1
81340	3	377427	7	NULL	NULL	0	NULL	iSP	GeneOrProtein		is					immunoreactive substance P	GeneOrProtein				NULL		0	NULL	NULL	NULL	NULL	NULL	Noxious mechanical stimuli , but not thermal stimuli , increased the release of immunoreactive substance P ( iSP ) .	manualset1
81343	1	377428	7	NULL	NULL	NULL	NULL	Noxious stimuli	ExperimentalFactor		excite					contralateral topographical projection 	Process	system with 			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Noxious stimuli also excite a system with contralateral topographical projection , high synaptic security and termination in lamina IV .	manualset1
81344	2	377428	7	NULL	NULL	NULL	NULL	Noxious stimuli	ExperimentalFactor		excite					lamina IV	Cell	system with high synaptic security			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Noxious stimuli also excite a system with contralateral topographical projection , high synaptic security and termination in lamina IV .	manualset1
81345	3	377428	7	NULL	NULL	0	NULL	Noxious stimuli	ExperimentalFactor		excite					lamina IV	Cell	termination in			NULL		0	NULL	NULL	NULL	NULL	NULL	Noxious stimuli also excite a system with contralateral topographical projection , high synaptic security and termination in lamina IV .	manualset1
81346	1	377432	7	NULL	NULL	0	NULL	enzymes	Protein		protective against					oxidative stress	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nuclear factor erythroid-derived 2-like 2 ( Nrf2 ) controls the expression of several enzymes that are protective against oxidative stress .	manualset1
81347	2	377432	7	NULL	NULL	0	NULL	Nrf2	Protein		controls					statement 1	Process	expression of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nuclear factor erythroid-derived 2-like 2 ( Nrf2 ) controls the expression of several enzymes that are protective against oxidative stress .	manualset1
81348	3	377432	7	NULL	NULL	NULL	NULL	Nrf2	Protein		is					Nuclear factor erythroid-derived 2-like 2	Protein				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nuclear factor erythroid-derived 2-like 2 ( Nrf2 ) controls the expression of several enzymes that are protective against oxidative stress .	manualset1
81349	1	377433	7	NULL	NULL	0	NULL	Nuclear proteins	Protein		isolated from					enterocytes	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Nuclear proteins isolated from enterocytes showed increased binding of the HNF-1 alpha complex with a concomitant decrease in the HNF-1 beta-containing complex to the SIF3 element both during the suckling-weaning developmental transition and Caco-2 cell differentiation .	manualset1
81350	2	377433	7	NULL	NULL	0	NULL	HNF-1 alpha complex	Protein		bind					SIF3 element	Gene				NULL		0	NULL	NULL	NULL	NULL	NULL	Nuclear proteins isolated from enterocytes showed increased binding of the HNF-1 alpha complex with a concomitant decrease in the HNF-1 beta-containing complex to the SIF3 element both during the suckling-weaning developmental transition and Caco-2 cell differentiation .	manualset1
81351	3	377433	7	NULL	NULL	0	NULL	Nuclear proteins	Protein		increase					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nuclear proteins isolated from enterocytes showed increased binding of the HNF-1 alpha complex with a concomitant decrease in the HNF-1 beta-containing complex to the SIF3 element both during the suckling-weaning developmental transition and Caco-2 cell differentiation .	manualset1
81352	4	377433	7	NULL	NULL	0	NULL	HNF-1 beta-containing complex	Protein		bind					SIF3 element	Gene				NULL		0	NULL	NULL	NULL	NULL	NULL	Nuclear proteins isolated from enterocytes showed increased binding of the HNF-1 alpha complex with a concomitant decrease in the HNF-1 beta-containing complex to the SIF3 element both during the suckling-weaning developmental transition and Caco-2 cell differentiation .	manualset1
81353	5	377433	7	NULL	NULL	0	NULL	Nuclear proteins	Protein		decrease					statement 4	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nuclear proteins isolated from enterocytes showed increased binding of the HNF-1 alpha complex with a concomitant decrease in the HNF-1 beta-containing complex to the SIF3 element both during the suckling-weaning developmental transition and Caco-2 cell differentiation .	manualset1
81354	6	377433	7	NULL	NULL	0	NULL	statement 3	Process		during					suckling-weaning developmental transition	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nuclear proteins isolated from enterocytes showed increased binding of the HNF-1 alpha complex with a concomitant decrease in the HNF-1 beta-containing complex to the SIF3 element both during the suckling-weaning developmental transition and Caco-2 cell differentiation .	manualset1
81355	7	377433	7	NULL	NULL	0	NULL	statement 3	Process		during					Caco-2 cell	Cell	differentiation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nuclear proteins isolated from enterocytes showed increased binding of the HNF-1 alpha complex with a concomitant decrease in the HNF-1 beta-containing complex to the SIF3 element both during the suckling-weaning developmental transition and Caco-2 cell differentiation .	manualset1
81356	8	377433	7	NULL	NULL	0	NULL	statement 5	Process		during					suckling-weaning developmental transition	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nuclear proteins isolated from enterocytes showed increased binding of the HNF-1 alpha complex with a concomitant decrease in the HNF-1 beta-containing complex to the SIF3 element both during the suckling-weaning developmental transition and Caco-2 cell differentiation .	manualset1
81357	9	377433	7	NULL	NULL	0	NULL	statement 5	Process		during					Caco-2 cell	Cell	differentiation of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nuclear proteins isolated from enterocytes showed increased binding of the HNF-1 alpha complex with a concomitant decrease in the HNF-1 beta-containing complex to the SIF3 element both during the suckling-weaning developmental transition and Caco-2 cell differentiation .	manualset1
81369	1	377434	7	NULL	NULL	0	NULL	Nuclear ribonucleoprotein complexes	Protein		contain					U1 RNA	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	NULL	NULL	Nuclear ribonucleoprotein complexes containing U1 and U2 RNA .	manualset1
81374	2	377434	7	NULL	NULL	0	NULL	Nuclear ribonucleoprotein complexes	Protein		contain					U2 RNA	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	NULL	NULL	Nuclear ribonucleoprotein complexes containing U1 and U2 RNA .	manualset1
81378	1	377435	7	NULL	NULL	0	NULL	phorbol ester 	NonProteinOrNucleicAcidChemical		induce					interleukin 1 beta	Protein	transcription of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nuclear run-on analysis showed that phorbol ester induced the transcription of interleukin 1 beta but did not induce it in the presence of cycloheximide .	manualset1
81381	2	377435	7	NULL	NULL	0	NULL	phorbol ester	NonProteinOrNucleicAcidChemical		does not induce					cycloheximide	NonProteinOrNucleicAcidChemical	in the presence of			NULL		0	NULL	NULL	NULL	NULL	NULL	Nuclear run-on analysis showed that phorbol ester induced the transcription of interleukin 1 beta but did not induce it in the presence of cycloheximide .	manualset1
81572	1	377436	7	NULL	NULL	0	NULL	Nuclear tau	Protein		immunoreactivity in					presenile dementia with motor neuron disease	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	Nuclear tau immunoreactivity in presenile dementia with motor neuron disease : a case report .	manualset1
81573	1	377438	7	NULL	NULL	NULL	NULL	VTs	Protein		stabilize					preproET-1 mRNA transcripts	NucleicAcidSubstance	labile			NULL	endothelial cells	NULL	NULL	NULL	NULL	NULL	NULL	Nuclear transcription and actinomycin D chase experiments indicated that VTs stabilize labile preproET-1 mRNA transcripts in endothelial cells .	manualset1
81574	1	377441	7	NULL	NULL	0	NULL	Nucleoli	CellComponent		is a type of					subnuclear organelles	CellComponent				NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleoli are prominent subnuclear organelles , and are known to be hubs of ribosome synthesis .	manualset1
81575	2	377441	7	NULL	NULL	0	NULL	Nucleoli	CellComponent		hubs of					ribosome synthesis	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleoli are prominent subnuclear organelles , and are known to be hubs of ribosome synthesis .	manualset1
81576	1	377442	7	NULL	NULL	0	NULL	NRTIs	NonProteinOrNucleicAcidChemical		used against					HIV	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleoside reverse transcriptase inhibitors ( NRTIs ) used against the human immunodeficiency virus ( HIV ) need to be activated intracellularly to their triphosphate moiety to inhibit HIV replication .	manualset1
81577	2	377442	7	NULL	NULL	0	NULL	statement 1	Process		activated to					triphosphate moiety	NonProteinOrNucleicAcidChemical	intracellularly			NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleoside reverse transcriptase inhibitors ( NRTIs ) used against the human immunodeficiency virus ( HIV ) need to be activated intracellularly to their triphosphate moiety to inhibit HIV replication .	manualset1
81578	3	377442	7	NULL	NULL	0	NULL	statement 2	Process		inhibit					HIV replication	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleoside reverse transcriptase inhibitors ( NRTIs ) used against the human immunodeficiency virus ( HIV ) need to be activated intracellularly to their triphosphate moiety to inhibit HIV replication .	manualset1
81579	4	377442	7	NULL	NULL	0	NULL	NRTIs	NonProteinOrNucleicAcidChemical		is					Nucleoside reverse transcriptase inhibitors	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleoside reverse transcriptase inhibitors ( NRTIs ) used against the human immunodeficiency virus ( HIV ) need to be activated intracellularly to their triphosphate moiety to inhibit HIV replication .	manualset1
81580	5	377442	7	NULL	NULL	0	NULL	HIV	Organism		is					human immunodeficiency virus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleoside reverse transcriptase inhibitors ( NRTIs ) used against the human immunodeficiency virus ( HIV ) need to be activated intracellularly to their triphosphate moiety to inhibit HIV replication .	manualset1
81581	1	377443	7	NULL	NULL	NULL	NULL	H2B	Protein	Nucleosomal peptides in histone regions	recognized by			10-33		CD4 T cells	Cell				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nucleosomal peptides in histone regions H2B ( 10-33 ) , H4 ( 16-39 ) ( and overlapping H4 ( 14-28 ) ) , H4 ( 71-94 ) , and H3 ( 91-105 ) ( and overlapping H3 ( 100-114 ) ) were recurrently recognized by CD4 T cells from the patients with lupus .	manualset1
81709	2	377443	7	NULL	NULL	0	NULL	H4	Protein	Nucleosomal peptides in histone regions	recognized by			16-39		CD4 T cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleosomal peptides in histone regions H2B ( 10-33 ) , H4 ( 16-39 ) ( and overlapping H4 ( 14-28 ) ) , H4 ( 71-94 ) , and H3 ( 91-105 ) ( and overlapping H3 ( 100-114 ) ) were recurrently recognized by CD4 T cells from the patients with lupus .	manualset1
81710	3	377443	7	NULL	NULL	0	NULL	overlapping H4	Protein	Nucleosomal peptides in histone regions	recognized by			14-28		CD4 T cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleosomal peptides in histone regions H2B ( 10-33 ) , H4 ( 16-39 ) ( and overlapping H4 ( 14-28 ) ) , H4 ( 71-94 ) , and H3 ( 91-105 ) ( and overlapping H3 ( 100-114 ) ) were recurrently recognized by CD4 T cells from the patients with lupus .	manualset1
81711	4	377443	7	NULL	NULL	0	NULL	H4	Protein	Nucleosomal peptides in histone regions	recognized by			71-94		CD4 T cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleosomal peptides in histone regions H2B ( 10-33 ) , H4 ( 16-39 ) ( and overlapping H4 ( 14-28 ) ) , H4 ( 71-94 ) , and H3 ( 91-105 ) ( and overlapping H3 ( 100-114 ) ) were recurrently recognized by CD4 T cells from the patients with lupus .	manualset1
81712	5	377443	7	NULL	NULL	0	NULL	H3	Protein	Nucleosomal peptides in histone regions	recognized by			91-105		CD4 T cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleosomal peptides in histone regions H2B ( 10-33 ) , H4 ( 16-39 ) ( and overlapping H4 ( 14-28 ) ) , H4 ( 71-94 ) , and H3 ( 91-105 ) ( and overlapping H3 ( 100-114 ) ) were recurrently recognized by CD4 T cells from the patients with lupus .	manualset1
81713	6	377443	7	NULL	NULL	0	NULL	overlapping H3	Protein	Nucleosomal peptides in histone regions	recognized by			100-114		CD4 T cells	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleosomal peptides in histone regions H2B ( 10-33 ) , H4 ( 16-39 ) ( and overlapping H4 ( 14-28 ) ) , H4 ( 71-94 ) , and H3 ( 91-105 ) ( and overlapping H3 ( 100-114 ) ) were recurrently recognized by CD4 T cells from the patients with lupus .	manualset1
81714	7	377443	7	NULL	NULL	0	NULL	statement 1	Process		occur from					lupus	Disease	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleosomal peptides in histone regions H2B ( 10-33 ) , H4 ( 16-39 ) ( and overlapping H4 ( 14-28 ) ) , H4 ( 71-94 ) , and H3 ( 91-105 ) ( and overlapping H3 ( 100-114 ) ) were recurrently recognized by CD4 T cells from the patients with lupus .	manualset1
81715	8	377443	7	NULL	NULL	NULL	NULL	statement 2	Process		occur from					lupus	Disease	patients with			NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nucleosomal peptides in histone regions H2B ( 10-33 ) , H4 ( 16-39 ) ( and overlapping H4 ( 14-28 ) ) , H4 ( 71-94 ) , and H3 ( 91-105 ) ( and overlapping H3 ( 100-114 ) ) were recurrently recognized by CD4 T cells from the patients with lupus .	manualset1
81716	9	377443	7	NULL	NULL	0	NULL	statement 3	Process		occur from					lupus	Disease	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleosomal peptides in histone regions H2B ( 10-33 ) , H4 ( 16-39 ) ( and overlapping H4 ( 14-28 ) ) , H4 ( 71-94 ) , and H3 ( 91-105 ) ( and overlapping H3 ( 100-114 ) ) were recurrently recognized by CD4 T cells from the patients with lupus .	manualset1
81717	10	377443	7	NULL	NULL	0	NULL	statement 4	Process		occur from					lupus	Disease	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleosomal peptides in histone regions H2B ( 10-33 ) , H4 ( 16-39 ) ( and overlapping H4 ( 14-28 ) ) , H4 ( 71-94 ) , and H3 ( 91-105 ) ( and overlapping H3 ( 100-114 ) ) were recurrently recognized by CD4 T cells from the patients with lupus .	manualset1
81718	11	377443	7	NULL	NULL	0	NULL	statement 5	Process		occur from					lupus	Disease	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleosomal peptides in histone regions H2B ( 10-33 ) , H4 ( 16-39 ) ( and overlapping H4 ( 14-28 ) ) , H4 ( 71-94 ) , and H3 ( 91-105 ) ( and overlapping H3 ( 100-114 ) ) were recurrently recognized by CD4 T cells from the patients with lupus .	manualset1
81719	12	377443	7	NULL	NULL	0	NULL	statement 6	Process		occur from					lupus	Disease	patients with			NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleosomal peptides in histone regions H2B ( 10-33 ) , H4 ( 16-39 ) ( and overlapping H4 ( 14-28 ) ) , H4 ( 71-94 ) , and H3 ( 91-105 ) ( and overlapping H3 ( 100-114 ) ) were recurrently recognized by CD4 T cells from the patients with lupus .	manualset1
81720	1	377444	7	NULL	NULL	0	NULL	Nucleosome assembly proteins	Protein		important role in					chromatin remodeling	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleosome assembly proteins play important roles in chromatin remodeling , which determines gene expression , cell proliferation and terminal differentiation .	manualset1
81721	2	377444	7	NULL	NULL	NULL	NULL	statement 1	Process		determines					gene expression	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nucleosome assembly proteins play important roles in chromatin remodeling , which determines gene expression , cell proliferation and terminal differentiation .	manualset1
81722	3	377444	7	NULL	NULL	NULL	NULL	statement 1	Process		determines					cell proliferation	Process				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Nucleosome assembly proteins play important roles in chromatin remodeling , which determines gene expression , cell proliferation and terminal differentiation .	manualset1
81723	4	377444	7	NULL	NULL	0	NULL	statement 1	Process		determines					terminal differentiation	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleosome assembly proteins play important roles in chromatin remodeling , which determines gene expression , cell proliferation and terminal differentiation .	manualset1
81724	1	377445	7	NULL	NULL	0	NULL	NER	Process	Eukaryotes	involves					multiple gene products	Gene				NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleotide excision repair ( NER ) in eukaryotes is a biochemically complex process involving multiple gene products .	manualset1
81725	2	377445	7	NULL	NULL	0	NULL	NER	Process		is a type of					biochemically complex process	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleotide excision repair ( NER ) in eukaryotes is a biochemically complex process involving multiple gene products .	manualset1
81726	3	377445	7	NULL	NULL	0	NULL	NER	Process		is					Nucleotide excision repair	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleotide excision repair ( NER ) in eukaryotes is a biochemically complex process involving multiple gene products .	manualset1
81727	1	377446	7	NULL	NULL	0	NULL	beta-luffin	Protein		is a type of					ribosome-inactivating protein	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleotide sequence of cDNA encoding beta-luffin , another ribosome-inactivating protein from Luffa cylindrica .	manualset1
81728	2	377446	7	NULL	NULL	0	NULL	beta-luffin	Protein		is obtained from					Luffa cylindrica	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Nucleotide sequence of cDNA encoding beta-luffin , another ribosome-inactivating protein from Luffa cylindrica .	manualset1
81883	1	377448	7	NULL	NULL	0	NULL	CEH-10	GeneOrProtein		regulates					CEH-10	GeneOrProtein	its own expression of			NULL		0	NULL	NULL	NULL	NULL	NULL	Null mutants also fail to express CEH-10 , suggesting that CEH-10 regulates its own expression .	manualset1
81897	1	377455	7	NULL	NULL	0	NULL	GAST-like genes	Gene		identified in					plant species	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	Numerous GAST-like genes have been identified in various plant species .	manualset1
81898	1	377457	7	NULL	NULL	NULL	NULL	microglia	Cell	cells with the appearance of 	express		constitutively			class I MHC antigens	Protein				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Numerous cells with the appearance of microglia were found to constitutively express class I MHC antigens , while only rare cells expressed class II ( Ia ) antigens .	manualset1
81899	2	377457	7	NULL	NULL	NULL	NULL	rare cells	Cell		express					class II ( Ia ) antigen	Protein				NULL		NULL	NULL	NULL	NULL	NULL	NULL	Numerous cells with the appearance of microglia were found to constitutively express class I MHC antigens , while only rare cells expressed class II ( Ia ) antigens .	manualset1
81900	1	377458	7	NULL	NULL	0	NULL	neuronal heterotopias	Disease		associated with					ectopic ependymal cavities	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	Numerous neuronal heterotopias associated with ectopic ependymal cavities were observed in the vermis in one case .	manualset1
81901	2	377458	7	NULL	NULL	0	NULL	statement 1	Process		occur in					vermis	BodyPart				NULL		0	NULL	NULL	NULL	NULL	NULL	Numerous neuronal heterotopias associated with ectopic ependymal cavities were observed in the vermis in one case .	manualset1
81647	1	387313	11	NULL	NULL	0	NULL	 lesion	MedicalFinding		does not respond to					nafcillin	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The lesion failed to respond to nafcillin alone or combination therapy with hyperbaric oxygen , but showed slow , steady improvement with long-term clindamycin .	manualset1
81648	2	387313	11	NULL	NULL	0	NULL	lesion	MedicalFinding		showed improvement with		 slow;;steady			clindamycin	NonProteinOrNucleicAcidChemical	 long-term			NULL		0	NULL	NULL	NULL	NULL	NULL	The lesion failed to respond to nafcillin alone or combination therapy with hyperbaric oxygen , but showed slow , steady improvement with long-term clindamycin .	manualset1
81649	1	387314	11	NULL	NULL	0	NULL	lesions	MedicalFinding		are					umbilicated	AnatomicalPart	centrally			NULL		0	NULL	NULL	NULL	NULL	NULL	The lesions were centrally umbilicated , resembling molluscum contagiosum , but clearly distinct from Tyson 's glands .	manualset1
81650	2	387314	11	NULL	NULL	0	NULL	 lesions	MedicalFinding		 resemble					molluscum contagiosum	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	The lesions were centrally umbilicated , resembling molluscum contagiosum , but clearly distinct from Tyson 's glands .	manualset1
81651	3	387314	11	NULL	NULL	0	NULL	lesions	MedicalFinding		distinct from		clearly			Tyson 's gland	AnatomicalPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The lesions were centrally umbilicated , resembling molluscum contagiosum , but clearly distinct from Tyson 's glands .	manualset1
81652	1	387315	11	NULL	NULL	0	NULL	 lesions	MedicalFinding		located in					posterolateral thalamus	AnatomicalPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The lesions were located mainly in the posterolateral thalamus including posteromedial part of the internal capsule ( thalamic pain ) , however , they were located outside of the thalamus in some cases ( suprathalamic pain ) .	manualset1
81653	2	387315	11	NULL	NULL	0	NULL	lesions	MedicalFinding		occurs					thalamus	AnatomicalPart	outside			NULL		0	NULL	NULL	NULL	NULL	NULL	The lesions were located mainly in the posterolateral thalamus including posteromedial part of the internal capsule ( thalamic pain ) , however , they were located outside of the thalamus in some cases ( suprathalamic pain ) .	manualset1
81654	3	387315	11	NULL	NULL	0	NULL	statement 1	MedicalFinding		causes					thalamic pain	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	The lesions were located mainly in the posterolateral thalamus including posteromedial part of the internal capsule ( thalamic pain ) , however , they were located outside of the thalamus in some cases ( suprathalamic pain ) .	manualset1
81655	4	387315	11	NULL	NULL	0	NULL	statement 2	MedicalFinding		causes					suprathalamic pain	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	The lesions were located mainly in the posterolateral thalamus including posteromedial part of the internal capsule ( thalamic pain ) , however , they were located outside of the thalamus in some cases ( suprathalamic pain ) .	manualset1
81656	1	387316	11	NULL	NULL	0	NULL	pigs	Organism		infected with					virulent strain	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	The lesions were more strongly expressed in the pigs infected with the virulent strain .	manualset1
81657	2	387316	11	NULL	NULL	0	NULL	lesions	MedicalFinding		expressed in		strongly			statement 1	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	The lesions were more strongly expressed in the pigs infected with the virulent strain .	manualset1
81658	1	387318	11	NULL	NULL	0	NULL	leucocyte migration inhibition	BiologicalProcess		is					LMI	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	The leucocyte migration inhibition ( LMI ) was determined in an assay after in vitro challenge with beta-lactoglobulin .	manualset1
81659	1	387319	11	NULL	NULL	0	NULL	leukemia	Disease		is specific to 					strain	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	The leukemia is strain-specific and causes the death of its recipients within 9 days .	manualset1
81660	2	387319	11	NULL	NULL	0	NULL	leukemia	Disease		causes					death	BiologicalProcess	recipient			NULL		0	NULL	NULL	NULL	NULL	NULL	The leukemia is strain-specific and causes the death of its recipients within 9 days .	manualset1
81661	1	387320	11	NULL	NULL	0	NULL	DcCB1 mRNA	NucleicAcidSubstance		is high in					 somatic embryo	Organism part	heart-shaped stage;;globular-shaped stage			NULL		0	NULL	NULL	NULL	NULL	NULL	The level of DcCB1 mRNAs was high in somatic embryos at globular and heart-shaped stages but low in torpedo-shaped somatic embryos .	manualset1
81662	2	387320	11	NULL	NULL	0	NULL	DcCB1 mRNA	NucleicAcidSubstance		is low in					somatic embryo	Organism part	 torpedo-shaped			NULL		0	NULL	NULL	NULL	NULL	NULL	The level of DcCB1 mRNAs was high in somatic embryos at globular and heart-shaped stages but low in torpedo-shaped somatic embryos .	manualset1
81663	1	387321	11	NULL	NULL	NULL	NULL	F antigen	Protein	LNC of MRL/1	increases with		progressively			age	QuantityOrMeasure				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The level of F antigen on LNC of MRL/1 , but not on those of MRL/n mice , increased progressively with age and reached its maximum at 4 mo of age .	manualset1
81667	1	387323	11	NULL	NULL	0	NULL	c-Myc 	Protein		decreased in					ErbB2	Protein	absence of 			NULL		0	NULL	NULL	NULL	NULL	NULL	The level of c-Myc and D-cyclins , proteins involved in p27KiP1 sequestration , decreased in the absence of functional ErbB2 .	manualset1
81668	2	387323	11	NULL	NULL	0	NULL	D-cyclins	Protein		decreased in					ErbB2	Protein	absence of 			NULL		0	NULL	NULL	NULL	NULL	NULL	The level of c-Myc and D-cyclins , proteins involved in p27KiP1 sequestration , decreased in the absence of functional ErbB2 .	manualset1
81669	3	387323	11	NULL	NULL	0	NULL	c-Myc	Protein		involved in					sequestration	BiologicalProcess	p27KiP1			NULL		0	NULL	NULL	NULL	NULL	NULL	The level of c-Myc and D-cyclins , proteins involved in p27KiP1 sequestration , decreased in the absence of functional ErbB2 .	manualset1
81670	4	387323	11	NULL	NULL	0	NULL	D-cyclin	Protein		involved in					sequestration	BiologicalProcess	p27KiP1			NULL		0	NULL	NULL	NULL	NULL	NULL	The level of c-Myc and D-cyclins , proteins involved in p27KiP1 sequestration , decreased in the absence of functional ErbB2 .	manualset1
81671	1	387324	11	NULL	NULL	0	NULL	BMP-2	GeneOrProtein	recombinant;;human	upregulate					connexin43 mRNA	NucleicAcidSubstance				NULL		0	NULL	NULL	NULL	NULL	NULL	The level of connexin43 mRNA is maximally upregulated 48 h after treatment with recombinant human BMP-2 with corresponding changes in protein expression .	manualset1
81672	1	387325	11	NULL	NULL	0	NULL	education													NULL		0	NULL	NULL	NULL	NULL	NULL	The level of education is related to exposure to media as well as the use of family planning methods , and negatively related to the degree of apprehension .	manualset1
81673	1	387326	11	NULL	NULL	0	NULL	infectious pancreatic necrosis virus	Organism		is					IPNV	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	The level of infection by infectious pancreatic necrosis virus ( IPNV ) of kidney macrophages from 12 asymptomatic carrier Atlantic salmon post-smolts was studied .	manualset1
81674	2	387326	11	NULL	NULL	0	NULL	IPNV	Organism		infect					macrophages	Cell	kidney			NULL		0	NULL	NULL	NULL	NULL	NULL	The level of infection by infectious pancreatic necrosis virus ( IPNV ) of kidney macrophages from 12 asymptomatic carrier Atlantic salmon post-smolts was studied .	manualset1
81675	1	387329	11	NULL	NULL	0	NULL	lymphocytes	cell	peritoneal	decreased in					 mice	Organism	Lsp1 ( - / - )			NULL		0	NULL	NULL	NULL	NULL	NULL	The level of peritoneal lymphocytes is decreased in Lsp1 ( - / - ) mice without affecting a particular lymphocytic subset .	manualset1
81676	1	387331	11	NULL	NULL	0	NULL	osteocalcin	Protein		is a marker of					vitamin K2	NonProteinOrNucleicAcidChemical	bone			NULL		0	NULL	NULL	NULL	NULL	NULL	The level of undercarboxylated osteocalcin is recognized as a marker of vitamin K2 bone .	manualset1
81677	1	387334	11	NULL	NULL	NULL	NULL	P450	GeneOrProtein		express					RNA	NucleicAcidSubstance				NULL	fetal hamsters	NULL	NULL	NULL	NULL	NULL	NULL	The levels of RNA expression of both P450s in fetal hamsters were less than 30 % of nonpregnant adult values .	manualset1
81678	1	387338	11	NULL	NULL	0	NULL	ammonium	NonProteinOrNucleicAcidChemical	in cells	reduce the level of					nirB transcript	GeneOrProtein				NULL		0	NULL	NULL	NULL	NULL	NULL	The levels of nirB and ntcB transcripts were low in cells growing on ammonium and increased upon transfer of ammonium-grown cells to nitrate-containing medium .	manualset1
81679	2	387338	11	NULL	NULL	0	NULL	ammonium	NonProteinOrNucleicAcidChemical	in cells	reduce the level of					ntcB transcript	GeneOrProtein				NULL		0	NULL	NULL	NULL	NULL	NULL	The levels of nirB and ntcB transcripts were low in cells growing on ammonium and increased upon transfer of ammonium-grown cells to nitrate-containing medium .	manualset1
81680	3	387338	11	NULL	NULL	0	NULL	nitrate	NonProteinOrNucleicAcidChemical	in cells	increased in the level of					nirB transcript	GeneOrProtein				NULL		0	NULL	NULL	NULL	NULL	NULL	The levels of nirB and ntcB transcripts were low in cells growing on ammonium and increased upon transfer of ammonium-grown cells to nitrate-containing medium .	manualset1
81681	4	387338	11	NULL	NULL	0	NULL	nitrate	NonProteinOrNucleicAcidChemical	in cells	increased in the level of					ntcB transcript\t	GeneOrProtein				NULL		0	NULL	NULL	NULL	NULL	NULL	The levels of nirB and ntcB transcripts were low in cells growing on ammonium and increased upon transfer of ammonium-grown cells to nitrate-containing medium .	manualset1
81682	1	387343	11	NULL	NULL	0	NULL	 lhp1 cyp71	Gene	double mutant	showed					phenotypes	RelationshipPhrase	 severe			NULL		0	NULL	NULL	NULL	NULL	NULL	The lhp1 cyp71 double mutant showed more severe phenotypes than the single mutants , suggesting that AtCYP71 and LHP1 synergistically control plant development .	manualset1
81683	2	387343	11	NULL	NULL	0	NULL	AtCYP71	GeneOrProtein		control 					development	BiologicalProcess	plant			NULL		0	NULL	NULL	NULL	NULL	NULL	The lhp1 cyp71 double mutant showed more severe phenotypes than the single mutants , suggesting that AtCYP71 and LHP1 synergistically control plant development .	manualset1
81684	3	387343	11	NULL	NULL	0	NULL	LHP1	GeneOrProtein		controls					development	BiologicalProcess	plant			NULL		0	NULL	NULL	NULL	NULL	NULL	The lhp1 cyp71 double mutant showed more severe phenotypes than the single mutants , suggesting that AtCYP71 and LHP1 synergistically control plant development .	manualset1
81685	4	387343	11	NULL	NULL	0	NULL	statement 2	Process		is synergistic with					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The lhp1 cyp71 double mutant showed more severe phenotypes than the single mutants , suggesting that AtCYP71 and LHP1 synergistically control plant development .	manualset1
81686	1	387345	11	NULL	NULL	0	NULL	collagenase	GeneOrProtein	fibroblast	has binding site for		putative			 zinc	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The library was screened with an oligonucleotide probe constructed from the putative zinc-binding region of fibroblast collagenase .	manualset1
81687	1	387348	11	NULL	NULL	0	NULL	 ligK gene	Gene		encoding				684-bp open reading frame	polypeptide	PartOfProtein				NULL		0	NULL	NULL	NULL	NULL	NULL	The ligK gene consists of a 684-bp open reading frame encoding a polypeptide with a molecular mass of 24,131 Da .	manualset1
81688	1	387368	11	NULL	NULL	0	NULL	symptomatic epilepsy	Disease	frequency	increased in					elderly population	PersonGroup				NULL		0	NULL	NULL	NULL	NULL	NULL	The literature analysis and our own notices showed that the frequency of symptomatic epilepsy in the elderly population increased .	manualset1
81689	1	387369	11	NULL	NULL	0	NULL	allergic reaction	BiologicalProcess		occurs to					amide 	chemical	local anesthetics			NULL		0	NULL	NULL	NULL	NULL	NULL	The literature demonstrates that an allergic reaction to amide local anesthetics can occur and a thorough history , intradermal testing , and subcutaneous challenge are reasonable approaches to determine a safe agent for subsequent use .	manualset1
81691	1	387378	11	NULL	NULL	0	NULL	 liver	AnatomicalPart		has the capacity to					regenerate	BiologicalProcess	unlimited			NULL		0	NULL	NULL	NULL	NULL	NULL	The liver is an exceptional organ , not only because of its unique anatomical and physiological characteristics , but also because of its unlimited regenerative capacity .	manualset1
81692	1	387380	11	NULL	NULL	0	NULL	transplantation	MedicalProcedureOrDevice	liver 	treats					ATTR amyloidosis	Disease	hereditary			NULL		0	NULL	NULL	NULL	NULL	NULL	The liver transplantation for hereditary ATTR amyloidosis has become a well-established treatment , because the main source of serum variant TTR is shut out .	manualset1
81693	1	387382	11	NULL	NULL	0	NULL	immunoglobulin isotypes			appear in		locally 			 urinary tract	AnatomicalPart	ascending pyelonephritis			NULL		0	NULL	NULL	NULL	NULL	NULL	The local appearance of various immunoglobulin ( Ig ) isotypes in the urinary tract during ascending pyelonephritis was studied in rats experimentally infected with Corynebacterium renale .	manualset1
81694	1	387385	11	NULL	NULL	0	NULL	cobalamin-binding protein	Protein		produces in		locally 			SS	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	The local production of cobalamin-binding proteins in SS was sufficient to achieve concentrations in saliva comparable to the control group .	manualset1
81695	1	387386	11	NULL	NULL	0	NULL	ICP 4	Protein		localized in					infected cells	Cell	herpes simplex virus type 1			NULL		0	NULL	NULL	NULL	NULL	NULL	The localization of ICP 4 , ICP 8 , DNA polymerase and alkaline exonuclease within herpes simplex virus type 1 ( HSV ) - infected cells has been examined by immunofluorescence using specific antibodies to these proteins .	manualset1
81697	1	387392	11	NULL	NULL	0	NULL	GSK3 beta	Protein		hyperphosphorylate					substrate	Protein		 Ser/Thr pentad-repeats		NULL		0	NULL	NULL	NULL	NULL	NULL	The location of this oxyanion binding site in the substrate binding cleft indicates direct coupling of P +4 phosphate-primed substrate binding and catalytic activation , explains the ability of GSK3 beta to processively hyperphosphorylate substrates with Ser/Thr pentad-repeats , and suggests a mechanism for autoinhibition in which the phosphorylated N terminus binds as a competitive pseudosubstrate with phospho-Ser 9 occupying the P +4 site .	manualset1
81698	1	387407	11	NULL	NULL	0	NULL	loss of function	MolecularProcess	 Jhdm2a	results in					obesity	MedicalFinding	mice			NULL		0	NULL	NULL	NULL	NULL	NULL	The loss of Jhdm2a function results in obesity and hyperlipidemia in mice .	manualset1
81699	2	387407	11	NULL	NULL	0	NULL	loss of function	MolecularProcess	 Jhdm2a	results in					hyperlipidemia	MedicalFinding	mice			NULL		0	NULL	NULL	NULL	NULL	NULL	The loss of Jhdm2a function results in obesity and hyperlipidemia in mice .	manualset1
81700	3	387407	11	NULL	NULL	0	NULL	statement 1	Process		occurs along with					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The loss of Jhdm2a function results in obesity and hyperlipidemia in mice .	manualset1
81701	1	387408	11	NULL	NULL	0	NULL	loss of activity	MolecularProcess	PSII	reversed by					Ca ( 2 + )	NonProteinOrNucleicAcidChemical	external medium			NULL		0	NULL	NULL	NULL	NULL	NULL	The loss of PSII activity is reversible by addition of submillimolar amounts of either Ca ( 2 + ) or Na ( + ) to the external medium but not by the addition of any other cation .	manualset1
81702	2	387408	11	NULL	NULL	0	NULL	loss of activity	MolecularProcess	PSII	reversed by					Na ( + )	NonProteinOrNucleicAcidChemical	external medium			NULL		0	NULL	NULL	NULL	NULL	NULL	The loss of PSII activity is reversible by addition of submillimolar amounts of either Ca ( 2 + ) or Na ( + ) to the external medium but not by the addition of any other cation .	manualset1
81703	3	387408	11	NULL	NULL	0	NULL	statement 1	Process		is an alternative to					statement 2	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The loss of PSII activity is reversible by addition of submillimolar amounts of either Ca ( 2 + ) or Na ( + ) to the external medium but not by the addition of any other cation .	manualset1
81704	1	387410	11	NULL	NULL	0	NULL	GAT-1	Protein		is a type of 					GABA transporter	Protein	neuronal			NULL		0	NULL	NULL	NULL	NULL	NULL	The loss of inhibition was accompanied by loss of subclasses of inhibitory interneurons labeled by cholecystokinin and the neuronal GABA transporter GAT-1 , which project axo-somatic and axo-axonic GABAergic inhibitory terminals to granule cells and axon initial segments .	manualset1
81705	2	387410	11	NULL	NULL	0	NULL	GAT-1	Protein		project					 inhibitory terminals	PartOfProtein	axo-somatic;;axo-axonic GABAergic;;granule cells			NULL		0	NULL	NULL	NULL	NULL	NULL	The loss of inhibition was accompanied by loss of subclasses of inhibitory interneurons labeled by cholecystokinin and the neuronal GABA transporter GAT-1 , which project axo-somatic and axo-axonic GABAergic inhibitory terminals to granule cells and axon initial segments .	manualset1
81706	1	387411	11	NULL	NULL	0	NULL	glaucoma	Disease		leads to					loss of sight	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The loss of sight in glaucoma is due to the permanent optic nerve damage which is the result of a chronic elevated intraocular pressure .	manualset1
81707	2	387411	11	NULL	NULL	0	NULL	statement 1	MedicalFinding		is due to					optic nerve damage	MedicalFinding	permanent 			NULL		0	NULL	NULL	NULL	NULL	NULL	The loss of sight in glaucoma is due to the permanent optic nerve damage which is the result of a chronic elevated intraocular pressure .	manualset1
81708	3	387411	11	NULL	NULL	NULL	NULL	intraocular pressure	BiologicalProcess	chronic	damages		permanently 			optic nerve	AnatomicalPart				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The loss of sight in glaucoma is due to the permanent optic nerve damage which is the result of a chronic elevated intraocular pressure .	manualset1
81729	1	387419	11	NULL	NULL	0	NULL	calmodulin	Protein		activates					Ca-ATPase	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	The lower affinity of Met 145-oxidized calmodulin toward the target peptide correlates with experimentally observed lowering of calmodulin-activated Ca-ATPase activity when oxidized calmodulin from aged rat brains is used .	manualset1
81730	1	387420	11	NULL	NULL	0	NULL	PsaK	Protein		is lower in					PSI	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	The lower amount of PsaK present in PSI * may explain its higher electrophoretic mobility .	manualset1
81731	1	387421	11	NULL	NULL	0	NULL	ethylene	NonProteinOrNucleicAcidChemical		is a type of 					hydrocarbon	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The lower hydrocarbons ( ethylene , ethane , and propylene ) were also converted to methane at about 300 degrees C. Conversion of benzene was also possible when other hydrocarbons were present at high concentrations .	manualset1
81732	2	387421	11	NULL	NULL	0	NULL	 ethane	NonProteinOrNucleicAcidChemical		is a type of 					hydrocarbon	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The lower hydrocarbons ( ethylene , ethane , and propylene ) were also converted to methane at about 300 degrees C. Conversion of benzene was also possible when other hydrocarbons were present at high concentrations .	manualset1
81733	3	387421	11	NULL	NULL	0	NULL	propylene	NonProteinOrNucleicAcidChemical		is a type of 					hydrocarbon	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The lower hydrocarbons ( ethylene , ethane , and propylene ) were also converted to methane at about 300 degrees C. Conversion of benzene was also possible when other hydrocarbons were present at high concentrations .	manualset1
81734	4	387421	11	NULL	NULL	0	NULL	ethylene	NonProteinOrNucleicAcidChemical		is converted to					methane	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The lower hydrocarbons ( ethylene , ethane , and propylene ) were also converted to methane at about 300 degrees C. Conversion of benzene was also possible when other hydrocarbons were present at high concentrations .	manualset1
81735	5	387421	11	NULL	NULL	0	NULL	ethane	NonProteinOrNucleicAcidChemical		is converted to					methane	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The lower hydrocarbons ( ethylene , ethane , and propylene ) were also converted to methane at about 300 degrees C. Conversion of benzene was also possible when other hydrocarbons were present at high concentrations .	manualset1
81736	6	387421	11	NULL	NULL	0	NULL	propylene	NonProteinOrNucleicAcidChemical		is converted to					methane	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The lower hydrocarbons ( ethylene , ethane , and propylene ) were also converted to methane at about 300 degrees C. Conversion of benzene was also possible when other hydrocarbons were present at high concentrations .	manualset1
81737	7	387421	11	NULL	NULL	0	NULL	benzene	NonProteinOrNucleicAcidChemical		is converted to					methane	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The lower hydrocarbons ( ethylene , ethane , and propylene ) were also converted to methane at about 300 degrees C. Conversion of benzene was also possible when other hydrocarbons were present at high concentrations .	manualset1
81738	1	387425	11	NULL	NULL	0	NULL	angiotensin II 	Protein	low	has no effect on					water intake	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The lowest doses of angiotensin II ( 25 and 50 micrograms/kg SC ) had no significant effect on either water intake or urine output .	manualset1
81739	2	387425	11	NULL	NULL	0	NULL	angiotensin II	Protein	low	has no effect on					urine output	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The lowest doses of angiotensin II ( 25 and 50 micrograms/kg SC ) had no significant effect on either water intake or urine output .	manualset1
81740	1	387428	11	NULL	NULL	0	NULL	 lubricants	Chemical		are based on					 mineral hydrocarbon	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The lubricants were based on mineral hydrocarbon fractions .	manualset1
81741	1	387434	11	NULL	NULL	0	NULL	lung ball	MedicalFinding		is a type of 					pulmonary aspergillosis	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	The lung ball is a special type of pulmonary aspergillosis ( PA ) occurring often after chemotherapy for leukemia .	manualset1
81742	2	387434	11	NULL	NULL	0	NULL	pulmonary aspergillosis	Disease		is					PA	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	The lung ball is a special type of pulmonary aspergillosis ( PA ) occurring often after chemotherapy for leukemia .	manualset1
81743	3	387434	11	NULL	NULL	0	NULL	pulmonary aspergillosis	Disease		occurs after					leukemia	Disease	chemotherapy for			NULL		0	NULL	NULL	NULL	NULL	NULL	The lung ball is a special type of pulmonary aspergillosis ( PA ) occurring often after chemotherapy for leukemia .	manualset1
81744	1	387437	11	NULL	NULL	0	NULL	acidic forms	Organism	lung	eliminated by					neuraminidase	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	The lung preparation also contained more acidic forms ( pI = 4 -- 5 ) , which were eliminated by treatment with neuraminidase .	manualset1
81745	1	387438	11	NULL	NULL	0	NULL	oxymetholone	NonProteinOrNucleicAcidChemical		has					luteolytic activity	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The luteolytic activity of oxymetholone , and anabolic steroid , has been evaluated in 10 women .	manualset1
81746	1	387447	11	NULL	NULL	0	NULL	macrogamonts	cell		have a					nucleus	CellComponent	large			NULL		0	NULL	NULL	NULL	NULL	NULL	The macrogamonts develop below the nucleus of the host cell and have a large nucleus with a prominent nucleolus .	manualset1
81747	1	387453	11	NULL	NULL	0	NULL	magnetic urokinase	Protein		has 					fibrinolytic activity	BiologicalProcess	high			NULL		0	NULL	NULL	NULL	NULL	NULL	The magnetic urokinase dispersed in saline and exerted high fibrinolytic activity ( 13.8 X 10 ( 4 ) IU/mg protein ) , and was readily recovered from saline by magnetic force of 250 Oe .	manualset1
81748	1	387460	11	NULL	NULL	0	NULL	yohimbine	NonProteinOrNucleicAcidChemical		induces					reinstatement	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The magnitude of yohimbine-induced reinstatement was similar regardless of the presence or absence of the cocaine-paired stimulus .	manualset1
81750	1	387475	11	NULL	NULL	0	NULL	staphylococcus	Organism		causes					sepsis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The main pathogene of sepsis at present is staphylococcus .	manualset1
81751	1	387479	11	NULL	NULL	0	NULL	anastomotic construction	MedicalFinding	colon;;rectum	include					dehiscence	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	The main serious risks of anastomotic construction in the colon and rectum include dehiscence and stricture formation .	manualset1
81752	2	387479	11	NULL	NULL	0	NULL	anastomotic construction	MedicalFinding	colon;;rectum\t	include					stricture formation	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	The main serious risks of anastomotic construction in the colon and rectum include dehiscence and stricture formation .	manualset1
81753	1	387483	11	NULL	NULL	0	NULL	maize	Organism		is a synonym of					Zea mays	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	The maize ( Zea mays ) genome appears to contain at least 17 different CycD genes , and they fall into the subgroups previously described for other plants .	manualset1
81754	2	387483	11	NULL	NULL	0	NULL	maize	Organism		contain					CycD gene	Gene				NULL		0	NULL	NULL	NULL	NULL	NULL	The maize ( Zea mays ) genome appears to contain at least 17 different CycD genes , and they fall into the subgroups previously described for other plants .	manualset1
81755	1	387486	11	NULL	NULL	0	NULL	ampullate gland	AnatomicalPart	major	is present in					Latrodectus hesperus	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	The major ampullate gland of Latrodectus hesperus ( black widow ) is similar in morphology to those found in the Araneid spiders .	manualset1
81756	2	387486	11	NULL	NULL	0	NULL	ampullate gland	AnatomicalPart	Latrodectus hesperus	similar to		morphological 			ampullate gland	AnatomicalPart	Araneid spider			NULL		0	NULL	NULL	NULL	NULL	NULL	The major ampullate gland of Latrodectus hesperus ( black widow ) is similar in morphology to those found in the Araneid spiders .	manualset1
81757	1	387487	11	NULL	NULL	0	NULL	carbonyl reduction	MolecularProcess		is a part of 					 biotransformation	BiologicalProcess	major			NULL		0	NULL	NULL	NULL	NULL	NULL	The major biotransformation pathways are carbonyl reduction , O-methylation at C-3 ' , O-methylation after aromatic hydroxylation at the position C-2 ' on phenyl B ring and O-demethylation on A ring .	manualset1
81758	2	387487	11	NULL	NULL	0	NULL	O-methylation	MolecularProcess		is a part of 				C-3 '	biotransformation	BiologicalProcess	major			NULL		0	NULL	NULL	NULL	NULL	NULL	The major biotransformation pathways are carbonyl reduction , O-methylation at C-3 ' , O-methylation after aromatic hydroxylation at the position C-2 ' on phenyl B ring and O-demethylation on A ring .	manualset1
81759	3	387487	11	NULL	NULL	0	NULL	 phenyl B ring	Chemical	C-2 '	undergoes					hydroxylation	MolecularProcess	aromatic			NULL		0	NULL	NULL	NULL	NULL	NULL	The major biotransformation pathways are carbonyl reduction , O-methylation at C-3 ' , O-methylation after aromatic hydroxylation at the position C-2 ' on phenyl B ring and O-demethylation on A ring .	manualset1
81760	4	387487	11	NULL	NULL	0	NULL	statement 3	Chemical		undergoes					O-methylation	MolecularProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	The major biotransformation pathways are carbonyl reduction , O-methylation at C-3 ' , O-methylation after aromatic hydroxylation at the position C-2 ' on phenyl B ring and O-demethylation on A ring .	manualset1
81761	5	387487	11	NULL	NULL	0	NULL	statement 4	Process		occurs after					statement 3	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The major biotransformation pathways are carbonyl reduction , O-methylation at C-3 ' , O-methylation after aromatic hydroxylation at the position C-2 ' on phenyl B ring and O-demethylation on A ring .	manualset1
81762	6	387487	11	NULL	NULL	0	NULL	A ring	Chemical		undergoes					O-demethylation 	MolecularProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	The major biotransformation pathways are carbonyl reduction , O-methylation at C-3 ' , O-methylation after aromatic hydroxylation at the position C-2 ' on phenyl B ring and O-demethylation on A ring .	manualset1
81763	7	387487	11	NULL	NULL	0	NULL	statement 4	Process		is a part of 					biotransformation	BiologicalProcess	major			NULL		0	NULL	NULL	NULL	NULL	NULL	The major biotransformation pathways are carbonyl reduction , O-methylation at C-3 ' , O-methylation after aromatic hydroxylation at the position C-2 ' on phenyl B ring and O-demethylation on A ring .	manualset1
81764	8	387487	11	NULL	NULL	0	NULL	statement 6	Process		is a part of 					biotransformation	BiologicalProcess	major			NULL		0	NULL	NULL	NULL	NULL	NULL	The major biotransformation pathways are carbonyl reduction , O-methylation at C-3 ' , O-methylation after aromatic hydroxylation at the position C-2 ' on phenyl B ring and O-demethylation on A ring .	manualset1
81765	1	387488	11	NULL	NULL	NULL	NULL	death	BiologicalProcess	hemophiliacs	is related to		cause			bleeding	BiologicalProcess				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The major causes of death not related to AIDS in hemophiliacs were bleeding , liver cirrhosis , and liver cancer .	manualset1
81766	2	387488	11	NULL	NULL	NULL	NULL	death	BiologicalProcess	hemophiliacs	is related to		cause			liver cirrhosis	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The major causes of death not related to AIDS in hemophiliacs were bleeding , liver cirrhosis , and liver cancer .	manualset1
81767	3	387488	11	NULL	NULL	NULL	NULL	death	BiologicalProcess	hemophiliacs	is related to		cause			liver cancer	MedicalFinding				NULL		NULL	NULL	NULL	NULL	NULL	NULL	The major causes of death not related to AIDS in hemophiliacs were bleeding , liver cirrhosis , and liver cancer .	manualset1
81768	4	387488	11	NULL	NULL	0	NULL	death	BiologicalProcess	hemophiliacs	is not related to		cause			AIDS	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The major causes of death not related to AIDS in hemophiliacs were bleeding , liver cirrhosis , and liver cancer .	manualset1
81769	1	387489	11	NULL	NULL	0	NULL	atrial natriuretic peptide	GeneOrProtein		is					ANP	GeneOrProtein				NULL		0	NULL	NULL	NULL	NULL	NULL	The major class of atrial natriuretic peptide ( ANP ) receptors was isolated from cultured vascular smooth muscle cells , and a partial amino acid sequence was obtained .	manualset1
81770	2	387489	11	NULL	NULL	0	NULL	atrial natriuretic peptide receptor	GeneOrProtein		is isolated from					vascular smooth muscle cell	Cell	cultured			NULL		0	NULL	NULL	NULL	NULL	NULL	The major class of atrial natriuretic peptide ( ANP ) receptors was isolated from cultured vascular smooth muscle cells , and a partial amino acid sequence was obtained .	manualset1
81771	1	387490	11	NULL	NULL	NULL	NULL	rose water	Chemical		obtained from					bud	AnatomicalPart	cultivar Ranisahiba 			NULL		NULL	NULL	NULL	NULL	NULL	NULL	The major components of rose water volatiles obtained from the bud , half bloom and full bloom stages of cultivar ` Ranisahiba ' were phenyl ethyl alcohol ( 66.2-79 .0 % ) , geraniol ( 3.3-6 .6 % ) and citronellol ( 1.8-5 .5 % ) .	manualset1
81772	2	387490	11	NULL	NULL	NULL	NULL	rose water	Chemical		obtained from					 half bloom	AnatomicalPart	cultivar Ranisahiba			NULL		NULL	NULL	NULL	NULL	NULL	NULL	The major components of rose water volatiles obtained from the bud , half bloom and full bloom stages of cultivar ` Ranisahiba ' were phenyl ethyl alcohol ( 66.2-79 .0 % ) , geraniol ( 3.3-6 .6 % ) and citronellol ( 1.8-5 .5 % ) .	manualset1
81773	3	387490	11	NULL	NULL	NULL	NULL	rose water	Chemical		obtained from					full bloom	AnatomicalPart	cultivar Ranisahiba			NULL		NULL	NULL	NULL	NULL	NULL	NULL	The major components of rose water volatiles obtained from the bud , half bloom and full bloom stages of cultivar ` Ranisahiba ' were phenyl ethyl alcohol ( 66.2-79 .0 % ) , geraniol ( 3.3-6 .6 % ) and citronellol ( 1.8-5 .5 % ) .	manualset1
81774	4	387490	11	NULL	NULL	0	NULL	rose water	Chemical	volatiles of	composed of 					phenyl ethyl alcohol	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The major components of rose water volatiles obtained from the bud , half bloom and full bloom stages of cultivar ` Ranisahiba ' were phenyl ethyl alcohol ( 66.2-79 .0 % ) , geraniol ( 3.3-6 .6 % ) and citronellol ( 1.8-5 .5 % ) .	manualset1
81775	5	387490	11	NULL	NULL	0	NULL	rose water	Chemical	volatiles of	composed of 					geraniol	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The major components of rose water volatiles obtained from the bud , half bloom and full bloom stages of cultivar ` Ranisahiba ' were phenyl ethyl alcohol ( 66.2-79 .0 % ) , geraniol ( 3.3-6 .6 % ) and citronellol ( 1.8-5 .5 % ) .	manualset1
81776	6	387490	11	NULL	NULL	0	NULL	rose water	Chemical	volatiles of	composed of 					citronellol 	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The major components of rose water volatiles obtained from the bud , half bloom and full bloom stages of cultivar ` Ranisahiba ' were phenyl ethyl alcohol ( 66.2-79 .0 % ) , geraniol ( 3.3-6 .6 % ) and citronellol ( 1.8-5 .5 % ) .	manualset1
81777	1	387492	11	NULL	NULL	0	NULL	triathlon	Process		contains					running stage	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The major decrease in plasma volume was during the running stage of the triathlon during which it decreased by 6.2 % + / - 1.7 % , of which 3.0 % + / - 1.8 % was attributable to exercise alone .	manualset1
81778	2	387492	11	NULL	NULL	0	NULL	statement 1	Process		reduces					volume	Quantity	plasma			NULL		0	NULL	NULL	NULL	NULL	NULL	The major decrease in plasma volume was during the running stage of the triathlon during which it decreased by 6.2 % + / - 1.7 % , of which 3.0 % + / - 1.8 % was attributable to exercise alone .	manualset1
81779	1	387494	11	NULL	NULL	0	NULL	silty sediment 	EnvironmentalFactor		is rich in					omega-3 PUFAs	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The major difference in the fatty acid composition of M. plumulosa cultured on silty sediment compared to amphipods cultured on a sand substrate and both fed Sera micron was an increase in the ratio of omega-3 to omega-6 PUFAs , indicating that the silty sediment provides additional food sources rich in omega-3 PUFAs .	manualset1
81780	1	387495	11	NULL	NULL	0	NULL	transplantation immunology	MedicalProcedureOrDevice		aims on					allograft transplants	AnatomicalPart	tolerance to			NULL		0	NULL	NULL	NULL	NULL	NULL	The major goal of transplantation immunology is to develop tolerance to allograft transplants and long-term drug-free survival .	manualset1
81781	2	387495	11	NULL	NULL	0	NULL	transplantation immunology	MedicalProcedureOrDevice		aims on					drug-free survival	BiologicalProcess	long-term			NULL		0	NULL	NULL	NULL	NULL	NULL	The major goal of transplantation immunology is to develop tolerance to allograft transplants and long-term drug-free survival .	manualset1
81782	1	387496	11	NULL	NULL	0	NULL	trauma	MedicalFinding		is an indication for					amputation	MedicalFinding	upper limb			NULL		0	NULL	NULL	NULL	NULL	NULL	The major indication for upper limb amputation was trauma and post-fracture splintage gangrene ( 57 % ) .	manualset1
81783	2	387496	11	NULL	NULL	0	NULL	splintage gangrene	MedicalFinding	post-fracture	is an indication for					amputation	MedicalFinding	upper limb			NULL		0	NULL	NULL	NULL	NULL	NULL	The major indication for upper limb amputation was trauma and post-fracture splintage gangrene ( 57 % ) .	manualset1
81785	1	387504	11	NULL	NULL	0	NULL	 emphysema	MedicalFinding		is a type of 					lung disease	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	The major underlying lung diseases associated with SSP were emphysema ( 22 patients ) and tuberculosis ( 21 patients ) .	manualset1
81786	2	387504	11	NULL	NULL	0	NULL	tuberculosis	MedicalFinding		is a type of 					lung disease	Disease				NULL		0	NULL	NULL	NULL	NULL	NULL	The major underlying lung diseases associated with SSP were emphysema ( 22 patients ) and tuberculosis ( 21 patients ) .	manualset1
81787	3	387504	11	NULL	NULL	0	NULL	emphysema 	MedicalFinding		is associated with					SSP	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The major underlying lung diseases associated with SSP were emphysema ( 22 patients ) and tuberculosis ( 21 patients ) .	manualset1
81788	4	387504	11	NULL	NULL	0	NULL	tuberculosis	MedicalFinding		is associated with					SSP	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The major underlying lung diseases associated with SSP were emphysema ( 22 patients ) and tuberculosis ( 21 patients ) .	manualset1
81789	1	387506	11	NULL	NULL	0	NULL	compounds	Chemical		transport					membrane	CellComponent	across			NULL		0	NULL	NULL	NULL	NULL	NULL	The majority of ABC domains energize the transport of compounds across the membranes .	manualset1
81790	2	387506	11	NULL	NULL	0	NULL	ABC domain	PartOfProtein		energize					statement 1	Process				NULL		0	NULL	NULL	NULL	NULL	NULL	The majority of ABC domains energize the transport of compounds across the membranes .	manualset1
81791	1	387507	11	NULL	NULL	0	NULL	IC neurons	cell		increases					action potential	Process	current-evoked			NULL		0	NULL	NULL	NULL	NULL	NULL	The majority of IC neurons ( 66 % ) displayed an increase in current-evoked action potentials ( Positive Gain ) .	manualset1
81792	1	387508	11	NULL	NULL	0	NULL	human gene	Gene	majority	are conserved among					mammals	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	The majority of human genes are conserved among mammals , but some gene families have undergone extensive expansion in particular lineages .	manualset1
81793	1	387509	11	NULL	NULL	0	NULL	squamous cell carcinoma	MedicalFinding	majority	is a type of 					tumor	MedicalFinding	induced			NULL		0	NULL	NULL	NULL	NULL	NULL	The majority of induced tumors were squamous cell carcinomas .	manualset1
81794	1	387515	11	NULL	NULL	0	NULL	ANAE	Protein		are active in					membrane	CellComponent	lymphocytes			NULL		0	NULL	NULL	NULL	NULL	NULL	The majority of the ANAE activity in lymphocytes was found to be membrane bound .	manualset1
81795	1	387516	11	NULL	NULL	NULL	NULL	Golgi tendon organ	AnatomicalPart	majority of	does not produce					discharge	Chemical	spontaneous			NULL		NULL	NULL	NULL	NULL	NULL	NULL	The majority of the Golgi tendon organs , pressure receptors , and the elementary dynamic and static receptors of the muscle spindles did not produce spontaneous discharges .	manualset1
81796	2	387516	11	NULL	NULL	NULL	NULL	pressure receptor	AnatomicalPart	majority	does not produce					discharge	Chemical	spontaneous			NULL		NULL	NULL	NULL	NULL	NULL	NULL	The majority of the Golgi tendon organs , pressure receptors , and the elementary dynamic and static receptors of the muscle spindles did not produce spontaneous discharges .	manualset1
81797	3	387516	11	NULL	NULL	NULL	NULL	dynamic receptor	AnatomicalPart	muscle spindles	does not produce					discharge	Chemical	spontaneous			NULL		NULL	NULL	NULL	NULL	NULL	NULL	The majority of the Golgi tendon organs , pressure receptors , and the elementary dynamic and static receptors of the muscle spindles did not produce spontaneous discharges .	manualset1
81798	4	387516	11	NULL	NULL	NULL	NULL	static receptor	AnatomicalPart	muscle spindles	does not produce					discharge	Chemical	spontaneous			NULL		NULL	NULL	NULL	NULL	NULL	NULL	The majority of the Golgi tendon organs , pressure receptors , and the elementary dynamic and static receptors of the muscle spindles did not produce spontaneous discharges .	manualset1
81799	1	387518	11	NULL	NULL	0	NULL	Bacillus	Organism		is a type of 					bacteria	Organism	airborne			NULL		0	NULL	NULL	NULL	NULL	NULL	The majority of the airborne bacteria belonged to the genera Bacillus , Micrococcus , and Staphylococcus , but a total of 37 different genera were identified in the air .	manualset1
81800	2	387518	11	NULL	NULL	0	NULL	Micrococcus	Organism		is a type of 					bacteria	Organism	airborne			NULL		0	NULL	NULL	NULL	NULL	NULL	The majority of the airborne bacteria belonged to the genera Bacillus , Micrococcus , and Staphylococcus , but a total of 37 different genera were identified in the air .	manualset1
81801	3	387518	11	NULL	NULL	0	NULL	Staphylococcus	Organism		is a type of 					bacteria	Organism	airborne			NULL		0	NULL	NULL	NULL	NULL	NULL	The majority of the airborne bacteria belonged to the genera Bacillus , Micrococcus , and Staphylococcus , but a total of 37 different genera were identified in the air .	manualset1
81802	1	387524	11	NULL	NULL	0	NULL	gastric ulcer	MedicalFinding	coexisting	occurres in					pyloric gland area	AnatomicalPart	antrofundic border			NULL		0	NULL	NULL	NULL	NULL	NULL	The majority of these coexisting gastric ulcers occurred in the pyloric gland area adjacent to the antrofundic border , and all the duodenal ulcers in the proximal duodenum .	manualset1
81803	2	387524	11	NULL	NULL	0	NULL	duodenal ulcers	MedicalFinding		occurred in					duodenum	AnatomicalPart	proximal 			NULL		0	NULL	NULL	NULL	NULL	NULL	The majority of these coexisting gastric ulcers occurred in the pyloric gland area adjacent to the antrofundic border , and all the duodenal ulcers in the proximal duodenum .	manualset1
81804	1	387525	11	NULL	NULL	0	NULL	teratomas	MedicalFinding	majority	are					solid	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The majority of these teratomas are solid or mixed cystic and solid external caudal masses .	manualset1
81805	2	387525	11	NULL	NULL	0	NULL	teratomas	MedicalFinding	majority of	are					cystic	MedicalFinding	mixed			NULL		0	NULL	NULL	NULL	NULL	NULL	The majority of these teratomas are solid or mixed cystic and solid external caudal masses .	manualset1
81806	3	387525	11	NULL	NULL	0	NULL	statement 1	MedicalFinding		is an alternative to					statement 2	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The majority of these teratomas are solid or mixed cystic and solid external caudal masses .	manualset1
81807	4	387525	11	NULL	NULL	0	NULL	teratomas	MedicalFinding	majority of	have					solid caudal mass	AnatomicalPart	external 			NULL		0	NULL	NULL	NULL	NULL	NULL	The majority of these teratomas are solid or mixed cystic and solid external caudal masses .	manualset1
81808	1	387528	11	NULL	NULL	0	NULL	deformities	MedicalFinding	vertebral 	are					asymptomatic	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The majority of vertebral deformities are asymptomatic and thus definition is normally based on radiographic appearance .	manualset1
81810	1	387532	11	NULL	NULL	0	NULL	lethality	BiologicalProcess	male	is suppressed by					mutations	MolecularProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	The male lethality is suppressed by mutations that force all animals into the XO mode of both processes .	manualset1
81811	1	387535	11	NULL	NULL	0	NULL	malignant cells	cell		can avoid initiation of 					Mvarphi	Cell				NULL		0	NULL	NULL	NULL	NULL	NULL	The malignant cells can thereby avoid initiation of potentially dangerous Mvarphi functions and create favorable conditions for tumor progression .	manualset1
81814	2	387535	11	NULL	NULL	0	NULL	statement 1	Process		is favorable for					tumor progression	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	The malignant cells can thereby avoid initiation of potentially dangerous Mvarphi functions and create favorable conditions for tumor progression .	manualset1
81816	1	387541	11	NULL	NULL	0	NULL	bone graft	MedicalProcedureOrDevice	iliac crest	widened					manubrium	AnatomicalPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The manubrium was widened using an iliac crest bone graft , stabilised using internal fixation plates and reconstructed with a pectoral muscle flap .	manualset1
81850	1	387544	11	NULL	NULL	0	NULL	Dysidea avara	Organism		is a type of					marine sponge	Organism				NULL		0	NULL	NULL	NULL	NULL	NULL	The marine sponge Dysidea avara contained avarol ( 1 ) and avarone ( 2 ) .	manualset1
81851	2	387544	11	NULL	NULL	0	NULL	Dysidea avara	Organism		contains					avarol	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The marine sponge Dysidea avara contained avarol ( 1 ) and avarone ( 2 ) .	manualset1
81852	3	387544	11	NULL	NULL	0	NULL	Dysidea avara	Organism		contains					avarone	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The marine sponge Dysidea avara contained avarol ( 1 ) and avarone ( 2 ) .	manualset1
81853	1	387549	11	NULL	NULL	0	NULL	lymphocytic choriomeningitis virus	Organism		causes					massive inflammation	MedicalFinding	cerebrospinal fluid;;adult mice			NULL		0	NULL	NULL	NULL	NULL	NULL	The massive inflammation of the cerebrospinal fluid ( CSF ) which occurs in adult mice injected with lymphocytic choriomeningitis virus ( LCMV ) has been analyzed by flow microfluorometry ( FMF ) .	manualset1
81854	1	387552	11	NULL	NULL	0	NULL	humerus 	AnatomicalPart		has more strength than		material			tibiotarsus	AnatomicalPart				NULL		0	NULL	NULL	NULL	NULL	NULL	The material strength of the humerus was greater than the tibiotarsus ; this difference in strength was reflected in both the collagen and mineral matrix biochemistry .	manualset1
81855	1	387554	11	NULL	NULL	0	NULL	 immune response	BiologicalProcess	maternal	effects					 platelet GPIb	CellComponent	fetal			NULL		0	NULL	NULL	NULL	NULL	NULL	The maternal immune response to fetal platelet GPIb causes frequent miscarriage in mice that can be prevented by intravenous IgG and anti-FcRn therapies .	manualset1
81856	2	387554	11	NULL	NULL	0	NULL	statement 1	process		causes					miscarriage	BiologicalProcess	 mice			NULL		0	NULL	NULL	NULL	NULL	NULL	The maternal immune response to fetal platelet GPIb causes frequent miscarriage in mice that can be prevented by intravenous IgG and anti-FcRn therapies .	manualset1
81857	3	387554	11	NULL	NULL	0	NULL	IgG	Protein	intravenous	treats					miscarriage	BiologicalProcess	mice			NULL		0	NULL	NULL	NULL	NULL	NULL	The maternal immune response to fetal platelet GPIb causes frequent miscarriage in mice that can be prevented by intravenous IgG and anti-FcRn therapies .	manualset1
81858	1	387559	11	NULL	NULL	0	NULL	VSV G protein	Protein	wild-type;;mature	is a					trimer	Protein	noncovalently associated			NULL		0	NULL	NULL	NULL	NULL	NULL	The mature wild-type VSV G protein is a noncovalently associated trimer .	manualset1
81859	1	387560	11	NULL	NULL	0	NULL	mau gene cluster	Gene		encode 					mauJ product	PartOfProtein	polypeptide			NULL		0	NULL	NULL	NULL	NULL	NULL	The mauJ product is the only polypeptide encoded by the mau gene cluster which is predicted to be cytoplasmic .	manualset1
81860	1	387561	11	NULL	NULL	0	NULL	maxillary tuberosity region	AnatomicalPart		is involved in					preprosthetic surgery	MedicalProcedureOrDevice				NULL		0	NULL	NULL	NULL	NULL	NULL	The maxillary tuberosity region is becoming increasingly involved in preprosthetic surgery as part of a comprehensive implant treatment planning .	manualset1
81861	1	387595	11	NULL	NULL	0	NULL	 Maalox 	NonProteinOrNucleicAcidChemical		produces 					bilesalt	chemical	less			NULL		0	NULL	NULL	NULL	NULL	NULL	The mean bile salt concentration of those treated with Maalox ( 0.24 mM ) , Meciadanol ( 0.24 mM ) , or sucralfate ( 0.35 mM ) was significantly lower than those treated with nasogastric aspiration ( 0.87 mM ) alone ( P less than 0.01 ) .	manualset1
81862	2	387595	11	NULL	NULL	0	NULL	Meciadanol	NonProteinOrNucleicAcidChemical		produces					bilesalt	chemical	less			NULL		0	NULL	NULL	NULL	NULL	NULL	The mean bile salt concentration of those treated with Maalox ( 0.24 mM ) , Meciadanol ( 0.24 mM ) , or sucralfate ( 0.35 mM ) was significantly lower than those treated with nasogastric aspiration ( 0.87 mM ) alone ( P less than 0.01 ) .	manualset1
81863	3	387595	11	NULL	NULL	0	NULL	sucralfate	NonProteinOrNucleicAcidChemical		produces					bilesalt	chemical	less			NULL		0	NULL	NULL	NULL	NULL	NULL	The mean bile salt concentration of those treated with Maalox ( 0.24 mM ) , Meciadanol ( 0.24 mM ) , or sucralfate ( 0.35 mM ) was significantly lower than those treated with nasogastric aspiration ( 0.87 mM ) alone ( P less than 0.01 ) .	manualset1
81864	4	387595	11	NULL	NULL	0	NULL	nasogastric aspiration	AnatomicalPart		produces					bilesalt	chemical	more			NULL		0	NULL	NULL	NULL	NULL	NULL	The mean bile salt concentration of those treated with Maalox ( 0.24 mM ) , Meciadanol ( 0.24 mM ) , or sucralfate ( 0.35 mM ) was significantly lower than those treated with nasogastric aspiration ( 0.87 mM ) alone ( P less than 0.01 ) .	manualset1
81865	1	387611	11	NULL	NULL	0	NULL	FSH	chemical	high	higher the severity of					liver cirrhosis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The mean percentage increase of FSH and LH was higher the greater the severity of liver cirrhosis .	manualset1
81866	2	387611	11	NULL	NULL	0	NULL	LH	chemical	high	higher the severity of					liver cirrhosis	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The mean percentage increase of FSH and LH was higher the greater the severity of liver cirrhosis .	manualset1
81867	1	387620	11	NULL	NULL	0	NULL	 infection	MedicalFinding	central nervous system	onsets 					epilepsy	MedicalFinding				NULL		0	NULL	NULL	NULL	NULL	NULL	The mean time of onset of epilepsy after central nervous system infection was 1.4 + / - 0.9 years ( range 0-19 years ) .	manualset1
81868	1	387626	11	NULL	NULL	0	NULL	measles-mumps-rubella vaccine 	MedicalProcedureOrDevice		has					biosafety	BiologicalProcess	high			NULL		0	NULL	NULL	NULL	NULL	NULL	The measles-mumps-rubella ( MMR ) vaccine has been very effective in the elimination of disease and has high biosafety .	manualset1
81869	2	387626	11	NULL	NULL	0	NULL	measles-mumps-rubella	MedicalProcedureOrDevice		is					MMR	MedicalProcedureOrDevice				NULL		0	NULL	NULL	NULL	NULL	NULL	The measles-mumps-rubella ( MMR ) vaccine has been very effective in the elimination of disease and has high biosafety .	manualset1
81870	1	387641	11	NULL	NULL	0	NULL	phosphate	NonProteinOrNucleicAcidChemical	intestine	transports via					proton symporter	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	The mechanism of the transport of phosphate in the intestine is via a proton symporter whilst in the parotid gland it is effected by a Na + coupled transporter .	manualset1
81871	2	387641	11	NULL	NULL	0	NULL	phosphate	NonProteinOrNucleicAcidChemical	parotid gland	transports via					Na + coupled transporter	Protein				NULL		0	NULL	NULL	NULL	NULL	NULL	The mechanism of the transport of phosphate in the intestine is via a proton symporter whilst in the parotid gland it is effected by a Na + coupled transporter .	manualset1
81873	1	387642	11	NULL	NULL	0	NULL	12-O-tetradecanoylphorbol 13-acetate	NonProteinOrNucleicAcidChemical		induces					 inflammation	BiologicalProcess	psoriasis-like			NULL		0	NULL	NULL	NULL	NULL	NULL	The mechanism underlying this increased sensitivity of Pglyrp2 ( - / - ) mice to 12-O-tetradecanoylphorbol 13-acetate-induced psoriasis-like inflammation is reduced recruitment of regulatory T cells to the skin and enhanced production and activation of Th17 cells in the skin in Pglyrp2 ( - / - ) mice , which results in more severe inflammation and keratinocyte proliferation .	manualset1
81874	2	387642	11	NULL	NULL	0	NULL	Pglyrp2 ( - / - ) mice	Organism		is sensitivity to					statement 1	process				NULL		0	NULL	NULL	NULL	NULL	NULL	The mechanism underlying this increased sensitivity of Pglyrp2 ( - / - ) mice to 12-O-tetradecanoylphorbol 13-acetate-induced psoriasis-like inflammation is reduced recruitment of regulatory T cells to the skin and enhanced production and activation of Th17 cells in the skin in Pglyrp2 ( - / - ) mice , which results in more severe inflammation and keratinocyte proliferation .	manualset1
81875	3	387642	11	NULL	NULL	0	NULL	T cells	cell	regulatory 	recruited to					skin 	Body part				NULL		0	NULL	NULL	NULL	NULL	NULL	The mechanism underlying this increased sensitivity of Pglyrp2 ( - / - ) mice to 12-O-tetradecanoylphorbol 13-acetate-induced psoriasis-like inflammation is reduced recruitment of regulatory T cells to the skin and enhanced production and activation of Th17 cells in the skin in Pglyrp2 ( - / - ) mice , which results in more severe inflammation and keratinocyte proliferation .	manualset1
81876	4	387642	11	NULL	NULL	0	NULL	statement 3	BiologicalProcess		produces					Th17 cells	cells	skin			NULL	Pglyrp2 ( - / - ) mice	0	NULL	NULL	NULL	NULL	NULL	The mechanism underlying this increased sensitivity of Pglyrp2 ( - / - ) mice to 12-O-tetradecanoylphorbol 13-acetate-induced psoriasis-like inflammation is reduced recruitment of regulatory T cells to the skin and enhanced production and activation of Th17 cells in the skin in Pglyrp2 ( - / - ) mice , which results in more severe inflammation and keratinocyte proliferation .	manualset1
81877	5	387642	11	NULL	NULL	0	NULL	statement 3	BiologicalProcess		activates					Th17 cell	cells	skin			NULL	Pglyrp2 ( - / - ) mice	0	NULL	NULL	NULL	NULL	NULL	The mechanism underlying this increased sensitivity of Pglyrp2 ( - / - ) mice to 12-O-tetradecanoylphorbol 13-acetate-induced psoriasis-like inflammation is reduced recruitment of regulatory T cells to the skin and enhanced production and activation of Th17 cells in the skin in Pglyrp2 ( - / - ) mice , which results in more severe inflammation and keratinocyte proliferation .	manualset1
81878	6	387642	11	NULL	NULL	0	NULL	statement 4	BiologicalProcess		occurs along with					statement 5	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	The mechanism underlying this increased sensitivity of Pglyrp2 ( - / - ) mice to 12-O-tetradecanoylphorbol 13-acetate-induced psoriasis-like inflammation is reduced recruitment of regulatory T cells to the skin and enhanced production and activation of Th17 cells in the skin in Pglyrp2 ( - / - ) mice , which results in more severe inflammation and keratinocyte proliferation .	manualset1
81879	7	387642	11	NULL	NULL	0	NULL	statement 6	BiologicalProcess		results in					inflammation	BiologicalProcess	severe			NULL		0	NULL	NULL	NULL	NULL	NULL	The mechanism underlying this increased sensitivity of Pglyrp2 ( - / - ) mice to 12-O-tetradecanoylphorbol 13-acetate-induced psoriasis-like inflammation is reduced recruitment of regulatory T cells to the skin and enhanced production and activation of Th17 cells in the skin in Pglyrp2 ( - / - ) mice , which results in more severe inflammation and keratinocyte proliferation .	manualset1
81880	8	387642	11	NULL	NULL	0	NULL	statement 6	BiologicalProcess		results in					proliferation	BiologicalProcess	keratinocyte 			NULL		0	NULL	NULL	NULL	NULL	NULL	The mechanism underlying this increased sensitivity of Pglyrp2 ( - / - ) mice to 12-O-tetradecanoylphorbol 13-acetate-induced psoriasis-like inflammation is reduced recruitment of regulatory T cells to the skin and enhanced production and activation of Th17 cells in the skin in Pglyrp2 ( - / - ) mice , which results in more severe inflammation and keratinocyte proliferation .	manualset1
81881	1	387644	11	NULL	NULL	0	NULL	electrotransfer	MolecularProcess	DNA	include					electropermeabilization	MolecularProcess	cell			NULL		0	NULL	NULL	NULL	NULL	NULL	The mechanisms involved in DNA electrotransfer , which include cell electropermeabilization and DNA electrophoresis , are also surveyed .	manualset1
81882	2	387644	11	NULL	NULL	0	NULL	electrotransfer	MolecularProcess	DNA	include					electrophoresis	MolecularProcess	DNA			NULL		0	NULL	NULL	NULL	NULL	NULL	The mechanisms involved in DNA electrotransfer , which include cell electropermeabilization and DNA electrophoresis , are also surveyed .	manualset1
81887	1	387668	11	NULL	NULL	0	NULL	melanocortin-1 receptor gene	Gene		undergoes					polymorphism	BiologicalProcess				NULL		0	NULL	NULL	NULL	NULL	NULL	The melanocortin-1 receptor gene polymorphism and association with human skin cancer .	manualset1
81889	2	387668	11	NULL	NULL	0	NULL	statement 1	BiologicalProcess		associated with		may			skin cancer	MedicalFinding	human			NULL		0	NULL	NULL	NULL	NULL	NULL	The melanocortin-1 receptor gene polymorphism and association with human skin cancer .	manualset1
81890	1	387669	11	NULL	NULL	0	NULL	regulators of G-protein signaling	Protein		act as					GTPase-activating protein	Protein	Galpha subunit;;in vitro			NULL		0	NULL	NULL	NULL	NULL	NULL	The members of a recently identified protein family termed regulators of G-protein signaling ( RGS ) act as GTPase-activating proteins for certain Galpha subunits in vitro , but their physiological effects in cells are uncertain in the face of similar biochemical activity and overlapping patterns of tissue expression .	manualset1
81891	1	387670	11	NULL	NULL	0	NULL	humidifier	Chemical	membrane	produces					humidification	MolecularProcess	good			NULL		0	NULL	NULL	NULL	NULL	NULL	The membrane humidifier could produce good humidification .	manualset1
81892	1	387676	11	NULL	NULL	0	NULL	messenger RNA	NucleicAcid	outer membrane protein	are more stable than					messenger RNA	NucleicAcid	bulk of			NULL	 E. coli 	0	NULL	NULL	NULL	NULL	NULL	The messenger RNAs for the outer membrane proteins in E. coli are more stable than the bulk of the messenger RNA s ( Hirashima et al. , 1973 ) .	manualset1
81894	1	387682	11	NULL	NULL	0	NULL	phenobarbital	NonProteinOrNucleicAcidChemical		induce					microsomes	CellComponent	rat liver 			NULL		0	NULL	NULL	NULL	NULL	NULL	The metabolism of Odapipam has been studied with phenobarbital-induced rat liver microsomes , followed by analysis with normal-phase hplc in combination with particle-beam mass spectrometry .	manualset1
81895	1	387683	11	NULL	NULL	0	NULL	rat	Organism		metabolise					pteroylglutamic acid	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The metabolism of pteroylglutamic acid by the rat .	manualset1
81896	1	387688	11	NULL	NULL	0	NULL	metal sites	CellComponent	sarcoplasmic reticulum membrane	bind		highest affinity			lanthanide ions	Ion				NULL		0	NULL	NULL	NULL	NULL	NULL	The metal sites on sarcoplasmic reticulum membranes that bind lanthanide ions with the highest affinity are not the ATPase Ca2 + transport sites .	manualset1
81902	1	387743	11	NULL	NULL	0	NULL	methoxy methyl group	NonProteinOrNucleicAcidChemical	MTBE	 oxidized to					formaldehyde	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The methoxy methyl group of MTBE was oxidized to formaldehyde and ultimately to CO2 .	manualset1
81903	2	387743	11	NULL	NULL	0	NULL	formaldehyde	NonProteinOrNucleicAcidChemical		converted into					CO2	NonProteinOrNucleicAcidChemical				NULL		0	NULL	NULL	NULL	NULL	NULL	The methoxy methyl group of MTBE was oxidized to formaldehyde and ultimately to CO2 .	manualset1
81904	1	387744	11	NULL	NULL	0	NULL	methyl substitution	MolecularProcess	C9;;C10	increased the expression of					T antigen	Protein	adenovirus infected cells			NULL		0	NULL	NULL	NULL	NULL	NULL	The methyl substitution at positions C9 or C10 increased the T antigen expression of adenovirus infected cells .	manualset1
81905	1	387745	11	NULL	NULL	0	NULL	mice	Organism	early postnatal	sensitive to					radiation	EnvironmentalFactor				NULL		0	NULL	NULL	NULL	NULL	NULL	The mice in the early postnatal period were most sensitive to the life-shortening effect of radiation .	manualset1
82033	1	397631	5	NULL	NULL	NULL	NULL	( NHC ) AuCl ) complexes	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( ( NHC ) AuCl ) complexes ( NHC = N-heterocyclic carbene ) , in conjunction with a silver salt , were found to efficiently catalyze the rearrangement of allylic acetates under both conventional and microwave-assisted heating .
	manualset2
82035	3	397631	5	NULL	NULL	NULL	NULL	N-heterocyclic carbene	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( ( NHC ) AuCl ) complexes ( NHC = N-heterocyclic carbene ) , in conjunction with a silver salt , were found to efficiently catalyze the rearrangement of allylic acetates under both conventional and microwave-assisted heating .
	manualset2
82036	4	397631	5	NULL	NULL	NULL	NULL	silver salt	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( ( NHC ) AuCl ) complexes ( NHC = N-heterocyclic carbene ) , in conjunction with a silver salt , were found to efficiently catalyze the rearrangement of allylic acetates under both conventional and microwave-assisted heating .
	manualset2
82037	5	397631	5	NULL	NULL	0	NULL	rearrangement	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( ( NHC ) AuCl ) complexes ( NHC = N-heterocyclic carbene ) , in conjunction with a silver salt , were found to efficiently catalyze the rearrangement of allylic acetates under both conventional and microwave-assisted heating .
	manualset2
82038	6	397631	5	NULL	NULL	NULL	NULL	allylic acetates	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( ( NHC ) AuCl ) complexes ( NHC = N-heterocyclic carbene ) , in conjunction with a silver salt , were found to efficiently catalyze the rearrangement of allylic acetates under both conventional and microwave-assisted heating .
	manualset2
82039	7	397631	5	NULL	NULL	0	NULL	heating	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	( ( NHC ) AuCl ) complexes ( NHC = N-heterocyclic carbene ) , in conjunction with a silver salt , were found to efficiently catalyze the rearrangement of allylic acetates under both conventional and microwave-assisted heating .
	manualset2
82547	2	397631	5	NULL	NULL	0	NULL	NHC	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	( ( NHC ) AuCl ) complexes ( NHC = N-heterocyclic carbene ) , in conjunction with a silver salt , were found to efficiently catalyze the rearrangement of allylic acetates under both conventional and microwave-assisted heating .
	manualset2
82040	1	397632	5	NULL	NULL	0	NULL	Germapect	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( 1st experiences with the antitussive Germapect in the treatment of pulmonary tuberculosis ) .
	manualset2
82041	2	397632	5	NULL	NULL	NULL	NULL	treatment	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( 1st experiences with the antitussive Germapect in the treatment of pulmonary tuberculosis ) .
	manualset2
82042	3	397632	5	NULL	NULL	NULL	NULL	pulmonary tuberculosis	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( 1st experiences with the antitussive Germapect in the treatment of pulmonary tuberculosis ) .
	manualset2
82043	1	397633	5	NULL	NULL	0	NULL	treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Advances in the treatment of algodystrophy ) .
	manualset2
82044	2	397633	5	NULL	NULL	0	NULL	algodystrophy	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Advances in the treatment of algodystrophy ) .
	manualset2
82045	1	397634	5	NULL	NULL	NULL	NULL	CMV DNA levels	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , CMV DNA levels were consistently higher when targeted at the smaller amplicon , providing additional evidence for the fragmentation of viral DNA .
	manualset2
82047	2	397634	5	NULL	NULL	NULL	NULL	amplicon	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , CMV DNA levels were consistently higher when targeted at the smaller amplicon , providing additional evidence for the fragmentation of viral DNA .
	manualset2
82048	3	397634	5	NULL	NULL	NULL	NULL	fragmentation	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , CMV DNA levels were consistently higher when targeted at the smaller amplicon , providing additional evidence for the fragmentation of viral DNA .
	manualset2
82049	4	397634	5	NULL	NULL	NULL	NULL	viral DNA	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , CMV DNA levels were consistently higher when targeted at the smaller amplicon , providing additional evidence for the fragmentation of viral DNA .
	manualset2
82050	1	397635	5	NULL	NULL	0	NULL	CSF	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , CSF increases in the left Sylvian fissure were negatively correlated with the reduction percentage of depressive symptoms at discharge .
	manualset2
82051	2	397635	5	NULL	NULL	NULL	NULL	Sylvian fissure	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , CSF increases in the left Sylvian fissure were negatively correlated with the reduction percentage of depressive symptoms at discharge .
	manualset2
82052	3	397635	5	NULL	NULL	NULL	NULL	depressive symptoms	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , CSF increases in the left Sylvian fissure were negatively correlated with the reduction percentage of depressive symptoms at discharge .
	manualset2
82053	1	397636	5	NULL	NULL	NULL	NULL	Chinese hamster	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , Chinese hamster V79 lung fibroblasts depleted of glutathione display enhanced cytotoxicity on exposure to NO. ( ABSTRACT TRUNCATED AT 250 WORDS )
	manualset2
82054	2	397636	5	NULL	NULL	NULL	NULL	V79 lung fibroblasts	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , Chinese hamster V79 lung fibroblasts depleted of glutathione display enhanced cytotoxicity on exposure to NO. ( ABSTRACT TRUNCATED AT 250 WORDS )
	manualset2
82057	3	397636	5	NULL	NULL	NULL	NULL	glutathione	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , Chinese hamster V79 lung fibroblasts depleted of glutathione display enhanced cytotoxicity on exposure to NO. ( ABSTRACT TRUNCATED AT 250 WORDS )
	manualset2
82058	4	397636	5	NULL	NULL	NULL	NULL	cytotoxicity	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , Chinese hamster V79 lung fibroblasts depleted of glutathione display enhanced cytotoxicity on exposure to NO. ( ABSTRACT TRUNCATED AT 250 WORDS )
	manualset2
82548	5	397636	5	NULL	NULL	0	NULL	exposure	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , Chinese hamster V79 lung fibroblasts depleted of glutathione display enhanced cytotoxicity on exposure to NO. ( ABSTRACT TRUNCATED AT 250 WORDS )
	manualset2
81909	1	397637	5	NULL	NULL	0	NULL	EDCL	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , EDCL did not alter the expression of bax in HepG2 cells but did selectively downregulate the expression of bcl-2 and bcl-xl , resulting in an increase in the ratio of bax : bcl-2 and bax : bcl-xl .
	manualset2
81910	3	397637	5	NULL	NULL	NULL	NULL	bax	Molecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , EDCL did not alter the expression of bax in HepG2 cells but did selectively downregulate the expression of bcl-2 and bcl-xl , resulting in an increase in the ratio of bax : bcl-2 and bax : bcl-xl .
	manualset2
81911	4	397637	5	NULL	NULL	NULL	NULL	HepG2	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , EDCL did not alter the expression of bax in HepG2 cells but did selectively downregulate the expression of bcl-2 and bcl-xl , resulting in an increase in the ratio of bax : bcl-2 and bax : bcl-xl .
	manualset2
81912	5	397637	5	NULL	NULL	NULL	NULL	bcl-2	Molecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , EDCL did not alter the expression of bax in HepG2 cells but did selectively downregulate the expression of bcl-2 and bcl-xl , resulting in an increase in the ratio of bax : bcl-2 and bax : bcl-xl .
	manualset2
81913	6	397637	5	NULL	NULL	NULL	NULL	bcl-xl	Molecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , EDCL did not alter the expression of bax in HepG2 cells but did selectively downregulate the expression of bcl-2 and bcl-xl , resulting in an increase in the ratio of bax : bcl-2 and bax : bcl-xl .
	manualset2
81954	7	397637	5	NULL	NULL	NULL	NULL	bax : bcl-2	Molecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , EDCL did not alter the expression of bax in HepG2 cells but did selectively downregulate the expression of bcl-2 and bcl-xl , resulting in an increase in the ratio of bax : bcl-2 and bax : bcl-xl .
	manualset2
81955	8	397637	5	NULL	NULL	NULL	NULL	bax : bcl-xl	Molecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , EDCL did not alter the expression of bax in HepG2 cells but did selectively downregulate the expression of bcl-2 and bcl-xl , resulting in an increase in the ratio of bax : bcl-2 and bax : bcl-xl .
	manualset2
82549	2	397637	5	NULL	NULL	0	NULL	expression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , EDCL did not alter the expression of bax in HepG2 cells but did selectively downregulate the expression of bcl-2 and bcl-xl , resulting in an increase in the ratio of bax : bcl-2 and bax : bcl-xl .
	manualset2
81914	1	397638	5	NULL	NULL	NULL	NULL	IFN-alpha	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , IFN-alpha markedly induced a 4.7-kb transcript that hybridized to a PKC-epsilon-specific , but not to a PKC-eta-specific , cDNA probe .
	manualset2
81919	3	397638	5	NULL	NULL	NULL	NULL	cDNA probe	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , IFN-alpha markedly induced a 4.7-kb transcript that hybridized to a PKC-epsilon-specific , but not to a PKC-eta-specific , cDNA probe .
	manualset2
82531	2	397638	5	NULL	NULL	NULL	NULL	4.7-kb transcript	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , IFN-alpha markedly induced a 4.7-kb transcript that hybridized to a PKC-epsilon-specific , but not to a PKC-eta-specific , cDNA probe .
	manualset2
81920	1	397639	5	NULL	NULL	NULL	NULL	L-1MT addition	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , L-1MT addition allowed C. trachomatis to undergo secondary differentiation , albeit with limited productive multiplication of the bacterium .
	manualset2
81921	2	397639	5	NULL	NULL	NULL	NULL	C. trachomatis	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , L-1MT addition allowed C. trachomatis to undergo secondary differentiation , albeit with limited productive multiplication of the bacterium .
	manualset2
81922	3	397639	5	NULL	NULL	NULL	NULL	secondary differentiation	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , L-1MT addition allowed C. trachomatis to undergo secondary differentiation , albeit with limited productive multiplication of the bacterium .
	manualset2
81923	5	397639	5	NULL	NULL	NULL	NULL	bacterium	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , L-1MT addition allowed C. trachomatis to undergo secondary differentiation , albeit with limited productive multiplication of the bacterium .
	manualset2
81956	4	397639	5	NULL	NULL	NULL	NULL	productive multiplication	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , L-1MT addition allowed C. trachomatis to undergo secondary differentiation , albeit with limited productive multiplication of the bacterium .
	manualset2
81924	1	397640	5	NULL	NULL	NULL	NULL	NKT cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , NKT cells from mice pre-challenged with alpha-GalCer in vivo showed little cytokine production and reduced proliferation in vitro .
	manualset2
81925	2	397640	5	NULL	NULL	0	NULL	mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , NKT cells from mice pre-challenged with alpha-GalCer in vivo showed little cytokine production and reduced proliferation in vitro .
	manualset2
81926	3	397640	5	NULL	NULL	NULL	NULL	alpha-GalCer	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , NKT cells from mice pre-challenged with alpha-GalCer in vivo showed little cytokine production and reduced proliferation in vitro .
	manualset2
81927	4	397640	5	NULL	NULL	NULL	NULL	cytokine production	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , NKT cells from mice pre-challenged with alpha-GalCer in vivo showed little cytokine production and reduced proliferation in vitro .
	manualset2
81928	5	397640	5	NULL	NULL	NULL	NULL	reduced proliferation	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , NKT cells from mice pre-challenged with alpha-GalCer in vivo showed little cytokine production and reduced proliferation in vitro .
	manualset2
81929	1	397641	5	NULL	NULL	0	NULL	RASSF6	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , RASSF6 is often downregulated in primary human tumors .
	manualset2
81930	2	397641	5	NULL	NULL	NULL	NULL	human tumors	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , RASSF6 is often downregulated in primary human tumors .
	manualset2
81932	1	397642	5	NULL	NULL	NULL	NULL	TLR activation	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , TLR activation is capable of modulating the adaptive immune response with a bias towards a Th1 T-cell response .
	manualset2
81935	2	397642	5	NULL	NULL	NULL	NULL	adaptive immune response	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , TLR activation is capable of modulating the adaptive immune response with a bias towards a Th1 T-cell response .
	manualset2
81936	3	397642	5	NULL	NULL	NULL	NULL	Th1 T-cell response	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , TLR activation is capable of modulating the adaptive immune response with a bias towards a Th1 T-cell response .
	manualset2
81937	2	397643	5	NULL	NULL	NULL	NULL	diabetes-induced alterations	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , Western blot data indicated that the diabetes-induced alterations in the cardiac ryanodine receptor Ca ( 2 + ) release channel 's hyperphosphorylation decreased the FKBP12 .6 protein level .
	manualset2
81938	4	397643	5	NULL	NULL	NULL	NULL	Ca ( 2 + ) release channel	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , Western blot data indicated that the diabetes-induced alterations in the cardiac ryanodine receptor Ca ( 2 + ) release channel 's hyperphosphorylation decreased the FKBP12 .6 protein level .
	manualset2
81941	5	397643	5	NULL	NULL	NULL	NULL	hyperphosphorylation	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , Western blot data indicated that the diabetes-induced alterations in the cardiac ryanodine receptor Ca ( 2 + ) release channel 's hyperphosphorylation decreased the FKBP12 .6 protein level .
	manualset2
81942	6	397643	5	NULL	NULL	NULL	NULL	FKBP12 .6 protein level	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , Western blot data indicated that the diabetes-induced alterations in the cardiac ryanodine receptor Ca ( 2 + ) release channel 's hyperphosphorylation decreased the FKBP12 .6 protein level .
	manualset2
81960	1	397643	5	NULL	NULL	NULL	NULL	Western blot data	PublishedSourceOfInformation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , Western blot data indicated that the diabetes-induced alterations in the cardiac ryanodine receptor Ca ( 2 + ) release channel 's hyperphosphorylation decreased the FKBP12 .6 protein level .
	manualset2
81961	3	397643	5	NULL	NULL	NULL	NULL	cardiac ryanodine receptor	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , Western blot data indicated that the diabetes-induced alterations in the cardiac ryanodine receptor Ca ( 2 + ) release channel 's hyperphosphorylation decreased the FKBP12 .6 protein level .
	manualset2
81943	2	397644	5	NULL	NULL	NULL	NULL	adult stem cell population	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , ablation of the adult stem cell population leads to concomitant loss of PBK/TOPK-positive cells in the SEZ .
	manualset2
81944	4	397644	5	NULL	NULL	NULL	NULL	PBK/TOPK-positive cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , ablation of the adult stem cell population leads to concomitant loss of PBK/TOPK-positive cells in the SEZ .
	manualset2
81945	5	397644	5	NULL	NULL	NULL	NULL	SEZ	AnatomicalPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , ablation of the adult stem cell population leads to concomitant loss of PBK/TOPK-positive cells in the SEZ .
	manualset2
81946	1	397644	5	NULL	NULL	NULL	NULL	ablation	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , ablation of the adult stem cell population leads to concomitant loss of PBK/TOPK-positive cells in the SEZ .
	manualset2
81963	3	397644	5	NULL	NULL	NULL	NULL	concomitant loss	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , ablation of the adult stem cell population leads to concomitant loss of PBK/TOPK-positive cells in the SEZ .
	manualset2
81947	1	397645	5	NULL	NULL	NULL	NULL	pseudo-PBs	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , abnormally large pseudo-PBs , as large as four times the normal PB sizes , were observed .
	manualset2
81965	2	397645	5	NULL	NULL	0	NULL	PB	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , abnormally large pseudo-PBs , as large as four times the normal PB sizes , were observed .
	manualset2
81948	3	397646	5	NULL	NULL	NULL	NULL	intracellular free Ca ( 2 + )	Ion												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , activation of these receptors was found to increase the steady-state level of intracellular free Ca ( 2 + ) in EECs and the frequency of beating of cardiomyocytes .
	manualset2
81949	4	397646	5	NULL	NULL	NULL	NULL	EECs	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , activation of these receptors was found to increase the steady-state level of intracellular free Ca ( 2 + ) in EECs and the frequency of beating of cardiomyocytes .
	manualset2
81967	1	397646	5	NULL	NULL	0	NULL	activation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , activation of these receptors was found to increase the steady-state level of intracellular free Ca ( 2 + ) in EECs and the frequency of beating of cardiomyocytes .
	manualset2
81968	2	397646	5	NULL	NULL	0	NULL	receptors	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , activation of these receptors was found to increase the steady-state level of intracellular free Ca ( 2 + ) in EECs and the frequency of beating of cardiomyocytes .
	manualset2
81971	5	397646	5	NULL	NULL	NULL	NULL	beating	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , activation of these receptors was found to increase the steady-state level of intracellular free Ca ( 2 + ) in EECs and the frequency of beating of cardiomyocytes .
	manualset2
82555	6	397646	5	NULL	NULL	0	NULL	cardiomyocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , activation of these receptors was found to increase the steady-state level of intracellular free Ca ( 2 + ) in EECs and the frequency of beating of cardiomyocytes .
	manualset2
81972	1	397647	5	NULL	NULL	NULL	NULL	adoptive transfer experiments	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , adoptive transfer experiments have revealed that activated liver lymphocytes may migrate to other organs to inhibit tumor growth , such as the lungs and kidneys .
	manualset2
81973	2	397647	5	NULL	NULL	NULL	NULL	activated liver lymphocytes	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , adoptive transfer experiments have revealed that activated liver lymphocytes may migrate to other organs to inhibit tumor growth , such as the lungs and kidneys .
	manualset2
81976	3	397647	5	NULL	NULL	NULL	NULL	organs	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , adoptive transfer experiments have revealed that activated liver lymphocytes may migrate to other organs to inhibit tumor growth , such as the lungs and kidneys .
	manualset2
81977	4	397647	5	NULL	NULL	NULL	NULL	tumor growth	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , adoptive transfer experiments have revealed that activated liver lymphocytes may migrate to other organs to inhibit tumor growth , such as the lungs and kidneys .
	manualset2
81979	5	397647	5	NULL	NULL	NULL	NULL	lungs	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , adoptive transfer experiments have revealed that activated liver lymphocytes may migrate to other organs to inhibit tumor growth , such as the lungs and kidneys .
	manualset2
81980	6	397647	5	NULL	NULL	NULL	NULL	kidneys	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , adoptive transfer experiments have revealed that activated liver lymphocytes may migrate to other organs to inhibit tumor growth , such as the lungs and kidneys .
	manualset2
81981	1	397648	5	NULL	NULL	0	NULL	airway remodeling	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , airway remodeling changes were significantly reduced with TSA compared to vehicle-treated mice , with fewer goblet cells ( p & lt ; 0.05 ) , less subepithelial collagen deposition ( p & lt ; 0.05 ) and attenuated airway hyperresponsiveness at the highest methacholine dose .
	manualset2
81982	2	397648	5	NULL	NULL	0	NULL	TSA	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , airway remodeling changes were significantly reduced with TSA compared to vehicle-treated mice , with fewer goblet cells ( p & lt ; 0.05 ) , less subepithelial collagen deposition ( p & lt ; 0.05 ) and attenuated airway hyperresponsiveness at the highest methacholine dose .
	manualset2
81983	3	397648	5	NULL	NULL	NULL	NULL	 vehicle-treated mice	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , airway remodeling changes were significantly reduced with TSA compared to vehicle-treated mice , with fewer goblet cells ( p & lt ; 0.05 ) , less subepithelial collagen deposition ( p & lt ; 0.05 ) and attenuated airway hyperresponsiveness at the highest methacholine dose .
	manualset2
81984	4	397648	5	NULL	NULL	0	NULL	goblet cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , airway remodeling changes were significantly reduced with TSA compared to vehicle-treated mice , with fewer goblet cells ( p & lt ; 0.05 ) , less subepithelial collagen deposition ( p & lt ; 0.05 ) and attenuated airway hyperresponsiveness at the highest methacholine dose .
	manualset2
81985	5	397648	5	NULL	NULL	NULL	NULL	subepithelial collagen deposition	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , airway remodeling changes were significantly reduced with TSA compared to vehicle-treated mice , with fewer goblet cells ( p & lt ; 0.05 ) , less subepithelial collagen deposition ( p & lt ; 0.05 ) and attenuated airway hyperresponsiveness at the highest methacholine dose .
	manualset2
81987	6	397648	5	NULL	NULL	NULL	NULL	airway hyperresponsiveness	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , airway remodeling changes were significantly reduced with TSA compared to vehicle-treated mice , with fewer goblet cells ( p & lt ; 0.05 ) , less subepithelial collagen deposition ( p & lt ; 0.05 ) and attenuated airway hyperresponsiveness at the highest methacholine dose .
	manualset2
81988	7	397648	5	NULL	NULL	NULL	NULL	methacholine	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , airway remodeling changes were significantly reduced with TSA compared to vehicle-treated mice , with fewer goblet cells ( p & lt ; 0.05 ) , less subepithelial collagen deposition ( p & lt ; 0.05 ) and attenuated airway hyperresponsiveness at the highest methacholine dose .
	manualset2
81989	1	397649	5	NULL	NULL	0	NULL	acetic acid	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , an interesting effect of acetic acid as an additive is uncovered that facilitates catalyst activation .
	manualset2
81990	2	397649	5	NULL	NULL	NULL	NULL	catalyst activation	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , an interesting effect of acetic acid as an additive is uncovered that facilitates catalyst activation .
	manualset2
81992	1	397650	5	NULL	NULL	NULL	NULL	tissue factor	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Role of tissue factor in atherothrombosis ) .
	manualset2
81993	2	397650	5	NULL	NULL	0	NULL	atherothrombosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Role of tissue factor in atherothrombosis ) .
	manualset2
81994	1	397651	5	NULL	NULL	NULL	NULL	phytohemagglutinin ( PHA ) - activated T-cell lysates	CellComponent												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , analysis of phytohemagglutinin ( PHA ) - activated T-cell lysates for LHRH by RIA demonstrated that the mean concentration of LHRH in PHA-activated T-cells increased from 45 + / - 4.5 to 64 + / - 7 pg/10 ( 6 ) cells after 24 h of culture and from 47 + / - 3.6 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.01 ) after 48 h. While the LHRH concentration in PHA-activated cells increased over the last 24 h of culture h from 64 + / - 7 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.001 ) , there was no change in mean concentration of LHRH in T-cells kept in medium alone .
	manualset2
81998	2	397651	5	NULL	NULL	NULL	NULL	LHRH	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , analysis of phytohemagglutinin ( PHA ) - activated T-cell lysates for LHRH by RIA demonstrated that the mean concentration of LHRH in PHA-activated T-cells increased from 45 + / - 4.5 to 64 + / - 7 pg/10 ( 6 ) cells after 24 h of culture and from 47 + / - 3.6 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.01 ) after 48 h. While the LHRH concentration in PHA-activated cells increased over the last 24 h of culture h from 64 + / - 7 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.001 ) , there was no change in mean concentration of LHRH in T-cells kept in medium alone .
	manualset2
81999	3	397651	5	NULL	NULL	NULL	NULL	RIA	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , analysis of phytohemagglutinin ( PHA ) - activated T-cell lysates for LHRH by RIA demonstrated that the mean concentration of LHRH in PHA-activated T-cells increased from 45 + / - 4.5 to 64 + / - 7 pg/10 ( 6 ) cells after 24 h of culture and from 47 + / - 3.6 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.01 ) after 48 h. While the LHRH concentration in PHA-activated cells increased over the last 24 h of culture h from 64 + / - 7 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.001 ) , there was no change in mean concentration of LHRH in T-cells kept in medium alone .
	manualset2
82000	4	397651	5	NULL	NULL	NULL	NULL	LHRH	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , analysis of phytohemagglutinin ( PHA ) - activated T-cell lysates for LHRH by RIA demonstrated that the mean concentration of LHRH in PHA-activated T-cells increased from 45 + / - 4.5 to 64 + / - 7 pg/10 ( 6 ) cells after 24 h of culture and from 47 + / - 3.6 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.01 ) after 48 h. While the LHRH concentration in PHA-activated cells increased over the last 24 h of culture h from 64 + / - 7 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.001 ) , there was no change in mean concentration of LHRH in T-cells kept in medium alone .
	manualset2
82059	6	397651	5	NULL	NULL	NULL	NULL	45 + / - 4.5 pg/10 ( 6 ) cells	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , analysis of phytohemagglutinin ( PHA ) - activated T-cell lysates for LHRH by RIA demonstrated that the mean concentration of LHRH in PHA-activated T-cells increased from 45 + / - 4.5 to 64 + / - 7 pg/10 ( 6 ) cells after 24 h of culture and from 47 + / - 3.6 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.01 ) after 48 h. While the LHRH concentration in PHA-activated cells increased over the last 24 h of culture h from 64 + / - 7 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.001 ) , there was no change in mean concentration of LHRH in T-cells kept in medium alone .
	manualset2
82060	7	397651	5	NULL	NULL	NULL	NULL	64 + / - 7 pg/10 ( 6 ) cells	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , analysis of phytohemagglutinin ( PHA ) - activated T-cell lysates for LHRH by RIA demonstrated that the mean concentration of LHRH in PHA-activated T-cells increased from 45 + / - 4.5 to 64 + / - 7 pg/10 ( 6 ) cells after 24 h of culture and from 47 + / - 3.6 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.01 ) after 48 h. While the LHRH concentration in PHA-activated cells increased over the last 24 h of culture h from 64 + / - 7 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.001 ) , there was no change in mean concentration of LHRH in T-cells kept in medium alone .
	manualset2
82062	8	397651	5	NULL	NULL	NULL	NULL	24 h	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , analysis of phytohemagglutinin ( PHA ) - activated T-cell lysates for LHRH by RIA demonstrated that the mean concentration of LHRH in PHA-activated T-cells increased from 45 + / - 4.5 to 64 + / - 7 pg/10 ( 6 ) cells after 24 h of culture and from 47 + / - 3.6 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.01 ) after 48 h. While the LHRH concentration in PHA-activated cells increased over the last 24 h of culture h from 64 + / - 7 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.001 ) , there was no change in mean concentration of LHRH in T-cells kept in medium alone .
	manualset2
82063	9	397651	5	NULL	NULL	NULL	NULL	47 + / - 3.6 pg/10 ( 6 ) cells	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , analysis of phytohemagglutinin ( PHA ) - activated T-cell lysates for LHRH by RIA demonstrated that the mean concentration of LHRH in PHA-activated T-cells increased from 45 + / - 4.5 to 64 + / - 7 pg/10 ( 6 ) cells after 24 h of culture and from 47 + / - 3.6 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.01 ) after 48 h. While the LHRH concentration in PHA-activated cells increased over the last 24 h of culture h from 64 + / - 7 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.001 ) , there was no change in mean concentration of LHRH in T-cells kept in medium alone .
	manualset2
82064	10	397651	5	NULL	NULL	NULL	NULL	117 + / - 11.8 pg/10 ( 6 ) cells	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , analysis of phytohemagglutinin ( PHA ) - activated T-cell lysates for LHRH by RIA demonstrated that the mean concentration of LHRH in PHA-activated T-cells increased from 45 + / - 4.5 to 64 + / - 7 pg/10 ( 6 ) cells after 24 h of culture and from 47 + / - 3.6 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.01 ) after 48 h. While the LHRH concentration in PHA-activated cells increased over the last 24 h of culture h from 64 + / - 7 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.001 ) , there was no change in mean concentration of LHRH in T-cells kept in medium alone .
	manualset2
82066	11	397651	5	NULL	NULL	NULL	NULL	48 h	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , analysis of phytohemagglutinin ( PHA ) - activated T-cell lysates for LHRH by RIA demonstrated that the mean concentration of LHRH in PHA-activated T-cells increased from 45 + / - 4.5 to 64 + / - 7 pg/10 ( 6 ) cells after 24 h of culture and from 47 + / - 3.6 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.01 ) after 48 h. While the LHRH concentration in PHA-activated cells increased over the last 24 h of culture h from 64 + / - 7 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.001 ) , there was no change in mean concentration of LHRH in T-cells kept in medium alone .
	manualset2
82067	12	397651	5	NULL	NULL	NULL	NULL	LHRH concentration	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , analysis of phytohemagglutinin ( PHA ) - activated T-cell lysates for LHRH by RIA demonstrated that the mean concentration of LHRH in PHA-activated T-cells increased from 45 + / - 4.5 to 64 + / - 7 pg/10 ( 6 ) cells after 24 h of culture and from 47 + / - 3.6 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.01 ) after 48 h. While the LHRH concentration in PHA-activated cells increased over the last 24 h of culture h from 64 + / - 7 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.001 ) , there was no change in mean concentration of LHRH in T-cells kept in medium alone .
	manualset2
82068	13	397651	5	NULL	NULL	NULL	NULL	PHA-activated cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , analysis of phytohemagglutinin ( PHA ) - activated T-cell lysates for LHRH by RIA demonstrated that the mean concentration of LHRH in PHA-activated T-cells increased from 45 + / - 4.5 to 64 + / - 7 pg/10 ( 6 ) cells after 24 h of culture and from 47 + / - 3.6 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.01 ) after 48 h. While the LHRH concentration in PHA-activated cells increased over the last 24 h of culture h from 64 + / - 7 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.001 ) , there was no change in mean concentration of LHRH in T-cells kept in medium alone .
	manualset2
82070	14	397651	5	NULL	NULL	NULL	NULL	24 h	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , analysis of phytohemagglutinin ( PHA ) - activated T-cell lysates for LHRH by RIA demonstrated that the mean concentration of LHRH in PHA-activated T-cells increased from 45 + / - 4.5 to 64 + / - 7 pg/10 ( 6 ) cells after 24 h of culture and from 47 + / - 3.6 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.01 ) after 48 h. While the LHRH concentration in PHA-activated cells increased over the last 24 h of culture h from 64 + / - 7 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.001 ) , there was no change in mean concentration of LHRH in T-cells kept in medium alone .
	manualset2
82071	15	397651	5	NULL	NULL	NULL	NULL	64 + / - 7 pg/10 ( 6 ) cells	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , analysis of phytohemagglutinin ( PHA ) - activated T-cell lysates for LHRH by RIA demonstrated that the mean concentration of LHRH in PHA-activated T-cells increased from 45 + / - 4.5 to 64 + / - 7 pg/10 ( 6 ) cells after 24 h of culture and from 47 + / - 3.6 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.01 ) after 48 h. While the LHRH concentration in PHA-activated cells increased over the last 24 h of culture h from 64 + / - 7 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.001 ) , there was no change in mean concentration of LHRH in T-cells kept in medium alone .
	manualset2
82072	16	397651	5	NULL	NULL	NULL	NULL	117 + / - 11.8 pg/10 ( 6 ) cells	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , analysis of phytohemagglutinin ( PHA ) - activated T-cell lysates for LHRH by RIA demonstrated that the mean concentration of LHRH in PHA-activated T-cells increased from 45 + / - 4.5 to 64 + / - 7 pg/10 ( 6 ) cells after 24 h of culture and from 47 + / - 3.6 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.01 ) after 48 h. While the LHRH concentration in PHA-activated cells increased over the last 24 h of culture h from 64 + / - 7 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.001 ) , there was no change in mean concentration of LHRH in T-cells kept in medium alone .
	manualset2
82074	17	397651	5	NULL	NULL	NULL	NULL	LHRH 	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , analysis of phytohemagglutinin ( PHA ) - activated T-cell lysates for LHRH by RIA demonstrated that the mean concentration of LHRH in PHA-activated T-cells increased from 45 + / - 4.5 to 64 + / - 7 pg/10 ( 6 ) cells after 24 h of culture and from 47 + / - 3.6 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.01 ) after 48 h. While the LHRH concentration in PHA-activated cells increased over the last 24 h of culture h from 64 + / - 7 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.001 ) , there was no change in mean concentration of LHRH in T-cells kept in medium alone .
	manualset2
82075	19	397651	5	NULL	NULL	NULL	NULL	T-cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , analysis of phytohemagglutinin ( PHA ) - activated T-cell lysates for LHRH by RIA demonstrated that the mean concentration of LHRH in PHA-activated T-cells increased from 45 + / - 4.5 to 64 + / - 7 pg/10 ( 6 ) cells after 24 h of culture and from 47 + / - 3.6 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.01 ) after 48 h. While the LHRH concentration in PHA-activated cells increased over the last 24 h of culture h from 64 + / - 7 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.001 ) , there was no change in mean concentration of LHRH in T-cells kept in medium alone .
	manualset2
82556	5	397651	5	NULL	NULL	0	NULL	PHA-activated T-cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , analysis of phytohemagglutinin ( PHA ) - activated T-cell lysates for LHRH by RIA demonstrated that the mean concentration of LHRH in PHA-activated T-cells increased from 45 + / - 4.5 to 64 + / - 7 pg/10 ( 6 ) cells after 24 h of culture and from 47 + / - 3.6 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.01 ) after 48 h. While the LHRH concentration in PHA-activated cells increased over the last 24 h of culture h from 64 + / - 7 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.001 ) , there was no change in mean concentration of LHRH in T-cells kept in medium alone .
	manualset2
82557	18	397651	5	NULL	NULL	0	NULL	T-cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , analysis of phytohemagglutinin ( PHA ) - activated T-cell lysates for LHRH by RIA demonstrated that the mean concentration of LHRH in PHA-activated T-cells increased from 45 + / - 4.5 to 64 + / - 7 pg/10 ( 6 ) cells after 24 h of culture and from 47 + / - 3.6 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.01 ) after 48 h. While the LHRH concentration in PHA-activated cells increased over the last 24 h of culture h from 64 + / - 7 to 117 + / - 11.8 pg/10 ( 6 ) cells ( P & lt ; 0.001 ) , there was no change in mean concentration of LHRH in T-cells kept in medium alone .
	manualset2
82003	2	397652	5	NULL	NULL	NULL	NULL	syndrome	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , as executive functions are thought to be spared in this syndrome , TGA provides an opportunity to examine the impact of a massive `` pure '' memory impairment on PM .
	manualset2
82004	3	397652	5	NULL	NULL	NULL	NULL	TGA	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , as executive functions are thought to be spared in this syndrome , TGA provides an opportunity to examine the impact of a massive `` pure '' memory impairment on PM .
	manualset2
82005	4	397652	5	NULL	NULL	NULL	NULL	memory impairment	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , as executive functions are thought to be spared in this syndrome , TGA provides an opportunity to examine the impact of a massive `` pure '' memory impairment on PM .
	manualset2
82006	5	397652	5	NULL	NULL	NULL	NULL	PM	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , as executive functions are thought to be spared in this syndrome , TGA provides an opportunity to examine the impact of a massive `` pure '' memory impairment on PM .
	manualset2
82550	1	397652	5	NULL	NULL	0	NULL	executive functions	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , as executive functions are thought to be spared in this syndrome , TGA provides an opportunity to examine the impact of a massive `` pure '' memory impairment on PM .
	manualset2
82008	1	397653	5	NULL	NULL	NULL	NULL	bioinformatics analysis	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , bioinformatics analysis predicted an increased significance of binding site clusters in the CRMs of h 1 , eve 1 , run 1 and ftz 1when Hkb was incorporated in the analysis , indicating that Hkb plays a direct role in these CRMs .
	manualset2
82022	2	397653	5	NULL	NULL	NULL	NULL	binding site clusters	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , bioinformatics analysis predicted an increased significance of binding site clusters in the CRMs of h 1 , eve 1 , run 1 and ftz 1when Hkb was incorporated in the analysis , indicating that Hkb plays a direct role in these CRMs .
	manualset2
82024	3	397653	5	NULL	NULL	NULL	NULL	CRMs	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , bioinformatics analysis predicted an increased significance of binding site clusters in the CRMs of h 1 , eve 1 , run 1 and ftz 1when Hkb was incorporated in the analysis , indicating that Hkb plays a direct role in these CRMs .
	manualset2
82025	4	397653	5	NULL	NULL	NULL	NULL	h 1	Gene												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , bioinformatics analysis predicted an increased significance of binding site clusters in the CRMs of h 1 , eve 1 , run 1 and ftz 1when Hkb was incorporated in the analysis , indicating that Hkb plays a direct role in these CRMs .
	manualset2
82026	5	397653	5	NULL	NULL	NULL	NULL	eve 1	Gene												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , bioinformatics analysis predicted an increased significance of binding site clusters in the CRMs of h 1 , eve 1 , run 1 and ftz 1when Hkb was incorporated in the analysis , indicating that Hkb plays a direct role in these CRMs .
	manualset2
82027	6	397653	5	NULL	NULL	NULL	NULL	run 1	Gene												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , bioinformatics analysis predicted an increased significance of binding site clusters in the CRMs of h 1 , eve 1 , run 1 and ftz 1when Hkb was incorporated in the analysis , indicating that Hkb plays a direct role in these CRMs .
	manualset2
82028	7	397653	5	NULL	NULL	NULL	NULL	ftz 1	Gene												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , bioinformatics analysis predicted an increased significance of binding site clusters in the CRMs of h 1 , eve 1 , run 1 and ftz 1when Hkb was incorporated in the analysis , indicating that Hkb plays a direct role in these CRMs .
	manualset2
82029	8	397653	5	NULL	NULL	NULL	NULL	Hkb	GeneOrProtein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , bioinformatics analysis predicted an increased significance of binding site clusters in the CRMs of h 1 , eve 1 , run 1 and ftz 1when Hkb was incorporated in the analysis , indicating that Hkb plays a direct role in these CRMs .
	manualset2
82030	9	397653	5	NULL	NULL	NULL	NULL	analysis	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , bioinformatics analysis predicted an increased significance of binding site clusters in the CRMs of h 1 , eve 1 , run 1 and ftz 1when Hkb was incorporated in the analysis , indicating that Hkb plays a direct role in these CRMs .
	manualset2
82031	10	397653	5	NULL	NULL	NULL	NULL	Hkb	GeneOrProtein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , bioinformatics analysis predicted an increased significance of binding site clusters in the CRMs of h 1 , eve 1 , run 1 and ftz 1when Hkb was incorporated in the analysis , indicating that Hkb plays a direct role in these CRMs .
	manualset2
82032	11	397653	5	NULL	NULL	NULL	NULL	CRMs	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , bioinformatics analysis predicted an increased significance of binding site clusters in the CRMs of h 1 , eve 1 , run 1 and ftz 1when Hkb was incorporated in the analysis , indicating that Hkb plays a direct role in these CRMs .
	manualset2
82009	1	397654	5	NULL	NULL	NULL	NULL	c-kit mRNA	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , c-kit mRNA and protein were down-regulated during erythroid differentiation .
	manualset2
82010	2	397654	5	NULL	NULL	NULL	NULL	c-kit protein	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , c-kit mRNA and protein were down-regulated during erythroid differentiation .
	manualset2
82012	3	397654	5	NULL	NULL	NULL	NULL	erythroid differentiation	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , c-kit mRNA and protein were down-regulated during erythroid differentiation .
	manualset2
82014	1	397655	5	NULL	NULL	NULL	NULL	carbonyl modification	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , carbonyl modification of HCNP-pp may be involved in pathophysiological alterations associated with deterioration in the learning and memory in the brain seen in SAMP8 .
	manualset2
82015	2	397655	5	NULL	NULL	0	NULL	HCNP-pp	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , carbonyl modification of HCNP-pp may be involved in pathophysiological alterations associated with deterioration in the learning and memory in the brain seen in SAMP8 .
	manualset2
82016	3	397655	5	NULL	NULL	NULL	NULL	pathophysiological alterations	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , carbonyl modification of HCNP-pp may be involved in pathophysiological alterations associated with deterioration in the learning and memory in the brain seen in SAMP8 .
	manualset2
82017	4	397655	5	NULL	NULL	0	NULL	deterioration	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , carbonyl modification of HCNP-pp may be involved in pathophysiological alterations associated with deterioration in the learning and memory in the brain seen in SAMP8 .
	manualset2
82018	5	397655	5	NULL	NULL	NULL	NULL	learning and memory	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , carbonyl modification of HCNP-pp may be involved in pathophysiological alterations associated with deterioration in the learning and memory in the brain seen in SAMP8 .
	manualset2
82020	6	397655	5	NULL	NULL	NULL	NULL	brain	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , carbonyl modification of HCNP-pp may be involved in pathophysiological alterations associated with deterioration in the learning and memory in the brain seen in SAMP8 .
	manualset2
82021	4	397655	5	NULL	NULL	NULL	NULL	SAMP8	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , carbonyl modification of HCNP-pp may be involved in pathophysiological alterations associated with deterioration in the learning and memory in the brain seen in SAMP8 .
	manualset2
82076	1	397656	5	NULL	NULL	NULL	NULL	cell surface biotinylation experiments	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , cell surface biotinylation experiments showed that - calpain was clearly detected among the cell surface proteins .
	manualset2
82079	2	397656	5	NULL	NULL	NULL	NULL	calpain	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , cell surface biotinylation experiments showed that - calpain was clearly detected among the cell surface proteins .
	manualset2
82080	3	397656	5	NULL	NULL	NULL	NULL	cell surface proteins	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , cell surface biotinylation experiments showed that - calpain was clearly detected among the cell surface proteins .
	manualset2
82083	1	397657	5	NULL	NULL	0	NULL	chemoimmunotherapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , chemoimmunotherapy containing rituximab has led to significant increases in complete response and progression-free survival rates for patients with both previously untreated and relapsed or refractory chronic lymphocytic leukemia ( CLL ) .
	manualset2
82084	2	397657	5	NULL	NULL	NULL	NULL	rituximab	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , chemoimmunotherapy containing rituximab has led to significant increases in complete response and progression-free survival rates for patients with both previously untreated and relapsed or refractory chronic lymphocytic leukemia ( CLL ) .
	manualset2
82085	3	397657	5	NULL	NULL	0	NULL	response	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , chemoimmunotherapy containing rituximab has led to significant increases in complete response and progression-free survival rates for patients with both previously untreated and relapsed or refractory chronic lymphocytic leukemia ( CLL ) .
	manualset2
82086	4	397657	5	NULL	NULL	0	NULL	progression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , chemoimmunotherapy containing rituximab has led to significant increases in complete response and progression-free survival rates for patients with both previously untreated and relapsed or refractory chronic lymphocytic leukemia ( CLL ) .
	manualset2
82087	5	397657	5	NULL	NULL	NULL	NULL	survival rates	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , chemoimmunotherapy containing rituximab has led to significant increases in complete response and progression-free survival rates for patients with both previously untreated and relapsed or refractory chronic lymphocytic leukemia ( CLL ) .
	manualset2
82088	6	397657	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , chemoimmunotherapy containing rituximab has led to significant increases in complete response and progression-free survival rates for patients with both previously untreated and relapsed or refractory chronic lymphocytic leukemia ( CLL ) .
	manualset2
82089	7	397657	5	NULL	NULL	NULL	NULL	refractory chronic lymphocytic leukemia	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , chemoimmunotherapy containing rituximab has led to significant increases in complete response and progression-free survival rates for patients with both previously untreated and relapsed or refractory chronic lymphocytic leukemia ( CLL ) .
	manualset2
82090	1	397658	5	NULL	NULL	NULL	NULL	class I-directed cytotoxicity	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , class I-directed cytotoxicity failed to develop in the absence of CD4 ( + ) T cells .
	manualset2
82091	2	397658	5	NULL	NULL	NULL	NULL	CD4 ( + ) T cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , class I-directed cytotoxicity failed to develop in the absence of CD4 ( + ) T cells .
	manualset2
82093	1	397659	5	NULL	NULL	0	NULL	co-expression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , co-expression of Pax-6 did not enhance promoter activity .
	manualset2
82094	2	397659	5	NULL	NULL	0	NULL	Pax-6	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , co-expression of Pax-6 did not enhance promoter activity .
	manualset2
82095	3	397659	5	NULL	NULL	NULL	NULL	promoter activity	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , co-expression of Pax-6 did not enhance promoter activity .
	manualset2
82097	1	397660	5	NULL	NULL	0	NULL	competition	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , competition between SMILE and the coactivator peroxisome proliferator-activated receptor ( PGC-1 ) on CREBH transactivation has been demonstrated in vitro and in vivo .
	manualset2
82098	2	397660	5	NULL	NULL	0	NULL	SMILE	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , competition between SMILE and the coactivator peroxisome proliferator-activated receptor ( PGC-1 ) on CREBH transactivation has been demonstrated in vitro and in vivo .
	manualset2
82099	3	397660	5	NULL	NULL	NULL	NULL	coactivator peroxisome proliferator-activated receptor ( PGC-1 )	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , competition between SMILE and the coactivator peroxisome proliferator-activated receptor ( PGC-1 ) on CREBH transactivation has been demonstrated in vitro and in vivo .
	manualset2
82104	8	397660	5	NULL	NULL	NULL	NULL	CREBH transactivation	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , competition between SMILE and the coactivator peroxisome proliferator-activated receptor ( PGC-1 ) on CREBH transactivation has been demonstrated in vitro and in vivo .
	manualset2
82106	1	397661	5	NULL	NULL	NULL	NULL	vitamin E	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Role of vitamin E in adaptation and stress processes in premature infants ) .
	manualset2
82107	2	397661	5	NULL	NULL	NULL	NULL	adaptation and stress processes	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Role of vitamin E in adaptation and stress processes in premature infants ) .
	manualset2
82110	3	397661	5	NULL	NULL	NULL	NULL	premature infants	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Role of vitamin E in adaptation and stress processes in premature infants ) .
	manualset2
82111	1	397662	5	NULL	NULL	NULL	NULL	dDAVP	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , dDAVP potentiated CRF and neither its own ACTH-releasing action nor its potentiation of CRF were sensitive to previous VI - or V2-receptor blockade .
	manualset2
82112	2	397662	5	NULL	NULL	0	NULL	CRF	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , dDAVP potentiated CRF and neither its own ACTH-releasing action nor its potentiation of CRF were sensitive to previous VI - or V2-receptor blockade .
	manualset2
82113	3	397662	5	NULL	NULL	NULL	NULL	ACTH-releasing action	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , dDAVP potentiated CRF and neither its own ACTH-releasing action nor its potentiation of CRF were sensitive to previous VI - or V2-receptor blockade .
	manualset2
82115	4	397662	5	NULL	NULL	NULL	NULL	potentiation of CRF	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , dDAVP potentiated CRF and neither its own ACTH-releasing action nor its potentiation of CRF were sensitive to previous VI - or V2-receptor blockade .
	manualset2
82117	5	397662	5	NULL	NULL	NULL	NULL	VI - or V2-receptor blockade	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , dDAVP potentiated CRF and neither its own ACTH-releasing action nor its potentiation of CRF were sensitive to previous VI - or V2-receptor blockade .
	manualset2
82119	1	397663	5	NULL	NULL	0	NULL	Annexin V	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , double staining with Annexin V and PI revealed that hMTERF4 knockdown increased necrosis but not apoptosis .
	manualset2
82120	2	397663	5	NULL	NULL	0	NULL	PI	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , double staining with Annexin V and PI revealed that hMTERF4 knockdown increased necrosis but not apoptosis .
	manualset2
82121	3	397663	5	NULL	NULL	NULL	NULL	hMTERF4 knockdown	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , double staining with Annexin V and PI revealed that hMTERF4 knockdown increased necrosis but not apoptosis .
	manualset2
82122	4	397663	5	NULL	NULL	NULL	NULL	necrosis	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , double staining with Annexin V and PI revealed that hMTERF4 knockdown increased necrosis but not apoptosis .
	manualset2
82123	5	397663	5	NULL	NULL	NULL	NULL	apoptosis	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , double staining with Annexin V and PI revealed that hMTERF4 knockdown increased necrosis but not apoptosis .
	manualset2
82128	1	397664	5	NULL	NULL	NULL	NULL	low-income areas	UnproperNamedGeographicalLocation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , dynamic market forces will gradually reduce the quality of care in low-income areas while both access and quality of care will be even better in high-income areas .
	manualset2
82131	2	397664	5	NULL	NULL	NULL	NULL	high-income areas	UnproperNamedGeographicalLocation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , dynamic market forces will gradually reduce the quality of care in low-income areas while both access and quality of care will be even better in high-income areas .
	manualset2
82132	1	397665	5	NULL	NULL	0	NULL	mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , each of the nonspecifically protected mice of both the BALB/c and P/J strains developed immunity to rechallenge with viable L. major .
	manualset2
82133	2	397665	5	NULL	NULL	NULL	NULL	BALB/c and P/J strains	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , each of the nonspecifically protected mice of both the BALB/c and P/J strains developed immunity to rechallenge with viable L. major .
	manualset2
82136	3	397665	5	NULL	NULL	NULL	NULL	immunity	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , each of the nonspecifically protected mice of both the BALB/c and P/J strains developed immunity to rechallenge with viable L. major .
	manualset2
82137	4	397665	5	NULL	NULL	NULL	NULL	viable L. major	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , each of the nonspecifically protected mice of both the BALB/c and P/J strains developed immunity to rechallenge with viable L. major .
	manualset2
82138	2	397666	5	NULL	NULL	NULL	NULL	Fxr-null mice	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , experiments with Fxr-null mice suggest that cholesterol feeding can down-regulate ASBT expression through a pathway independent of FXR .
	manualset2
82140	1	397666	5	NULL	NULL	0	NULL	experiments	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , experiments with Fxr-null mice suggest that cholesterol feeding can down-regulate ASBT expression through a pathway independent of FXR .
	manualset2
82141	3	397666	5	NULL	NULL	NULL	NULL	cholesterol feeding	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , experiments with Fxr-null mice suggest that cholesterol feeding can down-regulate ASBT expression through a pathway independent of FXR .
	manualset2
82142	4	397666	5	NULL	NULL	NULL	NULL	ASBT expression	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , experiments with Fxr-null mice suggest that cholesterol feeding can down-regulate ASBT expression through a pathway independent of FXR .
	manualset2
82144	5	397666	5	NULL	NULL	NULL	NULL	pathway independent of FXR	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , experiments with Fxr-null mice suggest that cholesterol feeding can down-regulate ASBT expression through a pathway independent of FXR .
	manualset2
82146	1	397667	5	NULL	NULL	NULL	NULL	low-energy conformations ( LECs )	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , from superpositions of low-energy conformations ( LECs ) of 1 , 2 , and ( S ) -6 al , it was concluded that a common binding conformation ( LEC II ; Figure 10B ) may exist and that differences in binding to the SU receptor and in the mechanism of insulin release between repaglinide and the two SUs may be due to specific hydrophobic differences .
	manualset2
82150	3	397667	5	NULL	NULL	NULL	NULL	LEC II	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , from superpositions of low-energy conformations ( LECs ) of 1 , 2 , and ( S ) -6 al , it was concluded that a common binding conformation ( LEC II ; Figure 10B ) may exist and that differences in binding to the SU receptor and in the mechanism of insulin release between repaglinide and the two SUs may be due to specific hydrophobic differences .
	manualset2
82151	4	397667	5	NULL	NULL	NULL	NULL	SU receptor	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , from superpositions of low-energy conformations ( LECs ) of 1 , 2 , and ( S ) -6 al , it was concluded that a common binding conformation ( LEC II ; Figure 10B ) may exist and that differences in binding to the SU receptor and in the mechanism of insulin release between repaglinide and the two SUs may be due to specific hydrophobic differences .
	manualset2
82153	5	397667	5	NULL	NULL	NULL	NULL	mechanism of insulin release	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , from superpositions of low-energy conformations ( LECs ) of 1 , 2 , and ( S ) -6 al , it was concluded that a common binding conformation ( LEC II ; Figure 10B ) may exist and that differences in binding to the SU receptor and in the mechanism of insulin release between repaglinide and the two SUs may be due to specific hydrophobic differences .
	manualset2
82154	6	397667	5	NULL	NULL	NULL	NULL	repaglinide	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , from superpositions of low-energy conformations ( LECs ) of 1 , 2 , and ( S ) -6 al , it was concluded that a common binding conformation ( LEC II ; Figure 10B ) may exist and that differences in binding to the SU receptor and in the mechanism of insulin release between repaglinide and the two SUs may be due to specific hydrophobic differences .
	manualset2
82155	7	397667	5	NULL	NULL	NULL	NULL	SUs	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , from superpositions of low-energy conformations ( LECs ) of 1 , 2 , and ( S ) -6 al , it was concluded that a common binding conformation ( LEC II ; Figure 10B ) may exist and that differences in binding to the SU receptor and in the mechanism of insulin release between repaglinide and the two SUs may be due to specific hydrophobic differences .
	manualset2
82551	2	397667	5	NULL	NULL	0	NULL	common binding conformation	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , from superpositions of low-energy conformations ( LECs ) of 1 , 2 , and ( S ) -6 al , it was concluded that a common binding conformation ( LEC II ; Figure 10B ) may exist and that differences in binding to the SU receptor and in the mechanism of insulin release between repaglinide and the two SUs may be due to specific hydrophobic differences .
	manualset2
82552	8	397667	5	NULL	NULL	0	NULL	hydrophobic differences	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , from superpositions of low-energy conformations ( LECs ) of 1 , 2 , and ( S ) -6 al , it was concluded that a common binding conformation ( LEC II ; Figure 10B ) may exist and that differences in binding to the SU receptor and in the mechanism of insulin release between repaglinide and the two SUs may be due to specific hydrophobic differences .
	manualset2
82156	1	397668	5	NULL	NULL	NULL	NULL	immature B cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , immature B cells have been widely shown to be hypersensitive to tolerance induction .
	manualset2
82157	2	397668	5	NULL	NULL	NULL	NULL	tolerance induction	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , immature B cells have been widely shown to be hypersensitive to tolerance induction .
	manualset2
82159	3	397669	5	NULL	NULL	NULL	NULL	rehabilitation programs	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Round table discussion : the psychological aspect of rehabilitation programs ) .
	manualset2
82553	1	397669	5	NULL	NULL	NULL	NULL	Round table discussion	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Round table discussion : the psychological aspect of rehabilitation programs ) .
	manualset2
82554	2	397669	5	NULL	NULL	0	NULL	psychological aspect	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Round table discussion : the psychological aspect of rehabilitation programs ) .
	manualset2
82160	1	397670	5	NULL	NULL	NULL	NULL	intact cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in intact cells addition of 1 mM selenate stimulated tyrosyl phosphorylation of 210 - , 170 - , 120 - , 95 - , 70 - , and 60-kDa proteins but failed to stimulate insulin receptor kinase activity , suggesting that selenate stimulated other tyrosine kinase .
	manualset2
82161	2	397670	5	NULL	NULL	NULL	NULL	addition	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in intact cells addition of 1 mM selenate stimulated tyrosyl phosphorylation of 210 - , 170 - , 120 - , 95 - , 70 - , and 60-kDa proteins but failed to stimulate insulin receptor kinase activity , suggesting that selenate stimulated other tyrosine kinase .
	manualset2
82162	3	397670	5	NULL	NULL	NULL	NULL	1 mM selenate	NonProteinOrNucleicAcidChemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in intact cells addition of 1 mM selenate stimulated tyrosyl phosphorylation of 210 - , 170 - , 120 - , 95 - , 70 - , and 60-kDa proteins but failed to stimulate insulin receptor kinase activity , suggesting that selenate stimulated other tyrosine kinase .
	manualset2
82163	4	397670	5	NULL	NULL	NULL	NULL	tyrosyl phosphorylation	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in intact cells addition of 1 mM selenate stimulated tyrosyl phosphorylation of 210 - , 170 - , 120 - , 95 - , 70 - , and 60-kDa proteins but failed to stimulate insulin receptor kinase activity , suggesting that selenate stimulated other tyrosine kinase .
	manualset2
82165	6	397670	5	NULL	NULL	NULL	NULL	stimulate	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in intact cells addition of 1 mM selenate stimulated tyrosyl phosphorylation of 210 - , 170 - , 120 - , 95 - , 70 - , and 60-kDa proteins but failed to stimulate insulin receptor kinase activity , suggesting that selenate stimulated other tyrosine kinase .
	manualset2
82166	7	397670	5	NULL	NULL	NULL	NULL	insulin receptor kinase activity	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in intact cells addition of 1 mM selenate stimulated tyrosyl phosphorylation of 210 - , 170 - , 120 - , 95 - , 70 - , and 60-kDa proteins but failed to stimulate insulin receptor kinase activity , suggesting that selenate stimulated other tyrosine kinase .
	manualset2
82170	8	397670	5	NULL	NULL	NULL	NULL	selenate	NonProteinOrNucleicAcidChemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in intact cells addition of 1 mM selenate stimulated tyrosyl phosphorylation of 210 - , 170 - , 120 - , 95 - , 70 - , and 60-kDa proteins but failed to stimulate insulin receptor kinase activity , suggesting that selenate stimulated other tyrosine kinase .
	manualset2
82171	9	397670	5	NULL	NULL	NULL	NULL	tyrosine kinase	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in intact cells addition of 1 mM selenate stimulated tyrosyl phosphorylation of 210 - , 170 - , 120 - , 95 - , 70 - , and 60-kDa proteins but failed to stimulate insulin receptor kinase activity , suggesting that selenate stimulated other tyrosine kinase .
	manualset2
82535	5	397670	5	NULL	NULL	NULL	NULL	210 - , 170 - , 120 - , 95 - , 70 - , and 60-kDa proteins	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in intact cells addition of 1 mM selenate stimulated tyrosyl phosphorylation of 210 - , 170 - , 120 - , 95 - , 70 - , and 60-kDa proteins but failed to stimulate insulin receptor kinase activity , suggesting that selenate stimulated other tyrosine kinase .
	manualset2
82173	1	397671	5	NULL	NULL	0	NULL	media	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , in media with physiological concentrations of glucose or pyruvate , A2E significantly inhibited phagocytosis .
	manualset2
82174	2	397671	5	NULL	NULL	NULL	NULL	physiological concentrations	ExperimentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in media with physiological concentrations of glucose or pyruvate , A2E significantly inhibited phagocytosis .
	manualset2
82175	3	397671	5	NULL	NULL	NULL	NULL	glucose	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in media with physiological concentrations of glucose or pyruvate , A2E significantly inhibited phagocytosis .
	manualset2
82176	4	397671	5	NULL	NULL	NULL	NULL	pyruvate	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in media with physiological concentrations of glucose or pyruvate , A2E significantly inhibited phagocytosis .
	manualset2
82177	5	397671	5	NULL	NULL	0	NULL	A2E	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , in media with physiological concentrations of glucose or pyruvate , A2E significantly inhibited phagocytosis .
	manualset2
82178	6	397671	5	NULL	NULL	0	NULL	phagocytosis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , in media with physiological concentrations of glucose or pyruvate , A2E significantly inhibited phagocytosis .
	manualset2
82179	1	397672	5	NULL	NULL	NULL	NULL	platelets and endothelial cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in platelets and endothelial cells , the enzyme activity was localized in the membrane fraction and was distinct from cytosolic glutathione-S-transferases .
	manualset2
82181	2	397672	5	NULL	NULL	NULL	NULL	enzyme activity	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in platelets and endothelial cells , the enzyme activity was localized in the membrane fraction and was distinct from cytosolic glutathione-S-transferases .
	manualset2
82183	3	397672	5	NULL	NULL	NULL	NULL	membrane fraction	CellComponent												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in platelets and endothelial cells , the enzyme activity was localized in the membrane fraction and was distinct from cytosolic glutathione-S-transferases .
	manualset2
82186	4	397672	5	NULL	NULL	NULL	NULL	cytosolic glutathione-S-transferases	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in platelets and endothelial cells , the enzyme activity was localized in the membrane fraction and was distinct from cytosolic glutathione-S-transferases .
	manualset2
82187	1	397673	5	NULL	NULL	0	NULL	response	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , in response to DNA damage , p53 and hnRNP K are recruited to the promoters of p53-responsive genes in a mutually dependent manner .
	manualset2
82188	2	397673	5	NULL	NULL	NULL	NULL	DNA damage	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in response to DNA damage , p53 and hnRNP K are recruited to the promoters of p53-responsive genes in a mutually dependent manner .
	manualset2
82190	4	397673	5	NULL	NULL	0	NULL	p53	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , in response to DNA damage , p53 and hnRNP K are recruited to the promoters of p53-responsive genes in a mutually dependent manner .
	manualset2
82191	5	397673	5	NULL	NULL	0	NULL	hnRNP K	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , in response to DNA damage , p53 and hnRNP K are recruited to the promoters of p53-responsive genes in a mutually dependent manner .
	manualset2
82192	6	397673	5	NULL	NULL	NULL	NULL	promoters of p53-responsive genes	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in response to DNA damage , p53 and hnRNP K are recruited to the promoters of p53-responsive genes in a mutually dependent manner .
	manualset2
82195	1	397674	5	NULL	NULL	NULL	NULL	S447X polymorphism	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in the case of the S447X polymorphism , 447Ter carriers had a lower postprandial response for small TRL-RP , large TRL-B48 , and small TRL-RP .
	manualset2
82197	2	397674	5	NULL	NULL	NULL	NULL	447Ter carriers	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in the case of the S447X polymorphism , 447Ter carriers had a lower postprandial response for small TRL-RP , large TRL-B48 , and small TRL-RP .
	manualset2
82198	3	397674	5	NULL	NULL	NULL	NULL	postprandial response	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in the case of the S447X polymorphism , 447Ter carriers had a lower postprandial response for small TRL-RP , large TRL-B48 , and small TRL-RP .
	manualset2
82200	4	397674	5	NULL	NULL	NULL	NULL	TRL-RP	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in the case of the S447X polymorphism , 447Ter carriers had a lower postprandial response for small TRL-RP , large TRL-B48 , and small TRL-RP .
	manualset2
82201	5	397674	5	NULL	NULL	NULL	NULL	TRL-B48	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in the case of the S447X polymorphism , 447Ter carriers had a lower postprandial response for small TRL-RP , large TRL-B48 , and small TRL-RP .
	manualset2
82202	6	397674	5	NULL	NULL	NULL	NULL	TRL-RP	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in the case of the S447X polymorphism , 447Ter carriers had a lower postprandial response for small TRL-RP , large TRL-B48 , and small TRL-RP .
	manualset2
82203	1	397675	5	NULL	NULL	NULL	NULL	vitamin E	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in the group treated with vitamin E , distinct recovery of EEG potentials at three hours after recirculation was apparent .
	manualset2
82204	2	397675	5	NULL	NULL	0	NULL	EEG	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , in the group treated with vitamin E , distinct recovery of EEG potentials at three hours after recirculation was apparent .
	manualset2
82205	3	397675	5	NULL	NULL	0	NULL	potentials	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , in the group treated with vitamin E , distinct recovery of EEG potentials at three hours after recirculation was apparent .
	manualset2
82206	4	397675	5	NULL	NULL	NULL	NULL	three hours	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in the group treated with vitamin E , distinct recovery of EEG potentials at three hours after recirculation was apparent .
	manualset2
82207	5	397675	5	NULL	NULL	0	NULL	recirculation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , in the group treated with vitamin E , distinct recovery of EEG potentials at three hours after recirculation was apparent .
	manualset2
82208	1	397676	5	NULL	NULL	NULL	NULL	p53 gene	Gene												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in the light of previous findings that the p53 gene in most UNPCs is in the wild-type configuration , mechanisms other than mutation may be responsible for stabilisation of the p53 protein in UNPCs .
	manualset2
82210	2	397676	5	NULL	NULL	NULL	NULL	UNPCs	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in the light of previous findings that the p53 gene in most UNPCs is in the wild-type configuration , mechanisms other than mutation may be responsible for stabilisation of the p53 protein in UNPCs .
	manualset2
82212	3	397676	5	NULL	NULL	NULL	NULL	mechanisms	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in the light of previous findings that the p53 gene in most UNPCs is in the wild-type configuration , mechanisms other than mutation may be responsible for stabilisation of the p53 protein in UNPCs .
	manualset2
82213	4	397676	5	NULL	NULL	NULL	NULL	mutation	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in the light of previous findings that the p53 gene in most UNPCs is in the wild-type configuration , mechanisms other than mutation may be responsible for stabilisation of the p53 protein in UNPCs .
	manualset2
82214	5	397676	5	NULL	NULL	NULL	NULL	stabilisation	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in the light of previous findings that the p53 gene in most UNPCs is in the wild-type configuration , mechanisms other than mutation may be responsible for stabilisation of the p53 protein in UNPCs .
	manualset2
82215	6	397676	5	NULL	NULL	NULL	NULL	p53 protein	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in the light of previous findings that the p53 gene in most UNPCs is in the wild-type configuration , mechanisms other than mutation may be responsible for stabilisation of the p53 protein in UNPCs .
	manualset2
82217	7	397676	5	NULL	NULL	NULL	NULL	UNPCs	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , in the light of previous findings that the p53 gene in most UNPCs is in the wild-type configuration , mechanisms other than mutation may be responsible for stabilisation of the p53 protein in UNPCs .
	manualset2
82218	1	397677	5	NULL	NULL	NULL	NULL	apple juice	Food												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , it was not possible to acidify apple juice to a pH of 2.0 to completely inhibit enzymatic browning .
	manualset2
82220	2	397677	5	NULL	NULL	NULL	NULL	pH of 2.0	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , it was not possible to acidify apple juice to a pH of 2.0 to completely inhibit enzymatic browning .
	manualset2
82223	3	397677	5	NULL	NULL	NULL	NULL	enzymatic browning	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , it was not possible to acidify apple juice to a pH of 2.0 to completely inhibit enzymatic browning .
	manualset2
82224	1	397678	5	NULL	NULL	NULL	NULL	mRNA 	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , mRNA and protein levels of E-cadherin ( CDH1 ) were decreased in siRNA microinjected blastocysts .
	manualset2
82226	3	397678	5	NULL	NULL	NULL	NULL	E-cadherin ( CDH1 )	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , mRNA and protein levels of E-cadherin ( CDH1 ) were decreased in siRNA microinjected blastocysts .
	manualset2
82228	4	397678	5	NULL	NULL	NULL	NULL	siRNA microinjected blastocysts	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , mRNA and protein levels of E-cadherin ( CDH1 ) were decreased in siRNA microinjected blastocysts .
	manualset2
82558	2	397678	5	NULL	NULL	NULL	NULL	protein 	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , mRNA and protein levels of E-cadherin ( CDH1 ) were decreased in siRNA microinjected blastocysts .
	manualset2
82230	1	397679	5	NULL	NULL	0	NULL	Rubiaceae	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Rubiaceae ) is an important component of the ayurvedic system of medicine .
	manualset2
82231	2	397679	5	NULL	NULL	NULL	NULL	important component	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Rubiaceae ) is an important component of the ayurvedic system of medicine .
	manualset2
82232	3	397679	5	NULL	NULL	NULL	NULL	ayurvedic system of medicine	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Rubiaceae ) is an important component of the ayurvedic system of medicine .
	manualset2
82236	2	397680	5	NULL	NULL	NULL	NULL	agar	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , minimal inhibitory concentration and minimal lethal concentration for different bacterial species in presence of agar were significantly lower than those observed in presence of tween 80 or ethanol .
	manualset2
82237	3	397680	5	NULL	NULL	NULL	NULL	tween 80	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , minimal inhibitory concentration and minimal lethal concentration for different bacterial species in presence of agar were significantly lower than those observed in presence of tween 80 or ethanol .
	manualset2
82238	4	397680	5	NULL	NULL	NULL	NULL	ethanol	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , minimal inhibitory concentration and minimal lethal concentration for different bacterial species in presence of agar were significantly lower than those observed in presence of tween 80 or ethanol .
	manualset2
82239	1	397680	5	NULL	NULL	NULL	NULL	bacterial species	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , minimal inhibitory concentration and minimal lethal concentration for different bacterial species in presence of agar were significantly lower than those observed in presence of tween 80 or ethanol .
	manualset2
82240	1	397681	5	NULL	NULL	NULL	NULL	mutant yeast cells	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , mutant yeast cells show increased susceptibility to a nitrosative challenge , whereas their resistance to oxidative stress is unimpaired .
	manualset2
82242	2	397681	5	NULL	NULL	NULL	NULL	increased susceptibility	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , mutant yeast cells show increased susceptibility to a nitrosative challenge , whereas their resistance to oxidative stress is unimpaired .
	manualset2
82243	3	397681	5	NULL	NULL	NULL	NULL	nitrosative challenge	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , mutant yeast cells show increased susceptibility to a nitrosative challenge , whereas their resistance to oxidative stress is unimpaired .
	manualset2
82244	4	397681	5	NULL	NULL	NULL	NULL	resistance to oxidative stress	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , mutant yeast cells show increased susceptibility to a nitrosative challenge , whereas their resistance to oxidative stress is unimpaired .
	manualset2
82246	1	397682	5	NULL	NULL	0	NULL	mutation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , mutation at the tyrosine phosphorylation site in the cytoplasmic domain of C-CAM1 did not obliterate C-CAM1 's growth suppression function , suggesting that tyrosine phosphorylation is not involved in the signal transduction pathway leading to cell growth suppression .
	manualset2
82247	2	397682	5	NULL	NULL	NULL	NULL	tyrosine phosphorylation site	PartOfProtein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , mutation at the tyrosine phosphorylation site in the cytoplasmic domain of C-CAM1 did not obliterate C-CAM1 's growth suppression function , suggesting that tyrosine phosphorylation is not involved in the signal transduction pathway leading to cell growth suppression .
	manualset2
82250	3	397682	5	NULL	NULL	NULL	NULL	cytoplasmic domain	PartOfProtein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , mutation at the tyrosine phosphorylation site in the cytoplasmic domain of C-CAM1 did not obliterate C-CAM1 's growth suppression function , suggesting that tyrosine phosphorylation is not involved in the signal transduction pathway leading to cell growth suppression .
	manualset2
82251	4	397682	5	NULL	NULL	NULL	NULL	C-CAM1	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , mutation at the tyrosine phosphorylation site in the cytoplasmic domain of C-CAM1 did not obliterate C-CAM1 's growth suppression function , suggesting that tyrosine phosphorylation is not involved in the signal transduction pathway leading to cell growth suppression .
	manualset2
82252	5	397682	5	NULL	NULL	NULL	NULL	C-CAM1	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , mutation at the tyrosine phosphorylation site in the cytoplasmic domain of C-CAM1 did not obliterate C-CAM1 's growth suppression function , suggesting that tyrosine phosphorylation is not involved in the signal transduction pathway leading to cell growth suppression .
	manualset2
82253	6	397682	5	NULL	NULL	NULL	NULL	growth suppression function	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , mutation at the tyrosine phosphorylation site in the cytoplasmic domain of C-CAM1 did not obliterate C-CAM1 's growth suppression function , suggesting that tyrosine phosphorylation is not involved in the signal transduction pathway leading to cell growth suppression .
	manualset2
82256	7	397682	5	NULL	NULL	NULL	NULL	tyrosine phosphorylation	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , mutation at the tyrosine phosphorylation site in the cytoplasmic domain of C-CAM1 did not obliterate C-CAM1 's growth suppression function , suggesting that tyrosine phosphorylation is not involved in the signal transduction pathway leading to cell growth suppression .
	manualset2
82258	8	397682	5	NULL	NULL	NULL	NULL	signal transduction pathway	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , mutation at the tyrosine phosphorylation site in the cytoplasmic domain of C-CAM1 did not obliterate C-CAM1 's growth suppression function , suggesting that tyrosine phosphorylation is not involved in the signal transduction pathway leading to cell growth suppression .
	manualset2
82259	9	397682	5	NULL	NULL	NULL	NULL	cell growth suppression	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , mutation at the tyrosine phosphorylation site in the cytoplasmic domain of C-CAM1 did not obliterate C-CAM1 's growth suppression function , suggesting that tyrosine phosphorylation is not involved in the signal transduction pathway leading to cell growth suppression .
	manualset2
82263	1	397683	5	NULL	NULL	NULL	NULL	nicotine	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , nicotine modulates cognitive networks involved in attention and learning/memory .
	manualset2
82264	2	397683	5	NULL	NULL	NULL	NULL	cognitive networks	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , nicotine modulates cognitive networks involved in attention and learning/memory .
	manualset2
82266	3	397683	5	NULL	NULL	NULL	NULL	attention	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , nicotine modulates cognitive networks involved in attention and learning/memory .
	manualset2
82267	4	397683	5	NULL	NULL	NULL	NULL	learning/memory	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , nicotine modulates cognitive networks involved in attention and learning/memory .
	manualset2
82269	1	397684	5	NULL	NULL	NULL	NULL	time	Time												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , nuclear grade was associated with time to recurrence ( P = 0.004 ) in patients who underwent complete surgical resection ( n = 159 ) .
	manualset2
82270	3	397684	5	NULL	NULL	NULL	NULL	patients	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , nuclear grade was associated with time to recurrence ( P = 0.004 ) in patients who underwent complete surgical resection ( n = 159 ) .
	manualset2
82271	2	397684	5	NULL	NULL	NULL	NULL	recurrence	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , nuclear grade was associated with time to recurrence ( P = 0.004 ) in patients who underwent complete surgical resection ( n = 159 ) .
	manualset2
82272	4	397684	5	NULL	NULL	NULL	NULL	surgical resection	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , nuclear grade was associated with time to recurrence ( P = 0.004 ) in patients who underwent complete surgical resection ( n = 159 ) .
	manualset2
82273	1	397685	5	NULL	NULL	NULL	NULL	IAP elements	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , one of the IAP elements ( belonging to the LS1 subfamily ) is specifically hypomethylated in the DNA of the immunogenic cells .
	manualset2
82275	2	397685	5	NULL	NULL	NULL	NULL	LS1 subfamily	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , one of the IAP elements ( belonging to the LS1 subfamily ) is specifically hypomethylated in the DNA of the immunogenic cells .
	manualset2
82278	3	397685	5	NULL	NULL	NULL	NULL	DNA	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , one of the IAP elements ( belonging to the LS1 subfamily ) is specifically hypomethylated in the DNA of the immunogenic cells .
	manualset2
82559	4	397685	5	NULL	NULL	0	NULL	immunogenic cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , one of the IAP elements ( belonging to the LS1 subfamily ) is specifically hypomethylated in the DNA of the immunogenic cells .
	manualset2
82280	1	397686	5	NULL	NULL	0	NULL	oocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , oocytes cultured with FSH maintained trans-zonal projections of cumulus cells .
	manualset2
82281	2	397686	5	NULL	NULL	0	NULL	FSH	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , oocytes cultured with FSH maintained trans-zonal projections of cumulus cells .
	manualset2
82282	3	397686	5	NULL	NULL	NULL	NULL	trans-zonal projections	CellComponent												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , oocytes cultured with FSH maintained trans-zonal projections of cumulus cells .
	manualset2
82283	4	397686	5	NULL	NULL	NULL	NULL	cumulus cell	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , oocytes cultured with FSH maintained trans-zonal projections of cumulus cells .
	manualset2
82285	1	397687	5	NULL	NULL	NULL	NULL	oral administration	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , oral administration of loratadine at a dose of 10 mg/kg for 7 days also significantly inhibited the histamine-induced scratching behavior in the same animals .
	manualset2
82286	2	397687	5	NULL	NULL	0	NULL	loratadine	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , oral administration of loratadine at a dose of 10 mg/kg for 7 days also significantly inhibited the histamine-induced scratching behavior in the same animals .
	manualset2
82287	3	397687	5	NULL	NULL	0	NULL	10 mg/kg	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , oral administration of loratadine at a dose of 10 mg/kg for 7 days also significantly inhibited the histamine-induced scratching behavior in the same animals .
	manualset2
82288	4	397687	5	NULL	NULL	NULL	NULL	7 days	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , oral administration of loratadine at a dose of 10 mg/kg for 7 days also significantly inhibited the histamine-induced scratching behavior in the same animals .
	manualset2
82289	5	397687	5	NULL	NULL	NULL	NULL	histamine-induced scratching behavior	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , oral administration of loratadine at a dose of 10 mg/kg for 7 days also significantly inhibited the histamine-induced scratching behavior in the same animals .
	manualset2
82291	6	397687	5	NULL	NULL	NULL	NULL	animals	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , oral administration of loratadine at a dose of 10 mg/kg for 7 days also significantly inhibited the histamine-induced scratching behavior in the same animals .
	manualset2
82292	1	397688	5	NULL	NULL	0	NULL	pH	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , pH changes correlated with the 3NP-induced inhibition of succinate dehydrogenase and preceded striatum lesions .
	manualset2
82293	2	397688	5	NULL	NULL	NULL	NULL	3NP	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , pH changes correlated with the 3NP-induced inhibition of succinate dehydrogenase and preceded striatum lesions .
	manualset2
82294	3	397688	5	NULL	NULL	NULL	NULL	3NP-induced inhibition	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , pH changes correlated with the 3NP-induced inhibition of succinate dehydrogenase and preceded striatum lesions .
	manualset2
82295	4	397688	5	NULL	NULL	0	NULL	succinate dehydrogenase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , pH changes correlated with the 3NP-induced inhibition of succinate dehydrogenase and preceded striatum lesions .
	manualset2
82296	5	397688	5	NULL	NULL	NULL	NULL	striatum lesions	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , pH changes correlated with the 3NP-induced inhibition of succinate dehydrogenase and preceded striatum lesions .
	manualset2
82298	2	397689	5	NULL	NULL	NULL	NULL	L1210/CPA cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , pretreatment of L1210/CPA cells with the ADH inhibitor , diethyl aminobenzaldehyde ( DEAB ) , resulted in potentiation of the SDA response .
	manualset2
82299	3	397689	5	NULL	NULL	NULL	NULL	ADH inhibitor	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , pretreatment of L1210/CPA cells with the ADH inhibitor , diethyl aminobenzaldehyde ( DEAB ) , resulted in potentiation of the SDA response .
	manualset2
82300	4	397689	5	NULL	NULL	NULL	NULL	diethyl aminobenzaldehyde  ( DEAB )	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , pretreatment of L1210/CPA cells with the ADH inhibitor , diethyl aminobenzaldehyde ( DEAB ) , resulted in potentiation of the SDA response .
	manualset2
82302	5	397689	5	NULL	NULL	NULL	NULL	potentiation	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , pretreatment of L1210/CPA cells with the ADH inhibitor , diethyl aminobenzaldehyde ( DEAB ) , resulted in potentiation of the SDA response .
	manualset2
82303	6	397689	5	NULL	NULL	NULL	NULL	SDA response	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , pretreatment of L1210/CPA cells with the ADH inhibitor , diethyl aminobenzaldehyde ( DEAB ) , resulted in potentiation of the SDA response .
	manualset2
82537	1	397689	5	NULL	NULL	0	NULL	pretreatment	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , pretreatment of L1210/CPA cells with the ADH inhibitor , diethyl aminobenzaldehyde ( DEAB ) , resulted in potentiation of the SDA response .
	manualset2
82305	1	397690	5	NULL	NULL	NULL	NULL	qualitative examination	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , qualitative examination of the recognition trial revealed the presence of `` atypical recognition errors '' that were endorsed with significantly higher frequency by the suspect effort patients .
	manualset2
82306	4	397690	5	NULL	NULL	NULL	NULL	patients	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , qualitative examination of the recognition trial revealed the presence of `` atypical recognition errors '' that were endorsed with significantly higher frequency by the suspect effort patients .
	manualset2
82307	2	397690	5	NULL	NULL	NULL	NULL	recognition trial	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , qualitative examination of the recognition trial revealed the presence of `` atypical recognition errors '' that were endorsed with significantly higher frequency by the suspect effort patients .
	manualset2
82309	1	397691	5	NULL	NULL	0	NULL	quercetin	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , quercetin conjugation by different in vitro models from corresponding origins may differ significantly .
	manualset2
82310	2	397691	5	NULL	NULL	0	NULL	conjugation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , quercetin conjugation by different in vitro models from corresponding origins may differ significantly .
	manualset2
82311	1	397692	5	NULL	NULL	0	NULL	dieldrin	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , regardless of whether dieldrin was present or not , removal of vanadate 24 h before fixation of the colonies caused a slight decrease in the transformation frequency .
	manualset2
82312	2	397692	5	NULL	NULL	NULL	NULL	vanadate	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , regardless of whether dieldrin was present or not , removal of vanadate 24 h before fixation of the colonies caused a slight decrease in the transformation frequency .
	manualset2
82313	3	397692	5	NULL	NULL	NULL	NULL	24 h	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , regardless of whether dieldrin was present or not , removal of vanadate 24 h before fixation of the colonies caused a slight decrease in the transformation frequency .
	manualset2
82314	4	397692	5	NULL	NULL	0	NULL	fixation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , regardless of whether dieldrin was present or not , removal of vanadate 24 h before fixation of the colonies caused a slight decrease in the transformation frequency .
	manualset2
82315	5	397692	5	NULL	NULL	0	NULL	colonies	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , regardless of whether dieldrin was present or not , removal of vanadate 24 h before fixation of the colonies caused a slight decrease in the transformation frequency .
	manualset2
82316	6	397692	5	NULL	NULL	0	NULL	transformation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , regardless of whether dieldrin was present or not , removal of vanadate 24 h before fixation of the colonies caused a slight decrease in the transformation frequency .
	manualset2
82317	1	397693	5	NULL	NULL	NULL	NULL	 management attention	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , results to date , suggest that management attention must expand from its historical focus on infra-structure provision to incorporate diffuse sources of faecal indicator loading which present a new set of management and modelling challenges .
	manualset2
82527	2	397693	5	NULL	NULL	0	NULL	focus	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , results to date , suggest that management attention must expand from its historical focus on infra-structure provision to incorporate diffuse sources of faecal indicator loading which present a new set of management and modelling challenges .
	manualset2
82528	3	397693	5	NULL	NULL	NULL	NULL	infra-structure provision	Facility												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , results to date , suggest that management attention must expand from its historical focus on infra-structure provision to incorporate diffuse sources of faecal indicator loading which present a new set of management and modelling challenges .
	manualset2
82530	4	397693	5	NULL	NULL	NULL	NULL	challenges	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , results to date , suggest that management attention must expand from its historical focus on infra-structure provision to incorporate diffuse sources of faecal indicator loading which present a new set of management and modelling challenges .
	manualset2
82318	1	397694	5	NULL	NULL	NULL	NULL	sequence	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , some sequence similarities in the 5 ' - flanking region are found between the corticotropin/beta-lipotropin precursor gene and the mouse alpha-globin and beta-globin genes , all of which are negatively regulated by glucocorticoids .
	manualset2
82319	3	397694	5	NULL	NULL	NULL	NULL	corticotropin/beta-lipotropin precursor	Gene												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , some sequence similarities in the 5 ' - flanking region are found between the corticotropin/beta-lipotropin precursor gene and the mouse alpha-globin and beta-globin genes , all of which are negatively regulated by glucocorticoids .
	manualset2
82320	4	397694	5	NULL	NULL	NULL	NULL	mouse	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , some sequence similarities in the 5 ' - flanking region are found between the corticotropin/beta-lipotropin precursor gene and the mouse alpha-globin and beta-globin genes , all of which are negatively regulated by glucocorticoids .
	manualset2
82321	2	397694	5	NULL	NULL	NULL	NULL	5 ' - flanking region	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , some sequence similarities in the 5 ' - flanking region are found between the corticotropin/beta-lipotropin precursor gene and the mouse alpha-globin and beta-globin genes , all of which are negatively regulated by glucocorticoids .
	manualset2
82322	6	397694	5	NULL	NULL	NULL	NULL	beta-globin	Gene												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , some sequence similarities in the 5 ' - flanking region are found between the corticotropin/beta-lipotropin precursor gene and the mouse alpha-globin and beta-globin genes , all of which are negatively regulated by glucocorticoids .
	manualset2
82324	8	397694	5	NULL	NULL	NULL	NULL	glucocorticoids	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , some sequence similarities in the 5 ' - flanking region are found between the corticotropin/beta-lipotropin precursor gene and the mouse alpha-globin and beta-globin genes , all of which are negatively regulated by glucocorticoids .
	manualset2
82325	5	397694	5	NULL	NULL	0	NULL	alpha-globin	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , some sequence similarities in the 5 ' - flanking region are found between the corticotropin/beta-lipotropin precursor gene and the mouse alpha-globin and beta-globin genes , all of which are negatively regulated by glucocorticoids .
	manualset2
82326	1	397695	5	NULL	NULL	0	NULL	behavioral acquisition	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , studies of blocking show that behavioral acquisition in response to one component can be hindered or blocked by pretraining with the other component .
	manualset2
82327	2	397695	5	NULL	NULL	0	NULL	response	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , studies of blocking show that behavioral acquisition in response to one component can be hindered or blocked by pretraining with the other component .
	manualset2
82328	3	397695	5	NULL	NULL	0	NULL	component	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , studies of blocking show that behavioral acquisition in response to one component can be hindered or blocked by pretraining with the other component .
	manualset2
82329	4	397695	5	NULL	NULL	0	NULL	component	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , studies of blocking show that behavioral acquisition in response to one component can be hindered or blocked by pretraining with the other component .
	manualset2
82330	1	397696	5	NULL	NULL	NULL	NULL	Ad2 E1A products	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ad2 E1A products repress transcription activated by the immunoglobulin heavy chain enhancer in chimeric recombinants , which are either stably integrated in the genome of lymphoid cells or are present as episomes .
	manualset2
82331	2	397696	5	NULL	NULL	0	NULL	repress	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ad2 E1A products repress transcription activated by the immunoglobulin heavy chain enhancer in chimeric recombinants , which are either stably integrated in the genome of lymphoid cells or are present as episomes .
	manualset2
82332	3	397696	5	NULL	NULL	0	NULL	transcription	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ad2 E1A products repress transcription activated by the immunoglobulin heavy chain enhancer in chimeric recombinants , which are either stably integrated in the genome of lymphoid cells or are present as episomes .
	manualset2
82333	4	397696	5	NULL	NULL	NULL	NULL	immunoglobulin heavy chain enhancer	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ad2 E1A products repress transcription activated by the immunoglobulin heavy chain enhancer in chimeric recombinants , which are either stably integrated in the genome of lymphoid cells or are present as episomes .
	manualset2
82334	5	397696	5	NULL	NULL	0	NULL	chimeric recombinants	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ad2 E1A products repress transcription activated by the immunoglobulin heavy chain enhancer in chimeric recombinants , which are either stably integrated in the genome of lymphoid cells or are present as episomes .
	manualset2
82335	6	397696	5	NULL	NULL	0	NULL	genome	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ad2 E1A products repress transcription activated by the immunoglobulin heavy chain enhancer in chimeric recombinants , which are either stably integrated in the genome of lymphoid cells or are present as episomes .
	manualset2
82336	7	397696	5	NULL	NULL	0	NULL	lymphoid cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ad2 E1A products repress transcription activated by the immunoglobulin heavy chain enhancer in chimeric recombinants , which are either stably integrated in the genome of lymphoid cells or are present as episomes .
	manualset2
82337	8	397696	5	NULL	NULL	0	NULL	episomes	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ad2 E1A products repress transcription activated by the immunoglobulin heavy chain enhancer in chimeric recombinants , which are either stably integrated in the genome of lymphoid cells or are present as episomes .
	manualset2
82338	1	397697	5	NULL	NULL	NULL	NULL	Danish Folkeskole	Facility												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Danish Folkeskole , which is the Danish municipal primary and lower secondary school , uses the principle of differentiated teaching , integrating information technology , and there are no recommended textbooks in the curriculum .
	manualset2
82339	2	397697	5	NULL	NULL	0	NULL	school	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the Danish Folkeskole , which is the Danish municipal primary and lower secondary school , uses the principle of differentiated teaching , integrating information technology , and there are no recommended textbooks in the curriculum .
	manualset2
82340	3	397697	5	NULL	NULL	NULL	NULL	information technology	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Danish Folkeskole , which is the Danish municipal primary and lower secondary school , uses the principle of differentiated teaching , integrating information technology , and there are no recommended textbooks in the curriculum .
	manualset2
82342	4	397697	5	NULL	NULL	NULL	NULL	textbooks	PublishedSourceOfInformation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Danish Folkeskole , which is the Danish municipal primary and lower secondary school , uses the principle of differentiated teaching , integrating information technology , and there are no recommended textbooks in the curriculum .
	manualset2
82343	5	397697	5	NULL	NULL	NULL	NULL	curriculum	PublishedSourceOfInformation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Danish Folkeskole , which is the Danish municipal primary and lower secondary school , uses the principle of differentiated teaching , integrating information technology , and there are no recommended textbooks in the curriculum .
	manualset2
82345	1	397698	5	NULL	NULL	0	NULL	Km	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the Km in whites was inversely related to plasma renin activity ( r = 0.50 ; P less than 0.005 ) .
	manualset2
82346	2	397698	5	NULL	NULL	0	NULL	whites	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the Km in whites was inversely related to plasma renin activity ( r = 0.50 ; P less than 0.005 ) .
	manualset2
82347	3	397698	5	NULL	NULL	NULL	NULL	plasma renin activity	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Km in whites was inversely related to plasma renin activity ( r = 0.50 ; P less than 0.005 ) .
	manualset2
82348	4	397698	5	NULL	NULL	NULL	NULL	r = 0.50	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Km in whites was inversely related to plasma renin activity ( r = 0.50 ; P less than 0.005 ) .
	manualset2
82349	5	397698	5	NULL	NULL	NULL	NULL	0.005	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Km in whites was inversely related to plasma renin activity ( r = 0.50 ; P less than 0.005 ) .
	manualset2
82350	1	397699	5	NULL	NULL	0	NULL	Ncorr value	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ncorr value for the copolymer ( MA ratio MAPTAC = 56 : 44 ) became much smaller by the neutralization of MA residues in the copolymer with sodium hydroxide , and comparable to those for neutral polymers such as poly ( ethylene glycol ) and poly ( N-vinylpyrrolidone ) and zwitterionic polymers such as poly ( 2-methacryloyloxyethyl phosphorylcholine ) ( PMPC ) and poly ( 3-sulfo-N , N-dimethyl-N - ( 3 ' - methacryloylaminopropyl ) propanaminium inner salt ) .
	manualset2
82351	2	397699	5	NULL	NULL	NULL	NULL	copolymer	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ncorr value for the copolymer ( MA ratio MAPTAC = 56 : 44 ) became much smaller by the neutralization of MA residues in the copolymer with sodium hydroxide , and comparable to those for neutral polymers such as poly ( ethylene glycol ) and poly ( N-vinylpyrrolidone ) and zwitterionic polymers such as poly ( 2-methacryloyloxyethyl phosphorylcholine ) ( PMPC ) and poly ( 3-sulfo-N , N-dimethyl-N - ( 3 ' - methacryloylaminopropyl ) propanaminium inner salt ) .
	manualset2
82353	3	397699	5	NULL	NULL	NULL	NULL	MA	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ncorr value for the copolymer ( MA ratio MAPTAC = 56 : 44 ) became much smaller by the neutralization of MA residues in the copolymer with sodium hydroxide , and comparable to those for neutral polymers such as poly ( ethylene glycol ) and poly ( N-vinylpyrrolidone ) and zwitterionic polymers such as poly ( 2-methacryloyloxyethyl phosphorylcholine ) ( PMPC ) and poly ( 3-sulfo-N , N-dimethyl-N - ( 3 ' - methacryloylaminopropyl ) propanaminium inner salt ) .
	manualset2
82354	4	397699	5	NULL	NULL	NULL	NULL	MAPTAC	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ncorr value for the copolymer ( MA ratio MAPTAC = 56 : 44 ) became much smaller by the neutralization of MA residues in the copolymer with sodium hydroxide , and comparable to those for neutral polymers such as poly ( ethylene glycol ) and poly ( N-vinylpyrrolidone ) and zwitterionic polymers such as poly ( 2-methacryloyloxyethyl phosphorylcholine ) ( PMPC ) and poly ( 3-sulfo-N , N-dimethyl-N - ( 3 ' - methacryloylaminopropyl ) propanaminium inner salt ) .
	manualset2
82355	5	397699	5	NULL	NULL	NULL	NULL	MA ratio MAPTAC = 56 : 44	Relationship												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ncorr value for the copolymer ( MA ratio MAPTAC = 56 : 44 ) became much smaller by the neutralization of MA residues in the copolymer with sodium hydroxide , and comparable to those for neutral polymers such as poly ( ethylene glycol ) and poly ( N-vinylpyrrolidone ) and zwitterionic polymers such as poly ( 2-methacryloyloxyethyl phosphorylcholine ) ( PMPC ) and poly ( 3-sulfo-N , N-dimethyl-N - ( 3 ' - methacryloylaminopropyl ) propanaminium inner salt ) .
	manualset2
82356	6	397699	5	NULL	NULL	0	NULL	neutralization	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ncorr value for the copolymer ( MA ratio MAPTAC = 56 : 44 ) became much smaller by the neutralization of MA residues in the copolymer with sodium hydroxide , and comparable to those for neutral polymers such as poly ( ethylene glycol ) and poly ( N-vinylpyrrolidone ) and zwitterionic polymers such as poly ( 2-methacryloyloxyethyl phosphorylcholine ) ( PMPC ) and poly ( 3-sulfo-N , N-dimethyl-N - ( 3 ' - methacryloylaminopropyl ) propanaminium inner salt ) .
	manualset2
82357	7	397699	5	NULL	NULL	NULL	NULL	MA	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ncorr value for the copolymer ( MA ratio MAPTAC = 56 : 44 ) became much smaller by the neutralization of MA residues in the copolymer with sodium hydroxide , and comparable to those for neutral polymers such as poly ( ethylene glycol ) and poly ( N-vinylpyrrolidone ) and zwitterionic polymers such as poly ( 2-methacryloyloxyethyl phosphorylcholine ) ( PMPC ) and poly ( 3-sulfo-N , N-dimethyl-N - ( 3 ' - methacryloylaminopropyl ) propanaminium inner salt ) .
	manualset2
82358	8	397699	5	NULL	NULL	NULL	NULL	copolymer	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ncorr value for the copolymer ( MA ratio MAPTAC = 56 : 44 ) became much smaller by the neutralization of MA residues in the copolymer with sodium hydroxide , and comparable to those for neutral polymers such as poly ( ethylene glycol ) and poly ( N-vinylpyrrolidone ) and zwitterionic polymers such as poly ( 2-methacryloyloxyethyl phosphorylcholine ) ( PMPC ) and poly ( 3-sulfo-N , N-dimethyl-N - ( 3 ' - methacryloylaminopropyl ) propanaminium inner salt ) .
	manualset2
82359	9	397699	5	NULL	NULL	0	NULL	sodium hydroxide	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ncorr value for the copolymer ( MA ratio MAPTAC = 56 : 44 ) became much smaller by the neutralization of MA residues in the copolymer with sodium hydroxide , and comparable to those for neutral polymers such as poly ( ethylene glycol ) and poly ( N-vinylpyrrolidone ) and zwitterionic polymers such as poly ( 2-methacryloyloxyethyl phosphorylcholine ) ( PMPC ) and poly ( 3-sulfo-N , N-dimethyl-N - ( 3 ' - methacryloylaminopropyl ) propanaminium inner salt ) .
	manualset2
82360	10	397699	5	NULL	NULL	NULL	NULL	neutral polymers	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ncorr value for the copolymer ( MA ratio MAPTAC = 56 : 44 ) became much smaller by the neutralization of MA residues in the copolymer with sodium hydroxide , and comparable to those for neutral polymers such as poly ( ethylene glycol ) and poly ( N-vinylpyrrolidone ) and zwitterionic polymers such as poly ( 2-methacryloyloxyethyl phosphorylcholine ) ( PMPC ) and poly ( 3-sulfo-N , N-dimethyl-N - ( 3 ' - methacryloylaminopropyl ) propanaminium inner salt ) .
	manualset2
82361	11	397699	5	NULL	NULL	NULL	NULL	poly ( ethylene glycol )	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ncorr value for the copolymer ( MA ratio MAPTAC = 56 : 44 ) became much smaller by the neutralization of MA residues in the copolymer with sodium hydroxide , and comparable to those for neutral polymers such as poly ( ethylene glycol ) and poly ( N-vinylpyrrolidone ) and zwitterionic polymers such as poly ( 2-methacryloyloxyethyl phosphorylcholine ) ( PMPC ) and poly ( 3-sulfo-N , N-dimethyl-N - ( 3 ' - methacryloylaminopropyl ) propanaminium inner salt ) .
	manualset2
82362	12	397699	5	NULL	NULL	NULL	NULL	poly ( N-vinylpyrrolidone )	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ncorr value for the copolymer ( MA ratio MAPTAC = 56 : 44 ) became much smaller by the neutralization of MA residues in the copolymer with sodium hydroxide , and comparable to those for neutral polymers such as poly ( ethylene glycol ) and poly ( N-vinylpyrrolidone ) and zwitterionic polymers such as poly ( 2-methacryloyloxyethyl phosphorylcholine ) ( PMPC ) and poly ( 3-sulfo-N , N-dimethyl-N - ( 3 ' - methacryloylaminopropyl ) propanaminium inner salt ) .
	manualset2
82363	13	397699	5	NULL	NULL	NULL	NULL	zwitterionic polymers	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ncorr value for the copolymer ( MA ratio MAPTAC = 56 : 44 ) became much smaller by the neutralization of MA residues in the copolymer with sodium hydroxide , and comparable to those for neutral polymers such as poly ( ethylene glycol ) and poly ( N-vinylpyrrolidone ) and zwitterionic polymers such as poly ( 2-methacryloyloxyethyl phosphorylcholine ) ( PMPC ) and poly ( 3-sulfo-N , N-dimethyl-N - ( 3 ' - methacryloylaminopropyl ) propanaminium inner salt ) .
	manualset2
82364	14	397699	5	NULL	NULL	NULL	NULL	poly ( 2-methacryloyloxyethyl phosphorylcholine )	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ncorr value for the copolymer ( MA ratio MAPTAC = 56 : 44 ) became much smaller by the neutralization of MA residues in the copolymer with sodium hydroxide , and comparable to those for neutral polymers such as poly ( ethylene glycol ) and poly ( N-vinylpyrrolidone ) and zwitterionic polymers such as poly ( 2-methacryloyloxyethyl phosphorylcholine ) ( PMPC ) and poly ( 3-sulfo-N , N-dimethyl-N - ( 3 ' - methacryloylaminopropyl ) propanaminium inner salt ) .
	manualset2
82365	15	397699	5	NULL	NULL	NULL	NULL	PMPC 	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ncorr value for the copolymer ( MA ratio MAPTAC = 56 : 44 ) became much smaller by the neutralization of MA residues in the copolymer with sodium hydroxide , and comparable to those for neutral polymers such as poly ( ethylene glycol ) and poly ( N-vinylpyrrolidone ) and zwitterionic polymers such as poly ( 2-methacryloyloxyethyl phosphorylcholine ) ( PMPC ) and poly ( 3-sulfo-N , N-dimethyl-N - ( 3 ' - methacryloylaminopropyl ) propanaminium inner salt ) .
	manualset2
82366	16	397699	5	NULL	NULL	NULL	NULL	poly ( 3-sulfo-N , N-dimethyl-N - ( 3 ' - methacryloylaminopropyl ) propanaminium inner salt )	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the Ncorr value for the copolymer ( MA ratio MAPTAC = 56 : 44 ) became much smaller by the neutralization of MA residues in the copolymer with sodium hydroxide , and comparable to those for neutral polymers such as poly ( ethylene glycol ) and poly ( N-vinylpyrrolidone ) and zwitterionic polymers such as poly ( 2-methacryloyloxyethyl phosphorylcholine ) ( PMPC ) and poly ( 3-sulfo-N , N-dimethyl-N - ( 3 ' - methacryloylaminopropyl ) propanaminium inner salt ) .
	manualset2
82367	1	397700	5	NULL	NULL	0	NULL	QPCR assay	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the QPCR assay identifies how much amplifiable DNA is in a sample and thus has the potential to predict PCR success in downstream applications such as STR analysis .
	manualset2
82368	2	397700	5	NULL	NULL	0	NULL	DNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the QPCR assay identifies how much amplifiable DNA is in a sample and thus has the potential to predict PCR success in downstream applications such as STR analysis .
	manualset2
82369	3	397700	5	NULL	NULL	0	NULL	sample	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the QPCR assay identifies how much amplifiable DNA is in a sample and thus has the potential to predict PCR success in downstream applications such as STR analysis .
	manualset2
82370	4	397700	5	NULL	NULL	0	NULL	PCR	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the QPCR assay identifies how much amplifiable DNA is in a sample and thus has the potential to predict PCR success in downstream applications such as STR analysis .
	manualset2
82371	5	397700	5	NULL	NULL	0	NULL	applications	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the QPCR assay identifies how much amplifiable DNA is in a sample and thus has the potential to predict PCR success in downstream applications such as STR analysis .
	manualset2
82372	6	397700	5	NULL	NULL	0	NULL	STR analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the QPCR assay identifies how much amplifiable DNA is in a sample and thus has the potential to predict PCR success in downstream applications such as STR analysis .
	manualset2
82373	1	397701	5	NULL	NULL	0	NULL	endothelium	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the abnormal endothelium function can be corrected by tempol treatment , but this seems to involve mechanisms partly independent of NO .
	manualset2
82374	2	397701	5	NULL	NULL	0	NULL	function	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the abnormal endothelium function can be corrected by tempol treatment , but this seems to involve mechanisms partly independent of NO .
	manualset2
82375	3	397701	5	NULL	NULL	0	NULL	tempol treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the abnormal endothelium function can be corrected by tempol treatment , but this seems to involve mechanisms partly independent of NO .
	manualset2
82376	4	397701	5	NULL	NULL	0	NULL	mechanisms	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the abnormal endothelium function can be corrected by tempol treatment , but this seems to involve mechanisms partly independent of NO .
	manualset2
82377	5	397701	5	NULL	NULL	NULL	NULL	NO	NonProteinOrNucleicAcidChemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the abnormal endothelium function can be corrected by tempol treatment , but this seems to involve mechanisms partly independent of NO .
	manualset2
82378	1	397702	5	NULL	NULL	NULL	NULL	aminoethylated mutant proteins	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the aminoethylated mutant proteins form isolable complexes with a transition state analog , but with compromised stabilities .
	manualset2
82379	2	397702	5	NULL	NULL	NULL	NULL	isolable complexes	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the aminoethylated mutant proteins form isolable complexes with a transition state analog , but with compromised stabilities .
	manualset2
82380	3	397702	5	NULL	NULL	NULL	NULL	transition state analog	Molecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the aminoethylated mutant proteins form isolable complexes with a transition state analog , but with compromised stabilities .
	manualset2
82382	1	397703	5	NULL	NULL	0	NULL	mercury	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the amount of mercury released with the time kept constant was almost independent of the pumping flow rate up to 8 L/min .
	manualset2
82383	2	397703	5	NULL	NULL	0	NULL	time	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the amount of mercury released with the time kept constant was almost independent of the pumping flow rate up to 8 L/min .
	manualset2
82384	3	397703	5	NULL	NULL	0	NULL	8 L/min	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the amount of mercury released with the time kept constant was almost independent of the pumping flow rate up to 8 L/min .
	manualset2
82385	1	397704	5	NULL	NULL	0	NULL	antioxidant	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the antioxidant activity was evaluated through DPPH scavenging activity , reducing power , - carotene bleaching inhibition and TBARS formation inhibition .
	manualset2
82386	2	397704	5	NULL	NULL	0	NULL	activity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the antioxidant activity was evaluated through DPPH scavenging activity , reducing power , - carotene bleaching inhibition and TBARS formation inhibition .
	manualset2
82387	3	397704	5	NULL	NULL	NULL	NULL	DPPH	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the antioxidant activity was evaluated through DPPH scavenging activity , reducing power , - carotene bleaching inhibition and TBARS formation inhibition .
	manualset2
82388	4	397704	5	NULL	NULL	NULL	NULL	scavenging activity	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the antioxidant activity was evaluated through DPPH scavenging activity , reducing power , - carotene bleaching inhibition and TBARS formation inhibition .
	manualset2
82389	5	397704	5	NULL	NULL	NULL	NULL	carotene	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the antioxidant activity was evaluated through DPPH scavenging activity , reducing power , - carotene bleaching inhibition and TBARS formation inhibition .
	manualset2
82390	6	397704	5	NULL	NULL	0	NULL	inhibition	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the antioxidant activity was evaluated through DPPH scavenging activity , reducing power , - carotene bleaching inhibition and TBARS formation inhibition .
	manualset2
82391	7	397704	5	NULL	NULL	NULL	NULL	TBARS	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the antioxidant activity was evaluated through DPPH scavenging activity , reducing power , - carotene bleaching inhibition and TBARS formation inhibition .
	manualset2
82392	8	397704	5	NULL	NULL	0	NULL	formation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the antioxidant activity was evaluated through DPPH scavenging activity , reducing power , - carotene bleaching inhibition and TBARS formation inhibition .
	manualset2
82393	9	397704	5	NULL	NULL	0	NULL	inhibition	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the antioxidant activity was evaluated through DPPH scavenging activity , reducing power , - carotene bleaching inhibition and TBARS formation inhibition .
	manualset2
82394	1	397705	5	NULL	NULL	0	NULL	data	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the data suggest that female-specific regulation of dsx RNA processing occurs by promoting the usage of the female splice acceptor site , rather than by repressing the usage of the alternative male-specific splice acceptor .
	manualset2
82395	2	397705	5	NULL	NULL	0	NULL	female	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the data suggest that female-specific regulation of dsx RNA processing occurs by promoting the usage of the female splice acceptor site , rather than by repressing the usage of the alternative male-specific splice acceptor .
	manualset2
82396	3	397705	5	NULL	NULL	0	NULL	regulation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the data suggest that female-specific regulation of dsx RNA processing occurs by promoting the usage of the female splice acceptor site , rather than by repressing the usage of the alternative male-specific splice acceptor .
	manualset2
82397	4	397705	5	NULL	NULL	0	NULL	dsx RNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the data suggest that female-specific regulation of dsx RNA processing occurs by promoting the usage of the female splice acceptor site , rather than by repressing the usage of the alternative male-specific splice acceptor .
	manualset2
82398	5	397705	5	NULL	NULL	0	NULL	processing	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the data suggest that female-specific regulation of dsx RNA processing occurs by promoting the usage of the female splice acceptor site , rather than by repressing the usage of the alternative male-specific splice acceptor .
	manualset2
82399	6	397705	5	NULL	NULL	0	NULL	female	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the data suggest that female-specific regulation of dsx RNA processing occurs by promoting the usage of the female splice acceptor site , rather than by repressing the usage of the alternative male-specific splice acceptor .
	manualset2
82400	7	397705	5	NULL	NULL	NULL	NULL	splice acceptor site	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the data suggest that female-specific regulation of dsx RNA processing occurs by promoting the usage of the female splice acceptor site , rather than by repressing the usage of the alternative male-specific splice acceptor .
	manualset2
82401	8	397705	5	NULL	NULL	0	NULL	male	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the data suggest that female-specific regulation of dsx RNA processing occurs by promoting the usage of the female splice acceptor site , rather than by repressing the usage of the alternative male-specific splice acceptor .
	manualset2
82402	9	397705	5	NULL	NULL	0	NULL	splice acceptor	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the data suggest that female-specific regulation of dsx RNA processing occurs by promoting the usage of the female splice acceptor site , rather than by repressing the usage of the alternative male-specific splice acceptor .
	manualset2
82403	1	397706	5	NULL	NULL	0	NULL	PD game	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the decision of which PD game type to investigate ( whether all PD games , PD-Chicken boundary games or Donor & Recipient games ) is important for discussing network reciprocity .
	manualset2
82404	2	397706	5	NULL	NULL	0	NULL	PD games	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the decision of which PD game type to investigate ( whether all PD games , PD-Chicken boundary games or Donor & Recipient games ) is important for discussing network reciprocity .
	manualset2
82405	3	397706	5	NULL	NULL	0	NULL	PD-Chicken boundary games	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the decision of which PD game type to investigate ( whether all PD games , PD-Chicken boundary games or Donor & Recipient games ) is important for discussing network reciprocity .
	manualset2
82406	4	397706	5	NULL	NULL	NULL	NULL	Donor & Recipient games	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the decision of which PD game type to investigate ( whether all PD games , PD-Chicken boundary games or Donor & Recipient games ) is important for discussing network reciprocity .
	manualset2
82407	5	397706	5	NULL	NULL	0	NULL	network	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the decision of which PD game type to investigate ( whether all PD games , PD-Chicken boundary games or Donor & Recipient games ) is important for discussing network reciprocity .
	manualset2
82408	6	397706	5	NULL	NULL	0	NULL	reciprocity	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the decision of which PD game type to investigate ( whether all PD games , PD-Chicken boundary games or Donor & Recipient games ) is important for discussing network reciprocity .
	manualset2
82409	1	397707	5	NULL	NULL	0	NULL	Sarcoma	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Sarcoma of the abdominal wall ruptured during labor ) .
	manualset2
82410	2	397707	5	NULL	NULL	0	NULL	abdominal wall	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( Sarcoma of the abdominal wall ruptured during labor ) .
	manualset2
82411	3	397707	5	NULL	NULL	0	NULL	labor	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Sarcoma of the abdominal wall ruptured during labor ) .
	manualset2
82412	1	397708	5	NULL	NULL	0	NULL	expression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the expression of adipophilin as a 37 kDa N-terminally truncated protein is higher in the gastrocnemius than in the quadriceps of C57BL/6J mice , especially after an 8-week high-fat diet .
	manualset2
82413	2	397708	5	NULL	NULL	0	NULL	adipophilin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the expression of adipophilin as a 37 kDa N-terminally truncated protein is higher in the gastrocnemius than in the quadriceps of C57BL/6J mice , especially after an 8-week high-fat diet .
	manualset2
82414	3	397708	5	NULL	NULL	0	NULL	37 kDa	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the expression of adipophilin as a 37 kDa N-terminally truncated protein is higher in the gastrocnemius than in the quadriceps of C57BL/6J mice , especially after an 8-week high-fat diet .
	manualset2
82415	4	397708	5	NULL	NULL	NULL	NULL	N-terminally truncated protein	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the expression of adipophilin as a 37 kDa N-terminally truncated protein is higher in the gastrocnemius than in the quadriceps of C57BL/6J mice , especially after an 8-week high-fat diet .
	manualset2
82416	5	397708	5	NULL	NULL	0	NULL	gastrocnemius	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the expression of adipophilin as a 37 kDa N-terminally truncated protein is higher in the gastrocnemius than in the quadriceps of C57BL/6J mice , especially after an 8-week high-fat diet .
	manualset2
82417	6	397708	5	NULL	NULL	0	NULL	quadriceps	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the expression of adipophilin as a 37 kDa N-terminally truncated protein is higher in the gastrocnemius than in the quadriceps of C57BL/6J mice , especially after an 8-week high-fat diet .
	manualset2
82418	7	397708	5	NULL	NULL	0	NULL	C57BL/6J mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the expression of adipophilin as a 37 kDa N-terminally truncated protein is higher in the gastrocnemius than in the quadriceps of C57BL/6J mice , especially after an 8-week high-fat diet .
	manualset2
82419	8	397708	5	NULL	NULL	NULL	NULL	8-week	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the expression of adipophilin as a 37 kDa N-terminally truncated protein is higher in the gastrocnemius than in the quadriceps of C57BL/6J mice , especially after an 8-week high-fat diet .
	manualset2
82420	9	397708	5	NULL	NULL	NULL	NULL	high-fat diet	Food												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the expression of adipophilin as a 37 kDa N-terminally truncated protein is higher in the gastrocnemius than in the quadriceps of C57BL/6J mice , especially after an 8-week high-fat diet .
	manualset2
82422	1	397709	5	NULL	NULL	0	NULL	expression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the expression of the different A-type cyclin genes responded differently upon a block at mid-S phase by DNA synthesis inhibitors .
	manualset2
82423	2	397709	5	NULL	NULL	NULL	NULL	A-type cyclin	Gene												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the expression of the different A-type cyclin genes responded differently upon a block at mid-S phase by DNA synthesis inhibitors .
	manualset2
82424	3	397709	5	NULL	NULL	NULL	NULL	block	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the expression of the different A-type cyclin genes responded differently upon a block at mid-S phase by DNA synthesis inhibitors .
	manualset2
82425	4	397709	5	NULL	NULL	NULL	NULL	mid-S phase	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the expression of the different A-type cyclin genes responded differently upon a block at mid-S phase by DNA synthesis inhibitors .
	manualset2
82426	5	397709	5	NULL	NULL	NULL	NULL	DNA synthesis inhibitors	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the expression of the different A-type cyclin genes responded differently upon a block at mid-S phase by DNA synthesis inhibitors .
	manualset2
82429	1	397710	5	NULL	NULL	0	NULL	experience	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the increased experience with reduced-intensity allogeneic progenitor cell transplantation allows offering this option to physically fit patients .
	manualset2
82430	2	397710	5	NULL	NULL	NULL	NULL	allogeneic progenitor	Relationship												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the increased experience with reduced-intensity allogeneic progenitor cell transplantation allows offering this option to physically fit patients .
	manualset2
82431	3	397710	5	NULL	NULL	0	NULL	cell	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the increased experience with reduced-intensity allogeneic progenitor cell transplantation allows offering this option to physically fit patients .
	manualset2
82432	4	397710	5	NULL	NULL	0	NULL	transplantation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the increased experience with reduced-intensity allogeneic progenitor cell transplantation allows offering this option to physically fit patients .
	manualset2
82433	5	397710	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the increased experience with reduced-intensity allogeneic progenitor cell transplantation allows offering this option to physically fit patients .
	manualset2
82434	1	397711	5	NULL	NULL	NULL	NULL	cocaine	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the issue is somewhat unclear regarding cocaine and the place preference paradigm .
	manualset2
82435	2	397711	5	NULL	NULL	NULL	NULL	preference paradigm	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the issue is somewhat unclear regarding cocaine and the place preference paradigm .
	manualset2
82437	1	397712	5	NULL	NULL	0	NULL	survivors	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the majority of survivors suffer long-term side-effects due to severe management modalities .
	manualset2
82438	2	397712	5	NULL	NULL	NULL	NULL	long-term side-effects	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the majority of survivors suffer long-term side-effects due to severe management modalities .
	manualset2
82439	1	397713	5	NULL	NULL	0	NULL	SLAM/SLAM	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the negative effect of SLAM/SLAM interactions on CD40L-induced DC activation was also detected in the presence of lipopolysaccharide ( LPS ) .
	manualset2
82440	2	397713	5	NULL	NULL	0	NULL	interactions	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the negative effect of SLAM/SLAM interactions on CD40L-induced DC activation was also detected in the presence of lipopolysaccharide ( LPS ) .
	manualset2
82441	3	397713	5	NULL	NULL	0	NULL	CD40L	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the negative effect of SLAM/SLAM interactions on CD40L-induced DC activation was also detected in the presence of lipopolysaccharide ( LPS ) .
	manualset2
82442	4	397713	5	NULL	NULL	0	NULL	DC	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the negative effect of SLAM/SLAM interactions on CD40L-induced DC activation was also detected in the presence of lipopolysaccharide ( LPS ) .
	manualset2
82443	5	397713	5	NULL	NULL	0	NULL	activation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the negative effect of SLAM/SLAM interactions on CD40L-induced DC activation was also detected in the presence of lipopolysaccharide ( LPS ) .
	manualset2
82444	6	397713	5	NULL	NULL	NULL	NULL	lipopolysaccharide	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the negative effect of SLAM/SLAM interactions on CD40L-induced DC activation was also detected in the presence of lipopolysaccharide ( LPS ) .
	manualset2
82445	7	397713	5	NULL	NULL	NULL	NULL	LPS	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the negative effect of SLAM/SLAM interactions on CD40L-induced DC activation was also detected in the presence of lipopolysaccharide ( LPS ) .
	manualset2
82446	1	397714	5	NULL	NULL	0	NULL	rat	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the nude rat CD8 + subset contained a substantial number of OX22 - cells which were nearly absent in normal rats .
	manualset2
82447	2	397714	5	NULL	NULL	0	NULL	CD8 +	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the nude rat CD8 + subset contained a substantial number of OX22 - cells which were nearly absent in normal rats .
	manualset2
82448	3	397714	5	NULL	NULL	0	NULL	OX22 - cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the nude rat CD8 + subset contained a substantial number of OX22 - cells which were nearly absent in normal rats .
	manualset2
82449	4	397714	5	NULL	NULL	0	NULL	rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the nude rat CD8 + subset contained a substantial number of OX22 - cells which were nearly absent in normal rats .
	manualset2
82450	1	397715	5	NULL	NULL	0	NULL	pain	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the pain-relieved groups 2 and 4b performed statistically significantly better in PASAT than the pain-suffering groups 3 and 4a .
	manualset2
82451	2	397715	5	NULL	NULL	0	NULL	groups	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the pain-relieved groups 2 and 4b performed statistically significantly better in PASAT than the pain-suffering groups 3 and 4a .
	manualset2
82452	3	397715	5	NULL	NULL	0	NULL	PASAT	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the pain-relieved groups 2 and 4b performed statistically significantly better in PASAT than the pain-suffering groups 3 and 4a .
	manualset2
82453	4	397715	5	NULL	NULL	0	NULL	pain	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the pain-relieved groups 2 and 4b performed statistically significantly better in PASAT than the pain-suffering groups 3 and 4a .
	manualset2
82454	5	397715	5	NULL	NULL	0	NULL	groups	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the pain-relieved groups 2 and 4b performed statistically significantly better in PASAT than the pain-suffering groups 3 and 4a .
	manualset2
82455	1	397716	5	NULL	NULL	0	NULL	phase	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the phase coupling between multiple low-frequency signals is likely to produce a high rate of false positives when CFC is evaluated using bivariate methods .
	manualset2
82456	2	397716	5	NULL	NULL	NULL	NULL	 low-frequency signals	LaboratoryExperimentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the phase coupling between multiple low-frequency signals is likely to produce a high rate of false positives when CFC is evaluated using bivariate methods .
	manualset2
82457	3	397716	5	NULL	NULL	0	NULL	produce	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the phase coupling between multiple low-frequency signals is likely to produce a high rate of false positives when CFC is evaluated using bivariate methods .
	manualset2
82458	4	397716	5	NULL	NULL	NULL	NULL	CFC	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the phase coupling between multiple low-frequency signals is likely to produce a high rate of false positives when CFC is evaluated using bivariate methods .
	manualset2
82543	5	397716	5	NULL	NULL	0	NULL	bivariate methods	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the phase coupling between multiple low-frequency signals is likely to produce a high rate of false positives when CFC is evaluated using bivariate methods .
	manualset2
82459	1	397717	5	NULL	NULL	0	NULL	prevention	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Secondary prevention of cerebral infarct ) .
	manualset2
82460	2	397717	5	NULL	NULL	0	NULL	cerebral infarct	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Secondary prevention of cerebral infarct ) .
	manualset2
82461	1	397718	5	NULL	NULL	0	NULL	genes	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the presence of multiple genes for these rGH-related proteins is suggested by the large family of immunoreactive gene products identified after cell-free translation of messenger RNA derived from the pituitary .
	manualset2
82462	2	397718	5	NULL	NULL	0	NULL	rGH	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the presence of multiple genes for these rGH-related proteins is suggested by the large family of immunoreactive gene products identified after cell-free translation of messenger RNA derived from the pituitary .
	manualset2
82463	3	397718	5	NULL	NULL	0	NULL	proteins	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the presence of multiple genes for these rGH-related proteins is suggested by the large family of immunoreactive gene products identified after cell-free translation of messenger RNA derived from the pituitary .
	manualset2
82464	5	397718	5	NULL	NULL	NULL	NULL	immunoreactive gene products	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the presence of multiple genes for these rGH-related proteins is suggested by the large family of immunoreactive gene products identified after cell-free translation of messenger RNA derived from the pituitary .
	manualset2
82466	6	397718	5	NULL	NULL	0	NULL	cell	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the presence of multiple genes for these rGH-related proteins is suggested by the large family of immunoreactive gene products identified after cell-free translation of messenger RNA derived from the pituitary .
	manualset2
82467	7	397718	5	NULL	NULL	0	NULL	translation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the presence of multiple genes for these rGH-related proteins is suggested by the large family of immunoreactive gene products identified after cell-free translation of messenger RNA derived from the pituitary .
	manualset2
82468	8	397718	5	NULL	NULL	0	NULL	messenger RNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the presence of multiple genes for these rGH-related proteins is suggested by the large family of immunoreactive gene products identified after cell-free translation of messenger RNA derived from the pituitary .
	manualset2
82469	9	397718	5	NULL	NULL	0	NULL	pituitary	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the presence of multiple genes for these rGH-related proteins is suggested by the large family of immunoreactive gene products identified after cell-free translation of messenger RNA derived from the pituitary .
	manualset2
82544	4	397718	5	NULL	NULL	0	NULL	family	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the presence of multiple genes for these rGH-related proteins is suggested by the large family of immunoreactive gene products identified after cell-free translation of messenger RNA derived from the pituitary .
	manualset2
82470	1	397719	5	NULL	NULL	0	NULL	dysplasia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the present study showed that more consensus scoring on either the degree of dysplasia , assessment of risk or the presence of each morphological characteristic by a panel should be encouraged .
	manualset2
82545	2	397719	5	NULL	NULL	0	NULL	assessment	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the present study showed that more consensus scoring on either the degree of dysplasia , assessment of risk or the presence of each morphological characteristic by a panel should be encouraged .
	manualset2
82471	1	397720	5	NULL	NULL	NULL	NULL	acetyl-ACP	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the rate of acetyl-ACP-primed fatty acid synthesis was inhibited significantly by cerulenin , indicating that the slow utilization of acetyl-ACP was predominantly by 3-oxoacyl-ACP synthase I. In light-incubated isolated chloroplasts with high rates of fatty acid synthesis ( greater than 800 nmol.h-1 .
	manualset2
82472	2	397720	5	NULL	NULL	NULL	NULL	fatty acid	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the rate of acetyl-ACP-primed fatty acid synthesis was inhibited significantly by cerulenin , indicating that the slow utilization of acetyl-ACP was predominantly by 3-oxoacyl-ACP synthase I. In light-incubated isolated chloroplasts with high rates of fatty acid synthesis ( greater than 800 nmol.h-1 .
	manualset2
82473	3	397720	5	NULL	NULL	0	NULL	synthesis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the rate of acetyl-ACP-primed fatty acid synthesis was inhibited significantly by cerulenin , indicating that the slow utilization of acetyl-ACP was predominantly by 3-oxoacyl-ACP synthase I. In light-incubated isolated chloroplasts with high rates of fatty acid synthesis ( greater than 800 nmol.h-1 .
	manualset2
82474	4	397720	5	NULL	NULL	NULL	NULL	cerulenin	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the rate of acetyl-ACP-primed fatty acid synthesis was inhibited significantly by cerulenin , indicating that the slow utilization of acetyl-ACP was predominantly by 3-oxoacyl-ACP synthase I. In light-incubated isolated chloroplasts with high rates of fatty acid synthesis ( greater than 800 nmol.h-1 .
	manualset2
82475	5	397720	5	NULL	NULL	NULL	NULL	acetyl-ACP	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the rate of acetyl-ACP-primed fatty acid synthesis was inhibited significantly by cerulenin , indicating that the slow utilization of acetyl-ACP was predominantly by 3-oxoacyl-ACP synthase I. In light-incubated isolated chloroplasts with high rates of fatty acid synthesis ( greater than 800 nmol.h-1 .
	manualset2
82476	6	397720	5	NULL	NULL	0	NULL	3-oxoacyl-ACP synthase I	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the rate of acetyl-ACP-primed fatty acid synthesis was inhibited significantly by cerulenin , indicating that the slow utilization of acetyl-ACP was predominantly by 3-oxoacyl-ACP synthase I. In light-incubated isolated chloroplasts with high rates of fatty acid synthesis ( greater than 800 nmol.h-1 .
	manualset2
82477	7	397720	5	NULL	NULL	0	NULL	light	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the rate of acetyl-ACP-primed fatty acid synthesis was inhibited significantly by cerulenin , indicating that the slow utilization of acetyl-ACP was predominantly by 3-oxoacyl-ACP synthase I. In light-incubated isolated chloroplasts with high rates of fatty acid synthesis ( greater than 800 nmol.h-1 .
	manualset2
82478	8	397720	5	NULL	NULL	0	NULL	chloroplasts	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the rate of acetyl-ACP-primed fatty acid synthesis was inhibited significantly by cerulenin , indicating that the slow utilization of acetyl-ACP was predominantly by 3-oxoacyl-ACP synthase I. In light-incubated isolated chloroplasts with high rates of fatty acid synthesis ( greater than 800 nmol.h-1 .
	manualset2
82479	9	397720	5	NULL	NULL	NULL	NULL	fatty acid	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the rate of acetyl-ACP-primed fatty acid synthesis was inhibited significantly by cerulenin , indicating that the slow utilization of acetyl-ACP was predominantly by 3-oxoacyl-ACP synthase I. In light-incubated isolated chloroplasts with high rates of fatty acid synthesis ( greater than 800 nmol.h-1 .
	manualset2
82480	10	397720	5	NULL	NULL	0	NULL	synthesis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the rate of acetyl-ACP-primed fatty acid synthesis was inhibited significantly by cerulenin , indicating that the slow utilization of acetyl-ACP was predominantly by 3-oxoacyl-ACP synthase I. In light-incubated isolated chloroplasts with high rates of fatty acid synthesis ( greater than 800 nmol.h-1 .
	manualset2
82481	11	397720	5	NULL	NULL	0	NULL	800 nmol.h-1	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the rate of acetyl-ACP-primed fatty acid synthesis was inhibited significantly by cerulenin , indicating that the slow utilization of acetyl-ACP was predominantly by 3-oxoacyl-ACP synthase I. In light-incubated isolated chloroplasts with high rates of fatty acid synthesis ( greater than 800 nmol.h-1 .
	manualset2
82482	1	397721	5	NULL	NULL	0	NULL	dissociation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the results show that the dissociation of water on Fe ( 100 ) is a non-activated process : 0.16 eV for the zero-coverage limit and 0.03 eV when surface oxygen is present .
	manualset2
82483	2	397721	5	NULL	NULL	0	NULL	water	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the results show that the dissociation of water on Fe ( 100 ) is a non-activated process : 0.16 eV for the zero-coverage limit and 0.03 eV when surface oxygen is present .
	manualset2
82484	3	397721	5	NULL	NULL	0	NULL	Fe	Atom												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the results show that the dissociation of water on Fe ( 100 ) is a non-activated process : 0.16 eV for the zero-coverage limit and 0.03 eV when surface oxygen is present .
	manualset2
82485	5	397721	5	NULL	NULL	NULL	NULL	0.16 eV	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the results show that the dissociation of water on Fe ( 100 ) is a non-activated process : 0.16 eV for the zero-coverage limit and 0.03 eV when surface oxygen is present .
	manualset2
82486	6	397721	5	NULL	NULL	NULL	NULL	0.03 eV	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the results show that the dissociation of water on Fe ( 100 ) is a non-activated process : 0.16 eV for the zero-coverage limit and 0.03 eV when surface oxygen is present .
	manualset2
82487	7	397721	5	NULL	NULL	NULL	NULL	oxygen	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the results show that the dissociation of water on Fe ( 100 ) is a non-activated process : 0.16 eV for the zero-coverage limit and 0.03 eV when surface oxygen is present .
	manualset2
82546	4	397721	5	NULL	NULL	0	NULL	non-activated process	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the results show that the dissociation of water on Fe ( 100 ) is a non-activated process : 0.16 eV for the zero-coverage limit and 0.03 eV when surface oxygen is present .
	manualset2
82488	1	397722	5	NULL	NULL	0	NULL	spicules	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the spicules end as fairly large ovoid knobs , and vulvar flaps are present in the females .
	manualset2
82489	2	397722	5	NULL	NULL	0	NULL	ovoid knobs	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the spicules end as fairly large ovoid knobs , and vulvar flaps are present in the females .
	manualset2
82490	3	397722	5	NULL	NULL	0	NULL	vulvar flaps	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the spicules end as fairly large ovoid knobs , and vulvar flaps are present in the females .
	manualset2
82491	4	397722	5	NULL	NULL	0	NULL	females	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the spicules end as fairly large ovoid knobs , and vulvar flaps are present in the females .
	manualset2
82492	1	397723	5	NULL	NULL	0	NULL	neuron	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the three neuron groups that were immunoreactive for both PV and CB , immunoreactive for PV alone and immunoreactive for CB alone were heterogeneous in their structural features such as shape and size , and no particular difference was found in their structural features among these three groups .
	manualset2
82493	2	397723	5	NULL	NULL	0	NULL	immunoreactive	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the three neuron groups that were immunoreactive for both PV and CB , immunoreactive for PV alone and immunoreactive for CB alone were heterogeneous in their structural features such as shape and size , and no particular difference was found in their structural features among these three groups .
	manualset2
82494	3	397723	5	NULL	NULL	0	NULL	PV	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the three neuron groups that were immunoreactive for both PV and CB , immunoreactive for PV alone and immunoreactive for CB alone were heterogeneous in their structural features such as shape and size , and no particular difference was found in their structural features among these three groups .
	manualset2
82495	4	397723	5	NULL	NULL	0	NULL	CB	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the three neuron groups that were immunoreactive for both PV and CB , immunoreactive for PV alone and immunoreactive for CB alone were heterogeneous in their structural features such as shape and size , and no particular difference was found in their structural features among these three groups .
	manualset2
82496	5	397723	5	NULL	NULL	0	NULL	immunoreactive	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the three neuron groups that were immunoreactive for both PV and CB , immunoreactive for PV alone and immunoreactive for CB alone were heterogeneous in their structural features such as shape and size , and no particular difference was found in their structural features among these three groups .
	manualset2
82497	6	397723	5	NULL	NULL	0	NULL	PV	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the three neuron groups that were immunoreactive for both PV and CB , immunoreactive for PV alone and immunoreactive for CB alone were heterogeneous in their structural features such as shape and size , and no particular difference was found in their structural features among these three groups .
	manualset2
82498	7	397723	5	NULL	NULL	0	NULL	immunoreactive	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the three neuron groups that were immunoreactive for both PV and CB , immunoreactive for PV alone and immunoreactive for CB alone were heterogeneous in their structural features such as shape and size , and no particular difference was found in their structural features among these three groups .
	manualset2
82499	8	397723	5	NULL	NULL	0	NULL	CB	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the three neuron groups that were immunoreactive for both PV and CB , immunoreactive for PV alone and immunoreactive for CB alone were heterogeneous in their structural features such as shape and size , and no particular difference was found in their structural features among these three groups .
	manualset2
82500	1	397724	5	NULL	NULL	NULL	NULL	pentylenetetrazol	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the threshold for pentylenetetrazol ( PTZ ) clonic convulsions was also increased in response to DPA administration .
	manualset2
82501	2	397724	5	NULL	NULL	NULL	NULL	PTZ	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the threshold for pentylenetetrazol ( PTZ ) clonic convulsions was also increased in response to DPA administration .
	manualset2
82502	3	397724	5	NULL	NULL	0	NULL	clonic convulsions	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the threshold for pentylenetetrazol ( PTZ ) clonic convulsions was also increased in response to DPA administration .
	manualset2
82503	4	397724	5	NULL	NULL	0	NULL	response	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the threshold for pentylenetetrazol ( PTZ ) clonic convulsions was also increased in response to DPA administration .
	manualset2
82504	5	397724	5	NULL	NULL	NULL	NULL	DPA	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the threshold for pentylenetetrazol ( PTZ ) clonic convulsions was also increased in response to DPA administration .
	manualset2
82505	6	397724	5	NULL	NULL	0	NULL	administration	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the threshold for pentylenetetrazol ( PTZ ) clonic convulsions was also increased in response to DPA administration .
	manualset2
82506	1	397725	5	NULL	NULL	0	NULL	dosages	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Advantages of different dosages of active metabolites in the follow-up of azathioprine treatment for Crohn disease ) .
	manualset2
82507	2	397725	5	NULL	NULL	NULL	NULL	active metabolites	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Advantages of different dosages of active metabolites in the follow-up of azathioprine treatment for Crohn disease ) .
	manualset2
82508	3	397725	5	NULL	NULL	NULL	NULL	azathioprine	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Advantages of different dosages of active metabolites in the follow-up of azathioprine treatment for Crohn disease ) .
	manualset2
82509	4	397725	5	NULL	NULL	0	NULL	treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Advantages of different dosages of active metabolites in the follow-up of azathioprine treatment for Crohn disease ) .
	manualset2
82510	5	397725	5	NULL	NULL	0	NULL	Crohn disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Advantages of different dosages of active metabolites in the follow-up of azathioprine treatment for Crohn disease ) .
	manualset2
82511	1	397726	5	NULL	NULL	NULL	NULL	Selection	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Selection of school sites with reference to traffic noise in cities ) .
	manualset2
82512	2	397726	5	NULL	NULL	0	NULL	school	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	( Selection of school sites with reference to traffic noise in cities ) .
	manualset2
82513	3	397726	5	NULL	NULL	0	NULL	traffic	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	( Selection of school sites with reference to traffic noise in cities ) .
	manualset2
82514	4	397726	5	NULL	NULL	0	NULL	noise	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	( Selection of school sites with reference to traffic noise in cities ) .
	manualset2
82515	1	397727	5	NULL	NULL	0	NULL	tumor	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the tumor displayed evidence of close relations with the thymus capsule ; the possibility that it may arise from the thymic stroma is considered .
	manualset2
82516	2	397727	5	NULL	NULL	0	NULL	relations	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the tumor displayed evidence of close relations with the thymus capsule ; the possibility that it may arise from the thymic stroma is considered .
	manualset2
82517	3	397727	5	NULL	NULL	0	NULL	thymus	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the tumor displayed evidence of close relations with the thymus capsule ; the possibility that it may arise from the thymic stroma is considered .
	manualset2
82518	4	397727	5	NULL	NULL	0	NULL	capsule	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the tumor displayed evidence of close relations with the thymus capsule ; the possibility that it may arise from the thymic stroma is considered .
	manualset2
82519	5	397727	5	NULL	NULL	NULL	NULL	thymic stroma	AnatomicalPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , the tumor displayed evidence of close relations with the thymus capsule ; the possibility that it may arise from the thymic stroma is considered .
	manualset2
82520	1	397728	5	NULL	NULL	0	NULL	water	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the water content was quantified using a PCA approach .
	manualset2
82521	2	397728	5	NULL	NULL	0	NULL	PCA	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , the water content was quantified using a PCA approach .
	manualset2
82522	1	397729	5	NULL	NULL	0	NULL	P-D MTs	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , there appeared to be a bias in the P-D MTs , with slightly more plus ends oriented distally .
	manualset2
82523	1	397730	5	NULL	NULL	NULL	NULL	magnetic mismatch negativity ( MMNm )	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , there was an increase of magnetic mismatch negativity ( MMNm ) amplitude in attended conditions and a simultaneous decrease in unattended conditions after water drinking .
	manualset2
82525	2	397730	5	NULL	NULL	NULL	NULL	water drinking	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , there was an increase of magnetic mismatch negativity ( MMNm ) amplitude in attended conditions and a simultaneous decrease in unattended conditions after water drinking .
	manualset2
82538	1	397731	5	NULL	NULL	0	NULL	nicotinic acid	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , these results indicate that nicotinic acid is a potent antidote to treat GMX1777 overdose .
	manualset2
82539	2	397731	5	NULL	NULL	NULL	NULL	potent antidote	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , these results indicate that nicotinic acid is a potent antidote to treat GMX1777 overdose .
	manualset2
82540	3	397731	5	NULL	NULL	0	NULL	treat	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , these results indicate that nicotinic acid is a potent antidote to treat GMX1777 overdose .
	manualset2
82541	4	397731	5	NULL	NULL	NULL	NULL	GMX1777 overdose	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , these results indicate that nicotinic acid is a potent antidote to treat GMX1777 overdose .
	manualset2
82560	1	397732	5	NULL	NULL	0	NULL	agonist affinity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this is the first demonstration that agonist affinity of a GPCR and the affinity of arrestin binding to the phosphorylated receptor are regulated by distinct receptor phosphodomains .
	manualset2
82561	2	397732	5	NULL	NULL	0	NULL	GPCR	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this is the first demonstration that agonist affinity of a GPCR and the affinity of arrestin binding to the phosphorylated receptor are regulated by distinct receptor phosphodomains .
	manualset2
82562	3	397732	5	NULL	NULL	0	NULL	affinity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this is the first demonstration that agonist affinity of a GPCR and the affinity of arrestin binding to the phosphorylated receptor are regulated by distinct receptor phosphodomains .
	manualset2
82563	4	397732	5	NULL	NULL	0	NULL	arrestin binding	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this is the first demonstration that agonist affinity of a GPCR and the affinity of arrestin binding to the phosphorylated receptor are regulated by distinct receptor phosphodomains .
	manualset2
82564	5	397732	5	NULL	NULL	0	NULL	phosphorylated receptor	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this is the first demonstration that agonist affinity of a GPCR and the affinity of arrestin binding to the phosphorylated receptor are regulated by distinct receptor phosphodomains .
	manualset2
83232	6	397732	5	NULL	NULL	0	NULL	distinct receptor phosphodomains	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this is the first demonstration that agonist affinity of a GPCR and the affinity of arrestin binding to the phosphorylated receptor are regulated by distinct receptor phosphodomains .
	manualset2
82565	1	397733	5	NULL	NULL	0	NULL	patient	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this patient also had a wheeze , eosinophilia , elevation of the serum IgE level , and was positive for specific IgE to Mucor .
	manualset2
82566	2	397733	5	NULL	NULL	0	NULL	wheeze	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this patient also had a wheeze , eosinophilia , elevation of the serum IgE level , and was positive for specific IgE to Mucor .
	manualset2
82567	3	397733	5	NULL	NULL	0	NULL	eosinophilia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this patient also had a wheeze , eosinophilia , elevation of the serum IgE level , and was positive for specific IgE to Mucor .
	manualset2
82568	4	397733	5	NULL	NULL	0	NULL	elevation of the serum IgE level	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this patient also had a wheeze , eosinophilia , elevation of the serum IgE level , and was positive for specific IgE to Mucor .
	manualset2
82569	5	397733	5	NULL	NULL	0	NULL	IgE	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this patient also had a wheeze , eosinophilia , elevation of the serum IgE level , and was positive for specific IgE to Mucor .
	manualset2
82570	6	397733	5	NULL	NULL	0	NULL	Mucor	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this patient also had a wheeze , eosinophilia , elevation of the serum IgE level , and was positive for specific IgE to Mucor .
	manualset2
82571	1	397734	5	NULL	NULL	0	NULL	rescue	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this rescue depends on both the clathrin-binding and J domains , suggesting that the ability of Aux to bind clathrin and the Hsc70 ATPase is essential for sperm formation .
	manualset2
82572	2	397734	5	NULL	NULL	0	NULL	clathrin-binding	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this rescue depends on both the clathrin-binding and J domains , suggesting that the ability of Aux to bind clathrin and the Hsc70 ATPase is essential for sperm formation .
	manualset2
82573	3	397734	5	NULL	NULL	0	NULL	J domains	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this rescue depends on both the clathrin-binding and J domains , suggesting that the ability of Aux to bind clathrin and the Hsc70 ATPase is essential for sperm formation .
	manualset2
82574	4	397734	5	NULL	NULL	0	NULL	Aux	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this rescue depends on both the clathrin-binding and J domains , suggesting that the ability of Aux to bind clathrin and the Hsc70 ATPase is essential for sperm formation .
	manualset2
82575	5	397734	5	NULL	NULL	0	NULL	bind	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this rescue depends on both the clathrin-binding and J domains , suggesting that the ability of Aux to bind clathrin and the Hsc70 ATPase is essential for sperm formation .
	manualset2
82576	6	397734	5	NULL	NULL	0	NULL	clathrin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this rescue depends on both the clathrin-binding and J domains , suggesting that the ability of Aux to bind clathrin and the Hsc70 ATPase is essential for sperm formation .
	manualset2
82577	7	397734	5	NULL	NULL	0	NULL	Hsc70 ATPase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this rescue depends on both the clathrin-binding and J domains , suggesting that the ability of Aux to bind clathrin and the Hsc70 ATPase is essential for sperm formation .
	manualset2
82578	8	397734	5	NULL	NULL	0	NULL	sperm formation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this rescue depends on both the clathrin-binding and J domains , suggesting that the ability of Aux to bind clathrin and the Hsc70 ATPase is essential for sperm formation .
	manualset2
82579	1	397735	5	NULL	NULL	0	NULL	catecholamines ( NE and EPI )	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this study also examined the possible relationships between catecholamines ( NE and EPI ) and 8-isoprostane and between IL-2 and 8-isoprostane following a combined physical and psychological challenge .
	manualset2
82580	2	397735	5	NULL	NULL	0	NULL	8-isoprostane	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this study also examined the possible relationships between catecholamines ( NE and EPI ) and 8-isoprostane and between IL-2 and 8-isoprostane following a combined physical and psychological challenge .
	manualset2
82581	3	397735	5	NULL	NULL	0	NULL	IL-2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this study also examined the possible relationships between catecholamines ( NE and EPI ) and 8-isoprostane and between IL-2 and 8-isoprostane following a combined physical and psychological challenge .
	manualset2
82582	4	397735	5	NULL	NULL	0	NULL	8-isoprostane	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this study also examined the possible relationships between catecholamines ( NE and EPI ) and 8-isoprostane and between IL-2 and 8-isoprostane following a combined physical and psychological challenge .
	manualset2
82583	5	397735	5	NULL	NULL	0	NULL	physical and psychological challenge	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , this study also examined the possible relationships between catecholamines ( NE and EPI ) and 8-isoprostane and between IL-2 and 8-isoprostane following a combined physical and psychological challenge .
	manualset2
82584	1	397736	5	NULL	NULL	0	NULL	titration	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , titration of this group is linked with marked spectroscopic changes unique to CIP .
	manualset2
82585	2	397736	5	NULL	NULL	0	NULL	spectroscopic changes	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , titration of this group is linked with marked spectroscopic changes unique to CIP .
	manualset2
82586	3	397736	5	NULL	NULL	0	NULL	CIP	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , titration of this group is linked with marked spectroscopic changes unique to CIP .
	manualset2
82587	1	397737	5	NULL	NULL	0	NULL	Sensitivity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Sensitivity to acidity of aphthous virus strains non pathogenic for swine ) .
	manualset2
82588	2	397737	5	NULL	NULL	NULL	NULL	acidity	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Sensitivity to acidity of aphthous virus strains non pathogenic for swine ) .
	manualset2
82589	3	397737	5	NULL	NULL	0	NULL	aphthous virus strains	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Sensitivity to acidity of aphthous virus strains non pathogenic for swine ) .
	manualset2
82590	4	397737	5	NULL	NULL	0	NULL	swine	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Sensitivity to acidity of aphthous virus strains non pathogenic for swine ) .
	manualset2
82591	1	397738	5	NULL	NULL	0	NULL	anti-inflammatory action	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , to confirm the anti-inflammatory action of PPAR activated by baicalin , we used lipopolysaccharide ( LPS ) - treated cells and mice .
	manualset2
82592	2	397738	5	NULL	NULL	0	NULL	PPAR	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , to confirm the anti-inflammatory action of PPAR activated by baicalin , we used lipopolysaccharide ( LPS ) - treated cells and mice .
	manualset2
82593	3	397738	5	NULL	NULL	0	NULL	baicalin	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , to confirm the anti-inflammatory action of PPAR activated by baicalin , we used lipopolysaccharide ( LPS ) - treated cells and mice .
	manualset2
82594	4	397738	5	NULL	NULL	0	NULL	lipopolysaccharide ( LPS ) - treated cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , to confirm the anti-inflammatory action of PPAR activated by baicalin , we used lipopolysaccharide ( LPS ) - treated cells and mice .
	manualset2
82595	5	397738	5	NULL	NULL	0	NULL	mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , to confirm the anti-inflammatory action of PPAR activated by baicalin , we used lipopolysaccharide ( LPS ) - treated cells and mice .
	manualset2
82596	1	397739	5	NULL	NULL	0	NULL	treatment	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , treatment with the non-promoting mitogens 4-O-methyl-TPA and Ca-ionophore A 23187 did not result in any alterations of the matrix composition .
	manualset2
82597	2	397739	5	NULL	NULL	0	NULL	non-promoting mitogens 4-O-methyl-TPA	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , treatment with the non-promoting mitogens 4-O-methyl-TPA and Ca-ionophore A 23187 did not result in any alterations of the matrix composition .
	manualset2
82598	3	397739	5	NULL	NULL	0	NULL	non-promoting mitogens Ca-ionophore A 23187	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , treatment with the non-promoting mitogens 4-O-methyl-TPA and Ca-ionophore A 23187 did not result in any alterations of the matrix composition .
	manualset2
82599	4	397739	5	NULL	NULL	0	NULL	matrix composition	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , treatment with the non-promoting mitogens 4-O-methyl-TPA and Ca-ionophore A 23187 did not result in any alterations of the matrix composition .
	manualset2
82600	1	397740	5	NULL	NULL	0	NULL	tremor power	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , tremor power accounted for a significant part of variance in the contralateral striatum , suggesting a relationship between this PD symptom and the degeneration of the dopaminergic system .
	manualset2
82601	2	397740	5	NULL	NULL	0	NULL	contralateral striatum	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , tremor power accounted for a significant part of variance in the contralateral striatum , suggesting a relationship between this PD symptom and the degeneration of the dopaminergic system .
	manualset2
82602	3	397740	5	NULL	NULL	0	NULL	PD symptom	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , tremor power accounted for a significant part of variance in the contralateral striatum , suggesting a relationship between this PD symptom and the degeneration of the dopaminergic system .
	manualset2
82603	4	397740	5	NULL	NULL	0	NULL	degeneration of the dopaminergic system 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , tremor power accounted for a significant part of variance in the contralateral striatum , suggesting a relationship between this PD symptom and the degeneration of the dopaminergic system .
	manualset2
82604	1	397741	5	NULL	NULL	0	NULL	high affinity binding	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we compare two of these double sites and show that high affinity binding of GATA-1 to a reporter gene does not necessarily induce transactivation , namely the sequence of the DNA-binding site can alter the ability of GATA-1 to stimulate transcription .
	manualset2
82605	2	397741	5	NULL	NULL	0	NULL	GATA-1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we compare two of these double sites and show that high affinity binding of GATA-1 to a reporter gene does not necessarily induce transactivation , namely the sequence of the DNA-binding site can alter the ability of GATA-1 to stimulate transcription .
	manualset2
82606	3	397741	5	NULL	NULL	0	NULL	transactivation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we compare two of these double sites and show that high affinity binding of GATA-1 to a reporter gene does not necessarily induce transactivation , namely the sequence of the DNA-binding site can alter the ability of GATA-1 to stimulate transcription .
	manualset2
82607	4	397741	5	NULL	NULL	NULL	NULL	sequence of the DNA-binding site	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , we compare two of these double sites and show that high affinity binding of GATA-1 to a reporter gene does not necessarily induce transactivation , namely the sequence of the DNA-binding site can alter the ability of GATA-1 to stimulate transcription .
	manualset2
82608	5	397741	5	NULL	NULL	0	NULL	GATA-1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we compare two of these double sites and show that high affinity binding of GATA-1 to a reporter gene does not necessarily induce transactivation , namely the sequence of the DNA-binding site can alter the ability of GATA-1 to stimulate transcription .
	manualset2
82609	6	397741	5	NULL	NULL	0	NULL	transcription	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we compare two of these double sites and show that high affinity binding of GATA-1 to a reporter gene does not necessarily induce transactivation , namely the sequence of the DNA-binding site can alter the ability of GATA-1 to stimulate transcription .
	manualset2
82610	1	397742	5	NULL	NULL	0	NULL	alk1 expression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we demonstrate that alk1 expression requires blood flow , and despite normal levels of shear stress , some flow-responsive genes are dysregulated in alk1 mutant arterial endothelial cells .
	manualset2
82611	3	397742	5	NULL	NULL	NULL	NULL	shear stress	ExperimentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , we demonstrate that alk1 expression requires blood flow , and despite normal levels of shear stress , some flow-responsive genes are dysregulated in alk1 mutant arterial endothelial cells .
	manualset2
82612	4	397742	5	NULL	NULL	NULL	NULL	flow-responsive genes	Gene												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , we demonstrate that alk1 expression requires blood flow , and despite normal levels of shear stress , some flow-responsive genes are dysregulated in alk1 mutant arterial endothelial cells .
	manualset2
82613	5	397742	5	NULL	NULL	NULL	NULL	alk1 mutant arterial endothelial cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , we demonstrate that alk1 expression requires blood flow , and despite normal levels of shear stress , some flow-responsive genes are dysregulated in alk1 mutant arterial endothelial cells .
	manualset2
82614	2	397742	5	NULL	NULL	0	NULL	blood flow	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we demonstrate that alk1 expression requires blood flow , and despite normal levels of shear stress , some flow-responsive genes are dysregulated in alk1 mutant arterial endothelial cells .
	manualset2
82615	1	397743	5	NULL	NULL	0	NULL	Bcl-2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we have targeted Bcl-2 specifically to either the ER or the outer mitochondrial membrane to test whether induction of apoptosis by Bcl-2 is dependent upon its localization within either of these membranes .
	manualset2
82616	2	397743	5	NULL	NULL	0	NULL	ER	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we have targeted Bcl-2 specifically to either the ER or the outer mitochondrial membrane to test whether induction of apoptosis by Bcl-2 is dependent upon its localization within either of these membranes .
	manualset2
82617	3	397743	5	NULL	NULL	0	NULL	outer mitochondrial membrane	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we have targeted Bcl-2 specifically to either the ER or the outer mitochondrial membrane to test whether induction of apoptosis by Bcl-2 is dependent upon its localization within either of these membranes .
	manualset2
82618	4	397743	5	NULL	NULL	0	NULL	induction of apoptosis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we have targeted Bcl-2 specifically to either the ER or the outer mitochondrial membrane to test whether induction of apoptosis by Bcl-2 is dependent upon its localization within either of these membranes .
	manualset2
82619	5	397743	5	NULL	NULL	0	NULL	Bcl-2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we have targeted Bcl-2 specifically to either the ER or the outer mitochondrial membrane to test whether induction of apoptosis by Bcl-2 is dependent upon its localization within either of these membranes .
	manualset2
82620	6	397743	5	NULL	NULL	0	NULL	localization	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we have targeted Bcl-2 specifically to either the ER or the outer mitochondrial membrane to test whether induction of apoptosis by Bcl-2 is dependent upon its localization within either of these membranes .
	manualset2
82621	7	397743	5	NULL	NULL	0	NULL	membranes	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we have targeted Bcl-2 specifically to either the ER or the outer mitochondrial membrane to test whether induction of apoptosis by Bcl-2 is dependent upon its localization within either of these membranes .
	manualset2
82622	1	397744	5	NULL	NULL	0	NULL	isolate	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we planned to isolate and identify the neuroprotective agent from LBP using chromatographic methods .
	manualset2
82623	2	397744	5	NULL	NULL	0	NULL	identify	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we planned to isolate and identify the neuroprotective agent from LBP using chromatographic methods .
	manualset2
82624	3	397744	5	NULL	NULL	0	NULL	neuroprotective agent	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we planned to isolate and identify the neuroprotective agent from LBP using chromatographic methods .
	manualset2
82625	4	397744	5	NULL	NULL	0	NULL	LBP	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we planned to isolate and identify the neuroprotective agent from LBP using chromatographic methods .
	manualset2
82626	5	397744	5	NULL	NULL	0	NULL	chromatographic methods	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we planned to isolate and identify the neuroprotective agent from LBP using chromatographic methods .
	manualset2
82628	1	397745	5	NULL	NULL	NULL	NULL	STU	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , we present evidence that STU serves as an important regulator mediating the control of cell proliferation by GA possibly through two cyclin-dependent kinase inhibitors , SIM and SMR1 .
	manualset2
82630	2	397745	5	NULL	NULL	NULL	NULL	important regulator	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , we present evidence that STU serves as an important regulator mediating the control of cell proliferation by GA possibly through two cyclin-dependent kinase inhibitors , SIM and SMR1 .
	manualset2
82631	3	397745	5	NULL	NULL	NULL	NULL	control of cell proliferation	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , we present evidence that STU serves as an important regulator mediating the control of cell proliferation by GA possibly through two cyclin-dependent kinase inhibitors , SIM and SMR1 .
	manualset2
82633	4	397745	5	NULL	NULL	NULL	NULL	GA	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , we present evidence that STU serves as an important regulator mediating the control of cell proliferation by GA possibly through two cyclin-dependent kinase inhibitors , SIM and SMR1 .
	manualset2
82634	5	397745	5	NULL	NULL	NULL	NULL	cyclin-dependent kinase inhibitors	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , we present evidence that STU serves as an important regulator mediating the control of cell proliferation by GA possibly through two cyclin-dependent kinase inhibitors , SIM and SMR1 .
	manualset2
82635	6	397745	5	NULL	NULL	NULL	NULL	SIM	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , we present evidence that STU serves as an important regulator mediating the control of cell proliferation by GA possibly through two cyclin-dependent kinase inhibitors , SIM and SMR1 .
	manualset2
82636	7	397745	5	NULL	NULL	NULL	NULL	SMR1	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , we present evidence that STU serves as an important regulator mediating the control of cell proliferation by GA possibly through two cyclin-dependent kinase inhibitors , SIM and SMR1 .
	manualset2
82637	1	397746	5	NULL	NULL	NULL	NULL	CsgG	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , we show that CsgG belongs to the nascent class of helical outer-membrane macromolecular exporters .
	manualset2
82639	2	397746	5	NULL	NULL	NULL	NULL	helical outer-membrane macromolecular exporters	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , we show that CsgG belongs to the nascent class of helical outer-membrane macromolecular exporters .
	manualset2
82640	1	397747	5	NULL	NULL	0	NULL	Serological types of strains of B. pertussis	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Serological types of strains of B. pertussis isolated in the Warsaw area and evaluation of their histamine-sensitisation potential for mice ) .
	manualset2
82641	2	397747	5	NULL	NULL	0	NULL	Warsaw area	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	( Serological types of strains of B. pertussis isolated in the Warsaw area and evaluation of their histamine-sensitisation potential for mice ) .
	manualset2
82642	3	397747	5	NULL	NULL	0	NULL	evaluation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Serological types of strains of B. pertussis isolated in the Warsaw area and evaluation of their histamine-sensitisation potential for mice ) .
	manualset2
82643	4	397747	5	NULL	NULL	0	NULL	histamine-sensitisation potential	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Serological types of strains of B. pertussis isolated in the Warsaw area and evaluation of their histamine-sensitisation potential for mice ) .
	manualset2
82644	5	397747	5	NULL	NULL	0	NULL	mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Serological types of strains of B. pertussis isolated in the Warsaw area and evaluation of their histamine-sensitisation potential for mice ) .
	manualset2
82645	1	397748	5	NULL	NULL	0	NULL	c-Jun	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we show that a mutated form of c-Jun lacking the transactivation domain ( TAM-67 ) was a much stronger activator of the IL-6 promoter than c-Jun .
	manualset2
82646	2	397748	5	NULL	NULL	0	NULL	transactivation domain ( TAM-67 )	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we show that a mutated form of c-Jun lacking the transactivation domain ( TAM-67 ) was a much stronger activator of the IL-6 promoter than c-Jun .
	manualset2
82647	3	397748	5	NULL	NULL	0	NULL	stronger activator	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we show that a mutated form of c-Jun lacking the transactivation domain ( TAM-67 ) was a much stronger activator of the IL-6 promoter than c-Jun .
	manualset2
82648	4	397748	5	NULL	NULL	0	NULL	IL-6 promoter	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we show that a mutated form of c-Jun lacking the transactivation domain ( TAM-67 ) was a much stronger activator of the IL-6 promoter than c-Jun .
	manualset2
82649	5	397748	5	NULL	NULL	0	NULL	c-Jun	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we show that a mutated form of c-Jun lacking the transactivation domain ( TAM-67 ) was a much stronger activator of the IL-6 promoter than c-Jun .
	manualset2
82650	1	397749	5	NULL	NULL	0	NULL	RASSF2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we showed that RASSF2 and MST2 do indeed colocalize , but whereas RASSF2 alone is nuclear , the presence of MST1 or MST2 results in colocalization in the cytoplasm .
	manualset2
82651	2	397749	5	NULL	NULL	0	NULL	MST2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , we showed that RASSF2 and MST2 do indeed colocalize , but whereas RASSF2 alone is nuclear , the presence of MST1 or MST2 results in colocalization in the cytoplasm .
	manualset2
82653	3	397749	5	NULL	NULL	NULL	NULL	RASSF2	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , we showed that RASSF2 and MST2 do indeed colocalize , but whereas RASSF2 alone is nuclear , the presence of MST1 or MST2 results in colocalization in the cytoplasm .
	manualset2
82654	4	397749	5	NULL	NULL	NULL	NULL	MST1	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , we showed that RASSF2 and MST2 do indeed colocalize , but whereas RASSF2 alone is nuclear , the presence of MST1 or MST2 results in colocalization in the cytoplasm .
	manualset2
82655	5	397749	5	NULL	NULL	NULL	NULL	MST2	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , we showed that RASSF2 and MST2 do indeed colocalize , but whereas RASSF2 alone is nuclear , the presence of MST1 or MST2 results in colocalization in the cytoplasm .
	manualset2
82656	6	397749	5	NULL	NULL	NULL	NULL	colocalization	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , we showed that RASSF2 and MST2 do indeed colocalize , but whereas RASSF2 alone is nuclear , the presence of MST1 or MST2 results in colocalization in the cytoplasm .
	manualset2
82657	7	397749	5	NULL	NULL	NULL	NULL	cytoplasm	CellComponent												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , we showed that RASSF2 and MST2 do indeed colocalize , but whereas RASSF2 alone is nuclear , the presence of MST1 or MST2 results in colocalization in the cytoplasm .
	manualset2
82658	1	397750	5	NULL	NULL	0	NULL	 western blotting	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , western blotting was performed to evaluate the expression of NFB and COX-2 in testes .
	manualset2
82660	2	397750	5	NULL	NULL	NULL	NULL	expression	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , western blotting was performed to evaluate the expression of NFB and COX-2 in testes .
	manualset2
82661	3	397750	5	NULL	NULL	NULL	NULL	NFB	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , western blotting was performed to evaluate the expression of NFB and COX-2 in testes .
	manualset2
82662	4	397750	5	NULL	NULL	NULL	NULL	COX-2	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , western blotting was performed to evaluate the expression of NFB and COX-2 in testes .
	manualset2
82663	5	397750	5	NULL	NULL	NULL	NULL	testes	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , western blotting was performed to evaluate the expression of NFB and COX-2 in testes .
	manualset2
82664	1	397751	5	NULL	NULL	0	NULL	endocytosis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , when endocytosis and lysosomal destabilization were inhibited , inflammasome activity was diminished , supporting the notion that nanoparticles rupture lysosomal compartments and behave as ` danger signals ' ( Hornung V , Bauernfeind F , Halle A , Samstad EO , Kono H , Rock KL , et al. .
	manualset2
82665	2	397751	5	NULL	NULL	0	NULL	lysosomal destabilization	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , when endocytosis and lysosomal destabilization were inhibited , inflammasome activity was diminished , supporting the notion that nanoparticles rupture lysosomal compartments and behave as ` danger signals ' ( Hornung V , Bauernfeind F , Halle A , Samstad EO , Kono H , Rock KL , et al. .
	manualset2
82666	3	397751	5	NULL	NULL	0	NULL	inflammasome activity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , when endocytosis and lysosomal destabilization were inhibited , inflammasome activity was diminished , supporting the notion that nanoparticles rupture lysosomal compartments and behave as ` danger signals ' ( Hornung V , Bauernfeind F , Halle A , Samstad EO , Kono H , Rock KL , et al. .
	manualset2
82669	4	397751	5	NULL	NULL	NULL	NULL	lysosomal compartments	CellComponent												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , when endocytosis and lysosomal destabilization were inhibited , inflammasome activity was diminished , supporting the notion that nanoparticles rupture lysosomal compartments and behave as ` danger signals ' ( Hornung V , Bauernfeind F , Halle A , Samstad EO , Kono H , Rock KL , et al. .
	manualset2
82670	5	397751	5	NULL	NULL	NULL	NULL	danger signals	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , when endocytosis and lysosomal destabilization were inhibited , inflammasome activity was diminished , supporting the notion that nanoparticles rupture lysosomal compartments and behave as ` danger signals ' ( Hornung V , Bauernfeind F , Halle A , Samstad EO , Kono H , Rock KL , et al. .
	manualset2
82671	1	397752	5	NULL	NULL	0	NULL	accumulation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , while the accumulation of CD8 + T cells in the neural parenchyma was significantly delayed in both CXCR3 - and CXCR3/CCR5-deficient mice , more CD8 + T cells were found in the parenchyma of double-deficient mice when these were analyzed around the time when the difference in clinical outcome becomes manifest .
	manualset2
82672	2	397752	5	NULL	NULL	0	NULL	CD8 + T cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , while the accumulation of CD8 + T cells in the neural parenchyma was significantly delayed in both CXCR3 - and CXCR3/CCR5-deficient mice , more CD8 + T cells were found in the parenchyma of double-deficient mice when these were analyzed around the time when the difference in clinical outcome becomes manifest .
	manualset2
82673	3	397752	5	NULL	NULL	0	NULL	neural parenchyma	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , while the accumulation of CD8 + T cells in the neural parenchyma was significantly delayed in both CXCR3 - and CXCR3/CCR5-deficient mice , more CD8 + T cells were found in the parenchyma of double-deficient mice when these were analyzed around the time when the difference in clinical outcome becomes manifest .
	manualset2
82674	4	397752	5	NULL	NULL	NULL	NULL	CXCR3 - and CXCR3/CCR5-deficient mice	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , while the accumulation of CD8 + T cells in the neural parenchyma was significantly delayed in both CXCR3 - and CXCR3/CCR5-deficient mice , more CD8 + T cells were found in the parenchyma of double-deficient mice when these were analyzed around the time when the difference in clinical outcome becomes manifest .
	manualset2
82675	5	397752	5	NULL	NULL	0	NULL	CD8 + T cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , while the accumulation of CD8 + T cells in the neural parenchyma was significantly delayed in both CXCR3 - and CXCR3/CCR5-deficient mice , more CD8 + T cells were found in the parenchyma of double-deficient mice when these were analyzed around the time when the difference in clinical outcome becomes manifest .
	manualset2
82676	6	397752	5	NULL	NULL	0	NULL	parenchyma	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , while the accumulation of CD8 + T cells in the neural parenchyma was significantly delayed in both CXCR3 - and CXCR3/CCR5-deficient mice , more CD8 + T cells were found in the parenchyma of double-deficient mice when these were analyzed around the time when the difference in clinical outcome becomes manifest .
	manualset2
82677	7	397752	5	NULL	NULL	0	NULL	double-deficient mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , while the accumulation of CD8 + T cells in the neural parenchyma was significantly delayed in both CXCR3 - and CXCR3/CCR5-deficient mice , more CD8 + T cells were found in the parenchyma of double-deficient mice when these were analyzed around the time when the difference in clinical outcome becomes manifest .
	manualset2
82678	8	397752	5	NULL	NULL	NULL	NULL	around the time	TimePoint												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore , while the accumulation of CD8 + T cells in the neural parenchyma was significantly delayed in both CXCR3 - and CXCR3/CCR5-deficient mice , more CD8 + T cells were found in the parenchyma of double-deficient mice when these were analyzed around the time when the difference in clinical outcome becomes manifest .
	manualset2
82679	9	397752	5	NULL	NULL	0	NULL	clinical outcome	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore , while the accumulation of CD8 + T cells in the neural parenchyma was significantly delayed in both CXCR3 - and CXCR3/CCR5-deficient mice , more CD8 + T cells were found in the parenchyma of double-deficient mice when these were analyzed around the time when the difference in clinical outcome becomes manifest .
	manualset2
82743	1	397753	5	NULL	NULL	0	NULL	Ang II	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore Ang II and CGP 42112 have no effect on nitroprusside-stimulated cGMP levels in these cells , thus ruling out interactions between the AT2 receptor and soluble guanylate cyclase .
	manualset2
82744	2	397753	5	NULL	NULL	0	NULL	CGP 42112	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore Ang II and CGP 42112 have no effect on nitroprusside-stimulated cGMP levels in these cells , thus ruling out interactions between the AT2 receptor and soluble guanylate cyclase .
	manualset2
82745	3	397753	5	NULL	NULL	NULL	NULL	nitroprusside-stimulated cGMP levels	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Furthermore Ang II and CGP 42112 have no effect on nitroprusside-stimulated cGMP levels in these cells , thus ruling out interactions between the AT2 receptor and soluble guanylate cyclase .
	manualset2
82746	4	397753	5	NULL	NULL	0	NULL	cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore Ang II and CGP 42112 have no effect on nitroprusside-stimulated cGMP levels in these cells , thus ruling out interactions between the AT2 receptor and soluble guanylate cyclase .
	manualset2
82747	5	397753	5	NULL	NULL	0	NULL	interactions	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore Ang II and CGP 42112 have no effect on nitroprusside-stimulated cGMP levels in these cells , thus ruling out interactions between the AT2 receptor and soluble guanylate cyclase .
	manualset2
82748	6	397753	5	NULL	NULL	0	NULL	AT2 receptor	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore Ang II and CGP 42112 have no effect on nitroprusside-stimulated cGMP levels in these cells , thus ruling out interactions between the AT2 receptor and soluble guanylate cyclase .
	manualset2
82749	7	397753	5	NULL	NULL	0	NULL	soluble guanylate cyclase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore Ang II and CGP 42112 have no effect on nitroprusside-stimulated cGMP levels in these cells , thus ruling out interactions between the AT2 receptor and soluble guanylate cyclase .
	manualset2
82750	1	397754	5	NULL	NULL	0	NULL	cell lines	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore cell lines derived from IL-7 transgenic mice may provide a novel source of rare factor-dependent bipotent stem cells .
	manualset2
82751	2	397754	5	NULL	NULL	0	NULL	IL-7 transgenic mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore cell lines derived from IL-7 transgenic mice may provide a novel source of rare factor-dependent bipotent stem cells .
	manualset2
82752	3	397754	5	NULL	NULL	0	NULL	factor-dependent bipotent stem cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore cell lines derived from IL-7 transgenic mice may provide a novel source of rare factor-dependent bipotent stem cells .
	manualset2
82753	1	397755	5	NULL	NULL	0	NULL	hypoalbuminemia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore hypoalbuminemia due to severe anorexia might have enhanced the occurrence of the disease .
	manualset2
82754	2	397755	5	NULL	NULL	0	NULL	severe anorexia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore hypoalbuminemia due to severe anorexia might have enhanced the occurrence of the disease .
	manualset2
82755	3	397755	5	NULL	NULL	0	NULL	occurrence	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore hypoalbuminemia due to severe anorexia might have enhanced the occurrence of the disease .
	manualset2
82756	4	397755	5	NULL	NULL	0	NULL	disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore hypoalbuminemia due to severe anorexia might have enhanced the occurrence of the disease .
	manualset2
82757	1	397756	5	NULL	NULL	0	NULL	Serum hormonal activities	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Serum hormonal activities in normal women and in patients with breast cancer ) .
	manualset2
82758	2	397756	5	NULL	NULL	0	NULL	normal women	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( Serum hormonal activities in normal women and in patients with breast cancer ) .
	manualset2
82759	3	397756	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( Serum hormonal activities in normal women and in patients with breast cancer ) .
	manualset2
82760	4	397756	5	NULL	NULL	0	NULL	breast cancer	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Serum hormonal activities in normal women and in patients with breast cancer ) .
	manualset2
82761	1	397757	5	NULL	NULL	0	NULL	 palisade ending-MIF unit	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore the ` palisade ending-MIF unit ' may be part of a sensory feedback system in eye muscles , which should be considered in association with the causes and treatment of strabismus .
	manualset2
82762	2	397757	5	NULL	NULL	0	NULL	sensory feedback system	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore the ` palisade ending-MIF unit ' may be part of a sensory feedback system in eye muscles , which should be considered in association with the causes and treatment of strabismus .
	manualset2
82763	3	397757	5	NULL	NULL	0	NULL	eye muscles	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore the ` palisade ending-MIF unit ' may be part of a sensory feedback system in eye muscles , which should be considered in association with the causes and treatment of strabismus .
	manualset2
82764	4	397757	5	NULL	NULL	0	NULL	causes	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore the ` palisade ending-MIF unit ' may be part of a sensory feedback system in eye muscles , which should be considered in association with the causes and treatment of strabismus .
	manualset2
82765	5	397757	5	NULL	NULL	0	NULL	treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore the ` palisade ending-MIF unit ' may be part of a sensory feedback system in eye muscles , which should be considered in association with the causes and treatment of strabismus .
	manualset2
82766	6	397757	5	NULL	NULL	0	NULL	strabismus	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Furthermore the ` palisade ending-MIF unit ' may be part of a sensory feedback system in eye muscles , which should be considered in association with the causes and treatment of strabismus .
	manualset2
82767	1	397758	5	NULL	NULL	0	NULL	Fusarium oxysporum homogenates	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Fusarium oxysporum homogenates and jasmonate induce limited sanguinarine accumulation in Argemone mexicana cell cultures .
	manualset2
82768	2	397758	5	NULL	NULL	0	NULL	jasmonate	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Fusarium oxysporum homogenates and jasmonate induce limited sanguinarine accumulation in Argemone mexicana cell cultures .
	manualset2
82769	3	397758	5	NULL	NULL	0	NULL	sanguinarine accumulation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Fusarium oxysporum homogenates and jasmonate induce limited sanguinarine accumulation in Argemone mexicana cell cultures .
	manualset2
82770	4	397758	5	NULL	NULL	0	NULL	Argemone mexicana cell cultures	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Fusarium oxysporum homogenates and jasmonate induce limited sanguinarine accumulation in Argemone mexicana cell cultures .
	manualset2
82771	1	397759	5	NULL	NULL	0	NULL	Fusion	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Fusion of secretion signals to the reporter cloned in a shuttle vector , pBPnuc1 , resulted in halo formation around colonies of Mycobacterium smegmatis and Mycobacterium tuberculosis grown on DNase agar plates containing Methyl Green indicator dye .
	manualset2
82772	2	397759	5	NULL	NULL	0	NULL	secretion signals	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Fusion of secretion signals to the reporter cloned in a shuttle vector , pBPnuc1 , resulted in halo formation around colonies of Mycobacterium smegmatis and Mycobacterium tuberculosis grown on DNase agar plates containing Methyl Green indicator dye .
	manualset2
82773	3	397759	5	NULL	NULL	0	NULL	reporter	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Fusion of secretion signals to the reporter cloned in a shuttle vector , pBPnuc1 , resulted in halo formation around colonies of Mycobacterium smegmatis and Mycobacterium tuberculosis grown on DNase agar plates containing Methyl Green indicator dye .
	manualset2
82774	4	397759	5	NULL	NULL	NULL	NULL	shuttle vector , pBPnuc1 	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Fusion of secretion signals to the reporter cloned in a shuttle vector , pBPnuc1 , resulted in halo formation around colonies of Mycobacterium smegmatis and Mycobacterium tuberculosis grown on DNase agar plates containing Methyl Green indicator dye .
	manualset2
82775	5	397759	5	NULL	NULL	0	NULL	halo formation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Fusion of secretion signals to the reporter cloned in a shuttle vector , pBPnuc1 , resulted in halo formation around colonies of Mycobacterium smegmatis and Mycobacterium tuberculosis grown on DNase agar plates containing Methyl Green indicator dye .
	manualset2
82776	6	397759	5	NULL	NULL	0	NULL	colonies of Mycobacterium smegmatis	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Fusion of secretion signals to the reporter cloned in a shuttle vector , pBPnuc1 , resulted in halo formation around colonies of Mycobacterium smegmatis and Mycobacterium tuberculosis grown on DNase agar plates containing Methyl Green indicator dye .
	manualset2
82777	7	397759	5	NULL	NULL	0	NULL	Mycobacterium tuberculosis	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Fusion of secretion signals to the reporter cloned in a shuttle vector , pBPnuc1 , resulted in halo formation around colonies of Mycobacterium smegmatis and Mycobacterium tuberculosis grown on DNase agar plates containing Methyl Green indicator dye .
	manualset2
82778	8	397759	5	NULL	NULL	0	NULL	DNase agar plates	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Fusion of secretion signals to the reporter cloned in a shuttle vector , pBPnuc1 , resulted in halo formation around colonies of Mycobacterium smegmatis and Mycobacterium tuberculosis grown on DNase agar plates containing Methyl Green indicator dye .
	manualset2
82779	9	397759	5	NULL	NULL	0	NULL	Methyl Green indicator dye	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Fusion of secretion signals to the reporter cloned in a shuttle vector , pBPnuc1 , resulted in halo formation around colonies of Mycobacterium smegmatis and Mycobacterium tuberculosis grown on DNase agar plates containing Methyl Green indicator dye .
	manualset2
82781	1	397760	5	NULL	NULL	NULL	NULL	designing models of care and infrastructure	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Future policy directions include designing models of care and infrastructure that enable patients and their family carers to balance life and illness , and aligning patient-centred care not only within health services but also with community and social support services .
	manualset2
82783	2	397760	5	NULL	NULL	NULL	NULL	patients	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Future policy directions include designing models of care and infrastructure that enable patients and their family carers to balance life and illness , and aligning patient-centred care not only within health services but also with community and social support services .
	manualset2
82784	3	397760	5	NULL	NULL	NULL	NULL	family carers	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Future policy directions include designing models of care and infrastructure that enable patients and their family carers to balance life and illness , and aligning patient-centred care not only within health services but also with community and social support services .
	manualset2
82786	4	397760	5	NULL	NULL	NULL	NULL	life	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Future policy directions include designing models of care and infrastructure that enable patients and their family carers to balance life and illness , and aligning patient-centred care not only within health services but also with community and social support services .
	manualset2
82787	5	397760	5	NULL	NULL	NULL	NULL	illness	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Future policy directions include designing models of care and infrastructure that enable patients and their family carers to balance life and illness , and aligning patient-centred care not only within health services but also with community and social support services .
	manualset2
82788	6	397760	5	NULL	NULL	NULL	NULL	patient-centred care	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Future policy directions include designing models of care and infrastructure that enable patients and their family carers to balance life and illness , and aligning patient-centred care not only within health services but also with community and social support services .
	manualset2
82789	7	397760	5	NULL	NULL	NULL	NULL	health services	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Future policy directions include designing models of care and infrastructure that enable patients and their family carers to balance life and illness , and aligning patient-centred care not only within health services but also with community and social support services .
	manualset2
82790	8	397760	5	NULL	NULL	NULL	NULL	community	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Future policy directions include designing models of care and infrastructure that enable patients and their family carers to balance life and illness , and aligning patient-centred care not only within health services but also with community and social support services .
	manualset2
82791	9	397760	5	NULL	NULL	NULL	NULL	social support services	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Future policy directions include designing models of care and infrastructure that enable patients and their family carers to balance life and illness , and aligning patient-centred care not only within health services but also with community and social support services .
	manualset2
82792	1	397761	5	NULL	NULL	0	NULL	Future research	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Future research should be aimed at developing vaccines that approach the ideal as closely as possible and which are directed against diseases not yet controlled by vaccination and against newly emerging diseases .
	manualset2
82794	3	397761	5	NULL	NULL	0	NULL	diseases	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Future research should be aimed at developing vaccines that approach the ideal as closely as possible and which are directed against diseases not yet controlled by vaccination and against newly emerging diseases .
	manualset2
82795	4	397761	5	NULL	NULL	0	NULL	vaccination	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Future research should be aimed at developing vaccines that approach the ideal as closely as possible and which are directed against diseases not yet controlled by vaccination and against newly emerging diseases .
	manualset2
82796	5	397761	5	NULL	NULL	0	NULL	newly emerging diseases	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Future research should be aimed at developing vaccines that approach the ideal as closely as possible and which are directed against diseases not yet controlled by vaccination and against newly emerging diseases .
	manualset2
83114	2	397761	5	NULL	NULL	0	NULL	vaccines	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Future research should be aimed at developing vaccines that approach the ideal as closely as possible and which are directed against diseases not yet controlled by vaccination and against newly emerging diseases .
	manualset2
82797	1	397762	5	NULL	NULL	NULL	NULL	Future studies	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Future studies should assess primarily the efficacy and safety of aspirin in essential thrombocythemia , and test the possible use of more aggressive antithrombotic strategies in high-risk polycythemic patients .
	manualset2
82798	2	397762	5	NULL	NULL	NULL	NULL	efficacy and safety	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Future studies should assess primarily the efficacy and safety of aspirin in essential thrombocythemia , and test the possible use of more aggressive antithrombotic strategies in high-risk polycythemic patients .
	manualset2
82800	3	397762	5	NULL	NULL	NULL	NULL	aspirin	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Future studies should assess primarily the efficacy and safety of aspirin in essential thrombocythemia , and test the possible use of more aggressive antithrombotic strategies in high-risk polycythemic patients .
	manualset2
82801	4	397762	5	NULL	NULL	NULL	NULL	essential thrombocythemia	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Future studies should assess primarily the efficacy and safety of aspirin in essential thrombocythemia , and test the possible use of more aggressive antithrombotic strategies in high-risk polycythemic patients .
	manualset2
82802	5	397762	5	NULL	NULL	NULL	NULL	test	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Future studies should assess primarily the efficacy and safety of aspirin in essential thrombocythemia , and test the possible use of more aggressive antithrombotic strategies in high-risk polycythemic patients .
	manualset2
82803	6	397762	5	NULL	NULL	NULL	NULL	more aggressive antithrombotic strategies	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Future studies should assess primarily the efficacy and safety of aspirin in essential thrombocythemia , and test the possible use of more aggressive antithrombotic strategies in high-risk polycythemic patients .
	manualset2
82804	7	397762	5	NULL	NULL	NULL	NULL	high-risk polycythemic patients	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Future studies should assess primarily the efficacy and safety of aspirin in essential thrombocythemia , and test the possible use of more aggressive antithrombotic strategies in high-risk polycythemic patients .
	manualset2
82805	1	397763	5	NULL	NULL	0	NULL	complex relationship	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	Future studies should shed new light on the complex relationship between HPTMs and human development .
	manualset2
82806	2	397763	5	NULL	NULL	0	NULL	HPTMs	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Future studies should shed new light on the complex relationship between HPTMs and human development .
	manualset2
82807	3	397763	5	NULL	NULL	0	NULL	human	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Future studies should shed new light on the complex relationship between HPTMs and human development .
	manualset2
82808	4	397763	5	NULL	NULL	0	NULL	development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Future studies should shed new light on the complex relationship between HPTMs and human development .
	manualset2
82809	1	397764	5	NULL	NULL	0	NULL	theoretical developments	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Future theoretical developments that move away from an abstract foundation embedded in cost-benefit tradeoffs and toward phenotypic integration of source-sink relationships will improve our ability to merge observations and theory .
	manualset2
82810	2	397764	5	NULL	NULL	0	NULL	abstract foundation	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Future theoretical developments that move away from an abstract foundation embedded in cost-benefit tradeoffs and toward phenotypic integration of source-sink relationships will improve our ability to merge observations and theory .
	manualset2
82811	3	397764	5	NULL	NULL	0	NULL	cost-benefit tradeoffs	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Future theoretical developments that move away from an abstract foundation embedded in cost-benefit tradeoffs and toward phenotypic integration of source-sink relationships will improve our ability to merge observations and theory .
	manualset2
82812	4	397764	5	NULL	NULL	0	NULL	phenotypic integration	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Future theoretical developments that move away from an abstract foundation embedded in cost-benefit tradeoffs and toward phenotypic integration of source-sink relationships will improve our ability to merge observations and theory .
	manualset2
82813	5	397764	5	NULL	NULL	0	NULL	source-sink relationships	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	Future theoretical developments that move away from an abstract foundation embedded in cost-benefit tradeoffs and toward phenotypic integration of source-sink relationships will improve our ability to merge observations and theory .
	manualset2
82814	6	397764	5	NULL	NULL	0	NULL	observations	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Future theoretical developments that move away from an abstract foundation embedded in cost-benefit tradeoffs and toward phenotypic integration of source-sink relationships will improve our ability to merge observations and theory .
	manualset2
82815	7	397764	5	NULL	NULL	0	NULL	theory	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Future theoretical developments that move away from an abstract foundation embedded in cost-benefit tradeoffs and toward phenotypic integration of source-sink relationships will improve our ability to merge observations and theory .
	manualset2
82816	1	397765	5	NULL	NULL	0	NULL	Serum level	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	( Serum level of alpha-1 antitrypsin in patients with sarcoidosis ) .
	manualset2
82817	2	397765	5	NULL	NULL	0	NULL	alpha-1 antitrypsin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	( Serum level of alpha-1 antitrypsin in patients with sarcoidosis ) .
	manualset2
82818	3	397765	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( Serum level of alpha-1 antitrypsin in patients with sarcoidosis ) .
	manualset2
82819	4	397765	5	NULL	NULL	0	NULL	sarcoidosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Serum level of alpha-1 antitrypsin in patients with sarcoidosis ) .
	manualset2
82820	1	397766	5	NULL	NULL	0	NULL	local bone regeneration	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Future of local bone regeneration - Protein versus gene therapy .
	manualset2
82821	2	397766	5	NULL	NULL	0	NULL	Protein therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Future of local bone regeneration - Protein versus gene therapy .
	manualset2
82822	3	397766	5	NULL	NULL	0	NULL	gene therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Future of local bone regeneration - Protein versus gene therapy .
	manualset2
82823	1	397767	5	NULL	NULL	0	NULL	GA	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	GA has been shown to reduce alpha-synuclein induced neurotoxicity in a fly model of Parkinson 's disease .
	manualset2
82824	2	397767	5	NULL	NULL	0	NULL	alpha-synuclein induced neurotoxicity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GA has been shown to reduce alpha-synuclein induced neurotoxicity in a fly model of Parkinson 's disease .
	manualset2
82825	3	397767	5	NULL	NULL	0	NULL	fly model	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	GA has been shown to reduce alpha-synuclein induced neurotoxicity in a fly model of Parkinson 's disease .
	manualset2
82826	4	397767	5	NULL	NULL	0	NULL	Parkinson 's disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	GA has been shown to reduce alpha-synuclein induced neurotoxicity in a fly model of Parkinson 's disease .
	manualset2
82827	1	397768	5	NULL	NULL	0	NULL	GABA	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	GABA hyperpolarizes hippocampal CA1 and CA3 pyramidal cells through activation of GABAB postsynaptic receptors .
	manualset2
82828	2	397768	5	NULL	NULL	0	NULL	 hippocampal CA1 and CA3 pyramidal cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	GABA hyperpolarizes hippocampal CA1 and CA3 pyramidal cells through activation of GABAB postsynaptic receptors .
	manualset2
82829	3	397768	5	NULL	NULL	0	NULL	activation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GABA hyperpolarizes hippocampal CA1 and CA3 pyramidal cells through activation of GABAB postsynaptic receptors .
	manualset2
82830	4	397768	5	NULL	NULL	0	NULL	GABAB postsynaptic receptors	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GABA hyperpolarizes hippocampal CA1 and CA3 pyramidal cells through activation of GABAB postsynaptic receptors .
	manualset2
82831	1	397769	5	NULL	NULL	0	NULL	GABA levels	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	GABA levels in controls were 803 + / - 98 ( n = 7 ) and in demented patients 702 + / - 98 ( n = 7 ) pmol/ml .
	manualset2
82832	2	397769	5	NULL	NULL	0	NULL	controls	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	GABA levels in controls were 803 + / - 98 ( n = 7 ) and in demented patients 702 + / - 98 ( n = 7 ) pmol/ml .
	manualset2
82833	3	397769	5	NULL	NULL	0	NULL	803 + / - 98 ( n = 7 )	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	GABA levels in controls were 803 + / - 98 ( n = 7 ) and in demented patients 702 + / - 98 ( n = 7 ) pmol/ml .
	manualset2
82834	4	397769	5	NULL	NULL	0	NULL	demented patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	GABA levels in controls were 803 + / - 98 ( n = 7 ) and in demented patients 702 + / - 98 ( n = 7 ) pmol/ml .
	manualset2
82835	5	397769	5	NULL	NULL	0	NULL	702 + / - 98 ( n = 7 ) pmol/ml	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	GABA levels in controls were 803 + / - 98 ( n = 7 ) and in demented patients 702 + / - 98 ( n = 7 ) pmol/ml .
	manualset2
82836	1	397770	5	NULL	NULL	0	NULL	GABAB receptors	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GABAB receptors are abundant on dendritic spines , where they dampen postsynaptic excitability and inhibit Ca2 + influx through NMDA receptors when activated by spillover of GABA from neighboring GABAergic terminals .
	manualset2
82837	2	397770	5	NULL	NULL	0	NULL	dendritic spines	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	GABAB receptors are abundant on dendritic spines , where they dampen postsynaptic excitability and inhibit Ca2 + influx through NMDA receptors when activated by spillover of GABA from neighboring GABAergic terminals .
	manualset2
82838	3	397770	5	NULL	NULL	0	NULL	postsynaptic excitability	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GABAB receptors are abundant on dendritic spines , where they dampen postsynaptic excitability and inhibit Ca2 + influx through NMDA receptors when activated by spillover of GABA from neighboring GABAergic terminals .
	manualset2
82839	4	397770	5	NULL	NULL	0	NULL	inhibit	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GABAB receptors are abundant on dendritic spines , where they dampen postsynaptic excitability and inhibit Ca2 + influx through NMDA receptors when activated by spillover of GABA from neighboring GABAergic terminals .
	manualset2
82840	5	397770	5	NULL	NULL	0	NULL	Ca2 + influx	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GABAB receptors are abundant on dendritic spines , where they dampen postsynaptic excitability and inhibit Ca2 + influx through NMDA receptors when activated by spillover of GABA from neighboring GABAergic terminals .
	manualset2
82841	6	397770	5	NULL	NULL	0	NULL	NMDA receptors	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GABAB receptors are abundant on dendritic spines , where they dampen postsynaptic excitability and inhibit Ca2 + influx through NMDA receptors when activated by spillover of GABA from neighboring GABAergic terminals .
	manualset2
82842	7	397770	5	NULL	NULL	0	NULL	spillover	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GABAB receptors are abundant on dendritic spines , where they dampen postsynaptic excitability and inhibit Ca2 + influx through NMDA receptors when activated by spillover of GABA from neighboring GABAergic terminals .
	manualset2
82843	8	397770	5	NULL	NULL	0	NULL	GABA	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	GABAB receptors are abundant on dendritic spines , where they dampen postsynaptic excitability and inhibit Ca2 + influx through NMDA receptors when activated by spillover of GABA from neighboring GABAergic terminals .
	manualset2
82844	9	397770	5	NULL	NULL	0	NULL	GABAergic terminals	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	GABAB receptors are abundant on dendritic spines , where they dampen postsynaptic excitability and inhibit Ca2 + influx through NMDA receptors when activated by spillover of GABA from neighboring GABAergic terminals .
	manualset2
82845	1	397771	5	NULL	NULL	0	NULL	GABAergic agents	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	GABAergic agents prevent alpha-melanocyte stimulating hormone induced anxiety and anorexia in rats .
	manualset2
82846	2	397771	5	NULL	NULL	NULL	NULL	alpha-melanocyte stimulating hormone	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	GABAergic agents prevent alpha-melanocyte stimulating hormone induced anxiety and anorexia in rats .
	manualset2
82847	3	397771	5	NULL	NULL	0	NULL	anxiety	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	GABAergic agents prevent alpha-melanocyte stimulating hormone induced anxiety and anorexia in rats .
	manualset2
82848	4	397771	5	NULL	NULL	0	NULL	anorexia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	GABAergic agents prevent alpha-melanocyte stimulating hormone induced anxiety and anorexia in rats .
	manualset2
82849	5	397771	5	NULL	NULL	0	NULL	rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	GABAergic agents prevent alpha-melanocyte stimulating hormone induced anxiety and anorexia in rats .
	manualset2
82850	1	397772	5	NULL	NULL	0	NULL	GAD	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GAD in beta-cells is associated with a vesicular compartment , similar to the GABA vesicles .
	manualset2
82851	2	397772	5	NULL	NULL	0	NULL	beta-cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	GAD in beta-cells is associated with a vesicular compartment , similar to the GABA vesicles .
	manualset2
82852	3	397772	5	NULL	NULL	0	NULL	vesicular compartment	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	GAD in beta-cells is associated with a vesicular compartment , similar to the GABA vesicles .
	manualset2
82853	4	397772	5	NULL	NULL	0	NULL	GABA vesicles	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	GAD in beta-cells is associated with a vesicular compartment , similar to the GABA vesicles .
	manualset2
82854	1	397773	5	NULL	NULL	0	NULL	GAS	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	GAS was produced more copiously and more quickly by rostral PVN lesion than by lesion of the ventromedial ( VMH ) or dorsomedial ( DMH ) nucleus , and nearly as much by caudal PVN lesion .
	manualset2
82855	2	397773	5	NULL	NULL	0	NULL	rostral PVN lesion	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	GAS was produced more copiously and more quickly by rostral PVN lesion than by lesion of the ventromedial ( VMH ) or dorsomedial ( DMH ) nucleus , and nearly as much by caudal PVN lesion .
	manualset2
82856	3	397773	5	NULL	NULL	0	NULL	 lesion of the ventromedial ( VMH )	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	GAS was produced more copiously and more quickly by rostral PVN lesion than by lesion of the ventromedial ( VMH ) or dorsomedial ( DMH ) nucleus , and nearly as much by caudal PVN lesion .
	manualset2
82857	4	397773	5	NULL	NULL	0	NULL	dorsomedial ( DMH ) nucleus	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	GAS was produced more copiously and more quickly by rostral PVN lesion than by lesion of the ventromedial ( VMH ) or dorsomedial ( DMH ) nucleus , and nearly as much by caudal PVN lesion .
	manualset2
82858	5	397773	5	NULL	NULL	0	NULL	caudal PVN lesion	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	GAS was produced more copiously and more quickly by rostral PVN lesion than by lesion of the ventromedial ( VMH ) or dorsomedial ( DMH ) nucleus , and nearly as much by caudal PVN lesion .
	manualset2
82859	1	397774	5	NULL	NULL	0	NULL	GATA6 reporter gene	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	GATA6 reporter gene reveals myocardial phenotypic heterogeneity that is related to variations in gap junction coupling .
	manualset2
82860	2	397774	5	NULL	NULL	0	NULL	myocardial phenotypic heterogeneity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	GATA6 reporter gene reveals myocardial phenotypic heterogeneity that is related to variations in gap junction coupling .
	manualset2
82861	3	397774	5	NULL	NULL	0	NULL	gap junction coupling	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GATA6 reporter gene reveals myocardial phenotypic heterogeneity that is related to variations in gap junction coupling .
	manualset2
82862	1	397775	5	NULL	NULL	0	NULL	benign neoplasms of the parotid gland	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Several cases of benign neoplasms of the parotid gland ( excluding pleiomorphic adenomas ) ) .
	manualset2
82863	2	397775	5	NULL	NULL	0	NULL	pleiomorphic adenomas	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Several cases of benign neoplasms of the parotid gland ( excluding pleiomorphic adenomas ) ) .
	manualset2
82864	1	397776	5	NULL	NULL	0	NULL	GC number	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	GC number , proliferation , apoptosis , differentiation ( loss of OCT4 , DMRT1 expression , DMRT1 re-expression , GC migration ) and aggregation were evaluated at various foetal and postnatal ages .
	manualset2
82865	2	397776	5	NULL	NULL	0	NULL	proliferation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GC number , proliferation , apoptosis , differentiation ( loss of OCT4 , DMRT1 expression , DMRT1 re-expression , GC migration ) and aggregation were evaluated at various foetal and postnatal ages .
	manualset2
82866	3	397776	5	NULL	NULL	0	NULL	apoptosis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GC number , proliferation , apoptosis , differentiation ( loss of OCT4 , DMRT1 expression , DMRT1 re-expression , GC migration ) and aggregation were evaluated at various foetal and postnatal ages .
	manualset2
82867	4	397776	5	NULL	NULL	0	NULL	differentiation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GC number , proliferation , apoptosis , differentiation ( loss of OCT4 , DMRT1 expression , DMRT1 re-expression , GC migration ) and aggregation were evaluated at various foetal and postnatal ages .
	manualset2
82868	5	397776	5	NULL	NULL	0	NULL	loss of OCT4	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GC number , proliferation , apoptosis , differentiation ( loss of OCT4 , DMRT1 expression , DMRT1 re-expression , GC migration ) and aggregation were evaluated at various foetal and postnatal ages .
	manualset2
82869	6	397776	5	NULL	NULL	0	NULL	DMRT1 expression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GC number , proliferation , apoptosis , differentiation ( loss of OCT4 , DMRT1 expression , DMRT1 re-expression , GC migration ) and aggregation were evaluated at various foetal and postnatal ages .
	manualset2
82870	7	397776	5	NULL	NULL	0	NULL	DMRT1 re-expression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GC number , proliferation , apoptosis , differentiation ( loss of OCT4 , DMRT1 expression , DMRT1 re-expression , GC migration ) and aggregation were evaluated at various foetal and postnatal ages .
	manualset2
82871	8	397776	5	NULL	NULL	0	NULL	GC migration	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GC number , proliferation , apoptosis , differentiation ( loss of OCT4 , DMRT1 expression , DMRT1 re-expression , GC migration ) and aggregation were evaluated at various foetal and postnatal ages .
	manualset2
82872	9	397776	5	NULL	NULL	0	NULL	aggregation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GC number , proliferation , apoptosis , differentiation ( loss of OCT4 , DMRT1 expression , DMRT1 re-expression , GC migration ) and aggregation were evaluated at various foetal and postnatal ages .
	manualset2
82873	10	397776	5	NULL	NULL	0	NULL	foetal and postnatal ages	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	GC number , proliferation , apoptosis , differentiation ( loss of OCT4 , DMRT1 expression , DMRT1 re-expression , GC migration ) and aggregation were evaluated at various foetal and postnatal ages .
	manualset2
82874	1	397777	5	NULL	NULL	0	NULL	GCN5	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GCN5 phosphorylated by activities in cellular extracts could be dephosphorylated by AtPP2C-6-6 in vitro .
	manualset2
82875	2	397777	5	NULL	NULL	0	NULL	cellular extracts	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	GCN5 phosphorylated by activities in cellular extracts could be dephosphorylated by AtPP2C-6-6 in vitro .
	manualset2
82876	3	397777	5	NULL	NULL	0	NULL	AtPP2C-6-6	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GCN5 phosphorylated by activities in cellular extracts could be dephosphorylated by AtPP2C-6-6 in vitro .
	manualset2
82877	1	397778	5	NULL	NULL	0	NULL	GC/MS systems	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	GC/MS systems are on the bench but still in the game .
	manualset2
82878	1	397779	5	NULL	NULL	0	NULL	GDC-0449 ( 25 and 50M )	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	GDC-0449 ( 25 and 50M ) inhibited concentration-dependent cell growth in HCC and H1339 cells .
	manualset2
82879	2	397779	5	NULL	NULL	0	NULL	concentration-dependent cell growth	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GDC-0449 ( 25 and 50M ) inhibited concentration-dependent cell growth in HCC and H1339 cells .
	manualset2
82880	3	397779	5	NULL	NULL	0	NULL	HCC cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	GDC-0449 ( 25 and 50M ) inhibited concentration-dependent cell growth in HCC and H1339 cells .
	manualset2
82881	4	397779	5	NULL	NULL	0	NULL	H1339 cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	GDC-0449 ( 25 and 50M ) inhibited concentration-dependent cell growth in HCC and H1339 cells .
	manualset2
82882	1	397780	5	NULL	NULL	0	NULL	GGA ( Golgi-localizing , gamma-adaptin ear homology domain , ARF-binding ) proteins	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GGA ( Golgi-localizing , gamma-adaptin ear homology domain , ARF-binding ) proteins are potential effectors of ADP-ribosylation factors , are associated with the trans-Golgi network ( TGN ) , and are involved in protein transport from this compartment .
	manualset2
82883	2	397780	5	NULL	NULL	0	NULL	potential effectors	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GGA ( Golgi-localizing , gamma-adaptin ear homology domain , ARF-binding ) proteins are potential effectors of ADP-ribosylation factors , are associated with the trans-Golgi network ( TGN ) , and are involved in protein transport from this compartment .
	manualset2
82884	3	397780	5	NULL	NULL	0	NULL	ADP-ribosylation factors	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GGA ( Golgi-localizing , gamma-adaptin ear homology domain , ARF-binding ) proteins are potential effectors of ADP-ribosylation factors , are associated with the trans-Golgi network ( TGN ) , and are involved in protein transport from this compartment .
	manualset2
82885	4	397780	5	NULL	NULL	0	NULL	trans-Golgi network ( TGN )	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	GGA ( Golgi-localizing , gamma-adaptin ear homology domain , ARF-binding ) proteins are potential effectors of ADP-ribosylation factors , are associated with the trans-Golgi network ( TGN ) , and are involved in protein transport from this compartment .
	manualset2
82886	5	397780	5	NULL	NULL	0	NULL	protein transport 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GGA ( Golgi-localizing , gamma-adaptin ear homology domain , ARF-binding ) proteins are potential effectors of ADP-ribosylation factors , are associated with the trans-Golgi network ( TGN ) , and are involved in protein transport from this compartment .
	manualset2
82887	6	397780	5	NULL	NULL	0	NULL	compartment	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	GGA ( Golgi-localizing , gamma-adaptin ear homology domain , ARF-binding ) proteins are potential effectors of ADP-ribosylation factors , are associated with the trans-Golgi network ( TGN ) , and are involved in protein transport from this compartment .
	manualset2
82888	1	397781	5	NULL	NULL	NULL	NULL	GI and SF AEs	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	GI and SF AEs were highest for subjects treated with ropinirole , while individuals treated with pramipexole exhibited the highest incidence of cognitive AEs .
	manualset2
82890	2	397781	5	NULL	NULL	NULL	NULL	subjects	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	GI and SF AEs were highest for subjects treated with ropinirole , while individuals treated with pramipexole exhibited the highest incidence of cognitive AEs .
	manualset2
82891	3	397781	5	NULL	NULL	NULL	NULL	ropinirole	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	GI and SF AEs were highest for subjects treated with ropinirole , while individuals treated with pramipexole exhibited the highest incidence of cognitive AEs .
	manualset2
82892	4	397781	5	NULL	NULL	NULL	NULL	individuals	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	GI and SF AEs were highest for subjects treated with ropinirole , while individuals treated with pramipexole exhibited the highest incidence of cognitive AEs .
	manualset2
82893	5	397781	5	NULL	NULL	NULL	NULL	pramipexole	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	GI and SF AEs were highest for subjects treated with ropinirole , while individuals treated with pramipexole exhibited the highest incidence of cognitive AEs .
	manualset2
82894	6	397781	5	NULL	NULL	0	NULL	cognitive AEs	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	GI and SF AEs were highest for subjects treated with ropinirole , while individuals treated with pramipexole exhibited the highest incidence of cognitive AEs .
	manualset2
82895	1	397782	5	NULL	NULL	0	NULL	GLTP specificity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GLTP specificity encompasses both sphingoid - and glycerol-based glycolipids , but with a strict requirement that the initial sugar residue be beta-linked to the hydrophobic lipid backbone .
	manualset2
82896	2	397782	5	NULL	NULL	0	NULL	sphingoid - and glycerol-based glycolipids	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	GLTP specificity encompasses both sphingoid - and glycerol-based glycolipids , but with a strict requirement that the initial sugar residue be beta-linked to the hydrophobic lipid backbone .
	manualset2
82897	3	397782	5	NULL	NULL	0	NULL	sugar residue	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	GLTP specificity encompasses both sphingoid - and glycerol-based glycolipids , but with a strict requirement that the initial sugar residue be beta-linked to the hydrophobic lipid backbone .
	manualset2
82898	4	397782	5	NULL	NULL	0	NULL	hydrophobic lipid backbone	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	GLTP specificity encompasses both sphingoid - and glycerol-based glycolipids , but with a strict requirement that the initial sugar residue be beta-linked to the hydrophobic lipid backbone .
	manualset2
82899	1	397783	5	NULL	NULL	0	NULL	cellular immunity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Several indices of the state of cellular immunity in amyloidosis ( experimental-clinical study ) ) .
	manualset2
82900	2	397783	5	NULL	NULL	0	NULL	amyloidosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Several indices of the state of cellular immunity in amyloidosis ( experimental-clinical study ) ) .
	manualset2
82901	3	397783	5	NULL	NULL	0	NULL	experimental-clinical study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Several indices of the state of cellular immunity in amyloidosis ( experimental-clinical study ) ) .
	manualset2
82902	1	397784	5	NULL	NULL	0	NULL	GLU treatment	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	GLU treatment caused time-dependent degeneration of outer hair cells ( OHCs ) in conjunction with a temporal increase of NOS activity in the organ of Corti .
	manualset2
82903	2	397784	5	NULL	NULL	0	NULL	time-dependent degeneration	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GLU treatment caused time-dependent degeneration of outer hair cells ( OHCs ) in conjunction with a temporal increase of NOS activity in the organ of Corti .
	manualset2
82904	3	397784	5	NULL	NULL	0	NULL	outer hair cells ( OHCs )	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	GLU treatment caused time-dependent degeneration of outer hair cells ( OHCs ) in conjunction with a temporal increase of NOS activity in the organ of Corti .
	manualset2
82905	4	397784	5	NULL	NULL	0	NULL	NOS activity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GLU treatment caused time-dependent degeneration of outer hair cells ( OHCs ) in conjunction with a temporal increase of NOS activity in the organ of Corti .
	manualset2
82906	5	397784	5	NULL	NULL	0	NULL	organ of Corti	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	GLU treatment caused time-dependent degeneration of outer hair cells ( OHCs ) in conjunction with a temporal increase of NOS activity in the organ of Corti .
	manualset2
82907	1	397785	5	NULL	NULL	0	NULL	GLUT4 levels	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GLUT4 levels were measured in whole membranes isolated from a variety of tissues in 4 and 20-week-old NZO and control NZC mice by Western blotting using a specific antibody to the C terminal end of the protein .
	manualset2
82908	2	397785	5	NULL	NULL	0	NULL	whole membranes	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	GLUT4 levels were measured in whole membranes isolated from a variety of tissues in 4 and 20-week-old NZO and control NZC mice by Western blotting using a specific antibody to the C terminal end of the protein .
	manualset2
82909	3	397785	5	NULL	NULL	0	NULL	tissues	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	GLUT4 levels were measured in whole membranes isolated from a variety of tissues in 4 and 20-week-old NZO and control NZC mice by Western blotting using a specific antibody to the C terminal end of the protein .
	manualset2
82910	4	397785	5	NULL	NULL	0	NULL	4 and 20-week-old NZO	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	GLUT4 levels were measured in whole membranes isolated from a variety of tissues in 4 and 20-week-old NZO and control NZC mice by Western blotting using a specific antibody to the C terminal end of the protein .
	manualset2
82911	5	397785	5	NULL	NULL	0	NULL	 control NZC mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	GLUT4 levels were measured in whole membranes isolated from a variety of tissues in 4 and 20-week-old NZO and control NZC mice by Western blotting using a specific antibody to the C terminal end of the protein .
	manualset2
82912	6	397785	5	NULL	NULL	0	NULL	Western blotting	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	GLUT4 levels were measured in whole membranes isolated from a variety of tissues in 4 and 20-week-old NZO and control NZC mice by Western blotting using a specific antibody to the C terminal end of the protein .
	manualset2
82913	7	397785	5	NULL	NULL	0	NULL	specific antibody	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GLUT4 levels were measured in whole membranes isolated from a variety of tissues in 4 and 20-week-old NZO and control NZC mice by Western blotting using a specific antibody to the C terminal end of the protein .
	manualset2
82914	8	397785	5	NULL	NULL	0	NULL	C terminal end	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	GLUT4 levels were measured in whole membranes isolated from a variety of tissues in 4 and 20-week-old NZO and control NZC mice by Western blotting using a specific antibody to the C terminal end of the protein .
	manualset2
82915	9	397785	5	NULL	NULL	0	NULL	protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GLUT4 levels were measured in whole membranes isolated from a variety of tissues in 4 and 20-week-old NZO and control NZC mice by Western blotting using a specific antibody to the C terminal end of the protein .
	manualset2
82916	1	397786	5	NULL	NULL	0	NULL	GPA	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	GPA was used as a biological cover for the following indications : problematic wound healing , 13 cases ; non-healing burns , 12 cases ; carcinoma , 4 cases ; unstable scar , 2 cases ; shortage of skin , 2 cases .
	manualset2
82917	2	397786	5	NULL	NULL	NULL	NULL	problematic wound healing	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	GPA was used as a biological cover for the following indications : problematic wound healing , 13 cases ; non-healing burns , 12 cases ; carcinoma , 4 cases ; unstable scar , 2 cases ; shortage of skin , 2 cases .
	manualset2
82918	3	397786	5	NULL	NULL	NULL	NULL	13 cases	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	GPA was used as a biological cover for the following indications : problematic wound healing , 13 cases ; non-healing burns , 12 cases ; carcinoma , 4 cases ; unstable scar , 2 cases ; shortage of skin , 2 cases .
	manualset2
82919	4	397786	5	NULL	NULL	0	NULL	non-healing burns	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	GPA was used as a biological cover for the following indications : problematic wound healing , 13 cases ; non-healing burns , 12 cases ; carcinoma , 4 cases ; unstable scar , 2 cases ; shortage of skin , 2 cases .
	manualset2
82920	5	397786	5	NULL	NULL	NULL	NULL	12 cases	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	GPA was used as a biological cover for the following indications : problematic wound healing , 13 cases ; non-healing burns , 12 cases ; carcinoma , 4 cases ; unstable scar , 2 cases ; shortage of skin , 2 cases .
	manualset2
82921	6	397786	5	NULL	NULL	0	NULL	carcinoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	GPA was used as a biological cover for the following indications : problematic wound healing , 13 cases ; non-healing burns , 12 cases ; carcinoma , 4 cases ; unstable scar , 2 cases ; shortage of skin , 2 cases .
	manualset2
82922	7	397786	5	NULL	NULL	NULL	NULL	4 cases	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	GPA was used as a biological cover for the following indications : problematic wound healing , 13 cases ; non-healing burns , 12 cases ; carcinoma , 4 cases ; unstable scar , 2 cases ; shortage of skin , 2 cases .
	manualset2
82923	8	397786	5	NULL	NULL	0	NULL	unstable scar	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	GPA was used as a biological cover for the following indications : problematic wound healing , 13 cases ; non-healing burns , 12 cases ; carcinoma , 4 cases ; unstable scar , 2 cases ; shortage of skin , 2 cases .
	manualset2
82924	9	397786	5	NULL	NULL	NULL	NULL	2 cases	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	GPA was used as a biological cover for the following indications : problematic wound healing , 13 cases ; non-healing burns , 12 cases ; carcinoma , 4 cases ; unstable scar , 2 cases ; shortage of skin , 2 cases .
	manualset2
82925	10	397786	5	NULL	NULL	0	NULL	shortage of skin	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	GPA was used as a biological cover for the following indications : problematic wound healing , 13 cases ; non-healing burns , 12 cases ; carcinoma , 4 cases ; unstable scar , 2 cases ; shortage of skin , 2 cases .
	manualset2
82926	11	397786	5	NULL	NULL	NULL	NULL	2 cases	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	GPA was used as a biological cover for the following indications : problematic wound healing , 13 cases ; non-healing burns , 12 cases ; carcinoma , 4 cases ; unstable scar , 2 cases ; shortage of skin , 2 cases .
	manualset2
82927	1	397787	5	NULL	NULL	0	NULL	GPAT6	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GPAT6 is a member of the Arabidopsis GPAT family , which is crucial for cutin biosynthesis in sepals and petals .
	manualset2
82928	2	397787	5	NULL	NULL	0	NULL	member	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GPAT6 is a member of the Arabidopsis GPAT family , which is crucial for cutin biosynthesis in sepals and petals .
	manualset2
82929	3	397787	5	NULL	NULL	0	NULL	Arabidopsis GPAT family	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GPAT6 is a member of the Arabidopsis GPAT family , which is crucial for cutin biosynthesis in sepals and petals .
	manualset2
82930	4	397787	5	NULL	NULL	0	NULL	cutin biosynthesis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GPAT6 is a member of the Arabidopsis GPAT family , which is crucial for cutin biosynthesis in sepals and petals .
	manualset2
82931	5	397787	5	NULL	NULL	0	NULL	sepals	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	GPAT6 is a member of the Arabidopsis GPAT family , which is crucial for cutin biosynthesis in sepals and petals .
	manualset2
82932	6	397787	5	NULL	NULL	0	NULL	petals	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	GPAT6 is a member of the Arabidopsis GPAT family , which is crucial for cutin biosynthesis in sepals and petals .
	manualset2
82933	1	397788	5	NULL	NULL	0	NULL	GRFs	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	GRFs of the crush - injured animals showed earlier improvement compared to the experimental animals , whose overall GRF patterns failed to recover as well as the crush group .
	manualset2
82934	2	397788	5	NULL	NULL	0	NULL	crush - injured animals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	GRFs of the crush - injured animals showed earlier improvement compared to the experimental animals , whose overall GRF patterns failed to recover as well as the crush group .
	manualset2
82935	3	397788	5	NULL	NULL	0	NULL	earlier improvement	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GRFs of the crush - injured animals showed earlier improvement compared to the experimental animals , whose overall GRF patterns failed to recover as well as the crush group .
	manualset2
82936	4	397788	5	NULL	NULL	0	NULL	experimental animals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	GRFs of the crush - injured animals showed earlier improvement compared to the experimental animals , whose overall GRF patterns failed to recover as well as the crush group .
	manualset2
82937	5	397788	5	NULL	NULL	0	NULL	GRF patterns	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	GRFs of the crush - injured animals showed earlier improvement compared to the experimental animals , whose overall GRF patterns failed to recover as well as the crush group .
	manualset2
82938	6	397788	5	NULL	NULL	0	NULL	recover	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GRFs of the crush - injured animals showed earlier improvement compared to the experimental animals , whose overall GRF patterns failed to recover as well as the crush group .
	manualset2
82939	7	397788	5	NULL	NULL	0	NULL	crush group	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	GRFs of the crush - injured animals showed earlier improvement compared to the experimental animals , whose overall GRF patterns failed to recover as well as the crush group .
	manualset2
82940	1	397789	5	NULL	NULL	0	NULL	GSK-3 beta	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GSK-3 beta , along with CDK5 , is responsible for most of the abnormal hyperphosphorylation of the microtubule-binding protein tau observed in Alzheimer 's disease .
	manualset2
82941	2	397789	5	NULL	NULL	0	NULL	CDK5	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GSK-3 beta , along with CDK5 , is responsible for most of the abnormal hyperphosphorylation of the microtubule-binding protein tau observed in Alzheimer 's disease .
	manualset2
82942	3	397789	5	NULL	NULL	0	NULL	abnormal hyperphosphorylation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GSK-3 beta , along with CDK5 , is responsible for most of the abnormal hyperphosphorylation of the microtubule-binding protein tau observed in Alzheimer 's disease .
	manualset2
82943	4	397789	5	NULL	NULL	0	NULL	microtubule-binding protein tau	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GSK-3 beta , along with CDK5 , is responsible for most of the abnormal hyperphosphorylation of the microtubule-binding protein tau observed in Alzheimer 's disease .
	manualset2
82944	5	397789	5	NULL	NULL	0	NULL	Alzheimer 's disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	GSK-3 beta , along with CDK5 , is responsible for most of the abnormal hyperphosphorylation of the microtubule-binding protein tau observed in Alzheimer 's disease .
	manualset2
82945	1	397790	5	NULL	NULL	0	NULL	GSK232802A treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	GSK232802A treatment produced a small but sustained weight loss ( 4.6 1.0 % , P & lt ; 0.0001 ) and reduced adiposity ( P & lt ; 0.0001 ) , which was due at least in part to a suppression of food intake ( 3.6 3.7 % , P & lt ; 0.0001 ) .
	manualset2
82946	2	397790	5	NULL	NULL	NULL	NULL	sustained weight loss	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	GSK232802A treatment produced a small but sustained weight loss ( 4.6 1.0 % , P & lt ; 0.0001 ) and reduced adiposity ( P & lt ; 0.0001 ) , which was due at least in part to a suppression of food intake ( 3.6 3.7 % , P & lt ; 0.0001 ) .
	manualset2
82947	4	397790	5	NULL	NULL	NULL	NULL	reduced adiposity	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	GSK232802A treatment produced a small but sustained weight loss ( 4.6 1.0 % , P & lt ; 0.0001 ) and reduced adiposity ( P & lt ; 0.0001 ) , which was due at least in part to a suppression of food intake ( 3.6 3.7 % , P & lt ; 0.0001 ) .
	manualset2
82948	6	397790	5	NULL	NULL	NULL	NULL	suppression	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	GSK232802A treatment produced a small but sustained weight loss ( 4.6 1.0 % , P & lt ; 0.0001 ) and reduced adiposity ( P & lt ; 0.0001 ) , which was due at least in part to a suppression of food intake ( 3.6 3.7 % , P & lt ; 0.0001 ) .
	manualset2
82949	7	397790	5	NULL	NULL	NULL	NULL	food intake	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	GSK232802A treatment produced a small but sustained weight loss ( 4.6 1.0 % , P & lt ; 0.0001 ) and reduced adiposity ( P & lt ; 0.0001 ) , which was due at least in part to a suppression of food intake ( 3.6 3.7 % , P & lt ; 0.0001 ) .
	manualset2
83170	3	397790	5	NULL	NULL	0	NULL	( 4.6 1.0 % , P & lt ; 0.0001 )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	GSK232802A treatment produced a small but sustained weight loss ( 4.6 1.0 % , P & lt ; 0.0001 ) and reduced adiposity ( P & lt ; 0.0001 ) , which was due at least in part to a suppression of food intake ( 3.6 3.7 % , P & lt ; 0.0001 ) .
	manualset2
83171	5	397790	5	NULL	NULL	0	NULL	 ( P & lt ; 0.0001 )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	GSK232802A treatment produced a small but sustained weight loss ( 4.6 1.0 % , P & lt ; 0.0001 ) and reduced adiposity ( P & lt ; 0.0001 ) , which was due at least in part to a suppression of food intake ( 3.6 3.7 % , P & lt ; 0.0001 ) .
	manualset2
83172	8	397790	5	NULL	NULL	0	NULL	 ( 3.6 3.7 % , P & lt ; 0.0001 )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	GSK232802A treatment produced a small but sustained weight loss ( 4.6 1.0 % , P & lt ; 0.0001 ) and reduced adiposity ( P & lt ; 0.0001 ) , which was due at least in part to a suppression of food intake ( 3.6 3.7 % , P & lt ; 0.0001 ) .
	manualset2
82950	1	397791	5	NULL	NULL	0	NULL	GTN	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	GTN ( 1 mg sub-lingually ) had no significant effect on bleeding time 90-100 min following either placebo or GR32191B .
	manualset2
82951	2	397791	5	NULL	NULL	0	NULL	significant effect	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	GTN ( 1 mg sub-lingually ) had no significant effect on bleeding time 90-100 min following either placebo or GR32191B .
	manualset2
82952	3	397791	5	NULL	NULL	0	NULL	bleeding time 90-100 min	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	GTN ( 1 mg sub-lingually ) had no significant effect on bleeding time 90-100 min following either placebo or GR32191B .
	manualset2
82953	4	397791	5	NULL	NULL	0	NULL	placebo	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	GTN ( 1 mg sub-lingually ) had no significant effect on bleeding time 90-100 min following either placebo or GR32191B .
	manualset2
82954	5	397791	5	NULL	NULL	0	NULL	GR32191B	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	GTN ( 1 mg sub-lingually ) had no significant effect on bleeding time 90-100 min following either placebo or GR32191B .
	manualset2
82955	1	397792	5	NULL	NULL	0	NULL	GUS	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GUS is required to degrade glycosaminoglycans ( GAGs ) , including heparan sulfate ( HS ) , dermatan sulfate ( DS ) , and chondroitin-4 , 6 - sulfate ( CS ) .
	manualset2
82956	2	397792	5	NULL	NULL	0	NULL	degrade	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GUS is required to degrade glycosaminoglycans ( GAGs ) , including heparan sulfate ( HS ) , dermatan sulfate ( DS ) , and chondroitin-4 , 6 - sulfate ( CS ) .
	manualset2
82957	3	397792	5	NULL	NULL	0	NULL	glycosaminoglycans ( GAGs )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	GUS is required to degrade glycosaminoglycans ( GAGs ) , including heparan sulfate ( HS ) , dermatan sulfate ( DS ) , and chondroitin-4 , 6 - sulfate ( CS ) .
	manualset2
82958	4	397792	5	NULL	NULL	0	NULL	heparan sulfate ( HS )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	GUS is required to degrade glycosaminoglycans ( GAGs ) , including heparan sulfate ( HS ) , dermatan sulfate ( DS ) , and chondroitin-4 , 6 - sulfate ( CS ) .
	manualset2
82959	5	397792	5	NULL	NULL	0	NULL	dermatan sulfate ( DS )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	GUS is required to degrade glycosaminoglycans ( GAGs ) , including heparan sulfate ( HS ) , dermatan sulfate ( DS ) , and chondroitin-4 , 6 - sulfate ( CS ) .
	manualset2
82960	6	397792	5	NULL	NULL	0	NULL	chondroitin-4 , 6 - sulfate ( CS )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	GUS is required to degrade glycosaminoglycans ( GAGs ) , including heparan sulfate ( HS ) , dermatan sulfate ( DS ) , and chondroitin-4 , 6 - sulfate ( CS ) .
	manualset2
82965	1	397794	5	NULL	NULL	0	NULL	GXMs	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	GXMs from typical serotype A and serotype D isolates were excellent inhibitors of factor serum 3 .
	manualset2
82966	2	397794	5	NULL	NULL	0	NULL	typical serotype A	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	GXMs from typical serotype A and serotype D isolates were excellent inhibitors of factor serum 3 .
	manualset2
82967	3	397794	5	NULL	NULL	0	NULL	serotype D isolates	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	GXMs from typical serotype A and serotype D isolates were excellent inhibitors of factor serum 3 .
	manualset2
82968	4	397794	5	NULL	NULL	NULL	NULL	excellent inhibitors	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	GXMs from typical serotype A and serotype D isolates were excellent inhibitors of factor serum 3 .
	manualset2
82969	5	397794	5	NULL	NULL	0	NULL	factor serum 3	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GXMs from typical serotype A and serotype D isolates were excellent inhibitors of factor serum 3 .
	manualset2
82970	1	397795	5	NULL	NULL	NULL	NULL	Gain - and loss-of-function analyses	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gain - and loss-of-function analyses show that sphingosine kinases affect trafficking of the G protein-coupled receptor Rhodopsin and the light-sensitive transient receptor potential ( TRP ) channel by modulating the levels of dihydrosphingosine 1 phosphate ( DHS1P ) and sphingosine 1 phosphate ( S1P ) .
	manualset2
82971	2	397795	5	NULL	NULL	0	NULL	sphingosine kinases	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Gain - and loss-of-function analyses show that sphingosine kinases affect trafficking of the G protein-coupled receptor Rhodopsin and the light-sensitive transient receptor potential ( TRP ) channel by modulating the levels of dihydrosphingosine 1 phosphate ( DHS1P ) and sphingosine 1 phosphate ( S1P ) .
	manualset2
82972	3	397795	5	NULL	NULL	0	NULL	 trafficking	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gain - and loss-of-function analyses show that sphingosine kinases affect trafficking of the G protein-coupled receptor Rhodopsin and the light-sensitive transient receptor potential ( TRP ) channel by modulating the levels of dihydrosphingosine 1 phosphate ( DHS1P ) and sphingosine 1 phosphate ( S1P ) .
	manualset2
82973	4	397795	5	NULL	NULL	0	NULL	G protein-coupled receptor Rhodopsin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Gain - and loss-of-function analyses show that sphingosine kinases affect trafficking of the G protein-coupled receptor Rhodopsin and the light-sensitive transient receptor potential ( TRP ) channel by modulating the levels of dihydrosphingosine 1 phosphate ( DHS1P ) and sphingosine 1 phosphate ( S1P ) .
	manualset2
82974	5	397795	5	NULL	NULL	0	NULL	light-sensitive transient receptor potential ( TRP ) channel	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Gain - and loss-of-function analyses show that sphingosine kinases affect trafficking of the G protein-coupled receptor Rhodopsin and the light-sensitive transient receptor potential ( TRP ) channel by modulating the levels of dihydrosphingosine 1 phosphate ( DHS1P ) and sphingosine 1 phosphate ( S1P ) .
	manualset2
82975	6	397795	5	NULL	NULL	0	NULL	dihydrosphingosine 1 phosphate ( DHS1P )	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Gain - and loss-of-function analyses show that sphingosine kinases affect trafficking of the G protein-coupled receptor Rhodopsin and the light-sensitive transient receptor potential ( TRP ) channel by modulating the levels of dihydrosphingosine 1 phosphate ( DHS1P ) and sphingosine 1 phosphate ( S1P ) .
	manualset2
82976	7	397795	5	NULL	NULL	0	NULL	sphingosine 1 phosphate ( S1P )	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Gain - and loss-of-function analyses show that sphingosine kinases affect trafficking of the G protein-coupled receptor Rhodopsin and the light-sensitive transient receptor potential ( TRP ) channel by modulating the levels of dihydrosphingosine 1 phosphate ( DHS1P ) and sphingosine 1 phosphate ( S1P ) .
	manualset2
83227	1	397796	5	NULL	NULL	0	NULL	cross-functional commitment	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gaining cross-functional commitment for a comprehensive PPE program not only will move the improvement process forward , but also will ensure the company benefits from optimal cost and performance advantages that positively impact the bottom line .
	manualset2
83228	2	397796	5	NULL	NULL	0	NULL	comprehensive PPE program	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gaining cross-functional commitment for a comprehensive PPE program not only will move the improvement process forward , but also will ensure the company benefits from optimal cost and performance advantages that positively impact the bottom line .
	manualset2
83230	3	397796	5	NULL	NULL	0	NULL	improvement process	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Gaining cross-functional commitment for a comprehensive PPE program not only will move the improvement process forward , but also will ensure the company benefits from optimal cost and performance advantages that positively impact the bottom line .
	manualset2
83231	4	397796	5	NULL	NULL	NULL	NULL	performance advantages	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gaining cross-functional commitment for a comprehensive PPE program not only will move the improvement process forward , but also will ensure the company benefits from optimal cost and performance advantages that positively impact the bottom line .
	manualset2
82977	1	397797	5	NULL	NULL	0	NULL	3p	Chromosome												NULL		0	NULL	NULL	NULL	NULL	NULL	Gains of 3p were detected in 4/55 ( 7 % ) WDET , no WDEC , but notably in 3/6 ( 50 % ) PDEC ( OR 23.6 ; P = 0.003 ) .
	manualset2
82978	2	397797	5	NULL	NULL	0	NULL	4/55 ( 7 % ) WDET	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gains of 3p were detected in 4/55 ( 7 % ) WDET , no WDEC , but notably in 3/6 ( 50 % ) PDEC ( OR 23.6 ; P = 0.003 ) .
	manualset2
82979	3	397797	5	NULL	NULL	0	NULL	WDEC	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gains of 3p were detected in 4/55 ( 7 % ) WDET , no WDEC , but notably in 3/6 ( 50 % ) PDEC ( OR 23.6 ; P = 0.003 ) .
	manualset2
82980	4	397797	5	NULL	NULL	0	NULL	3/6 ( 50 % ) PDEC	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gains of 3p were detected in 4/55 ( 7 % ) WDET , no WDEC , but notably in 3/6 ( 50 % ) PDEC ( OR 23.6 ; P = 0.003 ) .
	manualset2
82981	5	397797	5	NULL	NULL	0	NULL	23.6 ; P = 0.003	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Gains of 3p were detected in 4/55 ( 7 % ) WDET , no WDEC , but notably in 3/6 ( 50 % ) PDEC ( OR 23.6 ; P = 0.003 ) .
	manualset2
83173	1	397798	5	NULL	NULL	0	NULL	quicker bill collection	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Gains outweigh costs of quicker bill collection .
	manualset2
82982	1	397799	5	NULL	NULL	0	NULL	Gal-1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Gal-1 is up-regulated in hepatocarcinoma cells , although its role in liver pathophysiology remains uncertain .
	manualset2
82983	2	397799	5	NULL	NULL	0	NULL	hepatocarcinoma cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Gal-1 is up-regulated in hepatocarcinoma cells , although its role in liver pathophysiology remains uncertain .
	manualset2
82984	3	397799	5	NULL	NULL	NULL	NULL	liver pathophysiology	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gal-1 is up-regulated in hepatocarcinoma cells , although its role in liver pathophysiology remains uncertain .
	manualset2
82985	1	397800	5	NULL	NULL	0	NULL	Galactorrhea	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Galactorrhea , oligo/amenorrhea , and hyperprolactinemia in patients with craniopharyngiomas .
	manualset2
82986	2	397800	5	NULL	NULL	0	NULL	oligo/amenorrhea	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Galactorrhea , oligo/amenorrhea , and hyperprolactinemia in patients with craniopharyngiomas .
	manualset2
82987	3	397800	5	NULL	NULL	0	NULL	hyperprolactinemia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Galactorrhea , oligo/amenorrhea , and hyperprolactinemia in patients with craniopharyngiomas .
	manualset2
82988	4	397800	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Galactorrhea , oligo/amenorrhea , and hyperprolactinemia in patients with craniopharyngiomas .
	manualset2
82989	5	397800	5	NULL	NULL	0	NULL	craniopharyngiomas	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Galactorrhea , oligo/amenorrhea , and hyperprolactinemia in patients with craniopharyngiomas .
	manualset2
82990	1	397801	5	NULL	NULL	0	NULL	Gallbladder cancer	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gallbladder cancer and liver transplantation .
	manualset2
82991	2	397801	5	NULL	NULL	0	NULL	liver transplantation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Gallbladder cancer and liver transplantation .
	manualset2
82992	1	397802	5	NULL	NULL	0	NULL	Gallbladder perforation	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gallbladder perforation with contained empyema diagnosed by CT but missed by sonography and hepatobiliary scintigraphy .
	manualset2
82993	2	397802	5	NULL	NULL	0	NULL	contained empyema	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gallbladder perforation with contained empyema diagnosed by CT but missed by sonography and hepatobiliary scintigraphy .
	manualset2
82994	3	397802	5	NULL	NULL	NULL	NULL	CT	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gallbladder perforation with contained empyema diagnosed by CT but missed by sonography and hepatobiliary scintigraphy .
	manualset2
82995	4	397802	5	NULL	NULL	0	NULL	sonography	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Gallbladder perforation with contained empyema diagnosed by CT but missed by sonography and hepatobiliary scintigraphy .
	manualset2
82996	5	397802	5	NULL	NULL	0	NULL	hepatobiliary scintigraphy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Gallbladder perforation with contained empyema diagnosed by CT but missed by sonography and hepatobiliary scintigraphy .
	manualset2
82997	1	397803	5	NULL	NULL	0	NULL	Gambogenic acid	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Gambogenic acid significantly inhibited cell proliferation and induced apoptosis .
	manualset2
82998	2	397803	5	NULL	NULL	0	NULL	cell proliferation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gambogenic acid significantly inhibited cell proliferation and induced apoptosis .
	manualset2
82999	3	397803	5	NULL	NULL	0	NULL	apoptosis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gambogenic acid significantly inhibited cell proliferation and induced apoptosis .
	manualset2
83000	1	397804	5	NULL	NULL	0	NULL	Gamma scintigraphic studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gamma scintigraphic studies demonstrated that CaP capsules could pass through the stomach and small intestine intact and could release drug in colon .
	manualset2
83001	2	397804	5	NULL	NULL	0	NULL	CaP capsules	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Gamma scintigraphic studies demonstrated that CaP capsules could pass through the stomach and small intestine intact and could release drug in colon .
	manualset2
83002	3	397804	5	NULL	NULL	0	NULL	stomach	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Gamma scintigraphic studies demonstrated that CaP capsules could pass through the stomach and small intestine intact and could release drug in colon .
	manualset2
83003	4	397804	5	NULL	NULL	0	NULL	small intestine	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Gamma scintigraphic studies demonstrated that CaP capsules could pass through the stomach and small intestine intact and could release drug in colon .
	manualset2
83004	5	397804	5	NULL	NULL	NULL	NULL	release	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gamma scintigraphic studies demonstrated that CaP capsules could pass through the stomach and small intestine intact and could release drug in colon .
	manualset2
83005	6	397804	5	NULL	NULL	0	NULL	drug	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Gamma scintigraphic studies demonstrated that CaP capsules could pass through the stomach and small intestine intact and could release drug in colon .
	manualset2
83006	7	397804	5	NULL	NULL	0	NULL	colon	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Gamma scintigraphic studies demonstrated that CaP capsules could pass through the stomach and small intestine intact and could release drug in colon .
	manualset2
83007	1	397805	5	NULL	NULL	0	NULL	Ganglioside pattern	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Ganglioside pattern was altered only in the 2 month rats , showing a reduction of GM1 and GM1a in the synaptosomal fraction and of GD1a in the microsomal fraction .
	manualset2
83008	2	397805	5	NULL	NULL	0	NULL	rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Ganglioside pattern was altered only in the 2 month rats , showing a reduction of GM1 and GM1a in the synaptosomal fraction and of GD1a in the microsomal fraction .
	manualset2
83009	3	397805	5	NULL	NULL	0	NULL	GM1	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Ganglioside pattern was altered only in the 2 month rats , showing a reduction of GM1 and GM1a in the synaptosomal fraction and of GD1a in the microsomal fraction .
	manualset2
83010	4	397805	5	NULL	NULL	0	NULL	GM1a	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Ganglioside pattern was altered only in the 2 month rats , showing a reduction of GM1 and GM1a in the synaptosomal fraction and of GD1a in the microsomal fraction .
	manualset2
83011	5	397805	5	NULL	NULL	0	NULL	synaptosomal fraction	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Ganglioside pattern was altered only in the 2 month rats , showing a reduction of GM1 and GM1a in the synaptosomal fraction and of GD1a in the microsomal fraction .
	manualset2
83012	6	397805	5	NULL	NULL	0	NULL	GD1a	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Ganglioside pattern was altered only in the 2 month rats , showing a reduction of GM1 and GM1a in the synaptosomal fraction and of GD1a in the microsomal fraction .
	manualset2
83013	7	397805	5	NULL	NULL	0	NULL	microsomal fraction	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Ganglioside pattern was altered only in the 2 month rats , showing a reduction of GM1 and GM1a in the synaptosomal fraction and of GD1a in the microsomal fraction .
	manualset2
83014	1	397806	5	NULL	NULL	NULL	NULL	Gap junctions	AnatomicalPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gap junctions appear among myocardiocytes , confirming the myogenic theory of heart contractions .
	manualset2
83015	2	397806	5	NULL	NULL	0	NULL	myocardiocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Gap junctions appear among myocardiocytes , confirming the myogenic theory of heart contractions .
	manualset2
83016	3	397806	5	NULL	NULL	0	NULL	myogenic theory of heart contractions	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gap junctions appear among myocardiocytes , confirming the myogenic theory of heart contractions .
	manualset2
83017	1	397807	5	NULL	NULL	0	NULL	Gas-phase peptide sequencing	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gas-phase peptide sequencing by TEMPO-mediated radical generation .
	manualset2
83018	2	397807	5	NULL	NULL	NULL	NULL	TEMPO-mediated radical generation	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gas-phase peptide sequencing by TEMPO-mediated radical generation .
	manualset2
83019	1	397808	5	NULL	NULL	0	NULL	Gas-phase reactivity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gas-phase reactivity of metavanadate ( VO3 ) - towards methanol and ethanol : experiment and theory .
	manualset2
83020	2	397808	5	NULL	NULL	0	NULL	metavanadate ( VO3 ) -	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	Gas-phase reactivity of metavanadate ( VO3 ) - towards methanol and ethanol : experiment and theory .
	manualset2
83021	3	397808	5	NULL	NULL	0	NULL	methanol	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Gas-phase reactivity of metavanadate ( VO3 ) - towards methanol and ethanol : experiment and theory .
	manualset2
83022	4	397808	5	NULL	NULL	0	NULL	ethanol	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Gas-phase reactivity of metavanadate ( VO3 ) - towards methanol and ethanol : experiment and theory .
	manualset2
83023	5	397808	5	NULL	NULL	0	NULL	experiment	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gas-phase reactivity of metavanadate ( VO3 ) - towards methanol and ethanol : experiment and theory .
	manualset2
83024	6	397808	5	NULL	NULL	0	NULL	theory	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Gas-phase reactivity of metavanadate ( VO3 ) - towards methanol and ethanol : experiment and theory .
	manualset2
83025	1	397809	5	NULL	NULL	0	NULL	Gas	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Gas and solid sampling can be performed through the reactor bed with their composition profiles determined at steady state .
	manualset2
83026	2	397809	5	NULL	NULL	0	NULL	solid sampling	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gas and solid sampling can be performed through the reactor bed with their composition profiles determined at steady state .
	manualset2
83027	3	397809	5	NULL	NULL	0	NULL	reactor bed	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	Gas and solid sampling can be performed through the reactor bed with their composition profiles determined at steady state .
	manualset2
83028	4	397809	5	NULL	NULL	0	NULL	composition profiles													NULL		0	NULL	NULL	NULL	NULL	NULL	Gas and solid sampling can be performed through the reactor bed with their composition profiles determined at steady state .
	manualset2
83029	1	397810	5	NULL	NULL	0	NULL	children	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( Should we vaccinate children against influenza ? ) .
	manualset2
83030	2	397810	5	NULL	NULL	0	NULL	influenza	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Should we vaccinate children against influenza ? ) .
	manualset2
83031	1	397811	5	NULL	NULL	0	NULL	Gaseous environments	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Gaseous environments modify physiology in the brewing yeast Saccharomyces cerevisiae during batch alcoholic fermentation .
	manualset2
83032	2	397811	5	NULL	NULL	NULL	NULL	physiology	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gaseous environments modify physiology in the brewing yeast Saccharomyces cerevisiae during batch alcoholic fermentation .
	manualset2
83033	3	397811	5	NULL	NULL	0	NULL	brewing yeast Saccharomyces cerevisiae	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Gaseous environments modify physiology in the brewing yeast Saccharomyces cerevisiae during batch alcoholic fermentation .
	manualset2
83034	4	397811	5	NULL	NULL	NULL	NULL	batch alcoholic fermentation	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gaseous environments modify physiology in the brewing yeast Saccharomyces cerevisiae during batch alcoholic fermentation .
	manualset2
83037	1	397812	5	NULL	NULL	NULL	NULL	72 and 30 degrees F	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gasoline vehicles included normal particle mass ( particulate matter ( PM ) ) emitters ( tested at 72 and 30 degrees F ) , `` black '' and `` white '' smokers , and a new-technology vehicle ( tested at 72 degrees F ) .
	manualset2
83040	2	397812	5	NULL	NULL	NULL	NULL	72 degrees F	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gasoline vehicles included normal particle mass ( particulate matter ( PM ) ) emitters ( tested at 72 and 30 degrees F ) , `` black '' and `` white '' smokers , and a new-technology vehicle ( tested at 72 degrees F ) .
	manualset2
83041	1	397813	5	NULL	NULL	0	NULL	Gastric cancer	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastric cancer is the second leading cause of cancer death worldwide .
	manualset2
83042	2	397813	5	NULL	NULL	0	NULL	cancer death	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastric cancer is the second leading cause of cancer death worldwide .
	manualset2
83043	3	397813	5	NULL	NULL	0	NULL	worldwide	UnproperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastric cancer is the second leading cause of cancer death worldwide .
	manualset2
83044	1	397814	5	NULL	NULL	0	NULL	Gastric duplications	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastric duplications account for 2 % to 7 % of all gastrointestinal duplications .
	manualset2
83045	2	397814	5	NULL	NULL	0	NULL	2 % to 7 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastric duplications account for 2 % to 7 % of all gastrointestinal duplications .
	manualset2
83046	3	397814	5	NULL	NULL	0	NULL	gastrointestinal duplications	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastric duplications account for 2 % to 7 % of all gastrointestinal duplications .
	manualset2
83047	1	397815	5	NULL	NULL	0	NULL	Gastrin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastrin and cholecystokinin levels in rats fed soya bean trypsin inhibitor .
	manualset2
83048	2	397815	5	NULL	NULL	0	NULL	cholecystokinin levels	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastrin and cholecystokinin levels in rats fed soya bean trypsin inhibitor .
	manualset2
83049	3	397815	5	NULL	NULL	0	NULL	rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastrin and cholecystokinin levels in rats fed soya bean trypsin inhibitor .
	manualset2
83050	4	397815	5	NULL	NULL	0	NULL	soya bean trypsin inhibitor	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastrin and cholecystokinin levels in rats fed soya bean trypsin inhibitor .
	manualset2
83051	1	397816	5	NULL	NULL	0	NULL	Gastroccult reagent	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastroccult reagent was used every 4 h to detect blood in gastric juice in 41 ICU patients at risk of GI bleeding ( GB ) and receiving antacid prophylaxis ( gastric pH greater than 3.5 ) .
	manualset2
83052	3	397816	5	NULL	NULL	NULL	NULL	blood	Tissue												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gastroccult reagent was used every 4 h to detect blood in gastric juice in 41 ICU patients at risk of GI bleeding ( GB ) and receiving antacid prophylaxis ( gastric pH greater than 3.5 ) .
	manualset2
83053	4	397816	5	NULL	NULL	NULL	NULL	gastric juice	NonProteinOrNucleicAcidChemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gastroccult reagent was used every 4 h to detect blood in gastric juice in 41 ICU patients at risk of GI bleeding ( GB ) and receiving antacid prophylaxis ( gastric pH greater than 3.5 ) .
	manualset2
83054	5	397816	5	NULL	NULL	NULL	NULL	41 ICU patients	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gastroccult reagent was used every 4 h to detect blood in gastric juice in 41 ICU patients at risk of GI bleeding ( GB ) and receiving antacid prophylaxis ( gastric pH greater than 3.5 ) .
	manualset2
83055	6	397816	5	NULL	NULL	NULL	NULL	GI bleeding ( GB )	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gastroccult reagent was used every 4 h to detect blood in gastric juice in 41 ICU patients at risk of GI bleeding ( GB ) and receiving antacid prophylaxis ( gastric pH greater than 3.5 ) .
	manualset2
83056	7	397816	5	NULL	NULL	NULL	NULL	antacid prophylaxis	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gastroccult reagent was used every 4 h to detect blood in gastric juice in 41 ICU patients at risk of GI bleeding ( GB ) and receiving antacid prophylaxis ( gastric pH greater than 3.5 ) .
	manualset2
83057	8	397816	5	NULL	NULL	NULL	NULL	gastric pH greater than 3.5	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gastroccult reagent was used every 4 h to detect blood in gastric juice in 41 ICU patients at risk of GI bleeding ( GB ) and receiving antacid prophylaxis ( gastric pH greater than 3.5 ) .
	manualset2
83233	2	397816	5	NULL	NULL	NULL	NULL	every 4 h	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gastroccult reagent was used every 4 h to detect blood in gastric juice in 41 ICU patients at risk of GI bleeding ( GB ) and receiving antacid prophylaxis ( gastric pH greater than 3.5 ) .
	manualset2
83058	1	397817	5	NULL	NULL	0	NULL	Gastroenterologists	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastroenterologists have , in spite of these facts , addressed this scientific field surprisingly late , in contrast to veterinarians , for whom the fermentative production of SCFAs has been acknowledged as a principal mechanism of intestinal digestion in plant-eating animals for decades .
	manualset2
83060	2	397817	5	NULL	NULL	0	NULL	veterinarians	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastroenterologists have , in spite of these facts , addressed this scientific field surprisingly late , in contrast to veterinarians , for whom the fermentative production of SCFAs has been acknowledged as a principal mechanism of intestinal digestion in plant-eating animals for decades .
	manualset2
83061	3	397817	5	NULL	NULL	0	NULL	fermentative production	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastroenterologists have , in spite of these facts , addressed this scientific field surprisingly late , in contrast to veterinarians , for whom the fermentative production of SCFAs has been acknowledged as a principal mechanism of intestinal digestion in plant-eating animals for decades .
	manualset2
83062	4	397817	5	NULL	NULL	0	NULL	SCFAs	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastroenterologists have , in spite of these facts , addressed this scientific field surprisingly late , in contrast to veterinarians , for whom the fermentative production of SCFAs has been acknowledged as a principal mechanism of intestinal digestion in plant-eating animals for decades .
	manualset2
83063	5	397817	5	NULL	NULL	0	NULL	principal mechanism	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastroenterologists have , in spite of these facts , addressed this scientific field surprisingly late , in contrast to veterinarians , for whom the fermentative production of SCFAs has been acknowledged as a principal mechanism of intestinal digestion in plant-eating animals for decades .
	manualset2
83064	6	397817	5	NULL	NULL	0	NULL	intestinal digestion	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastroenterologists have , in spite of these facts , addressed this scientific field surprisingly late , in contrast to veterinarians , for whom the fermentative production of SCFAs has been acknowledged as a principal mechanism of intestinal digestion in plant-eating animals for decades .
	manualset2
83065	7	397817	5	NULL	NULL	0	NULL	plant-eating animals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastroenterologists have , in spite of these facts , addressed this scientific field surprisingly late , in contrast to veterinarians , for whom the fermentative production of SCFAs has been acknowledged as a principal mechanism of intestinal digestion in plant-eating animals for decades .
	manualset2
83066	8	397817	5	NULL	NULL	0	NULL	decades	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastroenterologists have , in spite of these facts , addressed this scientific field surprisingly late , in contrast to veterinarians , for whom the fermentative production of SCFAs has been acknowledged as a principal mechanism of intestinal digestion in plant-eating animals for decades .
	manualset2
83067	1	397818	5	NULL	NULL	0	NULL	Gastrointestinal disease outcomes	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastrointestinal disease outcomes are also more severe , due to under-nutrition and lack of intervention strategies in these regions .
	manualset2
83068	2	397818	5	NULL	NULL	0	NULL	under-nutrition	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastrointestinal disease outcomes are also more severe , due to under-nutrition and lack of intervention strategies in these regions .
	manualset2
83069	3	397818	5	NULL	NULL	0	NULL	lack of intervention strategies	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastrointestinal disease outcomes are also more severe , due to under-nutrition and lack of intervention strategies in these regions .
	manualset2
83070	4	397818	5	NULL	NULL	0	NULL	regions	UnproperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastrointestinal disease outcomes are also more severe , due to under-nutrition and lack of intervention strategies in these regions .
	manualset2
83071	1	397819	5	NULL	NULL	0	NULL	Sialolithiasis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Sialolithiasis of the parotid gland -- case report ) .
	manualset2
83072	2	397819	5	NULL	NULL	0	NULL	parotid gland	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( Sialolithiasis of the parotid gland -- case report ) .
	manualset2
83174	3	397819	5	NULL	NULL	0	NULL	case report	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	( Sialolithiasis of the parotid gland -- case report ) .
	manualset2
83074	1	397820	5	NULL	NULL	0	NULL	Gastrointestinal flora	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastrointestinal flora and its alterations in critical illness .
	manualset2
83075	2	397820	5	NULL	NULL	0	NULL	critical illness	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastrointestinal flora and its alterations in critical illness .
	manualset2
83076	1	397821	5	NULL	NULL	0	NULL	Gastrointestinal perforation	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastrointestinal perforation early after peripheral blood stem cell transplantation for AL amyloidosis .
	manualset2
83077	2	397821	5	NULL	NULL	0	NULL	peripheral blood stem cell transplantation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastrointestinal perforation early after peripheral blood stem cell transplantation for AL amyloidosis .
	manualset2
83078	3	397821	5	NULL	NULL	0	NULL	AL amyloidosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastrointestinal perforation early after peripheral blood stem cell transplantation for AL amyloidosis .
	manualset2
83079	1	397822	5	NULL	NULL	NULL	NULL	Gastrointestinal transit	Time												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gastrointestinal transit of 14C-labeled nutrients was unchanged in hypophagic rats , suggesting a postabsorptive mechanism controlled the hypophagia .
	manualset2
83080	2	397822	5	NULL	NULL	0	NULL	14C-labeled nutrients	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastrointestinal transit of 14C-labeled nutrients was unchanged in hypophagic rats , suggesting a postabsorptive mechanism controlled the hypophagia .
	manualset2
83081	3	397822	5	NULL	NULL	0	NULL	hypophagic rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastrointestinal transit of 14C-labeled nutrients was unchanged in hypophagic rats , suggesting a postabsorptive mechanism controlled the hypophagia .
	manualset2
83082	4	397822	5	NULL	NULL	0	NULL	postabsorptive mechanism	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastrointestinal transit of 14C-labeled nutrients was unchanged in hypophagic rats , suggesting a postabsorptive mechanism controlled the hypophagia .
	manualset2
83083	5	397822	5	NULL	NULL	0	NULL	hypophagia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gastrointestinal transit of 14C-labeled nutrients was unchanged in hypophagic rats , suggesting a postabsorptive mechanism controlled the hypophagia .
	manualset2
83084	1	397823	5	NULL	NULL	0	NULL	Gel filtration chromatography	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gel filtration chromatography and sucrose gradient sedimentation studies indicate that in solution , native TnsB is a monomer of nonspherical shape .
	manualset2
83085	2	397823	5	NULL	NULL	0	NULL	sucrose gradient sedimentation studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gel filtration chromatography and sucrose gradient sedimentation studies indicate that in solution , native TnsB is a monomer of nonspherical shape .
	manualset2
83086	3	397823	5	NULL	NULL	0	NULL	solution	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Gel filtration chromatography and sucrose gradient sedimentation studies indicate that in solution , native TnsB is a monomer of nonspherical shape .
	manualset2
83087	4	397823	5	NULL	NULL	0	NULL	native TnsB	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Gel filtration chromatography and sucrose gradient sedimentation studies indicate that in solution , native TnsB is a monomer of nonspherical shape .
	manualset2
83088	5	397823	5	NULL	NULL	0	NULL	monomer	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Gel filtration chromatography and sucrose gradient sedimentation studies indicate that in solution , native TnsB is a monomer of nonspherical shape .
	manualset2
83089	1	397824	5	NULL	NULL	0	NULL	efficient delivery	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Gelatin nanocarrier enables efficient delivery and phototoxicity of hypocrellin B against a mice tumor model .
	manualset2
83090	2	397824	5	NULL	NULL	0	NULL	phototoxicity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gelatin nanocarrier enables efficient delivery and phototoxicity of hypocrellin B against a mice tumor model .
	manualset2
83091	3	397824	5	NULL	NULL	0	NULL	hypocrellin B	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Gelatin nanocarrier enables efficient delivery and phototoxicity of hypocrellin B against a mice tumor model .
	manualset2
83092	4	397824	5	NULL	NULL	0	NULL	mice tumor model	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Gelatin nanocarrier enables efficient delivery and phototoxicity of hypocrellin B against a mice tumor model .
	manualset2
83093	1	397825	5	NULL	NULL	0	NULL	Geminin 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Geminin prevents rereplication during xenopus development .
	manualset2
83094	2	397825	5	NULL	NULL	0	NULL	rereplication	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Geminin prevents rereplication during xenopus development .
	manualset2
83095	3	397825	5	NULL	NULL	0	NULL	xenopus development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Geminin prevents rereplication during xenopus development .
	manualset2
83096	1	397826	5	NULL	NULL	0	NULL	children 's	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Gender labels and play styles : their relative contribution to children 's selection of playmates .
	manualset2
83097	2	397826	5	NULL	NULL	0	NULL	selection	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gender labels and play styles : their relative contribution to children 's selection of playmates .
	manualset2
83098	3	397826	5	NULL	NULL	0	NULL	playmates	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Gender labels and play styles : their relative contribution to children 's selection of playmates .
	manualset2
83099	1	397827	5	NULL	NULL	0	NULL	iliac artery	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( Sign of the iliac artery in patients with large gynecologic tumors ) .
	manualset2
83100	2	397827	5	NULL	NULL	0	NULL	 patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( Sign of the iliac artery in patients with large gynecologic tumors ) .
	manualset2
83101	3	397827	5	NULL	NULL	0	NULL	large gynecologic tumors	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Sign of the iliac artery in patients with large gynecologic tumors ) .
	manualset2
83102	1	397828	5	NULL	NULL	0	NULL	Gene arrays	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene arrays in lymphoma : Where will they fit in ?
	manualset2
83103	2	397828	5	NULL	NULL	0	NULL	lymphoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene arrays in lymphoma : Where will they fit in ?
	manualset2
83104	1	397829	5	NULL	NULL	0	NULL	Gene coexpression network topology	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene coexpression network topology of cardiac development , hypertrophy , and failure .
	manualset2
83105	2	397829	5	NULL	NULL	0	NULL	cardiac development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene coexpression network topology of cardiac development , hypertrophy , and failure .
	manualset2
83106	3	397829	5	NULL	NULL	NULL	NULL	hypertrophy	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene coexpression network topology of cardiac development , hypertrophy , and failure .
	manualset2
83107	4	397829	5	NULL	NULL	0	NULL	failure	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene coexpression network topology of cardiac development , hypertrophy , and failure .
	manualset2
83108	1	397830	5	NULL	NULL	0	NULL	Gene delivery	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene delivery of l-caldesmon protects cytoskeletal cell membrane integrity against adenovirus infection independently of myosin ATPase and actin assembly .
	manualset2
83109	2	397830	5	NULL	NULL	0	NULL	l-caldesmon	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene delivery of l-caldesmon protects cytoskeletal cell membrane integrity against adenovirus infection independently of myosin ATPase and actin assembly .
	manualset2
83110	3	397830	5	NULL	NULL	0	NULL	cytoskeletal cell membrane integrity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene delivery of l-caldesmon protects cytoskeletal cell membrane integrity against adenovirus infection independently of myosin ATPase and actin assembly .
	manualset2
83111	4	397830	5	NULL	NULL	0	NULL	adenovirus infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene delivery of l-caldesmon protects cytoskeletal cell membrane integrity against adenovirus infection independently of myosin ATPase and actin assembly .
	manualset2
83112	5	397830	5	NULL	NULL	0	NULL	myosin ATPase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene delivery of l-caldesmon protects cytoskeletal cell membrane integrity against adenovirus infection independently of myosin ATPase and actin assembly .
	manualset2
83113	6	397830	5	NULL	NULL	0	NULL	actin assembly	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene delivery of l-caldesmon protects cytoskeletal cell membrane integrity against adenovirus infection independently of myosin ATPase and actin assembly .
	manualset2
82680	2	397831	14	13	NULL	NULL	NULL	poliovirion RNA	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene duplications in poliovirion RNA .
	manualset3
83115	1	397831	14	13	NULL	0	NULL	Gene duplications	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene duplications in poliovirion RNA .
	manualset3
82681	1	397832	14	13	NULL	NULL	NULL	real-time ( kinetic ) RT-PCR	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression analyses using real-time ( kinetic ) RT-PCR were performed to monitor the transcriptional evolution of EGFR ligands EGF , TGF , AR , BTC , EPI , NRG and HB-EGF in experimental modes induced to exhibit acquired resistance to the mono-HER1 inhibitor CTX , the mono-HER2 inhibitor trastuzumab ( Tzb ) or the dual HER1/HER2 inhibitor lapatinib ( LPT ) .
	manualset3
82682	2	397832	14	13	NULL	NULL	NULL	EGFR ligands	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression analyses using real-time ( kinetic ) RT-PCR were performed to monitor the transcriptional evolution of EGFR ligands EGF , TGF , AR , BTC , EPI , NRG and HB-EGF in experimental modes induced to exhibit acquired resistance to the mono-HER1 inhibitor CTX , the mono-HER2 inhibitor trastuzumab ( Tzb ) or the dual HER1/HER2 inhibitor lapatinib ( LPT ) .
	manualset3
82683	3	397832	14	13	NULL	0	NULL	EGF	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expression analyses using real-time ( kinetic ) RT-PCR were performed to monitor the transcriptional evolution of EGFR ligands EGF , TGF , AR , BTC , EPI , NRG and HB-EGF in experimental modes induced to exhibit acquired resistance to the mono-HER1 inhibitor CTX , the mono-HER2 inhibitor trastuzumab ( Tzb ) or the dual HER1/HER2 inhibitor lapatinib ( LPT ) .
	manualset3
82684	4	397832	14	13	NULL	0	NULL	TGF 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expression analyses using real-time ( kinetic ) RT-PCR were performed to monitor the transcriptional evolution of EGFR ligands EGF , TGF , AR , BTC , EPI , NRG and HB-EGF in experimental modes induced to exhibit acquired resistance to the mono-HER1 inhibitor CTX , the mono-HER2 inhibitor trastuzumab ( Tzb ) or the dual HER1/HER2 inhibitor lapatinib ( LPT ) .
	manualset3
82685	5	397832	14	13	NULL	0	NULL	AR	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expression analyses using real-time ( kinetic ) RT-PCR were performed to monitor the transcriptional evolution of EGFR ligands EGF , TGF , AR , BTC , EPI , NRG and HB-EGF in experimental modes induced to exhibit acquired resistance to the mono-HER1 inhibitor CTX , the mono-HER2 inhibitor trastuzumab ( Tzb ) or the dual HER1/HER2 inhibitor lapatinib ( LPT ) .
	manualset3
82686	6	397832	14	13	NULL	0	NULL	BTC	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expression analyses using real-time ( kinetic ) RT-PCR were performed to monitor the transcriptional evolution of EGFR ligands EGF , TGF , AR , BTC , EPI , NRG and HB-EGF in experimental modes induced to exhibit acquired resistance to the mono-HER1 inhibitor CTX , the mono-HER2 inhibitor trastuzumab ( Tzb ) or the dual HER1/HER2 inhibitor lapatinib ( LPT ) .
	manualset3
82687	7	397832	14	13	NULL	0	NULL	EPI	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expression analyses using real-time ( kinetic ) RT-PCR were performed to monitor the transcriptional evolution of EGFR ligands EGF , TGF , AR , BTC , EPI , NRG and HB-EGF in experimental modes induced to exhibit acquired resistance to the mono-HER1 inhibitor CTX , the mono-HER2 inhibitor trastuzumab ( Tzb ) or the dual HER1/HER2 inhibitor lapatinib ( LPT ) .
	manualset3
82688	8	397832	14	13	NULL	0	NULL	NRG	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expression analyses using real-time ( kinetic ) RT-PCR were performed to monitor the transcriptional evolution of EGFR ligands EGF , TGF , AR , BTC , EPI , NRG and HB-EGF in experimental modes induced to exhibit acquired resistance to the mono-HER1 inhibitor CTX , the mono-HER2 inhibitor trastuzumab ( Tzb ) or the dual HER1/HER2 inhibitor lapatinib ( LPT ) .
	manualset3
82689	9	397832	14	13	NULL	0	NULL	HB-EGF 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expression analyses using real-time ( kinetic ) RT-PCR were performed to monitor the transcriptional evolution of EGFR ligands EGF , TGF , AR , BTC , EPI , NRG and HB-EGF in experimental modes induced to exhibit acquired resistance to the mono-HER1 inhibitor CTX , the mono-HER2 inhibitor trastuzumab ( Tzb ) or the dual HER1/HER2 inhibitor lapatinib ( LPT ) .
	manualset3
82691	10	397832	14	13	NULL	NULL	NULL	mono-HER2 inhibitor trastuzumab ( Tzb ) 	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression analyses using real-time ( kinetic ) RT-PCR were performed to monitor the transcriptional evolution of EGFR ligands EGF , TGF , AR , BTC , EPI , NRG and HB-EGF in experimental modes induced to exhibit acquired resistance to the mono-HER1 inhibitor CTX , the mono-HER2 inhibitor trastuzumab ( Tzb ) or the dual HER1/HER2 inhibitor lapatinib ( LPT ) .
	manualset3
82692	11	397832	14	13	NULL	NULL	NULL	 mono-HER1 inhibitor CTX	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression analyses using real-time ( kinetic ) RT-PCR were performed to monitor the transcriptional evolution of EGFR ligands EGF , TGF , AR , BTC , EPI , NRG and HB-EGF in experimental modes induced to exhibit acquired resistance to the mono-HER1 inhibitor CTX , the mono-HER2 inhibitor trastuzumab ( Tzb ) or the dual HER1/HER2 inhibitor lapatinib ( LPT ) .
	manualset3
82696	12	397832	14	13	NULL	NULL	NULL	dual HER1/HER2 inhibitor lapatinib ( LPT ) 	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression analyses using real-time ( kinetic ) RT-PCR were performed to monitor the transcriptional evolution of EGFR ligands EGF , TGF , AR , BTC , EPI , NRG and HB-EGF in experimental modes induced to exhibit acquired resistance to the mono-HER1 inhibitor CTX , the mono-HER2 inhibitor trastuzumab ( Tzb ) or the dual HER1/HER2 inhibitor lapatinib ( LPT ) .
	manualset3
83116	13	397832	14	13	NULL	NULL	NULL	Gene expression analyses	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression analyses using real-time ( kinetic ) RT-PCR were performed to monitor the transcriptional evolution of EGFR ligands EGF , TGF , AR , BTC , EPI , NRG and HB-EGF in experimental modes induced to exhibit acquired resistance to the mono-HER1 inhibitor CTX , the mono-HER2 inhibitor trastuzumab ( Tzb ) or the dual HER1/HER2 inhibitor lapatinib ( LPT ) .
	manualset3
83117	14	397832	14	13	NULL	NULL	NULL	transcriptional evolution 	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression analyses using real-time ( kinetic ) RT-PCR were performed to monitor the transcriptional evolution of EGFR ligands EGF , TGF , AR , BTC , EPI , NRG and HB-EGF in experimental modes induced to exhibit acquired resistance to the mono-HER1 inhibitor CTX , the mono-HER2 inhibitor trastuzumab ( Tzb ) or the dual HER1/HER2 inhibitor lapatinib ( LPT ) .
	manualset3
83118	15	397832	14	13	NULL	NULL	NULL	acquired resistance 	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression analyses using real-time ( kinetic ) RT-PCR were performed to monitor the transcriptional evolution of EGFR ligands EGF , TGF , AR , BTC , EPI , NRG and HB-EGF in experimental modes induced to exhibit acquired resistance to the mono-HER1 inhibitor CTX , the mono-HER2 inhibitor trastuzumab ( Tzb ) or the dual HER1/HER2 inhibitor lapatinib ( LPT ) .
	manualset3
84551	16	397832	14	13	NULL	0	NULL	experimental modes 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expression analyses using real-time ( kinetic ) RT-PCR were performed to monitor the transcriptional evolution of EGFR ligands EGF , TGF , AR , BTC , EPI , NRG and HB-EGF in experimental modes induced to exhibit acquired resistance to the mono-HER1 inhibitor CTX , the mono-HER2 inhibitor trastuzumab ( Tzb ) or the dual HER1/HER2 inhibitor lapatinib ( LPT ) .
	manualset3
82698	1	397833	14	13	NULL	NULL	NULL	histone acetylation and methylation	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression is controlled by epigenetic mechanisms such as histone acetylation and methylation , and recent studies have revealed that key developmental steps are regulated by the trimethylation of histone H3 lysine 4 ( H3K4me3 ) and lysine 27 ( H3K27me3 ) .
	manualset3
82701	2	397833	14	13	NULL	NULL	NULL	trimethylation	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression is controlled by epigenetic mechanisms such as histone acetylation and methylation , and recent studies have revealed that key developmental steps are regulated by the trimethylation of histone H3 lysine 4 ( H3K4me3 ) and lysine 27 ( H3K27me3 ) .
	manualset3
82702	3	397833	14	13	NULL	NULL	NULL	histone H3 lysine 4	AminoAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression is controlled by epigenetic mechanisms such as histone acetylation and methylation , and recent studies have revealed that key developmental steps are regulated by the trimethylation of histone H3 lysine 4 ( H3K4me3 ) and lysine 27 ( H3K27me3 ) .
	manualset3
82703	4	397833	14	13	NULL	NULL	NULL	H3K4me3	AminoAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression is controlled by epigenetic mechanisms such as histone acetylation and methylation , and recent studies have revealed that key developmental steps are regulated by the trimethylation of histone H3 lysine 4 ( H3K4me3 ) and lysine 27 ( H3K27me3 ) .
	manualset3
82704	5	397833	14	13	NULL	NULL	NULL	lysine 27	AminoAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression is controlled by epigenetic mechanisms such as histone acetylation and methylation , and recent studies have revealed that key developmental steps are regulated by the trimethylation of histone H3 lysine 4 ( H3K4me3 ) and lysine 27 ( H3K27me3 ) .
	manualset3
82705	6	397833	14	13	NULL	NULL	NULL	H3K27me3	AminoAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression is controlled by epigenetic mechanisms such as histone acetylation and methylation , and recent studies have revealed that key developmental steps are regulated by the trimethylation of histone H3 lysine 4 ( H3K4me3 ) and lysine 27 ( H3K27me3 ) .
	manualset3
83119	7	397833	14	13	NULL	NULL	NULL	Gene expression 	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression is controlled by epigenetic mechanisms such as histone acetylation and methylation , and recent studies have revealed that key developmental steps are regulated by the trimethylation of histone H3 lysine 4 ( H3K4me3 ) and lysine 27 ( H3K27me3 ) .
	manualset3
83120	8	397833	14	13	NULL	NULL	NULL	epigenetic mechanisms 	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression is controlled by epigenetic mechanisms such as histone acetylation and methylation , and recent studies have revealed that key developmental steps are regulated by the trimethylation of histone H3 lysine 4 ( H3K4me3 ) and lysine 27 ( H3K27me3 ) .
	manualset3
83121	9	397833	14	13	NULL	NULL	NULL	key developmental steps	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression is controlled by epigenetic mechanisms such as histone acetylation and methylation , and recent studies have revealed that key developmental steps are regulated by the trimethylation of histone H3 lysine 4 ( H3K4me3 ) and lysine 27 ( H3K27me3 ) .
	manualset3
83122	10	397833	14	13	NULL	NULL	NULL	recent studies 	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression is controlled by epigenetic mechanisms such as histone acetylation and methylation , and recent studies have revealed that key developmental steps are regulated by the trimethylation of histone H3 lysine 4 ( H3K4me3 ) and lysine 27 ( H3K27me3 ) .
	manualset3
82706	1	397834	14	13	NULL	0	NULL	CYP3A4	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expression of CYP3A4 , ABC-transporters ( MDR1 and MRP1-MRP5 ) and hPXR in three different human colon carcinoma cell lines .
	manualset3
82707	2	397834	14	13	NULL	0	NULL	MDR1	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expression of CYP3A4 , ABC-transporters ( MDR1 and MRP1-MRP5 ) and hPXR in three different human colon carcinoma cell lines .
	manualset3
82708	3	397834	14	13	NULL	NULL	NULL	ABC-transporters	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression of CYP3A4 , ABC-transporters ( MDR1 and MRP1-MRP5 ) and hPXR in three different human colon carcinoma cell lines .
	manualset3
82709	4	397834	14	13	NULL	NULL	NULL	MRP1-MRP5	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression of CYP3A4 , ABC-transporters ( MDR1 and MRP1-MRP5 ) and hPXR in three different human colon carcinoma cell lines .
	manualset3
82711	6	397834	14	13	NULL	0	NULL	hPXR	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expression of CYP3A4 , ABC-transporters ( MDR1 and MRP1-MRP5 ) and hPXR in three different human colon carcinoma cell lines .
	manualset3
82712	7	397834	14	13	NULL	0	NULL	human colon carcinoma cell lines	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expression of CYP3A4 , ABC-transporters ( MDR1 and MRP1-MRP5 ) and hPXR in three different human colon carcinoma cell lines .
	manualset3
83123	8	397834	14	13	NULL	0	NULL	Gene expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expression of CYP3A4 , ABC-transporters ( MDR1 and MRP1-MRP5 ) and hPXR in three different human colon carcinoma cell lines .
	manualset3
82713	1	397835	14	13	NULL	0	NULL	S. cerevisiae	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expression profiling and phenotype analyses of S. cerevisiae in response to changing copper reveals six genes with new roles in copper and iron metabolism .
	manualset3
82714	2	397835	14	13	NULL	NULL	NULL	Gene expression profiling 	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression profiling and phenotype analyses of S. cerevisiae in response to changing copper reveals six genes with new roles in copper and iron metabolism .
	manualset3
82715	3	397835	14	13	NULL	NULL	NULL	phenotype analyses	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression profiling and phenotype analyses of S. cerevisiae in response to changing copper reveals six genes with new roles in copper and iron metabolism .
	manualset3
82716	4	397835	14	13	NULL	NULL	NULL	response to changing copper 	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expression profiling and phenotype analyses of S. cerevisiae in response to changing copper reveals six genes with new roles in copper and iron metabolism .
	manualset3
83124	5	397835	14	13	NULL	0	NULL	six genes	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expression profiling and phenotype analyses of S. cerevisiae in response to changing copper reveals six genes with new roles in copper and iron metabolism .
	manualset3
83125	6	397835	14	13	NULL	0	NULL	copper and iron metabolism 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expression profiling and phenotype analyses of S. cerevisiae in response to changing copper reveals six genes with new roles in copper and iron metabolism .
	manualset3
82717	1	397836	14	13	NULL	0	NULL	TH 	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expressions of TH , GAD67 , and GluT1 were decreased , and those of TPH , beta-tubulin III , and S-100beta were increased by treatment with just ODNs , indicating the importance of the endogenous effect of HIF-1alpha on neuronal differentiation .
	manualset3
82718	2	397836	14	13	NULL	0	NULL	GAD67	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expressions of TH , GAD67 , and GluT1 were decreased , and those of TPH , beta-tubulin III , and S-100beta were increased by treatment with just ODNs , indicating the importance of the endogenous effect of HIF-1alpha on neuronal differentiation .
	manualset3
82719	3	397836	14	13	NULL	0	NULL	GluT1	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expressions of TH , GAD67 , and GluT1 were decreased , and those of TPH , beta-tubulin III , and S-100beta were increased by treatment with just ODNs , indicating the importance of the endogenous effect of HIF-1alpha on neuronal differentiation .
	manualset3
82720	4	397836	14	13	NULL	0	NULL	TPH	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expressions of TH , GAD67 , and GluT1 were decreased , and those of TPH , beta-tubulin III , and S-100beta were increased by treatment with just ODNs , indicating the importance of the endogenous effect of HIF-1alpha on neuronal differentiation .
	manualset3
82721	5	397836	14	13	NULL	0	NULL	beta-tubulin III 	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expressions of TH , GAD67 , and GluT1 were decreased , and those of TPH , beta-tubulin III , and S-100beta were increased by treatment with just ODNs , indicating the importance of the endogenous effect of HIF-1alpha on neuronal differentiation .
	manualset3
82722	6	397836	14	13	NULL	0	NULL	S-100beta	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expressions of TH , GAD67 , and GluT1 were decreased , and those of TPH , beta-tubulin III , and S-100beta were increased by treatment with just ODNs , indicating the importance of the endogenous effect of HIF-1alpha on neuronal differentiation .
	manualset3
82723	7	397836	14	13	NULL	NULL	NULL	treatment with just ODNs 	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expressions of TH , GAD67 , and GluT1 were decreased , and those of TPH , beta-tubulin III , and S-100beta were increased by treatment with just ODNs , indicating the importance of the endogenous effect of HIF-1alpha on neuronal differentiation .
	manualset3
82724	8	397836	14	13	NULL	0	NULL	HIF-1alpha	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expressions of TH , GAD67 , and GluT1 were decreased , and those of TPH , beta-tubulin III , and S-100beta were increased by treatment with just ODNs , indicating the importance of the endogenous effect of HIF-1alpha on neuronal differentiation .
	manualset3
82725	9	397836	14	13	NULL	0	NULL	neuronal differentiation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expressions of TH , GAD67 , and GluT1 were decreased , and those of TPH , beta-tubulin III , and S-100beta were increased by treatment with just ODNs , indicating the importance of the endogenous effect of HIF-1alpha on neuronal differentiation .
	manualset3
83126	10	397836	14	13	NULL	0	NULL	Gene expressions	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expressions of TH , GAD67 , and GluT1 were decreased , and those of TPH , beta-tubulin III , and S-100beta were increased by treatment with just ODNs , indicating the importance of the endogenous effect of HIF-1alpha on neuronal differentiation .
	manualset3
83127	11	397836	14	13	NULL	0	NULL	endogenous effect	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expressions of TH , GAD67 , and GluT1 were decreased , and those of TPH , beta-tubulin III , and S-100beta were increased by treatment with just ODNs , indicating the importance of the endogenous effect of HIF-1alpha on neuronal differentiation .
	manualset3
82726	1	397837	14	13	NULL	NULL	NULL	partial pressure	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Significance of partial pressure of respiratory gas in the pulmonary alveoli and in arterial blood in respiratory function tests ; research in pulmonary tuberculosis ) .
	manualset3
82727	2	397837	14	13	NULL	0	NULL	pulmonary alveoli	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( Significance of partial pressure of respiratory gas in the pulmonary alveoli and in arterial blood in respiratory function tests ; research in pulmonary tuberculosis ) .
	manualset3
82728	3	397837	14	13	NULL	0	NULL	arterial blood	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( Significance of partial pressure of respiratory gas in the pulmonary alveoli and in arterial blood in respiratory function tests ; research in pulmonary tuberculosis ) .
	manualset3
82729	4	397837	14	13	NULL	0	NULL	pulmonary tuberculosis 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Significance of partial pressure of respiratory gas in the pulmonary alveoli and in arterial blood in respiratory function tests ; research in pulmonary tuberculosis ) .
	manualset3
83128	5	397837	14	13	NULL	0	NULL	respiratory function tests	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Significance of partial pressure of respiratory gas in the pulmonary alveoli and in arterial blood in respiratory function tests ; research in pulmonary tuberculosis ) .
	manualset3
84552	6	397837	14	13	NULL	0	NULL	respiratory gas	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( Significance of partial pressure of respiratory gas in the pulmonary alveoli and in arterial blood in respiratory function tests ; research in pulmonary tuberculosis ) .
	manualset3
82730	1	397838	14	13	NULL	0	NULL	X-gal staining	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expressions were visualized by both the quality of enzymatic color reaction using X-gal staining and by the quantification of the substrate chlorophenol red galactopyranoside ( CPRG ) in enucleated eyes on day 2 after gene transfer .
	manualset3
82731	2	397838	14	13	NULL	0	NULL	chlorophenol red galactopyranoside	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expressions were visualized by both the quality of enzymatic color reaction using X-gal staining and by the quantification of the substrate chlorophenol red galactopyranoside ( CPRG ) in enucleated eyes on day 2 after gene transfer .
	manualset3
82732	3	397838	14	13	NULL	0	NULL	CPRG	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expressions were visualized by both the quality of enzymatic color reaction using X-gal staining and by the quantification of the substrate chlorophenol red galactopyranoside ( CPRG ) in enucleated eyes on day 2 after gene transfer .
	manualset3
82733	4	397838	14	13	NULL	NULL	NULL	enucleated eyes	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expressions were visualized by both the quality of enzymatic color reaction using X-gal staining and by the quantification of the substrate chlorophenol red galactopyranoside ( CPRG ) in enucleated eyes on day 2 after gene transfer .
	manualset3
82734	5	397838	14	13	NULL	NULL	NULL	on day 2 after gene transfer	TimePoint												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene expressions were visualized by both the quality of enzymatic color reaction using X-gal staining and by the quantification of the substrate chlorophenol red galactopyranoside ( CPRG ) in enucleated eyes on day 2 after gene transfer .
	manualset3
83129	6	397838	14	13	NULL	0	NULL	Gene expressions	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expressions were visualized by both the quality of enzymatic color reaction using X-gal staining and by the quantification of the substrate chlorophenol red galactopyranoside ( CPRG ) in enucleated eyes on day 2 after gene transfer .
	manualset3
83130	7	397838	14	13	NULL	0	NULL	enzymatic color reaction 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expressions were visualized by both the quality of enzymatic color reaction using X-gal staining and by the quantification of the substrate chlorophenol red galactopyranoside ( CPRG ) in enucleated eyes on day 2 after gene transfer .
	manualset3
83131	8	397838	14	13	NULL	0	NULL	quantification of the substrate 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene expressions were visualized by both the quality of enzymatic color reaction using X-gal staining and by the quantification of the substrate chlorophenol red galactopyranoside ( CPRG ) in enucleated eyes on day 2 after gene transfer .
	manualset3
82735	1	397839	14	13	NULL	0	NULL	Gene therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene therapy : recent progress in the clinical oncology arena .
	manualset3
82736	2	397839	14	13	NULL	NULL	NULL	clinical oncology	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gene therapy : recent progress in the clinical oncology arena .
	manualset3
82737	1	397840	14	13	NULL	0	NULL	Gene therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene therapy for optic nerve disease .
	manualset3
82738	2	397840	14	13	NULL	0	NULL	optic nerve disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gene therapy for optic nerve disease .
	manualset3
82739	1	397841	14	13	NULL	NULL	NULL	Genealogy	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genealogy of the spontaneously hypertensive rat and Wistar-Kyoto rat strains : implications for studies of inherited hypertension .
	manualset3
82740	2	397841	14	13	NULL	NULL	NULL	spontaneously hypertensive rat 	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genealogy of the spontaneously hypertensive rat and Wistar-Kyoto rat strains : implications for studies of inherited hypertension .
	manualset3
82741	3	397841	14	13	NULL	0	NULL	Wistar-Kyoto rat 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genealogy of the spontaneously hypertensive rat and Wistar-Kyoto rat strains : implications for studies of inherited hypertension .
	manualset3
82742	4	397841	14	13	NULL	NULL	NULL	inherited hypertension	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genealogy of the spontaneously hypertensive rat and Wistar-Kyoto rat strains : implications for studies of inherited hypertension .
	manualset3
83132	5	397841	14	13	NULL	0	NULL	 implications for studies 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genealogy of the spontaneously hypertensive rat and Wistar-Kyoto rat strains : implications for studies of inherited hypertension .
	manualset3
83133	1	397842	14	13	NULL	0	NULL	General activation 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	General activation of all major basal ganglia regions during locomotion is more likely to provide a dynamic background for cortical signal processing rather than to directly control precise movements .
	manualset3
83134	2	397842	14	13	NULL	0	NULL	all major basal ganglia regions	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	General activation of all major basal ganglia regions during locomotion is more likely to provide a dynamic background for cortical signal processing rather than to directly control precise movements .
	manualset3
83135	3	397842	14	13	NULL	0	NULL	 locomotion	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	General activation of all major basal ganglia regions during locomotion is more likely to provide a dynamic background for cortical signal processing rather than to directly control precise movements .
	manualset3
83136	4	397842	14	13	NULL	0	NULL	cortical signal processing 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	General activation of all major basal ganglia regions during locomotion is more likely to provide a dynamic background for cortical signal processing rather than to directly control precise movements .
	manualset3
83137	5	397842	14	13	NULL	0	NULL	precise movements	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	General activation of all major basal ganglia regions during locomotion is more likely to provide a dynamic background for cortical signal processing rather than to directly control precise movements .
	manualset3
83138	1	397843	14	13	NULL	NULL	NULL	General vacuole index ( total vacuole number in a patient )	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	General vacuole index ( total vacuole number in a patient ) for left eyes was analyzed further .
	manualset3
83139	2	397843	14	13	NULL	0	NULL	left eyes	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	General vacuole index ( total vacuole number in a patient ) for left eyes was analyzed further .
	manualset3
83140	1	397844	14	13	NULL	0	NULL	General practice	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	General practice : still waiting for green-paper .
	manualset3
83141	2	397844	14	13	NULL	0	NULL	green-paper	PublicationOrCitation												NULL		0	NULL	NULL	NULL	NULL	NULL	General practice : still waiting for green-paper .
	manualset3
83151	1	397846	14	13	NULL	NULL	NULL	General surgeon	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	General surgeon , biologist , professor .
	manualset3
83152	2	397846	14	13	NULL	0	NULL	biologist	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	General surgeon , biologist , professor .
	manualset3
83153	3	397846	14	13	NULL	0	NULL	professor 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	General surgeon , biologist , professor .
	manualset3
83154	1	397847	14	13	NULL	0	NULL	Generalizability analyses	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Generalizability analyses suggest that while variability in PN ratings can be attributed to the choice of rater , candidate scores are reproducible over the 10-encounter CSA .
	manualset3
83155	2	397847	14	13	NULL	0	NULL	PN ratings	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Generalizability analyses suggest that while variability in PN ratings can be attributed to the choice of rater , candidate scores are reproducible over the 10-encounter CSA .
	manualset3
83156	3	397847	14	13	NULL	0	NULL	choice of rater	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Generalizability analyses suggest that while variability in PN ratings can be attributed to the choice of rater , candidate scores are reproducible over the 10-encounter CSA .
	manualset3
83157	4	397847	14	13	NULL	0	NULL	candidate scores	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Generalizability analyses suggest that while variability in PN ratings can be attributed to the choice of rater , candidate scores are reproducible over the 10-encounter CSA .
	manualset3
83158	5	397847	14	13	NULL	0	NULL	10-encounter CSA	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Generalizability analyses suggest that while variability in PN ratings can be attributed to the choice of rater , candidate scores are reproducible over the 10-encounter CSA .
	manualset3
83159	1	397848	14	13	NULL	0	NULL	Silent myocardial infarction 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Silent myocardial infarction ) .
	manualset3
83160	1	397849	14	13	NULL	0	NULL	Generalized morphea	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Generalized morphea and lichen sclerosus et atrophicus successfully treated with sulphasalazine .
	manualset3
83161	2	397849	14	13	NULL	0	NULL	lichen sclerosus et atrophicus	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Generalized morphea and lichen sclerosus et atrophicus successfully treated with sulphasalazine .
	manualset3
83163	3	397849	14	13	NULL	NULL	NULL	sulphasalazine	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generalized morphea and lichen sclerosus et atrophicus successfully treated with sulphasalazine .
	manualset3
83164	1	397850	14	13	NULL	NULL	NULL	fetus	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generally , in the fetus , FcR expression was lower than in the adult while in the neonate it approached values found later in life .
	manualset3
83165	2	397850	14	13	NULL	NULL	NULL	FcR expression	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generally , in the fetus , FcR expression was lower than in the adult while in the neonate it approached values found later in life .
	manualset3
83166	3	397850	14	13	NULL	NULL	NULL	adult	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generally , in the fetus , FcR expression was lower than in the adult while in the neonate it approached values found later in life .
	manualset3
83167	4	397850	14	13	NULL	NULL	NULL	neonate	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generally , in the fetus , FcR expression was lower than in the adult while in the neonate it approached values found later in life .
	manualset3
83168	5	397850	14	13	NULL	0	NULL	approached values	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Generally , in the fetus , FcR expression was lower than in the adult while in the neonate it approached values found later in life .
	manualset3
83169	6	397850	14	13	NULL	0	NULL	found later in life	TimePoint												NULL		0	NULL	NULL	NULL	NULL	NULL	Generally , in the fetus , FcR expression was lower than in the adult while in the neonate it approached values found later in life .
	manualset3
83176	1	397851	14	13	NULL	NULL	NULL	retrogenes	Gene												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generally , retrogenes emerge `` out of the testis , '' because they are often initially transcribed in testis and later evolve stronger and sometimes more diverse spatial expression patterns .
	manualset3
83177	2	397851	14	13	NULL	0	NULL	 out of the testis	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Generally , retrogenes emerge `` out of the testis , '' because they are often initially transcribed in testis and later evolve stronger and sometimes more diverse spatial expression patterns .
	manualset3
83179	3	397851	14	13	NULL	NULL	NULL	testis	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generally , retrogenes emerge `` out of the testis , '' because they are often initially transcribed in testis and later evolve stronger and sometimes more diverse spatial expression patterns .
	manualset3
83181	4	397851	14	13	NULL	NULL	NULL	sometimes more diverse spatial expression patterns	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generally , retrogenes emerge `` out of the testis , '' because they are often initially transcribed in testis and later evolve stronger and sometimes more diverse spatial expression patterns .
	manualset3
83182	1	397852	14	13	NULL	0	NULL	time delay	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Generally speaking , time delay is a prevailing phenomenon in aquatic environments , since the production of allelopathic substance by competitive species is not instantaneous , but mediated by some time lag required for maturity of species .
	manualset3
83183	2	397852	14	13	NULL	0	NULL	aquatic environments	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Generally speaking , time delay is a prevailing phenomenon in aquatic environments , since the production of allelopathic substance by competitive species is not instantaneous , but mediated by some time lag required for maturity of species .
	manualset3
83184	3	397852	14	13	NULL	0	NULL	production of allelopathic substance 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Generally speaking , time delay is a prevailing phenomenon in aquatic environments , since the production of allelopathic substance by competitive species is not instantaneous , but mediated by some time lag required for maturity of species .
	manualset3
83185	4	397852	14	13	NULL	0	NULL	competitive species	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Generally speaking , time delay is a prevailing phenomenon in aquatic environments , since the production of allelopathic substance by competitive species is not instantaneous , but mediated by some time lag required for maturity of species .
	manualset3
83186	5	397852	14	13	NULL	0	NULL	some time lag 	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Generally speaking , time delay is a prevailing phenomenon in aquatic environments , since the production of allelopathic substance by competitive species is not instantaneous , but mediated by some time lag required for maturity of species .
	manualset3
83187	6	397852	14	13	NULL	0	NULL	maturity of species 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Generally speaking , time delay is a prevailing phenomenon in aquatic environments , since the production of allelopathic substance by competitive species is not instantaneous , but mediated by some time lag required for maturity of species .
	manualset3
83188	1	397853	14	13	NULL	NULL	NULL	total plate counts	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generally speaking , total plate counts and lactic acid bacteria counts of all treatments slightly increased , with CHL being the lowest .
	manualset3
83189	2	397853	14	13	NULL	NULL	NULL	lactic acid bacteria counts	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generally speaking , total plate counts and lactic acid bacteria counts of all treatments slightly increased , with CHL being the lowest .
	manualset3
83191	4	397853	14	13	NULL	0	NULL	CHL	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Generally speaking , total plate counts and lactic acid bacteria counts of all treatments slightly increased , with CHL being the lowest .
	manualset3
83192	3	397853	14	13	NULL	0	NULL	treatments	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Generally speaking , total plate counts and lactic acid bacteria counts of all treatments slightly increased , with CHL being the lowest .
	manualset3
83193	1	397854	14	13	NULL	0	NULL	Generation in vitro	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Generation in vitro of alloreactive lymphocytes is suppressed by the addition of spleen cells from mice infected with lymphocytic choriomeningitis virus .
	manualset3
83194	2	397854	14	13	NULL	0	NULL	alloreactive lymphocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Generation in vitro of alloreactive lymphocytes is suppressed by the addition of spleen cells from mice infected with lymphocytic choriomeningitis virus .
	manualset3
83196	3	397854	14	13	NULL	NULL	NULL	spleen cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generation in vitro of alloreactive lymphocytes is suppressed by the addition of spleen cells from mice infected with lymphocytic choriomeningitis virus .
	manualset3
83197	4	397854	14	13	NULL	NULL	NULL	mice infected 	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generation in vitro of alloreactive lymphocytes is suppressed by the addition of spleen cells from mice infected with lymphocytic choriomeningitis virus .
	manualset3
83199	5	397854	14	13	NULL	NULL	NULL	lymphocytic choriomeningitis virus	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generation in vitro of alloreactive lymphocytes is suppressed by the addition of spleen cells from mice infected with lymphocytic choriomeningitis virus .
	manualset3
83200	1	397855	14	13	NULL	0	NULL	Generation of CTL	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Generation of CTL was accelerated in animals that had been previously primed in vivo by skin grafting .
	manualset3
83201	2	397855	14	13	NULL	0	NULL	animals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Generation of CTL was accelerated in animals that had been previously primed in vivo by skin grafting .
	manualset3
83203	3	397855	14	13	NULL	NULL	NULL	skin grafting	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generation of CTL was accelerated in animals that had been previously primed in vivo by skin grafting .
	manualset3
83204	1	397856	14	13	NULL	0	NULL	Silicone elastomer prosthesis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Silicone elastomer prosthesis of the common bile duct .
	manualset3
83205	2	397856	14	13	NULL	0	NULL	common bile duct	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( Silicone elastomer prosthesis of the common bile duct .
	manualset3
83206	1	397857	14	13	NULL	NULL	NULL	genetic engineering	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generation of genetic engineering monoclonal antibodies against prion protein .
	manualset3
83207	2	397857	14	13	NULL	NULL	NULL	monoclonal antibodies	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generation of genetic engineering monoclonal antibodies against prion protein .
	manualset3
83208	3	397857	14	13	NULL	0	NULL	prion protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Generation of genetic engineering monoclonal antibodies against prion protein .
	manualset3
83234	4	397857	14	13	NULL	0	NULL	Generation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Generation of genetic engineering monoclonal antibodies against prion protein .
	manualset3
83209	1	397858	14	13	NULL	NULL	NULL	new neurons	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generation of new neurons is of particular interest because of the potential to treat diseases of the nervous system , such as neurodegenerative disorders and spinal cord injuries , with cell replacement therapy .
	manualset3
83210	2	397858	14	13	NULL	0	NULL	nervous system	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Generation of new neurons is of particular interest because of the potential to treat diseases of the nervous system , such as neurodegenerative disorders and spinal cord injuries , with cell replacement therapy .
	manualset3
83211	3	397858	14	13	NULL	NULL	NULL	neurodegenerative disorders	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generation of new neurons is of particular interest because of the potential to treat diseases of the nervous system , such as neurodegenerative disorders and spinal cord injuries , with cell replacement therapy .
	manualset3
83212	4	397858	14	13	NULL	0	NULL	potential to treat diseases	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Generation of new neurons is of particular interest because of the potential to treat diseases of the nervous system , such as neurodegenerative disorders and spinal cord injuries , with cell replacement therapy .
	manualset3
83213	5	397858	14	13	NULL	0	NULL	spinal cord injuries	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Generation of new neurons is of particular interest because of the potential to treat diseases of the nervous system , such as neurodegenerative disorders and spinal cord injuries , with cell replacement therapy .
	manualset3
83214	6	397858	14	13	NULL	0	NULL	cell replacement therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Generation of new neurons is of particular interest because of the potential to treat diseases of the nervous system , such as neurodegenerative disorders and spinal cord injuries , with cell replacement therapy .
	manualset3
83235	7	397858	14	13	NULL	0	NULL	Generation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Generation of new neurons is of particular interest because of the potential to treat diseases of the nervous system , such as neurodegenerative disorders and spinal cord injuries , with cell replacement therapy .
	manualset3
83215	1	397859	14	13	NULL	NULL	NULL	Generation	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generation of replication-competent and - defective HSV vectors .
	manualset3
83216	2	397859	14	13	NULL	0	NULL	replication-competent and - defective HSV vectors	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Generation of replication-competent and - defective HSV vectors .
	manualset3
83217	1	397860	14	13	NULL	NULL	NULL	Mitonyssoides stercoralis	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generic and specific synonymy of Mitonyssoides stercoralis Yunker , Lukoschus , and Giesen , 1990 with Coprolactistus whitakeri Radovsky and Krantz , 1998 ( Acari : Mesostigmata : Macronyssidae ) .
	manualset3
83218	2	397860	14	13	NULL	0	NULL	Yunker	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Generic and specific synonymy of Mitonyssoides stercoralis Yunker , Lukoschus , and Giesen , 1990 with Coprolactistus whitakeri Radovsky and Krantz , 1998 ( Acari : Mesostigmata : Macronyssidae ) .
	manualset3
83219	3	397860	14	13	NULL	0	NULL	Lukoschus	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Generic and specific synonymy of Mitonyssoides stercoralis Yunker , Lukoschus , and Giesen , 1990 with Coprolactistus whitakeri Radovsky and Krantz , 1998 ( Acari : Mesostigmata : Macronyssidae ) .
	manualset3
83220	4	397860	14	13	NULL	0	NULL	Giesen	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Generic and specific synonymy of Mitonyssoides stercoralis Yunker , Lukoschus , and Giesen , 1990 with Coprolactistus whitakeri Radovsky and Krantz , 1998 ( Acari : Mesostigmata : Macronyssidae ) .
	manualset3
83221	5	397860	14	13	NULL	0	NULL	1990	TimePoint												NULL		0	NULL	NULL	NULL	NULL	NULL	Generic and specific synonymy of Mitonyssoides stercoralis Yunker , Lukoschus , and Giesen , 1990 with Coprolactistus whitakeri Radovsky and Krantz , 1998 ( Acari : Mesostigmata : Macronyssidae ) .
	manualset3
83222	6	397860	14	13	NULL	0	NULL	Coprolactistus whitakeri	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Generic and specific synonymy of Mitonyssoides stercoralis Yunker , Lukoschus , and Giesen , 1990 with Coprolactistus whitakeri Radovsky and Krantz , 1998 ( Acari : Mesostigmata : Macronyssidae ) .
	manualset3
83223	7	397860	14	13	NULL	0	NULL	Radovsky	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Generic and specific synonymy of Mitonyssoides stercoralis Yunker , Lukoschus , and Giesen , 1990 with Coprolactistus whitakeri Radovsky and Krantz , 1998 ( Acari : Mesostigmata : Macronyssidae ) .
	manualset3
83224	8	397860	14	13	NULL	0	NULL	Krantz	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Generic and specific synonymy of Mitonyssoides stercoralis Yunker , Lukoschus , and Giesen , 1990 with Coprolactistus whitakeri Radovsky and Krantz , 1998 ( Acari : Mesostigmata : Macronyssidae ) .
	manualset3
83225	9	397860	14	13	NULL	0	NULL	1998 	TimePoint												NULL		0	NULL	NULL	NULL	NULL	NULL	Generic and specific synonymy of Mitonyssoides stercoralis Yunker , Lukoschus , and Giesen , 1990 with Coprolactistus whitakeri Radovsky and Krantz , 1998 ( Acari : Mesostigmata : Macronyssidae ) .
	manualset3
83226	10	397860	14	13	NULL	NULL	NULL	Acari : Mesostigmata : Macronyssidae	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Generic and specific synonymy of Mitonyssoides stercoralis Yunker , Lukoschus , and Giesen , 1990 with Coprolactistus whitakeri Radovsky and Krantz , 1998 ( Acari : Mesostigmata : Macronyssidae ) .
	manualset3
83236	1	397861	14	13	NULL	0	NULL	Genes	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Genes and development : molecular and logical themes .
	manualset3
83237	2	397861	14	13	NULL	0	NULL	development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Genes and development : molecular and logical themes .
	manualset3
83238	3	397861	14	13	NULL	NULL	NULL	molecular and logical themes	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genes and development : molecular and logical themes .
	manualset3
83243	1	397863	14	13	NULL	0	NULL	Genes 	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Genes encoding other potential virulence factors ( ace , efaA ( fs ) , ccf and cpd ) were frequently detected .
	manualset3
83244	2	397863	14	13	NULL	0	NULL	potential virulence factors	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Genes encoding other potential virulence factors ( ace , efaA ( fs ) , ccf and cpd ) were frequently detected .
	manualset3
83245	3	397863	14	13	NULL	0	NULL	ace	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Genes encoding other potential virulence factors ( ace , efaA ( fs ) , ccf and cpd ) were frequently detected .
	manualset3
83246	4	397863	14	13	NULL	0	NULL	efaA ( fs )	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Genes encoding other potential virulence factors ( ace , efaA ( fs ) , ccf and cpd ) were frequently detected .
	manualset3
83247	5	397863	14	13	NULL	0	NULL	ccf	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Genes encoding other potential virulence factors ( ace , efaA ( fs ) , ccf and cpd ) were frequently detected .
	manualset3
83248	6	397863	14	13	NULL	0	NULL	cpd 	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Genes encoding other potential virulence factors ( ace , efaA ( fs ) , ccf and cpd ) were frequently detected .
	manualset3
83249	1	397864	14	13	NULL	0	NULL	Genes 	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Genes for the pathways involved in biological nitrogen fixation ( the nif gene cluster ) , nod genes including nodABC , and genes for the type III protein secretion system ( T3SS ) are present .
	manualset3
83250	2	397864	14	13	NULL	0	NULL	pathways 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Genes for the pathways involved in biological nitrogen fixation ( the nif gene cluster ) , nod genes including nodABC , and genes for the type III protein secretion system ( T3SS ) are present .
	manualset3
83251	3	397864	14	13	NULL	0	NULL	biological nitrogen fixation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Genes for the pathways involved in biological nitrogen fixation ( the nif gene cluster ) , nod genes including nodABC , and genes for the type III protein secretion system ( T3SS ) are present .
	manualset3
83252	4	397864	14	13	NULL	0	NULL	nif gene cluster	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Genes for the pathways involved in biological nitrogen fixation ( the nif gene cluster ) , nod genes including nodABC , and genes for the type III protein secretion system ( T3SS ) are present .
	manualset3
83253	5	397864	14	13	NULL	0	NULL	nod genes	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Genes for the pathways involved in biological nitrogen fixation ( the nif gene cluster ) , nod genes including nodABC , and genes for the type III protein secretion system ( T3SS ) are present .
	manualset3
83254	6	397864	14	13	NULL	0	NULL	nodABC	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Genes for the pathways involved in biological nitrogen fixation ( the nif gene cluster ) , nod genes including nodABC , and genes for the type III protein secretion system ( T3SS ) are present .
	manualset3
83255	7	397864	14	13	NULL	0	NULL	genes for the type III protein secretion system ( T3SS )	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Genes for the pathways involved in biological nitrogen fixation ( the nif gene cluster ) , nod genes including nodABC , and genes for the type III protein secretion system ( T3SS ) are present .
	manualset3
83256	1	397865	14	13	NULL	NULL	NULL	Genetic components	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic , spatial , and temporal components of precise spawning synchrony in reef building corals of the Montastraea annularis species complex .
	manualset3
83257	2	397865	14	13	NULL	NULL	NULL	spatial components	GeographicalLocation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic , spatial , and temporal components of precise spawning synchrony in reef building corals of the Montastraea annularis species complex .
	manualset3
83258	3	397865	14	13	NULL	NULL	NULL	temporal components	Time												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic , spatial , and temporal components of precise spawning synchrony in reef building corals of the Montastraea annularis species complex .
	manualset3
83259	4	397865	14	13	NULL	0	NULL	precise spawning synchrony	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic , spatial , and temporal components of precise spawning synchrony in reef building corals of the Montastraea annularis species complex .
	manualset3
83260	5	397865	14	13	NULL	0	NULL	reef building corals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic , spatial , and temporal components of precise spawning synchrony in reef building corals of the Montastraea annularis species complex .
	manualset3
83261	6	397865	14	13	NULL	0	NULL	Montastraea annularis species complex	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic , spatial , and temporal components of precise spawning synchrony in reef building corals of the Montastraea annularis species complex .
	manualset3
83262	1	397866	14	13	NULL	NULL	NULL	five active constitutents	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Simultaneous determination of five active constitutents in Xiaochaihu Tang by HPLC ) .
	manualset3
83263	2	397866	14	13	NULL	0	NULL	Xiaochaihu Tang 	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	( Simultaneous determination of five active constitutents in Xiaochaihu Tang by HPLC ) .
	manualset3
83264	3	397866	14	13	NULL	0	NULL	HPLC	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Simultaneous determination of five active constitutents in Xiaochaihu Tang by HPLC ) .
	manualset3
83481	4	397866	14	13	NULL	0	NULL	 Simultaneous determination	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Simultaneous determination of five active constitutents in Xiaochaihu Tang by HPLC ) .
	manualset3
83265	1	397867	14	13	NULL	0	NULL	Genetic ablation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic ablation of serum opacity factor ( SOF ) , a virulence determinant of S. pyogenes , reduced binding by approximately 50 % , and a recombinant peptide of SOF inhibited binding of fibulin-1 to streptococci by approximately 45 % .
	manualset3
83266	2	397867	14	13	NULL	0	NULL	serum opacity factor ( SOF )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic ablation of serum opacity factor ( SOF ) , a virulence determinant of S. pyogenes , reduced binding by approximately 50 % , and a recombinant peptide of SOF inhibited binding of fibulin-1 to streptococci by approximately 45 % .
	manualset3
83267	3	397867	14	13	NULL	NULL	NULL	a virulence determinant	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic ablation of serum opacity factor ( SOF ) , a virulence determinant of S. pyogenes , reduced binding by approximately 50 % , and a recombinant peptide of SOF inhibited binding of fibulin-1 to streptococci by approximately 45 % .
	manualset3
83268	4	397867	14	13	NULL	0	NULL	S. pyogenes	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic ablation of serum opacity factor ( SOF ) , a virulence determinant of S. pyogenes , reduced binding by approximately 50 % , and a recombinant peptide of SOF inhibited binding of fibulin-1 to streptococci by approximately 45 % .
	manualset3
83270	5	397867	14	13	NULL	NULL	NULL	approximately 50 %	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic ablation of serum opacity factor ( SOF ) , a virulence determinant of S. pyogenes , reduced binding by approximately 50 % , and a recombinant peptide of SOF inhibited binding of fibulin-1 to streptococci by approximately 45 % .
	manualset3
83271	6	397867	14	13	NULL	NULL	NULL	recombinant peptide	AminoAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic ablation of serum opacity factor ( SOF ) , a virulence determinant of S. pyogenes , reduced binding by approximately 50 % , and a recombinant peptide of SOF inhibited binding of fibulin-1 to streptococci by approximately 45 % .
	manualset3
83272	7	397867	14	13	NULL	NULL	NULL	 SOF	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic ablation of serum opacity factor ( SOF ) , a virulence determinant of S. pyogenes , reduced binding by approximately 50 % , and a recombinant peptide of SOF inhibited binding of fibulin-1 to streptococci by approximately 45 % .
	manualset3
83274	8	397867	14	13	NULL	NULL	NULL	fibulin-1	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic ablation of serum opacity factor ( SOF ) , a virulence determinant of S. pyogenes , reduced binding by approximately 50 % , and a recombinant peptide of SOF inhibited binding of fibulin-1 to streptococci by approximately 45 % .
	manualset3
83275	9	397867	14	13	NULL	NULL	NULL	streptococci 	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic ablation of serum opacity factor ( SOF ) , a virulence determinant of S. pyogenes , reduced binding by approximately 50 % , and a recombinant peptide of SOF inhibited binding of fibulin-1 to streptococci by approximately 45 % .
	manualset3
83276	10	397867	14	13	NULL	NULL	NULL	approximately 45 % 	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic ablation of serum opacity factor ( SOF ) , a virulence determinant of S. pyogenes , reduced binding by approximately 50 % , and a recombinant peptide of SOF inhibited binding of fibulin-1 to streptococci by approximately 45 % .
	manualset3
83277	1	397868	14	13	NULL	NULL	NULL	Genetic algorithm interval partial least squares regression 	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic algorithm interval partial least squares regression combined successive projections algorithm for variable selection in near-infrared quantitative analysis of pigment in cucumber leaves .
	manualset3
83278	2	397868	14	13	NULL	NULL	NULL	successive projections algorithm	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic algorithm interval partial least squares regression combined successive projections algorithm for variable selection in near-infrared quantitative analysis of pigment in cucumber leaves .
	manualset3
83279	3	397868	14	13	NULL	0	NULL	variable selection	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic algorithm interval partial least squares regression combined successive projections algorithm for variable selection in near-infrared quantitative analysis of pigment in cucumber leaves .
	manualset3
83280	4	397868	14	13	NULL	NULL	NULL	near-infrared quantitative analysis	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic algorithm interval partial least squares regression combined successive projections algorithm for variable selection in near-infrared quantitative analysis of pigment in cucumber leaves .
	manualset3
83281	5	397868	14	13	NULL	0	NULL	pigment in cucumber leaves	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic algorithm interval partial least squares regression combined successive projections algorithm for variable selection in near-infrared quantitative analysis of pigment in cucumber leaves .
	manualset3
83282	1	397869	14	13	NULL	NULL	NULL	Genetic alterations	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic alterations in chromosome 10q24 .3 and glutathione S-transferase omega 2 gene polymorphism in ovarian cancer .
	manualset3
83283	2	397869	14	13	NULL	0	NULL	chromosome 10q24 .3	Chromosome												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic alterations in chromosome 10q24 .3 and glutathione S-transferase omega 2 gene polymorphism in ovarian cancer .
	manualset3
83285	3	397869	14	13	NULL	NULL	NULL	glutathione S-transferase omega 2 gene polymorphism	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic alterations in chromosome 10q24 .3 and glutathione S-transferase omega 2 gene polymorphism in ovarian cancer .
	manualset3
83286	4	397869	14	13	NULL	NULL	NULL	ovarian cancer	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic alterations in chromosome 10q24 .3 and glutathione S-transferase omega 2 gene polymorphism in ovarian cancer .
	manualset3
83287	1	397870	14	13	NULL	0	NULL	Genetic alterations	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic alterations in chronic ulcerative colitis-associated adenoma-like DALMs are similar to non-colitic sporadic adenomas .
	manualset3
83288	2	397870	14	13	NULL	0	NULL	chronic ulcerative colitis-associated adenoma-like DALMs	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic alterations in chronic ulcerative colitis-associated adenoma-like DALMs are similar to non-colitic sporadic adenomas .
	manualset3
83289	3	397870	14	13	NULL	0	NULL	non-colitic sporadic adenomas	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic alterations in chronic ulcerative colitis-associated adenoma-like DALMs are similar to non-colitic sporadic adenomas .
	manualset3
83489	1	397871	14	13	NULL	0	NULL	Genetic analyses	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analyses in asthma : current concepts and future directions .
	manualset3
83490	2	397871	14	13	NULL	0	NULL	asthma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analyses in asthma : current concepts and future directions .
	manualset3
83491	3	397871	14	13	NULL	0	NULL	current concepts	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analyses in asthma : current concepts and future directions .
	manualset3
83493	4	397871	14	13	NULL	0	NULL	future directions	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analyses in asthma : current concepts and future directions .
	manualset3
83501	1	397872	14	13	NULL	0	NULL	Genetic analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analysis in mice identifies cysteamine as a novel partner for artemisinin in the treatment of malaria .
	manualset3
83502	2	397872	14	13	NULL	0	NULL	 mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analysis in mice identifies cysteamine as a novel partner for artemisinin in the treatment of malaria .
	manualset3
83504	3	397872	14	13	NULL	0	NULL	 cysteamine	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analysis in mice identifies cysteamine as a novel partner for artemisinin in the treatment of malaria .
	manualset3
83507	4	397872	14	13	NULL	0	NULL	artemisinin	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analysis in mice identifies cysteamine as a novel partner for artemisinin in the treatment of malaria .
	manualset3
83510	5	397872	14	13	NULL	NULL	NULL	malaria	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic analysis in mice identifies cysteamine as a novel partner for artemisinin in the treatment of malaria .
	manualset3
83600	6	397872	14	13	NULL	0	NULL	treatment 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analysis in mice identifies cysteamine as a novel partner for artemisinin in the treatment of malaria .
	manualset3
83512	1	397873	14	13	NULL	0	NULL	Genetic analysis 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analysis indicated that the cfiA gene was present in some but not all of the isolates with high MICs to the carbapenems .
	manualset3
83513	2	397873	14	13	NULL	0	NULL	cfiA gene 	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analysis indicated that the cfiA gene was present in some but not all of the isolates with high MICs to the carbapenems .
	manualset3
83523	3	397873	14	13	NULL	0	NULL	isolates	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analysis indicated that the cfiA gene was present in some but not all of the isolates with high MICs to the carbapenems .
	manualset3
83525	4	397873	14	13	NULL	NULL	NULL	high MICs	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic analysis indicated that the cfiA gene was present in some but not all of the isolates with high MICs to the carbapenems .
	manualset3
83527	5	397873	14	13	NULL	0	NULL	carbapenems 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analysis indicated that the cfiA gene was present in some but not all of the isolates with high MICs to the carbapenems .
	manualset3
83536	1	397874	14	13	NULL	0	NULL	Genetic analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analysis of the additional sex combs locus of Drosophila melanogaster .
	manualset3
83546	2	397874	14	13	NULL	NULL	NULL	additional sex combs locus	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic analysis of the additional sex combs locus of Drosophila melanogaster .
	manualset3
83547	3	397874	14	13	NULL	0	NULL	Drosophila melanogaster	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analysis of the additional sex combs locus of Drosophila melanogaster .
	manualset3
83551	1	397875	14	13	NULL	0	NULL	Genetic analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analysis of turbot pathogenic Streptococcus parauberis strains by ribotyping and random amplified polymorphic DNA .
	manualset3
83555	1	397875	14	13	NULL	0	NULL	turbot pathogenic Streptococcus parauberis strains	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analysis of turbot pathogenic Streptococcus parauberis strains by ribotyping and random amplified polymorphic DNA .
	manualset3
83556	3	397875	14	13	NULL	0	NULL	ribotyping	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analysis of turbot pathogenic Streptococcus parauberis strains by ribotyping and random amplified polymorphic DNA .
	manualset3
83558	4	397875	14	13	NULL	0	NULL	random amplified polymorphic DNA 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analysis of turbot pathogenic Streptococcus parauberis strains by ribotyping and random amplified polymorphic DNA .
	manualset3
83561	1	397876	14	13	NULL	0	NULL	Genetic analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analysis that reveals a monoclonal T-cell population is also relevant .
	manualset3
83564	2	397876	14	13	NULL	0	NULL	monoclonal T-cell population 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic analysis that reveals a monoclonal T-cell population is also relevant .
	manualset3
83569	1	397877	14	13	NULL	0	NULL	Simultaneous occurrence	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Simultaneous occurrence of excessive myopic fundus changes , cataract , corneal opacity and elastoma diffusum Dubreuilh ) .
	manualset3
83572	2	397877	14	13	NULL	NULL	NULL	excessive myopic fundus changes 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Simultaneous occurrence of excessive myopic fundus changes , cataract , corneal opacity and elastoma diffusum Dubreuilh ) .
	manualset3
83574	3	397877	14	13	NULL	0	NULL	cataract	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Simultaneous occurrence of excessive myopic fundus changes , cataract , corneal opacity and elastoma diffusum Dubreuilh ) .
	manualset3
83577	4	397877	14	13	NULL	NULL	NULL	corneal opacity	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Simultaneous occurrence of excessive myopic fundus changes , cataract , corneal opacity and elastoma diffusum Dubreuilh ) .
	manualset3
83578	5	397877	14	13	NULL	0	NULL	elastoma diffusum	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Simultaneous occurrence of excessive myopic fundus changes , cataract , corneal opacity and elastoma diffusum Dubreuilh ) .
	manualset3
83579	6	397877	14	13	NULL	0	NULL	Dubreuilh 	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	( Simultaneous occurrence of excessive myopic fundus changes , cataract , corneal opacity and elastoma diffusum Dubreuilh ) .
	manualset3
83582	3	397878	14	13	NULL	0	NULL	thymidine-dependent mutants of pneumococcus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic and biochemical properties of thymidine-dependent mutants of pneumococcus .
	manualset3
83583	1	397879	14	13	NULL	0	NULL	Genetic study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic and functional study of the IPO5 gene in schizophrenia .
	manualset3
83584	2	397879	14	13	NULL	0	NULL	functional study 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic and functional study of the IPO5 gene in schizophrenia .
	manualset3
83585	3	397879	14	13	NULL	0	NULL	 IPO5 gene	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic and functional study of the IPO5 gene in schizophrenia .
	manualset3
83586	4	397879	14	13	NULL	0	NULL	schizophrenia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic and functional study of the IPO5 gene in schizophrenia .
	manualset3
83589	1	397880	14	13	NULL	0	NULL	Genetic studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic and molecular genetic studies in the diagnosis of myeloid diseases .
	manualset3
83590	2	397880	14	13	NULL	NULL	NULL	molecular genetic studies	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic and molecular genetic studies in the diagnosis of myeloid diseases .
	manualset3
83592	3	397880	14	13	NULL	0	NULL	diagnosis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic and molecular genetic studies in the diagnosis of myeloid diseases .
	manualset3
83593	4	397880	14	13	NULL	0	NULL	myeloid diseases	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic and molecular genetic studies in the diagnosis of myeloid diseases .
	manualset3
83994	1	397881	14	13	NULL	0	NULL	Genetic animal models	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic animal models : focus on schizophrenia .
	manualset3
83995	2	397881	14	13	NULL	0	NULL	schizophrenia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic animal models : focus on schizophrenia .
	manualset3
83996	1	397882	14	13	NULL	0	NULL	Genetic characterisation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic characterisation of six Sarcocystis species from reindeer ( Rangifer tarandus tarandus ) in Norway based on the small subunit rRNA gene .
	manualset3
83997	2	397882	14	13	NULL	0	NULL	six	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic characterisation of six Sarcocystis species from reindeer ( Rangifer tarandus tarandus ) in Norway based on the small subunit rRNA gene .
	manualset3
83998	3	397882	14	13	NULL	0	NULL	Sarcocystis species 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic characterisation of six Sarcocystis species from reindeer ( Rangifer tarandus tarandus ) in Norway based on the small subunit rRNA gene .
	manualset3
83999	4	397882	14	13	NULL	0	NULL	reindeer ( Rangifer tarandus tarandus )	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic characterisation of six Sarcocystis species from reindeer ( Rangifer tarandus tarandus ) in Norway based on the small subunit rRNA gene .
	manualset3
84000	5	397882	14	13	NULL	0	NULL	Norway	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic characterisation of six Sarcocystis species from reindeer ( Rangifer tarandus tarandus ) in Norway based on the small subunit rRNA gene .
	manualset3
84001	6	397882	14	13	NULL	0	NULL	small subunit rRNA gene	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic characterisation of six Sarcocystis species from reindeer ( Rangifer tarandus tarandus ) in Norway based on the small subunit rRNA gene .
	manualset3
84002	1	397883	14	13	NULL	0	NULL	Genetic characterization	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic characterization of equine arteritis virus during persistent infection of stallions .
	manualset3
84003	2	397883	14	13	NULL	0	NULL	equine arteritis virus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic characterization of equine arteritis virus during persistent infection of stallions .
	manualset3
84004	3	397883	14	13	NULL	0	NULL	persistent infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic characterization of equine arteritis virus during persistent infection of stallions .
	manualset3
84005	4	397883	14	13	NULL	0	NULL	stallions	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic characterization of equine arteritis virus during persistent infection of stallions .
	manualset3
84006	1	397884	14	13	NULL	0	NULL	Genetic data	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic data suggest that Stp1 acts either at , or above , the level of Ras2 , possibly on the Ira proteins .
	manualset3
84007	2	397884	14	13	NULL	NULL	NULL	 Stp1	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic data suggest that Stp1 acts either at , or above , the level of Ras2 , possibly on the Ira proteins .
	manualset3
84008	3	397884	14	13	NULL	NULL	NULL	Ras2 	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic data suggest that Stp1 acts either at , or above , the level of Ras2 , possibly on the Ira proteins .
	manualset3
84009	3	397884	14	13	NULL	0	NULL	Ira proteins 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic data suggest that Stp1 acts either at , or above , the level of Ras2 , possibly on the Ira proteins .
	manualset3
84010	1	397885	14	13	NULL	0	NULL	Single-dose 	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	( Single-dose and high-volume Bretschneider cardioplegic solution for congenital heart surgery ) .
	manualset3
84011	2	397885	14	13	NULL	0	NULL	high-volume 	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	( Single-dose and high-volume Bretschneider cardioplegic solution for congenital heart surgery ) .
	manualset3
84012	3	397885	14	13	NULL	0	NULL	Bretschneider cardioplegic solution	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( Single-dose and high-volume Bretschneider cardioplegic solution for congenital heart surgery ) .
	manualset3
84013	4	397885	14	13	NULL	0	NULL	congenital heart surgery 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Single-dose and high-volume Bretschneider cardioplegic solution for congenital heart surgery ) .
	manualset3
84014	1	397886	14	13	NULL	NULL	NULL	Genetic differentiation 	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic differentiation was highest between BC and the South Cascades , and intermediate between BC and the North Cascades .
	manualset3
84015	2	397886	14	13	NULL	NULL	NULL	BC	ProperNamedGeographicalLocation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic differentiation was highest between BC and the South Cascades , and intermediate between BC and the North Cascades .
	manualset3
84016	3	397886	14	13	NULL	0	NULL	South Cascades	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic differentiation was highest between BC and the South Cascades , and intermediate between BC and the North Cascades .
	manualset3
84017	4	397886	14	13	NULL	0	NULL	BC	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic differentiation was highest between BC and the South Cascades , and intermediate between BC and the North Cascades .
	manualset3
84018	5	397886	14	13	NULL	0	NULL	North Cascades	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic differentiation was highest between BC and the South Cascades , and intermediate between BC and the North Cascades .
	manualset3
84019	1	397887	14	13	NULL	0	NULL	Genetic diversity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic diversity and population structure of Salvia miltiorrhiza Bge in China revealed by ISSR and SRAP .
	manualset3
84021	3	397887	14	13	NULL	0	NULL	Salvia miltiorrhiza Bge	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic diversity and population structure of Salvia miltiorrhiza Bge in China revealed by ISSR and SRAP .
	manualset3
84022	4	397887	14	13	NULL	0	NULL	China	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic diversity and population structure of Salvia miltiorrhiza Bge in China revealed by ISSR and SRAP .
	manualset3
84023	5	397887	14	13	NULL	NULL	NULL	ISSR	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic diversity and population structure of Salvia miltiorrhiza Bge in China revealed by ISSR and SRAP .
	manualset3
84024	6	397887	14	13	NULL	0	NULL	SRAP	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic diversity and population structure of Salvia miltiorrhiza Bge in China revealed by ISSR and SRAP .
	manualset3
84025	1	397888	14	13	NULL	0	NULL	Genetic information	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic information and the life-span of laboratory animal models .
	manualset3
84026	2	397888	14	13	NULL	NULL	NULL	life-span	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic information and the life-span of laboratory animal models .
	manualset3
84027	3	397888	14	13	NULL	0	NULL	 laboratory animal models	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic information and the life-span of laboratory animal models .
	manualset3
84028	1	397889	14	13	NULL	0	NULL	Genetic inhibition	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic inhibition of NAD ( P ) H oxidase or administration of uric acid ( a peroxynitrite scavenger ) or N ( G ) - nitro-l-arginine methyl ester ( nonselective NO synthase inhibitor ) significantly attenuated Ang II-induced PA700 nitration , 26S proteasome activation , and reduction of GTP cyclohydrolase I and BH4 .
	manualset3
84029	2	397889	14	13	NULL	0	NULL	NAD ( P ) H oxidase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic inhibition of NAD ( P ) H oxidase or administration of uric acid ( a peroxynitrite scavenger ) or N ( G ) - nitro-l-arginine methyl ester ( nonselective NO synthase inhibitor ) significantly attenuated Ang II-induced PA700 nitration , 26S proteasome activation , and reduction of GTP cyclohydrolase I and BH4 .
	manualset3
84030	3	397889	14	13	NULL	0	NULL	administration	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic inhibition of NAD ( P ) H oxidase or administration of uric acid ( a peroxynitrite scavenger ) or N ( G ) - nitro-l-arginine methyl ester ( nonselective NO synthase inhibitor ) significantly attenuated Ang II-induced PA700 nitration , 26S proteasome activation , and reduction of GTP cyclohydrolase I and BH4 .
	manualset3
84031	4	397889	14	13	NULL	0	NULL	uric acid ( a peroxynitrite scavenger ) 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic inhibition of NAD ( P ) H oxidase or administration of uric acid ( a peroxynitrite scavenger ) or N ( G ) - nitro-l-arginine methyl ester ( nonselective NO synthase inhibitor ) significantly attenuated Ang II-induced PA700 nitration , 26S proteasome activation , and reduction of GTP cyclohydrolase I and BH4 .
	manualset3
84032	5	397889	14	13	NULL	0	NULL	N ( G ) - nitro-l-arginine methyl ester ( nonselective NO synthase inhibitor )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic inhibition of NAD ( P ) H oxidase or administration of uric acid ( a peroxynitrite scavenger ) or N ( G ) - nitro-l-arginine methyl ester ( nonselective NO synthase inhibitor ) significantly attenuated Ang II-induced PA700 nitration , 26S proteasome activation , and reduction of GTP cyclohydrolase I and BH4 .
	manualset3
84035	6	397889	14	13	NULL	NULL	NULL	Ang II-induced PA700 nitration	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic inhibition of NAD ( P ) H oxidase or administration of uric acid ( a peroxynitrite scavenger ) or N ( G ) - nitro-l-arginine methyl ester ( nonselective NO synthase inhibitor ) significantly attenuated Ang II-induced PA700 nitration , 26S proteasome activation , and reduction of GTP cyclohydrolase I and BH4 .
	manualset3
84036	7	397889	14	13	NULL	NULL	NULL	26S proteasome activation	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic inhibition of NAD ( P ) H oxidase or administration of uric acid ( a peroxynitrite scavenger ) or N ( G ) - nitro-l-arginine methyl ester ( nonselective NO synthase inhibitor ) significantly attenuated Ang II-induced PA700 nitration , 26S proteasome activation , and reduction of GTP cyclohydrolase I and BH4 .
	manualset3
84039	8	397889	14	13	NULL	NULL	NULL	reduction of GTP cyclohydrolase I and BH4	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic inhibition of NAD ( P ) H oxidase or administration of uric acid ( a peroxynitrite scavenger ) or N ( G ) - nitro-l-arginine methyl ester ( nonselective NO synthase inhibitor ) significantly attenuated Ang II-induced PA700 nitration , 26S proteasome activation , and reduction of GTP cyclohydrolase I and BH4 .
	manualset3
84041	1	397890	14	13	NULL	0	NULL	Genetic instability	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic instability and p53 mutations in metastatic foci of mouse urinary bladder carcinomas induced by N-butyl-N - ( 4-hydroxybutyl ) nitrosamine .
	manualset3
84042	2	397890	14	13	NULL	NULL	NULL	p53 mutations	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic instability and p53 mutations in metastatic foci of mouse urinary bladder carcinomas induced by N-butyl-N - ( 4-hydroxybutyl ) nitrosamine .
	manualset3
84044	4	397890	14	13	NULL	0	NULL	metastatic foci	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic instability and p53 mutations in metastatic foci of mouse urinary bladder carcinomas induced by N-butyl-N - ( 4-hydroxybutyl ) nitrosamine .
	manualset3
84045	5	397890	14	13	NULL	0	NULL	mouse	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic instability and p53 mutations in metastatic foci of mouse urinary bladder carcinomas induced by N-butyl-N - ( 4-hydroxybutyl ) nitrosamine .
	manualset3
84046	6	397890	14	13	NULL	0	NULL	urinary bladder carcinomas	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic instability and p53 mutations in metastatic foci of mouse urinary bladder carcinomas induced by N-butyl-N - ( 4-hydroxybutyl ) nitrosamine .
	manualset3
84047	7	397890	14	13	NULL	0	NULL	N-butyl-N - ( 4-hydroxybutyl ) nitrosamine 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic instability and p53 mutations in metastatic foci of mouse urinary bladder carcinomas induced by N-butyl-N - ( 4-hydroxybutyl ) nitrosamine .
	manualset3
84048	1	397891	14	13	NULL	0	NULL	Genetic instability	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic instability of microsatellite sequences in non-small cell lung cancers .
	manualset3
84049	2	397891	14	13	NULL	0	NULL	microsatellite sequences	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic instability of microsatellite sequences in non-small cell lung cancers .
	manualset3
84050	3	397891	14	13	NULL	0	NULL	non-small cell lung cancers	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic instability of microsatellite sequences in non-small cell lung cancers .
	manualset3
84051	1	397892	14	13	NULL	NULL	NULL	Genetic interactions 	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic interactions in the - adrenoceptor/G-protein signal transduction pathway and survival after coronary artery bypass grafting : a pilot study .
	manualset3
84052	2	397892	14	13	NULL	0	NULL	adrenoceptor/G-protein signal transduction pathway	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic interactions in the - adrenoceptor/G-protein signal transduction pathway and survival after coronary artery bypass grafting : a pilot study .
	manualset3
84053	3	397892	14	13	NULL	NULL	NULL	survival	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic interactions in the - adrenoceptor/G-protein signal transduction pathway and survival after coronary artery bypass grafting : a pilot study .
	manualset3
84054	4	397892	14	13	NULL	0	NULL	coronary artery bypass grafting 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic interactions in the - adrenoceptor/G-protein signal transduction pathway and survival after coronary artery bypass grafting : a pilot study .
	manualset3
84055	5	397892	14	13	NULL	0	NULL	pilot study 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic interactions in the - adrenoceptor/G-protein signal transduction pathway and survival after coronary artery bypass grafting : a pilot study .
	manualset3
84056	1	397893	14	13	NULL	NULL	NULL	Genetic polymorphims	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic polymorphims in promoter region of osteopontin gene may be a marker reflecting hepatitis activity in chronic hepatitis C patients .
	manualset3
84057	2	397893	14	13	NULL	0	NULL	promoter region	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic polymorphims in promoter region of osteopontin gene may be a marker reflecting hepatitis activity in chronic hepatitis C patients .
	manualset3
84058	3	397893	14	13	NULL	0	NULL	osteopontin gene	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic polymorphims in promoter region of osteopontin gene may be a marker reflecting hepatitis activity in chronic hepatitis C patients .
	manualset3
84059	4	397893	14	13	NULL	NULL	NULL	hepatitis activity	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic polymorphims in promoter region of osteopontin gene may be a marker reflecting hepatitis activity in chronic hepatitis C patients .
	manualset3
84060	5	397893	14	13	NULL	0	NULL	chronic hepatitis C	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic polymorphims in promoter region of osteopontin gene may be a marker reflecting hepatitis activity in chronic hepatitis C patients .
	manualset3
84061	6	397893	14	13	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic polymorphims in promoter region of osteopontin gene may be a marker reflecting hepatitis activity in chronic hepatitis C patients .
	manualset3
84062	1	397894	14	13	NULL	NULL	NULL	Genetic predisposition	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic predisposition to breast cancer : past , present , and future .
	manualset3
84063	2	397894	14	13	NULL	0	NULL	breast cancer	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic predisposition to breast cancer : past , present , and future .
	manualset3
84064	3	397894	14	13	NULL	0	NULL	past 	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic predisposition to breast cancer : past , present , and future .
	manualset3
84065	4	397894	14	13	NULL	0	NULL	present	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic predisposition to breast cancer : past , present , and future .
	manualset3
84066	5	397894	14	13	NULL	0	NULL	future	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic predisposition to breast cancer : past , present , and future .
	manualset3
84067	1	397895	14	13	NULL	0	NULL	Genetic restriction	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic restriction of HIV-1 pathogenesis to AIDS by promoter alleles of IL10 .
	manualset3
84069	3	397895	14	13	NULL	NULL	NULL	HIV-1 pathogenesis	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic restriction of HIV-1 pathogenesis to AIDS by promoter alleles of IL10 .
	manualset3
84070	4	397895	14	13	NULL	0	NULL	AIDS	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic restriction of HIV-1 pathogenesis to AIDS by promoter alleles of IL10 .
	manualset3
84071	5	397895	14	13	NULL	0	NULL	promoter alleles of IL10	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic restriction of HIV-1 pathogenesis to AIDS by promoter alleles of IL10 .
	manualset3
84072	1	397896	14	13	NULL	0	NULL	Genetic studies 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic studies on MTP mitogenicity revealed that 90 % of responder DBA/2J X nonresponder C3H/HeJ F1 hybrids had intermediate mitogenic activity .
	manualset3
84073	2	397896	14	13	NULL	NULL	NULL	MTP mitogenicity	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic studies on MTP mitogenicity revealed that 90 % of responder DBA/2J X nonresponder C3H/HeJ F1 hybrids had intermediate mitogenic activity .
	manualset3
84074	4	397896	14	13	NULL	NULL	NULL	90 %	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic studies on MTP mitogenicity revealed that 90 % of responder DBA/2J X nonresponder C3H/HeJ F1 hybrids had intermediate mitogenic activity .
	manualset3
84075	5	397896	14	13	NULL	NULL	NULL	responder DBA/2J X nonresponder C3H/HeJ F1 hybrids	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic studies on MTP mitogenicity revealed that 90 % of responder DBA/2J X nonresponder C3H/HeJ F1 hybrids had intermediate mitogenic activity .
	manualset3
84077	6	397896	14	13	NULL	NULL	NULL	mitogenic activity	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic studies on MTP mitogenicity revealed that 90 % of responder DBA/2J X nonresponder C3H/HeJ F1 hybrids had intermediate mitogenic activity .
	manualset3
84079	1	397897	14	13	NULL	0	NULL	Genetic variation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic variation in phosphorus ( P ) efficiency exists among wheat ( Triticum aestivum ) and barley ( Hordeum vulgare ) genotypes , but the underlying mechanisms for the variation remain elusive .
	manualset3
84080	1	397897	14	13	NULL	NULL	NULL	phosphorus ( P ) efficiency	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic variation in phosphorus ( P ) efficiency exists among wheat ( Triticum aestivum ) and barley ( Hordeum vulgare ) genotypes , but the underlying mechanisms for the variation remain elusive .
	manualset3
84081	3	397897	14	13	NULL	0	NULL	wheat ( Triticum aestivum ) 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic variation in phosphorus ( P ) efficiency exists among wheat ( Triticum aestivum ) and barley ( Hordeum vulgare ) genotypes , but the underlying mechanisms for the variation remain elusive .
	manualset3
84082	4	397897	14	13	NULL	0	NULL	barley ( Hordeum vulgare ) genotypes	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic variation in phosphorus ( P ) efficiency exists among wheat ( Triticum aestivum ) and barley ( Hordeum vulgare ) genotypes , but the underlying mechanisms for the variation remain elusive .
	manualset3
84083	5	397897	14	13	NULL	NULL	NULL	underlying mechanisms for the variation	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic variation in phosphorus ( P ) efficiency exists among wheat ( Triticum aestivum ) and barley ( Hordeum vulgare ) genotypes , but the underlying mechanisms for the variation remain elusive .
	manualset3
84084	1	397898	14	13	NULL	0	NULL	Genetic variation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic variation in the promoter of the lactase gene ( LCT ) is known to be associated with lactase production and is therefore a genetic determinant for either lactase deficiency or lactase persistence during adulthood .
	manualset3
84085	2	397898	14	13	NULL	0	NULL	 promoter of the lactase gene ( LCT )	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic variation in the promoter of the lactase gene ( LCT ) is known to be associated with lactase production and is therefore a genetic determinant for either lactase deficiency or lactase persistence during adulthood .
	manualset3
84086	3	397898	14	13	NULL	0	NULL	lactase production 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic variation in the promoter of the lactase gene ( LCT ) is known to be associated with lactase production and is therefore a genetic determinant for either lactase deficiency or lactase persistence during adulthood .
	manualset3
84087	4	397898	14	13	NULL	0	NULL	lactase deficiency	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic variation in the promoter of the lactase gene ( LCT ) is known to be associated with lactase production and is therefore a genetic determinant for either lactase deficiency or lactase persistence during adulthood .
	manualset3
84088	5	397898	14	13	NULL	0	NULL	lactase persistence 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetic variation in the promoter of the lactase gene ( LCT ) is known to be associated with lactase production and is therefore a genetic determinant for either lactase deficiency or lactase persistence during adulthood .
	manualset3
84100	6	397898	14	13	NULL	NULL	NULL	adulthood	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic variation in the promoter of the lactase gene ( LCT ) is known to be associated with lactase production and is therefore a genetic determinant for either lactase deficiency or lactase persistence during adulthood .
	manualset3
84101	7	397898	14	13	NULL	NULL	NULL	genetic determinant 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetic variation in the promoter of the lactase gene ( LCT ) is known to be associated with lactase production and is therefore a genetic determinant for either lactase deficiency or lactase persistence during adulthood .
	manualset3
84090	1	397899	14	13	NULL	NULL	NULL	Genetics of Parthenogenesis	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetics of Parthenogenesis in DROSOPHILA MELANOGASTER .
	manualset3
84091	2	397899	14	13	NULL	NULL	NULL	DROSOPHILA MELANOGASTER 	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetics of Parthenogenesis in DROSOPHILA MELANOGASTER .
	manualset3
84092	1	397900	14	13	NULL	NULL	NULL	Genetics	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetics of aryl hydrocarbon hydroxylase induction in mice : additive inheritance in crosses between C3H-HeJ and DBA-2J .
	manualset3
84093	2	397900	14	13	NULL	NULL	NULL	aryl hydrocarbon hydroxylase	Gene												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetics of aryl hydrocarbon hydroxylase induction in mice : additive inheritance in crosses between C3H-HeJ and DBA-2J .
	manualset3
84094	3	397900	14	13	NULL	NULL	NULL	induction	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genetics of aryl hydrocarbon hydroxylase induction in mice : additive inheritance in crosses between C3H-HeJ and DBA-2J .
	manualset3
84095	4	397900	14	13	NULL	0	NULL	mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetics of aryl hydrocarbon hydroxylase induction in mice : additive inheritance in crosses between C3H-HeJ and DBA-2J .
	manualset3
84096	5	397900	14	13	NULL	0	NULL	additive inheritance	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetics of aryl hydrocarbon hydroxylase induction in mice : additive inheritance in crosses between C3H-HeJ and DBA-2J .
	manualset3
84097	6	397900	14	13	NULL	0	NULL	crosses 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetics of aryl hydrocarbon hydroxylase induction in mice : additive inheritance in crosses between C3H-HeJ and DBA-2J .
	manualset3
84098	7	397900	14	13	NULL	0	NULL	C3H-HeJ	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetics of aryl hydrocarbon hydroxylase induction in mice : additive inheritance in crosses between C3H-HeJ and DBA-2J .
	manualset3
84099	8	397900	14	13	NULL	0	NULL	 DBA-2J	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genetics of aryl hydrocarbon hydroxylase induction in mice : additive inheritance in crosses between C3H-HeJ and DBA-2J .
	manualset3
84102	1	397901	14	13	NULL	0	NULL	Sinonasal mucosal melanoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Sinonasal mucosal melanoma ) .
	manualset3
84103	1	397902	14	13	NULL	NULL	NULL	Genistein	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genistein and C3 transferase toxin did not elevate the cellular cAMP levels .
	manualset3
84104	2	397902	14	13	NULL	0	NULL	C3 transferase toxin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Genistein and C3 transferase toxin did not elevate the cellular cAMP levels .
	manualset3
84105	3	397902	14	13	NULL	NULL	NULL	cellular cAMP 	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genistein and C3 transferase toxin did not elevate the cellular cAMP levels .
	manualset3
84114	4	397902	14	13	NULL	0	NULL	 levels 	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Genistein and C3 transferase toxin did not elevate the cellular cAMP levels .
	manualset3
84107	1	397903	14	13	NULL	0	NULL	Genistein	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Genistein induced significant increases in the number of FSH cells ( by 21 % ) and LH cells ( by 20 % ) per mm ( 2 ) compared to corresponding controls .
	manualset3
84108	2	397903	14	13	NULL	0	NULL	FSH cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Genistein induced significant increases in the number of FSH cells ( by 21 % ) and LH cells ( by 20 % ) per mm ( 2 ) compared to corresponding controls .
	manualset3
84109	3	397903	14	13	NULL	NULL	NULL	by 21% per mm (2)	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genistein induced significant increases in the number of FSH cells ( by 21 % ) and LH cells ( by 20 % ) per mm ( 2 ) compared to corresponding controls .
	manualset3
84110	4	397903	14	13	NULL	NULL	NULL	LH cells 	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genistein induced significant increases in the number of FSH cells ( by 21 % ) and LH cells ( by 20 % ) per mm ( 2 ) compared to corresponding controls .
	manualset3
84111	5	397903	14	13	NULL	NULL	NULL	by 20% per mm (2)	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genistein induced significant increases in the number of FSH cells ( by 21 % ) and LH cells ( by 20 % ) per mm ( 2 ) compared to corresponding controls .
	manualset3
84113	6	397903	14	13	NULL	NULL	NULL	corresponding controls	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genistein induced significant increases in the number of FSH cells ( by 21 % ) and LH cells ( by 20 % ) per mm ( 2 ) compared to corresponding controls .
	manualset3
84115	1	397904	14	13	NULL	0	NULL	Genome-wide association studies ( GWAS )	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genome-wide association studies ( GWAS ) have led to the identification of more than 100 common , low-penetrance loci for cancer .
	manualset3
84116	2	397904	14	13	NULL	NULL	NULL	identification	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genome-wide association studies ( GWAS ) have led to the identification of more than 100 common , low-penetrance loci for cancer .
	manualset3
84117	3	397904	14	13	NULL	0	NULL	more than 100 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genome-wide association studies ( GWAS ) have led to the identification of more than 100 common , low-penetrance loci for cancer .
	manualset3
84118	4	397904	14	13	NULL	NULL	NULL	low-penetrance loci	Gene												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genome-wide association studies ( GWAS ) have led to the identification of more than 100 common , low-penetrance loci for cancer .
	manualset3
84119	5	397904	14	13	NULL	0	NULL	cancer 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Genome-wide association studies ( GWAS ) have led to the identification of more than 100 common , low-penetrance loci for cancer .
	manualset3
84120	1	397905	14	13	NULL	0	NULL	Genome-wide association study 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genome-wide association study of PR interval .
	manualset3
84121	2	397905	14	13	NULL	NULL	NULL	PR interval	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genome-wide association study of PR interval .
	manualset3
84134	1	397907	14	13	NULL	0	NULL	Genomic analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genomic analysis of the major bovine milk protein genes .
	manualset3
84135	2	397907	14	13	NULL	0	NULL	bovine	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genomic analysis of the major bovine milk protein genes .
	manualset3
84136	3	397907	14	13	NULL	0	NULL	milk protein genes	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Genomic analysis of the major bovine milk protein genes .
	manualset3
84143	1	397909	14	13	NULL	0	NULL	Genomic maps	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Genomic maps of long noncoding RNA occupancy reveal principles of RNA-chromatin interactions .
	manualset3
84144	2	397909	14	13	NULL	NULL	NULL	long noncoding RNA occupancy	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genomic maps of long noncoding RNA occupancy reveal principles of RNA-chromatin interactions .
	manualset3
84145	3	397909	14	13	NULL	NULL	NULL	principles of RNA-chromatin interactions	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genomic maps of long noncoding RNA occupancy reveal principles of RNA-chromatin interactions .
	manualset3
84146	1	397910	14	13	NULL	NULL	NULL	Airflowmeter	MedicalDevice												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Airflowmeter -- a simple apparatus for lung function tests ) .
	manualset3
84147	2	397910	14	13	NULL	0	NULL	lung function tests	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Airflowmeter -- a simple apparatus for lung function tests ) .
	manualset3
84148	1	397911	14	13	NULL	0	NULL	Situation-simulating games	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Situation-simulating games in the teaching of obstetrics ) .
	manualset3
84209	2	397911	14	13	NULL	0	NULL	teaching 	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Situation-simulating games in the teaching of obstetrics ) .
	manualset3
84210	3	397911	14	13	NULL	NULL	NULL	obstetrics 	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Situation-simulating games in the teaching of obstetrics ) .
	manualset3
84149	1	397912	14	13	NULL	NULL	NULL	Genomic profiling 	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genomic profiling of peripheral T-cell lymphoma , unspecified , and anaplastic large T-cell lymphoma delineates novel recurrent chromosomal alterations .
	manualset3
84150	2	397912	14	13	NULL	NULL	NULL	peripheral T-cell lymphoma 	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genomic profiling of peripheral T-cell lymphoma , unspecified , and anaplastic large T-cell lymphoma delineates novel recurrent chromosomal alterations .
	manualset3
84151	3	397912	14	13	NULL	0	NULL	anaplastic large T-cell lymphoma 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Genomic profiling of peripheral T-cell lymphoma , unspecified , and anaplastic large T-cell lymphoma delineates novel recurrent chromosomal alterations .
	manualset3
84152	4	397912	14	13	NULL	0	NULL	novel recurrent chromosomal alterations	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Genomic profiling of peripheral T-cell lymphoma , unspecified , and anaplastic large T-cell lymphoma delineates novel recurrent chromosomal alterations .
	manualset3
84153	1	397913	14	13	NULL	0	NULL	Genomic profiling	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genomic profiling of plasmablastic lymphoma using array comparative genomic hybridization ( aCGH ) : revealing significant overlapping genomic lesions with diffuse large B-cell lymphoma .
	manualset3
84154	2	397913	14	13	NULL	0	NULL	plasmablastic lymphoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Genomic profiling of plasmablastic lymphoma using array comparative genomic hybridization ( aCGH ) : revealing significant overlapping genomic lesions with diffuse large B-cell lymphoma .
	manualset3
84155	3	397913	14	13	NULL	0	NULL	 array comparative genomic hybridization ( aCGH ) 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genomic profiling of plasmablastic lymphoma using array comparative genomic hybridization ( aCGH ) : revealing significant overlapping genomic lesions with diffuse large B-cell lymphoma .
	manualset3
84156	4	397913	14	13	NULL	0	NULL	overlapping genomic lesions	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Genomic profiling of plasmablastic lymphoma using array comparative genomic hybridization ( aCGH ) : revealing significant overlapping genomic lesions with diffuse large B-cell lymphoma .
	manualset3
84157	5	397913	14	13	NULL	0	NULL	diffuse large B-cell lymphoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Genomic profiling of plasmablastic lymphoma using array comparative genomic hybridization ( aCGH ) : revealing significant overlapping genomic lesions with diffuse large B-cell lymphoma .
	manualset3
84158	1	397914	14	13	NULL	NULL	NULL	Genoprotective properties	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genoprotective properties in BTK-8L correlate to some extent with the lowering of the death rate of experimental animals at the early stage of intoxication by chlorofos at the prophylactic injection of the preparation , which , nevertheless , was not so significant , as in the case of intoxication by tetrachloromethane .
	manualset3
84159	2	397914	14	13	NULL	0	NULL	BTK-8L	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Genoprotective properties in BTK-8L correlate to some extent with the lowering of the death rate of experimental animals at the early stage of intoxication by chlorofos at the prophylactic injection of the preparation , which , nevertheless , was not so significant , as in the case of intoxication by tetrachloromethane .
	manualset3
84160	3	397914	14	13	NULL	NULL	NULL	lowering of the death rate	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genoprotective properties in BTK-8L correlate to some extent with the lowering of the death rate of experimental animals at the early stage of intoxication by chlorofos at the prophylactic injection of the preparation , which , nevertheless , was not so significant , as in the case of intoxication by tetrachloromethane .
	manualset3
84161	4	397914	14	13	NULL	0	NULL	experimental animals 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Genoprotective properties in BTK-8L correlate to some extent with the lowering of the death rate of experimental animals at the early stage of intoxication by chlorofos at the prophylactic injection of the preparation , which , nevertheless , was not so significant , as in the case of intoxication by tetrachloromethane .
	manualset3
84162	5	397914	14	13	NULL	0	NULL	early stage of intoxication	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Genoprotective properties in BTK-8L correlate to some extent with the lowering of the death rate of experimental animals at the early stage of intoxication by chlorofos at the prophylactic injection of the preparation , which , nevertheless , was not so significant , as in the case of intoxication by tetrachloromethane .
	manualset3
84163	6	397914	14	13	NULL	0	NULL	chlorofos 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Genoprotective properties in BTK-8L correlate to some extent with the lowering of the death rate of experimental animals at the early stage of intoxication by chlorofos at the prophylactic injection of the preparation , which , nevertheless , was not so significant , as in the case of intoxication by tetrachloromethane .
	manualset3
84164	7	397914	14	13	NULL	0	NULL	prophylactic injection	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Genoprotective properties in BTK-8L correlate to some extent with the lowering of the death rate of experimental animals at the early stage of intoxication by chlorofos at the prophylactic injection of the preparation , which , nevertheless , was not so significant , as in the case of intoxication by tetrachloromethane .
	manualset3
84165	8	397914	14	13	NULL	NULL	NULL	intoxication 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genoprotective properties in BTK-8L correlate to some extent with the lowering of the death rate of experimental animals at the early stage of intoxication by chlorofos at the prophylactic injection of the preparation , which , nevertheless , was not so significant , as in the case of intoxication by tetrachloromethane .
	manualset3
84166	9	397914	14	13	NULL	0	NULL	tetrachloromethane	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Genoprotective properties in BTK-8L correlate to some extent with the lowering of the death rate of experimental animals at the early stage of intoxication by chlorofos at the prophylactic injection of the preparation , which , nevertheless , was not so significant , as in the case of intoxication by tetrachloromethane .
	manualset3
84167	1	397915	14	13	NULL	0	NULL	Genotypes	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Genotypes of the two loci were identified by direct sequencing , and for site 85 of the mtLSU locus , three allele-specific PCR assays were used .
	manualset3
84168	2	397915	14	13	NULL	NULL	NULL	two	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genotypes of the two loci were identified by direct sequencing , and for site 85 of the mtLSU locus , three allele-specific PCR assays were used .
	manualset3
84169	3	397915	14	13	NULL	0	NULL	loci	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Genotypes of the two loci were identified by direct sequencing , and for site 85 of the mtLSU locus , three allele-specific PCR assays were used .
	manualset3
84170	4	397915	14	13	NULL	0	NULL	direct sequencing	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genotypes of the two loci were identified by direct sequencing , and for site 85 of the mtLSU locus , three allele-specific PCR assays were used .
	manualset3
84171	5	397915	14	13	NULL	NULL	NULL	site 85 of the mtLSU locus 	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genotypes of the two loci were identified by direct sequencing , and for site 85 of the mtLSU locus , three allele-specific PCR assays were used .
	manualset3
84173	6	397915	14	13	NULL	NULL	NULL	three	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genotypes of the two loci were identified by direct sequencing , and for site 85 of the mtLSU locus , three allele-specific PCR assays were used .
	manualset3
84174	7	397915	14	13	NULL	NULL	NULL	allele-specific PCR assays 	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genotypes of the two loci were identified by direct sequencing , and for site 85 of the mtLSU locus , three allele-specific PCR assays were used .
	manualset3
84175	1	397916	14	13	NULL	0	NULL	Genotypic and phenotypic analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genotypic and phenotypic analysis of Mycoplasma fermentans strains isolated from different host tissues .
	manualset3
84176	2	397916	14	13	NULL	NULL	NULL	Mycoplasma fermentans strains	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genotypic and phenotypic analysis of Mycoplasma fermentans strains isolated from different host tissues .
	manualset3
84177	3	397916	14	13	NULL	0	NULL	different host tissues	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Genotypic and phenotypic analysis of Mycoplasma fermentans strains isolated from different host tissues .
	manualset3
84178	1	397917	14	13	NULL	0	NULL	Genotypic and phenotypic stability	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Genotypic and phenotypic stability of Helicobacter pylori markers in a nine-year follow-up study of patients with noneradicated infection .
	manualset3
84179	2	397917	14	13	NULL	0	NULL	Helicobacter pylori markers 	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Genotypic and phenotypic stability of Helicobacter pylori markers in a nine-year follow-up study of patients with noneradicated infection .
	manualset3
84180	3	397917	14	13	NULL	0	NULL	nine-year	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Genotypic and phenotypic stability of Helicobacter pylori markers in a nine-year follow-up study of patients with noneradicated infection .
	manualset3
84181	4	397917	14	13	NULL	0	NULL	follow-up study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genotypic and phenotypic stability of Helicobacter pylori markers in a nine-year follow-up study of patients with noneradicated infection .
	manualset3
84182	5	397917	14	13	NULL	0	NULL	patients 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Genotypic and phenotypic stability of Helicobacter pylori markers in a nine-year follow-up study of patients with noneradicated infection .
	manualset3
84183	6	397917	14	13	NULL	0	NULL	noneradicated infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Genotypic and phenotypic stability of Helicobacter pylori markers in a nine-year follow-up study of patients with noneradicated infection .
	manualset3
84184	1	397918	14	13	NULL	0	NULL	Genotyping or phenotyping 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Genotyping or phenotyping needs to be introduced in clinical laboratories .
	manualset3
84185	2	397918	14	13	NULL	NULL	NULL	clinical laboratories	Facility												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Genotyping or phenotyping needs to be introduced in clinical laboratories .
	manualset3
84186	1	397919	14	13	NULL	0	NULL	Gentamicin	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Gentamicin ( 2.5 microgram/ml ) , kanamycin ( 31.2 microgram/ml ) , neomycin ( 62.5 microgram/ml ) , and tobramycin ( 2.5 microgram/ml ) were the only antibacterials tested which controlled microbial growth without affecting sperm viability for up to 24 hr storage at 5 C. Tobramycin maintained fertility equal to that of the non-antibiotic control up to 24 hr storage .
	manualset3
84187	2	397919	14	13	NULL	0	NULL	2.5 microgram/ml	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gentamicin ( 2.5 microgram/ml ) , kanamycin ( 31.2 microgram/ml ) , neomycin ( 62.5 microgram/ml ) , and tobramycin ( 2.5 microgram/ml ) were the only antibacterials tested which controlled microbial growth without affecting sperm viability for up to 24 hr storage at 5 C. Tobramycin maintained fertility equal to that of the non-antibiotic control up to 24 hr storage .
	manualset3
84188	3	397919	14	13	NULL	0	NULL	kanamycin 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Gentamicin ( 2.5 microgram/ml ) , kanamycin ( 31.2 microgram/ml ) , neomycin ( 62.5 microgram/ml ) , and tobramycin ( 2.5 microgram/ml ) were the only antibacterials tested which controlled microbial growth without affecting sperm viability for up to 24 hr storage at 5 C. Tobramycin maintained fertility equal to that of the non-antibiotic control up to 24 hr storage .
	manualset3
84189	4	397919	14	13	NULL	0	NULL	 31.2 microgram/ml	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gentamicin ( 2.5 microgram/ml ) , kanamycin ( 31.2 microgram/ml ) , neomycin ( 62.5 microgram/ml ) , and tobramycin ( 2.5 microgram/ml ) were the only antibacterials tested which controlled microbial growth without affecting sperm viability for up to 24 hr storage at 5 C. Tobramycin maintained fertility equal to that of the non-antibiotic control up to 24 hr storage .
	manualset3
84190	5	397919	14	13	NULL	0	NULL	 neomycin 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Gentamicin ( 2.5 microgram/ml ) , kanamycin ( 31.2 microgram/ml ) , neomycin ( 62.5 microgram/ml ) , and tobramycin ( 2.5 microgram/ml ) were the only antibacterials tested which controlled microbial growth without affecting sperm viability for up to 24 hr storage at 5 C. Tobramycin maintained fertility equal to that of the non-antibiotic control up to 24 hr storage .
	manualset3
84191	6	397919	14	13	NULL	NULL	NULL	62.5 microgram/ml 	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gentamicin ( 2.5 microgram/ml ) , kanamycin ( 31.2 microgram/ml ) , neomycin ( 62.5 microgram/ml ) , and tobramycin ( 2.5 microgram/ml ) were the only antibacterials tested which controlled microbial growth without affecting sperm viability for up to 24 hr storage at 5 C. Tobramycin maintained fertility equal to that of the non-antibiotic control up to 24 hr storage .
	manualset3
84192	7	397919	14	13	NULL	0	NULL	tobramycin	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Gentamicin ( 2.5 microgram/ml ) , kanamycin ( 31.2 microgram/ml ) , neomycin ( 62.5 microgram/ml ) , and tobramycin ( 2.5 microgram/ml ) were the only antibacterials tested which controlled microbial growth without affecting sperm viability for up to 24 hr storage at 5 C. Tobramycin maintained fertility equal to that of the non-antibiotic control up to 24 hr storage .
	manualset3
84193	8	397919	14	13	NULL	0	NULL	2.5 microgram/ml 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gentamicin ( 2.5 microgram/ml ) , kanamycin ( 31.2 microgram/ml ) , neomycin ( 62.5 microgram/ml ) , and tobramycin ( 2.5 microgram/ml ) were the only antibacterials tested which controlled microbial growth without affecting sperm viability for up to 24 hr storage at 5 C. Tobramycin maintained fertility equal to that of the non-antibiotic control up to 24 hr storage .
	manualset3
84194	9	397919	14	13	NULL	0	NULL	antibacterials	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Gentamicin ( 2.5 microgram/ml ) , kanamycin ( 31.2 microgram/ml ) , neomycin ( 62.5 microgram/ml ) , and tobramycin ( 2.5 microgram/ml ) were the only antibacterials tested which controlled microbial growth without affecting sperm viability for up to 24 hr storage at 5 C. Tobramycin maintained fertility equal to that of the non-antibiotic control up to 24 hr storage .
	manualset3
84195	10	397919	14	13	NULL	NULL	NULL	microbial growth	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gentamicin ( 2.5 microgram/ml ) , kanamycin ( 31.2 microgram/ml ) , neomycin ( 62.5 microgram/ml ) , and tobramycin ( 2.5 microgram/ml ) were the only antibacterials tested which controlled microbial growth without affecting sperm viability for up to 24 hr storage at 5 C. Tobramycin maintained fertility equal to that of the non-antibiotic control up to 24 hr storage .
	manualset3
84196	11	397919	14	13	NULL	NULL	NULL	sperm viability	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gentamicin ( 2.5 microgram/ml ) , kanamycin ( 31.2 microgram/ml ) , neomycin ( 62.5 microgram/ml ) , and tobramycin ( 2.5 microgram/ml ) were the only antibacterials tested which controlled microbial growth without affecting sperm viability for up to 24 hr storage at 5 C. Tobramycin maintained fertility equal to that of the non-antibiotic control up to 24 hr storage .
	manualset3
84197	12	397919	14	13	NULL	0	NULL	24 hr	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Gentamicin ( 2.5 microgram/ml ) , kanamycin ( 31.2 microgram/ml ) , neomycin ( 62.5 microgram/ml ) , and tobramycin ( 2.5 microgram/ml ) were the only antibacterials tested which controlled microbial growth without affecting sperm viability for up to 24 hr storage at 5 C. Tobramycin maintained fertility equal to that of the non-antibiotic control up to 24 hr storage .
	manualset3
84198	13	397919	14	13	NULL	0	NULL	5 C	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Gentamicin ( 2.5 microgram/ml ) , kanamycin ( 31.2 microgram/ml ) , neomycin ( 62.5 microgram/ml ) , and tobramycin ( 2.5 microgram/ml ) were the only antibacterials tested which controlled microbial growth without affecting sperm viability for up to 24 hr storage at 5 C. Tobramycin maintained fertility equal to that of the non-antibiotic control up to 24 hr storage .
	manualset3
84199	14	397919	14	13	NULL	0	NULL	Tobramycin	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Gentamicin ( 2.5 microgram/ml ) , kanamycin ( 31.2 microgram/ml ) , neomycin ( 62.5 microgram/ml ) , and tobramycin ( 2.5 microgram/ml ) were the only antibacterials tested which controlled microbial growth without affecting sperm viability for up to 24 hr storage at 5 C. Tobramycin maintained fertility equal to that of the non-antibiotic control up to 24 hr storage .
	manualset3
84200	15	397919	14	13	NULL	NULL	NULL	fertility 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gentamicin ( 2.5 microgram/ml ) , kanamycin ( 31.2 microgram/ml ) , neomycin ( 62.5 microgram/ml ) , and tobramycin ( 2.5 microgram/ml ) were the only antibacterials tested which controlled microbial growth without affecting sperm viability for up to 24 hr storage at 5 C. Tobramycin maintained fertility equal to that of the non-antibiotic control up to 24 hr storage .
	manualset3
84201	16	397919	14	13	NULL	NULL	NULL	non-antibiotic control 	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gentamicin ( 2.5 microgram/ml ) , kanamycin ( 31.2 microgram/ml ) , neomycin ( 62.5 microgram/ml ) , and tobramycin ( 2.5 microgram/ml ) were the only antibacterials tested which controlled microbial growth without affecting sperm viability for up to 24 hr storage at 5 C. Tobramycin maintained fertility equal to that of the non-antibiotic control up to 24 hr storage .
	manualset3
84202	17	397919	14	13	NULL	0	NULL	24 hr 	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Gentamicin ( 2.5 microgram/ml ) , kanamycin ( 31.2 microgram/ml ) , neomycin ( 62.5 microgram/ml ) , and tobramycin ( 2.5 microgram/ml ) were the only antibacterials tested which controlled microbial growth without affecting sperm viability for up to 24 hr storage at 5 C. Tobramycin maintained fertility equal to that of the non-antibiotic control up to 24 hr storage .
	manualset3
84203	1	397920	14	13	NULL	0	NULL	Geobacillus stearothermophilus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Geobacillus stearothermophilus has been used under mesophilic and static cultivation conditions using wool as the main carbon source .
	manualset3
84204	2	397920	14	13	NULL	0	NULL	mesophilic and static cultivation conditions	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Geobacillus stearothermophilus has been used under mesophilic and static cultivation conditions using wool as the main carbon source .
	manualset3
84205	3	397920	14	13	NULL	NULL	NULL	wool	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Geobacillus stearothermophilus has been used under mesophilic and static cultivation conditions using wool as the main carbon source .
	manualset3
84206	4	397920	14	13	NULL	0	NULL	carbon 	Atom												NULL		0	NULL	NULL	NULL	NULL	NULL	Geobacillus stearothermophilus has been used under mesophilic and static cultivation conditions using wool as the main carbon source .
	manualset3
84229	1	397921	14	13	NULL	0	NULL	Slovak 	Language												NULL		0	NULL	NULL	NULL	NULL	NULL	( Slovak verbal audiometry ) .
	manualset3
84230	2	397921	14	13	NULL	0	NULL	verbal audiometry 	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	( Slovak verbal audiometry ) .
	manualset3
84231	1	397922	14	13	NULL	0	NULL	George Eliot	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	George Eliot and specific learning disorders .
	manualset3
84232	2	397922	14	13	NULL	0	NULL	specific learning disorders	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	George Eliot and specific learning disorders .
	manualset3
84233	1	397923	14	13	NULL	0	NULL	Gestational diabetes mellitus ( GDM )	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gestational diabetes mellitus ( GDM ) is a risk factor for both Type 2 diabetes ( DM2 ) and insulin-resistance syndrome ( IRS ) .
	manualset3
84234	2	397923	14	13	NULL	0	NULL	risk factor	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gestational diabetes mellitus ( GDM ) is a risk factor for both Type 2 diabetes ( DM2 ) and insulin-resistance syndrome ( IRS ) .
	manualset3
84235	3	397923	14	13	NULL	0	NULL	 Type 2 diabetes ( DM2 ) 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gestational diabetes mellitus ( GDM ) is a risk factor for both Type 2 diabetes ( DM2 ) and insulin-resistance syndrome ( IRS ) .
	manualset3
84236	4	397923	14	13	NULL	0	NULL	insulin-resistance syndrome ( IRS )	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gestational diabetes mellitus ( GDM ) is a risk factor for both Type 2 diabetes ( DM2 ) and insulin-resistance syndrome ( IRS ) .
	manualset3
84237	1	397924	14	13	NULL	0	NULL	Giant cell arteritis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Giant cell arteritis of the uterus and adnexa .
	manualset3
84238	2	397924	14	13	NULL	0	NULL	uterus	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Giant cell arteritis of the uterus and adnexa .
	manualset3
84239	3	397924	14	13	NULL	0	NULL	adnexa	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Giant cell arteritis of the uterus and adnexa .
	manualset3
84240	1	397925	14	13	NULL	0	NULL	Giant cell pneumonia 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Giant cell pneumonia is a rare and uncommon type of lung infection developing as a complication of measles , especially in immunocompromised patients , whether their immune systems are affected primarily or whether they have acquired immune defects .
	manualset3
84241	2	397925	14	13	NULL	0	NULL	lung infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Giant cell pneumonia is a rare and uncommon type of lung infection developing as a complication of measles , especially in immunocompromised patients , whether their immune systems are affected primarily or whether they have acquired immune defects .
	manualset3
84242	3	397925	14	13	NULL	NULL	NULL	complication of measles	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Giant cell pneumonia is a rare and uncommon type of lung infection developing as a complication of measles , especially in immunocompromised patients , whether their immune systems are affected primarily or whether they have acquired immune defects .
	manualset3
84243	4	397925	14	13	NULL	0	NULL	 immunocompromised patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Giant cell pneumonia is a rare and uncommon type of lung infection developing as a complication of measles , especially in immunocompromised patients , whether their immune systems are affected primarily or whether they have acquired immune defects .
	manualset3
84244	5	397925	14	13	NULL	NULL	NULL	immune systems	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Giant cell pneumonia is a rare and uncommon type of lung infection developing as a complication of measles , especially in immunocompromised patients , whether their immune systems are affected primarily or whether they have acquired immune defects .
	manualset3
84245	6	397925	14	13	NULL	0	NULL	acquired immune defects	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Giant cell pneumonia is a rare and uncommon type of lung infection developing as a complication of measles , especially in immunocompromised patients , whether their immune systems are affected primarily or whether they have acquired immune defects .
	manualset3
84246	1	397926	14	13	NULL	0	NULL	Giardia lamblia	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Giardia lamblia was the most frequent species found .
	manualset3
84248	1	397927	14	13	NULL	0	NULL	Small bridges with inlay and attachment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Small bridges with inlay and attachment : the prosthetic solution for limited tooth gaps ) .
	manualset3
84249	2	397927	14	13	NULL	NULL	NULL	prosthetic solution	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Small bridges with inlay and attachment : the prosthetic solution for limited tooth gaps ) .
	manualset3
84250	3	397927	14	13	NULL	0	NULL	limited tooth gaps	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Small bridges with inlay and attachment : the prosthetic solution for limited tooth gaps ) .
	manualset3
84251	1	397928	14	13	NULL	0	NULL	Gilding the lilly	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Gilding the lilly : comments on the training based model .
	manualset3
84252	2	397928	14	13	NULL	0	NULL	training based model 	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Gilding the lilly : comments on the training based model .
	manualset3
84253	1	397929	14	13	NULL	0	NULL	Gilts 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Gilts exhibited elevated concentrations of NE in the olfactory bulbs ( OB ) , hypothalamus , pons , and corpus trapezoideum-locus ceruleus ( LC ) compared to lower concentrations in corresponding areas of sows .
	manualset3
84254	2	397929	14	13	NULL	NULL	NULL	elevated concentrations 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gilts exhibited elevated concentrations of NE in the olfactory bulbs ( OB ) , hypothalamus , pons , and corpus trapezoideum-locus ceruleus ( LC ) compared to lower concentrations in corresponding areas of sows .
	manualset3
84255	3	397929	14	13	NULL	0	NULL	NE	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Gilts exhibited elevated concentrations of NE in the olfactory bulbs ( OB ) , hypothalamus , pons , and corpus trapezoideum-locus ceruleus ( LC ) compared to lower concentrations in corresponding areas of sows .
	manualset3
84256	4	397929	14	13	NULL	NULL	NULL	olfactory bulbs ( OB )	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gilts exhibited elevated concentrations of NE in the olfactory bulbs ( OB ) , hypothalamus , pons , and corpus trapezoideum-locus ceruleus ( LC ) compared to lower concentrations in corresponding areas of sows .
	manualset3
84257	5	397929	14	13	NULL	NULL	NULL	hypothalamus	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gilts exhibited elevated concentrations of NE in the olfactory bulbs ( OB ) , hypothalamus , pons , and corpus trapezoideum-locus ceruleus ( LC ) compared to lower concentrations in corresponding areas of sows .
	manualset3
84258	6	397929	14	13	NULL	NULL	NULL	 pons	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gilts exhibited elevated concentrations of NE in the olfactory bulbs ( OB ) , hypothalamus , pons , and corpus trapezoideum-locus ceruleus ( LC ) compared to lower concentrations in corresponding areas of sows .
	manualset3
84259	7	397929	14	13	NULL	NULL	NULL	corpus trapezoideum-locus ceruleus ( LC )	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gilts exhibited elevated concentrations of NE in the olfactory bulbs ( OB ) , hypothalamus , pons , and corpus trapezoideum-locus ceruleus ( LC ) compared to lower concentrations in corresponding areas of sows .
	manualset3
84260	8	397929	14	13	NULL	NULL	NULL	lower concentrations	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gilts exhibited elevated concentrations of NE in the olfactory bulbs ( OB ) , hypothalamus , pons , and corpus trapezoideum-locus ceruleus ( LC ) compared to lower concentrations in corresponding areas of sows .
	manualset3
84261	9	397929	14	13	NULL	NULL	NULL	corresponding areas	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gilts exhibited elevated concentrations of NE in the olfactory bulbs ( OB ) , hypothalamus , pons , and corpus trapezoideum-locus ceruleus ( LC ) compared to lower concentrations in corresponding areas of sows .
	manualset3
84262	10	397929	14	13	NULL	0	NULL	sows	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Gilts exhibited elevated concentrations of NE in the olfactory bulbs ( OB ) , hypothalamus , pons , and corpus trapezoideum-locus ceruleus ( LC ) compared to lower concentrations in corresponding areas of sows .
	manualset3
84263	1	397930	14	13	NULL	0	NULL	Gilts 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Gilts remained on their respective experimental diets and with their penmates throughout the nursery , growing , and finishing phases .
	manualset3
84264	2	397930	14	13	NULL	0	NULL	respective experimental diets 	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	Gilts remained on their respective experimental diets and with their penmates throughout the nursery , growing , and finishing phases .
	manualset3
84265	3	397930	14	13	NULL	0	NULL	penmates 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Gilts remained on their respective experimental diets and with their penmates throughout the nursery , growing , and finishing phases .
	manualset3
84266	4	397930	14	13	NULL	NULL	NULL	nursery  phase	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gilts remained on their respective experimental diets and with their penmates throughout the nursery , growing , and finishing phases .
	manualset3
84267	5	397930	14	13	NULL	NULL	NULL	growing phase	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gilts remained on their respective experimental diets and with their penmates throughout the nursery , growing , and finishing phases .
	manualset3
84268	6	397930	14	13	NULL	NULL	NULL	finishing phase	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gilts remained on their respective experimental diets and with their penmates throughout the nursery , growing , and finishing phases .
	manualset3
84506	3	397931	14	13	NULL	0	NULL	 increased morbidity 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Given a certain severity of crash and of injury , it is unclear whether acute and/or chronic alcohol use leads to increased morbidity , mortality or a more complicated hospital course after motor vehicle collisions .
	manualset3
84507	4	397931	14	13	NULL	0	NULL	mortality	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Given a certain severity of crash and of injury , it is unclear whether acute and/or chronic alcohol use leads to increased morbidity , mortality or a more complicated hospital course after motor vehicle collisions .
	manualset3
84508	5	397931	14	13	NULL	0	NULL	more complicated hospital course	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Given a certain severity of crash and of injury , it is unclear whether acute and/or chronic alcohol use leads to increased morbidity , mortality or a more complicated hospital course after motor vehicle collisions .
	manualset3
84509	6	397931	14	13	NULL	NULL	NULL	motor vehicle collisions	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given a certain severity of crash and of injury , it is unclear whether acute and/or chronic alcohol use leads to increased morbidity , mortality or a more complicated hospital course after motor vehicle collisions .
	manualset3
84510	7	397931	14	13	NULL	NULL	NULL	certain severity of crash and of injury	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given a certain severity of crash and of injury , it is unclear whether acute and/or chronic alcohol use leads to increased morbidity , mortality or a more complicated hospital course after motor vehicle collisions .
	manualset3
85426	1	397931	14	13	NULL	NULL	NULL	acute and/or chronic alcohol use	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given a certain severity of crash and of injury , it is unclear whether acute and/or chronic alcohol use leads to increased morbidity , mortality or a more complicated hospital course after motor vehicle collisions .
	manualset3
84511	1	397932	14	13	NULL	0	NULL	current findings	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Given our current findings , and because a number of risk factors for sporadic AD serve to lower levels of sAPP - in brains of AD patients , inadequate sAPP - levels may be sufficient to polarize APP processing towards the amyloidogenic , A-producing route .
	manualset3
84512	2	397932	14	13	NULL	NULL	NULL	risk factors	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given our current findings , and because a number of risk factors for sporadic AD serve to lower levels of sAPP - in brains of AD patients , inadequate sAPP - levels may be sufficient to polarize APP processing towards the amyloidogenic , A-producing route .
	manualset3
84513	3	397932	14	13	NULL	NULL	NULL	sporadic AD	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given our current findings , and because a number of risk factors for sporadic AD serve to lower levels of sAPP - in brains of AD patients , inadequate sAPP - levels may be sufficient to polarize APP processing towards the amyloidogenic , A-producing route .
	manualset3
84514	4	397932	14	13	NULL	NULL	NULL	 levels of sAPP	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given our current findings , and because a number of risk factors for sporadic AD serve to lower levels of sAPP - in brains of AD patients , inadequate sAPP - levels may be sufficient to polarize APP processing towards the amyloidogenic , A-producing route .
	manualset3
84515	5	397932	14	13	NULL	0	NULL	brains	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Given our current findings , and because a number of risk factors for sporadic AD serve to lower levels of sAPP - in brains of AD patients , inadequate sAPP - levels may be sufficient to polarize APP processing towards the amyloidogenic , A-producing route .
	manualset3
84516	6	397932	14	13	NULL	0	NULL	AD patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Given our current findings , and because a number of risk factors for sporadic AD serve to lower levels of sAPP - in brains of AD patients , inadequate sAPP - levels may be sufficient to polarize APP processing towards the amyloidogenic , A-producing route .
	manualset3
84517	7	397932	14	13	NULL	NULL	NULL	inadequate sAPP - levels	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given our current findings , and because a number of risk factors for sporadic AD serve to lower levels of sAPP - in brains of AD patients , inadequate sAPP - levels may be sufficient to polarize APP processing towards the amyloidogenic , A-producing route .
	manualset3
84518	8	397932	14	13	NULL	NULL	NULL	APP processing	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given our current findings , and because a number of risk factors for sporadic AD serve to lower levels of sAPP - in brains of AD patients , inadequate sAPP - levels may be sufficient to polarize APP processing towards the amyloidogenic , A-producing route .
	manualset3
84519	9	397932	14	13	NULL	NULL	NULL	amyloidogenic , A-producing route	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given our current findings , and because a number of risk factors for sporadic AD serve to lower levels of sAPP - in brains of AD patients , inadequate sAPP - levels may be sufficient to polarize APP processing towards the amyloidogenic , A-producing route .
	manualset3
84521	1	397933	14	13	NULL	0	NULL	species x 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Given species x and y , the ordinal binary character cxy of M is defined by cxy ( s ) = 1 if and only if M ( s , x ) & lt ; M ( s , y ) , for all species s. In this paper we present several results concerning the inference of evolutionary trees or phylogenies from ordinal assertions .
	manualset3
84522	2	397933	14	13	NULL	0	NULL	species y	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Given species x and y , the ordinal binary character cxy of M is defined by cxy ( s ) = 1 if and only if M ( s , x ) & lt ; M ( s , y ) , for all species s. In this paper we present several results concerning the inference of evolutionary trees or phylogenies from ordinal assertions .
	manualset3
84523	3	397933	14	13	NULL	0	NULL	ordinal binary character cxy of M 	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Given species x and y , the ordinal binary character cxy of M is defined by cxy ( s ) = 1 if and only if M ( s , x ) & lt ; M ( s , y ) , for all species s. In this paper we present several results concerning the inference of evolutionary trees or phylogenies from ordinal assertions .
	manualset3
84525	5	397933	14	13	NULL	0	NULL	1	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Given species x and y , the ordinal binary character cxy of M is defined by cxy ( s ) = 1 if and only if M ( s , x ) & lt ; M ( s , y ) , for all species s. In this paper we present several results concerning the inference of evolutionary trees or phylogenies from ordinal assertions .
	manualset3
84528	8	397933	14	13	NULL	NULL	NULL	species s	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given species x and y , the ordinal binary character cxy of M is defined by cxy ( s ) = 1 if and only if M ( s , x ) & lt ; M ( s , y ) , for all species s. In this paper we present several results concerning the inference of evolutionary trees or phylogenies from ordinal assertions .
	manualset3
84529	9	397933	14	13	NULL	0	NULL	paper	PublicationOrCitation												NULL		0	NULL	NULL	NULL	NULL	NULL	Given species x and y , the ordinal binary character cxy of M is defined by cxy ( s ) = 1 if and only if M ( s , x ) & lt ; M ( s , y ) , for all species s. In this paper we present several results concerning the inference of evolutionary trees or phylogenies from ordinal assertions .
	manualset3
84531	11	397933	14	13	NULL	NULL	NULL	inference of evolutionary trees 	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given species x and y , the ordinal binary character cxy of M is defined by cxy ( s ) = 1 if and only if M ( s , x ) & lt ; M ( s , y ) , for all species s. In this paper we present several results concerning the inference of evolutionary trees or phylogenies from ordinal assertions .
	manualset3
84532	12	397933	14	13	NULL	NULL	NULL	phylogenies from ordinal assertions	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given species x and y , the ordinal binary character cxy of M is defined by cxy ( s ) = 1 if and only if M ( s , x ) & lt ; M ( s , y ) , for all species s. In this paper we present several results concerning the inference of evolutionary trees or phylogenies from ordinal assertions .
	manualset3
84533	1	397934	14	13	NULL	0	NULL	PP1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Given that PP1 controls fusion , the SNARE complexes that accumulate in glc7 mutants likely represent trans-SNARE complexes .
	manualset3
84534	2	397934	14	13	NULL	0	NULL	fusion	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Given that PP1 controls fusion , the SNARE complexes that accumulate in glc7 mutants likely represent trans-SNARE complexes .
	manualset3
84535	3	397934	14	13	NULL	NULL	NULL	SNARE complexes	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given that PP1 controls fusion , the SNARE complexes that accumulate in glc7 mutants likely represent trans-SNARE complexes .
	manualset3
84536	4	397934	14	13	NULL	0	NULL	glc7 mutants	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Given that PP1 controls fusion , the SNARE complexes that accumulate in glc7 mutants likely represent trans-SNARE complexes .
	manualset3
84537	5	397934	14	13	NULL	NULL	NULL	trans-SNARE complexes	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given that PP1 controls fusion , the SNARE complexes that accumulate in glc7 mutants likely represent trans-SNARE complexes .
	manualset3
84538	1	397935	14	13	NULL	0	NULL	PPAR ligands	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Given that PPAR ligands are currently used in medicine as hypolipidemic drugs with excellent tolerance and limited toxicity , PPARalpha activation might offer a novel and potentially low-toxic approach for the treatment of tumor-associated angiogenesis and cancer .
	manualset3
84539	2	397935	14	13	NULL	NULL	NULL	medicine	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given that PPAR ligands are currently used in medicine as hypolipidemic drugs with excellent tolerance and limited toxicity , PPARalpha activation might offer a novel and potentially low-toxic approach for the treatment of tumor-associated angiogenesis and cancer .
	manualset3
84540	3	397935	14	13	NULL	NULL	NULL	hypolipidemic drugs	Drug												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given that PPAR ligands are currently used in medicine as hypolipidemic drugs with excellent tolerance and limited toxicity , PPARalpha activation might offer a novel and potentially low-toxic approach for the treatment of tumor-associated angiogenesis and cancer .
	manualset3
84541	4	397935	14	13	NULL	0	NULL	excellent tolerance	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Given that PPAR ligands are currently used in medicine as hypolipidemic drugs with excellent tolerance and limited toxicity , PPARalpha activation might offer a novel and potentially low-toxic approach for the treatment of tumor-associated angiogenesis and cancer .
	manualset3
84542	5	397935	14	13	NULL	0	NULL	limited toxicity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Given that PPAR ligands are currently used in medicine as hypolipidemic drugs with excellent tolerance and limited toxicity , PPARalpha activation might offer a novel and potentially low-toxic approach for the treatment of tumor-associated angiogenesis and cancer .
	manualset3
84543	6	397935	14	13	NULL	0	NULL	PPARalpha activation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Given that PPAR ligands are currently used in medicine as hypolipidemic drugs with excellent tolerance and limited toxicity , PPARalpha activation might offer a novel and potentially low-toxic approach for the treatment of tumor-associated angiogenesis and cancer .
	manualset3
84544	7	397935	14	13	NULL	0	NULL	novel and potentially low-toxic approach 	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Given that PPAR ligands are currently used in medicine as hypolipidemic drugs with excellent tolerance and limited toxicity , PPARalpha activation might offer a novel and potentially low-toxic approach for the treatment of tumor-associated angiogenesis and cancer .
	manualset3
84545	8	397935	14	13	NULL	0	NULL	tumor-associated angiogenesis 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Given that PPAR ligands are currently used in medicine as hypolipidemic drugs with excellent tolerance and limited toxicity , PPARalpha activation might offer a novel and potentially low-toxic approach for the treatment of tumor-associated angiogenesis and cancer .
	manualset3
84546	9	397935	14	13	NULL	0	NULL	cancer	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Given that PPAR ligands are currently used in medicine as hypolipidemic drugs with excellent tolerance and limited toxicity , PPARalpha activation might offer a novel and potentially low-toxic approach for the treatment of tumor-associated angiogenesis and cancer .
	manualset3
85427	10	397935	14	13	NULL	0	NULL	treatment 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Given that PPAR ligands are currently used in medicine as hypolipidemic drugs with excellent tolerance and limited toxicity , PPARalpha activation might offer a novel and potentially low-toxic approach for the treatment of tumor-associated angiogenesis and cancer .
	manualset3
84547	1	397936	14	13	NULL	NULL	NULL	Soft-tissue changes	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Soft-tissue changes in the metacarpal area in chronic polyarthritis ) .
	manualset3
84548	2	397936	14	13	NULL	0	NULL	metacarpal area	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( Soft-tissue changes in the metacarpal area in chronic polyarthritis ) .
	manualset3
84549	3	397936	14	13	NULL	0	NULL	chronic polyarthritis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Soft-tissue changes in the metacarpal area in chronic polyarthritis ) .
	manualset3
84561	1	397938	14	13	NULL	NULL	NULL	kinetics of the peptides	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given the different kinetics of the peptides , a mathematical model was necessary to analyze the oral glucose tolerance test ( OGTT ) data of insulin , C-peptide , and proinsulin in 55 healthy ( NGT ) , 30 impaired glucose-tolerant ( IGT ) , and 31 type 2 diabetic ( T2DM ) subjects .
	manualset3
84562	2	397938	14	13	NULL	0	NULL	mathematical model	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the different kinetics of the peptides , a mathematical model was necessary to analyze the oral glucose tolerance test ( OGTT ) data of insulin , C-peptide , and proinsulin in 55 healthy ( NGT ) , 30 impaired glucose-tolerant ( IGT ) , and 31 type 2 diabetic ( T2DM ) subjects .
	manualset3
84563	3	397938	14	13	NULL	0	NULL	oral glucose tolerance test ( OGTT ) data of insulin	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the different kinetics of the peptides , a mathematical model was necessary to analyze the oral glucose tolerance test ( OGTT ) data of insulin , C-peptide , and proinsulin in 55 healthy ( NGT ) , 30 impaired glucose-tolerant ( IGT ) , and 31 type 2 diabetic ( T2DM ) subjects .
	manualset3
84564	4	397938	14	13	NULL	NULL	NULL	oral glucose tolerance test ( OGTT ) data of C-peptide	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given the different kinetics of the peptides , a mathematical model was necessary to analyze the oral glucose tolerance test ( OGTT ) data of insulin , C-peptide , and proinsulin in 55 healthy ( NGT ) , 30 impaired glucose-tolerant ( IGT ) , and 31 type 2 diabetic ( T2DM ) subjects .
	manualset3
84565	5	397938	14	13	NULL	0	NULL	oral glucose tolerance test ( OGTT ) data of proinsulin	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the different kinetics of the peptides , a mathematical model was necessary to analyze the oral glucose tolerance test ( OGTT ) data of insulin , C-peptide , and proinsulin in 55 healthy ( NGT ) , 30 impaired glucose-tolerant ( IGT ) , and 31 type 2 diabetic ( T2DM ) subjects .
	manualset3
84566	6	397938	14	13	NULL	0	NULL	55	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the different kinetics of the peptides , a mathematical model was necessary to analyze the oral glucose tolerance test ( OGTT ) data of insulin , C-peptide , and proinsulin in 55 healthy ( NGT ) , 30 impaired glucose-tolerant ( IGT ) , and 31 type 2 diabetic ( T2DM ) subjects .
	manualset3
84567	7	397938	14	13	NULL	0	NULL	healthy ( NGT ) subjects	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the different kinetics of the peptides , a mathematical model was necessary to analyze the oral glucose tolerance test ( OGTT ) data of insulin , C-peptide , and proinsulin in 55 healthy ( NGT ) , 30 impaired glucose-tolerant ( IGT ) , and 31 type 2 diabetic ( T2DM ) subjects .
	manualset3
84568	8	397938	14	13	NULL	0	NULL	30	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the different kinetics of the peptides , a mathematical model was necessary to analyze the oral glucose tolerance test ( OGTT ) data of insulin , C-peptide , and proinsulin in 55 healthy ( NGT ) , 30 impaired glucose-tolerant ( IGT ) , and 31 type 2 diabetic ( T2DM ) subjects .
	manualset3
84569	9	397938	14	13	NULL	0	NULL	impaired glucose-tolerant ( IGT ) subjects 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the different kinetics of the peptides , a mathematical model was necessary to analyze the oral glucose tolerance test ( OGTT ) data of insulin , C-peptide , and proinsulin in 55 healthy ( NGT ) , 30 impaired glucose-tolerant ( IGT ) , and 31 type 2 diabetic ( T2DM ) subjects .
	manualset3
84570	10	397938	14	13	NULL	0	NULL	31	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the different kinetics of the peptides , a mathematical model was necessary to analyze the oral glucose tolerance test ( OGTT ) data of insulin , C-peptide , and proinsulin in 55 healthy ( NGT ) , 30 impaired glucose-tolerant ( IGT ) , and 31 type 2 diabetic ( T2DM ) subjects .
	manualset3
84571	11	397938	14	13	NULL	0	NULL	type 2 diabetic ( T2DM ) subjects	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the different kinetics of the peptides , a mathematical model was necessary to analyze the oral glucose tolerance test ( OGTT ) data of insulin , C-peptide , and proinsulin in 55 healthy ( NGT ) , 30 impaired glucose-tolerant ( IGT ) , and 31 type 2 diabetic ( T2DM ) subjects .
	manualset3
84572	1	397939	14	13	NULL	0	NULL	CALLA 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the fact that CALLA is completely modulated on the surface of lymphoid cells , we have employed pre-embedding immunogold techniques at electron-microscopical level and demonstrated that J5 monoclonal antibody ( MoAb ) - mediated modulation of CALLA expression on the lymphoblastic cell line NALM-6 is a specific , rapid process , closely resembling receptor-mediated endocytosis .
	manualset3
84573	2	397939	14	13	NULL	0	NULL	surface of lymphoid cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the fact that CALLA is completely modulated on the surface of lymphoid cells , we have employed pre-embedding immunogold techniques at electron-microscopical level and demonstrated that J5 monoclonal antibody ( MoAb ) - mediated modulation of CALLA expression on the lymphoblastic cell line NALM-6 is a specific , rapid process , closely resembling receptor-mediated endocytosis .
	manualset3
84574	3	397939	14	13	NULL	NULL	NULL	pre-embedding immunogold techniques  at electron-microscopical level	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given the fact that CALLA is completely modulated on the surface of lymphoid cells , we have employed pre-embedding immunogold techniques at electron-microscopical level and demonstrated that J5 monoclonal antibody ( MoAb ) - mediated modulation of CALLA expression on the lymphoblastic cell line NALM-6 is a specific , rapid process , closely resembling receptor-mediated endocytosis .
	manualset3
84575	4	397939	14	13	NULL	0	NULL	J5 monoclonal antibody ( MoAb ) 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the fact that CALLA is completely modulated on the surface of lymphoid cells , we have employed pre-embedding immunogold techniques at electron-microscopical level and demonstrated that J5 monoclonal antibody ( MoAb ) - mediated modulation of CALLA expression on the lymphoblastic cell line NALM-6 is a specific , rapid process , closely resembling receptor-mediated endocytosis .
	manualset3
84576	5	397939	14	13	NULL	0	NULL	CALLA expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the fact that CALLA is completely modulated on the surface of lymphoid cells , we have employed pre-embedding immunogold techniques at electron-microscopical level and demonstrated that J5 monoclonal antibody ( MoAb ) - mediated modulation of CALLA expression on the lymphoblastic cell line NALM-6 is a specific , rapid process , closely resembling receptor-mediated endocytosis .
	manualset3
84577	6	397939	14	13	NULL	0	NULL	lymphoblastic cell line NALM-6	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the fact that CALLA is completely modulated on the surface of lymphoid cells , we have employed pre-embedding immunogold techniques at electron-microscopical level and demonstrated that J5 monoclonal antibody ( MoAb ) - mediated modulation of CALLA expression on the lymphoblastic cell line NALM-6 is a specific , rapid process , closely resembling receptor-mediated endocytosis .
	manualset3
84578	7	397939	14	13	NULL	0	NULL	receptor-mediated endocytosis	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the fact that CALLA is completely modulated on the surface of lymphoid cells , we have employed pre-embedding immunogold techniques at electron-microscopical level and demonstrated that J5 monoclonal antibody ( MoAb ) - mediated modulation of CALLA expression on the lymphoblastic cell line NALM-6 is a specific , rapid process , closely resembling receptor-mediated endocytosis .
	manualset3
84580	2	397940	14	13	NULL	NULL	NULL	health care	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given the imbalances and inefficiencies of market forces in health care , perverse incentives that have strengthened resistance to change , and secrecy when it comes to adverse event information , however , it is likely that policy initiatives will continue to play an important role in the transformation of the industry to more highly reliable , safer levels of care .
	manualset3
84677	3	397940	14	13	NULL	0	NULL	safer levels of care 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the imbalances and inefficiencies of market forces in health care , perverse incentives that have strengthened resistance to change , and secrecy when it comes to adverse event information , however , it is likely that policy initiatives will continue to play an important role in the transformation of the industry to more highly reliable , safer levels of care .
	manualset3
84678	4	397940	14	13	NULL	0	NULL	industry	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the imbalances and inefficiencies of market forces in health care , perverse incentives that have strengthened resistance to change , and secrecy when it comes to adverse event information , however , it is likely that policy initiatives will continue to play an important role in the transformation of the industry to more highly reliable , safer levels of care .
	manualset3
84773	1	397940	14	13	NULL	0	NULL	transformation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the imbalances and inefficiencies of market forces in health care , perverse incentives that have strengthened resistance to change , and secrecy when it comes to adverse event information , however , it is likely that policy initiatives will continue to play an important role in the transformation of the industry to more highly reliable , safer levels of care .
	manualset3
84581	1	397941	14	13	NULL	0	NULL	urolithiasis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the influence of the composition of the urolithiasis for its treatment , we must insist on the collection of the greater number of samples for its analysis , although the epidemiologic data and the study of the urinary sediment can be used in the practice .
	manualset3
84582	2	397941	14	13	NULL	0	NULL	samples	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the influence of the composition of the urolithiasis for its treatment , we must insist on the collection of the greater number of samples for its analysis , although the epidemiologic data and the study of the urinary sediment can be used in the practice .
	manualset3
84583	3	397941	14	13	NULL	0	NULL	 analysis 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the influence of the composition of the urolithiasis for its treatment , we must insist on the collection of the greater number of samples for its analysis , although the epidemiologic data and the study of the urinary sediment can be used in the practice .
	manualset3
84584	4	397941	14	13	NULL	0	NULL	 treatment 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the influence of the composition of the urolithiasis for its treatment , we must insist on the collection of the greater number of samples for its analysis , although the epidemiologic data and the study of the urinary sediment can be used in the practice .
	manualset3
84585	5	397941	14	13	NULL	0	NULL	epidemiologic data 	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the influence of the composition of the urolithiasis for its treatment , we must insist on the collection of the greater number of samples for its analysis , although the epidemiologic data and the study of the urinary sediment can be used in the practice .
	manualset3
84586	6	397941	14	13	NULL	0	NULL	study of the urinary sediment 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the influence of the composition of the urolithiasis for its treatment , we must insist on the collection of the greater number of samples for its analysis , although the epidemiologic data and the study of the urinary sediment can be used in the practice .
	manualset3
84587	1	397942	14	13	NULL	NULL	NULL	Patient Protection and Affordable Care Act ( PPACA ) 	PublishedSourceOfInformation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given the passage of the Patient Protection and Affordable Care Act ( PPACA ) of 2010 , researchers and policy makers must agree on the model that best monitors and evaluates these new policy initiatives .
	manualset3
84588	2	397942	14	13	NULL	0	NULL	2010	TimePoint												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the passage of the Patient Protection and Affordable Care Act ( PPACA ) of 2010 , researchers and policy makers must agree on the model that best monitors and evaluates these new policy initiatives .
	manualset3
84589	3	397942	14	13	NULL	0	NULL	researchers 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the passage of the Patient Protection and Affordable Care Act ( PPACA ) of 2010 , researchers and policy makers must agree on the model that best monitors and evaluates these new policy initiatives .
	manualset3
84590	4	397942	14	13	NULL	0	NULL	policy makers	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the passage of the Patient Protection and Affordable Care Act ( PPACA ) of 2010 , researchers and policy makers must agree on the model that best monitors and evaluates these new policy initiatives .
	manualset3
84591	5	397942	14	13	NULL	0	NULL	model	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the passage of the Patient Protection and Affordable Care Act ( PPACA ) of 2010 , researchers and policy makers must agree on the model that best monitors and evaluates these new policy initiatives .
	manualset3
84592	6	397942	14	13	NULL	0	NULL	new policy initiatives	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the passage of the Patient Protection and Affordable Care Act ( PPACA ) of 2010 , researchers and policy makers must agree on the model that best monitors and evaluates these new policy initiatives .
	manualset3
84593	1	397943	14	13	NULL	0	NULL	glycyphyllin	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the reported level of activity it is unlikely that glycyphyllin would provide direct antioxidant protection in tissues affected by oxidative stress .
	manualset3
84594	2	397943	14	13	NULL	0	NULL	antioxidant protection	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the reported level of activity it is unlikely that glycyphyllin would provide direct antioxidant protection in tissues affected by oxidative stress .
	manualset3
84595	3	397943	14	13	NULL	0	NULL	tissues	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the reported level of activity it is unlikely that glycyphyllin would provide direct antioxidant protection in tissues affected by oxidative stress .
	manualset3
84596	4	397943	14	13	NULL	0	NULL	oxidative stress	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Given the reported level of activity it is unlikely that glycyphyllin would provide direct antioxidant protection in tissues affected by oxidative stress .
	manualset3
84597	1	397944	14	13	NULL	0	NULL	wide variety of disease states	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Given their roles in such a wide variety of disease states , protein kinases are rapidly becoming extremely attractive targets for drug discovery , probably second only to heterotrimeric G protein-coupled receptors ( eg , angiotensin II ) .
	manualset3
84598	2	397944	14	13	NULL	NULL	NULL	protein kinases	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given their roles in such a wide variety of disease states , protein kinases are rapidly becoming extremely attractive targets for drug discovery , probably second only to heterotrimeric G protein-coupled receptors ( eg , angiotensin II ) .
	manualset3
84599	3	397944	14	13	NULL	NULL	NULL	attractive targets	LaboratoryExperimentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given their roles in such a wide variety of disease states , protein kinases are rapidly becoming extremely attractive targets for drug discovery , probably second only to heterotrimeric G protein-coupled receptors ( eg , angiotensin II ) .
	manualset3
84600	4	397944	14	13	NULL	0	NULL	drug discovery	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Given their roles in such a wide variety of disease states , protein kinases are rapidly becoming extremely attractive targets for drug discovery , probably second only to heterotrimeric G protein-coupled receptors ( eg , angiotensin II ) .
	manualset3
84601	5	397944	14	13	NULL	NULL	NULL	heterotrimeric G protein-coupled receptors	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Given their roles in such a wide variety of disease states , protein kinases are rapidly becoming extremely attractive targets for drug discovery , probably second only to heterotrimeric G protein-coupled receptors ( eg , angiotensin II ) .
	manualset3
84602	6	397944	14	13	NULL	0	NULL	angiotensin II 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Given their roles in such a wide variety of disease states , protein kinases are rapidly becoming extremely attractive targets for drug discovery , probably second only to heterotrimeric G protein-coupled receptors ( eg , angiotensin II ) .
	manualset3
84603	1	397945	14	13	NULL	0	NULL	Glasses	Thing												NULL		0	NULL	NULL	NULL	NULL	NULL	Glasses with a large laser effect : Nd-phosphate and Nd-fluorophosphate .
	manualset3
84604	2	397945	14	13	NULL	0	NULL	Nd-phosphate	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Glasses with a large laser effect : Nd-phosphate and Nd-fluorophosphate .
	manualset3
84605	3	397945	14	13	NULL	0	NULL	Nd-fluorophosphate	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Glasses with a large laser effect : Nd-phosphate and Nd-fluorophosphate .
	manualset3
84606	1	397946	14	13	NULL	0	NULL	Glatiramer acetate-specific T cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Glatiramer acetate-specific T cells in the brain express T helper 2/3 cytokines and brain-derived neurotrophic factor in situ .
	manualset3
84607	2	397946	14	13	NULL	0	NULL	brain	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Glatiramer acetate-specific T cells in the brain express T helper 2/3 cytokines and brain-derived neurotrophic factor in situ .
	manualset3
84608	3	397946	14	13	NULL	NULL	NULL	T helper 2/3 cytokines	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glatiramer acetate-specific T cells in the brain express T helper 2/3 cytokines and brain-derived neurotrophic factor in situ .
	manualset3
84610	4	397946	14	13	NULL	NULL	NULL	brain-derived neurotrophic factor 	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glatiramer acetate-specific T cells in the brain express T helper 2/3 cytokines and brain-derived neurotrophic factor in situ .
	manualset3
84611	1	397947	14	13	NULL	0	NULL	Glaucoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Glaucoma in the developing world .
	manualset3
84612	2	397947	14	13	NULL	0	NULL	developing world	GeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Glaucoma in the developing world .
	manualset3
84613	1	397948	14	13	NULL	0	NULL	GlcN	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	GlcN completely abolished glycogen synthesis in the liver .
	manualset3
84614	2	397948	14	13	NULL	0	NULL	glycogen synthesis 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	GlcN completely abolished glycogen synthesis in the liver .
	manualset3
84615	3	397948	14	13	NULL	0	NULL	liver 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	GlcN completely abolished glycogen synthesis in the liver .
	manualset3
84616	1	397949	14	13	NULL	NULL	NULL	Gleason grade	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gleason grade has been linked to a number of clinical end points , including clinical stage , progression to metastatic disease , and survival .
	manualset3
84617	2	397949	14	13	NULL	0	NULL	clinical end points	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gleason grade has been linked to a number of clinical end points , including clinical stage , progression to metastatic disease , and survival .
	manualset3
84618	3	397949	14	13	NULL	0	NULL	clinical stage	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gleason grade has been linked to a number of clinical end points , including clinical stage , progression to metastatic disease , and survival .
	manualset3
84619	4	397949	14	13	NULL	0	NULL	progression to metastatic disease	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gleason grade has been linked to a number of clinical end points , including clinical stage , progression to metastatic disease , and survival .
	manualset3
84620	6	397949	14	13	NULL	0	NULL	survival 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gleason grade has been linked to a number of clinical end points , including clinical stage , progression to metastatic disease , and survival .
	manualset3
84621	1	397950	14	13	NULL	0	NULL	Glenohumeral range of motion deficits	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Glenohumeral range of motion deficits and posterior shoulder tightness in throwers with pathologic internal impingement .
	manualset3
84622	2	397950	14	13	NULL	0	NULL	posterior shoulder tightness	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Glenohumeral range of motion deficits and posterior shoulder tightness in throwers with pathologic internal impingement .
	manualset3
84623	3	397950	14	13	NULL	0	NULL	 throwers	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Glenohumeral range of motion deficits and posterior shoulder tightness in throwers with pathologic internal impingement .
	manualset3
84624	4	397950	14	13	NULL	0	NULL	pathologic internal impingement	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Glenohumeral range of motion deficits and posterior shoulder tightness in throwers with pathologic internal impingement .
	manualset3
84625	1	397951	14	13	NULL	NULL	NULL	Gli/Ci proteins	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gli/Ci proteins possess a nuclear localization signal ( NLS ) and a nuclear export signal ( NES ) , both of which are key signatures for controlling nucleocytoplasmic shuttling .
	manualset3
84626	2	397951	14	13	NULL	0	NULL	nuclear localization signal ( NLS )	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gli/Ci proteins possess a nuclear localization signal ( NLS ) and a nuclear export signal ( NES ) , both of which are key signatures for controlling nucleocytoplasmic shuttling .
	manualset3
84627	3	397951	14	13	NULL	0	NULL	nuclear export signal ( NES )	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gli/Ci proteins possess a nuclear localization signal ( NLS ) and a nuclear export signal ( NES ) , both of which are key signatures for controlling nucleocytoplasmic shuttling .
	manualset3
84629	4	397951	14	13	NULL	NULL	NULL	nucleocytoplasmic shuttling	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gli/Ci proteins possess a nuclear localization signal ( NLS ) and a nuclear export signal ( NES ) , both of which are key signatures for controlling nucleocytoplasmic shuttling .
	manualset3
84630	1	397952	14	13	NULL	0	NULL	Glibenclamide	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Glibenclamide and tetraethylammonium chloride ( TEA ) also did not influence the relaxation induced by the compounds .
	manualset3
84631	2	397952	14	13	NULL	0	NULL	tetraethylammonium chloride ( TEA )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Glibenclamide and tetraethylammonium chloride ( TEA ) also did not influence the relaxation induced by the compounds .
	manualset3
84632	3	397952	14	13	NULL	0	NULL	relaxation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Glibenclamide and tetraethylammonium chloride ( TEA ) also did not influence the relaxation induced by the compounds .
	manualset3
84633	4	397952	14	13	NULL	0	NULL	compounds	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Glibenclamide and tetraethylammonium chloride ( TEA ) also did not influence the relaxation induced by the compounds .
	manualset3
84634	1	397953	14	13	NULL	NULL	NULL	Gliomatosis cerebri is an infrequent tumor of neuroepithelial origin	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gliomatosis cerebri is an infrequent tumor of neuroepithelial origin presenting with deterioration of cognitive functions , behavioral and mental changes , motor weakness , headache , and seizures .
	manualset3
84636	3	397953	14	13	NULL	0	NULL	deterioration of cognitive functions	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gliomatosis cerebri is an infrequent tumor of neuroepithelial origin presenting with deterioration of cognitive functions , behavioral and mental changes , motor weakness , headache , and seizures .
	manualset3
84637	4	397953	14	13	NULL	NULL	NULL	behavioral and mental changes	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gliomatosis cerebri is an infrequent tumor of neuroepithelial origin presenting with deterioration of cognitive functions , behavioral and mental changes , motor weakness , headache , and seizures .
	manualset3
84638	5	397953	14	13	NULL	0	NULL	motor weakness	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gliomatosis cerebri is an infrequent tumor of neuroepithelial origin presenting with deterioration of cognitive functions , behavioral and mental changes , motor weakness , headache , and seizures .
	manualset3
84639	6	397953	14	13	NULL	0	NULL	headache	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gliomatosis cerebri is an infrequent tumor of neuroepithelial origin presenting with deterioration of cognitive functions , behavioral and mental changes , motor weakness , headache , and seizures .
	manualset3
84640	7	397953	14	13	NULL	0	NULL	seizures	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gliomatosis cerebri is an infrequent tumor of neuroepithelial origin presenting with deterioration of cognitive functions , behavioral and mental changes , motor weakness , headache , and seizures .
	manualset3
84641	1	397954	14	13	NULL	0	NULL	Gliotoxin	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Gliotoxin stimulates the apoptosis of human and rat hepatic stellate cells and enhances the resolution of liver fibrosis in rats .
	manualset3
84642	2	397954	14	13	NULL	NULL	NULL	apoptosis 	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gliotoxin stimulates the apoptosis of human and rat hepatic stellate cells and enhances the resolution of liver fibrosis in rats .
	manualset3
84643	3	397954	14	13	NULL	NULL	NULL	human hepatic stellate cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gliotoxin stimulates the apoptosis of human and rat hepatic stellate cells and enhances the resolution of liver fibrosis in rats .
	manualset3
84644	4	397954	14	13	NULL	0	NULL	rat hepatic stellate cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Gliotoxin stimulates the apoptosis of human and rat hepatic stellate cells and enhances the resolution of liver fibrosis in rats .
	manualset3
84645	5	397954	14	13	NULL	0	NULL	liver fibrosis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gliotoxin stimulates the apoptosis of human and rat hepatic stellate cells and enhances the resolution of liver fibrosis in rats .
	manualset3
84646	6	397954	14	13	NULL	0	NULL	 rats 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Gliotoxin stimulates the apoptosis of human and rat hepatic stellate cells and enhances the resolution of liver fibrosis in rats .
	manualset3
84647	1	397955	14	13	NULL	0	NULL	Global analysis of the variations	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Global analysis of the variations introduced on pyridine , pyrimidine and thiazole rings of this tricyclic system showed an increases of diuretic and natriuretic activities when the formal charge on N9a and C9b increases .
	manualset3
84648	2	397955	14	13	NULL	0	NULL	pyridine	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Global analysis of the variations introduced on pyridine , pyrimidine and thiazole rings of this tricyclic system showed an increases of diuretic and natriuretic activities when the formal charge on N9a and C9b increases .
	manualset3
84649	3	397955	14	13	NULL	0	NULL	pyrimidine	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Global analysis of the variations introduced on pyridine , pyrimidine and thiazole rings of this tricyclic system showed an increases of diuretic and natriuretic activities when the formal charge on N9a and C9b increases .
	manualset3
84650	4	397955	14	13	NULL	0	NULL	thiazole rings 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Global analysis of the variations introduced on pyridine , pyrimidine and thiazole rings of this tricyclic system showed an increases of diuretic and natriuretic activities when the formal charge on N9a and C9b increases .
	manualset3
84651	5	397955	14	13	NULL	NULL	NULL	N9a	Atom												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Global analysis of the variations introduced on pyridine , pyrimidine and thiazole rings of this tricyclic system showed an increases of diuretic and natriuretic activities when the formal charge on N9a and C9b increases .
	manualset3
84652	6	397955	14	13	NULL	NULL	NULL	C9b	Atom												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Global analysis of the variations introduced on pyridine , pyrimidine and thiazole rings of this tricyclic system showed an increases of diuretic and natriuretic activities when the formal charge on N9a and C9b increases .
	manualset3
84653	7	397955	14	13	NULL	0	NULL	diuretic activities	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Global analysis of the variations introduced on pyridine , pyrimidine and thiazole rings of this tricyclic system showed an increases of diuretic and natriuretic activities when the formal charge on N9a and C9b increases .
	manualset3
84654	8	397955	14	13	NULL	0	NULL	natriuretic activities	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Global analysis of the variations introduced on pyridine , pyrimidine and thiazole rings of this tricyclic system showed an increases of diuretic and natriuretic activities when the formal charge on N9a and C9b increases .
	manualset3
84655	1	397956	14	13	NULL	0	NULL	Global cooling	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Global cooling after the eruption of Mount Pinatubo : a test of climate feedback by water vapor .
	manualset3
84656	2	397956	14	13	NULL	0	NULL	eruption	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Global cooling after the eruption of Mount Pinatubo : a test of climate feedback by water vapor .
	manualset3
84657	3	397956	14	13	NULL	0	NULL	Mount Pinatubo	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Global cooling after the eruption of Mount Pinatubo : a test of climate feedback by water vapor .
	manualset3
84658	4	397956	14	13	NULL	0	NULL	climate	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Global cooling after the eruption of Mount Pinatubo : a test of climate feedback by water vapor .
	manualset3
84659	5	397956	14	13	NULL	0	NULL	water vapor 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Global cooling after the eruption of Mount Pinatubo : a test of climate feedback by water vapor .
	manualset3
84660	1	397957	14	13	NULL	0	NULL	Global left ventricular wall motion	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Global left ventricular wall motion in patients with persisting or resolved thrombus was similar during follow-up .
	manualset3
84661	2	397957	14	13	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Global left ventricular wall motion in patients with persisting or resolved thrombus was similar during follow-up .
	manualset3
84662	3	397957	14	13	NULL	0	NULL	persisting or resolved thrombus	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Global left ventricular wall motion in patients with persisting or resolved thrombus was similar during follow-up .
	manualset3
84663	4	397957	14	13	NULL	0	NULL	follow-up	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Global left ventricular wall motion in patients with persisting or resolved thrombus was similar during follow-up .
	manualset3
84664	1	397958	14	13	NULL	0	NULL	Global parsimony analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Global parsimony analysis recovers a monophyletic Bradoriida as the sister group to crown crustaceans .
	manualset3
84665	2	397958	14	13	NULL	0	NULL	monophyletic Bradoriida 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Global parsimony analysis recovers a monophyletic Bradoriida as the sister group to crown crustaceans .
	manualset3
84666	3	397958	14	13	NULL	0	NULL	sister group	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Global parsimony analysis recovers a monophyletic Bradoriida as the sister group to crown crustaceans .
	manualset3
84667	4	397958	14	13	NULL	0	NULL	crown crustaceans	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Global parsimony analysis recovers a monophyletic Bradoriida as the sister group to crown crustaceans .
	manualset3
84668	1	397959	14	13	NULL	0	NULL	Global theory	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Global theory and the nature of risk , Part I. How orthodox managed care stifles innovation .
	manualset3
84671	3	397959	14	13	NULL	NULL	NULL	orthodox	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Global theory and the nature of risk , Part I. How orthodox managed care stifles innovation .
	manualset3
84673	1	397960	14	13	NULL	NULL	NULL	Global Quality of Life	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Global Quality of Life slightly improved after masitinib therapy and did not predicted depression improvement .
	manualset3
84675	2	397960	14	13	NULL	NULL	NULL	masitinib therapy	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Global Quality of Life slightly improved after masitinib therapy and did not predicted depression improvement .
	manualset3
84676	3	397960	14	13	NULL	NULL	NULL	depression improvement 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Global Quality of Life slightly improved after masitinib therapy and did not predicted depression improvement .
	manualset3
84679	1	397961	14	13	NULL	0	NULL	 diagnosis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Some problems in the diagnosis , treatment and prevention of ischemic heart disease ) .
	manualset3
84680	2	397961	14	13	NULL	0	NULL	treatment 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Some problems in the diagnosis , treatment and prevention of ischemic heart disease ) .
	manualset3
84681	3	397961	14	13	NULL	0	NULL	prevention	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Some problems in the diagnosis , treatment and prevention of ischemic heart disease ) .
	manualset3
84682	4	397961	14	13	NULL	0	NULL	 ischemic heart disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Some problems in the diagnosis , treatment and prevention of ischemic heart disease ) .
	manualset3
84689	1	397963	14	13	NULL	0	NULL	Glomerular charge and size selectivity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Glomerular charge and size selectivity assessed by changes in salt intake in type 2 diabetic patients .
	manualset3
84690	2	397963	14	13	NULL	NULL	NULL	salt intake	Food												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glomerular charge and size selectivity assessed by changes in salt intake in type 2 diabetic patients .
	manualset3
84691	4	397963	14	13	NULL	NULL	NULL	 type 2 diabetic patients	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glomerular charge and size selectivity assessed by changes in salt intake in type 2 diabetic patients .
	manualset3
84693	1	397964	14	13	NULL	0	NULL	Glucagon-induced changes	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucagon-induced changes in fructose 2 , 6-bisphosphate and 6-phosphofructo-2-kinase in cultured rat foetal hepatocytes .
	manualset3
84694	2	397964	14	13	NULL	NULL	NULL	fructose 2 , 6-bisphosphate	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glucagon-induced changes in fructose 2 , 6-bisphosphate and 6-phosphofructo-2-kinase in cultured rat foetal hepatocytes .
	manualset3
84695	3	397964	14	13	NULL	0	NULL	6-phosphofructo-2-kinase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucagon-induced changes in fructose 2 , 6-bisphosphate and 6-phosphofructo-2-kinase in cultured rat foetal hepatocytes .
	manualset3
84696	4	397964	14	13	NULL	0	NULL	cultured rat foetal hepatocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucagon-induced changes in fructose 2 , 6-bisphosphate and 6-phosphofructo-2-kinase in cultured rat foetal hepatocytes .
	manualset3
84697	1	397965	14	13	NULL	NULL	NULL	Glucocorticoids 	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glucocorticoids , the end-products of the hypothalamic-pituitary - adrenal ( HPA ) axis , influence the functions of virtually all organs and tissues through the nuclear glucocorticoid receptor ( GR ) .
	manualset3
84698	2	397965	14	13	NULL	0	NULL	hypothalamic-pituitary - adrenal ( HPA ) axis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucocorticoids , the end-products of the hypothalamic-pituitary - adrenal ( HPA ) axis , influence the functions of virtually all organs and tissues through the nuclear glucocorticoid receptor ( GR ) .
	manualset3
84700	3	397965	14	13	NULL	NULL	NULL	 functions of virtually all organs and tissues 	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glucocorticoids , the end-products of the hypothalamic-pituitary - adrenal ( HPA ) axis , influence the functions of virtually all organs and tissues through the nuclear glucocorticoid receptor ( GR ) .
	manualset3
84702	4	397965	14	13	NULL	NULL	NULL	nuclear glucocorticoid receptor ( GR ) 	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glucocorticoids , the end-products of the hypothalamic-pituitary - adrenal ( HPA ) axis , influence the functions of virtually all organs and tissues through the nuclear glucocorticoid receptor ( GR ) .
	manualset3
84703	1	397966	14	13	NULL	NULL	NULL	Glucocorticoids	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glucocorticoids acting through the glucocorticoid receptor ( GR ) inhibit TNF-induced lethal inflammation .
	manualset3
84704	2	397966	14	13	NULL	0	NULL	glucocorticoid receptor ( GR ) 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucocorticoids acting through the glucocorticoid receptor ( GR ) inhibit TNF-induced lethal inflammation .
	manualset3
84705	3	397966	14	13	NULL	NULL	NULL	TNF-induced lethal inflammation	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glucocorticoids acting through the glucocorticoid receptor ( GR ) inhibit TNF-induced lethal inflammation .
	manualset3
84707	1	397967	14	13	NULL	NULL	NULL	Glucose	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glucose and xylose were co-utilized , and transport studies suggested that there was a common transport system for both sugars .
	manualset3
84708	2	397967	14	13	NULL	NULL	NULL	xylose	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glucose and xylose were co-utilized , and transport studies suggested that there was a common transport system for both sugars .
	manualset3
84709	3	397967	14	13	NULL	0	NULL	transport studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucose and xylose were co-utilized , and transport studies suggested that there was a common transport system for both sugars .
	manualset3
84710	4	397967	14	13	NULL	0	NULL	common transport system	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucose and xylose were co-utilized , and transport studies suggested that there was a common transport system for both sugars .
	manualset3
84711	5	397967	14	13	NULL	NULL	NULL	both sugars	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glucose and xylose were co-utilized , and transport studies suggested that there was a common transport system for both sugars .
	manualset3
84712	1	397968	14	13	NULL	NULL	NULL	Glucose 	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glucose had no such effect , although this carbohydrate and L-proline were transported in similar fashions .
	manualset3
84713	2	397968	14	13	NULL	NULL	NULL	carbohydrate	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glucose had no such effect , although this carbohydrate and L-proline were transported in similar fashions .
	manualset3
84714	3	397968	14	13	NULL	NULL	NULL	L-proline	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glucose had no such effect , although this carbohydrate and L-proline were transported in similar fashions .
	manualset3
84715	4	397968	14	13	NULL	0	NULL	 transported in similar fashions	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucose had no such effect , although this carbohydrate and L-proline were transported in similar fashions .
	manualset3
84716	1	397969	14	13	NULL	0	NULL	Glucose intolerance	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucose intolerance was associated with the risk of gallstones independent of obesity .
	manualset3
84717	2	397969	14	13	NULL	0	NULL	risk of gallstones	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucose intolerance was associated with the risk of gallstones independent of obesity .
	manualset3
84718	3	397969	14	13	NULL	0	NULL	obesity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucose intolerance was associated with the risk of gallstones independent of obesity .
	manualset3
84719	1	397970	14	13	NULL	0	NULL	Glucose metabolism	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucose metabolism , which was also studied for the plaque samples , was not significantly affected by presence of any of the 2 detergents , indicating that the amounts of xylitol in toothpastes were presumably too low to give clinical significant effects , even when mild detergents are used .
	manualset3
84720	2	397970	14	13	NULL	0	NULL	plaque samples	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucose metabolism , which was also studied for the plaque samples , was not significantly affected by presence of any of the 2 detergents , indicating that the amounts of xylitol in toothpastes were presumably too low to give clinical significant effects , even when mild detergents are used .
	manualset3
84721	3	397970	14	13	NULL	0	NULL	2	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucose metabolism , which was also studied for the plaque samples , was not significantly affected by presence of any of the 2 detergents , indicating that the amounts of xylitol in toothpastes were presumably too low to give clinical significant effects , even when mild detergents are used .
	manualset3
84722	4	397970	14	13	NULL	0	NULL	detergents	Thing												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucose metabolism , which was also studied for the plaque samples , was not significantly affected by presence of any of the 2 detergents , indicating that the amounts of xylitol in toothpastes were presumably too low to give clinical significant effects , even when mild detergents are used .
	manualset3
84723	5	397970	14	13	NULL	0	NULL	xylitol	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucose metabolism , which was also studied for the plaque samples , was not significantly affected by presence of any of the 2 detergents , indicating that the amounts of xylitol in toothpastes were presumably too low to give clinical significant effects , even when mild detergents are used .
	manualset3
84724	6	397970	14	13	NULL	0	NULL	toothpastes	Thing												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucose metabolism , which was also studied for the plaque samples , was not significantly affected by presence of any of the 2 detergents , indicating that the amounts of xylitol in toothpastes were presumably too low to give clinical significant effects , even when mild detergents are used .
	manualset3
84726	8	397970	14	13	NULL	NULL	NULL	clinical significant effects 	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glucose metabolism , which was also studied for the plaque samples , was not significantly affected by presence of any of the 2 detergents , indicating that the amounts of xylitol in toothpastes were presumably too low to give clinical significant effects , even when mild detergents are used .
	manualset3
84727	9	397970	14	13	NULL	0	NULL	mild detergents	Thing												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucose metabolism , which was also studied for the plaque samples , was not significantly affected by presence of any of the 2 detergents , indicating that the amounts of xylitol in toothpastes were presumably too low to give clinical significant effects , even when mild detergents are used .
	manualset3
84729	1	397971	14	13	NULL	NULL	NULL	study 	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Some progress in study on mind and brain ) .
	manualset3
84730	2	397971	14	13	NULL	NULL	NULL	mind	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Some progress in study on mind and brain ) .
	manualset3
84731	3	397971	14	13	NULL	NULL	NULL	brain	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Some progress in study on mind and brain ) .
	manualset3
84732	1	397972	14	13	NULL	0	NULL	Glucose tolerance	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucose tolerance improved after the barley meal , with the peak OGTT plasma glucose concentration being 0.7 mmol/L lower than that after the rice meal ( 7.7 + / - 0.4 v 8.4 + / - 0.3 mmol/L , P & lt ; .05 ) .
	manualset3
84733	2	397972	14	13	NULL	0	NULL	barley meal	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucose tolerance improved after the barley meal , with the peak OGTT plasma glucose concentration being 0.7 mmol/L lower than that after the rice meal ( 7.7 + / - 0.4 v 8.4 + / - 0.3 mmol/L , P & lt ; .05 ) .
	manualset3
84734	3	397972	14	13	NULL	0	NULL	peak OGTT plasma glucose concentration 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucose tolerance improved after the barley meal , with the peak OGTT plasma glucose concentration being 0.7 mmol/L lower than that after the rice meal ( 7.7 + / - 0.4 v 8.4 + / - 0.3 mmol/L , P & lt ; .05 ) .
	manualset3
84735	4	397972	14	13	NULL	0	NULL	0.7 mmol/L 	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucose tolerance improved after the barley meal , with the peak OGTT plasma glucose concentration being 0.7 mmol/L lower than that after the rice meal ( 7.7 + / - 0.4 v 8.4 + / - 0.3 mmol/L , P & lt ; .05 ) .
	manualset3
84736	5	397972	14	13	NULL	0	NULL	rice meal	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	Glucose tolerance improved after the barley meal , with the peak OGTT plasma glucose concentration being 0.7 mmol/L lower than that after the rice meal ( 7.7 + / - 0.4 v 8.4 + / - 0.3 mmol/L , P & lt ; .05 ) .
	manualset3
84737	6	397972	14	13	NULL	NULL	NULL	7.7 + / - 0.4 v 8.4 + / - 0.3 mmol/L , P & lt ; .05 	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glucose tolerance improved after the barley meal , with the peak OGTT plasma glucose concentration being 0.7 mmol/L lower than that after the rice meal ( 7.7 + / - 0.4 v 8.4 + / - 0.3 mmol/L , P & lt ; .05 ) .
	manualset3
84738	1	397973	14	13	NULL	0	NULL	Glutamate-gated channels 	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate-gated channels mediate fundamental brain processes , yet the mechanisms by which the neurotransmitter controls channel activation are incompletely understood .
	manualset3
84739	2	397973	14	13	NULL	0	NULL	fundamental brain processes	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate-gated channels mediate fundamental brain processes , yet the mechanisms by which the neurotransmitter controls channel activation are incompletely understood .
	manualset3
84740	3	397973	14	13	NULL	0	NULL	mechanisms 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate-gated channels mediate fundamental brain processes , yet the mechanisms by which the neurotransmitter controls channel activation are incompletely understood .
	manualset3
84741	4	397973	14	13	NULL	0	NULL	neurotransmitter controls channel activation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate-gated channels mediate fundamental brain processes , yet the mechanisms by which the neurotransmitter controls channel activation are incompletely understood .
	manualset3
84742	1	397974	14	13	NULL	0	NULL	Glutamate dehydrogenase ( GDH ) 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate dehydrogenase ( GDH ) is a homohexameric enzyme that catalyzes the reversible oxidative deamination of l-glutamate to 2-oxoglutarate .
	manualset3
84743	2	397974	14	13	NULL	0	NULL	homohexameric enzyme	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate dehydrogenase ( GDH ) is a homohexameric enzyme that catalyzes the reversible oxidative deamination of l-glutamate to 2-oxoglutarate .
	manualset3
84744	3	397974	14	13	NULL	NULL	NULL	reversible oxidative deamination	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glutamate dehydrogenase ( GDH ) is a homohexameric enzyme that catalyzes the reversible oxidative deamination of l-glutamate to 2-oxoglutarate .
	manualset3
84745	4	397974	14	13	NULL	NULL	NULL	l-glutamate	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glutamate dehydrogenase ( GDH ) is a homohexameric enzyme that catalyzes the reversible oxidative deamination of l-glutamate to 2-oxoglutarate .
	manualset3
84746	5	397974	14	13	NULL	NULL	NULL	2-oxoglutarate	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glutamate dehydrogenase ( GDH ) is a homohexameric enzyme that catalyzes the reversible oxidative deamination of l-glutamate to 2-oxoglutarate .
	manualset3
84752	1	397976	14	13	NULL	NULL	NULL	Glutamate	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glutamate was oxidized via the tricarboxylic acid cycle .
	manualset3
84753	2	397976	14	13	NULL	0	NULL	oxidized	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate was oxidized via the tricarboxylic acid cycle .
	manualset3
84754	3	397976	14	13	NULL	0	NULL	tricarboxylic acid cycle	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamate was oxidized via the tricarboxylic acid cycle .
	manualset3
84755	1	397977	14	13	NULL	0	NULL	Glutamatergic medications	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamatergic medications for the treatment of drug and behavioral addictions .
	manualset3
84756	2	397977	14	13	NULL	0	NULL	treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamatergic medications for the treatment of drug and behavioral addictions .
	manualset3
84757	3	397977	14	13	NULL	0	NULL	drug and behavioral addictions	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Glutamatergic medications for the treatment of drug and behavioral addictions .
	manualset3
84758	1	397978	14	13	NULL	NULL	NULL	Glutathione effects	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glutathione effects on toxicity and uptake of mercuric chloride and sodium arsenite in rabbit renal cortical slices .
	manualset3
84759	2	397978	14	13	NULL	0	NULL	 toxicity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Glutathione effects on toxicity and uptake of mercuric chloride and sodium arsenite in rabbit renal cortical slices .
	manualset3
84760	3	397978	14	13	NULL	0	NULL	mercuric chloride	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Glutathione effects on toxicity and uptake of mercuric chloride and sodium arsenite in rabbit renal cortical slices .
	manualset3
84761	4	397978	14	13	NULL	0	NULL	sodium arsenite	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Glutathione effects on toxicity and uptake of mercuric chloride and sodium arsenite in rabbit renal cortical slices .
	manualset3
85429	5	397978	14	13	NULL	0	NULL	rabbit renal cortical slices	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Glutathione effects on toxicity and uptake of mercuric chloride and sodium arsenite in rabbit renal cortical slices .
	manualset3
85430	6	397978	14	13	NULL	0	NULL	uptake	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Glutathione effects on toxicity and uptake of mercuric chloride and sodium arsenite in rabbit renal cortical slices .
	manualset3
84762	1	397979	14	13	NULL	NULL	NULL	Glycan-modifying bacteria-derived soluble factors	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glycan-modifying bacteria-derived soluble factors from Bacteroides thetaiotaomicron and Lactobacillus casei inhibit rotavirus infection in human intestinal cells .
	manualset3
84763	2	397979	14	13	NULL	0	NULL	Bacteroides thetaiotaomicron	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycan-modifying bacteria-derived soluble factors from Bacteroides thetaiotaomicron and Lactobacillus casei inhibit rotavirus infection in human intestinal cells .
	manualset3
84764	3	397979	14	13	NULL	0	NULL	Lactobacillus casei	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycan-modifying bacteria-derived soluble factors from Bacteroides thetaiotaomicron and Lactobacillus casei inhibit rotavirus infection in human intestinal cells .
	manualset3
84765	4	397979	14	13	NULL	0	NULL	rotavirus infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycan-modifying bacteria-derived soluble factors from Bacteroides thetaiotaomicron and Lactobacillus casei inhibit rotavirus infection in human intestinal cells .
	manualset3
84766	5	397979	14	13	NULL	0	NULL	human intestinal cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycan-modifying bacteria-derived soluble factors from Bacteroides thetaiotaomicron and Lactobacillus casei inhibit rotavirus infection in human intestinal cells .
	manualset3
84767	1	397980	14	13	NULL	NULL	NULL	Glycans	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glycans released by peptide N-glycosidase were resolved by Bio-Gel P-4 gel filtration into two fractions : a low molecular mass mannose-rich fraction and a high molecular mass galactose and N-acetylglucosamine-rich fraction .
	manualset3
84768	2	397980	14	13	NULL	0	NULL	peptide N-glycosidase	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycans released by peptide N-glycosidase were resolved by Bio-Gel P-4 gel filtration into two fractions : a low molecular mass mannose-rich fraction and a high molecular mass galactose and N-acetylglucosamine-rich fraction .
	manualset3
84769	3	397980	14	13	NULL	0	NULL	Bio-Gel P-4 gel filtration	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycans released by peptide N-glycosidase were resolved by Bio-Gel P-4 gel filtration into two fractions : a low molecular mass mannose-rich fraction and a high molecular mass galactose and N-acetylglucosamine-rich fraction .
	manualset3
84770	4	397980	14	13	NULL	0	NULL	two fractions	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycans released by peptide N-glycosidase were resolved by Bio-Gel P-4 gel filtration into two fractions : a low molecular mass mannose-rich fraction and a high molecular mass galactose and N-acetylglucosamine-rich fraction .
	manualset3
84771	5	397980	14	13	NULL	NULL	NULL	a low molecular mass mannose-rich fraction 	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glycans released by peptide N-glycosidase were resolved by Bio-Gel P-4 gel filtration into two fractions : a low molecular mass mannose-rich fraction and a high molecular mass galactose and N-acetylglucosamine-rich fraction .
	manualset3
84772	6	397980	14	13	NULL	0	NULL	 a high molecular mass galactose and N-acetylglucosamine-rich fraction	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycans released by peptide N-glycosidase were resolved by Bio-Gel P-4 gel filtration into two fractions : a low molecular mass mannose-rich fraction and a high molecular mass galactose and N-acetylglucosamine-rich fraction .
	manualset3
84876	1	397981	14	13	NULL	0	NULL	Glycerol kinase deficiency	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycerol kinase deficiency : compartmental considerations regarding pathogenesis and clinical heterogeneity .
	manualset3
84877	2	397981	14	13	NULL	0	NULL	pathogenesis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycerol kinase deficiency : compartmental considerations regarding pathogenesis and clinical heterogeneity .
	manualset3
84878	3	397981	14	13	NULL	0	NULL	clinical heterogeneity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycerol kinase deficiency : compartmental considerations regarding pathogenesis and clinical heterogeneity .
	manualset3
84879	1	397982	14	13	NULL	0	NULL	Glycoalkaloids	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycoalkaloids are involved in the resistance of potatoes to pathogens and pests , but they also have implications for human health and nutrition .
	manualset3
84880	2	397982	14	13	NULL	NULL	NULL	resistance of potatoes	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glycoalkaloids are involved in the resistance of potatoes to pathogens and pests , but they also have implications for human health and nutrition .
	manualset3
84881	3	397982	14	13	NULL	0	NULL	pathogens	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycoalkaloids are involved in the resistance of potatoes to pathogens and pests , but they also have implications for human health and nutrition .
	manualset3
84882	4	397982	14	13	NULL	NULL	NULL	pests	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glycoalkaloids are involved in the resistance of potatoes to pathogens and pests , but they also have implications for human health and nutrition .
	manualset3
84883	5	397982	14	13	NULL	NULL	NULL	human health	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glycoalkaloids are involved in the resistance of potatoes to pathogens and pests , but they also have implications for human health and nutrition .
	manualset3
84884	6	397982	14	13	NULL	0	NULL	nutrition	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycoalkaloids are involved in the resistance of potatoes to pathogens and pests , but they also have implications for human health and nutrition .
	manualset3
84885	1	397983	14	13	NULL	NULL	NULL	Glycolipid-protein interaction	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glycolipid-protein interaction in the mechanism of signal transduction : studies with a photoactivable ganglioside analog .
	manualset3
84886	2	397983	14	13	NULL	0	NULL	mechanism of signal transduction	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycolipid-protein interaction in the mechanism of signal transduction : studies with a photoactivable ganglioside analog .
	manualset3
84887	3	397983	14	13	NULL	0	NULL	studies 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycolipid-protein interaction in the mechanism of signal transduction : studies with a photoactivable ganglioside analog .
	manualset3
84888	4	397983	14	13	NULL	0	NULL	photoactivable ganglioside analog	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycolipid-protein interaction in the mechanism of signal transduction : studies with a photoactivable ganglioside analog .
	manualset3
84889	1	397984	14	13	NULL	0	NULL	Glycolipids	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycolipids with gluco stereochemistry are the most prevalent .
	manualset3
84890	2	397984	14	13	NULL	0	NULL	gluco stereochemistry	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycolipids with gluco stereochemistry are the most prevalent .
	manualset3
84891	1	397985	14	13	NULL	0	NULL	Glycophorin A 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycophorin A is specific for the erythroid lineage of cells , and leukocytes have a major sialoglycoprotein , also called leukosialin or sialophorin .
	manualset3
84892	2	397985	14	13	NULL	0	NULL	erythroid lineage of cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycophorin A is specific for the erythroid lineage of cells , and leukocytes have a major sialoglycoprotein , also called leukosialin or sialophorin .
	manualset3
84893	3	397985	14	13	NULL	0	NULL	leukocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycophorin A is specific for the erythroid lineage of cells , and leukocytes have a major sialoglycoprotein , also called leukosialin or sialophorin .
	manualset3
84894	4	397985	14	13	NULL	0	NULL	major sialoglycoprotein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycophorin A is specific for the erythroid lineage of cells , and leukocytes have a major sialoglycoprotein , also called leukosialin or sialophorin .
	manualset3
84895	5	397985	14	13	NULL	0	NULL	leukosialin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycophorin A is specific for the erythroid lineage of cells , and leukocytes have a major sialoglycoprotein , also called leukosialin or sialophorin .
	manualset3
84896	6	397985	14	13	NULL	0	NULL	sialophorin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycophorin A is specific for the erythroid lineage of cells , and leukocytes have a major sialoglycoprotein , also called leukosialin or sialophorin .
	manualset3
84897	1	397986	14	13	NULL	0	NULL	Glycoprotein biosynthesis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycoprotein biosynthesis in liver mitochondria .
	manualset3
84898	2	397986	14	13	NULL	NULL	NULL	 liver mitochondria	CellComponent												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glycoprotein biosynthesis in liver mitochondria .
	manualset3
84899	1	397987	14	13	NULL	NULL	NULL	Glycoproteins	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glycoproteins synthesized in SCO cells are released into the ventricular CSF where they aggregate , in a highly ordered fashion , forming an elongated supramacromolecular structure known as the Reissner 's fiber ( RF ) .
	manualset3
84900	2	397987	14	13	NULL	0	NULL	SCO cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycoproteins synthesized in SCO cells are released into the ventricular CSF where they aggregate , in a highly ordered fashion , forming an elongated supramacromolecular structure known as the Reissner 's fiber ( RF ) .
	manualset3
84901	3	397987	14	13	NULL	NULL	NULL	ventricular CSF	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glycoproteins synthesized in SCO cells are released into the ventricular CSF where they aggregate , in a highly ordered fashion , forming an elongated supramacromolecular structure known as the Reissner 's fiber ( RF ) .
	manualset3
84902	4	397987	14	13	NULL	NULL	NULL	elongated supramacromolecular structure	AnatomicalPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Glycoproteins synthesized in SCO cells are released into the ventricular CSF where they aggregate , in a highly ordered fashion , forming an elongated supramacromolecular structure known as the Reissner 's fiber ( RF ) .
	manualset3
85431	5	397987	14	13	NULL	0	NULL	Reissner 's fiber ( RF )	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycoproteins synthesized in SCO cells are released into the ventricular CSF where they aggregate , in a highly ordered fashion , forming an elongated supramacromolecular structure known as the Reissner 's fiber ( RF ) .
	manualset3
84903	1	397988	14	13	NULL	0	NULL	Glycosylation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycosylation and high-level secretion of human tumor necrosis factor-beta in recombinant baculovirus-infected insect cells .
	manualset3
84904	2	397988	14	13	NULL	0	NULL	secretion	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycosylation and high-level secretion of human tumor necrosis factor-beta in recombinant baculovirus-infected insect cells .
	manualset3
84905	3	397988	14	13	NULL	0	NULL	 human tumor necrosis factor-beta	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycosylation and high-level secretion of human tumor necrosis factor-beta in recombinant baculovirus-infected insect cells .
	manualset3
84906	4	397988	14	13	NULL	0	NULL	recombinant baculovirus-infected insect cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Glycosylation and high-level secretion of human tumor necrosis factor-beta in recombinant baculovirus-infected insect cells .
	manualset3
84907	1	397989	14	13	NULL	0	NULL	GnRH	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	GnRH levels were determined at various times during an estrogen/progesterone ( E/P ) - induced LH surge .
	manualset3
84908	2	397989	14	13	NULL	NULL	NULL	estrogen/progesterone ( E/P ) - induced LH surge	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	GnRH levels were determined at various times during an estrogen/progesterone ( E/P ) - induced LH surge .
	manualset3
84910	1	397990	14	13	NULL	NULL	NULL	simple flow reactor	Facility												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Go with the flow : A simple flow reactor has been developed to accommodate highly absorbing ( RuL ( 3 ) ) ( 2 + ) photosensitizers for light-starved photoredox reactions .
	manualset3
84911	2	397990	14	13	NULL	0	NULL	( RuL ( 3 ) ) ( 2 + ) photosensitizers	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Go with the flow : A simple flow reactor has been developed to accommodate highly absorbing ( RuL ( 3 ) ) ( 2 + ) photosensitizers for light-starved photoredox reactions .
	manualset3
84912	3	397990	14	13	NULL	0	NULL	light-starved photoredox reactions	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Go with the flow : A simple flow reactor has been developed to accommodate highly absorbing ( RuL ( 3 ) ) ( 2 + ) photosensitizers for light-starved photoredox reactions .
	manualset3
84913	1	397991	14	13	NULL	0	NULL	Goals of therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Goals of therapy are different in lower risk patients than in higher risk .
	manualset3
84914	2	397991	14	13	NULL	0	NULL	lower risk patients 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Goals of therapy are different in lower risk patients than in higher risk .
	manualset3
84915	3	397991	14	13	NULL	0	NULL	higher risk patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Goals of therapy are different in lower risk patients than in higher risk .
	manualset3
84916	1	397992	14	13	NULL	0	NULL	Goals of treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Goals of treatment involve improving hypotension without excessive supine hypertension , relieving orthostatic symptoms , and improving standing time .
	manualset3
84917	2	397992	14	13	NULL	NULL	NULL	improving hypotension	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Goals of treatment involve improving hypotension without excessive supine hypertension , relieving orthostatic symptoms , and improving standing time .
	manualset3
84918	3	397992	14	13	NULL	NULL	NULL	supine hypertension	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Goals of treatment involve improving hypotension without excessive supine hypertension , relieving orthostatic symptoms , and improving standing time .
	manualset3
84919	4	397992	14	13	NULL	NULL	NULL	orthostatic symptoms	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Goals of treatment involve improving hypotension without excessive supine hypertension , relieving orthostatic symptoms , and improving standing time .
	manualset3
84920	5	397992	14	13	NULL	NULL	NULL	standing time	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Goals of treatment involve improving hypotension without excessive supine hypertension , relieving orthostatic symptoms , and improving standing time .
	manualset3
84921	1	397993	14	13	NULL	NULL	NULL	Alkaline	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Alkaline earth chelates from hydrolytically cleavable chelate constituents , I. On the calcium chelate of the N-glucoside of dimethylamino-alpha , alpha ' - dicarboxylic acid ( iminodiacetic acid ) ) .
	manualset3
84922	4	397993	14	13	NULL	NULL	NULL	hydrolytically cleavable chelate constituents	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Alkaline earth chelates from hydrolytically cleavable chelate constituents , I. On the calcium chelate of the N-glucoside of dimethylamino-alpha , alpha ' - dicarboxylic acid ( iminodiacetic acid ) ) .
	manualset3
85009	3	397993	14	13	NULL	0	NULL	calcium chelate of the N-glucoside of dimethylamino-alpha , alpha ' - dicarboxylic acid ( iminodiacetic acid ) )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( Alkaline earth chelates from hydrolytically cleavable chelate constituents , I. On the calcium chelate of the N-glucoside of dimethylamino-alpha , alpha ' - dicarboxylic acid ( iminodiacetic acid ) ) .
	manualset3
85270	2	397993	14	13	NULL	0	NULL	chelates	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( Alkaline earth chelates from hydrolytically cleavable chelate constituents , I. On the calcium chelate of the N-glucoside of dimethylamino-alpha , alpha ' - dicarboxylic acid ( iminodiacetic acid ) ) .
	manualset3
85010	1	397994	14	13	NULL	0	NULL	Spectrophotometric determination	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Spectrophotometric determination of tabletted allacil , methylthiouracil and hexamidine ) .
	manualset3
85011	2	397994	14	13	NULL	0	NULL	tabletted allacil	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( Spectrophotometric determination of tabletted allacil , methylthiouracil and hexamidine ) .
	manualset3
85012	3	397994	14	13	NULL	0	NULL	methylthiouracil	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( Spectrophotometric determination of tabletted allacil , methylthiouracil and hexamidine ) .
	manualset3
85013	4	397994	14	13	NULL	0	NULL	hexamidine 	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( Spectrophotometric determination of tabletted allacil , methylthiouracil and hexamidine ) .
	manualset3
85014	1	397995	14	13	NULL	0	NULL	Gold phosphides	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Gold phosphides show unique optical or semiconductor properties and there are extensive high technology applications , e.g. in laser diodes , etc. .
	manualset3
85015	2	397995	14	13	NULL	NULL	NULL	high technology applications	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gold phosphides show unique optical or semiconductor properties and there are extensive high technology applications , e.g. in laser diodes , etc. .
	manualset3
85016	3	397995	14	13	NULL	NULL	NULL	laser diodes	Facility												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gold phosphides show unique optical or semiconductor properties and there are extensive high technology applications , e.g. in laser diodes , etc. .
	manualset3
85017	1	397996	14	13	NULL	0	NULL	Gonadal dysgenesis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gonadal dysgenesis is an infrequent cause for primary amenorrhoea .
	manualset3
85018	2	397996	14	13	NULL	0	NULL	primary amenorrhoea	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gonadal dysgenesis is an infrequent cause for primary amenorrhoea .
	manualset3
85019	1	397997	14	13	NULL	NULL	NULL	Gonadal function	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gonadal function in young women with Down syndrome .
	manualset3
85020	2	397997	14	13	NULL	0	NULL	young women	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Gonadal function in young women with Down syndrome .
	manualset3
85021	3	397997	14	13	NULL	0	NULL	Down syndrome	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gonadal function in young women with Down syndrome .
	manualset3
85022	1	397998	14	13	NULL	0	NULL	Gonadosomatic index ( GSI )	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gonadosomatic index ( GSI ) , sperm quality , plasma sex steroids ( 11-keto testosterone ( 11-KT ) ; testosterone ( T ) ; estradiol-17beta ( E2 ) ) were evaluated on 10 to 24 fish fed on each diet .
	manualset3
85023	2	397998	14	13	NULL	0	NULL	sperm quality	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gonadosomatic index ( GSI ) , sperm quality , plasma sex steroids ( 11-keto testosterone ( 11-KT ) ; testosterone ( T ) ; estradiol-17beta ( E2 ) ) were evaluated on 10 to 24 fish fed on each diet .
	manualset3
85024	3	397998	14	13	NULL	0	NULL	 plasma sex steroids ( 11-keto testosterone ( 11-KT ) ; testosterone ( T ) ; estradiol-17beta ( E2 ) )	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Gonadosomatic index ( GSI ) , sperm quality , plasma sex steroids ( 11-keto testosterone ( 11-KT ) ; testosterone ( T ) ; estradiol-17beta ( E2 ) ) were evaluated on 10 to 24 fish fed on each diet .
	manualset3
85025	4	397998	14	13	NULL	NULL	NULL	10 to 24	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gonadosomatic index ( GSI ) , sperm quality , plasma sex steroids ( 11-keto testosterone ( 11-KT ) ; testosterone ( T ) ; estradiol-17beta ( E2 ) ) were evaluated on 10 to 24 fish fed on each diet .
	manualset3
85026	5	397998	14	13	NULL	NULL	NULL	fish fed on each diet 	Food												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gonadosomatic index ( GSI ) , sperm quality , plasma sex steroids ( 11-keto testosterone ( 11-KT ) ; testosterone ( T ) ; estradiol-17beta ( E2 ) ) were evaluated on 10 to 24 fish fed on each diet .
	manualset3
85028	1	397999	14	13	NULL	0	NULL	Gonadotrophin pulsatility	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gonadotrophin pulsatility in girls with the Turner syndrome : modulation by exogenous sex steroids .
	manualset3
85029	2	397999	14	13	NULL	0	NULL	girls	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Gonadotrophin pulsatility in girls with the Turner syndrome : modulation by exogenous sex steroids .
	manualset3
85030	3	397999	14	13	NULL	0	NULL	Turner syndrome	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gonadotrophin pulsatility in girls with the Turner syndrome : modulation by exogenous sex steroids .
	manualset3
85031	4	397999	14	13	NULL	NULL	NULL	 exogenous sex steroids	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gonadotrophin pulsatility in girls with the Turner syndrome : modulation by exogenous sex steroids .
	manualset3
85432	5	397999	14	13	NULL	0	NULL	modulation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Gonadotrophin pulsatility in girls with the Turner syndrome : modulation by exogenous sex steroids .
	manualset3
85032	1	398000	14	13	NULL	0	NULL	Gonadotropin-treated ewes	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Gonadotropin-treated ewes demonstrated estrus approximately 24 h earlier than control ewes and , therefore , exhibited an accelerated estradiol-17beta surge and rise in circulating progesterone .
	manualset3
85033	2	398000	14	13	NULL	0	NULL	estrus	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Gonadotropin-treated ewes demonstrated estrus approximately 24 h earlier than control ewes and , therefore , exhibited an accelerated estradiol-17beta surge and rise in circulating progesterone .
	manualset3
85034	3	398000	14	13	NULL	0	NULL	24 h	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Gonadotropin-treated ewes demonstrated estrus approximately 24 h earlier than control ewes and , therefore , exhibited an accelerated estradiol-17beta surge and rise in circulating progesterone .
	manualset3
85035	4	398000	14	13	NULL	0	NULL	control ewes	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Gonadotropin-treated ewes demonstrated estrus approximately 24 h earlier than control ewes and , therefore , exhibited an accelerated estradiol-17beta surge and rise in circulating progesterone .
	manualset3
85036	5	398000	14	13	NULL	0	NULL	estradiol-17beta surge	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gonadotropin-treated ewes demonstrated estrus approximately 24 h earlier than control ewes and , therefore , exhibited an accelerated estradiol-17beta surge and rise in circulating progesterone .
	manualset3
85037	6	398000	14	13	NULL	0	NULL	rise in circulating progesterone	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gonadotropin-treated ewes demonstrated estrus approximately 24 h earlier than control ewes and , therefore , exhibited an accelerated estradiol-17beta surge and rise in circulating progesterone .
	manualset3
85038	1	398001	14	13	NULL	0	NULL	103 %	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Good accuracy and recoveries of 103 % were calculated using the fast direct determination technique .
	manualset3
85039	2	398001	14	13	NULL	0	NULL	fast direct determination technique	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Good accuracy and recoveries of 103 % were calculated using the fast direct determination technique .
	manualset3
85040	1	398002	14	13	NULL	NULL	NULL	 insilico hot spot predictions	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Good agreement between the insilico hot spot predictions and the experimentally observed positions of the polar hydrogen bond forming functional groups and hydrophobic portions was obtained .
	manualset3
85041	2	398002	14	13	NULL	NULL	NULL	experimentally observed positions 	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Good agreement between the insilico hot spot predictions and the experimentally observed positions of the polar hydrogen bond forming functional groups and hydrophobic portions was obtained .
	manualset3
85042	3	398002	14	13	NULL	NULL	NULL	 polar hydrogen bond forming functional groups	Atom												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Good agreement between the insilico hot spot predictions and the experimentally observed positions of the polar hydrogen bond forming functional groups and hydrophobic portions was obtained .
	manualset3
85436	4	398002	14	13	NULL	0	NULL	hydrophobic portions	Atom												NULL		0	NULL	NULL	NULL	NULL	NULL	Good agreement between the insilico hot spot predictions and the experimentally observed positions of the polar hydrogen bond forming functional groups and hydrophobic portions was obtained .
	manualset3
85044	1	398003	14	13	NULL	0	NULL	Good birth	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Good birth and infertility : a long-awaited homebirth .
	manualset3
85045	2	398003	14	13	NULL	0	NULL	infertility	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Good birth and infertility : a long-awaited homebirth .
	manualset3
85046	3	398003	14	13	NULL	0	NULL	 a long-awaited homebirth	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Good birth and infertility : a long-awaited homebirth .
	manualset3
85047	1	398004	14	13	NULL	NULL	NULL	Spermatozoal granuloma	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Spermatozoal granuloma as a possible cause of hydrocele ) .
	manualset3
85048	2	398004	14	13	NULL	0	NULL	hydrocele	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Spermatozoal granuloma as a possible cause of hydrocele ) .
	manualset3
85049	1	398005	14	13	NULL	0	NULL	Good communication skills	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Good communication skills and sensitivity are essential to discuss the patient 's needs and preferences and suggest solutions that are safe and legally defensible .
	manualset3
85050	2	398005	14	13	NULL	0	NULL	sensitivity	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Good communication skills and sensitivity are essential to discuss the patient 's needs and preferences and suggest solutions that are safe and legally defensible .
	manualset3
85051	3	398005	14	13	NULL	NULL	NULL	patient 's needs	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Good communication skills and sensitivity are essential to discuss the patient 's needs and preferences and suggest solutions that are safe and legally defensible .
	manualset3
85052	4	398005	14	13	NULL	NULL	NULL	solutions	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Good communication skills and sensitivity are essential to discuss the patient 's needs and preferences and suggest solutions that are safe and legally defensible .
	manualset3
85053	1	398006	14	13	NULL	0	NULL	Good computer	Thing												NULL		0	NULL	NULL	NULL	NULL	NULL	Good computer -- bad computer .
	manualset3
85054	2	398006	14	13	NULL	0	NULL	bad computer	Thing												NULL		0	NULL	NULL	NULL	NULL	NULL	Good computer -- bad computer .
	manualset3
85055	1	398007	14	13	NULL	NULL	NULL	Good cycle control	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Good cycle control and effective contraception was achieved with the two LNG preparations , however , the cycle control results were less favorable with EE/NET 20/500 .
	manualset3
85056	2	398007	14	13	NULL	NULL	NULL	effective contraception	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Good cycle control and effective contraception was achieved with the two LNG preparations , however , the cycle control results were less favorable with EE/NET 20/500 .
	manualset3
85057	3	398007	14	13	NULL	0	NULL	two	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Good cycle control and effective contraception was achieved with the two LNG preparations , however , the cycle control results were less favorable with EE/NET 20/500 .
	manualset3
85058	4	398007	14	13	NULL	0	NULL	LNG preparations	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Good cycle control and effective contraception was achieved with the two LNG preparations , however , the cycle control results were less favorable with EE/NET 20/500 .
	manualset3
85059	5	398007	14	13	NULL	NULL	NULL	cycle control results 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Good cycle control and effective contraception was achieved with the two LNG preparations , however , the cycle control results were less favorable with EE/NET 20/500 .
	manualset3
85060	6	398007	14	13	NULL	0	NULL	EE/NET 20/500	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Good cycle control and effective contraception was achieved with the two LNG preparations , however , the cycle control results were less favorable with EE/NET 20/500 .
	manualset3
85061	1	398008	14	13	NULL	0	NULL	data	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Good precision is obtained when data are acquired for approximately 1 min per sample .
	manualset3
85062	2	398008	14	13	NULL	0	NULL	1 min per sample	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Good precision is obtained when data are acquired for approximately 1 min per sample .
	manualset3
85063	1	398009	14	13	NULL	NULL	NULL	Good recoveries ( 72-129 % )	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Good recoveries ( 72-129 % ) , and low limits of detection ( 0.4-5 .5 ng L ( -1 ) ) and quantification ( 1.1-18 .2 ng L ( -1 ) ) were achieved for all selected pesticides .
	manualset3
85064	2	398009	14	13	NULL	0	NULL	low limits of detection ( 0.4-5 .5 ng L ( -1 ) )	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Good recoveries ( 72-129 % ) , and low limits of detection ( 0.4-5 .5 ng L ( -1 ) ) and quantification ( 1.1-18 .2 ng L ( -1 ) ) were achieved for all selected pesticides .
	manualset3
85065	3	398009	14	13	NULL	0	NULL	quantification ( 1.1-18 .2 ng L ( -1 ) )	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Good recoveries ( 72-129 % ) , and low limits of detection ( 0.4-5 .5 ng L ( -1 ) ) and quantification ( 1.1-18 .2 ng L ( -1 ) ) were achieved for all selected pesticides .
	manualset3
85066	4	398009	14	13	NULL	0	NULL	all selected pesticides	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Good recoveries ( 72-129 % ) , and low limits of detection ( 0.4-5 .5 ng L ( -1 ) ) and quantification ( 1.1-18 .2 ng L ( -1 ) ) were achieved for all selected pesticides .
	manualset3
85067	1	398010	14	13	NULL	0	NULL	Good staining	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Good staining was obtained with ethanol - , glutaraldehyde - , or Carnoy 's - fixed material but not with formalin or Bouin 's fixation .
	manualset3
85068	2	398010	14	13	NULL	NULL	NULL	ethanol -fixed material	Tissue												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Good staining was obtained with ethanol - , glutaraldehyde - , or Carnoy 's - fixed material but not with formalin or Bouin 's fixation .
	manualset3
85069	3	398010	14	13	NULL	0	NULL	glutaraldehyde -fixed material 	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Good staining was obtained with ethanol - , glutaraldehyde - , or Carnoy 's - fixed material but not with formalin or Bouin 's fixation .
	manualset3
85070	4	398010	14	13	NULL	0	NULL	Carnoy 's - fixed material	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Good staining was obtained with ethanol - , glutaraldehyde - , or Carnoy 's - fixed material but not with formalin or Bouin 's fixation .
	manualset3
85071	5	398010	14	13	NULL	0	NULL	formalin fixation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Good staining was obtained with ethanol - , glutaraldehyde - , or Carnoy 's - fixed material but not with formalin or Bouin 's fixation .
	manualset3
85072	6	398010	14	13	NULL	0	NULL	Bouin 's fixation 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Good staining was obtained with ethanol - , glutaraldehyde - , or Carnoy 's - fixed material but not with formalin or Bouin 's fixation .
	manualset3
85073	1	398011	14	13	NULL	0	NULL	Goodpasture 's original article	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Goodpasture 's original article is reviewed with particular reference to the possible etiological relationship of influenza virus infection and the subsequent development of this strange , poorly understood disorder .
	manualset3
85075	2	398011	14	13	NULL	NULL	NULL	influenza virus infection	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Goodpasture 's original article is reviewed with particular reference to the possible etiological relationship of influenza virus infection and the subsequent development of this strange , poorly understood disorder .
	manualset3
85076	3	398011	14	13	NULL	NULL	NULL	disorder	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Goodpasture 's original article is reviewed with particular reference to the possible etiological relationship of influenza virus infection and the subsequent development of this strange , poorly understood disorder .
	manualset3
85077	1	398012	14	13	NULL	0	NULL	Gout 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Gout in the geriatric patient is a disease affecting women , commonly associated with diuretic usage , often involves the fingers , may be complicated by the development of masses of uric acid crystals ( tophi ) in soft tissues , and is frequently polyarticular .
	manualset3
85078	2	398012	14	13	NULL	0	NULL	geriatric patient	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Gout in the geriatric patient is a disease affecting women , commonly associated with diuretic usage , often involves the fingers , may be complicated by the development of masses of uric acid crystals ( tophi ) in soft tissues , and is frequently polyarticular .
	manualset3
85079	3	398012	14	13	NULL	0	NULL	women	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Gout in the geriatric patient is a disease affecting women , commonly associated with diuretic usage , often involves the fingers , may be complicated by the development of masses of uric acid crystals ( tophi ) in soft tissues , and is frequently polyarticular .
	manualset3
85080	4	398012	14	13	NULL	0	NULL	diuretic usage	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Gout in the geriatric patient is a disease affecting women , commonly associated with diuretic usage , often involves the fingers , may be complicated by the development of masses of uric acid crystals ( tophi ) in soft tissues , and is frequently polyarticular .
	manualset3
85081	5	398012	14	13	NULL	0	NULL	fingers	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Gout in the geriatric patient is a disease affecting women , commonly associated with diuretic usage , often involves the fingers , may be complicated by the development of masses of uric acid crystals ( tophi ) in soft tissues , and is frequently polyarticular .
	manualset3
85082	6	398012	14	13	NULL	0	NULL	development of masses of uric acid crystals ( tophi )	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gout in the geriatric patient is a disease affecting women , commonly associated with diuretic usage , often involves the fingers , may be complicated by the development of masses of uric acid crystals ( tophi ) in soft tissues , and is frequently polyarticular .
	manualset3
85083	7	398012	14	13	NULL	0	NULL	soft tissues	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Gout in the geriatric patient is a disease affecting women , commonly associated with diuretic usage , often involves the fingers , may be complicated by the development of masses of uric acid crystals ( tophi ) in soft tissues , and is frequently polyarticular .
	manualset3
85084	8	398012	14	13	NULL	0	NULL	polyarticular 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gout in the geriatric patient is a disease affecting women , commonly associated with diuretic usage , often involves the fingers , may be complicated by the development of masses of uric acid crystals ( tophi ) in soft tissues , and is frequently polyarticular .
	manualset3
85085	1	398013	14	13	NULL	0	NULL	Spontaneous rupture of the ureter	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Spontaneous rupture of the ureter caused by metastatic ureteric tumor : a case report ) .
	manualset3
85086	2	398013	14	13	NULL	0	NULL	metastatic ureteric tumor	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Spontaneous rupture of the ureter caused by metastatic ureteric tumor : a case report ) .
	manualset3
85087	3	398013	14	13	NULL	0	NULL	a case report	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	( Spontaneous rupture of the ureter caused by metastatic ureteric tumor : a case report ) .
	manualset3
85088	1	398014	14	13	NULL	0	NULL	Governmental policy statements	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Governmental policy statements on population : an inventory .
	manualset3
85089	2	398014	14	13	NULL	0	NULL	population	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Governmental policy statements on population : an inventory .
	manualset3
85090	1	398015	14	13	NULL	0	NULL	Graded intravenous infusions of vasopressin	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Graded intravenous infusions of vasopressin induced greater increases in MABP and mesenteric vascular resistance and a greater decrease in mesenteric blood flow in males .
	manualset3
85091	2	398015	14	13	NULL	0	NULL	greater increases in MABP	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Graded intravenous infusions of vasopressin induced greater increases in MABP and mesenteric vascular resistance and a greater decrease in mesenteric blood flow in males .
	manualset3
85092	3	398015	14	13	NULL	0	NULL	mesenteric vascular resistance	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Graded intravenous infusions of vasopressin induced greater increases in MABP and mesenteric vascular resistance and a greater decrease in mesenteric blood flow in males .
	manualset3
85093	4	398015	14	13	NULL	0	NULL	greater decrease in mesenteric blood flow	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Graded intravenous infusions of vasopressin induced greater increases in MABP and mesenteric vascular resistance and a greater decrease in mesenteric blood flow in males .
	manualset3
85094	5	398015	14	13	NULL	0	NULL	males	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Graded intravenous infusions of vasopressin induced greater increases in MABP and mesenteric vascular resistance and a greater decrease in mesenteric blood flow in males .
	manualset3
85095	1	398016	14	13	NULL	0	NULL	Graded responsibility and autonomy	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Graded responsibility and autonomy are integral features of medical education .
	manualset3
85096	2	398016	14	13	NULL	NULL	NULL	medical education	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Graded responsibility and autonomy are integral features of medical education .
	manualset3
85097	1	398017	14	13	NULL	NULL	NULL	Gradual facial palsy	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gradual facial palsy and intrapetrous internal carotid aneurysm : a case report .
	manualset3
85098	2	398017	14	13	NULL	NULL	NULL	intrapetrous internal carotid aneurysm	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gradual facial palsy and intrapetrous internal carotid aneurysm : a case report .
	manualset3
85099	3	398017	14	13	NULL	0	NULL	a case report	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Gradual facial palsy and intrapetrous internal carotid aneurysm : a case report .
	manualset3
85100	1	398018	14	13	NULL	0	NULL	Graft thrombogenicity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Graft thrombogenicity was assessed by changes in platelet function , isotope labeled platelet studies and scanning electron microscopy .
	manualset3
85101	2	398018	14	13	NULL	NULL	NULL	changes in platelet function	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Graft thrombogenicity was assessed by changes in platelet function , isotope labeled platelet studies and scanning electron microscopy .
	manualset3
85102	3	398018	14	13	NULL	0	NULL	isotope labeled platelet studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Graft thrombogenicity was assessed by changes in platelet function , isotope labeled platelet studies and scanning electron microscopy .
	manualset3
85103	4	398018	14	13	NULL	0	NULL	 scanning electron microscopy	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	Graft thrombogenicity was assessed by changes in platelet function , isotope labeled platelet studies and scanning electron microscopy .
	manualset3
85104	1	398019	14	13	NULL	0	NULL	Graft versus host disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Graft versus host disease-dependent decreases in salivary IgA levels were sought in labial gland saliva samples from bone marrow transplant recipients .
	manualset3
85105	2	398019	14	13	NULL	0	NULL	salivary IgA levels	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Graft versus host disease-dependent decreases in salivary IgA levels were sought in labial gland saliva samples from bone marrow transplant recipients .
	manualset3
85106	3	398019	14	13	NULL	0	NULL	labial gland saliva samples	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Graft versus host disease-dependent decreases in salivary IgA levels were sought in labial gland saliva samples from bone marrow transplant recipients .
	manualset3
85107	4	398019	14	13	NULL	0	NULL	bone marrow transplant recipients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Graft versus host disease-dependent decreases in salivary IgA levels were sought in labial gland saliva samples from bone marrow transplant recipients .
	manualset3
85108	1	398020	14	13	NULL	0	NULL	Graft versus host disease ( GVHD ) 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Graft versus host disease ( GVHD ) is one of the obstacles encountered in allogeneic bone marrow transplantation ( alloBMT ) and has a direct impact on the transplant outcome and survival .
	manualset3
85109	2	398020	14	13	NULL	0	NULL	allogeneic bone marrow transplantation ( alloBMT ) 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Graft versus host disease ( GVHD ) is one of the obstacles encountered in allogeneic bone marrow transplantation ( alloBMT ) and has a direct impact on the transplant outcome and survival .
	manualset3
85110	3	398020	14	13	NULL	0	NULL	 transplant outcome and survival 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Graft versus host disease ( GVHD ) is one of the obstacles encountered in allogeneic bone marrow transplantation ( alloBMT ) and has a direct impact on the transplant outcome and survival .
	manualset3
85111	1	398021	14	13	NULL	0	NULL	Gram-positive bacteria	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Gram-positive bacteria and fungus accounted for 22.1 % ( 25/113 ) and 21.2 % ( 24/113 ) of the isolated strains , respectively .
	manualset3
85112	2	398021	14	13	NULL	NULL	NULL	fungus	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gram-positive bacteria and fungus accounted for 22.1 % ( 25/113 ) and 21.2 % ( 24/113 ) of the isolated strains , respectively .
	manualset3
85113	3	398021	14	13	NULL	0	NULL	22.1 % ( 25/113 )	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gram-positive bacteria and fungus accounted for 22.1 % ( 25/113 ) and 21.2 % ( 24/113 ) of the isolated strains , respectively .
	manualset3
85114	4	398021	14	13	NULL	0	NULL	21.2 % ( 24/113 )	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gram-positive bacteria and fungus accounted for 22.1 % ( 25/113 ) and 21.2 % ( 24/113 ) of the isolated strains , respectively .
	manualset3
85115	5	398021	14	13	NULL	0	NULL	isolated strains	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Gram-positive bacteria and fungus accounted for 22.1 % ( 25/113 ) and 21.2 % ( 24/113 ) of the isolated strains , respectively .
	manualset3
85116	1	398022	14	13	NULL	0	NULL	Gram-positive bloodstream infections	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gram-positive bloodstream infections in liver transplant recipients : incidence , risk factors , and impact on survival .
	manualset3
85117	2	398022	14	13	NULL	0	NULL	liver transplant recipients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Gram-positive bloodstream infections in liver transplant recipients : incidence , risk factors , and impact on survival .
	manualset3
85118	3	398022	14	13	NULL	0	NULL	 incidence	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gram-positive bloodstream infections in liver transplant recipients : incidence , risk factors , and impact on survival .
	manualset3
85119	4	398022	14	13	NULL	0	NULL	risk factors 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gram-positive bloodstream infections in liver transplant recipients : incidence , risk factors , and impact on survival .
	manualset3
85120	5	398022	14	13	NULL	0	NULL	impact on survival 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gram-positive bloodstream infections in liver transplant recipients : incidence , risk factors , and impact on survival .
	manualset3
85121	1	398023	14	13	NULL	0	NULL	Gram negative diplococci 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Gram negative diplococci grown on selective media and which are catalase , oxidase , DNase , nitrate reduction positive , glucose , maltose , sucrose and lactose fermentation negative , were diagnosed as M. catarrhalis .
	manualset3
85122	3	398023	14	13	NULL	NULL	NULL	catalase	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gram negative diplococci grown on selective media and which are catalase , oxidase , DNase , nitrate reduction positive , glucose , maltose , sucrose and lactose fermentation negative , were diagnosed as M. catarrhalis .
	manualset3
85124	4	398023	14	13	NULL	NULL	NULL	oxidase	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gram negative diplococci grown on selective media and which are catalase , oxidase , DNase , nitrate reduction positive , glucose , maltose , sucrose and lactose fermentation negative , were diagnosed as M. catarrhalis .
	manualset3
85126	2	398023	14	13	NULL	NULL	NULL	DNase	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gram negative diplococci grown on selective media and which are catalase , oxidase , DNase , nitrate reduction positive , glucose , maltose , sucrose and lactose fermentation negative , were diagnosed as M. catarrhalis .
	manualset3
85127	5	398023	14	13	NULL	NULL	NULL	nitrate	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gram negative diplococci grown on selective media and which are catalase , oxidase , DNase , nitrate reduction positive , glucose , maltose , sucrose and lactose fermentation negative , were diagnosed as M. catarrhalis .
	manualset3
85128	6	398023	14	13	NULL	NULL	NULL	glucose 	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gram negative diplococci grown on selective media and which are catalase , oxidase , DNase , nitrate reduction positive , glucose , maltose , sucrose and lactose fermentation negative , were diagnosed as M. catarrhalis .
	manualset3
85129	7	398023	14	13	NULL	NULL	NULL	maltose	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gram negative diplococci grown on selective media and which are catalase , oxidase , DNase , nitrate reduction positive , glucose , maltose , sucrose and lactose fermentation negative , were diagnosed as M. catarrhalis .
	manualset3
85130	8	398023	14	13	NULL	NULL	NULL	sucrose	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gram negative diplococci grown on selective media and which are catalase , oxidase , DNase , nitrate reduction positive , glucose , maltose , sucrose and lactose fermentation negative , were diagnosed as M. catarrhalis .
	manualset3
85131	9	398023	14	13	NULL	NULL	NULL	lactose	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Gram negative diplococci grown on selective media and which are catalase , oxidase , DNase , nitrate reduction positive , glucose , maltose , sucrose and lactose fermentation negative , were diagnosed as M. catarrhalis .
	manualset3
85132	10	398023	14	13	NULL	0	NULL	M. catarrhalis	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Gram negative diplococci grown on selective media and which are catalase , oxidase , DNase , nitrate reduction positive , glucose , maltose , sucrose and lactose fermentation negative , were diagnosed as M. catarrhalis .
	manualset3
85133	1	398024	14	13	NULL	0	NULL	 Spread of excitation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Spread of excitation from the ventromedial hypothalamus to the limbic-reticular structure of the brain ) .
	manualset3
85134	2	398024	14	13	NULL	0	NULL	ventromedial hypothalamus	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( Spread of excitation from the ventromedial hypothalamus to the limbic-reticular structure of the brain ) .
	manualset3
85135	3	398024	14	13	NULL	0	NULL	limbic-reticular structure of the brain	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( Spread of excitation from the ventromedial hypothalamus to the limbic-reticular structure of the brain ) .
	manualset3
85136	1	398025	14	13	NULL	0	NULL	Grammar	Language												NULL		0	NULL	NULL	NULL	NULL	NULL	Grammar and syntax for UVAL-MED are defined and its features as a language-independent tool are discussed .
	manualset3
85137	2	398025	14	13	NULL	0	NULL	syntax	Language												NULL		0	NULL	NULL	NULL	NULL	NULL	Grammar and syntax for UVAL-MED are defined and its features as a language-independent tool are discussed .
	manualset3
85138	3	398025	14	13	NULL	0	NULL	UVAL-MED	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Grammar and syntax for UVAL-MED are defined and its features as a language-independent tool are discussed .
	manualset3
85139	4	398025	14	13	NULL	0	NULL	language-independent tool	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Grammar and syntax for UVAL-MED are defined and its features as a language-independent tool are discussed .
	manualset3
85140	1	398026	14	13	NULL	0	NULL	Granular acute lymphoblastic leukemia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Granular acute lymphoblastic leukemia in an adult patient .
	manualset3
85141	2	398026	14	13	NULL	NULL	NULL	adult patient	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Granular acute lymphoblastic leukemia in an adult patient .
	manualset3
85142	1	398027	14	13	NULL	0	NULL	Granulocyte antibodies	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Granulocyte antibodies are important in the pathogenesis of neonatal granulocytopenia , in some varieties of idiopathic granulocytopenia , and in transfusion reactions , particularly since the development of leukocyte transfusion therapy for granulocytopenic patients .
	manualset3
85143	2	398027	14	13	NULL	0	NULL	pathogenesis of neonatal granulocytopenia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Granulocyte antibodies are important in the pathogenesis of neonatal granulocytopenia , in some varieties of idiopathic granulocytopenia , and in transfusion reactions , particularly since the development of leukocyte transfusion therapy for granulocytopenic patients .
	manualset3
85144	3	398027	14	13	NULL	NULL	NULL	idiopathic granulocytopenia	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Granulocyte antibodies are important in the pathogenesis of neonatal granulocytopenia , in some varieties of idiopathic granulocytopenia , and in transfusion reactions , particularly since the development of leukocyte transfusion therapy for granulocytopenic patients .
	manualset3
85145	4	398027	14	13	NULL	NULL	NULL	 transfusion reactions 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Granulocyte antibodies are important in the pathogenesis of neonatal granulocytopenia , in some varieties of idiopathic granulocytopenia , and in transfusion reactions , particularly since the development of leukocyte transfusion therapy for granulocytopenic patients .
	manualset3
85146	5	398027	14	13	NULL	NULL	NULL	leukocyte transfusion therapy	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Granulocyte antibodies are important in the pathogenesis of neonatal granulocytopenia , in some varieties of idiopathic granulocytopenia , and in transfusion reactions , particularly since the development of leukocyte transfusion therapy for granulocytopenic patients .
	manualset3
85147	6	398027	14	13	NULL	0	NULL	granulocytopenic patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Granulocyte antibodies are important in the pathogenesis of neonatal granulocytopenia , in some varieties of idiopathic granulocytopenia , and in transfusion reactions , particularly since the development of leukocyte transfusion therapy for granulocytopenic patients .
	manualset3
85148	1	398028	14	13	NULL	0	NULL	Granulocyte macrophage colony-stimulating factor ( GM-CSF )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Granulocyte macrophage colony-stimulating factor ( GM-CSF ) has been shown to be an effective vaccine adjuvant because it enhances antigen processing and presentation by dendritic cells .
	manualset3
85149	2	398028	14	13	NULL	0	NULL	effective vaccine adjuvant	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Granulocyte macrophage colony-stimulating factor ( GM-CSF ) has been shown to be an effective vaccine adjuvant because it enhances antigen processing and presentation by dendritic cells .
	manualset3
85150	3	398028	14	13	NULL	0	NULL	antigen processing and presentation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Granulocyte macrophage colony-stimulating factor ( GM-CSF ) has been shown to be an effective vaccine adjuvant because it enhances antigen processing and presentation by dendritic cells .
	manualset3
85151	4	398028	14	13	NULL	0	NULL	dendritic cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Granulocyte macrophage colony-stimulating factor ( GM-CSF ) has been shown to be an effective vaccine adjuvant because it enhances antigen processing and presentation by dendritic cells .
	manualset3
85152	1	398029	14	13	NULL	0	NULL	Granulocytic sarcoma ( chloroma )	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Granulocytic sarcoma ( chloroma ) is a rare solid tumor of myelogenous stem cells , usually appearing in patients with acute myelogenous leukemia and less commonly in patients with chronic myelogenous leukemia or myeloproliferative disorders .
	manualset3
85153	2	398029	14	13	NULL	NULL	NULL	rare solid tumor	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Granulocytic sarcoma ( chloroma ) is a rare solid tumor of myelogenous stem cells , usually appearing in patients with acute myelogenous leukemia and less commonly in patients with chronic myelogenous leukemia or myeloproliferative disorders .
	manualset3
85154	3	398029	14	13	NULL	0	NULL	myelogenous stem cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Granulocytic sarcoma ( chloroma ) is a rare solid tumor of myelogenous stem cells , usually appearing in patients with acute myelogenous leukemia and less commonly in patients with chronic myelogenous leukemia or myeloproliferative disorders .
	manualset3
85155	4	398029	14	13	NULL	0	NULL	patients 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Granulocytic sarcoma ( chloroma ) is a rare solid tumor of myelogenous stem cells , usually appearing in patients with acute myelogenous leukemia and less commonly in patients with chronic myelogenous leukemia or myeloproliferative disorders .
	manualset3
85156	5	398029	14	13	NULL	0	NULL	acute myelogenous leukemia 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Granulocytic sarcoma ( chloroma ) is a rare solid tumor of myelogenous stem cells , usually appearing in patients with acute myelogenous leukemia and less commonly in patients with chronic myelogenous leukemia or myeloproliferative disorders .
	manualset3
85157	6	398029	14	13	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Granulocytic sarcoma ( chloroma ) is a rare solid tumor of myelogenous stem cells , usually appearing in patients with acute myelogenous leukemia and less commonly in patients with chronic myelogenous leukemia or myeloproliferative disorders .
	manualset3
85158	7	398029	14	13	NULL	0	NULL	chronic myelogenous leukemia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Granulocytic sarcoma ( chloroma ) is a rare solid tumor of myelogenous stem cells , usually appearing in patients with acute myelogenous leukemia and less commonly in patients with chronic myelogenous leukemia or myeloproliferative disorders .
	manualset3
85159	8	398029	14	13	NULL	0	NULL	myeloproliferative disorders	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Granulocytic sarcoma ( chloroma ) is a rare solid tumor of myelogenous stem cells , usually appearing in patients with acute myelogenous leukemia and less commonly in patients with chronic myelogenous leukemia or myeloproliferative disorders .
	manualset3
85160	1	398030	14	13	NULL	0	NULL	Granulocytic sarcoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Granulocytic sarcoma of the testis .
	manualset3
85161	2	398030	14	13	NULL	0	NULL	testis 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Granulocytic sarcoma of the testis .
	manualset3
83290	1	398031	5	NULL	NULL	0	NULL	Graves ' disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Graves ' disease also resolved but without specific treatment with either antithyroid drugs or radioactive iodine .
	manualset3
83291	2	398031	5	NULL	NULL	0	NULL	specific treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Graves ' disease also resolved but without specific treatment with either antithyroid drugs or radioactive iodine .
	manualset3
83292	3	398031	5	NULL	NULL	0	NULL	antithyroid drugs	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Graves ' disease also resolved but without specific treatment with either antithyroid drugs or radioactive iodine .
	manualset3
83293	4	398031	5	NULL	NULL	0	NULL	radioactive iodine	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Graves ' disease also resolved but without specific treatment with either antithyroid drugs or radioactive iodine .
	manualset3
83294	1	398032	5	NULL	NULL	0	NULL	time savings	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Greater autonomy and time savings ) .
	manualset3
83295	1	398033	5	NULL	NULL	0	NULL	young	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Greater opportunities for the young and women in socioeconomic areas will tend to increase participation in decisions which will moderate fertility .
	manualset3
83296	2	398033	5	NULL	NULL	0	NULL	women	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Greater opportunities for the young and women in socioeconomic areas will tend to increase participation in decisions which will moderate fertility .
	manualset3
83297	3	398033	5	NULL	NULL	0	NULL	socioeconomic areas	UnproperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Greater opportunities for the young and women in socioeconomic areas will tend to increase participation in decisions which will moderate fertility .
	manualset3
83298	4	398033	5	NULL	NULL	0	NULL	increase participation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Greater opportunities for the young and women in socioeconomic areas will tend to increase participation in decisions which will moderate fertility .
	manualset3
83299	5	398033	5	NULL	NULL	0	NULL	decisions	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Greater opportunities for the young and women in socioeconomic areas will tend to increase participation in decisions which will moderate fertility .
	manualset3
83300	6	398033	5	NULL	NULL	0	NULL	moderate fertility	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Greater opportunities for the young and women in socioeconomic areas will tend to increase participation in decisions which will moderate fertility .
	manualset3
83301	1	398034	5	NULL	NULL	0	NULL	Greater attention	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Greater attention has been focused on the criteria for listing patients for transplantation and for allocation of organs .
	manualset3
83302	2	398034	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Greater attention has been focused on the criteria for listing patients for transplantation and for allocation of organs .
	manualset3
83303	3	398034	5	NULL	NULL	NULL	NULL	transplantation	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Greater attention has been focused on the criteria for listing patients for transplantation and for allocation of organs .
	manualset3
83304	4	398034	5	NULL	NULL	0	NULL	allocation 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Greater attention has been focused on the criteria for listing patients for transplantation and for allocation of organs .
	manualset3
83305	5	398034	5	NULL	NULL	0	NULL	organs	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Greater attention has been focused on the criteria for listing patients for transplantation and for allocation of organs .
	manualset3
83306	1	398035	5	NULL	NULL	0	NULL	Green sulfur bacteria	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Green sulfur bacteria utilize reduced inorganic sulfur compounds ( sulfide , thiosulfate , and/or sulfur ) as electron sources for their anoxygenic photosynthetic growth .
	manualset3
83307	2	398035	5	NULL	NULL	0	NULL	reduced inorganic sulfur compounds ( sulfide , thiosulfate , and/or sulfur )	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Green sulfur bacteria utilize reduced inorganic sulfur compounds ( sulfide , thiosulfate , and/or sulfur ) as electron sources for their anoxygenic photosynthetic growth .
	manualset3
83308	3	398035	5	NULL	NULL	0	NULL	electron sources	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Green sulfur bacteria utilize reduced inorganic sulfur compounds ( sulfide , thiosulfate , and/or sulfur ) as electron sources for their anoxygenic photosynthetic growth .
	manualset3
83309	4	398035	5	NULL	NULL	0	NULL	anoxygenic photosynthetic growth	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Green sulfur bacteria utilize reduced inorganic sulfur compounds ( sulfide , thiosulfate , and/or sulfur ) as electron sources for their anoxygenic photosynthetic growth .
	manualset3
83310	1	398036	5	NULL	NULL	0	NULL	Green tea consumption	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Green tea consumption tended to reduce aortic lesion formation by 31 % ( 24 + / - 3.2 % versus 35 + / - 5.7 % for control animals P = 0.11 ) , while black tea , vitamin E and beta-carotene had no effect .
	manualset3
83311	2	398036	5	NULL	NULL	0	NULL	reduce aortic lesion formation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Green tea consumption tended to reduce aortic lesion formation by 31 % ( 24 + / - 3.2 % versus 35 + / - 5.7 % for control animals P = 0.11 ) , while black tea , vitamin E and beta-carotene had no effect .
	manualset3
83312	3	398036	5	NULL	NULL	0	NULL	31 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Green tea consumption tended to reduce aortic lesion formation by 31 % ( 24 + / - 3.2 % versus 35 + / - 5.7 % for control animals P = 0.11 ) , while black tea , vitamin E and beta-carotene had no effect .
	manualset3
83313	4	398036	5	NULL	NULL	0	NULL	( 24 + / - 3.2 % versus 35 + / - 5.7 % for control animals P = 0.11 )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Green tea consumption tended to reduce aortic lesion formation by 31 % ( 24 + / - 3.2 % versus 35 + / - 5.7 % for control animals P = 0.11 ) , while black tea , vitamin E and beta-carotene had no effect .
	manualset3
83314	5	398036	5	NULL	NULL	0	NULL	black tea	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Green tea consumption tended to reduce aortic lesion formation by 31 % ( 24 + / - 3.2 % versus 35 + / - 5.7 % for control animals P = 0.11 ) , while black tea , vitamin E and beta-carotene had no effect .
	manualset3
83315	6	398036	5	NULL	NULL	0	NULL	vitamin E	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Green tea consumption tended to reduce aortic lesion formation by 31 % ( 24 + / - 3.2 % versus 35 + / - 5.7 % for control animals P = 0.11 ) , while black tea , vitamin E and beta-carotene had no effect .
	manualset3
83316	7	398036	5	NULL	NULL	0	NULL	beta-carotene	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Green tea consumption tended to reduce aortic lesion formation by 31 % ( 24 + / - 3.2 % versus 35 + / - 5.7 % for control animals P = 0.11 ) , while black tea , vitamin E and beta-carotene had no effect .
	manualset3
83317	1	398037	5	NULL	NULL	NULL	NULL	Green tea ( Camellia sinensis )	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Green tea ( Camellia sinensis ) is rich in catechins , of which ( - ) - epigallocatechin-3-gallate ( EGCG ) is the most abundant .
	manualset3
83319	2	398037	5	NULL	NULL	NULL	NULL	catechins	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Green tea ( Camellia sinensis ) is rich in catechins , of which ( - ) - epigallocatechin-3-gallate ( EGCG ) is the most abundant .
	manualset3
83320	3	398037	5	NULL	NULL	NULL	NULL	 ( - ) - epigallocatechin-3-gallate ( EGCG )	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Green tea ( Camellia sinensis ) is rich in catechins , of which ( - ) - epigallocatechin-3-gallate ( EGCG ) is the most abundant .
	manualset3
83321	1	398038	5	NULL	NULL	0	NULL	Green space	UnproperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Green space , health inequality and pregnancy .
	manualset3
83322	2	398038	5	NULL	NULL	0	NULL	health inequality	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Green space , health inequality and pregnancy .
	manualset3
83323	3	398038	5	NULL	NULL	0	NULL	pregnancy	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Green space , health inequality and pregnancy .
	manualset3
83324	1	398039	5	NULL	NULL	0	NULL	Gregory Bisson	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Gregory Bisson and Jeffrey Stringer discuss the implications of a new study showing how loss to follow-up affects the effectiveness of a public sector HIV program in Cte d'Ivoire .
	manualset3
83325	2	398039	5	NULL	NULL	0	NULL	Jeffrey Stringer	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Gregory Bisson and Jeffrey Stringer discuss the implications of a new study showing how loss to follow-up affects the effectiveness of a public sector HIV program in Cte d'Ivoire .
	manualset3
83326	3	398039	5	NULL	NULL	0	NULL	implications	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Gregory Bisson and Jeffrey Stringer discuss the implications of a new study showing how loss to follow-up affects the effectiveness of a public sector HIV program in Cte d'Ivoire .
	manualset3
83327	4	398039	5	NULL	NULL	0	NULL	new study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gregory Bisson and Jeffrey Stringer discuss the implications of a new study showing how loss to follow-up affects the effectiveness of a public sector HIV program in Cte d'Ivoire .
	manualset3
83328	5	398039	5	NULL	NULL	0	NULL	follow-up	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Gregory Bisson and Jeffrey Stringer discuss the implications of a new study showing how loss to follow-up affects the effectiveness of a public sector HIV program in Cte d'Ivoire .
	manualset3
83329	6	398039	5	NULL	NULL	0	NULL	public sector HIV program	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gregory Bisson and Jeffrey Stringer discuss the implications of a new study showing how loss to follow-up affects the effectiveness of a public sector HIV program in Cte d'Ivoire .
	manualset3
83330	7	398039	5	NULL	NULL	0	NULL	Cte d'Ivoire	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Gregory Bisson and Jeffrey Stringer discuss the implications of a new study showing how loss to follow-up affects the effectiveness of a public sector HIV program in Cte d'Ivoire .
	manualset3
83331	1	398040	5	NULL	NULL	0	NULL	Grimelius reactivity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Grimelius reactivity was identical to chromogranin immunoreactivity in all cases except that more cells in the tumors and in the normal islets were positive for chromogranin .
	manualset3
83332	2	398040	5	NULL	NULL	0	NULL	chromogranin immunoreactivity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Grimelius reactivity was identical to chromogranin immunoreactivity in all cases except that more cells in the tumors and in the normal islets were positive for chromogranin .
	manualset3
83333	3	398040	5	NULL	NULL	0	NULL	more cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Grimelius reactivity was identical to chromogranin immunoreactivity in all cases except that more cells in the tumors and in the normal islets were positive for chromogranin .
	manualset3
83334	4	398040	5	NULL	NULL	0	NULL	tumors	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Grimelius reactivity was identical to chromogranin immunoreactivity in all cases except that more cells in the tumors and in the normal islets were positive for chromogranin .
	manualset3
83335	5	398040	5	NULL	NULL	0	NULL	normal islets	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Grimelius reactivity was identical to chromogranin immunoreactivity in all cases except that more cells in the tumors and in the normal islets were positive for chromogranin .
	manualset3
83336	6	398040	5	NULL	NULL	0	NULL	chromogranin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Grimelius reactivity was identical to chromogranin immunoreactivity in all cases except that more cells in the tumors and in the normal islets were positive for chromogranin .
	manualset3
83338	1	398041	5	NULL	NULL	NULL	NULL	occlusion	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( State of the art : posture and occlusion ) .
	manualset3
83339	1	398042	5	NULL	NULL	0	NULL	Ground beef products	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	Ground beef products are susceptible to contamination with Escherichia coli O157 : H7 .
	manualset3
83340	2	398042	5	NULL	NULL	0	NULL	contamination	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Ground beef products are susceptible to contamination with Escherichia coli O157 : H7 .
	manualset3
83341	3	398042	5	NULL	NULL	0	NULL	Escherichia coli O157 : H7	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Ground beef products are susceptible to contamination with Escherichia coli O157 : H7 .
	manualset3
83342	1	398043	5	NULL	NULL	NULL	NULL	Ground glass opacification	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Ground glass opacification was present in seven , while basal honey-combing was also evident in seven patients .
	manualset3
83343	2	398043	5	NULL	NULL	0	NULL	seven	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Ground glass opacification was present in seven , while basal honey-combing was also evident in seven patients .
	manualset3
83344	3	398043	5	NULL	NULL	0	NULL	basal honey-combing	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Ground glass opacification was present in seven , while basal honey-combing was also evident in seven patients .
	manualset3
83345	4	398043	5	NULL	NULL	0	NULL	seven patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Ground glass opacification was present in seven , while basal honey-combing was also evident in seven patients .
	manualset3
83346	1	398044	5	NULL	NULL	0	NULL	Groundwater	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Groundwater contaminated with arsenic must be treated to meet stringent drinking water standards or guideline values .
	manualset3
83347	2	398044	5	NULL	NULL	0	NULL	arsenic	Atom												NULL		0	NULL	NULL	NULL	NULL	NULL	Groundwater contaminated with arsenic must be treated to meet stringent drinking water standards or guideline values .
	manualset3
83348	3	398044	5	NULL	NULL	0	NULL	stringent drinking water standards	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Groundwater contaminated with arsenic must be treated to meet stringent drinking water standards or guideline values .
	manualset3
83349	4	398044	5	NULL	NULL	0	NULL	guideline values	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Groundwater contaminated with arsenic must be treated to meet stringent drinking water standards or guideline values .
	manualset3
83350	1	398045	5	NULL	NULL	0	NULL	Group 2 and group 3 patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Group 2 and group 3 patients had higher fasting intragastric bile acid concentrations than group 1 ( p less than 0.01 in both cases ) .
	manualset3
83351	2	398045	5	NULL	NULL	0	NULL	higher fasting intragastric bile acid concentrations	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Group 2 and group 3 patients had higher fasting intragastric bile acid concentrations than group 1 ( p less than 0.01 in both cases ) .
	manualset3
83352	3	398045	5	NULL	NULL	0	NULL	group 1	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Group 2 and group 3 patients had higher fasting intragastric bile acid concentrations than group 1 ( p less than 0.01 in both cases ) .
	manualset3
83353	4	398045	5	NULL	NULL	0	NULL	 p less than 0.01	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Group 2 and group 3 patients had higher fasting intragastric bile acid concentrations than group 1 ( p less than 0.01 in both cases ) .
	manualset3
83354	1	398046	5	NULL	NULL	0	NULL	Group 3 cats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Group 3 cats demonstrated the highest detectable antibody response to the vaccine antigen as determined by ELISA and Western blot analysis .
	manualset3
83355	2	398046	5	NULL	NULL	0	NULL	highest detectable antibody response	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Group 3 cats demonstrated the highest detectable antibody response to the vaccine antigen as determined by ELISA and Western blot analysis .
	manualset3
83356	3	398046	5	NULL	NULL	0	NULL	vaccine antigen	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Group 3 cats demonstrated the highest detectable antibody response to the vaccine antigen as determined by ELISA and Western blot analysis .
	manualset3
83357	4	398046	5	NULL	NULL	0	NULL	ELISA 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Group 3 cats demonstrated the highest detectable antibody response to the vaccine antigen as determined by ELISA and Western blot analysis .
	manualset3
83358	5	398046	5	NULL	NULL	0	NULL	Western blot analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Group 3 cats demonstrated the highest detectable antibody response to the vaccine antigen as determined by ELISA and Western blot analysis .
	manualset3
83359	1	398047	5	NULL	NULL	0	NULL	mouth cavity	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( State of the mouth cavity in patients with inflammatory intestinal diseases ) .
	manualset3
83360	2	398047	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( State of the mouth cavity in patients with inflammatory intestinal diseases ) .
	manualset3
83361	3	398047	5	NULL	NULL	0	NULL	inflammatory intestinal diseases	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( State of the mouth cavity in patients with inflammatory intestinal diseases ) .
	manualset3
83362	1	398048	5	NULL	NULL	0	NULL	Group B animals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Group B animals also had improved thymic function as assessed by thymic weight , the total number of thymic lymphocytes/gland and mitogenic reactivity of thymic lymphocytes to PHA and Con A. The experiments indicate that high arginine levels in IVH solutions improve wound healing and thymic immune function following injury .
	manualset3
83363	2	398048	5	NULL	NULL	0	NULL	improved thymic function	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Group B animals also had improved thymic function as assessed by thymic weight , the total number of thymic lymphocytes/gland and mitogenic reactivity of thymic lymphocytes to PHA and Con A. The experiments indicate that high arginine levels in IVH solutions improve wound healing and thymic immune function following injury .
	manualset3
83364	3	398048	5	NULL	NULL	NULL	NULL	thymic weight	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Group B animals also had improved thymic function as assessed by thymic weight , the total number of thymic lymphocytes/gland and mitogenic reactivity of thymic lymphocytes to PHA and Con A. The experiments indicate that high arginine levels in IVH solutions improve wound healing and thymic immune function following injury .
	manualset3
83365	4	398048	5	NULL	NULL	0	NULL	total number of thymic lymphocytes/gland	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Group B animals also had improved thymic function as assessed by thymic weight , the total number of thymic lymphocytes/gland and mitogenic reactivity of thymic lymphocytes to PHA and Con A. The experiments indicate that high arginine levels in IVH solutions improve wound healing and thymic immune function following injury .
	manualset3
83366	5	398048	5	NULL	NULL	0	NULL	mitogenic reactivity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Group B animals also had improved thymic function as assessed by thymic weight , the total number of thymic lymphocytes/gland and mitogenic reactivity of thymic lymphocytes to PHA and Con A. The experiments indicate that high arginine levels in IVH solutions improve wound healing and thymic immune function following injury .
	manualset3
83367	6	398048	5	NULL	NULL	0	NULL	thymic lymphocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Group B animals also had improved thymic function as assessed by thymic weight , the total number of thymic lymphocytes/gland and mitogenic reactivity of thymic lymphocytes to PHA and Con A. The experiments indicate that high arginine levels in IVH solutions improve wound healing and thymic immune function following injury .
	manualset3
83368	7	398048	5	NULL	NULL	0	NULL	PHA	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Group B animals also had improved thymic function as assessed by thymic weight , the total number of thymic lymphocytes/gland and mitogenic reactivity of thymic lymphocytes to PHA and Con A. The experiments indicate that high arginine levels in IVH solutions improve wound healing and thymic immune function following injury .
	manualset3
83369	8	398048	5	NULL	NULL	0	NULL	Con A	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Group B animals also had improved thymic function as assessed by thymic weight , the total number of thymic lymphocytes/gland and mitogenic reactivity of thymic lymphocytes to PHA and Con A. The experiments indicate that high arginine levels in IVH solutions improve wound healing and thymic immune function following injury .
	manualset3
83370	9	398048	5	NULL	NULL	0	NULL	experiments 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Group B animals also had improved thymic function as assessed by thymic weight , the total number of thymic lymphocytes/gland and mitogenic reactivity of thymic lymphocytes to PHA and Con A. The experiments indicate that high arginine levels in IVH solutions improve wound healing and thymic immune function following injury .
	manualset3
83371	10	398048	5	NULL	NULL	0	NULL	high arginine levels	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Group B animals also had improved thymic function as assessed by thymic weight , the total number of thymic lymphocytes/gland and mitogenic reactivity of thymic lymphocytes to PHA and Con A. The experiments indicate that high arginine levels in IVH solutions improve wound healing and thymic immune function following injury .
	manualset3
83372	11	398048	5	NULL	NULL	0	NULL	IVH solutions	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Group B animals also had improved thymic function as assessed by thymic weight , the total number of thymic lymphocytes/gland and mitogenic reactivity of thymic lymphocytes to PHA and Con A. The experiments indicate that high arginine levels in IVH solutions improve wound healing and thymic immune function following injury .
	manualset3
83373	12	398048	5	NULL	NULL	0	NULL	improve wound healing	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Group B animals also had improved thymic function as assessed by thymic weight , the total number of thymic lymphocytes/gland and mitogenic reactivity of thymic lymphocytes to PHA and Con A. The experiments indicate that high arginine levels in IVH solutions improve wound healing and thymic immune function following injury .
	manualset3
83374	13	398048	5	NULL	NULL	0	NULL	thymic immune function	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Group B animals also had improved thymic function as assessed by thymic weight , the total number of thymic lymphocytes/gland and mitogenic reactivity of thymic lymphocytes to PHA and Con A. The experiments indicate that high arginine levels in IVH solutions improve wound healing and thymic immune function following injury .
	manualset3
83375	14	398048	5	NULL	NULL	0	NULL	injury	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Group B animals also had improved thymic function as assessed by thymic weight , the total number of thymic lymphocytes/gland and mitogenic reactivity of thymic lymphocytes to PHA and Con A. The experiments indicate that high arginine levels in IVH solutions improve wound healing and thymic immune function following injury .
	manualset3
83376	1	398049	5	NULL	NULL	0	NULL	Group II ( postincisional group ) 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Group II ( postincisional group ) received the same drug mixture after surgery .
	manualset3
83377	2	398049	5	NULL	NULL	0	NULL	drug mixture	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Group II ( postincisional group ) received the same drug mixture after surgery .
	manualset3
83378	3	398049	5	NULL	NULL	0	NULL	surgery	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Group II ( postincisional group ) received the same drug mixture after surgery .
	manualset3
83379	1	398050	5	NULL	NULL	NULL	NULL	Group differences	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Group differences are analyzed through a cultural lens in which different interpretive norms can generate expectations for either nondirectiveness or directiveness .
	manualset3
83380	2	398050	5	NULL	NULL	NULL	NULL	cultural lens	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Group differences are analyzed through a cultural lens in which different interpretive norms can generate expectations for either nondirectiveness or directiveness .
	manualset3
83381	3	398050	5	NULL	NULL	NULL	NULL	different interpretive norms 	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Group differences are analyzed through a cultural lens in which different interpretive norms can generate expectations for either nondirectiveness or directiveness .
	manualset3
83382	1	398051	5	NULL	NULL	0	NULL	Groups 3-6 rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Groups 3-6 rats were given DMH at a dose of ( 20mg/kg body weight subcutaneously ) once a week for 15 weeks to induce colonic tumors .
	manualset3
83383	2	398051	5	NULL	NULL	0	NULL	DMH 	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Groups 3-6 rats were given DMH at a dose of ( 20mg/kg body weight subcutaneously ) once a week for 15 weeks to induce colonic tumors .
	manualset3
83384	3	398051	5	NULL	NULL	NULL	NULL	dose	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Groups 3-6 rats were given DMH at a dose of ( 20mg/kg body weight subcutaneously ) once a week for 15 weeks to induce colonic tumors .
	manualset3
83385	4	398051	5	NULL	NULL	0	NULL	20mg/kg body weight	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Groups 3-6 rats were given DMH at a dose of ( 20mg/kg body weight subcutaneously ) once a week for 15 weeks to induce colonic tumors .
	manualset3
83386	5	398051	5	NULL	NULL	0	NULL	once a week	TimePoint												NULL		0	NULL	NULL	NULL	NULL	NULL	Groups 3-6 rats were given DMH at a dose of ( 20mg/kg body weight subcutaneously ) once a week for 15 weeks to induce colonic tumors .
	manualset3
83387	6	398051	5	NULL	NULL	NULL	NULL	15 weeks	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Groups 3-6 rats were given DMH at a dose of ( 20mg/kg body weight subcutaneously ) once a week for 15 weeks to induce colonic tumors .
	manualset3
83388	7	398051	5	NULL	NULL	0	NULL	colonic tumors	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Groups 3-6 rats were given DMH at a dose of ( 20mg/kg body weight subcutaneously ) once a week for 15 weeks to induce colonic tumors .
	manualset3
83389	1	398052	5	NULL	NULL	0	NULL	Groups of Ile-de-France ewes	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Groups of Ile-de-France ewes were maintained in two nutritional states ( restricted and well fed ) under a simulated annual photoperiod of 8-16 h of light per day over two breeding seasons .
	manualset3
83390	3	398052	5	NULL	NULL	NULL	NULL	simulated annual photoperiod	LaboratoryExperimentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Groups of Ile-de-France ewes were maintained in two nutritional states ( restricted and well fed ) under a simulated annual photoperiod of 8-16 h of light per day over two breeding seasons .
	manualset3
83391	4	398052	5	NULL	NULL	NULL	NULL	8-16 h of light per day	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Groups of Ile-de-France ewes were maintained in two nutritional states ( restricted and well fed ) under a simulated annual photoperiod of 8-16 h of light per day over two breeding seasons .
	manualset3
83392	5	398052	5	NULL	NULL	NULL	NULL	two breeding seasons	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Groups of Ile-de-France ewes were maintained in two nutritional states ( restricted and well fed ) under a simulated annual photoperiod of 8-16 h of light per day over two breeding seasons .
	manualset3
83777	2	398052	5	NULL	NULL	0	NULL	 two nutritional states ( restricted and well fed )	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	Groups of Ile-de-France ewes were maintained in two nutritional states ( restricted and well fed ) under a simulated annual photoperiod of 8-16 h of light per day over two breeding seasons .
	manualset3
83393	1	398053	5	NULL	NULL	0	NULL	diatom species	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Growing alone , no effect was found , but in co-culture with a single diatom species , the bacteria reduced the diatom effect on flow through the bioreactors seen earlier , however did not reduce the extent of their growth .
	manualset3
83394	2	398053	5	NULL	NULL	0	NULL	bacteria	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Growing alone , no effect was found , but in co-culture with a single diatom species , the bacteria reduced the diatom effect on flow through the bioreactors seen earlier , however did not reduce the extent of their growth .
	manualset3
83395	3	398053	5	NULL	NULL	0	NULL	diatom effect 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Growing alone , no effect was found , but in co-culture with a single diatom species , the bacteria reduced the diatom effect on flow through the bioreactors seen earlier , however did not reduce the extent of their growth .
	manualset3
83396	4	398053	5	NULL	NULL	0	NULL	bioreactors 	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	Growing alone , no effect was found , but in co-culture with a single diatom species , the bacteria reduced the diatom effect on flow through the bioreactors seen earlier , however did not reduce the extent of their growth .
	manualset3
83397	5	398053	5	NULL	NULL	0	NULL	growth	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Growing alone , no effect was found , but in co-culture with a single diatom species , the bacteria reduced the diatom effect on flow through the bioreactors seen earlier , however did not reduce the extent of their growth .
	manualset3
83398	1	398054	5	NULL	NULL	0	NULL	Static flatfoot	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Static flatfoot in children and adolescents ) .
	manualset3
83399	2	398054	5	NULL	NULL	0	NULL	children	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( Static flatfoot in children and adolescents ) .
	manualset3
83400	3	398054	5	NULL	NULL	0	NULL	adolescents	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( Static flatfoot in children and adolescents ) .
	manualset3
83401	1	398055	5	NULL	NULL	0	NULL	significant proportion	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Growing evidence indicates that a significant proportion of individuals with TBI demonstrate an inability to recognize affective information from the face , voice , bodily movement , and posture .
	manualset3
83402	2	398055	5	NULL	NULL	0	NULL	individuals	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Growing evidence indicates that a significant proportion of individuals with TBI demonstrate an inability to recognize affective information from the face , voice , bodily movement , and posture .
	manualset3
83403	3	398055	5	NULL	NULL	0	NULL	TBI	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Growing evidence indicates that a significant proportion of individuals with TBI demonstrate an inability to recognize affective information from the face , voice , bodily movement , and posture .
	manualset3
83404	4	398055	5	NULL	NULL	0	NULL	recognize affective information	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Growing evidence indicates that a significant proportion of individuals with TBI demonstrate an inability to recognize affective information from the face , voice , bodily movement , and posture .
	manualset3
83405	5	398055	5	NULL	NULL	0	NULL	face	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Growing evidence indicates that a significant proportion of individuals with TBI demonstrate an inability to recognize affective information from the face , voice , bodily movement , and posture .
	manualset3
83406	6	398055	5	NULL	NULL	0	NULL	bodily movement	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Growing evidence indicates that a significant proportion of individuals with TBI demonstrate an inability to recognize affective information from the face , voice , bodily movement , and posture .
	manualset3
83407	7	398055	5	NULL	NULL	0	NULL	posture	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Growing evidence indicates that a significant proportion of individuals with TBI demonstrate an inability to recognize affective information from the face , voice , bodily movement , and posture .
	manualset3
83408	1	398056	5	NULL	NULL	0	NULL	heme-mediated injury	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Growing evidence suggests that heme-mediated injury may contribute to the pathogenesis of CNS hemorrhage .
	manualset3
83409	2	398056	5	NULL	NULL	0	NULL	pathogenesis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Growing evidence suggests that heme-mediated injury may contribute to the pathogenesis of CNS hemorrhage .
	manualset3
83410	3	398056	5	NULL	NULL	0	NULL	CNS hemorrhage	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Growing evidence suggests that heme-mediated injury may contribute to the pathogenesis of CNS hemorrhage .
	manualset3
83411	1	398057	5	NULL	NULL	0	NULL	Growth hormone ( GH )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth hormone ( GH ) exerts sexually dimorphic effects on liver gene transcription that are regulated by the temporal pattern of pituitary GH release ; this release is intermittent in male rats and nearly continuous in females .
	manualset3
83412	2	398057	5	NULL	NULL	0	NULL	sexually dimorphic effects	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth hormone ( GH ) exerts sexually dimorphic effects on liver gene transcription that are regulated by the temporal pattern of pituitary GH release ; this release is intermittent in male rats and nearly continuous in females .
	manualset3
83413	3	398057	5	NULL	NULL	0	NULL	liver gene transcription	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth hormone ( GH ) exerts sexually dimorphic effects on liver gene transcription that are regulated by the temporal pattern of pituitary GH release ; this release is intermittent in male rats and nearly continuous in females .
	manualset3
83414	4	398057	5	NULL	NULL	NULL	NULL	temporal pattern of pituitary GH release	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Growth hormone ( GH ) exerts sexually dimorphic effects on liver gene transcription that are regulated by the temporal pattern of pituitary GH release ; this release is intermittent in male rats and nearly continuous in females .
	manualset3
83415	5	398057	5	NULL	NULL	0	NULL	release	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth hormone ( GH ) exerts sexually dimorphic effects on liver gene transcription that are regulated by the temporal pattern of pituitary GH release ; this release is intermittent in male rats and nearly continuous in females .
	manualset3
83416	6	398057	5	NULL	NULL	0	NULL	male rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth hormone ( GH ) exerts sexually dimorphic effects on liver gene transcription that are regulated by the temporal pattern of pituitary GH release ; this release is intermittent in male rats and nearly continuous in females .
	manualset3
83417	7	398057	5	NULL	NULL	0	NULL	females	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth hormone ( GH ) exerts sexually dimorphic effects on liver gene transcription that are regulated by the temporal pattern of pituitary GH release ; this release is intermittent in male rats and nearly continuous in females .
	manualset3
83418	1	398058	5	NULL	NULL	0	NULL	Growth hormone	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth hormone and insulin-like growth factor I regulate collagen gene expression and extracellular collagen in cultures of avian skin fibroblasts .
	manualset3
83419	2	398058	5	NULL	NULL	0	NULL	insulin-like growth factor I 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth hormone and insulin-like growth factor I regulate collagen gene expression and extracellular collagen in cultures of avian skin fibroblasts .
	manualset3
83420	3	398058	5	NULL	NULL	0	NULL	collagen gene expression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth hormone and insulin-like growth factor I regulate collagen gene expression and extracellular collagen in cultures of avian skin fibroblasts .
	manualset3
83421	4	398058	5	NULL	NULL	0	NULL	extracellular collagen	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth hormone and insulin-like growth factor I regulate collagen gene expression and extracellular collagen in cultures of avian skin fibroblasts .
	manualset3
83422	5	398058	5	NULL	NULL	0	NULL	cultures	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth hormone and insulin-like growth factor I regulate collagen gene expression and extracellular collagen in cultures of avian skin fibroblasts .
	manualset3
83423	6	398058	5	NULL	NULL	0	NULL	avian skin fibroblasts	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth hormone and insulin-like growth factor I regulate collagen gene expression and extracellular collagen in cultures of avian skin fibroblasts .
	manualset3
83424	1	398059	5	NULL	NULL	0	NULL	Growth hormone	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth hormone promotes early initiation of hepatocyte growth factor gene expression in the liver of hypophysectomized rats after partial hepatectomy .
	manualset3
83425	2	398059	5	NULL	NULL	0	NULL	early initiation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth hormone promotes early initiation of hepatocyte growth factor gene expression in the liver of hypophysectomized rats after partial hepatectomy .
	manualset3
83426	3	398059	5	NULL	NULL	0	NULL	hepatocyte growth factor gene expression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth hormone promotes early initiation of hepatocyte growth factor gene expression in the liver of hypophysectomized rats after partial hepatectomy .
	manualset3
83427	4	398059	5	NULL	NULL	0	NULL	liver	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth hormone promotes early initiation of hepatocyte growth factor gene expression in the liver of hypophysectomized rats after partial hepatectomy .
	manualset3
83428	5	398059	5	NULL	NULL	0	NULL	hypophysectomized rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth hormone promotes early initiation of hepatocyte growth factor gene expression in the liver of hypophysectomized rats after partial hepatectomy .
	manualset3
83429	6	398059	5	NULL	NULL	0	NULL	partial hepatectomy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth hormone promotes early initiation of hepatocyte growth factor gene expression in the liver of hypophysectomized rats after partial hepatectomy .
	manualset3
83430	1	398060	5	NULL	NULL	0	NULL	Growth	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth in managed care enrollment potentially creates incentives for health plans to become involved in public health activities , such as health promotion and disease prevention interventions , and care for vulnerable populations .
	manualset3
83431	2	398060	5	NULL	NULL	0	NULL	managed care enrollment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth in managed care enrollment potentially creates incentives for health plans to become involved in public health activities , such as health promotion and disease prevention interventions , and care for vulnerable populations .
	manualset3
83432	3	398060	5	NULL	NULL	0	NULL	 health plans	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth in managed care enrollment potentially creates incentives for health plans to become involved in public health activities , such as health promotion and disease prevention interventions , and care for vulnerable populations .
	manualset3
83433	4	398060	5	NULL	NULL	NULL	NULL	public health activities	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Growth in managed care enrollment potentially creates incentives for health plans to become involved in public health activities , such as health promotion and disease prevention interventions , and care for vulnerable populations .
	manualset3
83434	5	398060	5	NULL	NULL	0	NULL	health promotion	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth in managed care enrollment potentially creates incentives for health plans to become involved in public health activities , such as health promotion and disease prevention interventions , and care for vulnerable populations .
	manualset3
83435	6	398060	5	NULL	NULL	0	NULL	disease prevention interventions	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth in managed care enrollment potentially creates incentives for health plans to become involved in public health activities , such as health promotion and disease prevention interventions , and care for vulnerable populations .
	manualset3
83436	7	398060	5	NULL	NULL	0	NULL	care	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth in managed care enrollment potentially creates incentives for health plans to become involved in public health activities , such as health promotion and disease prevention interventions , and care for vulnerable populations .
	manualset3
83437	8	398060	5	NULL	NULL	0	NULL	vulnerable populations	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth in managed care enrollment potentially creates incentives for health plans to become involved in public health activities , such as health promotion and disease prevention interventions , and care for vulnerable populations .
	manualset3
83438	1	398061	5	NULL	NULL	0	NULL	Growth inhibition	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth inhibition was due to SE-induced programmed cell death ( apoptosis ) as shown by propidium iodide staining and the appearance of the characteristic ladder pattern of DNA fragmentation .
	manualset3
83439	2	398061	5	NULL	NULL	0	NULL	SE-induced programmed cell death ( apoptosis )	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth inhibition was due to SE-induced programmed cell death ( apoptosis ) as shown by propidium iodide staining and the appearance of the characteristic ladder pattern of DNA fragmentation .
	manualset3
83440	3	398061	5	NULL	NULL	0	NULL	propidium iodide staining	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth inhibition was due to SE-induced programmed cell death ( apoptosis ) as shown by propidium iodide staining and the appearance of the characteristic ladder pattern of DNA fragmentation .
	manualset3
83441	4	398061	5	NULL	NULL	0	NULL	characteristic ladder pattern of DNA fragmentation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth inhibition was due to SE-induced programmed cell death ( apoptosis ) as shown by propidium iodide staining and the appearance of the characteristic ladder pattern of DNA fragmentation .
	manualset3
83442	1	398062	5	NULL	NULL	0	NULL	Growth patterns	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth patterns of bone marrow in complete remission from ANLL often had depressed colony numbers .
	manualset3
83443	2	398062	5	NULL	NULL	0	NULL	bone marrow	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth patterns of bone marrow in complete remission from ANLL often had depressed colony numbers .
	manualset3
83444	3	398062	5	NULL	NULL	0	NULL	complete remission	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth patterns of bone marrow in complete remission from ANLL often had depressed colony numbers .
	manualset3
83445	4	398062	5	NULL	NULL	0	NULL	ANLL	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth patterns of bone marrow in complete remission from ANLL often had depressed colony numbers .
	manualset3
83446	5	398062	5	NULL	NULL	0	NULL	depressed colony numbers	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth patterns of bone marrow in complete remission from ANLL often had depressed colony numbers .
	manualset3
83447	1	398063	5	NULL	NULL	NULL	NULL	Growth rate	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Growth rate was greater in pigs previously fed lysine-restricted diets than well-fed pigs although it did not reach a significant level during realimentation .
	manualset3
83448	2	398063	5	NULL	NULL	0	NULL	pigs	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth rate was greater in pigs previously fed lysine-restricted diets than well-fed pigs although it did not reach a significant level during realimentation .
	manualset3
83449	3	398063	5	NULL	NULL	0	NULL	 lysine-restricted diets	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth rate was greater in pigs previously fed lysine-restricted diets than well-fed pigs although it did not reach a significant level during realimentation .
	manualset3
83450	4	398063	5	NULL	NULL	0	NULL	well-fed pigs	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth rate was greater in pigs previously fed lysine-restricted diets than well-fed pigs although it did not reach a significant level during realimentation .
	manualset3
83451	5	398063	5	NULL	NULL	0	NULL	realimentation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth rate was greater in pigs previously fed lysine-restricted diets than well-fed pigs although it did not reach a significant level during realimentation .
	manualset3
83452	1	398064	5	NULL	NULL	0	NULL	Growth regulated peptide ( GRO-alpha ) 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth regulated peptide ( GRO-alpha ) is chemotactic for neutrophils .
	manualset3
83453	2	398064	5	NULL	NULL	0	NULL	neutrophils	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth regulated peptide ( GRO-alpha ) is chemotactic for neutrophils .
	manualset3
83454	1	398065	5	NULL	NULL	0	NULL	Growth stimulation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth stimulation by NGF could be completely reversed by neutralizing anti-NGF antibody and by the tyrosine kinase inhibitor genistein .
	manualset3
83455	2	398065	5	NULL	NULL	0	NULL	NGF	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth stimulation by NGF could be completely reversed by neutralizing anti-NGF antibody and by the tyrosine kinase inhibitor genistein .
	manualset3
83456	3	398065	5	NULL	NULL	0	NULL	anti-NGF antibody	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth stimulation by NGF could be completely reversed by neutralizing anti-NGF antibody and by the tyrosine kinase inhibitor genistein .
	manualset3
83457	4	398065	5	NULL	NULL	0	NULL	tyrosine kinase inhibitor genistein	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth stimulation by NGF could be completely reversed by neutralizing anti-NGF antibody and by the tyrosine kinase inhibitor genistein .
	manualset3
83458	1	398066	5	NULL	NULL	0	NULL	Growth studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth studies showed that M. pusillus had the capacity to utilize ammonium N , nitrate N , amino N , and urea .
	manualset3
83459	2	398066	5	NULL	NULL	0	NULL	M. pusillus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth studies showed that M. pusillus had the capacity to utilize ammonium N , nitrate N , amino N , and urea .
	manualset3
83460	3	398066	5	NULL	NULL	NULL	NULL	ammonium N	Ion												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Growth studies showed that M. pusillus had the capacity to utilize ammonium N , nitrate N , amino N , and urea .
	manualset3
83461	4	398066	5	NULL	NULL	NULL	NULL	nitrate N	Ion												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Growth studies showed that M. pusillus had the capacity to utilize ammonium N , nitrate N , amino N , and urea .
	manualset3
83462	5	398066	5	NULL	NULL	NULL	NULL	amino N	Ion												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Growth studies showed that M. pusillus had the capacity to utilize ammonium N , nitrate N , amino N , and urea .
	manualset3
83463	6	398066	5	NULL	NULL	0	NULL	urea	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Growth studies showed that M. pusillus had the capacity to utilize ammonium N , nitrate N , amino N , and urea .
	manualset3
83464	1	398067	5	NULL	NULL	0	NULL	Guanidine hydrochloride	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Guanidine hydrochloride exerts dual effects on the tryptophan synthase alpha 2 beta 2 complex as a cation activator and as a modulator of the active site conformation .
	manualset3
83465	2	398067	5	NULL	NULL	0	NULL	dual effects	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Guanidine hydrochloride exerts dual effects on the tryptophan synthase alpha 2 beta 2 complex as a cation activator and as a modulator of the active site conformation .
	manualset3
83466	3	398067	5	NULL	NULL	0	NULL	tryptophan synthase alpha 2 beta 2 complex	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Guanidine hydrochloride exerts dual effects on the tryptophan synthase alpha 2 beta 2 complex as a cation activator and as a modulator of the active site conformation .
	manualset3
83467	4	398067	5	NULL	NULL	0	NULL	cation activator	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Guanidine hydrochloride exerts dual effects on the tryptophan synthase alpha 2 beta 2 complex as a cation activator and as a modulator of the active site conformation .
	manualset3
83468	5	398067	5	NULL	NULL	0	NULL	 modulator of the active site conformation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Guanidine hydrochloride exerts dual effects on the tryptophan synthase alpha 2 beta 2 complex as a cation activator and as a modulator of the active site conformation .
	manualset3
83469	1	398068	5	NULL	NULL	0	NULL	Guided dilatation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Guided dilatation and transurethral resection in one session for treatment of post-prostatectomy obstructive complications .
	manualset3
83470	2	398068	5	NULL	NULL	0	NULL	transurethral resection	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Guided dilatation and transurethral resection in one session for treatment of post-prostatectomy obstructive complications .
	manualset3
83471	3	398068	5	NULL	NULL	0	NULL	treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Guided dilatation and transurethral resection in one session for treatment of post-prostatectomy obstructive complications .
	manualset3
83472	4	398068	5	NULL	NULL	0	NULL	post-prostatectomy obstructive complications	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Guided dilatation and transurethral resection in one session for treatment of post-prostatectomy obstructive complications .
	manualset3
83473	1	398069	5	NULL	NULL	0	NULL	guidelines	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Guidelines for establishing a maternal serum alpha-fetoprotein screening program .
	manualset3
83474	2	398069	5	NULL	NULL	0	NULL	maternal serum alpha-fetoprotein screening program	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Guidelines for establishing a maternal serum alpha-fetoprotein screening program .
	manualset3
83475	1	398070	5	NULL	NULL	0	NULL	maternal mortality	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Statistical review of maternal mortality in North-Moravian region in 1965-1974 and consequent conclusions ( author 's transl ) ) .
	manualset3
83476	2	398070	5	NULL	NULL	0	NULL	North-Moravian region	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	( Statistical review of maternal mortality in North-Moravian region in 1965-1974 and consequent conclusions ( author 's transl ) ) .
	manualset3
83477	3	398070	5	NULL	NULL	0	NULL	1965-1974	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	( Statistical review of maternal mortality in North-Moravian region in 1965-1974 and consequent conclusions ( author 's transl ) ) .
	manualset3
83478	1	398071	5	NULL	NULL	0	NULL	Guidelines	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Guidelines for the clinical application of the LCP .
	manualset3
83479	2	398071	5	NULL	NULL	0	NULL	clinical application	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Guidelines for the clinical application of the LCP .
	manualset3
83480	3	398071	5	NULL	NULL	0	NULL	LCP	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	Guidelines for the clinical application of the LCP .
	manualset3
83482	1	398072	5	NULL	NULL	0	NULL	Guidelines	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Guidelines for the documentation and verification of measles , rubella , and congenital rubella syndrome elimination in the region of the Americas .
	manualset3
83483	2	398072	5	NULL	NULL	NULL	NULL	documentation and verification	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Guidelines for the documentation and verification of measles , rubella , and congenital rubella syndrome elimination in the region of the Americas .
	manualset3
83484	3	398072	5	NULL	NULL	NULL	NULL	measles , rubella , and congenital rubella syndrome elimination	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Guidelines for the documentation and verification of measles , rubella , and congenital rubella syndrome elimination in the region of the Americas .
	manualset3
83485	4	398072	5	NULL	NULL	NULL	NULL	region	UnproperNamedGeographicalLocation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Guidelines for the documentation and verification of measles , rubella , and congenital rubella syndrome elimination in the region of the Americas .
	manualset3
83486	5	398072	5	NULL	NULL	NULL	NULL	Americas	ProperNamedGeographicalLocation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Guidelines for the documentation and verification of measles , rubella , and congenital rubella syndrome elimination in the region of the Americas .
	manualset3
83487	1	398073	5	NULL	NULL	0	NULL	Guinea pig	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Guinea pig brainstem preparations possessed specific binding sites for ( 3H ) 5-HT but specific ( 3H ) spiperone binding was low and inconsistent .
	manualset3
83488	2	398073	5	NULL	NULL	0	NULL	brainstem preparations	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Guinea pig brainstem preparations possessed specific binding sites for ( 3H ) 5-HT but specific ( 3H ) spiperone binding was low and inconsistent .
	manualset3
83492	3	398073	5	NULL	NULL	0	NULL	possessed specific binding sites	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Guinea pig brainstem preparations possessed specific binding sites for ( 3H ) 5-HT but specific ( 3H ) spiperone binding was low and inconsistent .
	manualset3
83494	4	398073	5	NULL	NULL	0	NULL	( 3H ) 5-HT	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Guinea pig brainstem preparations possessed specific binding sites for ( 3H ) 5-HT but specific ( 3H ) spiperone binding was low and inconsistent .
	manualset3
83495	5	398073	5	NULL	NULL	0	NULL	specific ( 3H ) spiperone binding	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Guinea pig brainstem preparations possessed specific binding sites for ( 3H ) 5-HT but specific ( 3H ) spiperone binding was low and inconsistent .
	manualset3
83496	1	398074	5	NULL	NULL	0	NULL	Gynaecological examination	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gynaecological examination , USG and CT showed small hypoplastic uterus and rudimentary ovaries .
	manualset3
83497	2	398074	5	NULL	NULL	0	NULL	USG	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gynaecological examination , USG and CT showed small hypoplastic uterus and rudimentary ovaries .
	manualset3
83498	3	398074	5	NULL	NULL	0	NULL	CT	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Gynaecological examination , USG and CT showed small hypoplastic uterus and rudimentary ovaries .
	manualset3
83499	4	398074	5	NULL	NULL	0	NULL	small hypoplastic uterus	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gynaecological examination , USG and CT showed small hypoplastic uterus and rudimentary ovaries .
	manualset3
83500	5	398074	5	NULL	NULL	0	NULL	rudimentary ovaries	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Gynaecological examination , USG and CT showed small hypoplastic uterus and rudimentary ovaries .
	manualset3
83503	1	398075	5	NULL	NULL	0	NULL	H. pylori	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	H. pylori LPS in part mediates the binding of the bacterium to laminin , and interferes with gastric cell receptor-laminin interaction , thereby potentially contributing to the loss of mucosal integrity .
	manualset3
83505	2	398075	5	NULL	NULL	0	NULL	LPS	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	H. pylori LPS in part mediates the binding of the bacterium to laminin , and interferes with gastric cell receptor-laminin interaction , thereby potentially contributing to the loss of mucosal integrity .
	manualset3
83506	3	398075	5	NULL	NULL	0	NULL	binding	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	H. pylori LPS in part mediates the binding of the bacterium to laminin , and interferes with gastric cell receptor-laminin interaction , thereby potentially contributing to the loss of mucosal integrity .
	manualset3
83508	4	398075	5	NULL	NULL	0	NULL	bacterium	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	H. pylori LPS in part mediates the binding of the bacterium to laminin , and interferes with gastric cell receptor-laminin interaction , thereby potentially contributing to the loss of mucosal integrity .
	manualset3
83509	5	398075	5	NULL	NULL	0	NULL	laminin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	H. pylori LPS in part mediates the binding of the bacterium to laminin , and interferes with gastric cell receptor-laminin interaction , thereby potentially contributing to the loss of mucosal integrity .
	manualset3
83511	6	398075	5	NULL	NULL	0	NULL	gastric cell receptor-laminin interaction	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	H. pylori LPS in part mediates the binding of the bacterium to laminin , and interferes with gastric cell receptor-laminin interaction , thereby potentially contributing to the loss of mucosal integrity .
	manualset3
83514	7	398075	5	NULL	NULL	0	NULL	mucosal integrity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	H. pylori LPS in part mediates the binding of the bacterium to laminin , and interferes with gastric cell receptor-laminin interaction , thereby potentially contributing to the loss of mucosal integrity .
	manualset3
83515	1	398076	5	NULL	NULL	0	NULL	H ( 2 ) O ( 2 ) production	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	H ( 2 ) O ( 2 ) production and changes in glutathione , catalase , and peroxidase were followed in whole-leaf extracts from the susceptible ( AlgS ( Algerian/4 * ( F14 ) Man .
	manualset3
83516	2	398076	5	NULL	NULL	0	NULL	glutathione	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	H ( 2 ) O ( 2 ) production and changes in glutathione , catalase , and peroxidase were followed in whole-leaf extracts from the susceptible ( AlgS ( Algerian/4 * ( F14 ) Man .
	manualset3
83517	3	398076	5	NULL	NULL	0	NULL	catalase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	H ( 2 ) O ( 2 ) production and changes in glutathione , catalase , and peroxidase were followed in whole-leaf extracts from the susceptible ( AlgS ( Algerian/4 * ( F14 ) Man .
	manualset3
83518	4	398076	5	NULL	NULL	0	NULL	peroxidase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	H ( 2 ) O ( 2 ) production and changes in glutathione , catalase , and peroxidase were followed in whole-leaf extracts from the susceptible ( AlgS ( Algerian/4 * ( F14 ) Man .
	manualset3
83519	5	398076	5	NULL	NULL	0	NULL	whole-leaf extracts	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	H ( 2 ) O ( 2 ) production and changes in glutathione , catalase , and peroxidase were followed in whole-leaf extracts from the susceptible ( AlgS ( Algerian/4 * ( F14 ) Man .
	manualset3
83520	6	398076	5	NULL	NULL	0	NULL	susceptible ( AlgS ( Algerian/4 * ( F14 ) Man	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	H ( 2 ) O ( 2 ) production and changes in glutathione , catalase , and peroxidase were followed in whole-leaf extracts from the susceptible ( AlgS ( Algerian/4 * ( F14 ) Man .
	manualset3
83521	1	398077	5	NULL	NULL	0	NULL	H ( 2 ) O } ( 3 )	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	H ( 2 ) O } ( 3 ) , ( SbI ( 3 ) ( MTZD ) ) ( 4 ) , ( ( NMeMBZT ) SbI ( 2 ) ( mu ( 2 ) - I ) ( 2 ) ( mu ( 2 ) - S-NMeMBZT ) SbI ( 2 ) ( NMeMBZT ) ) ( 5 ) , { ( SbI ( 3 ) ( tHPMT ) ( 3 ) ) .
	manualset3
83522	2	398077	5	NULL	NULL	NULL	NULL	( SbI ( 3 ) ( MTZD ) ) ( 4 )	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	H ( 2 ) O } ( 3 ) , ( SbI ( 3 ) ( MTZD ) ) ( 4 ) , ( ( NMeMBZT ) SbI ( 2 ) ( mu ( 2 ) - I ) ( 2 ) ( mu ( 2 ) - S-NMeMBZT ) SbI ( 2 ) ( NMeMBZT ) ) ( 5 ) , { ( SbI ( 3 ) ( tHPMT ) ( 3 ) ) .
	manualset3
83524	3	398077	5	NULL	NULL	0	NULL	( ( NMeMBZT ) SbI ( 2 ) ( mu ( 2 ) - I ) ( 2 ) ( mu ( 2 ) - S-NMeMBZT ) SbI ( 2 ) ( NMeMBZT ) ) ( 5 ) 	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	H ( 2 ) O } ( 3 ) , ( SbI ( 3 ) ( MTZD ) ) ( 4 ) , ( ( NMeMBZT ) SbI ( 2 ) ( mu ( 2 ) - I ) ( 2 ) ( mu ( 2 ) - S-NMeMBZT ) SbI ( 2 ) ( NMeMBZT ) ) ( 5 ) , { ( SbI ( 3 ) ( tHPMT ) ( 3 ) ) .
	manualset3
83526	4	398077	5	NULL	NULL	0	NULL	{ ( SbI ( 3 ) ( tHPMT ) ( 3 ) )	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	H ( 2 ) O } ( 3 ) , ( SbI ( 3 ) ( MTZD ) ) ( 4 ) , ( ( NMeMBZT ) SbI ( 2 ) ( mu ( 2 ) - I ) ( 2 ) ( mu ( 2 ) - S-NMeMBZT ) SbI ( 2 ) ( NMeMBZT ) ) ( 5 ) , { ( SbI ( 3 ) ( tHPMT ) ( 3 ) ) .
	manualset3
83528	1	398078	5	NULL	NULL	0	NULL	Alpha-fetoprotein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	( Alpha-fetoprotein ( author 's transl ) ) .
	manualset3
83529	1	398079	5	NULL	NULL	NULL	NULL	H complex concentration	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	H complex concentration was found up to 25 microM whether the reaction was followed by probe displacement or the quenching of AT .
	manualset3
83530	2	398079	5	NULL	NULL	0	NULL	25 microM	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	H complex concentration was found up to 25 microM whether the reaction was followed by probe displacement or the quenching of AT .
	manualset3
83531	3	398079	5	NULL	NULL	0	NULL	reaction 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	H complex concentration was found up to 25 microM whether the reaction was followed by probe displacement or the quenching of AT .
	manualset3
83532	4	398079	5	NULL	NULL	NULL	NULL	probe displacement	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	H complex concentration was found up to 25 microM whether the reaction was followed by probe displacement or the quenching of AT .
	manualset3
83533	5	398079	5	NULL	NULL	0	NULL	quenching of AT	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	H complex concentration was found up to 25 microM whether the reaction was followed by probe displacement or the quenching of AT .
	manualset3
83534	1	398080	5	NULL	NULL	0	NULL	H pylori infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	H pylori infection was detected in 85 % of patients versus 76.7 % for control subjects .
	manualset3
83535	2	398080	5	NULL	NULL	0	NULL	85 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	H pylori infection was detected in 85 % of patients versus 76.7 % for control subjects .
	manualset3
83537	3	398080	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	H pylori infection was detected in 85 % of patients versus 76.7 % for control subjects .
	manualset3
83538	4	398080	5	NULL	NULL	0	NULL	76.7 % 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	H pylori infection was detected in 85 % of patients versus 76.7 % for control subjects .
	manualset3
83539	5	398080	5	NULL	NULL	0	NULL	control subjects	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	H pylori infection was detected in 85 % of patients versus 76.7 % for control subjects .
	manualset3
83540	1	398081	5	NULL	NULL	0	NULL	H2-M	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	H2-M , a facilitator of MHC class II peptide loading , and its negative modulator H2-O are differentially expressed in response to proinflammatory cytokines .
	manualset3
83541	2	398081	5	NULL	NULL	0	NULL	facilitator 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	H2-M , a facilitator of MHC class II peptide loading , and its negative modulator H2-O are differentially expressed in response to proinflammatory cytokines .
	manualset3
83542	3	398081	5	NULL	NULL	0	NULL	MHC class II peptide loading	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	H2-M , a facilitator of MHC class II peptide loading , and its negative modulator H2-O are differentially expressed in response to proinflammatory cytokines .
	manualset3
83543	4	398081	5	NULL	NULL	0	NULL	negative modulator H2-O	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	H2-M , a facilitator of MHC class II peptide loading , and its negative modulator H2-O are differentially expressed in response to proinflammatory cytokines .
	manualset3
83544	5	398081	5	NULL	NULL	0	NULL	response 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	H2-M , a facilitator of MHC class II peptide loading , and its negative modulator H2-O are differentially expressed in response to proinflammatory cytokines .
	manualset3
83545	6	398081	5	NULL	NULL	0	NULL	proinflammatory cytokines	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	H2-M , a facilitator of MHC class II peptide loading , and its negative modulator H2-O are differentially expressed in response to proinflammatory cytokines .
	manualset3
83548	1	398082	5	NULL	NULL	NULL	NULL	H2mfpp	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	H2mfpp and its complexes Sn ( Hmfpp ) ( C2H5 ) 2Cl and Sn3 ( Hmfpp ) ( mfpp ) ( C6H5 ) 3Cl6 are shown by the Salmonella-microsome assay to be mutagenic substances in the presence of a metabolic activation system .
	manualset3
83549	2	398082	5	NULL	NULL	NULL	NULL	Sn ( Hmfpp ) ( C2H5 ) 2Cl	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	H2mfpp and its complexes Sn ( Hmfpp ) ( C2H5 ) 2Cl and Sn3 ( Hmfpp ) ( mfpp ) ( C6H5 ) 3Cl6 are shown by the Salmonella-microsome assay to be mutagenic substances in the presence of a metabolic activation system .
	manualset3
83550	3	398082	5	NULL	NULL	0	NULL	Sn3 ( Hmfpp ) ( mfpp ) ( C6H5 ) 3Cl6	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	H2mfpp and its complexes Sn ( Hmfpp ) ( C2H5 ) 2Cl and Sn3 ( Hmfpp ) ( mfpp ) ( C6H5 ) 3Cl6 are shown by the Salmonella-microsome assay to be mutagenic substances in the presence of a metabolic activation system .
	manualset3
83552	4	398082	5	NULL	NULL	0	NULL	Salmonella-microsome assay	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	H2mfpp and its complexes Sn ( Hmfpp ) ( C2H5 ) 2Cl and Sn3 ( Hmfpp ) ( mfpp ) ( C6H5 ) 3Cl6 are shown by the Salmonella-microsome assay to be mutagenic substances in the presence of a metabolic activation system .
	manualset3
83553	5	398082	5	NULL	NULL	0	NULL	mutagenic substances	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	H2mfpp and its complexes Sn ( Hmfpp ) ( C2H5 ) 2Cl and Sn3 ( Hmfpp ) ( mfpp ) ( C6H5 ) 3Cl6 are shown by the Salmonella-microsome assay to be mutagenic substances in the presence of a metabolic activation system .
	manualset3
83554	6	398082	5	NULL	NULL	0	NULL	metabolic activation system	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	H2mfpp and its complexes Sn ( Hmfpp ) ( C2H5 ) 2Cl and Sn3 ( Hmfpp ) ( mfpp ) ( C6H5 ) 3Cl6 are shown by the Salmonella-microsome assay to be mutagenic substances in the presence of a metabolic activation system .
	manualset3
83557	1	398083	5	NULL	NULL	0	NULL	H3 .3	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	H3 .3 is also incorporated during decondensation of the Drosophila sperm pronucleus , indicating a direct role in chromatin remodeling upon fertilization .
	manualset3
83559	2	398083	5	NULL	NULL	0	NULL	decondensation 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	H3 .3 is also incorporated during decondensation of the Drosophila sperm pronucleus , indicating a direct role in chromatin remodeling upon fertilization .
	manualset3
83560	3	398083	5	NULL	NULL	0	NULL	Drosophila sperm pronucleus	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	H3 .3 is also incorporated during decondensation of the Drosophila sperm pronucleus , indicating a direct role in chromatin remodeling upon fertilization .
	manualset3
83562	4	398083	5	NULL	NULL	0	NULL	direct role	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	H3 .3 is also incorporated during decondensation of the Drosophila sperm pronucleus , indicating a direct role in chromatin remodeling upon fertilization .
	manualset3
83563	5	398083	5	NULL	NULL	0	NULL	chromatin remodeling	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	H3 .3 is also incorporated during decondensation of the Drosophila sperm pronucleus , indicating a direct role in chromatin remodeling upon fertilization .
	manualset3
83565	6	398083	5	NULL	NULL	0	NULL	fertilization	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	H3 .3 is also incorporated during decondensation of the Drosophila sperm pronucleus , indicating a direct role in chromatin remodeling upon fertilization .
	manualset3
83566	1	398084	5	NULL	NULL	0	NULL	HABC	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	HABC responded better than HPC and HGF to CAP treated root slices , and HPC response was higher than that of HGF .
	manualset3
83567	2	398084	5	NULL	NULL	0	NULL	HPC	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	HABC responded better than HPC and HGF to CAP treated root slices , and HPC response was higher than that of HGF .
	manualset3
83568	3	398084	5	NULL	NULL	0	NULL	HGF	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	HABC responded better than HPC and HGF to CAP treated root slices , and HPC response was higher than that of HGF .
	manualset3
83570	4	398084	5	NULL	NULL	0	NULL	CAP treated root slices	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	HABC responded better than HPC and HGF to CAP treated root slices , and HPC response was higher than that of HGF .
	manualset3
83571	5	398084	5	NULL	NULL	0	NULL	HPC response	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HABC responded better than HPC and HGF to CAP treated root slices , and HPC response was higher than that of HGF .
	manualset3
83573	6	398084	5	NULL	NULL	0	NULL	HGF	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	HABC responded better than HPC and HGF to CAP treated root slices , and HPC response was higher than that of HGF .
	manualset3
83575	1	398085	5	NULL	NULL	0	NULL	HAVAb 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HAVAb was in 75 % of the cases , its meaning was of post-contact with HAV .
	manualset3
83576	2	398085	5	NULL	NULL	0	NULL	75 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	HAVAb was in 75 % of the cases , its meaning was of post-contact with HAV .
	manualset3
83587	3	398085	5	NULL	NULL	0	NULL	post-contact	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HAVAb was in 75 % of the cases , its meaning was of post-contact with HAV .
	manualset3
83588	4	398085	5	NULL	NULL	0	NULL	HAV	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	HAVAb was in 75 % of the cases , its meaning was of post-contact with HAV .
	manualset3
83591	1	398086	5	NULL	NULL	0	NULL	HBO	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	HBO was most effective when whole-body and regional hypoxia was applied simultaneously .
	manualset3
83594	2	398086	5	NULL	NULL	0	NULL	whole-body	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	HBO was most effective when whole-body and regional hypoxia was applied simultaneously .
	manualset3
83595	3	398086	5	NULL	NULL	0	NULL	regional hypoxia	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HBO was most effective when whole-body and regional hypoxia was applied simultaneously .
	manualset3
83596	1	398087	5	NULL	NULL	NULL	NULL	psychotherapy	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Status of the psychotherapy in general practice ? ) .
	manualset3
83597	2	398087	5	NULL	NULL	0	NULL	general practice	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Status of the psychotherapy in general practice ? ) .
	manualset3
83598	1	398088	5	NULL	NULL	0	NULL	HBV-related hepatocellular carcinoma susceptibility gene KIF1B	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	HBV-related hepatocellular carcinoma susceptibility gene KIF1B is not associated with development of chronic hepatitis B .
	manualset3
83599	2	398088	5	NULL	NULL	0	NULL	development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HBV-related hepatocellular carcinoma susceptibility gene KIF1B is not associated with development of chronic hepatitis B .
	manualset3
83601	3	398088	5	NULL	NULL	0	NULL	chronic hepatitis B	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	HBV-related hepatocellular carcinoma susceptibility gene KIF1B is not associated with development of chronic hepatitis B .
	manualset3
83602	1	398089	5	NULL	NULL	0	NULL	HCC	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	HCC recurred after an occlusion of the reservoir in 18 patients .
	manualset3
83603	2	398089	5	NULL	NULL	NULL	NULL	occlusion of the reservoir	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HCC recurred after an occlusion of the reservoir in 18 patients .
	manualset3
83604	3	398089	5	NULL	NULL	NULL	NULL	18 patients	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HCC recurred after an occlusion of the reservoir in 18 patients .
	manualset3
83605	1	398090	5	NULL	NULL	0	NULL	HCF-1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HCF-1 is a highly conserved and abundant chromatin-associated host cell factor required for transcriptional activation of herpes simplex virus immediate-early genes by the virion protein VP16 .
	manualset3
83606	2	398090	5	NULL	NULL	0	NULL	highly conserved and abundant chromatin-associated host cell factor	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HCF-1 is a highly conserved and abundant chromatin-associated host cell factor required for transcriptional activation of herpes simplex virus immediate-early genes by the virion protein VP16 .
	manualset3
83607	3	398090	5	NULL	NULL	0	NULL	transcriptional activation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HCF-1 is a highly conserved and abundant chromatin-associated host cell factor required for transcriptional activation of herpes simplex virus immediate-early genes by the virion protein VP16 .
	manualset3
83608	4	398090	5	NULL	NULL	0	NULL	herpes simplex virus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	HCF-1 is a highly conserved and abundant chromatin-associated host cell factor required for transcriptional activation of herpes simplex virus immediate-early genes by the virion protein VP16 .
	manualset3
83609	5	398090	5	NULL	NULL	0	NULL	immediate-early genes	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	HCF-1 is a highly conserved and abundant chromatin-associated host cell factor required for transcriptional activation of herpes simplex virus immediate-early genes by the virion protein VP16 .
	manualset3
83610	6	398090	5	NULL	NULL	0	NULL	virion protein VP16	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HCF-1 is a highly conserved and abundant chromatin-associated host cell factor required for transcriptional activation of herpes simplex virus immediate-early genes by the virion protein VP16 .
	manualset3
83611	1	398091	5	NULL	NULL	0	NULL	HCMV infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	HCMV infection resulted in increased Sp1 mRNA expression , protein levels , and DNA binding activity .
	manualset3
83612	2	398091	5	NULL	NULL	0	NULL	Sp1 mRNA expression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HCMV infection resulted in increased Sp1 mRNA expression , protein levels , and DNA binding activity .
	manualset3
83613	3	398091	5	NULL	NULL	0	NULL	protein levels	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	HCMV infection resulted in increased Sp1 mRNA expression , protein levels , and DNA binding activity .
	manualset3
83614	4	398091	5	NULL	NULL	0	NULL	DNA binding activity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HCMV infection resulted in increased Sp1 mRNA expression , protein levels , and DNA binding activity .
	manualset3
83615	1	398092	5	NULL	NULL	0	NULL	HDAC8	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HDAC8 enhanced endocytosis , acidification , and penetration of the incoming virus .
	manualset3
83616	2	398092	5	NULL	NULL	0	NULL	endocytosis 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HDAC8 enhanced endocytosis , acidification , and penetration of the incoming virus .
	manualset3
83617	3	398092	5	NULL	NULL	0	NULL	acidification 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HDAC8 enhanced endocytosis , acidification , and penetration of the incoming virus .
	manualset3
83618	4	398092	5	NULL	NULL	0	NULL	penetration 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HDAC8 enhanced endocytosis , acidification , and penetration of the incoming virus .
	manualset3
83619	5	398092	5	NULL	NULL	0	NULL	incoming virus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	HDAC8 enhanced endocytosis , acidification , and penetration of the incoming virus .
	manualset3
83620	1	398093	5	NULL	NULL	0	NULL	HDL-C : LDL-C ratios	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	HDL-C : LDL-C ratios increased significantly in the estrogen and raloxifene groups ( range 9-29 % ) .
	manualset3
83621	2	398093	5	NULL	NULL	NULL	NULL	estrogen and raloxifene groups	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HDL-C : LDL-C ratios increased significantly in the estrogen and raloxifene groups ( range 9-29 % ) .
	manualset3
83622	3	398093	5	NULL	NULL	0	NULL	range 9-29 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	HDL-C : LDL-C ratios increased significantly in the estrogen and raloxifene groups ( range 9-29 % ) .
	manualset3
83623	1	398094	5	NULL	NULL	0	NULL	Stem cell regulation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Stem cell regulation in plants ) .
	manualset3
83624	2	398094	5	NULL	NULL	0	NULL	plants	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Stem cell regulation in plants ) .
	manualset3
83625	1	398095	5	NULL	NULL	0	NULL	HER-2 / neu-overexpressing breast cancer cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	HER-2 / neu-overexpressing breast cancer cells are more resistant to the chemotherapeutic agent paclitaxel ( Taxol ) than low-HER-2 / neu-expressing breast cancer cells , and the adenoviral type 5 EIA can down-regulate HER-2 / neu overexpression .
	manualset3
83626	2	398095	5	NULL	NULL	0	NULL	resistant	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HER-2 / neu-overexpressing breast cancer cells are more resistant to the chemotherapeutic agent paclitaxel ( Taxol ) than low-HER-2 / neu-expressing breast cancer cells , and the adenoviral type 5 EIA can down-regulate HER-2 / neu overexpression .
	manualset3
83627	3	398095	5	NULL	NULL	0	NULL	chemotherapeutic agent paclitaxel ( Taxol )	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	HER-2 / neu-overexpressing breast cancer cells are more resistant to the chemotherapeutic agent paclitaxel ( Taxol ) than low-HER-2 / neu-expressing breast cancer cells , and the adenoviral type 5 EIA can down-regulate HER-2 / neu overexpression .
	manualset3
83628	4	398095	5	NULL	NULL	0	NULL	low-HER-2 / neu-expressing breast cancer cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	HER-2 / neu-overexpressing breast cancer cells are more resistant to the chemotherapeutic agent paclitaxel ( Taxol ) than low-HER-2 / neu-expressing breast cancer cells , and the adenoviral type 5 EIA can down-regulate HER-2 / neu overexpression .
	manualset3
83629	5	398095	5	NULL	NULL	0	NULL	adenoviral type 5 EIA	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	HER-2 / neu-overexpressing breast cancer cells are more resistant to the chemotherapeutic agent paclitaxel ( Taxol ) than low-HER-2 / neu-expressing breast cancer cells , and the adenoviral type 5 EIA can down-regulate HER-2 / neu overexpression .
	manualset3
83630	6	398095	5	NULL	NULL	0	NULL	HER-2 / neu overexpression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HER-2 / neu-overexpressing breast cancer cells are more resistant to the chemotherapeutic agent paclitaxel ( Taxol ) than low-HER-2 / neu-expressing breast cancer cells , and the adenoviral type 5 EIA can down-regulate HER-2 / neu overexpression .
	manualset3
83631	1	398096	5	NULL	NULL	0	NULL	HERV ( Human Endogenous Retrovirus )	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	HERV ( Human Endogenous Retrovirus ) - encoded envelope proteins are implicated in the development of the placenta .
	manualset3
83632	2	398096	5	NULL	NULL	0	NULL	envelope proteins	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HERV ( Human Endogenous Retrovirus ) - encoded envelope proteins are implicated in the development of the placenta .
	manualset3
83633	3	398096	5	NULL	NULL	0	NULL	development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HERV ( Human Endogenous Retrovirus ) - encoded envelope proteins are implicated in the development of the placenta .
	manualset3
83634	4	398096	5	NULL	NULL	0	NULL	placenta	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	HERV ( Human Endogenous Retrovirus ) - encoded envelope proteins are implicated in the development of the placenta .
	manualset3
83635	1	398097	5	NULL	NULL	0	NULL	HEW-NIH dtente	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	HEW-NIH dtente , plus other matters .
	manualset3
83636	1	398098	5	NULL	NULL	0	NULL	HEX1-N2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HEX1-N2 is approximately 3-fold less active in Mn ( 2 + ) - containing buffers and exhibits & lt ; 5 % activity in the presence of Co ( 2 + ) , Zn ( 2 + ) , or Ca ( 2 + ) .
	manualset3
83637	2	398098	5	NULL	NULL	0	NULL	3-fold less active	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	HEX1-N2 is approximately 3-fold less active in Mn ( 2 + ) - containing buffers and exhibits & lt ; 5 % activity in the presence of Co ( 2 + ) , Zn ( 2 + ) , or Ca ( 2 + ) .
	manualset3
83638	3	398098	5	NULL	NULL	0	NULL	Mn ( 2 + ) - containing buffers	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	HEX1-N2 is approximately 3-fold less active in Mn ( 2 + ) - containing buffers and exhibits & lt ; 5 % activity in the presence of Co ( 2 + ) , Zn ( 2 + ) , or Ca ( 2 + ) .
	manualset3
83639	4	398098	5	NULL	NULL	0	NULL	5 % activity	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	HEX1-N2 is approximately 3-fold less active in Mn ( 2 + ) - containing buffers and exhibits & lt ; 5 % activity in the presence of Co ( 2 + ) , Zn ( 2 + ) , or Ca ( 2 + ) .
	manualset3
83640	5	398098	5	NULL	NULL	0	NULL	Co ( 2 + )	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	HEX1-N2 is approximately 3-fold less active in Mn ( 2 + ) - containing buffers and exhibits & lt ; 5 % activity in the presence of Co ( 2 + ) , Zn ( 2 + ) , or Ca ( 2 + ) .
	manualset3
83641	6	398098	5	NULL	NULL	0	NULL	Zn ( 2 + )	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	HEX1-N2 is approximately 3-fold less active in Mn ( 2 + ) - containing buffers and exhibits & lt ; 5 % activity in the presence of Co ( 2 + ) , Zn ( 2 + ) , or Ca ( 2 + ) .
	manualset3
83642	7	398098	5	NULL	NULL	0	NULL	Ca ( 2 + )	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	HEX1-N2 is approximately 3-fold less active in Mn ( 2 + ) - containing buffers and exhibits & lt ; 5 % activity in the presence of Co ( 2 + ) , Zn ( 2 + ) , or Ca ( 2 + ) .
	manualset3
83643	1	398099	5	NULL	NULL	0	NULL	HEp-2 cell monolayers	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	HEp-2 cell monolayers were cocultured with intracellular Staphylococcus aureus , and changes in gene expression were profiled using DNA microarrays .
	manualset3
83644	2	398099	5	NULL	NULL	0	NULL	intracellular Staphylococcus aureus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	HEp-2 cell monolayers were cocultured with intracellular Staphylococcus aureus , and changes in gene expression were profiled using DNA microarrays .
	manualset3
83645	3	398099	5	NULL	NULL	0	NULL	changes in gene expression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HEp-2 cell monolayers were cocultured with intracellular Staphylococcus aureus , and changes in gene expression were profiled using DNA microarrays .
	manualset3
83646	4	398099	5	NULL	NULL	0	NULL	DNA microarrays	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	HEp-2 cell monolayers were cocultured with intracellular Staphylococcus aureus , and changes in gene expression were profiled using DNA microarrays .
	manualset3
83647	1	398100	5	NULL	NULL	0	NULL	HG stimulation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HG stimulation of VEGF synthesis is prevented by captopril , an inhibitor of angiotensin-converting enzyme , and , by losartan , a specific antagonist of angiotensin type 1 receptor ( AT1 ) , suggesting that VEGF synthesis is mediated by Ang II .
	manualset3
83648	2	398100	5	NULL	NULL	0	NULL	VEGF synthesis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HG stimulation of VEGF synthesis is prevented by captopril , an inhibitor of angiotensin-converting enzyme , and , by losartan , a specific antagonist of angiotensin type 1 receptor ( AT1 ) , suggesting that VEGF synthesis is mediated by Ang II .
	manualset3
83649	3	398100	5	NULL	NULL	0	NULL	captopril 	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	HG stimulation of VEGF synthesis is prevented by captopril , an inhibitor of angiotensin-converting enzyme , and , by losartan , a specific antagonist of angiotensin type 1 receptor ( AT1 ) , suggesting that VEGF synthesis is mediated by Ang II .
	manualset3
83650	4	398100	5	NULL	NULL	0	NULL	inhibitor of angiotensin-converting enzyme	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	HG stimulation of VEGF synthesis is prevented by captopril , an inhibitor of angiotensin-converting enzyme , and , by losartan , a specific antagonist of angiotensin type 1 receptor ( AT1 ) , suggesting that VEGF synthesis is mediated by Ang II .
	manualset3
83651	5	398100	5	NULL	NULL	0	NULL	losartan	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	HG stimulation of VEGF synthesis is prevented by captopril , an inhibitor of angiotensin-converting enzyme , and , by losartan , a specific antagonist of angiotensin type 1 receptor ( AT1 ) , suggesting that VEGF synthesis is mediated by Ang II .
	manualset3
83652	6	398100	5	NULL	NULL	0	NULL	specific antagonist of angiotensin type 1 receptor ( AT1 ) 	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	HG stimulation of VEGF synthesis is prevented by captopril , an inhibitor of angiotensin-converting enzyme , and , by losartan , a specific antagonist of angiotensin type 1 receptor ( AT1 ) , suggesting that VEGF synthesis is mediated by Ang II .
	manualset3
83653	7	398100	5	NULL	NULL	0	NULL	VEGF synthesis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HG stimulation of VEGF synthesis is prevented by captopril , an inhibitor of angiotensin-converting enzyme , and , by losartan , a specific antagonist of angiotensin type 1 receptor ( AT1 ) , suggesting that VEGF synthesis is mediated by Ang II .
	manualset3
83654	8	398100	5	NULL	NULL	0	NULL	Ang II	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HG stimulation of VEGF synthesis is prevented by captopril , an inhibitor of angiotensin-converting enzyme , and , by losartan , a specific antagonist of angiotensin type 1 receptor ( AT1 ) , suggesting that VEGF synthesis is mediated by Ang II .
	manualset3
83655	1	398101	5	NULL	NULL	0	NULL	HGF mRNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	HGF mRNA was elevated following obstruction and showed increased expression 1 day after decompression , peaking at 2 days of repair .
	manualset3
83656	2	398101	5	NULL	NULL	0	NULL	obstruction	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	HGF mRNA was elevated following obstruction and showed increased expression 1 day after decompression , peaking at 2 days of repair .
	manualset3
83657	3	398101	5	NULL	NULL	0	NULL	increased expression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HGF mRNA was elevated following obstruction and showed increased expression 1 day after decompression , peaking at 2 days of repair .
	manualset3
83658	4	398101	5	NULL	NULL	0	NULL	1 day	TimePoint												NULL		0	NULL	NULL	NULL	NULL	NULL	HGF mRNA was elevated following obstruction and showed increased expression 1 day after decompression , peaking at 2 days of repair .
	manualset3
83659	5	398101	5	NULL	NULL	NULL	NULL	decompression 	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HGF mRNA was elevated following obstruction and showed increased expression 1 day after decompression , peaking at 2 days of repair .
	manualset3
83660	6	398101	5	NULL	NULL	0	NULL	2 days	TimePoint												NULL		0	NULL	NULL	NULL	NULL	NULL	HGF mRNA was elevated following obstruction and showed increased expression 1 day after decompression , peaking at 2 days of repair .
	manualset3
83661	7	398101	5	NULL	NULL	0	NULL	repair	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HGF mRNA was elevated following obstruction and showed increased expression 1 day after decompression , peaking at 2 days of repair .
	manualset3
83662	1	398102	5	NULL	NULL	0	NULL	HIF-1 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HIF-1 and mechanisms of hypoxia sensing .
	manualset3
83663	2	398102	5	NULL	NULL	NULL	NULL	mechanisms	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HIF-1 and mechanisms of hypoxia sensing .
	manualset3
83664	3	398102	5	NULL	NULL	0	NULL	hypoxia sensing	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HIF-1 and mechanisms of hypoxia sensing .
	manualset3
83665	1	398103	5	NULL	NULL	0	NULL	Stiff man syndrome	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Stiff man syndrome ( Moersch and Woltman syndrome ) .
	manualset3
83666	2	398103	5	NULL	NULL	0	NULL	Moersch and Woltman syndrome	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Stiff man syndrome ( Moersch and Woltman syndrome ) .
	manualset3
83667	1	398104	5	NULL	NULL	0	NULL	HIV-1	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	HIV-1 acquires resistance to two classes of antiviral drugs through homologous recombination .
	manualset3
83668	2	398104	5	NULL	NULL	0	NULL	resistance 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HIV-1 acquires resistance to two classes of antiviral drugs through homologous recombination .
	manualset3
83669	3	398104	5	NULL	NULL	0	NULL	antiviral drugs	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	HIV-1 acquires resistance to two classes of antiviral drugs through homologous recombination .
	manualset3
83670	4	398104	5	NULL	NULL	0	NULL	homologous recombination	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HIV-1 acquires resistance to two classes of antiviral drugs through homologous recombination .
	manualset3
83671	1	398105	5	NULL	NULL	0	NULL	HIV-1 transcription	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HIV-1 transcription is activated by HIV-1 Tat protein , which recruits cyclin-dependent kinase 9 ( CDK9 ) / cyclin T1 and other host transcriptional coactivators to the HIV-1 promoter .
	manualset3
83672	2	398105	5	NULL	NULL	0	NULL	HIV-1 Tat protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HIV-1 transcription is activated by HIV-1 Tat protein , which recruits cyclin-dependent kinase 9 ( CDK9 ) / cyclin T1 and other host transcriptional coactivators to the HIV-1 promoter .
	manualset3
83673	3	398105	5	NULL	NULL	0	NULL	cyclin-dependent kinase 9 ( CDK9 ) / cyclin T1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HIV-1 transcription is activated by HIV-1 Tat protein , which recruits cyclin-dependent kinase 9 ( CDK9 ) / cyclin T1 and other host transcriptional coactivators to the HIV-1 promoter .
	manualset3
83674	4	398105	5	NULL	NULL	0	NULL	host transcriptional coactivators	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HIV-1 transcription is activated by HIV-1 Tat protein , which recruits cyclin-dependent kinase 9 ( CDK9 ) / cyclin T1 and other host transcriptional coactivators to the HIV-1 promoter .
	manualset3
83675	5	398105	5	NULL	NULL	0	NULL	HIV-1 promoter	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	HIV-1 transcription is activated by HIV-1 Tat protein , which recruits cyclin-dependent kinase 9 ( CDK9 ) / cyclin T1 and other host transcriptional coactivators to the HIV-1 promoter .
	manualset3
83676	1	398106	5	NULL	NULL	0	NULL	HIV infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	HIV infection : treatment outcomes in older and younger adults .
	manualset3
83677	2	398106	5	NULL	NULL	0	NULL	treatment outcomes	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	HIV infection : treatment outcomes in older and younger adults .
	manualset3
83678	3	398106	5	NULL	NULL	0	NULL	older and younger adults	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	HIV infection : treatment outcomes in older and younger adults .
	manualset3
83679	1	398107	5	NULL	NULL	0	NULL	HIV transmission	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HIV transmission has been facilitated by ( a ) concomitant sexually transmitted diseases ( STDs ) , ( b ) the presence of social conditions that create core groups who have frequent and numerous partners , ( c ) sexual practices associated with bleeding ( i.e. , trauma , sex during menses ) as well as noncircumcision , ( d ) cervical ectopy , and ( e ) anal sex .
	manualset3
83680	2	398107	5	NULL	NULL	0	NULL	concomitant sexually transmitted diseases ( STDs )	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	HIV transmission has been facilitated by ( a ) concomitant sexually transmitted diseases ( STDs ) , ( b ) the presence of social conditions that create core groups who have frequent and numerous partners , ( c ) sexual practices associated with bleeding ( i.e. , trauma , sex during menses ) as well as noncircumcision , ( d ) cervical ectopy , and ( e ) anal sex .
	manualset3
83681	3	398107	5	NULL	NULL	NULL	NULL	social conditions	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HIV transmission has been facilitated by ( a ) concomitant sexually transmitted diseases ( STDs ) , ( b ) the presence of social conditions that create core groups who have frequent and numerous partners , ( c ) sexual practices associated with bleeding ( i.e. , trauma , sex during menses ) as well as noncircumcision , ( d ) cervical ectopy , and ( e ) anal sex .
	manualset3
83682	4	398107	5	NULL	NULL	0	NULL	core groups	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	HIV transmission has been facilitated by ( a ) concomitant sexually transmitted diseases ( STDs ) , ( b ) the presence of social conditions that create core groups who have frequent and numerous partners , ( c ) sexual practices associated with bleeding ( i.e. , trauma , sex during menses ) as well as noncircumcision , ( d ) cervical ectopy , and ( e ) anal sex .
	manualset3
83683	5	398107	5	NULL	NULL	0	NULL	frequent and numerous partners	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	HIV transmission has been facilitated by ( a ) concomitant sexually transmitted diseases ( STDs ) , ( b ) the presence of social conditions that create core groups who have frequent and numerous partners , ( c ) sexual practices associated with bleeding ( i.e. , trauma , sex during menses ) as well as noncircumcision , ( d ) cervical ectopy , and ( e ) anal sex .
	manualset3
83684	6	398107	5	NULL	NULL	NULL	NULL	sexual practices associated with bleeding	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HIV transmission has been facilitated by ( a ) concomitant sexually transmitted diseases ( STDs ) , ( b ) the presence of social conditions that create core groups who have frequent and numerous partners , ( c ) sexual practices associated with bleeding ( i.e. , trauma , sex during menses ) as well as noncircumcision , ( d ) cervical ectopy , and ( e ) anal sex .
	manualset3
83686	7	398107	5	NULL	NULL	NULL	NULL	trauma	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HIV transmission has been facilitated by ( a ) concomitant sexually transmitted diseases ( STDs ) , ( b ) the presence of social conditions that create core groups who have frequent and numerous partners , ( c ) sexual practices associated with bleeding ( i.e. , trauma , sex during menses ) as well as noncircumcision , ( d ) cervical ectopy , and ( e ) anal sex .
	manualset3
83687	8	398107	5	NULL	NULL	NULL	NULL	sex during menses	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HIV transmission has been facilitated by ( a ) concomitant sexually transmitted diseases ( STDs ) , ( b ) the presence of social conditions that create core groups who have frequent and numerous partners , ( c ) sexual practices associated with bleeding ( i.e. , trauma , sex during menses ) as well as noncircumcision , ( d ) cervical ectopy , and ( e ) anal sex .
	manualset3
83689	9	398107	5	NULL	NULL	NULL	NULL	noncircumcision	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HIV transmission has been facilitated by ( a ) concomitant sexually transmitted diseases ( STDs ) , ( b ) the presence of social conditions that create core groups who have frequent and numerous partners , ( c ) sexual practices associated with bleeding ( i.e. , trauma , sex during menses ) as well as noncircumcision , ( d ) cervical ectopy , and ( e ) anal sex .
	manualset3
83690	10	398107	5	NULL	NULL	NULL	NULL	cervical ectopy	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HIV transmission has been facilitated by ( a ) concomitant sexually transmitted diseases ( STDs ) , ( b ) the presence of social conditions that create core groups who have frequent and numerous partners , ( c ) sexual practices associated with bleeding ( i.e. , trauma , sex during menses ) as well as noncircumcision , ( d ) cervical ectopy , and ( e ) anal sex .
	manualset3
83691	11	398107	5	NULL	NULL	NULL	NULL	anal sex	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HIV transmission has been facilitated by ( a ) concomitant sexually transmitted diseases ( STDs ) , ( b ) the presence of social conditions that create core groups who have frequent and numerous partners , ( c ) sexual practices associated with bleeding ( i.e. , trauma , sex during menses ) as well as noncircumcision , ( d ) cervical ectopy , and ( e ) anal sex .
	manualset3
83692	1	398108	5	NULL	NULL	0	NULL	HLA allotyping	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	HLA allotyping strongly suggested C2 depression associated with a C4BQ0 allele .
	manualset3
83693	2	398108	5	NULL	NULL	0	NULL	C2 depression	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	HLA allotyping strongly suggested C2 depression associated with a C4BQ0 allele .
	manualset3
83694	3	398108	5	NULL	NULL	0	NULL	C4BQ0 allele	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	HLA allotyping strongly suggested C2 depression associated with a C4BQ0 allele .
	manualset3
83695	1	398109	5	NULL	NULL	0	NULL	HLA	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HLA is the most informative system in all three populations , followed by PGM1 , with the rhesus blood group the next most useful in the whites and ` coloured 's , whereas ABO is the next most useful in the blacks .
	manualset3
83697	2	398109	5	NULL	NULL	NULL	NULL	three populations	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HLA is the most informative system in all three populations , followed by PGM1 , with the rhesus blood group the next most useful in the whites and ` coloured 's , whereas ABO is the next most useful in the blacks .
	manualset3
83698	3	398109	5	NULL	NULL	NULL	NULL	PGM1	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HLA is the most informative system in all three populations , followed by PGM1 , with the rhesus blood group the next most useful in the whites and ` coloured 's , whereas ABO is the next most useful in the blacks .
	manualset3
83699	4	398109	5	NULL	NULL	NULL	NULL	rhesus blood group	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HLA is the most informative system in all three populations , followed by PGM1 , with the rhesus blood group the next most useful in the whites and ` coloured 's , whereas ABO is the next most useful in the blacks .
	manualset3
83700	5	398109	5	NULL	NULL	NULL	NULL	whites and ` coloured 's	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HLA is the most informative system in all three populations , followed by PGM1 , with the rhesus blood group the next most useful in the whites and ` coloured 's , whereas ABO is the next most useful in the blacks .
	manualset3
83701	6	398109	5	NULL	NULL	NULL	NULL	ABO	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HLA is the most informative system in all three populations , followed by PGM1 , with the rhesus blood group the next most useful in the whites and ` coloured 's , whereas ABO is the next most useful in the blacks .
	manualset3
83702	7	398109	5	NULL	NULL	NULL	NULL	blacks	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HLA is the most informative system in all three populations , followed by PGM1 , with the rhesus blood group the next most useful in the whites and ` coloured 's , whereas ABO is the next most useful in the blacks .
	manualset3
83703	1	398110	5	NULL	NULL	0	NULL	HMGB1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HMGB1 interacts with human topoisomerase IIalpha and stimulates its catalytic activity .
	manualset3
83704	2	398110	5	NULL	NULL	0	NULL	human topoisomerase IIalpha	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HMGB1 interacts with human topoisomerase IIalpha and stimulates its catalytic activity .
	manualset3
83705	3	398110	5	NULL	NULL	0	NULL	catalytic activity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HMGB1 interacts with human topoisomerase IIalpha and stimulates its catalytic activity .
	manualset3
83706	1	398111	5	NULL	NULL	0	NULL	Storage	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Storage and blood coagulation in methylcellulose treated rats ) .
	manualset3
83707	2	398111	5	NULL	NULL	0	NULL	blood coagulation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Storage and blood coagulation in methylcellulose treated rats ) .
	manualset3
83708	3	398111	5	NULL	NULL	0	NULL	methylcellulose treated rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Storage and blood coagulation in methylcellulose treated rats ) .
	manualset3
83709	1	398112	5	NULL	NULL	0	NULL	HNa	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	HNa or LNa significantly increased or decreased MAP but had no effects on resting RSNA in SHR and had no effects on resting MAP and RSNA in WKY rats .
	manualset3
83710	2	398112	5	NULL	NULL	0	NULL	LNa	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	HNa or LNa significantly increased or decreased MAP but had no effects on resting RSNA in SHR and had no effects on resting MAP and RSNA in WKY rats .
	manualset3
83711	3	398112	5	NULL	NULL	0	NULL	MAP	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	HNa or LNa significantly increased or decreased MAP but had no effects on resting RSNA in SHR and had no effects on resting MAP and RSNA in WKY rats .
	manualset3
83712	4	398112	5	NULL	NULL	0	NULL	resting RSNA	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HNa or LNa significantly increased or decreased MAP but had no effects on resting RSNA in SHR and had no effects on resting MAP and RSNA in WKY rats .
	manualset3
83713	5	398112	5	NULL	NULL	0	NULL	SHR	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	HNa or LNa significantly increased or decreased MAP but had no effects on resting RSNA in SHR and had no effects on resting MAP and RSNA in WKY rats .
	manualset3
83714	6	398112	5	NULL	NULL	0	NULL	resting MAP	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	HNa or LNa significantly increased or decreased MAP but had no effects on resting RSNA in SHR and had no effects on resting MAP and RSNA in WKY rats .
	manualset3
83715	7	398112	5	NULL	NULL	0	NULL	RSNA	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HNa or LNa significantly increased or decreased MAP but had no effects on resting RSNA in SHR and had no effects on resting MAP and RSNA in WKY rats .
	manualset3
83716	8	398112	5	NULL	NULL	0	NULL	WKY rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	HNa or LNa significantly increased or decreased MAP but had no effects on resting RSNA in SHR and had no effects on resting MAP and RSNA in WKY rats .
	manualset3
83717	1	398113	5	NULL	NULL	0	NULL	HPV 16 and 18 DNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	HPV 16 and 18 DNA and virus-encoded antigens , L1 and E6 were found highly prevalent in these cervical carcinomas .
	manualset3
83718	2	398113	5	NULL	NULL	NULL	NULL	virus-encoded antigens , L1 and E6 	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HPV 16 and 18 DNA and virus-encoded antigens , L1 and E6 were found highly prevalent in these cervical carcinomas .
	manualset3
83719	3	398113	5	NULL	NULL	0	NULL	cervical carcinomas	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	HPV 16 and 18 DNA and virus-encoded antigens , L1 and E6 were found highly prevalent in these cervical carcinomas .
	manualset3
83720	1	398114	5	NULL	NULL	0	NULL	HPV infections	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	HPV infections are transient but on average last for more than one year suggesting that HPV has developed means to evade host immunity .
	manualset3
83721	2	398114	5	NULL	NULL	0	NULL	one year	TimePoint												NULL		0	NULL	NULL	NULL	NULL	NULL	HPV infections are transient but on average last for more than one year suggesting that HPV has developed means to evade host immunity .
	manualset3
83722	3	398114	5	NULL	NULL	0	NULL	HPV	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	HPV infections are transient but on average last for more than one year suggesting that HPV has developed means to evade host immunity .
	manualset3
83723	4	398114	5	NULL	NULL	0	NULL	host immunity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HPV infections are transient but on average last for more than one year suggesting that HPV has developed means to evade host immunity .
	manualset3
83724	1	398115	5	NULL	NULL	NULL	NULL	HSV-1 antigen	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HSV-1 antigen , glycoprotein D ( gD ) and regulatory protein ICP27 were detected in 8-18 % of the hypodiploid fraction of PHA-stimulated , HSV-1-infected lymphocytes .
	manualset3
83725	2	398115	5	NULL	NULL	0	NULL	glycoprotein D ( gD )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HSV-1 antigen , glycoprotein D ( gD ) and regulatory protein ICP27 were detected in 8-18 % of the hypodiploid fraction of PHA-stimulated , HSV-1-infected lymphocytes .
	manualset3
83726	3	398115	5	NULL	NULL	0	NULL	regulatory protein ICP27	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HSV-1 antigen , glycoprotein D ( gD ) and regulatory protein ICP27 were detected in 8-18 % of the hypodiploid fraction of PHA-stimulated , HSV-1-infected lymphocytes .
	manualset3
83727	4	398115	5	NULL	NULL	0	NULL	8-18 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	HSV-1 antigen , glycoprotein D ( gD ) and regulatory protein ICP27 were detected in 8-18 % of the hypodiploid fraction of PHA-stimulated , HSV-1-infected lymphocytes .
	manualset3
83728	5	398115	5	NULL	NULL	0	NULL	hypodiploid fraction	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	HSV-1 antigen , glycoprotein D ( gD ) and regulatory protein ICP27 were detected in 8-18 % of the hypodiploid fraction of PHA-stimulated , HSV-1-infected lymphocytes .
	manualset3
83729	6	398115	5	NULL	NULL	0	NULL	PHA-stimulated , HSV-1-infected lymphocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	HSV-1 antigen , glycoprotein D ( gD ) and regulatory protein ICP27 were detected in 8-18 % of the hypodiploid fraction of PHA-stimulated , HSV-1-infected lymphocytes .
	manualset3
83730	1	398116	5	NULL	NULL	0	NULL	HSV-2 positive individuals	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	HSV-2 positive individuals were found seropositive to HSV-1 in approximately 95 % of the cases .
	manualset3
83731	2	398116	5	NULL	NULL	0	NULL	HSV-1	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	HSV-2 positive individuals were found seropositive to HSV-1 in approximately 95 % of the cases .
	manualset3
83732	3	398116	5	NULL	NULL	0	NULL	95 % of the cases	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	HSV-2 positive individuals were found seropositive to HSV-1 in approximately 95 % of the cases .
	manualset3
83733	1	398117	5	NULL	NULL	0	NULL	HTP N-oxide ( HTPNO )	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	HTP N-oxide ( HTPNO ) exhibits a relatively weak effect on DA uptake .
	manualset3
83734	3	398117	5	NULL	NULL	NULL	NULL	DA uptake	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	HTP N-oxide ( HTPNO ) exhibits a relatively weak effect on DA uptake .
	manualset3
83735	2	398117	5	NULL	NULL	0	NULL	weak effect	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	HTP N-oxide ( HTPNO ) exhibits a relatively weak effect on DA uptake .
	manualset3
83736	1	398118	5	NULL	NULL	0	NULL	HVC	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	HVC receives new neurons in adulthood .
	manualset3
83737	2	398118	5	NULL	NULL	0	NULL	new neurons	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	HVC receives new neurons in adulthood .
	manualset3
83738	3	398118	5	NULL	NULL	0	NULL	adulthood	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	HVC receives new neurons in adulthood .
	manualset3
83739	1	398119	5	NULL	NULL	0	NULL	Mycobacterium paratuberculosis	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Strain of Mycobacterium paratuberculosis ; observations on its isolation and on its pathogenic activity ) .
	manualset3
83740	2	398119	5	NULL	NULL	0	NULL	observations	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Strain of Mycobacterium paratuberculosis ; observations on its isolation and on its pathogenic activity ) .
	manualset3
83741	3	398119	5	NULL	NULL	NULL	NULL	isolation	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Strain of Mycobacterium paratuberculosis ; observations on its isolation and on its pathogenic activity ) .
	manualset3
83742	4	398119	5	NULL	NULL	0	NULL	pathogenic activity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Strain of Mycobacterium paratuberculosis ; observations on its isolation and on its pathogenic activity ) .
	manualset3
83743	1	398120	5	NULL	NULL	0	NULL	HYAL-1 ( hyaluronoglucosaminidase-1 ) 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HYAL-1 ( hyaluronoglucosaminidase-1 ) belongs to the hyaluronidase family of enzymes that degrade hyaluronic acid .
	manualset3
83744	2	398120	5	NULL	NULL	0	NULL	hyaluronidase family	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HYAL-1 ( hyaluronoglucosaminidase-1 ) belongs to the hyaluronidase family of enzymes that degrade hyaluronic acid .
	manualset3
83745	3	398120	5	NULL	NULL	0	NULL	enzymes	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HYAL-1 ( hyaluronoglucosaminidase-1 ) belongs to the hyaluronidase family of enzymes that degrade hyaluronic acid .
	manualset3
83746	4	398120	5	NULL	NULL	0	NULL	hyaluronic acid	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	HYAL-1 ( hyaluronoglucosaminidase-1 ) belongs to the hyaluronidase family of enzymes that degrade hyaluronic acid .
	manualset3
83747	1	398121	5	NULL	NULL	0	NULL	Habitat associations	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Habitat associations , reproduction and diet of the Guinean tilapia Tilapia guineensis of the Gambia River floodplains .
	manualset3
83748	2	398121	5	NULL	NULL	0	NULL	reproduction	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Habitat associations , reproduction and diet of the Guinean tilapia Tilapia guineensis of the Gambia River floodplains .
	manualset3
83749	3	398121	5	NULL	NULL	0	NULL	diet	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	Habitat associations , reproduction and diet of the Guinean tilapia Tilapia guineensis of the Gambia River floodplains .
	manualset3
83750	4	398121	5	NULL	NULL	0	NULL	Guinean tilapia Tilapia guineensis	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Habitat associations , reproduction and diet of the Guinean tilapia Tilapia guineensis of the Gambia River floodplains .
	manualset3
83751	5	398121	5	NULL	NULL	0	NULL	Gambia River floodplains	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Habitat associations , reproduction and diet of the Guinean tilapia Tilapia guineensis of the Gambia River floodplains .
	manualset3
83752	1	398122	5	NULL	NULL	0	NULL	Haemangiosarcoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemangiosarcoma was diagnosed on biopsy .
	manualset3
83753	2	398122	5	NULL	NULL	0	NULL	biopsy	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemangiosarcoma was diagnosed on biopsy .
	manualset3
83754	1	398123	5	NULL	NULL	0	NULL	Haematological toxicity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Haematological toxicity was common ( about 40 % of the children , 11 in the twice - and 19 in the once-daily group ) but never severe .
	manualset3
83755	2	398123	5	NULL	NULL	0	NULL	 40 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Haematological toxicity was common ( about 40 % of the children , 11 in the twice - and 19 in the once-daily group ) but never severe .
	manualset3
83756	3	398123	5	NULL	NULL	0	NULL	 children	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Haematological toxicity was common ( about 40 % of the children , 11 in the twice - and 19 in the once-daily group ) but never severe .
	manualset3
83757	4	398123	5	NULL	NULL	0	NULL	11 in the twice - and 19 in the once-daily group	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Haematological toxicity was common ( about 40 % of the children , 11 in the twice - and 19 in the once-daily group ) but never severe .
	manualset3
83758	1	398124	5	NULL	NULL	0	NULL	Haemocyte lysate	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemocyte lysate was able to activate the plasma proPO indicating location of the prophenoloxidase activating enzyme ( PPAE ) in hemocytes .
	manualset3
83759	2	398124	5	NULL	NULL	0	NULL	plasma proPO	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemocyte lysate was able to activate the plasma proPO indicating location of the prophenoloxidase activating enzyme ( PPAE ) in hemocytes .
	manualset3
83760	3	398124	5	NULL	NULL	0	NULL	 prophenoloxidase activating enzyme ( PPAE )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemocyte lysate was able to activate the plasma proPO indicating location of the prophenoloxidase activating enzyme ( PPAE ) in hemocytes .
	manualset3
83761	4	398124	5	NULL	NULL	0	NULL	hemocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemocyte lysate was able to activate the plasma proPO indicating location of the prophenoloxidase activating enzyme ( PPAE ) in hemocytes .
	manualset3
83762	1	398125	5	NULL	NULL	0	NULL	Haemodynamic changes	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemodynamic changes following carotid occlusion : MRI angiography and transcranial Doppler patterns .
	manualset3
83763	2	398125	5	NULL	NULL	0	NULL	carotid occlusion	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemodynamic changes following carotid occlusion : MRI angiography and transcranial Doppler patterns .
	manualset3
83764	3	398125	5	NULL	NULL	0	NULL	MRI angiography	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemodynamic changes following carotid occlusion : MRI angiography and transcranial Doppler patterns .
	manualset3
83765	4	398125	5	NULL	NULL	0	NULL	transcranial Doppler patterns	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemodynamic changes following carotid occlusion : MRI angiography and transcranial Doppler patterns .
	manualset3
83766	1	398126	5	NULL	NULL	0	NULL	Haemodynamics	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemodynamics in early essential hypertension -- still an area of controversy .
	manualset3
83767	2	398126	5	NULL	NULL	0	NULL	early essential hypertension	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemodynamics in early essential hypertension -- still an area of controversy .
	manualset3
83768	1	398127	5	NULL	NULL	0	NULL	Haemolytic assays	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemolytic assays were conducted to investigate the activation of the human serum complement system via the classical and alternative pathways .
	manualset3
83769	2	398127	5	NULL	NULL	0	NULL	activation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemolytic assays were conducted to investigate the activation of the human serum complement system via the classical and alternative pathways .
	manualset3
83770	3	398127	5	NULL	NULL	0	NULL	human serum complement system	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemolytic assays were conducted to investigate the activation of the human serum complement system via the classical and alternative pathways .
	manualset3
83771	4	398127	5	NULL	NULL	0	NULL	classical and alternative pathways	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemolytic assays were conducted to investigate the activation of the human serum complement system via the classical and alternative pathways .
	manualset3
83772	1	398128	5	NULL	NULL	0	NULL	Haemophilus aphrophilus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemophilus aphrophilus isolated from blood .
	manualset3
83773	2	398128	5	NULL	NULL	0	NULL	blood	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemophilus aphrophilus isolated from blood .
	manualset3
83775	1	398130	5	NULL	NULL	0	NULL	Haemorrhagic thrombocythemia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemorrhagic thrombocythemia : a clinical and laboratory study .
	manualset3
83776	2	398130	5	NULL	NULL	0	NULL	clinical and laboratory study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Haemorrhagic thrombocythemia : a clinical and laboratory study .
	manualset3
83778	1	398131	5	NULL	NULL	0	NULL	Haghighi S	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Haghighi S , Lekman A , Nilsson S , Blomqvist M , Andersen O. Myelin glycosphingolipid immunoreactivity and CSF levels in multiple sclerosis .
	manualset3
83779	2	398131	5	NULL	NULL	0	NULL	Lekman A	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Haghighi S , Lekman A , Nilsson S , Blomqvist M , Andersen O. Myelin glycosphingolipid immunoreactivity and CSF levels in multiple sclerosis .
	manualset3
83780	3	398131	5	NULL	NULL	0	NULL	Nilsson S	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Haghighi S , Lekman A , Nilsson S , Blomqvist M , Andersen O. Myelin glycosphingolipid immunoreactivity and CSF levels in multiple sclerosis .
	manualset3
83781	4	398131	5	NULL	NULL	0	NULL	Blomqvist M	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Haghighi S , Lekman A , Nilsson S , Blomqvist M , Andersen O. Myelin glycosphingolipid immunoreactivity and CSF levels in multiple sclerosis .
	manualset3
83782	5	398131	5	NULL	NULL	0	NULL	Andersen O	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Haghighi S , Lekman A , Nilsson S , Blomqvist M , Andersen O. Myelin glycosphingolipid immunoreactivity and CSF levels in multiple sclerosis .
	manualset3
83783	6	398131	5	NULL	NULL	0	NULL	Myelin glycosphingolipid immunoreactivity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Haghighi S , Lekman A , Nilsson S , Blomqvist M , Andersen O. Myelin glycosphingolipid immunoreactivity and CSF levels in multiple sclerosis .
	manualset3
83784	7	398131	5	NULL	NULL	0	NULL	CSF levels	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Haghighi S , Lekman A , Nilsson S , Blomqvist M , Andersen O. Myelin glycosphingolipid immunoreactivity and CSF levels in multiple sclerosis .
	manualset3
83785	8	398131	5	NULL	NULL	0	NULL	multiple sclerosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Haghighi S , Lekman A , Nilsson S , Blomqvist M , Andersen O. Myelin glycosphingolipid immunoreactivity and CSF levels in multiple sclerosis .
	manualset3
83786	1	398132	5	NULL	NULL	0	NULL	Hair follicle delivery systems	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hair follicle delivery systems are described , such as liposomes and viral vectors for gene therapy .
	manualset3
83787	2	398132	5	NULL	NULL	NULL	NULL	liposomes	LaboratoryExperimentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hair follicle delivery systems are described , such as liposomes and viral vectors for gene therapy .
	manualset3
83788	3	398132	5	NULL	NULL	0	NULL	viral vectors	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Hair follicle delivery systems are described , such as liposomes and viral vectors for gene therapy .
	manualset3
83789	4	398132	5	NULL	NULL	0	NULL	gene therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hair follicle delivery systems are described , such as liposomes and viral vectors for gene therapy .
	manualset3
83790	1	398133	5	NULL	NULL	0	NULL	Hair follicles	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hair follicles : kinetic concepts and human disease .
	manualset3
83791	2	398133	5	NULL	NULL	0	NULL	kinetic concepts	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hair follicles : kinetic concepts and human disease .
	manualset3
83792	3	398133	5	NULL	NULL	0	NULL	human disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hair follicles : kinetic concepts and human disease .
	manualset3
83793	1	398134	5	NULL	NULL	0	NULL	Hair pellets	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hair pellets of 10 New Zealand rabbits were prepared and shaped as 1 x 1 x 1-cm cubes with the help of fibrin sealant , then inserted subcutaneously .
	manualset3
83794	2	398134	5	NULL	NULL	0	NULL	10 New Zealand rabbits	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hair pellets of 10 New Zealand rabbits were prepared and shaped as 1 x 1 x 1-cm cubes with the help of fibrin sealant , then inserted subcutaneously .
	manualset3
83795	3	398134	5	NULL	NULL	0	NULL	1 x 1 x 1-cm cubes	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hair pellets of 10 New Zealand rabbits were prepared and shaped as 1 x 1 x 1-cm cubes with the help of fibrin sealant , then inserted subcutaneously .
	manualset3
83796	4	398134	5	NULL	NULL	0	NULL	fibrin sealant	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Hair pellets of 10 New Zealand rabbits were prepared and shaped as 1 x 1 x 1-cm cubes with the help of fibrin sealant , then inserted subcutaneously .
	manualset3
83797	1	398135	5	NULL	NULL	0	NULL	Hairy cell leukemia hemopathy	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hairy cell leukemia hemopathy is a rare lymphod hemopathy type B. 8 cases are reported and diagnosed at Hpital Aziza Othmana over a period of 20 years between 1979 and 1999 , 7 men and one women .
	manualset3
83798	2	398135	5	NULL	NULL	0	NULL	 rare lymphod hemopathy type B	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hairy cell leukemia hemopathy is a rare lymphod hemopathy type B. 8 cases are reported and diagnosed at Hpital Aziza Othmana over a period of 20 years between 1979 and 1999 , 7 men and one women .
	manualset3
83799	3	398135	5	NULL	NULL	NULL	NULL	8 cases	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hairy cell leukemia hemopathy is a rare lymphod hemopathy type B. 8 cases are reported and diagnosed at Hpital Aziza Othmana over a period of 20 years between 1979 and 1999 , 7 men and one women .
	manualset3
83800	4	398135	5	NULL	NULL	0	NULL	Hpital Aziza Othmana	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Hairy cell leukemia hemopathy is a rare lymphod hemopathy type B. 8 cases are reported and diagnosed at Hpital Aziza Othmana over a period of 20 years between 1979 and 1999 , 7 men and one women .
	manualset3
83801	5	398135	5	NULL	NULL	NULL	NULL	20 years	Time												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hairy cell leukemia hemopathy is a rare lymphod hemopathy type B. 8 cases are reported and diagnosed at Hpital Aziza Othmana over a period of 20 years between 1979 and 1999 , 7 men and one women .
	manualset3
83802	7	398135	5	NULL	NULL	NULL	NULL	7 men	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hairy cell leukemia hemopathy is a rare lymphod hemopathy type B. 8 cases are reported and diagnosed at Hpital Aziza Othmana over a period of 20 years between 1979 and 1999 , 7 men and one women .
	manualset3
83803	8	398135	5	NULL	NULL	NULL	NULL	one women	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hairy cell leukemia hemopathy is a rare lymphod hemopathy type B. 8 cases are reported and diagnosed at Hpital Aziza Othmana over a period of 20 years between 1979 and 1999 , 7 men and one women .
	manualset3
84550	6	398135	5	NULL	NULL	0	NULL	between 1979 and 1999	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Hairy cell leukemia hemopathy is a rare lymphod hemopathy type B. 8 cases are reported and diagnosed at Hpital Aziza Othmana over a period of 20 years between 1979 and 1999 , 7 men and one women .
	manualset3
83804	1	398136	5	NULL	NULL	0	NULL	Half of patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Half of patients with IF mutation had a rapid evolution to ESRD , and half recovered .
	manualset3
83805	2	398136	5	NULL	NULL	0	NULL	IF mutation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Half of patients with IF mutation had a rapid evolution to ESRD , and half recovered .
	manualset3
83806	3	398136	5	NULL	NULL	0	NULL	rapid evolution	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Half of patients with IF mutation had a rapid evolution to ESRD , and half recovered .
	manualset3
83807	4	398136	5	NULL	NULL	0	NULL	ESRD	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Half of patients with IF mutation had a rapid evolution to ESRD , and half recovered .
	manualset3
83808	1	398137	5	NULL	NULL	0	NULL	Structure-activity study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Structure-activity study of the HindIII-I fragment of the L-IVP strain of vaccinia virus genome .
	manualset3
83809	2	398137	5	NULL	NULL	0	NULL	HindIII-I fragment of the L-IVP strain of vaccinia virus genome	Chromosome												NULL		0	NULL	NULL	NULL	NULL	NULL	( Structure-activity study of the HindIII-I fragment of the L-IVP strain of vaccinia virus genome .
	manualset3
83810	1	398138	5	NULL	NULL	0	NULL	 probes	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Half of the probes matched , and half did not match , an item in the preceding memory set .
	manualset3
83811	2	398138	5	NULL	NULL	0	NULL	preceding memory set	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Half of the probes matched , and half did not match , an item in the preceding memory set .
	manualset3
83812	1	398139	5	NULL	NULL	0	NULL	Half the groups of experimental and control animals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Half the groups of experimental and control animals were also subjected to daily endurance or uphill running exercise to determine the possible preventive effects of exercise .
	manualset3
83813	2	398139	5	NULL	NULL	0	NULL	daily endurance	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Half the groups of experimental and control animals were also subjected to daily endurance or uphill running exercise to determine the possible preventive effects of exercise .
	manualset3
83814	3	398139	5	NULL	NULL	0	NULL	uphill running exercise	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Half the groups of experimental and control animals were also subjected to daily endurance or uphill running exercise to determine the possible preventive effects of exercise .
	manualset3
83815	4	398139	5	NULL	NULL	NULL	NULL	 possible preventive effects of exercise	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Half the groups of experimental and control animals were also subjected to daily endurance or uphill running exercise to determine the possible preventive effects of exercise .
	manualset3
83816	1	398140	5	NULL	NULL	0	NULL	monkeys	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Half the monkeys in each group were offered milk ad lib , and half were given restricted quantities .
	manualset3
83817	2	398140	5	NULL	NULL	0	NULL	each group	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Half the monkeys in each group were offered milk ad lib , and half were given restricted quantities .
	manualset3
83818	3	398140	5	NULL	NULL	0	NULL	milk ad lib	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	Half the monkeys in each group were offered milk ad lib , and half were given restricted quantities .
	manualset3
83819	4	398140	5	NULL	NULL	0	NULL	restricted quantities	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Half the monkeys in each group were offered milk ad lib , and half were given restricted quantities .
	manualset3
83820	1	398141	5	NULL	NULL	0	NULL	Hallux varus	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hallux varus : a step-wise approach for correction .
	manualset3
83821	2	398141	5	NULL	NULL	0	NULL	correction	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hallux varus : a step-wise approach for correction .
	manualset3
83822	1	398142	5	NULL	NULL	0	NULL	Haloperidol 	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Haloperidol , a typical antipsychotic , is the most commonly prescribed medication for the treatment of mental health problems such as agitation and psychosis .
	manualset3
83823	2	398142	5	NULL	NULL	0	NULL	typical antipsychotic	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Haloperidol , a typical antipsychotic , is the most commonly prescribed medication for the treatment of mental health problems such as agitation and psychosis .
	manualset3
83824	3	398142	5	NULL	NULL	0	NULL	most commonly prescribed medication	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Haloperidol , a typical antipsychotic , is the most commonly prescribed medication for the treatment of mental health problems such as agitation and psychosis .
	manualset3
83825	4	398142	5	NULL	NULL	0	NULL	treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Haloperidol , a typical antipsychotic , is the most commonly prescribed medication for the treatment of mental health problems such as agitation and psychosis .
	manualset3
83826	5	398142	5	NULL	NULL	0	NULL	mental health problems	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Haloperidol , a typical antipsychotic , is the most commonly prescribed medication for the treatment of mental health problems such as agitation and psychosis .
	manualset3
83827	6	398142	5	NULL	NULL	0	NULL	agitation	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Haloperidol , a typical antipsychotic , is the most commonly prescribed medication for the treatment of mental health problems such as agitation and psychosis .
	manualset3
83828	7	398142	5	NULL	NULL	0	NULL	psychosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Haloperidol , a typical antipsychotic , is the most commonly prescribed medication for the treatment of mental health problems such as agitation and psychosis .
	manualset3
83829	1	398143	5	NULL	NULL	0	NULL	Haloperidol catalepsy	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Haloperidol catalepsy was increased only by ivc histamine .
	manualset3
83830	2	398143	5	NULL	NULL	0	NULL	ivc histamine	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Haloperidol catalepsy was increased only by ivc histamine .
	manualset3
83831	1	398144	5	NULL	NULL	0	NULL	Haloperidol 	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Haloperidol exerts its therapeutic effects basically by acting on dopamine receptors .
	manualset3
83832	2	398144	5	NULL	NULL	0	NULL	therapeutic effects	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Haloperidol exerts its therapeutic effects basically by acting on dopamine receptors .
	manualset3
83833	3	398144	5	NULL	NULL	0	NULL	dopamine receptors	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Haloperidol exerts its therapeutic effects basically by acting on dopamine receptors .
	manualset3
83834	1	398145	5	NULL	NULL	0	NULL	Haloperidol treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Haloperidol treatment significantly increased dyskinetic movements and striatal dopamine D2 receptor density compared with controls .
	manualset3
83835	2	398145	5	NULL	NULL	NULL	NULL	dyskinetic movements	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Haloperidol treatment significantly increased dyskinetic movements and striatal dopamine D2 receptor density compared with controls .
	manualset3
83836	3	398145	5	NULL	NULL	0	NULL	striatal dopamine D2 receptor density	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Haloperidol treatment significantly increased dyskinetic movements and striatal dopamine D2 receptor density compared with controls .
	manualset3
83837	4	398145	5	NULL	NULL	0	NULL	controls	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Haloperidol treatment significantly increased dyskinetic movements and striatal dopamine D2 receptor density compared with controls .
	manualset3
83838	1	398146	5	NULL	NULL	0	NULL	Studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies of pregnanediol in urine .
	manualset3
83839	2	398146	5	NULL	NULL	0	NULL	pregnanediol	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies of pregnanediol in urine .
	manualset3
83840	3	398146	5	NULL	NULL	0	NULL	urine	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies of pregnanediol in urine .
	manualset3
83841	1	398147	5	NULL	NULL	NULL	NULL	Hamartoma	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hamartoma of the mitral valve with blood cysts : a rare tumor detected by echocardiography .
	manualset3
83842	2	398147	5	NULL	NULL	0	NULL	mitral valve	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hamartoma of the mitral valve with blood cysts : a rare tumor detected by echocardiography .
	manualset3
83843	3	398147	5	NULL	NULL	0	NULL	blood cysts	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hamartoma of the mitral valve with blood cysts : a rare tumor detected by echocardiography .
	manualset3
83844	4	398147	5	NULL	NULL	0	NULL	rare tumor	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hamartoma of the mitral valve with blood cysts : a rare tumor detected by echocardiography .
	manualset3
83845	5	398147	5	NULL	NULL	0	NULL	echocardiography	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hamartoma of the mitral valve with blood cysts : a rare tumor detected by echocardiography .
	manualset3
83846	1	398148	5	NULL	NULL	0	NULL	Hamycin	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hamycin incorporated into liposomes containing phosphatidylcholine ( SPC ) and phosphatidic acid ( PA ) had reduced toxicity and an enhanced antifungal activity in experimental aspergillosis in balb/c mice .
	manualset3
83847	2	398148	5	NULL	NULL	NULL	NULL	liposomes	CellComponent												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hamycin incorporated into liposomes containing phosphatidylcholine ( SPC ) and phosphatidic acid ( PA ) had reduced toxicity and an enhanced antifungal activity in experimental aspergillosis in balb/c mice .
	manualset3
83848	5	398148	5	NULL	NULL	NULL	NULL	 reduced toxicity	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hamycin incorporated into liposomes containing phosphatidylcholine ( SPC ) and phosphatidic acid ( PA ) had reduced toxicity and an enhanced antifungal activity in experimental aspergillosis in balb/c mice .
	manualset3
83849	6	398148	5	NULL	NULL	NULL	NULL	enhanced antifungal activity	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hamycin incorporated into liposomes containing phosphatidylcholine ( SPC ) and phosphatidic acid ( PA ) had reduced toxicity and an enhanced antifungal activity in experimental aspergillosis in balb/c mice .
	manualset3
83850	7	398148	5	NULL	NULL	NULL	NULL	experimental aspergillosis	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hamycin incorporated into liposomes containing phosphatidylcholine ( SPC ) and phosphatidic acid ( PA ) had reduced toxicity and an enhanced antifungal activity in experimental aspergillosis in balb/c mice .
	manualset3
83851	8	398148	5	NULL	NULL	NULL	NULL	balb/c mice	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hamycin incorporated into liposomes containing phosphatidylcholine ( SPC ) and phosphatidic acid ( PA ) had reduced toxicity and an enhanced antifungal activity in experimental aspergillosis in balb/c mice .
	manualset3
84501	3	398148	5	NULL	NULL	0	NULL	phosphatidylcholine ( SPC )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hamycin incorporated into liposomes containing phosphatidylcholine ( SPC ) and phosphatidic acid ( PA ) had reduced toxicity and an enhanced antifungal activity in experimental aspergillosis in balb/c mice .
	manualset3
84502	4	398148	5	NULL	NULL	0	NULL	phosphatidic acid ( PA )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hamycin incorporated into liposomes containing phosphatidylcholine ( SPC ) and phosphatidic acid ( PA ) had reduced toxicity and an enhanced antifungal activity in experimental aspergillosis in balb/c mice .
	manualset3
83852	1	398149	5	NULL	NULL	0	NULL	Hand et al	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hand et al. argued for the importance of including launch site in analyses of target word fixation durations .
	manualset3
83853	2	398149	5	NULL	NULL	0	NULL	launch site	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Hand et al. argued for the importance of including launch site in analyses of target word fixation durations .
	manualset3
83854	3	398149	5	NULL	NULL	0	NULL	target word fixation durations	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Hand et al. argued for the importance of including launch site in analyses of target word fixation durations .
	manualset3
83855	1	398150	5	NULL	NULL	0	NULL	Hand volume	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hand volume , GS ( J ) , GS ( C ) and PS of the dominant hand were respectively 3.6 + / - 4.1 % , 6.6 + / - 9.2 % , 11.7 + / - 11.2 % , and 8.0 + / - 13.2 % higher than those of the non-dominant hand ( p & lt ; 0.001 ) .
	manualset3
83856	2	398150	5	NULL	NULL	0	NULL	GS ( J )	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hand volume , GS ( J ) , GS ( C ) and PS of the dominant hand were respectively 3.6 + / - 4.1 % , 6.6 + / - 9.2 % , 11.7 + / - 11.2 % , and 8.0 + / - 13.2 % higher than those of the non-dominant hand ( p & lt ; 0.001 ) .
	manualset3
83857	3	398150	5	NULL	NULL	0	NULL	GS ( C )	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hand volume , GS ( J ) , GS ( C ) and PS of the dominant hand were respectively 3.6 + / - 4.1 % , 6.6 + / - 9.2 % , 11.7 + / - 11.2 % , and 8.0 + / - 13.2 % higher than those of the non-dominant hand ( p & lt ; 0.001 ) .
	manualset3
83858	4	398150	5	NULL	NULL	0	NULL	PS	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hand volume , GS ( J ) , GS ( C ) and PS of the dominant hand were respectively 3.6 + / - 4.1 % , 6.6 + / - 9.2 % , 11.7 + / - 11.2 % , and 8.0 + / - 13.2 % higher than those of the non-dominant hand ( p & lt ; 0.001 ) .
	manualset3
83859	5	398150	5	NULL	NULL	0	NULL	dominant hand	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hand volume , GS ( J ) , GS ( C ) and PS of the dominant hand were respectively 3.6 + / - 4.1 % , 6.6 + / - 9.2 % , 11.7 + / - 11.2 % , and 8.0 + / - 13.2 % higher than those of the non-dominant hand ( p & lt ; 0.001 ) .
	manualset3
83860	6	398150	5	NULL	NULL	0	NULL	3.6 + / - 4.1 % , 6.6 + / - 9.2 % , 11.7 + / - 11.2 % , and 8.0 + / - 13.2 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hand volume , GS ( J ) , GS ( C ) and PS of the dominant hand were respectively 3.6 + / - 4.1 % , 6.6 + / - 9.2 % , 11.7 + / - 11.2 % , and 8.0 + / - 13.2 % higher than those of the non-dominant hand ( p & lt ; 0.001 ) .
	manualset3
83861	7	398150	5	NULL	NULL	0	NULL	non-dominant hand	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hand volume , GS ( J ) , GS ( C ) and PS of the dominant hand were respectively 3.6 + / - 4.1 % , 6.6 + / - 9.2 % , 11.7 + / - 11.2 % , and 8.0 + / - 13.2 % higher than those of the non-dominant hand ( p & lt ; 0.001 ) .
	manualset3
83862	8	398150	5	NULL	NULL	0	NULL	p & lt ; 0.001	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hand volume , GS ( J ) , GS ( C ) and PS of the dominant hand were respectively 3.6 + / - 4.1 % , 6.6 + / - 9.2 % , 11.7 + / - 11.2 % , and 8.0 + / - 13.2 % higher than those of the non-dominant hand ( p & lt ; 0.001 ) .
	manualset3
83863	1	398151	5	NULL	NULL	0	NULL	Hangover	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hangover may be related to propensity to develop alcohol use disorders ( AUDs ) .
	manualset3
83864	2	398151	5	NULL	NULL	0	NULL	propensity 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hangover may be related to propensity to develop alcohol use disorders ( AUDs ) .
	manualset3
83865	3	398151	5	NULL	NULL	0	NULL	alcohol use disorders ( AUDs )	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hangover may be related to propensity to develop alcohol use disorders ( AUDs ) .
	manualset3
83866	1	398152	5	NULL	NULL	0	NULL	Hans Krebs	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Hans Krebs : nineteen nineteen and after .
	manualset3
83867	2	398152	5	NULL	NULL	0	NULL	nineteen nineteen	TimePoint												NULL		0	NULL	NULL	NULL	NULL	NULL	Hans Krebs : nineteen nineteen and after .
	manualset3
83868	1	398153	5	NULL	NULL	0	NULL	Hardware schematics	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Hardware schematics , layout files , and software are freely available .
	manualset3
83869	2	398153	5	NULL	NULL	0	NULL	layout files	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Hardware schematics , layout files , and software are freely available .
	manualset3
83870	3	398153	5	NULL	NULL	0	NULL	software	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Hardware schematics , layout files , and software are freely available .
	manualset3
83871	1	398154	5	NULL	NULL	0	NULL	technical difficulties	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Having solved the technical difficulties of bulk manufacture of IgG concentrates for intravenous use , our attention should now be directed towards preventing viral contamination by both modifying the manufacturing processes and screening the donors for evidence of disease .
	manualset3
83872	2	398154	5	NULL	NULL	0	NULL	bulk manufacture	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Having solved the technical difficulties of bulk manufacture of IgG concentrates for intravenous use , our attention should now be directed towards preventing viral contamination by both modifying the manufacturing processes and screening the donors for evidence of disease .
	manualset3
83873	3	398154	5	NULL	NULL	0	NULL	IgG concentrates	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Having solved the technical difficulties of bulk manufacture of IgG concentrates for intravenous use , our attention should now be directed towards preventing viral contamination by both modifying the manufacturing processes and screening the donors for evidence of disease .
	manualset3
83874	4	398154	5	NULL	NULL	0	NULL	attention	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Having solved the technical difficulties of bulk manufacture of IgG concentrates for intravenous use , our attention should now be directed towards preventing viral contamination by both modifying the manufacturing processes and screening the donors for evidence of disease .
	manualset3
83875	5	398154	5	NULL	NULL	0	NULL	viral contamination	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Having solved the technical difficulties of bulk manufacture of IgG concentrates for intravenous use , our attention should now be directed towards preventing viral contamination by both modifying the manufacturing processes and screening the donors for evidence of disease .
	manualset3
83876	6	398154	5	NULL	NULL	0	NULL	manufacturing processes	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Having solved the technical difficulties of bulk manufacture of IgG concentrates for intravenous use , our attention should now be directed towards preventing viral contamination by both modifying the manufacturing processes and screening the donors for evidence of disease .
	manualset3
83877	7	398154	5	NULL	NULL	0	NULL	donors	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Having solved the technical difficulties of bulk manufacture of IgG concentrates for intravenous use , our attention should now be directed towards preventing viral contamination by both modifying the manufacturing processes and screening the donors for evidence of disease .
	manualset3
83878	8	398154	5	NULL	NULL	0	NULL	evidence of disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Having solved the technical difficulties of bulk manufacture of IgG concentrates for intravenous use , our attention should now be directed towards preventing viral contamination by both modifying the manufacturing processes and screening the donors for evidence of disease .
	manualset3
83879	1	398155	5	NULL	NULL	0	NULL	Hazard analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hazard analysis and risk assessment techniques are utilized within many private sector industries and government agencies , including the medical device and pharmaceutical industry , within a structured process to control human injuries and environmental and property damage .
	manualset3
83880	2	398155	5	NULL	NULL	0	NULL	risk assessment techniques	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hazard analysis and risk assessment techniques are utilized within many private sector industries and government agencies , including the medical device and pharmaceutical industry , within a structured process to control human injuries and environmental and property damage .
	manualset3
83881	3	398155	5	NULL	NULL	0	NULL	private sector industries and government agencies	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Hazard analysis and risk assessment techniques are utilized within many private sector industries and government agencies , including the medical device and pharmaceutical industry , within a structured process to control human injuries and environmental and property damage .
	manualset3
83882	4	398155	5	NULL	NULL	0	NULL	medical device	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	Hazard analysis and risk assessment techniques are utilized within many private sector industries and government agencies , including the medical device and pharmaceutical industry , within a structured process to control human injuries and environmental and property damage .
	manualset3
83883	5	398155	5	NULL	NULL	0	NULL	pharmaceutical industry	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Hazard analysis and risk assessment techniques are utilized within many private sector industries and government agencies , including the medical device and pharmaceutical industry , within a structured process to control human injuries and environmental and property damage .
	manualset3
83884	6	398155	5	NULL	NULL	0	NULL	structured process	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Hazard analysis and risk assessment techniques are utilized within many private sector industries and government agencies , including the medical device and pharmaceutical industry , within a structured process to control human injuries and environmental and property damage .
	manualset3
83885	7	398155	5	NULL	NULL	NULL	NULL	human injuries	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hazard analysis and risk assessment techniques are utilized within many private sector industries and government agencies , including the medical device and pharmaceutical industry , within a structured process to control human injuries and environmental and property damage .
	manualset3
83886	8	398155	5	NULL	NULL	NULL	NULL	 environmental and property damage	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hazard analysis and risk assessment techniques are utilized within many private sector industries and government agencies , including the medical device and pharmaceutical industry , within a structured process to control human injuries and environmental and property damage .
	manualset3
83889	1	398157	5	NULL	NULL	0	NULL	comatose	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	He became comatose , requiring ventilatory support , and exhibited abnormalities of some brainstem reflexes prior to treatment .
	manualset3
83890	2	398157	5	NULL	NULL	0	NULL	ventilatory support	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	He became comatose , requiring ventilatory support , and exhibited abnormalities of some brainstem reflexes prior to treatment .
	manualset3
83891	3	398157	5	NULL	NULL	0	NULL	brainstem reflexes	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	He became comatose , requiring ventilatory support , and exhibited abnormalities of some brainstem reflexes prior to treatment .
	manualset3
83892	4	398157	5	NULL	NULL	0	NULL	treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	He became comatose , requiring ventilatory support , and exhibited abnormalities of some brainstem reflexes prior to treatment .
	manualset3
83893	1	398158	5	NULL	NULL	0	NULL	Studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on metabolites of baicalin in human urine ) .
	manualset3
83894	2	398158	5	NULL	NULL	0	NULL	metabolites	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on metabolites of baicalin in human urine ) .
	manualset3
83895	3	398158	5	NULL	NULL	0	NULL	baicalin	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on metabolites of baicalin in human urine ) .
	manualset3
83896	4	398158	5	NULL	NULL	0	NULL	human urine	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on metabolites of baicalin in human urine ) .
	manualset3
83897	1	398159	5	NULL	NULL	0	NULL	four treatment phases	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	He completed four treatment phases : 6 weeks of detraining , 10 weeks of weight lifting , 10 weeks of running , and 10 weeks of weight lifting .
	manualset3
83898	2	398159	5	NULL	NULL	0	NULL	6 weeks of detraining	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	He completed four treatment phases : 6 weeks of detraining , 10 weeks of weight lifting , 10 weeks of running , and 10 weeks of weight lifting .
	manualset3
83899	3	398159	5	NULL	NULL	0	NULL	10 weeks of weight lifting	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	He completed four treatment phases : 6 weeks of detraining , 10 weeks of weight lifting , 10 weeks of running , and 10 weeks of weight lifting .
	manualset3
83900	4	398159	5	NULL	NULL	0	NULL	10 weeks of running	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	He completed four treatment phases : 6 weeks of detraining , 10 weeks of weight lifting , 10 weeks of running , and 10 weeks of weight lifting .
	manualset3
83901	5	398159	5	NULL	NULL	0	NULL	10 weeks of weight lifting	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	He completed four treatment phases : 6 weeks of detraining , 10 weeks of weight lifting , 10 weeks of running , and 10 weeks of weight lifting .
	manualset3
83902	1	398160	5	NULL	NULL	0	NULL	explanatory model	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	He devised an explanatory model of this disease , indicating its origin as the variable alteration of the relationship between what he termed thymo and noopsyche .
	manualset3
83903	2	398160	5	NULL	NULL	0	NULL	disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	He devised an explanatory model of this disease , indicating its origin as the variable alteration of the relationship between what he termed thymo and noopsyche .
	manualset3
83904	3	398160	5	NULL	NULL	0	NULL	variable alteration	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	He devised an explanatory model of this disease , indicating its origin as the variable alteration of the relationship between what he termed thymo and noopsyche .
	manualset3
83905	4	398160	5	NULL	NULL	0	NULL	relationship	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	He devised an explanatory model of this disease , indicating its origin as the variable alteration of the relationship between what he termed thymo and noopsyche .
	manualset3
83906	5	398160	5	NULL	NULL	NULL	NULL	thymo and noopsyche	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	He devised an explanatory model of this disease , indicating its origin as the variable alteration of the relationship between what he termed thymo and noopsyche .
	manualset3
83907	1	398161	5	NULL	NULL	0	NULL	white forelock	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	He exhibited white forelock , hypopigmented macules and patches , heterochromia irides , and dystopia canthorum .
	manualset3
83908	2	398161	5	NULL	NULL	0	NULL	hypopigmented macules and patches	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	He exhibited white forelock , hypopigmented macules and patches , heterochromia irides , and dystopia canthorum .
	manualset3
83909	3	398161	5	NULL	NULL	0	NULL	heterochromia irides	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	He exhibited white forelock , hypopigmented macules and patches , heterochromia irides , and dystopia canthorum .
	manualset3
83910	4	398161	5	NULL	NULL	0	NULL	dystopia canthorum	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	He exhibited white forelock , hypopigmented macules and patches , heterochromia irides , and dystopia canthorum .
	manualset3
83911	1	398162	5	NULL	NULL	0	NULL	 anti-tumor necrosis factor ( TNF ) alpha therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	He had never received anti-tumor necrosis factor ( TNF ) alpha therapy .
	manualset3
83912	1	398163	5	NULL	NULL	0	NULL	Studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on pathophysiological principles of thinking disorders in schizophrenia by means of a motor method with verbal stimuli ) .
	manualset3
83913	2	398163	5	NULL	NULL	0	NULL	pathophysiological principles	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on pathophysiological principles of thinking disorders in schizophrenia by means of a motor method with verbal stimuli ) .
	manualset3
83914	3	398163	5	NULL	NULL	0	NULL	thinking disorders	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on pathophysiological principles of thinking disorders in schizophrenia by means of a motor method with verbal stimuli ) .
	manualset3
83915	4	398163	5	NULL	NULL	0	NULL	schizophrenia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on pathophysiological principles of thinking disorders in schizophrenia by means of a motor method with verbal stimuli ) .
	manualset3
83916	5	398163	5	NULL	NULL	0	NULL	motor method with verbal stimuli	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on pathophysiological principles of thinking disorders in schizophrenia by means of a motor method with verbal stimuli ) .
	manualset3
83917	1	398164	5	NULL	NULL	0	NULL	5 FC ( 5-fluorocytosine ) 	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	He is on 5 FC ( 5-fluorocytosine ) , Minomycin ( minocycline hydrochloride ) , and Baktar ( trimethoprim-sulfamethoxazole ) .
	manualset3
83918	2	398164	5	NULL	NULL	0	NULL	Minomycin ( minocycline hydrochloride ) 	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	He is on 5 FC ( 5-fluorocytosine ) , Minomycin ( minocycline hydrochloride ) , and Baktar ( trimethoprim-sulfamethoxazole ) .
	manualset3
83919	3	398164	5	NULL	NULL	0	NULL	Baktar ( trimethoprim-sulfamethoxazole )	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	He is on 5 FC ( 5-fluorocytosine ) , Minomycin ( minocycline hydrochloride ) , and Baktar ( trimethoprim-sulfamethoxazole ) .
	manualset3
84493	1	398165	5	NULL	NULL	0	NULL	recent relevant directions	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	He outlines recent relevant directions of the Joint Commission on Accreditation of Healthcare Organizations , especially the shift to continuous quality improvement and the organization of the 1995 standards around major functions such as improving performance .
	manualset3
84494	2	398165	5	NULL	NULL	0	NULL	Joint Commission	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	He outlines recent relevant directions of the Joint Commission on Accreditation of Healthcare Organizations , especially the shift to continuous quality improvement and the organization of the 1995 standards around major functions such as improving performance .
	manualset3
84495	3	398165	5	NULL	NULL	0	NULL	Accreditation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	He outlines recent relevant directions of the Joint Commission on Accreditation of Healthcare Organizations , especially the shift to continuous quality improvement and the organization of the 1995 standards around major functions such as improving performance .
	manualset3
84496	4	398165	5	NULL	NULL	0	NULL	Healthcare Organizations	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	He outlines recent relevant directions of the Joint Commission on Accreditation of Healthcare Organizations , especially the shift to continuous quality improvement and the organization of the 1995 standards around major functions such as improving performance .
	manualset3
84497	5	398165	5	NULL	NULL	0	NULL	continuous quality improvement	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	He outlines recent relevant directions of the Joint Commission on Accreditation of Healthcare Organizations , especially the shift to continuous quality improvement and the organization of the 1995 standards around major functions such as improving performance .
	manualset3
84498	6	398165	5	NULL	NULL	0	NULL	organization	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	He outlines recent relevant directions of the Joint Commission on Accreditation of Healthcare Organizations , especially the shift to continuous quality improvement and the organization of the 1995 standards around major functions such as improving performance .
	manualset3
84499	7	398165	5	NULL	NULL	0	NULL	1995 standards	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	He outlines recent relevant directions of the Joint Commission on Accreditation of Healthcare Organizations , especially the shift to continuous quality improvement and the organization of the 1995 standards around major functions such as improving performance .
	manualset3
84500	8	398165	5	NULL	NULL	0	NULL	major functions such as improving performance	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	He outlines recent relevant directions of the Joint Commission on Accreditation of Healthcare Organizations , especially the shift to continuous quality improvement and the organization of the 1995 standards around major functions such as improving performance .
	manualset3
83920	1	398166	5	NULL	NULL	0	NULL	symptoms	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	He presented all the symptoms : urethritis , conjunctivitis , arthritis , balanitis circinata and keratodermia .
	manualset3
83921	2	398166	5	NULL	NULL	0	NULL	urethritis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	He presented all the symptoms : urethritis , conjunctivitis , arthritis , balanitis circinata and keratodermia .
	manualset3
83922	3	398166	5	NULL	NULL	0	NULL	conjunctivitis 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	He presented all the symptoms : urethritis , conjunctivitis , arthritis , balanitis circinata and keratodermia .
	manualset3
83923	4	398166	5	NULL	NULL	0	NULL	arthritis 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	He presented all the symptoms : urethritis , conjunctivitis , arthritis , balanitis circinata and keratodermia .
	manualset3
83924	5	398166	5	NULL	NULL	0	NULL	balanitis circinata	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	He presented all the symptoms : urethritis , conjunctivitis , arthritis , balanitis circinata and keratodermia .
	manualset3
83925	6	398166	5	NULL	NULL	0	NULL	keratodermia 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	He presented all the symptoms : urethritis , conjunctivitis , arthritis , balanitis circinata and keratodermia .
	manualset3
83926	1	398167	5	NULL	NULL	0	NULL	establishment of psychiatric hospitals	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	He proposed the establishment of psychiatric hospitals in order to eliminate the hospitalization of the sick in the same building as healthy and to permit the application of specific forms of treatment .
	manualset3
83927	2	398167	5	NULL	NULL	0	NULL	hospitalization 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	He proposed the establishment of psychiatric hospitals in order to eliminate the hospitalization of the sick in the same building as healthy and to permit the application of specific forms of treatment .
	manualset3
83928	3	398167	5	NULL	NULL	0	NULL	sick 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	He proposed the establishment of psychiatric hospitals in order to eliminate the hospitalization of the sick in the same building as healthy and to permit the application of specific forms of treatment .
	manualset3
83929	4	398167	5	NULL	NULL	0	NULL	same building	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	He proposed the establishment of psychiatric hospitals in order to eliminate the hospitalization of the sick in the same building as healthy and to permit the application of specific forms of treatment .
	manualset3
83930	5	398167	5	NULL	NULL	NULL	NULL	application	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	He proposed the establishment of psychiatric hospitals in order to eliminate the hospitalization of the sick in the same building as healthy and to permit the application of specific forms of treatment .
	manualset3
83931	6	398167	5	NULL	NULL	0	NULL	specific forms of treatment 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	He proposed the establishment of psychiatric hospitals in order to eliminate the hospitalization of the sick in the same building as healthy and to permit the application of specific forms of treatment .
	manualset3
83932	1	398168	5	NULL	NULL	0	NULL	2 courses of CDDP/TXT chemotherapy ( cisplatin 75 mg/m2 , docetaxel 80 mg/m2 )	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	He received 2 courses of CDDP/TXT chemotherapy ( cisplatin 75 mg/m2 , docetaxel 80 mg/m2 ) and achieved a partial response , but his carcinoma of the pancreas recurred .
	manualset3
83933	2	398168	5	NULL	NULL	0	NULL	partial response	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	He received 2 courses of CDDP/TXT chemotherapy ( cisplatin 75 mg/m2 , docetaxel 80 mg/m2 ) and achieved a partial response , but his carcinoma of the pancreas recurred .
	manualset3
83934	3	398168	5	NULL	NULL	NULL	NULL	carcinoma of the pancreas	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	He received 2 courses of CDDP/TXT chemotherapy ( cisplatin 75 mg/m2 , docetaxel 80 mg/m2 ) and achieved a partial response , but his carcinoma of the pancreas recurred .
	manualset3
83936	1	398169	5	NULL	NULL	0	NULL	recurrence of a similar episode	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	He recovered completely , but the recurrence of a similar episode with associated cardiomyopathy and dicarboxylic aciduria at 10 months of age led to the recognition of a fatty acid oxidation defect .
	manualset3
83937	2	398169	5	NULL	NULL	0	NULL	associated cardiomyopathy and dicarboxylic aciduria	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	He recovered completely , but the recurrence of a similar episode with associated cardiomyopathy and dicarboxylic aciduria at 10 months of age led to the recognition of a fatty acid oxidation defect .
	manualset3
83938	3	398169	5	NULL	NULL	0	NULL	10 months of age	TimePoint												NULL		0	NULL	NULL	NULL	NULL	NULL	He recovered completely , but the recurrence of a similar episode with associated cardiomyopathy and dicarboxylic aciduria at 10 months of age led to the recognition of a fatty acid oxidation defect .
	manualset3
83939	4	398169	5	NULL	NULL	0	NULL	recognition	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	He recovered completely , but the recurrence of a similar episode with associated cardiomyopathy and dicarboxylic aciduria at 10 months of age led to the recognition of a fatty acid oxidation defect .
	manualset3
83940	5	398169	5	NULL	NULL	0	NULL	fatty acid oxidation defect	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	He recovered completely , but the recurrence of a similar episode with associated cardiomyopathy and dicarboxylic aciduria at 10 months of age led to the recognition of a fatty acid oxidation defect .
	manualset3
83941	1	398170	5	NULL	NULL	0	NULL	studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on the causative agent of Hyuga-feveri ; cultivation of rickettsia-like organisms isolated from metacercariae of Stellantchasumus falcatus in tissue culture cell and their antigenic relation to Rickettsia sennetsu ( author 's transl ) ) .
	manualset3
83942	2	398170	5	NULL	NULL	0	NULL	causative agent of Hyuga-feveri	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on the causative agent of Hyuga-feveri ; cultivation of rickettsia-like organisms isolated from metacercariae of Stellantchasumus falcatus in tissue culture cell and their antigenic relation to Rickettsia sennetsu ( author 's transl ) ) .
	manualset3
83943	3	398170	5	NULL	NULL	0	NULL	cultivation 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on the causative agent of Hyuga-feveri ; cultivation of rickettsia-like organisms isolated from metacercariae of Stellantchasumus falcatus in tissue culture cell and their antigenic relation to Rickettsia sennetsu ( author 's transl ) ) .
	manualset3
83944	4	398170	5	NULL	NULL	0	NULL	rickettsia-like organisms	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on the causative agent of Hyuga-feveri ; cultivation of rickettsia-like organisms isolated from metacercariae of Stellantchasumus falcatus in tissue culture cell and their antigenic relation to Rickettsia sennetsu ( author 's transl ) ) .
	manualset3
83945	5	398170	5	NULL	NULL	0	NULL	metacercariae of Stellantchasumus falcatus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on the causative agent of Hyuga-feveri ; cultivation of rickettsia-like organisms isolated from metacercariae of Stellantchasumus falcatus in tissue culture cell and their antigenic relation to Rickettsia sennetsu ( author 's transl ) ) .
	manualset3
83946	6	398170	5	NULL	NULL	0	NULL	tissue culture cell	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on the causative agent of Hyuga-feveri ; cultivation of rickettsia-like organisms isolated from metacercariae of Stellantchasumus falcatus in tissue culture cell and their antigenic relation to Rickettsia sennetsu ( author 's transl ) ) .
	manualset3
83947	7	398170	5	NULL	NULL	0	NULL	antigenic relation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on the causative agent of Hyuga-feveri ; cultivation of rickettsia-like organisms isolated from metacercariae of Stellantchasumus falcatus in tissue culture cell and their antigenic relation to Rickettsia sennetsu ( author 's transl ) ) .
	manualset3
83948	8	398170	5	NULL	NULL	0	NULL	Rickettsia sennetsu	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on the causative agent of Hyuga-feveri ; cultivation of rickettsia-like organisms isolated from metacercariae of Stellantchasumus falcatus in tissue culture cell and their antigenic relation to Rickettsia sennetsu ( author 's transl ) ) .
	manualset3
83949	1	398171	5	NULL	NULL	NULL	NULL	pontine hemorrhage	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	He subsequently developed a pontine hemorrhage and acute hydrocephalus and died secondary to transtentorial herniation .
	manualset3
83950	2	398171	5	NULL	NULL	0	NULL	acute hydrocephalus	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	He subsequently developed a pontine hemorrhage and acute hydrocephalus and died secondary to transtentorial herniation .
	manualset3
83952	4	398171	5	NULL	NULL	NULL	NULL	transtentorial herniation	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	He subsequently developed a pontine hemorrhage and acute hydrocephalus and died secondary to transtentorial herniation .
	manualset3
83953	1	398172	5	NULL	NULL	0	NULL	ethanol intake	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	He successfully reduced his ethanol intake over a 3-month period , but he was unable to sustain abstinence .
	manualset3
83954	2	398172	5	NULL	NULL	0	NULL	over a 3-month period	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	He successfully reduced his ethanol intake over a 3-month period , but he was unable to sustain abstinence .
	manualset3
83955	3	398172	5	NULL	NULL	0	NULL	sustain abstinence	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	He successfully reduced his ethanol intake over a 3-month period , but he was unable to sustain abstinence .
	manualset3
83956	1	398173	5	NULL	NULL	0	NULL	BD with oral ulcer , genital ulcer , papular skin lesion , deep vein thrombosis ( DVT ) and positive pathergy reaction	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	He was diagnosed as having BD with oral ulcer , genital ulcer , papular skin lesion , deep vein thrombosis ( DVT ) and positive pathergy reaction .
	manualset3
83957	1	398174	5	NULL	NULL	0	NULL	heparin-induced thrombocytopenia and thrombosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	He was found to have developed heparin-induced thrombocytopenia and thrombosis , confirmed by high levels of heparin-platelet factor 4-antibody on enzyme-linked immunosorbent assay ( ELISA ) .
	manualset3
83958	2	398174	5	NULL	NULL	0	NULL	high levels of heparin-platelet factor 4-antibody	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	He was found to have developed heparin-induced thrombocytopenia and thrombosis , confirmed by high levels of heparin-platelet factor 4-antibody on enzyme-linked immunosorbent assay ( ELISA ) .
	manualset3
83959	3	398174	5	NULL	NULL	0	NULL	enzyme-linked immunosorbent assay ( ELISA )	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	He was found to have developed heparin-induced thrombocytopenia and thrombosis , confirmed by high levels of heparin-platelet factor 4-antibody on enzyme-linked immunosorbent assay ( ELISA ) .
	manualset3
83960	1	398175	5	NULL	NULL	0	NULL	pediatric dentist	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	He was initially evaluated by a pediatric dentist and epidermal dysplasia syndromes were considered , but insensitivity to pain was suspected after a skeletal survey revealed an unrecognized skull fracture .
	manualset3
83961	2	398175	5	NULL	NULL	0	NULL	epidermal dysplasia syndromes	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	He was initially evaluated by a pediatric dentist and epidermal dysplasia syndromes were considered , but insensitivity to pain was suspected after a skeletal survey revealed an unrecognized skull fracture .
	manualset3
83962	3	398175	5	NULL	NULL	0	NULL	insensitivity to pain	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	He was initially evaluated by a pediatric dentist and epidermal dysplasia syndromes were considered , but insensitivity to pain was suspected after a skeletal survey revealed an unrecognized skull fracture .
	manualset3
83963	4	398175	5	NULL	NULL	0	NULL	skeletal survey	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	He was initially evaluated by a pediatric dentist and epidermal dysplasia syndromes were considered , but insensitivity to pain was suspected after a skeletal survey revealed an unrecognized skull fracture .
	manualset3
83964	5	398175	5	NULL	NULL	0	NULL	 unrecognized skull fracture	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	He was initially evaluated by a pediatric dentist and epidermal dysplasia syndromes were considered , but insensitivity to pain was suspected after a skeletal survey revealed an unrecognized skull fracture .
	manualset3
83965	1	398176	5	NULL	NULL	0	NULL	pretreated	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	He was pretreated with 300 mg of aspirin , 600 mg of clopidogrel , and was taken to the catheterization laboratory .
	manualset3
83966	2	398176	5	NULL	NULL	0	NULL	 300 mg of aspirin 	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	He was pretreated with 300 mg of aspirin , 600 mg of clopidogrel , and was taken to the catheterization laboratory .
	manualset3
83967	3	398176	5	NULL	NULL	0	NULL	600 mg of clopidogrel	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	He was pretreated with 300 mg of aspirin , 600 mg of clopidogrel , and was taken to the catheterization laboratory .
	manualset3
83968	4	398176	5	NULL	NULL	0	NULL	catheterization laboratory	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	He was pretreated with 300 mg of aspirin , 600 mg of clopidogrel , and was taken to the catheterization laboratory .
	manualset3
83969	1	398177	5	NULL	NULL	0	NULL	chemotherapy ( CHOP )	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	He was treated with chemotherapy ( CHOP ) and radiation , and achieved complete remission .
	manualset3
83970	2	398177	5	NULL	NULL	0	NULL	radiation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	He was treated with chemotherapy ( CHOP ) and radiation , and achieved complete remission .
	manualset3
83971	3	398177	5	NULL	NULL	0	NULL	complete remission	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	He was treated with chemotherapy ( CHOP ) and radiation , and achieved complete remission .
	manualset3
83972	1	398178	5	NULL	NULL	0	NULL	Head louse	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Head louse and other common infections in schools : head teachers ' use of an information pack .
	manualset3
83973	2	398178	5	NULL	NULL	0	NULL	other common infections	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Head louse and other common infections in schools : head teachers ' use of an information pack .
	manualset3
83974	3	398178	5	NULL	NULL	0	NULL	schools	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Head louse and other common infections in schools : head teachers ' use of an information pack .
	manualset3
83975	4	398178	5	NULL	NULL	0	NULL	head teachers '	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Head louse and other common infections in schools : head teachers ' use of an information pack .
	manualset3
83976	5	398178	5	NULL	NULL	0	NULL	information pack	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Head louse and other common infections in schools : head teachers ' use of an information pack .
	manualset3
83977	1	398179	5	NULL	NULL	0	NULL	Health	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Health , illness , and immigration .
	manualset3
83978	2	398179	5	NULL	NULL	0	NULL	illness 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Health , illness , and immigration .
	manualset3
83979	3	398179	5	NULL	NULL	0	NULL	immigration	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Health , illness , and immigration .
	manualset3
83980	1	398180	5	NULL	NULL	0	NULL	Health care delivery system	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Health care delivery system in France : effects on surgical education .
	manualset3
83981	2	398180	5	NULL	NULL	0	NULL	France	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Health care delivery system in France : effects on surgical education .
	manualset3
83982	3	398180	5	NULL	NULL	NULL	NULL	surgical education	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Health care delivery system in France : effects on surgical education .
	manualset3
83983	1	398181	5	NULL	NULL	0	NULL	Health care delivery	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Health care delivery to homeless youth was often nonanticipatory , inconsistent and perceived as discriminatory .
	manualset3
83984	2	398181	5	NULL	NULL	0	NULL	homeless youth	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Health care delivery to homeless youth was often nonanticipatory , inconsistent and perceived as discriminatory .
	manualset3
83985	1	398182	5	NULL	NULL	0	NULL	Health services research	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Health services research comes of age : three new volumes document the history , development , and present state of the field .
	manualset3
83986	2	398182	5	NULL	NULL	0	NULL	age	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Health services research comes of age : three new volumes document the history , development , and present state of the field .
	manualset3
83987	3	398182	5	NULL	NULL	0	NULL	three new volumes document	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Health services research comes of age : three new volumes document the history , development , and present state of the field .
	manualset3
83988	4	398182	5	NULL	NULL	0	NULL	history	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Health services research comes of age : three new volumes document the history , development , and present state of the field .
	manualset3
83989	5	398182	5	NULL	NULL	0	NULL	present state of the field	UnproperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Health services research comes of age : three new volumes document the history , development , and present state of the field .
	manualset3
83990	1	398183	5	NULL	NULL	0	NULL	Healthcare organizations	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Healthcare organizations must adopt a new paradigm of care that holds patient safety as a core value and practice .
	manualset3
83991	2	398183	5	NULL	NULL	0	NULL	new paradigm of care	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Healthcare organizations must adopt a new paradigm of care that holds patient safety as a core value and practice .
	manualset3
83992	3	398183	5	NULL	NULL	0	NULL	holds patient safety	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Healthcare organizations must adopt a new paradigm of care that holds patient safety as a core value and practice .
	manualset3
83993	4	398183	5	NULL	NULL	0	NULL	core value and practice	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Healthcare organizations must adopt a new paradigm of care that holds patient safety as a core value and practice .
	manualset3
84211	1	398184	5	NULL	NULL	0	NULL	Studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on the formation of antibodies against antigens in protein extracts of psoriatic scales from the patients with psoriatic arthritis ) .
	manualset3
84212	2	398184	5	NULL	NULL	0	NULL	formation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on the formation of antibodies against antigens in protein extracts of psoriatic scales from the patients with psoriatic arthritis ) .
	manualset3
84213	3	398184	5	NULL	NULL	0	NULL	antibodies	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on the formation of antibodies against antigens in protein extracts of psoriatic scales from the patients with psoriatic arthritis ) .
	manualset3
84214	4	398184	5	NULL	NULL	0	NULL	antigens	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on the formation of antibodies against antigens in protein extracts of psoriatic scales from the patients with psoriatic arthritis ) .
	manualset3
84215	5	398184	5	NULL	NULL	0	NULL	protein extracts	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on the formation of antibodies against antigens in protein extracts of psoriatic scales from the patients with psoriatic arthritis ) .
	manualset3
84216	6	398184	5	NULL	NULL	0	NULL	psoriatic scales	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on the formation of antibodies against antigens in protein extracts of psoriatic scales from the patients with psoriatic arthritis ) .
	manualset3
84217	7	398184	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on the formation of antibodies against antigens in protein extracts of psoriatic scales from the patients with psoriatic arthritis ) .
	manualset3
84218	8	398184	5	NULL	NULL	0	NULL	psoriatic arthritis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on the formation of antibodies against antigens in protein extracts of psoriatic scales from the patients with psoriatic arthritis ) .
	manualset3
84219	1	398185	5	NULL	NULL	0	NULL	Healthcare professionals	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Healthcare professionals should be aware that not all men ( or women ) conform to the social stereotypes of masculinity ( or femininity ) .
	manualset3
84220	2	398185	5	NULL	NULL	0	NULL	men ( or women )	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Healthcare professionals should be aware that not all men ( or women ) conform to the social stereotypes of masculinity ( or femininity ) .
	manualset3
84221	3	398185	5	NULL	NULL	0	NULL	social stereotypes	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Healthcare professionals should be aware that not all men ( or women ) conform to the social stereotypes of masculinity ( or femininity ) .
	manualset3
84222	4	398185	5	NULL	NULL	0	NULL	masculinity ( or femininity )	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Healthcare professionals should be aware that not all men ( or women ) conform to the social stereotypes of masculinity ( or femininity ) .
	manualset3
84223	1	398186	5	NULL	NULL	0	NULL	Healthy vegetarians	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Healthy vegetarians ( 12 male , 12 female ) consumed nine capsules daily of either DHA ( 1.62 g/d ) or corn oil for 6 wk .
	manualset3
84224	2	398186	5	NULL	NULL	0	NULL	 ( 12 male , 12 female )	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Healthy vegetarians ( 12 male , 12 female ) consumed nine capsules daily of either DHA ( 1.62 g/d ) or corn oil for 6 wk .
	manualset3
84225	3	398186	5	NULL	NULL	NULL	NULL	nine capsules	Molecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Healthy vegetarians ( 12 male , 12 female ) consumed nine capsules daily of either DHA ( 1.62 g/d ) or corn oil for 6 wk .
	manualset3
84226	4	398186	5	NULL	NULL	0	NULL	DHA ( 1.62 g/d )	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Healthy vegetarians ( 12 male , 12 female ) consumed nine capsules daily of either DHA ( 1.62 g/d ) or corn oil for 6 wk .
	manualset3
84227	5	398186	5	NULL	NULL	0	NULL	corn oil	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Healthy vegetarians ( 12 male , 12 female ) consumed nine capsules daily of either DHA ( 1.62 g/d ) or corn oil for 6 wk .
	manualset3
84228	6	398186	5	NULL	NULL	0	NULL	6 wk	TimePoint												NULL		0	NULL	NULL	NULL	NULL	NULL	Healthy vegetarians ( 12 male , 12 female ) consumed nine capsules daily of either DHA ( 1.62 g/d ) or corn oil for 6 wk .
	manualset3
84269	1	398187	5	NULL	NULL	0	NULL	Hearing aid benefit	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hearing aid benefit related to the POGO amplification formula , evaluated from insertion gain measurements of two BTE hearing aids .
	manualset3
84270	2	398187	5	NULL	NULL	0	NULL	POGO amplification formula	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Hearing aid benefit related to the POGO amplification formula , evaluated from insertion gain measurements of two BTE hearing aids .
	manualset3
84271	3	398187	5	NULL	NULL	0	NULL	 insertion gain measurements	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hearing aid benefit related to the POGO amplification formula , evaluated from insertion gain measurements of two BTE hearing aids .
	manualset3
84272	4	398187	5	NULL	NULL	0	NULL	two BTE hearing aids	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	Hearing aid benefit related to the POGO amplification formula , evaluated from insertion gain measurements of two BTE hearing aids .
	manualset3
84273	1	398188	5	NULL	NULL	0	NULL	Heart rate	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heart rate , oxygen consumption ( VO2 ) , respiratory exchange ratio ( RER ) , and ratings of perceived exertion ( RPE ) were measured during the preload , and blood glucose and lactate were measured before and after the preload and time-trial .
	manualset3
84274	2	398188	5	NULL	NULL	0	NULL	oxygen consumption ( VO2 )	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heart rate , oxygen consumption ( VO2 ) , respiratory exchange ratio ( RER ) , and ratings of perceived exertion ( RPE ) were measured during the preload , and blood glucose and lactate were measured before and after the preload and time-trial .
	manualset3
84275	3	398188	5	NULL	NULL	0	NULL	respiratory exchange ratio ( RER )	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heart rate , oxygen consumption ( VO2 ) , respiratory exchange ratio ( RER ) , and ratings of perceived exertion ( RPE ) were measured during the preload , and blood glucose and lactate were measured before and after the preload and time-trial .
	manualset3
84276	4	398188	5	NULL	NULL	0	NULL	ratings of perceived exertion ( RPE )	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heart rate , oxygen consumption ( VO2 ) , respiratory exchange ratio ( RER ) , and ratings of perceived exertion ( RPE ) were measured during the preload , and blood glucose and lactate were measured before and after the preload and time-trial .
	manualset3
84277	5	398188	5	NULL	NULL	0	NULL	preload	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Heart rate , oxygen consumption ( VO2 ) , respiratory exchange ratio ( RER ) , and ratings of perceived exertion ( RPE ) were measured during the preload , and blood glucose and lactate were measured before and after the preload and time-trial .
	manualset3
84278	6	398188	5	NULL	NULL	0	NULL	blood glucose	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Heart rate , oxygen consumption ( VO2 ) , respiratory exchange ratio ( RER ) , and ratings of perceived exertion ( RPE ) were measured during the preload , and blood glucose and lactate were measured before and after the preload and time-trial .
	manualset3
84279	7	398188	5	NULL	NULL	0	NULL	lactate	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Heart rate , oxygen consumption ( VO2 ) , respiratory exchange ratio ( RER ) , and ratings of perceived exertion ( RPE ) were measured during the preload , and blood glucose and lactate were measured before and after the preload and time-trial .
	manualset3
84280	8	398188	5	NULL	NULL	0	NULL	 preload	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Heart rate , oxygen consumption ( VO2 ) , respiratory exchange ratio ( RER ) , and ratings of perceived exertion ( RPE ) were measured during the preload , and blood glucose and lactate were measured before and after the preload and time-trial .
	manualset3
84281	9	398188	5	NULL	NULL	0	NULL	time-trial	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Heart rate , oxygen consumption ( VO2 ) , respiratory exchange ratio ( RER ) , and ratings of perceived exertion ( RPE ) were measured during the preload , and blood glucose and lactate were measured before and after the preload and time-trial .
	manualset3
84282	1	398189	5	NULL	NULL	0	NULL	Heart rate	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heart rate , pupil size , pupillary light reflex , BIS scores , and blood pressure were measured every 2min before and for 30min after drug administration .
	manualset3
84283	2	398189	5	NULL	NULL	0	NULL	pupillary light reflex	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heart rate , pupil size , pupillary light reflex , BIS scores , and blood pressure were measured every 2min before and for 30min after drug administration .
	manualset3
84284	3	398189	5	NULL	NULL	0	NULL	BIS scores	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heart rate , pupil size , pupillary light reflex , BIS scores , and blood pressure were measured every 2min before and for 30min after drug administration .
	manualset3
84285	4	398189	5	NULL	NULL	0	NULL	blood pressure	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heart rate , pupil size , pupillary light reflex , BIS scores , and blood pressure were measured every 2min before and for 30min after drug administration .
	manualset3
84286	5	398189	5	NULL	NULL	0	NULL	2min 	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Heart rate , pupil size , pupillary light reflex , BIS scores , and blood pressure were measured every 2min before and for 30min after drug administration .
	manualset3
84287	6	398189	5	NULL	NULL	0	NULL	30min	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Heart rate , pupil size , pupillary light reflex , BIS scores , and blood pressure were measured every 2min before and for 30min after drug administration .
	manualset3
84288	7	398189	5	NULL	NULL	0	NULL	drug administration	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heart rate , pupil size , pupillary light reflex , BIS scores , and blood pressure were measured every 2min before and for 30min after drug administration .
	manualset3
84289	1	398190	5	NULL	NULL	0	NULL	Hearts	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hearts of aged animals contained significantly ( P & lt ; 0.05 ; ANOVA ) more proANF 1-98 , proANF 31-67 , and ANF than hearts of adult animals .
	manualset3
84290	2	398190	5	NULL	NULL	0	NULL	aged animals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hearts of aged animals contained significantly ( P & lt ; 0.05 ; ANOVA ) more proANF 1-98 , proANF 31-67 , and ANF than hearts of adult animals .
	manualset3
84291	3	398190	5	NULL	NULL	0	NULL	P & lt ; 0.05 ; ANOVA	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hearts of aged animals contained significantly ( P & lt ; 0.05 ; ANOVA ) more proANF 1-98 , proANF 31-67 , and ANF than hearts of adult animals .
	manualset3
84292	4	398190	5	NULL	NULL	0	NULL	proANF 1-98	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hearts of aged animals contained significantly ( P & lt ; 0.05 ; ANOVA ) more proANF 1-98 , proANF 31-67 , and ANF than hearts of adult animals .
	manualset3
84293	5	398190	5	NULL	NULL	0	NULL	proANF 31-67	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hearts of aged animals contained significantly ( P & lt ; 0.05 ; ANOVA ) more proANF 1-98 , proANF 31-67 , and ANF than hearts of adult animals .
	manualset3
84294	6	398190	5	NULL	NULL	0	NULL	ANF	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hearts of aged animals contained significantly ( P & lt ; 0.05 ; ANOVA ) more proANF 1-98 , proANF 31-67 , and ANF than hearts of adult animals .
	manualset3
84295	7	398190	5	NULL	NULL	0	NULL	hearts	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hearts of aged animals contained significantly ( P & lt ; 0.05 ; ANOVA ) more proANF 1-98 , proANF 31-67 , and ANF than hearts of adult animals .
	manualset3
84296	8	398190	5	NULL	NULL	0	NULL	adult animals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hearts of aged animals contained significantly ( P & lt ; 0.05 ; ANOVA ) more proANF 1-98 , proANF 31-67 , and ANF than hearts of adult animals .
	manualset3
84297	1	398191	5	NULL	NULL	0	NULL	Studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on the mechanism of action of so-called radiation-protective agents and agents against radiation damage ) .
	manualset3
84298	2	398191	5	NULL	NULL	0	NULL	mechanism of action	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on the mechanism of action of so-called radiation-protective agents and agents against radiation damage ) .
	manualset3
84299	3	398191	5	NULL	NULL	0	NULL	radiation-protective agents	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on the mechanism of action of so-called radiation-protective agents and agents against radiation damage ) .
	manualset3
84300	4	398191	5	NULL	NULL	NULL	NULL	agents against radiation damage	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Studies on the mechanism of action of so-called radiation-protective agents and agents against radiation damage ) .
	manualset3
84301	1	398192	5	NULL	NULL	0	NULL	Hearts	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hearts were removed and mitochondria were isolated .
	manualset3
84302	2	398192	5	NULL	NULL	0	NULL	mitochondria	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Hearts were removed and mitochondria were isolated .
	manualset3
84303	1	398193	5	NULL	NULL	0	NULL	Heat-shock activation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat-shock activation of the mutant HNF1B variants P328L329del and A263insGG resulted in malformations of various organs and the affected larvae developed large edemas .
	manualset3
84304	2	398193	5	NULL	NULL	0	NULL	mutant HNF1B variants P328L329del and A263insGG	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat-shock activation of the mutant HNF1B variants P328L329del and A263insGG resulted in malformations of various organs and the affected larvae developed large edemas .
	manualset3
84305	3	398193	5	NULL	NULL	0	NULL	malformations	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat-shock activation of the mutant HNF1B variants P328L329del and A263insGG resulted in malformations of various organs and the affected larvae developed large edemas .
	manualset3
84306	4	398193	5	NULL	NULL	0	NULL	various organs	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat-shock activation of the mutant HNF1B variants P328L329del and A263insGG resulted in malformations of various organs and the affected larvae developed large edemas .
	manualset3
84307	5	398193	5	NULL	NULL	0	NULL	affected larvae	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat-shock activation of the mutant HNF1B variants P328L329del and A263insGG resulted in malformations of various organs and the affected larvae developed large edemas .
	manualset3
84308	6	398193	5	NULL	NULL	0	NULL	edemas	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat-shock activation of the mutant HNF1B variants P328L329del and A263insGG resulted in malformations of various organs and the affected larvae developed large edemas .
	manualset3
84309	1	398194	5	NULL	NULL	0	NULL	Heat-stressed 44-59-day-old quails	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat-stressed 44-59-day-old quails elevated their Tb to as much as an average 44.1 degrees C in Ta of about 45 degrees C. The obtained growth model and a gradual development of the body temperature regulation mechanism in king quails followed the known strategy of development , typical for precocial birds .
	manualset3
84310	2	398194	5	NULL	NULL	NULL	NULL	Tb	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Heat-stressed 44-59-day-old quails elevated their Tb to as much as an average 44.1 degrees C in Ta of about 45 degrees C. The obtained growth model and a gradual development of the body temperature regulation mechanism in king quails followed the known strategy of development , typical for precocial birds .
	manualset3
84311	3	398194	5	NULL	NULL	0	NULL	44.1 degrees C	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat-stressed 44-59-day-old quails elevated their Tb to as much as an average 44.1 degrees C in Ta of about 45 degrees C. The obtained growth model and a gradual development of the body temperature regulation mechanism in king quails followed the known strategy of development , typical for precocial birds .
	manualset3
84312	4	398194	5	NULL	NULL	0	NULL	Ta	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat-stressed 44-59-day-old quails elevated their Tb to as much as an average 44.1 degrees C in Ta of about 45 degrees C. The obtained growth model and a gradual development of the body temperature regulation mechanism in king quails followed the known strategy of development , typical for precocial birds .
	manualset3
84313	5	398194	5	NULL	NULL	0	NULL	45 degrees C	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat-stressed 44-59-day-old quails elevated their Tb to as much as an average 44.1 degrees C in Ta of about 45 degrees C. The obtained growth model and a gradual development of the body temperature regulation mechanism in king quails followed the known strategy of development , typical for precocial birds .
	manualset3
84314	6	398194	5	NULL	NULL	0	NULL	obtained growth model 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat-stressed 44-59-day-old quails elevated their Tb to as much as an average 44.1 degrees C in Ta of about 45 degrees C. The obtained growth model and a gradual development of the body temperature regulation mechanism in king quails followed the known strategy of development , typical for precocial birds .
	manualset3
84315	7	398194	5	NULL	NULL	0	NULL	gradual development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat-stressed 44-59-day-old quails elevated their Tb to as much as an average 44.1 degrees C in Ta of about 45 degrees C. The obtained growth model and a gradual development of the body temperature regulation mechanism in king quails followed the known strategy of development , typical for precocial birds .
	manualset3
84316	8	398194	5	NULL	NULL	0	NULL	body temperature regulation mechanism	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat-stressed 44-59-day-old quails elevated their Tb to as much as an average 44.1 degrees C in Ta of about 45 degrees C. The obtained growth model and a gradual development of the body temperature regulation mechanism in king quails followed the known strategy of development , typical for precocial birds .
	manualset3
84317	9	398194	5	NULL	NULL	0	NULL	king quails	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat-stressed 44-59-day-old quails elevated their Tb to as much as an average 44.1 degrees C in Ta of about 45 degrees C. The obtained growth model and a gradual development of the body temperature regulation mechanism in king quails followed the known strategy of development , typical for precocial birds .
	manualset3
84318	10	398194	5	NULL	NULL	0	NULL	known strategy	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat-stressed 44-59-day-old quails elevated their Tb to as much as an average 44.1 degrees C in Ta of about 45 degrees C. The obtained growth model and a gradual development of the body temperature regulation mechanism in king quails followed the known strategy of development , typical for precocial birds .
	manualset3
84319	11	398194	5	NULL	NULL	0	NULL	development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat-stressed 44-59-day-old quails elevated their Tb to as much as an average 44.1 degrees C in Ta of about 45 degrees C. The obtained growth model and a gradual development of the body temperature regulation mechanism in king quails followed the known strategy of development , typical for precocial birds .
	manualset3
84320	12	398194	5	NULL	NULL	0	NULL	precocial birds	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat-stressed 44-59-day-old quails elevated their Tb to as much as an average 44.1 degrees C in Ta of about 45 degrees C. The obtained growth model and a gradual development of the body temperature regulation mechanism in king quails followed the known strategy of development , typical for precocial birds .
	manualset3
84321	1	398195	5	NULL	NULL	0	NULL	Heat protection	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat protection was principally reflected in an increased Dq on the 45 degrees C survival curve ; for example , with 100 mM L-alanine , the Dq increased from approximately equal to 20 ( control ) to 30 min at 45 degrees C. Hyperthermia of 1 h at temperatures between 42 degrees C and 45 degrees C indicated that 100 mM alanine had shifted the isotoxic temperature by 0.5 degrees C. Comparable heat protection was also observed with D-alanine and amino acid dimers , such as alanyl-alanine or alanyl-leucine .
	manualset3
84322	2	398195	5	NULL	NULL	0	NULL	increased Dq	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat protection was principally reflected in an increased Dq on the 45 degrees C survival curve ; for example , with 100 mM L-alanine , the Dq increased from approximately equal to 20 ( control ) to 30 min at 45 degrees C. Hyperthermia of 1 h at temperatures between 42 degrees C and 45 degrees C indicated that 100 mM alanine had shifted the isotoxic temperature by 0.5 degrees C. Comparable heat protection was also observed with D-alanine and amino acid dimers , such as alanyl-alanine or alanyl-leucine .
	manualset3
84323	3	398195	5	NULL	NULL	0	NULL	45 degrees C survival curve	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat protection was principally reflected in an increased Dq on the 45 degrees C survival curve ; for example , with 100 mM L-alanine , the Dq increased from approximately equal to 20 ( control ) to 30 min at 45 degrees C. Hyperthermia of 1 h at temperatures between 42 degrees C and 45 degrees C indicated that 100 mM alanine had shifted the isotoxic temperature by 0.5 degrees C. Comparable heat protection was also observed with D-alanine and amino acid dimers , such as alanyl-alanine or alanyl-leucine .
	manualset3
84324	4	398195	5	NULL	NULL	0	NULL	100 mM L-alanine	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat protection was principally reflected in an increased Dq on the 45 degrees C survival curve ; for example , with 100 mM L-alanine , the Dq increased from approximately equal to 20 ( control ) to 30 min at 45 degrees C. Hyperthermia of 1 h at temperatures between 42 degrees C and 45 degrees C indicated that 100 mM alanine had shifted the isotoxic temperature by 0.5 degrees C. Comparable heat protection was also observed with D-alanine and amino acid dimers , such as alanyl-alanine or alanyl-leucine .
	manualset3
84325	5	398195	5	NULL	NULL	0	NULL	Dq	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat protection was principally reflected in an increased Dq on the 45 degrees C survival curve ; for example , with 100 mM L-alanine , the Dq increased from approximately equal to 20 ( control ) to 30 min at 45 degrees C. Hyperthermia of 1 h at temperatures between 42 degrees C and 45 degrees C indicated that 100 mM alanine had shifted the isotoxic temperature by 0.5 degrees C. Comparable heat protection was also observed with D-alanine and amino acid dimers , such as alanyl-alanine or alanyl-leucine .
	manualset3
84326	6	398195	5	NULL	NULL	0	NULL	20 ( control ) to 30 min at 45 degrees C	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat protection was principally reflected in an increased Dq on the 45 degrees C survival curve ; for example , with 100 mM L-alanine , the Dq increased from approximately equal to 20 ( control ) to 30 min at 45 degrees C. Hyperthermia of 1 h at temperatures between 42 degrees C and 45 degrees C indicated that 100 mM alanine had shifted the isotoxic temperature by 0.5 degrees C. Comparable heat protection was also observed with D-alanine and amino acid dimers , such as alanyl-alanine or alanyl-leucine .
	manualset3
84327	7	398195	5	NULL	NULL	0	NULL	Hyperthermia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat protection was principally reflected in an increased Dq on the 45 degrees C survival curve ; for example , with 100 mM L-alanine , the Dq increased from approximately equal to 20 ( control ) to 30 min at 45 degrees C. Hyperthermia of 1 h at temperatures between 42 degrees C and 45 degrees C indicated that 100 mM alanine had shifted the isotoxic temperature by 0.5 degrees C. Comparable heat protection was also observed with D-alanine and amino acid dimers , such as alanyl-alanine or alanyl-leucine .
	manualset3
84328	8	398195	5	NULL	NULL	0	NULL	1 h	TimePoint												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat protection was principally reflected in an increased Dq on the 45 degrees C survival curve ; for example , with 100 mM L-alanine , the Dq increased from approximately equal to 20 ( control ) to 30 min at 45 degrees C. Hyperthermia of 1 h at temperatures between 42 degrees C and 45 degrees C indicated that 100 mM alanine had shifted the isotoxic temperature by 0.5 degrees C. Comparable heat protection was also observed with D-alanine and amino acid dimers , such as alanyl-alanine or alanyl-leucine .
	manualset3
84329	9	398195	5	NULL	NULL	0	NULL	temperatures between 42 degrees C and 45 degrees C	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat protection was principally reflected in an increased Dq on the 45 degrees C survival curve ; for example , with 100 mM L-alanine , the Dq increased from approximately equal to 20 ( control ) to 30 min at 45 degrees C. Hyperthermia of 1 h at temperatures between 42 degrees C and 45 degrees C indicated that 100 mM alanine had shifted the isotoxic temperature by 0.5 degrees C. Comparable heat protection was also observed with D-alanine and amino acid dimers , such as alanyl-alanine or alanyl-leucine .
	manualset3
84330	10	398195	5	NULL	NULL	0	NULL	100 mM alanine	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat protection was principally reflected in an increased Dq on the 45 degrees C survival curve ; for example , with 100 mM L-alanine , the Dq increased from approximately equal to 20 ( control ) to 30 min at 45 degrees C. Hyperthermia of 1 h at temperatures between 42 degrees C and 45 degrees C indicated that 100 mM alanine had shifted the isotoxic temperature by 0.5 degrees C. Comparable heat protection was also observed with D-alanine and amino acid dimers , such as alanyl-alanine or alanyl-leucine .
	manualset3
84331	11	398195	5	NULL	NULL	0	NULL	isotoxic temperature	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat protection was principally reflected in an increased Dq on the 45 degrees C survival curve ; for example , with 100 mM L-alanine , the Dq increased from approximately equal to 20 ( control ) to 30 min at 45 degrees C. Hyperthermia of 1 h at temperatures between 42 degrees C and 45 degrees C indicated that 100 mM alanine had shifted the isotoxic temperature by 0.5 degrees C. Comparable heat protection was also observed with D-alanine and amino acid dimers , such as alanyl-alanine or alanyl-leucine .
	manualset3
84332	12	398195	5	NULL	NULL	0	NULL	0.5 degrees C	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat protection was principally reflected in an increased Dq on the 45 degrees C survival curve ; for example , with 100 mM L-alanine , the Dq increased from approximately equal to 20 ( control ) to 30 min at 45 degrees C. Hyperthermia of 1 h at temperatures between 42 degrees C and 45 degrees C indicated that 100 mM alanine had shifted the isotoxic temperature by 0.5 degrees C. Comparable heat protection was also observed with D-alanine and amino acid dimers , such as alanyl-alanine or alanyl-leucine .
	manualset3
84333	13	398195	5	NULL	NULL	0	NULL	Comparable heat protection	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat protection was principally reflected in an increased Dq on the 45 degrees C survival curve ; for example , with 100 mM L-alanine , the Dq increased from approximately equal to 20 ( control ) to 30 min at 45 degrees C. Hyperthermia of 1 h at temperatures between 42 degrees C and 45 degrees C indicated that 100 mM alanine had shifted the isotoxic temperature by 0.5 degrees C. Comparable heat protection was also observed with D-alanine and amino acid dimers , such as alanyl-alanine or alanyl-leucine .
	manualset3
84334	14	398195	5	NULL	NULL	0	NULL	D-alanine	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat protection was principally reflected in an increased Dq on the 45 degrees C survival curve ; for example , with 100 mM L-alanine , the Dq increased from approximately equal to 20 ( control ) to 30 min at 45 degrees C. Hyperthermia of 1 h at temperatures between 42 degrees C and 45 degrees C indicated that 100 mM alanine had shifted the isotoxic temperature by 0.5 degrees C. Comparable heat protection was also observed with D-alanine and amino acid dimers , such as alanyl-alanine or alanyl-leucine .
	manualset3
84335	15	398195	5	NULL	NULL	0	NULL	amino acid dimers , such as alanyl-alanine or alanyl-leucine	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat protection was principally reflected in an increased Dq on the 45 degrees C survival curve ; for example , with 100 mM L-alanine , the Dq increased from approximately equal to 20 ( control ) to 30 min at 45 degrees C. Hyperthermia of 1 h at temperatures between 42 degrees C and 45 degrees C indicated that 100 mM alanine had shifted the isotoxic temperature by 0.5 degrees C. Comparable heat protection was also observed with D-alanine and amino acid dimers , such as alanyl-alanine or alanyl-leucine .
	manualset3
84336	1	398196	5	NULL	NULL	0	NULL	Heat shock	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat shock to embryonal carcinoma cells PCC4 at 45 degrees C for 30 min resulted in the differentiation of cells although heat shock response was induced on exposure to 42 degrees C for 60 min .
	manualset3
84337	2	398196	5	NULL	NULL	0	NULL	embryonal carcinoma cells PCC4 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat shock to embryonal carcinoma cells PCC4 at 45 degrees C for 30 min resulted in the differentiation of cells although heat shock response was induced on exposure to 42 degrees C for 60 min .
	manualset3
84338	3	398196	5	NULL	NULL	0	NULL	45 degrees C 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat shock to embryonal carcinoma cells PCC4 at 45 degrees C for 30 min resulted in the differentiation of cells although heat shock response was induced on exposure to 42 degrees C for 60 min .
	manualset3
84339	4	398196	5	NULL	NULL	0	NULL	30 min	TimePoint												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat shock to embryonal carcinoma cells PCC4 at 45 degrees C for 30 min resulted in the differentiation of cells although heat shock response was induced on exposure to 42 degrees C for 60 min .
	manualset3
84340	5	398196	5	NULL	NULL	0	NULL	differentiation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat shock to embryonal carcinoma cells PCC4 at 45 degrees C for 30 min resulted in the differentiation of cells although heat shock response was induced on exposure to 42 degrees C for 60 min .
	manualset3
84341	6	398196	5	NULL	NULL	0	NULL	cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat shock to embryonal carcinoma cells PCC4 at 45 degrees C for 30 min resulted in the differentiation of cells although heat shock response was induced on exposure to 42 degrees C for 60 min .
	manualset3
84342	7	398196	5	NULL	NULL	0	NULL	heat shock response	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat shock to embryonal carcinoma cells PCC4 at 45 degrees C for 30 min resulted in the differentiation of cells although heat shock response was induced on exposure to 42 degrees C for 60 min .
	manualset3
84343	8	398196	5	NULL	NULL	0	NULL	42 degrees C	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat shock to embryonal carcinoma cells PCC4 at 45 degrees C for 30 min resulted in the differentiation of cells although heat shock response was induced on exposure to 42 degrees C for 60 min .
	manualset3
84344	9	398196	5	NULL	NULL	0	NULL	60 min	TimePoint												NULL		0	NULL	NULL	NULL	NULL	NULL	Heat shock to embryonal carcinoma cells PCC4 at 45 degrees C for 30 min resulted in the differentiation of cells although heat shock response was induced on exposure to 42 degrees C for 60 min .
	manualset3
84345	1	398197	5	NULL	NULL	0	NULL	lidocaine	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Heating lidocaine appears to prevent painful injection .
	manualset3
84346	2	398197	5	NULL	NULL	0	NULL	painful injection	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Heating lidocaine appears to prevent painful injection .
	manualset3
84347	1	398198	5	NULL	NULL	0	NULL	ethylene oxide sterilization	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heating during ethylene oxide sterilization also resulted in reduced viscosity and breakdown .
	manualset3
84348	2	398198	5	NULL	NULL	NULL	NULL	reduced viscosity and breakdown	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Heating during ethylene oxide sterilization also resulted in reduced viscosity and breakdown .
	manualset3
84349	2	398199	5	NULL	NULL	NULL	NULL	lipoid-reagin	Molecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Heating the lipoid-reagin precipitate to 100 degrees for 1 minute destroys the sensitizing film of reagin globulin ; the avidity for complement disappears simultaneously .
	manualset3
84350	3	398199	5	NULL	NULL	NULL	NULL	100 degrees	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Heating the lipoid-reagin precipitate to 100 degrees for 1 minute destroys the sensitizing film of reagin globulin ; the avidity for complement disappears simultaneously .
	manualset3
84351	4	398199	5	NULL	NULL	NULL	NULL	1 minute	TimePoint												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Heating the lipoid-reagin precipitate to 100 degrees for 1 minute destroys the sensitizing film of reagin globulin ; the avidity for complement disappears simultaneously .
	manualset3
84353	5	398199	5	NULL	NULL	0	NULL	reagin globulin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Heating the lipoid-reagin precipitate to 100 degrees for 1 minute destroys the sensitizing film of reagin globulin ; the avidity for complement disappears simultaneously .
	manualset3
84354	6	398199	5	NULL	NULL	0	NULL	avidity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heating the lipoid-reagin precipitate to 100 degrees for 1 minute destroys the sensitizing film of reagin globulin ; the avidity for complement disappears simultaneously .
	manualset3
84355	7	398199	5	NULL	NULL	0	NULL	complement	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Heating the lipoid-reagin precipitate to 100 degrees for 1 minute destroys the sensitizing film of reagin globulin ; the avidity for complement disappears simultaneously .
	manualset3
84503	1	398199	5	NULL	NULL	0	NULL	Heating	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Heating the lipoid-reagin precipitate to 100 degrees for 1 minute destroys the sensitizing film of reagin globulin ; the avidity for complement disappears simultaneously .
	manualset3
84356	1	398200	5	NULL	NULL	0	NULL	Heavy meromyosin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Heavy meromyosin induces sliding movements between antiparallel actin filaments .
	manualset3
84357	2	398200	5	NULL	NULL	0	NULL	sliding movements	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heavy meromyosin induces sliding movements between antiparallel actin filaments .
	manualset3
84358	3	398200	5	NULL	NULL	NULL	NULL	antiparallel actin filaments	CellComponent												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Heavy meromyosin induces sliding movements between antiparallel actin filaments .
	manualset3
84359	1	398201	5	NULL	NULL	0	NULL	Studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on uric acid metabolism in various skin diseases ( supplemental report ) .
	manualset3
84360	2	398201	5	NULL	NULL	0	NULL	uric acid metabolism	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on uric acid metabolism in various skin diseases ( supplemental report ) .
	manualset3
84361	3	398201	5	NULL	NULL	0	NULL	skin diseases	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on uric acid metabolism in various skin diseases ( supplemental report ) .
	manualset3
84362	4	398201	5	NULL	NULL	0	NULL	supplemental report	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	( Studies on uric acid metabolism in various skin diseases ( supplemental report ) .
	manualset3
84363	1	398202	5	NULL	NULL	0	NULL	Heifers	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Heifers fed accelerated diets had a higher average daily gain ( 933 vs. 778 g/d ) and calved earlier ( 21.7 vs. 24.6 mo ) than did heifers fed control diets .
	manualset3
84364	2	398202	5	NULL	NULL	0	NULL	accelerated diets	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	Heifers fed accelerated diets had a higher average daily gain ( 933 vs. 778 g/d ) and calved earlier ( 21.7 vs. 24.6 mo ) than did heifers fed control diets .
	manualset3
84365	3	398202	5	NULL	NULL	0	NULL	 higher average daily gain ( 933 vs. 778 g/d )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Heifers fed accelerated diets had a higher average daily gain ( 933 vs. 778 g/d ) and calved earlier ( 21.7 vs. 24.6 mo ) than did heifers fed control diets .
	manualset3
84366	4	398202	5	NULL	NULL	0	NULL	calved earlier ( 21.7 vs. 24.6 mo )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Heifers fed accelerated diets had a higher average daily gain ( 933 vs. 778 g/d ) and calved earlier ( 21.7 vs. 24.6 mo ) than did heifers fed control diets .
	manualset3
84367	5	398202	5	NULL	NULL	0	NULL	heifers	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Heifers fed accelerated diets had a higher average daily gain ( 933 vs. 778 g/d ) and calved earlier ( 21.7 vs. 24.6 mo ) than did heifers fed control diets .
	manualset3
84368	6	398202	5	NULL	NULL	0	NULL	control diets	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	Heifers fed accelerated diets had a higher average daily gain ( 933 vs. 778 g/d ) and calved earlier ( 21.7 vs. 24.6 mo ) than did heifers fed control diets .
	manualset3
84369	1	398203	5	NULL	NULL	0	NULL	Heifers	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Heifers were injected in the area of the supramammary lymph nodes with vaccine or placebo twice before calving and observed and sampled throughout their first lactation .
	manualset3
84370	2	398203	5	NULL	NULL	0	NULL	area of the supramammary lymph nodes	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Heifers were injected in the area of the supramammary lymph nodes with vaccine or placebo twice before calving and observed and sampled throughout their first lactation .
	manualset3
84371	3	398203	5	NULL	NULL	0	NULL	vaccine	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Heifers were injected in the area of the supramammary lymph nodes with vaccine or placebo twice before calving and observed and sampled throughout their first lactation .
	manualset3
84372	4	398203	5	NULL	NULL	0	NULL	placebo	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Heifers were injected in the area of the supramammary lymph nodes with vaccine or placebo twice before calving and observed and sampled throughout their first lactation .
	manualset3
84373	5	398203	5	NULL	NULL	0	NULL	first lactation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heifers were injected in the area of the supramammary lymph nodes with vaccine or placebo twice before calving and observed and sampled throughout their first lactation .
	manualset3
84374	1	398204	5	NULL	NULL	0	NULL	Heifers	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Heifers were inseminated at 6 h and 16 h after onset of estrus .
	manualset3
84375	2	398204	5	NULL	NULL	0	NULL	6 h and 16 h	TimePoint												NULL		0	NULL	NULL	NULL	NULL	NULL	Heifers were inseminated at 6 h and 16 h after onset of estrus .
	manualset3
84376	3	398204	5	NULL	NULL	0	NULL	estrus	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heifers were inseminated at 6 h and 16 h after onset of estrus .
	manualset3
84377	1	398205	5	NULL	NULL	0	NULL	Height gain	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Height gain can be successfully achieved in these patients with growth hormone treatment .
	manualset3
84378	2	398205	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Height gain can be successfully achieved in these patients with growth hormone treatment .
	manualset3
84379	3	398205	5	NULL	NULL	0	NULL	growth hormone treatment	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Height gain can be successfully achieved in these patients with growth hormone treatment .
	manualset3
84380	1	398206	5	NULL	NULL	0	NULL	Helicity propensity and interaction	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Helicity propensity and interaction of synthetic peptides from heptad-repeat domains of herpes simplex virus 1 glycoprotein H : a circular dichroism study .
	manualset3
84381	2	398206	5	NULL	NULL	0	NULL	synthetic peptides	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Helicity propensity and interaction of synthetic peptides from heptad-repeat domains of herpes simplex virus 1 glycoprotein H : a circular dichroism study .
	manualset3
84382	3	398206	5	NULL	NULL	0	NULL	heptad-repeat domains	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Helicity propensity and interaction of synthetic peptides from heptad-repeat domains of herpes simplex virus 1 glycoprotein H : a circular dichroism study .
	manualset3
84383	4	398206	5	NULL	NULL	0	NULL	herpes simplex virus 1 glycoprotein H	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Helicity propensity and interaction of synthetic peptides from heptad-repeat domains of herpes simplex virus 1 glycoprotein H : a circular dichroism study .
	manualset3
84384	5	398206	5	NULL	NULL	0	NULL	circular dichroism study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Helicity propensity and interaction of synthetic peptides from heptad-repeat domains of herpes simplex virus 1 glycoprotein H : a circular dichroism study .
	manualset3
84385	1	398207	5	NULL	NULL	0	NULL	Helicobacter pylori	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Helicobacter pylori induces the release of alpha-defensin by human granulocytes .
	manualset3
84386	2	398207	5	NULL	NULL	0	NULL	alpha-defensin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Helicobacter pylori induces the release of alpha-defensin by human granulocytes .
	manualset3
84387	3	398207	5	NULL	NULL	0	NULL	human granulocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Helicobacter pylori induces the release of alpha-defensin by human granulocytes .
	manualset3
84388	1	398208	5	NULL	NULL	0	NULL	Helicobacter pylori infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Helicobacter pylori infection : a risk factor for ischaemic cerebrovascular disease and carotid atheroma .
	manualset3
84389	2	398208	5	NULL	NULL	0	NULL	ischaemic cerebrovascular disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Helicobacter pylori infection : a risk factor for ischaemic cerebrovascular disease and carotid atheroma .
	manualset3
84390	3	398208	5	NULL	NULL	0	NULL	carotid atheroma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Helicobacter pylori infection : a risk factor for ischaemic cerebrovascular disease and carotid atheroma .
	manualset3
84391	1	398209	5	NULL	NULL	0	NULL	Helicobacter pylori	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Helicobacter pylori is the definitive carcinogen for stomach cancer and is known to induce proinflammatory cytokines , such as tumor necrosis factor-alpha ( TNF-alpha ) and interleukin-1 ( IL-1 ) in the stomach .
	manualset3
84392	2	398209	5	NULL	NULL	0	NULL	definitive carcinogen	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Helicobacter pylori is the definitive carcinogen for stomach cancer and is known to induce proinflammatory cytokines , such as tumor necrosis factor-alpha ( TNF-alpha ) and interleukin-1 ( IL-1 ) in the stomach .
	manualset3
84393	3	398209	5	NULL	NULL	0	NULL	stomach cancer	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Helicobacter pylori is the definitive carcinogen for stomach cancer and is known to induce proinflammatory cytokines , such as tumor necrosis factor-alpha ( TNF-alpha ) and interleukin-1 ( IL-1 ) in the stomach .
	manualset3
84394	4	398209	5	NULL	NULL	0	NULL	proinflammatory cytokines	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Helicobacter pylori is the definitive carcinogen for stomach cancer and is known to induce proinflammatory cytokines , such as tumor necrosis factor-alpha ( TNF-alpha ) and interleukin-1 ( IL-1 ) in the stomach .
	manualset3
84395	5	398209	5	NULL	NULL	0	NULL	tumor necrosis factor-alpha ( TNF-alpha )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Helicobacter pylori is the definitive carcinogen for stomach cancer and is known to induce proinflammatory cytokines , such as tumor necrosis factor-alpha ( TNF-alpha ) and interleukin-1 ( IL-1 ) in the stomach .
	manualset3
84396	6	398209	5	NULL	NULL	0	NULL	interleukin-1 ( IL-1 )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Helicobacter pylori is the definitive carcinogen for stomach cancer and is known to induce proinflammatory cytokines , such as tumor necrosis factor-alpha ( TNF-alpha ) and interleukin-1 ( IL-1 ) in the stomach .
	manualset3
84397	7	398209	5	NULL	NULL	0	NULL	stomach	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Helicobacter pylori is the definitive carcinogen for stomach cancer and is known to induce proinflammatory cytokines , such as tumor necrosis factor-alpha ( TNF-alpha ) and interleukin-1 ( IL-1 ) in the stomach .
	manualset3
84398	1	398210	5	NULL	NULL	0	NULL	Study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study of Morita therapy -- including an experience in participating a joint study program for young psychiatrists from Japan and Korea ) .
	manualset3
84399	2	398210	5	NULL	NULL	0	NULL	Morita therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study of Morita therapy -- including an experience in participating a joint study program for young psychiatrists from Japan and Korea ) .
	manualset3
84400	3	398210	5	NULL	NULL	0	NULL	experience	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study of Morita therapy -- including an experience in participating a joint study program for young psychiatrists from Japan and Korea ) .
	manualset3
84401	4	398210	5	NULL	NULL	0	NULL	joint study program	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study of Morita therapy -- including an experience in participating a joint study program for young psychiatrists from Japan and Korea ) .
	manualset3
84402	5	398210	5	NULL	NULL	0	NULL	young psychiatrists	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study of Morita therapy -- including an experience in participating a joint study program for young psychiatrists from Japan and Korea ) .
	manualset3
84403	6	398210	5	NULL	NULL	0	NULL	Japan and Korea	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study of Morita therapy -- including an experience in participating a joint study program for young psychiatrists from Japan and Korea ) .
	manualset3
84404	1	398211	5	NULL	NULL	0	NULL	Hema-Strip HIV-1 / 2	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hema-Strip HIV-1 / 2 is a one-step rapid test for the detection of anti-HIV-1 / 2 antibodies in whole blood .
	manualset3
84405	2	398211	5	NULL	NULL	0	NULL	one-step rapid test	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hema-Strip HIV-1 / 2 is a one-step rapid test for the detection of anti-HIV-1 / 2 antibodies in whole blood .
	manualset3
84406	3	398211	5	NULL	NULL	0	NULL	detection	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hema-Strip HIV-1 / 2 is a one-step rapid test for the detection of anti-HIV-1 / 2 antibodies in whole blood .
	manualset3
84407	4	398211	5	NULL	NULL	0	NULL	anti-HIV-1 / 2 antibodies	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hema-Strip HIV-1 / 2 is a one-step rapid test for the detection of anti-HIV-1 / 2 antibodies in whole blood .
	manualset3
84408	5	398211	5	NULL	NULL	0	NULL	whole blood	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Hema-Strip HIV-1 / 2 is a one-step rapid test for the detection of anti-HIV-1 / 2 antibodies in whole blood .
	manualset3
84409	1	398212	5	NULL	NULL	0	NULL	Hemangiomatosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemangiomatosis of the liver is growing in the last decades , because of the abdominal imaging progresses : brain CT scan , MRI .
	manualset3
84410	2	398212	5	NULL	NULL	0	NULL	liver	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemangiomatosis of the liver is growing in the last decades , because of the abdominal imaging progresses : brain CT scan , MRI .
	manualset3
84411	3	398212	5	NULL	NULL	0	NULL	last decades	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemangiomatosis of the liver is growing in the last decades , because of the abdominal imaging progresses : brain CT scan , MRI .
	manualset3
84412	4	398212	5	NULL	NULL	NULL	NULL	abdominal imaging progresses	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hemangiomatosis of the liver is growing in the last decades , because of the abdominal imaging progresses : brain CT scan , MRI .
	manualset3
84413	5	398212	5	NULL	NULL	NULL	NULL	brain CT scan	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hemangiomatosis of the liver is growing in the last decades , because of the abdominal imaging progresses : brain CT scan , MRI .
	manualset3
84414	6	398212	5	NULL	NULL	0	NULL	MRI	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemangiomatosis of the liver is growing in the last decades , because of the abdominal imaging progresses : brain CT scan , MRI .
	manualset3
84415	1	398213	5	NULL	NULL	0	NULL	Hemangiopericytoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemangiopericytoma of the orbit treated with conservative surgery and radiotherapy .
	manualset3
84416	2	398213	5	NULL	NULL	0	NULL	orbit	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemangiopericytoma of the orbit treated with conservative surgery and radiotherapy .
	manualset3
84417	3	398213	5	NULL	NULL	NULL	NULL	conservative surgery and radiotherapy 	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hemangiopericytoma of the orbit treated with conservative surgery and radiotherapy .
	manualset3
84418	1	398214	5	NULL	NULL	0	NULL	Hemato-vascular origins	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemato-vascular origins of endothelial progenitor cells ?
	manualset3
84419	2	398214	5	NULL	NULL	0	NULL	endothelial progenitor cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemato-vascular origins of endothelial progenitor cells ?
	manualset3
84420	1	398215	5	NULL	NULL	0	NULL	Hematological malignancie	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hematological malignancies in the island of Sardinia , 1974-1993 : age and sex distributions and temporal changes in incidence .
	manualset3
84421	2	398215	5	NULL	NULL	0	NULL	island of Sardinia	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Hematological malignancies in the island of Sardinia , 1974-1993 : age and sex distributions and temporal changes in incidence .
	manualset3
84422	3	398215	5	NULL	NULL	0	NULL	1974-1993	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Hematological malignancies in the island of Sardinia , 1974-1993 : age and sex distributions and temporal changes in incidence .
	manualset3
84423	4	398215	5	NULL	NULL	0	NULL	age and sex distributions	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Hematological malignancies in the island of Sardinia , 1974-1993 : age and sex distributions and temporal changes in incidence .
	manualset3
84424	5	398215	5	NULL	NULL	0	NULL	temporal changes in incidence	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Hematological malignancies in the island of Sardinia , 1974-1993 : age and sex distributions and temporal changes in incidence .
	manualset3
84425	1	398216	5	NULL	NULL	0	NULL	Hematopoietic SCT	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hematopoietic SCT became an established therapy for such disorders .
	manualset3
84426	2	398216	5	NULL	NULL	0	NULL	established therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hematopoietic SCT became an established therapy for such disorders .
	manualset3
84427	3	398216	5	NULL	NULL	0	NULL	disorders	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hematopoietic SCT became an established therapy for such disorders .
	manualset3
84428	1	398217	5	NULL	NULL	0	NULL	Hematopoietic stem/progenitor cells ( HSPCs )	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Hematopoietic stem/progenitor cells ( HSPCs ) in placental/umbilical cord blood ( CB ) , which is neonatal peripheral blood , have increasingly been used for hematopoietic stem cell transplantations .
	manualset3
84429	2	398217	5	NULL	NULL	0	NULL	placental/umbilical cord blood ( CB )	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Hematopoietic stem/progenitor cells ( HSPCs ) in placental/umbilical cord blood ( CB ) , which is neonatal peripheral blood , have increasingly been used for hematopoietic stem cell transplantations .
	manualset3
84430	3	398217	5	NULL	NULL	0	NULL	neonatal peripheral blood	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Hematopoietic stem/progenitor cells ( HSPCs ) in placental/umbilical cord blood ( CB ) , which is neonatal peripheral blood , have increasingly been used for hematopoietic stem cell transplantations .
	manualset3
84431	4	398217	5	NULL	NULL	0	NULL	hematopoietic stem cell transplantations	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hematopoietic stem/progenitor cells ( HSPCs ) in placental/umbilical cord blood ( CB ) , which is neonatal peripheral blood , have increasingly been used for hematopoietic stem cell transplantations .
	manualset3
84432	1	398218	5	NULL	NULL	0	NULL	Hematuria	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hematuria was relatively frequent ( 33 % in the Fraxiparine group and 28 % in the Calciparine group ) , however these rates were related to prostatic and urinary incontinence surgery .
	manualset3
84433	2	398218	5	NULL	NULL	0	NULL	33 % in the Fraxiparine group	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hematuria was relatively frequent ( 33 % in the Fraxiparine group and 28 % in the Calciparine group ) , however these rates were related to prostatic and urinary incontinence surgery .
	manualset3
84434	3	398218	5	NULL	NULL	0	NULL	28 % in the Calciparine group	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hematuria was relatively frequent ( 33 % in the Fraxiparine group and 28 % in the Calciparine group ) , however these rates were related to prostatic and urinary incontinence surgery .
	manualset3
84435	4	398218	5	NULL	NULL	0	NULL	prostatic and urinary incontinence surgery	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hematuria was relatively frequent ( 33 % in the Fraxiparine group and 28 % in the Calciparine group ) , however these rates were related to prostatic and urinary incontinence surgery .
	manualset3
84436	1	398219	5	NULL	NULL	0	NULL	Heme oxygenase-1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Heme oxygenase-1 stabilizes the blood-spinal cord barrier and limits oxidative stress and white matter damage in the acutely injured murine spinal cord .
	manualset3
84437	2	398219	5	NULL	NULL	0	NULL	blood-spinal cord barrier	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Heme oxygenase-1 stabilizes the blood-spinal cord barrier and limits oxidative stress and white matter damage in the acutely injured murine spinal cord .
	manualset3
84438	3	398219	5	NULL	NULL	0	NULL	oxidative stress	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Heme oxygenase-1 stabilizes the blood-spinal cord barrier and limits oxidative stress and white matter damage in the acutely injured murine spinal cord .
	manualset3
84439	4	398219	5	NULL	NULL	0	NULL	white matter damage	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Heme oxygenase-1 stabilizes the blood-spinal cord barrier and limits oxidative stress and white matter damage in the acutely injured murine spinal cord .
	manualset3
84440	5	398219	5	NULL	NULL	0	NULL	acutely injured murine spinal cord	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Heme oxygenase-1 stabilizes the blood-spinal cord barrier and limits oxidative stress and white matter damage in the acutely injured murine spinal cord .
	manualset3
84441	1	398220	5	NULL	NULL	0	NULL	Hemodialysis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemodialysis elicited marked reduction in early diastolic lateral mitral annular and midlateral myocardial velocities ( 6.9 + / - 3.2 to 6.3 + / - 2.9 cm/s , P & lt ; 0.04 and 6.7 + / - 0.3 to 5.5 + / - 2 cm/s , P & lt ; 0.001 , respectively ) .
	manualset3
84442	2	398220	5	NULL	NULL	0	NULL	early diastolic lateral mitral annular and midlateral myocardial velocities	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemodialysis elicited marked reduction in early diastolic lateral mitral annular and midlateral myocardial velocities ( 6.9 + / - 3.2 to 6.3 + / - 2.9 cm/s , P & lt ; 0.04 and 6.7 + / - 0.3 to 5.5 + / - 2 cm/s , P & lt ; 0.001 , respectively ) .
	manualset3
84443	3	398220	5	NULL	NULL	0	NULL	6.9 + / - 3.2 to 6.3 + / - 2.9 cm/s , P & lt ; 0.04 and 6.7 + / - 0.3 to 5.5 + / - 2 cm/s , P & lt ; 0.001	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemodialysis elicited marked reduction in early diastolic lateral mitral annular and midlateral myocardial velocities ( 6.9 + / - 3.2 to 6.3 + / - 2.9 cm/s , P & lt ; 0.04 and 6.7 + / - 0.3 to 5.5 + / - 2 cm/s , P & lt ; 0.001 , respectively ) .
	manualset3
84444	1	398221	5	NULL	NULL	0	NULL	Hemodynamic data	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemodynamic data indicated that LV function in group A was enhanced during the development of the hypertrophy .
	manualset3
84445	2	398221	5	NULL	NULL	0	NULL	LV function	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemodynamic data indicated that LV function in group A was enhanced during the development of the hypertrophy .
	manualset3
84446	3	398221	5	NULL	NULL	0	NULL	group A	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemodynamic data indicated that LV function in group A was enhanced during the development of the hypertrophy .
	manualset3
84447	4	398221	5	NULL	NULL	0	NULL	development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemodynamic data indicated that LV function in group A was enhanced during the development of the hypertrophy .
	manualset3
84448	5	398221	5	NULL	NULL	0	NULL	hypertrophy	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemodynamic data indicated that LV function in group A was enhanced during the development of the hypertrophy .
	manualset3
84449	1	398222	5	NULL	NULL	0	NULL	Hemodynamic improvement	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemodynamic improvement was sustained in both dogs at the time of recatheterization 3 months later .
	manualset3
84450	2	398222	5	NULL	NULL	0	NULL	both dogs	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemodynamic improvement was sustained in both dogs at the time of recatheterization 3 months later .
	manualset3
84451	3	398222	5	NULL	NULL	0	NULL	recatheterization	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemodynamic improvement was sustained in both dogs at the time of recatheterization 3 months later .
	manualset3
84452	4	398222	5	NULL	NULL	0	NULL	3 months later	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemodynamic improvement was sustained in both dogs at the time of recatheterization 3 months later .
	manualset3
84453	1	398223	5	NULL	NULL	0	NULL	Hemofiltration	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemofiltration in human sepsis : evidence for elimination of immunomodulatory substances .
	manualset3
84454	2	398223	5	NULL	NULL	0	NULL	human sepsis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemofiltration in human sepsis : evidence for elimination of immunomodulatory substances .
	manualset3
84455	3	398223	5	NULL	NULL	NULL	NULL	elimination	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hemofiltration in human sepsis : evidence for elimination of immunomodulatory substances .
	manualset3
84456	4	398223	5	NULL	NULL	0	NULL	immunomodulatory substances	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemofiltration in human sepsis : evidence for elimination of immunomodulatory substances .
	manualset3
84457	1	398224	5	NULL	NULL	0	NULL	Hemoglobin G Saskatoon	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemoglobin G Saskatoon : beta-22Glu -- Ala .
	manualset3
84458	2	398224	5	NULL	NULL	0	NULL	beta-22Glu -- Ala	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemoglobin G Saskatoon : beta-22Glu -- Ala .
	manualset3
84459	1	398225	5	NULL	NULL	0	NULL	Hemoglobin ( Hb ) variants	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemoglobin ( Hb ) variants caused by an elongation of the beta-globin chain are rare .
	manualset3
84460	2	398225	5	NULL	NULL	0	NULL	elongation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemoglobin ( Hb ) variants caused by an elongation of the beta-globin chain are rare .
	manualset3
84461	3	398225	5	NULL	NULL	0	NULL	beta-globin chain	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemoglobin ( Hb ) variants caused by an elongation of the beta-globin chain are rare .
	manualset3
84462	1	398226	5	NULL	NULL	0	NULL	Hemoglobin Rainier ( beta ( 145 ) tyrosine -- ) histidine )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemoglobin Rainier ( beta ( 145 ) tyrosine -- ) histidine ) is an abnormal hemoglobin associated with increased oxygen affinity , decreased heme-heme interaction , presence of a Bohr effect , and erythrocytosis , but without obvious clinical sequelae .
	manualset3
84463	2	398226	5	NULL	NULL	0	NULL	abnormal hemoglobin associated with increased oxygen affinity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemoglobin Rainier ( beta ( 145 ) tyrosine -- ) histidine ) is an abnormal hemoglobin associated with increased oxygen affinity , decreased heme-heme interaction , presence of a Bohr effect , and erythrocytosis , but without obvious clinical sequelae .
	manualset3
84464	3	398226	5	NULL	NULL	0	NULL	heme-heme interaction	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemoglobin Rainier ( beta ( 145 ) tyrosine -- ) histidine ) is an abnormal hemoglobin associated with increased oxygen affinity , decreased heme-heme interaction , presence of a Bohr effect , and erythrocytosis , but without obvious clinical sequelae .
	manualset3
84465	4	398226	5	NULL	NULL	0	NULL	Bohr effect	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemoglobin Rainier ( beta ( 145 ) tyrosine -- ) histidine ) is an abnormal hemoglobin associated with increased oxygen affinity , decreased heme-heme interaction , presence of a Bohr effect , and erythrocytosis , but without obvious clinical sequelae .
	manualset3
84466	5	398226	5	NULL	NULL	0	NULL	erythrocytosis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemoglobin Rainier ( beta ( 145 ) tyrosine -- ) histidine ) is an abnormal hemoglobin associated with increased oxygen affinity , decreased heme-heme interaction , presence of a Bohr effect , and erythrocytosis , but without obvious clinical sequelae .
	manualset3
84467	6	398226	5	NULL	NULL	NULL	NULL	obvious clinical sequelae	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hemoglobin Rainier ( beta ( 145 ) tyrosine -- ) histidine ) is an abnormal hemoglobin associated with increased oxygen affinity , decreased heme-heme interaction , presence of a Bohr effect , and erythrocytosis , but without obvious clinical sequelae .
	manualset3
84468	1	398227	5	NULL	NULL	0	NULL	Hemojuvelin ( Hjv )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemojuvelin ( Hjv ) , a member of the repulsive-guidance molecule ( RGM ) family , upregulates transcription of the iron regulatory hormone hepcidin by activating the bone morphogenetic protein ( BMP ) signaling pathway in mammalian cells .
	manualset3
84469	2	398227	5	NULL	NULL	0	NULL	memeber of repulsive-guidance molecule ( RGM ) family	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemojuvelin ( Hjv ) , a member of the repulsive-guidance molecule ( RGM ) family , upregulates transcription of the iron regulatory hormone hepcidin by activating the bone morphogenetic protein ( BMP ) signaling pathway in mammalian cells .
	manualset3
84470	3	398227	5	NULL	NULL	0	NULL	transcription	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemojuvelin ( Hjv ) , a member of the repulsive-guidance molecule ( RGM ) family , upregulates transcription of the iron regulatory hormone hepcidin by activating the bone morphogenetic protein ( BMP ) signaling pathway in mammalian cells .
	manualset3
84471	4	398227	5	NULL	NULL	0	NULL	iron regulatory hormone hepcidin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemojuvelin ( Hjv ) , a member of the repulsive-guidance molecule ( RGM ) family , upregulates transcription of the iron regulatory hormone hepcidin by activating the bone morphogenetic protein ( BMP ) signaling pathway in mammalian cells .
	manualset3
84472	5	398227	5	NULL	NULL	0	NULL	bone morphogenetic protein ( BMP ) signaling pathway	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemojuvelin ( Hjv ) , a member of the repulsive-guidance molecule ( RGM ) family , upregulates transcription of the iron regulatory hormone hepcidin by activating the bone morphogenetic protein ( BMP ) signaling pathway in mammalian cells .
	manualset3
84473	6	398227	5	NULL	NULL	0	NULL	mammalian cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemojuvelin ( Hjv ) , a member of the repulsive-guidance molecule ( RGM ) family , upregulates transcription of the iron regulatory hormone hepcidin by activating the bone morphogenetic protein ( BMP ) signaling pathway in mammalian cells .
	manualset3
84474	1	398228	5	NULL	NULL	0	NULL	Hemolymph oxygen content	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemolymph oxygen content fell dramatically at 9 degrees C to values between 2 % and 12 % of ambient water O ( 2 ) content and had a maximum Po ( 2 ) of around 20 mmHg .
	manualset3
84475	2	398228	5	NULL	NULL	0	NULL	9 degrees C	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemolymph oxygen content fell dramatically at 9 degrees C to values between 2 % and 12 % of ambient water O ( 2 ) content and had a maximum Po ( 2 ) of around 20 mmHg .
	manualset3
84476	3	398228	5	NULL	NULL	0	NULL	values between 2 % and 12 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemolymph oxygen content fell dramatically at 9 degrees C to values between 2 % and 12 % of ambient water O ( 2 ) content and had a maximum Po ( 2 ) of around 20 mmHg .
	manualset3
84477	4	398228	5	NULL	NULL	0	NULL	ambient water O ( 2 ) content	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemolymph oxygen content fell dramatically at 9 degrees C to values between 2 % and 12 % of ambient water O ( 2 ) content and had a maximum Po ( 2 ) of around 20 mmHg .
	manualset3
84478	5	398228	5	NULL	NULL	0	NULL	maximum Po ( 2 )	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemolymph oxygen content fell dramatically at 9 degrees C to values between 2 % and 12 % of ambient water O ( 2 ) content and had a maximum Po ( 2 ) of around 20 mmHg .
	manualset3
84479	6	398228	5	NULL	NULL	0	NULL	20 mmHg	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemolymph oxygen content fell dramatically at 9 degrees C to values between 2 % and 12 % of ambient water O ( 2 ) content and had a maximum Po ( 2 ) of around 20 mmHg .
	manualset3
84480	1	398229	5	NULL	NULL	0	NULL	Hemolysis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemolysis , lipemia and icterus in specimens for arterial blood gas analysis .
	manualset3
84481	2	398229	5	NULL	NULL	0	NULL	lipemia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemolysis , lipemia and icterus in specimens for arterial blood gas analysis .
	manualset3
84482	3	398229	5	NULL	NULL	0	NULL	icterus	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemolysis , lipemia and icterus in specimens for arterial blood gas analysis .
	manualset3
84483	4	398229	5	NULL	NULL	NULL	NULL	specimens	Tissue												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hemolysis , lipemia and icterus in specimens for arterial blood gas analysis .
	manualset3
84484	5	398229	5	NULL	NULL	0	NULL	arterial blood gas analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemolysis , lipemia and icterus in specimens for arterial blood gas analysis .
	manualset3
84485	1	398230	5	NULL	NULL	0	NULL	Hemolysis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemolysis occurring after exposure to oxygen under high pressure .
	manualset3
84486	2	398230	5	NULL	NULL	0	NULL	exposure	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemolysis occurring after exposure to oxygen under high pressure .
	manualset3
84487	3	398230	5	NULL	NULL	0	NULL	oxygen	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemolysis occurring after exposure to oxygen under high pressure .
	manualset3
84488	4	398230	5	NULL	NULL	0	NULL	high pressure	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemolysis occurring after exposure to oxygen under high pressure .
	manualset3
84774	1	398231	5	NULL	NULL	0	NULL	Hemolytic activities	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemolytic activities in the central cornea were compared with hemolytic activities in the peripheral cornea for each of the following complement components : C1 , C4 , C2 , C3 , C5 , C6 , and C7 .
	manualset3
84775	2	398231	5	NULL	NULL	0	NULL	central cornea	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemolytic activities in the central cornea were compared with hemolytic activities in the peripheral cornea for each of the following complement components : C1 , C4 , C2 , C3 , C5 , C6 , and C7 .
	manualset3
84776	3	398231	5	NULL	NULL	0	NULL	hemolytic activities	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemolytic activities in the central cornea were compared with hemolytic activities in the peripheral cornea for each of the following complement components : C1 , C4 , C2 , C3 , C5 , C6 , and C7 .
	manualset3
84777	4	398231	5	NULL	NULL	0	NULL	peripheral cornea	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemolytic activities in the central cornea were compared with hemolytic activities in the peripheral cornea for each of the following complement components : C1 , C4 , C2 , C3 , C5 , C6 , and C7 .
	manualset3
84778	5	398231	5	NULL	NULL	NULL	NULL	complement components : C1 , C4 , C2 , C3 , C5 , C6 , and C7	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hemolytic activities in the central cornea were compared with hemolytic activities in the peripheral cornea for each of the following complement components : C1 , C4 , C2 , C3 , C5 , C6 , and C7 .
	manualset3
84779	1	398232	5	NULL	NULL	0	NULL	Hemophilia A ( HA )	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemophilia A ( HA ) is caused by mutation in factor VIII ( FVIII ) gene in humans ; it leads to inadequate synthesis of active protein .
	manualset3
84780	2	398232	5	NULL	NULL	0	NULL	mutation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemophilia A ( HA ) is caused by mutation in factor VIII ( FVIII ) gene in humans ; it leads to inadequate synthesis of active protein .
	manualset3
84781	3	398232	5	NULL	NULL	0	NULL	factor VIII ( FVIII ) gene	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemophilia A ( HA ) is caused by mutation in factor VIII ( FVIII ) gene in humans ; it leads to inadequate synthesis of active protein .
	manualset3
84782	4	398232	5	NULL	NULL	0	NULL	humans	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemophilia A ( HA ) is caused by mutation in factor VIII ( FVIII ) gene in humans ; it leads to inadequate synthesis of active protein .
	manualset3
84783	5	398232	5	NULL	NULL	0	NULL	inadequate synthesis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemophilia A ( HA ) is caused by mutation in factor VIII ( FVIII ) gene in humans ; it leads to inadequate synthesis of active protein .
	manualset3
84784	6	398232	5	NULL	NULL	0	NULL	active protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemophilia A ( HA ) is caused by mutation in factor VIII ( FVIII ) gene in humans ; it leads to inadequate synthesis of active protein .
	manualset3
84785	1	398233	5	NULL	NULL	0	NULL	autopsy case	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( An autopsy case of lung cancer accompanied by pneumoperitoneum ) .
	manualset3
84786	2	398233	5	NULL	NULL	0	NULL	lung cancer	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( An autopsy case of lung cancer accompanied by pneumoperitoneum ) .
	manualset3
84787	3	398233	5	NULL	NULL	0	NULL	pneumoperitoneum	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( An autopsy case of lung cancer accompanied by pneumoperitoneum ) .
	manualset3
84788	1	398234	5	NULL	NULL	0	NULL	Study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study of influenza infection in organ cultures of human embryonic trachea ) .
	manualset3
84789	2	398234	5	NULL	NULL	0	NULL	influenza infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study of influenza infection in organ cultures of human embryonic trachea ) .
	manualset3
84790	3	398234	5	NULL	NULL	0	NULL	organ cultures of human embryonic trachea	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study of influenza infection in organ cultures of human embryonic trachea ) .
	manualset3
84791	1	398235	5	NULL	NULL	0	NULL	Hemorrhage	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhage is not as severe as in patients with hemophilia A or B. Data are presented suggesting that hemorrhage may , in part , be associated with aspirin use .
	manualset3
84792	2	398235	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhage is not as severe as in patients with hemophilia A or B. Data are presented suggesting that hemorrhage may , in part , be associated with aspirin use .
	manualset3
84793	3	398235	5	NULL	NULL	0	NULL	hemophilia A or B	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhage is not as severe as in patients with hemophilia A or B. Data are presented suggesting that hemorrhage may , in part , be associated with aspirin use .
	manualset3
84794	4	398235	5	NULL	NULL	0	NULL	Data	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhage is not as severe as in patients with hemophilia A or B. Data are presented suggesting that hemorrhage may , in part , be associated with aspirin use .
	manualset3
84795	5	398235	5	NULL	NULL	0	NULL	hemorrhage	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhage is not as severe as in patients with hemophilia A or B. Data are presented suggesting that hemorrhage may , in part , be associated with aspirin use .
	manualset3
84796	6	398235	5	NULL	NULL	NULL	NULL	aspirin	Drug												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hemorrhage is not as severe as in patients with hemophilia A or B. Data are presented suggesting that hemorrhage may , in part , be associated with aspirin use .
	manualset3
84797	1	398236	5	NULL	NULL	0	NULL	Hemorrhagic complications	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhagic complications in patients treated with anticoagulant doses of a low molecular weight heparin ( enoxaparin ) in routine hospital practice .
	manualset3
84798	2	398236	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhagic complications in patients treated with anticoagulant doses of a low molecular weight heparin ( enoxaparin ) in routine hospital practice .
	manualset3
84799	3	398236	5	NULL	NULL	NULL	NULL	anticoagulant doses	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hemorrhagic complications in patients treated with anticoagulant doses of a low molecular weight heparin ( enoxaparin ) in routine hospital practice .
	manualset3
84800	5	398236	5	NULL	NULL	NULL	NULL	routine hospital practice	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hemorrhagic complications in patients treated with anticoagulant doses of a low molecular weight heparin ( enoxaparin ) in routine hospital practice .
	manualset3
84801	4	398236	5	NULL	NULL	0	NULL	low molecular weight heparin ( enoxaparin )	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhagic complications in patients treated with anticoagulant doses of a low molecular weight heparin ( enoxaparin ) in routine hospital practice .
	manualset3
84802	1	398237	5	NULL	NULL	0	NULL	Hemorrhagic cystitis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhagic cystitis can occur 6 months to 10 years after pelvic irradiation .
	manualset3
84803	2	398237	5	NULL	NULL	0	NULL	6 months to 10 years	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhagic cystitis can occur 6 months to 10 years after pelvic irradiation .
	manualset3
84804	3	398237	5	NULL	NULL	0	NULL	pelvic irradiation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhagic cystitis can occur 6 months to 10 years after pelvic irradiation .
	manualset3
84805	1	398238	5	NULL	NULL	0	NULL	Hemorrhagic lumbar synovial facet cyst	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhagic lumbar synovial facet cyst secondary to anticoagulation therapy .
	manualset3
84806	2	398238	5	NULL	NULL	0	NULL	anticoagulation therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhagic lumbar synovial facet cyst secondary to anticoagulation therapy .
	manualset3
84807	1	398239	5	NULL	NULL	0	NULL	Hemorrhagic shock	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhagic shock renders patients susceptible to the development of acute lung injury in response to a second inflammatory stimulus by as yet unclear mechanisms .
	manualset3
84808	2	398239	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhagic shock renders patients susceptible to the development of acute lung injury in response to a second inflammatory stimulus by as yet unclear mechanisms .
	manualset3
84809	3	398239	5	NULL	NULL	0	NULL	development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhagic shock renders patients susceptible to the development of acute lung injury in response to a second inflammatory stimulus by as yet unclear mechanisms .
	manualset3
84810	4	398239	5	NULL	NULL	0	NULL	acute lung injury	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhagic shock renders patients susceptible to the development of acute lung injury in response to a second inflammatory stimulus by as yet unclear mechanisms .
	manualset3
84811	5	398239	5	NULL	NULL	0	NULL	response	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhagic shock renders patients susceptible to the development of acute lung injury in response to a second inflammatory stimulus by as yet unclear mechanisms .
	manualset3
84812	6	398239	5	NULL	NULL	0	NULL	second inflammatory stimulus	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhagic shock renders patients susceptible to the development of acute lung injury in response to a second inflammatory stimulus by as yet unclear mechanisms .
	manualset3
84813	7	398239	5	NULL	NULL	0	NULL	unclear mechanisms	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hemorrhagic shock renders patients susceptible to the development of acute lung injury in response to a second inflammatory stimulus by as yet unclear mechanisms .
	manualset3
84814	1	398240	5	NULL	NULL	0	NULL	EFhd2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , EFhd2 regulates the BCR-elicited calcium flux through a calcium-dependent positive feedback mechanism in WEHI231 cells .
	manualset3
84815	2	398240	5	NULL	NULL	0	NULL	BCR-elicited calcium flux	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , EFhd2 regulates the BCR-elicited calcium flux through a calcium-dependent positive feedback mechanism in WEHI231 cells .
	manualset3
84816	3	398240	5	NULL	NULL	0	NULL	calcium-dependent positive feedback mechanism	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , EFhd2 regulates the BCR-elicited calcium flux through a calcium-dependent positive feedback mechanism in WEHI231 cells .
	manualset3
84817	4	398240	5	NULL	NULL	0	NULL	WEHI231 cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , EFhd2 regulates the BCR-elicited calcium flux through a calcium-dependent positive feedback mechanism in WEHI231 cells .
	manualset3
84818	1	398241	5	NULL	NULL	NULL	NULL	TRAIL-agonist compounds	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hence , TRAIL-agonist compounds have the potential of being excellent cancer therapeutic agents with minimal cytotoxicity .
	manualset3
84819	2	398241	5	NULL	NULL	NULL	NULL	excellent cancer therapeutic agents	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hence , TRAIL-agonist compounds have the potential of being excellent cancer therapeutic agents with minimal cytotoxicity .
	manualset3
84820	3	398241	5	NULL	NULL	0	NULL	minimal cytotoxicity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , TRAIL-agonist compounds have the potential of being excellent cancer therapeutic agents with minimal cytotoxicity .
	manualset3
84821	1	398242	5	NULL	NULL	NULL	NULL	compounds	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hence , compounds that bind phosphorus in the bowel are often necessary .
	manualset3
84822	2	398242	5	NULL	NULL	0	NULL	bind	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , compounds that bind phosphorus in the bowel are often necessary .
	manualset3
84823	3	398242	5	NULL	NULL	0	NULL	phosphorus	Atom												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , compounds that bind phosphorus in the bowel are often necessary .
	manualset3
84824	4	398242	5	NULL	NULL	0	NULL	bowel	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , compounds that bind phosphorus in the bowel are often necessary .
	manualset3
84825	1	398243	5	NULL	NULL	0	NULL	Study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study of the factors responsible for the etiology of pressure sores ) .
	manualset3
84826	2	398243	5	NULL	NULL	0	NULL	 factors	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study of the factors responsible for the etiology of pressure sores ) .
	manualset3
84827	3	398243	5	NULL	NULL	0	NULL	etiology	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study of the factors responsible for the etiology of pressure sores ) .
	manualset3
84828	4	398243	5	NULL	NULL	0	NULL	pressure sores	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study of the factors responsible for the etiology of pressure sores ) .
	manualset3
84829	1	398244	5	NULL	NULL	0	NULL	inadequate sleep	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , inadequate sleep is associated with development of obesity .
	manualset3
84830	2	398244	5	NULL	NULL	0	NULL	development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , inadequate sleep is associated with development of obesity .
	manualset3
84831	3	398244	5	NULL	NULL	0	NULL	obesity	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , inadequate sleep is associated with development of obesity .
	manualset3
84832	1	398245	5	NULL	NULL	0	NULL	suppression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , suppression of glial proinflammatory responses can significantly reduce opioid withdrawal , while improving analgesia .
	manualset3
84833	2	398245	5	NULL	NULL	0	NULL	glial proinflammatory responses	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , suppression of glial proinflammatory responses can significantly reduce opioid withdrawal , while improving analgesia .
	manualset3
84834	3	398245	5	NULL	NULL	NULL	NULL	opioid withdrawal	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hence , suppression of glial proinflammatory responses can significantly reduce opioid withdrawal , while improving analgesia .
	manualset3
84835	4	398245	5	NULL	NULL	NULL	NULL	analgesia	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hence , suppression of glial proinflammatory responses can significantly reduce opioid withdrawal , while improving analgesia .
	manualset3
84836	1	398246	5	NULL	NULL	0	NULL	 low-affinity A2A agonists CVT-3146 and CVT-3033	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , the low-affinity A2A agonists CVT-3146 and CVT-3033 may prove to be superior to currently available high-affinity agonists as coronary vasodilators during myocardial imaging with radionuclide agents .
	manualset3
84837	2	398246	5	NULL	NULL	0	NULL	currently available high-affinity agonists	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , the low-affinity A2A agonists CVT-3146 and CVT-3033 may prove to be superior to currently available high-affinity agonists as coronary vasodilators during myocardial imaging with radionuclide agents .
	manualset3
84838	3	398246	5	NULL	NULL	0	NULL	coronary vasodilators	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , the low-affinity A2A agonists CVT-3146 and CVT-3033 may prove to be superior to currently available high-affinity agonists as coronary vasodilators during myocardial imaging with radionuclide agents .
	manualset3
84839	4	398246	5	NULL	NULL	0	NULL	myocardial imaging	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , the low-affinity A2A agonists CVT-3146 and CVT-3033 may prove to be superior to currently available high-affinity agonists as coronary vasodilators during myocardial imaging with radionuclide agents .
	manualset3
84840	5	398246	5	NULL	NULL	0	NULL	radionuclide agents	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , the low-affinity A2A agonists CVT-3146 and CVT-3033 may prove to be superior to currently available high-affinity agonists as coronary vasodilators during myocardial imaging with radionuclide agents .
	manualset3
84841	1	398247	5	NULL	NULL	0	NULL	senile myoclonic epilepsy of Genton	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , the senile myoclonic epilepsy of Genton is an easily recognizable newer epileptic syndrome of the older Down syndrome patient .
	manualset3
84842	2	398247	5	NULL	NULL	0	NULL	epileptic syndrome	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , the senile myoclonic epilepsy of Genton is an easily recognizable newer epileptic syndrome of the older Down syndrome patient .
	manualset3
84843	3	398247	5	NULL	NULL	0	NULL	older Down syndrome patient	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , the senile myoclonic epilepsy of Genton is an easily recognizable newer epileptic syndrome of the older Down syndrome patient .
	manualset3
84844	1	398248	5	NULL	NULL	NULL	NULL	warfarin	Drug												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hence , warfarin is significantly underused in clinical practice , with only half of warfarin-treated patients actually achieving therapeutic anticoagulation in routine clinical practice .
	manualset3
84845	2	398248	5	NULL	NULL	0	NULL	clinical practice	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , warfarin is significantly underused in clinical practice , with only half of warfarin-treated patients actually achieving therapeutic anticoagulation in routine clinical practice .
	manualset3
84846	3	398248	5	NULL	NULL	0	NULL	warfarin-treated patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , warfarin is significantly underused in clinical practice , with only half of warfarin-treated patients actually achieving therapeutic anticoagulation in routine clinical practice .
	manualset3
84847	4	398248	5	NULL	NULL	0	NULL	therapeutic anticoagulation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , warfarin is significantly underused in clinical practice , with only half of warfarin-treated patients actually achieving therapeutic anticoagulation in routine clinical practice .
	manualset3
84848	5	398248	5	NULL	NULL	0	NULL	routine clinical practice	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hence , warfarin is significantly underused in clinical practice , with only half of warfarin-treated patients actually achieving therapeutic anticoagulation in routine clinical practice .
	manualset3
84849	1	398249	5	NULL	NULL	0	NULL	Heparin affinity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin affinity of factor VIIa : implications on the physiological inhibition by antithrombin and clearance of recombinant factor VIIa .
	manualset3
84850	2	398249	5	NULL	NULL	0	NULL	factor VIIa	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin affinity of factor VIIa : implications on the physiological inhibition by antithrombin and clearance of recombinant factor VIIa .
	manualset3
84851	3	398249	5	NULL	NULL	0	NULL	implications	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin affinity of factor VIIa : implications on the physiological inhibition by antithrombin and clearance of recombinant factor VIIa .
	manualset3
84852	4	398249	5	NULL	NULL	0	NULL	physiological inhibition	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin affinity of factor VIIa : implications on the physiological inhibition by antithrombin and clearance of recombinant factor VIIa .
	manualset3
84853	5	398249	5	NULL	NULL	0	NULL	antithrombin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin affinity of factor VIIa : implications on the physiological inhibition by antithrombin and clearance of recombinant factor VIIa .
	manualset3
84854	6	398249	5	NULL	NULL	0	NULL	clearance	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin affinity of factor VIIa : implications on the physiological inhibition by antithrombin and clearance of recombinant factor VIIa .
	manualset3
84855	7	398249	5	NULL	NULL	0	NULL	recombinant factor VIIa	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin affinity of factor VIIa : implications on the physiological inhibition by antithrombin and clearance of recombinant factor VIIa .
	manualset3
84856	1	398250	5	NULL	NULL	0	NULL	Heparin	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin and nitric oxide ( NO ) attenuate changes to the pulmonary vasculature caused by prolonged hypoxia .
	manualset3
84857	2	398250	5	NULL	NULL	0	NULL	nitric oxide ( NO )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin and nitric oxide ( NO ) attenuate changes to the pulmonary vasculature caused by prolonged hypoxia .
	manualset3
84858	3	398250	5	NULL	NULL	0	NULL	pulmonary vasculature	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin and nitric oxide ( NO ) attenuate changes to the pulmonary vasculature caused by prolonged hypoxia .
	manualset3
84859	4	398250	5	NULL	NULL	0	NULL	prolonged hypoxia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin and nitric oxide ( NO ) attenuate changes to the pulmonary vasculature caused by prolonged hypoxia .
	manualset3
84860	1	398251	5	NULL	NULL	NULL	NULL	Heparin and suramin treatment	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Heparin and suramin treatment of these advanced embryos ( stage 4 ) revealed a dose-dependent inhibition on the regression of Hensen 's node and formation of mesodermal derivatives such as somites .
	manualset3
84861	2	398251	5	NULL	NULL	0	NULL	advanced embryos ( stage 4 )	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin and suramin treatment of these advanced embryos ( stage 4 ) revealed a dose-dependent inhibition on the regression of Hensen 's node and formation of mesodermal derivatives such as somites .
	manualset3
84862	3	398251	5	NULL	NULL	0	NULL	dose-dependent inhibition	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin and suramin treatment of these advanced embryos ( stage 4 ) revealed a dose-dependent inhibition on the regression of Hensen 's node and formation of mesodermal derivatives such as somites .
	manualset3
84863	4	398251	5	NULL	NULL	0	NULL	regression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin and suramin treatment of these advanced embryos ( stage 4 ) revealed a dose-dependent inhibition on the regression of Hensen 's node and formation of mesodermal derivatives such as somites .
	manualset3
84864	5	398251	5	NULL	NULL	0	NULL	Hensen 's node	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin and suramin treatment of these advanced embryos ( stage 4 ) revealed a dose-dependent inhibition on the regression of Hensen 's node and formation of mesodermal derivatives such as somites .
	manualset3
84865	6	398251	5	NULL	NULL	0	NULL	formation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin and suramin treatment of these advanced embryos ( stage 4 ) revealed a dose-dependent inhibition on the regression of Hensen 's node and formation of mesodermal derivatives such as somites .
	manualset3
84866	7	398251	5	NULL	NULL	NULL	NULL	mesodermal derivatives	AnatomicalPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Heparin and suramin treatment of these advanced embryos ( stage 4 ) revealed a dose-dependent inhibition on the regression of Hensen 's node and formation of mesodermal derivatives such as somites .
	manualset3
85498	8	398251	5	NULL	NULL	0	NULL	somites	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin and suramin treatment of these advanced embryos ( stage 4 ) revealed a dose-dependent inhibition on the regression of Hensen 's node and formation of mesodermal derivatives such as somites .
	manualset3
84867	1	398252	5	NULL	NULL	NULL	NULL	Heparin	Drug												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Heparin as an anti-inflammatory agent : it 's no GAG to forget about chemokines .
	manualset3
84868	2	398252	5	NULL	NULL	NULL	NULL	anti-inflammatory agent	Drug												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Heparin as an anti-inflammatory agent : it 's no GAG to forget about chemokines .
	manualset3
84869	3	398252	5	NULL	NULL	0	NULL	GAG	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin as an anti-inflammatory agent : it 's no GAG to forget about chemokines .
	manualset3
84870	4	398252	5	NULL	NULL	0	NULL	chemokines	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin as an anti-inflammatory agent : it 's no GAG to forget about chemokines .
	manualset3
84871	1	398253	5	NULL	NULL	0	NULL	 LDL receptors	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study on LDL receptors of liver non-parenchymal cells in hypertriglyceridemic rats induced by high carbohydrate diet ) .
	manualset3
84872	2	398253	5	NULL	NULL	0	NULL	liver non-parenchymal cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study on LDL receptors of liver non-parenchymal cells in hypertriglyceridemic rats induced by high carbohydrate diet ) .
	manualset3
84873	3	398253	5	NULL	NULL	0	NULL	hypertriglyceridemic rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study on LDL receptors of liver non-parenchymal cells in hypertriglyceridemic rats induced by high carbohydrate diet ) .
	manualset3
84874	4	398253	5	NULL	NULL	0	NULL	high carbohydrate diet	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study on LDL receptors of liver non-parenchymal cells in hypertriglyceridemic rats induced by high carbohydrate diet ) .
	manualset3
84875	1	398254	5	NULL	NULL	0	NULL	Heparin	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin inhibits the HDLp binding , indicating that positively charged groups are involved in the HDLp-fat body interaction .
	manualset3
84923	2	398254	5	NULL	NULL	0	NULL	HDLp	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin inhibits the HDLp binding , indicating that positively charged groups are involved in the HDLp-fat body interaction .
	manualset3
84924	3	398254	5	NULL	NULL	0	NULL	positively charged groups	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin inhibits the HDLp binding , indicating that positively charged groups are involved in the HDLp-fat body interaction .
	manualset3
84925	4	398254	5	NULL	NULL	0	NULL	HDLp-fat body interaction	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin inhibits the HDLp binding , indicating that positively charged groups are involved in the HDLp-fat body interaction .
	manualset3
84926	1	398255	5	NULL	NULL	0	NULL	Heparin levels	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin levels may be used as an alternative for heparin monitoring but plasma levels of argatroban are not commercially available .
	manualset3
84927	2	398255	5	NULL	NULL	0	NULL	heparin	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin levels may be used as an alternative for heparin monitoring but plasma levels of argatroban are not commercially available .
	manualset3
84928	3	398255	5	NULL	NULL	0	NULL	plasma levels	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin levels may be used as an alternative for heparin monitoring but plasma levels of argatroban are not commercially available .
	manualset3
84929	4	398255	5	NULL	NULL	0	NULL	argatroban	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Heparin levels may be used as an alternative for heparin monitoring but plasma levels of argatroban are not commercially available .
	manualset3
84930	1	398256	5	NULL	NULL	0	NULL	Hepatic Cd accumulation	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatic Cd accumulation was linked to decreased cco-1 and sod-1 gene expression , whereas Cu accumulation was associated with a decrease in CCO enzymatic activity and an increase in total protein concentration and in cco-1 , mts and hsp-70 gene expression levels .
	manualset3
84931	2	398256	5	NULL	NULL	0	NULL	decreased cco-1 and sod-1 gene expression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatic Cd accumulation was linked to decreased cco-1 and sod-1 gene expression , whereas Cu accumulation was associated with a decrease in CCO enzymatic activity and an increase in total protein concentration and in cco-1 , mts and hsp-70 gene expression levels .
	manualset3
84932	3	398256	5	NULL	NULL	NULL	NULL	Cu accumulation	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hepatic Cd accumulation was linked to decreased cco-1 and sod-1 gene expression , whereas Cu accumulation was associated with a decrease in CCO enzymatic activity and an increase in total protein concentration and in cco-1 , mts and hsp-70 gene expression levels .
	manualset3
84933	4	398256	5	NULL	NULL	0	NULL	CCO enzymatic activity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatic Cd accumulation was linked to decreased cco-1 and sod-1 gene expression , whereas Cu accumulation was associated with a decrease in CCO enzymatic activity and an increase in total protein concentration and in cco-1 , mts and hsp-70 gene expression levels .
	manualset3
84934	5	398256	5	NULL	NULL	0	NULL	total protein concentration	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatic Cd accumulation was linked to decreased cco-1 and sod-1 gene expression , whereas Cu accumulation was associated with a decrease in CCO enzymatic activity and an increase in total protein concentration and in cco-1 , mts and hsp-70 gene expression levels .
	manualset3
84935	6	398256	5	NULL	NULL	0	NULL	cco-1 , mts and hsp-70 gene expression levels	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatic Cd accumulation was linked to decreased cco-1 and sod-1 gene expression , whereas Cu accumulation was associated with a decrease in CCO enzymatic activity and an increase in total protein concentration and in cco-1 , mts and hsp-70 gene expression levels .
	manualset3
84936	1	398257	5	NULL	NULL	0	NULL	Hepatic abscess	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatic abscess presenting as severe fatigue and anemia .
	manualset3
84937	2	398257	5	NULL	NULL	0	NULL	severe fatigue	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatic abscess presenting as severe fatigue and anemia .
	manualset3
84938	3	398257	5	NULL	NULL	0	NULL	anemia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatic abscess presenting as severe fatigue and anemia .
	manualset3
84939	1	398258	5	NULL	NULL	0	NULL	Hepatic iron loading	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatic iron loading in patients with compound heterozygous HFE mutations .
	manualset3
84940	2	398258	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatic iron loading in patients with compound heterozygous HFE mutations .
	manualset3
84941	3	398258	5	NULL	NULL	0	NULL	compound heterozygous HFE mutations	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatic iron loading in patients with compound heterozygous HFE mutations .
	manualset3
84942	1	398259	5	NULL	NULL	0	NULL	Hepatic lesions	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatic lesions and bacterial changes in mice during infection of Fusobacterium necrophorum .
	manualset3
84943	2	398259	5	NULL	NULL	0	NULL	bacterial changes	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatic lesions and bacterial changes in mice during infection of Fusobacterium necrophorum .
	manualset3
84944	3	398259	5	NULL	NULL	0	NULL	mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatic lesions and bacterial changes in mice during infection of Fusobacterium necrophorum .
	manualset3
84945	4	398259	5	NULL	NULL	NULL	NULL	infection	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hepatic lesions and bacterial changes in mice during infection of Fusobacterium necrophorum .
	manualset3
84946	5	398259	5	NULL	NULL	0	NULL	Fusobacterium necrophorum	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatic lesions and bacterial changes in mice during infection of Fusobacterium necrophorum .
	manualset3
84947	1	398260	5	NULL	NULL	0	NULL	Study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study on linkage between polymorphism of interleukin 6 gene -572 C/G and susceptibility to myocardial infarction ) .
	manualset3
84948	2	398260	5	NULL	NULL	0	NULL	linkage	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study on linkage between polymorphism of interleukin 6 gene -572 C/G and susceptibility to myocardial infarction ) .
	manualset3
84949	3	398260	5	NULL	NULL	0	NULL	polymorphism	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study on linkage between polymorphism of interleukin 6 gene -572 C/G and susceptibility to myocardial infarction ) .
	manualset3
84950	4	398260	5	NULL	NULL	0	NULL	interleukin 6 gene -572 C/G	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study on linkage between polymorphism of interleukin 6 gene -572 C/G and susceptibility to myocardial infarction ) .
	manualset3
84951	5	398260	5	NULL	NULL	0	NULL	susceptibility	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study on linkage between polymorphism of interleukin 6 gene -572 C/G and susceptibility to myocardial infarction ) .
	manualset3
84952	6	398260	5	NULL	NULL	0	NULL	myocardial infarction	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Study on linkage between polymorphism of interleukin 6 gene -572 C/G and susceptibility to myocardial infarction ) .
	manualset3
84953	1	398261	5	NULL	NULL	0	NULL	Hepatic stellate cells ( HpSTCs )	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatic stellate cells ( HpSTCs ) are major regulators of hepatic fibrogenesis in adults .
	manualset3
84954	2	398261	5	NULL	NULL	0	NULL	major regulators	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatic stellate cells ( HpSTCs ) are major regulators of hepatic fibrogenesis in adults .
	manualset3
84955	3	398261	5	NULL	NULL	0	NULL	hepatic fibrogenesis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatic stellate cells ( HpSTCs ) are major regulators of hepatic fibrogenesis in adults .
	manualset3
84956	4	398261	5	NULL	NULL	0	NULL	adults	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatic stellate cells ( HpSTCs ) are major regulators of hepatic fibrogenesis in adults .
	manualset3
84957	1	398262	5	NULL	NULL	0	NULL	Hepatitis B virus ( HBV ) infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatitis B virus ( HBV ) infection , one of the major health priorities , accounts approximately for 350 million chronic cases and a global total of 33 million people were living with human immunodeficiency virus ( HIV ) in the world.Co-infection with HIV and the HBV presents a significant challenge to health care providers , with different prevalence rates in different parts of the world .
	manualset3
84958	3	398262	5	NULL	NULL	NULL	NULL	350 million chronic cases	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hepatitis B virus ( HBV ) infection , one of the major health priorities , accounts approximately for 350 million chronic cases and a global total of 33 million people were living with human immunodeficiency virus ( HIV ) in the world.Co-infection with HIV and the HBV presents a significant challenge to health care providers , with different prevalence rates in different parts of the world .
	manualset3
84959	4	398262	5	NULL	NULL	NULL	NULL	33 million people	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hepatitis B virus ( HBV ) infection , one of the major health priorities , accounts approximately for 350 million chronic cases and a global total of 33 million people were living with human immunodeficiency virus ( HIV ) in the world.Co-infection with HIV and the HBV presents a significant challenge to health care providers , with different prevalence rates in different parts of the world .
	manualset3
84960	5	398262	5	NULL	NULL	NULL	NULL	human immunodeficiency virus ( HIV )	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hepatitis B virus ( HBV ) infection , one of the major health priorities , accounts approximately for 350 million chronic cases and a global total of 33 million people were living with human immunodeficiency virus ( HIV ) in the world.Co-infection with HIV and the HBV presents a significant challenge to health care providers , with different prevalence rates in different parts of the world .
	manualset3
84961	6	398262	5	NULL	NULL	NULL	NULL	world	UnproperNamedGeographicalLocation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hepatitis B virus ( HBV ) infection , one of the major health priorities , accounts approximately for 350 million chronic cases and a global total of 33 million people were living with human immunodeficiency virus ( HIV ) in the world.Co-infection with HIV and the HBV presents a significant challenge to health care providers , with different prevalence rates in different parts of the world .
	manualset3
84962	7	398262	5	NULL	NULL	NULL	NULL	Co-infection with HIV and the HBV	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hepatitis B virus ( HBV ) infection , one of the major health priorities , accounts approximately for 350 million chronic cases and a global total of 33 million people were living with human immunodeficiency virus ( HIV ) in the world.Co-infection with HIV and the HBV presents a significant challenge to health care providers , with different prevalence rates in different parts of the world .
	manualset3
84965	8	398262	5	NULL	NULL	NULL	NULL	health care providers	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hepatitis B virus ( HBV ) infection , one of the major health priorities , accounts approximately for 350 million chronic cases and a global total of 33 million people were living with human immunodeficiency virus ( HIV ) in the world.Co-infection with HIV and the HBV presents a significant challenge to health care providers , with different prevalence rates in different parts of the world .
	manualset3
84967	9	398262	5	NULL	NULL	NULL	NULL	different parts of the world	UnproperNamedGeographicalLocation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hepatitis B virus ( HBV ) infection , one of the major health priorities , accounts approximately for 350 million chronic cases and a global total of 33 million people were living with human immunodeficiency virus ( HIV ) in the world.Co-infection with HIV and the HBV presents a significant challenge to health care providers , with different prevalence rates in different parts of the world .
	manualset3
85433	2	398262	5	NULL	NULL	0	NULL	major health priorities	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatitis B virus ( HBV ) infection , one of the major health priorities , accounts approximately for 350 million chronic cases and a global total of 33 million people were living with human immunodeficiency virus ( HIV ) in the world.Co-infection with HIV and the HBV presents a significant challenge to health care providers , with different prevalence rates in different parts of the world .
	manualset3
84969	1	398263	5	NULL	NULL	0	NULL	Hepatitis B virus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatitis B virus alters the antioxidant system in transgenic mice and sensitizes hepatocytes to Fas signaling .
	manualset3
84970	2	398263	5	NULL	NULL	0	NULL	antioxidant system	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatitis B virus alters the antioxidant system in transgenic mice and sensitizes hepatocytes to Fas signaling .
	manualset3
84971	3	398263	5	NULL	NULL	0	NULL	transgenic mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatitis B virus alters the antioxidant system in transgenic mice and sensitizes hepatocytes to Fas signaling .
	manualset3
84972	4	398263	5	NULL	NULL	0	NULL	hepatocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatitis B virus alters the antioxidant system in transgenic mice and sensitizes hepatocytes to Fas signaling .
	manualset3
84973	5	398263	5	NULL	NULL	0	NULL	Fas signaling	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatitis B virus alters the antioxidant system in transgenic mice and sensitizes hepatocytes to Fas signaling .
	manualset3
84974	1	398264	5	NULL	NULL	NULL	NULL	Hepatitis C prevalence	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hepatitis C prevalence and needle/syringe sharing behaviors in recent onset injecting drug users .
	manualset3
84975	2	398264	5	NULL	NULL	0	NULL	needle/syringe sharing behaviors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatitis C prevalence and needle/syringe sharing behaviors in recent onset injecting drug users .
	manualset3
84976	3	398264	5	NULL	NULL	0	NULL	drug users	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatitis C prevalence and needle/syringe sharing behaviors in recent onset injecting drug users .
	manualset3
84977	1	398265	5	NULL	NULL	0	NULL	Hepatitis C virus ( HCV )	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatitis C virus ( HCV ) has a high propensity for persistence .
	manualset3
84978	2	398265	5	NULL	NULL	0	NULL	high propensity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatitis C virus ( HCV ) has a high propensity for persistence .
	manualset3
84979	3	398265	5	NULL	NULL	0	NULL	persistence 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatitis C virus ( HCV ) has a high propensity for persistence .
	manualset3
84980	1	398266	5	NULL	NULL	0	NULL	Hepatoblastoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatoblastoma , thrombocytosis , and increased thrombopoietin .
	manualset3
84981	2	398266	5	NULL	NULL	0	NULL	thrombocytosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatoblastoma , thrombocytosis , and increased thrombopoietin .
	manualset3
84982	3	398266	5	NULL	NULL	0	NULL	increased thrombopoietin	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatoblastoma , thrombocytosis , and increased thrombopoietin .
	manualset3
84983	1	398267	5	NULL	NULL	0	NULL	Hepatocellular necrosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocellular necrosis , fibrosis and microsomal activity determine the hepatic pharmacokinetics of basic drugs in right-heart-failure-induced liver damage .
	manualset3
84984	2	398267	5	NULL	NULL	0	NULL	fibrosis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocellular necrosis , fibrosis and microsomal activity determine the hepatic pharmacokinetics of basic drugs in right-heart-failure-induced liver damage .
	manualset3
84985	3	398267	5	NULL	NULL	0	NULL	microsomal activity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocellular necrosis , fibrosis and microsomal activity determine the hepatic pharmacokinetics of basic drugs in right-heart-failure-induced liver damage .
	manualset3
84986	4	398267	5	NULL	NULL	0	NULL	hepatic pharmacokinetics	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocellular necrosis , fibrosis and microsomal activity determine the hepatic pharmacokinetics of basic drugs in right-heart-failure-induced liver damage .
	manualset3
84987	5	398267	5	NULL	NULL	NULL	NULL	basic drugs	Drug												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hepatocellular necrosis , fibrosis and microsomal activity determine the hepatic pharmacokinetics of basic drugs in right-heart-failure-induced liver damage .
	manualset3
84988	6	398267	5	NULL	NULL	0	NULL	right-heart-failure-induced liver damage	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocellular necrosis , fibrosis and microsomal activity determine the hepatic pharmacokinetics of basic drugs in right-heart-failure-induced liver damage .
	manualset3
84989	1	398268	5	NULL	NULL	0	NULL	Hepatocyte-specific knockout	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocyte-specific knockout of - catenin inhibited CAR agonists-induced hepatocyte proliferation in male mice .
	manualset3
84990	2	398268	5	NULL	NULL	0	NULL	catenin	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocyte-specific knockout of - catenin inhibited CAR agonists-induced hepatocyte proliferation in male mice .
	manualset3
84991	3	398268	5	NULL	NULL	0	NULL	CAR agonists-induced hepatocyte proliferation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocyte-specific knockout of - catenin inhibited CAR agonists-induced hepatocyte proliferation in male mice .
	manualset3
84992	4	398268	5	NULL	NULL	0	NULL	male mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocyte-specific knockout of - catenin inhibited CAR agonists-induced hepatocyte proliferation in male mice .
	manualset3
84993	1	398269	5	NULL	NULL	0	NULL	Hepatocyte nuclear factor 4 alpha ( HNF4 alpha )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocyte nuclear factor 4 alpha ( HNF4 alpha ) is a member of the nuclear receptor superfamily and is expressed in several endodermal tissues .
	manualset3
84994	2	398269	5	NULL	NULL	0	NULL	nuclear receptor superfamily	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocyte nuclear factor 4 alpha ( HNF4 alpha ) is a member of the nuclear receptor superfamily and is expressed in several endodermal tissues .
	manualset3
84995	3	398269	5	NULL	NULL	0	NULL	endodermal tissues	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocyte nuclear factor 4 alpha ( HNF4 alpha ) is a member of the nuclear receptor superfamily and is expressed in several endodermal tissues .
	manualset3
84996	1	398270	5	NULL	NULL	0	NULL	Hepatocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocytes derived from embryonic stem cells ( ESCs ) are expected to be useful for basic research and clinical applications .
	manualset3
84997	2	398270	5	NULL	NULL	0	NULL	embryonic stem cells ( ESCs )	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocytes derived from embryonic stem cells ( ESCs ) are expected to be useful for basic research and clinical applications .
	manualset3
84998	3	398270	5	NULL	NULL	0	NULL	basic research	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocytes derived from embryonic stem cells ( ESCs ) are expected to be useful for basic research and clinical applications .
	manualset3
84999	4	398270	5	NULL	NULL	0	NULL	clinical applications	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocytes derived from embryonic stem cells ( ESCs ) are expected to be useful for basic research and clinical applications .
	manualset3
85000	1	398271	5	NULL	NULL	0	NULL	Hepatocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocytes obtained from ( RHA ) Wistar rats by collagenase perfusion were seeded onto non-woven filamentous sheets of polyglycolic acid 1 x 3 cm in size and 2 mm thickness to a density of 500 , 000 cells/cm2 .
	manualset3
85001	2	398271	5	NULL	NULL	0	NULL	( RHA ) Wistar rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocytes obtained from ( RHA ) Wistar rats by collagenase perfusion were seeded onto non-woven filamentous sheets of polyglycolic acid 1 x 3 cm in size and 2 mm thickness to a density of 500 , 000 cells/cm2 .
	manualset3
85002	3	398271	5	NULL	NULL	0	NULL	collagenase perfusion	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocytes obtained from ( RHA ) Wistar rats by collagenase perfusion were seeded onto non-woven filamentous sheets of polyglycolic acid 1 x 3 cm in size and 2 mm thickness to a density of 500 , 000 cells/cm2 .
	manualset3
85003	4	398271	5	NULL	NULL	0	NULL	non-woven filamentous sheets	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocytes obtained from ( RHA ) Wistar rats by collagenase perfusion were seeded onto non-woven filamentous sheets of polyglycolic acid 1 x 3 cm in size and 2 mm thickness to a density of 500 , 000 cells/cm2 .
	manualset3
85004	5	398271	5	NULL	NULL	0	NULL	polyglycolic acid	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatocytes obtained from ( RHA ) Wistar rats by collagenase perfusion were seeded onto non-woven filamentous sheets of polyglycolic acid 1 x 3 cm in size and 2 mm thickness to a density of 500 , 000 cells/cm2 .
	manualset3
85005	6	398271	5	NULL	NULL	NULL	NULL	1 x 3 cm in size	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hepatocytes obtained from ( RHA ) Wistar rats by collagenase perfusion were seeded onto non-woven filamentous sheets of polyglycolic acid 1 x 3 cm in size and 2 mm thickness to a density of 500 , 000 cells/cm2 .
	manualset3
85006	7	398271	5	NULL	NULL	NULL	NULL	2 mm thickness	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hepatocytes obtained from ( RHA ) Wistar rats by collagenase perfusion were seeded onto non-woven filamentous sheets of polyglycolic acid 1 x 3 cm in size and 2 mm thickness to a density of 500 , 000 cells/cm2 .
	manualset3
85007	8	398271	5	NULL	NULL	NULL	NULL	density of 500 , 000 cells/cm2	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hepatocytes obtained from ( RHA ) Wistar rats by collagenase perfusion were seeded onto non-woven filamentous sheets of polyglycolic acid 1 x 3 cm in size and 2 mm thickness to a density of 500 , 000 cells/cm2 .
	manualset3
85008	1	398272	5	NULL	NULL	0	NULL	Hepatoma cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatoma cells were infected with AdB17 or AdB17-beta with AdLacZ , an adenovirus expressing beta-galactosidase , as a control .
	manualset3
85412	2	398272	5	NULL	NULL	NULL	NULL	AdB17	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hepatoma cells were infected with AdB17 or AdB17-beta with AdLacZ , an adenovirus expressing beta-galactosidase , as a control .
	manualset3
85413	3	398272	5	NULL	NULL	0	NULL	AdB17-beta with AdLacZ	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatoma cells were infected with AdB17 or AdB17-beta with AdLacZ , an adenovirus expressing beta-galactosidase , as a control .
	manualset3
85414	4	398272	5	NULL	NULL	0	NULL	adenovirus expressing beta-galactosidase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatoma cells were infected with AdB17 or AdB17-beta with AdLacZ , an adenovirus expressing beta-galactosidase , as a control .
	manualset3
85415	5	398272	5	NULL	NULL	NULL	NULL	control	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hepatoma cells were infected with AdB17 or AdB17-beta with AdLacZ , an adenovirus expressing beta-galactosidase , as a control .
	manualset3
85162	1	398273	5	NULL	NULL	0	NULL	Hepatoregenerative role	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatoregenerative role of bone morphogenetic protein-9 .
	manualset3
85163	2	398273	5	NULL	NULL	0	NULL	bone morphogenetic protein-9	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatoregenerative role of bone morphogenetic protein-9 .
	manualset3
85164	1	398274	5	NULL	NULL	0	NULL	Hepatosplanchnic blood flow control	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatosplanchnic blood flow control and oxygen extraction are modified by the underlying mechanism of impaired perfusion .
	manualset3
85165	2	398274	5	NULL	NULL	0	NULL	oxygen extraction	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatosplanchnic blood flow control and oxygen extraction are modified by the underlying mechanism of impaired perfusion .
	manualset3
85166	3	398274	5	NULL	NULL	0	NULL	underlying mechanism	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatosplanchnic blood flow control and oxygen extraction are modified by the underlying mechanism of impaired perfusion .
	manualset3
85167	4	398274	5	NULL	NULL	0	NULL	impaired perfusion	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatosplanchnic blood flow control and oxygen extraction are modified by the underlying mechanism of impaired perfusion .
	manualset3
85168	1	398275	5	NULL	NULL	0	NULL	Hepatosplenomegaly	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatosplenomegaly was diagnosed by USG examination .
	manualset3
85169	2	398275	5	NULL	NULL	0	NULL	USG examination	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hepatosplenomegaly was diagnosed by USG examination .
	manualset3
85170	1	398276	5	NULL	NULL	NULL	NULL	adrenal mass	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Her general condition has markedly improved and her adrenal mass and meningioma are being closely observed now .
	manualset3
85171	2	398276	5	NULL	NULL	0	NULL	meningioma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Her general condition has markedly improved and her adrenal mass and meningioma are being closely observed now .
	manualset3
85172	1	398277	5	NULL	NULL	NULL	NULL	hemoglobin level	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Her hemoglobin level was 8.3 g/dl .
	manualset3
85173	2	398277	5	NULL	NULL	0	NULL	8.3 g/dl	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Her hemoglobin level was 8.3 g/dl .
	manualset3
85174	1	398278	5	NULL	NULL	0	NULL	serum calcium level	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Her serum calcium level ranged from 9.0 to 10.0 mg/dL , which caused difficulties in performing vitamin D injection therapy .
	manualset3
85175	2	398278	5	NULL	NULL	0	NULL	9.0 to 10.0 mg/dL	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Her serum calcium level ranged from 9.0 to 10.0 mg/dL , which caused difficulties in performing vitamin D injection therapy .
	manualset3
85176	3	398278	5	NULL	NULL	0	NULL	vitamin D injection therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Her serum calcium level ranged from 9.0 to 10.0 mg/dL , which caused difficulties in performing vitamin D injection therapy .
	manualset3
85177	1	398279	5	NULL	NULL	NULL	NULL	sister aged two months	Person												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Her sister aged two months received porcine calcitonin for three weeks , during which clinical improvement , no change in the serum level of alkaline phosphatase and a marked decrease of the excretion of hydroxyproline were recorded .
	manualset3
85179	2	398279	5	NULL	NULL	NULL	NULL	porcine calcitonin	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Her sister aged two months received porcine calcitonin for three weeks , during which clinical improvement , no change in the serum level of alkaline phosphatase and a marked decrease of the excretion of hydroxyproline were recorded .
	manualset3
85180	3	398279	5	NULL	NULL	NULL	NULL	three weeks	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Her sister aged two months received porcine calcitonin for three weeks , during which clinical improvement , no change in the serum level of alkaline phosphatase and a marked decrease of the excretion of hydroxyproline were recorded .
	manualset3
85181	4	398279	5	NULL	NULL	NULL	NULL	clinical improvement	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Her sister aged two months received porcine calcitonin for three weeks , during which clinical improvement , no change in the serum level of alkaline phosphatase and a marked decrease of the excretion of hydroxyproline were recorded .
	manualset3
85182	5	398279	5	NULL	NULL	NULL	NULL	serum level	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Her sister aged two months received porcine calcitonin for three weeks , during which clinical improvement , no change in the serum level of alkaline phosphatase and a marked decrease of the excretion of hydroxyproline were recorded .
	manualset3
85183	6	398279	5	NULL	NULL	NULL	NULL	alkaline phosphatase	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Her sister aged two months received porcine calcitonin for three weeks , during which clinical improvement , no change in the serum level of alkaline phosphatase and a marked decrease of the excretion of hydroxyproline were recorded .
	manualset3
85184	7	398279	5	NULL	NULL	NULL	NULL	excretion	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Her sister aged two months received porcine calcitonin for three weeks , during which clinical improvement , no change in the serum level of alkaline phosphatase and a marked decrease of the excretion of hydroxyproline were recorded .
	manualset3
85185	8	398279	5	NULL	NULL	NULL	NULL	hydroxyproline	AminoAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Her sister aged two months received porcine calcitonin for three weeks , during which clinical improvement , no change in the serum level of alkaline phosphatase and a marked decrease of the excretion of hydroxyproline were recorded .
	manualset3
85186	1	398280	5	NULL	NULL	0	NULL	purification	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , I report a method that was originally designed for purification of large amounts of nucleotides using anion-exchanging resin but has shown the promise of enriching phosphorylated peptides .
	manualset3
85187	2	398280	5	NULL	NULL	0	NULL	nucleotides	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , I report a method that was originally designed for purification of large amounts of nucleotides using anion-exchanging resin but has shown the promise of enriching phosphorylated peptides .
	manualset3
85188	3	398280	5	NULL	NULL	0	NULL	anion-exchanging resin	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , I report a method that was originally designed for purification of large amounts of nucleotides using anion-exchanging resin but has shown the promise of enriching phosphorylated peptides .
	manualset3
85189	4	398280	5	NULL	NULL	0	NULL	phosphorylated peptides	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , I report a method that was originally designed for purification of large amounts of nucleotides using anion-exchanging resin but has shown the promise of enriching phosphorylated peptides .
	manualset3
85190	1	398281	5	NULL	NULL	0	NULL	MRP	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , MRP was detected in several types of epithelia , muscle cells , and macrophages .
	manualset3
85191	2	398281	5	NULL	NULL	0	NULL	epithelia	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , MRP was detected in several types of epithelia , muscle cells , and macrophages .
	manualset3
85192	3	398281	5	NULL	NULL	0	NULL	muscle cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , MRP was detected in several types of epithelia , muscle cells , and macrophages .
	manualset3
85193	4	398281	5	NULL	NULL	0	NULL	macrophages	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , MRP was detected in several types of epithelia , muscle cells , and macrophages .
	manualset3
85194	1	398282	5	NULL	NULL	0	NULL	metastatic renal cell carcinoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , a case of metastatic renal cell carcinoma to muscle and jejunum is reported .
	manualset3
85195	2	398282	5	NULL	NULL	0	NULL	muscle	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , a case of metastatic renal cell carcinoma to muscle and jejunum is reported .
	manualset3
85196	3	398282	5	NULL	NULL	0	NULL	jejunum	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , a case of metastatic renal cell carcinoma to muscle and jejunum is reported .
	manualset3
85197	1	398283	5	NULL	NULL	0	NULL	recent data	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , based upon the recent data , mainly obtained from the DT40 system , we discuss several new aspects on mechanisms by which BCR signals are propagated and modified .
	manualset3
85198	2	398283	5	NULL	NULL	0	NULL	DT40 system	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , based upon the recent data , mainly obtained from the DT40 system , we discuss several new aspects on mechanisms by which BCR signals are propagated and modified .
	manualset3
85199	3	398283	5	NULL	NULL	0	NULL	BCR signals	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , based upon the recent data , mainly obtained from the DT40 system , we discuss several new aspects on mechanisms by which BCR signals are propagated and modified .
	manualset3
85200	1	398284	5	NULL	NULL	0	NULL	Subcutaneous traumatic gallbladder rupture	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Subcutaneous traumatic gallbladder rupture ) .
	manualset3
85416	1	398285	5	NULL	NULL	0	NULL	altimetry-derived variation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , for the first time , we have further used the altimetry-derived variation of water level for estimating the fluctuation of water storage as an addition to the present in situ water storage estimation systems to be used in remote areas and in emergency situation such as in the events flooding monitoring and for studying the effect of climate change .
	manualset3
85417	2	398285	5	NULL	NULL	0	NULL	water level	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , for the first time , we have further used the altimetry-derived variation of water level for estimating the fluctuation of water storage as an addition to the present in situ water storage estimation systems to be used in remote areas and in emergency situation such as in the events flooding monitoring and for studying the effect of climate change .
	manualset3
85418	3	398285	5	NULL	NULL	0	NULL	fluctuation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , for the first time , we have further used the altimetry-derived variation of water level for estimating the fluctuation of water storage as an addition to the present in situ water storage estimation systems to be used in remote areas and in emergency situation such as in the events flooding monitoring and for studying the effect of climate change .
	manualset3
85419	4	398285	5	NULL	NULL	0	NULL	water storage	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , for the first time , we have further used the altimetry-derived variation of water level for estimating the fluctuation of water storage as an addition to the present in situ water storage estimation systems to be used in remote areas and in emergency situation such as in the events flooding monitoring and for studying the effect of climate change .
	manualset3
85420	5	398285	5	NULL	NULL	0	NULL	addition	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , for the first time , we have further used the altimetry-derived variation of water level for estimating the fluctuation of water storage as an addition to the present in situ water storage estimation systems to be used in remote areas and in emergency situation such as in the events flooding monitoring and for studying the effect of climate change .
	manualset3
85421	6	398285	5	NULL	NULL	0	NULL	situ water storage estimation systems	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , for the first time , we have further used the altimetry-derived variation of water level for estimating the fluctuation of water storage as an addition to the present in situ water storage estimation systems to be used in remote areas and in emergency situation such as in the events flooding monitoring and for studying the effect of climate change .
	manualset3
85422	7	398285	5	NULL	NULL	0	NULL	remote areas	UnproperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , for the first time , we have further used the altimetry-derived variation of water level for estimating the fluctuation of water storage as an addition to the present in situ water storage estimation systems to be used in remote areas and in emergency situation such as in the events flooding monitoring and for studying the effect of climate change .
	manualset3
85423	8	398285	5	NULL	NULL	0	NULL	emergency situation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , for the first time , we have further used the altimetry-derived variation of water level for estimating the fluctuation of water storage as an addition to the present in situ water storage estimation systems to be used in remote areas and in emergency situation such as in the events flooding monitoring and for studying the effect of climate change .
	manualset3
85424	9	398285	5	NULL	NULL	0	NULL	events flooding monitoring	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , for the first time , we have further used the altimetry-derived variation of water level for estimating the fluctuation of water storage as an addition to the present in situ water storage estimation systems to be used in remote areas and in emergency situation such as in the events flooding monitoring and for studying the effect of climate change .
	manualset3
85425	10	398285	5	NULL	NULL	0	NULL	climate change	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , for the first time , we have further used the altimetry-derived variation of water level for estimating the fluctuation of water storage as an addition to the present in situ water storage estimation systems to be used in remote areas and in emergency situation such as in the events flooding monitoring and for studying the effect of climate change .
	manualset3
85201	1	398286	5	NULL	NULL	0	NULL	scintigraphy	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , scintigraphy is superior to all other imaging procedures in the evaluation of bile flow situations .
	manualset3
85202	2	398286	5	NULL	NULL	0	NULL	imaging procedures	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , scintigraphy is superior to all other imaging procedures in the evaluation of bile flow situations .
	manualset3
85203	3	398286	5	NULL	NULL	0	NULL	evaluation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , scintigraphy is superior to all other imaging procedures in the evaluation of bile flow situations .
	manualset3
85204	4	398286	5	NULL	NULL	0	NULL	bile flow situations	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , scintigraphy is superior to all other imaging procedures in the evaluation of bile flow situations .
	manualset3
85205	1	398287	5	NULL	NULL	0	NULL	authors	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , the authors present a case of a drug-resistant epilepsy patient with a complex phenotype where a diagnosis of CTX was done and showed a significant reduction in seizure frequency after chenodeoxycholic acid supplementation .
	manualset3
85206	2	398287	5	NULL	NULL	0	NULL	case	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , the authors present a case of a drug-resistant epilepsy patient with a complex phenotype where a diagnosis of CTX was done and showed a significant reduction in seizure frequency after chenodeoxycholic acid supplementation .
	manualset3
85207	3	398287	5	NULL	NULL	0	NULL	drug-resistant epilepsy patient	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , the authors present a case of a drug-resistant epilepsy patient with a complex phenotype where a diagnosis of CTX was done and showed a significant reduction in seizure frequency after chenodeoxycholic acid supplementation .
	manualset3
85208	4	398287	5	NULL	NULL	0	NULL	complex phenotype	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , the authors present a case of a drug-resistant epilepsy patient with a complex phenotype where a diagnosis of CTX was done and showed a significant reduction in seizure frequency after chenodeoxycholic acid supplementation .
	manualset3
85209	5	398287	5	NULL	NULL	NULL	NULL	diagnosis	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , the authors present a case of a drug-resistant epilepsy patient with a complex phenotype where a diagnosis of CTX was done and showed a significant reduction in seizure frequency after chenodeoxycholic acid supplementation .
	manualset3
85210	6	398287	5	NULL	NULL	0	NULL	CTX	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , the authors present a case of a drug-resistant epilepsy patient with a complex phenotype where a diagnosis of CTX was done and showed a significant reduction in seizure frequency after chenodeoxycholic acid supplementation .
	manualset3
85211	7	398287	5	NULL	NULL	0	NULL	significant reduction	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , the authors present a case of a drug-resistant epilepsy patient with a complex phenotype where a diagnosis of CTX was done and showed a significant reduction in seizure frequency after chenodeoxycholic acid supplementation .
	manualset3
85212	8	398287	5	NULL	NULL	0	NULL	seizure frequency	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , the authors present a case of a drug-resistant epilepsy patient with a complex phenotype where a diagnosis of CTX was done and showed a significant reduction in seizure frequency after chenodeoxycholic acid supplementation .
	manualset3
85213	9	398287	5	NULL	NULL	0	NULL	chenodeoxycholic acid supplementation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , the authors present a case of a drug-resistant epilepsy patient with a complex phenotype where a diagnosis of CTX was done and showed a significant reduction in seizure frequency after chenodeoxycholic acid supplementation .
	manualset3
85214	1	398288	5	NULL	NULL	NULL	NULL	oxygen concentration	ExperimentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , the effects of oxygen concentration and temperature on the kinetic isotope effects with deuterated choline have been investigated .
	manualset3
85215	2	398288	5	NULL	NULL	0	NULL	temperature	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , the effects of oxygen concentration and temperature on the kinetic isotope effects with deuterated choline have been investigated .
	manualset3
85216	3	398288	5	NULL	NULL	0	NULL	kinetic isotope effects	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , the effects of oxygen concentration and temperature on the kinetic isotope effects with deuterated choline have been investigated .
	manualset3
85217	4	398288	5	NULL	NULL	0	NULL	deuterated choline	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , the effects of oxygen concentration and temperature on the kinetic isotope effects with deuterated choline have been investigated .
	manualset3
85218	1	398289	5	NULL	NULL	0	NULL	two genes	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , two genes are identified , ARE1 and ARE2 , that encode ACAT-related enzymes in yeast .
	manualset3
85219	2	398289	5	NULL	NULL	0	NULL	ARE1	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , two genes are identified , ARE1 and ARE2 , that encode ACAT-related enzymes in yeast .
	manualset3
85220	3	398289	5	NULL	NULL	0	NULL	ARE2	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , two genes are identified , ARE1 and ARE2 , that encode ACAT-related enzymes in yeast .
	manualset3
85221	4	398289	5	NULL	NULL	0	NULL	encode	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , two genes are identified , ARE1 and ARE2 , that encode ACAT-related enzymes in yeast .
	manualset3
85222	5	398289	5	NULL	NULL	0	NULL	ACAT-related enzymes	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , two genes are identified , ARE1 and ARE2 , that encode ACAT-related enzymes in yeast .
	manualset3
85223	6	398289	5	NULL	NULL	0	NULL	yeast	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , two genes are identified , ARE1 and ARE2 , that encode ACAT-related enzymes in yeast .
	manualset3
85224	1	398290	5	NULL	NULL	0	NULL	viruses	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , viruses are detected using an immunoassay sandwich approach with the reporting antibodies tagged to liposomes .
	manualset3
85225	2	398290	5	NULL	NULL	0	NULL	immunoassay sandwich approach	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , viruses are detected using an immunoassay sandwich approach with the reporting antibodies tagged to liposomes .
	manualset3
85226	3	398290	5	NULL	NULL	0	NULL	reporting antibodies	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , viruses are detected using an immunoassay sandwich approach with the reporting antibodies tagged to liposomes .
	manualset3
85227	4	398290	5	NULL	NULL	0	NULL	liposomes	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , viruses are detected using an immunoassay sandwich approach with the reporting antibodies tagged to liposomes .
	manualset3
85228	1	398291	5	NULL	NULL	NULL	NULL	constitutive monocyte TLR2 expression	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we analyzed constitutive monocyte TLR2 expression and evaluated the expression profiles of the proximal downstream adapter molecule myeloid differentiation factor 88 ( MyD88 ) .
	manualset3
85230	2	398291	5	NULL	NULL	NULL	NULL	proximal downstream adapter molecule myeloid differentiation factor 88 ( MyD88 )	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we analyzed constitutive monocyte TLR2 expression and evaluated the expression profiles of the proximal downstream adapter molecule myeloid differentiation factor 88 ( MyD88 ) .
	manualset3
85231	1	398292	5	NULL	NULL	0	NULL	Subrenal capsule assay	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Subrenal capsule assay in normal mice immunosuppressed by cyclosporin A ) .
	manualset3
85232	2	398292	5	NULL	NULL	0	NULL	normal mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Subrenal capsule assay in normal mice immunosuppressed by cyclosporin A ) .
	manualset3
85233	3	398292	5	NULL	NULL	0	NULL	cyclosporin A	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( Subrenal capsule assay in normal mice immunosuppressed by cyclosporin A ) .
	manualset3
85234	1	398293	5	NULL	NULL	NULL	NULL	Toll-like receptor-IL-1 receptor signaling components	Molecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we analyzed the Toll-like receptor-IL-1 receptor signaling components involved in the post-transcriptional regulation of IB - with mutated estrogen receptor ( ER ( T2 ) ) fusion proteins .
	manualset3
85235	2	398293	5	NULL	NULL	0	NULL	post-transcriptional regulation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we analyzed the Toll-like receptor-IL-1 receptor signaling components involved in the post-transcriptional regulation of IB - with mutated estrogen receptor ( ER ( T2 ) ) fusion proteins .
	manualset3
85236	3	398293	5	NULL	NULL	0	NULL	IB	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we analyzed the Toll-like receptor-IL-1 receptor signaling components involved in the post-transcriptional regulation of IB - with mutated estrogen receptor ( ER ( T2 ) ) fusion proteins .
	manualset3
85237	4	398293	5	NULL	NULL	0	NULL	mutated estrogen receptor ( ER ( T2 ) ) fusion proteins	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we analyzed the Toll-like receptor-IL-1 receptor signaling components involved in the post-transcriptional regulation of IB - with mutated estrogen receptor ( ER ( T2 ) ) fusion proteins .
	manualset3
85238	1	398294	5	NULL	NULL	0	NULL	electrophysiological and imaging techniques	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we combine a variety of electrophysiological and imaging techniques and computational modeling to elucidate the mechanisms underlying these spatial and temporal properties of waves in developing mouse retina .
	manualset3
85239	2	398294	5	NULL	NULL	0	NULL	computational modeling	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we combine a variety of electrophysiological and imaging techniques and computational modeling to elucidate the mechanisms underlying these spatial and temporal properties of waves in developing mouse retina .
	manualset3
85240	3	398294	5	NULL	NULL	0	NULL	mechanisms	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we combine a variety of electrophysiological and imaging techniques and computational modeling to elucidate the mechanisms underlying these spatial and temporal properties of waves in developing mouse retina .
	manualset3
85241	4	398294	5	NULL	NULL	0	NULL	spatial and temporal properties	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we combine a variety of electrophysiological and imaging techniques and computational modeling to elucidate the mechanisms underlying these spatial and temporal properties of waves in developing mouse retina .
	manualset3
85242	5	398294	5	NULL	NULL	0	NULL	waves	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we combine a variety of electrophysiological and imaging techniques and computational modeling to elucidate the mechanisms underlying these spatial and temporal properties of waves in developing mouse retina .
	manualset3
85243	6	398294	5	NULL	NULL	0	NULL	developing mouse retina	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we combine a variety of electrophysiological and imaging techniques and computational modeling to elucidate the mechanisms underlying these spatial and temporal properties of waves in developing mouse retina .
	manualset3
85244	1	398295	5	NULL	NULL	0	NULL	nocturnal dynamics	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we compared nocturnal dynamics in plasma concentrations of ACTH/cortisol in 7 patients with Cushing 's disease with those of 7 healthy controls matched in age and sex with the patients .
	manualset3
85246	2	398295	5	NULL	NULL	NULL	NULL	ACTH	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we compared nocturnal dynamics in plasma concentrations of ACTH/cortisol in 7 patients with Cushing 's disease with those of 7 healthy controls matched in age and sex with the patients .
	manualset3
85247	4	398295	5	NULL	NULL	0	NULL	7 patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we compared nocturnal dynamics in plasma concentrations of ACTH/cortisol in 7 patients with Cushing 's disease with those of 7 healthy controls matched in age and sex with the patients .
	manualset3
85248	5	398295	5	NULL	NULL	0	NULL	Cushing 's disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we compared nocturnal dynamics in plasma concentrations of ACTH/cortisol in 7 patients with Cushing 's disease with those of 7 healthy controls matched in age and sex with the patients .
	manualset3
85249	6	398295	5	NULL	NULL	0	NULL	7 healthy controls	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we compared nocturnal dynamics in plasma concentrations of ACTH/cortisol in 7 patients with Cushing 's disease with those of 7 healthy controls matched in age and sex with the patients .
	manualset3
85250	7	398295	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we compared nocturnal dynamics in plasma concentrations of ACTH/cortisol in 7 patients with Cushing 's disease with those of 7 healthy controls matched in age and sex with the patients .
	manualset3
85437	3	398295	5	NULL	NULL	0	NULL	cortisol	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we compared nocturnal dynamics in plasma concentrations of ACTH/cortisol in 7 patients with Cushing 's disease with those of 7 healthy controls matched in age and sex with the patients .
	manualset3
85499	8	398295	5	NULL	NULL	0	NULL	plasma concentrations	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we compared nocturnal dynamics in plasma concentrations of ACTH/cortisol in 7 patients with Cushing 's disease with those of 7 healthy controls matched in age and sex with the patients .
	manualset3
85251	1	398296	5	NULL	NULL	0	NULL	postoperative electrophysiological changes	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we compared the postoperative electrophysiological changes in resting hand tremor after 32 ablations and 12 DBS implantations in patients with severe tremor-dominant idiopathic Parkinson 's disease ( PD ) and essential tremor ( ET ) .
	manualset3
85252	2	398296	5	NULL	NULL	0	NULL	resting hand tremor	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we compared the postoperative electrophysiological changes in resting hand tremor after 32 ablations and 12 DBS implantations in patients with severe tremor-dominant idiopathic Parkinson 's disease ( PD ) and essential tremor ( ET ) .
	manualset3
85253	3	398296	5	NULL	NULL	0	NULL	32 ablations	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we compared the postoperative electrophysiological changes in resting hand tremor after 32 ablations and 12 DBS implantations in patients with severe tremor-dominant idiopathic Parkinson 's disease ( PD ) and essential tremor ( ET ) .
	manualset3
85254	4	398296	5	NULL	NULL	0	NULL	12 DBS implantations	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we compared the postoperative electrophysiological changes in resting hand tremor after 32 ablations and 12 DBS implantations in patients with severe tremor-dominant idiopathic Parkinson 's disease ( PD ) and essential tremor ( ET ) .
	manualset3
85255	5	398296	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we compared the postoperative electrophysiological changes in resting hand tremor after 32 ablations and 12 DBS implantations in patients with severe tremor-dominant idiopathic Parkinson 's disease ( PD ) and essential tremor ( ET ) .
	manualset3
85256	6	398296	5	NULL	NULL	0	NULL	severe tremor-dominant idiopathic Parkinson 's disease ( PD )	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we compared the postoperative electrophysiological changes in resting hand tremor after 32 ablations and 12 DBS implantations in patients with severe tremor-dominant idiopathic Parkinson 's disease ( PD ) and essential tremor ( ET ) .
	manualset3
85257	7	398296	5	NULL	NULL	0	NULL	essential tremor ( ET )	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we compared the postoperative electrophysiological changes in resting hand tremor after 32 ablations and 12 DBS implantations in patients with severe tremor-dominant idiopathic Parkinson 's disease ( PD ) and essential tremor ( ET ) .
	manualset3
85258	1	398297	5	NULL	NULL	0	NULL	mechanism	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we define the mechanism by which ORF45 activates RSKs .
	manualset3
85259	2	398297	5	NULL	NULL	0	NULL	ORF45	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we define the mechanism by which ORF45 activates RSKs .
	manualset3
85260	3	398297	5	NULL	NULL	0	NULL	RSKs	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we define the mechanism by which ORF45 activates RSKs .
	manualset3
85261	1	398298	5	NULL	NULL	0	NULL	role	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we defined the role of CXCR5 in the development of mucosal tertiary lymphoid tissue and gastric inflammation in a mouse model of chronic H. pylori infection .
	manualset3
85262	2	398298	5	NULL	NULL	0	NULL	CXCR5	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we defined the role of CXCR5 in the development of mucosal tertiary lymphoid tissue and gastric inflammation in a mouse model of chronic H. pylori infection .
	manualset3
85263	3	398298	5	NULL	NULL	0	NULL	development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we defined the role of CXCR5 in the development of mucosal tertiary lymphoid tissue and gastric inflammation in a mouse model of chronic H. pylori infection .
	manualset3
85264	4	398298	5	NULL	NULL	0	NULL	mucosal tertiary lymphoid tissue	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we defined the role of CXCR5 in the development of mucosal tertiary lymphoid tissue and gastric inflammation in a mouse model of chronic H. pylori infection .
	manualset3
85265	5	398298	5	NULL	NULL	0	NULL	gastric inflammation	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we defined the role of CXCR5 in the development of mucosal tertiary lymphoid tissue and gastric inflammation in a mouse model of chronic H. pylori infection .
	manualset3
85266	6	398298	5	NULL	NULL	0	NULL	mouse model	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we defined the role of CXCR5 in the development of mucosal tertiary lymphoid tissue and gastric inflammation in a mouse model of chronic H. pylori infection .
	manualset3
85267	7	398298	5	NULL	NULL	0	NULL	chronic H. pylori infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we defined the role of CXCR5 in the development of mucosal tertiary lymphoid tissue and gastric inflammation in a mouse model of chronic H. pylori infection .
	manualset3
85268	1	398299	5	NULL	NULL	0	NULL	Mrc1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we demonstrate that Mrc1 functions constitutively to promote normal replication fork progression .
	manualset3
85269	2	398299	5	NULL	NULL	0	NULL	normal replication fork progression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we demonstrate that Mrc1 functions constitutively to promote normal replication fork progression .
	manualset3
85271	1	398300	5	NULL	NULL	NULL	NULL	vertical and lateral integration	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we demonstrate the vertical and lateral integration of ZnO nanowires into arrays that are capable of producing sufficient power to operate real devices .
	manualset3
85272	2	398300	5	NULL	NULL	0	NULL	ZnO nanowires	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we demonstrate the vertical and lateral integration of ZnO nanowires into arrays that are capable of producing sufficient power to operate real devices .
	manualset3
85273	3	398300	5	NULL	NULL	0	NULL	arrays	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we demonstrate the vertical and lateral integration of ZnO nanowires into arrays that are capable of producing sufficient power to operate real devices .
	manualset3
85274	4	398300	5	NULL	NULL	0	NULL	sufficient power	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we demonstrate the vertical and lateral integration of ZnO nanowires into arrays that are capable of producing sufficient power to operate real devices .
	manualset3
85275	5	398300	5	NULL	NULL	0	NULL	real devices	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we demonstrate the vertical and lateral integration of ZnO nanowires into arrays that are capable of producing sufficient power to operate real devices .
	manualset3
85276	1	398301	5	NULL	NULL	0	NULL	routine nursing	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Subtle violence in routine nursing ) .
	manualset3
85277	1	398302	5	NULL	NULL	NULL	NULL	novel and highly conserved paralog of adiponectin	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we describe a novel and highly conserved paralog of adiponectin designated as C1q/TNF-related protein ( CTRP ) 9 .
	manualset3
85278	2	398302	5	NULL	NULL	0	NULL	C1q/TNF-related protein ( CTRP ) 9	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we describe a novel and highly conserved paralog of adiponectin designated as C1q/TNF-related protein ( CTRP ) 9 .
	manualset3
85279	1	398303	5	NULL	NULL	0	NULL	novel bacterium	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we describe a novel bacterium , strain TUD-YJ37 ( T ) , which can accumulate polyhydroxybutyrate ( PHB ) to more than 85 % ( w/w ) dry cell weight .
	manualset3
85280	2	398303	5	NULL	NULL	0	NULL	strain TUD-YJ37 ( T )	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we describe a novel bacterium , strain TUD-YJ37 ( T ) , which can accumulate polyhydroxybutyrate ( PHB ) to more than 85 % ( w/w ) dry cell weight .
	manualset3
85281	3	398303	5	NULL	NULL	0	NULL	polyhydroxybutyrate ( PHB )	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we describe a novel bacterium , strain TUD-YJ37 ( T ) , which can accumulate polyhydroxybutyrate ( PHB ) to more than 85 % ( w/w ) dry cell weight .
	manualset3
85282	4	398303	5	NULL	NULL	0	NULL	85 % ( w/w ) dry cell weight	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we describe a novel bacterium , strain TUD-YJ37 ( T ) , which can accumulate polyhydroxybutyrate ( PHB ) to more than 85 % ( w/w ) dry cell weight .
	manualset3
85283	1	398304	5	NULL	NULL	0	NULL	novel cell biological mechanism	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we describe a novel cell biological mechanism that disperses membrane fragments over large distances through the Drosophila imaginal disc epithelium .
	manualset3
85284	2	398304	5	NULL	NULL	0	NULL	membrane fragments	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we describe a novel cell biological mechanism that disperses membrane fragments over large distances through the Drosophila imaginal disc epithelium .
	manualset3
85286	4	398304	5	NULL	NULL	NULL	NULL	Drosophila imaginal disc epithelium	Tissue												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we describe a novel cell biological mechanism that disperses membrane fragments over large distances through the Drosophila imaginal disc epithelium .
	manualset3
85438	3	398304	5	NULL	NULL	0	NULL	large distances	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we describe a novel cell biological mechanism that disperses membrane fragments over large distances through the Drosophila imaginal disc epithelium .
	manualset3
85287	1	398305	5	NULL	NULL	0	NULL	novel protein molecular weight markers	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we describe novel protein molecular weight markers in which a prestaining procedure is no longer needed .
	manualset3
85288	2	398305	5	NULL	NULL	0	NULL	prestaining procedure	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we describe novel protein molecular weight markers in which a prestaining procedure is no longer needed .
	manualset3
85289	1	398306	5	NULL	NULL	0	NULL	 isolation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we describe the isolation of the CMP-Neu5Ac hydroxylase from A. rubens gonads using anion exchange chromatography and chromatography on immobilized cytochrome b ( 5 ) .
	manualset3
85290	2	398306	5	NULL	NULL	0	NULL	CMP-Neu5Ac hydroxylase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we describe the isolation of the CMP-Neu5Ac hydroxylase from A. rubens gonads using anion exchange chromatography and chromatography on immobilized cytochrome b ( 5 ) .
	manualset3
85291	3	398306	5	NULL	NULL	0	NULL	A. rubens gonads	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we describe the isolation of the CMP-Neu5Ac hydroxylase from A. rubens gonads using anion exchange chromatography and chromatography on immobilized cytochrome b ( 5 ) .
	manualset3
85292	4	398306	5	NULL	NULL	0	NULL	anion exchange chromatography	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we describe the isolation of the CMP-Neu5Ac hydroxylase from A. rubens gonads using anion exchange chromatography and chromatography on immobilized cytochrome b ( 5 ) .
	manualset3
85293	5	398306	5	NULL	NULL	0	NULL	chromatography on immobilized cytochrome b ( 5 )	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we describe the isolation of the CMP-Neu5Ac hydroxylase from A. rubens gonads using anion exchange chromatography and chromatography on immobilized cytochrome b ( 5 ) .
	manualset3
85294	1	398307	5	NULL	NULL	0	NULL	functions	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we evaluated the functions of the two major signaling pathways , the signal transducers and activators of transcription 1 and 3 ( STAT1/3 ) and the Src-homology tyrosine phosphatase 2 ( SHP2 ) - Ras-ERK , emanating from the common signal transducer , gp130 , in the gastrointestinal tract .
	manualset3
85295	2	398307	5	NULL	NULL	NULL	NULL	major signaling pathways	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we evaluated the functions of the two major signaling pathways , the signal transducers and activators of transcription 1 and 3 ( STAT1/3 ) and the Src-homology tyrosine phosphatase 2 ( SHP2 ) - Ras-ERK , emanating from the common signal transducer , gp130 , in the gastrointestinal tract .
	manualset3
85296	3	398307	5	NULL	NULL	NULL	NULL	signal transducers and activators of transcription 1 and 3 ( STAT1/3 )	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we evaluated the functions of the two major signaling pathways , the signal transducers and activators of transcription 1 and 3 ( STAT1/3 ) and the Src-homology tyrosine phosphatase 2 ( SHP2 ) - Ras-ERK , emanating from the common signal transducer , gp130 , in the gastrointestinal tract .
	manualset3
85298	4	398307	5	NULL	NULL	NULL	NULL	Src-homology tyrosine phosphatase 2 ( SHP2 ) - Ras-ERKB signaling pathway	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we evaluated the functions of the two major signaling pathways , the signal transducers and activators of transcription 1 and 3 ( STAT1/3 ) and the Src-homology tyrosine phosphatase 2 ( SHP2 ) - Ras-ERK , emanating from the common signal transducer , gp130 , in the gastrointestinal tract .
	manualset3
85299	5	398307	5	NULL	NULL	NULL	NULL	common signal transducer	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we evaluated the functions of the two major signaling pathways , the signal transducers and activators of transcription 1 and 3 ( STAT1/3 ) and the Src-homology tyrosine phosphatase 2 ( SHP2 ) - Ras-ERK , emanating from the common signal transducer , gp130 , in the gastrointestinal tract .
	manualset3
85300	6	398307	5	NULL	NULL	NULL	NULL	gp130	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we evaluated the functions of the two major signaling pathways , the signal transducers and activators of transcription 1 and 3 ( STAT1/3 ) and the Src-homology tyrosine phosphatase 2 ( SHP2 ) - Ras-ERK , emanating from the common signal transducer , gp130 , in the gastrointestinal tract .
	manualset3
85301	7	398307	5	NULL	NULL	NULL	NULL	gastrointestinal tract	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we evaluated the functions of the two major signaling pathways , the signal transducers and activators of transcription 1 and 3 ( STAT1/3 ) and the Src-homology tyrosine phosphatase 2 ( SHP2 ) - Ras-ERK , emanating from the common signal transducer , gp130 , in the gastrointestinal tract .
	manualset3
85302	1	398308	5	NULL	NULL	0	NULL	cellular distribution	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we examined cellular distribution of Daxx by sub-cellular fractionation and immunofluorescent localization of endogenous protein , using SH-SY5Y neuroblastoma cell line previously reported to exhibit cytoplasmic translocation of Daxx after oxidative stress and beta-amyloid exposure .
	manualset3
85303	2	398308	5	NULL	NULL	0	NULL	Daxx	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we examined cellular distribution of Daxx by sub-cellular fractionation and immunofluorescent localization of endogenous protein , using SH-SY5Y neuroblastoma cell line previously reported to exhibit cytoplasmic translocation of Daxx after oxidative stress and beta-amyloid exposure .
	manualset3
85304	3	398308	5	NULL	NULL	0	NULL	sub-cellular fractionation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we examined cellular distribution of Daxx by sub-cellular fractionation and immunofluorescent localization of endogenous protein , using SH-SY5Y neuroblastoma cell line previously reported to exhibit cytoplasmic translocation of Daxx after oxidative stress and beta-amyloid exposure .
	manualset3
85305	4	398308	5	NULL	NULL	0	NULL	immunofluorescent localization	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we examined cellular distribution of Daxx by sub-cellular fractionation and immunofluorescent localization of endogenous protein , using SH-SY5Y neuroblastoma cell line previously reported to exhibit cytoplasmic translocation of Daxx after oxidative stress and beta-amyloid exposure .
	manualset3
85306	5	398308	5	NULL	NULL	0	NULL	endogenous protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we examined cellular distribution of Daxx by sub-cellular fractionation and immunofluorescent localization of endogenous protein , using SH-SY5Y neuroblastoma cell line previously reported to exhibit cytoplasmic translocation of Daxx after oxidative stress and beta-amyloid exposure .
	manualset3
85307	6	398308	5	NULL	NULL	0	NULL	SH-SY5Y neuroblastoma cell line	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we examined cellular distribution of Daxx by sub-cellular fractionation and immunofluorescent localization of endogenous protein , using SH-SY5Y neuroblastoma cell line previously reported to exhibit cytoplasmic translocation of Daxx after oxidative stress and beta-amyloid exposure .
	manualset3
85308	7	398308	5	NULL	NULL	0	NULL	cytoplasmic translocation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we examined cellular distribution of Daxx by sub-cellular fractionation and immunofluorescent localization of endogenous protein , using SH-SY5Y neuroblastoma cell line previously reported to exhibit cytoplasmic translocation of Daxx after oxidative stress and beta-amyloid exposure .
	manualset3
85309	8	398308	5	NULL	NULL	0	NULL	Daxx	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we examined cellular distribution of Daxx by sub-cellular fractionation and immunofluorescent localization of endogenous protein , using SH-SY5Y neuroblastoma cell line previously reported to exhibit cytoplasmic translocation of Daxx after oxidative stress and beta-amyloid exposure .
	manualset3
85310	9	398308	5	NULL	NULL	0	NULL	oxidative stress	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we examined cellular distribution of Daxx by sub-cellular fractionation and immunofluorescent localization of endogenous protein , using SH-SY5Y neuroblastoma cell line previously reported to exhibit cytoplasmic translocation of Daxx after oxidative stress and beta-amyloid exposure .
	manualset3
85311	10	398308	5	NULL	NULL	0	NULL	beta-amyloid exposure	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we examined cellular distribution of Daxx by sub-cellular fractionation and immunofluorescent localization of endogenous protein , using SH-SY5Y neuroblastoma cell line previously reported to exhibit cytoplasmic translocation of Daxx after oxidative stress and beta-amyloid exposure .
	manualset3
85312	1	398309	5	NULL	NULL	0	NULL	antisense oligonucleotide ( AS ) therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we examined the effects of an antisense oligonucleotide ( AS ) therapy directed against SHIP2 on whole body insulin sensitivity and insulin action in liver and muscle tissue in a dietary rodent model of the metabolic syndrome , the high-fat-fed ( HF ) rat .
	manualset3
85313	2	398309	5	NULL	NULL	0	NULL	SHIP2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we examined the effects of an antisense oligonucleotide ( AS ) therapy directed against SHIP2 on whole body insulin sensitivity and insulin action in liver and muscle tissue in a dietary rodent model of the metabolic syndrome , the high-fat-fed ( HF ) rat .
	manualset3
85314	3	398309	5	NULL	NULL	0	NULL	whole body insulin sensitivity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we examined the effects of an antisense oligonucleotide ( AS ) therapy directed against SHIP2 on whole body insulin sensitivity and insulin action in liver and muscle tissue in a dietary rodent model of the metabolic syndrome , the high-fat-fed ( HF ) rat .
	manualset3
85315	4	398309	5	NULL	NULL	0	NULL	insulin action	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we examined the effects of an antisense oligonucleotide ( AS ) therapy directed against SHIP2 on whole body insulin sensitivity and insulin action in liver and muscle tissue in a dietary rodent model of the metabolic syndrome , the high-fat-fed ( HF ) rat .
	manualset3
85316	5	398309	5	NULL	NULL	0	NULL	liver	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we examined the effects of an antisense oligonucleotide ( AS ) therapy directed against SHIP2 on whole body insulin sensitivity and insulin action in liver and muscle tissue in a dietary rodent model of the metabolic syndrome , the high-fat-fed ( HF ) rat .
	manualset3
85317	6	398309	5	NULL	NULL	0	NULL	muscle tissue	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we examined the effects of an antisense oligonucleotide ( AS ) therapy directed against SHIP2 on whole body insulin sensitivity and insulin action in liver and muscle tissue in a dietary rodent model of the metabolic syndrome , the high-fat-fed ( HF ) rat .
	manualset3
85318	7	398309	5	NULL	NULL	0	NULL	dietary rodent model	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we examined the effects of an antisense oligonucleotide ( AS ) therapy directed against SHIP2 on whole body insulin sensitivity and insulin action in liver and muscle tissue in a dietary rodent model of the metabolic syndrome , the high-fat-fed ( HF ) rat .
	manualset3
85319	8	398309	5	NULL	NULL	0	NULL	metabolic syndrome	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we examined the effects of an antisense oligonucleotide ( AS ) therapy directed against SHIP2 on whole body insulin sensitivity and insulin action in liver and muscle tissue in a dietary rodent model of the metabolic syndrome , the high-fat-fed ( HF ) rat .
	manualset3
85320	9	398309	5	NULL	NULL	0	NULL	high-fat-fed ( HF ) rat	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we examined the effects of an antisense oligonucleotide ( AS ) therapy directed against SHIP2 on whole body insulin sensitivity and insulin action in liver and muscle tissue in a dietary rodent model of the metabolic syndrome , the high-fat-fed ( HF ) rat .
	manualset3
85321	1	398310	5	NULL	NULL	0	NULL	Notch-mediated regulation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we focus on recent advances in our understanding of Notch-mediated regulation of cardiac development with specific attention to the formation of the cardiac outflow tract .
	manualset3
85322	2	398310	5	NULL	NULL	0	NULL	cardiac development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we focus on recent advances in our understanding of Notch-mediated regulation of cardiac development with specific attention to the formation of the cardiac outflow tract .
	manualset3
85323	3	398310	5	NULL	NULL	0	NULL	specific attention	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we focus on recent advances in our understanding of Notch-mediated regulation of cardiac development with specific attention to the formation of the cardiac outflow tract .
	manualset3
85324	4	398310	5	NULL	NULL	0	NULL	formation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we focus on recent advances in our understanding of Notch-mediated regulation of cardiac development with specific attention to the formation of the cardiac outflow tract .
	manualset3
85325	5	398310	5	NULL	NULL	0	NULL	cardiac outflow tract	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we focus on recent advances in our understanding of Notch-mediated regulation of cardiac development with specific attention to the formation of the cardiac outflow tract .
	manualset3
85326	1	398311	5	NULL	NULL	0	NULL	Successful treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Successful treatment of cystoid macular edema with etanercept in a patient with rheumatoid arthritis associated panuveitis ) .
	manualset3
85327	2	398311	5	NULL	NULL	0	NULL	cystoid macular edema	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Successful treatment of cystoid macular edema with etanercept in a patient with rheumatoid arthritis associated panuveitis ) .
	manualset3
85328	3	398311	5	NULL	NULL	0	NULL	etanercept	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( Successful treatment of cystoid macular edema with etanercept in a patient with rheumatoid arthritis associated panuveitis ) .
	manualset3
85329	4	398311	5	NULL	NULL	0	NULL	patient	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( Successful treatment of cystoid macular edema with etanercept in a patient with rheumatoid arthritis associated panuveitis ) .
	manualset3
85330	5	398311	5	NULL	NULL	0	NULL	rheumatoid arthritis associated panuveitis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Successful treatment of cystoid macular edema with etanercept in a patient with rheumatoid arthritis associated panuveitis ) .
	manualset3
85331	1	398312	5	NULL	NULL	0	NULL	ADH1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we have examined the involvement of ADH1 and ADH4 in embryonic adrenal function by using transgenic mouse technology and immunohistochemistry .
	manualset3
85332	2	398312	5	NULL	NULL	0	NULL	ADH4	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we have examined the involvement of ADH1 and ADH4 in embryonic adrenal function by using transgenic mouse technology and immunohistochemistry .
	manualset3
85333	3	398312	5	NULL	NULL	0	NULL	embryonic adrenal function	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we have examined the involvement of ADH1 and ADH4 in embryonic adrenal function by using transgenic mouse technology and immunohistochemistry .
	manualset3
85334	4	398312	5	NULL	NULL	0	NULL	transgenic mouse technology	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we have examined the involvement of ADH1 and ADH4 in embryonic adrenal function by using transgenic mouse technology and immunohistochemistry .
	manualset3
85335	5	398312	5	NULL	NULL	0	NULL	immunohistochemistry	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we have examined the involvement of ADH1 and ADH4 in embryonic adrenal function by using transgenic mouse technology and immunohistochemistry .
	manualset3
85336	1	398313	5	NULL	NULL	0	NULL	role	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we have further elucidated the role of MMP-13 in tumor invasion by examining its expression in invasive malignant tumors of the female genital tract .
	manualset3
85337	2	398313	5	NULL	NULL	0	NULL	MMP-13	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we have further elucidated the role of MMP-13 in tumor invasion by examining its expression in invasive malignant tumors of the female genital tract .
	manualset3
85338	3	398313	5	NULL	NULL	0	NULL	tumor invasion	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we have further elucidated the role of MMP-13 in tumor invasion by examining its expression in invasive malignant tumors of the female genital tract .
	manualset3
85339	4	398313	5	NULL	NULL	0	NULL	expression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we have further elucidated the role of MMP-13 in tumor invasion by examining its expression in invasive malignant tumors of the female genital tract .
	manualset3
85340	5	398313	5	NULL	NULL	0	NULL	invasive malignant tumors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we have further elucidated the role of MMP-13 in tumor invasion by examining its expression in invasive malignant tumors of the female genital tract .
	manualset3
85341	6	398313	5	NULL	NULL	0	NULL	female genital tract	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we have further elucidated the role of MMP-13 in tumor invasion by examining its expression in invasive malignant tumors of the female genital tract .
	manualset3
85342	1	398314	5	NULL	NULL	0	NULL	atomic force microsopy ( AFM )	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we have used atomic force microsopy ( AFM ) to study the effects of MBP and P2 on lipid bilayers .
	manualset3
85343	2	398314	5	NULL	NULL	0	NULL	study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we have used atomic force microsopy ( AFM ) to study the effects of MBP and P2 on lipid bilayers .
	manualset3
85344	3	398314	5	NULL	NULL	0	NULL	MBP	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we have used atomic force microsopy ( AFM ) to study the effects of MBP and P2 on lipid bilayers .
	manualset3
85345	4	398314	5	NULL	NULL	0	NULL	P2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we have used atomic force microsopy ( AFM ) to study the effects of MBP and P2 on lipid bilayers .
	manualset3
85346	5	398314	5	NULL	NULL	NULL	NULL	lipid bilayers	CellComponent												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we have used atomic force microsopy ( AFM ) to study the effects of MBP and P2 on lipid bilayers .
	manualset3
85347	1	398315	5	NULL	NULL	NULL	NULL	RKIP dimer formation	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we identify RKIP dimer formation as an important mechanistic feature in the target switch from Raf1 to GRK2 .
	manualset3
85349	2	398315	5	NULL	NULL	NULL	NULL	target switch	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we identify RKIP dimer formation as an important mechanistic feature in the target switch from Raf1 to GRK2 .
	manualset3
85350	3	398315	5	NULL	NULL	NULL	NULL	Raf1	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we identify RKIP dimer formation as an important mechanistic feature in the target switch from Raf1 to GRK2 .
	manualset3
85351	4	398315	5	NULL	NULL	NULL	NULL	GRK2	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we identify RKIP dimer formation as an important mechanistic feature in the target switch from Raf1 to GRK2 .
	manualset3
85352	1	398316	5	NULL	NULL	0	NULL	nakiterpiosin	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we identify nakiterpiosin as a novel antimitotic drug that targets microtubules .
	manualset3
85353	2	398316	5	NULL	NULL	0	NULL	novel antimitotic drug	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we identify nakiterpiosin as a novel antimitotic drug that targets microtubules .
	manualset3
85354	3	398316	5	NULL	NULL	0	NULL	microtubules	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we identify nakiterpiosin as a novel antimitotic drug that targets microtubules .
	manualset3
85355	1	398317	5	NULL	NULL	0	NULL	 interactive computer application	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we introduce an interactive computer application with a graphical interface , for the purpose of educating students about DP .
	manualset3
85356	2	398317	5	NULL	NULL	NULL	NULL	graphical interface	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we introduce an interactive computer application with a graphical interface , for the purpose of educating students about DP .
	manualset3
85357	3	398317	5	NULL	NULL	0	NULL	students	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we introduce an interactive computer application with a graphical interface , for the purpose of educating students about DP .
	manualset3
85358	4	398317	5	NULL	NULL	0	NULL	DP	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we introduce an interactive computer application with a graphical interface , for the purpose of educating students about DP .
	manualset3
85359	1	398318	5	NULL	NULL	0	NULL	investigation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( An investigation on the prevalence of internet addiction disorder in middle school students of Hunan province ) .
	manualset3
85360	2	398318	5	NULL	NULL	0	NULL	internet addiction disorder	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( An investigation on the prevalence of internet addiction disorder in middle school students of Hunan province ) .
	manualset3
85361	3	398318	5	NULL	NULL	0	NULL	middle school students	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( An investigation on the prevalence of internet addiction disorder in middle school students of Hunan province ) .
	manualset3
85362	4	398318	5	NULL	NULL	0	NULL	Hunan province	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	( An investigation on the prevalence of internet addiction disorder in middle school students of Hunan province ) .
	manualset3
85363	1	398319	5	NULL	NULL	0	NULL	Suppression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Suppression of pituitary-adrenal axis by triamcinolone acetonide in asthmatics ) .
	manualset3
85364	2	398319	5	NULL	NULL	0	NULL	pituitary-adrenal axis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Suppression of pituitary-adrenal axis by triamcinolone acetonide in asthmatics ) .
	manualset3
85365	3	398319	5	NULL	NULL	0	NULL	triamcinolone acetonide	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( Suppression of pituitary-adrenal axis by triamcinolone acetonide in asthmatics ) .
	manualset3
85366	4	398319	5	NULL	NULL	0	NULL	asthmatics	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( Suppression of pituitary-adrenal axis by triamcinolone acetonide in asthmatics ) .
	manualset3
85367	1	398320	5	NULL	NULL	0	NULL	activating role	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we investigated the activating role of the second and third extracellular loop of the human adenosine A1 receptor .
	manualset3
85368	2	398320	5	NULL	NULL	0	NULL	second and third extracellular loop	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we investigated the activating role of the second and third extracellular loop of the human adenosine A1 receptor .
	manualset3
85369	3	398320	5	NULL	NULL	0	NULL	human adenosine A1 receptor	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we investigated the activating role of the second and third extracellular loop of the human adenosine A1 receptor .
	manualset3
85370	1	398321	5	NULL	NULL	0	NULL	ecologically relevant levels	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we investigated the effects of ecologically relevant levels of UVR on the transmission of the intertidal trematode Maritrema novaezealandensis from its first intermediate snail host ( Zeacumantus subcarinatus ) to its second intermediate amphipod host ( Paracalliope novizealandiae ) .
	manualset3
85371	2	398321	5	NULL	NULL	0	NULL	UVR	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we investigated the effects of ecologically relevant levels of UVR on the transmission of the intertidal trematode Maritrema novaezealandensis from its first intermediate snail host ( Zeacumantus subcarinatus ) to its second intermediate amphipod host ( Paracalliope novizealandiae ) .
	manualset3
85372	3	398321	5	NULL	NULL	0	NULL	transmission	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we investigated the effects of ecologically relevant levels of UVR on the transmission of the intertidal trematode Maritrema novaezealandensis from its first intermediate snail host ( Zeacumantus subcarinatus ) to its second intermediate amphipod host ( Paracalliope novizealandiae ) .
	manualset3
85373	4	398321	5	NULL	NULL	0	NULL	 intertidal trematode Maritrema novaezealandensis	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we investigated the effects of ecologically relevant levels of UVR on the transmission of the intertidal trematode Maritrema novaezealandensis from its first intermediate snail host ( Zeacumantus subcarinatus ) to its second intermediate amphipod host ( Paracalliope novizealandiae ) .
	manualset3
85374	5	398321	5	NULL	NULL	NULL	NULL	 Zeacumantus subcarinatus	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we investigated the effects of ecologically relevant levels of UVR on the transmission of the intertidal trematode Maritrema novaezealandensis from its first intermediate snail host ( Zeacumantus subcarinatus ) to its second intermediate amphipod host ( Paracalliope novizealandiae ) .
	manualset3
85375	6	398321	5	NULL	NULL	NULL	NULL	Paracalliope novizealandiae	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we investigated the effects of ecologically relevant levels of UVR on the transmission of the intertidal trematode Maritrema novaezealandensis from its first intermediate snail host ( Zeacumantus subcarinatus ) to its second intermediate amphipod host ( Paracalliope novizealandiae ) .
	manualset3
85377	1	398322	5	NULL	NULL	NULL	NULL	extracts of anterior and posterior cockroach midguts	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we partially purified extracts of anterior and posterior cockroach midguts , using HPLC coupled with radioimmunoassay , and found , among multiple FMRFamide-like immunoreactive fractions , one fraction co-eluting with LMS in both regions .
	manualset3
85378	2	398322	5	NULL	NULL	NULL	NULL	HPLC coupled with radioimmunoassay	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we partially purified extracts of anterior and posterior cockroach midguts , using HPLC coupled with radioimmunoassay , and found , among multiple FMRFamide-like immunoreactive fractions , one fraction co-eluting with LMS in both regions .
	manualset3
85379	3	398322	5	NULL	NULL	NULL	NULL	FMRFamide-like immunoreactive fractions	CellComponent												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we partially purified extracts of anterior and posterior cockroach midguts , using HPLC coupled with radioimmunoassay , and found , among multiple FMRFamide-like immunoreactive fractions , one fraction co-eluting with LMS in both regions .
	manualset3
85380	4	398322	5	NULL	NULL	NULL	NULL	one fraction	CellComponent												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we partially purified extracts of anterior and posterior cockroach midguts , using HPLC coupled with radioimmunoassay , and found , among multiple FMRFamide-like immunoreactive fractions , one fraction co-eluting with LMS in both regions .
	manualset3
85381	1	398323	5	NULL	NULL	0	NULL	visualized current-clamp recordings	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we performed visualized current-clamp recordings to determine the effects of repeated cocaine administration on the membrane excitability of mPFC pyramidal neurons in rat brain slices .
	manualset3
85382	2	398323	5	NULL	NULL	0	NULL	repeated cocaine administration	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we performed visualized current-clamp recordings to determine the effects of repeated cocaine administration on the membrane excitability of mPFC pyramidal neurons in rat brain slices .
	manualset3
85383	3	398323	5	NULL	NULL	0	NULL	membrane excitability	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we performed visualized current-clamp recordings to determine the effects of repeated cocaine administration on the membrane excitability of mPFC pyramidal neurons in rat brain slices .
	manualset3
85384	4	398323	5	NULL	NULL	0	NULL	mPFC pyramidal neurons	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we performed visualized current-clamp recordings to determine the effects of repeated cocaine administration on the membrane excitability of mPFC pyramidal neurons in rat brain slices .
	manualset3
85385	5	398323	5	NULL	NULL	0	NULL	rat brain slices	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we performed visualized current-clamp recordings to determine the effects of repeated cocaine administration on the membrane excitability of mPFC pyramidal neurons in rat brain slices .
	manualset3
85386	1	398324	5	NULL	NULL	0	NULL	direct proteomic approach	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we present a direct proteomic approach , used to study the degree of iodination of mouse Tg without any preliminary purification .
	manualset3
85387	2	398324	5	NULL	NULL	0	NULL	study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we present a direct proteomic approach , used to study the degree of iodination of mouse Tg without any preliminary purification .
	manualset3
85388	3	398324	5	NULL	NULL	0	NULL	degree of iodination	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we present a direct proteomic approach , used to study the degree of iodination of mouse Tg without any preliminary purification .
	manualset3
85389	4	398324	5	NULL	NULL	0	NULL	mouse Tg	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we present a direct proteomic approach , used to study the degree of iodination of mouse Tg without any preliminary purification .
	manualset3
85390	5	398324	5	NULL	NULL	0	NULL	preliminary purification	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we present a direct proteomic approach , used to study the degree of iodination of mouse Tg without any preliminary purification .
	manualset3
85391	1	398325	5	NULL	NULL	0	NULL	unusual case	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we present an unusual case of unilateral leg calciphylaxis in the setting of relative chronic arterial insufficiency of the affected extremity secondary to steal syndrome .
	manualset3
85392	2	398325	5	NULL	NULL	0	NULL	unilateral leg calciphylaxis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we present an unusual case of unilateral leg calciphylaxis in the setting of relative chronic arterial insufficiency of the affected extremity secondary to steal syndrome .
	manualset3
85393	3	398325	5	NULL	NULL	0	NULL	relative chronic arterial insufficiency	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we present an unusual case of unilateral leg calciphylaxis in the setting of relative chronic arterial insufficiency of the affected extremity secondary to steal syndrome .
	manualset3
85394	4	398325	5	NULL	NULL	0	NULL	steal syndrome	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we present an unusual case of unilateral leg calciphylaxis in the setting of relative chronic arterial insufficiency of the affected extremity secondary to steal syndrome .
	manualset3
85395	1	398326	5	NULL	NULL	0	NULL	critical role	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we present evidence identifying a critical role for Hsp90 in TGFbeta signaling .
	manualset3
85396	2	398326	5	NULL	NULL	0	NULL	Hsp90	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we present evidence identifying a critical role for Hsp90 in TGFbeta signaling .
	manualset3
85397	3	398326	5	NULL	NULL	0	NULL	TGFbeta signaling	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we present evidence identifying a critical role for Hsp90 in TGFbeta signaling .
	manualset3
85398	1	398327	5	NULL	NULL	NULL	NULL	simple DNA gate architecture	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we propose a simple DNA gate architecture that appears suitable for practical synthesis of large-scale circuits involving possibly thousands of gates .
	manualset3
85399	2	398327	5	NULL	NULL	0	NULL	practical synthesis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we propose a simple DNA gate architecture that appears suitable for practical synthesis of large-scale circuits involving possibly thousands of gates .
	manualset3
85402	1	398328	5	NULL	NULL	0	NULL	case	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report a case of spondylitis due to brucella in an elderly male .
	manualset3
85403	2	398328	5	NULL	NULL	0	NULL	spondylitis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report a case of spondylitis due to brucella in an elderly male .
	manualset3
85404	3	398328	5	NULL	NULL	0	NULL	brucella	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report a case of spondylitis due to brucella in an elderly male .
	manualset3
85405	4	398328	5	NULL	NULL	0	NULL	elderly male	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report a case of spondylitis due to brucella in an elderly male .
	manualset3
85406	1	398329	5	NULL	NULL	0	NULL	miR expression profile	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report changes in miR expression profile in hepatocellular carcinomas ( HCCs ) developed in male Fisher rats-fed folic acid , methionine , and choline-deficient ( FMD ) diet .
	manualset3
85407	2	398329	5	NULL	NULL	0	NULL	hepatocellular carcinomas ( HCCs )	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report changes in miR expression profile in hepatocellular carcinomas ( HCCs ) developed in male Fisher rats-fed folic acid , methionine , and choline-deficient ( FMD ) diet .
	manualset3
85408	3	398329	5	NULL	NULL	0	NULL	male Fisher rats-fed folic acid , methionine , and choline-deficient ( FMD ) diet	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report changes in miR expression profile in hepatocellular carcinomas ( HCCs ) developed in male Fisher rats-fed folic acid , methionine , and choline-deficient ( FMD ) diet .
	manualset3
85409	1	398330	5	NULL	NULL	0	NULL	Surgery	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgery on the smoking habits of juveniles ) .
	manualset3
85410	2	398330	5	NULL	NULL	0	NULL	smoking habits	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgery on the smoking habits of juveniles ) .
	manualset3
85411	3	398330	5	NULL	NULL	0	NULL	juveniles	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgery on the smoking habits of juveniles ) .
	manualset3
85439	1	398331	5	NULL	NULL	0	NULL	GATA-2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that GATA-2 is expressed in a substantial proportion of prostate cancers and that high expression of GATA-2 is associated with biochemical recurrence and distant metastatic progression in a validation set of 203 cancers .
	manualset3
85440	2	398331	5	NULL	NULL	0	NULL	prostate cancers	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that GATA-2 is expressed in a substantial proportion of prostate cancers and that high expression of GATA-2 is associated with biochemical recurrence and distant metastatic progression in a validation set of 203 cancers .
	manualset3
85441	3	398331	5	NULL	NULL	0	NULL	high expression	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that GATA-2 is expressed in a substantial proportion of prostate cancers and that high expression of GATA-2 is associated with biochemical recurrence and distant metastatic progression in a validation set of 203 cancers .
	manualset3
85442	4	398331	5	NULL	NULL	0	NULL	GATA-2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that GATA-2 is expressed in a substantial proportion of prostate cancers and that high expression of GATA-2 is associated with biochemical recurrence and distant metastatic progression in a validation set of 203 cancers .
	manualset3
85443	5	398331	5	NULL	NULL	0	NULL	biochemical recurrence and distant metastatic progression	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that GATA-2 is expressed in a substantial proportion of prostate cancers and that high expression of GATA-2 is associated with biochemical recurrence and distant metastatic progression in a validation set of 203 cancers .
	manualset3
85444	6	398331	5	NULL	NULL	NULL	NULL	validation set	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we report that GATA-2 is expressed in a substantial proportion of prostate cancers and that high expression of GATA-2 is associated with biochemical recurrence and distant metastatic progression in a validation set of 203 cancers .
	manualset3
86455	7	398331	5	NULL	NULL	0	NULL	203 cancers	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that GATA-2 is expressed in a substantial proportion of prostate cancers and that high expression of GATA-2 is associated with biochemical recurrence and distant metastatic progression in a validation set of 203 cancers .
	manualset3
85445	1	398332	5	NULL	NULL	0	NULL	HBXIP	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that HBXIP contributes to protecting breast cancer cells from CDC by upregulating membrane-bound complement regulatory protein ( mCRPs ) , including CD46 , CD55 and CD59 .
	manualset3
85446	2	398332	5	NULL	NULL	0	NULL	breast cancer cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that HBXIP contributes to protecting breast cancer cells from CDC by upregulating membrane-bound complement regulatory protein ( mCRPs ) , including CD46 , CD55 and CD59 .
	manualset3
85447	3	398332	5	NULL	NULL	0	NULL	CDC	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that HBXIP contributes to protecting breast cancer cells from CDC by upregulating membrane-bound complement regulatory protein ( mCRPs ) , including CD46 , CD55 and CD59 .
	manualset3
85448	4	398332	5	NULL	NULL	0	NULL	membrane-bound complement regulatory protein ( mCRPs )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that HBXIP contributes to protecting breast cancer cells from CDC by upregulating membrane-bound complement regulatory protein ( mCRPs ) , including CD46 , CD55 and CD59 .
	manualset3
85449	5	398332	5	NULL	NULL	0	NULL	CD46	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that HBXIP contributes to protecting breast cancer cells from CDC by upregulating membrane-bound complement regulatory protein ( mCRPs ) , including CD46 , CD55 and CD59 .
	manualset3
85450	6	398332	5	NULL	NULL	0	NULL	CD55	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that HBXIP contributes to protecting breast cancer cells from CDC by upregulating membrane-bound complement regulatory protein ( mCRPs ) , including CD46 , CD55 and CD59 .
	manualset3
85451	7	398332	5	NULL	NULL	0	NULL	CD59	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that HBXIP contributes to protecting breast cancer cells from CDC by upregulating membrane-bound complement regulatory protein ( mCRPs ) , including CD46 , CD55 and CD59 .
	manualset3
85452	1	398333	5	NULL	NULL	0	NULL	Shank proteins	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that Shank proteins also bind to Homer .
	manualset3
85453	2	398333	5	NULL	NULL	0	NULL	Homer	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that Shank proteins also bind to Homer .
	manualset3
85454	1	398334	5	NULL	NULL	0	NULL	activation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that activation of P2Y ( 2 ) receptors by extracellular UTP inhibits the IGF-I-induced p110alpha-PI3K activation .
	manualset3
85455	2	398334	5	NULL	NULL	0	NULL	P2Y ( 2 ) receptors	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that activation of P2Y ( 2 ) receptors by extracellular UTP inhibits the IGF-I-induced p110alpha-PI3K activation .
	manualset3
85456	3	398334	5	NULL	NULL	0	NULL	extracellular UTP	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that activation of P2Y ( 2 ) receptors by extracellular UTP inhibits the IGF-I-induced p110alpha-PI3K activation .
	manualset3
85457	4	398334	5	NULL	NULL	0	NULL	IGF-I-induced p110alpha-PI3K activation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that activation of P2Y ( 2 ) receptors by extracellular UTP inhibits the IGF-I-induced p110alpha-PI3K activation .
	manualset3
85458	1	398335	5	NULL	NULL	0	NULL	glucose levels	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that glucose levels are significantly lower in bulk tumor specimens than those in normal tissues of the same tissue origins .
	manualset3
85459	2	398335	5	NULL	NULL	0	NULL	bulk tumor specimens	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that glucose levels are significantly lower in bulk tumor specimens than those in normal tissues of the same tissue origins .
	manualset3
85460	3	398335	5	NULL	NULL	0	NULL	normal tissues	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that glucose levels are significantly lower in bulk tumor specimens than those in normal tissues of the same tissue origins .
	manualset3
85461	4	398335	5	NULL	NULL	0	NULL	same tissue origins	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that glucose levels are significantly lower in bulk tumor specimens than those in normal tissues of the same tissue origins .
	manualset3
85462	1	398336	5	NULL	NULL	0	NULL	iPLA ( 2 ) expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that iPLA ( 2 ) expression increases in the vascular tunica media upon carotid artery ligation and that neointima formation is suppressed by genetic deletion of iPLA ( 2 ) or by inhibiting its activity or expression via perivascular delivery of bromoenol lactone or of antisense oligonucleotides , respectively .
	manualset3
85463	2	398336	5	NULL	NULL	0	NULL	vascular tunica media	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that iPLA ( 2 ) expression increases in the vascular tunica media upon carotid artery ligation and that neointima formation is suppressed by genetic deletion of iPLA ( 2 ) or by inhibiting its activity or expression via perivascular delivery of bromoenol lactone or of antisense oligonucleotides , respectively .
	manualset3
85464	3	398336	5	NULL	NULL	0	NULL	carotid artery ligation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that iPLA ( 2 ) expression increases in the vascular tunica media upon carotid artery ligation and that neointima formation is suppressed by genetic deletion of iPLA ( 2 ) or by inhibiting its activity or expression via perivascular delivery of bromoenol lactone or of antisense oligonucleotides , respectively .
	manualset3
85465	4	398336	5	NULL	NULL	0	NULL	neointima formation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that iPLA ( 2 ) expression increases in the vascular tunica media upon carotid artery ligation and that neointima formation is suppressed by genetic deletion of iPLA ( 2 ) or by inhibiting its activity or expression via perivascular delivery of bromoenol lactone or of antisense oligonucleotides , respectively .
	manualset3
85466	5	398336	5	NULL	NULL	NULL	NULL	genetic deletion	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we report that iPLA ( 2 ) expression increases in the vascular tunica media upon carotid artery ligation and that neointima formation is suppressed by genetic deletion of iPLA ( 2 ) or by inhibiting its activity or expression via perivascular delivery of bromoenol lactone or of antisense oligonucleotides , respectively .
	manualset3
85467	7	398336	5	NULL	NULL	NULL	NULL	activity or expression via perivascular delivery	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we report that iPLA ( 2 ) expression increases in the vascular tunica media upon carotid artery ligation and that neointima formation is suppressed by genetic deletion of iPLA ( 2 ) or by inhibiting its activity or expression via perivascular delivery of bromoenol lactone or of antisense oligonucleotides , respectively .
	manualset3
85468	8	398336	5	NULL	NULL	NULL	NULL	bromoenol lactone	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we report that iPLA ( 2 ) expression increases in the vascular tunica media upon carotid artery ligation and that neointima formation is suppressed by genetic deletion of iPLA ( 2 ) or by inhibiting its activity or expression via perivascular delivery of bromoenol lactone or of antisense oligonucleotides , respectively .
	manualset3
85469	9	398336	5	NULL	NULL	NULL	NULL	antisense oligonucleotides	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we report that iPLA ( 2 ) expression increases in the vascular tunica media upon carotid artery ligation and that neointima formation is suppressed by genetic deletion of iPLA ( 2 ) or by inhibiting its activity or expression via perivascular delivery of bromoenol lactone or of antisense oligonucleotides , respectively .
	manualset3
86456	6	398336	5	NULL	NULL	0	NULL	iPLA ( 2 )	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that iPLA ( 2 ) expression increases in the vascular tunica media upon carotid artery ligation and that neointima formation is suppressed by genetic deletion of iPLA ( 2 ) or by inhibiting its activity or expression via perivascular delivery of bromoenol lactone or of antisense oligonucleotides , respectively .
	manualset3
85470	1	398337	5	NULL	NULL	0	NULL	maternally contributed fat facets ( faf ; a homolog of USP9X/FAM )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that maternally contributed fat facets ( faf ; a homolog of USP9X/FAM ) is essential for proper interpretation of the zygotic Decapentaplegic ( Dpp ) morphogen gradient that patterns the embryonic dorsal-ventral axis .
	manualset3
85471	2	398337	5	NULL	NULL	0	NULL	proper interpretation	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that maternally contributed fat facets ( faf ; a homolog of USP9X/FAM ) is essential for proper interpretation of the zygotic Decapentaplegic ( Dpp ) morphogen gradient that patterns the embryonic dorsal-ventral axis .
	manualset3
85479	3	398337	5	NULL	NULL	0	NULL	zygotic Decapentaplegic ( Dpp ) morphogen gradient	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that maternally contributed fat facets ( faf ; a homolog of USP9X/FAM ) is essential for proper interpretation of the zygotic Decapentaplegic ( Dpp ) morphogen gradient that patterns the embryonic dorsal-ventral axis .
	manualset3
85480	4	398337	5	NULL	NULL	0	NULL	embryonic dorsal-ventral axis	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that maternally contributed fat facets ( faf ; a homolog of USP9X/FAM ) is essential for proper interpretation of the zygotic Decapentaplegic ( Dpp ) morphogen gradient that patterns the embryonic dorsal-ventral axis .
	manualset3
85481	1	398338	5	NULL	NULL	0	NULL	nuclear import	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that the nuclear import of the various CtBP proteins and splice isoforms is differentially regulated .
	manualset3
85482	2	398338	5	NULL	NULL	0	NULL	CtBP proteins	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that the nuclear import of the various CtBP proteins and splice isoforms is differentially regulated .
	manualset3
85483	3	398338	5	NULL	NULL	0	NULL	splice isoforms	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that the nuclear import of the various CtBP proteins and splice isoforms is differentially regulated .
	manualset3
85484	1	398339	5	NULL	NULL	0	NULL	type 1 T helper cell-like effector cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that type 1 T helper cell-like effector cells that arose in tumor-bearing hosts progressively expressed programmed death 1 during tumor growth .
	manualset3
85485	2	398339	5	NULL	NULL	0	NULL	tumor-bearing hosts	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that type 1 T helper cell-like effector cells that arose in tumor-bearing hosts progressively expressed programmed death 1 during tumor growth .
	manualset3
85486	3	398339	5	NULL	NULL	0	NULL	programmed death 1	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that type 1 T helper cell-like effector cells that arose in tumor-bearing hosts progressively expressed programmed death 1 during tumor growth .
	manualset3
85487	4	398339	5	NULL	NULL	0	NULL	tumor growth	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report that type 1 T helper cell-like effector cells that arose in tumor-bearing hosts progressively expressed programmed death 1 during tumor growth .
	manualset3
85488	1	398340	5	NULL	NULL	0	NULL	metallo -- lactamase HVO_2763	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report the characterisation of this metallo -- lactamase HVO_2763 in the halophilic archaeon Haloferax volcanii .
	manualset3
85489	2	398340	5	NULL	NULL	0	NULL	halophilic archaeon Haloferax volcanii	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report the characterisation of this metallo -- lactamase HVO_2763 in the halophilic archaeon Haloferax volcanii .
	manualset3
85490	1	398341	5	NULL	NULL	0	NULL	Surgical aspects	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgical aspects of chronic kidney failure and transplantation .
	manualset3
85491	2	398341	5	NULL	NULL	0	NULL	chronic kidney failure	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgical aspects of chronic kidney failure and transplantation .
	manualset3
85492	3	398341	5	NULL	NULL	0	NULL	transplantation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgical aspects of chronic kidney failure and transplantation .
	manualset3
85493	2	398342	5	NULL	NULL	NULL	NULL	novel TCS	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we report the characterization of this novel TCS , designated as RapA1/A2 ( regulation of both actinorhodin and a type I polyketide ) , using genetic and proteomic approaches .
	manualset3
85494	3	398342	5	NULL	NULL	0	NULL	RapA1/A2 ( regulation of both actinorhodin and a type I polyketide )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report the characterization of this novel TCS , designated as RapA1/A2 ( regulation of both actinorhodin and a type I polyketide ) , using genetic and proteomic approaches .
	manualset3
85495	1	398342	5	NULL	NULL	0	NULL	characterization	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report the characterization of this novel TCS , designated as RapA1/A2 ( regulation of both actinorhodin and a type I polyketide ) , using genetic and proteomic approaches .
	manualset3
85496	4	398342	5	NULL	NULL	0	NULL	genetic and proteomic approaches	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report the characterization of this novel TCS , designated as RapA1/A2 ( regulation of both actinorhodin and a type I polyketide ) , using genetic and proteomic approaches .
	manualset3
85497	1	398343	5	NULL	NULL	0	NULL	first study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report the first study of synonymous and nonsynonymous substitution rates on plant sex chromosomes .
	manualset3
85509	2	398343	5	NULL	NULL	NULL	NULL	synonymous and nonsynonymous substitution rates	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we report the first study of synonymous and nonsynonymous substitution rates on plant sex chromosomes .
	manualset3
85510	3	398343	5	NULL	NULL	0	NULL	plant sex chromosomes	Chromosome												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report the first study of synonymous and nonsynonymous substitution rates on plant sex chromosomes .
	manualset3
85512	1	398344	5	NULL	NULL	0	NULL	identification	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report the identification of a new tomato XET gene , LeXET2 , that shows a different spatial expression and diametrically opposite pattern of auxin regulation from LeEXT .
	manualset3
85513	2	398344	5	NULL	NULL	0	NULL	new tomato XET gene , LeXET2	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report the identification of a new tomato XET gene , LeXET2 , that shows a different spatial expression and diametrically opposite pattern of auxin regulation from LeEXT .
	manualset3
85515	3	398344	5	NULL	NULL	0	NULL	different spatial expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report the identification of a new tomato XET gene , LeXET2 , that shows a different spatial expression and diametrically opposite pattern of auxin regulation from LeEXT .
	manualset3
85516	4	398344	5	NULL	NULL	0	NULL	diametrically opposite pattern of auxin regulation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report the identification of a new tomato XET gene , LeXET2 , that shows a different spatial expression and diametrically opposite pattern of auxin regulation from LeEXT .
	manualset3
85517	5	398344	5	NULL	NULL	0	NULL	LeEXT	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we report the identification of a new tomato XET gene , LeXET2 , that shows a different spatial expression and diametrically opposite pattern of auxin regulation from LeEXT .
	manualset3
85518	1	398345	5	NULL	NULL	0	NULL	behavioural and neuroimaging studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we review recent behavioural and neuroimaging studies on adolescent development of the self-concept .
	manualset3
85519	2	398345	5	NULL	NULL	0	NULL	adolescent development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we review recent behavioural and neuroimaging studies on adolescent development of the self-concept .
	manualset3
85520	3	398345	5	NULL	NULL	0	NULL	self-concept	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we review recent behavioural and neuroimaging studies on adolescent development of the self-concept .
	manualset3
85521	1	398346	5	NULL	NULL	0	NULL	molecular pathways	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we review recent insights into the molecular pathways regulating trophoblast lineage segregation , stem cell maintenance , and subtype differentiation .
	manualset3
85522	2	398346	5	NULL	NULL	0	NULL	trophoblast lineage segregation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we review recent insights into the molecular pathways regulating trophoblast lineage segregation , stem cell maintenance , and subtype differentiation .
	manualset3
85523	3	398346	5	NULL	NULL	0	NULL	stem cell maintenance	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we review recent insights into the molecular pathways regulating trophoblast lineage segregation , stem cell maintenance , and subtype differentiation .
	manualset3
85524	4	398346	5	NULL	NULL	0	NULL	subtype differentiation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we review recent insights into the molecular pathways regulating trophoblast lineage segregation , stem cell maintenance , and subtype differentiation .
	manualset3
85533	3	398347	5	NULL	NULL	NULL	NULL	cytokines	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we review the key factors that generate such diversity , as well as the cytokines and transcription factors that are differentially expressed in pathogenic and nonpathogenic Th17 cells .
	manualset3
85534	4	398347	5	NULL	NULL	NULL	NULL	transcription factors	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we review the key factors that generate such diversity , as well as the cytokines and transcription factors that are differentially expressed in pathogenic and nonpathogenic Th17 cells .
	manualset3
85535	5	398347	5	NULL	NULL	NULL	NULL	pathogenic and nonpathogenic Th17 cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we review the key factors that generate such diversity , as well as the cytokines and transcription factors that are differentially expressed in pathogenic and nonpathogenic Th17 cells .
	manualset3
86460	1	398347	5	NULL	NULL	NULL	NULL	key factors	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we review the key factors that generate such diversity , as well as the cytokines and transcription factors that are differentially expressed in pathogenic and nonpathogenic Th17 cells .
	manualset3
86461	2	398347	5	NULL	NULL	NULL	NULL	diversity	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we review the key factors that generate such diversity , as well as the cytokines and transcription factors that are differentially expressed in pathogenic and nonpathogenic Th17 cells .
	manualset3
85537	1	398348	5	NULL	NULL	NULL	NULL	medicinal and industrial applications	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we review the medicinal and industrial applications of saffron .
	manualset3
85576	2	398348	5	NULL	NULL	NULL	NULL	saffron	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we review the medicinal and industrial applications of saffron .
	manualset3
85577	1	398349	5	NULL	NULL	NULL	NULL	 novel biodegradable thermosensitive implant	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we show a novel biodegradable thermosensitive implant composed of poly ( ethylene glycol ) monomethyl ether ( mPEG ) and poly ( lactic-co-glycolic acid ) ( PLGA ) copolymer as a sol-gel drug delivery system for treating bone infection .
	manualset3
85578	2	398349	5	NULL	NULL	0	NULL	poly ( ethylene glycol ) monomethyl ether ( mPEG )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show a novel biodegradable thermosensitive implant composed of poly ( ethylene glycol ) monomethyl ether ( mPEG ) and poly ( lactic-co-glycolic acid ) ( PLGA ) copolymer as a sol-gel drug delivery system for treating bone infection .
	manualset3
85579	3	398349	5	NULL	NULL	0	NULL	poly ( lactic-co-glycolic acid ) ( PLGA ) copolymer	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show a novel biodegradable thermosensitive implant composed of poly ( ethylene glycol ) monomethyl ether ( mPEG ) and poly ( lactic-co-glycolic acid ) ( PLGA ) copolymer as a sol-gel drug delivery system for treating bone infection .
	manualset3
85580	4	398349	5	NULL	NULL	0	NULL	sol-gel drug delivery system	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show a novel biodegradable thermosensitive implant composed of poly ( ethylene glycol ) monomethyl ether ( mPEG ) and poly ( lactic-co-glycolic acid ) ( PLGA ) copolymer as a sol-gel drug delivery system for treating bone infection .
	manualset3
85581	5	398349	5	NULL	NULL	0	NULL	bone infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show a novel biodegradable thermosensitive implant composed of poly ( ethylene glycol ) monomethyl ether ( mPEG ) and poly ( lactic-co-glycolic acid ) ( PLGA ) copolymer as a sol-gel drug delivery system for treating bone infection .
	manualset3
85582	1	398350	5	NULL	NULL	0	NULL	immunofluorescence experiments	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show by immunofluorescence experiments , in cells exposed to ROS , the involvement of MutY glycosylase homolog ( MUTYH ) and DNA pol lambda in the repair of A : 8 - oxo-G mispairs .
	manualset3
85583	2	398350	5	NULL	NULL	0	NULL	cells exposed to ROS	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show by immunofluorescence experiments , in cells exposed to ROS , the involvement of MutY glycosylase homolog ( MUTYH ) and DNA pol lambda in the repair of A : 8 - oxo-G mispairs .
	manualset3
85584	3	398350	5	NULL	NULL	0	NULL	MutY glycosylase homolog ( MUTYH )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show by immunofluorescence experiments , in cells exposed to ROS , the involvement of MutY glycosylase homolog ( MUTYH ) and DNA pol lambda in the repair of A : 8 - oxo-G mispairs .
	manualset3
85585	4	398350	5	NULL	NULL	0	NULL	DNA pol lambda	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show by immunofluorescence experiments , in cells exposed to ROS , the involvement of MutY glycosylase homolog ( MUTYH ) and DNA pol lambda in the repair of A : 8 - oxo-G mispairs .
	manualset3
85586	5	398350	5	NULL	NULL	0	NULL	repair	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show by immunofluorescence experiments , in cells exposed to ROS , the involvement of MutY glycosylase homolog ( MUTYH ) and DNA pol lambda in the repair of A : 8 - oxo-G mispairs .
	manualset3
85587	6	398350	5	NULL	NULL	NULL	NULL	A : 8 - oxo-G mispairs	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we show by immunofluorescence experiments , in cells exposed to ROS , the involvement of MutY glycosylase homolog ( MUTYH ) and DNA pol lambda in the repair of A : 8 - oxo-G mispairs .
	manualset3
85588	1	398351	5	NULL	NULL	0	NULL	Surgical closure	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgical closure of perforations of the palate ( suction perforations ) ) .
	manualset3
85589	2	398351	5	NULL	NULL	0	NULL	perforations of the palate ( suction perforations )	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgical closure of perforations of the palate ( suction perforations ) ) .
	manualset3
85590	1	398352	5	NULL	NULL	0	NULL	elevated mutation levels	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show elevated mutation levels in single cells from Drosophila melanogaster S2 and mouse embryonic fibroblast populations after treatment with the powerful mutagen N-ethyl-N-nitrosourea .
	manualset3
85591	2	398352	5	NULL	NULL	NULL	NULL	single cells from Drosophila melanogaster S2	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we show elevated mutation levels in single cells from Drosophila melanogaster S2 and mouse embryonic fibroblast populations after treatment with the powerful mutagen N-ethyl-N-nitrosourea .
	manualset3
85592	3	398352	5	NULL	NULL	NULL	NULL	mouse embryonic fibroblast populations	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we show elevated mutation levels in single cells from Drosophila melanogaster S2 and mouse embryonic fibroblast populations after treatment with the powerful mutagen N-ethyl-N-nitrosourea .
	manualset3
85593	4	398352	5	NULL	NULL	0	NULL	treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show elevated mutation levels in single cells from Drosophila melanogaster S2 and mouse embryonic fibroblast populations after treatment with the powerful mutagen N-ethyl-N-nitrosourea .
	manualset3
85594	5	398352	5	NULL	NULL	0	NULL	powerful mutagen N-ethyl-N-nitrosourea	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show elevated mutation levels in single cells from Drosophila melanogaster S2 and mouse embryonic fibroblast populations after treatment with the powerful mutagen N-ethyl-N-nitrosourea .
	manualset3
85595	1	398353	5	NULL	NULL	0	NULL	possession	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that , paradoxically , possession of the varepsilon4 allele confers a cognitive advantage on tasks mediated by the frontal lobe , and that young carriers of the varepsilon4 allele show larger cognitive benefit from procholinergic nicotinic stimulation .
	manualset3
85596	2	398353	5	NULL	NULL	0	NULL	varepsilon4 allele	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that , paradoxically , possession of the varepsilon4 allele confers a cognitive advantage on tasks mediated by the frontal lobe , and that young carriers of the varepsilon4 allele show larger cognitive benefit from procholinergic nicotinic stimulation .
	manualset3
85597	3	398353	5	NULL	NULL	0	NULL	cognitive advantage	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that , paradoxically , possession of the varepsilon4 allele confers a cognitive advantage on tasks mediated by the frontal lobe , and that young carriers of the varepsilon4 allele show larger cognitive benefit from procholinergic nicotinic stimulation .
	manualset3
85598	4	398353	5	NULL	NULL	0	NULL	frontal lobe	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that , paradoxically , possession of the varepsilon4 allele confers a cognitive advantage on tasks mediated by the frontal lobe , and that young carriers of the varepsilon4 allele show larger cognitive benefit from procholinergic nicotinic stimulation .
	manualset3
85599	5	398353	5	NULL	NULL	0	NULL	young carriers of the varepsilon4 allele	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that , paradoxically , possession of the varepsilon4 allele confers a cognitive advantage on tasks mediated by the frontal lobe , and that young carriers of the varepsilon4 allele show larger cognitive benefit from procholinergic nicotinic stimulation .
	manualset3
85600	6	398353	5	NULL	NULL	0	NULL	cognitive benefit	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that , paradoxically , possession of the varepsilon4 allele confers a cognitive advantage on tasks mediated by the frontal lobe , and that young carriers of the varepsilon4 allele show larger cognitive benefit from procholinergic nicotinic stimulation .
	manualset3
85601	7	398353	5	NULL	NULL	0	NULL	 procholinergic nicotinic stimulation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that , paradoxically , possession of the varepsilon4 allele confers a cognitive advantage on tasks mediated by the frontal lobe , and that young carriers of the varepsilon4 allele show larger cognitive benefit from procholinergic nicotinic stimulation .
	manualset3
86484	8	398353	5	NULL	NULL	0	NULL	tasks	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that , paradoxically , possession of the varepsilon4 allele confers a cognitive advantage on tasks mediated by the frontal lobe , and that young carriers of the varepsilon4 allele show larger cognitive benefit from procholinergic nicotinic stimulation .
	manualset3
85602	1	398354	5	NULL	NULL	0	NULL	viewing of natural scenes	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that during viewing of natural scenes , microscopic eye movements carry out a crucial information-processing step : they remove predictable correlations in natural scenes by equalizing the spatial power of the retinal image within the frequency range of ganglion cells ' peak sensitivity .
	manualset3
85603	2	398354	5	NULL	NULL	0	NULL	microscopic eye movements	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that during viewing of natural scenes , microscopic eye movements carry out a crucial information-processing step : they remove predictable correlations in natural scenes by equalizing the spatial power of the retinal image within the frequency range of ganglion cells ' peak sensitivity .
	manualset3
85604	3	398354	5	NULL	NULL	NULL	NULL	information-processing step	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we show that during viewing of natural scenes , microscopic eye movements carry out a crucial information-processing step : they remove predictable correlations in natural scenes by equalizing the spatial power of the retinal image within the frequency range of ganglion cells ' peak sensitivity .
	manualset3
85605	4	398354	5	NULL	NULL	NULL	NULL	predictable correlations	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we show that during viewing of natural scenes , microscopic eye movements carry out a crucial information-processing step : they remove predictable correlations in natural scenes by equalizing the spatial power of the retinal image within the frequency range of ganglion cells ' peak sensitivity .
	manualset3
86398	5	398354	5	NULL	NULL	0	NULL	spatial power of the retinal image	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that during viewing of natural scenes , microscopic eye movements carry out a crucial information-processing step : they remove predictable correlations in natural scenes by equalizing the spatial power of the retinal image within the frequency range of ganglion cells ' peak sensitivity .
	manualset3
86399	6	398354	5	NULL	NULL	0	NULL	frequency range	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that during viewing of natural scenes , microscopic eye movements carry out a crucial information-processing step : they remove predictable correlations in natural scenes by equalizing the spatial power of the retinal image within the frequency range of ganglion cells ' peak sensitivity .
	manualset3
86400	7	398354	5	NULL	NULL	0	NULL	ganglion cells ' peak sensitivity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that during viewing of natural scenes , microscopic eye movements carry out a crucial information-processing step : they remove predictable correlations in natural scenes by equalizing the spatial power of the retinal image within the frequency range of ganglion cells ' peak sensitivity .
	manualset3
85626	1	398355	5	NULL	NULL	NULL	NULL	endogenous mp53 knockdown	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we show that endogenous mp53 knockdown enhanced cell migration and phosphorylation of ERK in DU145 prostate cancer cells .
	manualset3
85627	3	398355	5	NULL	NULL	NULL	NULL	phosphorylation of ERK	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we show that endogenous mp53 knockdown enhanced cell migration and phosphorylation of ERK in DU145 prostate cancer cells .
	manualset3
85628	4	398355	5	NULL	NULL	NULL	NULL	DU145 prostate cancer cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we show that endogenous mp53 knockdown enhanced cell migration and phosphorylation of ERK in DU145 prostate cancer cells .
	manualset3
85629	2	398355	5	NULL	NULL	0	NULL	cell migration	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that endogenous mp53 knockdown enhanced cell migration and phosphorylation of ERK in DU145 prostate cancer cells .
	manualset3
85607	1	398356	5	NULL	NULL	NULL	NULL	mPTP opening	AnatomicalPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we show that mPTP opening acts as an initiating event to stimulate Bax translocation to mitochondria .
	manualset3
85608	2	398356	5	NULL	NULL	0	NULL	initiating event	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that mPTP opening acts as an initiating event to stimulate Bax translocation to mitochondria .
	manualset3
85609	3	398356	5	NULL	NULL	0	NULL	Bax translocation to mitochondria	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that mPTP opening acts as an initiating event to stimulate Bax translocation to mitochondria .
	manualset3
85610	1	398357	5	NULL	NULL	0	NULL	mda-7	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that mda-7 and IL-19 bind to the previously described IL-20R complex , composed by cytokine receptor family 2-8 / IL-20Ralpha and DIRS1/IL -20 Rbeta ( type I IL-20R ) .
	manualset3
85611	2	398357	5	NULL	NULL	0	NULL	IL-19	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that mda-7 and IL-19 bind to the previously described IL-20R complex , composed by cytokine receptor family 2-8 / IL-20Ralpha and DIRS1/IL -20 Rbeta ( type I IL-20R ) .
	manualset3
85612	3	398357	5	NULL	NULL	0	NULL	IL-20R complex	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that mda-7 and IL-19 bind to the previously described IL-20R complex , composed by cytokine receptor family 2-8 / IL-20Ralpha and DIRS1/IL -20 Rbeta ( type I IL-20R ) .
	manualset3
85613	4	398357	5	NULL	NULL	0	NULL	cytokine receptor family 2-8 / IL-20Ralpha	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that mda-7 and IL-19 bind to the previously described IL-20R complex , composed by cytokine receptor family 2-8 / IL-20Ralpha and DIRS1/IL -20 Rbeta ( type I IL-20R ) .
	manualset3
85614	5	398357	5	NULL	NULL	0	NULL	DIRS1/IL -20 Rbeta ( type I IL-20R )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that mda-7 and IL-19 bind to the previously described IL-20R complex , composed by cytokine receptor family 2-8 / IL-20Ralpha and DIRS1/IL -20 Rbeta ( type I IL-20R ) .
	manualset3
85615	1	398358	5	NULL	NULL	0	NULL	semaphorin 3A ( Sema3A ) expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that semaphorin 3A ( Sema3A ) expression overcomes the proinvasive and prometastatic resistance observed upon angiogenesis reduction by the small-molecule tyrosine inhibitor sunitinib in both pancreatic neuroendocrine tumors ( PNETs ) in RIP-Tag2 mice and cervical carcinomas in HPV16/E2 mice .
	manualset3
85616	2	398358	5	NULL	NULL	NULL	NULL	proinvasive and prometastatic resistance	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we show that semaphorin 3A ( Sema3A ) expression overcomes the proinvasive and prometastatic resistance observed upon angiogenesis reduction by the small-molecule tyrosine inhibitor sunitinib in both pancreatic neuroendocrine tumors ( PNETs ) in RIP-Tag2 mice and cervical carcinomas in HPV16/E2 mice .
	manualset3
85617	3	398358	5	NULL	NULL	NULL	NULL	angiogenesis reduction	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we show that semaphorin 3A ( Sema3A ) expression overcomes the proinvasive and prometastatic resistance observed upon angiogenesis reduction by the small-molecule tyrosine inhibitor sunitinib in both pancreatic neuroendocrine tumors ( PNETs ) in RIP-Tag2 mice and cervical carcinomas in HPV16/E2 mice .
	manualset3
85618	4	398358	5	NULL	NULL	0	NULL	 small-molecule tyrosine inhibitor sunitinib	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that semaphorin 3A ( Sema3A ) expression overcomes the proinvasive and prometastatic resistance observed upon angiogenesis reduction by the small-molecule tyrosine inhibitor sunitinib in both pancreatic neuroendocrine tumors ( PNETs ) in RIP-Tag2 mice and cervical carcinomas in HPV16/E2 mice .
	manualset3
85619	5	398358	5	NULL	NULL	0	NULL	pancreatic neuroendocrine tumors ( PNETs )	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that semaphorin 3A ( Sema3A ) expression overcomes the proinvasive and prometastatic resistance observed upon angiogenesis reduction by the small-molecule tyrosine inhibitor sunitinib in both pancreatic neuroendocrine tumors ( PNETs ) in RIP-Tag2 mice and cervical carcinomas in HPV16/E2 mice .
	manualset3
85620	6	398358	5	NULL	NULL	0	NULL	RIP-Tag2 mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that semaphorin 3A ( Sema3A ) expression overcomes the proinvasive and prometastatic resistance observed upon angiogenesis reduction by the small-molecule tyrosine inhibitor sunitinib in both pancreatic neuroendocrine tumors ( PNETs ) in RIP-Tag2 mice and cervical carcinomas in HPV16/E2 mice .
	manualset3
85621	7	398358	5	NULL	NULL	0	NULL	cervical carcinomas	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that semaphorin 3A ( Sema3A ) expression overcomes the proinvasive and prometastatic resistance observed upon angiogenesis reduction by the small-molecule tyrosine inhibitor sunitinib in both pancreatic neuroendocrine tumors ( PNETs ) in RIP-Tag2 mice and cervical carcinomas in HPV16/E2 mice .
	manualset3
85622	8	398358	5	NULL	NULL	0	NULL	HPV16/E2 mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that semaphorin 3A ( Sema3A ) expression overcomes the proinvasive and prometastatic resistance observed upon angiogenesis reduction by the small-molecule tyrosine inhibitor sunitinib in both pancreatic neuroendocrine tumors ( PNETs ) in RIP-Tag2 mice and cervical carcinomas in HPV16/E2 mice .
	manualset3
85623	1	398359	5	NULL	NULL	0	NULL	catenin pathway	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the - catenin pathway is active in the limb-forming area in mouse embryos .
	manualset3
85624	2	398359	5	NULL	NULL	0	NULL	limb-forming area	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the - catenin pathway is active in the limb-forming area in mouse embryos .
	manualset3
85625	3	398359	5	NULL	NULL	0	NULL	mouse embryos	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the - catenin pathway is active in the limb-forming area in mouse embryos .
	manualset3
85660	1	398360	5	NULL	NULL	0	NULL	HSCs	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the HSCs from the embryonic aorta are the most potently supported HSCs in UG stromal clone co-cultures and that contact is required for the maintenance and expansion of embryo-derived HSCs .
	manualset3
85661	2	398360	5	NULL	NULL	0	NULL	embryonic aorta	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the HSCs from the embryonic aorta are the most potently supported HSCs in UG stromal clone co-cultures and that contact is required for the maintenance and expansion of embryo-derived HSCs .
	manualset3
85662	3	398360	5	NULL	NULL	0	NULL	HSCs	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the HSCs from the embryonic aorta are the most potently supported HSCs in UG stromal clone co-cultures and that contact is required for the maintenance and expansion of embryo-derived HSCs .
	manualset3
85664	4	398360	5	NULL	NULL	0	NULL	UG stromal clone co-cultures	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the HSCs from the embryonic aorta are the most potently supported HSCs in UG stromal clone co-cultures and that contact is required for the maintenance and expansion of embryo-derived HSCs .
	manualset3
85666	5	398360	5	NULL	NULL	0	NULL	maintenance and expansion of embryo-derived HSCs	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the HSCs from the embryonic aorta are the most potently supported HSCs in UG stromal clone co-cultures and that contact is required for the maintenance and expansion of embryo-derived HSCs .
	manualset3
85670	1	398361	5	NULL	NULL	0	NULL	allogeneic stimulation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the allogeneic stimulation also induces the appearance in the low molecular weight fraction of the serum ( 1000-110 , 000 MW ) of an inhibitor which blocks the PBA activity of the complex without affecting the PBA activity of LPS or dextran sulphate .
	manualset3
85674	2	398361	5	NULL	NULL	0	NULL	appearance	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the allogeneic stimulation also induces the appearance in the low molecular weight fraction of the serum ( 1000-110 , 000 MW ) of an inhibitor which blocks the PBA activity of the complex without affecting the PBA activity of LPS or dextran sulphate .
	manualset3
85675	3	398361	5	NULL	NULL	0	NULL	low molecular weight fraction of the serum ( 1000-110 , 000 MW )	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the allogeneic stimulation also induces the appearance in the low molecular weight fraction of the serum ( 1000-110 , 000 MW ) of an inhibitor which blocks the PBA activity of the complex without affecting the PBA activity of LPS or dextran sulphate .
	manualset3
85677	4	398361	5	NULL	NULL	0	NULL	inhibitor	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the allogeneic stimulation also induces the appearance in the low molecular weight fraction of the serum ( 1000-110 , 000 MW ) of an inhibitor which blocks the PBA activity of the complex without affecting the PBA activity of LPS or dextran sulphate .
	manualset3
85679	5	398361	5	NULL	NULL	0	NULL	PBA activity of the complex	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the allogeneic stimulation also induces the appearance in the low molecular weight fraction of the serum ( 1000-110 , 000 MW ) of an inhibitor which blocks the PBA activity of the complex without affecting the PBA activity of LPS or dextran sulphate .
	manualset3
85697	6	398361	5	NULL	NULL	0	NULL	PBA activity of LPS or dextran sulphate	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the allogeneic stimulation also induces the appearance in the low molecular weight fraction of the serum ( 1000-110 , 000 MW ) of an inhibitor which blocks the PBA activity of the complex without affecting the PBA activity of LPS or dextran sulphate .
	manualset3
85698	1	398362	5	NULL	NULL	0	NULL	Surgical indications	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgical indications in ileus ) .
	manualset3
85699	2	398362	5	NULL	NULL	0	NULL	ileus	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgical indications in ileus ) .
	manualset3
85939	1	398363	5	NULL	NULL	0	NULL	coexpression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the coexpression of another HCMV glycoprotein , gO , with gH/gL in human fibroblasts interferes with HCMV entry into fibroblasts but not epithelial cells .
	manualset3
85940	2	398363	5	NULL	NULL	0	NULL	HCMV glycoprotein , gO	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the coexpression of another HCMV glycoprotein , gO , with gH/gL in human fibroblasts interferes with HCMV entry into fibroblasts but not epithelial cells .
	manualset3
85941	3	398363	5	NULL	NULL	0	NULL	gH/gL	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the coexpression of another HCMV glycoprotein , gO , with gH/gL in human fibroblasts interferes with HCMV entry into fibroblasts but not epithelial cells .
	manualset3
85942	4	398363	5	NULL	NULL	0	NULL	human fibroblasts	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the coexpression of another HCMV glycoprotein , gO , with gH/gL in human fibroblasts interferes with HCMV entry into fibroblasts but not epithelial cells .
	manualset3
85943	5	398363	5	NULL	NULL	0	NULL	HCMV	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the coexpression of another HCMV glycoprotein , gO , with gH/gL in human fibroblasts interferes with HCMV entry into fibroblasts but not epithelial cells .
	manualset3
85944	6	398363	5	NULL	NULL	0	NULL	fibroblasts	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the coexpression of another HCMV glycoprotein , gO , with gH/gL in human fibroblasts interferes with HCMV entry into fibroblasts but not epithelial cells .
	manualset3
85945	7	398363	5	NULL	NULL	0	NULL	epithelial cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the coexpression of another HCMV glycoprotein , gO , with gH/gL in human fibroblasts interferes with HCMV entry into fibroblasts but not epithelial cells .
	manualset3
85946	1	398364	5	NULL	NULL	0	NULL	decreased FA synthesis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the decreased FA synthesis in liver is balanced by an equal increase in nonhepatic tissues , primarily adipose tissue .
	manualset3
85947	2	398364	5	NULL	NULL	0	NULL	liver	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the decreased FA synthesis in liver is balanced by an equal increase in nonhepatic tissues , primarily adipose tissue .
	manualset3
85948	3	398364	5	NULL	NULL	0	NULL	nonhepatic tissues	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the decreased FA synthesis in liver is balanced by an equal increase in nonhepatic tissues , primarily adipose tissue .
	manualset3
85949	4	398364	5	NULL	NULL	0	NULL	adipose tissue	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the decreased FA synthesis in liver is balanced by an equal increase in nonhepatic tissues , primarily adipose tissue .
	manualset3
85950	1	398365	5	NULL	NULL	0	NULL	interleukin-1 receptor-associated kinase ( IRAK ) / Pelle-like kinase gene SHORT SUSPENSOR ( SSP )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the interleukin-1 receptor-associated kinase ( IRAK ) / Pelle-like kinase gene SHORT SUSPENSOR ( SSP ) regulates this pathway through a previously unknown parent-of-origin effect .
	manualset3
85951	2	398365	5	NULL	NULL	0	NULL	pathway	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the interleukin-1 receptor-associated kinase ( IRAK ) / Pelle-like kinase gene SHORT SUSPENSOR ( SSP ) regulates this pathway through a previously unknown parent-of-origin effect .
	manualset3
85952	3	398365	5	NULL	NULL	0	NULL	parent-of-origin effect	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we show that the interleukin-1 receptor-associated kinase ( IRAK ) / Pelle-like kinase gene SHORT SUSPENSOR ( SSP ) regulates this pathway through a previously unknown parent-of-origin effect .
	manualset3
85953	1	398366	5	NULL	NULL	0	NULL	gene expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we sought to identify gene expression in the medial prefrontal cortex ( mPFC ) of mice associated with PPI using a laser microdissection and microarray analysis-based approach .
	manualset3
85954	2	398366	5	NULL	NULL	0	NULL	medial prefrontal cortex ( mPFC )	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we sought to identify gene expression in the medial prefrontal cortex ( mPFC ) of mice associated with PPI using a laser microdissection and microarray analysis-based approach .
	manualset3
85955	3	398366	5	NULL	NULL	0	NULL	mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we sought to identify gene expression in the medial prefrontal cortex ( mPFC ) of mice associated with PPI using a laser microdissection and microarray analysis-based approach .
	manualset3
85956	4	398366	5	NULL	NULL	0	NULL	PPI	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we sought to identify gene expression in the medial prefrontal cortex ( mPFC ) of mice associated with PPI using a laser microdissection and microarray analysis-based approach .
	manualset3
85957	5	398366	5	NULL	NULL	0	NULL	laser microdissection	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we sought to identify gene expression in the medial prefrontal cortex ( mPFC ) of mice associated with PPI using a laser microdissection and microarray analysis-based approach .
	manualset3
85958	6	398366	5	NULL	NULL	0	NULL	microarray analysis-based approach	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we sought to identify gene expression in the medial prefrontal cortex ( mPFC ) of mice associated with PPI using a laser microdissection and microarray analysis-based approach .
	manualset3
85959	1	398367	5	NULL	NULL	0	NULL	intracellular localisation of siRNA and Argonaute 2 ( Ago2 )	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we studied the intracellular localisation of siRNA and Argonaute 2 ( Ago2 ) , the major component of the RNA interference ( RNAi ) machinery , by density gradient centrifugation and fluorescence microscopy after PS-stimulated delivery or transfection with Lipofectamine 2000 .
	manualset3
85960	2	398367	5	NULL	NULL	0	NULL	RNA interference ( RNAi ) machinery	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we studied the intracellular localisation of siRNA and Argonaute 2 ( Ago2 ) , the major component of the RNA interference ( RNAi ) machinery , by density gradient centrifugation and fluorescence microscopy after PS-stimulated delivery or transfection with Lipofectamine 2000 .
	manualset3
85961	3	398367	5	NULL	NULL	0	NULL	density gradient centrifugation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we studied the intracellular localisation of siRNA and Argonaute 2 ( Ago2 ) , the major component of the RNA interference ( RNAi ) machinery , by density gradient centrifugation and fluorescence microscopy after PS-stimulated delivery or transfection with Lipofectamine 2000 .
	manualset3
85962	4	398367	5	NULL	NULL	0	NULL	fluorescence microscopy	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we studied the intracellular localisation of siRNA and Argonaute 2 ( Ago2 ) , the major component of the RNA interference ( RNAi ) machinery , by density gradient centrifugation and fluorescence microscopy after PS-stimulated delivery or transfection with Lipofectamine 2000 .
	manualset3
85963	5	398367	5	NULL	NULL	0	NULL	PS-stimulated delivery	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we studied the intracellular localisation of siRNA and Argonaute 2 ( Ago2 ) , the major component of the RNA interference ( RNAi ) machinery , by density gradient centrifugation and fluorescence microscopy after PS-stimulated delivery or transfection with Lipofectamine 2000 .
	manualset3
85964	6	398367	5	NULL	NULL	0	NULL	transfection with Lipofectamine 2000	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we studied the intracellular localisation of siRNA and Argonaute 2 ( Ago2 ) , the major component of the RNA interference ( RNAi ) machinery , by density gradient centrifugation and fluorescence microscopy after PS-stimulated delivery or transfection with Lipofectamine 2000 .
	manualset3
85965	1	398368	5	NULL	NULL	0	NULL	 hypothesis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we test the hypothesis that BMSCs suppress immune responses by Fas-mediated apoptosis of activated lymphocytes and find both Fas and FasL expression by primary BMSCs .
	manualset3
85966	2	398368	5	NULL	NULL	0	NULL	BMSCs	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we test the hypothesis that BMSCs suppress immune responses by Fas-mediated apoptosis of activated lymphocytes and find both Fas and FasL expression by primary BMSCs .
	manualset3
85967	3	398368	5	NULL	NULL	0	NULL	immune responses	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we test the hypothesis that BMSCs suppress immune responses by Fas-mediated apoptosis of activated lymphocytes and find both Fas and FasL expression by primary BMSCs .
	manualset3
85968	4	398368	5	NULL	NULL	0	NULL	Fas-mediated apoptosis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we test the hypothesis that BMSCs suppress immune responses by Fas-mediated apoptosis of activated lymphocytes and find both Fas and FasL expression by primary BMSCs .
	manualset3
85969	5	398368	5	NULL	NULL	0	NULL	activated lymphocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we test the hypothesis that BMSCs suppress immune responses by Fas-mediated apoptosis of activated lymphocytes and find both Fas and FasL expression by primary BMSCs .
	manualset3
85970	6	398368	5	NULL	NULL	0	NULL	Fas and FasL expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we test the hypothesis that BMSCs suppress immune responses by Fas-mediated apoptosis of activated lymphocytes and find both Fas and FasL expression by primary BMSCs .
	manualset3
85971	7	398368	5	NULL	NULL	0	NULL	primary BMSCs	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we test the hypothesis that BMSCs suppress immune responses by Fas-mediated apoptosis of activated lymphocytes and find both Fas and FasL expression by primary BMSCs .
	manualset3
85972	1	398369	5	NULL	NULL	0	NULL	NIRS	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we tested the applicability of imaging NIRS to the discrimination of cryptic species by using the ants Tetramorium caespitum and T. impurum .
	manualset3
85973	2	398369	5	NULL	NULL	0	NULL	discrimination of cryptic species	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we tested the applicability of imaging NIRS to the discrimination of cryptic species by using the ants Tetramorium caespitum and T. impurum .
	manualset3
85974	3	398369	5	NULL	NULL	0	NULL	ants Tetramorium caespitum	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we tested the applicability of imaging NIRS to the discrimination of cryptic species by using the ants Tetramorium caespitum and T. impurum .
	manualset3
85975	4	398369	5	NULL	NULL	0	NULL	T. impurum	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we tested the applicability of imaging NIRS to the discrimination of cryptic species by using the ants Tetramorium caespitum and T. impurum .
	manualset3
85976	1	398370	5	NULL	NULL	0	NULL	 rodent model	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we use a rodent model of an aversive cue-induced cessation of feeding .
	manualset3
85977	2	398370	5	NULL	NULL	0	NULL	aversive cue-induced cessation of feeding	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we use a rodent model of an aversive cue-induced cessation of feeding .
	manualset3
85978	1	398371	5	NULL	NULL	NULL	NULL	acute in vivo genetic manipulation of synaptic proteins	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we use acute in vivo genetic manipulation of synaptic proteins to investigate the molecular basis for presynaptic long-term potentiation ( LTP ) at hippocampal mossy fiber synapses .
	manualset3
85979	2	398371	5	NULL	NULL	0	NULL	presynaptic long-term potentiation ( LTP )	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we use acute in vivo genetic manipulation of synaptic proteins to investigate the molecular basis for presynaptic long-term potentiation ( LTP ) at hippocampal mossy fiber synapses .
	manualset3
85980	3	398371	5	NULL	NULL	0	NULL	hippocampal mossy fiber synapses	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we use acute in vivo genetic manipulation of synaptic proteins to investigate the molecular basis for presynaptic long-term potentiation ( LTP ) at hippocampal mossy fiber synapses .
	manualset3
85981	1	398372	5	NULL	NULL	0	NULL	chemical probing	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we use chemical probing to show that interaction sites with the 40S subunit and eIF3 are conserved between HCV and HCV-like IRESs .
	manualset3
85982	2	398372	5	NULL	NULL	NULL	NULL	interaction sites with the 40S subunit and eIF3	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we use chemical probing to show that interaction sites with the 40S subunit and eIF3 are conserved between HCV and HCV-like IRESs .
	manualset3
85983	3	398372	5	NULL	NULL	NULL	NULL	HCV	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we use chemical probing to show that interaction sites with the 40S subunit and eIF3 are conserved between HCV and HCV-like IRESs .
	manualset3
87582	4	398372	5	NULL	NULL	0	NULL	HCV-like IRESs	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we use chemical probing to show that interaction sites with the 40S subunit and eIF3 are conserved between HCV and HCV-like IRESs .
	manualset3
85984	1	398373	5	NULL	NULL	NULL	NULL	Surgical protocol	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Surgical protocol and intraoperative considerations in interventions on the testis ) .
	manualset3
85985	3	398373	5	NULL	NULL	NULL	NULL	interventions on the testis	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Surgical protocol and intraoperative considerations in interventions on the testis ) .
	manualset3
86485	2	398373	5	NULL	NULL	NULL	NULL	intraoperative considerations	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Surgical protocol and intraoperative considerations in interventions on the testis ) .
	manualset3
85986	1	398374	5	NULL	NULL	0	NULL	precursor ion scanning MS	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we use precursor ion scanning MS to identify five previously unknown sites in MSK1 : Thr630 , Ser647 , Ser657 , Ser695 and Thr700 .
	manualset3
85987	2	398374	5	NULL	NULL	0	NULL	MSK1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we use precursor ion scanning MS to identify five previously unknown sites in MSK1 : Thr630 , Ser647 , Ser657 , Ser695 and Thr700 .
	manualset3
85988	3	398374	5	NULL	NULL	0	NULL	Thr630	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we use precursor ion scanning MS to identify five previously unknown sites in MSK1 : Thr630 , Ser647 , Ser657 , Ser695 and Thr700 .
	manualset3
85989	4	398374	5	NULL	NULL	0	NULL	Ser647	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we use precursor ion scanning MS to identify five previously unknown sites in MSK1 : Thr630 , Ser647 , Ser657 , Ser695 and Thr700 .
	manualset3
85990	5	398374	5	NULL	NULL	0	NULL	Ser657	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we use precursor ion scanning MS to identify five previously unknown sites in MSK1 : Thr630 , Ser647 , Ser657 , Ser695 and Thr700 .
	manualset3
85991	6	398374	5	NULL	NULL	0	NULL	Ser695	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we use precursor ion scanning MS to identify five previously unknown sites in MSK1 : Thr630 , Ser647 , Ser657 , Ser695 and Thr700 .
	manualset3
85992	7	398374	5	NULL	NULL	0	NULL	Thr700	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we use precursor ion scanning MS to identify five previously unknown sites in MSK1 : Thr630 , Ser647 , Ser657 , Ser695 and Thr700 .
	manualset3
85993	2	398375	5	NULL	NULL	NULL	NULL	non-cellular solid-state compartment	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we will focus on studies concerning a common theme , which is the central importance of the non-cellular solid-state compartment as a master regulator of the malignant phenotype .
	manualset3
85994	3	398375	5	NULL	NULL	NULL	NULL	master regulator	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we will focus on studies concerning a common theme , which is the central importance of the non-cellular solid-state compartment as a master regulator of the malignant phenotype .
	manualset3
85995	4	398375	5	NULL	NULL	NULL	NULL	malignant phenotype	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here , we will focus on studies concerning a common theme , which is the central importance of the non-cellular solid-state compartment as a master regulator of the malignant phenotype .
	manualset3
86401	1	398375	5	NULL	NULL	0	NULL	studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here , we will focus on studies concerning a common theme , which is the central importance of the non-cellular solid-state compartment as a master regulator of the malignant phenotype .
	manualset3
85996	1	398376	5	NULL	NULL	NULL	NULL	physiological field , immunology	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here I show that one physiological field , immunology , offers a theory that makes possible a biological individuation based on physiological grounds .
	manualset3
85997	2	398376	5	NULL	NULL	0	NULL	theory	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Here I show that one physiological field , immunology , offers a theory that makes possible a biological individuation based on physiological grounds .
	manualset3
86340	3	398376	5	NULL	NULL	0	NULL	biological individuation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here I show that one physiological field , immunology , offers a theory that makes possible a biological individuation based on physiological grounds .
	manualset3
86402	4	398376	5	NULL	NULL	0	NULL	physiological grounds	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here I show that one physiological field , immunology , offers a theory that makes possible a biological individuation based on physiological grounds .
	manualset3
85998	1	398377	5	NULL	NULL	0	NULL	chimeric model system	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here a chimeric model system consisting of human cytochrome P450 3A4 and the soluble reductase domain of CYP102A1 from Bacillus megaterium ( BMR ) is used to study the relationship between electron transfer and the coupling efficiency in substrate monoxygenation .
	manualset3
85999	2	398377	5	NULL	NULL	0	NULL	human cytochrome P450 3A4	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here a chimeric model system consisting of human cytochrome P450 3A4 and the soluble reductase domain of CYP102A1 from Bacillus megaterium ( BMR ) is used to study the relationship between electron transfer and the coupling efficiency in substrate monoxygenation .
	manualset3
86000	3	398377	5	NULL	NULL	0	NULL	soluble reductase domain of CYP102A1	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here a chimeric model system consisting of human cytochrome P450 3A4 and the soluble reductase domain of CYP102A1 from Bacillus megaterium ( BMR ) is used to study the relationship between electron transfer and the coupling efficiency in substrate monoxygenation .
	manualset3
86001	4	398377	5	NULL	NULL	0	NULL	Bacillus megaterium ( BMR )	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here a chimeric model system consisting of human cytochrome P450 3A4 and the soluble reductase domain of CYP102A1 from Bacillus megaterium ( BMR ) is used to study the relationship between electron transfer and the coupling efficiency in substrate monoxygenation .
	manualset3
86002	5	398377	5	NULL	NULL	0	NULL	relationship	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	Here a chimeric model system consisting of human cytochrome P450 3A4 and the soluble reductase domain of CYP102A1 from Bacillus megaterium ( BMR ) is used to study the relationship between electron transfer and the coupling efficiency in substrate monoxygenation .
	manualset3
86003	6	398377	5	NULL	NULL	NULL	NULL	electron transfer	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here a chimeric model system consisting of human cytochrome P450 3A4 and the soluble reductase domain of CYP102A1 from Bacillus megaterium ( BMR ) is used to study the relationship between electron transfer and the coupling efficiency in substrate monoxygenation .
	manualset3
86486	7	398377	5	NULL	NULL	0	NULL	coupling efficiency	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here a chimeric model system consisting of human cytochrome P450 3A4 and the soluble reductase domain of CYP102A1 from Bacillus megaterium ( BMR ) is used to study the relationship between electron transfer and the coupling efficiency in substrate monoxygenation .
	manualset3
86487	8	398377	5	NULL	NULL	0	NULL	 substrate monoxygenation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here a chimeric model system consisting of human cytochrome P450 3A4 and the soluble reductase domain of CYP102A1 from Bacillus megaterium ( BMR ) is used to study the relationship between electron transfer and the coupling efficiency in substrate monoxygenation .
	manualset3
86004	1	398378	5	NULL	NULL	0	NULL	transparietojejunal endoscopic investigation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here a transparietojejunal endoscopic investigation is proposed that permits direct sight of the anastomosis , biliary sampling for cultural examination and dilatative type therapeutic maneuvers , biopsies or extractions of residual stones from the bile ways that would not otherwise be possible without further surgery .
	manualset3
86005	2	398378	5	NULL	NULL	NULL	NULL	direct sight of the anastomosis	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here a transparietojejunal endoscopic investigation is proposed that permits direct sight of the anastomosis , biliary sampling for cultural examination and dilatative type therapeutic maneuvers , biopsies or extractions of residual stones from the bile ways that would not otherwise be possible without further surgery .
	manualset3
86006	3	398378	5	NULL	NULL	0	NULL	biliary sampling	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here a transparietojejunal endoscopic investigation is proposed that permits direct sight of the anastomosis , biliary sampling for cultural examination and dilatative type therapeutic maneuvers , biopsies or extractions of residual stones from the bile ways that would not otherwise be possible without further surgery .
	manualset3
86007	4	398378	5	NULL	NULL	0	NULL	cultural examination	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here a transparietojejunal endoscopic investigation is proposed that permits direct sight of the anastomosis , biliary sampling for cultural examination and dilatative type therapeutic maneuvers , biopsies or extractions of residual stones from the bile ways that would not otherwise be possible without further surgery .
	manualset3
86008	5	398378	5	NULL	NULL	0	NULL	dilatative type therapeutic maneuvers	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Here a transparietojejunal endoscopic investigation is proposed that permits direct sight of the anastomosis , biliary sampling for cultural examination and dilatative type therapeutic maneuvers , biopsies or extractions of residual stones from the bile ways that would not otherwise be possible without further surgery .
	manualset3
86009	6	398378	5	NULL	NULL	0	NULL	biopsies or extractions of residual stones from the bile	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Here a transparietojejunal endoscopic investigation is proposed that permits direct sight of the anastomosis , biliary sampling for cultural examination and dilatative type therapeutic maneuvers , biopsies or extractions of residual stones from the bile ways that would not otherwise be possible without further surgery .
	manualset3
86010	7	398378	5	NULL	NULL	0	NULL	surgery	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Here a transparietojejunal endoscopic investigation is proposed that permits direct sight of the anastomosis , biliary sampling for cultural examination and dilatative type therapeutic maneuvers , biopsies or extractions of residual stones from the bile ways that would not otherwise be possible without further surgery .
	manualset3
86011	1	398379	5	NULL	NULL	0	NULL	unusual complication of the treatment	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here an unusual complication of the treatment is reported : multiple tender subcutaneous nodules developed where the catgut was embedded over the lower abdomen and both medial thighs 1 month after treatment .
	manualset3
86020	2	398379	5	NULL	NULL	NULL	NULL	multiple tender subcutaneous nodules	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here an unusual complication of the treatment is reported : multiple tender subcutaneous nodules developed where the catgut was embedded over the lower abdomen and both medial thighs 1 month after treatment .
	manualset3
86021	3	398379	5	NULL	NULL	NULL	NULL	catgut	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here an unusual complication of the treatment is reported : multiple tender subcutaneous nodules developed where the catgut was embedded over the lower abdomen and both medial thighs 1 month after treatment .
	manualset3
86028	4	398379	5	NULL	NULL	0	NULL	lower abdomen	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here an unusual complication of the treatment is reported : multiple tender subcutaneous nodules developed where the catgut was embedded over the lower abdomen and both medial thighs 1 month after treatment .
	manualset3
86032	5	398379	5	NULL	NULL	0	NULL	medial thighs	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here an unusual complication of the treatment is reported : multiple tender subcutaneous nodules developed where the catgut was embedded over the lower abdomen and both medial thighs 1 month after treatment .
	manualset3
86033	6	398379	5	NULL	NULL	0	NULL	1 month after treatment	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Here an unusual complication of the treatment is reported : multiple tender subcutaneous nodules developed where the catgut was embedded over the lower abdomen and both medial thighs 1 month after treatment .
	manualset3
86036	1	398380	5	NULL	NULL	0	NULL	ARABIDOPSIS THALIANA HOMEOBOX GENE1 ( ATH1 ) gene	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here it is reported that the ARABIDOPSIS THALIANA HOMEOBOX GENE1 ( ATH1 ) gene , which belongs to the BELL1-like homeodomain gene family , is a new member participating in regulating pedicel orientation in the class-I KNOX network .
	manualset3
86037	2	398380	5	NULL	NULL	0	NULL	BELL1-like homeodomain gene family	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here it is reported that the ARABIDOPSIS THALIANA HOMEOBOX GENE1 ( ATH1 ) gene , which belongs to the BELL1-like homeodomain gene family , is a new member participating in regulating pedicel orientation in the class-I KNOX network .
	manualset3
86038	3	398380	5	NULL	NULL	0	NULL	new member	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here it is reported that the ARABIDOPSIS THALIANA HOMEOBOX GENE1 ( ATH1 ) gene , which belongs to the BELL1-like homeodomain gene family , is a new member participating in regulating pedicel orientation in the class-I KNOX network .
	manualset3
86039	4	398380	5	NULL	NULL	0	NULL	pedicel orientation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here it is reported that the ARABIDOPSIS THALIANA HOMEOBOX GENE1 ( ATH1 ) gene , which belongs to the BELL1-like homeodomain gene family , is a new member participating in regulating pedicel orientation in the class-I KNOX network .
	manualset3
86040	5	398380	5	NULL	NULL	0	NULL	class-I KNOX network	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here it is reported that the ARABIDOPSIS THALIANA HOMEOBOX GENE1 ( ATH1 ) gene , which belongs to the BELL1-like homeodomain gene family , is a new member participating in regulating pedicel orientation in the class-I KNOX network .
	manualset3
86041	1	398381	5	NULL	NULL	0	NULL	Xa21 homologs	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we attempted to determine the existence of Xa21 homologs in other wild rice species and rice cultivars and the sequence differences between the homologs .
	manualset3
86042	2	398381	5	NULL	NULL	0	NULL	wild rice species	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we attempted to determine the existence of Xa21 homologs in other wild rice species and rice cultivars and the sequence differences between the homologs .
	manualset3
86043	3	398381	5	NULL	NULL	0	NULL	rice cultivars	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we attempted to determine the existence of Xa21 homologs in other wild rice species and rice cultivars and the sequence differences between the homologs .
	manualset3
86044	4	398381	5	NULL	NULL	0	NULL	sequence differences between the homologs	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we attempted to determine the existence of Xa21 homologs in other wild rice species and rice cultivars and the sequence differences between the homologs .
	manualset3
86488	5	398381	5	NULL	NULL	0	NULL	existence	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we attempted to determine the existence of Xa21 homologs in other wild rice species and rice cultivars and the sequence differences between the homologs .
	manualset3
86048	1	398382	5	NULL	NULL	0	NULL	data	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we collated data from 331 experiments in 255 healthy volunteers over a 23-year period , in which subcutaneous abdominal adipose tissue metabolism was studied by measurements of arterio-venous differences after an overnight fast .
	manualset3
86050	2	398382	5	NULL	NULL	0	NULL	331 experiments	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we collated data from 331 experiments in 255 healthy volunteers over a 23-year period , in which subcutaneous abdominal adipose tissue metabolism was studied by measurements of arterio-venous differences after an overnight fast .
	manualset3
86051	3	398382	5	NULL	NULL	0	NULL	255 healthy volunteers	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we collated data from 331 experiments in 255 healthy volunteers over a 23-year period , in which subcutaneous abdominal adipose tissue metabolism was studied by measurements of arterio-venous differences after an overnight fast .
	manualset3
86052	4	398382	5	NULL	NULL	0	NULL	23-year period	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we collated data from 331 experiments in 255 healthy volunteers over a 23-year period , in which subcutaneous abdominal adipose tissue metabolism was studied by measurements of arterio-venous differences after an overnight fast .
	manualset3
86053	5	398382	5	NULL	NULL	0	NULL	subcutaneous abdominal adipose tissue metabolism	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we collated data from 331 experiments in 255 healthy volunteers over a 23-year period , in which subcutaneous abdominal adipose tissue metabolism was studied by measurements of arterio-venous differences after an overnight fast .
	manualset3
86054	6	398382	5	NULL	NULL	0	NULL	measurements of arterio-venous differences	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we collated data from 331 experiments in 255 healthy volunteers over a 23-year period , in which subcutaneous abdominal adipose tissue metabolism was studied by measurements of arterio-venous differences after an overnight fast .
	manualset3
86056	7	398382	5	NULL	NULL	0	NULL	overnight fast	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we collated data from 331 experiments in 255 healthy volunteers over a 23-year period , in which subcutaneous abdominal adipose tissue metabolism was studied by measurements of arterio-venous differences after an overnight fast .
	manualset3
86057	1	398383	5	NULL	NULL	0	NULL	role	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we deal with its role in the biosynthesis of the subclasses of ethanolamine - and choline-containing phosphoglycerides ( EPG , CPG , respectively ) .
	manualset3
86058	2	398383	5	NULL	NULL	0	NULL	 biosynthesis of the subclasses of ethanolamine	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we deal with its role in the biosynthesis of the subclasses of ethanolamine - and choline-containing phosphoglycerides ( EPG , CPG , respectively ) .
	manualset3
86059	3	398383	5	NULL	NULL	0	NULL	 biosynthesis of the subclasses of  choline-containing phosphoglycerides ( EPG , CPG , respectively )	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we deal with its role in the biosynthesis of the subclasses of ethanolamine - and choline-containing phosphoglycerides ( EPG , CPG , respectively ) .
	manualset3
86098	1	398384	5	NULL	NULL	0	NULL	Surgical treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgical treatment of malignant neoplasms of the pancreatoduodenal zone ) .
	manualset3
86100	2	398384	5	NULL	NULL	0	NULL	malignant neoplasms	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgical treatment of malignant neoplasms of the pancreatoduodenal zone ) .
	manualset3
86102	3	398384	5	NULL	NULL	0	NULL	pancreatoduodenal zone	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgical treatment of malignant neoplasms of the pancreatoduodenal zone ) .
	manualset3
86105	1	398385	5	NULL	NULL	0	NULL	input logic	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we define the input logic and transcriptional output of the stringent response in the oligotroph , Caulobacter crescentus .
	manualset3
86106	2	398385	5	NULL	NULL	0	NULL	transcriptional output	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we define the input logic and transcriptional output of the stringent response in the oligotroph , Caulobacter crescentus .
	manualset3
86107	3	398385	5	NULL	NULL	0	NULL	stringent response	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we define the input logic and transcriptional output of the stringent response in the oligotroph , Caulobacter crescentus .
	manualset3
86108	4	398385	5	NULL	NULL	0	NULL	oligotroph	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we define the input logic and transcriptional output of the stringent response in the oligotroph , Caulobacter crescentus .
	manualset3
86109	5	398385	5	NULL	NULL	0	NULL	Caulobacter crescentus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we define the input logic and transcriptional output of the stringent response in the oligotroph , Caulobacter crescentus .
	manualset3
86147	1	398386	5	NULL	NULL	NULL	NULL	overexpression of NCAM ( CD56 )	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we demonstrate , that the overexpression of NCAM ( CD56 ) is specific for ischemic damage as compaired to other heart diseases including congestive cardiomyopathy , hypertrophic obstrutive cardiomyopathy , myocarditis and sarcoidosis .
	manualset3
86148	2	398386	5	NULL	NULL	0	NULL	ischemic damage	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we demonstrate , that the overexpression of NCAM ( CD56 ) is specific for ischemic damage as compaired to other heart diseases including congestive cardiomyopathy , hypertrophic obstrutive cardiomyopathy , myocarditis and sarcoidosis .
	manualset3
86149	3	398386	5	NULL	NULL	0	NULL	heart diseases	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we demonstrate , that the overexpression of NCAM ( CD56 ) is specific for ischemic damage as compaired to other heart diseases including congestive cardiomyopathy , hypertrophic obstrutive cardiomyopathy , myocarditis and sarcoidosis .
	manualset3
86150	4	398386	5	NULL	NULL	0	NULL	congestive cardiomyopathy	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we demonstrate , that the overexpression of NCAM ( CD56 ) is specific for ischemic damage as compaired to other heart diseases including congestive cardiomyopathy , hypertrophic obstrutive cardiomyopathy , myocarditis and sarcoidosis .
	manualset3
86151	5	398386	5	NULL	NULL	0	NULL	hypertrophic obstrutive cardiomyopathy	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we demonstrate , that the overexpression of NCAM ( CD56 ) is specific for ischemic damage as compaired to other heart diseases including congestive cardiomyopathy , hypertrophic obstrutive cardiomyopathy , myocarditis and sarcoidosis .
	manualset3
86152	6	398386	5	NULL	NULL	0	NULL	myocarditis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we demonstrate , that the overexpression of NCAM ( CD56 ) is specific for ischemic damage as compaired to other heart diseases including congestive cardiomyopathy , hypertrophic obstrutive cardiomyopathy , myocarditis and sarcoidosis .
	manualset3
86153	7	398386	5	NULL	NULL	0	NULL	sarcoidosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we demonstrate , that the overexpression of NCAM ( CD56 ) is specific for ischemic damage as compaired to other heart diseases including congestive cardiomyopathy , hypertrophic obstrutive cardiomyopathy , myocarditis and sarcoidosis .
	manualset3
86154	1	398387	5	NULL	NULL	0	NULL	lipopeptides	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we demonstrate that lipopeptides also constitute adjuvants for mucosal immunizations .
	manualset3
86155	2	398387	5	NULL	NULL	0	NULL	adjuvants	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we demonstrate that lipopeptides also constitute adjuvants for mucosal immunizations .
	manualset3
86156	3	398387	5	NULL	NULL	0	NULL	mucosal immunizations	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we demonstrate that lipopeptides also constitute adjuvants for mucosal immunizations .
	manualset3
86157	1	398388	5	NULL	NULL	0	NULL	LipA levels	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we demonstrate that the reduced LipA levels are due to the absence of four genes , skfABCD , located in the prophage 1 region .
	manualset3
86158	2	398388	5	NULL	NULL	NULL	NULL	four genes	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we demonstrate that the reduced LipA levels are due to the absence of four genes , skfABCD , located in the prophage 1 region .
	manualset3
86159	3	398388	5	NULL	NULL	0	NULL	skfABCD	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we demonstrate that the reduced LipA levels are due to the absence of four genes , skfABCD , located in the prophage 1 region .
	manualset3
86160	4	398388	5	NULL	NULL	0	NULL	prophage 1 region	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we demonstrate that the reduced LipA levels are due to the absence of four genes , skfABCD , located in the prophage 1 region .
	manualset3
86161	1	398389	5	NULL	NULL	0	NULL	p1-30	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we demonstrate the ability of p1-30 to act in synergy with IL-2 , -4 , -9 , and -15 .
	manualset3
86162	3	398389	5	NULL	NULL	NULL	NULL	IL-2 , -4 , -9 , and -15	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we demonstrate the ability of p1-30 to act in synergy with IL-2 , -4 , -9 , and -15 .
	manualset3
86489	2	398389	5	NULL	NULL	0	NULL	synergy 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we demonstrate the ability of p1-30 to act in synergy with IL-2 , -4 , -9 , and -15 .
	manualset3
86163	1	398390	5	NULL	NULL	0	NULL	CAP approach , called biotinylated CAP ( Bio-CAP )	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe a new CAP approach , called biotinylated CAP ( Bio-CAP ) , which eliminates the requirement for specialized equipment while dramatically improving and simplifying the CxxC-based DNA affinity purification .
	manualset3
86164	2	398390	5	NULL	NULL	0	NULL	specialized equipment	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe a new CAP approach , called biotinylated CAP ( Bio-CAP ) , which eliminates the requirement for specialized equipment while dramatically improving and simplifying the CxxC-based DNA affinity purification .
	manualset3
86165	3	398390	5	NULL	NULL	0	NULL	CxxC-based DNA affinity purification	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe a new CAP approach , called biotinylated CAP ( Bio-CAP ) , which eliminates the requirement for specialized equipment while dramatically improving and simplifying the CxxC-based DNA affinity purification .
	manualset3
86166	1	398391	5	NULL	NULL	0	NULL	novel database termed MaxQB	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe a novel database termed MaxQB that stores and displays collections of large proteomics projects and allows joint analysis and comparison .
	manualset3
86167	2	398391	5	NULL	NULL	0	NULL	large proteomics projects	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe a novel database termed MaxQB that stores and displays collections of large proteomics projects and allows joint analysis and comparison .
	manualset3
86168	3	398391	5	NULL	NULL	0	NULL	joint analysis and comparison	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe a novel database termed MaxQB that stores and displays collections of large proteomics projects and allows joint analysis and comparison .
	manualset3
86169	1	398392	5	NULL	NULL	0	NULL	DNA lesions	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe a procedure to quantify DNA lesions recognized by the bacterial formamido-pyrimidine-DNA glycosylases ( Fpg protein ) .
	manualset3
86170	2	398392	5	NULL	NULL	0	NULL	bacterial formamido-pyrimidine-DNA glycosylases ( Fpg protein )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe a procedure to quantify DNA lesions recognized by the bacterial formamido-pyrimidine-DNA glycosylases ( Fpg protein ) .
	manualset3
86171	1	398393	5	NULL	NULL	0	NULL	Surgical treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgical treatment of myocardial infarct in complications .
	manualset3
86172	2	398393	5	NULL	NULL	0	NULL	myocardial infarct	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgical treatment of myocardial infarct in complications .
	manualset3
86173	3	398393	5	NULL	NULL	0	NULL	complications	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surgical treatment of myocardial infarct in complications .
	manualset3
86174	1	398394	5	NULL	NULL	0	NULL	catalysis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe an advance in the catalysis of the overall splitting of water under visible light : the new catalyst is a solid solution of gallium and zinc nitrogen oxide , ( Ga ( 1-x ) Zn ( x ) ) ( N ( 1-x ) O ( x ) ) , modified with nanoparticles of a mixed oxide of rhodium and chromium .
	manualset3
86175	2	398394	5	NULL	NULL	0	NULL	splitting of water under visible light	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe an advance in the catalysis of the overall splitting of water under visible light : the new catalyst is a solid solution of gallium and zinc nitrogen oxide , ( Ga ( 1-x ) Zn ( x ) ) ( N ( 1-x ) O ( x ) ) , modified with nanoparticles of a mixed oxide of rhodium and chromium .
	manualset3
86176	3	398394	5	NULL	NULL	NULL	NULL	new catalyst	NonProteinOrNucleicAcidChemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we describe an advance in the catalysis of the overall splitting of water under visible light : the new catalyst is a solid solution of gallium and zinc nitrogen oxide , ( Ga ( 1-x ) Zn ( x ) ) ( N ( 1-x ) O ( x ) ) , modified with nanoparticles of a mixed oxide of rhodium and chromium .
	manualset3
86177	4	398394	5	NULL	NULL	NULL	NULL	solid solution of gallium and zinc nitrogen oxide , ( Ga ( 1-x ) Zn ( x ) ) ( N ( 1-x ) O ( x ) )	NonProteinOrNucleicAcidChemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we describe an advance in the catalysis of the overall splitting of water under visible light : the new catalyst is a solid solution of gallium and zinc nitrogen oxide , ( Ga ( 1-x ) Zn ( x ) ) ( N ( 1-x ) O ( x ) ) , modified with nanoparticles of a mixed oxide of rhodium and chromium .
	manualset3
86178	5	398394	5	NULL	NULL	NULL	NULL	nanoparticles of a mixed oxide of rhodium and chromium	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we describe an advance in the catalysis of the overall splitting of water under visible light : the new catalyst is a solid solution of gallium and zinc nitrogen oxide , ( Ga ( 1-x ) Zn ( x ) ) ( N ( 1-x ) O ( x ) ) , modified with nanoparticles of a mixed oxide of rhodium and chromium .
	manualset3
86341	1	398395	5	NULL	NULL	0	NULL	five stages	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe five stages of insular gyral and sulcal development closely related to gestational age : stage 1 : appearance of the first sulcus at 13-17 GWs , stage 2 : development of the periinsular sulci at 18-19 GWs , stage 3 : central sulci and opercularization of the insula at 20-22 GWs , stage 4 : covering of the posterior insula at 24-26 GWs , stage 5 : closure of the sylvian fissure at 27-28 GWs .
	manualset3
86342	2	398395	5	NULL	NULL	0	NULL	insular gyral and sulcal development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe five stages of insular gyral and sulcal development closely related to gestational age : stage 1 : appearance of the first sulcus at 13-17 GWs , stage 2 : development of the periinsular sulci at 18-19 GWs , stage 3 : central sulci and opercularization of the insula at 20-22 GWs , stage 4 : covering of the posterior insula at 24-26 GWs , stage 5 : closure of the sylvian fissure at 27-28 GWs .
	manualset3
86343	3	398395	5	NULL	NULL	0	NULL	gestational age	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe five stages of insular gyral and sulcal development closely related to gestational age : stage 1 : appearance of the first sulcus at 13-17 GWs , stage 2 : development of the periinsular sulci at 18-19 GWs , stage 3 : central sulci and opercularization of the insula at 20-22 GWs , stage 4 : covering of the posterior insula at 24-26 GWs , stage 5 : closure of the sylvian fissure at 27-28 GWs .
	manualset3
86344	4	398395	5	NULL	NULL	0	NULL	stage 1	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe five stages of insular gyral and sulcal development closely related to gestational age : stage 1 : appearance of the first sulcus at 13-17 GWs , stage 2 : development of the periinsular sulci at 18-19 GWs , stage 3 : central sulci and opercularization of the insula at 20-22 GWs , stage 4 : covering of the posterior insula at 24-26 GWs , stage 5 : closure of the sylvian fissure at 27-28 GWs .
	manualset3
86345	5	398395	5	NULL	NULL	0	NULL	appearance of the first sulcus at 13-17 GWs	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe five stages of insular gyral and sulcal development closely related to gestational age : stage 1 : appearance of the first sulcus at 13-17 GWs , stage 2 : development of the periinsular sulci at 18-19 GWs , stage 3 : central sulci and opercularization of the insula at 20-22 GWs , stage 4 : covering of the posterior insula at 24-26 GWs , stage 5 : closure of the sylvian fissure at 27-28 GWs .
	manualset3
86346	6	398395	5	NULL	NULL	0	NULL	stage 2	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe five stages of insular gyral and sulcal development closely related to gestational age : stage 1 : appearance of the first sulcus at 13-17 GWs , stage 2 : development of the periinsular sulci at 18-19 GWs , stage 3 : central sulci and opercularization of the insula at 20-22 GWs , stage 4 : covering of the posterior insula at 24-26 GWs , stage 5 : closure of the sylvian fissure at 27-28 GWs .
	manualset3
86347	7	398395	5	NULL	NULL	0	NULL	development of the periinsular sulci at 18-19 GWs	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe five stages of insular gyral and sulcal development closely related to gestational age : stage 1 : appearance of the first sulcus at 13-17 GWs , stage 2 : development of the periinsular sulci at 18-19 GWs , stage 3 : central sulci and opercularization of the insula at 20-22 GWs , stage 4 : covering of the posterior insula at 24-26 GWs , stage 5 : closure of the sylvian fissure at 27-28 GWs .
	manualset3
86348	8	398395	5	NULL	NULL	0	NULL	stage 3	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe five stages of insular gyral and sulcal development closely related to gestational age : stage 1 : appearance of the first sulcus at 13-17 GWs , stage 2 : development of the periinsular sulci at 18-19 GWs , stage 3 : central sulci and opercularization of the insula at 20-22 GWs , stage 4 : covering of the posterior insula at 24-26 GWs , stage 5 : closure of the sylvian fissure at 27-28 GWs .
	manualset3
86349	9	398395	5	NULL	NULL	0	NULL	central sulci and opercularization of the insula at 20-22 GWs	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe five stages of insular gyral and sulcal development closely related to gestational age : stage 1 : appearance of the first sulcus at 13-17 GWs , stage 2 : development of the periinsular sulci at 18-19 GWs , stage 3 : central sulci and opercularization of the insula at 20-22 GWs , stage 4 : covering of the posterior insula at 24-26 GWs , stage 5 : closure of the sylvian fissure at 27-28 GWs .
	manualset3
86350	10	398395	5	NULL	NULL	0	NULL	stage 4	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe five stages of insular gyral and sulcal development closely related to gestational age : stage 1 : appearance of the first sulcus at 13-17 GWs , stage 2 : development of the periinsular sulci at 18-19 GWs , stage 3 : central sulci and opercularization of the insula at 20-22 GWs , stage 4 : covering of the posterior insula at 24-26 GWs , stage 5 : closure of the sylvian fissure at 27-28 GWs .
	manualset3
86351	11	398395	5	NULL	NULL	0	NULL	covering of the posterior insula at 24-26 GWs	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe five stages of insular gyral and sulcal development closely related to gestational age : stage 1 : appearance of the first sulcus at 13-17 GWs , stage 2 : development of the periinsular sulci at 18-19 GWs , stage 3 : central sulci and opercularization of the insula at 20-22 GWs , stage 4 : covering of the posterior insula at 24-26 GWs , stage 5 : closure of the sylvian fissure at 27-28 GWs .
	manualset3
86352	12	398395	5	NULL	NULL	0	NULL	stage 5	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe five stages of insular gyral and sulcal development closely related to gestational age : stage 1 : appearance of the first sulcus at 13-17 GWs , stage 2 : development of the periinsular sulci at 18-19 GWs , stage 3 : central sulci and opercularization of the insula at 20-22 GWs , stage 4 : covering of the posterior insula at 24-26 GWs , stage 5 : closure of the sylvian fissure at 27-28 GWs .
	manualset3
86353	13	398395	5	NULL	NULL	0	NULL	closure of the sylvian fissure at 27-28 GWs	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe five stages of insular gyral and sulcal development closely related to gestational age : stage 1 : appearance of the first sulcus at 13-17 GWs , stage 2 : development of the periinsular sulci at 18-19 GWs , stage 3 : central sulci and opercularization of the insula at 20-22 GWs , stage 4 : covering of the posterior insula at 24-26 GWs , stage 5 : closure of the sylvian fissure at 27-28 GWs .
	manualset3
86179	1	398396	5	NULL	NULL	NULL	NULL	mass precision	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we describe how mass precision for each peptide increases successively by considering all associated measurements , starting from the MS peak and proceeding to its chromatographic elution profile , isotope envelope , and stable isotope pair in SILAC measurements .
	manualset3
86180	2	398396	5	NULL	NULL	0	NULL	peptide	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe how mass precision for each peptide increases successively by considering all associated measurements , starting from the MS peak and proceeding to its chromatographic elution profile , isotope envelope , and stable isotope pair in SILAC measurements .
	manualset3
86181	3	398396	5	NULL	NULL	NULL	NULL	MS peak	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we describe how mass precision for each peptide increases successively by considering all associated measurements , starting from the MS peak and proceeding to its chromatographic elution profile , isotope envelope , and stable isotope pair in SILAC measurements .
	manualset3
86182	4	398396	5	NULL	NULL	NULL	NULL	chromatographic elution profile	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we describe how mass precision for each peptide increases successively by considering all associated measurements , starting from the MS peak and proceeding to its chromatographic elution profile , isotope envelope , and stable isotope pair in SILAC measurements .
	manualset3
86183	5	398396	5	NULL	NULL	NULL	NULL	isotope envelope	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we describe how mass precision for each peptide increases successively by considering all associated measurements , starting from the MS peak and proceeding to its chromatographic elution profile , isotope envelope , and stable isotope pair in SILAC measurements .
	manualset3
86184	6	398396	5	NULL	NULL	NULL	NULL	stable isotope pair in SILAC measurements	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we describe how mass precision for each peptide increases successively by considering all associated measurements , starting from the MS peak and proceeding to its chromatographic elution profile , isotope envelope , and stable isotope pair in SILAC measurements .
	manualset3
86185	1	398397	5	NULL	NULL	0	NULL	young male	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe the case of young male with , long-standing progressive vitiligo , presenting with congestive cardiac failure due to dilated cardiomyopathy and primary hypothyroidism .
	manualset3
86186	2	398397	5	NULL	NULL	0	NULL	 long-standing progressive vitiligo	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe the case of young male with , long-standing progressive vitiligo , presenting with congestive cardiac failure due to dilated cardiomyopathy and primary hypothyroidism .
	manualset3
86187	3	398397	5	NULL	NULL	0	NULL	congestive cardiac failure	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe the case of young male with , long-standing progressive vitiligo , presenting with congestive cardiac failure due to dilated cardiomyopathy and primary hypothyroidism .
	manualset3
86188	4	398397	5	NULL	NULL	0	NULL	dilated cardiomyopathy	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe the case of young male with , long-standing progressive vitiligo , presenting with congestive cardiac failure due to dilated cardiomyopathy and primary hypothyroidism .
	manualset3
86189	5	398397	5	NULL	NULL	0	NULL	primary hypothyroidism	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe the case of young male with , long-standing progressive vitiligo , presenting with congestive cardiac failure due to dilated cardiomyopathy and primary hypothyroidism .
	manualset3
86190	1	398398	5	NULL	NULL	NULL	NULL	cryptic chromosomally encoded 34-kDa cytolysin A hemolysin of Salmonella enterica serovar Typhi ( ClyA )	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we describe the cryptic chromosomally encoded 34-kDa cytolysin A hemolysin of Salmonella enterica serovar Typhi ( ClyA ) as a novel export system for the expression of heterologous antigens in the supernatant of attenuated Salmonella serovar Typhi live-vector vaccine strains .
	manualset3
86191	2	398398	5	NULL	NULL	0	NULL	novel export system	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe the cryptic chromosomally encoded 34-kDa cytolysin A hemolysin of Salmonella enterica serovar Typhi ( ClyA ) as a novel export system for the expression of heterologous antigens in the supernatant of attenuated Salmonella serovar Typhi live-vector vaccine strains .
	manualset3
86192	3	398398	5	NULL	NULL	0	NULL	expression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe the cryptic chromosomally encoded 34-kDa cytolysin A hemolysin of Salmonella enterica serovar Typhi ( ClyA ) as a novel export system for the expression of heterologous antigens in the supernatant of attenuated Salmonella serovar Typhi live-vector vaccine strains .
	manualset3
86193	4	398398	5	NULL	NULL	0	NULL	heterologous antigens	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe the cryptic chromosomally encoded 34-kDa cytolysin A hemolysin of Salmonella enterica serovar Typhi ( ClyA ) as a novel export system for the expression of heterologous antigens in the supernatant of attenuated Salmonella serovar Typhi live-vector vaccine strains .
	manualset3
86194	5	398398	5	NULL	NULL	0	NULL	attenuated Salmonella serovar Typhi live-vector vaccine strains	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe the cryptic chromosomally encoded 34-kDa cytolysin A hemolysin of Salmonella enterica serovar Typhi ( ClyA ) as a novel export system for the expression of heterologous antigens in the supernatant of attenuated Salmonella serovar Typhi live-vector vaccine strains .
	manualset3
86195	1	398399	5	NULL	NULL	0	NULL	expression pattern of HTm4	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe the expression pattern of HTm4 in peripheral blood cells using gene expression microarray technology , and in normal foetal and adult human tissues , as well as adult human cancers , using tissue microarray technology .
	manualset3
86196	2	398399	5	NULL	NULL	0	NULL	peripheral blood cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe the expression pattern of HTm4 in peripheral blood cells using gene expression microarray technology , and in normal foetal and adult human tissues , as well as adult human cancers , using tissue microarray technology .
	manualset3
86197	3	398399	5	NULL	NULL	0	NULL	gene expression microarray technology	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe the expression pattern of HTm4 in peripheral blood cells using gene expression microarray technology , and in normal foetal and adult human tissues , as well as adult human cancers , using tissue microarray technology .
	manualset3
86198	4	398399	5	NULL	NULL	0	NULL	normal foetal and adult human tissues	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe the expression pattern of HTm4 in peripheral blood cells using gene expression microarray technology , and in normal foetal and adult human tissues , as well as adult human cancers , using tissue microarray technology .
	manualset3
86199	5	398399	5	NULL	NULL	0	NULL	adult human cancers	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe the expression pattern of HTm4 in peripheral blood cells using gene expression microarray technology , and in normal foetal and adult human tissues , as well as adult human cancers , using tissue microarray technology .
	manualset3
86200	6	398399	5	NULL	NULL	0	NULL	tissue microarray technology	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we describe the expression pattern of HTm4 in peripheral blood cells using gene expression microarray technology , and in normal foetal and adult human tissues , as well as adult human cancers , using tissue microarray technology .
	manualset3
86201	1	398400	5	NULL	NULL	0	NULL	de novo spine formation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we develop an approach to induce and monitor de novo spine formation in real time using combined two-photon laser-scanning microscopy and two-photon laser uncaging of glutamate .
	manualset3
86202	2	398400	5	NULL	NULL	0	NULL	real time	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we develop an approach to induce and monitor de novo spine formation in real time using combined two-photon laser-scanning microscopy and two-photon laser uncaging of glutamate .
	manualset3
86203	3	398400	5	NULL	NULL	NULL	NULL	two-photon laser-scanning microscopy	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we develop an approach to induce and monitor de novo spine formation in real time using combined two-photon laser-scanning microscopy and two-photon laser uncaging of glutamate .
	manualset3
86493	4	398400	5	NULL	NULL	0	NULL	two-photon laser uncaging of glutamate	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we develop an approach to induce and monitor de novo spine formation in real time using combined two-photon laser-scanning microscopy and two-photon laser uncaging of glutamate .
	manualset3
86204	1	398401	5	NULL	NULL	0	NULL	studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we disclose studies examining the use of large amplitude voltage excitations ( applied for short periods of time ) to cause fragmentation of the ions of interest .
	manualset3
86205	2	398401	5	NULL	NULL	0	NULL	large amplitude voltage excitations	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we disclose studies examining the use of large amplitude voltage excitations ( applied for short periods of time ) to cause fragmentation of the ions of interest .
	manualset3
86206	3	398401	5	NULL	NULL	0	NULL	short periods of time	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we disclose studies examining the use of large amplitude voltage excitations ( applied for short periods of time ) to cause fragmentation of the ions of interest .
	manualset3
86207	4	398401	5	NULL	NULL	0	NULL	fragmentation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we disclose studies examining the use of large amplitude voltage excitations ( applied for short periods of time ) to cause fragmentation of the ions of interest .
	manualset3
86208	5	398401	5	NULL	NULL	0	NULL	ions	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we disclose studies examining the use of large amplitude voltage excitations ( applied for short periods of time ) to cause fragmentation of the ions of interest .
	manualset3
86209	1	398402	5	NULL	NULL	0	NULL	mechanisms of RUNX3	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we discuss recent breakthroughs in our understanding of the mechanisms of RUNX3 in gastric malignancy and comment on possible future trends and perspectives .
	manualset3
86210	2	398402	5	NULL	NULL	0	NULL	gastric malignancy	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we discuss recent breakthroughs in our understanding of the mechanisms of RUNX3 in gastric malignancy and comment on possible future trends and perspectives .
	manualset3
87583	3	398402	5	NULL	NULL	0	NULL	breakthroughs in our understanding	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we discuss recent breakthroughs in our understanding of the mechanisms of RUNX3 in gastric malignancy and comment on possible future trends and perspectives .
	manualset3
86211	1	398403	5	NULL	NULL	0	NULL	distribution	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine the distribution of cannabinoid receptors and endocannabinoid-hydrolyzing enzymes within pain modulatory circuits together with behavioral , neurochemical , and neurophysiological studies that suggest a role for endocannabinoid signaling in pain modulation .
	manualset3
86212	2	398403	5	NULL	NULL	0	NULL	cannabinoid receptors	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine the distribution of cannabinoid receptors and endocannabinoid-hydrolyzing enzymes within pain modulatory circuits together with behavioral , neurochemical , and neurophysiological studies that suggest a role for endocannabinoid signaling in pain modulation .
	manualset3
86213	3	398403	5	NULL	NULL	0	NULL	endocannabinoid-hydrolyzing enzymes	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine the distribution of cannabinoid receptors and endocannabinoid-hydrolyzing enzymes within pain modulatory circuits together with behavioral , neurochemical , and neurophysiological studies that suggest a role for endocannabinoid signaling in pain modulation .
	manualset3
86214	4	398403	5	NULL	NULL	0	NULL	 pain modulatory circuits	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine the distribution of cannabinoid receptors and endocannabinoid-hydrolyzing enzymes within pain modulatory circuits together with behavioral , neurochemical , and neurophysiological studies that suggest a role for endocannabinoid signaling in pain modulation .
	manualset3
86215	5	398403	5	NULL	NULL	0	NULL	behavioral studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine the distribution of cannabinoid receptors and endocannabinoid-hydrolyzing enzymes within pain modulatory circuits together with behavioral , neurochemical , and neurophysiological studies that suggest a role for endocannabinoid signaling in pain modulation .
	manualset3
86216	6	398403	5	NULL	NULL	0	NULL	neurochemical studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine the distribution of cannabinoid receptors and endocannabinoid-hydrolyzing enzymes within pain modulatory circuits together with behavioral , neurochemical , and neurophysiological studies that suggest a role for endocannabinoid signaling in pain modulation .
	manualset3
86217	7	398403	5	NULL	NULL	0	NULL	neurophysiological studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine the distribution of cannabinoid receptors and endocannabinoid-hydrolyzing enzymes within pain modulatory circuits together with behavioral , neurochemical , and neurophysiological studies that suggest a role for endocannabinoid signaling in pain modulation .
	manualset3
86218	8	398403	5	NULL	NULL	0	NULL	role	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine the distribution of cannabinoid receptors and endocannabinoid-hydrolyzing enzymes within pain modulatory circuits together with behavioral , neurochemical , and neurophysiological studies that suggest a role for endocannabinoid signaling in pain modulation .
	manualset3
86219	9	398403	5	NULL	NULL	0	NULL	endocannabinoid signaling	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine the distribution of cannabinoid receptors and endocannabinoid-hydrolyzing enzymes within pain modulatory circuits together with behavioral , neurochemical , and neurophysiological studies that suggest a role for endocannabinoid signaling in pain modulation .
	manualset3
86220	10	398403	5	NULL	NULL	0	NULL	pain modulation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine the distribution of cannabinoid receptors and endocannabinoid-hydrolyzing enzymes within pain modulatory circuits together with behavioral , neurochemical , and neurophysiological studies that suggest a role for endocannabinoid signaling in pain modulation .
	manualset3
86221	1	398404	5	NULL	NULL	0	NULL	partner preference formation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine the effects on partner preference formation in male prairie voles of neurochemical manipulations in the ventral tegmental area ( VTA ) , a major source of dopamine to brain regions implicated in pair bonding .
	manualset3
86222	2	398404	5	NULL	NULL	0	NULL	male prairie voles	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine the effects on partner preference formation in male prairie voles of neurochemical manipulations in the ventral tegmental area ( VTA ) , a major source of dopamine to brain regions implicated in pair bonding .
	manualset3
86223	3	398404	5	NULL	NULL	0	NULL	neurochemical manipulations	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine the effects on partner preference formation in male prairie voles of neurochemical manipulations in the ventral tegmental area ( VTA ) , a major source of dopamine to brain regions implicated in pair bonding .
	manualset3
86224	4	398404	5	NULL	NULL	0	NULL	ventral tegmental area ( VTA )	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine the effects on partner preference formation in male prairie voles of neurochemical manipulations in the ventral tegmental area ( VTA ) , a major source of dopamine to brain regions implicated in pair bonding .
	manualset3
86225	5	398404	5	NULL	NULL	0	NULL	dopamine	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine the effects on partner preference formation in male prairie voles of neurochemical manipulations in the ventral tegmental area ( VTA ) , a major source of dopamine to brain regions implicated in pair bonding .
	manualset3
86226	6	398404	5	NULL	NULL	0	NULL	brain regions implicated in pair bonding	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine the effects on partner preference formation in male prairie voles of neurochemical manipulations in the ventral tegmental area ( VTA ) , a major source of dopamine to brain regions implicated in pair bonding .
	manualset3
86227	1	398405	5	NULL	NULL	0	NULL	stimulation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine their stimulation of antigen-specific CD4 ( + ) T cells , critical for protective immunity against tumors or infectious disease .
	manualset3
86228	2	398405	5	NULL	NULL	0	NULL	antigen-specific CD4 ( + ) T cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine their stimulation of antigen-specific CD4 ( + ) T cells , critical for protective immunity against tumors or infectious disease .
	manualset3
86229	3	398405	5	NULL	NULL	0	NULL	protective immunity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine their stimulation of antigen-specific CD4 ( + ) T cells , critical for protective immunity against tumors or infectious disease .
	manualset3
86230	4	398405	5	NULL	NULL	0	NULL	tumors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine their stimulation of antigen-specific CD4 ( + ) T cells , critical for protective immunity against tumors or infectious disease .
	manualset3
86231	5	398405	5	NULL	NULL	0	NULL	infectious disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examine their stimulation of antigen-specific CD4 ( + ) T cells , critical for protective immunity against tumors or infectious disease .
	manualset3
86232	1	398406	5	NULL	NULL	0	NULL	captopril , an angiotensin converting enzyme inhibitor	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examined effects of captopril , an angiotensin converting enzyme inhibitor , on serum lipid levels and oxygen consumption rate in mitochondria isolated from heart of rabbits treated by hypercholesterolemic diet .
	manualset3
86233	2	398406	5	NULL	NULL	0	NULL	serum lipid levels	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examined effects of captopril , an angiotensin converting enzyme inhibitor , on serum lipid levels and oxygen consumption rate in mitochondria isolated from heart of rabbits treated by hypercholesterolemic diet .
	manualset3
86234	3	398406	5	NULL	NULL	0	NULL	oxygen consumption rate	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examined effects of captopril , an angiotensin converting enzyme inhibitor , on serum lipid levels and oxygen consumption rate in mitochondria isolated from heart of rabbits treated by hypercholesterolemic diet .
	manualset3
86235	4	398406	5	NULL	NULL	0	NULL	mitochondria	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examined effects of captopril , an angiotensin converting enzyme inhibitor , on serum lipid levels and oxygen consumption rate in mitochondria isolated from heart of rabbits treated by hypercholesterolemic diet .
	manualset3
86236	5	398406	5	NULL	NULL	0	NULL	heart 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examined effects of captopril , an angiotensin converting enzyme inhibitor , on serum lipid levels and oxygen consumption rate in mitochondria isolated from heart of rabbits treated by hypercholesterolemic diet .
	manualset3
86237	6	398406	5	NULL	NULL	0	NULL	rabbits	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examined effects of captopril , an angiotensin converting enzyme inhibitor , on serum lipid levels and oxygen consumption rate in mitochondria isolated from heart of rabbits treated by hypercholesterolemic diet .
	manualset3
86238	7	398406	5	NULL	NULL	0	NULL	hypercholesterolemic diet	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we examined effects of captopril , an angiotensin converting enzyme inhibitor , on serum lipid levels and oxygen consumption rate in mitochondria isolated from heart of rabbits treated by hypercholesterolemic diet .
	manualset3
86239	1	398407	5	NULL	NULL	0	NULL	role	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we explored the role of CD8 ( + ) T-cells in T. cruzi-elicited heart injury in C57BL/6 mice infected with the Colombian strain .
	manualset3
86240	2	398407	5	NULL	NULL	0	NULL	CD8 ( + ) T-cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we explored the role of CD8 ( + ) T-cells in T. cruzi-elicited heart injury in C57BL/6 mice infected with the Colombian strain .
	manualset3
86241	3	398407	5	NULL	NULL	0	NULL	T. cruzi-elicited heart injury	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we explored the role of CD8 ( + ) T-cells in T. cruzi-elicited heart injury in C57BL/6 mice infected with the Colombian strain .
	manualset3
86242	4	398407	5	NULL	NULL	0	NULL	C57BL/6 mice infected with the Colombian strain	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we explored the role of CD8 ( + ) T-cells in T. cruzi-elicited heart injury in C57BL/6 mice infected with the Colombian strain .
	manualset3
86243	1	398408	5	NULL	NULL	0	NULL	influenza virus reporter cell line	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we generated an influenza virus reporter cell line in which the luciferase gene was driven by the influenza virus promoter and screened a small compound library ( NCI Diversity Set II ) .
	manualset3
86244	2	398408	5	NULL	NULL	0	NULL	luciferase gene	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we generated an influenza virus reporter cell line in which the luciferase gene was driven by the influenza virus promoter and screened a small compound library ( NCI Diversity Set II ) .
	manualset3
86245	3	398408	5	NULL	NULL	0	NULL	influenza virus promoter	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we generated an influenza virus reporter cell line in which the luciferase gene was driven by the influenza virus promoter and screened a small compound library ( NCI Diversity Set II ) .
	manualset3
86246	4	398408	5	NULL	NULL	0	NULL	small compound library ( NCI Diversity Set II )	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we generated an influenza virus reporter cell line in which the luciferase gene was driven by the influenza virus promoter and screened a small compound library ( NCI Diversity Set II ) .
	manualset3
86247	1	398409	5	NULL	NULL	0	NULL	FLAG-fused Orai1 protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we have purified the FLAG-fused Orai1 protein , determined its tetrameric stoichiometry , and reconstructed its three-dimensional structure at 21-A resolution from 3681 automatically selected particle images , taken with an electron microscope .
	manualset3
86248	2	398409	5	NULL	NULL	0	NULL	tetrameric stoichiometry	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we have purified the FLAG-fused Orai1 protein , determined its tetrameric stoichiometry , and reconstructed its three-dimensional structure at 21-A resolution from 3681 automatically selected particle images , taken with an electron microscope .
	manualset3
86249	3	398409	5	NULL	NULL	0	NULL	three-dimensional structure	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we have purified the FLAG-fused Orai1 protein , determined its tetrameric stoichiometry , and reconstructed its three-dimensional structure at 21-A resolution from 3681 automatically selected particle images , taken with an electron microscope .
	manualset3
86250	4	398409	5	NULL	NULL	0	NULL	21-A resolution	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we have purified the FLAG-fused Orai1 protein , determined its tetrameric stoichiometry , and reconstructed its three-dimensional structure at 21-A resolution from 3681 automatically selected particle images , taken with an electron microscope .
	manualset3
86251	5	398409	5	NULL	NULL	0	NULL	3681 automatically selected particle images	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we have purified the FLAG-fused Orai1 protein , determined its tetrameric stoichiometry , and reconstructed its three-dimensional structure at 21-A resolution from 3681 automatically selected particle images , taken with an electron microscope .
	manualset3
86252	6	398409	5	NULL	NULL	0	NULL	electron microscope	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we have purified the FLAG-fused Orai1 protein , determined its tetrameric stoichiometry , and reconstructed its three-dimensional structure at 21-A resolution from 3681 automatically selected particle images , taken with an electron microscope .
	manualset3
86253	1	398410	5	NULL	NULL	0	NULL	Survival	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Survival of intestinal bacilli in oil-polluted sea water ) .
	manualset3
86254	2	398410	5	NULL	NULL	0	NULL	intestinal bacilli	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Survival of intestinal bacilli in oil-polluted sea water ) .
	manualset3
86255	3	398410	5	NULL	NULL	0	NULL	oil-polluted sea water	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( Survival of intestinal bacilli in oil-polluted sea water ) .
	manualset3
86256	1	398411	5	NULL	NULL	0	NULL	novel mass spectrometry-based imaging technique called cation-enhanced nanostructure-initiator mass spectrometry ( NIMS )	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we have used a novel mass spectrometry-based imaging technique called cation-enhanced nanostructure-initiator mass spectrometry ( NIMS ) for the in situ detection of intact cholesterol molecules from biological tissues .
	manualset3
86257	3	398411	5	NULL	NULL	NULL	NULL	intact cholesterol molecules	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we have used a novel mass spectrometry-based imaging technique called cation-enhanced nanostructure-initiator mass spectrometry ( NIMS ) for the in situ detection of intact cholesterol molecules from biological tissues .
	manualset3
86258	3	398411	5	NULL	NULL	0	NULL	biological tissues	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we have used a novel mass spectrometry-based imaging technique called cation-enhanced nanostructure-initiator mass spectrometry ( NIMS ) for the in situ detection of intact cholesterol molecules from biological tissues .
	manualset3
87584	2	398411	5	NULL	NULL	0	NULL	in situ detection	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we have used a novel mass spectrometry-based imaging technique called cation-enhanced nanostructure-initiator mass spectrometry ( NIMS ) for the in situ detection of intact cholesterol molecules from biological tissues .
	manualset3
86259	1	398412	5	NULL	NULL	0	NULL	LXR activation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we investigated the influence of LXR activation on intracellular cholesterol trafficking in primary human macrophages .
	manualset3
86260	2	398412	5	NULL	NULL	0	NULL	intracellular cholesterol trafficking	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we investigated the influence of LXR activation on intracellular cholesterol trafficking in primary human macrophages .
	manualset3
86261	3	398412	5	NULL	NULL	0	NULL	primary human macrophages	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we investigated the influence of LXR activation on intracellular cholesterol trafficking in primary human macrophages .
	manualset3
86262	1	398413	5	NULL	NULL	0	NULL	receptors	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we investigated the presence and characteristics of such receptors in the rat LSO by means of whole-cell patch-clamp recordings in combination with pharmacology .
	manualset3
86263	2	398413	5	NULL	NULL	0	NULL	rat LSO	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we investigated the presence and characteristics of such receptors in the rat LSO by means of whole-cell patch-clamp recordings in combination with pharmacology .
	manualset3
86264	3	398413	5	NULL	NULL	0	NULL	whole-cell patch-clamp recordings	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we investigated the presence and characteristics of such receptors in the rat LSO by means of whole-cell patch-clamp recordings in combination with pharmacology .
	manualset3
86265	4	398413	5	NULL	NULL	0	NULL	pharmacology	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we investigated the presence and characteristics of such receptors in the rat LSO by means of whole-cell patch-clamp recordings in combination with pharmacology .
	manualset3
86266	1	398414	5	NULL	NULL	0	NULL	time constants	Unit												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we note that the time constants involved in this latter type of field sensitivity are much longer than those in organisms that make use of the earth 's magnetic field for navigation .
	manualset3
86267	2	398414	5	NULL	NULL	0	NULL	field sensitivity	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we note that the time constants involved in this latter type of field sensitivity are much longer than those in organisms that make use of the earth 's magnetic field for navigation .
	manualset3
86268	3	398414	5	NULL	NULL	0	NULL	organisms	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we note that the time constants involved in this latter type of field sensitivity are much longer than those in organisms that make use of the earth 's magnetic field for navigation .
	manualset3
86269	4	398414	5	NULL	NULL	0	NULL	earth 's magnetic field	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we note that the time constants involved in this latter type of field sensitivity are much longer than those in organisms that make use of the earth 's magnetic field for navigation .
	manualset3
86270	5	398414	5	NULL	NULL	0	NULL	navigation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we note that the time constants involved in this latter type of field sensitivity are much longer than those in organisms that make use of the earth 's magnetic field for navigation .
	manualset3
86271	1	398415	5	NULL	NULL	0	NULL	whole-cell patch-clamp recordings	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we performed whole-cell patch clamp recordings from CA1 stratum radiatum interneurons in rat brain slices to investigate the effect of the eCB anandamide on excitatory synapses as well as the involvement of Group I metabotropic glutamate receptors ( mGluRs ) , which have been reported to produce eCBs endogenously .
	manualset3
86272	2	398415	5	NULL	NULL	0	NULL	CA1 stratum radiatum interneurons	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we performed whole-cell patch clamp recordings from CA1 stratum radiatum interneurons in rat brain slices to investigate the effect of the eCB anandamide on excitatory synapses as well as the involvement of Group I metabotropic glutamate receptors ( mGluRs ) , which have been reported to produce eCBs endogenously .
	manualset3
86273	3	398415	5	NULL	NULL	0	NULL	rat brain slices	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we performed whole-cell patch clamp recordings from CA1 stratum radiatum interneurons in rat brain slices to investigate the effect of the eCB anandamide on excitatory synapses as well as the involvement of Group I metabotropic glutamate receptors ( mGluRs ) , which have been reported to produce eCBs endogenously .
	manualset3
86274	4	398415	5	NULL	NULL	NULL	NULL	eCB anandamide	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we performed whole-cell patch clamp recordings from CA1 stratum radiatum interneurons in rat brain slices to investigate the effect of the eCB anandamide on excitatory synapses as well as the involvement of Group I metabotropic glutamate receptors ( mGluRs ) , which have been reported to produce eCBs endogenously .
	manualset3
86275	5	398415	5	NULL	NULL	0	NULL	excitatory synapses	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we performed whole-cell patch clamp recordings from CA1 stratum radiatum interneurons in rat brain slices to investigate the effect of the eCB anandamide on excitatory synapses as well as the involvement of Group I metabotropic glutamate receptors ( mGluRs ) , which have been reported to produce eCBs endogenously .
	manualset3
86276	6	398415	5	NULL	NULL	0	NULL	Group I metabotropic glutamate receptors ( mGluRs )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we performed whole-cell patch clamp recordings from CA1 stratum radiatum interneurons in rat brain slices to investigate the effect of the eCB anandamide on excitatory synapses as well as the involvement of Group I metabotropic glutamate receptors ( mGluRs ) , which have been reported to produce eCBs endogenously .
	manualset3
86277	7	398415	5	NULL	NULL	0	NULL	eCBs	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we performed whole-cell patch clamp recordings from CA1 stratum radiatum interneurons in rat brain slices to investigate the effect of the eCB anandamide on excitatory synapses as well as the involvement of Group I metabotropic glutamate receptors ( mGluRs ) , which have been reported to produce eCBs endogenously .
	manualset3
86278	1	398416	5	NULL	NULL	NULL	NULL	PEM case	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we present a PEM case with R1150W polymorphism in SCN9A and a five-year remission was achieved by chemical lumbar sympathectomy ( CLS ) .
	manualset3
86279	2	398416	5	NULL	NULL	0	NULL	R1150W polymorphism	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present a PEM case with R1150W polymorphism in SCN9A and a five-year remission was achieved by chemical lumbar sympathectomy ( CLS ) .
	manualset3
86280	3	398416	5	NULL	NULL	0	NULL	SCN9A	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present a PEM case with R1150W polymorphism in SCN9A and a five-year remission was achieved by chemical lumbar sympathectomy ( CLS ) .
	manualset3
86281	4	398416	5	NULL	NULL	0	NULL	five-year remission	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present a PEM case with R1150W polymorphism in SCN9A and a five-year remission was achieved by chemical lumbar sympathectomy ( CLS ) .
	manualset3
86282	5	398416	5	NULL	NULL	0	NULL	chemical lumbar sympathectomy ( CLS )	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present a PEM case with R1150W polymorphism in SCN9A and a five-year remission was achieved by chemical lumbar sympathectomy ( CLS ) .
	manualset3
86283	1	398417	5	NULL	NULL	0	NULL	theoretical argument	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present a theoretical argument that motion differences can account for the direction of bias seen in humans .
	manualset3
86284	2	398417	5	NULL	NULL	0	NULL	motion differences	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present a theoretical argument that motion differences can account for the direction of bias seen in humans .
	manualset3
86285	3	398417	5	NULL	NULL	0	NULL	bias	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present a theoretical argument that motion differences can account for the direction of bias seen in humans .
	manualset3
86286	4	398417	5	NULL	NULL	0	NULL	humans	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present a theoretical argument that motion differences can account for the direction of bias seen in humans .
	manualset3
86287	1	398418	5	NULL	NULL	0	NULL	behavioral data	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present behavioral data and experiments from within nests of an ambrosia beetle , Xyleborinus saxesenii .
	manualset3
86288	2	398418	5	NULL	NULL	0	NULL	experiments	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present behavioral data and experiments from within nests of an ambrosia beetle , Xyleborinus saxesenii .
	manualset3
86289	3	398418	5	NULL	NULL	0	NULL	nests	Thing												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present behavioral data and experiments from within nests of an ambrosia beetle , Xyleborinus saxesenii .
	manualset3
86290	4	398418	5	NULL	NULL	0	NULL	ambrosia beetle , Xyleborinus saxesenii	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present behavioral data and experiments from within nests of an ambrosia beetle , Xyleborinus saxesenii .
	manualset3
86291	1	398419	5	NULL	NULL	0	NULL	Anaerobic organisms	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Anaerobic organisms , bacteremia and septicemia ) .
	manualset3
86292	2	398419	5	NULL	NULL	0	NULL	bacteremia	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Anaerobic organisms , bacteremia and septicemia ) .
	manualset3
86293	3	398419	5	NULL	NULL	0	NULL	septicemia	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Anaerobic organisms , bacteremia and septicemia ) .
	manualset3
86294	1	398420	5	NULL	NULL	0	NULL	Surviving case	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surviving case of Legionella pneumonia showing a high level of serum KL-6 and complicated with rhabdomyolysis ) .
	manualset3
86295	2	398420	5	NULL	NULL	0	NULL	Legionella pneumonia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surviving case of Legionella pneumonia showing a high level of serum KL-6 and complicated with rhabdomyolysis ) .
	manualset3
86296	3	398420	5	NULL	NULL	0	NULL	high level	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surviving case of Legionella pneumonia showing a high level of serum KL-6 and complicated with rhabdomyolysis ) .
	manualset3
86297	4	398420	5	NULL	NULL	0	NULL	serum KL-6	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surviving case of Legionella pneumonia showing a high level of serum KL-6 and complicated with rhabdomyolysis ) .
	manualset3
86298	5	398420	5	NULL	NULL	0	NULL	rhabdomyolysis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Surviving case of Legionella pneumonia showing a high level of serum KL-6 and complicated with rhabdomyolysis ) .
	manualset3
86299	1	398421	5	NULL	NULL	NULL	NULL	location of a second prostate cancer susceptibility gene	Gene												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we present evidence for the location of a second prostate cancer susceptibility gene , which by heterogeneity estimates accounts for approximately 16 % of HPC cases .
	manualset3
86300	2	398421	5	NULL	NULL	0	NULL	heterogeneity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present evidence for the location of a second prostate cancer susceptibility gene , which by heterogeneity estimates accounts for approximately 16 % of HPC cases .
	manualset3
86301	3	398421	5	NULL	NULL	0	NULL	16 % of HPC cases	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present evidence for the location of a second prostate cancer susceptibility gene , which by heterogeneity estimates accounts for approximately 16 % of HPC cases .
	manualset3
86302	1	398422	5	NULL	NULL	0	NULL	seven co-crystal structures of PDE4	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present seven co-crystal structures of PDE4 and bound inhibitors that show the regulatory domain closed across the active site , thereby revealing the structural basis of PDE4 regulation .
	manualset3
86303	2	398422	5	NULL	NULL	0	NULL	bound inhibitors	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present seven co-crystal structures of PDE4 and bound inhibitors that show the regulatory domain closed across the active site , thereby revealing the structural basis of PDE4 regulation .
	manualset3
86304	3	398422	5	NULL	NULL	0	NULL	regulatory domain	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present seven co-crystal structures of PDE4 and bound inhibitors that show the regulatory domain closed across the active site , thereby revealing the structural basis of PDE4 regulation .
	manualset3
86305	4	398422	5	NULL	NULL	0	NULL	active site	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present seven co-crystal structures of PDE4 and bound inhibitors that show the regulatory domain closed across the active site , thereby revealing the structural basis of PDE4 regulation .
	manualset3
86306	5	398422	5	NULL	NULL	0	NULL	PDE4 regulation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present seven co-crystal structures of PDE4 and bound inhibitors that show the regulatory domain closed across the active site , thereby revealing the structural basis of PDE4 regulation .
	manualset3
86307	1	398423	5	NULL	NULL	0	NULL	rationale	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present the rationale and details of this approach , typical experimental results and necessary precautions .
	manualset3
86308	2	398423	5	NULL	NULL	0	NULL	typical experimental results	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present the rationale and details of this approach , typical experimental results and necessary precautions .
	manualset3
86309	3	398423	5	NULL	NULL	0	NULL	necessary precautions	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we present the rationale and details of this approach , typical experimental results and necessary precautions .
	manualset3
86310	1	398424	5	NULL	NULL	0	NULL	Val	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we propose that Val , Thr , and Ile are `` isosteric residues ' because they all contain a beta-branched side-chain .
	manualset3
86311	2	398424	5	NULL	NULL	0	NULL	Thr	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we propose that Val , Thr , and Ile are `` isosteric residues ' because they all contain a beta-branched side-chain .
	manualset3
86312	3	398424	5	NULL	NULL	0	NULL	Ile	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we propose that Val , Thr , and Ile are `` isosteric residues ' because they all contain a beta-branched side-chain .
	manualset3
86313	4	398424	5	NULL	NULL	0	NULL	isosteric residues	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we propose that Val , Thr , and Ile are `` isosteric residues ' because they all contain a beta-branched side-chain .
	manualset3
86314	5	398424	5	NULL	NULL	0	NULL	beta-branched side-chain	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we propose that Val , Thr , and Ile are `` isosteric residues ' because they all contain a beta-branched side-chain .
	manualset3
86315	1	398425	5	NULL	NULL	NULL	NULL	sparse overcomplete linear representations	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we provide an example of how sparse overcomplete linear representations can directly solve difficult acoustic signal processing problems , using as an example monaural source separation using solely the cues provided by the differential filtering imposed on a source by its path from its origin to the cochlea ( the head-related transfer function ( HRTF ) ) .
	manualset3
86316	2	398425	5	NULL	NULL	NULL	NULL	acoustic signal processing	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we provide an example of how sparse overcomplete linear representations can directly solve difficult acoustic signal processing problems , using as an example monaural source separation using solely the cues provided by the differential filtering imposed on a source by its path from its origin to the cochlea ( the head-related transfer function ( HRTF ) ) .
	manualset3
86317	3	398425	5	NULL	NULL	0	NULL	monaural source separation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we provide an example of how sparse overcomplete linear representations can directly solve difficult acoustic signal processing problems , using as an example monaural source separation using solely the cues provided by the differential filtering imposed on a source by its path from its origin to the cochlea ( the head-related transfer function ( HRTF ) ) .
	manualset3
86318	4	398425	5	NULL	NULL	0	NULL	differential filtering	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we provide an example of how sparse overcomplete linear representations can directly solve difficult acoustic signal processing problems , using as an example monaural source separation using solely the cues provided by the differential filtering imposed on a source by its path from its origin to the cochlea ( the head-related transfer function ( HRTF ) ) .
	manualset3
86319	5	398425	5	NULL	NULL	0	NULL	cochlea	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we provide an example of how sparse overcomplete linear representations can directly solve difficult acoustic signal processing problems , using as an example monaural source separation using solely the cues provided by the differential filtering imposed on a source by its path from its origin to the cochlea ( the head-related transfer function ( HRTF ) ) .
	manualset3
86320	6	398425	5	NULL	NULL	0	NULL	head-related transfer function ( HRTF )	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we provide an example of how sparse overcomplete linear representations can directly solve difficult acoustic signal processing problems , using as an example monaural source separation using solely the cues provided by the differential filtering imposed on a source by its path from its origin to the cochlea ( the head-related transfer function ( HRTF ) ) .
	manualset3
86321	1	398426	5	NULL	NULL	0	NULL	concentration-dependent interactions	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we provide evidence that concentration-dependent interactions involving a network of these proteins are sufficient to determine the outcome of PKM splicing .
	manualset3
86322	2	398426	5	NULL	NULL	0	NULL	network	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we provide evidence that concentration-dependent interactions involving a network of these proteins are sufficient to determine the outcome of PKM splicing .
	manualset3
86323	3	398426	5	NULL	NULL	0	NULL	proteins	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we provide evidence that concentration-dependent interactions involving a network of these proteins are sufficient to determine the outcome of PKM splicing .
	manualset3
86324	4	398426	5	NULL	NULL	0	NULL	PKM splicing	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we provide evidence that concentration-dependent interactions involving a network of these proteins are sufficient to determine the outcome of PKM splicing .
	manualset3
86325	1	398427	5	NULL	NULL	0	NULL	TFW-induced switch	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we provide evidence that the TFW-induced switch in Numb isoforms regulates Notch signaling strength and Notch target gene expression .
	manualset3
86326	2	398427	5	NULL	NULL	0	NULL	Numb isoforms	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we provide evidence that the TFW-induced switch in Numb isoforms regulates Notch signaling strength and Notch target gene expression .
	manualset3
86327	3	398427	5	NULL	NULL	0	NULL	Notch signaling strength	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we provide evidence that the TFW-induced switch in Numb isoforms regulates Notch signaling strength and Notch target gene expression .
	manualset3
86328	4	398427	5	NULL	NULL	0	NULL	Notch target gene expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we provide evidence that the TFW-induced switch in Numb isoforms regulates Notch signaling strength and Notch target gene expression .
	manualset3
86329	1	398428	5	NULL	NULL	0	NULL	Helix-Loop-Helix-COE transcription factor Collier	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we provide first molecular evidence that the Helix-Loop-Helix-COE transcription factor Collier fulfills this role by directly activating the expression of the segment polarity gene hedgehog in the posterior part of the intercalary segment .
	manualset3
86330	2	398428	5	NULL	NULL	0	NULL	expression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we provide first molecular evidence that the Helix-Loop-Helix-COE transcription factor Collier fulfills this role by directly activating the expression of the segment polarity gene hedgehog in the posterior part of the intercalary segment .
	manualset3
86331	3	398428	5	NULL	NULL	0	NULL	segment polarity gene hedgehog	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we provide first molecular evidence that the Helix-Loop-Helix-COE transcription factor Collier fulfills this role by directly activating the expression of the segment polarity gene hedgehog in the posterior part of the intercalary segment .
	manualset3
86332	4	398428	5	NULL	NULL	0	NULL	posterior part of the intercalary segment	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we provide first molecular evidence that the Helix-Loop-Helix-COE transcription factor Collier fulfills this role by directly activating the expression of the segment polarity gene hedgehog in the posterior part of the intercalary segment .
	manualset3
86333	1	398429	5	NULL	NULL	0	NULL	4-year old female	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report a 4-year old female with idiopathic renal hypouricemia who presented with macroscopic hematuria due to obstructive calcium oxalate urolithiasis .
	manualset3
86334	2	398429	5	NULL	NULL	0	NULL	idiopathic renal hypouricemia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report a 4-year old female with idiopathic renal hypouricemia who presented with macroscopic hematuria due to obstructive calcium oxalate urolithiasis .
	manualset3
86335	3	398429	5	NULL	NULL	0	NULL	macroscopic hematuria	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report a 4-year old female with idiopathic renal hypouricemia who presented with macroscopic hematuria due to obstructive calcium oxalate urolithiasis .
	manualset3
86336	4	398429	5	NULL	NULL	0	NULL	obstructive calcium oxalate urolithiasis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report a 4-year old female with idiopathic renal hypouricemia who presented with macroscopic hematuria due to obstructive calcium oxalate urolithiasis .
	manualset3
86337	1	398430	5	NULL	NULL	0	NULL	Susceptibilities of Pseudomonas species	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Susceptibilities of Pseudomonas species to aminoglycosides and tetracyclines ) .
	manualset3
86338	2	398430	5	NULL	NULL	0	NULL	aminoglycosides	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( Susceptibilities of Pseudomonas species to aminoglycosides and tetracyclines ) .
	manualset3
86339	3	398430	5	NULL	NULL	0	NULL	tetracyclines	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( Susceptibilities of Pseudomonas species to aminoglycosides and tetracyclines ) .
	manualset3
85472	1	398431	14	13	NULL	NULL	NULL	novel conceptualisation	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report a novel conceptualisation of impulsivity based on ` waiting ' and ` stopping ' efficiency with explanatory value in defining the psychological and neural basis of impulsivity and the high co-morbidity of brain disorders such as ADHD and drug addiction .
	manualset3
85474	3	398431	14	13	NULL	NULL	NULL	` waiting ' and ` stopping ' efficiency	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report a novel conceptualisation of impulsivity based on ` waiting ' and ` stopping ' efficiency with explanatory value in defining the psychological and neural basis of impulsivity and the high co-morbidity of brain disorders such as ADHD and drug addiction .
	manualset3
85475	4	398431	14	13	NULL	NULL	NULL	psychological and neural basis of impulsivity	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report a novel conceptualisation of impulsivity based on ` waiting ' and ` stopping ' efficiency with explanatory value in defining the psychological and neural basis of impulsivity and the high co-morbidity of brain disorders such as ADHD and drug addiction .
	manualset3
85476	5	398431	14	13	NULL	0	NULL	 high co-morbidity of brain disorders 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report a novel conceptualisation of impulsivity based on ` waiting ' and ` stopping ' efficiency with explanatory value in defining the psychological and neural basis of impulsivity and the high co-morbidity of brain disorders such as ADHD and drug addiction .
	manualset3
85477	6	398431	14	13	NULL	NULL	NULL	ADHD	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report a novel conceptualisation of impulsivity based on ` waiting ' and ` stopping ' efficiency with explanatory value in defining the psychological and neural basis of impulsivity and the high co-morbidity of brain disorders such as ADHD and drug addiction .
	manualset3
85478	7	398431	14	13	NULL	0	NULL	drug addiction	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report a novel conceptualisation of impulsivity based on ` waiting ' and ` stopping ' efficiency with explanatory value in defining the psychological and neural basis of impulsivity and the high co-morbidity of brain disorders such as ADHD and drug addiction .
	manualset3
85500	2	398431	14	13	NULL	0	NULL	impulsivity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report a novel conceptualisation of impulsivity based on ` waiting ' and ` stopping ' efficiency with explanatory value in defining the psychological and neural basis of impulsivity and the high co-morbidity of brain disorders such as ADHD and drug addiction .
	manualset3
85501	1	398432	14	13	NULL	0	NULL	general strategy	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report an unexpected and general strategy that is based on the requirement for specific cohorts of inhibitory histone methyltransferases ( HMTs ) to impose gene-specific gatekeeper functions that prevent unliganded nuclear receptors and other classes of regulated transcription factors from binding to their target gene promoters and causing constitutive gene activation in the absence of stimulating signals .
	manualset3
85502	2	398432	14	13	NULL	0	NULL	cohorts of inhibitory histone methyltransferases ( HMTs )	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report an unexpected and general strategy that is based on the requirement for specific cohorts of inhibitory histone methyltransferases ( HMTs ) to impose gene-specific gatekeeper functions that prevent unliganded nuclear receptors and other classes of regulated transcription factors from binding to their target gene promoters and causing constitutive gene activation in the absence of stimulating signals .
	manualset3
85503	3	398432	14	13	NULL	0	NULL	gene-specific gatekeeper functions 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report an unexpected and general strategy that is based on the requirement for specific cohorts of inhibitory histone methyltransferases ( HMTs ) to impose gene-specific gatekeeper functions that prevent unliganded nuclear receptors and other classes of regulated transcription factors from binding to their target gene promoters and causing constitutive gene activation in the absence of stimulating signals .
	manualset3
85504	4	398432	14	13	NULL	0	NULL	unliganded nuclear receptors 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report an unexpected and general strategy that is based on the requirement for specific cohorts of inhibitory histone methyltransferases ( HMTs ) to impose gene-specific gatekeeper functions that prevent unliganded nuclear receptors and other classes of regulated transcription factors from binding to their target gene promoters and causing constitutive gene activation in the absence of stimulating signals .
	manualset3
85505	5	398432	14	13	NULL	0	NULL	classes of regulated transcription factors	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report an unexpected and general strategy that is based on the requirement for specific cohorts of inhibitory histone methyltransferases ( HMTs ) to impose gene-specific gatekeeper functions that prevent unliganded nuclear receptors and other classes of regulated transcription factors from binding to their target gene promoters and causing constitutive gene activation in the absence of stimulating signals .
	manualset3
85506	6	398432	14	13	NULL	0	NULL	 target gene promoters 	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report an unexpected and general strategy that is based on the requirement for specific cohorts of inhibitory histone methyltransferases ( HMTs ) to impose gene-specific gatekeeper functions that prevent unliganded nuclear receptors and other classes of regulated transcription factors from binding to their target gene promoters and causing constitutive gene activation in the absence of stimulating signals .
	manualset3
85507	7	398432	14	13	NULL	NULL	NULL	 constitutive gene activation	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report an unexpected and general strategy that is based on the requirement for specific cohorts of inhibitory histone methyltransferases ( HMTs ) to impose gene-specific gatekeeper functions that prevent unliganded nuclear receptors and other classes of regulated transcription factors from binding to their target gene promoters and causing constitutive gene activation in the absence of stimulating signals .
	manualset3
85508	8	398432	14	13	NULL	0	NULL	stimulating signals	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report an unexpected and general strategy that is based on the requirement for specific cohorts of inhibitory histone methyltransferases ( HMTs ) to impose gene-specific gatekeeper functions that prevent unliganded nuclear receptors and other classes of regulated transcription factors from binding to their target gene promoters and causing constitutive gene activation in the absence of stimulating signals .
	manualset3
85511	1	398433	14	13	NULL	0	NULL	hypoxia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report effects of hypoxia on human monocyte-derived macrophage ( HMDM ) secreted glycosaminoglycans ( GAG ) , and its interaction with LDL .
	manualset3
85514	2	398433	14	13	NULL	0	NULL	human monocyte-derived macrophage ( HMDM )	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report effects of hypoxia on human monocyte-derived macrophage ( HMDM ) secreted glycosaminoglycans ( GAG ) , and its interaction with LDL .
	manualset3
85525	3	398433	14	13	NULL	0	NULL	glycosaminoglycans ( GAG )	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report effects of hypoxia on human monocyte-derived macrophage ( HMDM ) secreted glycosaminoglycans ( GAG ) , and its interaction with LDL .
	manualset3
85526	4	398433	14	13	NULL	0	NULL	interaction	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report effects of hypoxia on human monocyte-derived macrophage ( HMDM ) secreted glycosaminoglycans ( GAG ) , and its interaction with LDL .
	manualset3
85527	5	398433	14	13	NULL	0	NULL	LDL 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report effects of hypoxia on human monocyte-derived macrophage ( HMDM ) secreted glycosaminoglycans ( GAG ) , and its interaction with LDL .
	manualset3
85528	1	398435	14	13	NULL	0	NULL	HOF1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report on the roles of HOF1 , BNI1 , and BNR1 in cytokinesis , focusing on Hof1p .
	manualset3
85529	2	398435	14	13	NULL	0	NULL	BNI1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report on the roles of HOF1 , BNI1 , and BNR1 in cytokinesis , focusing on Hof1p .
	manualset3
85530	3	398435	14	13	NULL	0	NULL	BNR1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report on the roles of HOF1 , BNI1 , and BNR1 in cytokinesis , focusing on Hof1p .
	manualset3
85531	4	398435	14	13	NULL	0	NULL	cytokinesis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report on the roles of HOF1 , BNI1 , and BNR1 in cytokinesis , focusing on Hof1p .
	manualset3
85532	5	398435	14	13	NULL	0	NULL	Hof1p 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report on the roles of HOF1 , BNI1 , and BNR1 in cytokinesis , focusing on Hof1p .
	manualset3
85538	1	398436	14	13	NULL	0	NULL	mice infected with a recombinant spleen focus-forming retrovirus ( SFFV )	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report that , in mice infected with a recombinant spleen focus-forming retrovirus ( SFFV ) expressing an oncogenic erythropoietin receptor ( EpoR ) , there was an increase in platelet count preceding the ensuing erythrocytosis .
	manualset3
85539	2	398436	14	13	NULL	0	NULL	oncogenic erythropoietin receptor ( EpoR )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report that , in mice infected with a recombinant spleen focus-forming retrovirus ( SFFV ) expressing an oncogenic erythropoietin receptor ( EpoR ) , there was an increase in platelet count preceding the ensuing erythrocytosis .
	manualset3
85540	3	398436	14	13	NULL	0	NULL	increase in platelet count	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report that , in mice infected with a recombinant spleen focus-forming retrovirus ( SFFV ) expressing an oncogenic erythropoietin receptor ( EpoR ) , there was an increase in platelet count preceding the ensuing erythrocytosis .
	manualset3
85541	4	398436	14	13	NULL	0	NULL	erythrocytosis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report that , in mice infected with a recombinant spleen focus-forming retrovirus ( SFFV ) expressing an oncogenic erythropoietin receptor ( EpoR ) , there was an increase in platelet count preceding the ensuing erythrocytosis .
	manualset3
85542	1	398437	14	13	NULL	0	NULL	E2F-1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report that E2F-1 is actively degraded by the ubiquitin-proteasome pathway .
	manualset3
85543	2	398437	14	13	NULL	0	NULL	ubiquitin-proteasome pathway	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report that E2F-1 is actively degraded by the ubiquitin-proteasome pathway .
	manualset3
85544	1	398438	14	13	NULL	0	NULL	GATA-1	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report that GATA-1 , SCL , and Klf1 form an erythroid core transcriptional network by co-occupying & gt ; 300 genes .
	manualset3
85545	2	398438	14	13	NULL	0	NULL	SCL	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report that GATA-1 , SCL , and Klf1 form an erythroid core transcriptional network by co-occupying & gt ; 300 genes .
	manualset3
85546	3	398438	14	13	NULL	0	NULL	Klf1	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report that GATA-1 , SCL , and Klf1 form an erythroid core transcriptional network by co-occupying & gt ; 300 genes .
	manualset3
85547	4	398438	14	13	NULL	0	NULL	erythroid core transcriptional network	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report that GATA-1 , SCL , and Klf1 form an erythroid core transcriptional network by co-occupying & gt ; 300 genes .
	manualset3
85548	5	398438	14	13	NULL	NULL	NULL	300 genes	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report that GATA-1 , SCL , and Klf1 form an erythroid core transcriptional network by co-occupying & gt ; 300 genes .
	manualset3
85549	1	398439	14	13	NULL	0	NULL	HSV type 1 ( HSV-1 )	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report that HSV type 1 ( HSV-1 ) induces persistent activation of transcription factor NF-kappa B , a critical regulator of genes involved in inflammation , by activating the I kappa B kinase ( IKK ) in the early phase of infection .
	manualset3
85550	2	398439	14	13	NULL	NULL	NULL	activation of transcription factor 	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report that HSV type 1 ( HSV-1 ) induces persistent activation of transcription factor NF-kappa B , a critical regulator of genes involved in inflammation , by activating the I kappa B kinase ( IKK ) in the early phase of infection .
	manualset3
85551	4	398439	14	13	NULL	NULL	NULL	critical regulator of genes 	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report that HSV type 1 ( HSV-1 ) induces persistent activation of transcription factor NF-kappa B , a critical regulator of genes involved in inflammation , by activating the I kappa B kinase ( IKK ) in the early phase of infection .
	manualset3
85552	5	398439	14	13	NULL	NULL	NULL	 inflammation 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report that HSV type 1 ( HSV-1 ) induces persistent activation of transcription factor NF-kappa B , a critical regulator of genes involved in inflammation , by activating the I kappa B kinase ( IKK ) in the early phase of infection .
	manualset3
85553	6	398439	14	13	NULL	NULL	NULL	activating the I kappa B kinase ( IKK )	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report that HSV type 1 ( HSV-1 ) induces persistent activation of transcription factor NF-kappa B , a critical regulator of genes involved in inflammation , by activating the I kappa B kinase ( IKK ) in the early phase of infection .
	manualset3
85554	7	398439	14	13	NULL	NULL	NULL	early phase	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report that HSV type 1 ( HSV-1 ) induces persistent activation of transcription factor NF-kappa B , a critical regulator of genes involved in inflammation , by activating the I kappa B kinase ( IKK ) in the early phase of infection .
	manualset3
85555	8	398439	14	13	NULL	NULL	NULL	infection	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report that HSV type 1 ( HSV-1 ) induces persistent activation of transcription factor NF-kappa B , a critical regulator of genes involved in inflammation , by activating the I kappa B kinase ( IKK ) in the early phase of infection .
	manualset3
86124	3	398439	14	13	NULL	0	NULL	NF-kappa B	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report that HSV type 1 ( HSV-1 ) induces persistent activation of transcription factor NF-kappa B , a critical regulator of genes involved in inflammation , by activating the I kappa B kinase ( IKK ) in the early phase of infection .
	manualset3
85556	1	398440	14	13	NULL	NULL	NULL	endogenous local signaling	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report that only endogenous local signaling at D ( 1 ) dopamine receptors is needed for rostral generation of excessive eating , potentially implicating a direct output pathway contribution .
	manualset3
85557	2	398440	14	13	NULL	0	NULL	 D ( 1 ) dopamine receptors	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report that only endogenous local signaling at D ( 1 ) dopamine receptors is needed for rostral generation of excessive eating , potentially implicating a direct output pathway contribution .
	manualset3
85558	3	398440	14	13	NULL	NULL	NULL	rostral generation	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report that only endogenous local signaling at D ( 1 ) dopamine receptors is needed for rostral generation of excessive eating , potentially implicating a direct output pathway contribution .
	manualset3
85559	5	398440	14	13	NULL	NULL	NULL	output pathway	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report that only endogenous local signaling at D ( 1 ) dopamine receptors is needed for rostral generation of excessive eating , potentially implicating a direct output pathway contribution .
	manualset3
86125	4	398440	14	13	NULL	0	NULL	excessive eating	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report that only endogenous local signaling at D ( 1 ) dopamine receptors is needed for rostral generation of excessive eating , potentially implicating a direct output pathway contribution .
	manualset3
85560	1	398441	14	13	NULL	0	NULL	crystal structure	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report the crystal structure of a squid core complexin-SNARE complex at 2.95-A resolution .
	manualset3
85561	2	398441	14	13	NULL	0	NULL	squid core complexin-SNARE complex	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report the crystal structure of a squid core complexin-SNARE complex at 2.95-A resolution .
	manualset3
85562	3	398441	14	13	NULL	0	NULL	2.95-A resolution	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report the crystal structure of a squid core complexin-SNARE complex at 2.95-A resolution .
	manualset3
85563	1	398442	14	13	NULL	0	NULL	crystal structure	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report the crystal structure of the kinase domain of SnRK2 .6 at 2.6 - resolution .
	manualset3
85564	2	398442	14	13	NULL	0	NULL	kinase domain of SnRK2 .6	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report the crystal structure of the kinase domain of SnRK2 .6 at 2.6 - resolution .
	manualset3
85565	3	398442	14	13	NULL	0	NULL	2.6 - resolution 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report the crystal structure of the kinase domain of SnRK2 .6 at 2.6 - resolution .
	manualset3
85566	1	398443	14	13	NULL	0	NULL	optimisation of immunofluorescent staining	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report the optimisation of immunofluorescent staining for cell surface and intracellular antigens using three-colour flow cytometric analysis to measure the frequency of rat CD3 ( + ) 4 ( + ) T-cells that produce IFN-gamma , IL-4 and IL-10 .
	manualset3
85567	2	398443	14	13	NULL	NULL	NULL	cell surface antigens	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report the optimisation of immunofluorescent staining for cell surface and intracellular antigens using three-colour flow cytometric analysis to measure the frequency of rat CD3 ( + ) 4 ( + ) T-cells that produce IFN-gamma , IL-4 and IL-10 .
	manualset3
85568	3	398443	14	13	NULL	0	NULL	three-colour flow cytometric analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report the optimisation of immunofluorescent staining for cell surface and intracellular antigens using three-colour flow cytometric analysis to measure the frequency of rat CD3 ( + ) 4 ( + ) T-cells that produce IFN-gamma , IL-4 and IL-10 .
	manualset3
85569	4	398443	14	13	NULL	0	NULL	rat CD3 ( + ) 4 ( + ) T-cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report the optimisation of immunofluorescent staining for cell surface and intracellular antigens using three-colour flow cytometric analysis to measure the frequency of rat CD3 ( + ) 4 ( + ) T-cells that produce IFN-gamma , IL-4 and IL-10 .
	manualset3
85570	5	398443	14	13	NULL	0	NULL	IFN-gamma	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report the optimisation of immunofluorescent staining for cell surface and intracellular antigens using three-colour flow cytometric analysis to measure the frequency of rat CD3 ( + ) 4 ( + ) T-cells that produce IFN-gamma , IL-4 and IL-10 .
	manualset3
85571	6	398443	14	13	NULL	0	NULL	IL-4	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report the optimisation of immunofluorescent staining for cell surface and intracellular antigens using three-colour flow cytometric analysis to measure the frequency of rat CD3 ( + ) 4 ( + ) T-cells that produce IFN-gamma , IL-4 and IL-10 .
	manualset3
85572	7	398443	14	13	NULL	0	NULL	 IL-10	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report the optimisation of immunofluorescent staining for cell surface and intracellular antigens using three-colour flow cytometric analysis to measure the frequency of rat CD3 ( + ) 4 ( + ) T-cells that produce IFN-gamma , IL-4 and IL-10 .
	manualset3
86126	8	398443	14	13	NULL	0	NULL	intracellular antigens	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report the optimisation of immunofluorescent staining for cell surface and intracellular antigens using three-colour flow cytometric analysis to measure the frequency of rat CD3 ( + ) 4 ( + ) T-cells that produce IFN-gamma , IL-4 and IL-10 .
	manualset3
85573	1	398444	14	13	NULL	0	NULL	resection	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report the successful complete resection of a giant , local recurrent chondrosarcoma of the chest wall ( max .
	manualset3
85574	2	398444	14	13	NULL	0	NULL	 giant , local recurrent chondrosarcoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report the successful complete resection of a giant , local recurrent chondrosarcoma of the chest wall ( max .
	manualset3
85575	3	398444	14	13	NULL	0	NULL	chest wall 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report the successful complete resection of a giant , local recurrent chondrosarcoma of the chest wall ( max .
	manualset3
85634	1	398445	14	13	NULL	0	NULL	three types	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report three types of responses to EFS in human isolated colon circular muscle : monophasic cholinergic contraction during EFS , biphasic response ( nitrergic relaxation during EFS followed by cholinergic contraction after termination of EFS ) and triphasic response ( cholinergic contraction followed by nitrergic relaxation during EFS and a tachykininergic contraction after EFS ) .
	manualset3
85636	3	398445	14	13	NULL	NULL	NULL	human isolated colon circular muscle	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report three types of responses to EFS in human isolated colon circular muscle : monophasic cholinergic contraction during EFS , biphasic response ( nitrergic relaxation during EFS followed by cholinergic contraction after termination of EFS ) and triphasic response ( cholinergic contraction followed by nitrergic relaxation during EFS and a tachykininergic contraction after EFS ) .
	manualset3
85637	4	398445	14	13	NULL	NULL	NULL	monophasic cholinergic contraction during EFS 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report three types of responses to EFS in human isolated colon circular muscle : monophasic cholinergic contraction during EFS , biphasic response ( nitrergic relaxation during EFS followed by cholinergic contraction after termination of EFS ) and triphasic response ( cholinergic contraction followed by nitrergic relaxation during EFS and a tachykininergic contraction after EFS ) .
	manualset3
85639	6	398445	14	13	NULL	0	NULL	biphasic response	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report three types of responses to EFS in human isolated colon circular muscle : monophasic cholinergic contraction during EFS , biphasic response ( nitrergic relaxation during EFS followed by cholinergic contraction after termination of EFS ) and triphasic response ( cholinergic contraction followed by nitrergic relaxation during EFS and a tachykininergic contraction after EFS ) .
	manualset3
85640	7	398445	14	13	NULL	NULL	NULL	nitrergic relaxation during EFS	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report three types of responses to EFS in human isolated colon circular muscle : monophasic cholinergic contraction during EFS , biphasic response ( nitrergic relaxation during EFS followed by cholinergic contraction after termination of EFS ) and triphasic response ( cholinergic contraction followed by nitrergic relaxation during EFS and a tachykininergic contraction after EFS ) .
	manualset3
85641	8	398445	14	13	NULL	0	NULL	cholinergic contraction after termination of EFS	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report three types of responses to EFS in human isolated colon circular muscle : monophasic cholinergic contraction during EFS , biphasic response ( nitrergic relaxation during EFS followed by cholinergic contraction after termination of EFS ) and triphasic response ( cholinergic contraction followed by nitrergic relaxation during EFS and a tachykininergic contraction after EFS ) .
	manualset3
85642	9	398445	14	13	NULL	0	NULL	triphasic response 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report three types of responses to EFS in human isolated colon circular muscle : monophasic cholinergic contraction during EFS , biphasic response ( nitrergic relaxation during EFS followed by cholinergic contraction after termination of EFS ) and triphasic response ( cholinergic contraction followed by nitrergic relaxation during EFS and a tachykininergic contraction after EFS ) .
	manualset3
85643	10	398445	14	13	NULL	0	NULL	cholinergic contraction followed by nitrergic relaxation during EFS	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report three types of responses to EFS in human isolated colon circular muscle : monophasic cholinergic contraction during EFS , biphasic response ( nitrergic relaxation during EFS followed by cholinergic contraction after termination of EFS ) and triphasic response ( cholinergic contraction followed by nitrergic relaxation during EFS and a tachykininergic contraction after EFS ) .
	manualset3
85644	11	398445	14	13	NULL	0	NULL	tachykininergic contraction after EFS	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we report three types of responses to EFS in human isolated colon circular muscle : monophasic cholinergic contraction during EFS , biphasic response ( nitrergic relaxation during EFS followed by cholinergic contraction after termination of EFS ) and triphasic response ( cholinergic contraction followed by nitrergic relaxation during EFS and a tachykininergic contraction after EFS ) .
	manualset3
86127	2	398445	14	13	NULL	NULL	NULL	responses to EFS	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we report three types of responses to EFS in human isolated colon circular muscle : monophasic cholinergic contraction during EFS , biphasic response ( nitrergic relaxation during EFS followed by cholinergic contraction after termination of EFS ) and triphasic response ( cholinergic contraction followed by nitrergic relaxation during EFS and a tachykininergic contraction after EFS ) .
	manualset3
85653	1	398448	14	13	NULL	NULL	NULL	non-native fish pathogens	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we review the most important non-native fish and shellfish pathogens in European waters and their global impacts on wild fish host populations .
	manualset3
85654	2	398448	14	13	NULL	0	NULL	shellfish pathogens	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we review the most important non-native fish and shellfish pathogens in European waters and their global impacts on wild fish host populations .
	manualset3
85655	3	398448	14	13	NULL	0	NULL	European waters	GeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we review the most important non-native fish and shellfish pathogens in European waters and their global impacts on wild fish host populations .
	manualset3
85656	4	398448	14	13	NULL	0	NULL	wild fish host populations 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we review the most important non-native fish and shellfish pathogens in European waters and their global impacts on wild fish host populations .
	manualset3
85657	1	398449	14	13	NULL	0	NULL	Stat-1 nuclear accumulation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show inhibition of Stat-1 nuclear accumulation in cells that express ICP27 .
	manualset3
85658	2	398449	14	13	NULL	0	NULL	 cells that express ICP27	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show inhibition of Stat-1 nuclear accumulation in cells that express ICP27 .
	manualset3
85659	1	398450	14	13	NULL	NULL	NULL	Synergistic protective effect of testicular cells	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Synergistic protective effect of testicular cells expressing Fas ligand and cyclosporine A on the survival of islet allografts ) .
	manualset3
85663	2	398450	14	13	NULL	0	NULL	 Fas ligand	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	( Synergistic protective effect of testicular cells expressing Fas ligand and cyclosporine A on the survival of islet allografts ) .
	manualset3
85665	3	398450	14	13	NULL	0	NULL	cyclosporine A	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( Synergistic protective effect of testicular cells expressing Fas ligand and cyclosporine A on the survival of islet allografts ) .
	manualset3
85667	4	398450	14	13	NULL	0	NULL	survival of islet allografts	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Synergistic protective effect of testicular cells expressing Fas ligand and cyclosporine A on the survival of islet allografts ) .
	manualset3
85668	1	398451	14	13	NULL	0	NULL	 ADC protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that ADC protein was increasingly expressed at early stages of hop internode culture ( 12h ) .
	manualset3
85669	2	398451	14	13	NULL	0	NULL	early stages	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that ADC protein was increasingly expressed at early stages of hop internode culture ( 12h ) .
	manualset3
85671	3	398451	14	13	NULL	0	NULL	hop internode culture	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that ADC protein was increasingly expressed at early stages of hop internode culture ( 12h ) .
	manualset3
85672	4	398451	14	13	NULL	0	NULL	12h	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that ADC protein was increasingly expressed at early stages of hop internode culture ( 12h ) .
	manualset3
85673	1	398452	14	13	NULL	0	NULL	AcrS	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that AcrS represses other multidrug efflux genes , acrAB , which encode a major efflux system in Escherichia coli .
	manualset3
85676	2	398452	14	13	NULL	0	NULL	multidrug efflux genes 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that AcrS represses other multidrug efflux genes , acrAB , which encode a major efflux system in Escherichia coli .
	manualset3
85678	3	398452	14	13	NULL	0	NULL	acrAB	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that AcrS represses other multidrug efflux genes , acrAB , which encode a major efflux system in Escherichia coli .
	manualset3
85680	4	398452	14	13	NULL	0	NULL	major efflux system	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that AcrS represses other multidrug efflux genes , acrAB , which encode a major efflux system in Escherichia coli .
	manualset3
85681	5	398452	14	13	NULL	0	NULL	Escherichia coli	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that AcrS represses other multidrug efflux genes , acrAB , which encode a major efflux system in Escherichia coli .
	manualset3
85682	1	398453	14	13	NULL	0	NULL	Ad-specific CTLs	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that Ad-specific CTLs recognize the early region 2 proteins DNA polymerase ( Pol ) and DNA-binding protein ( DBP ) .
	manualset3
85683	2	398453	14	13	NULL	NULL	NULL	2	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we show that Ad-specific CTLs recognize the early region 2 proteins DNA polymerase ( Pol ) and DNA-binding protein ( DBP ) .
	manualset3
85684	3	398453	14	13	NULL	0	NULL	 DNA polymerase ( Pol )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that Ad-specific CTLs recognize the early region 2 proteins DNA polymerase ( Pol ) and DNA-binding protein ( DBP ) .
	manualset3
85685	4	398453	14	13	NULL	0	NULL	DNA-binding protein ( DBP )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that Ad-specific CTLs recognize the early region 2 proteins DNA polymerase ( Pol ) and DNA-binding protein ( DBP ) .
	manualset3
86130	2	398453	14	13	NULL	0	NULL	proteins	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that Ad-specific CTLs recognize the early region 2 proteins DNA polymerase ( Pol ) and DNA-binding protein ( DBP ) .
	manualset3
85686	1	398454	14	13	NULL	0	NULL	CD94	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that CD94 , a molecule preferentially expressed by NK cells , is essential for the resistance of C57BL/6 mice to mousepox , a disease caused by the Orthopoxvirus ectromelia virus .
	manualset3
85687	2	398454	14	13	NULL	0	NULL	molecule preferentially expressed	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that CD94 , a molecule preferentially expressed by NK cells , is essential for the resistance of C57BL/6 mice to mousepox , a disease caused by the Orthopoxvirus ectromelia virus .
	manualset3
85688	3	398454	14	13	NULL	0	NULL	NK cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that CD94 , a molecule preferentially expressed by NK cells , is essential for the resistance of C57BL/6 mice to mousepox , a disease caused by the Orthopoxvirus ectromelia virus .
	manualset3
85689	4	398454	14	13	NULL	0	NULL	resistance	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that CD94 , a molecule preferentially expressed by NK cells , is essential for the resistance of C57BL/6 mice to mousepox , a disease caused by the Orthopoxvirus ectromelia virus .
	manualset3
85690	5	398454	14	13	NULL	0	NULL	C57BL/6 mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that CD94 , a molecule preferentially expressed by NK cells , is essential for the resistance of C57BL/6 mice to mousepox , a disease caused by the Orthopoxvirus ectromelia virus .
	manualset3
85691	6	398454	14	13	NULL	0	NULL	mousepox	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that CD94 , a molecule preferentially expressed by NK cells , is essential for the resistance of C57BL/6 mice to mousepox , a disease caused by the Orthopoxvirus ectromelia virus .
	manualset3
85692	7	398454	14	13	NULL	0	NULL	disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that CD94 , a molecule preferentially expressed by NK cells , is essential for the resistance of C57BL/6 mice to mousepox , a disease caused by the Orthopoxvirus ectromelia virus .
	manualset3
85693	8	398454	14	13	NULL	0	NULL	Orthopoxvirus ectromelia virus 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that CD94 , a molecule preferentially expressed by NK cells , is essential for the resistance of C57BL/6 mice to mousepox , a disease caused by the Orthopoxvirus ectromelia virus .
	manualset3
85694	1	398455	14	13	NULL	NULL	NULL	HA scaffolds	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we show that HA scaffolds were stable cell carriers and had the potential to generate volume-retaining tissue .
	manualset3
85696	2	398455	14	13	NULL	NULL	NULL	volume-retaining tissue	Tissue												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we show that HA scaffolds were stable cell carriers and had the potential to generate volume-retaining tissue .
	manualset3
85700	1	398456	14	13	NULL	0	NULL	 LPS	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that LPS induces nuclear expression of c-Rel/p50 heterodimers as well as p50/p65 ( NF-kappa B ) kappa B DNA-binding complexes in human monocytic THP-1 cells .
	manualset3
85701	2	398456	14	13	NULL	0	NULL	nuclear expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that LPS induces nuclear expression of c-Rel/p50 heterodimers as well as p50/p65 ( NF-kappa B ) kappa B DNA-binding complexes in human monocytic THP-1 cells .
	manualset3
85702	3	398456	14	13	NULL	NULL	NULL	c-Rel/p50 heterodimers	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we show that LPS induces nuclear expression of c-Rel/p50 heterodimers as well as p50/p65 ( NF-kappa B ) kappa B DNA-binding complexes in human monocytic THP-1 cells .
	manualset3
85703	4	398456	14	13	NULL	0	NULL	p50/p65 ( NF-kappa B ) kappa B DNA-binding complexes	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that LPS induces nuclear expression of c-Rel/p50 heterodimers as well as p50/p65 ( NF-kappa B ) kappa B DNA-binding complexes in human monocytic THP-1 cells .
	manualset3
85704	5	398456	14	13	NULL	0	NULL	human monocytic THP-1 cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that LPS induces nuclear expression of c-Rel/p50 heterodimers as well as p50/p65 ( NF-kappa B ) kappa B DNA-binding complexes in human monocytic THP-1 cells .
	manualset3
85705	1	398457	14	13	NULL	NULL	NULL	MLS0315771	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we show that MLS0315771 , a potent MPI inhibitor from the benzoisothiazolone series , diverts Man-6-P toward glycosylation in various cell lines including fibroblasts from CDG-Ia patients and improves N-glycosylation .
	manualset3
85706	2	398457	14	13	NULL	NULL	NULL	MPI inhibitor	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we show that MLS0315771 , a potent MPI inhibitor from the benzoisothiazolone series , diverts Man-6-P toward glycosylation in various cell lines including fibroblasts from CDG-Ia patients and improves N-glycosylation .
	manualset3
85707	3	398457	14	13	NULL	NULL	NULL	 benzoisothiazolone series	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we show that MLS0315771 , a potent MPI inhibitor from the benzoisothiazolone series , diverts Man-6-P toward glycosylation in various cell lines including fibroblasts from CDG-Ia patients and improves N-glycosylation .
	manualset3
85708	4	398457	14	13	NULL	NULL	NULL	Man-6-P	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we show that MLS0315771 , a potent MPI inhibitor from the benzoisothiazolone series , diverts Man-6-P toward glycosylation in various cell lines including fibroblasts from CDG-Ia patients and improves N-glycosylation .
	manualset3
85709	5	398457	14	13	NULL	NULL	NULL	glycosylation	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we show that MLS0315771 , a potent MPI inhibitor from the benzoisothiazolone series , diverts Man-6-P toward glycosylation in various cell lines including fibroblasts from CDG-Ia patients and improves N-glycosylation .
	manualset3
85710	6	398457	14	13	NULL	NULL	NULL	various cell lines 	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we show that MLS0315771 , a potent MPI inhibitor from the benzoisothiazolone series , diverts Man-6-P toward glycosylation in various cell lines including fibroblasts from CDG-Ia patients and improves N-glycosylation .
	manualset3
85711	7	398457	14	13	NULL	0	NULL	fibroblasts 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that MLS0315771 , a potent MPI inhibitor from the benzoisothiazolone series , diverts Man-6-P toward glycosylation in various cell lines including fibroblasts from CDG-Ia patients and improves N-glycosylation .
	manualset3
85712	8	398457	14	13	NULL	0	NULL	CDG-Ia patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that MLS0315771 , a potent MPI inhibitor from the benzoisothiazolone series , diverts Man-6-P toward glycosylation in various cell lines including fibroblasts from CDG-Ia patients and improves N-glycosylation .
	manualset3
85713	9	398457	14	13	NULL	0	NULL	N-glycosylation 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that MLS0315771 , a potent MPI inhibitor from the benzoisothiazolone series , diverts Man-6-P toward glycosylation in various cell lines including fibroblasts from CDG-Ia patients and improves N-glycosylation .
	manualset3
85714	1	398458	14	13	NULL	0	NULL	mutations	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that both mutations constitutively activate the mammalian target of rapamycin ( mTOR ) signaling pathway .
	manualset3
85715	2	398458	14	13	NULL	0	NULL	mammalian target of rapamycin ( mTOR ) signaling pathway 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that both mutations constitutively activate the mammalian target of rapamycin ( mTOR ) signaling pathway .
	manualset3
85716	1	398459	14	13	NULL	0	NULL	chimeric PRL receptors	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that chimeric PRL receptors that contain the transmembrane and cytoplasmic domains of the IL-2R beta or beta c-chains transduce in response to PRL tyrosine phosphorylation and activation of Jak1 and Jak2 , respectively .
	manualset3
85717	2	398459	14	13	NULL	0	NULL	transmembrane domains of the IL-2R beta or beta c-chains	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that chimeric PRL receptors that contain the transmembrane and cytoplasmic domains of the IL-2R beta or beta c-chains transduce in response to PRL tyrosine phosphorylation and activation of Jak1 and Jak2 , respectively .
	manualset3
85718	3	398459	14	13	NULL	0	NULL	cytoplasmic domains of the IL-2R beta or beta c-chains	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that chimeric PRL receptors that contain the transmembrane and cytoplasmic domains of the IL-2R beta or beta c-chains transduce in response to PRL tyrosine phosphorylation and activation of Jak1 and Jak2 , respectively .
	manualset3
85719	4	398459	14	13	NULL	0	NULL	PRL tyrosine phosphorylation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that chimeric PRL receptors that contain the transmembrane and cytoplasmic domains of the IL-2R beta or beta c-chains transduce in response to PRL tyrosine phosphorylation and activation of Jak1 and Jak2 , respectively .
	manualset3
85720	5	398459	14	13	NULL	0	NULL	activation of Jak1 and Jak2	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that chimeric PRL receptors that contain the transmembrane and cytoplasmic domains of the IL-2R beta or beta c-chains transduce in response to PRL tyrosine phosphorylation and activation of Jak1 and Jak2 , respectively .
	manualset3
85721	1	398460	14	13	NULL	0	NULL	clam p82 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that clam p82 is related to Xenopus CPEB , an RNA-binding protein that interacts with the U-rich cytoplasmic polyadenylation elements ( CPEs ) of maternal mRNAs and promotes their polyadenylation .
	manualset3
85722	2	398460	14	13	NULL	0	NULL	Xenopus CPEB	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that clam p82 is related to Xenopus CPEB , an RNA-binding protein that interacts with the U-rich cytoplasmic polyadenylation elements ( CPEs ) of maternal mRNAs and promotes their polyadenylation .
	manualset3
85723	3	398460	14	13	NULL	0	NULL	RNA-binding protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that clam p82 is related to Xenopus CPEB , an RNA-binding protein that interacts with the U-rich cytoplasmic polyadenylation elements ( CPEs ) of maternal mRNAs and promotes their polyadenylation .
	manualset3
85724	4	398460	14	13	NULL	0	NULL	U-rich cytoplasmic polyadenylation elements ( CPEs ) of maternal mRNAs	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that clam p82 is related to Xenopus CPEB , an RNA-binding protein that interacts with the U-rich cytoplasmic polyadenylation elements ( CPEs ) of maternal mRNAs and promotes their polyadenylation .
	manualset3
85725	5	398460	14	13	NULL	0	NULL	polyadenylation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that clam p82 is related to Xenopus CPEB , an RNA-binding protein that interacts with the U-rich cytoplasmic polyadenylation elements ( CPEs ) of maternal mRNAs and promotes their polyadenylation .
	manualset3
85726	1	398461	14	13	NULL	0	NULL	 commensal microbiota 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that encounter with commensal microbiota results in the peripheral generation of T ( reg ) cells rather than pathogenic effectors .
	manualset3
85727	2	398461	14	13	NULL	0	NULL	peripheral generation of T ( reg ) cells 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that encounter with commensal microbiota results in the peripheral generation of T ( reg ) cells rather than pathogenic effectors .
	manualset3
85728	3	398461	14	13	NULL	0	NULL	pathogenic effectors	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that encounter with commensal microbiota results in the peripheral generation of T ( reg ) cells rather than pathogenic effectors .
	manualset3
85729	1	398462	14	13	NULL	0	NULL	mTOR	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that mTOR is necessary for the maintenance of mitochondrial oxidative function .
	manualset3
85730	2	398462	14	13	NULL	NULL	NULL	maintenance of mitochondrial oxidative function function 	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we show that mTOR is necessary for the maintenance of mitochondrial oxidative function .
	manualset3
85731	1	398463	14	13	NULL	NULL	NULL	Mcm proteins	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we show that the Mcm proteins of budding yeast are abundant and are quantitatively found in a chromatin-enriched fraction specifically during the G1 phase of the cell cycle .
	manualset3
85732	2	398463	14	13	NULL	0	NULL	budding yeast	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that the Mcm proteins of budding yeast are abundant and are quantitatively found in a chromatin-enriched fraction specifically during the G1 phase of the cell cycle .
	manualset3
85733	3	398463	14	13	NULL	0	NULL	chromatin-enriched fraction 	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that the Mcm proteins of budding yeast are abundant and are quantitatively found in a chromatin-enriched fraction specifically during the G1 phase of the cell cycle .
	manualset3
85734	4	398463	14	13	NULL	0	NULL	G1 phase of the cell cycle	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that the Mcm proteins of budding yeast are abundant and are quantitatively found in a chromatin-enriched fraction specifically during the G1 phase of the cell cycle .
	manualset3
85735	1	398464	14	13	NULL	NULL	NULL	color octet mechanism 	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we show that the color octet mechanism reproduces the RHIC data for J/psi production in pp collisions with respect to the p ( T ) distribution , the rapidity distribution , and the total cross section at square root = 200 GeV .
	manualset3
85736	2	398464	14	13	NULL	NULL	NULL	data 	PublishedSourceOfInformation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we show that the color octet mechanism reproduces the RHIC data for J/psi production in pp collisions with respect to the p ( T ) distribution , the rapidity distribution , and the total cross section at square root = 200 GeV .
	manualset3
85737	6	398464	14	13	NULL	NULL	NULL	square root = 200 GeV	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we show that the color octet mechanism reproduces the RHIC data for J/psi production in pp collisions with respect to the p ( T ) distribution , the rapidity distribution , and the total cross section at square root = 200 GeV .
	manualset3
86131	3	398464	14	13	NULL	NULL	NULL	J/psi production 	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we show that the color octet mechanism reproduces the RHIC data for J/psi production in pp collisions with respect to the p ( T ) distribution , the rapidity distribution , and the total cross section at square root = 200 GeV .
	manualset3
86132	4	398464	14	13	NULL	NULL	NULL	pp collisions	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we show that the color octet mechanism reproduces the RHIC data for J/psi production in pp collisions with respect to the p ( T ) distribution , the rapidity distribution , and the total cross section at square root = 200 GeV .
	manualset3
86133	5	398464	14	13	NULL	NULL	NULL	p ( T ) distribution	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we show that the color octet mechanism reproduces the RHIC data for J/psi production in pp collisions with respect to the p ( T ) distribution , the rapidity distribution , and the total cross section at square root = 200 GeV .
	manualset3
86143	7	398464	14	13	NULL	0	NULL	RHIC	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that the color octet mechanism reproduces the RHIC data for J/psi production in pp collisions with respect to the p ( T ) distribution , the rapidity distribution , and the total cross section at square root = 200 GeV .
	manualset3
86144	8	398464	14	13	NULL	0	NULL	rapidity distribution	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that the color octet mechanism reproduces the RHIC data for J/psi production in pp collisions with respect to the p ( T ) distribution , the rapidity distribution , and the total cross section at square root = 200 GeV .
	manualset3
86145	9	398464	14	13	NULL	0	NULL	total cross section	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that the color octet mechanism reproduces the RHIC data for J/psi production in pp collisions with respect to the p ( T ) distribution , the rapidity distribution , and the total cross section at square root = 200 GeV .
	manualset3
85738	1	398465	14	13	NULL	0	NULL	neoplastic cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that the neoplastic cells of many human breast cancers express the ROR1 protein and high-level expression of ROR1 in breast adenocarcinoma was associated with aggressive disease .
	manualset3
85739	2	398465	14	13	NULL	0	NULL	human breast cancers	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that the neoplastic cells of many human breast cancers express the ROR1 protein and high-level expression of ROR1 in breast adenocarcinoma was associated with aggressive disease .
	manualset3
85740	3	398465	14	13	NULL	0	NULL	ROR1 protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that the neoplastic cells of many human breast cancers express the ROR1 protein and high-level expression of ROR1 in breast adenocarcinoma was associated with aggressive disease .
	manualset3
85741	4	398465	14	13	NULL	0	NULL	high-level expression of ROR1	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that the neoplastic cells of many human breast cancers express the ROR1 protein and high-level expression of ROR1 in breast adenocarcinoma was associated with aggressive disease .
	manualset3
85742	5	398465	14	13	NULL	0	NULL	breast adenocarcinoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that the neoplastic cells of many human breast cancers express the ROR1 protein and high-level expression of ROR1 in breast adenocarcinoma was associated with aggressive disease .
	manualset3
85743	6	398465	14	13	NULL	0	NULL	aggressive disease	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that the neoplastic cells of many human breast cancers express the ROR1 protein and high-level expression of ROR1 in breast adenocarcinoma was associated with aggressive disease .
	manualset3
85744	1	398466	14	13	NULL	0	NULL	vitellogenin mRNA-binding protein ( VitRNABP )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that the vitellogenin mRNA-binding protein ( VitRNABP ) is vigilin .
	manualset3
85745	2	398466	14	13	NULL	0	NULL	vigilin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we show that the vitellogenin mRNA-binding protein ( VitRNABP ) is vigilin .
	manualset3
85746	1	398467	14	13	NULL	0	NULL	human insulin ( HI )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we studied the role of human insulin ( HI ) in breast milk as a modulator of the immune response to insulin .
	manualset3
85747	2	398467	14	13	NULL	NULL	NULL	breast milk 	Food												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we studied the role of human insulin ( HI ) in breast milk as a modulator of the immune response to insulin .
	manualset3
85748	3	398467	14	13	NULL	0	NULL	immune response	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we studied the role of human insulin ( HI ) in breast milk as a modulator of the immune response to insulin .
	manualset3
85749	4	398467	14	13	NULL	0	NULL	 insulin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we studied the role of human insulin ( HI ) in breast milk as a modulator of the immune response to insulin .
	manualset3
85752	1	398468	14	13	NULL	0	NULL	pattern of expression of certain genes	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we summarise the pattern of expression of certain genes involved in the eye network that have been isolated in planarians , such as Otx , Pax-6 , Six , Rax and opsin .
	manualset3
85753	2	398468	14	13	NULL	0	NULL	eye network	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we summarise the pattern of expression of certain genes involved in the eye network that have been isolated in planarians , such as Otx , Pax-6 , Six , Rax and opsin .
	manualset3
85754	3	398468	14	13	NULL	0	NULL	planarians	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we summarise the pattern of expression of certain genes involved in the eye network that have been isolated in planarians , such as Otx , Pax-6 , Six , Rax and opsin .
	manualset3
85755	4	398468	14	13	NULL	0	NULL	Otx	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we summarise the pattern of expression of certain genes involved in the eye network that have been isolated in planarians , such as Otx , Pax-6 , Six , Rax and opsin .
	manualset3
85756	5	398468	14	13	NULL	0	NULL	Pax-6	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we summarise the pattern of expression of certain genes involved in the eye network that have been isolated in planarians , such as Otx , Pax-6 , Six , Rax and opsin .
	manualset3
85757	6	398468	14	13	NULL	0	NULL	Six	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we summarise the pattern of expression of certain genes involved in the eye network that have been isolated in planarians , such as Otx , Pax-6 , Six , Rax and opsin .
	manualset3
85758	7	398468	14	13	NULL	0	NULL	Rax	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we summarise the pattern of expression of certain genes involved in the eye network that have been isolated in planarians , such as Otx , Pax-6 , Six , Rax and opsin .
	manualset3
85759	8	398468	14	13	NULL	0	NULL	opsin	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we summarise the pattern of expression of certain genes involved in the eye network that have been isolated in planarians , such as Otx , Pax-6 , Six , Rax and opsin .
	manualset3
85760	1	398469	14	13	NULL	0	NULL	 immunogenicity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we tested the immunogenicity and protective effectiveness of attenuated F18ac ( + ) non-ETEC vaccine candidate strain against challenge infection with F4ac ( + ) ETEC strain by quantitative phenotypic analysis of small intestinal leukocyte subsets in weaned pigs .
	manualset3
85761	2	398469	14	13	NULL	0	NULL	protective effectiveness 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we tested the immunogenicity and protective effectiveness of attenuated F18ac ( + ) non-ETEC vaccine candidate strain against challenge infection with F4ac ( + ) ETEC strain by quantitative phenotypic analysis of small intestinal leukocyte subsets in weaned pigs .
	manualset3
85762	3	398469	14	13	NULL	0	NULL	attenuated F18ac ( + ) non-ETEC vaccine candidate strain	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we tested the immunogenicity and protective effectiveness of attenuated F18ac ( + ) non-ETEC vaccine candidate strain against challenge infection with F4ac ( + ) ETEC strain by quantitative phenotypic analysis of small intestinal leukocyte subsets in weaned pigs .
	manualset3
85763	4	398469	14	13	NULL	0	NULL	challenge infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we tested the immunogenicity and protective effectiveness of attenuated F18ac ( + ) non-ETEC vaccine candidate strain against challenge infection with F4ac ( + ) ETEC strain by quantitative phenotypic analysis of small intestinal leukocyte subsets in weaned pigs .
	manualset3
85764	5	398469	14	13	NULL	0	NULL	F4ac ( + ) ETEC strain	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we tested the immunogenicity and protective effectiveness of attenuated F18ac ( + ) non-ETEC vaccine candidate strain against challenge infection with F4ac ( + ) ETEC strain by quantitative phenotypic analysis of small intestinal leukocyte subsets in weaned pigs .
	manualset3
85765	6	398469	14	13	NULL	0	NULL	quantitative phenotypic analysis 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we tested the immunogenicity and protective effectiveness of attenuated F18ac ( + ) non-ETEC vaccine candidate strain against challenge infection with F4ac ( + ) ETEC strain by quantitative phenotypic analysis of small intestinal leukocyte subsets in weaned pigs .
	manualset3
85766	7	398469	14	13	NULL	0	NULL	small intestinal leukocyte subsets	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we tested the immunogenicity and protective effectiveness of attenuated F18ac ( + ) non-ETEC vaccine candidate strain against challenge infection with F4ac ( + ) ETEC strain by quantitative phenotypic analysis of small intestinal leukocyte subsets in weaned pigs .
	manualset3
85767	8	398469	14	13	NULL	0	NULL	weaned pigs	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we tested the immunogenicity and protective effectiveness of attenuated F18ac ( + ) non-ETEC vaccine candidate strain against challenge infection with F4ac ( + ) ETEC strain by quantitative phenotypic analysis of small intestinal leukocyte subsets in weaned pigs .
	manualset3
85768	1	398470	14	13	NULL	0	NULL	 Synthesis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Synthesis of porcine brain natriuretic peptide ( BNP-26 ) and an analog ) .
	manualset3
85769	2	398470	14	13	NULL	NULL	NULL	porcine brain natriuretic peptide ( BNP-26 )	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Synthesis of porcine brain natriuretic peptide ( BNP-26 ) and an analog ) .
	manualset3
85770	3	398470	14	13	NULL	NULL	NULL	analog	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Synthesis of porcine brain natriuretic peptide ( BNP-26 ) and an analog ) .
	manualset3
85777	1	398472	14	13	NULL	NULL	NULL	fiber taper waveguide	Facility												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we use a fiber taper waveguide to perform direct optical spectroscopy of a system consisting of a quantum dot embedded in a microdisk .
	manualset3
85778	2	398472	14	13	NULL	NULL	NULL	optical spectroscopy	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we use a fiber taper waveguide to perform direct optical spectroscopy of a system consisting of a quantum dot embedded in a microdisk .
	manualset3
85779	4	398472	14	13	NULL	NULL	NULL	microdisk 	Facility												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we use a fiber taper waveguide to perform direct optical spectroscopy of a system consisting of a quantum dot embedded in a microdisk .
	manualset3
86134	3	398472	14	13	NULL	0	NULL	quantum dot \t	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we use a fiber taper waveguide to perform direct optical spectroscopy of a system consisting of a quantum dot embedded in a microdisk .
	manualset3
85780	1	398473	14	13	NULL	NULL	NULL	genetic recapture data	PublishedSourceOfInformation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we used genetic recapture data to quantify male site fidelity at a colony of Antarctic fur seals where an aerial walkway provides unprecedented access and individual positions are determined daily to 1 m accuracy .
	manualset3
85781	2	398473	14	13	NULL	0	NULL	male site fidelity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we used genetic recapture data to quantify male site fidelity at a colony of Antarctic fur seals where an aerial walkway provides unprecedented access and individual positions are determined daily to 1 m accuracy .
	manualset3
85782	3	398473	14	13	NULL	0	NULL	 colony of Antarctic fur seals 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we used genetic recapture data to quantify male site fidelity at a colony of Antarctic fur seals where an aerial walkway provides unprecedented access and individual positions are determined daily to 1 m accuracy .
	manualset3
85783	4	398473	14	13	NULL	NULL	NULL	 aerial walkway	Thing												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we used genetic recapture data to quantify male site fidelity at a colony of Antarctic fur seals where an aerial walkway provides unprecedented access and individual positions are determined daily to 1 m accuracy .
	manualset3
85784	5	398473	14	13	NULL	0	NULL	daily	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we used genetic recapture data to quantify male site fidelity at a colony of Antarctic fur seals where an aerial walkway provides unprecedented access and individual positions are determined daily to 1 m accuracy .
	manualset3
85785	6	398473	14	13	NULL	NULL	NULL	1 m 	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Here we used genetic recapture data to quantify male site fidelity at a colony of Antarctic fur seals where an aerial walkway provides unprecedented access and individual positions are determined daily to 1 m accuracy .
	manualset3
85786	1	398474	14	13	NULL	0	NULL	intrahippocampal microinfusion	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we used intrahippocampal microinfusion of BDNF to analyze its effects on functional and structural synaptic plasticity induced by subsequent mossy fiber HFS sufficient to induce LTP in adult rats , in vivo .
	manualset3
85787	2	398474	14	13	NULL	0	NULL	BDNF	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we used intrahippocampal microinfusion of BDNF to analyze its effects on functional and structural synaptic plasticity induced by subsequent mossy fiber HFS sufficient to induce LTP in adult rats , in vivo .
	manualset3
85788	3	398474	14	13	NULL	0	NULL	functional and structural synaptic plasticity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we used intrahippocampal microinfusion of BDNF to analyze its effects on functional and structural synaptic plasticity induced by subsequent mossy fiber HFS sufficient to induce LTP in adult rats , in vivo .
	manualset3
85789	4	398474	14	13	NULL	0	NULL	mossy fiber	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we used intrahippocampal microinfusion of BDNF to analyze its effects on functional and structural synaptic plasticity induced by subsequent mossy fiber HFS sufficient to induce LTP in adult rats , in vivo .
	manualset3
85790	5	398474	14	13	NULL	0	NULL	HFS	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we used intrahippocampal microinfusion of BDNF to analyze its effects on functional and structural synaptic plasticity induced by subsequent mossy fiber HFS sufficient to induce LTP in adult rats , in vivo .
	manualset3
85791	6	398474	14	13	NULL	0	NULL	LTP	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we used intrahippocampal microinfusion of BDNF to analyze its effects on functional and structural synaptic plasticity induced by subsequent mossy fiber HFS sufficient to induce LTP in adult rats , in vivo .
	manualset3
85792	7	398474	14	13	NULL	0	NULL	adult rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we used intrahippocampal microinfusion of BDNF to analyze its effects on functional and structural synaptic plasticity induced by subsequent mossy fiber HFS sufficient to induce LTP in adult rats , in vivo .
	manualset3
85793	1	398475	14	13	NULL	0	NULL	linkage group selection	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we used linkage group selection and Solexa whole-genome resequencing to investigate the genetic basis of resistance to component drugs of ACTs .
	manualset3
85794	2	398475	14	13	NULL	0	NULL	Solexa whole-genome resequencing	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we used linkage group selection and Solexa whole-genome resequencing to investigate the genetic basis of resistance to component drugs of ACTs .
	manualset3
85795	3	398475	14	13	NULL	0	NULL	genetic basis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we used linkage group selection and Solexa whole-genome resequencing to investigate the genetic basis of resistance to component drugs of ACTs .
	manualset3
85796	4	398475	14	13	NULL	0	NULL	resistance 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we used linkage group selection and Solexa whole-genome resequencing to investigate the genetic basis of resistance to component drugs of ACTs .
	manualset3
85797	5	398475	14	13	NULL	0	NULL	component drugs	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we used linkage group selection and Solexa whole-genome resequencing to investigate the genetic basis of resistance to component drugs of ACTs .
	manualset3
85798	6	398475	14	13	NULL	0	NULL	ACTs	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Here we used linkage group selection and Solexa whole-genome resequencing to investigate the genetic basis of resistance to component drugs of ACTs .
	manualset3
85799	1	398476	14	13	NULL	0	NULL	Hereditary angioedema ( HAE )	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary angioedema ( HAE ) is a rare disorder characterized by recurrent attacks of swelling that may involve multiple anatomical locations .
	manualset3
85800	3	398476	14	13	NULL	0	NULL	recurrent attacks of swelling 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary angioedema ( HAE ) is a rare disorder characterized by recurrent attacks of swelling that may involve multiple anatomical locations .
	manualset3
85801	2	398476	14	13	NULL	0	NULL	 rare disorder	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary angioedema ( HAE ) is a rare disorder characterized by recurrent attacks of swelling that may involve multiple anatomical locations .
	manualset3
85802	4	398476	14	13	NULL	0	NULL	multiple anatomical locations	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary angioedema ( HAE ) is a rare disorder characterized by recurrent attacks of swelling that may involve multiple anatomical locations .
	manualset3
85803	1	398477	14	13	NULL	0	NULL	Hereditary inclusion body myopathy ( HIBM )	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary inclusion body myopathy ( HIBM ) is a young-adult onset autosomal recessive disorder caused by a hypomorphic rate limiting enzyme of sialic acid biosynthesis .
	manualset3
85804	2	398477	14	13	NULL	0	NULL	young-adult onset autosomal recessive disorder	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary inclusion body myopathy ( HIBM ) is a young-adult onset autosomal recessive disorder caused by a hypomorphic rate limiting enzyme of sialic acid biosynthesis .
	manualset3
85805	3	398477	14	13	NULL	0	NULL	hypomorphic rate limiting enzyme	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary inclusion body myopathy ( HIBM ) is a young-adult onset autosomal recessive disorder caused by a hypomorphic rate limiting enzyme of sialic acid biosynthesis .
	manualset3
85806	4	398477	14	13	NULL	0	NULL	sialic acid biosynthesis 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary inclusion body myopathy ( HIBM ) is a young-adult onset autosomal recessive disorder caused by a hypomorphic rate limiting enzyme of sialic acid biosynthesis .
	manualset3
85807	1	398478	14	13	NULL	0	NULL	Hereditary nonpolyposis colorectal cancer ( HNPCC )	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary nonpolyposis colorectal cancer ( HNPCC ) is a major cancer susceptibility syndrome known to be caused by the inheritance of mutations in DNA mismatch repair genes , such as hMSH2 , hMLH1 , hPMS1 and hPMS2 .
	manualset3
85808	2	398478	14	13	NULL	0	NULL	major cancer susceptibility syndrome	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary nonpolyposis colorectal cancer ( HNPCC ) is a major cancer susceptibility syndrome known to be caused by the inheritance of mutations in DNA mismatch repair genes , such as hMSH2 , hMLH1 , hPMS1 and hPMS2 .
	manualset3
85809	3	398478	14	13	NULL	0	NULL	inheritance of mutations	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary nonpolyposis colorectal cancer ( HNPCC ) is a major cancer susceptibility syndrome known to be caused by the inheritance of mutations in DNA mismatch repair genes , such as hMSH2 , hMLH1 , hPMS1 and hPMS2 .
	manualset3
85810	4	398478	14	13	NULL	0	NULL	DNA mismatch repair genes	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary nonpolyposis colorectal cancer ( HNPCC ) is a major cancer susceptibility syndrome known to be caused by the inheritance of mutations in DNA mismatch repair genes , such as hMSH2 , hMLH1 , hPMS1 and hPMS2 .
	manualset3
85811	5	398478	14	13	NULL	0	NULL	hMSH2	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary nonpolyposis colorectal cancer ( HNPCC ) is a major cancer susceptibility syndrome known to be caused by the inheritance of mutations in DNA mismatch repair genes , such as hMSH2 , hMLH1 , hPMS1 and hPMS2 .
	manualset3
85812	6	398478	14	13	NULL	0	NULL	hMLH1 	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary nonpolyposis colorectal cancer ( HNPCC ) is a major cancer susceptibility syndrome known to be caused by the inheritance of mutations in DNA mismatch repair genes , such as hMSH2 , hMLH1 , hPMS1 and hPMS2 .
	manualset3
85813	7	398478	14	13	NULL	0	NULL	hPMS1	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary nonpolyposis colorectal cancer ( HNPCC ) is a major cancer susceptibility syndrome known to be caused by the inheritance of mutations in DNA mismatch repair genes , such as hMSH2 , hMLH1 , hPMS1 and hPMS2 .
	manualset3
85814	8	398478	14	13	NULL	0	NULL	hPMS2 	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary nonpolyposis colorectal cancer ( HNPCC ) is a major cancer susceptibility syndrome known to be caused by the inheritance of mutations in DNA mismatch repair genes , such as hMSH2 , hMLH1 , hPMS1 and hPMS2 .
	manualset3
85815	1	398479	14	13	NULL	0	NULL	Hereditary spherocytosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary spherocytosis and elliptocytosis erythrocytes show a normal transbilayer phospholipid distribution .
	manualset3
85816	2	398479	14	13	NULL	0	NULL	elliptocytosis erythrocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary spherocytosis and elliptocytosis erythrocytes show a normal transbilayer phospholipid distribution .
	manualset3
85817	3	398479	14	13	NULL	0	NULL	normal transbilayer phospholipid distribution	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hereditary spherocytosis and elliptocytosis erythrocytes show a normal transbilayer phospholipid distribution .
	manualset3
85823	1	398481	14	13	NULL	NULL	NULL	Synthesis of quinolines	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Synthesis of quinolines from safrole ) .
	manualset3
85824	2	398481	14	13	NULL	0	NULL	safrole	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( Synthesis of quinolines from safrole ) .
	manualset3
85830	1	398483	14	13	NULL	0	NULL	hispolon	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Herein , we report our findings that hispolon inhibited breast and bladder cancer cell growth , regardless of p53 status .
	manualset3
85831	2	398483	14	13	NULL	0	NULL	 breast and bladder cancer cell growth	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Herein , we report our findings that hispolon inhibited breast and bladder cancer cell growth , regardless of p53 status .
	manualset3
85832	3	398483	14	13	NULL	0	NULL	p53	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Herein , we report our findings that hispolon inhibited breast and bladder cancer cell growth , regardless of p53 status .
	manualset3
85833	1	398484	14	13	NULL	NULL	NULL	epigenetic findings	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Herein , we review relevant epigenetic findings associated with psoriasis , and provide clues and directions for further studies in this field .
	manualset3
85834	2	398484	14	13	NULL	NULL	NULL	psoriasis	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Herein , we review relevant epigenetic findings associated with psoriasis , and provide clues and directions for further studies in this field .
	manualset3
86146	3	398484	14	13	NULL	0	NULL	studies 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Herein , we review relevant epigenetic findings associated with psoriasis , and provide clues and directions for further studies in this field .
	manualset3
85836	1	398485	14	13	NULL	0	NULL	SrTiO ( 3 ) 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Herein we show that metallic interfaces can be realized in SrTiO ( 3 ) - based heterostructures with various insulating overlayers of amorphous LaAlO ( 3 ) , SrTiO ( 3 ) , and yttria-stabilized zirconia films .
	manualset3
85837	2	398485	14	13	NULL	0	NULL	 amorphous LaAlO ( 3 ) 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Herein we show that metallic interfaces can be realized in SrTiO ( 3 ) - based heterostructures with various insulating overlayers of amorphous LaAlO ( 3 ) , SrTiO ( 3 ) , and yttria-stabilized zirconia films .
	manualset3
85838	3	398485	14	13	NULL	0	NULL	SrTiO ( 3 )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Herein we show that metallic interfaces can be realized in SrTiO ( 3 ) - based heterostructures with various insulating overlayers of amorphous LaAlO ( 3 ) , SrTiO ( 3 ) , and yttria-stabilized zirconia films .
	manualset3
85839	4	398485	14	13	NULL	NULL	NULL	yttria-stabilized zirconia films	Facility												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Herein we show that metallic interfaces can be realized in SrTiO ( 3 ) - based heterostructures with various insulating overlayers of amorphous LaAlO ( 3 ) , SrTiO ( 3 ) , and yttria-stabilized zirconia films .
	manualset3
85846	1	398487	14	13	NULL	NULL	NULL	Herniography	MedicalDevice												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Herniography , computed tomography ( CT ) , and magnetic resonance ( MR ) imaging are also helpful in diagnosis .
	manualset3
85847	2	398487	14	13	NULL	NULL	NULL	computed tomography ( CT ) 	MedicalDevice												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Herniography , computed tomography ( CT ) , and magnetic resonance ( MR ) imaging are also helpful in diagnosis .
	manualset3
85848	3	398487	14	13	NULL	NULL	NULL	magnetic resonance ( MR ) imaging	MedicalDevice												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Herniography , computed tomography ( CT ) , and magnetic resonance ( MR ) imaging are also helpful in diagnosis .
	manualset3
85849	4	398487	14	13	NULL	0	NULL	diagnosis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Herniography , computed tomography ( CT ) , and magnetic resonance ( MR ) imaging are also helpful in diagnosis .
	manualset3
85850	1	398488	14	13	NULL	NULL	NULL	Systems for financing and delivery 	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Systems for financing and delivery of dental care ) .
	manualset3
85851	2	398488	14	13	NULL	0	NULL	dental care	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Systems for financing and delivery of dental care ) .
	manualset3
85852	1	398489	14	13	NULL	NULL	NULL	Herpes simplex virus type 1 infection	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Herpes simplex virus type 1 infection activates the Epstein-Barr virus replicative cycle via a CREB-dependent mechanism .
	manualset3
85853	2	398489	14	13	NULL	0	NULL	Epstein-Barr virus replicative cycle	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Herpes simplex virus type 1 infection activates the Epstein-Barr virus replicative cycle via a CREB-dependent mechanism .
	manualset3
85854	3	398489	14	13	NULL	0	NULL	 CREB-dependent mechanism	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Herpes simplex virus type 1 infection activates the Epstein-Barr virus replicative cycle via a CREB-dependent mechanism .
	manualset3
85855	1	398490	14	13	NULL	0	NULL	Herpes simplex virus type 2 meningitis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Herpes simplex virus type 2 meningitis and associated genital lesions in a three-year-old child .
	manualset3
85856	2	398490	14	13	NULL	0	NULL	genital lesions	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Herpes simplex virus type 2 meningitis and associated genital lesions in a three-year-old child .
	manualset3
85857	3	398490	14	13	NULL	0	NULL	three-year-old child	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Herpes simplex virus type 2 meningitis and associated genital lesions in a three-year-old child .
	manualset3
85858	1	398491	14	13	NULL	0	NULL	Heteroaromatic synthesis 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Heteroaromatic synthesis via olefin cross-metathesis : entry to polysubstituted pyridines .
	manualset3
85859	2	398491	14	13	NULL	0	NULL	olefin cross-metathesis	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Heteroaromatic synthesis via olefin cross-metathesis : entry to polysubstituted pyridines .
	manualset3
85861	3	398491	14	13	NULL	0	NULL	polysubstituted pyridines	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Heteroaromatic synthesis via olefin cross-metathesis : entry to polysubstituted pyridines .
	manualset3
85862	1	398492	14	13	NULL	0	NULL	Heterochromatisation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterochromatisation as a change of chromosome cycle .
	manualset3
85863	2	398492	14	13	NULL	0	NULL	chromosome cycle	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterochromatisation as a change of chromosome cycle .
	manualset3
85864	1	398493	14	13	NULL	0	NULL	Heteroduplex analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Heteroduplex analysis and restriction endonuclease mapping experiments indicate that the LpE family is more closely related to the B-C than the A-D family of early histone genes .
	manualset3
85865	2	398493	14	13	NULL	0	NULL	restriction endonuclease mapping experiments	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Heteroduplex analysis and restriction endonuclease mapping experiments indicate that the LpE family is more closely related to the B-C than the A-D family of early histone genes .
	manualset3
85866	3	398493	14	13	NULL	0	NULL	LpE family	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Heteroduplex analysis and restriction endonuclease mapping experiments indicate that the LpE family is more closely related to the B-C than the A-D family of early histone genes .
	manualset3
85867	4	398493	14	13	NULL	0	NULL	B-C family	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Heteroduplex analysis and restriction endonuclease mapping experiments indicate that the LpE family is more closely related to the B-C than the A-D family of early histone genes .
	manualset3
85868	5	398493	14	13	NULL	0	NULL	A-D family of early histone genes	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Heteroduplex analysis and restriction endonuclease mapping experiments indicate that the LpE family is more closely related to the B-C than the A-D family of early histone genes .
	manualset3
85873	1	398495	14	13	NULL	0	NULL	Heterogeneous nuclear RNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterogeneous nuclear RNA is normally complexed with a specific set of proteins , forming ribonucleoprotein particles termed hnRNP .
	manualset3
85874	2	398495	14	13	NULL	0	NULL	specific set of proteins	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterogeneous nuclear RNA is normally complexed with a specific set of proteins , forming ribonucleoprotein particles termed hnRNP .
	manualset3
85875	3	398495	14	13	NULL	0	NULL	ribonucleoprotein particles	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterogeneous nuclear RNA is normally complexed with a specific set of proteins , forming ribonucleoprotein particles termed hnRNP .
	manualset3
85876	4	398495	14	13	NULL	0	NULL	hnRNP	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterogeneous nuclear RNA is normally complexed with a specific set of proteins , forming ribonucleoprotein particles termed hnRNP .
	manualset3
85877	1	398496	14	13	NULL	0	NULL	Heterogeneous ribonucleoprotein C	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterogeneous ribonucleoprotein C displays a repressor activity mediated by T-cell intracellular antigen-1-related / like protein to modulate Fas exon 6 splicing through a mechanism involving Hu antigen R .
	manualset3
85878	2	398496	14	13	NULL	0	NULL	repressor activity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterogeneous ribonucleoprotein C displays a repressor activity mediated by T-cell intracellular antigen-1-related / like protein to modulate Fas exon 6 splicing through a mechanism involving Hu antigen R .
	manualset3
85879	3	398496	14	13	NULL	0	NULL	T-cell intracellular antigen-1-related / like protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterogeneous ribonucleoprotein C displays a repressor activity mediated by T-cell intracellular antigen-1-related / like protein to modulate Fas exon 6 splicing through a mechanism involving Hu antigen R .
	manualset3
85880	4	398496	14	13	NULL	0	NULL	Fas exon 6 splicing	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterogeneous ribonucleoprotein C displays a repressor activity mediated by T-cell intracellular antigen-1-related / like protein to modulate Fas exon 6 splicing through a mechanism involving Hu antigen R .
	manualset3
85881	5	398496	14	13	NULL	0	NULL	Hu antigen R	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterogeneous ribonucleoprotein C displays a repressor activity mediated by T-cell intracellular antigen-1-related / like protein to modulate Fas exon 6 splicing through a mechanism involving Hu antigen R .
	manualset3
85882	1	398497	14	13	NULL	0	NULL	Heterokaryosis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterokaryosis in Fusarium oxysporum f. sp .
	manualset3
85883	2	398497	14	13	NULL	0	NULL	Fusarium oxysporum f. sp	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterokaryosis in Fusarium oxysporum f. sp .
	manualset3
85884	1	398498	14	13	NULL	0	NULL	Heterologous expression of lipoprotein-associated phospholipase A2 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterologous expression of lipoprotein-associated phospholipase A2 in different expression systems .
	manualset3
86140	2	398498	14	13	NULL	0	NULL	 different expression systems	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterologous expression of lipoprotein-associated phospholipase A2 in different expression systems .
	manualset3
85885	1	398499	14	13	NULL	0	NULL	Heterooligomerization	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterooligomerization of human dopamine receptor 2 and somatostatin receptor 2 Co-immunoprecipitation and fluorescence resonance energy transfer analysis .
	manualset3
85886	2	398499	14	13	NULL	0	NULL	human dopamine receptor 2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterooligomerization of human dopamine receptor 2 and somatostatin receptor 2 Co-immunoprecipitation and fluorescence resonance energy transfer analysis .
	manualset3
85887	3	398499	14	13	NULL	0	NULL	somatostatin receptor 2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterooligomerization of human dopamine receptor 2 and somatostatin receptor 2 Co-immunoprecipitation and fluorescence resonance energy transfer analysis .
	manualset3
85888	4	398499	14	13	NULL	0	NULL	Co-immunoprecipitation 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterooligomerization of human dopamine receptor 2 and somatostatin receptor 2 Co-immunoprecipitation and fluorescence resonance energy transfer analysis .
	manualset3
85889	5	398499	14	13	NULL	0	NULL	fluorescence resonance energy transfer analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterooligomerization of human dopamine receptor 2 and somatostatin receptor 2 Co-immunoprecipitation and fluorescence resonance energy transfer analysis .
	manualset3
85890	1	398500	14	13	NULL	0	NULL	Heterophile antibodies	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterophile antibodies and the diagnosis of Rocky Mountain spotted fever .
	manualset3
85891	2	398500	14	13	NULL	NULL	NULL	diagnosis 	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Heterophile antibodies and the diagnosis of Rocky Mountain spotted fever .
	manualset3
85894	3	398500	14	13	NULL	0	NULL	Rocky Mountain spotted fever	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterophile antibodies and the diagnosis of Rocky Mountain spotted fever .
	manualset3
85895	1	398501	14	13	NULL	NULL	NULL	Heterotopic bone	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Heterotopic bone in the abdominal wall due to metastatic transitional cell carcinoma in a dog .
	manualset3
85896	2	398501	14	13	NULL	0	NULL	abdominal wall 	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterotopic bone in the abdominal wall due to metastatic transitional cell carcinoma in a dog .
	manualset3
85897	3	398501	14	13	NULL	0	NULL	metastatic transitional cell carcinoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterotopic bone in the abdominal wall due to metastatic transitional cell carcinoma in a dog .
	manualset3
85898	4	398501	14	13	NULL	0	NULL	dog	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Heterotopic bone in the abdominal wall due to metastatic transitional cell carcinoma in a dog .
	manualset3
85899	1	398502	14	13	NULL	0	NULL	Hexafluorocyclobutene ( HFCB )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hexafluorocyclobutene ( HFCB ) , a reactive organohalogen gas , causes overwhelming pulmonary oedema .
	manualset3
85900	2	398502	14	13	NULL	0	NULL	reactive organohalogen gas	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hexafluorocyclobutene ( HFCB ) , a reactive organohalogen gas , causes overwhelming pulmonary oedema .
	manualset3
85901	3	398502	14	13	NULL	0	NULL	overwhelming pulmonary oedema	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hexafluorocyclobutene ( HFCB ) , a reactive organohalogen gas , causes overwhelming pulmonary oedema .
	manualset3
85902	1	398503	14	13	NULL	0	NULL	T cell non-Hodgkin 's lymphoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( T cell non-Hodgkin 's lymphoma of the external auditory canal ) .
	manualset3
85903	2	398503	14	13	NULL	0	NULL	external auditory canal 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( T cell non-Hodgkin 's lymphoma of the external auditory canal ) .
	manualset3
85904	1	398504	14	13	NULL	0	NULL	Hexokinase ( EC 2.7.1.1 ) 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hexokinase ( EC 2.7.1.1 ) , NAD-dependent malate dehydrogenase ( EC 1.1.1.37 ) , malic enzyme ( EC 1.1.1.40 ) , lactate dehydrogenase ( EC 1.1.1.27 ) , alcohol dehydrogenase ( EC 1.1.1.1 ) and succinate dehydrogenase ( EC 1.3.99.1 ) were not detectable .
	manualset3
85905	2	398504	14	13	NULL	0	NULL	NAD-dependent malate dehydrogenase ( EC 1.1.1.37 )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hexokinase ( EC 2.7.1.1 ) , NAD-dependent malate dehydrogenase ( EC 1.1.1.37 ) , malic enzyme ( EC 1.1.1.40 ) , lactate dehydrogenase ( EC 1.1.1.27 ) , alcohol dehydrogenase ( EC 1.1.1.1 ) and succinate dehydrogenase ( EC 1.3.99.1 ) were not detectable .
	manualset3
85906	3	398504	14	13	NULL	0	NULL	malic enzyme ( EC 1.1.1.40 )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hexokinase ( EC 2.7.1.1 ) , NAD-dependent malate dehydrogenase ( EC 1.1.1.37 ) , malic enzyme ( EC 1.1.1.40 ) , lactate dehydrogenase ( EC 1.1.1.27 ) , alcohol dehydrogenase ( EC 1.1.1.1 ) and succinate dehydrogenase ( EC 1.3.99.1 ) were not detectable .
	manualset3
85907	4	398504	14	13	NULL	0	NULL	lactate dehydrogenase ( EC 1.1.1.27 )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hexokinase ( EC 2.7.1.1 ) , NAD-dependent malate dehydrogenase ( EC 1.1.1.37 ) , malic enzyme ( EC 1.1.1.40 ) , lactate dehydrogenase ( EC 1.1.1.27 ) , alcohol dehydrogenase ( EC 1.1.1.1 ) and succinate dehydrogenase ( EC 1.3.99.1 ) were not detectable .
	manualset3
85908	5	398504	14	13	NULL	0	NULL	alcohol dehydrogenase ( EC 1.1.1.1 ) 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hexokinase ( EC 2.7.1.1 ) , NAD-dependent malate dehydrogenase ( EC 1.1.1.37 ) , malic enzyme ( EC 1.1.1.40 ) , lactate dehydrogenase ( EC 1.1.1.27 ) , alcohol dehydrogenase ( EC 1.1.1.1 ) and succinate dehydrogenase ( EC 1.3.99.1 ) were not detectable .
	manualset3
85909	6	398504	14	13	NULL	0	NULL	succinate dehydrogenase ( EC 1.3.99.1 )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hexokinase ( EC 2.7.1.1 ) , NAD-dependent malate dehydrogenase ( EC 1.1.1.37 ) , malic enzyme ( EC 1.1.1.40 ) , lactate dehydrogenase ( EC 1.1.1.27 ) , alcohol dehydrogenase ( EC 1.1.1.1 ) and succinate dehydrogenase ( EC 1.3.99.1 ) were not detectable .
	manualset3
85910	1	398505	14	13	NULL	0	NULL	Hexose-monophosphate shunt ( HMS ) activity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hexose-monophosphate shunt ( HMS ) activity , myelo-peroxidase - ( MPO ) - mediated iodination and random mobility in human polymorphonuclear leukocytes ( PMNs ) were studied in the presence of lignocaine .
	manualset3
85911	2	398505	14	13	NULL	0	NULL	myelo-peroxidase - ( MPO ) - mediated iodination	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hexose-monophosphate shunt ( HMS ) activity , myelo-peroxidase - ( MPO ) - mediated iodination and random mobility in human polymorphonuclear leukocytes ( PMNs ) were studied in the presence of lignocaine .
	manualset3
85912	3	398505	14	13	NULL	NULL	NULL	random mobility 	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hexose-monophosphate shunt ( HMS ) activity , myelo-peroxidase - ( MPO ) - mediated iodination and random mobility in human polymorphonuclear leukocytes ( PMNs ) were studied in the presence of lignocaine .
	manualset3
85913	4	398505	14	13	NULL	0	NULL	human polymorphonuclear leukocytes ( PMNs )	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Hexose-monophosphate shunt ( HMS ) activity , myelo-peroxidase - ( MPO ) - mediated iodination and random mobility in human polymorphonuclear leukocytes ( PMNs ) were studied in the presence of lignocaine .
	manualset3
85914	5	398505	14	13	NULL	0	NULL	lignocaine	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Hexose-monophosphate shunt ( HMS ) activity , myelo-peroxidase - ( MPO ) - mediated iodination and random mobility in human polymorphonuclear leukocytes ( PMNs ) were studied in the presence of lignocaine .
	manualset3
85915	1	398506	14	13	NULL	NULL	NULL	Hierarchical clustering of the 17 miRNAs expression profiles	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hierarchical clustering of the 17 miRNAs expression profiles showed that individuals with active TB clustered independently of individuals with LTBI or from healthy controls .
	manualset3
85917	3	398506	14	13	NULL	0	NULL	 individuals	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hierarchical clustering of the 17 miRNAs expression profiles showed that individuals with active TB clustered independently of individuals with LTBI or from healthy controls .
	manualset3
85918	4	398506	14	13	NULL	0	NULL	active TB	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hierarchical clustering of the 17 miRNAs expression profiles showed that individuals with active TB clustered independently of individuals with LTBI or from healthy controls .
	manualset3
85919	5	398506	14	13	NULL	NULL	NULL	individuals with LTBI 	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hierarchical clustering of the 17 miRNAs expression profiles showed that individuals with active TB clustered independently of individuals with LTBI or from healthy controls .
	manualset3
85920	6	398506	14	13	NULL	0	NULL	healthy controls	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hierarchical clustering of the 17 miRNAs expression profiles showed that individuals with active TB clustered independently of individuals with LTBI or from healthy controls .
	manualset3
85921	1	398507	14	13	NULL	0	NULL	High-content screening ( HCS ) 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	High-content screening ( HCS ) , historically limited to drug-development companies , is now a powerful and affordable technology for academic researchers .
	manualset3
85922	2	398507	14	13	NULL	0	NULL	drug-development companies	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	High-content screening ( HCS ) , historically limited to drug-development companies , is now a powerful and affordable technology for academic researchers .
	manualset3
85923	3	398507	14	13	NULL	NULL	NULL	powerful and affordable technology	Facility												NULL		NULL	NULL	NULL	NULL	NULL	NULL	High-content screening ( HCS ) , historically limited to drug-development companies , is now a powerful and affordable technology for academic researchers .
	manualset3
85924	4	398507	14	13	NULL	0	NULL	academic researchers	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	High-content screening ( HCS ) , historically limited to drug-development companies , is now a powerful and affordable technology for academic researchers .
	manualset3
85928	1	398509	14	13	NULL	0	NULL	High-dose intravenous methylprednisolone pulse therapy 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	High-dose intravenous methylprednisolone pulse therapy in systemic lupus erythematosus .
	manualset3
85929	2	398509	14	13	NULL	0	NULL	systemic lupus erythematosus 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	High-dose intravenous methylprednisolone pulse therapy in systemic lupus erythematosus .
	manualset3
85930	1	398510	14	13	NULL	0	NULL	High-flow cardiopulmonary bypass	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	High-flow cardiopulmonary bypass , vasodilating inhalation anesthesia and continuation of Inderal therapy may account for our results .
	manualset3
85931	2	398510	14	13	NULL	0	NULL	vasodilating inhalation anesthesia	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	High-flow cardiopulmonary bypass , vasodilating inhalation anesthesia and continuation of Inderal therapy may account for our results .
	manualset3
85932	3	398510	14	13	NULL	0	NULL	Inderal therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	High-flow cardiopulmonary bypass , vasodilating inhalation anesthesia and continuation of Inderal therapy may account for our results .
	manualset3
85933	1	398511	14	13	NULL	0	NULL	High-passage poorly differentiated cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	High-passage poorly differentiated cells were refractory to PTHRP .
	manualset3
85934	2	398511	14	13	NULL	0	NULL	PTHRP	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	High-passage poorly differentiated cells were refractory to PTHRP .
	manualset3
85935	1	398512	14	13	NULL	NULL	NULL	( 2 , 3 , 4 , 4-Tetramethylcyclopentyl ) methyl acetate 	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( 2 , 3 , 4 , 4-Tetramethylcyclopentyl ) methyl acetate , a sex pheromone from the obscure mealybug : first example of a new structural class of monoterpenes .
	manualset3
85936	2	398512	14	13	NULL	NULL	NULL	sex pheromone	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( 2 , 3 , 4 , 4-Tetramethylcyclopentyl ) methyl acetate , a sex pheromone from the obscure mealybug : first example of a new structural class of monoterpenes .
	manualset3
85937	3	398512	14	13	NULL	0	NULL	obscure mealybug	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( 2 , 3 , 4 , 4-Tetramethylcyclopentyl ) methyl acetate , a sex pheromone from the obscure mealybug : first example of a new structural class of monoterpenes .
	manualset3
85938	4	398512	14	13	NULL	NULL	NULL	structural class of monoterpenes 	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( 2 , 3 , 4 , 4-Tetramethylcyclopentyl ) methyl acetate , a sex pheromone from the obscure mealybug : first example of a new structural class of monoterpenes .
	manualset3
86012	1	398513	14	13	NULL	0	NULL	Analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Analysis of immune response to Japanese encephalitis virus infection in mice : effect of cyclosporin A on the production of HI antibody and interferon ) .
	manualset3
86013	2	398513	14	13	NULL	0	NULL	immune response to Japanese encephalitis virus infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Analysis of immune response to Japanese encephalitis virus infection in mice : effect of cyclosporin A on the production of HI antibody and interferon ) .
	manualset3
86014	3	398513	14	13	NULL	0	NULL	mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Analysis of immune response to Japanese encephalitis virus infection in mice : effect of cyclosporin A on the production of HI antibody and interferon ) .
	manualset3
86015	4	398513	14	13	NULL	0	NULL	cyclosporin A	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( Analysis of immune response to Japanese encephalitis virus infection in mice : effect of cyclosporin A on the production of HI antibody and interferon ) .
	manualset3
86016	5	398513	14	13	NULL	0	NULL	production of HI antibody	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Analysis of immune response to Japanese encephalitis virus infection in mice : effect of cyclosporin A on the production of HI antibody and interferon ) .
	manualset3
86017	6	398513	14	13	NULL	NULL	NULL	production of interferon 	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Analysis of immune response to Japanese encephalitis virus infection in mice : effect of cyclosporin A on the production of HI antibody and interferon ) .
	manualset3
86022	1	398515	14	13	NULL	0	NULL	High-performance liquid chromatographic determination	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	High-performance liquid chromatographic determination of lansoprazole and its metabolites in human serum and urine .
	manualset3
86023	2	398515	14	13	NULL	0	NULL	lansoprazole	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	High-performance liquid chromatographic determination of lansoprazole and its metabolites in human serum and urine .
	manualset3
86024	3	398515	14	13	NULL	0	NULL	metabolites	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	High-performance liquid chromatographic determination of lansoprazole and its metabolites in human serum and urine .
	manualset3
86025	4	398515	14	13	NULL	0	NULL	human serum	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	High-performance liquid chromatographic determination of lansoprazole and its metabolites in human serum and urine .
	manualset3
86026	5	398515	14	13	NULL	0	NULL	urine	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	High-performance liquid chromatographic determination of lansoprazole and its metabolites in human serum and urine .
	manualset3
86027	1	398516	14	13	NULL	0	NULL	High-performance liquid chromatographic microdetermination	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	High-performance liquid chromatographic microdetermination of indoprofen in human milk .
	manualset3
86029	2	398516	14	13	NULL	0	NULL	indoprofen	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	High-performance liquid chromatographic microdetermination of indoprofen in human milk .
	manualset3
86030	3	398516	14	13	NULL	0	NULL	human milk 	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	High-performance liquid chromatographic microdetermination of indoprofen in human milk .
	manualset3
86031	1	398517	14	13	NULL	0	NULL	High-pressure liquid chromatographic assays	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	High-pressure liquid chromatographic assays of dopamine and its primary metabolites , homovanillic acid and 3 , 4-dihydroxyphenylacetic acid , showed normal findings .
	manualset3
86034	2	398517	14	13	NULL	NULL	NULL	dopamine	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	High-pressure liquid chromatographic assays of dopamine and its primary metabolites , homovanillic acid and 3 , 4-dihydroxyphenylacetic acid , showed normal findings .
	manualset3
86035	3	398517	14	13	NULL	0	NULL	primary metabolites	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	High-pressure liquid chromatographic assays of dopamine and its primary metabolites , homovanillic acid and 3 , 4-dihydroxyphenylacetic acid , showed normal findings .
	manualset3
86045	4	398517	14	13	NULL	0	NULL	 homovanillic acid	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	High-pressure liquid chromatographic assays of dopamine and its primary metabolites , homovanillic acid and 3 , 4-dihydroxyphenylacetic acid , showed normal findings .
	manualset3
86046	5	398517	14	13	NULL	0	NULL	3 , 4-dihydroxyphenylacetic acid	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	High-pressure liquid chromatographic assays of dopamine and its primary metabolites , homovanillic acid and 3 , 4-dihydroxyphenylacetic acid , showed normal findings .
	manualset3
86047	6	398517	14	13	NULL	NULL	NULL	normal findings 	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	High-pressure liquid chromatographic assays of dopamine and its primary metabolites , homovanillic acid and 3 , 4-dihydroxyphenylacetic acid , showed normal findings .
	manualset3
86049	1	398518	14	13	NULL	0	NULL	High-resolution bone imaging 	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	High-resolution bone imaging has made tremendous progress in the recent past .
	manualset3
86055	3	398518	14	13	NULL	NULL	NULL	recent past	Time												NULL		NULL	NULL	NULL	NULL	NULL	NULL	High-resolution bone imaging has made tremendous progress in the recent past .
	manualset3
86060	1	398519	14	13	NULL	0	NULL	High-resolution subsurface water-ice distributions 	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	High-resolution subsurface water-ice distributions on Mars .
	manualset3
86061	2	398519	14	13	NULL	NULL	NULL	Mars	GeographicalLocation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	High-resolution subsurface water-ice distributions on Mars .
	manualset3
86067	1	398521	14	13	NULL	0	NULL	High-sensitivity C-reactive protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	High-sensitivity C-reactive protein , statin therapy , and risks of atrial fibrillation : an exploratory analysis of the JUPITER trial .
	manualset3
86068	2	398521	14	13	NULL	0	NULL	statin therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	High-sensitivity C-reactive protein , statin therapy , and risks of atrial fibrillation : an exploratory analysis of the JUPITER trial .
	manualset3
86069	3	398521	14	13	NULL	0	NULL	 risks of atrial fibrillation 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	High-sensitivity C-reactive protein , statin therapy , and risks of atrial fibrillation : an exploratory analysis of the JUPITER trial .
	manualset3
86070	4	398521	14	13	NULL	0	NULL	exploratory analysis of the JUPITER trial	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	High-sensitivity C-reactive protein , statin therapy , and risks of atrial fibrillation : an exploratory analysis of the JUPITER trial .
	manualset3
86080	1	398524	14	13	NULL	NULL	NULL	simultaneous three-dimensional T ( 2 )	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	High accuracy for simultaneous three-dimensional T ( 2 ) and apparent diffusion coefficient measurements are demonstrated , while also providing morphologic three-dimensional images without blurring or distortion in reasonable scan times .
	manualset3
86081	2	398524	14	13	NULL	0	NULL	apparent diffusion coefficient measurements	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	High accuracy for simultaneous three-dimensional T ( 2 ) and apparent diffusion coefficient measurements are demonstrated , while also providing morphologic three-dimensional images without blurring or distortion in reasonable scan times .
	manualset3
86082	3	398524	14	13	NULL	NULL	NULL	morphologic three-dimensional images	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	High accuracy for simultaneous three-dimensional T ( 2 ) and apparent diffusion coefficient measurements are demonstrated , while also providing morphologic three-dimensional images without blurring or distortion in reasonable scan times .
	manualset3
86083	4	398524	14	13	NULL	NULL	NULL	reasonable scan times 	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	High accuracy for simultaneous three-dimensional T ( 2 ) and apparent diffusion coefficient measurements are demonstrated , while also providing morphologic three-dimensional images without blurring or distortion in reasonable scan times .
	manualset3
86084	1	398525	14	13	NULL	0	NULL	High content cellular immune profiling	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	High content cellular immune profiling reveals differences between rhesus monkeys and men .
	manualset3
86085	2	398525	14	13	NULL	0	NULL	rhesus monkeys	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	High content cellular immune profiling reveals differences between rhesus monkeys and men .
	manualset3
86086	3	398525	14	13	NULL	0	NULL	men	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	High content cellular immune profiling reveals differences between rhesus monkeys and men .
	manualset3
86087	1	398526	14	13	NULL	0	NULL	High deletion frequency	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	High deletion frequency of the complete AZFa sequence in men with Sertoli-cell-only syndrome .
	manualset3
86088	2	398526	14	13	NULL	0	NULL	complete AZFa sequence	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	High deletion frequency of the complete AZFa sequence in men with Sertoli-cell-only syndrome .
	manualset3
86089	3	398526	14	13	NULL	NULL	NULL	men	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	High deletion frequency of the complete AZFa sequence in men with Sertoli-cell-only syndrome .
	manualset3
86090	4	398526	14	13	NULL	0	NULL	Sertoli-cell-only syndrome	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	High deletion frequency of the complete AZFa sequence in men with Sertoli-cell-only syndrome .
	manualset3
86091	1	398527	14	13	NULL	0	NULL	High density lipoprotein deficiency 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	High density lipoprotein deficiency and foam cell accumulation in mice with targeted disruption of ATP-binding cassette transporter-1 .
	manualset3
86092	2	398527	14	13	NULL	0	NULL	foam cell accumulation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	High density lipoprotein deficiency and foam cell accumulation in mice with targeted disruption of ATP-binding cassette transporter-1 .
	manualset3
86093	3	398527	14	13	NULL	0	NULL	mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	High density lipoprotein deficiency and foam cell accumulation in mice with targeted disruption of ATP-binding cassette transporter-1 .
	manualset3
86094	4	398527	14	13	NULL	0	NULL	ATP-binding cassette transporter-1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	High density lipoprotein deficiency and foam cell accumulation in mice with targeted disruption of ATP-binding cassette transporter-1 .
	manualset3
86095	1	398528	14	13	NULL	NULL	NULL	High doses of myelosuppressive chemotherapy	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	High doses of myelosuppressive chemotherapy or radiation have been used in preparative regimens with the goal of preventing graft rejection and eradicating malignancy .
	manualset3
86096	2	398528	14	13	NULL	0	NULL	radiation 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	High doses of myelosuppressive chemotherapy or radiation have been used in preparative regimens with the goal of preventing graft rejection and eradicating malignancy .
	manualset3
86097	3	398528	14	13	NULL	0	NULL	preparative regimens	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	High doses of myelosuppressive chemotherapy or radiation have been used in preparative regimens with the goal of preventing graft rejection and eradicating malignancy .
	manualset3
86099	4	398528	14	13	NULL	0	NULL	graft rejection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	High doses of myelosuppressive chemotherapy or radiation have been used in preparative regimens with the goal of preventing graft rejection and eradicating malignancy .
	manualset3
86101	5	398528	14	13	NULL	0	NULL	malignancy	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	High doses of myelosuppressive chemotherapy or radiation have been used in preparative regimens with the goal of preventing graft rejection and eradicating malignancy .
	manualset3
86141	1	398530	14	13	NULL	NULL	NULL	LEGAL RULINGS 	PublishedSourceOfInformation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( THE RIGHT TO DECREE LEGAL RULINGS FOR PLANTS NEEDING SUPERVISION .
	manualset3
86142	2	398530	14	13	NULL	NULL	NULL	PLANTS	Facility												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( THE RIGHT TO DECREE LEGAL RULINGS FOR PLANTS NEEDING SUPERVISION .
	manualset3
86354	1	398531	13	NULL	NULL	0	NULL	High field T2-weighted sequences	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	High field T2-weighted sequences disclosed hypersignal bilateral and symmetrically located exclusively at substantia nigra ( 3 cases ) , exclusively at globus pallidus ( 1case ) and simultaneously at substantia nigra , globus pallidus and nigro-strital interconnections ( 1case ) .
	manualset3
86355	2	398531	13	NULL	NULL	0	NULL	substantia nigra	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	High field T2-weighted sequences disclosed hypersignal bilateral and symmetrically located exclusively at substantia nigra ( 3 cases ) , exclusively at globus pallidus ( 1case ) and simultaneously at substantia nigra , globus pallidus and nigro-strital interconnections ( 1case ) .
	manualset3
86356	3	398531	13	NULL	NULL	0	NULL	3 cases	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	High field T2-weighted sequences disclosed hypersignal bilateral and symmetrically located exclusively at substantia nigra ( 3 cases ) , exclusively at globus pallidus ( 1case ) and simultaneously at substantia nigra , globus pallidus and nigro-strital interconnections ( 1case ) .
	manualset3
86357	4	398531	13	NULL	NULL	0	NULL	globus pallidus	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	High field T2-weighted sequences disclosed hypersignal bilateral and symmetrically located exclusively at substantia nigra ( 3 cases ) , exclusively at globus pallidus ( 1case ) and simultaneously at substantia nigra , globus pallidus and nigro-strital interconnections ( 1case ) .
	manualset3
86358	5	398531	13	NULL	NULL	0	NULL	1case	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	High field T2-weighted sequences disclosed hypersignal bilateral and symmetrically located exclusively at substantia nigra ( 3 cases ) , exclusively at globus pallidus ( 1case ) and simultaneously at substantia nigra , globus pallidus and nigro-strital interconnections ( 1case ) .
	manualset3
86359	6	398531	13	NULL	NULL	0	NULL	substantia nigra	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	High field T2-weighted sequences disclosed hypersignal bilateral and symmetrically located exclusively at substantia nigra ( 3 cases ) , exclusively at globus pallidus ( 1case ) and simultaneously at substantia nigra , globus pallidus and nigro-strital interconnections ( 1case ) .
	manualset3
86360	7	398531	13	NULL	NULL	0	NULL	globus pallidus 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	High field T2-weighted sequences disclosed hypersignal bilateral and symmetrically located exclusively at substantia nigra ( 3 cases ) , exclusively at globus pallidus ( 1case ) and simultaneously at substantia nigra , globus pallidus and nigro-strital interconnections ( 1case ) .
	manualset3
86361	8	398531	13	NULL	NULL	0	NULL	nigro-strital interconnections	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	High field T2-weighted sequences disclosed hypersignal bilateral and symmetrically located exclusively at substantia nigra ( 3 cases ) , exclusively at globus pallidus ( 1case ) and simultaneously at substantia nigra , globus pallidus and nigro-strital interconnections ( 1case ) .
	manualset3
86362	9	398531	13	NULL	NULL	0	NULL	1case	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	High field T2-weighted sequences disclosed hypersignal bilateral and symmetrically located exclusively at substantia nigra ( 3 cases ) , exclusively at globus pallidus ( 1case ) and simultaneously at substantia nigra , globus pallidus and nigro-strital interconnections ( 1case ) .
	manualset3
86363	1	398532	13	NULL	NULL	0	NULL	High huAbeta/heme ratio	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	High huAbeta/heme ratio increases the peroxidase activity .
	manualset3
86364	2	398532	13	NULL	NULL	0	NULL	peroxidase activity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	High huAbeta/heme ratio increases the peroxidase activity .
	manualset3
86365	1	398533	13	NULL	NULL	0	NULL	High intake of palatable food	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	High intake of palatable food predicts binge-eating independent of susceptibility to obesity : an animal model of lean vs obese binge-eating and obesity with and without binge-eating .
	manualset3
86366	2	398533	13	NULL	NULL	0	NULL	binge-eating 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	High intake of palatable food predicts binge-eating independent of susceptibility to obesity : an animal model of lean vs obese binge-eating and obesity with and without binge-eating .
	manualset3
86367	3	398533	13	NULL	NULL	0	NULL	susceptibility to obesity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	High intake of palatable food predicts binge-eating independent of susceptibility to obesity : an animal model of lean vs obese binge-eating and obesity with and without binge-eating .
	manualset3
86368	4	398533	13	NULL	NULL	0	NULL	animal model	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	High intake of palatable food predicts binge-eating independent of susceptibility to obesity : an animal model of lean vs obese binge-eating and obesity with and without binge-eating .
	manualset3
86369	5	398533	13	NULL	NULL	0	NULL	lean vs obese binge-eating	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	High intake of palatable food predicts binge-eating independent of susceptibility to obesity : an animal model of lean vs obese binge-eating and obesity with and without binge-eating .
	manualset3
86370	6	398533	13	NULL	NULL	0	NULL	obesity with and without binge-eating	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	High intake of palatable food predicts binge-eating independent of susceptibility to obesity : an animal model of lean vs obese binge-eating and obesity with and without binge-eating .
	manualset3
86371	1	398534	13	NULL	NULL	NULL	NULL	HU protein 	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	High levels of HU protein ( 136 molecules/oriC ) restrain the free superhelicity .
	manualset3
86372	2	398534	13	NULL	NULL	0	NULL	136 molecules/oriC 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	High levels of HU protein ( 136 molecules/oriC ) restrain the free superhelicity .
	manualset3
86373	3	398534	13	NULL	NULL	0	NULL	 superhelicity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	High levels of HU protein ( 136 molecules/oriC ) restrain the free superhelicity .
	manualset3
86374	1	398535	13	NULL	NULL	0	NULL	High levels of soluble endothelial protein C receptor ( EPCR )	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	High levels of soluble endothelial protein C receptor ( EPCR ) induce coagulation dysfunction by inhibiting protein C activation , and activated protein C ( APC ) activity .
	manualset3
86375	2	398535	13	NULL	NULL	0	NULL	coagulation dysfunction	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	High levels of soluble endothelial protein C receptor ( EPCR ) induce coagulation dysfunction by inhibiting protein C activation , and activated protein C ( APC ) activity .
	manualset3
86376	3	398535	13	NULL	NULL	0	NULL	protein C activation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	High levels of soluble endothelial protein C receptor ( EPCR ) induce coagulation dysfunction by inhibiting protein C activation , and activated protein C ( APC ) activity .
	manualset3
86377	4	398535	13	NULL	NULL	0	NULL	activated protein C ( APC ) activity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	High levels of soluble endothelial protein C receptor ( EPCR ) induce coagulation dysfunction by inhibiting protein C activation , and activated protein C ( APC ) activity .
	manualset3
86378	1	398536	13	NULL	NULL	0	NULL	High levels of sunshine exposure	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	High levels of sunshine exposure reduced risk of rectal cancer among those diagnosed when & lt ; 60 years of age ( OR = 0.62 , 95 % CI = 0.42-0 .93 ) .
	manualset3
86379	2	398536	13	NULL	NULL	0	NULL	risk of rectal cancer	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	High levels of sunshine exposure reduced risk of rectal cancer among those diagnosed when & lt ; 60 years of age ( OR = 0.62 , 95 % CI = 0.42-0 .93 ) .
	manualset3
86380	3	398536	13	NULL	NULL	0	NULL	60 years of age 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	High levels of sunshine exposure reduced risk of rectal cancer among those diagnosed when & lt ; 60 years of age ( OR = 0.62 , 95 % CI = 0.42-0 .93 ) .
	manualset3
86381	4	398536	13	NULL	NULL	0	NULL	( OR = 0.62 , 95 % CI = 0.42-0 .93 )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	High levels of sunshine exposure reduced risk of rectal cancer among those diagnosed when & lt ; 60 years of age ( OR = 0.62 , 95 % CI = 0.42-0 .93 ) .
	manualset3
86382	1	398537	13	NULL	NULL	NULL	NULL	High neuroleptic dosage	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	High neuroleptic dosage was found to be associated with increased reaction time , reduced span of apprehension , low basal skin conductance level , and reduced skin conductance reactivity .
	manualset3
86383	2	398537	13	NULL	NULL	0	NULL	increased reaction time	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	High neuroleptic dosage was found to be associated with increased reaction time , reduced span of apprehension , low basal skin conductance level , and reduced skin conductance reactivity .
	manualset3
86384	3	398537	13	NULL	NULL	0	NULL	reduced span of apprehension	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	High neuroleptic dosage was found to be associated with increased reaction time , reduced span of apprehension , low basal skin conductance level , and reduced skin conductance reactivity .
	manualset3
86385	4	398537	13	NULL	NULL	0	NULL	low basal skin conductance level	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	High neuroleptic dosage was found to be associated with increased reaction time , reduced span of apprehension , low basal skin conductance level , and reduced skin conductance reactivity .
	manualset3
86386	5	398537	13	NULL	NULL	0	NULL	reduced skin conductance reactivity 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	High neuroleptic dosage was found to be associated with increased reaction time , reduced span of apprehension , low basal skin conductance level , and reduced skin conductance reactivity .
	manualset3
86387	1	398538	13	NULL	NULL	0	NULL	High neutrophilia 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	High neutrophilia ( 150 , 000-240 , 000 white blood cell count ) observed in two patients with non-small cell lung cancer led us to run the present trial .
	manualset3
86388	2	398538	13	NULL	NULL	0	NULL	150 , 000-240 , 000 white blood cell count	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	High neutrophilia ( 150 , 000-240 , 000 white blood cell count ) observed in two patients with non-small cell lung cancer led us to run the present trial .
	manualset3
86389	3	398538	13	NULL	NULL	0	NULL	two patients	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	High neutrophilia ( 150 , 000-240 , 000 white blood cell count ) observed in two patients with non-small cell lung cancer led us to run the present trial .
	manualset3
86390	4	398538	13	NULL	NULL	0	NULL	non-small cell lung cancer 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	High neutrophilia ( 150 , 000-240 , 000 white blood cell count ) observed in two patients with non-small cell lung cancer led us to run the present trial .
	manualset3
86391	1	398539	13	NULL	NULL	0	NULL	High prevalence of human rhinovirus C infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	High prevalence of human rhinovirus C infection in Thai children with acute lower respiratory tract disease .
	manualset3
86392	2	398539	13	NULL	NULL	0	NULL	Thai children	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	High prevalence of human rhinovirus C infection in Thai children with acute lower respiratory tract disease .
	manualset3
86393	3	398539	13	NULL	NULL	0	NULL	acute lower respiratory tract disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	High prevalence of human rhinovirus C infection in Thai children with acute lower respiratory tract disease .
	manualset3
86394	1	398540	13	NULL	NULL	0	NULL	proline	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	High proline concentration in the youngest uppermost leaves contributed to their protection from drought , which was associated with low degree of senescence .
	manualset3
86395	2	398540	13	NULL	NULL	0	NULL	youngest uppermost leaves	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	High proline concentration in the youngest uppermost leaves contributed to their protection from drought , which was associated with low degree of senescence .
	manualset3
86396	3	398540	13	NULL	NULL	NULL	NULL	drought	EnvironmentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	High proline concentration in the youngest uppermost leaves contributed to their protection from drought , which was associated with low degree of senescence .
	manualset3
86397	4	398540	13	NULL	NULL	0	NULL	low degree of senescence	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	High proline concentration in the youngest uppermost leaves contributed to their protection from drought , which was associated with low degree of senescence .
	manualset3
86403	1	398541	13	NULL	NULL	NULL	NULL	High resolution images of the computed full wave field 	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	High resolution images of the computed full wave field provide insights into the spiked and rounded features seen in sonic booms that have propagated through turbulence .
	manualset3
86404	2	398541	13	NULL	NULL	0	NULL	sonic booms 	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	High resolution images of the computed full wave field provide insights into the spiked and rounded features seen in sonic booms that have propagated through turbulence .
	manualset3
86405	3	398541	13	NULL	NULL	0	NULL	turbulence 	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	High resolution images of the computed full wave field provide insights into the spiked and rounded features seen in sonic booms that have propagated through turbulence .
	manualset3
86406	1	398542	13	NULL	NULL	0	NULL	bacterioplankton communities	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	High similarities of the bacterioplankton communities across several hundred kilometers were observed in the surface water using RNA - and DNA-based fingerprints .
	manualset3
86407	2	398542	13	NULL	NULL	0	NULL	several hundred kilometers	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	High similarities of the bacterioplankton communities across several hundred kilometers were observed in the surface water using RNA - and DNA-based fingerprints .
	manualset3
86408	3	398542	13	NULL	NULL	0	NULL	surface water	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	High similarities of the bacterioplankton communities across several hundred kilometers were observed in the surface water using RNA - and DNA-based fingerprints .
	manualset3
86409	4	398542	13	NULL	NULL	0	NULL	RNA -based fingerprints	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	High similarities of the bacterioplankton communities across several hundred kilometers were observed in the surface water using RNA - and DNA-based fingerprints .
	manualset3
86410	5	398542	13	NULL	NULL	0	NULL	DNA-based fingerprints 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	High similarities of the bacterioplankton communities across several hundred kilometers were observed in the surface water using RNA - and DNA-based fingerprints .
	manualset3
86411	1	398543	13	NULL	NULL	0	NULL	similarities	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	High similarities were observed in helminth populations of two groups of states : 1 ) Alabama , Mississippi , Arkansas , Virginia , and Tennessee ; and 2 ) Tennessee , Kentucky , and Illinois .
	manualset3
86412	2	398543	13	NULL	NULL	0	NULL	helminth populations 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	High similarities were observed in helminth populations of two groups of states : 1 ) Alabama , Mississippi , Arkansas , Virginia , and Tennessee ; and 2 ) Tennessee , Kentucky , and Illinois .
	manualset3
86413	3	398543	13	NULL	NULL	0	NULL	 two groups of states	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	High similarities were observed in helminth populations of two groups of states : 1 ) Alabama , Mississippi , Arkansas , Virginia , and Tennessee ; and 2 ) Tennessee , Kentucky , and Illinois .
	manualset3
86414	4	398543	13	NULL	NULL	NULL	NULL	Alabama , Mississippi , Arkansas , Virginia , and Tennessee	ProperNamedGeographicalLocation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	High similarities were observed in helminth populations of two groups of states : 1 ) Alabama , Mississippi , Arkansas , Virginia , and Tennessee ; and 2 ) Tennessee , Kentucky , and Illinois .
	manualset3
86415	5	398543	13	NULL	NULL	0	NULL	Tennessee , Kentucky , and Illinois 	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	High similarities were observed in helminth populations of two groups of states : 1 ) Alabama , Mississippi , Arkansas , Virginia , and Tennessee ; and 2 ) Tennessee , Kentucky , and Illinois .
	manualset3
86416	1	398544	13	NULL	NULL	0	NULL	High street oral surgeons 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	High street oral surgeons -- if the USA catches a cold will the UK get pneumonia ?
	manualset3
86417	2	398544	13	NULL	NULL	0	NULL	USA	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	High street oral surgeons -- if the USA catches a cold will the UK get pneumonia ?
	manualset3
86418	3	398544	13	NULL	NULL	0	NULL	cold 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	High street oral surgeons -- if the USA catches a cold will the UK get pneumonia ?
	manualset3
86419	4	398544	13	NULL	NULL	0	NULL	UK	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	High street oral surgeons -- if the USA catches a cold will the UK get pneumonia ?
	manualset3
86420	5	398544	13	NULL	NULL	0	NULL	pneumonia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	High street oral surgeons -- if the USA catches a cold will the UK get pneumonia ?
	manualset3
86421	1	398545	13	NULL	NULL	0	NULL	university graduates	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	High unemployment of university graduates , a growing factor in developing and developed nations , is pointed to as a major stress during a university education in the late 1970s .
	manualset3
86422	2	398545	13	NULL	NULL	0	NULL	 developing nations 	UnproperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	High unemployment of university graduates , a growing factor in developing and developed nations , is pointed to as a major stress during a university education in the late 1970s .
	manualset3
86423	3	398545	13	NULL	NULL	0	NULL	developed nations 	UnproperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	High unemployment of university graduates , a growing factor in developing and developed nations , is pointed to as a major stress during a university education in the late 1970s .
	manualset3
86424	4	398545	13	NULL	NULL	0	NULL	major stress	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	High unemployment of university graduates , a growing factor in developing and developed nations , is pointed to as a major stress during a university education in the late 1970s .
	manualset3
86425	5	398545	13	NULL	NULL	0	NULL	university education	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	High unemployment of university graduates , a growing factor in developing and developed nations , is pointed to as a major stress during a university education in the late 1970s .
	manualset3
86426	6	398545	13	NULL	NULL	0	NULL	late 1970s	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	High unemployment of university graduates , a growing factor in developing and developed nations , is pointed to as a major stress during a university education in the late 1970s .
	manualset3
86427	1	398546	13	NULL	NULL	0	NULL	Higher DPP4 gene expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher DPP4 gene expression in VAT and its relationship with the plasma lipid profile may be explained by actually unknown DPP4 biological effect or , to another extent , may also be a marker of VAT inflammation known to be associated with metabolic disturbances .
	manualset3
86428	2	398546	13	NULL	NULL	0	NULL	VAT	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher DPP4 gene expression in VAT and its relationship with the plasma lipid profile may be explained by actually unknown DPP4 biological effect or , to another extent , may also be a marker of VAT inflammation known to be associated with metabolic disturbances .
	manualset3
86429	3	398546	13	NULL	NULL	NULL	NULL	plasma lipid profile 	CellComponent												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Higher DPP4 gene expression in VAT and its relationship with the plasma lipid profile may be explained by actually unknown DPP4 biological effect or , to another extent , may also be a marker of VAT inflammation known to be associated with metabolic disturbances .
	manualset3
86430	4	398546	13	NULL	NULL	0	NULL	DPP4 biological effect	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher DPP4 gene expression in VAT and its relationship with the plasma lipid profile may be explained by actually unknown DPP4 biological effect or , to another extent , may also be a marker of VAT inflammation known to be associated with metabolic disturbances .
	manualset3
86431	5	398546	13	NULL	NULL	0	NULL	VAT inflammation	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher DPP4 gene expression in VAT and its relationship with the plasma lipid profile may be explained by actually unknown DPP4 biological effect or , to another extent , may also be a marker of VAT inflammation known to be associated with metabolic disturbances .
	manualset3
86432	6	398546	13	NULL	NULL	0	NULL	metabolic disturbances	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher DPP4 gene expression in VAT and its relationship with the plasma lipid profile may be explained by actually unknown DPP4 biological effect or , to another extent , may also be a marker of VAT inflammation known to be associated with metabolic disturbances .
	manualset3
86433	7	398546	13	NULL	NULL	0	NULL	relationship	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher DPP4 gene expression in VAT and its relationship with the plasma lipid profile may be explained by actually unknown DPP4 biological effect or , to another extent , may also be a marker of VAT inflammation known to be associated with metabolic disturbances .
	manualset3
86434	1	398547	13	NULL	NULL	0	NULL	Ki-67 expression 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher Ki-67 expression in immunostaining and RT-PCR was more often seen in grade 3 tumors ( p & lt ; 0.001 and p = 0.026 , respectively ) .
	manualset3
86435	2	398547	13	NULL	NULL	0	NULL	immunostaining	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher Ki-67 expression in immunostaining and RT-PCR was more often seen in grade 3 tumors ( p & lt ; 0.001 and p = 0.026 , respectively ) .
	manualset3
86436	3	398547	13	NULL	NULL	0	NULL	RT-PCR	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher Ki-67 expression in immunostaining and RT-PCR was more often seen in grade 3 tumors ( p & lt ; 0.001 and p = 0.026 , respectively ) .
	manualset3
86437	4	398547	13	NULL	NULL	0	NULL	grade 3 tumors	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher Ki-67 expression in immunostaining and RT-PCR was more often seen in grade 3 tumors ( p & lt ; 0.001 and p = 0.026 , respectively ) .
	manualset3
86438	5	398547	13	NULL	NULL	0	NULL	 p & lt ; 0.001 and p = 0.026 , respectively	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher Ki-67 expression in immunostaining and RT-PCR was more often seen in grade 3 tumors ( p & lt ; 0.001 and p = 0.026 , respectively ) .
	manualset3
86439	1	398548	13	NULL	NULL	0	NULL	Higher fees	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher fees have been implemented for rural transports and air ambulance services .
	manualset3
86440	2	398548	13	NULL	NULL	0	NULL	rural transports 	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher fees have been implemented for rural transports and air ambulance services .
	manualset3
86441	3	398548	13	NULL	NULL	0	NULL	air ambulance services	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher fees have been implemented for rural transports and air ambulance services .
	manualset3
86442	1	398549	13	NULL	NULL	NULL	NULL	Higher kidney weights	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Higher kidney weights , correlating to renal tubule hypertrophy in the 0.6 mg/kg group , were observed for parental males and females in the 0.125 and 0.6 mg / ( kgday ) groups .
	manualset3
86443	2	398549	13	NULL	NULL	0	NULL	renal tubule hypertrophy	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher kidney weights , correlating to renal tubule hypertrophy in the 0.6 mg/kg group , were observed for parental males and females in the 0.125 and 0.6 mg / ( kgday ) groups .
	manualset3
86444	3	398549	13	NULL	NULL	NULL	NULL	0.6 mg/kg group	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Higher kidney weights , correlating to renal tubule hypertrophy in the 0.6 mg/kg group , were observed for parental males and females in the 0.125 and 0.6 mg / ( kgday ) groups .
	manualset3
86445	4	398549	13	NULL	NULL	0	NULL	parental males	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher kidney weights , correlating to renal tubule hypertrophy in the 0.6 mg/kg group , were observed for parental males and females in the 0.125 and 0.6 mg / ( kgday ) groups .
	manualset3
86446	5	398549	13	NULL	NULL	NULL	NULL	parental females	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Higher kidney weights , correlating to renal tubule hypertrophy in the 0.6 mg/kg group , were observed for parental males and females in the 0.125 and 0.6 mg / ( kgday ) groups .
	manualset3
86447	6	398549	13	NULL	NULL	0	NULL	0.125 mg / ( kgday ) group	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher kidney weights , correlating to renal tubule hypertrophy in the 0.6 mg/kg group , were observed for parental males and females in the 0.125 and 0.6 mg / ( kgday ) groups .
	manualset3
86448	7	398549	13	NULL	NULL	0	NULL	0.6 mg / ( kgday ) group	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher kidney weights , correlating to renal tubule hypertrophy in the 0.6 mg/kg group , were observed for parental males and females in the 0.125 and 0.6 mg / ( kgday ) groups .
	manualset3
86449	1	398550	13	NULL	NULL	0	NULL	Higher neuroticism scores	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher neuroticism scores also attenuated the decrease in negative affect across time .
	manualset3
86450	2	398550	13	NULL	NULL	0	NULL	 decrease in negative affect	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher neuroticism scores also attenuated the decrease in negative affect across time .
	manualset3
86451	3	398550	13	NULL	NULL	0	NULL	time	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher neuroticism scores also attenuated the decrease in negative affect across time .
	manualset3
86452	1	398551	13	NULL	NULL	0	NULL	Higher rates of refractory infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher rates of refractory infection , serious morbidity , and attributable death occurred in the VREF cohort and were partially mediated by the lack of effective antimicrobial therapy .
	manualset3
86453	2	398551	13	NULL	NULL	0	NULL	serious morbidity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher rates of refractory infection , serious morbidity , and attributable death occurred in the VREF cohort and were partially mediated by the lack of effective antimicrobial therapy .
	manualset3
86454	3	398551	13	NULL	NULL	0	NULL	attributable death	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher rates of refractory infection , serious morbidity , and attributable death occurred in the VREF cohort and were partially mediated by the lack of effective antimicrobial therapy .
	manualset3
86462	4	398551	13	NULL	NULL	0	NULL	VREF cohort	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher rates of refractory infection , serious morbidity , and attributable death occurred in the VREF cohort and were partially mediated by the lack of effective antimicrobial therapy .
	manualset3
86463	5	398551	13	NULL	NULL	0	NULL	antimicrobial therapy 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher rates of refractory infection , serious morbidity , and attributable death occurred in the VREF cohort and were partially mediated by the lack of effective antimicrobial therapy .
	manualset3
86464	1	398552	13	NULL	NULL	NULL	NULL	urban setting	UnproperNamedGeographicalLocation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Higher rates were found in urban than rural setting and , to a lesser degree , for women than men .
	manualset3
86465	2	398552	13	NULL	NULL	0	NULL	rural setting	UnproperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher rates were found in urban than rural setting and , to a lesser degree , for women than men .
	manualset3
86466	3	398552	13	NULL	NULL	0	NULL	women	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher rates were found in urban than rural setting and , to a lesser degree , for women than men .
	manualset3
86467	4	398552	13	NULL	NULL	0	NULL	men	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher rates were found in urban than rural setting and , to a lesser degree , for women than men .
	manualset3
86468	1	398553	13	NULL	NULL	0	NULL	Higher susceptibility to peroxidation in heart 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher susceptibility to peroxidation in heart , thymus and pancreas was also found in the sucrose-fed group v. the starch-fed group .
	manualset3
86469	2	398553	13	NULL	NULL	0	NULL	Higher susceptibility to peroxidation in thymus	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher susceptibility to peroxidation in heart , thymus and pancreas was also found in the sucrose-fed group v. the starch-fed group .
	manualset3
86470	3	398553	13	NULL	NULL	0	NULL	Higher susceptibility to peroxidation in pancreas	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher susceptibility to peroxidation in heart , thymus and pancreas was also found in the sucrose-fed group v. the starch-fed group .
	manualset3
86471	4	398553	13	NULL	NULL	0	NULL	sucrose-fed group	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher susceptibility to peroxidation in heart , thymus and pancreas was also found in the sucrose-fed group v. the starch-fed group .
	manualset3
86472	5	398553	13	NULL	NULL	0	NULL	starch-fed group	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher susceptibility to peroxidation in heart , thymus and pancreas was also found in the sucrose-fed group v. the starch-fed group .
	manualset3
86473	1	398554	13	NULL	NULL	0	NULL	Higher values of seminiferous tubule diameters	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher values of seminiferous tubule diameters and all types of spermatogenic cells including mature-phase spermatozoa were found during the breeding season .
	manualset3
86474	2	398554	13	NULL	NULL	0	NULL	all types of spermatogenic cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher values of seminiferous tubule diameters and all types of spermatogenic cells including mature-phase spermatozoa were found during the breeding season .
	manualset3
86475	3	398554	13	NULL	NULL	0	NULL	mature-phase spermatozoa	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher values of seminiferous tubule diameters and all types of spermatogenic cells including mature-phase spermatozoa were found during the breeding season .
	manualset3
86476	4	398554	13	NULL	NULL	0	NULL	breeding season	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Higher values of seminiferous tubule diameters and all types of spermatogenic cells including mature-phase spermatozoa were found during the breeding season .
	manualset3
86477	1	398555	13	NULL	NULL	0	NULL	Highest 3H-naloxone binding	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest 3H-naloxone binding occurs in the inferior olive in fetuses at midgestation , compared to the interpeduncular nucleus in infants .
	manualset3
86478	2	398555	13	NULL	NULL	0	NULL	inferior olive	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest 3H-naloxone binding occurs in the inferior olive in fetuses at midgestation , compared to the interpeduncular nucleus in infants .
	manualset3
86479	3	398555	13	NULL	NULL	0	NULL	fetuses	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest 3H-naloxone binding occurs in the inferior olive in fetuses at midgestation , compared to the interpeduncular nucleus in infants .
	manualset3
86480	4	398555	13	NULL	NULL	0	NULL	midgestation	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest 3H-naloxone binding occurs in the inferior olive in fetuses at midgestation , compared to the interpeduncular nucleus in infants .
	manualset3
86481	5	398555	13	NULL	NULL	0	NULL	interpeduncular nucleus	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest 3H-naloxone binding occurs in the inferior olive in fetuses at midgestation , compared to the interpeduncular nucleus in infants .
	manualset3
86482	6	398555	13	NULL	NULL	0	NULL	infants	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest 3H-naloxone binding occurs in the inferior olive in fetuses at midgestation , compared to the interpeduncular nucleus in infants .
	manualset3
86483	1	398556	13	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest levels were seen in patients with active systemic JRA ( mean value 2419 U/ml ) while patients with pauciarticular JRA and B27 + JRA had the lowest sIL-2R levels ( 1167 and 1045 U/ml , respectively ) .
	manualset3
86490	2	398556	13	NULL	NULL	0	NULL	active systemic JRA	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest levels were seen in patients with active systemic JRA ( mean value 2419 U/ml ) while patients with pauciarticular JRA and B27 + JRA had the lowest sIL-2R levels ( 1167 and 1045 U/ml , respectively ) .
	manualset3
86491	3	398556	13	NULL	NULL	0	NULL	 mean value 2419 U/ml	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest levels were seen in patients with active systemic JRA ( mean value 2419 U/ml ) while patients with pauciarticular JRA and B27 + JRA had the lowest sIL-2R levels ( 1167 and 1045 U/ml , respectively ) .
	manualset3
86492	4	398556	13	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest levels were seen in patients with active systemic JRA ( mean value 2419 U/ml ) while patients with pauciarticular JRA and B27 + JRA had the lowest sIL-2R levels ( 1167 and 1045 U/ml , respectively ) .
	manualset3
86494	5	398556	13	NULL	NULL	0	NULL	pauciarticular JRA	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest levels were seen in patients with active systemic JRA ( mean value 2419 U/ml ) while patients with pauciarticular JRA and B27 + JRA had the lowest sIL-2R levels ( 1167 and 1045 U/ml , respectively ) .
	manualset3
86495	6	398556	13	NULL	NULL	0	NULL	B27 + JRA	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest levels were seen in patients with active systemic JRA ( mean value 2419 U/ml ) while patients with pauciarticular JRA and B27 + JRA had the lowest sIL-2R levels ( 1167 and 1045 U/ml , respectively ) .
	manualset3
86496	7	398556	13	NULL	NULL	0	NULL	lowest sIL-2R levels	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest levels were seen in patients with active systemic JRA ( mean value 2419 U/ml ) while patients with pauciarticular JRA and B27 + JRA had the lowest sIL-2R levels ( 1167 and 1045 U/ml , respectively ) .
	manualset3
86497	8	398556	13	NULL	NULL	0	NULL	1167 U/ml	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest levels were seen in patients with active systemic JRA ( mean value 2419 U/ml ) while patients with pauciarticular JRA and B27 + JRA had the lowest sIL-2R levels ( 1167 and 1045 U/ml , respectively ) .
	manualset3
86498	9	398556	13	NULL	NULL	0	NULL	1045 U/ml	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest levels were seen in patients with active systemic JRA ( mean value 2419 U/ml ) while patients with pauciarticular JRA and B27 + JRA had the lowest sIL-2R levels ( 1167 and 1045 U/ml , respectively ) .
	manualset3
86499	1	398557	13	NULL	NULL	0	NULL	pyrene mineralization	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest pyrene mineralization rates and extents ( more than 60 % after 20 days ) were obtained when pyrene was in contact with composted soil from the curing stage .
	manualset3
86500	2	398557	13	NULL	NULL	0	NULL	 more than 60 %	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest pyrene mineralization rates and extents ( more than 60 % after 20 days ) were obtained when pyrene was in contact with composted soil from the curing stage .
	manualset3
86501	3	398557	13	NULL	NULL	NULL	NULL	after 20 days 	TimePoint												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Highest pyrene mineralization rates and extents ( more than 60 % after 20 days ) were obtained when pyrene was in contact with composted soil from the curing stage .
	manualset3
86502	4	398557	13	NULL	NULL	NULL	NULL	pyrene	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Highest pyrene mineralization rates and extents ( more than 60 % after 20 days ) were obtained when pyrene was in contact with composted soil from the curing stage .
	manualset3
86503	5	398557	13	NULL	NULL	0	NULL	composted soil	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest pyrene mineralization rates and extents ( more than 60 % after 20 days ) were obtained when pyrene was in contact with composted soil from the curing stage .
	manualset3
86504	6	398557	13	NULL	NULL	0	NULL	curing stage	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest pyrene mineralization rates and extents ( more than 60 % after 20 days ) were obtained when pyrene was in contact with composted soil from the curing stage .
	manualset3
86505	1	398558	13	NULL	NULL	0	NULL	printed fuel cell	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest stability was obtained for a printed fuel cell using osmium complexes as mediators of glucose oxidation by aldose dehydrogenase , and oxygen reduction by T. hirsuta laccase , maintaining cell voltage above 200mV for 137h at pH 5 .
	manualset3
86506	2	398558	13	NULL	NULL	0	NULL	osmium complexes	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest stability was obtained for a printed fuel cell using osmium complexes as mediators of glucose oxidation by aldose dehydrogenase , and oxygen reduction by T. hirsuta laccase , maintaining cell voltage above 200mV for 137h at pH 5 .
	manualset3
86507	3	398558	13	NULL	NULL	0	NULL	mediators	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest stability was obtained for a printed fuel cell using osmium complexes as mediators of glucose oxidation by aldose dehydrogenase , and oxygen reduction by T. hirsuta laccase , maintaining cell voltage above 200mV for 137h at pH 5 .
	manualset3
86508	4	398558	13	NULL	NULL	0	NULL	glucose oxidation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest stability was obtained for a printed fuel cell using osmium complexes as mediators of glucose oxidation by aldose dehydrogenase , and oxygen reduction by T. hirsuta laccase , maintaining cell voltage above 200mV for 137h at pH 5 .
	manualset3
86509	5	398558	13	NULL	NULL	0	NULL	aldose dehydrogenase 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest stability was obtained for a printed fuel cell using osmium complexes as mediators of glucose oxidation by aldose dehydrogenase , and oxygen reduction by T. hirsuta laccase , maintaining cell voltage above 200mV for 137h at pH 5 .
	manualset3
86510	6	398558	13	NULL	NULL	0	NULL	oxygen reduction 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest stability was obtained for a printed fuel cell using osmium complexes as mediators of glucose oxidation by aldose dehydrogenase , and oxygen reduction by T. hirsuta laccase , maintaining cell voltage above 200mV for 137h at pH 5 .
	manualset3
86511	7	398558	13	NULL	NULL	0	NULL	T. hirsuta laccase	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest stability was obtained for a printed fuel cell using osmium complexes as mediators of glucose oxidation by aldose dehydrogenase , and oxygen reduction by T. hirsuta laccase , maintaining cell voltage above 200mV for 137h at pH 5 .
	manualset3
86512	8	398558	13	NULL	NULL	0	NULL	cell 	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest stability was obtained for a printed fuel cell using osmium complexes as mediators of glucose oxidation by aldose dehydrogenase , and oxygen reduction by T. hirsuta laccase , maintaining cell voltage above 200mV for 137h at pH 5 .
	manualset3
86513	9	398558	13	NULL	NULL	0	NULL	voltage above 200mV	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest stability was obtained for a printed fuel cell using osmium complexes as mediators of glucose oxidation by aldose dehydrogenase , and oxygen reduction by T. hirsuta laccase , maintaining cell voltage above 200mV for 137h at pH 5 .
	manualset3
86514	10	398558	13	NULL	NULL	0	NULL	137h	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest stability was obtained for a printed fuel cell using osmium complexes as mediators of glucose oxidation by aldose dehydrogenase , and oxygen reduction by T. hirsuta laccase , maintaining cell voltage above 200mV for 137h at pH 5 .
	manualset3
86515	11	398558	13	NULL	NULL	0	NULL	pH 5	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Highest stability was obtained for a printed fuel cell using osmium complexes as mediators of glucose oxidation by aldose dehydrogenase , and oxygen reduction by T. hirsuta laccase , maintaining cell voltage above 200mV for 137h at pH 5 .
	manualset3
86516	1	398559	13	NULL	NULL	0	NULL	modified vaccinia virus Ankara ( MVA )	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly attenuated modified vaccinia virus Ankara ( MVA ) as an effective recombinant vector : a murine tumor model .
	manualset3
86517	2	398559	13	NULL	NULL	NULL	NULL	recombinant vector	LaboratoryExperimentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Highly attenuated modified vaccinia virus Ankara ( MVA ) as an effective recombinant vector : a murine tumor model .
	manualset3
86518	3	398559	13	NULL	NULL	0	NULL	 murine tumor model 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly attenuated modified vaccinia virus Ankara ( MVA ) as an effective recombinant vector : a murine tumor model .
	manualset3
86519	1	398560	13	NULL	NULL	NULL	NULL	Highly conserved regions	AminoAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Highly conserved regions were observed among the deduced amino acid sequences of AT1 , AT2 , chicken erythroblast and rabbit and human skeletal muscle ADP-ribosyltransferases , and rodent T-cell surface antigen RT6 .
	manualset3
86520	2	398560	13	NULL	NULL	NULL	NULL	amino acid sequences of AT1	AminoAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Highly conserved regions were observed among the deduced amino acid sequences of AT1 , AT2 , chicken erythroblast and rabbit and human skeletal muscle ADP-ribosyltransferases , and rodent T-cell surface antigen RT6 .
	manualset3
86521	3	398560	13	NULL	NULL	NULL	NULL	AT2	AminoAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Highly conserved regions were observed among the deduced amino acid sequences of AT1 , AT2 , chicken erythroblast and rabbit and human skeletal muscle ADP-ribosyltransferases , and rodent T-cell surface antigen RT6 .
	manualset3
86522	4	398560	13	NULL	NULL	NULL	NULL	chicken erythroblast ADP-ribosyltransferase	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Highly conserved regions were observed among the deduced amino acid sequences of AT1 , AT2 , chicken erythroblast and rabbit and human skeletal muscle ADP-ribosyltransferases , and rodent T-cell surface antigen RT6 .
	manualset3
86523	5	398560	13	NULL	NULL	0	NULL	rabbit ADP-ribosyltransferase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly conserved regions were observed among the deduced amino acid sequences of AT1 , AT2 , chicken erythroblast and rabbit and human skeletal muscle ADP-ribosyltransferases , and rodent T-cell surface antigen RT6 .
	manualset3
86524	6	398560	13	NULL	NULL	0	NULL	human skeletal muscle ADP-ribosyltransferase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly conserved regions were observed among the deduced amino acid sequences of AT1 , AT2 , chicken erythroblast and rabbit and human skeletal muscle ADP-ribosyltransferases , and rodent T-cell surface antigen RT6 .
	manualset3
86525	7	398560	13	NULL	NULL	0	NULL	rodent T-cell surface antigen RT6	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly conserved regions were observed among the deduced amino acid sequences of AT1 , AT2 , chicken erythroblast and rabbit and human skeletal muscle ADP-ribosyltransferases , and rodent T-cell surface antigen RT6 .
	manualset3
86526	1	398561	13	NULL	NULL	0	NULL	Highly crystalline nanostructured multilayered assemblies	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly crystalline nanostructured multilayered assemblies were formed , which revealed a very rich polymorphism of micro - and macro-structures depending on the chemical structure of the bile acid and the properties of the cosolvent ( EtOH or DMSO ) used .
	manualset3
86527	2	398561	13	NULL	NULL	NULL	NULL	polymorphism	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Highly crystalline nanostructured multilayered assemblies were formed , which revealed a very rich polymorphism of micro - and macro-structures depending on the chemical structure of the bile acid and the properties of the cosolvent ( EtOH or DMSO ) used .
	manualset3
86528	3	398561	13	NULL	NULL	NULL	NULL	micro -structures	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Highly crystalline nanostructured multilayered assemblies were formed , which revealed a very rich polymorphism of micro - and macro-structures depending on the chemical structure of the bile acid and the properties of the cosolvent ( EtOH or DMSO ) used .
	manualset3
86529	4	398561	13	NULL	NULL	NULL	NULL	macro-structures	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Highly crystalline nanostructured multilayered assemblies were formed , which revealed a very rich polymorphism of micro - and macro-structures depending on the chemical structure of the bile acid and the properties of the cosolvent ( EtOH or DMSO ) used .
	manualset3
86530	5	398561	13	NULL	NULL	0	NULL	chemical structure of the bile acid	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly crystalline nanostructured multilayered assemblies were formed , which revealed a very rich polymorphism of micro - and macro-structures depending on the chemical structure of the bile acid and the properties of the cosolvent ( EtOH or DMSO ) used .
	manualset3
86531	6	398561	13	NULL	NULL	0	NULL	cosolvent ( EtOH or DMSO )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly crystalline nanostructured multilayered assemblies were formed , which revealed a very rich polymorphism of micro - and macro-structures depending on the chemical structure of the bile acid and the properties of the cosolvent ( EtOH or DMSO ) used .
	manualset3
86532	1	398562	13	NULL	NULL	0	NULL	enantioselective hydrogenation of enol ester phosphonates	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly enantioselective hydrogenation of enol ester phosphonates catalyzed by rhodium phosphine-phosphite complexes .
	manualset3
86533	2	398562	13	NULL	NULL	0	NULL	rhodium phosphine-phosphite complexes	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly enantioselective hydrogenation of enol ester phosphonates catalyzed by rhodium phosphine-phosphite complexes .
	manualset3
86534	1	398563	13	NULL	NULL	NULL	NULL	lipidated C14 HSA	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Highly lipidated C14 HSA ( C14 , fatty acid side-chains with 14 carbon atoms ) was not itself mitogenic : unlike HSA it localized heavily to the red pulp as well as to cells of dendritic form in the splenic white pulp .
	manualset3
86535	2	398563	13	NULL	NULL	0	NULL	C14 , fatty acid side-chains with 14 carbon atoms 	Atom												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly lipidated C14 HSA ( C14 , fatty acid side-chains with 14 carbon atoms ) was not itself mitogenic : unlike HSA it localized heavily to the red pulp as well as to cells of dendritic form in the splenic white pulp .
	manualset3
86536	3	398563	13	NULL	NULL	NULL	NULL	HSA	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Highly lipidated C14 HSA ( C14 , fatty acid side-chains with 14 carbon atoms ) was not itself mitogenic : unlike HSA it localized heavily to the red pulp as well as to cells of dendritic form in the splenic white pulp .
	manualset3
86537	4	398563	13	NULL	NULL	0	NULL	red pulp	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly lipidated C14 HSA ( C14 , fatty acid side-chains with 14 carbon atoms ) was not itself mitogenic : unlike HSA it localized heavily to the red pulp as well as to cells of dendritic form in the splenic white pulp .
	manualset3
86538	5	398563	13	NULL	NULL	0	NULL	cells of dendritic form	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly lipidated C14 HSA ( C14 , fatty acid side-chains with 14 carbon atoms ) was not itself mitogenic : unlike HSA it localized heavily to the red pulp as well as to cells of dendritic form in the splenic white pulp .
	manualset3
86539	6	398563	13	NULL	NULL	0	NULL	splenic white pulp	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly lipidated C14 HSA ( C14 , fatty acid side-chains with 14 carbon atoms ) was not itself mitogenic : unlike HSA it localized heavily to the red pulp as well as to cells of dendritic form in the splenic white pulp .
	manualset3
86540	1	398564	13	NULL	NULL	NULL	NULL	Temperature	EnvironmentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Temperature of adaptation and regeneration in vivo of various molecular species of lecithins of rainbow trout ( Salmo gairdneri R. ) tissues ) .
	manualset3
86541	2	398564	13	NULL	NULL	0	NULL	adaptation 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Temperature of adaptation and regeneration in vivo of various molecular species of lecithins of rainbow trout ( Salmo gairdneri R. ) tissues ) .
	manualset3
86542	3	398564	13	NULL	NULL	0	NULL	regeneration	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Temperature of adaptation and regeneration in vivo of various molecular species of lecithins of rainbow trout ( Salmo gairdneri R. ) tissues ) .
	manualset3
86543	4	398564	13	NULL	NULL	NULL	NULL	various molecular species of lecithins	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Temperature of adaptation and regeneration in vivo of various molecular species of lecithins of rainbow trout ( Salmo gairdneri R. ) tissues ) .
	manualset3
86544	5	398564	13	NULL	NULL	0	NULL	rainbow trout ( Salmo gairdneri R. ) tissues	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	( Temperature of adaptation and regeneration in vivo of various molecular species of lecithins of rainbow trout ( Salmo gairdneri R. ) tissues ) .
	manualset3
86545	1	398565	13	NULL	NULL	0	NULL	Highly motivated patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly motivated patients had greater improvement on the Stereotypy Linear Analog Scale and Stereotypy Severity Scale scales compared with less motivated patients , but motivation had no impact on the Child Global Assessment Scale .
	manualset3
86546	2	398565	13	NULL	NULL	0	NULL	greater improvement	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly motivated patients had greater improvement on the Stereotypy Linear Analog Scale and Stereotypy Severity Scale scales compared with less motivated patients , but motivation had no impact on the Child Global Assessment Scale .
	manualset3
86547	3	398565	13	NULL	NULL	0	NULL	Stereotypy Linear Analog Scale	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly motivated patients had greater improvement on the Stereotypy Linear Analog Scale and Stereotypy Severity Scale scales compared with less motivated patients , but motivation had no impact on the Child Global Assessment Scale .
	manualset3
86548	4	398565	13	NULL	NULL	0	NULL	Stereotypy Severity Scale scales	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly motivated patients had greater improvement on the Stereotypy Linear Analog Scale and Stereotypy Severity Scale scales compared with less motivated patients , but motivation had no impact on the Child Global Assessment Scale .
	manualset3
86549	5	398565	13	NULL	NULL	0	NULL	less motivated patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly motivated patients had greater improvement on the Stereotypy Linear Analog Scale and Stereotypy Severity Scale scales compared with less motivated patients , but motivation had no impact on the Child Global Assessment Scale .
	manualset3
86550	6	398565	13	NULL	NULL	0	NULL	Child Global Assessment Scale	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly motivated patients had greater improvement on the Stereotypy Linear Analog Scale and Stereotypy Severity Scale scales compared with less motivated patients , but motivation had no impact on the Child Global Assessment Scale .
	manualset3
86551	1	398566	13	NULL	NULL	0	NULL	Highly pathogenic infections	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly pathogenic infections , with long-lived infective stages , tend to produce cyclic behavior in their host populations .
	manualset3
86552	2	398566	13	NULL	NULL	0	NULL	long-lived infective stages	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly pathogenic infections , with long-lived infective stages , tend to produce cyclic behavior in their host populations .
	manualset3
86553	3	398566	13	NULL	NULL	0	NULL	cyclic behavior	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly pathogenic infections , with long-lived infective stages , tend to produce cyclic behavior in their host populations .
	manualset3
86554	4	398566	13	NULL	NULL	0	NULL	host populations	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly pathogenic infections , with long-lived infective stages , tend to produce cyclic behavior in their host populations .
	manualset3
86555	1	398567	13	NULL	NULL	0	NULL	Highly sensitive molecularly imprinted electrochemical sensor	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly sensitive molecularly imprinted electrochemical sensor based on the double amplification by an inorganic Prussian blue catalytic polymer and the enzymatic effect of glucose oxidase .
	manualset3
86556	2	398567	13	NULL	NULL	0	NULL	double amplification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly sensitive molecularly imprinted electrochemical sensor based on the double amplification by an inorganic Prussian blue catalytic polymer and the enzymatic effect of glucose oxidase .
	manualset3
86557	3	398567	13	NULL	NULL	0	NULL	inorganic Prussian blue catalytic polymer	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly sensitive molecularly imprinted electrochemical sensor based on the double amplification by an inorganic Prussian blue catalytic polymer and the enzymatic effect of glucose oxidase .
	manualset3
86558	4	398567	13	NULL	NULL	0	NULL	 enzymatic effect of glucose oxidase	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly sensitive molecularly imprinted electrochemical sensor based on the double amplification by an inorganic Prussian blue catalytic polymer and the enzymatic effect of glucose oxidase .
	manualset3
86559	1	398568	13	NULL	NULL	NULL	NULL	Highly successful antimicrobial measures 	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Highly successful antimicrobial measures that would reduce the number of diseased sibs independent of the distribution of susceptible sibs could produce a dissociation of the gene-to - `` rheumatic '' relationship and thus explains the declining ascertainment bias .
	manualset3
86560	2	398568	13	NULL	NULL	0	NULL	diseased sibs	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly successful antimicrobial measures that would reduce the number of diseased sibs independent of the distribution of susceptible sibs could produce a dissociation of the gene-to - `` rheumatic '' relationship and thus explains the declining ascertainment bias .
	manualset3
86561	3	398568	13	NULL	NULL	0	NULL	distribution	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly successful antimicrobial measures that would reduce the number of diseased sibs independent of the distribution of susceptible sibs could produce a dissociation of the gene-to - `` rheumatic '' relationship and thus explains the declining ascertainment bias .
	manualset3
86562	4	398568	13	NULL	NULL	0	NULL	 susceptible sibs	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly successful antimicrobial measures that would reduce the number of diseased sibs independent of the distribution of susceptible sibs could produce a dissociation of the gene-to - `` rheumatic '' relationship and thus explains the declining ascertainment bias .
	manualset3
86563	5	398568	13	NULL	NULL	NULL	NULL	dissociation 	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Highly successful antimicrobial measures that would reduce the number of diseased sibs independent of the distribution of susceptible sibs could produce a dissociation of the gene-to - `` rheumatic '' relationship and thus explains the declining ascertainment bias .
	manualset3
86564	6	398568	13	NULL	NULL	NULL	NULL	gene-to - `` rheumatic '' relationship	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Highly successful antimicrobial measures that would reduce the number of diseased sibs independent of the distribution of susceptible sibs could produce a dissociation of the gene-to - `` rheumatic '' relationship and thus explains the declining ascertainment bias .
	manualset3
86565	7	398568	13	NULL	NULL	NULL	NULL	declining ascertainment bias 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Highly successful antimicrobial measures that would reduce the number of diseased sibs independent of the distribution of susceptible sibs could produce a dissociation of the gene-to - `` rheumatic '' relationship and thus explains the declining ascertainment bias .
	manualset3
86566	1	398569	13	NULL	NULL	0	NULL	pi-conjugation extension	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly unusual effects of pi-conjugation extension on the molecular linear and quadratic nonlinear optical properties of ruthenium ( II ) ammine complexes .
	manualset3
86567	2	398569	13	NULL	NULL	0	NULL	ruthenium ( II ) ammine complexes 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly unusual effects of pi-conjugation extension on the molecular linear and quadratic nonlinear optical properties of ruthenium ( II ) ammine complexes .
	manualset3
86568	3	398569	13	NULL	NULL	0	NULL	 molecular linear properties	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly unusual effects of pi-conjugation extension on the molecular linear and quadratic nonlinear optical properties of ruthenium ( II ) ammine complexes .
	manualset3
86569	4	398569	13	NULL	NULL	0	NULL	quadratic nonlinear optical properties 	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Highly unusual effects of pi-conjugation extension on the molecular linear and quadratic nonlinear optical properties of ruthenium ( II ) ammine complexes .
	manualset3
86570	1	398570	13	NULL	NULL	NULL	NULL	Hilbert transform	PublishedSourceOfInformation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hilbert transform is used to combine multiple channel measurements and the adaptive rule based decision process is used to eliminate spurious beats .
	manualset3
86571	2	398570	13	NULL	NULL	NULL	NULL	multiple channel measurements	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hilbert transform is used to combine multiple channel measurements and the adaptive rule based decision process is used to eliminate spurious beats .
	manualset3
86572	3	398570	13	NULL	NULL	NULL	NULL	adaptive rule based decision process	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hilbert transform is used to combine multiple channel measurements and the adaptive rule based decision process is used to eliminate spurious beats .
	manualset3
86574	1	398571	13	NULL	NULL	0	NULL	Hindsight	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hindsight rather than foresight : reality versus the EU draft guideline on pharmaceuticals in the environment .
	manualset3
86575	2	398571	13	NULL	NULL	0	NULL	foresight	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hindsight rather than foresight : reality versus the EU draft guideline on pharmaceuticals in the environment .
	manualset3
86576	3	398571	13	NULL	NULL	0	NULL	EU draft guideline	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Hindsight rather than foresight : reality versus the EU draft guideline on pharmaceuticals in the environment .
	manualset3
86577	4	398571	13	NULL	NULL	0	NULL	pharmaceuticals	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hindsight rather than foresight : reality versus the EU draft guideline on pharmaceuticals in the environment .
	manualset3
86578	5	398571	13	NULL	NULL	0	NULL	environment	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Hindsight rather than foresight : reality versus the EU draft guideline on pharmaceuticals in the environment .
	manualset3
86579	1	398572	13	NULL	NULL	0	NULL	 Termination of pregnancy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Termination of pregnancy , a very difficult question ) .
	manualset3
86580	1	398573	13	NULL	NULL	0	NULL	Hippocampal slices	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hippocampal slices ( 450 microm ) generate epileptiform bursts of an interictal nature when perfused with a zero magnesium medium containing 4-aminopyridine ( 50 microM ) .
	manualset3
86581	2	398573	13	NULL	NULL	0	NULL	450 microm	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hippocampal slices ( 450 microm ) generate epileptiform bursts of an interictal nature when perfused with a zero magnesium medium containing 4-aminopyridine ( 50 microM ) .
	manualset3
86582	3	398573	13	NULL	NULL	0	NULL	generate epileptiform bursts of an interictal nature 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hippocampal slices ( 450 microm ) generate epileptiform bursts of an interictal nature when perfused with a zero magnesium medium containing 4-aminopyridine ( 50 microM ) .
	manualset3
86583	4	398573	13	NULL	NULL	0	NULL	zero magnesium medium	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Hippocampal slices ( 450 microm ) generate epileptiform bursts of an interictal nature when perfused with a zero magnesium medium containing 4-aminopyridine ( 50 microM ) .
	manualset3
86584	5	398573	13	NULL	NULL	NULL	NULL	4-aminopyridine	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hippocampal slices ( 450 microm ) generate epileptiform bursts of an interictal nature when perfused with a zero magnesium medium containing 4-aminopyridine ( 50 microM ) .
	manualset3
86585	6	398573	13	NULL	NULL	NULL	NULL	50 microM	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hippocampal slices ( 450 microm ) generate epileptiform bursts of an interictal nature when perfused with a zero magnesium medium containing 4-aminopyridine ( 50 microM ) .
	manualset3
86586	1	398574	13	NULL	NULL	0	NULL	 generalised fair innings approach 	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	His ` generalised fair innings approach ' on the one hand , and the severity approach on the other , are two ways of incorporating concerns for fairness in economic evaluation of health care .
	manualset3
86587	2	398574	13	NULL	NULL	0	NULL	 severity approach 	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	His ` generalised fair innings approach ' on the one hand , and the severity approach on the other , are two ways of incorporating concerns for fairness in economic evaluation of health care .
	manualset3
86588	3	398574	13	NULL	NULL	0	NULL	two ways of incorporating concerns for fairness	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	His ` generalised fair innings approach ' on the one hand , and the severity approach on the other , are two ways of incorporating concerns for fairness in economic evaluation of health care .
	manualset3
86589	4	398574	13	NULL	NULL	0	NULL	economic evaluation of health care	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	His ` generalised fair innings approach ' on the one hand , and the severity approach on the other , are two ways of incorporating concerns for fairness in economic evaluation of health care .
	manualset3
86590	1	398575	13	NULL	NULL	NULL	NULL	serum creatine kinase ( CK ) level 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	His serum creatine kinase ( CK ) level was extremely elevated , and chest X-ray revealed bilateral hilar lymphadenopathy and small nodules in bilateral lung fields .
	manualset3
86591	2	398575	13	NULL	NULL	0	NULL	chest X-ray 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	His serum creatine kinase ( CK ) level was extremely elevated , and chest X-ray revealed bilateral hilar lymphadenopathy and small nodules in bilateral lung fields .
	manualset3
86592	3	398575	13	NULL	NULL	0	NULL	bilateral hilar lymphadenopathy	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	His serum creatine kinase ( CK ) level was extremely elevated , and chest X-ray revealed bilateral hilar lymphadenopathy and small nodules in bilateral lung fields .
	manualset3
86593	4	398575	13	NULL	NULL	NULL	NULL	small nodules in bilateral lung fields	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	His serum creatine kinase ( CK ) level was extremely elevated , and chest X-ray revealed bilateral hilar lymphadenopathy and small nodules in bilateral lung fields .
	manualset3
86594	1	398576	13	NULL	NULL	0	NULL	theory of `` determinant spreading ''	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	His theory of `` determinant spreading '' is one of the cornerstones of our modern understanding of autoimmunity .
	manualset3
86595	2	398576	13	NULL	NULL	0	NULL	modern understanding	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	His theory of `` determinant spreading '' is one of the cornerstones of our modern understanding of autoimmunity .
	manualset3
86596	3	398576	13	NULL	NULL	0	NULL	autoimmunity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	His theory of `` determinant spreading '' is one of the cornerstones of our modern understanding of autoimmunity .
	manualset3
86597	1	398577	13	NULL	NULL	0	NULL	young wife	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	His young wife presented him with a daughter Bianca , and a son Gaspare , but in 1861 she died , leaving him with the responsibility of rearing the children .
	manualset3
86598	2	398577	13	NULL	NULL	0	NULL	daughter Bianca	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	His young wife presented him with a daughter Bianca , and a son Gaspare , but in 1861 she died , leaving him with the responsibility of rearing the children .
	manualset3
86599	3	398577	13	NULL	NULL	0	NULL	son Gaspare	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	His young wife presented him with a daughter Bianca , and a son Gaspare , but in 1861 she died , leaving him with the responsibility of rearing the children .
	manualset3
86600	4	398577	13	NULL	NULL	0	NULL	1861	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	His young wife presented him with a daughter Bianca , and a son Gaspare , but in 1861 she died , leaving him with the responsibility of rearing the children .
	manualset3
86601	5	398577	13	NULL	NULL	0	NULL	died	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	His young wife presented him with a daughter Bianca , and a son Gaspare , but in 1861 she died , leaving him with the responsibility of rearing the children .
	manualset3
86602	6	398577	13	NULL	NULL	0	NULL	children	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	His young wife presented him with a daughter Bianca , and a son Gaspare , but in 1861 she died , leaving him with the responsibility of rearing the children .
	manualset3
86603	1	398578	13	NULL	NULL	0	NULL	His1	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	His1 and His2 are distantly related , spindle-shaped haloviruses belonging to the novel virus group , Salterprovirus .
	manualset3
86604	2	398578	13	NULL	NULL	0	NULL	His2	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	His1 and His2 are distantly related , spindle-shaped haloviruses belonging to the novel virus group , Salterprovirus .
	manualset3
86605	3	398578	13	NULL	NULL	0	NULL	spindle-shaped haloviruses	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	His1 and His2 are distantly related , spindle-shaped haloviruses belonging to the novel virus group , Salterprovirus .
	manualset3
86606	4	398578	13	NULL	NULL	0	NULL	novel virus group , Salterprovirus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	His1 and His2 are distantly related , spindle-shaped haloviruses belonging to the novel virus group , Salterprovirus .
	manualset3
86607	1	398579	13	NULL	NULL	0	NULL	His373 in flavocytochrome b2	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	His373 in flavocytochrome b2 has been proposed to act as an active site base during the oxidation of lactate to pyruvate , most likely by removing the lactate hydroxyl proton .
	manualset3
86608	2	398579	13	NULL	NULL	0	NULL	active site base	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	His373 in flavocytochrome b2 has been proposed to act as an active site base during the oxidation of lactate to pyruvate , most likely by removing the lactate hydroxyl proton .
	manualset3
86609	3	398579	13	NULL	NULL	0	NULL	 oxidation of lactate to pyruvate 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	His373 in flavocytochrome b2 has been proposed to act as an active site base during the oxidation of lactate to pyruvate , most likely by removing the lactate hydroxyl proton .
	manualset3
86610	4	398579	13	NULL	NULL	0	NULL	removing the lactate hydroxyl proton	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	His373 in flavocytochrome b2 has been proposed to act as an active site base during the oxidation of lactate to pyruvate , most likely by removing the lactate hydroxyl proton .
	manualset3
86611	1	398580	13	NULL	NULL	0	NULL	Terminology	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	( Terminology and classification of automobile injuries ) .
	manualset3
86612	2	398580	13	NULL	NULL	0	NULL	classification	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	( Terminology and classification of automobile injuries ) .
	manualset3
86613	3	398580	13	NULL	NULL	0	NULL	automobile injuries	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Terminology and classification of automobile injuries ) .
	manualset3
86614	1	398581	13	NULL	NULL	0	NULL	Histamine-induced surface expression of P-selectin 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Histamine-induced surface expression of P-selectin was blocked by the histamine H2 receptor antagonist cimetidine .
	manualset3
86615	2	398581	13	NULL	NULL	0	NULL	histamine H2 receptor antagonist cimetidine	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Histamine-induced surface expression of P-selectin was blocked by the histamine H2 receptor antagonist cimetidine .
	manualset3
86616	1	398582	13	NULL	NULL	0	NULL	Histamine release	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Histamine release by the calcium ionophore ( A 23187 ) added to cells at intervals before the addition of calcium did not show significant decay .7 .
	manualset3
86617	2	398582	13	NULL	NULL	0	NULL	calcium ionophore ( A 23187 ) 	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Histamine release by the calcium ionophore ( A 23187 ) added to cells at intervals before the addition of calcium did not show significant decay .7 .
	manualset3
86618	3	398582	13	NULL	NULL	0	NULL	cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Histamine release by the calcium ionophore ( A 23187 ) added to cells at intervals before the addition of calcium did not show significant decay .7 .
	manualset3
86619	4	398582	13	NULL	NULL	0	NULL	intervals	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Histamine release by the calcium ionophore ( A 23187 ) added to cells at intervals before the addition of calcium did not show significant decay .7 .
	manualset3
86620	5	398582	13	NULL	NULL	NULL	NULL	calcium	Atom												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Histamine release by the calcium ionophore ( A 23187 ) added to cells at intervals before the addition of calcium did not show significant decay .7 .
	manualset3
86621	6	398582	13	NULL	NULL	0	NULL	significant decay .7	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histamine release by the calcium ionophore ( A 23187 ) added to cells at intervals before the addition of calcium did not show significant decay .7 .
	manualset3
86622	1	398583	13	NULL	NULL	0	NULL	Histidine	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Histidine , which is known to activate motility of starfish sperm , also raised the ( pH ) i during the motility activation .
	manualset3
86623	2	398583	13	NULL	NULL	0	NULL	motility of starfish sperm	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Histidine , which is known to activate motility of starfish sperm , also raised the ( pH ) i during the motility activation .
	manualset3
86624	3	398583	13	NULL	NULL	NULL	NULL	( pH ) i 	ExperimentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Histidine , which is known to activate motility of starfish sperm , also raised the ( pH ) i during the motility activation .
	manualset3
86625	4	398583	13	NULL	NULL	0	NULL	motility activation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Histidine , which is known to activate motility of starfish sperm , also raised the ( pH ) i during the motility activation .
	manualset3
86626	1	398584	13	NULL	NULL	0	NULL	Histidine	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Histidine and tryptamine also gave products upon UV irradiation that competed with TCDD .
	manualset3
86627	2	398584	13	NULL	NULL	0	NULL	tryptamine	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Histidine and tryptamine also gave products upon UV irradiation that competed with TCDD .
	manualset3
86628	3	398584	13	NULL	NULL	0	NULL	UV irradiation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histidine and tryptamine also gave products upon UV irradiation that competed with TCDD .
	manualset3
86629	4	398584	13	NULL	NULL	0	NULL	TCDD	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Histidine and tryptamine also gave products upon UV irradiation that competed with TCDD .
	manualset3
86630	1	398585	13	NULL	NULL	0	NULL	Histochemical changes 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Histochemical changes in enzymes of energy metabolism in the dentate gyrus accompany deafferentation and synaptic reorganization .
	manualset3
86631	2	398585	13	NULL	NULL	0	NULL	enzymes of energy metabolism	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Histochemical changes in enzymes of energy metabolism in the dentate gyrus accompany deafferentation and synaptic reorganization .
	manualset3
86632	3	398585	13	NULL	NULL	0	NULL	dentate gyrus	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Histochemical changes in enzymes of energy metabolism in the dentate gyrus accompany deafferentation and synaptic reorganization .
	manualset3
86633	4	398585	13	NULL	NULL	0	NULL	deafferentation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Histochemical changes in enzymes of energy metabolism in the dentate gyrus accompany deafferentation and synaptic reorganization .
	manualset3
86634	5	398585	13	NULL	NULL	0	NULL	 synaptic reorganization	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Histochemical changes in enzymes of energy metabolism in the dentate gyrus accompany deafferentation and synaptic reorganization .
	manualset3
86635	1	398586	13	NULL	NULL	0	NULL	Histochemical demonstration 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histochemical demonstration of alpha-glucan phosphorylase activity in the human axillary apocrine sweat gland .
	manualset3
86636	2	398586	13	NULL	NULL	0	NULL	alpha-glucan phosphorylase activity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Histochemical demonstration of alpha-glucan phosphorylase activity in the human axillary apocrine sweat gland .
	manualset3
86637	3	398586	13	NULL	NULL	0	NULL	human axillary apocrine sweat gland	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Histochemical demonstration of alpha-glucan phosphorylase activity in the human axillary apocrine sweat gland .
	manualset3
86638	1	398587	13	NULL	NULL	0	NULL	Histocompatibility antigens	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Histocompatibility antigens on mouse spermatozoa .
	manualset3
86639	2	398587	13	NULL	NULL	0	NULL	mouse spermatozoa	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Histocompatibility antigens on mouse spermatozoa .
	manualset3
86640	1	398588	13	NULL	NULL	0	NULL	Association	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( The Association should be the information center ) .
	manualset3
86641	2	398588	13	NULL	NULL	0	NULL	 information center	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	( The Association should be the information center ) .
	manualset3
86642	1	398589	13	NULL	NULL	0	NULL	Histologic analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologic analysis demonstrated an intact endothelial surface in the stenotic segments , confirmed by the demonstration of factor VIII production by these cells .
	manualset3
86643	2	398589	13	NULL	NULL	0	NULL	intact endothelial surface in the stenotic segments	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologic analysis demonstrated an intact endothelial surface in the stenotic segments , confirmed by the demonstration of factor VIII production by these cells .
	manualset3
86644	3	398589	13	NULL	NULL	NULL	NULL	 factor VIII production	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Histologic analysis demonstrated an intact endothelial surface in the stenotic segments , confirmed by the demonstration of factor VIII production by these cells .
	manualset3
86645	4	398589	13	NULL	NULL	0	NULL	 cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologic analysis demonstrated an intact endothelial surface in the stenotic segments , confirmed by the demonstration of factor VIII production by these cells .
	manualset3
86646	1	398590	13	NULL	NULL	0	NULL	Histologic appearances of tumors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologic appearances of tumors remained constant in subsequent passages .
	manualset3
86647	2	398590	13	NULL	NULL	0	NULL	subsequent passages	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologic appearances of tumors remained constant in subsequent passages .
	manualset3
86648	1	398591	13	NULL	NULL	0	NULL	Histologic evaluation of hepatic biopsy specimens	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologic evaluation of hepatic biopsy specimens from the 2 dogs revealed granulomatous hepatitis in the Basset Hound and lymphocytic hepatitis with fibrosis and copper accumulation in the Doberman Pinscher .
	manualset3
86650	3	398591	13	NULL	NULL	0	NULL	granulomatous hepatitis 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologic evaluation of hepatic biopsy specimens from the 2 dogs revealed granulomatous hepatitis in the Basset Hound and lymphocytic hepatitis with fibrosis and copper accumulation in the Doberman Pinscher .
	manualset3
86651	4	398591	13	NULL	NULL	0	NULL	Basset Hound 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologic evaluation of hepatic biopsy specimens from the 2 dogs revealed granulomatous hepatitis in the Basset Hound and lymphocytic hepatitis with fibrosis and copper accumulation in the Doberman Pinscher .
	manualset3
86652	5	398591	13	NULL	NULL	0	NULL	lymphocytic hepatitis with fibrosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologic evaluation of hepatic biopsy specimens from the 2 dogs revealed granulomatous hepatitis in the Basset Hound and lymphocytic hepatitis with fibrosis and copper accumulation in the Doberman Pinscher .
	manualset3
86653	6	398591	13	NULL	NULL	0	NULL	copper accumulation	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologic evaluation of hepatic biopsy specimens from the 2 dogs revealed granulomatous hepatitis in the Basset Hound and lymphocytic hepatitis with fibrosis and copper accumulation in the Doberman Pinscher .
	manualset3
86654	7	398591	13	NULL	NULL	0	NULL	Doberman Pinscher	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologic evaluation of hepatic biopsy specimens from the 2 dogs revealed granulomatous hepatitis in the Basset Hound and lymphocytic hepatitis with fibrosis and copper accumulation in the Doberman Pinscher .
	manualset3
89565	8	398591	13	NULL	NULL	0	NULL	 2 dogs	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologic evaluation of hepatic biopsy specimens from the 2 dogs revealed granulomatous hepatitis in the Basset Hound and lymphocytic hepatitis with fibrosis and copper accumulation in the Doberman Pinscher .
	manualset3
86649	1	398592	13	NULL	NULL	NULL	NULL	Histologic examination	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Histologic examination showed a histological pattern of interstitial granulomatous dermatitis .
	manualset3
86658	2	398592	13	NULL	NULL	NULL	NULL	histological pattern 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Histologic examination showed a histological pattern of interstitial granulomatous dermatitis .
	manualset3
86731	3	398592	13	NULL	NULL	0	NULL	interstitial granulomatous dermatitis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologic examination showed a histological pattern of interstitial granulomatous dermatitis .
	manualset3
86738	1	398593	13	NULL	NULL	0	NULL	Histologic examination	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologic examination showed that epididymal adipocyte size was smaller in mice fed the HF + 3 % CO. .
	manualset3
86740	2	398593	13	NULL	NULL	0	NULL	epididymal adipocyte	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologic examination showed that epididymal adipocyte size was smaller in mice fed the HF + 3 % CO. .
	manualset3
86741	3	398593	13	NULL	NULL	0	NULL	size	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologic examination showed that epididymal adipocyte size was smaller in mice fed the HF + 3 % CO. .
	manualset3
86743	4	398593	13	NULL	NULL	0	NULL	mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologic examination showed that epididymal adipocyte size was smaller in mice fed the HF + 3 % CO. .
	manualset3
86744	5	398593	13	NULL	NULL	0	NULL	HF + 3 % CO	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologic examination showed that epididymal adipocyte size was smaller in mice fed the HF + 3 % CO. .
	manualset3
86746	1	398594	13	NULL	NULL	0	NULL	Histological analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological analysis of the aneurysm wall showed non-caseating granulomata .
	manualset3
86749	2	398594	13	NULL	NULL	0	NULL	aneurysm wall 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological analysis of the aneurysm wall showed non-caseating granulomata .
	manualset3
86750	3	398594	13	NULL	NULL	0	NULL	non-caseating granulomata	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological analysis of the aneurysm wall showed non-caseating granulomata .
	manualset3
86752	1	398595	13	NULL	NULL	0	NULL	Histological analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological analysis revealed well-differentiated HCC in both of the tumors .
	manualset3
86755	2	398595	13	NULL	NULL	0	NULL	well-differentiated HCC 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological analysis revealed well-differentiated HCC in both of the tumors .
	manualset3
86759	3	398595	13	NULL	NULL	NULL	NULL	tumors	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Histological analysis revealed well-differentiated HCC in both of the tumors .
	manualset3
86765	1	398596	13	NULL	NULL	0	NULL	Histological and immunocytochemical studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological and immunocytochemical studies showed good survival of both PN and VM grafts .
	manualset3
86766	2	398596	13	NULL	NULL	NULL	NULL	good survival	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Histological and immunocytochemical studies showed good survival of both PN and VM grafts .
	manualset3
86771	3	398596	13	NULL	NULL	0	NULL	PN grafts	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological and immunocytochemical studies showed good survival of both PN and VM grafts .
	manualset3
86772	4	398596	13	NULL	NULL	0	NULL	 VM grafts	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological and immunocytochemical studies showed good survival of both PN and VM grafts .
	manualset3
86776	1	398597	13	NULL	NULL	0	NULL	Histological changes 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological changes in bladders of patients submitted to ifosfamide chemotherapy even with mesna prophylaxis .
	manualset3
86777	2	398597	13	NULL	NULL	NULL	NULL	bladders	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Histological changes in bladders of patients submitted to ifosfamide chemotherapy even with mesna prophylaxis .
	manualset3
86778	4	398597	13	NULL	NULL	NULL	NULL	ifosfamide chemotherapy	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Histological changes in bladders of patients submitted to ifosfamide chemotherapy even with mesna prophylaxis .
	manualset3
86781	5	398597	13	NULL	NULL	NULL	NULL	mesna prophylaxis 	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Histological changes in bladders of patients submitted to ifosfamide chemotherapy even with mesna prophylaxis .
	manualset3
86782	3	398597	13	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological changes in bladders of patients submitted to ifosfamide chemotherapy even with mesna prophylaxis .
	manualset3
86785	1	398598	13	NULL	NULL	0	NULL	Histological diagnosis of the lesions	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological diagnosis of the lesions revealed : astrocytomas in 14 patients , oligodendroglioma in one , ependymoma in one , arteriovenous malformations in two , radionecrosis in one , cryptococcal abscess in one , demyelinating disease in three , and infarctions in three .
	manualset3
86786	2	398598	13	NULL	NULL	0	NULL	astrocytomas	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological diagnosis of the lesions revealed : astrocytomas in 14 patients , oligodendroglioma in one , ependymoma in one , arteriovenous malformations in two , radionecrosis in one , cryptococcal abscess in one , demyelinating disease in three , and infarctions in three .
	manualset3
86788	3	398598	13	NULL	NULL	0	NULL	14 patients	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological diagnosis of the lesions revealed : astrocytomas in 14 patients , oligodendroglioma in one , ependymoma in one , arteriovenous malformations in two , radionecrosis in one , cryptococcal abscess in one , demyelinating disease in three , and infarctions in three .
	manualset3
86789	4	398598	13	NULL	NULL	0	NULL	oligodendroglioma 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological diagnosis of the lesions revealed : astrocytomas in 14 patients , oligodendroglioma in one , ependymoma in one , arteriovenous malformations in two , radionecrosis in one , cryptococcal abscess in one , demyelinating disease in three , and infarctions in three .
	manualset3
86790	5	398598	13	NULL	NULL	0	NULL	one	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological diagnosis of the lesions revealed : astrocytomas in 14 patients , oligodendroglioma in one , ependymoma in one , arteriovenous malformations in two , radionecrosis in one , cryptococcal abscess in one , demyelinating disease in three , and infarctions in three .
	manualset3
86791	6	398598	13	NULL	NULL	0	NULL	 ependymoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological diagnosis of the lesions revealed : astrocytomas in 14 patients , oligodendroglioma in one , ependymoma in one , arteriovenous malformations in two , radionecrosis in one , cryptococcal abscess in one , demyelinating disease in three , and infarctions in three .
	manualset3
86792	7	398598	13	NULL	NULL	0	NULL	one 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological diagnosis of the lesions revealed : astrocytomas in 14 patients , oligodendroglioma in one , ependymoma in one , arteriovenous malformations in two , radionecrosis in one , cryptococcal abscess in one , demyelinating disease in three , and infarctions in three .
	manualset3
86793	8	398598	13	NULL	NULL	0	NULL	arteriovenous malformations	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological diagnosis of the lesions revealed : astrocytomas in 14 patients , oligodendroglioma in one , ependymoma in one , arteriovenous malformations in two , radionecrosis in one , cryptococcal abscess in one , demyelinating disease in three , and infarctions in three .
	manualset3
86794	9	398598	13	NULL	NULL	0	NULL	two	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological diagnosis of the lesions revealed : astrocytomas in 14 patients , oligodendroglioma in one , ependymoma in one , arteriovenous malformations in two , radionecrosis in one , cryptococcal abscess in one , demyelinating disease in three , and infarctions in three .
	manualset3
86796	10	398598	13	NULL	NULL	0	NULL	radionecrosis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological diagnosis of the lesions revealed : astrocytomas in 14 patients , oligodendroglioma in one , ependymoma in one , arteriovenous malformations in two , radionecrosis in one , cryptococcal abscess in one , demyelinating disease in three , and infarctions in three .
	manualset3
86797	11	398598	13	NULL	NULL	0	NULL	 one	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological diagnosis of the lesions revealed : astrocytomas in 14 patients , oligodendroglioma in one , ependymoma in one , arteriovenous malformations in two , radionecrosis in one , cryptococcal abscess in one , demyelinating disease in three , and infarctions in three .
	manualset3
86799	12	398598	13	NULL	NULL	0	NULL	cryptococcal abscess	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological diagnosis of the lesions revealed : astrocytomas in 14 patients , oligodendroglioma in one , ependymoma in one , arteriovenous malformations in two , radionecrosis in one , cryptococcal abscess in one , demyelinating disease in three , and infarctions in three .
	manualset3
86800	13	398598	13	NULL	NULL	0	NULL	one	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological diagnosis of the lesions revealed : astrocytomas in 14 patients , oligodendroglioma in one , ependymoma in one , arteriovenous malformations in two , radionecrosis in one , cryptococcal abscess in one , demyelinating disease in three , and infarctions in three .
	manualset3
86802	14	398598	13	NULL	NULL	0	NULL	demyelinating disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological diagnosis of the lesions revealed : astrocytomas in 14 patients , oligodendroglioma in one , ependymoma in one , arteriovenous malformations in two , radionecrosis in one , cryptococcal abscess in one , demyelinating disease in three , and infarctions in three .
	manualset3
86803	15	398598	13	NULL	NULL	0	NULL	three	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological diagnosis of the lesions revealed : astrocytomas in 14 patients , oligodendroglioma in one , ependymoma in one , arteriovenous malformations in two , radionecrosis in one , cryptococcal abscess in one , demyelinating disease in three , and infarctions in three .
	manualset3
86804	16	398598	13	NULL	NULL	0	NULL	infarctions	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological diagnosis of the lesions revealed : astrocytomas in 14 patients , oligodendroglioma in one , ependymoma in one , arteriovenous malformations in two , radionecrosis in one , cryptococcal abscess in one , demyelinating disease in three , and infarctions in three .
	manualset3
86806	17	398598	13	NULL	NULL	0	NULL	three 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological diagnosis of the lesions revealed : astrocytomas in 14 patients , oligodendroglioma in one , ependymoma in one , arteriovenous malformations in two , radionecrosis in one , cryptococcal abscess in one , demyelinating disease in three , and infarctions in three .
	manualset3
86809	1	398599	13	NULL	NULL	0	NULL	Analysis of late components	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Analysis of late components of evoked potentials arising in the paramedian lobule of the cerebellum in response to stimulation of nerves and the cerebral cortex ) .
	manualset3
86810	2	398599	13	NULL	NULL	0	NULL	evoked potentials 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Analysis of late components of evoked potentials arising in the paramedian lobule of the cerebellum in response to stimulation of nerves and the cerebral cortex ) .
	manualset3
86811	3	398599	13	NULL	NULL	0	NULL	paramedian lobule of the cerebellum	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( Analysis of late components of evoked potentials arising in the paramedian lobule of the cerebellum in response to stimulation of nerves and the cerebral cortex ) .
	manualset3
86812	4	398599	13	NULL	NULL	0	NULL	stimulation of nerves	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Analysis of late components of evoked potentials arising in the paramedian lobule of the cerebellum in response to stimulation of nerves and the cerebral cortex ) .
	manualset3
86813	5	398599	13	NULL	NULL	0	NULL	cerebral cortex	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( Analysis of late components of evoked potentials arising in the paramedian lobule of the cerebellum in response to stimulation of nerves and the cerebral cortex ) .
	manualset3
86814	1	398600	13	NULL	NULL	0	NULL	C-cell system of the thyroid	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	( The C-cell system of the thyroid in rats following a flight on the Kosmos 1667 biosatellite ) .
	manualset3
86815	2	398600	13	NULL	NULL	0	NULL	rats 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( The C-cell system of the thyroid in rats following a flight on the Kosmos 1667 biosatellite ) .
	manualset3
86816	3	398600	13	NULL	NULL	0	NULL	Kosmos 1667 biosatellite	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	( The C-cell system of the thyroid in rats following a flight on the Kosmos 1667 biosatellite ) .
	manualset3
86818	1	398601	13	NULL	NULL	0	NULL	Histological examination	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological examination demonstrated bladder endometriosis sparing the urothelium .
	manualset3
86819	2	398601	13	NULL	NULL	0	NULL	bladder endometriosis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological examination demonstrated bladder endometriosis sparing the urothelium .
	manualset3
86820	3	398601	13	NULL	NULL	0	NULL	urothelium	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological examination demonstrated bladder endometriosis sparing the urothelium .
	manualset3
86821	1	398602	13	NULL	NULL	0	NULL	Histological lesions	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological lesions comprised of fragmentation of elastic fibers as well as extensive loss of elastic layers .
	manualset3
86822	2	398602	13	NULL	NULL	NULL	NULL	fragmentation of elastic fibers	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Histological lesions comprised of fragmentation of elastic fibers as well as extensive loss of elastic layers .
	manualset3
86823	3	398602	13	NULL	NULL	0	NULL	extensive loss of elastic layers	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological lesions comprised of fragmentation of elastic fibers as well as extensive loss of elastic layers .
	manualset3
86824	1	398603	13	NULL	NULL	0	NULL	Histological studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological studies and TEM revealed that Y. enterocolitica selectively invaded the PP via M cells but not via other cells of the FAE .
	manualset3
86825	2	398603	13	NULL	NULL	0	NULL	TEM	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological studies and TEM revealed that Y. enterocolitica selectively invaded the PP via M cells but not via other cells of the FAE .
	manualset3
86826	3	398603	13	NULL	NULL	0	NULL	Y. enterocolitica 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological studies and TEM revealed that Y. enterocolitica selectively invaded the PP via M cells but not via other cells of the FAE .
	manualset3
86827	4	398603	13	NULL	NULL	0	NULL	PP	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological studies and TEM revealed that Y. enterocolitica selectively invaded the PP via M cells but not via other cells of the FAE .
	manualset3
86828	5	398603	13	NULL	NULL	0	NULL	M cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological studies and TEM revealed that Y. enterocolitica selectively invaded the PP via M cells but not via other cells of the FAE .
	manualset3
86829	6	398603	13	NULL	NULL	0	NULL	other cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological studies and TEM revealed that Y. enterocolitica selectively invaded the PP via M cells but not via other cells of the FAE .
	manualset3
86830	7	398603	13	NULL	NULL	0	NULL	FAE 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Histological studies and TEM revealed that Y. enterocolitica selectively invaded the PP via M cells but not via other cells of the FAE .
	manualset3
86831	1	398604	13	NULL	NULL	0	NULL	tumors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologically , tumors were classified as MALT-type lymphoma .
	manualset3
86832	2	398604	13	NULL	NULL	0	NULL	MALT-type lymphoma 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Histologically , tumors were classified as MALT-type lymphoma .
	manualset3
86833	1	398605	13	NULL	NULL	0	NULL	Histology	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Histology revealed fibrocystic change in 66 , fibroadenoma in 27 , radial scar/complex sclerosing lesion in 23 , atypical ductal hyperplasia only in eight , and a variety of unusual benign lesions in 13 .
	manualset3
86834	2	398605	13	NULL	NULL	0	NULL	fibrocystic change	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histology revealed fibrocystic change in 66 , fibroadenoma in 27 , radial scar/complex sclerosing lesion in 23 , atypical ductal hyperplasia only in eight , and a variety of unusual benign lesions in 13 .
	manualset3
86835	3	398605	13	NULL	NULL	0	NULL	66	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histology revealed fibrocystic change in 66 , fibroadenoma in 27 , radial scar/complex sclerosing lesion in 23 , atypical ductal hyperplasia only in eight , and a variety of unusual benign lesions in 13 .
	manualset3
86836	4	398605	13	NULL	NULL	0	NULL	fibroadenoma	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histology revealed fibrocystic change in 66 , fibroadenoma in 27 , radial scar/complex sclerosing lesion in 23 , atypical ductal hyperplasia only in eight , and a variety of unusual benign lesions in 13 .
	manualset3
86837	5	398605	13	NULL	NULL	0	NULL	27	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histology revealed fibrocystic change in 66 , fibroadenoma in 27 , radial scar/complex sclerosing lesion in 23 , atypical ductal hyperplasia only in eight , and a variety of unusual benign lesions in 13 .
	manualset3
86838	6	398605	13	NULL	NULL	0	NULL	radial scar/complex sclerosing lesion 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histology revealed fibrocystic change in 66 , fibroadenoma in 27 , radial scar/complex sclerosing lesion in 23 , atypical ductal hyperplasia only in eight , and a variety of unusual benign lesions in 13 .
	manualset3
86839	7	398605	13	NULL	NULL	0	NULL	23	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histology revealed fibrocystic change in 66 , fibroadenoma in 27 , radial scar/complex sclerosing lesion in 23 , atypical ductal hyperplasia only in eight , and a variety of unusual benign lesions in 13 .
	manualset3
86840	8	398605	13	NULL	NULL	0	NULL	atypical ductal hyperplasia 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histology revealed fibrocystic change in 66 , fibroadenoma in 27 , radial scar/complex sclerosing lesion in 23 , atypical ductal hyperplasia only in eight , and a variety of unusual benign lesions in 13 .
	manualset3
86841	9	398605	13	NULL	NULL	0	NULL	eight	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histology revealed fibrocystic change in 66 , fibroadenoma in 27 , radial scar/complex sclerosing lesion in 23 , atypical ductal hyperplasia only in eight , and a variety of unusual benign lesions in 13 .
	manualset3
86842	10	398605	13	NULL	NULL	0	NULL	variety of unusual benign lesions 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histology revealed fibrocystic change in 66 , fibroadenoma in 27 , radial scar/complex sclerosing lesion in 23 , atypical ductal hyperplasia only in eight , and a variety of unusual benign lesions in 13 .
	manualset3
86843	11	398605	13	NULL	NULL	0	NULL	13	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histology revealed fibrocystic change in 66 , fibroadenoma in 27 , radial scar/complex sclerosing lesion in 23 , atypical ductal hyperplasia only in eight , and a variety of unusual benign lesions in 13 .
	manualset3
86844	1	398606	13	NULL	NULL	0	NULL	Histone acetyltransferases	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Histone acetyltransferases as regulators of nonhistone proteins : the role of interferon regulatory factor acetylation on gene transcription .
	manualset3
86845	2	398606	13	NULL	NULL	0	NULL	regulators of nonhistone proteins 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Histone acetyltransferases as regulators of nonhistone proteins : the role of interferon regulatory factor acetylation on gene transcription .
	manualset3
86846	3	398606	13	NULL	NULL	0	NULL	interferon regulatory factor acetylation 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Histone acetyltransferases as regulators of nonhistone proteins : the role of interferon regulatory factor acetylation on gene transcription .
	manualset3
86847	4	398606	13	NULL	NULL	0	NULL	gene transcription	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Histone acetyltransferases as regulators of nonhistone proteins : the role of interferon regulatory factor acetylation on gene transcription .
	manualset3
86848	1	398607	13	NULL	NULL	0	NULL	Histone deacetylase ( HDAC ) inhibitors	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Histone deacetylase ( HDAC ) inhibitors attenuate cardiac hypertrophy by suppressing autophagy .
	manualset3
86849	2	398607	13	NULL	NULL	0	NULL	cardiac hypertrophy	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histone deacetylase ( HDAC ) inhibitors attenuate cardiac hypertrophy by suppressing autophagy .
	manualset3
86850	3	398607	13	NULL	NULL	0	NULL	autophagy	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Histone deacetylase ( HDAC ) inhibitors attenuate cardiac hypertrophy by suppressing autophagy .
	manualset3
86851	1	398608	13	NULL	NULL	0	NULL	Histone deacetylase inhibitors	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Histone deacetylase inhibitors decrease DNA methyltransferase-3B messenger RNA stability and down-regulate de novo DNA methyltransferase activity in human endometrial cells .
	manualset3
86852	2	398608	13	NULL	NULL	0	NULL	DNA methyltransferase-3B messenger RNA stability	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Histone deacetylase inhibitors decrease DNA methyltransferase-3B messenger RNA stability and down-regulate de novo DNA methyltransferase activity in human endometrial cells .
	manualset3
86853	3	398608	13	NULL	NULL	0	NULL	de novo DNA methyltransferase activity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Histone deacetylase inhibitors decrease DNA methyltransferase-3B messenger RNA stability and down-regulate de novo DNA methyltransferase activity in human endometrial cells .
	manualset3
86854	4	398608	13	NULL	NULL	0	NULL	 human endometrial cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Histone deacetylase inhibitors decrease DNA methyltransferase-3B messenger RNA stability and down-regulate de novo DNA methyltransferase activity in human endometrial cells .
	manualset3
86855	1	398609	13	NULL	NULL	0	NULL	Histopathologic examination	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Histopathologic examination confirmed that excision of the tumor was complete .
	manualset3
86856	2	398609	13	NULL	NULL	0	NULL	excision of the tumor was complete	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histopathologic examination confirmed that excision of the tumor was complete .
	manualset3
86857	1	398610	13	NULL	NULL	0	NULL	Histopathologic studies	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Histopathologic studies indicate that laminitis is associated with changes of the vasculature .
	manualset3
86858	2	398610	13	NULL	NULL	0	NULL	laminitis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Histopathologic studies indicate that laminitis is associated with changes of the vasculature .
	manualset3
86859	3	398610	13	NULL	NULL	0	NULL	changes of the vasculature	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histopathologic studies indicate that laminitis is associated with changes of the vasculature .
	manualset3
86860	1	398611	13	NULL	NULL	0	NULL	Histopathological analysis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Histopathological analysis established the diagnosis as peritoneal pseudomyxoma .
	manualset3
86861	2	398611	13	NULL	NULL	0	NULL	diagnosis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Histopathological analysis established the diagnosis as peritoneal pseudomyxoma .
	manualset3
86862	3	398611	13	NULL	NULL	0	NULL	peritoneal pseudomyxoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Histopathological analysis established the diagnosis as peritoneal pseudomyxoma .
	manualset3
86863	1	398612	13	NULL	NULL	NULL	NULL	Histopathological changes 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Histopathological changes in the bile - or acid-perfused esophagus were consistent with the findings associated with reflux esophagitis .
	manualset3
86864	3	398612	13	NULL	NULL	NULL	NULL	findings	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Histopathological changes in the bile - or acid-perfused esophagus were consistent with the findings associated with reflux esophagitis .
	manualset3
86865	4	398612	13	NULL	NULL	NULL	NULL	reflux esophagitis	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Histopathological changes in the bile - or acid-perfused esophagus were consistent with the findings associated with reflux esophagitis .
	manualset3
86866	2	398612	13	NULL	NULL	0	NULL	bile - or acid-perfused esophagus 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Histopathological changes in the bile - or acid-perfused esophagus were consistent with the findings associated with reflux esophagitis .
	manualset3
86867	1	398613	13	NULL	NULL	NULL	NULL	Histopathological examination	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Histopathological examination of the tumor indicated well differentiated adenocarcinoma compatible with the metastasis from the previous descending colon cancer .
	manualset3
86868	2	398613	13	NULL	NULL	0	NULL	tumor	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histopathological examination of the tumor indicated well differentiated adenocarcinoma compatible with the metastasis from the previous descending colon cancer .
	manualset3
86869	3	398613	13	NULL	NULL	0	NULL	well differentiated adenocarcinoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Histopathological examination of the tumor indicated well differentiated adenocarcinoma compatible with the metastasis from the previous descending colon cancer .
	manualset3
86870	4	398613	13	NULL	NULL	0	NULL	metastasis 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Histopathological examination of the tumor indicated well differentiated adenocarcinoma compatible with the metastasis from the previous descending colon cancer .
	manualset3
86871	5	398613	13	NULL	NULL	0	NULL	descending colon cancer 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Histopathological examination of the tumor indicated well differentiated adenocarcinoma compatible with the metastasis from the previous descending colon cancer .
	manualset3
86872	1	398614	13	NULL	NULL	0	NULL	Histopathological studies	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Histopathological studies proved the tissue compatibility of ALOME to be safe .
	manualset3
86873	2	398614	13	NULL	NULL	0	NULL	 tissue compatibility	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histopathological studies proved the tissue compatibility of ALOME to be safe .
	manualset3
86874	3	398614	13	NULL	NULL	0	NULL	ALOME	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Histopathological studies proved the tissue compatibility of ALOME to be safe .
	manualset3
86875	4	398614	13	NULL	NULL	0	NULL	 safe	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Histopathological studies proved the tissue compatibility of ALOME to be safe .
	manualset3
86876	1	398615	13	NULL	NULL	0	NULL	Histopathology and cell proliferation analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Histopathology and cell proliferation analysis demonstrated a compound - and sex-specific onset of preneoplastic lesions .
	manualset3
86877	2	398615	13	NULL	NULL	NULL	NULL	compound - and sex-specific onset of preneoplastic lesions	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Histopathology and cell proliferation analysis demonstrated a compound - and sex-specific onset of preneoplastic lesions .
	manualset3
86879	1	398616	13	NULL	NULL	0	NULL	role of Ca ( 2 + ) signals	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Historically , much of the research effort in this area has focused on the role of Ca ( 2 + ) signals in cell-cycle progression .
	manualset3
86880	2	398616	13	NULL	NULL	NULL	NULL	cell-cycle progression	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Historically , much of the research effort in this area has focused on the role of Ca ( 2 + ) signals in cell-cycle progression .
	manualset3
86936	3	398616	13	NULL	NULL	0	NULL	research effort 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Historically , much of the research effort in this area has focused on the role of Ca ( 2 + ) signals in cell-cycle progression .
	manualset3
86881	1	398617	13	NULL	NULL	NULL	NULL	History of pathology	PublishedSourceOfInformation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	History of pathology in California .
	manualset3
86882	2	398617	13	NULL	NULL	0	NULL	California	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	History of pathology in California .
	manualset3
86883	1	398618	13	NULL	NULL	NULL	NULL	History of risk factors	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	History of risk factors , especially of snoring and sleeping habits was recorded with structured questionnaire during interview .
	manualset3
86884	2	398618	13	NULL	NULL	0	NULL	snoring and sleeping habits	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	History of risk factors , especially of snoring and sleeping habits was recorded with structured questionnaire during interview .
	manualset3
86885	3	398618	13	NULL	NULL	0	NULL	structured questionnaire during interview	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	History of risk factors , especially of snoring and sleeping habits was recorded with structured questionnaire during interview .
	manualset3
86886	1	398619	13	NULL	NULL	0	NULL	Hodgkin lymphoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hodgkin lymphoma in temporal association with growth hormone replacement .
	manualset3
86887	2	398619	13	NULL	NULL	0	NULL	temporal association 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hodgkin lymphoma in temporal association with growth hormone replacement .
	manualset3
86888	3	398619	13	NULL	NULL	0	NULL	growth hormone replacement	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hodgkin lymphoma in temporal association with growth hormone replacement .
	manualset3
86889	1	398620	13	NULL	NULL	0	NULL	Hoffman 's plastic lymphangitis of the penis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hoffman 's plastic lymphangitis of the penis is a benign , uncommon entity whose aetiology is still unknown .
	manualset3
86890	2	398620	13	NULL	NULL	0	NULL	benign	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hoffman 's plastic lymphangitis of the penis is a benign , uncommon entity whose aetiology is still unknown .
	manualset3
86891	3	398620	13	NULL	NULL	0	NULL	aetiology	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Hoffman 's plastic lymphangitis of the penis is a benign , uncommon entity whose aetiology is still unknown .
	manualset3
86892	1	398621	13	NULL	NULL	NULL	NULL	Home-based intervention	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Home-based intervention has been shown to provide long-term cost benefit in a range of chronic illnesses ; however , the role of home visits by respiratory therapists ( RT ) in COPD management has not been evaluated .
	manualset3
86893	2	398621	13	NULL	NULL	NULL	NULL	range of chronic illnesses	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Home-based intervention has been shown to provide long-term cost benefit in a range of chronic illnesses ; however , the role of home visits by respiratory therapists ( RT ) in COPD management has not been evaluated .
	manualset3
86894	3	398621	13	NULL	NULL	0	NULL	home visits by respiratory therapists ( RT )	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Home-based intervention has been shown to provide long-term cost benefit in a range of chronic illnesses ; however , the role of home visits by respiratory therapists ( RT ) in COPD management has not been evaluated .
	manualset3
86895	4	398621	13	NULL	NULL	0	NULL	COPD management 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Home-based intervention has been shown to provide long-term cost benefit in a range of chronic illnesses ; however , the role of home visits by respiratory therapists ( RT ) in COPD management has not been evaluated .
	manualset3
86896	1	398622	13	NULL	NULL	0	NULL	Home care company	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Home care company is single source for purchase of epoprostenol .
	manualset3
86897	2	398622	13	NULL	NULL	0	NULL	single source for purchase	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Home care company is single source for purchase of epoprostenol .
	manualset3
86898	3	398622	13	NULL	NULL	0	NULL	epoprostenol	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Home care company is single source for purchase of epoprostenol .
	manualset3
86899	1	398623	13	NULL	NULL	0	NULL	Home health aides 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Home health aides were offered to half of a group of 227 low-income diabetic clinic patients ; in the group offered aides , fasting blood sugar ( FBS ) declined when compared to control group ( 10.1 mg/dl vs an increase of 5.1 mg/dl ) , and missed clinic appointments and emergency room use also decreased .
	manualset3
86900	2	398623	13	NULL	NULL	0	NULL	half of a group of 227	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Home health aides were offered to half of a group of 227 low-income diabetic clinic patients ; in the group offered aides , fasting blood sugar ( FBS ) declined when compared to control group ( 10.1 mg/dl vs an increase of 5.1 mg/dl ) , and missed clinic appointments and emergency room use also decreased .
	manualset3
86901	3	398623	13	NULL	NULL	0	NULL	low-income diabetic clinic patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Home health aides were offered to half of a group of 227 low-income diabetic clinic patients ; in the group offered aides , fasting blood sugar ( FBS ) declined when compared to control group ( 10.1 mg/dl vs an increase of 5.1 mg/dl ) , and missed clinic appointments and emergency room use also decreased .
	manualset3
86902	4	398623	13	NULL	NULL	0	NULL	group offered aides	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Home health aides were offered to half of a group of 227 low-income diabetic clinic patients ; in the group offered aides , fasting blood sugar ( FBS ) declined when compared to control group ( 10.1 mg/dl vs an increase of 5.1 mg/dl ) , and missed clinic appointments and emergency room use also decreased .
	manualset3
86903	5	398623	13	NULL	NULL	0	NULL	fasting blood sugar ( FBS ) declined	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Home health aides were offered to half of a group of 227 low-income diabetic clinic patients ; in the group offered aides , fasting blood sugar ( FBS ) declined when compared to control group ( 10.1 mg/dl vs an increase of 5.1 mg/dl ) , and missed clinic appointments and emergency room use also decreased .
	manualset3
86904	6	398623	13	NULL	NULL	0	NULL	control group	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Home health aides were offered to half of a group of 227 low-income diabetic clinic patients ; in the group offered aides , fasting blood sugar ( FBS ) declined when compared to control group ( 10.1 mg/dl vs an increase of 5.1 mg/dl ) , and missed clinic appointments and emergency room use also decreased .
	manualset3
86905	7	398623	13	NULL	NULL	0	NULL	10.1 mg/dl vs an increase of 5.1 mg/dl 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Home health aides were offered to half of a group of 227 low-income diabetic clinic patients ; in the group offered aides , fasting blood sugar ( FBS ) declined when compared to control group ( 10.1 mg/dl vs an increase of 5.1 mg/dl ) , and missed clinic appointments and emergency room use also decreased .
	manualset3
86906	8	398623	13	NULL	NULL	0	NULL	clinic appointments	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Home health aides were offered to half of a group of 227 low-income diabetic clinic patients ; in the group offered aides , fasting blood sugar ( FBS ) declined when compared to control group ( 10.1 mg/dl vs an increase of 5.1 mg/dl ) , and missed clinic appointments and emergency room use also decreased .
	manualset3
86907	9	398623	13	NULL	NULL	0	NULL	emergency room	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Home health aides were offered to half of a group of 227 low-income diabetic clinic patients ; in the group offered aides , fasting blood sugar ( FBS ) declined when compared to control group ( 10.1 mg/dl vs an increase of 5.1 mg/dl ) , and missed clinic appointments and emergency room use also decreased .
	manualset3
86908	1	398624	13	NULL	NULL	0	NULL	Home visits	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Home visits were also conducted after discharge to assess the home care environment and give instant consultation , providing holistic health care with sustained quality of care .
	manualset3
86909	2	398624	13	NULL	NULL	0	NULL	discharge	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Home visits were also conducted after discharge to assess the home care environment and give instant consultation , providing holistic health care with sustained quality of care .
	manualset3
86910	3	398624	13	NULL	NULL	0	NULL	home care environment 	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Home visits were also conducted after discharge to assess the home care environment and give instant consultation , providing holistic health care with sustained quality of care .
	manualset3
86911	4	398624	13	NULL	NULL	0	NULL	 instant consultation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Home visits were also conducted after discharge to assess the home care environment and give instant consultation , providing holistic health care with sustained quality of care .
	manualset3
86912	5	398624	13	NULL	NULL	NULL	NULL	holistic health care 	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Home visits were also conducted after discharge to assess the home care environment and give instant consultation , providing holistic health care with sustained quality of care .
	manualset3
86913	6	398624	13	NULL	NULL	0	NULL	sustained quality of care	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Home visits were also conducted after discharge to assess the home care environment and give instant consultation , providing holistic health care with sustained quality of care .
	manualset3
86914	1	398625	13	NULL	NULL	0	NULL	Homeowner attitudes	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Homeowner attitudes and practices towards residential landscape management in ohio , USA .
	manualset3
86915	2	398625	13	NULL	NULL	0	NULL	practices	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Homeowner attitudes and practices towards residential landscape management in ohio , USA .
	manualset3
86916	3	398625	13	NULL	NULL	0	NULL	residential landscape management	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Homeowner attitudes and practices towards residential landscape management in ohio , USA .
	manualset3
86917	4	398625	13	NULL	NULL	0	NULL	ohio , USA	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Homeowner attitudes and practices towards residential landscape management in ohio , USA .
	manualset3
86918	1	398626	13	NULL	NULL	0	NULL	mechanisms	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Homing in on mechanisms linking breast density to breast cancer risk .
	manualset3
86919	2	398626	13	NULL	NULL	0	NULL	breast density	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Homing in on mechanisms linking breast density to breast cancer risk .
	manualset3
86920	3	398626	13	NULL	NULL	0	NULL	breast cancer risk	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Homing in on mechanisms linking breast density to breast cancer risk .
	manualset3
86921	1	398627	13	NULL	NULL	0	NULL	Homocysteine levels	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Homocysteine levels and coronary heart disease in Syria .
	manualset3
86922	2	398627	13	NULL	NULL	0	NULL	coronary heart disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Homocysteine levels and coronary heart disease in Syria .
	manualset3
86923	3	398627	13	NULL	NULL	0	NULL	Syria	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Homocysteine levels and coronary heart disease in Syria .
	manualset3
86924	1	398628	13	NULL	NULL	0	NULL	Homogenous glycine receptor expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Homogenous glycine receptor expression in cortical plate neurons and Cajal-Retzius cells of neonatal rat cerebral cortex .
	manualset3
86925	2	398628	13	NULL	NULL	0	NULL	cortical plate neurons	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Homogenous glycine receptor expression in cortical plate neurons and Cajal-Retzius cells of neonatal rat cerebral cortex .
	manualset3
86926	3	398628	13	NULL	NULL	0	NULL	Cajal-Retzius cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Homogenous glycine receptor expression in cortical plate neurons and Cajal-Retzius cells of neonatal rat cerebral cortex .
	manualset3
86927	4	398628	13	NULL	NULL	0	NULL	neonatal rat cerebral cortex	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Homogenous glycine receptor expression in cortical plate neurons and Cajal-Retzius cells of neonatal rat cerebral cortex .
	manualset3
86928	1	398629	13	NULL	NULL	0	NULL	Homologous recombination	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Homologous recombination is a conserved molecular process that has primarily evolved for the repair of double-stranded DNA breaks and stalled replication forks .
	manualset3
86929	2	398629	13	NULL	NULL	0	NULL	molecular process	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Homologous recombination is a conserved molecular process that has primarily evolved for the repair of double-stranded DNA breaks and stalled replication forks .
	manualset3
86930	3	398629	13	NULL	NULL	NULL	NULL	repair of double-stranded DNA breaks	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Homologous recombination is a conserved molecular process that has primarily evolved for the repair of double-stranded DNA breaks and stalled replication forks .
	manualset3
86931	4	398629	13	NULL	NULL	0	NULL	stalled replication forks	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Homologous recombination is a conserved molecular process that has primarily evolved for the repair of double-stranded DNA breaks and stalled replication forks .
	manualset3
86932	1	398630	13	NULL	NULL	0	NULL	Homologous transient transfection experiments	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Homologous transient transfection experiments were conducted employing a 0.9-kb fragment of the 5 ' flanking region of the human CRH gene coupled to the luciferase reporter gene , using Ishikawa human endometrial cells .
	manualset3
86933	2	398630	13	NULL	NULL	NULL	NULL	 0.9-kb fragment of the 5 ' flanking region of the human CRH gene	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Homologous transient transfection experiments were conducted employing a 0.9-kb fragment of the 5 ' flanking region of the human CRH gene coupled to the luciferase reporter gene , using Ishikawa human endometrial cells .
	manualset3
86934	3	398630	13	NULL	NULL	0	NULL	luciferase reporter gene	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Homologous transient transfection experiments were conducted employing a 0.9-kb fragment of the 5 ' flanking region of the human CRH gene coupled to the luciferase reporter gene , using Ishikawa human endometrial cells .
	manualset3
86935	4	398630	13	NULL	NULL	0	NULL	Ishikawa human endometrial cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Homologous transient transfection experiments were conducted employing a 0.9-kb fragment of the 5 ' flanking region of the human CRH gene coupled to the luciferase reporter gene , using Ishikawa human endometrial cells .
	manualset3
86999	1	398631	13	NULL	NULL	0	NULL	Homologs 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Homologs of the recently described mouse pro genes , that transfer sensitivity to promotion of neoplastic transformation by tumor promoters , have been cloned from a genomic library of the human nasopharyngeal carcinoma ( NPC ) cell line CNE2 .
	manualset3
87000	2	398631	13	NULL	NULL	0	NULL	mouse pro genes 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Homologs of the recently described mouse pro genes , that transfer sensitivity to promotion of neoplastic transformation by tumor promoters , have been cloned from a genomic library of the human nasopharyngeal carcinoma ( NPC ) cell line CNE2 .
	manualset3
87001	3	398631	13	NULL	NULL	NULL	NULL	neoplastic transformation	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Homologs of the recently described mouse pro genes , that transfer sensitivity to promotion of neoplastic transformation by tumor promoters , have been cloned from a genomic library of the human nasopharyngeal carcinoma ( NPC ) cell line CNE2 .
	manualset3
87002	4	398631	13	NULL	NULL	0	NULL	tumor promoters 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Homologs of the recently described mouse pro genes , that transfer sensitivity to promotion of neoplastic transformation by tumor promoters , have been cloned from a genomic library of the human nasopharyngeal carcinoma ( NPC ) cell line CNE2 .
	manualset3
87003	5	398631	13	NULL	NULL	NULL	NULL	genomic library	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Homologs of the recently described mouse pro genes , that transfer sensitivity to promotion of neoplastic transformation by tumor promoters , have been cloned from a genomic library of the human nasopharyngeal carcinoma ( NPC ) cell line CNE2 .
	manualset3
87004	6	398631	13	NULL	NULL	0	NULL	human nasopharyngeal carcinoma ( NPC ) cell line CNE2	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Homologs of the recently described mouse pro genes , that transfer sensitivity to promotion of neoplastic transformation by tumor promoters , have been cloned from a genomic library of the human nasopharyngeal carcinoma ( NPC ) cell line CNE2 .
	manualset3
87005	1	398632	13	NULL	NULL	0	NULL	Homology modeling	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Homology modeling of human methylmalonyl-CoA mutase : a structural basis for point mutations causing methylmalonic aciduria .
	manualset3
87006	2	398632	13	NULL	NULL	0	NULL	human methylmalonyl-CoA mutase 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Homology modeling of human methylmalonyl-CoA mutase : a structural basis for point mutations causing methylmalonic aciduria .
	manualset3
87007	3	398632	13	NULL	NULL	0	NULL	point mutations 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Homology modeling of human methylmalonyl-CoA mutase : a structural basis for point mutations causing methylmalonic aciduria .
	manualset3
87008	4	398632	13	NULL	NULL	0	NULL	methylmalonic aciduria	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Homology modeling of human methylmalonyl-CoA mutase : a structural basis for point mutations causing methylmalonic aciduria .
	manualset3
87009	1	398633	13	NULL	NULL	0	NULL	Homology models 	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Homology models were constructed using the crystal structure of a bacterial homolog , the leucine transporter from Aquifex aeolicus , as the template and three slightly different sequence alignments .
	manualset3
87010	2	398633	13	NULL	NULL	NULL	NULL	crystal structure of a bacterial homolog	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Homology models were constructed using the crystal structure of a bacterial homolog , the leucine transporter from Aquifex aeolicus , as the template and three slightly different sequence alignments .
	manualset3
87011	3	398633	13	NULL	NULL	0	NULL	leucine transporter	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Homology models were constructed using the crystal structure of a bacterial homolog , the leucine transporter from Aquifex aeolicus , as the template and three slightly different sequence alignments .
	manualset3
87012	4	398633	13	NULL	NULL	0	NULL	 Aquifex aeolicus 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Homology models were constructed using the crystal structure of a bacterial homolog , the leucine transporter from Aquifex aeolicus , as the template and three slightly different sequence alignments .
	manualset3
87013	5	398633	13	NULL	NULL	NULL	NULL	template 	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Homology models were constructed using the crystal structure of a bacterial homolog , the leucine transporter from Aquifex aeolicus , as the template and three slightly different sequence alignments .
	manualset3
87014	6	398633	13	NULL	NULL	0	NULL	three 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Homology models were constructed using the crystal structure of a bacterial homolog , the leucine transporter from Aquifex aeolicus , as the template and three slightly different sequence alignments .
	manualset3
87015	7	398633	13	NULL	NULL	0	NULL	sequence alignments	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Homology models were constructed using the crystal structure of a bacterial homolog , the leucine transporter from Aquifex aeolicus , as the template and three slightly different sequence alignments .
	manualset3
87016	1	398634	13	NULL	NULL	0	NULL	Hookworm anemia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hookworm anemia , a deficiency disease .
	manualset3
87017	2	398634	13	NULL	NULL	0	NULL	deficiency disease 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hookworm anemia , a deficiency disease .
	manualset3
87018	1	398635	13	NULL	NULL	NULL	NULL	Hormonal changes	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hormonal changes during salinity-induced leaf senescence in tomato ( Solanum lycopersicum L. ) .
	manualset3
87019	2	398635	13	NULL	NULL	0	NULL	salinity-induced leaf senescence 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hormonal changes during salinity-induced leaf senescence in tomato ( Solanum lycopersicum L. ) .
	manualset3
87020	3	398635	13	NULL	NULL	0	NULL	tomato ( Solanum lycopersicum L. ) 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hormonal changes during salinity-induced leaf senescence in tomato ( Solanum lycopersicum L. ) .
	manualset3
87021	1	398636	13	NULL	NULL	0	NULL	The active metabolite of leflunomide A771726	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( The active metabolite of leflunomide A771726 inhibits proliferation and collagen synthesis of hepatic stellate cell ) .
	manualset3
87022	2	398636	13	NULL	NULL	0	NULL	proliferation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The active metabolite of leflunomide A771726 inhibits proliferation and collagen synthesis of hepatic stellate cell ) .
	manualset3
87023	3	398636	13	NULL	NULL	0	NULL	 collagen synthesis 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The active metabolite of leflunomide A771726 inhibits proliferation and collagen synthesis of hepatic stellate cell ) .
	manualset3
87024	4	398636	13	NULL	NULL	0	NULL	hepatic stellate cell 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	( The active metabolite of leflunomide A771726 inhibits proliferation and collagen synthesis of hepatic stellate cell ) .
	manualset3
87025	1	398637	13	NULL	NULL	NULL	NULL	Hormonal factors	Molecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hormonal factors may have a permissive role in thrombus formation or neoplastic vascular invasion .
	manualset3
87026	2	398637	13	NULL	NULL	NULL	NULL	thrombus formation	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hormonal factors may have a permissive role in thrombus formation or neoplastic vascular invasion .
	manualset3
87027	3	398637	13	NULL	NULL	0	NULL	 neoplastic vascular invasion	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hormonal factors may have a permissive role in thrombus formation or neoplastic vascular invasion .
	manualset3
87028	1	398638	13	NULL	NULL	NULL	NULL	Hormonal stimulation	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hormonal stimulation of ribosomal RNA synthesis in Achlya ambisexualis .
	manualset3
87029	2	398638	13	NULL	NULL	0	NULL	ribosomal RNA synthesis 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hormonal stimulation of ribosomal RNA synthesis in Achlya ambisexualis .
	manualset3
87030	3	398638	13	NULL	NULL	0	NULL	Achlya ambisexualis	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hormonal stimulation of ribosomal RNA synthesis in Achlya ambisexualis .
	manualset3
87031	1	398639	13	NULL	NULL	0	NULL	Hormone replacement therapy 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hormone replacement therapy to develop secondary sexual characteristics has been used for years whereas several growth promoting agents undergo clinical trials at the moment .
	manualset3
87032	2	398639	13	NULL	NULL	0	NULL	develop secondary sexual characteristics	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hormone replacement therapy to develop secondary sexual characteristics has been used for years whereas several growth promoting agents undergo clinical trials at the moment .
	manualset3
87033	3	398639	13	NULL	NULL	0	NULL	years	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Hormone replacement therapy to develop secondary sexual characteristics has been used for years whereas several growth promoting agents undergo clinical trials at the moment .
	manualset3
87034	4	398639	13	NULL	NULL	0	NULL	several growth promoting agents	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hormone replacement therapy to develop secondary sexual characteristics has been used for years whereas several growth promoting agents undergo clinical trials at the moment .
	manualset3
87035	5	398639	13	NULL	NULL	0	NULL	clinical trials 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hormone replacement therapy to develop secondary sexual characteristics has been used for years whereas several growth promoting agents undergo clinical trials at the moment .
	manualset3
87036	1	398640	13	NULL	NULL	0	NULL	Hormone therapy 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hormone therapy of such cancer has so far been only mildly active , probably because we do not understand the role and mechanism of action of FSH and FSHR in the hypothalamo-pituitary-ovarian axis in development of such cancer .
	manualset3
87037	2	398640	13	NULL	NULL	0	NULL	cancer 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hormone therapy of such cancer has so far been only mildly active , probably because we do not understand the role and mechanism of action of FSH and FSHR in the hypothalamo-pituitary-ovarian axis in development of such cancer .
	manualset3
87038	3	398640	13	NULL	NULL	0	NULL	mechanism of action of FSH 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hormone therapy of such cancer has so far been only mildly active , probably because we do not understand the role and mechanism of action of FSH and FSHR in the hypothalamo-pituitary-ovarian axis in development of such cancer .
	manualset3
87039	4	398640	13	NULL	NULL	0	NULL	mechanism of action of FSHR	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hormone therapy of such cancer has so far been only mildly active , probably because we do not understand the role and mechanism of action of FSH and FSHR in the hypothalamo-pituitary-ovarian axis in development of such cancer .
	manualset3
87040	5	398640	13	NULL	NULL	0	NULL	hypothalamo-pituitary-ovarian axis	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hormone therapy of such cancer has so far been only mildly active , probably because we do not understand the role and mechanism of action of FSH and FSHR in the hypothalamo-pituitary-ovarian axis in development of such cancer .
	manualset3
87041	6	398640	13	NULL	NULL	0	NULL	development of such cancer 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hormone therapy of such cancer has so far been only mildly active , probably because we do not understand the role and mechanism of action of FSH and FSHR in the hypothalamo-pituitary-ovarian axis in development of such cancer .
	manualset3
87042	1	398641	13	NULL	NULL	0	NULL	Hospital admission blood pressure	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hospital admission blood pressure : a predictor for hypertension following endotracheal intubation .
	manualset3
87043	2	398641	13	NULL	NULL	0	NULL	hypertension	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hospital admission blood pressure : a predictor for hypertension following endotracheal intubation .
	manualset3
87044	3	398641	13	NULL	NULL	0	NULL	endotracheal intubation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hospital admission blood pressure : a predictor for hypertension following endotracheal intubation .
	manualset3
87045	1	398642	13	NULL	NULL	0	NULL	Hospital trust director	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Hospital trust director is cleared of dishonesty in case of misdiagnosed diabetes .
	manualset3
87046	2	398642	13	NULL	NULL	0	NULL	dishonesty	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hospital trust director is cleared of dishonesty in case of misdiagnosed diabetes .
	manualset3
87047	3	398642	13	NULL	NULL	0	NULL	 diabetes	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hospital trust director is cleared of dishonesty in case of misdiagnosed diabetes .
	manualset3
87048	1	398643	13	NULL	NULL	0	NULL	Hospitalization	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hospitalization of the mother as a necessary measure for the prevention of physical and psycho-affective disorders in the hospitalized child ) .
	manualset3
87049	2	398643	13	NULL	NULL	NULL	NULL	mother	Person												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hospitalization of the mother as a necessary measure for the prevention of physical and psycho-affective disorders in the hospitalized child ) .
	manualset3
87050	3	398643	13	NULL	NULL	NULL	NULL	prevention 	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hospitalization of the mother as a necessary measure for the prevention of physical and psycho-affective disorders in the hospitalized child ) .
	manualset3
87051	4	398643	13	NULL	NULL	0	NULL	hospitalized child 	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Hospitalization of the mother as a necessary measure for the prevention of physical and psycho-affective disorders in the hospitalized child ) .
	manualset3
87052	5	398643	13	NULL	NULL	0	NULL	physical and psycho-affective disorders	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hospitalization of the mother as a necessary measure for the prevention of physical and psycho-affective disorders in the hospitalized child ) .
	manualset3
87053	1	398644	13	NULL	NULL	0	NULL	lipid peroxidation 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The activity of the lipid peroxidation processes in the mucosa of the rat small intestine and its morphofunctional state under acute irradiation and the administration of combined preparations created on a base of highly dispersed silica ) .
	manualset3
87054	2	398644	13	NULL	NULL	0	NULL	mucosa of the rat small intestine 	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	( The activity of the lipid peroxidation processes in the mucosa of the rat small intestine and its morphofunctional state under acute irradiation and the administration of combined preparations created on a base of highly dispersed silica ) .
	manualset3
87055	3	398644	13	NULL	NULL	NULL	NULL	acute irradiation	LaboratoryExperimentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The activity of the lipid peroxidation processes in the mucosa of the rat small intestine and its morphofunctional state under acute irradiation and the administration of combined preparations created on a base of highly dispersed silica ) .
	manualset3
87056	4	398644	13	NULL	NULL	NULL	NULL	administration of combined preparations	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The activity of the lipid peroxidation processes in the mucosa of the rat small intestine and its morphofunctional state under acute irradiation and the administration of combined preparations created on a base of highly dispersed silica ) .
	manualset3
87057	5	398644	13	NULL	NULL	0	NULL	silica	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( The activity of the lipid peroxidation processes in the mucosa of the rat small intestine and its morphofunctional state under acute irradiation and the administration of combined preparations created on a base of highly dispersed silica ) .
	manualset3
87058	1	398645	13	NULL	NULL	0	NULL	Host-derived adiponectin 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Host-derived adiponectin is tumor-suppressive and a novel therapeutic target for multiple myeloma and the associated bone disease .
	manualset3
87059	2	398645	13	NULL	NULL	0	NULL	tumor-suppressive 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Host-derived adiponectin is tumor-suppressive and a novel therapeutic target for multiple myeloma and the associated bone disease .
	manualset3
87060	3	398645	13	NULL	NULL	0	NULL	novel therapeutic target	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Host-derived adiponectin is tumor-suppressive and a novel therapeutic target for multiple myeloma and the associated bone disease .
	manualset3
87061	4	398645	13	NULL	NULL	0	NULL	multiple myeloma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Host-derived adiponectin is tumor-suppressive and a novel therapeutic target for multiple myeloma and the associated bone disease .
	manualset3
87062	5	398645	13	NULL	NULL	0	NULL	bone disease 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Host-derived adiponectin is tumor-suppressive and a novel therapeutic target for multiple myeloma and the associated bone disease .
	manualset3
87063	1	398646	13	NULL	NULL	0	NULL	Host defense pathways 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Host defense pathways against fungi : the basis for vaccines and immunotherapy .
	manualset3
87064	2	398646	13	NULL	NULL	0	NULL	fungi	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Host defense pathways against fungi : the basis for vaccines and immunotherapy .
	manualset3
87065	3	398646	13	NULL	NULL	NULL	NULL	vaccines	Molecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Host defense pathways against fungi : the basis for vaccines and immunotherapy .
	manualset3
87066	4	398646	13	NULL	NULL	0	NULL	immunotherapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Host defense pathways against fungi : the basis for vaccines and immunotherapy .
	manualset3
87067	1	398647	13	NULL	NULL	0	NULL	Host populations	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Host populations , transmission efficiency , and therefore pathogen amplification vary spatially , thereby creating a heterogeneous surface that may be defined by remote sensing and statistical tools .
	manualset3
87068	2	398647	13	NULL	NULL	0	NULL	transmission efficiency	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Host populations , transmission efficiency , and therefore pathogen amplification vary spatially , thereby creating a heterogeneous surface that may be defined by remote sensing and statistical tools .
	manualset3
87069	3	398647	13	NULL	NULL	NULL	NULL	pathogen 	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Host populations , transmission efficiency , and therefore pathogen amplification vary spatially , thereby creating a heterogeneous surface that may be defined by remote sensing and statistical tools .
	manualset3
87070	4	398647	13	NULL	NULL	0	NULL	amplification 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Host populations , transmission efficiency , and therefore pathogen amplification vary spatially , thereby creating a heterogeneous surface that may be defined by remote sensing and statistical tools .
	manualset3
87071	5	398647	13	NULL	NULL	0	NULL	 heterogeneous surface	GeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Host populations , transmission efficiency , and therefore pathogen amplification vary spatially , thereby creating a heterogeneous surface that may be defined by remote sensing and statistical tools .
	manualset3
87072	6	398647	13	NULL	NULL	0	NULL	remote sensing 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Host populations , transmission efficiency , and therefore pathogen amplification vary spatially , thereby creating a heterogeneous surface that may be defined by remote sensing and statistical tools .
	manualset3
87073	7	398647	13	NULL	NULL	0	NULL	statistical tools	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Host populations , transmission efficiency , and therefore pathogen amplification vary spatially , thereby creating a heterogeneous surface that may be defined by remote sensing and statistical tools .
	manualset3
87074	1	398648	13	NULL	NULL	0	NULL	Host 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Host resistance against Candida alibcans infection in mice with adjuvant induced arthritis .
	manualset3
87075	2	398648	13	NULL	NULL	0	NULL	 resistance	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Host resistance against Candida alibcans infection in mice with adjuvant induced arthritis .
	manualset3
87076	3	398648	13	NULL	NULL	0	NULL	Candida alibcans infection 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Host resistance against Candida alibcans infection in mice with adjuvant induced arthritis .
	manualset3
87077	4	398648	13	NULL	NULL	0	NULL	mice 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Host resistance against Candida alibcans infection in mice with adjuvant induced arthritis .
	manualset3
87078	5	398648	13	NULL	NULL	0	NULL	adjuvant induced arthritis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Host resistance against Candida alibcans infection in mice with adjuvant induced arthritis .
	manualset3
87079	1	398649	13	NULL	NULL	0	NULL	Hotspots	GeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Hotspots of intraspecific diversity have been observed in most species , often within areas of putative Pleistocene refugia .
	manualset3
87080	2	398649	13	NULL	NULL	0	NULL	intraspecific diversity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hotspots of intraspecific diversity have been observed in most species , often within areas of putative Pleistocene refugia .
	manualset3
87081	3	398649	13	NULL	NULL	0	NULL	species	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hotspots of intraspecific diversity have been observed in most species , often within areas of putative Pleistocene refugia .
	manualset3
87082	4	398649	13	NULL	NULL	NULL	NULL	areas of putative Pleistocene refugia 	ProperNamedGeographicalLocation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hotspots of intraspecific diversity have been observed in most species , often within areas of putative Pleistocene refugia .
	manualset3
87083	1	398650	13	NULL	NULL	0	NULL	Household products	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Household products containing acids , alkalies or detergents : toxic effects and their treatment .
	manualset3
87084	2	398650	13	NULL	NULL	0	NULL	acids 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Household products containing acids , alkalies or detergents : toxic effects and their treatment .
	manualset3
87085	3	398650	13	NULL	NULL	0	NULL	alkalies	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Household products containing acids , alkalies or detergents : toxic effects and their treatment .
	manualset3
87086	4	398650	13	NULL	NULL	0	NULL	detergents	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Household products containing acids , alkalies or detergents : toxic effects and their treatment .
	manualset3
87087	5	398650	13	NULL	NULL	0	NULL	 toxic effects 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Household products containing acids , alkalies or detergents : toxic effects and their treatment .
	manualset3
87088	6	398650	13	NULL	NULL	0	NULL	 treatment 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Household products containing acids , alkalies or detergents : toxic effects and their treatment .
	manualset3
87089	1	398651	13	NULL	NULL	0	NULL	 poise	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	How to keep your poise under pressure .
	manualset3
87179	2	398651	13	NULL	NULL	0	NULL	 pressure	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	How to keep your poise under pressure .
	manualset3
87090	1	398652	13	NULL	NULL	0	NULL	 anti-anginous	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The anti-anginous action of FT-9 ) .
	manualset3
87091	2	398652	13	NULL	NULL	0	NULL	FT-9 	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( The anti-anginous action of FT-9 ) .
	manualset3
87092	1	398653	13	NULL	NULL	0	NULL	ZAP 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	How ZAP recognizes its target RNA has been unclear .
	manualset3
87093	2	398653	13	NULL	NULL	0	NULL	RNA 	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	How ZAP recognizes its target RNA has been unclear .
	manualset3
87094	1	398654	13	NULL	NULL	0	NULL	midwife	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	How a midwife can change attitudes .
	manualset3
87095	2	398654	13	NULL	NULL	0	NULL	attitudes	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	How a midwife can change attitudes .
	manualset3
87096	1	398655	13	NULL	NULL	0	NULL	aerobic glycolysis	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	How aerobic glycolysis and apoptosis resistance are linked remains to be elucidated .
	manualset3
87097	2	398655	13	NULL	NULL	0	NULL	apoptosis resistance	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	How aerobic glycolysis and apoptosis resistance are linked remains to be elucidated .
	manualset3
87098	1	398656	13	NULL	NULL	NULL	NULL	organs	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	How are the regular patterns of organs established along a plant stem and howare the transitions between different patterns regulated ?
	manualset3
87099	2	398656	13	NULL	NULL	NULL	NULL	plant stem	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	How are the regular patterns of organs established along a plant stem and howare the transitions between different patterns regulated ?
	manualset3
87101	3	398656	13	NULL	NULL	NULL	NULL	transitions 	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	How are the regular patterns of organs established along a plant stem and howare the transitions between different patterns regulated ?
	manualset3
87102	1	398657	13	NULL	NULL	0	NULL	roots 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	How do roots manage to simultaneously communicate with neighboring plants , and with symbiotic and pathogenic organisms within this crowded rhizosphere ?
	manualset3
87104	2	398657	13	NULL	NULL	0	NULL	neighboring plants	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	How do roots manage to simultaneously communicate with neighboring plants , and with symbiotic and pathogenic organisms within this crowded rhizosphere ?
	manualset3
87106	3	398657	13	NULL	NULL	0	NULL	symbiotic organisms	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	How do roots manage to simultaneously communicate with neighboring plants , and with symbiotic and pathogenic organisms within this crowded rhizosphere ?
	manualset3
87108	4	398657	13	NULL	NULL	0	NULL	pathogenic organisms 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	How do roots manage to simultaneously communicate with neighboring plants , and with symbiotic and pathogenic organisms within this crowded rhizosphere ?
	manualset3
87114	5	398657	13	NULL	NULL	0	NULL	rhizosphere	GeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	How do roots manage to simultaneously communicate with neighboring plants , and with symbiotic and pathogenic organisms within this crowded rhizosphere ?
	manualset3
87118	1	398658	13	NULL	NULL	0	NULL	data	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	How do we collect data for surveillance of wound infection ?
	manualset3
87119	2	398658	13	NULL	NULL	NULL	NULL	surveillance	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	How do we collect data for surveillance of wound infection ?
	manualset3
87120	3	398658	13	NULL	NULL	0	NULL	wound infection 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	How do we collect data for surveillance of wound infection ?
	manualset3
87124	1	398659	13	NULL	NULL	0	NULL	ammonium	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	How does ammonium dynamically interact with benzene in aqueous media ?
	manualset3
87125	2	398659	13	NULL	NULL	0	NULL	benzene	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	How does ammonium dynamically interact with benzene in aqueous media ?
	manualset3
87126	3	398659	13	NULL	NULL	0	NULL	aqueous media	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	How does ammonium dynamically interact with benzene in aqueous media ?
	manualset3
87131	1	398660	13	NULL	NULL	0	NULL	 photoreceptor cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	How photoreceptor cells respond to light .
	manualset3
87132	2	398660	13	NULL	NULL	0	NULL	 light 	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	How photoreceptor cells respond to light .
	manualset3
87183	1	398661	13	NULL	NULL	0	NULL	antialgesic action	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The antialgesic action of hyaluronidase in the treatment of medicinal apical parodontitis after filling of the canal ) .
	manualset3
87184	2	398661	13	NULL	NULL	0	NULL	hyaluronidase 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	( The antialgesic action of hyaluronidase in the treatment of medicinal apical parodontitis after filling of the canal ) .
	manualset3
87187	3	398661	13	NULL	NULL	0	NULL	treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The antialgesic action of hyaluronidase in the treatment of medicinal apical parodontitis after filling of the canal ) .
	manualset3
87189	4	398661	13	NULL	NULL	0	NULL	medicinal apical parodontitis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The antialgesic action of hyaluronidase in the treatment of medicinal apical parodontitis after filling of the canal ) .
	manualset3
87190	5	398661	13	NULL	NULL	0	NULL	filling of the canal 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The antialgesic action of hyaluronidase in the treatment of medicinal apical parodontitis after filling of the canal ) .
	manualset3
87194	1	398662	13	NULL	NULL	0	NULL	future doctors	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	How prepared are our future doctors for HIV/AIDS ?
	manualset3
87195	2	398662	13	NULL	NULL	0	NULL	 HIV/AIDS	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	How prepared are our future doctors for HIV/AIDS ?
	manualset3
87200	1	398663	13	NULL	NULL	0	NULL	H1N1 influenza	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	How the H1N1 influenza epidemic spread among university students in Japan : experience from Shinshu University .
	manualset3
87203	2	398663	13	NULL	NULL	0	NULL	 epidemic spread	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	How the H1N1 influenza epidemic spread among university students in Japan : experience from Shinshu University .
	manualset3
87204	3	398663	13	NULL	NULL	0	NULL	university students	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	How the H1N1 influenza epidemic spread among university students in Japan : experience from Shinshu University .
	manualset3
87205	4	398663	13	NULL	NULL	0	NULL	Japan	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	How the H1N1 influenza epidemic spread among university students in Japan : experience from Shinshu University .
	manualset3
87208	5	398663	13	NULL	NULL	0	NULL	Shinshu University	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	How the H1N1 influenza epidemic spread among university students in Japan : experience from Shinshu University .
	manualset3
87209	1	398664	13	NULL	NULL	0	NULL	cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	How these cells maintain their identity , restricted localization , and fate is unknown and is fundamental to the control of BP and homeostasis of fluid and electrolytes .
	manualset3
87213	2	398664	13	NULL	NULL	0	NULL	localization	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	How these cells maintain their identity , restricted localization , and fate is unknown and is fundamental to the control of BP and homeostasis of fluid and electrolytes .
	manualset3
87216	3	398664	13	NULL	NULL	NULL	NULL	BP	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	How these cells maintain their identity , restricted localization , and fate is unknown and is fundamental to the control of BP and homeostasis of fluid and electrolytes .
	manualset3
87217	4	398664	13	NULL	NULL	0	NULL	homeostasis of fluid 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	How these cells maintain their identity , restricted localization , and fate is unknown and is fundamental to the control of BP and homeostasis of fluid and electrolytes .
	manualset3
87219	5	398664	13	NULL	NULL	0	NULL	electrolytes	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	How these cells maintain their identity , restricted localization , and fate is unknown and is fundamental to the control of BP and homeostasis of fluid and electrolytes .
	manualset3
87221	1	398665	13	NULL	NULL	0	NULL	ACA 	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	How these changes and the multiple other provisions of the ACA will affect young adults during the next decade is uncertain , but it has the potential to lead to earlier diagnosis of cancer , less invasive cancer therapy , better quality of survival , and higher cure rates .
	manualset3
87223	2	398665	13	NULL	NULL	0	NULL	young adults	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	How these changes and the multiple other provisions of the ACA will affect young adults during the next decade is uncertain , but it has the potential to lead to earlier diagnosis of cancer , less invasive cancer therapy , better quality of survival , and higher cure rates .
	manualset3
87225	3	398665	13	NULL	NULL	0	NULL	decade 	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	How these changes and the multiple other provisions of the ACA will affect young adults during the next decade is uncertain , but it has the potential to lead to earlier diagnosis of cancer , less invasive cancer therapy , better quality of survival , and higher cure rates .
	manualset3
87231	4	398665	13	NULL	NULL	0	NULL	diagnosis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	How these changes and the multiple other provisions of the ACA will affect young adults during the next decade is uncertain , but it has the potential to lead to earlier diagnosis of cancer , less invasive cancer therapy , better quality of survival , and higher cure rates .
	manualset3
87233	5	398665	13	NULL	NULL	0	NULL	cancer	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	How these changes and the multiple other provisions of the ACA will affect young adults during the next decade is uncertain , but it has the potential to lead to earlier diagnosis of cancer , less invasive cancer therapy , better quality of survival , and higher cure rates .
	manualset3
87234	6	398665	13	NULL	NULL	0	NULL	 less invasive cancer therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	How these changes and the multiple other provisions of the ACA will affect young adults during the next decade is uncertain , but it has the potential to lead to earlier diagnosis of cancer , less invasive cancer therapy , better quality of survival , and higher cure rates .
	manualset3
87236	7	398665	13	NULL	NULL	0	NULL	better quality of survival	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	How these changes and the multiple other provisions of the ACA will affect young adults during the next decade is uncertain , but it has the potential to lead to earlier diagnosis of cancer , less invasive cancer therapy , better quality of survival , and higher cure rates .
	manualset3
87237	8	398665	13	NULL	NULL	0	NULL	higher cure rates 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	How these changes and the multiple other provisions of the ACA will affect young adults during the next decade is uncertain , but it has the potential to lead to earlier diagnosis of cancer , less invasive cancer therapy , better quality of survival , and higher cure rates .
	manualset3
87262	1	398666	13	NULL	NULL	0	NULL	HCV	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Howerver , even in cases of tight association , the mechanisms through which HCV may promote or induce extrahepatic manifestations remain unclear and merit further investigations .
	manualset3
87264	2	398666	13	NULL	NULL	0	NULL	mechanisms 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Howerver , even in cases of tight association , the mechanisms through which HCV may promote or induce extrahepatic manifestations remain unclear and merit further investigations .
	manualset3
87267	3	398666	13	NULL	NULL	0	NULL	extrahepatic manifestations	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Howerver , even in cases of tight association , the mechanisms through which HCV may promote or induce extrahepatic manifestations remain unclear and merit further investigations .
	manualset3
87268	4	398666	13	NULL	NULL	0	NULL	 investigations	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Howerver , even in cases of tight association , the mechanisms through which HCV may promote or induce extrahepatic manifestations remain unclear and merit further investigations .
	manualset3
87275	1	398667	13	NULL	NULL	0	NULL	 ( 125I ) iodoarylazidoprazosin photoaffinity labeling 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , ( 125I ) iodoarylazidoprazosin photoaffinity labeling of the chimeric Pgp and its binding competition with cyclosporin A , showed that cyclosporin A competed for the photoaffinity labeling .
	manualset3
87276	2	398667	13	NULL	NULL	0	NULL	chimeric Pgp	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , ( 125I ) iodoarylazidoprazosin photoaffinity labeling of the chimeric Pgp and its binding competition with cyclosporin A , showed that cyclosporin A competed for the photoaffinity labeling .
	manualset3
87277	3	398667	13	NULL	NULL	0	NULL	 binding 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , ( 125I ) iodoarylazidoprazosin photoaffinity labeling of the chimeric Pgp and its binding competition with cyclosporin A , showed that cyclosporin A competed for the photoaffinity labeling .
	manualset3
87278	4	398667	13	NULL	NULL	0	NULL	cyclosporin A	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , ( 125I ) iodoarylazidoprazosin photoaffinity labeling of the chimeric Pgp and its binding competition with cyclosporin A , showed that cyclosporin A competed for the photoaffinity labeling .
	manualset3
87279	5	398667	13	NULL	NULL	0	NULL	cyclosporin A	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , ( 125I ) iodoarylazidoprazosin photoaffinity labeling of the chimeric Pgp and its binding competition with cyclosporin A , showed that cyclosporin A competed for the photoaffinity labeling .
	manualset3
87280	6	398667	13	NULL	NULL	0	NULL	 photoaffinity labeling 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , ( 125I ) iodoarylazidoprazosin photoaffinity labeling of the chimeric Pgp and its binding competition with cyclosporin A , showed that cyclosporin A competed for the photoaffinity labeling .
	manualset3
87281	1	398668	13	NULL	NULL	0	NULL	pyrexia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , his pyrexia continued and he developed repeating visual and hearing impairment reacting to steroid .
	manualset3
87282	2	398668	13	NULL	NULL	0	NULL	visual and hearing impairment 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , his pyrexia continued and he developed repeating visual and hearing impairment reacting to steroid .
	manualset3
87283	3	398668	13	NULL	NULL	NULL	NULL	steroid	NonProteinOrNucleicAcidChemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , his pyrexia continued and he developed repeating visual and hearing impairment reacting to steroid .
	manualset3
87284	1	398669	13	NULL	NULL	0	NULL	AGEP	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , our case describes the rare presentation of AGEP induced by erlotinib .
	manualset3
87285	2	398669	13	NULL	NULL	0	NULL	erlotinib	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , our case describes the rare presentation of AGEP induced by erlotinib .
	manualset3
87286	1	398670	13	NULL	NULL	0	NULL	urban populations 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , our focus will be on some of the more vulnerable urban populations who are most profoundly affected by SDH .
	manualset3
87287	2	398670	13	NULL	NULL	NULL	NULL	 SDH 	EnvironmentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , our focus will be on some of the more vulnerable urban populations who are most profoundly affected by SDH .
	manualset3
87288	1	398671	13	NULL	NULL	NULL	NULL	 courtship regulation 	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , their acute physiological roles in courtship regulation still largely remain unknown .
	manualset3
87289	1	398672	13	NULL	NULL	0	NULL	reproducibility	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , their reproducibility varied highly ( CV 9-40 % ) .
	manualset3
87290	2	398672	13	NULL	NULL	0	NULL	CV 9-40 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , their reproducibility varied highly ( CV 9-40 % ) .
	manualset3
87291	1	398673	13	NULL	NULL	0	NULL	1 month	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	However , 1 month after the chemotherapy , she developed ALL .
	manualset3
87292	2	398673	13	NULL	NULL	0	NULL	chemotherapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , 1 month after the chemotherapy , she developed ALL .
	manualset3
87293	3	398673	13	NULL	NULL	0	NULL	 ALL	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , 1 month after the chemotherapy , she developed ALL .
	manualset3
87294	1	398674	13	NULL	NULL	0	NULL	3 - ( methylthio ) catechol	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , 3 - ( methylthio ) catechol is a very poor substrate for catechol 1 , 2-dioxygenase ( 0.8 % of the rate of catechol ) , but it is a potent competitive inhibitor ( Ki = 0.6 microM ) .
	manualset3
87295	2	398674	13	NULL	NULL	0	NULL	catechol 1 , 2-dioxygenase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , 3 - ( methylthio ) catechol is a very poor substrate for catechol 1 , 2-dioxygenase ( 0.8 % of the rate of catechol ) , but it is a potent competitive inhibitor ( Ki = 0.6 microM ) .
	manualset3
87296	3	398674	13	NULL	NULL	0	NULL	0.8 % of the rate of catechol 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , 3 - ( methylthio ) catechol is a very poor substrate for catechol 1 , 2-dioxygenase ( 0.8 % of the rate of catechol ) , but it is a potent competitive inhibitor ( Ki = 0.6 microM ) .
	manualset3
87297	4	398674	13	NULL	NULL	0	NULL	inhibitor	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , 3 - ( methylthio ) catechol is a very poor substrate for catechol 1 , 2-dioxygenase ( 0.8 % of the rate of catechol ) , but it is a potent competitive inhibitor ( Ki = 0.6 microM ) .
	manualset3
87298	5	398674	13	NULL	NULL	0	NULL	Ki = 0.6 microM	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , 3 - ( methylthio ) catechol is a very poor substrate for catechol 1 , 2-dioxygenase ( 0.8 % of the rate of catechol ) , but it is a potent competitive inhibitor ( Ki = 0.6 microM ) .
	manualset3
87299	1	398675	13	NULL	NULL	0	NULL	Analysis of properties of single molecules 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Analysis of properties of single molecules in vivo or ... why small fish is better than empty dish ) .
	manualset3
87300	2	398675	13	NULL	NULL	NULL	NULL	fish	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Analysis of properties of single molecules in vivo or ... why small fish is better than empty dish ) .
	manualset3
87301	3	398675	13	NULL	NULL	0	NULL	dish	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	( Analysis of properties of single molecules in vivo or ... why small fish is better than empty dish ) .
	manualset3
87302	1	398676	13	NULL	NULL	0	NULL	cyclic AMP	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	( The biological role of cyclic AMP ) .
	manualset3
87652	2	398676	13	NULL	NULL	0	NULL	biological role 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The biological role of cyclic AMP ) .
	manualset3
87303	1	398677	13	NULL	NULL	0	NULL	8 weeks	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	However , 8 weeks after implantation the UBM-treated defect area showed significantly greater ( p & lt ; 0.05 ) regional systolic contraction compared to the myocardial defects repaired with by Dacron ( 3.3 + / - 1.3 % vs. -1.8 + / - 1.1 % ; respectively ) .
	manualset3
87304	2	398677	13	NULL	NULL	NULL	NULL	implantation	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , 8 weeks after implantation the UBM-treated defect area showed significantly greater ( p & lt ; 0.05 ) regional systolic contraction compared to the myocardial defects repaired with by Dacron ( 3.3 + / - 1.3 % vs. -1.8 + / - 1.1 % ; respectively ) .
	manualset3
87305	3	398677	13	NULL	NULL	0	NULL	UBM-treated defect area 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , 8 weeks after implantation the UBM-treated defect area showed significantly greater ( p & lt ; 0.05 ) regional systolic contraction compared to the myocardial defects repaired with by Dacron ( 3.3 + / - 1.3 % vs. -1.8 + / - 1.1 % ; respectively ) .
	manualset3
87306	4	398677	13	NULL	NULL	0	NULL	p & lt ; 0.05	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , 8 weeks after implantation the UBM-treated defect area showed significantly greater ( p & lt ; 0.05 ) regional systolic contraction compared to the myocardial defects repaired with by Dacron ( 3.3 + / - 1.3 % vs. -1.8 + / - 1.1 % ; respectively ) .
	manualset3
87307	5	398677	13	NULL	NULL	0	NULL	regional systolic contraction 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , 8 weeks after implantation the UBM-treated defect area showed significantly greater ( p & lt ; 0.05 ) regional systolic contraction compared to the myocardial defects repaired with by Dacron ( 3.3 + / - 1.3 % vs. -1.8 + / - 1.1 % ; respectively ) .
	manualset3
87308	6	398677	13	NULL	NULL	0	NULL	myocardial defects 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , 8 weeks after implantation the UBM-treated defect area showed significantly greater ( p & lt ; 0.05 ) regional systolic contraction compared to the myocardial defects repaired with by Dacron ( 3.3 + / - 1.3 % vs. -1.8 + / - 1.1 % ; respectively ) .
	manualset3
87309	7	398677	13	NULL	NULL	0	NULL	Dacron	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , 8 weeks after implantation the UBM-treated defect area showed significantly greater ( p & lt ; 0.05 ) regional systolic contraction compared to the myocardial defects repaired with by Dacron ( 3.3 + / - 1.3 % vs. -1.8 + / - 1.1 % ; respectively ) .
	manualset3
87310	8	398677	13	NULL	NULL	0	NULL	3.3 + / - 1.3 % vs. -1.8 + / - 1.1 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , 8 weeks after implantation the UBM-treated defect area showed significantly greater ( p & lt ; 0.05 ) regional systolic contraction compared to the myocardial defects repaired with by Dacron ( 3.3 + / - 1.3 % vs. -1.8 + / - 1.1 % ; respectively ) .
	manualset3
87311	1	398678	13	NULL	NULL	0	NULL	ALA pentyl ester	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , ALA pentyl ester slightly increased the in vivo PpIX fluorescence in early ( pre ) malignant lesions in hairless mouse skin compared to ALA. .
	manualset3
87312	2	398678	13	NULL	NULL	NULL	NULL	 PpIX fluorescence	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , ALA pentyl ester slightly increased the in vivo PpIX fluorescence in early ( pre ) malignant lesions in hairless mouse skin compared to ALA. .
	manualset3
87313	3	398678	13	NULL	NULL	NULL	NULL	early ( pre ) malignant lesions	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , ALA pentyl ester slightly increased the in vivo PpIX fluorescence in early ( pre ) malignant lesions in hairless mouse skin compared to ALA. .
	manualset3
87314	4	398678	13	NULL	NULL	0	NULL	hairless mouse skin 	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	However , ALA pentyl ester slightly increased the in vivo PpIX fluorescence in early ( pre ) malignant lesions in hairless mouse skin compared to ALA. .
	manualset3
87315	5	398678	13	NULL	NULL	0	NULL	ALA	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , ALA pentyl ester slightly increased the in vivo PpIX fluorescence in early ( pre ) malignant lesions in hairless mouse skin compared to ALA. .
	manualset3
87316	1	398679	13	NULL	NULL	0	NULL	AMG517 	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , AMG517 , a TRPV1 antagonist , presents several clinical limitations that include the induction of severe hyperthermia .
	manualset3
87317	2	398679	13	NULL	NULL	0	NULL	TRPV1 antagonist	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , AMG517 , a TRPV1 antagonist , presents several clinical limitations that include the induction of severe hyperthermia .
	manualset3
87318	3	398679	13	NULL	NULL	0	NULL	clinical limitations	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , AMG517 , a TRPV1 antagonist , presents several clinical limitations that include the induction of severe hyperthermia .
	manualset3
87319	4	398679	13	NULL	NULL	0	NULL	severe hyperthermia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , AMG517 , a TRPV1 antagonist , presents several clinical limitations that include the induction of severe hyperthermia .
	manualset3
87320	1	398680	13	NULL	NULL	0	NULL	AngII 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , AngII did increase O2 * - when the tissue strips were preincubated with the NO scavenger 2 - ( 4-carboxyphenyl ) -4 , 4 , 5 , 5 - tetramethylimidazoline-1-oxyl-3-oxide ( carboxy-PTIO ) , indicating that cross-talk of O2 * - from mTAL to the VR occurred but was normally inhibited by NO. .
	manualset3
87321	2	398680	13	NULL	NULL	0	NULL	O2 *	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	However , AngII did increase O2 * - when the tissue strips were preincubated with the NO scavenger 2 - ( 4-carboxyphenyl ) -4 , 4 , 5 , 5 - tetramethylimidazoline-1-oxyl-3-oxide ( carboxy-PTIO ) , indicating that cross-talk of O2 * - from mTAL to the VR occurred but was normally inhibited by NO. .
	manualset3
87322	3	398680	13	NULL	NULL	NULL	NULL	tissue	Tissue												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , AngII did increase O2 * - when the tissue strips were preincubated with the NO scavenger 2 - ( 4-carboxyphenyl ) -4 , 4 , 5 , 5 - tetramethylimidazoline-1-oxyl-3-oxide ( carboxy-PTIO ) , indicating that cross-talk of O2 * - from mTAL to the VR occurred but was normally inhibited by NO. .
	manualset3
87323	4	398680	13	NULL	NULL	NULL	NULL	NO scavenger	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , AngII did increase O2 * - when the tissue strips were preincubated with the NO scavenger 2 - ( 4-carboxyphenyl ) -4 , 4 , 5 , 5 - tetramethylimidazoline-1-oxyl-3-oxide ( carboxy-PTIO ) , indicating that cross-talk of O2 * - from mTAL to the VR occurred but was normally inhibited by NO. .
	manualset3
87326	5	398680	13	NULL	NULL	0	NULL	2 - ( 4-carboxyphenyl ) -4 , 4 , 5 , 5 - tetramethylimidazoline-1-oxyl-3-oxide ( carboxy-PTIO )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , AngII did increase O2 * - when the tissue strips were preincubated with the NO scavenger 2 - ( 4-carboxyphenyl ) -4 , 4 , 5 , 5 - tetramethylimidazoline-1-oxyl-3-oxide ( carboxy-PTIO ) , indicating that cross-talk of O2 * - from mTAL to the VR occurred but was normally inhibited by NO. .
	manualset3
87327	6	398680	13	NULL	NULL	NULL	NULL	cross-talk of O2 *	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , AngII did increase O2 * - when the tissue strips were preincubated with the NO scavenger 2 - ( 4-carboxyphenyl ) -4 , 4 , 5 , 5 - tetramethylimidazoline-1-oxyl-3-oxide ( carboxy-PTIO ) , indicating that cross-talk of O2 * - from mTAL to the VR occurred but was normally inhibited by NO. .
	manualset3
87328	7	398680	13	NULL	NULL	0	NULL	mTAL	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , AngII did increase O2 * - when the tissue strips were preincubated with the NO scavenger 2 - ( 4-carboxyphenyl ) -4 , 4 , 5 , 5 - tetramethylimidazoline-1-oxyl-3-oxide ( carboxy-PTIO ) , indicating that cross-talk of O2 * - from mTAL to the VR occurred but was normally inhibited by NO. .
	manualset3
87329	8	398680	13	NULL	NULL	0	NULL	VR	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , AngII did increase O2 * - when the tissue strips were preincubated with the NO scavenger 2 - ( 4-carboxyphenyl ) -4 , 4 , 5 , 5 - tetramethylimidazoline-1-oxyl-3-oxide ( carboxy-PTIO ) , indicating that cross-talk of O2 * - from mTAL to the VR occurred but was normally inhibited by NO. .
	manualset3
87330	9	398680	13	NULL	NULL	0	NULL	NO	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , AngII did increase O2 * - when the tissue strips were preincubated with the NO scavenger 2 - ( 4-carboxyphenyl ) -4 , 4 , 5 , 5 - tetramethylimidazoline-1-oxyl-3-oxide ( carboxy-PTIO ) , indicating that cross-talk of O2 * - from mTAL to the VR occurred but was normally inhibited by NO. .
	manualset3
87331	1	398681	13	NULL	NULL	0	NULL	Arabidopsis	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Arabidopsis showed a higher number of significantly altered mass features than Thellungiella .
	manualset3
87332	2	398681	13	NULL	NULL	0	NULL	Thellungiella 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Arabidopsis showed a higher number of significantly altered mass features than Thellungiella .
	manualset3
87333	3	398681	13	NULL	NULL	NULL	NULL	features 	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , Arabidopsis showed a higher number of significantly altered mass features than Thellungiella .
	manualset3
87653	4	398681	13	NULL	NULL	0	NULL	higher number 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Arabidopsis showed a higher number of significantly altered mass features than Thellungiella .
	manualset3
87334	1	398682	13	NULL	NULL	0	NULL	Au nanoparticles	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Au nanoparticles undergo charge equilibration with TiO ( 2 ) nanoparticles and shift the apparent Fermi level of the composite to more negative potentials .
	manualset3
87335	2	398682	13	NULL	NULL	NULL	NULL	charge equilibration	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , Au nanoparticles undergo charge equilibration with TiO ( 2 ) nanoparticles and shift the apparent Fermi level of the composite to more negative potentials .
	manualset3
87336	3	398682	13	NULL	NULL	0	NULL	TiO ( 2 ) nanoparticles	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Au nanoparticles undergo charge equilibration with TiO ( 2 ) nanoparticles and shift the apparent Fermi level of the composite to more negative potentials .
	manualset3
87654	4	398682	13	NULL	NULL	0	NULL	apparent Fermi level 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Au nanoparticles undergo charge equilibration with TiO ( 2 ) nanoparticles and shift the apparent Fermi level of the composite to more negative potentials .
	manualset3
87655	5	398682	13	NULL	NULL	0	NULL	negative potentials	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Au nanoparticles undergo charge equilibration with TiO ( 2 ) nanoparticles and shift the apparent Fermi level of the composite to more negative potentials .
	manualset3
87337	1	398683	13	NULL	NULL	0	NULL	BAPTA-AM	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , BAPTA-AM did not interfere with the ER-stress response pathway that triggers the expression of GRP 78 .
	manualset3
87338	2	398683	13	NULL	NULL	0	NULL	ER-stress response pathway	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , BAPTA-AM did not interfere with the ER-stress response pathway that triggers the expression of GRP 78 .
	manualset3
87339	3	398683	13	NULL	NULL	0	NULL	expression of GRP 78	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , BAPTA-AM did not interfere with the ER-stress response pathway that triggers the expression of GRP 78 .
	manualset3
87340	1	398684	13	NULL	NULL	0	NULL	GABAergic afferents 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , GABAergic afferents account for only a fraction of A15 synaptic input and do not appear to vary with season .
	manualset3
87341	2	398684	13	NULL	NULL	0	NULL	A15 synaptic input	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , GABAergic afferents account for only a fraction of A15 synaptic input and do not appear to vary with season .
	manualset3
87342	3	398684	13	NULL	NULL	0	NULL	season	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , GABAergic afferents account for only a fraction of A15 synaptic input and do not appear to vary with season .
	manualset3
87343	1	398685	13	NULL	NULL	0	NULL	 IK	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , IK has a nonlinear dependence on ( V-EK ) well described by the Goldman-Hodgkin-Katz equation that determines the voltage dependence of gK .
	manualset3
87344	2	398685	13	NULL	NULL	0	NULL	V-EK	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , IK has a nonlinear dependence on ( V-EK ) well described by the Goldman-Hodgkin-Katz equation that determines the voltage dependence of gK .
	manualset3
87345	3	398685	13	NULL	NULL	0	NULL	Goldman-Hodgkin-Katz equation 	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	However , IK has a nonlinear dependence on ( V-EK ) well described by the Goldman-Hodgkin-Katz equation that determines the voltage dependence of gK .
	manualset3
87346	4	398685	13	NULL	NULL	NULL	NULL	voltage dependence	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , IK has a nonlinear dependence on ( V-EK ) well described by the Goldman-Hodgkin-Katz equation that determines the voltage dependence of gK .
	manualset3
87347	5	398685	13	NULL	NULL	0	NULL	 gK 	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , IK has a nonlinear dependence on ( V-EK ) well described by the Goldman-Hodgkin-Katz equation that determines the voltage dependence of gK .
	manualset3
87656	6	398685	13	NULL	NULL	0	NULL	 nonlinear dependence 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , IK has a nonlinear dependence on ( V-EK ) well described by the Goldman-Hodgkin-Katz equation that determines the voltage dependence of gK .
	manualset3
87348	1	398686	13	NULL	NULL	0	NULL	IgE antibodies	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , IgE antibodies to a serum dilution of 1 : 200 specific for several components of the leaf extract were seen in serum from the dog that had anaphylactic shock after exposure to sap .
	manualset3
87349	2	398686	13	NULL	NULL	NULL	NULL	serum dilution of 1 : 200	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , IgE antibodies to a serum dilution of 1 : 200 specific for several components of the leaf extract were seen in serum from the dog that had anaphylactic shock after exposure to sap .
	manualset3
87350	3	398686	13	NULL	NULL	NULL	NULL	components of the leaf extract 	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , IgE antibodies to a serum dilution of 1 : 200 specific for several components of the leaf extract were seen in serum from the dog that had anaphylactic shock after exposure to sap .
	manualset3
87351	4	398686	13	NULL	NULL	NULL	NULL	serum 	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , IgE antibodies to a serum dilution of 1 : 200 specific for several components of the leaf extract were seen in serum from the dog that had anaphylactic shock after exposure to sap .
	manualset3
87352	5	398686	13	NULL	NULL	0	NULL	dog	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , IgE antibodies to a serum dilution of 1 : 200 specific for several components of the leaf extract were seen in serum from the dog that had anaphylactic shock after exposure to sap .
	manualset3
87353	6	398686	13	NULL	NULL	0	NULL	anaphylactic shock	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , IgE antibodies to a serum dilution of 1 : 200 specific for several components of the leaf extract were seen in serum from the dog that had anaphylactic shock after exposure to sap .
	manualset3
87354	7	398686	13	NULL	NULL	0	NULL	sap 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , IgE antibodies to a serum dilution of 1 : 200 specific for several components of the leaf extract were seen in serum from the dog that had anaphylactic shock after exposure to sap .
	manualset3
87355	1	398687	13	NULL	NULL	0	NULL	Japanese patients 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Japanese patients undergoing dialysis might be less tolerant of sevelamer treatment , and it is likely to cause hypocalcemia because their dietary Ca intake is less than that in European and American patients .
	manualset3
87356	2	398687	13	NULL	NULL	0	NULL	dialysis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Japanese patients undergoing dialysis might be less tolerant of sevelamer treatment , and it is likely to cause hypocalcemia because their dietary Ca intake is less than that in European and American patients .
	manualset3
87357	3	398687	13	NULL	NULL	0	NULL	sevelamer treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Japanese patients undergoing dialysis might be less tolerant of sevelamer treatment , and it is likely to cause hypocalcemia because their dietary Ca intake is less than that in European and American patients .
	manualset3
87358	4	398687	13	NULL	NULL	0	NULL	hypocalcemia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Japanese patients undergoing dialysis might be less tolerant of sevelamer treatment , and it is likely to cause hypocalcemia because their dietary Ca intake is less than that in European and American patients .
	manualset3
87359	5	398687	13	NULL	NULL	0	NULL	Ca intake	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Japanese patients undergoing dialysis might be less tolerant of sevelamer treatment , and it is likely to cause hypocalcemia because their dietary Ca intake is less than that in European and American patients .
	manualset3
87360	6	398687	13	NULL	NULL	0	NULL	European patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Japanese patients undergoing dialysis might be less tolerant of sevelamer treatment , and it is likely to cause hypocalcemia because their dietary Ca intake is less than that in European and American patients .
	manualset3
87361	7	398687	13	NULL	NULL	0	NULL	American patients 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Japanese patients undergoing dialysis might be less tolerant of sevelamer treatment , and it is likely to cause hypocalcemia because their dietary Ca intake is less than that in European and American patients .
	manualset3
87362	1	398688	13	NULL	NULL	0	NULL	Mg2 +	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Mg2 + enhanced equally by a factor of 3 affinities of high - and low-affinity binding sites as evidenced by SMS 201.995 displacement curves without modifying the ratio between high and low affinity sites .
	manualset3
87363	2	398688	13	NULL	NULL	0	NULL	SMS 201.995 displacement curves	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Mg2 + enhanced equally by a factor of 3 affinities of high - and low-affinity binding sites as evidenced by SMS 201.995 displacement curves without modifying the ratio between high and low affinity sites .
	manualset3
87659	3	398688	13	NULL	NULL	0	NULL	factor of 3 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Mg2 + enhanced equally by a factor of 3 affinities of high - and low-affinity binding sites as evidenced by SMS 201.995 displacement curves without modifying the ratio between high and low affinity sites .
	manualset3
87660	4	398688	13	NULL	NULL	NULL	NULL	high - and low-affinity binding sites 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , Mg2 + enhanced equally by a factor of 3 affinities of high - and low-affinity binding sites as evidenced by SMS 201.995 displacement curves without modifying the ratio between high and low affinity sites .
	manualset3
87661	5	398688	13	NULL	NULL	0	NULL	ratio	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Mg2 + enhanced equally by a factor of 3 affinities of high - and low-affinity binding sites as evidenced by SMS 201.995 displacement curves without modifying the ratio between high and low affinity sites .
	manualset3
87662	6	398688	13	NULL	NULL	0	NULL	high and low affinity sites 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Mg2 + enhanced equally by a factor of 3 affinities of high - and low-affinity binding sites as evidenced by SMS 201.995 displacement curves without modifying the ratio between high and low affinity sites .
	manualset3
87364	1	398689	13	NULL	NULL	0	NULL	North American signal crayfish Pacifastacus leniusculus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , North American signal crayfish Pacifastacus leniusculus were recently discovered in a water-course that has been repeatedly hit by the plague .
	manualset3
87365	2	398689	13	NULL	NULL	0	NULL	water-course	GeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , North American signal crayfish Pacifastacus leniusculus were recently discovered in a water-course that has been repeatedly hit by the plague .
	manualset3
87366	3	398689	13	NULL	NULL	0	NULL	plague	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , North American signal crayfish Pacifastacus leniusculus were recently discovered in a water-course that has been repeatedly hit by the plague .
	manualset3
87367	1	398690	13	NULL	NULL	0	NULL	PBP2a	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , PBP2a did not cross-link the peptide stems of glycan chains in vitro .
	manualset3
87368	2	398690	13	NULL	NULL	0	NULL	cross-link	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , PBP2a did not cross-link the peptide stems of glycan chains in vitro .
	manualset3
87369	3	398690	13	NULL	NULL	0	NULL	peptide stems of glycan chains	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	However , PBP2a did not cross-link the peptide stems of glycan chains in vitro .
	manualset3
87370	1	398691	13	NULL	NULL	0	NULL	PPCM	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , PPCM differs from autoimmune IDCM in that ( a ) it is associated with unique sets of autoantibodies and autoantigens , ( b ) it has a relatively rapid onset , and ( c ) it exclusively affects pregnant women .
	manualset3
87371	2	398691	13	NULL	NULL	0	NULL	autoimmune IDCM 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , PPCM differs from autoimmune IDCM in that ( a ) it is associated with unique sets of autoantibodies and autoantigens , ( b ) it has a relatively rapid onset , and ( c ) it exclusively affects pregnant women .
	manualset3
87372	3	398691	13	NULL	NULL	0	NULL	autoantibodies	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , PPCM differs from autoimmune IDCM in that ( a ) it is associated with unique sets of autoantibodies and autoantigens , ( b ) it has a relatively rapid onset , and ( c ) it exclusively affects pregnant women .
	manualset3
87373	4	398691	13	NULL	NULL	0	NULL	autoantigens	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , PPCM differs from autoimmune IDCM in that ( a ) it is associated with unique sets of autoantibodies and autoantigens , ( b ) it has a relatively rapid onset , and ( c ) it exclusively affects pregnant women .
	manualset3
87374	5	398691	13	NULL	NULL	0	NULL	rapid onset	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , PPCM differs from autoimmune IDCM in that ( a ) it is associated with unique sets of autoantibodies and autoantigens , ( b ) it has a relatively rapid onset , and ( c ) it exclusively affects pregnant women .
	manualset3
87375	6	398691	13	NULL	NULL	0	NULL	pregnant women 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , PPCM differs from autoimmune IDCM in that ( a ) it is associated with unique sets of autoantibodies and autoantigens , ( b ) it has a relatively rapid onset , and ( c ) it exclusively affects pregnant women .
	manualset3
87376	1	398692	13	NULL	NULL	0	NULL	Thy-1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Thy-1 was never expressed until the total age of 10 weeks .
	manualset3
87377	2	398692	13	NULL	NULL	0	NULL	age of 10 weeks 	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Thy-1 was never expressed until the total age of 10 weeks .
	manualset3
87378	1	398693	13	NULL	NULL	0	NULL	Yamanouchi	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Yamanouchi and Pfizer discontinued the co-development and marketing agreement for conivaptan .
	manualset3
87379	2	398693	13	NULL	NULL	0	NULL	Pfizer	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Yamanouchi and Pfizer discontinued the co-development and marketing agreement for conivaptan .
	manualset3
87380	3	398693	13	NULL	NULL	0	NULL	marketing agreement	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Yamanouchi and Pfizer discontinued the co-development and marketing agreement for conivaptan .
	manualset3
87381	4	398693	13	NULL	NULL	0	NULL	conivaptan	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , Yamanouchi and Pfizer discontinued the co-development and marketing agreement for conivaptan .
	manualset3
87382	1	398694	13	NULL	NULL	NULL	NULL	Nesselt number	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , a bulk Nesselt number should not be used to estimate heat loss from a live sheep in a hot environment if the windspeed is below about 4 m s-1 because the relation between mean surface temperature , Nusselt number and convective heat flux is not unique .
	manualset3
87383	2	398694	13	NULL	NULL	NULL	NULL	heat loss 	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , a bulk Nesselt number should not be used to estimate heat loss from a live sheep in a hot environment if the windspeed is below about 4 m s-1 because the relation between mean surface temperature , Nusselt number and convective heat flux is not unique .
	manualset3
87384	3	398694	13	NULL	NULL	0	NULL	live sheep	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , a bulk Nesselt number should not be used to estimate heat loss from a live sheep in a hot environment if the windspeed is below about 4 m s-1 because the relation between mean surface temperature , Nusselt number and convective heat flux is not unique .
	manualset3
87385	4	398694	13	NULL	NULL	0	NULL	hot environment 	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , a bulk Nesselt number should not be used to estimate heat loss from a live sheep in a hot environment if the windspeed is below about 4 m s-1 because the relation between mean surface temperature , Nusselt number and convective heat flux is not unique .
	manualset3
87386	5	398694	13	NULL	NULL	0	NULL	windspeed	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , a bulk Nesselt number should not be used to estimate heat loss from a live sheep in a hot environment if the windspeed is below about 4 m s-1 because the relation between mean surface temperature , Nusselt number and convective heat flux is not unique .
	manualset3
87387	6	398694	13	NULL	NULL	0	NULL	 4 m s-1 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , a bulk Nesselt number should not be used to estimate heat loss from a live sheep in a hot environment if the windspeed is below about 4 m s-1 because the relation between mean surface temperature , Nusselt number and convective heat flux is not unique .
	manualset3
87388	7	398694	13	NULL	NULL	0	NULL	mean surface temperature	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , a bulk Nesselt number should not be used to estimate heat loss from a live sheep in a hot environment if the windspeed is below about 4 m s-1 because the relation between mean surface temperature , Nusselt number and convective heat flux is not unique .
	manualset3
87389	8	398694	13	NULL	NULL	NULL	NULL	Nusselt number	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , a bulk Nesselt number should not be used to estimate heat loss from a live sheep in a hot environment if the windspeed is below about 4 m s-1 because the relation between mean surface temperature , Nusselt number and convective heat flux is not unique .
	manualset3
87390	9	398694	13	NULL	NULL	0	NULL	convective heat flux	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , a bulk Nesselt number should not be used to estimate heat loss from a live sheep in a hot environment if the windspeed is below about 4 m s-1 because the relation between mean surface temperature , Nusselt number and convective heat flux is not unique .
	manualset3
87391	1	398695	13	NULL	NULL	NULL	NULL	onset of caudal cranial nerve symptoms	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , a case with a sudden onset of caudal cranial nerve symptoms , before evident symptoms due to subarachnoid hemorrhage , has never been reported previously .
	manualset3
87392	2	398695	13	NULL	NULL	NULL	NULL	symptoms due to subarachnoid hemorrhage	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , a case with a sudden onset of caudal cranial nerve symptoms , before evident symptoms due to subarachnoid hemorrhage , has never been reported previously .
	manualset3
87393	1	398696	13	NULL	NULL	0	NULL	ALVAC-GM-CSF	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , a combination of ALVAC-GM-CSF and ALVAC-IL12 had no synergistic effect .
	manualset3
87394	2	398696	13	NULL	NULL	0	NULL	ALVAC-IL12	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , a combination of ALVAC-GM-CSF and ALVAC-IL12 had no synergistic effect .
	manualset3
87395	1	398697	13	NULL	NULL	0	NULL	reliance	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , a concern with reliance upon steady-state drug concentrations is that it ignores events occurring while the pathogen is exposed to intermittent suboptimal systemic drug concentrations prior to the attainment of a steady state .
	manualset3
87396	2	398697	13	NULL	NULL	NULL	NULL	steady-state drug concentrations	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , a concern with reliance upon steady-state drug concentrations is that it ignores events occurring while the pathogen is exposed to intermittent suboptimal systemic drug concentrations prior to the attainment of a steady state .
	manualset3
87397	3	398697	13	NULL	NULL	0	NULL	 pathogen 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , a concern with reliance upon steady-state drug concentrations is that it ignores events occurring while the pathogen is exposed to intermittent suboptimal systemic drug concentrations prior to the attainment of a steady state .
	manualset3
87398	4	398697	13	NULL	NULL	NULL	NULL	suboptimal systemic drug concentrations 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , a concern with reliance upon steady-state drug concentrations is that it ignores events occurring while the pathogen is exposed to intermittent suboptimal systemic drug concentrations prior to the attainment of a steady state .
	manualset3
87399	5	398697	13	NULL	NULL	NULL	NULL	steady state	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , a concern with reliance upon steady-state drug concentrations is that it ignores events occurring while the pathogen is exposed to intermittent suboptimal systemic drug concentrations prior to the attainment of a steady state .
	manualset3
87400	1	398698	13	NULL	NULL	0	NULL	evidence 	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , a growing body of evidence suggests that intracellular peptide hormone , either internalized or synthesized in situ , can exert physiologically relevant effects .
	manualset3
87401	2	398698	13	NULL	NULL	0	NULL	peptide hormone	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , a growing body of evidence suggests that intracellular peptide hormone , either internalized or synthesized in situ , can exert physiologically relevant effects .
	manualset3
87402	3	398698	13	NULL	NULL	NULL	NULL	internalized 	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , a growing body of evidence suggests that intracellular peptide hormone , either internalized or synthesized in situ , can exert physiologically relevant effects .
	manualset3
87403	4	398698	13	NULL	NULL	0	NULL	synthesized 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , a growing body of evidence suggests that intracellular peptide hormone , either internalized or synthesized in situ , can exert physiologically relevant effects .
	manualset3
87404	1	398699	13	NULL	NULL	0	NULL	null mutation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , a likely null mutation in the Shab K ( + ) channel gene ( Shab ( 3 ) ) reduces I ( K ) but does not eliminate it .
	manualset3
87405	2	398699	13	NULL	NULL	0	NULL	Shab K ( + ) channel gene ( Shab ( 3 ) )	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	However , a likely null mutation in the Shab K ( + ) channel gene ( Shab ( 3 ) ) reduces I ( K ) but does not eliminate it .
	manualset3
87406	3	398699	13	NULL	NULL	0	NULL	I ( K )	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , a likely null mutation in the Shab K ( + ) channel gene ( Shab ( 3 ) ) reduces I ( K ) but does not eliminate it .
	manualset3
87407	1	398700	13	NULL	NULL	0	NULL	tunicamycin	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , a possible effect of tunicamycin on the expression of the Ca channel as an alternative mechanism can not be excluded .
	manualset3
87408	2	398700	13	NULL	NULL	0	NULL	expression of the Ca channel	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , a possible effect of tunicamycin on the expression of the Ca channel as an alternative mechanism can not be excluded .
	manualset3
87409	3	398700	13	NULL	NULL	0	NULL	mechanism	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , a possible effect of tunicamycin on the expression of the Ca channel as an alternative mechanism can not be excluded .
	manualset3
87410	1	398701	13	NULL	NULL	0	NULL	 24-h recording period	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	However , across the 24-h recording period IL-6 knockout mice spent approximately 30 % more time in rapid eye movements sleep ( REMS ) than did C57BL/6J mice .
	manualset3
87411	2	398701	13	NULL	NULL	0	NULL	IL-6 knockout mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , across the 24-h recording period IL-6 knockout mice spent approximately 30 % more time in rapid eye movements sleep ( REMS ) than did C57BL/6J mice .
	manualset3
87412	3	398701	13	NULL	NULL	0	NULL	30 % more time 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , across the 24-h recording period IL-6 knockout mice spent approximately 30 % more time in rapid eye movements sleep ( REMS ) than did C57BL/6J mice .
	manualset3
87413	4	398701	13	NULL	NULL	0	NULL	rapid eye movements sleep ( REMS ) 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , across the 24-h recording period IL-6 knockout mice spent approximately 30 % more time in rapid eye movements sleep ( REMS ) than did C57BL/6J mice .
	manualset3
87414	5	398701	13	NULL	NULL	0	NULL	C57BL/6J mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , across the 24-h recording period IL-6 knockout mice spent approximately 30 % more time in rapid eye movements sleep ( REMS ) than did C57BL/6J mice .
	manualset3
87415	1	398702	13	NULL	NULL	0	NULL	activation of p53	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , activation of p53 was suppressed by SP600125 ; therefore the function of p53 was possibly controlled by JNK as well .
	manualset3
87416	2	398702	13	NULL	NULL	0	NULL	SP600125	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , activation of p53 was suppressed by SP600125 ; therefore the function of p53 was possibly controlled by JNK as well .
	manualset3
87417	3	398702	13	NULL	NULL	0	NULL	function of p53	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , activation of p53 was suppressed by SP600125 ; therefore the function of p53 was possibly controlled by JNK as well .
	manualset3
87418	4	398702	13	NULL	NULL	0	NULL	JNK	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , activation of p53 was suppressed by SP600125 ; therefore the function of p53 was possibly controlled by JNK as well .
	manualset3
87419	1	398703	13	NULL	NULL	0	NULL	acute tubular necrosis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , acute tubular necrosis was present both in IR non-treated and IR+FTY 720-treated groups .
	manualset3
87420	2	398703	13	NULL	NULL	NULL	NULL	IR non-treated group	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , acute tubular necrosis was present both in IR non-treated and IR+FTY 720-treated groups .
	manualset3
87421	3	398703	13	NULL	NULL	NULL	NULL	IR+FTY 720-treated group	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , acute tubular necrosis was present both in IR non-treated and IR+FTY 720-treated groups .
	manualset3
87422	1	398704	13	NULL	NULL	NULL	NULL	ischemia	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , after in vitro ischemia on hippocampal slices , both EAAs and PEA concentrations increased , but with different temporal patterns .
	manualset3
87423	2	398704	13	NULL	NULL	0	NULL	hippocampal slices	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , after in vitro ischemia on hippocampal slices , both EAAs and PEA concentrations increased , but with different temporal patterns .
	manualset3
87424	3	398704	13	NULL	NULL	0	NULL	EAAs	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , after in vitro ischemia on hippocampal slices , both EAAs and PEA concentrations increased , but with different temporal patterns .
	manualset3
87425	4	398704	13	NULL	NULL	0	NULL	PEA	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , after in vitro ischemia on hippocampal slices , both EAAs and PEA concentrations increased , but with different temporal patterns .
	manualset3
87426	5	398704	13	NULL	NULL	0	NULL	 temporal patterns	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , after in vitro ischemia on hippocampal slices , both EAAs and PEA concentrations increased , but with different temporal patterns .
	manualset3
87427	1	398705	13	NULL	NULL	0	NULL	indomethacin administration	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , after indomethacin administration , only hypertensive patients showed a significant reduction in the 24-hour sodium excretion ( from 417 + / - 61 to 317 + / - 49 mEq , p less than 0.05 ) , so that the difference between this value and the corresponding value of normotensive subjects ( 453 + / - 79 mEq ) became significant ( p less than 0.05 ) .
	manualset3
87428	2	398705	13	NULL	NULL	0	NULL	hypertensive patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , after indomethacin administration , only hypertensive patients showed a significant reduction in the 24-hour sodium excretion ( from 417 + / - 61 to 317 + / - 49 mEq , p less than 0.05 ) , so that the difference between this value and the corresponding value of normotensive subjects ( 453 + / - 79 mEq ) became significant ( p less than 0.05 ) .
	manualset3
87429	3	398705	13	NULL	NULL	0	NULL	24-hour	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	However , after indomethacin administration , only hypertensive patients showed a significant reduction in the 24-hour sodium excretion ( from 417 + / - 61 to 317 + / - 49 mEq , p less than 0.05 ) , so that the difference between this value and the corresponding value of normotensive subjects ( 453 + / - 79 mEq ) became significant ( p less than 0.05 ) .
	manualset3
87430	4	398705	13	NULL	NULL	0	NULL	sodium excretion	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , after indomethacin administration , only hypertensive patients showed a significant reduction in the 24-hour sodium excretion ( from 417 + / - 61 to 317 + / - 49 mEq , p less than 0.05 ) , so that the difference between this value and the corresponding value of normotensive subjects ( 453 + / - 79 mEq ) became significant ( p less than 0.05 ) .
	manualset3
87431	5	398705	13	NULL	NULL	NULL	NULL	417 + / - 61 to 317 + / - 49 mEq 	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , after indomethacin administration , only hypertensive patients showed a significant reduction in the 24-hour sodium excretion ( from 417 + / - 61 to 317 + / - 49 mEq , p less than 0.05 ) , so that the difference between this value and the corresponding value of normotensive subjects ( 453 + / - 79 mEq ) became significant ( p less than 0.05 ) .
	manualset3
87432	6	398705	13	NULL	NULL	0	NULL	normotensive subjects	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , after indomethacin administration , only hypertensive patients showed a significant reduction in the 24-hour sodium excretion ( from 417 + / - 61 to 317 + / - 49 mEq , p less than 0.05 ) , so that the difference between this value and the corresponding value of normotensive subjects ( 453 + / - 79 mEq ) became significant ( p less than 0.05 ) .
	manualset3
87433	7	398705	13	NULL	NULL	0	NULL	453 + / - 79 mEq	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , after indomethacin administration , only hypertensive patients showed a significant reduction in the 24-hour sodium excretion ( from 417 + / - 61 to 317 + / - 49 mEq , p less than 0.05 ) , so that the difference between this value and the corresponding value of normotensive subjects ( 453 + / - 79 mEq ) became significant ( p less than 0.05 ) .
	manualset3
87434	8	398705	13	NULL	NULL	0	NULL	p less than 0.05	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , after indomethacin administration , only hypertensive patients showed a significant reduction in the 24-hour sodium excretion ( from 417 + / - 61 to 317 + / - 49 mEq , p less than 0.05 ) , so that the difference between this value and the corresponding value of normotensive subjects ( 453 + / - 79 mEq ) became significant ( p less than 0.05 ) .
	manualset3
89563	9	398705	13	NULL	NULL	0	NULL	p less than 0.05	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , after indomethacin administration , only hypertensive patients showed a significant reduction in the 24-hour sodium excretion ( from 417 + / - 61 to 317 + / - 49 mEq , p less than 0.05 ) , so that the difference between this value and the corresponding value of normotensive subjects ( 453 + / - 79 mEq ) became significant ( p less than 0.05 ) .
	manualset3
87435	1	398706	13	NULL	NULL	0	NULL	urethane treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , after urethane treatment , most strains carrying the Pas1 ( s ) allele show an intermediate ( 1-4 tumors/mouse ) instead of a highly susceptible ( 15-30 tumors/mouse ) lung tumor phenotype .
	manualset3
87436	2	398706	13	NULL	NULL	0	NULL	strains carrying the Pas1 ( s ) allele	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , after urethane treatment , most strains carrying the Pas1 ( s ) allele show an intermediate ( 1-4 tumors/mouse ) instead of a highly susceptible ( 15-30 tumors/mouse ) lung tumor phenotype .
	manualset3
87437	3	398706	13	NULL	NULL	0	NULL	 intermediate ( 1-4 tumors/mouse ) lung tumor phenotype 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , after urethane treatment , most strains carrying the Pas1 ( s ) allele show an intermediate ( 1-4 tumors/mouse ) instead of a highly susceptible ( 15-30 tumors/mouse ) lung tumor phenotype .
	manualset3
87438	4	398706	13	NULL	NULL	0	NULL	highly susceptible ( 15-30 tumors/mouse ) lung tumor phenotype 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , after urethane treatment , most strains carrying the Pas1 ( s ) allele show an intermediate ( 1-4 tumors/mouse ) instead of a highly susceptible ( 15-30 tumors/mouse ) lung tumor phenotype .
	manualset3
87439	1	398707	13	NULL	NULL	NULL	NULL	non-esterified fatty acid parameters	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , all non-esterified fatty acid parameters showed only modest inverse correlation with liver transaminases .
	manualset3
87440	2	398707	13	NULL	NULL	NULL	NULL	modest inverse correlation	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , all non-esterified fatty acid parameters showed only modest inverse correlation with liver transaminases .
	manualset3
87441	3	398707	13	NULL	NULL	NULL	NULL	liver transaminases	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , all non-esterified fatty acid parameters showed only modest inverse correlation with liver transaminases .
	manualset3
87442	1	398708	13	NULL	NULL	0	NULL	analytes	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , analytes that form protonated molecular ions , such as reserpine , also show higher signal intensities when a ground loop is introduced into the system .
	manualset3
87443	2	398708	13	NULL	NULL	NULL	NULL	protonated molecular ions	Ion												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , analytes that form protonated molecular ions , such as reserpine , also show higher signal intensities when a ground loop is introduced into the system .
	manualset3
87444	3	398708	13	NULL	NULL	0	NULL	 reserpine	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , analytes that form protonated molecular ions , such as reserpine , also show higher signal intensities when a ground loop is introduced into the system .
	manualset3
87445	4	398708	13	NULL	NULL	0	NULL	ground loop	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , analytes that form protonated molecular ions , such as reserpine , also show higher signal intensities when a ground loop is introduced into the system .
	manualset3
87446	5	398708	13	NULL	NULL	0	NULL	system	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , analytes that form protonated molecular ions , such as reserpine , also show higher signal intensities when a ground loop is introduced into the system .
	manualset3
87447	1	398709	13	NULL	NULL	0	NULL	androgens 	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , androgens are not widely used for these indications because of the side effects associated with these drugs .
	manualset3
87448	2	398709	13	NULL	NULL	0	NULL	 indications	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , androgens are not widely used for these indications because of the side effects associated with these drugs .
	manualset3
87449	3	398709	13	NULL	NULL	0	NULL	side effects 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , androgens are not widely used for these indications because of the side effects associated with these drugs .
	manualset3
87450	4	398709	13	NULL	NULL	0	NULL	drugs	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , androgens are not widely used for these indications because of the side effects associated with these drugs .
	manualset3
87451	1	398710	13	NULL	NULL	NULL	NULL	antisense ODN-mediated depletion of mitogen-activated protein kinases	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , antisense ODN-mediated depletion of mitogen-activated protein kinases from the cells showed that their expression was necessary for terminal differentiation .
	manualset3
87452	2	398710	13	NULL	NULL	0	NULL	cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , antisense ODN-mediated depletion of mitogen-activated protein kinases from the cells showed that their expression was necessary for terminal differentiation .
	manualset3
87453	3	398710	13	NULL	NULL	0	NULL	expression 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , antisense ODN-mediated depletion of mitogen-activated protein kinases from the cells showed that their expression was necessary for terminal differentiation .
	manualset3
87454	4	398710	13	NULL	NULL	0	NULL	terminal differentiation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , antisense ODN-mediated depletion of mitogen-activated protein kinases from the cells showed that their expression was necessary for terminal differentiation .
	manualset3
87455	1	398711	13	NULL	NULL	0	NULL	central thermoregulatory action	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The central thermoregulatory action of cholecystokinin-8 and prostaglandin E1 ) .
	manualset3
87456	2	398711	13	NULL	NULL	0	NULL	cholecystokinin-8 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	( The central thermoregulatory action of cholecystokinin-8 and prostaglandin E1 ) .
	manualset3
87457	3	398711	13	NULL	NULL	0	NULL	prostaglandin E1	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( The central thermoregulatory action of cholecystokinin-8 and prostaglandin E1 ) .
	manualset3
87458	1	398712	13	NULL	NULL	0	NULL	membrane-interacting agents	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , application of membrane-interacting agents like tris ( hydroxymethyl ) aminomethane ( Tris ) - hydrochloride , ethylenediaminetetraacetate ( Na salt ) ( EDTA ) , divalent cations , and sublethal doses of the cationic antibacterial agents polymyxin B and chlorhexidine induced specific fluorescent labeling of envelope proteins and lipids but not of cytoplasmic compounds , with the exception of a soluble protein with a molecular weight of 46 , 000 in sodium dodecyl sulfate-polyacrylamide gel electrophoresis .
	manualset3
87459	2	398712	13	NULL	NULL	NULL	NULL	tris ( hydroxymethyl ) aminomethane ( Tris ) - hydrochloride	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , application of membrane-interacting agents like tris ( hydroxymethyl ) aminomethane ( Tris ) - hydrochloride , ethylenediaminetetraacetate ( Na salt ) ( EDTA ) , divalent cations , and sublethal doses of the cationic antibacterial agents polymyxin B and chlorhexidine induced specific fluorescent labeling of envelope proteins and lipids but not of cytoplasmic compounds , with the exception of a soluble protein with a molecular weight of 46 , 000 in sodium dodecyl sulfate-polyacrylamide gel electrophoresis .
	manualset3
87460	3	398712	13	NULL	NULL	0	NULL	ethylenediaminetetraacetate ( Na salt ) ( EDTA ) 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , application of membrane-interacting agents like tris ( hydroxymethyl ) aminomethane ( Tris ) - hydrochloride , ethylenediaminetetraacetate ( Na salt ) ( EDTA ) , divalent cations , and sublethal doses of the cationic antibacterial agents polymyxin B and chlorhexidine induced specific fluorescent labeling of envelope proteins and lipids but not of cytoplasmic compounds , with the exception of a soluble protein with a molecular weight of 46 , 000 in sodium dodecyl sulfate-polyacrylamide gel electrophoresis .
	manualset3
87461	4	398712	13	NULL	NULL	0	NULL	divalent cations 	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	However , application of membrane-interacting agents like tris ( hydroxymethyl ) aminomethane ( Tris ) - hydrochloride , ethylenediaminetetraacetate ( Na salt ) ( EDTA ) , divalent cations , and sublethal doses of the cationic antibacterial agents polymyxin B and chlorhexidine induced specific fluorescent labeling of envelope proteins and lipids but not of cytoplasmic compounds , with the exception of a soluble protein with a molecular weight of 46 , 000 in sodium dodecyl sulfate-polyacrylamide gel electrophoresis .
	manualset3
87462	5	398712	13	NULL	NULL	NULL	NULL	cationic antibacterial agents 	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , application of membrane-interacting agents like tris ( hydroxymethyl ) aminomethane ( Tris ) - hydrochloride , ethylenediaminetetraacetate ( Na salt ) ( EDTA ) , divalent cations , and sublethal doses of the cationic antibacterial agents polymyxin B and chlorhexidine induced specific fluorescent labeling of envelope proteins and lipids but not of cytoplasmic compounds , with the exception of a soluble protein with a molecular weight of 46 , 000 in sodium dodecyl sulfate-polyacrylamide gel electrophoresis .
	manualset3
87463	6	398712	13	NULL	NULL	0	NULL	polymyxin B	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , application of membrane-interacting agents like tris ( hydroxymethyl ) aminomethane ( Tris ) - hydrochloride , ethylenediaminetetraacetate ( Na salt ) ( EDTA ) , divalent cations , and sublethal doses of the cationic antibacterial agents polymyxin B and chlorhexidine induced specific fluorescent labeling of envelope proteins and lipids but not of cytoplasmic compounds , with the exception of a soluble protein with a molecular weight of 46 , 000 in sodium dodecyl sulfate-polyacrylamide gel electrophoresis .
	manualset3
87464	7	398712	13	NULL	NULL	0	NULL	chlorhexidine 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , application of membrane-interacting agents like tris ( hydroxymethyl ) aminomethane ( Tris ) - hydrochloride , ethylenediaminetetraacetate ( Na salt ) ( EDTA ) , divalent cations , and sublethal doses of the cationic antibacterial agents polymyxin B and chlorhexidine induced specific fluorescent labeling of envelope proteins and lipids but not of cytoplasmic compounds , with the exception of a soluble protein with a molecular weight of 46 , 000 in sodium dodecyl sulfate-polyacrylamide gel electrophoresis .
	manualset3
87465	8	398712	13	NULL	NULL	0	NULL	specific fluorescent labeling of envelope proteins and lipids	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , application of membrane-interacting agents like tris ( hydroxymethyl ) aminomethane ( Tris ) - hydrochloride , ethylenediaminetetraacetate ( Na salt ) ( EDTA ) , divalent cations , and sublethal doses of the cationic antibacterial agents polymyxin B and chlorhexidine induced specific fluorescent labeling of envelope proteins and lipids but not of cytoplasmic compounds , with the exception of a soluble protein with a molecular weight of 46 , 000 in sodium dodecyl sulfate-polyacrylamide gel electrophoresis .
	manualset3
87466	9	398712	13	NULL	NULL	0	NULL	cytoplasmic compounds	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , application of membrane-interacting agents like tris ( hydroxymethyl ) aminomethane ( Tris ) - hydrochloride , ethylenediaminetetraacetate ( Na salt ) ( EDTA ) , divalent cations , and sublethal doses of the cationic antibacterial agents polymyxin B and chlorhexidine induced specific fluorescent labeling of envelope proteins and lipids but not of cytoplasmic compounds , with the exception of a soluble protein with a molecular weight of 46 , 000 in sodium dodecyl sulfate-polyacrylamide gel electrophoresis .
	manualset3
87467	10	398712	13	NULL	NULL	0	NULL	soluble protein with a molecular weight of 46 , 000 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , application of membrane-interacting agents like tris ( hydroxymethyl ) aminomethane ( Tris ) - hydrochloride , ethylenediaminetetraacetate ( Na salt ) ( EDTA ) , divalent cations , and sublethal doses of the cationic antibacterial agents polymyxin B and chlorhexidine induced specific fluorescent labeling of envelope proteins and lipids but not of cytoplasmic compounds , with the exception of a soluble protein with a molecular weight of 46 , 000 in sodium dodecyl sulfate-polyacrylamide gel electrophoresis .
	manualset3
87468	11	398712	13	NULL	NULL	0	NULL	sodium dodecyl sulfate-polyacrylamide gel electrophoresis 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , application of membrane-interacting agents like tris ( hydroxymethyl ) aminomethane ( Tris ) - hydrochloride , ethylenediaminetetraacetate ( Na salt ) ( EDTA ) , divalent cations , and sublethal doses of the cationic antibacterial agents polymyxin B and chlorhexidine induced specific fluorescent labeling of envelope proteins and lipids but not of cytoplasmic compounds , with the exception of a soluble protein with a molecular weight of 46 , 000 in sodium dodecyl sulfate-polyacrylamide gel electrophoresis .
	manualset3
89566	12	398712	13	NULL	NULL	0	NULL	sublethal doses	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , application of membrane-interacting agents like tris ( hydroxymethyl ) aminomethane ( Tris ) - hydrochloride , ethylenediaminetetraacetate ( Na salt ) ( EDTA ) , divalent cations , and sublethal doses of the cationic antibacterial agents polymyxin B and chlorhexidine induced specific fluorescent labeling of envelope proteins and lipids but not of cytoplasmic compounds , with the exception of a soluble protein with a molecular weight of 46 , 000 in sodium dodecyl sulfate-polyacrylamide gel electrophoresis .
	manualset3
87469	1	398713	13	NULL	NULL	0	NULL	apyrase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , apyrase , an ATPase and ADPase , did not inhibit the shear-induced ( Ca2 + ) i responses in standard medium ( no added ATP or ADP ) , suggesting that the shear-induced ( Ca2 + ) i response is not due to ATP released by endothelial cells .
	manualset3
87470	2	398713	13	NULL	NULL	0	NULL	ATPase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , apyrase , an ATPase and ADPase , did not inhibit the shear-induced ( Ca2 + ) i responses in standard medium ( no added ATP or ADP ) , suggesting that the shear-induced ( Ca2 + ) i response is not due to ATP released by endothelial cells .
	manualset3
87471	3	398713	13	NULL	NULL	0	NULL	ADPase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , apyrase , an ATPase and ADPase , did not inhibit the shear-induced ( Ca2 + ) i responses in standard medium ( no added ATP or ADP ) , suggesting that the shear-induced ( Ca2 + ) i response is not due to ATP released by endothelial cells .
	manualset3
87472	4	398713	13	NULL	NULL	0	NULL	shear-induced ( Ca2 + ) i responses 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , apyrase , an ATPase and ADPase , did not inhibit the shear-induced ( Ca2 + ) i responses in standard medium ( no added ATP or ADP ) , suggesting that the shear-induced ( Ca2 + ) i response is not due to ATP released by endothelial cells .
	manualset3
87473	5	398713	13	NULL	NULL	0	NULL	standard medium ( no added ATP or ADP )	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , apyrase , an ATPase and ADPase , did not inhibit the shear-induced ( Ca2 + ) i responses in standard medium ( no added ATP or ADP ) , suggesting that the shear-induced ( Ca2 + ) i response is not due to ATP released by endothelial cells .
	manualset3
87474	6	398713	13	NULL	NULL	0	NULL	shear-induced ( Ca2 + ) i response	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , apyrase , an ATPase and ADPase , did not inhibit the shear-induced ( Ca2 + ) i responses in standard medium ( no added ATP or ADP ) , suggesting that the shear-induced ( Ca2 + ) i response is not due to ATP released by endothelial cells .
	manualset3
87475	7	398713	13	NULL	NULL	0	NULL	ATP	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , apyrase , an ATPase and ADPase , did not inhibit the shear-induced ( Ca2 + ) i responses in standard medium ( no added ATP or ADP ) , suggesting that the shear-induced ( Ca2 + ) i response is not due to ATP released by endothelial cells .
	manualset3
87476	8	398713	13	NULL	NULL	0	NULL	endothelial cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , apyrase , an ATPase and ADPase , did not inhibit the shear-induced ( Ca2 + ) i responses in standard medium ( no added ATP or ADP ) , suggesting that the shear-induced ( Ca2 + ) i response is not due to ATP released by endothelial cells .
	manualset3
87477	1	398714	13	NULL	NULL	0	NULL	 frontal electrodes	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , at the frontal electrodes , late positivity ( probably a P3a ) only appeared in valid-invalid trials , indicating that invalid trials are analyzed as novel-like stimuli .
	manualset3
87478	2	398714	13	NULL	NULL	0	NULL	valid-invalid trials	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , at the frontal electrodes , late positivity ( probably a P3a ) only appeared in valid-invalid trials , indicating that invalid trials are analyzed as novel-like stimuli .
	manualset3
87479	3	398714	13	NULL	NULL	0	NULL	invalid trials are analyzed	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , at the frontal electrodes , late positivity ( probably a P3a ) only appeared in valid-invalid trials , indicating that invalid trials are analyzed as novel-like stimuli .
	manualset3
87480	4	398714	13	NULL	NULL	0	NULL	novel-like stimuli	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , at the frontal electrodes , late positivity ( probably a P3a ) only appeared in valid-invalid trials , indicating that invalid trials are analyzed as novel-like stimuli .
	manualset3
87481	1	398715	13	NULL	NULL	0	NULL	( 1 microM ) NT ( 8-13 )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , at the highest concentration studied ( 1 microM ) NT ( 8-13 ) was associated with a rapid increase ( 130 % ) in striatal dopamine release .
	manualset3
87482	2	398715	13	NULL	NULL	0	NULL	130 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , at the highest concentration studied ( 1 microM ) NT ( 8-13 ) was associated with a rapid increase ( 130 % ) in striatal dopamine release .
	manualset3
87483	3	398715	13	NULL	NULL	0	NULL	striatal dopamine release	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , at the highest concentration studied ( 1 microM ) NT ( 8-13 ) was associated with a rapid increase ( 130 % ) in striatal dopamine release .
	manualset3
87484	1	398716	13	NULL	NULL	0	NULL	clomipramine	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , because clomipramine is an effective treatment , information about the drug 's neurochemical effect could enhance the understanding of canine CD .
	manualset3
87485	2	398716	13	NULL	NULL	0	NULL	treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , because clomipramine is an effective treatment , information about the drug 's neurochemical effect could enhance the understanding of canine CD .
	manualset3
87486	3	398716	13	NULL	NULL	0	NULL	drug 's neurochemical effect	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , because clomipramine is an effective treatment , information about the drug 's neurochemical effect could enhance the understanding of canine CD .
	manualset3
87487	4	398716	13	NULL	NULL	0	NULL	canine CD	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , because clomipramine is an effective treatment , information about the drug 's neurochemical effect could enhance the understanding of canine CD .
	manualset3
87488	1	398717	13	NULL	NULL	0	NULL	 29 and 84 ( early milking phase ) 	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	However , between d 29 and 84 ( early milking phase ) , mean daily milk yield was greater in LD1X does than in DD1X does ( 2.6 0.1 kg vs. 2.1 0.1 kg ; P = 0.001 ) .
	manualset3
87489	2	398717	13	NULL	NULL	0	NULL	mean daily milk yield	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , between d 29 and 84 ( early milking phase ) , mean daily milk yield was greater in LD1X does than in DD1X does ( 2.6 0.1 kg vs. 2.1 0.1 kg ; P = 0.001 ) .
	manualset3
87490	3	398717	13	NULL	NULL	0	NULL	LD1X	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , between d 29 and 84 ( early milking phase ) , mean daily milk yield was greater in LD1X does than in DD1X does ( 2.6 0.1 kg vs. 2.1 0.1 kg ; P = 0.001 ) .
	manualset3
87491	4	398717	13	NULL	NULL	0	NULL	 DD1X 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , between d 29 and 84 ( early milking phase ) , mean daily milk yield was greater in LD1X does than in DD1X does ( 2.6 0.1 kg vs. 2.1 0.1 kg ; P = 0.001 ) .
	manualset3
87492	5	398717	13	NULL	NULL	0	NULL	( 2.6 0.1 kg vs. 2.1 0.1 kg ; P = 0.001 )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , between d 29 and 84 ( early milking phase ) , mean daily milk yield was greater in LD1X does than in DD1X does ( 2.6 0.1 kg vs. 2.1 0.1 kg ; P = 0.001 ) .
	manualset3
87493	1	398718	13	NULL	NULL	0	NULL	meaning	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , both meaning and forgiveness conferred mental health benefits for all three groups .
	manualset3
87494	2	398718	13	NULL	NULL	0	NULL	forgiveness 	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , both meaning and forgiveness conferred mental health benefits for all three groups .
	manualset3
87495	3	398718	13	NULL	NULL	0	NULL	mental health benefits	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , both meaning and forgiveness conferred mental health benefits for all three groups .
	manualset3
87496	4	398718	13	NULL	NULL	0	NULL	three groups	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , both meaning and forgiveness conferred mental health benefits for all three groups .
	manualset3
87497	1	398719	13	NULL	NULL	0	NULL	D137-L 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , both D137-L and E139-L had fusion activities equivalent to that of wild-type G protein after exposure to a pH of 5.7 or below .
	manualset3
87498	2	398719	13	NULL	NULL	0	NULL	E139-L	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , both D137-L and E139-L had fusion activities equivalent to that of wild-type G protein after exposure to a pH of 5.7 or below .
	manualset3
87499	3	398719	13	NULL	NULL	0	NULL	wild-type G protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , both D137-L and E139-L had fusion activities equivalent to that of wild-type G protein after exposure to a pH of 5.7 or below .
	manualset3
87500	4	398719	13	NULL	NULL	NULL	NULL	exposure 	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , both D137-L and E139-L had fusion activities equivalent to that of wild-type G protein after exposure to a pH of 5.7 or below .
	manualset3
87719	5	398719	13	NULL	NULL	0	NULL	pH of 5.7 or below	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , both D137-L and E139-L had fusion activities equivalent to that of wild-type G protein after exposure to a pH of 5.7 or below .
	manualset3
87501	1	398720	13	NULL	NULL	0	NULL	radioprotectant B-190	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( The characteristic of radioprotective properties of a radioprotectant B-190 at its administration after radiation ) .
	manualset3
87502	2	398720	13	NULL	NULL	NULL	NULL	administration 	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The characteristic of radioprotective properties of a radioprotectant B-190 at its administration after radiation ) .
	manualset3
87503	3	398720	13	NULL	NULL	0	NULL	 radiation 	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	( The characteristic of radioprotective properties of a radioprotectant B-190 at its administration after radiation ) .
	manualset3
87504	1	398721	13	NULL	NULL	NULL	NULL	stimuli	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , both forms of stimuli also activate other receptors .
	manualset3
87505	2	398721	13	NULL	NULL	0	NULL	activate other receptors	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , both forms of stimuli also activate other receptors .
	manualset3
87506	1	398722	13	NULL	NULL	NULL	NULL	80 pg/ml	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , by adding 80 pg/ml naloxone to the culture system containing 600 pg/ml beta-endorphin , the inhibitory effect of beta-endorphin on spontaneous GVBD could be reversed completely .
	manualset3
87507	2	398722	13	NULL	NULL	0	NULL	naloxone	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , by adding 80 pg/ml naloxone to the culture system containing 600 pg/ml beta-endorphin , the inhibitory effect of beta-endorphin on spontaneous GVBD could be reversed completely .
	manualset3
87508	3	398722	13	NULL	NULL	0	NULL	culture system	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , by adding 80 pg/ml naloxone to the culture system containing 600 pg/ml beta-endorphin , the inhibitory effect of beta-endorphin on spontaneous GVBD could be reversed completely .
	manualset3
87509	4	398722	13	NULL	NULL	NULL	NULL	600 pg/ml 	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , by adding 80 pg/ml naloxone to the culture system containing 600 pg/ml beta-endorphin , the inhibitory effect of beta-endorphin on spontaneous GVBD could be reversed completely .
	manualset3
87510	5	398722	13	NULL	NULL	0	NULL	beta-endorphin	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	However , by adding 80 pg/ml naloxone to the culture system containing 600 pg/ml beta-endorphin , the inhibitory effect of beta-endorphin on spontaneous GVBD could be reversed completely .
	manualset3
87511	6	398722	13	NULL	NULL	0	NULL	beta-endorphin	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	However , by adding 80 pg/ml naloxone to the culture system containing 600 pg/ml beta-endorphin , the inhibitory effect of beta-endorphin on spontaneous GVBD could be reversed completely .
	manualset3
87512	7	398722	13	NULL	NULL	NULL	NULL	GVBD	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , by adding 80 pg/ml naloxone to the culture system containing 600 pg/ml beta-endorphin , the inhibitory effect of beta-endorphin on spontaneous GVBD could be reversed completely .
	manualset3
87513	1	398723	13	NULL	NULL	NULL	NULL	 zyxin SNP	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , by single marker association , several of the zyxin SNP were significantly associated with carotenoid or NO ( 2 ) ( - ) + NO ( 3 ) ( - ) concentrations .
	manualset3
87514	2	398723	13	NULL	NULL	0	NULL	carotenoid	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , by single marker association , several of the zyxin SNP were significantly associated with carotenoid or NO ( 2 ) ( - ) + NO ( 3 ) ( - ) concentrations .
	manualset3
87515	3	398723	13	NULL	NULL	0	NULL	NO ( 2 ) ( - ) + NO ( 3 ) ( - )	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	However , by single marker association , several of the zyxin SNP were significantly associated with carotenoid or NO ( 2 ) ( - ) + NO ( 3 ) ( - ) concentrations .
	manualset3
89567	4	398723	13	NULL	NULL	0	NULL	single marker association	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , by single marker association , several of the zyxin SNP were significantly associated with carotenoid or NO ( 2 ) ( - ) + NO ( 3 ) ( - ) concentrations .
	manualset3
87516	1	398724	13	NULL	NULL	0	NULL	methods of data analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , by supervised methods of data analysis , we were able to select a set of genes that may differentiate between hereditary and sporadic tumors .
	manualset3
87517	2	398724	13	NULL	NULL	0	NULL	set of genes 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , by supervised methods of data analysis , we were able to select a set of genes that may differentiate between hereditary and sporadic tumors .
	manualset3
87518	3	398724	13	NULL	NULL	0	NULL	hereditary tumors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , by supervised methods of data analysis , we were able to select a set of genes that may differentiate between hereditary and sporadic tumors .
	manualset3
87519	4	398724	13	NULL	NULL	0	NULL	sporadic tumors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , by supervised methods of data analysis , we were able to select a set of genes that may differentiate between hereditary and sporadic tumors .
	manualset3
87520	1	398725	13	NULL	NULL	NULL	NULL	techniques	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , by using appropriate techniques , physicians can help patients quit smoking , even when office visits are limited .
	manualset3
87521	2	398725	13	NULL	NULL	0	NULL	physicians	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , by using appropriate techniques , physicians can help patients quit smoking , even when office visits are limited .
	manualset3
87522	3	398725	13	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , by using appropriate techniques , physicians can help patients quit smoking , even when office visits are limited .
	manualset3
87523	4	398725	13	NULL	NULL	NULL	NULL	office visits	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , by using appropriate techniques , physicians can help patients quit smoking , even when office visits are limited .
	manualset3
87524	1	398726	13	NULL	NULL	0	NULL	cardiac index	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , cardiac index and left ventricular end-diastolic pressure were unchanged by whole-body cooling .
	manualset3
87525	2	398726	13	NULL	NULL	0	NULL	left ventricular end-diastolic pressure	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , cardiac index and left ventricular end-diastolic pressure were unchanged by whole-body cooling .
	manualset3
87526	3	398726	13	NULL	NULL	NULL	NULL	whole-body 	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , cardiac index and left ventricular end-diastolic pressure were unchanged by whole-body cooling .
	manualset3
87527	1	398727	13	NULL	NULL	0	NULL	 changes of transcript patterns	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , causal links between physiological effects and changes of transcript patterns , for the most part , are still unresolved .
	manualset3
87720	2	398727	13	NULL	NULL	0	NULL	causal links 	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	However , causal links between physiological effects and changes of transcript patterns , for the most part , are still unresolved .
	manualset3
87721	3	398727	13	NULL	NULL	0	NULL	physiological effects	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , causal links between physiological effects and changes of transcript patterns , for the most part , are still unresolved .
	manualset3
87528	1	398728	13	NULL	NULL	0	NULL	 interpretation	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , caution should be used in the interpretation of increased cardiovascular disease risk , as it does not necessarily translate into early increased mortality .
	manualset3
87529	2	398728	13	NULL	NULL	0	NULL	cardiovascular disease risk	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , caution should be used in the interpretation of increased cardiovascular disease risk , as it does not necessarily translate into early increased mortality .
	manualset3
87530	3	398728	13	NULL	NULL	0	NULL	mortality	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , caution should be used in the interpretation of increased cardiovascular disease risk , as it does not necessarily translate into early increased mortality .
	manualset3
87531	1	398729	13	NULL	NULL	NULL	NULL	central anorexigenic action	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , central anorexigenic action of leptin is clearly diminished in aging , most likely due to the impaired leptin signal transduction .
	manualset3
87532	2	398729	13	NULL	NULL	0	NULL	aging	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , central anorexigenic action of leptin is clearly diminished in aging , most likely due to the impaired leptin signal transduction .
	manualset3
87533	3	398729	13	NULL	NULL	0	NULL	leptin signal transduction	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , central anorexigenic action of leptin is clearly diminished in aging , most likely due to the impaired leptin signal transduction .
	manualset3
87722	4	398729	13	NULL	NULL	0	NULL	leptin 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , central anorexigenic action of leptin is clearly diminished in aging , most likely due to the impaired leptin signal transduction .
	manualset3
87723	1	398731	13	NULL	NULL	NULL	NULL	challenges 	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , challenges associated with early vascularization of transplanted islet grafts and long-term islet survival remain .
	manualset3
87724	2	398731	13	NULL	NULL	NULL	NULL	early vascularization 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , challenges associated with early vascularization of transplanted islet grafts and long-term islet survival remain .
	manualset3
87725	3	398731	13	NULL	NULL	NULL	NULL	transplanted islet grafts	Tissue												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , challenges associated with early vascularization of transplanted islet grafts and long-term islet survival remain .
	manualset3
87726	4	398731	13	NULL	NULL	0	NULL	long-term islet survival	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , challenges associated with early vascularization of transplanted islet grafts and long-term islet survival remain .
	manualset3
87727	1	398732	13	NULL	NULL	NULL	NULL	challenges	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , challenges still lie ahead .
	manualset3
87728	1	398733	13	NULL	NULL	0	NULL	chemotherapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , chemotherapy is often cost-prohibitive in our setting as mirrored by limited use ( 17.6 % ) .
	manualset3
87729	2	398733	13	NULL	NULL	0	NULL	17.6 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , chemotherapy is often cost-prohibitive in our setting as mirrored by limited use ( 17.6 % ) .
	manualset3
87730	1	398734	13	NULL	NULL	0	NULL	choline metabolism	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , choline metabolism was altered in rats , as indicated by decreases in betaine and increases in phosphocholine with the concomitant induction of betaine-homocysteine methyltransferase and choline kinase gene expression .
	manualset3
87731	2	398734	13	NULL	NULL	0	NULL	 rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , choline metabolism was altered in rats , as indicated by decreases in betaine and increases in phosphocholine with the concomitant induction of betaine-homocysteine methyltransferase and choline kinase gene expression .
	manualset3
87732	3	398734	13	NULL	NULL	NULL	NULL	betaine	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , choline metabolism was altered in rats , as indicated by decreases in betaine and increases in phosphocholine with the concomitant induction of betaine-homocysteine methyltransferase and choline kinase gene expression .
	manualset3
87733	4	398734	13	NULL	NULL	0	NULL	phosphocholine	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , choline metabolism was altered in rats , as indicated by decreases in betaine and increases in phosphocholine with the concomitant induction of betaine-homocysteine methyltransferase and choline kinase gene expression .
	manualset3
87734	5	398734	13	NULL	NULL	0	NULL	betaine-homocysteine methyltransferase gene expression 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , choline metabolism was altered in rats , as indicated by decreases in betaine and increases in phosphocholine with the concomitant induction of betaine-homocysteine methyltransferase and choline kinase gene expression .
	manualset3
87735	6	398734	13	NULL	NULL	0	NULL	choline kinase gene expression 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , choline metabolism was altered in rats , as indicated by decreases in betaine and increases in phosphocholine with the concomitant induction of betaine-homocysteine methyltransferase and choline kinase gene expression .
	manualset3
87736	1	398735	13	NULL	NULL	0	NULL	clinical cholera infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , clinical cholera infection gave rise to detectable serum antibody responses to soluble hemagglutinin in only 2 of 10 Bangladeshi patients or 1 of 17 cholera-infected North American volunteers .
	manualset3
87737	2	398735	13	NULL	NULL	NULL	NULL	serum antibody responses	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , clinical cholera infection gave rise to detectable serum antibody responses to soluble hemagglutinin in only 2 of 10 Bangladeshi patients or 1 of 17 cholera-infected North American volunteers .
	manualset3
87738	3	398735	13	NULL	NULL	NULL	NULL	soluble hemagglutinin	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , clinical cholera infection gave rise to detectable serum antibody responses to soluble hemagglutinin in only 2 of 10 Bangladeshi patients or 1 of 17 cholera-infected North American volunteers .
	manualset3
87739	4	398735	13	NULL	NULL	0	NULL	2 of 10 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , clinical cholera infection gave rise to detectable serum antibody responses to soluble hemagglutinin in only 2 of 10 Bangladeshi patients or 1 of 17 cholera-infected North American volunteers .
	manualset3
87740	5	398735	13	NULL	NULL	0	NULL	Bangladeshi patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , clinical cholera infection gave rise to detectable serum antibody responses to soluble hemagglutinin in only 2 of 10 Bangladeshi patients or 1 of 17 cholera-infected North American volunteers .
	manualset3
87741	6	398735	13	NULL	NULL	0	NULL	1 of 17	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , clinical cholera infection gave rise to detectable serum antibody responses to soluble hemagglutinin in only 2 of 10 Bangladeshi patients or 1 of 17 cholera-infected North American volunteers .
	manualset3
87742	7	398735	13	NULL	NULL	0	NULL	cholera-infected North American volunteers	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , clinical cholera infection gave rise to detectable serum antibody responses to soluble hemagglutinin in only 2 of 10 Bangladeshi patients or 1 of 17 cholera-infected North American volunteers .
	manualset3
87743	1	398736	13	NULL	NULL	0	NULL	mRNA expressions	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , combining mRNA expressions of genes coding for detoxification enzymes along with enzyme activities will be more useful biomarkers of stress .
	manualset3
87744	2	398736	13	NULL	NULL	0	NULL	genes coding for detoxification enzymes	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , combining mRNA expressions of genes coding for detoxification enzymes along with enzyme activities will be more useful biomarkers of stress .
	manualset3
87745	3	398736	13	NULL	NULL	0	NULL	enzyme activities	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , combining mRNA expressions of genes coding for detoxification enzymes along with enzyme activities will be more useful biomarkers of stress .
	manualset3
87746	4	398736	13	NULL	NULL	0	NULL	biomarkers	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , combining mRNA expressions of genes coding for detoxification enzymes along with enzyme activities will be more useful biomarkers of stress .
	manualset3
87747	5	398736	13	NULL	NULL	NULL	NULL	stress	EnvironmentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , combining mRNA expressions of genes coding for detoxification enzymes along with enzyme activities will be more useful biomarkers of stress .
	manualset3
87748	1	398737	13	NULL	NULL	0	NULL	standard C-Support Vector Machine ( C-SVM )	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , comparing to standard C-Support Vector Machine ( C-SVM ) , its formulation is more complicated , up until now there are no effective methods on solving accurate on-line learning for it .
	manualset3
87749	2	398737	13	NULL	NULL	0	NULL	formulation 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , comparing to standard C-Support Vector Machine ( C-SVM ) , its formulation is more complicated , up until now there are no effective methods on solving accurate on-line learning for it .
	manualset3
87750	3	398737	13	NULL	NULL	NULL	NULL	methods	PublishedSourceOfInformation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , comparing to standard C-Support Vector Machine ( C-SVM ) , its formulation is more complicated , up until now there are no effective methods on solving accurate on-line learning for it .
	manualset3
87751	4	398737	13	NULL	NULL	0	NULL	on-line learning	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , comparing to standard C-Support Vector Machine ( C-SVM ) , its formulation is more complicated , up until now there are no effective methods on solving accurate on-line learning for it .
	manualset3
87752	1	398738	13	NULL	NULL	0	NULL	conductance 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , conductance is low when deeply torpid animals are thermo-conforming probably because of peripheral vasoconstriction .
	manualset3
87753	2	398738	13	NULL	NULL	0	NULL	animals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , conductance is low when deeply torpid animals are thermo-conforming probably because of peripheral vasoconstriction .
	manualset3
87754	3	398738	13	NULL	NULL	0	NULL	peripheral vasoconstriction 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , conductance is low when deeply torpid animals are thermo-conforming probably because of peripheral vasoconstriction .
	manualset3
87755	1	398739	13	NULL	NULL	0	NULL	confusion	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , confusion exists about the purpose of ultrasound scans currently available .
	manualset3
87756	2	398739	13	NULL	NULL	0	NULL	ultrasound scans	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , confusion exists about the purpose of ultrasound scans currently available .
	manualset3
87757	1	398740	13	NULL	NULL	0	NULL	 conservation of synteny	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , conservation of synteny across the cereal genomes , in combination with new maize resources , has now made positional cloning in maize feasible .
	manualset3
87758	2	398740	13	NULL	NULL	NULL	NULL	cereal genomes 	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , conservation of synteny across the cereal genomes , in combination with new maize resources , has now made positional cloning in maize feasible .
	manualset3
87759	3	398740	13	NULL	NULL	0	NULL	maize	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , conservation of synteny across the cereal genomes , in combination with new maize resources , has now made positional cloning in maize feasible .
	manualset3
87760	4	398740	13	NULL	NULL	0	NULL	positional cloning	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , conservation of synteny across the cereal genomes , in combination with new maize resources , has now made positional cloning in maize feasible .
	manualset3
87761	5	398740	13	NULL	NULL	0	NULL	maize 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , conservation of synteny across the cereal genomes , in combination with new maize resources , has now made positional cloning in maize feasible .
	manualset3
87762	1	398741	13	NULL	NULL	0	NULL	contributions	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	However , contributions had already appeared in the 1950s showing - albeit indirectly - that isolated mitochondria bound Ca ( 2 + ) actively .
	manualset3
87763	2	398741	13	NULL	NULL	0	NULL	1950s	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	However , contributions had already appeared in the 1950s showing - albeit indirectly - that isolated mitochondria bound Ca ( 2 + ) actively .
	manualset3
87764	3	398741	13	NULL	NULL	0	NULL	mitochondria 	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	However , contributions had already appeared in the 1950s showing - albeit indirectly - that isolated mitochondria bound Ca ( 2 + ) actively .
	manualset3
87765	4	398741	13	NULL	NULL	0	NULL	Ca ( 2 + )	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	However , contributions had already appeared in the 1950s showing - albeit indirectly - that isolated mitochondria bound Ca ( 2 + ) actively .
	manualset3
87766	1	398742	13	NULL	NULL	0	NULL	 interactions between subunits 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , cooperative interactions between subunits also affect the voltage dependence of channel opening , and these interactions can be altered by making substitutions at uncharged residues in the S4 region .
	manualset3
87767	2	398742	13	NULL	NULL	NULL	NULL	voltage dependence	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , cooperative interactions between subunits also affect the voltage dependence of channel opening , and these interactions can be altered by making substitutions at uncharged residues in the S4 region .
	manualset3
87768	3	398742	13	NULL	NULL	0	NULL	channel opening	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , cooperative interactions between subunits also affect the voltage dependence of channel opening , and these interactions can be altered by making substitutions at uncharged residues in the S4 region .
	manualset3
87769	4	398742	13	NULL	NULL	0	NULL	 interactions	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , cooperative interactions between subunits also affect the voltage dependence of channel opening , and these interactions can be altered by making substitutions at uncharged residues in the S4 region .
	manualset3
87770	5	398742	13	NULL	NULL	0	NULL	substitutions	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , cooperative interactions between subunits also affect the voltage dependence of channel opening , and these interactions can be altered by making substitutions at uncharged residues in the S4 region .
	manualset3
87771	6	398742	13	NULL	NULL	0	NULL	uncharged residues in the S4 region	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , cooperative interactions between subunits also affect the voltage dependence of channel opening , and these interactions can be altered by making substitutions at uncharged residues in the S4 region .
	manualset3
87890	1	398743	13	NULL	NULL	0	NULL	clinical course	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The clinical course of acute brain injuries in deep cranial wounds ) .
	manualset3
87891	2	398743	13	NULL	NULL	0	NULL	acute brain injuries 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The clinical course of acute brain injuries in deep cranial wounds ) .
	manualset3
87892	3	398743	13	NULL	NULL	0	NULL	cranial wounds	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The clinical course of acute brain injuries in deep cranial wounds ) .
	manualset3
87893	1	398744	13	NULL	NULL	0	NULL	NO production 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , despite elevated NO production by murine cells , blockage of NO synthesis with the l-arginine analog N-monomethyl-l-arginine only partially rescued chlamydial growth , suggesting the presence of another IFN-gamma-inducible antichlamydial mechanism unique to murine cells .
	manualset3
87894	2	398744	13	NULL	NULL	0	NULL	murine cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , despite elevated NO production by murine cells , blockage of NO synthesis with the l-arginine analog N-monomethyl-l-arginine only partially rescued chlamydial growth , suggesting the presence of another IFN-gamma-inducible antichlamydial mechanism unique to murine cells .
	manualset3
87895	3	398744	13	NULL	NULL	0	NULL	NO synthesis	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , despite elevated NO production by murine cells , blockage of NO synthesis with the l-arginine analog N-monomethyl-l-arginine only partially rescued chlamydial growth , suggesting the presence of another IFN-gamma-inducible antichlamydial mechanism unique to murine cells .
	manualset3
87896	4	398744	13	NULL	NULL	NULL	NULL	l-arginine analog N-monomethyl-l-arginine	Molecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , despite elevated NO production by murine cells , blockage of NO synthesis with the l-arginine analog N-monomethyl-l-arginine only partially rescued chlamydial growth , suggesting the presence of another IFN-gamma-inducible antichlamydial mechanism unique to murine cells .
	manualset3
87897	5	398744	13	NULL	NULL	0	NULL	chlamydial growth	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , despite elevated NO production by murine cells , blockage of NO synthesis with the l-arginine analog N-monomethyl-l-arginine only partially rescued chlamydial growth , suggesting the presence of another IFN-gamma-inducible antichlamydial mechanism unique to murine cells .
	manualset3
87898	6	398744	13	NULL	NULL	0	NULL	IFN-gamma-inducible antichlamydial mechanism	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , despite elevated NO production by murine cells , blockage of NO synthesis with the l-arginine analog N-monomethyl-l-arginine only partially rescued chlamydial growth , suggesting the presence of another IFN-gamma-inducible antichlamydial mechanism unique to murine cells .
	manualset3
87899	7	398744	13	NULL	NULL	0	NULL	murine cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , despite elevated NO production by murine cells , blockage of NO synthesis with the l-arginine analog N-monomethyl-l-arginine only partially rescued chlamydial growth , suggesting the presence of another IFN-gamma-inducible antichlamydial mechanism unique to murine cells .
	manualset3
87900	1	398745	13	NULL	NULL	0	NULL	molecular activation mechanism ( s )	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , despite such advances in our understanding of the molecular activation mechanism ( s ) and physiological functions of NDR kinases in yeast and invertebrates , most biological NDR substrates still remain to be identified .
	manualset3
87901	2	398745	13	NULL	NULL	NULL	NULL	physiological functions 	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , despite such advances in our understanding of the molecular activation mechanism ( s ) and physiological functions of NDR kinases in yeast and invertebrates , most biological NDR substrates still remain to be identified .
	manualset3
87902	3	398745	13	NULL	NULL	0	NULL	NDR kinases	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , despite such advances in our understanding of the molecular activation mechanism ( s ) and physiological functions of NDR kinases in yeast and invertebrates , most biological NDR substrates still remain to be identified .
	manualset3
87903	4	398745	13	NULL	NULL	0	NULL	yeast 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , despite such advances in our understanding of the molecular activation mechanism ( s ) and physiological functions of NDR kinases in yeast and invertebrates , most biological NDR substrates still remain to be identified .
	manualset3
87904	5	398745	13	NULL	NULL	0	NULL	invertebrates	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , despite such advances in our understanding of the molecular activation mechanism ( s ) and physiological functions of NDR kinases in yeast and invertebrates , most biological NDR substrates still remain to be identified .
	manualset3
87905	6	398745	13	NULL	NULL	0	NULL	biological NDR substrates	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , despite such advances in our understanding of the molecular activation mechanism ( s ) and physiological functions of NDR kinases in yeast and invertebrates , most biological NDR substrates still remain to be identified .
	manualset3
87906	1	398746	13	NULL	NULL	0	NULL	ligand	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , different ligand specificities of MDC1-FHA have been reported , and no structure is available .
	manualset3
87907	2	398746	13	NULL	NULL	0	NULL	MDC1-FHA 	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , different ligand specificities of MDC1-FHA have been reported , and no structure is available .
	manualset3
87908	1	398747	13	NULL	NULL	NULL	NULL	 comparisons	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , direct comparisons have shown that eradication rates achieved by dual therapy are not as high as those achieved by triple therapy .
	manualset3
87909	2	398747	13	NULL	NULL	0	NULL	 eradication rates	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , direct comparisons have shown that eradication rates achieved by dual therapy are not as high as those achieved by triple therapy .
	manualset3
87910	3	398747	13	NULL	NULL	0	NULL	dual therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , direct comparisons have shown that eradication rates achieved by dual therapy are not as high as those achieved by triple therapy .
	manualset3
87911	4	398747	13	NULL	NULL	0	NULL	triple therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , direct comparisons have shown that eradication rates achieved by dual therapy are not as high as those achieved by triple therapy .
	manualset3
87912	1	398748	13	NULL	NULL	NULL	NULL	artifact 	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , doubt remains whether this may be an artifact of education bias in the screening tests used .
	manualset3
87913	2	398748	13	NULL	NULL	0	NULL	education bias	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , doubt remains whether this may be an artifact of education bias in the screening tests used .
	manualset3
87914	3	398748	13	NULL	NULL	0	NULL	screening tests	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , doubt remains whether this may be an artifact of education bias in the screening tests used .
	manualset3
88184	4	398748	13	NULL	NULL	0	NULL	doubt	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , doubt remains whether this may be an artifact of education bias in the screening tests used .
	manualset3
87915	1	398749	13	NULL	NULL	0	NULL	differentiation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , doubts can be raised about their differentiation as separate species .
	manualset3
87916	2	398749	13	NULL	NULL	0	NULL	species	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , doubts can be raised about their differentiation as separate species .
	manualset3
87917	1	398750	13	NULL	NULL	NULL	NULL	routine drug susceptibility testing	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , due to technical difficulties , routine drug susceptibility testing of Mycobacterium tuberculosis for pyrazinamide is , in many laboratories , not performed .
	manualset3
87918	2	398750	13	NULL	NULL	0	NULL	Mycobacterium tuberculosis	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , due to technical difficulties , routine drug susceptibility testing of Mycobacterium tuberculosis for pyrazinamide is , in many laboratories , not performed .
	manualset3
87919	3	398750	13	NULL	NULL	NULL	NULL	pyrazinamide 	Drug												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , due to technical difficulties , routine drug susceptibility testing of Mycobacterium tuberculosis for pyrazinamide is , in many laboratories , not performed .
	manualset3
87920	4	398750	13	NULL	NULL	0	NULL	laboratories 	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , due to technical difficulties , routine drug susceptibility testing of Mycobacterium tuberculosis for pyrazinamide is , in many laboratories , not performed .
	manualset3
88185	5	398750	13	NULL	NULL	0	NULL	technical difficulties	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , due to technical difficulties , routine drug susceptibility testing of Mycobacterium tuberculosis for pyrazinamide is , in many laboratories , not performed .
	manualset3
87921	1	398751	13	NULL	NULL	NULL	NULL	early larval life	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , during early larval life , in the prelude to a free-swimming existence , the innervation fields of motorneurons become restricted to a more limited sector of each muscle block , with individual motorneurons reaching predominantly ventral , medial , or dorsal regions .
	manualset3
87922	2	398751	13	NULL	NULL	0	NULL	 free-swimming existence	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , during early larval life , in the prelude to a free-swimming existence , the innervation fields of motorneurons become restricted to a more limited sector of each muscle block , with individual motorneurons reaching predominantly ventral , medial , or dorsal regions .
	manualset3
87923	3	398751	13	NULL	NULL	0	NULL	innervation fields 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , during early larval life , in the prelude to a free-swimming existence , the innervation fields of motorneurons become restricted to a more limited sector of each muscle block , with individual motorneurons reaching predominantly ventral , medial , or dorsal regions .
	manualset3
87924	4	398751	13	NULL	NULL	NULL	NULL	motorneurons	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , during early larval life , in the prelude to a free-swimming existence , the innervation fields of motorneurons become restricted to a more limited sector of each muscle block , with individual motorneurons reaching predominantly ventral , medial , or dorsal regions .
	manualset3
87925	5	398751	13	NULL	NULL	NULL	NULL	muscle block	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , during early larval life , in the prelude to a free-swimming existence , the innervation fields of motorneurons become restricted to a more limited sector of each muscle block , with individual motorneurons reaching predominantly ventral , medial , or dorsal regions .
	manualset3
87926	6	398751	13	NULL	NULL	NULL	NULL	motorneurons	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , during early larval life , in the prelude to a free-swimming existence , the innervation fields of motorneurons become restricted to a more limited sector of each muscle block , with individual motorneurons reaching predominantly ventral , medial , or dorsal regions .
	manualset3
87927	7	398751	13	NULL	NULL	0	NULL	ventral regions	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , during early larval life , in the prelude to a free-swimming existence , the innervation fields of motorneurons become restricted to a more limited sector of each muscle block , with individual motorneurons reaching predominantly ventral , medial , or dorsal regions .
	manualset3
87928	8	398751	13	NULL	NULL	0	NULL	medial regions	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , during early larval life , in the prelude to a free-swimming existence , the innervation fields of motorneurons become restricted to a more limited sector of each muscle block , with individual motorneurons reaching predominantly ventral , medial , or dorsal regions .
	manualset3
87929	9	398751	13	NULL	NULL	0	NULL	dorsal regions 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , during early larval life , in the prelude to a free-swimming existence , the innervation fields of motorneurons become restricted to a more limited sector of each muscle block , with individual motorneurons reaching predominantly ventral , medial , or dorsal regions .
	manualset3
87930	1	398752	13	NULL	NULL	0	NULL	dust formulations 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , dust formulations are difficult to apply and require specialized equipment .
	manualset3
87931	2	398752	13	NULL	NULL	0	NULL	equipment	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , dust formulations are difficult to apply and require specialized equipment .
	manualset3
88186	1	398753	13	NULL	NULL	NULL	NULL	electron pairs	Atom												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , electron pairs emitted by the core-resonant channel also share their energy continuously to jointly conserve the energy of the complete process .
	manualset3
89536	2	398753	13	NULL	NULL	0	NULL	core-resonant channel 	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , electron pairs emitted by the core-resonant channel also share their energy continuously to jointly conserve the energy of the complete process .
	manualset3
89537	3	398753	13	NULL	NULL	0	NULL	energy	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , electron pairs emitted by the core-resonant channel also share their energy continuously to jointly conserve the energy of the complete process .
	manualset3
89538	4	398753	13	NULL	NULL	0	NULL	energy	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , electron pairs emitted by the core-resonant channel also share their energy continuously to jointly conserve the energy of the complete process .
	manualset3
89539	5	398753	13	NULL	NULL	0	NULL	process	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , electron pairs emitted by the core-resonant channel also share their energy continuously to jointly conserve the energy of the complete process .
	manualset3
87932	1	398754	13	NULL	NULL	0	NULL	clinical significance	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The clinical significance of findings in microscopic urinalysis ) .
	manualset3
87933	2	398754	13	NULL	NULL	0	NULL	microscopic urinalysis 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The clinical significance of findings in microscopic urinalysis ) .
	manualset3
87934	1	398755	13	NULL	NULL	0	NULL	electrophysiological studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , electrophysiological studies revealed no alteration in the Ca ( 2 + ) current density , the frequency and amplitude of miniature excitatory postsynaptic currents , and the basal synaptic transmission in the mutant hippocampus .
	manualset3
87935	2	398755	13	NULL	NULL	NULL	NULL	Ca ( 2 + ) current density	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , electrophysiological studies revealed no alteration in the Ca ( 2 + ) current density , the frequency and amplitude of miniature excitatory postsynaptic currents , and the basal synaptic transmission in the mutant hippocampus .
	manualset3
87936	3	398755	13	NULL	NULL	0	NULL	frequency 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , electrophysiological studies revealed no alteration in the Ca ( 2 + ) current density , the frequency and amplitude of miniature excitatory postsynaptic currents , and the basal synaptic transmission in the mutant hippocampus .
	manualset3
87937	4	398755	13	NULL	NULL	NULL	NULL	amplitude 	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , electrophysiological studies revealed no alteration in the Ca ( 2 + ) current density , the frequency and amplitude of miniature excitatory postsynaptic currents , and the basal synaptic transmission in the mutant hippocampus .
	manualset3
87938	5	398755	13	NULL	NULL	0	NULL	 miniature excitatory postsynaptic currents	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , electrophysiological studies revealed no alteration in the Ca ( 2 + ) current density , the frequency and amplitude of miniature excitatory postsynaptic currents , and the basal synaptic transmission in the mutant hippocampus .
	manualset3
87939	6	398755	13	NULL	NULL	0	NULL	 basal synaptic transmission	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , electrophysiological studies revealed no alteration in the Ca ( 2 + ) current density , the frequency and amplitude of miniature excitatory postsynaptic currents , and the basal synaptic transmission in the mutant hippocampus .
	manualset3
87940	7	398755	13	NULL	NULL	NULL	NULL	mutant hippocampus	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , electrophysiological studies revealed no alteration in the Ca ( 2 + ) current density , the frequency and amplitude of miniature excitatory postsynaptic currents , and the basal synaptic transmission in the mutant hippocampus .
	manualset3
87941	1	398756	13	NULL	NULL	NULL	NULL	 evaluation	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , evaluation of student learning for this kind of simulation focuses mainly on the content and outcome of learning , rather than on the process of learning through student engagement .
	manualset3
87942	2	398756	13	NULL	NULL	NULL	NULL	student 	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , evaluation of student learning for this kind of simulation focuses mainly on the content and outcome of learning , rather than on the process of learning through student engagement .
	manualset3
87943	3	398756	13	NULL	NULL	NULL	NULL	learning	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , evaluation of student learning for this kind of simulation focuses mainly on the content and outcome of learning , rather than on the process of learning through student engagement .
	manualset3
87944	4	398756	13	NULL	NULL	NULL	NULL	simulation 	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , evaluation of student learning for this kind of simulation focuses mainly on the content and outcome of learning , rather than on the process of learning through student engagement .
	manualset3
87945	5	398756	13	NULL	NULL	0	NULL	learning	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , evaluation of student learning for this kind of simulation focuses mainly on the content and outcome of learning , rather than on the process of learning through student engagement .
	manualset3
87946	6	398756	13	NULL	NULL	0	NULL	learning	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , evaluation of student learning for this kind of simulation focuses mainly on the content and outcome of learning , rather than on the process of learning through student engagement .
	manualset3
87947	7	398756	13	NULL	NULL	0	NULL	 student	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , evaluation of student learning for this kind of simulation focuses mainly on the content and outcome of learning , rather than on the process of learning through student engagement .
	manualset3
87948	1	398757	13	NULL	NULL	0	NULL	women 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , even among women at low risk of recurrence , omitting guideline therapy placed them at elevated risk of recurrence .
	manualset3
87949	2	398757	13	NULL	NULL	0	NULL	low risk of recurrence	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , even among women at low risk of recurrence , omitting guideline therapy placed them at elevated risk of recurrence .
	manualset3
87950	3	398757	13	NULL	NULL	0	NULL	omitting guideline therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , even among women at low risk of recurrence , omitting guideline therapy placed them at elevated risk of recurrence .
	manualset3
87951	4	398757	13	NULL	NULL	0	NULL	elevated risk of recurrence 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , even among women at low risk of recurrence , omitting guideline therapy placed them at elevated risk of recurrence .
	manualset3
87952	1	398758	13	NULL	NULL	0	NULL	strains	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , even in strains overproducing L32 mRNA , e.g. from a cDNA copy of the gene , little accumulation of L32 is observed after a brief pulse label .
	manualset3
87953	2	398758	13	NULL	NULL	0	NULL	L32 mRNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , even in strains overproducing L32 mRNA , e.g. from a cDNA copy of the gene , little accumulation of L32 is observed after a brief pulse label .
	manualset3
87954	3	398758	13	NULL	NULL	NULL	NULL	 cDNA copy 	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , even in strains overproducing L32 mRNA , e.g. from a cDNA copy of the gene , little accumulation of L32 is observed after a brief pulse label .
	manualset3
87955	4	398758	13	NULL	NULL	0	NULL	 gene	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	However , even in strains overproducing L32 mRNA , e.g. from a cDNA copy of the gene , little accumulation of L32 is observed after a brief pulse label .
	manualset3
87956	5	398758	13	NULL	NULL	NULL	NULL	 accumulation	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , even in strains overproducing L32 mRNA , e.g. from a cDNA copy of the gene , little accumulation of L32 is observed after a brief pulse label .
	manualset3
87957	6	398758	13	NULL	NULL	NULL	NULL	L32	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , even in strains overproducing L32 mRNA , e.g. from a cDNA copy of the gene , little accumulation of L32 is observed after a brief pulse label .
	manualset3
87958	7	398758	13	NULL	NULL	0	NULL	pulse label 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , even in strains overproducing L32 mRNA , e.g. from a cDNA copy of the gene , little accumulation of L32 is observed after a brief pulse label .
	manualset3
87959	1	398759	13	NULL	NULL	0	NULL	angiographic studies 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , even the most careful angiographic studies do not always totally define the lesion and the surgeon must be prepared to find unexpected vascular relationships at operation .
	manualset3
87960	2	398759	13	NULL	NULL	0	NULL	 lesion	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , even the most careful angiographic studies do not always totally define the lesion and the surgeon must be prepared to find unexpected vascular relationships at operation .
	manualset3
87961	3	398759	13	NULL	NULL	0	NULL	surgeon	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , even the most careful angiographic studies do not always totally define the lesion and the surgeon must be prepared to find unexpected vascular relationships at operation .
	manualset3
87962	4	398759	13	NULL	NULL	0	NULL	relationships	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	However , even the most careful angiographic studies do not always totally define the lesion and the surgeon must be prepared to find unexpected vascular relationships at operation .
	manualset3
87963	5	398759	13	NULL	NULL	0	NULL	operation 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , even the most careful angiographic studies do not always totally define the lesion and the surgeon must be prepared to find unexpected vascular relationships at operation .
	manualset3
87964	1	398760	13	NULL	NULL	NULL	NULL	fasting urine calcium excretions 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , fasting urine calcium and magnesium excretions were higher in hypercalciuric calcium stone formers than in healthy control or time-control subjects .
	manualset3
87965	2	398760	13	NULL	NULL	0	NULL	fasting urine magnesium excretions 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , fasting urine calcium and magnesium excretions were higher in hypercalciuric calcium stone formers than in healthy control or time-control subjects .
	manualset3
87966	3	398760	13	NULL	NULL	0	NULL	hypercalciuric calcium stone formers 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , fasting urine calcium and magnesium excretions were higher in hypercalciuric calcium stone formers than in healthy control or time-control subjects .
	manualset3
87967	4	398760	13	NULL	NULL	0	NULL	healthy control	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , fasting urine calcium and magnesium excretions were higher in hypercalciuric calcium stone formers than in healthy control or time-control subjects .
	manualset3
87968	5	398760	13	NULL	NULL	0	NULL	time-control subjects	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , fasting urine calcium and magnesium excretions were higher in hypercalciuric calcium stone formers than in healthy control or time-control subjects .
	manualset3
87969	1	398761	13	NULL	NULL	0	NULL	XPY	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , feeding XPY alone tended to increase total tract digestibility of organic matter , N , neutral detergent fiber , and acid detergent fiber .
	manualset3
87970	2	398761	13	NULL	NULL	0	NULL	tract digestibility 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , feeding XPY alone tended to increase total tract digestibility of organic matter , N , neutral detergent fiber , and acid detergent fiber .
	manualset3
87971	3	398761	13	NULL	NULL	0	NULL	organic matter	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , feeding XPY alone tended to increase total tract digestibility of organic matter , N , neutral detergent fiber , and acid detergent fiber .
	manualset3
87972	4	398761	13	NULL	NULL	NULL	NULL	N , neutral detergent fiber	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , feeding XPY alone tended to increase total tract digestibility of organic matter , N , neutral detergent fiber , and acid detergent fiber .
	manualset3
87973	5	398761	13	NULL	NULL	NULL	NULL	acid detergent fiber 	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , feeding XPY alone tended to increase total tract digestibility of organic matter , N , neutral detergent fiber , and acid detergent fiber .
	manualset3
87974	1	398762	13	NULL	NULL	0	NULL	quantitative assessment measures 	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , few , if any , quantitative assessment measures exist ; most descriptions in the literature are qualitative , and this has limited the scope and robustness of research into the problem .
	manualset3
87975	2	398762	13	NULL	NULL	NULL	NULL	descriptions in the literature	PublishedSourceOfInformation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , few , if any , quantitative assessment measures exist ; most descriptions in the literature are qualitative , and this has limited the scope and robustness of research into the problem .
	manualset3
87976	3	398762	13	NULL	NULL	0	NULL	scope	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , few , if any , quantitative assessment measures exist ; most descriptions in the literature are qualitative , and this has limited the scope and robustness of research into the problem .
	manualset3
87977	4	398762	13	NULL	NULL	0	NULL	research	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , few , if any , quantitative assessment measures exist ; most descriptions in the literature are qualitative , and this has limited the scope and robustness of research into the problem .
	manualset3
87978	1	398763	13	NULL	NULL	0	NULL	 Analysis 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Analysis of spermatogenesis in senescence-accelerated mice ) .
	manualset3
87979	2	398763	13	NULL	NULL	0	NULL	spermatogenesis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Analysis of spermatogenesis in senescence-accelerated mice ) .
	manualset3
87980	3	398763	13	NULL	NULL	0	NULL	senescence-accelerated mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Analysis of spermatogenesis in senescence-accelerated mice ) .
	manualset3
87981	1	398764	13	NULL	NULL	NULL	NULL	compliance	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The compliance of the respiratory system in healthy and respiratory ill newborns after birth and its prognostic value for ventilatory support ( author 's transl ) ) .
	manualset3
87982	2	398764	13	NULL	NULL	0	NULL	respiratory system 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( The compliance of the respiratory system in healthy and respiratory ill newborns after birth and its prognostic value for ventilatory support ( author 's transl ) ) .
	manualset3
87983	3	398764	13	NULL	NULL	0	NULL	 healthy	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( The compliance of the respiratory system in healthy and respiratory ill newborns after birth and its prognostic value for ventilatory support ( author 's transl ) ) .
	manualset3
87984	4	398764	13	NULL	NULL	0	NULL	respiratory ill newborns	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( The compliance of the respiratory system in healthy and respiratory ill newborns after birth and its prognostic value for ventilatory support ( author 's transl ) ) .
	manualset3
87985	5	398764	13	NULL	NULL	NULL	NULL	birth	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The compliance of the respiratory system in healthy and respiratory ill newborns after birth and its prognostic value for ventilatory support ( author 's transl ) ) .
	manualset3
87986	6	398764	13	NULL	NULL	0	NULL	prognostic value	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The compliance of the respiratory system in healthy and respiratory ill newborns after birth and its prognostic value for ventilatory support ( author 's transl ) ) .
	manualset3
87987	7	398764	13	NULL	NULL	0	NULL	ventilatory support	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The compliance of the respiratory system in healthy and respiratory ill newborns after birth and its prognostic value for ventilatory support ( author 's transl ) ) .
	manualset3
87988	1	398765	13	NULL	NULL	0	NULL	flavonoids	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , flavonoids with 7-methoxy or 8-hydroxyl groups on the A ring showed only anti-aromatase activity .
	manualset3
87989	2	398765	13	NULL	NULL	0	NULL	7-methoxy or 8-hydroxyl groups	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , flavonoids with 7-methoxy or 8-hydroxyl groups on the A ring showed only anti-aromatase activity .
	manualset3
87990	3	398765	13	NULL	NULL	0	NULL	anti-aromatase activity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , flavonoids with 7-methoxy or 8-hydroxyl groups on the A ring showed only anti-aromatase activity .
	manualset3
87991	1	398766	13	NULL	NULL	0	NULL	immunisation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , following immunisation with xenogenic K562 cells , devils did produce cytotoxic responses and antibodies against this foreign tumor cell line .
	manualset3
87992	2	398766	13	NULL	NULL	0	NULL	xenogenic K562 cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , following immunisation with xenogenic K562 cells , devils did produce cytotoxic responses and antibodies against this foreign tumor cell line .
	manualset3
87993	3	398766	13	NULL	NULL	0	NULL	devils	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , following immunisation with xenogenic K562 cells , devils did produce cytotoxic responses and antibodies against this foreign tumor cell line .
	manualset3
87994	4	398766	13	NULL	NULL	0	NULL	cytotoxic responses	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , following immunisation with xenogenic K562 cells , devils did produce cytotoxic responses and antibodies against this foreign tumor cell line .
	manualset3
87995	5	398766	13	NULL	NULL	NULL	NULL	 antibodies 	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , following immunisation with xenogenic K562 cells , devils did produce cytotoxic responses and antibodies against this foreign tumor cell line .
	manualset3
87996	6	398766	13	NULL	NULL	0	NULL	foreign tumor cell line	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , following immunisation with xenogenic K562 cells , devils did produce cytotoxic responses and antibodies against this foreign tumor cell line .
	manualset3
87997	1	398767	13	NULL	NULL	0	NULL	mutant of M. fortuitum	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , for a mutant of M. fortuitum ( gamma 27 ) with virtually nonexistent beta-lactamase production , the antibiotics still had relatively high MICs ( for instance , benzylpenicillin and cephaloridine had MICs of 64 and 32 micrograms/ml , respectively ) .
	manualset3
87998	2	398767	13	NULL	NULL	0	NULL	gamma 27	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , for a mutant of M. fortuitum ( gamma 27 ) with virtually nonexistent beta-lactamase production , the antibiotics still had relatively high MICs ( for instance , benzylpenicillin and cephaloridine had MICs of 64 and 32 micrograms/ml , respectively ) .
	manualset3
87999	3	398767	13	NULL	NULL	0	NULL	beta-lactamase production	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , for a mutant of M. fortuitum ( gamma 27 ) with virtually nonexistent beta-lactamase production , the antibiotics still had relatively high MICs ( for instance , benzylpenicillin and cephaloridine had MICs of 64 and 32 micrograms/ml , respectively ) .
	manualset3
88000	4	398767	13	NULL	NULL	0	NULL	 antibiotics	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , for a mutant of M. fortuitum ( gamma 27 ) with virtually nonexistent beta-lactamase production , the antibiotics still had relatively high MICs ( for instance , benzylpenicillin and cephaloridine had MICs of 64 and 32 micrograms/ml , respectively ) .
	manualset3
88001	5	398767	13	NULL	NULL	NULL	NULL	MICs	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , for a mutant of M. fortuitum ( gamma 27 ) with virtually nonexistent beta-lactamase production , the antibiotics still had relatively high MICs ( for instance , benzylpenicillin and cephaloridine had MICs of 64 and 32 micrograms/ml , respectively ) .
	manualset3
88002	6	398767	13	NULL	NULL	0	NULL	benzylpenicillin	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , for a mutant of M. fortuitum ( gamma 27 ) with virtually nonexistent beta-lactamase production , the antibiotics still had relatively high MICs ( for instance , benzylpenicillin and cephaloridine had MICs of 64 and 32 micrograms/ml , respectively ) .
	manualset3
88003	7	398767	13	NULL	NULL	0	NULL	cephaloridine	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , for a mutant of M. fortuitum ( gamma 27 ) with virtually nonexistent beta-lactamase production , the antibiotics still had relatively high MICs ( for instance , benzylpenicillin and cephaloridine had MICs of 64 and 32 micrograms/ml , respectively ) .
	manualset3
88004	8	398767	13	NULL	NULL	0	NULL	MICs 	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , for a mutant of M. fortuitum ( gamma 27 ) with virtually nonexistent beta-lactamase production , the antibiotics still had relatively high MICs ( for instance , benzylpenicillin and cephaloridine had MICs of 64 and 32 micrograms/ml , respectively ) .
	manualset3
88005	9	398767	13	NULL	NULL	0	NULL	64 micrograms/ml	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , for a mutant of M. fortuitum ( gamma 27 ) with virtually nonexistent beta-lactamase production , the antibiotics still had relatively high MICs ( for instance , benzylpenicillin and cephaloridine had MICs of 64 and 32 micrograms/ml , respectively ) .
	manualset3
88006	10	398767	13	NULL	NULL	NULL	NULL	32 micrograms/ml 	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , for a mutant of M. fortuitum ( gamma 27 ) with virtually nonexistent beta-lactamase production , the antibiotics still had relatively high MICs ( for instance , benzylpenicillin and cephaloridine had MICs of 64 and 32 micrograms/ml , respectively ) .
	manualset3
88007	1	398768	13	NULL	NULL	0	NULL	first-generation adolescents	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , for first - and second-generation adolescents , participation in extracurricular activities is associated with higher rather than lower odds of violence compared to their non-participating counterparts .
	manualset3
88008	2	398768	13	NULL	NULL	0	NULL	second-generation adolescents	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , for first - and second-generation adolescents , participation in extracurricular activities is associated with higher rather than lower odds of violence compared to their non-participating counterparts .
	manualset3
88009	3	398768	13	NULL	NULL	NULL	NULL	extracurricular activities	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , for first - and second-generation adolescents , participation in extracurricular activities is associated with higher rather than lower odds of violence compared to their non-participating counterparts .
	manualset3
88010	4	398768	13	NULL	NULL	NULL	NULL	violence	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , for first - and second-generation adolescents , participation in extracurricular activities is associated with higher rather than lower odds of violence compared to their non-participating counterparts .
	manualset3
88011	5	398768	13	NULL	NULL	0	NULL	non-participating counterparts	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , for first - and second-generation adolescents , participation in extracurricular activities is associated with higher rather than lower odds of violence compared to their non-participating counterparts .
	manualset3
88012	1	398769	13	NULL	NULL	0	NULL	loci in LD	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , for loci in LD , GIA is often positive , suggesting that assignment can be improved by combining markers into haplotypes .
	manualset3
88013	2	398769	13	NULL	NULL	NULL	NULL	GIA	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , for loci in LD , GIA is often positive , suggesting that assignment can be improved by combining markers into haplotypes .
	manualset3
88014	3	398769	13	NULL	NULL	NULL	NULL	markers	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , for loci in LD , GIA is often positive , suggesting that assignment can be improved by combining markers into haplotypes .
	manualset3
88015	4	398769	13	NULL	NULL	0	NULL	haplotypes	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , for loci in LD , GIA is often positive , suggesting that assignment can be improved by combining markers into haplotypes .
	manualset3
88016	1	398770	13	NULL	NULL	0	NULL	infectious diseases	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , for many infectious diseases T cells are an important part of naturally acquired protective immune responses , and inducing these by vaccination has been the aim of much research .
	manualset3
88017	2	398770	13	NULL	NULL	0	NULL	T cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , for many infectious diseases T cells are an important part of naturally acquired protective immune responses , and inducing these by vaccination has been the aim of much research .
	manualset3
88018	3	398770	13	NULL	NULL	0	NULL	naturally acquired protective immune responses 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , for many infectious diseases T cells are an important part of naturally acquired protective immune responses , and inducing these by vaccination has been the aim of much research .
	manualset3
88019	4	398770	13	NULL	NULL	0	NULL	vaccination	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , for many infectious diseases T cells are an important part of naturally acquired protective immune responses , and inducing these by vaccination has been the aim of much research .
	manualset3
88020	5	398770	13	NULL	NULL	0	NULL	research	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , for many infectious diseases T cells are an important part of naturally acquired protective immune responses , and inducing these by vaccination has been the aim of much research .
	manualset3
88021	1	398771	13	NULL	NULL	0	NULL	traditional curriculums	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	( The construction of collective portfolios in traditional curriculums : an innovative approach in teaching-learning ) .
	manualset3
88022	2	398771	13	NULL	NULL	NULL	NULL	 innovative approach	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The construction of collective portfolios in traditional curriculums : an innovative approach in teaching-learning ) .
	manualset3
88023	3	398771	13	NULL	NULL	0	NULL	teaching-learning 	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The construction of collective portfolios in traditional curriculums : an innovative approach in teaching-learning ) .
	manualset3
88024	1	398772	13	NULL	NULL	0	NULL	studies 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , future studies should consider adopting a framework that explicitly accounts for the genealogical effects of population subdivision and empirical sampling schemes .
	manualset3
88025	2	398772	13	NULL	NULL	0	NULL	 framework	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	However , future studies should consider adopting a framework that explicitly accounts for the genealogical effects of population subdivision and empirical sampling schemes .
	manualset3
88026	3	398772	13	NULL	NULL	0	NULL	genealogical effects	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , future studies should consider adopting a framework that explicitly accounts for the genealogical effects of population subdivision and empirical sampling schemes .
	manualset3
88027	4	398772	13	NULL	NULL	0	NULL	population	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , future studies should consider adopting a framework that explicitly accounts for the genealogical effects of population subdivision and empirical sampling schemes .
	manualset3
88028	5	398772	13	NULL	NULL	0	NULL	subdivision	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , future studies should consider adopting a framework that explicitly accounts for the genealogical effects of population subdivision and empirical sampling schemes .
	manualset3
88029	6	398772	13	NULL	NULL	0	NULL	empirical sampling schemes 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , future studies should consider adopting a framework that explicitly accounts for the genealogical effects of population subdivision and empirical sampling schemes .
	manualset3
88030	1	398773	13	NULL	NULL	0	NULL	gibberellin 	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , gibberellin regulates expression of GID1 , GA20ox , and GA3ox , and there is also evidence that it regulates DELLA expression .
	manualset3
88031	2	398773	13	NULL	NULL	0	NULL	expression of GID1	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , gibberellin regulates expression of GID1 , GA20ox , and GA3ox , and there is also evidence that it regulates DELLA expression .
	manualset3
88032	3	398773	13	NULL	NULL	0	NULL	expression of GA20ox	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , gibberellin regulates expression of GID1 , GA20ox , and GA3ox , and there is also evidence that it regulates DELLA expression .
	manualset3
88033	4	398773	13	NULL	NULL	0	NULL	expression of GA3ox	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , gibberellin regulates expression of GID1 , GA20ox , and GA3ox , and there is also evidence that it regulates DELLA expression .
	manualset3
88034	5	398773	13	NULL	NULL	0	NULL	DELLA expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , gibberellin regulates expression of GID1 , GA20ox , and GA3ox , and there is also evidence that it regulates DELLA expression .
	manualset3
88035	1	398774	13	NULL	NULL	0	NULL	hemodialysis patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , hemodialysis patients and hemophiliacs were at higher risk of having HCV infection , since the prevalences were , respectively , 35.1 and 42.4 % in comparison with the blood donors ' prevalence ( 1.1 % ) .
	manualset3
88036	2	398774	13	NULL	NULL	0	NULL	 hemophiliacs	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , hemodialysis patients and hemophiliacs were at higher risk of having HCV infection , since the prevalences were , respectively , 35.1 and 42.4 % in comparison with the blood donors ' prevalence ( 1.1 % ) .
	manualset3
88037	3	398774	13	NULL	NULL	0	NULL	risk of having HCV infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , hemodialysis patients and hemophiliacs were at higher risk of having HCV infection , since the prevalences were , respectively , 35.1 and 42.4 % in comparison with the blood donors ' prevalence ( 1.1 % ) .
	manualset3
88038	4	398774	13	NULL	NULL	0	NULL	 35.1 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , hemodialysis patients and hemophiliacs were at higher risk of having HCV infection , since the prevalences were , respectively , 35.1 and 42.4 % in comparison with the blood donors ' prevalence ( 1.1 % ) .
	manualset3
88039	5	398774	13	NULL	NULL	0	NULL	42.4 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , hemodialysis patients and hemophiliacs were at higher risk of having HCV infection , since the prevalences were , respectively , 35.1 and 42.4 % in comparison with the blood donors ' prevalence ( 1.1 % ) .
	manualset3
88040	6	398774	13	NULL	NULL	0	NULL	comparison	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	However , hemodialysis patients and hemophiliacs were at higher risk of having HCV infection , since the prevalences were , respectively , 35.1 and 42.4 % in comparison with the blood donors ' prevalence ( 1.1 % ) .
	manualset3
88041	7	398774	13	NULL	NULL	0	NULL	blood donors	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , hemodialysis patients and hemophiliacs were at higher risk of having HCV infection , since the prevalences were , respectively , 35.1 and 42.4 % in comparison with the blood donors ' prevalence ( 1.1 % ) .
	manualset3
88042	8	398774	13	NULL	NULL	0	NULL	prevalence 	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , hemodialysis patients and hemophiliacs were at higher risk of having HCV infection , since the prevalences were , respectively , 35.1 and 42.4 % in comparison with the blood donors ' prevalence ( 1.1 % ) .
	manualset3
88043	9	398774	13	NULL	NULL	0	NULL	prevalences	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , hemodialysis patients and hemophiliacs were at higher risk of having HCV infection , since the prevalences were , respectively , 35.1 and 42.4 % in comparison with the blood donors ' prevalence ( 1.1 % ) .
	manualset3
88044	10	398774	13	NULL	NULL	0	NULL	1.1 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , hemodialysis patients and hemophiliacs were at higher risk of having HCV infection , since the prevalences were , respectively , 35.1 and 42.4 % in comparison with the blood donors ' prevalence ( 1.1 % ) .
	manualset3
88045	1	398775	13	NULL	NULL	NULL	NULL	 higher doses of naltrexone	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , higher doses of naltrexone ( 3.0 and 10.0 mg/kg ) increased latencies of both shocked and unshocked mice .
	manualset3
88047	2	398775	13	NULL	NULL	NULL	NULL	3.0 mg/kg	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , higher doses of naltrexone ( 3.0 and 10.0 mg/kg ) increased latencies of both shocked and unshocked mice .
	manualset3
88048	3	398775	13	NULL	NULL	NULL	NULL	10.0 mg/kg	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , higher doses of naltrexone ( 3.0 and 10.0 mg/kg ) increased latencies of both shocked and unshocked mice .
	manualset3
88049	4	398775	13	NULL	NULL	NULL	NULL	shocked  mice	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , higher doses of naltrexone ( 3.0 and 10.0 mg/kg ) increased latencies of both shocked and unshocked mice .
	manualset3
88050	5	398775	13	NULL	NULL	NULL	NULL	unshocked mice	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , higher doses of naltrexone ( 3.0 and 10.0 mg/kg ) increased latencies of both shocked and unshocked mice .
	manualset3
88051	1	398776	13	NULL	NULL	0	NULL	DA neurons	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , how DA neurons encode negative events in the environment is still unclear because some DA neurons appear to be depressed and others excited by aversive stimuli .
	manualset3
88052	2	398776	13	NULL	NULL	NULL	NULL	negative events	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , how DA neurons encode negative events in the environment is still unclear because some DA neurons appear to be depressed and others excited by aversive stimuli .
	manualset3
88053	3	398776	13	NULL	NULL	0	NULL	environment	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , how DA neurons encode negative events in the environment is still unclear because some DA neurons appear to be depressed and others excited by aversive stimuli .
	manualset3
88054	4	398776	13	NULL	NULL	0	NULL	DA neurons	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , how DA neurons encode negative events in the environment is still unclear because some DA neurons appear to be depressed and others excited by aversive stimuli .
	manualset3
88055	5	398776	13	NULL	NULL	NULL	NULL	 aversive stimuli 	EnvironmentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , how DA neurons encode negative events in the environment is still unclear because some DA neurons appear to be depressed and others excited by aversive stimuli .
	manualset3
88056	1	398777	13	NULL	NULL	0	NULL	ice water	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , ice water applied to the roots , which reduces root pressure , rapidly diminished exudation rate .
	manualset3
88057	2	398777	13	NULL	NULL	0	NULL	roots 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , ice water applied to the roots , which reduces root pressure , rapidly diminished exudation rate .
	manualset3
88058	3	398777	13	NULL	NULL	0	NULL	root pressure	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , ice water applied to the roots , which reduces root pressure , rapidly diminished exudation rate .
	manualset3
88059	4	398777	13	NULL	NULL	0	NULL	exudation rate	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , ice water applied to the roots , which reduces root pressure , rapidly diminished exudation rate .
	manualset3
88060	1	398778	13	NULL	NULL	0	NULL	intensive therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , if intensive therapy is combined with a hypoglycemia prevention program , the percentage of HbA1c can be maintained below risk values for the onset or progression of complications , and the frequency of hypoglycemia can be kept low .
	manualset3
88061	2	398778	13	NULL	NULL	0	NULL	hypoglycemia prevention program	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , if intensive therapy is combined with a hypoglycemia prevention program , the percentage of HbA1c can be maintained below risk values for the onset or progression of complications , and the frequency of hypoglycemia can be kept low .
	manualset3
88062	3	398778	13	NULL	NULL	0	NULL	 percentage of HbA1c	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , if intensive therapy is combined with a hypoglycemia prevention program , the percentage of HbA1c can be maintained below risk values for the onset or progression of complications , and the frequency of hypoglycemia can be kept low .
	manualset3
88063	4	398778	13	NULL	NULL	0	NULL	risk values	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , if intensive therapy is combined with a hypoglycemia prevention program , the percentage of HbA1c can be maintained below risk values for the onset or progression of complications , and the frequency of hypoglycemia can be kept low .
	manualset3
88064	5	398778	13	NULL	NULL	0	NULL	onset or progression of complications	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , if intensive therapy is combined with a hypoglycemia prevention program , the percentage of HbA1c can be maintained below risk values for the onset or progression of complications , and the frequency of hypoglycemia can be kept low .
	manualset3
88065	6	398778	13	NULL	NULL	0	NULL	frequency of hypoglycemia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , if intensive therapy is combined with a hypoglycemia prevention program , the percentage of HbA1c can be maintained below risk values for the onset or progression of complications , and the frequency of hypoglycemia can be kept low .
	manualset3
88066	1	398779	13	NULL	NULL	0	NULL	ocular toxoplasmosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( The cost of ocular toxoplasmosis ) .
	manualset3
88293	2	398779	13	NULL	NULL	0	NULL	cost	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The cost of ocular toxoplasmosis ) .
	manualset3
88067	1	398780	13	NULL	NULL	0	NULL	70 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in 70 % of asthmatics with BA exacerbation leukocyte sensitivity to CO2 inhibition diminished .
	manualset3
88068	2	398780	13	NULL	NULL	0	NULL	asthmatics	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in 70 % of asthmatics with BA exacerbation leukocyte sensitivity to CO2 inhibition diminished .
	manualset3
88069	3	398780	13	NULL	NULL	0	NULL	BA	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in 70 % of asthmatics with BA exacerbation leukocyte sensitivity to CO2 inhibition diminished .
	manualset3
88070	4	398780	13	NULL	NULL	0	NULL	leukocyte sensitivity to CO2 inhibition 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in 70 % of asthmatics with BA exacerbation leukocyte sensitivity to CO2 inhibition diminished .
	manualset3
88071	1	398781	13	NULL	NULL	0	NULL	 AMPK ( - / - ) MEFs	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in AMPK ( - / - ) MEFs transduced with DN AMPK , MMP-9 expression was suppressed .
	manualset3
88072	2	398781	13	NULL	NULL	0	NULL	DN AMPK	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in AMPK ( - / - ) MEFs transduced with DN AMPK , MMP-9 expression was suppressed .
	manualset3
88073	3	398781	13	NULL	NULL	0	NULL	MMP-9 expression 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in AMPK ( - / - ) MEFs transduced with DN AMPK , MMP-9 expression was suppressed .
	manualset3
88074	1	398782	13	NULL	NULL	0	NULL	RASMC serum	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in RASMC serum stimulated DNA synthesis and further increased the IC50 value for LPS-stimulated inhibition of thymidine incorporation ( 57.3 + / - 7.8 micrograms ml-1 ) .
	manualset3
88075	2	398782	13	NULL	NULL	0	NULL	DNA synthesis	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in RASMC serum stimulated DNA synthesis and further increased the IC50 value for LPS-stimulated inhibition of thymidine incorporation ( 57.3 + / - 7.8 micrograms ml-1 ) .
	manualset3
88076	3	398782	13	NULL	NULL	0	NULL	IC50 value	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in RASMC serum stimulated DNA synthesis and further increased the IC50 value for LPS-stimulated inhibition of thymidine incorporation ( 57.3 + / - 7.8 micrograms ml-1 ) .
	manualset3
88077	4	398782	13	NULL	NULL	0	NULL	LPS-stimulated inhibition of thymidine incorporation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in RASMC serum stimulated DNA synthesis and further increased the IC50 value for LPS-stimulated inhibition of thymidine incorporation ( 57.3 + / - 7.8 micrograms ml-1 ) .
	manualset3
88078	5	398782	13	NULL	NULL	0	NULL	 57.3 + / - 7.8 micrograms ml-1 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in RASMC serum stimulated DNA synthesis and further increased the IC50 value for LPS-stimulated inhibition of thymidine incorporation ( 57.3 + / - 7.8 micrograms ml-1 ) .
	manualset3
88079	1	398783	13	NULL	NULL	0	NULL	humid atmosphere	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in a humid atmosphere , heat treatment would transform TCP and TTCP into HA by hydrolytic reactions .
	manualset3
88080	2	398783	13	NULL	NULL	0	NULL	heat treatment 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in a humid atmosphere , heat treatment would transform TCP and TTCP into HA by hydrolytic reactions .
	manualset3
88081	3	398783	13	NULL	NULL	0	NULL	TCP	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in a humid atmosphere , heat treatment would transform TCP and TTCP into HA by hydrolytic reactions .
	manualset3
88082	4	398783	13	NULL	NULL	0	NULL	TTCP	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in a humid atmosphere , heat treatment would transform TCP and TTCP into HA by hydrolytic reactions .
	manualset3
88083	5	398783	13	NULL	NULL	0	NULL	HA	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in a humid atmosphere , heat treatment would transform TCP and TTCP into HA by hydrolytic reactions .
	manualset3
88084	6	398783	13	NULL	NULL	0	NULL	hydrolytic reactions	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in a humid atmosphere , heat treatment would transform TCP and TTCP into HA by hydrolytic reactions .
	manualset3
88085	1	398784	13	NULL	NULL	NULL	NULL	a two-sided clinical scenario	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , in a two-sided clinical scenario ( eg , a trial comparing similar treatments ) the prerandomisation design is potentially highly inefficient ; the refusal rate was much higher for prerandomisation to standard treatment than for conventional two-sided informed consent .
	manualset3
88086	2	398784	13	NULL	NULL	NULL	NULL	a trial comparing similar treatments	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , in a two-sided clinical scenario ( eg , a trial comparing similar treatments ) the prerandomisation design is potentially highly inefficient ; the refusal rate was much higher for prerandomisation to standard treatment than for conventional two-sided informed consent .
	manualset3
88087	3	398784	13	NULL	NULL	0	NULL	prerandomisation design	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in a two-sided clinical scenario ( eg , a trial comparing similar treatments ) the prerandomisation design is potentially highly inefficient ; the refusal rate was much higher for prerandomisation to standard treatment than for conventional two-sided informed consent .
	manualset3
88088	4	398784	13	NULL	NULL	0	NULL	refusal rate	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in a two-sided clinical scenario ( eg , a trial comparing similar treatments ) the prerandomisation design is potentially highly inefficient ; the refusal rate was much higher for prerandomisation to standard treatment than for conventional two-sided informed consent .
	manualset3
88089	5	398784	13	NULL	NULL	0	NULL	prerandomisation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in a two-sided clinical scenario ( eg , a trial comparing similar treatments ) the prerandomisation design is potentially highly inefficient ; the refusal rate was much higher for prerandomisation to standard treatment than for conventional two-sided informed consent .
	manualset3
88090	6	398784	13	NULL	NULL	0	NULL	standard treatment 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in a two-sided clinical scenario ( eg , a trial comparing similar treatments ) the prerandomisation design is potentially highly inefficient ; the refusal rate was much higher for prerandomisation to standard treatment than for conventional two-sided informed consent .
	manualset3
88091	7	398784	13	NULL	NULL	0	NULL	conventional two-sided informed consent	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in a two-sided clinical scenario ( eg , a trial comparing similar treatments ) the prerandomisation design is potentially highly inefficient ; the refusal rate was much higher for prerandomisation to standard treatment than for conventional two-sided informed consent .
	manualset3
88092	1	398785	13	NULL	NULL	0	NULL	sub-active dose of the selective 5-HT reuptake inhibitor citalopram 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in combination with a sub-active dose of the selective 5-HT reuptake inhibitor citalopram , inducing ~ 50 % 5-HT reuptake inhibition , PNU-282987 has shown marked antidepressant-like effects in the mFST .
	manualset3
88093	2	398785	13	NULL	NULL	0	NULL	~ 50 %	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in combination with a sub-active dose of the selective 5-HT reuptake inhibitor citalopram , inducing ~ 50 % 5-HT reuptake inhibition , PNU-282987 has shown marked antidepressant-like effects in the mFST .
	manualset3
88094	3	398785	13	NULL	NULL	NULL	NULL	5-HT reuptake inhibition	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , in combination with a sub-active dose of the selective 5-HT reuptake inhibitor citalopram , inducing ~ 50 % 5-HT reuptake inhibition , PNU-282987 has shown marked antidepressant-like effects in the mFST .
	manualset3
88095	4	398785	13	NULL	NULL	0	NULL	 PNU-282987 	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in combination with a sub-active dose of the selective 5-HT reuptake inhibitor citalopram , inducing ~ 50 % 5-HT reuptake inhibition , PNU-282987 has shown marked antidepressant-like effects in the mFST .
	manualset3
88096	5	398785	13	NULL	NULL	0	NULL	antidepressant-like effects	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in combination with a sub-active dose of the selective 5-HT reuptake inhibitor citalopram , inducing ~ 50 % 5-HT reuptake inhibition , PNU-282987 has shown marked antidepressant-like effects in the mFST .
	manualset3
88097	6	398785	13	NULL	NULL	0	NULL	mFST	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in combination with a sub-active dose of the selective 5-HT reuptake inhibitor citalopram , inducing ~ 50 % 5-HT reuptake inhibition , PNU-282987 has shown marked antidepressant-like effects in the mFST .
	manualset3
88098	1	398786	13	NULL	NULL	0	NULL	female rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in intact female rats only MA1 was formed , although the amount of MA , formed in females was much less than in males .
	manualset3
88099	2	398786	13	NULL	NULL	0	NULL	MA1	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in intact female rats only MA1 was formed , although the amount of MA , formed in females was much less than in males .
	manualset3
88100	3	398786	13	NULL	NULL	0	NULL	amount of MA	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in intact female rats only MA1 was formed , although the amount of MA , formed in females was much less than in males .
	manualset3
88101	4	398786	13	NULL	NULL	0	NULL	females	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in intact female rats only MA1 was formed , although the amount of MA , formed in females was much less than in males .
	manualset3
88102	5	398786	13	NULL	NULL	0	NULL	 males	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in intact female rats only MA1 was formed , although the amount of MA , formed in females was much less than in males .
	manualset3
88103	1	398787	13	NULL	NULL	0	NULL	HIV-1	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in many cases , it has been found that HIV-1 can enhance the level of expression and hence the life cycle of other viruses independently of immunosuppression through specific interactions with the viruses .
	manualset3
88104	2	398787	13	NULL	NULL	0	NULL	level of expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in many cases , it has been found that HIV-1 can enhance the level of expression and hence the life cycle of other viruses independently of immunosuppression through specific interactions with the viruses .
	manualset3
88105	3	398787	13	NULL	NULL	NULL	NULL	life cycle 	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , in many cases , it has been found that HIV-1 can enhance the level of expression and hence the life cycle of other viruses independently of immunosuppression through specific interactions with the viruses .
	manualset3
88106	4	398787	13	NULL	NULL	0	NULL	viruses 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in many cases , it has been found that HIV-1 can enhance the level of expression and hence the life cycle of other viruses independently of immunosuppression through specific interactions with the viruses .
	manualset3
88107	5	398787	13	NULL	NULL	0	NULL	immunosuppression	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in many cases , it has been found that HIV-1 can enhance the level of expression and hence the life cycle of other viruses independently of immunosuppression through specific interactions with the viruses .
	manualset3
88108	6	398787	13	NULL	NULL	0	NULL	interactions	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in many cases , it has been found that HIV-1 can enhance the level of expression and hence the life cycle of other viruses independently of immunosuppression through specific interactions with the viruses .
	manualset3
88109	7	398787	13	NULL	NULL	0	NULL	viruses	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in many cases , it has been found that HIV-1 can enhance the level of expression and hence the life cycle of other viruses independently of immunosuppression through specific interactions with the viruses .
	manualset3
89672	8	398787	13	NULL	NULL	0	NULL	many cases	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in many cases , it has been found that HIV-1 can enhance the level of expression and hence the life cycle of other viruses independently of immunosuppression through specific interactions with the viruses .
	manualset3
88110	1	398788	13	NULL	NULL	0	NULL	occipital structures	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in occipital and occipitotemporal structures , only beta , gamma , and high-gamma amplitudes were robustly strengthened by memory load .
	manualset3
88111	2	398788	13	NULL	NULL	0	NULL	occipitotemporal structures	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in occipital and occipitotemporal structures , only beta , gamma , and high-gamma amplitudes were robustly strengthened by memory load .
	manualset3
88112	3	398788	13	NULL	NULL	NULL	NULL	beta amplitudes	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , in occipital and occipitotemporal structures , only beta , gamma , and high-gamma amplitudes were robustly strengthened by memory load .
	manualset3
88294	4	398788	13	NULL	NULL	0	NULL	gamma amplitudes 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in occipital and occipitotemporal structures , only beta , gamma , and high-gamma amplitudes were robustly strengthened by memory load .
	manualset3
88295	5	398788	13	NULL	NULL	0	NULL	high-gamma amplitudes	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in occipital and occipitotemporal structures , only beta , gamma , and high-gamma amplitudes were robustly strengthened by memory load .
	manualset3
88296	6	398788	13	NULL	NULL	0	NULL	memory load	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in occipital and occipitotemporal structures , only beta , gamma , and high-gamma amplitudes were robustly strengthened by memory load .
	manualset3
88113	1	398789	13	NULL	NULL	0	NULL	decision	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in order to take any decision about sports eligibility , sports physicians should perform an initial accurate staging of the bicuspid aortic valve , taking into account hemodynamic factors , aortic complications and associated significant cardiovascular anomalies .
	manualset3
88114	2	398789	13	NULL	NULL	0	NULL	sports physicians	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in order to take any decision about sports eligibility , sports physicians should perform an initial accurate staging of the bicuspid aortic valve , taking into account hemodynamic factors , aortic complications and associated significant cardiovascular anomalies .
	manualset3
88132	3	398789	13	NULL	NULL	0	NULL	staging	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in order to take any decision about sports eligibility , sports physicians should perform an initial accurate staging of the bicuspid aortic valve , taking into account hemodynamic factors , aortic complications and associated significant cardiovascular anomalies .
	manualset3
88133	4	398789	13	NULL	NULL	0	NULL	bicuspid aortic valve	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in order to take any decision about sports eligibility , sports physicians should perform an initial accurate staging of the bicuspid aortic valve , taking into account hemodynamic factors , aortic complications and associated significant cardiovascular anomalies .
	manualset3
88134	5	398789	13	NULL	NULL	0	NULL	hemodynamic factors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in order to take any decision about sports eligibility , sports physicians should perform an initial accurate staging of the bicuspid aortic valve , taking into account hemodynamic factors , aortic complications and associated significant cardiovascular anomalies .
	manualset3
88135	6	398789	13	NULL	NULL	0	NULL	aortic complications	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in order to take any decision about sports eligibility , sports physicians should perform an initial accurate staging of the bicuspid aortic valve , taking into account hemodynamic factors , aortic complications and associated significant cardiovascular anomalies .
	manualset3
88136	7	398789	13	NULL	NULL	0	NULL	cardiovascular anomalies	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in order to take any decision about sports eligibility , sports physicians should perform an initial accurate staging of the bicuspid aortic valve , taking into account hemodynamic factors , aortic complications and associated significant cardiovascular anomalies .
	manualset3
88137	1	398790	13	NULL	NULL	0	NULL	B subunit	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in other preparations of the B subunit , there was an additional inhibitory effect due to small contaminations with the A subunit , which caused increases in intracellular cyclic adenosine monophosphate ( cAMP ) levels and concomitant growth inhibition .
	manualset3
88138	2	398790	13	NULL	NULL	NULL	NULL	contaminations 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , in other preparations of the B subunit , there was an additional inhibitory effect due to small contaminations with the A subunit , which caused increases in intracellular cyclic adenosine monophosphate ( cAMP ) levels and concomitant growth inhibition .
	manualset3
88139	3	398790	13	NULL	NULL	0	NULL	A subunit 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in other preparations of the B subunit , there was an additional inhibitory effect due to small contaminations with the A subunit , which caused increases in intracellular cyclic adenosine monophosphate ( cAMP ) levels and concomitant growth inhibition .
	manualset3
88141	5	398790	13	NULL	NULL	0	NULL	growth inhibition	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in other preparations of the B subunit , there was an additional inhibitory effect due to small contaminations with the A subunit , which caused increases in intracellular cyclic adenosine monophosphate ( cAMP ) levels and concomitant growth inhibition .
	manualset3
89675	6	398790	13	NULL	NULL	0	NULL	intracellular cyclic adenosine monophosphate ( cAMP ) levels	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in other preparations of the B subunit , there was an additional inhibitory effect due to small contaminations with the A subunit , which caused increases in intracellular cyclic adenosine monophosphate ( cAMP ) levels and concomitant growth inhibition .
	manualset3
88140	1	398791	13	NULL	NULL	NULL	NULL	 hypercholesterolemia	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , in refractory hypercholesterolemia combination therapy may be required .
	manualset3
88142	2	398791	13	NULL	NULL	0	NULL	combination therapy 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in refractory hypercholesterolemia combination therapy may be required .
	manualset3
88143	1	398792	13	NULL	NULL	0	NULL	serum-free conditions 	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in serum-free conditions , the rate of enzyme degradation is doubled with no change in the pinocytic rate of the cells .
	manualset3
88144	2	398792	13	NULL	NULL	NULL	NULL	 rate of enzyme degradation 	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , in serum-free conditions , the rate of enzyme degradation is doubled with no change in the pinocytic rate of the cells .
	manualset3
88145	3	398792	13	NULL	NULL	0	NULL	pinocytic rate	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in serum-free conditions , the rate of enzyme degradation is doubled with no change in the pinocytic rate of the cells .
	manualset3
88146	4	398792	13	NULL	NULL	0	NULL	 cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in serum-free conditions , the rate of enzyme degradation is doubled with no change in the pinocytic rate of the cells .
	manualset3
88147	1	398793	13	NULL	NULL	0	NULL	translation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in the absence of late translation the L1 pre-mRNA was aberrantly spliced .
	manualset3
88148	2	398793	13	NULL	NULL	0	NULL	L1 pre-mRNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in the absence of late translation the L1 pre-mRNA was aberrantly spliced .
	manualset3
88149	1	398794	13	NULL	NULL	0	NULL	rose bengal group	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in the illuminated rose bengal group , electrophysiological changes ( inversion of the terminal portion of the T wave and an increase in Q-T interval ) were observed within 11.8 + / - 2.1 seconds ( i.e. , less than 60 beats ) .
	manualset3
88150	2	398794	13	NULL	NULL	NULL	NULL	electrophysiological changes	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , in the illuminated rose bengal group , electrophysiological changes ( inversion of the terminal portion of the T wave and an increase in Q-T interval ) were observed within 11.8 + / - 2.1 seconds ( i.e. , less than 60 beats ) .
	manualset3
88151	3	398794	13	NULL	NULL	NULL	NULL	inversion 	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , in the illuminated rose bengal group , electrophysiological changes ( inversion of the terminal portion of the T wave and an increase in Q-T interval ) were observed within 11.8 + / - 2.1 seconds ( i.e. , less than 60 beats ) .
	manualset3
88152	4	398794	13	NULL	NULL	NULL	NULL	Q-T interval 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , in the illuminated rose bengal group , electrophysiological changes ( inversion of the terminal portion of the T wave and an increase in Q-T interval ) were observed within 11.8 + / - 2.1 seconds ( i.e. , less than 60 beats ) .
	manualset3
88153	5	398794	13	NULL	NULL	0	NULL	11.8 + / - 2.1 seconds 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in the illuminated rose bengal group , electrophysiological changes ( inversion of the terminal portion of the T wave and an increase in Q-T interval ) were observed within 11.8 + / - 2.1 seconds ( i.e. , less than 60 beats ) .
	manualset3
88154	6	398794	13	NULL	NULL	0	NULL	less than 60 beats	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in the illuminated rose bengal group , electrophysiological changes ( inversion of the terminal portion of the T wave and an increase in Q-T interval ) were observed within 11.8 + / - 2.1 seconds ( i.e. , less than 60 beats ) .
	manualset3
89540	7	398794	13	NULL	NULL	0	NULL	T wave	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in the illuminated rose bengal group , electrophysiological changes ( inversion of the terminal portion of the T wave and an increase in Q-T interval ) were observed within 11.8 + / - 2.1 seconds ( i.e. , less than 60 beats ) .
	manualset3
88155	1	398795	13	NULL	NULL	NULL	NULL	artificial articular cartilage-PVA-hydrogel 	NonProteinOrNucleicAcidChemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The development of a kind of artificial articular cartilage-PVA-hydrogel ) .
	manualset3
88297	2	398795	13	NULL	NULL	0	NULL	development	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( The development of a kind of artificial articular cartilage-PVA-hydrogel ) .
	manualset3
88156	1	398796	13	NULL	NULL	0	NULL	positive control cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in the positive control cells treated with gliotoxin and PMA ( phorbol 12 myristate-13 acetate ) , a significant increase in apoptotic and necrotic cells was seen .
	manualset3
88157	2	398796	13	NULL	NULL	0	NULL	 gliotoxin	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in the positive control cells treated with gliotoxin and PMA ( phorbol 12 myristate-13 acetate ) , a significant increase in apoptotic and necrotic cells was seen .
	manualset3
88158	3	398796	13	NULL	NULL	0	NULL	 PMA ( phorbol 12 myristate-13 acetate )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in the positive control cells treated with gliotoxin and PMA ( phorbol 12 myristate-13 acetate ) , a significant increase in apoptotic and necrotic cells was seen .
	manualset3
88159	4	398796	13	NULL	NULL	0	NULL	apoptotic cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in the positive control cells treated with gliotoxin and PMA ( phorbol 12 myristate-13 acetate ) , a significant increase in apoptotic and necrotic cells was seen .
	manualset3
88160	5	398796	13	NULL	NULL	0	NULL	necrotic cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in the positive control cells treated with gliotoxin and PMA ( phorbol 12 myristate-13 acetate ) , a significant increase in apoptotic and necrotic cells was seen .
	manualset3
88161	1	398797	13	NULL	NULL	0	NULL	EGF	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in the presence of EGF , overexpression of ERMBMPs induced remarkable microvillar elongation in A431 cells .
	manualset3
88162	2	398797	13	NULL	NULL	0	NULL	overexpression of ERMBMPs	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in the presence of EGF , overexpression of ERMBMPs induced remarkable microvillar elongation in A431 cells .
	manualset3
88163	3	398797	13	NULL	NULL	0	NULL	microvillar elongation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in the presence of EGF , overexpression of ERMBMPs induced remarkable microvillar elongation in A431 cells .
	manualset3
88164	4	398797	13	NULL	NULL	0	NULL	A431 cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in the presence of EGF , overexpression of ERMBMPs induced remarkable microvillar elongation in A431 cells .
	manualset3
88165	1	398798	13	NULL	NULL	NULL	NULL	pressures	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , in the range of pressures over 10 ( -5 ) Torr the measured tritium counting rate was found to be getting smaller than the expected with increase in tritium pressure .
	manualset3
88166	2	398798	13	NULL	NULL	0	NULL	tritium counting rate	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in the range of pressures over 10 ( -5 ) Torr the measured tritium counting rate was found to be getting smaller than the expected with increase in tritium pressure .
	manualset3
88167	3	398798	13	NULL	NULL	0	NULL	tritium pressure	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in the range of pressures over 10 ( -5 ) Torr the measured tritium counting rate was found to be getting smaller than the expected with increase in tritium pressure .
	manualset3
88298	4	398798	13	NULL	NULL	0	NULL	 10 ( -5 ) Torr	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in the range of pressures over 10 ( -5 ) Torr the measured tritium counting rate was found to be getting smaller than the expected with increase in tritium pressure .
	manualset3
88168	1	398799	13	NULL	NULL	NULL	NULL	research field	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , in the research field , we emphasize the need to look for other methods to improve reverse cholesterol transport , irrespective of HDL-C levels .
	manualset3
88169	2	398799	13	NULL	NULL	NULL	NULL	 methods	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , in the research field , we emphasize the need to look for other methods to improve reverse cholesterol transport , irrespective of HDL-C levels .
	manualset3
88170	3	398799	13	NULL	NULL	NULL	NULL	cholesterol transport	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , in the research field , we emphasize the need to look for other methods to improve reverse cholesterol transport , irrespective of HDL-C levels .
	manualset3
88171	4	398799	13	NULL	NULL	0	NULL	HDL-C levels	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , in the research field , we emphasize the need to look for other methods to improve reverse cholesterol transport , irrespective of HDL-C levels .
	manualset3
88172	1	398800	13	NULL	NULL	0	NULL	new class of agents	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , introduction of the new class of agents that target beta-glucan synthase ( echinocandins ) has invigorated the prospects of combination therapy .
	manualset3
88173	2	398800	13	NULL	NULL	0	NULL	beta-glucan synthase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , introduction of the new class of agents that target beta-glucan synthase ( echinocandins ) has invigorated the prospects of combination therapy .
	manualset3
88174	3	398800	13	NULL	NULL	0	NULL	echinocandins	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , introduction of the new class of agents that target beta-glucan synthase ( echinocandins ) has invigorated the prospects of combination therapy .
	manualset3
88175	4	398800	13	NULL	NULL	0	NULL	combination therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , introduction of the new class of agents that target beta-glucan synthase ( echinocandins ) has invigorated the prospects of combination therapy .
	manualset3
88176	1	398801	13	NULL	NULL	0	NULL	ionophores	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , ionophores ( 200 mM ) in conjunction with TPA ( 20 ng/ml ) induced release of NKCF .
	manualset3
88177	2	398801	13	NULL	NULL	0	NULL	 200 mM 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , ionophores ( 200 mM ) in conjunction with TPA ( 20 ng/ml ) induced release of NKCF .
	manualset3
88178	3	398801	13	NULL	NULL	0	NULL	TPA 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , ionophores ( 200 mM ) in conjunction with TPA ( 20 ng/ml ) induced release of NKCF .
	manualset3
88179	4	398801	13	NULL	NULL	0	NULL	20 ng/ml 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , ionophores ( 200 mM ) in conjunction with TPA ( 20 ng/ml ) induced release of NKCF .
	manualset3
88180	5	398801	13	NULL	NULL	0	NULL	release of NKCF	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , ionophores ( 200 mM ) in conjunction with TPA ( 20 ng/ml ) induced release of NKCF .
	manualset3
88181	1	398802	13	NULL	NULL	NULL	NULL	diagnosis	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The diagnosis of pregnancy ) .
	manualset3
88182	2	398802	13	NULL	NULL	0	NULL	pregnancy	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The diagnosis of pregnancy ) .
	manualset3
88183	1	398803	13	NULL	NULL	0	NULL	FDA 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it is expected that the FDA will soon include cantharidin on its `` Bulk Substances List , '' which would permit physicians or pharmacists to compound cantharidin to be used in the office for individual patients .
	manualset3
88215	2	398803	13	NULL	NULL	0	NULL	cantharidin 	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it is expected that the FDA will soon include cantharidin on its `` Bulk Substances List , '' which would permit physicians or pharmacists to compound cantharidin to be used in the office for individual patients .
	manualset3
88216	3	398803	13	NULL	NULL	0	NULL	Bulk Substances List 	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it is expected that the FDA will soon include cantharidin on its `` Bulk Substances List , '' which would permit physicians or pharmacists to compound cantharidin to be used in the office for individual patients .
	manualset3
88217	4	398803	13	NULL	NULL	0	NULL	physicians	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it is expected that the FDA will soon include cantharidin on its `` Bulk Substances List , '' which would permit physicians or pharmacists to compound cantharidin to be used in the office for individual patients .
	manualset3
88218	5	398803	13	NULL	NULL	0	NULL	pharmacists	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it is expected that the FDA will soon include cantharidin on its `` Bulk Substances List , '' which would permit physicians or pharmacists to compound cantharidin to be used in the office for individual patients .
	manualset3
88219	6	398803	13	NULL	NULL	0	NULL	cantharidin	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it is expected that the FDA will soon include cantharidin on its `` Bulk Substances List , '' which would permit physicians or pharmacists to compound cantharidin to be used in the office for individual patients .
	manualset3
88220	7	398803	13	NULL	NULL	0	NULL	office	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it is expected that the FDA will soon include cantharidin on its `` Bulk Substances List , '' which would permit physicians or pharmacists to compound cantharidin to be used in the office for individual patients .
	manualset3
88221	8	398803	13	NULL	NULL	0	NULL	individual patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it is expected that the FDA will soon include cantharidin on its `` Bulk Substances List , '' which would permit physicians or pharmacists to compound cantharidin to be used in the office for individual patients .
	manualset3
88222	1	398804	13	NULL	NULL	0	NULL	PHN 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it is much less effective against PHN , which occurs more commonly and more severely in older patients .
	manualset3
88223	2	398804	13	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it is much less effective against PHN , which occurs more commonly and more severely in older patients .
	manualset3
88224	1	398805	13	NULL	NULL	0	NULL	arginine	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it is not known whether such high concentrations of arginine are unique for porcine allantoic fluid or whether they represent an important physiological phenomenon for mammals .
	manualset3
88225	2	398805	13	NULL	NULL	0	NULL	porcine allantoic fluid	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it is not known whether such high concentrations of arginine are unique for porcine allantoic fluid or whether they represent an important physiological phenomenon for mammals .
	manualset3
88226	3	398805	13	NULL	NULL	0	NULL	physiological phenomenon	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it is not known whether such high concentrations of arginine are unique for porcine allantoic fluid or whether they represent an important physiological phenomenon for mammals .
	manualset3
88227	4	398805	13	NULL	NULL	0	NULL	mammals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it is not known whether such high concentrations of arginine are unique for porcine allantoic fluid or whether they represent an important physiological phenomenon for mammals .
	manualset3
88244	5	398805	13	NULL	NULL	0	NULL	concentrations	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it is not known whether such high concentrations of arginine are unique for porcine allantoic fluid or whether they represent an important physiological phenomenon for mammals .
	manualset3
88228	1	398806	13	NULL	NULL	NULL	NULL	training	EnvironmentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , it is unclear how different forms of training affect the response of these hormones .
	manualset3
88229	2	398806	13	NULL	NULL	NULL	NULL	hormones	NonProteinOrNucleicAcidChemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , it is unclear how different forms of training affect the response of these hormones .
	manualset3
88230	1	398807	13	NULL	NULL	0	NULL	KIBRA	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it is unclear whether or how KIBRA is connected to the Hippo pathway in mammalian cells .
	manualset3
88231	2	398807	13	NULL	NULL	0	NULL	Hippo pathway	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it is unclear whether or how KIBRA is connected to the Hippo pathway in mammalian cells .
	manualset3
88232	3	398807	13	NULL	NULL	0	NULL	mammalian cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it is unclear whether or how KIBRA is connected to the Hippo pathway in mammalian cells .
	manualset3
88233	1	398808	13	NULL	NULL	0	NULL	patients 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it remains unclear whether patients with hematological disorders are at a higher risk of B19 infection .
	manualset3
88234	2	398808	13	NULL	NULL	0	NULL	hematological disorders	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it remains unclear whether patients with hematological disorders are at a higher risk of B19 infection .
	manualset3
88235	3	398808	13	NULL	NULL	0	NULL	risk of B19 infection 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it remains unclear whether patients with hematological disorders are at a higher risk of B19 infection .
	manualset3
88236	1	398809	13	NULL	NULL	0	NULL	zoledronic acid monotherapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it was markedly regressed after zoledronic acid monotherapy , and the patient 's symptoms almost disappeared .
	manualset3
88237	2	398809	13	NULL	NULL	0	NULL	patient 's symptoms	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it was markedly regressed after zoledronic acid monotherapy , and the patient 's symptoms almost disappeared .
	manualset3
88238	2	398810	13	NULL	NULL	NULL	NULL	axonal stump	CellComponent												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , it was not the absolute length of the axonal stump that determined the response to transection , but rather its length relative to the lengths of the cell 's other processes .
	manualset3
88239	3	398810	13	NULL	NULL	NULL	NULL	transection	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , it was not the absolute length of the axonal stump that determined the response to transection , but rather its length relative to the lengths of the cell 's other processes .
	manualset3
88240	1	398810	13	NULL	NULL	0	NULL	length	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it was not the absolute length of the axonal stump that determined the response to transection , but rather its length relative to the lengths of the cell 's other processes .
	manualset3
88241	4	398810	13	NULL	NULL	0	NULL	length 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it was not the absolute length of the axonal stump that determined the response to transection , but rather its length relative to the lengths of the cell 's other processes .
	manualset3
88242	5	398810	13	NULL	NULL	0	NULL	lengths 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it was not the absolute length of the axonal stump that determined the response to transection , but rather its length relative to the lengths of the cell 's other processes .
	manualset3
88243	6	398810	13	NULL	NULL	0	NULL	cell 's other processes	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	However , it was not the absolute length of the axonal stump that determined the response to transection , but rather its length relative to the lengths of the cell 's other processes .
	manualset3
88245	1	398811	13	NULL	NULL	0	NULL	renin inhibitors	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , large differences between the potencies of renin inhibitors as measured in human and marmoset plasma were observed .
	manualset3
88246	2	398811	13	NULL	NULL	NULL	NULL	human plasma	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , large differences between the potencies of renin inhibitors as measured in human and marmoset plasma were observed .
	manualset3
88247	3	398811	13	NULL	NULL	0	NULL	 marmoset plasma	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , large differences between the potencies of renin inhibitors as measured in human and marmoset plasma were observed .
	manualset3
88248	1	398812	13	NULL	NULL	NULL	NULL	field gradients 	LaboratoryExperimentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , later it was recognized that field gradients or inhomogeneous fields were not necessary to separate large DNA fragments , and nowadays , PFGE is generally used to mean pulsed-field gel electrophoresis , i.e. , all kinds of methods involving switching ( pulsing ) of fields to separate large DNAs .
	manualset3
88249	2	398812	13	NULL	NULL	NULL	NULL	inhomogeneous fields	LaboratoryExperimentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , later it was recognized that field gradients or inhomogeneous fields were not necessary to separate large DNA fragments , and nowadays , PFGE is generally used to mean pulsed-field gel electrophoresis , i.e. , all kinds of methods involving switching ( pulsing ) of fields to separate large DNAs .
	manualset3
88250	3	398812	13	NULL	NULL	0	NULL	DNA fragments	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , later it was recognized that field gradients or inhomogeneous fields were not necessary to separate large DNA fragments , and nowadays , PFGE is generally used to mean pulsed-field gel electrophoresis , i.e. , all kinds of methods involving switching ( pulsing ) of fields to separate large DNAs .
	manualset3
88251	4	398812	13	NULL	NULL	0	NULL	PFGE 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , later it was recognized that field gradients or inhomogeneous fields were not necessary to separate large DNA fragments , and nowadays , PFGE is generally used to mean pulsed-field gel electrophoresis , i.e. , all kinds of methods involving switching ( pulsing ) of fields to separate large DNAs .
	manualset3
88252	5	398812	13	NULL	NULL	0	NULL	pulsed-field gel electrophoresis 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , later it was recognized that field gradients or inhomogeneous fields were not necessary to separate large DNA fragments , and nowadays , PFGE is generally used to mean pulsed-field gel electrophoresis , i.e. , all kinds of methods involving switching ( pulsing ) of fields to separate large DNAs .
	manualset3
88253	6	398812	13	NULL	NULL	0	NULL	methods involving switching ( pulsing ) of fields	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , later it was recognized that field gradients or inhomogeneous fields were not necessary to separate large DNA fragments , and nowadays , PFGE is generally used to mean pulsed-field gel electrophoresis , i.e. , all kinds of methods involving switching ( pulsing ) of fields to separate large DNAs .
	manualset3
88254	7	398812	13	NULL	NULL	0	NULL	DNAs	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , later it was recognized that field gradients or inhomogeneous fields were not necessary to separate large DNA fragments , and nowadays , PFGE is generally used to mean pulsed-field gel electrophoresis , i.e. , all kinds of methods involving switching ( pulsing ) of fields to separate large DNAs .
	manualset3
88255	1	398813	13	NULL	NULL	0	NULL	learning	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , learning to choose advantageously was moderated by sex of participant .
	manualset3
88257	3	398813	13	NULL	NULL	0	NULL	 participant	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , learning to choose advantageously was moderated by sex of participant .
	manualset3
88258	1	398814	13	NULL	NULL	NULL	NULL	 linear acceleration	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , linear acceleration can be received by otolith organ and produce a sensation that is different from that on Earth .
	manualset3
88259	2	398814	13	NULL	NULL	0	NULL	otolith organ	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , linear acceleration can be received by otolith organ and produce a sensation that is different from that on Earth .
	manualset3
88260	3	398814	13	NULL	NULL	0	NULL	sensation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , linear acceleration can be received by otolith organ and produce a sensation that is different from that on Earth .
	manualset3
88261	4	398814	13	NULL	NULL	0	NULL	Earth	GeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , linear acceleration can be received by otolith organ and produce a sensation that is different from that on Earth .
	manualset3
88262	1	398815	13	NULL	NULL	0	NULL	veins of vascular brain tumors 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( The draining veins of vascular brain tumors in serial angiograms ) .
	manualset3
88263	2	398815	13	NULL	NULL	0	NULL	angiograms	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The draining veins of vascular brain tumors in serial angiograms ) .
	manualset3
88264	1	398816	13	NULL	NULL	0	NULL	Agrobacterium	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , little is known regarding Agrobacterium persistence in tree species .
	manualset3
88265	2	398816	13	NULL	NULL	0	NULL	persistence	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , little is known regarding Agrobacterium persistence in tree species .
	manualset3
88266	3	398816	13	NULL	NULL	0	NULL	 tree species 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , little is known regarding Agrobacterium persistence in tree species .
	manualset3
88267	1	398817	13	NULL	NULL	0	NULL	macrophages	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , macrophages of acutely and chronically stressed mice showed inhibition of NO after incubation with MK886 in-vitro .
	manualset3
88268	2	398817	13	NULL	NULL	0	NULL	mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , macrophages of acutely and chronically stressed mice showed inhibition of NO after incubation with MK886 in-vitro .
	manualset3
88269	3	398817	13	NULL	NULL	0	NULL	 inhibition of NO	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , macrophages of acutely and chronically stressed mice showed inhibition of NO after incubation with MK886 in-vitro .
	manualset3
88270	4	398817	13	NULL	NULL	0	NULL	incubation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , macrophages of acutely and chronically stressed mice showed inhibition of NO after incubation with MK886 in-vitro .
	manualset3
88271	5	398817	13	NULL	NULL	0	NULL	MK886	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , macrophages of acutely and chronically stressed mice showed inhibition of NO after incubation with MK886 in-vitro .
	manualset3
88272	1	398818	13	NULL	NULL	0	NULL	male knockout mice 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , male knockout mice are subfertile and produce sperm with abnormal heads .
	manualset3
88273	2	398818	13	NULL	NULL	0	NULL	subfertile	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , male knockout mice are subfertile and produce sperm with abnormal heads .
	manualset3
88274	3	398818	13	NULL	NULL	0	NULL	 sperm	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , male knockout mice are subfertile and produce sperm with abnormal heads .
	manualset3
88275	4	398818	13	NULL	NULL	0	NULL	abnormal heads	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	However , male knockout mice are subfertile and produce sperm with abnormal heads .
	manualset3
88276	1	398819	13	NULL	NULL	0	NULL	malignant neoplasms	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , malignant neoplasms could be differentiated from benign neoplasms in 88 % of the cases .
	manualset3
88277	2	398819	13	NULL	NULL	0	NULL	benign neoplasms	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , malignant neoplasms could be differentiated from benign neoplasms in 88 % of the cases .
	manualset3
88278	3	398819	13	NULL	NULL	0	NULL	88 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , malignant neoplasms could be differentiated from benign neoplasms in 88 % of the cases .
	manualset3
88279	4	398819	13	NULL	NULL	0	NULL	 cases	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , malignant neoplasms could be differentiated from benign neoplasms in 88 % of the cases .
	manualset3
88280	1	398820	13	NULL	NULL	0	NULL	disease ( stage IV compared with stage IIIB )	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , more advanced disease ( stage IV compared with stage IIIB ) was associated with lower SOD activity .
	manualset3
88281	2	398820	13	NULL	NULL	0	NULL	SOD activity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , more advanced disease ( stage IV compared with stage IIIB ) was associated with lower SOD activity .
	manualset3
88282	1	398821	13	NULL	NULL	0	NULL	mortality	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , mortality and post-operative stay are not increased .
	manualset3
88283	2	398821	13	NULL	NULL	0	NULL	post-operative stay	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , mortality and post-operative stay are not increased .
	manualset3
88284	1	398822	13	NULL	NULL	0	NULL	12-deoxyphorbol 13-phenylacetate 20-acetate	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neither 12-deoxyphorbol 13-phenylacetate 20-acetate , which selectively activates cPKC-beta , nor ingenol 3 , 20-dibenzoate , which selectively activates nPKC-epsilon , exerted such an effect .
	manualset3
88285	2	398822	13	NULL	NULL	0	NULL	cPKC-beta	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neither 12-deoxyphorbol 13-phenylacetate 20-acetate , which selectively activates cPKC-beta , nor ingenol 3 , 20-dibenzoate , which selectively activates nPKC-epsilon , exerted such an effect .
	manualset3
88286	3	398822	13	NULL	NULL	0	NULL	ingenol 3 , 20-dibenzoate	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neither 12-deoxyphorbol 13-phenylacetate 20-acetate , which selectively activates cPKC-beta , nor ingenol 3 , 20-dibenzoate , which selectively activates nPKC-epsilon , exerted such an effect .
	manualset3
88287	4	398822	13	NULL	NULL	0	NULL	nPKC-epsilon	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neither 12-deoxyphorbol 13-phenylacetate 20-acetate , which selectively activates cPKC-beta , nor ingenol 3 , 20-dibenzoate , which selectively activates nPKC-epsilon , exerted such an effect .
	manualset3
88288	1	398823	13	NULL	NULL	NULL	NULL	age	Time												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , neither advanced age nor severity of COPD , body mass index , or comorbidity significantly correlated with the total cost .
	manualset3
88289	2	398823	13	NULL	NULL	0	NULL	severity of COPD	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neither advanced age nor severity of COPD , body mass index , or comorbidity significantly correlated with the total cost .
	manualset3
88290	3	398823	13	NULL	NULL	0	NULL	body mass index	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neither advanced age nor severity of COPD , body mass index , or comorbidity significantly correlated with the total cost .
	manualset3
88291	4	398823	13	NULL	NULL	0	NULL	comorbidity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neither advanced age nor severity of COPD , body mass index , or comorbidity significantly correlated with the total cost .
	manualset3
88292	5	398823	13	NULL	NULL	0	NULL	cost	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neither advanced age nor severity of COPD , body mass index , or comorbidity significantly correlated with the total cost .
	manualset3
88299	1	398824	13	NULL	NULL	0	NULL	PMB	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neither free PMB nor the PMB-IgG conjugate could protect mice challenged with endotoxin 2 h after administration .
	manualset3
88300	2	398824	13	NULL	NULL	0	NULL	 PMB-IgG conjugate	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neither free PMB nor the PMB-IgG conjugate could protect mice challenged with endotoxin 2 h after administration .
	manualset3
88301	3	398824	13	NULL	NULL	0	NULL	mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neither free PMB nor the PMB-IgG conjugate could protect mice challenged with endotoxin 2 h after administration .
	manualset3
88302	4	398824	13	NULL	NULL	0	NULL	 endotoxin 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neither free PMB nor the PMB-IgG conjugate could protect mice challenged with endotoxin 2 h after administration .
	manualset3
88303	5	398824	13	NULL	NULL	0	NULL	2 h	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neither free PMB nor the PMB-IgG conjugate could protect mice challenged with endotoxin 2 h after administration .
	manualset3
88304	6	398824	13	NULL	NULL	0	NULL	administration	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neither free PMB nor the PMB-IgG conjugate could protect mice challenged with endotoxin 2 h after administration .
	manualset3
88305	1	398825	13	NULL	NULL	0	NULL	2	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neither of the 2 enriched environments proved consistent superiority or inferiority across all traits .
	manualset3
88306	2	398825	13	NULL	NULL	0	NULL	environments	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neither of the 2 enriched environments proved consistent superiority or inferiority across all traits .
	manualset3
88307	3	398825	13	NULL	NULL	NULL	NULL	 superiority	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , neither of the 2 enriched environments proved consistent superiority or inferiority across all traits .
	manualset3
88494	4	398825	13	NULL	NULL	0	NULL	 inferiority	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neither of the 2 enriched environments proved consistent superiority or inferiority across all traits .
	manualset3
88495	5	398825	13	NULL	NULL	0	NULL	traits	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neither of the 2 enriched environments proved consistent superiority or inferiority across all traits .
	manualset3
88308	1	398826	13	NULL	NULL	0	NULL	 neutralization	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neutralization of TNF-alpha by specific anti-TNF-alpha antibody had no effect on FasL-induced apoptosis .
	manualset3
88309	2	398826	13	NULL	NULL	0	NULL	TNF-alpha	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neutralization of TNF-alpha by specific anti-TNF-alpha antibody had no effect on FasL-induced apoptosis .
	manualset3
88310	3	398826	13	NULL	NULL	0	NULL	anti-TNF-alpha antibody	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neutralization of TNF-alpha by specific anti-TNF-alpha antibody had no effect on FasL-induced apoptosis .
	manualset3
88311	4	398826	13	NULL	NULL	0	NULL	FasL-induced apoptosis 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , neutralization of TNF-alpha by specific anti-TNF-alpha antibody had no effect on FasL-induced apoptosis .
	manualset3
88312	1	398827	13	NULL	NULL	0	NULL	 nitrogenase activity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , nitrogenase activity under oxic conditions was impaired in strain CSAV135 ( cox3 ) and undetectable in strain CSAV141 ( cox2 cox3 ) .
	manualset3
88313	2	398827	13	NULL	NULL	0	NULL	oxic conditions	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , nitrogenase activity under oxic conditions was impaired in strain CSAV135 ( cox3 ) and undetectable in strain CSAV141 ( cox2 cox3 ) .
	manualset3
88314	3	398827	13	NULL	NULL	0	NULL	strain CSAV135 ( cox3 ) 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , nitrogenase activity under oxic conditions was impaired in strain CSAV135 ( cox3 ) and undetectable in strain CSAV141 ( cox2 cox3 ) .
	manualset3
88315	4	398827	13	NULL	NULL	0	NULL	strain CSAV141 ( cox2 cox3 ) 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , nitrogenase activity under oxic conditions was impaired in strain CSAV135 ( cox3 ) and undetectable in strain CSAV141 ( cox2 cox3 ) .
	manualset3
88316	1	398828	13	NULL	NULL	0	NULL	 MVD differences	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no MVD differences were detected between CLL subgroups subdivided according to the above-mentioned prognostic factors .
	manualset3
88317	2	398828	13	NULL	NULL	0	NULL	CLL subgroups	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no MVD differences were detected between CLL subgroups subdivided according to the above-mentioned prognostic factors .
	manualset3
88318	3	398828	13	NULL	NULL	0	NULL	prognostic factors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no MVD differences were detected between CLL subgroups subdivided according to the above-mentioned prognostic factors .
	manualset3
88319	1	398829	13	NULL	NULL	0	NULL	epithelial defect 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no obvious overlying epithelial defect was detected and an intermittent leakage through micro-perforations in the corneal epithelium was the probable cause of the variable appearance .
	manualset3
88320	2	398829	13	NULL	NULL	0	NULL	leakage	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no obvious overlying epithelial defect was detected and an intermittent leakage through micro-perforations in the corneal epithelium was the probable cause of the variable appearance .
	manualset3
88321	3	398829	13	NULL	NULL	0	NULL	micro-perforations 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no obvious overlying epithelial defect was detected and an intermittent leakage through micro-perforations in the corneal epithelium was the probable cause of the variable appearance .
	manualset3
88322	4	398829	13	NULL	NULL	0	NULL	corneal epithelium	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no obvious overlying epithelial defect was detected and an intermittent leakage through micro-perforations in the corneal epithelium was the probable cause of the variable appearance .
	manualset3
88323	5	398829	13	NULL	NULL	0	NULL	appearance 	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no obvious overlying epithelial defect was detected and an intermittent leakage through micro-perforations in the corneal epithelium was the probable cause of the variable appearance .
	manualset3
88324	1	398830	13	NULL	NULL	0	NULL	scientific study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no scientific study has examined the influence of the time of day when strength training is performed on hormonal adaptations .
	manualset3
88325	2	398830	13	NULL	NULL	0	NULL	 influence 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no scientific study has examined the influence of the time of day when strength training is performed on hormonal adaptations .
	manualset3
88326	3	398830	13	NULL	NULL	0	NULL	time of day	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no scientific study has examined the influence of the time of day when strength training is performed on hormonal adaptations .
	manualset3
88327	4	398830	13	NULL	NULL	0	NULL	 strength	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no scientific study has examined the influence of the time of day when strength training is performed on hormonal adaptations .
	manualset3
88328	5	398830	13	NULL	NULL	0	NULL	training	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no scientific study has examined the influence of the time of day when strength training is performed on hormonal adaptations .
	manualset3
88329	6	398830	13	NULL	NULL	0	NULL	hormonal adaptations	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no scientific study has examined the influence of the time of day when strength training is performed on hormonal adaptations .
	manualset3
88330	1	398831	13	NULL	NULL	0	NULL	consequences	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( The economic consequences of work accidents .
	manualset3
88331	2	398831	13	NULL	NULL	0	NULL	work accidents	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The economic consequences of work accidents .
	manualset3
88332	1	398832	13	NULL	NULL	0	NULL	( 3H ) leucine incorporation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no significant difference in ( 3H ) leucine incorporation was observed before or during the initial Ca2 + transport response observed by Halloran and DeLuca , i.e. , at 1.0 , 3.0 , and 6.5 h following an injection of 1 , 25-dihydroxyvitamin D3 .
	manualset3
88333	2	398832	13	NULL	NULL	0	NULL	Ca2 + transport response	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no significant difference in ( 3H ) leucine incorporation was observed before or during the initial Ca2 + transport response observed by Halloran and DeLuca , i.e. , at 1.0 , 3.0 , and 6.5 h following an injection of 1 , 25-dihydroxyvitamin D3 .
	manualset3
88334	3	398832	13	NULL	NULL	0	NULL	Halloran	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no significant difference in ( 3H ) leucine incorporation was observed before or during the initial Ca2 + transport response observed by Halloran and DeLuca , i.e. , at 1.0 , 3.0 , and 6.5 h following an injection of 1 , 25-dihydroxyvitamin D3 .
	manualset3
88335	4	398832	13	NULL	NULL	0	NULL	DeLuca	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no significant difference in ( 3H ) leucine incorporation was observed before or during the initial Ca2 + transport response observed by Halloran and DeLuca , i.e. , at 1.0 , 3.0 , and 6.5 h following an injection of 1 , 25-dihydroxyvitamin D3 .
	manualset3
88336	5	398832	13	NULL	NULL	0	NULL	1.0 h	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no significant difference in ( 3H ) leucine incorporation was observed before or during the initial Ca2 + transport response observed by Halloran and DeLuca , i.e. , at 1.0 , 3.0 , and 6.5 h following an injection of 1 , 25-dihydroxyvitamin D3 .
	manualset3
88337	6	398832	13	NULL	NULL	0	NULL	3.0 h	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no significant difference in ( 3H ) leucine incorporation was observed before or during the initial Ca2 + transport response observed by Halloran and DeLuca , i.e. , at 1.0 , 3.0 , and 6.5 h following an injection of 1 , 25-dihydroxyvitamin D3 .
	manualset3
88338	7	398832	13	NULL	NULL	0	NULL	6.5 h 	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no significant difference in ( 3H ) leucine incorporation was observed before or during the initial Ca2 + transport response observed by Halloran and DeLuca , i.e. , at 1.0 , 3.0 , and 6.5 h following an injection of 1 , 25-dihydroxyvitamin D3 .
	manualset3
88339	8	398832	13	NULL	NULL	0	NULL	injection 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no significant difference in ( 3H ) leucine incorporation was observed before or during the initial Ca2 + transport response observed by Halloran and DeLuca , i.e. , at 1.0 , 3.0 , and 6.5 h following an injection of 1 , 25-dihydroxyvitamin D3 .
	manualset3
88340	9	398832	13	NULL	NULL	0	NULL	1 , 25-dihydroxyvitamin D3	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no significant difference in ( 3H ) leucine incorporation was observed before or during the initial Ca2 + transport response observed by Halloran and DeLuca , i.e. , at 1.0 , 3.0 , and 6.5 h following an injection of 1 , 25-dihydroxyvitamin D3 .
	manualset3
88341	1	398833	13	NULL	NULL	0	NULL	virulence	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no significant virulence differences were observed between wild type , mutant and reconstituted strains in a murine model of pulmonary aspergillosis .
	manualset3
88342	2	398833	13	NULL	NULL	0	NULL	wild type strains 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no significant virulence differences were observed between wild type , mutant and reconstituted strains in a murine model of pulmonary aspergillosis .
	manualset3
88343	3	398833	13	NULL	NULL	0	NULL	mutant strains	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no significant virulence differences were observed between wild type , mutant and reconstituted strains in a murine model of pulmonary aspergillosis .
	manualset3
88344	4	398833	13	NULL	NULL	0	NULL	reconstituted strains	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no significant virulence differences were observed between wild type , mutant and reconstituted strains in a murine model of pulmonary aspergillosis .
	manualset3
88345	5	398833	13	NULL	NULL	NULL	NULL	murine model 	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , no significant virulence differences were observed between wild type , mutant and reconstituted strains in a murine model of pulmonary aspergillosis .
	manualset3
88346	6	398833	13	NULL	NULL	0	NULL	pulmonary aspergillosis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , no significant virulence differences were observed between wild type , mutant and reconstituted strains in a murine model of pulmonary aspergillosis .
	manualset3
88347	1	398834	13	NULL	NULL	0	NULL	32 ( + ) DPZn	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	However , notably 32 ( + ) DPZn achieved remarkably higher ( 1 ) O ( 2 ) - induced cytotoxicity against LLC cells than PIX .
	manualset3
88348	2	398834	13	NULL	NULL	0	NULL	( 1 ) O ( 2 ) 	Atom												NULL		0	NULL	NULL	NULL	NULL	NULL	However , notably 32 ( + ) DPZn achieved remarkably higher ( 1 ) O ( 2 ) - induced cytotoxicity against LLC cells than PIX .
	manualset3
88350	3	398834	13	NULL	NULL	0	NULL	cytotoxicity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , notably 32 ( + ) DPZn achieved remarkably higher ( 1 ) O ( 2 ) - induced cytotoxicity against LLC cells than PIX .
	manualset3
88351	4	398834	13	NULL	NULL	0	NULL	LLC cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , notably 32 ( + ) DPZn achieved remarkably higher ( 1 ) O ( 2 ) - induced cytotoxicity against LLC cells than PIX .
	manualset3
88352	5	398834	13	NULL	NULL	0	NULL	PIX	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , notably 32 ( + ) DPZn achieved remarkably higher ( 1 ) O ( 2 ) - induced cytotoxicity against LLC cells than PIX .
	manualset3
88365	1	398835	13	NULL	NULL	NULL	NULL	mouse models	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , now that we have mouse or large-animal models for most forms of NCL , we can investigate pathogenesis and compare what happens in the brain in different types of the disease .
	manualset3
88367	2	398835	13	NULL	NULL	NULL	NULL	large-animal models	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , now that we have mouse or large-animal models for most forms of NCL , we can investigate pathogenesis and compare what happens in the brain in different types of the disease .
	manualset3
88371	3	398835	13	NULL	NULL	0	NULL	NCL	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , now that we have mouse or large-animal models for most forms of NCL , we can investigate pathogenesis and compare what happens in the brain in different types of the disease .
	manualset3
88372	4	398835	13	NULL	NULL	0	NULL	 pathogenesis 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , now that we have mouse or large-animal models for most forms of NCL , we can investigate pathogenesis and compare what happens in the brain in different types of the disease .
	manualset3
88373	5	398835	13	NULL	NULL	0	NULL	brain 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , now that we have mouse or large-animal models for most forms of NCL , we can investigate pathogenesis and compare what happens in the brain in different types of the disease .
	manualset3
88379	6	398835	13	NULL	NULL	0	NULL	disease 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , now that we have mouse or large-animal models for most forms of NCL , we can investigate pathogenesis and compare what happens in the brain in different types of the disease .
	manualset3
88384	1	398836	13	NULL	NULL	0	NULL	 biofilm bacteria	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , on suspension of the biofilm bacteria , glycocalyx-mediated resistance was lost .
	manualset3
88385	2	398836	13	NULL	NULL	0	NULL	glycocalyx-mediated resistance	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , on suspension of the biofilm bacteria , glycocalyx-mediated resistance was lost .
	manualset3
88386	3	398836	13	NULL	NULL	0	NULL	 suspension	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	However , on suspension of the biofilm bacteria , glycocalyx-mediated resistance was lost .
	manualset3
88388	1	398837	13	NULL	NULL	0	NULL	mind 	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , one should been in mind that systemic heparinization itself carries a potential risk of hemorrhage .
	manualset3
88389	2	398837	13	NULL	NULL	0	NULL	heparinization 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , one should been in mind that systemic heparinization itself carries a potential risk of hemorrhage .
	manualset3
88390	3	398837	13	NULL	NULL	0	NULL	 risk of hemorrhage 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , one should been in mind that systemic heparinization itself carries a potential risk of hemorrhage .
	manualset3
88391	1	398838	13	NULL	NULL	0	NULL	 minority	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only a minority of familial gastric cancers can be accounted for by CDH1 mutations .
	manualset3
88392	2	398838	13	NULL	NULL	0	NULL	familial gastric cancers	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only a minority of familial gastric cancers can be accounted for by CDH1 mutations .
	manualset3
88393	3	398838	13	NULL	NULL	0	NULL	CDH1 mutations	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only a minority of familial gastric cancers can be accounted for by CDH1 mutations .
	manualset3
88394	1	398839	13	NULL	NULL	NULL	NULL	small fraction ( 0.07-0 .32 % )	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , only a small fraction ( 0.07-0 .32 % ) of the TFIIIB70 from these sources results in the synthesis of full-length RNA .
	manualset3
88397	2	398839	13	NULL	NULL	0	NULL	TFIIIB70	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only a small fraction ( 0.07-0 .32 % ) of the TFIIIB70 from these sources results in the synthesis of full-length RNA .
	manualset3
88399	3	398839	13	NULL	NULL	0	NULL	synthesis of full-length RNA	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only a small fraction ( 0.07-0 .32 % ) of the TFIIIB70 from these sources results in the synthesis of full-length RNA .
	manualset3
88423	1	398840	13	NULL	NULL	0	NULL	adrenoblockaders	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( The effect of adrenoblockaders on the rate of H3-catecholamine synthesis and uptake in the rat seminal duct ) .
	manualset3
88424	2	398840	13	NULL	NULL	0	NULL	rate	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	( The effect of adrenoblockaders on the rate of H3-catecholamine synthesis and uptake in the rat seminal duct ) .
	manualset3
88425	3	398840	13	NULL	NULL	0	NULL	H3-catecholamine synthesis	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The effect of adrenoblockaders on the rate of H3-catecholamine synthesis and uptake in the rat seminal duct ) .
	manualset3
88426	4	398840	13	NULL	NULL	0	NULL	uptake	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The effect of adrenoblockaders on the rate of H3-catecholamine synthesis and uptake in the rat seminal duct ) .
	manualset3
88427	5	398840	13	NULL	NULL	0	NULL	rat seminal duct 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( The effect of adrenoblockaders on the rate of H3-catecholamine synthesis and uptake in the rat seminal duct ) .
	manualset3
88428	1	398841	13	NULL	NULL	0	NULL	 works 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only few works focus their attention on its seeds , which constitute a major byproduct of the tomato processing industry .
	manualset3
88430	3	398841	13	NULL	NULL	0	NULL	attention	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only few works focus their attention on its seeds , which constitute a major byproduct of the tomato processing industry .
	manualset3
88431	4	398841	13	NULL	NULL	0	NULL	seeds	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only few works focus their attention on its seeds , which constitute a major byproduct of the tomato processing industry .
	manualset3
88433	5	398841	13	NULL	NULL	0	NULL	tomato processing industry	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only few works focus their attention on its seeds , which constitute a major byproduct of the tomato processing industry .
	manualset3
88434	1	398842	13	NULL	NULL	0	NULL	JNK1 isoform 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only the JNK1 isoform was phosphorylated and , as determined in single knock-out mice , was necessary for Mkp1 induction by M-CSF or LPS .
	manualset3
88435	2	398842	13	NULL	NULL	0	NULL	single knock-out mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only the JNK1 isoform was phosphorylated and , as determined in single knock-out mice , was necessary for Mkp1 induction by M-CSF or LPS .
	manualset3
88436	3	398842	13	NULL	NULL	0	NULL	Mkp1 induction	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only the JNK1 isoform was phosphorylated and , as determined in single knock-out mice , was necessary for Mkp1 induction by M-CSF or LPS .
	manualset3
88437	4	398842	13	NULL	NULL	0	NULL	M-CSF 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only the JNK1 isoform was phosphorylated and , as determined in single knock-out mice , was necessary for Mkp1 induction by M-CSF or LPS .
	manualset3
88441	5	398842	13	NULL	NULL	0	NULL	 LPS	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only the JNK1 isoform was phosphorylated and , as determined in single knock-out mice , was necessary for Mkp1 induction by M-CSF or LPS .
	manualset3
88445	1	398843	13	NULL	NULL	0	NULL	mutated peptide	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only the mutated peptide could induce specific CTL expansion from PBL .
	manualset3
88446	2	398843	13	NULL	NULL	0	NULL	CTL expansion	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only the mutated peptide could induce specific CTL expansion from PBL .
	manualset3
88447	3	398843	13	NULL	NULL	0	NULL	PBL	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only the mutated peptide could induce specific CTL expansion from PBL .
	manualset3
88448	1	398844	13	NULL	NULL	0	NULL	three-quarters 	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only three-quarters of all strokes can be attributable to known causal risk factors .
	manualset3
88449	2	398844	13	NULL	NULL	0	NULL	strokes	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only three-quarters of all strokes can be attributable to known causal risk factors .
	manualset3
88450	3	398844	13	NULL	NULL	0	NULL	risk factors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , only three-quarters of all strokes can be attributable to known causal risk factors .
	manualset3
88451	1	398845	13	NULL	NULL	0	NULL	peritoneal exudate cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , peritoneal exudate cells continued to respond to exogenous beta carotene in vitro to produce additional cytotoxic materials .
	manualset3
88452	2	398845	13	NULL	NULL	0	NULL	beta carotene 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , peritoneal exudate cells continued to respond to exogenous beta carotene in vitro to produce additional cytotoxic materials .
	manualset3
88453	3	398845	13	NULL	NULL	0	NULL	cytotoxic materials	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , peritoneal exudate cells continued to respond to exogenous beta carotene in vitro to produce additional cytotoxic materials .
	manualset3
88454	1	398846	13	NULL	NULL	0	NULL	 phylogenetic analysis 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , phylogenetic analysis of rpoD gene sequences showed that strain M1 ( T ) exhibited high sequence similarity only with respect to Pseudomonas psycrophila ( 97.42 % ) and P. fragi ( 96.40 % ) and DNA-DNA hybridization experiments between the Antarctic isolate M1 ( T ) and the type strains of these two closely related species revealed relatedness values of 58 and 57 % , respectively .
	manualset3
88455	2	398846	13	NULL	NULL	0	NULL	 rpoD gene sequences 	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , phylogenetic analysis of rpoD gene sequences showed that strain M1 ( T ) exhibited high sequence similarity only with respect to Pseudomonas psycrophila ( 97.42 % ) and P. fragi ( 96.40 % ) and DNA-DNA hybridization experiments between the Antarctic isolate M1 ( T ) and the type strains of these two closely related species revealed relatedness values of 58 and 57 % , respectively .
	manualset3
88456	3	398846	13	NULL	NULL	0	NULL	strain M1 ( T )	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , phylogenetic analysis of rpoD gene sequences showed that strain M1 ( T ) exhibited high sequence similarity only with respect to Pseudomonas psycrophila ( 97.42 % ) and P. fragi ( 96.40 % ) and DNA-DNA hybridization experiments between the Antarctic isolate M1 ( T ) and the type strains of these two closely related species revealed relatedness values of 58 and 57 % , respectively .
	manualset3
88457	4	398846	13	NULL	NULL	NULL	NULL	sequence similarity	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , phylogenetic analysis of rpoD gene sequences showed that strain M1 ( T ) exhibited high sequence similarity only with respect to Pseudomonas psycrophila ( 97.42 % ) and P. fragi ( 96.40 % ) and DNA-DNA hybridization experiments between the Antarctic isolate M1 ( T ) and the type strains of these two closely related species revealed relatedness values of 58 and 57 % , respectively .
	manualset3
88478	5	398846	13	NULL	NULL	0	NULL	Pseudomonas psycrophila	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , phylogenetic analysis of rpoD gene sequences showed that strain M1 ( T ) exhibited high sequence similarity only with respect to Pseudomonas psycrophila ( 97.42 % ) and P. fragi ( 96.40 % ) and DNA-DNA hybridization experiments between the Antarctic isolate M1 ( T ) and the type strains of these two closely related species revealed relatedness values of 58 and 57 % , respectively .
	manualset3
88479	6	398846	13	NULL	NULL	0	NULL	97.42 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , phylogenetic analysis of rpoD gene sequences showed that strain M1 ( T ) exhibited high sequence similarity only with respect to Pseudomonas psycrophila ( 97.42 % ) and P. fragi ( 96.40 % ) and DNA-DNA hybridization experiments between the Antarctic isolate M1 ( T ) and the type strains of these two closely related species revealed relatedness values of 58 and 57 % , respectively .
	manualset3
88480	7	398846	13	NULL	NULL	0	NULL	P. fragi	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , phylogenetic analysis of rpoD gene sequences showed that strain M1 ( T ) exhibited high sequence similarity only with respect to Pseudomonas psycrophila ( 97.42 % ) and P. fragi ( 96.40 % ) and DNA-DNA hybridization experiments between the Antarctic isolate M1 ( T ) and the type strains of these two closely related species revealed relatedness values of 58 and 57 % , respectively .
	manualset3
88481	8	398846	13	NULL	NULL	0	NULL	96.40 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , phylogenetic analysis of rpoD gene sequences showed that strain M1 ( T ) exhibited high sequence similarity only with respect to Pseudomonas psycrophila ( 97.42 % ) and P. fragi ( 96.40 % ) and DNA-DNA hybridization experiments between the Antarctic isolate M1 ( T ) and the type strains of these two closely related species revealed relatedness values of 58 and 57 % , respectively .
	manualset3
88482	9	398846	13	NULL	NULL	0	NULL	 DNA-DNA hybridization experiments	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , phylogenetic analysis of rpoD gene sequences showed that strain M1 ( T ) exhibited high sequence similarity only with respect to Pseudomonas psycrophila ( 97.42 % ) and P. fragi ( 96.40 % ) and DNA-DNA hybridization experiments between the Antarctic isolate M1 ( T ) and the type strains of these two closely related species revealed relatedness values of 58 and 57 % , respectively .
	manualset3
88484	10	398846	13	NULL	NULL	0	NULL	Antarctic isolate M1 ( T ) 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , phylogenetic analysis of rpoD gene sequences showed that strain M1 ( T ) exhibited high sequence similarity only with respect to Pseudomonas psycrophila ( 97.42 % ) and P. fragi ( 96.40 % ) and DNA-DNA hybridization experiments between the Antarctic isolate M1 ( T ) and the type strains of these two closely related species revealed relatedness values of 58 and 57 % , respectively .
	manualset3
88485	11	398846	13	NULL	NULL	0	NULL	strains	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , phylogenetic analysis of rpoD gene sequences showed that strain M1 ( T ) exhibited high sequence similarity only with respect to Pseudomonas psycrophila ( 97.42 % ) and P. fragi ( 96.40 % ) and DNA-DNA hybridization experiments between the Antarctic isolate M1 ( T ) and the type strains of these two closely related species revealed relatedness values of 58 and 57 % , respectively .
	manualset3
88486	12	398846	13	NULL	NULL	NULL	NULL	species	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , phylogenetic analysis of rpoD gene sequences showed that strain M1 ( T ) exhibited high sequence similarity only with respect to Pseudomonas psycrophila ( 97.42 % ) and P. fragi ( 96.40 % ) and DNA-DNA hybridization experiments between the Antarctic isolate M1 ( T ) and the type strains of these two closely related species revealed relatedness values of 58 and 57 % , respectively .
	manualset3
88487	13	398846	13	NULL	NULL	0	NULL	 relatedness values	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , phylogenetic analysis of rpoD gene sequences showed that strain M1 ( T ) exhibited high sequence similarity only with respect to Pseudomonas psycrophila ( 97.42 % ) and P. fragi ( 96.40 % ) and DNA-DNA hybridization experiments between the Antarctic isolate M1 ( T ) and the type strains of these two closely related species revealed relatedness values of 58 and 57 % , respectively .
	manualset3
88488	14	398846	13	NULL	NULL	0	NULL	58 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , phylogenetic analysis of rpoD gene sequences showed that strain M1 ( T ) exhibited high sequence similarity only with respect to Pseudomonas psycrophila ( 97.42 % ) and P. fragi ( 96.40 % ) and DNA-DNA hybridization experiments between the Antarctic isolate M1 ( T ) and the type strains of these two closely related species revealed relatedness values of 58 and 57 % , respectively .
	manualset3
88489	15	398846	13	NULL	NULL	0	NULL	57 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , phylogenetic analysis of rpoD gene sequences showed that strain M1 ( T ) exhibited high sequence similarity only with respect to Pseudomonas psycrophila ( 97.42 % ) and P. fragi ( 96.40 % ) and DNA-DNA hybridization experiments between the Antarctic isolate M1 ( T ) and the type strains of these two closely related species revealed relatedness values of 58 and 57 % , respectively .
	manualset3
88490	1	398847	13	NULL	NULL	0	NULL	physiologic tissue oxygenation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , physiologic tissue oxygenation on its own is not enough to prevent toxicity after perfusion .
	manualset3
88491	2	398847	13	NULL	NULL	0	NULL	toxicity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , physiologic tissue oxygenation on its own is not enough to prevent toxicity after perfusion .
	manualset3
88496	3	398847	13	NULL	NULL	0	NULL	perfusion	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , physiologic tissue oxygenation on its own is not enough to prevent toxicity after perfusion .
	manualset3
88497	1	398848	13	NULL	NULL	0	NULL	 plasma total cholesterol 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , plasma total cholesterol and HDL-cholesterol levels were significantly increased and plasma triglyceride levels were slightly decreased in the pioglitazone + NO-1886 group , compared with the values in the pioglitazone-alone group .
	manualset3
88499	2	398848	13	NULL	NULL	0	NULL	 HDL-cholesterol levels	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , plasma total cholesterol and HDL-cholesterol levels were significantly increased and plasma triglyceride levels were slightly decreased in the pioglitazone + NO-1886 group , compared with the values in the pioglitazone-alone group .
	manualset3
88501	3	398848	13	NULL	NULL	0	NULL	plasma triglyceride levels	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , plasma total cholesterol and HDL-cholesterol levels were significantly increased and plasma triglyceride levels were slightly decreased in the pioglitazone + NO-1886 group , compared with the values in the pioglitazone-alone group .
	manualset3
88504	5	398848	13	NULL	NULL	0	NULL	values	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , plasma total cholesterol and HDL-cholesterol levels were significantly increased and plasma triglyceride levels were slightly decreased in the pioglitazone + NO-1886 group , compared with the values in the pioglitazone-alone group .
	manualset3
88505	6	398848	13	NULL	NULL	NULL	NULL	pioglitazone-alone group	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , plasma total cholesterol and HDL-cholesterol levels were significantly increased and plasma triglyceride levels were slightly decreased in the pioglitazone + NO-1886 group , compared with the values in the pioglitazone-alone group .
	manualset3
91081	7	398848	13	NULL	NULL	0	NULL	 pioglitazone + NO-1886 group	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , plasma total cholesterol and HDL-cholesterol levels were significantly increased and plasma triglyceride levels were slightly decreased in the pioglitazone + NO-1886 group , compared with the values in the pioglitazone-alone group .
	manualset3
88503	1	398849	13	NULL	NULL	NULL	NULL	 pretreatment	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , pretreatment with PD98059 had no effect on EPAS1 phosphorylation during hypoxia , suggesting that MAPK targets other proteins that are critical for the trans-activation of EPAS1 .
	manualset3
88511	2	398849	13	NULL	NULL	0	NULL	PD98059	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , pretreatment with PD98059 had no effect on EPAS1 phosphorylation during hypoxia , suggesting that MAPK targets other proteins that are critical for the trans-activation of EPAS1 .
	manualset3
88512	3	398849	13	NULL	NULL	0	NULL	EPAS1 phosphorylation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , pretreatment with PD98059 had no effect on EPAS1 phosphorylation during hypoxia , suggesting that MAPK targets other proteins that are critical for the trans-activation of EPAS1 .
	manualset3
88514	4	398849	13	NULL	NULL	0	NULL	hypoxia	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , pretreatment with PD98059 had no effect on EPAS1 phosphorylation during hypoxia , suggesting that MAPK targets other proteins that are critical for the trans-activation of EPAS1 .
	manualset3
88516	5	398849	13	NULL	NULL	0	NULL	MAPK targets	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , pretreatment with PD98059 had no effect on EPAS1 phosphorylation during hypoxia , suggesting that MAPK targets other proteins that are critical for the trans-activation of EPAS1 .
	manualset3
88517	6	398849	13	NULL	NULL	NULL	NULL	 proteins	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , pretreatment with PD98059 had no effect on EPAS1 phosphorylation during hypoxia , suggesting that MAPK targets other proteins that are critical for the trans-activation of EPAS1 .
	manualset3
88519	7	398849	13	NULL	NULL	0	NULL	trans-activation of EPAS1	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , pretreatment with PD98059 had no effect on EPAS1 phosphorylation during hypoxia , suggesting that MAPK targets other proteins that are critical for the trans-activation of EPAS1 .
	manualset3
88523	1	398850	13	NULL	NULL	0	NULL	all-trans retinoid acid	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	( The effect of all-trans retinoid acid and sodium selenite ( Na2SeO3 ) on VEGF and its receptor expression in HL-60 cells ) .
	manualset3
88524	2	398850	13	NULL	NULL	0	NULL	sodium selenite ( Na2SeO3 ) 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( The effect of all-trans retinoid acid and sodium selenite ( Na2SeO3 ) on VEGF and its receptor expression in HL-60 cells ) .
	manualset3
88526	3	398850	13	NULL	NULL	0	NULL	VEGF	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	( The effect of all-trans retinoid acid and sodium selenite ( Na2SeO3 ) on VEGF and its receptor expression in HL-60 cells ) .
	manualset3
88528	4	398850	13	NULL	NULL	0	NULL	receptor expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The effect of all-trans retinoid acid and sodium selenite ( Na2SeO3 ) on VEGF and its receptor expression in HL-60 cells ) .
	manualset3
88529	5	398850	13	NULL	NULL	0	NULL	HL-60 cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	( The effect of all-trans retinoid acid and sodium selenite ( Na2SeO3 ) on VEGF and its receptor expression in HL-60 cells ) .
	manualset3
88542	1	398851	13	NULL	NULL	0	NULL	research 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , previous research did not test whether motion sickness increases anticipatory nausea only by increasing the base rate of posttreatment nausea and vomiting ( which has traditionally served as the unconditioned stimulus in the conditioning model for anticipatory nausea ) or , alternatively , whether motion sickness might facilitate the association of external stimuli to posttreatment nausea and vomiting .
	manualset3
88544	2	398851	13	NULL	NULL	0	NULL	motion sickness 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , previous research did not test whether motion sickness increases anticipatory nausea only by increasing the base rate of posttreatment nausea and vomiting ( which has traditionally served as the unconditioned stimulus in the conditioning model for anticipatory nausea ) or , alternatively , whether motion sickness might facilitate the association of external stimuli to posttreatment nausea and vomiting .
	manualset3
88546	3	398851	13	NULL	NULL	NULL	NULL	anticipatory nausea 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , previous research did not test whether motion sickness increases anticipatory nausea only by increasing the base rate of posttreatment nausea and vomiting ( which has traditionally served as the unconditioned stimulus in the conditioning model for anticipatory nausea ) or , alternatively , whether motion sickness might facilitate the association of external stimuli to posttreatment nausea and vomiting .
	manualset3
88548	4	398851	13	NULL	NULL	0	NULL	rate of posttreatment nausea 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , previous research did not test whether motion sickness increases anticipatory nausea only by increasing the base rate of posttreatment nausea and vomiting ( which has traditionally served as the unconditioned stimulus in the conditioning model for anticipatory nausea ) or , alternatively , whether motion sickness might facilitate the association of external stimuli to posttreatment nausea and vomiting .
	manualset3
88549	5	398851	13	NULL	NULL	0	NULL	vomiting	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , previous research did not test whether motion sickness increases anticipatory nausea only by increasing the base rate of posttreatment nausea and vomiting ( which has traditionally served as the unconditioned stimulus in the conditioning model for anticipatory nausea ) or , alternatively , whether motion sickness might facilitate the association of external stimuli to posttreatment nausea and vomiting .
	manualset3
88550	6	398851	13	NULL	NULL	0	NULL	 stimulus	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , previous research did not test whether motion sickness increases anticipatory nausea only by increasing the base rate of posttreatment nausea and vomiting ( which has traditionally served as the unconditioned stimulus in the conditioning model for anticipatory nausea ) or , alternatively , whether motion sickness might facilitate the association of external stimuli to posttreatment nausea and vomiting .
	manualset3
88552	7	398851	13	NULL	NULL	NULL	NULL	conditioning model	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , previous research did not test whether motion sickness increases anticipatory nausea only by increasing the base rate of posttreatment nausea and vomiting ( which has traditionally served as the unconditioned stimulus in the conditioning model for anticipatory nausea ) or , alternatively , whether motion sickness might facilitate the association of external stimuli to posttreatment nausea and vomiting .
	manualset3
88553	8	398851	13	NULL	NULL	0	NULL	anticipatory nausea 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , previous research did not test whether motion sickness increases anticipatory nausea only by increasing the base rate of posttreatment nausea and vomiting ( which has traditionally served as the unconditioned stimulus in the conditioning model for anticipatory nausea ) or , alternatively , whether motion sickness might facilitate the association of external stimuli to posttreatment nausea and vomiting .
	manualset3
88554	9	398851	13	NULL	NULL	0	NULL	motion sickness	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , previous research did not test whether motion sickness increases anticipatory nausea only by increasing the base rate of posttreatment nausea and vomiting ( which has traditionally served as the unconditioned stimulus in the conditioning model for anticipatory nausea ) or , alternatively , whether motion sickness might facilitate the association of external stimuli to posttreatment nausea and vomiting .
	manualset3
88555	10	398851	13	NULL	NULL	0	NULL	stimuli	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , previous research did not test whether motion sickness increases anticipatory nausea only by increasing the base rate of posttreatment nausea and vomiting ( which has traditionally served as the unconditioned stimulus in the conditioning model for anticipatory nausea ) or , alternatively , whether motion sickness might facilitate the association of external stimuli to posttreatment nausea and vomiting .
	manualset3
88556	11	398851	13	NULL	NULL	0	NULL	posttreatment nausea	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , previous research did not test whether motion sickness increases anticipatory nausea only by increasing the base rate of posttreatment nausea and vomiting ( which has traditionally served as the unconditioned stimulus in the conditioning model for anticipatory nausea ) or , alternatively , whether motion sickness might facilitate the association of external stimuli to posttreatment nausea and vomiting .
	manualset3
88557	12	398851	13	NULL	NULL	0	NULL	vomiting	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , previous research did not test whether motion sickness increases anticipatory nausea only by increasing the base rate of posttreatment nausea and vomiting ( which has traditionally served as the unconditioned stimulus in the conditioning model for anticipatory nausea ) or , alternatively , whether motion sickness might facilitate the association of external stimuli to posttreatment nausea and vomiting .
	manualset3
88558	1	398852	13	NULL	NULL	0	NULL	studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , previous studies of Ca ( i ) ( 2 + ) handling have been limited to recordings from the heart surface during short-duration ventricular fibrillation .
	manualset3
88559	2	398852	13	NULL	NULL	0	NULL	Ca ( i ) ( 2 + ) 	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	However , previous studies of Ca ( i ) ( 2 + ) handling have been limited to recordings from the heart surface during short-duration ventricular fibrillation .
	manualset3
88560	3	398852	13	NULL	NULL	0	NULL	 recordings 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , previous studies of Ca ( i ) ( 2 + ) handling have been limited to recordings from the heart surface during short-duration ventricular fibrillation .
	manualset3
88561	4	398852	13	NULL	NULL	0	NULL	heart surface 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , previous studies of Ca ( i ) ( 2 + ) handling have been limited to recordings from the heart surface during short-duration ventricular fibrillation .
	manualset3
88562	5	398852	13	NULL	NULL	0	NULL	short-duration	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	However , previous studies of Ca ( i ) ( 2 + ) handling have been limited to recordings from the heart surface during short-duration ventricular fibrillation .
	manualset3
88563	6	398852	13	NULL	NULL	0	NULL	ventricular fibrillation	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , previous studies of Ca ( i ) ( 2 + ) handling have been limited to recordings from the heart surface during short-duration ventricular fibrillation .
	manualset3
88564	1	398853	13	NULL	NULL	0	NULL	period	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	However , prolonging the period of breath holding prior to exhalation reduced DLCO ( exhaled ) values at all lung volumes when non-uniform diffusion was simulated , but did not affect DLCO ( exhaled ) when only nonuniform ventilation was simulated .
	manualset3
88565	2	398853	13	NULL	NULL	0	NULL	 breath holding	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , prolonging the period of breath holding prior to exhalation reduced DLCO ( exhaled ) values at all lung volumes when non-uniform diffusion was simulated , but did not affect DLCO ( exhaled ) when only nonuniform ventilation was simulated .
	manualset3
88566	3	398853	13	NULL	NULL	0	NULL	exhalation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , prolonging the period of breath holding prior to exhalation reduced DLCO ( exhaled ) values at all lung volumes when non-uniform diffusion was simulated , but did not affect DLCO ( exhaled ) when only nonuniform ventilation was simulated .
	manualset3
88567	4	398853	13	NULL	NULL	0	NULL	DLCO ( exhaled ) values	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , prolonging the period of breath holding prior to exhalation reduced DLCO ( exhaled ) values at all lung volumes when non-uniform diffusion was simulated , but did not affect DLCO ( exhaled ) when only nonuniform ventilation was simulated .
	manualset3
88568	5	398853	13	NULL	NULL	0	NULL	lung volumes	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , prolonging the period of breath holding prior to exhalation reduced DLCO ( exhaled ) values at all lung volumes when non-uniform diffusion was simulated , but did not affect DLCO ( exhaled ) when only nonuniform ventilation was simulated .
	manualset3
88569	6	398853	13	NULL	NULL	0	NULL	diffusion 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , prolonging the period of breath holding prior to exhalation reduced DLCO ( exhaled ) values at all lung volumes when non-uniform diffusion was simulated , but did not affect DLCO ( exhaled ) when only nonuniform ventilation was simulated .
	manualset3
88570	7	398853	13	NULL	NULL	0	NULL	DLCO ( exhaled ) 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , prolonging the period of breath holding prior to exhalation reduced DLCO ( exhaled ) values at all lung volumes when non-uniform diffusion was simulated , but did not affect DLCO ( exhaled ) when only nonuniform ventilation was simulated .
	manualset3
88571	8	398853	13	NULL	NULL	0	NULL	ventilation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , prolonging the period of breath holding prior to exhalation reduced DLCO ( exhaled ) values at all lung volumes when non-uniform diffusion was simulated , but did not affect DLCO ( exhaled ) when only nonuniform ventilation was simulated .
	manualset3
88572	1	398854	13	NULL	NULL	0	NULL	promoter assays	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , promoter assays suggest multiple elements present in the p14ARF promoter and argue against the idea that the ARF promoter has a unique ability to distinguish between aberrant and physiological levels of E2F1 .
	manualset3
88573	2	398854	13	NULL	NULL	0	NULL	elements 	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , promoter assays suggest multiple elements present in the p14ARF promoter and argue against the idea that the ARF promoter has a unique ability to distinguish between aberrant and physiological levels of E2F1 .
	manualset3
88574	3	398854	13	NULL	NULL	0	NULL	p14ARF promoter	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , promoter assays suggest multiple elements present in the p14ARF promoter and argue against the idea that the ARF promoter has a unique ability to distinguish between aberrant and physiological levels of E2F1 .
	manualset3
88575	4	398854	13	NULL	NULL	0	NULL	idea	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , promoter assays suggest multiple elements present in the p14ARF promoter and argue against the idea that the ARF promoter has a unique ability to distinguish between aberrant and physiological levels of E2F1 .
	manualset3
88576	5	398854	13	NULL	NULL	0	NULL	ARF promoter	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , promoter assays suggest multiple elements present in the p14ARF promoter and argue against the idea that the ARF promoter has a unique ability to distinguish between aberrant and physiological levels of E2F1 .
	manualset3
88577	6	398854	13	NULL	NULL	0	NULL	E2F1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , promoter assays suggest multiple elements present in the p14ARF promoter and argue against the idea that the ARF promoter has a unique ability to distinguish between aberrant and physiological levels of E2F1 .
	manualset3
88578	1	398855	13	NULL	NULL	0	NULL	protein localization studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , protein localization studies show that the R. sphaeroides chemotaxis proteins are organized into two distinct sensory clusters -- one containing transmembrane receptors located at the cell poles and the other containing soluble chemoreceptors located in the cytoplasm .
	manualset3
88579	2	398855	13	NULL	NULL	NULL	NULL	R. sphaeroides chemotaxis proteins	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , protein localization studies show that the R. sphaeroides chemotaxis proteins are organized into two distinct sensory clusters -- one containing transmembrane receptors located at the cell poles and the other containing soluble chemoreceptors located in the cytoplasm .
	manualset3
88580	3	398855	13	NULL	NULL	0	NULL	two	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , protein localization studies show that the R. sphaeroides chemotaxis proteins are organized into two distinct sensory clusters -- one containing transmembrane receptors located at the cell poles and the other containing soluble chemoreceptors located in the cytoplasm .
	manualset3
88581	4	398855	13	NULL	NULL	0	NULL	sensory clusters 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , protein localization studies show that the R. sphaeroides chemotaxis proteins are organized into two distinct sensory clusters -- one containing transmembrane receptors located at the cell poles and the other containing soluble chemoreceptors located in the cytoplasm .
	manualset3
88582	5	398855	13	NULL	NULL	0	NULL	transmembrane receptors	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , protein localization studies show that the R. sphaeroides chemotaxis proteins are organized into two distinct sensory clusters -- one containing transmembrane receptors located at the cell poles and the other containing soluble chemoreceptors located in the cytoplasm .
	manualset3
88583	6	398855	13	NULL	NULL	0	NULL	 cell poles	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	However , protein localization studies show that the R. sphaeroides chemotaxis proteins are organized into two distinct sensory clusters -- one containing transmembrane receptors located at the cell poles and the other containing soluble chemoreceptors located in the cytoplasm .
	manualset3
88584	7	398855	13	NULL	NULL	0	NULL	soluble chemoreceptors	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , protein localization studies show that the R. sphaeroides chemotaxis proteins are organized into two distinct sensory clusters -- one containing transmembrane receptors located at the cell poles and the other containing soluble chemoreceptors located in the cytoplasm .
	manualset3
88585	8	398855	13	NULL	NULL	0	NULL	cytoplasm	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	However , protein localization studies show that the R. sphaeroides chemotaxis proteins are organized into two distinct sensory clusters -- one containing transmembrane receptors located at the cell poles and the other containing soluble chemoreceptors located in the cytoplasm .
	manualset3
88586	1	398856	13	NULL	NULL	0	NULL	pseudophakia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , pseudophakia changes the physiology of the eye and immediate changes include release of inflammatory cytokines .
	manualset3
88587	2	398856	13	NULL	NULL	0	NULL	physiology 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , pseudophakia changes the physiology of the eye and immediate changes include release of inflammatory cytokines .
	manualset3
88588	3	398856	13	NULL	NULL	0	NULL	 eye 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , pseudophakia changes the physiology of the eye and immediate changes include release of inflammatory cytokines .
	manualset3
88589	4	398856	13	NULL	NULL	0	NULL	inflammatory cytokines	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , pseudophakia changes the physiology of the eye and immediate changes include release of inflammatory cytokines .
	manualset3
88590	1	398857	13	NULL	NULL	0	NULL	punctal and canalicular agenesis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , punctal and canalicular agenesis is not among these reported abnormalities .
	manualset3
88591	2	398857	13	NULL	NULL	0	NULL	abnormalities	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , punctal and canalicular agenesis is not among these reported abnormalities .
	manualset3
88592	1	398858	13	NULL	NULL	0	NULL	evidence	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , recent evidence indicates that , instead , sarcolemmal LCFA transport mediated by CD36 in concert with FABPpm provides a major site of flux control .
	manualset3
88593	2	398858	13	NULL	NULL	0	NULL	sarcolemmal LCFA transport	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , recent evidence indicates that , instead , sarcolemmal LCFA transport mediated by CD36 in concert with FABPpm provides a major site of flux control .
	manualset3
88594	3	398858	13	NULL	NULL	0	NULL	CD36	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , recent evidence indicates that , instead , sarcolemmal LCFA transport mediated by CD36 in concert with FABPpm provides a major site of flux control .
	manualset3
88595	4	398858	13	NULL	NULL	0	NULL	FABPpm	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , recent evidence indicates that , instead , sarcolemmal LCFA transport mediated by CD36 in concert with FABPpm provides a major site of flux control .
	manualset3
88596	5	398858	13	NULL	NULL	0	NULL	site	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , recent evidence indicates that , instead , sarcolemmal LCFA transport mediated by CD36 in concert with FABPpm provides a major site of flux control .
	manualset3
88597	6	398858	13	NULL	NULL	0	NULL	 flux 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , recent evidence indicates that , instead , sarcolemmal LCFA transport mediated by CD36 in concert with FABPpm provides a major site of flux control .
	manualset3
88598	1	398859	13	NULL	NULL	0	NULL	 metal ions	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	( The effect of metal ions on the phosphate-containing moiety of thrombokinase ) .
	manualset3
88599	2	398859	13	NULL	NULL	0	NULL	phosphate-containing moiety 	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	( The effect of metal ions on the phosphate-containing moiety of thrombokinase ) .
	manualset3
88600	3	398859	13	NULL	NULL	0	NULL	 thrombokinase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	( The effect of metal ions on the phosphate-containing moiety of thrombokinase ) .
	manualset3
88601	1	398860	13	NULL	NULL	0	NULL	evidence 	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , recent evidence suggests a nonredundant unique role for IL-15 in the establishment and perhaps maintenance of peripheral natural killer ( NK ) cell populations in vivo .
	manualset3
88602	2	398860	13	NULL	NULL	0	NULL	IL-15 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , recent evidence suggests a nonredundant unique role for IL-15 in the establishment and perhaps maintenance of peripheral natural killer ( NK ) cell populations in vivo .
	manualset3
88603	3	398860	13	NULL	NULL	0	NULL	establishment 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , recent evidence suggests a nonredundant unique role for IL-15 in the establishment and perhaps maintenance of peripheral natural killer ( NK ) cell populations in vivo .
	manualset3
88604	4	398860	13	NULL	NULL	0	NULL	maintenance 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , recent evidence suggests a nonredundant unique role for IL-15 in the establishment and perhaps maintenance of peripheral natural killer ( NK ) cell populations in vivo .
	manualset3
88605	5	398860	13	NULL	NULL	0	NULL	peripheral natural killer ( NK ) cell populations 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , recent evidence suggests a nonredundant unique role for IL-15 in the establishment and perhaps maintenance of peripheral natural killer ( NK ) cell populations in vivo .
	manualset3
88606	1	398861	13	NULL	NULL	0	NULL	 studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , recent studies suggest that DDAH may regulate eNOS activity and endothelial function through both ADMA-dependent and - independent mechanisms .
	manualset3
88607	2	398861	13	NULL	NULL	0	NULL	DDAH	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , recent studies suggest that DDAH may regulate eNOS activity and endothelial function through both ADMA-dependent and - independent mechanisms .
	manualset3
88608	3	398861	13	NULL	NULL	NULL	NULL	eNOS activity	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , recent studies suggest that DDAH may regulate eNOS activity and endothelial function through both ADMA-dependent and - independent mechanisms .
	manualset3
88609	4	398861	13	NULL	NULL	0	NULL	endothelial function	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , recent studies suggest that DDAH may regulate eNOS activity and endothelial function through both ADMA-dependent and - independent mechanisms .
	manualset3
88610	5	398861	13	NULL	NULL	0	NULL	ADMA-dependent mechanisms 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , recent studies suggest that DDAH may regulate eNOS activity and endothelial function through both ADMA-dependent and - independent mechanisms .
	manualset3
88611	6	398861	13	NULL	NULL	NULL	NULL	ADMA-independent mechanisms	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , recent studies suggest that DDAH may regulate eNOS activity and endothelial function through both ADMA-dependent and - independent mechanisms .
	manualset3
88612	1	398862	13	NULL	NULL	0	NULL	results 	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , results from in-gel and Western blot analysis suggested that expression of recombinant GsiA in Rosetta ( DE3 ) provides an efficient source in soluble form .
	manualset3
88613	2	398862	13	NULL	NULL	0	NULL	in-gel analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , results from in-gel and Western blot analysis suggested that expression of recombinant GsiA in Rosetta ( DE3 ) provides an efficient source in soluble form .
	manualset3
88614	3	398862	13	NULL	NULL	0	NULL	Western blot analysis 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , results from in-gel and Western blot analysis suggested that expression of recombinant GsiA in Rosetta ( DE3 ) provides an efficient source in soluble form .
	manualset3
88615	4	398862	13	NULL	NULL	0	NULL	 expression of recombinant GsiA	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , results from in-gel and Western blot analysis suggested that expression of recombinant GsiA in Rosetta ( DE3 ) provides an efficient source in soluble form .
	manualset3
88616	5	398862	13	NULL	NULL	0	NULL	Rosetta ( DE3 ) 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , results from in-gel and Western blot analysis suggested that expression of recombinant GsiA in Rosetta ( DE3 ) provides an efficient source in soluble form .
	manualset3
88617	6	398862	13	NULL	NULL	0	NULL	source	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , results from in-gel and Western blot analysis suggested that expression of recombinant GsiA in Rosetta ( DE3 ) provides an efficient source in soluble form .
	manualset3
88618	1	398863	13	NULL	NULL	0	NULL	 banding procedures	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , routine banding procedures , by themselves , provide only limited information about the identity of marker chromosomes .
	manualset3
88619	2	398863	13	NULL	NULL	0	NULL	information	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , routine banding procedures , by themselves , provide only limited information about the identity of marker chromosomes .
	manualset3
88620	3	398863	13	NULL	NULL	0	NULL	 marker chromosomes	Chromosome												NULL		0	NULL	NULL	NULL	NULL	NULL	However , routine banding procedures , by themselves , provide only limited information about the identity of marker chromosomes .
	manualset3
88621	1	398864	13	NULL	NULL	0	NULL	schizophrenia diagnosis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , schizophrenia diagnosis was a strong predictor ( p & lt ; 0.0005 ) of the abundance of a truncated 50 kDa GR protein isoform , putative GR-D1 , which was increased in schizophrenia cases ( 80.4 % ) relative to controls .
	manualset3
88622	2	398864	13	NULL	NULL	0	NULL	predictor	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , schizophrenia diagnosis was a strong predictor ( p & lt ; 0.0005 ) of the abundance of a truncated 50 kDa GR protein isoform , putative GR-D1 , which was increased in schizophrenia cases ( 80.4 % ) relative to controls .
	manualset3
88623	3	398864	13	NULL	NULL	0	NULL	 p & lt ; 0.0005 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , schizophrenia diagnosis was a strong predictor ( p & lt ; 0.0005 ) of the abundance of a truncated 50 kDa GR protein isoform , putative GR-D1 , which was increased in schizophrenia cases ( 80.4 % ) relative to controls .
	manualset3
88624	4	398864	13	NULL	NULL	0	NULL	truncated 50 kDa GR protein isoform	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , schizophrenia diagnosis was a strong predictor ( p & lt ; 0.0005 ) of the abundance of a truncated 50 kDa GR protein isoform , putative GR-D1 , which was increased in schizophrenia cases ( 80.4 % ) relative to controls .
	manualset3
88625	5	398864	13	NULL	NULL	0	NULL	putative GR-D1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , schizophrenia diagnosis was a strong predictor ( p & lt ; 0.0005 ) of the abundance of a truncated 50 kDa GR protein isoform , putative GR-D1 , which was increased in schizophrenia cases ( 80.4 % ) relative to controls .
	manualset3
88626	6	398864	13	NULL	NULL	0	NULL	schizophrenia cases	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , schizophrenia diagnosis was a strong predictor ( p & lt ; 0.0005 ) of the abundance of a truncated 50 kDa GR protein isoform , putative GR-D1 , which was increased in schizophrenia cases ( 80.4 % ) relative to controls .
	manualset3
88627	7	398864	13	NULL	NULL	0	NULL	80.4 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , schizophrenia diagnosis was a strong predictor ( p & lt ; 0.0005 ) of the abundance of a truncated 50 kDa GR protein isoform , putative GR-D1 , which was increased in schizophrenia cases ( 80.4 % ) relative to controls .
	manualset3
88628	8	398864	13	NULL	NULL	0	NULL	 controls 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , schizophrenia diagnosis was a strong predictor ( p & lt ; 0.0005 ) of the abundance of a truncated 50 kDa GR protein isoform , putative GR-D1 , which was increased in schizophrenia cases ( 80.4 % ) relative to controls .
	manualset3
88629	1	398865	13	NULL	NULL	NULL	NULL	scopolamine 	Drug												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , scopolamine dose-dependently facilitated the striatal ECF dopamine induced by the DAT inhibitor GBR12909 at a dose of 0.5 mg/kg .
	manualset3
88630	2	398865	13	NULL	NULL	0	NULL	striatal ECF dopamine	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , scopolamine dose-dependently facilitated the striatal ECF dopamine induced by the DAT inhibitor GBR12909 at a dose of 0.5 mg/kg .
	manualset3
88631	3	398865	13	NULL	NULL	0	NULL	DAT inhibitor GBR12909	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , scopolamine dose-dependently facilitated the striatal ECF dopamine induced by the DAT inhibitor GBR12909 at a dose of 0.5 mg/kg .
	manualset3
88632	4	398865	13	NULL	NULL	0	NULL	dose of 0.5 mg/kg	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , scopolamine dose-dependently facilitated the striatal ECF dopamine induced by the DAT inhibitor GBR12909 at a dose of 0.5 mg/kg .
	manualset3
88784	1	398866	13	NULL	NULL	0	NULL	weight control program	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The effects of a weight control program with competence ) .
	manualset3
88785	2	398866	13	NULL	NULL	0	NULL	competence 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( The effects of a weight control program with competence ) .
	manualset3
88788	1	398867	13	NULL	NULL	0	NULL	screening	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , screening for antituberculosis compounds by using GFP driven by the heat shock promoter , hsp60 , has been of limited utility due to the low signal-to-noise ratio .
	manualset3
88795	2	398867	13	NULL	NULL	0	NULL	antituberculosis compounds	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , screening for antituberculosis compounds by using GFP driven by the heat shock promoter , hsp60 , has been of limited utility due to the low signal-to-noise ratio .
	manualset3
88796	3	398867	13	NULL	NULL	0	NULL	GFP	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , screening for antituberculosis compounds by using GFP driven by the heat shock promoter , hsp60 , has been of limited utility due to the low signal-to-noise ratio .
	manualset3
88800	4	398867	13	NULL	NULL	NULL	NULL	heat shock promoter , hsp60	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , screening for antituberculosis compounds by using GFP driven by the heat shock promoter , hsp60 , has been of limited utility due to the low signal-to-noise ratio .
	manualset3
88805	5	398867	13	NULL	NULL	0	NULL	signal-to-noise ratio	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , screening for antituberculosis compounds by using GFP driven by the heat shock promoter , hsp60 , has been of limited utility due to the low signal-to-noise ratio .
	manualset3
88837	1	398868	13	NULL	NULL	NULL	NULL	sensory tuning properties	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , sensory tuning properties in these areas , especially during wakefulness , and their relation to perception , are poorly understood .
	manualset3
88838	2	398868	13	NULL	NULL	0	NULL	areas	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , sensory tuning properties in these areas , especially during wakefulness , and their relation to perception , are poorly understood .
	manualset3
88846	3	398868	13	NULL	NULL	0	NULL	wakefulness	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , sensory tuning properties in these areas , especially during wakefulness , and their relation to perception , are poorly understood .
	manualset3
88847	4	398868	13	NULL	NULL	NULL	NULL	perception 	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , sensory tuning properties in these areas , especially during wakefulness , and their relation to perception , are poorly understood .
	manualset3
88849	1	398869	13	NULL	NULL	0	NULL	dysarthria 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , severe dysarthria and myoclonic jerks in a patient with hemiparesis should be considered as warning signs to indicate the herald hemiparesis with subsequent severe brainstem infarction .
	manualset3
88850	2	398869	13	NULL	NULL	0	NULL	myoclonic jerks	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , severe dysarthria and myoclonic jerks in a patient with hemiparesis should be considered as warning signs to indicate the herald hemiparesis with subsequent severe brainstem infarction .
	manualset3
88852	3	398869	13	NULL	NULL	0	NULL	patient	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , severe dysarthria and myoclonic jerks in a patient with hemiparesis should be considered as warning signs to indicate the herald hemiparesis with subsequent severe brainstem infarction .
	manualset3
88856	4	398869	13	NULL	NULL	0	NULL	hemiparesis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , severe dysarthria and myoclonic jerks in a patient with hemiparesis should be considered as warning signs to indicate the herald hemiparesis with subsequent severe brainstem infarction .
	manualset3
88861	5	398869	13	NULL	NULL	0	NULL	warning signs	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , severe dysarthria and myoclonic jerks in a patient with hemiparesis should be considered as warning signs to indicate the herald hemiparesis with subsequent severe brainstem infarction .
	manualset3
88862	6	398869	13	NULL	NULL	0	NULL	herald hemiparesis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , severe dysarthria and myoclonic jerks in a patient with hemiparesis should be considered as warning signs to indicate the herald hemiparesis with subsequent severe brainstem infarction .
	manualset3
88863	7	398869	13	NULL	NULL	0	NULL	severe brainstem infarction	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , severe dysarthria and myoclonic jerks in a patient with hemiparesis should be considered as warning signs to indicate the herald hemiparesis with subsequent severe brainstem infarction .
	manualset3
88864	1	398870	13	NULL	NULL	0	NULL	cross-protection	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , significant cross-protection was observed when serotype II and III strains were analyzed in the model .
	manualset3
88865	2	398870	13	NULL	NULL	0	NULL	serotype II strains	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , significant cross-protection was observed when serotype II and III strains were analyzed in the model .
	manualset3
88866	3	398870	13	NULL	NULL	0	NULL	serotype III strains	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , significant cross-protection was observed when serotype II and III strains were analyzed in the model .
	manualset3
88867	4	398870	13	NULL	NULL	NULL	NULL	model	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , significant cross-protection was observed when serotype II and III strains were analyzed in the model .
	manualset3
88868	1	398871	13	NULL	NULL	0	NULL	RT-PCR	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , since RT-PCR generally lacks the specificity of sequencing or serology , the most practical application of RT-PCR methods for subtype identification is either to target a few of the most important subtypes such as H5 and H7 or to use it in situations where a specific strain is being targeted , such as during an outbreak or with experimental samples .
	manualset3
88872	2	398871	13	NULL	NULL	0	NULL	sequencing	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , since RT-PCR generally lacks the specificity of sequencing or serology , the most practical application of RT-PCR methods for subtype identification is either to target a few of the most important subtypes such as H5 and H7 or to use it in situations where a specific strain is being targeted , such as during an outbreak or with experimental samples .
	manualset3
88873	3	398871	13	NULL	NULL	NULL	NULL	serology	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , since RT-PCR generally lacks the specificity of sequencing or serology , the most practical application of RT-PCR methods for subtype identification is either to target a few of the most important subtypes such as H5 and H7 or to use it in situations where a specific strain is being targeted , such as during an outbreak or with experimental samples .
	manualset3
88875	4	398871	13	NULL	NULL	0	NULL	RT-PCR methods	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , since RT-PCR generally lacks the specificity of sequencing or serology , the most practical application of RT-PCR methods for subtype identification is either to target a few of the most important subtypes such as H5 and H7 or to use it in situations where a specific strain is being targeted , such as during an outbreak or with experimental samples .
	manualset3
88876	5	398871	13	NULL	NULL	0	NULL	subtype identification	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , since RT-PCR generally lacks the specificity of sequencing or serology , the most practical application of RT-PCR methods for subtype identification is either to target a few of the most important subtypes such as H5 and H7 or to use it in situations where a specific strain is being targeted , such as during an outbreak or with experimental samples .
	manualset3
88881	6	398871	13	NULL	NULL	0	NULL	H5	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , since RT-PCR generally lacks the specificity of sequencing or serology , the most practical application of RT-PCR methods for subtype identification is either to target a few of the most important subtypes such as H5 and H7 or to use it in situations where a specific strain is being targeted , such as during an outbreak or with experimental samples .
	manualset3
88882	7	398871	13	NULL	NULL	0	NULL	H7	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , since RT-PCR generally lacks the specificity of sequencing or serology , the most practical application of RT-PCR methods for subtype identification is either to target a few of the most important subtypes such as H5 and H7 or to use it in situations where a specific strain is being targeted , such as during an outbreak or with experimental samples .
	manualset3
88883	8	398871	13	NULL	NULL	0	NULL	strain	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , since RT-PCR generally lacks the specificity of sequencing or serology , the most practical application of RT-PCR methods for subtype identification is either to target a few of the most important subtypes such as H5 and H7 or to use it in situations where a specific strain is being targeted , such as during an outbreak or with experimental samples .
	manualset3
88884	9	398871	13	NULL	NULL	0	NULL	outbreak 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , since RT-PCR generally lacks the specificity of sequencing or serology , the most practical application of RT-PCR methods for subtype identification is either to target a few of the most important subtypes such as H5 and H7 or to use it in situations where a specific strain is being targeted , such as during an outbreak or with experimental samples .
	manualset3
88885	10	398871	13	NULL	NULL	0	NULL	experimental samples 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , since RT-PCR generally lacks the specificity of sequencing or serology , the most practical application of RT-PCR methods for subtype identification is either to target a few of the most important subtypes such as H5 and H7 or to use it in situations where a specific strain is being targeted , such as during an outbreak or with experimental samples .
	manualset3
88900	1	398872	13	NULL	NULL	NULL	NULL	 immobilization	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , single immobilization significantly decreased beta ( 2 ) - AR mRNA levels both in left atria and ventricles compared to acute cold stress .
	manualset3
88901	2	398872	13	NULL	NULL	0	NULL	beta ( 2 ) - AR mRNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , single immobilization significantly decreased beta ( 2 ) - AR mRNA levels both in left atria and ventricles compared to acute cold stress .
	manualset3
88902	3	398872	13	NULL	NULL	0	NULL	left atria	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , single immobilization significantly decreased beta ( 2 ) - AR mRNA levels both in left atria and ventricles compared to acute cold stress .
	manualset3
88903	4	398872	13	NULL	NULL	0	NULL	ventricles	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , single immobilization significantly decreased beta ( 2 ) - AR mRNA levels both in left atria and ventricles compared to acute cold stress .
	manualset3
88904	5	398872	13	NULL	NULL	0	NULL	cold stress	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , single immobilization significantly decreased beta ( 2 ) - AR mRNA levels both in left atria and ventricles compared to acute cold stress .
	manualset3
88905	1	398873	13	NULL	NULL	0	NULL	 sodium channels	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , sodium channels were detected only in axon patches .
	manualset3
88906	2	398873	13	NULL	NULL	0	NULL	axon patches	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , sodium channels were detected only in axon patches .
	manualset3
88907	1	398874	13	NULL	NULL	0	NULL	activities 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , some activities were located in high molecular weight complexes , and methods that disrupted these complexes ( such as treatment with sodium dodecyl sulfate at elevated temperature ) destroyed enzyme activity .
	manualset3
88908	2	398874	13	NULL	NULL	0	NULL	 high molecular weight complexes	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , some activities were located in high molecular weight complexes , and methods that disrupted these complexes ( such as treatment with sodium dodecyl sulfate at elevated temperature ) destroyed enzyme activity .
	manualset3
88909	3	398874	13	NULL	NULL	NULL	NULL	methods	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , some activities were located in high molecular weight complexes , and methods that disrupted these complexes ( such as treatment with sodium dodecyl sulfate at elevated temperature ) destroyed enzyme activity .
	manualset3
88910	4	398874	13	NULL	NULL	0	NULL	complexes	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , some activities were located in high molecular weight complexes , and methods that disrupted these complexes ( such as treatment with sodium dodecyl sulfate at elevated temperature ) destroyed enzyme activity .
	manualset3
88911	5	398874	13	NULL	NULL	0	NULL	treatment	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , some activities were located in high molecular weight complexes , and methods that disrupted these complexes ( such as treatment with sodium dodecyl sulfate at elevated temperature ) destroyed enzyme activity .
	manualset3
88912	6	398874	13	NULL	NULL	0	NULL	sodium dodecyl sulfate	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , some activities were located in high molecular weight complexes , and methods that disrupted these complexes ( such as treatment with sodium dodecyl sulfate at elevated temperature ) destroyed enzyme activity .
	manualset3
88913	7	398874	13	NULL	NULL	0	NULL	temperature 	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , some activities were located in high molecular weight complexes , and methods that disrupted these complexes ( such as treatment with sodium dodecyl sulfate at elevated temperature ) destroyed enzyme activity .
	manualset3
88914	8	398874	13	NULL	NULL	0	NULL	enzyme activity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , some activities were located in high molecular weight complexes , and methods that disrupted these complexes ( such as treatment with sodium dodecyl sulfate at elevated temperature ) destroyed enzyme activity .
	manualset3
88915	1	398875	13	NULL	NULL	NULL	NULL	 effects	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The effects of iodized sodium tetrachloride on certain fungi ) .
	manualset3
88916	2	398875	13	NULL	NULL	0	NULL	iodized sodium tetrachloride	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( The effects of iodized sodium tetrachloride on certain fungi ) .
	manualset3
88917	3	398875	13	NULL	NULL	0	NULL	fungi 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( The effects of iodized sodium tetrachloride on certain fungi ) .
	manualset3
88918	1	398876	13	NULL	NULL	0	NULL	targets	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , specific targets for calmodulin action have not been thoroughly addressed .
	manualset3
88919	2	398876	13	NULL	NULL	0	NULL	calmodulin action	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , specific targets for calmodulin action have not been thoroughly addressed .
	manualset3
88920	1	398877	13	NULL	NULL	0	NULL	 neurotransmitter release	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , spontaneous neurotransmitter release was stable ( both in frequency and amplitude ) throughout the period of antibody exposure .
	manualset3
88921	2	398877	13	NULL	NULL	0	NULL	frequency	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , spontaneous neurotransmitter release was stable ( both in frequency and amplitude ) throughout the period of antibody exposure .
	manualset3
88922	3	398877	13	NULL	NULL	0	NULL	 amplitude	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , spontaneous neurotransmitter release was stable ( both in frequency and amplitude ) throughout the period of antibody exposure .
	manualset3
88923	4	398877	13	NULL	NULL	0	NULL	period	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	However , spontaneous neurotransmitter release was stable ( both in frequency and amplitude ) throughout the period of antibody exposure .
	manualset3
88924	5	398877	13	NULL	NULL	NULL	NULL	antibody	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , spontaneous neurotransmitter release was stable ( both in frequency and amplitude ) throughout the period of antibody exposure .
	manualset3
88926	6	398877	13	NULL	NULL	0	NULL	exposure	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , spontaneous neurotransmitter release was stable ( both in frequency and amplitude ) throughout the period of antibody exposure .
	manualset3
88927	1	398878	13	NULL	NULL	0	NULL	 statistical analyses	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , statistical analyses substantiated the observation that the bases of the sinuses and raphes were the valvular regions particularly prone to the development of cartilage .
	manualset3
88928	2	398878	13	NULL	NULL	0	NULL	observation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , statistical analyses substantiated the observation that the bases of the sinuses and raphes were the valvular regions particularly prone to the development of cartilage .
	manualset3
88929	3	398878	13	NULL	NULL	NULL	NULL	bases of the sinuses	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , statistical analyses substantiated the observation that the bases of the sinuses and raphes were the valvular regions particularly prone to the development of cartilage .
	manualset3
88930	4	398878	13	NULL	NULL	0	NULL	raphes	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , statistical analyses substantiated the observation that the bases of the sinuses and raphes were the valvular regions particularly prone to the development of cartilage .
	manualset3
88931	5	398878	13	NULL	NULL	0	NULL	valvular regions	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , statistical analyses substantiated the observation that the bases of the sinuses and raphes were the valvular regions particularly prone to the development of cartilage .
	manualset3
88932	6	398878	13	NULL	NULL	0	NULL	development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , statistical analyses substantiated the observation that the bases of the sinuses and raphes were the valvular regions particularly prone to the development of cartilage .
	manualset3
88933	7	398878	13	NULL	NULL	0	NULL	cartilage	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	However , statistical analyses substantiated the observation that the bases of the sinuses and raphes were the valvular regions particularly prone to the development of cartilage .
	manualset3
88934	1	398879	13	NULL	NULL	0	NULL	structurally and mechanistically dissimilar inhibitors	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , structurally and mechanistically dissimilar inhibitors of protein methylation and coexpression of protein arginine methyltransferase 1 did not influence Nox activity .
	manualset3
88941	2	398879	13	NULL	NULL	0	NULL	protein methylation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , structurally and mechanistically dissimilar inhibitors of protein methylation and coexpression of protein arginine methyltransferase 1 did not influence Nox activity .
	manualset3
88942	3	398879	13	NULL	NULL	0	NULL	coexpression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , structurally and mechanistically dissimilar inhibitors of protein methylation and coexpression of protein arginine methyltransferase 1 did not influence Nox activity .
	manualset3
88943	4	398879	13	NULL	NULL	0	NULL	 protein arginine methyltransferase 1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , structurally and mechanistically dissimilar inhibitors of protein methylation and coexpression of protein arginine methyltransferase 1 did not influence Nox activity .
	manualset3
88944	5	398879	13	NULL	NULL	0	NULL	Nox activity 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , structurally and mechanistically dissimilar inhibitors of protein methylation and coexpression of protein arginine methyltransferase 1 did not influence Nox activity .
	manualset3
90008	6	398879	13	NULL	NULL	0	NULL	influence	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , structurally and mechanistically dissimilar inhibitors of protein methylation and coexpression of protein arginine methyltransferase 1 did not influence Nox activity .
	manualset3
88945	1	398880	13	NULL	NULL	0	NULL	interconnections	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , such interconnections have remained elusive due to the difficulty in separating the intra - and extraribosomal roles of ribosome biogenesis factors .
	manualset3
88946	2	398880	13	NULL	NULL	0	NULL	intraribosomal roles	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , such interconnections have remained elusive due to the difficulty in separating the intra - and extraribosomal roles of ribosome biogenesis factors .
	manualset3
88947	3	398880	13	NULL	NULL	0	NULL	extraribosomal roles	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , such interconnections have remained elusive due to the difficulty in separating the intra - and extraribosomal roles of ribosome biogenesis factors .
	manualset3
88948	4	398880	13	NULL	NULL	0	NULL	ribosome biogenesis factors	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , such interconnections have remained elusive due to the difficulty in separating the intra - and extraribosomal roles of ribosome biogenesis factors .
	manualset3
88949	1	398881	13	NULL	NULL	NULL	NULL	support 	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , such support was predicated on the specialty 's highlighting particular legitimating discourses and practices at the expense of others , and in framing this in terms of specific policy concerns around an ageing population .
	manualset3
88950	2	398881	13	NULL	NULL	0	NULL	discourses	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , such support was predicated on the specialty 's highlighting particular legitimating discourses and practices at the expense of others , and in framing this in terms of specific policy concerns around an ageing population .
	manualset3
88951	3	398881	13	NULL	NULL	0	NULL	practices	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , such support was predicated on the specialty 's highlighting particular legitimating discourses and practices at the expense of others , and in framing this in terms of specific policy concerns around an ageing population .
	manualset3
88952	4	398881	13	NULL	NULL	0	NULL	policy	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , such support was predicated on the specialty 's highlighting particular legitimating discourses and practices at the expense of others , and in framing this in terms of specific policy concerns around an ageing population .
	manualset3
88953	5	398881	13	NULL	NULL	0	NULL	ageing population	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , such support was predicated on the specialty 's highlighting particular legitimating discourses and practices at the expense of others , and in framing this in terms of specific policy concerns around an ageing population .
	manualset3
88954	1	398882	13	NULL	NULL	0	NULL	sulphated insulin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , sulphated insulin bound to liver membranes with an affinity more closely resembling that for adipocytes rather than hepatocytes .
	manualset3
88955	2	398882	13	NULL	NULL	0	NULL	liver membranes	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , sulphated insulin bound to liver membranes with an affinity more closely resembling that for adipocytes rather than hepatocytes .
	manualset3
88956	3	398882	13	NULL	NULL	0	NULL	affinity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , sulphated insulin bound to liver membranes with an affinity more closely resembling that for adipocytes rather than hepatocytes .
	manualset3
88957	4	398882	13	NULL	NULL	0	NULL	adipocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , sulphated insulin bound to liver membranes with an affinity more closely resembling that for adipocytes rather than hepatocytes .
	manualset3
88958	5	398882	13	NULL	NULL	0	NULL	hepatocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , sulphated insulin bound to liver membranes with an affinity more closely resembling that for adipocytes rather than hepatocytes .
	manualset3
88959	1	398883	13	NULL	NULL	0	NULL	synaptic circuit mechanisms	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , synaptic circuit mechanisms underlying the OS sharpening remain unclear .
	manualset3
88960	2	398883	13	NULL	NULL	0	NULL	OS sharpening 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , synaptic circuit mechanisms underlying the OS sharpening remain unclear .
	manualset3
88961	1	398884	13	NULL	NULL	0	NULL	syncollin-deficient mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , syncollin-deficient mice reacted to caerulein hyperstimulation with a more severe pancreatitis .
	manualset3
88962	2	398884	13	NULL	NULL	0	NULL	caerulein	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	However , syncollin-deficient mice reacted to caerulein hyperstimulation with a more severe pancreatitis .
	manualset3
88963	3	398884	13	NULL	NULL	0	NULL	hyperstimulation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , syncollin-deficient mice reacted to caerulein hyperstimulation with a more severe pancreatitis .
	manualset3
88964	4	398884	13	NULL	NULL	0	NULL	pancreatitis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , syncollin-deficient mice reacted to caerulein hyperstimulation with a more severe pancreatitis .
	manualset3
88965	1	398885	13	NULL	NULL	0	NULL	etiology	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	( The etiology of chronic anti-HBc-positive hepatitis ) .
	manualset3
88966	2	398885	13	NULL	NULL	0	NULL	 chronic anti-HBc-positive hepatitis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( The etiology of chronic anti-HBc-positive hepatitis ) .
	manualset3
88967	1	398886	13	NULL	NULL	0	NULL	telmisartan	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , telmisartan showed better tolerability than ramipril in ONTARGET , with less cough and angioedema .
	manualset3
88968	2	398886	13	NULL	NULL	0	NULL	tolerability	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , telmisartan showed better tolerability than ramipril in ONTARGET , with less cough and angioedema .
	manualset3
88969	3	398886	13	NULL	NULL	0	NULL	ramipril	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , telmisartan showed better tolerability than ramipril in ONTARGET , with less cough and angioedema .
	manualset3
88970	4	398886	13	NULL	NULL	0	NULL	ONTARGET	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , telmisartan showed better tolerability than ramipril in ONTARGET , with less cough and angioedema .
	manualset3
88971	5	398886	13	NULL	NULL	0	NULL	cough 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , telmisartan showed better tolerability than ramipril in ONTARGET , with less cough and angioedema .
	manualset3
88972	6	398886	13	NULL	NULL	0	NULL	angioedema	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , telmisartan showed better tolerability than ramipril in ONTARGET , with less cough and angioedema .
	manualset3
88973	1	398887	13	NULL	NULL	0	NULL	 CGN treatments	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the CGN treatments did not affect the antibody response to BA nor to SRBC differently between L and H line chicks .
	manualset3
88974	2	398887	13	NULL	NULL	NULL	NULL	antibody response	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the CGN treatments did not affect the antibody response to BA nor to SRBC differently between L and H line chicks .
	manualset3
88975	3	398887	13	NULL	NULL	0	NULL	BA	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the CGN treatments did not affect the antibody response to BA nor to SRBC differently between L and H line chicks .
	manualset3
88976	4	398887	13	NULL	NULL	0	NULL	 SRBC	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the CGN treatments did not affect the antibody response to BA nor to SRBC differently between L and H line chicks .
	manualset3
88977	5	398887	13	NULL	NULL	0	NULL	L line chicks	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the CGN treatments did not affect the antibody response to BA nor to SRBC differently between L and H line chicks .
	manualset3
88978	6	398887	13	NULL	NULL	0	NULL	H line chicks	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the CGN treatments did not affect the antibody response to BA nor to SRBC differently between L and H line chicks .
	manualset3
89028	1	398888	13	NULL	NULL	0	NULL	ISO/IEC Guide 58	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the ISO/IEC Guide 58 , for the setting up and operation of a laboratory accreditation body , specifies that inspectors should have appropriate technical knowledge of the specific calibrations , tests or types of calibration or tests for which accreditation is sought .
	manualset3
89035	3	398888	13	NULL	NULL	0	NULL	operation 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the ISO/IEC Guide 58 , for the setting up and operation of a laboratory accreditation body , specifies that inspectors should have appropriate technical knowledge of the specific calibrations , tests or types of calibration or tests for which accreditation is sought .
	manualset3
89049	4	398888	13	NULL	NULL	0	NULL	laboratory accreditation body	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the ISO/IEC Guide 58 , for the setting up and operation of a laboratory accreditation body , specifies that inspectors should have appropriate technical knowledge of the specific calibrations , tests or types of calibration or tests for which accreditation is sought .
	manualset3
89050	5	398888	13	NULL	NULL	0	NULL	inspectors 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the ISO/IEC Guide 58 , for the setting up and operation of a laboratory accreditation body , specifies that inspectors should have appropriate technical knowledge of the specific calibrations , tests or types of calibration or tests for which accreditation is sought .
	manualset3
89052	6	398888	13	NULL	NULL	0	NULL	 technical knowledge 	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the ISO/IEC Guide 58 , for the setting up and operation of a laboratory accreditation body , specifies that inspectors should have appropriate technical knowledge of the specific calibrations , tests or types of calibration or tests for which accreditation is sought .
	manualset3
89053	7	398888	13	NULL	NULL	0	NULL	 calibrations 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the ISO/IEC Guide 58 , for the setting up and operation of a laboratory accreditation body , specifies that inspectors should have appropriate technical knowledge of the specific calibrations , tests or types of calibration or tests for which accreditation is sought .
	manualset3
89055	8	398888	13	NULL	NULL	0	NULL	tests	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the ISO/IEC Guide 58 , for the setting up and operation of a laboratory accreditation body , specifies that inspectors should have appropriate technical knowledge of the specific calibrations , tests or types of calibration or tests for which accreditation is sought .
	manualset3
89056	9	398888	13	NULL	NULL	0	NULL	calibration	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the ISO/IEC Guide 58 , for the setting up and operation of a laboratory accreditation body , specifies that inspectors should have appropriate technical knowledge of the specific calibrations , tests or types of calibration or tests for which accreditation is sought .
	manualset3
89057	10	398888	13	NULL	NULL	0	NULL	tests 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the ISO/IEC Guide 58 , for the setting up and operation of a laboratory accreditation body , specifies that inspectors should have appropriate technical knowledge of the specific calibrations , tests or types of calibration or tests for which accreditation is sought .
	manualset3
89058	11	398888	13	NULL	NULL	0	NULL	accreditation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the ISO/IEC Guide 58 , for the setting up and operation of a laboratory accreditation body , specifies that inspectors should have appropriate technical knowledge of the specific calibrations , tests or types of calibration or tests for which accreditation is sought .
	manualset3
89066	1	398889	13	NULL	NULL	0	NULL	Kcec values	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the Kcec values of the enkephalin peptides under all temperature conditions studied were positive with an eluent composed of water-50 mM NH4OAc/AcOH , pH 5.2-acetonitrile ( 5 : 2 : 3 , v/v ) and therefore the chromatographic component dominates the retention process with these small peptides under these conditions .
	manualset3
89067	2	398889	13	NULL	NULL	0	NULL	enkephalin peptides	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the Kcec values of the enkephalin peptides under all temperature conditions studied were positive with an eluent composed of water-50 mM NH4OAc/AcOH , pH 5.2-acetonitrile ( 5 : 2 : 3 , v/v ) and therefore the chromatographic component dominates the retention process with these small peptides under these conditions .
	manualset3
89069	3	398889	13	NULL	NULL	0	NULL	temperature conditions	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the Kcec values of the enkephalin peptides under all temperature conditions studied were positive with an eluent composed of water-50 mM NH4OAc/AcOH , pH 5.2-acetonitrile ( 5 : 2 : 3 , v/v ) and therefore the chromatographic component dominates the retention process with these small peptides under these conditions .
	manualset3
89071	5	398889	13	NULL	NULL	NULL	NULL	water-50 mM NH4OAc/AcOH	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the Kcec values of the enkephalin peptides under all temperature conditions studied were positive with an eluent composed of water-50 mM NH4OAc/AcOH , pH 5.2-acetonitrile ( 5 : 2 : 3 , v/v ) and therefore the chromatographic component dominates the retention process with these small peptides under these conditions .
	manualset3
89074	8	398889	13	NULL	NULL	0	NULL	pH 5.2	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the Kcec values of the enkephalin peptides under all temperature conditions studied were positive with an eluent composed of water-50 mM NH4OAc/AcOH , pH 5.2-acetonitrile ( 5 : 2 : 3 , v/v ) and therefore the chromatographic component dominates the retention process with these small peptides under these conditions .
	manualset3
89078	9	398889	13	NULL	NULL	0	NULL	acetonitrile 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the Kcec values of the enkephalin peptides under all temperature conditions studied were positive with an eluent composed of water-50 mM NH4OAc/AcOH , pH 5.2-acetonitrile ( 5 : 2 : 3 , v/v ) and therefore the chromatographic component dominates the retention process with these small peptides under these conditions .
	manualset3
89079	10	398889	13	NULL	NULL	0	NULL	5 : 2 : 3 , v/v	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the Kcec values of the enkephalin peptides under all temperature conditions studied were positive with an eluent composed of water-50 mM NH4OAc/AcOH , pH 5.2-acetonitrile ( 5 : 2 : 3 , v/v ) and therefore the chromatographic component dominates the retention process with these small peptides under these conditions .
	manualset3
89081	11	398889	13	NULL	NULL	0	NULL	component	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the Kcec values of the enkephalin peptides under all temperature conditions studied were positive with an eluent composed of water-50 mM NH4OAc/AcOH , pH 5.2-acetonitrile ( 5 : 2 : 3 , v/v ) and therefore the chromatographic component dominates the retention process with these small peptides under these conditions .
	manualset3
89082	12	398889	13	NULL	NULL	0	NULL	retention process	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the Kcec values of the enkephalin peptides under all temperature conditions studied were positive with an eluent composed of water-50 mM NH4OAc/AcOH , pH 5.2-acetonitrile ( 5 : 2 : 3 , v/v ) and therefore the chromatographic component dominates the retention process with these small peptides under these conditions .
	manualset3
89083	13	398889	13	NULL	NULL	0	NULL	peptides	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the Kcec values of the enkephalin peptides under all temperature conditions studied were positive with an eluent composed of water-50 mM NH4OAc/AcOH , pH 5.2-acetonitrile ( 5 : 2 : 3 , v/v ) and therefore the chromatographic component dominates the retention process with these small peptides under these conditions .
	manualset3
89086	14	398889	13	NULL	NULL	0	NULL	conditions	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the Kcec values of the enkephalin peptides under all temperature conditions studied were positive with an eluent composed of water-50 mM NH4OAc/AcOH , pH 5.2-acetonitrile ( 5 : 2 : 3 , v/v ) and therefore the chromatographic component dominates the retention process with these small peptides under these conditions .
	manualset3
89087	1	398890	13	NULL	NULL	0	NULL	NR3B mRNA expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the NR3B mRNA expression was significantly up-regulated by the factors 9.11 ( P & lt ; 0.001 ) , 10.07 ( P & lt ; 0.001 ) and 4.08 ( P & lt ; 0.05 ) in abstinent , addicted and methadone maintained subjects , respectively relative to control group .
	manualset3
89090	2	398890	13	NULL	NULL	0	NULL	9.11 ( P & lt ; 0.001 ) 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the NR3B mRNA expression was significantly up-regulated by the factors 9.11 ( P & lt ; 0.001 ) , 10.07 ( P & lt ; 0.001 ) and 4.08 ( P & lt ; 0.05 ) in abstinent , addicted and methadone maintained subjects , respectively relative to control group .
	manualset3
89091	3	398890	13	NULL	NULL	0	NULL	 10.07 ( P & lt ; 0.001 )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the NR3B mRNA expression was significantly up-regulated by the factors 9.11 ( P & lt ; 0.001 ) , 10.07 ( P & lt ; 0.001 ) and 4.08 ( P & lt ; 0.05 ) in abstinent , addicted and methadone maintained subjects , respectively relative to control group .
	manualset3
89092	4	398890	13	NULL	NULL	0	NULL	4.08 ( P & lt ; 0.05 )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the NR3B mRNA expression was significantly up-regulated by the factors 9.11 ( P & lt ; 0.001 ) , 10.07 ( P & lt ; 0.001 ) and 4.08 ( P & lt ; 0.05 ) in abstinent , addicted and methadone maintained subjects , respectively relative to control group .
	manualset3
89093	5	398890	13	NULL	NULL	0	NULL	abstinent subjects	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the NR3B mRNA expression was significantly up-regulated by the factors 9.11 ( P & lt ; 0.001 ) , 10.07 ( P & lt ; 0.001 ) and 4.08 ( P & lt ; 0.05 ) in abstinent , addicted and methadone maintained subjects , respectively relative to control group .
	manualset3
89095	6	398890	13	NULL	NULL	0	NULL	addicted subjects	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the NR3B mRNA expression was significantly up-regulated by the factors 9.11 ( P & lt ; 0.001 ) , 10.07 ( P & lt ; 0.001 ) and 4.08 ( P & lt ; 0.05 ) in abstinent , addicted and methadone maintained subjects , respectively relative to control group .
	manualset3
89097	7	398890	13	NULL	NULL	0	NULL	methadone maintained subjects	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the NR3B mRNA expression was significantly up-regulated by the factors 9.11 ( P & lt ; 0.001 ) , 10.07 ( P & lt ; 0.001 ) and 4.08 ( P & lt ; 0.05 ) in abstinent , addicted and methadone maintained subjects , respectively relative to control group .
	manualset3
89098	8	398890	13	NULL	NULL	0	NULL	control group	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the NR3B mRNA expression was significantly up-regulated by the factors 9.11 ( P & lt ; 0.001 ) , 10.07 ( P & lt ; 0.001 ) and 4.08 ( P & lt ; 0.05 ) in abstinent , addicted and methadone maintained subjects , respectively relative to control group .
	manualset3
89100	9	398890	13	NULL	NULL	0	NULL	factors	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the NR3B mRNA expression was significantly up-regulated by the factors 9.11 ( P & lt ; 0.001 ) , 10.07 ( P & lt ; 0.001 ) and 4.08 ( P & lt ; 0.05 ) in abstinent , addicted and methadone maintained subjects , respectively relative to control group .
	manualset3
89225	1	398891	13	NULL	NULL	NULL	NULL	RNA content	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the RNA content ( cytophotometry ) and the total protein content ( cytophotometry and micro-interferometry ) are relatively low in the tumor cells .
	manualset3
89226	2	398891	13	NULL	NULL	0	NULL	cytophotometry	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the RNA content ( cytophotometry ) and the total protein content ( cytophotometry and micro-interferometry ) are relatively low in the tumor cells .
	manualset3
89227	3	398891	13	NULL	NULL	0	NULL	protein content 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the RNA content ( cytophotometry ) and the total protein content ( cytophotometry and micro-interferometry ) are relatively low in the tumor cells .
	manualset3
89228	4	398891	13	NULL	NULL	0	NULL	cytophotometry	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the RNA content ( cytophotometry ) and the total protein content ( cytophotometry and micro-interferometry ) are relatively low in the tumor cells .
	manualset3
89229	5	398891	13	NULL	NULL	0	NULL	micro-interferometry 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the RNA content ( cytophotometry ) and the total protein content ( cytophotometry and micro-interferometry ) are relatively low in the tumor cells .
	manualset3
89230	6	398891	13	NULL	NULL	0	NULL	tumor cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the RNA content ( cytophotometry ) and the total protein content ( cytophotometry and micro-interferometry ) are relatively low in the tumor cells .
	manualset3
89231	1	398892	13	NULL	NULL	0	NULL	T-cadherin amino acid motif 	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the T-cadherin amino acid motif has been well conserved through evolution in vertebrates , suggesting that T-cadherin may have biological significance in higher animals .
	manualset3
89232	2	398892	13	NULL	NULL	0	NULL	 evolution	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the T-cadherin amino acid motif has been well conserved through evolution in vertebrates , suggesting that T-cadherin may have biological significance in higher animals .
	manualset3
89233	3	398892	13	NULL	NULL	0	NULL	vertebrates	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the T-cadherin amino acid motif has been well conserved through evolution in vertebrates , suggesting that T-cadherin may have biological significance in higher animals .
	manualset3
89234	4	398892	13	NULL	NULL	0	NULL	T-cadherin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the T-cadherin amino acid motif has been well conserved through evolution in vertebrates , suggesting that T-cadherin may have biological significance in higher animals .
	manualset3
89235	5	398892	13	NULL	NULL	0	NULL	biological significance	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the T-cadherin amino acid motif has been well conserved through evolution in vertebrates , suggesting that T-cadherin may have biological significance in higher animals .
	manualset3
89236	6	398892	13	NULL	NULL	0	NULL	animals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the T-cadherin amino acid motif has been well conserved through evolution in vertebrates , suggesting that T-cadherin may have biological significance in higher animals .
	manualset3
89237	1	398893	13	NULL	NULL	0	NULL	X-ray cocrystal structure	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the X-ray cocrystal structure of the antithrombin-pentasaccharide complex shows that Trp49 does not contact the bound saccharide .
	manualset3
89238	2	398893	13	NULL	NULL	0	NULL	antithrombin-pentasaccharide complex	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the X-ray cocrystal structure of the antithrombin-pentasaccharide complex shows that Trp49 does not contact the bound saccharide .
	manualset3
89239	3	398893	13	NULL	NULL	0	NULL	Trp49	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the X-ray cocrystal structure of the antithrombin-pentasaccharide complex shows that Trp49 does not contact the bound saccharide .
	manualset3
89240	4	398893	13	NULL	NULL	0	NULL	saccharide 	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the X-ray cocrystal structure of the antithrombin-pentasaccharide complex shows that Trp49 does not contact the bound saccharide .
	manualset3
89241	1	398894	13	NULL	NULL	0	NULL	future 	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	( The future of the medical profession ) .
	manualset3
89242	2	398894	13	NULL	NULL	0	NULL	medical profession	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	( The future of the medical profession ) .
	manualset3
89243	1	398895	13	NULL	NULL	0	NULL	agglomerates	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the agglomerates had a smaller fractal dimension ( D ( f ) = 1.28 0.08 ) ( i.e. , loosely bound ) and were found to be cytotoxic to the HaCaT cells , with a significant decrease in cell viability occurring at 25 g/mL and higher .
	manualset3
89244	2	398895	13	NULL	NULL	0	NULL	smaller fractal dimension ( D ( f ) = 1.28 0.08 ) 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the agglomerates had a smaller fractal dimension ( D ( f ) = 1.28 0.08 ) ( i.e. , loosely bound ) and were found to be cytotoxic to the HaCaT cells , with a significant decrease in cell viability occurring at 25 g/mL and higher .
	manualset3
89245	3	398895	13	NULL	NULL	0	NULL	HaCaT cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the agglomerates had a smaller fractal dimension ( D ( f ) = 1.28 0.08 ) ( i.e. , loosely bound ) and were found to be cytotoxic to the HaCaT cells , with a significant decrease in cell viability occurring at 25 g/mL and higher .
	manualset3
89246	4	398895	13	NULL	NULL	0	NULL	cell viability	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the agglomerates had a smaller fractal dimension ( D ( f ) = 1.28 0.08 ) ( i.e. , loosely bound ) and were found to be cytotoxic to the HaCaT cells , with a significant decrease in cell viability occurring at 25 g/mL and higher .
	manualset3
89247	5	398895	13	NULL	NULL	0	NULL	25 g/mL 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the agglomerates had a smaller fractal dimension ( D ( f ) = 1.28 0.08 ) ( i.e. , loosely bound ) and were found to be cytotoxic to the HaCaT cells , with a significant decrease in cell viability occurring at 25 g/mL and higher .
	manualset3
89248	1	398896	13	NULL	NULL	0	NULL	antigenic epitopes	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the antigenic epitopes of human spermatozoa , which induced antibody production , are xenogenic for the mouse , and therefore there is a possibility that there is a difference in recognized antigenic epitopes in humans as isotypic and in mice as xenogenic .
	manualset3
89249	2	398896	13	NULL	NULL	0	NULL	human spermatozoa 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the antigenic epitopes of human spermatozoa , which induced antibody production , are xenogenic for the mouse , and therefore there is a possibility that there is a difference in recognized antigenic epitopes in humans as isotypic and in mice as xenogenic .
	manualset3
89250	3	398896	13	NULL	NULL	NULL	NULL	antibody production	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the antigenic epitopes of human spermatozoa , which induced antibody production , are xenogenic for the mouse , and therefore there is a possibility that there is a difference in recognized antigenic epitopes in humans as isotypic and in mice as xenogenic .
	manualset3
89251	4	398896	13	NULL	NULL	0	NULL	mouse 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the antigenic epitopes of human spermatozoa , which induced antibody production , are xenogenic for the mouse , and therefore there is a possibility that there is a difference in recognized antigenic epitopes in humans as isotypic and in mice as xenogenic .
	manualset3
89252	5	398896	13	NULL	NULL	0	NULL	antigenic epitopes	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the antigenic epitopes of human spermatozoa , which induced antibody production , are xenogenic for the mouse , and therefore there is a possibility that there is a difference in recognized antigenic epitopes in humans as isotypic and in mice as xenogenic .
	manualset3
89253	6	398896	13	NULL	NULL	0	NULL	humans	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the antigenic epitopes of human spermatozoa , which induced antibody production , are xenogenic for the mouse , and therefore there is a possibility that there is a difference in recognized antigenic epitopes in humans as isotypic and in mice as xenogenic .
	manualset3
89254	7	398896	13	NULL	NULL	0	NULL	mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the antigenic epitopes of human spermatozoa , which induced antibody production , are xenogenic for the mouse , and therefore there is a possibility that there is a difference in recognized antigenic epitopes in humans as isotypic and in mice as xenogenic .
	manualset3
89255	1	398897	13	NULL	NULL	0	NULL	aptamer	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the aptamer does not completely block small synthetic substrate cleavage , although it does slow the rate of cleavage .
	manualset3
89256	2	398897	13	NULL	NULL	0	NULL	substrate cleavage	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the aptamer does not completely block small synthetic substrate cleavage , although it does slow the rate of cleavage .
	manualset3
89257	3	398897	13	NULL	NULL	0	NULL	rate	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the aptamer does not completely block small synthetic substrate cleavage , although it does slow the rate of cleavage .
	manualset3
89258	4	398897	13	NULL	NULL	0	NULL	cleavage	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the aptamer does not completely block small synthetic substrate cleavage , although it does slow the rate of cleavage .
	manualset3
89259	1	398898	13	NULL	NULL	0	NULL	 bursting activity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the bursting activity elicited by d-amphetamine was blocked in the presence of ouabain or in the medium containing potassium-free , low sodium solutions .
	manualset3
89260	2	398898	13	NULL	NULL	0	NULL	d-amphetamine	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the bursting activity elicited by d-amphetamine was blocked in the presence of ouabain or in the medium containing potassium-free , low sodium solutions .
	manualset3
89261	3	398898	13	NULL	NULL	0	NULL	ouabain	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the bursting activity elicited by d-amphetamine was blocked in the presence of ouabain or in the medium containing potassium-free , low sodium solutions .
	manualset3
89262	4	398898	13	NULL	NULL	0	NULL	medium 	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the bursting activity elicited by d-amphetamine was blocked in the presence of ouabain or in the medium containing potassium-free , low sodium solutions .
	manualset3
89263	5	398898	13	NULL	NULL	0	NULL	potassium-free solutions 	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the bursting activity elicited by d-amphetamine was blocked in the presence of ouabain or in the medium containing potassium-free , low sodium solutions .
	manualset3
89264	6	398898	13	NULL	NULL	0	NULL	low sodium solutions	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the bursting activity elicited by d-amphetamine was blocked in the presence of ouabain or in the medium containing potassium-free , low sodium solutions .
	manualset3
89265	1	398899	13	NULL	NULL	0	NULL	 carba-analogue compound 4	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the carba-analogue compound 4 is almost ineffective .
	manualset3
89266	1	398900	13	NULL	NULL	0	NULL	cationized ferritin	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the cationized ferritin binding was preserved in the endothelial cells of the arterioles with an increased vascular permeability .
	manualset3
89267	2	398900	13	NULL	NULL	0	NULL	endothelial cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the cationized ferritin binding was preserved in the endothelial cells of the arterioles with an increased vascular permeability .
	manualset3
89268	3	398900	13	NULL	NULL	0	NULL	arterioles	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the cationized ferritin binding was preserved in the endothelial cells of the arterioles with an increased vascular permeability .
	manualset3
89269	4	398900	13	NULL	NULL	0	NULL	vascular permeability	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the cationized ferritin binding was preserved in the endothelial cells of the arterioles with an increased vascular permeability .
	manualset3
89270	1	398901	13	NULL	NULL	0	NULL	cell-free assay 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the cell-free assay provides an incomplete representation of the assembly and regulation of the NADPH oxidase in vivo , and it has become necessary to develop methods for introducing biomolecules , such as peptides , into intact neutrophils where their effects can be investigated .
	manualset3
89271	2	398901	13	NULL	NULL	NULL	NULL	assembly 	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the cell-free assay provides an incomplete representation of the assembly and regulation of the NADPH oxidase in vivo , and it has become necessary to develop methods for introducing biomolecules , such as peptides , into intact neutrophils where their effects can be investigated .
	manualset3
89272	3	398901	13	NULL	NULL	0	NULL	regulation of the NADPH oxidase	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the cell-free assay provides an incomplete representation of the assembly and regulation of the NADPH oxidase in vivo , and it has become necessary to develop methods for introducing biomolecules , such as peptides , into intact neutrophils where their effects can be investigated .
	manualset3
89273	4	398901	13	NULL	NULL	0	NULL	methods 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the cell-free assay provides an incomplete representation of the assembly and regulation of the NADPH oxidase in vivo , and it has become necessary to develop methods for introducing biomolecules , such as peptides , into intact neutrophils where their effects can be investigated .
	manualset3
89274	5	398901	13	NULL	NULL	0	NULL	biomolecules	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the cell-free assay provides an incomplete representation of the assembly and regulation of the NADPH oxidase in vivo , and it has become necessary to develop methods for introducing biomolecules , such as peptides , into intact neutrophils where their effects can be investigated .
	manualset3
89275	6	398901	13	NULL	NULL	0	NULL	peptides	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the cell-free assay provides an incomplete representation of the assembly and regulation of the NADPH oxidase in vivo , and it has become necessary to develop methods for introducing biomolecules , such as peptides , into intact neutrophils where their effects can be investigated .
	manualset3
89276	7	398901	13	NULL	NULL	0	NULL	neutrophils	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the cell-free assay provides an incomplete representation of the assembly and regulation of the NADPH oxidase in vivo , and it has become necessary to develop methods for introducing biomolecules , such as peptides , into intact neutrophils where their effects can be investigated .
	manualset3
89277	8	398901	13	NULL	NULL	0	NULL	effects	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the cell-free assay provides an incomplete representation of the assembly and regulation of the NADPH oxidase in vivo , and it has become necessary to develop methods for introducing biomolecules , such as peptides , into intact neutrophils where their effects can be investigated .
	manualset3
89278	1	398902	13	NULL	NULL	0	NULL	question	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the central question of why it took these populations approximately 100 , 000 years to disperse from Africa to other regions of the world has never been clearly resolved .
	manualset3
89279	2	398902	13	NULL	NULL	0	NULL	populations	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the central question of why it took these populations approximately 100 , 000 years to disperse from Africa to other regions of the world has never been clearly resolved .
	manualset3
89280	3	398902	13	NULL	NULL	0	NULL	100 , 000 years	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the central question of why it took these populations approximately 100 , 000 years to disperse from Africa to other regions of the world has never been clearly resolved .
	manualset3
89281	4	398902	13	NULL	NULL	0	NULL	Africa	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the central question of why it took these populations approximately 100 , 000 years to disperse from Africa to other regions of the world has never been clearly resolved .
	manualset3
89282	5	398902	13	NULL	NULL	NULL	NULL	regions 	GeographicalLocation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the central question of why it took these populations approximately 100 , 000 years to disperse from Africa to other regions of the world has never been clearly resolved .
	manualset3
89283	6	398902	13	NULL	NULL	0	NULL	 world 	GeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the central question of why it took these populations approximately 100 , 000 years to disperse from Africa to other regions of the world has never been clearly resolved .
	manualset3
89284	1	398903	13	NULL	NULL	0	NULL	chemical preparation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the chemical preparation of scanning electron microscope ( SEM ) specimens , although adequate for low-resolution imaging of superficial detail , is not the true representation of the chemistry and composition of the sample , as extraction and aggregation artefacts as a result of dehydrating and cross-linking agents are abundant .
	manualset3
89285	2	398903	13	NULL	NULL	0	NULL	scanning electron microscope ( SEM ) specimens	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the chemical preparation of scanning electron microscope ( SEM ) specimens , although adequate for low-resolution imaging of superficial detail , is not the true representation of the chemistry and composition of the sample , as extraction and aggregation artefacts as a result of dehydrating and cross-linking agents are abundant .
	manualset3
89286	3	398903	13	NULL	NULL	0	NULL	low-resolution imaging 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the chemical preparation of scanning electron microscope ( SEM ) specimens , although adequate for low-resolution imaging of superficial detail , is not the true representation of the chemistry and composition of the sample , as extraction and aggregation artefacts as a result of dehydrating and cross-linking agents are abundant .
	manualset3
89287	4	398903	13	NULL	NULL	NULL	NULL	chemistry of the sample	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the chemical preparation of scanning electron microscope ( SEM ) specimens , although adequate for low-resolution imaging of superficial detail , is not the true representation of the chemistry and composition of the sample , as extraction and aggregation artefacts as a result of dehydrating and cross-linking agents are abundant .
	manualset3
89288	5	398903	13	NULL	NULL	0	NULL	composition of the sample	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the chemical preparation of scanning electron microscope ( SEM ) specimens , although adequate for low-resolution imaging of superficial detail , is not the true representation of the chemistry and composition of the sample , as extraction and aggregation artefacts as a result of dehydrating and cross-linking agents are abundant .
	manualset3
89289	6	398903	13	NULL	NULL	0	NULL	extraction 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the chemical preparation of scanning electron microscope ( SEM ) specimens , although adequate for low-resolution imaging of superficial detail , is not the true representation of the chemistry and composition of the sample , as extraction and aggregation artefacts as a result of dehydrating and cross-linking agents are abundant .
	manualset3
89290	7	398903	13	NULL	NULL	0	NULL	aggregation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the chemical preparation of scanning electron microscope ( SEM ) specimens , although adequate for low-resolution imaging of superficial detail , is not the true representation of the chemistry and composition of the sample , as extraction and aggregation artefacts as a result of dehydrating and cross-linking agents are abundant .
	manualset3
89291	8	398903	13	NULL	NULL	0	NULL	artefacts	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the chemical preparation of scanning electron microscope ( SEM ) specimens , although adequate for low-resolution imaging of superficial detail , is not the true representation of the chemistry and composition of the sample , as extraction and aggregation artefacts as a result of dehydrating and cross-linking agents are abundant .
	manualset3
89292	9	398903	13	NULL	NULL	0	NULL	dehydrating agents 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the chemical preparation of scanning electron microscope ( SEM ) specimens , although adequate for low-resolution imaging of superficial detail , is not the true representation of the chemistry and composition of the sample , as extraction and aggregation artefacts as a result of dehydrating and cross-linking agents are abundant .
	manualset3
89293	10	398903	13	NULL	NULL	0	NULL	cross-linking agents	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the chemical preparation of scanning electron microscope ( SEM ) specimens , although adequate for low-resolution imaging of superficial detail , is not the true representation of the chemistry and composition of the sample , as extraction and aggregation artefacts as a result of dehydrating and cross-linking agents are abundant .
	manualset3
89294	1	398904	13	NULL	NULL	0	NULL	comparison 	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the comparison of the steady-state level of the pyruvate dehydrogenase system in the presence of different substrates in various metabolic conditions provides some evidence that accumulation of acetyl-CoA and high level of NADH may promote the phosphorylation of pyruvate dehydrogenase .
	manualset3
89295	2	398904	13	NULL	NULL	0	NULL	 steady-state level	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the comparison of the steady-state level of the pyruvate dehydrogenase system in the presence of different substrates in various metabolic conditions provides some evidence that accumulation of acetyl-CoA and high level of NADH may promote the phosphorylation of pyruvate dehydrogenase .
	manualset3
89296	3	398904	13	NULL	NULL	NULL	NULL	pyruvate dehydrogenase system 	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the comparison of the steady-state level of the pyruvate dehydrogenase system in the presence of different substrates in various metabolic conditions provides some evidence that accumulation of acetyl-CoA and high level of NADH may promote the phosphorylation of pyruvate dehydrogenase .
	manualset3
89297	4	398904	13	NULL	NULL	0	NULL	substrates 	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the comparison of the steady-state level of the pyruvate dehydrogenase system in the presence of different substrates in various metabolic conditions provides some evidence that accumulation of acetyl-CoA and high level of NADH may promote the phosphorylation of pyruvate dehydrogenase .
	manualset3
89298	5	398904	13	NULL	NULL	0	NULL	conditions 	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the comparison of the steady-state level of the pyruvate dehydrogenase system in the presence of different substrates in various metabolic conditions provides some evidence that accumulation of acetyl-CoA and high level of NADH may promote the phosphorylation of pyruvate dehydrogenase .
	manualset3
89299	6	398904	13	NULL	NULL	0	NULL	evidence 	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the comparison of the steady-state level of the pyruvate dehydrogenase system in the presence of different substrates in various metabolic conditions provides some evidence that accumulation of acetyl-CoA and high level of NADH may promote the phosphorylation of pyruvate dehydrogenase .
	manualset3
89300	7	398904	13	NULL	NULL	0	NULL	accumulation 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the comparison of the steady-state level of the pyruvate dehydrogenase system in the presence of different substrates in various metabolic conditions provides some evidence that accumulation of acetyl-CoA and high level of NADH may promote the phosphorylation of pyruvate dehydrogenase .
	manualset3
89301	8	398904	13	NULL	NULL	0	NULL	acetyl-CoA 	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the comparison of the steady-state level of the pyruvate dehydrogenase system in the presence of different substrates in various metabolic conditions provides some evidence that accumulation of acetyl-CoA and high level of NADH may promote the phosphorylation of pyruvate dehydrogenase .
	manualset3
89302	9	398904	13	NULL	NULL	0	NULL	 NADH	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the comparison of the steady-state level of the pyruvate dehydrogenase system in the presence of different substrates in various metabolic conditions provides some evidence that accumulation of acetyl-CoA and high level of NADH may promote the phosphorylation of pyruvate dehydrogenase .
	manualset3
89303	10	398904	13	NULL	NULL	0	NULL	 phosphorylation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the comparison of the steady-state level of the pyruvate dehydrogenase system in the presence of different substrates in various metabolic conditions provides some evidence that accumulation of acetyl-CoA and high level of NADH may promote the phosphorylation of pyruvate dehydrogenase .
	manualset3
89304	11	398904	13	NULL	NULL	0	NULL	pyruvate dehydrogenase 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the comparison of the steady-state level of the pyruvate dehydrogenase system in the presence of different substrates in various metabolic conditions provides some evidence that accumulation of acetyl-CoA and high level of NADH may promote the phosphorylation of pyruvate dehydrogenase .
	manualset3
89305	1	398905	13	NULL	NULL	0	NULL	concept	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the concept of grief in children after the loss of a sibling or a parent has been accepted only recently .
	manualset3
89306	2	398905	13	NULL	NULL	0	NULL	grief	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the concept of grief in children after the loss of a sibling or a parent has been accepted only recently .
	manualset3
89307	3	398905	13	NULL	NULL	0	NULL	children	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the concept of grief in children after the loss of a sibling or a parent has been accepted only recently .
	manualset3
89308	4	398905	13	NULL	NULL	0	NULL	loss	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the concept of grief in children after the loss of a sibling or a parent has been accepted only recently .
	manualset3
89309	5	398905	13	NULL	NULL	NULL	NULL	 sibling	Person												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the concept of grief in children after the loss of a sibling or a parent has been accepted only recently .
	manualset3
89310	6	398905	13	NULL	NULL	NULL	NULL	parent	Person												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the concept of grief in children after the loss of a sibling or a parent has been accepted only recently .
	manualset3
89323	1	398906	13	NULL	NULL	0	NULL	conformational change	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the conformational change of BSA at pH values above pH 8 has to be taken into account .
	manualset3
89325	2	398906	13	NULL	NULL	0	NULL	BSA	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the conformational change of BSA at pH values above pH 8 has to be taken into account .
	manualset3
89327	3	398906	13	NULL	NULL	NULL	NULL	pH values	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the conformational change of BSA at pH values above pH 8 has to be taken into account .
	manualset3
89328	4	398906	13	NULL	NULL	0	NULL	pH 8	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the conformational change of BSA at pH values above pH 8 has to be taken into account .
	manualset3
89337	1	398907	13	NULL	NULL	0	NULL	consequences of stigmatization	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the consequences of stigmatization were class related in that the lower the class , the greater the chance that the XYY individual would spend time in the penal as well as the medical system of society .
	manualset3
89341	2	398907	13	NULL	NULL	0	NULL	 class	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the consequences of stigmatization were class related in that the lower the class , the greater the chance that the XYY individual would spend time in the penal as well as the medical system of society .
	manualset3
89343	3	398907	13	NULL	NULL	0	NULL	 XYY individual	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the consequences of stigmatization were class related in that the lower the class , the greater the chance that the XYY individual would spend time in the penal as well as the medical system of society .
	manualset3
89344	4	398907	13	NULL	NULL	0	NULL	time	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the consequences of stigmatization were class related in that the lower the class , the greater the chance that the XYY individual would spend time in the penal as well as the medical system of society .
	manualset3
89345	5	398907	13	NULL	NULL	NULL	NULL	 medical system of society	Facility												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the consequences of stigmatization were class related in that the lower the class , the greater the chance that the XYY individual would spend time in the penal as well as the medical system of society .
	manualset3
91082	6	398907	13	NULL	NULL	0	NULL	 penal system of society	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the consequences of stigmatization were class related in that the lower the class , the greater the chance that the XYY individual would spend time in the penal as well as the medical system of society .
	manualset3
89347	1	398908	13	NULL	NULL	0	NULL	efficacy of the antibiotic	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the control efficacy of the antibiotic against Phytophthora infection was somewhat less than that of metalaxyl .
	manualset3
89348	2	398908	13	NULL	NULL	0	NULL	Phytophthora infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the control efficacy of the antibiotic against Phytophthora infection was somewhat less than that of metalaxyl .
	manualset3
89349	3	398908	13	NULL	NULL	0	NULL	metalaxyl	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the control efficacy of the antibiotic against Phytophthora infection was somewhat less than that of metalaxyl .
	manualset3
89350	1	398909	13	NULL	NULL	0	NULL	correlation	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the correlation between lethality and connectivity is relatively weak , and some highly connected proteins can be removed without noticeable phenotypic effect .
	manualset3
89351	2	398909	13	NULL	NULL	0	NULL	lethality	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the correlation between lethality and connectivity is relatively weak , and some highly connected proteins can be removed without noticeable phenotypic effect .
	manualset3
89352	3	398909	13	NULL	NULL	0	NULL	connectivity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the correlation between lethality and connectivity is relatively weak , and some highly connected proteins can be removed without noticeable phenotypic effect .
	manualset3
89353	4	398909	13	NULL	NULL	0	NULL	 proteins	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the correlation between lethality and connectivity is relatively weak , and some highly connected proteins can be removed without noticeable phenotypic effect .
	manualset3
89354	5	398909	13	NULL	NULL	0	NULL	phenotypic effect	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the correlation between lethality and connectivity is relatively weak , and some highly connected proteins can be removed without noticeable phenotypic effect .
	manualset3
89356	1	398910	13	NULL	NULL	0	NULL	correlation	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the correlation between levels of TNF and PMN counts in pleural fluid of patients with parapneumonic effusion has not been previously evaluated .
	manualset3
89357	2	398910	13	NULL	NULL	0	NULL	TNF counts	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the correlation between levels of TNF and PMN counts in pleural fluid of patients with parapneumonic effusion has not been previously evaluated .
	manualset3
89358	3	398910	13	NULL	NULL	0	NULL	PMN counts	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the correlation between levels of TNF and PMN counts in pleural fluid of patients with parapneumonic effusion has not been previously evaluated .
	manualset3
89359	4	398910	13	NULL	NULL	0	NULL	pleural fluid	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the correlation between levels of TNF and PMN counts in pleural fluid of patients with parapneumonic effusion has not been previously evaluated .
	manualset3
89360	5	398910	13	NULL	NULL	0	NULL	 patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the correlation between levels of TNF and PMN counts in pleural fluid of patients with parapneumonic effusion has not been previously evaluated .
	manualset3
89361	6	398910	13	NULL	NULL	0	NULL	parapneumonic effusion	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the correlation between levels of TNF and PMN counts in pleural fluid of patients with parapneumonic effusion has not been previously evaluated .
	manualset3
89362	1	398911	13	NULL	NULL	NULL	NULL	cost	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the cost and time required performing the intracellular calcium HTS assays in the 384-well format can be prohibitive for HTS campaigns of greater than 1 x 10 ( 6 ) wells .
	manualset3
89364	2	398911	13	NULL	NULL	0	NULL	time	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the cost and time required performing the intracellular calcium HTS assays in the 384-well format can be prohibitive for HTS campaigns of greater than 1 x 10 ( 6 ) wells .
	manualset3
89365	3	398911	13	NULL	NULL	0	NULL	intracellular calcium HTS assays	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the cost and time required performing the intracellular calcium HTS assays in the 384-well format can be prohibitive for HTS campaigns of greater than 1 x 10 ( 6 ) wells .
	manualset3
89383	4	398911	13	NULL	NULL	0	NULL	384-well format 	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the cost and time required performing the intracellular calcium HTS assays in the 384-well format can be prohibitive for HTS campaigns of greater than 1 x 10 ( 6 ) wells .
	manualset3
89387	5	398911	13	NULL	NULL	0	NULL	HTS campaigns	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the cost and time required performing the intracellular calcium HTS assays in the 384-well format can be prohibitive for HTS campaigns of greater than 1 x 10 ( 6 ) wells .
	manualset3
89388	6	398911	13	NULL	NULL	0	NULL	1 x 10 ( 6 ) wells	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the cost and time required performing the intracellular calcium HTS assays in the 384-well format can be prohibitive for HTS campaigns of greater than 1 x 10 ( 6 ) wells .
	manualset3
89390	1	398912	13	NULL	NULL	0	NULL	implementation process	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( The implementation process of a new model of intensive rehabilitation in a hospital setting : the development of an innovative practice within the context of integration of settings , services and treatment models ) .
	manualset3
89391	2	398912	13	NULL	NULL	NULL	NULL	a new model of intensive rehabilitation 	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The implementation process of a new model of intensive rehabilitation in a hospital setting : the development of an innovative practice within the context of integration of settings , services and treatment models ) .
	manualset3
89392	3	398912	13	NULL	NULL	0	NULL	hospital setting	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The implementation process of a new model of intensive rehabilitation in a hospital setting : the development of an innovative practice within the context of integration of settings , services and treatment models ) .
	manualset3
89393	4	398912	13	NULL	NULL	0	NULL	development	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( The implementation process of a new model of intensive rehabilitation in a hospital setting : the development of an innovative practice within the context of integration of settings , services and treatment models ) .
	manualset3
89395	5	398912	13	NULL	NULL	0	NULL	innovative practice 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The implementation process of a new model of intensive rehabilitation in a hospital setting : the development of an innovative practice within the context of integration of settings , services and treatment models ) .
	manualset3
89398	6	398912	13	NULL	NULL	NULL	NULL	integration of settings	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The implementation process of a new model of intensive rehabilitation in a hospital setting : the development of an innovative practice within the context of integration of settings , services and treatment models ) .
	manualset3
89401	7	398912	13	NULL	NULL	0	NULL	services	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The implementation process of a new model of intensive rehabilitation in a hospital setting : the development of an innovative practice within the context of integration of settings , services and treatment models ) .
	manualset3
89402	8	398912	13	NULL	NULL	0	NULL	treatment models	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The implementation process of a new model of intensive rehabilitation in a hospital setting : the development of an innovative practice within the context of integration of settings , services and treatment models ) .
	manualset3
89404	1	398913	13	NULL	NULL	0	NULL	difference	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the critical difference between ACL and MCL is still unclear in their healing potential and cellular response .
	manualset3
89407	2	398913	13	NULL	NULL	0	NULL	ACL	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the critical difference between ACL and MCL is still unclear in their healing potential and cellular response .
	manualset3
89408	3	398913	13	NULL	NULL	0	NULL	MCL 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the critical difference between ACL and MCL is still unclear in their healing potential and cellular response .
	manualset3
89409	4	398913	13	NULL	NULL	0	NULL	healing potential	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the critical difference between ACL and MCL is still unclear in their healing potential and cellular response .
	manualset3
89410	5	398913	13	NULL	NULL	0	NULL	cellular response 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the critical difference between ACL and MCL is still unclear in their healing potential and cellular response .
	manualset3
89411	1	398914	13	NULL	NULL	0	NULL	data 	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the data suggested that if health care providers provide women with information regarding their personal breast cancer risk and make a personalized recommendation for their breast cancer screening , greater compliance with screening guidelines would occur .
	manualset3
89412	2	398914	13	NULL	NULL	0	NULL	health care providers 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the data suggested that if health care providers provide women with information regarding their personal breast cancer risk and make a personalized recommendation for their breast cancer screening , greater compliance with screening guidelines would occur .
	manualset3
89413	3	398914	13	NULL	NULL	0	NULL	women	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the data suggested that if health care providers provide women with information regarding their personal breast cancer risk and make a personalized recommendation for their breast cancer screening , greater compliance with screening guidelines would occur .
	manualset3
89415	4	398914	13	NULL	NULL	0	NULL	information 	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the data suggested that if health care providers provide women with information regarding their personal breast cancer risk and make a personalized recommendation for their breast cancer screening , greater compliance with screening guidelines would occur .
	manualset3
89417	5	398914	13	NULL	NULL	0	NULL	personal breast cancer risk	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the data suggested that if health care providers provide women with information regarding their personal breast cancer risk and make a personalized recommendation for their breast cancer screening , greater compliance with screening guidelines would occur .
	manualset3
89418	6	398914	13	NULL	NULL	0	NULL	personalized recommendation 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the data suggested that if health care providers provide women with information regarding their personal breast cancer risk and make a personalized recommendation for their breast cancer screening , greater compliance with screening guidelines would occur .
	manualset3
89420	7	398914	13	NULL	NULL	0	NULL	breast cancer screening 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the data suggested that if health care providers provide women with information regarding their personal breast cancer risk and make a personalized recommendation for their breast cancer screening , greater compliance with screening guidelines would occur .
	manualset3
89424	8	398914	13	NULL	NULL	0	NULL	compliance	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the data suggested that if health care providers provide women with information regarding their personal breast cancer risk and make a personalized recommendation for their breast cancer screening , greater compliance with screening guidelines would occur .
	manualset3
89425	9	398914	13	NULL	NULL	0	NULL	screening guidelines	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the data suggested that if health care providers provide women with information regarding their personal breast cancer risk and make a personalized recommendation for their breast cancer screening , greater compliance with screening guidelines would occur .
	manualset3
89426	1	398915	13	NULL	NULL	NULL	NULL	ubiquitin E3 ligases	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the dedicated ubiquitin E3 ligases targeting mitochondria for autophagy have not been revealed .
	manualset3
89427	2	398915	13	NULL	NULL	0	NULL	mitochondria	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the dedicated ubiquitin E3 ligases targeting mitochondria for autophagy have not been revealed .
	manualset3
89428	3	398915	13	NULL	NULL	0	NULL	autophagy 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the dedicated ubiquitin E3 ligases targeting mitochondria for autophagy have not been revealed .
	manualset3
89429	1	398916	13	NULL	NULL	0	NULL	detection limits	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the detection limits depend considerably on the size of the HA oligomer with larger oligomers being less sensitively detectable .
	manualset3
89431	2	398916	13	NULL	NULL	0	NULL	size	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the detection limits depend considerably on the size of the HA oligomer with larger oligomers being less sensitively detectable .
	manualset3
89433	3	398916	13	NULL	NULL	0	NULL	HA oligomer	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the detection limits depend considerably on the size of the HA oligomer with larger oligomers being less sensitively detectable .
	manualset3
89434	4	398916	13	NULL	NULL	0	NULL	oligomers	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the detection limits depend considerably on the size of the HA oligomer with larger oligomers being less sensitively detectable .
	manualset3
89437	1	398917	13	NULL	NULL	0	NULL	diagnostic accuracy	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the diagnostic accuracy of individual imaging techniques is still limited .
	manualset3
89438	2	398917	13	NULL	NULL	0	NULL	individual imaging techniques	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the diagnostic accuracy of individual imaging techniques is still limited .
	manualset3
89440	1	398918	13	NULL	NULL	0	NULL	inconsistency	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the dispute about the inconsistency of data concerning the site-specific mechanism of colorectal carcinoma does exist , and more evidence about molecular events of carcinogenesis and targeted therapy needs to be collected to definitely confirm the conception .
	manualset3
89441	2	398918	13	NULL	NULL	0	NULL	data	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the dispute about the inconsistency of data concerning the site-specific mechanism of colorectal carcinoma does exist , and more evidence about molecular events of carcinogenesis and targeted therapy needs to be collected to definitely confirm the conception .
	manualset3
89443	3	398918	13	NULL	NULL	NULL	NULL	site-specific mechanism 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the dispute about the inconsistency of data concerning the site-specific mechanism of colorectal carcinoma does exist , and more evidence about molecular events of carcinogenesis and targeted therapy needs to be collected to definitely confirm the conception .
	manualset3
89444	4	398918	13	NULL	NULL	0	NULL	colorectal carcinoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the dispute about the inconsistency of data concerning the site-specific mechanism of colorectal carcinoma does exist , and more evidence about molecular events of carcinogenesis and targeted therapy needs to be collected to definitely confirm the conception .
	manualset3
89447	5	398918	13	NULL	NULL	0	NULL	evidence	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the dispute about the inconsistency of data concerning the site-specific mechanism of colorectal carcinoma does exist , and more evidence about molecular events of carcinogenesis and targeted therapy needs to be collected to definitely confirm the conception .
	manualset3
89448	6	398918	13	NULL	NULL	0	NULL	molecular events	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the dispute about the inconsistency of data concerning the site-specific mechanism of colorectal carcinoma does exist , and more evidence about molecular events of carcinogenesis and targeted therapy needs to be collected to definitely confirm the conception .
	manualset3
89449	7	398918	13	NULL	NULL	0	NULL	carcinogenesis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the dispute about the inconsistency of data concerning the site-specific mechanism of colorectal carcinoma does exist , and more evidence about molecular events of carcinogenesis and targeted therapy needs to be collected to definitely confirm the conception .
	manualset3
89450	8	398918	13	NULL	NULL	0	NULL	targeted therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the dispute about the inconsistency of data concerning the site-specific mechanism of colorectal carcinoma does exist , and more evidence about molecular events of carcinogenesis and targeted therapy needs to be collected to definitely confirm the conception .
	manualset3
89451	9	398918	13	NULL	NULL	0	NULL	conception	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the dispute about the inconsistency of data concerning the site-specific mechanism of colorectal carcinoma does exist , and more evidence about molecular events of carcinogenesis and targeted therapy needs to be collected to definitely confirm the conception .
	manualset3
89455	1	398919	13	NULL	NULL	0	NULL	dissociation constant ( K ( d ) )	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the dissociation constant ( K ( d ) ) for the interaction between TIAR RRM2 and the WNV 3 ' ( - ) SL RNA was 1.5 x 10 ( -8 ) , while that for TIA-1 RRM2 was 1.12 x 10 ( -7 ) .
	manualset3
89457	2	398919	13	NULL	NULL	0	NULL	 interaction	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the dissociation constant ( K ( d ) ) for the interaction between TIAR RRM2 and the WNV 3 ' ( - ) SL RNA was 1.5 x 10 ( -8 ) , while that for TIA-1 RRM2 was 1.12 x 10 ( -7 ) .
	manualset3
89460	3	398919	13	NULL	NULL	NULL	NULL	TIAR RRM2	PartOfProtein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the dissociation constant ( K ( d ) ) for the interaction between TIAR RRM2 and the WNV 3 ' ( - ) SL RNA was 1.5 x 10 ( -8 ) , while that for TIA-1 RRM2 was 1.12 x 10 ( -7 ) .
	manualset3
89461	4	398919	13	NULL	NULL	0	NULL	WNV 3 ' ( - ) SL RNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the dissociation constant ( K ( d ) ) for the interaction between TIAR RRM2 and the WNV 3 ' ( - ) SL RNA was 1.5 x 10 ( -8 ) , while that for TIA-1 RRM2 was 1.12 x 10 ( -7 ) .
	manualset3
89463	5	398919	13	NULL	NULL	0	NULL	1.5 x 10 ( -8 ) 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the dissociation constant ( K ( d ) ) for the interaction between TIAR RRM2 and the WNV 3 ' ( - ) SL RNA was 1.5 x 10 ( -8 ) , while that for TIA-1 RRM2 was 1.12 x 10 ( -7 ) .
	manualset3
89464	6	398919	13	NULL	NULL	NULL	NULL	TIA-1 RRM2	PartOfProtein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the dissociation constant ( K ( d ) ) for the interaction between TIAR RRM2 and the WNV 3 ' ( - ) SL RNA was 1.5 x 10 ( -8 ) , while that for TIA-1 RRM2 was 1.12 x 10 ( -7 ) .
	manualset3
89466	7	398919	13	NULL	NULL	0	NULL	1.12 x 10 ( -7 )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the dissociation constant ( K ( d ) ) for the interaction between TIAR RRM2 and the WNV 3 ' ( - ) SL RNA was 1.5 x 10 ( -8 ) , while that for TIA-1 RRM2 was 1.12 x 10 ( -7 ) .
	manualset3
89474	1	398920	13	NULL	NULL	0	NULL	H1c haplotype	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect is not strong , and the H1c haplotype is not involved , suggesting a mechanism that is distinct to that involved in the associated tauopathies and may be explained by the H1/H2 inversion .
	manualset3
89476	2	398920	13	NULL	NULL	0	NULL	mechanism	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect is not strong , and the H1c haplotype is not involved , suggesting a mechanism that is distinct to that involved in the associated tauopathies and may be explained by the H1/H2 inversion .
	manualset3
89481	3	398920	13	NULL	NULL	0	NULL	tauopathies	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect is not strong , and the H1c haplotype is not involved , suggesting a mechanism that is distinct to that involved in the associated tauopathies and may be explained by the H1/H2 inversion .
	manualset3
89482	4	398920	13	NULL	NULL	0	NULL	H1/H2 inversion	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect is not strong , and the H1c haplotype is not involved , suggesting a mechanism that is distinct to that involved in the associated tauopathies and may be explained by the H1/H2 inversion .
	manualset3
89494	5	398920	13	NULL	NULL	0	NULL	effect	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect is not strong , and the H1c haplotype is not involved , suggesting a mechanism that is distinct to that involved in the associated tauopathies and may be explained by the H1/H2 inversion .
	manualset3
89487	1	398921	13	NULL	NULL	0	NULL	BMP-4 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect of BMP-4 on the release of VEGF by ARPE-19 cells has not been studied .
	manualset3
89488	2	398921	13	NULL	NULL	0	NULL	VEGF	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect of BMP-4 on the release of VEGF by ARPE-19 cells has not been studied .
	manualset3
89491	3	398921	13	NULL	NULL	0	NULL	ARPE-19 cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect of BMP-4 on the release of VEGF by ARPE-19 cells has not been studied .
	manualset3
89493	4	398921	13	NULL	NULL	0	NULL	effect	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect of BMP-4 on the release of VEGF by ARPE-19 cells has not been studied .
	manualset3
89495	1	398922	13	NULL	NULL	0	NULL	effect	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect of dialyzer reuse has never been assessed in an uncontrolled clinical practice setting .
	manualset3
89496	2	398922	13	NULL	NULL	0	NULL	dialyzer	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect of dialyzer reuse has never been assessed in an uncontrolled clinical practice setting .
	manualset3
89497	3	398922	13	NULL	NULL	0	NULL	clinical practice setting	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect of dialyzer reuse has never been assessed in an uncontrolled clinical practice setting .
	manualset3
89498	1	398923	13	NULL	NULL	0	NULL	 preoperative treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The importance of pre - and postoperative treatment for success in plastic tubal surgery ) .
	manualset3
89499	2	398923	13	NULL	NULL	0	NULL	 postoperative treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The importance of pre - and postoperative treatment for success in plastic tubal surgery ) .
	manualset3
89500	3	398923	13	NULL	NULL	0	NULL	 plastic tubal surgery 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The importance of pre - and postoperative treatment for success in plastic tubal surgery ) .
	manualset3
89501	1	398924	13	NULL	NULL	0	NULL	effect	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect of nitrogen on the synthesis of this toxin remains unclear because of the literature contradictory data .
	manualset3
89502	2	398924	13	NULL	NULL	0	NULL	nitrogen	Atom												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect of nitrogen on the synthesis of this toxin remains unclear because of the literature contradictory data .
	manualset3
89503	3	398924	13	NULL	NULL	0	NULL	synthesis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect of nitrogen on the synthesis of this toxin remains unclear because of the literature contradictory data .
	manualset3
89504	4	398924	13	NULL	NULL	0	NULL	 toxin	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect of nitrogen on the synthesis of this toxin remains unclear because of the literature contradictory data .
	manualset3
89505	5	398924	13	NULL	NULL	0	NULL	literature contradictory data	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect of nitrogen on the synthesis of this toxin remains unclear because of the literature contradictory data .
	manualset3
89506	1	398925	13	NULL	NULL	0	NULL	effect	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect of the lindane + permethrin mixture was not significantly different than individual components of this mixture .
	manualset3
89507	2	398925	13	NULL	NULL	0	NULL	lindane + permethrin mixture	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect of the lindane + permethrin mixture was not significantly different than individual components of this mixture .
	manualset3
89508	3	398925	13	NULL	NULL	NULL	NULL	components	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the effect of the lindane + permethrin mixture was not significantly different than individual components of this mixture .
	manualset3
89509	4	398925	13	NULL	NULL	0	NULL	mixture	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect of the lindane + permethrin mixture was not significantly different than individual components of this mixture .
	manualset3
89510	1	398926	13	NULL	NULL	0	NULL	infrared laser light	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect of transient infrared laser light on neurotransmission in the CNS is still largely unknown .
	manualset3
89511	2	398926	13	NULL	NULL	0	NULL	neurotransmission	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect of transient infrared laser light on neurotransmission in the CNS is still largely unknown .
	manualset3
89512	3	398926	13	NULL	NULL	0	NULL	effect	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect of transient infrared laser light on neurotransmission in the CNS is still largely unknown .
	manualset3
89513	4	398926	13	NULL	NULL	0	NULL	 CNS 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the effect of transient infrared laser light on neurotransmission in the CNS is still largely unknown .
	manualset3
89535	1	398927	13	NULL	NULL	0	NULL	social norms campaigns	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the efficacy of social norms campaigns has been mixed .
	manualset3
89541	2	398927	13	NULL	NULL	0	NULL	efficacy	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the efficacy of social norms campaigns has been mixed .
	manualset3
89514	1	398928	13	NULL	NULL	0	NULL	eggs 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the eggs were more resistant to the C. molmol effect than the adult snails , embryogenesis began to stop at 20 ppm and eggs were all killed at 60 & 80 ppm .
	manualset3
89515	2	398928	13	NULL	NULL	0	NULL	resistant 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the eggs were more resistant to the C. molmol effect than the adult snails , embryogenesis began to stop at 20 ppm and eggs were all killed at 60 & 80 ppm .
	manualset3
89516	3	398928	13	NULL	NULL	0	NULL	C. molmol 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the eggs were more resistant to the C. molmol effect than the adult snails , embryogenesis began to stop at 20 ppm and eggs were all killed at 60 & 80 ppm .
	manualset3
89517	4	398928	13	NULL	NULL	0	NULL	effect 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the eggs were more resistant to the C. molmol effect than the adult snails , embryogenesis began to stop at 20 ppm and eggs were all killed at 60 & 80 ppm .
	manualset3
89518	5	398928	13	NULL	NULL	0	NULL	adult snails	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the eggs were more resistant to the C. molmol effect than the adult snails , embryogenesis began to stop at 20 ppm and eggs were all killed at 60 & 80 ppm .
	manualset3
89519	6	398928	13	NULL	NULL	0	NULL	embryogenesis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the eggs were more resistant to the C. molmol effect than the adult snails , embryogenesis began to stop at 20 ppm and eggs were all killed at 60 & 80 ppm .
	manualset3
89520	7	398928	13	NULL	NULL	0	NULL	20 ppm	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the eggs were more resistant to the C. molmol effect than the adult snails , embryogenesis began to stop at 20 ppm and eggs were all killed at 60 & 80 ppm .
	manualset3
89521	8	398928	13	NULL	NULL	0	NULL	eggs	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the eggs were more resistant to the C. molmol effect than the adult snails , embryogenesis began to stop at 20 ppm and eggs were all killed at 60 & 80 ppm .
	manualset3
89522	9	398928	13	NULL	NULL	0	NULL	60 & 80 ppm	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the eggs were more resistant to the C. molmol effect than the adult snails , embryogenesis began to stop at 20 ppm and eggs were all killed at 60 & 80 ppm .
	manualset3
89523	1	398929	13	NULL	NULL	0	NULL	erythrocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the erythrocytes tend to become saturated , and this phenomenon causes a nonlinear relationship between B-Pb and uptake and between metabolic and toxic effects and B-Pb .
	manualset3
89524	2	398929	13	NULL	NULL	0	NULL	phenomenon	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the erythrocytes tend to become saturated , and this phenomenon causes a nonlinear relationship between B-Pb and uptake and between metabolic and toxic effects and B-Pb .
	manualset3
89525	3	398929	13	NULL	NULL	0	NULL	nonlinear relationship	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the erythrocytes tend to become saturated , and this phenomenon causes a nonlinear relationship between B-Pb and uptake and between metabolic and toxic effects and B-Pb .
	manualset3
89526	4	398929	13	NULL	NULL	NULL	NULL	B-Pb	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the erythrocytes tend to become saturated , and this phenomenon causes a nonlinear relationship between B-Pb and uptake and between metabolic and toxic effects and B-Pb .
	manualset3
89527	5	398929	13	NULL	NULL	0	NULL	uptake	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the erythrocytes tend to become saturated , and this phenomenon causes a nonlinear relationship between B-Pb and uptake and between metabolic and toxic effects and B-Pb .
	manualset3
89528	6	398929	13	NULL	NULL	NULL	NULL	metabolic effects	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the erythrocytes tend to become saturated , and this phenomenon causes a nonlinear relationship between B-Pb and uptake and between metabolic and toxic effects and B-Pb .
	manualset3
89529	7	398929	13	NULL	NULL	0	NULL	toxic effects	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the erythrocytes tend to become saturated , and this phenomenon causes a nonlinear relationship between B-Pb and uptake and between metabolic and toxic effects and B-Pb .
	manualset3
89530	8	398929	13	NULL	NULL	0	NULL	B-Pb	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the erythrocytes tend to become saturated , and this phenomenon causes a nonlinear relationship between B-Pb and uptake and between metabolic and toxic effects and B-Pb .
	manualset3
89531	1	398930	13	NULL	NULL	0	NULL	harvest-induced selection 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the exact form of harvest-induced selection is generally unknown and the effects of harvest on trait variability remain unexplored .
	manualset3
89532	2	398930	13	NULL	NULL	0	NULL	effects	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the exact form of harvest-induced selection is generally unknown and the effects of harvest on trait variability remain unexplored .
	manualset3
89533	3	398930	13	NULL	NULL	NULL	NULL	harvest	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the exact form of harvest-induced selection is generally unknown and the effects of harvest on trait variability remain unexplored .
	manualset3
89534	4	398930	13	NULL	NULL	0	NULL	trait variability	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the exact form of harvest-induced selection is generally unknown and the effects of harvest on trait variability remain unexplored .
	manualset3
89542	1	398931	13	NULL	NULL	0	NULL	follicles	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the excess follicles formed shortly after birth did not persist into puberty and both adult rh-ActA - and vehicle-treated animals demonstrated normal fertility .
	manualset3
89543	2	398931	13	NULL	NULL	NULL	NULL	birth	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the excess follicles formed shortly after birth did not persist into puberty and both adult rh-ActA - and vehicle-treated animals demonstrated normal fertility .
	manualset3
89544	3	398931	13	NULL	NULL	NULL	NULL	puberty	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the excess follicles formed shortly after birth did not persist into puberty and both adult rh-ActA - and vehicle-treated animals demonstrated normal fertility .
	manualset3
89545	4	398931	13	NULL	NULL	0	NULL	adult rh-ActA-treated animals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the excess follicles formed shortly after birth did not persist into puberty and both adult rh-ActA - and vehicle-treated animals demonstrated normal fertility .
	manualset3
89546	5	398931	13	NULL	NULL	0	NULL	vehicle-treated animals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the excess follicles formed shortly after birth did not persist into puberty and both adult rh-ActA - and vehicle-treated animals demonstrated normal fertility .
	manualset3
89547	6	398931	13	NULL	NULL	0	NULL	fertility 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the excess follicles formed shortly after birth did not persist into puberty and both adult rh-ActA - and vehicle-treated animals demonstrated normal fertility .
	manualset3
89548	1	398932	13	NULL	NULL	0	NULL	Analyzing spatial-temporal dynamics	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Analyzing spatial-temporal dynamics of the ecological niche : a marten ( Martes martes ) population case study ) .
	manualset3
89549	2	398932	13	NULL	NULL	0	NULL	marten ( Martes martes ) 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Analyzing spatial-temporal dynamics of the ecological niche : a marten ( Martes martes ) population case study ) .
	manualset3
89550	3	398932	13	NULL	NULL	0	NULL	population case study 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Analyzing spatial-temporal dynamics of the ecological niche : a marten ( Martes martes ) population case study ) .
	manualset3
90968	4	398932	13	NULL	NULL	0	NULL	 ecological niche 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Analyzing spatial-temporal dynamics of the ecological niche : a marten ( Martes martes ) population case study ) .
	manualset3
89551	1	398933	13	NULL	NULL	0	NULL	antibacterial activity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The in vitro antibacterial activity of cefozopran against clinically isolated bacteria ) .
	manualset3
89552	2	398933	13	NULL	NULL	0	NULL	cefozopran	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( The in vitro antibacterial activity of cefozopran against clinically isolated bacteria ) .
	manualset3
89553	3	398933	13	NULL	NULL	0	NULL	bacteria	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( The in vitro antibacterial activity of cefozopran against clinically isolated bacteria ) .
	manualset3
89554	1	398934	13	NULL	NULL	0	NULL	fatty acid composition	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the fatty acid composition of the brown adipose tissue , in the 3rd generation , was similar to that observed in the 1st and 2nd generation .
	manualset3
89555	2	398934	13	NULL	NULL	0	NULL	brown adipose tissue 	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the fatty acid composition of the brown adipose tissue , in the 3rd generation , was similar to that observed in the 1st and 2nd generation .
	manualset3
89556	3	398934	13	NULL	NULL	0	NULL	 3rd generation	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the fatty acid composition of the brown adipose tissue , in the 3rd generation , was similar to that observed in the 1st and 2nd generation .
	manualset3
89557	4	398934	13	NULL	NULL	0	NULL	 1st generation	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the fatty acid composition of the brown adipose tissue , in the 3rd generation , was similar to that observed in the 1st and 2nd generation .
	manualset3
89558	5	398934	13	NULL	NULL	0	NULL	2nd generation	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the fatty acid composition of the brown adipose tissue , in the 3rd generation , was similar to that observed in the 1st and 2nd generation .
	manualset3
89559	1	398935	13	NULL	NULL	0	NULL	answer	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the final answer will require a clinical randomized trial in the management of carcinoma of the nasopharynx .
	manualset3
89561	3	398935	13	NULL	NULL	0	NULL	management	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the final answer will require a clinical randomized trial in the management of carcinoma of the nasopharynx .
	manualset3
89562	4	398935	13	NULL	NULL	0	NULL	carcinoma of the nasopharynx	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the final answer will require a clinical randomized trial in the management of carcinoma of the nasopharynx .
	manualset3
90969	5	398935	13	NULL	NULL	0	NULL	clinical randomized trial	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the final answer will require a clinical randomized trial in the management of carcinoma of the nasopharynx .
	manualset3
89560	2	398936	13	NULL	NULL	NULL	NULL	implementation 	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the implementation of hypothermia in the treatment of stroke patients is still far from routine clinical practice .
	manualset3
89570	3	398936	13	NULL	NULL	0	NULL	hypothermia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the implementation of hypothermia in the treatment of stroke patients is still far from routine clinical practice .
	manualset3
89571	4	398936	13	NULL	NULL	0	NULL	treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the implementation of hypothermia in the treatment of stroke patients is still far from routine clinical practice .
	manualset3
89572	5	398936	13	NULL	NULL	0	NULL	stroke patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the implementation of hypothermia in the treatment of stroke patients is still far from routine clinical practice .
	manualset3
89573	6	398936	13	NULL	NULL	0	NULL	routine clinical practice	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the implementation of hypothermia in the treatment of stroke patients is still far from routine clinical practice .
	manualset3
89574	1	398937	13	NULL	NULL	0	NULL	improvements in blood pressure 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the improvements in blood pressure and lipids demonstrated in the intervention group suggest that grapefruit should be further evaluated in the context of obesity and cardiovascular disease prevention .
	manualset3
89575	2	398937	13	NULL	NULL	0	NULL	 improvements in lipids	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the improvements in blood pressure and lipids demonstrated in the intervention group suggest that grapefruit should be further evaluated in the context of obesity and cardiovascular disease prevention .
	manualset3
89576	3	398937	13	NULL	NULL	0	NULL	intervention group	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the improvements in blood pressure and lipids demonstrated in the intervention group suggest that grapefruit should be further evaluated in the context of obesity and cardiovascular disease prevention .
	manualset3
89577	4	398937	13	NULL	NULL	0	NULL	grapefruit	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the improvements in blood pressure and lipids demonstrated in the intervention group suggest that grapefruit should be further evaluated in the context of obesity and cardiovascular disease prevention .
	manualset3
89578	5	398937	13	NULL	NULL	0	NULL	obesity prevention 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the improvements in blood pressure and lipids demonstrated in the intervention group suggest that grapefruit should be further evaluated in the context of obesity and cardiovascular disease prevention .
	manualset3
89579	6	398937	13	NULL	NULL	0	NULL	cardiovascular disease prevention	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the improvements in blood pressure and lipids demonstrated in the intervention group suggest that grapefruit should be further evaluated in the context of obesity and cardiovascular disease prevention .
	manualset3
89580	1	398938	13	NULL	NULL	NULL	NULL	incidence	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the incidence of nutritional rickets and the incidence and prevalence of hereditary rickets in Scandinavia are unknown .
	manualset3
89581	2	398938	13	NULL	NULL	0	NULL	nutritional rickets	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the incidence of nutritional rickets and the incidence and prevalence of hereditary rickets in Scandinavia are unknown .
	manualset3
89582	3	398938	13	NULL	NULL	NULL	NULL	incidence 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the incidence of nutritional rickets and the incidence and prevalence of hereditary rickets in Scandinavia are unknown .
	manualset3
89583	4	398938	13	NULL	NULL	NULL	NULL	prevalence	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the incidence of nutritional rickets and the incidence and prevalence of hereditary rickets in Scandinavia are unknown .
	manualset3
89584	5	398938	13	NULL	NULL	0	NULL	hereditary rickets	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the incidence of nutritional rickets and the incidence and prevalence of hereditary rickets in Scandinavia are unknown .
	manualset3
89585	6	398938	13	NULL	NULL	0	NULL	Scandinavia	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the incidence of nutritional rickets and the incidence and prevalence of hereditary rickets in Scandinavia are unknown .
	manualset3
89586	1	398939	13	NULL	NULL	0	NULL	influence	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the influence of cool storage of cat spermatozoa on subsequent in vitro embryo development and quality after IVF requires further investigation .
	manualset3
89587	2	398939	13	NULL	NULL	0	NULL	cool storage	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the influence of cool storage of cat spermatozoa on subsequent in vitro embryo development and quality after IVF requires further investigation .
	manualset3
89588	3	398939	13	NULL	NULL	0	NULL	cat spermatozoa	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the influence of cool storage of cat spermatozoa on subsequent in vitro embryo development and quality after IVF requires further investigation .
	manualset3
89589	4	398939	13	NULL	NULL	0	NULL	embryo development 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the influence of cool storage of cat spermatozoa on subsequent in vitro embryo development and quality after IVF requires further investigation .
	manualset3
89590	5	398939	13	NULL	NULL	0	NULL	embryo quality	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the influence of cool storage of cat spermatozoa on subsequent in vitro embryo development and quality after IVF requires further investigation .
	manualset3
89591	6	398939	13	NULL	NULL	0	NULL	IVF 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the influence of cool storage of cat spermatozoa on subsequent in vitro embryo development and quality after IVF requires further investigation .
	manualset3
89592	7	398939	13	NULL	NULL	NULL	NULL	investigation	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the influence of cool storage of cat spermatozoa on subsequent in vitro embryo development and quality after IVF requires further investigation .
	manualset3
89593	1	398940	13	NULL	NULL	0	NULL	 influence	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the influence of cultivar in the rhizosphere was the opposite to that in the phyllosphere , and the higher number and activity of E. coli O157 cells in the rhizosphere may be a consequence of them not being able to gain entry to the plant as effectively .
	manualset3
89594	2	398940	13	NULL	NULL	0	NULL	cultivar	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the influence of cultivar in the rhizosphere was the opposite to that in the phyllosphere , and the higher number and activity of E. coli O157 cells in the rhizosphere may be a consequence of them not being able to gain entry to the plant as effectively .
	manualset3
89595	3	398940	13	NULL	NULL	0	NULL	rhizosphere	GeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the influence of cultivar in the rhizosphere was the opposite to that in the phyllosphere , and the higher number and activity of E. coli O157 cells in the rhizosphere may be a consequence of them not being able to gain entry to the plant as effectively .
	manualset3
89596	4	398940	13	NULL	NULL	0	NULL	phyllosphere	GeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the influence of cultivar in the rhizosphere was the opposite to that in the phyllosphere , and the higher number and activity of E. coli O157 cells in the rhizosphere may be a consequence of them not being able to gain entry to the plant as effectively .
	manualset3
89597	5	398940	13	NULL	NULL	0	NULL	number	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the influence of cultivar in the rhizosphere was the opposite to that in the phyllosphere , and the higher number and activity of E. coli O157 cells in the rhizosphere may be a consequence of them not being able to gain entry to the plant as effectively .
	manualset3
89598	6	398940	13	NULL	NULL	0	NULL	activity 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the influence of cultivar in the rhizosphere was the opposite to that in the phyllosphere , and the higher number and activity of E. coli O157 cells in the rhizosphere may be a consequence of them not being able to gain entry to the plant as effectively .
	manualset3
89599	7	398940	13	NULL	NULL	0	NULL	E. coli O157 cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the influence of cultivar in the rhizosphere was the opposite to that in the phyllosphere , and the higher number and activity of E. coli O157 cells in the rhizosphere may be a consequence of them not being able to gain entry to the plant as effectively .
	manualset3
89600	8	398940	13	NULL	NULL	0	NULL	rhizosphere	GeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the influence of cultivar in the rhizosphere was the opposite to that in the phyllosphere , and the higher number and activity of E. coli O157 cells in the rhizosphere may be a consequence of them not being able to gain entry to the plant as effectively .
	manualset3
89601	9	398940	13	NULL	NULL	0	NULL	consequence	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the influence of cultivar in the rhizosphere was the opposite to that in the phyllosphere , and the higher number and activity of E. coli O157 cells in the rhizosphere may be a consequence of them not being able to gain entry to the plant as effectively .
	manualset3
89603	10	398940	13	NULL	NULL	0	NULL	 plant	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the influence of cultivar in the rhizosphere was the opposite to that in the phyllosphere , and the higher number and activity of E. coli O157 cells in the rhizosphere may be a consequence of them not being able to gain entry to the plant as effectively .
	manualset3
90970	11	398940	13	NULL	NULL	0	NULL	entry	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the influence of cultivar in the rhizosphere was the opposite to that in the phyllosphere , and the higher number and activity of E. coli O157 cells in the rhizosphere may be a consequence of them not being able to gain entry to the plant as effectively .
	manualset3
89604	1	398941	13	NULL	NULL	0	NULL	 information	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the information obtained thus far has been from only subtype B from North America and Europe , and little is known about other subtypes whose V3 amino acids differ by as much as 50 % from subtype B V3 .
	manualset3
89605	2	398941	13	NULL	NULL	0	NULL	subtype B	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the information obtained thus far has been from only subtype B from North America and Europe , and little is known about other subtypes whose V3 amino acids differ by as much as 50 % from subtype B V3 .
	manualset3
89606	3	398941	13	NULL	NULL	0	NULL	North America	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the information obtained thus far has been from only subtype B from North America and Europe , and little is known about other subtypes whose V3 amino acids differ by as much as 50 % from subtype B V3 .
	manualset3
89607	4	398941	13	NULL	NULL	0	NULL	Europe	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the information obtained thus far has been from only subtype B from North America and Europe , and little is known about other subtypes whose V3 amino acids differ by as much as 50 % from subtype B V3 .
	manualset3
89608	5	398941	13	NULL	NULL	0	NULL	subtypes	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the information obtained thus far has been from only subtype B from North America and Europe , and little is known about other subtypes whose V3 amino acids differ by as much as 50 % from subtype B V3 .
	manualset3
89609	6	398941	13	NULL	NULL	0	NULL	V3 amino acids	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the information obtained thus far has been from only subtype B from North America and Europe , and little is known about other subtypes whose V3 amino acids differ by as much as 50 % from subtype B V3 .
	manualset3
89610	7	398941	13	NULL	NULL	0	NULL	50 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the information obtained thus far has been from only subtype B from North America and Europe , and little is known about other subtypes whose V3 amino acids differ by as much as 50 % from subtype B V3 .
	manualset3
89611	8	398941	13	NULL	NULL	0	NULL	subtype B V3 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the information obtained thus far has been from only subtype B from North America and Europe , and little is known about other subtypes whose V3 amino acids differ by as much as 50 % from subtype B V3 .
	manualset3
89612	1	398942	13	NULL	NULL	0	NULL	 influence	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( The influence of different forms of coenzyme on the 4th structure of succinylized aspartate-transaminase ) .
	manualset3
89613	2	398942	13	NULL	NULL	0	NULL	coenzyme	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( The influence of different forms of coenzyme on the 4th structure of succinylized aspartate-transaminase ) .
	manualset3
89614	3	398942	13	NULL	NULL	0	NULL	4th structure	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	( The influence of different forms of coenzyme on the 4th structure of succinylized aspartate-transaminase ) .
	manualset3
89615	4	398942	13	NULL	NULL	0	NULL	succinylized aspartate-transaminase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	( The influence of different forms of coenzyme on the 4th structure of succinylized aspartate-transaminase ) .
	manualset3
89616	1	398943	13	NULL	NULL	0	NULL	 inhibition	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the inhibition occurred even in the absence of extracellular IPAR if the cells had been preincubated with IPAR .
	manualset3
89617	2	398943	13	NULL	NULL	NULL	NULL	extracellular IPAR	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the inhibition occurred even in the absence of extracellular IPAR if the cells had been preincubated with IPAR .
	manualset3
89618	3	398943	13	NULL	NULL	0	NULL	cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the inhibition occurred even in the absence of extracellular IPAR if the cells had been preincubated with IPAR .
	manualset3
89619	4	398943	13	NULL	NULL	0	NULL	 IPAR	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the inhibition occurred even in the absence of extracellular IPAR if the cells had been preincubated with IPAR .
	manualset3
89620	1	398944	13	NULL	NULL	0	NULL	iodinated alpha 1-adrenergic antagonist HEAT	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the iodinated alpha 1-adrenergic antagonist HEAT ( ( 2-beta ( 4-hydroxyphenyl ) - ethylaminomethyl ) - tetralone ) , BE 2254 ) , a radioligand with high affinity and specificity , provides autoradiographs with a higher signal to noise ratio .
	manualset3
89621	2	398944	13	NULL	NULL	0	NULL	( 2-beta ( 4-hydroxyphenyl ) - ethylaminomethyl ) - tetralone )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the iodinated alpha 1-adrenergic antagonist HEAT ( ( 2-beta ( 4-hydroxyphenyl ) - ethylaminomethyl ) - tetralone ) , BE 2254 ) , a radioligand with high affinity and specificity , provides autoradiographs with a higher signal to noise ratio .
	manualset3
89622	3	398944	13	NULL	NULL	0	NULL	BE 2254	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the iodinated alpha 1-adrenergic antagonist HEAT ( ( 2-beta ( 4-hydroxyphenyl ) - ethylaminomethyl ) - tetralone ) , BE 2254 ) , a radioligand with high affinity and specificity , provides autoradiographs with a higher signal to noise ratio .
	manualset3
89623	4	398944	13	NULL	NULL	0	NULL	radioligand	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the iodinated alpha 1-adrenergic antagonist HEAT ( ( 2-beta ( 4-hydroxyphenyl ) - ethylaminomethyl ) - tetralone ) , BE 2254 ) , a radioligand with high affinity and specificity , provides autoradiographs with a higher signal to noise ratio .
	manualset3
89624	5	398944	13	NULL	NULL	0	NULL	affinity	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the iodinated alpha 1-adrenergic antagonist HEAT ( ( 2-beta ( 4-hydroxyphenyl ) - ethylaminomethyl ) - tetralone ) , BE 2254 ) , a radioligand with high affinity and specificity , provides autoradiographs with a higher signal to noise ratio .
	manualset3
89625	6	398944	13	NULL	NULL	0	NULL	specificity	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the iodinated alpha 1-adrenergic antagonist HEAT ( ( 2-beta ( 4-hydroxyphenyl ) - ethylaminomethyl ) - tetralone ) , BE 2254 ) , a radioligand with high affinity and specificity , provides autoradiographs with a higher signal to noise ratio .
	manualset3
89626	7	398944	13	NULL	NULL	0	NULL	autoradiographs 	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the iodinated alpha 1-adrenergic antagonist HEAT ( ( 2-beta ( 4-hydroxyphenyl ) - ethylaminomethyl ) - tetralone ) , BE 2254 ) , a radioligand with high affinity and specificity , provides autoradiographs with a higher signal to noise ratio .
	manualset3
89627	8	398944	13	NULL	NULL	NULL	NULL	signal to noise ratio	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the iodinated alpha 1-adrenergic antagonist HEAT ( ( 2-beta ( 4-hydroxyphenyl ) - ethylaminomethyl ) - tetralone ) , BE 2254 ) , a radioligand with high affinity and specificity , provides autoradiographs with a higher signal to noise ratio .
	manualset3
89628	1	398945	13	NULL	NULL	NULL	NULL	non-invasive biomarkers	Molecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the lack of early non-invasive biomarkers has hampered our ability to diagnose kidney diseases as early as possible , and subsequently , to initiate timely , effective , and appropriate treatment .
	manualset3
89629	2	398945	13	NULL	NULL	0	NULL	kidney diseases	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the lack of early non-invasive biomarkers has hampered our ability to diagnose kidney diseases as early as possible , and subsequently , to initiate timely , effective , and appropriate treatment .
	manualset3
89630	3	398945	13	NULL	NULL	0	NULL	treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the lack of early non-invasive biomarkers has hampered our ability to diagnose kidney diseases as early as possible , and subsequently , to initiate timely , effective , and appropriate treatment .
	manualset3
89644	1	398946	13	NULL	NULL	0	NULL	DBP	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the lower DBP could not be explained statistically by any of the variables measured .
	manualset3
89648	2	398946	13	NULL	NULL	NULL	NULL	 variables 	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the lower DBP could not be explained statistically by any of the variables measured .
	manualset3
89649	1	398947	13	NULL	NULL	0	NULL	mRNA of the inhibin alpha subunit	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the mRNA of the inhibin alpha subunit was not expressed in any of these .
	manualset3
89650	1	398948	13	NULL	NULL	0	NULL	 mineral constitution	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the main mineral constitution of sintered bovine bone-hydroxyapatite ( Ca10 ( PO4 ) 6 ( OH ) 2 , HAP ) seems to be too stable in vivo .
	manualset3
89651	2	398948	13	NULL	NULL	0	NULL	 bovine bone-hydroxyapatite	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the main mineral constitution of sintered bovine bone-hydroxyapatite ( Ca10 ( PO4 ) 6 ( OH ) 2 , HAP ) seems to be too stable in vivo .
	manualset3
89652	3	398948	13	NULL	NULL	0	NULL	Ca10 ( PO4 ) 6 ( OH ) 2 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the main mineral constitution of sintered bovine bone-hydroxyapatite ( Ca10 ( PO4 ) 6 ( OH ) 2 , HAP ) seems to be too stable in vivo .
	manualset3
89653	4	398948	13	NULL	NULL	0	NULL	HAP	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the main mineral constitution of sintered bovine bone-hydroxyapatite ( Ca10 ( PO4 ) 6 ( OH ) 2 , HAP ) seems to be too stable in vivo .
	manualset3
89654	1	398949	13	NULL	NULL	0	NULL	route of transmission 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the major route of transmission remains poorly understood .
	manualset3
89655	1	398950	13	NULL	NULL	0	NULL	penetrance 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the marked incomplete penetrance and the gender bias indicate some additional genetic and/or environmental factors to disease expression .
	manualset3
89659	2	398950	13	NULL	NULL	0	NULL	gender bias	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the marked incomplete penetrance and the gender bias indicate some additional genetic and/or environmental factors to disease expression .
	manualset3
89669	3	398950	13	NULL	NULL	0	NULL	genetic factors	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the marked incomplete penetrance and the gender bias indicate some additional genetic and/or environmental factors to disease expression .
	manualset3
89670	4	398950	13	NULL	NULL	0	NULL	environmental factors 	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the marked incomplete penetrance and the gender bias indicate some additional genetic and/or environmental factors to disease expression .
	manualset3
89671	5	398950	13	NULL	NULL	0	NULL	disease expression	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the marked incomplete penetrance and the gender bias indicate some additional genetic and/or environmental factors to disease expression .
	manualset3
89682	1	398951	13	NULL	NULL	0	NULL	mechanism	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the mechanism by which aspirin affect platelets other than by prostaglandin blockade is unclear .
	manualset3
89683	2	398951	13	NULL	NULL	0	NULL	aspirin	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the mechanism by which aspirin affect platelets other than by prostaglandin blockade is unclear .
	manualset3
89684	3	398951	13	NULL	NULL	0	NULL	platelets	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the mechanism by which aspirin affect platelets other than by prostaglandin blockade is unclear .
	manualset3
89685	4	398951	13	NULL	NULL	0	NULL	prostaglandin blockade	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the mechanism by which aspirin affect platelets other than by prostaglandin blockade is unclear .
	manualset3
89686	1	398952	13	NULL	NULL	0	NULL	 influence	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The influence of estrogens upon the mitotic activity and DNA synthesis in the adrenal glands of the castrated mice ) .
	manualset3
89687	2	398952	13	NULL	NULL	0	NULL	estrogens 	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( The influence of estrogens upon the mitotic activity and DNA synthesis in the adrenal glands of the castrated mice ) .
	manualset3
89688	3	398952	13	NULL	NULL	0	NULL	mitotic activity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The influence of estrogens upon the mitotic activity and DNA synthesis in the adrenal glands of the castrated mice ) .
	manualset3
89689	4	398952	13	NULL	NULL	NULL	NULL	DNA synthesis	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The influence of estrogens upon the mitotic activity and DNA synthesis in the adrenal glands of the castrated mice ) .
	manualset3
89690	5	398952	13	NULL	NULL	0	NULL	adrenal glands	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( The influence of estrogens upon the mitotic activity and DNA synthesis in the adrenal glands of the castrated mice ) .
	manualset3
89691	6	398952	13	NULL	NULL	0	NULL	castrated mice 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( The influence of estrogens upon the mitotic activity and DNA synthesis in the adrenal glands of the castrated mice ) .
	manualset3
89692	1	398953	13	NULL	NULL	0	NULL	mechanism	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the mechanism by which gJ prevents apoptosis is not understood , and it is not known whether gJ mediates additional cellular effects .
	manualset3
89693	2	398953	13	NULL	NULL	0	NULL	gJ	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the mechanism by which gJ prevents apoptosis is not understood , and it is not known whether gJ mediates additional cellular effects .
	manualset3
89694	3	398953	13	NULL	NULL	NULL	NULL	apoptosis	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the mechanism by which gJ prevents apoptosis is not understood , and it is not known whether gJ mediates additional cellular effects .
	manualset3
89695	4	398953	13	NULL	NULL	0	NULL	gJ 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the mechanism by which gJ prevents apoptosis is not understood , and it is not known whether gJ mediates additional cellular effects .
	manualset3
89696	5	398953	13	NULL	NULL	0	NULL	cellular effects	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the mechanism by which gJ prevents apoptosis is not understood , and it is not known whether gJ mediates additional cellular effects .
	manualset3
89697	1	398954	13	NULL	NULL	NULL	NULL	mechanisms	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the mechanisms by which TMS interferes with neural activities , especially in terms of theoretical aspects , are totally unknown .
	manualset3
89698	2	398954	13	NULL	NULL	0	NULL	TMS	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the mechanisms by which TMS interferes with neural activities , especially in terms of theoretical aspects , are totally unknown .
	manualset3
89699	3	398954	13	NULL	NULL	0	NULL	neural activities	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the mechanisms by which TMS interferes with neural activities , especially in terms of theoretical aspects , are totally unknown .
	manualset3
89700	4	398954	13	NULL	NULL	NULL	NULL	theoretical aspects	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the mechanisms by which TMS interferes with neural activities , especially in terms of theoretical aspects , are totally unknown .
	manualset3
89701	1	398955	13	NULL	NULL	NULL	NULL	mechanisms	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the mechanisms by which chromosomes recognize their homologous partners are poorly understood .
	manualset3
89702	2	398955	13	NULL	NULL	0	NULL	chromosomes	Chromosome												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the mechanisms by which chromosomes recognize their homologous partners are poorly understood .
	manualset3
89703	3	398955	13	NULL	NULL	0	NULL	homologous partners	Chromosome												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the mechanisms by which chromosomes recognize their homologous partners are poorly understood .
	manualset3
89704	1	398956	13	NULL	NULL	NULL	NULL	mechanisms	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the mechanisms of interaction of these hormones in NPY neurons are largely unknown .
	manualset3
89705	2	398956	13	NULL	NULL	0	NULL	 interaction	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the mechanisms of interaction of these hormones in NPY neurons are largely unknown .
	manualset3
89706	3	398956	13	NULL	NULL	0	NULL	hormones	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the mechanisms of interaction of these hormones in NPY neurons are largely unknown .
	manualset3
89707	4	398956	13	NULL	NULL	0	NULL	NPY neurons	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the mechanisms of interaction of these hormones in NPY neurons are largely unknown .
	manualset3
89708	1	398957	13	NULL	NULL	0	NULL	 Hebeloma	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the monophyly of Hebeloma can not be rejected outright given ITS and nLSU-rDNA data .
	manualset3
89709	2	398957	13	NULL	NULL	0	NULL	ITS	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the monophyly of Hebeloma can not be rejected outright given ITS and nLSU-rDNA data .
	manualset3
89710	3	398957	13	NULL	NULL	0	NULL	nLSU-rDNA data	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the monophyly of Hebeloma can not be rejected outright given ITS and nLSU-rDNA data .
	manualset3
90971	4	398957	13	NULL	NULL	0	NULL	monophyly	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the monophyly of Hebeloma can not be rejected outright given ITS and nLSU-rDNA data .
	manualset3
89711	1	398958	13	NULL	NULL	0	NULL	wild-type strains 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the most significant difference among the wild-type strains grown under conditions promoting capsule formation was the ability to invade fish cell lines , which was significantly higher than when the same strains were grown under conditions which did not promote capsule formation .
	manualset3
89712	2	398958	13	NULL	NULL	0	NULL	conditions 	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the most significant difference among the wild-type strains grown under conditions promoting capsule formation was the ability to invade fish cell lines , which was significantly higher than when the same strains were grown under conditions which did not promote capsule formation .
	manualset3
89713	3	398958	13	NULL	NULL	0	NULL	capsule formation 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the most significant difference among the wild-type strains grown under conditions promoting capsule formation was the ability to invade fish cell lines , which was significantly higher than when the same strains were grown under conditions which did not promote capsule formation .
	manualset3
89714	4	398958	13	NULL	NULL	0	NULL	fish cell lines	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the most significant difference among the wild-type strains grown under conditions promoting capsule formation was the ability to invade fish cell lines , which was significantly higher than when the same strains were grown under conditions which did not promote capsule formation .
	manualset3
89715	5	398958	13	NULL	NULL	0	NULL	 strains 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the most significant difference among the wild-type strains grown under conditions promoting capsule formation was the ability to invade fish cell lines , which was significantly higher than when the same strains were grown under conditions which did not promote capsule formation .
	manualset3
89716	6	398958	13	NULL	NULL	0	NULL	conditions	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the most significant difference among the wild-type strains grown under conditions promoting capsule formation was the ability to invade fish cell lines , which was significantly higher than when the same strains were grown under conditions which did not promote capsule formation .
	manualset3
89717	7	398958	13	NULL	NULL	0	NULL	capsule formation 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the most significant difference among the wild-type strains grown under conditions promoting capsule formation was the ability to invade fish cell lines , which was significantly higher than when the same strains were grown under conditions which did not promote capsule formation .
	manualset3
89718	1	398959	13	NULL	NULL	0	NULL	influence	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( The influence of mechanical forces and age on the remodelling of the spongy bone in lumbar vertebrae and in the neck of the femur .
	manualset3
89719	2	398959	13	NULL	NULL	NULL	NULL	mechanical forces	EnvironmentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The influence of mechanical forces and age on the remodelling of the spongy bone in lumbar vertebrae and in the neck of the femur .
	manualset3
89720	3	398959	13	NULL	NULL	0	NULL	age 	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	( The influence of mechanical forces and age on the remodelling of the spongy bone in lumbar vertebrae and in the neck of the femur .
	manualset3
89721	4	398959	13	NULL	NULL	NULL	NULL	 spongy bone in lumbar vertebrae	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The influence of mechanical forces and age on the remodelling of the spongy bone in lumbar vertebrae and in the neck of the femur .
	manualset3
89723	6	398959	13	NULL	NULL	0	NULL	neck of the femur	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( The influence of mechanical forces and age on the remodelling of the spongy bone in lumbar vertebrae and in the neck of the femur .
	manualset3
89724	1	398960	13	NULL	NULL	NULL	NULL	new technique 	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the new technique of transhepatic pancreatic vein catheterization , supplemented by determination of local hormone gradients , allows preoperative localization of even small tumors .
	manualset3
89725	2	398960	13	NULL	NULL	0	NULL	 transhepatic pancreatic vein catheterization	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the new technique of transhepatic pancreatic vein catheterization , supplemented by determination of local hormone gradients , allows preoperative localization of even small tumors .
	manualset3
89726	3	398960	13	NULL	NULL	NULL	NULL	hormone gradients	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the new technique of transhepatic pancreatic vein catheterization , supplemented by determination of local hormone gradients , allows preoperative localization of even small tumors .
	manualset3
89727	4	398960	13	NULL	NULL	NULL	NULL	preoperative localization	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the new technique of transhepatic pancreatic vein catheterization , supplemented by determination of local hormone gradients , allows preoperative localization of even small tumors .
	manualset3
89728	5	398960	13	NULL	NULL	0	NULL	tumors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the new technique of transhepatic pancreatic vein catheterization , supplemented by determination of local hormone gradients , allows preoperative localization of even small tumors .
	manualset3
89729	1	398961	13	NULL	NULL	0	NULL	sequence homology 	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the overall sequence homology among the conserved regions of RPA1 from different species is significantly lower than that observed in the corresponding beta ' - like subunits of class II and III RNA polymerase .
	manualset3
89730	2	398961	13	NULL	NULL	NULL	NULL	 conserved regions of RPA1	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the overall sequence homology among the conserved regions of RPA1 from different species is significantly lower than that observed in the corresponding beta ' - like subunits of class II and III RNA polymerase .
	manualset3
89732	4	398961	13	NULL	NULL	0	NULL	species	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the overall sequence homology among the conserved regions of RPA1 from different species is significantly lower than that observed in the corresponding beta ' - like subunits of class II and III RNA polymerase .
	manualset3
89733	5	398961	13	NULL	NULL	0	NULL	beta ' - like subunits of class II RNA polymerase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the overall sequence homology among the conserved regions of RPA1 from different species is significantly lower than that observed in the corresponding beta ' - like subunits of class II and III RNA polymerase .
	manualset3
89734	6	398961	13	NULL	NULL	NULL	NULL	 beta ' - like subunits of class III RNA polymerase	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the overall sequence homology among the conserved regions of RPA1 from different species is significantly lower than that observed in the corresponding beta ' - like subunits of class II and III RNA polymerase .
	manualset3
89735	1	398962	13	NULL	NULL	0	NULL	persistence	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the persistence of the oral antiallergic ( anti-PCA ) effects of azelastine for 24 h ( ID50 = 3.7 mg/kg ) does not seem to be associated with its antihistaminic or antiserotonin activities .
	manualset3
89736	2	398962	13	NULL	NULL	0	NULL	oral antiallergic ( anti-PCA ) effects	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the persistence of the oral antiallergic ( anti-PCA ) effects of azelastine for 24 h ( ID50 = 3.7 mg/kg ) does not seem to be associated with its antihistaminic or antiserotonin activities .
	manualset3
89737	3	398962	13	NULL	NULL	0	NULL	azelastine	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the persistence of the oral antiallergic ( anti-PCA ) effects of azelastine for 24 h ( ID50 = 3.7 mg/kg ) does not seem to be associated with its antihistaminic or antiserotonin activities .
	manualset3
89738	4	398962	13	NULL	NULL	0	NULL	24 h	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the persistence of the oral antiallergic ( anti-PCA ) effects of azelastine for 24 h ( ID50 = 3.7 mg/kg ) does not seem to be associated with its antihistaminic or antiserotonin activities .
	manualset3
89739	5	398962	13	NULL	NULL	0	NULL	ID50 = 3.7 mg/kg	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the persistence of the oral antiallergic ( anti-PCA ) effects of azelastine for 24 h ( ID50 = 3.7 mg/kg ) does not seem to be associated with its antihistaminic or antiserotonin activities .
	manualset3
89740	6	398962	13	NULL	NULL	0	NULL	antihistaminic activities	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the persistence of the oral antiallergic ( anti-PCA ) effects of azelastine for 24 h ( ID50 = 3.7 mg/kg ) does not seem to be associated with its antihistaminic or antiserotonin activities .
	manualset3
89741	7	398962	13	NULL	NULL	0	NULL	antiserotonin activities	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the persistence of the oral antiallergic ( anti-PCA ) effects of azelastine for 24 h ( ID50 = 3.7 mg/kg ) does not seem to be associated with its antihistaminic or antiserotonin activities .
	manualset3
89742	1	398963	13	NULL	NULL	NULL	NULL	position 	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the position of this nucleotide change makes it highly unlikely that it could be causative for Mbius syndrome in this patient because it does not affect known splicing sequences .
	manualset3
89743	2	398963	13	NULL	NULL	0	NULL	nucleotide change	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the position of this nucleotide change makes it highly unlikely that it could be causative for Mbius syndrome in this patient because it does not affect known splicing sequences .
	manualset3
89744	3	398963	13	NULL	NULL	0	NULL	Mbius syndrome	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the position of this nucleotide change makes it highly unlikely that it could be causative for Mbius syndrome in this patient because it does not affect known splicing sequences .
	manualset3
89745	4	398963	13	NULL	NULL	NULL	NULL	patient 	Person												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the position of this nucleotide change makes it highly unlikely that it could be causative for Mbius syndrome in this patient because it does not affect known splicing sequences .
	manualset3
89746	5	398963	13	NULL	NULL	0	NULL	splicing sequences	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the position of this nucleotide change makes it highly unlikely that it could be causative for Mbius syndrome in this patient because it does not affect known splicing sequences .
	manualset3
89747	1	398964	13	NULL	NULL	NULL	NULL	influence	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the potential influence of neuropsychological factors on pancreatic cancer has not been investigated to date .
	manualset3
89748	2	398964	13	NULL	NULL	0	NULL	 neuropsychological factors 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the potential influence of neuropsychological factors on pancreatic cancer has not been investigated to date .
	manualset3
89749	3	398964	13	NULL	NULL	0	NULL	pancreatic cancer	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the potential influence of neuropsychological factors on pancreatic cancer has not been investigated to date .
	manualset3
89750	4	398964	13	NULL	NULL	0	NULL	date	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the potential influence of neuropsychological factors on pancreatic cancer has not been investigated to date .
	manualset3
89751	1	398965	13	NULL	NULL	0	NULL	risk	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the potential risk of inducing an atrial and/or ventricular tachyarrhythmia and the consequences of lowering ventricular filling pressures and systemic vascular resistances should be born in mind ; when using this therapeutic association , the authors suggest starting treatment with low doses of dobutamine ( 5/kg/min ) and enoximone ( 0.5 - 1 mg/kg ) with hemodynamic control and steadily increasing the doses , depending on the results obtained .
	manualset3
89752	2	398965	13	NULL	NULL	0	NULL	atrial tachyarrhythmia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the potential risk of inducing an atrial and/or ventricular tachyarrhythmia and the consequences of lowering ventricular filling pressures and systemic vascular resistances should be born in mind ; when using this therapeutic association , the authors suggest starting treatment with low doses of dobutamine ( 5/kg/min ) and enoximone ( 0.5 - 1 mg/kg ) with hemodynamic control and steadily increasing the doses , depending on the results obtained .
	manualset3
89753	3	398965	13	NULL	NULL	0	NULL	ventricular tachyarrhythmia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the potential risk of inducing an atrial and/or ventricular tachyarrhythmia and the consequences of lowering ventricular filling pressures and systemic vascular resistances should be born in mind ; when using this therapeutic association , the authors suggest starting treatment with low doses of dobutamine ( 5/kg/min ) and enoximone ( 0.5 - 1 mg/kg ) with hemodynamic control and steadily increasing the doses , depending on the results obtained .
	manualset3
89754	4	398965	13	NULL	NULL	0	NULL	consequences	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the potential risk of inducing an atrial and/or ventricular tachyarrhythmia and the consequences of lowering ventricular filling pressures and systemic vascular resistances should be born in mind ; when using this therapeutic association , the authors suggest starting treatment with low doses of dobutamine ( 5/kg/min ) and enoximone ( 0.5 - 1 mg/kg ) with hemodynamic control and steadily increasing the doses , depending on the results obtained .
	manualset3
89755	5	398965	13	NULL	NULL	0	NULL	ventricular filling pressures 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the potential risk of inducing an atrial and/or ventricular tachyarrhythmia and the consequences of lowering ventricular filling pressures and systemic vascular resistances should be born in mind ; when using this therapeutic association , the authors suggest starting treatment with low doses of dobutamine ( 5/kg/min ) and enoximone ( 0.5 - 1 mg/kg ) with hemodynamic control and steadily increasing the doses , depending on the results obtained .
	manualset3
89756	6	398965	13	NULL	NULL	0	NULL	systemic vascular resistances 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the potential risk of inducing an atrial and/or ventricular tachyarrhythmia and the consequences of lowering ventricular filling pressures and systemic vascular resistances should be born in mind ; when using this therapeutic association , the authors suggest starting treatment with low doses of dobutamine ( 5/kg/min ) and enoximone ( 0.5 - 1 mg/kg ) with hemodynamic control and steadily increasing the doses , depending on the results obtained .
	manualset3
89757	7	398965	13	NULL	NULL	0	NULL	mind	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the potential risk of inducing an atrial and/or ventricular tachyarrhythmia and the consequences of lowering ventricular filling pressures and systemic vascular resistances should be born in mind ; when using this therapeutic association , the authors suggest starting treatment with low doses of dobutamine ( 5/kg/min ) and enoximone ( 0.5 - 1 mg/kg ) with hemodynamic control and steadily increasing the doses , depending on the results obtained .
	manualset3
89758	8	398965	13	NULL	NULL	0	NULL	therapeutic association	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the potential risk of inducing an atrial and/or ventricular tachyarrhythmia and the consequences of lowering ventricular filling pressures and systemic vascular resistances should be born in mind ; when using this therapeutic association , the authors suggest starting treatment with low doses of dobutamine ( 5/kg/min ) and enoximone ( 0.5 - 1 mg/kg ) with hemodynamic control and steadily increasing the doses , depending on the results obtained .
	manualset3
89759	9	398965	13	NULL	NULL	0	NULL	authors	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the potential risk of inducing an atrial and/or ventricular tachyarrhythmia and the consequences of lowering ventricular filling pressures and systemic vascular resistances should be born in mind ; when using this therapeutic association , the authors suggest starting treatment with low doses of dobutamine ( 5/kg/min ) and enoximone ( 0.5 - 1 mg/kg ) with hemodynamic control and steadily increasing the doses , depending on the results obtained .
	manualset3
89760	10	398965	13	NULL	NULL	0	NULL	treatment 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the potential risk of inducing an atrial and/or ventricular tachyarrhythmia and the consequences of lowering ventricular filling pressures and systemic vascular resistances should be born in mind ; when using this therapeutic association , the authors suggest starting treatment with low doses of dobutamine ( 5/kg/min ) and enoximone ( 0.5 - 1 mg/kg ) with hemodynamic control and steadily increasing the doses , depending on the results obtained .
	manualset3
89761	11	398965	13	NULL	NULL	NULL	NULL	low doses	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the potential risk of inducing an atrial and/or ventricular tachyarrhythmia and the consequences of lowering ventricular filling pressures and systemic vascular resistances should be born in mind ; when using this therapeutic association , the authors suggest starting treatment with low doses of dobutamine ( 5/kg/min ) and enoximone ( 0.5 - 1 mg/kg ) with hemodynamic control and steadily increasing the doses , depending on the results obtained .
	manualset3
89762	12	398965	13	NULL	NULL	0	NULL	5/kg/min	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the potential risk of inducing an atrial and/or ventricular tachyarrhythmia and the consequences of lowering ventricular filling pressures and systemic vascular resistances should be born in mind ; when using this therapeutic association , the authors suggest starting treatment with low doses of dobutamine ( 5/kg/min ) and enoximone ( 0.5 - 1 mg/kg ) with hemodynamic control and steadily increasing the doses , depending on the results obtained .
	manualset3
89763	13	398965	13	NULL	NULL	0	NULL	enoximone	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the potential risk of inducing an atrial and/or ventricular tachyarrhythmia and the consequences of lowering ventricular filling pressures and systemic vascular resistances should be born in mind ; when using this therapeutic association , the authors suggest starting treatment with low doses of dobutamine ( 5/kg/min ) and enoximone ( 0.5 - 1 mg/kg ) with hemodynamic control and steadily increasing the doses , depending on the results obtained .
	manualset3
89764	14	398965	13	NULL	NULL	0	NULL	0.5 - 1 mg/kg 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the potential risk of inducing an atrial and/or ventricular tachyarrhythmia and the consequences of lowering ventricular filling pressures and systemic vascular resistances should be born in mind ; when using this therapeutic association , the authors suggest starting treatment with low doses of dobutamine ( 5/kg/min ) and enoximone ( 0.5 - 1 mg/kg ) with hemodynamic control and steadily increasing the doses , depending on the results obtained .
	manualset3
89765	15	398965	13	NULL	NULL	0	NULL	hemodynamic control	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the potential risk of inducing an atrial and/or ventricular tachyarrhythmia and the consequences of lowering ventricular filling pressures and systemic vascular resistances should be born in mind ; when using this therapeutic association , the authors suggest starting treatment with low doses of dobutamine ( 5/kg/min ) and enoximone ( 0.5 - 1 mg/kg ) with hemodynamic control and steadily increasing the doses , depending on the results obtained .
	manualset3
89766	16	398965	13	NULL	NULL	NULL	NULL	low doses	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the potential risk of inducing an atrial and/or ventricular tachyarrhythmia and the consequences of lowering ventricular filling pressures and systemic vascular resistances should be born in mind ; when using this therapeutic association , the authors suggest starting treatment with low doses of dobutamine ( 5/kg/min ) and enoximone ( 0.5 - 1 mg/kg ) with hemodynamic control and steadily increasing the doses , depending on the results obtained .
	manualset3
91216	17	398965	13	NULL	NULL	0	NULL	dobutamine	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the potential risk of inducing an atrial and/or ventricular tachyarrhythmia and the consequences of lowering ventricular filling pressures and systemic vascular resistances should be born in mind ; when using this therapeutic association , the authors suggest starting treatment with low doses of dobutamine ( 5/kg/min ) and enoximone ( 0.5 - 1 mg/kg ) with hemodynamic control and steadily increasing the doses , depending on the results obtained .
	manualset3
89767	1	398966	13	NULL	NULL	NULL	NULL	 C18 : 3 	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the presence of C18 : 3 made differences more obvious between mixtures than the presence of C18 : 1 or C18 : 2 .
	manualset3
89768	2	398966	13	NULL	NULL	0	NULL	mixtures	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the presence of C18 : 3 made differences more obvious between mixtures than the presence of C18 : 1 or C18 : 2 .
	manualset3
89769	3	398966	13	NULL	NULL	NULL	NULL	C18 : 1 	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the presence of C18 : 3 made differences more obvious between mixtures than the presence of C18 : 1 or C18 : 2 .
	manualset3
89770	4	398966	13	NULL	NULL	NULL	NULL	C18 : 2 	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the presence of C18 : 3 made differences more obvious between mixtures than the presence of C18 : 1 or C18 : 2 .
	manualset3
89771	1	398967	13	NULL	NULL	0	NULL	 HCO ( 3 ) ( - )	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the presence of HCO ( 3 ) ( - ) / CO ( 2 ) stimulates the Cl ( - ) - transporting activity of SLC26A9 in Xenopus laevis oocytes or SLC26A9-transduced COS-7 cells .
	manualset3
89772	2	398967	13	NULL	NULL	0	NULL	CO ( 2 )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the presence of HCO ( 3 ) ( - ) / CO ( 2 ) stimulates the Cl ( - ) - transporting activity of SLC26A9 in Xenopus laevis oocytes or SLC26A9-transduced COS-7 cells .
	manualset3
89773	3	398967	13	NULL	NULL	0	NULL	Cl ( - ) - transporting activity 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the presence of HCO ( 3 ) ( - ) / CO ( 2 ) stimulates the Cl ( - ) - transporting activity of SLC26A9 in Xenopus laevis oocytes or SLC26A9-transduced COS-7 cells .
	manualset3
89774	4	398967	13	NULL	NULL	0	NULL	SLC26A9	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the presence of HCO ( 3 ) ( - ) / CO ( 2 ) stimulates the Cl ( - ) - transporting activity of SLC26A9 in Xenopus laevis oocytes or SLC26A9-transduced COS-7 cells .
	manualset3
89775	5	398967	13	NULL	NULL	0	NULL	Xenopus laevis oocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the presence of HCO ( 3 ) ( - ) / CO ( 2 ) stimulates the Cl ( - ) - transporting activity of SLC26A9 in Xenopus laevis oocytes or SLC26A9-transduced COS-7 cells .
	manualset3
89776	6	398967	13	NULL	NULL	0	NULL	SLC26A9-transduced COS-7 cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the presence of HCO ( 3 ) ( - ) / CO ( 2 ) stimulates the Cl ( - ) - transporting activity of SLC26A9 in Xenopus laevis oocytes or SLC26A9-transduced COS-7 cells .
	manualset3
89777	1	398968	13	NULL	NULL	0	NULL	radiobiological parameters	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the radiobiological parameters of the different tumors and normal tissues are typically not taken into account during dose prescription and optimization of a treatment plan or during plan evaluation .
	manualset3
89778	2	398968	13	NULL	NULL	0	NULL	 tumors 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the radiobiological parameters of the different tumors and normal tissues are typically not taken into account during dose prescription and optimization of a treatment plan or during plan evaluation .
	manualset3
89779	3	398968	13	NULL	NULL	0	NULL	tissues 	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the radiobiological parameters of the different tumors and normal tissues are typically not taken into account during dose prescription and optimization of a treatment plan or during plan evaluation .
	manualset3
89780	4	398968	13	NULL	NULL	0	NULL	dose prescription	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the radiobiological parameters of the different tumors and normal tissues are typically not taken into account during dose prescription and optimization of a treatment plan or during plan evaluation .
	manualset3
89781	5	398968	13	NULL	NULL	0	NULL	dose optimization	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the radiobiological parameters of the different tumors and normal tissues are typically not taken into account during dose prescription and optimization of a treatment plan or during plan evaluation .
	manualset3
89782	6	398968	13	NULL	NULL	0	NULL	treatment plan	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the radiobiological parameters of the different tumors and normal tissues are typically not taken into account during dose prescription and optimization of a treatment plan or during plan evaluation .
	manualset3
89783	7	398968	13	NULL	NULL	0	NULL	plan evaluation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the radiobiological parameters of the different tumors and normal tissues are typically not taken into account during dose prescription and optimization of a treatment plan or during plan evaluation .
	manualset3
89784	1	398969	13	NULL	NULL	0	NULL	literature	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the recent literature indicates that radical surgery combined with maximal radiotherapy dosage and modification of the chemotherapy schedules used in children may be required to improve the prognosis for adults with Wilms ' tumor .
	manualset3
89785	2	398969	13	NULL	NULL	0	NULL	radical surgery	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the recent literature indicates that radical surgery combined with maximal radiotherapy dosage and modification of the chemotherapy schedules used in children may be required to improve the prognosis for adults with Wilms ' tumor .
	manualset3
89786	3	398969	13	NULL	NULL	0	NULL	radiotherapy dosage	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the recent literature indicates that radical surgery combined with maximal radiotherapy dosage and modification of the chemotherapy schedules used in children may be required to improve the prognosis for adults with Wilms ' tumor .
	manualset3
89787	4	398969	13	NULL	NULL	0	NULL	chemotherapy schedules	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the recent literature indicates that radical surgery combined with maximal radiotherapy dosage and modification of the chemotherapy schedules used in children may be required to improve the prognosis for adults with Wilms ' tumor .
	manualset3
89788	5	398969	13	NULL	NULL	0	NULL	children	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the recent literature indicates that radical surgery combined with maximal radiotherapy dosage and modification of the chemotherapy schedules used in children may be required to improve the prognosis for adults with Wilms ' tumor .
	manualset3
89789	6	398969	13	NULL	NULL	0	NULL	prognosis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the recent literature indicates that radical surgery combined with maximal radiotherapy dosage and modification of the chemotherapy schedules used in children may be required to improve the prognosis for adults with Wilms ' tumor .
	manualset3
89790	7	398969	13	NULL	NULL	0	NULL	adults	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the recent literature indicates that radical surgery combined with maximal radiotherapy dosage and modification of the chemotherapy schedules used in children may be required to improve the prognosis for adults with Wilms ' tumor .
	manualset3
89791	8	398969	13	NULL	NULL	0	NULL	Wilms ' tumor	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the recent literature indicates that radical surgery combined with maximal radiotherapy dosage and modification of the chemotherapy schedules used in children may be required to improve the prognosis for adults with Wilms ' tumor .
	manualset3
89792	1	398970	13	NULL	NULL	0	NULL	relation	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the relation between these factors and arrhythmia has hitherto not been systematically explored .
	manualset3
89793	2	398970	13	NULL	NULL	0	NULL	 factors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the relation between these factors and arrhythmia has hitherto not been systematically explored .
	manualset3
89794	3	398970	13	NULL	NULL	0	NULL	arrhythmia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the relation between these factors and arrhythmia has hitherto not been systematically explored .
	manualset3
89795	1	398971	13	NULL	NULL	0	NULL	 relationship	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the relationship between digit ratio and cognition , and spatial cognition in particular , has produced mixed results .
	manualset3
89796	2	398971	13	NULL	NULL	0	NULL	 digit ratio 	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the relationship between digit ratio and cognition , and spatial cognition in particular , has produced mixed results .
	manualset3
89797	3	398971	13	NULL	NULL	0	NULL	cognition	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the relationship between digit ratio and cognition , and spatial cognition in particular , has produced mixed results .
	manualset3
89798	4	398971	13	NULL	NULL	NULL	NULL	spatial cognition	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the relationship between digit ratio and cognition , and spatial cognition in particular , has produced mixed results .
	manualset3
89799	1	398972	13	NULL	NULL	0	NULL	abundance 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the relative abundance of three POMC-end products ( i.e. lys-gamma1-MSH , acetyl-alpha-MSH , and CLIP fragment ) was higher in the HD subset .
	manualset3
89800	2	398972	13	NULL	NULL	0	NULL	POMC-end products	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the relative abundance of three POMC-end products ( i.e. lys-gamma1-MSH , acetyl-alpha-MSH , and CLIP fragment ) was higher in the HD subset .
	manualset3
89801	3	398972	13	NULL	NULL	0	NULL	 lys-gamma1-MSH	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the relative abundance of three POMC-end products ( i.e. lys-gamma1-MSH , acetyl-alpha-MSH , and CLIP fragment ) was higher in the HD subset .
	manualset3
89802	4	398972	13	NULL	NULL	0	NULL	acetyl-alpha-MSH	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the relative abundance of three POMC-end products ( i.e. lys-gamma1-MSH , acetyl-alpha-MSH , and CLIP fragment ) was higher in the HD subset .
	manualset3
89803	5	398972	13	NULL	NULL	0	NULL	CLIP fragment	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the relative abundance of three POMC-end products ( i.e. lys-gamma1-MSH , acetyl-alpha-MSH , and CLIP fragment ) was higher in the HD subset .
	manualset3
89804	6	398972	13	NULL	NULL	NULL	NULL	HD subset	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the relative abundance of three POMC-end products ( i.e. lys-gamma1-MSH , acetyl-alpha-MSH , and CLIP fragment ) was higher in the HD subset .
	manualset3
89805	1	398973	13	NULL	NULL	0	NULL	peroxisomal import experiment 	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the results of an in vitro peroxisomal import experiment showed that the mutation of L9P , L13P , V17P , and A20P caused loss of the PTS function .
	manualset3
89806	2	398973	13	NULL	NULL	0	NULL	mutation of L9P 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the results of an in vitro peroxisomal import experiment showed that the mutation of L9P , L13P , V17P , and A20P caused loss of the PTS function .
	manualset3
89807	3	398973	13	NULL	NULL	0	NULL	mutation of  L13P	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the results of an in vitro peroxisomal import experiment showed that the mutation of L9P , L13P , V17P , and A20P caused loss of the PTS function .
	manualset3
89808	4	398973	13	NULL	NULL	0	NULL	mutation of  V17P	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the results of an in vitro peroxisomal import experiment showed that the mutation of L9P , L13P , V17P , and A20P caused loss of the PTS function .
	manualset3
89809	5	398973	13	NULL	NULL	0	NULL	 mutation of A20P	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the results of an in vitro peroxisomal import experiment showed that the mutation of L9P , L13P , V17P , and A20P caused loss of the PTS function .
	manualset3
89810	6	398973	13	NULL	NULL	0	NULL	PTS function	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the results of an in vitro peroxisomal import experiment showed that the mutation of L9P , L13P , V17P , and A20P caused loss of the PTS function .
	manualset3
89811	1	398974	13	NULL	NULL	0	NULL	OCT-4 protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the role of the OCT-4 protein in seminomas has not been clarified .
	manualset3
89812	2	398974	13	NULL	NULL	0	NULL	seminomas	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the role of the OCT-4 protein in seminomas has not been clarified .
	manualset3
89813	3	398974	13	NULL	NULL	0	NULL	 role	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the role of the OCT-4 protein in seminomas has not been clarified .
	manualset3
89814	1	398975	13	NULL	NULL	0	NULL	role	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the role that these animals play in the transmission cycle of the Leishmania spp .
	manualset3
89815	2	398975	13	NULL	NULL	0	NULL	animals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the role that these animals play in the transmission cycle of the Leishmania spp .
	manualset3
89816	3	398975	13	NULL	NULL	NULL	NULL	transmission cycle	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the role that these animals play in the transmission cycle of the Leishmania spp .
	manualset3
89817	4	398975	13	NULL	NULL	0	NULL	Leishmania spp	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the role that these animals play in the transmission cycle of the Leishmania spp .
	manualset3
89818	1	398976	13	NULL	NULL	0	NULL	mechanism	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The mechanism of glucan-induced agglutination of Actinomyces viscosus ( author 's transl ) ) .
	manualset3
89819	2	398976	13	NULL	NULL	NULL	NULL	glucan-induced agglutination	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The mechanism of glucan-induced agglutination of Actinomyces viscosus ( author 's transl ) ) .
	manualset3
89820	3	398976	13	NULL	NULL	0	NULL	Actinomyces viscosus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( The mechanism of glucan-induced agglutination of Actinomyces viscosus ( author 's transl ) ) .
	manualset3
89821	4	398976	13	NULL	NULL	0	NULL	 author 's	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( The mechanism of glucan-induced agglutination of Actinomyces viscosus ( author 's transl ) ) .
	manualset3
89822	1	398977	13	NULL	NULL	0	NULL	treatment	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the same treatment decreased the amount of 4-methylthio-3-butenylisothiocyanate ( MTBITC ) , a major isothiocyanate in radish sprout and the activity of myrosinase , an enzyme related to produce isothiocyanates .
	manualset3
89823	2	398977	13	NULL	NULL	0	NULL	4-methylthio-3-butenylisothiocyanate ( MTBITC )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the same treatment decreased the amount of 4-methylthio-3-butenylisothiocyanate ( MTBITC ) , a major isothiocyanate in radish sprout and the activity of myrosinase , an enzyme related to produce isothiocyanates .
	manualset3
89824	3	398977	13	NULL	NULL	0	NULL	amount 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the same treatment decreased the amount of 4-methylthio-3-butenylisothiocyanate ( MTBITC ) , a major isothiocyanate in radish sprout and the activity of myrosinase , an enzyme related to produce isothiocyanates .
	manualset3
89825	4	398977	13	NULL	NULL	NULL	NULL	 a major isothiocyanate	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the same treatment decreased the amount of 4-methylthio-3-butenylisothiocyanate ( MTBITC ) , a major isothiocyanate in radish sprout and the activity of myrosinase , an enzyme related to produce isothiocyanates .
	manualset3
89826	5	398977	13	NULL	NULL	0	NULL	radish sprout 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the same treatment decreased the amount of 4-methylthio-3-butenylisothiocyanate ( MTBITC ) , a major isothiocyanate in radish sprout and the activity of myrosinase , an enzyme related to produce isothiocyanates .
	manualset3
89827	6	398977	13	NULL	NULL	0	NULL	activity of myrosinase	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the same treatment decreased the amount of 4-methylthio-3-butenylisothiocyanate ( MTBITC ) , a major isothiocyanate in radish sprout and the activity of myrosinase , an enzyme related to produce isothiocyanates .
	manualset3
89828	7	398977	13	NULL	NULL	0	NULL	enzyme	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the same treatment decreased the amount of 4-methylthio-3-butenylisothiocyanate ( MTBITC ) , a major isothiocyanate in radish sprout and the activity of myrosinase , an enzyme related to produce isothiocyanates .
	manualset3
89829	8	398977	13	NULL	NULL	0	NULL	isothiocyanates	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the same treatment decreased the amount of 4-methylthio-3-butenylisothiocyanate ( MTBITC ) , a major isothiocyanate in radish sprout and the activity of myrosinase , an enzyme related to produce isothiocyanates .
	manualset3
89830	1	398978	13	NULL	NULL	0	NULL	scale shift 	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the scale shift was similar between the LRCpH and the CIpH .
	manualset3
89831	2	398978	13	NULL	NULL	0	NULL	LRCpH	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the scale shift was similar between the LRCpH and the CIpH .
	manualset3
89832	3	398978	13	NULL	NULL	0	NULL	CIpH	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the scale shift was similar between the LRCpH and the CIpH .
	manualset3
89833	1	398979	13	NULL	NULL	NULL	NULL	severe cases	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the severe cases and those occurring in high risk patient must be treated ( ciprofloxacin or ceftriaxone ) .
	manualset3
89834	2	398979	13	NULL	NULL	NULL	NULL	high risk patient 	Person												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the severe cases and those occurring in high risk patient must be treated ( ciprofloxacin or ceftriaxone ) .
	manualset3
89835	3	398979	13	NULL	NULL	0	NULL	ciprofloxacin	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the severe cases and those occurring in high risk patient must be treated ( ciprofloxacin or ceftriaxone ) .
	manualset3
89836	4	398979	13	NULL	NULL	0	NULL	ceftriaxone	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the severe cases and those occurring in high risk patient must be treated ( ciprofloxacin or ceftriaxone ) .
	manualset3
89837	1	398980	13	NULL	NULL	0	NULL	signal intensities	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the signal intensities for IL-1mRNA and protein in the epithelium were significantly decreased after marsupialization which relived intracystic pressure .
	manualset3
89838	2	398980	13	NULL	NULL	0	NULL	IL-1mRNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the signal intensities for IL-1mRNA and protein in the epithelium were significantly decreased after marsupialization which relived intracystic pressure .
	manualset3
89839	3	398980	13	NULL	NULL	0	NULL	 IL-1 protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the signal intensities for IL-1mRNA and protein in the epithelium were significantly decreased after marsupialization which relived intracystic pressure .
	manualset3
89840	4	398980	13	NULL	NULL	0	NULL	epithelium	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the signal intensities for IL-1mRNA and protein in the epithelium were significantly decreased after marsupialization which relived intracystic pressure .
	manualset3
89841	5	398980	13	NULL	NULL	0	NULL	marsupialization	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the signal intensities for IL-1mRNA and protein in the epithelium were significantly decreased after marsupialization which relived intracystic pressure .
	manualset3
89842	6	398980	13	NULL	NULL	0	NULL	intracystic pressure	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the signal intensities for IL-1mRNA and protein in the epithelium were significantly decreased after marsupialization which relived intracystic pressure .
	manualset3
89843	1	398981	13	NULL	NULL	NULL	NULL	CNS sites	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the specific CNS sites where ANG II inhibits baroreflexes are not completely understood .
	manualset3
89844	2	398981	13	NULL	NULL	0	NULL	ANG II	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the specific CNS sites where ANG II inhibits baroreflexes are not completely understood .
	manualset3
89845	3	398981	13	NULL	NULL	0	NULL	baroreflexes	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the specific CNS sites where ANG II inhibits baroreflexes are not completely understood .
	manualset3
89932	1	398982	13	NULL	NULL	0	NULL	role	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the specific role of sPLA ( 2 ) - IIA in phosgene-induced acute lung injury remains unidentified .
	manualset3
89933	2	398982	13	NULL	NULL	0	NULL	sPLA ( 2 ) - IIA 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the specific role of sPLA ( 2 ) - IIA in phosgene-induced acute lung injury remains unidentified .
	manualset3
89934	3	398982	13	NULL	NULL	0	NULL	phosgene-induced acute lung injury	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the specific role of sPLA ( 2 ) - IIA in phosgene-induced acute lung injury remains unidentified .
	manualset3
89935	1	398983	13	NULL	NULL	NULL	NULL	 surface area of rough endoplasmic reticulum per unit volume 	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the surface area of rough endoplasmic reticulum per unit volume of the supraoptic nucleus cell did differ significantly between the two age groups over the course of the experiment .
	manualset3
89936	2	398983	13	NULL	NULL	0	NULL	 supraoptic nucleus cell	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the surface area of rough endoplasmic reticulum per unit volume of the supraoptic nucleus cell did differ significantly between the two age groups over the course of the experiment .
	manualset3
89941	3	398983	13	NULL	NULL	0	NULL	two age groups 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the surface area of rough endoplasmic reticulum per unit volume of the supraoptic nucleus cell did differ significantly between the two age groups over the course of the experiment .
	manualset3
89942	4	398983	13	NULL	NULL	0	NULL	course	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the surface area of rough endoplasmic reticulum per unit volume of the supraoptic nucleus cell did differ significantly between the two age groups over the course of the experiment .
	manualset3
89943	5	398983	13	NULL	NULL	0	NULL	experiment	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the surface area of rough endoplasmic reticulum per unit volume of the supraoptic nucleus cell did differ significantly between the two age groups over the course of the experiment .
	manualset3
89944	1	398984	13	NULL	NULL	0	NULL	medico-social problem	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The medico-social problem in recovery from poliomyelitis ) .
	manualset3
89945	2	398984	13	NULL	NULL	0	NULL	 recovery	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The medico-social problem in recovery from poliomyelitis ) .
	manualset3
89946	3	398984	13	NULL	NULL	0	NULL	poliomyelitis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( The medico-social problem in recovery from poliomyelitis ) .
	manualset3
89947	1	398985	13	NULL	NULL	0	NULL	 time constant	Unit												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the time constant of recovery of Raw from MCh constriction was increased from control ( 40 + / - 3 s ) to 57 + / - 10 s after bradykinin infusion ( P = 0.03 ) .
	manualset3
89948	2	398985	13	NULL	NULL	0	NULL	recovery of Raw 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the time constant of recovery of Raw from MCh constriction was increased from control ( 40 + / - 3 s ) to 57 + / - 10 s after bradykinin infusion ( P = 0.03 ) .
	manualset3
89949	3	398985	13	NULL	NULL	0	NULL	MCh constriction 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the time constant of recovery of Raw from MCh constriction was increased from control ( 40 + / - 3 s ) to 57 + / - 10 s after bradykinin infusion ( P = 0.03 ) .
	manualset3
89950	4	398985	13	NULL	NULL	0	NULL	control ( 40 + / - 3 s ) to 57 + / - 10 s	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the time constant of recovery of Raw from MCh constriction was increased from control ( 40 + / - 3 s ) to 57 + / - 10 s after bradykinin infusion ( P = 0.03 ) .
	manualset3
89951	5	398985	13	NULL	NULL	0	NULL	bradykinin infusion	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the time constant of recovery of Raw from MCh constriction was increased from control ( 40 + / - 3 s ) to 57 + / - 10 s after bradykinin infusion ( P = 0.03 ) .
	manualset3
89952	6	398985	13	NULL	NULL	0	NULL	P = 0.03 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the time constant of recovery of Raw from MCh constriction was increased from control ( 40 + / - 3 s ) to 57 + / - 10 s after bradykinin infusion ( P = 0.03 ) .
	manualset3
89953	1	398986	13	NULL	NULL	0	NULL	tumors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the tumors were negative for synaptophysin and neurofilament proteins , unlike most islet cell tumors .
	manualset3
89954	2	398986	13	NULL	NULL	0	NULL	synaptophysin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the tumors were negative for synaptophysin and neurofilament proteins , unlike most islet cell tumors .
	manualset3
89955	3	398986	13	NULL	NULL	0	NULL	neurofilament proteins	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the tumors were negative for synaptophysin and neurofilament proteins , unlike most islet cell tumors .
	manualset3
89956	4	398986	13	NULL	NULL	0	NULL	islet cell tumors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the tumors were negative for synaptophysin and neurofilament proteins , unlike most islet cell tumors .
	manualset3
89957	1	398987	13	NULL	NULL	0	NULL	two	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the two extended wear groups did not differ significantly ( P ) 0.2 .
	manualset3
89958	2	398987	13	NULL	NULL	NULL	NULL	extended wear groups	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the two extended wear groups did not differ significantly ( P ) 0.2 .
	manualset3
89959	3	398987	13	NULL	NULL	0	NULL	( P ) 0.2	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the two extended wear groups did not differ significantly ( P ) 0.2 .
	manualset3
89960	1	398988	13	NULL	NULL	NULL	NULL	 vertical concentration distributions	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the vertical concentration distributions of soluble copper seem not affected much by the variation of sediment concentrations .
	manualset3
89961	2	398988	13	NULL	NULL	NULL	NULL	soluble copper	Atom												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the vertical concentration distributions of soluble copper seem not affected much by the variation of sediment concentrations .
	manualset3
89962	3	398988	13	NULL	NULL	0	NULL	variation 	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the vertical concentration distributions of soluble copper seem not affected much by the variation of sediment concentrations .
	manualset3
89963	4	398988	13	NULL	NULL	0	NULL	sediment concentrations 	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the vertical concentration distributions of soluble copper seem not affected much by the variation of sediment concentrations .
	manualset3
89964	1	398989	13	NULL	NULL	0	NULL	volume	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the volume reduction compared with equivalent BNR systems with SSTs will not be large ( 40-60 % ) , but the cost of the membranes can be offset against sludge thickening and stabilisation costs .
	manualset3
89965	2	398989	13	NULL	NULL	0	NULL	 reduction	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the volume reduction compared with equivalent BNR systems with SSTs will not be large ( 40-60 % ) , but the cost of the membranes can be offset against sludge thickening and stabilisation costs .
	manualset3
89966	3	398989	13	NULL	NULL	0	NULL	BNR systems	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the volume reduction compared with equivalent BNR systems with SSTs will not be large ( 40-60 % ) , but the cost of the membranes can be offset against sludge thickening and stabilisation costs .
	manualset3
89967	4	398989	13	NULL	NULL	0	NULL	SSTs	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the volume reduction compared with equivalent BNR systems with SSTs will not be large ( 40-60 % ) , but the cost of the membranes can be offset against sludge thickening and stabilisation costs .
	manualset3
89968	5	398989	13	NULL	NULL	0	NULL	large ( 40-60 % )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the volume reduction compared with equivalent BNR systems with SSTs will not be large ( 40-60 % ) , but the cost of the membranes can be offset against sludge thickening and stabilisation costs .
	manualset3
89969	6	398989	13	NULL	NULL	0	NULL	cost	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the volume reduction compared with equivalent BNR systems with SSTs will not be large ( 40-60 % ) , but the cost of the membranes can be offset against sludge thickening and stabilisation costs .
	manualset3
89970	7	398989	13	NULL	NULL	0	NULL	 membranes 	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the volume reduction compared with equivalent BNR systems with SSTs will not be large ( 40-60 % ) , but the cost of the membranes can be offset against sludge thickening and stabilisation costs .
	manualset3
89971	8	398989	13	NULL	NULL	0	NULL	sludge thickening	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the volume reduction compared with equivalent BNR systems with SSTs will not be large ( 40-60 % ) , but the cost of the membranes can be offset against sludge thickening and stabilisation costs .
	manualset3
89972	9	398989	13	NULL	NULL	0	NULL	stabilisation costs 	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the volume reduction compared with equivalent BNR systems with SSTs will not be large ( 40-60 % ) , but the cost of the membranes can be offset against sludge thickening and stabilisation costs .
	manualset3
89973	1	398990	13	NULL	NULL	NULL	NULL	xenogeneic CDRs 	PartOfProtein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the xenogeneic CDRs of the humanized antibodies may evoke anti-idiotypic ( anti-Id ) response in patients .
	manualset3
89974	2	398990	13	NULL	NULL	NULL	NULL	humanized antibodies	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , the xenogeneic CDRs of the humanized antibodies may evoke anti-idiotypic ( anti-Id ) response in patients .
	manualset3
89975	3	398990	13	NULL	NULL	0	NULL	anti-idiotypic ( anti-Id ) response 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the xenogeneic CDRs of the humanized antibodies may evoke anti-idiotypic ( anti-Id ) response in patients .
	manualset3
89976	4	398990	13	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , the xenogeneic CDRs of the humanized antibodies may evoke anti-idiotypic ( anti-Id ) response in patients .
	manualset3
89977	1	398991	13	NULL	NULL	0	NULL	rehabilitation training	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( The need for organized advanced rehabilitation training for handicapped adults as a condition of occupational success ) .
	manualset3
89978	2	398991	13	NULL	NULL	NULL	NULL	handicapped adults	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The need for organized advanced rehabilitation training for handicapped adults as a condition of occupational success ) .
	manualset3
89979	3	398991	13	NULL	NULL	0	NULL	condition	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( The need for organized advanced rehabilitation training for handicapped adults as a condition of occupational success ) .
	manualset3
89980	4	398991	13	NULL	NULL	NULL	NULL	occupational success	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The need for organized advanced rehabilitation training for handicapped adults as a condition of occupational success ) .
	manualset3
89981	1	398992	13	NULL	NULL	0	NULL	differences 	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there are no significant differences between scutellarin-treated group and S. miltiorrhiza-treated group ( P & gt ; 0.05 ) .
	manualset3
89982	2	398992	13	NULL	NULL	0	NULL	 scutellarin-treated group	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there are no significant differences between scutellarin-treated group and S. miltiorrhiza-treated group ( P & gt ; 0.05 ) .
	manualset3
89983	3	398992	13	NULL	NULL	0	NULL	 S. miltiorrhiza-treated group	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there are no significant differences between scutellarin-treated group and S. miltiorrhiza-treated group ( P & gt ; 0.05 ) .
	manualset3
89984	4	398992	13	NULL	NULL	0	NULL	P & gt ; 0.05	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there are no significant differences between scutellarin-treated group and S. miltiorrhiza-treated group ( P & gt ; 0.05 ) .
	manualset3
89985	1	398993	13	NULL	NULL	NULL	NULL	 indication	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , there has been some indication that cue integration may be affected by characteristics of the visual stimulus .
	manualset3
89986	2	398993	13	NULL	NULL	NULL	NULL	cue integration	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , there has been some indication that cue integration may be affected by characteristics of the visual stimulus .
	manualset3
89987	3	398993	13	NULL	NULL	NULL	NULL	visual stimulus 	EnvironmentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , there has been some indication that cue integration may be affected by characteristics of the visual stimulus .
	manualset3
89988	1	398994	13	NULL	NULL	0	NULL	 lack	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is a lack of data on tumors , regarding the relationship between N-myc gene amplification and proliferation activity .
	manualset3
89989	2	398994	13	NULL	NULL	0	NULL	data on tumors	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is a lack of data on tumors , regarding the relationship between N-myc gene amplification and proliferation activity .
	manualset3
89990	3	398994	13	NULL	NULL	0	NULL	relationship 	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is a lack of data on tumors , regarding the relationship between N-myc gene amplification and proliferation activity .
	manualset3
89991	4	398994	13	NULL	NULL	0	NULL	 N-myc gene amplification	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is a lack of data on tumors , regarding the relationship between N-myc gene amplification and proliferation activity .
	manualset3
89992	5	398994	13	NULL	NULL	0	NULL	 proliferation activity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is a lack of data on tumors , regarding the relationship between N-myc gene amplification and proliferation activity .
	manualset3
89993	1	398995	13	NULL	NULL	0	NULL	stimulation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is a possibility that long-term stimulation of neurogenesis might exhaust the proliferation potentials of neuronal progenitors .
	manualset3
89994	2	398995	13	NULL	NULL	0	NULL	neurogenesis 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is a possibility that long-term stimulation of neurogenesis might exhaust the proliferation potentials of neuronal progenitors .
	manualset3
89995	3	398995	13	NULL	NULL	0	NULL	 proliferation 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is a possibility that long-term stimulation of neurogenesis might exhaust the proliferation potentials of neuronal progenitors .
	manualset3
89996	4	398995	13	NULL	NULL	NULL	NULL	neuronal progenitors 	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , there is a possibility that long-term stimulation of neurogenesis might exhaust the proliferation potentials of neuronal progenitors .
	manualset3
89997	1	398996	13	NULL	NULL	0	NULL	documentation	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is no documentation that systematic screening will have a positive effect on morbidity and mortality , owing to the lack of randomised clinical trials .
	manualset3
89998	2	398996	13	NULL	NULL	0	NULL	systematic screening 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is no documentation that systematic screening will have a positive effect on morbidity and mortality , owing to the lack of randomised clinical trials .
	manualset3
89999	3	398996	13	NULL	NULL	0	NULL	effect	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is no documentation that systematic screening will have a positive effect on morbidity and mortality , owing to the lack of randomised clinical trials .
	manualset3
90000	4	398996	13	NULL	NULL	0	NULL	morbidity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is no documentation that systematic screening will have a positive effect on morbidity and mortality , owing to the lack of randomised clinical trials .
	manualset3
90001	5	398996	13	NULL	NULL	0	NULL	mortality	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is no documentation that systematic screening will have a positive effect on morbidity and mortality , owing to the lack of randomised clinical trials .
	manualset3
90002	6	398996	13	NULL	NULL	0	NULL	randomised clinical trials	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is no documentation that systematic screening will have a positive effect on morbidity and mortality , owing to the lack of randomised clinical trials .
	manualset3
90003	1	398997	13	NULL	NULL	0	NULL	evidence	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is no evidence that initiation of treatment , or increases in dose of opioids or sedatives , is associated with precipitation of death .
	manualset3
90004	2	398997	13	NULL	NULL	0	NULL	initiation of treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is no evidence that initiation of treatment , or increases in dose of opioids or sedatives , is associated with precipitation of death .
	manualset3
90005	3	398997	13	NULL	NULL	0	NULL	dose of opioids 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is no evidence that initiation of treatment , or increases in dose of opioids or sedatives , is associated with precipitation of death .
	manualset3
90006	4	398997	13	NULL	NULL	0	NULL	dose of sedatives	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is no evidence that initiation of treatment , or increases in dose of opioids or sedatives , is associated with precipitation of death .
	manualset3
90007	5	398997	13	NULL	NULL	0	NULL	precipitation of death	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is no evidence that initiation of treatment , or increases in dose of opioids or sedatives , is associated with precipitation of death .
	manualset3
90009	1	398998	13	NULL	NULL	0	NULL	influence	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is no mention of the influence of hemoglobinopathy on the ZPP test value .
	manualset3
90010	2	398998	13	NULL	NULL	0	NULL	hemoglobinopathy 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is no mention of the influence of hemoglobinopathy on the ZPP test value .
	manualset3
90011	3	398998	13	NULL	NULL	0	NULL	ZPP test value	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there is no mention of the influence of hemoglobinopathy on the ZPP test value .
	manualset3
90012	1	398999	13	NULL	NULL	0	NULL	trend	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there was a trend for antigen-specific proliferative responses of peripheral blood mononuclear cells ( PBMC ) from booster vaccinates to be reduced compared to responses of PBMC from single vaccinates .
	manualset3
90013	2	398999	13	NULL	NULL	0	NULL	antigen-specific proliferative responses	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there was a trend for antigen-specific proliferative responses of peripheral blood mononuclear cells ( PBMC ) from booster vaccinates to be reduced compared to responses of PBMC from single vaccinates .
	manualset3
90014	3	398999	13	NULL	NULL	0	NULL	peripheral blood mononuclear cells ( PBMC )	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there was a trend for antigen-specific proliferative responses of peripheral blood mononuclear cells ( PBMC ) from booster vaccinates to be reduced compared to responses of PBMC from single vaccinates .
	manualset3
90015	4	398999	13	NULL	NULL	0	NULL	booster vaccinates 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there was a trend for antigen-specific proliferative responses of peripheral blood mononuclear cells ( PBMC ) from booster vaccinates to be reduced compared to responses of PBMC from single vaccinates .
	manualset3
90016	5	398999	13	NULL	NULL	0	NULL	responses 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there was a trend for antigen-specific proliferative responses of peripheral blood mononuclear cells ( PBMC ) from booster vaccinates to be reduced compared to responses of PBMC from single vaccinates .
	manualset3
90017	6	398999	13	NULL	NULL	0	NULL	PBMC	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there was a trend for antigen-specific proliferative responses of peripheral blood mononuclear cells ( PBMC ) from booster vaccinates to be reduced compared to responses of PBMC from single vaccinates .
	manualset3
90018	7	398999	13	NULL	NULL	0	NULL	single vaccinates	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there was a trend for antigen-specific proliferative responses of peripheral blood mononuclear cells ( PBMC ) from booster vaccinates to be reduced compared to responses of PBMC from single vaccinates .
	manualset3
90019	1	399000	13	NULL	NULL	0	NULL	correlation 	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there was no correlation between the colony-forming efficiency and the initial number of peripheral platelets or bone marrow megakaryocytes that contained growth-promoting factor .
	manualset3
90020	2	399000	13	NULL	NULL	0	NULL	colony-forming efficiency	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there was no correlation between the colony-forming efficiency and the initial number of peripheral platelets or bone marrow megakaryocytes that contained growth-promoting factor .
	manualset3
90021	3	399000	13	NULL	NULL	NULL	NULL	 initial number	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , there was no correlation between the colony-forming efficiency and the initial number of peripheral platelets or bone marrow megakaryocytes that contained growth-promoting factor .
	manualset3
90022	4	399000	13	NULL	NULL	0	NULL	peripheral platelets	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there was no correlation between the colony-forming efficiency and the initial number of peripheral platelets or bone marrow megakaryocytes that contained growth-promoting factor .
	manualset3
90023	5	399000	13	NULL	NULL	0	NULL	bone marrow megakaryocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there was no correlation between the colony-forming efficiency and the initial number of peripheral platelets or bone marrow megakaryocytes that contained growth-promoting factor .
	manualset3
90024	6	399000	13	NULL	NULL	0	NULL	growth-promoting factor 	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there was no correlation between the colony-forming efficiency and the initial number of peripheral platelets or bone marrow megakaryocytes that contained growth-promoting factor .
	manualset3
90025	1	399001	13	NULL	NULL	0	NULL	correlation	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there was no full correlation between ` retinoblastoma pathway ' inactivation and TA-p73 expression .
	manualset3
90026	2	399001	13	NULL	NULL	NULL	NULL	  ` retinoblastoma pathway ' inactivation	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , there was no full correlation between ` retinoblastoma pathway ' inactivation and TA-p73 expression .
	manualset3
90027	3	399001	13	NULL	NULL	0	NULL	TA-p73 expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , there was no full correlation between ` retinoblastoma pathway ' inactivation and TA-p73 expression .
	manualset3
90028	1	399002	13	NULL	NULL	0	NULL	oral administration	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these changes were prevented by oral administration of PSK .
	manualset3
90029	2	399002	13	NULL	NULL	0	NULL	PSK	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these changes were prevented by oral administration of PSK .
	manualset3
90030	1	399003	13	NULL	NULL	0	NULL	concentrations	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these concentrations can inhibit the isolation of this microorganism but not its urease activity .
	manualset3
90031	2	399003	13	NULL	NULL	0	NULL	isolation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these concentrations can inhibit the isolation of this microorganism but not its urease activity .
	manualset3
90032	3	399003	13	NULL	NULL	0	NULL	 microorganism	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these concentrations can inhibit the isolation of this microorganism but not its urease activity .
	manualset3
90033	4	399003	13	NULL	NULL	0	NULL	urease activity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these concentrations can inhibit the isolation of this microorganism but not its urease activity .
	manualset3
90034	1	399004	13	NULL	NULL	0	NULL	factors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these different factors may elicit the same temporary or permanent response in that degenerating germ cells become more common , multinucleate giant germ cells form by coalescence of spermatocytes or spermatids , the ratio of germ cells to Sertoli cells is reduced , and spermatozoan production is adversely affected .
	manualset3
90035	2	399004	13	NULL	NULL	NULL	NULL	temporary or permanent response	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , these different factors may elicit the same temporary or permanent response in that degenerating germ cells become more common , multinucleate giant germ cells form by coalescence of spermatocytes or spermatids , the ratio of germ cells to Sertoli cells is reduced , and spermatozoan production is adversely affected .
	manualset3
90036	3	399004	13	NULL	NULL	NULL	NULL	degenerating germ cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , these different factors may elicit the same temporary or permanent response in that degenerating germ cells become more common , multinucleate giant germ cells form by coalescence of spermatocytes or spermatids , the ratio of germ cells to Sertoli cells is reduced , and spermatozoan production is adversely affected .
	manualset3
90037	4	399004	13	NULL	NULL	0	NULL	multinucleate giant germ cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these different factors may elicit the same temporary or permanent response in that degenerating germ cells become more common , multinucleate giant germ cells form by coalescence of spermatocytes or spermatids , the ratio of germ cells to Sertoli cells is reduced , and spermatozoan production is adversely affected .
	manualset3
90038	5	399004	13	NULL	NULL	0	NULL	coalescence	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these different factors may elicit the same temporary or permanent response in that degenerating germ cells become more common , multinucleate giant germ cells form by coalescence of spermatocytes or spermatids , the ratio of germ cells to Sertoli cells is reduced , and spermatozoan production is adversely affected .
	manualset3
90039	6	399004	13	NULL	NULL	0	NULL	spermatocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these different factors may elicit the same temporary or permanent response in that degenerating germ cells become more common , multinucleate giant germ cells form by coalescence of spermatocytes or spermatids , the ratio of germ cells to Sertoli cells is reduced , and spermatozoan production is adversely affected .
	manualset3
90040	7	399004	13	NULL	NULL	0	NULL	 spermatids	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these different factors may elicit the same temporary or permanent response in that degenerating germ cells become more common , multinucleate giant germ cells form by coalescence of spermatocytes or spermatids , the ratio of germ cells to Sertoli cells is reduced , and spermatozoan production is adversely affected .
	manualset3
90041	8	399004	13	NULL	NULL	0	NULL	ratio of germ cells to Sertoli cells 	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these different factors may elicit the same temporary or permanent response in that degenerating germ cells become more common , multinucleate giant germ cells form by coalescence of spermatocytes or spermatids , the ratio of germ cells to Sertoli cells is reduced , and spermatozoan production is adversely affected .
	manualset3
90042	9	399004	13	NULL	NULL	0	NULL	spermatozoan production	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these different factors may elicit the same temporary or permanent response in that degenerating germ cells become more common , multinucleate giant germ cells form by coalescence of spermatocytes or spermatids , the ratio of germ cells to Sertoli cells is reduced , and spermatozoan production is adversely affected .
	manualset3
90043	1	399005	13	NULL	NULL	NULL	NULL	ethnic-related differences 	Relationship												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , these ethnic and gender-related differences were similar to those previously reported for ESRD in the general population .
	manualset3
90044	2	399005	13	NULL	NULL	0	NULL	ESRD	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these ethnic and gender-related differences were similar to those previously reported for ESRD in the general population .
	manualset3
90045	3	399005	13	NULL	NULL	NULL	NULL	 general population 	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , these ethnic and gender-related differences were similar to those previously reported for ESRD in the general population .
	manualset3
90972	4	399005	13	NULL	NULL	0	NULL	gender-related differences	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these ethnic and gender-related differences were similar to those previously reported for ESRD in the general population .
	manualset3
90046	1	399006	13	NULL	NULL	0	NULL	modalities 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these modalities only provide anatomical information of the coronary artery .
	manualset3
90047	2	399006	13	NULL	NULL	NULL	NULL	anatomical information	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , these modalities only provide anatomical information of the coronary artery .
	manualset3
90048	3	399006	13	NULL	NULL	0	NULL	 coronary artery	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these modalities only provide anatomical information of the coronary artery .
	manualset3
90049	1	399007	13	NULL	NULL	0	NULL	studies 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these studies were conducted in university teaching hospitals whereas a significant proportion of training in Ireland takes place in peripheral hospitals which provide a different training environment .
	manualset3
90050	2	399007	13	NULL	NULL	0	NULL	university teaching hospitals	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these studies were conducted in university teaching hospitals whereas a significant proportion of training in Ireland takes place in peripheral hospitals which provide a different training environment .
	manualset3
90051	3	399007	13	NULL	NULL	0	NULL	proportion	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these studies were conducted in university teaching hospitals whereas a significant proportion of training in Ireland takes place in peripheral hospitals which provide a different training environment .
	manualset3
90052	4	399007	13	NULL	NULL	0	NULL	training	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these studies were conducted in university teaching hospitals whereas a significant proportion of training in Ireland takes place in peripheral hospitals which provide a different training environment .
	manualset3
90053	5	399007	13	NULL	NULL	0	NULL	Ireland	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these studies were conducted in university teaching hospitals whereas a significant proportion of training in Ireland takes place in peripheral hospitals which provide a different training environment .
	manualset3
90054	6	399007	13	NULL	NULL	NULL	NULL	 peripheral hospitals	Facility												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , these studies were conducted in university teaching hospitals whereas a significant proportion of training in Ireland takes place in peripheral hospitals which provide a different training environment .
	manualset3
90055	7	399007	13	NULL	NULL	0	NULL	training environment 	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	However , these studies were conducted in university teaching hospitals whereas a significant proportion of training in Ireland takes place in peripheral hospitals which provide a different training environment .
	manualset3
90056	1	399008	13	NULL	NULL	0	NULL	 information 	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	However , they can give information of a more general nature - much in the same way as measurements of tension may do , for example - and the patterns can also tell us what structural regularities are no longer present during contraction .
	manualset3
90057	2	399008	13	NULL	NULL	NULL	NULL	measurements of tension	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , they can give information of a more general nature - much in the same way as measurements of tension may do , for example - and the patterns can also tell us what structural regularities are no longer present during contraction .
	manualset3
90058	3	399008	13	NULL	NULL	0	NULL	 patterns	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , they can give information of a more general nature - much in the same way as measurements of tension may do , for example - and the patterns can also tell us what structural regularities are no longer present during contraction .
	manualset3
90059	4	399008	13	NULL	NULL	NULL	NULL	general nature	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , they can give information of a more general nature - much in the same way as measurements of tension may do , for example - and the patterns can also tell us what structural regularities are no longer present during contraction .
	manualset3
90060	5	399008	13	NULL	NULL	0	NULL	contraction	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , they can give information of a more general nature - much in the same way as measurements of tension may do , for example - and the patterns can also tell us what structural regularities are no longer present during contraction .
	manualset3
91217	6	399008	13	NULL	NULL	0	NULL	structural regularities	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , they can give information of a more general nature - much in the same way as measurements of tension may do , for example - and the patterns can also tell us what structural regularities are no longer present during contraction .
	manualset3
90061	1	399009	13	NULL	NULL	NULL	NULL	allogeneic transplantation 	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , they have been clinically beneficial in allogeneic transplantation and in delayed erythropoiesis post-transplantation .
	manualset3
90062	2	399009	13	NULL	NULL	0	NULL	erythropoiesis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , they have been clinically beneficial in allogeneic transplantation and in delayed erythropoiesis post-transplantation .
	manualset3
90063	3	399009	13	NULL	NULL	0	NULL	post-transplantation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , they have been clinically beneficial in allogeneic transplantation and in delayed erythropoiesis post-transplantation .
	manualset3
90064	1	399010	13	NULL	NULL	0	NULL	treatment 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , they have not been employed in the treatment of central hyperthyroidism .
	manualset3
90065	2	399010	13	NULL	NULL	NULL	NULL	central hyperthyroidism	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , they have not been employed in the treatment of central hyperthyroidism .
	manualset3
90066	1	399011	13	NULL	NULL	0	NULL	 risk factors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , they suggest for the first time that individual risk factors related to the HPA axis predict stereotypic behavior following enrichment-removal , and that previously-enriched mice have lasting motivational differences from standard-raised mice , suggesting sustained behavioural effects related to the frustration of enrichment-loss .
	manualset3
90067	2	399011	13	NULL	NULL	0	NULL	HPA axis	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , they suggest for the first time that individual risk factors related to the HPA axis predict stereotypic behavior following enrichment-removal , and that previously-enriched mice have lasting motivational differences from standard-raised mice , suggesting sustained behavioural effects related to the frustration of enrichment-loss .
	manualset3
90068	3	399011	13	NULL	NULL	NULL	NULL	stereotypic behavior	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , they suggest for the first time that individual risk factors related to the HPA axis predict stereotypic behavior following enrichment-removal , and that previously-enriched mice have lasting motivational differences from standard-raised mice , suggesting sustained behavioural effects related to the frustration of enrichment-loss .
	manualset3
90069	4	399011	13	NULL	NULL	0	NULL	enrichment-removal 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , they suggest for the first time that individual risk factors related to the HPA axis predict stereotypic behavior following enrichment-removal , and that previously-enriched mice have lasting motivational differences from standard-raised mice , suggesting sustained behavioural effects related to the frustration of enrichment-loss .
	manualset3
90070	5	399011	13	NULL	NULL	0	NULL	 mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , they suggest for the first time that individual risk factors related to the HPA axis predict stereotypic behavior following enrichment-removal , and that previously-enriched mice have lasting motivational differences from standard-raised mice , suggesting sustained behavioural effects related to the frustration of enrichment-loss .
	manualset3
90071	6	399011	13	NULL	NULL	NULL	NULL	motivational differences	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , they suggest for the first time that individual risk factors related to the HPA axis predict stereotypic behavior following enrichment-removal , and that previously-enriched mice have lasting motivational differences from standard-raised mice , suggesting sustained behavioural effects related to the frustration of enrichment-loss .
	manualset3
90072	7	399011	13	NULL	NULL	0	NULL	mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , they suggest for the first time that individual risk factors related to the HPA axis predict stereotypic behavior following enrichment-removal , and that previously-enriched mice have lasting motivational differences from standard-raised mice , suggesting sustained behavioural effects related to the frustration of enrichment-loss .
	manualset3
90073	8	399011	13	NULL	NULL	0	NULL	behavioural effects 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , they suggest for the first time that individual risk factors related to the HPA axis predict stereotypic behavior following enrichment-removal , and that previously-enriched mice have lasting motivational differences from standard-raised mice , suggesting sustained behavioural effects related to the frustration of enrichment-loss .
	manualset3
90074	9	399011	13	NULL	NULL	NULL	NULL	frustration of enrichment-loss	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , they suggest for the first time that individual risk factors related to the HPA axis predict stereotypic behavior following enrichment-removal , and that previously-enriched mice have lasting motivational differences from standard-raised mice , suggesting sustained behavioural effects related to the frustration of enrichment-loss .
	manualset3
90076	1	399012	13	NULL	NULL	0	NULL	case	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , this case differs in that the patient had no preexisting gynecologic conditions at the time of hysterectomy and bilateral salpingo-oophorectomy to account for residual ovarian tissue .
	manualset3
90077	2	399012	13	NULL	NULL	0	NULL	patient	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , this case differs in that the patient had no preexisting gynecologic conditions at the time of hysterectomy and bilateral salpingo-oophorectomy to account for residual ovarian tissue .
	manualset3
90078	3	399012	13	NULL	NULL	NULL	NULL	gynecologic conditions	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , this case differs in that the patient had no preexisting gynecologic conditions at the time of hysterectomy and bilateral salpingo-oophorectomy to account for residual ovarian tissue .
	manualset3
90079	4	399012	13	NULL	NULL	0	NULL	time 	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	However , this case differs in that the patient had no preexisting gynecologic conditions at the time of hysterectomy and bilateral salpingo-oophorectomy to account for residual ovarian tissue .
	manualset3
90080	5	399012	13	NULL	NULL	0	NULL	hysterectomy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , this case differs in that the patient had no preexisting gynecologic conditions at the time of hysterectomy and bilateral salpingo-oophorectomy to account for residual ovarian tissue .
	manualset3
90081	6	399012	13	NULL	NULL	NULL	NULL	bilateral salpingo-oophorectomy 	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , this case differs in that the patient had no preexisting gynecologic conditions at the time of hysterectomy and bilateral salpingo-oophorectomy to account for residual ovarian tissue .
	manualset3
90082	7	399012	13	NULL	NULL	NULL	NULL	 residual ovarian tissue	Tissue												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , this case differs in that the patient had no preexisting gynecologic conditions at the time of hysterectomy and bilateral salpingo-oophorectomy to account for residual ovarian tissue .
	manualset3
90083	1	399013	13	NULL	NULL	0	NULL	fragment	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , this fragment did not contain the oprD structural gene as judged by its inability to hybridize with an oligonucleotide corresponding to the N-terminal amino acid sequence of OprD .
	manualset3
90084	2	399013	13	NULL	NULL	0	NULL	oprD structural gene 	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	However , this fragment did not contain the oprD structural gene as judged by its inability to hybridize with an oligonucleotide corresponding to the N-terminal amino acid sequence of OprD .
	manualset3
90086	4	399013	13	NULL	NULL	0	NULL	oligonucleotide	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , this fragment did not contain the oprD structural gene as judged by its inability to hybridize with an oligonucleotide corresponding to the N-terminal amino acid sequence of OprD .
	manualset3
90087	5	399013	13	NULL	NULL	0	NULL	N-terminal amino acid sequence of OprD	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	However , this fragment did not contain the oprD structural gene as judged by its inability to hybridize with an oligonucleotide corresponding to the N-terminal amino acid sequence of OprD .
	manualset3
90088	1	399014	13	NULL	NULL	NULL	NULL	prior history of depression	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , those with prior history of depression may face a re-emergence of depression during this transition while others may experience a first episode of depression in their lives .
	manualset3
90090	3	399014	13	NULL	NULL	NULL	NULL	 re-emergence of depression 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , those with prior history of depression may face a re-emergence of depression during this transition while others may experience a first episode of depression in their lives .
	manualset3
90092	5	399014	13	NULL	NULL	0	NULL	transition	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , those with prior history of depression may face a re-emergence of depression during this transition while others may experience a first episode of depression in their lives .
	manualset3
90093	6	399014	13	NULL	NULL	0	NULL	experience	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , those with prior history of depression may face a re-emergence of depression during this transition while others may experience a first episode of depression in their lives .
	manualset3
90094	7	399014	13	NULL	NULL	0	NULL	first episode of depression 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , those with prior history of depression may face a re-emergence of depression during this transition while others may experience a first episode of depression in their lives .
	manualset3
90095	8	399014	13	NULL	NULL	0	NULL	lives	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , those with prior history of depression may face a re-emergence of depression during this transition while others may experience a first episode of depression in their lives .
	manualset3
90096	1	399015	13	NULL	NULL	0	NULL	attention 	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , though much attention has been given to infrapopliteal intervention , the importance of identifying preprocedural infrapopliteal variants remains underappreciated .
	manualset3
90097	2	399015	13	NULL	NULL	0	NULL	 infrapopliteal intervention 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , though much attention has been given to infrapopliteal intervention , the importance of identifying preprocedural infrapopliteal variants remains underappreciated .
	manualset3
90098	3	399015	13	NULL	NULL	NULL	NULL	preprocedural infrapopliteal variants	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , though much attention has been given to infrapopliteal intervention , the importance of identifying preprocedural infrapopliteal variants remains underappreciated .
	manualset3
90099	1	399016	13	NULL	NULL	0	NULL	three of the four individuals	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , three of the four individuals developed extensive areas of acanthosis nigricans beginning in early childhood , suffer from severe neurological impairments , and have survived past infancy without prolonged life-support measures .
	manualset3
90100	2	399016	13	NULL	NULL	0	NULL	areas of acanthosis nigricans	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , three of the four individuals developed extensive areas of acanthosis nigricans beginning in early childhood , suffer from severe neurological impairments , and have survived past infancy without prolonged life-support measures .
	manualset3
90101	3	399016	13	NULL	NULL	NULL	NULL	early childhood	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , three of the four individuals developed extensive areas of acanthosis nigricans beginning in early childhood , suffer from severe neurological impairments , and have survived past infancy without prolonged life-support measures .
	manualset3
90102	4	399016	13	NULL	NULL	0	NULL	neurological impairments 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , three of the four individuals developed extensive areas of acanthosis nigricans beginning in early childhood , suffer from severe neurological impairments , and have survived past infancy without prolonged life-support measures .
	manualset3
90103	5	399016	13	NULL	NULL	0	NULL	 infancy 	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	However , three of the four individuals developed extensive areas of acanthosis nigricans beginning in early childhood , suffer from severe neurological impairments , and have survived past infancy without prolonged life-support measures .
	manualset3
90104	6	399016	13	NULL	NULL	0	NULL	life-support measures	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , three of the four individuals developed extensive areas of acanthosis nigricans beginning in early childhood , suffer from severe neurological impairments , and have survived past infancy without prolonged life-support measures .
	manualset3
90105	1	399017	13	NULL	NULL	0	NULL	date 	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	However , to date only a limited number of P450s have been identified and characterized in legumes .
	manualset3
90106	2	399017	13	NULL	NULL	0	NULL	number 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , to date only a limited number of P450s have been identified and characterized in legumes .
	manualset3
90107	3	399017	13	NULL	NULL	0	NULL	P450s 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , to date only a limited number of P450s have been identified and characterized in legumes .
	manualset3
90108	4	399017	13	NULL	NULL	0	NULL	legumes	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , to date only a limited number of P450s have been identified and characterized in legumes .
	manualset3
90109	1	399018	13	NULL	NULL	0	NULL	molecular details 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , to understand the molecular details of microglia activation , future work is required .
	manualset3
90110	2	399018	13	NULL	NULL	NULL	NULL	microglia activation	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , to understand the molecular details of microglia activation , future work is required .
	manualset3
90111	3	399018	13	NULL	NULL	0	NULL	future work	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , to understand the molecular details of microglia activation , future work is required .
	manualset3
90112	1	399019	13	NULL	NULL	0	NULL	two	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , two misdiagnoses have been also described , showing the need for further development and improvement in the accuracy , efficiency and efficacy of DNA analysis in single cells .
	manualset3
90113	2	399019	13	NULL	NULL	0	NULL	development in the accuracy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , two misdiagnoses have been also described , showing the need for further development and improvement in the accuracy , efficiency and efficacy of DNA analysis in single cells .
	manualset3
90114	3	399019	13	NULL	NULL	0	NULL	improvement in the accuracy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , two misdiagnoses have been also described , showing the need for further development and improvement in the accuracy , efficiency and efficacy of DNA analysis in single cells .
	manualset3
90115	4	399019	13	NULL	NULL	0	NULL	efficiency of DNA analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , two misdiagnoses have been also described , showing the need for further development and improvement in the accuracy , efficiency and efficacy of DNA analysis in single cells .
	manualset3
90116	5	399019	13	NULL	NULL	0	NULL	efficacy of DNA analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , two misdiagnoses have been also described , showing the need for further development and improvement in the accuracy , efficiency and efficacy of DNA analysis in single cells .
	manualset3
90117	6	399019	13	NULL	NULL	NULL	NULL	single cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , two misdiagnoses have been also described , showing the need for further development and improvement in the accuracy , efficiency and efficacy of DNA analysis in single cells .
	manualset3
91240	7	399019	13	NULL	NULL	0	NULL	 misdiagnoses 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , two misdiagnoses have been also described , showing the need for further development and improvement in the accuracy , efficiency and efficacy of DNA analysis in single cells .
	manualset3
90118	1	399020	13	NULL	NULL	0	NULL	nurse	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( The nurse and the community ) .
	manualset3
90119	2	399020	13	NULL	NULL	0	NULL	community	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( The nurse and the community ) .
	manualset3
90120	1	399021	13	NULL	NULL	0	NULL	exons 1-CAT hybrid mRNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However , unexpectedly exons 1-CAT hybrid mRNA in JEG-3 cells was not induced by forskolin .
	manualset3
90121	2	399021	13	NULL	NULL	0	NULL	JEG-3 cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , unexpectedly exons 1-CAT hybrid mRNA in JEG-3 cells was not induced by forskolin .
	manualset3
90122	3	399021	13	NULL	NULL	0	NULL	forskolin	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , unexpectedly exons 1-CAT hybrid mRNA in JEG-3 cells was not induced by forskolin .
	manualset3
90123	1	399022	13	NULL	NULL	0	NULL	C7H9 + 	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	However , unlike for C7H9 + both the bishomo square pyramidal structure 3 and the trishomocyclopropenium type structure 4 were found to be minima on the potential energy surface of C8H9 + .
	manualset3
90124	2	399022	13	NULL	NULL	0	NULL	bishomo square pyramidal structure 3 	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	However , unlike for C7H9 + both the bishomo square pyramidal structure 3 and the trishomocyclopropenium type structure 4 were found to be minima on the potential energy surface of C8H9 + .
	manualset3
90125	3	399022	13	NULL	NULL	0	NULL	trishomocyclopropenium type structure 4 	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	However , unlike for C7H9 + both the bishomo square pyramidal structure 3 and the trishomocyclopropenium type structure 4 were found to be minima on the potential energy surface of C8H9 + .
	manualset3
90126	4	399022	13	NULL	NULL	0	NULL	minima	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , unlike for C7H9 + both the bishomo square pyramidal structure 3 and the trishomocyclopropenium type structure 4 were found to be minima on the potential energy surface of C8H9 + .
	manualset3
90127	5	399022	13	NULL	NULL	NULL	NULL	potential energy surface	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , unlike for C7H9 + both the bishomo square pyramidal structure 3 and the trishomocyclopropenium type structure 4 were found to be minima on the potential energy surface of C8H9 + .
	manualset3
90128	6	399022	13	NULL	NULL	0	NULL	C8H9 +	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	However , unlike for C7H9 + both the bishomo square pyramidal structure 3 and the trishomocyclopropenium type structure 4 were found to be minima on the potential energy surface of C8H9 + .
	manualset3
90129	1	399023	13	NULL	NULL	0	NULL	cGMP	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we demonstrate that cGMP can directly activate PDE5 without phosphorylation in platelet cytosol , most likely via binding to the regulatory GAF domains .
	manualset3
90130	2	399023	13	NULL	NULL	0	NULL	PDE5	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we demonstrate that cGMP can directly activate PDE5 without phosphorylation in platelet cytosol , most likely via binding to the regulatory GAF domains .
	manualset3
90131	3	399023	13	NULL	NULL	0	NULL	phosphorylation 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we demonstrate that cGMP can directly activate PDE5 without phosphorylation in platelet cytosol , most likely via binding to the regulatory GAF domains .
	manualset3
90132	4	399023	13	NULL	NULL	0	NULL	platelet cytosol	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we demonstrate that cGMP can directly activate PDE5 without phosphorylation in platelet cytosol , most likely via binding to the regulatory GAF domains .
	manualset3
90133	5	399023	13	NULL	NULL	0	NULL	binding	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we demonstrate that cGMP can directly activate PDE5 without phosphorylation in platelet cytosol , most likely via binding to the regulatory GAF domains .
	manualset3
90134	6	399023	13	NULL	NULL	0	NULL	regulatory GAF domains	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we demonstrate that cGMP can directly activate PDE5 without phosphorylation in platelet cytosol , most likely via binding to the regulatory GAF domains .
	manualset3
90135	1	399024	13	NULL	NULL	0	NULL	DYS287 YAP + individuals	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we did find DYS287 YAP + individuals who harbored the DYS199 C allele in one Native American population , the Mixe , and in one Asian group , the Tibetans .
	manualset3
90136	2	399024	13	NULL	NULL	NULL	NULL	 DYS199 C allele	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , we did find DYS287 YAP + individuals who harbored the DYS199 C allele in one Native American population , the Mixe , and in one Asian group , the Tibetans .
	manualset3
90137	3	399024	13	NULL	NULL	NULL	NULL	one Native American population	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , we did find DYS287 YAP + individuals who harbored the DYS199 C allele in one Native American population , the Mixe , and in one Asian group , the Tibetans .
	manualset3
90138	4	399024	13	NULL	NULL	0	NULL	Mixe	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we did find DYS287 YAP + individuals who harbored the DYS199 C allele in one Native American population , the Mixe , and in one Asian group , the Tibetans .
	manualset3
90139	5	399024	13	NULL	NULL	0	NULL	one Asian group	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we did find DYS287 YAP + individuals who harbored the DYS199 C allele in one Native American population , the Mixe , and in one Asian group , the Tibetans .
	manualset3
90140	6	399024	13	NULL	NULL	0	NULL	Tibetans	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we did find DYS287 YAP + individuals who harbored the DYS199 C allele in one Native American population , the Mixe , and in one Asian group , the Tibetans .
	manualset3
90141	1	399025	13	NULL	NULL	0	NULL	mouse chow	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we discovered that most normal mouse chow contains casein .
	manualset3
90142	2	399025	13	NULL	NULL	0	NULL	casein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we discovered that most normal mouse chow contains casein .
	manualset3
90143	1	399026	13	NULL	NULL	0	NULL	evidence	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we failed to detect evidence of strong positive selection in any of the cas genes .
	manualset3
90144	2	399026	13	NULL	NULL	0	NULL	selection	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we failed to detect evidence of strong positive selection in any of the cas genes .
	manualset3
90145	3	399026	13	NULL	NULL	0	NULL	cas genes	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we failed to detect evidence of strong positive selection in any of the cas genes .
	manualset3
90146	1	399027	13	NULL	NULL	0	NULL	steroid hormone	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we now know that this steroid hormone activates multiple signaling pathways to affect neuronal excitability and gene transcription .
	manualset3
90147	2	399027	13	NULL	NULL	NULL	NULL	multiple signaling pathways 	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , we now know that this steroid hormone activates multiple signaling pathways to affect neuronal excitability and gene transcription .
	manualset3
90148	3	399027	13	NULL	NULL	0	NULL	neuronal excitability	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we now know that this steroid hormone activates multiple signaling pathways to affect neuronal excitability and gene transcription .
	manualset3
90149	4	399027	13	NULL	NULL	0	NULL	gene transcription	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we now know that this steroid hormone activates multiple signaling pathways to affect neuronal excitability and gene transcription .
	manualset3
90150	1	399028	13	NULL	NULL	0	NULL	 surface scatter	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we show that surface scatter can be treated very similarly to conventional wavefront aberrations .
	manualset3
90151	2	399028	13	NULL	NULL	0	NULL	wavefront aberrations 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we show that surface scatter can be treated very similarly to conventional wavefront aberrations .
	manualset3
90152	1	399029	13	NULL	NULL	0	NULL	cell-associated gp41 molecules 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we suggest that only a minority of cell-associated gp41 molecules - those destined for incorporation into virions - has 3 MSDs and the minor ectodomain .
	manualset3
90153	2	399029	13	NULL	NULL	0	NULL	incorporation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we suggest that only a minority of cell-associated gp41 molecules - those destined for incorporation into virions - has 3 MSDs and the minor ectodomain .
	manualset3
90154	3	399029	13	NULL	NULL	0	NULL	virions 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we suggest that only a minority of cell-associated gp41 molecules - those destined for incorporation into virions - has 3 MSDs and the minor ectodomain .
	manualset3
90155	4	399029	13	NULL	NULL	0	NULL	3 MSDs	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we suggest that only a minority of cell-associated gp41 molecules - those destined for incorporation into virions - has 3 MSDs and the minor ectodomain .
	manualset3
90156	5	399029	13	NULL	NULL	NULL	NULL	minor ectodomain	PartOfProtein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , we suggest that only a minority of cell-associated gp41 molecules - those destined for incorporation into virions - has 3 MSDs and the minor ectodomain .
	manualset3
90157	1	399030	13	NULL	NULL	0	NULL	protein crystals	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we were able to obtain protein crystals suited for X-ray structure determination from flavodoxin expressed as an intein-CBD fusion protein , but not from flavodoxin expressed with a C-terminal His ( 6 ) - tag .
	manualset3
90158	2	399030	13	NULL	NULL	0	NULL	X-ray structure determination	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we were able to obtain protein crystals suited for X-ray structure determination from flavodoxin expressed as an intein-CBD fusion protein , but not from flavodoxin expressed with a C-terminal His ( 6 ) - tag .
	manualset3
90159	3	399030	13	NULL	NULL	0	NULL	flavodoxin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we were able to obtain protein crystals suited for X-ray structure determination from flavodoxin expressed as an intein-CBD fusion protein , but not from flavodoxin expressed with a C-terminal His ( 6 ) - tag .
	manualset3
90160	4	399030	13	NULL	NULL	0	NULL	intein-CBD fusion protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , we were able to obtain protein crystals suited for X-ray structure determination from flavodoxin expressed as an intein-CBD fusion protein , but not from flavodoxin expressed with a C-terminal His ( 6 ) - tag .
	manualset3
90161	5	399030	13	NULL	NULL	NULL	NULL	flavodoxin expressed with a C-terminal His ( 6 ) - tag	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , we were able to obtain protein crystals suited for X-ray structure determination from flavodoxin expressed as an intein-CBD fusion protein , but not from flavodoxin expressed with a C-terminal His ( 6 ) - tag .
	manualset3
90188	1	399031	13	NULL	NULL	0	NULL	ventilator settings	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , what is true for ventilator settings should also be true for extracorporeal procedures : studies will have to demonstrate a convincing risk-benefit ratio .
	manualset3
90189	2	399031	13	NULL	NULL	NULL	NULL	extracorporeal procedures	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , what is true for ventilator settings should also be true for extracorporeal procedures : studies will have to demonstrate a convincing risk-benefit ratio .
	manualset3
90190	3	399031	13	NULL	NULL	0	NULL	studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , what is true for ventilator settings should also be true for extracorporeal procedures : studies will have to demonstrate a convincing risk-benefit ratio .
	manualset3
90191	4	399031	13	NULL	NULL	0	NULL	risk-benefit ratio	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , what is true for ventilator settings should also be true for extracorporeal procedures : studies will have to demonstrate a convincing risk-benefit ratio .
	manualset3
90192	1	399032	13	NULL	NULL	0	NULL	level	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when divided according to potential level of IL-10 production , the group of potentially high IL-10 producers among the CD patients demonstrated significantly lower levels of antitissue transglutaminase antibodies compared to potentially low IL-10 producers ( p = 0.01 ) .
	manualset3
90193	2	399032	13	NULL	NULL	0	NULL	 IL-10 production	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when divided according to potential level of IL-10 production , the group of potentially high IL-10 producers among the CD patients demonstrated significantly lower levels of antitissue transglutaminase antibodies compared to potentially low IL-10 producers ( p = 0.01 ) .
	manualset3
90194	3	399032	13	NULL	NULL	NULL	NULL	group 	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , when divided according to potential level of IL-10 production , the group of potentially high IL-10 producers among the CD patients demonstrated significantly lower levels of antitissue transglutaminase antibodies compared to potentially low IL-10 producers ( p = 0.01 ) .
	manualset3
90195	4	399032	13	NULL	NULL	0	NULL	IL-10 producers	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when divided according to potential level of IL-10 production , the group of potentially high IL-10 producers among the CD patients demonstrated significantly lower levels of antitissue transglutaminase antibodies compared to potentially low IL-10 producers ( p = 0.01 ) .
	manualset3
90196	5	399032	13	NULL	NULL	0	NULL	CD patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when divided according to potential level of IL-10 production , the group of potentially high IL-10 producers among the CD patients demonstrated significantly lower levels of antitissue transglutaminase antibodies compared to potentially low IL-10 producers ( p = 0.01 ) .
	manualset3
90197	6	399032	13	NULL	NULL	0	NULL	 levels	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when divided according to potential level of IL-10 production , the group of potentially high IL-10 producers among the CD patients demonstrated significantly lower levels of antitissue transglutaminase antibodies compared to potentially low IL-10 producers ( p = 0.01 ) .
	manualset3
90198	7	399032	13	NULL	NULL	NULL	NULL	antitissue transglutaminase antibodies	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , when divided according to potential level of IL-10 production , the group of potentially high IL-10 producers among the CD patients demonstrated significantly lower levels of antitissue transglutaminase antibodies compared to potentially low IL-10 producers ( p = 0.01 ) .
	manualset3
90199	8	399032	13	NULL	NULL	0	NULL	IL-10 producers	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when divided according to potential level of IL-10 production , the group of potentially high IL-10 producers among the CD patients demonstrated significantly lower levels of antitissue transglutaminase antibodies compared to potentially low IL-10 producers ( p = 0.01 ) .
	manualset3
90200	9	399032	13	NULL	NULL	0	NULL	p = 0.01	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when divided according to potential level of IL-10 production , the group of potentially high IL-10 producers among the CD patients demonstrated significantly lower levels of antitissue transglutaminase antibodies compared to potentially low IL-10 producers ( p = 0.01 ) .
	manualset3
90201	1	399033	13	NULL	NULL	0	NULL	histamine	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when histamine was present in combination with isoproterenol or forskolin 4-DAMP mustard treatment shifted the concentration-effect curves for oxo-M to the right only about 3.5-fold .
	manualset3
90202	2	399033	13	NULL	NULL	NULL	NULL	isoproterenol 	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , when histamine was present in combination with isoproterenol or forskolin 4-DAMP mustard treatment shifted the concentration-effect curves for oxo-M to the right only about 3.5-fold .
	manualset3
90203	3	399033	13	NULL	NULL	NULL	NULL	 forskolin	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , when histamine was present in combination with isoproterenol or forskolin 4-DAMP mustard treatment shifted the concentration-effect curves for oxo-M to the right only about 3.5-fold .
	manualset3
90204	4	399033	13	NULL	NULL	NULL	NULL	4-DAMP mustard	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , when histamine was present in combination with isoproterenol or forskolin 4-DAMP mustard treatment shifted the concentration-effect curves for oxo-M to the right only about 3.5-fold .
	manualset3
90205	5	399033	13	NULL	NULL	0	NULL	treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when histamine was present in combination with isoproterenol or forskolin 4-DAMP mustard treatment shifted the concentration-effect curves for oxo-M to the right only about 3.5-fold .
	manualset3
90206	6	399033	13	NULL	NULL	NULL	NULL	concentration-effect curves	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , when histamine was present in combination with isoproterenol or forskolin 4-DAMP mustard treatment shifted the concentration-effect curves for oxo-M to the right only about 3.5-fold .
	manualset3
90207	7	399033	13	NULL	NULL	0	NULL	 oxo-M 	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when histamine was present in combination with isoproterenol or forskolin 4-DAMP mustard treatment shifted the concentration-effect curves for oxo-M to the right only about 3.5-fold .
	manualset3
90208	8	399033	13	NULL	NULL	0	NULL	3.5-fold 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when histamine was present in combination with isoproterenol or forskolin 4-DAMP mustard treatment shifted the concentration-effect curves for oxo-M to the right only about 3.5-fold .
	manualset3
90209	1	399034	13	NULL	NULL	0	NULL	lysis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when lysis was induced by the isolated C5b-9 membrane attack mechanism , bypassing the requirement for C3 binding , only type III PNH cells exhibited greater than normal lysis .
	manualset3
90210	2	399034	13	NULL	NULL	NULL	NULL	C5b-9 	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , when lysis was induced by the isolated C5b-9 membrane attack mechanism , bypassing the requirement for C3 binding , only type III PNH cells exhibited greater than normal lysis .
	manualset3
90211	3	399034	13	NULL	NULL	NULL	NULL	membrane attack mechanism	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , when lysis was induced by the isolated C5b-9 membrane attack mechanism , bypassing the requirement for C3 binding , only type III PNH cells exhibited greater than normal lysis .
	manualset3
90226	5	399034	13	NULL	NULL	0	NULL	C3 binding	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when lysis was induced by the isolated C5b-9 membrane attack mechanism , bypassing the requirement for C3 binding , only type III PNH cells exhibited greater than normal lysis .
	manualset3
90227	6	399034	13	NULL	NULL	0	NULL	type III PNH cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when lysis was induced by the isolated C5b-9 membrane attack mechanism , bypassing the requirement for C3 binding , only type III PNH cells exhibited greater than normal lysis .
	manualset3
90228	7	399034	13	NULL	NULL	0	NULL	lysis 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when lysis was induced by the isolated C5b-9 membrane attack mechanism , bypassing the requirement for C3 binding , only type III PNH cells exhibited greater than normal lysis .
	manualset3
90229	1	399035	13	NULL	NULL	0	NULL	peripheral blood mononuclear cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when peripheral blood mononuclear cells and B lymphocytes are isolated from BLV-infected animals and incubated in the presence of activating reagents , such as phorbol ester , the expression of BLV is markedly enhanced .
	manualset3
90230	2	399035	13	NULL	NULL	0	NULL	B lymphocytes 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when peripheral blood mononuclear cells and B lymphocytes are isolated from BLV-infected animals and incubated in the presence of activating reagents , such as phorbol ester , the expression of BLV is markedly enhanced .
	manualset3
90231	3	399035	13	NULL	NULL	0	NULL	BLV-infected animals 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when peripheral blood mononuclear cells and B lymphocytes are isolated from BLV-infected animals and incubated in the presence of activating reagents , such as phorbol ester , the expression of BLV is markedly enhanced .
	manualset3
90232	4	399035	13	NULL	NULL	NULL	NULL	activating reagents	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , when peripheral blood mononuclear cells and B lymphocytes are isolated from BLV-infected animals and incubated in the presence of activating reagents , such as phorbol ester , the expression of BLV is markedly enhanced .
	manualset3
90233	5	399035	13	NULL	NULL	0	NULL	 phorbol ester	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when peripheral blood mononuclear cells and B lymphocytes are isolated from BLV-infected animals and incubated in the presence of activating reagents , such as phorbol ester , the expression of BLV is markedly enhanced .
	manualset3
90234	6	399035	13	NULL	NULL	0	NULL	expression of BLV 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when peripheral blood mononuclear cells and B lymphocytes are isolated from BLV-infected animals and incubated in the presence of activating reagents , such as phorbol ester , the expression of BLV is markedly enhanced .
	manualset3
90235	1	399036	13	NULL	NULL	0	NULL	pathogenesis 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The pathogenesis of CD4 ( + ) ; T cells infiltrated into the spinal cord in rat SNL model ) .
	manualset3
90236	2	399036	13	NULL	NULL	NULL	NULL	CD4 ( + ) ; T cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The pathogenesis of CD4 ( + ) ; T cells infiltrated into the spinal cord in rat SNL model ) .
	manualset3
90238	4	399036	13	NULL	NULL	0	NULL	spinal cord	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( The pathogenesis of CD4 ( + ) ; T cells infiltrated into the spinal cord in rat SNL model ) .
	manualset3
90239	5	399036	13	NULL	NULL	0	NULL	rat SNL model 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( The pathogenesis of CD4 ( + ) ; T cells infiltrated into the spinal cord in rat SNL model ) .
	manualset3
90240	1	399037	13	NULL	NULL	0	NULL	 mice 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when tested in mice bearing tumor cells expressing mesothelin , the antitumor activity of the bivalent immunotoxin is very similar to the activity of the lower affinity monovalent immunotoxin .
	manualset3
90241	2	399037	13	NULL	NULL	0	NULL	tumor cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when tested in mice bearing tumor cells expressing mesothelin , the antitumor activity of the bivalent immunotoxin is very similar to the activity of the lower affinity monovalent immunotoxin .
	manualset3
90242	3	399037	13	NULL	NULL	0	NULL	 mesothelin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when tested in mice bearing tumor cells expressing mesothelin , the antitumor activity of the bivalent immunotoxin is very similar to the activity of the lower affinity monovalent immunotoxin .
	manualset3
90244	4	399037	13	NULL	NULL	0	NULL	antitumor activity 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when tested in mice bearing tumor cells expressing mesothelin , the antitumor activity of the bivalent immunotoxin is very similar to the activity of the lower affinity monovalent immunotoxin .
	manualset3
90246	5	399037	13	NULL	NULL	NULL	NULL	bivalent immunotoxin	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , when tested in mice bearing tumor cells expressing mesothelin , the antitumor activity of the bivalent immunotoxin is very similar to the activity of the lower affinity monovalent immunotoxin .
	manualset3
90249	6	399037	13	NULL	NULL	NULL	NULL	activity	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , when tested in mice bearing tumor cells expressing mesothelin , the antitumor activity of the bivalent immunotoxin is very similar to the activity of the lower affinity monovalent immunotoxin .
	manualset3
90250	7	399037	13	NULL	NULL	0	NULL	affinity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when tested in mice bearing tumor cells expressing mesothelin , the antitumor activity of the bivalent immunotoxin is very similar to the activity of the lower affinity monovalent immunotoxin .
	manualset3
90251	8	399037	13	NULL	NULL	NULL	NULL	monovalent immunotoxin	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , when tested in mice bearing tumor cells expressing mesothelin , the antitumor activity of the bivalent immunotoxin is very similar to the activity of the lower affinity monovalent immunotoxin .
	manualset3
90266	1	399038	13	NULL	NULL	0	NULL	electrode	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when the electrode was placed on the nasal ala , the threshold was significantly lower , an ideal biphasic configuration was present in almost all cases ( 97.5 per cent ) of normal volunteers and it was easier to identify the waveform .
	manualset3
90268	2	399038	13	NULL	NULL	0	NULL	nasal ala	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when the electrode was placed on the nasal ala , the threshold was significantly lower , an ideal biphasic configuration was present in almost all cases ( 97.5 per cent ) of normal volunteers and it was easier to identify the waveform .
	manualset3
90270	3	399038	13	NULL	NULL	0	NULL	 threshold 	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when the electrode was placed on the nasal ala , the threshold was significantly lower , an ideal biphasic configuration was present in almost all cases ( 97.5 per cent ) of normal volunteers and it was easier to identify the waveform .
	manualset3
90272	4	399038	13	NULL	NULL	NULL	NULL	biphasic configuration 	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , when the electrode was placed on the nasal ala , the threshold was significantly lower , an ideal biphasic configuration was present in almost all cases ( 97.5 per cent ) of normal volunteers and it was easier to identify the waveform .
	manualset3
90273	5	399038	13	NULL	NULL	0	NULL	 cases	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when the electrode was placed on the nasal ala , the threshold was significantly lower , an ideal biphasic configuration was present in almost all cases ( 97.5 per cent ) of normal volunteers and it was easier to identify the waveform .
	manualset3
90274	6	399038	13	NULL	NULL	0	NULL	97.5 per cent	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when the electrode was placed on the nasal ala , the threshold was significantly lower , an ideal biphasic configuration was present in almost all cases ( 97.5 per cent ) of normal volunteers and it was easier to identify the waveform .
	manualset3
90275	7	399038	13	NULL	NULL	0	NULL	volunteers	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when the electrode was placed on the nasal ala , the threshold was significantly lower , an ideal biphasic configuration was present in almost all cases ( 97.5 per cent ) of normal volunteers and it was easier to identify the waveform .
	manualset3
90276	8	399038	13	NULL	NULL	0	NULL	waveform	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when the electrode was placed on the nasal ala , the threshold was significantly lower , an ideal biphasic configuration was present in almost all cases ( 97.5 per cent ) of normal volunteers and it was easier to identify the waveform .
	manualset3
90278	1	399039	13	NULL	NULL	0	NULL	 two	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when the two tasks vary randomly from trial to trial , effects of spatial predictability carry over to the perceptual task .
	manualset3
90279	2	399039	13	NULL	NULL	0	NULL	tasks	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when the two tasks vary randomly from trial to trial , effects of spatial predictability carry over to the perceptual task .
	manualset3
90280	3	399039	13	NULL	NULL	0	NULL	trial	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when the two tasks vary randomly from trial to trial , effects of spatial predictability carry over to the perceptual task .
	manualset3
90281	4	399039	13	NULL	NULL	0	NULL	trial 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when the two tasks vary randomly from trial to trial , effects of spatial predictability carry over to the perceptual task .
	manualset3
90282	5	399039	13	NULL	NULL	0	NULL	effects	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when the two tasks vary randomly from trial to trial , effects of spatial predictability carry over to the perceptual task .
	manualset3
90283	6	399039	13	NULL	NULL	NULL	NULL	spatial predictability	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , when the two tasks vary randomly from trial to trial , effects of spatial predictability carry over to the perceptual task .
	manualset3
90284	7	399039	13	NULL	NULL	0	NULL	task	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , when the two tasks vary randomly from trial to trial , effects of spatial predictability carry over to the perceptual task .
	manualset3
90285	1	399040	13	NULL	NULL	0	NULL	depression	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , whether depression interferes with the cardioprotection of IPC during myocardial ischemia/reperfusion and their underlying mechanisms remain largely unknown .
	manualset3
90286	2	399040	13	NULL	NULL	NULL	NULL	 cardioprotection of IPC	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , whether depression interferes with the cardioprotection of IPC during myocardial ischemia/reperfusion and their underlying mechanisms remain largely unknown .
	manualset3
90288	4	399040	13	NULL	NULL	0	NULL	myocardial ischemia/reperfusion 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , whether depression interferes with the cardioprotection of IPC during myocardial ischemia/reperfusion and their underlying mechanisms remain largely unknown .
	manualset3
90289	5	399040	13	NULL	NULL	0	NULL	mechanisms	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , whether depression interferes with the cardioprotection of IPC during myocardial ischemia/reperfusion and their underlying mechanisms remain largely unknown .
	manualset3
90290	1	399041	13	NULL	NULL	0	NULL	G ( q ) - PLC pathway 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , whether the G ( q ) - PLC pathway is the main regulator of TRPC4/5 channels and how other G proteins may regulate these channels are poorly understood .
	manualset3
90291	2	399041	13	NULL	NULL	0	NULL	regulator	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , whether the G ( q ) - PLC pathway is the main regulator of TRPC4/5 channels and how other G proteins may regulate these channels are poorly understood .
	manualset3
90292	3	399041	13	NULL	NULL	0	NULL	TRPC4/5 channels	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , whether the G ( q ) - PLC pathway is the main regulator of TRPC4/5 channels and how other G proteins may regulate these channels are poorly understood .
	manualset3
90293	4	399041	13	NULL	NULL	0	NULL	G proteins 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , whether the G ( q ) - PLC pathway is the main regulator of TRPC4/5 channels and how other G proteins may regulate these channels are poorly understood .
	manualset3
90296	5	399041	13	NULL	NULL	0	NULL	channels	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However , whether the G ( q ) - PLC pathway is the main regulator of TRPC4/5 channels and how other G proteins may regulate these channels are poorly understood .
	manualset3
90297	1	399042	13	NULL	NULL	0	NULL	specificity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , while the specificity of 4-74-6 is stringent , 2-96-12 cross-reacts with many evolutionarily related cytochromes c. Such a marked difference in specificity of antibodies with overlapping epitopes may represent unique antibody immunodiversity .
	manualset3
90298	2	399042	13	NULL	NULL	0	NULL	4-74-6 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , while the specificity of 4-74-6 is stringent , 2-96-12 cross-reacts with many evolutionarily related cytochromes c. Such a marked difference in specificity of antibodies with overlapping epitopes may represent unique antibody immunodiversity .
	manualset3
90301	3	399042	13	NULL	NULL	0	NULL	2-96-12	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , while the specificity of 4-74-6 is stringent , 2-96-12 cross-reacts with many evolutionarily related cytochromes c. Such a marked difference in specificity of antibodies with overlapping epitopes may represent unique antibody immunodiversity .
	manualset3
90308	4	399042	13	NULL	NULL	0	NULL	cytochromes c	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However , while the specificity of 4-74-6 is stringent , 2-96-12 cross-reacts with many evolutionarily related cytochromes c. Such a marked difference in specificity of antibodies with overlapping epitopes may represent unique antibody immunodiversity .
	manualset3
90309	5	399042	13	NULL	NULL	0	NULL	 difference	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	However , while the specificity of 4-74-6 is stringent , 2-96-12 cross-reacts with many evolutionarily related cytochromes c. Such a marked difference in specificity of antibodies with overlapping epitopes may represent unique antibody immunodiversity .
	manualset3
90311	6	399042	13	NULL	NULL	0	NULL	specificity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , while the specificity of 4-74-6 is stringent , 2-96-12 cross-reacts with many evolutionarily related cytochromes c. Such a marked difference in specificity of antibodies with overlapping epitopes may represent unique antibody immunodiversity .
	manualset3
90312	7	399042	13	NULL	NULL	NULL	NULL	 antibodies	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , while the specificity of 4-74-6 is stringent , 2-96-12 cross-reacts with many evolutionarily related cytochromes c. Such a marked difference in specificity of antibodies with overlapping epitopes may represent unique antibody immunodiversity .
	manualset3
90313	8	399042	13	NULL	NULL	NULL	NULL	 overlapping epitopes	Molecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , while the specificity of 4-74-6 is stringent , 2-96-12 cross-reacts with many evolutionarily related cytochromes c. Such a marked difference in specificity of antibodies with overlapping epitopes may represent unique antibody immunodiversity .
	manualset3
90315	9	399042	13	NULL	NULL	0	NULL	antibody immunodiversity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However , while the specificity of 4-74-6 is stringent , 2-96-12 cross-reacts with many evolutionarily related cytochromes c. Such a marked difference in specificity of antibodies with overlapping epitopes may represent unique antibody immunodiversity .
	manualset3
90318	1	399043	13	NULL	NULL	0	NULL	 iron	Atom												NULL		0	NULL	NULL	NULL	NULL	NULL	However , why iron accumulates and in what oxidation state iron it accumulates in the brain of PS-exposed rats has not been well elucidated .
	manualset3
90322	2	399043	13	NULL	NULL	NULL	NULL	oxidation state iron	Ion												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , why iron accumulates and in what oxidation state iron it accumulates in the brain of PS-exposed rats has not been well elucidated .
	manualset3
90323	3	399043	13	NULL	NULL	0	NULL	brain	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	However , why iron accumulates and in what oxidation state iron it accumulates in the brain of PS-exposed rats has not been well elucidated .
	manualset3
90324	4	399043	13	NULL	NULL	0	NULL	PS-exposed rats 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However , why iron accumulates and in what oxidation state iron it accumulates in the brain of PS-exposed rats has not been well elucidated .
	manualset3
90325	1	399044	13	NULL	NULL	0	NULL	improvements	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , with the improvements in atherectomy technology , namely plaque excision and laser plaque ablation , the full spectrum of arterial occlusive lesions may now be addressed by percutaneous means with excellent limb salvage rates .
	manualset3
90328	2	399044	13	NULL	NULL	NULL	NULL	atherectomy technology	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , with the improvements in atherectomy technology , namely plaque excision and laser plaque ablation , the full spectrum of arterial occlusive lesions may now be addressed by percutaneous means with excellent limb salvage rates .
	manualset3
90332	3	399044	13	NULL	NULL	0	NULL	plaque excision	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , with the improvements in atherectomy technology , namely plaque excision and laser plaque ablation , the full spectrum of arterial occlusive lesions may now be addressed by percutaneous means with excellent limb salvage rates .
	manualset3
90334	4	399044	13	NULL	NULL	0	NULL	laser plaque ablation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , with the improvements in atherectomy technology , namely plaque excision and laser plaque ablation , the full spectrum of arterial occlusive lesions may now be addressed by percutaneous means with excellent limb salvage rates .
	manualset3
90336	5	399044	13	NULL	NULL	0	NULL	spectrum of arterial occlusive lesions	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , with the improvements in atherectomy technology , namely plaque excision and laser plaque ablation , the full spectrum of arterial occlusive lesions may now be addressed by percutaneous means with excellent limb salvage rates .
	manualset3
90337	6	399044	13	NULL	NULL	0	NULL	limb salvage rates	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However , with the improvements in atherectomy technology , namely plaque excision and laser plaque ablation , the full spectrum of arterial occlusive lesions may now be addressed by percutaneous means with excellent limb salvage rates .
	manualset3
91239	7	399044	13	NULL	NULL	NULL	NULL	percutaneous means	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , with the improvements in atherectomy technology , namely plaque excision and laser plaque ablation , the full spectrum of arterial occlusive lesions may now be addressed by percutaneous means with excellent limb salvage rates .
	manualset3
90339	1	399045	13	NULL	NULL	NULL	NULL	 patient	Person												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The patient and the informed consent ) .
	manualset3
90342	2	399045	13	NULL	NULL	NULL	NULL	 informed consent	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The patient and the informed consent ) .
	manualset3
90345	1	399046	13	NULL	NULL	0	NULL	identifications	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However , with the recent advances in the identifications of unique molecular signatures for CSCs along with ongoing clinical trials targeting CSCs , it is possible to use targeted nanotechnology-based strategies in the management of different types of cancers .
	manualset3
90346	2	399046	13	NULL	NULL	NULL	NULL	unique molecular signatures	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However , with the recent advances in the identifications of unique molecular signatures for CSCs along with ongoing clinical trials targeting CSCs , it is possible to use targeted nanotechnology-based strategies in the management of different types of cancers .
	manualset3
90347	3	399046	13	NULL	NULL	0	NULL	CSCs	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	However , with the recent advances in the identifications of unique molecular signatures for CSCs along with ongoing clinical trials targeting CSCs , it is possible to use targeted nanotechnology-based strategies in the management of different types of cancers .
	manualset3
90348	4	399046	13	NULL	NULL	0	NULL	clinical trials targeting CSCs	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However , with the recent advances in the identifications of unique molecular signatures for CSCs along with ongoing clinical trials targeting CSCs , it is possible to use targeted nanotechnology-based strategies in the management of different types of cancers .
	manualset3
90349	5	399046	13	NULL	NULL	0	NULL	nanotechnology-based strategies	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , with the recent advances in the identifications of unique molecular signatures for CSCs along with ongoing clinical trials targeting CSCs , it is possible to use targeted nanotechnology-based strategies in the management of different types of cancers .
	manualset3
90350	6	399046	13	NULL	NULL	0	NULL	management	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However , with the recent advances in the identifications of unique molecular signatures for CSCs along with ongoing clinical trials targeting CSCs , it is possible to use targeted nanotechnology-based strategies in the management of different types of cancers .
	manualset3
90351	7	399046	13	NULL	NULL	0	NULL	types of cancers 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	However , with the recent advances in the identifications of unique molecular signatures for CSCs along with ongoing clinical trials targeting CSCs , it is possible to use targeted nanotechnology-based strategies in the management of different types of cancers .
	manualset3
90356	1	399047	13	NULL	NULL	0	NULL	4 ' - O-allyl ether of hygromycin A aglycone 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However a 4 ' - O-allyl ether of hygromycin A aglycone showed an equivalent MIC to hygromycin A , while having a less potent IC50 in the cell free assay .
	manualset3
90357	2	399047	13	NULL	NULL	0	NULL	MIC	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However a 4 ' - O-allyl ether of hygromycin A aglycone showed an equivalent MIC to hygromycin A , while having a less potent IC50 in the cell free assay .
	manualset3
90358	3	399047	13	NULL	NULL	0	NULL	hygromycin A	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However a 4 ' - O-allyl ether of hygromycin A aglycone showed an equivalent MIC to hygromycin A , while having a less potent IC50 in the cell free assay .
	manualset3
90359	4	399047	13	NULL	NULL	0	NULL	 IC50 	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However a 4 ' - O-allyl ether of hygromycin A aglycone showed an equivalent MIC to hygromycin A , while having a less potent IC50 in the cell free assay .
	manualset3
90360	5	399047	13	NULL	NULL	0	NULL	cell free assay	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However a 4 ' - O-allyl ether of hygromycin A aglycone showed an equivalent MIC to hygromycin A , while having a less potent IC50 in the cell free assay .
	manualset3
90361	1	399048	13	NULL	NULL	0	NULL	methods	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However both methods need very expensive instruments like HPLC and/or Bactec-460 Tb radiometric system .
	manualset3
90362	2	399048	13	NULL	NULL	0	NULL	instruments	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However both methods need very expensive instruments like HPLC and/or Bactec-460 Tb radiometric system .
	manualset3
90363	3	399048	13	NULL	NULL	0	NULL	HPLC 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	However both methods need very expensive instruments like HPLC and/or Bactec-460 Tb radiometric system .
	manualset3
90364	4	399048	13	NULL	NULL	0	NULL	Bactec-460 Tb radiometric system 	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However both methods need very expensive instruments like HPLC and/or Bactec-460 Tb radiometric system .
	manualset3
90365	1	399049	13	NULL	NULL	0	NULL	postoperative pain group	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However in the acute postoperative pain group other factors such as depletion of endorphins by drugs used for anesthesia or due to surgical stress can not be excluded .
	manualset3
90366	2	399049	13	NULL	NULL	0	NULL	factors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However in the acute postoperative pain group other factors such as depletion of endorphins by drugs used for anesthesia or due to surgical stress can not be excluded .
	manualset3
90367	3	399049	13	NULL	NULL	0	NULL	depletion of endorphins 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However in the acute postoperative pain group other factors such as depletion of endorphins by drugs used for anesthesia or due to surgical stress can not be excluded .
	manualset3
90368	4	399049	13	NULL	NULL	0	NULL	drugs	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	However in the acute postoperative pain group other factors such as depletion of endorphins by drugs used for anesthesia or due to surgical stress can not be excluded .
	manualset3
90369	5	399049	13	NULL	NULL	0	NULL	anesthesia	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However in the acute postoperative pain group other factors such as depletion of endorphins by drugs used for anesthesia or due to surgical stress can not be excluded .
	manualset3
90370	6	399049	13	NULL	NULL	0	NULL	 surgical stress	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However in the acute postoperative pain group other factors such as depletion of endorphins by drugs used for anesthesia or due to surgical stress can not be excluded .
	manualset3
90372	2	399050	13	NULL	NULL	0	NULL	durations 	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	However in this study the durations of vecuronium action in patients who required further hemodialysis therapy were also shorter than those during kidney transplantation .
	manualset3
90373	3	399050	13	NULL	NULL	NULL	NULL	vecuronium action	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However in this study the durations of vecuronium action in patients who required further hemodialysis therapy were also shorter than those during kidney transplantation .
	manualset3
90375	5	399050	13	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However in this study the durations of vecuronium action in patients who required further hemodialysis therapy were also shorter than those during kidney transplantation .
	manualset3
90376	6	399050	13	NULL	NULL	0	NULL	hemodialysis therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However in this study the durations of vecuronium action in patients who required further hemodialysis therapy were also shorter than those during kidney transplantation .
	manualset3
90377	7	399050	13	NULL	NULL	0	NULL	kidney transplantation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However in this study the durations of vecuronium action in patients who required further hemodialysis therapy were also shorter than those during kidney transplantation .
	manualset3
90378	1	399051	13	NULL	NULL	NULL	NULL	non-phosphorylated peptides	AminoAcidPeptide												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However it can bind to some non-phosphorylated peptides containing one or more aspartic acid residues and/or glutamic acid residues .
	manualset3
90379	2	399051	13	NULL	NULL	0	NULL	one or more aspartic acid residues	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However it can bind to some non-phosphorylated peptides containing one or more aspartic acid residues and/or glutamic acid residues .
	manualset3
90380	3	399051	13	NULL	NULL	0	NULL	glutamic acid residues	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	However it can bind to some non-phosphorylated peptides containing one or more aspartic acid residues and/or glutamic acid residues .
	manualset3
90381	1	399052	13	NULL	NULL	0	NULL	molecules	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	However some molecules are able to block in vitro the interaction between a rhinovirus and its receptor : anti-receptor antibodies , soluble ICAM-1 , capsid-binding agents .
	manualset3
90382	2	399052	13	NULL	NULL	0	NULL	 interaction	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However some molecules are able to block in vitro the interaction between a rhinovirus and its receptor : anti-receptor antibodies , soluble ICAM-1 , capsid-binding agents .
	manualset3
90383	3	399052	13	NULL	NULL	0	NULL	rhinovirus 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	However some molecules are able to block in vitro the interaction between a rhinovirus and its receptor : anti-receptor antibodies , soluble ICAM-1 , capsid-binding agents .
	manualset3
90384	4	399052	13	NULL	NULL	0	NULL	receptor	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However some molecules are able to block in vitro the interaction between a rhinovirus and its receptor : anti-receptor antibodies , soluble ICAM-1 , capsid-binding agents .
	manualset3
90385	5	399052	13	NULL	NULL	0	NULL	anti-receptor antibodies	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However some molecules are able to block in vitro the interaction between a rhinovirus and its receptor : anti-receptor antibodies , soluble ICAM-1 , capsid-binding agents .
	manualset3
90386	6	399052	13	NULL	NULL	0	NULL	soluble ICAM-1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However some molecules are able to block in vitro the interaction between a rhinovirus and its receptor : anti-receptor antibodies , soluble ICAM-1 , capsid-binding agents .
	manualset3
90389	7	399052	13	NULL	NULL	0	NULL	capsid-binding agents	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However some molecules are able to block in vitro the interaction between a rhinovirus and its receptor : anti-receptor antibodies , soluble ICAM-1 , capsid-binding agents .
	manualset3
90390	1	399053	13	NULL	NULL	0	NULL	alcoholism	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The present state of alcoholism treatment in Poland ) .
	manualset3
90391	2	399053	13	NULL	NULL	0	NULL	treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The present state of alcoholism treatment in Poland ) .
	manualset3
90392	3	399053	13	NULL	NULL	0	NULL	Poland	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	( The present state of alcoholism treatment in Poland ) .
	manualset3
90394	5	399053	13	NULL	NULL	0	NULL	state	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( The present state of alcoholism treatment in Poland ) .
	manualset3
90395	1	399054	13	NULL	NULL	0	NULL	mechanism	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However the mechanism by which AIRE controls gene expression is currently unknown and the function of its domains , in particular of its PHD fingers is still elusive and controversial .
	manualset3
90405	2	399054	13	NULL	NULL	0	NULL	AIRE	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	However the mechanism by which AIRE controls gene expression is currently unknown and the function of its domains , in particular of its PHD fingers is still elusive and controversial .
	manualset3
90407	3	399054	13	NULL	NULL	0	NULL	gene expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However the mechanism by which AIRE controls gene expression is currently unknown and the function of its domains , in particular of its PHD fingers is still elusive and controversial .
	manualset3
90408	4	399054	13	NULL	NULL	0	NULL	 function	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	However the mechanism by which AIRE controls gene expression is currently unknown and the function of its domains , in particular of its PHD fingers is still elusive and controversial .
	manualset3
90409	5	399054	13	NULL	NULL	0	NULL	domains 	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	However the mechanism by which AIRE controls gene expression is currently unknown and the function of its domains , in particular of its PHD fingers is still elusive and controversial .
	manualset3
90410	6	399054	13	NULL	NULL	0	NULL	PHD fingers	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	However the mechanism by which AIRE controls gene expression is currently unknown and the function of its domains , in particular of its PHD fingers is still elusive and controversial .
	manualset3
90414	1	399055	13	NULL	NULL	NULL	NULL	order of activity	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However the order of activity MOR ) MFI ) BEA ) FAU seems to be related to the size of the pores , which may suggest the involvement of a confinement effect in the zeolites cavities .
	manualset3
90415	2	399055	13	NULL	NULL	0	NULL	MOR 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However the order of activity MOR ) MFI ) BEA ) FAU seems to be related to the size of the pores , which may suggest the involvement of a confinement effect in the zeolites cavities .
	manualset3
90417	3	399055	13	NULL	NULL	0	NULL	MFI	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However the order of activity MOR ) MFI ) BEA ) FAU seems to be related to the size of the pores , which may suggest the involvement of a confinement effect in the zeolites cavities .
	manualset3
90418	4	399055	13	NULL	NULL	0	NULL	BEA	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However the order of activity MOR ) MFI ) BEA ) FAU seems to be related to the size of the pores , which may suggest the involvement of a confinement effect in the zeolites cavities .
	manualset3
90419	5	399055	13	NULL	NULL	0	NULL	FAU 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	However the order of activity MOR ) MFI ) BEA ) FAU seems to be related to the size of the pores , which may suggest the involvement of a confinement effect in the zeolites cavities .
	manualset3
90421	6	399055	13	NULL	NULL	0	NULL	size of the pores	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	However the order of activity MOR ) MFI ) BEA ) FAU seems to be related to the size of the pores , which may suggest the involvement of a confinement effect in the zeolites cavities .
	manualset3
90424	7	399055	13	NULL	NULL	0	NULL	involvement 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However the order of activity MOR ) MFI ) BEA ) FAU seems to be related to the size of the pores , which may suggest the involvement of a confinement effect in the zeolites cavities .
	manualset3
90425	8	399055	13	NULL	NULL	0	NULL	confinement effect	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	However the order of activity MOR ) MFI ) BEA ) FAU seems to be related to the size of the pores , which may suggest the involvement of a confinement effect in the zeolites cavities .
	manualset3
90427	9	399055	13	NULL	NULL	0	NULL	zeolites cavities	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	However the order of activity MOR ) MFI ) BEA ) FAU seems to be related to the size of the pores , which may suggest the involvement of a confinement effect in the zeolites cavities .
	manualset3
90473	1	399056	13	NULL	NULL	NULL	NULL	hyponatremia warrant	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	However the potentially severe affects of hyponatremia warrant close monitoring of these patients and the establishment of methods to prevent this problem from occurring .
	manualset3
90475	3	399056	13	NULL	NULL	0	NULL	monitoring	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However the potentially severe affects of hyponatremia warrant close monitoring of these patients and the establishment of methods to prevent this problem from occurring .
	manualset3
90476	4	399056	13	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	However the potentially severe affects of hyponatremia warrant close monitoring of these patients and the establishment of methods to prevent this problem from occurring .
	manualset3
90477	5	399056	13	NULL	NULL	0	NULL	 establishment of methods 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	However the potentially severe affects of hyponatremia warrant close monitoring of these patients and the establishment of methods to prevent this problem from occurring .
	manualset3
91076	6	399056	13	NULL	NULL	0	NULL	problem	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	However the potentially severe affects of hyponatremia warrant close monitoring of these patients and the establishment of methods to prevent this problem from occurring .
	manualset3
90478	1	399057	13	NULL	NULL	0	NULL	HoxB5 mRNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	HoxB5 mRNA colocalized with flk1 expression in differentiating embryoid bodies , and HoxB5 potently transactivated the flk1 promoter in an HBE-dependent fashion in transient-transfection assays .
	manualset3
90479	2	399057	13	NULL	NULL	0	NULL	flk1 expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HoxB5 mRNA colocalized with flk1 expression in differentiating embryoid bodies , and HoxB5 potently transactivated the flk1 promoter in an HBE-dependent fashion in transient-transfection assays .
	manualset3
90480	3	399057	13	NULL	NULL	0	NULL	embryoid bodies	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	HoxB5 mRNA colocalized with flk1 expression in differentiating embryoid bodies , and HoxB5 potently transactivated the flk1 promoter in an HBE-dependent fashion in transient-transfection assays .
	manualset3
90481	4	399057	13	NULL	NULL	0	NULL	HoxB5 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	HoxB5 mRNA colocalized with flk1 expression in differentiating embryoid bodies , and HoxB5 potently transactivated the flk1 promoter in an HBE-dependent fashion in transient-transfection assays .
	manualset3
90482	5	399057	13	NULL	NULL	0	NULL	flk1 promoter 	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	HoxB5 mRNA colocalized with flk1 expression in differentiating embryoid bodies , and HoxB5 potently transactivated the flk1 promoter in an HBE-dependent fashion in transient-transfection assays .
	manualset3
90483	6	399057	13	NULL	NULL	0	NULL	HBE-dependent fashion	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	HoxB5 mRNA colocalized with flk1 expression in differentiating embryoid bodies , and HoxB5 potently transactivated the flk1 promoter in an HBE-dependent fashion in transient-transfection assays .
	manualset3
90484	7	399057	13	NULL	NULL	0	NULL	transient-transfection assays 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	HoxB5 mRNA colocalized with flk1 expression in differentiating embryoid bodies , and HoxB5 potently transactivated the flk1 promoter in an HBE-dependent fashion in transient-transfection assays .
	manualset3
90485	1	399058	13	NULL	NULL	0	NULL	Hp	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hp administrated orally along with Cd injection for 21 days , significantly revert back the status of oxidative stress markers , Cd concentration in testis , improved status of antioxidant markers and membrane bound enzymes in the testis to near normal level .
	manualset3
90486	2	399058	13	NULL	NULL	0	NULL	Cd injection	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hp administrated orally along with Cd injection for 21 days , significantly revert back the status of oxidative stress markers , Cd concentration in testis , improved status of antioxidant markers and membrane bound enzymes in the testis to near normal level .
	manualset3
90487	3	399058	13	NULL	NULL	0	NULL	21 days	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Hp administrated orally along with Cd injection for 21 days , significantly revert back the status of oxidative stress markers , Cd concentration in testis , improved status of antioxidant markers and membrane bound enzymes in the testis to near normal level .
	manualset3
90488	4	399058	13	NULL	NULL	0	NULL	 status of oxidative stress markers	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hp administrated orally along with Cd injection for 21 days , significantly revert back the status of oxidative stress markers , Cd concentration in testis , improved status of antioxidant markers and membrane bound enzymes in the testis to near normal level .
	manualset3
90489	5	399058	13	NULL	NULL	0	NULL	Cd concentration in testis 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hp administrated orally along with Cd injection for 21 days , significantly revert back the status of oxidative stress markers , Cd concentration in testis , improved status of antioxidant markers and membrane bound enzymes in the testis to near normal level .
	manualset3
90490	6	399058	13	NULL	NULL	0	NULL	status of antioxidant markers	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hp administrated orally along with Cd injection for 21 days , significantly revert back the status of oxidative stress markers , Cd concentration in testis , improved status of antioxidant markers and membrane bound enzymes in the testis to near normal level .
	manualset3
90491	7	399058	13	NULL	NULL	0	NULL	membrane bound enzymes 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hp administrated orally along with Cd injection for 21 days , significantly revert back the status of oxidative stress markers , Cd concentration in testis , improved status of antioxidant markers and membrane bound enzymes in the testis to near normal level .
	manualset3
90492	8	399058	13	NULL	NULL	0	NULL	testis 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hp administrated orally along with Cd injection for 21 days , significantly revert back the status of oxidative stress markers , Cd concentration in testis , improved status of antioxidant markers and membrane bound enzymes in the testis to near normal level .
	manualset3
90493	9	399058	13	NULL	NULL	0	NULL	level 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hp administrated orally along with Cd injection for 21 days , significantly revert back the status of oxidative stress markers , Cd concentration in testis , improved status of antioxidant markers and membrane bound enzymes in the testis to near normal level .
	manualset3
90494	1	399059	13	NULL	NULL	0	NULL	Hsp70	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hsp70 was strongly induced in all exposure groups , which also included bisphenol A and diallylphthalate .
	manualset3
90495	2	399059	13	NULL	NULL	0	NULL	exposure groups	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hsp70 was strongly induced in all exposure groups , which also included bisphenol A and diallylphthalate .
	manualset3
90496	3	399059	13	NULL	NULL	0	NULL	bisphenol A	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hsp70 was strongly induced in all exposure groups , which also included bisphenol A and diallylphthalate .
	manualset3
90497	4	399059	13	NULL	NULL	0	NULL	 diallylphthalate	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hsp70 was strongly induced in all exposure groups , which also included bisphenol A and diallylphthalate .
	manualset3
90498	1	399060	13	NULL	NULL	0	NULL	Human B cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Human B cells express two closely related immunoglobulin G receptors , FcRIIb1 and FcRIIb2 , which differ by a 19 amino acid insertion in the cytoplasmic tail of FcRIIb1 .
	manualset3
90499	2	399060	13	NULL	NULL	0	NULL	two 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Human B cells express two closely related immunoglobulin G receptors , FcRIIb1 and FcRIIb2 , which differ by a 19 amino acid insertion in the cytoplasmic tail of FcRIIb1 .
	manualset3
90500	3	399060	13	NULL	NULL	0	NULL	immunoglobulin G receptors	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Human B cells express two closely related immunoglobulin G receptors , FcRIIb1 and FcRIIb2 , which differ by a 19 amino acid insertion in the cytoplasmic tail of FcRIIb1 .
	manualset3
90501	4	399060	13	NULL	NULL	0	NULL	FcRIIb1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human B cells express two closely related immunoglobulin G receptors , FcRIIb1 and FcRIIb2 , which differ by a 19 amino acid insertion in the cytoplasmic tail of FcRIIb1 .
	manualset3
90502	5	399060	13	NULL	NULL	0	NULL	FcRIIb2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human B cells express two closely related immunoglobulin G receptors , FcRIIb1 and FcRIIb2 , which differ by a 19 amino acid insertion in the cytoplasmic tail of FcRIIb1 .
	manualset3
90503	6	399060	13	NULL	NULL	0	NULL	19 amino acid insertion	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human B cells express two closely related immunoglobulin G receptors , FcRIIb1 and FcRIIb2 , which differ by a 19 amino acid insertion in the cytoplasmic tail of FcRIIb1 .
	manualset3
90504	7	399060	13	NULL	NULL	0	NULL	cytoplasmic tail of FcRIIb1 	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human B cells express two closely related immunoglobulin G receptors , FcRIIb1 and FcRIIb2 , which differ by a 19 amino acid insertion in the cytoplasmic tail of FcRIIb1 .
	manualset3
90505	1	399061	13	NULL	NULL	0	NULL	Human CysC	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human CysC also increased the number of neurospheres formed from embryonic brain , and thus it increases the number of neural stem/precursor cells in a manner similar to glycosylated rat CysC .
	manualset3
90506	2	399061	13	NULL	NULL	NULL	NULL	number of neurospheres	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human CysC also increased the number of neurospheres formed from embryonic brain , and thus it increases the number of neural stem/precursor cells in a manner similar to glycosylated rat CysC .
	manualset3
90507	3	399061	13	NULL	NULL	0	NULL	embryonic brain	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Human CysC also increased the number of neurospheres formed from embryonic brain , and thus it increases the number of neural stem/precursor cells in a manner similar to glycosylated rat CysC .
	manualset3
90508	4	399061	13	NULL	NULL	NULL	NULL	number of neural stem/precursor cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human CysC also increased the number of neurospheres formed from embryonic brain , and thus it increases the number of neural stem/precursor cells in a manner similar to glycosylated rat CysC .
	manualset3
90509	5	399061	13	NULL	NULL	0	NULL	glycosylated rat CysC	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human CysC also increased the number of neurospheres formed from embryonic brain , and thus it increases the number of neural stem/precursor cells in a manner similar to glycosylated rat CysC .
	manualset3
90510	1	399062	13	NULL	NULL	0	NULL	Human Cytomegalovirus ( HCMV ) infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Human Cytomegalovirus ( HCMV ) infection induces several metabolic activities that have been found to be important for viral replication .
	manualset3
90511	2	399062	13	NULL	NULL	NULL	NULL	metabolic activities 	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human Cytomegalovirus ( HCMV ) infection induces several metabolic activities that have been found to be important for viral replication .
	manualset3
90512	3	399062	13	NULL	NULL	0	NULL	viral replication	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human Cytomegalovirus ( HCMV ) infection induces several metabolic activities that have been found to be important for viral replication .
	manualset3
90513	1	399063	13	NULL	NULL	0	NULL	Human EEG activity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human EEG activity in the conventional frequency range of 1-30 c/s is a well-established entity .
	manualset3
90514	2	399063	13	NULL	NULL	0	NULL	frequency range	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Human EEG activity in the conventional frequency range of 1-30 c/s is a well-established entity .
	manualset3
90515	3	399063	13	NULL	NULL	0	NULL	1-30 c/s 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Human EEG activity in the conventional frequency range of 1-30 c/s is a well-established entity .
	manualset3
90516	4	399063	13	NULL	NULL	NULL	NULL	well-established entity	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human EEG activity in the conventional frequency range of 1-30 c/s is a well-established entity .
	manualset3
90517	1	399064	13	NULL	NULL	0	NULL	 problem of cervical ribs	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The problem of cervical ribs in internal medicine ) .
	manualset3
90518	2	399064	13	NULL	NULL	NULL	NULL	internal medicine	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The problem of cervical ribs in internal medicine ) .
	manualset3
90519	1	399065	13	NULL	NULL	0	NULL	Human Immunodeficiency virus type 1 Nef	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human Immunodeficiency virus type 1 Nef potently induces apoptosis in primary human brain microvascular endothelial cells via the activation of caspases .
	manualset3
90520	2	399065	13	NULL	NULL	NULL	NULL	apoptosis	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human Immunodeficiency virus type 1 Nef potently induces apoptosis in primary human brain microvascular endothelial cells via the activation of caspases .
	manualset3
90521	3	399065	13	NULL	NULL	0	NULL	primary human brain microvascular endothelial cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Human Immunodeficiency virus type 1 Nef potently induces apoptosis in primary human brain microvascular endothelial cells via the activation of caspases .
	manualset3
90522	4	399065	13	NULL	NULL	0	NULL	activation of caspases	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human Immunodeficiency virus type 1 Nef potently induces apoptosis in primary human brain microvascular endothelial cells via the activation of caspases .
	manualset3
90523	1	399066	13	NULL	NULL	0	NULL	Human LDL 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human LDL was oxidized in the presence of CuSO ( 4 ) ( ox-LDL ) .
	manualset3
90524	2	399066	13	NULL	NULL	0	NULL	 CuSO ( 4 )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Human LDL was oxidized in the presence of CuSO ( 4 ) ( ox-LDL ) .
	manualset3
90525	3	399066	13	NULL	NULL	0	NULL	ox-LDL 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human LDL was oxidized in the presence of CuSO ( 4 ) ( ox-LDL ) .
	manualset3
90526	1	399067	13	NULL	NULL	0	NULL	Human NEIL2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human NEIL2 , one of five oxidized base-specific DNA glycosylases , is unique in preferentially repairing oxidative damage in transcribed genes .
	manualset3
90527	2	399067	13	NULL	NULL	0	NULL	one of five oxidized base-specific DNA glycosylases	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human NEIL2 , one of five oxidized base-specific DNA glycosylases , is unique in preferentially repairing oxidative damage in transcribed genes .
	manualset3
90528	3	399067	13	NULL	NULL	NULL	NULL	oxidative damage 	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human NEIL2 , one of five oxidized base-specific DNA glycosylases , is unique in preferentially repairing oxidative damage in transcribed genes .
	manualset3
90529	4	399067	13	NULL	NULL	0	NULL	genes	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Human NEIL2 , one of five oxidized base-specific DNA glycosylases , is unique in preferentially repairing oxidative damage in transcribed genes .
	manualset3
90530	1	399068	13	NULL	NULL	0	NULL	Human P450c17	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human P450c17 is expressed in a cAMP-responsive , cell-specific , developmentally programmed fashion , but little is known about its transcriptional regulation .
	manualset3
90531	2	399068	13	NULL	NULL	NULL	NULL	cAMP-responsive fashion	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human P450c17 is expressed in a cAMP-responsive , cell-specific , developmentally programmed fashion , but little is known about its transcriptional regulation .
	manualset3
90532	3	399068	13	NULL	NULL	NULL	NULL	cell-specific fashion	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human P450c17 is expressed in a cAMP-responsive , cell-specific , developmentally programmed fashion , but little is known about its transcriptional regulation .
	manualset3
90533	4	399068	13	NULL	NULL	NULL	NULL	developmentally programmed fashion	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human P450c17 is expressed in a cAMP-responsive , cell-specific , developmentally programmed fashion , but little is known about its transcriptional regulation .
	manualset3
90534	5	399068	13	NULL	NULL	0	NULL	 transcriptional regulation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human P450c17 is expressed in a cAMP-responsive , cell-specific , developmentally programmed fashion , but little is known about its transcriptional regulation .
	manualset3
90535	1	399069	13	NULL	NULL	0	NULL	Human RhAG ammonia channel	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human RhAG ammonia channel is impaired by the Phe65Ser mutation in overhydrated stomatocytic red cells .
	manualset3
90536	2	399069	13	NULL	NULL	0	NULL	Phe65Ser mutation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human RhAG ammonia channel is impaired by the Phe65Ser mutation in overhydrated stomatocytic red cells .
	manualset3
90537	3	399069	13	NULL	NULL	0	NULL	stomatocytic red cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Human RhAG ammonia channel is impaired by the Phe65Ser mutation in overhydrated stomatocytic red cells .
	manualset3
90538	1	399070	13	NULL	NULL	0	NULL	Human atrial natriuretic factor ( ANF ) levels 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Human atrial natriuretic factor ( ANF ) levels were measured before and after peritoneovenous shunt implantation in 10 cirrhotic patients with ascites , in whom sodium retention is a major clinical problem .
	manualset3
90539	2	399070	13	NULL	NULL	0	NULL	 peritoneovenous shunt implantation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Human atrial natriuretic factor ( ANF ) levels were measured before and after peritoneovenous shunt implantation in 10 cirrhotic patients with ascites , in whom sodium retention is a major clinical problem .
	manualset3
90540	3	399070	13	NULL	NULL	0	NULL	10 cirrhotic patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Human atrial natriuretic factor ( ANF ) levels were measured before and after peritoneovenous shunt implantation in 10 cirrhotic patients with ascites , in whom sodium retention is a major clinical problem .
	manualset3
90541	4	399070	13	NULL	NULL	0	NULL	ascites	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Human atrial natriuretic factor ( ANF ) levels were measured before and after peritoneovenous shunt implantation in 10 cirrhotic patients with ascites , in whom sodium retention is a major clinical problem .
	manualset3
90542	5	399070	13	NULL	NULL	0	NULL	sodium retention	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Human atrial natriuretic factor ( ANF ) levels were measured before and after peritoneovenous shunt implantation in 10 cirrhotic patients with ascites , in whom sodium retention is a major clinical problem .
	manualset3
90543	6	399070	13	NULL	NULL	NULL	NULL	major clinical problem 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human atrial natriuretic factor ( ANF ) levels were measured before and after peritoneovenous shunt implantation in 10 cirrhotic patients with ascites , in whom sodium retention is a major clinical problem .
	manualset3
90544	1	399071	13	NULL	NULL	0	NULL	Human calmodulin	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Human calmodulin is encoded by three genes CALM1 , CALM2 and CALM3 located on different chromosomes .
	manualset3
90545	2	399071	13	NULL	NULL	0	NULL	three	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Human calmodulin is encoded by three genes CALM1 , CALM2 and CALM3 located on different chromosomes .
	manualset3
90546	3	399071	13	NULL	NULL	NULL	NULL	genes	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human calmodulin is encoded by three genes CALM1 , CALM2 and CALM3 located on different chromosomes .
	manualset3
90547	4	399071	13	NULL	NULL	0	NULL	CALM1	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Human calmodulin is encoded by three genes CALM1 , CALM2 and CALM3 located on different chromosomes .
	manualset3
90548	5	399071	13	NULL	NULL	0	NULL	CALM2	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Human calmodulin is encoded by three genes CALM1 , CALM2 and CALM3 located on different chromosomes .
	manualset3
90549	6	399071	13	NULL	NULL	0	NULL	CALM3 	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Human calmodulin is encoded by three genes CALM1 , CALM2 and CALM3 located on different chromosomes .
	manualset3
90550	7	399071	13	NULL	NULL	0	NULL	chromosomes 	Chromosome												NULL		0	NULL	NULL	NULL	NULL	NULL	Human calmodulin is encoded by three genes CALM1 , CALM2 and CALM3 located on different chromosomes .
	manualset3
90551	1	399072	13	NULL	NULL	0	NULL	Human carboxypeptidase D ( CPD )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human carboxypeptidase D ( CPD ) is a 180-kDa type I membrane protein with three tandem active site domains .
	manualset3
90552	2	399072	13	NULL	NULL	0	NULL	180-kDa type I membrane protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human carboxypeptidase D ( CPD ) is a 180-kDa type I membrane protein with three tandem active site domains .
	manualset3
90553	3	399072	13	NULL	NULL	0	NULL	three	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Human carboxypeptidase D ( CPD ) is a 180-kDa type I membrane protein with three tandem active site domains .
	manualset3
90554	4	399072	13	NULL	NULL	0	NULL	tandem active site domains	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human carboxypeptidase D ( CPD ) is a 180-kDa type I membrane protein with three tandem active site domains .
	manualset3
90555	1	399073	13	NULL	NULL	NULL	NULL	Human cerebellar hypoplasia	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human cerebellar hypoplasia : a syndrome of diverse causes .
	manualset3
90556	2	399073	13	NULL	NULL	0	NULL	syndrome	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Human cerebellar hypoplasia : a syndrome of diverse causes .
	manualset3
90557	3	399073	13	NULL	NULL	0	NULL	causes	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Human cerebellar hypoplasia : a syndrome of diverse causes .
	manualset3
90558	1	399074	13	NULL	NULL	NULL	NULL	problem of individuality	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The problem of individuality in taxonomy ) .
	manualset3
90559	2	399074	13	NULL	NULL	0	NULL	taxonomy	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	( The problem of individuality in taxonomy ) .
	manualset3
90560	1	399075	13	NULL	NULL	0	NULL	Human chondrocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Human chondrocytes that overexpressed IL-1RII were resistant to IL-1-induced IL-1beta mRNA accumulation and inhibition of proteoglycan synthesis .
	manualset3
90561	2	399075	13	NULL	NULL	0	NULL	 IL-1RII	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human chondrocytes that overexpressed IL-1RII were resistant to IL-1-induced IL-1beta mRNA accumulation and inhibition of proteoglycan synthesis .
	manualset3
90562	3	399075	13	NULL	NULL	0	NULL	IL-1-induced IL-1beta mRNA accumulation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human chondrocytes that overexpressed IL-1RII were resistant to IL-1-induced IL-1beta mRNA accumulation and inhibition of proteoglycan synthesis .
	manualset3
90563	4	399075	13	NULL	NULL	0	NULL	inhibition of proteoglycan synthesis	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human chondrocytes that overexpressed IL-1RII were resistant to IL-1-induced IL-1beta mRNA accumulation and inhibition of proteoglycan synthesis .
	manualset3
90564	1	399076	13	NULL	NULL	0	NULL	Human chorionic gonadotropin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human chorionic gonadotropin in lung and lung tumors .
	manualset3
90565	2	399076	13	NULL	NULL	0	NULL	lung	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Human chorionic gonadotropin in lung and lung tumors .
	manualset3
90566	3	399076	13	NULL	NULL	0	NULL	lung tumors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Human chorionic gonadotropin in lung and lung tumors .
	manualset3
90567	1	399077	13	NULL	NULL	0	NULL	Human chorionic gonadotropin levels	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Human chorionic gonadotropin levels were 33.25-174315 .5 IU/l .
	manualset3
90568	2	399077	13	NULL	NULL	0	NULL	33.25-174315 .5 IU/l	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Human chorionic gonadotropin levels were 33.25-174315 .5 IU/l .
	manualset3
90569	1	399078	13	NULL	NULL	0	NULL	Human eIF4AIII 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human eIF4AIII interacts with an eIF4G-like partner , NOM1 , revealing an evolutionarily conserved function outside the exon junction complex .
	manualset3
90570	2	399078	13	NULL	NULL	0	NULL	eIF4G-like partner	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human eIF4AIII interacts with an eIF4G-like partner , NOM1 , revealing an evolutionarily conserved function outside the exon junction complex .
	manualset3
90571	3	399078	13	NULL	NULL	0	NULL	NOM1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human eIF4AIII interacts with an eIF4G-like partner , NOM1 , revealing an evolutionarily conserved function outside the exon junction complex .
	manualset3
90572	4	399078	13	NULL	NULL	0	NULL	function 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human eIF4AIII interacts with an eIF4G-like partner , NOM1 , revealing an evolutionarily conserved function outside the exon junction complex .
	manualset3
90573	5	399078	13	NULL	NULL	0	NULL	exon junction complex	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Human eIF4AIII interacts with an eIF4G-like partner , NOM1 , revealing an evolutionarily conserved function outside the exon junction complex .
	manualset3
90574	1	399079	13	NULL	NULL	0	NULL	Human enhancer of invasion-cluster ( HEI-C )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human enhancer of invasion-cluster ( HEI-C ) , encoding a novel evolutionarily conserved coiled-coil protein , was isolated in a screen for human genes that induce agar invasion in S. cerevisiae .
	manualset3
90575	2	399079	13	NULL	NULL	0	NULL	 coiled-coil protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human enhancer of invasion-cluster ( HEI-C ) , encoding a novel evolutionarily conserved coiled-coil protein , was isolated in a screen for human genes that induce agar invasion in S. cerevisiae .
	manualset3
90576	3	399079	13	NULL	NULL	0	NULL	screen	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Human enhancer of invasion-cluster ( HEI-C ) , encoding a novel evolutionarily conserved coiled-coil protein , was isolated in a screen for human genes that induce agar invasion in S. cerevisiae .
	manualset3
90577	4	399079	13	NULL	NULL	0	NULL	human genes 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Human enhancer of invasion-cluster ( HEI-C ) , encoding a novel evolutionarily conserved coiled-coil protein , was isolated in a screen for human genes that induce agar invasion in S. cerevisiae .
	manualset3
90578	5	399079	13	NULL	NULL	0	NULL	agar invasion	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human enhancer of invasion-cluster ( HEI-C ) , encoding a novel evolutionarily conserved coiled-coil protein , was isolated in a screen for human genes that induce agar invasion in S. cerevisiae .
	manualset3
90579	6	399079	13	NULL	NULL	0	NULL	S. cerevisiae 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Human enhancer of invasion-cluster ( HEI-C ) , encoding a novel evolutionarily conserved coiled-coil protein , was isolated in a screen for human genes that induce agar invasion in S. cerevisiae .
	manualset3
90580	1	399080	13	NULL	NULL	0	NULL	Human fibrinogen	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human fibrinogen specifically binds hyaluronic acid .
	manualset3
90581	2	399080	13	NULL	NULL	0	NULL	hyaluronic acid	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Human fibrinogen specifically binds hyaluronic acid .
	manualset3
90582	1	399081	13	NULL	NULL	0	NULL	Human fibroblasts	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Human fibroblasts were cultured in the absence and presence of cadmium sulfide nanoparticles to evaluate cytotoxicity and cell compatibility .
	manualset3
90583	2	399081	13	NULL	NULL	NULL	NULL	 presence of cadmium sulfide nanoparticles	ExperimentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human fibroblasts were cultured in the absence and presence of cadmium sulfide nanoparticles to evaluate cytotoxicity and cell compatibility .
	manualset3
90584	3	399081	13	NULL	NULL	NULL	NULL	absence of cadmium sulfide nanoparticles 	ExperimentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human fibroblasts were cultured in the absence and presence of cadmium sulfide nanoparticles to evaluate cytotoxicity and cell compatibility .
	manualset3
90586	5	399081	13	NULL	NULL	0	NULL	 cytotoxicity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human fibroblasts were cultured in the absence and presence of cadmium sulfide nanoparticles to evaluate cytotoxicity and cell compatibility .
	manualset3
90587	6	399081	13	NULL	NULL	0	NULL	cell compatibility	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human fibroblasts were cultured in the absence and presence of cadmium sulfide nanoparticles to evaluate cytotoxicity and cell compatibility .
	manualset3
90588	1	399082	13	NULL	NULL	0	NULL	Human gyrovirus DNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Human gyrovirus DNA in human blood , Italy .
	manualset3
90589	2	399082	13	NULL	NULL	0	NULL	human blood	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Human gyrovirus DNA in human blood , Italy .
	manualset3
90590	3	399082	13	NULL	NULL	0	NULL	 Italy	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Human gyrovirus DNA in human blood , Italy .
	manualset3
90591	1	399083	13	NULL	NULL	0	NULL	Human infants	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Human infants use prosodic cues present in speech to extract language regularities , and it has been suggested that this capacity is anchored in more general mechanisms that are shared across mammals .
	manualset3
90592	2	399083	13	NULL	NULL	NULL	NULL	prosodic cues 	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human infants use prosodic cues present in speech to extract language regularities , and it has been suggested that this capacity is anchored in more general mechanisms that are shared across mammals .
	manualset3
90593	3	399083	13	NULL	NULL	0	NULL	speech 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Human infants use prosodic cues present in speech to extract language regularities , and it has been suggested that this capacity is anchored in more general mechanisms that are shared across mammals .
	manualset3
90594	4	399083	13	NULL	NULL	0	NULL	 language regularities	Language												NULL		0	NULL	NULL	NULL	NULL	NULL	Human infants use prosodic cues present in speech to extract language regularities , and it has been suggested that this capacity is anchored in more general mechanisms that are shared across mammals .
	manualset3
90595	5	399083	13	NULL	NULL	0	NULL	capacity	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Human infants use prosodic cues present in speech to extract language regularities , and it has been suggested that this capacity is anchored in more general mechanisms that are shared across mammals .
	manualset3
90596	6	399083	13	NULL	NULL	0	NULL	mechanisms 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human infants use prosodic cues present in speech to extract language regularities , and it has been suggested that this capacity is anchored in more general mechanisms that are shared across mammals .
	manualset3
90597	7	399083	13	NULL	NULL	0	NULL	mammals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Human infants use prosodic cues present in speech to extract language regularities , and it has been suggested that this capacity is anchored in more general mechanisms that are shared across mammals .
	manualset3
90598	1	399084	13	NULL	NULL	0	NULL	Human leukocyte antigen-G ( HLA-G )	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Human leukocyte antigen-G ( HLA-G ) is an MHC class I gene of particular interest in reproductive biology because of its specific expression on fetal cytotrophoblast cells , and its reported involvement both in protection of the developing fetus from destruction by the maternal immune response and in the prevention of maternal pre-eclampsia .
	manualset3
90599	2	399084	13	NULL	NULL	0	NULL	 MHC class I gene 	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Human leukocyte antigen-G ( HLA-G ) is an MHC class I gene of particular interest in reproductive biology because of its specific expression on fetal cytotrophoblast cells , and its reported involvement both in protection of the developing fetus from destruction by the maternal immune response and in the prevention of maternal pre-eclampsia .
	manualset3
90600	3	399084	13	NULL	NULL	0	NULL	reproductive biology	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Human leukocyte antigen-G ( HLA-G ) is an MHC class I gene of particular interest in reproductive biology because of its specific expression on fetal cytotrophoblast cells , and its reported involvement both in protection of the developing fetus from destruction by the maternal immune response and in the prevention of maternal pre-eclampsia .
	manualset3
90601	4	399084	13	NULL	NULL	0	NULL	expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human leukocyte antigen-G ( HLA-G ) is an MHC class I gene of particular interest in reproductive biology because of its specific expression on fetal cytotrophoblast cells , and its reported involvement both in protection of the developing fetus from destruction by the maternal immune response and in the prevention of maternal pre-eclampsia .
	manualset3
90602	5	399084	13	NULL	NULL	0	NULL	fetal cytotrophoblast cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Human leukocyte antigen-G ( HLA-G ) is an MHC class I gene of particular interest in reproductive biology because of its specific expression on fetal cytotrophoblast cells , and its reported involvement both in protection of the developing fetus from destruction by the maternal immune response and in the prevention of maternal pre-eclampsia .
	manualset3
90603	6	399084	13	NULL	NULL	NULL	NULL	involvement	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human leukocyte antigen-G ( HLA-G ) is an MHC class I gene of particular interest in reproductive biology because of its specific expression on fetal cytotrophoblast cells , and its reported involvement both in protection of the developing fetus from destruction by the maternal immune response and in the prevention of maternal pre-eclampsia .
	manualset3
90604	7	399084	13	NULL	NULL	0	NULL	protection 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human leukocyte antigen-G ( HLA-G ) is an MHC class I gene of particular interest in reproductive biology because of its specific expression on fetal cytotrophoblast cells , and its reported involvement both in protection of the developing fetus from destruction by the maternal immune response and in the prevention of maternal pre-eclampsia .
	manualset3
90605	8	399084	13	NULL	NULL	NULL	NULL	developing fetus 	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human leukocyte antigen-G ( HLA-G ) is an MHC class I gene of particular interest in reproductive biology because of its specific expression on fetal cytotrophoblast cells , and its reported involvement both in protection of the developing fetus from destruction by the maternal immune response and in the prevention of maternal pre-eclampsia .
	manualset3
90606	9	399084	13	NULL	NULL	NULL	NULL	destruction	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human leukocyte antigen-G ( HLA-G ) is an MHC class I gene of particular interest in reproductive biology because of its specific expression on fetal cytotrophoblast cells , and its reported involvement both in protection of the developing fetus from destruction by the maternal immune response and in the prevention of maternal pre-eclampsia .
	manualset3
90607	10	399084	13	NULL	NULL	NULL	NULL	maternal immune response 	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human leukocyte antigen-G ( HLA-G ) is an MHC class I gene of particular interest in reproductive biology because of its specific expression on fetal cytotrophoblast cells , and its reported involvement both in protection of the developing fetus from destruction by the maternal immune response and in the prevention of maternal pre-eclampsia .
	manualset3
90608	11	399084	13	NULL	NULL	NULL	NULL	prevention 	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human leukocyte antigen-G ( HLA-G ) is an MHC class I gene of particular interest in reproductive biology because of its specific expression on fetal cytotrophoblast cells , and its reported involvement both in protection of the developing fetus from destruction by the maternal immune response and in the prevention of maternal pre-eclampsia .
	manualset3
90609	12	399084	13	NULL	NULL	NULL	NULL	maternal pre-eclampsia	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human leukocyte antigen-G ( HLA-G ) is an MHC class I gene of particular interest in reproductive biology because of its specific expression on fetal cytotrophoblast cells , and its reported involvement both in protection of the developing fetus from destruction by the maternal immune response and in the prevention of maternal pre-eclampsia .
	manualset3
90610	1	399085	13	NULL	NULL	0	NULL	production	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( The production of alcohol and the growth rate of baker 's yeast cultivated in the presence of air ) .
	manualset3
90611	2	399085	13	NULL	NULL	0	NULL	alcohol 	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	( The production of alcohol and the growth rate of baker 's yeast cultivated in the presence of air ) .
	manualset3
90612	3	399085	13	NULL	NULL	0	NULL	growth rate	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	( The production of alcohol and the growth rate of baker 's yeast cultivated in the presence of air ) .
	manualset3
90613	4	399085	13	NULL	NULL	0	NULL	baker 's yeast	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( The production of alcohol and the growth rate of baker 's yeast cultivated in the presence of air ) .
	manualset3
90614	5	399085	13	NULL	NULL	0	NULL	presence	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( The production of alcohol and the growth rate of baker 's yeast cultivated in the presence of air ) .
	manualset3
90615	6	399085	13	NULL	NULL	0	NULL	air	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	( The production of alcohol and the growth rate of baker 's yeast cultivated in the presence of air ) .
	manualset3
90739	1	399086	13	NULL	NULL	0	NULL	Human long-term bone marrow cultures	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Human long-term bone marrow cultures allow persistence of hematopoietic stem cells in vitro for several weeks .
	manualset3
90740	2	399086	13	NULL	NULL	0	NULL	persistence	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human long-term bone marrow cultures allow persistence of hematopoietic stem cells in vitro for several weeks .
	manualset3
90741	3	399086	13	NULL	NULL	0	NULL	hematopoietic stem cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Human long-term bone marrow cultures allow persistence of hematopoietic stem cells in vitro for several weeks .
	manualset3
90742	4	399086	13	NULL	NULL	NULL	NULL	several weeks	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human long-term bone marrow cultures allow persistence of hematopoietic stem cells in vitro for several weeks .
	manualset3
90743	1	399087	13	NULL	NULL	0	NULL	Human malignant T cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Human malignant T cells capable of inducing an immunoglobulin class switch .
	manualset3
90745	3	399087	13	NULL	NULL	NULL	NULL	 immunoglobulin class switch	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human malignant T cells capable of inducing an immunoglobulin class switch .
	manualset3
90746	1	399088	13	NULL	NULL	0	NULL	Human monocyte-derived macrophages	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Human monocyte-derived macrophages treated with recombinant IFN-gamma ( rIFN-gamma ) and control cells were assessed for three distinct effector functions , all mediated by Fc receptors .
	manualset3
90749	2	399088	13	NULL	NULL	0	NULL	recombinant IFN-gamma ( rIFN-gamma )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human monocyte-derived macrophages treated with recombinant IFN-gamma ( rIFN-gamma ) and control cells were assessed for three distinct effector functions , all mediated by Fc receptors .
	manualset3
90750	3	399088	13	NULL	NULL	0	NULL	control cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Human monocyte-derived macrophages treated with recombinant IFN-gamma ( rIFN-gamma ) and control cells were assessed for three distinct effector functions , all mediated by Fc receptors .
	manualset3
90751	4	399088	13	NULL	NULL	0	NULL	 effector functions 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human monocyte-derived macrophages treated with recombinant IFN-gamma ( rIFN-gamma ) and control cells were assessed for three distinct effector functions , all mediated by Fc receptors .
	manualset3
90752	5	399088	13	NULL	NULL	NULL	NULL	 Fc receptors	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human monocyte-derived macrophages treated with recombinant IFN-gamma ( rIFN-gamma ) and control cells were assessed for three distinct effector functions , all mediated by Fc receptors .
	manualset3
90755	1	399089	13	NULL	NULL	0	NULL	Human paleopathology 	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Human paleopathology has the potential of enriching what we can reconstruct about the lives of our recent and ancient ancestors .
	manualset3
90761	2	399089	13	NULL	NULL	0	NULL	lives 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human paleopathology has the potential of enriching what we can reconstruct about the lives of our recent and ancient ancestors .
	manualset3
90763	3	399089	13	NULL	NULL	NULL	NULL	recent ancestors	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human paleopathology has the potential of enriching what we can reconstruct about the lives of our recent and ancient ancestors .
	manualset3
91077	4	399089	13	NULL	NULL	0	NULL	ancient ancestors	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Human paleopathology has the potential of enriching what we can reconstruct about the lives of our recent and ancient ancestors .
	manualset3
90766	1	399090	13	NULL	NULL	0	NULL	Human pancreatic kallikrein 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human pancreatic kallikrein ( H. Panc .
	manualset3
90767	2	399090	13	NULL	NULL	0	NULL	H. Panc . 	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Human pancreatic kallikrein ( H. Panc .
	manualset3
90768	1	399091	13	NULL	NULL	0	NULL	Human parvovirus B19 infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Human parvovirus B19 infection during pregnancy can result in fetal hydrops and death .
	manualset3
90769	2	399091	13	NULL	NULL	0	NULL	pregnancy	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Human parvovirus B19 infection during pregnancy can result in fetal hydrops and death .
	manualset3
90770	3	399091	13	NULL	NULL	NULL	NULL	 fetal hydrops	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human parvovirus B19 infection during pregnancy can result in fetal hydrops and death .
	manualset3
90771	4	399091	13	NULL	NULL	0	NULL	death	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Human parvovirus B19 infection during pregnancy can result in fetal hydrops and death .
	manualset3
90772	1	399092	13	NULL	NULL	0	NULL	Human recombinant palmitoyl-protein thioesterase-1 ( PPT1 ) 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human recombinant palmitoyl-protein thioesterase-1 ( PPT1 ) for preclinical evaluation of enzyme replacement therapy for infantile neuronal ceroid lipofuscinosis .
	manualset3
90773	2	399092	13	NULL	NULL	NULL	NULL	preclinical evaluation	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human recombinant palmitoyl-protein thioesterase-1 ( PPT1 ) for preclinical evaluation of enzyme replacement therapy for infantile neuronal ceroid lipofuscinosis .
	manualset3
90774	3	399092	13	NULL	NULL	0	NULL	enzyme replacement therapy 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Human recombinant palmitoyl-protein thioesterase-1 ( PPT1 ) for preclinical evaluation of enzyme replacement therapy for infantile neuronal ceroid lipofuscinosis .
	manualset3
90775	4	399092	13	NULL	NULL	NULL	NULL	 infantile neuronal ceroid lipofuscinosis 	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human recombinant palmitoyl-protein thioesterase-1 ( PPT1 ) for preclinical evaluation of enzyme replacement therapy for infantile neuronal ceroid lipofuscinosis .
	manualset3
90776	1	399093	13	NULL	NULL	0	NULL	Human red blood cells ( H-RBC ) 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Human red blood cells ( H-RBC ) , sensitized by specific rabbit antihuman hemolysin , showed a significant increase in susceptibility to complement lysis after rigidification of the membrane lipid layer by incorporation of cholesterol ( p less than 0.001 ) .
	manualset3
90777	2	399093	13	NULL	NULL	0	NULL	rabbit antihuman hemolysin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human red blood cells ( H-RBC ) , sensitized by specific rabbit antihuman hemolysin , showed a significant increase in susceptibility to complement lysis after rigidification of the membrane lipid layer by incorporation of cholesterol ( p less than 0.001 ) .
	manualset3
90778	3	399093	13	NULL	NULL	0	NULL	 susceptibility	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Human red blood cells ( H-RBC ) , sensitized by specific rabbit antihuman hemolysin , showed a significant increase in susceptibility to complement lysis after rigidification of the membrane lipid layer by incorporation of cholesterol ( p less than 0.001 ) .
	manualset3
90779	4	399093	13	NULL	NULL	0	NULL	complement lysis 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human red blood cells ( H-RBC ) , sensitized by specific rabbit antihuman hemolysin , showed a significant increase in susceptibility to complement lysis after rigidification of the membrane lipid layer by incorporation of cholesterol ( p less than 0.001 ) .
	manualset3
90780	5	399093	13	NULL	NULL	0	NULL	rigidification 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human red blood cells ( H-RBC ) , sensitized by specific rabbit antihuman hemolysin , showed a significant increase in susceptibility to complement lysis after rigidification of the membrane lipid layer by incorporation of cholesterol ( p less than 0.001 ) .
	manualset3
90781	6	399093	13	NULL	NULL	0	NULL	membrane lipid layer 	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Human red blood cells ( H-RBC ) , sensitized by specific rabbit antihuman hemolysin , showed a significant increase in susceptibility to complement lysis after rigidification of the membrane lipid layer by incorporation of cholesterol ( p less than 0.001 ) .
	manualset3
90782	7	399093	13	NULL	NULL	0	NULL	incorporation of cholesterol	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human red blood cells ( H-RBC ) , sensitized by specific rabbit antihuman hemolysin , showed a significant increase in susceptibility to complement lysis after rigidification of the membrane lipid layer by incorporation of cholesterol ( p less than 0.001 ) .
	manualset3
90783	8	399093	13	NULL	NULL	0	NULL	p less than 0.001 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Human red blood cells ( H-RBC ) , sensitized by specific rabbit antihuman hemolysin , showed a significant increase in susceptibility to complement lysis after rigidification of the membrane lipid layer by incorporation of cholesterol ( p less than 0.001 ) .
	manualset3
90784	1	399094	13	NULL	NULL	0	NULL	Human ribonucleotide reductase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human ribonucleotide reductase was less sensitive to the inhibitory effects of A1110U and its iron-complex .
	manualset3
90785	2	399094	13	NULL	NULL	NULL	NULL	inhibitory effects	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Human ribonucleotide reductase was less sensitive to the inhibitory effects of A1110U and its iron-complex .
	manualset3
90786	3	399094	13	NULL	NULL	0	NULL	 A1110U	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Human ribonucleotide reductase was less sensitive to the inhibitory effects of A1110U and its iron-complex .
	manualset3
90787	4	399094	13	NULL	NULL	0	NULL	iron-complex	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Human ribonucleotide reductase was less sensitive to the inhibitory effects of A1110U and its iron-complex .
	manualset3
90788	1	399095	13	NULL	NULL	0	NULL	Human ribosomal protein L7	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human ribosomal protein L7 incorporates an ER-binding characteristic .
	manualset3
90789	2	399095	13	NULL	NULL	0	NULL	ER-binding characteristic	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human ribosomal protein L7 incorporates an ER-binding characteristic .
	manualset3
90790	1	399096	13	NULL	NULL	0	NULL	 promotion	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The promotion of plant growth by ultraviolet radiation ) .
	manualset3
90791	2	399096	13	NULL	NULL	0	NULL	plant growth	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The promotion of plant growth by ultraviolet radiation ) .
	manualset3
90792	3	399096	13	NULL	NULL	0	NULL	 ultraviolet radiation	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	( The promotion of plant growth by ultraviolet radiation ) .
	manualset3
90793	1	399097	13	NULL	NULL	0	NULL	Human serum holo-transferrin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human serum holo-transferrin was labeled with 99mTc using pre-reduction with 2-mercaptoethanol .
	manualset3
90794	2	399097	13	NULL	NULL	0	NULL	99mTc	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Human serum holo-transferrin was labeled with 99mTc using pre-reduction with 2-mercaptoethanol .
	manualset3
90795	3	399097	13	NULL	NULL	0	NULL	 pre-reduction	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human serum holo-transferrin was labeled with 99mTc using pre-reduction with 2-mercaptoethanol .
	manualset3
90796	4	399097	13	NULL	NULL	0	NULL	2-mercaptoethanol	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Human serum holo-transferrin was labeled with 99mTc using pre-reduction with 2-mercaptoethanol .
	manualset3
90797	1	399098	13	NULL	NULL	0	NULL	Human splenic marginal zone B cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Human splenic marginal zone B cells lack expression of activation-induced cytidine deaminase .
	manualset3
90798	2	399098	13	NULL	NULL	0	NULL	 expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Human splenic marginal zone B cells lack expression of activation-induced cytidine deaminase .
	manualset3
90799	3	399098	13	NULL	NULL	0	NULL	activation-induced cytidine deaminase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Human splenic marginal zone B cells lack expression of activation-induced cytidine deaminase .
	manualset3
90800	1	399099	13	NULL	NULL	0	NULL	Huntington 's disease 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Huntington 's disease : seeing the pathogenic process through a genetic lens .
	manualset3
90801	2	399099	13	NULL	NULL	0	NULL	pathogenic process	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Huntington 's disease : seeing the pathogenic process through a genetic lens .
	manualset3
90802	3	399099	13	NULL	NULL	NULL	NULL	 genetic lens	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Huntington 's disease : seeing the pathogenic process through a genetic lens .
	manualset3
90803	1	399100	13	NULL	NULL	0	NULL	Hyaluronic acid ( HA )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyaluronic acid ( HA ) is a natural biopolymer with unique physiochemical and biological properties and finds a wide range of applications in biomedical and cosmetic fields .
	manualset3
90804	2	399100	13	NULL	NULL	NULL	NULL	natural biopolymer	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hyaluronic acid ( HA ) is a natural biopolymer with unique physiochemical and biological properties and finds a wide range of applications in biomedical and cosmetic fields .
	manualset3
90805	3	399100	13	NULL	NULL	0	NULL	applications	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyaluronic acid ( HA ) is a natural biopolymer with unique physiochemical and biological properties and finds a wide range of applications in biomedical and cosmetic fields .
	manualset3
90806	4	399100	13	NULL	NULL	0	NULL	biomedical fields	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyaluronic acid ( HA ) is a natural biopolymer with unique physiochemical and biological properties and finds a wide range of applications in biomedical and cosmetic fields .
	manualset3
90807	5	399100	13	NULL	NULL	0	NULL	cosmetic fields	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyaluronic acid ( HA ) is a natural biopolymer with unique physiochemical and biological properties and finds a wide range of applications in biomedical and cosmetic fields .
	manualset3
90808	1	399101	13	NULL	NULL	0	NULL	Hyaluronic acid 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyaluronic acid and glycerol are viable carriers for demineralized bone matrices .
	manualset3
90809	2	399101	13	NULL	NULL	0	NULL	glycerol	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyaluronic acid and glycerol are viable carriers for demineralized bone matrices .
	manualset3
90810	3	399101	13	NULL	NULL	0	NULL	carriers	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyaluronic acid and glycerol are viable carriers for demineralized bone matrices .
	manualset3
90811	4	399101	13	NULL	NULL	NULL	NULL	demineralized bone matrices	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hyaluronic acid and glycerol are viable carriers for demineralized bone matrices .
	manualset3
90812	1	399102	13	NULL	NULL	NULL	NULL	Hybrid poplar response	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hybrid poplar and forest soil response to municipal and industrial by-products : a greenhouse study .
	manualset3
90813	2	399102	13	NULL	NULL	0	NULL	forest soil response	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Hybrid poplar and forest soil response to municipal and industrial by-products : a greenhouse study .
	manualset3
90814	3	399102	13	NULL	NULL	0	NULL	municipal by-products	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hybrid poplar and forest soil response to municipal and industrial by-products : a greenhouse study .
	manualset3
90815	4	399102	13	NULL	NULL	0	NULL	industrial by-products	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hybrid poplar and forest soil response to municipal and industrial by-products : a greenhouse study .
	manualset3
90816	5	399102	13	NULL	NULL	0	NULL	greenhouse study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hybrid poplar and forest soil response to municipal and industrial by-products : a greenhouse study .
	manualset3
90817	1	399103	13	NULL	NULL	0	NULL	Anatomical studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Anatomical studies on the structure of joints of the foot in south Kyushu Japanese .
	manualset3
90818	2	399103	13	NULL	NULL	0	NULL	structure of joints of the foot 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Anatomical studies on the structure of joints of the foot in south Kyushu Japanese .
	manualset3
90819	3	399103	13	NULL	NULL	0	NULL	south Kyushu Japanese	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( Anatomical studies on the structure of joints of the foot in south Kyushu Japanese .
	manualset3
90820	1	399104	13	NULL	NULL	0	NULL	Hybridization	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hybridization both on Southern blots and in situ as well as sequence analysis show that this subset is most closely related , as expected , to sequences on HSA 17 .
	manualset3
90821	2	399104	13	NULL	NULL	0	NULL	 Southern blots	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hybridization both on Southern blots and in situ as well as sequence analysis show that this subset is most closely related , as expected , to sequences on HSA 17 .
	manualset3
90822	3	399104	13	NULL	NULL	0	NULL	sequence analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hybridization both on Southern blots and in situ as well as sequence analysis show that this subset is most closely related , as expected , to sequences on HSA 17 .
	manualset3
90823	4	399104	13	NULL	NULL	0	NULL	subset	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Hybridization both on Southern blots and in situ as well as sequence analysis show that this subset is most closely related , as expected , to sequences on HSA 17 .
	manualset3
90824	5	399104	13	NULL	NULL	0	NULL	sequences on HSA 17	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Hybridization both on Southern blots and in situ as well as sequence analysis show that this subset is most closely related , as expected , to sequences on HSA 17 .
	manualset3
90825	1	399105	13	NULL	NULL	0	NULL	Hydration	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydration and ionization of CO2 is facilitated by elevated hydrostatic pressure because a negative volume change ( delta V & lt ; 0 ) accompanies the chemical reaction .
	manualset3
90826	2	399105	13	NULL	NULL	0	NULL	 ionization 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydration and ionization of CO2 is facilitated by elevated hydrostatic pressure because a negative volume change ( delta V & lt ; 0 ) accompanies the chemical reaction .
	manualset3
90827	3	399105	13	NULL	NULL	0	NULL	CO2	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydration and ionization of CO2 is facilitated by elevated hydrostatic pressure because a negative volume change ( delta V & lt ; 0 ) accompanies the chemical reaction .
	manualset3
90828	4	399105	13	NULL	NULL	NULL	NULL	hydrostatic pressure	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hydration and ionization of CO2 is facilitated by elevated hydrostatic pressure because a negative volume change ( delta V & lt ; 0 ) accompanies the chemical reaction .
	manualset3
90829	5	399105	13	NULL	NULL	NULL	NULL	negative volume change 	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hydration and ionization of CO2 is facilitated by elevated hydrostatic pressure because a negative volume change ( delta V & lt ; 0 ) accompanies the chemical reaction .
	manualset3
90830	6	399105	13	NULL	NULL	0	NULL	delta V & lt ; 0	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydration and ionization of CO2 is facilitated by elevated hydrostatic pressure because a negative volume change ( delta V & lt ; 0 ) accompanies the chemical reaction .
	manualset3
90831	7	399105	13	NULL	NULL	0	NULL	chemical reaction	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydration and ionization of CO2 is facilitated by elevated hydrostatic pressure because a negative volume change ( delta V & lt ; 0 ) accompanies the chemical reaction .
	manualset3
90832	1	399106	13	NULL	NULL	NULL	NULL	Hydrodynamic calculations	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hydrodynamic calculations lead to the conclusion that chymotryptic ( or ethylenediaminetetraacetic acid ) myosin S1 in solution ( hydrated ) , at 1-5 degrees C , can be modeled as a prolate ellipsoid , with an axial ratio lying between p = 1.0 and 2.5 ( major axis between 100.5 A , for p = 1.0 , and 162.5 A , for p = 2.5 ) .
	manualset3
90833	2	399106	13	NULL	NULL	0	NULL	conclusion	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrodynamic calculations lead to the conclusion that chymotryptic ( or ethylenediaminetetraacetic acid ) myosin S1 in solution ( hydrated ) , at 1-5 degrees C , can be modeled as a prolate ellipsoid , with an axial ratio lying between p = 1.0 and 2.5 ( major axis between 100.5 A , for p = 1.0 , and 162.5 A , for p = 2.5 ) .
	manualset3
90834	3	399106	13	NULL	NULL	0	NULL	ethylenediaminetetraacetic acid	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrodynamic calculations lead to the conclusion that chymotryptic ( or ethylenediaminetetraacetic acid ) myosin S1 in solution ( hydrated ) , at 1-5 degrees C , can be modeled as a prolate ellipsoid , with an axial ratio lying between p = 1.0 and 2.5 ( major axis between 100.5 A , for p = 1.0 , and 162.5 A , for p = 2.5 ) .
	manualset3
90835	4	399106	13	NULL	NULL	NULL	NULL	chymotryptic myosin S1 in solution	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hydrodynamic calculations lead to the conclusion that chymotryptic ( or ethylenediaminetetraacetic acid ) myosin S1 in solution ( hydrated ) , at 1-5 degrees C , can be modeled as a prolate ellipsoid , with an axial ratio lying between p = 1.0 and 2.5 ( major axis between 100.5 A , for p = 1.0 , and 162.5 A , for p = 2.5 ) .
	manualset3
90837	6	399106	13	NULL	NULL	0	NULL	1-5 degrees C	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrodynamic calculations lead to the conclusion that chymotryptic ( or ethylenediaminetetraacetic acid ) myosin S1 in solution ( hydrated ) , at 1-5 degrees C , can be modeled as a prolate ellipsoid , with an axial ratio lying between p = 1.0 and 2.5 ( major axis between 100.5 A , for p = 1.0 , and 162.5 A , for p = 2.5 ) .
	manualset3
90838	7	399106	13	NULL	NULL	NULL	NULL	prolate ellipsoid	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hydrodynamic calculations lead to the conclusion that chymotryptic ( or ethylenediaminetetraacetic acid ) myosin S1 in solution ( hydrated ) , at 1-5 degrees C , can be modeled as a prolate ellipsoid , with an axial ratio lying between p = 1.0 and 2.5 ( major axis between 100.5 A , for p = 1.0 , and 162.5 A , for p = 2.5 ) .
	manualset3
90839	8	399106	13	NULL	NULL	0	NULL	axial ratio	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrodynamic calculations lead to the conclusion that chymotryptic ( or ethylenediaminetetraacetic acid ) myosin S1 in solution ( hydrated ) , at 1-5 degrees C , can be modeled as a prolate ellipsoid , with an axial ratio lying between p = 1.0 and 2.5 ( major axis between 100.5 A , for p = 1.0 , and 162.5 A , for p = 2.5 ) .
	manualset3
90840	9	399106	13	NULL	NULL	0	NULL	between p = 1.0 and 2.5 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrodynamic calculations lead to the conclusion that chymotryptic ( or ethylenediaminetetraacetic acid ) myosin S1 in solution ( hydrated ) , at 1-5 degrees C , can be modeled as a prolate ellipsoid , with an axial ratio lying between p = 1.0 and 2.5 ( major axis between 100.5 A , for p = 1.0 , and 162.5 A , for p = 2.5 ) .
	manualset3
90841	10	399106	13	NULL	NULL	NULL	NULL	major axis	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hydrodynamic calculations lead to the conclusion that chymotryptic ( or ethylenediaminetetraacetic acid ) myosin S1 in solution ( hydrated ) , at 1-5 degrees C , can be modeled as a prolate ellipsoid , with an axial ratio lying between p = 1.0 and 2.5 ( major axis between 100.5 A , for p = 1.0 , and 162.5 A , for p = 2.5 ) .
	manualset3
90842	11	399106	13	NULL	NULL	0	NULL	100.5 A , for p = 1.0	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrodynamic calculations lead to the conclusion that chymotryptic ( or ethylenediaminetetraacetic acid ) myosin S1 in solution ( hydrated ) , at 1-5 degrees C , can be modeled as a prolate ellipsoid , with an axial ratio lying between p = 1.0 and 2.5 ( major axis between 100.5 A , for p = 1.0 , and 162.5 A , for p = 2.5 ) .
	manualset3
90843	12	399106	13	NULL	NULL	0	NULL	162.5 A , for p = 2.5	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrodynamic calculations lead to the conclusion that chymotryptic ( or ethylenediaminetetraacetic acid ) myosin S1 in solution ( hydrated ) , at 1-5 degrees C , can be modeled as a prolate ellipsoid , with an axial ratio lying between p = 1.0 and 2.5 ( major axis between 100.5 A , for p = 1.0 , and 162.5 A , for p = 2.5 ) .
	manualset3
90844	1	399107	13	NULL	NULL	0	NULL	Hydrogels 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogels have been synthesized starting from water solutions of carboxymethylcellulose sodium salt and hydroxyethylcellulose , chemically crosslinked with divinylsulphone .
	manualset3
90845	2	399107	13	NULL	NULL	0	NULL	water solutions	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogels have been synthesized starting from water solutions of carboxymethylcellulose sodium salt and hydroxyethylcellulose , chemically crosslinked with divinylsulphone .
	manualset3
90846	3	399107	13	NULL	NULL	0	NULL	carboxymethylcellulose sodium salt	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogels have been synthesized starting from water solutions of carboxymethylcellulose sodium salt and hydroxyethylcellulose , chemically crosslinked with divinylsulphone .
	manualset3
90847	4	399107	13	NULL	NULL	0	NULL	hydroxyethylcellulose	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogels have been synthesized starting from water solutions of carboxymethylcellulose sodium salt and hydroxyethylcellulose , chemically crosslinked with divinylsulphone .
	manualset3
90848	5	399107	13	NULL	NULL	0	NULL	divinylsulphone	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogels have been synthesized starting from water solutions of carboxymethylcellulose sodium salt and hydroxyethylcellulose , chemically crosslinked with divinylsulphone .
	manualset3
90849	1	399108	13	NULL	NULL	0	NULL	Hydrogen-deuterium exchange experiments	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen-deuterium exchange experiments were performed to map with higher resolution the conformational changes induced by metal binding .
	manualset3
90851	3	399108	13	NULL	NULL	NULL	NULL	higher resolution	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hydrogen-deuterium exchange experiments were performed to map with higher resolution the conformational changes induced by metal binding .
	manualset3
90852	4	399108	13	NULL	NULL	0	NULL	conformational changes	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen-deuterium exchange experiments were performed to map with higher resolution the conformational changes induced by metal binding .
	manualset3
90853	5	399108	13	NULL	NULL	0	NULL	metal binding	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen-deuterium exchange experiments were performed to map with higher resolution the conformational changes induced by metal binding .
	manualset3
90854	1	399109	13	NULL	NULL	0	NULL	Hydrogen-isotopic compositions 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen-isotopic compositions of carbonate and maskelynite in Allan Hills ( ALH ) 84001 were measured by secondary ion mass spectrometry ( SIMS ) .
	manualset3
90855	2	399109	13	NULL	NULL	0	NULL	carbonate	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen-isotopic compositions of carbonate and maskelynite in Allan Hills ( ALH ) 84001 were measured by secondary ion mass spectrometry ( SIMS ) .
	manualset3
90856	3	399109	13	NULL	NULL	0	NULL	maskelynite	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen-isotopic compositions of carbonate and maskelynite in Allan Hills ( ALH ) 84001 were measured by secondary ion mass spectrometry ( SIMS ) .
	manualset3
90857	4	399109	13	NULL	NULL	0	NULL	Allan Hills ( ALH ) 84001	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen-isotopic compositions of carbonate and maskelynite in Allan Hills ( ALH ) 84001 were measured by secondary ion mass spectrometry ( SIMS ) .
	manualset3
90858	5	399109	13	NULL	NULL	0	NULL	secondary ion mass spectrometry ( SIMS )	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen-isotopic compositions of carbonate and maskelynite in Allan Hills ( ALH ) 84001 were measured by secondary ion mass spectrometry ( SIMS ) .
	manualset3
90859	1	399110	13	NULL	NULL	0	NULL	reaction	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The reaction of the circulation following intravenous application of bradykinin in man ) .
	manualset3
90860	2	399110	13	NULL	NULL	0	NULL	circulation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The reaction of the circulation following intravenous application of bradykinin in man ) .
	manualset3
90861	3	399110	13	NULL	NULL	0	NULL	intravenous application	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The reaction of the circulation following intravenous application of bradykinin in man ) .
	manualset3
90862	4	399110	13	NULL	NULL	0	NULL	bradykinin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	( The reaction of the circulation following intravenous application of bradykinin in man ) .
	manualset3
90863	5	399110	13	NULL	NULL	NULL	NULL	man	Person												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The reaction of the circulation following intravenous application of bradykinin in man ) .
	manualset3
90864	1	399111	13	NULL	NULL	0	NULL	Hydrogen bonding	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen bonding in water clusters and their ionized counterparts .
	manualset3
90865	2	399111	13	NULL	NULL	0	NULL	water clusters	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen bonding in water clusters and their ionized counterparts .
	manualset3
90866	3	399111	13	NULL	NULL	0	NULL	ionized counterparts	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen bonding in water clusters and their ionized counterparts .
	manualset3
90867	1	399112	13	NULL	NULL	0	NULL	Hydrogen bonds	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen bonds between water molecules and carboxylate O atoms link neighbouring ( 4 , 4 ) networks , yielding a three-dimensional alpha-polonium net .
	manualset3
90868	2	399112	13	NULL	NULL	0	NULL	water molecules 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen bonds between water molecules and carboxylate O atoms link neighbouring ( 4 , 4 ) networks , yielding a three-dimensional alpha-polonium net .
	manualset3
90869	3	399112	13	NULL	NULL	0	NULL	carboxylate O atoms	Atom												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen bonds between water molecules and carboxylate O atoms link neighbouring ( 4 , 4 ) networks , yielding a three-dimensional alpha-polonium net .
	manualset3
90872	6	399112	13	NULL	NULL	0	NULL	three-dimensional alpha-polonium net	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen bonds between water molecules and carboxylate O atoms link neighbouring ( 4 , 4 ) networks , yielding a three-dimensional alpha-polonium net .
	manualset3
92370	4	399112	13	NULL	NULL	0	NULL	neighbouring ( 4 , 4 ) networks	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen bonds between water molecules and carboxylate O atoms link neighbouring ( 4 , 4 ) networks , yielding a three-dimensional alpha-polonium net .
	manualset3
90871	1	399113	13	NULL	NULL	NULL	NULL	Hydrogen peroxide	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hydrogen peroxide stimulated bone resorption in a concentration-dependent manner in calvarial organ cultures with a maximal effect at 1 mumol/L ( 45Ca release ; treated/control = 1.6 + / - 0.07 ; p & lt ; 0.001 from control ) .
	manualset3
90873	2	399113	13	NULL	NULL	0	NULL	bone resorption	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen peroxide stimulated bone resorption in a concentration-dependent manner in calvarial organ cultures with a maximal effect at 1 mumol/L ( 45Ca release ; treated/control = 1.6 + / - 0.07 ; p & lt ; 0.001 from control ) .
	manualset3
90874	3	399113	13	NULL	NULL	0	NULL	concentration-dependent manner	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen peroxide stimulated bone resorption in a concentration-dependent manner in calvarial organ cultures with a maximal effect at 1 mumol/L ( 45Ca release ; treated/control = 1.6 + / - 0.07 ; p & lt ; 0.001 from control ) .
	manualset3
90875	4	399113	13	NULL	NULL	0	NULL	calvarial organ cultures	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen peroxide stimulated bone resorption in a concentration-dependent manner in calvarial organ cultures with a maximal effect at 1 mumol/L ( 45Ca release ; treated/control = 1.6 + / - 0.07 ; p & lt ; 0.001 from control ) .
	manualset3
90876	5	399113	13	NULL	NULL	0	NULL	effect at 1 mumol/L	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen peroxide stimulated bone resorption in a concentration-dependent manner in calvarial organ cultures with a maximal effect at 1 mumol/L ( 45Ca release ; treated/control = 1.6 + / - 0.07 ; p & lt ; 0.001 from control ) .
	manualset3
90877	6	399113	13	NULL	NULL	0	NULL	45Ca release	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen peroxide stimulated bone resorption in a concentration-dependent manner in calvarial organ cultures with a maximal effect at 1 mumol/L ( 45Ca release ; treated/control = 1.6 + / - 0.07 ; p & lt ; 0.001 from control ) .
	manualset3
90878	7	399113	13	NULL	NULL	0	NULL	treated/control = 1.6 + / - 0.07 ; p & lt ; 0.001 from control	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen peroxide stimulated bone resorption in a concentration-dependent manner in calvarial organ cultures with a maximal effect at 1 mumol/L ( 45Ca release ; treated/control = 1.6 + / - 0.07 ; p & lt ; 0.001 from control ) .
	manualset3
90879	1	399114	13	NULL	NULL	0	NULL	Hydrogen sulfide	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen sulfide : its production and functions .
	manualset3
90880	2	399114	13	NULL	NULL	0	NULL	production 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen sulfide : its production and functions .
	manualset3
90881	3	399114	13	NULL	NULL	0	NULL	functions	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen sulfide : its production and functions .
	manualset3
90882	1	399115	13	NULL	NULL	NULL	NULL	Hydrogen transfer reaction	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hydrogen transfer reaction on the surface of an oxide catalyst .
	manualset3
90883	2	399115	13	NULL	NULL	0	NULL	surface of an oxide catalyst	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrogen transfer reaction on the surface of an oxide catalyst .
	manualset3
90884	1	399116	13	NULL	NULL	NULL	NULL	Hydrolysis	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hydrolysis of trehalose in yeast depends on neutral trehalase and acid trehalase ( Ath1 ) .
	manualset3
90885	2	399116	13	NULL	NULL	NULL	NULL	trehalose	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hydrolysis of trehalose in yeast depends on neutral trehalase and acid trehalase ( Ath1 ) .
	manualset3
90886	3	399116	13	NULL	NULL	0	NULL	yeast	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrolysis of trehalose in yeast depends on neutral trehalase and acid trehalase ( Ath1 ) .
	manualset3
90887	4	399116	13	NULL	NULL	NULL	NULL	neutral trehalase	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hydrolysis of trehalose in yeast depends on neutral trehalase and acid trehalase ( Ath1 ) .
	manualset3
90888	5	399116	13	NULL	NULL	NULL	NULL	acid trehalase ( Ath1 )	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hydrolysis of trehalose in yeast depends on neutral trehalase and acid trehalase ( Ath1 ) .
	manualset3
90889	1	399117	13	NULL	NULL	0	NULL	Hydrolytic kinetics	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrolytic kinetics of lithospermic acid B extracted from roots of Salvia miltiorrhiza .
	manualset3
90890	2	399117	13	NULL	NULL	0	NULL	lithospermic acid B	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrolytic kinetics of lithospermic acid B extracted from roots of Salvia miltiorrhiza .
	manualset3
90891	3	399117	13	NULL	NULL	0	NULL	 roots	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrolytic kinetics of lithospermic acid B extracted from roots of Salvia miltiorrhiza .
	manualset3
90892	4	399117	13	NULL	NULL	0	NULL	Salvia miltiorrhiza	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrolytic kinetics of lithospermic acid B extracted from roots of Salvia miltiorrhiza .
	manualset3
90893	1	399118	13	NULL	NULL	0	NULL	Hydrotalcite-like catalysts	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrotalcite-like catalysts were synthesized by coprecipitation and modified co-precipitation by the impregnation method and those were promoted by the addition of noble metals .
	manualset3
90894	2	399118	13	NULL	NULL	0	NULL	coprecipitation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrotalcite-like catalysts were synthesized by coprecipitation and modified co-precipitation by the impregnation method and those were promoted by the addition of noble metals .
	manualset3
90895	3	399118	13	NULL	NULL	0	NULL	co-precipitation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrotalcite-like catalysts were synthesized by coprecipitation and modified co-precipitation by the impregnation method and those were promoted by the addition of noble metals .
	manualset3
90896	4	399118	13	NULL	NULL	0	NULL	 impregnation method	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrotalcite-like catalysts were synthesized by coprecipitation and modified co-precipitation by the impregnation method and those were promoted by the addition of noble metals .
	manualset3
90897	5	399118	13	NULL	NULL	0	NULL	addition	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydrotalcite-like catalysts were synthesized by coprecipitation and modified co-precipitation by the impregnation method and those were promoted by the addition of noble metals .
	manualset3
90898	6	399118	13	NULL	NULL	NULL	NULL	noble metals 	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hydrotalcite-like catalysts were synthesized by coprecipitation and modified co-precipitation by the impregnation method and those were promoted by the addition of noble metals .
	manualset3
90899	1	399119	13	NULL	NULL	0	NULL	Hydroxy-naphthoquinones	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydroxy-naphthoquinones are competitive inhibitors of the cytochrome bc ( 1 ) complex that bind to the ubiquinol oxidation site between cytochrome b and the iron-sulfur protein and presumably mimic a transition state in the ubiquinol oxidation reaction catalyzed by the enzyme .
	manualset3
90900	2	399119	13	NULL	NULL	NULL	NULL	competitive inhibitors	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hydroxy-naphthoquinones are competitive inhibitors of the cytochrome bc ( 1 ) complex that bind to the ubiquinol oxidation site between cytochrome b and the iron-sulfur protein and presumably mimic a transition state in the ubiquinol oxidation reaction catalyzed by the enzyme .
	manualset3
90901	3	399119	13	NULL	NULL	0	NULL	cytochrome bc ( 1 ) complex	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydroxy-naphthoquinones are competitive inhibitors of the cytochrome bc ( 1 ) complex that bind to the ubiquinol oxidation site between cytochrome b and the iron-sulfur protein and presumably mimic a transition state in the ubiquinol oxidation reaction catalyzed by the enzyme .
	manualset3
90902	4	399119	13	NULL	NULL	0	NULL	bind	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydroxy-naphthoquinones are competitive inhibitors of the cytochrome bc ( 1 ) complex that bind to the ubiquinol oxidation site between cytochrome b and the iron-sulfur protein and presumably mimic a transition state in the ubiquinol oxidation reaction catalyzed by the enzyme .
	manualset3
90903	5	399119	13	NULL	NULL	0	NULL	 ubiquinol oxidation site	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydroxy-naphthoquinones are competitive inhibitors of the cytochrome bc ( 1 ) complex that bind to the ubiquinol oxidation site between cytochrome b and the iron-sulfur protein and presumably mimic a transition state in the ubiquinol oxidation reaction catalyzed by the enzyme .
	manualset3
90904	6	399119	13	NULL	NULL	0	NULL	cytochrome b	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydroxy-naphthoquinones are competitive inhibitors of the cytochrome bc ( 1 ) complex that bind to the ubiquinol oxidation site between cytochrome b and the iron-sulfur protein and presumably mimic a transition state in the ubiquinol oxidation reaction catalyzed by the enzyme .
	manualset3
90905	7	399119	13	NULL	NULL	0	NULL	iron-sulfur protein 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydroxy-naphthoquinones are competitive inhibitors of the cytochrome bc ( 1 ) complex that bind to the ubiquinol oxidation site between cytochrome b and the iron-sulfur protein and presumably mimic a transition state in the ubiquinol oxidation reaction catalyzed by the enzyme .
	manualset3
90906	8	399119	13	NULL	NULL	0	NULL	transition state	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydroxy-naphthoquinones are competitive inhibitors of the cytochrome bc ( 1 ) complex that bind to the ubiquinol oxidation site between cytochrome b and the iron-sulfur protein and presumably mimic a transition state in the ubiquinol oxidation reaction catalyzed by the enzyme .
	manualset3
90907	9	399119	13	NULL	NULL	0	NULL	ubiquinol oxidation reaction	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydroxy-naphthoquinones are competitive inhibitors of the cytochrome bc ( 1 ) complex that bind to the ubiquinol oxidation site between cytochrome b and the iron-sulfur protein and presumably mimic a transition state in the ubiquinol oxidation reaction catalyzed by the enzyme .
	manualset3
90908	10	399119	13	NULL	NULL	0	NULL	 enzyme	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydroxy-naphthoquinones are competitive inhibitors of the cytochrome bc ( 1 ) complex that bind to the ubiquinol oxidation site between cytochrome b and the iron-sulfur protein and presumably mimic a transition state in the ubiquinol oxidation reaction catalyzed by the enzyme .
	manualset3
90909	1	399120	13	NULL	NULL	0	NULL	Hydroxyl derivative 7b	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydroxyl derivative 7b showed the highest reactivity toward thiols and showed the strongest cytotoxicity in Hela S3 cells among the three derivatives having a different protecting group at the tert-hydroxyl group .
	manualset3
90910	2	399120	13	NULL	NULL	0	NULL	reactivity	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydroxyl derivative 7b showed the highest reactivity toward thiols and showed the strongest cytotoxicity in Hela S3 cells among the three derivatives having a different protecting group at the tert-hydroxyl group .
	manualset3
90911	3	399120	13	NULL	NULL	0	NULL	thiols 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydroxyl derivative 7b showed the highest reactivity toward thiols and showed the strongest cytotoxicity in Hela S3 cells among the three derivatives having a different protecting group at the tert-hydroxyl group .
	manualset3
90912	4	399120	13	NULL	NULL	0	NULL	cytotoxicity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydroxyl derivative 7b showed the highest reactivity toward thiols and showed the strongest cytotoxicity in Hela S3 cells among the three derivatives having a different protecting group at the tert-hydroxyl group .
	manualset3
90913	5	399120	13	NULL	NULL	0	NULL	Hela S3 cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydroxyl derivative 7b showed the highest reactivity toward thiols and showed the strongest cytotoxicity in Hela S3 cells among the three derivatives having a different protecting group at the tert-hydroxyl group .
	manualset3
90914	6	399120	13	NULL	NULL	0	NULL	three	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydroxyl derivative 7b showed the highest reactivity toward thiols and showed the strongest cytotoxicity in Hela S3 cells among the three derivatives having a different protecting group at the tert-hydroxyl group .
	manualset3
90915	7	399120	13	NULL	NULL	0	NULL	derivatives 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydroxyl derivative 7b showed the highest reactivity toward thiols and showed the strongest cytotoxicity in Hela S3 cells among the three derivatives having a different protecting group at the tert-hydroxyl group .
	manualset3
90916	8	399120	13	NULL	NULL	NULL	NULL	protecting group 	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hydroxyl derivative 7b showed the highest reactivity toward thiols and showed the strongest cytotoxicity in Hela S3 cells among the three derivatives having a different protecting group at the tert-hydroxyl group .
	manualset3
90917	9	399120	13	NULL	NULL	0	NULL	tert-hydroxyl group 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hydroxyl derivative 7b showed the highest reactivity toward thiols and showed the strongest cytotoxicity in Hela S3 cells among the three derivatives having a different protecting group at the tert-hydroxyl group .
	manualset3
90918	1	399121	13	NULL	NULL	NULL	NULL	Hyper-Raman scattering	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hyper-Raman scattering enhanced by anisotropic dimer plasmons on artificial nanostructures .
	manualset3
90920	3	399121	13	NULL	NULL	NULL	NULL	artificial nanostructures 	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hyper-Raman scattering enhanced by anisotropic dimer plasmons on artificial nanostructures .
	manualset3
91078	4	399121	13	NULL	NULL	0	NULL	 anisotropic dimer plasmons	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyper-Raman scattering enhanced by anisotropic dimer plasmons on artificial nanostructures .
	manualset3
90919	1	399122	13	NULL	NULL	NULL	NULL	Hyperandrogenemia	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hyperandrogenemia and hyperinsulinemia are conditions whose significance in terms of increasing both endometrial and breast cancer risks is increasingly recognized .
	manualset3
90921	2	399122	13	NULL	NULL	0	NULL	hyperinsulinemia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperandrogenemia and hyperinsulinemia are conditions whose significance in terms of increasing both endometrial and breast cancer risks is increasingly recognized .
	manualset3
90922	3	399122	13	NULL	NULL	0	NULL	conditions 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperandrogenemia and hyperinsulinemia are conditions whose significance in terms of increasing both endometrial and breast cancer risks is increasingly recognized .
	manualset3
90923	4	399122	13	NULL	NULL	0	NULL	significance	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperandrogenemia and hyperinsulinemia are conditions whose significance in terms of increasing both endometrial and breast cancer risks is increasingly recognized .
	manualset3
90924	5	399122	13	NULL	NULL	0	NULL	endometrial cancer risks	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperandrogenemia and hyperinsulinemia are conditions whose significance in terms of increasing both endometrial and breast cancer risks is increasingly recognized .
	manualset3
90925	6	399122	13	NULL	NULL	0	NULL	breast cancer risks	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperandrogenemia and hyperinsulinemia are conditions whose significance in terms of increasing both endometrial and breast cancer risks is increasingly recognized .
	manualset3
90926	1	399123	13	NULL	NULL	0	NULL	Hypercalcemia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypercalcemia , on the other hand , can be associated with increased extraosseous calcium and phosphate deposition leading to vascular calcification with an attendant mortality and morbidity .
	manualset3
90927	2	399123	13	NULL	NULL	NULL	NULL	extraosseous calcium	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hypercalcemia , on the other hand , can be associated with increased extraosseous calcium and phosphate deposition leading to vascular calcification with an attendant mortality and morbidity .
	manualset3
90928	3	399123	13	NULL	NULL	NULL	NULL	phosphate deposition	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hypercalcemia , on the other hand , can be associated with increased extraosseous calcium and phosphate deposition leading to vascular calcification with an attendant mortality and morbidity .
	manualset3
90929	4	399123	13	NULL	NULL	0	NULL	vascular calcification	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypercalcemia , on the other hand , can be associated with increased extraosseous calcium and phosphate deposition leading to vascular calcification with an attendant mortality and morbidity .
	manualset3
90930	5	399123	13	NULL	NULL	0	NULL	attendant	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypercalcemia , on the other hand , can be associated with increased extraosseous calcium and phosphate deposition leading to vascular calcification with an attendant mortality and morbidity .
	manualset3
90931	6	399123	13	NULL	NULL	0	NULL	mortality	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypercalcemia , on the other hand , can be associated with increased extraosseous calcium and phosphate deposition leading to vascular calcification with an attendant mortality and morbidity .
	manualset3
90932	7	399123	13	NULL	NULL	0	NULL	morbidity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypercalcemia , on the other hand , can be associated with increased extraosseous calcium and phosphate deposition leading to vascular calcification with an attendant mortality and morbidity .
	manualset3
90933	1	399124	13	NULL	NULL	0	NULL	Hyperfractionated radiotherapy 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperfractionated radiotherapy followed by adjuvant chemotherapy for nasopharyngeal cancer : report of seven cases .
	manualset3
90934	2	399124	13	NULL	NULL	0	NULL	adjuvant chemotherapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperfractionated radiotherapy followed by adjuvant chemotherapy for nasopharyngeal cancer : report of seven cases .
	manualset3
90935	3	399124	13	NULL	NULL	0	NULL	nasopharyngeal cancer	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperfractionated radiotherapy followed by adjuvant chemotherapy for nasopharyngeal cancer : report of seven cases .
	manualset3
90936	4	399124	13	NULL	NULL	0	NULL	report	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperfractionated radiotherapy followed by adjuvant chemotherapy for nasopharyngeal cancer : report of seven cases .
	manualset3
90937	5	399124	13	NULL	NULL	0	NULL	seven	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperfractionated radiotherapy followed by adjuvant chemotherapy for nasopharyngeal cancer : report of seven cases .
	manualset3
90938	6	399124	13	NULL	NULL	0	NULL	cases	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperfractionated radiotherapy followed by adjuvant chemotherapy for nasopharyngeal cancer : report of seven cases .
	manualset3
90939	1	399125	13	NULL	NULL	0	NULL	Hyperglycemia 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperglycemia promotes the intracellular generation of superoxide anion and hydrogen peroxide , both of which have been linked to the activation of the mitochondrial apoptosis program .
	manualset3
90940	2	399125	13	NULL	NULL	0	NULL	intracellular generation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperglycemia promotes the intracellular generation of superoxide anion and hydrogen peroxide , both of which have been linked to the activation of the mitochondrial apoptosis program .
	manualset3
90941	3	399125	13	NULL	NULL	0	NULL	superoxide anion	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperglycemia promotes the intracellular generation of superoxide anion and hydrogen peroxide , both of which have been linked to the activation of the mitochondrial apoptosis program .
	manualset3
90942	4	399125	13	NULL	NULL	0	NULL	 hydrogen peroxide	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperglycemia promotes the intracellular generation of superoxide anion and hydrogen peroxide , both of which have been linked to the activation of the mitochondrial apoptosis program .
	manualset3
90944	6	399125	13	NULL	NULL	0	NULL	mitochondrial apoptosis program	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperglycemia promotes the intracellular generation of superoxide anion and hydrogen peroxide , both of which have been linked to the activation of the mitochondrial apoptosis program .
	manualset3
91079	7	399125	13	NULL	NULL	0	NULL	 activation 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperglycemia promotes the intracellular generation of superoxide anion and hydrogen peroxide , both of which have been linked to the activation of the mitochondrial apoptosis program .
	manualset3
90943	1	399126	13	NULL	NULL	NULL	NULL	Hyperleptinemia	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hyperleptinemia was associated with insulin resistance ( r = -0.57 ; P & lt ; 0.0001 ) and high waist to hip ratio ( r = 0.75 ; P & lt ; 0.0001 ) only in men .
	manualset3
90945	2	399126	13	NULL	NULL	0	NULL	insulin resistance	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperleptinemia was associated with insulin resistance ( r = -0.57 ; P & lt ; 0.0001 ) and high waist to hip ratio ( r = 0.75 ; P & lt ; 0.0001 ) only in men .
	manualset3
90946	3	399126	13	NULL	NULL	0	NULL	 r = -0.57 ; P & lt ; 0.0001	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperleptinemia was associated with insulin resistance ( r = -0.57 ; P & lt ; 0.0001 ) and high waist to hip ratio ( r = 0.75 ; P & lt ; 0.0001 ) only in men .
	manualset3
90947	4	399126	13	NULL	NULL	NULL	NULL	high waist to hip ratio ( r = 0.75 ; P & lt ; 0.0001 )	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hyperleptinemia was associated with insulin resistance ( r = -0.57 ; P & lt ; 0.0001 ) and high waist to hip ratio ( r = 0.75 ; P & lt ; 0.0001 ) only in men .
	manualset3
90948	5	399126	13	NULL	NULL	0	NULL	men	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperleptinemia was associated with insulin resistance ( r = -0.57 ; P & lt ; 0.0001 ) and high waist to hip ratio ( r = 0.75 ; P & lt ; 0.0001 ) only in men .
	manualset3
90949	1	399127	13	NULL	NULL	0	NULL	Hyperosmolar non-ketotic diabetic coma	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperosmolar non-ketotic diabetic coma following leptospirosis -- a case report .
	manualset3
90950	2	399127	13	NULL	NULL	0	NULL	leptospirosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperosmolar non-ketotic diabetic coma following leptospirosis -- a case report .
	manualset3
90951	3	399127	13	NULL	NULL	0	NULL	a case report 	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperosmolar non-ketotic diabetic coma following leptospirosis -- a case report .
	manualset3
90952	1	399128	13	NULL	NULL	0	NULL	regulation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The regulation of serum albumin in physiological and pathological conditions ( author 's transl ) ) .
	manualset3
90953	2	399128	13	NULL	NULL	0	NULL	serum albumin 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	( The regulation of serum albumin in physiological and pathological conditions ( author 's transl ) ) .
	manualset3
90954	3	399128	13	NULL	NULL	0	NULL	 physiological conditions	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The regulation of serum albumin in physiological and pathological conditions ( author 's transl ) ) .
	manualset3
90955	4	399128	13	NULL	NULL	0	NULL	pathological conditions	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The regulation of serum albumin in physiological and pathological conditions ( author 's transl ) ) .
	manualset3
90956	5	399128	13	NULL	NULL	0	NULL	author 's	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( The regulation of serum albumin in physiological and pathological conditions ( author 's transl ) ) .
	manualset3
90957	1	399129	13	NULL	NULL	0	NULL	Hyperphosphorylation 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperphosphorylation was dependent on L-voltage dependent Ca ( 2 + ) channels ( L-VDCC ) , N-methyl-d-aspartate ( NMDA ) and metabotropic glutamate receptors , as demonstrated by the specific inhibitors verapamil , DL-AP5 and MCPG , respectively .
	manualset3
90958	2	399129	13	NULL	NULL	0	NULL	L-voltage dependent Ca ( 2 + ) channels ( L-VDCC )	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperphosphorylation was dependent on L-voltage dependent Ca ( 2 + ) channels ( L-VDCC ) , N-methyl-d-aspartate ( NMDA ) and metabotropic glutamate receptors , as demonstrated by the specific inhibitors verapamil , DL-AP5 and MCPG , respectively .
	manualset3
90959	3	399129	13	NULL	NULL	0	NULL	N-methyl-d-aspartate ( NMDA )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperphosphorylation was dependent on L-voltage dependent Ca ( 2 + ) channels ( L-VDCC ) , N-methyl-d-aspartate ( NMDA ) and metabotropic glutamate receptors , as demonstrated by the specific inhibitors verapamil , DL-AP5 and MCPG , respectively .
	manualset3
90960	4	399129	13	NULL	NULL	NULL	NULL	metabotropic glutamate receptors	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hyperphosphorylation was dependent on L-voltage dependent Ca ( 2 + ) channels ( L-VDCC ) , N-methyl-d-aspartate ( NMDA ) and metabotropic glutamate receptors , as demonstrated by the specific inhibitors verapamil , DL-AP5 and MCPG , respectively .
	manualset3
90961	5	399129	13	NULL	NULL	0	NULL	inhibitors	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperphosphorylation was dependent on L-voltage dependent Ca ( 2 + ) channels ( L-VDCC ) , N-methyl-d-aspartate ( NMDA ) and metabotropic glutamate receptors , as demonstrated by the specific inhibitors verapamil , DL-AP5 and MCPG , respectively .
	manualset3
90962	6	399129	13	NULL	NULL	0	NULL	verapamil	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperphosphorylation was dependent on L-voltage dependent Ca ( 2 + ) channels ( L-VDCC ) , N-methyl-d-aspartate ( NMDA ) and metabotropic glutamate receptors , as demonstrated by the specific inhibitors verapamil , DL-AP5 and MCPG , respectively .
	manualset3
90963	7	399129	13	NULL	NULL	0	NULL	DL-AP5	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperphosphorylation was dependent on L-voltage dependent Ca ( 2 + ) channels ( L-VDCC ) , N-methyl-d-aspartate ( NMDA ) and metabotropic glutamate receptors , as demonstrated by the specific inhibitors verapamil , DL-AP5 and MCPG , respectively .
	manualset3
91080	8	399129	13	NULL	NULL	0	NULL	MCPG	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperphosphorylation was dependent on L-voltage dependent Ca ( 2 + ) channels ( L-VDCC ) , N-methyl-d-aspartate ( NMDA ) and metabotropic glutamate receptors , as demonstrated by the specific inhibitors verapamil , DL-AP5 and MCPG , respectively .
	manualset3
90964	1	399130	13	NULL	NULL	0	NULL	Hyperpolarization	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperpolarization was accompanied by a concomitant decrease in the membrane input resistance ( control = 16.6 + / - 2.8 Momega ; 10 ( -4 ) M 5-HT = 6.4 + / - 1.3 MD ; n = 6 , P & lt ; 0.05 ) and time constant ( control = 60.3 + / - 13.1 ms ; 10 ( -4 ) M 5-HT = 16.0 + / - 4.4 ms , n = 6 , P & lt ; 0.05 ) .
	manualset3
90965	2	399130	13	NULL	NULL	0	NULL	membrane input resistance	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperpolarization was accompanied by a concomitant decrease in the membrane input resistance ( control = 16.6 + / - 2.8 Momega ; 10 ( -4 ) M 5-HT = 6.4 + / - 1.3 MD ; n = 6 , P & lt ; 0.05 ) and time constant ( control = 60.3 + / - 13.1 ms ; 10 ( -4 ) M 5-HT = 16.0 + / - 4.4 ms , n = 6 , P & lt ; 0.05 ) .
	manualset3
90966	3	399130	13	NULL	NULL	0	NULL	control = 16.6 + / - 2.8 Momega ; 10 ( -4 ) M 5-HT = 6.4 + / - 1.3 MD ; n = 6 , P & lt ; 0.05	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperpolarization was accompanied by a concomitant decrease in the membrane input resistance ( control = 16.6 + / - 2.8 Momega ; 10 ( -4 ) M 5-HT = 6.4 + / - 1.3 MD ; n = 6 , P & lt ; 0.05 ) and time constant ( control = 60.3 + / - 13.1 ms ; 10 ( -4 ) M 5-HT = 16.0 + / - 4.4 ms , n = 6 , P & lt ; 0.05 ) .
	manualset3
90967	4	399130	13	NULL	NULL	0	NULL	time constant ( control = 60.3 + / - 13.1 ms ; 10 ( -4 ) M 5-HT = 16.0 + / - 4.4 ms , n = 6 , P & lt ; 0.05 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperpolarization was accompanied by a concomitant decrease in the membrane input resistance ( control = 16.6 + / - 2.8 Momega ; 10 ( -4 ) M 5-HT = 6.4 + / - 1.3 MD ; n = 6 , P & lt ; 0.05 ) and time constant ( control = 60.3 + / - 13.1 ms ; 10 ( -4 ) M 5-HT = 16.0 + / - 4.4 ms , n = 6 , P & lt ; 0.05 ) .
	manualset3
91092	1	399131	13	NULL	NULL	0	NULL	Hypertension-dependent cerebrovascular changes	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypertension-dependent cerebrovascular changes were documented primarily in brain pial arteries , whereas no information is so far available concerning changes of peripheral nerve vascularization in hypertension .
	manualset3
91093	2	399131	13	NULL	NULL	0	NULL	brain pial arteries	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypertension-dependent cerebrovascular changes were documented primarily in brain pial arteries , whereas no information is so far available concerning changes of peripheral nerve vascularization in hypertension .
	manualset3
91094	3	399131	13	NULL	NULL	0	NULL	information	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypertension-dependent cerebrovascular changes were documented primarily in brain pial arteries , whereas no information is so far available concerning changes of peripheral nerve vascularization in hypertension .
	manualset3
91095	4	399131	13	NULL	NULL	0	NULL	changes of peripheral nerve vascularization	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypertension-dependent cerebrovascular changes were documented primarily in brain pial arteries , whereas no information is so far available concerning changes of peripheral nerve vascularization in hypertension .
	manualset3
91096	5	399131	13	NULL	NULL	0	NULL	hypertension 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypertension-dependent cerebrovascular changes were documented primarily in brain pial arteries , whereas no information is so far available concerning changes of peripheral nerve vascularization in hypertension .
	manualset3
91097	1	399132	13	NULL	NULL	0	NULL	Hypertension	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypertension is very prevalent in chronic kidney disease and critical for its prognosis .
	manualset3
91098	2	399132	13	NULL	NULL	0	NULL	chronic kidney disease 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypertension is very prevalent in chronic kidney disease and critical for its prognosis .
	manualset3
91099	3	399132	13	NULL	NULL	0	NULL	prognosis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypertension is very prevalent in chronic kidney disease and critical for its prognosis .
	manualset3
91100	1	399133	13	NULL	NULL	0	NULL	Hypertension	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypertension remains the most common complication associated with cyclosporine administration in heart transplant recipients .
	manualset3
91101	2	399133	13	NULL	NULL	0	NULL	complication 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypertension remains the most common complication associated with cyclosporine administration in heart transplant recipients .
	manualset3
91102	3	399133	13	NULL	NULL	0	NULL	cyclosporine administration	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypertension remains the most common complication associated with cyclosporine administration in heart transplant recipients .
	manualset3
91103	4	399133	13	NULL	NULL	0	NULL	heart transplant recipients 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypertension remains the most common complication associated with cyclosporine administration in heart transplant recipients .
	manualset3
91104	1	399134	13	NULL	NULL	0	NULL	partial thickness facial burns 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypertrophic scarring after partial thickness facial burns is common when epithelialization takes longer than 3 weeks .
	manualset3
91105	2	399134	13	NULL	NULL	0	NULL	epithelialization	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypertrophic scarring after partial thickness facial burns is common when epithelialization takes longer than 3 weeks .
	manualset3
91106	3	399134	13	NULL	NULL	0	NULL	3 weeks 	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypertrophic scarring after partial thickness facial burns is common when epithelialization takes longer than 3 weeks .
	manualset3
98569	4	399134	13	NULL	NULL	0	NULL	Hypertrophic scarring	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypertrophic scarring after partial thickness facial burns is common when epithelialization takes longer than 3 weeks .
	manualset3
91107	1	399135	13	NULL	NULL	0	NULL	Hyperuricemic nephropathy 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperuricemic nephropathy can progress to the permanent renal damage even in infancy in partial hypoxanthine-guanine phosphoribosyltransferase ( HPRT ) deficiency .
	manualset3
91108	2	399135	13	NULL	NULL	0	NULL	progress 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperuricemic nephropathy can progress to the permanent renal damage even in infancy in partial hypoxanthine-guanine phosphoribosyltransferase ( HPRT ) deficiency .
	manualset3
91109	3	399135	13	NULL	NULL	0	NULL	permanent renal damage 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperuricemic nephropathy can progress to the permanent renal damage even in infancy in partial hypoxanthine-guanine phosphoribosyltransferase ( HPRT ) deficiency .
	manualset3
91110	4	399135	13	NULL	NULL	0	NULL	infancy	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperuricemic nephropathy can progress to the permanent renal damage even in infancy in partial hypoxanthine-guanine phosphoribosyltransferase ( HPRT ) deficiency .
	manualset3
91111	5	399135	13	NULL	NULL	0	NULL	 partial hypoxanthine-guanine phosphoribosyltransferase ( HPRT ) deficiency	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyperuricemic nephropathy can progress to the permanent renal damage even in infancy in partial hypoxanthine-guanine phosphoribosyltransferase ( HPRT ) deficiency .
	manualset3
91112	1	399136	13	NULL	NULL	0	NULL	Hypnosis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypnosis using a communication device to increase magnetic resonance imaging tolerance with a claustrophobic patient .
	manualset3
91113	2	399136	13	NULL	NULL	0	NULL	communication device	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypnosis using a communication device to increase magnetic resonance imaging tolerance with a claustrophobic patient .
	manualset3
91114	3	399136	13	NULL	NULL	0	NULL	magnetic resonance imaging tolerance	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypnosis using a communication device to increase magnetic resonance imaging tolerance with a claustrophobic patient .
	manualset3
91115	4	399136	13	NULL	NULL	0	NULL	claustrophobic patient	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypnosis using a communication device to increase magnetic resonance imaging tolerance with a claustrophobic patient .
	manualset3
91116	1	399137	13	NULL	NULL	0	NULL	relationship	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	( The relationship between occupational stress and serum glycosylated hemoglobin A1c level ) .
	manualset3
91117	2	399137	13	NULL	NULL	0	NULL	occupational stress	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	( The relationship between occupational stress and serum glycosylated hemoglobin A1c level ) .
	manualset3
91118	3	399137	13	NULL	NULL	0	NULL	serum glycosylated hemoglobin A1c level	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The relationship between occupational stress and serum glycosylated hemoglobin A1c level ) .
	manualset3
91119	1	399138	13	NULL	NULL	0	NULL	Hypobaric-hypoxic exposure	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypobaric-hypoxic exposure and histochemical responses of soleus muscle fibers in the rat .
	manualset3
91120	2	399138	13	NULL	NULL	0	NULL	histochemical responses 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypobaric-hypoxic exposure and histochemical responses of soleus muscle fibers in the rat .
	manualset3
91121	3	399138	13	NULL	NULL	0	NULL	soleus muscle fibers	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypobaric-hypoxic exposure and histochemical responses of soleus muscle fibers in the rat .
	manualset3
91122	4	399138	13	NULL	NULL	0	NULL	rat 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypobaric-hypoxic exposure and histochemical responses of soleus muscle fibers in the rat .
	manualset3
91123	1	399139	13	NULL	NULL	0	NULL	Hypocalcemia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypocalcemia after intravenous bisphosphonate : lesson to be learned .
	manualset3
91124	2	399139	13	NULL	NULL	0	NULL	intravenous bisphosphonate	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypocalcemia after intravenous bisphosphonate : lesson to be learned .
	manualset3
91125	3	399139	13	NULL	NULL	0	NULL	lesson	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypocalcemia after intravenous bisphosphonate : lesson to be learned .
	manualset3
91126	1	399140	13	NULL	NULL	0	NULL	Hypocalcemia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypocalcemia in metastatic bone disease : metabolic and radionuclide studies of a case .
	manualset3
91127	2	399140	13	NULL	NULL	0	NULL	metastatic bone disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypocalcemia in metastatic bone disease : metabolic and radionuclide studies of a case .
	manualset3
91128	3	399140	13	NULL	NULL	0	NULL	 metabolic studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypocalcemia in metastatic bone disease : metabolic and radionuclide studies of a case .
	manualset3
91129	4	399140	13	NULL	NULL	0	NULL	radionuclide studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypocalcemia in metastatic bone disease : metabolic and radionuclide studies of a case .
	manualset3
91130	5	399140	13	NULL	NULL	NULL	NULL	 case	Person												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hypocalcemia in metastatic bone disease : metabolic and radionuclide studies of a case .
	manualset3
91131	1	399141	13	NULL	NULL	0	NULL	Hypochaeris 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypochaeris ( consisting of H. glabra , H. radicata , H. arachnoidea , and H. salzmanniana ) .
	manualset3
91132	2	399141	13	NULL	NULL	0	NULL	H. glabra	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypochaeris ( consisting of H. glabra , H. radicata , H. arachnoidea , and H. salzmanniana ) .
	manualset3
91133	3	399141	13	NULL	NULL	0	NULL	H. radicata	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypochaeris ( consisting of H. glabra , H. radicata , H. arachnoidea , and H. salzmanniana ) .
	manualset3
91134	4	399141	13	NULL	NULL	0	NULL	H. arachnoidea	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypochaeris ( consisting of H. glabra , H. radicata , H. arachnoidea , and H. salzmanniana ) .
	manualset3
91135	5	399141	13	NULL	NULL	0	NULL	H. salzmanniana 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypochaeris ( consisting of H. glabra , H. radicata , H. arachnoidea , and H. salzmanniana ) .
	manualset3
91136	1	399142	13	NULL	NULL	0	NULL	Hypohidrotic ectodermal dysplasia 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypohidrotic ectodermal dysplasia : a genealogic , stereomicroscope , and scanning electron microscope study .
	manualset3
91137	2	399142	13	NULL	NULL	0	NULL	genealogic study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypohidrotic ectodermal dysplasia : a genealogic , stereomicroscope , and scanning electron microscope study .
	manualset3
91138	3	399142	13	NULL	NULL	0	NULL	 stereomicroscope study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypohidrotic ectodermal dysplasia : a genealogic , stereomicroscope , and scanning electron microscope study .
	manualset3
91139	4	399142	13	NULL	NULL	0	NULL	scanning electron microscope study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypohidrotic ectodermal dysplasia : a genealogic , stereomicroscope , and scanning electron microscope study .
	manualset3
91140	1	399143	13	NULL	NULL	0	NULL	Hyporeflexia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyporeflexia in workers chronically exposed to organophosphate insecticides .
	manualset3
91141	2	399143	13	NULL	NULL	0	NULL	workers 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyporeflexia in workers chronically exposed to organophosphate insecticides .
	manualset3
91142	3	399143	13	NULL	NULL	0	NULL	organophosphate insecticides	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Hyporeflexia in workers chronically exposed to organophosphate insecticides .
	manualset3
91143	1	399144	13	NULL	NULL	0	NULL	Hypothalamic ER mRNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothalamic ER mRNA was decreased in response to melatonin in both intact and ovariectomized animals by 25 % .
	manualset3
91144	2	399144	13	NULL	NULL	0	NULL	response to melatonin 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothalamic ER mRNA was decreased in response to melatonin in both intact and ovariectomized animals by 25 % .
	manualset3
91145	3	399144	13	NULL	NULL	0	NULL	intact animals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothalamic ER mRNA was decreased in response to melatonin in both intact and ovariectomized animals by 25 % .
	manualset3
91146	4	399144	13	NULL	NULL	0	NULL	ovariectomized animals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothalamic ER mRNA was decreased in response to melatonin in both intact and ovariectomized animals by 25 % .
	manualset3
91147	5	399144	13	NULL	NULL	0	NULL	25 % 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothalamic ER mRNA was decreased in response to melatonin in both intact and ovariectomized animals by 25 % .
	manualset3
91148	1	399145	13	NULL	NULL	0	NULL	Hypothalamic blood flow	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothalamic blood flow remains unaltered following chronic nitric oxide synthase blockade in rats .
	manualset3
91149	2	399145	13	NULL	NULL	0	NULL	chronic nitric oxide synthase blockade	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothalamic blood flow remains unaltered following chronic nitric oxide synthase blockade in rats .
	manualset3
91150	3	399145	13	NULL	NULL	0	NULL	rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothalamic blood flow remains unaltered following chronic nitric oxide synthase blockade in rats .
	manualset3
91151	1	399146	13	NULL	NULL	0	NULL	Hypothalamic preparations	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothalamic preparations exhibited the greatest insulin binding .
	manualset3
91152	2	399146	13	NULL	NULL	0	NULL	insulin binding 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothalamic preparations exhibited the greatest insulin binding .
	manualset3
91153	1	399147	13	NULL	NULL	0	NULL	nitric oxide	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( The release of nitric oxide from organic nitroso compounds in the body of animals ) .
	manualset3
91154	2	399147	13	NULL	NULL	0	NULL	organic nitroso compounds	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( The release of nitric oxide from organic nitroso compounds in the body of animals ) .
	manualset3
91155	3	399147	13	NULL	NULL	NULL	NULL	body of animals	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The release of nitric oxide from organic nitroso compounds in the body of animals ) .
	manualset3
91156	1	399148	13	NULL	NULL	0	NULL	Hypothermic preservation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothermic preservation effect on mammalian cells of type III antifreeze proteins from notched-fin eelpout .
	manualset3
91157	2	399148	13	NULL	NULL	NULL	NULL	effect	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hypothermic preservation effect on mammalian cells of type III antifreeze proteins from notched-fin eelpout .
	manualset3
91158	3	399148	13	NULL	NULL	0	NULL	 mammalian cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothermic preservation effect on mammalian cells of type III antifreeze proteins from notched-fin eelpout .
	manualset3
91159	4	399148	13	NULL	NULL	0	NULL	type III antifreeze proteins 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothermic preservation effect on mammalian cells of type III antifreeze proteins from notched-fin eelpout .
	manualset3
91160	5	399148	13	NULL	NULL	0	NULL	notched-fin eelpout	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothermic preservation effect on mammalian cells of type III antifreeze proteins from notched-fin eelpout .
	manualset3
91161	1	399149	13	NULL	NULL	0	NULL	Hypotheses	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypotheses were : ( a ) the quality of mother-daughter attachment will mediate the relationship between their social support and drug use and ( b ) the effects of mothers ' and daughters ' chronic stress on their drug use is mediated by their social support which , in turn , is also mediated by the quality of their attachment after taking into account socio-demographic variables .
	manualset3
91163	3	399149	13	NULL	NULL	NULL	NULL	quality of mother-daughter attachment	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hypotheses were : ( a ) the quality of mother-daughter attachment will mediate the relationship between their social support and drug use and ( b ) the effects of mothers ' and daughters ' chronic stress on their drug use is mediated by their social support which , in turn , is also mediated by the quality of their attachment after taking into account socio-demographic variables .
	manualset3
91164	4	399149	13	NULL	NULL	0	NULL	relationship	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypotheses were : ( a ) the quality of mother-daughter attachment will mediate the relationship between their social support and drug use and ( b ) the effects of mothers ' and daughters ' chronic stress on their drug use is mediated by their social support which , in turn , is also mediated by the quality of their attachment after taking into account socio-demographic variables .
	manualset3
91165	5	399149	13	NULL	NULL	NULL	NULL	drug use	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hypotheses were : ( a ) the quality of mother-daughter attachment will mediate the relationship between their social support and drug use and ( b ) the effects of mothers ' and daughters ' chronic stress on their drug use is mediated by their social support which , in turn , is also mediated by the quality of their attachment after taking into account socio-demographic variables .
	manualset3
91166	6	399149	13	NULL	NULL	0	NULL	effects of mothers ' and daughters ' chronic stress 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypotheses were : ( a ) the quality of mother-daughter attachment will mediate the relationship between their social support and drug use and ( b ) the effects of mothers ' and daughters ' chronic stress on their drug use is mediated by their social support which , in turn , is also mediated by the quality of their attachment after taking into account socio-demographic variables .
	manualset3
91167	7	399149	13	NULL	NULL	NULL	NULL	drug use	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hypotheses were : ( a ) the quality of mother-daughter attachment will mediate the relationship between their social support and drug use and ( b ) the effects of mothers ' and daughters ' chronic stress on their drug use is mediated by their social support which , in turn , is also mediated by the quality of their attachment after taking into account socio-demographic variables .
	manualset3
91168	8	399149	13	NULL	NULL	0	NULL	quality of their attachment 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypotheses were : ( a ) the quality of mother-daughter attachment will mediate the relationship between their social support and drug use and ( b ) the effects of mothers ' and daughters ' chronic stress on their drug use is mediated by their social support which , in turn , is also mediated by the quality of their attachment after taking into account socio-demographic variables .
	manualset3
91169	9	399149	13	NULL	NULL	NULL	NULL	socio-demographic variables	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hypotheses were : ( a ) the quality of mother-daughter attachment will mediate the relationship between their social support and drug use and ( b ) the effects of mothers ' and daughters ' chronic stress on their drug use is mediated by their social support which , in turn , is also mediated by the quality of their attachment after taking into account socio-demographic variables .
	manualset3
98570	10	399149	13	NULL	NULL	0	NULL	social support	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypotheses were : ( a ) the quality of mother-daughter attachment will mediate the relationship between their social support and drug use and ( b ) the effects of mothers ' and daughters ' chronic stress on their drug use is mediated by their social support which , in turn , is also mediated by the quality of their attachment after taking into account socio-demographic variables .
	manualset3
91170	1	399150	13	NULL	NULL	0	NULL	Hypothesis 3 	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothesis 3 did not contribute to the explanation of forest age effects on NEP .
	manualset3
91171	2	399150	13	NULL	NULL	0	NULL	explanation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothesis 3 did not contribute to the explanation of forest age effects on NEP .
	manualset3
91172	3	399150	13	NULL	NULL	0	NULL	forest age effects	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothesis 3 did not contribute to the explanation of forest age effects on NEP .
	manualset3
91173	4	399150	13	NULL	NULL	0	NULL	NEP 	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothesis 3 did not contribute to the explanation of forest age effects on NEP .
	manualset3
91174	1	399151	13	NULL	NULL	0	NULL	Hypothyroid larvae	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothyroid larvae were produced by rearing the animals , beginning at stage 48 , in a 0.01 % solution of propylthiouracil ( PTU ) , a treatment that blocks synthesis of thyroid hormone .
	manualset3
91175	2	399151	13	NULL	NULL	0	NULL	animals 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothyroid larvae were produced by rearing the animals , beginning at stage 48 , in a 0.01 % solution of propylthiouracil ( PTU ) , a treatment that blocks synthesis of thyroid hormone .
	manualset3
91176	3	399151	13	NULL	NULL	0	NULL	stage 48	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothyroid larvae were produced by rearing the animals , beginning at stage 48 , in a 0.01 % solution of propylthiouracil ( PTU ) , a treatment that blocks synthesis of thyroid hormone .
	manualset3
91177	4	399151	13	NULL	NULL	0	NULL	0.01 % solution	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothyroid larvae were produced by rearing the animals , beginning at stage 48 , in a 0.01 % solution of propylthiouracil ( PTU ) , a treatment that blocks synthesis of thyroid hormone .
	manualset3
91178	5	399151	13	NULL	NULL	0	NULL	 propylthiouracil ( PTU )	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothyroid larvae were produced by rearing the animals , beginning at stage 48 , in a 0.01 % solution of propylthiouracil ( PTU ) , a treatment that blocks synthesis of thyroid hormone .
	manualset3
91179	6	399151	13	NULL	NULL	0	NULL	treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothyroid larvae were produced by rearing the animals , beginning at stage 48 , in a 0.01 % solution of propylthiouracil ( PTU ) , a treatment that blocks synthesis of thyroid hormone .
	manualset3
91180	7	399151	13	NULL	NULL	NULL	NULL	synthesis of thyroid hormone	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hypothyroid larvae were produced by rearing the animals , beginning at stage 48 , in a 0.01 % solution of propylthiouracil ( PTU ) , a treatment that blocks synthesis of thyroid hormone .
	manualset3
91181	1	399152	13	NULL	NULL	0	NULL	Hypothyroidism	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothyroidism is a typical low rennin HT form showing a better antihypertensive response to CCB and diuretics ; indeed in hypothyroidism a low-sodium diet seems further to improve BP control .
	manualset3
91182	2	399152	13	NULL	NULL	0	NULL	low rennin HT	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothyroidism is a typical low rennin HT form showing a better antihypertensive response to CCB and diuretics ; indeed in hypothyroidism a low-sodium diet seems further to improve BP control .
	manualset3
91183	3	399152	13	NULL	NULL	0	NULL	antihypertensive response	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothyroidism is a typical low rennin HT form showing a better antihypertensive response to CCB and diuretics ; indeed in hypothyroidism a low-sodium diet seems further to improve BP control .
	manualset3
91184	4	399152	13	NULL	NULL	0	NULL	 CCB	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothyroidism is a typical low rennin HT form showing a better antihypertensive response to CCB and diuretics ; indeed in hypothyroidism a low-sodium diet seems further to improve BP control .
	manualset3
91185	5	399152	13	NULL	NULL	0	NULL	diuretics	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothyroidism is a typical low rennin HT form showing a better antihypertensive response to CCB and diuretics ; indeed in hypothyroidism a low-sodium diet seems further to improve BP control .
	manualset3
91186	6	399152	13	NULL	NULL	0	NULL	hypothyroidism	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothyroidism is a typical low rennin HT form showing a better antihypertensive response to CCB and diuretics ; indeed in hypothyroidism a low-sodium diet seems further to improve BP control .
	manualset3
91187	7	399152	13	NULL	NULL	0	NULL	low-sodium diet	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothyroidism is a typical low rennin HT form showing a better antihypertensive response to CCB and diuretics ; indeed in hypothyroidism a low-sodium diet seems further to improve BP control .
	manualset3
91188	8	399152	13	NULL	NULL	0	NULL	BP	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypothyroidism is a typical low rennin HT form showing a better antihypertensive response to CCB and diuretics ; indeed in hypothyroidism a low-sodium diet seems further to improve BP control .
	manualset3
91189	1	399153	13	NULL	NULL	0	NULL	Hypoxia-induced acidosis 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia-induced acidosis uncouples the STIM-Orai calcium signaling complex .
	manualset3
91190	2	399153	13	NULL	NULL	0	NULL	STIM-Orai calcium signaling complex	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia-induced acidosis uncouples the STIM-Orai calcium signaling complex .
	manualset3
91191	1	399154	13	NULL	NULL	0	NULL	Hypoxia-induced expression of C1q	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia-induced expression of C1q , a subcomponent of the complement system , in cultured rat PC12 cells .
	manualset3
91192	2	399154	13	NULL	NULL	0	NULL	a subcomponent of the complement system	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia-induced expression of C1q , a subcomponent of the complement system , in cultured rat PC12 cells .
	manualset3
91193	3	399154	13	NULL	NULL	0	NULL	cultured rat PC12 cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia-induced expression of C1q , a subcomponent of the complement system , in cultured rat PC12 cells .
	manualset3
91194	1	399155	13	NULL	NULL	0	NULL	Hypoxia-induced suppression of automaticity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia-induced suppression of automaticity was reversed completely by 5 mM glucose , and partially by 40 mM valine .
	manualset3
91195	2	399155	13	NULL	NULL	0	NULL	5 mM glucose	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia-induced suppression of automaticity was reversed completely by 5 mM glucose , and partially by 40 mM valine .
	manualset3
91196	3	399155	13	NULL	NULL	0	NULL	40 mM valine	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia-induced suppression of automaticity was reversed completely by 5 mM glucose , and partially by 40 mM valine .
	manualset3
91197	1	399156	13	NULL	NULL	NULL	NULL	Hypoxia inducible factor ( HIF ) 	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hypoxia inducible factor ( HIF ) , the most potent regulator of VEGF , is a heterodimer of a constitutively expressed beta subunit and an oxygen-regulated alpha subunit ( HIF-alpha ) .
	manualset3
91198	2	399156	13	NULL	NULL	NULL	NULL	 regulator of VEGF 	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hypoxia inducible factor ( HIF ) , the most potent regulator of VEGF , is a heterodimer of a constitutively expressed beta subunit and an oxygen-regulated alpha subunit ( HIF-alpha ) .
	manualset3
91199	3	399156	13	NULL	NULL	NULL	NULL	heterodimer	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hypoxia inducible factor ( HIF ) , the most potent regulator of VEGF , is a heterodimer of a constitutively expressed beta subunit and an oxygen-regulated alpha subunit ( HIF-alpha ) .
	manualset3
91200	4	399156	13	NULL	NULL	0	NULL	beta subunit	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia inducible factor ( HIF ) , the most potent regulator of VEGF , is a heterodimer of a constitutively expressed beta subunit and an oxygen-regulated alpha subunit ( HIF-alpha ) .
	manualset3
91201	5	399156	13	NULL	NULL	0	NULL	xygen-regulated alpha subunit ( HIF-alpha )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia inducible factor ( HIF ) , the most potent regulator of VEGF , is a heterodimer of a constitutively expressed beta subunit and an oxygen-regulated alpha subunit ( HIF-alpha ) .
	manualset3
91202	1	399157	13	NULL	NULL	NULL	NULL	Hypoxia	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Hypoxia was determined biochemically by ATP and phosphocreatine ( PCr ) levels .
	manualset3
91203	2	399157	13	NULL	NULL	0	NULL	ATP levels  	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia was determined biochemically by ATP and phosphocreatine ( PCr ) levels .
	manualset3
91204	3	399157	13	NULL	NULL	0	NULL	phosphocreatine ( PCr ) levels	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Hypoxia was determined biochemically by ATP and phosphocreatine ( PCr ) levels .
	manualset3
91205	1	399158	13	NULL	NULL	0	NULL	I-cell disease ( mucolipidosis II ) 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	I-cell disease ( mucolipidosis II ) is a fatal childhood disorder affecting the expression of multiple lysosomal acid hydrolases .
	manualset3
91206	2	399158	13	NULL	NULL	0	NULL	fatal childhood disorder	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	I-cell disease ( mucolipidosis II ) is a fatal childhood disorder affecting the expression of multiple lysosomal acid hydrolases .
	manualset3
91207	3	399158	13	NULL	NULL	0	NULL	expression of multiple lysosomal acid hydrolases	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	I-cell disease ( mucolipidosis II ) is a fatal childhood disorder affecting the expression of multiple lysosomal acid hydrolases .
	manualset3
91208	1	399159	13	NULL	NULL	0	NULL	Antigenic differences	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Antigenic differences between parasite lines detected by crossed immunoelectrophoresis .
	manualset3
91209	2	399159	13	NULL	NULL	0	NULL	parasite lines	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Antigenic differences between parasite lines detected by crossed immunoelectrophoresis .
	manualset3
91210	3	399159	13	NULL	NULL	0	NULL	crossed immunoelectrophoresis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Antigenic differences between parasite lines detected by crossed immunoelectrophoresis .
	manualset3
90393	1	399160	13	NULL	NULL	NULL	NULL	Dependence 	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	I. Dependence on composition of the configurational stability of deoxyribonucleic acids .
	manualset3
91241	2	399160	13	NULL	NULL	0	NULL	composition	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Dependence on composition of the configurational stability of deoxyribonucleic acids .
	manualset3
91242	3	399160	13	NULL	NULL	0	NULL	configurational stability 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Dependence on composition of the configurational stability of deoxyribonucleic acids .
	manualset3
91243	4	399160	13	NULL	NULL	0	NULL	 deoxyribonucleic acids 	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Dependence on composition of the configurational stability of deoxyribonucleic acids .
	manualset3
91244	1	399161	13	NULL	NULL	0	NULL	Differences	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Differences in reactivity with Poly ( U ) and Poly - ( A ) Poly ( U ) .
	manualset3
91245	2	399161	13	NULL	NULL	0	NULL	reactivity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Differences in reactivity with Poly ( U ) and Poly - ( A ) Poly ( U ) .
	manualset3
91246	3	399161	13	NULL	NULL	0	NULL	Poly ( U )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Differences in reactivity with Poly ( U ) and Poly - ( A ) Poly ( U ) .
	manualset3
91247	4	399161	13	NULL	NULL	0	NULL	Poly - ( A ) Poly ( U )	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Differences in reactivity with Poly ( U ) and Poly - ( A ) Poly ( U ) .
	manualset3
91248	1	399162	13	NULL	NULL	0	NULL	role	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The role of B72 .3 125-I monoclonal antibody in the radioimmunoguided surgery of colorectal neoplasms ) .
	manualset3
91249	2	399162	13	NULL	NULL	0	NULL	B72 .3 125-I monoclonal antibody	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	( The role of B72 .3 125-I monoclonal antibody in the radioimmunoguided surgery of colorectal neoplasms ) .
	manualset3
91250	3	399162	13	NULL	NULL	0	NULL	radioimmunoguided surgery 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The role of B72 .3 125-I monoclonal antibody in the radioimmunoguided surgery of colorectal neoplasms ) .
	manualset3
91251	4	399162	13	NULL	NULL	0	NULL	colorectal neoplasms	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( The role of B72 .3 125-I monoclonal antibody in the radioimmunoguided surgery of colorectal neoplasms ) .
	manualset3
91252	1	399163	13	NULL	NULL	0	NULL	Effect	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Effect of 8-methoxypsoralen on the epidermal patch test in allergic contact eczema ) .
	manualset3
91253	2	399163	13	NULL	NULL	0	NULL	8-methoxypsoralen	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Effect of 8-methoxypsoralen on the epidermal patch test in allergic contact eczema ) .
	manualset3
91254	3	399163	13	NULL	NULL	0	NULL	epidermal patch test	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Effect of 8-methoxypsoralen on the epidermal patch test in allergic contact eczema ) .
	manualset3
91255	4	399163	13	NULL	NULL	0	NULL	allergic contact eczema	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Effect of 8-methoxypsoralen on the epidermal patch test in allergic contact eczema ) .
	manualset3
91256	1	399164	13	NULL	NULL	0	NULL	Isolation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Isolation and characterization of the virus .
	manualset3
91257	2	399164	13	NULL	NULL	0	NULL	characterization 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Isolation and characterization of the virus .
	manualset3
91258	3	399164	13	NULL	NULL	0	NULL	virus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Isolation and characterization of the virus .
	manualset3
91259	1	399165	13	NULL	NULL	0	NULL	Observations	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Observations on H 10 Z tumor short term tissue cultures .
	manualset3
91260	2	399165	13	NULL	NULL	0	NULL	H 10 Z tumor short term tissue cultures	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Observations on H 10 Z tumor short term tissue cultures .
	manualset3
91261	1	399166	13	NULL	NULL	NULL	NULL	Regional fibrinolysis	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	I. Regional fibrinolysis ( cerebral , of the upper extremity and of the lower extremity ) caused by `` arterial '' administration of nicotinic acid ) .
	manualset3
91262	2	399166	13	NULL	NULL	0	NULL	 cerebral , of the upper extremity	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Regional fibrinolysis ( cerebral , of the upper extremity and of the lower extremity ) caused by `` arterial '' administration of nicotinic acid ) .
	manualset3
91263	3	399166	13	NULL	NULL	0	NULL	cerebral of the lower extremity	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Regional fibrinolysis ( cerebral , of the upper extremity and of the lower extremity ) caused by `` arterial '' administration of nicotinic acid ) .
	manualset3
91264	4	399166	13	NULL	NULL	NULL	NULL	`` arterial '' administration	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	I. Regional fibrinolysis ( cerebral , of the upper extremity and of the lower extremity ) caused by `` arterial '' administration of nicotinic acid ) .
	manualset3
91265	5	399166	13	NULL	NULL	0	NULL	nicotinic acid 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Regional fibrinolysis ( cerebral , of the upper extremity and of the lower extremity ) caused by `` arterial '' administration of nicotinic acid ) .
	manualset3
91266	1	399167	13	NULL	NULL	0	NULL	Cytological changes	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Cytological changes associated with the exposure of Escherichia coli to colistin sulfate .
	manualset3
91267	2	399167	13	NULL	NULL	0	NULL	exposure	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Cytological changes associated with the exposure of Escherichia coli to colistin sulfate .
	manualset3
91268	3	399167	13	NULL	NULL	0	NULL	Escherichia coli 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Cytological changes associated with the exposure of Escherichia coli to colistin sulfate .
	manualset3
91269	4	399167	13	NULL	NULL	0	NULL	colistin sulfate	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Cytological changes associated with the exposure of Escherichia coli to colistin sulfate .
	manualset3
91270	1	399168	13	NULL	NULL	0	NULL	T-T interactions	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Collaborative T-T interactions in the immunoregulation of B cell differentiation .
	manualset3
91271	2	399168	13	NULL	NULL	0	NULL	 immunoregulation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Collaborative T-T interactions in the immunoregulation of B cell differentiation .
	manualset3
91272	3	399168	13	NULL	NULL	0	NULL	B cell differentiation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Collaborative T-T interactions in the immunoregulation of B cell differentiation .
	manualset3
91273	1	399169	13	NULL	NULL	0	NULL	 role 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The role of D2 lymphadenectomy in the surgical treatment of gastric carcinoma ) .
	manualset3
91274	2	399169	13	NULL	NULL	0	NULL	D2 lymphadenectomy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The role of D2 lymphadenectomy in the surgical treatment of gastric carcinoma ) .
	manualset3
91275	3	399169	13	NULL	NULL	0	NULL	surgical treatment 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The role of D2 lymphadenectomy in the surgical treatment of gastric carcinoma ) .
	manualset3
91276	4	399169	13	NULL	NULL	0	NULL	gastric carcinoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( The role of D2 lymphadenectomy in the surgical treatment of gastric carcinoma ) .
	manualset3
91277	1	399170	13	NULL	NULL	0	NULL	Clinical studies 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Clinical and statistical studies on the effect of dentition on the hearing organ and hearing in 5000 patients treated in an otolaryngologic clinic ) .
	manualset3
91278	2	399170	13	NULL	NULL	0	NULL	statistical studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Clinical and statistical studies on the effect of dentition on the hearing organ and hearing in 5000 patients treated in an otolaryngologic clinic ) .
	manualset3
91279	3	399170	13	NULL	NULL	0	NULL	effect	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Clinical and statistical studies on the effect of dentition on the hearing organ and hearing in 5000 patients treated in an otolaryngologic clinic ) .
	manualset3
91280	4	399170	13	NULL	NULL	0	NULL	dentition 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Clinical and statistical studies on the effect of dentition on the hearing organ and hearing in 5000 patients treated in an otolaryngologic clinic ) .
	manualset3
91281	5	399170	13	NULL	NULL	0	NULL	hearing organ 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Clinical and statistical studies on the effect of dentition on the hearing organ and hearing in 5000 patients treated in an otolaryngologic clinic ) .
	manualset3
91282	6	399170	13	NULL	NULL	0	NULL	 hearing	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Clinical and statistical studies on the effect of dentition on the hearing organ and hearing in 5000 patients treated in an otolaryngologic clinic ) .
	manualset3
91283	7	399170	13	NULL	NULL	0	NULL	5000	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Clinical and statistical studies on the effect of dentition on the hearing organ and hearing in 5000 patients treated in an otolaryngologic clinic ) .
	manualset3
91284	8	399170	13	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Clinical and statistical studies on the effect of dentition on the hearing organ and hearing in 5000 patients treated in an otolaryngologic clinic ) .
	manualset3
91285	9	399170	13	NULL	NULL	0	NULL	otolaryngologic clinic	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Clinical and statistical studies on the effect of dentition on the hearing organ and hearing in 5000 patients treated in an otolaryngologic clinic ) .
	manualset3
91286	1	399171	13	NULL	NULL	NULL	NULL	Alterations 	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	I. Alterations in the metabolism of xenobiotic compounds and D-glucuronic acid pathway .
	manualset3
91287	2	399171	13	NULL	NULL	0	NULL	metabolism of xenobiotic compounds	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Alterations in the metabolism of xenobiotic compounds and D-glucuronic acid pathway .
	manualset3
91288	3	399171	13	NULL	NULL	0	NULL	D-glucuronic acid pathway	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Alterations in the metabolism of xenobiotic compounds and D-glucuronic acid pathway .
	manualset3
91289	1	399172	13	NULL	NULL	0	NULL	 Development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Development of collicular responses to optic stimulation ) .
	manualset3
91290	2	399172	13	NULL	NULL	0	NULL	collicular responses	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Development of collicular responses to optic stimulation ) .
	manualset3
91291	3	399172	13	NULL	NULL	0	NULL	optic stimulation 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	I. Development of collicular responses to optic stimulation ) .
	manualset3
91292	1	399173	13	NULL	NULL	0	NULL	( vti ) 	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	I ( vti ) showed a half-maximal activation around -102 mV with a slope factor of 25 mV .
	manualset3
91293	2	399173	13	NULL	NULL	0	NULL	half-maximal activation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	I ( vti ) showed a half-maximal activation around -102 mV with a slope factor of 25 mV .
	manualset3
91294	3	399173	13	NULL	NULL	0	NULL	-102 mV 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	I ( vti ) showed a half-maximal activation around -102 mV with a slope factor of 25 mV .
	manualset3
91295	4	399173	13	NULL	NULL	0	NULL	slope factor of 25 mV	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	I ( vti ) showed a half-maximal activation around -102 mV with a slope factor of 25 mV .
	manualset3
91296	1	399174	13	NULL	NULL	0	NULL	present issue of Current Drug Targets	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	I guest-edited the present issue of Current Drug Targets aiming to bring together a number of leading experts in the field of cancer chemoprevention , who would systematically review the evidence ; discuss the clinical and experimental data ; highlight new approaches and promising directions for future research .
	manualset3
91297	2	399174	13	NULL	NULL	0	NULL	number of leading experts	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	I guest-edited the present issue of Current Drug Targets aiming to bring together a number of leading experts in the field of cancer chemoprevention , who would systematically review the evidence ; discuss the clinical and experimental data ; highlight new approaches and promising directions for future research .
	manualset3
91298	3	399174	13	NULL	NULL	0	NULL	field of cancer chemoprevention	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	I guest-edited the present issue of Current Drug Targets aiming to bring together a number of leading experts in the field of cancer chemoprevention , who would systematically review the evidence ; discuss the clinical and experimental data ; highlight new approaches and promising directions for future research .
	manualset3
91299	4	399174	13	NULL	NULL	0	NULL	evidence	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	I guest-edited the present issue of Current Drug Targets aiming to bring together a number of leading experts in the field of cancer chemoprevention , who would systematically review the evidence ; discuss the clinical and experimental data ; highlight new approaches and promising directions for future research .
	manualset3
91300	5	399174	13	NULL	NULL	0	NULL	clinical and experimental data	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	I guest-edited the present issue of Current Drug Targets aiming to bring together a number of leading experts in the field of cancer chemoprevention , who would systematically review the evidence ; discuss the clinical and experimental data ; highlight new approaches and promising directions for future research .
	manualset3
91301	6	399174	13	NULL	NULL	NULL	NULL	new approaches	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	I guest-edited the present issue of Current Drug Targets aiming to bring together a number of leading experts in the field of cancer chemoprevention , who would systematically review the evidence ; discuss the clinical and experimental data ; highlight new approaches and promising directions for future research .
	manualset3
91302	7	399174	13	NULL	NULL	0	NULL	promising directions	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	I guest-edited the present issue of Current Drug Targets aiming to bring together a number of leading experts in the field of cancer chemoprevention , who would systematically review the evidence ; discuss the clinical and experimental data ; highlight new approaches and promising directions for future research .
	manualset3
91303	8	399174	13	NULL	NULL	0	NULL	future research	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	I guest-edited the present issue of Current Drug Targets aiming to bring together a number of leading experts in the field of cancer chemoprevention , who would systematically review the evidence ; discuss the clinical and experimental data ; highlight new approaches and promising directions for future research .
	manualset3
91304	1	399175	13	NULL	NULL	0	NULL	legitimacy 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	I am particularly concerned with the legitimacy these justifications have in the eyes of project beneficiaries .
	manualset3
91305	2	399175	13	NULL	NULL	0	NULL	 justifications	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	I am particularly concerned with the legitimacy these justifications have in the eyes of project beneficiaries .
	manualset3
91306	3	399175	13	NULL	NULL	0	NULL	eyes	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	I am particularly concerned with the legitimacy these justifications have in the eyes of project beneficiaries .
	manualset3
91307	4	399175	13	NULL	NULL	0	NULL	project beneficiaries	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	I am particularly concerned with the legitimacy these justifications have in the eyes of project beneficiaries .
	manualset3
91308	1	399176	13	NULL	NULL	0	NULL	pattern of mortality	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	I examined the pattern of mortality in the Donner Party , a group of emigrants who became trapped with inadequate food stores in the winter snows of the Sierra Nevada mountains in 1846-1847 .
	manualset3
91309	2	399176	13	NULL	NULL	0	NULL	Donner Party	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	I examined the pattern of mortality in the Donner Party , a group of emigrants who became trapped with inadequate food stores in the winter snows of the Sierra Nevada mountains in 1846-1847 .
	manualset3
91310	3	399176	13	NULL	NULL	0	NULL	a group of emigrants 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	I examined the pattern of mortality in the Donner Party , a group of emigrants who became trapped with inadequate food stores in the winter snows of the Sierra Nevada mountains in 1846-1847 .
	manualset3
91311	4	399176	13	NULL	NULL	NULL	NULL	food stores	Food												NULL		NULL	NULL	NULL	NULL	NULL	NULL	I examined the pattern of mortality in the Donner Party , a group of emigrants who became trapped with inadequate food stores in the winter snows of the Sierra Nevada mountains in 1846-1847 .
	manualset3
91312	5	399176	13	NULL	NULL	0	NULL	winter snows	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	I examined the pattern of mortality in the Donner Party , a group of emigrants who became trapped with inadequate food stores in the winter snows of the Sierra Nevada mountains in 1846-1847 .
	manualset3
91313	6	399176	13	NULL	NULL	0	NULL	 Sierra Nevada mountains	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	I examined the pattern of mortality in the Donner Party , a group of emigrants who became trapped with inadequate food stores in the winter snows of the Sierra Nevada mountains in 1846-1847 .
	manualset3
91314	7	399176	13	NULL	NULL	0	NULL	1846-1847	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	I examined the pattern of mortality in the Donner Party , a group of emigrants who became trapped with inadequate food stores in the winter snows of the Sierra Nevada mountains in 1846-1847 .
	manualset3
91315	1	399177	13	NULL	NULL	NULL	NULL	active participant	Person												NULL		NULL	NULL	NULL	NULL	NULL	NULL	I have been an active participant and eyewitness , and take full responsibility for attempting to write an early history at a time when most of the contributors are still alive .
	manualset3
91316	2	399177	13	NULL	NULL	0	NULL	eyewitness	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	I have been an active participant and eyewitness , and take full responsibility for attempting to write an early history at a time when most of the contributors are still alive .
	manualset3
91317	3	399177	13	NULL	NULL	0	NULL	responsibility	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	I have been an active participant and eyewitness , and take full responsibility for attempting to write an early history at a time when most of the contributors are still alive .
	manualset3
91318	4	399177	13	NULL	NULL	0	NULL	 time	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	I have been an active participant and eyewitness , and take full responsibility for attempting to write an early history at a time when most of the contributors are still alive .
	manualset3
91319	5	399177	13	NULL	NULL	0	NULL	contributors	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	I have been an active participant and eyewitness , and take full responsibility for attempting to write an early history at a time when most of the contributors are still alive .
	manualset3
91320	6	399177	13	NULL	NULL	0	NULL	alive	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	I have been an active participant and eyewitness , and take full responsibility for attempting to write an early history at a time when most of the contributors are still alive .
	manualset3
92130	7	399177	13	NULL	NULL	0	NULL	early history	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	I have been an active participant and eyewitness , and take full responsibility for attempting to write an early history at a time when most of the contributors are still alive .
	manualset3
91321	1	399178	13	NULL	NULL	0	NULL	perspectives	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	I hope to provide new perspectives and experimental approaches that go beyond the current state of the art to foster an understanding of eutherian embryogenesis and provide clues for the efficient production of somatic cells for cell therapy .
	manualset3
91322	2	399178	13	NULL	NULL	0	NULL	experimental approaches 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	I hope to provide new perspectives and experimental approaches that go beyond the current state of the art to foster an understanding of eutherian embryogenesis and provide clues for the efficient production of somatic cells for cell therapy .
	manualset3
91323	3	399178	13	NULL	NULL	0	NULL	 current state of the art	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	I hope to provide new perspectives and experimental approaches that go beyond the current state of the art to foster an understanding of eutherian embryogenesis and provide clues for the efficient production of somatic cells for cell therapy .
	manualset3
91324	4	399178	13	NULL	NULL	0	NULL	eutherian embryogenesis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	I hope to provide new perspectives and experimental approaches that go beyond the current state of the art to foster an understanding of eutherian embryogenesis and provide clues for the efficient production of somatic cells for cell therapy .
	manualset3
91325	5	399178	13	NULL	NULL	0	NULL	clues	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	I hope to provide new perspectives and experimental approaches that go beyond the current state of the art to foster an understanding of eutherian embryogenesis and provide clues for the efficient production of somatic cells for cell therapy .
	manualset3
91326	6	399178	13	NULL	NULL	0	NULL	efficient production 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	I hope to provide new perspectives and experimental approaches that go beyond the current state of the art to foster an understanding of eutherian embryogenesis and provide clues for the efficient production of somatic cells for cell therapy .
	manualset3
91327	7	399178	13	NULL	NULL	0	NULL	somatic cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	I hope to provide new perspectives and experimental approaches that go beyond the current state of the art to foster an understanding of eutherian embryogenesis and provide clues for the efficient production of somatic cells for cell therapy .
	manualset3
91328	8	399178	13	NULL	NULL	0	NULL	cell therapy 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	I hope to provide new perspectives and experimental approaches that go beyond the current state of the art to foster an understanding of eutherian embryogenesis and provide clues for the efficient production of somatic cells for cell therapy .
	manualset3
91329	1	399179	13	NULL	NULL	0	NULL	Anemia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Anemia following partial gastrectomy ) .
	manualset3
91330	2	399179	13	NULL	NULL	0	NULL	 partial gastrectomy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Anemia following partial gastrectomy ) .
	manualset3
91331	1	399180	13	NULL	NULL	0	NULL	role	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The role of bone marrow stromal cells in apoptosis in myelodysplastic syndrome ) .
	manualset3
91332	2	399180	13	NULL	NULL	0	NULL	bone marrow stromal cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	( The role of bone marrow stromal cells in apoptosis in myelodysplastic syndrome ) .
	manualset3
91333	3	399180	13	NULL	NULL	0	NULL	apoptosis 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The role of bone marrow stromal cells in apoptosis in myelodysplastic syndrome ) .
	manualset3
91334	4	399180	13	NULL	NULL	0	NULL	myelodysplastic syndrome	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( The role of bone marrow stromal cells in apoptosis in myelodysplastic syndrome ) .
	manualset3
91335	1	399181	13	NULL	NULL	0	NULL	emotions	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	I will argue that emotions are constitutively and discursively relevant features of the evaluative experience of persons .
	manualset3
91336	2	399181	13	NULL	NULL	0	NULL	features	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	I will argue that emotions are constitutively and discursively relevant features of the evaluative experience of persons .
	manualset3
91337	3	399181	13	NULL	NULL	NULL	NULL	evaluative experience	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	I will argue that emotions are constitutively and discursively relevant features of the evaluative experience of persons .
	manualset3
91338	4	399181	13	NULL	NULL	0	NULL	persons	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	I will argue that emotions are constitutively and discursively relevant features of the evaluative experience of persons .
	manualset3
91339	1	399182	13	NULL	NULL	NULL	NULL	IAEA/WHO TLD postal dose audit service	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	IAEA/WHO TLD postal dose audit service and high precision measurements for radiotherapy level dosimetry .
	manualset3
91340	2	399182	13	NULL	NULL	0	NULL	precision measurements	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	IAEA/WHO TLD postal dose audit service and high precision measurements for radiotherapy level dosimetry .
	manualset3
91341	3	399182	13	NULL	NULL	0	NULL	radiotherapy level dosimetry	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	IAEA/WHO TLD postal dose audit service and high precision measurements for radiotherapy level dosimetry .
	manualset3
91342	1	399183	13	NULL	NULL	0	NULL	IBD patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IBD patients may require long-term immunosuppression , and therefore should be considered candidates for vaccination against new HBV infection as well as prophylaxis against HBV reactivation prior to immunosuppressive therapy .
	manualset3
91343	2	399183	13	NULL	NULL	0	NULL	long-term immunosuppression	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	IBD patients may require long-term immunosuppression , and therefore should be considered candidates for vaccination against new HBV infection as well as prophylaxis against HBV reactivation prior to immunosuppressive therapy .
	manualset3
91344	3	399183	13	NULL	NULL	0	NULL	candidates	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IBD patients may require long-term immunosuppression , and therefore should be considered candidates for vaccination against new HBV infection as well as prophylaxis against HBV reactivation prior to immunosuppressive therapy .
	manualset3
91345	4	399183	13	NULL	NULL	0	NULL	vaccination 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	IBD patients may require long-term immunosuppression , and therefore should be considered candidates for vaccination against new HBV infection as well as prophylaxis against HBV reactivation prior to immunosuppressive therapy .
	manualset3
91346	5	399183	13	NULL	NULL	0	NULL	 HBV infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IBD patients may require long-term immunosuppression , and therefore should be considered candidates for vaccination against new HBV infection as well as prophylaxis against HBV reactivation prior to immunosuppressive therapy .
	manualset3
91347	6	399183	13	NULL	NULL	0	NULL	prophylaxis 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	IBD patients may require long-term immunosuppression , and therefore should be considered candidates for vaccination against new HBV infection as well as prophylaxis against HBV reactivation prior to immunosuppressive therapy .
	manualset3
91348	7	399183	13	NULL	NULL	0	NULL	HBV reactivation 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IBD patients may require long-term immunosuppression , and therefore should be considered candidates for vaccination against new HBV infection as well as prophylaxis against HBV reactivation prior to immunosuppressive therapy .
	manualset3
91349	8	399183	13	NULL	NULL	0	NULL	immunosuppressive therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	IBD patients may require long-term immunosuppression , and therefore should be considered candidates for vaccination against new HBV infection as well as prophylaxis against HBV reactivation prior to immunosuppressive therapy .
	manualset3
91350	1	399184	13	NULL	NULL	0	NULL	ICI 182 780 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	ICI 182 780 did not suppress E2-stimulated IGF-I mRNA expression and 100 nM ICI 182 780 enhanced ( 93 % , p & lt ; 0.05 ) IGF-I mRNA levels in BSC cultures .
	manualset3
91351	2	399184	13	NULL	NULL	0	NULL	E2-stimulated IGF-I mRNA expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	ICI 182 780 did not suppress E2-stimulated IGF-I mRNA expression and 100 nM ICI 182 780 enhanced ( 93 % , p & lt ; 0.05 ) IGF-I mRNA levels in BSC cultures .
	manualset3
91352	3	399184	13	NULL	NULL	0	NULL	100 nM	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	ICI 182 780 did not suppress E2-stimulated IGF-I mRNA expression and 100 nM ICI 182 780 enhanced ( 93 % , p & lt ; 0.05 ) IGF-I mRNA levels in BSC cultures .
	manualset3
91353	4	399184	13	NULL	NULL	0	NULL	ICI 182 780	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	ICI 182 780 did not suppress E2-stimulated IGF-I mRNA expression and 100 nM ICI 182 780 enhanced ( 93 % , p & lt ; 0.05 ) IGF-I mRNA levels in BSC cultures .
	manualset3
91354	5	399184	13	NULL	NULL	0	NULL	93 % , p & lt ; 0.05	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	ICI 182 780 did not suppress E2-stimulated IGF-I mRNA expression and 100 nM ICI 182 780 enhanced ( 93 % , p & lt ; 0.05 ) IGF-I mRNA levels in BSC cultures .
	manualset3
91355	6	399184	13	NULL	NULL	0	NULL	 IGF-I mRNA levels	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	ICI 182 780 did not suppress E2-stimulated IGF-I mRNA expression and 100 nM ICI 182 780 enhanced ( 93 % , p & lt ; 0.05 ) IGF-I mRNA levels in BSC cultures .
	manualset3
91356	7	399184	13	NULL	NULL	0	NULL	BSC cultures	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	ICI 182 780 did not suppress E2-stimulated IGF-I mRNA expression and 100 nM ICI 182 780 enhanced ( 93 % , p & lt ; 0.05 ) IGF-I mRNA levels in BSC cultures .
	manualset3
91357	1	399185	13	NULL	NULL	0	NULL	ICW	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	ICW was similar in both groups but the ICW to ECW ratio was significantly higher in the athletes compared to the recreational sportsmen ( 0.67 + / - 0.16 vs 0.54 + / - 0.07 , p & lt ; 0.01 ) .
	manualset3
91358	2	399185	13	NULL	NULL	0	NULL	both groups	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	ICW was similar in both groups but the ICW to ECW ratio was significantly higher in the athletes compared to the recreational sportsmen ( 0.67 + / - 0.16 vs 0.54 + / - 0.07 , p & lt ; 0.01 ) .
	manualset3
91359	3	399185	13	NULL	NULL	0	NULL	ICW to ECW ratio	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	ICW was similar in both groups but the ICW to ECW ratio was significantly higher in the athletes compared to the recreational sportsmen ( 0.67 + / - 0.16 vs 0.54 + / - 0.07 , p & lt ; 0.01 ) .
	manualset3
91360	4	399185	13	NULL	NULL	0	NULL	athletes 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	ICW was similar in both groups but the ICW to ECW ratio was significantly higher in the athletes compared to the recreational sportsmen ( 0.67 + / - 0.16 vs 0.54 + / - 0.07 , p & lt ; 0.01 ) .
	manualset3
91361	5	399185	13	NULL	NULL	0	NULL	recreational sportsmen	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	ICW was similar in both groups but the ICW to ECW ratio was significantly higher in the athletes compared to the recreational sportsmen ( 0.67 + / - 0.16 vs 0.54 + / - 0.07 , p & lt ; 0.01 ) .
	manualset3
91362	6	399185	13	NULL	NULL	0	NULL	0.67 + / - 0.16 vs 0.54 + / - 0.07 , p & lt ; 0.01	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	ICW was similar in both groups but the ICW to ECW ratio was significantly higher in the athletes compared to the recreational sportsmen ( 0.67 + / - 0.16 vs 0.54 + / - 0.07 , p & lt ; 0.01 ) .
	manualset3
91363	1	399186	13	NULL	NULL	0	NULL	IFN	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IFN arrests the growth of Burkitt Lymphoma derived cell line Daudi cells in the G1 phase .
	manualset3
91364	2	399186	13	NULL	NULL	0	NULL	growth	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IFN arrests the growth of Burkitt Lymphoma derived cell line Daudi cells in the G1 phase .
	manualset3
91365	3	399186	13	NULL	NULL	0	NULL	Burkitt Lymphoma derived cell line Daudi cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IFN arrests the growth of Burkitt Lymphoma derived cell line Daudi cells in the G1 phase .
	manualset3
91366	4	399186	13	NULL	NULL	0	NULL	G1 phase	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IFN arrests the growth of Burkitt Lymphoma derived cell line Daudi cells in the G1 phase .
	manualset3
91367	1	399187	13	NULL	NULL	0	NULL	IGF-II	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IGF-II was more effective than IGF-I in competitively displacing both labeled ligands .
	manualset3
91368	2	399187	13	NULL	NULL	0	NULL	IGF-I	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IGF-II was more effective than IGF-I in competitively displacing both labeled ligands .
	manualset3
91369	3	399187	13	NULL	NULL	0	NULL	labeled ligands	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IGF-II was more effective than IGF-I in competitively displacing both labeled ligands .
	manualset3
91370	1	399188	13	NULL	NULL	0	NULL	 role	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( The role of the general practitioner in the control of cancer ) .
	manualset3
91371	2	399188	13	NULL	NULL	0	NULL	general practitioner	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	( The role of the general practitioner in the control of cancer ) .
	manualset3
91372	3	399188	13	NULL	NULL	0	NULL	cancer	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( The role of the general practitioner in the control of cancer ) .
	manualset3
91373	1	399189	13	NULL	NULL	0	NULL	IGFBP-2 mRNA levels	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-2 mRNA levels remained high at the contusion site in the presence of either drug , but the increase was blocked in the cortex temporal to the impact by MK-801 .
	manualset3
91374	2	399189	13	NULL	NULL	0	NULL	 contusion site	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-2 mRNA levels remained high at the contusion site in the presence of either drug , but the increase was blocked in the cortex temporal to the impact by MK-801 .
	manualset3
91375	3	399189	13	NULL	NULL	0	NULL	drug	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-2 mRNA levels remained high at the contusion site in the presence of either drug , but the increase was blocked in the cortex temporal to the impact by MK-801 .
	manualset3
91376	4	399189	13	NULL	NULL	0	NULL	cortex temporal	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-2 mRNA levels remained high at the contusion site in the presence of either drug , but the increase was blocked in the cortex temporal to the impact by MK-801 .
	manualset3
91377	5	399189	13	NULL	NULL	0	NULL	 impact	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-2 mRNA levels remained high at the contusion site in the presence of either drug , but the increase was blocked in the cortex temporal to the impact by MK-801 .
	manualset3
91378	6	399189	13	NULL	NULL	0	NULL	MK-801	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-2 mRNA levels remained high at the contusion site in the presence of either drug , but the increase was blocked in the cortex temporal to the impact by MK-801 .
	manualset3
91379	7	399189	13	NULL	NULL	0	NULL	presence	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	IGFBP-2 mRNA levels remained high at the contusion site in the presence of either drug , but the increase was blocked in the cortex temporal to the impact by MK-801 .
	manualset3
91380	1	399190	13	NULL	NULL	0	NULL	IGFs	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IGFs are important positive modulators of overall body and muscle growth in different species .
	manualset3
91381	2	399190	13	NULL	NULL	0	NULL	positive modulators	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IGFs are important positive modulators of overall body and muscle growth in different species .
	manualset3
91382	3	399190	13	NULL	NULL	0	NULL	 overall body	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	IGFs are important positive modulators of overall body and muscle growth in different species .
	manualset3
91383	4	399190	13	NULL	NULL	0	NULL	muscle growth 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IGFs are important positive modulators of overall body and muscle growth in different species .
	manualset3
91384	5	399190	13	NULL	NULL	0	NULL	species	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	IGFs are important positive modulators of overall body and muscle growth in different species .
	manualset3
91385	1	399191	13	NULL	NULL	0	NULL	IHD	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	IHD correlated with SA ( r = 0.25-0 .27 , p = 0.006-0 .0026 ) , only in the 74 year age group .
	manualset3
91386	2	399191	13	NULL	NULL	0	NULL	SA ( r = 0.25-0 .27 , p = 0.006-0 .0026 )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	IHD correlated with SA ( r = 0.25-0 .27 , p = 0.006-0 .0026 ) , only in the 74 year age group .
	manualset3
91387	3	399191	13	NULL	NULL	0	NULL	74 year age group	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IHD correlated with SA ( r = 0.25-0 .27 , p = 0.006-0 .0026 ) , only in the 74 year age group .
	manualset3
91388	1	399192	13	NULL	NULL	0	NULL	RIAMAT T4 kit	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	II : RIAMAT T4 kit ( author 's transl ) ) .
	manualset3
91389	2	399192	13	NULL	NULL	0	NULL	author 's	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	II : RIAMAT T4 kit ( author 's transl ) ) .
	manualset3
91390	1	399193	13	NULL	NULL	0	NULL	IISs	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	IISs propagate to L2/3 via activation of L2/3 interneurons but not pyramidal cells , which are mostly quiescent at this phase .
	manualset3
91391	2	399193	13	NULL	NULL	0	NULL	L2/3	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IISs propagate to L2/3 via activation of L2/3 interneurons but not pyramidal cells , which are mostly quiescent at this phase .
	manualset3
91392	3	399193	13	NULL	NULL	0	NULL	 activation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IISs propagate to L2/3 via activation of L2/3 interneurons but not pyramidal cells , which are mostly quiescent at this phase .
	manualset3
91393	4	399193	13	NULL	NULL	0	NULL	L2/3 interneurons	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IISs propagate to L2/3 via activation of L2/3 interneurons but not pyramidal cells , which are mostly quiescent at this phase .
	manualset3
91394	5	399193	13	NULL	NULL	0	NULL	 pyramidal cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IISs propagate to L2/3 via activation of L2/3 interneurons but not pyramidal cells , which are mostly quiescent at this phase .
	manualset3
91395	6	399193	13	NULL	NULL	0	NULL	phase	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IISs propagate to L2/3 via activation of L2/3 interneurons but not pyramidal cells , which are mostly quiescent at this phase .
	manualset3
91396	1	399194	13	NULL	NULL	NULL	NULL	IK	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	IK , IR recorded in GH3/B6 cells and ERG currents in CHO cells were compared using similar experimental conditions ( same pulse protocols and isotonic KCl as extracellular solution ) .
	manualset3
91397	2	399194	13	NULL	NULL	0	NULL	IR 	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	IK , IR recorded in GH3/B6 cells and ERG currents in CHO cells were compared using similar experimental conditions ( same pulse protocols and isotonic KCl as extracellular solution ) .
	manualset3
91398	3	399194	13	NULL	NULL	0	NULL	GH3/B6 cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IK , IR recorded in GH3/B6 cells and ERG currents in CHO cells were compared using similar experimental conditions ( same pulse protocols and isotonic KCl as extracellular solution ) .
	manualset3
91399	4	399194	13	NULL	NULL	0	NULL	ERG currents 	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	IK , IR recorded in GH3/B6 cells and ERG currents in CHO cells were compared using similar experimental conditions ( same pulse protocols and isotonic KCl as extracellular solution ) .
	manualset3
91400	5	399194	13	NULL	NULL	0	NULL	 CHO cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IK , IR recorded in GH3/B6 cells and ERG currents in CHO cells were compared using similar experimental conditions ( same pulse protocols and isotonic KCl as extracellular solution ) .
	manualset3
91401	6	399194	13	NULL	NULL	0	NULL	experimental conditions	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	IK , IR recorded in GH3/B6 cells and ERG currents in CHO cells were compared using similar experimental conditions ( same pulse protocols and isotonic KCl as extracellular solution ) .
	manualset3
91402	7	399194	13	NULL	NULL	0	NULL	pulse protocols	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	IK , IR recorded in GH3/B6 cells and ERG currents in CHO cells were compared using similar experimental conditions ( same pulse protocols and isotonic KCl as extracellular solution ) .
	manualset3
91403	8	399194	13	NULL	NULL	0	NULL	isotonic KCl	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	IK , IR recorded in GH3/B6 cells and ERG currents in CHO cells were compared using similar experimental conditions ( same pulse protocols and isotonic KCl as extracellular solution ) .
	manualset3
91404	9	399194	13	NULL	NULL	0	NULL	extracellular solution 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	IK , IR recorded in GH3/B6 cells and ERG currents in CHO cells were compared using similar experimental conditions ( same pulse protocols and isotonic KCl as extracellular solution ) .
	manualset3
91405	1	399195	13	NULL	NULL	0	NULL	IK2 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IK2 inhibits development of malaria sporozoites present in the mosquito salivary glands .
	manualset3
91406	2	399195	13	NULL	NULL	0	NULL	development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IK2 inhibits development of malaria sporozoites present in the mosquito salivary glands .
	manualset3
91407	3	399195	13	NULL	NULL	0	NULL	malaria sporozoites 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IK2 inhibits development of malaria sporozoites present in the mosquito salivary glands .
	manualset3
91408	4	399195	13	NULL	NULL	0	NULL	mosquito salivary glands 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	IK2 inhibits development of malaria sporozoites present in the mosquito salivary glands .
	manualset3
91409	1	399196	13	NULL	NULL	0	NULL	IL-1 / IL-1 receptor complex signaling 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 / IL-1 receptor complex signaling requires adaptor proteins , e.g. , the IL-1 receptor brain-specific accessory protein ( AcPb ) .
	manualset3
91410	2	399196	13	NULL	NULL	0	NULL	adaptor proteins	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 / IL-1 receptor complex signaling requires adaptor proteins , e.g. , the IL-1 receptor brain-specific accessory protein ( AcPb ) .
	manualset3
91411	3	399196	13	NULL	NULL	0	NULL	IL-1 receptor brain-specific accessory protein ( AcPb ) 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 / IL-1 receptor complex signaling requires adaptor proteins , e.g. , the IL-1 receptor brain-specific accessory protein ( AcPb ) .
	manualset3
91412	1	399197	13	NULL	NULL	0	NULL	 role	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( The role of the pharmacist in the management of the operating room ) .
	manualset3
91413	2	399197	13	NULL	NULL	0	NULL	pharmacist	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	( The role of the pharmacist in the management of the operating room ) .
	manualset3
91414	3	399197	13	NULL	NULL	0	NULL	management 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( The role of the pharmacist in the management of the operating room ) .
	manualset3
91415	4	399197	13	NULL	NULL	0	NULL	operating room 	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	( The role of the pharmacist in the management of the operating room ) .
	manualset3
91416	1	399198	13	NULL	NULL	0	NULL	IL-1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 activation of NF-B was inhibited by NPY treatment , as observed by confocal microscopy and Western blotting analysis of nuclear translocation of NF-B p65 subunit , leading to the decrease of NO synthesis .
	manualset3
91417	2	399198	13	NULL	NULL	0	NULL	 activation of NF-B	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 activation of NF-B was inhibited by NPY treatment , as observed by confocal microscopy and Western blotting analysis of nuclear translocation of NF-B p65 subunit , leading to the decrease of NO synthesis .
	manualset3
91418	3	399198	13	NULL	NULL	0	NULL	NPY	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 activation of NF-B was inhibited by NPY treatment , as observed by confocal microscopy and Western blotting analysis of nuclear translocation of NF-B p65 subunit , leading to the decrease of NO synthesis .
	manualset3
91419	4	399198	13	NULL	NULL	0	NULL	 treatment	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 activation of NF-B was inhibited by NPY treatment , as observed by confocal microscopy and Western blotting analysis of nuclear translocation of NF-B p65 subunit , leading to the decrease of NO synthesis .
	manualset3
91420	5	399198	13	NULL	NULL	0	NULL	 confocal microscopy 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 activation of NF-B was inhibited by NPY treatment , as observed by confocal microscopy and Western blotting analysis of nuclear translocation of NF-B p65 subunit , leading to the decrease of NO synthesis .
	manualset3
91421	6	399198	13	NULL	NULL	0	NULL	Western blotting analysis 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 activation of NF-B was inhibited by NPY treatment , as observed by confocal microscopy and Western blotting analysis of nuclear translocation of NF-B p65 subunit , leading to the decrease of NO synthesis .
	manualset3
91422	7	399198	13	NULL	NULL	0	NULL	 nuclear translocation 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 activation of NF-B was inhibited by NPY treatment , as observed by confocal microscopy and Western blotting analysis of nuclear translocation of NF-B p65 subunit , leading to the decrease of NO synthesis .
	manualset3
91423	8	399198	13	NULL	NULL	0	NULL	NF-B p65 subunit 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 activation of NF-B was inhibited by NPY treatment , as observed by confocal microscopy and Western blotting analysis of nuclear translocation of NF-B p65 subunit , leading to the decrease of NO synthesis .
	manualset3
91424	9	399198	13	NULL	NULL	0	NULL	decrease of NO synthesis	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 activation of NF-B was inhibited by NPY treatment , as observed by confocal microscopy and Western blotting analysis of nuclear translocation of NF-B p65 subunit , leading to the decrease of NO synthesis .
	manualset3
91425	1	399199	13	NULL	NULL	0	NULL	IL-1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 and TNF-alpha induced mRNA expression of c-jun while IL-17 had no effect .
	manualset3
91426	2	399199	13	NULL	NULL	0	NULL	TNF-alpha	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 and TNF-alpha induced mRNA expression of c-jun while IL-17 had no effect .
	manualset3
91427	3	399199	13	NULL	NULL	0	NULL	mRNA expression of c-jun	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 and TNF-alpha induced mRNA expression of c-jun while IL-17 had no effect .
	manualset3
91428	4	399199	13	NULL	NULL	0	NULL	IL-17	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 and TNF-alpha induced mRNA expression of c-jun while IL-17 had no effect .
	manualset3
91429	1	399200	13	NULL	NULL	0	NULL	IL-1 beta	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 beta is secreted by activated murine macrophages as biologically inactive precursor .
	manualset3
91430	2	399200	13	NULL	NULL	0	NULL	murine macrophages 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 beta is secreted by activated murine macrophages as biologically inactive precursor .
	manualset3
91431	3	399200	13	NULL	NULL	0	NULL	biologically inactive precursor	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 beta is secreted by activated murine macrophages as biologically inactive precursor .
	manualset3
91432	1	399201	13	NULL	NULL	NULL	NULL	IL-1	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	IL-1 is a pro-inflammatory cytokine consisted of two molecular species , IL-1alpha and IL-1beta , and the IL-1 receptor antagonist ( IL-1Ra ) is a natural inhibitor of both molecules .
	manualset3
91433	2	399201	13	NULL	NULL	NULL	NULL	pro-inflammatory cytokine	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	IL-1 is a pro-inflammatory cytokine consisted of two molecular species , IL-1alpha and IL-1beta , and the IL-1 receptor antagonist ( IL-1Ra ) is a natural inhibitor of both molecules .
	manualset3
91434	3	399201	13	NULL	NULL	0	NULL	two	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 is a pro-inflammatory cytokine consisted of two molecular species , IL-1alpha and IL-1beta , and the IL-1 receptor antagonist ( IL-1Ra ) is a natural inhibitor of both molecules .
	manualset3
91435	4	399201	13	NULL	NULL	0	NULL	molecular species 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 is a pro-inflammatory cytokine consisted of two molecular species , IL-1alpha and IL-1beta , and the IL-1 receptor antagonist ( IL-1Ra ) is a natural inhibitor of both molecules .
	manualset3
91436	5	399201	13	NULL	NULL	0	NULL	IL-1alpha 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 is a pro-inflammatory cytokine consisted of two molecular species , IL-1alpha and IL-1beta , and the IL-1 receptor antagonist ( IL-1Ra ) is a natural inhibitor of both molecules .
	manualset3
91437	6	399201	13	NULL	NULL	0	NULL	IL-1beta	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 is a pro-inflammatory cytokine consisted of two molecular species , IL-1alpha and IL-1beta , and the IL-1 receptor antagonist ( IL-1Ra ) is a natural inhibitor of both molecules .
	manualset3
91438	7	399201	13	NULL	NULL	0	NULL	IL-1 receptor antagonist ( IL-1Ra )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 is a pro-inflammatory cytokine consisted of two molecular species , IL-1alpha and IL-1beta , and the IL-1 receptor antagonist ( IL-1Ra ) is a natural inhibitor of both molecules .
	manualset3
91439	8	399201	13	NULL	NULL	0	NULL	natural inhibitor	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 is a pro-inflammatory cytokine consisted of two molecular species , IL-1alpha and IL-1beta , and the IL-1 receptor antagonist ( IL-1Ra ) is a natural inhibitor of both molecules .
	manualset3
91440	9	399201	13	NULL	NULL	0	NULL	molecules	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-1 is a pro-inflammatory cytokine consisted of two molecular species , IL-1alpha and IL-1beta , and the IL-1 receptor antagonist ( IL-1Ra ) is a natural inhibitor of both molecules .
	manualset3
91441	1	399202	13	NULL	NULL	0	NULL	IL-12 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-12 protects against coxsackievirus B3-induced myocarditis by increasing IFN-gamma and macrophage and neutrophil populations in the heart .
	manualset3
91442	2	399202	13	NULL	NULL	0	NULL	coxsackievirus B3-induced myocarditis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-12 protects against coxsackievirus B3-induced myocarditis by increasing IFN-gamma and macrophage and neutrophil populations in the heart .
	manualset3
91443	3	399202	13	NULL	NULL	0	NULL	IFN-gamma 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-12 protects against coxsackievirus B3-induced myocarditis by increasing IFN-gamma and macrophage and neutrophil populations in the heart .
	manualset3
91444	4	399202	13	NULL	NULL	0	NULL	macrophage populations	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-12 protects against coxsackievirus B3-induced myocarditis by increasing IFN-gamma and macrophage and neutrophil populations in the heart .
	manualset3
91445	5	399202	13	NULL	NULL	0	NULL	neutrophil populations	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-12 protects against coxsackievirus B3-induced myocarditis by increasing IFN-gamma and macrophage and neutrophil populations in the heart .
	manualset3
91446	6	399202	13	NULL	NULL	0	NULL	heart	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-12 protects against coxsackievirus B3-induced myocarditis by increasing IFN-gamma and macrophage and neutrophil populations in the heart .
	manualset3
91447	1	399203	13	NULL	NULL	0	NULL	IL-13	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-13 induces mucin production by stimulating epidermal growth factor receptors and by activating neutrophils .
	manualset3
91448	2	399203	13	NULL	NULL	0	NULL	mucin production 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-13 induces mucin production by stimulating epidermal growth factor receptors and by activating neutrophils .
	manualset3
91449	3	399203	13	NULL	NULL	0	NULL	epidermal growth factor receptors	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-13 induces mucin production by stimulating epidermal growth factor receptors and by activating neutrophils .
	manualset3
91450	4	399203	13	NULL	NULL	0	NULL	neutrophils	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-13 induces mucin production by stimulating epidermal growth factor receptors and by activating neutrophils .
	manualset3
91451	1	399204	13	NULL	NULL	0	NULL	IL-17 expression 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-17 expression by mycobacteria-specific disease site T cells was not detected in healthy , M.tb-infected persons , or patients with TB pericarditis .
	manualset3
91452	2	399204	13	NULL	NULL	0	NULL	mycobacteria-specific disease site T cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-17 expression by mycobacteria-specific disease site T cells was not detected in healthy , M.tb-infected persons , or patients with TB pericarditis .
	manualset3
91453	3	399204	13	NULL	NULL	0	NULL	healthy persons	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-17 expression by mycobacteria-specific disease site T cells was not detected in healthy , M.tb-infected persons , or patients with TB pericarditis .
	manualset3
91454	4	399204	13	NULL	NULL	0	NULL	M.tb-infected persons	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-17 expression by mycobacteria-specific disease site T cells was not detected in healthy , M.tb-infected persons , or patients with TB pericarditis .
	manualset3
91455	5	399204	13	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-17 expression by mycobacteria-specific disease site T cells was not detected in healthy , M.tb-infected persons , or patients with TB pericarditis .
	manualset3
91456	6	399204	13	NULL	NULL	0	NULL	TB pericarditis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-17 expression by mycobacteria-specific disease site T cells was not detected in healthy , M.tb-infected persons , or patients with TB pericarditis .
	manualset3
91457	1	399205	13	NULL	NULL	0	NULL	IL-18	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-18 produced by DCs and macrophages acts in an autocrine manner and augments IL-12-induced IFN-gamma production by DCs as also observed in T and NK cells .
	manualset3
91458	2	399205	13	NULL	NULL	0	NULL	DCs	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-18 produced by DCs and macrophages acts in an autocrine manner and augments IL-12-induced IFN-gamma production by DCs as also observed in T and NK cells .
	manualset3
91459	3	399205	13	NULL	NULL	0	NULL	macrophages	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-18 produced by DCs and macrophages acts in an autocrine manner and augments IL-12-induced IFN-gamma production by DCs as also observed in T and NK cells .
	manualset3
91461	5	399205	13	NULL	NULL	0	NULL	autocrine manner 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-18 produced by DCs and macrophages acts in an autocrine manner and augments IL-12-induced IFN-gamma production by DCs as also observed in T and NK cells .
	manualset3
91462	6	399205	13	NULL	NULL	0	NULL	IL-12-induced IFN-gamma production	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-18 produced by DCs and macrophages acts in an autocrine manner and augments IL-12-induced IFN-gamma production by DCs as also observed in T and NK cells .
	manualset3
91463	7	399205	13	NULL	NULL	0	NULL	DCs 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-18 produced by DCs and macrophages acts in an autocrine manner and augments IL-12-induced IFN-gamma production by DCs as also observed in T and NK cells .
	manualset3
91464	8	399205	13	NULL	NULL	0	NULL	T cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-18 produced by DCs and macrophages acts in an autocrine manner and augments IL-12-induced IFN-gamma production by DCs as also observed in T and NK cells .
	manualset3
91465	9	399205	13	NULL	NULL	0	NULL	NK cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-18 produced by DCs and macrophages acts in an autocrine manner and augments IL-12-induced IFN-gamma production by DCs as also observed in T and NK cells .
	manualset3
91466	1	399206	13	NULL	NULL	0	NULL	IL-2-dependent T effector cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-2-dependent T effector cells usually die when deprived of growth factor .
	manualset3
91467	2	399206	13	NULL	NULL	0	NULL	growth factor	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-2-dependent T effector cells usually die when deprived of growth factor .
	manualset3
91468	1	399207	13	NULL	NULL	0	NULL	small RNAs 	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	( The small RNAs in plant immunity ) .
	manualset3
91469	2	399207	13	NULL	NULL	0	NULL	plant	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( The small RNAs in plant immunity ) .
	manualset3
91470	3	399207	13	NULL	NULL	0	NULL	immunity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The small RNAs in plant immunity ) .
	manualset3
91471	1	399208	13	NULL	NULL	0	NULL	IL-2 levels 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-2 , IL-10 , TNF-alpha , C3 , and C4 levels were significantly elevated in the patient group .
	manualset3
91472	2	399208	13	NULL	NULL	0	NULL	IL-10 levels	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-2 , IL-10 , TNF-alpha , C3 , and C4 levels were significantly elevated in the patient group .
	manualset3
91473	3	399208	13	NULL	NULL	0	NULL	TNF-alpha levels	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-2 , IL-10 , TNF-alpha , C3 , and C4 levels were significantly elevated in the patient group .
	manualset3
91474	4	399208	13	NULL	NULL	0	NULL	C3 levels	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-2 , IL-10 , TNF-alpha , C3 , and C4 levels were significantly elevated in the patient group .
	manualset3
92438	5	399208	13	NULL	NULL	0	NULL	patient group	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-2 , IL-10 , TNF-alpha , C3 , and C4 levels were significantly elevated in the patient group .
	manualset3
91475	1	399209	13	NULL	NULL	0	NULL	IL-2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-2 and IL-4 stimulated the expression of MEK1 and c-Fos and induced T cell resistance .
	manualset3
91476	2	399209	13	NULL	NULL	0	NULL	IL-4 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-2 and IL-4 stimulated the expression of MEK1 and c-Fos and induced T cell resistance .
	manualset3
91477	3	399209	13	NULL	NULL	0	NULL	expression of MEK1	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-2 and IL-4 stimulated the expression of MEK1 and c-Fos and induced T cell resistance .
	manualset3
91478	4	399209	13	NULL	NULL	0	NULL	expression of c-Fos	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-2 and IL-4 stimulated the expression of MEK1 and c-Fos and induced T cell resistance .
	manualset3
91479	5	399209	13	NULL	NULL	0	NULL	T cell resistance	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-2 and IL-4 stimulated the expression of MEK1 and c-Fos and induced T cell resistance .
	manualset3
91480	1	399210	13	NULL	NULL	0	NULL	IL-27 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-27 regulates IL-12 responsiveness of naive CD4 + T cells through Stat1-dependent and - independent mechanisms .
	manualset3
91481	2	399210	13	NULL	NULL	0	NULL	IL-12 responsiveness	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-27 regulates IL-12 responsiveness of naive CD4 + T cells through Stat1-dependent and - independent mechanisms .
	manualset3
91482	3	399210	13	NULL	NULL	0	NULL	naive CD4 + T cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-27 regulates IL-12 responsiveness of naive CD4 + T cells through Stat1-dependent and - independent mechanisms .
	manualset3
91483	4	399210	13	NULL	NULL	0	NULL	 Stat1-dependent mechanisms 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-27 regulates IL-12 responsiveness of naive CD4 + T cells through Stat1-dependent and - independent mechanisms .
	manualset3
91484	5	399210	13	NULL	NULL	0	NULL	Stat1- independent mechanisms	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-27 regulates IL-12 responsiveness of naive CD4 + T cells through Stat1-dependent and - independent mechanisms .
	manualset3
91485	1	399211	13	NULL	NULL	0	NULL	IL-4 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-4 and interferon-gamma production in children with atopic disease .
	manualset3
91486	2	399211	13	NULL	NULL	0	NULL	interferon-gamma	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-4 and interferon-gamma production in children with atopic disease .
	manualset3
91487	3	399211	13	NULL	NULL	0	NULL	production	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-4 and interferon-gamma production in children with atopic disease .
	manualset3
91488	4	399211	13	NULL	NULL	0	NULL	children	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-4 and interferon-gamma production in children with atopic disease .
	manualset3
91489	5	399211	13	NULL	NULL	0	NULL	 atopic disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-4 and interferon-gamma production in children with atopic disease .
	manualset3
91490	1	399212	13	NULL	NULL	0	NULL	IL-4 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-4 inhibited the spontaneous proliferation found in three cases , but stimulated proliferation after CD40 crosslinking .
	manualset3
91491	2	399212	13	NULL	NULL	0	NULL	spontaneous proliferation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-4 inhibited the spontaneous proliferation found in three cases , but stimulated proliferation after CD40 crosslinking .
	manualset3
91492	3	399212	13	NULL	NULL	0	NULL	three cases	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-4 inhibited the spontaneous proliferation found in three cases , but stimulated proliferation after CD40 crosslinking .
	manualset3
91493	4	399212	13	NULL	NULL	0	NULL	proliferation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-4 inhibited the spontaneous proliferation found in three cases , but stimulated proliferation after CD40 crosslinking .
	manualset3
91494	5	399212	13	NULL	NULL	0	NULL	CD40 crosslinking 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-4 inhibited the spontaneous proliferation found in three cases , but stimulated proliferation after CD40 crosslinking .
	manualset3
91495	1	399213	13	NULL	NULL	0	NULL	IL-5-producing T cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-5-producing T cells that induce airway eosinophilia and hyperresponsiveness are suppressed by dexamethasone and cyclosporin A in mice .
	manualset3
91496	2	399213	13	NULL	NULL	0	NULL	airway eosinophilia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-5-producing T cells that induce airway eosinophilia and hyperresponsiveness are suppressed by dexamethasone and cyclosporin A in mice .
	manualset3
91497	3	399213	13	NULL	NULL	0	NULL	hyperresponsiveness	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-5-producing T cells that induce airway eosinophilia and hyperresponsiveness are suppressed by dexamethasone and cyclosporin A in mice .
	manualset3
91498	4	399213	13	NULL	NULL	0	NULL	dexamethasone	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-5-producing T cells that induce airway eosinophilia and hyperresponsiveness are suppressed by dexamethasone and cyclosporin A in mice .
	manualset3
91499	5	399213	13	NULL	NULL	0	NULL	cyclosporin A	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-5-producing T cells that induce airway eosinophilia and hyperresponsiveness are suppressed by dexamethasone and cyclosporin A in mice .
	manualset3
91500	6	399213	13	NULL	NULL	0	NULL	 mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-5-producing T cells that induce airway eosinophilia and hyperresponsiveness are suppressed by dexamethasone and cyclosporin A in mice .
	manualset3
91501	1	399214	13	NULL	NULL	0	NULL	IL-5 mRNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-5 and IL-13 mRNA were increased in lung tissue of OA-challenged Dcn ( + / + ) mice .
	manualset3
91502	2	399214	13	NULL	NULL	0	NULL	IL-13 mRNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-5 and IL-13 mRNA were increased in lung tissue of OA-challenged Dcn ( + / + ) mice .
	manualset3
91503	3	399214	13	NULL	NULL	0	NULL	lung tissue	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-5 and IL-13 mRNA were increased in lung tissue of OA-challenged Dcn ( + / + ) mice .
	manualset3
91504	4	399214	13	NULL	NULL	0	NULL	OA-challenged Dcn ( + / + ) mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-5 and IL-13 mRNA were increased in lung tissue of OA-challenged Dcn ( + / + ) mice .
	manualset3
91505	1	399215	13	NULL	NULL	0	NULL	IL-5 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-5 is produced by both hematopoietic and non-hematopoietic cells including T cells , granulocytes , and natural helper cells .
	manualset3
91506	2	399215	13	NULL	NULL	0	NULL	hematopoietic cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-5 is produced by both hematopoietic and non-hematopoietic cells including T cells , granulocytes , and natural helper cells .
	manualset3
91507	3	399215	13	NULL	NULL	0	NULL	non-hematopoietic cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-5 is produced by both hematopoietic and non-hematopoietic cells including T cells , granulocytes , and natural helper cells .
	manualset3
91508	4	399215	13	NULL	NULL	0	NULL	T cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-5 is produced by both hematopoietic and non-hematopoietic cells including T cells , granulocytes , and natural helper cells .
	manualset3
91509	5	399215	13	NULL	NULL	0	NULL	granulocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-5 is produced by both hematopoietic and non-hematopoietic cells including T cells , granulocytes , and natural helper cells .
	manualset3
91510	6	399215	13	NULL	NULL	0	NULL	natural helper cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-5 is produced by both hematopoietic and non-hematopoietic cells including T cells , granulocytes , and natural helper cells .
	manualset3
91511	1	399216	13	NULL	NULL	0	NULL	IL-6	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-6 also activated the MAPK signaling pathway in adipocytes through the association with its receptor .
	manualset3
91512	2	399216	13	NULL	NULL	0	NULL	MAPK signaling pathway	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-6 also activated the MAPK signaling pathway in adipocytes through the association with its receptor .
	manualset3
91513	3	399216	13	NULL	NULL	0	NULL	adipocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-6 also activated the MAPK signaling pathway in adipocytes through the association with its receptor .
	manualset3
91514	4	399216	13	NULL	NULL	0	NULL	association	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-6 also activated the MAPK signaling pathway in adipocytes through the association with its receptor .
	manualset3
91515	5	399216	13	NULL	NULL	0	NULL	receptor	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-6 also activated the MAPK signaling pathway in adipocytes through the association with its receptor .
	manualset3
91516	1	399217	13	NULL	NULL	0	NULL	state	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( The state of the field of hygiene in medicine .
	manualset3
91517	2	399217	13	NULL	NULL	0	NULL	field of hygiene	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	( The state of the field of hygiene in medicine .
	manualset3
91518	3	399217	13	NULL	NULL	0	NULL	medicine	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	( The state of the field of hygiene in medicine .
	manualset3
91519	1	399218	13	NULL	NULL	0	NULL	IL-6 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-6 or TNF also significantly reduced plasma membrane-associated caveolin-1 .
	manualset3
91520	2	399218	13	NULL	NULL	0	NULL	TNF 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-6 or TNF also significantly reduced plasma membrane-associated caveolin-1 .
	manualset3
91521	3	399218	13	NULL	NULL	0	NULL	plasma membrane-associated caveolin-1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-6 or TNF also significantly reduced plasma membrane-associated caveolin-1 .
	manualset3
91522	1	399219	13	NULL	NULL	0	NULL	IL-6 production	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-6 production in response to size-fractioned PM exposures failed to show evidence of relative importance of particle sizes in their abilities to induce proinflammatory responses .
	manualset3
91523	2	399219	13	NULL	NULL	0	NULL	response 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-6 production in response to size-fractioned PM exposures failed to show evidence of relative importance of particle sizes in their abilities to induce proinflammatory responses .
	manualset3
91524	3	399219	13	NULL	NULL	0	NULL	size-fractioned PM exposures	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-6 production in response to size-fractioned PM exposures failed to show evidence of relative importance of particle sizes in their abilities to induce proinflammatory responses .
	manualset3
91525	4	399219	13	NULL	NULL	0	NULL	evidence	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-6 production in response to size-fractioned PM exposures failed to show evidence of relative importance of particle sizes in their abilities to induce proinflammatory responses .
	manualset3
91526	5	399219	13	NULL	NULL	0	NULL	relative importance	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-6 production in response to size-fractioned PM exposures failed to show evidence of relative importance of particle sizes in their abilities to induce proinflammatory responses .
	manualset3
91527	6	399219	13	NULL	NULL	0	NULL	particle sizes	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-6 production in response to size-fractioned PM exposures failed to show evidence of relative importance of particle sizes in their abilities to induce proinflammatory responses .
	manualset3
91528	7	399219	13	NULL	NULL	0	NULL	abilities 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-6 production in response to size-fractioned PM exposures failed to show evidence of relative importance of particle sizes in their abilities to induce proinflammatory responses .
	manualset3
91529	8	399219	13	NULL	NULL	0	NULL	proinflammatory responses	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL-6 production in response to size-fractioned PM exposures failed to show evidence of relative importance of particle sizes in their abilities to induce proinflammatory responses .
	manualset3
91530	1	399220	13	NULL	NULL	0	NULL	IL 1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IL 1 in combination with ionomycin ( iono/rIL 1 ) stimulated a proliferative response that was associated with the production of IL 4 as measured by lymphokine bioassay and mRNA studies .
	manualset3
91531	2	399220	13	NULL	NULL	0	NULL	ionomycin	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	IL 1 in combination with ionomycin ( iono/rIL 1 ) stimulated a proliferative response that was associated with the production of IL 4 as measured by lymphokine bioassay and mRNA studies .
	manualset3
91532	3	399220	13	NULL	NULL	0	NULL	iono/rIL 1	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IL 1 in combination with ionomycin ( iono/rIL 1 ) stimulated a proliferative response that was associated with the production of IL 4 as measured by lymphokine bioassay and mRNA studies .
	manualset3
91533	4	399220	13	NULL	NULL	NULL	NULL	proliferative response	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	IL 1 in combination with ionomycin ( iono/rIL 1 ) stimulated a proliferative response that was associated with the production of IL 4 as measured by lymphokine bioassay and mRNA studies .
	manualset3
91534	5	399220	13	NULL	NULL	0	NULL	production of IL 4	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IL 1 in combination with ionomycin ( iono/rIL 1 ) stimulated a proliferative response that was associated with the production of IL 4 as measured by lymphokine bioassay and mRNA studies .
	manualset3
91535	6	399220	13	NULL	NULL	0	NULL	 lymphokine bioassay 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	IL 1 in combination with ionomycin ( iono/rIL 1 ) stimulated a proliferative response that was associated with the production of IL 4 as measured by lymphokine bioassay and mRNA studies .
	manualset3
91536	7	399220	13	NULL	NULL	0	NULL	mRNA studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	IL 1 in combination with ionomycin ( iono/rIL 1 ) stimulated a proliferative response that was associated with the production of IL 4 as measured by lymphokine bioassay and mRNA studies .
	manualset3
91537	1	399221	13	NULL	NULL	0	NULL	IMPLICATIONS	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IMPLICATIONS : Complications , particularly when they involve organs other than just the heart , increase mortality and prolong the length of hospital stay after heart surgery , independent of a patient 's preoperative risk factors and the duration of cardiopulmonary bypass .
	manualset3
91538	2	399221	13	NULL	NULL	0	NULL	Complications	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IMPLICATIONS : Complications , particularly when they involve organs other than just the heart , increase mortality and prolong the length of hospital stay after heart surgery , independent of a patient 's preoperative risk factors and the duration of cardiopulmonary bypass .
	manualset3
91539	3	399221	13	NULL	NULL	0	NULL	organs	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	IMPLICATIONS : Complications , particularly when they involve organs other than just the heart , increase mortality and prolong the length of hospital stay after heart surgery , independent of a patient 's preoperative risk factors and the duration of cardiopulmonary bypass .
	manualset3
91540	4	399221	13	NULL	NULL	0	NULL	heart 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	IMPLICATIONS : Complications , particularly when they involve organs other than just the heart , increase mortality and prolong the length of hospital stay after heart surgery , independent of a patient 's preoperative risk factors and the duration of cardiopulmonary bypass .
	manualset3
91541	5	399221	13	NULL	NULL	0	NULL	 mortality	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IMPLICATIONS : Complications , particularly when they involve organs other than just the heart , increase mortality and prolong the length of hospital stay after heart surgery , independent of a patient 's preoperative risk factors and the duration of cardiopulmonary bypass .
	manualset3
91542	6	399221	13	NULL	NULL	0	NULL	length of hospital stay	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	IMPLICATIONS : Complications , particularly when they involve organs other than just the heart , increase mortality and prolong the length of hospital stay after heart surgery , independent of a patient 's preoperative risk factors and the duration of cardiopulmonary bypass .
	manualset3
91543	7	399221	13	NULL	NULL	0	NULL	 heart surgery	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	IMPLICATIONS : Complications , particularly when they involve organs other than just the heart , increase mortality and prolong the length of hospital stay after heart surgery , independent of a patient 's preoperative risk factors and the duration of cardiopulmonary bypass .
	manualset3
91544	8	399221	13	NULL	NULL	0	NULL	patient 's preoperative risk factors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IMPLICATIONS : Complications , particularly when they involve organs other than just the heart , increase mortality and prolong the length of hospital stay after heart surgery , independent of a patient 's preoperative risk factors and the duration of cardiopulmonary bypass .
	manualset3
91545	9	399221	13	NULL	NULL	0	NULL	duration	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	IMPLICATIONS : Complications , particularly when they involve organs other than just the heart , increase mortality and prolong the length of hospital stay after heart surgery , independent of a patient 's preoperative risk factors and the duration of cardiopulmonary bypass .
	manualset3
91546	10	399221	13	NULL	NULL	0	NULL	cardiopulmonary bypass	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	IMPLICATIONS : Complications , particularly when they involve organs other than just the heart , increase mortality and prolong the length of hospital stay after heart surgery , independent of a patient 's preoperative risk factors and the duration of cardiopulmonary bypass .
	manualset3
91547	1	399222	13	NULL	NULL	0	NULL	IMPLICATIONS 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IMPLICATIONS : We describe three patients with difficult airways in which fiberoptic endotracheal intubation was used to insert breathing tubes into the patients ' windpipes .
	manualset3
91548	2	399222	13	NULL	NULL	0	NULL	three 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	IMPLICATIONS : We describe three patients with difficult airways in which fiberoptic endotracheal intubation was used to insert breathing tubes into the patients ' windpipes .
	manualset3
91549	3	399222	13	NULL	NULL	0	NULL	patients 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IMPLICATIONS : We describe three patients with difficult airways in which fiberoptic endotracheal intubation was used to insert breathing tubes into the patients ' windpipes .
	manualset3
91550	4	399222	13	NULL	NULL	0	NULL	difficult airways	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IMPLICATIONS : We describe three patients with difficult airways in which fiberoptic endotracheal intubation was used to insert breathing tubes into the patients ' windpipes .
	manualset3
91551	5	399222	13	NULL	NULL	0	NULL	 fiberoptic endotracheal intubation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	IMPLICATIONS : We describe three patients with difficult airways in which fiberoptic endotracheal intubation was used to insert breathing tubes into the patients ' windpipes .
	manualset3
91552	6	399222	13	NULL	NULL	0	NULL	breathing tubes	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	IMPLICATIONS : We describe three patients with difficult airways in which fiberoptic endotracheal intubation was used to insert breathing tubes into the patients ' windpipes .
	manualset3
91553	7	399222	13	NULL	NULL	0	NULL	 patients ' 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IMPLICATIONS : We describe three patients with difficult airways in which fiberoptic endotracheal intubation was used to insert breathing tubes into the patients ' windpipes .
	manualset3
91554	8	399222	13	NULL	NULL	0	NULL	 windpipes	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	IMPLICATIONS : We describe three patients with difficult airways in which fiberoptic endotracheal intubation was used to insert breathing tubes into the patients ' windpipes .
	manualset3
91555	1	399223	13	NULL	NULL	0	NULL	rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	IN rats , a contractile threshold dose of ONO-802 was similar from day 15 to day 21 of pregnancy .
	manualset3
91556	2	399223	13	NULL	NULL	0	NULL	contractile threshold dose	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	IN rats , a contractile threshold dose of ONO-802 was similar from day 15 to day 21 of pregnancy .
	manualset3
91557	3	399223	13	NULL	NULL	0	NULL	 ONO-802	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	IN rats , a contractile threshold dose of ONO-802 was similar from day 15 to day 21 of pregnancy .
	manualset3
91558	4	399223	13	NULL	NULL	0	NULL	day 15 to day 21 	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	IN rats , a contractile threshold dose of ONO-802 was similar from day 15 to day 21 of pregnancy .
	manualset3
91559	5	399223	13	NULL	NULL	0	NULL	pregnancy	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IN rats , a contractile threshold dose of ONO-802 was similar from day 15 to day 21 of pregnancy .
	manualset3
91560	1	399224	13	NULL	NULL	0	NULL	INA	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	INA is usually localized in the uterine cervix , but , when multifocal lesions are present , the latter is almost always involved .
	manualset3
91561	2	399224	13	NULL	NULL	0	NULL	uterine cervix	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	INA is usually localized in the uterine cervix , but , when multifocal lesions are present , the latter is almost always involved .
	manualset3
91562	3	399224	13	NULL	NULL	0	NULL	 multifocal lesions	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	INA is usually localized in the uterine cervix , but , when multifocal lesions are present , the latter is almost always involved .
	manualset3
91563	1	399225	13	NULL	NULL	0	NULL	INTRODUCTION	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	INTRODUCTION : Coronary artery disease ( CAD ) is one of the major causes of morbidity and mortality worldwide , exerting a huge economic burden .
	manualset3
91564	2	399225	13	NULL	NULL	0	NULL	Coronary artery disease ( CAD )	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	INTRODUCTION : Coronary artery disease ( CAD ) is one of the major causes of morbidity and mortality worldwide , exerting a huge economic burden .
	manualset3
91565	3	399225	13	NULL	NULL	NULL	NULL	one of the major causes of morbidity	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	INTRODUCTION : Coronary artery disease ( CAD ) is one of the major causes of morbidity and mortality worldwide , exerting a huge economic burden .
	manualset3
91566	4	399225	13	NULL	NULL	0	NULL	mortality	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	INTRODUCTION : Coronary artery disease ( CAD ) is one of the major causes of morbidity and mortality worldwide , exerting a huge economic burden .
	manualset3
91567	5	399225	13	NULL	NULL	0	NULL	worldwide	GeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	INTRODUCTION : Coronary artery disease ( CAD ) is one of the major causes of morbidity and mortality worldwide , exerting a huge economic burden .
	manualset3
91568	6	399225	13	NULL	NULL	0	NULL	economic burden	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	INTRODUCTION : Coronary artery disease ( CAD ) is one of the major causes of morbidity and mortality worldwide , exerting a huge economic burden .
	manualset3
91569	1	399226	13	NULL	NULL	0	NULL	INTRODUCTION	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	INTRODUCTION : Juvenile polyposis syndrome ( JPS ) is a rare , autosomal dominant condition .
	manualset3
91570	2	399226	13	NULL	NULL	0	NULL	Juvenile polyposis syndrome ( JPS )	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	INTRODUCTION : Juvenile polyposis syndrome ( JPS ) is a rare , autosomal dominant condition .
	manualset3
91571	3	399226	13	NULL	NULL	0	NULL	autosomal dominant condition	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	INTRODUCTION : Juvenile polyposis syndrome ( JPS ) is a rare , autosomal dominant condition .
	manualset3
91572	1	399227	13	NULL	NULL	0	NULL	study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( The study of iron metabolism in irradiated dogs with increased erythropoietic function ) .
	manualset3
91573	2	399227	13	NULL	NULL	0	NULL	 iron metabolism	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The study of iron metabolism in irradiated dogs with increased erythropoietic function ) .
	manualset3
91574	3	399227	13	NULL	NULL	0	NULL	irradiated dogs	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( The study of iron metabolism in irradiated dogs with increased erythropoietic function ) .
	manualset3
91575	4	399227	13	NULL	NULL	0	NULL	erythropoietic function	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The study of iron metabolism in irradiated dogs with increased erythropoietic function ) .
	manualset3
91576	1	399228	13	NULL	NULL	0	NULL	INTRODUCTION	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	INTRODUCTIONWe describe here a procedure for introducing loxP sites into the mammalian genome .
	manualset3
91577	2	399228	13	NULL	NULL	0	NULL	 procedure	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	INTRODUCTIONWe describe here a procedure for introducing loxP sites into the mammalian genome .
	manualset3
91578	3	399228	13	NULL	NULL	0	NULL	loxP sites	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	INTRODUCTIONWe describe here a procedure for introducing loxP sites into the mammalian genome .
	manualset3
91579	4	399228	13	NULL	NULL	0	NULL	mammalian genome	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	INTRODUCTIONWe describe here a procedure for introducing loxP sites into the mammalian genome .
	manualset3
91580	1	399229	13	NULL	NULL	0	NULL	IOM	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	IOM is established as effective to predict an increased risk of the adverse outcomes of paraparesis , paraplegia , and quadriplegia in spinal surgery ( 4 Class I and 7 Class II studies ) .
	manualset3
91581	2	399229	13	NULL	NULL	0	NULL	risk	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IOM is established as effective to predict an increased risk of the adverse outcomes of paraparesis , paraplegia , and quadriplegia in spinal surgery ( 4 Class I and 7 Class II studies ) .
	manualset3
91582	3	399229	13	NULL	NULL	0	NULL	adverse outcomes of paraparesis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IOM is established as effective to predict an increased risk of the adverse outcomes of paraparesis , paraplegia , and quadriplegia in spinal surgery ( 4 Class I and 7 Class II studies ) .
	manualset3
91583	4	399229	13	NULL	NULL	0	NULL	paraplegia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IOM is established as effective to predict an increased risk of the adverse outcomes of paraparesis , paraplegia , and quadriplegia in spinal surgery ( 4 Class I and 7 Class II studies ) .
	manualset3
91584	5	399229	13	NULL	NULL	0	NULL	quadriplegia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IOM is established as effective to predict an increased risk of the adverse outcomes of paraparesis , paraplegia , and quadriplegia in spinal surgery ( 4 Class I and 7 Class II studies ) .
	manualset3
91585	6	399229	13	NULL	NULL	0	NULL	spinal surgery	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	IOM is established as effective to predict an increased risk of the adverse outcomes of paraparesis , paraplegia , and quadriplegia in spinal surgery ( 4 Class I and 7 Class II studies ) .
	manualset3
91586	7	399229	13	NULL	NULL	0	NULL	4 Class I and 7 Class II studies 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	IOM is established as effective to predict an increased risk of the adverse outcomes of paraparesis , paraplegia , and quadriplegia in spinal surgery ( 4 Class I and 7 Class II studies ) .
	manualset3
91587	1	399230	13	NULL	NULL	0	NULL	IPANEMA	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	IPANEMA , a research platform devoted to ancient and historical materials ( archaeology , cultural heritage , palaeontology and past environments ) , is currently being set up at the synchrotron facility SOLEIL ( Saint-Aubin , France ; SOLEIL opened to users in January 2008 ) .
	manualset3
91588	2	399230	13	NULL	NULL	0	NULL	a research platform	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	IPANEMA , a research platform devoted to ancient and historical materials ( archaeology , cultural heritage , palaeontology and past environments ) , is currently being set up at the synchrotron facility SOLEIL ( Saint-Aubin , France ; SOLEIL opened to users in January 2008 ) .
	manualset3
91589	3	399230	13	NULL	NULL	0	NULL	ancient materials	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	IPANEMA , a research platform devoted to ancient and historical materials ( archaeology , cultural heritage , palaeontology and past environments ) , is currently being set up at the synchrotron facility SOLEIL ( Saint-Aubin , France ; SOLEIL opened to users in January 2008 ) .
	manualset3
91590	4	399230	13	NULL	NULL	0	NULL	 historical materials	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	IPANEMA , a research platform devoted to ancient and historical materials ( archaeology , cultural heritage , palaeontology and past environments ) , is currently being set up at the synchrotron facility SOLEIL ( Saint-Aubin , France ; SOLEIL opened to users in January 2008 ) .
	manualset3
91591	5	399230	13	NULL	NULL	0	NULL	archaeology	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	IPANEMA , a research platform devoted to ancient and historical materials ( archaeology , cultural heritage , palaeontology and past environments ) , is currently being set up at the synchrotron facility SOLEIL ( Saint-Aubin , France ; SOLEIL opened to users in January 2008 ) .
	manualset3
91592	6	399230	13	NULL	NULL	0	NULL	cultural heritage	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	IPANEMA , a research platform devoted to ancient and historical materials ( archaeology , cultural heritage , palaeontology and past environments ) , is currently being set up at the synchrotron facility SOLEIL ( Saint-Aubin , France ; SOLEIL opened to users in January 2008 ) .
	manualset3
91593	7	399230	13	NULL	NULL	0	NULL	palaeontology	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	IPANEMA , a research platform devoted to ancient and historical materials ( archaeology , cultural heritage , palaeontology and past environments ) , is currently being set up at the synchrotron facility SOLEIL ( Saint-Aubin , France ; SOLEIL opened to users in January 2008 ) .
	manualset3
91594	8	399230	13	NULL	NULL	0	NULL	 past environments	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	IPANEMA , a research platform devoted to ancient and historical materials ( archaeology , cultural heritage , palaeontology and past environments ) , is currently being set up at the synchrotron facility SOLEIL ( Saint-Aubin , France ; SOLEIL opened to users in January 2008 ) .
	manualset3
91595	9	399230	13	NULL	NULL	0	NULL	synchrotron facility	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	IPANEMA , a research platform devoted to ancient and historical materials ( archaeology , cultural heritage , palaeontology and past environments ) , is currently being set up at the synchrotron facility SOLEIL ( Saint-Aubin , France ; SOLEIL opened to users in January 2008 ) .
	manualset3
91596	10	399230	13	NULL	NULL	0	NULL	SOLEIL 	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	IPANEMA , a research platform devoted to ancient and historical materials ( archaeology , cultural heritage , palaeontology and past environments ) , is currently being set up at the synchrotron facility SOLEIL ( Saint-Aubin , France ; SOLEIL opened to users in January 2008 ) .
	manualset3
91597	11	399230	13	NULL	NULL	0	NULL	Saint-Aubin	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	IPANEMA , a research platform devoted to ancient and historical materials ( archaeology , cultural heritage , palaeontology and past environments ) , is currently being set up at the synchrotron facility SOLEIL ( Saint-Aubin , France ; SOLEIL opened to users in January 2008 ) .
	manualset3
91598	12	399230	13	NULL	NULL	0	NULL	France	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	IPANEMA , a research platform devoted to ancient and historical materials ( archaeology , cultural heritage , palaeontology and past environments ) , is currently being set up at the synchrotron facility SOLEIL ( Saint-Aubin , France ; SOLEIL opened to users in January 2008 ) .
	manualset3
91599	13	399230	13	NULL	NULL	0	NULL	SOLEIL 	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	IPANEMA , a research platform devoted to ancient and historical materials ( archaeology , cultural heritage , palaeontology and past environments ) , is currently being set up at the synchrotron facility SOLEIL ( Saint-Aubin , France ; SOLEIL opened to users in January 2008 ) .
	manualset3
91600	14	399230	13	NULL	NULL	0	NULL	 users	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IPANEMA , a research platform devoted to ancient and historical materials ( archaeology , cultural heritage , palaeontology and past environments ) , is currently being set up at the synchrotron facility SOLEIL ( Saint-Aubin , France ; SOLEIL opened to users in January 2008 ) .
	manualset3
91601	15	399230	13	NULL	NULL	0	NULL	January 2008 	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	IPANEMA , a research platform devoted to ancient and historical materials ( archaeology , cultural heritage , palaeontology and past environments ) , is currently being set up at the synchrotron facility SOLEIL ( Saint-Aubin , France ; SOLEIL opened to users in January 2008 ) .
	manualset3
91602	1	399231	13	NULL	NULL	0	NULL	IRES-mediated translation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IRES-mediated translation of cellular messenger RNA operates in eIF2 - independent manner during stress .
	manualset3
91603	2	399231	13	NULL	NULL	0	NULL	cellular messenger RNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	IRES-mediated translation of cellular messenger RNA operates in eIF2 - independent manner during stress .
	manualset3
91604	3	399231	13	NULL	NULL	0	NULL	eIF2 - independent manner	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IRES-mediated translation of cellular messenger RNA operates in eIF2 - independent manner during stress .
	manualset3
91605	4	399231	13	NULL	NULL	0	NULL	 stress 	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	IRES-mediated translation of cellular messenger RNA operates in eIF2 - independent manner during stress .
	manualset3
91606	1	399232	13	NULL	NULL	NULL	NULL	Ibuprofen metabolite profiling 	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Ibuprofen metabolite profiling using a combination of SPE/column-trapping and HPLC-micro-coil NMR .
	manualset3
91607	2	399232	13	NULL	NULL	0	NULL	SPE/column-trapping	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Ibuprofen metabolite profiling using a combination of SPE/column-trapping and HPLC-micro-coil NMR .
	manualset3
91608	3	399232	13	NULL	NULL	0	NULL	HPLC-micro-coil NMR	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Ibuprofen metabolite profiling using a combination of SPE/column-trapping and HPLC-micro-coil NMR .
	manualset3
91609	4	399232	13	NULL	NULL	0	NULL	 combination	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Ibuprofen metabolite profiling using a combination of SPE/column-trapping and HPLC-micro-coil NMR .
	manualset3
91610	1	399233	13	NULL	NULL	0	NULL	Ibutilide-induced cardioversion 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Ibutilide-induced cardioversion of atrial fibrillation during pregnancy .
	manualset3
91611	2	399233	13	NULL	NULL	0	NULL	atrial fibrillation	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Ibutilide-induced cardioversion of atrial fibrillation during pregnancy .
	manualset3
91612	3	399233	13	NULL	NULL	0	NULL	pregnancy	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Ibutilide-induced cardioversion of atrial fibrillation during pregnancy .
	manualset3
91613	1	399234	13	NULL	NULL	0	NULL	 teaching	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( The teaching of anatomy in the United States ) .
	manualset3
91614	2	399234	13	NULL	NULL	0	NULL	anatomy	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	( The teaching of anatomy in the United States ) .
	manualset3
91615	3	399234	13	NULL	NULL	0	NULL	United States	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	( The teaching of anatomy in the United States ) .
	manualset3
91616	1	399235	13	NULL	NULL	0	NULL	Ictal blindness	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Ictal blindness was the solitary epileptic phenomenon in only two children .
	manualset3
91617	2	399235	13	NULL	NULL	0	NULL	solitary epileptic phenomenon	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Ictal blindness was the solitary epileptic phenomenon in only two children .
	manualset3
91618	3	399235	13	NULL	NULL	0	NULL	two	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Ictal blindness was the solitary epileptic phenomenon in only two children .
	manualset3
91619	4	399235	13	NULL	NULL	0	NULL	children	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Ictal blindness was the solitary epileptic phenomenon in only two children .
	manualset3
91620	1	399236	13	NULL	NULL	0	NULL	reconstruction	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Ideally , reconstruction of lower extremity soft tissue defects includes not only an esthetically pleasing 3-dimensional shape and solid anchoring to the underlying structures to resist shear forces , but should also address the restoration of sensation .
	manualset3
91621	2	399236	13	NULL	NULL	0	NULL	lower extremity soft tissue defects	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Ideally , reconstruction of lower extremity soft tissue defects includes not only an esthetically pleasing 3-dimensional shape and solid anchoring to the underlying structures to resist shear forces , but should also address the restoration of sensation .
	manualset3
91622	3	399236	13	NULL	NULL	0	NULL	esthetically pleasing 3-dimensional shape	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Ideally , reconstruction of lower extremity soft tissue defects includes not only an esthetically pleasing 3-dimensional shape and solid anchoring to the underlying structures to resist shear forces , but should also address the restoration of sensation .
	manualset3
91623	4	399236	13	NULL	NULL	0	NULL	underlying structures	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Ideally , reconstruction of lower extremity soft tissue defects includes not only an esthetically pleasing 3-dimensional shape and solid anchoring to the underlying structures to resist shear forces , but should also address the restoration of sensation .
	manualset3
91624	5	399236	13	NULL	NULL	0	NULL	resist shear forces	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Ideally , reconstruction of lower extremity soft tissue defects includes not only an esthetically pleasing 3-dimensional shape and solid anchoring to the underlying structures to resist shear forces , but should also address the restoration of sensation .
	manualset3
91625	6	399236	13	NULL	NULL	0	NULL	restoration of sensation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Ideally , reconstruction of lower extremity soft tissue defects includes not only an esthetically pleasing 3-dimensional shape and solid anchoring to the underlying structures to resist shear forces , but should also address the restoration of sensation .
	manualset3
91626	1	399237	13	NULL	NULL	0	NULL	doctor 	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Ideally , the doctor will inform the patient fully on the proposed treatment so as to assure the patient 's right to participate intelligently and freely in the decisions regarding his treatment .
	manualset3
91627	2	399237	13	NULL	NULL	0	NULL	patient	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Ideally , the doctor will inform the patient fully on the proposed treatment so as to assure the patient 's right to participate intelligently and freely in the decisions regarding his treatment .
	manualset3
91628	3	399237	13	NULL	NULL	0	NULL	treatment 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Ideally , the doctor will inform the patient fully on the proposed treatment so as to assure the patient 's right to participate intelligently and freely in the decisions regarding his treatment .
	manualset3
91629	4	399237	13	NULL	NULL	0	NULL	 patient 's	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Ideally , the doctor will inform the patient fully on the proposed treatment so as to assure the patient 's right to participate intelligently and freely in the decisions regarding his treatment .
	manualset3
91630	5	399237	13	NULL	NULL	NULL	NULL	decisions	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Ideally , the doctor will inform the patient fully on the proposed treatment so as to assure the patient 's right to participate intelligently and freely in the decisions regarding his treatment .
	manualset3
91631	6	399237	13	NULL	NULL	0	NULL	 treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Ideally , the doctor will inform the patient fully on the proposed treatment so as to assure the patient 's right to participate intelligently and freely in the decisions regarding his treatment .
	manualset3
91632	1	399238	13	NULL	NULL	0	NULL	diagnostic approach	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Ideally the diagnostic approach to an individual patient will be highly tailored , not only in regard to the nature of the pulmonary lesion , but also to his or her overall medical and social situation .
	manualset3
91633	2	399238	13	NULL	NULL	0	NULL	individual patient	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Ideally the diagnostic approach to an individual patient will be highly tailored , not only in regard to the nature of the pulmonary lesion , but also to his or her overall medical and social situation .
	manualset3
91634	3	399238	13	NULL	NULL	0	NULL	nature of the pulmonary lesion	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Ideally the diagnostic approach to an individual patient will be highly tailored , not only in regard to the nature of the pulmonary lesion , but also to his or her overall medical and social situation .
	manualset3
91635	4	399238	13	NULL	NULL	0	NULL	medical situation 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Ideally the diagnostic approach to an individual patient will be highly tailored , not only in regard to the nature of the pulmonary lesion , but also to his or her overall medical and social situation .
	manualset3
91636	5	399238	13	NULL	NULL	NULL	NULL	social situation	EnvironmentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Ideally the diagnostic approach to an individual patient will be highly tailored , not only in regard to the nature of the pulmonary lesion , but also to his or her overall medical and social situation .
	manualset3
91637	1	399239	13	NULL	NULL	0	NULL	Identical effects	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identical effects of the peptides were observed in identified gastric-related and unlabeled DMV neurons .
	manualset3
91638	2	399239	13	NULL	NULL	0	NULL	peptides 	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	Identical effects of the peptides were observed in identified gastric-related and unlabeled DMV neurons .
	manualset3
91639	3	399239	13	NULL	NULL	0	NULL	gastric-related neurons	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Identical effects of the peptides were observed in identified gastric-related and unlabeled DMV neurons .
	manualset3
91640	4	399239	13	NULL	NULL	0	NULL	unlabeled DMV neurons	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Identical effects of the peptides were observed in identified gastric-related and unlabeled DMV neurons .
	manualset3
91641	1	399240	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification and characterization of a rat hepatic oncofetal membrane glycoprotein .
	manualset3
91642	2	399240	13	NULL	NULL	0	NULL	characterization	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification and characterization of a rat hepatic oncofetal membrane glycoprotein .
	manualset3
91643	3	399240	13	NULL	NULL	0	NULL	rat hepatic oncofetal membrane glycoprotein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification and characterization of a rat hepatic oncofetal membrane glycoprotein .
	manualset3
91644	1	399241	13	NULL	NULL	0	NULL	Identification 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification and characterization of metal ion binding sites in RNA .
	manualset3
91645	2	399241	13	NULL	NULL	0	NULL	characterization	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification and characterization of metal ion binding sites in RNA .
	manualset3
91646	3	399241	13	NULL	NULL	0	NULL	 metal ion binding sites in RNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification and characterization of metal ion binding sites in RNA .
	manualset3
91647	1	399242	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification and molecular mapping of two QTLs with major effects for resistance to Fusarium head blight in wheat .
	manualset3
91648	2	399242	13	NULL	NULL	0	NULL	molecular mapping	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification and molecular mapping of two QTLs with major effects for resistance to Fusarium head blight in wheat .
	manualset3
91649	3	399242	13	NULL	NULL	0	NULL	two	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification and molecular mapping of two QTLs with major effects for resistance to Fusarium head blight in wheat .
	manualset3
91650	4	399242	13	NULL	NULL	0	NULL	QTLs	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification and molecular mapping of two QTLs with major effects for resistance to Fusarium head blight in wheat .
	manualset3
91651	5	399242	13	NULL	NULL	0	NULL	major effects for resistance	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification and molecular mapping of two QTLs with major effects for resistance to Fusarium head blight in wheat .
	manualset3
91652	6	399242	13	NULL	NULL	0	NULL	Fusarium head blight	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification and molecular mapping of two QTLs with major effects for resistance to Fusarium head blight in wheat .
	manualset3
91653	7	399242	13	NULL	NULL	0	NULL	wheat	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification and molecular mapping of two QTLs with major effects for resistance to Fusarium head blight in wheat .
	manualset3
91654	1	399243	13	NULL	NULL	0	NULL	teaching role	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( The teaching role of the midwife ) .
	manualset3
91655	2	399243	13	NULL	NULL	0	NULL	midwife	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	( The teaching role of the midwife ) .
	manualset3
91656	1	399244	13	NULL	NULL	0	NULL	Identification 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification and nucleotide sequence of the heat shock protein 60 ( GroEL ) gene of Bacteroides forsythus .
	manualset3
91657	2	399244	13	NULL	NULL	NULL	NULL	nucleotide sequence of the heat shock protein 60 ( GroEL ) gene 	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Identification and nucleotide sequence of the heat shock protein 60 ( GroEL ) gene of Bacteroides forsythus .
	manualset3
91658	3	399244	13	NULL	NULL	0	NULL	Bacteroides forsythus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification and nucleotide sequence of the heat shock protein 60 ( GroEL ) gene of Bacteroides forsythus .
	manualset3
91659	1	399245	13	NULL	NULL	0	NULL	Identification 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Acinetobacter species isolated from clinical specimens by amplified ribosomal DNA restriction analysis .
	manualset3
91660	2	399245	13	NULL	NULL	0	NULL	Acinetobacter species	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Acinetobacter species isolated from clinical specimens by amplified ribosomal DNA restriction analysis .
	manualset3
91661	3	399245	13	NULL	NULL	NULL	NULL	clinical specimens 	AnatomicalPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Identification of Acinetobacter species isolated from clinical specimens by amplified ribosomal DNA restriction analysis .
	manualset3
91662	4	399245	13	NULL	NULL	0	NULL	amplified ribosomal DNA restriction analysis 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Acinetobacter species isolated from clinical specimens by amplified ribosomal DNA restriction analysis .
	manualset3
91663	1	399246	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Candida dubliniensis based on temperature and utilization of xylose and alpha-methyl-D-glucoside as determined with the API 20C AUX and vitek YBC systems .
	manualset3
91664	2	399246	13	NULL	NULL	0	NULL	Candida dubliniensis	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Candida dubliniensis based on temperature and utilization of xylose and alpha-methyl-D-glucoside as determined with the API 20C AUX and vitek YBC systems .
	manualset3
91665	3	399246	13	NULL	NULL	0	NULL	temperature	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Candida dubliniensis based on temperature and utilization of xylose and alpha-methyl-D-glucoside as determined with the API 20C AUX and vitek YBC systems .
	manualset3
91666	4	399246	13	NULL	NULL	0	NULL	utilization of xylose	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Candida dubliniensis based on temperature and utilization of xylose and alpha-methyl-D-glucoside as determined with the API 20C AUX and vitek YBC systems .
	manualset3
91667	5	399246	13	NULL	NULL	0	NULL	 utilization of alpha-methyl-D-glucoside	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Candida dubliniensis based on temperature and utilization of xylose and alpha-methyl-D-glucoside as determined with the API 20C AUX and vitek YBC systems .
	manualset3
91668	6	399246	13	NULL	NULL	0	NULL	API 20C AUX	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Candida dubliniensis based on temperature and utilization of xylose and alpha-methyl-D-glucoside as determined with the API 20C AUX and vitek YBC systems .
	manualset3
91669	7	399246	13	NULL	NULL	0	NULL	vitek YBC systems	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Candida dubliniensis based on temperature and utilization of xylose and alpha-methyl-D-glucoside as determined with the API 20C AUX and vitek YBC systems .
	manualset3
91670	1	399247	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of NEEP21 as a - amyloid precursor protein-interacting protein in vivo that modulates amyloidogenic processing in vitro .
	manualset3
91671	2	399247	13	NULL	NULL	0	NULL	NEEP21	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of NEEP21 as a - amyloid precursor protein-interacting protein in vivo that modulates amyloidogenic processing in vitro .
	manualset3
91672	3	399247	13	NULL	NULL	0	NULL	a - amyloid precursor protein-interacting protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of NEEP21 as a - amyloid precursor protein-interacting protein in vivo that modulates amyloidogenic processing in vitro .
	manualset3
98571	4	399247	13	NULL	NULL	NULL	NULL	amyloidogenic processing	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Identification of NEEP21 as a - amyloid precursor protein-interacting protein in vivo that modulates amyloidogenic processing in vitro .
	manualset3
91673	1	399248	13	NULL	NULL	0	NULL	Identification 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Plum pox virus Determinants Implicated in Specific Interactions with Different Prunus spp .
	manualset3
91674	2	399248	13	NULL	NULL	0	NULL	Plum pox virus Determinants	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Plum pox virus Determinants Implicated in Specific Interactions with Different Prunus spp .
	manualset3
91675	3	399248	13	NULL	NULL	0	NULL	Specific Interactions	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Plum pox virus Determinants Implicated in Specific Interactions with Different Prunus spp .
	manualset3
91676	4	399248	13	NULL	NULL	0	NULL	Different Prunus spp	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Plum pox virus Determinants Implicated in Specific Interactions with Different Prunus spp .
	manualset3
91677	1	399249	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of SOX3 as an XX male sex reversal gene in mice and humans .
	manualset3
91678	2	399249	13	NULL	NULL	0	NULL	SOX3	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of SOX3 as an XX male sex reversal gene in mice and humans .
	manualset3
91679	3	399249	13	NULL	NULL	0	NULL	XX male sex reversal gene	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of SOX3 as an XX male sex reversal gene in mice and humans .
	manualset3
91680	4	399249	13	NULL	NULL	0	NULL	 mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of SOX3 as an XX male sex reversal gene in mice and humans .
	manualset3
91681	5	399249	13	NULL	NULL	0	NULL	humans	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of SOX3 as an XX male sex reversal gene in mice and humans .
	manualset3
91682	1	399250	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Staphylococcus aureus ( food laboratories ) : microscopic observation , catalase activity , coagulase production , thermonuclease production , and ( optional ) lysostaphin sensitivity .
	manualset3
91683	2	399250	13	NULL	NULL	0	NULL	Staphylococcus aureus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Staphylococcus aureus ( food laboratories ) : microscopic observation , catalase activity , coagulase production , thermonuclease production , and ( optional ) lysostaphin sensitivity .
	manualset3
91684	3	399250	13	NULL	NULL	0	NULL	food laboratories	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Staphylococcus aureus ( food laboratories ) : microscopic observation , catalase activity , coagulase production , thermonuclease production , and ( optional ) lysostaphin sensitivity .
	manualset3
91685	4	399250	13	NULL	NULL	0	NULL	microscopic observation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Staphylococcus aureus ( food laboratories ) : microscopic observation , catalase activity , coagulase production , thermonuclease production , and ( optional ) lysostaphin sensitivity .
	manualset3
91686	5	399250	13	NULL	NULL	0	NULL	catalase activity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Staphylococcus aureus ( food laboratories ) : microscopic observation , catalase activity , coagulase production , thermonuclease production , and ( optional ) lysostaphin sensitivity .
	manualset3
91687	6	399250	13	NULL	NULL	0	NULL	 coagulase production 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Staphylococcus aureus ( food laboratories ) : microscopic observation , catalase activity , coagulase production , thermonuclease production , and ( optional ) lysostaphin sensitivity .
	manualset3
91688	7	399250	13	NULL	NULL	0	NULL	thermonuclease production	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Staphylococcus aureus ( food laboratories ) : microscopic observation , catalase activity , coagulase production , thermonuclease production , and ( optional ) lysostaphin sensitivity .
	manualset3
91689	8	399250	13	NULL	NULL	0	NULL	lysostaphin sensitivity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of Staphylococcus aureus ( food laboratories ) : microscopic observation , catalase activity , coagulase production , thermonuclease production , and ( optional ) lysostaphin sensitivity .
	manualset3
91690	1	399251	13	NULL	NULL	0	NULL	Identification 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a diacylglycerol acyltransferase 2 gene involved in pheromone biosynthesis activating neuropeptide stimulated pheromone production in Bombyx mori .
	manualset3
91691	2	399251	13	NULL	NULL	0	NULL	diacylglycerol acyltransferase 2 gene	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a diacylglycerol acyltransferase 2 gene involved in pheromone biosynthesis activating neuropeptide stimulated pheromone production in Bombyx mori .
	manualset3
91692	3	399251	13	NULL	NULL	0	NULL	pheromone biosynthesis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a diacylglycerol acyltransferase 2 gene involved in pheromone biosynthesis activating neuropeptide stimulated pheromone production in Bombyx mori .
	manualset3
91693	4	399251	13	NULL	NULL	0	NULL	neuropeptide	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a diacylglycerol acyltransferase 2 gene involved in pheromone biosynthesis activating neuropeptide stimulated pheromone production in Bombyx mori .
	manualset3
91694	5	399251	13	NULL	NULL	0	NULL	pheromone production	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a diacylglycerol acyltransferase 2 gene involved in pheromone biosynthesis activating neuropeptide stimulated pheromone production in Bombyx mori .
	manualset3
91695	6	399251	13	NULL	NULL	0	NULL	Bombyx mori 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a diacylglycerol acyltransferase 2 gene involved in pheromone biosynthesis activating neuropeptide stimulated pheromone production in Bombyx mori .
	manualset3
91696	1	399252	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a dominant form in a blood smear provides a clue to diagnosis .
	manualset3
91697	2	399252	13	NULL	NULL	0	NULL	dominant form	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a dominant form in a blood smear provides a clue to diagnosis .
	manualset3
91698	3	399252	13	NULL	NULL	0	NULL	blood smear	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a dominant form in a blood smear provides a clue to diagnosis .
	manualset3
91699	4	399252	13	NULL	NULL	0	NULL	diagnosis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a dominant form in a blood smear provides a clue to diagnosis .
	manualset3
91700	5	399252	13	NULL	NULL	0	NULL	clue	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a dominant form in a blood smear provides a clue to diagnosis .
	manualset3
91701	1	399253	13	NULL	NULL	0	NULL	technique of obtaining gastric juice	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The technique of obtaining gastric juice from dogs with a small Pavlov 's pouch ) .
	manualset3
91702	2	399253	13	NULL	NULL	0	NULL	dogs	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( The technique of obtaining gastric juice from dogs with a small Pavlov 's pouch ) .
	manualset3
91703	3	399253	13	NULL	NULL	0	NULL	small Pavlov 's pouch	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( The technique of obtaining gastric juice from dogs with a small Pavlov 's pouch ) .
	manualset3
91704	1	399254	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a novel proinflammatory human skin-homing V9V2 T cell subset with a potential role in psoriasis .
	manualset3
91705	2	399254	13	NULL	NULL	0	NULL	a novel proinflammatory human skin-homing V9V2 T cell subset	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a novel proinflammatory human skin-homing V9V2 T cell subset with a potential role in psoriasis .
	manualset3
91706	3	399254	13	NULL	NULL	0	NULL	potential role	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a novel proinflammatory human skin-homing V9V2 T cell subset with a potential role in psoriasis .
	manualset3
91707	4	399254	13	NULL	NULL	0	NULL	psoriasis 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a novel proinflammatory human skin-homing V9V2 T cell subset with a potential role in psoriasis .
	manualset3
91708	1	399255	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a protein that interacts with the golli-myelin basic protein and with nuclear LIM interactor in the nervous system .
	manualset3
91709	2	399255	13	NULL	NULL	0	NULL	protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a protein that interacts with the golli-myelin basic protein and with nuclear LIM interactor in the nervous system .
	manualset3
91710	3	399255	13	NULL	NULL	0	NULL	 golli-myelin basic protein 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a protein that interacts with the golli-myelin basic protein and with nuclear LIM interactor in the nervous system .
	manualset3
91711	4	399255	13	NULL	NULL	0	NULL	nuclear LIM interactor	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a protein that interacts with the golli-myelin basic protein and with nuclear LIM interactor in the nervous system .
	manualset3
91712	5	399255	13	NULL	NULL	0	NULL	nervous system	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of a protein that interacts with the golli-myelin basic protein and with nuclear LIM interactor in the nervous system .
	manualset3
91713	1	399256	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of additional target sites downstream of COX may benefit the ) 27 , 000 patients whom die annually from cirrhosis in the United States alone .
	manualset3
91714	2	399256	13	NULL	NULL	0	NULL	 target sites downstream of COX	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of additional target sites downstream of COX may benefit the ) 27 , 000 patients whom die annually from cirrhosis in the United States alone .
	manualset3
91715	3	399256	13	NULL	NULL	0	NULL	 benefit	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of additional target sites downstream of COX may benefit the ) 27 , 000 patients whom die annually from cirrhosis in the United States alone .
	manualset3
91716	4	399256	13	NULL	NULL	0	NULL	27 , 000	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of additional target sites downstream of COX may benefit the ) 27 , 000 patients whom die annually from cirrhosis in the United States alone .
	manualset3
91717	5	399256	13	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of additional target sites downstream of COX may benefit the ) 27 , 000 patients whom die annually from cirrhosis in the United States alone .
	manualset3
91719	7	399256	13	NULL	NULL	0	NULL	cirrhosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of additional target sites downstream of COX may benefit the ) 27 , 000 patients whom die annually from cirrhosis in the United States alone .
	manualset3
91720	8	399256	13	NULL	NULL	0	NULL	United States	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of additional target sites downstream of COX may benefit the ) 27 , 000 patients whom die annually from cirrhosis in the United States alone .
	manualset3
91721	1	399257	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of amino acid residues essential for the substrate specificity of Flavobacterium sp .
	manualset3
91722	2	399257	13	NULL	NULL	0	NULL	 amino acid residues	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of amino acid residues essential for the substrate specificity of Flavobacterium sp .
	manualset3
91723	3	399257	13	NULL	NULL	0	NULL	substrate specificity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of amino acid residues essential for the substrate specificity of Flavobacterium sp .
	manualset3
91724	4	399257	13	NULL	NULL	0	NULL	Flavobacterium sp	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of amino acid residues essential for the substrate specificity of Flavobacterium sp .
	manualset3
91725	1	399258	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of beta-hemolytic streptococci isolated from hospitalized children in Baghdad .
	manualset3
91726	2	399258	13	NULL	NULL	0	NULL	beta-hemolytic streptococci 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of beta-hemolytic streptococci isolated from hospitalized children in Baghdad .
	manualset3
91727	3	399258	13	NULL	NULL	NULL	NULL	children	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Identification of beta-hemolytic streptococci isolated from hospitalized children in Baghdad .
	manualset3
91728	4	399258	13	NULL	NULL	0	NULL	Baghdad	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of beta-hemolytic streptococci isolated from hospitalized children in Baghdad .
	manualset3
91729	1	399259	13	NULL	NULL	0	NULL	Identification 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of beta adrenoreceptors during thymocyte ontogeny in mice .
	manualset3
91730	2	399259	13	NULL	NULL	0	NULL	beta adrenoreceptors	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of beta adrenoreceptors during thymocyte ontogeny in mice .
	manualset3
91731	3	399259	13	NULL	NULL	0	NULL	thymocyte ontogeny	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of beta adrenoreceptors during thymocyte ontogeny in mice .
	manualset3
91732	4	399259	13	NULL	NULL	0	NULL	mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of beta adrenoreceptors during thymocyte ontogeny in mice .
	manualset3
91733	1	399260	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of bovine brain calcium binding proteins .
	manualset3
91734	2	399260	13	NULL	NULL	0	NULL	bovine brain calcium binding proteins	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of bovine brain calcium binding proteins .
	manualset3
91735	1	399261	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of genetic parameters associated with disease progression in plasma cell myeloma .
	manualset3
91736	2	399261	13	NULL	NULL	0	NULL	genetic parameters	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of genetic parameters associated with disease progression in plasma cell myeloma .
	manualset3
91737	3	399261	13	NULL	NULL	0	NULL	disease progression	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of genetic parameters associated with disease progression in plasma cell myeloma .
	manualset3
91738	4	399261	13	NULL	NULL	0	NULL	plasma cell myeloma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of genetic parameters associated with disease progression in plasma cell myeloma .
	manualset3
91739	1	399262	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of homocystinuric newborns is hindered by the pitfalls of neonatal screening programs .
	manualset3
91740	2	399262	13	NULL	NULL	0	NULL	homocystinuric newborns	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of homocystinuric newborns is hindered by the pitfalls of neonatal screening programs .
	manualset3
91741	3	399262	13	NULL	NULL	0	NULL	 neonatal screening programs	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of homocystinuric newborns is hindered by the pitfalls of neonatal screening programs .
	manualset3
91743	1	399263	13	NULL	NULL	0	NULL	aprophen	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( The use of aprophen in internal diseases ) .
	manualset3
91744	2	399263	13	NULL	NULL	0	NULL	 internal diseases	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( The use of aprophen in internal diseases ) .
	manualset3
91745	1	399264	13	NULL	NULL	0	NULL	Identification 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of intimin alleles in pathogenic Escherichia coli by PCR-restriction fragment length polymorphism analysis .
	manualset3
91746	2	399264	13	NULL	NULL	0	NULL	 intimin alleles 	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of intimin alleles in pathogenic Escherichia coli by PCR-restriction fragment length polymorphism analysis .
	manualset3
91747	3	399264	13	NULL	NULL	0	NULL	pathogenic Escherichia coli	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of intimin alleles in pathogenic Escherichia coli by PCR-restriction fragment length polymorphism analysis .
	manualset3
91749	4	399264	13	NULL	NULL	0	NULL	PCR-restriction fragment length polymorphism analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of intimin alleles in pathogenic Escherichia coli by PCR-restriction fragment length polymorphism analysis .
	manualset3
91750	1	399265	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of macrophages in sections of rabbit lung using acetoacetylated lipoproteins .
	manualset3
91751	2	399265	13	NULL	NULL	0	NULL	macrophages	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of macrophages in sections of rabbit lung using acetoacetylated lipoproteins .
	manualset3
91752	3	399265	13	NULL	NULL	0	NULL	sections of rabbit lung 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of macrophages in sections of rabbit lung using acetoacetylated lipoproteins .
	manualset3
91753	4	399265	13	NULL	NULL	0	NULL	acetoacetylated lipoproteins	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of macrophages in sections of rabbit lung using acetoacetylated lipoproteins .
	manualset3
91754	1	399266	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of muscle-specific calpain and beta-sarcoglycan genes in progressive autosomal recessive muscular dystrophies .
	manualset3
91755	2	399266	13	NULL	NULL	NULL	NULL	muscle-specific calpain gene	Gene												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Identification of muscle-specific calpain and beta-sarcoglycan genes in progressive autosomal recessive muscular dystrophies .
	manualset3
91756	3	399266	13	NULL	NULL	NULL	NULL	beta-sarcoglycan gene	Gene												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Identification of muscle-specific calpain and beta-sarcoglycan genes in progressive autosomal recessive muscular dystrophies .
	manualset3
91757	4	399266	13	NULL	NULL	0	NULL	 progressive autosomal recessive muscular dystrophies	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of muscle-specific calpain and beta-sarcoglycan genes in progressive autosomal recessive muscular dystrophies .
	manualset3
91758	1	399267	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of several clinical isolates of dermatophytes based on the nucleotide sequence of internal transcribed spacer 1 ( ITS 1 ) in nuclear ribosomal DNA .
	manualset3
91759	2	399267	13	NULL	NULL	0	NULL	clinical isolates of dermatophytes	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of several clinical isolates of dermatophytes based on the nucleotide sequence of internal transcribed spacer 1 ( ITS 1 ) in nuclear ribosomal DNA .
	manualset3
91760	3	399267	13	NULL	NULL	0	NULL	nucleotide sequence of internal transcribed spacer 1 ( ITS 1 ) 	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of several clinical isolates of dermatophytes based on the nucleotide sequence of internal transcribed spacer 1 ( ITS 1 ) in nuclear ribosomal DNA .
	manualset3
91761	4	399267	13	NULL	NULL	0	NULL	nuclear ribosomal DNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of several clinical isolates of dermatophytes based on the nucleotide sequence of internal transcribed spacer 1 ( ITS 1 ) in nuclear ribosomal DNA .
	manualset3
91762	1	399268	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of the gene encoding sulfopyruvate decarboxylase , an enzyme involved in biosynthesis of coenzyme M .
	manualset3
91763	2	399268	13	NULL	NULL	NULL	NULL	gene 	Gene												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Identification of the gene encoding sulfopyruvate decarboxylase , an enzyme involved in biosynthesis of coenzyme M .
	manualset3
91764	4	399268	13	NULL	NULL	NULL	NULL	enzyme	Gene												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Identification of the gene encoding sulfopyruvate decarboxylase , an enzyme involved in biosynthesis of coenzyme M .
	manualset3
92466	5	399268	13	NULL	NULL	NULL	NULL	 biosynthesis of coenzyme M	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Identification of the gene encoding sulfopyruvate decarboxylase , an enzyme involved in biosynthesis of coenzyme M .
	manualset3
92471	3	399268	13	NULL	NULL	0	NULL	sulfopyruvate decarboxylase	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of the gene encoding sulfopyruvate decarboxylase , an enzyme involved in biosynthesis of coenzyme M .
	manualset3
91765	1	399269	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of the molecular lesions covering the gamut of MFS clinical variability should allow the construction of genotype/phenotype correlations .
	manualset3
91766	2	399269	13	NULL	NULL	0	NULL	molecular lesions 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of the molecular lesions covering the gamut of MFS clinical variability should allow the construction of genotype/phenotype correlations .
	manualset3
91767	3	399269	13	NULL	NULL	0	NULL	gamut of MFS clinical variability	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of the molecular lesions covering the gamut of MFS clinical variability should allow the construction of genotype/phenotype correlations .
	manualset3
91768	4	399269	13	NULL	NULL	0	NULL	construction	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of the molecular lesions covering the gamut of MFS clinical variability should allow the construction of genotype/phenotype correlations .
	manualset3
91769	5	399269	13	NULL	NULL	0	NULL	genotype/phenotype correlations 	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of the molecular lesions covering the gamut of MFS clinical variability should allow the construction of genotype/phenotype correlations .
	manualset3
91770	1	399270	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of the molecular mechanisms of VSMC activation is crucial in understanding the initiation of vascular restenosis .
	manualset3
91771	2	399270	13	NULL	NULL	0	NULL	molecular mechanisms 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of the molecular mechanisms of VSMC activation is crucial in understanding the initiation of vascular restenosis .
	manualset3
91772	3	399270	13	NULL	NULL	0	NULL	VSMC activation 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of the molecular mechanisms of VSMC activation is crucial in understanding the initiation of vascular restenosis .
	manualset3
91773	4	399270	13	NULL	NULL	0	NULL	initiation of vascular restenosis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of the molecular mechanisms of VSMC activation is crucial in understanding the initiation of vascular restenosis .
	manualset3
91774	1	399271	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of these proteins and their binding affinities for Abeta are needed to assess their potential role in the pathogenesis of Alzheimer 's disease .
	manualset3
91775	2	399271	13	NULL	NULL	0	NULL	 proteins	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of these proteins and their binding affinities for Abeta are needed to assess their potential role in the pathogenesis of Alzheimer 's disease .
	manualset3
91776	3	399271	13	NULL	NULL	0	NULL	binding affinities	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of these proteins and their binding affinities for Abeta are needed to assess their potential role in the pathogenesis of Alzheimer 's disease .
	manualset3
91777	4	399271	13	NULL	NULL	0	NULL	 Abeta 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of these proteins and their binding affinities for Abeta are needed to assess their potential role in the pathogenesis of Alzheimer 's disease .
	manualset3
91778	5	399271	13	NULL	NULL	0	NULL	potential role	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of these proteins and their binding affinities for Abeta are needed to assess their potential role in the pathogenesis of Alzheimer 's disease .
	manualset3
91779	6	399271	13	NULL	NULL	0	NULL	 pathogenesis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of these proteins and their binding affinities for Abeta are needed to assess their potential role in the pathogenesis of Alzheimer 's disease .
	manualset3
91780	7	399271	13	NULL	NULL	0	NULL	Alzheimer 's disease 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of these proteins and their binding affinities for Abeta are needed to assess their potential role in the pathogenesis of Alzheimer 's disease .
	manualset3
91781	1	399272	13	NULL	NULL	0	NULL	Anemia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Anemia in chronic renal insufficiency and chronic failure ) .
	manualset3
91782	2	399272	13	NULL	NULL	0	NULL	chronic renal insufficiency	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Anemia in chronic renal insufficiency and chronic failure ) .
	manualset3
91783	3	399272	13	NULL	NULL	0	NULL	chronic failure	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Anemia in chronic renal insufficiency and chronic failure ) .
	manualset3
91784	1	399273	13	NULL	NULL	0	NULL	corticosteroids	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( The use of corticosteroids in intensive care unit ( author 's transl ) ) .
	manualset3
91785	2	399273	13	NULL	NULL	0	NULL	intensive care unit	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	( The use of corticosteroids in intensive care unit ( author 's transl ) ) .
	manualset3
91786	3	399273	13	NULL	NULL	0	NULL	author 's	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	( The use of corticosteroids in intensive care unit ( author 's transl ) ) .
	manualset3
91787	1	399274	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of two regulatory elements within the promoter region of the mouse connexin 43 gene .
	manualset3
91788	2	399274	13	NULL	NULL	0	NULL	two regulatory elements	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of two regulatory elements within the promoter region of the mouse connexin 43 gene .
	manualset3
91789	3	399274	13	NULL	NULL	0	NULL	promoter region of the mouse connexin 43 gene	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of two regulatory elements within the promoter region of the mouse connexin 43 gene .
	manualset3
91790	1	399275	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of very few cynomolgus monkey-specific framework region residues suggests a role for cynomolgus monkey antibodies as donators of variable regions to chimeric monoclonal antibodies for utilisation in human therapy with human constant ( C ) regions .
	manualset3
91791	2	399275	13	NULL	NULL	0	NULL	 cynomolgus monkey-specific framework region residues	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of very few cynomolgus monkey-specific framework region residues suggests a role for cynomolgus monkey antibodies as donators of variable regions to chimeric monoclonal antibodies for utilisation in human therapy with human constant ( C ) regions .
	manualset3
91792	3	399275	13	NULL	NULL	0	NULL	role	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of very few cynomolgus monkey-specific framework region residues suggests a role for cynomolgus monkey antibodies as donators of variable regions to chimeric monoclonal antibodies for utilisation in human therapy with human constant ( C ) regions .
	manualset3
91793	4	399275	13	NULL	NULL	NULL	NULL	cynomolgus monkey antibodies	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Identification of very few cynomolgus monkey-specific framework region residues suggests a role for cynomolgus monkey antibodies as donators of variable regions to chimeric monoclonal antibodies for utilisation in human therapy with human constant ( C ) regions .
	manualset3
91794	5	399275	13	NULL	NULL	0	NULL	donators of variable regions	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of very few cynomolgus monkey-specific framework region residues suggests a role for cynomolgus monkey antibodies as donators of variable regions to chimeric monoclonal antibodies for utilisation in human therapy with human constant ( C ) regions .
	manualset3
91795	6	399275	13	NULL	NULL	0	NULL	chimeric monoclonal antibodies	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of very few cynomolgus monkey-specific framework region residues suggests a role for cynomolgus monkey antibodies as donators of variable regions to chimeric monoclonal antibodies for utilisation in human therapy with human constant ( C ) regions .
	manualset3
91796	7	399275	13	NULL	NULL	0	NULL	utilisation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of very few cynomolgus monkey-specific framework region residues suggests a role for cynomolgus monkey antibodies as donators of variable regions to chimeric monoclonal antibodies for utilisation in human therapy with human constant ( C ) regions .
	manualset3
91797	8	399275	13	NULL	NULL	0	NULL	human therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of very few cynomolgus monkey-specific framework region residues suggests a role for cynomolgus monkey antibodies as donators of variable regions to chimeric monoclonal antibodies for utilisation in human therapy with human constant ( C ) regions .
	manualset3
91798	9	399275	13	NULL	NULL	NULL	NULL	human constant ( C ) regions	AminoAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Identification of very few cynomolgus monkey-specific framework region residues suggests a role for cynomolgus monkey antibodies as donators of variable regions to chimeric monoclonal antibodies for utilisation in human therapy with human constant ( C ) regions .
	manualset3
91799	1	399276	13	NULL	NULL	0	NULL	Identification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of viruses in a study of acute respiratory tract infection in children from Uruguay .
	manualset3
91800	2	399276	13	NULL	NULL	0	NULL	viruses	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of viruses in a study of acute respiratory tract infection in children from Uruguay .
	manualset3
91801	3	399276	13	NULL	NULL	NULL	NULL	study 	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Identification of viruses in a study of acute respiratory tract infection in children from Uruguay .
	manualset3
91802	4	399276	13	NULL	NULL	0	NULL	acute respiratory tract infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of viruses in a study of acute respiratory tract infection in children from Uruguay .
	manualset3
91803	5	399276	13	NULL	NULL	0	NULL	children	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of viruses in a study of acute respiratory tract infection in children from Uruguay .
	manualset3
91804	6	399276	13	NULL	NULL	0	NULL	Uruguay	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Identification of viruses in a study of acute respiratory tract infection in children from Uruguay .
	manualset3
91805	1	399277	13	NULL	NULL	0	NULL	epitopes	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Identifying epitopes that elicit a major histocompatibility complex ( MHC ) - restricted T-cell response is critical for designing vaccines for infectious diseases and cancers .
	manualset3
91806	2	399277	13	NULL	NULL	0	NULL	major histocompatibility complex ( MHC ) - restricted T-cell response	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identifying epitopes that elicit a major histocompatibility complex ( MHC ) - restricted T-cell response is critical for designing vaccines for infectious diseases and cancers .
	manualset3
91807	3	399277	13	NULL	NULL	0	NULL	designing vaccines	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Identifying epitopes that elicit a major histocompatibility complex ( MHC ) - restricted T-cell response is critical for designing vaccines for infectious diseases and cancers .
	manualset3
91808	4	399277	13	NULL	NULL	0	NULL	infectious diseases 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Identifying epitopes that elicit a major histocompatibility complex ( MHC ) - restricted T-cell response is critical for designing vaccines for infectious diseases and cancers .
	manualset3
91809	5	399277	13	NULL	NULL	0	NULL	cancers	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Identifying epitopes that elicit a major histocompatibility complex ( MHC ) - restricted T-cell response is critical for designing vaccines for infectious diseases and cancers .
	manualset3
91810	1	399278	13	NULL	NULL	0	NULL	hypoxemia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Identifying hypoxemia in children admitted for adenotonsillectomy .
	manualset3
91811	2	399278	13	NULL	NULL	0	NULL	children 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Identifying hypoxemia in children admitted for adenotonsillectomy .
	manualset3
91812	3	399278	13	NULL	NULL	0	NULL	 adenotonsillectomy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Identifying hypoxemia in children admitted for adenotonsillectomy .
	manualset3
91813	1	399279	13	NULL	NULL	0	NULL	intracellular targets	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Identifying the appropriate intracellular targets and understanding the signal transduction pathways in which these molecules participate are critical to this process .
	manualset3
91814	2	399279	13	NULL	NULL	0	NULL	signal transduction pathways	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identifying the appropriate intracellular targets and understanding the signal transduction pathways in which these molecules participate are critical to this process .
	manualset3
91815	3	399279	13	NULL	NULL	0	NULL	molecules	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Identifying the appropriate intracellular targets and understanding the signal transduction pathways in which these molecules participate are critical to this process .
	manualset3
91816	4	399279	13	NULL	NULL	0	NULL	 process	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identifying the appropriate intracellular targets and understanding the signal transduction pathways in which these molecules participate are critical to this process .
	manualset3
91817	1	399280	13	NULL	NULL	0	NULL	role 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identifying the role of Refilins in organizing perinuclear actin networks provides additional insight in the process of intracellular mechanotransduction that regulate changes in cellular phenotype such as those observed during EMT .
	manualset3
91818	2	399280	13	NULL	NULL	0	NULL	Refilins	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Identifying the role of Refilins in organizing perinuclear actin networks provides additional insight in the process of intracellular mechanotransduction that regulate changes in cellular phenotype such as those observed during EMT .
	manualset3
91823	3	399280	13	NULL	NULL	0	NULL	perinuclear actin networks 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identifying the role of Refilins in organizing perinuclear actin networks provides additional insight in the process of intracellular mechanotransduction that regulate changes in cellular phenotype such as those observed during EMT .
	manualset3
91824	4	399280	13	NULL	NULL	0	NULL	process of intracellular mechanotransduction	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identifying the role of Refilins in organizing perinuclear actin networks provides additional insight in the process of intracellular mechanotransduction that regulate changes in cellular phenotype such as those observed during EMT .
	manualset3
91826	5	399280	13	NULL	NULL	0	NULL	changes in cellular phenotype	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identifying the role of Refilins in organizing perinuclear actin networks provides additional insight in the process of intracellular mechanotransduction that regulate changes in cellular phenotype such as those observed during EMT .
	manualset3
91827	6	399280	13	NULL	NULL	0	NULL	EMT	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Identifying the role of Refilins in organizing perinuclear actin networks provides additional insight in the process of intracellular mechanotransduction that regulate changes in cellular phenotype such as those observed during EMT .
	manualset3
91830	1	399281	13	NULL	NULL	0	NULL	Idiopathic intracranial hypertension	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Idiopathic intracranial hypertension and anticardolipin antibodies .
	manualset3
91832	2	399281	13	NULL	NULL	0	NULL	 anticardolipin antibodies	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Idiopathic intracranial hypertension and anticardolipin antibodies .
	manualset3
91834	1	399282	13	NULL	NULL	0	NULL	Idiopathic portal hypertension 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Idiopathic portal hypertension : a case report .
	manualset3
91836	2	399282	13	NULL	NULL	0	NULL	a case report	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Idiopathic portal hypertension : a case report .
	manualset3
91839	1	399283	13	NULL	NULL	0	NULL	pathogenesis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If , as has been suggested , the pathogenesis of wound healing and tumor stroma generation is similar and dependent on fibrin deposition , then the types and amounts of fibrin deposited in wounds and tumors might also be expected to be similar .
	manualset3
91841	2	399283	13	NULL	NULL	0	NULL	wound healing 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If , as has been suggested , the pathogenesis of wound healing and tumor stroma generation is similar and dependent on fibrin deposition , then the types and amounts of fibrin deposited in wounds and tumors might also be expected to be similar .
	manualset3
91842	3	399283	13	NULL	NULL	0	NULL	tumor stroma generation	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If , as has been suggested , the pathogenesis of wound healing and tumor stroma generation is similar and dependent on fibrin deposition , then the types and amounts of fibrin deposited in wounds and tumors might also be expected to be similar .
	manualset3
91843	4	399283	13	NULL	NULL	0	NULL	fibrin deposition	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	If , as has been suggested , the pathogenesis of wound healing and tumor stroma generation is similar and dependent on fibrin deposition , then the types and amounts of fibrin deposited in wounds and tumors might also be expected to be similar .
	manualset3
91844	5	399283	13	NULL	NULL	0	NULL	types of fibrin	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	If , as has been suggested , the pathogenesis of wound healing and tumor stroma generation is similar and dependent on fibrin deposition , then the types and amounts of fibrin deposited in wounds and tumors might also be expected to be similar .
	manualset3
91845	6	399283	13	NULL	NULL	0	NULL	amounts of fibrin	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	If , as has been suggested , the pathogenesis of wound healing and tumor stroma generation is similar and dependent on fibrin deposition , then the types and amounts of fibrin deposited in wounds and tumors might also be expected to be similar .
	manualset3
91846	7	399283	13	NULL	NULL	0	NULL	wounds	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If , as has been suggested , the pathogenesis of wound healing and tumor stroma generation is similar and dependent on fibrin deposition , then the types and amounts of fibrin deposited in wounds and tumors might also be expected to be similar .
	manualset3
91847	8	399283	13	NULL	NULL	0	NULL	tumors 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If , as has been suggested , the pathogenesis of wound healing and tumor stroma generation is similar and dependent on fibrin deposition , then the types and amounts of fibrin deposited in wounds and tumors might also be expected to be similar .
	manualset3
91848	1	399284	13	NULL	NULL	0	NULL	PIU	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	If PIU and these co-occurring disorders could be explained by shared risk factors or better as secondary disorders is largely unknown .
	manualset3
91849	2	399284	13	NULL	NULL	0	NULL	 disorders	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If PIU and these co-occurring disorders could be explained by shared risk factors or better as secondary disorders is largely unknown .
	manualset3
91850	3	399284	13	NULL	NULL	0	NULL	risk factors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If PIU and these co-occurring disorders could be explained by shared risk factors or better as secondary disorders is largely unknown .
	manualset3
91851	4	399284	13	NULL	NULL	0	NULL	secondary disorders 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If PIU and these co-occurring disorders could be explained by shared risk factors or better as secondary disorders is largely unknown .
	manualset3
91852	1	399285	13	NULL	NULL	0	NULL	male 	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	If a male has a paternity of less than unity , then another male or other males must have gained the lost paternity .
	manualset3
91855	2	399285	13	NULL	NULL	0	NULL	paternity of less than unity	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	If a male has a paternity of less than unity , then another male or other males must have gained the lost paternity .
	manualset3
91856	3	399285	13	NULL	NULL	0	NULL	male 	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	If a male has a paternity of less than unity , then another male or other males must have gained the lost paternity .
	manualset3
91857	4	399285	13	NULL	NULL	0	NULL	males	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	If a male has a paternity of less than unity , then another male or other males must have gained the lost paternity .
	manualset3
91860	5	399285	13	NULL	NULL	0	NULL	paternity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	If a male has a paternity of less than unity , then another male or other males must have gained the lost paternity .
	manualset3
91861	1	399286	13	NULL	NULL	0	NULL	patient	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	If a patient is predicted to derive little advantage from chemotherapy in the adjuvant setting , it is equally unlikely that an advantage will be seen with neoadjuvant chemotherapy .
	manualset3
91863	2	399286	13	NULL	NULL	0	NULL	 chemotherapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If a patient is predicted to derive little advantage from chemotherapy in the adjuvant setting , it is equally unlikely that an advantage will be seen with neoadjuvant chemotherapy .
	manualset3
91864	3	399286	13	NULL	NULL	0	NULL	adjuvant setting	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If a patient is predicted to derive little advantage from chemotherapy in the adjuvant setting , it is equally unlikely that an advantage will be seen with neoadjuvant chemotherapy .
	manualset3
91865	4	399286	13	NULL	NULL	0	NULL	neoadjuvant chemotherapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If a patient is predicted to derive little advantage from chemotherapy in the adjuvant setting , it is equally unlikely that an advantage will be seen with neoadjuvant chemotherapy .
	manualset3
91867	5	399286	13	NULL	NULL	0	NULL	advantage	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If a patient is predicted to derive little advantage from chemotherapy in the adjuvant setting , it is equally unlikely that an advantage will be seen with neoadjuvant chemotherapy .
	manualset3
91868	6	399286	13	NULL	NULL	0	NULL	 advantage 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If a patient is predicted to derive little advantage from chemotherapy in the adjuvant setting , it is equally unlikely that an advantage will be seen with neoadjuvant chemotherapy .
	manualset3
91869	1	399287	13	NULL	NULL	0	NULL	working diagnosis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If a working diagnosis of congestive heart failure was made only on the basis of the most common probability , and the fluid supply was restricted , HHNKDC would readily occur or be aggravated by the dehydration iatrogenically produced .
	manualset3
91870	2	399287	13	NULL	NULL	0	NULL	 congestive heart failure 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If a working diagnosis of congestive heart failure was made only on the basis of the most common probability , and the fluid supply was restricted , HHNKDC would readily occur or be aggravated by the dehydration iatrogenically produced .
	manualset3
91871	3	399287	13	NULL	NULL	0	NULL	common probability	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	If a working diagnosis of congestive heart failure was made only on the basis of the most common probability , and the fluid supply was restricted , HHNKDC would readily occur or be aggravated by the dehydration iatrogenically produced .
	manualset3
91872	4	399287	13	NULL	NULL	NULL	NULL	fluid 	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	If a working diagnosis of congestive heart failure was made only on the basis of the most common probability , and the fluid supply was restricted , HHNKDC would readily occur or be aggravated by the dehydration iatrogenically produced .
	manualset3
91873	5	399287	13	NULL	NULL	0	NULL	HHNKDC 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If a working diagnosis of congestive heart failure was made only on the basis of the most common probability , and the fluid supply was restricted , HHNKDC would readily occur or be aggravated by the dehydration iatrogenically produced .
	manualset3
91874	6	399287	13	NULL	NULL	0	NULL	dehydration	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If a working diagnosis of congestive heart failure was made only on the basis of the most common probability , and the fluid supply was restricted , HHNKDC would readily occur or be aggravated by the dehydration iatrogenically produced .
	manualset3
91875	1	399288	13	NULL	NULL	0	NULL	 interferometer	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	If an interferometer is available for quantitative wave-front analysis on the production line , the point-spread function may quite easily be computed from an interferogram of the wave front in the back focal plane of a micro-objective .
	manualset3
91877	2	399288	13	NULL	NULL	0	NULL	quantitative wave-front analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	If an interferometer is available for quantitative wave-front analysis on the production line , the point-spread function may quite easily be computed from an interferogram of the wave front in the back focal plane of a micro-objective .
	manualset3
91895	3	399288	13	NULL	NULL	0	NULL	production line 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If an interferometer is available for quantitative wave-front analysis on the production line , the point-spread function may quite easily be computed from an interferogram of the wave front in the back focal plane of a micro-objective .
	manualset3
91896	4	399288	13	NULL	NULL	0	NULL	point-spread function 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If an interferometer is available for quantitative wave-front analysis on the production line , the point-spread function may quite easily be computed from an interferogram of the wave front in the back focal plane of a micro-objective .
	manualset3
91897	5	399288	13	NULL	NULL	0	NULL	interferogram of the wave front 	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	If an interferometer is available for quantitative wave-front analysis on the production line , the point-spread function may quite easily be computed from an interferogram of the wave front in the back focal plane of a micro-objective .
	manualset3
91898	6	399288	13	NULL	NULL	0	NULL	back focal plane 	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	If an interferometer is available for quantitative wave-front analysis on the production line , the point-spread function may quite easily be computed from an interferogram of the wave front in the back focal plane of a micro-objective .
	manualset3
91899	7	399288	13	NULL	NULL	0	NULL	micro-objective	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	If an interferometer is available for quantitative wave-front analysis on the production line , the point-spread function may quite easily be computed from an interferogram of the wave front in the back focal plane of a micro-objective .
	manualset3
91900	1	399289	13	NULL	NULL	0	NULL	bladder cancer	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	If bladder cancer is caused by agents present in the urine , as is widely believed , this mechanism may also protect against carcinogenesis .
	manualset3
91901	2	399289	13	NULL	NULL	0	NULL	 agents	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	If bladder cancer is caused by agents present in the urine , as is widely believed , this mechanism may also protect against carcinogenesis .
	manualset3
91902	3	399289	13	NULL	NULL	0	NULL	urine	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	If bladder cancer is caused by agents present in the urine , as is widely believed , this mechanism may also protect against carcinogenesis .
	manualset3
91903	4	399289	13	NULL	NULL	0	NULL	mechanism 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If bladder cancer is caused by agents present in the urine , as is widely believed , this mechanism may also protect against carcinogenesis .
	manualset3
91904	5	399289	13	NULL	NULL	0	NULL	 carcinogenesis 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	If bladder cancer is caused by agents present in the urine , as is widely believed , this mechanism may also protect against carcinogenesis .
	manualset3
91905	1	399290	13	NULL	NULL	0	NULL	combination therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If combination therapy with OAD is not successful in achieving HbA1c values & lt ; 6.5 % , insulin therapy is required either in combination with OADs as a bedtime regimen or as intensive insulin therapy using both basal and short-term acting insulins .
	manualset3
91906	2	399290	13	NULL	NULL	0	NULL	OAD 	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	If combination therapy with OAD is not successful in achieving HbA1c values & lt ; 6.5 % , insulin therapy is required either in combination with OADs as a bedtime regimen or as intensive insulin therapy using both basal and short-term acting insulins .
	manualset3
91907	3	399290	13	NULL	NULL	0	NULL	HbA1c values	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If combination therapy with OAD is not successful in achieving HbA1c values & lt ; 6.5 % , insulin therapy is required either in combination with OADs as a bedtime regimen or as intensive insulin therapy using both basal and short-term acting insulins .
	manualset3
91908	4	399290	13	NULL	NULL	0	NULL	6.5 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	If combination therapy with OAD is not successful in achieving HbA1c values & lt ; 6.5 % , insulin therapy is required either in combination with OADs as a bedtime regimen or as intensive insulin therapy using both basal and short-term acting insulins .
	manualset3
91909	5	399290	13	NULL	NULL	0	NULL	 insulin therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If combination therapy with OAD is not successful in achieving HbA1c values & lt ; 6.5 % , insulin therapy is required either in combination with OADs as a bedtime regimen or as intensive insulin therapy using both basal and short-term acting insulins .
	manualset3
91910	6	399290	13	NULL	NULL	0	NULL	combination	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If combination therapy with OAD is not successful in achieving HbA1c values & lt ; 6.5 % , insulin therapy is required either in combination with OADs as a bedtime regimen or as intensive insulin therapy using both basal and short-term acting insulins .
	manualset3
91911	7	399290	13	NULL	NULL	0	NULL	OADs	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	If combination therapy with OAD is not successful in achieving HbA1c values & lt ; 6.5 % , insulin therapy is required either in combination with OADs as a bedtime regimen or as intensive insulin therapy using both basal and short-term acting insulins .
	manualset3
91912	8	399290	13	NULL	NULL	0	NULL	bedtime regimen	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If combination therapy with OAD is not successful in achieving HbA1c values & lt ; 6.5 % , insulin therapy is required either in combination with OADs as a bedtime regimen or as intensive insulin therapy using both basal and short-term acting insulins .
	manualset3
91913	9	399290	13	NULL	NULL	0	NULL	intensive insulin therapy 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If combination therapy with OAD is not successful in achieving HbA1c values & lt ; 6.5 % , insulin therapy is required either in combination with OADs as a bedtime regimen or as intensive insulin therapy using both basal and short-term acting insulins .
	manualset3
91914	10	399290	13	NULL	NULL	NULL	NULL	 insulins 	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	If combination therapy with OAD is not successful in achieving HbA1c values & lt ; 6.5 % , insulin therapy is required either in combination with OADs as a bedtime regimen or as intensive insulin therapy using both basal and short-term acting insulins .
	manualset3
91915	1	399291	13	NULL	NULL	0	NULL	delivery modules	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If developed , delivery modules would bring targeting molecules across the BBB to their respective active sites .
	manualset3
91916	2	399291	13	NULL	NULL	0	NULL	targeting molecules	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	If developed , delivery modules would bring targeting molecules across the BBB to their respective active sites .
	manualset3
91917	3	399291	13	NULL	NULL	NULL	NULL	BBB	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	If developed , delivery modules would bring targeting molecules across the BBB to their respective active sites .
	manualset3
91918	4	399291	13	NULL	NULL	0	NULL	active sites 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	If developed , delivery modules would bring targeting molecules across the BBB to their respective active sites .
	manualset3
91919	1	399292	13	NULL	NULL	0	NULL	heparanase 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	If heparanase is the answer , what is the question ?
	manualset3
91920	2	399292	13	NULL	NULL	0	NULL	answer 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If heparanase is the answer , what is the question ?
	manualset3
91921	3	399292	13	NULL	NULL	0	NULL	question	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If heparanase is the answer , what is the question ?
	manualset3
91922	1	399293	13	NULL	NULL	0	NULL	stapedius reflex 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The use of the stapedius reflex in the fitting of hearing aids ( author transl ) ) .
	manualset3
91923	2	399293	13	NULL	NULL	0	NULL	hearing aids 	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	( The use of the stapedius reflex in the fitting of hearing aids ( author transl ) ) .
	manualset3
91924	3	399293	13	NULL	NULL	0	NULL	author	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	( The use of the stapedius reflex in the fitting of hearing aids ( author transl ) ) .
	manualset3
91926	1	399294	13	NULL	NULL	0	NULL	perceptual phenomenon	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	If it is agreed that this perceptual phenomenon is causally linked to the activity of nerve cells , the state jumps would have to occur in conjunction with changes in neural activity somewhere in the nervous system .
	manualset3
91927	2	399294	13	NULL	NULL	0	NULL	activity of nerve cells	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	If it is agreed that this perceptual phenomenon is causally linked to the activity of nerve cells , the state jumps would have to occur in conjunction with changes in neural activity somewhere in the nervous system .
	manualset3
91929	3	399294	13	NULL	NULL	0	NULL	conjunction	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If it is agreed that this perceptual phenomenon is causally linked to the activity of nerve cells , the state jumps would have to occur in conjunction with changes in neural activity somewhere in the nervous system .
	manualset3
91931	4	399294	13	NULL	NULL	0	NULL	neural activity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	If it is agreed that this perceptual phenomenon is causally linked to the activity of nerve cells , the state jumps would have to occur in conjunction with changes in neural activity somewhere in the nervous system .
	manualset3
91932	5	399294	13	NULL	NULL	0	NULL	nervous system 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	If it is agreed that this perceptual phenomenon is causally linked to the activity of nerve cells , the state jumps would have to occur in conjunction with changes in neural activity somewhere in the nervous system .
	manualset3
91933	1	399295	13	NULL	NULL	0	NULL	hair 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	If it were possible to pool all hair belonging to an individual prior to DNA analysis , then this effort could not only be reduced , but the number of hair for an STR-approach could also be increased .
	manualset3
91934	2	399295	13	NULL	NULL	0	NULL	individual	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	If it were possible to pool all hair belonging to an individual prior to DNA analysis , then this effort could not only be reduced , but the number of hair for an STR-approach could also be increased .
	manualset3
91935	3	399295	13	NULL	NULL	0	NULL	prior to DNA analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	If it were possible to pool all hair belonging to an individual prior to DNA analysis , then this effort could not only be reduced , but the number of hair for an STR-approach could also be increased .
	manualset3
91936	4	399295	13	NULL	NULL	0	NULL	effort 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If it were possible to pool all hair belonging to an individual prior to DNA analysis , then this effort could not only be reduced , but the number of hair for an STR-approach could also be increased .
	manualset3
91937	5	399295	13	NULL	NULL	0	NULL	number of hair	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	If it were possible to pool all hair belonging to an individual prior to DNA analysis , then this effort could not only be reduced , but the number of hair for an STR-approach could also be increased .
	manualset3
91938	6	399295	13	NULL	NULL	0	NULL	STR-approach	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	If it were possible to pool all hair belonging to an individual prior to DNA analysis , then this effort could not only be reduced , but the number of hair for an STR-approach could also be increased .
	manualset3
91939	1	399296	13	NULL	NULL	0	NULL	 left portal ducts 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	If left portal ducts are inaccessible by division of the main portal fissure because of a retroportal location , then an anastomosis in the anterior portion of the umbilical fissure may give adequate drainage .
	manualset3
91940	2	399296	13	NULL	NULL	0	NULL	division	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If left portal ducts are inaccessible by division of the main portal fissure because of a retroportal location , then an anastomosis in the anterior portion of the umbilical fissure may give adequate drainage .
	manualset3
91941	3	399296	13	NULL	NULL	0	NULL	main portal fissure 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	If left portal ducts are inaccessible by division of the main portal fissure because of a retroportal location , then an anastomosis in the anterior portion of the umbilical fissure may give adequate drainage .
	manualset3
91942	4	399296	13	NULL	NULL	0	NULL	retroportal location	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	If left portal ducts are inaccessible by division of the main portal fissure because of a retroportal location , then an anastomosis in the anterior portion of the umbilical fissure may give adequate drainage .
	manualset3
91943	5	399296	13	NULL	NULL	0	NULL	 anastomosis 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If left portal ducts are inaccessible by division of the main portal fissure because of a retroportal location , then an anastomosis in the anterior portion of the umbilical fissure may give adequate drainage .
	manualset3
91944	6	399296	13	NULL	NULL	0	NULL	anterior portion of the umbilical fissure	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	If left portal ducts are inaccessible by division of the main portal fissure because of a retroportal location , then an anastomosis in the anterior portion of the umbilical fissure may give adequate drainage .
	manualset3
91945	7	399296	13	NULL	NULL	0	NULL	adequate drainage	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	If left portal ducts are inaccessible by division of the main portal fissure because of a retroportal location , then an anastomosis in the anterior portion of the umbilical fissure may give adequate drainage .
	manualset3
91946	1	399297	13	NULL	NULL	0	NULL	metal chloride 	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	If metal chloride or nitrate salts are used in the reaction with the LDH then co-intercalation of either the Cl ( - ) or NO ( 3 ) ( - ) anions is observed .
	manualset3
91947	2	399297	13	NULL	NULL	0	NULL	 nitrate salts	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	If metal chloride or nitrate salts are used in the reaction with the LDH then co-intercalation of either the Cl ( - ) or NO ( 3 ) ( - ) anions is observed .
	manualset3
91948	3	399297	13	NULL	NULL	0	NULL	reaction	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If metal chloride or nitrate salts are used in the reaction with the LDH then co-intercalation of either the Cl ( - ) or NO ( 3 ) ( - ) anions is observed .
	manualset3
91949	4	399297	13	NULL	NULL	0	NULL	LDH	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	If metal chloride or nitrate salts are used in the reaction with the LDH then co-intercalation of either the Cl ( - ) or NO ( 3 ) ( - ) anions is observed .
	manualset3
91950	5	399297	13	NULL	NULL	0	NULL	co-intercalation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If metal chloride or nitrate salts are used in the reaction with the LDH then co-intercalation of either the Cl ( - ) or NO ( 3 ) ( - ) anions is observed .
	manualset3
91951	6	399297	13	NULL	NULL	0	NULL	Cl ( - )	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	If metal chloride or nitrate salts are used in the reaction with the LDH then co-intercalation of either the Cl ( - ) or NO ( 3 ) ( - ) anions is observed .
	manualset3
91952	7	399297	13	NULL	NULL	0	NULL	NO ( 3 ) ( - ) anions	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	If metal chloride or nitrate salts are used in the reaction with the LDH then co-intercalation of either the Cl ( - ) or NO ( 3 ) ( - ) anions is observed .
	manualset3
91959	1	399298	13	NULL	NULL	0	NULL	GVHD	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	If more effective control of GVHD can be accomplished , marrow transplantation between MLC-reactive individuals may become feasible .
	manualset3
91960	2	399298	13	NULL	NULL	0	NULL	marrow transplantation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If more effective control of GVHD can be accomplished , marrow transplantation between MLC-reactive individuals may become feasible .
	manualset3
91961	3	399298	13	NULL	NULL	0	NULL	MLC-reactive individuals	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	If more effective control of GVHD can be accomplished , marrow transplantation between MLC-reactive individuals may become feasible .
	manualset3
91964	1	399299	13	NULL	NULL	0	NULL	energy	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	If most of the energy of the inconsistencies is limited to a certain region of kappa-space , increased sampling density ( oversampling ) in this region can be especially effective in reducing motion artifacts .
	manualset3
91965	2	399299	13	NULL	NULL	0	NULL	inconsistencies 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If most of the energy of the inconsistencies is limited to a certain region of kappa-space , increased sampling density ( oversampling ) in this region can be especially effective in reducing motion artifacts .
	manualset3
91966	3	399299	13	NULL	NULL	NULL	NULL	certain region of kappa-space	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	If most of the energy of the inconsistencies is limited to a certain region of kappa-space , increased sampling density ( oversampling ) in this region can be especially effective in reducing motion artifacts .
	manualset3
91967	4	399299	13	NULL	NULL	0	NULL	sampling density ( oversampling )	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	If most of the energy of the inconsistencies is limited to a certain region of kappa-space , increased sampling density ( oversampling ) in this region can be especially effective in reducing motion artifacts .
	manualset3
91968	5	399299	13	NULL	NULL	0	NULL	reducing motion artifacts 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If most of the energy of the inconsistencies is limited to a certain region of kappa-space , increased sampling density ( oversampling ) in this region can be especially effective in reducing motion artifacts .
	manualset3
91969	1	399300	13	NULL	NULL	NULL	NULL	agents 	Drug												NULL		NULL	NULL	NULL	NULL	NULL	NULL	If recent results consistently show the superiority of these agents over tamoxifen , the therapeutic strategies of AIs in adjuvant setting are still debated .
	manualset3
91970	2	399300	13	NULL	NULL	0	NULL	 tamoxifen	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	If recent results consistently show the superiority of these agents over tamoxifen , the therapeutic strategies of AIs in adjuvant setting are still debated .
	manualset3
91971	3	399300	13	NULL	NULL	0	NULL	therapeutic strategies	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If recent results consistently show the superiority of these agents over tamoxifen , the therapeutic strategies of AIs in adjuvant setting are still debated .
	manualset3
91972	4	399300	13	NULL	NULL	0	NULL	AIs 	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	If recent results consistently show the superiority of these agents over tamoxifen , the therapeutic strategies of AIs in adjuvant setting are still debated .
	manualset3
91973	5	399300	13	NULL	NULL	0	NULL	adjuvant setting	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If recent results consistently show the superiority of these agents over tamoxifen , the therapeutic strategies of AIs in adjuvant setting are still debated .
	manualset3
91974	1	399301	13	NULL	NULL	0	NULL	salt fluoridation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If salt fluoridation could also be generalized , caries levels could be reduced to a fraction of their initial values .
	manualset3
91975	2	399301	13	NULL	NULL	0	NULL	 caries levels	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If salt fluoridation could also be generalized , caries levels could be reduced to a fraction of their initial values .
	manualset3
91976	3	399301	13	NULL	NULL	0	NULL	fraction of their initial values	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	If salt fluoridation could also be generalized , caries levels could be reduced to a fraction of their initial values .
	manualset3
91977	1	399302	13	NULL	NULL	0	NULL	hip 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	If screened only at the hip or spine , 17.9 / 27.3 % with osteopenia and 1.3 / 2.9 % with osteoporosis at either site would be diagnosed as normal .
	manualset3
91978	2	399302	13	NULL	NULL	0	NULL	 spine	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	If screened only at the hip or spine , 17.9 / 27.3 % with osteopenia and 1.3 / 2.9 % with osteoporosis at either site would be diagnosed as normal .
	manualset3
91979	3	399302	13	NULL	NULL	0	NULL	 17.9 / 27.3 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	If screened only at the hip or spine , 17.9 / 27.3 % with osteopenia and 1.3 / 2.9 % with osteoporosis at either site would be diagnosed as normal .
	manualset3
91980	4	399302	13	NULL	NULL	0	NULL	osteopenia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If screened only at the hip or spine , 17.9 / 27.3 % with osteopenia and 1.3 / 2.9 % with osteoporosis at either site would be diagnosed as normal .
	manualset3
91981	5	399302	13	NULL	NULL	0	NULL	1.3 / 2.9 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	If screened only at the hip or spine , 17.9 / 27.3 % with osteopenia and 1.3 / 2.9 % with osteoporosis at either site would be diagnosed as normal .
	manualset3
91982	6	399302	13	NULL	NULL	0	NULL	osteoporosis at either site	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If screened only at the hip or spine , 17.9 / 27.3 % with osteopenia and 1.3 / 2.9 % with osteoporosis at either site would be diagnosed as normal .
	manualset3
91983	1	399303	13	NULL	NULL	0	NULL	value of CT	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	( The value of CT in the differential diagnostic evaluation of masses in the left upper abdominal quadrant ( author 's transl ) ) .
	manualset3
91984	2	399303	13	NULL	NULL	0	NULL	differential diagnostic evaluation 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The value of CT in the differential diagnostic evaluation of masses in the left upper abdominal quadrant ( author 's transl ) ) .
	manualset3
91985	3	399303	13	NULL	NULL	0	NULL	masses in the left upper abdominal quadrant 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( The value of CT in the differential diagnostic evaluation of masses in the left upper abdominal quadrant ( author 's transl ) ) .
	manualset3
91986	4	399303	13	NULL	NULL	0	NULL	author 's	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	( The value of CT in the differential diagnostic evaluation of masses in the left upper abdominal quadrant ( author 's transl ) ) .
	manualset3
91988	2	399304	13	NULL	NULL	0	NULL	nitric oxide donors	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	If so , it will be interesting to study whether nitric oxide donors and/or nitric oxide precursors can be given together with estrogen , statins , or essential fatty acids to potentiate their benefit in osteoporosis .
	manualset3
91989	3	399304	13	NULL	NULL	0	NULL	nitric oxide precursors 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	If so , it will be interesting to study whether nitric oxide donors and/or nitric oxide precursors can be given together with estrogen , statins , or essential fatty acids to potentiate their benefit in osteoporosis .
	manualset3
91990	4	399304	13	NULL	NULL	0	NULL	estrogen 	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	If so , it will be interesting to study whether nitric oxide donors and/or nitric oxide precursors can be given together with estrogen , statins , or essential fatty acids to potentiate their benefit in osteoporosis .
	manualset3
91991	5	399304	13	NULL	NULL	0	NULL	statins	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	If so , it will be interesting to study whether nitric oxide donors and/or nitric oxide precursors can be given together with estrogen , statins , or essential fatty acids to potentiate their benefit in osteoporosis .
	manualset3
91992	6	399304	13	NULL	NULL	0	NULL	essential fatty acids	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	If so , it will be interesting to study whether nitric oxide donors and/or nitric oxide precursors can be given together with estrogen , statins , or essential fatty acids to potentiate their benefit in osteoporosis .
	manualset3
91993	7	399304	13	NULL	NULL	0	NULL	osteoporosis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If so , it will be interesting to study whether nitric oxide donors and/or nitric oxide precursors can be given together with estrogen , statins , or essential fatty acids to potentiate their benefit in osteoporosis .
	manualset3
91994	1	399305	13	NULL	NULL	0	NULL	crustal extraction 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If so , such crustal extraction should have left a chemical fingerprint in the isotopic composition of the mantle .
	manualset3
91995	2	399305	13	NULL	NULL	0	NULL	 chemical fingerprint 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If so , such crustal extraction should have left a chemical fingerprint in the isotopic composition of the mantle .
	manualset3
91996	3	399305	13	NULL	NULL	0	NULL	isotopic composition	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	If so , such crustal extraction should have left a chemical fingerprint in the isotopic composition of the mantle .
	manualset3
91997	4	399305	13	NULL	NULL	0	NULL	mantle	GeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	If so , such crustal extraction should have left a chemical fingerprint in the isotopic composition of the mantle .
	manualset3
91998	1	399306	13	NULL	NULL	0	NULL	chest picture 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If the chest picture is abnormal , further investigations will be required and , according to the results , preventive treatment or polychemotherapy for tuberculosis disease will be administered .
	manualset3
91999	2	399306	13	NULL	NULL	0	NULL	investigations 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If the chest picture is abnormal , further investigations will be required and , according to the results , preventive treatment or polychemotherapy for tuberculosis disease will be administered .
	manualset3
92000	3	399306	13	NULL	NULL	0	NULL	preventive treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If the chest picture is abnormal , further investigations will be required and , according to the results , preventive treatment or polychemotherapy for tuberculosis disease will be administered .
	manualset3
92001	4	399306	13	NULL	NULL	0	NULL	polychemotherapy 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If the chest picture is abnormal , further investigations will be required and , according to the results , preventive treatment or polychemotherapy for tuberculosis disease will be administered .
	manualset3
92002	5	399306	13	NULL	NULL	0	NULL	tuberculosis disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	If the chest picture is abnormal , further investigations will be required and , according to the results , preventive treatment or polychemotherapy for tuberculosis disease will be administered .
	manualset3
92003	1	399307	13	NULL	NULL	0	NULL	fiber	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	If the fiber and obstacle only interact via excluded volume , there are small corrections to the Brownian ratchet predictions which suggest that tip fluctuations play a minor role .
	manualset3
92004	2	399307	13	NULL	NULL	0	NULL	obstacle 	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	If the fiber and obstacle only interact via excluded volume , there are small corrections to the Brownian ratchet predictions which suggest that tip fluctuations play a minor role .
	manualset3
92005	3	399307	13	NULL	NULL	0	NULL	volume	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	If the fiber and obstacle only interact via excluded volume , there are small corrections to the Brownian ratchet predictions which suggest that tip fluctuations play a minor role .
	manualset3
92006	4	399307	13	NULL	NULL	0	NULL	corrections	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If the fiber and obstacle only interact via excluded volume , there are small corrections to the Brownian ratchet predictions which suggest that tip fluctuations play a minor role .
	manualset3
92007	5	399307	13	NULL	NULL	0	NULL	 Brownian ratchet predictions	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	If the fiber and obstacle only interact via excluded volume , there are small corrections to the Brownian ratchet predictions which suggest that tip fluctuations play a minor role .
	manualset3
92008	6	399307	13	NULL	NULL	0	NULL	tip fluctuations	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If the fiber and obstacle only interact via excluded volume , there are small corrections to the Brownian ratchet predictions which suggest that tip fluctuations play a minor role .
	manualset3
92009	1	399308	13	NULL	NULL	0	NULL	gene 	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	If the gene encodes a protein that is closely related to known proteins , gene identification is aided by matching similarity of potential translation products to those target proteins .
	manualset3
92010	2	399308	13	NULL	NULL	0	NULL	protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	If the gene encodes a protein that is closely related to known proteins , gene identification is aided by matching similarity of potential translation products to those target proteins .
	manualset3
92011	3	399308	13	NULL	NULL	0	NULL	proteins	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	If the gene encodes a protein that is closely related to known proteins , gene identification is aided by matching similarity of potential translation products to those target proteins .
	manualset3
92012	4	399308	13	NULL	NULL	0	NULL	gene identification 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	If the gene encodes a protein that is closely related to known proteins , gene identification is aided by matching similarity of potential translation products to those target proteins .
	manualset3
92013	5	399308	13	NULL	NULL	0	NULL	similarity	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	If the gene encodes a protein that is closely related to known proteins , gene identification is aided by matching similarity of potential translation products to those target proteins .
	manualset3
92014	6	399308	13	NULL	NULL	0	NULL	potential translation products 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	If the gene encodes a protein that is closely related to known proteins , gene identification is aided by matching similarity of potential translation products to those target proteins .
	manualset3
92015	7	399308	13	NULL	NULL	0	NULL	target proteins	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	If the gene encodes a protein that is closely related to known proteins , gene identification is aided by matching similarity of potential translation products to those target proteins .
	manualset3
92016	1	399309	13	NULL	NULL	0	NULL	 pre-ablation bridging strategy 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If the latter approach is chosen , a pre-ablation bridging strategy of enoxaparin 1mg/kg twice daily is reasonable in selected patients unless the patient 's bleeding risk dictates using a lower dose regimen ( 0.5 mg/kg twice daily ) or avoiding bridging altogether .
	manualset3
92017	2	399309	13	NULL	NULL	0	NULL	enoxaparin	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	If the latter approach is chosen , a pre-ablation bridging strategy of enoxaparin 1mg/kg twice daily is reasonable in selected patients unless the patient 's bleeding risk dictates using a lower dose regimen ( 0.5 mg/kg twice daily ) or avoiding bridging altogether .
	manualset3
92018	3	399309	13	NULL	NULL	0	NULL	1mg/kg twice daily	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	If the latter approach is chosen , a pre-ablation bridging strategy of enoxaparin 1mg/kg twice daily is reasonable in selected patients unless the patient 's bleeding risk dictates using a lower dose regimen ( 0.5 mg/kg twice daily ) or avoiding bridging altogether .
	manualset3
92019	4	399309	13	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	If the latter approach is chosen , a pre-ablation bridging strategy of enoxaparin 1mg/kg twice daily is reasonable in selected patients unless the patient 's bleeding risk dictates using a lower dose regimen ( 0.5 mg/kg twice daily ) or avoiding bridging altogether .
	manualset3
92020	5	399309	13	NULL	NULL	0	NULL	patient 's	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	If the latter approach is chosen , a pre-ablation bridging strategy of enoxaparin 1mg/kg twice daily is reasonable in selected patients unless the patient 's bleeding risk dictates using a lower dose regimen ( 0.5 mg/kg twice daily ) or avoiding bridging altogether .
	manualset3
92021	6	399309	13	NULL	NULL	0	NULL	bleeding risk	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If the latter approach is chosen , a pre-ablation bridging strategy of enoxaparin 1mg/kg twice daily is reasonable in selected patients unless the patient 's bleeding risk dictates using a lower dose regimen ( 0.5 mg/kg twice daily ) or avoiding bridging altogether .
	manualset3
92022	7	399309	13	NULL	NULL	0	NULL	lower dose regimen	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If the latter approach is chosen , a pre-ablation bridging strategy of enoxaparin 1mg/kg twice daily is reasonable in selected patients unless the patient 's bleeding risk dictates using a lower dose regimen ( 0.5 mg/kg twice daily ) or avoiding bridging altogether .
	manualset3
92023	8	399309	13	NULL	NULL	0	NULL	0.5 mg/kg twice daily	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	If the latter approach is chosen , a pre-ablation bridging strategy of enoxaparin 1mg/kg twice daily is reasonable in selected patients unless the patient 's bleeding risk dictates using a lower dose regimen ( 0.5 mg/kg twice daily ) or avoiding bridging altogether .
	manualset3
92024	1	399310	13	NULL	NULL	0	NULL	 leachate	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	If the leachate continues to migrate at this apparent rate , it will take more than 100 years to reach the water table .
	manualset3
92025	2	399310	13	NULL	NULL	0	NULL	apparent rate	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	If the leachate continues to migrate at this apparent rate , it will take more than 100 years to reach the water table .
	manualset3
92026	3	399310	13	NULL	NULL	0	NULL	100 years	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	If the leachate continues to migrate at this apparent rate , it will take more than 100 years to reach the water table .
	manualset3
92027	4	399310	13	NULL	NULL	0	NULL	water table	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	If the leachate continues to migrate at this apparent rate , it will take more than 100 years to reach the water table .
	manualset3
92028	1	399311	13	NULL	NULL	0	NULL	neoplastic cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	If the neoplastic cells on slides are mixed with nonneoplastic lymphocytes , cells of interest are isolated by microdissection .
	manualset3
92029	2	399311	13	NULL	NULL	0	NULL	slides	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	If the neoplastic cells on slides are mixed with nonneoplastic lymphocytes , cells of interest are isolated by microdissection .
	manualset3
92030	3	399311	13	NULL	NULL	0	NULL	nonneoplastic lymphocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	If the neoplastic cells on slides are mixed with nonneoplastic lymphocytes , cells of interest are isolated by microdissection .
	manualset3
92031	4	399311	13	NULL	NULL	0	NULL	cells of interest	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	If the neoplastic cells on slides are mixed with nonneoplastic lymphocytes , cells of interest are isolated by microdissection .
	manualset3
92032	5	399311	13	NULL	NULL	0	NULL	microdissection	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	If the neoplastic cells on slides are mixed with nonneoplastic lymphocytes , cells of interest are isolated by microdissection .
	manualset3
92033	1	399312	13	NULL	NULL	0	NULL	patient 's condition	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If the patient 's condition permits , it may be useful to opacify the dilated segment in order to study the nature of the obstacle .
	manualset3
92034	2	399312	13	NULL	NULL	0	NULL	dilated segment	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	If the patient 's condition permits , it may be useful to opacify the dilated segment in order to study the nature of the obstacle .
	manualset3
92035	3	399312	13	NULL	NULL	0	NULL	nature of the obstacle	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If the patient 's condition permits , it may be useful to opacify the dilated segment in order to study the nature of the obstacle .
	manualset3
92036	1	399313	13	NULL	NULL	0	NULL	value 	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	( The value of MRI for diagnosis of recurrence of rectal carcinoma after surgical resection ) .
	manualset3
92037	2	399313	13	NULL	NULL	0	NULL	MRI	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The value of MRI for diagnosis of recurrence of rectal carcinoma after surgical resection ) .
	manualset3
92038	3	399313	13	NULL	NULL	0	NULL	diagnosis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The value of MRI for diagnosis of recurrence of rectal carcinoma after surgical resection ) .
	manualset3
92039	4	399313	13	NULL	NULL	NULL	NULL	recurrence of rectal carcinoma	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The value of MRI for diagnosis of recurrence of rectal carcinoma after surgical resection ) .
	manualset3
92040	5	399313	13	NULL	NULL	0	NULL	surgical resection	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The value of MRI for diagnosis of recurrence of rectal carcinoma after surgical resection ) .
	manualset3
92041	1	399314	13	NULL	NULL	0	NULL	 time span 	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	If the time span of risk of perinatal death is defined as the period from 20 weeks gestation through 27 days after birth , 97 out of 100 infants born in California during 1959 were born alive and survived the first month of life .
	manualset3
92042	2	399314	13	NULL	NULL	0	NULL	risk of perinatal death	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If the time span of risk of perinatal death is defined as the period from 20 weeks gestation through 27 days after birth , 97 out of 100 infants born in California during 1959 were born alive and survived the first month of life .
	manualset3
92043	3	399314	13	NULL	NULL	0	NULL	period	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	If the time span of risk of perinatal death is defined as the period from 20 weeks gestation through 27 days after birth , 97 out of 100 infants born in California during 1959 were born alive and survived the first month of life .
	manualset3
92044	4	399314	13	NULL	NULL	0	NULL	20 weeks gestation through 27 days after birth	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	If the time span of risk of perinatal death is defined as the period from 20 weeks gestation through 27 days after birth , 97 out of 100 infants born in California during 1959 were born alive and survived the first month of life .
	manualset3
92045	5	399314	13	NULL	NULL	0	NULL	97 out of 100	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	If the time span of risk of perinatal death is defined as the period from 20 weeks gestation through 27 days after birth , 97 out of 100 infants born in California during 1959 were born alive and survived the first month of life .
	manualset3
92046	6	399314	13	NULL	NULL	0	NULL	infants 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	If the time span of risk of perinatal death is defined as the period from 20 weeks gestation through 27 days after birth , 97 out of 100 infants born in California during 1959 were born alive and survived the first month of life .
	manualset3
92047	7	399314	13	NULL	NULL	0	NULL	California	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	If the time span of risk of perinatal death is defined as the period from 20 weeks gestation through 27 days after birth , 97 out of 100 infants born in California during 1959 were born alive and survived the first month of life .
	manualset3
92048	8	399314	13	NULL	NULL	0	NULL	1959 	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	If the time span of risk of perinatal death is defined as the period from 20 weeks gestation through 27 days after birth , 97 out of 100 infants born in California during 1959 were born alive and survived the first month of life .
	manualset3
92049	9	399314	13	NULL	NULL	0	NULL	alive	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If the time span of risk of perinatal death is defined as the period from 20 weeks gestation through 27 days after birth , 97 out of 100 infants born in California during 1959 were born alive and survived the first month of life .
	manualset3
92050	10	399314	13	NULL	NULL	0	NULL	first month of life	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	If the time span of risk of perinatal death is defined as the period from 20 weeks gestation through 27 days after birth , 97 out of 100 infants born in California during 1959 were born alive and survived the first month of life .
	manualset3
92051	1	399315	13	NULL	NULL	0	NULL	factors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If these factors are absent , another chronic illness known to cause hypoglycemia may be the source .
	manualset3
92052	2	399315	13	NULL	NULL	0	NULL	chronic illness	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If these factors are absent , another chronic illness known to cause hypoglycemia may be the source .
	manualset3
92053	3	399315	13	NULL	NULL	0	NULL	hypoglycemia 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If these factors are absent , another chronic illness known to cause hypoglycemia may be the source .
	manualset3
98572	4	399315	13	NULL	NULL	0	NULL	 source	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If these factors are absent , another chronic illness known to cause hypoglycemia may be the source .
	manualset3
92054	1	399316	13	NULL	NULL	0	NULL	washin-washout effect 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If this , so-called , washin-washout effect is substantial it may interfere with the diagnosis , as a major part of breath HCN may originate from the respiratory tract , due to recent exposure , and not from systemic exposure .
	manualset3
92055	2	399316	13	NULL	NULL	0	NULL	 diagnosis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If this , so-called , washin-washout effect is substantial it may interfere with the diagnosis , as a major part of breath HCN may originate from the respiratory tract , due to recent exposure , and not from systemic exposure .
	manualset3
92056	3	399316	13	NULL	NULL	0	NULL	major part of breath HCN 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	If this , so-called , washin-washout effect is substantial it may interfere with the diagnosis , as a major part of breath HCN may originate from the respiratory tract , due to recent exposure , and not from systemic exposure .
	manualset3
92057	4	399316	13	NULL	NULL	0	NULL	respiratory tract	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	If this , so-called , washin-washout effect is substantial it may interfere with the diagnosis , as a major part of breath HCN may originate from the respiratory tract , due to recent exposure , and not from systemic exposure .
	manualset3
92058	5	399316	13	NULL	NULL	NULL	NULL	recent exposure	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	If this , so-called , washin-washout effect is substantial it may interfere with the diagnosis , as a major part of breath HCN may originate from the respiratory tract , due to recent exposure , and not from systemic exposure .
	manualset3
92059	6	399316	13	NULL	NULL	0	NULL	systemic exposure	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	If this , so-called , washin-washout effect is substantial it may interfere with the diagnosis , as a major part of breath HCN may originate from the respiratory tract , due to recent exposure , and not from systemic exposure .
	manualset3
92060	1	399317	13	NULL	NULL	0	NULL	prophylactic infusion therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If this can be achieved , we may be able to look forward to prophylactic infusion therapy for patients with severe FVIII deficiency and eliminate the significant complications that continue to occur even with prompt treatment of hemorrhage and thrombosis .
	manualset3
92061	2	399317	13	NULL	NULL	0	NULL	patients 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	If this can be achieved , we may be able to look forward to prophylactic infusion therapy for patients with severe FVIII deficiency and eliminate the significant complications that continue to occur even with prompt treatment of hemorrhage and thrombosis .
	manualset3
92062	3	399317	13	NULL	NULL	0	NULL	severe FVIII deficiency	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If this can be achieved , we may be able to look forward to prophylactic infusion therapy for patients with severe FVIII deficiency and eliminate the significant complications that continue to occur even with prompt treatment of hemorrhage and thrombosis .
	manualset3
92063	4	399317	13	NULL	NULL	0	NULL	significant complications	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If this can be achieved , we may be able to look forward to prophylactic infusion therapy for patients with severe FVIII deficiency and eliminate the significant complications that continue to occur even with prompt treatment of hemorrhage and thrombosis .
	manualset3
92064	5	399317	13	NULL	NULL	0	NULL	treatment 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	If this can be achieved , we may be able to look forward to prophylactic infusion therapy for patients with severe FVIII deficiency and eliminate the significant complications that continue to occur even with prompt treatment of hemorrhage and thrombosis .
	manualset3
92065	6	399317	13	NULL	NULL	0	NULL	hemorrhage	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If this can be achieved , we may be able to look forward to prophylactic infusion therapy for patients with severe FVIII deficiency and eliminate the significant complications that continue to occur even with prompt treatment of hemorrhage and thrombosis .
	manualset3
92066	7	399317	13	NULL	NULL	0	NULL	thrombosis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	If this can be achieved , we may be able to look forward to prophylactic infusion therapy for patients with severe FVIII deficiency and eliminate the significant complications that continue to occur even with prompt treatment of hemorrhage and thrombosis .
	manualset3
92067	1	399318	13	NULL	NULL	0	NULL	amidation reaction	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	If true , this would seem to imply that the amidation reaction of the Glut-tRNA ( Gln ) complex was the evolutionary precursor of the direct tRNA ( Gln ) aminoacylation pathway .
	manualset3
92068	2	399318	13	NULL	NULL	0	NULL	Glut-tRNA ( Gln ) complex	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	If true , this would seem to imply that the amidation reaction of the Glut-tRNA ( Gln ) complex was the evolutionary precursor of the direct tRNA ( Gln ) aminoacylation pathway .
	manualset3
92069	3	399318	13	NULL	NULL	0	NULL	evolutionary precursor	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	If true , this would seem to imply that the amidation reaction of the Glut-tRNA ( Gln ) complex was the evolutionary precursor of the direct tRNA ( Gln ) aminoacylation pathway .
	manualset3
92070	4	399318	13	NULL	NULL	0	NULL	direct tRNA ( Gln ) aminoacylation pathway	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	If true , this would seem to imply that the amidation reaction of the Glut-tRNA ( Gln ) complex was the evolutionary precursor of the direct tRNA ( Gln ) aminoacylation pathway .
	manualset3
92071	1	399319	13	NULL	NULL	0	NULL	IgE cross reactivity 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	IgE cross reactivity between reindeer and bovine milk beta-lactoglobulins in cow 's milk allergic patients .
	manualset3
92072	2	399319	13	NULL	NULL	0	NULL	reindeer milk beta-lactoglobulins	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IgE cross reactivity between reindeer and bovine milk beta-lactoglobulins in cow 's milk allergic patients .
	manualset3
92073	3	399319	13	NULL	NULL	0	NULL	bovine milk beta-lactoglobulins	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IgE cross reactivity between reindeer and bovine milk beta-lactoglobulins in cow 's milk allergic patients .
	manualset3
92074	4	399319	13	NULL	NULL	0	NULL	cow 's milk allergic patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IgE cross reactivity between reindeer and bovine milk beta-lactoglobulins in cow 's milk allergic patients .
	manualset3
92075	1	399320	13	NULL	NULL	0	NULL	IgG4	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	IgG4 bound to SG components were found in the sera of the common reaction group at the levels of 24 and 48 kD , but , in one severe case , no bands were observed , although the total IgG was very high .
	manualset3
92076	2	399320	13	NULL	NULL	0	NULL	SG components	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	IgG4 bound to SG components were found in the sera of the common reaction group at the levels of 24 and 48 kD , but , in one severe case , no bands were observed , although the total IgG was very high .
	manualset3
92077	3	399320	13	NULL	NULL	0	NULL	sera	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	IgG4 bound to SG components were found in the sera of the common reaction group at the levels of 24 and 48 kD , but , in one severe case , no bands were observed , although the total IgG was very high .
	manualset3
92078	4	399320	13	NULL	NULL	0	NULL	common reaction group	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	IgG4 bound to SG components were found in the sera of the common reaction group at the levels of 24 and 48 kD , but , in one severe case , no bands were observed , although the total IgG was very high .
	manualset3
92079	5	399320	13	NULL	NULL	0	NULL	levels of 24 and 48 kD	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	IgG4 bound to SG components were found in the sera of the common reaction group at the levels of 24 and 48 kD , but , in one severe case , no bands were observed , although the total IgG was very high .
	manualset3
92080	6	399320	13	NULL	NULL	0	NULL	one severe case	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IgG4 bound to SG components were found in the sera of the common reaction group at the levels of 24 and 48 kD , but , in one severe case , no bands were observed , although the total IgG was very high .
	manualset3
92081	7	399320	13	NULL	NULL	0	NULL	total IgG was very high 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	IgG4 bound to SG components were found in the sera of the common reaction group at the levels of 24 and 48 kD , but , in one severe case , no bands were observed , although the total IgG was very high .
	manualset3
92082	1	399321	13	NULL	NULL	NULL	NULL	IgM concentrations	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	IgM concentrations were significantly ( P = .002 ) higher in the affected dogs ( median 1.95 mg/mL ) than in the control dogs ( median 1.12 mg/mL ) .
	manualset3
92083	2	399321	13	NULL	NULL	0	NULL	 ( P = .002 )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	IgM concentrations were significantly ( P = .002 ) higher in the affected dogs ( median 1.95 mg/mL ) than in the control dogs ( median 1.12 mg/mL ) .
	manualset3
92084	3	399321	13	NULL	NULL	0	NULL	dogs	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	IgM concentrations were significantly ( P = .002 ) higher in the affected dogs ( median 1.95 mg/mL ) than in the control dogs ( median 1.12 mg/mL ) .
	manualset3
92085	4	399321	13	NULL	NULL	0	NULL	median 1.95 mg/mL 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	IgM concentrations were significantly ( P = .002 ) higher in the affected dogs ( median 1.95 mg/mL ) than in the control dogs ( median 1.12 mg/mL ) .
	manualset3
92086	5	399321	13	NULL	NULL	0	NULL	control dogs	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	IgM concentrations were significantly ( P = .002 ) higher in the affected dogs ( median 1.95 mg/mL ) than in the control dogs ( median 1.12 mg/mL ) .
	manualset3
92087	6	399321	13	NULL	NULL	0	NULL	median 1.12 mg/mL	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	IgM concentrations were significantly ( P = .002 ) higher in the affected dogs ( median 1.95 mg/mL ) than in the control dogs ( median 1.12 mg/mL ) .
	manualset3
92088	1	399322	13	NULL	NULL	0	NULL	diffusion-related NaCl effect	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Ignoring the presumably diffusion-related NaCl effect on carbon isotope ratios results in an overestimation of nocturnal CO ( 2 ) gain in comparison to an isotope versus nocturnal CO ( 2 ) gain calibration established previously for C ( 3 ) and CAM species grown under well-watered conditions .
	manualset3
92089	2	399322	13	NULL	NULL	0	NULL	carbon isotope ratios	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Ignoring the presumably diffusion-related NaCl effect on carbon isotope ratios results in an overestimation of nocturnal CO ( 2 ) gain in comparison to an isotope versus nocturnal CO ( 2 ) gain calibration established previously for C ( 3 ) and CAM species grown under well-watered conditions .
	manualset3
92090	3	399322	13	NULL	NULL	0	NULL	overestimation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Ignoring the presumably diffusion-related NaCl effect on carbon isotope ratios results in an overestimation of nocturnal CO ( 2 ) gain in comparison to an isotope versus nocturnal CO ( 2 ) gain calibration established previously for C ( 3 ) and CAM species grown under well-watered conditions .
	manualset3
92091	4	399322	13	NULL	NULL	0	NULL	nocturnal CO ( 2 ) gain	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Ignoring the presumably diffusion-related NaCl effect on carbon isotope ratios results in an overestimation of nocturnal CO ( 2 ) gain in comparison to an isotope versus nocturnal CO ( 2 ) gain calibration established previously for C ( 3 ) and CAM species grown under well-watered conditions .
	manualset3
92092	5	399322	13	NULL	NULL	0	NULL	comparison	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	Ignoring the presumably diffusion-related NaCl effect on carbon isotope ratios results in an overestimation of nocturnal CO ( 2 ) gain in comparison to an isotope versus nocturnal CO ( 2 ) gain calibration established previously for C ( 3 ) and CAM species grown under well-watered conditions .
	manualset3
92093	6	399322	13	NULL	NULL	0	NULL	isotope versus nocturnal CO ( 2 ) gain calibration	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Ignoring the presumably diffusion-related NaCl effect on carbon isotope ratios results in an overestimation of nocturnal CO ( 2 ) gain in comparison to an isotope versus nocturnal CO ( 2 ) gain calibration established previously for C ( 3 ) and CAM species grown under well-watered conditions .
	manualset3
92094	7	399322	13	NULL	NULL	0	NULL	C ( 3 ) species	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Ignoring the presumably diffusion-related NaCl effect on carbon isotope ratios results in an overestimation of nocturnal CO ( 2 ) gain in comparison to an isotope versus nocturnal CO ( 2 ) gain calibration established previously for C ( 3 ) and CAM species grown under well-watered conditions .
	manualset3
92095	8	399322	13	NULL	NULL	0	NULL	CAM species	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Ignoring the presumably diffusion-related NaCl effect on carbon isotope ratios results in an overestimation of nocturnal CO ( 2 ) gain in comparison to an isotope versus nocturnal CO ( 2 ) gain calibration established previously for C ( 3 ) and CAM species grown under well-watered conditions .
	manualset3
92096	9	399322	13	NULL	NULL	0	NULL	conditions	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Ignoring the presumably diffusion-related NaCl effect on carbon isotope ratios results in an overestimation of nocturnal CO ( 2 ) gain in comparison to an isotope versus nocturnal CO ( 2 ) gain calibration established previously for C ( 3 ) and CAM species grown under well-watered conditions .
	manualset3
92097	1	399323	13	NULL	NULL	NULL	NULL	value of sex chromatin	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( The value of sex chromatin in the hormone therapy of breast tumors ) .
	manualset3
92098	2	399323	13	NULL	NULL	0	NULL	 hormone therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( The value of sex chromatin in the hormone therapy of breast tumors ) .
	manualset3
92099	3	399323	13	NULL	NULL	0	NULL	breast tumors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( The value of sex chromatin in the hormone therapy of breast tumors ) .
	manualset3
92100	1	399324	13	NULL	NULL	0	NULL	Image stacks	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Image stacks ( 5 benign , 7 malignant tumors ) were analyzed by established software ( principal component analysis PCA , hyperspectral classification , spectral profiles ) .
	manualset3
92101	2	399324	13	NULL	NULL	0	NULL	5	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Image stacks ( 5 benign , 7 malignant tumors ) were analyzed by established software ( principal component analysis PCA , hyperspectral classification , spectral profiles ) .
	manualset3
92102	3	399324	13	NULL	NULL	0	NULL	benign tumors 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Image stacks ( 5 benign , 7 malignant tumors ) were analyzed by established software ( principal component analysis PCA , hyperspectral classification , spectral profiles ) .
	manualset3
92103	4	399324	13	NULL	NULL	0	NULL	7	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Image stacks ( 5 benign , 7 malignant tumors ) were analyzed by established software ( principal component analysis PCA , hyperspectral classification , spectral profiles ) .
	manualset3
92104	5	399324	13	NULL	NULL	0	NULL	 malignant tumors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Image stacks ( 5 benign , 7 malignant tumors ) were analyzed by established software ( principal component analysis PCA , hyperspectral classification , spectral profiles ) .
	manualset3
92105	6	399324	13	NULL	NULL	0	NULL	software	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Image stacks ( 5 benign , 7 malignant tumors ) were analyzed by established software ( principal component analysis PCA , hyperspectral classification , spectral profiles ) .
	manualset3
92106	7	399324	13	NULL	NULL	0	NULL	principal component analysis PCA	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Image stacks ( 5 benign , 7 malignant tumors ) were analyzed by established software ( principal component analysis PCA , hyperspectral classification , spectral profiles ) .
	manualset3
92107	8	399324	13	NULL	NULL	0	NULL	 hyperspectral classification	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Image stacks ( 5 benign , 7 malignant tumors ) were analyzed by established software ( principal component analysis PCA , hyperspectral classification , spectral profiles ) .
	manualset3
92108	9	399324	13	NULL	NULL	0	NULL	spectral profiles	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	Image stacks ( 5 benign , 7 malignant tumors ) were analyzed by established software ( principal component analysis PCA , hyperspectral classification , spectral profiles ) .
	manualset3
92109	1	399325	13	NULL	NULL	0	NULL	Images of tooth slices	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Images of tooth slices were also visually examined under magnification and dye penetration along the tooth/restoration interface was scored .
	manualset3
92110	2	399325	13	NULL	NULL	0	NULL	magnification	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Images of tooth slices were also visually examined under magnification and dye penetration along the tooth/restoration interface was scored .
	manualset3
92111	3	399325	13	NULL	NULL	0	NULL	dye penetration	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Images of tooth slices were also visually examined under magnification and dye penetration along the tooth/restoration interface was scored .
	manualset3
92112	4	399325	13	NULL	NULL	0	NULL	tooth/restoration interface	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Images of tooth slices were also visually examined under magnification and dye penetration along the tooth/restoration interface was scored .
	manualset3
92113	1	399326	13	NULL	NULL	0	NULL	Images	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Images were taken using single breath-hold and ECG triggering .
	manualset3
92114	2	399326	13	NULL	NULL	0	NULL	single breath-hold 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Images were taken using single breath-hold and ECG triggering .
	manualset3
92115	3	399326	13	NULL	NULL	0	NULL	 ECG triggering	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Images were taken using single breath-hold and ECG triggering .
	manualset3
92116	1	399327	13	NULL	NULL	0	NULL	topic	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging is the topic of 1998 with advances in the areas of ultrasound .
	manualset3
92117	2	399327	13	NULL	NULL	0	NULL	1998	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging is the topic of 1998 with advances in the areas of ultrasound .
	manualset3
92118	3	399327	13	NULL	NULL	0	NULL	areas of ultrasound	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging is the topic of 1998 with advances in the areas of ultrasound .
	manualset3
98573	4	399327	13	NULL	NULL	0	NULL	Imaging	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging is the topic of 1998 with advances in the areas of ultrasound .
	manualset3
92119	1	399328	13	NULL	NULL	0	NULL	 important role 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging plays an important role in LDLT programs by providing robust evaluation of potential donors to ensure that only anatomically suitable donors with no significant co-existing pathology are selected and that crucial information that allows detailed preoperative planning is available .
	manualset3
92120	2	399328	13	NULL	NULL	0	NULL	LDLT programs	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging plays an important role in LDLT programs by providing robust evaluation of potential donors to ensure that only anatomically suitable donors with no significant co-existing pathology are selected and that crucial information that allows detailed preoperative planning is available .
	manualset3
92121	3	399328	13	NULL	NULL	0	NULL	 robust evaluation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging plays an important role in LDLT programs by providing robust evaluation of potential donors to ensure that only anatomically suitable donors with no significant co-existing pathology are selected and that crucial information that allows detailed preoperative planning is available .
	manualset3
92122	4	399328	13	NULL	NULL	0	NULL	potential donors	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging plays an important role in LDLT programs by providing robust evaluation of potential donors to ensure that only anatomically suitable donors with no significant co-existing pathology are selected and that crucial information that allows detailed preoperative planning is available .
	manualset3
92123	5	399328	13	NULL	NULL	NULL	NULL	suitable donors	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imaging plays an important role in LDLT programs by providing robust evaluation of potential donors to ensure that only anatomically suitable donors with no significant co-existing pathology are selected and that crucial information that allows detailed preoperative planning is available .
	manualset3
92124	6	399328	13	NULL	NULL	0	NULL	pathology 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging plays an important role in LDLT programs by providing robust evaluation of potential donors to ensure that only anatomically suitable donors with no significant co-existing pathology are selected and that crucial information that allows detailed preoperative planning is available .
	manualset3
92125	7	399328	13	NULL	NULL	0	NULL	crucial information	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging plays an important role in LDLT programs by providing robust evaluation of potential donors to ensure that only anatomically suitable donors with no significant co-existing pathology are selected and that crucial information that allows detailed preoperative planning is available .
	manualset3
98574	8	399328	13	NULL	NULL	0	NULL	Imaging 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging plays an important role in LDLT programs by providing robust evaluation of potential donors to ensure that only anatomically suitable donors with no significant co-existing pathology are selected and that crucial information that allows detailed preoperative planning is available .
	manualset3
92126	1	399329	13	NULL	NULL	0	NULL	hematopoietic stem cell transplantation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging in hematopoietic stem cell transplantation .
	manualset3
98575	2	399329	13	NULL	NULL	0	NULL	Imaging	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging in hematopoietic stem cell transplantation .
	manualset3
92127	2	399330	13	NULL	NULL	NULL	NULL	acute neurological conditions 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imaging of acute neurological conditions in pregnancy and the puerperium .
	manualset3
92128	3	399330	13	NULL	NULL	NULL	NULL	pregnancy	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imaging of acute neurological conditions in pregnancy and the puerperium .
	manualset3
92129	4	399330	13	NULL	NULL	NULL	NULL	puerperium	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imaging of acute neurological conditions in pregnancy and the puerperium .
	manualset3
94202	1	399330	13	NULL	NULL	NULL	NULL	Imaging	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imaging of acute neurological conditions in pregnancy and the puerperium .
	manualset3
92397	2	399331	13	NULL	NULL	NULL	NULL	primary penile cancer	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imaging of primary penile cancer and metastatic lymphadenopathy can help optimize planning of both primary tumor resection and treatment for lymph node metastases .
	manualset3
92406	3	399331	13	NULL	NULL	NULL	NULL	metastatic lymphadenopathy	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imaging of primary penile cancer and metastatic lymphadenopathy can help optimize planning of both primary tumor resection and treatment for lymph node metastases .
	manualset3
92410	5	399331	13	NULL	NULL	NULL	NULL	primary tumor resection	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imaging of primary penile cancer and metastatic lymphadenopathy can help optimize planning of both primary tumor resection and treatment for lymph node metastases .
	manualset3
92411	6	399331	13	NULL	NULL	NULL	NULL	treatment 	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imaging of primary penile cancer and metastatic lymphadenopathy can help optimize planning of both primary tumor resection and treatment for lymph node metastases .
	manualset3
92412	7	399331	13	NULL	NULL	NULL	NULL	lymph node metastases 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imaging of primary penile cancer and metastatic lymphadenopathy can help optimize planning of both primary tumor resection and treatment for lymph node metastases .
	manualset3
94203	1	399331	13	NULL	NULL	0	NULL	Imaging	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging of primary penile cancer and metastatic lymphadenopathy can help optimize planning of both primary tumor resection and treatment for lymph node metastases .
	manualset3
94204	4	399331	13	NULL	NULL	0	NULL	optimize planning	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging of primary penile cancer and metastatic lymphadenopathy can help optimize planning of both primary tumor resection and treatment for lymph node metastases .
	manualset3
92414	4	399332	13	NULL	NULL	NULL	NULL	protease functions	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imaging of protease functions -- current guide to spotting cysteine cathepsins in classical and novel scenes of action in mammalian epithelial cells and tissues .
	manualset3
92419	2	399332	13	NULL	NULL	0	NULL	cysteine cathepsins	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging of protease functions -- current guide to spotting cysteine cathepsins in classical and novel scenes of action in mammalian epithelial cells and tissues .
	manualset3
92421	5	399332	13	NULL	NULL	NULL	NULL	classical scenes of action	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imaging of protease functions -- current guide to spotting cysteine cathepsins in classical and novel scenes of action in mammalian epithelial cells and tissues .
	manualset3
92422	6	399332	13	NULL	NULL	NULL	NULL	novel scenes of action	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imaging of protease functions -- current guide to spotting cysteine cathepsins in classical and novel scenes of action in mammalian epithelial cells and tissues .
	manualset3
92423	7	399332	13	NULL	NULL	NULL	NULL	mammalian epithelial cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imaging of protease functions -- current guide to spotting cysteine cathepsins in classical and novel scenes of action in mammalian epithelial cells and tissues .
	manualset3
92424	8	399332	13	NULL	NULL	NULL	NULL	mammalian epithelial tissues	Tissue												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imaging of protease functions -- current guide to spotting cysteine cathepsins in classical and novel scenes of action in mammalian epithelial cells and tissues .
	manualset3
94205	1	399332	13	NULL	NULL	0	NULL	Imaging	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging of protease functions -- current guide to spotting cysteine cathepsins in classical and novel scenes of action in mammalian epithelial cells and tissues .
	manualset3
94206	3	399332	13	NULL	NULL	NULL	NULL	guide	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imaging of protease functions -- current guide to spotting cysteine cathepsins in classical and novel scenes of action in mammalian epithelial cells and tissues .
	manualset3
92425	1	399333	13	NULL	NULL	NULL	NULL	Imaging of the vascular system	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imaging of the vascular system revealed vessels down to the caliber of capillaries , and the digital three-dimensional data obtained from the scans allowed for virtual cutting , amplification , and scaling without destroying the sample .
	manualset3
92428	2	399333	13	NULL	NULL	0	NULL	vessels 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging of the vascular system revealed vessels down to the caliber of capillaries , and the digital three-dimensional data obtained from the scans allowed for virtual cutting , amplification , and scaling without destroying the sample .
	manualset3
92430	3	399333	13	NULL	NULL	0	NULL	caliber of capillaries	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging of the vascular system revealed vessels down to the caliber of capillaries , and the digital three-dimensional data obtained from the scans allowed for virtual cutting , amplification , and scaling without destroying the sample .
	manualset3
92497	4	399333	13	NULL	NULL	0	NULL	digital three-dimensional data	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging of the vascular system revealed vessels down to the caliber of capillaries , and the digital three-dimensional data obtained from the scans allowed for virtual cutting , amplification , and scaling without destroying the sample .
	manualset3
92502	5	399333	13	NULL	NULL	0	NULL	scans 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging of the vascular system revealed vessels down to the caliber of capillaries , and the digital three-dimensional data obtained from the scans allowed for virtual cutting , amplification , and scaling without destroying the sample .
	manualset3
92508	7	399333	13	NULL	NULL	NULL	NULL	 amplification 	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imaging of the vascular system revealed vessels down to the caliber of capillaries , and the digital three-dimensional data obtained from the scans allowed for virtual cutting , amplification , and scaling without destroying the sample .
	manualset3
92509	8	399333	13	NULL	NULL	NULL	NULL	sample	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Imaging of the vascular system revealed vessels down to the caliber of capillaries , and the digital three-dimensional data obtained from the scans allowed for virtual cutting , amplification , and scaling without destroying the sample .
	manualset3
94208	6	399333	13	NULL	NULL	0	NULL	 virtual cutting	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Imaging of the vascular system revealed vessels down to the caliber of capillaries , and the digital three-dimensional data obtained from the scans allowed for virtual cutting , amplification , and scaling without destroying the sample .
	manualset3
92512	1	399334	13	NULL	NULL	0	NULL	historical development	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( Then and now ; the historical development of the theory of pernicious anemia Biermer ) .
	manualset3
92516	2	399334	13	NULL	NULL	0	NULL	theory	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	( Then and now ; the historical development of the theory of pernicious anemia Biermer ) .
	manualset3
92517	3	399334	13	NULL	NULL	0	NULL	pernicious anemia Biermer	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Then and now ; the historical development of the theory of pernicious anemia Biermer ) .
	manualset3
96842	4	399334	13	NULL	NULL	0	NULL	Then	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	( Then and now ; the historical development of the theory of pernicious anemia Biermer ) .
	manualset3
96843	5	399334	13	NULL	NULL	0	NULL	now	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	( Then and now ; the historical development of the theory of pernicious anemia Biermer ) .
	manualset3
92518	1	399335	13	NULL	NULL	0	NULL	Iminoazophenol 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Iminoazophenol appended calix ( 4 ) arene/thiacalix ( 4 ) arene derivatives 1 and 2 of cone and 3 of 1 , 3-alternate conformation have been synthesized and examined for their chromogenic anion recognition abilities towards different anions like fluoride , chloride , bromide , iodide , acetate , dihydrogenphosphate , nitrate and hydrogensulphate by UV-vis spectroscopy .
	manualset3
92519	2	399335	13	NULL	NULL	NULL	NULL	 calix ( 4 ) arene/thiacalix ( 4 ) arene derivatives 1	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Iminoazophenol appended calix ( 4 ) arene/thiacalix ( 4 ) arene derivatives 1 and 2 of cone and 3 of 1 , 3-alternate conformation have been synthesized and examined for their chromogenic anion recognition abilities towards different anions like fluoride , chloride , bromide , iodide , acetate , dihydrogenphosphate , nitrate and hydrogensulphate by UV-vis spectroscopy .
	manualset3
92520	3	399335	13	NULL	NULL	NULL	NULL	 calix ( 4 ) arene/thiacalix ( 4 ) arene derivatives 2	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Iminoazophenol appended calix ( 4 ) arene/thiacalix ( 4 ) arene derivatives 1 and 2 of cone and 3 of 1 , 3-alternate conformation have been synthesized and examined for their chromogenic anion recognition abilities towards different anions like fluoride , chloride , bromide , iodide , acetate , dihydrogenphosphate , nitrate and hydrogensulphate by UV-vis spectroscopy .
	manualset3
92522	5	399335	13	NULL	NULL	0	NULL	 3 of 1 , 3-alternate conformation	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Iminoazophenol appended calix ( 4 ) arene/thiacalix ( 4 ) arene derivatives 1 and 2 of cone and 3 of 1 , 3-alternate conformation have been synthesized and examined for their chromogenic anion recognition abilities towards different anions like fluoride , chloride , bromide , iodide , acetate , dihydrogenphosphate , nitrate and hydrogensulphate by UV-vis spectroscopy .
	manualset3
92523	6	399335	13	NULL	NULL	0	NULL	chromogenic anion 	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	Iminoazophenol appended calix ( 4 ) arene/thiacalix ( 4 ) arene derivatives 1 and 2 of cone and 3 of 1 , 3-alternate conformation have been synthesized and examined for their chromogenic anion recognition abilities towards different anions like fluoride , chloride , bromide , iodide , acetate , dihydrogenphosphate , nitrate and hydrogensulphate by UV-vis spectroscopy .
	manualset3
92524	7	399335	13	NULL	NULL	0	NULL	recognition abilities	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Iminoazophenol appended calix ( 4 ) arene/thiacalix ( 4 ) arene derivatives 1 and 2 of cone and 3 of 1 , 3-alternate conformation have been synthesized and examined for their chromogenic anion recognition abilities towards different anions like fluoride , chloride , bromide , iodide , acetate , dihydrogenphosphate , nitrate and hydrogensulphate by UV-vis spectroscopy .
	manualset3
92525	8	399335	13	NULL	NULL	0	NULL	anions	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	Iminoazophenol appended calix ( 4 ) arene/thiacalix ( 4 ) arene derivatives 1 and 2 of cone and 3 of 1 , 3-alternate conformation have been synthesized and examined for their chromogenic anion recognition abilities towards different anions like fluoride , chloride , bromide , iodide , acetate , dihydrogenphosphate , nitrate and hydrogensulphate by UV-vis spectroscopy .
	manualset3
92526	9	399335	13	NULL	NULL	0	NULL	fluoride	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	Iminoazophenol appended calix ( 4 ) arene/thiacalix ( 4 ) arene derivatives 1 and 2 of cone and 3 of 1 , 3-alternate conformation have been synthesized and examined for their chromogenic anion recognition abilities towards different anions like fluoride , chloride , bromide , iodide , acetate , dihydrogenphosphate , nitrate and hydrogensulphate by UV-vis spectroscopy .
	manualset3
92527	10	399335	13	NULL	NULL	0	NULL	 chloride	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	Iminoazophenol appended calix ( 4 ) arene/thiacalix ( 4 ) arene derivatives 1 and 2 of cone and 3 of 1 , 3-alternate conformation have been synthesized and examined for their chromogenic anion recognition abilities towards different anions like fluoride , chloride , bromide , iodide , acetate , dihydrogenphosphate , nitrate and hydrogensulphate by UV-vis spectroscopy .
	manualset3
92528	11	399335	13	NULL	NULL	0	NULL	bromide	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	Iminoazophenol appended calix ( 4 ) arene/thiacalix ( 4 ) arene derivatives 1 and 2 of cone and 3 of 1 , 3-alternate conformation have been synthesized and examined for their chromogenic anion recognition abilities towards different anions like fluoride , chloride , bromide , iodide , acetate , dihydrogenphosphate , nitrate and hydrogensulphate by UV-vis spectroscopy .
	manualset3
92529	12	399335	13	NULL	NULL	0	NULL	 iodide	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	Iminoazophenol appended calix ( 4 ) arene/thiacalix ( 4 ) arene derivatives 1 and 2 of cone and 3 of 1 , 3-alternate conformation have been synthesized and examined for their chromogenic anion recognition abilities towards different anions like fluoride , chloride , bromide , iodide , acetate , dihydrogenphosphate , nitrate and hydrogensulphate by UV-vis spectroscopy .
	manualset3
92530	13	399335	13	NULL	NULL	0	NULL	acetate	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	Iminoazophenol appended calix ( 4 ) arene/thiacalix ( 4 ) arene derivatives 1 and 2 of cone and 3 of 1 , 3-alternate conformation have been synthesized and examined for their chromogenic anion recognition abilities towards different anions like fluoride , chloride , bromide , iodide , acetate , dihydrogenphosphate , nitrate and hydrogensulphate by UV-vis spectroscopy .
	manualset3
92531	14	399335	13	NULL	NULL	0	NULL	dihydrogenphosphate 	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	Iminoazophenol appended calix ( 4 ) arene/thiacalix ( 4 ) arene derivatives 1 and 2 of cone and 3 of 1 , 3-alternate conformation have been synthesized and examined for their chromogenic anion recognition abilities towards different anions like fluoride , chloride , bromide , iodide , acetate , dihydrogenphosphate , nitrate and hydrogensulphate by UV-vis spectroscopy .
	manualset3
92532	15	399335	13	NULL	NULL	0	NULL	nitrate	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	Iminoazophenol appended calix ( 4 ) arene/thiacalix ( 4 ) arene derivatives 1 and 2 of cone and 3 of 1 , 3-alternate conformation have been synthesized and examined for their chromogenic anion recognition abilities towards different anions like fluoride , chloride , bromide , iodide , acetate , dihydrogenphosphate , nitrate and hydrogensulphate by UV-vis spectroscopy .
	manualset3
92533	16	399335	13	NULL	NULL	0	NULL	hydrogensulphate 	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	Iminoazophenol appended calix ( 4 ) arene/thiacalix ( 4 ) arene derivatives 1 and 2 of cone and 3 of 1 , 3-alternate conformation have been synthesized and examined for their chromogenic anion recognition abilities towards different anions like fluoride , chloride , bromide , iodide , acetate , dihydrogenphosphate , nitrate and hydrogensulphate by UV-vis spectroscopy .
	manualset3
92534	17	399335	13	NULL	NULL	0	NULL	UV-vis spectroscopy	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Iminoazophenol appended calix ( 4 ) arene/thiacalix ( 4 ) arene derivatives 1 and 2 of cone and 3 of 1 , 3-alternate conformation have been synthesized and examined for their chromogenic anion recognition abilities towards different anions like fluoride , chloride , bromide , iodide , acetate , dihydrogenphosphate , nitrate and hydrogensulphate by UV-vis spectroscopy .
	manualset3
92577	1	399336	13	NULL	NULL	NULL	NULL	Immediate effects	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immediate and long-term effects of addition of exercise to a 16-week very low calorie diet on low-grade inflammation in obese , insulin-dependent type 2 diabetic patients .
	manualset3
92578	2	399336	13	NULL	NULL	NULL	NULL	 long-term effects 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immediate and long-term effects of addition of exercise to a 16-week very low calorie diet on low-grade inflammation in obese , insulin-dependent type 2 diabetic patients .
	manualset3
92579	3	399336	13	NULL	NULL	0	NULL	addition of exercise 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Immediate and long-term effects of addition of exercise to a 16-week very low calorie diet on low-grade inflammation in obese , insulin-dependent type 2 diabetic patients .
	manualset3
92580	4	399336	13	NULL	NULL	0	NULL	16-week	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Immediate and long-term effects of addition of exercise to a 16-week very low calorie diet on low-grade inflammation in obese , insulin-dependent type 2 diabetic patients .
	manualset3
92581	5	399336	13	NULL	NULL	0	NULL	low calorie diet	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	Immediate and long-term effects of addition of exercise to a 16-week very low calorie diet on low-grade inflammation in obese , insulin-dependent type 2 diabetic patients .
	manualset3
92582	6	399336	13	NULL	NULL	0	NULL	low-grade inflammation 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immediate and long-term effects of addition of exercise to a 16-week very low calorie diet on low-grade inflammation in obese , insulin-dependent type 2 diabetic patients .
	manualset3
92583	7	399336	13	NULL	NULL	0	NULL	obese patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immediate and long-term effects of addition of exercise to a 16-week very low calorie diet on low-grade inflammation in obese , insulin-dependent type 2 diabetic patients .
	manualset3
92584	8	399336	13	NULL	NULL	0	NULL	insulin-dependent type 2 diabetic patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immediate and long-term effects of addition of exercise to a 16-week very low calorie diet on low-grade inflammation in obese , insulin-dependent type 2 diabetic patients .
	manualset3
92585	2	399337	13	NULL	NULL	NULL	NULL	larger initial specimens	Tissue												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immediate re-sampling , or larger initial specimens would have salvaged the procedure in most instances of failure .
	manualset3
92586	2	399337	13	NULL	NULL	0	NULL	procedure	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immediate re-sampling , or larger initial specimens would have salvaged the procedure in most instances of failure .
	manualset3
92587	3	399337	13	NULL	NULL	0	NULL	instances of failure	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immediate re-sampling , or larger initial specimens would have salvaged the procedure in most instances of failure .
	manualset3
94209	1	399337	13	NULL	NULL	0	NULL	Immediate re-sampling	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immediate re-sampling , or larger initial specimens would have salvaged the procedure in most instances of failure .
	manualset3
92588	1	399338	13	NULL	NULL	0	NULL	Immobilization	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immobilization of protamine to the inner lumen of cellulose hollow fibers has been shown useful in preventing both heparin - and protamine-induced complications during an extracorporeal blood circulation procedure .
	manualset3
92589	2	399338	13	NULL	NULL	0	NULL	protamine	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immobilization of protamine to the inner lumen of cellulose hollow fibers has been shown useful in preventing both heparin - and protamine-induced complications during an extracorporeal blood circulation procedure .
	manualset3
92590	3	399338	13	NULL	NULL	NULL	NULL	inner lumen of cellulose hollow fibers	Facility												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immobilization of protamine to the inner lumen of cellulose hollow fibers has been shown useful in preventing both heparin - and protamine-induced complications during an extracorporeal blood circulation procedure .
	manualset3
92591	4	399338	13	NULL	NULL	0	NULL	heparin-induced complications 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immobilization of protamine to the inner lumen of cellulose hollow fibers has been shown useful in preventing both heparin - and protamine-induced complications during an extracorporeal blood circulation procedure .
	manualset3
92592	5	399338	13	NULL	NULL	0	NULL	protamine-induced complications	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immobilization of protamine to the inner lumen of cellulose hollow fibers has been shown useful in preventing both heparin - and protamine-induced complications during an extracorporeal blood circulation procedure .
	manualset3
92593	6	399338	13	NULL	NULL	0	NULL	 extracorporeal blood circulation procedure 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immobilization of protamine to the inner lumen of cellulose hollow fibers has been shown useful in preventing both heparin - and protamine-induced complications during an extracorporeal blood circulation procedure .
	manualset3
92594	1	399339	13	NULL	NULL	0	NULL	Immune cytokine inhibition 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immune cytokine inhibition of beta-adrenergic agonist stimulated cyclic AMP generation in cardiac myocytes .
	manualset3
92595	2	399339	13	NULL	NULL	0	NULL	beta-adrenergic agonist	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Immune cytokine inhibition of beta-adrenergic agonist stimulated cyclic AMP generation in cardiac myocytes .
	manualset3
92596	3	399339	13	NULL	NULL	0	NULL	cyclic AMP generation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immune cytokine inhibition of beta-adrenergic agonist stimulated cyclic AMP generation in cardiac myocytes .
	manualset3
92597	4	399339	13	NULL	NULL	0	NULL	cardiac myocytes 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Immune cytokine inhibition of beta-adrenergic agonist stimulated cyclic AMP generation in cardiac myocytes .
	manualset3
92598	1	399340	13	NULL	NULL	0	NULL	Therapeutic action	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Therapeutic and prophylactic action of succimer in experimental subacute lead acetate poisoning ) .
	manualset3
92599	2	399340	13	NULL	NULL	0	NULL	prophylactic action 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Therapeutic and prophylactic action of succimer in experimental subacute lead acetate poisoning ) .
	manualset3
92600	3	399340	13	NULL	NULL	0	NULL	succimer	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( Therapeutic and prophylactic action of succimer in experimental subacute lead acetate poisoning ) .
	manualset3
92601	4	399340	13	NULL	NULL	NULL	NULL	experimental subacute lead acetate poisoning	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Therapeutic and prophylactic action of succimer in experimental subacute lead acetate poisoning ) .
	manualset3
92602	1	399341	13	NULL	NULL	0	NULL	Immune factors 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immune factors such as cellular immunity , autoimmunity , and inflammation may play a pathogenic role in Alzheimer 's disease ( AD ) , a neurodegenerative disorder .
	manualset3
92603	2	399341	13	NULL	NULL	NULL	NULL	cellular immunity	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immune factors such as cellular immunity , autoimmunity , and inflammation may play a pathogenic role in Alzheimer 's disease ( AD ) , a neurodegenerative disorder .
	manualset3
92604	3	399341	13	NULL	NULL	0	NULL	autoimmunity 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immune factors such as cellular immunity , autoimmunity , and inflammation may play a pathogenic role in Alzheimer 's disease ( AD ) , a neurodegenerative disorder .
	manualset3
92605	4	399341	13	NULL	NULL	0	NULL	inflammation 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immune factors such as cellular immunity , autoimmunity , and inflammation may play a pathogenic role in Alzheimer 's disease ( AD ) , a neurodegenerative disorder .
	manualset3
92606	5	399341	13	NULL	NULL	0	NULL	pathogenic role	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immune factors such as cellular immunity , autoimmunity , and inflammation may play a pathogenic role in Alzheimer 's disease ( AD ) , a neurodegenerative disorder .
	manualset3
92607	6	399341	13	NULL	NULL	0	NULL	Alzheimer 's disease ( AD )	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Immune factors such as cellular immunity , autoimmunity , and inflammation may play a pathogenic role in Alzheimer 's disease ( AD ) , a neurodegenerative disorder .
	manualset3
92608	7	399341	13	NULL	NULL	0	NULL	neurodegenerative disorder 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Immune factors such as cellular immunity , autoimmunity , and inflammation may play a pathogenic role in Alzheimer 's disease ( AD ) , a neurodegenerative disorder .
	manualset3
92609	1	399342	13	NULL	NULL	0	NULL	Immune reactivity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immune reactivity of the purified hemagglutinin of measles virus .
	manualset3
92610	2	399342	13	NULL	NULL	0	NULL	hemagglutinin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immune reactivity of the purified hemagglutinin of measles virus .
	manualset3
92611	3	399342	13	NULL	NULL	0	NULL	 measles virus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Immune reactivity of the purified hemagglutinin of measles virus .
	manualset3
92612	1	399343	13	NULL	NULL	0	NULL	Immunisation coverage	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunisation coverage with 3 doses of oral polio vaccine ( OPV ) was less than 10 % during 1974-80 when immunisation was a clinic based activity .
	manualset3
92613	2	399343	13	NULL	NULL	0	NULL	3 doses of oral polio vaccine ( OPV ) 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunisation coverage with 3 doses of oral polio vaccine ( OPV ) was less than 10 % during 1974-80 when immunisation was a clinic based activity .
	manualset3
92614	3	399343	13	NULL	NULL	0	NULL	less than 10 % 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunisation coverage with 3 doses of oral polio vaccine ( OPV ) was less than 10 % during 1974-80 when immunisation was a clinic based activity .
	manualset3
92615	4	399343	13	NULL	NULL	0	NULL	1974-80	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunisation coverage with 3 doses of oral polio vaccine ( OPV ) was less than 10 % during 1974-80 when immunisation was a clinic based activity .
	manualset3
92616	5	399343	13	NULL	NULL	0	NULL	 immunisation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunisation coverage with 3 doses of oral polio vaccine ( OPV ) was less than 10 % during 1974-80 when immunisation was a clinic based activity .
	manualset3
92617	6	399343	13	NULL	NULL	0	NULL	 clinic based activity	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunisation coverage with 3 doses of oral polio vaccine ( OPV ) was less than 10 % during 1974-80 when immunisation was a clinic based activity .
	manualset3
92618	1	399344	13	NULL	NULL	0	NULL	Immunization 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization against a dominant tumor antigen abrogates immunogenicity of the tumor .
	manualset3
92619	2	399344	13	NULL	NULL	0	NULL	dominant tumor antigen	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization against a dominant tumor antigen abrogates immunogenicity of the tumor .
	manualset3
92620	3	399344	13	NULL	NULL	0	NULL	immunogenicity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization against a dominant tumor antigen abrogates immunogenicity of the tumor .
	manualset3
92621	4	399344	13	NULL	NULL	0	NULL	tumor	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization against a dominant tumor antigen abrogates immunogenicity of the tumor .
	manualset3
92622	1	399345	13	NULL	NULL	0	NULL	Immunization 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization of children with asthma against pneumococcal infection with polysaccharide vaccine or combined immunization against pneumococcal infection and influenza reduced rate of asthma exacerbations and led to formation of immunity to vaccine strains of Streptococcus pneumoniae .
	manualset3
92623	2	399345	13	NULL	NULL	0	NULL	children	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization of children with asthma against pneumococcal infection with polysaccharide vaccine or combined immunization against pneumococcal infection and influenza reduced rate of asthma exacerbations and led to formation of immunity to vaccine strains of Streptococcus pneumoniae .
	manualset3
92624	3	399345	13	NULL	NULL	0	NULL	asthma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization of children with asthma against pneumococcal infection with polysaccharide vaccine or combined immunization against pneumococcal infection and influenza reduced rate of asthma exacerbations and led to formation of immunity to vaccine strains of Streptococcus pneumoniae .
	manualset3
92625	4	399345	13	NULL	NULL	0	NULL	pneumococcal infection 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization of children with asthma against pneumococcal infection with polysaccharide vaccine or combined immunization against pneumococcal infection and influenza reduced rate of asthma exacerbations and led to formation of immunity to vaccine strains of Streptococcus pneumoniae .
	manualset3
92626	5	399345	13	NULL	NULL	0	NULL	polysaccharide vaccine	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization of children with asthma against pneumococcal infection with polysaccharide vaccine or combined immunization against pneumococcal infection and influenza reduced rate of asthma exacerbations and led to formation of immunity to vaccine strains of Streptococcus pneumoniae .
	manualset3
92627	6	399345	13	NULL	NULL	0	NULL	immunization 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization of children with asthma against pneumococcal infection with polysaccharide vaccine or combined immunization against pneumococcal infection and influenza reduced rate of asthma exacerbations and led to formation of immunity to vaccine strains of Streptococcus pneumoniae .
	manualset3
92628	7	399345	13	NULL	NULL	0	NULL	pneumococcal infection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization of children with asthma against pneumococcal infection with polysaccharide vaccine or combined immunization against pneumococcal infection and influenza reduced rate of asthma exacerbations and led to formation of immunity to vaccine strains of Streptococcus pneumoniae .
	manualset3
92629	8	399345	13	NULL	NULL	0	NULL	influenza	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization of children with asthma against pneumococcal infection with polysaccharide vaccine or combined immunization against pneumococcal infection and influenza reduced rate of asthma exacerbations and led to formation of immunity to vaccine strains of Streptococcus pneumoniae .
	manualset3
92630	9	399345	13	NULL	NULL	0	NULL	rate of asthma exacerbations	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization of children with asthma against pneumococcal infection with polysaccharide vaccine or combined immunization against pneumococcal infection and influenza reduced rate of asthma exacerbations and led to formation of immunity to vaccine strains of Streptococcus pneumoniae .
	manualset3
92631	10	399345	13	NULL	NULL	0	NULL	formation of immunity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization of children with asthma against pneumococcal infection with polysaccharide vaccine or combined immunization against pneumococcal infection and influenza reduced rate of asthma exacerbations and led to formation of immunity to vaccine strains of Streptococcus pneumoniae .
	manualset3
92632	11	399345	13	NULL	NULL	0	NULL	vaccine strains of Streptococcus pneumoniae 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization of children with asthma against pneumococcal infection with polysaccharide vaccine or combined immunization against pneumococcal infection and influenza reduced rate of asthma exacerbations and led to formation of immunity to vaccine strains of Streptococcus pneumoniae .
	manualset3
92633	1	399346	13	NULL	NULL	0	NULL	Immunization	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization with rgp96-tumor antigen complexes significantly inhibited B16 tumor growth compared with either rgp96 or tumor antigens alone and led to enhancement of tumor-specific T-cell activities , which was found similar to that of tumor tissue derived gp96 .
	manualset3
92634	2	399346	13	NULL	NULL	0	NULL	rgp96-tumor antigen complexes 	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization with rgp96-tumor antigen complexes significantly inhibited B16 tumor growth compared with either rgp96 or tumor antigens alone and led to enhancement of tumor-specific T-cell activities , which was found similar to that of tumor tissue derived gp96 .
	manualset3
92635	3	399346	13	NULL	NULL	0	NULL	 B16 tumor growth	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization with rgp96-tumor antigen complexes significantly inhibited B16 tumor growth compared with either rgp96 or tumor antigens alone and led to enhancement of tumor-specific T-cell activities , which was found similar to that of tumor tissue derived gp96 .
	manualset3
92636	4	399346	13	NULL	NULL	0	NULL	rgp96	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization with rgp96-tumor antigen complexes significantly inhibited B16 tumor growth compared with either rgp96 or tumor antigens alone and led to enhancement of tumor-specific T-cell activities , which was found similar to that of tumor tissue derived gp96 .
	manualset3
92637	5	399346	13	NULL	NULL	0	NULL	 tumor antigens	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization with rgp96-tumor antigen complexes significantly inhibited B16 tumor growth compared with either rgp96 or tumor antigens alone and led to enhancement of tumor-specific T-cell activities , which was found similar to that of tumor tissue derived gp96 .
	manualset3
92638	6	399346	13	NULL	NULL	0	NULL	 enhancement 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization with rgp96-tumor antigen complexes significantly inhibited B16 tumor growth compared with either rgp96 or tumor antigens alone and led to enhancement of tumor-specific T-cell activities , which was found similar to that of tumor tissue derived gp96 .
	manualset3
92639	7	399346	13	NULL	NULL	0	NULL	tumor-specific T-cell activities 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunization with rgp96-tumor antigen complexes significantly inhibited B16 tumor growth compared with either rgp96 or tumor antigens alone and led to enhancement of tumor-specific T-cell activities , which was found similar to that of tumor tissue derived gp96 .
	manualset3
92641	8	399346	13	NULL	NULL	NULL	NULL	tumor tissue	Tissue												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunization with rgp96-tumor antigen complexes significantly inhibited B16 tumor growth compared with either rgp96 or tumor antigens alone and led to enhancement of tumor-specific T-cell activities , which was found similar to that of tumor tissue derived gp96 .
	manualset3
92642	9	399346	13	NULL	NULL	NULL	NULL	gp96	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunization with rgp96-tumor antigen complexes significantly inhibited B16 tumor growth compared with either rgp96 or tumor antigens alone and led to enhancement of tumor-specific T-cell activities , which was found similar to that of tumor tissue derived gp96 .
	manualset3
92643	1	399347	13	NULL	NULL	0	NULL	Immunoarchitecture 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoarchitecture of eutopic remnants was indistinguishable from that of intact spleens and total nucleated cell counts remained proportional to weight .
	manualset3
92644	2	399347	13	NULL	NULL	0	NULL	eutopic remnants	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoarchitecture of eutopic remnants was indistinguishable from that of intact spleens and total nucleated cell counts remained proportional to weight .
	manualset3
92645	3	399347	13	NULL	NULL	0	NULL	intact spleens	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoarchitecture of eutopic remnants was indistinguishable from that of intact spleens and total nucleated cell counts remained proportional to weight .
	manualset3
92646	4	399347	13	NULL	NULL	0	NULL	total nucleated cell counts	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoarchitecture of eutopic remnants was indistinguishable from that of intact spleens and total nucleated cell counts remained proportional to weight .
	manualset3
92647	5	399347	13	NULL	NULL	0	NULL	proportional to weight	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoarchitecture of eutopic remnants was indistinguishable from that of intact spleens and total nucleated cell counts remained proportional to weight .
	manualset3
92648	1	399348	13	NULL	NULL	0	NULL	Immunoassays 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoassays of the 1st and 2nd levels were investigated in patients with acute radiation disease 12-36 mos .
	manualset3
92649	2	399348	13	NULL	NULL	0	NULL	1st level	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoassays of the 1st and 2nd levels were investigated in patients with acute radiation disease 12-36 mos .
	manualset3
92650	3	399348	13	NULL	NULL	0	NULL	2nd level	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoassays of the 1st and 2nd levels were investigated in patients with acute radiation disease 12-36 mos .
	manualset3
92651	4	399348	13	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoassays of the 1st and 2nd levels were investigated in patients with acute radiation disease 12-36 mos .
	manualset3
92652	5	399348	13	NULL	NULL	0	NULL	acute radiation disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoassays of the 1st and 2nd levels were investigated in patients with acute radiation disease 12-36 mos .
	manualset3
92653	6	399348	13	NULL	NULL	0	NULL	12-36 mos	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoassays of the 1st and 2nd levels were investigated in patients with acute radiation disease 12-36 mos .
	manualset3
92654	1	399349	13	NULL	NULL	0	NULL	( 2 ) A short region	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	( 2 ) A short region , largely uniform in length , which was located immediately 5 ' to each rTU .
	manualset3
92655	2	399349	13	NULL	NULL	0	NULL	 length	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	( 2 ) A short region , largely uniform in length , which was located immediately 5 ' to each rTU .
	manualset3
92656	3	399349	13	NULL	NULL	0	NULL	5 ' to each rTU 	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	( 2 ) A short region , largely uniform in length , which was located immediately 5 ' to each rTU .
	manualset3
92657	1	399350	13	NULL	NULL	0	NULL	 Anesthetic properties	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Anesthetic properties of a new inhibitor of glutaminergic transmission in the central nervous system , riluzole ) .
	manualset3
92658	2	399350	13	NULL	NULL	0	NULL	a new inhibitor of glutaminergic transmission	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( Anesthetic properties of a new inhibitor of glutaminergic transmission in the central nervous system , riluzole ) .
	manualset3
92659	3	399350	13	NULL	NULL	0	NULL	 central nervous system	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( Anesthetic properties of a new inhibitor of glutaminergic transmission in the central nervous system , riluzole ) .
	manualset3
92660	4	399350	13	NULL	NULL	NULL	NULL	riluzole	Drug												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Anesthetic properties of a new inhibitor of glutaminergic transmission in the central nervous system , riluzole ) .
	manualset3
92661	1	399351	13	NULL	NULL	0	NULL	Therapeutic effects	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Therapeutic effects and histological findings during administration of the cytostatic agent bleomycin ) .
	manualset3
92662	2	399351	13	NULL	NULL	0	NULL	histological findings 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Therapeutic effects and histological findings during administration of the cytostatic agent bleomycin ) .
	manualset3
92663	3	399351	13	NULL	NULL	0	NULL	 administration 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Therapeutic effects and histological findings during administration of the cytostatic agent bleomycin ) .
	manualset3
92664	4	399351	13	NULL	NULL	0	NULL	cytostatic agent bleomycin 	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( Therapeutic effects and histological findings during administration of the cytostatic agent bleomycin ) .
	manualset3
92665	1	399352	13	NULL	NULL	0	NULL	Immunoblot analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot analysis demonstrated that type I - , IV - , and V-collagen-binding polypeptides ( CBPs ) were detected in the heated and unheated preparations from both Treponema denticola ATCC 33520 and T. socranskii subsp .
	manualset3
92666	2	399352	13	NULL	NULL	0	NULL	type I-collagen-binding polypeptides	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot analysis demonstrated that type I - , IV - , and V-collagen-binding polypeptides ( CBPs ) were detected in the heated and unheated preparations from both Treponema denticola ATCC 33520 and T. socranskii subsp .
	manualset3
92667	3	399352	13	NULL	NULL	0	NULL	type IV-collagen-binding polypeptides	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot analysis demonstrated that type I - , IV - , and V-collagen-binding polypeptides ( CBPs ) were detected in the heated and unheated preparations from both Treponema denticola ATCC 33520 and T. socranskii subsp .
	manualset3
92668	4	399352	13	NULL	NULL	0	NULL	type V-collagen-binding polypeptides	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot analysis demonstrated that type I - , IV - , and V-collagen-binding polypeptides ( CBPs ) were detected in the heated and unheated preparations from both Treponema denticola ATCC 33520 and T. socranskii subsp .
	manualset3
92669	5	399352	13	NULL	NULL	0	NULL	CBPs	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot analysis demonstrated that type I - , IV - , and V-collagen-binding polypeptides ( CBPs ) were detected in the heated and unheated preparations from both Treponema denticola ATCC 33520 and T. socranskii subsp .
	manualset3
92670	6	399352	13	NULL	NULL	0	NULL	 preparations	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot analysis demonstrated that type I - , IV - , and V-collagen-binding polypeptides ( CBPs ) were detected in the heated and unheated preparations from both Treponema denticola ATCC 33520 and T. socranskii subsp .
	manualset3
92671	7	399352	13	NULL	NULL	0	NULL	Treponema denticola ATCC 33520 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot analysis demonstrated that type I - , IV - , and V-collagen-binding polypeptides ( CBPs ) were detected in the heated and unheated preparations from both Treponema denticola ATCC 33520 and T. socranskii subsp .
	manualset3
92672	8	399352	13	NULL	NULL	0	NULL	T. socranskii subsp	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot analysis demonstrated that type I - , IV - , and V-collagen-binding polypeptides ( CBPs ) were detected in the heated and unheated preparations from both Treponema denticola ATCC 33520 and T. socranskii subsp .
	manualset3
92673	1	399353	13	NULL	NULL	0	NULL	Immunoblot analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot analysis identifies the released pertussis toxin substrate as alpha subunits of Gi2 , Gi3 , and G ( o ) in the resolved supernatant .
	manualset3
92674	2	399353	13	NULL	NULL	0	NULL	pertussis toxin 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot analysis identifies the released pertussis toxin substrate as alpha subunits of Gi2 , Gi3 , and G ( o ) in the resolved supernatant .
	manualset3
92675	3	399353	13	NULL	NULL	0	NULL	substrate	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot analysis identifies the released pertussis toxin substrate as alpha subunits of Gi2 , Gi3 , and G ( o ) in the resolved supernatant .
	manualset3
92676	4	399353	13	NULL	NULL	0	NULL	alpha subunit of Gi2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot analysis identifies the released pertussis toxin substrate as alpha subunits of Gi2 , Gi3 , and G ( o ) in the resolved supernatant .
	manualset3
92677	5	399353	13	NULL	NULL	0	NULL	 alpha subunits of Gi3	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot analysis identifies the released pertussis toxin substrate as alpha subunits of Gi2 , Gi3 , and G ( o ) in the resolved supernatant .
	manualset3
92678	6	399353	13	NULL	NULL	0	NULL	alpha subunits of G ( o )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot analysis identifies the released pertussis toxin substrate as alpha subunits of Gi2 , Gi3 , and G ( o ) in the resolved supernatant .
	manualset3
92679	7	399353	13	NULL	NULL	NULL	NULL	 supernatant 	CellComponent												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunoblot analysis identifies the released pertussis toxin substrate as alpha subunits of Gi2 , Gi3 , and G ( o ) in the resolved supernatant .
	manualset3
92680	1	399354	13	NULL	NULL	0	NULL	Immunoblot 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot and RNA analysis revealed decreases in P450 2C11 apoprotein and its corresponding mRNA in liver from deficient rats that was prevented by inclusion of ATRA in the deficient diet .
	manualset3
92681	2	399354	13	NULL	NULL	0	NULL	RNA analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot and RNA analysis revealed decreases in P450 2C11 apoprotein and its corresponding mRNA in liver from deficient rats that was prevented by inclusion of ATRA in the deficient diet .
	manualset3
92682	3	399354	13	NULL	NULL	0	NULL	P450 2C11 apoprotein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot and RNA analysis revealed decreases in P450 2C11 apoprotein and its corresponding mRNA in liver from deficient rats that was prevented by inclusion of ATRA in the deficient diet .
	manualset3
92683	4	399354	13	NULL	NULL	0	NULL	mRNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot and RNA analysis revealed decreases in P450 2C11 apoprotein and its corresponding mRNA in liver from deficient rats that was prevented by inclusion of ATRA in the deficient diet .
	manualset3
92684	5	399354	13	NULL	NULL	0	NULL	liver 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot and RNA analysis revealed decreases in P450 2C11 apoprotein and its corresponding mRNA in liver from deficient rats that was prevented by inclusion of ATRA in the deficient diet .
	manualset3
92685	6	399354	13	NULL	NULL	0	NULL	deficient rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot and RNA analysis revealed decreases in P450 2C11 apoprotein and its corresponding mRNA in liver from deficient rats that was prevented by inclusion of ATRA in the deficient diet .
	manualset3
92686	7	399354	13	NULL	NULL	0	NULL	inclusion	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot and RNA analysis revealed decreases in P450 2C11 apoprotein and its corresponding mRNA in liver from deficient rats that was prevented by inclusion of ATRA in the deficient diet .
	manualset3
92687	8	399354	13	NULL	NULL	0	NULL	ATRA	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot and RNA analysis revealed decreases in P450 2C11 apoprotein and its corresponding mRNA in liver from deficient rats that was prevented by inclusion of ATRA in the deficient diet .
	manualset3
92688	9	399354	13	NULL	NULL	0	NULL	deficient diet	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblot and RNA analysis revealed decreases in P450 2C11 apoprotein and its corresponding mRNA in liver from deficient rats that was prevented by inclusion of ATRA in the deficient diet .
	manualset3
92690	1	399355	13	NULL	NULL	0	NULL	Immunoblotting	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblotting of endogenous PKC phosphorylation confirmed PKC2 activation in response to IGF-II .
	manualset3
92691	2	399355	13	NULL	NULL	0	NULL	endogenous PKC phosphorylation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblotting of endogenous PKC phosphorylation confirmed PKC2 activation in response to IGF-II .
	manualset3
92692	3	399355	13	NULL	NULL	0	NULL	PKC2 activation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblotting of endogenous PKC phosphorylation confirmed PKC2 activation in response to IGF-II .
	manualset3
92693	4	399355	13	NULL	NULL	0	NULL	response	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblotting of endogenous PKC phosphorylation confirmed PKC2 activation in response to IGF-II .
	manualset3
92694	5	399355	13	NULL	NULL	0	NULL	IGF-II 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoblotting of endogenous PKC phosphorylation confirmed PKC2 activation in response to IGF-II .
	manualset3
92695	1	399356	13	NULL	NULL	0	NULL	Immunocharacterization	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocharacterization with beta-catenin , E-cadherin , cytokeratins ( AE1/AE3 ) , epithelial membrane antigen , S-100 protein , smooth muscle actin , and vimentin was also performed .
	manualset3
92696	2	399356	13	NULL	NULL	0	NULL	beta-catenin 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocharacterization with beta-catenin , E-cadherin , cytokeratins ( AE1/AE3 ) , epithelial membrane antigen , S-100 protein , smooth muscle actin , and vimentin was also performed .
	manualset3
92697	3	399356	13	NULL	NULL	0	NULL	E-cadherin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocharacterization with beta-catenin , E-cadherin , cytokeratins ( AE1/AE3 ) , epithelial membrane antigen , S-100 protein , smooth muscle actin , and vimentin was also performed .
	manualset3
92698	4	399356	13	NULL	NULL	0	NULL	cytokeratins ( AE1/AE3 ) 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocharacterization with beta-catenin , E-cadherin , cytokeratins ( AE1/AE3 ) , epithelial membrane antigen , S-100 protein , smooth muscle actin , and vimentin was also performed .
	manualset3
92699	5	399356	13	NULL	NULL	0	NULL	epithelial membrane antigen	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocharacterization with beta-catenin , E-cadherin , cytokeratins ( AE1/AE3 ) , epithelial membrane antigen , S-100 protein , smooth muscle actin , and vimentin was also performed .
	manualset3
92700	6	399356	13	NULL	NULL	0	NULL	S-100 protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocharacterization with beta-catenin , E-cadherin , cytokeratins ( AE1/AE3 ) , epithelial membrane antigen , S-100 protein , smooth muscle actin , and vimentin was also performed .
	manualset3
92701	7	399356	13	NULL	NULL	0	NULL	smooth muscle actin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocharacterization with beta-catenin , E-cadherin , cytokeratins ( AE1/AE3 ) , epithelial membrane antigen , S-100 protein , smooth muscle actin , and vimentin was also performed .
	manualset3
92702	8	399356	13	NULL	NULL	0	NULL	vimentin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocharacterization with beta-catenin , E-cadherin , cytokeratins ( AE1/AE3 ) , epithelial membrane antigen , S-100 protein , smooth muscle actin , and vimentin was also performed .
	manualset3
92703	1	399357	13	NULL	NULL	0	NULL	Immunochemical studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunochemical studies of heat-shock protein 80 of Histoplasma capsulatum .
	manualset3
92704	2	399357	13	NULL	NULL	0	NULL	heat-shock protein 80	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunochemical studies of heat-shock protein 80 of Histoplasma capsulatum .
	manualset3
92705	3	399357	13	NULL	NULL	0	NULL	Histoplasma capsulatum	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunochemical studies of heat-shock protein 80 of Histoplasma capsulatum .
	manualset3
92706	1	399358	13	NULL	NULL	0	NULL	Immunochemical studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunochemical studies with monoclonal antibodies against rat liver cytochrome P450 isoenzymes of the gene families 1A , 2B , 3A , and 4A confirmed that bromopropylate is a phenobarbitone-type inducer in the mouse liver .
	manualset3
92707	2	399358	13	NULL	NULL	0	NULL	monoclonal antibodies	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunochemical studies with monoclonal antibodies against rat liver cytochrome P450 isoenzymes of the gene families 1A , 2B , 3A , and 4A confirmed that bromopropylate is a phenobarbitone-type inducer in the mouse liver .
	manualset3
92708	3	399358	13	NULL	NULL	0	NULL	rat liver cytochrome P450 isoenzymes	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunochemical studies with monoclonal antibodies against rat liver cytochrome P450 isoenzymes of the gene families 1A , 2B , 3A , and 4A confirmed that bromopropylate is a phenobarbitone-type inducer in the mouse liver .
	manualset3
92709	4	399358	13	NULL	NULL	0	NULL	gene families 1A	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunochemical studies with monoclonal antibodies against rat liver cytochrome P450 isoenzymes of the gene families 1A , 2B , 3A , and 4A confirmed that bromopropylate is a phenobarbitone-type inducer in the mouse liver .
	manualset3
92710	5	399358	13	NULL	NULL	0	NULL	gene families 2B	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunochemical studies with monoclonal antibodies against rat liver cytochrome P450 isoenzymes of the gene families 1A , 2B , 3A , and 4A confirmed that bromopropylate is a phenobarbitone-type inducer in the mouse liver .
	manualset3
92711	6	399358	13	NULL	NULL	0	NULL	gene families 3A	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunochemical studies with monoclonal antibodies against rat liver cytochrome P450 isoenzymes of the gene families 1A , 2B , 3A , and 4A confirmed that bromopropylate is a phenobarbitone-type inducer in the mouse liver .
	manualset3
92712	7	399358	13	NULL	NULL	0	NULL	gene families 4A	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunochemical studies with monoclonal antibodies against rat liver cytochrome P450 isoenzymes of the gene families 1A , 2B , 3A , and 4A confirmed that bromopropylate is a phenobarbitone-type inducer in the mouse liver .
	manualset3
92713	8	399358	13	NULL	NULL	0	NULL	bromopropylate	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunochemical studies with monoclonal antibodies against rat liver cytochrome P450 isoenzymes of the gene families 1A , 2B , 3A , and 4A confirmed that bromopropylate is a phenobarbitone-type inducer in the mouse liver .
	manualset3
92714	9	399358	13	NULL	NULL	0	NULL	phenobarbitone-type inducer	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunochemical studies with monoclonal antibodies against rat liver cytochrome P450 isoenzymes of the gene families 1A , 2B , 3A , and 4A confirmed that bromopropylate is a phenobarbitone-type inducer in the mouse liver .
	manualset3
92715	10	399358	13	NULL	NULL	0	NULL	mouse liver	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunochemical studies with monoclonal antibodies against rat liver cytochrome P450 isoenzymes of the gene families 1A , 2B , 3A , and 4A confirmed that bromopropylate is a phenobarbitone-type inducer in the mouse liver .
	manualset3
92716	1	399359	13	NULL	NULL	0	NULL	Therapeutic management	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Therapeutic management of peptic ulcer bleeding ) .
	manualset3
92717	2	399359	13	NULL	NULL	0	NULL	peptic ulcer bleeding	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Therapeutic management of peptic ulcer bleeding ) .
	manualset3
92718	1	399360	13	NULL	NULL	0	NULL	Immunocytochemical localization studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocytochemical localization studies found estrogen receptor alpha ( ERalpha ) and estrogen receptor beta ( ERbeta ) in cortical neurons and glia .
	manualset3
92719	2	399360	13	NULL	NULL	0	NULL	estrogen receptor alpha ( ERalpha ) 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocytochemical localization studies found estrogen receptor alpha ( ERalpha ) and estrogen receptor beta ( ERbeta ) in cortical neurons and glia .
	manualset3
92720	3	399360	13	NULL	NULL	0	NULL	estrogen receptor beta ( ERbeta )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocytochemical localization studies found estrogen receptor alpha ( ERalpha ) and estrogen receptor beta ( ERbeta ) in cortical neurons and glia .
	manualset3
92721	4	399360	13	NULL	NULL	0	NULL	cortical neurons	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocytochemical localization studies found estrogen receptor alpha ( ERalpha ) and estrogen receptor beta ( ERbeta ) in cortical neurons and glia .
	manualset3
92722	5	399360	13	NULL	NULL	0	NULL	 glia	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocytochemical localization studies found estrogen receptor alpha ( ERalpha ) and estrogen receptor beta ( ERbeta ) in cortical neurons and glia .
	manualset3
92723	1	399361	13	NULL	NULL	0	NULL	Immunocytochemistry	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocytochemistry of the taurine biosynthesis enzyme , cysteine sulfinate decarboxylase , in the cerebellum : evidence for a glial localization .
	manualset3
92724	2	399361	13	NULL	NULL	0	NULL	taurine biosynthesis enzyme	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocytochemistry of the taurine biosynthesis enzyme , cysteine sulfinate decarboxylase , in the cerebellum : evidence for a glial localization .
	manualset3
92725	3	399361	13	NULL	NULL	0	NULL	cysteine sulfinate decarboxylase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocytochemistry of the taurine biosynthesis enzyme , cysteine sulfinate decarboxylase , in the cerebellum : evidence for a glial localization .
	manualset3
92726	4	399361	13	NULL	NULL	0	NULL	cerebellum	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocytochemistry of the taurine biosynthesis enzyme , cysteine sulfinate decarboxylase , in the cerebellum : evidence for a glial localization .
	manualset3
92728	5	399361	13	NULL	NULL	NULL	NULL	glial localization	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunocytochemistry of the taurine biosynthesis enzyme , cysteine sulfinate decarboxylase , in the cerebellum : evidence for a glial localization .
	manualset3
94210	6	399361	13	NULL	NULL	0	NULL	evidence	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocytochemistry of the taurine biosynthesis enzyme , cysteine sulfinate decarboxylase , in the cerebellum : evidence for a glial localization .
	manualset3
92729	1	399362	13	NULL	NULL	0	NULL	Immunocytochemistry	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocytochemistry showed that the distribution of beacon protein followed that of beacon mRNA .
	manualset3
92730	2	399362	13	NULL	NULL	0	NULL	 distribution	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocytochemistry showed that the distribution of beacon protein followed that of beacon mRNA .
	manualset3
92731	3	399362	13	NULL	NULL	0	NULL	beacon protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocytochemistry showed that the distribution of beacon protein followed that of beacon mRNA .
	manualset3
92732	4	399362	13	NULL	NULL	0	NULL	beacon mRNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunocytochemistry showed that the distribution of beacon protein followed that of beacon mRNA .
	manualset3
92733	1	399363	13	NULL	NULL	0	NULL	Immunoelectron microscopy	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoelectron microscopy demonstrated that CgA and SgIII were specifically colocalized in large secretory granules in male rat gonadotropes , which possess large-type and small-type granules .
	manualset3
92734	2	399363	13	NULL	NULL	0	NULL	CgA	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoelectron microscopy demonstrated that CgA and SgIII were specifically colocalized in large secretory granules in male rat gonadotropes , which possess large-type and small-type granules .
	manualset3
92735	3	399363	13	NULL	NULL	0	NULL	 SgIII	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoelectron microscopy demonstrated that CgA and SgIII were specifically colocalized in large secretory granules in male rat gonadotropes , which possess large-type and small-type granules .
	manualset3
92736	4	399363	13	NULL	NULL	0	NULL	large secretory granules	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoelectron microscopy demonstrated that CgA and SgIII were specifically colocalized in large secretory granules in male rat gonadotropes , which possess large-type and small-type granules .
	manualset3
92737	5	399363	13	NULL	NULL	0	NULL	male rat gonadotropes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoelectron microscopy demonstrated that CgA and SgIII were specifically colocalized in large secretory granules in male rat gonadotropes , which possess large-type and small-type granules .
	manualset3
92738	6	399363	13	NULL	NULL	0	NULL	large-type granules	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoelectron microscopy demonstrated that CgA and SgIII were specifically colocalized in large secretory granules in male rat gonadotropes , which possess large-type and small-type granules .
	manualset3
92739	7	399363	13	NULL	NULL	0	NULL	small-type granules	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoelectron microscopy demonstrated that CgA and SgIII were specifically colocalized in large secretory granules in male rat gonadotropes , which possess large-type and small-type granules .
	manualset3
92740	1	399364	13	NULL	NULL	0	NULL	Immunofluorescence 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence and in vitro ( ( 35 ) S ) GTPgammaS autoradiography of rat tissue sections containing the PBN revealed the presence of cannabinoid receptors and their functional capability to couple to their G-proteins after incubation with the endocannabinoid 2-arachidonoyl glycerol ( 2-AG ) .
	manualset3
92741	2	399364	13	NULL	NULL	NULL	NULL	 in vitro ( ( 35 ) S ) GTPgammaS autoradiography	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunofluorescence and in vitro ( ( 35 ) S ) GTPgammaS autoradiography of rat tissue sections containing the PBN revealed the presence of cannabinoid receptors and their functional capability to couple to their G-proteins after incubation with the endocannabinoid 2-arachidonoyl glycerol ( 2-AG ) .
	manualset3
92742	3	399364	13	NULL	NULL	0	NULL	rat tissue sections	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence and in vitro ( ( 35 ) S ) GTPgammaS autoradiography of rat tissue sections containing the PBN revealed the presence of cannabinoid receptors and their functional capability to couple to their G-proteins after incubation with the endocannabinoid 2-arachidonoyl glycerol ( 2-AG ) .
	manualset3
92743	4	399364	13	NULL	NULL	0	NULL	PBN 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence and in vitro ( ( 35 ) S ) GTPgammaS autoradiography of rat tissue sections containing the PBN revealed the presence of cannabinoid receptors and their functional capability to couple to their G-proteins after incubation with the endocannabinoid 2-arachidonoyl glycerol ( 2-AG ) .
	manualset3
92744	5	399364	13	NULL	NULL	0	NULL	cannabinoid receptors	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence and in vitro ( ( 35 ) S ) GTPgammaS autoradiography of rat tissue sections containing the PBN revealed the presence of cannabinoid receptors and their functional capability to couple to their G-proteins after incubation with the endocannabinoid 2-arachidonoyl glycerol ( 2-AG ) .
	manualset3
92745	6	399364	13	NULL	NULL	0	NULL	 functional capability	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence and in vitro ( ( 35 ) S ) GTPgammaS autoradiography of rat tissue sections containing the PBN revealed the presence of cannabinoid receptors and their functional capability to couple to their G-proteins after incubation with the endocannabinoid 2-arachidonoyl glycerol ( 2-AG ) .
	manualset3
92746	7	399364	13	NULL	NULL	0	NULL	G-proteins 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence and in vitro ( ( 35 ) S ) GTPgammaS autoradiography of rat tissue sections containing the PBN revealed the presence of cannabinoid receptors and their functional capability to couple to their G-proteins after incubation with the endocannabinoid 2-arachidonoyl glycerol ( 2-AG ) .
	manualset3
92747	8	399364	13	NULL	NULL	0	NULL	incubation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence and in vitro ( ( 35 ) S ) GTPgammaS autoradiography of rat tissue sections containing the PBN revealed the presence of cannabinoid receptors and their functional capability to couple to their G-proteins after incubation with the endocannabinoid 2-arachidonoyl glycerol ( 2-AG ) .
	manualset3
92748	9	399364	13	NULL	NULL	0	NULL	endocannabinoid 2-arachidonoyl glycerol ( 2-AG )	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence and in vitro ( ( 35 ) S ) GTPgammaS autoradiography of rat tissue sections containing the PBN revealed the presence of cannabinoid receptors and their functional capability to couple to their G-proteins after incubation with the endocannabinoid 2-arachidonoyl glycerol ( 2-AG ) .
	manualset3
94211	5	399364	13	NULL	NULL	0	NULL	presence	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence and in vitro ( ( 35 ) S ) GTPgammaS autoradiography of rat tissue sections containing the PBN revealed the presence of cannabinoid receptors and their functional capability to couple to their G-proteins after incubation with the endocannabinoid 2-arachidonoyl glycerol ( 2-AG ) .
	manualset3
92749	1	399365	13	NULL	NULL	0	NULL	Immunofluorescence 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence demonstrated that HUVEC expressed AHR and ER but lacked ER and the involvement of AHR and ER on the effects of PCB126 was examined by the addition of AHR and ER antagonists .
	manualset3
92750	2	399365	13	NULL	NULL	0	NULL	HUVEC 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence demonstrated that HUVEC expressed AHR and ER but lacked ER and the involvement of AHR and ER on the effects of PCB126 was examined by the addition of AHR and ER antagonists .
	manualset3
92751	3	399365	13	NULL	NULL	0	NULL	AHR	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence demonstrated that HUVEC expressed AHR and ER but lacked ER and the involvement of AHR and ER on the effects of PCB126 was examined by the addition of AHR and ER antagonists .
	manualset3
92752	4	399365	13	NULL	NULL	0	NULL	 ER	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence demonstrated that HUVEC expressed AHR and ER but lacked ER and the involvement of AHR and ER on the effects of PCB126 was examined by the addition of AHR and ER antagonists .
	manualset3
92753	5	399365	13	NULL	NULL	0	NULL	ER 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence demonstrated that HUVEC expressed AHR and ER but lacked ER and the involvement of AHR and ER on the effects of PCB126 was examined by the addition of AHR and ER antagonists .
	manualset3
92754	6	399365	13	NULL	NULL	0	NULL	involvement 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence demonstrated that HUVEC expressed AHR and ER but lacked ER and the involvement of AHR and ER on the effects of PCB126 was examined by the addition of AHR and ER antagonists .
	manualset3
92755	7	399365	13	NULL	NULL	0	NULL	AHR	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence demonstrated that HUVEC expressed AHR and ER but lacked ER and the involvement of AHR and ER on the effects of PCB126 was examined by the addition of AHR and ER antagonists .
	manualset3
92756	8	399365	13	NULL	NULL	0	NULL	ER	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence demonstrated that HUVEC expressed AHR and ER but lacked ER and the involvement of AHR and ER on the effects of PCB126 was examined by the addition of AHR and ER antagonists .
	manualset3
92757	9	399365	13	NULL	NULL	0	NULL	PCB126	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence demonstrated that HUVEC expressed AHR and ER but lacked ER and the involvement of AHR and ER on the effects of PCB126 was examined by the addition of AHR and ER antagonists .
	manualset3
92759	10	399365	13	NULL	NULL	0	NULL	addition	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence demonstrated that HUVEC expressed AHR and ER but lacked ER and the involvement of AHR and ER on the effects of PCB126 was examined by the addition of AHR and ER antagonists .
	manualset3
92760	11	399365	13	NULL	NULL	0	NULL	AHR antagonists 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence demonstrated that HUVEC expressed AHR and ER but lacked ER and the involvement of AHR and ER on the effects of PCB126 was examined by the addition of AHR and ER antagonists .
	manualset3
92761	12	399365	13	NULL	NULL	0	NULL	ER antagonists	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence demonstrated that HUVEC expressed AHR and ER but lacked ER and the involvement of AHR and ER on the effects of PCB126 was examined by the addition of AHR and ER antagonists .
	manualset3
92762	1	399366	13	NULL	NULL	0	NULL	Immunofluorescence 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence observations show that TrkA-GFP is found mainly in cell surface membrane ruffles and in endosomes .
	manualset3
92763	2	399366	13	NULL	NULL	0	NULL	 observations	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence observations show that TrkA-GFP is found mainly in cell surface membrane ruffles and in endosomes .
	manualset3
92764	3	399366	13	NULL	NULL	0	NULL	 TrkA-GFP 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence observations show that TrkA-GFP is found mainly in cell surface membrane ruffles and in endosomes .
	manualset3
92765	4	399366	13	NULL	NULL	0	NULL	cell surface membrane ruffles 	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence observations show that TrkA-GFP is found mainly in cell surface membrane ruffles and in endosomes .
	manualset3
92766	5	399366	13	NULL	NULL	0	NULL	endosomes	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence observations show that TrkA-GFP is found mainly in cell surface membrane ruffles and in endosomes .
	manualset3
92767	1	399367	13	NULL	NULL	0	NULL	Immunofluorescence	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence of sarcomeric a-actin was enhanced and its expression increased dose - and time-dependently in T3-treated cultured heart myocytes .
	manualset3
92768	2	399367	13	NULL	NULL	0	NULL	 sarcomeric a-actin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence of sarcomeric a-actin was enhanced and its expression increased dose - and time-dependently in T3-treated cultured heart myocytes .
	manualset3
92769	3	399367	13	NULL	NULL	0	NULL	expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence of sarcomeric a-actin was enhanced and its expression increased dose - and time-dependently in T3-treated cultured heart myocytes .
	manualset3
92770	4	399367	13	NULL	NULL	0	NULL	dose	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence of sarcomeric a-actin was enhanced and its expression increased dose - and time-dependently in T3-treated cultured heart myocytes .
	manualset3
92771	5	399367	13	NULL	NULL	0	NULL	T3-treated cultured heart myocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunofluorescence of sarcomeric a-actin was enhanced and its expression increased dose - and time-dependently in T3-treated cultured heart myocytes .
	manualset3
92772	1	399368	13	NULL	NULL	NULL	NULL	Immunogenicity	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunogenicity of Bacteroides isolated from mice : relationship between immunogenicity and cell wall antigens .
	manualset3
92773	2	399368	13	NULL	NULL	0	NULL	Bacteroides	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunogenicity of Bacteroides isolated from mice : relationship between immunogenicity and cell wall antigens .
	manualset3
92774	3	399368	13	NULL	NULL	0	NULL	mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunogenicity of Bacteroides isolated from mice : relationship between immunogenicity and cell wall antigens .
	manualset3
92775	4	399368	13	NULL	NULL	0	NULL	relationship	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunogenicity of Bacteroides isolated from mice : relationship between immunogenicity and cell wall antigens .
	manualset3
92776	5	399368	13	NULL	NULL	NULL	NULL	immunogenicity	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunogenicity of Bacteroides isolated from mice : relationship between immunogenicity and cell wall antigens .
	manualset3
92777	6	399368	13	NULL	NULL	0	NULL	cell wall antigens	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunogenicity of Bacteroides isolated from mice : relationship between immunogenicity and cell wall antigens .
	manualset3
92778	1	399369	13	NULL	NULL	NULL	NULL	Immunogenicity 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunogenicity of well-characterized synthetic Plasmodium falciparum multiple antigen peptide conjugates .
	manualset3
92779	2	399369	13	NULL	NULL	0	NULL	 synthetic Plasmodium falciparum multiple antigen peptide conjugates	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunogenicity of well-characterized synthetic Plasmodium falciparum multiple antigen peptide conjugates .
	manualset3
92780	1	399370	13	NULL	NULL	0	NULL	Immunoglobulin E antibodies 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoglobulin E antibodies to ingested cereal flour components : studies with sera from subjects with asthma and eczema .
	manualset3
92781	2	399370	13	NULL	NULL	0	NULL	cereal flour components	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoglobulin E antibodies to ingested cereal flour components : studies with sera from subjects with asthma and eczema .
	manualset3
92782	3	399370	13	NULL	NULL	0	NULL	sera	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoglobulin E antibodies to ingested cereal flour components : studies with sera from subjects with asthma and eczema .
	manualset3
92783	5	399370	13	NULL	NULL	NULL	NULL	subjects with asthma	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunoglobulin E antibodies to ingested cereal flour components : studies with sera from subjects with asthma and eczema .
	manualset3
92784	6	399370	13	NULL	NULL	NULL	NULL	subjects with eczema	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunoglobulin E antibodies to ingested cereal flour components : studies with sera from subjects with asthma and eczema .
	manualset3
94213	4	399370	13	NULL	NULL	0	NULL	studies	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoglobulin E antibodies to ingested cereal flour components : studies with sera from subjects with asthma and eczema .
	manualset3
92794	1	399371	13	NULL	NULL	NULL	NULL	Immunoglobulin G	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunoglobulin G may be prepared by different methods for intravenous infusion and administered as replacement therapy for hypogammaglobulinemia .
	manualset3
92795	2	399371	13	NULL	NULL	0	NULL	different methods	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoglobulin G may be prepared by different methods for intravenous infusion and administered as replacement therapy for hypogammaglobulinemia .
	manualset3
92796	3	399371	13	NULL	NULL	0	NULL	intravenous infusion 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoglobulin G may be prepared by different methods for intravenous infusion and administered as replacement therapy for hypogammaglobulinemia .
	manualset3
92797	4	399371	13	NULL	NULL	0	NULL	replacement therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoglobulin G may be prepared by different methods for intravenous infusion and administered as replacement therapy for hypogammaglobulinemia .
	manualset3
92799	5	399371	13	NULL	NULL	0	NULL	hypogammaglobulinemia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoglobulin G may be prepared by different methods for intravenous infusion and administered as replacement therapy for hypogammaglobulinemia .
	manualset3
92802	1	399372	13	NULL	NULL	0	NULL	Immunoglobulin G4-related systemic disease ( IgG4-RSD )	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoglobulin G4-related systemic disease ( IgG4-RSD ) is a recently defined emerging entity characterized by a diffuse or mass forming inflammatory reaction rich in IgG4-positive plasma cells associated with fibrosclerosis and obliterative phlebitis .
	manualset3
92803	2	399372	13	NULL	NULL	0	NULL	emerging entity	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoglobulin G4-related systemic disease ( IgG4-RSD ) is a recently defined emerging entity characterized by a diffuse or mass forming inflammatory reaction rich in IgG4-positive plasma cells associated with fibrosclerosis and obliterative phlebitis .
	manualset3
92804	3	399372	13	NULL	NULL	0	NULL	diffuse or mass forming inflammatory reaction	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoglobulin G4-related systemic disease ( IgG4-RSD ) is a recently defined emerging entity characterized by a diffuse or mass forming inflammatory reaction rich in IgG4-positive plasma cells associated with fibrosclerosis and obliterative phlebitis .
	manualset3
92805	4	399372	13	NULL	NULL	0	NULL	IgG4-positive plasma cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoglobulin G4-related systemic disease ( IgG4-RSD ) is a recently defined emerging entity characterized by a diffuse or mass forming inflammatory reaction rich in IgG4-positive plasma cells associated with fibrosclerosis and obliterative phlebitis .
	manualset3
92806	5	399372	13	NULL	NULL	0	NULL	fibrosclerosis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoglobulin G4-related systemic disease ( IgG4-RSD ) is a recently defined emerging entity characterized by a diffuse or mass forming inflammatory reaction rich in IgG4-positive plasma cells associated with fibrosclerosis and obliterative phlebitis .
	manualset3
92808	6	399372	13	NULL	NULL	0	NULL	obliterative phlebitis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoglobulin G4-related systemic disease ( IgG4-RSD ) is a recently defined emerging entity characterized by a diffuse or mass forming inflammatory reaction rich in IgG4-positive plasma cells associated with fibrosclerosis and obliterative phlebitis .
	manualset3
92811	1	399373	13	NULL	NULL	0	NULL	Immunohistochemical study 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical , electrophysiological , and electron microscopical study of rat fungiform taste buds after regeneration of chorda tympani through the non-gustatory lingual nerve .
	manualset3
92812	2	399373	13	NULL	NULL	0	NULL	electrophysiological study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical , electrophysiological , and electron microscopical study of rat fungiform taste buds after regeneration of chorda tympani through the non-gustatory lingual nerve .
	manualset3
92813	3	399373	13	NULL	NULL	0	NULL	electron microscopical study 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical , electrophysiological , and electron microscopical study of rat fungiform taste buds after regeneration of chorda tympani through the non-gustatory lingual nerve .
	manualset3
92814	4	399373	13	NULL	NULL	0	NULL	rat fungiform taste buds	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical , electrophysiological , and electron microscopical study of rat fungiform taste buds after regeneration of chorda tympani through the non-gustatory lingual nerve .
	manualset3
92815	5	399373	13	NULL	NULL	0	NULL	regeneration 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical , electrophysiological , and electron microscopical study of rat fungiform taste buds after regeneration of chorda tympani through the non-gustatory lingual nerve .
	manualset3
92816	6	399373	13	NULL	NULL	0	NULL	chorda tympani 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical , electrophysiological , and electron microscopical study of rat fungiform taste buds after regeneration of chorda tympani through the non-gustatory lingual nerve .
	manualset3
92817	7	399373	13	NULL	NULL	0	NULL	non-gustatory lingual nerve	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical , electrophysiological , and electron microscopical study of rat fungiform taste buds after regeneration of chorda tympani through the non-gustatory lingual nerve .
	manualset3
92818	1	399374	13	NULL	NULL	0	NULL	Immunohistochemical analyses	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analyses were performed on multiple sections of ML specimens to evaluate Pgp expression .
	manualset3
92819	2	399374	13	NULL	NULL	0	NULL	multiple sections of ML specimens	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analyses were performed on multiple sections of ML specimens to evaluate Pgp expression .
	manualset3
92820	3	399374	13	NULL	NULL	0	NULL	Pgp expression 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analyses were performed on multiple sections of ML specimens to evaluate Pgp expression .
	manualset3
92822	1	399375	13	NULL	NULL	0	NULL	Immunohistochemical analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis in 172 cases of breast tissues showed that the positive rate of CacyBP protein expression in normal breast tissues ( NBT ) ( 89.3 % ) was higher than that in invasive ductal carcinoma ( IDC ) ( 56.1 % ) ( P & lt ; 0.05 ) .
	manualset3
92823	2	399375	13	NULL	NULL	0	NULL	172 cases	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis in 172 cases of breast tissues showed that the positive rate of CacyBP protein expression in normal breast tissues ( NBT ) ( 89.3 % ) was higher than that in invasive ductal carcinoma ( IDC ) ( 56.1 % ) ( P & lt ; 0.05 ) .
	manualset3
92824	3	399375	13	NULL	NULL	0	NULL	breast tissues	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis in 172 cases of breast tissues showed that the positive rate of CacyBP protein expression in normal breast tissues ( NBT ) ( 89.3 % ) was higher than that in invasive ductal carcinoma ( IDC ) ( 56.1 % ) ( P & lt ; 0.05 ) .
	manualset3
92825	4	399375	13	NULL	NULL	0	NULL	positive rate	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis in 172 cases of breast tissues showed that the positive rate of CacyBP protein expression in normal breast tissues ( NBT ) ( 89.3 % ) was higher than that in invasive ductal carcinoma ( IDC ) ( 56.1 % ) ( P & lt ; 0.05 ) .
	manualset3
92826	5	399375	13	NULL	NULL	0	NULL	CacyBP protein expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis in 172 cases of breast tissues showed that the positive rate of CacyBP protein expression in normal breast tissues ( NBT ) ( 89.3 % ) was higher than that in invasive ductal carcinoma ( IDC ) ( 56.1 % ) ( P & lt ; 0.05 ) .
	manualset3
92827	6	399375	13	NULL	NULL	0	NULL	normal breast tissues ( NBT ) 	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis in 172 cases of breast tissues showed that the positive rate of CacyBP protein expression in normal breast tissues ( NBT ) ( 89.3 % ) was higher than that in invasive ductal carcinoma ( IDC ) ( 56.1 % ) ( P & lt ; 0.05 ) .
	manualset3
92828	7	399375	13	NULL	NULL	0	NULL	 89.3 % 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis in 172 cases of breast tissues showed that the positive rate of CacyBP protein expression in normal breast tissues ( NBT ) ( 89.3 % ) was higher than that in invasive ductal carcinoma ( IDC ) ( 56.1 % ) ( P & lt ; 0.05 ) .
	manualset3
92829	8	399375	13	NULL	NULL	0	NULL	invasive ductal carcinoma ( IDC )	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis in 172 cases of breast tissues showed that the positive rate of CacyBP protein expression in normal breast tissues ( NBT ) ( 89.3 % ) was higher than that in invasive ductal carcinoma ( IDC ) ( 56.1 % ) ( P & lt ; 0.05 ) .
	manualset3
92830	9	399375	13	NULL	NULL	0	NULL	( 56.1 % ) ( P & lt ; 0.05 ) 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis in 172 cases of breast tissues showed that the positive rate of CacyBP protein expression in normal breast tissues ( NBT ) ( 89.3 % ) was higher than that in invasive ductal carcinoma ( IDC ) ( 56.1 % ) ( P & lt ; 0.05 ) .
	manualset3
92831	1	399376	13	NULL	NULL	0	NULL	Immunohistochemical analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis of 14-3-3 sigma and related proteins in hyperplastic and neoplastic breast lesions , with particular reference to early carcinogenesis .
	manualset3
92832	2	399376	13	NULL	NULL	0	NULL	14-3-3 sigma	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis of 14-3-3 sigma and related proteins in hyperplastic and neoplastic breast lesions , with particular reference to early carcinogenesis .
	manualset3
92833	3	399376	13	NULL	NULL	0	NULL	 related proteins	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis of 14-3-3 sigma and related proteins in hyperplastic and neoplastic breast lesions , with particular reference to early carcinogenesis .
	manualset3
92834	4	399376	13	NULL	NULL	0	NULL	hyperplastic breast lesions	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis of 14-3-3 sigma and related proteins in hyperplastic and neoplastic breast lesions , with particular reference to early carcinogenesis .
	manualset3
92835	5	399376	13	NULL	NULL	0	NULL	neoplastic breast lesions	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis of 14-3-3 sigma and related proteins in hyperplastic and neoplastic breast lesions , with particular reference to early carcinogenesis .
	manualset3
92836	7	399376	13	NULL	NULL	NULL	NULL	 carcinogenesis	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis of 14-3-3 sigma and related proteins in hyperplastic and neoplastic breast lesions , with particular reference to early carcinogenesis .
	manualset3
94214	6	399376	13	NULL	NULL	0	NULL	reference	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis of 14-3-3 sigma and related proteins in hyperplastic and neoplastic breast lesions , with particular reference to early carcinogenesis .
	manualset3
92837	1	399377	13	NULL	NULL	0	NULL	Immunohistochemical analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis revealed a strong nuclear Snail staining in mock-transfected cells compared with a significantly reduced nuclear staining and translocation to the cytoplasm in P-cadherin-overexpressing cells .
	manualset3
92838	2	399377	13	NULL	NULL	0	NULL	 strong nuclear Snail staining	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis revealed a strong nuclear Snail staining in mock-transfected cells compared with a significantly reduced nuclear staining and translocation to the cytoplasm in P-cadherin-overexpressing cells .
	manualset3
92839	3	399377	13	NULL	NULL	0	NULL	 mock-transfected cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis revealed a strong nuclear Snail staining in mock-transfected cells compared with a significantly reduced nuclear staining and translocation to the cytoplasm in P-cadherin-overexpressing cells .
	manualset3
92840	4	399377	13	NULL	NULL	0	NULL	nuclear staining	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis revealed a strong nuclear Snail staining in mock-transfected cells compared with a significantly reduced nuclear staining and translocation to the cytoplasm in P-cadherin-overexpressing cells .
	manualset3
92841	5	399377	13	NULL	NULL	0	NULL	translocation to the cytoplasm 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis revealed a strong nuclear Snail staining in mock-transfected cells compared with a significantly reduced nuclear staining and translocation to the cytoplasm in P-cadherin-overexpressing cells .
	manualset3
92842	6	399377	13	NULL	NULL	0	NULL	P-cadherin-overexpressing cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical analysis revealed a strong nuclear Snail staining in mock-transfected cells compared with a significantly reduced nuclear staining and translocation to the cytoplasm in P-cadherin-overexpressing cells .
	manualset3
92843	1	399378	13	NULL	NULL	0	NULL	Therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Therapy and survival in thyroid tumors ) .
	manualset3
92844	2	399378	13	NULL	NULL	0	NULL	survival	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Therapy and survival in thyroid tumors ) .
	manualset3
92845	3	399378	13	NULL	NULL	0	NULL	thyroid tumors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Therapy and survival in thyroid tumors ) .
	manualset3
92846	1	399379	13	NULL	NULL	0	NULL	Immunohistochemical detection 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical detection of gastric mucin in normal and disease states .
	manualset3
92847	2	399379	13	NULL	NULL	0	NULL	gastric mucin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical detection of gastric mucin in normal and disease states .
	manualset3
92848	3	399379	13	NULL	NULL	0	NULL	normal states	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical detection of gastric mucin in normal and disease states .
	manualset3
92849	4	399379	13	NULL	NULL	0	NULL	disease states	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical detection of gastric mucin in normal and disease states .
	manualset3
92850	1	399380	13	NULL	NULL	0	NULL	Immunohistochemical detection	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical detection of the protein , Fos , was used to identify neurons in the brain activated following a volume load in conscious rabbits with doxorubicin-induced congestive cardiomyopathy .
	manualset3
92851	2	399380	13	NULL	NULL	0	NULL	 protein , Fos	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical detection of the protein , Fos , was used to identify neurons in the brain activated following a volume load in conscious rabbits with doxorubicin-induced congestive cardiomyopathy .
	manualset3
92852	3	399380	13	NULL	NULL	0	NULL	neurons	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical detection of the protein , Fos , was used to identify neurons in the brain activated following a volume load in conscious rabbits with doxorubicin-induced congestive cardiomyopathy .
	manualset3
92853	4	399380	13	NULL	NULL	0	NULL	brain	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical detection of the protein , Fos , was used to identify neurons in the brain activated following a volume load in conscious rabbits with doxorubicin-induced congestive cardiomyopathy .
	manualset3
92854	5	399380	13	NULL	NULL	0	NULL	 volume load	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical detection of the protein , Fos , was used to identify neurons in the brain activated following a volume load in conscious rabbits with doxorubicin-induced congestive cardiomyopathy .
	manualset3
92855	6	399380	13	NULL	NULL	0	NULL	conscious rabbits	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical detection of the protein , Fos , was used to identify neurons in the brain activated following a volume load in conscious rabbits with doxorubicin-induced congestive cardiomyopathy .
	manualset3
92856	7	399380	13	NULL	NULL	0	NULL	doxorubicin-induced congestive cardiomyopathy	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical detection of the protein , Fos , was used to identify neurons in the brain activated following a volume load in conscious rabbits with doxorubicin-induced congestive cardiomyopathy .
	manualset3
92857	1	399381	13	NULL	NULL	0	NULL	Immunohistochemical staining 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical staining for estrogen receptors in the endometrium was positive in all but one treated gilts , and negative to weakly positive in control gilts .
	manualset3
92858	2	399381	13	NULL	NULL	0	NULL	estrogen receptors	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical staining for estrogen receptors in the endometrium was positive in all but one treated gilts , and negative to weakly positive in control gilts .
	manualset3
92859	3	399381	13	NULL	NULL	0	NULL	endometrium	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical staining for estrogen receptors in the endometrium was positive in all but one treated gilts , and negative to weakly positive in control gilts .
	manualset3
92860	5	399381	13	NULL	NULL	NULL	NULL	gilts	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunohistochemical staining for estrogen receptors in the endometrium was positive in all but one treated gilts , and negative to weakly positive in control gilts .
	manualset3
92861	6	399381	13	NULL	NULL	NULL	NULL	control gilts	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunohistochemical staining for estrogen receptors in the endometrium was positive in all but one treated gilts , and negative to weakly positive in control gilts .
	manualset3
92862	4	399381	13	NULL	NULL	0	NULL	one 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical staining for estrogen receptors in the endometrium was positive in all but one treated gilts , and negative to weakly positive in control gilts .
	manualset3
92863	1	399382	13	NULL	NULL	0	NULL	Immunohistochemical staining	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical staining with a monoclonal antibody ( DO-7 ) and a polyclonal antibody ( CM-1 ) to p53 protein ( both wild type and mutant ) on formalin-fixed paraffin sections showed a strong correlation with malignancy grade .
	manualset3
92864	2	399382	13	NULL	NULL	0	NULL	monoclonal antibody ( DO-7 )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical staining with a monoclonal antibody ( DO-7 ) and a polyclonal antibody ( CM-1 ) to p53 protein ( both wild type and mutant ) on formalin-fixed paraffin sections showed a strong correlation with malignancy grade .
	manualset3
92865	3	399382	13	NULL	NULL	0	NULL	polyclonal antibody ( CM-1 )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical staining with a monoclonal antibody ( DO-7 ) and a polyclonal antibody ( CM-1 ) to p53 protein ( both wild type and mutant ) on formalin-fixed paraffin sections showed a strong correlation with malignancy grade .
	manualset3
92866	4	399382	13	NULL	NULL	0	NULL	p53 protein ( both wild type and mutant )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical staining with a monoclonal antibody ( DO-7 ) and a polyclonal antibody ( CM-1 ) to p53 protein ( both wild type and mutant ) on formalin-fixed paraffin sections showed a strong correlation with malignancy grade .
	manualset3
92867	5	399382	13	NULL	NULL	NULL	NULL	formalin-fixed paraffin sections 	Facility												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunohistochemical staining with a monoclonal antibody ( DO-7 ) and a polyclonal antibody ( CM-1 ) to p53 protein ( both wild type and mutant ) on formalin-fixed paraffin sections showed a strong correlation with malignancy grade .
	manualset3
92868	6	399382	13	NULL	NULL	0	NULL	correlation	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical staining with a monoclonal antibody ( DO-7 ) and a polyclonal antibody ( CM-1 ) to p53 protein ( both wild type and mutant ) on formalin-fixed paraffin sections showed a strong correlation with malignancy grade .
	manualset3
92869	7	399382	13	NULL	NULL	0	NULL	malignancy grade	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical staining with a monoclonal antibody ( DO-7 ) and a polyclonal antibody ( CM-1 ) to p53 protein ( both wild type and mutant ) on formalin-fixed paraffin sections showed a strong correlation with malignancy grade .
	manualset3
92870	1	399383	13	NULL	NULL	0	NULL	Immunohistochemical stains 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical stains for synaptophysin and chromogranin demonstrated diffuse , strong positivity uniformly throughout the tumor , even in the more conventional-appearing areas .
	manualset3
92871	2	399383	13	NULL	NULL	0	NULL	synaptophysin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical stains for synaptophysin and chromogranin demonstrated diffuse , strong positivity uniformly throughout the tumor , even in the more conventional-appearing areas .
	manualset3
92872	3	399383	13	NULL	NULL	0	NULL	chromogranin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical stains for synaptophysin and chromogranin demonstrated diffuse , strong positivity uniformly throughout the tumor , even in the more conventional-appearing areas .
	manualset3
92873	5	399383	13	NULL	NULL	NULL	NULL	tumor 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunohistochemical stains for synaptophysin and chromogranin demonstrated diffuse , strong positivity uniformly throughout the tumor , even in the more conventional-appearing areas .
	manualset3
92874	6	399383	13	NULL	NULL	NULL	NULL	conventional-appearing areas 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunohistochemical stains for synaptophysin and chromogranin demonstrated diffuse , strong positivity uniformly throughout the tumor , even in the more conventional-appearing areas .
	manualset3
92875	4	399383	13	NULL	NULL	0	NULL	positivity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical stains for synaptophysin and chromogranin demonstrated diffuse , strong positivity uniformly throughout the tumor , even in the more conventional-appearing areas .
	manualset3
92876	1	399384	13	NULL	NULL	0	NULL	Immunohistochemical study 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical study on neuroglia identified by the monoclonal antibody against a macrophage differentiation antigen ( Mac-1 ) .
	manualset3
92877	2	399384	13	NULL	NULL	0	NULL	neuroglia	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical study on neuroglia identified by the monoclonal antibody against a macrophage differentiation antigen ( Mac-1 ) .
	manualset3
92878	3	399384	13	NULL	NULL	0	NULL	monoclonal antibody	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical study on neuroglia identified by the monoclonal antibody against a macrophage differentiation antigen ( Mac-1 ) .
	manualset3
92879	4	399384	13	NULL	NULL	0	NULL	macrophage differentiation antigen ( Mac-1 )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemical study on neuroglia identified by the monoclonal antibody against a macrophage differentiation antigen ( Mac-1 ) .
	manualset3
92881	2	399385	13	NULL	NULL	0	NULL	tumor cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemically , the tumor cells were labeled by antibodies against neurofilament protein , synaptophysin , glial fibrillary acidic protein and S-100 protein antigen , but were negative for chromogranin A , cytokeratin and desmin .
	manualset3
92882	3	399385	13	NULL	NULL	0	NULL	antibodies	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemically , the tumor cells were labeled by antibodies against neurofilament protein , synaptophysin , glial fibrillary acidic protein and S-100 protein antigen , but were negative for chromogranin A , cytokeratin and desmin .
	manualset3
92883	4	399385	13	NULL	NULL	0	NULL	neurofilament protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemically , the tumor cells were labeled by antibodies against neurofilament protein , synaptophysin , glial fibrillary acidic protein and S-100 protein antigen , but were negative for chromogranin A , cytokeratin and desmin .
	manualset3
92884	5	399385	13	NULL	NULL	0	NULL	synaptophysin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemically , the tumor cells were labeled by antibodies against neurofilament protein , synaptophysin , glial fibrillary acidic protein and S-100 protein antigen , but were negative for chromogranin A , cytokeratin and desmin .
	manualset3
92885	6	399385	13	NULL	NULL	0	NULL	glial fibrillary acidic protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemically , the tumor cells were labeled by antibodies against neurofilament protein , synaptophysin , glial fibrillary acidic protein and S-100 protein antigen , but were negative for chromogranin A , cytokeratin and desmin .
	manualset3
92886	7	399385	13	NULL	NULL	NULL	NULL	 S-100 protein antigen	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunohistochemically , the tumor cells were labeled by antibodies against neurofilament protein , synaptophysin , glial fibrillary acidic protein and S-100 protein antigen , but were negative for chromogranin A , cytokeratin and desmin .
	manualset3
92887	8	399385	13	NULL	NULL	0	NULL	 chromogranin A	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemically , the tumor cells were labeled by antibodies against neurofilament protein , synaptophysin , glial fibrillary acidic protein and S-100 protein antigen , but were negative for chromogranin A , cytokeratin and desmin .
	manualset3
92888	9	399385	13	NULL	NULL	0	NULL	cytokeratin 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemically , the tumor cells were labeled by antibodies against neurofilament protein , synaptophysin , glial fibrillary acidic protein and S-100 protein antigen , but were negative for chromogranin A , cytokeratin and desmin .
	manualset3
92889	10	399385	13	NULL	NULL	0	NULL	desmin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunohistochemically , the tumor cells were labeled by antibodies against neurofilament protein , synaptophysin , glial fibrillary acidic protein and S-100 protein antigen , but were negative for chromogranin A , cytokeratin and desmin .
	manualset3
92890	1	399386	13	NULL	NULL	0	NULL	Immunolabeling	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunolabeling of SSPE and wild-type measles viruses in ferret brain cell culture .
	manualset3
92891	2	399386	13	NULL	NULL	0	NULL	SSPE	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunolabeling of SSPE and wild-type measles viruses in ferret brain cell culture .
	manualset3
92892	3	399386	13	NULL	NULL	0	NULL	wild-type measles viruses	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunolabeling of SSPE and wild-type measles viruses in ferret brain cell culture .
	manualset3
92893	4	399386	13	NULL	NULL	0	NULL	ferret brain cell culture 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunolabeling of SSPE and wild-type measles viruses in ferret brain cell culture .
	manualset3
92894	1	399387	13	NULL	NULL	0	NULL	Immunologic criteria	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunologic criteria are poor predictors of virologic outcome : implications for HIV treatment monitoring in resource-limited settings .
	manualset3
92895	2	399387	13	NULL	NULL	NULL	NULL	 predictors of virologic outcome	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunologic criteria are poor predictors of virologic outcome : implications for HIV treatment monitoring in resource-limited settings .
	manualset3
92896	3	399387	13	NULL	NULL	0	NULL	implications 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunologic criteria are poor predictors of virologic outcome : implications for HIV treatment monitoring in resource-limited settings .
	manualset3
92897	4	399387	13	NULL	NULL	0	NULL	HIV treatment 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunologic criteria are poor predictors of virologic outcome : implications for HIV treatment monitoring in resource-limited settings .
	manualset3
92898	5	399387	13	NULL	NULL	0	NULL	resource-limited settings 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunologic criteria are poor predictors of virologic outcome : implications for HIV treatment monitoring in resource-limited settings .
	manualset3
92899	1	399388	13	NULL	NULL	0	NULL	Immunologic mechanisms	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunologic mechanisms and aberrations of the RAS have been long considered contributors to the disorder .
	manualset3
92900	2	399388	13	NULL	NULL	0	NULL	aberrations	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunologic mechanisms and aberrations of the RAS have been long considered contributors to the disorder .
	manualset3
92901	3	399388	13	NULL	NULL	0	NULL	RAS	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunologic mechanisms and aberrations of the RAS have been long considered contributors to the disorder .
	manualset3
92902	4	399388	13	NULL	NULL	0	NULL	contributors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunologic mechanisms and aberrations of the RAS have been long considered contributors to the disorder .
	manualset3
92903	5	399388	13	NULL	NULL	0	NULL	 disorder	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunologic mechanisms and aberrations of the RAS have been long considered contributors to the disorder .
	manualset3
92905	1	399389	13	NULL	NULL	0	NULL	Immunological-focused microarray gene expression analysis 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunological-focused microarray gene expression analysis showed that only the CD72 gene was significantly downregulated in the 12-month RSV-treated mice compared to age-matched controls .
	manualset3
92906	2	399389	13	NULL	NULL	0	NULL	 CD72 gene 	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunological-focused microarray gene expression analysis showed that only the CD72 gene was significantly downregulated in the 12-month RSV-treated mice compared to age-matched controls .
	manualset3
92907	3	399389	13	NULL	NULL	0	NULL	12-month RSV-treated mice 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunological-focused microarray gene expression analysis showed that only the CD72 gene was significantly downregulated in the 12-month RSV-treated mice compared to age-matched controls .
	manualset3
92908	4	399389	13	NULL	NULL	0	NULL	age-matched controls	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunological-focused microarray gene expression analysis showed that only the CD72 gene was significantly downregulated in the 12-month RSV-treated mice compared to age-matched controls .
	manualset3
92909	1	399390	13	NULL	NULL	0	NULL	Immunological aspects	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunological aspects of transfer amyloidosis .
	manualset3
92910	2	399390	13	NULL	NULL	0	NULL	transfer amyloidosis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunological aspects of transfer amyloidosis .
	manualset3
92911	1	399391	13	NULL	NULL	0	NULL	Immunological response	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunological response related to photodynamic therapy ( PDT ) is one of the basic elements that influence on the efficiency of this cancer treatment method .
	manualset3
92912	2	399391	13	NULL	NULL	0	NULL	photodynamic therapy ( PDT )	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunological response related to photodynamic therapy ( PDT ) is one of the basic elements that influence on the efficiency of this cancer treatment method .
	manualset3
92913	3	399391	13	NULL	NULL	0	NULL	basic elements	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunological response related to photodynamic therapy ( PDT ) is one of the basic elements that influence on the efficiency of this cancer treatment method .
	manualset3
92915	5	399391	13	NULL	NULL	NULL	NULL	efficiency	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunological response related to photodynamic therapy ( PDT ) is one of the basic elements that influence on the efficiency of this cancer treatment method .
	manualset3
92916	6	399391	13	NULL	NULL	NULL	NULL	cancer treatment method	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunological response related to photodynamic therapy ( PDT ) is one of the basic elements that influence on the efficiency of this cancer treatment method .
	manualset3
92917	1	399392	13	NULL	NULL	0	NULL	Immunological studies 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunological studies indicate that the Mr-24 , 500 subunits present in GST III ( pI 7.9 ) are distinct from those present in GST IV ( pI 6.4 ) and V ( pI 5.7 ) .
	manualset3
92918	2	399392	13	NULL	NULL	0	NULL	Mr-24 , 500 subunits	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunological studies indicate that the Mr-24 , 500 subunits present in GST III ( pI 7.9 ) are distinct from those present in GST IV ( pI 6.4 ) and V ( pI 5.7 ) .
	manualset3
92919	3	399392	13	NULL	NULL	0	NULL	GST III ( pI 7.9 ) 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunological studies indicate that the Mr-24 , 500 subunits present in GST III ( pI 7.9 ) are distinct from those present in GST IV ( pI 6.4 ) and V ( pI 5.7 ) .
	manualset3
92920	4	399392	13	NULL	NULL	0	NULL	GST IV ( pI 6.4 )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunological studies indicate that the Mr-24 , 500 subunits present in GST III ( pI 7.9 ) are distinct from those present in GST IV ( pI 6.4 ) and V ( pI 5.7 ) .
	manualset3
92922	5	399392	13	NULL	NULL	0	NULL	GST V ( pI 5.7 )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunological studies indicate that the Mr-24 , 500 subunits present in GST III ( pI 7.9 ) are distinct from those present in GST IV ( pI 6.4 ) and V ( pI 5.7 ) .
	manualset3
92923	1	399393	13	NULL	NULL	0	NULL	Immunological variations	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunological variations of albumin as a function of the degradation stage ) .
	manualset3
92924	2	399393	13	NULL	NULL	0	NULL	albumin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunological variations of albumin as a function of the degradation stage ) .
	manualset3
92925	3	399393	13	NULL	NULL	NULL	NULL	function of the degradation stage	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunological variations of albumin as a function of the degradation stage ) .
	manualset3
92926	1	399394	13	NULL	NULL	NULL	NULL	food allergy	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunologically mediated food allergy : the importance of food challenge procedures .
	manualset3
92927	2	399394	13	NULL	NULL	0	NULL	importance	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunologically mediated food allergy : the importance of food challenge procedures .
	manualset3
92928	3	399394	13	NULL	NULL	0	NULL	food challenge procedures	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunologically mediated food allergy : the importance of food challenge procedures .
	manualset3
92929	1	399395	13	NULL	NULL	0	NULL	Immunoperoxidase studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoperoxidase studies using antibodies LN1 , LN2 , and L26 confirmed the presence of B cells in thymomas , particularly those with germinal centers .
	manualset3
92930	2	399395	13	NULL	NULL	0	NULL	antibodies LN1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoperoxidase studies using antibodies LN1 , LN2 , and L26 confirmed the presence of B cells in thymomas , particularly those with germinal centers .
	manualset3
92931	3	399395	13	NULL	NULL	0	NULL	antibodies LN2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoperoxidase studies using antibodies LN1 , LN2 , and L26 confirmed the presence of B cells in thymomas , particularly those with germinal centers .
	manualset3
92932	4	399395	13	NULL	NULL	0	NULL	antibodies L26	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoperoxidase studies using antibodies LN1 , LN2 , and L26 confirmed the presence of B cells in thymomas , particularly those with germinal centers .
	manualset3
92933	6	399395	13	NULL	NULL	NULL	NULL	B cells	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunoperoxidase studies using antibodies LN1 , LN2 , and L26 confirmed the presence of B cells in thymomas , particularly those with germinal centers .
	manualset3
92934	7	399395	13	NULL	NULL	NULL	NULL	thymomas	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunoperoxidase studies using antibodies LN1 , LN2 , and L26 confirmed the presence of B cells in thymomas , particularly those with germinal centers .
	manualset3
92935	8	399395	13	NULL	NULL	NULL	NULL	germinal centers	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunoperoxidase studies using antibodies LN1 , LN2 , and L26 confirmed the presence of B cells in thymomas , particularly those with germinal centers .
	manualset3
92936	5	399395	13	NULL	NULL	0	NULL	presence 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoperoxidase studies using antibodies LN1 , LN2 , and L26 confirmed the presence of B cells in thymomas , particularly those with germinal centers .
	manualset3
92937	1	399396	13	NULL	NULL	0	NULL	Immunopositivity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunopositivity was detected in the tumors tested as follows : KIT , 100 % ; CD34 , 75 % ; PKCtheta , 21 % ; PDGFRA , 90 % ; and smooth muscle actin , 6 % .
	manualset3
92938	2	399396	13	NULL	NULL	0	NULL	tumors 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunopositivity was detected in the tumors tested as follows : KIT , 100 % ; CD34 , 75 % ; PKCtheta , 21 % ; PDGFRA , 90 % ; and smooth muscle actin , 6 % .
	manualset3
92939	3	399396	13	NULL	NULL	0	NULL	KIT	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunopositivity was detected in the tumors tested as follows : KIT , 100 % ; CD34 , 75 % ; PKCtheta , 21 % ; PDGFRA , 90 % ; and smooth muscle actin , 6 % .
	manualset3
92940	4	399396	13	NULL	NULL	0	NULL	100 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunopositivity was detected in the tumors tested as follows : KIT , 100 % ; CD34 , 75 % ; PKCtheta , 21 % ; PDGFRA , 90 % ; and smooth muscle actin , 6 % .
	manualset3
92941	5	399396	13	NULL	NULL	0	NULL	CD34	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunopositivity was detected in the tumors tested as follows : KIT , 100 % ; CD34 , 75 % ; PKCtheta , 21 % ; PDGFRA , 90 % ; and smooth muscle actin , 6 % .
	manualset3
92942	6	399396	13	NULL	NULL	0	NULL	75 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunopositivity was detected in the tumors tested as follows : KIT , 100 % ; CD34 , 75 % ; PKCtheta , 21 % ; PDGFRA , 90 % ; and smooth muscle actin , 6 % .
	manualset3
92943	7	399396	13	NULL	NULL	0	NULL	PKCtheta	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunopositivity was detected in the tumors tested as follows : KIT , 100 % ; CD34 , 75 % ; PKCtheta , 21 % ; PDGFRA , 90 % ; and smooth muscle actin , 6 % .
	manualset3
92944	8	399396	13	NULL	NULL	0	NULL	 21 % 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunopositivity was detected in the tumors tested as follows : KIT , 100 % ; CD34 , 75 % ; PKCtheta , 21 % ; PDGFRA , 90 % ; and smooth muscle actin , 6 % .
	manualset3
92945	9	399396	13	NULL	NULL	0	NULL	 PDGFRA	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunopositivity was detected in the tumors tested as follows : KIT , 100 % ; CD34 , 75 % ; PKCtheta , 21 % ; PDGFRA , 90 % ; and smooth muscle actin , 6 % .
	manualset3
92946	10	399396	13	NULL	NULL	0	NULL	90 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunopositivity was detected in the tumors tested as follows : KIT , 100 % ; CD34 , 75 % ; PKCtheta , 21 % ; PDGFRA , 90 % ; and smooth muscle actin , 6 % .
	manualset3
92947	11	399396	13	NULL	NULL	0	NULL	smooth muscle actin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunopositivity was detected in the tumors tested as follows : KIT , 100 % ; CD34 , 75 % ; PKCtheta , 21 % ; PDGFRA , 90 % ; and smooth muscle actin , 6 % .
	manualset3
92948	12	399396	13	NULL	NULL	0	NULL	 6 % 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunopositivity was detected in the tumors tested as follows : KIT , 100 % ; CD34 , 75 % ; PKCtheta , 21 % ; PDGFRA , 90 % ; and smooth muscle actin , 6 % .
	manualset3
92949	1	399397	13	NULL	NULL	0	NULL	Immunoprecipitation analyses	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation analyses of B-CLL sera allow detection of several high molecular weight bands and of a 78 kDa band that represents a soluble form of CD44st and is 4 kDa lower than a similar band ( 82 kDa ) detected in B-CLL cell lysates .
	manualset3
92950	2	399397	13	NULL	NULL	0	NULL	B-CLL sera	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation analyses of B-CLL sera allow detection of several high molecular weight bands and of a 78 kDa band that represents a soluble form of CD44st and is 4 kDa lower than a similar band ( 82 kDa ) detected in B-CLL cell lysates .
	manualset3
92951	3	399397	13	NULL	NULL	0	NULL	detection	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation analyses of B-CLL sera allow detection of several high molecular weight bands and of a 78 kDa band that represents a soluble form of CD44st and is 4 kDa lower than a similar band ( 82 kDa ) detected in B-CLL cell lysates .
	manualset3
92953	4	399397	13	NULL	NULL	0	NULL	several high molecular weight bands	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation analyses of B-CLL sera allow detection of several high molecular weight bands and of a 78 kDa band that represents a soluble form of CD44st and is 4 kDa lower than a similar band ( 82 kDa ) detected in B-CLL cell lysates .
	manualset3
92954	5	399397	13	NULL	NULL	NULL	NULL	78 kDa band	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation analyses of B-CLL sera allow detection of several high molecular weight bands and of a 78 kDa band that represents a soluble form of CD44st and is 4 kDa lower than a similar band ( 82 kDa ) detected in B-CLL cell lysates .
	manualset3
92955	6	399397	13	NULL	NULL	0	NULL	soluble form of CD44st	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation analyses of B-CLL sera allow detection of several high molecular weight bands and of a 78 kDa band that represents a soluble form of CD44st and is 4 kDa lower than a similar band ( 82 kDa ) detected in B-CLL cell lysates .
	manualset3
92956	7	399397	13	NULL	NULL	0	NULL	 4 kDa lower than a similar band ( 82 kDa ) 	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation analyses of B-CLL sera allow detection of several high molecular weight bands and of a 78 kDa band that represents a soluble form of CD44st and is 4 kDa lower than a similar band ( 82 kDa ) detected in B-CLL cell lysates .
	manualset3
92958	8	399397	13	NULL	NULL	0	NULL	B-CLL cell lysates	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation analyses of B-CLL sera allow detection of several high molecular weight bands and of a 78 kDa band that represents a soluble form of CD44st and is 4 kDa lower than a similar band ( 82 kDa ) detected in B-CLL cell lysates .
	manualset3
92963	1	399398	13	NULL	NULL	0	NULL	Immunoprecipitation analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation analysis of radiolabeled conditioned medium revealed a specific Mr 25 , 000 band only after acidification .
	manualset3
92964	2	399398	13	NULL	NULL	NULL	NULL	conditioned medium	ExperimentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation analysis of radiolabeled conditioned medium revealed a specific Mr 25 , 000 band only after acidification .
	manualset3
92965	3	399398	13	NULL	NULL	0	NULL	Mr 25 , 000 band	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation analysis of radiolabeled conditioned medium revealed a specific Mr 25 , 000 band only after acidification .
	manualset3
92966	4	399398	13	NULL	NULL	0	NULL	acidification 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation analysis of radiolabeled conditioned medium revealed a specific Mr 25 , 000 band only after acidification .
	manualset3
92976	1	399399	13	NULL	NULL	0	NULL	Immunoprecipitation experiments	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation experiments using peptide-specific anti-SBE antibodies showed that SBEIIb and starch phosphorylase each coimmunoprecipitated with SBEI in a phosphorylation-dependent manner , suggesting that these enzymes may form protein complexes within the amyloplast in vivo .
	manualset3
92977	2	399399	13	NULL	NULL	0	NULL	peptide-specific anti-SBE antibodies	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation experiments using peptide-specific anti-SBE antibodies showed that SBEIIb and starch phosphorylase each coimmunoprecipitated with SBEI in a phosphorylation-dependent manner , suggesting that these enzymes may form protein complexes within the amyloplast in vivo .
	manualset3
92978	3	399399	13	NULL	NULL	0	NULL	SBEIIb 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation experiments using peptide-specific anti-SBE antibodies showed that SBEIIb and starch phosphorylase each coimmunoprecipitated with SBEI in a phosphorylation-dependent manner , suggesting that these enzymes may form protein complexes within the amyloplast in vivo .
	manualset3
92979	4	399399	13	NULL	NULL	0	NULL	starch phosphorylase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation experiments using peptide-specific anti-SBE antibodies showed that SBEIIb and starch phosphorylase each coimmunoprecipitated with SBEI in a phosphorylation-dependent manner , suggesting that these enzymes may form protein complexes within the amyloplast in vivo .
	manualset3
92980	5	399399	13	NULL	NULL	0	NULL	SBEI	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation experiments using peptide-specific anti-SBE antibodies showed that SBEIIb and starch phosphorylase each coimmunoprecipitated with SBEI in a phosphorylation-dependent manner , suggesting that these enzymes may form protein complexes within the amyloplast in vivo .
	manualset3
92981	6	399399	13	NULL	NULL	0	NULL	 phosphorylation-dependent manner	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation experiments using peptide-specific anti-SBE antibodies showed that SBEIIb and starch phosphorylase each coimmunoprecipitated with SBEI in a phosphorylation-dependent manner , suggesting that these enzymes may form protein complexes within the amyloplast in vivo .
	manualset3
92982	7	399399	13	NULL	NULL	0	NULL	enzymes	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation experiments using peptide-specific anti-SBE antibodies showed that SBEIIb and starch phosphorylase each coimmunoprecipitated with SBEI in a phosphorylation-dependent manner , suggesting that these enzymes may form protein complexes within the amyloplast in vivo .
	manualset3
92983	8	399399	13	NULL	NULL	0	NULL	protein complexes	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation experiments using peptide-specific anti-SBE antibodies showed that SBEIIb and starch phosphorylase each coimmunoprecipitated with SBEI in a phosphorylation-dependent manner , suggesting that these enzymes may form protein complexes within the amyloplast in vivo .
	manualset3
92984	9	399399	13	NULL	NULL	0	NULL	amyloplast	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation experiments using peptide-specific anti-SBE antibodies showed that SBEIIb and starch phosphorylase each coimmunoprecipitated with SBEI in a phosphorylation-dependent manner , suggesting that these enzymes may form protein complexes within the amyloplast in vivo .
	manualset3
92985	1	399400	13	NULL	NULL	0	NULL	Immunoprecipitation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation of MS2-tagged NCL 3 ` UTR was used to screen for endogenous repressors of nucleolin synthesis .
	manualset3
92986	2	399400	13	NULL	NULL	0	NULL	MS2-tagged NCL 3 ` UTR	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation of MS2-tagged NCL 3 ` UTR was used to screen for endogenous repressors of nucleolin synthesis .
	manualset3
92987	3	399400	13	NULL	NULL	0	NULL	endogenous repressors	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation of MS2-tagged NCL 3 ` UTR was used to screen for endogenous repressors of nucleolin synthesis .
	manualset3
92988	4	399400	13	NULL	NULL	0	NULL	nucleolin synthesis 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation of MS2-tagged NCL 3 ` UTR was used to screen for endogenous repressors of nucleolin synthesis .
	manualset3
92989	1	399401	13	NULL	NULL	0	NULL	Immunoprecipitation 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation of their livers followed by autoradiographic analysis showed the presence of 32P in small molecular weight apo-B .
	manualset3
92990	2	399401	13	NULL	NULL	0	NULL	livers 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation of their livers followed by autoradiographic analysis showed the presence of 32P in small molecular weight apo-B .
	manualset3
92991	3	399401	13	NULL	NULL	0	NULL	autoradiographic analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation of their livers followed by autoradiographic analysis showed the presence of 32P in small molecular weight apo-B .
	manualset3
92992	4	399401	13	NULL	NULL	0	NULL	32P	Atom												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation of their livers followed by autoradiographic analysis showed the presence of 32P in small molecular weight apo-B .
	manualset3
92993	5	399401	13	NULL	NULL	0	NULL	small molecular weight apo-B 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprecipitation of their livers followed by autoradiographic analysis showed the presence of 32P in small molecular weight apo-B .
	manualset3
92994	1	399402	13	NULL	NULL	0	NULL	Immunoprofile	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprofile of Hodgkin 's lymphoma in India .
	manualset3
92995	2	399402	13	NULL	NULL	0	NULL	Hodgkin 's lymphoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprofile of Hodgkin 's lymphoma in India .
	manualset3
92996	3	399402	13	NULL	NULL	0	NULL	India 	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprofile of Hodgkin 's lymphoma in India .
	manualset3
92997	1	399403	13	NULL	NULL	0	NULL	Immunoprophylaxis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprophylaxis with Simulect ( basiliximab ) in pediatric kidney transplant recipients : results from routine clinical practice at 5 kidney transplant units .
	manualset3
92998	2	399403	13	NULL	NULL	0	NULL	Simulect ( basiliximab ) 	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprophylaxis with Simulect ( basiliximab ) in pediatric kidney transplant recipients : results from routine clinical practice at 5 kidney transplant units .
	manualset3
92999	3	399403	13	NULL	NULL	0	NULL	pediatric kidney transplant recipients 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoprophylaxis with Simulect ( basiliximab ) in pediatric kidney transplant recipients : results from routine clinical practice at 5 kidney transplant units .
	manualset3
93000	5	399403	13	NULL	NULL	NULL	NULL	routine clinical practice	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunoprophylaxis with Simulect ( basiliximab ) in pediatric kidney transplant recipients : results from routine clinical practice at 5 kidney transplant units .
	manualset3
93001	6	399403	13	NULL	NULL	NULL	NULL	5 kidney transplant units	Facility												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunoprophylaxis with Simulect ( basiliximab ) in pediatric kidney transplant recipients : results from routine clinical practice at 5 kidney transplant units .
	manualset3
93002	4	399403	13	NULL	NULL	NULL	NULL	 results	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunoprophylaxis with Simulect ( basiliximab ) in pediatric kidney transplant recipients : results from routine clinical practice at 5 kidney transplant units .
	manualset3
93020	1	399404	13	NULL	NULL	0	NULL	Immunoreactive ( i ) TxB2 	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive ( i ) TxB2 was measured in plasma or Fluosol-43 obtained from rats prior to and after injection of Salmonella enteritidis endotoxin ( 20 mg/kg ) .
	manualset3
93021	2	399404	13	NULL	NULL	0	NULL	 plasma 	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive ( i ) TxB2 was measured in plasma or Fluosol-43 obtained from rats prior to and after injection of Salmonella enteritidis endotoxin ( 20 mg/kg ) .
	manualset3
93022	3	399404	13	NULL	NULL	0	NULL	Fluosol-43	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive ( i ) TxB2 was measured in plasma or Fluosol-43 obtained from rats prior to and after injection of Salmonella enteritidis endotoxin ( 20 mg/kg ) .
	manualset3
93023	4	399404	13	NULL	NULL	0	NULL	rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive ( i ) TxB2 was measured in plasma or Fluosol-43 obtained from rats prior to and after injection of Salmonella enteritidis endotoxin ( 20 mg/kg ) .
	manualset3
93024	5	399404	13	NULL	NULL	0	NULL	injection	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive ( i ) TxB2 was measured in plasma or Fluosol-43 obtained from rats prior to and after injection of Salmonella enteritidis endotoxin ( 20 mg/kg ) .
	manualset3
93025	6	399404	13	NULL	NULL	0	NULL	Salmonella enteritidis endotoxin	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive ( i ) TxB2 was measured in plasma or Fluosol-43 obtained from rats prior to and after injection of Salmonella enteritidis endotoxin ( 20 mg/kg ) .
	manualset3
93026	7	399404	13	NULL	NULL	0	NULL	20 mg/kg	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive ( i ) TxB2 was measured in plasma or Fluosol-43 obtained from rats prior to and after injection of Salmonella enteritidis endotoxin ( 20 mg/kg ) .
	manualset3
93027	1	399405	13	NULL	NULL	0	NULL	Therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Therapy of intestinal infections with paromomycin ) .
	manualset3
93028	2	399405	13	NULL	NULL	0	NULL	intestinal infections	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Therapy of intestinal infections with paromomycin ) .
	manualset3
93029	3	399405	13	NULL	NULL	0	NULL	paromomycin	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( Therapy of intestinal infections with paromomycin ) .
	manualset3
93030	1	399406	13	NULL	NULL	0	NULL	Immunoreactive bradykinin ( IRBK )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive bradykinin ( IRBK ) was measured in the perfusate and the basal level was found to be constant for up to 3 h. Ten min perfusions of the hearts with ET-1 at concentrations of 0.2-20 pM produced a dose-related suppression of kinin outflow by over 90 % ( P & lt ; 0.05 ) .
	manualset3
93031	2	399406	13	NULL	NULL	0	NULL	perfusate level  	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive bradykinin ( IRBK ) was measured in the perfusate and the basal level was found to be constant for up to 3 h. Ten min perfusions of the hearts with ET-1 at concentrations of 0.2-20 pM produced a dose-related suppression of kinin outflow by over 90 % ( P & lt ; 0.05 ) .
	manualset3
93032	3	399406	13	NULL	NULL	0	NULL	basal level	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive bradykinin ( IRBK ) was measured in the perfusate and the basal level was found to be constant for up to 3 h. Ten min perfusions of the hearts with ET-1 at concentrations of 0.2-20 pM produced a dose-related suppression of kinin outflow by over 90 % ( P & lt ; 0.05 ) .
	manualset3
93033	4	399406	13	NULL	NULL	0	NULL	3 h	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive bradykinin ( IRBK ) was measured in the perfusate and the basal level was found to be constant for up to 3 h. Ten min perfusions of the hearts with ET-1 at concentrations of 0.2-20 pM produced a dose-related suppression of kinin outflow by over 90 % ( P & lt ; 0.05 ) .
	manualset3
93034	5	399406	13	NULL	NULL	0	NULL	Ten min	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive bradykinin ( IRBK ) was measured in the perfusate and the basal level was found to be constant for up to 3 h. Ten min perfusions of the hearts with ET-1 at concentrations of 0.2-20 pM produced a dose-related suppression of kinin outflow by over 90 % ( P & lt ; 0.05 ) .
	manualset3
93035	6	399406	13	NULL	NULL	0	NULL	perfusions	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive bradykinin ( IRBK ) was measured in the perfusate and the basal level was found to be constant for up to 3 h. Ten min perfusions of the hearts with ET-1 at concentrations of 0.2-20 pM produced a dose-related suppression of kinin outflow by over 90 % ( P & lt ; 0.05 ) .
	manualset3
93036	7	399406	13	NULL	NULL	0	NULL	 hearts 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive bradykinin ( IRBK ) was measured in the perfusate and the basal level was found to be constant for up to 3 h. Ten min perfusions of the hearts with ET-1 at concentrations of 0.2-20 pM produced a dose-related suppression of kinin outflow by over 90 % ( P & lt ; 0.05 ) .
	manualset3
93037	8	399406	13	NULL	NULL	NULL	NULL	ET-1	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunoreactive bradykinin ( IRBK ) was measured in the perfusate and the basal level was found to be constant for up to 3 h. Ten min perfusions of the hearts with ET-1 at concentrations of 0.2-20 pM produced a dose-related suppression of kinin outflow by over 90 % ( P & lt ; 0.05 ) .
	manualset3
93038	9	399406	13	NULL	NULL	0	NULL	concentrations of 0.2-20 pM	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive bradykinin ( IRBK ) was measured in the perfusate and the basal level was found to be constant for up to 3 h. Ten min perfusions of the hearts with ET-1 at concentrations of 0.2-20 pM produced a dose-related suppression of kinin outflow by over 90 % ( P & lt ; 0.05 ) .
	manualset3
93039	10	399406	13	NULL	NULL	NULL	NULL	dose-related suppression of kinin outflow  	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunoreactive bradykinin ( IRBK ) was measured in the perfusate and the basal level was found to be constant for up to 3 h. Ten min perfusions of the hearts with ET-1 at concentrations of 0.2-20 pM produced a dose-related suppression of kinin outflow by over 90 % ( P & lt ; 0.05 ) .
	manualset3
93040	11	399406	13	NULL	NULL	0	NULL	over 90 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive bradykinin ( IRBK ) was measured in the perfusate and the basal level was found to be constant for up to 3 h. Ten min perfusions of the hearts with ET-1 at concentrations of 0.2-20 pM produced a dose-related suppression of kinin outflow by over 90 % ( P & lt ; 0.05 ) .
	manualset3
93041	12	399406	13	NULL	NULL	0	NULL	P & lt ; 0.05 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive bradykinin ( IRBK ) was measured in the perfusate and the basal level was found to be constant for up to 3 h. Ten min perfusions of the hearts with ET-1 at concentrations of 0.2-20 pM produced a dose-related suppression of kinin outflow by over 90 % ( P & lt ; 0.05 ) .
	manualset3
93042	1	399407	13	NULL	NULL	0	NULL	Immunoreactive cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive cells were found in about 2/3 of the tumors .
	manualset3
93043	2	399407	13	NULL	NULL	0	NULL	2/3 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive cells were found in about 2/3 of the tumors .
	manualset3
93044	3	399407	13	NULL	NULL	0	NULL	 tumors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunoreactive cells were found in about 2/3 of the tumors .
	manualset3
93045	1	399408	13	NULL	NULL	0	NULL	Immunosenescence	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunosenescence is characterized by reduced levels of the peripheral naive T cell pool derived from thymus and the loss of immature B lineage cells in the bone marrow .
	manualset3
93046	2	399408	13	NULL	NULL	NULL	NULL	reduced levels	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunosenescence is characterized by reduced levels of the peripheral naive T cell pool derived from thymus and the loss of immature B lineage cells in the bone marrow .
	manualset3
93047	3	399408	13	NULL	NULL	0	NULL	peripheral naive T cell pool	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunosenescence is characterized by reduced levels of the peripheral naive T cell pool derived from thymus and the loss of immature B lineage cells in the bone marrow .
	manualset3
93048	4	399408	13	NULL	NULL	0	NULL	thymus 	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunosenescence is characterized by reduced levels of the peripheral naive T cell pool derived from thymus and the loss of immature B lineage cells in the bone marrow .
	manualset3
93049	5	399408	13	NULL	NULL	0	NULL	loss 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunosenescence is characterized by reduced levels of the peripheral naive T cell pool derived from thymus and the loss of immature B lineage cells in the bone marrow .
	manualset3
93050	6	399408	13	NULL	NULL	0	NULL	immature B lineage cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunosenescence is characterized by reduced levels of the peripheral naive T cell pool derived from thymus and the loss of immature B lineage cells in the bone marrow .
	manualset3
93051	7	399408	13	NULL	NULL	0	NULL	bone marrow	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunosenescence is characterized by reduced levels of the peripheral naive T cell pool derived from thymus and the loss of immature B lineage cells in the bone marrow .
	manualset3
93052	1	399409	13	NULL	NULL	0	NULL	Immunostaining	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunostaining and protein tagging demonstrated that only Dmc1p formed strong DSB-dependent foci on meiotic chromatin , whereas the distribution of Rad51p was diffuse within nuclei .
	manualset3
93053	2	399409	13	NULL	NULL	0	NULL	 protein tagging	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunostaining and protein tagging demonstrated that only Dmc1p formed strong DSB-dependent foci on meiotic chromatin , whereas the distribution of Rad51p was diffuse within nuclei .
	manualset3
93054	3	399409	13	NULL	NULL	0	NULL	Dmc1p	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunostaining and protein tagging demonstrated that only Dmc1p formed strong DSB-dependent foci on meiotic chromatin , whereas the distribution of Rad51p was diffuse within nuclei .
	manualset3
93055	4	399409	13	NULL	NULL	0	NULL	DSB-dependent foci on meiotic chromatin	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunostaining and protein tagging demonstrated that only Dmc1p formed strong DSB-dependent foci on meiotic chromatin , whereas the distribution of Rad51p was diffuse within nuclei .
	manualset3
93056	5	399409	13	NULL	NULL	0	NULL	distribution 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunostaining and protein tagging demonstrated that only Dmc1p formed strong DSB-dependent foci on meiotic chromatin , whereas the distribution of Rad51p was diffuse within nuclei .
	manualset3
93057	6	399409	13	NULL	NULL	0	NULL	Rad51p	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunostaining and protein tagging demonstrated that only Dmc1p formed strong DSB-dependent foci on meiotic chromatin , whereas the distribution of Rad51p was diffuse within nuclei .
	manualset3
93059	7	399409	13	NULL	NULL	NULL	NULL	nuclei 	CellComponent												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Immunostaining and protein tagging demonstrated that only Dmc1p formed strong DSB-dependent foci on meiotic chromatin , whereas the distribution of Rad51p was diffuse within nuclei .
	manualset3
93060	1	399410	13	NULL	NULL	0	NULL	Immunostaining 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunostaining with HIK1083 and anti-lysozyme antibody was examined under light and electron microscopes .
	manualset3
93061	2	399410	13	NULL	NULL	0	NULL	HIK1083	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunostaining with HIK1083 and anti-lysozyme antibody was examined under light and electron microscopes .
	manualset3
93062	3	399410	13	NULL	NULL	0	NULL	anti-lysozyme antibody	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunostaining with HIK1083 and anti-lysozyme antibody was examined under light and electron microscopes .
	manualset3
93063	4	399410	13	NULL	NULL	0	NULL	 light microscopes	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunostaining with HIK1083 and anti-lysozyme antibody was examined under light and electron microscopes .
	manualset3
93064	5	399410	13	NULL	NULL	0	NULL	electron microscopes	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunostaining with HIK1083 and anti-lysozyme antibody was examined under light and electron microscopes .
	manualset3
93065	1	399411	13	NULL	NULL	0	NULL	Immunotoxic effects	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunotoxic effects of diethylstilbestrol ( DES ) and cadmium chloride ( CAD ) on host resistance : comparison with cyclophosphamide ( CPS ) .
	manualset3
93066	2	399411	13	NULL	NULL	0	NULL	diethylstilbestrol ( DES ) 	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunotoxic effects of diethylstilbestrol ( DES ) and cadmium chloride ( CAD ) on host resistance : comparison with cyclophosphamide ( CPS ) .
	manualset3
93067	3	399411	13	NULL	NULL	0	NULL	cadmium chloride ( CAD )	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunotoxic effects of diethylstilbestrol ( DES ) and cadmium chloride ( CAD ) on host resistance : comparison with cyclophosphamide ( CPS ) .
	manualset3
93068	4	399411	13	NULL	NULL	0	NULL	host resistance	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunotoxic effects of diethylstilbestrol ( DES ) and cadmium chloride ( CAD ) on host resistance : comparison with cyclophosphamide ( CPS ) .
	manualset3
93069	5	399411	13	NULL	NULL	0	NULL	comparison	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunotoxic effects of diethylstilbestrol ( DES ) and cadmium chloride ( CAD ) on host resistance : comparison with cyclophosphamide ( CPS ) .
	manualset3
93070	6	399411	13	NULL	NULL	0	NULL	 cyclophosphamide ( CPS )	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Immunotoxic effects of diethylstilbestrol ( DES ) and cadmium chloride ( CAD ) on host resistance : comparison with cyclophosphamide ( CPS ) .
	manualset3
93071	1	399412	13	NULL	NULL	0	NULL	 Impact 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of DOTS compared with DOTS-plus on multidrug resistant tuberculosis and tuberculosis deaths : decision analysis .
	manualset3
93072	2	399412	13	NULL	NULL	0	NULL	DOTS	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of DOTS compared with DOTS-plus on multidrug resistant tuberculosis and tuberculosis deaths : decision analysis .
	manualset3
93073	3	399412	13	NULL	NULL	0	NULL	DOTS-plus	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of DOTS compared with DOTS-plus on multidrug resistant tuberculosis and tuberculosis deaths : decision analysis .
	manualset3
93074	4	399412	13	NULL	NULL	0	NULL	multidrug resistant tuberculosis deaths 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of DOTS compared with DOTS-plus on multidrug resistant tuberculosis and tuberculosis deaths : decision analysis .
	manualset3
93075	5	399412	13	NULL	NULL	0	NULL	 tuberculosis deaths	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of DOTS compared with DOTS-plus on multidrug resistant tuberculosis and tuberculosis deaths : decision analysis .
	manualset3
93076	6	399412	13	NULL	NULL	0	NULL	decision analysis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of DOTS compared with DOTS-plus on multidrug resistant tuberculosis and tuberculosis deaths : decision analysis .
	manualset3
93078	3	399413	13	NULL	NULL	NULL	NULL	anorexia nervosa	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Impact of broadening definitions of anorexia nervosa on sample characteristics .
	manualset3
93079	4	399413	13	NULL	NULL	NULL	NULL	sample characteristics 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Impact of broadening definitions of anorexia nervosa on sample characteristics .
	manualset3
93080	2	399413	13	NULL	NULL	0	NULL	broadening definitions 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of broadening definitions of anorexia nervosa on sample characteristics .
	manualset3
93090	1	399413	13	NULL	NULL	0	NULL	Impact	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of broadening definitions of anorexia nervosa on sample characteristics .
	manualset3
93081	1	399414	13	NULL	NULL	NULL	NULL	Impact of changes	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Impact of changes in catheter management on infectious complications among children with central venous catheters .
	manualset3
93082	2	399414	13	NULL	NULL	0	NULL	catheter management	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of changes in catheter management on infectious complications among children with central venous catheters .
	manualset3
93083	3	399414	13	NULL	NULL	0	NULL	infectious complications	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of changes in catheter management on infectious complications among children with central venous catheters .
	manualset3
93084	4	399414	13	NULL	NULL	0	NULL	children	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of changes in catheter management on infectious complications among children with central venous catheters .
	manualset3
93085	5	399414	13	NULL	NULL	0	NULL	central venous catheters 	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of changes in catheter management on infectious complications among children with central venous catheters .
	manualset3
93086	2	399415	13	NULL	NULL	NULL	NULL	chronic kidney disease	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Impact of chronic kidney disease on carotid plaque vulnerability .
	manualset3
93087	2	399415	13	NULL	NULL	0	NULL	carotid plaque vulnerability	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of chronic kidney disease on carotid plaque vulnerability .
	manualset3
93088	1	399415	13	NULL	NULL	NULL	NULL	Impact	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Impact of chronic kidney disease on carotid plaque vulnerability .
	manualset3
93091	1	399416	13	NULL	NULL	NULL	NULL	Impact	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Impact of congenital color vision deficiency on education and unintentional injuries : findings from the 1958 British birth cohort .
	manualset3
93092	2	399416	13	NULL	NULL	0	NULL	congenital color vision deficiency 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of congenital color vision deficiency on education and unintentional injuries : findings from the 1958 British birth cohort .
	manualset3
93093	3	399416	13	NULL	NULL	0	NULL	education	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of congenital color vision deficiency on education and unintentional injuries : findings from the 1958 British birth cohort .
	manualset3
93094	4	399416	13	NULL	NULL	0	NULL	unintentional injuries	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of congenital color vision deficiency on education and unintentional injuries : findings from the 1958 British birth cohort .
	manualset3
93095	5	399416	13	NULL	NULL	0	NULL	findings	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of congenital color vision deficiency on education and unintentional injuries : findings from the 1958 British birth cohort .
	manualset3
93096	6	399416	13	NULL	NULL	0	NULL	1958	Time												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of congenital color vision deficiency on education and unintentional injuries : findings from the 1958 British birth cohort .
	manualset3
93097	7	399416	13	NULL	NULL	0	NULL	British birth cohort 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of congenital color vision deficiency on education and unintentional injuries : findings from the 1958 British birth cohort .
	manualset3
93098	1	399417	13	NULL	NULL	NULL	NULL	Impact	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Impact of depressive symptoms on visceral sensitivity among patients with different subtypes of irritable bowel syndrome .
	manualset3
93099	2	399417	13	NULL	NULL	0	NULL	depressive symptoms	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of depressive symptoms on visceral sensitivity among patients with different subtypes of irritable bowel syndrome .
	manualset3
93100	3	399417	13	NULL	NULL	0	NULL	visceral sensitivity 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of depressive symptoms on visceral sensitivity among patients with different subtypes of irritable bowel syndrome .
	manualset3
93101	4	399417	13	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of depressive symptoms on visceral sensitivity among patients with different subtypes of irritable bowel syndrome .
	manualset3
93102	5	399417	13	NULL	NULL	0	NULL	different subtypes of irritable bowel syndrome	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of depressive symptoms on visceral sensitivity among patients with different subtypes of irritable bowel syndrome .
	manualset3
93103	1	399418	13	NULL	NULL	0	NULL	Impact	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of different case definitions for acute otitis media on the efficacy estimates of a pneumococcal conjugate vaccine .
	manualset3
93104	2	399418	13	NULL	NULL	NULL	NULL	different case definitions 	PublishedSourceOfInformation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Impact of different case definitions for acute otitis media on the efficacy estimates of a pneumococcal conjugate vaccine .
	manualset3
93105	3	399418	13	NULL	NULL	0	NULL	acute otitis media	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of different case definitions for acute otitis media on the efficacy estimates of a pneumococcal conjugate vaccine .
	manualset3
93106	4	399418	13	NULL	NULL	0	NULL	efficacy estimates 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of different case definitions for acute otitis media on the efficacy estimates of a pneumococcal conjugate vaccine .
	manualset3
93107	5	399418	13	NULL	NULL	0	NULL	pneumococcal conjugate vaccine	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of different case definitions for acute otitis media on the efficacy estimates of a pneumococcal conjugate vaccine .
	manualset3
93108	1	399419	13	NULL	NULL	0	NULL	Impact	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of global transcriptional regulation by ArcA , ArcB , Cra , Crp , Cya , Fnr , and Mlc on glucose catabolism in Escherichia coli .
	manualset3
93109	2	399419	13	NULL	NULL	0	NULL	global transcriptional regulation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of global transcriptional regulation by ArcA , ArcB , Cra , Crp , Cya , Fnr , and Mlc on glucose catabolism in Escherichia coli .
	manualset3
93110	3	399419	13	NULL	NULL	0	NULL	ArcA	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of global transcriptional regulation by ArcA , ArcB , Cra , Crp , Cya , Fnr , and Mlc on glucose catabolism in Escherichia coli .
	manualset3
93111	4	399419	13	NULL	NULL	0	NULL	ArcB	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of global transcriptional regulation by ArcA , ArcB , Cra , Crp , Cya , Fnr , and Mlc on glucose catabolism in Escherichia coli .
	manualset3
93112	5	399419	13	NULL	NULL	0	NULL	Cra	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of global transcriptional regulation by ArcA , ArcB , Cra , Crp , Cya , Fnr , and Mlc on glucose catabolism in Escherichia coli .
	manualset3
93113	6	399419	13	NULL	NULL	0	NULL	Crp	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of global transcriptional regulation by ArcA , ArcB , Cra , Crp , Cya , Fnr , and Mlc on glucose catabolism in Escherichia coli .
	manualset3
93114	7	399419	13	NULL	NULL	0	NULL	Cya	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of global transcriptional regulation by ArcA , ArcB , Cra , Crp , Cya , Fnr , and Mlc on glucose catabolism in Escherichia coli .
	manualset3
93115	8	399419	13	NULL	NULL	0	NULL	Fnr	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of global transcriptional regulation by ArcA , ArcB , Cra , Crp , Cya , Fnr , and Mlc on glucose catabolism in Escherichia coli .
	manualset3
93116	9	399419	13	NULL	NULL	0	NULL	Mlc	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of global transcriptional regulation by ArcA , ArcB , Cra , Crp , Cya , Fnr , and Mlc on glucose catabolism in Escherichia coli .
	manualset3
93117	10	399419	13	NULL	NULL	0	NULL	glucose catabolism	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of global transcriptional regulation by ArcA , ArcB , Cra , Crp , Cya , Fnr , and Mlc on glucose catabolism in Escherichia coli .
	manualset3
93118	11	399419	13	NULL	NULL	0	NULL	Escherichia coli 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of global transcriptional regulation by ArcA , ArcB , Cra , Crp , Cya , Fnr , and Mlc on glucose catabolism in Escherichia coli .
	manualset3
93119	1	399420	13	NULL	NULL	0	NULL	Impact 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of heat stress exposure during meiotic maturation on oocyte , surrounding cumulus cell , and embryo RNA populations .
	manualset3
93120	2	399420	13	NULL	NULL	0	NULL	heat stress exposure	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of heat stress exposure during meiotic maturation on oocyte , surrounding cumulus cell , and embryo RNA populations .
	manualset3
93121	3	399420	13	NULL	NULL	0	NULL	meiotic maturation 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of heat stress exposure during meiotic maturation on oocyte , surrounding cumulus cell , and embryo RNA populations .
	manualset3
93122	4	399420	13	NULL	NULL	0	NULL	 oocyte	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of heat stress exposure during meiotic maturation on oocyte , surrounding cumulus cell , and embryo RNA populations .
	manualset3
93123	5	399420	13	NULL	NULL	0	NULL	surrounding cumulus cell 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of heat stress exposure during meiotic maturation on oocyte , surrounding cumulus cell , and embryo RNA populations .
	manualset3
93124	6	399420	13	NULL	NULL	0	NULL	embryo RNA populations	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of heat stress exposure during meiotic maturation on oocyte , surrounding cumulus cell , and embryo RNA populations .
	manualset3
93125	1	399421	13	NULL	NULL	0	NULL	Impact	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of kidney cancer surgery on oncologic and kidney functional outcomes .
	manualset3
93126	2	399421	13	NULL	NULL	0	NULL	kidney cancer surgery	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of kidney cancer surgery on oncologic and kidney functional outcomes .
	manualset3
93127	3	399421	13	NULL	NULL	0	NULL	oncologic outcomes	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of kidney cancer surgery on oncologic and kidney functional outcomes .
	manualset3
93128	4	399421	13	NULL	NULL	0	NULL	kidney functional outcomes	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of kidney cancer surgery on oncologic and kidney functional outcomes .
	manualset3
93129	1	399422	13	NULL	NULL	0	NULL	Impact	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of mass media on adolescent sexual behavior : the chicken or the egg ? .
	manualset3
93130	2	399422	13	NULL	NULL	0	NULL	mass media 	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of mass media on adolescent sexual behavior : the chicken or the egg ? .
	manualset3
93131	3	399422	13	NULL	NULL	0	NULL	adolescent sexual behavior	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of mass media on adolescent sexual behavior : the chicken or the egg ? .
	manualset3
93132	4	399422	13	NULL	NULL	0	NULL	chicken	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of mass media on adolescent sexual behavior : the chicken or the egg ? .
	manualset3
93133	5	399422	13	NULL	NULL	0	NULL	egg	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of mass media on adolescent sexual behavior : the chicken or the egg ? .
	manualset3
93134	1	399423	13	NULL	NULL	0	NULL	Impact	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of omega-3 polyunsaturated fatty acids on coronary plaque instability : an integrated backscatter intravascular ultrasound study .
	manualset3
93135	2	399423	13	NULL	NULL	0	NULL	omega-3 polyunsaturated fatty acids	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of omega-3 polyunsaturated fatty acids on coronary plaque instability : an integrated backscatter intravascular ultrasound study .
	manualset3
93136	3	399423	13	NULL	NULL	0	NULL	coronary plaque instability	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of omega-3 polyunsaturated fatty acids on coronary plaque instability : an integrated backscatter intravascular ultrasound study .
	manualset3
93137	4	399423	13	NULL	NULL	NULL	NULL	backscatter intravascular ultrasound study 	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Impact of omega-3 polyunsaturated fatty acids on coronary plaque instability : an integrated backscatter intravascular ultrasound study .
	manualset3
93138	1	399424	13	NULL	NULL	0	NULL	Impact	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of practice guidelines on support surface selection , incidence of pressure ulcers , and fiscal dollars .
	manualset3
93139	2	399424	13	NULL	NULL	0	NULL	practice guidelines	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of practice guidelines on support surface selection , incidence of pressure ulcers , and fiscal dollars .
	manualset3
93140	3	399424	13	NULL	NULL	0	NULL	support surface selection	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of practice guidelines on support surface selection , incidence of pressure ulcers , and fiscal dollars .
	manualset3
93141	4	399424	13	NULL	NULL	0	NULL	incidence of pressure ulcers	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of practice guidelines on support surface selection , incidence of pressure ulcers , and fiscal dollars .
	manualset3
93142	5	399424	13	NULL	NULL	0	NULL	fiscal dollars	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of practice guidelines on support surface selection , incidence of pressure ulcers , and fiscal dollars .
	manualset3
93143	1	399425	13	NULL	NULL	0	NULL	Thoracic pain	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Thoracic pain caused by coronary insufficiency ) .
	manualset3
93144	2	399425	13	NULL	NULL	0	NULL	coronary insufficiency	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Thoracic pain caused by coronary insufficiency ) .
	manualset3
93145	1	399426	13	NULL	NULL	0	NULL	Impact	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of practitioner 's training in the management of alcohol dependence : a quasi-experimental 18-month follow-up study .
	manualset3
93146	2	399426	13	NULL	NULL	0	NULL	 practitioner 's	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of practitioner 's training in the management of alcohol dependence : a quasi-experimental 18-month follow-up study .
	manualset3
93147	3	399426	13	NULL	NULL	0	NULL	training	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of practitioner 's training in the management of alcohol dependence : a quasi-experimental 18-month follow-up study .
	manualset3
93148	4	399426	13	NULL	NULL	0	NULL	 management of alcohol dependence	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Impact of practitioner 's training in the management of alcohol dependence : a quasi-experimental 18-month follow-up study .
	manualset3
93149	5	399426	13	NULL	NULL	NULL	NULL	a quasi-experimental 18-month follow-up study	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Impact of practitioner 's training in the management of alcohol dependence : a quasi-experimental 18-month follow-up study .
	manualset3
93150	1	399427	13	NULL	NULL	NULL	NULL	cardiovascular responsiveness	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Impaired cardiovascular responsiveness in liver disease .
	manualset3
93151	2	399427	13	NULL	NULL	0	NULL	liver disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Impaired cardiovascular responsiveness in liver disease .
	manualset3
93152	1	399428	13	NULL	NULL	NULL	NULL	 catecholaminergic signalling	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Impaired catecholaminergic signalling of B lymphocytes in patients with chronic rheumatic diseases .
	manualset3
93153	2	399428	13	NULL	NULL	0	NULL	B lymphocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Impaired catecholaminergic signalling of B lymphocytes in patients with chronic rheumatic diseases .
	manualset3
93154	3	399428	13	NULL	NULL	0	NULL	 patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Impaired catecholaminergic signalling of B lymphocytes in patients with chronic rheumatic diseases .
	manualset3
93155	4	399428	13	NULL	NULL	0	NULL	chronic rheumatic diseases	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Impaired catecholaminergic signalling of B lymphocytes in patients with chronic rheumatic diseases .
	manualset3
93156	1	399429	13	NULL	NULL	NULL	NULL	dentofacial development 	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Impaired dentofacial development after radiotherapy of a non-Hodgkin lymphoma : report of case .
	manualset3
93157	2	399429	13	NULL	NULL	0	NULL	 radiotherapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Impaired dentofacial development after radiotherapy of a non-Hodgkin lymphoma : report of case .
	manualset3
93158	3	399429	13	NULL	NULL	0	NULL	non-Hodgkin lymphoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Impaired dentofacial development after radiotherapy of a non-Hodgkin lymphoma : report of case .
	manualset3
93159	4	399429	13	NULL	NULL	0	NULL	report of case	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Impaired dentofacial development after radiotherapy of a non-Hodgkin lymphoma : report of case .
	manualset3
93160	1	399430	13	NULL	NULL	NULL	NULL	insulin binding	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Impaired insulin binding to isolated adipocytes in experimental diabetic ketoacidosis .
	manualset3
93161	2	399430	13	NULL	NULL	NULL	NULL	adipocytes	Cell												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Impaired insulin binding to isolated adipocytes in experimental diabetic ketoacidosis .
	manualset3
93162	3	399430	13	NULL	NULL	0	NULL	experimental diabetic ketoacidosis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impaired insulin binding to isolated adipocytes in experimental diabetic ketoacidosis .
	manualset3
93163	1	399431	13	NULL	NULL	0	NULL	Impairment determinations	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impairment determinations , return to work readiness , and wage replacement are unique components of medical services in the workers ' compensation system .
	manualset3
93164	2	399431	13	NULL	NULL	NULL	NULL	return to work readiness	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Impairment determinations , return to work readiness , and wage replacement are unique components of medical services in the workers ' compensation system .
	manualset3
93166	4	399431	13	NULL	NULL	0	NULL	wage replacement	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Impairment determinations , return to work readiness , and wage replacement are unique components of medical services in the workers ' compensation system .
	manualset3
93167	5	399431	13	NULL	NULL	0	NULL	unique components	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Impairment determinations , return to work readiness , and wage replacement are unique components of medical services in the workers ' compensation system .
	manualset3
93168	6	399431	13	NULL	NULL	NULL	NULL	medical services	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Impairment determinations , return to work readiness , and wage replacement are unique components of medical services in the workers ' compensation system .
	manualset3
93169	7	399431	13	NULL	NULL	0	NULL	workers	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Impairment determinations , return to work readiness , and wage replacement are unique components of medical services in the workers ' compensation system .
	manualset3
93170	8	399431	13	NULL	NULL	0	NULL	compensation system	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Impairment determinations , return to work readiness , and wage replacement are unique components of medical services in the workers ' compensation system .
	manualset3
93171	1	399432	13	NULL	NULL	0	NULL	Implementation of chemoprophylaxis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Implementation of chemoprophylaxis of leprosy in the Southern Marquesas with a single dose of 25 mg per kg rifampin .
	manualset3
93172	2	399432	13	NULL	NULL	0	NULL	 leprosy	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Implementation of chemoprophylaxis of leprosy in the Southern Marquesas with a single dose of 25 mg per kg rifampin .
	manualset3
93173	3	399432	13	NULL	NULL	0	NULL	Southern Marquesas 	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	Implementation of chemoprophylaxis of leprosy in the Southern Marquesas with a single dose of 25 mg per kg rifampin .
	manualset3
93174	4	399432	13	NULL	NULL	0	NULL	single dose	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	Implementation of chemoprophylaxis of leprosy in the Southern Marquesas with a single dose of 25 mg per kg rifampin .
	manualset3
93175	5	399432	13	NULL	NULL	0	NULL	25 mg per kg 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Implementation of chemoprophylaxis of leprosy in the Southern Marquesas with a single dose of 25 mg per kg rifampin .
	manualset3
93176	6	399432	13	NULL	NULL	0	NULL	rifampin	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Implementation of chemoprophylaxis of leprosy in the Southern Marquesas with a single dose of 25 mg per kg rifampin .
	manualset3
93177	1	399433	13	NULL	NULL	NULL	NULL	Implication	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Implication of the melanocortin-3 receptor in the regulation of food intake .
	manualset3
93178	2	399433	13	NULL	NULL	0	NULL	melanocortin-3 receptor	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Implication of the melanocortin-3 receptor in the regulation of food intake .
	manualset3
93179	3	399433	13	NULL	NULL	0	NULL	regulation of food intake	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Implication of the melanocortin-3 receptor in the regulation of food intake .
	manualset3
93180	1	399434	13	NULL	NULL	0	NULL	Implications 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Implications for IOR , object perception , and attentional capture are discussed .
	manualset3
93181	2	399434	13	NULL	NULL	0	NULL	IOR 	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	Implications for IOR , object perception , and attentional capture are discussed .
	manualset3
93182	3	399434	13	NULL	NULL	0	NULL	object perception	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Implications for IOR , object perception , and attentional capture are discussed .
	manualset3
93183	4	399434	13	NULL	NULL	0	NULL	attentional capture	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Implications for IOR , object perception , and attentional capture are discussed .
	manualset3
93184	1	399435	13	NULL	NULL	0	NULL	Implications	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Implications for an evaluation of student drinking behaviors are discussed .
	manualset3
93185	2	399435	13	NULL	NULL	0	NULL	evaluation 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Implications for an evaluation of student drinking behaviors are discussed .
	manualset3
93186	3	399435	13	NULL	NULL	0	NULL	student	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Implications for an evaluation of student drinking behaviors are discussed .
	manualset3
93187	4	399435	13	NULL	NULL	0	NULL	drinking behaviors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Implications for an evaluation of student drinking behaviors are discussed .
	manualset3
93188	1	399436	13	NULL	NULL	0	NULL	Implications	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Implications for diagnosis of human neoplasms .
	manualset3
93189	2	399436	13	NULL	NULL	0	NULL	diagnosis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Implications for diagnosis of human neoplasms .
	manualset3
93190	3	399436	13	NULL	NULL	0	NULL	human neoplasms	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Implications for diagnosis of human neoplasms .
	manualset3
93191	1	399437	13	NULL	NULL	0	NULL	Implications	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Implications for the design of integrated , multimedia , entertainment-education campaigns and integrated evaluation designs are discussed .
	manualset3
93192	2	399437	13	NULL	NULL	0	NULL	 design	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Implications for the design of integrated , multimedia , entertainment-education campaigns and integrated evaluation designs are discussed .
	manualset3
93193	3	399437	13	NULL	NULL	0	NULL	 multimedia	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Implications for the design of integrated , multimedia , entertainment-education campaigns and integrated evaluation designs are discussed .
	manualset3
93194	4	399437	13	NULL	NULL	0	NULL	entertainment-education campaigns 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Implications for the design of integrated , multimedia , entertainment-education campaigns and integrated evaluation designs are discussed .
	manualset3
93195	5	399437	13	NULL	NULL	0	NULL	evaluation designs	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Implications for the design of integrated , multimedia , entertainment-education campaigns and integrated evaluation designs are discussed .
	manualset3
93196	1	399438	13	NULL	NULL	0	NULL	Implicit overcompensation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Implicit overcompensation : the influence of negative self-instructions on performance of a self-paced motor task .
	manualset3
93197	2	399438	13	NULL	NULL	0	NULL	influence of negative self-instructions	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Implicit overcompensation : the influence of negative self-instructions on performance of a self-paced motor task .
	manualset3
93198	3	399438	13	NULL	NULL	0	NULL	performance	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Implicit overcompensation : the influence of negative self-instructions on performance of a self-paced motor task .
	manualset3
93199	4	399438	13	NULL	NULL	0	NULL	self-paced motor task 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Implicit overcompensation : the influence of negative self-instructions on performance of a self-paced motor task .
	manualset3
93200	1	399439	13	NULL	NULL	0	NULL	Importance	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Importance of sagittally reformatted images in CT evaluation of spondylolisthesis .
	manualset3
93201	2	399439	13	NULL	NULL	0	NULL	images	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Importance of sagittally reformatted images in CT evaluation of spondylolisthesis .
	manualset3
93202	3	399439	13	NULL	NULL	NULL	NULL	CT evaluation	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Importance of sagittally reformatted images in CT evaluation of spondylolisthesis .
	manualset3
93203	4	399439	13	NULL	NULL	0	NULL	spondylolisthesis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Importance of sagittally reformatted images in CT evaluation of spondylolisthesis .
	manualset3
93204	1	399440	13	NULL	NULL	0	NULL	Importance	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Importance of serum source for the in vitro replicative senescence of human bone marrow derived mesenchymal stem cells .
	manualset3
93205	2	399440	13	NULL	NULL	0	NULL	serum source	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Importance of serum source for the in vitro replicative senescence of human bone marrow derived mesenchymal stem cells .
	manualset3
93206	3	399440	13	NULL	NULL	0	NULL	replicative senescence 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Importance of serum source for the in vitro replicative senescence of human bone marrow derived mesenchymal stem cells .
	manualset3
93207	4	399440	13	NULL	NULL	0	NULL	human bone marrow derived mesenchymal stem cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Importance of serum source for the in vitro replicative senescence of human bone marrow derived mesenchymal stem cells .
	manualset3
93208	1	399441	13	NULL	NULL	0	NULL	Angiofibroma of nasal cavity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Angiofibroma of nasal cavity in a woman ) .
	manualset3
93209	2	399441	13	NULL	NULL	0	NULL	woman	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	( Angiofibroma of nasal cavity in a woman ) .
	manualset3
93210	1	399442	13	NULL	NULL	0	NULL	Thoughts	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Thoughts on hypoproteinemia in surgery ) .
	manualset3
93211	2	399442	13	NULL	NULL	0	NULL	hypoproteinemia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Thoughts on hypoproteinemia in surgery ) .
	manualset3
93212	3	399442	13	NULL	NULL	0	NULL	surgery	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Thoughts on hypoproteinemia in surgery ) .
	manualset3
93213	1	399443	13	NULL	NULL	0	NULL	Importance	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Importance of the carboxy-terminal 25 amino acid residues of lung collectins in interactions with lipids and alveolar type II cells .
	manualset3
93214	2	399443	13	NULL	NULL	0	NULL	carboxy-terminal 25 amino acid residues	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Importance of the carboxy-terminal 25 amino acid residues of lung collectins in interactions with lipids and alveolar type II cells .
	manualset3
93215	3	399443	13	NULL	NULL	0	NULL	lung collectins	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Importance of the carboxy-terminal 25 amino acid residues of lung collectins in interactions with lipids and alveolar type II cells .
	manualset3
93216	4	399443	13	NULL	NULL	0	NULL	interactions	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Importance of the carboxy-terminal 25 amino acid residues of lung collectins in interactions with lipids and alveolar type II cells .
	manualset3
93217	5	399443	13	NULL	NULL	0	NULL	lipids	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Importance of the carboxy-terminal 25 amino acid residues of lung collectins in interactions with lipids and alveolar type II cells .
	manualset3
93218	6	399443	13	NULL	NULL	0	NULL	 alveolar type II cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Importance of the carboxy-terminal 25 amino acid residues of lung collectins in interactions with lipids and alveolar type II cells .
	manualset3
93219	1	399444	13	NULL	NULL	0	NULL	Important aspects	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Important aspects of differential diagnosis are presented based on a study of the literature which should help the ENT specialist discriminate between hyperfunctional and hypofunctional dysphonia , which is very important for therapy .
	manualset3
93220	2	399444	13	NULL	NULL	0	NULL	 differential diagnosis 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Important aspects of differential diagnosis are presented based on a study of the literature which should help the ENT specialist discriminate between hyperfunctional and hypofunctional dysphonia , which is very important for therapy .
	manualset3
93221	3	399444	13	NULL	NULL	0	NULL	study	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Important aspects of differential diagnosis are presented based on a study of the literature which should help the ENT specialist discriminate between hyperfunctional and hypofunctional dysphonia , which is very important for therapy .
	manualset3
93222	4	399444	13	NULL	NULL	0	NULL	literature	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Important aspects of differential diagnosis are presented based on a study of the literature which should help the ENT specialist discriminate between hyperfunctional and hypofunctional dysphonia , which is very important for therapy .
	manualset3
93223	5	399444	13	NULL	NULL	0	NULL	ENT specialist 	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Important aspects of differential diagnosis are presented based on a study of the literature which should help the ENT specialist discriminate between hyperfunctional and hypofunctional dysphonia , which is very important for therapy .
	manualset3
93224	6	399444	13	NULL	NULL	0	NULL	hyperfunctional dysphonia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Important aspects of differential diagnosis are presented based on a study of the literature which should help the ENT specialist discriminate between hyperfunctional and hypofunctional dysphonia , which is very important for therapy .
	manualset3
93225	7	399444	13	NULL	NULL	0	NULL	hypofunctional dysphonia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Important aspects of differential diagnosis are presented based on a study of the literature which should help the ENT specialist discriminate between hyperfunctional and hypofunctional dysphonia , which is very important for therapy .
	manualset3
93226	8	399444	13	NULL	NULL	0	NULL	therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Important aspects of differential diagnosis are presented based on a study of the literature which should help the ENT specialist discriminate between hyperfunctional and hypofunctional dysphonia , which is very important for therapy .
	manualset3
93227	1	399445	13	NULL	NULL	0	NULL	Important aspects 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Important aspects of the dengue epidemics during the period 1995-2006 have been analyzed here , using epidemiological , clinical and laboratory data .
	manualset3
93228	2	399445	13	NULL	NULL	0	NULL	dengue epidemics	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Important aspects of the dengue epidemics during the period 1995-2006 have been analyzed here , using epidemiological , clinical and laboratory data .
	manualset3
93229	3	399445	13	NULL	NULL	0	NULL	period 1995-2006	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Important aspects of the dengue epidemics during the period 1995-2006 have been analyzed here , using epidemiological , clinical and laboratory data .
	manualset3
93230	4	399445	13	NULL	NULL	0	NULL	epidemiological data 	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Important aspects of the dengue epidemics during the period 1995-2006 have been analyzed here , using epidemiological , clinical and laboratory data .
	manualset3
93231	5	399445	13	NULL	NULL	0	NULL	clinical data 	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Important aspects of the dengue epidemics during the period 1995-2006 have been analyzed here , using epidemiological , clinical and laboratory data .
	manualset3
93232	6	399445	13	NULL	NULL	0	NULL	laboratory data	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Important aspects of the dengue epidemics during the period 1995-2006 have been analyzed here , using epidemiological , clinical and laboratory data .
	manualset3
93233	1	399446	13	NULL	NULL	0	NULL	Important implications 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Important implications can be derived for the design and interpretation of experiments to characterize weak interactions , which are potentially important for brain processing .
	manualset3
93234	2	399446	13	NULL	NULL	NULL	NULL	design of experiments	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Important implications can be derived for the design and interpretation of experiments to characterize weak interactions , which are potentially important for brain processing .
	manualset3
93235	3	399446	13	NULL	NULL	0	NULL	interpretation of experiments	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Important implications can be derived for the design and interpretation of experiments to characterize weak interactions , which are potentially important for brain processing .
	manualset3
93236	4	399446	13	NULL	NULL	NULL	NULL	 weak interactions	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Important implications can be derived for the design and interpretation of experiments to characterize weak interactions , which are potentially important for brain processing .
	manualset3
93237	5	399446	13	NULL	NULL	0	NULL	brain processing	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Important implications can be derived for the design and interpretation of experiments to characterize weak interactions , which are potentially important for brain processing .
	manualset3
93238	1	399447	13	NULL	NULL	0	NULL	Important limitations	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Important limitations of these vectors are that recombinant gene expression is transient and inflammation occurs at the site of gene transfer .
	manualset3
93239	2	399447	13	NULL	NULL	0	NULL	vectors	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Important limitations of these vectors are that recombinant gene expression is transient and inflammation occurs at the site of gene transfer .
	manualset3
93240	3	399447	13	NULL	NULL	0	NULL	recombinant gene expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Important limitations of these vectors are that recombinant gene expression is transient and inflammation occurs at the site of gene transfer .
	manualset3
93241	4	399447	13	NULL	NULL	0	NULL	inflammation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Important limitations of these vectors are that recombinant gene expression is transient and inflammation occurs at the site of gene transfer .
	manualset3
93242	5	399447	13	NULL	NULL	0	NULL	site of gene transfer 	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Important limitations of these vectors are that recombinant gene expression is transient and inflammation occurs at the site of gene transfer .
	manualset3
93243	1	399448	13	NULL	NULL	0	NULL	Important pretreatment characteristics	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Important pretreatment characteristics that favor response are ambulatory status , female , less than 50 years old , no prior chemotherapy and no liver or brain metastases .
	manualset3
93244	2	399448	13	NULL	NULL	NULL	NULL	favor response	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Important pretreatment characteristics that favor response are ambulatory status , female , less than 50 years old , no prior chemotherapy and no liver or brain metastases .
	manualset3
93245	3	399448	13	NULL	NULL	0	NULL	ambulatory status	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Important pretreatment characteristics that favor response are ambulatory status , female , less than 50 years old , no prior chemotherapy and no liver or brain metastases .
	manualset3
93246	4	399448	13	NULL	NULL	0	NULL	female	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	Important pretreatment characteristics that favor response are ambulatory status , female , less than 50 years old , no prior chemotherapy and no liver or brain metastases .
	manualset3
93247	5	399448	13	NULL	NULL	0	NULL	less than 50 years old	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Important pretreatment characteristics that favor response are ambulatory status , female , less than 50 years old , no prior chemotherapy and no liver or brain metastases .
	manualset3
93248	6	399448	13	NULL	NULL	0	NULL	chemotherapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Important pretreatment characteristics that favor response are ambulatory status , female , less than 50 years old , no prior chemotherapy and no liver or brain metastases .
	manualset3
93249	7	399448	13	NULL	NULL	0	NULL	liver  metastases	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Important pretreatment characteristics that favor response are ambulatory status , female , less than 50 years old , no prior chemotherapy and no liver or brain metastases .
	manualset3
93250	8	399448	13	NULL	NULL	0	NULL	brain metastases	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Important pretreatment characteristics that favor response are ambulatory status , female , less than 50 years old , no prior chemotherapy and no liver or brain metastases .
	manualset3
93251	1	399449	13	NULL	NULL	0	NULL	Important risk factors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Important risk factors for transmission of cholera were almost equally prevalent in the majority of both types of cholera cases .
	manualset3
93252	2	399449	13	NULL	NULL	0	NULL	transmission of cholera 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Important risk factors for transmission of cholera were almost equally prevalent in the majority of both types of cholera cases .
	manualset3
93253	3	399449	13	NULL	NULL	NULL	NULL	majority of both types of cholera cases	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Important risk factors for transmission of cholera were almost equally prevalent in the majority of both types of cholera cases .
	manualset3
93254	1	399450	13	NULL	NULL	0	NULL	HCV replicon replication	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , HCV replicon replication was efficiently inhibited by the allosteric ribozyme .
	manualset3
93255	2	399450	13	NULL	NULL	NULL	NULL	allosteric ribozyme	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Importantly , HCV replicon replication was efficiently inhibited by the allosteric ribozyme .
	manualset3
93256	1	399451	13	NULL	NULL	0	NULL	IC87114 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , IC87114 reduced cytokine production by memory T cells from healthy and allergic donors and from inflammatory arthritis patients .
	manualset3
93257	2	399451	13	NULL	NULL	0	NULL	cytokine production	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , IC87114 reduced cytokine production by memory T cells from healthy and allergic donors and from inflammatory arthritis patients .
	manualset3
93258	3	399451	13	NULL	NULL	0	NULL	memory T cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , IC87114 reduced cytokine production by memory T cells from healthy and allergic donors and from inflammatory arthritis patients .
	manualset3
93259	4	399451	13	NULL	NULL	0	NULL	healthy donors	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , IC87114 reduced cytokine production by memory T cells from healthy and allergic donors and from inflammatory arthritis patients .
	manualset3
93260	5	399451	13	NULL	NULL	0	NULL	allergic donors	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , IC87114 reduced cytokine production by memory T cells from healthy and allergic donors and from inflammatory arthritis patients .
	manualset3
93261	6	399451	13	NULL	NULL	0	NULL	 inflammatory arthritis patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , IC87114 reduced cytokine production by memory T cells from healthy and allergic donors and from inflammatory arthritis patients .
	manualset3
93262	1	399452	13	NULL	NULL	0	NULL	Three dimensional analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Three dimensional analysis of noninvasive ductal carcinoma of the breast using immunohistochemical staining technique of laminin ) .
	manualset3
93263	2	399452	13	NULL	NULL	0	NULL	noninvasive ductal carcinoma of the breast	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Three dimensional analysis of noninvasive ductal carcinoma of the breast using immunohistochemical staining technique of laminin ) .
	manualset3
93264	3	399452	13	NULL	NULL	0	NULL	immunohistochemical staining technique	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Three dimensional analysis of noninvasive ductal carcinoma of the breast using immunohistochemical staining technique of laminin ) .
	manualset3
93265	4	399452	13	NULL	NULL	0	NULL	 laminin 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	( Three dimensional analysis of noninvasive ductal carcinoma of the breast using immunohistochemical staining technique of laminin ) .
	manualset3
93266	1	399453	13	NULL	NULL	NULL	NULL	alternative pre-mRNA	NucleicAcid												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Importantly , alternative pre-mRNA splicing is kept under spatiotemporal control by circulating hormones and cellular activity , as well as being differentially modified during development and in different tissues .
	manualset3
93267	2	399453	13	NULL	NULL	0	NULL	spatiotemporal control 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , alternative pre-mRNA splicing is kept under spatiotemporal control by circulating hormones and cellular activity , as well as being differentially modified during development and in different tissues .
	manualset3
93268	3	399453	13	NULL	NULL	NULL	NULL	hormones	NonProteinOrNucleicAcidChemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Importantly , alternative pre-mRNA splicing is kept under spatiotemporal control by circulating hormones and cellular activity , as well as being differentially modified during development and in different tissues .
	manualset3
93269	4	399453	13	NULL	NULL	0	NULL	 cellular activity 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , alternative pre-mRNA splicing is kept under spatiotemporal control by circulating hormones and cellular activity , as well as being differentially modified during development and in different tissues .
	manualset3
93270	5	399453	13	NULL	NULL	0	NULL	development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , alternative pre-mRNA splicing is kept under spatiotemporal control by circulating hormones and cellular activity , as well as being differentially modified during development and in different tissues .
	manualset3
93271	6	399453	13	NULL	NULL	0	NULL	different tissues	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , alternative pre-mRNA splicing is kept under spatiotemporal control by circulating hormones and cellular activity , as well as being differentially modified during development and in different tissues .
	manualset3
93272	1	399454	13	NULL	NULL	0	NULL	steatotic livers	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , although steatotic livers were much more susceptible to IRI than lean livers , by most measures there was no statistical difference between the level of IRI to steatotic or lean livers when complement was inhibited .
	manualset3
93273	2	399454	13	NULL	NULL	0	NULL	IRI	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , although steatotic livers were much more susceptible to IRI than lean livers , by most measures there was no statistical difference between the level of IRI to steatotic or lean livers when complement was inhibited .
	manualset3
93274	3	399454	13	NULL	NULL	0	NULL	lean livers	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , although steatotic livers were much more susceptible to IRI than lean livers , by most measures there was no statistical difference between the level of IRI to steatotic or lean livers when complement was inhibited .
	manualset3
93275	4	399454	13	NULL	NULL	0	NULL	measures	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , although steatotic livers were much more susceptible to IRI than lean livers , by most measures there was no statistical difference between the level of IRI to steatotic or lean livers when complement was inhibited .
	manualset3
93276	5	399454	13	NULL	NULL	0	NULL	statistical difference	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , although steatotic livers were much more susceptible to IRI than lean livers , by most measures there was no statistical difference between the level of IRI to steatotic or lean livers when complement was inhibited .
	manualset3
93277	6	399454	13	NULL	NULL	0	NULL	level of IRI	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , although steatotic livers were much more susceptible to IRI than lean livers , by most measures there was no statistical difference between the level of IRI to steatotic or lean livers when complement was inhibited .
	manualset3
93278	7	399454	13	NULL	NULL	0	NULL	steatotic livers	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , although steatotic livers were much more susceptible to IRI than lean livers , by most measures there was no statistical difference between the level of IRI to steatotic or lean livers when complement was inhibited .
	manualset3
93279	8	399454	13	NULL	NULL	0	NULL	lean livers	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , although steatotic livers were much more susceptible to IRI than lean livers , by most measures there was no statistical difference between the level of IRI to steatotic or lean livers when complement was inhibited .
	manualset3
93280	9	399454	13	NULL	NULL	0	NULL	complement	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , although steatotic livers were much more susceptible to IRI than lean livers , by most measures there was no statistical difference between the level of IRI to steatotic or lean livers when complement was inhibited .
	manualset3
93281	1	399455	13	NULL	NULL	0	NULL	genetic studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , genetic studies , as well as molecular cloning strategies , recently identified epithelial ion channels as the gatekeepers of active Ca2 + and Mg2 + reabsorption .
	manualset3
93282	2	399455	13	NULL	NULL	0	NULL	molecular cloning strategies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , genetic studies , as well as molecular cloning strategies , recently identified epithelial ion channels as the gatekeepers of active Ca2 + and Mg2 + reabsorption .
	manualset3
93283	3	399455	13	NULL	NULL	NULL	NULL	epithelial ion channels	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Importantly , genetic studies , as well as molecular cloning strategies , recently identified epithelial ion channels as the gatekeepers of active Ca2 + and Mg2 + reabsorption .
	manualset3
93284	4	399455	13	NULL	NULL	0	NULL	gatekeepers	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , genetic studies , as well as molecular cloning strategies , recently identified epithelial ion channels as the gatekeepers of active Ca2 + and Mg2 + reabsorption .
	manualset3
93285	5	399455	13	NULL	NULL	0	NULL	active Ca2 + reabsorption	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , genetic studies , as well as molecular cloning strategies , recently identified epithelial ion channels as the gatekeepers of active Ca2 + and Mg2 + reabsorption .
	manualset3
93286	6	399455	13	NULL	NULL	0	NULL	active Mg2 + reabsorption	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , genetic studies , as well as molecular cloning strategies , recently identified epithelial ion channels as the gatekeepers of active Ca2 + and Mg2 + reabsorption .
	manualset3
93342	2	399456	13	NULL	NULL	NULL	NULL	 Golgi fragmentation	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Importantly , in addition to Golgi fragmentation , increased F-actin content in the absence of FMNL1 also led to cation-independent mannose 6-phosphate receptor dispersal , lysosomal enlargement and missorting of cathepsin D. Taken together , our data support a model in which FMNL1 regulates cellular F-actin levels required to maintain structural integrity of the Golgi complex and lysosomes .
	manualset3
93343	3	399456	13	NULL	NULL	NULL	NULL	F-actin content	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Importantly , in addition to Golgi fragmentation , increased F-actin content in the absence of FMNL1 also led to cation-independent mannose 6-phosphate receptor dispersal , lysosomal enlargement and missorting of cathepsin D. Taken together , our data support a model in which FMNL1 regulates cellular F-actin levels required to maintain structural integrity of the Golgi complex and lysosomes .
	manualset3
93344	5	399456	13	NULL	NULL	NULL	NULL	FMNL1 	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Importantly , in addition to Golgi fragmentation , increased F-actin content in the absence of FMNL1 also led to cation-independent mannose 6-phosphate receptor dispersal , lysosomal enlargement and missorting of cathepsin D. Taken together , our data support a model in which FMNL1 regulates cellular F-actin levels required to maintain structural integrity of the Golgi complex and lysosomes .
	manualset3
93345	6	399456	13	NULL	NULL	NULL	NULL	cation-independent mannose 6-phosphate receptor dispersal	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Importantly , in addition to Golgi fragmentation , increased F-actin content in the absence of FMNL1 also led to cation-independent mannose 6-phosphate receptor dispersal , lysosomal enlargement and missorting of cathepsin D. Taken together , our data support a model in which FMNL1 regulates cellular F-actin levels required to maintain structural integrity of the Golgi complex and lysosomes .
	manualset3
93346	7	399456	13	NULL	NULL	NULL	NULL	 lysosomal enlargement	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Importantly , in addition to Golgi fragmentation , increased F-actin content in the absence of FMNL1 also led to cation-independent mannose 6-phosphate receptor dispersal , lysosomal enlargement and missorting of cathepsin D. Taken together , our data support a model in which FMNL1 regulates cellular F-actin levels required to maintain structural integrity of the Golgi complex and lysosomes .
	manualset3
93347	8	399456	13	NULL	NULL	NULL	NULL	cathepsin D	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Importantly , in addition to Golgi fragmentation , increased F-actin content in the absence of FMNL1 also led to cation-independent mannose 6-phosphate receptor dispersal , lysosomal enlargement and missorting of cathepsin D. Taken together , our data support a model in which FMNL1 regulates cellular F-actin levels required to maintain structural integrity of the Golgi complex and lysosomes .
	manualset3
93348	9	399456	13	NULL	NULL	NULL	NULL	data 	PublishedSourceOfInformation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Importantly , in addition to Golgi fragmentation , increased F-actin content in the absence of FMNL1 also led to cation-independent mannose 6-phosphate receptor dispersal , lysosomal enlargement and missorting of cathepsin D. Taken together , our data support a model in which FMNL1 regulates cellular F-actin levels required to maintain structural integrity of the Golgi complex and lysosomes .
	manualset3
93349	10	399456	13	NULL	NULL	NULL	NULL	 model	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Importantly , in addition to Golgi fragmentation , increased F-actin content in the absence of FMNL1 also led to cation-independent mannose 6-phosphate receptor dispersal , lysosomal enlargement and missorting of cathepsin D. Taken together , our data support a model in which FMNL1 regulates cellular F-actin levels required to maintain structural integrity of the Golgi complex and lysosomes .
	manualset3
93350	11	399456	13	NULL	NULL	NULL	NULL	FMNL1 	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Importantly , in addition to Golgi fragmentation , increased F-actin content in the absence of FMNL1 also led to cation-independent mannose 6-phosphate receptor dispersal , lysosomal enlargement and missorting of cathepsin D. Taken together , our data support a model in which FMNL1 regulates cellular F-actin levels required to maintain structural integrity of the Golgi complex and lysosomes .
	manualset3
93352	12	399456	13	NULL	NULL	NULL	NULL	cellular F-actin levels	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Importantly , in addition to Golgi fragmentation , increased F-actin content in the absence of FMNL1 also led to cation-independent mannose 6-phosphate receptor dispersal , lysosomal enlargement and missorting of cathepsin D. Taken together , our data support a model in which FMNL1 regulates cellular F-actin levels required to maintain structural integrity of the Golgi complex and lysosomes .
	manualset3
93353	13	399456	13	NULL	NULL	NULL	NULL	structural integrity	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Importantly , in addition to Golgi fragmentation , increased F-actin content in the absence of FMNL1 also led to cation-independent mannose 6-phosphate receptor dispersal , lysosomal enlargement and missorting of cathepsin D. Taken together , our data support a model in which FMNL1 regulates cellular F-actin levels required to maintain structural integrity of the Golgi complex and lysosomes .
	manualset3
93354	13	399456	13	NULL	NULL	0	NULL	Golgi complex	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , in addition to Golgi fragmentation , increased F-actin content in the absence of FMNL1 also led to cation-independent mannose 6-phosphate receptor dispersal , lysosomal enlargement and missorting of cathepsin D. Taken together , our data support a model in which FMNL1 regulates cellular F-actin levels required to maintain structural integrity of the Golgi complex and lysosomes .
	manualset3
93355	14	399456	13	NULL	NULL	0	NULL	lysosomes	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , in addition to Golgi fragmentation , increased F-actin content in the absence of FMNL1 also led to cation-independent mannose 6-phosphate receptor dispersal , lysosomal enlargement and missorting of cathepsin D. Taken together , our data support a model in which FMNL1 regulates cellular F-actin levels required to maintain structural integrity of the Golgi complex and lysosomes .
	manualset3
93356	1	399456	13	NULL	NULL	0	NULL	addition 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , in addition to Golgi fragmentation , increased F-actin content in the absence of FMNL1 also led to cation-independent mannose 6-phosphate receptor dispersal , lysosomal enlargement and missorting of cathepsin D. Taken together , our data support a model in which FMNL1 regulates cellular F-actin levels required to maintain structural integrity of the Golgi complex and lysosomes .
	manualset3
93357	4	399456	13	NULL	NULL	0	NULL	 absence	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , in addition to Golgi fragmentation , increased F-actin content in the absence of FMNL1 also led to cation-independent mannose 6-phosphate receptor dispersal , lysosomal enlargement and missorting of cathepsin D. Taken together , our data support a model in which FMNL1 regulates cellular F-actin levels required to maintain structural integrity of the Golgi complex and lysosomes .
	manualset3
93358	1	399457	13	NULL	NULL	0	NULL	 results	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , our results establish the enhanced antitumor activity in vivo of the i-leader C-terminal truncated mutants , especially in a desmotic fibroblast-embedded lung carcinoma model in mice .
	manualset3
93359	2	399457	13	NULL	NULL	0	NULL	antitumor activity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , our results establish the enhanced antitumor activity in vivo of the i-leader C-terminal truncated mutants , especially in a desmotic fibroblast-embedded lung carcinoma model in mice .
	manualset3
93360	3	399457	13	NULL	NULL	0	NULL	i-leader C-terminal truncated mutants	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , our results establish the enhanced antitumor activity in vivo of the i-leader C-terminal truncated mutants , especially in a desmotic fibroblast-embedded lung carcinoma model in mice .
	manualset3
93361	4	399457	13	NULL	NULL	0	NULL	desmotic fibroblast-embedded lung carcinoma model	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , our results establish the enhanced antitumor activity in vivo of the i-leader C-terminal truncated mutants , especially in a desmotic fibroblast-embedded lung carcinoma model in mice .
	manualset3
93362	5	399457	13	NULL	NULL	0	NULL	mice 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , our results establish the enhanced antitumor activity in vivo of the i-leader C-terminal truncated mutants , especially in a desmotic fibroblast-embedded lung carcinoma model in mice .
	manualset3
93363	1	399458	13	NULL	NULL	0	NULL	platelet adhesiveness	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , platelet adhesiveness , abnormal before treatment 77.2 + / - 1.3 % ( normal less than 70 % ) , improved throughout the study to 57.8 + / - 1.3 % after 36 months of gliclazide .
	manualset3
93364	2	399458	13	NULL	NULL	0	NULL	treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , platelet adhesiveness , abnormal before treatment 77.2 + / - 1.3 % ( normal less than 70 % ) , improved throughout the study to 57.8 + / - 1.3 % after 36 months of gliclazide .
	manualset3
93365	3	399458	13	NULL	NULL	0	NULL	77.2 + / - 1.3 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , platelet adhesiveness , abnormal before treatment 77.2 + / - 1.3 % ( normal less than 70 % ) , improved throughout the study to 57.8 + / - 1.3 % after 36 months of gliclazide .
	manualset3
93366	4	399458	13	NULL	NULL	0	NULL	normal less than 70 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , platelet adhesiveness , abnormal before treatment 77.2 + / - 1.3 % ( normal less than 70 % ) , improved throughout the study to 57.8 + / - 1.3 % after 36 months of gliclazide .
	manualset3
93367	5	399458	13	NULL	NULL	0	NULL	study	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , platelet adhesiveness , abnormal before treatment 77.2 + / - 1.3 % ( normal less than 70 % ) , improved throughout the study to 57.8 + / - 1.3 % after 36 months of gliclazide .
	manualset3
93368	6	399458	13	NULL	NULL	0	NULL	57.8 + / - 1.3 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , platelet adhesiveness , abnormal before treatment 77.2 + / - 1.3 % ( normal less than 70 % ) , improved throughout the study to 57.8 + / - 1.3 % after 36 months of gliclazide .
	manualset3
93369	7	399458	13	NULL	NULL	0	NULL	 36 months	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , platelet adhesiveness , abnormal before treatment 77.2 + / - 1.3 % ( normal less than 70 % ) , improved throughout the study to 57.8 + / - 1.3 % after 36 months of gliclazide .
	manualset3
93370	8	399458	13	NULL	NULL	0	NULL	gliclazide	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , platelet adhesiveness , abnormal before treatment 77.2 + / - 1.3 % ( normal less than 70 % ) , improved throughout the study to 57.8 + / - 1.3 % after 36 months of gliclazide .
	manualset3
93371	1	399459	13	NULL	NULL	0	NULL	 quinupristin	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , quinupristin/dalfopristin shows similar activity against methicillin-susceptible and - resistant strains of S. aureus , and streptococci with benzylpenicillin ( penicillin G ) - or erythromycin-acquired resistance .
	manualset3
93372	2	399459	13	NULL	NULL	0	NULL	dalfopristin	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , quinupristin/dalfopristin shows similar activity against methicillin-susceptible and - resistant strains of S. aureus , and streptococci with benzylpenicillin ( penicillin G ) - or erythromycin-acquired resistance .
	manualset3
93373	3	399459	13	NULL	NULL	0	NULL	 activity	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , quinupristin/dalfopristin shows similar activity against methicillin-susceptible and - resistant strains of S. aureus , and streptococci with benzylpenicillin ( penicillin G ) - or erythromycin-acquired resistance .
	manualset3
93374	4	399459	13	NULL	NULL	0	NULL	methicillin-susceptible strains of S. aureus 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , quinupristin/dalfopristin shows similar activity against methicillin-susceptible and - resistant strains of S. aureus , and streptococci with benzylpenicillin ( penicillin G ) - or erythromycin-acquired resistance .
	manualset3
93375	5	399459	13	NULL	NULL	0	NULL	 methicillin- resistant strains of S. aureus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , quinupristin/dalfopristin shows similar activity against methicillin-susceptible and - resistant strains of S. aureus , and streptococci with benzylpenicillin ( penicillin G ) - or erythromycin-acquired resistance .
	manualset3
93376	6	399459	13	NULL	NULL	0	NULL	streptococci	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , quinupristin/dalfopristin shows similar activity against methicillin-susceptible and - resistant strains of S. aureus , and streptococci with benzylpenicillin ( penicillin G ) - or erythromycin-acquired resistance .
	manualset3
93377	7	399459	13	NULL	NULL	0	NULL	benzylpenicillin ( penicillin G )-acquired resistance	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , quinupristin/dalfopristin shows similar activity against methicillin-susceptible and - resistant strains of S. aureus , and streptococci with benzylpenicillin ( penicillin G ) - or erythromycin-acquired resistance .
	manualset3
93378	8	399459	13	NULL	NULL	0	NULL	erythromycin-acquired resistance	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , quinupristin/dalfopristin shows similar activity against methicillin-susceptible and - resistant strains of S. aureus , and streptococci with benzylpenicillin ( penicillin G ) - or erythromycin-acquired resistance .
	manualset3
93379	1	399460	13	NULL	NULL	0	NULL	Ets2 ( A72/A72 ) allele 	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the Ets2 ( A72/A72 ) allele resulted in decreased expression of inflammatory response genes , including TNF-alpha , CCL3 , matrix metalloprotease 9 , integrin alpha ( M ) , and Bcl-X in alveolar macrophage .
	manualset3
93380	2	399460	13	NULL	NULL	0	NULL	 expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the Ets2 ( A72/A72 ) allele resulted in decreased expression of inflammatory response genes , including TNF-alpha , CCL3 , matrix metalloprotease 9 , integrin alpha ( M ) , and Bcl-X in alveolar macrophage .
	manualset3
93381	3	399460	13	NULL	NULL	0	NULL	 inflammatory response genes	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the Ets2 ( A72/A72 ) allele resulted in decreased expression of inflammatory response genes , including TNF-alpha , CCL3 , matrix metalloprotease 9 , integrin alpha ( M ) , and Bcl-X in alveolar macrophage .
	manualset3
93382	4	399460	13	NULL	NULL	0	NULL	TNF-alpha	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the Ets2 ( A72/A72 ) allele resulted in decreased expression of inflammatory response genes , including TNF-alpha , CCL3 , matrix metalloprotease 9 , integrin alpha ( M ) , and Bcl-X in alveolar macrophage .
	manualset3
93383	5	399460	13	NULL	NULL	0	NULL	CCL3	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the Ets2 ( A72/A72 ) allele resulted in decreased expression of inflammatory response genes , including TNF-alpha , CCL3 , matrix metalloprotease 9 , integrin alpha ( M ) , and Bcl-X in alveolar macrophage .
	manualset3
93384	6	399460	13	NULL	NULL	0	NULL	 matrix metalloprotease 9	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the Ets2 ( A72/A72 ) allele resulted in decreased expression of inflammatory response genes , including TNF-alpha , CCL3 , matrix metalloprotease 9 , integrin alpha ( M ) , and Bcl-X in alveolar macrophage .
	manualset3
93385	7	399460	13	NULL	NULL	0	NULL	integrin alpha ( M )	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the Ets2 ( A72/A72 ) allele resulted in decreased expression of inflammatory response genes , including TNF-alpha , CCL3 , matrix metalloprotease 9 , integrin alpha ( M ) , and Bcl-X in alveolar macrophage .
	manualset3
93386	8	399460	13	NULL	NULL	0	NULL	Bcl-X	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the Ets2 ( A72/A72 ) allele resulted in decreased expression of inflammatory response genes , including TNF-alpha , CCL3 , matrix metalloprotease 9 , integrin alpha ( M ) , and Bcl-X in alveolar macrophage .
	manualset3
93387	9	399460	13	NULL	NULL	0	NULL	alveolar macrophage	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the Ets2 ( A72/A72 ) allele resulted in decreased expression of inflammatory response genes , including TNF-alpha , CCL3 , matrix metalloprotease 9 , integrin alpha ( M ) , and Bcl-X in alveolar macrophage .
	manualset3
93388	1	399461	13	NULL	NULL	0	NULL	XOR inhibitors	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the XOR inhibitors allopurinol and oxypurinol attenuate dysfunction caused by XOR in these disease states .
	manualset3
93389	2	399461	13	NULL	NULL	0	NULL	allopurinol	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the XOR inhibitors allopurinol and oxypurinol attenuate dysfunction caused by XOR in these disease states .
	manualset3
93390	3	399461	13	NULL	NULL	0	NULL	oxypurinol	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the XOR inhibitors allopurinol and oxypurinol attenuate dysfunction caused by XOR in these disease states .
	manualset3
93391	4	399461	13	NULL	NULL	0	NULL	dysfunction	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the XOR inhibitors allopurinol and oxypurinol attenuate dysfunction caused by XOR in these disease states .
	manualset3
93392	5	399461	13	NULL	NULL	0	NULL	XOR	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the XOR inhibitors allopurinol and oxypurinol attenuate dysfunction caused by XOR in these disease states .
	manualset3
93393	6	399461	13	NULL	NULL	0	NULL	disease states	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the XOR inhibitors allopurinol and oxypurinol attenuate dysfunction caused by XOR in these disease states .
	manualset3
93394	1	399462	13	NULL	NULL	0	NULL	siRNA-mediated reduction 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the siRNA-mediated reduction in cyclins resulted in decreased IC ( 50 ) ( 50 % inhibitory concentration ) values for both doxorubicin and etoposide .
	manualset3
93395	2	399462	13	NULL	NULL	0	NULL	cyclins	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the siRNA-mediated reduction in cyclins resulted in decreased IC ( 50 ) ( 50 % inhibitory concentration ) values for both doxorubicin and etoposide .
	manualset3
93396	3	399462	13	NULL	NULL	NULL	NULL	IC ( 50 ) values	QuantityOrMeasurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Importantly , the siRNA-mediated reduction in cyclins resulted in decreased IC ( 50 ) ( 50 % inhibitory concentration ) values for both doxorubicin and etoposide .
	manualset3
93397	4	399462	13	NULL	NULL	0	NULL	50 % inhibitory concentration	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the siRNA-mediated reduction in cyclins resulted in decreased IC ( 50 ) ( 50 % inhibitory concentration ) values for both doxorubicin and etoposide .
	manualset3
93398	5	399462	13	NULL	NULL	0	NULL	doxorubicin 	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the siRNA-mediated reduction in cyclins resulted in decreased IC ( 50 ) ( 50 % inhibitory concentration ) values for both doxorubicin and etoposide .
	manualset3
93399	6	399462	13	NULL	NULL	0	NULL	etoposide	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , the siRNA-mediated reduction in cyclins resulted in decreased IC ( 50 ) ( 50 % inhibitory concentration ) values for both doxorubicin and etoposide .
	manualset3
93400	1	399463	13	NULL	NULL	0	NULL	undifferentiated ASCs 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , we also show that undifferentiated ASCs and ASC-derived hepatic cells engraft robustly into the liver in a mouse model of toxic injury .
	manualset3
93401	2	399463	13	NULL	NULL	0	NULL	ASC-derived hepatic cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , we also show that undifferentiated ASCs and ASC-derived hepatic cells engraft robustly into the liver in a mouse model of toxic injury .
	manualset3
93402	3	399463	13	NULL	NULL	0	NULL	 liver	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , we also show that undifferentiated ASCs and ASC-derived hepatic cells engraft robustly into the liver in a mouse model of toxic injury .
	manualset3
93403	4	399463	13	NULL	NULL	0	NULL	mouse model 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , we also show that undifferentiated ASCs and ASC-derived hepatic cells engraft robustly into the liver in a mouse model of toxic injury .
	manualset3
93404	5	399463	13	NULL	NULL	0	NULL	 toxic injury	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , we also show that undifferentiated ASCs and ASC-derived hepatic cells engraft robustly into the liver in a mouse model of toxic injury .
	manualset3
93405	1	399464	13	NULL	NULL	0	NULL	role	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , we identify a role for endogenous Smac in overcoming XIAP to allow myotube death .
	manualset3
93406	2	399464	13	NULL	NULL	0	NULL	endogenous Smac	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , we identify a role for endogenous Smac in overcoming XIAP to allow myotube death .
	manualset3
93407	3	399464	13	NULL	NULL	0	NULL	XIAP	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , we identify a role for endogenous Smac in overcoming XIAP to allow myotube death .
	manualset3
93408	4	399464	13	NULL	NULL	0	NULL	myotube death	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Importantly , we identify a role for endogenous Smac in overcoming XIAP to allow myotube death .
	manualset3
93409	1	399465	13	NULL	NULL	0	NULL	prior studies	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Importing prior studies is best performed by creating a new order on the institution 's imaging system and then associating the DICOM objects from the prior study with it .
	manualset3
93410	2	399465	13	NULL	NULL	0	NULL	new order	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Importing prior studies is best performed by creating a new order on the institution 's imaging system and then associating the DICOM objects from the prior study with it .
	manualset3
93411	3	399465	13	NULL	NULL	0	NULL	 institution 's imaging system	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Importing prior studies is best performed by creating a new order on the institution 's imaging system and then associating the DICOM objects from the prior study with it .
	manualset3
93412	4	399465	13	NULL	NULL	0	NULL	DICOM objects	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Importing prior studies is best performed by creating a new order on the institution 's imaging system and then associating the DICOM objects from the prior study with it .
	manualset3
93413	5	399465	13	NULL	NULL	0	NULL	 prior study 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Importing prior studies is best performed by creating a new order on the institution 's imaging system and then associating the DICOM objects from the prior study with it .
	manualset3
93414	1	399466	13	NULL	NULL	0	NULL	Impressions	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impressions of plastic and maxillo-facial surgery in the Palestine war .
	manualset3
93415	2	399466	13	NULL	NULL	0	NULL	plastic surgery	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Impressions of plastic and maxillo-facial surgery in the Palestine war .
	manualset3
93416	3	399466	13	NULL	NULL	0	NULL	maxillo-facial surgery	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Impressions of plastic and maxillo-facial surgery in the Palestine war .
	manualset3
93417	4	399466	13	NULL	NULL	0	NULL	Palestine war 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Impressions of plastic and maxillo-facial surgery in the Palestine war .
	manualset3
93418	1	399467	13	NULL	NULL	0	NULL	Impressions	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Impressions were obtained with polyvinyl siloxane , and replicas were fabricated with the use of polyether impression material .
	manualset3
93419	2	399467	13	NULL	NULL	0	NULL	polyvinyl siloxane	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Impressions were obtained with polyvinyl siloxane , and replicas were fabricated with the use of polyether impression material .
	manualset3
93420	3	399467	13	NULL	NULL	0	NULL	replicas 	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	Impressions were obtained with polyvinyl siloxane , and replicas were fabricated with the use of polyether impression material .
	manualset3
93421	4	399467	13	NULL	NULL	0	NULL	polyether impression material	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	Impressions were obtained with polyvinyl siloxane , and replicas were fabricated with the use of polyether impression material .
	manualset3
93422	5	399467	13	NULL	NULL	0	NULL	 use	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Impressions were obtained with polyvinyl siloxane , and replicas were fabricated with the use of polyether impression material .
	manualset3
93423	1	399468	13	NULL	NULL	0	NULL	practice	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Improve your practice with effective telephone management .
	manualset3
93424	2	399468	13	NULL	NULL	0	NULL	telephone management 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Improve your practice with effective telephone management .
	manualset3
93425	1	399469	13	NULL	NULL	0	NULL	hearing	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Improved hearing was documented in 15 cases .
	manualset3
93426	2	399469	13	NULL	NULL	0	NULL	15 cases	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Improved hearing was documented in 15 cases .
	manualset3
93427	1	399470	13	NULL	NULL	0	NULL	Thrombendarterectomy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombendarterectomy of the carotid artery in the prevention of cerebrovascular insult ) .
	manualset3
93428	2	399470	13	NULL	NULL	0	NULL	 carotid artery	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombendarterectomy of the carotid artery in the prevention of cerebrovascular insult ) .
	manualset3
93429	3	399470	13	NULL	NULL	0	NULL	prevention	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombendarterectomy of the carotid artery in the prevention of cerebrovascular insult ) .
	manualset3
93430	4	399470	13	NULL	NULL	0	NULL	cerebrovascular insult 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombendarterectomy of the carotid artery in the prevention of cerebrovascular insult ) .
	manualset3
93431	1	399471	13	NULL	NULL	0	NULL	pectinase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Improved pectinase production in Penicillium griseoroseum recombinant strains .
	manualset3
93432	2	399471	13	NULL	NULL	0	NULL	production 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Improved pectinase production in Penicillium griseoroseum recombinant strains .
	manualset3
93433	3	399471	13	NULL	NULL	0	NULL	Penicillium griseoroseum recombinant strains	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Improved pectinase production in Penicillium griseoroseum recombinant strains .
	manualset3
93434	1	399472	13	NULL	NULL	0	NULL	 procedures	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Improved procedures for purification of the Bandeiraea simplicifolia I isolectins and Bandeiraea simplicifolia II lectin by affinity chromatography .
	manualset3
93435	2	399472	13	NULL	NULL	0	NULL	purification	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Improved procedures for purification of the Bandeiraea simplicifolia I isolectins and Bandeiraea simplicifolia II lectin by affinity chromatography .
	manualset3
93436	3	399472	13	NULL	NULL	0	NULL	Bandeiraea simplicifolia I isolectins	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Improved procedures for purification of the Bandeiraea simplicifolia I isolectins and Bandeiraea simplicifolia II lectin by affinity chromatography .
	manualset3
93437	4	399472	13	NULL	NULL	0	NULL	Bandeiraea simplicifolia II lectin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Improved procedures for purification of the Bandeiraea simplicifolia I isolectins and Bandeiraea simplicifolia II lectin by affinity chromatography .
	manualset3
93438	5	399472	13	NULL	NULL	0	NULL	affinity chromatography 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	Improved procedures for purification of the Bandeiraea simplicifolia I isolectins and Bandeiraea simplicifolia II lectin by affinity chromatography .
	manualset3
93439	1	399473	13	NULL	NULL	0	NULL	Improvement 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Improvement of malt modification by use of Rhizopus VII as starter culture .
	manualset3
93440	2	399473	13	NULL	NULL	0	NULL	malt modification 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Improvement of malt modification by use of Rhizopus VII as starter culture .
	manualset3
93441	3	399473	13	NULL	NULL	0	NULL	use	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Improvement of malt modification by use of Rhizopus VII as starter culture .
	manualset3
93442	4	399473	13	NULL	NULL	0	NULL	 Rhizopus VII	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Improvement of malt modification by use of Rhizopus VII as starter culture .
	manualset3
93443	5	399473	13	NULL	NULL	0	NULL	starter culture	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	Improvement of malt modification by use of Rhizopus VII as starter culture .
	manualset3
93444	1	399474	13	NULL	NULL	0	NULL	access	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Improving access to palliative care through an innovative quality improvement initiative : an opportunity for pay-for-performance .
	manualset3
93445	2	399474	13	NULL	NULL	NULL	NULL	palliative care	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Improving access to palliative care through an innovative quality improvement initiative : an opportunity for pay-for-performance .
	manualset3
93446	3	399474	13	NULL	NULL	0	NULL	 quality improvement initiative	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Improving access to palliative care through an innovative quality improvement initiative : an opportunity for pay-for-performance .
	manualset3
93447	4	399474	13	NULL	NULL	0	NULL	opportunity	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Improving access to palliative care through an innovative quality improvement initiative : an opportunity for pay-for-performance .
	manualset3
93448	5	399474	13	NULL	NULL	0	NULL	pay-for-performance	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Improving access to palliative care through an innovative quality improvement initiative : an opportunity for pay-for-performance .
	manualset3
93449	1	399475	13	NULL	NULL	0	NULL	clearance	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Improving clearance of the mutant protein is expected to prevent cellular dysfunction and neurodegeneration in HD .
	manualset3
93450	2	399475	13	NULL	NULL	0	NULL	mutant protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	Improving clearance of the mutant protein is expected to prevent cellular dysfunction and neurodegeneration in HD .
	manualset3
93451	3	399475	13	NULL	NULL	0	NULL	 cellular dysfunction	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	Improving clearance of the mutant protein is expected to prevent cellular dysfunction and neurodegeneration in HD .
	manualset3
93452	4	399475	13	NULL	NULL	0	NULL	neurodegeneration	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Improving clearance of the mutant protein is expected to prevent cellular dysfunction and neurodegeneration in HD .
	manualset3
93453	5	399475	13	NULL	NULL	0	NULL	HD	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	Improving clearance of the mutant protein is expected to prevent cellular dysfunction and neurodegeneration in HD .
	manualset3
93454	1	399476	13	NULL	NULL	0	NULL	Thrombocytosis 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombocytosis in ulcerative colitis and regional enteritis ) .
	manualset3
93455	2	399476	13	NULL	NULL	0	NULL	ulcerative colitis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombocytosis in ulcerative colitis and regional enteritis ) .
	manualset3
93456	3	399476	13	NULL	NULL	0	NULL	regional enteritis 	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombocytosis in ulcerative colitis and regional enteritis ) .
	manualset3
93457	1	399477	13	NULL	NULL	0	NULL	follow-up	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Improving the follow-up of positive hemoccult screening tests : an electronic intervention .
	manualset3
93458	2	399477	13	NULL	NULL	0	NULL	hemoccult screening tests	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Improving the follow-up of positive hemoccult screening tests : an electronic intervention .
	manualset3
93459	3	399477	13	NULL	NULL	0	NULL	electronic intervention	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	Improving the follow-up of positive hemoccult screening tests : an electronic intervention .
	manualset3
93460	1	399478	13	NULL	NULL	0	NULL	workforce	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Improving workforce is crucial to viability of Europe 's health services , commission says .
	manualset3
93461	2	399478	13	NULL	NULL	0	NULL	 viability	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	Improving workforce is crucial to viability of Europe 's health services , commission says .
	manualset3
93462	3	399478	13	NULL	NULL	0	NULL	Europe 's health services	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Improving workforce is crucial to viability of Europe 's health services , commission says .
	manualset3
93463	4	399478	13	NULL	NULL	0	NULL	 commission	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	Improving workforce is crucial to viability of Europe 's health services , commission says .
	manualset3
93464	1	399479	13	NULL	NULL	NULL	NULL	Impulsiveness	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	Impulsiveness and the prolactin response to d-fenfluramine .
	manualset3
93465	2	399479	13	NULL	NULL	0	NULL	 prolactin response	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	Impulsiveness and the prolactin response to d-fenfluramine .
	manualset3
93466	3	399479	13	NULL	NULL	0	NULL	d-fenfluramine	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	Impulsiveness and the prolactin response to d-fenfluramine .
	manualset3
93467	1	399480	13	NULL	NULL	0	NULL	ImuVert 	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	ImuVert , a biologic response modifier , is capable of activating mononuclear cells causing release of various cytokines .
	manualset3
93468	2	399480	13	NULL	NULL	0	NULL	biologic response modifier	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	ImuVert , a biologic response modifier , is capable of activating mononuclear cells causing release of various cytokines .
	manualset3
93469	3	399480	13	NULL	NULL	0	NULL	 mononuclear cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	ImuVert , a biologic response modifier , is capable of activating mononuclear cells causing release of various cytokines .
	manualset3
93470	4	399480	13	NULL	NULL	0	NULL	release of various cytokines 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	ImuVert , a biologic response modifier , is capable of activating mononuclear cells causing release of various cytokines .
	manualset3
93471	1	399481	13	NULL	NULL	0	NULL	In-stent restenosis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In-stent restenosis , thrombosis , and aneurysm formation are known complications .
	manualset3
93472	2	399481	13	NULL	NULL	0	NULL	 thrombosis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In-stent restenosis , thrombosis , and aneurysm formation are known complications .
	manualset3
93473	3	399481	13	NULL	NULL	0	NULL	aneurysm formation	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In-stent restenosis , thrombosis , and aneurysm formation are known complications .
	manualset3
93474	4	399481	13	NULL	NULL	0	NULL	complications	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In-stent restenosis , thrombosis , and aneurysm formation are known complications .
	manualset3
93475	1	399482	13	NULL	NULL	0	NULL	tiludronate	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro , tiludronate added to bone tissue culture inhibits calcium release , lysosomal enzyme secretion and collagen matrix degradation when induced by various stimulators of bone resorption .
	manualset3
93476	2	399482	13	NULL	NULL	0	NULL	bone tissue culture	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro , tiludronate added to bone tissue culture inhibits calcium release , lysosomal enzyme secretion and collagen matrix degradation when induced by various stimulators of bone resorption .
	manualset3
93477	3	399482	13	NULL	NULL	0	NULL	calcium release	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro , tiludronate added to bone tissue culture inhibits calcium release , lysosomal enzyme secretion and collagen matrix degradation when induced by various stimulators of bone resorption .
	manualset3
93478	4	399482	13	NULL	NULL	0	NULL	lysosomal enzyme secretion 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro , tiludronate added to bone tissue culture inhibits calcium release , lysosomal enzyme secretion and collagen matrix degradation when induced by various stimulators of bone resorption .
	manualset3
93479	5	399482	13	NULL	NULL	0	NULL	collagen matrix degradation 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro , tiludronate added to bone tissue culture inhibits calcium release , lysosomal enzyme secretion and collagen matrix degradation when induced by various stimulators of bone resorption .
	manualset3
93480	6	399482	13	NULL	NULL	0	NULL	various stimulators	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro , tiludronate added to bone tissue culture inhibits calcium release , lysosomal enzyme secretion and collagen matrix degradation when induced by various stimulators of bone resorption .
	manualset3
93481	7	399482	13	NULL	NULL	0	NULL	bone resorption	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro , tiludronate added to bone tissue culture inhibits calcium release , lysosomal enzyme secretion and collagen matrix degradation when induced by various stimulators of bone resorption .
	manualset3
93482	1	399483	13	NULL	NULL	0	NULL	effect 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro , we examined the effect of recombinant Ang-4 on endothelial cell migration in Boyden chambers .
	manualset3
93483	2	399483	13	NULL	NULL	0	NULL	recombinant Ang-4	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro , we examined the effect of recombinant Ang-4 on endothelial cell migration in Boyden chambers .
	manualset3
93484	3	399483	13	NULL	NULL	0	NULL	endothelial cell migration	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro , we examined the effect of recombinant Ang-4 on endothelial cell migration in Boyden chambers .
	manualset3
93485	4	399483	13	NULL	NULL	0	NULL	Boyden chambers	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro , we examined the effect of recombinant Ang-4 on endothelial cell migration in Boyden chambers .
	manualset3
93486	1	399484	13	NULL	NULL	0	NULL	activity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro activity of protegrin-1 and beta-defensin-1 , alone and in combination with isoniazid , against Mycobacterium tuberculosis .
	manualset3
93487	2	399484	13	NULL	NULL	0	NULL	protegrin-1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro activity of protegrin-1 and beta-defensin-1 , alone and in combination with isoniazid , against Mycobacterium tuberculosis .
	manualset3
93488	3	399484	13	NULL	NULL	0	NULL	beta-defensin-1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro activity of protegrin-1 and beta-defensin-1 , alone and in combination with isoniazid , against Mycobacterium tuberculosis .
	manualset3
93489	4	399484	13	NULL	NULL	0	NULL	combination	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro activity of protegrin-1 and beta-defensin-1 , alone and in combination with isoniazid , against Mycobacterium tuberculosis .
	manualset3
93490	5	399484	13	NULL	NULL	0	NULL	isoniazid	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro activity of protegrin-1 and beta-defensin-1 , alone and in combination with isoniazid , against Mycobacterium tuberculosis .
	manualset3
93491	6	399484	13	NULL	NULL	0	NULL	Mycobacterium tuberculosis	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro activity of protegrin-1 and beta-defensin-1 , alone and in combination with isoniazid , against Mycobacterium tuberculosis .
	manualset3
93492	1	399485	13	NULL	NULL	0	NULL	Thrombosis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombosis at the site of abdominal aortic aneurysm with repeated myocardial infarction ) .
	manualset3
93493	2	399485	13	NULL	NULL	0	NULL	site of abdominal aortic aneurysm	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombosis at the site of abdominal aortic aneurysm with repeated myocardial infarction ) .
	manualset3
93494	3	399485	13	NULL	NULL	0	NULL	myocardial infarction 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombosis at the site of abdominal aortic aneurysm with repeated myocardial infarction ) .
	manualset3
93495	1	399486	13	NULL	NULL	0	NULL	 complementation experiments	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo complementation experiments revealed that at least five cistrons were concerned with head formation and that at least six cistrons were concerned with tail formation in phi80 .
	manualset3
93496	2	399486	13	NULL	NULL	0	NULL	five	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo complementation experiments revealed that at least five cistrons were concerned with head formation and that at least six cistrons were concerned with tail formation in phi80 .
	manualset3
93497	3	399486	13	NULL	NULL	0	NULL	cistrons	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo complementation experiments revealed that at least five cistrons were concerned with head formation and that at least six cistrons were concerned with tail formation in phi80 .
	manualset3
93498	4	399486	13	NULL	NULL	0	NULL	head formation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo complementation experiments revealed that at least five cistrons were concerned with head formation and that at least six cistrons were concerned with tail formation in phi80 .
	manualset3
93499	5	399486	13	NULL	NULL	0	NULL	six	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo complementation experiments revealed that at least five cistrons were concerned with head formation and that at least six cistrons were concerned with tail formation in phi80 .
	manualset3
93500	6	399486	13	NULL	NULL	0	NULL	cistrons 	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo complementation experiments revealed that at least five cistrons were concerned with head formation and that at least six cistrons were concerned with tail formation in phi80 .
	manualset3
93501	7	399486	13	NULL	NULL	0	NULL	tail formation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo complementation experiments revealed that at least five cistrons were concerned with head formation and that at least six cistrons were concerned with tail formation in phi80 .
	manualset3
93502	8	399486	13	NULL	NULL	0	NULL	phi80 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo complementation experiments revealed that at least five cistrons were concerned with head formation and that at least six cistrons were concerned with tail formation in phi80 .
	manualset3
93503	1	399487	13	NULL	NULL	0	NULL	In vitro studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo studies of specific neuronal fast and slow transport components are presently reshaping our understanding of how the processes of vesicular and cytoskeletal transport are regulated in axons and dendrites .
	manualset3
93504	2	399487	13	NULL	NULL	0	NULL	in vivo studies 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo studies of specific neuronal fast and slow transport components are presently reshaping our understanding of how the processes of vesicular and cytoskeletal transport are regulated in axons and dendrites .
	manualset3
93505	3	399487	13	NULL	NULL	0	NULL	specific neuronal fast 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo studies of specific neuronal fast and slow transport components are presently reshaping our understanding of how the processes of vesicular and cytoskeletal transport are regulated in axons and dendrites .
	manualset3
93506	4	399487	13	NULL	NULL	0	NULL	transport components	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo studies of specific neuronal fast and slow transport components are presently reshaping our understanding of how the processes of vesicular and cytoskeletal transport are regulated in axons and dendrites .
	manualset3
93507	5	399487	13	NULL	NULL	0	NULL	understanding	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo studies of specific neuronal fast and slow transport components are presently reshaping our understanding of how the processes of vesicular and cytoskeletal transport are regulated in axons and dendrites .
	manualset3
93508	6	399487	13	NULL	NULL	0	NULL	processes	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo studies of specific neuronal fast and slow transport components are presently reshaping our understanding of how the processes of vesicular and cytoskeletal transport are regulated in axons and dendrites .
	manualset3
93509	7	399487	13	NULL	NULL	0	NULL	vesicular transport	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo studies of specific neuronal fast and slow transport components are presently reshaping our understanding of how the processes of vesicular and cytoskeletal transport are regulated in axons and dendrites .
	manualset3
93510	8	399487	13	NULL	NULL	0	NULL	cytoskeletal transport	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo studies of specific neuronal fast and slow transport components are presently reshaping our understanding of how the processes of vesicular and cytoskeletal transport are regulated in axons and dendrites .
	manualset3
93511	9	399487	13	NULL	NULL	0	NULL	axons	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo studies of specific neuronal fast and slow transport components are presently reshaping our understanding of how the processes of vesicular and cytoskeletal transport are regulated in axons and dendrites .
	manualset3
93512	10	399487	13	NULL	NULL	0	NULL	dendrites	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo studies of specific neuronal fast and slow transport components are presently reshaping our understanding of how the processes of vesicular and cytoskeletal transport are regulated in axons and dendrites .
	manualset3
93513	1	399488	13	NULL	NULL	0	NULL	In vitro suppression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo suppression of growth of rat liver epithelial tumor cells by antisense oligonucleotide against protein kinase C-alpha .
	manualset3
93514	2	399488	13	NULL	NULL	0	NULL	in vivo suppression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo suppression of growth of rat liver epithelial tumor cells by antisense oligonucleotide against protein kinase C-alpha .
	manualset3
93515	3	399488	13	NULL	NULL	0	NULL	growth	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo suppression of growth of rat liver epithelial tumor cells by antisense oligonucleotide against protein kinase C-alpha .
	manualset3
93516	4	399488	13	NULL	NULL	0	NULL	rat liver epithelial tumor cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo suppression of growth of rat liver epithelial tumor cells by antisense oligonucleotide against protein kinase C-alpha .
	manualset3
93517	5	399488	13	NULL	NULL	0	NULL	antisense oligonucleotide	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo suppression of growth of rat liver epithelial tumor cells by antisense oligonucleotide against protein kinase C-alpha .
	manualset3
93518	6	399488	13	NULL	NULL	0	NULL	protein kinase C-alpha	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro and in vivo suppression of growth of rat liver epithelial tumor cells by antisense oligonucleotide against protein kinase C-alpha .
	manualset3
93519	1	399489	13	NULL	NULL	0	NULL	In vitro antifungal activities	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro antifungal activities of bis ( alkylpyridinium ) alkane compounds against pathogenic yeasts and molds .
	manualset3
93520	2	399489	13	NULL	NULL	0	NULL	bis ( alkylpyridinium ) alkane compounds	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro antifungal activities of bis ( alkylpyridinium ) alkane compounds against pathogenic yeasts and molds .
	manualset3
93521	3	399489	13	NULL	NULL	0	NULL	pathogenic yeasts	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro antifungal activities of bis ( alkylpyridinium ) alkane compounds against pathogenic yeasts and molds .
	manualset3
93522	4	399489	13	NULL	NULL	0	NULL	pathogenic molds	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro antifungal activities of bis ( alkylpyridinium ) alkane compounds against pathogenic yeasts and molds .
	manualset3
93523	1	399490	13	NULL	NULL	0	NULL	In vitro antimicrobial activities	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro antimicrobial activities of the HPCS derivatives were evaluated by the Kirby-Bauer disc diffusion method and the macrotube dilution broth method .
	manualset3
93524	2	399490	13	NULL	NULL	0	NULL	HPCS derivatives 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro antimicrobial activities of the HPCS derivatives were evaluated by the Kirby-Bauer disc diffusion method and the macrotube dilution broth method .
	manualset3
93525	3	399490	13	NULL	NULL	0	NULL	Kirby-Bauer disc diffusion method	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro antimicrobial activities of the HPCS derivatives were evaluated by the Kirby-Bauer disc diffusion method and the macrotube dilution broth method .
	manualset3
93526	4	399490	13	NULL	NULL	0	NULL	macrotube dilution broth method	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro antimicrobial activities of the HPCS derivatives were evaluated by the Kirby-Bauer disc diffusion method and the macrotube dilution broth method .
	manualset3
93695	1	399491	13	NULL	NULL	0	NULL	In vitro antiviral activity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro antiviral activity of mycophenolic acid and its reversal by guanine-type compounds .
	manualset3
93696	2	399491	13	NULL	NULL	0	NULL	mycophenolic acid	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro antiviral activity of mycophenolic acid and its reversal by guanine-type compounds .
	manualset3
93697	3	399491	13	NULL	NULL	0	NULL	reversal	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro antiviral activity of mycophenolic acid and its reversal by guanine-type compounds .
	manualset3
93698	4	399491	13	NULL	NULL	0	NULL	 guanine-type compounds	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro antiviral activity of mycophenolic acid and its reversal by guanine-type compounds .
	manualset3
93699	1	399492	13	NULL	NULL	0	NULL	In vitro assays 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro assays were used to assess non-2OG TCAIs as inhibitors of purified PHD2 and FIH .
	manualset3
93700	2	399492	13	NULL	NULL	0	NULL	non-2OG TCAIs	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro assays were used to assess non-2OG TCAIs as inhibitors of purified PHD2 and FIH .
	manualset3
93701	3	399492	13	NULL	NULL	0	NULL	 inhibitors	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro assays were used to assess non-2OG TCAIs as inhibitors of purified PHD2 and FIH .
	manualset3
93702	4	399492	13	NULL	NULL	0	NULL	PHD2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro assays were used to assess non-2OG TCAIs as inhibitors of purified PHD2 and FIH .
	manualset3
93703	5	399492	13	NULL	NULL	0	NULL	FIH	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro assays were used to assess non-2OG TCAIs as inhibitors of purified PHD2 and FIH .
	manualset3
93704	1	399493	13	NULL	NULL	0	NULL	In vitro effect	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro effect of immune complex positive human sera on antibody dependent cellular cytotoxicity .
	manualset3
93705	2	399493	13	NULL	NULL	0	NULL	 immune complex	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro effect of immune complex positive human sera on antibody dependent cellular cytotoxicity .
	manualset3
93706	3	399493	13	NULL	NULL	0	NULL	human sera	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro effect of immune complex positive human sera on antibody dependent cellular cytotoxicity .
	manualset3
93707	4	399493	13	NULL	NULL	0	NULL	 antibody	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro effect of immune complex positive human sera on antibody dependent cellular cytotoxicity .
	manualset3
93708	5	399493	13	NULL	NULL	0	NULL	cellular cytotoxicity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro effect of immune complex positive human sera on antibody dependent cellular cytotoxicity .
	manualset3
93709	1	399494	13	NULL	NULL	0	NULL	Thrombotic changes	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombotic changes in hemostasis following streptokinase therapy in myocardial infarct ) .
	manualset3
93710	2	399494	13	NULL	NULL	0	NULL	hemostasis 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombotic changes in hemostasis following streptokinase therapy in myocardial infarct ) .
	manualset3
93711	3	399494	13	NULL	NULL	0	NULL	streptokinase therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombotic changes in hemostasis following streptokinase therapy in myocardial infarct ) .
	manualset3
93712	4	399494	13	NULL	NULL	0	NULL	myocardial infarct	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Thrombotic changes in hemostasis following streptokinase therapy in myocardial infarct ) .
	manualset3
93713	1	399495	13	NULL	NULL	NULL	NULL	In vitro effects	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In vitro effects of R-verapamil on the cytokine environment and T-lymphocyte proliferation when human T-lymphocyte activation takes place in the presence of acute myelogenous leukemia blasts .
	manualset3
93714	2	399495	13	NULL	NULL	0	NULL	 R-verapamil	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro effects of R-verapamil on the cytokine environment and T-lymphocyte proliferation when human T-lymphocyte activation takes place in the presence of acute myelogenous leukemia blasts .
	manualset3
93715	3	399495	13	NULL	NULL	0	NULL	cytokine environment	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro effects of R-verapamil on the cytokine environment and T-lymphocyte proliferation when human T-lymphocyte activation takes place in the presence of acute myelogenous leukemia blasts .
	manualset3
93716	4	399495	13	NULL	NULL	0	NULL	T-lymphocyte proliferation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro effects of R-verapamil on the cytokine environment and T-lymphocyte proliferation when human T-lymphocyte activation takes place in the presence of acute myelogenous leukemia blasts .
	manualset3
93717	5	399495	13	NULL	NULL	0	NULL	 human T-lymphocyte activation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro effects of R-verapamil on the cytokine environment and T-lymphocyte proliferation when human T-lymphocyte activation takes place in the presence of acute myelogenous leukemia blasts .
	manualset3
93718	6	399495	13	NULL	NULL	0	NULL	presence	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro effects of R-verapamil on the cytokine environment and T-lymphocyte proliferation when human T-lymphocyte activation takes place in the presence of acute myelogenous leukemia blasts .
	manualset3
93719	7	399495	13	NULL	NULL	0	NULL	acute myelogenous leukemia blasts	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro effects of R-verapamil on the cytokine environment and T-lymphocyte proliferation when human T-lymphocyte activation takes place in the presence of acute myelogenous leukemia blasts .
	manualset3
93720	1	399496	13	NULL	NULL	0	NULL	In vitro experiments	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro experiments using alkaline phosphatase and osteocalcin assays demonstrated the proliferation and differentiation of MSC into osteoblast-like cells , especially the direct contact between VEC and MSC .
	manualset3
93721	2	399496	13	NULL	NULL	0	NULL	alkaline phosphatase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro experiments using alkaline phosphatase and osteocalcin assays demonstrated the proliferation and differentiation of MSC into osteoblast-like cells , especially the direct contact between VEC and MSC .
	manualset3
93722	3	399496	13	NULL	NULL	0	NULL	osteocalcin assays	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro experiments using alkaline phosphatase and osteocalcin assays demonstrated the proliferation and differentiation of MSC into osteoblast-like cells , especially the direct contact between VEC and MSC .
	manualset3
93723	4	399496	13	NULL	NULL	0	NULL	proliferation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro experiments using alkaline phosphatase and osteocalcin assays demonstrated the proliferation and differentiation of MSC into osteoblast-like cells , especially the direct contact between VEC and MSC .
	manualset3
93724	5	399496	13	NULL	NULL	0	NULL	differentiation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro experiments using alkaline phosphatase and osteocalcin assays demonstrated the proliferation and differentiation of MSC into osteoblast-like cells , especially the direct contact between VEC and MSC .
	manualset3
93725	6	399496	13	NULL	NULL	0	NULL	MSC	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro experiments using alkaline phosphatase and osteocalcin assays demonstrated the proliferation and differentiation of MSC into osteoblast-like cells , especially the direct contact between VEC and MSC .
	manualset3
93726	7	399496	13	NULL	NULL	0	NULL	osteoblast-like cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro experiments using alkaline phosphatase and osteocalcin assays demonstrated the proliferation and differentiation of MSC into osteoblast-like cells , especially the direct contact between VEC and MSC .
	manualset3
93727	8	399496	13	NULL	NULL	0	NULL	contact	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro experiments using alkaline phosphatase and osteocalcin assays demonstrated the proliferation and differentiation of MSC into osteoblast-like cells , especially the direct contact between VEC and MSC .
	manualset3
93728	9	399496	13	NULL	NULL	0	NULL	VEC	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro experiments using alkaline phosphatase and osteocalcin assays demonstrated the proliferation and differentiation of MSC into osteoblast-like cells , especially the direct contact between VEC and MSC .
	manualset3
93729	10	399496	13	NULL	NULL	0	NULL	MSC	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro experiments using alkaline phosphatase and osteocalcin assays demonstrated the proliferation and differentiation of MSC into osteoblast-like cells , especially the direct contact between VEC and MSC .
	manualset3
93730	1	399497	13	NULL	NULL	0	NULL	In vitro growth of colonies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro growth of colonies of mitogen-stimulated mouse T lymphocytes : I. Conditions affecting colony formation ; II .
	manualset3
93731	2	399497	13	NULL	NULL	0	NULL	mitogen-stimulated mouse T lymphocytes 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro growth of colonies of mitogen-stimulated mouse T lymphocytes : I. Conditions affecting colony formation ; II .
	manualset3
93732	3	399497	13	NULL	NULL	0	NULL	Conditions 	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro growth of colonies of mitogen-stimulated mouse T lymphocytes : I. Conditions affecting colony formation ; II .
	manualset3
93733	4	399497	13	NULL	NULL	0	NULL	colony formation 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro growth of colonies of mitogen-stimulated mouse T lymphocytes : I. Conditions affecting colony formation ; II .
	manualset3
93734	1	399498	13	NULL	NULL	0	NULL	In vitro kinetic studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro kinetic studies revealed that these compounds are among the most effective APN/CD13 inhibitors found so far .
	manualset3
93735	2	399498	13	NULL	NULL	0	NULL	compounds	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro kinetic studies revealed that these compounds are among the most effective APN/CD13 inhibitors found so far .
	manualset3
93736	3	399498	13	NULL	NULL	0	NULL	effective APN/CD13 inhibitors	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro kinetic studies revealed that these compounds are among the most effective APN/CD13 inhibitors found so far .
	manualset3
93737	1	399499	13	NULL	NULL	0	NULL	In vitro lymphoma cell growth	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro lymphoma cell growth could be maintained in the presence of the growth factor for up to five weeks .
	manualset3
93738	2	399499	13	NULL	NULL	0	NULL	presence	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro lymphoma cell growth could be maintained in the presence of the growth factor for up to five weeks .
	manualset3
93739	3	399499	13	NULL	NULL	0	NULL	growth factor	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro lymphoma cell growth could be maintained in the presence of the growth factor for up to five weeks .
	manualset3
93740	4	399499	13	NULL	NULL	0	NULL	five weeks	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro lymphoma cell growth could be maintained in the presence of the growth factor for up to five weeks .
	manualset3
93741	1	399500	13	NULL	NULL	0	NULL	In vitro pharmacological purging	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro pharmacological purging of human bone marrow is enhanced by the use of lonidamine .
	manualset3
93742	2	399500	13	NULL	NULL	0	NULL	human bone marrow	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro pharmacological purging of human bone marrow is enhanced by the use of lonidamine .
	manualset3
93743	3	399500	13	NULL	NULL	NULL	NULL	use	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In vitro pharmacological purging of human bone marrow is enhanced by the use of lonidamine .
	manualset3
93744	4	399500	13	NULL	NULL	0	NULL	lonidamine	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro pharmacological purging of human bone marrow is enhanced by the use of lonidamine .
	manualset3
93745	1	399501	13	NULL	NULL	0	NULL	In vitro protein binding studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro protein binding studies suggest that AP-1 complexes are capable of binding to PE2A .
	manualset3
93746	2	399501	13	NULL	NULL	0	NULL	AP-1 complexes	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro protein binding studies suggest that AP-1 complexes are capable of binding to PE2A .
	manualset3
93747	4	399501	13	NULL	NULL	NULL	NULL	PE2A	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In vitro protein binding studies suggest that AP-1 complexes are capable of binding to PE2A .
	manualset3
93748	3	399501	13	NULL	NULL	0	NULL	binding	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro protein binding studies suggest that AP-1 complexes are capable of binding to PE2A .
	manualset3
93749	1	399502	13	NULL	NULL	0	NULL	In vitro selection	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro selection of NIH-3T3 cells for resistance to lymphotoxin induces resistance to activated macrophages and enhances tumorigenicity in vivo .
	manualset3
93750	2	399502	13	NULL	NULL	0	NULL	NIH-3T3 cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro selection of NIH-3T3 cells for resistance to lymphotoxin induces resistance to activated macrophages and enhances tumorigenicity in vivo .
	manualset3
93751	3	399502	13	NULL	NULL	0	NULL	resistance	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro selection of NIH-3T3 cells for resistance to lymphotoxin induces resistance to activated macrophages and enhances tumorigenicity in vivo .
	manualset3
93752	4	399502	13	NULL	NULL	0	NULL	lymphotoxin 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro selection of NIH-3T3 cells for resistance to lymphotoxin induces resistance to activated macrophages and enhances tumorigenicity in vivo .
	manualset3
93753	5	399502	13	NULL	NULL	0	NULL	resistance	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro selection of NIH-3T3 cells for resistance to lymphotoxin induces resistance to activated macrophages and enhances tumorigenicity in vivo .
	manualset3
93754	6	399502	13	NULL	NULL	0	NULL	macrophages	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro selection of NIH-3T3 cells for resistance to lymphotoxin induces resistance to activated macrophages and enhances tumorigenicity in vivo .
	manualset3
93755	7	399502	13	NULL	NULL	0	NULL	tumorigenicity in vivo 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro selection of NIH-3T3 cells for resistance to lymphotoxin induces resistance to activated macrophages and enhances tumorigenicity in vivo .
	manualset3
93756	1	399503	13	NULL	NULL	0	NULL	In vitro studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro studies of cell division have revealed similar mechanisms .
	manualset3
93757	2	399503	13	NULL	NULL	0	NULL	cell division	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro studies of cell division have revealed similar mechanisms .
	manualset3
93758	3	399503	13	NULL	NULL	0	NULL	similar mechanisms	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro studies of cell division have revealed similar mechanisms .
	manualset3
93759	1	399504	13	NULL	NULL	0	NULL	In vitro studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro studies of human breast carcinoma cells obtained by aspiration biopsy .
	manualset3
93760	2	399504	13	NULL	NULL	0	NULL	human breast carcinoma cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro studies of human breast carcinoma cells obtained by aspiration biopsy .
	manualset3
93761	3	399504	13	NULL	NULL	0	NULL	aspiration biopsy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro studies of human breast carcinoma cells obtained by aspiration biopsy .
	manualset3
93762	1	399505	13	NULL	NULL	0	NULL	In vitro studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro studies with crude membranes isolated from recombinant strains revealed that BRUCELLA : cyclic 1 , 2-beta-glucan synthetase was not inhibited by high concentrations of KCl or potassium glutamate even when expressed in AGROBACTERIUM : or RHIZOBIUM : backgrounds .
	manualset3
93763	2	399505	13	NULL	NULL	0	NULL	crude membranes	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro studies with crude membranes isolated from recombinant strains revealed that BRUCELLA : cyclic 1 , 2-beta-glucan synthetase was not inhibited by high concentrations of KCl or potassium glutamate even when expressed in AGROBACTERIUM : or RHIZOBIUM : backgrounds .
	manualset3
93764	3	399505	13	NULL	NULL	0	NULL	recombinant strains	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro studies with crude membranes isolated from recombinant strains revealed that BRUCELLA : cyclic 1 , 2-beta-glucan synthetase was not inhibited by high concentrations of KCl or potassium glutamate even when expressed in AGROBACTERIUM : or RHIZOBIUM : backgrounds .
	manualset3
93765	4	399505	13	NULL	NULL	0	NULL	 BRUCELLA	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro studies with crude membranes isolated from recombinant strains revealed that BRUCELLA : cyclic 1 , 2-beta-glucan synthetase was not inhibited by high concentrations of KCl or potassium glutamate even when expressed in AGROBACTERIUM : or RHIZOBIUM : backgrounds .
	manualset3
93766	5	399505	13	NULL	NULL	0	NULL	cyclic 1 , 2-beta-glucan synthetase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro studies with crude membranes isolated from recombinant strains revealed that BRUCELLA : cyclic 1 , 2-beta-glucan synthetase was not inhibited by high concentrations of KCl or potassium glutamate even when expressed in AGROBACTERIUM : or RHIZOBIUM : backgrounds .
	manualset3
93767	6	399505	13	NULL	NULL	0	NULL	high concentrations 	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro studies with crude membranes isolated from recombinant strains revealed that BRUCELLA : cyclic 1 , 2-beta-glucan synthetase was not inhibited by high concentrations of KCl or potassium glutamate even when expressed in AGROBACTERIUM : or RHIZOBIUM : backgrounds .
	manualset3
93768	7	399505	13	NULL	NULL	0	NULL	KCl	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro studies with crude membranes isolated from recombinant strains revealed that BRUCELLA : cyclic 1 , 2-beta-glucan synthetase was not inhibited by high concentrations of KCl or potassium glutamate even when expressed in AGROBACTERIUM : or RHIZOBIUM : backgrounds .
	manualset3
93769	8	399505	13	NULL	NULL	0	NULL	potassium glutamate	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro studies with crude membranes isolated from recombinant strains revealed that BRUCELLA : cyclic 1 , 2-beta-glucan synthetase was not inhibited by high concentrations of KCl or potassium glutamate even when expressed in AGROBACTERIUM : or RHIZOBIUM : backgrounds .
	manualset3
93770	9	399505	13	NULL	NULL	0	NULL	AGROBACTERIUM	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro studies with crude membranes isolated from recombinant strains revealed that BRUCELLA : cyclic 1 , 2-beta-glucan synthetase was not inhibited by high concentrations of KCl or potassium glutamate even when expressed in AGROBACTERIUM : or RHIZOBIUM : backgrounds .
	manualset3
93771	10	399505	13	NULL	NULL	0	NULL	RHIZOBIUM	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro studies with crude membranes isolated from recombinant strains revealed that BRUCELLA : cyclic 1 , 2-beta-glucan synthetase was not inhibited by high concentrations of KCl or potassium glutamate even when expressed in AGROBACTERIUM : or RHIZOBIUM : backgrounds .
	manualset3
93772	1	399506	13	NULL	NULL	0	NULL	In vitro tissue chambers	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro tissue chambers , like those used for electrophysiology , are usually continually perfused with the gassed buffer , but stopping the perfusion to add expensive chemicals or acquire imaging data is a common practice .
	manualset3
93773	2	399506	13	NULL	NULL	0	NULL	electrophysiology	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro tissue chambers , like those used for electrophysiology , are usually continually perfused with the gassed buffer , but stopping the perfusion to add expensive chemicals or acquire imaging data is a common practice .
	manualset3
93774	3	399506	13	NULL	NULL	0	NULL	gassed buffer	ExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro tissue chambers , like those used for electrophysiology , are usually continually perfused with the gassed buffer , but stopping the perfusion to add expensive chemicals or acquire imaging data is a common practice .
	manualset3
93775	4	399506	13	NULL	NULL	0	NULL	perfusion 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro tissue chambers , like those used for electrophysiology , are usually continually perfused with the gassed buffer , but stopping the perfusion to add expensive chemicals or acquire imaging data is a common practice .
	manualset3
93776	5	399506	13	NULL	NULL	0	NULL	expensive chemicals 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro tissue chambers , like those used for electrophysiology , are usually continually perfused with the gassed buffer , but stopping the perfusion to add expensive chemicals or acquire imaging data is a common practice .
	manualset3
93777	6	399506	13	NULL	NULL	0	NULL	imaging data 	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro tissue chambers , like those used for electrophysiology , are usually continually perfused with the gassed buffer , but stopping the perfusion to add expensive chemicals or acquire imaging data is a common practice .
	manualset3
93778	7	399506	13	NULL	NULL	0	NULL	common practice	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro tissue chambers , like those used for electrophysiology , are usually continually perfused with the gassed buffer , but stopping the perfusion to add expensive chemicals or acquire imaging data is a common practice .
	manualset3
93779	1	399507	13	NULL	NULL	0	NULL	In vitro translation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro translation directed by mRNA isolated from these cells has shown that the primary translation products are preprobactenecins of 23.5 and 21 kD , and are processed to polypeptides of 20 and 15.8 kD , respectively .
	manualset3
93780	2	399507	13	NULL	NULL	0	NULL	mRNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro translation directed by mRNA isolated from these cells has shown that the primary translation products are preprobactenecins of 23.5 and 21 kD , and are processed to polypeptides of 20 and 15.8 kD , respectively .
	manualset3
93781	3	399507	13	NULL	NULL	0	NULL	cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro translation directed by mRNA isolated from these cells has shown that the primary translation products are preprobactenecins of 23.5 and 21 kD , and are processed to polypeptides of 20 and 15.8 kD , respectively .
	manualset3
93782	4	399507	13	NULL	NULL	0	NULL	primary translation products	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro translation directed by mRNA isolated from these cells has shown that the primary translation products are preprobactenecins of 23.5 and 21 kD , and are processed to polypeptides of 20 and 15.8 kD , respectively .
	manualset3
93783	5	399507	13	NULL	NULL	0	NULL	 preprobactenecins 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro translation directed by mRNA isolated from these cells has shown that the primary translation products are preprobactenecins of 23.5 and 21 kD , and are processed to polypeptides of 20 and 15.8 kD , respectively .
	manualset3
93784	6	399507	13	NULL	NULL	0	NULL	23.5 kD	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro translation directed by mRNA isolated from these cells has shown that the primary translation products are preprobactenecins of 23.5 and 21 kD , and are processed to polypeptides of 20 and 15.8 kD , respectively .
	manualset3
93785	7	399507	13	NULL	NULL	0	NULL	21 kD	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro translation directed by mRNA isolated from these cells has shown that the primary translation products are preprobactenecins of 23.5 and 21 kD , and are processed to polypeptides of 20 and 15.8 kD , respectively .
	manualset3
93786	8	399507	13	NULL	NULL	NULL	NULL	polypeptides of 20 kD	AminoAcidPeptide												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In vitro translation directed by mRNA isolated from these cells has shown that the primary translation products are preprobactenecins of 23.5 and 21 kD , and are processed to polypeptides of 20 and 15.8 kD , respectively .
	manualset3
93787	9	399507	13	NULL	NULL	0	NULL	polypeptides of 15.8 kD	AminoAcidPeptide												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro translation directed by mRNA isolated from these cells has shown that the primary translation products are preprobactenecins of 23.5 and 21 kD , and are processed to polypeptides of 20 and 15.8 kD , respectively .
	manualset3
93788	1	399508	13	NULL	NULL	0	NULL	In vitro ubiquitination assay	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro ubiquitination assay showed that SCFbeta-TrCP but not SCFFBW4 increased ubiquitination of RCAN1 , dependent on H2O2 stimulation .
	manualset3
93789	2	399508	13	NULL	NULL	0	NULL	SCFbeta-TrCP	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro ubiquitination assay showed that SCFbeta-TrCP but not SCFFBW4 increased ubiquitination of RCAN1 , dependent on H2O2 stimulation .
	manualset3
93790	3	399508	13	NULL	NULL	0	NULL	SCFFBW4	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro ubiquitination assay showed that SCFbeta-TrCP but not SCFFBW4 increased ubiquitination of RCAN1 , dependent on H2O2 stimulation .
	manualset3
93791	4	399508	13	NULL	NULL	0	NULL	ubiquitination 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro ubiquitination assay showed that SCFbeta-TrCP but not SCFFBW4 increased ubiquitination of RCAN1 , dependent on H2O2 stimulation .
	manualset3
93792	5	399508	13	NULL	NULL	0	NULL	RCAN1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro ubiquitination assay showed that SCFbeta-TrCP but not SCFFBW4 increased ubiquitination of RCAN1 , dependent on H2O2 stimulation .
	manualset3
93793	6	399508	13	NULL	NULL	0	NULL	H2O2 stimulation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro ubiquitination assay showed that SCFbeta-TrCP but not SCFFBW4 increased ubiquitination of RCAN1 , dependent on H2O2 stimulation .
	manualset3
93794	1	399509	13	NULL	NULL	0	NULL	In vitro vs. in vivo tape stripping 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro vs. in vivo tape stripping : Validation of the porcine ear model and penetration assessment of novel sucrose stearate emulsions .
	manualset3
93795	2	399509	13	NULL	NULL	0	NULL	Validation 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro vs. in vivo tape stripping : Validation of the porcine ear model and penetration assessment of novel sucrose stearate emulsions .
	manualset3
93796	3	399509	13	NULL	NULL	NULL	NULL	porcine ear model 	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In vitro vs. in vivo tape stripping : Validation of the porcine ear model and penetration assessment of novel sucrose stearate emulsions .
	manualset3
93797	4	399509	13	NULL	NULL	0	NULL	penetration assessment	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro vs. in vivo tape stripping : Validation of the porcine ear model and penetration assessment of novel sucrose stearate emulsions .
	manualset3
93798	5	399509	13	NULL	NULL	0	NULL	novel sucrose stearate emulsions	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro vs. in vivo tape stripping : Validation of the porcine ear model and penetration assessment of novel sucrose stearate emulsions .
	manualset3
93799	1	399510	13	NULL	NULL	0	NULL	higher expression levels	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro we observed higher expression levels and sustained long-term expression of TK .007 , indicating lower nonspecific toxicity .
	manualset3
93800	2	399510	13	NULL	NULL	0	NULL	expression of TK .007	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro we observed higher expression levels and sustained long-term expression of TK .007 , indicating lower nonspecific toxicity .
	manualset3
93801	3	399510	13	NULL	NULL	0	NULL	lower nonspecific toxicity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In vitro we observed higher expression levels and sustained long-term expression of TK .007 , indicating lower nonspecific toxicity .
	manualset3
93802	1	399511	13	NULL	NULL	NULL	NULL	10 min	Time												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In vivo , 10 min of umbilical cord occlusion produced an increase in fetal blood ionized magnesium concentration in all animals ( P = 0.02 ) that was temporally related to the decrease in fetal blood pH. .
	manualset3
93803	2	399511	13	NULL	NULL	0	NULL	umbilical cord occlusion 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo , 10 min of umbilical cord occlusion produced an increase in fetal blood ionized magnesium concentration in all animals ( P = 0.02 ) that was temporally related to the decrease in fetal blood pH. .
	manualset3
93804	3	399511	13	NULL	NULL	NULL	NULL	increase in fetal blood ionized magnesium concentration	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In vivo , 10 min of umbilical cord occlusion produced an increase in fetal blood ionized magnesium concentration in all animals ( P = 0.02 ) that was temporally related to the decrease in fetal blood pH. .
	manualset3
93805	4	399511	13	NULL	NULL	0	NULL	animals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo , 10 min of umbilical cord occlusion produced an increase in fetal blood ionized magnesium concentration in all animals ( P = 0.02 ) that was temporally related to the decrease in fetal blood pH. .
	manualset3
93806	5	399511	13	NULL	NULL	0	NULL	P = 0.02	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo , 10 min of umbilical cord occlusion produced an increase in fetal blood ionized magnesium concentration in all animals ( P = 0.02 ) that was temporally related to the decrease in fetal blood pH. .
	manualset3
93807	6	399511	13	NULL	NULL	0	NULL	decrease in fetal blood pH	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo , 10 min of umbilical cord occlusion produced an increase in fetal blood ionized magnesium concentration in all animals ( P = 0.02 ) that was temporally related to the decrease in fetal blood pH. .
	manualset3
93808	1	399512	13	NULL	NULL	0	NULL	In vivo studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo , ex-vivo , and in vitro studies showed that TFF1 expression suppressed TNF -- mediated NF-B activation through the TNF receptor 1 ( TNFR1 ) / IB kinase ( IKK ) pathway .
	manualset3
93809	2	399512	13	NULL	NULL	0	NULL	ex-vivo studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo , ex-vivo , and in vitro studies showed that TFF1 expression suppressed TNF -- mediated NF-B activation through the TNF receptor 1 ( TNFR1 ) / IB kinase ( IKK ) pathway .
	manualset3
93810	3	399512	13	NULL	NULL	0	NULL	in vitro studies 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo , ex-vivo , and in vitro studies showed that TFF1 expression suppressed TNF -- mediated NF-B activation through the TNF receptor 1 ( TNFR1 ) / IB kinase ( IKK ) pathway .
	manualset3
93811	4	399512	13	NULL	NULL	0	NULL	TFF1 expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo , ex-vivo , and in vitro studies showed that TFF1 expression suppressed TNF -- mediated NF-B activation through the TNF receptor 1 ( TNFR1 ) / IB kinase ( IKK ) pathway .
	manualset3
93812	5	399512	13	NULL	NULL	0	NULL	TNF -- mediated NF-B activation 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo , ex-vivo , and in vitro studies showed that TFF1 expression suppressed TNF -- mediated NF-B activation through the TNF receptor 1 ( TNFR1 ) / IB kinase ( IKK ) pathway .
	manualset3
93813	6	399512	13	NULL	NULL	0	NULL	TNF receptor 1 ( TNFR1 ) / IB kinase ( IKK ) pathway	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo , ex-vivo , and in vitro studies showed that TFF1 expression suppressed TNF -- mediated NF-B activation through the TNF receptor 1 ( TNFR1 ) / IB kinase ( IKK ) pathway .
	manualset3
93814	1	399513	13	NULL	NULL	0	NULL	enzyme 	GeneOrProteinGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo , the enzyme but not the KOH solution produced shortening of p-aramid but not cellulose RFP recovered from the lungs .
	manualset3
93815	2	399513	13	NULL	NULL	0	NULL	 KOH solution 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo , the enzyme but not the KOH solution produced shortening of p-aramid but not cellulose RFP recovered from the lungs .
	manualset3
93816	3	399513	13	NULL	NULL	NULL	NULL	shortening of p-aramid 	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In vivo , the enzyme but not the KOH solution produced shortening of p-aramid but not cellulose RFP recovered from the lungs .
	manualset3
93817	4	399513	13	NULL	NULL	0	NULL	shortening of cellulose RFP	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo , the enzyme but not the KOH solution produced shortening of p-aramid but not cellulose RFP recovered from the lungs .
	manualset3
93818	5	399513	13	NULL	NULL	0	NULL	lungs	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo , the enzyme but not the KOH solution produced shortening of p-aramid but not cellulose RFP recovered from the lungs .
	manualset3
93819	1	399514	13	NULL	NULL	0	NULL	Tissue-phantom-dose relationship R ( t , F )	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	( Tissue-phantom-dose relationship R ( t , F ) for irradiation planning .
	manualset3
93820	2	399514	13	NULL	NULL	0	NULL	irradiation planning	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( Tissue-phantom-dose relationship R ( t , F ) for irradiation planning .
	manualset3
93821	1	399515	13	NULL	NULL	0	NULL	tumor growth	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo , tumor growth was significantly reduced and overall survival significantly prolonged in mice treated with EA as compared to untreated mice .
	manualset3
93822	2	399515	13	NULL	NULL	0	NULL	overall survival 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo , tumor growth was significantly reduced and overall survival significantly prolonged in mice treated with EA as compared to untreated mice .
	manualset3
93823	3	399515	13	NULL	NULL	0	NULL	mice 	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo , tumor growth was significantly reduced and overall survival significantly prolonged in mice treated with EA as compared to untreated mice .
	manualset3
93824	4	399515	13	NULL	NULL	0	NULL	EA	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo , tumor growth was significantly reduced and overall survival significantly prolonged in mice treated with EA as compared to untreated mice .
	manualset3
93825	5	399515	13	NULL	NULL	0	NULL	mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo , tumor growth was significantly reduced and overall survival significantly prolonged in mice treated with EA as compared to untreated mice .
	manualset3
93826	1	399516	13	NULL	NULL	0	NULL	In vivo administration	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo administration of anti-CD4 monoclonal antibody prolongs survival in longtailed macaques with experimental allergic encephalomyelitis .
	manualset3
93827	2	399516	13	NULL	NULL	0	NULL	 anti-CD4 monoclonal antibody	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo administration of anti-CD4 monoclonal antibody prolongs survival in longtailed macaques with experimental allergic encephalomyelitis .
	manualset3
93828	3	399516	13	NULL	NULL	0	NULL	survival	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo administration of anti-CD4 monoclonal antibody prolongs survival in longtailed macaques with experimental allergic encephalomyelitis .
	manualset3
93829	4	399516	13	NULL	NULL	0	NULL	longtailed macaques	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo administration of anti-CD4 monoclonal antibody prolongs survival in longtailed macaques with experimental allergic encephalomyelitis .
	manualset3
93830	5	399516	13	NULL	NULL	0	NULL	experimental allergic encephalomyelitis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo administration of anti-CD4 monoclonal antibody prolongs survival in longtailed macaques with experimental allergic encephalomyelitis .
	manualset3
93831	1	399517	13	NULL	NULL	0	NULL	In vivo assay	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo assay showed that gut trypsin activity from L ( 4 ) treated with M. oleifera flower extract decreased over time ( 0-1 , 440 min ) and was strongly inhibited ( 98.6 % ) after 310 min incubation ; acetylcholinesterase activity was not affected .
	manualset3
93832	2	399517	13	NULL	NULL	NULL	NULL	gut trypsin activity	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In vivo assay showed that gut trypsin activity from L ( 4 ) treated with M. oleifera flower extract decreased over time ( 0-1 , 440 min ) and was strongly inhibited ( 98.6 % ) after 310 min incubation ; acetylcholinesterase activity was not affected .
	manualset3
93833	3	399517	13	NULL	NULL	NULL	NULL	L ( 4 ) 	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In vivo assay showed that gut trypsin activity from L ( 4 ) treated with M. oleifera flower extract decreased over time ( 0-1 , 440 min ) and was strongly inhibited ( 98.6 % ) after 310 min incubation ; acetylcholinesterase activity was not affected .
	manualset3
93834	4	399517	13	NULL	NULL	0	NULL	M. oleifera flower extract	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo assay showed that gut trypsin activity from L ( 4 ) treated with M. oleifera flower extract decreased over time ( 0-1 , 440 min ) and was strongly inhibited ( 98.6 % ) after 310 min incubation ; acetylcholinesterase activity was not affected .
	manualset3
93835	5	399517	13	NULL	NULL	0	NULL	time ( 0-1 , 440 min ) 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo assay showed that gut trypsin activity from L ( 4 ) treated with M. oleifera flower extract decreased over time ( 0-1 , 440 min ) and was strongly inhibited ( 98.6 % ) after 310 min incubation ; acetylcholinesterase activity was not affected .
	manualset3
93836	6	399517	13	NULL	NULL	0	NULL	98.6 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo assay showed that gut trypsin activity from L ( 4 ) treated with M. oleifera flower extract decreased over time ( 0-1 , 440 min ) and was strongly inhibited ( 98.6 % ) after 310 min incubation ; acetylcholinesterase activity was not affected .
	manualset3
93837	7	399517	13	NULL	NULL	NULL	NULL	310 min	Time												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In vivo assay showed that gut trypsin activity from L ( 4 ) treated with M. oleifera flower extract decreased over time ( 0-1 , 440 min ) and was strongly inhibited ( 98.6 % ) after 310 min incubation ; acetylcholinesterase activity was not affected .
	manualset3
93838	8	399517	13	NULL	NULL	0	NULL	incubation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo assay showed that gut trypsin activity from L ( 4 ) treated with M. oleifera flower extract decreased over time ( 0-1 , 440 min ) and was strongly inhibited ( 98.6 % ) after 310 min incubation ; acetylcholinesterase activity was not affected .
	manualset3
93839	9	399517	13	NULL	NULL	0	NULL	acetylcholinesterase activity 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo assay showed that gut trypsin activity from L ( 4 ) treated with M. oleifera flower extract decreased over time ( 0-1 , 440 min ) and was strongly inhibited ( 98.6 % ) after 310 min incubation ; acetylcholinesterase activity was not affected .
	manualset3
93840	1	399518	13	NULL	NULL	0	NULL	In vivo competition experiments	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo competition experiments confirmed that the enhanced detection capability of EPTA-Gd was based specifically on ER targeting .
	manualset3
93841	2	399518	13	NULL	NULL	0	NULL	detection	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo competition experiments confirmed that the enhanced detection capability of EPTA-Gd was based specifically on ER targeting .
	manualset3
93842	3	399518	13	NULL	NULL	0	NULL	EPTA-Gd 	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo competition experiments confirmed that the enhanced detection capability of EPTA-Gd was based specifically on ER targeting .
	manualset3
93843	4	399518	13	NULL	NULL	0	NULL	ER targeting 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo competition experiments confirmed that the enhanced detection capability of EPTA-Gd was based specifically on ER targeting .
	manualset3
93844	1	399519	13	NULL	NULL	0	NULL	In vivo depletion experiments	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo depletion experiments show that CD4 + T cells are required for the SEB-triggered shock , while CD8 + cells suppress it .
	manualset3
93845	2	399519	13	NULL	NULL	0	NULL	CD4 + T cells 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo depletion experiments show that CD4 + T cells are required for the SEB-triggered shock , while CD8 + cells suppress it .
	manualset3
93846	3	399519	13	NULL	NULL	0	NULL	SEB-triggered shock	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo depletion experiments show that CD4 + T cells are required for the SEB-triggered shock , while CD8 + cells suppress it .
	manualset3
93847	4	399519	13	NULL	NULL	0	NULL	CD8 + cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo depletion experiments show that CD4 + T cells are required for the SEB-triggered shock , while CD8 + cells suppress it .
	manualset3
93848	1	399520	13	NULL	NULL	0	NULL	In vivo evidence	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo evidence for stimulation of placental , myometrial , and endometrial prostaglandin G/H synthase 2 by fetal cortisol replacement after fetal adrenalectomy .
	manualset3
93849	2	399520	13	NULL	NULL	0	NULL	stimulation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo evidence for stimulation of placental , myometrial , and endometrial prostaglandin G/H synthase 2 by fetal cortisol replacement after fetal adrenalectomy .
	manualset3
93850	3	399520	13	NULL	NULL	0	NULL	placental prostaglandin G/H synthase 2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo evidence for stimulation of placental , myometrial , and endometrial prostaglandin G/H synthase 2 by fetal cortisol replacement after fetal adrenalectomy .
	manualset3
93851	4	399520	13	NULL	NULL	0	NULL	myometrial prostaglandin G/H synthase 2 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo evidence for stimulation of placental , myometrial , and endometrial prostaglandin G/H synthase 2 by fetal cortisol replacement after fetal adrenalectomy .
	manualset3
93852	5	399520	13	NULL	NULL	0	NULL	endometrial prostaglandin G/H synthase 2 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo evidence for stimulation of placental , myometrial , and endometrial prostaglandin G/H synthase 2 by fetal cortisol replacement after fetal adrenalectomy .
	manualset3
93853	6	399520	13	NULL	NULL	0	NULL	fetal cortisol replacement	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo evidence for stimulation of placental , myometrial , and endometrial prostaglandin G/H synthase 2 by fetal cortisol replacement after fetal adrenalectomy .
	manualset3
93854	7	399520	13	NULL	NULL	0	NULL	 fetal adrenalectomy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo evidence for stimulation of placental , myometrial , and endometrial prostaglandin G/H synthase 2 by fetal cortisol replacement after fetal adrenalectomy .
	manualset3
94035	1	399521	13	NULL	NULL	NULL	NULL	In vivo hyperoxic exposure 	ExperimentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In vivo hyperoxic exposure increases cultured lung fibroblast proliferation and c-Ha-ras expression .
	manualset3
94037	2	399521	13	NULL	NULL	0	NULL	increases	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo hyperoxic exposure increases cultured lung fibroblast proliferation and c-Ha-ras expression .
	manualset3
94039	3	399521	13	NULL	NULL	0	NULL	 lung fibroblast proliferation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo hyperoxic exposure increases cultured lung fibroblast proliferation and c-Ha-ras expression .
	manualset3
94041	4	399521	13	NULL	NULL	0	NULL	c-Ha-ras expression 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo hyperoxic exposure increases cultured lung fibroblast proliferation and c-Ha-ras expression .
	manualset3
94146	1	399522	13	NULL	NULL	0	NULL	In vivo inoculation 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo inoculation of a low metastatic BW 5147 derived T-cell lymphoma variant into syngeneic mice , had led to the generation of a highly metastatic variant .
	manualset3
94147	2	399522	13	NULL	NULL	0	NULL	low metastatic BW 5147 derived T-cell lymphoma variant	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo inoculation of a low metastatic BW 5147 derived T-cell lymphoma variant into syngeneic mice , had led to the generation of a highly metastatic variant .
	manualset3
94148	3	399522	13	NULL	NULL	0	NULL	syngeneic mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo inoculation of a low metastatic BW 5147 derived T-cell lymphoma variant into syngeneic mice , had led to the generation of a highly metastatic variant .
	manualset3
94149	4	399522	13	NULL	NULL	0	NULL	generation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo inoculation of a low metastatic BW 5147 derived T-cell lymphoma variant into syngeneic mice , had led to the generation of a highly metastatic variant .
	manualset3
94150	5	399522	13	NULL	NULL	0	NULL	metastatic variant 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo inoculation of a low metastatic BW 5147 derived T-cell lymphoma variant into syngeneic mice , had led to the generation of a highly metastatic variant .
	manualset3
94151	1	399523	13	NULL	NULL	0	NULL	In vivo modulation of G proteins	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo modulation of G proteins and opioid receptor function by antisense oligodeoxynucleotides .
	manualset3
94152	2	399523	13	NULL	NULL	0	NULL	opioid receptor function	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo modulation of G proteins and opioid receptor function by antisense oligodeoxynucleotides .
	manualset3
94153	3	399523	13	NULL	NULL	0	NULL	antisense oligodeoxynucleotides	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo modulation of G proteins and opioid receptor function by antisense oligodeoxynucleotides .
	manualset3
94154	1	399524	13	NULL	NULL	0	NULL	In vivo occupancy	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo occupancy of the striatal dopamine uptake complex by various inhibitors does not predict their effects on locomotion .
	manualset3
94155	2	399524	13	NULL	NULL	NULL	NULL	 striatal dopamine uptake complex	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In vivo occupancy of the striatal dopamine uptake complex by various inhibitors does not predict their effects on locomotion .
	manualset3
94156	3	399524	13	NULL	NULL	0	NULL	various inhibitors	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo occupancy of the striatal dopamine uptake complex by various inhibitors does not predict their effects on locomotion .
	manualset3
94157	4	399524	13	NULL	NULL	NULL	NULL	 effects	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In vivo occupancy of the striatal dopamine uptake complex by various inhibitors does not predict their effects on locomotion .
	manualset3
94158	5	399524	13	NULL	NULL	0	NULL	locomotion	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo occupancy of the striatal dopamine uptake complex by various inhibitors does not predict their effects on locomotion .
	manualset3
94159	1	399525	13	NULL	NULL	0	NULL	In vivo solutions of thrombin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo solutions of thrombin were infused stereotactically into the right basal ganglia of rats .
	manualset3
94160	2	399525	13	NULL	NULL	NULL	NULL	right basal ganglia of rats	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In vivo solutions of thrombin were infused stereotactically into the right basal ganglia of rats .
	manualset3
94161	1	399526	13	NULL	NULL	0	NULL	In vivo study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo study showed that the expression of GM-CSF by RVJSB1175D/GM-CSF did not interfere with the HSV-1gD antibody production .
	manualset3
94162	2	399526	13	NULL	NULL	0	NULL	expression of GM-CSF 	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo study showed that the expression of GM-CSF by RVJSB1175D/GM-CSF did not interfere with the HSV-1gD antibody production .
	manualset3
94163	3	399526	13	NULL	NULL	0	NULL	RVJSB1175D/GM-CSF 	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo study showed that the expression of GM-CSF by RVJSB1175D/GM-CSF did not interfere with the HSV-1gD antibody production .
	manualset3
94164	4	399526	13	NULL	NULL	0	NULL	HSV-1gD antibody production	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo study showed that the expression of GM-CSF by RVJSB1175D/GM-CSF did not interfere with the HSV-1gD antibody production .
	manualset3
94165	1	399527	13	NULL	NULL	0	NULL	In vivo therapeutic gas delivery 	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo therapeutic gas delivery for neuroprotection with echogenic liposomes .
	manualset3
94166	2	399527	13	NULL	NULL	0	NULL	neuroprotection	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo therapeutic gas delivery for neuroprotection with echogenic liposomes .
	manualset3
94167	3	399527	13	NULL	NULL	0	NULL	echogenic liposomes	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In vivo therapeutic gas delivery for neuroprotection with echogenic liposomes .
	manualset3
94168	1	399528	13	NULL	NULL	0	NULL	In situ electron holography	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ electron holography showed that the oxide underwent reduction at elevated temperatures in a vacuum and was consequently reoxidized upon exposure to an oxygen flux at the same temperature .
	manualset3
94169	2	399528	13	NULL	NULL	0	NULL	oxide	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ electron holography showed that the oxide underwent reduction at elevated temperatures in a vacuum and was consequently reoxidized upon exposure to an oxygen flux at the same temperature .
	manualset3
94170	3	399528	13	NULL	NULL	0	NULL	reduction	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ electron holography showed that the oxide underwent reduction at elevated temperatures in a vacuum and was consequently reoxidized upon exposure to an oxygen flux at the same temperature .
	manualset3
94171	4	399528	13	NULL	NULL	0	NULL	temperatures 	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ electron holography showed that the oxide underwent reduction at elevated temperatures in a vacuum and was consequently reoxidized upon exposure to an oxygen flux at the same temperature .
	manualset3
94172	5	399528	13	NULL	NULL	0	NULL	vacuum	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ electron holography showed that the oxide underwent reduction at elevated temperatures in a vacuum and was consequently reoxidized upon exposure to an oxygen flux at the same temperature .
	manualset3
94173	6	399528	13	NULL	NULL	0	NULL	exposure	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ electron holography showed that the oxide underwent reduction at elevated temperatures in a vacuum and was consequently reoxidized upon exposure to an oxygen flux at the same temperature .
	manualset3
94174	7	399528	13	NULL	NULL	0	NULL	oxygen flux 	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ electron holography showed that the oxide underwent reduction at elevated temperatures in a vacuum and was consequently reoxidized upon exposure to an oxygen flux at the same temperature .
	manualset3
94175	8	399528	13	NULL	NULL	0	NULL	temperature	EnvironmentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ electron holography showed that the oxide underwent reduction at elevated temperatures in a vacuum and was consequently reoxidized upon exposure to an oxygen flux at the same temperature .
	manualset3
94176	1	399529	13	NULL	NULL	0	NULL	Angiographic diagnosis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Angiographic diagnosis of combined injuries of the spleen and left kidney ) .
	manualset3
94177	2	399529	13	NULL	NULL	0	NULL	injuries of the spleen	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Angiographic diagnosis of combined injuries of the spleen and left kidney ) .
	manualset3
94178	3	399529	13	NULL	NULL	0	NULL	injuries of the left kidney	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Angiographic diagnosis of combined injuries of the spleen and left kidney ) .
	manualset3
94179	1	399530	13	NULL	NULL	0	NULL	Tokyo	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	( Tokyo ) 86 , 79-86 ) and to the submandibular proline-rich protein precursor MSG1 of the mouse ( D. Tronik-Le Roux , M. Senorale-Pose , and F. Rougeon , manuscript in preparation ) .
	manualset3
94180	2	399530	13	NULL	NULL	0	NULL	86 , 79-86 	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	( Tokyo ) 86 , 79-86 ) and to the submandibular proline-rich protein precursor MSG1 of the mouse ( D. Tronik-Le Roux , M. Senorale-Pose , and F. Rougeon , manuscript in preparation ) .
	manualset3
94181	3	399530	13	NULL	NULL	0	NULL	submandibular proline-rich protein precursor MSG1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	( Tokyo ) 86 , 79-86 ) and to the submandibular proline-rich protein precursor MSG1 of the mouse ( D. Tronik-Le Roux , M. Senorale-Pose , and F. Rougeon , manuscript in preparation ) .
	manualset3
94182	4	399530	13	NULL	NULL	0	NULL	mouse	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	( Tokyo ) 86 , 79-86 ) and to the submandibular proline-rich protein precursor MSG1 of the mouse ( D. Tronik-Le Roux , M. Senorale-Pose , and F. Rougeon , manuscript in preparation ) .
	manualset3
94183	5	399530	13	NULL	NULL	0	NULL	 D. Tronik-Le Roux	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	( Tokyo ) 86 , 79-86 ) and to the submandibular proline-rich protein precursor MSG1 of the mouse ( D. Tronik-Le Roux , M. Senorale-Pose , and F. Rougeon , manuscript in preparation ) .
	manualset3
94184	6	399530	13	NULL	NULL	0	NULL	M. Senorale-Pose	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	( Tokyo ) 86 , 79-86 ) and to the submandibular proline-rich protein precursor MSG1 of the mouse ( D. Tronik-Le Roux , M. Senorale-Pose , and F. Rougeon , manuscript in preparation ) .
	manualset3
94185	7	399530	13	NULL	NULL	0	NULL	F. Rougeon	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	( Tokyo ) 86 , 79-86 ) and to the submandibular proline-rich protein precursor MSG1 of the mouse ( D. Tronik-Le Roux , M. Senorale-Pose , and F. Rougeon , manuscript in preparation ) .
	manualset3
94186	8	399530	13	NULL	NULL	0	NULL	manuscript	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	( Tokyo ) 86 , 79-86 ) and to the submandibular proline-rich protein precursor MSG1 of the mouse ( D. Tronik-Le Roux , M. Senorale-Pose , and F. Rougeon , manuscript in preparation ) .
	manualset3
94187	9	399530	13	NULL	NULL	0	NULL	preparation	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( Tokyo ) 86 , 79-86 ) and to the submandibular proline-rich protein precursor MSG1 of the mouse ( D. Tronik-Le Roux , M. Senorale-Pose , and F. Rougeon , manuscript in preparation ) .
	manualset3
86664	1	399531	5	NULL	NULL	0	NULL	In situ hybridization	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ hybridization shows that MeHsp90 is highly expressed in previtellogenic oocytes and its expression decreases with the progress of maturation , and finally stops in late-vitellogenic oocytes .
	manualset3
86665	2	399531	5	NULL	NULL	0	NULL	MeHsp90	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ hybridization shows that MeHsp90 is highly expressed in previtellogenic oocytes and its expression decreases with the progress of maturation , and finally stops in late-vitellogenic oocytes .
	manualset3
86666	3	399531	5	NULL	NULL	0	NULL	previtellogenic oocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ hybridization shows that MeHsp90 is highly expressed in previtellogenic oocytes and its expression decreases with the progress of maturation , and finally stops in late-vitellogenic oocytes .
	manualset3
86667	4	399531	5	NULL	NULL	NULL	NULL	expression	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In situ hybridization shows that MeHsp90 is highly expressed in previtellogenic oocytes and its expression decreases with the progress of maturation , and finally stops in late-vitellogenic oocytes .
	manualset3
86668	5	399531	5	NULL	NULL	0	NULL	progress	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ hybridization shows that MeHsp90 is highly expressed in previtellogenic oocytes and its expression decreases with the progress of maturation , and finally stops in late-vitellogenic oocytes .
	manualset3
86669	6	399531	5	NULL	NULL	0	NULL	maturation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ hybridization shows that MeHsp90 is highly expressed in previtellogenic oocytes and its expression decreases with the progress of maturation , and finally stops in late-vitellogenic oocytes .
	manualset3
86670	7	399531	5	NULL	NULL	0	NULL	late-vitellogenic oocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ hybridization shows that MeHsp90 is highly expressed in previtellogenic oocytes and its expression decreases with the progress of maturation , and finally stops in late-vitellogenic oocytes .
	manualset3
86671	1	399532	5	NULL	NULL	0	NULL	In situ proteomic profiling	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ proteomic profiling of tumors is a powerful technology with potential to enhance our understanding of tumor biology , but sources of variability due to patient and tumor heterogeneity are poorly understood and are the topic of this investigation .
	manualset3
86672	2	399532	5	NULL	NULL	0	NULL	tumors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ proteomic profiling of tumors is a powerful technology with potential to enhance our understanding of tumor biology , but sources of variability due to patient and tumor heterogeneity are poorly understood and are the topic of this investigation .
	manualset3
86673	3	399532	5	NULL	NULL	0	NULL	powerful technology	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ proteomic profiling of tumors is a powerful technology with potential to enhance our understanding of tumor biology , but sources of variability due to patient and tumor heterogeneity are poorly understood and are the topic of this investigation .
	manualset3
86674	4	399532	5	NULL	NULL	0	NULL	tumor biology	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ proteomic profiling of tumors is a powerful technology with potential to enhance our understanding of tumor biology , but sources of variability due to patient and tumor heterogeneity are poorly understood and are the topic of this investigation .
	manualset3
86675	5	399532	5	NULL	NULL	0	NULL	variability	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ proteomic profiling of tumors is a powerful technology with potential to enhance our understanding of tumor biology , but sources of variability due to patient and tumor heterogeneity are poorly understood and are the topic of this investigation .
	manualset3
86676	6	399532	5	NULL	NULL	0	NULL	patient	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ proteomic profiling of tumors is a powerful technology with potential to enhance our understanding of tumor biology , but sources of variability due to patient and tumor heterogeneity are poorly understood and are the topic of this investigation .
	manualset3
86677	7	399532	5	NULL	NULL	0	NULL	tumor heterogeneity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ proteomic profiling of tumors is a powerful technology with potential to enhance our understanding of tumor biology , but sources of variability due to patient and tumor heterogeneity are poorly understood and are the topic of this investigation .
	manualset3
86678	8	399532	5	NULL	NULL	0	NULL	investigation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ proteomic profiling of tumors is a powerful technology with potential to enhance our understanding of tumor biology , but sources of variability due to patient and tumor heterogeneity are poorly understood and are the topic of this investigation .
	manualset3
86679	1	399533	5	NULL	NULL	NULL	NULL	In situ steady-state , single-pass small intestine perfusions	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In situ steady-state , single-pass small intestine perfusions in rats were carried out to compare the effect of the bicarbonate and citrate World Health Organization oral rehydration solutions and a base precursor-free solution on intestinal water and electrolyte transport after inducing intestinal secretion with purified heat-stable Escherichia coli enterotoxin .
	manualset3
86680	2	399533	5	NULL	NULL	NULL	NULL	rats	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In situ steady-state , single-pass small intestine perfusions in rats were carried out to compare the effect of the bicarbonate and citrate World Health Organization oral rehydration solutions and a base precursor-free solution on intestinal water and electrolyte transport after inducing intestinal secretion with purified heat-stable Escherichia coli enterotoxin .
	manualset3
86681	3	399533	5	NULL	NULL	0	NULL	effect	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ steady-state , single-pass small intestine perfusions in rats were carried out to compare the effect of the bicarbonate and citrate World Health Organization oral rehydration solutions and a base precursor-free solution on intestinal water and electrolyte transport after inducing intestinal secretion with purified heat-stable Escherichia coli enterotoxin .
	manualset3
86682	4	399533	5	NULL	NULL	NULL	NULL	bicarbonate and citrate World Health Organization oral rehydration solutions	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In situ steady-state , single-pass small intestine perfusions in rats were carried out to compare the effect of the bicarbonate and citrate World Health Organization oral rehydration solutions and a base precursor-free solution on intestinal water and electrolyte transport after inducing intestinal secretion with purified heat-stable Escherichia coli enterotoxin .
	manualset3
86683	5	399533	5	NULL	NULL	NULL	NULL	base precursor-free solution	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In situ steady-state , single-pass small intestine perfusions in rats were carried out to compare the effect of the bicarbonate and citrate World Health Organization oral rehydration solutions and a base precursor-free solution on intestinal water and electrolyte transport after inducing intestinal secretion with purified heat-stable Escherichia coli enterotoxin .
	manualset3
86684	6	399533	5	NULL	NULL	0	NULL	intestinal water and electrolyte transport	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ steady-state , single-pass small intestine perfusions in rats were carried out to compare the effect of the bicarbonate and citrate World Health Organization oral rehydration solutions and a base precursor-free solution on intestinal water and electrolyte transport after inducing intestinal secretion with purified heat-stable Escherichia coli enterotoxin .
	manualset3
86685	7	399533	5	NULL	NULL	NULL	NULL	intestinal secretion	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In situ steady-state , single-pass small intestine perfusions in rats were carried out to compare the effect of the bicarbonate and citrate World Health Organization oral rehydration solutions and a base precursor-free solution on intestinal water and electrolyte transport after inducing intestinal secretion with purified heat-stable Escherichia coli enterotoxin .
	manualset3
86686	8	399533	5	NULL	NULL	0	NULL	purified heat-stable Escherichia coli enterotoxin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In situ steady-state , single-pass small intestine perfusions in rats were carried out to compare the effect of the bicarbonate and citrate World Health Organization oral rehydration solutions and a base precursor-free solution on intestinal water and electrolyte transport after inducing intestinal secretion with purified heat-stable Escherichia coli enterotoxin .
	manualset3
86687	1	399534	5	NULL	NULL	NULL	NULL	1904	TimePoint												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In 1904 , James Collier became the first to describe cerebellar tonsillar herniation as a `` false localizing sign '' often associated with intracranial tumors .
	manualset3
86688	2	399534	5	NULL	NULL	0	NULL	James Collier	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	In 1904 , James Collier became the first to describe cerebellar tonsillar herniation as a `` false localizing sign '' often associated with intracranial tumors .
	manualset3
86689	3	399534	5	NULL	NULL	0	NULL	cerebellar tonsillar herniation	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In 1904 , James Collier became the first to describe cerebellar tonsillar herniation as a `` false localizing sign '' often associated with intracranial tumors .
	manualset3
86690	4	399534	5	NULL	NULL	0	NULL	false localizing sign	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In 1904 , James Collier became the first to describe cerebellar tonsillar herniation as a `` false localizing sign '' often associated with intracranial tumors .
	manualset3
86691	5	399534	5	NULL	NULL	0	NULL	intracranial tumors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In 1904 , James Collier became the first to describe cerebellar tonsillar herniation as a `` false localizing sign '' often associated with intracranial tumors .
	manualset3
86692	1	399535	5	NULL	NULL	NULL	NULL	1969	TimePoint												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In 1969 , five cases of melioidosis in three separate outbreaks were diagnosed in nonhuman primates in the United States .
	manualset3
86693	2	399535	5	NULL	NULL	0	NULL	five cases	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In 1969 , five cases of melioidosis in three separate outbreaks were diagnosed in nonhuman primates in the United States .
	manualset3
86694	3	399535	5	NULL	NULL	0	NULL	melioidosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In 1969 , five cases of melioidosis in three separate outbreaks were diagnosed in nonhuman primates in the United States .
	manualset3
86695	4	399535	5	NULL	NULL	0	NULL	three separate outbreaks	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In 1969 , five cases of melioidosis in three separate outbreaks were diagnosed in nonhuman primates in the United States .
	manualset3
86696	5	399535	5	NULL	NULL	0	NULL	nonhuman primates	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In 1969 , five cases of melioidosis in three separate outbreaks were diagnosed in nonhuman primates in the United States .
	manualset3
86697	6	399535	5	NULL	NULL	0	NULL	United States	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In 1969 , five cases of melioidosis in three separate outbreaks were diagnosed in nonhuman primates in the United States .
	manualset3
86698	1	399536	5	NULL	NULL	0	NULL	1977	TimePoint												NULL		0	NULL	NULL	NULL	NULL	NULL	In 1977 , Fisher reported that in patients with possible normal-pressure hydrocephalus ( NPH ) , if the gait abnormality preceded dementia , surgery usually had a favorable outcome and vice versa .
	manualset3
86699	2	399536	5	NULL	NULL	0	NULL	Fisher	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	In 1977 , Fisher reported that in patients with possible normal-pressure hydrocephalus ( NPH ) , if the gait abnormality preceded dementia , surgery usually had a favorable outcome and vice versa .
	manualset3
86700	3	399536	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In 1977 , Fisher reported that in patients with possible normal-pressure hydrocephalus ( NPH ) , if the gait abnormality preceded dementia , surgery usually had a favorable outcome and vice versa .
	manualset3
86701	4	399536	5	NULL	NULL	0	NULL	normal-pressure hydrocephalus ( NPH )	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In 1977 , Fisher reported that in patients with possible normal-pressure hydrocephalus ( NPH ) , if the gait abnormality preceded dementia , surgery usually had a favorable outcome and vice versa .
	manualset3
86702	5	399536	5	NULL	NULL	0	NULL	gait abnormality	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In 1977 , Fisher reported that in patients with possible normal-pressure hydrocephalus ( NPH ) , if the gait abnormality preceded dementia , surgery usually had a favorable outcome and vice versa .
	manualset3
86703	6	399536	5	NULL	NULL	0	NULL	dementia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In 1977 , Fisher reported that in patients with possible normal-pressure hydrocephalus ( NPH ) , if the gait abnormality preceded dementia , surgery usually had a favorable outcome and vice versa .
	manualset3
86704	7	399536	5	NULL	NULL	0	NULL	surgery	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In 1977 , Fisher reported that in patients with possible normal-pressure hydrocephalus ( NPH ) , if the gait abnormality preceded dementia , surgery usually had a favorable outcome and vice versa .
	manualset3
86705	8	399536	5	NULL	NULL	0	NULL	favorable outcome	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In 1977 , Fisher reported that in patients with possible normal-pressure hydrocephalus ( NPH ) , if the gait abnormality preceded dementia , surgery usually had a favorable outcome and vice versa .
	manualset3
86706	1	399537	5	NULL	NULL	0	NULL	2004	TimePoint												NULL		0	NULL	NULL	NULL	NULL	NULL	In 2004 , Florida accounted for 11 % of the total number of acquired immunodeficiency syndrome ( AIDS ) cases in the United States , ranking third behind New York and California .
	manualset3
86707	2	399537	5	NULL	NULL	NULL	NULL	Florida	ProperNamedGeographicalLocation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In 2004 , Florida accounted for 11 % of the total number of acquired immunodeficiency syndrome ( AIDS ) cases in the United States , ranking third behind New York and California .
	manualset3
86708	3	399537	5	NULL	NULL	0	NULL	11 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In 2004 , Florida accounted for 11 % of the total number of acquired immunodeficiency syndrome ( AIDS ) cases in the United States , ranking third behind New York and California .
	manualset3
86709	4	399537	5	NULL	NULL	0	NULL	acquired immunodeficiency syndrome ( AIDS ) cases	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In 2004 , Florida accounted for 11 % of the total number of acquired immunodeficiency syndrome ( AIDS ) cases in the United States , ranking third behind New York and California .
	manualset3
86710	5	399537	5	NULL	NULL	0	NULL	United States	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In 2004 , Florida accounted for 11 % of the total number of acquired immunodeficiency syndrome ( AIDS ) cases in the United States , ranking third behind New York and California .
	manualset3
86711	6	399537	5	NULL	NULL	0	NULL	New York	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In 2004 , Florida accounted for 11 % of the total number of acquired immunodeficiency syndrome ( AIDS ) cases in the United States , ranking third behind New York and California .
	manualset3
86712	7	399537	5	NULL	NULL	0	NULL	California	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In 2004 , Florida accounted for 11 % of the total number of acquired immunodeficiency syndrome ( AIDS ) cases in the United States , ranking third behind New York and California .
	manualset3
86713	1	399538	5	NULL	NULL	0	NULL	2008	TimePoint												NULL		0	NULL	NULL	NULL	NULL	NULL	In 2008 , patients in the intensive care unit ( ICU ) at Danbury Hospital , Danbury , Connecticut , experienced 79 pressure ulcers .
	manualset3
86714	2	399538	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In 2008 , patients in the intensive care unit ( ICU ) at Danbury Hospital , Danbury , Connecticut , experienced 79 pressure ulcers .
	manualset3
86715	3	399538	5	NULL	NULL	0	NULL	intensive care unit ( ICU )	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	In 2008 , patients in the intensive care unit ( ICU ) at Danbury Hospital , Danbury , Connecticut , experienced 79 pressure ulcers .
	manualset3
86716	4	399538	5	NULL	NULL	0	NULL	Danbury Hospital	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	In 2008 , patients in the intensive care unit ( ICU ) at Danbury Hospital , Danbury , Connecticut , experienced 79 pressure ulcers .
	manualset3
86717	5	399538	5	NULL	NULL	0	NULL	Danbury	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In 2008 , patients in the intensive care unit ( ICU ) at Danbury Hospital , Danbury , Connecticut , experienced 79 pressure ulcers .
	manualset3
86718	6	399538	5	NULL	NULL	0	NULL	Connecticut	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In 2008 , patients in the intensive care unit ( ICU ) at Danbury Hospital , Danbury , Connecticut , experienced 79 pressure ulcers .
	manualset3
86719	7	399538	5	NULL	NULL	0	NULL	79 pressure ulcers	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In 2008 , patients in the intensive care unit ( ICU ) at Danbury Hospital , Danbury , Connecticut , experienced 79 pressure ulcers .
	manualset3
86720	1	399539	5	NULL	NULL	0	NULL	7 ( 50 % )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In 7 ( 50 % ) biological signs of pancreatitis were noted : mean amylase level 81 IU ( range 30-201 IU , normal value less than 40 IU ) , mean lipase level 949 IU ( range 468-2 , 000 IU , normal value less than 300 IU ) .
	manualset3
86721	2	399539	5	NULL	NULL	0	NULL	biological signs	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In 7 ( 50 % ) biological signs of pancreatitis were noted : mean amylase level 81 IU ( range 30-201 IU , normal value less than 40 IU ) , mean lipase level 949 IU ( range 468-2 , 000 IU , normal value less than 300 IU ) .
	manualset3
86722	3	399539	5	NULL	NULL	0	NULL	pancreatitis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In 7 ( 50 % ) biological signs of pancreatitis were noted : mean amylase level 81 IU ( range 30-201 IU , normal value less than 40 IU ) , mean lipase level 949 IU ( range 468-2 , 000 IU , normal value less than 300 IU ) .
	manualset3
86723	4	399539	5	NULL	NULL	0	NULL	mean amylase level 81 IU ( range 30-201 IU , normal value less than 40 IU )	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In 7 ( 50 % ) biological signs of pancreatitis were noted : mean amylase level 81 IU ( range 30-201 IU , normal value less than 40 IU ) , mean lipase level 949 IU ( range 468-2 , 000 IU , normal value less than 300 IU ) .
	manualset3
86724	5	399539	5	NULL	NULL	0	NULL	mean lipase level 949 IU ( range 468-2 , 000 IU , normal value less than 300 IU )	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In 7 ( 50 % ) biological signs of pancreatitis were noted : mean amylase level 81 IU ( range 30-201 IU , normal value less than 40 IU ) , mean lipase level 949 IU ( range 468-2 , 000 IU , normal value less than 300 IU ) .
	manualset3
86725	1	399540	5	NULL	NULL	0	NULL	expression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In ALL , the expression of CD58 was inversely correlated with the presence of a clinical tumoral syndrome ( p = 0.0009 ) , leucocytosis ( p = 0.005 ) , and the percent of peripheral blast cells ( p = 0.001 ) .
	manualset3
86726	2	399540	5	NULL	NULL	0	NULL	CD58	GeneOrProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	In ALL , the expression of CD58 was inversely correlated with the presence of a clinical tumoral syndrome ( p = 0.0009 ) , leucocytosis ( p = 0.005 ) , and the percent of peripheral blast cells ( p = 0.001 ) .
	manualset3
86727	3	399540	5	NULL	NULL	0	NULL	clinical tumoral syndrome	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In ALL , the expression of CD58 was inversely correlated with the presence of a clinical tumoral syndrome ( p = 0.0009 ) , leucocytosis ( p = 0.005 ) , and the percent of peripheral blast cells ( p = 0.001 ) .
	manualset3
86728	4	399540	5	NULL	NULL	0	NULL	( p = 0.0009 )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In ALL , the expression of CD58 was inversely correlated with the presence of a clinical tumoral syndrome ( p = 0.0009 ) , leucocytosis ( p = 0.005 ) , and the percent of peripheral blast cells ( p = 0.001 ) .
	manualset3
86729	5	399540	5	NULL	NULL	0	NULL	leucocytosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In ALL , the expression of CD58 was inversely correlated with the presence of a clinical tumoral syndrome ( p = 0.0009 ) , leucocytosis ( p = 0.005 ) , and the percent of peripheral blast cells ( p = 0.001 ) .
	manualset3
86730	6	399540	5	NULL	NULL	0	NULL	( p = 0.005 )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In ALL , the expression of CD58 was inversely correlated with the presence of a clinical tumoral syndrome ( p = 0.0009 ) , leucocytosis ( p = 0.005 ) , and the percent of peripheral blast cells ( p = 0.001 ) .
	manualset3
86732	7	399540	5	NULL	NULL	0	NULL	peripheral blast cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In ALL , the expression of CD58 was inversely correlated with the presence of a clinical tumoral syndrome ( p = 0.0009 ) , leucocytosis ( p = 0.005 ) , and the percent of peripheral blast cells ( p = 0.001 ) .
	manualset3
86733	8	399540	5	NULL	NULL	0	NULL	( p = 0.001 )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In ALL , the expression of CD58 was inversely correlated with the presence of a clinical tumoral syndrome ( p = 0.0009 ) , leucocytosis ( p = 0.005 ) , and the percent of peripheral blast cells ( p = 0.001 ) .
	manualset3
86734	1	399541	5	NULL	NULL	0	NULL	Brazil	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In Brazil , nursing professionals are trained based on the perspective of professional competencies .
	manualset3
86735	2	399541	5	NULL	NULL	0	NULL	nursing professionals	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In Brazil , nursing professionals are trained based on the perspective of professional competencies .
	manualset3
86736	3	399541	5	NULL	NULL	0	NULL	perspective	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In Brazil , nursing professionals are trained based on the perspective of professional competencies .
	manualset3
86737	4	399541	5	NULL	NULL	0	NULL	professional competencies	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In Brazil , nursing professionals are trained based on the perspective of professional competencies .
	manualset3
86739	1	399542	5	NULL	NULL	0	NULL	Canada	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In Canada , provincial and territorial laws address circumstances in which a substitute decision-maker may be appointed for an adult deemed legally incapable of making decisions in one or more areas of life .
	manualset3
86742	2	399542	5	NULL	NULL	0	NULL	provincial and territorial laws	IntellectualProduct												NULL		0	NULL	NULL	NULL	NULL	NULL	In Canada , provincial and territorial laws address circumstances in which a substitute decision-maker may be appointed for an adult deemed legally incapable of making decisions in one or more areas of life .
	manualset3
86745	3	399542	5	NULL	NULL	0	NULL	circumstances	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In Canada , provincial and territorial laws address circumstances in which a substitute decision-maker may be appointed for an adult deemed legally incapable of making decisions in one or more areas of life .
	manualset3
86747	4	399542	5	NULL	NULL	0	NULL	substitute decision-maker	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	In Canada , provincial and territorial laws address circumstances in which a substitute decision-maker may be appointed for an adult deemed legally incapable of making decisions in one or more areas of life .
	manualset3
86748	5	399542	5	NULL	NULL	0	NULL	adult	Person												NULL		0	NULL	NULL	NULL	NULL	NULL	In Canada , provincial and territorial laws address circumstances in which a substitute decision-maker may be appointed for an adult deemed legally incapable of making decisions in one or more areas of life .
	manualset3
86751	6	399542	5	NULL	NULL	0	NULL	making decisions	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In Canada , provincial and territorial laws address circumstances in which a substitute decision-maker may be appointed for an adult deemed legally incapable of making decisions in one or more areas of life .
	manualset3
86753	7	399542	5	NULL	NULL	NULL	NULL	life	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In Canada , provincial and territorial laws address circumstances in which a substitute decision-maker may be appointed for an adult deemed legally incapable of making decisions in one or more areas of life .
	manualset3
86754	1	399543	5	NULL	NULL	0	NULL	France	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In France , it is the official Veterinary Services who are responsible for food safety and who must respond to these demands .
	manualset3
86756	2	399543	5	NULL	NULL	0	NULL	 official Veterinary Services	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In France , it is the official Veterinary Services who are responsible for food safety and who must respond to these demands .
	manualset3
86757	3	399543	5	NULL	NULL	0	NULL	food safety	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In France , it is the official Veterinary Services who are responsible for food safety and who must respond to these demands .
	manualset3
86760	1	399544	5	NULL	NULL	0	NULL	France	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In France and in other European countries , however , a particular effect was observed early on that received various labels : disinhibitor , stimulant , antiautistic and anti-deficit , and that involved the beneficial action of certain neuroleptics on the negative symptoms of schizophrenia .
	manualset3
86761	2	399544	5	NULL	NULL	0	NULL	European countries	UnproperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In France and in other European countries , however , a particular effect was observed early on that received various labels : disinhibitor , stimulant , antiautistic and anti-deficit , and that involved the beneficial action of certain neuroleptics on the negative symptoms of schizophrenia .
	manualset3
86762	3	399544	5	NULL	NULL	0	NULL	particular effect	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In France and in other European countries , however , a particular effect was observed early on that received various labels : disinhibitor , stimulant , antiautistic and anti-deficit , and that involved the beneficial action of certain neuroleptics on the negative symptoms of schizophrenia .
	manualset3
86763	4	399544	5	NULL	NULL	0	NULL	disinhibitor	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In France and in other European countries , however , a particular effect was observed early on that received various labels : disinhibitor , stimulant , antiautistic and anti-deficit , and that involved the beneficial action of certain neuroleptics on the negative symptoms of schizophrenia .
	manualset3
86764	5	399544	5	NULL	NULL	0	NULL	stimulant	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In France and in other European countries , however , a particular effect was observed early on that received various labels : disinhibitor , stimulant , antiautistic and anti-deficit , and that involved the beneficial action of certain neuroleptics on the negative symptoms of schizophrenia .
	manualset3
86767	6	399544	5	NULL	NULL	NULL	NULL	antiautistic	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In France and in other European countries , however , a particular effect was observed early on that received various labels : disinhibitor , stimulant , antiautistic and anti-deficit , and that involved the beneficial action of certain neuroleptics on the negative symptoms of schizophrenia .
	manualset3
86768	7	399544	5	NULL	NULL	0	NULL	beneficial action	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In France and in other European countries , however , a particular effect was observed early on that received various labels : disinhibitor , stimulant , antiautistic and anti-deficit , and that involved the beneficial action of certain neuroleptics on the negative symptoms of schizophrenia .
	manualset3
86769	8	399544	5	NULL	NULL	0	NULL	neuroleptics	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	In France and in other European countries , however , a particular effect was observed early on that received various labels : disinhibitor , stimulant , antiautistic and anti-deficit , and that involved the beneficial action of certain neuroleptics on the negative symptoms of schizophrenia .
	manualset3
86770	9	399544	5	NULL	NULL	0	NULL	negative symptoms	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In France and in other European countries , however , a particular effect was observed early on that received various labels : disinhibitor , stimulant , antiautistic and anti-deficit , and that involved the beneficial action of certain neuroleptics on the negative symptoms of schizophrenia .
	manualset3
86773	10	399544	5	NULL	NULL	0	NULL	schizophrenia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In France and in other European countries , however , a particular effect was observed early on that received various labels : disinhibitor , stimulant , antiautistic and anti-deficit , and that involved the beneficial action of certain neuroleptics on the negative symptoms of schizophrenia .
	manualset3
89564	11	399544	5	NULL	NULL	0	NULL	anti-deficit	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In France and in other European countries , however , a particular effect was observed early on that received various labels : disinhibitor , stimulant , antiautistic and anti-deficit , and that involved the beneficial action of certain neuroleptics on the negative symptoms of schizophrenia .
	manualset3
86774	1	399545	5	NULL	NULL	0	NULL	women	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( Too many women currently live in danger ) .
	manualset3
86779	1	399546	5	NULL	NULL	0	NULL	Kanto	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In Kanto , Kinki and Chugoku/Shikoku Districts , however , proportion of atherothrombotic stroke was larger than that of lacunar stroke , which seemed to correspond to the higher frequency of patients with diabetes mellitus and hyperlipidemia in these 3 districts .
	manualset3
86780	2	399546	5	NULL	NULL	0	NULL	Kinki	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In Kanto , Kinki and Chugoku/Shikoku Districts , however , proportion of atherothrombotic stroke was larger than that of lacunar stroke , which seemed to correspond to the higher frequency of patients with diabetes mellitus and hyperlipidemia in these 3 districts .
	manualset3
86783	3	399546	5	NULL	NULL	0	NULL	Chugoku/Shikoku Districts	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In Kanto , Kinki and Chugoku/Shikoku Districts , however , proportion of atherothrombotic stroke was larger than that of lacunar stroke , which seemed to correspond to the higher frequency of patients with diabetes mellitus and hyperlipidemia in these 3 districts .
	manualset3
86784	4	399546	5	NULL	NULL	0	NULL	atherothrombotic stroke	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In Kanto , Kinki and Chugoku/Shikoku Districts , however , proportion of atherothrombotic stroke was larger than that of lacunar stroke , which seemed to correspond to the higher frequency of patients with diabetes mellitus and hyperlipidemia in these 3 districts .
	manualset3
86787	5	399546	5	NULL	NULL	0	NULL	lacunar stroke	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In Kanto , Kinki and Chugoku/Shikoku Districts , however , proportion of atherothrombotic stroke was larger than that of lacunar stroke , which seemed to correspond to the higher frequency of patients with diabetes mellitus and hyperlipidemia in these 3 districts .
	manualset3
86795	6	399546	5	NULL	NULL	0	NULL	higher frequency	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In Kanto , Kinki and Chugoku/Shikoku Districts , however , proportion of atherothrombotic stroke was larger than that of lacunar stroke , which seemed to correspond to the higher frequency of patients with diabetes mellitus and hyperlipidemia in these 3 districts .
	manualset3
86798	7	399546	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In Kanto , Kinki and Chugoku/Shikoku Districts , however , proportion of atherothrombotic stroke was larger than that of lacunar stroke , which seemed to correspond to the higher frequency of patients with diabetes mellitus and hyperlipidemia in these 3 districts .
	manualset3
86801	8	399546	5	NULL	NULL	0	NULL	diabetes mellitus	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In Kanto , Kinki and Chugoku/Shikoku Districts , however , proportion of atherothrombotic stroke was larger than that of lacunar stroke , which seemed to correspond to the higher frequency of patients with diabetes mellitus and hyperlipidemia in these 3 districts .
	manualset3
86805	9	399546	5	NULL	NULL	0	NULL	hyperlipidemia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In Kanto , Kinki and Chugoku/Shikoku Districts , however , proportion of atherothrombotic stroke was larger than that of lacunar stroke , which seemed to correspond to the higher frequency of patients with diabetes mellitus and hyperlipidemia in these 3 districts .
	manualset3
86807	10	399546	5	NULL	NULL	0	NULL	3 districts	UnproperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In Kanto , Kinki and Chugoku/Shikoku Districts , however , proportion of atherothrombotic stroke was larger than that of lacunar stroke , which seemed to correspond to the higher frequency of patients with diabetes mellitus and hyperlipidemia in these 3 districts .
	manualset3
86808	1	399547	5	NULL	NULL	0	NULL	MM	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In MM , the percentage of BM infiltration and Ki-67 index were positively associated with TRF2 , TANK1 and hTERT expression ( P 0.03 ) and negatively with TL ( P = 0.02 ) , whereas lactate dehydrogenase was significantly correlated with TRF2 mRNA ( P = 0.008 ) .
	manualset3
86817	2	399547	5	NULL	NULL	0	NULL	BM infiltration	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In MM , the percentage of BM infiltration and Ki-67 index were positively associated with TRF2 , TANK1 and hTERT expression ( P 0.03 ) and negatively with TL ( P = 0.02 ) , whereas lactate dehydrogenase was significantly correlated with TRF2 mRNA ( P = 0.008 ) .
	manualset3
86937	3	399547	5	NULL	NULL	0	NULL	Ki-67 index	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In MM , the percentage of BM infiltration and Ki-67 index were positively associated with TRF2 , TANK1 and hTERT expression ( P 0.03 ) and negatively with TL ( P = 0.02 ) , whereas lactate dehydrogenase was significantly correlated with TRF2 mRNA ( P = 0.008 ) .
	manualset3
86938	4	399547	5	NULL	NULL	0	NULL	TRF2 expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In MM , the percentage of BM infiltration and Ki-67 index were positively associated with TRF2 , TANK1 and hTERT expression ( P 0.03 ) and negatively with TL ( P = 0.02 ) , whereas lactate dehydrogenase was significantly correlated with TRF2 mRNA ( P = 0.008 ) .
	manualset3
86939	5	399547	5	NULL	NULL	0	NULL	TANK1 expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In MM , the percentage of BM infiltration and Ki-67 index were positively associated with TRF2 , TANK1 and hTERT expression ( P 0.03 ) and negatively with TL ( P = 0.02 ) , whereas lactate dehydrogenase was significantly correlated with TRF2 mRNA ( P = 0.008 ) .
	manualset3
86940	6	399547	5	NULL	NULL	0	NULL	hTERT expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In MM , the percentage of BM infiltration and Ki-67 index were positively associated with TRF2 , TANK1 and hTERT expression ( P 0.03 ) and negatively with TL ( P = 0.02 ) , whereas lactate dehydrogenase was significantly correlated with TRF2 mRNA ( P = 0.008 ) .
	manualset3
86941	7	399547	5	NULL	NULL	0	NULL	P 0.03	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In MM , the percentage of BM infiltration and Ki-67 index were positively associated with TRF2 , TANK1 and hTERT expression ( P 0.03 ) and negatively with TL ( P = 0.02 ) , whereas lactate dehydrogenase was significantly correlated with TRF2 mRNA ( P = 0.008 ) .
	manualset3
86942	8	399547	5	NULL	NULL	0	NULL	TL	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In MM , the percentage of BM infiltration and Ki-67 index were positively associated with TRF2 , TANK1 and hTERT expression ( P 0.03 ) and negatively with TL ( P = 0.02 ) , whereas lactate dehydrogenase was significantly correlated with TRF2 mRNA ( P = 0.008 ) .
	manualset3
86943	9	399547	5	NULL	NULL	NULL	NULL	P = 0.02	Measurement												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In MM , the percentage of BM infiltration and Ki-67 index were positively associated with TRF2 , TANK1 and hTERT expression ( P 0.03 ) and negatively with TL ( P = 0.02 ) , whereas lactate dehydrogenase was significantly correlated with TRF2 mRNA ( P = 0.008 ) .
	manualset3
86944	10	399547	5	NULL	NULL	0	NULL	lactate dehydrogenase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In MM , the percentage of BM infiltration and Ki-67 index were positively associated with TRF2 , TANK1 and hTERT expression ( P 0.03 ) and negatively with TL ( P = 0.02 ) , whereas lactate dehydrogenase was significantly correlated with TRF2 mRNA ( P = 0.008 ) .
	manualset3
86945	11	399547	5	NULL	NULL	0	NULL	TRF2 mRNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	In MM , the percentage of BM infiltration and Ki-67 index were positively associated with TRF2 , TANK1 and hTERT expression ( P 0.03 ) and negatively with TL ( P = 0.02 ) , whereas lactate dehydrogenase was significantly correlated with TRF2 mRNA ( P = 0.008 ) .
	manualset3
86946	12	399547	5	NULL	NULL	0	NULL	P = 0.008	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In MM , the percentage of BM infiltration and Ki-67 index were positively associated with TRF2 , TANK1 and hTERT expression ( P 0.03 ) and negatively with TL ( P = 0.02 ) , whereas lactate dehydrogenase was significantly correlated with TRF2 mRNA ( P = 0.008 ) .
	manualset3
86947	1	399548	5	NULL	NULL	NULL	NULL	P3	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In P3 , two out of nine amino acid changes occur in hydrophilic regions .
	manualset3
86948	2	399548	5	NULL	NULL	NULL	NULL	two out of nine amino acid changes	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In P3 , two out of nine amino acid changes occur in hydrophilic regions .
	manualset3
86949	3	399548	5	NULL	NULL	0	NULL	hydrophilic regions	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	In P3 , two out of nine amino acid changes occur in hydrophilic regions .
	manualset3
86950	1	399549	5	NULL	NULL	NULL	NULL	PD	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In PD , ERC atrophy , as measured on MRI , however , has received less attention , compared to hippocampal atrophy .
	manualset3
86951	2	399549	5	NULL	NULL	0	NULL	ERC atrophy	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In PD , ERC atrophy , as measured on MRI , however , has received less attention , compared to hippocampal atrophy .
	manualset3
86952	3	399549	5	NULL	NULL	NULL	NULL	MRI	MedicalDevice												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In PD , ERC atrophy , as measured on MRI , however , has received less attention , compared to hippocampal atrophy .
	manualset3
86953	4	399549	5	NULL	NULL	0	NULL	attention	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In PD , ERC atrophy , as measured on MRI , however , has received less attention , compared to hippocampal atrophy .
	manualset3
86954	5	399549	5	NULL	NULL	0	NULL	hippocampal atrophy	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In PD , ERC atrophy , as measured on MRI , however , has received less attention , compared to hippocampal atrophy .
	manualset3
86955	1	399550	5	NULL	NULL	0	NULL	Spain	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In Spain , a close relationship has been found between the yearly rate of aminopenicillin consumption and penicillin resistance .
	manualset3
86956	2	399550	5	NULL	NULL	0	NULL	close relationship	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	In Spain , a close relationship has been found between the yearly rate of aminopenicillin consumption and penicillin resistance .
	manualset3
86957	3	399550	5	NULL	NULL	0	NULL	yearly rate	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In Spain , a close relationship has been found between the yearly rate of aminopenicillin consumption and penicillin resistance .
	manualset3
86958	4	399550	5	NULL	NULL	0	NULL	aminopenicillin consumption	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In Spain , a close relationship has been found between the yearly rate of aminopenicillin consumption and penicillin resistance .
	manualset3
86959	5	399550	5	NULL	NULL	0	NULL	penicillin resistance	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In Spain , a close relationship has been found between the yearly rate of aminopenicillin consumption and penicillin resistance .
	manualset3
86960	1	399551	5	NULL	NULL	0	NULL	Xenopus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In Xenopus , Cdk1 phosphorylates Emi2 and both destabilizes and inactivates it , whereas Mos recruits PP2A phosphatase to antagonize the Cdk1 phosphorylation .
	manualset3
86961	2	399551	5	NULL	NULL	0	NULL	Cdk1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In Xenopus , Cdk1 phosphorylates Emi2 and both destabilizes and inactivates it , whereas Mos recruits PP2A phosphatase to antagonize the Cdk1 phosphorylation .
	manualset3
86962	3	399551	5	NULL	NULL	0	NULL	Emi2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In Xenopus , Cdk1 phosphorylates Emi2 and both destabilizes and inactivates it , whereas Mos recruits PP2A phosphatase to antagonize the Cdk1 phosphorylation .
	manualset3
86963	4	399551	5	NULL	NULL	0	NULL	Mos	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In Xenopus , Cdk1 phosphorylates Emi2 and both destabilizes and inactivates it , whereas Mos recruits PP2A phosphatase to antagonize the Cdk1 phosphorylation .
	manualset3
86964	5	399551	5	NULL	NULL	0	NULL	PP2A phosphatase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In Xenopus , Cdk1 phosphorylates Emi2 and both destabilizes and inactivates it , whereas Mos recruits PP2A phosphatase to antagonize the Cdk1 phosphorylation .
	manualset3
86965	6	399551	5	NULL	NULL	0	NULL	Cdk1 phosphorylation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In Xenopus , Cdk1 phosphorylates Emi2 and both destabilizes and inactivates it , whereas Mos recruits PP2A phosphatase to antagonize the Cdk1 phosphorylation .
	manualset3
86966	1	399552	5	NULL	NULL	0	NULL	B-Myb	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In accordance , B-Myb also elevates endogenous A ( 2B ) AR mRNA and receptor activity , and this activity decreases cell proliferation .
	manualset3
86967	2	399552	5	NULL	NULL	0	NULL	endogenous A ( 2B ) AR mRNA	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	In accordance , B-Myb also elevates endogenous A ( 2B ) AR mRNA and receptor activity , and this activity decreases cell proliferation .
	manualset3
86968	3	399552	5	NULL	NULL	0	NULL	receptor activity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In accordance , B-Myb also elevates endogenous A ( 2B ) AR mRNA and receptor activity , and this activity decreases cell proliferation .
	manualset3
86969	4	399552	5	NULL	NULL	0	NULL	activity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In accordance , B-Myb also elevates endogenous A ( 2B ) AR mRNA and receptor activity , and this activity decreases cell proliferation .
	manualset3
86970	5	399552	5	NULL	NULL	0	NULL	cell proliferation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In accordance , B-Myb also elevates endogenous A ( 2B ) AR mRNA and receptor activity , and this activity decreases cell proliferation .
	manualset3
86971	1	399553	5	NULL	NULL	0	NULL	age-associated telomere attrition rate	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In accordance , the age-associated telomere attrition rate was more prominent in families with members displaying longer telomeres at a young age ( r = -0.691 , P & lt ; 0.001 ) .
	manualset3
86972	2	399553	5	NULL	NULL	0	NULL	families	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In accordance , the age-associated telomere attrition rate was more prominent in families with members displaying longer telomeres at a young age ( r = -0.691 , P & lt ; 0.001 ) .
	manualset3
86973	3	399553	5	NULL	NULL	0	NULL	members	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In accordance , the age-associated telomere attrition rate was more prominent in families with members displaying longer telomeres at a young age ( r = -0.691 , P & lt ; 0.001 ) .
	manualset3
86974	4	399553	5	NULL	NULL	0	NULL	telomeres	Chromosome												NULL		0	NULL	NULL	NULL	NULL	NULL	In accordance , the age-associated telomere attrition rate was more prominent in families with members displaying longer telomeres at a young age ( r = -0.691 , P & lt ; 0.001 ) .
	manualset3
86975	5	399553	5	NULL	NULL	0	NULL	young age	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	In accordance , the age-associated telomere attrition rate was more prominent in families with members displaying longer telomeres at a young age ( r = -0.691 , P & lt ; 0.001 ) .
	manualset3
86976	6	399553	5	NULL	NULL	0	NULL	r = -0.691 , P & lt ; 0.001	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In accordance , the age-associated telomere attrition rate was more prominent in families with members displaying longer telomeres at a young age ( r = -0.691 , P & lt ; 0.001 ) .
	manualset3
86981	1	399555	5	NULL	NULL	NULL	NULL	determinations of phospholipase activity	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In agreement , determinations of phospholipase activity disclosed the presence of a phospholipase A2 in the fluid phase of synovial effusions .
	manualset3
86983	2	399555	5	NULL	NULL	NULL	NULL	phospholipase A2	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In agreement , determinations of phospholipase activity disclosed the presence of a phospholipase A2 in the fluid phase of synovial effusions .
	manualset3
86984	3	399555	5	NULL	NULL	NULL	NULL	fluid phase of synovial effusions	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In agreement , determinations of phospholipase activity disclosed the presence of a phospholipase A2 in the fluid phase of synovial effusions .
	manualset3
86985	1	399556	5	NULL	NULL	0	NULL	cardiomyocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In cardiomyocytes , Gq activates only one splice variant of one subtype of phospholipase Cbeta , specifically phospholipase Cbeta1b ( PLCbeta1b ) and PLCbeta1b is responsible for Gq mediated hypertrophic and apoptotic responses .
	manualset3
86986	2	399556	5	NULL	NULL	NULL	NULL	Gq	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In cardiomyocytes , Gq activates only one splice variant of one subtype of phospholipase Cbeta , specifically phospholipase Cbeta1b ( PLCbeta1b ) and PLCbeta1b is responsible for Gq mediated hypertrophic and apoptotic responses .
	manualset3
86987	3	399556	5	NULL	NULL	NULL	NULL	splice variant of one subtype of phospholipase Cbeta	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In cardiomyocytes , Gq activates only one splice variant of one subtype of phospholipase Cbeta , specifically phospholipase Cbeta1b ( PLCbeta1b ) and PLCbeta1b is responsible for Gq mediated hypertrophic and apoptotic responses .
	manualset3
86988	4	399556	5	NULL	NULL	0	NULL	phospholipase Cbeta1b ( PLCbeta1b )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In cardiomyocytes , Gq activates only one splice variant of one subtype of phospholipase Cbeta , specifically phospholipase Cbeta1b ( PLCbeta1b ) and PLCbeta1b is responsible for Gq mediated hypertrophic and apoptotic responses .
	manualset3
86989	5	399556	5	NULL	NULL	0	NULL	PLCbeta1b	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In cardiomyocytes , Gq activates only one splice variant of one subtype of phospholipase Cbeta , specifically phospholipase Cbeta1b ( PLCbeta1b ) and PLCbeta1b is responsible for Gq mediated hypertrophic and apoptotic responses .
	manualset3
86990	6	399556	5	NULL	NULL	NULL	NULL	Gq mediated hypertrophic responses	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In cardiomyocytes , Gq activates only one splice variant of one subtype of phospholipase Cbeta , specifically phospholipase Cbeta1b ( PLCbeta1b ) and PLCbeta1b is responsible for Gq mediated hypertrophic and apoptotic responses .
	manualset3
86991	7	399556	5	NULL	NULL	0	NULL	Gq mediated apoptotic responses	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In cardiomyocytes , Gq activates only one splice variant of one subtype of phospholipase Cbeta , specifically phospholipase Cbeta1b ( PLCbeta1b ) and PLCbeta1b is responsible for Gq mediated hypertrophic and apoptotic responses .
	manualset3
86992	1	399557	5	NULL	NULL	0	NULL	children	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In children , consumption of soy-based formulas and soy milk can lead to high levels of exposure to phytoestrogens with only limited data available concerning potential benefits or adverse effects .
	manualset3
86993	2	399557	5	NULL	NULL	0	NULL	consumption	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In children , consumption of soy-based formulas and soy milk can lead to high levels of exposure to phytoestrogens with only limited data available concerning potential benefits or adverse effects .
	manualset3
86994	3	399557	5	NULL	NULL	0	NULL	soy-based formulas	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	In children , consumption of soy-based formulas and soy milk can lead to high levels of exposure to phytoestrogens with only limited data available concerning potential benefits or adverse effects .
	manualset3
86995	4	399557	5	NULL	NULL	0	NULL	soy milk	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	In children , consumption of soy-based formulas and soy milk can lead to high levels of exposure to phytoestrogens with only limited data available concerning potential benefits or adverse effects .
	manualset3
86996	5	399557	5	NULL	NULL	NULL	NULL	high levels of exposure to phytoestrogens	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In children , consumption of soy-based formulas and soy milk can lead to high levels of exposure to phytoestrogens with only limited data available concerning potential benefits or adverse effects .
	manualset3
86997	6	399557	5	NULL	NULL	0	NULL	limited data	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	In children , consumption of soy-based formulas and soy milk can lead to high levels of exposure to phytoestrogens with only limited data available concerning potential benefits or adverse effects .
	manualset3
86998	7	399557	5	NULL	NULL	0	NULL	potential benefits or adverse effects	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In children , consumption of soy-based formulas and soy milk can lead to high levels of exposure to phytoestrogens with only limited data available concerning potential benefits or adverse effects .
	manualset3
87103	1	399558	5	NULL	NULL	0	NULL	antagonists	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In combination , these antagonists almost completely inhibited contraction to both agents .
	manualset3
87105	2	399558	5	NULL	NULL	0	NULL	contraction	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In combination , these antagonists almost completely inhibited contraction to both agents .
	manualset3
87107	3	399558	5	NULL	NULL	0	NULL	agents	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In combination , these antagonists almost completely inhibited contraction to both agents .
	manualset3
87109	1	399559	5	NULL	NULL	0	NULL	smaller plasma forms	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In comparison , smaller plasma forms circulating in blood bind platelets only under high fluid shear stress or induced by modulators .
	manualset3
87110	2	399559	5	NULL	NULL	0	NULL	blood	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	In comparison , smaller plasma forms circulating in blood bind platelets only under high fluid shear stress or induced by modulators .
	manualset3
87111	3	399559	5	NULL	NULL	0	NULL	platelets	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In comparison , smaller plasma forms circulating in blood bind platelets only under high fluid shear stress or induced by modulators .
	manualset3
87112	4	399559	5	NULL	NULL	0	NULL	high fluid shear stress	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	In comparison , smaller plasma forms circulating in blood bind platelets only under high fluid shear stress or induced by modulators .
	manualset3
87113	5	399559	5	NULL	NULL	0	NULL	modulators	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In comparison , smaller plasma forms circulating in blood bind platelets only under high fluid shear stress or induced by modulators .
	manualset3
87115	1	399560	5	NULL	NULL	0	NULL	CCK	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , CCK is a potential candidate as a physiological factor regulating insulin secretion in sheep .
	manualset3
87116	2	399560	5	NULL	NULL	0	NULL	potential candidate	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , CCK is a potential candidate as a physiological factor regulating insulin secretion in sheep .
	manualset3
87117	3	399560	5	NULL	NULL	0	NULL	physiological factor	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , CCK is a potential candidate as a physiological factor regulating insulin secretion in sheep .
	manualset3
87121	4	399560	5	NULL	NULL	0	NULL	insulin secretion	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , CCK is a potential candidate as a physiological factor regulating insulin secretion in sheep .
	manualset3
87122	5	399560	5	NULL	NULL	0	NULL	sheep	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , CCK is a potential candidate as a physiological factor regulating insulin secretion in sheep .
	manualset3
87123	1	399561	5	NULL	NULL	0	NULL	CHB patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , CHB patients with genotype B , G1896A , and A1762T/G1764A had a higher tendency to develop liver failure than patients with genotype C. Therefore , HBV genotyping and detecting G1896A and A1762T/G1764A mutations might have important clinical implications as predictive risk factors for hepatitis B-related acute-on-chronic liver failure .
	manualset3
87127	2	399561	5	NULL	NULL	0	NULL	genotype B , G1896A , and A1762T/G1764A	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , CHB patients with genotype B , G1896A , and A1762T/G1764A had a higher tendency to develop liver failure than patients with genotype C. Therefore , HBV genotyping and detecting G1896A and A1762T/G1764A mutations might have important clinical implications as predictive risk factors for hepatitis B-related acute-on-chronic liver failure .
	manualset3
87128	3	399561	5	NULL	NULL	0	NULL	liver failure	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , CHB patients with genotype B , G1896A , and A1762T/G1764A had a higher tendency to develop liver failure than patients with genotype C. Therefore , HBV genotyping and detecting G1896A and A1762T/G1764A mutations might have important clinical implications as predictive risk factors for hepatitis B-related acute-on-chronic liver failure .
	manualset3
87129	4	399561	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , CHB patients with genotype B , G1896A , and A1762T/G1764A had a higher tendency to develop liver failure than patients with genotype C. Therefore , HBV genotyping and detecting G1896A and A1762T/G1764A mutations might have important clinical implications as predictive risk factors for hepatitis B-related acute-on-chronic liver failure .
	manualset3
87130	5	399561	5	NULL	NULL	0	NULL	genotype C	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , CHB patients with genotype B , G1896A , and A1762T/G1764A had a higher tendency to develop liver failure than patients with genotype C. Therefore , HBV genotyping and detecting G1896A and A1762T/G1764A mutations might have important clinical implications as predictive risk factors for hepatitis B-related acute-on-chronic liver failure .
	manualset3
87133	6	399561	5	NULL	NULL	0	NULL	HBV genotyping	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , CHB patients with genotype B , G1896A , and A1762T/G1764A had a higher tendency to develop liver failure than patients with genotype C. Therefore , HBV genotyping and detecting G1896A and A1762T/G1764A mutations might have important clinical implications as predictive risk factors for hepatitis B-related acute-on-chronic liver failure .
	manualset3
87134	7	399561	5	NULL	NULL	0	NULL	G1896A and A1762T/G1764A mutations	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , CHB patients with genotype B , G1896A , and A1762T/G1764A had a higher tendency to develop liver failure than patients with genotype C. Therefore , HBV genotyping and detecting G1896A and A1762T/G1764A mutations might have important clinical implications as predictive risk factors for hepatitis B-related acute-on-chronic liver failure .
	manualset3
87135	8	399561	5	NULL	NULL	0	NULL	important clinical implications	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , CHB patients with genotype B , G1896A , and A1762T/G1764A had a higher tendency to develop liver failure than patients with genotype C. Therefore , HBV genotyping and detecting G1896A and A1762T/G1764A mutations might have important clinical implications as predictive risk factors for hepatitis B-related acute-on-chronic liver failure .
	manualset3
87136	9	399561	5	NULL	NULL	NULL	NULL	predictive risk factors	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , CHB patients with genotype B , G1896A , and A1762T/G1764A had a higher tendency to develop liver failure than patients with genotype C. Therefore , HBV genotyping and detecting G1896A and A1762T/G1764A mutations might have important clinical implications as predictive risk factors for hepatitis B-related acute-on-chronic liver failure .
	manualset3
87137	10	399561	5	NULL	NULL	0	NULL	hepatitis B-related acute-on-chronic liver failure	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , CHB patients with genotype B , G1896A , and A1762T/G1764A had a higher tendency to develop liver failure than patients with genotype C. Therefore , HBV genotyping and detecting G1896A and A1762T/G1764A mutations might have important clinical implications as predictive risk factors for hepatitis B-related acute-on-chronic liver failure .
	manualset3
87139	2	399562	5	NULL	NULL	0	NULL	Candida albicans ATCC 90028	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , Candida albicans ATCC 90028 possesses an alternative electron transfer chain and alternative oxidase , both absent in animal cells .
	manualset3
87140	3	399562	5	NULL	NULL	0	NULL	alternative electron transfer chain	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , Candida albicans ATCC 90028 possesses an alternative electron transfer chain and alternative oxidase , both absent in animal cells .
	manualset3
87141	4	399562	5	NULL	NULL	0	NULL	alternative oxidase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , Candida albicans ATCC 90028 possesses an alternative electron transfer chain and alternative oxidase , both absent in animal cells .
	manualset3
87142	5	399562	5	NULL	NULL	0	NULL	animal cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , Candida albicans ATCC 90028 possesses an alternative electron transfer chain and alternative oxidase , both absent in animal cells .
	manualset3
87143	1	399563	5	NULL	NULL	0	NULL	structure-based design	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Towards structure-based design of novel inhibitors for V-ATPase ) .
	manualset3
87144	2	399563	5	NULL	NULL	0	NULL	novel inhibitors	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( Towards structure-based design of novel inhibitors for V-ATPase ) .
	manualset3
87145	3	399563	5	NULL	NULL	0	NULL	V-ATPase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	( Towards structure-based design of novel inhibitors for V-ATPase ) .
	manualset3
87147	1	399564	5	NULL	NULL	NULL	NULL	ET-1 secretion	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , ET-1 secretion is increased by Prepro-ET-1 overexpression .
	manualset3
87148	2	399564	5	NULL	NULL	NULL	NULL	Prepro-ET-1 overexpression	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , ET-1 secretion is increased by Prepro-ET-1 overexpression .
	manualset3
87150	2	399565	5	NULL	NULL	0	NULL	HDAC activity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , HDAC activity is not essential for the strong transcriptional repressor activity mediated by the KRAB domain of Kox1 in particular and , presumably , by KRAB domains in general .
	manualset3
87151	3	399565	5	NULL	NULL	0	NULL	strong transcriptional repressor activity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , HDAC activity is not essential for the strong transcriptional repressor activity mediated by the KRAB domain of Kox1 in particular and , presumably , by KRAB domains in general .
	manualset3
87152	4	399565	5	NULL	NULL	0	NULL	KRAB domain	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , HDAC activity is not essential for the strong transcriptional repressor activity mediated by the KRAB domain of Kox1 in particular and , presumably , by KRAB domains in general .
	manualset3
87153	5	399565	5	NULL	NULL	0	NULL	Kox1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , HDAC activity is not essential for the strong transcriptional repressor activity mediated by the KRAB domain of Kox1 in particular and , presumably , by KRAB domains in general .
	manualset3
87154	6	399565	5	NULL	NULL	0	NULL	KRAB domains	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , HDAC activity is not essential for the strong transcriptional repressor activity mediated by the KRAB domain of Kox1 in particular and , presumably , by KRAB domains in general .
	manualset3
87156	2	399566	5	NULL	NULL	0	NULL	JAK2 exon 12 mutation analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , JAK2 exon 12 mutation analysis contributes to diagnostics in polycythemia vera or erythrocytosis .
	manualset3
87157	3	399566	5	NULL	NULL	0	NULL	diagnostics	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , JAK2 exon 12 mutation analysis contributes to diagnostics in polycythemia vera or erythrocytosis .
	manualset3
87158	4	399566	5	NULL	NULL	0	NULL	polycythemia vera or erythrocytosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , JAK2 exon 12 mutation analysis contributes to diagnostics in polycythemia vera or erythrocytosis .
	manualset3
87160	2	399567	5	NULL	NULL	0	NULL	MVs	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , MVs released from MSCs were found to exert a pro-survival effect on renal cells in vitro and in vivo , suggesting that MVs may contribute to renal protection conferred by MSCs .
	manualset3
87161	3	399567	5	NULL	NULL	0	NULL	MSCs	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , MVs released from MSCs were found to exert a pro-survival effect on renal cells in vitro and in vivo , suggesting that MVs may contribute to renal protection conferred by MSCs .
	manualset3
87162	4	399567	5	NULL	NULL	0	NULL	pro-survival effect	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , MVs released from MSCs were found to exert a pro-survival effect on renal cells in vitro and in vivo , suggesting that MVs may contribute to renal protection conferred by MSCs .
	manualset3
87163	5	399567	5	NULL	NULL	0	NULL	renal cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , MVs released from MSCs were found to exert a pro-survival effect on renal cells in vitro and in vivo , suggesting that MVs may contribute to renal protection conferred by MSCs .
	manualset3
87164	6	399567	5	NULL	NULL	0	NULL	MVs	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , MVs released from MSCs were found to exert a pro-survival effect on renal cells in vitro and in vivo , suggesting that MVs may contribute to renal protection conferred by MSCs .
	manualset3
87165	7	399567	5	NULL	NULL	0	NULL	renal protection	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , MVs released from MSCs were found to exert a pro-survival effect on renal cells in vitro and in vivo , suggesting that MVs may contribute to renal protection conferred by MSCs .
	manualset3
87166	8	399567	5	NULL	NULL	0	NULL	MSCs	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , MVs released from MSCs were found to exert a pro-survival effect on renal cells in vitro and in vivo , suggesting that MVs may contribute to renal protection conferred by MSCs .
	manualset3
87168	2	399568	5	NULL	NULL	0	NULL	SK	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , SK & F L-94901 discriminates hepatic cells and pituitary cells at the nuclear transport process .
	manualset3
87169	3	399568	5	NULL	NULL	0	NULL	F L-94901	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , SK & F L-94901 discriminates hepatic cells and pituitary cells at the nuclear transport process .
	manualset3
87170	4	399568	5	NULL	NULL	0	NULL	hepatic cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , SK & F L-94901 discriminates hepatic cells and pituitary cells at the nuclear transport process .
	manualset3
87171	5	399568	5	NULL	NULL	0	NULL	pituitary cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , SK & F L-94901 discriminates hepatic cells and pituitary cells at the nuclear transport process .
	manualset3
87172	6	399568	5	NULL	NULL	0	NULL	nuclear transport process	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , SK & F L-94901 discriminates hepatic cells and pituitary cells at the nuclear transport process .
	manualset3
87174	2	399569	5	NULL	NULL	NULL	NULL	TiO ( 2 ) nanotubes	Facility												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , TiO ( 2 ) nanotubes can modulate bone formation events at the bone-implant interface as to reach favorable molecular response and osseointegration ; in addition , the diameters of nanotubes can be precisely controlled in order to obtain better bone formation .
	manualset3
87175	3	399569	5	NULL	NULL	0	NULL	bone formation events	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , TiO ( 2 ) nanotubes can modulate bone formation events at the bone-implant interface as to reach favorable molecular response and osseointegration ; in addition , the diameters of nanotubes can be precisely controlled in order to obtain better bone formation .
	manualset3
87176	4	399569	5	NULL	NULL	0	NULL	bone-implant interface	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , TiO ( 2 ) nanotubes can modulate bone formation events at the bone-implant interface as to reach favorable molecular response and osseointegration ; in addition , the diameters of nanotubes can be precisely controlled in order to obtain better bone formation .
	manualset3
87177	5	399569	5	NULL	NULL	0	NULL	favorable molecular response	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , TiO ( 2 ) nanotubes can modulate bone formation events at the bone-implant interface as to reach favorable molecular response and osseointegration ; in addition , the diameters of nanotubes can be precisely controlled in order to obtain better bone formation .
	manualset3
87178	6	399569	5	NULL	NULL	0	NULL	osseointegration	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , TiO ( 2 ) nanotubes can modulate bone formation events at the bone-implant interface as to reach favorable molecular response and osseointegration ; in addition , the diameters of nanotubes can be precisely controlled in order to obtain better bone formation .
	manualset3
87180	7	399569	5	NULL	NULL	0	NULL	diameters	QuantityOrMeasurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , TiO ( 2 ) nanotubes can modulate bone formation events at the bone-implant interface as to reach favorable molecular response and osseointegration ; in addition , the diameters of nanotubes can be precisely controlled in order to obtain better bone formation .
	manualset3
87181	8	399569	5	NULL	NULL	0	NULL	nanotubes	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , TiO ( 2 ) nanotubes can modulate bone formation events at the bone-implant interface as to reach favorable molecular response and osseointegration ; in addition , the diameters of nanotubes can be precisely controlled in order to obtain better bone formation .
	manualset3
87182	9	399569	5	NULL	NULL	0	NULL	bone formation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , TiO ( 2 ) nanotubes can modulate bone formation events at the bone-implant interface as to reach favorable molecular response and osseointegration ; in addition , the diameters of nanotubes can be precisely controlled in order to obtain better bone formation .
	manualset3
87186	2	399570	5	NULL	NULL	0	NULL	12-week dietary fat modification	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , a 12-week dietary fat modification did not affect the investigated markers of oxidative stress and inflammation among subjects with the MetS in the LIPGENE study .
	manualset3
87188	3	399570	5	NULL	NULL	0	NULL	markers of oxidative stress and inflammation	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , a 12-week dietary fat modification did not affect the investigated markers of oxidative stress and inflammation among subjects with the MetS in the LIPGENE study .
	manualset3
87191	4	399570	5	NULL	NULL	0	NULL	subjects	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , a 12-week dietary fat modification did not affect the investigated markers of oxidative stress and inflammation among subjects with the MetS in the LIPGENE study .
	manualset3
87192	5	399570	5	NULL	NULL	0	NULL	MetS	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , a 12-week dietary fat modification did not affect the investigated markers of oxidative stress and inflammation among subjects with the MetS in the LIPGENE study .
	manualset3
87193	6	399570	5	NULL	NULL	0	NULL	LIPGENE study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , a 12-week dietary fat modification did not affect the investigated markers of oxidative stress and inflammation among subjects with the MetS in the LIPGENE study .
	manualset3
87197	2	399571	5	NULL	NULL	0	NULL	Roux-en-Y gastric bypass	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , after Roux-en-Y gastric bypass , energy economy hampers the weight loss process , probably through a low fat oxidation rate .
	manualset3
87198	3	399571	5	NULL	NULL	0	NULL	energy economy	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , after Roux-en-Y gastric bypass , energy economy hampers the weight loss process , probably through a low fat oxidation rate .
	manualset3
87199	4	399571	5	NULL	NULL	0	NULL	weight loss process	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , after Roux-en-Y gastric bypass , energy economy hampers the weight loss process , probably through a low fat oxidation rate .
	manualset3
87201	5	399571	5	NULL	NULL	0	NULL	low fat oxidation rate	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , after Roux-en-Y gastric bypass , energy economy hampers the weight loss process , probably through a low fat oxidation rate .
	manualset3
87206	2	399572	5	NULL	NULL	0	NULL	detailed mechanism	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , although the detailed mechanism for the anti-tumor activity of the P. cocos beta-glucan still needs further investigation , this study provides preliminary insights into its mode of action and perspectives of its development as a water-soluble anti-tumor agent .
	manualset3
87207	3	399572	5	NULL	NULL	0	NULL	anti-tumor activity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , although the detailed mechanism for the anti-tumor activity of the P. cocos beta-glucan still needs further investigation , this study provides preliminary insights into its mode of action and perspectives of its development as a water-soluble anti-tumor agent .
	manualset3
87210	4	399572	5	NULL	NULL	0	NULL	P. cocos beta-glucan	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , although the detailed mechanism for the anti-tumor activity of the P. cocos beta-glucan still needs further investigation , this study provides preliminary insights into its mode of action and perspectives of its development as a water-soluble anti-tumor agent .
	manualset3
87211	5	399572	5	NULL	NULL	0	NULL	investigation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , although the detailed mechanism for the anti-tumor activity of the P. cocos beta-glucan still needs further investigation , this study provides preliminary insights into its mode of action and perspectives of its development as a water-soluble anti-tumor agent .
	manualset3
87212	6	399572	5	NULL	NULL	0	NULL	study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , although the detailed mechanism for the anti-tumor activity of the P. cocos beta-glucan still needs further investigation , this study provides preliminary insights into its mode of action and perspectives of its development as a water-soluble anti-tumor agent .
	manualset3
87214	7	399572	5	NULL	NULL	0	NULL	preliminary insights	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , although the detailed mechanism for the anti-tumor activity of the P. cocos beta-glucan still needs further investigation , this study provides preliminary insights into its mode of action and perspectives of its development as a water-soluble anti-tumor agent .
	manualset3
87215	8	399572	5	NULL	NULL	0	NULL	mode of action	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , although the detailed mechanism for the anti-tumor activity of the P. cocos beta-glucan still needs further investigation , this study provides preliminary insights into its mode of action and perspectives of its development as a water-soluble anti-tumor agent .
	manualset3
87218	9	399572	5	NULL	NULL	0	NULL	water-soluble anti-tumor agent	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , although the detailed mechanism for the anti-tumor activity of the P. cocos beta-glucan still needs further investigation , this study provides preliminary insights into its mode of action and perspectives of its development as a water-soluble anti-tumor agent .
	manualset3
87222	2	399573	5	NULL	NULL	0	NULL	anaplerosis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , anaplerosis that enhances the supply and utilization of alpha-ketoglutarate in the tricarboxylic acid cycle appears to play an essential role in the generation of TDP .
	manualset3
87224	3	399573	5	NULL	NULL	0	NULL	supply and utilization	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , anaplerosis that enhances the supply and utilization of alpha-ketoglutarate in the tricarboxylic acid cycle appears to play an essential role in the generation of TDP .
	manualset3
87226	4	399573	5	NULL	NULL	0	NULL	alpha-ketoglutarate	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , anaplerosis that enhances the supply and utilization of alpha-ketoglutarate in the tricarboxylic acid cycle appears to play an essential role in the generation of TDP .
	manualset3
87227	5	399573	5	NULL	NULL	0	NULL	tricarboxylic acid cycle	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , anaplerosis that enhances the supply and utilization of alpha-ketoglutarate in the tricarboxylic acid cycle appears to play an essential role in the generation of TDP .
	manualset3
87228	6	399573	5	NULL	NULL	0	NULL	generation of TDP	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , anaplerosis that enhances the supply and utilization of alpha-ketoglutarate in the tricarboxylic acid cycle appears to play an essential role in the generation of TDP .
	manualset3
87229	1	399574	5	NULL	NULL	0	NULL	Toxic reaction	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Toxic reaction to bupivacaine ) .
	manualset3
87230	2	399574	5	NULL	NULL	0	NULL	bupivacaine	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	( Toxic reaction to bupivacaine ) .
	manualset3
87235	2	399575	5	NULL	NULL	0	NULL	antimelanoma MoAb	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , antimelanoma MoAb was of little help in radioimaging and stating this disease .
	manualset3
87238	3	399575	5	NULL	NULL	0	NULL	radioimaging	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , antimelanoma MoAb was of little help in radioimaging and stating this disease .
	manualset3
87239	4	399575	5	NULL	NULL	0	NULL	disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , antimelanoma MoAb was of little help in radioimaging and stating this disease .
	manualset3
87241	2	399576	5	NULL	NULL	0	NULL	cartilage	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , cartilage is an available , costless , reliable and technically easy to use graft material for functional reconstructions of the ossicular chain .
	manualset3
87242	3	399576	5	NULL	NULL	0	NULL	graft material	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , cartilage is an available , costless , reliable and technically easy to use graft material for functional reconstructions of the ossicular chain .
	manualset3
87243	4	399576	5	NULL	NULL	0	NULL	functional reconstructions	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , cartilage is an available , costless , reliable and technically easy to use graft material for functional reconstructions of the ossicular chain .
	manualset3
87244	5	399576	5	NULL	NULL	0	NULL	ossicular chain	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , cartilage is an available , costless , reliable and technically easy to use graft material for functional reconstructions of the ossicular chain .
	manualset3
87246	2	399577	5	NULL	NULL	NULL	NULL	claudin-6 immunohistochemistry	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , claudin-6 immunohistochemistry is of limited sensitivity and specificity for the diagnosis of AT/RT and does not correlate with clinical behavior .
	manualset3
87247	3	399577	5	NULL	NULL	0	NULL	limited sensitivity	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , claudin-6 immunohistochemistry is of limited sensitivity and specificity for the diagnosis of AT/RT and does not correlate with clinical behavior .
	manualset3
87248	4	399577	5	NULL	NULL	0	NULL	specificity	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , claudin-6 immunohistochemistry is of limited sensitivity and specificity for the diagnosis of AT/RT and does not correlate with clinical behavior .
	manualset3
87249	5	399577	5	NULL	NULL	0	NULL	 diagnosis of AT/RT	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , claudin-6 immunohistochemistry is of limited sensitivity and specificity for the diagnosis of AT/RT and does not correlate with clinical behavior .
	manualset3
87250	6	399577	5	NULL	NULL	0	NULL	clinical behavior	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , claudin-6 immunohistochemistry is of limited sensitivity and specificity for the diagnosis of AT/RT and does not correlate with clinical behavior .
	manualset3
87252	2	399578	5	NULL	NULL	0	NULL	consumption	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , consumption of drinking water , especially well water , with high nitrate levels can imply a genotoxic risk for humans as indicated by increased HPRT variant frequencies and by endogenous formation of carcinogenic N-nitroso compounds from nitrate-derived nitrite .
	manualset3
87253	3	399578	5	NULL	NULL	0	NULL	drinking water	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , consumption of drinking water , especially well water , with high nitrate levels can imply a genotoxic risk for humans as indicated by increased HPRT variant frequencies and by endogenous formation of carcinogenic N-nitroso compounds from nitrate-derived nitrite .
	manualset3
87254	4	399578	5	NULL	NULL	0	NULL	well water	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , consumption of drinking water , especially well water , with high nitrate levels can imply a genotoxic risk for humans as indicated by increased HPRT variant frequencies and by endogenous formation of carcinogenic N-nitroso compounds from nitrate-derived nitrite .
	manualset3
87255	5	399578	5	NULL	NULL	0	NULL	high nitrate levels	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , consumption of drinking water , especially well water , with high nitrate levels can imply a genotoxic risk for humans as indicated by increased HPRT variant frequencies and by endogenous formation of carcinogenic N-nitroso compounds from nitrate-derived nitrite .
	manualset3
87256	6	399578	5	NULL	NULL	0	NULL	genotoxic risk	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , consumption of drinking water , especially well water , with high nitrate levels can imply a genotoxic risk for humans as indicated by increased HPRT variant frequencies and by endogenous formation of carcinogenic N-nitroso compounds from nitrate-derived nitrite .
	manualset3
87257	7	399578	5	NULL	NULL	0	NULL	humans	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , consumption of drinking water , especially well water , with high nitrate levels can imply a genotoxic risk for humans as indicated by increased HPRT variant frequencies and by endogenous formation of carcinogenic N-nitroso compounds from nitrate-derived nitrite .
	manualset3
87258	8	399578	5	NULL	NULL	0	NULL	increased HPRT variant frequencies	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , consumption of drinking water , especially well water , with high nitrate levels can imply a genotoxic risk for humans as indicated by increased HPRT variant frequencies and by endogenous formation of carcinogenic N-nitroso compounds from nitrate-derived nitrite .
	manualset3
87259	9	399578	5	NULL	NULL	0	NULL	endogenous formation of carcinogenic N-nitroso compounds from nitrate-derived nitrite	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , consumption of drinking water , especially well water , with high nitrate levels can imply a genotoxic risk for humans as indicated by increased HPRT variant frequencies and by endogenous formation of carcinogenic N-nitroso compounds from nitrate-derived nitrite .
	manualset3
87261	2	399579	5	NULL	NULL	0	NULL	higher risk profile	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , despite a higher risk profile , CPS allowed longer balloon inflations and higher PTCA success rates compared to IABP .
	manualset3
87263	3	399579	5	NULL	NULL	0	NULL	CPS	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , despite a higher risk profile , CPS allowed longer balloon inflations and higher PTCA success rates compared to IABP .
	manualset3
87265	4	399579	5	NULL	NULL	0	NULL	longer balloon inflations	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , despite a higher risk profile , CPS allowed longer balloon inflations and higher PTCA success rates compared to IABP .
	manualset3
87266	5	399579	5	NULL	NULL	0	NULL	higher PTCA success rates	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , despite a higher risk profile , CPS allowed longer balloon inflations and higher PTCA success rates compared to IABP .
	manualset3
87269	6	399579	5	NULL	NULL	0	NULL	IABP	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , despite a higher risk profile , CPS allowed longer balloon inflations and higher PTCA success rates compared to IABP .
	manualset3
87271	2	399580	5	NULL	NULL	0	NULL	early controlled mobilization	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , early controlled mobilization using a hinged wrist splint may optimize the recovery period while retaining the desired arc of motion that is set intraoperatively .
	manualset3
87272	3	399580	5	NULL	NULL	0	NULL	hinged wrist splint	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , early controlled mobilization using a hinged wrist splint may optimize the recovery period while retaining the desired arc of motion that is set intraoperatively .
	manualset3
87273	4	399580	5	NULL	NULL	0	NULL	recovery period	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , early controlled mobilization using a hinged wrist splint may optimize the recovery period while retaining the desired arc of motion that is set intraoperatively .
	manualset3
87274	5	399580	5	NULL	NULL	0	NULL	desired arc of motion	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , early controlled mobilization using a hinged wrist splint may optimize the recovery period while retaining the desired arc of motion that is set intraoperatively .
	manualset3
87536	3	399581	5	NULL	NULL	NULL	NULL	DENV exposure	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , evidence for DENV exposure , presumably to DENV-2 , was identified in residents from Central Anatolian provinces of Ankara and Konya for the first time , however , seroreactivity detected against YFV could not be confirmed by PRNT .
	manualset3
87537	4	399581	5	NULL	NULL	0	NULL	DENV-2	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , evidence for DENV exposure , presumably to DENV-2 , was identified in residents from Central Anatolian provinces of Ankara and Konya for the first time , however , seroreactivity detected against YFV could not be confirmed by PRNT .
	manualset3
87538	5	399581	5	NULL	NULL	0	NULL	residents	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , evidence for DENV exposure , presumably to DENV-2 , was identified in residents from Central Anatolian provinces of Ankara and Konya for the first time , however , seroreactivity detected against YFV could not be confirmed by PRNT .
	manualset3
87539	6	399581	5	NULL	NULL	0	NULL	Central Anatolian provinces of Ankara and Konya	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , evidence for DENV exposure , presumably to DENV-2 , was identified in residents from Central Anatolian provinces of Ankara and Konya for the first time , however , seroreactivity detected against YFV could not be confirmed by PRNT .
	manualset3
87540	7	399581	5	NULL	NULL	0	NULL	seroreactivity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , evidence for DENV exposure , presumably to DENV-2 , was identified in residents from Central Anatolian provinces of Ankara and Konya for the first time , however , seroreactivity detected against YFV could not be confirmed by PRNT .
	manualset3
87541	8	399581	5	NULL	NULL	0	NULL	YFV	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , evidence for DENV exposure , presumably to DENV-2 , was identified in residents from Central Anatolian provinces of Ankara and Konya for the first time , however , seroreactivity detected against YFV could not be confirmed by PRNT .
	manualset3
87542	9	399581	5	NULL	NULL	0	NULL	PRNT	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , evidence for DENV exposure , presumably to DENV-2 , was identified in residents from Central Anatolian provinces of Ankara and Konya for the first time , however , seroreactivity detected against YFV could not be confirmed by PRNT .
	manualset3
87544	2	399582	5	NULL	NULL	0	NULL	high concentration	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , high concentration of porphyrin precursors had little impact on renal function .
	manualset3
87545	3	399582	5	NULL	NULL	0	NULL	porphyrin precursors	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , high concentration of porphyrin precursors had little impact on renal function .
	manualset3
87546	4	399582	5	NULL	NULL	0	NULL	renal function	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , high concentration of porphyrin precursors had little impact on renal function .
	manualset3
87547	1	399583	5	NULL	NULL	0	NULL	Toxicity standardization	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Toxicity and sanitary standardization of melamine cyanurate ( experimental data ) ) .
	manualset3
87548	3	399583	5	NULL	NULL	NULL	NULL	melamine cyanurate	SmallMolecule												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Toxicity and sanitary standardization of melamine cyanurate ( experimental data ) ) .
	manualset3
87549	4	399583	5	NULL	NULL	0	NULL	experimental data	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	( Toxicity and sanitary standardization of melamine cyanurate ( experimental data ) ) .
	manualset3
87550	2	399583	5	NULL	NULL	0	NULL	sanitary standardization	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Toxicity and sanitary standardization of melamine cyanurate ( experimental data ) ) .
	manualset3
87552	2	399584	5	NULL	NULL	0	NULL	tube	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , inserting the tube from the apex could shorten the treatment period .
	manualset3
87553	3	399584	5	NULL	NULL	0	NULL	apex	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , inserting the tube from the apex could shorten the treatment period .
	manualset3
87554	4	399584	5	NULL	NULL	0	NULL	treatment period	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , inserting the tube from the apex could shorten the treatment period .
	manualset3
87556	2	399585	5	NULL	NULL	0	NULL	delivery vehicle	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , it is of critical importance that the delivery vehicle prevents extensive aggregation of hypericin before injection and assures an efficient transfer to serum lipoproteins upon injection .
	manualset3
87557	3	399585	5	NULL	NULL	NULL	NULL	extensive aggregation	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , it is of critical importance that the delivery vehicle prevents extensive aggregation of hypericin before injection and assures an efficient transfer to serum lipoproteins upon injection .
	manualset3
87558	4	399585	5	NULL	NULL	0	NULL	hypericin	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , it is of critical importance that the delivery vehicle prevents extensive aggregation of hypericin before injection and assures an efficient transfer to serum lipoproteins upon injection .
	manualset3
87559	5	399585	5	NULL	NULL	0	NULL	injection	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , it is of critical importance that the delivery vehicle prevents extensive aggregation of hypericin before injection and assures an efficient transfer to serum lipoproteins upon injection .
	manualset3
87560	6	399585	5	NULL	NULL	0	NULL	efficient transfer	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , it is of critical importance that the delivery vehicle prevents extensive aggregation of hypericin before injection and assures an efficient transfer to serum lipoproteins upon injection .
	manualset3
87561	7	399585	5	NULL	NULL	0	NULL	serum lipoproteins	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , it is of critical importance that the delivery vehicle prevents extensive aggregation of hypericin before injection and assures an efficient transfer to serum lipoproteins upon injection .
	manualset3
87562	8	399585	5	NULL	NULL	0	NULL	injection	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , it is of critical importance that the delivery vehicle prevents extensive aggregation of hypericin before injection and assures an efficient transfer to serum lipoproteins upon injection .
	manualset3
87564	2	399586	5	NULL	NULL	0	NULL	nicotine	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , nicotine enhances the chemoatactiveness of VSMC .
	manualset3
87565	3	399586	5	NULL	NULL	0	NULL	chemoatactiveness	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , nicotine enhances the chemoatactiveness of VSMC .
	manualset3
87566	4	399586	5	NULL	NULL	0	NULL	VSMC	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , nicotine enhances the chemoatactiveness of VSMC .
	manualset3
87568	2	399587	5	NULL	NULL	0	NULL	techniques	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , none of the techniques evaluated in this study was effective in providing complete removal of filling material from the root canals .
	manualset3
87569	3	399587	5	NULL	NULL	0	NULL	study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , none of the techniques evaluated in this study was effective in providing complete removal of filling material from the root canals .
	manualset3
87570	4	399587	5	NULL	NULL	0	NULL	complete removal of filling material	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , none of the techniques evaluated in this study was effective in providing complete removal of filling material from the root canals .
	manualset3
87571	5	399587	5	NULL	NULL	0	NULL	root canals	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , none of the techniques evaluated in this study was effective in providing complete removal of filling material from the root canals .
	manualset3
87573	2	399588	5	NULL	NULL	0	NULL	objective assessment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , objective assessment of cough is practical in infants , enabling the pattern of cough in illness and in health to be studied further .
	manualset3
87574	3	399588	5	NULL	NULL	0	NULL	cough	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , objective assessment of cough is practical in infants , enabling the pattern of cough in illness and in health to be studied further .
	manualset3
87575	4	399588	5	NULL	NULL	0	NULL	infants	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , objective assessment of cough is practical in infants , enabling the pattern of cough in illness and in health to be studied further .
	manualset3
87576	5	399588	5	NULL	NULL	0	NULL	cough	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , objective assessment of cough is practical in infants , enabling the pattern of cough in illness and in health to be studied further .
	manualset3
87577	6	399588	5	NULL	NULL	0	NULL	illness	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , objective assessment of cough is practical in infants , enabling the pattern of cough in illness and in health to be studied further .
	manualset3
87578	7	399588	5	NULL	NULL	NULL	NULL	health	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , objective assessment of cough is practical in infants , enabling the pattern of cough in illness and in health to be studied further .
	manualset3
87580	2	399589	5	NULL	NULL	0	NULL	data	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our data provide evidence that adiponectin is up-regulated in vivo and in vitro in human and rodent myotubes in response to inflammatory stimuli .
	manualset3
87581	3	399589	5	NULL	NULL	0	NULL	adiponectin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our data provide evidence that adiponectin is up-regulated in vivo and in vitro in human and rodent myotubes in response to inflammatory stimuli .
	manualset3
87585	4	399589	5	NULL	NULL	0	NULL	human	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our data provide evidence that adiponectin is up-regulated in vivo and in vitro in human and rodent myotubes in response to inflammatory stimuli .
	manualset3
87586	5	399589	5	NULL	NULL	0	NULL	rodent myotubes	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our data provide evidence that adiponectin is up-regulated in vivo and in vitro in human and rodent myotubes in response to inflammatory stimuli .
	manualset3
87587	6	399589	5	NULL	NULL	0	NULL	inflammatory stimuli	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our data provide evidence that adiponectin is up-regulated in vivo and in vitro in human and rodent myotubes in response to inflammatory stimuli .
	manualset3
87589	2	399590	5	NULL	NULL	0	NULL	T. b. brucei invasion	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our data show that T. b. brucei invasion of the brain is related to that of leukocytes and that minocycline can ameliorate the disease in trypanosome-infected mice .
	manualset3
87590	3	399590	5	NULL	NULL	0	NULL	brain	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our data show that T. b. brucei invasion of the brain is related to that of leukocytes and that minocycline can ameliorate the disease in trypanosome-infected mice .
	manualset3
87591	4	399590	5	NULL	NULL	0	NULL	leukocytes	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our data show that T. b. brucei invasion of the brain is related to that of leukocytes and that minocycline can ameliorate the disease in trypanosome-infected mice .
	manualset3
87592	5	399590	5	NULL	NULL	0	NULL	minocycline	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our data show that T. b. brucei invasion of the brain is related to that of leukocytes and that minocycline can ameliorate the disease in trypanosome-infected mice .
	manualset3
87593	6	399590	5	NULL	NULL	0	NULL	disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our data show that T. b. brucei invasion of the brain is related to that of leukocytes and that minocycline can ameliorate the disease in trypanosome-infected mice .
	manualset3
87594	7	399590	5	NULL	NULL	0	NULL	trypanosome-infected mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our data show that T. b. brucei invasion of the brain is related to that of leukocytes and that minocycline can ameliorate the disease in trypanosome-infected mice .
	manualset3
87596	2	399591	5	NULL	NULL	0	NULL	data	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our data support a role for ER in lung ADCAs , proposing a role for ER in lungcarcinogenesis , especially among smokers .
	manualset3
87597	3	399591	5	NULL	NULL	0	NULL	ER	GeneOrProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our data support a role for ER in lung ADCAs , proposing a role for ER in lungcarcinogenesis , especially among smokers .
	manualset3
87598	4	399591	5	NULL	NULL	0	NULL	lung ADCAs	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our data support a role for ER in lung ADCAs , proposing a role for ER in lungcarcinogenesis , especially among smokers .
	manualset3
87599	5	399591	5	NULL	NULL	0	NULL	ER	GeneOrProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our data support a role for ER in lung ADCAs , proposing a role for ER in lungcarcinogenesis , especially among smokers .
	manualset3
87600	6	399591	5	NULL	NULL	NULL	NULL	lungcarcinogenesis	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , our data support a role for ER in lung ADCAs , proposing a role for ER in lungcarcinogenesis , especially among smokers .
	manualset3
87601	7	399591	5	NULL	NULL	0	NULL	smokers	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our data support a role for ER in lung ADCAs , proposing a role for ER in lungcarcinogenesis , especially among smokers .
	manualset3
87604	1	399592	5	NULL	NULL	NULL	NULL	beta-adrenoceptor stimulation	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , our findings confirm that beta-adrenoceptor stimulation is one condition where there may be an increased role of I ( Ks ) in action potential repolarisation .
	manualset3
87605	2	399592	5	NULL	NULL	NULL	NULL	role	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , our findings confirm that beta-adrenoceptor stimulation is one condition where there may be an increased role of I ( Ks ) in action potential repolarisation .
	manualset3
87606	3	399592	5	NULL	NULL	NULL	NULL	I ( Ks )	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , our findings confirm that beta-adrenoceptor stimulation is one condition where there may be an increased role of I ( Ks ) in action potential repolarisation .
	manualset3
87607	4	399592	5	NULL	NULL	NULL	NULL	action potential repolarisation	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , our findings confirm that beta-adrenoceptor stimulation is one condition where there may be an increased role of I ( Ks ) in action potential repolarisation .
	manualset3
87610	3	399593	5	NULL	NULL	0	NULL	expression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our findings indicate that expression of TGF-alpha gene and protein in normal blood eosinophils is differently regulated by GM-CSF and IL-3 .
	manualset3
87611	4	399593	5	NULL	NULL	0	NULL	TGF-alpha gene	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our findings indicate that expression of TGF-alpha gene and protein in normal blood eosinophils is differently regulated by GM-CSF and IL-3 .
	manualset3
87612	5	399593	5	NULL	NULL	0	NULL	TGF-alpha protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our findings indicate that expression of TGF-alpha gene and protein in normal blood eosinophils is differently regulated by GM-CSF and IL-3 .
	manualset3
87613	6	399593	5	NULL	NULL	0	NULL	normal blood eosinophils	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our findings indicate that expression of TGF-alpha gene and protein in normal blood eosinophils is differently regulated by GM-CSF and IL-3 .
	manualset3
87614	7	399593	5	NULL	NULL	0	NULL	GM-CSF	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our findings indicate that expression of TGF-alpha gene and protein in normal blood eosinophils is differently regulated by GM-CSF and IL-3 .
	manualset3
87615	8	399593	5	NULL	NULL	0	NULL	IL-3	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our findings indicate that expression of TGF-alpha gene and protein in normal blood eosinophils is differently regulated by GM-CSF and IL-3 .
	manualset3
87617	2	399594	5	NULL	NULL	NULL	NULL	results	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , our results imply a molecular mechanism for SAHA-induced apoptosis in BV-173 cells , which involves decreased protein expression levels of Bcr-Abl , c-Myc and HDAC3 .
	manualset3
87618	3	399594	5	NULL	NULL	0	NULL	molecular mechanism	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our results imply a molecular mechanism for SAHA-induced apoptosis in BV-173 cells , which involves decreased protein expression levels of Bcr-Abl , c-Myc and HDAC3 .
	manualset3
87619	4	399594	5	NULL	NULL	0	NULL	SAHA-induced apoptosis	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our results imply a molecular mechanism for SAHA-induced apoptosis in BV-173 cells , which involves decreased protein expression levels of Bcr-Abl , c-Myc and HDAC3 .
	manualset3
87620	5	399594	5	NULL	NULL	0	NULL	BV-173 cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our results imply a molecular mechanism for SAHA-induced apoptosis in BV-173 cells , which involves decreased protein expression levels of Bcr-Abl , c-Myc and HDAC3 .
	manualset3
87621	6	399594	5	NULL	NULL	0	NULL	protein expression levels	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our results imply a molecular mechanism for SAHA-induced apoptosis in BV-173 cells , which involves decreased protein expression levels of Bcr-Abl , c-Myc and HDAC3 .
	manualset3
87622	7	399594	5	NULL	NULL	0	NULL	Bcr-Abl	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our results imply a molecular mechanism for SAHA-induced apoptosis in BV-173 cells , which involves decreased protein expression levels of Bcr-Abl , c-Myc and HDAC3 .
	manualset3
87623	8	399594	5	NULL	NULL	0	NULL	c-Myc	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our results imply a molecular mechanism for SAHA-induced apoptosis in BV-173 cells , which involves decreased protein expression levels of Bcr-Abl , c-Myc and HDAC3 .
	manualset3
87624	9	399594	5	NULL	NULL	0	NULL	HDAC3	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our results imply a molecular mechanism for SAHA-induced apoptosis in BV-173 cells , which involves decreased protein expression levels of Bcr-Abl , c-Myc and HDAC3 .
	manualset3
87626	2	399595	5	NULL	NULL	0	NULL	results	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our results indicated that the knockdown of Cox-2 expression suppressed the proliferation and invasion of colorectal cancer cells both invitro and invivo .
	manualset3
87627	3	399595	5	NULL	NULL	0	NULL	 knockdown	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our results indicated that the knockdown of Cox-2 expression suppressed the proliferation and invasion of colorectal cancer cells both invitro and invivo .
	manualset3
87628	4	399595	5	NULL	NULL	0	NULL	Cox-2 expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our results indicated that the knockdown of Cox-2 expression suppressed the proliferation and invasion of colorectal cancer cells both invitro and invivo .
	manualset3
87629	5	399595	5	NULL	NULL	0	NULL	proliferation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our results indicated that the knockdown of Cox-2 expression suppressed the proliferation and invasion of colorectal cancer cells both invitro and invivo .
	manualset3
87630	6	399595	5	NULL	NULL	0	NULL	invasion	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our results indicated that the knockdown of Cox-2 expression suppressed the proliferation and invasion of colorectal cancer cells both invitro and invivo .
	manualset3
87631	7	399595	5	NULL	NULL	0	NULL	colorectal cancer cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , our results indicated that the knockdown of Cox-2 expression suppressed the proliferation and invasion of colorectal cancer cells both invitro and invivo .
	manualset3
87633	2	399596	5	NULL	NULL	0	NULL	oxidation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , oxidation of Trx1 and sustained Txnip expression in the lungs of newborn mice exposed to 85 % oxygen is likely to severely attenuate normal Trx1 function .
	manualset3
87634	3	399596	5	NULL	NULL	0	NULL	Trx1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , oxidation of Trx1 and sustained Txnip expression in the lungs of newborn mice exposed to 85 % oxygen is likely to severely attenuate normal Trx1 function .
	manualset3
87635	4	399596	5	NULL	NULL	0	NULL	sustained Txnip expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , oxidation of Trx1 and sustained Txnip expression in the lungs of newborn mice exposed to 85 % oxygen is likely to severely attenuate normal Trx1 function .
	manualset3
87636	5	399596	5	NULL	NULL	0	NULL	lungs	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , oxidation of Trx1 and sustained Txnip expression in the lungs of newborn mice exposed to 85 % oxygen is likely to severely attenuate normal Trx1 function .
	manualset3
87637	6	399596	5	NULL	NULL	0	NULL	newborn mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , oxidation of Trx1 and sustained Txnip expression in the lungs of newborn mice exposed to 85 % oxygen is likely to severely attenuate normal Trx1 function .
	manualset3
87638	7	399596	5	NULL	NULL	NULL	NULL	85 % oxygen	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , oxidation of Trx1 and sustained Txnip expression in the lungs of newborn mice exposed to 85 % oxygen is likely to severely attenuate normal Trx1 function .
	manualset3
87639	8	399596	5	NULL	NULL	0	NULL	normal Trx1 function	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , oxidation of Trx1 and sustained Txnip expression in the lungs of newborn mice exposed to 85 % oxygen is likely to severely attenuate normal Trx1 function .
	manualset3
87641	2	399597	5	NULL	NULL	0	NULL	p38 MAPK-induced myocardial ischemic injury	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , p38 MAPK-induced myocardial ischemic injury is not modulated by MK2 .
	manualset3
87642	3	399597	5	NULL	NULL	0	NULL	MK2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , p38 MAPK-induced myocardial ischemic injury is not modulated by MK2 .
	manualset3
87647	2	399599	5	NULL	NULL	0	NULL	sera	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , sera from AIH-1 patients reacted with the amino acids in the sequence 33-37 ( PQDGS ) of the N-terminal of UGT1A6 .
	manualset3
87648	3	399599	5	NULL	NULL	0	NULL	AIH-1 patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , sera from AIH-1 patients reacted with the amino acids in the sequence 33-37 ( PQDGS ) of the N-terminal of UGT1A6 .
	manualset3
87649	4	399599	5	NULL	NULL	0	NULL	amino acids	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , sera from AIH-1 patients reacted with the amino acids in the sequence 33-37 ( PQDGS ) of the N-terminal of UGT1A6 .
	manualset3
87650	5	399599	5	NULL	NULL	0	NULL	sequence 33-37 ( PQDGS )	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , sera from AIH-1 patients reacted with the amino acids in the sequence 33-37 ( PQDGS ) of the N-terminal of UGT1A6 .
	manualset3
87651	6	399599	5	NULL	NULL	0	NULL	N-terminal of UGT1A6	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , sera from AIH-1 patients reacted with the amino acids in the sequence 33-37 ( PQDGS ) of the N-terminal of UGT1A6 .
	manualset3
87658	2	399600	5	NULL	NULL	0	NULL	solid-state surface acidity measurement	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , solid-state surface acidity measurement of excipients and solid formulations using pH indicator probes as surrogates can be used to determine the ionization state of the drug and to predict the chemical stability profile of the drug in actual solid formulations .
	manualset3
87663	3	399600	5	NULL	NULL	0	NULL	excipients	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , solid-state surface acidity measurement of excipients and solid formulations using pH indicator probes as surrogates can be used to determine the ionization state of the drug and to predict the chemical stability profile of the drug in actual solid formulations .
	manualset3
87664	4	399600	5	NULL	NULL	NULL	NULL	solid formulations	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , solid-state surface acidity measurement of excipients and solid formulations using pH indicator probes as surrogates can be used to determine the ionization state of the drug and to predict the chemical stability profile of the drug in actual solid formulations .
	manualset3
87665	5	399600	5	NULL	NULL	NULL	NULL	pH indicator probes	Facility												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , solid-state surface acidity measurement of excipients and solid formulations using pH indicator probes as surrogates can be used to determine the ionization state of the drug and to predict the chemical stability profile of the drug in actual solid formulations .
	manualset3
87666	6	399600	5	NULL	NULL	NULL	NULL	surrogates	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , solid-state surface acidity measurement of excipients and solid formulations using pH indicator probes as surrogates can be used to determine the ionization state of the drug and to predict the chemical stability profile of the drug in actual solid formulations .
	manualset3
87667	7	399600	5	NULL	NULL	0	NULL	drug	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , solid-state surface acidity measurement of excipients and solid formulations using pH indicator probes as surrogates can be used to determine the ionization state of the drug and to predict the chemical stability profile of the drug in actual solid formulations .
	manualset3
87668	8	399600	5	NULL	NULL	0	NULL	drug	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , solid-state surface acidity measurement of excipients and solid formulations using pH indicator probes as surrogates can be used to determine the ionization state of the drug and to predict the chemical stability profile of the drug in actual solid formulations .
	manualset3
87669	9	399600	5	NULL	NULL	NULL	NULL	actual solid formulations	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , solid-state surface acidity measurement of excipients and solid formulations using pH indicator probes as surrogates can be used to determine the ionization state of the drug and to predict the chemical stability profile of the drug in actual solid formulations .
	manualset3
87671	2	399601	5	NULL	NULL	0	NULL	steroid saponins TTS-12 and TTS-15	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , steroid saponins TTS-12 and TTS-15 from Tribulus terrestris L. have significant in vitro antifungal activity against fluconazole-resistant fungi , especially TTS-12 also showed in vivo activity against fluconazole-resistant C. albicans .
	manualset3
87672	3	399601	5	NULL	NULL	0	NULL	Tribulus terrestris L.	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , steroid saponins TTS-12 and TTS-15 from Tribulus terrestris L. have significant in vitro antifungal activity against fluconazole-resistant fungi , especially TTS-12 also showed in vivo activity against fluconazole-resistant C. albicans .
	manualset3
87673	4	399601	5	NULL	NULL	0	NULL	in vitro antifungal activity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , steroid saponins TTS-12 and TTS-15 from Tribulus terrestris L. have significant in vitro antifungal activity against fluconazole-resistant fungi , especially TTS-12 also showed in vivo activity against fluconazole-resistant C. albicans .
	manualset3
87674	5	399601	5	NULL	NULL	0	NULL	fluconazole-resistant fungi	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , steroid saponins TTS-12 and TTS-15 from Tribulus terrestris L. have significant in vitro antifungal activity against fluconazole-resistant fungi , especially TTS-12 also showed in vivo activity against fluconazole-resistant C. albicans .
	manualset3
87675	6	399601	5	NULL	NULL	0	NULL	TTS-12	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , steroid saponins TTS-12 and TTS-15 from Tribulus terrestris L. have significant in vitro antifungal activity against fluconazole-resistant fungi , especially TTS-12 also showed in vivo activity against fluconazole-resistant C. albicans .
	manualset3
87676	7	399601	5	NULL	NULL	0	NULL	in vivo activity 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , steroid saponins TTS-12 and TTS-15 from Tribulus terrestris L. have significant in vitro antifungal activity against fluconazole-resistant fungi , especially TTS-12 also showed in vivo activity against fluconazole-resistant C. albicans .
	manualset3
87677	8	399601	5	NULL	NULL	0	NULL	fluconazole-resistant C. albicans	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , steroid saponins TTS-12 and TTS-15 from Tribulus terrestris L. have significant in vitro antifungal activity against fluconazole-resistant fungi , especially TTS-12 also showed in vivo activity against fluconazole-resistant C. albicans .
	manualset3
87679	2	399602	5	NULL	NULL	0	NULL	ADAM17 expression pattern	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the ADAM17 expression pattern and its role in shedding TGF-alpha from cultured human kidney cells suggest a role in the development of fibrosis .
	manualset3
87680	3	399602	5	NULL	NULL	0	NULL	role	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the ADAM17 expression pattern and its role in shedding TGF-alpha from cultured human kidney cells suggest a role in the development of fibrosis .
	manualset3
87681	4	399602	5	NULL	NULL	0	NULL	TGF-alpha	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the ADAM17 expression pattern and its role in shedding TGF-alpha from cultured human kidney cells suggest a role in the development of fibrosis .
	manualset3
87682	5	399602	5	NULL	NULL	0	NULL	cultured human kidney cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the ADAM17 expression pattern and its role in shedding TGF-alpha from cultured human kidney cells suggest a role in the development of fibrosis .
	manualset3
87683	6	399602	5	NULL	NULL	0	NULL	role	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the ADAM17 expression pattern and its role in shedding TGF-alpha from cultured human kidney cells suggest a role in the development of fibrosis .
	manualset3
87684	7	399602	5	NULL	NULL	0	NULL	development of fibrosis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the ADAM17 expression pattern and its role in shedding TGF-alpha from cultured human kidney cells suggest a role in the development of fibrosis .
	manualset3
87685	1	399603	5	NULL	NULL	0	NULL	Trabeculectomy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Trabeculectomy in glaucoma ) .
	manualset3
87686	2	399603	5	NULL	NULL	0	NULL	glaucoma	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Trabeculectomy in glaucoma ) .
	manualset3
87688	2	399604	5	NULL	NULL	0	NULL	IL-4 	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the absence of IL-4 enhanced GC reaction and specific antibody response of Th1-type .
	manualset3
87689	3	399604	5	NULL	NULL	0	NULL	GC reaction	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the absence of IL-4 enhanced GC reaction and specific antibody response of Th1-type .
	manualset3
87690	4	399604	5	NULL	NULL	0	NULL	specific antibody response	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the absence of IL-4 enhanced GC reaction and specific antibody response of Th1-type .
	manualset3
87691	5	399604	5	NULL	NULL	NULL	NULL	Th1-type antibodies	GeneOrProteinGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , the absence of IL-4 enhanced GC reaction and specific antibody response of Th1-type .
	manualset3
87693	2	399605	5	NULL	NULL	0	NULL	anterolateral thigh flap	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the anterolateral thigh flap is a versatile and dependable flap that can be adapted to any type of defect by modifying the flap design and composition .
	manualset3
87694	3	399605	5	NULL	NULL	0	NULL	versatile and dependable flap	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the anterolateral thigh flap is a versatile and dependable flap that can be adapted to any type of defect by modifying the flap design and composition .
	manualset3
87695	4	399605	5	NULL	NULL	0	NULL	defect	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the anterolateral thigh flap is a versatile and dependable flap that can be adapted to any type of defect by modifying the flap design and composition .
	manualset3
87697	2	399606	5	NULL	NULL	0	NULL	expression of YB-1	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the expression of YB-1 in the nucleus is related to carcinogenesis and the development of breast cancer .
	manualset3
87698	3	399606	5	NULL	NULL	0	NULL	nucleus	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the expression of YB-1 in the nucleus is related to carcinogenesis and the development of breast cancer .
	manualset3
87699	4	399606	5	NULL	NULL	0	NULL	carcinogenesis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the expression of YB-1 in the nucleus is related to carcinogenesis and the development of breast cancer .
	manualset3
87700	5	399606	5	NULL	NULL	0	NULL	 development of breast cancer	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the expression of YB-1 in the nucleus is related to carcinogenesis and the development of breast cancer .
	manualset3
87702	1	399607	5	NULL	NULL	NULL	NULL	glass fiber posts	MedicalDevice												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , the glass fiber posts proved excellent in flexural strengths and moduli .
	manualset3
87703	1	399608	5	NULL	NULL	0	NULL	new generation of PADPRP inhibitors	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the new generation of PADPRP inhibitors are at least 50-fold more effective than 3-aminobenzamide as chemopotentiators , and can be used at micromolar rather than millimolar concentrations in intact cells .
	manualset3
87704	2	399608	5	NULL	NULL	0	NULL	3-aminobenzamide	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the new generation of PADPRP inhibitors are at least 50-fold more effective than 3-aminobenzamide as chemopotentiators , and can be used at micromolar rather than millimolar concentrations in intact cells .
	manualset3
87705	3	399608	5	NULL	NULL	0	NULL	chemopotentiators	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the new generation of PADPRP inhibitors are at least 50-fold more effective than 3-aminobenzamide as chemopotentiators , and can be used at micromolar rather than millimolar concentrations in intact cells .
	manualset3
87706	4	399608	5	NULL	NULL	0	NULL	intact cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the new generation of PADPRP inhibitors are at least 50-fold more effective than 3-aminobenzamide as chemopotentiators , and can be used at micromolar rather than millimolar concentrations in intact cells .
	manualset3
87707	1	399609	5	NULL	NULL	0	NULL	present study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the present study demonstrates that antagonistic targeting of the histamine H ( 3 ) receptor decreases caloric intake in higher mammalian species .
	manualset3
87708	2	399609	5	NULL	NULL	0	NULL	histamine H ( 3 ) receptor	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the present study demonstrates that antagonistic targeting of the histamine H ( 3 ) receptor decreases caloric intake in higher mammalian species .
	manualset3
87709	3	399609	5	NULL	NULL	0	NULL	caloric intake	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the present study demonstrates that antagonistic targeting of the histamine H ( 3 ) receptor decreases caloric intake in higher mammalian species .
	manualset3
87710	4	399609	5	NULL	NULL	0	NULL	higher mammalian species	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the present study demonstrates that antagonistic targeting of the histamine H ( 3 ) receptor decreases caloric intake in higher mammalian species .
	manualset3
89568	5	399609	5	NULL	NULL	0	NULL	antagonistic targeting	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the present study demonstrates that antagonistic targeting of the histamine H ( 3 ) receptor decreases caloric intake in higher mammalian species .
	manualset3
87711	1	399610	5	NULL	NULL	0	NULL	present study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the present study shows that PTx-sensitivity of receptor-induced ERK1/2 activation could be a consequence of disinhibition of the adenylyl cyclase signaling pathway , which in turn causes inhibition of c-Raf-1 activation rather than indicating involvement of a PTx-sensitive G protein in this signaling pathway .
	manualset3
87712	2	399610	5	NULL	NULL	0	NULL	PTx-sensitivity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the present study shows that PTx-sensitivity of receptor-induced ERK1/2 activation could be a consequence of disinhibition of the adenylyl cyclase signaling pathway , which in turn causes inhibition of c-Raf-1 activation rather than indicating involvement of a PTx-sensitive G protein in this signaling pathway .
	manualset3
87713	3	399610	5	NULL	NULL	0	NULL	receptor-induced ERK1/2 activation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the present study shows that PTx-sensitivity of receptor-induced ERK1/2 activation could be a consequence of disinhibition of the adenylyl cyclase signaling pathway , which in turn causes inhibition of c-Raf-1 activation rather than indicating involvement of a PTx-sensitive G protein in this signaling pathway .
	manualset3
87714	4	399610	5	NULL	NULL	0	NULL	disinhibition of the adenylyl cyclase signaling pathway	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the present study shows that PTx-sensitivity of receptor-induced ERK1/2 activation could be a consequence of disinhibition of the adenylyl cyclase signaling pathway , which in turn causes inhibition of c-Raf-1 activation rather than indicating involvement of a PTx-sensitive G protein in this signaling pathway .
	manualset3
87715	5	399610	5	NULL	NULL	0	NULL	inhibition	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the present study shows that PTx-sensitivity of receptor-induced ERK1/2 activation could be a consequence of disinhibition of the adenylyl cyclase signaling pathway , which in turn causes inhibition of c-Raf-1 activation rather than indicating involvement of a PTx-sensitive G protein in this signaling pathway .
	manualset3
87716	6	399610	5	NULL	NULL	0	NULL	c-Raf-1 activation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the present study shows that PTx-sensitivity of receptor-induced ERK1/2 activation could be a consequence of disinhibition of the adenylyl cyclase signaling pathway , which in turn causes inhibition of c-Raf-1 activation rather than indicating involvement of a PTx-sensitive G protein in this signaling pathway .
	manualset3
87717	7	399610	5	NULL	NULL	0	NULL	PTx-sensitive G protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the present study shows that PTx-sensitivity of receptor-induced ERK1/2 activation could be a consequence of disinhibition of the adenylyl cyclase signaling pathway , which in turn causes inhibition of c-Raf-1 activation rather than indicating involvement of a PTx-sensitive G protein in this signaling pathway .
	manualset3
87718	8	399610	5	NULL	NULL	0	NULL	signaling pathway	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the present study shows that PTx-sensitivity of receptor-induced ERK1/2 activation could be a consequence of disinhibition of the adenylyl cyclase signaling pathway , which in turn causes inhibition of c-Raf-1 activation rather than indicating involvement of a PTx-sensitive G protein in this signaling pathway .
	manualset3
87773	1	399611	5	NULL	NULL	0	NULL	polysulfonate resin	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the properties of polysulfonate resin , such as particle shape and degree of cross-linking , and the deformation under compaction of fillers affect the physical properties and the drug release of the resinate tablets .
	manualset3
87774	2	399611	5	NULL	NULL	0	NULL	deformation under compaction of fillers	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the properties of polysulfonate resin , such as particle shape and degree of cross-linking , and the deformation under compaction of fillers affect the physical properties and the drug release of the resinate tablets .
	manualset3
87775	3	399611	5	NULL	NULL	0	NULL	drug	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the properties of polysulfonate resin , such as particle shape and degree of cross-linking , and the deformation under compaction of fillers affect the physical properties and the drug release of the resinate tablets .
	manualset3
87776	4	399611	5	NULL	NULL	0	NULL	resinate tablets	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the properties of polysulfonate resin , such as particle shape and degree of cross-linking , and the deformation under compaction of fillers affect the physical properties and the drug release of the resinate tablets .
	manualset3
87777	1	399612	5	NULL	NULL	0	NULL	study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the study highlighted the rise of non-albicans Candida species in our hospital with differential distribution in paediatric and adult wards and emergence of azole resistance .
	manualset3
87778	2	399612	5	NULL	NULL	0	NULL	non-albicans Candida species	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the study highlighted the rise of non-albicans Candida species in our hospital with differential distribution in paediatric and adult wards and emergence of azole resistance .
	manualset3
87779	3	399612	5	NULL	NULL	0	NULL	hospital	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the study highlighted the rise of non-albicans Candida species in our hospital with differential distribution in paediatric and adult wards and emergence of azole resistance .
	manualset3
87780	4	399612	5	NULL	NULL	0	NULL	differential distribution	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the study highlighted the rise of non-albicans Candida species in our hospital with differential distribution in paediatric and adult wards and emergence of azole resistance .
	manualset3
87781	5	399612	5	NULL	NULL	0	NULL	paediatric and adult wards	Facility												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the study highlighted the rise of non-albicans Candida species in our hospital with differential distribution in paediatric and adult wards and emergence of azole resistance .
	manualset3
87782	6	399612	5	NULL	NULL	0	NULL	azole resistance	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the study highlighted the rise of non-albicans Candida species in our hospital with differential distribution in paediatric and adult wards and emergence of azole resistance .
	manualset3
87783	1	399613	5	NULL	NULL	0	NULL	Tracheobronchial intracavitary localizations	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Tracheobronchial intracavitary localizations of Hodgkin 's disease ) .
	manualset3
87784	2	399613	5	NULL	NULL	0	NULL	Hodgkin 's disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Tracheobronchial intracavitary localizations of Hodgkin 's disease ) .
	manualset3
87785	1	399614	5	NULL	NULL	0	NULL	MTR profile	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the study of the MTR profile in this myelin lesion model demonstrates in vivo the loss of myelin and the presence of spontaneous remyelination .
	manualset3
87786	2	399614	5	NULL	NULL	NULL	NULL	myelin lesion model	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , the study of the MTR profile in this myelin lesion model demonstrates in vivo the loss of myelin and the presence of spontaneous remyelination .
	manualset3
87787	3	399614	5	NULL	NULL	0	NULL	loss of myelin	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the study of the MTR profile in this myelin lesion model demonstrates in vivo the loss of myelin and the presence of spontaneous remyelination .
	manualset3
87788	4	399614	5	NULL	NULL	0	NULL	spontaneous remyelination	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the study of the MTR profile in this myelin lesion model demonstrates in vivo the loss of myelin and the presence of spontaneous remyelination .
	manualset3
87789	1	399615	5	NULL	NULL	0	NULL	study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the study suggests that GSP are effective in ameliorating the damage to pancreatic tissue in experimental diabetes mellitus .
	manualset3
87790	2	399615	5	NULL	NULL	0	NULL	GSP	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the study suggests that GSP are effective in ameliorating the damage to pancreatic tissue in experimental diabetes mellitus .
	manualset3
87791	3	399615	5	NULL	NULL	0	NULL	pancreatic tissue	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the study suggests that GSP are effective in ameliorating the damage to pancreatic tissue in experimental diabetes mellitus .
	manualset3
87792	4	399615	5	NULL	NULL	0	NULL	experimental diabetes mellitus	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , the study suggests that GSP are effective in ameliorating the damage to pancreatic tissue in experimental diabetes mellitus .
	manualset3
87793	1	399616	5	NULL	NULL	0	NULL	study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , this study has demonstrated that the long and short cases/orals tested different aspects of student 's skills , and so reinforces the importance of retaining the short and long cases in undergraduate surgical examinations .
	manualset3
87794	2	399616	5	NULL	NULL	NULL	NULL	long and short cases/orals	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , this study has demonstrated that the long and short cases/orals tested different aspects of student 's skills , and so reinforces the importance of retaining the short and long cases in undergraduate surgical examinations .
	manualset3
87795	3	399616	5	NULL	NULL	NULL	NULL	student 's skills	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , this study has demonstrated that the long and short cases/orals tested different aspects of student 's skills , and so reinforces the importance of retaining the short and long cases in undergraduate surgical examinations .
	manualset3
87796	4	399616	5	NULL	NULL	NULL	NULL	short and long cases	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , this study has demonstrated that the long and short cases/orals tested different aspects of student 's skills , and so reinforces the importance of retaining the short and long cases in undergraduate surgical examinations .
	manualset3
87797	5	399616	5	NULL	NULL	NULL	NULL	undergraduate surgical examinations	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , this study has demonstrated that the long and short cases/orals tested different aspects of student 's skills , and so reinforces the importance of retaining the short and long cases in undergraduate surgical examinations .
	manualset3
87798	1	399617	5	NULL	NULL	0	NULL	study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , this study makes the novel observation that CRP induces IL-8 synthesis and secretion in HAEC via upregulation of NF-kappa B activity .
	manualset3
87799	2	399617	5	NULL	NULL	0	NULL	novel observation	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , this study makes the novel observation that CRP induces IL-8 synthesis and secretion in HAEC via upregulation of NF-kappa B activity .
	manualset3
87800	3	399617	5	NULL	NULL	0	NULL	CRP	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , this study makes the novel observation that CRP induces IL-8 synthesis and secretion in HAEC via upregulation of NF-kappa B activity .
	manualset3
87801	4	399617	5	NULL	NULL	0	NULL	IL-8 synthesis and secretion	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , this study makes the novel observation that CRP induces IL-8 synthesis and secretion in HAEC via upregulation of NF-kappa B activity .
	manualset3
87802	5	399617	5	NULL	NULL	0	NULL	HAEC	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , this study makes the novel observation that CRP induces IL-8 synthesis and secretion in HAEC via upregulation of NF-kappa B activity .
	manualset3
87803	6	399617	5	NULL	NULL	0	NULL	upregulation of NF-kappa B activity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , this study makes the novel observation that CRP induces IL-8 synthesis and secretion in HAEC via upregulation of NF-kappa B activity .
	manualset3
87804	1	399618	5	NULL	NULL	0	NULL	study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , this study shows that developmental increases occur not only in plasma leptin but also in hypothalamic Ob-Rb expression , suggesting that both are likely to influence the timing of puberty onset .
	manualset3
87805	2	399618	5	NULL	NULL	0	NULL	plasma leptin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , this study shows that developmental increases occur not only in plasma leptin but also in hypothalamic Ob-Rb expression , suggesting that both are likely to influence the timing of puberty onset .
	manualset3
87806	3	399618	5	NULL	NULL	0	NULL	hypothalamic Ob-Rb expression	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , this study shows that developmental increases occur not only in plasma leptin but also in hypothalamic Ob-Rb expression , suggesting that both are likely to influence the timing of puberty onset .
	manualset3
87807	4	399618	5	NULL	NULL	0	NULL	puberty onset	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , this study shows that developmental increases occur not only in plasma leptin but also in hypothalamic Ob-Rb expression , suggesting that both are likely to influence the timing of puberty onset .
	manualset3
89569	5	399618	5	NULL	NULL	0	NULL	developmental increases	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , this study shows that developmental increases occur not only in plasma leptin but also in hypothalamic Ob-Rb expression , suggesting that both are likely to influence the timing of puberty onset .
	manualset3
87808	1	399619	5	NULL	NULL	0	NULL	evidence	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we did not find any evidence for hepatotoxicity of risperidone rats .
	manualset3
87809	2	399619	5	NULL	NULL	0	NULL	hepatotoxicity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we did not find any evidence for hepatotoxicity of risperidone rats .
	manualset3
87810	3	399619	5	NULL	NULL	0	NULL	risperidone rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we did not find any evidence for hepatotoxicity of risperidone rats .
	manualset3
87811	1	399620	5	NULL	NULL	NULL	NULL	implications	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , we discuss implications for continued theorizing of the TNSB in light of the experiences of traditionally marginalized populations .
	manualset3
87812	2	399620	5	NULL	NULL	0	NULL	TNSB	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we discuss implications for continued theorizing of the TNSB in light of the experiences of traditionally marginalized populations .
	manualset3
87813	3	399620	5	NULL	NULL	0	NULL	traditionally marginalized populations	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we discuss implications for continued theorizing of the TNSB in light of the experiences of traditionally marginalized populations .
	manualset3
87814	1	399621	5	NULL	NULL	0	NULL	RECQL5	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we propose that RECQL5 stabilises the replication fork allowing replication to overcome the effects of thymidine and complete the cell cycle .
	manualset3
87815	2	399621	5	NULL	NULL	0	NULL	replication fork	NucleicAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we propose that RECQL5 stabilises the replication fork allowing replication to overcome the effects of thymidine and complete the cell cycle .
	manualset3
87816	3	399621	5	NULL	NULL	0	NULL	replication	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we propose that RECQL5 stabilises the replication fork allowing replication to overcome the effects of thymidine and complete the cell cycle .
	manualset3
87817	4	399621	5	NULL	NULL	0	NULL	effects	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we propose that RECQL5 stabilises the replication fork allowing replication to overcome the effects of thymidine and complete the cell cycle .
	manualset3
87818	5	399621	5	NULL	NULL	0	NULL	thymidine	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we propose that RECQL5 stabilises the replication fork allowing replication to overcome the effects of thymidine and complete the cell cycle .
	manualset3
87819	6	399621	5	NULL	NULL	0	NULL	cell cycle	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we propose that RECQL5 stabilises the replication fork allowing replication to overcome the effects of thymidine and complete the cell cycle .
	manualset3
87820	1	399622	5	NULL	NULL	0	NULL	non-linear dose-response effect	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we suggest non-linear dose-response effect of Halowax 1051 on steroidogenesis and steroidogenic enzymes activity and protein expression .
	manualset3
87821	2	399622	5	NULL	NULL	0	NULL	Halowax 1051	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we suggest non-linear dose-response effect of Halowax 1051 on steroidogenesis and steroidogenic enzymes activity and protein expression .
	manualset3
87822	3	399622	5	NULL	NULL	0	NULL	steroidogenesis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we suggest non-linear dose-response effect of Halowax 1051 on steroidogenesis and steroidogenic enzymes activity and protein expression .
	manualset3
87823	4	399622	5	NULL	NULL	0	NULL	steroidogenic enzymes activity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we suggest non-linear dose-response effect of Halowax 1051 on steroidogenesis and steroidogenic enzymes activity and protein expression .
	manualset3
87824	5	399622	5	NULL	NULL	0	NULL	protein expression	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we suggest non-linear dose-response effect of Halowax 1051 on steroidogenesis and steroidogenic enzymes activity and protein expression .
	manualset3
87825	1	399623	5	NULL	NULL	0	NULL	Antacids	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( Antacids and H2 antihistaminics for hyperacidity ) .
	manualset3
87826	2	399623	5	NULL	NULL	0	NULL	H2 antihistaminics	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( Antacids and H2 antihistaminics for hyperacidity ) .
	manualset3
87827	3	399623	5	NULL	NULL	0	NULL	hyperacidity	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Antacids and H2 antihistaminics for hyperacidity ) .
	manualset3
87828	1	399624	5	NULL	NULL	0	NULL	Transient elastography ( FibroScan )	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	( Transient elastography ( FibroScan ) for the non-invasive assessment of liver fibrosis : current status and perspectives ) .
	manualset3
87829	2	399624	5	NULL	NULL	0	NULL	non-invasive assessment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Transient elastography ( FibroScan ) for the non-invasive assessment of liver fibrosis : current status and perspectives ) .
	manualset3
87830	3	399624	5	NULL	NULL	0	NULL	liver fibrosis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Transient elastography ( FibroScan ) for the non-invasive assessment of liver fibrosis : current status and perspectives ) .
	manualset3
87831	4	399624	5	NULL	NULL	0	NULL	current status	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	( Transient elastography ( FibroScan ) for the non-invasive assessment of liver fibrosis : current status and perspectives ) .
	manualset3
87832	5	399624	5	NULL	NULL	0	NULL	perspectives	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	( Transient elastography ( FibroScan ) for the non-invasive assessment of liver fibrosis : current status and perspectives ) .
	manualset3
87833	1	399625	5	NULL	NULL	0	NULL	creatine	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we were able to demonstrate that the protective potential of creatine was primarily mediated by its impact on cellular energy metabolism and NMDA receptor function , along with reduced glutamate spillover , oxidative stress and subsequent excitotoxicity .
	manualset3
87834	2	399625	5	NULL	NULL	0	NULL	impact	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we were able to demonstrate that the protective potential of creatine was primarily mediated by its impact on cellular energy metabolism and NMDA receptor function , along with reduced glutamate spillover , oxidative stress and subsequent excitotoxicity .
	manualset3
87835	3	399625	5	NULL	NULL	0	NULL	cellular energy metabolism	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we were able to demonstrate that the protective potential of creatine was primarily mediated by its impact on cellular energy metabolism and NMDA receptor function , along with reduced glutamate spillover , oxidative stress and subsequent excitotoxicity .
	manualset3
87836	4	399625	5	NULL	NULL	0	NULL	NMDA receptor function	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we were able to demonstrate that the protective potential of creatine was primarily mediated by its impact on cellular energy metabolism and NMDA receptor function , along with reduced glutamate spillover , oxidative stress and subsequent excitotoxicity .
	manualset3
87837	5	399625	5	NULL	NULL	0	NULL	reduced glutamate spillover	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we were able to demonstrate that the protective potential of creatine was primarily mediated by its impact on cellular energy metabolism and NMDA receptor function , along with reduced glutamate spillover , oxidative stress and subsequent excitotoxicity .
	manualset3
87839	6	399625	5	NULL	NULL	0	NULL	oxidative stress	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we were able to demonstrate that the protective potential of creatine was primarily mediated by its impact on cellular energy metabolism and NMDA receptor function , along with reduced glutamate spillover , oxidative stress and subsequent excitotoxicity .
	manualset3
87840	7	399625	5	NULL	NULL	0	NULL	subsequent excitotoxicity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , we were able to demonstrate that the protective potential of creatine was primarily mediated by its impact on cellular energy metabolism and NMDA receptor function , along with reduced glutamate spillover , oxidative stress and subsequent excitotoxicity .
	manualset3
87841	1	399626	5	NULL	NULL	0	NULL	long periods of time ( 9.5 months to 2 years )	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , when given for long periods of time ( 9.5 months to 2 years ) , LTG was well tolerated in doses up to 400 mg/day and mean trough levels of 3.0 + / - 0.6 microgram/ml ; LTG has a favorable pharmacokinetic profile and appears to exhibit first-order linear kinetics during long-term chronic dosing ; LTG shows preliminary evidence of efficacy during long-term administration ; and to date , our patients represent the longest reported experience of continuous and closely monitored LTG therapy in the literature .
	manualset3
87842	2	399626	5	NULL	NULL	0	NULL	LTG	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , when given for long periods of time ( 9.5 months to 2 years ) , LTG was well tolerated in doses up to 400 mg/day and mean trough levels of 3.0 + / - 0.6 microgram/ml ; LTG has a favorable pharmacokinetic profile and appears to exhibit first-order linear kinetics during long-term chronic dosing ; LTG shows preliminary evidence of efficacy during long-term administration ; and to date , our patients represent the longest reported experience of continuous and closely monitored LTG therapy in the literature .
	manualset3
87843	3	399626	5	NULL	NULL	0	NULL	doses	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , when given for long periods of time ( 9.5 months to 2 years ) , LTG was well tolerated in doses up to 400 mg/day and mean trough levels of 3.0 + / - 0.6 microgram/ml ; LTG has a favorable pharmacokinetic profile and appears to exhibit first-order linear kinetics during long-term chronic dosing ; LTG shows preliminary evidence of efficacy during long-term administration ; and to date , our patients represent the longest reported experience of continuous and closely monitored LTG therapy in the literature .
	manualset3
87844	4	399626	5	NULL	NULL	0	NULL	400 mg/day	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , when given for long periods of time ( 9.5 months to 2 years ) , LTG was well tolerated in doses up to 400 mg/day and mean trough levels of 3.0 + / - 0.6 microgram/ml ; LTG has a favorable pharmacokinetic profile and appears to exhibit first-order linear kinetics during long-term chronic dosing ; LTG shows preliminary evidence of efficacy during long-term administration ; and to date , our patients represent the longest reported experience of continuous and closely monitored LTG therapy in the literature .
	manualset3
87845	5	399626	5	NULL	NULL	0	NULL	mean trough levels	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , when given for long periods of time ( 9.5 months to 2 years ) , LTG was well tolerated in doses up to 400 mg/day and mean trough levels of 3.0 + / - 0.6 microgram/ml ; LTG has a favorable pharmacokinetic profile and appears to exhibit first-order linear kinetics during long-term chronic dosing ; LTG shows preliminary evidence of efficacy during long-term administration ; and to date , our patients represent the longest reported experience of continuous and closely monitored LTG therapy in the literature .
	manualset3
87846	6	399626	5	NULL	NULL	0	NULL	3.0 + / - 0.6 microgram/ml	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , when given for long periods of time ( 9.5 months to 2 years ) , LTG was well tolerated in doses up to 400 mg/day and mean trough levels of 3.0 + / - 0.6 microgram/ml ; LTG has a favorable pharmacokinetic profile and appears to exhibit first-order linear kinetics during long-term chronic dosing ; LTG shows preliminary evidence of efficacy during long-term administration ; and to date , our patients represent the longest reported experience of continuous and closely monitored LTG therapy in the literature .
	manualset3
87847	7	399626	5	NULL	NULL	0	NULL	LTG	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , when given for long periods of time ( 9.5 months to 2 years ) , LTG was well tolerated in doses up to 400 mg/day and mean trough levels of 3.0 + / - 0.6 microgram/ml ; LTG has a favorable pharmacokinetic profile and appears to exhibit first-order linear kinetics during long-term chronic dosing ; LTG shows preliminary evidence of efficacy during long-term administration ; and to date , our patients represent the longest reported experience of continuous and closely monitored LTG therapy in the literature .
	manualset3
87848	8	399626	5	NULL	NULL	NULL	NULL	favorable pharmacokinetic profile	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , when given for long periods of time ( 9.5 months to 2 years ) , LTG was well tolerated in doses up to 400 mg/day and mean trough levels of 3.0 + / - 0.6 microgram/ml ; LTG has a favorable pharmacokinetic profile and appears to exhibit first-order linear kinetics during long-term chronic dosing ; LTG shows preliminary evidence of efficacy during long-term administration ; and to date , our patients represent the longest reported experience of continuous and closely monitored LTG therapy in the literature .
	manualset3
87849	9	399626	5	NULL	NULL	0	NULL	first-order linear kinetics	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , when given for long periods of time ( 9.5 months to 2 years ) , LTG was well tolerated in doses up to 400 mg/day and mean trough levels of 3.0 + / - 0.6 microgram/ml ; LTG has a favorable pharmacokinetic profile and appears to exhibit first-order linear kinetics during long-term chronic dosing ; LTG shows preliminary evidence of efficacy during long-term administration ; and to date , our patients represent the longest reported experience of continuous and closely monitored LTG therapy in the literature .
	manualset3
87850	10	399626	5	NULL	NULL	0	NULL	LTG	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , when given for long periods of time ( 9.5 months to 2 years ) , LTG was well tolerated in doses up to 400 mg/day and mean trough levels of 3.0 + / - 0.6 microgram/ml ; LTG has a favorable pharmacokinetic profile and appears to exhibit first-order linear kinetics during long-term chronic dosing ; LTG shows preliminary evidence of efficacy during long-term administration ; and to date , our patients represent the longest reported experience of continuous and closely monitored LTG therapy in the literature .
	manualset3
87851	11	399626	5	NULL	NULL	NULL	NULL	efficacy	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , when given for long periods of time ( 9.5 months to 2 years ) , LTG was well tolerated in doses up to 400 mg/day and mean trough levels of 3.0 + / - 0.6 microgram/ml ; LTG has a favorable pharmacokinetic profile and appears to exhibit first-order linear kinetics during long-term chronic dosing ; LTG shows preliminary evidence of efficacy during long-term administration ; and to date , our patients represent the longest reported experience of continuous and closely monitored LTG therapy in the literature .
	manualset3
87852	12	399626	5	NULL	NULL	0	NULL	long-term administration	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , when given for long periods of time ( 9.5 months to 2 years ) , LTG was well tolerated in doses up to 400 mg/day and mean trough levels of 3.0 + / - 0.6 microgram/ml ; LTG has a favorable pharmacokinetic profile and appears to exhibit first-order linear kinetics during long-term chronic dosing ; LTG shows preliminary evidence of efficacy during long-term administration ; and to date , our patients represent the longest reported experience of continuous and closely monitored LTG therapy in the literature .
	manualset3
87853	13	399626	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , when given for long periods of time ( 9.5 months to 2 years ) , LTG was well tolerated in doses up to 400 mg/day and mean trough levels of 3.0 + / - 0.6 microgram/ml ; LTG has a favorable pharmacokinetic profile and appears to exhibit first-order linear kinetics during long-term chronic dosing ; LTG shows preliminary evidence of efficacy during long-term administration ; and to date , our patients represent the longest reported experience of continuous and closely monitored LTG therapy in the literature .
	manualset3
87854	14	399626	5	NULL	NULL	0	NULL	experience	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , when given for long periods of time ( 9.5 months to 2 years ) , LTG was well tolerated in doses up to 400 mg/day and mean trough levels of 3.0 + / - 0.6 microgram/ml ; LTG has a favorable pharmacokinetic profile and appears to exhibit first-order linear kinetics during long-term chronic dosing ; LTG shows preliminary evidence of efficacy during long-term administration ; and to date , our patients represent the longest reported experience of continuous and closely monitored LTG therapy in the literature .
	manualset3
87855	15	399626	5	NULL	NULL	0	NULL	LTG therapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , when given for long periods of time ( 9.5 months to 2 years ) , LTG was well tolerated in doses up to 400 mg/day and mean trough levels of 3.0 + / - 0.6 microgram/ml ; LTG has a favorable pharmacokinetic profile and appears to exhibit first-order linear kinetics during long-term chronic dosing ; LTG shows preliminary evidence of efficacy during long-term administration ; and to date , our patients represent the longest reported experience of continuous and closely monitored LTG therapy in the literature .
	manualset3
87856	16	399626	5	NULL	NULL	0	NULL	literature	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , when given for long periods of time ( 9.5 months to 2 years ) , LTG was well tolerated in doses up to 400 mg/day and mean trough levels of 3.0 + / - 0.6 microgram/ml ; LTG has a favorable pharmacokinetic profile and appears to exhibit first-order linear kinetics during long-term chronic dosing ; LTG shows preliminary evidence of efficacy during long-term administration ; and to date , our patients represent the longest reported experience of continuous and closely monitored LTG therapy in the literature .
	manualset3
88115	17	399626	5	NULL	NULL	0	NULL	long-term chronic dosing	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , when given for long periods of time ( 9.5 months to 2 years ) , LTG was well tolerated in doses up to 400 mg/day and mean trough levels of 3.0 + / - 0.6 microgram/ml ; LTG has a favorable pharmacokinetic profile and appears to exhibit first-order linear kinetics during long-term chronic dosing ; LTG shows preliminary evidence of efficacy during long-term administration ; and to date , our patients represent the longest reported experience of continuous and closely monitored LTG therapy in the literature .
	manualset3
87857	1	399627	5	NULL	NULL	0	NULL	VE	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , while VE can not replace endoscopy of the tracheobronchial tree or the oesophagus , it is an accurate and non-invasive method for identifying endoluminal tumors , grading stenoses and visualizing the tracheobronchial tree beyond stenoses in a small number of patients who are not amenable to endoscopy .
	manualset3
87858	2	399627	5	NULL	NULL	0	NULL	endoscopy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , while VE can not replace endoscopy of the tracheobronchial tree or the oesophagus , it is an accurate and non-invasive method for identifying endoluminal tumors , grading stenoses and visualizing the tracheobronchial tree beyond stenoses in a small number of patients who are not amenable to endoscopy .
	manualset3
87859	3	399627	5	NULL	NULL	0	NULL	tracheobronchial tree	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , while VE can not replace endoscopy of the tracheobronchial tree or the oesophagus , it is an accurate and non-invasive method for identifying endoluminal tumors , grading stenoses and visualizing the tracheobronchial tree beyond stenoses in a small number of patients who are not amenable to endoscopy .
	manualset3
87860	4	399627	5	NULL	NULL	0	NULL	oesophagus	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , while VE can not replace endoscopy of the tracheobronchial tree or the oesophagus , it is an accurate and non-invasive method for identifying endoluminal tumors , grading stenoses and visualizing the tracheobronchial tree beyond stenoses in a small number of patients who are not amenable to endoscopy .
	manualset3
87861	5	399627	5	NULL	NULL	0	NULL	endoluminal tumors	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , while VE can not replace endoscopy of the tracheobronchial tree or the oesophagus , it is an accurate and non-invasive method for identifying endoluminal tumors , grading stenoses and visualizing the tracheobronchial tree beyond stenoses in a small number of patients who are not amenable to endoscopy .
	manualset3
87862	6	399627	5	NULL	NULL	0	NULL	grading stenoses	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , while VE can not replace endoscopy of the tracheobronchial tree or the oesophagus , it is an accurate and non-invasive method for identifying endoluminal tumors , grading stenoses and visualizing the tracheobronchial tree beyond stenoses in a small number of patients who are not amenable to endoscopy .
	manualset3
87863	7	399627	5	NULL	NULL	0	NULL	tracheobronchial tree	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , while VE can not replace endoscopy of the tracheobronchial tree or the oesophagus , it is an accurate and non-invasive method for identifying endoluminal tumors , grading stenoses and visualizing the tracheobronchial tree beyond stenoses in a small number of patients who are not amenable to endoscopy .
	manualset3
87864	8	399627	5	NULL	NULL	0	NULL	stenoses	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , while VE can not replace endoscopy of the tracheobronchial tree or the oesophagus , it is an accurate and non-invasive method for identifying endoluminal tumors , grading stenoses and visualizing the tracheobronchial tree beyond stenoses in a small number of patients who are not amenable to endoscopy .
	manualset3
87865	9	399627	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , while VE can not replace endoscopy of the tracheobronchial tree or the oesophagus , it is an accurate and non-invasive method for identifying endoluminal tumors , grading stenoses and visualizing the tracheobronchial tree beyond stenoses in a small number of patients who are not amenable to endoscopy .
	manualset3
87866	10	399627	5	NULL	NULL	0	NULL	endoscopy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , while VE can not replace endoscopy of the tracheobronchial tree or the oesophagus , it is an accurate and non-invasive method for identifying endoluminal tumors , grading stenoses and visualizing the tracheobronchial tree beyond stenoses in a small number of patients who are not amenable to endoscopy .
	manualset3
87867	1	399628	5	NULL	NULL	0	NULL	xenogeneic transplantation	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , xenogeneic transplantation of human PBSCs into NOD/SCID mice provides an excellent in vivo model to study human megakaryocytopoiesis and platelet production .
	manualset3
87868	2	399628	5	NULL	NULL	0	NULL	human PBSCs	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , xenogeneic transplantation of human PBSCs into NOD/SCID mice provides an excellent in vivo model to study human megakaryocytopoiesis and platelet production .
	manualset3
87869	3	399628	5	NULL	NULL	0	NULL	NOD/SCID mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , xenogeneic transplantation of human PBSCs into NOD/SCID mice provides an excellent in vivo model to study human megakaryocytopoiesis and platelet production .
	manualset3
87870	4	399628	5	NULL	NULL	NULL	NULL	 in vivo model	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In conclusion , xenogeneic transplantation of human PBSCs into NOD/SCID mice provides an excellent in vivo model to study human megakaryocytopoiesis and platelet production .
	manualset3
87871	5	399628	5	NULL	NULL	0	NULL	study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , xenogeneic transplantation of human PBSCs into NOD/SCID mice provides an excellent in vivo model to study human megakaryocytopoiesis and platelet production .
	manualset3
87872	6	399628	5	NULL	NULL	0	NULL	human megakaryocytopoiesis 	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , xenogeneic transplantation of human PBSCs into NOD/SCID mice provides an excellent in vivo model to study human megakaryocytopoiesis and platelet production .
	manualset3
87873	7	399628	5	NULL	NULL	0	NULL	platelet production	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , xenogeneic transplantation of human PBSCs into NOD/SCID mice provides an excellent in vivo model to study human megakaryocytopoiesis and platelet production .
	manualset3
87874	1	399629	5	NULL	NULL	0	NULL	zinc	Atom												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , zinc activates KATP by binding itself to extracellular His-326 and His-332 of the SUR1 subunit .
	manualset3
87875	2	399629	5	NULL	NULL	0	NULL	KATP	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , zinc activates KATP by binding itself to extracellular His-326 and His-332 of the SUR1 subunit .
	manualset3
87876	3	399629	5	NULL	NULL	0	NULL	extracellular His-326	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , zinc activates KATP by binding itself to extracellular His-326 and His-332 of the SUR1 subunit .
	manualset3
87877	4	399629	5	NULL	NULL	0	NULL	His-332	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , zinc activates KATP by binding itself to extracellular His-326 and His-332 of the SUR1 subunit .
	manualset3
87878	5	399629	5	NULL	NULL	0	NULL	SUR1 subunit	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In conclusion , zinc activates KATP by binding itself to extracellular His-326 and His-332 of the SUR1 subunit .
	manualset3
87879	1	399630	5	NULL	NULL	0	NULL	Ca ( 2 + )	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	In controls , Ca ( 2 + ) load required for mPTP opening averaged 11 + / - 4 microM mg ( -1 ) mitochondrial protein versus 116 + / - 6 in shams ( P & lt ; 0.0001 ) .
	manualset3
87880	2	399630	5	NULL	NULL	NULL	NULL	mPTP opening	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In controls , Ca ( 2 + ) load required for mPTP opening averaged 11 + / - 4 microM mg ( -1 ) mitochondrial protein versus 116 + / - 6 in shams ( P & lt ; 0.0001 ) .
	manualset3
87881	3	399630	5	NULL	NULL	0	NULL	11 + / - 4 microM mg ( -1 )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In controls , Ca ( 2 + ) load required for mPTP opening averaged 11 + / - 4 microM mg ( -1 ) mitochondrial protein versus 116 + / - 6 in shams ( P & lt ; 0.0001 ) .
	manualset3
87882	4	399630	5	NULL	NULL	0	NULL	mitochondrial protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In controls , Ca ( 2 + ) load required for mPTP opening averaged 11 + / - 4 microM mg ( -1 ) mitochondrial protein versus 116 + / - 6 in shams ( P & lt ; 0.0001 ) .
	manualset3
87883	5	399630	5	NULL	NULL	0	NULL	116 + / - 6	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In controls , Ca ( 2 + ) load required for mPTP opening averaged 11 + / - 4 microM mg ( -1 ) mitochondrial protein versus 116 + / - 6 in shams ( P & lt ; 0.0001 ) .
	manualset3
87884	6	399630	5	NULL	NULL	0	NULL	shams	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In controls , Ca ( 2 + ) load required for mPTP opening averaged 11 + / - 4 microM mg ( -1 ) mitochondrial protein versus 116 + / - 6 in shams ( P & lt ; 0.0001 ) .
	manualset3
87885	7	399630	5	NULL	NULL	0	NULL	P & lt ; 0.0001	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In controls , Ca ( 2 + ) load required for mPTP opening averaged 11 + / - 4 microM mg ( -1 ) mitochondrial protein versus 116 + / - 6 in shams ( P & lt ; 0.0001 ) .
	manualset3
88116	1	399631	5	NULL	NULL	0	NULL	eukaryotes	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In eukaryotes , manganese superoxide dismutase is a nuclear-encoded protein that scavenges superoxide radicals in the mitochondrial matrix .
	manualset3
88117	2	399631	5	NULL	NULL	0	NULL	manganese superoxide dismutase	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In eukaryotes , manganese superoxide dismutase is a nuclear-encoded protein that scavenges superoxide radicals in the mitochondrial matrix .
	manualset3
88118	3	399631	5	NULL	NULL	0	NULL	nuclear-encoded protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In eukaryotes , manganese superoxide dismutase is a nuclear-encoded protein that scavenges superoxide radicals in the mitochondrial matrix .
	manualset3
88119	4	399631	5	NULL	NULL	0	NULL	superoxide radicals	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In eukaryotes , manganese superoxide dismutase is a nuclear-encoded protein that scavenges superoxide radicals in the mitochondrial matrix .
	manualset3
88120	5	399631	5	NULL	NULL	0	NULL	mitochondrial matrix	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In eukaryotes , manganese superoxide dismutase is a nuclear-encoded protein that scavenges superoxide radicals in the mitochondrial matrix .
	manualset3
88121	1	399632	5	NULL	NULL	NULL	NULL	excised , inside-out patches	Facility												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In excised , inside-out patches , it was demonstrated that ATP currents were mediated by ATP-conductive channels , which were also activated by protein kinase A and blocked by the Cl - channel blocker diphenylamine-2-carboxylate under excised , inside-out conditions .
	manualset3
88122	2	399632	5	NULL	NULL	0	NULL	ATP currents	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In excised , inside-out patches , it was demonstrated that ATP currents were mediated by ATP-conductive channels , which were also activated by protein kinase A and blocked by the Cl - channel blocker diphenylamine-2-carboxylate under excised , inside-out conditions .
	manualset3
88123	3	399632	5	NULL	NULL	0	NULL	ATP-conductive channels	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In excised , inside-out patches , it was demonstrated that ATP currents were mediated by ATP-conductive channels , which were also activated by protein kinase A and blocked by the Cl - channel blocker diphenylamine-2-carboxylate under excised , inside-out conditions .
	manualset3
88124	4	399632	5	NULL	NULL	0	NULL	protein kinase A	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In excised , inside-out patches , it was demonstrated that ATP currents were mediated by ATP-conductive channels , which were also activated by protein kinase A and blocked by the Cl - channel blocker diphenylamine-2-carboxylate under excised , inside-out conditions .
	manualset3
88125	5	399632	5	NULL	NULL	0	NULL	Cl - channel blocker diphenylamine-2-carboxylate	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In excised , inside-out patches , it was demonstrated that ATP currents were mediated by ATP-conductive channels , which were also activated by protein kinase A and blocked by the Cl - channel blocker diphenylamine-2-carboxylate under excised , inside-out conditions .
	manualset3
88126	6	399632	5	NULL	NULL	NULL	NULL	excised , inside-out conditions	LaboratoryExperimentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In excised , inside-out patches , it was demonstrated that ATP currents were mediated by ATP-conductive channels , which were also activated by protein kinase A and blocked by the Cl - channel blocker diphenylamine-2-carboxylate under excised , inside-out conditions .
	manualset3
88127	1	399633	5	NULL	NULL	0	NULL	experiments	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In experiments in vitro against Mycobacterium tuberculosis , these compounds displayed minimum inhibitory concentration ( MIC ) values between several fold and several hundred fold greater than that of INH itself , on a molar basis , with some of the more active compounds having higher calculated values of log P. Among these derivatives , compound 1b , closely homologous to the INH metabolite 1a , N2-acetylisoniazid , provided unexpected protection in tuberculosis-infected mice .
	manualset3
88128	2	399633	5	NULL	NULL	NULL	NULL	Mycobacterium tuberculosis	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In experiments in vitro against Mycobacterium tuberculosis , these compounds displayed minimum inhibitory concentration ( MIC ) values between several fold and several hundred fold greater than that of INH itself , on a molar basis , with some of the more active compounds having higher calculated values of log P. Among these derivatives , compound 1b , closely homologous to the INH metabolite 1a , N2-acetylisoniazid , provided unexpected protection in tuberculosis-infected mice .
	manualset3
88129	3	399633	5	NULL	NULL	0	NULL	compounds	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In experiments in vitro against Mycobacterium tuberculosis , these compounds displayed minimum inhibitory concentration ( MIC ) values between several fold and several hundred fold greater than that of INH itself , on a molar basis , with some of the more active compounds having higher calculated values of log P. Among these derivatives , compound 1b , closely homologous to the INH metabolite 1a , N2-acetylisoniazid , provided unexpected protection in tuberculosis-infected mice .
	manualset3
88187	4	399633	5	NULL	NULL	0	NULL	minimum inhibitory concentration ( MIC ) values	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In experiments in vitro against Mycobacterium tuberculosis , these compounds displayed minimum inhibitory concentration ( MIC ) values between several fold and several hundred fold greater than that of INH itself , on a molar basis , with some of the more active compounds having higher calculated values of log P. Among these derivatives , compound 1b , closely homologous to the INH metabolite 1a , N2-acetylisoniazid , provided unexpected protection in tuberculosis-infected mice .
	manualset3
88188	5	399633	5	NULL	NULL	0	NULL	INH	Drug												NULL		0	NULL	NULL	NULL	NULL	NULL	In experiments in vitro against Mycobacterium tuberculosis , these compounds displayed minimum inhibitory concentration ( MIC ) values between several fold and several hundred fold greater than that of INH itself , on a molar basis , with some of the more active compounds having higher calculated values of log P. Among these derivatives , compound 1b , closely homologous to the INH metabolite 1a , N2-acetylisoniazid , provided unexpected protection in tuberculosis-infected mice .
	manualset3
88189	6	399633	5	NULL	NULL	0	NULL	molar basis	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In experiments in vitro against Mycobacterium tuberculosis , these compounds displayed minimum inhibitory concentration ( MIC ) values between several fold and several hundred fold greater than that of INH itself , on a molar basis , with some of the more active compounds having higher calculated values of log P. Among these derivatives , compound 1b , closely homologous to the INH metabolite 1a , N2-acetylisoniazid , provided unexpected protection in tuberculosis-infected mice .
	manualset3
88190	7	399633	5	NULL	NULL	0	NULL	active compounds	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In experiments in vitro against Mycobacterium tuberculosis , these compounds displayed minimum inhibitory concentration ( MIC ) values between several fold and several hundred fold greater than that of INH itself , on a molar basis , with some of the more active compounds having higher calculated values of log P. Among these derivatives , compound 1b , closely homologous to the INH metabolite 1a , N2-acetylisoniazid , provided unexpected protection in tuberculosis-infected mice .
	manualset3
88191	8	399633	5	NULL	NULL	0	NULL	log P	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In experiments in vitro against Mycobacterium tuberculosis , these compounds displayed minimum inhibitory concentration ( MIC ) values between several fold and several hundred fold greater than that of INH itself , on a molar basis , with some of the more active compounds having higher calculated values of log P. Among these derivatives , compound 1b , closely homologous to the INH metabolite 1a , N2-acetylisoniazid , provided unexpected protection in tuberculosis-infected mice .
	manualset3
88192	9	399633	5	NULL	NULL	0	NULL	derivatives	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In experiments in vitro against Mycobacterium tuberculosis , these compounds displayed minimum inhibitory concentration ( MIC ) values between several fold and several hundred fold greater than that of INH itself , on a molar basis , with some of the more active compounds having higher calculated values of log P. Among these derivatives , compound 1b , closely homologous to the INH metabolite 1a , N2-acetylisoniazid , provided unexpected protection in tuberculosis-infected mice .
	manualset3
88193	10	399633	5	NULL	NULL	0	NULL	compound 1b	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In experiments in vitro against Mycobacterium tuberculosis , these compounds displayed minimum inhibitory concentration ( MIC ) values between several fold and several hundred fold greater than that of INH itself , on a molar basis , with some of the more active compounds having higher calculated values of log P. Among these derivatives , compound 1b , closely homologous to the INH metabolite 1a , N2-acetylisoniazid , provided unexpected protection in tuberculosis-infected mice .
	manualset3
88194	11	399633	5	NULL	NULL	0	NULL	INH metabolite 1a	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In experiments in vitro against Mycobacterium tuberculosis , these compounds displayed minimum inhibitory concentration ( MIC ) values between several fold and several hundred fold greater than that of INH itself , on a molar basis , with some of the more active compounds having higher calculated values of log P. Among these derivatives , compound 1b , closely homologous to the INH metabolite 1a , N2-acetylisoniazid , provided unexpected protection in tuberculosis-infected mice .
	manualset3
88195	12	399633	5	NULL	NULL	0	NULL	N2-acetylisoniazid	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In experiments in vitro against Mycobacterium tuberculosis , these compounds displayed minimum inhibitory concentration ( MIC ) values between several fold and several hundred fold greater than that of INH itself , on a molar basis , with some of the more active compounds having higher calculated values of log P. Among these derivatives , compound 1b , closely homologous to the INH metabolite 1a , N2-acetylisoniazid , provided unexpected protection in tuberculosis-infected mice .
	manualset3
88196	13	399633	5	NULL	NULL	0	NULL	protection	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In experiments in vitro against Mycobacterium tuberculosis , these compounds displayed minimum inhibitory concentration ( MIC ) values between several fold and several hundred fold greater than that of INH itself , on a molar basis , with some of the more active compounds having higher calculated values of log P. Among these derivatives , compound 1b , closely homologous to the INH metabolite 1a , N2-acetylisoniazid , provided unexpected protection in tuberculosis-infected mice .
	manualset3
88197	14	399633	5	NULL	NULL	0	NULL	tuberculosis-infected mice	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In experiments in vitro against Mycobacterium tuberculosis , these compounds displayed minimum inhibitory concentration ( MIC ) values between several fold and several hundred fold greater than that of INH itself , on a molar basis , with some of the more active compounds having higher calculated values of log P. Among these derivatives , compound 1b , closely homologous to the INH metabolite 1a , N2-acetylisoniazid , provided unexpected protection in tuberculosis-infected mice .
	manualset3
88198	1	399634	5	NULL	NULL	0	NULL	45 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In fact , it has been estimated that approximately 45 % of epigenetic researchers today identify cancer/oncology as their main area of focus vis -- vis their epigenetic research efforts .
	manualset3
88199	2	399634	5	NULL	NULL	0	NULL	epigenetic researchers	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In fact , it has been estimated that approximately 45 % of epigenetic researchers today identify cancer/oncology as their main area of focus vis -- vis their epigenetic research efforts .
	manualset3
88200	3	399634	5	NULL	NULL	0	NULL	cancer/oncology	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In fact , it has been estimated that approximately 45 % of epigenetic researchers today identify cancer/oncology as their main area of focus vis -- vis their epigenetic research efforts .
	manualset3
88201	4	399634	5	NULL	NULL	0	NULL	main area of focus	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In fact , it has been estimated that approximately 45 % of epigenetic researchers today identify cancer/oncology as their main area of focus vis -- vis their epigenetic research efforts .
	manualset3
88202	5	399634	5	NULL	NULL	0	NULL	epigenetic research efforts	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In fact , it has been estimated that approximately 45 % of epigenetic researchers today identify cancer/oncology as their main area of focus vis -- vis their epigenetic research efforts .
	manualset3
88203	1	399635	5	NULL	NULL	0	NULL	spatial-temporal values	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In fact , these spatial-temporal values were stable during the time spent stroking and were higher or lower during the start , the turns ( in and out ) , and the finish .
	manualset3
88204	2	399635	5	NULL	NULL	0	NULL	time spent stroking	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	In fact , these spatial-temporal values were stable during the time spent stroking and were higher or lower during the start , the turns ( in and out ) , and the finish .
	manualset3
88205	3	399635	5	NULL	NULL	0	NULL	start	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In fact , these spatial-temporal values were stable during the time spent stroking and were higher or lower during the start , the turns ( in and out ) , and the finish .
	manualset3
88206	4	399635	5	NULL	NULL	0	NULL	turns ( in and out )	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In fact , these spatial-temporal values were stable during the time spent stroking and were higher or lower during the start , the turns ( in and out ) , and the finish .
	manualset3
88207	5	399635	5	NULL	NULL	0	NULL	finish	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In fact , these spatial-temporal values were stable during the time spent stroking and were higher or lower during the start , the turns ( in and out ) , and the finish .
	manualset3
88208	1	399636	5	NULL	NULL	0	NULL	females	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In females , the weight-related development of menarche leads to earlier menarche in obese girls than in normal weight girls .
	manualset3
88209	2	399636	5	NULL	NULL	0	NULL	weight-related development	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In females , the weight-related development of menarche leads to earlier menarche in obese girls than in normal weight girls .
	manualset3
88210	3	399636	5	NULL	NULL	0	NULL	menarche	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In females , the weight-related development of menarche leads to earlier menarche in obese girls than in normal weight girls .
	manualset3
88211	4	399636	5	NULL	NULL	0	NULL	earlier menarche	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In females , the weight-related development of menarche leads to earlier menarche in obese girls than in normal weight girls .
	manualset3
88212	5	399636	5	NULL	NULL	0	NULL	obese girls	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In females , the weight-related development of menarche leads to earlier menarche in obese girls than in normal weight girls .
	manualset3
88213	6	399636	5	NULL	NULL	0	NULL	normal weight girls	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In females , the weight-related development of menarche leads to earlier menarche in obese girls than in normal weight girls .
	manualset3
88214	1	399637	5	NULL	NULL	NULL	NULL	future	TimePoint												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In future , the choice of the ideal volume replacement regimen should not only be focused on its volume restoring properties , but additional effects ( e.g. on organ perfusion on , tissue oxygenation , inflammation , endothelial activation , capillary leakage ) should also be taken into account when treating hypovolemia in the critically ill .
	manualset3
88349	2	399637	5	NULL	NULL	NULL	NULL	 ideal volume replacement regimen	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In future , the choice of the ideal volume replacement regimen should not only be focused on its volume restoring properties , but additional effects ( e.g. on organ perfusion on , tissue oxygenation , inflammation , endothelial activation , capillary leakage ) should also be taken into account when treating hypovolemia in the critically ill .
	manualset3
88353	3	399637	5	NULL	NULL	0	NULL	additional effects	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In future , the choice of the ideal volume replacement regimen should not only be focused on its volume restoring properties , but additional effects ( e.g. on organ perfusion on , tissue oxygenation , inflammation , endothelial activation , capillary leakage ) should also be taken into account when treating hypovolemia in the critically ill .
	manualset3
88354	4	399637	5	NULL	NULL	0	NULL	organ perfusion	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In future , the choice of the ideal volume replacement regimen should not only be focused on its volume restoring properties , but additional effects ( e.g. on organ perfusion on , tissue oxygenation , inflammation , endothelial activation , capillary leakage ) should also be taken into account when treating hypovolemia in the critically ill .
	manualset3
88355	5	399637	5	NULL	NULL	NULL	NULL	tissue oxygenation	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In future , the choice of the ideal volume replacement regimen should not only be focused on its volume restoring properties , but additional effects ( e.g. on organ perfusion on , tissue oxygenation , inflammation , endothelial activation , capillary leakage ) should also be taken into account when treating hypovolemia in the critically ill .
	manualset3
88356	6	399637	5	NULL	NULL	0	NULL	inflammation 	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In future , the choice of the ideal volume replacement regimen should not only be focused on its volume restoring properties , but additional effects ( e.g. on organ perfusion on , tissue oxygenation , inflammation , endothelial activation , capillary leakage ) should also be taken into account when treating hypovolemia in the critically ill .
	manualset3
88357	7	399637	5	NULL	NULL	0	NULL	endothelial activation	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In future , the choice of the ideal volume replacement regimen should not only be focused on its volume restoring properties , but additional effects ( e.g. on organ perfusion on , tissue oxygenation , inflammation , endothelial activation , capillary leakage ) should also be taken into account when treating hypovolemia in the critically ill .
	manualset3
88358	8	399637	5	NULL	NULL	0	NULL	capillary leakage	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In future , the choice of the ideal volume replacement regimen should not only be focused on its volume restoring properties , but additional effects ( e.g. on organ perfusion on , tissue oxygenation , inflammation , endothelial activation , capillary leakage ) should also be taken into account when treating hypovolemia in the critically ill .
	manualset3
88359	9	399637	5	NULL	NULL	0	NULL	hypovolemia	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In future , the choice of the ideal volume replacement regimen should not only be focused on its volume restoring properties , but additional effects ( e.g. on organ perfusion on , tissue oxygenation , inflammation , endothelial activation , capillary leakage ) should also be taken into account when treating hypovolemia in the critically ill .
	manualset3
88360	10	399637	5	NULL	NULL	0	NULL	critically ill	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In future , the choice of the ideal volume replacement regimen should not only be focused on its volume restoring properties , but additional effects ( e.g. on organ perfusion on , tissue oxygenation , inflammation , endothelial activation , capillary leakage ) should also be taken into account when treating hypovolemia in the critically ill .
	manualset3
88361	11	399637	5	NULL	NULL	0	NULL	choice	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In future , the choice of the ideal volume replacement regimen should not only be focused on its volume restoring properties , but additional effects ( e.g. on organ perfusion on , tissue oxygenation , inflammation , endothelial activation , capillary leakage ) should also be taken into account when treating hypovolemia in the critically ill .
	manualset3
88362	1	399638	5	NULL	NULL	0	NULL	drug actions	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , drug actions on psi appear to be correlated with previously reported effects on Ca2 + transportation rather than oxidative phosphorylation associated with rat heart mitochondria .
	manualset3
88363	2	399638	5	NULL	NULL	0	NULL	psi	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , drug actions on psi appear to be correlated with previously reported effects on Ca2 + transportation rather than oxidative phosphorylation associated with rat heart mitochondria .
	manualset3
88364	3	399638	5	NULL	NULL	0	NULL	previously reported effects	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , drug actions on psi appear to be correlated with previously reported effects on Ca2 + transportation rather than oxidative phosphorylation associated with rat heart mitochondria .
	manualset3
88366	4	399638	5	NULL	NULL	NULL	NULL	Ca2 + transportation	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In general , drug actions on psi appear to be correlated with previously reported effects on Ca2 + transportation rather than oxidative phosphorylation associated with rat heart mitochondria .
	manualset3
88368	5	399638	5	NULL	NULL	0	NULL	oxidative phosphorylation	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , drug actions on psi appear to be correlated with previously reported effects on Ca2 + transportation rather than oxidative phosphorylation associated with rat heart mitochondria .
	manualset3
88369	6	399638	5	NULL	NULL	0	NULL	rat heart mitochondria	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , drug actions on psi appear to be correlated with previously reported effects on Ca2 + transportation rather than oxidative phosphorylation associated with rat heart mitochondria .
	manualset3
88370	1	399639	5	NULL	NULL	0	NULL	managed care	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , managed care has resulted in greater access to basic behavioral health and community-based services for children and adolescents , though access to inpatient hospital care has been reduced .
	manualset3
88374	2	399639	5	NULL	NULL	NULL	NULL	access to basic behavioral health	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In general , managed care has resulted in greater access to basic behavioral health and community-based services for children and adolescents , though access to inpatient hospital care has been reduced .
	manualset3
88375	3	399639	5	NULL	NULL	0	NULL	community-based services	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , managed care has resulted in greater access to basic behavioral health and community-based services for children and adolescents , though access to inpatient hospital care has been reduced .
	manualset3
88376	4	399639	5	NULL	NULL	0	NULL	children	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , managed care has resulted in greater access to basic behavioral health and community-based services for children and adolescents , though access to inpatient hospital care has been reduced .
	manualset3
88377	5	399639	5	NULL	NULL	0	NULL	adolescents	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , managed care has resulted in greater access to basic behavioral health and community-based services for children and adolescents , though access to inpatient hospital care has been reduced .
	manualset3
88378	6	399639	5	NULL	NULL	0	NULL	access to inpatient hospital care	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , managed care has resulted in greater access to basic behavioral health and community-based services for children and adolescents , though access to inpatient hospital care has been reduced .
	manualset3
88380	1	399640	5	NULL	NULL	0	NULL	patients	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , patients with higher level of ECP , ECP/Eo ratio , sIL-2R , sICAM-1 and with lower PC20H exhibited the higher risk of moderate asthma .
	manualset3
88381	2	399640	5	NULL	NULL	0	NULL	higher level of ECP , ECP/Eo ratio , sIL-2R , sICAM-1	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , patients with higher level of ECP , ECP/Eo ratio , sIL-2R , sICAM-1 and with lower PC20H exhibited the higher risk of moderate asthma .
	manualset3
88382	3	399640	5	NULL	NULL	0	NULL	lower PC20H	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , patients with higher level of ECP , ECP/Eo ratio , sIL-2R , sICAM-1 and with lower PC20H exhibited the higher risk of moderate asthma .
	manualset3
88383	4	399640	5	NULL	NULL	0	NULL	higher risk of moderate asthma	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , patients with higher level of ECP , ECP/Eo ratio , sIL-2R , sICAM-1 and with lower PC20H exhibited the higher risk of moderate asthma .
	manualset3
88387	1	399641	5	NULL	NULL	0	NULL	Transpharyngeal anterior atlanto-axial spondylodesis	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Transpharyngeal anterior atlanto-axial spondylodesis for old fractures of the odontoid process of the axis and compression of the spinal cord ) .
	manualset3
88395	2	399641	5	NULL	NULL	0	NULL	old fractures of the odontoid process of the axis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Transpharyngeal anterior atlanto-axial spondylodesis for old fractures of the odontoid process of the axis and compression of the spinal cord ) .
	manualset3
88396	3	399641	5	NULL	NULL	0	NULL	compression of the spinal cord	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Transpharyngeal anterior atlanto-axial spondylodesis for old fractures of the odontoid process of the axis and compression of the spinal cord ) .
	manualset3
88398	1	399642	5	NULL	NULL	0	NULL	physically abused children	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , physically abused children reported greater fear than nonabused children in response to all forms of interadult anger .
	manualset3
88400	2	399642	5	NULL	NULL	0	NULL	greater fear	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , physically abused children reported greater fear than nonabused children in response to all forms of interadult anger .
	manualset3
88401	3	399642	5	NULL	NULL	0	NULL	nonabused children	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , physically abused children reported greater fear than nonabused children in response to all forms of interadult anger .
	manualset3
88402	4	399642	5	NULL	NULL	0	NULL	response	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , physically abused children reported greater fear than nonabused children in response to all forms of interadult anger .
	manualset3
88403	5	399642	5	NULL	NULL	NULL	NULL	all forms of interadult anger	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In general , physically abused children reported greater fear than nonabused children in response to all forms of interadult anger .
	manualset3
88404	1	399643	5	NULL	NULL	0	NULL	non-marketed benefits	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , such non-marketed benefits provided by the case-study region more than compensate for the costs of forest maintenance .
	manualset3
88405	2	399643	5	NULL	NULL	0	NULL	case-study region	UnproperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , such non-marketed benefits provided by the case-study region more than compensate for the costs of forest maintenance .
	manualset3
88406	3	399643	5	NULL	NULL	0	NULL	compensate	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , such non-marketed benefits provided by the case-study region more than compensate for the costs of forest maintenance .
	manualset3
88407	4	399643	5	NULL	NULL	0	NULL	costs	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , such non-marketed benefits provided by the case-study region more than compensate for the costs of forest maintenance .
	manualset3
88408	5	399643	5	NULL	NULL	0	NULL	forest maintenance	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , such non-marketed benefits provided by the case-study region more than compensate for the costs of forest maintenance .
	manualset3
88409	1	399644	5	NULL	NULL	NULL	NULL	demographic factors	ExperimentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In general , the association between demographic factors and current HCV infection status was strengthened by use of latent-class analysis that combined data for markers of HCV infection , when compared with results of logistic regression analysis for each marker separately .
	manualset3
88410	2	399644	5	NULL	NULL	0	NULL	current HCV infection status	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , the association between demographic factors and current HCV infection status was strengthened by use of latent-class analysis that combined data for markers of HCV infection , when compared with results of logistic regression analysis for each marker separately .
	manualset3
88411	3	399644	5	NULL	NULL	0	NULL	latent-class analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , the association between demographic factors and current HCV infection status was strengthened by use of latent-class analysis that combined data for markers of HCV infection , when compared with results of logistic regression analysis for each marker separately .
	manualset3
88412	4	399644	5	NULL	NULL	0	NULL	data	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , the association between demographic factors and current HCV infection status was strengthened by use of latent-class analysis that combined data for markers of HCV infection , when compared with results of logistic regression analysis for each marker separately .
	manualset3
88413	5	399644	5	NULL	NULL	0	NULL	markers of HCV infection	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , the association between demographic factors and current HCV infection status was strengthened by use of latent-class analysis that combined data for markers of HCV infection , when compared with results of logistic regression analysis for each marker separately .
	manualset3
88414	6	399644	5	NULL	NULL	0	NULL	results	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , the association between demographic factors and current HCV infection status was strengthened by use of latent-class analysis that combined data for markers of HCV infection , when compared with results of logistic regression analysis for each marker separately .
	manualset3
88415	7	399644	5	NULL	NULL	0	NULL	logistic regression analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , the association between demographic factors and current HCV infection status was strengthened by use of latent-class analysis that combined data for markers of HCV infection , when compared with results of logistic regression analysis for each marker separately .
	manualset3
88416	8	399644	5	NULL	NULL	0	NULL	marker	Molecule												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , the association between demographic factors and current HCV infection status was strengthened by use of latent-class analysis that combined data for markers of HCV infection , when compared with results of logistic regression analysis for each marker separately .
	manualset3
88417	1	399645	5	NULL	NULL	0	NULL	Surgipro sutures	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , the new Surgipro sutures performed as good as Prolene sutures in terms of mechanical properties ; but there were some differences in fundamental properties between these two types of PP sutures , particularly in finer size PP sutures .
	manualset3
88418	2	399645	5	NULL	NULL	0	NULL	Prolene sutures	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , the new Surgipro sutures performed as good as Prolene sutures in terms of mechanical properties ; but there were some differences in fundamental properties between these two types of PP sutures , particularly in finer size PP sutures .
	manualset3
88419	3	399645	5	NULL	NULL	NULL	NULL	PP sutures	LaboratoryExperimentalFactor												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In general , the new Surgipro sutures performed as good as Prolene sutures in terms of mechanical properties ; but there were some differences in fundamental properties between these two types of PP sutures , particularly in finer size PP sutures .
	manualset3
88420	4	399645	5	NULL	NULL	0	NULL	finer size PP sutures	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	In general , the new Surgipro sutures performed as good as Prolene sutures in terms of mechanical properties ; but there were some differences in fundamental properties between these two types of PP sutures , particularly in finer size PP sutures .
	manualset3
88421	1	399646	5	NULL	NULL	0	NULL	goldfish	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In goldfish , unlike most teleosts , the vagal lobe is laminated , highly differentiated structure containing both sensory and motor layers .
	manualset3
88422	2	399646	5	NULL	NULL	0	NULL	teleosts	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In goldfish , unlike most teleosts , the vagal lobe is laminated , highly differentiated structure containing both sensory and motor layers .
	manualset3
88432	3	399646	5	NULL	NULL	0	NULL	vagal lobe	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In goldfish , unlike most teleosts , the vagal lobe is laminated , highly differentiated structure containing both sensory and motor layers .
	manualset3
88438	4	399646	5	NULL	NULL	0	NULL	sensory and motor layers	AnatomicalPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In goldfish , unlike most teleosts , the vagal lobe is laminated , highly differentiated structure containing both sensory and motor layers .
	manualset3
88439	1	399647	5	NULL	NULL	0	NULL	hamsters	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In hamsters , tocopherols were the only tocol readily detected in all tissues , except adipose during tocotrienol supplementation .
	manualset3
88440	2	399647	5	NULL	NULL	0	NULL	tocopherols	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In hamsters , tocopherols were the only tocol readily detected in all tissues , except adipose during tocotrienol supplementation .
	manualset3
88442	3	399647	5	NULL	NULL	0	NULL	tocol	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In hamsters , tocopherols were the only tocol readily detected in all tissues , except adipose during tocotrienol supplementation .
	manualset3
88443	4	399647	5	NULL	NULL	0	NULL	tissues	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	In hamsters , tocopherols were the only tocol readily detected in all tissues , except adipose during tocotrienol supplementation .
	manualset3
88444	5	399647	5	NULL	NULL	0	NULL	adipose	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	In hamsters , tocopherols were the only tocol readily detected in all tissues , except adipose during tocotrienol supplementation .
	manualset3
88458	6	399647	5	NULL	NULL	NULL	NULL	tocotrienol supplementation	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In hamsters , tocopherols were the only tocol readily detected in all tissues , except adipose during tocotrienol supplementation .
	manualset3
88459	1	399648	5	NULL	NULL	0	NULL	heart	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In heart , LDH-1 ( H4 ) was concentrated in mitochondria whereas LDH-5 ( M4 ) was present in both mitochondria and surrounding cytosol and organelles .
	manualset3
88460	2	399648	5	NULL	NULL	0	NULL	 LDH-1 ( H4 )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In heart , LDH-1 ( H4 ) was concentrated in mitochondria whereas LDH-5 ( M4 ) was present in both mitochondria and surrounding cytosol and organelles .
	manualset3
88461	3	399648	5	NULL	NULL	0	NULL	mitochondria	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In heart , LDH-1 ( H4 ) was concentrated in mitochondria whereas LDH-5 ( M4 ) was present in both mitochondria and surrounding cytosol and organelles .
	manualset3
88462	4	399648	5	NULL	NULL	0	NULL	LDH-5 ( M4 )	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In heart , LDH-1 ( H4 ) was concentrated in mitochondria whereas LDH-5 ( M4 ) was present in both mitochondria and surrounding cytosol and organelles .
	manualset3
88463	5	399648	5	NULL	NULL	0	NULL	mitochondria	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In heart , LDH-1 ( H4 ) was concentrated in mitochondria whereas LDH-5 ( M4 ) was present in both mitochondria and surrounding cytosol and organelles .
	manualset3
88464	6	399648	5	NULL	NULL	0	NULL	surrounding cytosol and organelles	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In heart , LDH-1 ( H4 ) was concentrated in mitochondria whereas LDH-5 ( M4 ) was present in both mitochondria and surrounding cytosol and organelles .
	manualset3
88465	1	399649	5	NULL	NULL	0	NULL	isolated , DNA synthesizing nuclei	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In isolated , DNA synthesizing nuclei , on the other hand , the slight inhibition of DNA synthesis by BTC is reversed merely by addition of Mg2 + .
	manualset3
88466	2	399649	5	NULL	NULL	0	NULL	slight inhibition of DNA synthesis	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In isolated , DNA synthesizing nuclei , on the other hand , the slight inhibition of DNA synthesis by BTC is reversed merely by addition of Mg2 + .
	manualset3
88467	3	399649	5	NULL	NULL	0	NULL	BTC	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In isolated , DNA synthesizing nuclei , on the other hand , the slight inhibition of DNA synthesis by BTC is reversed merely by addition of Mg2 + .
	manualset3
88468	4	399649	5	NULL	NULL	NULL	NULL	addition of Mg2 +	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In isolated , DNA synthesizing nuclei , on the other hand , the slight inhibition of DNA synthesis by BTC is reversed merely by addition of Mg2 + .
	manualset3
88470	1	399650	5	NULL	NULL	0	NULL	males	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , Chlam Ab were not significantly related to the outcome of semen analysis , including screening for ASA ( IgG and/or IgA ) in semen , and several parameters of sperm functional capacity .
	manualset3
88471	2	399650	5	NULL	NULL	0	NULL	Chlam Ab	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , Chlam Ab were not significantly related to the outcome of semen analysis , including screening for ASA ( IgG and/or IgA ) in semen , and several parameters of sperm functional capacity .
	manualset3
88472	3	399650	5	NULL	NULL	0	NULL	outcome	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , Chlam Ab were not significantly related to the outcome of semen analysis , including screening for ASA ( IgG and/or IgA ) in semen , and several parameters of sperm functional capacity .
	manualset3
88473	4	399650	5	NULL	NULL	0	NULL	semen analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , Chlam Ab were not significantly related to the outcome of semen analysis , including screening for ASA ( IgG and/or IgA ) in semen , and several parameters of sperm functional capacity .
	manualset3
88474	5	399650	5	NULL	NULL	0	NULL	screening for ASA ( IgG and/or IgA )	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , Chlam Ab were not significantly related to the outcome of semen analysis , including screening for ASA ( IgG and/or IgA ) in semen , and several parameters of sperm functional capacity .
	manualset3
88475	6	399650	5	NULL	NULL	NULL	NULL	semen	Tissue												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In males , Chlam Ab were not significantly related to the outcome of semen analysis , including screening for ASA ( IgG and/or IgA ) in semen , and several parameters of sperm functional capacity .
	manualset3
88476	7	399650	5	NULL	NULL	0	NULL	several parameters	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , Chlam Ab were not significantly related to the outcome of semen analysis , including screening for ASA ( IgG and/or IgA ) in semen , and several parameters of sperm functional capacity .
	manualset3
88477	8	399650	5	NULL	NULL	0	NULL	sperm functional capacity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , Chlam Ab were not significantly related to the outcome of semen analysis , including screening for ASA ( IgG and/or IgA ) in semen , and several parameters of sperm functional capacity .
	manualset3
88483	1	399651	5	NULL	NULL	0	NULL	males	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , higher BR was observed in childhood-adolescence age groups and at older ages , while in females a higher level of BR was observed during childhood .
	manualset3
88492	2	399651	5	NULL	NULL	0	NULL	higher BR	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , higher BR was observed in childhood-adolescence age groups and at older ages , while in females a higher level of BR was observed during childhood .
	manualset3
88493	3	399651	5	NULL	NULL	0	NULL	childhood-adolescence age groups	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , higher BR was observed in childhood-adolescence age groups and at older ages , while in females a higher level of BR was observed during childhood .
	manualset3
88498	4	399651	5	NULL	NULL	0	NULL	older ages	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , higher BR was observed in childhood-adolescence age groups and at older ages , while in females a higher level of BR was observed during childhood .
	manualset3
88500	5	399651	5	NULL	NULL	0	NULL	females	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , higher BR was observed in childhood-adolescence age groups and at older ages , while in females a higher level of BR was observed during childhood .
	manualset3
88502	6	399651	5	NULL	NULL	0	NULL	higher level of BR	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , higher BR was observed in childhood-adolescence age groups and at older ages , while in females a higher level of BR was observed during childhood .
	manualset3
88506	7	399651	5	NULL	NULL	0	NULL	childhood	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , higher BR was observed in childhood-adolescence age groups and at older ages , while in females a higher level of BR was observed during childhood .
	manualset3
88507	1	399652	5	NULL	NULL	0	NULL	males	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , neither a history of a previous primary nor a history of radiotherapy was associated significantly with lung cancer ; however , the numbers of exposed cases were small .
	manualset3
88508	2	399652	5	NULL	NULL	0	NULL	history	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , neither a history of a previous primary nor a history of radiotherapy was associated significantly with lung cancer ; however , the numbers of exposed cases were small .
	manualset3
88509	3	399652	5	NULL	NULL	0	NULL	history	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , neither a history of a previous primary nor a history of radiotherapy was associated significantly with lung cancer ; however , the numbers of exposed cases were small .
	manualset3
88510	4	399652	5	NULL	NULL	0	NULL	radiotherapy	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , neither a history of a previous primary nor a history of radiotherapy was associated significantly with lung cancer ; however , the numbers of exposed cases were small .
	manualset3
88513	5	399652	5	NULL	NULL	0	NULL	lung cancer	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , neither a history of a previous primary nor a history of radiotherapy was associated significantly with lung cancer ; however , the numbers of exposed cases were small .
	manualset3
88515	6	399652	5	NULL	NULL	0	NULL	numbers of exposed cases	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In males , neither a history of a previous primary nor a history of radiotherapy was associated significantly with lung cancer ; however , the numbers of exposed cases were small .
	manualset3
88518	1	399653	5	NULL	NULL	0	NULL	mammals	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In mammals , imprinted genes directly regulate placental function and nutrient distribution from mother to fetus ; however , none of the & gt ; 60 imprinted genes thus far reported in plants have been demonstrated to play an equivalent role in regulating the flow of resources to the embryo .
	manualset3
88520	2	399653	5	NULL	NULL	0	NULL	imprinted genes	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	In mammals , imprinted genes directly regulate placental function and nutrient distribution from mother to fetus ; however , none of the & gt ; 60 imprinted genes thus far reported in plants have been demonstrated to play an equivalent role in regulating the flow of resources to the embryo .
	manualset3
88521	3	399653	5	NULL	NULL	0	NULL	regulate placental function	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In mammals , imprinted genes directly regulate placental function and nutrient distribution from mother to fetus ; however , none of the & gt ; 60 imprinted genes thus far reported in plants have been demonstrated to play an equivalent role in regulating the flow of resources to the embryo .
	manualset3
88522	4	399653	5	NULL	NULL	0	NULL	nutrient distribution	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In mammals , imprinted genes directly regulate placental function and nutrient distribution from mother to fetus ; however , none of the & gt ; 60 imprinted genes thus far reported in plants have been demonstrated to play an equivalent role in regulating the flow of resources to the embryo .
	manualset3
88525	5	399653	5	NULL	NULL	0	NULL	mother	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In mammals , imprinted genes directly regulate placental function and nutrient distribution from mother to fetus ; however , none of the & gt ; 60 imprinted genes thus far reported in plants have been demonstrated to play an equivalent role in regulating the flow of resources to the embryo .
	manualset3
88527	6	399653	5	NULL	NULL	0	NULL	fetus	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In mammals , imprinted genes directly regulate placental function and nutrient distribution from mother to fetus ; however , none of the & gt ; 60 imprinted genes thus far reported in plants have been demonstrated to play an equivalent role in regulating the flow of resources to the embryo .
	manualset3
88530	7	399653	5	NULL	NULL	0	NULL	60 imprinted genes	Gene												NULL		0	NULL	NULL	NULL	NULL	NULL	In mammals , imprinted genes directly regulate placental function and nutrient distribution from mother to fetus ; however , none of the & gt ; 60 imprinted genes thus far reported in plants have been demonstrated to play an equivalent role in regulating the flow of resources to the embryo .
	manualset3
88531	8	399653	5	NULL	NULL	0	NULL	plants	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In mammals , imprinted genes directly regulate placental function and nutrient distribution from mother to fetus ; however , none of the & gt ; 60 imprinted genes thus far reported in plants have been demonstrated to play an equivalent role in regulating the flow of resources to the embryo .
	manualset3
88532	9	399653	5	NULL	NULL	0	NULL	equivalent role	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In mammals , imprinted genes directly regulate placental function and nutrient distribution from mother to fetus ; however , none of the & gt ; 60 imprinted genes thus far reported in plants have been demonstrated to play an equivalent role in regulating the flow of resources to the embryo .
	manualset3
88533	10	399653	5	NULL	NULL	0	NULL	flow of resources	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In mammals , imprinted genes directly regulate placental function and nutrient distribution from mother to fetus ; however , none of the & gt ; 60 imprinted genes thus far reported in plants have been demonstrated to play an equivalent role in regulating the flow of resources to the embryo .
	manualset3
88534	11	399653	5	NULL	NULL	0	NULL	embryo	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In mammals , imprinted genes directly regulate placental function and nutrient distribution from mother to fetus ; however , none of the & gt ; 60 imprinted genes thus far reported in plants have been demonstrated to play an equivalent role in regulating the flow of resources to the embryo .
	manualset3
88535	1	399654	5	NULL	NULL	0	NULL	men	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In men , the average length was 2.2 cm ( range 1.4-3 .8 cm ) , whereas in women the average length was 2.0 cm ( range 1.0-3 .2 cm ) ( P less than .01 ) .
	manualset3
88536	2	399654	5	NULL	NULL	0	NULL	average length	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In men , the average length was 2.2 cm ( range 1.4-3 .8 cm ) , whereas in women the average length was 2.0 cm ( range 1.0-3 .2 cm ) ( P less than .01 ) .
	manualset3
88537	3	399654	5	NULL	NULL	0	NULL	2.2 cm ( range 1.4-3 .8 cm )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In men , the average length was 2.2 cm ( range 1.4-3 .8 cm ) , whereas in women the average length was 2.0 cm ( range 1.0-3 .2 cm ) ( P less than .01 ) .
	manualset3
88538	4	399654	5	NULL	NULL	0	NULL	women	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In men , the average length was 2.2 cm ( range 1.4-3 .8 cm ) , whereas in women the average length was 2.0 cm ( range 1.0-3 .2 cm ) ( P less than .01 ) .
	manualset3
88539	5	399654	5	NULL	NULL	0	NULL	average length	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In men , the average length was 2.2 cm ( range 1.4-3 .8 cm ) , whereas in women the average length was 2.0 cm ( range 1.0-3 .2 cm ) ( P less than .01 ) .
	manualset3
88540	6	399654	5	NULL	NULL	0	NULL	2.0 cm ( range 1.0-3 .2 cm ) ( P less than .01 )	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In men , the average length was 2.2 cm ( range 1.4-3 .8 cm ) , whereas in women the average length was 2.0 cm ( range 1.0-3 .2 cm ) ( P less than .01 ) .
	manualset3
88541	1	399655	5	NULL	NULL	0	NULL	monkeys	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In monkeys , the selective KOR antagonist , nor-binaltorphimine ( nor-BNI ) , produces a long-lasting antagonism of the antinociceptive effects of U-50488H but not those of bremazocine , suggesting that KOR-mediated antinociception may occur through two distinct KORs .
	manualset3
88543	2	399655	5	NULL	NULL	0	NULL	selective KOR antagonist , nor-binaltorphimine ( nor-BNI )	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	In monkeys , the selective KOR antagonist , nor-binaltorphimine ( nor-BNI ) , produces a long-lasting antagonism of the antinociceptive effects of U-50488H but not those of bremazocine , suggesting that KOR-mediated antinociception may occur through two distinct KORs .
	manualset3
88545	3	399655	5	NULL	NULL	0	NULL	long-lasting antagonism	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In monkeys , the selective KOR antagonist , nor-binaltorphimine ( nor-BNI ) , produces a long-lasting antagonism of the antinociceptive effects of U-50488H but not those of bremazocine , suggesting that KOR-mediated antinociception may occur through two distinct KORs .
	manualset3
88547	4	399655	5	NULL	NULL	0	NULL	antinociceptive effects	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In monkeys , the selective KOR antagonist , nor-binaltorphimine ( nor-BNI ) , produces a long-lasting antagonism of the antinociceptive effects of U-50488H but not those of bremazocine , suggesting that KOR-mediated antinociception may occur through two distinct KORs .
	manualset3
88551	5	399655	5	NULL	NULL	0	NULL	U-50488H 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In monkeys , the selective KOR antagonist , nor-binaltorphimine ( nor-BNI ) , produces a long-lasting antagonism of the antinociceptive effects of U-50488H but not those of bremazocine , suggesting that KOR-mediated antinociception may occur through two distinct KORs .
	manualset3
88633	6	399655	5	NULL	NULL	0	NULL	bremazocine	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	In monkeys , the selective KOR antagonist , nor-binaltorphimine ( nor-BNI ) , produces a long-lasting antagonism of the antinociceptive effects of U-50488H but not those of bremazocine , suggesting that KOR-mediated antinociception may occur through two distinct KORs .
	manualset3
88634	7	399655	5	NULL	NULL	0	NULL	KOR-mediated antinociception	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In monkeys , the selective KOR antagonist , nor-binaltorphimine ( nor-BNI ) , produces a long-lasting antagonism of the antinociceptive effects of U-50488H but not those of bremazocine , suggesting that KOR-mediated antinociception may occur through two distinct KORs .
	manualset3
88635	8	399655	5	NULL	NULL	0	NULL	KORs	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In monkeys , the selective KOR antagonist , nor-binaltorphimine ( nor-BNI ) , produces a long-lasting antagonism of the antinociceptive effects of U-50488H but not those of bremazocine , suggesting that KOR-mediated antinociception may occur through two distinct KORs .
	manualset3
88636	1	399656	5	NULL	NULL	NULL	NULL	Traumatic false aneurysm	MedicalFinding												NULL		NULL	NULL	NULL	NULL	NULL	NULL	( Traumatic false aneurysm of the superior mesenteric artery with perforation into the duodenum ; surgery ; recovery ) .
	manualset3
88637	2	399656	5	NULL	NULL	0	NULL	superior mesenteric artery	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( Traumatic false aneurysm of the superior mesenteric artery with perforation into the duodenum ; surgery ; recovery ) .
	manualset3
88638	3	399656	5	NULL	NULL	0	NULL	perforation	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Traumatic false aneurysm of the superior mesenteric artery with perforation into the duodenum ; surgery ; recovery ) .
	manualset3
88639	4	399656	5	NULL	NULL	0	NULL	duodenum	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	( Traumatic false aneurysm of the superior mesenteric artery with perforation into the duodenum ; surgery ; recovery ) .
	manualset3
88640	5	399656	5	NULL	NULL	0	NULL	surgery	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Traumatic false aneurysm of the superior mesenteric artery with perforation into the duodenum ; surgery ; recovery ) .
	manualset3
88641	6	399656	5	NULL	NULL	0	NULL	recovery	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	( Traumatic false aneurysm of the superior mesenteric artery with perforation into the duodenum ; surgery ; recovery ) .
	manualset3
88642	1	399657	5	NULL	NULL	0	NULL	immunofluorescence study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In parallel , an immunofluorescence study of tight-junction protein expression of PND60 offspring from contaminated rats showed a disorganization of the tight-junction proteins claudin-2 and claudin-5 , specifically expressed in the proximal tubule and glomerulus , respectively .
	manualset3
88643	2	399657	5	NULL	NULL	NULL	NULL	tight-junction protein expression	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In parallel , an immunofluorescence study of tight-junction protein expression of PND60 offspring from contaminated rats showed a disorganization of the tight-junction proteins claudin-2 and claudin-5 , specifically expressed in the proximal tubule and glomerulus , respectively .
	manualset3
88644	3	399657	5	NULL	NULL	0	NULL	PND60 offspring	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In parallel , an immunofluorescence study of tight-junction protein expression of PND60 offspring from contaminated rats showed a disorganization of the tight-junction proteins claudin-2 and claudin-5 , specifically expressed in the proximal tubule and glomerulus , respectively .
	manualset3
88645	4	399657	5	NULL	NULL	0	NULL	contaminated rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In parallel , an immunofluorescence study of tight-junction protein expression of PND60 offspring from contaminated rats showed a disorganization of the tight-junction proteins claudin-2 and claudin-5 , specifically expressed in the proximal tubule and glomerulus , respectively .
	manualset3
88646	5	399657	5	NULL	NULL	0	NULL	disorganization of the tight-junction protein claudin-2	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In parallel , an immunofluorescence study of tight-junction protein expression of PND60 offspring from contaminated rats showed a disorganization of the tight-junction proteins claudin-2 and claudin-5 , specifically expressed in the proximal tubule and glomerulus , respectively .
	manualset3
88647	6	399657	5	NULL	NULL	0	NULL	disorganization of the tight-junction proteins claudin-5	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In parallel , an immunofluorescence study of tight-junction protein expression of PND60 offspring from contaminated rats showed a disorganization of the tight-junction proteins claudin-2 and claudin-5 , specifically expressed in the proximal tubule and glomerulus , respectively .
	manualset3
88648	7	399657	5	NULL	NULL	0	NULL	proximal tubule	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In parallel , an immunofluorescence study of tight-junction protein expression of PND60 offspring from contaminated rats showed a disorganization of the tight-junction proteins claudin-2 and claudin-5 , specifically expressed in the proximal tubule and glomerulus , respectively .
	manualset3
88649	8	399657	5	NULL	NULL	0	NULL	glomerulus	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In parallel , an immunofluorescence study of tight-junction protein expression of PND60 offspring from contaminated rats showed a disorganization of the tight-junction proteins claudin-2 and claudin-5 , specifically expressed in the proximal tubule and glomerulus , respectively .
	manualset3
88650	1	399658	5	NULL	NULL	0	NULL	multigram-scale diastereoselective diacetoxylation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , a multigram-scale diastereoselective diacetoxylation of methyl cinnamate ( 5.00 g ) was also accomplished in a few hours , maintaining the same efficiency as small-scale reaction .
	manualset3
88651	2	399658	5	NULL	NULL	0	NULL	methyl cinnamate ( 5.00 g ) 	SmallMolecule												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , a multigram-scale diastereoselective diacetoxylation of methyl cinnamate ( 5.00 g ) was also accomplished in a few hours , maintaining the same efficiency as small-scale reaction .
	manualset3
88652	3	399658	5	NULL	NULL	0	NULL	few hours	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , a multigram-scale diastereoselective diacetoxylation of methyl cinnamate ( 5.00 g ) was also accomplished in a few hours , maintaining the same efficiency as small-scale reaction .
	manualset3
88653	4	399658	5	NULL	NULL	0	NULL	efficiency	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , a multigram-scale diastereoselective diacetoxylation of methyl cinnamate ( 5.00 g ) was also accomplished in a few hours , maintaining the same efficiency as small-scale reaction .
	manualset3
88654	5	399658	5	NULL	NULL	0	NULL	small-scale reaction	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , a multigram-scale diastereoselective diacetoxylation of methyl cinnamate ( 5.00 g ) was also accomplished in a few hours , maintaining the same efficiency as small-scale reaction .
	manualset3
88655	1	399659	5	NULL	NULL	0	NULL	subgroup of NPY-I neurons	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , a subgroup of NPY-I neurons , distinguished by a higher percentage of unmyelinated axon coverage of the plasmalemmal surface , was present in young , but not aged , rats .
	manualset3
88656	2	399659	5	NULL	NULL	0	NULL	higher percentage	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , a subgroup of NPY-I neurons , distinguished by a higher percentage of unmyelinated axon coverage of the plasmalemmal surface , was present in young , but not aged , rats .
	manualset3
88657	3	399659	5	NULL	NULL	0	NULL	unmyelinated axon coverage of the plasmalemmal surface	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , a subgroup of NPY-I neurons , distinguished by a higher percentage of unmyelinated axon coverage of the plasmalemmal surface , was present in young , but not aged , rats .
	manualset3
88658	4	399659	5	NULL	NULL	0	NULL	young rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , a subgroup of NPY-I neurons , distinguished by a higher percentage of unmyelinated axon coverage of the plasmalemmal surface , was present in young , but not aged , rats .
	manualset3
88659	5	399659	5	NULL	NULL	0	NULL	aged , rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , a subgroup of NPY-I neurons , distinguished by a higher percentage of unmyelinated axon coverage of the plasmalemmal surface , was present in young , but not aged , rats .
	manualset3
88660	1	399660	5	NULL	NULL	0	NULL	accidental wounds	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , accidental wounds produced by used needles , especially needles contaminated with blood from Ag H be positive individuals , are frequently followed by clinical or serological evidence of viral hepatitis .
	manualset3
88661	2	399660	5	NULL	NULL	0	NULL	used needles	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , accidental wounds produced by used needles , especially needles contaminated with blood from Ag H be positive individuals , are frequently followed by clinical or serological evidence of viral hepatitis .
	manualset3
88662	3	399660	5	NULL	NULL	0	NULL	 needles	MedicalDevice												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , accidental wounds produced by used needles , especially needles contaminated with blood from Ag H be positive individuals , are frequently followed by clinical or serological evidence of viral hepatitis .
	manualset3
88663	4	399660	5	NULL	NULL	0	NULL	blood	Tissue												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , accidental wounds produced by used needles , especially needles contaminated with blood from Ag H be positive individuals , are frequently followed by clinical or serological evidence of viral hepatitis .
	manualset3
88664	5	399660	5	NULL	NULL	0	NULL	Ag H be positive individuals	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , accidental wounds produced by used needles , especially needles contaminated with blood from Ag H be positive individuals , are frequently followed by clinical or serological evidence of viral hepatitis .
	manualset3
88665	6	399660	5	NULL	NULL	0	NULL	clinical or serological evidence	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , accidental wounds produced by used needles , especially needles contaminated with blood from Ag H be positive individuals , are frequently followed by clinical or serological evidence of viral hepatitis .
	manualset3
88666	7	399660	5	NULL	NULL	0	NULL	viral hepatitis	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , accidental wounds produced by used needles , especially needles contaminated with blood from Ag H be positive individuals , are frequently followed by clinical or serological evidence of viral hepatitis .
	manualset3
88667	1	399661	5	NULL	NULL	0	NULL	pharmacological studies	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , pharmacological studies highlighted the crucial role for the neuropeptide oxytocin in social behavior and emotional perception .
	manualset3
88668	2	399661	5	NULL	NULL	0	NULL	crucial role	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , pharmacological studies highlighted the crucial role for the neuropeptide oxytocin in social behavior and emotional perception .
	manualset3
88669	3	399661	5	NULL	NULL	0	NULL	neuropeptide oxytocin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , pharmacological studies highlighted the crucial role for the neuropeptide oxytocin in social behavior and emotional perception .
	manualset3
88670	4	399661	5	NULL	NULL	0	NULL	social behavior	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , pharmacological studies highlighted the crucial role for the neuropeptide oxytocin in social behavior and emotional perception .
	manualset3
88671	5	399661	5	NULL	NULL	0	NULL	emotional perception	MentalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , pharmacological studies highlighted the crucial role for the neuropeptide oxytocin in social behavior and emotional perception .
	manualset3
88672	1	399662	5	NULL	NULL	0	NULL	phylogenetic methods	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , phylogenetic methods can quantitatively ( 1 ) test whether specific cognitive abilities are correlated with life history ( e.g. , lifespan ) , morphology ( e.g. , brain size ) , or socio-ecological variables ( e.g. , social system ) , ( 2 ) measure how strongly phylogenetic relatedness predicts the distribution of cognitive skills across species , and ( 3 ) estimate the ancestral state of a given cognitive trait using measures of cognitive performance from extant species .
	manualset3
88674	2	399662	5	NULL	NULL	NULL	NULL	specific cognitive abilities	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In particular , phylogenetic methods can quantitatively ( 1 ) test whether specific cognitive abilities are correlated with life history ( e.g. , lifespan ) , morphology ( e.g. , brain size ) , or socio-ecological variables ( e.g. , social system ) , ( 2 ) measure how strongly phylogenetic relatedness predicts the distribution of cognitive skills across species , and ( 3 ) estimate the ancestral state of a given cognitive trait using measures of cognitive performance from extant species .
	manualset3
88675	3	399662	5	NULL	NULL	NULL	NULL	life history ( e.g. , lifespan )	Duration												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In particular , phylogenetic methods can quantitatively ( 1 ) test whether specific cognitive abilities are correlated with life history ( e.g. , lifespan ) , morphology ( e.g. , brain size ) , or socio-ecological variables ( e.g. , social system ) , ( 2 ) measure how strongly phylogenetic relatedness predicts the distribution of cognitive skills across species , and ( 3 ) estimate the ancestral state of a given cognitive trait using measures of cognitive performance from extant species .
	manualset3
88676	4	399662	5	NULL	NULL	NULL	NULL	morphology ( e.g. , brain size )	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In particular , phylogenetic methods can quantitatively ( 1 ) test whether specific cognitive abilities are correlated with life history ( e.g. , lifespan ) , morphology ( e.g. , brain size ) , or socio-ecological variables ( e.g. , social system ) , ( 2 ) measure how strongly phylogenetic relatedness predicts the distribution of cognitive skills across species , and ( 3 ) estimate the ancestral state of a given cognitive trait using measures of cognitive performance from extant species .
	manualset3
88677	5	399662	5	NULL	NULL	NULL	NULL	socio-ecological variables ( e.g. , social system )	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In particular , phylogenetic methods can quantitatively ( 1 ) test whether specific cognitive abilities are correlated with life history ( e.g. , lifespan ) , morphology ( e.g. , brain size ) , or socio-ecological variables ( e.g. , social system ) , ( 2 ) measure how strongly phylogenetic relatedness predicts the distribution of cognitive skills across species , and ( 3 ) estimate the ancestral state of a given cognitive trait using measures of cognitive performance from extant species .
	manualset3
88679	6	399662	5	NULL	NULL	NULL	NULL	phylogenetic relatedness	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In particular , phylogenetic methods can quantitatively ( 1 ) test whether specific cognitive abilities are correlated with life history ( e.g. , lifespan ) , morphology ( e.g. , brain size ) , or socio-ecological variables ( e.g. , social system ) , ( 2 ) measure how strongly phylogenetic relatedness predicts the distribution of cognitive skills across species , and ( 3 ) estimate the ancestral state of a given cognitive trait using measures of cognitive performance from extant species .
	manualset3
88680	9	399662	5	NULL	NULL	0	NULL	distribution of cognitive skills	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , phylogenetic methods can quantitatively ( 1 ) test whether specific cognitive abilities are correlated with life history ( e.g. , lifespan ) , morphology ( e.g. , brain size ) , or socio-ecological variables ( e.g. , social system ) , ( 2 ) measure how strongly phylogenetic relatedness predicts the distribution of cognitive skills across species , and ( 3 ) estimate the ancestral state of a given cognitive trait using measures of cognitive performance from extant species .
	manualset3
88681	10	399662	5	NULL	NULL	0	NULL	species	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , phylogenetic methods can quantitatively ( 1 ) test whether specific cognitive abilities are correlated with life history ( e.g. , lifespan ) , morphology ( e.g. , brain size ) , or socio-ecological variables ( e.g. , social system ) , ( 2 ) measure how strongly phylogenetic relatedness predicts the distribution of cognitive skills across species , and ( 3 ) estimate the ancestral state of a given cognitive trait using measures of cognitive performance from extant species .
	manualset3
88683	11	399662	5	NULL	NULL	NULL	NULL	ancestral state	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In particular , phylogenetic methods can quantitatively ( 1 ) test whether specific cognitive abilities are correlated with life history ( e.g. , lifespan ) , morphology ( e.g. , brain size ) , or socio-ecological variables ( e.g. , social system ) , ( 2 ) measure how strongly phylogenetic relatedness predicts the distribution of cognitive skills across species , and ( 3 ) estimate the ancestral state of a given cognitive trait using measures of cognitive performance from extant species .
	manualset3
88684	12	399662	5	NULL	NULL	NULL	NULL	cognitive trait	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In particular , phylogenetic methods can quantitatively ( 1 ) test whether specific cognitive abilities are correlated with life history ( e.g. , lifespan ) , morphology ( e.g. , brain size ) , or socio-ecological variables ( e.g. , social system ) , ( 2 ) measure how strongly phylogenetic relatedness predicts the distribution of cognitive skills across species , and ( 3 ) estimate the ancestral state of a given cognitive trait using measures of cognitive performance from extant species .
	manualset3
88685	13	399662	5	NULL	NULL	NULL	NULL	cognitive performance	MentalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In particular , phylogenetic methods can quantitatively ( 1 ) test whether specific cognitive abilities are correlated with life history ( e.g. , lifespan ) , morphology ( e.g. , brain size ) , or socio-ecological variables ( e.g. , social system ) , ( 2 ) measure how strongly phylogenetic relatedness predicts the distribution of cognitive skills across species , and ( 3 ) estimate the ancestral state of a given cognitive trait using measures of cognitive performance from extant species .
	manualset3
88686	14	399662	5	NULL	NULL	NULL	NULL	extant species	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In particular , phylogenetic methods can quantitatively ( 1 ) test whether specific cognitive abilities are correlated with life history ( e.g. , lifespan ) , morphology ( e.g. , brain size ) , or socio-ecological variables ( e.g. , social system ) , ( 2 ) measure how strongly phylogenetic relatedness predicts the distribution of cognitive skills across species , and ( 3 ) estimate the ancestral state of a given cognitive trait using measures of cognitive performance from extant species .
	manualset3
88687	1	399663	5	NULL	NULL	0	NULL	examples	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , some examples such as the selective determination of inorganic and metallorganic species of different toxicity and the redox state speciation of multiply charged ions are discussed .
	manualset3
88688	2	399663	5	NULL	NULL	0	NULL	selective determination	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , some examples such as the selective determination of inorganic and metallorganic species of different toxicity and the redox state speciation of multiply charged ions are discussed .
	manualset3
88689	3	399663	5	NULL	NULL	0	NULL	inorganic and metallorganic species	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , some examples such as the selective determination of inorganic and metallorganic species of different toxicity and the redox state speciation of multiply charged ions are discussed .
	manualset3
88690	4	399663	5	NULL	NULL	0	NULL	toxicity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , some examples such as the selective determination of inorganic and metallorganic species of different toxicity and the redox state speciation of multiply charged ions are discussed .
	manualset3
88691	5	399663	5	NULL	NULL	NULL	NULL	redox state speciation	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In particular , some examples such as the selective determination of inorganic and metallorganic species of different toxicity and the redox state speciation of multiply charged ions are discussed .
	manualset3
88692	6	399663	5	NULL	NULL	0	NULL	multiply charged ions	Ion												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , some examples such as the selective determination of inorganic and metallorganic species of different toxicity and the redox state speciation of multiply charged ions are discussed .
	manualset3
88693	1	399664	5	NULL	NULL	0	NULL	EHHST	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the EHHST facilitates the computation of an asymptotic P-value instead of an empirical P-value , using simulations .
	manualset3
88694	2	399664	5	NULL	NULL	0	NULL	computation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the EHHST facilitates the computation of an asymptotic P-value instead of an empirical P-value , using simulations .
	manualset3
88695	3	399664	5	NULL	NULL	0	NULL	asymptotic P-value	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the EHHST facilitates the computation of an asymptotic P-value instead of an empirical P-value , using simulations .
	manualset3
88696	4	399664	5	NULL	NULL	0	NULL	empirical P-value	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the EHHST facilitates the computation of an asymptotic P-value instead of an empirical P-value , using simulations .
	manualset3
88697	5	399664	5	NULL	NULL	NULL	NULL	simulations	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In particular , the EHHST facilitates the computation of an asymptotic P-value instead of an empirical P-value , using simulations .
	manualset3
88698	1	399665	5	NULL	NULL	0	NULL	engineering	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the engineering of redox relays between roGFPs and redox enzymes allows control of probe specificity and enhancement of sensitivity .
	manualset3
88699	2	399665	5	NULL	NULL	NULL	NULL	redox relays	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In particular , the engineering of redox relays between roGFPs and redox enzymes allows control of probe specificity and enhancement of sensitivity .
	manualset3
88700	3	399665	5	NULL	NULL	0	NULL	roGFPs	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the engineering of redox relays between roGFPs and redox enzymes allows control of probe specificity and enhancement of sensitivity .
	manualset3
88701	4	399665	5	NULL	NULL	0	NULL	redox enzymes	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the engineering of redox relays between roGFPs and redox enzymes allows control of probe specificity and enhancement of sensitivity .
	manualset3
88702	5	399665	5	NULL	NULL	NULL	NULL	control of probe specificity	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In particular , the engineering of redox relays between roGFPs and redox enzymes allows control of probe specificity and enhancement of sensitivity .
	manualset3
88703	6	399665	5	NULL	NULL	0	NULL	enhancement of sensitivity	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the engineering of redox relays between roGFPs and redox enzymes allows control of probe specificity and enhancement of sensitivity .
	manualset3
88704	1	399666	5	NULL	NULL	0	NULL	focus	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the focus is on the unique properties of peptide selection by I-Ag7 that reveal the preferred binding motif of diabetogenic MHC molecules and its role in display of peptides derived from islet beta cells .
	manualset3
88705	2	399666	5	NULL	NULL	0	NULL	unique properties of peptide selection	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the focus is on the unique properties of peptide selection by I-Ag7 that reveal the preferred binding motif of diabetogenic MHC molecules and its role in display of peptides derived from islet beta cells .
	manualset3
88706	3	399666	5	NULL	NULL	0	NULL	I-Ag7	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the focus is on the unique properties of peptide selection by I-Ag7 that reveal the preferred binding motif of diabetogenic MHC molecules and its role in display of peptides derived from islet beta cells .
	manualset3
88707	4	399666	5	NULL	NULL	0	NULL	preferred binding motif	PartOfProtein												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the focus is on the unique properties of peptide selection by I-Ag7 that reveal the preferred binding motif of diabetogenic MHC molecules and its role in display of peptides derived from islet beta cells .
	manualset3
88708	5	399666	5	NULL	NULL	0	NULL	diabetogenic MHC molecules	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the focus is on the unique properties of peptide selection by I-Ag7 that reveal the preferred binding motif of diabetogenic MHC molecules and its role in display of peptides derived from islet beta cells .
	manualset3
88709	6	399666	5	NULL	NULL	0	NULL	 role	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the focus is on the unique properties of peptide selection by I-Ag7 that reveal the preferred binding motif of diabetogenic MHC molecules and its role in display of peptides derived from islet beta cells .
	manualset3
88710	7	399666	5	NULL	NULL	0	NULL	peptides derived from islet beta cells	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the focus is on the unique properties of peptide selection by I-Ag7 that reveal the preferred binding motif of diabetogenic MHC molecules and its role in display of peptides derived from islet beta cells .
	manualset3
88711	1	399667	5	NULL	NULL	0	NULL	 high percentages of positive sheep sera	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the high percentages of positive sheep sera in Martinique ( 15 % ) and Montserrat ( 11 % ) should be further investigated .
	manualset3
88712	2	399667	5	NULL	NULL	0	NULL	Martinique	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the high percentages of positive sheep sera in Martinique ( 15 % ) and Montserrat ( 11 % ) should be further investigated .
	manualset3
88713	3	399667	5	NULL	NULL	0	NULL	15 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the high percentages of positive sheep sera in Martinique ( 15 % ) and Montserrat ( 11 % ) should be further investigated .
	manualset3
88714	4	399667	5	NULL	NULL	0	NULL	Montserrat	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the high percentages of positive sheep sera in Martinique ( 15 % ) and Montserrat ( 11 % ) should be further investigated .
	manualset3
88715	5	399667	5	NULL	NULL	0	NULL	11 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the high percentages of positive sheep sera in Martinique ( 15 % ) and Montserrat ( 11 % ) should be further investigated .
	manualset3
88716	1	399668	5	NULL	NULL	NULL	NULL	substitution	MolecularProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In particular , the substitution of Thr220 by serine is unique to Pr1B .
	manualset3
88717	2	399668	5	NULL	NULL	0	NULL	Thr220	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the substitution of Thr220 by serine is unique to Pr1B .
	manualset3
88718	3	399668	5	NULL	NULL	0	NULL	serine	AminoAcid												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the substitution of Thr220 by serine is unique to Pr1B .
	manualset3
88719	4	399668	5	NULL	NULL	0	NULL	Pr1B	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , the substitution of Thr220 by serine is unique to Pr1B .
	manualset3
88720	1	399669	5	NULL	NULL	0	NULL	signal-to-noise ratio	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , to increase the signal-to-noise ratio and to mitigate the adverse effect of residual image misalignments , DTI data are often smoothed before VBA with an isotropic Gaussian kernel with a full width half maximum up to 16 x 16 x 16 mm ( 3 ) .
	manualset3
88721	2	399669	5	NULL	NULL	NULL	NULL	adverse effect	Process												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In particular , to increase the signal-to-noise ratio and to mitigate the adverse effect of residual image misalignments , DTI data are often smoothed before VBA with an isotropic Gaussian kernel with a full width half maximum up to 16 x 16 x 16 mm ( 3 ) .
	manualset3
88722	3	399669	5	NULL	NULL	0	NULL	residual image misalignments	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , to increase the signal-to-noise ratio and to mitigate the adverse effect of residual image misalignments , DTI data are often smoothed before VBA with an isotropic Gaussian kernel with a full width half maximum up to 16 x 16 x 16 mm ( 3 ) .
	manualset3
88723	4	399669	5	NULL	NULL	0	NULL	DTI data	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , to increase the signal-to-noise ratio and to mitigate the adverse effect of residual image misalignments , DTI data are often smoothed before VBA with an isotropic Gaussian kernel with a full width half maximum up to 16 x 16 x 16 mm ( 3 ) .
	manualset3
88724	5	399669	5	NULL	NULL	NULL	NULL	VBA	ResearchActivity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In particular , to increase the signal-to-noise ratio and to mitigate the adverse effect of residual image misalignments , DTI data are often smoothed before VBA with an isotropic Gaussian kernel with a full width half maximum up to 16 x 16 x 16 mm ( 3 ) .
	manualset3
88725	6	399669	5	NULL	NULL	NULL	NULL	isotropic Gaussian kernel	IntellectualProduct												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In particular , to increase the signal-to-noise ratio and to mitigate the adverse effect of residual image misalignments , DTI data are often smoothed before VBA with an isotropic Gaussian kernel with a full width half maximum up to 16 x 16 x 16 mm ( 3 ) .
	manualset3
88726	7	399669	5	NULL	NULL	0	NULL	full width half maximum up to 16 x 16 x 16 mm	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In particular , to increase the signal-to-noise ratio and to mitigate the adverse effect of residual image misalignments , DTI data are often smoothed before VBA with an isotropic Gaussian kernel with a full width half maximum up to 16 x 16 x 16 mm ( 3 ) .
	manualset3
88727	1	399670	5	NULL	NULL	0	NULL	photoreceptors 	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In photoreceptors , targeted toxin expression results in increased Fasciclin II and chaoptin but not IrreC-rst immunoreactivity .
	manualset3
88728	2	399670	5	NULL	NULL	0	NULL	targeted toxin expression	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In photoreceptors , targeted toxin expression results in increased Fasciclin II and chaoptin but not IrreC-rst immunoreactivity .
	manualset3
88729	3	399670	5	NULL	NULL	0	NULL	Fasciclin II	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In photoreceptors , targeted toxin expression results in increased Fasciclin II and chaoptin but not IrreC-rst immunoreactivity .
	manualset3
88730	4	399670	5	NULL	NULL	0	NULL	chaoptin	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In photoreceptors , targeted toxin expression results in increased Fasciclin II and chaoptin but not IrreC-rst immunoreactivity .
	manualset3
88731	5	399670	5	NULL	NULL	0	NULL	IrreC-rst immunoreactivity	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In photoreceptors , targeted toxin expression results in increased Fasciclin II and chaoptin but not IrreC-rst immunoreactivity .
	manualset3
88732	1	399671	5	NULL	NULL	0	NULL	plastids	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In plastids , at least six assembly factors are required for heme attachment to the apo-forms of cytochrome f and cytochrome c ( 6 ) in the thylakoid lumen .
	manualset3
88733	2	399671	5	NULL	NULL	0	NULL	six assembly factors	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In plastids , at least six assembly factors are required for heme attachment to the apo-forms of cytochrome f and cytochrome c ( 6 ) in the thylakoid lumen .
	manualset3
88734	3	399671	5	NULL	NULL	0	NULL	heme attachment	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In plastids , at least six assembly factors are required for heme attachment to the apo-forms of cytochrome f and cytochrome c ( 6 ) in the thylakoid lumen .
	manualset3
88735	4	399671	5	NULL	NULL	0	NULL	apo-forms of cytochrome f and cytochrome c	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In plastids , at least six assembly factors are required for heme attachment to the apo-forms of cytochrome f and cytochrome c ( 6 ) in the thylakoid lumen .
	manualset3
88736	5	399671	5	NULL	NULL	0	NULL	thylakoid lumen	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In plastids , at least six assembly factors are required for heme attachment to the apo-forms of cytochrome f and cytochrome c ( 6 ) in the thylakoid lumen .
	manualset3
88737	1	399672	5	NULL	NULL	0	NULL	scenario	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In principle , the scenario is prepared to make the most of this information for the analysis of the dynamics of signalling pathways .
	manualset3
88738	2	399672	5	NULL	NULL	0	NULL	information	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	In principle , the scenario is prepared to make the most of this information for the analysis of the dynamics of signalling pathways .
	manualset3
88739	3	399672	5	NULL	NULL	0	NULL	analysis	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In principle , the scenario is prepared to make the most of this information for the analysis of the dynamics of signalling pathways .
	manualset3
88740	4	399672	5	NULL	NULL	0	NULL	dynamics of signalling pathways	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In principle , the scenario is prepared to make the most of this information for the analysis of the dynamics of signalling pathways .
	manualset3
88741	1	399673	5	NULL	NULL	0	NULL	rodents	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In rodents , a cognitive anti-aging effect of DHEA and DHEAS has been observed but it is unclear whether this effect is mediated indirectly through conversion of these steroids to estradiol .
	manualset3
88742	2	399673	5	NULL	NULL	0	NULL	cognitive anti-aging effect	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In rodents , a cognitive anti-aging effect of DHEA and DHEAS has been observed but it is unclear whether this effect is mediated indirectly through conversion of these steroids to estradiol .
	manualset3
88743	3	399673	5	NULL	NULL	0	NULL	DHEA	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In rodents , a cognitive anti-aging effect of DHEA and DHEAS has been observed but it is unclear whether this effect is mediated indirectly through conversion of these steroids to estradiol .
	manualset3
88744	4	399673	5	NULL	NULL	0	NULL	DHEAS	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In rodents , a cognitive anti-aging effect of DHEA and DHEAS has been observed but it is unclear whether this effect is mediated indirectly through conversion of these steroids to estradiol .
	manualset3
88745	5	399673	5	NULL	NULL	0	NULL	effect	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In rodents , a cognitive anti-aging effect of DHEA and DHEAS has been observed but it is unclear whether this effect is mediated indirectly through conversion of these steroids to estradiol .
	manualset3
88746	6	399673	5	NULL	NULL	0	NULL	conversion	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In rodents , a cognitive anti-aging effect of DHEA and DHEAS has been observed but it is unclear whether this effect is mediated indirectly through conversion of these steroids to estradiol .
	manualset3
88747	7	399673	5	NULL	NULL	NULL	NULL	steroids	Chemical												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In rodents , a cognitive anti-aging effect of DHEA and DHEAS has been observed but it is unclear whether this effect is mediated indirectly through conversion of these steroids to estradiol .
	manualset3
88748	8	399673	5	NULL	NULL	0	NULL	estradiol 	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In rodents , a cognitive anti-aging effect of DHEA and DHEAS has been observed but it is unclear whether this effect is mediated indirectly through conversion of these steroids to estradiol .
	manualset3
88749	1	399674	5	NULL	NULL	0	NULL	serum	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In serum , most of the 125I-IGFBP-3 was in the 150 kDa fraction , while most 125I-IGFBP-3 in milk was in the 40 kDa fraction .
	manualset3
88750	2	399674	5	NULL	NULL	0	NULL	125I-IGFBP-3	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In serum , most of the 125I-IGFBP-3 was in the 150 kDa fraction , while most 125I-IGFBP-3 in milk was in the 40 kDa fraction .
	manualset3
88751	3	399674	5	NULL	NULL	0	NULL	150 kDa fraction	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In serum , most of the 125I-IGFBP-3 was in the 150 kDa fraction , while most 125I-IGFBP-3 in milk was in the 40 kDa fraction .
	manualset3
88752	4	399674	5	NULL	NULL	0	NULL	125I-IGFBP-3	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In serum , most of the 125I-IGFBP-3 was in the 150 kDa fraction , while most 125I-IGFBP-3 in milk was in the 40 kDa fraction .
	manualset3
88753	5	399674	5	NULL	NULL	0	NULL	milk	Food												NULL		0	NULL	NULL	NULL	NULL	NULL	In serum , most of the 125I-IGFBP-3 was in the 150 kDa fraction , while most 125I-IGFBP-3 in milk was in the 40 kDa fraction .
	manualset3
88754	6	399674	5	NULL	NULL	0	NULL	40 kDa fraction	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In serum , most of the 125I-IGFBP-3 was in the 150 kDa fraction , while most 125I-IGFBP-3 in milk was in the 40 kDa fraction .
	manualset3
88755	1	399675	5	NULL	NULL	0	NULL	seven ( Group I )	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In seven ( Group I ) predominantly unilateral disease was discovered by angiography ( renal-artery stenosis in six and hydronephrosis in one ) ; in the remaining seven ( Group II ) no rennal-artery abnormality was found .
	manualset3
88756	2	399675	5	NULL	NULL	0	NULL	unilateral disease	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In seven ( Group I ) predominantly unilateral disease was discovered by angiography ( renal-artery stenosis in six and hydronephrosis in one ) ; in the remaining seven ( Group II ) no rennal-artery abnormality was found .
	manualset3
88757	3	399675	5	NULL	NULL	0	NULL	angiography	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In seven ( Group I ) predominantly unilateral disease was discovered by angiography ( renal-artery stenosis in six and hydronephrosis in one ) ; in the remaining seven ( Group II ) no rennal-artery abnormality was found .
	manualset3
88758	4	399675	5	NULL	NULL	0	NULL	renal-artery stenosis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In seven ( Group I ) predominantly unilateral disease was discovered by angiography ( renal-artery stenosis in six and hydronephrosis in one ) ; in the remaining seven ( Group II ) no rennal-artery abnormality was found .
	manualset3
88759	5	399675	5	NULL	NULL	0	NULL	hydronephrosis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In seven ( Group I ) predominantly unilateral disease was discovered by angiography ( renal-artery stenosis in six and hydronephrosis in one ) ; in the remaining seven ( Group II ) no rennal-artery abnormality was found .
	manualset3
88760	6	399675	5	NULL	NULL	0	NULL	seven ( Group II ) 	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In seven ( Group I ) predominantly unilateral disease was discovered by angiography ( renal-artery stenosis in six and hydronephrosis in one ) ; in the remaining seven ( Group II ) no rennal-artery abnormality was found .
	manualset3
88761	7	399675	5	NULL	NULL	0	NULL	rennal-artery abnormality	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In seven ( Group I ) predominantly unilateral disease was discovered by angiography ( renal-artery stenosis in six and hydronephrosis in one ) ; in the remaining seven ( Group II ) no rennal-artery abnormality was found .
	manualset3
88762	1	399676	5	NULL	NULL	0	NULL	Treatment	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	( Treatment of acute lymphoblastic leukemia in adults using higher doses of cytostatic agents ) .
	manualset3
88763	2	399676	5	NULL	NULL	0	NULL	acute lymphoblastic leukemia	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	( Treatment of acute lymphoblastic leukemia in adults using higher doses of cytostatic agents ) .
	manualset3
88764	3	399676	5	NULL	NULL	0	NULL	adults	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	( Treatment of acute lymphoblastic leukemia in adults using higher doses of cytostatic agents ) .
	manualset3
88765	4	399676	5	NULL	NULL	0	NULL	higher doses	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	( Treatment of acute lymphoblastic leukemia in adults using higher doses of cytostatic agents ) .
	manualset3
88766	5	399676	5	NULL	NULL	0	NULL	cytostatic agents	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	( Treatment of acute lymphoblastic leukemia in adults using higher doses of cytostatic agents ) .
	manualset3
88767	1	399677	5	NULL	NULL	0	NULL	study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In short , this study showed that syndromes of HQD and HYD both displayed disturbed function of the vegetative nervous system , and their types and severities were correlated with the difference of Syndromes .
	manualset3
88768	2	399677	5	NULL	NULL	NULL	NULL	syndrome of HQD	Disease												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In short , this study showed that syndromes of HQD and HYD both displayed disturbed function of the vegetative nervous system , and their types and severities were correlated with the difference of Syndromes .
	manualset3
88769	3	399677	5	NULL	NULL	0	NULL	disturbed function	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In short , this study showed that syndromes of HQD and HYD both displayed disturbed function of the vegetative nervous system , and their types and severities were correlated with the difference of Syndromes .
	manualset3
88770	4	399677	5	NULL	NULL	NULL	NULL	vegetative nervous system	BodyPart												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In short , this study showed that syndromes of HQD and HYD both displayed disturbed function of the vegetative nervous system , and their types and severities were correlated with the difference of Syndromes .
	manualset3
88771	5	399677	5	NULL	NULL	0	NULL	types	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In short , this study showed that syndromes of HQD and HYD both displayed disturbed function of the vegetative nervous system , and their types and severities were correlated with the difference of Syndromes .
	manualset3
88772	6	399677	5	NULL	NULL	0	NULL	severities	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In short , this study showed that syndromes of HQD and HYD both displayed disturbed function of the vegetative nervous system , and their types and severities were correlated with the difference of Syndromes .
	manualset3
88773	7	399677	5	NULL	NULL	0	NULL	difference of Syndromes	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In short , this study showed that syndromes of HQD and HYD both displayed disturbed function of the vegetative nervous system , and their types and severities were correlated with the difference of Syndromes .
	manualset3
91211	8	399677	5	NULL	NULL	0	NULL	syndrome of HYD	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In short , this study showed that syndromes of HQD and HYD both displayed disturbed function of the vegetative nervous system , and their types and severities were correlated with the difference of Syndromes .
	manualset3
88774	1	399678	5	NULL	NULL	0	NULL	smokers ( n = 16 )	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In smokers ( n = 16 ) , the number of exfoliated cervicovaginal epithelial cells and leukocyte ascorbic acid levels was significantly higher ( p less than 0.01 , p less than 0.05 , respectively ) compared with nonsmokers ( n = 30 ) .
	manualset3
88775	2	399678	5	NULL	NULL	0	NULL	number	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In smokers ( n = 16 ) , the number of exfoliated cervicovaginal epithelial cells and leukocyte ascorbic acid levels was significantly higher ( p less than 0.01 , p less than 0.05 , respectively ) compared with nonsmokers ( n = 30 ) .
	manualset3
88776	3	399678	5	NULL	NULL	0	NULL	exfoliated cervicovaginal epithelial cells	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In smokers ( n = 16 ) , the number of exfoliated cervicovaginal epithelial cells and leukocyte ascorbic acid levels was significantly higher ( p less than 0.01 , p less than 0.05 , respectively ) compared with nonsmokers ( n = 30 ) .
	manualset3
88777	4	399678	5	NULL	NULL	0	NULL	leukocyte ascorbic acid levels	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In smokers ( n = 16 ) , the number of exfoliated cervicovaginal epithelial cells and leukocyte ascorbic acid levels was significantly higher ( p less than 0.01 , p less than 0.05 , respectively ) compared with nonsmokers ( n = 30 ) .
	manualset3
88778	5	399678	5	NULL	NULL	0	NULL	p less than 0.01	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In smokers ( n = 16 ) , the number of exfoliated cervicovaginal epithelial cells and leukocyte ascorbic acid levels was significantly higher ( p less than 0.01 , p less than 0.05 , respectively ) compared with nonsmokers ( n = 30 ) .
	manualset3
88779	6	399678	5	NULL	NULL	0	NULL	p less than 0.05	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In smokers ( n = 16 ) , the number of exfoliated cervicovaginal epithelial cells and leukocyte ascorbic acid levels was significantly higher ( p less than 0.01 , p less than 0.05 , respectively ) compared with nonsmokers ( n = 30 ) .
	manualset3
88780	7	399678	5	NULL	NULL	0	NULL	nonsmokers ( n = 30 )	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In smokers ( n = 16 ) , the number of exfoliated cervicovaginal epithelial cells and leukocyte ascorbic acid levels was significantly higher ( p less than 0.01 , p less than 0.05 , respectively ) compared with nonsmokers ( n = 30 ) .
	manualset3
88781	1	399679	5	NULL	NULL	0	NULL	smokers	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In smokers , sex influences the relationship between emphysema and clinical features .
	manualset3
88782	2	399679	5	NULL	NULL	NULL	NULL	sex	NamedEntity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In smokers , sex influences the relationship between emphysema and clinical features .
	manualset3
88783	3	399679	5	NULL	NULL	0	NULL	relationship	Relationship												NULL		0	NULL	NULL	NULL	NULL	NULL	In smokers , sex influences the relationship between emphysema and clinical features .
	manualset3
88786	4	399679	5	NULL	NULL	0	NULL	emphysema	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In smokers , sex influences the relationship between emphysema and clinical features .
	manualset3
88787	5	399679	5	NULL	NULL	0	NULL	clinical features	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In smokers , sex influences the relationship between emphysema and clinical features .
	manualset3
88789	1	399680	5	NULL	NULL	0	NULL	fermentation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In subsequent , fermentation with hydrolysate , maximal ethanol yield was attained after 24h with 0.368 % of sulfuric acid .
	manualset3
88790	2	399680	5	NULL	NULL	0	NULL	hydrolysate	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In subsequent , fermentation with hydrolysate , maximal ethanol yield was attained after 24h with 0.368 % of sulfuric acid .
	manualset3
88791	3	399680	5	NULL	NULL	0	NULL	maximal ethanol yield	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In subsequent , fermentation with hydrolysate , maximal ethanol yield was attained after 24h with 0.368 % of sulfuric acid .
	manualset3
88792	4	399680	5	NULL	NULL	0	NULL	 after 24h	Duration												NULL		0	NULL	NULL	NULL	NULL	NULL	In subsequent , fermentation with hydrolysate , maximal ethanol yield was attained after 24h with 0.368 % of sulfuric acid .
	manualset3
88793	5	399680	5	NULL	NULL	0	NULL	0.368 %	Measurement												NULL		0	NULL	NULL	NULL	NULL	NULL	In subsequent , fermentation with hydrolysate , maximal ethanol yield was attained after 24h with 0.368 % of sulfuric acid .
	manualset3
88794	6	399680	5	NULL	NULL	0	NULL	sulfuric acid	NonProteinOrNucleicAcidChemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In subsequent , fermentation with hydrolysate , maximal ethanol yield was attained after 24h with 0.368 % of sulfuric acid .
	manualset3
88798	1	399681	5	NULL	NULL	NULL	NULL	review	PublishedSourceOfInformation												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In sum , this review suggests that QSOX enzymes play a significant role in oxidative folding of a large variety of proteins in a wide range of multicellular organisms .
	manualset3
88799	2	399681	5	NULL	NULL	NULL	NULL	QSOX enzymes	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In sum , this review suggests that QSOX enzymes play a significant role in oxidative folding of a large variety of proteins in a wide range of multicellular organisms .
	manualset3
88801	3	399681	5	NULL	NULL	NULL	NULL	significant role	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In sum , this review suggests that QSOX enzymes play a significant role in oxidative folding of a large variety of proteins in a wide range of multicellular organisms .
	manualset3
88802	4	399681	5	NULL	NULL	NULL	NULL	oxidative folding of a large variety of proteins	BiologicalProcess												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In sum , this review suggests that QSOX enzymes play a significant role in oxidative folding of a large variety of proteins in a wide range of multicellular organisms .
	manualset3
88803	5	399681	5	NULL	NULL	NULL	NULL	wide range	Quantity												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In sum , this review suggests that QSOX enzymes play a significant role in oxidative folding of a large variety of proteins in a wide range of multicellular organisms .
	manualset3
88804	6	399681	5	NULL	NULL	NULL	NULL	multicellular organisms	Organism												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In sum , this review suggests that QSOX enzymes play a significant role in oxidative folding of a large variety of proteins in a wide range of multicellular organisms .
	manualset3
88806	1	399682	5	NULL	NULL	0	NULL	140 positive smears	LaboratoryExperimentalFactor												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , 140 positive smears were detected : 57 cases showed changes due to HPV , 63 LSIL , 15 HSIL , and 5 carcinomas .
	manualset3
88807	2	399682	5	NULL	NULL	0	NULL	57 cases	PersonGroup												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , 140 positive smears were detected : 57 cases showed changes due to HPV , 63 LSIL , 15 HSIL , and 5 carcinomas .
	manualset3
88808	3	399682	5	NULL	NULL	0	NULL	HPV	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , 140 positive smears were detected : 57 cases showed changes due to HPV , 63 LSIL , 15 HSIL , and 5 carcinomas .
	manualset3
88809	4	399682	5	NULL	NULL	0	NULL	63 LSIL	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , 140 positive smears were detected : 57 cases showed changes due to HPV , 63 LSIL , 15 HSIL , and 5 carcinomas .
	manualset3
88810	5	399682	5	NULL	NULL	0	NULL	15 HSIL	NamedEntity												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , 140 positive smears were detected : 57 cases showed changes due to HPV , 63 LSIL , 15 HSIL , and 5 carcinomas .
	manualset3
88811	6	399682	5	NULL	NULL	0	NULL	5 carcinomas	Disease												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , 140 positive smears were detected : 57 cases showed changes due to HPV , 63 LSIL , 15 HSIL , and 5 carcinomas .
	manualset3
88812	1	399683	5	NULL	NULL	0	NULL	cold-storage preservation with UW	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , cold-storage preservation with UW reduced endothelium-independent vascular relaxation by mechanisms other than competition with NO ; this requires further evaluation .
	manualset3
88813	2	399683	5	NULL	NULL	0	NULL	endothelium-independent vascular relaxation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , cold-storage preservation with UW reduced endothelium-independent vascular relaxation by mechanisms other than competition with NO ; this requires further evaluation .
	manualset3
88814	3	399683	5	NULL	NULL	0	NULL	mechanisms	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , cold-storage preservation with UW reduced endothelium-independent vascular relaxation by mechanisms other than competition with NO ; this requires further evaluation .
	manualset3
88815	4	399683	5	NULL	NULL	0	NULL	competition with NO	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , cold-storage preservation with UW reduced endothelium-independent vascular relaxation by mechanisms other than competition with NO ; this requires further evaluation .
	manualset3
88816	5	399683	5	NULL	NULL	0	NULL	evaluation	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , cold-storage preservation with UW reduced endothelium-independent vascular relaxation by mechanisms other than competition with NO ; this requires further evaluation .
	manualset3
88817	1	399684	5	NULL	NULL	0	NULL	distinct expression patterns	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , distinct expression patterns were shown for PKC isoenzymes alpha , beta I , beta II , delta , and epsilon in the mouse kidney .
	manualset3
88818	2	399684	5	NULL	NULL	NULL	NULL	PKC isoenzyme alpha	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In summary , distinct expression patterns were shown for PKC isoenzymes alpha , beta I , beta II , delta , and epsilon in the mouse kidney .
	manualset3
88819	3	399684	5	NULL	NULL	NULL	NULL	PKC isoenzyme beta I	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In summary , distinct expression patterns were shown for PKC isoenzymes alpha , beta I , beta II , delta , and epsilon in the mouse kidney .
	manualset3
88820	4	399684	5	NULL	NULL	NULL	NULL	PKC isoenzyme beta II	Protein												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In summary , distinct expression patterns were shown for PKC isoenzymes alpha , beta I , beta II , delta , and epsilon in the mouse kidney .
	manualset3
88821	5	399684	5	NULL	NULL	0	NULL	PKC isoenzyme delta	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , distinct expression patterns were shown for PKC isoenzymes alpha , beta I , beta II , delta , and epsilon in the mouse kidney .
	manualset3
88822	6	399684	5	NULL	NULL	0	NULL	PKC isoenzyme epsilon	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , distinct expression patterns were shown for PKC isoenzymes alpha , beta I , beta II , delta , and epsilon in the mouse kidney .
	manualset3
88823	7	399684	5	NULL	NULL	0	NULL	mouse kidney	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , distinct expression patterns were shown for PKC isoenzymes alpha , beta I , beta II , delta , and epsilon in the mouse kidney .
	manualset3
88824	1	399685	5	NULL	NULL	0	NULL	hepatic lesions	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , most hepatic lesions can be correctly characterized by supplemental use of enhanced sonography ; practitioners should nevertheless be aware of atypical phenomena to be able to critically evaluate the findings .
	manualset3
88825	2	399685	5	NULL	NULL	NULL	NULL	supplemental use of enhanced sonography	MedicalProcedure												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In summary , most hepatic lesions can be correctly characterized by supplemental use of enhanced sonography ; practitioners should nevertheless be aware of atypical phenomena to be able to critically evaluate the findings .
	manualset3
88826	3	399685	5	NULL	NULL	NULL	NULL	practitioners	PersonGroup												NULL		NULL	NULL	NULL	NULL	NULL	NULL	In summary , most hepatic lesions can be correctly characterized by supplemental use of enhanced sonography ; practitioners should nevertheless be aware of atypical phenomena to be able to critically evaluate the findings .
	manualset3
88827	4	399685	5	NULL	NULL	0	NULL	atypical phenomena	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , most hepatic lesions can be correctly characterized by supplemental use of enhanced sonography ; practitioners should nevertheless be aware of atypical phenomena to be able to critically evaluate the findings .
	manualset3
88828	5	399685	5	NULL	NULL	0	NULL	critically evaluate the findings	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , most hepatic lesions can be correctly characterized by supplemental use of enhanced sonography ; practitioners should nevertheless be aware of atypical phenomena to be able to critically evaluate the findings .
	manualset3
88829	1	399686	5	NULL	NULL	0	NULL	results	PublishedSourceOfInformation												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , our results suggest that the UL78 protein of HCMV traffics between the cell surface and cytoplasm , from where it might be recycled via early endosomes .
	manualset3
88830	2	399686	5	NULL	NULL	0	NULL	UL78 protein	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , our results suggest that the UL78 protein of HCMV traffics between the cell surface and cytoplasm , from where it might be recycled via early endosomes .
	manualset3
88831	3	399686	5	NULL	NULL	0	NULL	HCMV	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , our results suggest that the UL78 protein of HCMV traffics between the cell surface and cytoplasm , from where it might be recycled via early endosomes .
	manualset3
88832	4	399686	5	NULL	NULL	0	NULL	cell surface	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , our results suggest that the UL78 protein of HCMV traffics between the cell surface and cytoplasm , from where it might be recycled via early endosomes .
	manualset3
88833	5	399686	5	NULL	NULL	0	NULL	cytoplasm	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , our results suggest that the UL78 protein of HCMV traffics between the cell surface and cytoplasm , from where it might be recycled via early endosomes .
	manualset3
88834	6	399686	5	NULL	NULL	0	NULL	early endosomes	CellComponent												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , our results suggest that the UL78 protein of HCMV traffics between the cell surface and cytoplasm , from where it might be recycled via early endosomes .
	manualset3
88835	1	399687	5	NULL	NULL	0	NULL	study	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , our study shows that 5-HT is a potent regulator of human dendritic cell function , and that targeting serotoninergic receptors might be a promising approach for the treatment of inflammatory disorders .
	manualset3
88836	2	399687	5	NULL	NULL	0	NULL	5-HT	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , our study shows that 5-HT is a potent regulator of human dendritic cell function , and that targeting serotoninergic receptors might be a promising approach for the treatment of inflammatory disorders .
	manualset3
88839	3	399687	5	NULL	NULL	0	NULL	potent regulator	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , our study shows that 5-HT is a potent regulator of human dendritic cell function , and that targeting serotoninergic receptors might be a promising approach for the treatment of inflammatory disorders .
	manualset3
88840	4	399687	5	NULL	NULL	0	NULL	human dendritic cell function	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , our study shows that 5-HT is a potent regulator of human dendritic cell function , and that targeting serotoninergic receptors might be a promising approach for the treatment of inflammatory disorders .
	manualset3
88841	5	399687	5	NULL	NULL	0	NULL	serotoninergic receptors	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , our study shows that 5-HT is a potent regulator of human dendritic cell function , and that targeting serotoninergic receptors might be a promising approach for the treatment of inflammatory disorders .
	manualset3
88842	6	399687	5	NULL	NULL	0	NULL	promising approach	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , our study shows that 5-HT is a potent regulator of human dendritic cell function , and that targeting serotoninergic receptors might be a promising approach for the treatment of inflammatory disorders .
	manualset3
88843	7	399687	5	NULL	NULL	0	NULL	treatment of inflammatory disorders	MedicalProcedure												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , our study shows that 5-HT is a potent regulator of human dendritic cell function , and that targeting serotoninergic receptors might be a promising approach for the treatment of inflammatory disorders .
	manualset3
88844	1	399688	5	NULL	NULL	0	NULL	 second and third trimester pregnancy	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , second and third trimester pregnancy is associated with a normal circadian TSH rhythm .
	manualset3
88845	2	399688	5	NULL	NULL	0	NULL	normal circadian TSH rhythm	MolecularProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , second and third trimester pregnancy is associated with a normal circadian TSH rhythm .
	manualset3
88848	1	399689	5	NULL	NULL	0	NULL	supplemental i.v. crystalloids	Chemical												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , supplemental i.v. crystalloids were associated with a lower incidence of several PONV outcomes .
	manualset3
88851	2	399689	5	NULL	NULL	0	NULL	lower incidence of several PONV outcomes	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , supplemental i.v. crystalloids were associated with a lower incidence of several PONV outcomes .
	manualset3
88853	1	399690	5	NULL	NULL	0	NULL	GICA TP-IgM	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , the characteristics of GICA TP-IgM correspond to that of FTA-Abs TP-IgM ; this can be used as a serologic marker for the relapse and infection of syphilis in place of the conventional FTA-Abs IgM test .
	manualset3
88854	2	399690	5	NULL	NULL	0	NULL	FTA-Abs TP-IgM	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , the characteristics of GICA TP-IgM correspond to that of FTA-Abs TP-IgM ; this can be used as a serologic marker for the relapse and infection of syphilis in place of the conventional FTA-Abs IgM test .
	manualset3
88855	3	399690	5	NULL	NULL	0	NULL	serologic marker	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , the characteristics of GICA TP-IgM correspond to that of FTA-Abs TP-IgM ; this can be used as a serologic marker for the relapse and infection of syphilis in place of the conventional FTA-Abs IgM test .
	manualset3
88857	4	399690	5	NULL	NULL	0	NULL	relapse and infection of syphilis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , the characteristics of GICA TP-IgM correspond to that of FTA-Abs TP-IgM ; this can be used as a serologic marker for the relapse and infection of syphilis in place of the conventional FTA-Abs IgM test .
	manualset3
88858	5	399690	5	NULL	NULL	0	NULL	conventional FTA-Abs IgM test 	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , the characteristics of GICA TP-IgM correspond to that of FTA-Abs TP-IgM ; this can be used as a serologic marker for the relapse and infection of syphilis in place of the conventional FTA-Abs IgM test .
	manualset3
88859	1	399691	5	NULL	NULL	0	NULL	loss of 84 % of bulbospinal adrenergic neurones	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , the loss of 84 % of bulbospinal adrenergic neurones does not alter the ability of RVLM to maintain SNA and arterial pressure at rest in anaesthetized rats , but this loss reduces the sympathoexcitatory and pressor responses evoked by RVLM stimulation .
	manualset3
88860	2	399691	5	NULL	NULL	0	NULL	ability	Process												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , the loss of 84 % of bulbospinal adrenergic neurones does not alter the ability of RVLM to maintain SNA and arterial pressure at rest in anaesthetized rats , but this loss reduces the sympathoexcitatory and pressor responses evoked by RVLM stimulation .
	manualset3
88869	3	399691	5	NULL	NULL	0	NULL	RVLM	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , the loss of 84 % of bulbospinal adrenergic neurones does not alter the ability of RVLM to maintain SNA and arterial pressure at rest in anaesthetized rats , but this loss reduces the sympathoexcitatory and pressor responses evoked by RVLM stimulation .
	manualset3
88870	4	399691	5	NULL	NULL	0	NULL	SNA	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , the loss of 84 % of bulbospinal adrenergic neurones does not alter the ability of RVLM to maintain SNA and arterial pressure at rest in anaesthetized rats , but this loss reduces the sympathoexcitatory and pressor responses evoked by RVLM stimulation .
	manualset3
88871	5	399691	5	NULL	NULL	0	NULL	arterial pressure	Quantity												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , the loss of 84 % of bulbospinal adrenergic neurones does not alter the ability of RVLM to maintain SNA and arterial pressure at rest in anaesthetized rats , but this loss reduces the sympathoexcitatory and pressor responses evoked by RVLM stimulation .
	manualset3
88874	6	399691	5	NULL	NULL	0	NULL	anaesthetized rats	Organism												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , the loss of 84 % of bulbospinal adrenergic neurones does not alter the ability of RVLM to maintain SNA and arterial pressure at rest in anaesthetized rats , but this loss reduces the sympathoexcitatory and pressor responses evoked by RVLM stimulation .
	manualset3
88877	7	399691	5	NULL	NULL	0	NULL	sympathoexcitatory and pressor responses	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , the loss of 84 % of bulbospinal adrenergic neurones does not alter the ability of RVLM to maintain SNA and arterial pressure at rest in anaesthetized rats , but this loss reduces the sympathoexcitatory and pressor responses evoked by RVLM stimulation .
	manualset3
88878	8	399691	5	NULL	NULL	0	NULL	RVLM stimulation	BiologicalProcess												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , the loss of 84 % of bulbospinal adrenergic neurones does not alter the ability of RVLM to maintain SNA and arterial pressure at rest in anaesthetized rats , but this loss reduces the sympathoexcitatory and pressor responses evoked by RVLM stimulation .
	manualset3
88879	1	399692	5	NULL	NULL	0	NULL	prevalence and incidence of upper urinary tract calculi	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , the prevalence and incidence of upper urinary tract calculi in the Tajima area were considerably higher than those in the nationwide survey on urolithiasis in Japan conducted in 1985 .
	manualset3
88880	2	399692	5	NULL	NULL	0	NULL	Tajima area	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , the prevalence and incidence of upper urinary tract calculi in the Tajima area were considerably higher than those in the nationwide survey on urolithiasis in Japan conducted in 1985 .
	manualset3
88886	3	399692	5	NULL	NULL	0	NULL	nationwide survey	ResearchActivity												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , the prevalence and incidence of upper urinary tract calculi in the Tajima area were considerably higher than those in the nationwide survey on urolithiasis in Japan conducted in 1985 .
	manualset3
88887	4	399692	5	NULL	NULL	0	NULL	urolithiasis	MedicalFinding												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , the prevalence and incidence of upper urinary tract calculi in the Tajima area were considerably higher than those in the nationwide survey on urolithiasis in Japan conducted in 1985 .
	manualset3
88888	5	399692	5	NULL	NULL	0	NULL	Japan	ProperNamedGeographicalLocation												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , the prevalence and incidence of upper urinary tract calculi in the Tajima area were considerably higher than those in the nationwide survey on urolithiasis in Japan conducted in 1985 .
	manualset3
88889	6	399692	5	NULL	NULL	0	NULL	1985	TimePoint												NULL		0	NULL	NULL	NULL	NULL	NULL	In summary , the prevalence and incidence of upper urinary tract calculi in the Tajima area were considerably higher than those in the nationwide survey on urolithiasis in Japan conducted in 1985 .
	manualset3
88890	1	399693	5	NULL	NULL	0	NULL	testis	BodyPart												NULL		0	NULL	NULL	NULL	NULL	NULL	In testis , IMP1 and IMP3 were found mainly in the spermatogonia , whereas IMP2 was expressed in the immature Leydig cells .
	manualset3
88891	2	399693	5	NULL	NULL	0	NULL	IMP1	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In testis , IMP1 and IMP3 were found mainly in the spermatogonia , whereas IMP2 was expressed in the immature Leydig cells .
	manualset3
88892	3	399693	5	NULL	NULL	0	NULL	IMP3	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In testis , IMP1 and IMP3 were found mainly in the spermatogonia , whereas IMP2 was expressed in the immature Leydig cells .
	manualset3
88893	4	399693	5	NULL	NULL	0	NULL	spermatogonia	Cell												NULL		0	NULL	NULL	NULL	NULL	NULL	In testis , IMP1 and IMP3 were found mainly in the spermatogonia , whereas IMP2 was expressed in the immature Leydig cells .
	manualset3
88894	5	399693	5	NULL	NULL	0	NULL	IMP2	Protein												NULL		0	NULL	NULL	NULL	NULL	NULL	In testis , IMP1 and IMP3 were found mainly in the spermatogonia , whereas IMP2 was expressed in the immature Leydig cells .
	manualset3
88895	6	399693	5	NULL	NULL	0	NULL	immature Leydig cells	Cell				